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

6

Chapter 1

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 <13 (n = 159) 13/159 (8.2%) 11/159 (6.9%) 11/159 (6.9%) 35/159 (22%) 22/159 (13.8%) 0 12/159 (7.5%) 0 14/159 (8.8%) 4/159 (2.5%) 8/159 (5%) 4/159 (2.5%) 1/159 (0.6%) 29/159 (18.2%) 31/159 (19.5%)

Adolescent (n = 698) 78/601 (13.0%) 38/601 (6.3%) 2/698 (0.3%) 133/698 (19.1%) 142/698 (20.3%) 7/698 (1%) 22/698 (3.2%) 3/698 (0.4%) 30/698 (4.3%) 3/698 (0.4%) 22/698 (3.2%) 26/698 (3.7%) 48/698 (6.9%) 197/698 (28.2%) 65/698 (9.3%)

Total (n = 1231) 104/989 (10.5%) 64/989 (6.5%) 20/1231 (1.7%) 217/1231 (17.6%) 205/1231 (16.7%) 14/1231 (1.1%) 67/1231 (5.4%) 10/1231 (0.8%) 91/1231 (7.4%) 9/1231 (0.7%) 47/1231 (3.8%) 46/1231 (3.7%) 81/1231 (6.6%) 321/1231 (26.1%) 123/1231 (10.0%)

ACL, Anterior cruciate ligament; PCL, posterior cruciate ligament.

In 1273 children up to the age of 16 with knee trauma, soft tissue lesions accounted for 82% of the injuries, and hemarthrosis only occurred in 18%.47 Fewer cases of hemarthrosis occurred in younger children, whereas soft tissue injuries prevailed in these patients. The study also ascertained that, in the transition from childhood to adolescence, the pattern of injuries resulting in KEY POINTS hemarthrosis changed (Figure 1–4). The following section will Difficulties in diagnolook at the relative occurrence of sis of knee problems injury to specific anatomical knee in children components. These can be exam1. The pattern of injury ined as two categories: those that changes with age. arise as a result of acute trauma, 2. Accuracy of history and those that result from repetiand examination in tive microtrauma (i.e., overuse children is variable. injuries). Overuse arises from 3. Investigations often inadequate time for resolution fail to identify between stress episodes.48 In chilpathology in the dren the knee is the most comknee. mon site for overuse injuries.20 Soft Tissue Injuries Muscle Injury Acute muscle injuries to the knee are very common and usually self-limiting with resolution in a few weeks. Hamstring and quadriceps injuries are usually managed with physiotherapy and rest, ice, compression, and elevation. Chronic problems usually relate to recurrent injuries to the extensor mechanism and can be attributable to factors such as muscle imbalance and angular or torsional malalignment of the lower limb. Imbalance arises from weakness or low flexibility of the quadriceps muscles from inadequate conditioning or overtraining. Tendon and Ligament Injury Because ligaments are stronger than bone in young children, evidence of ligamentous disruption may be an indicator of a physeal fracture. Strain and sprain injuries account

for approximately 35% of knee injuries,7 of which MCL injuries are the most common. MCL injuries have been associated with Salter-Harris type III epiphyseal injuries of the tibia.49 ACL injuries usually are associated with fractures of the tibial spine in preadolescents. In an analysis of a series of publications on the use of arthroscopy performed in children after trauma,41–44,50–56 ACL injuries contribute to 16.7% of arthroscopic findings (see Table 1–3). In one series, ACL disruption was associated with tibial spine fractures in 80% of children under age 12.57 Mid-substance tears of the ACL have been reported in children as young as age 9, but the injury is more common in adolescents.47 The mechanisms of injury are usually hyperextension, sudden deceleration, or valgus and rotational force with the foot planted. In one study, 94% of ACL injuries were related to sport.55 ACL injuries have been associated with medial meniscal injuries. In one series, they coexisted in 6% of preadolescent hemarthroses and 18% of adolescent hemarthroses.50 At college level the incidence of ACL injuries has been explored in soccer and basketball. The incidence of ACL injuries in female college athletes is 0.31 per 1000 hours of combined practice and game time compared with 0.13 per 1000 in their male counterparts. Metzl and Micheli found that ACL injuries were increasing, with these trends being particularly evident in female soccer players.29 In one review, skeletally immature patients only account for 3–4% of all midsubstance tears of the ACL.58 Untreated ACL ruptures in skeletally immature patients fare poorly. However, reconstruction is not without the dangers of growth arrest, although a few cases have been reported.59,60 A variety of techniques that appear not to affect subsequent growth have been described.61–63 ACL injuries in children account for 10–65% of acute hemarthrosis in children.5 PCL injuries are very rare in children but may arise by a posteriorly directed force to the tibia on the femur with the knee flexed 90 degrees, or by a hyperextension injury of the knee. PCL injuries contribute to only 1% of arthroscopic findings in children (see Table 1–3).

8

Chapter 1

45 40

Percentage of injuries (%)

35 30 Extra articular fractures Internal Knee fractures Sprains with synovial tears Patellar dislocations Ligamentous or meniscal injury

25 20 15 10 5 0 0–10

11–12

13–16

Age group (years)

Figure 1–4 Trend of knee injury patterns resulting in hemarthrosis.47

Meniscal Injury Hede et al. reviewed 1215 meniscal injuries requiring open surgical treatment.64 In children 0 to 9 years of age, the incidence was 0.1 per 10,000 perKEY POINTS sons, but it increases to 5.2 per 10,000 persons between the ages Soft tissue injuries of 10 and 19. The peak inciabout the knee dence rises in those between 1. MCL and ACL ages 20 and 29. Trauma accountinjuries are common ed for 77% of childhood menisin children. cal injuries. Abdon30 reviewed 2. Sports involving operative findings in children rapid changes in under 18 who underwent menisdirection pose a cal surgery, and calculated an particular risk. annual incidence of menis3. Internal derangecectomy rate of 0.7 per 10,000 in ments are frequentthe 1960s to 2.5 per 10,000 ly associated with in the 1980s. However, this numhemarthrosis. ber should be lower at present 4. Ligament injuries, given the trend for meniscusfractures, and preserving surgical techniques. meniscal tears may Repair of meniscal tears in coexist. children should at least be attempted because patients with a meniscectomy at a young age have poor functional outcomes in the medium and long term.65 Long-term follow-up studies after total meniscectomy revealed that 37.5–63% of patients have fair to poor outcomes, with 87.5% demonstrating significant degenerative changes at radiography.66,67. In one study on meniscal injuries in a Chinese population, 22 of these patients had lateral meniscal lesions, 21 of which were discoid.44 Fractures Injuries of the knee most commonly result in physeal injuries because the ligaments are stronger than the

growth plates.68 Mechanically, the growth plate has only one third the strength of the surrounding ligaments.48 Hence, if fractures are not evident on plain anteroposterior and lateral radiographs in patients with open physes and a knee effusion, further investigations are warranted to identify possible fractures. Additional radiographs include valgus and varus stress views and tunnel and sunrise patellar views, and, if other injuries are suspected, magnetic resonance imaging may be indicated.69 With fractures around the knee, the biggest concern is growth disturbance, which may require surgery in more than 20% of cases.49 Fractures of the distal femoral physes represent less than 1% of all childhood fractures.1 The incidence is equal in boys and girls who partake in sports,1 especially sports that involve jumping. In younger children the main cause is high-velocity trauma such as road traffic accidents. Possibly for this reason, the degree of initial displacement in these injuries relates to the degree of growth disturbance more than to Salter-Harris grading.49 In 151 patients with a fracture of the distal femoral epiphysis, there was a strong male preponderance (6:1), with a mean age of injury at 12.3 years.70 Most of the injuries occurred in the 11–17 year age group (60.3%). Sports accounted for 59.6% of these injuries, road traffic accidents for 22.5%, and falls accounted for 17.9%. Less than 3% of these fractures were open, and most were Salter-Harris type II (43%). Peroneal nerve palsy was present in 7.2% of the fractures. Poor long-term results were reported in 35% of such fractures. After an average follow-up period of 8.2 years, 51% of patients clinically had deformity in the femur, 38.4% had limb shortening, 28.5% had lost some degree of knee motion, and ligamentous laxity was evident in 13.9%. Salter-Harris type II injuries to the distal femoral physes can result in significant long-term problems and are not a benign condition (Table 1–4).

Hyperextension force, high velocity trauma

Hyperextension force or direct trauma

Hyperextension force with rotation or direct blow

Violent flexion against a contracted quadriceps, or intensive jumping

Direct blow or sudden contraction of extensor apparatus

Periosteum stripped downward in continuity with the tendon Direct blow, shearing force to medial or lateral condyle, or flexion rotation injury of knee Forceful direct blow with hip and knee almost fully extended

Distal femoral physis

Proximal tibial physis

Tibial eminence

Tibial tuberosity

Patella

Sleeve fractures of the patella

RTAs, Road traffic accidents. * Based on Meyers and McKeever classification.71 † Based on Watson-Jones classification.85 ‡ Based on Grogan classification.86

Floating knee72

Osteochondral fractures

Mechanism of Injury

9 years

2.6% of fractured femora

7.4% of arthroscopic findings in children

Two thirds of patella fractures in children

11 years83

Unknown

Rare; only 6% of patellar fractures occur in children

14–15% of fractures about the knee

48% of fractures about the knee

Unknown

15 years

8-14 years

3% of physeal injuries

7% of physeal injuries and less than 1% of all childhood fractures

12 years70

14 years

Prevalence

Peak Onset

Summary of Distribution of Fractures about the Knee69

Fracture Site

Table 1–4

25–59.6% caused by sports 22.5–44% caused by RTAs 18% caused by falls Salter-Harris type I, 26% Salter-Harris type II, 43% Salter-Harris type III, 12% Salter-Harris type IV, 15% Salter-Harris type V, 4% 70 Salter-Harris type I, 15% Salter-Harris type II, 43% Salter-Harris type III, 22% Salter-Harris type IV, 17% Salter-Harris type V, 2% Type 1 nondisplaced, 15% Type 2 posterior hinge, 39% Type 3 fully displaced, 45%* Type 1 small fragment displaced up, 39% Type 2 whole lip hinged up, 17% Type 3 complete fracture through base, 43%† 53% caused by RTAs 28% caused by direct blow or falls 17% sports-related Superior, 15% Inferior, 38% Medial, 47% Lateral, 0%‡ Inferomedial fractures, 78% Lateral femoral fractures, 22% 73% caused by RTAs

Comments

58% have limb length discrepancy

39% of patellar dislocations associated with osteochondral fractures84

Can be mistaken for bipartite patella

Objective ligamentous laxity in 51–74%

Angular deformity in 28% Limb length discrepancy in 19% Neurovascular compromise in 6%

Angular deformity in 24–51% Limb length discrepancy in 32–38% Neurovascular compromise in 2.0–7.3%

Complications

Epidemiology of Pediatric Knee Injuries

9

10

Chapter 1

Complete fractures of the proximal tibial physes are rare because of stabilization by the collateral ligaments. Fractures may involve the anterior tibial tuberosity. There is an association with arterial injury and compartment syndromes. Most are Salter-Harris type II injuries and may cause genu valgum and varus (see Table 1–3). The mechanism of injury in fractures of the tibial eminence/avulsion of the tibial spine is either a direct blow or forced hyperextension with rotation. These fractures are most frequent in adolescents because of the relative weakness of the incompletely ossified tibial eminence. Meyers and McKeever classified71 fractures of the tibial eminence into type 1 nondisplaced, type 2 partial displaced or hinged, type 3 completely displaced, and type 4 comminuted. The overall prognosis for such fractures is good. Patellar subluxation or dislocation occurs in 1 in 1000 children aged 9–15,68 and 1 in 6 such patients develop recurrent dislocations. Approximately 5–39% of patellar dislocations are associated with osteochondral fractures69 when the ipsilateral leg pivots on the ground. The increase in valgus strain and lateral translational forces across the patellofemoral joint leads one of the contact surfaces to fracture. The mechanism of dislocation is twisting with the femur rotating medially with the foot planted or a direct blow to the medial aspect of the patella. Patellar injuries constitute the largest group of problems identified by arthroscopy in children (see Table 1–3). Osteochondral fractures of the patella are associated with dislocation or subluxation of the patella. Injuries to the patellofemoral joint from impact of the lateral femoral condyle against the medial patellar facet result in the aforementioned fracture. Osteochondral injuries, whether of the distal femur or the patella, constitute a significant proportion of childhood knee fractures, and may be found in 7.4% of arthroscopies. They are more common in preadolescents. Patellar fractures result from high-energy direct trauma to the patella or shear forces and avulsion forces through the patella. The common picture of patellar fractures in adults is rarely seen in children because of the cartilaginous makeup of the patella in youth. Sleeve fractures refer to avulsion fractures from either the patellar tendon or quadriceps insertion that can arise in children who participate in sports that involve jumping with sudden extension of the take-off knee. Sleeve fractures may be missed because the avulsed bony fragment is too small to be visualized on plain radiographs. Occasionally, congenital bipartite patella can be mistaken for these conditions.49 Tibial tuberosity fractures generally occur in adolescents who are involved in athletic jumping events. The average age of presentation is 13–16, with a male preponderance of 5:1. The vast majority of adolescent and pediatric knee injuries are trivial. Rarely, major road trauma may produce devastating injuries, such as floating knees or knee disarticulations. The mechanism of injury has been analyzed and identifies the bicycle being hit on the side by the bumper of the car with the cyclist’s leg extended.72 Secondary injuries are inevitable and can be life- or limb-threatening. Injuries of this severity are few and only represented 2.6% of all frac-

