The Pediatric and Adolescent Knee

1600 John F. Kennedy Boulevard, Suite 1800 Philadelphia, PA 19103-2899

THE PEDIATRIC AND ADOLESCENT KNEE

ISBN-13: 978-0-7216-0331-5 ISBN-10: 0-7216-0331-9

Copyright © 2006, Elsevier Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Permissions may be sought directly from Elsevier’s Health Sciences Rights Department in Philadelphia, PA, USA: phone: (+1) 215 239 3804, fax: (+1) 215 239 3805, e-mail: [email protected]. You may also complete your request online via the Elsevier homepage (http://www.elsevier.com), by selecting “Customer Support” and then “Obtaining Permissions.”

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

First Edition Library of Congress Cataloging-in-Publication Data The pediatric and adolescent knee / Lyle J. Micheli, Mininder S. Kocher [editors].–1st ed. p. cm. ISBN 0-7216-0331-9 1. Knee. 2. Knee–Diseases. 3. Knee–Care and hygiene. 4. Pediatric orthopedics. I. Micheli, Lyle J., 1940II. Kocher, Mininder S. RD 723.3.C43P42 2006 617.5182–dc22

2006040515

Acquisitions Editor: Elyse O’Grady Developmental Editor: Boris Ginsburgs Project Manager: David Saltzberg

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Preface Lyle J. Micheli, MD and Mininder S. Kocher, MD

In the preface to his 1979 textbook, The Injured Adolescent Knee, Dr. Jack Kennedy stated that “the adolescent knee is unlike the adult knee” and that he was “staggered” by the incidence of knee injuries in adolescent athletes.* A lot has changed for the pediatric and adolescent knee since 1979. Advances in technology such as arthroscopic surgery, magnetic resonance imaging, and minimally invasive repair techniques have allowed for greater recognition and improved management of knee injuries. Increased awareness that pediatric and adolescent athletes can sustain major knee injuries has resulted in earlier diagnosis and better management of these injuries. Old adages like “children don’t get serious knee injuries” and “just put it in a cast and it will heal in kids” have been dispelled. Increased participation in organized sports at younger ages and at higher competitive levels have resulted in dramatic increases in the incidence and severity of knee injuries in pediatric athletes. These injuries and their treatments will have important long-term ramifications in terms of risk of degenerative arthritis and disability later in life. Youth sports have also changed. Youth sports have become a big business with scouts at middle school games and adolescent athletes becoming professionals after high school. Pediatric and adolescent athletes can face an enormous amount of pressure to succeed from themselves, their peers, their coaches, and their parents. The negative effects of youth sports can be seen in psychological burnout, eating disorders, and the increasing use of ergogenic aids. However, the beneficial effects of youth sports are overwhelming. Physically, children have improved health with lower rates of obesity, heart disease, osteoporosis, and diabetes. Psychosocially, adolescent athletes have improved self-esteem, lower rates of recreational drug use, and lower rates of teen pregnancy. In this textbook, we have striven to give a comprehensive and useful overview of injuries and disorders of the pediatric and adolescent knee. The authors are experts in diverse fields, including pediatrics, orthopaedics, sports *

Kennedy, JC (ed): The Injured Adolescent Knee. Baltimore: The Williams and Wilkins Company, 1979.

medicine, exercise physiology, nutrition, rehabilitation, radiology, and anesthesia. General issues are presented, such as epidemiology of injuries, physical examination, anatomy, growth, and anesthesia. Issues of special interest in the pediatric and adolescent athlete, such as strength training, sports psychology, primary care issues, performance enhancing drugs, and the adolescent female athlete, are also highlighted. Specific injuries are thoroughly discussed, including patellofemoral dysfunction, extensor mechanism disorders, fractures, meniscal disorders, chondral injuries, osteochondritis dissecans, anterior cruciate ligament (ACL) and other ligament injuries, and tibial spine fracture. In addition, knee disorders, such as congenital knee deformities, angular deformities, infection, arthritis, and complex regional pain syndrome, are overviewed. Both surgical approaches and nonoperative approaches to management are emphasized. Technical notes are provided to pull out and emphasize how to do a specific technique. We would like to thank the authors for their excellent chapters and for providing their insight and pearls. We would like to thank our colleagues in the Division of Sports Medicine and the Department of Orthopaedic Surgery at Children’s Hospital. Most importantly, we would like to thank our pediatric and adolescent patients and their families, who have given us their trust in the management of their injuries. Dr. Kocher would like to specifically thank his guru, Dr. John Feagin, for inspiring and encouraging him to take on this project. He would like to thank his mentors, Drs. David Sabiston, Jr., John Hall, James Kasser, Richard Steadman, and Lyle Micheli, for their continued support and for being exemplary role models. Most importantly, he would like to thank his wife, Mich, and children, Sophia, Izzy, Calvin, and Ava, for their understanding and patience during this project. Dr. Micheli would like to thank his many mentors, teachers, colleagues, and fellows, each of whom has helped him to better grasp the special challenges of the child athlete. In addition, special thanks are due to all of the patients and parents who have patiently participated in this process. As always, his wife Anne has loyally supported

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the often excessive demands of combining an active clinical practice with academic and publishing efforts. We agree with Dr. Kennedy that the pediatric and adolescent knee is not a little adult knee. They are very differ-

ent in terms of growth, laxity, physiology, and anatomy. We hope that this book provides a comprehensive and useful framework for treating knee injuries in your young athletes and patients.

Foreword John A. Feagin, MD

Many years ago, The Injured Adolescent Knee was by edited by Dr. J.C. Kennedy* with contributions by Drs. Fowler, James, Larson, Roberts, and Salter—all giants of their generation and doctors who cared for adolescent patients and had visions for the betterment of the care of the adolescent knee. They chose a meaningful niche for making contributions to orthopedic literature. The Injured Adolescent Knee became a mainstay of my library and influenced my thought processes. The treatment of the adolescent knee is a discipline within the discipline of knee care. The adolescent and his or her knee deserve a special page in history and a special place in daily practice. Adolescents’ knees are different from those of adults. Also, adolescents’ parents, families, and coaches are involved and concerned. The future for the adolescent is forthcoming. The responsibility of all involved is ever present. Adolescents need all the expertise and advocacy that can be marshaled. We need this new book, The Pediatric and Adolescent Knee. This book prepares the physician for the responsibility of caring for the pediatric patient, the adolescent patient, and those concerned individuals who surround the patient. I recommend that you embrace the concepts contained in this book. Respect the pediatric and adolescent knee as a unique entity. Respect the child and the adolescent, the parents, the coaches and trainers, and the patient’s peers.

*

Kennedy, JC (ed): The Injured Adolescent Knee. Baltimore: The Williams and Wilkins Company, 1979.

They have entrusted you with the young person’s knee; this knee needs to function for many years. Your skill and knowledge are critical. They need to know and believe that you are their advocate—not just the surgeon. The concepts presented in the book are appropriate and useful. The body of knowledge is specialized. The contributors to The Pediatric and Adolescent Knee have brought the pediatric and adolescent knee into focus. You will use this knowledge and focus daily. The contributors to the book are outstanding in their fields. Their contributions will enrich your knowledge and expertise as you absorb the wisdom emanating from each chapter. To you, I recommend this book, The Pediatric and Adolescent Knee. The editors, Dr. Lyle J. Micheli and Dr. Mininder S. Kocher, are to be commended for recognizing the hiatus that had developed in our knowledge and filling it so admirably. Were Dr. J.C. Kennedy still with us, he would applaud the efforts of Drs. Kocher and Micheli and the addition that the contents of this book bring to our armamentarium. I know Dr. Larson will be proud of this extension of his original work. Thank you for your interest in The Pediatric and Adolescent Knee at this point in your career. The book, the rest of your practice—the rest of your journey—will benefit from your interest in the pediatric and adolescent knee. Godspeed.

Contributors

John A. Abraham, MD Resident Department of Orthopaedic Surgery Harvard Combined Orthopedic Residency Program; Department of Orthopaedic Surgery Children’s Hospital Boston Boston, Massachusetts Paolo Aglietti, MD Professor First Orthopaedic Clinic University of Florence Florence, Italy Jay C. Albright, MD Director of Pediatric Sports Medicine Medical Education Faculty Arnold Palmer Children’s Hospital; Pediatric Orthopaedic Surgery Orlando Regional Health Systems Orlando, Florida Allen F. Anderson, MD Tennessee Orthopaedic Alliance; Director Lipscomb Foundation for Education and Research Nashville, Tennessee Peter J. Apel, BA Stritch School of Medicine Loyola University, Chicago Maywood, Illinois Nigel M. Azer, MD Surgeon-in-Chief Washington Orthopaedic Center Washington, DC

Luke H. Balsamo, MD Bone and Joint Sports Medicine Institute Portsmouth Naval Hospital Portsmouth, Virginia David B. Bendor, PsyD (candidate) Postdoctoral Fellow Human Relations Service Wellesley, Massachusetts Charles B. Berde, MD, PhD Professor Department of Anaesthesia and Pediatrics Harvard Medical School; Chief Division of Pain Medicine Department of Anesthesiology, Perioperative and Pain Medicine Children’s Hospital Boston Boston, Massachusetts Treg D. Brown, MD Assistant Clinical Professor Department of Orthopaedic Surgery Tulane University New Orleans, Louisiana; Orthopaedic Surgeon Southern Illinois Orthopaedic Center Southern Orthopaedic Associates Herrin, Illinois Bernard Cahill, MD Past President (retired) American Orthopaedic Society of Sports Medicine Peoria, Illinois W. Dilworth Cannon, MD Professor Department of Orthopedic Surgery University of California, San Francisco San Francisco, California

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Contributors

Michelina Cassella, PT Lecturer on Orthopaedic Surgery Harvard Medical School Harvard University Cambridge, Massachusetts; Director Department of Physical Therapy and Occupational Therapy Services Children’s Hospital Boston Boston, Massachusetts Henry G. Chambers, MD Associate Clinical Professor Department of Orthopaedic Surgery University of California, San Diego; Chief of Staff Children’s Hospital and Health Center San Diego, California Antonio Ciardullo, MD First Orthopaedic Clinic University of Florence Cto Florence, Italy Jennifer L. Cook, MD Insall Scott Kelly Fellow Department of Orthopaedic Surgery Lenox Hill Hospital New York, New York Pierluigi Cuomo, MD First Orthopaedic Clinic University of Florence Cto Florence, Italy J.T. Davis, MD Department of Orthopaedics Tulane Institute of Sports Medicine Tulane University New Orleans, Louisiana Harvey N. Dulberg, PhD Private Practice of Sports Psychology Brookline, Massachusetts Pierre A. d’Hemecourt, MD Director of Primary Care Sports Medicine Fellowship Children’s Hospital Boston Boston, Massachusetts Avery D. Faigenbaum, EdD Associate Professor Department of Health and Exercise Science The College of New Jersey Ewing, New Jersey

John M. Flynn, MD Associate Professor Department of Orthopaedic Surgery University of Pennsylvania; Surgeon Department of Orthopaedic Surgery The Children’s Hospital of Philadelphia Philadelphia, Pennsylvania Peter J. Fowler, MD, FRCS Professor Department of Surgery University of Western Ontario London, Ontario, Canada John Franco, MD Fellow Santa Monica Sports and Orthopaedic Group Santa Monica, California Theodore J. Ganley, MD Assistant Professor Department of Orthopaedic Surgery University of Pennsylvania School of Medicine; Orthopaedic Director of Sports Medicine Department of Pediatric Orthopaedic Surgery The Children’s Hospital of Philadelphia Philadelphia, Pennsylvania Mark C. Gebhardt, MD Department of Orthopaedic Surgery Harvard Medical School; Chief Orthopaedic Surgery Orthopaedic Surgeon-in-Chief Department of Orthopaedic Surgery Beth Israel Deaconess Medical Center Boston, Massachusetts Peter G. Gerbino, II, MD Instructor Department of Orthopaedic Surgery Harvard Medical School; Assistant in Orthopaedic Surgery Department of Orthopedic Surgery Children’s Hospital Boston, Massachusetts Carl Gustafson, RPT, ATC, CSCS Division of Sports Medicine Children’s Hospital Boston Boston, Massachussetts; Sports and Physical Therapy Associates Wellesley, Massachusetts Vincenzo Guzzanti, MD Professore Ordinario di Ortopedia e Traumatologia Universita di Cassino; Primario Ortopedia e Traumatologia Ospedale Bambino Gesu—Roma Italia

Contributors

László Hangody, MD, PhD, DSc Clinical Professor Orthopaedic Clinic Debrecen Medical School Debrecen, Hungary; Orthopaedic Surgeon Orthopaedic and Traumatology Department Uzsoki Hospital Budapest, Hungary Christopher D. Harner, MD Professor Department of Surgery University of Pittsburgh; Medical Director Department of Orthopaedics University of Pittsburgh Medical Center for Sports Medicine Pittsburgh, Pennsylvania Richard Y. Hinton, MD, MPH, Med, PT Staff Orthopaedic Surgeon Director of Sports Medicine Department of Orthopaedic Surgery Union Memorial Hospital Baltimore, Maryland Charles P. Ho, PhD, MD California Advanced Imaging Atherton, California; Vail Imaging Center Vail, Colorado Christopher Iobst, MD Attending Physician Department of Orthopaedic Surgery Miami Children’s Hospital Miami, Florida Mary Lloyd Ireland, MD Team Physician Eastern Kentucky University Richmond, Kentucky; Consultant in Orthopaedic Surgery Shriner’s Hospital; President and Orthopaedic Surgeon Kentucky Sports Medicine Clinic Lexington, Kentucky Matthias Jacobi, MD Department of Orthopedic Surgery Hôpital cantonal Fribourg Fribourg, Switzerland Roland P. Jakob, MD Professor Medical Faculty University of Berne; Chief Orthopaedic Department Hôpital cantonal Switzerland

Diego Jaramillo, MD, MPH Professor Department of Radiology Hospital of the University of Pennsylvania; Radiologist-in-Chief and Chairman Department of Radiology Children’s Hospital of Philadelphia Philadelphia, Pennsylvania James R. Kasser, MD John E. Hall Professor of Orthopaedic Surgery Harvard Medical School; Orthopaedic Surgeon-in-Chief Department of Orthopaedic Surgery Children’s Hospital Boston Boston, Massachusetts Danielle A. Katz, MD Assistant Professor Department of Orthopedic Surgery SUNY Upstate Medical University Syracuse, New York Kevin E. Klingele, MD Assistant Clinical Professor Department of Orthopaedic Surgery The Ohio State University; Assistant Director Resident Education and Research Department of Orthopaedics Columbus Children’s Hospital Columbus, Ohio Mininder S. Kocher, MD, MPH Assistant Professor Department of Orthopaedic Surgery Harvard Medical School Harvard School of Public Health; Associate Director Department of Orthopaedic Surgery Division of Sports Medicine Children’s Hospital Boston Boston, Massachusetts Roger V. Larson, MD Associate Professor Department of Orthopaedic and Sports Medicine University of Washington Seattle, Washington Kevin H. Latz, MD Professor Department of Orthopaedic Surgery Children’s Mercy Hospital and Clinic; Assistant Professor University of Missouri, Kansas City Kansas City, Missouri

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Contributors

Ronald E. Losee, MD, ScD Private Practice; Ennis Academy of Orthopaedic Friends Ennis, Montana Anthony C. Luke, MD, MPH, CAQ(SM) Assistant Professor Department of Orthopaedics; Director Primary Care Sports Medicine Family and Community Medicine University of California, San Francisco San Francisco, California Nicola Maffulli, MD, MS, PhD, FRCS(Orth) Professor Department of Trauma and Orthopaedic Surgery Keele University School of Medicine; Consultant Department of Trauma and Orthopaedic Surgery University Hospital of North Staffordshire Stoke on Trent, Staffordshire, England Jung Y. Mah, MD, FRCSC Associate Clinical Professor Division of Orthopaedic Surgery Michael G. DeGroote School of Medicine McMaster University Hamilton, Ontario, Canada Bert R. Mandlebaum, MD Team Physician US Soccer and Pepperdine University; Director Santa Monica Orthopaedic Research and Education Foundation and Fellowship Santa Monica, California Lyle J. Micheli, MD O’Donnell Family Professor of Orthopaedic Sports Medicine and Director Division of Sports Medicine Harvard Medical School; Division of Sports Medicine Children’s Hospital Boston Boston, Massachusetts Tom Minas, MD, MS Associate Professor Harvard Medical School Boston, Massachusetts; Director Cartilage Repair Center Brigham and Women’s Hospital Chestnut Hill, Massachusetts

Paul J. Moroz, MD, MSc, FRCSC Assistant Professor Department of Orthopedic Surgery University of Ottawa; Attending Surgeon Division of Pediatric Orthopaedic Surgery Children’s Hospital of Eastern Ontario Ottawa, Ontario, Canada Martha Meaney Murray, MD Instructor Department of Orthopaedic Surgery Harvard Medical School; Orthopaedic Surgeon Department of Orthopedic Surgery Children’s Hospital Boston Boston, Massachusetts Michael F. Murray, MD Instructor in Medicine Harvard Medical School; Clinical Chief Division of Genetics Department of Medicine Brigham and Women’s Hospital Boston, Massachusetts Andrés T. Navedo-Rivera, MD Instructor Department of Anesthesia Harvard Medicine School; Assistant in Anesthesia Department of Anesthesia Children’s Hospital Boston Boston, Massachusetts Scott C. Nelson, MD Assistant Clinical Professor Department of Orthopaedic Surgery Loma Linda University School of Medicine Loma Linda, California; Medical Director Cure International Santo Domingo, Dominican Republic; Attending Surgeon Department of Orthopaedic Surgery Riverside County Regional Medical Center Moreno Valley, California Jason H. Nielson, MD Sports Medicine Fellow Department of Orthopaedics Division of Sports Medicine Harvard Medical School; Children’s Hospital Boston Boston, Massachusetts

Contributors

Michael J. O’Brien, MD Clinical Instructor Department of Sports Medicine Harvard Medical School; Staff Physician Department of Sports Medicine Children’s Hospital Boston; Staff Physician Department of Musculoskeletal Medicine Beth Israel Deaconess Medical Center Boston, Massachusetts Norman Y. Otsuka, MD, FRCSC, FACS Associate Clinical Professor Department of Orthopaedic Surgery David Geffen School of Medicine University of California, Los Angeles; Assistant Chief of Staff Shriner’s Hospitals for Children Los Angeles, California Susan M. Ott, MD Clinical Instructor and Team Physician Department of Athletics Florida Southern College Lakeland, Florida; Orthopedic Surgeon Department of Surgery South Florida Baptist Hospital Plant City, Florida George A. Paletta, Jr., MD Associate Professor Chief of Sports Medicine Department of Orthopaedic Surgery Washington University St. Louis, Missouri Ron Pfeiffer, EdD, LAT, ATC Professor Department of Kinesiology; Codirector Center for Orthopaedic and Biomechanics Research (COBR) Boise State University Boise, Idaho Gábor Ráthonyi, MD Orthopaedic Surgeon Orthopaedic and Traumatology Department Uzsoki Hospital Budapest, Hungary Kathleen Richard, PT, PCS Supervisor Outpatient Department Department of Physical Therapy Children’s Hospital Boston Boston, Massachusetts

William G. Rodkey, DVM Diplomate American College of Veterinary Science; Director Basic Science Research Steadman Hawkins Research Foundation Vail, Colorado Senthilkumar Sadhasivam, MD Assistant Professor Department of Anesthesia University of Cincinnati; Cincinnati Children’s Hospital Medical Center Cincinnati, Ohio Frederic Shapiro, MD Associate Professor Department of Orthopaedic Surgery Harvard Medical School; Attending Orthopaedic Surgeon Department of Orthopaedic Surgery; Research Associate Orthopaedic Research Laboratory Children’s Hospital Boston Boston, Massachusetts Krishn M. Sharma, MD Resident Department of Orthopaedic Surgery Union Memorial Hospital Baltimore, Maryland Kevin G. Shea, MD Center for Orthopaedics and Biomechanics Research Boise State University; St. Luke’s Children’s Hospital Boise, Idaho Angela D. Smith, MD Department of Orthopaedics The Children’s Hospital of Philadelphia Philadelphia, Pennsylvania Carl L. Stanitski, MD Professor Department of Orthopaedic Surgery Medical University of South Carolina; Children’s Hospital Charleston, South Carolina Deborah Stanitski, MD, FRCS(C) Professor Department of Orthopedic Surgery Medical University of South Carolina; Department of Orthopaedic Surgery Medical University of South Carolina Hospital Charleston, South Carolina

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Contributors

J. Richard Steadman, MD Clinical Professor University of Texas Southwestern Medical School Dallas, Texas; Orthopaedic Surgeon Steadman Hawkins Clinic; Chairman of the Board Steadman Hawkins Research Foundation Vail, Colorado Andrea Stracciolini, MD Lecturer in Sports Medicine Harvard Medical School; Department of Orthopaedic Surgery Division of Sports Medicine Children’s Hospital Boston Boston, Massachusetts Edward C. Sun, MD Staff Physician Spine Care Medical Group San Francisco Spine Institute Daly City, California Robert P. Sundel, MD Associate Professor Department of Pediatrics Harvard Medical School; Director of Rheumatology Department of Medicine Division of Immunology Children’s Hospital Boston Boston, Massachusetts John M. Tokish, MD Chief Sports Medicine; Head Team Physician US Air Force Academy Colorado Springs, Colorado

Brett L. Wasserlauf, MD Assistant Professor Department of Orthopedic Surgery University of Connecticut Farmington, Connecticut; Orthopaedic Surgery St. Francis Hospital Hartford, Connecticut Jason K.F. Wong, MBChB, MRCS (Ed) Lecturer Blond McIndoe Plastic and Reconstructive Surgery Laboratories The University of Manchester; Research Registrar Department of Burns and Plastic Surgery Central Manchester and Manchester Children’s University Hospitals NHS Trust Manchester, England Amy L. Woodward, MD, MPH Instructor Department of Pediatrics Harvard Medical School; Assistant in Medicine Rheumatology Program Children’s Hospital Boston Boston, Massachusetts Yi-Meng Yin, MD, PhD Chief Resident Department of Orthopaedics University of California, Los Angeles Los Angeles, California

Chapter 1

Epidemiology of Pediatric Knee Injuries Jason Wong

The growing child shows amazing resilience to repetitive minor external physical forces. As part of the learning process, children experience fall after fall without major detriment during everyday play. Childhood injuries, although mainly trivial, do vary in their severity and can affect a child’s growth and development. The knees provide a point of impact as soon as a child learns to crawl. As locomotion progressively develops, children become competent in walking, and the emphasis from falling backward onto the well-cushioned gluteal region shifts to falling forward so that the predominant body region of impact with the ground is the knee. The knee is the most common site of injury in most childhood sports.1 By understanding how to preserve knee function at an early age, it may be possible to limit the effects of injuries in later life. Injuries in children are usually minor and self-limiting. In young children, musculoskeletal tissues are generally more pliable and absorb much of the impact from external forces. Through adolescence, bone stiffness increases, and bone becomes less resilient to impact.2 Childhood knee injuries and their occurrence can be divided into those acquired through recreational and competitive sport and those acquired through accidents, such as road trauma. There are areas of transition where injuries are acquired through contact with roads and streets as part of a recreational activity such as in roller sports or cycling. Sports injuries are “acquired during a game or practice, causing one or more of the following: reduction of activity, the need for treatment or medical advice, and or negative social or economic consequences.”3 Major injuries can be defined as those injuries that require ongoing medical care or restricted participation for more than a month.4 Physical activity plays a significant role in the well-being of a child. Recently, there have been huge investments into promoting active lifestyles in children, and childhood competitive sport has become established. As a direct consequence, the number of sports-related (SR) knee injuries has increased.5 It is

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estimated that a quarter of all American children are injured per year.6 Common recreational activities include American football, basketball, cycling, roller sports, soccer, athletics, and Alpine activities. The growing knee involves a combination of musculoskeletal elements that can be subject to a vast array of acute and chronic injuries. It differs from the adult knee in that growth can be affected after injuries to the growth plates around the knee joint. The distal femoral physis represents the most active growth plate in the body. Approximately 0.9 cm per year of growth is attributable to this physis, providing 70% of the longitudinal growth of the femur.3 In comparison, the proximal tibial physis contributes approximately 0.6 cm per year to limb length, accounting for approximately 55% of the longitudinal growth of the tibia. Injury to these vulnerable areas can result in significant limb length discrepancy or angular deformities. This, coupled with difficulties associated in obtaining a diagnosis from young children, makes knee injuries in this age group particularly challenging. Hip pathology can present as knee pain in a child. Pain from conditions such as transient synovitis and slipped capital femoral epiphysis can be referred to the knee in children. Sports physicians should be aware of the extent of the problem and identify means to manage and take measures to prevent injuries to the knee. As already mentioned, sports injuries are increasing. The American Academy of Orthopaedic Surgeons identified more than 2.2 million fractures, dislocations, and soft tissue injuries related to five of the most popular childhood recreational pastimes.6 Unfortunately, to date, few well-conducted population studies have been performed to identify the scale of knee injuries in children. Most studies suffer from a lack of uniform epidemiological measurement and good exposure data. This chapter will highlight the scale of the problem within identified areas. 1

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Incidence of Injury The United States National Electronic Injury Surveillance System (NEISS)7 is an Internet-access database compiled by the U.S. Consumer Product Safety Commission (USCPSC). Initially, NEISS was to act as a database to log product-related injuries. However, since the year 2000, it has collected data on all injuries that present to 100 emergency rooms across the United States. The surveillance system detected 229,298 knee injuries in children under age 18 presenting to emergency rooms in the year 2001. There has been a steady increase in the number of incidences since NEISS was created (Figure 1–1), demonstrating a probable rise in concordance with organized sports in children. The vast majority of reported knee injuries are minor cuts and bruises and sprains (Figure 1–2). However, the most common injuries resulting in permanent and long-term disability are injuries of the knee.8 In one Danish study, the annual incidence of pediatric knee injuries was calculated at 13 per 100,000.9 This is probably a huge underestimation because a large proportion of trivial injuries are not reported. In addition to the statistics available from the NEISS database, the National Center for Health Statistics, part of the Centers for Disease Control and Prevention, conduct a yearly face-to-face household survey, collecting demographic and health data from a nationally representative sample of the civilian, noninstitutionalized population residing in the United States. This National Health Interview Survey (NHIS) determined that, in the period from 1997 to 1999, an estimated 7 million Americans per year received medical attention for sports-related injuries (25.9 injury episodes per 1000 persons). For 5- to 24-yearold Americans, this national estimate was nearly 42% higher than estimates based on sports-related injuries seen only

in emergency departments over a similar time frame. The highest average annual SR injury episode rates were for children ages 5 to 14 (59.3 injury episodes per 1000 persons) and persons between ages 15 and 24 (56.4 per 1000 persons). The SR injury episode rate for males was more than twice the rate for females. Basketball was the most frequently mentioned SR activity when the injury episode occurred, with a rate of approximately four injury events per 1000 persons.10 Influence of Age and Gender Analysis of NEISS data shows that knee injuries become more frequent in adolescence and then decrease through the transition into adulthood (Figure 1–3). Therefore most injuries arise when the child is at greatest risk of growth disturbance. Girls generally have a greater propensity to growth disturbance at an earlier age. Adolescent girls appear to have similar injury rates as boys in comparable activities,11 but with different injury patterns. More girls are taking part in school sports. This is an evolving area for the incidence of knee injury. Girls have greater joint laxity than boys and also have reduced muscle strength in comparison as they go through puberty. Anterior cruciate ligament (ACL) injuries are more frequent in adolescent girls, with male-to-female ratios varying from 1:2 to 1:8, depending on sport involvement.12 Potential risk factors include Q angle, femoral anteversion, genu valgum, external tibial torsion, femoral intercondylar notch shape and size, ACL thickness, hormonal influences, and training techniques. These factors may also contribute to the incidence of patellofemoral pain syndrome in females. Overuse injuries in female gymnasts have been explored, and factors related to patella malposition, extensor mechanism malalignment, muscular imbalance, and local

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Year Figure 1–1 NEISS annual incidence of knee injuries in children (ages 0–17).

Epidemiology of Pediatric Knee Injuries

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11% 29% Contusions Dislocations Fractures Lacerations Punctures Strains or sprains

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Figure 1–2 Distribution of knee injury types, NEISS database 2001.

deformities have been considered to predispose to extensor mechanism dysfunction.13 Sports that involve a predomKEY POINTS inantly female population, such as gymnastics, have identified 1. There is a steady knee injuries as a particular area of rise in childhood concern. Certain postures and knee injuries possimaneuvers in gymnastics, such as bly relating to parhigh-impact loading from vaultticipation in sports. ing, forced knee extension, and 2. Most injuries are knee flexion, predispose to knee sprains, contusions, injury. Common knee condior abrasions. tions in female gymnasts include 3. Many injuries are patellar pain, patellar subluxation not reported. and dislocation, patellar and 4. Some knee injuries quadriceps tendinopathy, Osgoodlead to ongoing Schlatter lesion, Sinding-Larsenproblems in future Johansson lesion, and synovial years. 14 plica. Caine et al. calculated a

knee injury rate in gymnasts of 0.273 per 1000 hours of training, accounting for 11% of all injuries acquired in their study,15 of which more than two thirds were acute injuries. The relative risk of injury in this group of athletes is related to the difficulty of the skills practiced and their intensity. Competition and advanced-level gymnasts have the greatest risk for injury.

Injury Risk Factors The risk factors for pediatric knee injuries are similar to those of adults. However, fewer investigations have studied the exact mechanical failing that leads to injury, given the spectrum of ages involved and the relative rarity of severe injuries. In general, children’s more flexible tissues are protective. Injury risk factors can be identified as either intrinsic or extrinsic. Intrinsic factors refer to anatomical and inherent contributions to injuries, whereas extrinsic risk

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Figure 1–3 NEISS incidence of knee injuries in 2001.

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factors are associated with biomechanical and environmental adversities that are often more amenable to change. Intrinsic Factors Several intrinsic risk factors for knee injury have been identified and shown to correlate with knee problems. Physical characteristics that predispose to knee problems have been explored. Specific to anterior knee pain and patellar tracking problems is the influence of the Q angle, that is, the angle of lateral traction of the quadriceps muscle complex on the patella. Hence the wider the pelvis, the more lateral the hip, the more medial the knee in relation to it, and the greater the lateral strain on the patella. Pronated hindfeet, limb length discrepancy, and a flat foot arch have also been advocated as risk factors. Hypermobility of the patella has a positive correlation with patellofemoral pain.16 Poor quadriceps and gastrocnemius muscle flexibility impaired reflex response time, especially of vastus medialis obliquus and vastus lateralis muscle.16 Developmental knee problems such as genu valgum and genu varum have also been implicated in making children’s knees more prone to injury. Extrinsic Factors Relatively greater forces have to be generated to cause injury to the more elastic tissues of the growing child. However, biomechanical abnormalities can similarly increase the risk of injury. Recurrent or single excessive loading from impact, rotational, valgus, varus, torsional, or translational forces put the knee at risk. Poor training KEY POINTS techniques, improper use of equipment, and poor child Intrinsic supervision have been identi1. Female gender fied as extrinsic risk factors for 2. Q angle knee injury. Potential areas for 3. Genu valgum/varum minimizing these risks could lie 4. Limb discrepancy in designing equipment speci5. Hypermobility of the fically for children or limiting patella their exposure to high-risk 6. Poor muscle flexisports. Other modifiable factors bility include enforcement of reguExtrinsic lations and rules in sports, 1. Single or recurrent making participation safer in excessive loading general. to knee Activities of Injury

2. Poor training techniques and conditioning 3. Poor supervision and coaching 4. Improper use of equipment or lack of safety equipment

In the United States, sports injuries account for nearly a quarter of all injuries in children and adolescents.17 In Britain, approximately 75% of healthy youngsters participate in organized sports.18 The most common sports that result in being admitted to an emergency department in the United States for a knee injury are American football, basketball, cycling, roller sports, soccer, and athletics (track

and field). Demographics differ across the world: For example, the Australian-based Victorian Injury Surveillance and Applied Research System19 identifies Australian rules football, soccer, basketball, cricket, and netball as the biggest factors in youth sports injuries. In that series, knee injuries accounted for 13% of injuries in Australian rules football, 22% in soccer, 8% in basketball, 7.5% in cricket, and 3% in netball. In a large study of pediatric sports injuries in Hong Kong, the most common sports involved were soccer, basketball, volleyball, athletics, and cycling. The knee was affected in 32% of the cases.20 All 37 soft tissue injuries to the knee resulted from ball games. Any sport that involves torsional, valgus, and varus forces puts the knee at risk. Repeated forceful extension and flexion also put strain on ligament and tendon attachments. This chapter will briefly discuss the main sports that produce knee injuries, with their relative contribution to the epidemiology of knee injuries (Table 1–1). Football In American football, injuries around the knee account for 12.7–36.5% of all injuries.21 Football claims the most injuries for a single sport in the pediatric population in the United States. In 2001, 315,820 injuries in children were reported to the NEISS. Of these, 9.1% were knee injuries (see Table 1–1). More than 75% of the injuries were sprains and contusions, with 5% being lacerations.7 The single most common site of injury from high school football was the knee, which accounted for 25% of all injuries.21 Injury levels were particularly high during contact practice and preseason practice. Adjusting footwear and ensuring good maintenance of playing fields reduce the risk of knee injury.21 Basketball In basketball, rapid acceleration, deceleration, and pivoting produce a high frequency of knee injuries. Collisions and falls are also numerous. In 2001, the NEISS database recorded 26,305 knee injuries in children, of which half were sprains and 6.8% were patellar dislocations.7 Ellison Table 1–1 NEISS Sports-Related Injuries and Knee Injuries in Children and Adolescents (0–17 Years) in 2001 Sport American football Basketball Cycling Roller sports (inline, roller, skateboard, and scooter) Soccer Athletics (track and field)

Total Number of Injuries

Number of Knee Injuries (%)

315,820

28,687 (9.1)

360,796 356,317 250,160

26,305 (7.3) 26,209 (7.4) 14,125 (5.6)

120,254 51,179

13,414 (11.1) 6182 (12.1)

Epidemiology of Pediatric Knee Injuries

reviewed 4966 basketball injuries that presented to the emergency room from the Canadian Hospitals Injury Reporting and Prevention Program (CHIRPP).22 They studied 5- to 19-year-olds and found that knee injuries accounted for 5.9% for males, and 6.7% for females, all of which were sustained in basketball. The greatest group at risk of knee injuries was 15- to 19-year-old female basketball players; their knee injuries accounted for 11% of all injuries. This is twice the proportion of knee injuries to their agematched male counterparts, which confirms observations by other authors23 that teenage female athletes seem to have more vulnerable knees. A review of basketball injuries at a Texas high school demonstrated a high rate of knee injuries requiring surgery.24 Collisions and overexertion injuries were the main culprits. Cycling The vast majority of knee injuries from cycling arise from falls in which the cyclist lacked adequate knee protection. The main areas of concern from cycling falls are head injuries, with most research concentrating in this area.25 Annually, 300 fatalities in children and adolescents under age 18 are attributed to cycling in the United States. In a Canadian-based study, 11% of serious pediatric trauma cases resulted from cycling incidents.26 The NEISS database reported 26,209 bicycle-associated knee injuries in 2001, of which a third were lacerations, 44% were contusions, and only 12% were sprains.7 Overuse injuries are also frequent in cyclists, and the knee has been identified as the most common site for injury.27 Roller Sports Inline skating is increasingly popular, with an incidence in pediatric trauma that surpasses that of all major childhood diseases.28 Knee injuries accounted for 10% of all injuries sustained. Of these, 94% were lacerations, sprains, abrasions, or other forms of soft tissue injury. In 2001, NEISS identified 81,345, 79,813, and approximately 89,002 inline/roller-skate-, skateboard-, and scooter-associated injuries, respectively, in children presenting to emergency rooms around the United States. This accounts for 14,125 knee injuries, of which 38% were contusions and abrasions and 25% were sprains. Skateboard injuries in the United States are estimated to account for 1500 child and adolescent hospitalizations per year. Scooter injuries increased by 700% between May and September 2000, according to USCPSC reports. The rise in their popularity was also reflected in injuries around the 2000 holiday season, because they were a popular choice of gift. Soccer The popularity of soccer around the world is well-recognized. In the United States the popularity of the sport has increased 60% in 9 years.29 The injury rates in children and adolescents vary from 0.5 injuries per 1000 hours of play to 32 injuries per 1000 hours of play.29 The former figure refers to injuries that prevented further participation in the sport,

5

whereas the latter figure refers to any traumatic incidents noted during sport. In soccer, lower limb injuries predominate, with approximately 60–70% classified as “minor injuries.” In 2001, NEISS reported 120,254 football-related injuries in the pediatric population. Of these, 11.2% involved the knee. This particular age group sustained 61.6% of all U.S. soccer injuries to the knee.7 Sprains and strains accounted for more than half of all these knee injuries, with simple abrasions and contusions contributing more than one fifth of the reported knee injuries in children. A Danish study on youth club soccer (12–18 years of age) found an incidence of knee injuries of 0.96 injuries per 1000 hours of soccer play, that is, 26% of injuries in soccer affect the knee.4 Some studies have identified soccer to be a dominant etiological factor in meniscal injuries in children.30 Other major knee injuries in soccer are ligament sprains, ruptures, and fractures, which are relatively less common. Athletics Track-and-field events are usually responsible for overuse injuries in the knee. In a previous study, we found that 8 of 12 cases of traction apophytes about the knee were in trackand-field athletes.20 In older athletes, 38% of overuse injuries were located to the knee.31 The NEISS reported 6182 knee injuries related to running and track-andfield–based events in children in the year 2001. Alpine Sports Knee injury figures from Alpine events reported on the NEISS database do not reflect the scale of the problem; only a few states have ski facilities, and for most people, visiting the slopes is a seasonal event. Up to 40% of injuries from the slopes are most likely not reported.32 Knee injuries in Alpine sports are frequent, with medial collateral ligament (MCL) strains being most common. A very large study by the University of Vermont, of 3,641,041 skiers, calculated injury rates of 4.27 per 1000 skier days in children, 2.93 per 1000 skier days in adolescents, and 2.69 per 1000 skier days in adults, highlighting children as a particular atrisk group.33 A factor contributing to the propensity for knee injuries are modern ski boots, which transmit torsional forces to the knee. In that study, knee injuries accounted for 25–38% of overall injuries. Contusions of the knee accounted for 11.2% of all injuries in children, with sprains of the MCL accounting for 7.9% and tibial fractures contributing to 4.9% of reported injuries. In adolescents the injury pattern is slightly different, with skier’s thumb being the most frequently reported injury. Contusions of the knee, MCL strain, and ACL injuries account for 6.1%, 6%, and 4.5% of the injuries, respectively. In adults, ACL injuries are far more common, and women are twice as likely to have ACL sprains. Snowboarding has increased in popularity and accounts for approximately 20% of visitors at U.S. ski resorts. Snowboarders are generally younger than skiers, with an average age of 20. Strain from hard boots, mostly worn during skiing, translate into greater torsional forces to the knee