tured femora admitted, with an average age of these patients of 9 years. Miscellaneous/Chronic Knee Problems Chronic or overuse injuries such as patellofemoral disorders vary in their severity, usually relating to the degree of patella malalignment, size of femoral condyles, and the opposing surKEY POINTS faces of the femur and patella. In its mildest form (lateral patellar Fractures about the compression syndrome), discomknee fort behind the patella is aggra1. Physeal injuries may vated by prolonged sitting or result in growth disstanding or knee flexion or turbances. extension. The effects of the 2. Severity of growth syndrome may be corrected by disturbance does exercises to strengthen the vasnot necessarily tus medialis and by thigh muscle relate to Salterstretching. At the more severe Harris grading. end of the spectrum, subluxation 3. Injuries can be and dislocation are infrequent associated with sequelae. neurovascular disYoung athletes rarely have ruption to vessels in true chondromalacia patellae popliteal fossa. (CMP) in the absence of trauma or underlying disease.1 CMP is both a clinical and a pathological diagnosis. At arthroscopy, most patients do not have evidence of articular damage, and the condition is possibly caused by stress from malalignment or a localized synovitis.49 The clinical diagnosis is made on the basis of generalized anterior knee pain and the impression of patellofemoral crepitus. Because of lack of clarity in its definition and diagnostic criteria, CMP is not universally accepted as a clinical condition.3,48 Osteochondritis dissecans (OCD) is multifactorial but can be associated with trauma. It can affect either the distal femur or the patella, and it is associated with intense physical training and high-level sport in young patients.73 More recent studies debate this relationship, finding no real athleticism and trauma in affected patients.49 Even the role of ischemia and avascular necrosis in its pathogenesis is debatable because the blood supply to the distal femur is rich, and patterns of bone infarction from diseases that cause embolization and small vessel disease show very different patterns. OCD of the patella frequently presents with unilateral symptoms, although one study found a bilateral picture emerging. The most common site for OCD at the knee is the lateral non-weight-bearing portion of the medial femoral condyle. Usually symptomatic only in adolescence, OCD occurs more frequently in boys (2:1) at the average age of 13.6 years74 and is bilateral in 20–30% of the patients. OCD accounts for 6.6% of arthroscopic findings, but it is rarely found in preadolescent patients. Traction apophysitis of the anterior tibial tuberosity (Osgood-Schlatter lesion) affects boys more than girls and is related to jumping activities. It is the result of repetitive microtrauma to the immature anterior tibial tuberosity. Girls affected with this lesion have an earlier age of onset (8–13 years) than boys. In boys, Osgood-Schlatter lesion

Epidemiology of Pediatric Knee Injuries

presents in those between age 10 and 15. The condition has been associated with low flexibility of the quadriceps muscles complex, is bilateral in 20–30% of patients, and may have a hereditary component.1,3 Jumping, squatting, and kneeling aggravate the condition. Immobilization of the knee may reduce recovery time,73 but recurrence rates of 60% have been described.3 Another common site for traction apophysitis is the inferior pole of the patella, giving rise to Sinding-LarsenJohansson lesion. The condition is self-limiting and affects a similar age group.18 Medial tibial stress syndrome results from stress fractures and inflammation of the periosteum, but it is rare in children. Rare conditions include knee tumors that are often recorded as sports-related injuries. Lewis KEY POINTS et al. reported a series of 22 knee tumors that presented as sportsOveruse injuries related knee injuries.75 Two of Patellofemoral probthese were malignant tumors in lems represent a specadolescents, hence the need for trum of disorders. awareness of rare and serious conImportant causes of ditions that affect the knee. chronic knee pain in These should be excluded when children include the the physician is presented with following: chronic injuries and abnormal 1. Chondromalacia radiographs. patellae Outcome

2. Osgood-Schlatter lesions 3. Sinding-LarsenJohansson lesions 4. Osteochondritis dissecans

In the short term, knee injuries in children produce a wide spectrum of disabilities. Children with internal derangement of the knee may require surgical intervention, and controversy still exists as to whether surgery should be delayed until the child is skeletally mature. For ACL injuries, there appears to be much variation in the way clinicians manage injuries in the skeletally immature patient, although there is an increasing trend to operate even in younger (below the age of 10) children.5 Meniscal-preserving surgery should be performed when possible, because meniscectomy leads to detrimental changes in the long term. Long-term followKEY POINTS up studies after total meniscectomy in children leave 29–77% of Surgical intervention children with persistent symp1. Surgery is rarely toms and 20–84% with radirequired for childographic evidence of joint degenhood knee comeration.65,76,77 Results of a study plaints. into sports-related knee injuries 2. Advancement in in children found that of all surgical techniques injuries that would go on to have challenge the tradilong-term problems, knee sprains tional fears of oper78 constitute 15% of this group. ating on skeletally Suggestions for Injury Prevention Through modification of intrinsic and extrinsic risk factors we can begin to formulate ways to

immature patients. 3. Better outcomes are associated with meniscal-preserving surgery than excision.

11

reduce childhood knee injuries. Intrinsic factors can rarely be modified directly, but training techniques and education, together with selective training of muscle groups, may reduce the risk of sports-related injury. In sports, warm-up exercises; proper, well-fitting equipment; and good supervision and coaching form the basis of a safe training environment. Coaches should emphasize proper techniques on how to jump and land while avoiding one-legged landings, as well as how to avoid out-of-control descent and straight-leg landings.79 Quadriceps and hamstring muscles should be gradually trained to react faster with improvement of muscle balance. Simple measures such as keeping on one’s toes allow safer pivoting in sports that involve rapid directional change. Prophylactic knee braces in children do not contribute much to the prevention of knee injuries and are not recommended by the American Academy of Pediatrics.80 Knee pads provide protection from direct injury but do not resist shear, torsional, and translational forces. Dynamic neuromuscular training improves knee stability in adults,81,82 but its application to children has not been demonstrated. Safe and supervised environments for competitive and recreational activities play a role in ensuring that injury levels are controlled. Rapid access to clinical and physiotherapy services also play a role in minimizing the disability associated with knee injuries. KEY POINTS Preparticipation screening of atrisk individuals may be a means Suggestions for injury to minimize the increasing inciprevention dence of childhood injuries. 1. Intrinsic and extrinIn summary, the incidence sic factors should of knee injuries in children and be modified when adolescents is increasing despite possible. better understanding and appre2. Proper techniques ciation of the effectiveness of for jumping, landing, training, supervision, education, and pivoting should and preventative provisions. be taught. Identification of these risk fac3. Safety promotion tors provides many avenues for and careful superviresearch into childhood knee sion may dampen injuries, which promises vast the rise of sportspotential and is greatly underinrelated injuries. vestigated. References 1. Smith AD, Tao SS: Knee injuries in young athletes. Clin Sports Med 14:629–650, 1995. 2. Maffulli N, Baxter-Jones AD: Common skeletal injuries in young athletes. Sports Med 19:137–149, 1995. 3. Davids JR: Pediatric knee: clinical assessment and common disorders. Pediatr Clin North Am 43:1067–1090, 1996. 4. Schmidt-Olsen S, Jorgensen U, Kaalund S, et al: Injuries among young soccer players. Am J Sports Med 19:273–275, 1991. 5. Kocher MS, Saxon HS, Hovis WD, et al: Management and complications of anterior cruciate ligament injuries in skeletally immature patients: survey of the Herodicus Society and The ACL Study Group. J Pediatr Orthop 22:452–457, 2002. 6. Hosalkar H, Lou J, Flynn J: Pediatric musculoskeletal trauma. Curr Opin Orthop 13:413–418, 2002. 7. US Consumer Product Safety Commission: National Electronic Injury Surveillance System (NEISS) database. 2001. Washington, DC. 8. Kujala UM, Nylund T, Taimela S: Acute injuries in orienteerers. Int J Sports Med 16:122–125, 1995.

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9. Skak SV, Jensen TT, Poulsen TD, et al: Epidemiology of knee injuries in children. Acta Orthop Scand 58:78–81, 1987. 10. Conn JM, Annest JL, Gilchrist J. Sports and recreation related injury episodes in the U.S. population, 1997–1999. Inj Prev 9:117–123; 2003. 11. Maffulli N, King JB, Helms P: Training in elite young athletes (the Training of Young Athletes [TOYA] Study): injuries, flexibility and isometric strength. Br J Sports Med 28:123–136, 1994. 12. Loud KJ, Micheli LJ: Common athletic injuries in adolescent girls. Curr Opin Pediatr 13:317–322, 2001. 13. Walsh WM, Huurman WW, Shelton GL: Overuse injuries of the knee and spine in girls’ gymnastics. Orthop Clin North Am 16:329–350, 1985. 14. Goldberg MJ: Gymnastic injuries. Orthop Clin North Am 11:717–726, 1980. 15. Caine D, Knutzen K, Howe W, et al: A three-year epidemiological study of injuries affecting young female gymnasts. Phys Ther Sport 4:10–23, 2003. 16. Witvrouw E, Lysens R, Bellemans J, et al: Intrinsic risk factors for the development of anterior knee pain in an athletic population. A twoyear prospective study. Am J Sports Med 28:480–489, 2000. 17. Ganley T, Pill S, Flynn J, et al: Pediatric and adolescent sports medicine. Curr Opin Orthop 12:456–461, 2001. 18. Maffulli N, Bruns W: Injuries in young athletes. Eur J Pediatr 159:59–63, 2000. 19. Routley V: Sports injuries in children: the five most commonly presented sports. Hazard 9:1-8, 1991. 20. Maffulli N, Bundoc RC, Chan KM, et al: Paediatric sports injuries in Hong Kong: a seven year survey. Br J Sports Med 30:218–221, 1996. 21. Halpern B, Thompson N, Curl WW, et al: High school football injuries: identifying the risk factors. Am J Sports Med 15:316–320, 1987. 22. Ellison L: Basketball injuries in the database of Canadian Hospitals Injury Reporting and Prevention Program (CHIRPP). Chronic Diseases in Canada 16:117–124, 1995. 23. Bylak J, Hutchinson MR: Common sports injuries in young tennis players. Sports Med 26:119–132, 1998. 24. Messina DF, Farney WC, DeLee JC: The incidence of injury in Texas high school basketball. A prospective study among male and female athletes. Am J Sports Med 27:294–299, 1999. 25. Dowd MD: Childhood injury prevention at home and play. Curr Opin Pediatr 11:578–582, 1999. 26. Osmond MH, Brennan-Barnes M, Shephard AL: A 4-year review of severe pediatric trauma in eastern Ontario: a descriptive analysis. J Trauma-Injury Infection Critical Care 52:8–12, 2002. 27. Wilber CA, Holland GJ, Madison RE, et al: An epidemiological analysis of overuse injuries among recreational cyclists. Int J Sports Med 16:201–206, 1995. 28. Nguyen D, Letts M: In-line skating injuries in children: a 10-year review. J Pediatr Orthop 21:613–618, 2001. 29. Metzl JD, Micheli LJ: Youth soccer: an epidemiologic perspective. Clin Sports Med 17:663–673, 1998. 30. Abdon P, Bauer M: Incidence of meniscal lesions in children. Increase associated with diagnostic arthroscopy. Acta Orthop Scand 60:710–711, 1989. 31. Clements K, Yates B, Curran M: The prevalence of chronic knee injury in triathletes. Br J Sports Med 33:214–216, 1999. 32. Heneved E: Skiing and snowboarding injuries in the year 2000. Wilderness Med 19:2002. 33. Deibert MC, Aronsson DD, Johnson RJ, et al: Skiing injuries in children, adolescents, and adults. J Bone Joint Surg Am 80:25–32, 1998. 34. Sutherland AG, Holmes JD, Myers S: Differing injury patterns in snowboarding and alpine skiing. Injury 27:423–425, 1996. 35. Bladin C, Giddings P, Robinson M: Australian snowboard injury data base study. A four-year prospective study. Am J Sports Med 21:701–704, 1993. 36. Atkinson T, Atkinson P: Knee injuries in motor vehicle collisions: a study of the National Accident Sampling System database for the years 1979–1995. Accid Anal Prev 32:779–786, 2000. 37. Ski G, Madro R: Knee joint injuries as a reconstructive factors in carto-pedestrian accidents. Forensic Sci Int 124:74–82, 2001. 38. Chard MD, Lachmann SM: Racquet sports—patterns of injury presenting to a sports injury clinic. Br J Sports Med 21:150–153, 1987.

39. Kwolek CJ, Sundaram S, Schwarcz TH, et al: Popliteal artery thrombosis associated with trampoline injuries and anterior knee dislocations in children. Am Surg 64:1183–1187, 1998. 40. Lonergan, GJ. Child abuse: the role of radiology, 2001, online at http://rad.usuhs.mil/rad/handouts/lonergan/osiabuse.html. 41. Harvell JC Jr., Fu FH, Stanitski CL: Diagnostic arthroscopy of the knee in children and adolescents. Orthopedics 12:1555–1560, 1989. 42. Vahasarja V, Kinnuen P, Serlo W: Arthroscopy of the acute traumatic knee in children. Prospective study of 138 cases. Acta Orthop Scand 64:580–582, 1993. 43. Matelic TM, Aronsson DD, Boyd DW Jr., et al: Acute hemarthrosis of the knee in children. Am J Sports Med 23:668–671, 1995. 44. Maffulli N, Chan KM, Bundoc RC, et al: Knee arthroscopy in Chinese children and adolescents: an eight-year prospective study. Arthroscopy 13:18–23, 1997. 45. Close BJ, Strouse PJ: MR of physeal fractures of the adolescent knee. Pediatr Radiol 30:756–762, 2000. 46. Zobel MS, Borrello JA, Siegel MJ, et al: Pediatric knee MR imaging: pattern of injuries in the immature skeleton. Radiology 190:397–401, 1994. 47. Wessel LM, Scholz S, Rusch M: Characteristic pattern and management of intra-articular knee lesions in different pediatric age groups. J Pediatr Orthop 21:14–19, 2001. 48. Stanitski CL: Pediatric and adolescent sports injuries. Clin Sports Med 16:613–633, 1997. 49. Steiner ME, Grana WA: The young athlete’s knee: recent advances. Clin Sports Med 7:527–546, 1988. 50. Stanitski CL, Harvell JC, Fu F: Observations on acute knee hemarthrosis in children and adolescents. J Pediatr Orthop 13:506–510, 1993. 51. Juhl M, Boe S: Arthroscopy in children, with special emphasis on meniscal lesions. Injury 17:171–173, 1986. 52. Bergstrom R, Gillquist J, Lysholm J, et al: Arthroscopy of the knee in children. J Pediatr Orthop 4:542–545, 1984. 53. Irha E, Vrdoljak J: Algorithm for establishing the indication for knee arthroscopy in children: a comparison of adolescent and preadolescent children. Knee Surg Sports Traumatol Arthrosc 8: 99–103, 2000 54. Ziv I, Carroll NC: The role of arthroscopy in children. J Pediatr Orthop 2:243–247, 1982. 55. Bak K, Wilbek H: Arthroscopy of the knee in children and adolescents. Scand J Med Sci Sports 2:92–95, 1992. 56. Angel KR, Hall DJ: The role of arthroscopy in children and adolescents. Arthroscopy 5:192–196, 1989. 57. Kellenberger R, von Laer L: Nonosseous lesions of the anterior cruciate ligaments in childhood and adolescence. Progr Pediatr Surg 25:123–131, 1990. 58. Nottage WM, Matsuura PA: Management of complete traumatic anterior cruciate ligament tears in the skeletally immature patient: current concepts and review of the literature. Arthroscopy 10:569–573, 1994. 59. Lipscomb A, Anderson A: Tears of the anterior cruciate ligament in adolescents. J Bone Joint Surg Am 68-A:19–28, 1986. 60. Koman J, Sanders J: Valgus deformity after reconstruction of the anterior cruciate ligament in a skeletally immature patient: a case report. J Bone Joint Surg Am 81-A:711–715, 1999. 61. Kim S, Ha K, Ahn J, et al: Anterior cruciate ligament reconstruction in the young patient without violation of the epiphyseal plate. Arthroscopy 15:792–795, 1999. 62. McCarroll JR, Rettig AC, Shelbourne KD: Anterior cruciate ligament injuries in the young athlete with open physes. Am J Sports Med 16:44–47, 1988. 63. Aichroth PM, Patel DV, Zorrilla P: The natural history and treatment of rupture of the anterior cruciate ligament in children and adolescents. A prospective review. J Bone Joint Surg Br 84:38–41, 2002. 64. Hede A, Jensen DB, Blyme P, et al: Epidemiology of meniscal lesions in the knee. 1,215 open operations in Copenhagen 1982–1984. Acta Orthop Scand 61:435–437, 1990. 65. Manzione M, Pizzutillo PD, Peoples AB, et al: Meniscectomy in children: a long-term follow-up study. Am J Sports Med 11:111–115, 1983. 66. Dai L, Zhang W, Xu Y: Meniscal injury in children: long-term results after meniscectomy. Knee Surg Sports Traumatol Arthrosc 5:77–79, 1997. 67. Wroble RR, Henderson RC, Campion ER, et al: Meniscectomy in children and adolescents. A long-term follow-up study. Clin Orthop 180–189, 1992.

Epidemiology of Pediatric Knee Injuries

68. Bruns W, Maffulli N: Lower limb injuries in children in sports. Clin Sports Med 19:637–662, 2000. 69. Beaty JH, Kumar A: Fractures about the knee in children. J Bone Joint Surg Am 76:1870–1880, 1994. 70. Eid AM, Hafez MA: Traumatic injuries of the distal femoral physis. Retrospective study on 151 cases. Injury 33:251–255, 2002. 71. Meyers MH, McKeever FM: Fracture of the intercondylar eminence of the tibia. J Bone Joint Surg Am 52-A:1677–1684, 1970. 72. Letts M, Vincent N, Gouw G: The “floating knee” in children. J Bone Joint Surg Br 68:442–446, 1986. 73. Maffulli N: Intensive training in young athletes. The orthopaedic surgeon’s viewpoint. Sports Med 9:229–243, 1990. 74. Bradley J, Dandy DJ: Osteochondritis dissecans and other lesions of the femoral condyles. J Bone Joint Surg Br 71:518–522, 1989. 75. Lewis MM, Reilly JF: Sports tumors. Am J Sports Med 15:362–365, 1987. 76. Vahvanen V, Aalto K: Meniscectomy in children. Acta Orthop Scand 50:791–795, 1979. 77. Medlar RC, Mandiberg JJ, Lyne ED: Meniscectomies in children. Report of long-term results (mean, 8.3 years) of 26 children. Am J Sports Med 8:87–92, 1980. 78. Marchi AG, Di Bello D, Messi G, et al: Permanent sequelae in sports injuries: a population based study. Arch Dis Child 81:324–328, 1999.

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79. Ireland ML: The female ACL: why is it more prone to injury? Orthop Clin North Am 33:637–651, 2002. 80. Martin TJ: Committee on Sports Medicine and Fitness: American Academy of Pediatrics: technical report: knee brace use in the young athlete. Pediatrics 108:503–507, 2001. 81. Hewett TE, Lindenfeld TN, Riccobene JV, et al: The effect of neuromuscular training on the incidence of knee injury in female athletes. A prospective study. Am J Sports Med 27:699–706, 1999. 82. Williams GN, Chmielewski T, Rudolph K, et al: Dynamic knee stability: current theory and implications for clinicians and scientists. J Orthop Sports Phys Ther 31:546–566, 2001. 83. Dai LY, Zhang WM: Fractures of the patella in children. Knee Surgery, Sports Traumatol, Arthrosc 7:243–245, 1999. 84. Nietosvaara Y, Aalto K, Kallio PE: Acute patellar dislocation in children: incidence and associated osteochondral fractures. J Pediatr Orthop 14:513–515, 1994. 85. Watson-Jones R: Fractures and Joint Injuries. Edinburgh, E. & S. Livingstone, 1955. 86. Grogan DP, Carey TP, Leffers D, et al: Avulsion fractures of the patella. J Pediatr Orthop 10:721–730, 1990.

Chapter 2

History and Physical Examination of the Child’s Knee Lyle Micheli

●

Kevin Latz

Obtaining a history and physical examination of a child with an acute injury or chronic problem of the knee can be a challenging endeavor for a number of reasons. Injured children are often not completely cooperative with their examiner and often cannot provide a history of their injury. Additionally, given their desire to return to their sport or activity, children will often underreport their symptoms. Despite these challenges, obtaining a thorough history and physical examination is vital to determine a correct diagnosis, and it has been shown to be superior to magnetic resonance imaging (MRI) in certain clinical conditions.1–3 This chapter will discuss general points relevant to obtaining an accurate history and performing a thorough physical on a skeletally immature patient. Specific conditions and their unique clinical findings will be discussed as well. History The examination of the pediatric knee should be preceded by a thorough problem-focused history. All skeletally immature patients are not equal. There is also a tremendous difference in obtaining the history of an injury or problem from a child versus an adolescent with regard both to the style of the interview and to the information solicited. Additionally, injury patterns differ between children and adolescents, and the questions should reflect these injury patterns.4 When examining a child, the majority of the questions regarding the etiology of the problem will necessarily be directed to the parent or caregiver. Similarly, questions involving objective findings or signs (e.g., the presence or absence of an effusion or ecchymosis) should be directed to the adult as well. Any positive history of an effusion should be further investigated. Consider asking, “Is the knee currently swollen?” to determine the family’s understanding of an effusion. Questions regarding symptoms should be 14

directed to the patient whenever possible. Children will often be more willing to talk to the examiner if they perceive rapport has been established between the examiner and their parent/caregiver. Conversely, the adolescent should be questioned regarding symptoms and signs. Although a child can certainly sustain injuries to the cruciate ligaments and menisci, an adolescent is more likely to sustain an injury to these structures. If an injury is suspected, specific details on the mechanism of the injury must be elicited. If the injury occurred during a sporting event, the type of playing surface and whether there was a collision is useful information to obtain. The patient should be questioned on whether he or she felt or heard a pop at the time of the injury, which would suggest an injury to the cruciate ligaments or the patellofemoral joint. If an effusion has developed, the rapidity of the onset of the effusion, as well as whether the effusion has been recurrent, can help differentiate between a cruciate ligament injury (immediate hemarthroses) and a meniscal injury or a repetitive stress injury. Whether the athlete was able to continue playing and/or leave the field under his or her own power, as well as whether the athlete has been able to return to his or her sport, can help determine the severity of the injury. If the symptoms are not the result of an injury, questions should focus on the initiation of any new sport or training regimen. As with the adult patient, symptoms, such as instability and pain, as well as activities and therapies that both alleviate and exacerbate the symptoms should be investigated. Physical Examination—General The clinical examination of the skeletally immature patient includes observation, palpation, and an examination of the ligamentous structures. The young child should be examined while wearing underwear. The adolescent should be examined while wearing shorts. Before examining a child, the caregiver and child should have a conversation of sufficient depth to

History and Physical Examination of the Child’s Knee

demonstrate to the child that the examiner can be trusted. In some situations a child is best examined in the lap of the caregiver. Additionally, the uninjured or nonpainful portion of the child’s limb should be examined first so as to further develop a relationship between the child and the examiner. Observation should include determination of the presence or absence of an effusion, muscle atrophy, or ecchymosis; range of motion; gait analysis; leg lengths; coronal and sagittal alignment of the limb; and patellar tracking. Suprapatellar swelling is consistent with an effusion and an intraarticular process, whereas swelling below the patella is consistent with overuse tendonitis. Range of motion should be observed with the child in a seated position and during the gait cycle. Ideally, the gait examination consists of watching the child walk, jog, and run up and down a hallway both toward and away from the examiner; however, incomplete cooperation from a fearful child is not unusual. Often this portion of the examination will need to be deferred until the end of the examination. Occasionally, gait can only be observed as a child is leaving the office, or not at all. Specific attention should be directed toward range of motion of the knee throughout the gait cycle. Leg lengths should be evaluated while the child is standing using blocks. Observation must also include an examination of the entire lower extremity in the coronal and sagittal planes to identify genu recurvatum, genu varum and valgum, pes planus, and hindfoot valgus. Adolescent genu varum is often accompanied by knee pain, whereas infantile genu varum is rarely associated with knee pain. Genu valgum lower extremity alignment can be associated with patellofemoral maltracking and patellofemoral pain, particularly when it is combined with pes planovalgus hindfoot alignment. Extremely obese patients often demonstrate dynamic painless genu valgum alignment. Finally, observation should also include inspection of the quadriceps for atrophy. In addition to demonstrating diminished rotation and abduction of the hip, patients with various hip conditions will often manifest quadriceps atrophy, as will patients with chronic knee pain. The examination should include palpation of the medial and lateral joint lines, the physis of the distal femur and proximal tibia, the superior and inferior poles of the patella, the patellar retinaculum, the synovial plicae, the patellar tendon, and the insertion of the patellar tendon at the tibial tubercle (Figure 2–1). Palpation KEY POINTS should also include provocative testing, that is, passive subluxaPhysical examination tion of the patella (apprehension (general) 5 test; Figure 2–2). 1. Initial examination of Stress testing of the anterior the injured child must and posterior cruciate ligaments not cause pain for and the medial and lateral colfear of losing the lateral ligaments and provocachild’s cooperation. tive testing of the menisci com2. Examination of the plete the physical examination. knee must be accomAny examination of the panied by examinaknee should include a thorough tion of the entire limb. examination of the hip, with spe3. Examination of the cific emphasis on passive internal hip is a vital compoand external rotation and passive nent of the knee abduction to identify primary examination. hip pathology with referred

15

Figure 2–1 Palpation of the joint line in the figure 4 position.

Figure 2–2 Demonstration of the apprehension test.

symptoms to the knee, such as slipped capital femoral epiphysis (SCFE) or Legg-Calvé-Perthes disease. Finally, generalized hypermobility criteria should be investigated in patients with patellar instability.6,7 Physical Examination—Specific Conditions Overuse Injuries of the Knee The majority of overuse injuries in the skeletally immature child occur in the knee, specifically in the extensor mechanism. Symptoms can localize to the superior pole of the patella, the inferior pole of the patella (Sinding-LarsenJohansson disease), the patellar tendon itself, or at the insertion of the patellar tendon on the proximal tibia (Osgood-Schlatter disease).8–10 Patients typically present between the ages of 11 and 15. The typical patient is an athlete involved in running, jumping sports, although overuse injuries can also occur in poorly conditioned patients who attempt to initiate physical activity. Symptoms typically are limited to pain localized to a specific site in the extensor mechanism; however, with chronic symptoms patients can also experience giving way episodes as a result of quadriceps weakness.