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than the soft boots used in snowboarding. Knee injuries are less prevalent in snowboarders, because of avoidance of high torque forces when the feet are in nonrelease bindings.34 Soft boots place approximately half the risk of injury to the knee when compared to hard boots. One resort in North Tahoe, California., noted a ski injury rate of 3.2 per 1000 skiers and a snowboard injury rate of 12.7 per 1000 snowboarders. Approximately 4–8% of injuries arise when a skier is waiting to enter or exit a ski lift, and these tend to be knee injuries. Knee injuries account for approximately 16.3% of the injuries in snowboarding, and in the low to intermediate level of snowboarders, it can account for as many as 28% of injuries. In a prospective Australian snowboarding study, the risk of knee injuries from snowboarding was approximately half that of skiing injuries,35 with the difference in footwear hypothesized as a major factor. Road Traffic Accidents As part of the National Accident Sampling System (NASS) database, knee injuries were recorded following motor vehicle collisions between 1979 and 1995.36 Knee injuries accounted for approximately 10% of all injuries following road traffic accidents. Of these, 50% were contusions. Minor injuries to the knee, such as abrasions, lacerations, and contusions, accounted for approximately 90% of all knee injuries, with fractures contributing to less than 2.5% of knee injuries. Tendon and ligament injuries accounted for approximately 25% of the injuries observed. Overall, 1% of the knee injuries occurred in patients under the age of 10, and 21% in patients between 10 and 20 years of age. The trend was similar for more severe injuries of the knee. Autopsy of pedestrian victims of road traffic accidents reveals that 80% of the victims have associated knee injuries caused by disruption to the knee through hyperextension and anterior dislocations.37 Miscellaneous Ball sports account for most knee injuries in children. Knee injuries are also frequent in racket sports and account for 20–25% of injuries sustained. Collateral ligament injuries prevail in squash and badminton, whereas patellofemoral problems are prevalent in tennis.38 Badminton players were also more prone to cruciate and meniscal injuries. Most injuries in youth tennis are overuse, presenting as pain and inflammation. Osgood-Schlatter lesion is apparent in yearround youth tennis players, and patellofemoral problems are frequent in young female players.23 Other significant observations from the NEISS database are that trampoline-related knee injuries pose a significant problem and are probably related to subsequent related falls. A total of 4370 knee injuries, representing 5.4% of trampoline-related injuries, were reported in 2001. Of these, 48% were sprains. Unusual injury patterns have been found in lower limb trampoline injuries in which anterior dislocations of the knee have been associated with popliteal vessel thrombosis.39 Child abuse can present as knee injuries. Metaphyseal fractures are fairly specific for cases of abuse, with the most

common site for these injuries around the knee. The mechanism of injury is from violent shearing through the bone from shaking.40 Healing in these areas takes place in a short time; therefore, early documentation is advised. Injury Characteristics Because of the various components of the knee joint, a number of sites can be affected by injury. The pattern of knee injury is different from adults, because ligaments and tendons are relatively stronger than bone in the growing child, with a prevalence of avulsion injuries. The pattern of knee injuries changes with age.9 Metaphyseal fractures are predominant in children before age 5. This changes over time, with a trend for a greater prevalence of tibial spine fractures and collateral ligament injuries. In a study in a relatively closed population, we calculated the relative knee injury rates in children up to the age of 14 (Table 1–2). The median age for ligament and physeal injuries in this group was 12. Assessment of the knee is easier in older children, with 55% accuracy in clinical assessment of preadolescents compared with 70% accuracy in adolescents.41 Clinical accuracy for ligamentous injuries was only 31%.42 The difficulty arises from unwitnessed injuries, a poor history from the child, and nonspecific physical signs. Investigation for specific pathology can often be fruitless. In a prospective study, only 71% of the children could actually recall the exact mechanism of injury that led to hemarthrosis.43 Of the osteochondral fractures found at arthroscopy, only 64% were evident on preoperative radiographs. Arthroscopy is still considered the gold standard for identifying internal knee derangement and causes of acute hemarthrosis in children. However, the clinician should be wary that a significant proportion of clinically indicated post-traumatic arthroscopies fail to reveal any pathology in children. When we quantitatively reviewed several articles on arthroscopy in this age group (Table 1–3), we discovered that 10% of arthroscopies are normal. However, our own prospective study showed that 26% of clinically indicated arthroscopies in children failed to reveal any pathology.44 Methods such as magnetic resonance imaging are constantly improving their diagnostic rate and are especially useful at highlighting nondisplaced fractures and soft tissue injuries around the knee45; however, they lack sensitivity in highlighting cruciate ligament injuries.46

Table 1–2 Annual Incidence of Knee Injuries in Children Aged 0–14(9) Type of Lesion Distal metaphyseal fractures Distal femoral physis Rupture of collateral ligaments Fracture of tibial eminence Proximal tibial physis Proximal metaphyseal fracture of the tibia

Annual Incidence per 100,000 2.0 1.0 0.7 3.0 1.2 5.6

Epidemiology of Pediatric Knee Injuries

Table 1–3

7

Quantitative Review Table of Arthroscopies Performed after Trauma in Children and Adolescents41–44,50–56

Lesion Site Medial meniscal Lateral meniscal Discoid meniscus Total mensical ACL tear or insertion fracture PCL tear Medial collateral Lateral collateral Osteochondral fractures Synovial tears Synovial plica Loose bodies Osteochondritis dissecans Patellar lesion/chondromalacia Normal

Children 1.05) is high, and the upper body to lower body ratio (pubis to top of head: pubis to bottom of foot) is also increased (>0.93).50 The athlete’s maturity is typically assessed using secondary sexual characteristics, most commonly breast and pubic hair development in females, and pubic hair development and genital development in males. Practically, the physician can assess Tanner staging by asking the athlete to select pictures of sexual characteristics that best match their physical development.51 Menarche usually occurs between 2 and 2.5 years after onset of thelarche (i.e., breast development), whereas growth in girls is usually ended by 1 to 1.5 years after menarche onset. Cardiovascular Examination For the cardiovascular screening examination (see Box 10–2), vital signs including pulse rate, respiratory rate, and brachial blood pressure in the sitting position should be checked for systemic hypertension, using age-adjusted tables. Radial and femoral artery pulses and possibly blood pressures in the upper and lower extremities should be checked to rule out coarctation of the aorta. Precordial auscultation with

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a stethoscope should be performed with the athlete in the supine, sitting, and standing positions.10 Listening to the heart with the athlete in the supine position and then standing is the most valuable maneuver to bring out murmurs associated with left ventricular outflow obstruction.52 Loud murmurs (grade 3 or more) and holosystolic, late systolic, systolic ejection with or without click, diastolic, or continuous murmurs warrant cardiac investigation.53 Hypertrophic cardiomyopathy is characterized by a harsh systolic ejection murmur that decreases with squatting and increases in intensity upon standing or during a Valsalva maneuver.54 Knee Examination Alignment The screening knee examination (Figure 10–1) begins by observing the lower extremity alignment. Lower extremity alignment changes during childhood. From age 2 onward, children have a valgus tibiofemoral alignment up to 15 degrees, peaking at age 6.55 Subsequently, this physiological genu valgum decreases until the completion of adolescence. Similarly, the angle of femoral anteversion at the hip, which can have rotational effects at the knee, begins at approximately 40 degree at birth but decreases progressively by age 10 and averages 15 degrees at skeletal maturity.56,57 Residual increased femoral anteversion may contribute to

malalignment of the knee, with girls having more patellar malalignment than males.58 Alignment of the knees can be assessed with the athlete standing with the ankles together to identify normal variants or abnormalities (e.g., genu valgum, genu varum, internal and external tibial torsion, and excessive femoral anteversion).59 The levels of the iliac crests can be quickly palpated to check for a leg length discrepancy. A standing flexion test enables evaluation of the back for asymmetries that suggest scoliosis. Observing alignment in the standing position with the ankles shoulder-width apart enables assessment of the height of the arches. When visualizing from behind, valgus positioning of the heel can be noted. When the athlete stands on the toes in this position, the heel usually goes into more varus with reconstitution of the arch of the foot, suggesting the midfoot is flexible. Pronation of the feet usually results in a compensatory internal rotation of the tibia and calcaneal eversion.60 If the athlete is unable to do so, or the arch remains flat, a more detailed examination of the foot and ankle should be performed to rule out problems such as tarsal coalition or spastic flatfoot. The presence of pes cavus or a high-arched foot suggests a biomechanically tight heel cord or plantar fascia, although an underlying neuromuscular disease should be ruled out. Leg-length discrepancies of less than 3% of the length of lower extremity were not associated with compensatory strategies.61

Figure 10–1 Screening maneuvers for lower extremity/knee problems. A more detailed knee examination for specific structures is performed as determined by history or screening. A, Observe lower extremity alignment. B, Toe raise.

Figure 10–1—Cont’d C, Observe gait. D, Squat. E, Observe duckwalk. F, Single-leg hop.

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A brief screening of gait and lower extremity function can be done by observing the athlete walking, squatting, duckwalking, and hopping. Abnormal position of the patellae and evidence of intoeing or outtoeing suggest a rotational deformity in the lower extremities. An antalgic lurching gait may suggest hip pathology, whereas toe walking can suggest tight heel cords or, more rarely, underlying neuromuscular disease. Inability to squat can indicate a problem with the hip or knee joint and warrants a more detailed examination. The single-leg hop test62,63 can be used to assess the functional and proprioceptive ability. Patellofemoral Joint The mobility and alignment of the patella in the trochlear groove can be assessed. The angle between the axis of the thigh, patella, and the tibia (Q-angle) can be measured in patients with patellofemoral problems. Although studies have shown strong relationships between structural measures and lower extremity injury in basketball players,64 the Q-angle alone has no clear correlation with incidence of patellofemoral disorders.65 Flexibility The strength and flexibility of major muscle groups, including the quadriceps, hamKEY POINTS strings, and adductors, are often considered modifiable risk facPhysical examination tors for sports injury.66,67 Typical 1. The physical examitests for flexibility (Figure 10–2) nation should have include (1) the Thomas test special focus on rulfor hip flexor tightness, (2) ing out any cardiothe quadriceps-inhibited flexion vascular or orthopeangle, or Ely’s test (greater or dic conditions, as equal than 10 degrees indicates well as evaluating tightness), (3) the popliteal concerns identified in angle test for hamstring, and (4) the athlete’s history. Ober’s test for the iliotibial 2. Anthropometric band. The expected range of measures and Tanner these measurements will vary staging help evaluate depending on the population the physical maturity assessed. For example, the flexiof the athlete. bility in dancers may be quite 3. Cardiac auscultation different than in football should be performed players. in a quiet area with Several studies have identian examination table, fied a spectrum of ligamentous with the athlete in the laxity among individuals. Athletes supine, sitting, and in general do not seem to be standing positions. more hypermobile compared with 4. The assessment of 68 nonathletes, although the cerlower extremity aligntain flexibility characteristics of ment and flexibility of athletes can preselect them muscle–tendon toward specific sports, such as groups should be gymnastics. The ligamentous laxincluded in the knee ity in children is also greater than examination. in adults. One must keep this in 5. The lower extremity mind when evaluating ligament function should be tests, especially the Lachman’s screened by observtest at a young age, because looseing gait, squat, and ness may represent increased single-leg hop. constitutional ligamentous laxity

rather than an ACL tear. Tests for constitutional joint laxity include thumb abduction to the forearm, hyperextension of the fifth metacarpophalangeal joint, hyperextension of the elbows and knees, and hyperflexion of the spine. These maneuvers can be used to calculate the Beighton score,68 or used individually to screen for constitutional ligamentous hyperlaxity.69 Hip and Ankle The examination of the hip and ankle can always be considered part of the knee examination. Internal and external range of motion of the hip can be performed with the athlete supine, the hip flexed 90 degrees, and the knee flexed 90 degrees. Pain on internal rotation of the hip warrants further investigation. The ankle can also be checked for range of motion, ligamentous stability, and ankle strength and stability. Follow-up Investigations Investigations are not ordered unless there is a concern identified on the physical examination. Screening electrocardiograms11 and echocardiograms70 are controversial and are not commonly done due to the resources necessary and its questionable cost-effectiveness.10,71 X-rays of both knees, including standing anteroposterior views, standing bentknee (or tunnel) views, lateral views, and Merchant view, are recommended if there are concerns of knee problems. Magnetic resonance imaging and isokinetic strength testing are considered, depending on the suspected pathology. Body composition testing has been done for elite athletes but is usually not necessary for high school athletes. Highly competitive athletes may also be evaluated for fitness, including maximal aerobic capacity testing (VO2 max). Training Recommendations Cross-sectional and longitudinal studies suggest that intensive training and competition do not negatively influence the growth of maturing athletes.72,73 However, volume and type of training are areas of particular concern because many of the injuries in young athletes are caused by overuse and overtraining. The athlete is advised to begin a preseason training program 6–8 weeks before the start of the season, including cardiovascular, flexibility, and strength exercises.74–76 A sports-specific training program can enhance performance and may decrease the risk of injury. Female athletes in deceleration or “cutting” sports should be referred to one of the validated ACL injury prevention regimens.77,78 Proprioception Proprioception is the afferent input that enables the detection of position and movement of limb segments in relation to one another. Patients with hypermobility of the knee have poorer proprioceptive feedback than controls, which may result in the athlete adopting unsound knee positions leading to injury.79 Similarly, athletes with ACL80 or posterior

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Figure 10–2 Flexibility tests. A, Thomas text (hip flexor). B, Ely’s test (quadriceps). C, Popliteal angle (hamstring). D, Ober’s test (iliotibial band).

cruciate ligament (PCL)81 deficiency have poorer proprioception. Proprioception may play a more significant role than pain in preventing injury.81 However, training to improve proprioception seems possible.82 A familial predisposition to ACL tears has been suggested, with individuals with an ACL tear being two times more likely to have a relative with an ACL tear compared with individuals without an ACL injury, and increased occurrence of 10% if the athlete has a first-degree relative with an ACL tear (OR = 2.03, 95% CI = 1.14–3.63).83 Similarly, the risk of tearing the opposite ACL is also approximately 10%.84

Many high school and college programs are enrolling their athletes in preventive ACL programs. This has shown some success in reducing the number of ACL injuries during the season. In soccer players the incidence of ACL tears differed from 1.15 injuries per team per season to 0.15 injuries per team per season when trained (RRR = 0.13).85,86 Another study in soccer players also demonstrated a decreased rate of lower leg injury (RRR = 0.77), including ACL injury with preseason training.87 It is hoped that a program of preseason conditioning including strength, flexibility, and proprioception training can help decrease significant injuries to the knee and ankle.76,77

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Equipment, Protection, Braces, and Orthotics

KEY POINTS Follow-up

During the PPE, equipment use 1. Appropriate evaluacan be discussed, and the athlete tion and follow-up should be encouraged to ensure should be arranged proper fit and condition of the for any athlete if seriequipment. Taping and bracing ous concerns are are recommended in some cases identified. to help prevent further injury in 2. Investigations are not a previously injured joint. For routinely necessary example, ankle braces or taping unless concerns are have been shown to be helpful identified. in ankle sprains.88 Research evi3. Proprioception exerdence does not support prophycise programs are lactic bracing of the knee to being implemented to reduce medial collateral ligaprevent ACL injuries ment (MCL)89 or ACL injuries. and ankle sprains. In college90,91 and high school92 4. Prophylactic ankle football players, there were no braces have shown significant differences found in some benefit for injury rates among braced and reducing ankle nonbraced competitors. However, sprains; however, a protective brace after injury prophylactic knee may allow an earlier and more braces have not been successful return to sports. shown to reduce the Foot orthotics are often used incidence of specific for foot or knee problems when injuries. alignment is a concern. Control of pronation at the midfoot and subtalar joint can affect the amount of internal rotation of the tibia, possibly reducing stress at the patellofemoral joint.93 If the athlete is asymptomatic, foot orthotics are unnecessary despite obvious pes planus94 or pes cavus, although appropriate footwear should be encouraged. Limitations It is important to recognize the limitations of the PPE. Criticisms of the PPE question the value,95 validity, reliability,96 cost-effectiveness,69,97 compliance, and lack of standardization10,98,99 of the examination. The ability to detect athletes at risk for sudden death, particularly from cardiac causes, is very limited, relying mainly on family history.7 The identification of relevant orthopedic and medical problems is better, ranging from 17% to 62% depending on the population and type of PPE performed.7 In addition, the reporting bias during history taking can lead to underreporting of problems. Athletes may feel uncomfortable answering specific health questions, especially those concerning sex, eating disorders, and drug use.25 These limitations can result in a false sense of security regarding the risk to an athlete when cleared in a PPE. More research needs to be done regarding the optimal, costeffective methods to screen for specific problems. Nevertheless, in a comprehensive form the PPE can be a valuable tool in providing health care to young individuals. Summary The preparticipation physical examination is a good starting point for the overall care of the athlete. Careful history

taking and proper screening examination should be performed to identify risk factors for injuries. Cardiac and orthopedic problems deserve special attention during the examination. Despite the limitations in fully meeting its primary and secondary objectives, the PPE presents a unique opportunity to reach the athlete with anticipatory care and guidance. The PPE needs continuing development to help achieve the ultimate goal of reducing the risk of injuries and making sports safer for young athletes.

References 1. Malina RM: Growth and maturation: Normal variation and effect of training. In: Gisolfi CV, Lamb DR (eds): Youth Exercise and Sports. Traverse City, Michigan: Cooper Publishing Group, 2001. 2. Pate RR, Trost SG, Levin S, et al: Sports participation and healthrelated behaviors among U.S. youth. Arch Pediatr Adolesc Med 154:904–911, 2000. 3. Bijur PE, Trumble A, Harel Y, et al: Sports and recreation injuries in U.S. children and adolescents. Arch Pediatr Adolesc Med 149:1009–1016, 1995. 4. Damore DT, Metzl JD, Ramundo M, et al: Patterns in childhood sports injury. Pediatr Emerg Care 19:65–67, 2003. 5. Garrick JG, Requa RK: Injuries in high school sports. Pediatrics 61:465–469, 1978. 6. McLain LG, Reynolds S: Sports injuries in a high school. Pediatrics 84:446–450, 1989. 7. American Medical Association: Athletic Preparticipation examinations for adolescents: Report of the board of trustees. Arch Pediatr Adolesc Med 148:93-98, 1994. 8. American Academy of Family Physicians, American Academy of Pediatrics, American College of Sports Medicine, American Medical Society for Sports Medicine, American Orthopaedic Society for Sports Medicine, American Osteopathic Academy of Sports Medicine: Preparticipation Physical Evaluation, Third Edition. Leawood, Kan.: The Physician and Sports Medicine, 2005, p 3. 9. Glover DW, Maron BJ: Profile of preparticipation cardiovascular screening for high school athletes. JAMA 279:1817–1819, 1998. 10. Maron BJ, Thompson PD, Puffer JC, et al: Cardiovascular preparticipation screening of competitive athletes. A statement for health professionals from the Sudden Death Committee (clinical cardiology) and Congenital Cardiac Defects Committee (cardiovascular disease in the young), American Heart Association. Circulation 94:850–856, 1996. 11. Fuller CM, McNulty CM, Spring DA, et al: Prospective screening of 5,615 high school athletes for risk of sudden cardiac death. Med Sci Sports Exerc 29:1131–1138, 1997. 12. Maron, BJ, Isner JM, McKenna WJ: The 26th Bethesda Conference: recommendations for determining eligibility for competition in athletes with cardiovascular abnormalities. J Am Coll Cardio 24:845–899, 1994. 13. American Academy of Pediatrics, Committee on Sport Medicine and Fitness: Medical conditions affecting sports participation. Pediatrics 107:1205–1209, 2001. 14. Smith J, Laskowski ER: The preparticipation physical examination: Mayo Clinic experience with 2,729 examinations. Mayo Clin Proc 73:419–429, 1998. 15. Risser WL, Hoffman HM, Bellah GG, et al: A cost-benefit analysis of preparticipation sports examination of adolescent athletes. J Sch Health 55:270–273, 1985. 16. Gallup EM: Law and the Team Physician. Champaign, Illinois: Human Kinetics, 1995. 17. Mitten MJ: Legal issues affecting medical clearance to resume play after mild brain injury. Clin J Sport Med 11:199–202, 2001. 18. Sideline preparedness for the team physician: a consensus statement. Med Sci Sports Exerc 33:846–849, 2001. 19. Bratton RL: Preparticipation screening of children for sports. Sports Med 24:300–307, 1997. 20. Rice SC, Schlotfeldt JD, Foley WE: The Athletic Health Care and Training Program: a comprehensive approach to the prevention and management of athletic injuries in high school. West J Med 142:352–357, 1985.

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21. DuRant RH, Seymore C, Linder CW, Jay S: The preparticipation examination of athletes: comparison of single and multiple examiners. Am J Dis Child 139:657–661, 1985. 22. Lysens R, Steverlynck A, Van den Auweele Y: The predictability of sports injuries. Sports Med 1:6–10, 1984. 23. Peltz JE, Haskell WL, Matheson GO: A comprehensive and costeffective preparticipation exam implemented on the World Wide Web. Med Sci Sports Exerc 31:1727–1740, 1999. 24. Maron BJ: Cardiovascular risks to young persons on the athletic field. Ann Intern Med 129:379–386, 1998. 25. Carek PJ, Futrell M, Hueston WJ: The preparticipation physical examination history: who has the correct answers? Clin J Sport Med 9:124–128, 1999. 26. Maron BJ, Gohman TE, Aeppli D: Prevalence of sudden cardiac death during competitive sports activities in Minnesota high school athletes. J Am Col Cardio 32:1881–1884, 1998. 27. Van Camp SP, Bloor CM, Mueller, et al: Nontraumatic sports death in high school and college athletes. Med Sci Sports Exerc 27:641–647, 1995. 28. Corrado D, Basso C, Schiavon M, et al: Screening for hypertrophic cardiomyopathy in young athletes. N Engl J Med 339:364–369, 1998. 29. Maron BJ, Shirani J, Poliac LC, et al: Sudden death in young competitive athletes. Clinical, demographic, and pathologic profiles. JAMA 276:199–204, 1996. 30. Pelliccia A, Maron BJ, Culasso F, et al: Athlete’s heart in women: echocardiographic characterization of highly trained elite female athletes. JAMA 276:211–215, 1996. 31. Gomez JE, Lantry BR, Saathoff KN: Current use of adequate preparticipation history forms for heart disease screening of high school athletes. Arch Pediatr Adolesc Med 153:723–726, 1999. 32. Viano DC, Bir CA, Cheney AK, et al: Prevention of commotio cordis in baseball: an evaluation of chest protectors. J Trauma 49:1023–1028, 2000. 33. Janda DH: Blunt impact to the chest and sudden death in young athletes. Clin J Sport Med 6:68, 1996. 34. Link MS, Maron BJ, Wang PJ, et al: Reduced risk of sudden death from chest wall blows (commotio cordis) with safety baseballs. Pediatrics 109:873–877, 2002. 35. Concussion in Sport (CIS) Group: Summary and agreement statement of the 1st International Symposium on Concussion in Sport, Vienna, 2001. Clin J Sport Med 12:6–11, 2002. 36. Practice parameter: The management of concussion in sports (summary statement). Report of the Quality Standards Subcommittee. Neurology 48:581–585,1997. 37. Lovell MR: The relevance of neuropsychologic testing for sportsrelated head injuries. Curr Sports Med Reports 1:7–11, 2002. 38. Collie A, Darby D, Maruff P: Computerised cognitive assessment of athletes with sports related head injury. Br J Sports Med 35:297–302, 2001. 39. Collins MW, Lovell MR, Iverson GL, et al: Cumulative effects of concussion in high school athletes. Neurosurgery 51(5):1175–1179, 2002. 40. Gerberich SG, Priest JD, Boen JR, et al: Concussion incidences and severity in secondary school varsity football players. Am J Public Health 73:1370–1375, 1983. 41. McCrory P: When to retire after concussion? Br J Sports Med 35:380–382, 2001. 42. AAP and AAO policy statement: Protective eyewear for young athletes. Pediatrics 98:311–313, 1996. 43. Nattiv A, Callahan LR, Kelman-Sherstinsky A: The female athlete triad. In: Ireland ML, Nattiv A (eds): The Female Athlete. Philadelphia: Elsevier Science, 2002, pp 223–235. 44. Koch JJ: Performance-enhancing substances and their use among adolescent athletes. Pediatr Rev 23, 2002. 45. Smith J, Dahm DL: Creatine use among a select population of high school athletes. Mayo Clin Proc 75:1257–1263, 2000. 46. Buckley W, Yesailis C, Friedl K, et al: Estimated prevalence of anabolic steroid use among high school seniors. JAMA 260:3441–3445, 1988. 47. Faigenbaum AD, Zaichkowsky LD, Gardner DE, et al: Anabolic steroid use by male and female middle school students. Pediatrics 101:E6, 1998. 48. McCarroll JR, Shelbourne KD, Porter DA: Patellar tendon graft reconstruction for midsubstance ACL rupture in junior high school athletes: an algorithm for management. AJSM 22:478–484, 1994. 49. Kocher MS, Micheli LJ, Zurakowski D, et al: Partial tears of the anterior cruciate ligament in children and adolescents. Am J Sports Med 30:697–703, 2002.

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50. Braverman AC: Exercise and the Marfan syndrome. Med. Sci Sports Exerc 30S:S387–S395, 1998. 51. Duke PM, Litt IF, Gross RT: Adolescents’ self-assessment of sexual maturation. Pediatrics 66:918–920, 1980. 52. McGrew CA: Insights into the AHA scientific statement concerning cardiovascular preparticipation screening of competitive athletes. Med Sci Sports Exerc 30:S351–S353, 1998. 53. Luckstead EF Sr:: Cardiac risk factors and participation guidelines for youth sports. Pediatr Clin North Am 49:681–707, 2002. 54. Drezner JA: Sudden cardiac death in young athletes: causes, athlete’s heart, and screening guidelines. Postgrad Med 108:37–50, 2000. 55. Salenius P, Vanka E: The development of tibiofemoral angle in children. J Bone Joint Surg Am 57:259, 1975. 56. Fabry G, MacEwen GD, Shands AR: Torsion of the femur. J Bone Joint Surg Am 55:1726–1738, 1973. 57. Bruce RW: Torsional and angular deformities. Common orthopedic problems I. Pediatr Clin North Am 43:867–881, 1996. 58. Vähäsarja V, Kinnuenen P, Lanning P, et al: Operative realignment of patellar malalignment in children. J Pediatr Orthop 15:281–285, 1995. 59. Staheli LT, Corbett M, Wyss C, et al: Lower-extremity rotational problems in children: normal values to guide management. J Bone Joint Surg Am 67:39–47, 1985. 60. Hintermann B, Nigg BM: Pronation in runners implications for injuries. Sports Med 26:169–176, 1998. 61. Song KM, Halliday SE, Little DG: The effect of limb-length discrepancy on gait. J Bone Joint Surg Am 79:1690–1698, 1997. 62. Birmingham TB: Test-reliability of lower extremity functional instability measures. Clin J Sports Med 10:264–268, 2000. 63. Fitzgerald GK, Lephart SM, Hwang JH, et al: Hop tests as predictors of dynamic knee stability. J Orthop Sports Phys Ther 31:588–597, 2001. 64. Shambaugh JP, Klein A, Herbert JH: Structural measures as predictors of injury basketball players. Med Sci Sports Exerc 23:522–527, 1991. 65. Post WR: Clinical evaluation of patients with patellofemoral disorders. Arthroscopy 15:841–851, 1999. 66. Smith AD, Stroud L, McQueen C: Flexibility and anterior knee pain in adolescent elite figure skaters. J Ped Orthop 11:77–82, 1991. 67. Hartig DE, Henderson JM: Increasing hamstring flexibility decreases lower extremity overuse injuries in military basic trainees. Am J Sports Med 27:173–176, 1999. 68. Decoster LC, Vailas JC, Lindsay RH, et al: Prevalence and features of joint hypermobility among adolescent athletes. Arch Pediatr Adolesc Med 151:989–992, 1997. 69. Micheli LJ, Greene HS, Cassella M, et al:Assessment of flexibility in young female skaters with the modified Marshall Test. J Pediatr Orthop 19:665–668, 1999. 70. Weidenbener EJ, Krauss MD, Waller BF, et al: Incorporation of screening echocardiography in the preparticipation exam. Clin J Sport Med 5:86–89, 1995. 71. Fuller CM: Cost effectiveness analysis of screening of high school athletes for risk of sudden cardiac death. Med Sci Sports Exerc 32:887–890, 2000. 72. Committee on Sports Medicine and Fitness, American Academy of Pediatrics: Intensive training and sports specialization in young athletes. Pediatrics 106:154–157, 2000. 73. Malina RM: Physical growth and biological maturation of young athletes. Exerc Sports Sci Rev 22:389–434, 1994. 74. Faigenbaum AD, Bradley DF: Strength training in the young athlete. Orthop Phys Ther Clin North Am 7:67–90, 1998. 75. Heidt RS Jr, Sweeterman, LM, Carlonas, RL, et al: Avoidance of soccer injuries with preseason conditioning. Am J Sports Med 28: 659-662, 2000. 76. Cahill, B., Griffith, E.: Effect of preseason conditioning on the incidence and severity of high school football knee injuries. Am J Sports Med 5:180-184, 1978. 77. Hewett TE, Lindenfeld TN, Riccobene JV, Noyes FR: The effect of neuromuscular training on the incidence of knee injury in female athletes. A prospective study. Am J Sports Med 27(6):699–706, 1999. 78. Mandelbaum B, Silvers HJ, Watanabe DS, et al: ACL prevention strategies in the female athlete and soccer: implementation of a neuromuscular training program to determine its efficacy on the incidence of ACL injury. American Orthopaedic Society for Sports Medicine Specialty Day 2002, Dallas, February 16, 2002.

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79. Hall MG, Ferrell WR, Sturrock RD, et al: The effect of the hypermobility syndrome on knee joint proprioception. Br J Rheumatol 34:121–125, 1995. 80. Borsa PA, Lephart SM, Irrgang JJ, et al: The effects of joint position and direction of joint motion on proprioceptive sensibility in anterior cruciate ligament-deficient athletes. Am J Sports Med 25:336–340, 1997. 81. Safran MR, Allen AA, Lephart SM, et al: Proprioception in the posterior cruciate ligament deficient knee. Knee Surg Sports Traumatol Arthrosc 7:310–317, 1999. 82. Bahr R, Bahr IA: Incidence of acute volleyball injuries:a prospective cohort study of injury mechanisms and risk factors. Scand J Med Sci Sports 7:166–171, 1997. 83. Fowler PJ, Flynn RK, Pedersen C, et al: The familial predisposition toward tearing the anterior cruciate ligament: a case-control study. Abstract. Annual Meeting of the American Academy of Orthopaedic Surgeons, News Orleans, February 9, 2003. 84. Fowler PJ, Pedersen C, Lebrun C, et al: The familial predisposition towards the anterior cruciate ligament tear. Abstract. 27th Annual Meeting of the American Orthopaedic Society for Sports Medicine, Keystone, Colorado, June 28, 2001. 85. Caraffa A, Cerulli G, Projetti M, et al: Prevention of anterior cruciate ligament injuries in soccer. A prospective controlled study of proprioceptive training. Knee Surg Sports Traumatol Arthrosc 4:19–21, 1996. 86. Cerulli G, Benoit DL, Caraffa A, et al: Proprioceptive training and prevention of anterior cruciate ligament injuries in soccer. J Orthop Sports Phys Ther 31:655–661, 2001. 87. Heidt RS Jr, Sweeterman LM, Carlonas RL, et al: Avoidance of soccer injuries with preseason conditioning. Am J Sports Med 28:659–662, 2000.

88. Lohrer H, Alt W, Gollhofer A: Neuromuscular properties and functional aspects of taped ankles. Am J Sports Med 27:69–75, 1999. 89. Albright JP, Powell JW, Smith W, et al: Medial collateral ligament knee sprains in college football. Effectiveness of preventive braces. Am J Sports Med 22:12–18, 1994. 90. Rovere GD, Haupt HA, Yates CS: Prophylactic knee bracing in college football. Am J Sports Med 15:111–116, 1987. 91. Albright JP, Powell JW, Smith W, et al: Medial collateral ligament knee sprains in college football. Effectiveness of preventive braces. Am J Sports Med 22:12–18, 1994. 92. Deppen RJ, Landfried MJ: Efficacy of prophylactic knee bracing in high school football players. J Orthop Sports Phys Ther 20:243–246, 1994. 93. Neptune RR, Wright IC, van den Bogert AJ: The influence of orthotic devices and vastus medialis strength and timing on patellofemoral loads during running. Clin Biomech 15:611–618, 2000. 94. Wenger DR, Mauldin D, Speck G, et al: Corrective shoes and inserts as treatment for flexible flatfoot in infants and children. J Bone Joint Surg Am 71:800–810, 1989. 95. Lyznicki JM, Nielsen NH, Schneider JF: Cardiovascular screening of student athletes. Am Fam Physician 62:765–784, 2000. 96. Carek PJ, Futrell M, Hueston WJ: The preparticipation physical examination history:who has the correct answers? Clin J Sport Med 9:124–128, 1999. 97. Risser WL, Hoffman HM, Bellah GG, et al: A cost-benefit analysis of preparticipation sports examination of adolescent athletes. J Sch Health 55:270–273, 1985. 98. Feinsten RA, Soileau EJ, Daniel WA Jr: A national survey of preparticipation physical examination requirements. Phys Sports Med 16:51–59, 1988. 99. Bradford BJ, Lyons CW: Preparticipation sports assessment in western Pennsylvania. J Adolesc Health 12:26–29, 1991.

Chapter 11

Anabolic Steroids and Other PerformanceEnhancing Substances in the Adolescent Athlete John M. Tokish

The use of androgenic anabolic steroids (AAS) and other substances to enhance performance and improve appearance has become mainstream. It is estimated that 1–3 million Americans have used anabolic steroids,1 with annual sales well in excess of $100 million. In addition, the socalled sports nutrition industry has also become an unregulated, burgeoning business, with annual sales estimated at $17.7 billion.2 This national phenomenon is reflected in today’s youth. By 1990, 250,000 high school students were users of AAS.3,4 Adolescent usage rates generally range between 4% and 12% among males and as high as 3% among females.5,6 Several studies note that a significant percentage of adolescents begin using AAS before the age of 10.7,8 Anabolic steroid use is associated with other high-risk behaviors such as substance abuse,6,9 unprotected sex, and suicidal ideation.10 Although anabolic steroids have received the most notoriety as ergogenic aids, other substances now garner attention as young athletes look for quick methods to improve performance and enhance appearance. Human growth hormone (hGH) is widely rumored as an anabolic agent, with use as high as 5% among teens.11 Amphetamines and other stimulants are commonly used in collegelevel athletes,12,13 as are over-the-counter supplements like creatine and androstenedione. Although little scientific data are available on many of these products with regard to use and effects, they are likely used at least as often as AAS, because many are legal, available, and aggressively marketed. Attempts have been made to affect the use and intention to use products like AAS by adolescents. Studies have shown that programs that emphasize “scare tactics” with

anabolic steroid use may actually increase interest and intention to use such products.14 A more effective approach to improving attitudes about potential AAS use emphasizes alternatives to AAS, such as strength training programs and nutritional education.15 Results of interventions like the Adolescents Training and Learning to Avoid Steroids (ATLAS) program16 have shown that a team-centered, sex-specific education program can be effective in reducing use rates of illicit drugs and anabolic steroids in the adolescent population. The ergogenic aid industry is poorly regulated but aggressively marketed. Much further study is warranted to provide data on the usage, effects, and health risks of these products. Androgenic Anabolic Steroids

KEY POINTS 1. 1–3 million Americans use anabolic steroids. 2. 4–12% of adolescents use steroids. 3. Steroid use is associated with other highrisk behaviors like substance abuse. 4. Up to 5% of high school students have used human growth hormone. 5. Team-centered education programs can be effective in reducing use rates in the adolescent population.