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The physical examination in these patients is remarkable for point tenderness at one or more of the aforementioned sites of the extensor mechanism. Swelling can occur in the infrapatellar region and can be quite pronounced, particularly with Osgood-Schlatter disease. Flexibility in the quadriceps and hamstrings is limited, and indeed one of the hallmarks of successful resolution of this condition is improving the flexibility of the quadriceps and hamstrings muscles.11 The identification of quadriceps contracture is accomplished by having the patient lie prone and flexing the knee while stabilizing the pelvis. The patient should be able to nearly touch the heel to the buttock. The rest of the clinical examination is usually unremarkable. Patellofemoral Pain Patellofemoral pain is a poorly understood condition commonly seen in the outpatient clinic. The typical patient provides a history of chronic pain without an antecedent traumatic event. Symptoms are limited to pain, although as with overuse injuries of the knee, chronic pain can lead to quadriceps weakness and giving way episodes. Pain occurs both at rest and with activity and is exacerbated by going up and particularly down stairs, as well as by sitting with the knee flexed for a prolonged period. The physical examination of these patients is often relatively unremarkable. Occasionally, in addition to the aforementioned diminished quadriceps flexibility, patients will demonstrate diminished hamstring flexibility as evidenced by a popliteal angle greater than 5 degrees or a straight leg raise test less than 90 degrees. Passively flexing the patient’s hip to 90 degrees and extending the ipsilateral knee determine the popliteal angle. The resultant angle between the thigh and leg is the popliteal angle. The straight leg raise test is accomplished by passively flexing a supine patient’s lower extremity while keeping the knee in full extension. The angle between the table and the hip is the angle in question. The rest of the physical examination is relatively unremarkable. Typically, there is not an effusion nor is there patellofemoral maltracking. Sometimes crepitus can be palpated at the inferior pole of the patella and also palpated with compression of the patella itself. Provocative testing of the patellofemoral joint by having a supine patient contract his or her quadriceps muscle while the examiner stabilizes the patella will often reproduce a patient’s symptoms of pain. Tests to determine patellofemoral tracking, quadriceps angle, and patellar mobility (described later) should also be performed on these patients. Any patient with suspected patellofemoral pain should be evaluated for painful synovial plicae. The plica most likely to cause pain is located medially and can typically be palpated as a longitudinal band one fingerbreadth medial to the patella and superior to the joint line (Figure 2–3). Pain as a result of a fibrotic medial synovial plica should be considered in any patient with suspected patellofemoral pain who does not improve with a supervised therapy program.12 Patellofemoral Instability Patellofemoral instability can be the result of an acute injury or a chronic process. In the setting of an acute injury the injury is usually the result of a direct medical blow to the

Figure 2–3 The plica, which is most likely to cause pain, is located medially and can typically be palpated as a longitudinal band one fingerbreadth medial to the patella and superior to the joint line.

knee that causes a lateral dislocation/subluxation. Instability can also result from very minimal trauma. Clinically, these patients demonstrate an effusion, medial retinacular tenderness, and a positive apprehension sign, although if the knee capsule was disrupted, the effusion may be difficult to appreciate. If pain or swelling persists, a chondral injury must be considered. Patients should be tested for generalized hypermobility because there is a protective effect against the occurrence of a chondral injury with hypermobility.13 Chronic patellofemoral instability is a continuum of disease from patella and femoral hypoplasia to patellofemoral dislocation. This process can be the result of an acute injury but is more commonly a congenital condition. Connective tissue disorders, such as Ehlers-Danlos, Larsen’s, and Marfan syndromes, as well as nail-patella syndrome, can involve the patellofemoral joint. Many pediatric patients with chronic patellofemoral instability do not experience pain even with chronic dislocations, although some patients will experience pain and giving way episodes. The clinical examination for patients with patellofemoral instability should include the inspection of the patellofemoral joint during active range of motion, evaluation of patella mobility, and determination of the quadriceps or Q angle. Determination of patellofemoral maltracking is best accomplished by palpating the medial and lateral borders of the patella in the femoral sulcus during active range of motion

History and Physical Examination of the Child’s Knee

of the knee with the patient in a seated position (Figure 2–4, A and B). In rare cases the patella is chronically laterally dislocated, although most patients have a reduced patellofemoral joint in full extension with subluxation or dislocation occurring at 20–30 degrees of active flexion. Patella mobility, specifically lateral retinacular contractures, can be identified by the passive patella tilt test and the patella glide test. The patella tilt test is accomplished by lifting the lateral border of the patella with the knee in extension. One should be able to lift the lateral border of the patella to neutral or past neutral (Figure 2–5, A and B).14–16 The patella glide test is similar to the apprehension test. The patella is divided into quadrants and passively subluxed both medially and laterally in approximately 30 degrees of flexion. Passive subluxation of greater than two quadrants laterally is suggestive of injury or laxity of the medial retinaculum, and passive subluxation medially of less than two quadrants is consistent with a lateral retinacular contracture (Figure 2–6, A and B).14–16 The quadriceps angle or Q angle is the angle formed between the quadriceps, the patella, and the patellar tendon in extension. Normal is considered <10 degrees in males and <15 degrees in females. A similar measurement is the tubercle sulcus angle, which is the angle formed between the same structures in 90 degrees of flexion (Figure 2–7, A and B).15,16 Zero degrees is considered normal as the tubercle rotates internally with flexion. Finally, maltracking of the patella can be identified via the lateral pull sign. This test is performed with contraction of the quadriceps

17

with the knee in extension. Migration of the patella superiorly or superolaterally in equal magnitudes is considered normal. Migration of the patella laterally with contraction of the quadriceps and the knee in extension is considered abnormal.15 With chronic dislocations, pediatric patients will develop a valgus limb, flexion contracture of the knee, and external rotation of the leg. Meniscal Pathology Although meniscal pathology in this age group is not common, pediatric orthopedic surgeons, pediatricians, and orthopedic surgeons who treat adolescents certainly will encounter this injury. Meniscal lesions can be divided into two groups: acute tears and congenital discoid menisci. As in the adult population, meniscal injuries are typically the result of a twisting injury on a flexed knee. Symptoms are typically limited to pain and occasional mechanical locking. Objectively, patients will often demonstrate lack of complete active extension, recurrent effusions, and joint line tenderness with palpation and with squatting. The diagnosis of a meniscus injury can be confirmed with a positive McMurray’s test or Apley compression test. McMurray’s test is performed with the patient supine with his or her hip and knee flexed to 90 degrees. The foot and leg is rotated from abduction and external rotation to adduction and internal rotation while palpating the medial and lateral joint line (Figure 2–8). The test is

Figure 2–4 A and B, Patellofemoral maltracking is best determined by palpating the medial and lateral borders of the patella in the femoral sulcus during active range of motion of the knee with the patient in a seated position.

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Figure 2–5 A and B, The patella tilt test. One should be able to lift the lateral border of the patella to neutral or past neutral.

considered positive if the examination produces an audible or palpable click with or without the development of pain.17 Children, however, can demonstrate a positive McMurray’s test without a corresponding meniscal injury.18 Alternatively, because adolescent meniscal tears are typically more peripheral than adult degenerative posterior horn tears, the meniscal injury can be detected with varus, valgus, or rotational stress applied to the knee at 30 degrees of flexion rather than 90 degrees of flexion used in McMurray’s test (Figure 2–9).3

Figure 2–6 A and B, Demonstration of the patella glide test.

History and Physical Examination of the Child’s Knee

19

Figure 2–7 A and B, The quadriceps angle (“Q angle”) is the angle formed among the quadriceps, the patella, and the patellar tendon in extension.

Figure 2–8 The medial McMurray test is performed by mounting the knee in forced external rotation while ranging the knee from full flexion to extension (resulting in longitudinal traction on the medial meniscus).

The Apley compression test is performed with the patient prone, the hip extended, and the knee flexed to 90 degrees. The foot is then rotated internally and externally while applying an axial force through the leg.17 Pain or clicking is consistent with a meniscus injury. Joint line tenderness with extreme knee flexion is consistent with a posterior horn tear, whereas joint line pain in full extension can be consistent with an anterior horn tear. Congenital meniscus pathology (“discoid meniscus”) is frequently without symptoms. Children will often provide a history of and readily demonstrate painless “clunking” in their knee with active range of motion. This “clunk” is often visible, audible, and palpable.19,20 Once torn, a discoid meniscus will have symptoms and objective findings, as listed previously. MRI of meniscal pathology has proved difficult in the pediatric population. Many authors have reported the

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Figure 2–9 The lateral McMurray test repeats the maneuver in Figure 2–8 with forced internal rotation.

unreliability of this modality, particularly with regard to the imaging of lateral meniscal lesions. A careful history and physical examination is thus vital.1–3,21 Ligamentous Injuries Previous authors have reported the increase in incidence of ligamentous injuries in skeletally immature patients.22–24 Typically, injuries to the cruciate ligaments are the result of a significant trauma, and usually the patient can provide a thorough detailed history for the injury. The injury is often the result of a hyperextension or valgus injury via a collision with another player, or a twisting injury. As noted previously, there is often an immediate effusion and usually the player is unable to continue playing. The injury to the cruciate ligament is often accompanied by a palpable or audible pop.25 Collateral ligament injuries can occur in isolation or in combination with injury to the cruciate ligaments. Collateral ligament injuries are identified by pain and instability with valgus and varus stressing of the knee in full extension and approximately 30 degrees of flexion. Valgus and varus stressing in full extension stresses the cruciate

ligaments and capsule, whereas valgus and varus stressing in 30 degrees of flexion isolates the collateral ligaments. Pain without instability with a valgus force applied to the limb is a grade I tear of the medial collateral ligament (MCL), whereas grades II and III are partial and complete tears, respectively. The lateral collateral ligament (LCL) is tested in similar fashion with a varus force applied to the limb in 0 and 30 degrees of flexion. MCL injuries can result in an effusion because a portion of the ligament is intraarticular. There are several examinations that can be used to identify an injury to the anterior cruciate ligament (ACL). Lachman’s test is performed by stabilizing the femur and with the knee slightly flexed and passively translating the tibia anteriorly (Technical Note 2–1). The amount of translation is quantified in millimeters: grade 1: 3–5 mm, grade 2: 6–10 mm, and grade 3: 11–15 mm. The quality of the endpoint, firm or soft, should also be noted.26 The pivot shift examination is another test to identify an ACL injury. In our experience, this is poorly tolerated in the acute setting; however, when accomplished successfully and with a positive result, it will reproduce a patient’s symptoms of instability. The test is performed by slightly internally rotating the limb in an extended position. While performing an axial load and a valgus stress to the knee, the knee is slowly flexed. A positive result indicative of an injury to the ACL is a palpable and audible clunk at approximately 30 degrees of flexion, which is the result of the posteriorly subluxed tibia sliding to its reduced position under the femoral condyle.27 The posterior cruciate ligament (PCL) is injured much less frequently than the ACL in the adult population and presumably in the pediatric and adolescent population as well. Diagnosis of this injury is frequently missed, and thus a high index of suspicion is warranted in those patients who sustain a classic PCL producing injury, that is, a posteriorly directed force to a flexed, planted knee (dashboard injury). These injuries also occur in combination with an ACL injury in knee dislocations. The injury is identified via the posterior drawer test.28 This test is performed with the knee flexed 90 degrees and the foot stabilized. While palpating the relationship of the anterior tibia to the femoral condyle, a posterior force is applied to the KEY POINTS proximal tibia. Normally, the tibia lies anterior to the medial Physical examination femoral condyle. Any alteration (specific conditions) of this relationship is diagnostic 1. Patellofemoral pain is of a PCL injury.25 The quadriassociated with ceps active test is another means diminished hamstring by which one can identify an and quadriceps injured PCL. With the patient flexibility. supine and the knee flexed to 2. McMurray’s test approximately 60 degrees, the should be performed patient attempts to extend the in 30 degrees of knee while keeping the foot flat flexion, in addition to on the examination table. 90 degrees of flexion, Anterior movement of the tibia to identify peripheral with this maneuver is diagnostic meniscal tears. 29 of a torn PCL. 3. Physiological laxity It is important to note that of children mandates side-to-side comparisons are side-to-side necessary. Children and adolescomparisons. cents have increased laxity versus Text continued on p. 25

History and Physical Examination of the Child’s Knee

TECHNICAL NOTE 2–1

Pivot Shift Examination Ronald E. Losee

The pivot shift is a dysfunction of the human knee that results from deficiency of the anterior cruciate ligament (ACL) and secondary restraining structures of the posterolateral corner of the joint. The deficiency is usually caused by trauma. The dysfunction is a posterior subluxation, then reduction, of the lateral femoral condyle off the lateral tibial plateau. During each dysfunctioning episode, either the subluxation or the reduction, or both, may be quiet or disturbing. A twist of the body toward the ipsilateral side of the dysfunctioning knee with the foot fixed will cause a subluxation. A twist of the body toward the contralateral side will cause a subluxated knee to reduce, usually in a more painful manner. When wrestling or testing, the body is fixed and the foot and tibia are free. Such testing then causes anterior subluxation,

then reduction of the lateral tibial plateau off, then back on, the lateral femoral condyle. Ivar Palmer made the first movie about this dysfunction in 1935. Marcel Lemaire first operated on a patient with the pivot shift dysfunction in 1967. Macintosh, Galway, and Beaupré labeled the dysfunction “the pivot shift” in 1971, and Losee radiographed it in 1969 (Figure 2–10) and cineradiographed it in 1975. It is critical to understand the mechanism of and the testing for the pivot shift because testing reproduces the very dysfunction that the patient wants fixed! A recent study by Kocher et al. emphasized the functional significance of the pivot shift phenomenon. In a cohort of patients who were at least 2 years post ACL reconstruction, associations of subjective functions and satisfactions were

Figure 2–10 Radiograph demonstrating anterior luxation of the tibia in the pivot/shift test. (Copyright 2003 Ronald E. Losee.)

Continued

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TECHNICAL NOTE 2–1

Pivot Shift Examination (Continued) found only with the pivot shift examination. No associations were found with the Lachman’s examination or instrumented knee laxity. This technical note seeks to emphasize the superior importance of pivot shift testing over the presently popularized Lachman’s test (Noulis) for this reason. Although this test, which is a simple variation of the anterior drawer test, does not do this, let us not abandon it; it does indicate ACL deficiency and joint laxity. Pivot shift tests will be described in such a way that the mechanics of the pivot shift should enhance understanding. MacIntosh Test The MacIntosh test is primarily a test for reduction (the knee is quietly subluxated, then reduced). While the patient lies supine on table, flex his or her left hip and knee 30 degrees by supporting

the foot in the left hand and the lateral side of the knee in the right. This relaxes the posterior capsule and allows space for the lateral femoral condyle to quietly sublux posteriorly by gravity off the lateral tibial plateau. Assist this by twisting the foot internally. A new fulcrum for further flexion forms where the posterolateral articular corner of the knee jams into the lateral femoral condyle (Figure 2–11, A). The examiner can carefully accentuate this by pulling the foot toward him or her and pushing the foot away, causing a valgus strain (Figure 2–11, B). This squeezing of the lateral compartment makes the test more recognizable to the patient and the uninitiated examiner. Vigorous squeezing causes pain. Further flexion makes the front of the joint open like a book instead of gliding. This opening advances Gerdy’s tubercle and stretches the iliotibial tract (ITT) (Figure 2–11, C).

108 flexion

458 flexion Figure 2–11 Sequential steps in MacIntosh test (see text). (Copyright 2003 Ronald E. Losee.)

Continued

History and Physical Examination of the Child’s Knee

TECHNICAL NOTE 2–1

Pivot Shift Examination (Continued)

Perform pivot shift tests while keeping the tibia strongly externally rotated.

If knee subluxates test is positive.

Figure 2–12 Twist-out test (Losee II). (Copyright 2003 Ronald E. Losee.)

At 40 degrees of flexion the intact and stretched ITT posteriorly passes the fulcrum and becomes a powerful vector of flexion that pulls the subluxated knee back into reduction. Thus we have a positive MacIntosh test! I classify the test as negative if there is no subluxation or reduction; grade I if the reduction glides; and grade II if there is jamming on reduction. A deficient ITT will result in a subluxation that will remain on flexion greater than 40–50 degrees and will be labeled as a false-negative test to the uninitiated.

40 degrees (the intact ITT no longer acts as a checking vector of flexion). The patient and the examiner will recognize this dysfunction in the ACL and secondary restraining structured-deficient knee. With full extension the tightening posterior capsule will subtly reduce the knee (Figure 2–13, C). If surgery is contemplated, it is smart to test for the “reversed pivot shift” and the adverse effect of a possible large “Q” angle.

Twist-Out Test (Liorzou’s “Losee II Test”)

Perform the MacIntosh test (as described previously) while trying to keep the knee from subluxating. This is done on the left knee by placing the thumb of the right hand (supporting the side of the knee) over Gerdy’s tubercle while grasping the back of the lateral femoral condylar area with the curved fingers (Figure 2–14, A and B). While testing, use the hand to retain the joint from subluxating, very much in the same manner as an extraarticular tenodesis would do. It should be easy to keep the knee from subluxating. If unable to do so, suspect the existence of a reversed pivot shift or a defect of the lateral femoral condyle.

As previously discussed for the left knee, let the knee subluxate as in the MacIntosh test. To emphasize the test, make a valgus strain by pushing the knee and pulling the foot (Figure 2–12). With the left hand, externally twist the foot and tibia. This will reduce the subluxed knee in a manner recognizable to both patient and examiner. It is a useful, sensitive test. Losee’s Test for Subluxation Again, the left knee: ensure reduction at the start by flexing the knee more than 50 degrees and twisting the foot and tibia outward. As in Figure 2–13, A, this will happen with an intact ITT. Again, to emphasize subluxation make a valgus strain by pushing the knee with the right hand and pulling the foot with the left. With authority, do this and let the knee extend (Figure 2–13, B). It will sublux under

‘Passive Retaining Test’ for Reversed Pivot Shift

Active Retaining Test for the Presence of the Adverse Effect of a Large ”Q” Angle Here, the examiner observes the “slingshot effect” (Figure 2–15) of the quadriceps apparatus on the ACL and secondarily restraining posterolateral Continued

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TECHNICAL NOTE 2–1

Pivot Shift Examination (Continued)

458 flexion

A

108 flexion

B

C Figure 2–13 In the Losee test for ACL insufficiency, the knee is initially fiexed to 45 degrees, reducing the tibia on the femur (A). Valgus with external rotation reproduces the subluxation as the knee extends (B) with relocation in full extension (C). (Copyright 2003 Ronald E. Losee.)

108 flexion

Twist foot and tibia externally. 108 flexion

Figure 2–14 Reversed pivot shift test (passive resistance test). (Copyright 2003 Ronald E. Losee)

Continued

History and Physical Examination of the Child’s Knee

25

TECHNICAL NOTE 2–1

Pivot Shift Examination (Continued)

Figure 2–15 Slingshot effect of the patella. (Copyright 2003 Ronald E. Losee.)

structurally deficient knee. In the range of sufficient flexion to relax the posterior capsule and within 40 degrees of flexion, contraction of the quadriceps can subluxate such a knee. This is a common mechanism of troublesome clinical subluxations. The quadriceps is a strong antagonist to the ACL, and increased lateral implantation of the patellar tendon magnifies the effect to the extent that surgical ACL reconstruction may be compromised. To test for this, instruct the patient to sit on a table with the knees flexed and legs dangling. Place your hand on the side of the knee, as described in the former passive retaining testing and attempt to prevent subluxation as the patient sharply kicks the knee into extension. It should be easy to prevent this. If you are unable to do so, the test is positive; consider what would happen to an ACL reconstruction! A possible solution that would make an ACL reconstruction feasible would be that of Ian Smiley, who transferred the insertion of the patellar ligament medially years ago.

adults, and thus it is the difference in excursion right versus left rather than the magnitude of excursion with these tests that is important.30 Many patients will demonstrate a greater than expected anterior translation on Lachman’s test and/or a positive pivot shift test without any history of trauma or damage to the cruciate ligaments. References 1. Kocher M, DiCanzio J, Zurakowski D, Micheli LJ: Diagnostic performance of clinical examination and selective magnetic resonance imaging in the evaluation of intraarticular knee disorders in children and adolescents. Am J Sports Med 29(3):292–296, 2001.

Suggested Readings 1. Anderson AF, Rennirt GW, Standeffer WC Jr: Clinical analysis of the pivot shift tests: description of the pivot drawer test. Am J Knee Surg 13(1):19–23, discussion 23–24, 2000. 2. Anderson AF, Snyder RB, Lipscomb AB Sr: Anterior cruciate ligament reconstruction using the semitendinosus and gracilis tendons augmented by the Losee iliotibial band tenodesis. A long-term study. Am J Sports Med 22(5):620–626, 1994. 3. Kocher MS, Steadman JR, Briggs KK, Sterett WI, Hawkins RJ: Relationships between objective assessment of ligament stability and subjective assessment of symptoms and function after anterior cruciate ligament reconstruction. Am J Sports Med 32(3):629–634, 2004. 4. Larson RL: Physical examination in the diagnosis of rotatory instability. Clin Orthop (172):38–44, 1983. 5. Losee RE: Concepts of the pivot shift. Clin Orthop (172):45–51, 1983. 6. Losee RE: Diagnosis of chronic injury to the anterior cruciate ligament. Orthop Clin North Am 16(1):83–97, review, 1985.

2. McDermott M, Bathgate B, Gillingham B, Hennrikus W: Correlation of MRI and arthroscopic diagnosis of knee pathology in children and adolescents. J Pediatr Orthop 18(5):675–678, 1998. 3. Stanitski C: Correlation of arthroscopic and clinical examinations with magnetic resonance imaging findings of injured knees in children and adolescents. Am J Sports Med 26(1):2–6, 1998. 4. Wessel L, Scholz S, Rusch M: Characteristic pattern and management of intra-articular knee lesions in different pediatric age groups. J Pediatr Orthop 21:14–19, 2001. 5. Dimon JH III: Apprehension test for subluxation of the patella. Clin Orthop Relat Res 103:39, 1974. 6. Carter C, Wilkinson J: Persistent joint laxity and congenital dislocation of the hip. J Bone Joint Surg Br 46:40–45, 1964. 7. Decoster L, Vailas J, Lindsay R, Williams G: Prevalence and features of joint hypermobility among adolescent athletes. Arch Pediatr Adolesc Med 151(10):989–992, 1997.

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8. Davids J: Pediatric knee clinical assessment and common disorders. Pediatr Clin North Am 43(5):1067–1090, 1996. 9. Saperstein A, Nicholas S: Pediatric and adolescent sports medicine. Pediatr Clin North Am 43(5):1013–1033, 1996. 10. Stanitski C: Anterior knee pain syndromes in the adolescent. J Bone Joint Surg Am 75(9):1407–1416, 1993. 11. Smith A, Stroud L, McQueen C: Flexibility and anterior knee pain in adolescent elite figure skaters. J Pediatr Orthop 11:77–82, 1991. 12. Dupont J: Synovial plicae of the knee. Clin Sports Med 16(1):87–122, 1997. 13. Stanitski C: Articular hypermobility and chondral injury in patients with acute patellar dislocation. Am J Sports Med 23(2):146–150, 1995. 14. Angletti P, Buzzi R, Insall J: Disorders of the patellofemoral joint. In Insall JA, Windsor, RE, Scott WN (eds): Surgery of the Knee, 2nd ed. New York: Churchill Livingston, 1993, pp 241–385. 15. Kolowich PA, Paulos LE, Rosenberg TD, Farnsworth S: Lateral release of the patella: indications and contraindications. Am J Sports Med 18:359–365, 1990. 16. Hughston J, Walsh W, Puddu G: Patella Subluxation and Dislocation. Philadelphia: WB Saunders Company, 1984. 17. Insall JA: Examination of the knee. In Insall JA (ed): Surgery of the Knee. New York: Churchill Livingston, 1984, p 191. 18. Walsh M, Bennet G: McMurray test in children. J Pediatr Orthop Part B 1:79–80, 1992. 19. Kaplan E: Discoid lateral meniscus of the knee joint; nature, mechanism and operative treatment. J Bone Joint Surg Am 39:77, 1957. 20. Bellner G, Dupont J, Larrain M: Lateral discoid meniscus in children. Arthroscopy: J Arthroscop Relat Surg 5:57, 1989.

21. Yoshitsugu T, Takaaki I, Shigehito Y, Hiroaki T, Shinji K: MRI highsignal intensity in the menisci of asymptomatic children. J Bone Joint Surg Br 80(3):463–467, 1998. 22. Stanitski C: Anterior cruciate ligament injury in the skeletally immature patient: diagnosis and treatment. J Am Acad Orthop Surgeons 3(3):146–158, 1995. 23. Shea K, Apel P, Pfeifer R: Anterior cruciate ligament injury in paediatric and adolescent patients: a review of basic science and clinical research. Sports Med 33(6):455–471, 2003. 24. Paletta G: Special considerations. Anterior cruciate ligament reconstruction in the skeletally immature. Orthop Clin North Am 34(1):65–77, 2003. 25. Ritchie JR, Miller MD, Harner CD: History and physical evaluation. In Fu FH, Harner Christopher D, Vince Kelly G (eds): Knee Surgery, vol 1. Baltimore, Philadelphia, Hong Kong, London, Munich, Sydney, Tokyo: Williams and Wilkins, 1994, p 254. 26. Torg J, Conrad W, Kalen V: Clinical diagnosis of the anterior cruciate ligament instability in the athlete. Am J Sports Med 4:84, 1976. 27. Galway R, Beaupre A, MacIntosh D: Pivot shift. J Bone Joint Surg Br 54:763, 1972. 28. Rubinstein R, Shelbourne K, McCarroll J, et al: The accuracy of the clinical examination in the setting of posterior cruciate ligament injuries. Am J Sports Med 22(4):550–557, 1994. 29. Daniel D, Stone M, Barnett P, Sachs R: The use of quadriceps active test to diagnose and measure posterior laxity of the knee. J Bone Joint Surg Am 70:386, 1988. 30. Flynn J, Mackenzie W, Kolstad K, et al: Objective evaluation of knee laxity in children. J Pediatr Orthop 20(2):259–263, 2000.