Androgenic anabolic steroids remain the most studied and concerning performance drug available. The data on these drugs are considerable with regard to use, effects, and side effects, and therefore make up the bulk of this chapter. From our knowledge of use rates 105

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and attitudes about these substances, we may make inferences regarding the future impact of other, less-studied products as they become available. This makes AAS the ideal focus for any study on the impact and effects of performance-enhancing drugs. The first use of steroids in American adolescents may have occurred in 1959 when a Texas physician reportedly administered Dianabol (methandrostenolone) to a high school football team.17 Studies from the 1980s suggested that 3.8% of high school students were current or former users of AAS.18 More recent data suggest that usage rates are on the rise, increasing 12% and 28% among twelfth graders and eighth graders, respectively, in 1998 alone.19 The following year was even more dramatic, with AAS usage by eighth grade boys increasing 56% from the previous year.16 The prevalence among high school boys has been consistent across several studies, with most showing AAS usage rates of 5–11%.3,20–22 The highest usage rate in this age group has been reported among high school football players,3,22,23 and rates do not seem to differ between rural and urban areas or with class size variation.9 Data from studies on younger students are no more encouraging. Faigenbaum et al.24 reported that usage rates among fifth, sixth, and seventh graders in Massachusetts averaged 2.7%, with near equal KEY POINTS distribution among boys and girls. Other studies have shown Anabolic steroid use that between 7% and 15% of 1. AAS usage rates conAAS users begin before the age tinue to climb among 7,8 of 10. In younger students, adolescents. gymnastics is the most common 2. Up to 15% of AAS sport associated with AAS use, users begin before with some suggesting that the the age of 10. side effect of stunted growth may 3. Gymnastics is the be a motivation for its use in this sport most commonly population.24 Such information associated with suggests that AAS intervention AAS use in programs begin before high children younger school and be targeted toward than age 10. both males and females. Basic Science AAS are chemically modified analogues of testosterone, the endogenous hormone primarily responsible for male sexual characteristics and muscle anabolism. This hormone was first isolated in 1935,25 and since then many attempts have been made to maximize the anabolic effects and minimize the androgenic effects of the drug. These attempts have included alkylation of the 17-alpha position or carboxylation of the 17-beta hydroxyl group on the sterol D ring. These analogues are much more slowly degraded than endogenous testosterone, resulting in a higher prolonged concentration of the analogue. The physiological action of AAS is thought to be similar to native testosterone. The molecule diffuses across the cell membrane after binding to a receptor. This complex then binds to the nucleus of a cell, stimulating messenger ribonucleic acid (RNA) synthesis, and leading to an increase in structural and contractile protein.26 In addition, AAS are thought to combat the catabolic effects of cortisol

through competitive inhibition of the glucocorticoid receptor, and to have a direct neural action through androgen receptors on alpha motor neurons.27 The normal adult testes secrete approximately 2.5 mg of testosterone per day. In contrast to this, bodybuilders have been reported to take 35–460 mg per day in various combinations.28,29 Performance Studies Very little data exist on the effects of anabolic steroid use in an adolescent population. However, there are several studies available on older populations.30–34 Although a few of these studies have shown minimal effect on body composition or strength,30,31 most show that supraphysiological doses of testosterone or its derivatives can lead to an increase in fat-free mass and muscle size and strength.32–34 In a prospective, placebo-controlled study of testosterone enanthate (TE) with and without exercise over a 10-week period, Bhasin et al.32 showed that weekly supraphysiological doses of TE increased triceps and leg area, as well as strength in the bench press (10 kg difference) and squat (17 kg difference) in subjects not engaged in strength training. In addition, those subjects assigned to TE administration and exercise had greater increases in fat-free mass (6 kg) and muscle size as well as strength (22 kg increase in bench press, 38 kg increase in squat), than those assigned to either no-exercise group. The authors concluded that supraphysiological doses of TE, especially when combined with strength training, lead to an increase in fat-free mass, muscle size, and strength in normal men. In another study of the effects of anabolic steroids on body composition and strength,34 21 weight-training men were randomly assigned in a double-blind fashion to either TE or placebo for 12 weeks, followed by a 12-week followup period. The TE group had significant increases in body weight, fat-free mass, arm girth, rectus femoris circumference, and libido over that of the placebo group. The TE group also experienced an increase in systolic blood pressure, frontal alopecia, mild acne, and subjective changes to personality, including increased aggression and irritability. The authors concluded that moderate doses of TE combined with weight training may result in short-term significant changes in upper body strength and composition, with changes to baseline health in some individuals. Forbes et al.33 also studied the effects of testosterone on healthy adult subjects and the effects on these individuals after the drug was stopped. These authors found that TE administration led to a progressive increase in lean body mass and a decrease in body fat. They also found that body composition reverted slowly toward normal when the injections were stopped, but they noted that the effects of the drug lingered for some time. They concluded that testosterone is a powerful anabolic agent that can have profound and lasting effects on body composition. Associations and Side Effects There have been a number of studies that have looked at associated behaviors and health risks in steroid users. These data are relatively consistent across these studies and show

Anabolic Steroids and Other Performance-Enhancing Substances in the Adolescent Athlete

that AAS use in adolescents is associated with lower selfesteem and disordered eating,6 poorer academic performance,35 substance abuse,6,9,23,29,35,36 engaging in unprotected sex,6 aggressive criminal behavior,23 depression,6 and suicidal ideation.10 Determining the specific health risks of AAS use is difficult. Because these drugs are illegal, there is a paucity of well-controlled studies available for review. Inconsistencies in type, dosing, and duration of use often make it difficult to draw statistically valid conclusions from the data that are available. In spite of this, a number of investigators have examined the consequences of AAS use. These studies support that AAS use likely has a causative role in hepatic cellular damage,37 gynecomastia,29 cardiovascular disease,38–40 and psychological disturbance.41,42 Specific to adolescents, these drugs also pose the risk of premature growth arrest.3,6,22 With regard to cardiovascular effects, there appears to be an association between an atherogenic blood lipid profile and endothelial dysfunction with steroid use.38–40 Ebenbichler et al.40 studied blood lipid profiles and flow-mediated dilatation (FMD) as an indicator for endothelial function in 20 male nonsmoking bodybuilders and compared their results to nonsmoking controls. The authors found that bodybuilders during a steroid cycle decreased high-density lipoprotein (HDL) and FMD, and that they suppressed luteinizing hormone and follicle-stimulating hormone levels compared with the controls. In addition, FMD was decreased both during and after completion of a steroid cycle. The authors concluded that intake of anabolic steroids is associated with both an atherogenic blood lipid profile and an endothelial dysfunction and thus may pose an increased KEY POINTS risk of atherosclerosis. Other studies have shown a relationship to Steroids: performance myocardial infarction.43,44 and side effects Another area of concern 1. Supraphysiological with AAS is the potential psydoses of AAS, chological effects associated with especially when 41 their use. Cooper et al. found combined with that anabolic steroid use directly strength training, caused significant disturbances in increase fat-free personality profile as assessed by mass, muscle size, the Diagnostic and Statistical and strength. Manual of Mental Disorders 2. AAS use in adoles(DSM3-R). Additionally, a study cents is associated by Midgley et al.42 showed that with lower selfanabolic steroid users reported esteem, disordered being significantly less in control eating, poorer acaof their aggression than subjects demic performance, in controls. Other studies have substance abuse, 6 noted increases in depression and depression, unpro45 dependence in adolescents. tected sex, and An additional, and perhaps suicidal ideation. underappreciated, health risk 3. Physiological side associated with the use of anaeffects include bolic steroids is that of infection hepatic cellular associated with needle sharing. damage, gyneco46 Rich et al. reported a 25% rate mastia, cardioof needle sharing among adolesvascular disease, cent anabolic steroid users. and premature Human immunodeficiency virus growth arrest. (HIV), hepatitis B and C, and

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abscesses have been documented among anabolic steroid injectors who share needles.47,48 Such health risks have led organizations like the American Academy of Pediatrics,49 the American College of Sports Medicine,50 and the National Strength and Conditioning Association51 to adopt strong stances condemning the use of AAS for performance enhancement. Motivation and Risk Factors for Use Among Adolescents Numerous studies have examined the motivation behind using AAS in adolescence. Several authors have noted that adolescent steroid use is part of a larger pattern of unhealthy lifestyle attitudes and behaviors.10,23,35 In young athletes the primary motivation appears to be performance improvement, whereas in nonathletes, appearance enhancement is the most commonly cited motivation.18,52 A theoretical model of AAS use and potential risk factors has been described.53 In this model, Goldberg et al. noted that AAS use was strongly influenced by peers, family, coaches, media, and sports figures,7 as well as by the perceived positive effects on strength and muscular size. Other possible risk factors include overestimation of use by peers, a win-at-allcosts attitude, the lack of information about the adverse effects of AAS, and belief in personal invulnerability to unwanted effects of these drugs.54 In another large study of adolescent health attitudes and their relation to AAS use, Irving et al6 noted that AAS use was strongly associated with social influences that encourage preoccupation and dissatisfaction with body weight. Irving and colleagues noted that AAS users were twice as likely to participate in a sport where there are specific perceived weight requirements. Steroid users were also more likely to have parents who are concerned about body weight, and male steroid users were more likely to have been teased about their weight by family members.6 Several studies have examined where adolescents get these illegal drugs.8,9,18 The most common sources are friends (30–65%), physicians (13–25%), coaches (16–30%), and parents (8–10%). With such strong social influences on adolescents, attempts to decrease intention to use anabolic steroids are recommended not only for athletes but also for significant others like peers, coaches, trainers, and parents.8,52 Interventions and Attempts to Decrease Usage among Adolescents Despite the now well-documented health risks and consequences associated with AAS use, the number of adolescents taking these drugs continues to grow.16,19 Methods to decrease usage among adolescents have included legislation, testing, education, and multidimensional intervention programs. From a legislative standpoint, attempts have been made to control distribution and possession of AAS. Under the 1988 Anti-Drug Abuse Act, the distribution or possession of AAS with intent to distribute them without a valid prescription is a felony offense. In addition, these drugs were added to Schedule III of the Controlled Substances

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Act of 1990.55 Interestingly, in one survey of high school athletes on reasons for not using AAS, only 5% of nonusers stated that they did not use because the drugs were illegal.8 Drug testing has been attempted in few high school districts.8 There are serious roadblocks to such testing: it is costly ($90–$120 per test)8 and although they have been upheld in the courts,56 there has been no prospective controlled study that has shown it to be effective.57 Nevertheless, the fear of getting caught or being tested has been cited as a reason for many AAS users to stop taking the drug.8 KEY POINTS Educational programs have also attempted to curb use rates, Risk factors for use and with mixed results. It has been attempts to curb use of shown that AAS users are more AAS familiar with the benefits of 1. Adolescents are steroids than nonusers, but motivated to use they are less familiar with the AAS because of a 3 risks. This finding has led many perceived increase to assume that increasing the in muscle size, knowledge of the risks would strength, and athletic lead to a decrease in usage rates. performance. One such program was begun by 2. AAS intent to use is 58 Goldberg et al. and aimed at strongly influenced high school football players in by peers, family, Oregon; it centered on an educacoaches, the media, tional program about steroids. and sports figures. Goldberg and colleagues found 3. Adolescent athletes that although such a program often possess a winimproved the understanding of at-all-costs attitude adverse effects associated with and a perception of use of AAS, it did not decrease personal invulnerabilintent to use. Furthermore, a ity to possible side second educational program by effects with drugs, 14 the same authors, that emphaoften making scare sized the harmful side effects of tactics about their AAS, appeared to have a use ineffective. rebound effect and actually 4. The possession of generated interest in the drugs AAS with intent to and increased intentions to distribute them withuse.59 More effective approaches out a valid prescripappear to employ alternatives to tion is a felony AAS use, such as strength trainoffense. ing techniques and nutritional 5. Drug testing has not counseling, in decreasing adolesbeen shown to be cents’ intention to use these effective, but many 15 drugs. users cite fear of getThe most effective program ting caught as a reato date in decreasing actual use son to stop. rates at the high school level is 6. The most effective 16 the ATLAS program. This proprograms to stop gram is a multidimensional usage include those interventional program consistthat are sex-specific, ing of classroom sessions, weight sports team– room training, and parent educentered, comprecation. It is a sex-specific, sports hensive educational team–centered approach based programs designed on social learning theory, and to redirect students’ uses an established social unit goal-directed (the sports team) to redirect stubehavior. dents’ goal-directed behavior.16

Peers direct a significant portion of the program, and the curriculum addresses the risk factors with AAS use, strength training, and sports nutrition.54 In addition, skills in how to refuse offers of AAS and other illicit drugs were taught and practiced. Weight room sessions are conducted weekly for 7 weeks and emphasize different strength training techniques, along with reinforcing other aspects of the curriculum. Finally, a single evening meeting is made available to parents to describe goals and to answer questions.54 The ATLAS program has resulted in increased understanding of AAS effects, greater belief in personal vulnerability to the adverse consequences of AAS, improved drug refusal skills, less belief in AAS-promoting media messages, increased belief in the team as an information source, improved perception of athletic abilities and strength training self-efficacy, improved nutrition and exercise behaviors, and reduced intentions to use AAS.54 Each of these goals has been maintained at 1 year after the intervention. Human Growth Hormone Although much less studied than AAS, there are increasing rumors that human growth hormone (hGH) is used as a performance-enhancing drug. Deficiency in hGH leads to small stature, whereas patients with an overabundance of the hormone have a condition called “gigantism” and are hallmarked by the large stature that justifies its name. This information alone is enough for many who seek increased size and strength to try this product as a performance enhancer. Because the drug is illegal without a prescription, well-controlled studies are lacking and its impact is unknown. One study has addressed the prevalence of use among adolescents.11 In this study of 432 Midwestern tenth graders, Ricket et al. reported that 5% of those surveyed responded that they had taken hGH. The users had a high association with AAS and reported first using the drug at 14–15 years of age. Most of the users in this study were unaware of any potential side effects. Much of the basic science of hGH remains unknown. The hormone is a large peptide that is secreted from the anterior pituitary gland. This secretion is regulated by a number of factors, including growth hormone–releasing hormone, sleep, exercise, L-dopa, and arginine.27 The halflife of this hormone is short, but it does stimulate the release of somatomedins, like the insulin-like growth factors. In addition, hGH stimulates the systemic breakdown of fat, called lipolysis, and hepatic gluconeogenesis.27 Performance studies in humans are lacking because of the illegal nature of the drug for performance issues. Animal studies have shown that administration of hGH leads to muscle hypertrophy, but this is not associated with increased strength.60 In patients with acromegaly, or gigantism, increases in hGH do lead to larger (but functionally weaker) muscles.60 Adolescents who take hGH do so because they believe it will build bigger and stronger muscles, prevent muscle catabolism after cessation of AAS use, or will protect muscle and tendons from injury.61 None of these perceptions have been shown with any validity. There has been one study done in elderly men with low endogenous hGH levels.62 This study by Taaffe et al. showed that hGH

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supplementation had no effect on muscle strength at any time in the study. Other data exist in critically ill populations63 that show that administration of hGH leads to higher mortality rates. Given this data, there appears to be no evidence that hGH is effective as a performance-enhancing drug. Side effects to hGH use include myopathic changes,60 water retention, carpal tunnel syndrome, and insulin resistance.64 This substance is banned by the International Olympic Committee (IOC) and the National Collegiate Athletic Association (NCAA) but awaits an accurate testing protocol.

KEY POINTS Human growth hormone 1. Up to 5% of the U.S. adolescent population has taken hGH. 2. Most users begin at 14–15 years old. 3. No study has shown any performance benefit with hGH supplementation. 4. Side effects of hGH use include myopathic changes, carpal tunnel syndrome, and insulin resistance. 5. The NCAA and IOC have banned hGH.

Amphetamines and Other Stimulants The use of stimulants as fat-loss supplements or performance enhancers has recently come under scrutiny with several deaths in professional athletes who were reportedly supplementing with these products. Ephedrine, a previously available over-the-counter herbal supplement that was banned in 2004, claims to increase metabolism, burn fat, and increase alertness. These claims have made it a popular supplement among pilots, truck drivers, and in the general population. Supplements such as the Chinese herb ma huang or guarana have similar actions to amphetamines. Little data are available on the usage rates among athletes. Green et al.12 performed a large KEY POINTS study of the NCAA and found that 2.5–3.7% of athletes used amphetStimulants amines, with 3.0–4.2% specifically 1. Stimulant use to using ephedrine. In contrast to this, enhance performBents et al.13 surveyed a Division I ance is alarmingly hockey league and found that high in some NCAA nearly half of players admitted to athletic populations. using ephedrine within the last 2. These drugs, related year. Such wide variation implies to catecholamines, that more study is needed. have been reported Amphetamines are chemieffective in fatigue cally related to the cateresistance, mood cholamines and have an indirect elevation, and anaeraction on catecholamine metabobic capacity. olism. In this way they stimulate 3. Ephedrine and other the release of norepinephrine stimulants have been from sympathetic nerves, resultassociated with ing in vasoconstriction and anxiety, ventricular increased blood pressure. In addidysrhythmias, tion, mood elevation and fatigue hypertension, and resistance have been reported death. 65 with the use of these drugs. 4. In 2002, the NCAA Several studies have evaluadded ephedrine to ated various stimulants as its list of banned ergogenic aids. Chandler et al.66 stimulants. showed that administration of

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Dexedrine resulted in improvements in quadriceps strength and anaerobic capacity, as well as time to exhaustion. Other authors have noted that administration of pseudoephedrine before cycle testing induced significant improvements in maximum torque, peak power, and improved lung function.67 Amphetamines have been associated with a number of negative side effects including anxiety, ventricular dysrhythmias, hypertension, hallucinations, and more recently, death. In addition, use among weight lifters has been associated with addiction.68 These health risks have moved the NCAA to add ephedrine to its list of banned stimulants in 2002. Androstenedione Androstenedione (andro) has gained enormous popularity as an over-the-counter ergogenic aid since Major League Baseball player Mark McGwire admitted to using it during the 1998 season, in which he broke the single-season record for home runs. Andro has been available since the 1930s and is marketed as being a “pro-hormone” that will naturally raise testosterone levels in the blood. As with many of these so-called natural nutritional supplements, the marketing is far more advanced than the science. Because andro is the immediate precursor to testosterone, any anabolic effect that KEY POINTS it may have is assumed to work in much the same way as testosAndrostenedione terone does. It is postulated that 1. Androstenedione is a if one increases the concentrapro-hormone that is tion of andro, the concentration marketed as a of testosterone will also be “pro-hormone” that increased. This claim has been will naturally raise evaluated by a number of studtestosterone levels in 69–75 ies, with the majority showblood and thereby ing no increase in testosterone improve athletic concentrations after supplemenperformance. 69–73 tation with andro. Two 2. Studies are mixed as 74,75 other studies did show an to whether andro will increase in testosterone with increase testosterone andro supplementation. All of in blood. the aforementioned studies 3. Studies universally have shown a disproportional agree that andro will increase in the female hormone, raise estrogen levels. estrogen. Although andro has 4. No study has been examined for performance shown any performenhancement or ability to affect ance enhancement body composition in a number with andro of trials,69,71,73 no study has supplementation. shown it to be effective in either 5. Side effects include area. alteration of blood Side effects with andro lipid profiles and a supplementation are similar to postulated downAAS use, with an alteration of regulation of 69,73,76 blood lipid profiles, and a testosterone postulated down-regulation of synthesis. testosterone synthesis.73 Creatine Since its introduction in 1992, creatine has become among the most popular nutritional supplements on the market.77

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According to the Nutrition Business Journal, sales for the year 2000 were estimated at more than $300 million in the United States alone, a three-fold increase since 1997. The first reported use of creatine by elite athletes occurred during the 1992 Barcelona Olympics78; it has since become popular in anaerobic sporting events. Several prevalence studies of its use among college athletes quote a usage rate of 41–48% among males.79,80 In a recent survey of NFL trainers and team physicians, all teams had players actively taking the supplement, with estimates of use averaging 33%, and reports as high as 90%.81 Basic Science Creatine is a naturally occurring compound made from the amino acids glycine, arginine, and methionine. Primarily synthesized in the liver, pancreas, and kidney, 95% of the creatine is stored in skeletal muscle. Exogenous sources of creatine include fresh fish and meat, but in small amounts that do not equal the estimated 2 g daily turnover.82 In its phosphorylated form, creatine contributes to the rapid resynthesis of adenosine triphosphate (ATP) during short duration maximal bouts of anaerobic exercise. This mechanism forms the basis for creatine supplementation. In 1992, Harris et al. showed that oral creatine supplementation resulted in a significant increase in the total creatine content of the quadriceps femoris muscle, in some subjects as high as 50%.83 Further studies by Balsom et al.84 have shown that creatine supplementation may put off or decrease anaerobic glycolysis during brief maximal exercise. These mechanisms may enhance anaerobic training, leading to strength and performance gains in these athletes. Performance Studies Human performance with creatine supplementation has been studied extensively. In weight lifters the number of repetitions at a specified percentage of single repetition maximum (1RM) goes up approximately 20–30% after a short-term creatine supplementation period.85–87 In cyclists, most studies have shown that creatine supplementation is effective in maintaining muscular force and power output.88–90 In swimming, performance has been measured with repeated short sprints of maximal intensity. Results have been mixed, with some studies showing a significant reduction in sprint times,91,92 whereas others have found the opposite and concluded that creatine supplementation is not effective in swimmers.93,94 Differences in these studies may be attributed to different outcome measures, the complex mechanics of the swimming stroke, or different supplementation regimens. In track-and-field sprinters, several studies have shown an improvement in average sprint times in the range of 1–2%,95–98 whereas authors of two other studies concluded that creatine had no effect on single sprint times.99,100 In terms of body composition changes, creatine supplementation appears to increase weight and lean body mass84,85 of around 1–2 kg over a short-term supplementation cycle. In summary, creatine can be an effective ergogenic supplement maximized when used for simple, short duration, maximal effort anaerobic events.

Side Effects Since the introduction of creatine in the early 1990s, there have been a number of isolated case reports of possible renal side effects associated with its use.101–103 Although commonly thought to lead to dehydration, to date, there has been no study that has demonstrated a negative side effect with the use of creatine in athletes. It should be cautioned, however, that the studies that have been done are mostly short-term, and in healthy individuals. One additional drawback to creatine deserves further mention. Because it is not classified as a drug, creatine is not under direct regulation by the Food and Drug Administration (FDA). This is a problem receiving much attention throughout the supplement industry, and although there is effort to control nutritional supplements in the United States, the quality of individual brands of creatine and other nutritional supplementation remain far from uniform. This lack of uniformity makes creatine difficult to study and even harder to control.

KEY POINTS Creatine 1. Creatine is a naturally occurring substance that regenerates ATP during maximum anaerobic exercise. 2. Creatine supplementation will increase creatine levels in the blood. 3. Creatine supplementation has been shown to be effective in improving performance in simple anaerobic events of short duration. 4. Side effects may include dehydration and muscle cramping, but no study has shown a negative side effect in athletes. 5. Like many supplements, creatine is not regulated by the FDA, and therefore individual brands may not be true to their labeled content.

Summary The use of steroids to enhance performance or improve appearance is a national common practice. Their use is often associated with numerous health risks and unhealthy behaviors. Adolescents use these drugs for both sports performance enhancement and improved physical appearance, and are under great influence from their parents, coaches, and peers. Interventions to decrease use of these drugs should be multidimensional and involve parents in educating teens to the alternatives of AAS use. Finally, such interventions should perhaps begin before high school, because a significant number of kids begin using these drugs before the age of 10. There are a number of other drugs and supplements that have become available more recently. Although the data on these products are not nearly as advanced as that pertaining to AAS, one can use the study of AAS as a framework for preparation for these other substances. Such a framework will help predict who is at risk to use these supplements, and approaches that will be effective in prevention. Unfortunately, parents, coaches, and sports medicine staff are often poorly educated about these substances, as well as their alternatives, and are therefore are not positive influences for these kids. Education and intervention programs are important deterrents to current and future performance-enhancing drugs.

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Chapter 12

Special Concerns in the Female Athlete Mary Lloyd Ireland

Young female athletes have a disturbingly high rate of anterior cruciate ligament (ACL) tears and anterior knee pain complaints. These gender differences are real and multifactorial. Anterior knee pain is a very common problem in repetitive training sports such as cheerleading, dance, and cross-country running. ACL tears are the plague of female adolescent basketball and soccer players. However, other conditions are more common in males, including OsgoodSchlatter disease and Sinding-Larsen-Johansson syndrome. Osteochondritis dissecans is 3–4 times more common in males than in females.1 Salter-Harris fractures of distal femur, proximal tibia, and tibial tubercle apophyseal injuries and tibial eminence fractures are more common in males than in females. ACL tears and anterior knee pain will be the focus of this chapter. The female athlete triad will be defined to increase awareness of this diagnosis, which is often made too late to provide a cure. Every year, more males and females participate in organized sports at the high school and college levels.2,3 According to the National Federation of State High School Associations, for the 2002–2003 season, 3,988,738 males and 2,856,358 females participated in high school athletics. Coed participation totaled 19,289 athletes. The progressive increase in sport participation by high school girls compared to boys is shown from the years 1971 to 20032 (Figure 12–1). In the 1971–1972 school year, athletes at the high school level were made up of 3,666,917 boys and 294,015 girls. By the 1980-1981 school year, boys made up 3,500,124 of the athletes and girls rose to 1,853,789. The ratio of boys to girls was 1.4:1 in 1999–2000. Between 1971 and 1994, the number of girls participating in high school sports compared to female students rose from 1 in 27 to 1 in 3.4,5 The National Collegiate Athletic Association (NCAA) in the three divisions of colleges for the years 2000–2001, reported 157,740 female and 217,115 male participants.6 The years from 1989 to 2001 are shown in groups of females, males with football, and males excluding football (Figure 12–2).

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Susan M. Ott

Ratios of males to females participating at the collegiate level in all divisions is 1.4:1. Since the passage of Title IX in 1972, there has been a progressive trend toward equalization of men and women at federally funded colleges. With football eliminated, the ratio comparing males and females competing in college is equal.3 Unfortunately, the number of knee injuries is also on the rise. At the high school level, Powell et al.3 reported the number of injuries over a 3-year period and serious knee injuries as the percentage of athletes undergoing knee surgery divided by the number of participants in their respective sports. The top two sports necessitating knee surgeries were girls’ basketball, followed by girls’ soccer. For knee surgeries the percentage of girls compared to boys in basketball was 4% and 2%, respectively; in soccer, 3.9% and 2%, respectively. In male-only sports the percentage of reported knee surgery cases was 2.4% in football and 2% in wrestling. The numbers and relative risk of knee-injured males and females were analyzed at Kentucky Sports Medicine (KSM) over a 13-year period (personal communication, unpublished). Genders were compared for three conditions, all knee diagnoses inclusive, plica syndrome, and ACL tears. The three diagnoses were evaluated in four age groups: younger than 15 years, high school age, college age, and older than age 23. Relative risk was calculated as the ratio of percentages of females to males in each of the four age groups. The relative risk was higher in females, younger than age 15, for all categories: plica (1.6), ACL injury (2.0), and all (1.4) (Table 12–1). Athletes undergoing ACL reconstruction at KSM were analyzed for relative risk. The ratios of females to males were 7:1 in younger than age 15 and 1.8:1 in high school age, 0.96 in college age, and 0.16 older than age 23. Athletes undergoing ACL reconstruction who were playing basketball and soccer when injured were further analyzed. For ACL reconstruction the relative risk in 113

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Figure 12–1 High school athletics participation survey, 1971–2003.

1989–1990 1990–1991 1991–1992 1992–1993 1993–1994 1994–1995 1995–1996 1996–1997 1997–1998 1998–1999 1999–2000 2000–2001

Ratio M:W 1.99 Ratio (M–Football):W 1.55 Ratio (%) W:M 50.4% Ratio (%) W:(M–Football) 64.6%

1.99 1.45 50.3% 68.8%

1.93 1.41 51.9% 70.8%

1.87 1.37 53.4% 72.7%

1.84 1.36 54.4% 73.8%

1.71 1.25 58.5% 80.0%

1.61 1.18 62.3% 84.4%

1.55 1.13 64.3% 88.2%

1.51 1.10 66.3% 90.7%

1.42 1.04 70.4% 96.2%

1.42 1.03 70.3% 97.2%

1.38 1.00 72.7% 99.6%

220,000 211,273

208,957

217,115 208,481

200,000

203,189

193,928 184,593

203,686

186,046 189,084

187,041

180,000 177,166

160,000

158,404

154,746

154,130 148,235

150,888

148,893

157,740

143,080

140,000

138,124

134,930

136,252

148,802

137,273 138,128

146,618

130,098 135,110 130,700

120,000 105,532 96,467

100,000

110,524

99,859

92,778

Women Men

89,212

80,000

Men without football

1989–1990 1990–1991 1991–1992 1992–1993 1993–1994 1994–1995 1995–1996 1996–1997 1997–1998 1998–1999 1999–2000 2000–2001

Men as % of total 66.5% Women as % of total 33.5%

66.6% 33.4%

65.9% 34.1%

65.2% 34.8%

64.8% 35.2%

63.1% 36.9%

61.6% 38.4%

60.9% 39.1%

60.1% 39.9%

58.7% 41.3%

58.7% 41.3%

57.9% 42.1%

Figure 12–2 Ratios of men to women in college sports, 1989–2001. (Data from National Collegiate Athletic Association [NCAA] Injury Surveillance System.)

381 628 276 1328 2613

181 423 221 1182 2007

Males 562 1051 497 2510 4620

Total 2.10 1.48 1.25 1.12 1.30

Ratio F:M 1.6 1.1 1.0 0.9

Relative Risk 65 370 166 474 1075

Females 56 444 303 1068 1871

Males 121 814 469 1542 2946

Total

ACL Diagnoses

Notes: 1. Age of each patient was determined as of the time the patient was originally diagnosed. 2. “High School” age group is ≥15 and 1 cm), is easily accessible, involves a weightbearing area, and has adequate cortical bone attached to the chondral surface, fixation should be attempted (Figures 23–21 and 23–22). This can be done via arthroscopy or arthrotomy with smooth or threaded Steinmann pins or screws countersunk below the articular surface. If the fracture fragment is small, loose, and from a non-weight-bearing region of the knee, then arthroscopic excision is recommended (Figure 23–23). The fragment’s crater should be debrided to stable edges, and the underlying subchondral bone should be perforated to encourage fibrocartilage formation. In patients with an osteochondral fracture after acute patellar dislocation, concomitant repair of the medial retinaculum at the time of fragment excision or fixation produces the best results. Postoperatively, patients treated by excision of the fragment can begin range-of-motion exercises immediately. Crutches may be necessary in the immediate postoperative period, but patients can progress to weight bearing as tolerated. If the patient has the fragment fixed, initial immobilization with

Figure 23–23 Excision of osteochondral fragment.

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protected weight bearing is necessary. Weight bearing is gradually progressed, and full weight bearing is allowed when the swelling has subsided and radiographs show evidence of fracture healing. Return to athletic activities is permitted when full range of motion is recovered and quadriceps strength is symmetrical. References

KEY POINTS 1. If the osteochondral fracture is greater than 1 cm and involves a weightbearing area, then fixation should be attempted. 2. In patients with an osteochondral fracture after an acute patellar dislocation, the medial retinaculum should be repaired at the fracture fixation.

1. Kocher MS, Micheli LJ: The pediatric knee: evaluation and treatment. In Insall JN, Scott WN (eds): Surgery of the knee, 3rd ed. New York: Churchill-Livingstone, 2001, pp 1356–1397. 2. Hangody L, Fules P: Autologous osteochondral mosaicplasty for the treatment of full-thickness defects of weight-bearing joints. J Bone Joint Surg Am 85(suppl 2):25–32, 2003. 3. Curl WW, Krome J, Gordon ES, et al: Cartilage injuries: a review of 31,516 knee arthroscopies. Arthroscopy 13:456–460, 1997. 4. Poole AR: What type of cartilage repair are we attempting to attain? J Bone Joint Surg Am 85(suppl 2):40–44, 2003. 5. Ochi M, Uchio Y, Kawasaki K, et al: Transplantation of cartilage-like tissue engineering in the treatment of cartilage defects of the knee. J Bone Joint Surg Br 84:571–578, 2002. 6. Brittberg M, Lindahl A, Nilsson A, et al: Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation. N Engl J Med 331:889–895, 1994. 7. Peterson L, Brittberg M, Kiviranta I, et al: Autologous chondrocyte transplantation. Biomechanics and long-term durability. Am J Sports Med 30:2–12, 2002. 8. Hangody L, Kish G, Karpati Z, et al: Arthroscopic autogenous osteochondral mosaicplasty for the treatment of femoral condylar articular defects. A preliminary report. Knee Surg Sports Traumatol Arthrosc 5:262–267, 1997.

9. Shelbourne KD, Jari S, Gray T: Outcome of untreated traumatic articular cartilage defects of the knee. J Bone Joint Surg Am 85(suppl 2):8–16, 2003. 10. Brittberg M, Winalski CS: Evaluation of cartilage injuries and repair. J Bone Joint Surg 85(suppl 2):58–69, 2003. 11. Outerbridge RE: The etiology of chondromalacia patellae. J Bone Joint Surg Br 43:752–759, 1961. 12. 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. 13. Messner K, Maletius W: The long-term prognosis for severe damage to weight-bearing cartilage in the knee: a 14-year clinical and radiographic follow-up in 28 young athletes. Acta Orthop Scand 67:165–168, 1996. 14. Nietosaara Y, Aalto K, Kallio PE: Acute patellar dislocation in children: Incidence and associated osteochondral fractures. J Pediatr Orthop 14:513–515, 1994. 15. Stanitski CL, Paletta GA: Articular cartilage injury with acute patellar dislocation in adolescents. Am J Sports Med 26(1):52–55, 1998. 16. Matelic TM, Aronsson DD, Boyd DW, et al: Acute hemarthrosis of the knee in children. Am J Sports Med 23:668–671, 1995. 17. Farmer JM, Martin DF, Boles CA, et al: Chondral and osteochondral injuries. Clin Sports Med 20:299–319, 2001. 18. Alleyne KR, Galloway MT: Management of osteochondral injuries of the knee. Clin Sports Med 20:343–363, 2001. 19. Birk GT, DeLee JC: Osteochondral injuries. Clin Sports Med 20:279–287, 2001. 20. Flachsmann R, Broom ND, Hardy AE, et al: Why is the adolescent joint particularly susceptible to osteochondral shear fracture? Clin Orthop Rel Res 381:212–221, 2000. 21. Bohndorf K: Imaging of acute injuries of the articular surfaces (chondral, osteochondral, and subchondral fractures). Skeletal Radiol 28:545–560,1999. 22. Wessel LM, Scholz S, Rusch M, et al: Hemarthrosis after trauma to the pediatric knee joint: what is the value of magnetic resonance imaging in the diagnostic algorithm? J Pediatr Orthop 21(3):338–342, 2001. 23. Menche DS, Vangsness CT, Pitman M, et al: The treatment of isolated articular cartilage lesions in the young individual. Instr Cours Lect 47:505–515, 1998.

Chapter 24

Anterior Cruciate Ligament Injuries Richard Y. Hinton

Anterior cruciate ligament (ACL) insufficiency in the skeletally immature is one of the most exciting areas of orthopedic sports medicine today. Improved diagnostics, increased professional and public awareness, and changes in sports participation have led to an increased recognition of ACL injuries among young athletes. The “best” treatment for these patients is controversial, and intervention must be tempered by a variety of factors unique to each young athlete and their sporting environment. The question of “what to do and when to do it” is often framed as a debate.1 A somewhat “conservative” pediatric orthopedic viewpoint is usually paired against a more “aggressive” adult sports medicine opinion. The former may underestimate the consequences of cumulative meniscal and articular cartilage damage while overestimating the risk of surgery-related leg length discrepancy. The latter may not appreciate the nuances of skeletal maturation and underestimate the risk of iatrogenic angular deformity. The treating physician must have a working knowledge of normal growth and development, injury risk factors, nonoperative options, and a complete armamentarium of surgical skills. The literature on ACL deficiency in the skeletally immature suffers from a lack of age-specific basic science, small clinical cohorts that often combine a variety of maturation levels and treatment interventions, and little information on outcomes into maturation. It must be remembered that “skeletal immaturity” represents a wide spectrum. What is best for the high level, postmenarchal 13-year-old female soccer player may not be best for the less athletic, 13-year-old boy next door. In this chapter, we will focus on ACL insufficiency in the skeletally immature with special emphasis on the young athlete. We will review the available literature, suggest the practical applications of this information, and discuss our experiences in diagnosis and treatment of these injuries.

●

Krishn M. Sharma

Embryology and Congenital Deformity Embryology During the sixth week of gestation the lower limb buds are well formed, and appreciable development of the knee joint begins. A rapid differentiation ensues, and over the next 2 weeks, all intraarticular structures become recognizable in their adult form.2–4 During days 44–45, at a crown rump length (CRL) of 15–16 mm, a homogenous, mesenchymal interzone is found between the chondrifying distal ends of the femur and tibia. During days 46–47, at a CRL of 16–19 mm, this interzone begins to differentiate. Cells that will form the menisci are densely packed toward the periphery. Facing the intercondylar fossa, obliquely oriented loose strands are now recognizable precursors to the cruciate ligaments. The early ACL is relatively ventral and progressively invaginates with the formation of the intercondylar notch. The ACL appears before joint capsular formation (days 50–52, at a CRL of 23.5–24.5 mm) and remains extrasynovial at all times. ACL development is temporally and spatially associated with that of the menisci. Their common blastemal origins and development suggest shared function. Congenital deficiencies of these structures are often seen in combination. By day 52, at a CRL of 26–27.5 mm the cruciate ligaments are distinct, well-oriented bands of connective tissue surrounded by loosely organized vascular elements.3,4 The formation of the ACL and other major knee structures is genetically programmed. Later, function, but not initial form, is dependent on motion and functional demands.5 Congenital Deformity Congenital absence of the ACLs can occur in isolation but most frequently travel with other knee joint anomalies, lower extremity dysplasias, or syndromic conditions. These may 317

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include congenital knee dislocation, congenital short femur, tibial/fibular dysplasia, lower extremity angular deformities, patella hypoplasia and instability, absence or congenital malformation of the menisci, tarsal coalition, absence of the posterior cruciate ligament (PCL), congenital thrombocytopenia, and absent radius syndrome.6–12 Congenital knee dislocation is related to absent or hypoplastic cruciate ligaments coupled with an environment of joint hyperextension.5 In addition to graded tibiofemoral luxation, there are often dysplastic changes in the intercondylar notch and tibial spines.5,13 Similar changes can occur with congenital cruciate absence without dislocation. Johansson et al.8 reported different radiographic deformities in isolated ACL versus combined ACL and PCL absence. The authors have found similar changes on arthroscopic examination (Figure 24–1, A and B).8 Congenital KEY POINTS absence rarely results in debilitating instability; however, in those 1. ACL development cases requiring reconstruction, is temporally and special attention must be given to spatially associated aggressive notchplasty and definwith that of the ing appropriate landmarks for menisci. Their tunnel placement. Congenital common blastemal cruciate dysfunction is a risk facorigins and develtor for knee subluxation during opment suggest 14 limb lengthening. If radiographic shared function. or clinical signs of absence are 2. Congenital absence present, diligence must be given to of the ACL is preventing knee subluxation durcommonly associing the lengthening period. ated with leg length Discoid and other aberrant menisdiscrepancies, cal forms also commonly travel meniscal malformawith congenital anomalies of the tions, and other cruciate ligaments. Associated deformities of the mechanical symptoms usually knee joint and lower resolve by addressing the meniscal extremity. 15,16 pathology. Anatomy and Biomechanics Anatomy The ACL is an intraarticular extrasynovial complex structure traversing from the inner wall of the posterolateral femoral condyle to insert anterior and lateral to the medial intercondylar tubercle of the tibia. The complex bony insertions are more than three times greater in area than the ligament at its mid-substance. The femoral and tibial origins have been delineated and described in detail for the adult ACL.2,17,18 Two studies19,20 have investigated the femoral and tibial origins of the ACL in the skeletally immature. Behr and associates19 have described the anatomy and histology of the femoral origin of the ACL in human fetal specimens (gestational ages 20–36 weeks) and skeletally immature knee samples (ages 5–15 years). In all specimens the ACL originated from the posterior epiphysis of the lateral femoral condyle immediately distal to the distal femoral physes. The origin was found to be completely epiphyseal. The distance from the most superior aspect of the femoral ACL origin to the physis averaged 2.66 +/− 0.18 mm, and there was no significant change in this relationship with growth of the femur. This

Figure 24–1 Posteroanterior (PA) radiograph of bent knee showing absence of ACL and PCL (A) and absence of ACL (B). (Reprinted with permission from Johansson E, Aparisi T: Missing cruciate ligament in congenital short femur. J Bone Joint Surg Am 65:1109–1115, 1983).

close association of ACL origin to the physis makes placing an adequate-sized tunnel in an anatomical fashion while remaining reliably all intraepiphyseal, a significant technical challenge. The “over-the-top position” was adjacent and immediately posterior to the distal femoral physis. Grooving of this area to move a graft more anterior could result in damage to the perichondral ring (Figure 24–2).

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ture girls, values for anterior limit, center point, and posterior limit of the ACL with relation to tibial anterior to posterior width were 28%, 46%, and 63%, and roof angle was 38 degrees. Corresponding values for adult females were 28%, 44%, and 60%, and roof angle was 35 degrees. For boys, the comparable values were 27%, 43%, and 59%, and roof angle was 40 degrees; for mature men the values were 28%, 44%, and 59%, and roof angle was 37 degrees. Although different in size, the anatomical landmarks for locating the appropriate tibial tunnel are proportionate in the adult and skeletally immature knee. Biomechanics

Figure 24–2 Posterior view of fetal specimen showing epiphyseal origin of ACL (curved arrow) and close proximity of over-the-top position and distal femoral physis (straight arrow). (Reprinted with permission from Behr CT, Potter HG, Paletta GA, Jr.: The relationship of the femoral origin of the ACL and the distal femoral physeal plate in the skeletally immature knee. An anatomic study. Am J Sports Med 29:781–787, 2001).

At gestational ages less than 24 weeks, the insertion of the ACL was confluent with the posterior femoral periosteum. From 24 to 36 weeks, there was a gradual establishment of an adultlike zonal insertion, with the ACL transitioning to fibrocartilage, minimal fibrocartilage, and then epiphyseal bone. Shea et al.20 measured the anterior limit, center point, posterior limit, and roof angle of the ACL with regard to the proximal tibia in a large group of skeletally immature children. They found little gender or age variability. In skeletally imma-

The ACL is most frequently divided into anteromedial and posterolateral bundles, named by their attachment points on the tibia. The smaller anteromedial bundle is tightest in flexion; the posterolateral bundle tightens as the knee moves into extension. Complete transaction of the anteromedial bundle may not be detectable on clinical examination.21,22 If a “partial tear” is associated with clinical laxity, it may result in a functionally complete injury. The natural history of partial ACL injury in children may differ from that of the adult, however. Kocher et al. found that only 31% of arthroscopically confirmed partial ACL injuries in children required reconstruction. The ACL is the primary restraint to anterior translation of the tibia on the femur and is the primary ligamentous stabilizer of the knee during jump, cut, and twist sporting activities. The ACL carries only small loads during normal daily function. Its complex microstructure allows low, commonly encountered forces to be taken up by relaxation of interligamentous crimp. As increasing forces are encountered, the stress/strain curve becomes more linear and more fibers are recruited.18 Anterior cruciate ligament failure occurs only in high-stress situations, which often combine large external loads and internal muscular forces. In the skeletally immature, the ACL is in the middle of a complex viscoelastic chain (Figure 24–3). Based on

Figure 24–3 The weak link is relative in the complex viscoelastic chain of the skeletally immature knee. (Adapted from Ligamentous injury of the knee. In Stanitski CL, DeLee JC, Drez D, Jr. [eds]: Pediatric and Adolescent Sports Medicine. Philadelphia: WB Saunders, 1994, pp 406–432.