Chapter 3

Developmental Anatomy of the Pediatric and Adolescent Knee Brett L. Wasserlauf

An understanding of the developmental anatomy of the knee is critical for the practitioner caring for pediatric and adolescent knee injuries. A thorough knowledge of the normal stages of development will help the physician to understand pathological processes in the growing child. As in all orthopedics, a firm grasp of the anatomical details will aid the clinician in assessing the knee in this unique group of patients. Embryology The complex interactions that contribute to early development of the appendicular skeleton have become better understood through the contributions of many authors.1–3 The human embryo begins morphological differentiation during the second gestational week, progressing to the formation of somites within the mesoderm by the end of the third gestational week. Localized differentiations of the lateral plate mesoderm thicken by cellular proliferation, lose their epithelial connections, and reaggregate as a mesenchymal cell mass comprising each presumptive limb bud. The definitive limb bud is established for the lower limb later than that of the upper limb. The close association of this mesenchyme with the inner surface of the ectoderm controls subsequent differentiation. The limb ectoderm establishes the apical ectodermal ridge, a structure responsible for the continual outgrowth and proximal-to-distal differentiation within the limb bud. Many transverse deficiencies arise from damage to a segment of the interaction of this ridge with the underlying mesoderm at the appropriate time. Intercalary deficiencies, in contrast, are probably caused by more localized damage to the inductive capacity of the apical ectodermal ridge for a certain skeletal component. These conditions may also a be result of defective differentiation in later stages.

●

George A. Paletta, Jr.

Within the early limb anlage, the mesenchymal cells elaborate extracellular matrix, enter the precartilage stage, and rapidly continue transformation into the cartilaginous anlage. Chondrification starts centrally and progresses toward the periphery of the mesenchymal anlage. The perichondrium differentiates at the periphery, surrounding the anlage. Interzones form at the sites of the presumptive joints. The perichondrium establishes continuity with the cartilaginous layers of the interzones. Subsequently, this continuity is lost across the joint as this tissue becomes fibroblastic and evolves into the joint capsule and ligaments. The primitive joint capsule differentiates from that interface of intermediate and deep mesoderm that gave rise to perichondrium and periosteum. The interzone has three layers: two parallel chondrogenic layers and an intermediate, less dense layer. The more peripheral regions of the interzone intermediate layer form synovial tissue. Blood vessels penetrate the evolving joint capsule to reach the blastemal synovium, but they do not usually penetrate the central joint regions. The intraarticular structures, such as the menisci and cruciate ligaments, appear as further cellular condensations in the intermediate mesenchyme. Once the basic contours and intraarticular structures are established, minute spaces appear KEY POINT in the intermediate zone and coalesce to form the joint cavity. Early in utero, joint Concomitant development motion enhances joint of innervated muscle creates modeling; however, final some early motion, enhancing joint contours are dicthe joint modeling process in tated by postnatal joint utero. Postnatally, joint motion motion and joint reactive and joint reaction forces dictate forces. the final joint contours. The 27

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blastemal cells destined to become articular surface become committed in early development and no longer function as basic epiphyseal cartilage. Growth Plates The physis, or growth plate, is a nearly uniform structure throughout the skeleton.4–7 HisKEY POINT tologically, the physis is composed of definitive zones, including The physis is composed the reserve zone, the proliferaof definitive zones that tive zone, and the hypertrophic remain essentially zone. This cytoarchitectural strucunchanged from early ture is essentially unchanged fetal life to skeletal from early fetal life to skeletal maturity. maturation. Macroscopically, the growth plates around the knee have some unique qualities.7 The physes of the distal femur and proximal tibia are horizontal or discoid. Each physis undergoes some contouring throughout development, but it generally retains its basic planar nature. A separate growth plate at the tibial tuberosity forms postnatally. This will ultimately coalesce with the proximal tibial physis. The magnetic resonance imaging (MRI) appearance of the growth plate of the normal knee in subjects of different ages has been evaluated and described in some detail.8 MRI is an important tool for accurately mapping premature physeal arrest in pathological conditions. Therefore an understanding of the appearance in normal subjects is essential. Four stages of physeal development were identified. Stage I is seen in children younger than 2 years of age. The appearance is characterized by a spherical or elliptical ossification center, with the bulk of the distal femoral epiphysis and the proximal tibial epiphysis being composed of cartilage. Between the ages of 2 and 12 (stage II), the ossification center has spread peripherally, replacing cartilage in all but two regions. These regions, a well-defined plate between the epiphysis and the metaphysis, and an area over the free edge of the bone as articular cartilage, become well defined. Stage III occurs generally after age 12, depending on the sex of the child, and corresponds to the process of growth plate closure. There is no further proliferation of cartilage, and the epiphyseal plate is gradually replaced with bone. Magnetic resonance signal characteristics of the growth plate can vary during this stage, with the cartilage band beginning to narrow in some regions. Stage IV represents complete closure and is seen in adolescents and young adults. This last stage occurs earlier in female than in male subjects. Patellofemoral Mechanism The embryology of the patellofemoral joint has been well described.9,10 At 4 weeks of gestation, the patellofemoral joint is an ectodermal sac stuffed with mesenchyme of somatic mesoderm. Mesenchymal condensations appear at 4–5 weeks in precartilage, and chondrification of the patella and femur begins at approximately 5 weeks of gestation. The joint space and ligamentum patella become evident by 6 weeks, and at 7 weeks, well-established patellar and distal femoral chondral models are present. By then, the patellar retinaculum is well formed. The original cartilage rudiments

of the joint proceed to form the articular surfaces of the femur, tibia, and patella. By 8 weeks in utero (the end of the embryonic period), the knee is present in its basic adult form. A well-developed patellar and quadriceps mechanism is present, and active joint motion has begun. The femoral sulcus is shaped embryologically in concert with this joint motion. Patellar ossification is equivalent to that of an epiphysis. The patella anlage is distinguishable within the quadriceps condensation by close aggregation of rounded cells at 7.5 weeks of gestation.11,12 It subsequently becomes a clearly definable cartilaginous anlage. In the embryo, before motor function, the knee develops in a position of 90 degrees of knee flexion. Thus the patella initially conforms to the distal aspect of the femoral condyles. A primitive joint plate forms in common with the distal femur. The subsequent mechanical behavior of the patella molds it and determines its ultimate shape. The patella increases in relative size up to the sixth fetal month, after which it increases at the same rate as the other bones.11 Initially the medial and lateral patellar facets are equal in size. However, by approximately 23 weeks of gestation, the patella has acquired lateral facet predominance, a characteristic of the adult patella.9,11 This characteristic is somewhat variable, however, and different facet configurations of the patella, ranging from medial/lateral facet equality to extreme lateral facet prominence, have been described. The medial facet itself shows the greatest anatomical variation. The odd facet, separated from the remainder of the medial facet by a small vertical ridge, develops after birth in response to functional loads applied to the knee. From a cartilaginous disc at birth, the patella consolidates from a variable number of ossification centers. The patella usually appears roentgenographically in children between ages 5 and 6, but it may be seen as early as age 2. The patella appears to be complete at approximately 2 years of age in children. Ossification proceeds in a centrifugal manner until full patellar maturity is reached at approximately 16–18 years of age. Early development of the trochlear surface of the femur appears to be primary and genetically determined.9 The basic morphology develops before fetal movement. The general adult form is achieved relatively early in fetal life, as early as 8 weeks of gestation. This development does not occur while in contact with the patella but appears to be in response to the quadriceps mechanism. However, further development of the trochlear surface, it is generally believed, is dependent on a complex series of interactions predicated on an intimate relationship to the patella.9,10 This reciprocal relationship between the patella and the trochlear groove is somewhat analogous to that seen between the femoral head and the acetabulum in the hip joint. Dysplasia of the patellofemoral joint occurs as a spectrum of disorders.13 At one end of this spectrum is congenital dislocation of the patella. The dislocation may be a result of abnormal muscle forces or early developmental anomalies. The dislocation itself, however, further contributes to continued abnormal development of the patellofemoral joint. Hypoplasia or marked dysplasia often occurs in this setting. The distal end of the femur may have a complete absence of a trochlear groove (Figure 3–1). This degree of abnormality is often associated with a syndrome, such as Down syndrome, Larsen’s syndrome, nail-patella syndrome, among others.10,13

Developmental Anatomy of the Pediatric and Adolescent Knee

Figure 3–1 Axial magnetic resonance image of congenital trochlear dysplasia. Note that the trochlea is convex.

Mild dysplasia is more common and is frequently seen in the general population. It is characterized by abnormal lateral deviation of the patella and quadriceps mechanism. Lateral contracture is present. Again, this occurs on a spectrum. In more extreme cases, such as those associated with congenital dislocation, a thick fibrous band tethers the patella to the lateral intermuscular septum. In mild dysplasia the fibrous tethering occurs to a lesser degree. The medial structures are abnormal as well. In general the degree of abnormality of the medial capsule and retinaculum is correlated directly with that of the lateral. Patella alta or patella infra may rarely occur as a developmental anomaly. More commonly these conditions are the result of acute trauma, surgery, or an imbalance of muscle forces at the knee joint. Menisci By the end of the embryonic period, at approximately 8 weeks of gestation, the menisci have formed from the interzone of the knee blastema.3,14,15 The menisci form in concert with the anterior cruciate ligament (ACL), capsule, and patella. They appear in almost their adult form, and intrauterine forces and active fetal motion contribute to the development of these structures. As intrauterine life progresses, the meniscal vascularity gradually diminishes, and there is continued progressive loss of vascularity from the postnatal period to preadolescence.14,15 This diminution in vascularity proceeds from the central area toward the periphery, with retention of vascular segments at the periphery. Clark and Ogden studied prenatal and postnatal cadaver knees to elucidate the developmental changes that occur in the menisci before skeletal maturity.15 Their protocol included observation of gross morphology, histological examination of the menisci and their ligaments, and comparison of surface areas of the menisci, both to their respective tibial plateaus and to each other. They found that the menisci

29

assumed their characteristic shapes early in prenatal development. The prenatal menisci were very cellular, and intrameniscal blood vessels were numerous. During the prenatal period, photomicrographs demonstrated a progressive decrease in cellularity, with a concomitant increase in intercellular matrix. After birth, gradual changes occurred, which included decreasing vascularity that progressed from the central to the peripheral margin, growth commensurate with the enlargement of the developing femur and tibia, and changes in the configuration of the menisci to accommodate changes in the femorotibial contact areas. The lateral meniscus tended to have more KEY POINTS developmental variation, but at no stage during development The menisci demondid it have a discoid shape. strate characteristic Throughout growth the ratios of adult shape early in the areas of each meniscus, both intrauterine life, with to their respective tibial plateau gradually decreasing and to each other, were fairly convascularity and cellu stant. Finally, the collagen fiber larity and alterations in arrangement within the meniscus collagen fiber arrangeappeared to change progressively ment occurring through in response to biomechanical early adolescence. function. The vascularity of the adult meniscus has been described by Arnoczky and Warren, who demonstrated a rich parameniscal capsular plexus in a study of older adult cadavers.16 The blood supply originated from the lateral, medial, and middle geniculate arteries, with the middle geniculate providing the main blood supply to the horn attachments. This work helped define the zones of meniscushealing potential based on the vascular supply to peripheral versus central segments. The menisci of the developing child have a greater vascular supply. The adult pattern described by Arnoczky and Warren is not achieved until early adulthood. The histological development of the meniscus has also been described.15 The characteristic cell contained within meniscal tissue has been termed the fibrochondrocyte. Its structure contains elements of both fibroblasts and chondrocytes. Along with the progressive decrease in cellularity in the developing meniscus, the cells undergo changes in both their structure and arrangement within the matrix. The cells undergo maturation, such that they become arranged in a more orderly fashion and their nuclei become smaller. A synovial membrane, which is five to six celllayers thick and contains cells with larger nuclei than those in the meniscal body, is characteristic of the embryonic meniscus. However, this layer progressively diminishes postnatally, becoming one to two cell-layers thick in children, and becoming virtually nonexistent in the adult meniscus. The changes in cellularity of the developing meniscus are accompanied by concomitant alterations in its matrix.15 Decreasing vascularity and cellularity are balanced by increasing collagen density, with the adult collagen concentration reached at age 10. The ratio of collagen to noncollagen protein increases with age, with this effect most marked in the neonatal and early childhood period. Approximately 75% of the organic matrix of the meniscus is composed of type I collagen. The arrangement of collagenous bundles develops in response to the mechanical environment. Collagen bundles in the more central

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portions are arranged radially, while the peripheral bundles are arranged longitudinally. This understanding of the developmental characteristics of the meniscus is clinically significant on several fronts. First, the vascularity, histological characteristics, and biomechanical composition of the developing meniscus may be responsible for its relative immunity from injury. Meniscus tears are uncommon in children. Furthermore, the developing meniscus may have greater reparative abilities than the menisci of adults. Therefore every effort should be made to preserve some or all of a traumatized meniscus in children and adolescents. Finally, confirmation that the lateral meniscus does not normally assume a discoid configuration during its development has altered our approach to this condition. Authors have speculated that partial excision of a KEY POINT discoid meniscus, a pathological entity, might improve its bioAt no stage in developmechanics, and, especially if done ment is the meniscus at an early age, might allow more discoid in shape. normal growth and develop15,17 ment. More recent work described the development of the transverse ligament of the knee. Investigations of embryos at 6–8 weeks of fetal development demonstrated a peripheral condensation of mesenchyme, located anteriorly to the primordia of the cruciate ligaments. This condensation was visualized as densely packed parallel strands of oval cells, which connected the medial and lateral menisci, by 8 weeks.18

Figure 3–2 Sagittal MRI of fetal knee demonstrating relationship of the femoral origin of the ACL to the distal femoral physis.