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environmental loading conditions and host maturation characteristics, different parts of this viscoelastic chain may be the “relative” weak link. The traditional thinking has been that ligament rupture does not occur before complete physeal closure. More recently the concept of relative weakness, load-dependent failure, and graduated age-related changes have gained acceptance.23 The age-dependent transition from tibial bony avulsion to intrasubstance tear appears to occur between ages 12 and 13, well before complete physeal closure.24,25 NOTE: The authors have seen intrasubstance tears in children as young as 4 years old, and many in the 6–14 age range. Other factors, such as notch width, energy levels, and mechanism of injury, may effect whether a tibial spine avulsion or intrasubstance tear KEY POINTS occurs.72 There are little normative data for ACL function in the 1. The relative skeletally immature. Animal studpositions of the 26–28 ies have reported significant femoral and tibial age-related changes in ligament insertions of the biomechanics. There are wellACL are established documented associations between early in developage and gender with generalized ment and are similar joint laxity.29 However, the relato those found in the tionship between joint laxity and adult knee. specific ligament function is 2. In the skeletally unclear. Hormonal influences on immature knee, the peripheral ligament function ACL is in the middle have been proposed as one possiof a complex visble factor contributing to gender coelastic chain. differences in ACL injury rates. If Failure mode this is the case, then gender- and depends on a myriad age-related changes in ACL funcof loading and host tion may be apparent as children characteristics. progress into and through puberty. 3. Anterior translation We have preliminarily reporand endpoint indices ted normative data for anterior show age and translation of the knee in schoolgender variations 30 age children. Progressing from during pubertal grades five through twelve, antedevelopment. rior translation (measured by standard KT2000 methods) shows age-related decreases for both boys and girls. Girls tended toward greater anterior translation and had statistically significantly greater endpoint compliance (Figure 24–4). Interestingly, there was no correlation between the overall Beighton scores for hyperlaxity and anterior translation and specifically no correlation between knee hyperextension greater than 10 degrees and anterior translation values. Injury Epidemiology and Risk Factors There are a growing number of small group reports on the diagnoses and treatment of interstitial ACL tears in the skeletally immature. Unfortunately, most lack the demographic data needed to generate true injury rates. In one of the few studies on adolescents containing demographic data, Souryal and Freeman31 reported an annual incidence rate of 16 per 1000 for intrasubstance ACL tears in a cohort of high school athletes. There has been an increase in par-

Figure 24–4 Anterior knee translation for school-age girls and boys.

ticipation by young girls in high knee-demand sports. Their increased participation, coupled with their inherently higher ACL injury risk, has led to an overall increase in ACL injury rates among the skeletally immature. The early specialization and highly competitive nature of many of today’s youth sports also place children at greater risk for knee injury. In this environment, there is a disproportionate amount of time spent in highly competitive game situations. Compared to practice time, game participation is associated with a higher risk of major musculoskeletal injuries.32,33 For many young children, specialized sports skills are being emphasized before they have the chance to develop core muscle strength and fundamental sport abilities.34 Studies are now pointing to deficient neuromuscular coordination in core areas, such as jumping, deceleration, and change of direction, as a key factor for ACL injuries.35,36 Injury Risk Factors Injury risks depend on factors associated with the host (the athlete), the environment (the social and physical environment in which the athlete participates), and the agent (in infectious disease: a bacterial, viral, or macrobacterial agent; in musculoskeletal injury: the exchange of injury).32 By partitioning risk factors into these three areas, more effective preventive programs can be instituted. The primary risk factor for ACL injury in the skeletally immature is participation in high knee-demand sports. In younger children, ACL injuries have sometimes been related to nonsport situations, including falls or motor vehicular accidents. The second greatest risk factor for ACL injuries in the skeletally immature may be gender. ACL injuries among older adolescent and young adult athletes involved in sports, such as soccer, basketball, and volleyball, are some of the most genderdriven conditions in all of orthopedics.35–38 Many of the proposed mechanisms placing adult females at higher risk for ACL injury would appear to be at work in immature girls and boys. These include relative weakness in core muscle strength, deficient neuromuscular coordination, smaller femoral notch width indices, smaller ACL size, lower extremity postural laxity, and decreased dynamic knee stiffness.35,36

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Injury Patterns

Natural History

In the skeletally immature, the ACL complex may fail at different sites, be partial or complete, occur in isolation or with other injuries, and be a frequent cause of acute hemarthrosis. Intrasubstance tears may occur in the midsubstance or near the femoral or tibial attachment. Bony avulsions are most frequent at the tibial spine, but isolated cases of femoral bone attachment have also been reported.39 Detectable laxity after healed avulsion injuries suggests some intrasubstance failure before bony avulsion.40–42 Partial ACL injuries have been reported with significantly higher frequency in skeletally immature children and adolescents than in adults.25,43 These injuries also appear to be more common in prepubescent than adolescent patients. The relative frequency of bony avulsions to intrasubstance tears is also age dependent but seems to cross over well before the time of complete physeal closure. In a group of 63 skeletally immature patients with ACL equivalent injuries, Kellenberger24 found that that 80% of the injuries in those less than 12 years of age involved tibial eminence fracture, while 90% of those over 12 years of age had intrasubstance tears. In a review of 70 children ages 7–18, Stanitski et al.25 found tibial spine fractures to be three times more common in those 7–12 years of age as compared to adolescents 13–18 years of age. ACL injury in the skeletally immature may be accompanied by other knee damage. These include meniscal tears, physeal fractures, patellar dislocation, and multiligamenKEY POINTS tous injuries. Of these, meniscal injury is by far the most common. 1. The growing In the adolescent athlete, Millett “frequency” of ACL 44 et al. and others have reported injuries in the acute concurrent meniscal tear skeletally immature patterns to be reflective of adults. is due to combinaTears occur acutely in 40–50% of tion of increased cases with lateral tears occurring injury recognition in higher frequency than medial and true increases tears. Preadolescents may suffer in injury rates. fewer associated meniscal tears at 2. Injury risks are best 25 the time of ACL injury. assessed utilizing a The presence of acute framework of host, hemarthrosis in the knee of the agent, and environskeletally immature athlete repmental factors. resents significant intraarticular 3. Major risk factors pathology, and ACL injury must for ACL injuries in always be ruled out. The potenthe young are tial causes of acute hemarthrosis participation in high include cruciate ligament injury, knee-demand avulsion fracture, osteochondral sports, female lesions, patella femoral instabilgender, and ity, meniscal tears, and intraarimmature ticular growth plate-related fracneuromuscular 25 tures. In Stanitski et al., 47% of development. the preadolescent group and 55% 4. Concurrent of the adolescents with acute meniscal damage is hemarthroses had partial or comcommon. plete ACL tears. Other studies 5. ACL injury is a have reported an association of common cause of ACL tears with acute hemarthroacute hemarthrosis sis in the skeletally immature to in the young athlete. 43–47 vary between 10–45%.

The natural history of the ACL-deficient knee in the young athlete is often one of recurrent instability, cumulative meniscal damage, and sports-related disability. Limited success with activity modification, poor compliance with rehabilitation and bracing, immature neuromuscular development, and weaker secondary restraints predispose many young patients to being “noncopers.” Although organized sports time may be modified to decrease knee stress, activities of daily living for children include running, jumping, and cutting movements in unorganized settings. Younger patients are more likely than adults to return to the same environment that led to the initial ACL injury. Since they are children, they have more time to accrue cumulative knee damage than adults, whose most active years are behind them. The idea of putting off reconstructive surgery until a safer time is understandable, yet often detrimental. Millett et al.44 reported on a group of 39 patients (ages 10–14, mean 13.6) undergoing either acute (less than 6 weeks after injury) or chronic (greater than 6 weeks after injury) ACL surgery. They found medial meniscal tears to be more common in the chronic group (36% versus 11%) and that significantly more of these medial meniscal tears required partial excision or repair (85% versus 40%). Aichroth et al.49 reviewed a population of 60 immature patients with arthroscopically confirmed ACL injuries. Thirty-three of these patients were initially treated conservatively and were followed prospectively over a 10-year period. Ten of the thirtythree subsequently underwent operative intervention for increasing instability. The remaining 23 nonoperative patients (11–15 years old, average 12.5) were followed for a mean of 72 months. Average Lysholm and Tegner scores fell from 78.6 and 6.7 at time of diagnosis to 52.4 and 4.2 at follow-up. Three of the 23 developed osteochondral fractures, and degenerative radiographic changes were seen in 43%. Graf et al. studied a group50 of 8 patients (average age 14.5 years) with acute ACL tears who were treated with a formal nonoperative program, including muscular rehabilitation, bracing, and a graduate return to sports. All eight patients developed functional instability. KEY POINTS Seven of the eight patients developed new meniscal tears at an 1. For a number of average of 15 months post-ACL developmental and 51 injury. McCarroll reported simibehavioral reasons, lar results in a group of 38 adolesmany young, cents treated nonoperatively with ACL-deficient rehabilitation, bracing, and activathletes are ity modification. At a mean folpredisposed to low-up of 29 months from initial being “noncopers.” injury, 37 of the 38 demonstrated 2. The natural history recurrent instability, and 27 had of the ACL-deficient developed new, symptomatic knee in the young meniscal tears. Only sixteen active athlete is attempted to return to their often one of previous level of competition, and recurrent instability, all complained of instability. cumulative 52 Mizuta et al. described their meniscal damage, findings in 18 patients (average and sports-related age 12.8 years, 16 girls and 2 boys) disability. with complete ACL tears treated

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conservatively and followed for an average of 57 months. Patients were allowed to return to preinjury sports once 90% quadriceps and hamstring strength had been reestablished and with the recommendation of functional brace use. Subjectively, all patients complained of pain, and 17 complained of instability or experienced giving way. Only one patient was able to return to the previous level of activity, 13 returned at a reduced level, and 4 were unable to return. Secondary meniscal tears were found in nine patients and radiographic signs of early arthritis in eleven. Injury Diagnosis The vast majority of ACL injury diagnoses can be made through the history. When the history is elicited, the young patient must focus on the most important issues. Parents and coaches should be included when available. The patient should be questioned for feelings of instability, ability to return to play, sensation of a “pop” at the time of injury, acute swelling, and the exact mechanism of injury. ACL tears usually occur in sudden decelerations, pivoting/cutting, and offbalance landings during organized sports participation. Symptoms from acute ACL injury can resolve remarkably quickly in the young. Swelling, pain, and gait deviations may return to normal within a few weeks. It may not be until high-demand sports are resumed that functional instability becomes apparent. Younger patients have a hard time telling the difference between the “instability” of patellar dislocation and that of ACL insufficiency, both in the acute and chronic situation. Both diagnoses must be fully investigated. Serial examinations should be utilized to allow time for the knee to calm down and the child time to warm to a more productive examination. It provides a better environment for patient and family education and allows the clinician an opportunity to better understand both patient and parental expectations. Acute surgery is rarely indicated, unless there is a locked knee or large osteochondral fracture, and preoperative therapy is integral to postreconstructive success. Thus some time is available to examine the whole child and check for generalized hypermobility, physiological knee laxity, and a sense of overall neuromuscular development. Adequate baseline radiographs and other information needed to assess skeletal maturity, preexisting conditions, and concurrent injuries can be obtained. This includes Tanner scaling, menstrual or maternal menstrual history if the patient is premenarcheal, and information on parental height and older sibling growth patterns. Standard radiographs should include weight-bearing anteroposterior (AP), and bent knee posterolateral (PL), lateral, and sunrise views. Special attention is given to the presence of avulsion fractures, lateral capsular avulsions, patellofemoral osteochondral fractures, and preexisting osteochondritis or Osgood-Schlatter disorder. In Tanner stages I, I, and III girls, and Tanner stage I–IV boys, left hand wrist and or lateral elbow films, long leg standing films, and scanograms may be obtained to establish baseline values for bone age, lower limb alignment and preexisting leg length inequalities. The authors do not routinely get stress views unless there is discrete tenderness along the physes, suggestion of physeal injury on standard films, or hemarthrosis without other explanation.

Placing the child at ease is important in obtaining a quality examination. The physical examination should begin with the contralateral uninjured knee to serve this purpose and to establish normative data for the child. Particular emphasis is give to anterior translation and endpoint compliance, physiological pivot shift, and patellar mobility. The involved leg examination begins with an overall assessment of the degree of injury and functional disability. An adequate examination does not require excessive flexion or repeatedly painful manipulations. The knee should be palpated in an anatomical fashion with special attention to the following: (1) a significant effusion, suggestive of acute hemarthrosis; (2)lateral joint line tenderness, suggesting meniscal tear and/or lateral compartment bone bruise; and (3) tenderness along medial patellofemoral ligament, retropatellar/lateral trochlear surfaces, or patella hypermobility/apprehension to suggest patellofemoral instability. McMurray’s test is not well tolerated in the acute setting. Meniscal damage should be suspected with discrete joint line tenderness or in rare cases of mechanical locking. All ligamentous stabilizers of the knee should be assessed for excursion and endpoint quality. Multiligamentous injuries can occur in the young patient, and misdiagnosis can be a cause of reconstructive failure. Varus/valgus motion should be checked in full extension and 20 to 30 degrees of flexion while palpating the joint line for gapping. The simplest test for PCL involvement is checking for the normal tibial stepoff. Increases in external tibial rotation at 30 or 90 degrees may be indicative of posterolateral corner or PCL involvement. The Lachman’s test is the most sensitive for assessing ACL function. Preformed in only 20 degrees of knee flexion and with minimal load, it is well tolerated even in the acute setting. The anterior drawer maneuver is less sensitive, easily compromised by hamstring contraction, and requires greater flexion of KEY POINTS the knee. The pivot shift is beneficial in that it often reproduces 1. Obtain adequate a sense of instability, which the information and patient experiences but may radiographs to have a hard time describing. It determine patient may not be well tolerated in the sexual/skeletal acute situation or with concurmaturation, rent medial collateral ligament preexisting (MCL) damage. Arthrometers conditions, or are useful in objectifying anterior concurrent injury. translation values and endpoint 2. Lachman’s test is compliances. A difference in the most sensitive translation of greater than 3 mm clinical test for ACL from injured to uninjured knees instability and is is suggestive of ACL injury. well tolerated even Historically, there have been in the acute setting. some concerns about the correla3. MRI is infrequently tions between clinical/arthrorequired to scopic and MRI findings in the diagnose an ACL young knee patient. However, tear but is helpful newer sequencing and diagnostic in determining acumen have improved the reliaconcurrent 8,43,45 53 bility a great deal. Lee et al. meniscal injury and have described the primary and to aid patient and secondary MRI findings suggesfamily education. tive of ACL tear in the skeletally

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immature patient. Primary findings included abnormal signal intensity within the ACL, discontinuity of the ligament, and Blumensaat’s angle of >9.5 degrees. Secondary criteria included lateral compartment bone bruise, anterior tibial displacement, uncovered posterior horn of the lateral meniscus, change in the posterior cruciate line, and posterior cruciate angle 10

Associated Tear Minimal Moderate Complete

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suture repair of the torn MCL and 5–6 weeks of immobilization. Subjective and clinical results were excellent to good for five patients and fair for one patient, who also had an associated ACL tear. Isolated MCL injury from an automobile accident has been reported in a 4-year-old child.82 In this case, primary repair with sutures and 4 weeks of immobilization produced an excellent result.

Although surgical treatment of MCL injury has been advocated in adults,83,84 recent trends have been toward nonoperative treatment for Grade I and Grade II isolated MCL injuries (Technical Note 25–1).71,85–89 Good outcomes of conservatively treated Grade III injuries of the MCL have been reported.90–92 Jones et al.93 described treatment of 24 high school football players with isolated Grade

TECHNICAL NOTE 25–1

Medial Collateral Ligament Sprain: Rehabilitation Program Pierre d’Hemecourt

Epidemiology and Pathophysiology Injuries to the MCL are common in contact and noncontact sports. This represents the most common ligamentous injury about the knee. Either a direct valgus blow or a rotational force can cause injury to this ligament. Basketball, soccer, football, hockey, and alpine skiing are typical sports causing these injuries. The MCL is a two-layered structure on the medial aspect of the tibiofemoral joint. The deep layer is attached to the medial meniscus, whereas the superficial layer is broad and stronger. The MCL is the primary restraint to valgus rotation of the knee. Secondary restraints include the ACL, PCL, and posteromedial capsule. Injury to the MCL may be associated with other ligamentous structures producing single or multiplanar instability. Double-ligament injury to the MCL and ACL is common in the alpine skier. Meniscus injuries may also occur. Furthermore, the child presents a unique situation with the epiphysis being weaker than the ligament and prone to injury, which may mimic a ligamentous strain. Thus, an epiphyseal injury is crucial to consider in this population. The MCL injury may be subdivided into grade I through III injuries. Grade I indicates a strain of the ligament without enough disruption to cause laxity on stress testing. A grade II injury represents a partial disruption with stress testing laxity of less than 5 mm. Grade III reflects a complete disruption of the ligament. Diagnosis The athlete will usually complain of pain on the medial aspect of the knee. This will often be aggravated in full extension or flexion beyond 90 degrees. Ambulation may occur with a partially flexed knee. With a grade III tear, there may be symptoms of instability. The physical examination is essential in the evaluation of MCL injuries. The examiner must

assess for coexisting ligamentous injury as well as meniscal, osteochondral, and physeal involvement. Single and multiplanar instability are considered because the latter is associated with more significant injury. Valgus stress testing is performed in extension and 20–30 degrees of flexion. Laxity in the flexed position is expected in single-plane instability. Laxity in full extension is considered an indicator of more severe injury to the posteromedial capsule, ACL, or PCL. Rotatory instability can be further confirmed with tests such as the Hughston posteromedial drawer sign (Figure 25–9). The patient is supine with a flexed knee and hip at 80 and 45 degrees, respectively. The examiner applies a posterior drawer force assessing excess posteromedial laxity. ACL and PCL laxity are independently tested. Plain x-rays are done to rule out osseous injury. MRI is usually not needed in a simple MCL injury. On the other hand, as the severity of the injury increases, the sensitivity of the physical examination for other injury may diminish. Here, the MRI may be helpful in delineating the degree of injury. Nonetheless, it is also still somewhat limited in the detection of meniscal and other ligamentous injury. Treatment and Prevention Isolated MCL injury is treated conservatively regardless of the grade. Immobilization is not used. The athlete may use crutch ambulation temporarily while there is an extension lag. Early mobilization with minimal resistance cycling and isometric quadriceps and hamstring strengthening are instituted. Ice and nonsteroidal antiinflammatory medication will enhance this phase. Functional hinged braces are used for 4–6 weeks in grade III tears and may be of some help in the rehabilitation of lessergrade tears. The return to athletics is determined by the lack of pain, a full range of motion and strength, as well Continued

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TECHNICAL NOTE 25–1

Medial Collateral Ligament Sprain: Rehabilitation Program (Continued)

Figure 25–9 Hughston posteromedial drawer sign.

as the ability of the athlete to perform sport-specific drills such as cutting and jumping. The athlete should also manifest minimal residual valgus laxity. Proximal tears may be associated with some residual laxity. In general, grade I injury requires 1–3 weeks of rehabilitation. Grade II tears may require 4–6 weeks. The grade III injuries may need 6–12 weeks of recovery. When MCL injuries are associated with cruciate ligament injury, the cruciate is usually treated operatively, whereas the MCL is treated conservatively. The use of functional hinged braces for prevention is somewhat controversial. There have been some positive trends noted with less MCL injury in football linemen. However, in “skilled” positions, such as running backs and kickers, there

may be an increased risk of injury to the MCL as well as the ACL. Furthermore, speed and agility may be adversely affected. Suggested Readings 1. Albright JP, Powell JW, Smith W, et al: Medial collateral ligament knee sprains in college football. Brace wear preferences and injury risk. Am J Sports Med 22:2–11, 1994. 2. Albright JP, Powell JW, Smith W, et al: Medial collateral ligament knee sprains in college football. Effectiveness of preventive braces. Am J Sports Med 22:12–18, 1994. 3. Albright JP, Saterbak A, Stokes J: Use of knee braces in sport. Current recommendation. Sports Med 20:281–301, 1995. 4. Barber FA. Snow skiing combined anterior cruciate ligament/medial collateral ligament disruptions. Arthroscopy 10:85–89, 1994.

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TECHNICAL NOTE 25–1

Medial Collateral Ligament Sprain: Rehabilitation Program (Continued) 5. Lundberg M, Odensten M, Thuomas KA, et al: The diagnostic validity of magnetic resonance imaging in acute knee injuries with hemarthrosis. A single-blinded evaluation in 69 patients using high-field MRI before arthroscopy. Int J Sports Med 17:218–222, 1996. 6. Paletta GA, Warren RF: Knee injuries and Alpine skiing. Treatment and rehabilitation. Sports Med 17:411–423, 1994.

III injuries of the MCL. These athletes were treated with an aggressive rehabilitation program, progressing from immobilization to muscle strengthening and agility exercises. In 22 cases, a stable knee was attained. The athletes returned to competitive sports an average of 34 days after their injury. Several recent studies have demonstrated good outcomes in adults with nonsurgical treatment of Grade III MCL injury.94 Reider et al.92 demonstrated good results in a series of Grade III MCL injuries with 5-year follow-up. Indelicato et al.87,88 have also demonstrated excellent results with nonoperative treatment of Grade III tears. Although some have suggested that nonoperative treatment of Grade III MCL injury will result in poor outcomes,95 the current literature supports conservative treatment for most isolated Grade III injuries.96 The results for treatment of most isolated MCL injuries are good with nonoperative programs in all age groups, and MCL healing will generally be adequate in 3–4 weeks for most Grade I and Grade II injuries.96,97 The ruptured MCL is supported by other structures, including the ACL and joint capsule. These structures may stabilize the knee during healing of the MCL and reduce stresses that impede healing. Operative treatment may be indicated if there is a displaced avulsion fracture.86 Some rehabilitation protocols include immobilization, either in full extension or 90 degrees of flexion,71,98 whereas others have advocated early motion without a period of casting or immobilization.99 In patients treated with early mobilization and weight bearing as tolerated, a low-profile knee brace with a medial and lateral hinge will provide some support to the knee while healing. A brief period of immobilization may be necessary in patients with significant discomfort. In a study of 51 athletes managed with an active rehabilitation program involving full or partial mobilization, athletes with Grade I and Grade II sprains returned to full participation after an average of 10.6 and 19.5 days, respectively.97 MCL injury is commonly seen in association with ACL injury in adults 39,100,101 and may occur in children and adolescents in association with tibial spine avulsions.39,41,102 Treatment for combined ACL/MCL injury is also controversial,103 with different studies recommending different treatment algorithms. Jokl et al.104 and Mok et al.105 suggested nonoperative treatment for these injuries. Some studies have suggested operative repair/reconstruction for both ligaments106,107 or operative repair of the MCL only.71,108 Recent studies have suggested that combined ACL/ MCL injuries

7. Reider B: Medial collateral ligament injuries in athletes. Sports Med 21:147–156, 1996. 8. Rubin DA, Kettering JM, Towers JD, et al: MR imaging of knees having isolated and combined ligament injuries. Am J Roentgenol 172:239–240, 1999.

should be treated with protective bracing and early motion to allow healing of the MCL. After motion has been restored and the risk of arthrofibrosis is reduced, the ACL should be reconstructed.99,109–111 Although these studies have focused on skeletally mature patents, similar treatments can be utilized in children and adolescents. In some cases, residual MCL laxity may be present after ACL reconstruction, and repair of the MCL has been recommended for select patients.71 The Lateral Collateral Ligament and the Posterolateral Corner Anatomy and Biomechanics

KEY POINTS 1. The medial aspect of the knee can be described as being composed of three layers, with the MCL existing in the deepest two layers. 2. The MCL is the primary static knee stabilizer with respect to valgus stress. 3. MCL injury may occur in young athletes, but the presence of a physeal fracture should always be suspected with a history of a valgus stress injury. 4. Careful physical examination can usually differentiate MCL injury from a physeal fracture. 5. The adult literature provides the best guidance for management of these injuries in young athletes. Conservative treatment is usually successful, even for high-grade injuries.

The lateral and posterolateral aspects of the knee were described by Andrews112 as the “dark side of the knee” because less was known about this region compared to other areas. Recent studies have defined the anatomy and biomechanics of this region.76,113–122 In addition to the LCL, numerous dynamic and static stabilizing structures contribute to the stability of the posterolateral corner. The static structures of the posterolateral corner include the LCL, posterolateral joint capsule, arcuate ligament complex, and the fabellofibular ligament. Several dynamic structures exist, including the popliteus, iliotibial band, lateral head of the gastrocnemius, and biceps femoris tendon.76,99,115–117,123 Seebacher et al.76 have described the posterolateral aspect of the knee using a three-layer model (Figure 25–10).

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Figure 25–10 Anatomy of the posterolateral corner of the knee. (From Seebacher JR, Inglis AE, Marshall JL, et al: The structure of the posterolateral aspect of the knee. J Bone Joint Surg Am 64[4]:536–541, 1982.)

The superficial layer (I) includes a contiguous sheath arising from the biceps tendon posteriorly and extending anteriorly to the iliotibial band. The next layer (II) is composed of the quadriceps retinaculum anteriorly, which extends posteriorly through the patellofemoral ligaments. Layer III—the deepest layer—includes the fabellofibular, arcuate, and lateral collateral ligaments, the popliteus tendon, and the lateral joint capsule with associated meniscal coronary ligaments. Anatomic variability of the posterolateral corner (PLC) is high, with absences of the arcuate or fabellofibular ligament present in 20% and 13% of the population, respectively.76 Although there is anatomic variability in the posterolateral corner, the popliteus complex (popliteus muscle and popliteofibular ligament) and LCL are consistent anatomic findings (Figure 25–10).115,122,124–126 The LCL originates from a ridge on the lateral femoral epicondyle, between the origins of the lateral head of the gastrocnemius and the tendon of the popliteus (Figure 25–11, A).118 The pear-shaped insertion of the LCL is on the V-shaped epiphyseal portion of the superolateral aspect of the fibula, proximal to the physis (Figure 25–11, B). The ligament has an elliptical cross-section, fanning out at its origin and insertion.118 The LCL and popliteofibular ligament have been studied by Maynard et al.127 and Wadia et al.122 The cross-sectional area of the popliteofibular ligament in adults is 6.9 ± 2.1 mm2, compared with 7.2 ± 2.7 mm2 for the LCL.127 Both of these structures are contained within the physeal envelope of the knee (Figures 25–2 and 25–12). The posterolateral structures of the knee are normally subjected to greater forces and are generally stronger than those of the medial knee.128 The role of the posterolateral ligament complex in determining knee stability continues to be

investigated. Several studies have concluded that the LCL and popliteus complex are two of the major structures that resist lateral opening and varus stress.* In addition, recent studies by Pasque et al.119 and Ullrich et al.113 have documented the importance of both the popliteus complex and LCL in providing tibial rotational stability. The LCL and the popliteus complex are likely the most important structures with respect to posterolateral knee stability. The dynamic behavior of the LCL and posterolateral complex has been well described by Meister et al.118 and Gollehon et al.129 The LCL is taut in full extension and loosens during flexion, providing maximal resistance to external rotation and posterior translation when the knee is in extension. At all angles of flexion, the LCL and posterolateral complex function together as the principal structures preventing varus and external rotation of the tibia, whereas the PCL is the principal structure preventing posterior translation. However, the LCL and posterolateral complex aid in the prevention of posterior translation when the knee is flexed less than 30 degrees.129 The LCL may also limit internal rotation at flexion angles from 60 to 105 degrees.118,129 Incidence and Mechanism of LCL and PLC Injury Lateral collateral ligament and posterolateral corner injuries are rare in skeletally immature patients, and the literature contains little research in this age group. Thus, treatment principles for these injuries will have to partially rely on the insight from adult studies. For adult patients, injury to the lateral and posterolateral structures of the knee *

References 70, 119, 125, 127, 129–131.

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Figure 25–12 Magnetic resonance imaging anatomy of a skeletally immature knee. The lateral collateral ligament and posterolateral complex are contained within the physeal envelope of the knee.

Figure 25–11 A, Insertion of the lateral head of the gastrocnemius (G), lateral collateral ligament (L), and popliteus (P ) on the ridge of the lateral femoral condyle. B, Insertion of the lateral collateral ligament on the fibular head (L). (From Meister BR, Michael SP, Moyer RA, et al: Anatomy and kinematics of the lateral collateral ligament of the knee. Am J Sports Med 28[6]:869–878, 2000.)

is much less common than MCL or ACL injury. Even though the incidence of isolated PLC injury is probably less than 2–3% of all knee injuries,128 a growing number of studies in adult patients have focused on these injuries.132–135 Isolated injury to the LCL is extremely uncommon; injury to the posterolateral structures is usually seen with other

injuries such as strains of the lateral fascia and iliotibial tract, biceps femoris tendon, or PCL.136 The orthopedic literature contains limited information concerning the frequency of these injuries in pediatric or adolescent populations. LCL or PLC injuries are rarely found in studies of knee injury in children.4,102,137 Injury to the PLC or LCL may occur from athletic competition, motor vehicle accidents, or knee dislocations.138 When injury to the LCL and posterolateral corner occurs, it is usually due to a medial blow to the extended knee and may involve external rotation. LCL and posterolateral injuries may also occur from noncontact hyperextension and external rotation, or from forceful deceleration with the lower leg planted.128,139 With injuries to the proximal fibular physis, laxity resembling LCL or posterolateral injury may be present.140 In cases of displaced fracture through the fibular physis, surgery may be necessary.140 Clinical Examination of the Patient with Suspected LCL or PLC Injury Evaluation of the patient’s gait and lower extremity alignment is important for both adults and skeletally immature patients. Adult patients may exhibit gait deviations, which include varus thrust and hyperextension of the knee.125,128 The overall alignment of the lower extremity should be evaluated because genu varum may increase the likelihood of a poor outcome. The acutely injured knee may exhibit ecchymosis and

Injury of the MCL, PCL, and Posterolateral Complex in Skeletally Immature Patients

pain over the posterolateral aspect or in the popliteal fossa region (Figure 25–13). A careful evaluation of neurovascular status is important because LCL and PLC injuries may be associated with peroneal nerve injury.128 The possibility of a spontaneously reduced knee dislocation should always be considered, and a thorough neurovascular exam is essential. Numerous tests have been described to assess laxity of the posterolateral knee complex. These tests evaluate the integrity of the LCL, the PLC, and the PCL and include the evaluation of translation, varus position, laxity, and external rotation. Each test should be compared to the contralateral knee in all patients.128 This is especially important because pediatric and adolescent patients often have physiological laxity. Veltri and Warren139 and others have provided comprehensive summaries of clinical tests of the PLC and LCL. A posterolateral corner injury will demonstrate increased varus laxity, external tibial rotation, and posterior translation. In cases of isolated posterolateral injury with an intact PCL, posterior translation will be most obvious at 20–30 degrees of flexion but will decrease significantly when the knee is flexed to 90 degrees. With combined posterolateral corner and PCL injury, significant posterior subluxation will occur at 90 degrees of flexion.128 Varus stress testing at 0 and 30 degrees will demonstrate laxity with LCL and posterolateral corner injury.117 A significant amount of varus laxity should raise suspicion of other injuries, including the PCL and ACL.138

387

In the posterolateral drawer test, the knee is placed in 80–90 degrees of flexion, with the foot in a fixed position of 15 degrees of external rotation. A force is exerted over the proximal anterolateral tibia to assess the posterior movement and outward tibial rotation.117 The sensitivity and specificity of this test are limited; therefore, other tests, as well as imaging, may be necessary to fully assess the knee.128,141,142 Another exam, the external rotation recurvatum test, is performed with the patient in a supine position.143 The great toe of each leg is elevated by the examiner, and the posture of the knee is evaluated. The knee will demonstrate varus, hyperextension, and external rotation of the tibia if a significant injury to the PLC is present. Other injuries may also be present, including injury to the ACL and/or PCL. The tibial external rotation test is performed with the patient in a supine or prone position. An outward rotation movement is applied to both feet at 30 and 90 degrees. A difference of outward rotation of more than 10 degrees is significant. A positive test at 30 degrees is considered more specific for a PLC injury, whereas a positive test at 90 degrees suggests a combined PLC and PCL injury.128,135,136 The reverse pivot shift test can also be used to evaluate the PLC, although comparison with the other extremity is important. This test may also be positive in a significant number of patients without injury, so the results should be interpreted with caution.138 Several descriptions of this test

Figure 25–13 Ecchymosis seen with posterolateral corner injury.

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exist. With the foot held in external rotation and the knee flexed to 90 degrees, the knee is extended. A palpable shift or jerk near full extension may occur as the posteriorly subluxated tibial plateau shifts anteriorly.117 The posterolateral external rotation test described by LaPrade and Terry117 is also useful for the evaluation and differentiation of isolated PLC and combined PLC and PCL injury (Figure 25–14).128 This test is performed with the knee at 30 degrees of flexion, starting in neutral rotation. A combined force of external rotation and posterior subluxation is applied at 30 degrees, then at 90 degrees. An isolated injury of the PLC is likely to demonstrate laxity at 30 degrees, whereas the posterior subluxation will be less obvious if the PCL is intact. In cases of combined PCL/PLC injury, the test will demonstrate laxity in 30 and 90 degrees.128 By correlating clinical findings with arthroscopy, LaPrade and Terry117 found that clinical exams are strong indicators of the likely area of injury. A positive reverse pivot shift test was associated with LCL, popliteal component, or midthird lateral capsular ligament, whereas a positive posterolateral external rotation test at 30 degrees was associated with injury to the LCL or lateral tendon of the gastrocnemius. In addition, an abnormal adduction at 30 degrees of flexion indicated injury of the posterior arcuate ligament. Treatment of LCL and PLC Injuries LCL injury is often associated with other ligamentous injury such as PLC injury, ACL tears, or PCL tears.128 PLC or PCL injuries are extremely rare in children, thus there are few reports of treatment for this injury. The natural history of LCL and PLC injury has not been well defined in skeletally immature patients. In pediatric patients, cast immobilization is probably a reasonable treatment option until studies support operative intervention. There is a report of a 4-yearold child with a LCL tear and a femur fracture treated with a spica cast, resulting in a good outcome.30 Treatment for the adolescent patient with this injury should follow the protocols established for adult patients. Some patients with low-grade injury may return to activities with little or no disability.128,144 Low-grade injuries with minimal laxity may be treated with immobilization for 2–4 weeks, followed by a rehabilitation program.128 In adults,

Figure 25–14 The posterolateral external rotation test described by LaPrade and Terry.117 With the knee in neutral rotation, the knee is flexed to 30 degrees. While the posterolateral aspect of the knee is palpated, a combined force of external rotation and posterior drawer is applied. Abnormal posterolateral subluxation is indicative of a posterolateral corner injury.

Kannus et al.144 demonstrated good outcomes for conservative treatment of Grade II injuries, but poor outcomes for nonsurgically treated Grade III injuries. For Grade III injuries, nonoperative treatment may yield poor outcomes; recent research has focused on early surgical reconstruction in these cases. Several authors have suggested that early reconstruction or primary repair of PLC injury yields better results than reconstructions that have been delayed.125 Numerous techniques have focused on reconstruction of the LCL and popliteus complex,145,146 but no technique has emerged as the “gold standard.” In recent studies of adults, an emphasis has been placed on anatomic reconstruction, focusing on recreating the natural anatomy and biomechanics of the PLC and/or LCL. Primary repair of injured structures or reduction of avulsed fragments should be the first objective of surgical repair,128 although this may not be possible in the chronically injured knee. Early intervention after the injury may allow for anatomic repair of injured and/or avulsed structures. In older or chronic injuries, these structures may not be readily identified, and soft-tissue reconstruction procedures may be more appropriate. Tibial avulsions of the popliteus can be reduced by simple screws or suturing,125 whereas avulsions of the femoral origins of the LCL and popliteus may require sutures through transosseous drill holes.128 Fibular disruption of the LCL or popliteofibular ligament can be addressed with sutures and reinforcement with the fabellofibular ligament, if present.125 More complex procedures to address PLC and LCL injuries have been described. These include augmentation of an acutely torn popliteus tendon by utilizing a portion of the iliotibial tract, fixed to the tibia via sutures passed through a drill hole.147 Reconstruction of the popliteofibular ligament can be accomplished by the use of a portion of the biceps femoris tendon fixed to the lateral femoral condyle (Technical Note 25–2).125 Advancement of the arcuate complex, if intact, has been used by some authors with fair to good results.141,142,148–152 With this technique, the structures of the lateral aspect of the knee, including the lateral head of the gastrocnemius, the popliteus tendon, the arcuate ligament, and the LCL are advanced proximally on the femur in line with the LCL to restore tension. The disadvantage of this procedure is that it may produce nonanatomic changes in the ligament biomechanics, which may lead to stretching and failure over time.128 Combination repairs of the LCL and popliteus have been described by Veltri and Warren.125 In this technique, reconstruction of the popliteus utilizes a single drill hole in the lateral femoral condyle and a split patellar tendon graft. The proximal aspect of the graft is secured in the femoral hole and fixed distally in two locations: on the posterior tibial and lateral fibula. This creates a reconstruction that approximates the anatomic course of the popliteus. To reconstruct the LCL, a portion of the biceps femoris tendon is released proximally and rerouted to the lateral femoral condyle and attached at the approximate isometric point on the lateral femoral condyle. This method is advantageous because it approximates normal anatomy and biomechanics.128 Isolated LCL rupture has been addressed by numerous authors, and techniques have been described to reconstruct this ligament using the biceps femoris tendon,125

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TECHNICAL NOTE 25–2

Posterior Cruciate Ligament Repair and Reconstruction Chris D. Harner

Indications PCL injuries in the preadolescent age group are quite rare compared to ACL injuries. Numerous papers1–3 have been written on ACL reconstruction in the skeletally immature individual focusing on graft choice, tunnel placement, and outcomes. Currently, there are no comparable data regarding PCL injuries in this age group. As a result, the decision-making process for treatment of these injuries is challenging. From the knowledge we have to date, the overall goal in the preadolescent with a PCL injury is repair of avulsions and delay of reconstruction until skeletal maturity if the patient remains asymptomatic. The primary indication for PCL surgery in children and adolescents is avulsion or peel-off injuries from the femoral insertion site (Figure 25–15).4–9 If displaced less than 5 mm, tibial avulsion injuries can be treated nonoperatively with immobilization in extension. If displacement is greater than 5 mm, open reduction internal fixation (ORIF) can be performed through a posterior approach. In children, femoral or tibial avulsions are often largely cartilaginous. Magnetic resonance imaging can be helpful to better delineate the injury pattern.10

Midsubstance injuries are more controversial, but fortunately are less common in this age group. The prognosis for nonoperative treatment of Grade I and II injuries is extremely favorable.11,12 Nonsurgical results for isolated Grade III injuries are less predictable.8 The PCL tibial tunnel used for traditional reconstruction crosses the growth plate more peripherally than the tunnel used in ACL reconstruction. Drilling through the physis at this location potentially poses greater risk for growth arrest and deformity.13 As a result, children with isolated midsubstance Grade I, II, or III PCL injuries should be managed nonoperatively. Often an exam under anesthesia may need to be performed because of difficulty in examining a child in the clinical setting (Figure 25–16). Treatment for Grade I and II injuries involves protective weight-bearing and quadriceps muscle rehabilitation. The majority of patients are able to return to sports in 2–4 weeks. Grade III injuries should be immobilized in full extension for 2–4 weeks. During this period of immobilization, they can begin quadriceps sets, straight leg raises, and mini-squats.9,14,15 Active assisted range of motion begins at 4 weeks. Resisted open-chain strengthening exercises for the hamstrings are contraindicated,

Figure 25–15 A 14-year-old running back sustained a hyperflexion knee injury. The patient had a Grade II posterior drawer on physical exam. A femoral “peel off” injury was seen at the time of surgery.

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TECHNICAL NOTE 25–2

Posterior Cruciate Ligament Repair and Reconstruction (Continued)

Figure 25–16 A 6-year-old fell off a trampoline and was unable to bear weight. A, MRI showed a complete disruption of the posterior cruciate ligament (PCL). B, An exam under anesthesia was performed and revealed a Grade III isolated PCL injury. The patient was placed in a cast in 5 degrees of flexion for 1 month. Five months after injury, the posterior drawer was 2+, and there were no symptoms according to the patient and his parents.

and individuals should rely on closed-chain exercises to improve hamstring strength. Patients are usually able to return to sports at approximately 3 months. Combined soft-tissue injuries including collateral ligaments, meniscal, or chondral lesions should be addressed early with surgical intervention, if necessary. PCL function should be monitored clinically. If signs and symptoms persist, PCL reconstruction should be considered at skeletal maturity (Figure 25–17).

Setup In children and adolescents, general anesthesia is often used. The patient is placed supine on the operating table with a lateral post and a sandbag to maintain the knee at 90 degrees flexion. Gravity flow is used for the arthroscopy. A tourniquet is applied over web roll to the lower extremity but is not generally inflated. A 70-degree arthroscope should be available. Continued

Injury of the MCL, PCL, and Posterolateral Complex in Skeletally Immature Patients

TECHNICAL NOTE 25–2

Posterior Cruciate Ligament Repair and Reconstruction (Continued) Pediatric PCL injury

Isolated

Grade I

II

4–6 wks of limited activities (“relative rest”) If difficult office exam, consider EUA

Combined

III

PCL/ PLC (⫺LCL) (⫹LCL)

4 wks of full extension to prevent posterior tibial subluxation Surgery if: • Young athlete w/closed growth plates • Femoral “peel-off” • Tibial avulsion displaced ⬎5 mm • Grade III PLRI on EUA

PCL/ MCL

PCL/ ACL/ medial/lateral corner (“dislocated knee”)

Surgery within 2 wks: • Acute repair of collaterals • Address meniscal and chondral injuries • Possible ACL reconstruction • Delay PCL reconstruction until skeletally mature if symptoms remain

Figure 25–17 Algorithm showing treatment regimens of posterior cruciate ligament injuries.

Technique Examination Under Anesthesia: A posterior drawer test should be performed at 90 degrees to assess the degree of posterior laxity. If translation is greater than 10 mm, posterolateral corner injury should be suspected. The posterolateral corner is examined after reducing the tibia on the femur at both 30 and 90 degrees and comparing the side-to-side difference in external rotation. Lachman’s and varus/valgus stress testing at 0 and 30 degrees should also be performed. For all tests, both knees should be examined for side-to-side comparison. Before surgery, a neurovascular exam should be performed. Arthroscopy: A superior lateral outflow portal is made in Langers lines. Standard anterior lateral and medial portals are made longitudinally. The portals should be slightly more lateral than normal to allow better access and visualization of the PCL femoral insertion site. A diagnostic arthroscopy is performed to rule out any meniscal or chondral lesions. The PCL avulsed fragment is identified and can often be retracted posteriorly and inferiorly. Placing the arthroscope through an additional posterior medial portal may help identify the PCL. A 70-degree arthroscope may be useful at this point if there is difficulty finding the PCL. Once identified, a curved spectrum (Linvatec) is placed through the lateral portal to pass OPDS

sutures at the PCL ligament-bone interface. At least two sutures should be passed. These sutures are retrieved from the lateral portal and are used as shuttles for no. 2 fiberwire (Arthrex). The sutures are then retrieved from the lateral portal. The PCL insertion site is debrided using a 4.5 synovator. Any fibrous tissue or loose chondral flaps should be removed. Two drill holes are made from the inside to the outside using a 2-mm drill through the lateral portal. The drill holes should be placed very close to the condyle-cartilage boundary to optimize tension on the reattached PCL. The drill holes should remain on the epiphyseal side of the growth plate if the growth plates are still open. A Beath pin is then placed from the lateral portal though the medial femoral condyle tunnel and out through the skin. An incision is made over the medial femoral condyle and taken down to the bone using the Beath pin as a guide. The no. 2 fiberwire sutures around the PCL are passed through the Beath needle, and the Beath needle is pulled from outside the medial femoral condyle. The sutures are then tied over a button on the medial femoral condyle with the knee flexed to 90 degrees while an anterior drawer is applied. Postoperative Management Patients are kept overnight in the hospital. The knee is immobilized in extension for 2–4 weeks, Continued

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TECHNICAL NOTE 25–2

Posterior Cruciate Ligament Repair and Reconstruction (Continued) and partial weight bearing is allowed. The postoperative rehabilitation focuses on strengthening the quadriceps through isometric quadriceps sets and straight leg raises. At 4 weeks, passive motion by a physical therapist can be done while maintaining anterior translation on the tibia. Return to sports is usually allowed 6 months postoperatively.

7. 8. 9.

References 1. Lo IK, Kirkley A, Fowler PJ, Miniaci A: The outcome of operatively treated anterior cruciate ligament disruptions in the skeletally immature child. Arthroscopy 13:627–634, 1997. 2. Andrews M, Noyes FR, Barber-Westin SD: Anterior cruciate ligament allograft reconstruction in the skeletally immature athlete. Am J Sports Med 22:48–54, 1994. 3. Aronowitz ER, Ganley TJ, Goode JR, et al: Anterior cruciate ligament reconstruction in adolescents with open physes. Am J Sports Med 28:168–175, 2000. 4. Sanders WE, Wilkins KE, Neidre A: Acute insufficiency of the posterior cruciate ligament in children. Two case reports. J Bone Joint Surg Am 62:129–131, 1980. 5. Frank C, Strother R: Isolated posterior cruciate ligament injury in a child: literature review and a case report. Can J Surg 32:373–374, 1989. 6. Itokazu M, Yamane T, Shoen S: Incomplete avulsion of the femoral attachment of the posterior cruciate ligament

bone–tendon–bone autografts,153 Achilles allografts,125,154 semitendinosis autografts,155 and quadriceps tendon autografts.145 With the exception of procedures using the biceps femoris tendon, these techniques employ a cephalocaudal oriented drill hole in the fibular head and a transverse drill hole on the femur. Fixation is achieved with interference screws, sutures, or both. These studies of reconstruction of the LCL have had good results in adults, but they are limited by their lack of pediatric and adolescent subjects. Injuries to the PLC or PCL are likely to occur at or near skeletal maturity; the concern about physeal arrest may not be a significant clinical problem.156 In adolescent cases, the use of standard adult techniques, which may employ drill holes at or near the physeal region, are probably appropriate. Although the authors do not have significant personal experience with these rare injuries in the skeletally immature, primary repair and reduction of avulsions of the LCL or popliteal complex could likely be performed in skeletally immature patients if care is taken to avoid placement of hardware or drill holes across the physis. For LCL reconstruction, techniques that use the attachment of the biceps femoris tendon have an advantage, in that they do not require a drill hole in the proximal fibula. Knowledge of the anatomy of the ligaments to be reconstructed and their relation to the physes is helpful to avoid iatrogenic growth disturbance. The reconstructive drill holes used for LCL and PLC reconstruction would be relatively small, thus reducing the risk of producing a significant physeal injury. Drill-hole positioning should consider the location of

10. 11. 12. 13. 14.

15.

with an osteochondral fragment in a twelve-year-old boy. Arch Orthop Trauma Surg 110:55–57, 1990. Lobenhoffer P, Wunsch L, Bosch U, Krettek C: Arthroscopic repair of the posterior cruciate ligament in a 3-year-old child. Arthroscopy 13:248–253, 1997. Harner CD, Hoher J: Evaluation and treatment of posterior cruciate ligament injuries. Am J Sports Med 26:471–482, 1998. Giffin J, Annunziata C, Harner CD: Posterior Cruciate Ligament Injuries in the Child. In Delee JC, Drez D, Miller MD (eds): Delee & Drez’s Orthopaedic Sports Medicine. Philadelphia: Saunders, 2003, pp 2106–2111. Clanton TO, DeLee JC, Sanders B, Neidre A: Knee ligament injuries in children. J Bone Joint Surg 61:1195–1201, 1979. Fowler PJ, Messieh SS: Isolated posterior cruciate ligament injuries in athletes. Am J Sports Med 15:553–557, 1987. Parolie JM, Bergfeld JA: Long-term results of nonoperative treatment of isolated posterior cruciate ligament injuries in the athlete. Am J Sports Med 14:35–38, 1986. Edwards TB, Greene CC, Baratta RV, et al: The effect of placing a tensioned graft across open growth plates. J Bone Joint Surg Am 83: 725–734, 2001. Shelbourne KD, Davis TJ, Patel DV: The natural history of acute, isolated, nonoperatively treated posterior cruciate ligament injuries. A prospective study. Am J Sports Med 27: 276–283, 1999. Ogata K, McCarthy JA: Measurements of length and tension patterns during reconstruction of the posterior cruciate ligament. Am J Sports Med 20:351–355, 1992.

the femoral, tibial, and fibular physeal regions. If drill-hole placement avoids the physis, surgical reconstructive techniques for addressing LCL and PLC injuries may be successful, but this has yet to be demonstrated in clinical or animal studies. Adolescents at or close to skeletal maturity can probably be safely treated as adults with minimal risk of growth complications. Recent studies of ACL reconstruction have demonstrated the potential for growth plate complication, and these issues will need to be discussed thoroughly with the patient and family before any reconstructive procedure.156–158 The Posterior Cruciate Ligament Anatomy The PCL originates from the anteromedial region of the intercondylar notch of the femur and courses posterolaterally to the posterior tibia. Anatomical studies have shown that the PCL has a large oblong femoral insertion, spanning nearly 3 cm in the adult (Figures 25–18 and 25–19).130,159 The PCL attaches posterior to the tibial eminence, approximately 10–15 mm inferior to the posterior tibial plateau and extending distally towards the proximal tibial physis.160 The PCL is 20–50% larger in cross-section than the ACL and fans out at its origin and insertion—so much so that the area of attachment is five times the size of the midsubstance crosssectional area. The midsubstance of the PCL is asymmetric, with larger diameters on the femoral end of the ligament.161

Injury of the MCL, PCL, and Posterolateral Complex in Skeletally Immature Patients

The PCL has been described as having two functional units: the posteromedial bundle and the anterolateral bundle (Figure 25–18 and 25–19).130,152,162–165 These two nonisometric parts of the PCL have slightly different roles in providing knee stability. From studies in adults, it was found that the anterolateral bundle is twice as large in cross-section and is stiffer and stronger than the posteromedial bundle.161,166 Biomechanics

393

KEY POINTS 1. The posterolateral structures of the knee are normally subjected to greater forces and are generally stronger than those of the medial knee. Injury to this region can produce significant function disability. 2. Numerous structures contribute to the dynamic and static stability of the posterolateral corner, including the LCL, the PCL, and structures of the posterolateal complex. 3. Injuries to the posterolateral structures are uncommon. Only a handful of cases exist in the pediatric literature. 4. Numerous physical exam techniques have been described to assess the posterolateral corner. 5. Most low-grade injuries can be treated conservatively, but highergrade injuries may require surgical intervention. Many different operative techniques have been reported, but no procedure has emerged as the “gold standard.”

The anatomy of the PCL determines its biomechanical properties. The PCL is nonisometric; throughout the motion of the knee, changes take place such that neither bundle dominates in restraining posterior tibial motion during flexion and extension.167 The larger anterolateral bundle tightens during flexion, whereas the posteromedial bundle tightens during extension.168 These biomechanical properties of the PCL provide a challenge for single graft reconstructions; thus some authors have advocated the use of two-band, double-femoral tunnel techniques.115 The PCL is the primary restraint to posterior translation of the tibia and also prevents external rotation of the knee when flexion is greater than 30 degrees.121,129,147 Sectioning of the PCL has been shown to modestly increase posterior laxity at full extension, but larger increases in laxity are seen with the knee in 90 degrees of flexion, suggesting that additional structures participate in resisting posterior drawer during extension.115,169 Despite the redundancy of other structures, the PCL is an important provider of knee stability. Several injury mechanisms for the PCL have been described. A common injury pattern occurs with a direct blow to the anterior aspect of the knee, such as striking the dashboard during an automobile accident.170 Another mechanism is a fall onto the flexed knee.138,170,171 Fowler and Messieh172 have described in injury pattern associated with hyperflexion of the knee. Another mechanism, a blow to the anterior knee while the foot is in firm contact with the ground, has been described by Kennedy et al.173

AL PM

AL PM

Figure 25–18 Origin and insertion of posterior cruciate ligament anterolateral (AL) and posteromedial (PM) bands. (From Harner CD, Hoher J: Evaluation and treatment of posterior cruciate ligament injuries. Am J Sports Med 26[3]:471–482, 1998.)

Figure 25–19 Anatomic pictures of anterolateral (AL) and posteromedial (PM) bundles of posterior cruciate ligament. (From Harner CD, Hoher J: Evaluation and treatment of posterior cruciate ligament injuries. Am J Sports Med 26[3]:471–482, 1998.)

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Incidence and Natural History of PCL Injuries PCL disruption is less common than ACL injury. Studies in adults have identified PCL injury in 3–20% of patients with knee injuries.138 Reports of isolated PCL injury are rare in children, with approximately 25 case reports in the literature. Because of the limited number of PCL injuries in skeletally immature patients, the natural history of this injury in pediatric populations is not well defined. There have been limited case reports in the literature of various PCL injuries, including isolated PCL injury,45,174 PCL tears in combination with other injuries,8,39 and avulsions of the tibial47,175 or femoral attachments.46,176,177 An incomplete avulsion of the origin of the PCL has also been reported in an adolescent.178 Studies of the natural history of isolated PCL injury in adult patients are unclear, with some reporting good outcomes172,179,180 and others demonstrating poor long-term knee function.181–184 Shelbourne et al.185 found that in athletically active patients with PCL injury at an average of 5.4 years, half were able to return to the same or higher level of sports, one third returned to a lower level of competition, and one sixth did not return to the same sport. For an average of 6.2 years, Parolie et al.179 followed 25 patients who had suffered isolated PCL injury and were treated nonoperatively. They found that 80% were satisfied with their knees and 84% had returned to their previous sport (68% at the same level of performance, 16% at a decreased level of performance). Interestingly, they found that patients who were unable to regain 100% of preinjury quadriceps strength were more likely to have a poor outcome and not to return to preinjury level of activity. Complications due to chronic PCL deficiency are not clearly defined but are understood to possibly include functional limitations,184 pain and articular degeneration,181 and articular cartilage defects.183 Reports of the natural history of PCL injury in children are extremely rare with limited case reports. One case report of nonoperative treatment in a 6-year-old boy found excellent functional outcome, despite clinical PCL laxity suggesting that at least short-term conservative management in children may be appropriate.45 Another case report of PCL deficiency in a 6-year-old reported chronic instability after an initial asymptomatic period lasting more than 4 years.174 At a follow-up examination 5 years after the injury, the boy reported acute anterior knee pain as well as occasional instability. A tear of the medial meniscus was found on MRI. These two case reports suggest that shortterm conservative treatment may be appropriate, but that complications may eventually develop. Evaluation and Management of PCL Injury Examination of the knee for PCL deficiency includes tests described for the posterolateral corner and LCL injury. If the PCL is torn, varus laxity, external tibial rotation, and posterior translation will be present at 90 degrees of flexion.139 The posterior drawer test at 90 degrees of flexion is very useful for evaluation of the PCL. Laxity or subluxation should be graded and compared with the contralateral knee, because pediatric patients often can have physiological laxity. With PCL examination, identification of starting and

endpoints is important because an unsuspected PCL injury can produce a false-positive anterior drawer if the tibia is sagging posteriorly. The endpoint quality of the ligamentous structures should be graded in addition to the overall laxity or displacement. In the normal knee, the tibial condyle is usually 10 mm anterior to the femoral condyle with the knee at 90 degrees of flexion. Grading of PCL laxity can be performed as indicated in Table 25–2. A Grade I posterior drawer will reveal the tibia to be located posteriorly 0–5 mm compared with the normal knee.139 Others have suggested grading that depends on the amount of “step off” of the medial tibial plateau in relation to the medial femoral condyle (Table 25–3).79 Treatment in Children Because of the limited data available concerning treatment of pediatric PCL injury, the adult literature serves as a useful guide. Veltri and Warren.139 have developed algorithms for the approach to PCL injury in adults. Isolated acute PCL tears with less than 10 mm of posterior laxity at 90 degrees of flexion should be treated with aggressive physical therapy and rehabilitation. Reconstruction should be done for severe tears with more than 10 to 15 mm of laxity or PCL injuries in the knee with multiple injuries. In adults, chronic PCL injuries initially should be treated with an aggressive physical therapy and rehabilitation. Most authors advocate repair of all PCL avulsions in children,46–48,160 although casting for nondisplaced fractures has shown good results.186 Treatment of midsubstance tears of the PCL presents problems unique to the immature skeleton. Standard adult procedures may result in iatrogenic damage to the physis, leading to premature growth arrest. However, the repair of an avulsion of the femoral attachment of the PCL in a child performed by Lobenhoffer et al.46 involved transphyseal tunnels and sutures; no complications were reported. In pediatric and adolescent patients, the risks of causing growth disturbances must be weighed against known complications of chronic PCL deficiency. From the few published case reports, it is advisable to treat PCL tears in children conservatively until skeletal maturity is approached, although intervention may be warranted if symptoms and instability persist.

Table 25–2

PCL Laxity Grading System

PCL Injury Grade I II III

Table 25–3

Posterior Displacement of Tibia Compared to Noninjury Knee (mm) 0–5 5–10 >10

“Step Off” Grading System

Step Off (mm)

Instability

+10 +5 0 (flush) −5

0 1 2 3

(normal) (mild) (moderate) (severe)

Injury of the MCL, PCL, and Posterolateral Complex in Skeletally Immature Patients

The unique biomechanical properties of the PCL pose a challenge to reconstruction because a single graft is unlikely to mimic natural anatomy. There is evidence that single-bundle grafts result in increased laxity,187,188 presumably due to their inability to approximate the natural PCL. Some authors have advocated a single graft placed in the approximate position of the anterolateral bundle only.168,187,189,190 With single-graft techniques, precise placement of the femoral tunnel is closely tied to functional outcome, more so than location of the tibial tunnel189; hence, this has been an area of interest. Single-graft reconstructions are frequently performed with allografts, but bone–tendon–bone and hamstring grafts are also used. Due to concerns about physeal damage to the tibial tubercle, bone–tendon–bone autografts are probably not a desirable choice for the skeletally immature. Double-tunnel techniques, with a single tibial tunnel but two femoral tunnels, have been described.191–194 This style of graft is thought to better approximate the natural biomechanics of the PCL, and there is evidence that these may be superior to single grafts.192,194 Paulos 193 advocates the outside-in technique so that the tunnels for the anterolateral and posteromedial bundles can be oriented to be collinear with their maximum tension vectors. Graft choices for the double bundle are numerous: semitendinosis, gracilis autograft,193,194 hamstring allograft,193 anterior tibialis allograft,195 or quadriceps tendon.128 Regardless of the technique in a double-tunnel reconstruction, each graft must be tensioned separately. Despite its biomechanical advantages, there are limits to the double-tunnel procedure, including a steep learning curve, a more prolonged surgical procedure, and the need for precise placement of each grafted bundle. The double-tunnel technique is more complex, but its supe- riority has been suggested in the literature.115,192 The use of

KEY POINTS 1. The PCL originates from the anteromedial region of the intercondylar notch of the femur and courses posterolaterally to the posterior tibia. It has been described as having two functional units: the posteromedial bundle and the anterolateral bundle. 2. The PCL is nonisometric. The larger anterolateral bundle tightens during flexion, and the posteromedial bundle tightens during extension. These anatomic features make reconstructive approaches challenging. 3. Several injury mechanisms for the PCL have been described. A common injury pattern occurs with a direct blow to the anterior aspect of the knee with the knee in flexion. 4. Reports of isolated PCL injury are rare in children, with approximately only 25 case reports in the literature. PCL injury is more commonly seen with multiple ligamentous injuries. 5. Because of the limited data available concerning treatment of pediatric PCL injury, the adult literature serves as a useful guide. 6. Reconstruction of the PCL is controversial, with some authors advocating double-graft techniques, whereas others argue that single-bundle grafts are sufficient.

395

single-versus double-bundle grafts for PCL continues to be an active area of research, and many questions remain unanswered. Conclusion The last 20 years have seen a slow but steady increase in articles on athletic knee injuries in skeletally immature athletes. Growing recognition of injury to these structures should lead to more research on ligamentous knee injury in skeletally immature athletes and development of algorithms for treatment because numerous questions remain unanswered. Natural history studies that describe the outcome of these injuries would be beneficial, but the rarity of these injuries makes these studies difficult. Pediatric patients have better outcomes than adults for many musculoskeletal injuries, but it remains to be demonstrated how these differences will affect treatment of MCL, LCL, PCL, and PLC injuries. Will younger patients respond better than adults to nonconservative treatment? Will immobilization allow for adequate healing without surgical reconstruction, which is required in adults for serious LCL/PLC injury? What criteria can be used to distinguish younger athletes, who will likely heal from soft-tissue injuries without surgery, from older athletes who will require operative reconstruction? Other issues that remain enigmatic are the risk of growth complications during ligament reconstruction and the likelihood of physeal arrest, leg-length discrepancy, or angular deformity. This topic remains controversial for the treatment of ACL injuries.156 As several authors have demonstrated, the potential for physeal injury exists during transphyseal ACL reconstruction.157,158 Current reconstructive procedures for the PCL, LCL, and PLC employ the use of intraosseous tunnels. It is unknown if transphyseal procedures will cause clinically significant deformities. These and other questions concerning ligamentous injury and treatment in the skeletally immature knee remain unanswered. References 1. Rang M: Children’s Fractures. Philadelphia: JB Lippincott, 1983. 2. Rang M: Children’s Fractures. Philadelphia: JB Lippincott, 1974. 3. Beaty JH, Kumar A: Fractures about the knee in children. J Bone Joint Surg Am 76(12):1870–1880, 1994. 4. Bertin KC, Goble EM: Ligament injuries associated with physeal fractures about the knee. Clin Orthop 177:188–195, 1983. 5. Close BJ, Strouse PJ: MR of physeal fractures of the adolescent knee. Pediatr Radiol 30(11):756–762, 2000. 6. Crawford AH: Fractures about the knee in children. Orthop Clin North Am 7(3):639–656, 1976. 7. Ehrlich MG, Strain RE Jr: Epiphyseal injuries about the knee. Orthop Clin North Am 10(1):91–103, 1979. 8. Goodrich A, Ballard A: Posterior cruciate ligament avulsion associated with ipsilateral femur fracture in a 10-year-old child. J Trauma 28(9):1393–1396, 1988. 9. Kennedy JC: The Injured Adolescent Knee. Baltimore: Williams and Wilkins, 1979. 10. Larson RL: Epiphyseal injuries in the adolescent athlete. Orthop Clin North Am 4(3):839–851, 1973. 11. Lombardo SJ, Harvey JP Jr: Fractures of the distal femoral epiphyses. Factors influencing prognosis: a review of thirty-four cases. J Bone Joint Surg Am 59(6):742–751, 1977. 12. Poulsen TD, Skak SV, Jensen TT: Epiphyseal fractures of the proximal tibia. Injury 20(2):111–113, 1989. 13. Salter RB: Textbook of Disorders and Injuries of the Musculoskeletal System. Baltimore: Williams and Wilkins, 1970. 14. Thomson JD, Stricker SJ, Williams MM: Fractures of the distal femoral epiphyseal plate. J Pediatr Orthop 15(4):474–478, 1995.

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186. Meyers MH: Isolated avulsion of the tibial attachment of the posterior cruciate ligament of the knee. J Bone Joint Surg Am 57(5):669–672, 1975. 187. Burns WC 2nd, Draganich LF, Pyevich M, et al: The effect of femoral tunnel position and graft tensioning technique on posterior laxity of the posterior cruciate ligament-reconstructed knee. Am J Sports Med 23(4):424–430, 1995. 188. Pearsall AT, Pyevich M, Draganich LF, et al: In vitro study of knee stability after posterior cruciate ligament reconstruction. Clin Orthop 327:264–271, 1996. 189. Galloway MT, Grood ES, Mehalik JN, et al: Posterior cruciate ligament reconstruction. An in vitro study of femoral and tibial graft placement. Am J Sports Med 24(4):437–445, 1996. 190. Harner CD, Xerogeanes JW, Livesay GA, et al: The human posterior cruciate ligament complex: an interdisciplinary study. Ligament morphology and biomechanical evaluation. Am J Sports Med 23(6):736–745, 1995. 191. Borden PS, Nyland JA, Caborn DN: Posterior cruciate ligament reconstruction (double bundle) using anterior tibialis tendon allograft. Arthroscopy 17(4):E14, 2001. 192. Nyland J, Hester P, Caborn DN: Double-bundle posterior cruciate ligament reconstruction with allograft tissue: 2-year postoperative outcomes. Knee Surg Sports Traumatol Arthrosc 10(5):274–279, 2002. 193. Paulos LE: Taansosseous reconstruction of the posterior cruciate ligament: single and double tunnel techniques. Operative Techniques in Sports Medicine 9(2):60–68, 2001. 194. Stahelin AC, Sudkamp NP, Weiler A: Anatomic double-bundle posterior cruciate ligament reconstruction using hamstring tendons. Arthroscopy 17(1):88–97, 2001. 195. Borden PS, Nyland JA, Caborn DN: Posterior cruciate ligament reconstruction (double bundle) using anterior tibialis tendon allograft. Arthroscopy 17(4):E14, 2001.

Chapter 26

Tibial Eminence Fractures Jay C. Albright

●

Henry Chambers

Avulsion fracture of the intercondylar eminence in the immature skeleton is a relatively rare injury, accounting for approximately 2% of knee injuries, or 3 per 100,000 children each year.1,2 Rarely occurring in children younger than 7 years, these injuries typically occur in the 8–14-year age range. They do occur after skeletal maturity but are usually associated with higher energy mechanisms and up to 67% of associated injuries.3–7 This chondroepiphyseal avulsion fracture occurs through the subchondral bone beneath the anterior cruciate ligament (ACL) insertion.8–11 Noyes has shown that as the bone fails, a stretch injury or elongation of the ACL occurs.10 This has led many authors to equate this injury with ACL injuries in adults.8,9,12–23 The terms tibial eminence fracture and tibial spine fracture have been used interchangeably. Tibial eminence refers to the intercondylar of the proximal tibia where two elevations of bone and cartilage reside; the medial eminence or elevation accepts fibers from the ACL as it inserts into its footprint on the proximal tibia. The lateral tibial eminence receives no such fibers or attachments. Both menisci insert into the tibia in this region between and adjacent to the medial and lateral spines, although there is no direct connection between the ACL and the menisci. The goal of treatment is to obtain a stable, painless knee. Controversy over the most appropriate technique remains. Fracture treatment techniques range from immobilization to closed reduction with cast immobilization to surgical reduction and fixation.* Entrapment of a portion of meniscus, intermeniscal ligament, or its attachments, as well as the combination of the ACL and lateral meniscal insertion, have been cited as blocks to reduction of the fracture.18,58–62 Avulsion fracture of the posterior tibial eminence, femoral attachment of the ACL, and posterior horn insertion of the medial meniscus have been reported but are 10 times less common than anterior tibial spine avulsions.63–68 *

References 6, 8, 9, 13, 17–20, 23–57.

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Diagnosis Signs and symptoms, including pain and effusion from hemarthrosis, are the typical presenting symptoms after injury. Reluctance to bear weight and decreased range of motion are present as well. Physical examination should also include testing to evaluate for the possibility of ligamentous or physeal injury and should occur only after radiographic assessment has been performed.2,69 Radiographic evaluation should consist of anteroposterior (AP) and lateral radiographs. The fracture will be best evaluated on the lateral radiograph. Evaluation of both views is essential because the fragment attached to the ACL may be large or merely a thin fleck of bone. In a few instances, stress radiographs, with or without sedation/anesthesia, are indicated when the determination between a ligamentous and physeal injury is being considered. Radiographs should also be utilized to evaluate for adequacy of reduction after any attempt at closed reduction. Although magnetic resonance imaging may be of value to determine associated injuries and its use has been advocated in adult tibial eminence fractures, its use in the pediatric population is limited.4 Computed tomography scanning can be used to evaluate displacement and adequacy of reduction after closed treatment of these injuries. Mechanism of Injury The classic description of this injury is a fall off a bicycle.2,8,9,63 There is an increasing incidence of tibial spine avulsion fractures associated with the increasing athletic participation of children at younger ages. Multiple trauma is the third most commonly cited mechanism.20,21,58 Anatomic studies and biomechanical studies show that the ligament fails in midsubstance in adults; only when a defect is made in the subchondral bone will an avulsion fracture of the tibial eminence be reproduced. The ACL frequently undergoes stretch injury with laxity after the injury.

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Classification Based on the degree of displacement, Meyers and McKeever8 proposed a classification of tibial spine fractures (Figure 26–1). • Type I: Minimal displacement of avulsed fragment from the proximal tibial physis (Figure 26–1, A). • Type II: Displacement of the anterior one third to one half of the fragment superiorly. However, it is still hinged posteriorly and remains in contact with the proximal tibia (Figure 26–1, B). • Type III: Displacement of the entire fragment with complete separation from the proximal tibial physis, associated with upward displacement and rotation (Figure 26–1, C). This classification was later modified by Zaricznyj30 to include type IV, which are comminuted fractures of the tibial eminence. Treatment Type I Most authors recommend closed treatment of this nondisplaced or minimally displaced injury with immobilization in a cast. The controversy lies in the position of immobilization ranging from full extension, 10 degrees, or 20 degrees of flexion. Meyers and McKeever9 recommended immobilization in 20 degrees of flexion after closed reduction in all type I and type II injuries. Bakalim and Wilppula56 report good success with no laxity in neutral to 10 degrees of flexion in 10 patients. Smillie70 believed that reduction was only possible with hyperextension and a large fragment. Hallam et al.51 also believed that hyperextension was necessary for maintenance of reduction in their series of eight patients. The casting of these injuries is recommended for 6–8 weeks with the initiation of range of motion and ambulation. Type II Most authors prefer to treat this injury with an attempt at closed reduction and casting.* If postreduction radiographs *

References 8, 9, 15, 17, 20–22, 27, 30, 56, 63, 70–74

Figure 26–1 Meyers and McKeever classification. A, Type I. B, Type II. C, Type III.

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show adequate reduction, the patient is left in the cast for 6 weeks with close follow-up using radiographs to rule out displacement. If an inadequate reduction is obtained closed, most recommend open or arthroscopic reduction and fixation. Kocher et al.58 found 47% of type II fractures to be unreducible by closed techniques and 26% of these to have meniscal entrapment. Operative reduction is advocated not only for those that fail to reduce, but also for those with concurrent meniscal or osteochondral injuries; this prevents loss of extension or reduction and allows for early mobilization.16,20,22,62,75 The cause of failure of reduction by closed means is debatable. Most authors have found that the medial meniscus, lateral meniscus, intermeniscal ligament, or a combination of the three is responsible, based on observational studies at the time of arthroscopic evaluation.18,58,60–62,68 Lowe et al.59 evaluated these injuries arthroscopically in 12 patients and found no meniscal or intermeniscal ligament entrapments. They found, in all cases, that the ACL and insertion of the lateral meniscus were attached to the fragment and thus concluded that the combination of the differential pull—ACL proximally and the meniscus laterally—prevented reduction. No other studies have noted similar findings. Type III/IV Molander et al.27 reported excellent clinical results with minimal loss of motion and pain after treatment of 14 of 17 type III fractures conservatively. They found no correlation between posttreatment projection of the tibial eminence and knee pain or even initial displacement. They also reported no instability in any of the patients. The patients in this study were treated in a heterogenous way: some were treated with immobilization in flexion, whereas others were left in full extension. There is also no mention of evaluation of reduction posttreatment. Meyers and McKeever8 and Zaricznyj30 recommended open reduction and fixation of displaced fractures using K-wires. All 13 patients healed, and although a second surgery was needed to remove the

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pins, only 1 also had excision of an unreduced fragment. Two patients had a 1+ anterior drawer at the time of followup as well. Recent articles agree that these displaced and comminuted fractures require surgical reduction and fixation. Significant comminution or minimal bony component of the avulsed piece, which defines the Type IV fracture, deserve mention. The minimal bony area of fixation presents a treatment challenge and makes closed reduction and casting difficult. McLennan75 arthroscopically evaluated 10 patients after treatment of type III fractures with closed reduction and casting, arthroscopic reduction, and arthroscopic reduction and internal fixation. The patients treated with arthroscopic reduction and fixation did far better at both arthroscopic assessment as well as functional assessments with International Knee Documentation Committee (IKDC), Tegner, and Lysholm ratings. Closed reduction may still be attempted8,9,70 but most commonly fail to adequately reduce the avulsion. Controversy still lies in the method or type of fixation used.

Mah et al.18,19 described an arthroscopic technique of reduction and fixation and followed nine patients for an average of 3.5 years after fixation of type III fractures with arthroscopic epiphyseal suture fixation. They found no sign of instability, clinically or subjectively. Lehman et al.47 later described, in a case report, an arthroscopic whip-stitch technique utilizing an ACL guide and arthroscopic suturing

Surgical Techniques Multiple surgical techniques have been reported in the literature, ranging from open reduction with K-wire or suture fixation to arthroscopic reduction with casting, K-wire, screws, cannulated screws (Figures 26–2 and 26–3), or suture fixation (Figure 26–4), either transphyseal or intraepiphyseal only (Technical Note 26–1). Suturing techniques and some arthroscopic K-wire and screw fixation techniques had good results but did not allow early mobilization.6,42,45,76 Hallam et al.51 found no need for fixation after arthroscopic reduction of the entrapped transverse meniscal ligament and used cylindrical casts in hyperextension in eight adolescents. This clinical and cadaveric study showed no evidence of increased tension on the ACL in hyperextension. Zaricznyj30 had good overall healing rates and results from Kirschner wire fixation but required prolonged immobilization and no weight bearing.

Figure 26–2 Depiction of transphyseal screw fixation.

Figure 26–3 Intraepiphyseal screw fixation. A, Depiction of screw placement. B, Anteroposterior radiograph of type III fracture postreduction and screw fixation.

(Continued)

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Figure 26–4 Suture fixation.

Figure 26–3—cont’d C, Latera radiograph of type III fracture postreduction and screw fixation.

with good results in one patient at 9 months. Postoperative protocol included casting for 4 weeks and then initiation of range of motion in a removable brace. He advocates his technique as a method to reduce or retension the ACL via the suturing of the ACL stump as part of the fixation to the tibia. Owens et al.77 described their experience with the treatment of type III fracture with a combined arthroscopic evaluation and reduction with a miniopen arthrotomy and suture fixation in the epiphysis only. They passed a suture over the tibial eminence fragment and tied the suture under tension through bone tunnels connected by a bony bridge on the anteromedial epiphysis. All the patients in their Text continued on p. 407

TECHNICAL NOTE 26–1

Arthroscopic Reduction and Internal Fixation of Tibial Spine Fractures: Epiphyseal Cannulated Screws Jennifer L. Cook • Lyle J. Micheli

Background A tibial spine avulsion in a child is, in effect, an injury to the anterior cruciate ligament (ACL) complex. Because it involves a bony avulsion of the ACL insertion, there may be a resultant instability of the knee as seen with a classic ACL tear. In the past, the McKeever classification system has been used to determine intervention and relative treatment of tibial spine fractures. According to this classification system, a type I tibial spine fracture is nondisplaced and is typically treated using long-leg cast immobilization for 5–6 weeks (Figure 26–5, A). The type II fracture (Figure 26–5, B) has a posterior hinge with the anterior portion elevated and is

treated with attempted closed reduction and casting, with open reduction if closed reduction fails. A type III fracture (Figure 26–5, C) is completely displaced and is treated with open reduction. However, it is our opinion that this approach is quite dated. Physical Examination In the case of a child with a tibial spine avulsion, a physical examination is first done to determine whether the child has a positive Lachman’s test. If the child does indeed have a positive test, suggesting disruption of the ACL complex at the Continued

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TECHNICAL NOTE 26–1

Arthroscopic Reduction and Internal Fixation of Tibial Spine Fractures: Epiphyseal Cannulated Screws (Continued)

Figure 26–5 McKeever classification system of tibial spine fractures.

bony site, then it is our opinion that an arthroscopic evaluation with internal reduction is necessary. However, if there is a tibial spine injury but the knee is stable (hence a negative Lachman’s test), the injury is conservatively managed by immobilizing the injured knee in approximately 30 degrees of flexion for approximately 4 weeks to allow for bony healing. This is followed by progressive therapy. In our experience, this methodology has resulted in satisfactory treatment. Setup In patients deemed to have an unstable lesion and thus undergoing arthroscopy, general anesthesia is used. A nonsterile tourniquet is applied high in the upper thigh. The patient is positioned supine. Preoperative antibiotics are administered before inflation of the tourniquet. Technique Examination Under Anesthesia: Examination confirms a positive Lachman’s sign. Arthroscopy: The leg is routinely prepped and draped. An Esmarch bandage is used for exsanguination. Arthroscopy is performed with a standard anterolateral viewing portal. There is always a hemarthrosis of the knee, which is immediately washed out before any attempt at arthroscopy is carried out. Diagnostic arthroscopy is then performed.

A second portal is made medially, and either an angled mechanical shaver or a straight small shaver is inserted through this portal. Debridement of the area at the base of the tibial spine avulsion is carried out, and all clots are removed. Inspection then delineates the size of the fracture fragment and whether it has become entrapped and is lying in such a way that attempted reduction will be blocked by either the medial or lateral menisci (Figure 26–6). Often the fragment is so large that it can also avulse the anterior attachment of the lateral meniscus, and less commonly, the medial meniscus. The base of the fracture is debrided using shavers and small curettes so that the fracture line can be identified exactly. Attempted reduction is performed. In our experience, this generally occurs with the tibia posteriorly translated and the knee flexed to about 40 degrees, which takes most of the tension off the ACL complex. Then, using an arthroscopic probe, an attempt is made to reduce the fragment into its bed. If the reduction is blocked by one of the menisci overlapping this area, we have found it satisfactory to do an outside-in suture into the anterior horn of the meniscus and to then simply apply traction transcutaneously through this loop suture to pull back the meniscus and allow the fracture to be reduced. Once an adequate and anatomic reduction has been attained under direct visualization with the arthroscope, it is our practice to maintain the Continued

Tibial Eminence Fractures

TECHNICAL NOTE 26–1

Arthroscopic Reduction and Internal Fixation of Tibial Spine Fractures: Epiphyseal Cannulated Screws (Continued) knee on the table in a reduced position, generally approximately 60–70 degrees of flexion. We then make two additional high parapatellar portals, just at the angle of the patella. These skirt both medially and laterally downward along the margin of the femoral condyle to help facilitate our screw insertion. We use the 3.5-mm cannulated screw system with lag screws. The guide pin is passed into the knee to the tibia through either the medial or lateral high parapatellar portal first. The second guide pin may then be placed again either through the medial or lateral high parapatellar portal.

Reduction of the fracture fragment is confirmed by fluoroscopy. Images are taken in both the anteroposterior (AP) and lateral directions. If the guide pins are in a satisfactory position as visualized with fluoroscopy, the cannulated screws are advanced sequentially across the fracture fragment into the subchondral bone (Figure 26–7). Once again, fluoroscopic AP and lateral views are taken, this time to ensure that the physeal plate has not been violated. When adequate reduction and internal fixation have been attained, the guide pins are removed. The flexion position of the knee is maintained. We generally flex and extend the knee gently until

Figure 26–6 Nonreduced tibial spine fracture.

Figure 26–7 Cannulated screws inserted into reduced fracture fragment.

Continued

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TECHNICAL NOTE 26–1

Arthroscopic Reduction and Internal Fixation of Tibial Spine Fractures: Epiphyseal Cannulated Screws (Continued) we determine the position where it seems that there is essentially no tension on the repair, usually between 40 and 60 degrees. Figure 27–8 shows the AP and lateral postoperative views. The tourniquet is then deflated, and a cylinder cast is applied while maintaining the no-tension position of the knee. Postoperative Management The cylinder cast immobilization is maintained for 4 weeks, at which time the cast is removed and x-rays are obtained. If the fracture reduction is satisfactory and there is evidence of early bone healing, we will generally place the patient into a frame-type dial brace such as

a Bledsoe brace and begin range of motion gently from –30 degrees of extension to 90 degrees of flexion. Repeat x-rays are obtained at 6–7 weeks following reduction. If there is evidence of good bone healing, we then progress with range-ofmotion exercises to the knee as well as strengthening, using a closed-chain strengthening exercise program and gentle assisted progressive range-ofmotion exercises. We will routinely remove the hardware from these knees at 1 year after the surgery. However, if there appears to be an associated arthrofibrosis developing, we will do an arthroscopic debridement on the knee and also remove the hardware at that time as early as 6 months postoperatively.

Figure 26–8 A, Anteroposterior postoperative view of the left knee.

Continued

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TECHNICAL NOTE 26–1

Arthroscopic Reduction and Internal Fixation of Tibial Spine Fractures: Epiphyseal Cannulated Screws (Continued)

Figure 26–8—cont’d

B, Lateral postoperative view of the left knee.