Ligaments Vascular mesenchyme isolated within the embryological knee joint is the precursor tissue of the cruciate ligaments and the menisci.3,19 Condensations of this tissue first appear at 7–8 weeks of development. Further differentiation into immature fibroblasts with fusiform nuclei and scanty cytoplasm occurs over the following weeks. The long axes of these fibroblasts parallel the course of the ligaments. The anterior and posterior cruciate ligaments are separate structures by 10 weeks of development. Over the next few weeks the ligaments become better differentiated from the adjacent tissues. Blood vessels are seen in the tissue surrounding the cruciate ligaments, and the attachment sites become more specialized. At 18 weeks the ACL and posterior cruciate ligament (PCL) stand almost alone, and a few vascular elements are noted within their substance. The following weeks are characterized by an increase in vascularity and the appearance of fat cells in the connective tissue anterior to the cruciate KEY POINT ligaments and inferior to the patella. This will become the The ACL and PCL infrapatellar fat pad. By 20 weeks achieve essentially adult of development the ACL and form by 20 weeks’ gesPCL resemble those of the adult. tation with little subseSubsequent development consists quent change in form of marked growth with little despite continued change in form. growth. The anatomical relationship of the anterior cruciate ligament femoral origin to the distal femoral physis in the skeletally immature knee has been defined (Figures 3–2 and 3–3).20 This relationship is particularly important because

Figure 3–3 Hematoxylin and eosin (H&E)-stained anatomical cross-section of 26 weeks’ gestational age fetal specimen demonstrating relationship of the femoral origin of the ACL to the distal femoral physis.

of the concern for iatrogenic injury to the distal femoral physeal plate during intraarticular ACL reconstruction in the skeletally immature knee. The authors studied human fetal specimens ages 20–36 weeks and skeletally immature knee specimens ages 5–15 years grossly, histologically, and

Developmental Anatomy of the Pediatric and Adolescent Knee

radiographically. The fetal ACL was found to develop as a confluence of ligament fibers with periosteum at 20 weeks, with vascular invasion into the epiphysis occurring at 24 weeks, and establishment of a secure epiphyseal attachment for the ACL being noted by 36 weeks. In all specimens the ACL origin was distal to the physis. In the fetus the distance from the most superior aspect of the ACL femoral origin to the distal femoral physis was 2.66 mm. There was not a significant change in KEY POINT this distance in adolescent specimens, which averaged 2.92 mm. The femoral origin of Furthermore, the over-the-top the ACL remains only position on the lateral femoral 2.6–2.9 mm distal to the condyle was noted to lie immedidistal femoral physis ately adjacent and posterior to throughout skeletal the physis, with only a layer of development. periosteum separating the two. These findings call into question the feasibility of some proposed techniques for ACL reconstruction in the skeletally immature knee. Some described techniques suggest creation of a femoral tunnel that remains entirely distal to the physis. A small margin for error exists between the physis and the attachment site. Drilling an all-epiphyseal horizontal tunnel of adequate size to accommodate a graft while remaining below the physis would appear to be technically challenging. Some surgeons have preferred the over-the-top position for graft placement. Descriptions of this technique include roughening the periosteum and creating a trough at the over-the-top position, to facilitate healing of the graft to bone and to improve the anatomical positioning of the graft. With only a layer of periosteum separating the femoral origin from the physis, these techniques would appear to put the femoral physis and the perichondral ring at risk for injury. Developmental abnormalities of the cruciate ligaments are often associated with other ipsilateral limb abnormalities, such as tibial or fibular hemimelia and congenital short femur. This fact is consistent with the dependence of each structure’s development on its surrounding anatomical and biomechanical environment. In the absence of normal cruciates, the intercondylar eminence of the tibia is aplastic. A developmental anomaly must be considered in the child with clinical instability if there is an associated limb anomaly such as hemimelia, leg-length discrepancy, or a ball-and-socket ankle; aplasia of the intercondylar eminence of the tibia on an anteroposterior radiograph; or no history of significant trauma preceding the instability.19 The developmental morphology of the medial collateral ligament insertion has been studied in a rabbit model.21 The tibial insertion is composed of five tissue layers, comprising a “ligamentous portion” and a “cortical portion.” The proportion of these layers changes dramatically during growth and maturation. In immature animals, MCL fibers enter the periosteum; in older animals, MCL fibers are cemented to the tibia by advancing mineral. The tibial attachment of the MCL is thus transferred from the periosteum to the cortex during growth. The authors suggested that the term periosteal insertion is imprecise in adults. Furthermore, the authors hypothesized that these structural changes account for the reported increase in tensile failure of this insertion near skeletal maturity.

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Tibial Tubercle The tibial tuberosity appears as a discrete structure at 12–15 weeks of fetal development.22 It does not have a recognizable growth plate until several months after birth. The evolution of the tuberosity into a definitive functional unit occurs as a continuum of development but has been divided into several stages by Ogden and Southwick.22 The prenatal phase has been divided into three stages. During stage I, no tibial tuberosity is present. The growth plate of the proximal tibia is transversely oriented. During stage II, concomitant with fibrovascular ingrowth and vascularization of the chondroepiphysis, an anterior outgrowth develops from the tibial chondroepiphysis. Stage III is characterized by distal displacement of the tuberosity by longitudinal growth at the proximal tibial physis, and anatomical separation from the proximal tibial physis by continued fibro-mesenchymal-vascular ingrowth. The postnatal development occurs in four subsequent stages. During stage IV, a separate growth plate associated with the tibial tuberosity develops. This subsequently coalesces with the primary proximal growth plate. Stage V demonstrates the appearance of a secondary ossification center in the distal portion of the tuberosity. During stage VI, the ossification centers of the tuberosity and the proximal tibial epiphysis coalesce. The final stage (stage VII) occurs with the closure of the contiguous growth plates of the proximal tibia and tuberosity. The tibial tuberosity represents an apophysis and, as such, has characteristic differences that distinguish its architecture from that of an epiphysis. Histologically the tuberosity growth plate develops three regions. Proximally the cytoarchitecture is analogous to the remainder of the proximal tibial growth plate, except that the cell columns are short, there is a greater degree of intercellular matrix, KEY POINTS and the lacunae are distorted by elongation. This region grades The tibial tubercle develimperceptibly into a fibrocartiops its own separate laginous zone with layers of hyaphysis that does not coaline cartilage, fibrocartilage, and lesce with the proximal bone being formed by membratibial physis until after nous ossification. The third (disthe appearance of the tal) region shows a transformation tubercle’s secondary from hyaline cartilage to fibrous center of ossification. tissue and, subsequently, to bone. The patellar tendon has its primary attachments toward the distal end of the tuberosity during early development. The outgrowth and relative distal displacement of the tuberosity during the later stages of development, however, results in a more proximal extent of insertion. This insertion becomes predominant during adolescence. The developmental anatomy of the tibial tuberosity has clinical implications for the skeletally immature patient. The fibrocartilaginous growth plate appears to be a structural adaptation to prevent avulsion of the tibial tuberosity away from the anterior tibial metaphysis. Despite this adaptation, Osgood-Schlatter disease occurs quite commonly in children before closure of the tibial tubercle apophysis. This disorder represents an avulsion of a portion of the developing ossification center and overlying hyaline cartilage. The resultant formation of callus causes the characteristic enlargement of the anterior portion of the tuberosity. Acute tibial tubercle

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avulsion fractures may occur as well, and they are most commonly seen in adolescents who are near skeletal maturity. Finally, because of the potential risk of recurvatum with violation of the tibial tuberosity growth plate, “bony” patellar tendon transfers in children before the closure of the physis are not recommended. Summary The anatomy of the pediatric and adolescent knee has unique characteristics compared to that of the adult knee. These differences carry relevant clinical implications in the treatment of injury to and conditions of the skeletally immature knee. Injury to the patellofemoral joint, menisci, ligaments, and tibial tuberosity occur in described patterns, and treatment options are adapted to the distinctive anatomy. Knowledge of the developmental anatomy of the knee will aid the clinician in diagnosis and treatment of this patient population. References 1. Gardner E, O’Rahilly R: The early development of the knee joint in staged human embryos. J Anat 102:289–299, 1968. 2. McDermott LJ: Development of the human knee joint. Arch Surg 705–719, 1938. 3. Ogden JA: Developmental and maturation of the neuromusculoskeletal system. In: Morrissy RT (ed): Lovell and Winter’s Pediatric Orthopaedics. Philadelphia: Lippincott, 1990, pp 1–33. 4. Brighton CT: Structure and function of the growth plate. Clin Orthop 22–32, 1978. 5. Brighton CT: The growth plate. Orthop Clin North Am 15:571–595, 1984. 6. Ogden JA: The uniqueness of growing bones. In: King RE (ed): Fractures in Children. Hagerstown, Md.: Lippincott, 1984, pp 30–52.

7. Ogden JA, Rosenberg LC: Defining the growth plate. In: Wiley JJ (ed): Behavior of the Growth Plate. New York: Raven, 1–15, 1988. 8. Harcke HT, Synder M, Caro PA, Bowen JR: Growth plate of the normal knee: evaluation with MR imaging. Radiology 183:119–123, 1992. 9. Fulkerson JP, Hungerford DS: Normal anatomy. In Fulkerson JP, Hungerford DS (ed): Disorders of the Patellofemoral Joint, 2nd ed. Baltimore: Williams & Wilkins, 1990, pp 1–24. 10. Stanitski CL: Patellofemoral mechanism. In: Drez D (ed): Pediatric and Adolescent Sports Medicine. Philadelphia: WB Saunders Company, 1994, pp 294–334. 11. Walmsley R: The development of the patella. J Anat 74:360–370, 1939–1940. 12. Gray DJ, Gardner E: Prenatal development of the human knee and superior tibiofibular joints. Am J Anat 86:235–287, 1950. 13. Eilert RE: Dysplasia of the patellofemoral joint in children. Am J Knee Surg 12:114–119, 1999. 14. Stanitski CL: Meniscal lesions. In: Drez D (ed): Pediatric and Adolescent Sports Medicine. Philadelphia: WB Saunders Company, 1994, 371–372. 15. Clark CR, Ogden JA: Development of the menisci of the human knee joint. Morphological changes and their potential role in childhood meniscal injury. J Bone Joint Surg Am 65:538–547, 1983. 16. Arnoczky SP, Warren RF: Microvasculature of the human meniscus. Am J Sports Med 10:90–95, 1982. 17. Andrish JT: Meniscal injuries in children and adolescents: diagnosis and management. J Am Acad Orthop Surg 4:231–237, 1996. 18. Ratajczak W: Transverse ligament of the knee in human embryos aged 7 and 8 weeks. Folia Morphol (Warsz) 60:323–331, 2001. 19. DeLee JC: Ligamentous injury of the knee. In: Drez D (ed): Pediatric and Adolescent Sports Medicine. Philadelphia: WB Saunders Company, 1994, pp 406–407. 20. Behr CT, Potter HG, Paletta GA, Jr: The relationship of the femoral origin of the anterior cruciate ligament and the distal femoral physeal plate in the skeletally immature knee. An anatomic study. Am J Sports Med 29:781–787, 2001. 21. Matyas JR, Bodie D, Andersen M, Frank CB: The developmental morphology of a “periosteal” ligament insertion: growth and maturation of the tibial insertion of the rabbit medial collateral ligament. J Orthop Res 8:412–424, 1990. 22. Ogden JA, Southwick WO: Osgood-Schlatter’s disease and tibial tuberosity development. Clin Orthop 180–189, 1976.

Chapter 4

Biology and Gene-Based Therapy Martha Meaney Murray

Optimal treatment of pediatric and adolescent knee disease and injury is founded on the understanding of the basic physiology and pathophysiology of the tissues. Molecular biology, tissue engineering, and genetics are now contributing to a long-established knowledge base composed of clinical observation, radiology, and cell biology. This chapter will address the major biological features of each of these tissues, and in the final section, will provide examples of how advances in tissue engineering and gene therapy will contribute to new treatments of the diseases of the knee. Bone Bone serves both a mechanical and a metabolic function. The mechanical role is to provide support, both of the limb itself, and also of the articular cartilage in the joint. The mineral structure of bone is similar to hydroxyapatite crystal with carbonate, sodium, and magnesium substitutions. It is this mineral phase that provides the compressive strength of the tissue. Disorders of the mineralization of bone lead to weakening of the bone and pathological fractures. Osteomalacia, also known as rickets in children, is caused by a relative decrease in calcium or phosphorus and is the result of defects in mineralization of the skeleton. This leads to thinning of the cortices of bone, decreases in the quantity of medullary bone, and thin and irregular trabeculae (Figure 4–1). Osteoporosis describes the problem of reduced bone mass with normal mineralization and structure (see Figure 4–1). The tensile strength of bone is provided by the type I collagen fibers found within the bone, which function like the reinforcing bars (REBAR) in concrete structures. Disorders in type I collagen synthesis, as found in osteogenesis imperfecta, also lead to problems in the mechanical strength of the bone and pathological fractures. The metabolic function of bone is to stabilize calcium homeostasis.1 Maintaining a stable level of calcium in the bloodstream is necessary for normal blood clotting,

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Michael F. Murray

neuromuscular responses, and growth and regeneration. Calcium and other ions are stored in the mineral component of bone, and their release is controlled by parathyroid hormone (PTH), 1,25 vitamin D, and calcitonin.2 Disturbances in vitamin D intake or synthesis can lead to impaired deposition of calcium in the bones, decreased bone mineralization, and osteomalacia in the pediatric knee. One of the key features of bone physiology is skeletal remodeling or turnover, in which bone is continually being resorbed and replaced with new tissue. Two principal cell types govern remodeling: osteoblasts (which make bone) and osteoclasts (which resorb bone). This process gives bone the ability to heal in response to injury, to incorporate bone graft materials, and to undergo distraction osteogenesis. Disorders in remodeling where more bone is resorbed than replaced lead to osteoporosis, while an impaired resorption response leads to osteopetrosis. Longitudinal bone growth at the knee occurs predominantly at the distal femoral and proximal tibial growth plates, or physes,3,4 while the patella forms with appositional growth on a cartilaginous anlage. The physis is the portion of the cartilage anlage of the bone that remains between the shaft of the bone (diaphysis and metaphysis) and the end of the bone (epiphysis). As growth continues, the physes narrow and then close in adolescence. Disorders of the growth plates, such as slipped capital femoral epiphysis (SCFE) or post-traumatic growth arrest, can thus cause growth abnormalities in the bone. Fractures occur in bone when the load placed on the bone is higher than the strength of the bone itself. The response to fracture is healing and regeneration, if conditions are favorable. Most fractures heal by secondary repair, which has four phases: hematoma formation, soft callus formation, hard callus formation, and endochondral ossification. 33

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Fractures can also heal by primary repair, where complete immobilization and exact reduction and compression at the fracture site (as in a greenstick fracture or using reduction and internal fixation) lead to direct bridging of new osteons across the fracture site. Articular Cartilage The principal function of articular cartilage is to provide almost frictionless movement for the joint surfaces.5,6 Lubrication of the joint is achieved as the water within the articular cartilage is squeezed onto the surface of the

KEY POINTS Bone 1. Bone serves both a mechanical and a metabolic function. 2. The metabolic function of bone is to stabilize calcium homeostasis. 3. Bone is continually being resorbed and replaced with new tissue. 4. Longitudinal bone growth at the knee occurs predominantly at the physes.