Results Our experience with this technique can be found in Kocher et al.1

series were able to return to sporting activity and reported no instability episodes (Technical Note 26–2). Lubowitz46 described arthroscopically assisted reduction and percutaneous cannulated screw fixation in adults through the anteromedial arthroscopic portal. This technique allows for early immobilization secondary to screw fixation when adequate bone is present. Despite the ability for early mobilization in these patients, there is also frequently a second operation to remove the implant. Recent authors have concentrated on techniques of suture passing and knot tying with small numbers and minimal clinical follow-up.29,42,47,50 Oohashi42 and Hara et al.50 independently described their

Reference 1. 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.

use of folded surgical steel as a suture passer through bone tunnels during suture fixation in separate case reports. Binnet et al.55 used a four-portal technique in arthroscopic screw fixation in adults and suture fixation in adolescents. They found good results in 21 total patients treated but had to remove 2 of the 13 patients treated with screw fixation secondary to prominent hardware. Reynders et al.37 used a toothed washer and screw with intraepiphyseal fixation through the anterior fracture line. They reported good results clinically in 26 patients at a minimum of 6 months follow-up, with 2 failures that went on to ACL reconstruction. Senekovic, and Veselko34 reported 16–69 months of follow-up Text continued on p. 413

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TECHNICAL NOTE 26–2

Arthroscopic Reduction and Fixation of Tibial Spine Fractures: Suture Fixation Norman Y. Otsuka • Yi-Meng Yin • Jung Y. Mah

Indications Tibial eminence or spine fractures are a relatively rare injury in the pediatric age group. Meyers and McKeever classified anterior tibial eminence fractures into three types: type I, non-displaced; type II, partially displaced or hinged posteriorly; and type III, completely displaced.1 Closed treatment is recommended for type I and II fractures.1,2 For displaced type III fractures, often the anterior horn of the lateral meniscus remains attached to the avulsed fragment, preventing closed reduction.3–5 Traditionally, an open reduction and internal fixation technique using an anteromedial arthrotomy is used.6–8 We perform an arthroscopic technique for reduction of tibial eminence fractures with fixation using absorbable sutures.5

thigh of the affected leg. The patient is placed supine with the affected leg in a leg holder. Standard arthroscopic instruments and monitors are used. Technique

Setup

Arthroscopy: The leg is exsanguinated with an Esmarch bandage. Arthroscopy is performed through the standard anterolateral portal for viewing, and the anteromedial portal for instrumentation (Figure 26–9). The fracture hematoma is first evacuated through the medial portal, and any portion of the anterior fat pad is removed for clear visualization of the fracture. Diagnostic arthroscopy is then carried out to ensure no associated pathology. The pattern of injury is noted, and any block to reduction, such as meniscal interposition or bony fragments, is corrected.

For younger patients, general anesthesia is used. A nonsterile tourniquet is applied on the upper

Reduction and Fixation: Reduction of the fracture is then performed using a hook with extension of

Growth plate

Arthroscopic portals

Anterior cruciate ligament Fracture

Incision for drill holes Growth plate

Figure 26–9 Arthroscopic portals and incision for drill holes.

Continued

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TECHNICAL NOTE 26–2

Arthroscopic Reduction and Fixation of Tibial Spine Fractures: Suture Fixation (Continued) the knee. An incision of 1 cm in length is made over the metaphyseal flare of the tibia, midpoint between the tibial tuberosity and medial border of the tibia proximal to the growth plate. Subperiosteal dissection through the incision is accomplished to clearly visualize the growth plate. All subsequent instrumentation is carried proximal to the growth plate. While holding the tibial eminence reduced, a threaded K-wire is passed using a drill guide from the new incision through the fracture under direct arthroscopic visualization. The K-

wire should protrude slightly to hold the fracture in place (Figure 26–10). Next, using a small fragment three-hole AO drill guide, a nonthreaded K-wire is passed parallel to the threaded K-wire (Figure 26–11). Another nonthreaded K-wire is then drilled through the third hole of the drill guide, such that the drill holes are medial and lateral to the threaded K-wire. The nonthreaded K-wires are then removed. Using the medial arthroscopy portal, a no. 1 Vicryl suture is passed into the knee and held with a grasper. A Hewson suture passer is then

Fracture

Incision

Threaded K-wire

Figure 26–10 Insertion of threaded K-wire into reduced fracture fragment.

Continued

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TECHNICAL NOTE 26–2

Arthroscopic Reduction and Fixation of Tibial Spine Fractures: Suture Fixation (Continued)

Fracture

Incision

Smooth K-wires

Threaded K-wire

Figure 26–11 Nonthreaded K-wires passed parallel and medial and lateral to threaded K-wire.

inserted through the medial drill hole and the end of the suture passed through the suture passer. The suture passer is then retrieved from the drill hole at the exterior of the knee (Figure 26–12). Similarly, the suture passer is used to bring the other loose end of the suture through the lateral drill hole. The suture is then pulled taut with reduction of the fracture visualized through the arthroscope. The suture is then tied (Figure 26–13). A reinforcement suture can be placed if necessary by pivoting the three-

hole drill guide around the threaded K-wire. After adequate fixation is obtained with anatomic reduction, the threaded K-wire is removed. Closure: The tourniquet is let down, and hemostasis is achieved. The arthroscopic portals and incision are closed with simple interrupted 4-0 nylon sutures. A long-leg cast in 30 degrees of flexion is then applied. Continued

Tibial Eminence Fractures

TECHNICAL NOTE 26–2

Arthroscopic Reduction and Fixation of Tibial Spine Fractures: Suture Fixation (Continued)

Fracture

Suture

Incision

Hewson suture passer

Threaded K-wire

Figure 26–12 Hewson passer through medial drill hole retrieving no. 1 Vicryl suture passed through anteromedial arthroscopic hole.

Postoperative Management

Results

Patients are generally kept overnight for pain control. They are kept in a long-leg cast for 2 weeks postoperatively. The cast is removed after 2 weeks. Patients are then mobilized and allowed to weight bear as tolerated, and range-of-motion exercises are started.

Arthroscopic management of type III tibial eminence fractures allows for anatomic reduction of these fractures with more rapid healing than conventional arthrotomy techniques. We have reported on nine children who were followed for an average of 3.5 years. All patients underwent KT1000 arthrometry with no knee laxity. All patients had excellent function with return to full activities.9 Continued

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TECHNICAL NOTE 26–2

Arthroscopic Reduction and Fixation of Tibial Spine Fractures: Suture Fixation (Continued)

Fracture

Knotted suture Threaded K-wire

Figure 26–13 Suture knotted with reduction of the fracture.

References 1. Meyers MH, McKeever FM: Fracture of the intercondylar eminence of the tibia. J Bone Joint Surg Am 41:209–222, 1959. 2. Bakalim G, Wilppula E: Closed treatment of fracture of the tibial spines. Injury 5:210–212, 1974. 3. Kocher MS, Micheli LJ, Gerbino P, et al: Tibial eminence fractures in children: prevalence of meniscal entrapment. Am J Sports Med 31:404–407, 2003. 4. Lowe J, Chaimsky G, Freedman A, et al: The anatomy of tibial eminence fractures: arthroscopic observations following failed closed reduction. J Bone Joint Surg Am 84:1933–1938, 2002. 5. Mah JY, Otsuka NY, McLean J: An arthroscopic technique for the reduction and fixation of tibial-eminence fractures. J Pediatr Orthop 16:119–121, 1996.

6. Torisu T: Isolated avulsion fracture of the tibial attachment of the posterior cruciate ligament. J Bone Joint Surg Am 59:68–72, 1977. 7. Zaricznyj B: Avulsion fracture of the tibial eminence: treatment by open reduction and pinning. J Bone Joint Surg Am 59:1111–1114, 1977. 8. Kocher M, Garg S, Micheli L: Physeal sparing reconstruction of the anterior cruciate ligament in skeletally immature prepubescent children and adolescents. JBJS 87A(11):2371–2379, 2005. 9. Mah JY, Adili A, Otsuka NY, et al: Follow-up study of arthroscopic reduction and fixation of type III tibial-eminence fractures. J Pediatr Orthop 18:475–477, 1998.

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for intraepiphyseal cannulated screw fixation in 32 patients with good overall results. Only one aseptic synovitis occurred and KT1000 results averaged 1.1 mm. Preferred Technique Type I fractures with little or no displacement may be treated nonoperatively in a long-leg cast in approximately 20 degrees of flexion for 6 weeks, followed by rehabilitation with motion and strengthening exercises. If there is a question as to the amount of displacement seen on plain radiographs, the we will obtain a computed tomography (CT) scan of the knee to further evaluate the injury (Figure 26–14). If more than minimal displacement exists, we recommend arthroscopic evaluation with anatomic reduction and fixation (Figure 26–15). Evaluation of the articular surface for extension into the weight-bearing surface and evaluation and treatment of blocks to reduction is recommended. This evaluation allows one to assess the amount of comminution and the amount of bone in the fracture fragment. If adequate bone is present, we prefer fixation through a miniopen approach with intraepiphyseal screw fixation with a single screw. This often will require a second procedure for screw removal after healing. If the fragment is either too comminuted, a very shallow fragment of bone, or a large fragment that can only be fixed with a screw by crossing the physis, suture is used through tibial bone tunnels as the preferred method of fixation after reduction through a miniopen approach.

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Approach After induction, sterile preparation, and drape, the knee is insufflated with lactated Ringer’s Solution and a long-acting anesthetic such as bupivacaine. Standard superolateral, inferomedial, and inferolateral peripatellar portals are established, and the knee is systematically evaluated to rule out associated pathology. The fracture fragment is then assessed, and the hematoma and fracture surfaces are debrided, taking a small amount of tibial cancellous bone to allow some countersinking of the fracture reduction without significant stepoff of articular cartilage. If an anatomic reduction can be obtained and if the surgeon is comfortable with arthroscopic techniques, then sutures or a screw are placed. If the reduction cannot be adequately performed via the arthroscope, then the arthroscopic instruments are removed and the inferomedial portal is extended into a medial peripatellar incision of 5–6 cm in length. The use of a headlight and fatpad retractors are very helpful during this stage. Screw Fixation Under direct visualization, the fracture is reduced with a dental pick or small pointed pusher. A peripatellar medial portal is used to place the K-wire for the cannulated screw at more of a right angle to the fracture. A second K-wire may be utilized to temporarily transfix the fracture in a reduced position. This K-wire tends to aim posterolaterally from the tibial spine. A partially threaded cancellous screw

Figure 26–14 Nonoperative treatment of a type II fracture. Injury anteroposterior (A) and lateral (B) radiographs. The displacement and hinging of the posterior aspect of the fracture is more evident on the lateral view.

(Continued)

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Figure 26–14—cont’d

C–E, Fracture after reduction is performed. F, Final follow-up lateral radiograph with good alignment.

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Figure 26–15 Type II fracture treated with an attempt at closed reduction and ultimately arthroscopic reduction and suture fixation. Postinjury anteroposterior (A) and lateral (B) plain radiographs show the fracture displacement again more evident on the lateral view. Sagittal (C) and coronal (D) reconstruction computed tomography scans of the fracture after attempted closed reduction and casting with significant displacement. (Continued)

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Figure 26–15—cont’d E and F, Meniscal entrapment into the fracture and the debrided fracture bed. G, Process of the suture repair of the fracture and the final arthroscopic reduction.

(Continued)

is then inserted, and a length is chosen that stops short of the physis. Suture Technique The anteromedial portion of the epiphysis in exposed, and parallel K-wires are passed into the medial and lateral sides of the footprint of the fracture. A no. 2 nonabsorbable

braided suture is then sutured in a whip-stitch fashion through the base of the ACL at the insertion onto the tibial spine. The free ends of the suture are then passed through the K-wire tunnels with a Hewson suture passer. Alternatively, an inside-out meniscus suture passer (Instrument Makar) can be used to pass the suture. The fracture is reduced and held into position while the suture is tied anteriorly over the bone bridge of the anteromedial

Tibial Eminence Fractures

Figure 26–15—cont’d

417

H–K, Postoperative radiographs and computed tomography scan with an anatomic reduction.

portion of the epiphysis. The reduction stability is checked, and additional suture is placed if needed. The wounds are then closed in a standard fashion. The patient is placed in a long-leg cast at 20 degrees of flexion for 4 weeks. Fluoroscopic views are obtained in the operating room, and a CT scan is ordered to document the adequacy of the reduction. Motion is then begun out of the cast. A standard ACL rehabilitation protocol is also initiated. Partial weight bearing is allowed in the initial postoperative cast. Complications Arthrofibrosis, extension block from malunion, nonunion, residual laxity and instability, and prominence or irritation

of fixation devices are all reported complications of treatment of tibial eminence fractures. Growth Arrest Mylle et al.43 reported growth arrest of the anterior proximal tibial physis in an 11-year-old girl, causing hyperextension 2 years after fixation. They recommended early removal of transepiphyseal screws if used in children with immature skeletons. No other authors report growth arrest as a complication and cite this possibility as a reason for not crossing the physis with a screw. There has been no reported case of growth arrest with suture fixation.

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Arthrofibrosis/Loss of Range of Motion Decreased range of motion and stiffness of the knee was found in two separate studies by Wiley and Baxter.12,22 A minimum 10-degree loss of extension was reported in 45% of treated patients in one study and 60% in a second study. They state that only 64% noticed the loss of motion. Both studies used a variety of closed- and open-reduction techniques with variable fixation techniques when employed. No attempt was made to quantify quality of maintenance of reduction. Binnet et al.55 had one case of arthrofibrosis secondary to delayed therapy from a vascular insult. Residual Laxity The early literature claimed that these fractures caused no long-term knee instability issues, even when the fracture fragment and the ACL were excised. However, more recent authors are recognizing the importance of the ACL and are reporting decreased stability with increased laxity postinjury.12,22,23,79 Smith79 reported some degree of ACL laxity in all 21 cases of tibial eminence fractures of types I, II, and III, despite reportedly anatomic reduction. Residual laxity is being reported in up to 64% of patients with anterior laxity at 4 years follow-up.23 Reynders et al.37 reported that only 3 of 26 type II and III patients did not have residual laxity at follow-up after arthroscopic cannulated screw fixation. In addition, 2 cases of type III injuries required ACL reconstruction within 3 years after injury. Although Willis et al.23, in a heterogeneous group of patients and treatments with 50% follow-up, reported no subjective symptoms of instability, 8 patients could not return to the level of previous activity and 5 of 50 patients had pain associated with the decrease in activity. They found no difference in the clinical and KT1000 outcomes between the 30 patients that had either closed treatment of type I, II and III fractures or were arthroscopically reduced and casted, and those treated with open reduction and fixation with a variety of methods. Owens77 found residual laxity in 3 of their 12 patients at follow-up on KT1000 measurements but reported no subjective instability. Wiley and Baxter22 also found that all injuries classified as type II or III had residual laxity averaging 3–4 mm greater for anterior drawer than the uninjured side, 3–10 years after injury. Laxity at follow-up has been reported in many patients despite anatomic reductions with or without countersinking.12 None of these patients had symptomatic instability or a positive pivot shift in the two studies by Wiley and Baxter.12,22 Ahmad et al.5 evaluated ACL function after treatment of tibial eminence fractures. They compared their patients to those that either had undergone ACL reconstruction with bone–patella–tendon–bone or had ACL deficiency at average follow-up of 5.2 years. They treated type I fractures with casting for 4–6 weeks, type II fractures with closed reduction and casting for 4–6 weeks, and type III fractures by open reduction with internal fixation using screws. No statistically significant differences between the fracture and reconstruction groups existed. They did find a significant difference in both laxity on KT1000 and proprioception in the ACL-deficient group. They surmised that closed or surgical reduction and

fixation of tibial eminence fractures in adults restore stability and proprioception to the knee. Malunion Malunion may lead to mechanical impingement within the notch during full extension.60,74,78,79 Repeat injury or avulsion of a fibrous union was reported by Lombardo80 in a 10-year-old patient 3 years after cast treatment of a type II fracture. If this causes symptoms, excision of the fragment and reinsertion of the ACL has been performed. It also may be difficult from the literature to distinguish the difference between loss of range of motion from arthrofibrosis and loss of motion from malunion and impingement from the displaced fragment. References

KEY POINTS 1. Avulsion fractures of the intercondylar eminence occur with sporting activities and play activities as well as motor vehicle accidents. 2. Diagnosis is made by physical examination and radiographs. 3. Classification of Meyers and McKeever can help in the treatment decision. A. Type I and II fractures may be treated with cast immobilization alone if the type II partly displaced fracture is reducible in extension. B. Confirm anatomic closed reduction with CT scan. C. Irreducible type II and all type III fractures should undergo surgical intervention with reduction and fixation. 4. Maintenance of anatomic reduction with or without fixation results is the most reliable outcome.

1. Luhmann SJ: Acute traumatic knee effusions in children and adolescents. J Pediatr Orthop 23:199–202, 2003. 2. Skak SV, Jensen TT, Poulsen TD, et al: Epidemiology of knee injuries in children. Acta Orthop Scand 58:78–81, 1987. 3. Delcogliano A, Chiossi S, Caporaso A, et al: Tibial intercondylar eminence fractures in adults: arthroscopic treatment. Knee Surg Sports Traumatol Arthrosc 11: 255–259, 2003. 4. Toye LR, Cummings, DP, Armendariz G: Adult tibial intercondylar eminence fracture: evaluation with MR imaging. Skeletal Radiol 31:46–48, 2002. 5. Ahmad CS, Stein BE, Jeshuran W, et al: Anterior cruciate ligament function after tibial eminence fracture in skeletally mature patients. Am J Sports Med 29:339–345, 2001. 6. van Loon T, Marti RK: A fracture of the intercondylar eminence of the tibia treated by arthroscopic fixation. Arthroscopy 7:385–388, 1991. 7. Kendall NS, Hsu SY, Chan KM: Fracture of the tibial spine in adults and children. A review of 31 cases. J Bone Joint Surg Br 74:848–852, 1992. 8. Meyers MH, McKeever FM: Fracture of the intercondylar eminence of the tibia. J Bone Joint Surg Am 41:209–222, 1959. 9. Meyers MH, McKeever FM: Fracture of the intercondylar eminence of the tibia. J Bone Joint Surg Am 52:1677–1684, 1970. 10. Noyes FR, DeLucas JL, Torvik PJ: Biomechanics of anterior cruciate ligament failure: an analysis of strain-rate sensitivity and mechanisms of failure in primates. J Bone Joint Surg Am 56:236–253, 1974. 11. Woo SL, Hollis JM, Adams DJ, et al: Tensile properties of the human femur-anterior cruciate ligament-tibia complex. The effects of specimen age and orientation. Am J Sports Med 19:217–225, 1991. 12. Baxter MP, Wiley JJ: Fractures of the tibial spine in children. An evaluation of knee stability. J Bone Joint Surg Br 70: 228–230, 1988. 13. Berg EE: Pediatric tibial eminence fractures: arthroscopic cannulated screw fixation. Arthroscopy 11:328–331, 1995.

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14. Clanton TO, DeLee JC, Sanders B, et al: Knee ligament injuries in children. J Bone Joint Surg Am 61:1195–1201, 1979. 15. Gronkvist H, Hirsch G, Johansson L: Fracture of the anterior tibial spine in children. J Pediatr Orthop 4:465–468, 1984. 16. Janarv PM, Westblad P, Johansson C, et al: Long-term follow-up of anterior tibial spine fractures in children. J Pediatr Orthop 15:63–68, 1995. 17. Lee YH, Chin LS, Wang NH, et al: Anterior tibial spine fracture in children: follow-up evaluation by biomechanical studies. Zhonghua Yi Xue Za Zhi (Taipei) 58:183–189, 1996. 18. Mah JY, Adili A, Otsuka NY, et al: Follow-up study of arthroscopic reduction and fixation of type III tibial-eminence fractures. J Pediatr Orthop 18:475–477, 1998. 19. Mah JY, Otsuka NY, McLean J: An arthroscopic technique for the reduction and fixation of tibial-eminence fractures. J Pediatr Orthop 16:119–121, 1996. 20. Oostvogel HJ, Klasen HJ, Reddingius RE: Fractures of the intercondylar eminence in children and adolescents. Arch Orthop Trauma Surg 107:242–247, 1988. 21. Pellacci F, Mignani G, Valdiserri L: Fractures of the intercondylar eminence of the tibia in children. Ital J Orthop Traumatol 12:441–446, 1986. 22. Wiley JJ, Baxter MP: Tibial spine fractures in children. Clin Orthop 255:54–60, 1990. 23. Willis RB, Blokker C, Stoll TM, et al: Long-term follow-up of anterior tibial eminence fractures. J Pediatr Orthop 13:361–364, 1993. 24. Bale RS, Banks AJ: Arthroscopically guided Kirschner wire fixation for fractures of the intercondylar eminence of the tibia. J R Coll Surg Edinb 40:260–262, 1995. 25. Jung YB, Yum JK, Koo BH: A new method for arthroscopic treatment of tibial eminence fractures with eyed Steinmann pins. Arthroscopy 15:672–675, 1999. 26. McLennan JG: The role of arthroscopic surgery in the treatment of fractures of the intercondylar eminence of the tibia. J Bone Joint Surg Br 64:477–480, 1982. 27. Molander ML, Wallin G, Wikstad I: Fracture of the intercondylar eminence of the tibia: a review of 35 patients. J Bone Joint Surg Br 63:89–91, 1981. 28. Mulhall KJ, Dowdall J, Grannell M, et al: Tibial spine fractures: an analysis of outcome in surgically treated type III injuries. Injury 30:289–292, 1999. 29. Yip DK, Wong JW, Chien EP, et al: Modified arthroscopic suture fixation of displaced tibial eminence fractures using a suture loop transporter. Arthroscopy 17:101–106, 2001. 30. Zaricznyj B: Avulsion fracture of the tibial eminence: treatment by open reduction and pinning. J Bone Joint Surg Am 59:1111–1114, 1977. 31. Walmsley JP: Fracture of the intercondylar eminence of the tibia treated by arthroscopic internal fixation. Equine Vet J 29:148–150, 1997. 32. Veselko M, Senekovic V, Tonin M: Simple and safe arthroscopic placement and removal of cannulated screw and washer for fixation of tibial avulsion fracture of the anterior cruciate ligament. Arthroscopy 12:258–262, 1996. 33. Tuompo P, Partio E, Rokkanen P: Bioabsorbable fixation in the treatment of proximal tibial osteotomies and fractures. A clinical study. Ann Chir Gynaecol 88:66–72, 1999. 34. Senekovic V, Veselko M: Anterograde arthroscopic fixation of avulsion fractures of the tibial eminence with a cannulated screw: five-year results. Arthroscopy 19:54–61, 2003. 35. Schmitgen GF, Utukuri MM: Arthroscopic treatment of tibial spine fractures in children: a review of three cases. Knee 7:115–119, 2000. 36. Roberts JM: Operative treatment of fractures about the knee. Orthop Clin North Am 21:365–379, 1990. 37. Reynders P, Reynders K, Broos P: Pediatric and adolescent tibial eminence fractures: arthroscopic cannulated screw fixation. J Trauma 53:49–54, 2002. 38. Prince AR, Moyer RA: Arthroscopic treatment of an avulsion fracture of the intercondylar eminence of the tibia. Case report. Am J Knee Surg 8:114–116, 1995. 39. Perez Carro L, Garcia Suarez G, Gomez Cimiano F: The arthroscopic knot technique for fracture of the tibia in children. Arthroscopy 10:698–699, 1994. 40. Osti L, Merlo F, Liu SH, et al: A simple modified arthroscopic procedure for fixation of displaced tibial eminence fractures. Arthroscopy 16:379–382, 2000. 41. Osti L, Merlo F, Bocchi L: Our experience in the arthroscopic treatment of fracture-avulsion of the tibial spine. Chir Organi Mov 82:295–299, 1997.

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42. Oohashi Y: A simple technique for arthroscopic suture fixation of displaced fracture of the intercondylar eminence of the tibia using folded surgical steels. Arthroscopy 17:1007–1011, 2001. 43. Mylle J, Reynders P, Broos P: Transepiphysial fixation of anterior cruciate avulsion in a child. Report of a complication and review of the literature. Arch Orthop Trauma Surg 112:101–103, 1993. 44. Medler RG, Jansson KA: Arthroscopic treatment of fractures of the tibial spine. Arthroscopy 10:292–295, 1994. 45. Matthews DE, Geissler WB: Arthroscopic suture fixation of displaced tibial eminence fractures. Arthroscopy 10:418–423, 1994. 46. Lubowitz JH, Grauer JD: Arthroscopic treatment of anterior cruciate ligament avulsion. Clin Orthop 294:242–246, 1993. 47. Lehman RA Jr, Murphy KP, Machen MS, et al: Modified arthroscopic suture fixation of a displaced tibial eminence fracture. Arthroscopy 19:6E, 2003. 48. Kogan MG, Marks P, Amendola A: Technique for arthroscopic suture fixation of displaced tibial intercondylar eminence fractures. Arthroscopy 13:301–306, 1997. 49. Kobayashi S, Terayama K: Arthroscopic reduction and fixation of a completely displaced fracture of the intercondylar eminence of the tibia. Arthroscopy 10:231–235, 1994. 50. Hara K, Kubo T, Shimizu C, et al: Arthroscopic reduction and fixation of avulsion fracture of the tibial attachment of the anterior cruciate ligament. Arthroscopy 17:1003–1006, 2001. 51. Hallam PJ, Fazal MA, Ashwood N, et al: An alternative to fixation of displaced fractures of the anterior intercondylar eminence in children. J Bone Joint Surg Br 84:579–582, 2002. 52. Geissler WB, Matthews DE: Arthroscopic suture fixation of displaced tibial eminence fractures. Orthopedics 16:331–333, 1993. 53. Fehnel DJ, Johnson R: Anterior cruciate injuries in the skeletally immature athlete: a review of treatment outcomes. Sports Med 29:51–63, 2000. 54. Doral MN, Atay OA, Leblebicioglu G, et al: Arthroscopic fixation of the fractures of the intercondylar eminence via transquadricipital tendinous portal. Knee Surg Sports Traumatol Arthrosc 9:346–349, 2001. 55. Binnet MS, Gurkan I, Yilmaz C, et al: Arthroscopic fixation of intercondylar eminence fractures using a 4-portal technique. Arthroscopy 17:450–460, 2001. 56. Bakalim G, Wilppula E: Closed treatment of fracture of the tibial spines. Injury 5:210–212, 1974. 57. Ando T, Nishihara K: Arthroscopic internal fixation of fractures of the intercondylar eminence of the tibia. Arthroscopy 12:616–622, 1996. 58. Kocher MS, Micheli LJ, Gerbino P, et al: Tibial eminence fractures in children: prevalence of meniscal entrapment. Am J Sports Med 31;404–407, 2003. 59. Lowe J, Chaimsky G, Freedman A, et al: The anatomy of tibial eminence fractures: arthroscopic observations following failed closed reduction. J Bone Joint Surg Am 84:1933–1938, 2002. 60. Burstein DB, Viola A, Fulkerson JP: Entrapment of the medial meniscus in a fracture of the tibial eminence. Arthroscopy 4:47–50, 1988. 61. Chandler JT, Miller TK: Tibial eminence fracture with meniscal entrapment. Arthroscopy 11:499–502, 1995. 62. Falstie-Jensen S, Sondergard Petersen PE: Incarceration of the meniscus in fractures of the intercondylar eminence of the tibia in children. Injury 15:236–238, 1984. 63. Roberts JM, Lovell WW: Fractures of the intercondylar eminence of the tibia. J Bone Joint Surg Am 52:827, 1970. 64. Ross AC, Chesterman PJ: Isolated avulsion of the tibial attachment of the posterior cruciate ligament in childhood. J Bone Joint Surg Br 68:747, 1986. 65. Goodrich A, Ballard A: Posterior cruciate ligament avulsion associated with ipsilateral femur fracture in a 10-year-old child. J Trauma 28:1393–1396, 1988. 66. Tohyama H, Kutsumi K, Yasuda K: Avulsion fracture at the femoral attachment of the anterior cruciate ligament after intercondylar eminence fracture of the tibia. Am J Sports Med 30:279–282, 2002. 67. Torisu T: Isolated avulsion fracture of the tibial attachment of the posterior cruciate ligament. J Bone Joint Surg Am 59:68–72, 1977. 68. Pauly T, Van Ende R: Avulsion fracture. Special type of meniscal damage. Arch Orthop Trauma Surg 108:325–326, 1989. 69. Hayes JM, Masear VR: Avulsion fracture of the tibial eminence associated with severe medial ligamentous injury in an adolescent. A case report and literature review. Am J Sports Med 12:330–333, 1984. 70. Smillie IS: Injuries of the Knee Joint. 5th ed. Edinburgh, ChurchillLivingstone, 1978.

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71. Blasier RD, Aronson J: Fractures in children. Curr Opin Pediatr 6:85–89, 1994. 72. Brunelli G: Fractures of the intercondylar tibial eminence. Ital J Orthop Traumatol 4:5–12, 1978. 73. Driessen MJ, Winkelman PA: Fractures of the intercondylar eminence of the tibia in childhood. Neth J Surg 36:69–72, 1984. 74. Fyfe IS, Jackson JP: Tibial intercondylar fractures in children: a review of the classification and the treatment of mal-union. Injury 13:165, 1981. 75. McLennan JG: Lessons learned after second-look arthroscopy in type III fractures of the tibial spine. J Pediatr Orthop 15:59–62, 1995. 76. Berg EE: Comminuted tibial eminence anterior cruciate ligament avulsion fractures: failure of arthroscopic treatment. Arthroscopy 9:446–450, 1993.

77. Owens BD, Crane GK, Plante T, et al: Treatment of type III tibial intercondylar eminence fractures in skeletally immature athletes. Am J Orthop 32:103–105, 2003. 78. Keys GW, Walters J: Nonunion of intercondylar eminence fracture of the tibia. J Trauma 28:870–871, 1988. 79. Sullivan DJ, Dines DM, Hershon SJ, et al: Natural history of a type III fracture of the intercondylar eminence of the tibia in an adult. A case report. Am J Sports Med 17:132–133, 1989. 80. Lombardo SJ: Avulsion of a fibrous union of the intercondylar eminence of the tibia. A case report. J Bone Joint Surg Am 76:1565–1568, 1994.

Chapter 27

Congenital Knee Deformities Kevin E. Klingele

Congenital Dislocation of the Knee Congenital dislocation of the knee is a rare spectrum of disease, affecting an estimated 1.7–6.8 of every 100,000 live births.1,2 First described by Chatelain in 1822, this disorder rarely presents as an isolated entity.3 Developmental hip dysplasia (DDH) has been reported to occur in nearly 50–100% of cases.4–10 Similarly, multiple foot anomalies have been reported, with clubfoot deformity occurring in over 40% of patients with congenital knee dislocation.4,7,10 More importantly, however, is the common association of disorders such as Larsen’s syndrome, arthrogryposis multiplex congenita, myelomeningocele, spondyloepiphyseal dysplasia, Ehler-Danlos syndrome, Down syndrome, Streeter’s syndrome, and the 49,XXXXY variant of Klinefelter’s syndrome. This has led many authors to characterize congenital knee dislocation as a so-called syndrome rather than a disorder, based on the many associated disease processes. Other associated clinical findings can include congenital elbow dislocation, torticollis, cleft lip/palate, cryptochordism, imperforate anus, camptodactyly, facial paralysis, scoliosis, angiomata, and strabismus. Congenital dislocation of the knee is thought to be approximately two to three times more likely to occur in females, with equal involvement of both limbs and bilateral involvement in approximately one third of all cases. Etiology The true cause of congenital dislocation of the knee is unknown. Theories include developmental or mesenchymal defects, endocrine disorders, genetic selection, and teratogenic agents. Although frequently associated with other hereditary disorders, a definite genetic etiology has not been found. Nevertheless, a review of 212 cases reported a 7% positive family history.11 In addition, one case report described a mother with three children, all of whom had congenital knee dislocation and different fathers.12 Early theories relate the condition to malposition in utero, with hyperextension at the knees due to extended

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James R. Kasser

periods of breech positioning and/or oligohydramnios.3,13,14 With such abnormal fetal positioning (Figure 27–1), the feet can lock onto the mandible or axilla, often producing secondary deformity. Breech presentation is more common in this population, occurring in up to 40% of newborns with congenital knee dislocation or hyperextension.7 Other early theories point toward birth trauma as the cause. Hyperextension of the knee during delivery, however, more commonly produces fractures of the distal femur and/or physis rather than dislocation. Katz et al.8 proposed that an absence of the cruciate ligaments leads to congenital dislocation. Subsequent authors refute this, claiming it to be a secondary finding not seen in all patients.5 Perhaps the most widely accepted theory relates to the universal finding of quadriceps muscle contracture in these patients. In a review of 135 cases, Middleton15 attributed fibrosis and contracture of the quadriceps muscle group to intrauterine fibrofatty degeneration. Ferris et al.6 proposed some period of intrauterine ischemia and subsequent compartment syndrome leading to fibrosis. Uhthoff and Ogata16 reported partial quadriceps fibrosis and an abnormal suprapatellar pouch in a 19.5-week-old spontaneously aborted fetus. Many authors agree that a shortened and fibrotic quadriceps muscle group is more than likely the cause, rather than the result, of congenital knee dislocation.5,16–19 Classification Congenital dislocation of the knee is a disorder characterized by varying levels of severity. The most commonly used classification system is a modified version of the system proposed by Leveuf and Pais in 1946.5 As seen in Figure 27–2, this system subclassifies congenital knee dislocation based simply on the tibiofemoral articular relationship. Grade I, or simple genu recurvatum, produces a knee that hyperextends 15–20 degrees and can be flexed 45–90 degrees. Radiographs show a normal relationship between femur and 421

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Figure 27–1 Congenital dislocation of the knee. A, Lateral view of the affected limb. B, Posterior view of the affected limb. Note the hyperextension deformity of the knee and ipsilateral hip dislocation. (Reprinted with permission from Tachdjian MO: Clinical Pediatric Orthopaedics. Stamford, Appleton and Lange, 1997, p 88.)

tibia without subluxation. Grade II disease produces anterior tibial subluxation with a knee that often feels unstable and hyperextends more than 15 degrees. Total anterior displacement of the tibia in relationship to the femur is considered Grade III. No contact exists between the femoral condyles and the dislocated proximal tibia. Other classification systems have been described. Carlson and O’Conner described three types of patients with congenital knee dislocations: those with isolated dislocations, those with multiple dislocations, and those with associated syndrome.20–22

dislocation are born with varying degrees of mild to severe hyperextension at the knee, with marked limitations to flexion (Figure 27–3). This can often be readily apparent to the physician, as well as to the parents and family. With severe disease, the proximal tibial surface may be felt lying anterior to the surface of the distal femur. The skin along the anterior knee surface may show deep, transverse creases or folds. Varying ability to correct the deformity may indicate milder disease or the reduction of a previous complete dislocation. Quadriceps atrophy is also seen. In addition, close evaluation of the hips and feet is warranted because of the frequent association of such conditions as DDH and clubfoot.4–10

Clinical Features A normal newborn presents with a posture of slight flexion at the hip and knee, related to age-appropriate hip and knee contracture. In contrast, children with congenital knee

Radiographic Findings Congenital knee dislocation can be diagnosed by prenatal ultrasound, with the earliest reported finding occurring at

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Figure 27–2 Classification of congenital dislocation of the knee. A, Grade I: minimal anterior displacement of the tibia. B, Grade II: moderate anterior subluxation of the tibia with remaining femorotibial contact. C, Grade III: complete anterior dislocation of the tibia without femorotibial contact. (Reprinted with permission from Tachdjian MO: Clinical Pediatric Orthopaedics. Stamford, Appleton and Lange, 1997, p 89.)

Figure 27–4 Lateral radiograph of congenital dislocation of the knee.

Figure 27–3 Clinical photograph of congenital dislocation of the knee. (Reprinted with permission from Morrissy RT, Weinstein SL: Lovell and Winter’s Pediatric Orthopaedics. 4th edition. Philadelphia, Lippincott-Raven, 1996, p 1062.)

19.5 weeks gestation.16,23 In the newborn with clinical findings supportive of such a disorder, anteroposterior and lateral radiographs confirm the suspicion (Figure 27–4). On the anteroposterior view, a valgus deformity may be seen with or without slight lateral subluxation of the tibia. The distal femur and proximal tibial ossification centers, normally present in a full-term infant’s x-ray, may be absent or hypoplastic due to a delay in development. Lateral radiographs are important to assess the tibiofemoral relationship. This allows adequate classification of the hyperextension deformity. Lateral views taken in both full extension and maximum flexion help verify and assess the reducibility of the dislocated knee. An exaggerated posterior tibial slope is also evident. Ultrasound may be useful in determining the tibiofemoral relationship if the epiphyses are unossified.

In older children, regardless of treatment, additional radiographic findings include hypoplasia of the intercondylar notch and tibial spines (suggestive of cruciate absence or aplasia); genu valgum with proximal tibial bowing; and patellar absence, hypoplasia, or elongation. Abnormality within the distal femur epiphysis is often secondary to longstanding joint hyperlaxity or valgus angulation. Knee arthrography has been reported to help determine pathology, treatment, and even outcome of congenital dislocation of the knee.10,24 With a better understanding of the existing pathology, however, few authors now advocate its use. Magnetic resonance imaging (MRI) can also be used to assess ligamentous and meniscal presence or integrity. Sedation for MRI is usually required for children 6 years of age and younger. Pathology All reported cases of congenital knee dislocation reiterate the significant shortening, fibrosis, and atrophy of the quadriceps muscle group. The lateral portion of the quadriceps group, along with the fascia lata, is primarily affected. Vastus medialis is often spared.5 Such lateral contraction may explain the rotatory subluxation and valgus deformity

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that can accompany the hyperextension. In addition, contracture of the anterior knee capsule is seen, and adhesions between the distal femur and overlying extensor mechanism may shrink or obliterate the suprapatellar pouch.7,10,25 The extent of such pathology will dictate the severity of the disorder and its response to treatment. Several reports describe anterior subluxation of the collateral ligaments and hamstring tendons.10,25,26 Approximately 50% of patients will present with lateral patellar dislocation. In addition, an absent or hypoplastic anterior cruciate ligament (ACL) can be seen, as well as an absent or shortened, tight posterior cruciate ligament (PCL).8,27 Meniscal hypoplasia has been reported.10 Neurovascular structures within the popliteal region are usually normal, and an exaggerated posterior tibial slope and flattening of the femoral epiphysis is often evident. Treatment Treatment of congenital knee dislocation depends on the classification, severity, and flexibility of the deformity. Regardless of the presentation, however, treatment should be started as soon as possible. Much like developmental hip dysplasia and clubfoot, an improved response to early institution of conservative treatment is seen.9,26 Conservative treatment consists of serial manipulations in an effort to improve flexion and reduce tibiofemoral subluxation or dislocation. Manual traction is applied first, followed by a posteriorly directed tibial force, an anteriorly directed femoral force, and then flexion once the joint surface is in contact. Daily to weekly manipulations have been suggested, each followed by either longleg casting or posterior splinting to maintain correction.* Femoral nerve blocks can be used to decrease resistance of the shortened and fibrotic quadriceps. Skin or skeletal traction may also help obtain flexion before casting. Children with Grade I or II disease but without associated disorders often respond to treatment within the first several weeks.6,28 Poor prognostic indicators for a positive response to conservative treatment include Grade III disease; associated syndromes such as arthrogryposis, Larsen’s syndrome, and DDH; and institution of treatment later than 3 months of age.6,7,9,10,28 Children with a normal tibiofemoral relationship and approximately 60–90 degrees of flexion should then be placed in nightly bivalved casts with daily stretching, or more commonly into a Pavlik-type harness. The harness is often beneficial because of the high association of DDH seen in these patients. In those without DDH, the harness can be discontinued once knee flexion of nearly normal, or 120 degrees, is achieved. If lateral subluxation exists, use of a Pavlik harness is contraindicated.29 Reports of spontaneous resolution in those with isolated knee dislocation have led some to suggest waiting at least 1 month before institution of treatment.13 In addition, acute reduction of a knee dislocation in a newborn less than 1 day old has been reported.9 Nevertheless, most now agree that children who will respond to conservative treatment will do so best with stretching, manipulation, and casting instituted as early as possible. For those who fail to achieve reduction of the tibiofemoral articulation or adequate knee flexion, opera*

References 5, 7, 9, 10, 13, 28.

tive open reduction is indicated. Timing of open reduction often relies on the patient’s medical status and the many confounding medical issues and their associated syndrome. Some advocate surgical reduction within the first 1–2 years of life.6,7,10 Others suggest reduction within 3–6 months, allowing more remodeling to occur.4,27 Regardless, the goal of operative treatment is to remove any obstacles to reduction, improve intraoperative knee flexion to at least 90 degrees, and correct factors that may lead to recurrence, instability, or future deformity. Varying levels of release are required. A significantly shortened and fibrotic quadriceps is always present along with a contracted anterior capsule. Extensive quadricepsplasty often requires sectioning of the fascia lata, release of the vastus lateralis off the intermuscular septum and femur, and sectioning of the anterior joint capsule. Multiple methods of quadriceps lengthening can be utilized, with a V–Y quadricepsplasty advocated (Technical Note 27–1). Often this will allow reduction of the tibiofemoral articulation and improved knee flexion. Femoral shortening provides an attractive alternative to the often extensive quadricepsplasty. Such technique limits the amount of required dissection, lengthening, and reconstruction of an already atrophic and thin quadriceps tendon. This technique is especially beneficial for simultaneous open reduction of ipsilateral hip and knee dislocations. Roy and Crawford22 have described a percutaneous technique of quadriceps recession, which when performed in the neonate, provided good results. Such a technique is proposed only in patients with coexisting deformity such as arthrogryposis multiplex congenital, Larsen’s syndrome, or myelomeningocele. Anterior subluxation of collateral ligaments and hamstring tendons may require mobilization of these structures. A tight and shortened posterior cruciate ligament may need release.27 If significant valgus deformity exists, posterior transposition and advancement of the medial collateral ligament (MCL) and pes anserinus complex may help prevent further deformity.10 In addition, associated hypoplasia or absence of the anterior cruciate ligament has led some to advocate physeal-sparing reconstruction to be done at the index procedure.8 Postoperatively, patients are immobilized to the degree of flexion that does not seem to compromise the vascular status of the limb or the incision site. Serial bracing or casting is often useful in the postoperative course as well, helping to improve and maintain knee flexion. In children with associated developmental dysplasia of the hip or multiple-joint instability, adequate treatment of the knee deformity should take place before harness placement or hip reduction.5,9,10 Lack of knee motion causes difficulty in applying a Pavlik harness, maintaining good hip position, and controlling hip rotation. Once knee flexion is obtained, with or without surgery, the child may be placed in a Pavlik harness, aiding in the treatment of both knee and hip pathology. Simultaneous open reductions can be performed. In children with coexisting clubfeet, manipulation and incorporation of the feet into long-leg casts can be done with the original casting (Technical Note 27-1).

Congenital Knee Deformities

TECHNICAL NOTE 27–1

Quadricepsplasty for Congenital Knee Dislocation Edward C. Sun • James R. Kasser

Curtis and Fisher1 distinguish three types of congenital dislocation of the knee: recurvatum, subluxation, and dislocation. The majority of those with recurvatum and subluxation will resolve satisfactorily with serial manipulation and splinting; however, those with dislocation often require surgical reduction. Our indication for surgery consists of those patients who failed a trial course of serial manipulation with (1) persistent anterior subluxation/dislocation of the tibia on the femur as visualized on a lateral radiograph or (2) failure to obtain 45 degrees of knee flexion. Pathological findings at surgery include quadriceps fibrosis, ablation of the suprapatellar pouch, anterior dislocation of the hamstring tendons and collateral ligaments, and femoral and tibial articular surface dysplasia. The anterior cruciate ligament has been reported as usually present,2 absent,3 elongated,4 or shortened.5 The patella is laterally subluxed about 50% of the time.1 To obtain a reduction, the following steps must be taken: free the quadriceps and the lateral retinaculum from the underlying femur, divide the anterior capsule, mobilize the collateral ligaments, and lengthen the quadriceps mechanism.

Technique The patient is positioned supine, and a midline longitudinal incision is made from the tibial tubercle to the middle of the thigh (Figure 27–5). The underlying quadriceps muscle, the patella, the patellar tendon, and the lateral retinaculum are sharply dissected. The subluxated hamstring tendons and the collateral ligaments should be identified. Fibrosis with a reduction in the bulk of the quadriceps muscle is frequently seen. We prefer to perform V-to-Y advancement of the quadriceps mechanism. The entire quadriceps tendon proximal to the patella should be exposed, and the medial and lateral fibers are detached from the tendon (Figure 27–6). A small amount of tendinous tissue should remain with the muscle to facilitate later repair. The incision is carried distally on each side of the patella to divide the medial and lateral retinaculum. The anterior capsule is then divided transversely to the medial and lateral collateral ligament. The ligamentous structures can then be mobilized so that they can be displaced posteriorly as the knee is flexed. If the tibia is in

Figure 27–5 A midline longitudinal incision is made from the tibial tubercle to the middle of the thigh. (Reprinted with permission from Morrissy RT, Weinstein SL: Atlas of Pediatric Orthopaedic Surgery. Philadelphia: Lippincott Williams & Wilkins, 2001, p 629.)

Continued

425

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TECHNICAL NOTE 27–1

Quadricepsplasty for Congenital Knee Dislocation (Continued)

Figure 27–6 The medial and lateral quadriceps fibers are attached from the quadriceps tendon. The medial retinaculum and lateral retinaculum are separated from the patella. A V-shaped incision is made in the quadriceps tendon. The knee joint is inspected. (Reprinted with permission from Morrissy RT, Weinstein SL: Atlas of Pediatric Orthopaedic Surgery. Philadelphia: Lippincott Williams & Wilkins, 2001, p 631.)

valgus and external rotation, the iliotibial band should be divided as well. In patients with a laterally subluxed patella, the release of the lateral portion of the patellar tendon or Goldthwait type procedure may be needed to centralize the patella over the femoral trochlea. At this point, the joint can be inspected (Figure 27–6). The menisci are usually intact, and the pathology in the cruciate ligaments is variable. The quadriceps muscle and the lateral retinaculum

should be mobilized from the underlying femur to obtain reduction and flexion of the dislocated tibia. This can be facilitated by dividing the posterior border of the lateralis and medialis sharply and freeing the muscle flap from the underlying femur. Reduction can usually be affected by flexing the knee. The amount of extension that permits redislocation should be noted. With the knee flexed about 40 degrees, the medialis and lateralis are reattached to the Continued

Congenital Knee Deformities

TECHNICAL NOTE 27–1

Quadricepsplasty for Congenital Knee Dislocation (Continued) quadriceps tendon in their new position, creating the V-to-Y advancement (Figure 27–7). The retinaculum does not require closure. The wound is closed, and the leg is immobilized in sufficient flexion so that there is no tendency for the tibia to subluxate anteriorly. We have found that 40 degrees of flexion is generally adequate. Postoperative Management The knee is immobilized for 6 weeks, and the patient is started on active and passive motion

exercises thereafter. Quadriceps stimulation exercises are emphasized. Results Most studies indicate that patients generally achieve flexion greater than 90 degrees with flexion contracture in the 0–15-degree range. Most have residual quadriceps weakness and residual instability with stress testing (pivot shift, varus/valgus stress). Most studies report good results if the surgery is performed early (10 years) and ankle range of motion is depending on age of normal. Hip range of motion onset. should be checked to see if flex2. The etiology of ion or internal rotation are lackBlount’s disease is ing or cause pain, possibly unknown. Mechaniindicative of a slipped capital cal factors associfemoral epiphysis. ated with excessive Radiographs should be fullbody weight leading length, standing AP films to to medial physeal assess the presence of tibial and overload are thought possibly femoral deformity. The to play a role in growth plate needs to be assessed by MRI or CT to determine the

Angular Deformity About the Knee in Children

presence or absence of a physeal bar. Lateral knee and tibial radiographs will ascertain the extent of a procurvatum deformity. Like the juvenile form, treatment is surgical. Because this is a growth disturbance, continued growth will worsen, not improve, the situation. The presence of associated femoral deformity is established, and the need and type of additional surgical correction are determined. Generally speaking, these children are very large and warrant relatively rigid fixation. Fibular and distal tibial osteotomy with gradual or acute correction is the treatment of choice. It should be remembered that closing wedge osteotomy shortens the limb, whereas opening wedge osteotomy (either acutely or gradually) does not do this. Generally speaking, if a physeal bar is identified, concurrent lateral epiphysiodesis of the tibia is indicated. Because there is little growth remaining, epiphysiodesis of the fibula is usually not necessary. Internal and external fixation each have their advocates. Internal fixation avoids the “contraption” factor but allows no postoperative adjustment, if required. If an acute opening wedge correction fixed externally does not heal, it is easily salvaged by compressing the osteotomy site and distracting it gradually. This is not possible with internal fixation. The other issue, which can be raised at any age, is that there is postoperative adjustability of external fixation that does not exist with internal fixation. However, external fixators of any type are external devices with pin sites, which must be cared for to avoid potential bone infection. Depending on the manner of pin insertion, ring sequestra are also possible, particularly in cortical diaphyseal bone. Recurrence and/or significant limb-length inequality are rare in adolescent Blount’s disease. The real issue for infantile, juvenile, and adolescent Blount’s disease is that its etiology remains enigmatic.

KEY POINTS

3.

4.

5.

6.

7.

8.

combination with biological factors. Langenskiold’s grading system for infantile tibia vara illustrates progressive physeal involvement and deformity, leading to complete medial physeal deformity and arrest in the most severe cases. In contrast to adolescent Blount’s disease, the infantile form is usually bilateral, often with varying side-to-side magnitudes of involvement. Lower extremity alignment radiographs are preferably done standing with the patella positioned directly anterior. Treatment of infantile Blount’s disease is usually surgical via osteotomy. Hemiepiphysiodesis and stapling may lead to unpredictable outcomes. Brace treatment for less severe deformities does not have predictable results. Noncompliance is a common problem during brace treatment. External fixator use with osteotomies allows postoperative alignment correction by fixator adjustments. Tibial deformity magnitude in adolescent Blount’s Disease is usually less than in the infantile type. Associated excessive distal femoral varus or valgus may be present in the juvenile and adolescent varieties.

449

References 1. Kling TF Jr., Hensinger RN: Angular and torsional deformities of the lower limbs in children. Clin Orthop 176:136–147, 1983. 2. Heath CH, Staheli LT: Normal limits of knee angle in white children—genu varum and genu valgum. J Pediatr Orthop 13:259–262, 1993. 3. Dietz FR, Merchant TC: Indications for osteotomy of the tibia in children. J Pediatr Orthop 10:486–490, 1990. 4. Scott CI: Achondroplastic and hypochondroplastic dwarfism. Clin Ortho 114:14–18, 1976. 5. Kozlowski K: Metaphyseal and spondylometaphyseal chondrodysplasias. Clin Orthop 114:83–93, 1976. 6. Kopits SE, Lindstrom JA, McKusick VA: Pseudoachondroplastic dysplasia: pathodynamics and management. Birth Defects Orig Artic Ser 10:341–352, 1974. 7. Sillence D: Osteogenesis imperfecta: an expanding panorama of variants. Clin Orthop 159:11–25, 1981. 8. Sheridan RM, Chiroff RT, Friedman EM: Operative and non-operative treatment of rachitic lower extremity deformities. A long-term study with forty-six year average follow-up. Clin Orthop 116:66–69, 1976. 9. Crutchlow WP, David DS, Whitsell J: Multiple skeletal complications in a case of chronic renal failure treated by kidney homotransplantation. Am J Med 50:309–394, 1971. 10. Cozen L: Fracture of the proximal portion of the tibia in children followed by valgus deformity. Surg Gynecol Obstet 97:183–188, 1953. 11. Tuten HR, Keeler KA, Gabos PG, et al: Posttraumatic tibia valga in children. A long-term follow-up note. J Bone Joint Surg Am 81:799–810, 1999. 12. Erlacher P: Peformierende prozesse der epiphysen gegend bei kinderm. Arch Orthop Unfallchiiv 20:81–96, 1922. 13. Langenskiold A: Tibia vara: a summary of 23 cases. Acta Orthop Scand 14(2):103, 1952. 14. Langenskiold A: Tibia vara. A critical review. Clin Orthop 246:195–207, 1989. 15. Blount WP: Tibia vara, osteochondrosis deformans tibiae. Curr Pract Orthop Surg 3:141–156, 1966. 16. Thompson GH, Carter JR: Late-onset tibia vara (Blount’s disease). Current concepts. Clin Orthop 255:24–35, 1990. 17. Thompson GH, Carter JR, Smith CW: Late-onset tibia vara: a comparative analysis. J Pediatr Orthop 4:185–194, 1984. 18. Cook SD, Lavernia CJ, Burke SW, et al: A biomechanical analysis of the etiology of tibia vara. J Pediatr Orthop 3:449–454, 1983. 19. Davids JR, Huskamp M, Bagley AM: A dynamic biomechanical analysis of the etiology of adolescent tibia vara. J Pediatr Orthop 16:461–488, 1996. 20. Stanitski DF, Stanitski CL, Trumble S: Depression of the medial tibial plateau in early-onset Blount disease: myth or reality? J Pediatr Orthop 19:265–269, 1999. 21. Thompson GH, Carter JR: Late-onset tibia vara (Blount’s disease). Current concepts. Clin Orthop 255:24–35, 1990. 22. Bowen RE, Dorey FJ, Moseley CF: Relative tibial and femoral varus as a predictor of progression of varus deformities of the lower limbs in young children. J Pediatr Orthop 22:105–111, 2002. 23. McCarthy JJ, Betz RR, Kim A, et al: Early radiographic differentiation of infantile tibia vara from physiologic bowing using the femoral-tibial ratio. J Pediatr Orthop, 21:545–548, 2001. 24. Greene WB: Infantile tibia vara. Instr Course Lect 42:525–538, 1993. 25. Levine AM, Drennan JC: Physiological bowing and tibia vara. The metaphyseal-diaphyseal angle in the measurement of bowleg deformities. J Bone Joint Surg Am 64:1158–1163, 1982. 26. Feldman MD, Schoenecker PL: Use of the metaphyseal-diaphyseal angle in the evaluation of bowed legs. J Bone Joint Surg Am 75:1602–1609, 1993. 27. Beck CL, Burke SW, Roberts JM, et al: Physeal bridge resection in infantile Blount disease. J Pediatr Orthop 7:161–163, 1987. 28. Choi IH, Kim CJ, Cho TJ, et al: Focal fibrocartilaginous dysplasia of long bones: report of eight additional cases and literature review. J Pediatr Orthop 20:421–427, 2000. 29. Raney EM, Topoleski TA, Yaghoubian R, et al: Orthotic treatment of infantile tibia vara. J Pediatr Orthop 18:670–674, 1998. 30. Richards BS, Katz DE, Sims JB: Effectiveness of brace treatment in early infantile Blount’s disease. J Pediatr Orthop 18:374–380, 1998.

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31. Doyle BS, Volk AG, Smith CF: Infantile Blount disease: long-term follow-up of surgically treated patients at skeletal maturity. J Pediatr Orthop 16:469–476, 1996. 32. Young NL, Davis RJ, Bell DF, et al: Electromyographic and nerve conduction changes after tibial lengthening by the Ilizarov method. J Pediatric Orthop 13:473–477, 1993. 33. Canale ST, Harper MC: Biotrigonometric analysis and practical applications of osteotomies of tibia in children. Instr Course Lect 30:85–101, 1981. 34. Rab GT: Oblique tibial osteotomy for Blount’s disease (tibia vara). J Pediatr Orthop 8:715–720, 1988. 35. Martin SD, Moran MC, Martin TL, et al: Proximal tibial osteotomy with compression plate fixation for tibia vara. J Pediatr Orthop 14:619–622, 1994. 36. Smith SL, Beckish ML, Winters SC, et al: Treatment of late-onset tibia vara using Afghan percutaneous osteotomy and orthofix external fixation. J Pediatr Orthop 20:606–610, 2000. 37. Alekberov C, Shevtsov VI, Karatosun V, et al: Treatment of tibia vara by the Ilizarov method. Clin Orthop 409:199–208, 2003.

38. Stanitski DF, Srivastava P, Stanitski CL: Correction of proximal tibial deformities in adolescents with the T-G arches external fixator. J Pediatr Orthop 18:512–517, 1998. 39. Rajacich N, Bell DF, Armstrong PF: Pediatric applications of the Ilizarov method. Clin Orthop 280:72–80, 1992. 40. Zuege RC, Kempken TG, Blount WP: Epiphyseal stapling for angular deformity at the knee. J Bone Joint Surg Am 61:320–329, 1979. 41. Stanitski CL: Correlation of arthroscopic and clinical examinations with magnetic resonance imaging findings of injured knees in children and adolescents. Am J Sports Med 26:2–6, 1998. 42. Gregosiewicz A, Wosko I, Kandzierski G, et al: Double-elevating osteotomy of tibiae in the treatment of severe cases of Blount’s disease. J Pediatr Orthop 9:178–181, 1989. 43. Kline SC, Bostrum M, Griffin PP: Femoral varus: an important component in late-onset Blount’s disease. J Pediatr Orthop 12:197–206, 1992. 44. Henderson RC: Tibia vara: a complication of adolescent obesity. J Pediatr 121:482–486, 1992.

Chapter 29

Infection Danielle A. Katz

Along with acute trauma and overuse injuries, infection can be a cause of knee pain in children and adolescents. Over the past century, there has been marked improvement in early diagnosis and appropriate treatment of musculoskeletal infections, leading to greatly improved outcomes. Nonetheless, the diagnosis can be difficult to make and often requires a high index of suspicion. Delayed diagnosis and treatment can lead to devastating results. This chapter will review the epidemiology, pathophysiology, diagnosis, and treatment of infections about the knee in pediatric patients. Osteomyelitis and Septic Arthritis Epidemiology Acute hematogenous osteomyelitis (AHO) and septic arthritis are most common in the first decade of life.1–3 Approximately 40% of cases of septic arthritis occur in the knee,4–7 and approximately 30% of cases of AHO occur about the knee (distal femur, proximal tibia, proximal fibula).8,9 Some reports indicate an equal prevalence between males and females, whereas others show a male predominance.7,8,10–13 Since the widespread availability of antibiotics in the 1940s, rates of fulminant osteomyelitis have decreased, whereas rates of subacute osteomyelitis have increased.1,8,14–16 Pathophysiology The development of osteomyelitis and septic arthritis is related to the bony, intraarticular, and vascular anatomy.2,14,16–18 AHO occurs when organisms from a bacteremia lodge in bone and proliferate more quickly than they can be cleared by the patient’s immune system. Morrissy and Haynes19 created a rabbit model in which to study AHO. They found that following the production of a bacteremia, the organisms could first be detected within the medullary canal of a long bone but that they were quickly cleared from this area. Fewer organisms were found to settle in the

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Mininder S. Kocher

metaphysis, but these quickly multiplied with the paucity of nearby phagocytic cells. Thus clinical manifestations of AHO typically begin in the metaphyses of long bones. In this region, the cancellous bone is permeated by terminal arterial branches emptying into venous sinusoids, resulting in a region of slow flow.2,14,16,18 Furthermore, in this area the vessels have small gaps that allow blood cells and bacteria to enter the extravascular space.2,14,18 Bacteria in the extravascular space are further removed from immune mediators and may serve as a nidus of infection.14 Bacteremia occurs in a variety of situations, but not all bacteremia leads to clinical infection.20 Infection occurs when there is imbalance between pathogenicity and host defenses. Many investigators believe that the establishment of clinical infection thus requires an additional insult to host defenses in the presence of bacteremia.20 One proposed mechanism is that trauma can alter the local environment sufficiently to allow the initiation of AHO.19–22 Rabbit models have found that a sufficiently large bacteremic load alone resulted in small, well-contained loci of AHO. When a physeal injury was created in the presence of the same degree of bacteremia, however, AHO consistently developed in the area underneath the injured physis. In addition, AHO developed in nearly all specimens with trauma and a bacteremic load not sufficient to produce AHO in the absence of trauma.19,20 Infection has effects on bone formation and resorption. Polymorphonuclear leukocytes (PMNs) are part of the body’s first-line defense against infection. PMNs release interleukin-1 (IL-1), which propagates inflammation and stimulates the release of prostaglandin E2 (PGE2). PGE2 is also released directly from Staphylococcus aureus. PGE2 stimulates bone resorption. Infection can result in bone necrosis, resulting in a sequestrum (area of necrosis). The arrangement of the sequestrum and the reactive new bone that forms around is called an involucrum.2,14,23,24 Infection that begins in the cancellous bone of the metaphysis may break through the cortex, which is thinner than 451

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that in the diaphysis. The periosteumin in children is quite thick and may serve to contain infection even after it has progressed through the cortex. This can result in a subperiosteal abscess. Although the periosteum is lifted up from the cortex, its viability is not impaired (because its blood supply enters superficially), and it continues to produce new bone. Sometimes, however, the infection continues through the periosteum. In some areas, this will allow spread into the surrounding soft tissues. At four locations (proximal femur, proximal humerus, proximal radius, distal tibia, and distal fibula) the metaphysis is within the capsule of the adjacent joint. In these areas, eruption of AHO through the periosteum can result in septic arthritis as well. Septic arthritis may also develop independent of osteomyelitis. The synovial lining of joints is a highly vascular tissue without a basement membrane.2,25,26 It filters out a transudate from the circulating blood to create synovial fluid. Therefore, it is possible to have direct seeding of a joint from bacteremia. Joints are able to clear a finite bacterial load.27 When this threshold is exceeded, bacteria proliferate rapidly within the nutrition-rich and relatively avascular intraarticular environment. The consequences of untreated or inadequately treated septic arthritis can be devastating because of the damage caused to KEY POINTS articular surfaces and intracapsular physes. Soon after the estab1. Bacteremia is the lishment of infection, there is loss most common of glycosaminoglycans from articsource of 28 ular cartilage. Subsequently osteomyelitis and there is a decrease in collagen septic arthritis. Local 28–31 content. This chondrolysis is trauma may be a believed to result from the effects contributing factor. of inflammatory cytokines that 2. AHO typically enter the joint in response to the begins in the metainfection or from proteolytic physis because of enzymes released by certain bacteslow blood flow and 2,29–34 ria (e.g., S. aureus). vascular gaps that Finally, both septic arthritis allow bacteria into and osteomyelitis may result from the extravascular direct inoculation as a result of space. trauma. Open fractures and direct 3. Infection causes penetrating trauma are the most bone necrosis. common routes of direct inocula4. Septic arthritis can tion leading to osteomyelitis and lead to destruction septic arthritis. Early and aggresof articular cartisive treatment has made many of lage and intracapthe adverse sequelae of direct sular physes. inoculation preventable. Diagnosis History Pain is the most frequent presenting symptom of musculoskeletal infection.9,12 Small children, however, may not be able to verbalize their pain and may present only with a history of limping or refusal to bear weight. Sometimes osteomyelitis or septic arthritis may cause a child to present with fever that has not yet been explained. Infants may simply have a history of being unusually fussy; less commonly, they present as systemically septic.

A history of trauma is not unusual.11 Concern for infection should be raised when the pain seems to be greater than would have been expected from the traumatic event, or when the pain worsens over the days following the injury instead of improving. The role of trauma in predisposing to osteomyelitis has been discussed in greater detail previously. Additionally, it is helpful to determine whether there has been recent or chronic illness. Recent illness may alert the physician to the possibility of infection (e.g., strep osteomyelitis or septic arthritis following strep throat) or transient immunosuppression (e.g., secondary to chickenpox), allowing the development of bone or joint infection.35 Recent antibiotic use may also mask symptoms of osteomyelitis or septic arthritis; partially treated or subacute infections are also being seen more often.1,8,14–16 Chronic illness or other causes for immunosuppression (e.g., human immunodeficiency virus, transplantation, steroid use) may also be risk factors for osteomyelitis and septic arthritis. Physical Examination As always, the physical examination begins with observation of the child. The general appearance may be variable depending on the extent and severity of infection. Sometimes the child will appear quite comfortable until the affected part is manipulated or the child is asked to bear weight. Often the patient is irritable and appears uncomfortable, but rarely do patients present systemically ill. Particularly in the small child, a great deal of information can be obtained from observation alone. The patient’s limp or refusal to bear weight or voluntarily move the affected extremity can be the only consistent finding on exam. An infected knee (either with septic arthritis or AHO) is frequently swollen and may be warm and erythematous. Classic signs of infection are dolor (pain), tumor (swelling), rubor (redness), and calor (warmth). The skin must be inspected because it may show evidence of direct inoculation of infection. The presence of other skin lesions may suggest the etiology of the symptoms (e.g., Lyme disease, psoriatic arthritis). Since the diagnosis is often not immediately apparent, it is important to examine the child’s hip, back, thigh, leg, ankle, and foot to localize the origin of the symptoms. Fever is a helpful finding in making the diagnosis, but not a necessary one.9,12 Tenderness to palpation is a consistent finding in both AHO and septic arthritis but may be difficult to ascertain in a young child who begins crying simply in response to the approach of the physician. In these cases, it may be helpful to instruct the parent how to perform the examination and KEY POINTS allow the parent to determine the area of maximal discomfort. 1. Pain is the most Septic arthritis results in an effucommon presenting sion and decreased range of symptom or sign of motion of the joint. An infected infection. knee typically lacks both full 2. Fever, although flexion and full extension. AHO often present, is not may result in a sympathetic a requirement for effusion in an adjacent joint or the diagnosis of may break through an intracapseptic arthritis or sular metaphysis to result in a osteomyelitis. concomitant septic arthritis.

Infection

453

Imaging

Ultrasound

Radiographs

Ultrasound has been used in the diagnosis of both septic arthritis and osteomyelitis.37,38 Ultrasound can confirm a clinical impression of joint effusion, particularly in joints not easily palpated.39 The knee joint is easily aspirated without imaging guidance, but ultrasound may be useful to guide aspiration of the hip. Ultrasound can also show areas

Radiographs are typically the first imaging study obtained in the evaluation of a possible septic arthritis or AHO. True anteroposterior (AP) and lateral views of the knee are imperative. A small effusion may only be detected on a true lateral view and obscured on an oblique view. An effusion is the primary radiographic finding in septic arthritis. Radiographic signs of AHO are subtle at first and become increasingly obvious with progression of the infectious process and bone destruction.36 Within approximately 3 days of the onset of symptoms, deep soft-tissue swelling adjacent to the metaphysis becomes noticeable (Figure 29–1). This is detected by observation that the soft-tissue swelling has displaced the lucent plane between muscle and bone away from the bone. Comparison views of the contralateral side in identical position may be required to identify this subtle change. Within a week of the onset of symptoms, the muscle swelling is more pronounced, and there may be obliteration of the lucent planes normally seen between muscles. A lytic lesion within the bone typically is not seen until 10–12 days after the onset of symptoms (Figure 29–2). If left untreated (or inadequately treated), chronic osteomyelitis may develop. Radiographically, this is evident by further bony destruction. If the cortical bone becomes devascularized and necrotic, it becomes a sequestrum, which is seen as an area of sclerosis on radiographs. When the adjacent periosteum responds with new bone formation around the sequestrum, an involucrum develops (Figure 29–3).2,14,36 Osteomyelitis typically does not cross an open physis, but of the processes radiographically found to cross the physis, AHO is the most common.

Figure 29–2 Lytic abscess associated with osteomyelitis.

Figure 29–1 Soft-tissue swelling of the leg associated with osteomyelitis.

Figure 29–3 Sequestrum associated with osteomyelitis.

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of subperiosteal fluid collection and may be useful in guiding aspiration or in determining the need for operative drainage and debridement of a subperiosteal abscess.37,40 Radionuclide Scintigraphy (Bone Scan) Radionuclide scintigraphy is a sensitive tool for the detection of septic arthritis and osteomyelitis.2,14,41–44 The most commonly used technique is a three-phase bone scan with technetium-99 labeled diphosphonate (Figure 29–4). The first phase is an image obtained immediately after injection that is essentially an angiogram. The second-phase image is obtained soon thereafter and is the “blood-pooling” phase in which accumulation in the soft tissues is best identified. This phase can be helpful in distinguishing cellulitis from osteomyelitis or septic arthritis. The third phase occurs after 2–4 hours and shows uptake into bony areas of high blood flow and bone formation. This phase is most helpful in the diagnosis of osteomyelitis and septic arthritis. It is important to recognize, however, that although radionuclide scintigraphy is sensitive for infection, it is not specific. Any process causing hyperemia and bone formation (including tumors, fracture, disuse osteopenia) may result in increased uptake on bone scan, also known as a “hot” scan. In children, the physes are such an area. Because osteomyelitis often has a metaphyseal location, it is particularly important to obtain “pinhole” images of areas suspicious for osteomyelitis to distinguish from the marked uptake of the adjacent physis. Generally in osteomyelitis, there is increased or decreased uptake extending beyond the limits of the capsular attachments. In septic arthritis, however, there is increased or decreased uptake on either side of the joint, but this is confined to and uniform within the limits of the capsule.44 Bone-scan images also can demonstrate areas of decreased uptake, also known as “cold” scans. This occurs

when there is decreased blood flow to an area, as may be seen with an abscess or sequestrum. More than one study has found that the positive predictive value of a “cold” bone scan was 100%.9,44 If the diagnosis is still unclear after a technetium bone scan, an indium-labeled white blood cell scan may be useful. In this technique, blood is drawn from the patient, and the white cells are labeled with indium and injected back into the patient’s circulatory system. Images obtained approximately 24 hours after reinfusion show areas of increased presence of white blood cells, which are more specific for infection than the technetium scans. Computed Tomography The role for computed tomography (CT) in the evaluation of AHO and septic arthritis about the knee is limited. CT can provide excellent detail of bony anatomy and may show soft-tissue involvement, but it exposes the child to radiation and does not show soft tissues as well as magnetic resonance imaging (MRI). The knee joint and adjacent metaphyses are usually aspirated without difficulty, but CT may be useful in guiding aspiration of less accessible locations (e.g., hip, spine). Magnetic Resonance Imaging MRI does not expose the patient to radiation and is very sensitive in demonstrating inflammation and fluid collections. MRI clearly shows joint effusions that can be the result of septic arthritis or may be a sympathetic response to osteomyelitis. Subperiosteal abscess may be visualized as a subperiosteal fluid collection on MRI. In acute osteomyelitis, the inflammation replaces the normal marrow fat. As a result, acute osteomyelitis gives rise to decreased signal intensity on T1-weighted images and increased signal intensity on T2-weighted images. Laboratory Studies

Figure 29–4 Bone scan demonstrating increased uptake in the distal femur associated with osteomyelitis.

KEY POINTS 1. Radiographs will not show bony destruction for 10–12 days after the onset of infection. 2. Ultrasound may be used to detect subperiosteal abscess. 3. Bone scan (radionuclide scintigraphy) is very sensitive, but not specific, for infection. 4. It is important to get “pinhole” images of bone scans to distinguish AHO from normal increased uptake of physes. 5. MRI is very sensitive for both AHO and septic arthritis.

Laboratory studies can be very useful in making the diagnosis of septic arthritis or osteomyelitis. Complete blood count (CBC) with differential may demonstrate an increased white blood cell count (WBC), increased platelet count, increased neutrophil count, and an increased number of immature cells (bandemia), but these are not reliable. Early in the course of infection these indices are often normal or only slightly elevated.9,45 More sensitive, however, are erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP).9,45,46 ESR rises within 48–72 hours of the onset of infection and may continue to increase for 3–5 days after the initiation of treatment. If treatment is effective, the ESR should no longer rise after 5 days of treatment, but may remain

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elevated for 2–3 weeks after treatment.45 Furthermore, ESR may be altered by conditions affecting red blood cells, including sickle cell disease and anemia, and in patients taking steroids. CRP rises within 6 hours after the onset of infection, peaks after approximately 50 hours, and typically returns to normal within 1 week of treatment. Because CRP rises and falls more quickly, it is a more timely indicator of both the onset and successful treatment of infection.2,45,47,48 Blood cultures identify the organism in approximately 30–50% of cases of AHO and septic arthritis.12,13,49 Although CRP and blood cultures are reliable indicators of infection, they do not indicate the source of infection. Cultures from the suspected bone and/or joint are useful in confirming the diagnosis and guiding appropriate treatment. In cases of suspected septic arthritis, the knee joint should be aspirated. Usually this is easily accomplished in the office or emergency room. In an older, cooperative adolescent, this may be accomplished with or without local anesthesia, whereas a younger or anxious child may require sedation. The knee may be aspirated through one or more possible sites. One approach is to have the knee extended and enter the knee medially or laterally, directing the needle under the patella. Another approach is to keep the knee flexed and to enter either anteromedially or anterolaterally through the “soft spots” at the level of the joint line adjacent to the patellar tendon. It is important to use a needle that is large enough to aspirate the thickened, purulent material; typically an 18-gauge needle is sufficient. The appearance of the fluid should be noted. Classically, infected synovial fluid is thick and cloudy. However, early on in the course of disease, the fluid may be clear. Conversely, cloudy fluid may be aspirated from joints with juvenile rheumatoid arthritis, rheumatic fever, or other inflammatory conditions. Aspiration of a rust-colored or bloody effusion may be seen after trauma, with a traumatic tap, with hemophilia, and with pigmented villonodular synovitis (PVNS). Any fluid obtained (even if it appears to be clear or only blood) should be sent for cell count with differential (determining the total number of white cells and the proportion of polymorphonuclear cells and monocytes)50, Gram stain, and culture and sensitivities. There are no clear boundaries above or below which the cell count definitively confirms or excludes the diagnosis of septic arthritis.51–53 Generally, a white count above 100,000 with more than 75% polymorphonuclear cells is very strongly suggestive of infection.50,54 Fewer than 20,000 white cells and fewer than 25% polymorphonuclear cells make infection much less likely,50 but certainly not impossible.4,53 Gram stain can provide useful information as to the likely causative organism and may be used to guide initial treatment while cultures are pending. Final cultures reveal the organism in 60–80% of cases,7,12,13,49 and determination of sensitivities helps ensure appropriate and successful treatment. Aspiration also is important in diagnosing and treating osteomyelitis. The physician should determine the point of maximal tenderness and aspirate at that site. If it is not possible to determine the most tender location, then ultrasound or CT may be useful adjuncts in guiding aspiration. If the differential diagnosis includes cellulitis without an underlying osteomyelitis, then the soft tissue should be aspirated as the needle is advanced. If purulent material is obtained,

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and radiographic studies have suggested no involvement of the underlying bone, then it may be prudent to stop to avoid introducing infection into the bone. Typically, however, there has been some imaging study that suggests bony infection or no material is aspirated from the soft tissues. In these cases, the needle should be advanced down to bone and an attempt made to aspirate any existing subperiosteal abscess. Any material obtained is sent for Gram stain, culture, and sensitivities. The needle is then advanced through the cortex and the bone aspirated. Usually this is easily accomplished, because most AHO is metaphyseal and the cortex in this region is thin. If the infection is diaphyseal in a larger child, it may not be possible to penetrate the cortex with a needle, and open biopsy may be required. Again, any material obtained is sent for Gram stain, culture, and sensitivities. In AHO, cultures are positive in 50–70% of cases.9,12,17 Organisms The same organisms tend to cause most osteomyelitis and septic arthritis, and the prevalence correlates with the age of the patient. When all cases of septic arthritis and AHO are considered, the most common causative organism is S. aureus.8,9,11,13,45 In addition to S. aureus, neonates often are infected with Group B streptococci or Gram-negative rods such as Eschericia coli.2,6,55,56 In children less than 10 years old, the incidence of Haemophilus influenzae is decreasing,57 and the incidence of Kingella kingae is increasing.58 Sexually active adolescents may develop infection from Neisseria gonorrhoeae. Patients with sickle-cell disease are more susceptible to infection with Salmonella.14 Staphylococcus aureus S. aureus is the most common cause of AHO and septic arthritis.* It appears on Gram stain as Gram-positive cocci in clusters. S. aureus usually can be treated successfully with semisynthetic penicillins (e.g., oxacillin, nafcillin) or first generation cephalosporins (e.g., cefazolin). Fortunately, methicillin-resistant S. aureus is uncommon in children, but it is usually treated with vancomycin when present. Streptococci Streptococci also are Gram-positive cocci, usually found in chains. Group A streptococci are frequently seen in children,9 whereas Group B streptococci are more commonly seen in neonates and infants.56 Streptococci are often treated successfully with penicillin or a first-generation cephalosporin. Haemophilus influenzae H. influenzae was a common source of infection in children under 5 years of age in the 1960s through the 1980s.2,59,61 Since routine vaccination of children against H. influenzae type B began in the 1990s, the incidence of AHO and septic arthritis resulting from this organism has dropped dramatically.57,58 H. influenzae may be treated with semisynthetic penicillins or cephalosporins. Today there is debate whether empiric treatment for this organism is necessary while awaiting culture results.57 *

References 8, 9, 13, 45 59, 60.

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Kingella kingae The incidence of K. kingae has increased over the past decade.58,62 This organism is found most often in children less than 5 years old. AHO from K. kingae may occur in the epiphysis rather than the metaphysis. Recovery of the organism in culture may be difficult, and results seem to be improved by placing the specimen in a BACTEC culture bottle (Becton Dickinson Microbiology Systems, Sparks, Maryland).63 The organisms are identified as Gram-negative coccobacilli in pairs or short chains. Successful treatment is usually achieved with penicillin, semisynthetic penicillins, or first-generation cephalosporins.2,58,62 Neisseria gonorrhoeae N. gonorrhoeae septic arthritis or AHO may be seen in sexually active adolescents. N. gonorrhoeae septic arthritis occurs most commonly in the knee. It is detected on Gram stain as intracellular Gram-negative diplococci. It is often sensitive to ceftriaxone. N. gonorrhoeae may be transmitted to a neonate via the birth canal and is not uncommon in this population. When seen in older children, however, the possibility of sexual abuse must be considered.2 Salmonella Salmonella is an uncommon cause of osteoarticular infections, except among patients with sickle-cell disease. Within this population, there is debate as to whether Salmonella or S. aureus is the most common pathogen. Salmonella infections may be multifocal with bilateral and symmetric involvement. Septic arthritis is less common than osteomyelitis in patients with sickle-cell disease, but when present, Salmonella is a common pathogen.10,64–69 Salmonella may be treated with a third-generation cephalosporin, Augmentin, Unasyn, or Bactrim.2 Differential Diagnosis The diagnosis of AHO or septic arthritis is not always an easy one. Other entities that may present with similar findings include juvenile rheumatoid arthritis and other autoimmune processes, Lyme disease, trauma, neoplasm, bone infarction (especially in patients with sickle-cell disease), and Henoch-Schönlein purpura. Juvenile Rheumatoid Arthritis Juvenile rheumatoid arthritis (JRA) can present in similar fashion to septic arthritis with pain, swelling, and erythema. There are some factors that may help distinguish between these two entities. With JRA, the onset of pain and swelling is typically more gradual, and the patient

KEY POINTS 1. Culture of aspirate (from septic arthritis or osteomyelitis) will demonstrate infection in 50–80% of cases. 2. S. aureus is the most common organism identified in both AHO and septic arthritis. 3. Neonates are more commonly infected with group B streptococcus or Gramnegative rods. 4. Incidence of K. kingae is increasing. 5. Patients with sicklecell disease are more susceptible to infection with Salmonella.

usually remains ambulatory. Pain is often worse in the morning. Range of motion is generally not limited except at the extremes of flexion and extension secondary to the swelling. More than one joint may be affected (pauciarticular, polyarticular), although the knee is the joint most commonly involved. ESR may be elevated. Rheumatoid factor and antinuclear antibody may be positive. Synovial fluid aspiration may be indistinguishable from septic arthritis. The fluid may be cloudy. It is often said that the white cell count is under 100,000 in JRA and greater than 100,000 in sepsis, but there is enough overlap that cell count is not a reliable indicator for differentiating between the two. JRA should be a diagnosis of exclusion. Initial treatment is with antiinflammatory medications. If unsuccessful, other medications used in treatment may include gold, methotrexate, or corticosteroids. If symptoms are severe and not responsive to medication, arthroscopic synovectomy may provide relief. If the patient is skeletally mature and debilitated by his or her arthritic knees, total knee arthroplasty becomes an option.2,14,70 Rheumatic Fever Rheumatic fever is diagnosed by the Jones criteria. The diagnosis is made when there are two major criteria, or one major and two minor criteria. Major criteria include arthritis, carditis, erythema marginatum, subcutaneous nodules, and chorea. Minor criteria include previous history of rheumatic fever, arthralgia, fever, increased ESR or CRP, and a prolonged PR interval on electrocardiogram. The history often includes group A streptococcus infection (evidenced by sore throat, rash, and/or fever) before the onset of joint symptoms. The knee is commonly involved, although the arthritis may be migratory. The pain tends to be severe and the swelling mild. Treatment traditionally has been with aspirin.2 Lyme Disease Lyme disease is transmitted by deer ticks (Ixodes dammini) that carry the spirochete Borrelia burgdorferi. The disease can have several manifestations. A common symptom is arthritis that may present acutely, similar to septic arthritis, but may also be less painful and more insidious in onset. As with JRA, multiple joints may be involved. Often there is a history of malaise, headache, fever, myalgia, and/or erythema migrans. There may be neurologic symptoms (including peripheral neuropathy and seventh cranial nerve palsy) and/or cardiac symptoms (myocarditis, atrioventricular block). ESR is elevated in Lyme disease; white blood cell count may be elevated. B. burgdorferi may be detected by enzyme-linked immunosorbent assay and Western blot analysis, but as with any test, both falsepositive and false-negative results are possible. Treatment generally is with amoxicillin or doxycycline. Intravenous ceftriaxone may be used when the response to oral agents is inadequate.52,71–74 Trauma A history of trauma may go along with the development of AHO or septic arthritis (see section about pathophysiology), and at times it may be difficult to determine whether a patient’s symptoms are from trauma, infection, or both. Laboratory tests and aspiration are helpful in making this

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distinction. Children with myelodysplasia or other forms of spinal cord injury form a population in which traumatic injury is often mistaken for infection. A red, swollen, warm lower extremity in a child with myelodysplasia is fractured, not infected, until proven otherwise.

involve the upper extremities and face. The musculoskeletal manifestations typically require symptomatic treatment, but the visceral manifestations may require medical management.2

Tumor

Treatment

Certain neoplasms may mimic AHO or septic arthritis. This may be particularly true around the knee because this is a common location for tumors. The radiographic appearance of both benign (e.g., nonossifying fibroma, osteoid osteoma, eosinophilic granuloma) and malignant (e.g., Ewing’s sarcoma, osteosarcoma) tumors may be indistinguishable from AHO. Neoplasms may cause sympathetic effusions in adjacent joints (e.g., epiphyseal lesions such as chondroblastoma), or may cause joint swelling directly (e.g., PVNS). Leukemia presents with musculoskeletal complaints 15–30% of the time. The metaphyses about the knee, ankle, and wrist are the most common sites of pain. A painful joint effusion may also be present. Children may present with fever, abnormal white blood cell count (increased or decreased), and/or an elevated ESR. Radiographs may reveal characteristic radiolucent metaphyseal bands, osteopenia, lytic or sclerotic lesions, and/or periosteal reaction.75–77

Appropriate antibiotics are critical to the successful and timely treatment of both AHO and septic arthritis. If osteomyelitis is detected early in the course of disease, before there is an abscess or necrotic bone (sequestrum or involucrum), then treatment with antibiotics alone may be sufficient. Initial treatment should be administered intravenously (IV). If the organism is sensitive to an oral antibiotic and ingestion of the antibiotic is reliable, then the route of administration may be changed from IV to oral when there have been clinical signs of improvement and the WBC, ESR, and/or CRP have begun to decrease. The total duration of antibiotic treatment is typically 4–6 weeks (see section about chronic osteomyelitis).7,60,81–84 If there is an abscess, sequestrum or involucrum, or lack of expected clinical improvement, then debridement is required as part of treatment. This is done through an open incision. If open debridement is required, then antibiotics should not be started until intraoperative cultures have been obtained. The area should be debrided of any infected or nonviable tissue, copiously irrigated, and closed over a drain that is left in place for 2–3 days. When debriding bone, the cortical window should be large enough to allow adequate debridement and should be oval in shape to minimize stress risers that could lead to pathologic fracture. The antibiotic regimen is the same as above (see section about chronic osteomyelitis).60,81,84,85 In the treatment of septic arthritis, mechanical removal of bacteria from the joint is essential. Because the intraarticular environment is relatively avascular and the joint’s capacity to clear high loads of bacteria is limited, treatment with antibiotics alone is not adequate. In addition, some pathogens (such as S. aureus) release proteolytic enzymes that can continue to damage the articular surface, even if the bacteria are killed. There have been reports of successful treatment of septic arthritis of the knee with serial aspirations and antibiotics.5,86 Two experimental models in rabbits have suggested that there may be less damage to articular cartilage following arthrotomy and irrigation in addition to the administration of antibiotics than after sequential needle aspirations and the use of antibiotics or antibiotics alone.32,87 Most orthopedic surgeons believe that optimal treatment includes arthrotomy or arthroscopy with a drain left in for 2–3 days postoperatively. Traditionally, septic joints have been treated with antibiotics and serial aspiration or arthrotomy. As indicated previously, antibiotics and serial aspirations may not be adequate treatment. With the advent of arthroscopy, another tool has become available as an option in the treatment of septic arthritis. Several studies have demonstrated the efficacy of arthroscopic irrigation and debridement of infected knees,88–92 and at least one has suggested that arthroscopy is preferable because of earlier functional recovery and less arthrofibrosis than with arthrotomy.91

Bone Infarction Children with sickle-cell disease may present with pain, swelling, and fever; it may be difficult to determine whether the source of the problem is a bone infarction or infection.64,78 Although bandemia and elevated ESR are more common in AHO, there is considerable overlap in the results of laboratory evaluation of AHO and bone infarction.64 Radiographs may show periosteal reaction in both situations. Bone scintigraphy may be helpful in making this distinction in that it is often (but not always) “hot” with infection and “cold” with infarction.64,68,79,80 White blood cell scan can also be used to clarify the picture by demonstrating increased uptake in infection but not infarction. Furthermore, infarction can precede infection, and the two conditions can coexist. Henoch-Schönlein Purpura Henoch-Schönlein purpura is a vasculitis for which the etiology is not well understood. It is associated with arthritis or arthralgia in approximately 75% of patients, and this may be the initial symptom. The knees and ankles are the joints most frequently affected. The effusion is typically small, and the tenderness is more along the ends of the long bones than over the joint itself. Other features associated with this condition include abdominal pain, nephritis, and a purpuric rash that usually starts below the waist and remains confined to the trunk and lower extremities but can

KEY POINTS 1. JRA must be a diagnosis of exclusion. 2. Lyme disease may present with arthritis or arthralgias. 3. Benign and malignant neoplasms can mimic septic arthritis and osteomyelitis. 4. It can be very difficult to distinguish a bone infarction from AHO in patients with sickle-cell disease. White blood cell scans may be helpful.

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Again, the postoperative course of antibiotics is similar to that for osteomyelitis. Initial administration is via a parenteral route. If the diagnosis was made early in the course of the disease, there is no evidence of osteomyelitis, and the pathogen is susceptible to an oral agent, then change to oral administration is appropriate when the child has shown clinical improvement and is able to tolerate oral medication. The total duration of antibiotic treatment is typically 3–6 weeks (see section about CPG-septic arthritis).7,60,82,83 Complications Untreated or inadequately treated septic arthritis and osteomyelitis can have devastating effects. Persistence of infection within a joint can lead to permanent destruction of the articular cartilage—predominantly from the cytokines released from leukoKEY POINTS cytes, but can also be from enzymes released by certain bac1. Osteomyelitis withteria (such as S. aureus). out abscess may be Fulminant osteomyelitis may treated with antibiresult in severe bony destruction. otics alone. Both AHO and septic arthritis, 2. Septic arthritis and if allowed to flourish, may result AHO with in systemic sepsis and even death. abscess/sequestrum/ Other potential complications of involucrum should AHO and septic arthritis can be treated with irriinclude damage to the growth gation, debridement, plate and a growth arrest that and antibiotics. may result in an angular defor3. Inadequate treatmity and/or leg-length discrepment can result in ancy. Leg-length discrepancy may severe destruction also result from overgrowth of of bone, joint, the involved extremity. Chronic and/or physis. osteomyelitis has become much less common but can still be difficult to eradicate.* Other Considerations

Neonatal Infections Neonatal septic arthritis and osteomyelitis may be difficult to diagnose, but delayed diagnosis can lead to disastrous sequelae. The neonate’s immune system is immature, and infection may be acquired from the child’s surroundings or mother. Typically the bone or joint is seeded by hematogenous spread. Since these children are nonverbal and nonambulatory, the presence of pain may not be easy to determine. Lack of movement of an extremity may be the only finding initially. Frequently the child will have a fever. A red, warm, swollen joint or extremity should be suspected of infection. The incidence of multifocal disease is higher than in older children, and these infants may become systemically ill in a relatively short period of time. Laboratory values may be less reliable in neonates, and therefore clinical suspicion must remain high. The organisms encountered differ somewhat from those found in older children. S. aureus is still the most common pathogen, but this is followed in frequency by group B Streptococcus and Gram-negative rods (e.g., E. coli). Candida albicans may develop as a superinfection. Aggressive treatment with debridement and antibiotics is important for successful results. Even with appropriate treatment, neonates still are at higher risk for long-term adverse sequelae.* Infected Prepatellar Bursitis The other infection commonly seen about the knee is infection of the prepatellar bursa. This presents with localized tenderness, swelling, erythema, and warmth directly over the patella. The diagnosis usually is made clinically. White blood cell count, ESR, and CRP may be elevated. Radiographs typically are unremarkable, although they may show prepatellar soft-tissue swelling. If the diagnosis is uncertain, the bursa may be aspirated. If mild and early in the course of disease, antibiotic treatment may be adequate. If there is an abscess or if there is not resolution of the infection with antibiotics alone, operative drainage and debridement is warranted.

Subacute Osteomyelitis Over the past half century, the incidence of chronic and fulminant osteomyelitis has decreased, and the incidence of subacute osteomyelitis has increased.1,8,14–16 Subacute osteomyelitis differs from AHO in that the pain, with or without a limp, is usually more insidious in onset, and systemic signs (such as fever) are not present. The white blood cell count may be normal or only slightly elevated, ESR often is elevated, and blood cultures usually are negative. Typically the lesion is detected on radiographs that show an eccentric, lytic lesion with geographic or permeative borders. Most often the lesions are metaphyseal but may also be epiphyseal. Sometimes there is an abscess present, known as a Brodie abscess. Initial treatment is often with a short course (48 hours) of IV antibiotics followed by oral antibiotics for 6 weeks. If this treatment is inadequate or if the diagnosis is uncertain, open biopsy and curettage may be indicated.†

Summary Infection about the knee must be considered as an etiology for knee pain in children and adolescents. History, physical examination, imaging, and laboratory studies must all be considered in making the diagnosis of AHO or septic arthritis. The differential diagnosis for the symptoms and signs associated with infection includes, but is not limited to, trauma, tumor, Lyme disease, JRA, and bone infarction. Early diagnosis and appropriate treatment may lead to resolution without long-term sequelae. Adverse sequelae may include arthritis, leg-length discrepancy, angular deformity, chronic infection, or systemic illness. A high index of suspicion must be maintained for considering infection in the differential diagnosis of knee pain in children.

*

References 2, 5, 14, 23, 85, 93. References 1, 2, 14, 15, 94–98.

†

*

References 2, 14, 55, 56, 99, 100.

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References 1. Dormans JP, Drummond DS: Pediatric hematogenous osteomyelitis: New trends in presentation, diagnosis, and treatment. J Am Assoc Orthop Surg 2:333–341, 1994. 2. Morrissy RT: Bone and joint sepsis. In Morrissy RT, Weinstein SL (eds): Lovell and Winter’s Pediatric Orthopaedics, vol 1. Philadelphia, Lippincott-Raven, 1996, pp 579–624. 3. Peltola H, Vahvanen V: A comparative study of osteomyelitis and purulent arthritis with special reference to aetiology and recovery. Infection 12:75–79, 1984. 4. Fink CW, Nelson JD: Septic arthritis and osteomyelitis in children. Clin Rheum Dis 12:423–435, 1986. 5. Howard JB, Highgenboten CL, Nelson JD: Residual effects of septic arthritis in infancy and childhood. JAMA 236:932–935, 1976. 6. Jackson MA, Nelson JD: Etiology and medical management of acute suppurative bone and joint infection in pediatric patients. J Pediatr Orthop 2:313–323, 1982. 7. Nelson JD, Bucholz RW, Kusmiesz H, et al: Benefits and risks of sequential parenteral-oral cephalosporin therapy for suppurative bone and joint infections. J Pediatr Orthop 2:255–262, 1982. 8. Craigen MAC, Watters J, Hackett JS: The changing epidemiology of osteomyelitis in children. J Bone Joint Surg Br 74:541–545, 1992. 9. Scott RJ, Christofersen MR, Robertson WW, et al: Acute osteomyelitis in children: A review of 116 cases. J Pediatr Orthop 10:649–652, 1990. 10. Adeyokunnu AA, Hendrickse RG: Salmonella osteomyelitis in childhood: A report of 63 cases seen in Nigerian children of whom 57 had sickle cell anemia. Arch Dis Child 55:175–184, 1980. 11. Dich VQ, Nelson JD, Haltalin KC: Osteomyelitis in infants and children: A review of 163 cases. Am J Dis Child 129:1273–1278, 1975. 12. Faden H, Grossi M: Acute osteomyelitis in children: Reassessment of etiologic agents and their clinical characteristics. Am J Dis Child 145:65–69, 1991. 13. Morrey BF, Bianco AJ, Rhodes KH: Septic arthritis in children. Orthop Clin North Am 6:923–934, 1975. 14. Herring JA: Bone and joint infections. In Herring JA (ed): Tachdjian’s Pediatric Orthopaedics, vol. 3. Philadelphia, WB Saunders Company, 2002, pp 1841–1877. 15. Jones NS, Anderson DJ, Stiles PJ: Osteomyelitis in a general hospital: A five-year study showing an increase in subacute osteomyelitis. J Bone Joint Surg Br 69:779–783, 1987. 16. Morrissy RT: Bone and joint sepsis in children. Instr Course Lect 31:49–61, 1982. 17. Ferguson AB: Acute and chronic osteomyelitis in children. Clin Orthop 96:51–56, 1973. 18. Trueta J: The three types of acute haematogenous osteomyelitis: A clinical and vascular study. J Bone Joint Surg Br 41:671–680, 1959. 19. Morrissy RT, Haynes DW: Acute hematogenous osteomyelitis: A model with trauma as an etiology. J Pediatr Orthop 9:447–456, 1989. 20. Whalen JL, Fitzgerald RH, Morrissy RT: A histological study of acute hematogenous osteomyelitis following physeal injuries in rabbits. J Bone Joint Surg Am 70:1383–1392, 1988. 21. Canale ST, Puhl J, Watson FM, Gillespie R: Acute osteomyelitis following closed fractures. J Bone Joint Surg Am 57:415–418, 1975. 22. Hardy AE, Nicol RO: Closed fractures complicated by acute hematogenous osteomyelitis. Clin Orthop 201:190–195, 1985. 23. Shaw BA, Kasser JR: Acute septic arthritis in infancy and childhood. Clin Orthop 257:212–225, 1990. 24. Tiku K, Tiku ML, Skosey JL: Interleukin 1 production by human polymorphonuclear neutrophils. J Immunol 136:3677–3685, 1986. 25. Dodge GR, Boesler EW, Jimenez SA: Expression of the basement membrane heparin sulfate proteoglycan (Perlecan) in human synovium and in cultured human synovial cells. Lab Invest 73:649–657, 1995. 26. Pollock LE, Lalor P, Revell PA: Type IV collagen and laminin in the synovial intimal layer: an immunohistochemical study. Rheumatol 9:277–280, 1990. 27. Johnson AH, Campbell WG, Callahan BC: Infection of rabbit knee joints after intra-articular injection of Staphylococcus aureus: comparison with joints injected with Staphylococcus albus. Am J Path 60:165–177, 1970. 28. Smith RL, Schurman DJ: Comparison of cartilage destruction between infectious and adjuvant arthritis. J Orthop Res 1:136–143, 1983. 29. Curtiss PH, Klein L: Destruction of articular cartilage in septic arthritis: In vitro studies. J Bone Joint Surg Am 45:797–806, 1963.

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30. Curtiss PH, Klein L: Destruction of articular cartilage in septic arthritis: In vivo studies. J Bone Joint Surg Am 47:1595–1604, 1965. 31. Curtiss PH: Cartilage damage in septic arthritis. Clin Orthop 64:87–90, 1969. 32. Daniel D, Akeson W, Amiel D, et al: Lavage of septic joints in rabbits: Effect of chondrolysis. J Bone Joint Surg 58A:393–395, 1976. 33. Dingle JT: The role of lysosomal enzymes in skeletal tissues. J Bone Joint Surg 55B:87–95, 1973. 34. Oronsky A, Ignarro L, Perper R: Release of cartilage mucopolysaccharide-degrading neutral protease from human leukocytes. J Exp Med 138:461–472, 1973. 35. Griebel M, Nahlen B, Jacobs RF, et al: Group A Streptococcal postvaricella osteomyelitis. J Pediatr Orthop 5:101–103, 1985. 36. Capitanio MA, Kirkpatrick JA: Early roentgen observations in acute osteomyelitis. AJR 108:488–496, 1970. 37. Howard CB, Einhorn M, Dagan R, et al: Ultrasound in diagnosis and management of acute haematogenous osteomyelitis in children. J Bone Joint Surg Br 75:79–82, 1993. 38. Mah ET, LeQuesne GW, Gent RJ, et al: Ultrasonic features of acute osteomyelitis in children. J Bone Joint Surg Br 76:969–974, 1994. 39. Shiv VK, Jain AK, Taneja K, et al: Sonography of hip joint in infective arthritis. Can Assoc Radiol 41:76–78, 1990. 40. Kaiser S, Rosenborg M: Early detection of subperiosteal abscesses by ultrasonography: A means for further successful treatment in pediatric osteomyelitis. Pediatr Radiol 24:336–339, 1994. 41. Bressler EL, Conway JJ, Weiss SC: Neonatal osteomyelitis examined by bone scintigraphy. Radiology 152:685–688, 1984. 42. Howie DW, Savage JP, Wilson TG, et al: The technetium phosphate bone scan in the diagnosis of osteomyelitis in childhood. J Bone Joint Surg Am 65:431–437, 1983. 43. Treves S, Khettry J, Broker FH, et al: Osteomyelitis: Early scintigraphic detection in children. Pediatrics 57:173–186, 1976. 44. Tuson CE, Hoffman EB, Mann MD: Isotope bone scanning for acute osteomyelitis and septic arthritis in children. J Bone Joint Surg Br 76:306–310, 1994. 45. Unkila-Kallio L, Kallio MJT, Eskola J, et al: Serum C-reactive protein, erythrocyte sedimentation rate, and white blood cell count in acute hematogenous osteomyelitis of children. Pediatrics 93:59–62, 1994. 46. McCarthy PL, Jekel JF, Dolan TF: Comparison of acute-phase reactants in pediatric patients with fever. Pediatrics 62:716–720, 1978. 47. Peltola H, Vahvanen V, Aalto K: Fever, C-reactive protein, and erythrocyte sedimentation rate in monitoring recovery from septic arthritis: A preliminary study. J Pediatr Orthop 4:170–174, 1984. 48. Pepys MB: C-reactive protein fifty years on. Lancet 1:653–656, 1981. 49. Wilson NIL, DiPaola M: Acute septic arthritis in infancy and childhood. J Bone Joint Surg Br 68:584–587, 1986. 50. Shmerling RH, Delbanco TL, Tosteson ANA, et al: Synovial fluid tests: What should be ordered? JAMA 264:1009–1014, 1990. 51. Baldassare AR, Chang F, Zuckner J: Markedly raised synovial fluid leukocyte counts not associated with infectious arthritis in children. Ann Rheum Dis 37:404–409, 1978. 52. Cristofaro RL, Appel MH, Gelb RI, Williams CL: Musculoskeletal manifestations of Lyme disease in children. J Pediatr Orthop 7:527–530, 1987. 53. Krey PR, Bailen DA: Synovial fluid leukocytosis: A study of extremes. Am J Med 67:436–442, 1979. 54. Nade S: Acute haematogenous osteomyelitis in infancy and childhood. J Bone Joint Surg Br 65:109–119, 1983. 55. Bergdahl S, Ekengren K, Eriksson M: Neonatal hematogenous osteomyelitis: Risk factors for long-term sequelae. J Pediatr Orthop 5:564–568, 1985. 56. Fox L, Sprunt K: Neonatal osteomyelitis. Pediatrics 62:535–542, 1978. 57. Bowerman SG, Green NE, Mencio GA: Decline of bone and joint infections attributable to Haemophilus influenzae type b. Clin Orthop 341:128–133, 1997. 58. Lundy DW, Kehl DK: Increasing prevalence of Kingella kingae in osteoarticular infections in young children. J Pediatr Orthop 18:262–267, 1998. 59. Lebel MH, Nelson JD: Haemophilus influenzae type b osteomyelitis in infants and children. Pediatr Infect Dis J 7:250–254, 1988. 60. Tetzlaff TR, McCracken GH, Nelson JD: Oral antibiotic therapy for skeletal infections of children: Therapy of osteomyelitis and suppurative arthritis. J Pediatr 92:485–490, 1978.

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61. Almquist EE: The changing epidemiology of septic arthritis in children. Clin Orthop 68:96–99, 1970. 62. Lacour M, Duarte M, Beutler A, et al: Osteoarticular infections due to Kingella kingae in children. Eur J Pediatr 150:612–618, 1991. 63. Yagupsky P, Dagan R, Howard CW, et al: High prevalence of Kingella kingae in joint fluid from children with septic arthritis revealed by the BACTEC blood culture system. J Clin Microbiol 30:1278–1281, 1992. 64. Anand AJ, Glatt AE: Salmonella osteomyelitis and arthritis in sickle cell disease. Semin Arthritis Rheum 24:211–221, 1994. 65. Burnett MW, Bass JW, Cook BA: Etiology of osteomyelitis complicating sickle cell disease. Pediatrics 101:296–297, 1998. 66. Epps CH, Bryant DD, Coles MJM, et al: Osteomyelitis in patients who have sickle-cell disease: Diagnosis and management. J Bone Joint Surg Am 73:1281–1294, 1991. 67. Hughes JG, Carroll DS: Salmonella osteomyelitis complicating sickle cell disease. Lancet 19:184–191, 1957. 68. Mallouh A, Talab Y: Bone and joint infection in patient with sickle cell disease. J Pediatr Orthop 5:158–162, 1985. 69. Piehl FC, Davis RJ, Prugh SI: Osteomyelitis in sickle cell disease. J Pediatr Orthop 13:225–227, 1993. 70. Kunnamo I, Kallio P, Pelkonen P, et al: Clinical signs and laboratory tests in the differential diagnosis of arthritis in children. Am J Dis Child 141:34–40, 1987. 71. Bakken LL, Case KL, Callister SM, et al: Performance of 45 laboratories participating in a proficiency testing program for Lyme disease serology. JAMA 268:891–895, 1992. 72. Culp RW, Eichenfield AH, Davidson RS, et al: Lyme arthritis I children: An orthopaedic perspective. J Bone Joint Surg 69A:96–99, 1987. 73. Feder HM, Hunt MS: Pitfalls in the diagnosis and treatment of Lyme disease in children. JAMA 274:66–68, 1995. 74. Rose CD, Fawcett PT, Eppes SC, et al: Pediatric Lyme arthritis: Clinical spectrum and outcome. J Pediatr Orthop 14:238–241, 1994. 75. Fink CW, Windmiller J, Sartain P: Arthritis as the presenting feature of childhood leukemia. Arthritis Rheum 15:347–349, 1972. 76. Jonsson OG, Sartain P, Ducore JM, et al: Bone pain as an initial symptom of childhood acute lymphoblastic leukemia: Association with nearly normal hematologic indexes. J Pediatr 117:233–237, 1990. 77. Rogalsky RJ, Black GB, Reed MH: Orthopaedic manifestations of leukemia in children. J Bone Joint Surg Am 68:494–501, 1986. 78. Dalton GP, Drummond DS, Davidson RS, et al: Bone infarction versus infection in sickle cell disease in children. J Pediatr Orthop 16:540–544, 1996. 79. Amndsen TR, Siegel MJ, Siegel BA: Osteomyelitis and infarction in sickle cell hemoglobinopathies: Differentiation by combined technetium and gallium scintigraphy. Radiology 153:807–812, 1984.

80. Rao S, Solomon N, Miller S, et al: Scintigraphic differentiation of bone infarction from osteomyelitis in children with sickle cell disease. J Pediatr 107:685–688, 1985. 81. Cole WG, Dalziel RE, Leitl S: Treatment of acute osteomyelitis in childhood. J Bone Joint Surg 64B:218–223, 1982. 82. Kolyvas E, Ahronheim G, Marks MI, et al: Oral antibiotic therapy of skeletal infections in children. Pediatrics 65:867–871, 1980. 83. Syrogiannopoulos GA, Nelson JD: Duration of antimicrobial therapy for acute suppurative osteoarticular infections. Lancet 1:37–40, 1988. 84. Vaughan PA, Newman NM, Rosman MA: Acute hematogenous osteomyelitis in children. J Pediatr Orthop 7:652–655, 1987. 85. LaMont RL, Anderson PA, Dajani AS, et al: Acute hematogenous osteomyelitis in children. J Pediatr Orthop 7:579–583, 1987. 86. Herndon WA, Knauer S, Sullivan JA, et al: Management of septic arthritis in children. J Pediatr Orthop 6:576–578, 1986. 87. Goldstein WM, Gleason TF, Barmada R: A comparison between arthrotomy and irrigation and multiple aspirations in the treatment of pyogenic arthritis: A histological study in a rabbit model. Orthopedics 6:1309–1314, 1983. 88. Ivey M, Clark R: Arthroscopic debridement of the knee for septic arthritis. Clin Orthop 199:201–206, 1985. 89. Jarrett MP, Grossman L, Sadler AH, et al: The role of arthroscopy in the treatment of septic arthritis. Arthritis Rheum 24:737–739, 1981. 90. Jerosch J, Hoffstetter I, Schroder M, et al: Septic arthritis: Arthroscopic management with local antibiotic treatment. Acta Orthop Belg 61:126–134, 1995. 91. Skyhar MJ, Mubarak SJ: Arthroscopic treatment of septic knees in children. J Pediatr Orthop 7:647–651, 1987. 92. Stanitski CL, Harvell JC, Fu FH: Arthroscopy in acute septic knees: Management in pediatric patients. Clin Orthop 241:209–212, 1989. 93. Welkon CJ, Long SS, Fisher MC, et al: Pyogenic arthritis in infants and children: a review of 95 cases. Pediatr Infect Dis 5:669–676, 1986. 94. Andrew TA, Porter K: Primary subacute epiphyseal osteomyelitis: A report of three cases. J Pediatr Orthop 5:155–157, 1985. 95. Gledhill RB: Subacute osteomyelitis in children. Clin Orthop 96:57–69, 1973. 96. Harris NH, Kirkaldy-Willis WH: Primary subacute pyogenic osteomyelitis. J Bone Joint Surg 47B:526–532, 1965. 97. King DM, Mayo KM: Subacute haematogenous osteomyelitis. J Bone Joint Surg Br 51:458–463, 1969. 98. Roberts JM, Drummond DS, Breed AL, et al: Subacute hematogenous osteomyelitis in children: A retrospective study. J Pediatr Orthop 2:249–254, 1982. 99. Frederiksen B, Christiansen P, Knudsen FU: Acute osteomyelitis and septic arthritis in the neonate, risk factors and outcome. Eur J Pediatr 152:577–580, 1993. 100. Knudsen CJM, Hoffman EB: Neonatal osteomyelitis. J Bone Joint Surg Br 72:846–851, 1990.

Chapter 30

Inflammatory Diseases of the Knee: Juvenile Rheumatoid Arthritis and Lyme Disease Amy L. Woodward

Rheumatological conditions of the knee differ fundamentally from many of the more common complaints of children and adolescents addressed in this volume. Arthritis and related processes tend to be indolent in onset and chronic in tempo, causing morbidity over time. Limping or a subtle loss of milestones thus is a more typical presentation than is pain or acute disability. Furthermore, the process is mediated by inflammatory and immunological mechanisms rather than by anatomical or mechanical disruption. The result is a characteristic pattern of symptoms that is readily differentiated from infectious or orthopedic pathology. The most common rheumatic disease affecting the pediatric and adolescent knee is inflammatory arthritis. This chapter will focus on the presentation and diagnosis of juvenile arthritis as it may affect the knee, highlighting the differential diagnosis, appropriate workup, and treatment. Lyme disease, often confused with both infectious and autoimmune causes of arthritis, will also be discussed in some detail. Rheumatological Approach to Knee Complaints When a child presents with a complaint referable to the knee, the list of possible etiologies is long and varied. In the absence of an obvious explanation such as known trauma, it is helpful to start the evaluation by categorizing the type of pain or discomfort according to the nature of onset (acute versus chronic), whether the knee is the only joint involved, and whether extraarticular signs or symptoms are present (Table 30–1). It is also important to remember that most normally active children will have a history of trauma during the preceding 24 hours. However, unless the trauma is significant (typically a football injury, automobile accident, or bicycle fall), it is more likely to have unmasked

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Robert P. Sundel

pre-existing pathology than it is to have caused a problem in the resilient tissues of a child’s knee. Thus, 10–20% of osteogenic sarcomas present after trauma, but in none of these cases does the accident represent anything more than a signpost for the problem. Inflammatory Pain As discussed in Chapter 2, key elements of the history that help identify the cause of pain include (1) timing of the pain; (2) nature of the pain with regard to alleviating and exacerbating factors, particularly response to activity; and (3) character of the pain, such as dull, sharp, radiating, or burning. In young or nonverbal children who are not able to articulate the specifics of their symptoms, observations from the parents and other caregivers substitute for the patient’s description. The single most characteristic feature of discomfort related to inflammatory processes is the classic morning stiffness of arthritis. Difficulties are also often reported after naps or other periods of inactivity such as long car rides or sitting in classes at school (the so-called theater sign). This is thought to be due to decreased hyaluronic acid in inflamed synovial fluid, leading to gelling and reduced lubrication at physiological temperatures. Thus, children with arthritis typically feel better after a warm bath or several minutes of activity. These help to raise the temperature within the joint, and as with motor oil in a car, returns the synovial fluid to the liquid state in which it lubricates most efficiently. Accordingly, a child with arthritis may suffer joint stiffness in the morning but may be quite comfortable exercising strenuously later in the day. It is decidedly 461

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Table 30–1

Categories of Musculoskeletal Pain Examples A.M. P.M. Nighttime Activity

Inflammatory Arthritis Mechanical Strains, sprains Bony Fractures

+++ + +/− ++

− +/−

Improves Worsens

++

++

++

Neuropathic

+

++

+++

No change No change

Crush injury

atypical for inflammatory arthritis to awaken children from sleep. Cold, damp weather, or swimming in cool water tend to be more difficult for children with arthritis, whereas warm weather generally relieves symptoms. An atypical symptom profile—especially nighttime pain or pain with activity—should raise suspicion of an alternative diagnosis, even in the setting of what appears clinically to be an arthritic joint. Differential Diagnosis of Knee Pain Mechanical Derangement The timing of mechanical pain is essentially the reverse of inflammatory pain: children typically feel well in the morning, but the more active they are, the more discomfort they feel. Rest and ice tend to alleviate mechanical symptoms, rather than the activity and heat that are typically salubrious in arthritis. Mechanical pain does not generally awaken children from sleep. The conditions discussed in the first 28 chapters of this book tend to cause pain of this nature. Bony Pain Pain originating in the osseous compartment tends to be constant and does not change significantly with activity. Bone pain raises concerns for infection, trauma, and also malignancy. Although inflammatory and mechanical pains do not usually awaken children at night, bony pain may, particularly when related to leukemia or other tumors. Consequently, when a history of nighttime awakening is elicited, special consideration must be given to possible oncological etiologies. Cytopenias are typically seen with leukemia, although a normal complete blood count does not absolutely exclude the possibility. Other tumors, such as sarcomas or metastatic neuroblastoma, are far less common, but they must be considered in children with more nighttime pain than morning stiffness. Neuropathic Pain Nerve pain tends to be worst at bedtime, when the usual distractions of daily activities disappear. In children old enough to describe the sensation, neuropathic pain typically has a burning or shooting character. It is also commonly associated with allodynia, severe hypersensitivity of overlying normal soft tissues. Although joints may be involved, neuropathic pain generally encompasses extraarticular areas as well and can follow a dermatomal distribution. Activity does not have a significant effect on neuropathic pain. This type of pain is relatively uncommon in children; when nerve

pathology due to severe trauma, tumors, or vasculitis cannot be identified, then pain syndromes, such as those discussed in Chapter 31, are often the cause of neuropathic pain. Pattern of Joint Involvement

KEY POINTS 1. Joint pain may be caused by softtissue damage, stretching of the joint capsule, bony lesions, or nerve injury. 2. Symptoms of arthritis are inflammatory in nature and are typically worse in the morning, improving with use.

In addition to categorizing the type of pain a child is experiencing, it is critical to determine whether the knee is the only joint affected. The potential causes of a monoarticular process differ significantly from those of a polyarticular condition, so careful examination of all the joints is mandatory, even when the patient is adamant that only the knee is involved. It is also important to determine the type of onset (sudden or gradual), duration of symptoms, and any associated systemic features such as fever or rash. The differential diagnosis will be discussed for monoarticular and polyarticular processes, as well as for arthritis associated with fever and other systemic signs or symptoms. Monoarthritis The potential etiologies of a monoarticular process in the knee may be narrowed down by consideration of the nature of onset and duration of symptoms. The differential diagnosis of monoarticular arthritis is reflected in Table 30–2. Acute Onset: When a monoarticular process involving pain and swelling of the knee starts acutely, traumatic injury must always be excluded. It is helpful if there has been clearly documented antecedent trauma, but this may be difficult to elicit in young children who are unable to verbalize specifics of the history. In patients with an underlying bleeding disorder such as hemophilia, routine daily activities may cause hemarthrosis. Once this possibility is excluded,

Table 30–2

Common Causes of Arthritis

Type

Cause

Monoarticular Acute onset

Septic arthritis Reactive arthritis Trauma Hemophilia Lyme disease Juvenile rheumatoid arthritis Other forms of chronic arthritis Lyme disease Tuberculosis (rare without pulmonary disease) Tumor (pigmented villonodular synovitis most common; rare) Juvenile rheumatoid arthritis Other forms of chronic arthritis Systemic autoimmune diseases (lupus, sarcoidosis) Arthritis associated with inflammatory bowel disease Viral arthritis

Chronic

Polyarticular

Inflammatory Diseases of the Knee: Juvenile Rheumatoid Arthritis and Lyme Disease

bacterial infections must be considered; unlike most types of inflammatory arthritis, in which delaying the diagnosis by days or weeks has few long-term implications, treatment of septic arthritis must not be postponed. A history of fever associated with a red, swollen, painful, or hot knee necessitates aspiration of the joint for cell count and culture (see Chapter 29). Postinfectious or “reactive arthritis” may involve the knee alone or multiple joints. Postinfectious arthritis typically causes less inflammation than most types of acute infection. It does not usually cause erythema overlying the joint, and although it may be uncomfortable, excruciating pain is uncommon. Reactive arthritis generally responds well to nonsteroidal antiinflammatory drugs and is typically transient. Lyme disease may also be difficult to distinguish clinically from septic arthritis, although generally it causes more indolent symptoms. Subacute Onset: Diagnostic considerations of an isolated, chronically swollen knee differ from those related to an acute arthritis. Bacterial infections are far less likely, whereas lower-grade infections (especially Lyme disease in endemic areas) must be ruled out. Chronic monoarthritis of the knee may also be caused by Mycobacterium tuberculosis, particularly in immunocompromised children. Within this category are also chronic forms of juvenile arthritis, especially pauciarticular juvenile rheumatoid arthritis (JRA), psoriatic arthritis, and juvenile spondyloarthritides. Rarer inflammatory arthropathies, such as arthritis due to sarcoidosis, may also cause monoarthritis involving the knee. Tumors of the cartilage and synovium, although extremely rare, are also more likely to present in an indolent manner (see Chapter 32). The most common of these, pigmented villonodular synovitis, typically causes a chronically painful and swollen knee. Arthrocentesis yielding bloody fluid increases the likelihood of an articular tumor. Polyarthritis When the knee is one of several involved joints, rheumatological conditions rise to the top of the differential diagnosis. Most common among these is polyarticular JRA, although other autoimmune diseases such as systemic lupus erythematosus and vasculitis typically involve multiple joints as well. Infections, on the other hand, are progressively less common as more joints are involved, with the exceptions of gonococcal arthritis in sexually active or abused children and salmonella arthritis in immunocompromised patients. Arthritis associated with systemic conditions, such as inflammatory bowel disease or cystic fibrosis, must also be considered. Usually, extraarticular involvement (such as a new murmur in rheumatic fever or KEY POINTS hives in serum sickness) offers a clue to these conditions. The pat1. Infection must be tern of joint involvement may excluded in a child also be suggestive: rheumatic with acute, febrile, fever, vasculitis, and serum sickmonoarthritis. ness characteristically cause a 2. Chronic arthritis is migratory polyarthritis, whereas most common when most other conditions cause addisymptoms involve tive or fixed involvement of mulmultiple joints or tiple joints. In general, children are indolent and with polyarticular arthritis are cause minimal pain. likely to benefit from consultation

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with a pediatric rheumatologist. The differential diagnosis for polyarticular arthritis is reviewed in Box 30–1. Juvenile Rheumatoid Arthritis As long as the cause of idiopathic inflammatory arthritis in children remains unknown, naming the condition will remain imprecise. Since its initial description by George Fredric Still in 1898, prolonged inflammation in a child’s joint has been called juvenile rheumatoid arthritis because of its superficial similarity to rheumatoid arthritis (RA) in adults. In fact, genetic and histopathological differences from RA, as well as important differences between various forms of JRA, have led to various other designations for this condition. For many years, persistent inflammatory arthritis in someone younger than 16 years was called juvenile chronic arthritis in Europe; more recently, the term juvenile idiopathic arthritis has been proposed. Thus, although we will use the term JRA to refer to arthritis in one or more joints lasting for at least 6 weeks in a child or adolescent, the discussion also applies to these other names for chronic inflammatory arthritis of children. Clinical Presentation/Diagnosis The diagnosis of JRA is defined clinically, not radiologically or pathologically, so the history and physical examination are central to identifying the condition. It is also important to distinguish arthritis from arthralgia. Arthritis is defined as decreased range of motion. Tenderness or pain on joint motion, or increased warmth of the joint, are aspects of the examination that reflect inflammation in the joint. In contrast, arthralgia is joint pain without signs of inflammation, which is a far more common and less specific condition. In addition, other forms of arthritis must be excluded before the diagnosis of JRA is established definitively. The diagnostic criteria established by the American College of Rheumatology (ACR) are listed in Box 30–2. There have been recent efforts to revise these criteria, but the ACR criteria will be retained for the purposes of this discussion. Epidemiology The reported incidence and prevalence of juvenile arthritis vary significantly worldwide. A review of 34 epidemiological studies found that the reported annual incidence of juvenile arthritis ranged from 0.008 to 0.226 per 1000 children, and the reported prevalence was 0.07 to 4.01 per 1000

Box 30–1 Arthritis Associated with Fever Reactive arthritis Serum sickness Rheumatic fever (migratory arthritis) Septic arthritis Juvenile rheumatoid arthritis, systemic onset Systemic autoimmune diseases (SLE, vasculitis) Inflammatory bowel disease Malignancies Periodic fever syndromes

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Box 30–2 Diagnostic Criteria for Juvenile Rheumatoid Arthritis (JRA) Onset at age