Schematic of osteomalacic or ricketic trabeculae (black ⫽ mineralized osteoid, grey ⫽ unmineralized bone)

Schematic of normal trabeculae (black ⫽ mineralized osteoid)

Additive Gene Treatment

cartilage when pressure is applied, providing a slippery surface with a coefficient of friction approximately one fifth that of ice on ice. Articular cartilage does not have nerves, lymphatics, or vascularity within its substance. Approximately 65% of the weight of cartilage is water,7,8 and the remaining components are type II collagen9,10 and proteoglycans, including hyaluronic acid, chondroitin sulfate, and glucosamine. There are five histological zones of articular cartilage: the lamina splendens, the superficial zone, the transitional zone, the radial or deep zone, and the calcified cartilage (Figure 4–2). The lamina splendens is a very thin, filamentous layer that covers the surface of the cartilage. The superficial zone is a densely fibrous layer populated by cells that resemble fibroblasts that maintains the hydration of the cartilage and filters nutrients and oxygen. The transitional zone has a large content of proteoglycan and is populated by rounded chondrocytes in lacunae. The radial zone is deeper, containing collagenous fibers oriented perpendicular to both the articular

DNA transgene

Schematic of osteoporotic bone (note decreased size of mineralized trabeculae)

Transgene messenger RNA

New protein product (novel or additive with endogenous)

Figure 4–1 Schematic of defects in bone mineralization. A, Schematic of normal bone trabeculae and mineralization. B, Schematic of osteomalacia, or rickets. Note the wide seams of uncalcified osteoid at the edges of the trabeculae. C, Schematic of osteoporotic bone. Note the decrease in volume of the trabeculae.

Subtractive Gene Treatment

DNA transgene

Non messenger RNA intermediate

ⴙ

Endogenous mRNA

Decreased protein product Lamina splendens

Superficial zone Transitional zone Radial or deep zone

Tidemark Calcified cartilage Figure 4–2 Schematic of articular cartilage demonstrating the five histological zones: the lamina splendens, the superficial zone, the transitional zone, the radial or deep zone, and the calcified cartilage.

Biology and Gene-Based Therapy

surface and the subchondral bone. This zone is separated from the underlying calcified layer by the tidemark. The calcified cartilage has few cells and is adherent to the underlying subchondral bone.11 In young articular cartilage, chondrocyte replication occurs in all the zones of the cartilage; however, as one approaches skeletal maturity, replication occurs only in the radial or deep zone of the cartilage. This change in proliferative activity may be one of the underlying reasons for differences in the healing capacity of pediatric and adult cartilage lesions, such as osteochondritis dissecans. In addition, water and proteoglycan content is highest in immature cartilage, decreasing during growth, whereas collagen content steadily increases until skeletal maturity.12,13 Unlike other connective tissues, articular cartilage is avascular, and the cells receive their nutrition by diffusion from the synovial fluid and underlying bone. It has long been believed that the failure of cartilage to spontaneously heal after injury is a result of the avascular nature of the tissue. A partial thickness injury of cartilage (as occurs in chondromalacia) results in a short period of cell proliferation and synthetic activity, which lasts only approximately 2 weeks, and the defect remains open.14 However, if the injury extends down to the underlying vascular bone, the response is notably different, with formation of a KEY POINTS fibrin clot in the defect, which is replaced by a fibrous membrane Cartilage and immature cartilage.11 This 1. The principal function finding is the basis for treatment of articular cartilage of chondral injury and osteochonis to provide almost dritis dissecans by drilling through frictionless movethe defect into the subchondral ment for the joint bone—the thought being that surfaces. the penetration of the underlying 2. In young articular vascular tissue will stimulate the cartilage, chondromore abundant repair process. cyte replication However, even with this stimulaoccurs in all the tion the new cartilage that forms zones of the has more type I collagen than cartilage. normal cartilage and is thought to 3. Unlike other connechave mechanical properties that tive tissues, articular are inferior to the native articular cartilage is avascular, cartilage. New therapies are under and the cells receive investigation, including the introtheir nutrition by duction of cultured chondrocytes diffusion from the beneath a periosteal sleeve, or synovial fluid and the placement of cells and growth underlying bone. factors into the defect. Musculotendinous Unit Skeletal muscle and the tendons that connect the muscle to bone are responsible for generation of motion of the knee joint. The major muscle groups that cross the knee joint are the extensor mechanism (quadriceps muscle/patellar tendon) and the flexor group (hamstring muscles and tendons). Additional muscles, including the popliteus and gastrocnemius muscles, also cross the joint and assist with knee motion. Most skeletal muscles contain both type I, slowtwitch, oxidative fibers (which function as endurance elements) and type II, fast-twitch fibers (which provide short

35

bursts of power). “Low-tension, high repetition” training (e.g., distance running) leads to improved function of type I fibers, whereas “high-tension, low repetition” training (e.g., power lifting) leads to improvements in type II fibers.15 The musculotendinous unit causes acceleration of joint and limb motion when the muscle undergoes a concentric contraction, which results in muscle shortening. Eccentric contractions, which generate force while the muscle is lengthening, result in deceleration of the limb. Muscle strains are more likely to occur during eccentric contractions. Imbalances in power generation between muscles can result in uneven loading of joint surfaces, cartilage overload, and pain. One example of this is in patellofemoral syndrome, where the vastus lateralis muscle of the quadriceps is typically stronger than the vastus medialis muscle. This contributes to lateral tilt and shift of the patella as it moves in the trochlear groove, resulting in lateral facet overload and pain. Tendons are composed primarily of type I collagen arranged in parallel bundles. Tendons attach to muscle at a specialized myotendinous junction, which has a highly convoluted surface area optimized for load transfer from muscle to tendon. Tendon inserts onto bone with another specialized junction, where the outer tendon fibers blend into the periosteum of the bone, and the inner fibers insert directly into the bone through four zones: tendon, fibrocartilage, mineralized fibrocartilage, and bone. Sharpey’s fibers are collagen fibers that extend directly from the tendon to the bone. During skeletal growth spurts, the musculotendinous unit is often unable to keep up with the growth of the underlying bone, thus muscle KEY POINTS tightness is exacerbated. This can manifest itself not only with Muscles and tendons muscle strains but also with 1. The musculotendistrain and injury at the insertion nous unit causes site of the tendon where overacceleration of joint load results in microtears and and limb motion when pain. One common example of the muscle underthis is Osgood-Schlatter disease, in goes a concentric which a tight quadriceps muscle contraction, which results in overload and pain at results in muscle the insertion site of the patellar shortening. tendon to the tibia. 2. Eccentric contracOccasionally in this disease, tions, which generate small pieces of bone can be force while the muspulled away from the tibia with cle is lengthening, the insertion of the tendon, result in deceleration resulting in bony prominences of the limb. and ossicle formation. Stretch3. Tendons are coming, which effectively lengthens posed primarily of the musculotendinous unit, can type I collagen often ameliorate or eliminate arranged in parallel the symptoms of these traction bundles. type of injuries. Ligaments Ligaments connect bone to bone and provide additional intrinsic stability to the knee joint, as well as proprioceptive feedback to the muscles surrounding the joint that enhance the dynamic stability of the knee.16 The cruciate and collateral ligaments are the major ligaments in the knee and

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connect the distal femur to the proximal tibia. Ligaments are composed predominantly of wavy bundles of type I collagen, which allow for a range of easy extensibility of the tissue (as the waviness straightens out) during a normal range of motion, and a strong resistance to further extension once the waviness is straight (thus preventing abnormal motion or instability of the joint).17 During growth, ligaments elongate throughout their length,18 unlike bone that grows at a few specific sites. The insertion site has rapid cell proliferation throughout growth, with incorporation of the collagen at the site into the adjacent bone. This allows the insertion site of the medial collateral ligament to remain metaphyseal during growth. Injury sites for ligaments vary KEY POINTS with age. In skeletally mature patients, the insertion site is often Ligaments stronger than the ligament itself, 1. Ligaments provide thus with excessive force the additional intrinsic ligament fails before the bone. stability to the knee However, in skeletally immature joint, as well as patients, the ligament substance is proprioceptive often stronger than the bone, and feedback to the a higher proportion of these muscles surrounding patients will present with a bony the joint. avulsion of the insertion site 2. Injury sites for ligarather than a purely ligamentous ments vary with age. injury.19

Meniscus The menisci serve as shock absorbers in the knee.20 They are C-shaped pieces of fibrocartilage with a triangular crosssection that increases the area of load transfer between the femur and tibia, thus effectively lowering the peak stresses across the articular cartilage and subchondral bone. In discoid lateral menisci, the normal C shape of the meniscus is filled in to some degree, and the central tissue can be more vulnerable to abnormal stress and tear. The meniscus is formed predominantly of type I collagen in a complex three-dimensional arrangement with circumferential and interweaving radial fibers. The blood supply of the meniscus is from the medial, middle, and lateral geniculate arteries.21,22 The immature meniscus is vascular, but by adolescence the capillary bed only penetrates the outer third of the meniscus, called the “red zone.” The inner two thirds KEY POINTS of the meniscus is avascular and called the “white zone.” The sucMeniscus cess rate of meniscal repair has 1. The menisci serve as been found to be dependent on shock absorbers in the location of the tear, with tears the knee. in the red zone more likely to 2. The immature menisheal than tears in the white zone. cus is vascular, but Because the younger meniscus by adolescence the has a larger red zone, this may be capillary bed only one reason that meniscal repair penetrates the outer has a higher success rate in this third of the meniscus, patient population than in the called the “red zone.” skeletally mature patients.

Healing Response to Injury Extraarticular Tissues Skeletal muscle, tendon, and ligaments that are extraarticular (i.e., outside the joint, such as the medial collateral ligament), heal in three similar stages: inflammation, proliferation, and remodeling.23–25 During the inflammation phase a hematoma forms at the site of injury and is invaded initially by inflammatory cells. The hematoma is then gradually invaded by reparative cells: myoblasts in muscle injury, and fibroblasts in ligament and tendon injuries. During the proliferative phase, these cells multiply, populate the injury site, and begin producing the functional tissue that heals the defect. During the remodeling phase the newly formed scar tissue becomes more and more like the original tissue, although it may never become identical. During the healing process the tissue is weaker than normal and needs protection; however, early motion is often beneficial because it is thought to help direct the remodeling process. Intraarticular Tissues Articular cartilage, menisci, and ligaments that are inside the joint (i.e., intraarticular, such as the anterior cruciate ligament) have a different response to injury. No hematoma is formed in the defect, a finding that has been attributed to the presence of fibrinolytic factors in the synovial fluid that prevent KEY POINTS blood clotting in the joint.26,27 Without this initial hematoma, Healing response to there is no substrate bridging injury the gap of injury for reparative 1. Skeletal muscle, tencells to migrate into and heal don, and ligaments the defect. This results in a that are extraarticular defective healing response in (i.e., outside the joint) all of these tissues. This probhave a predictable lem has recently started to be healing response addressed by placement of that typically leads a blood clot into the site of a to restoration of 28 meniscal tear and by other function of the tissue-engineering techniques tissue. designed to place a substitute for 2. Intraarticular tissues the hematoma/blood clot at the often have a defect in site of injury in articular cartithe healing process, lage, meniscal, and ligament and do not regain 29,30 defects. Although early normal function after results are promising, additional injury. work is needed. Gene-Based Therapy The goal of gene-based therapies is to either induce or suppress a specific gene’s expression in order to modify and treat a pathological process. This is typically accomplished by delivering new deoxyribonucleic acid (DNA) to target cells. This newly introduced DNA is called a “transgene” (Table 4–1). In its simplest form, gene therapy involves the transfer of DNA that codes for a specific protein into a cell, with the overall aim of curing or ameliorating a disease arising from either the absence or inadequate production of the

Biology and Gene-Based Therapy

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Table 4–1 Terms Commonly Used in Gene Therapy Vector Transfection Translation Transduction Transcription Transgene Ex vivo gene therapy In vivo gene therapy DNA RNA mRNA Intron Exon Gene Ribosome Transgene Plasmid Liposome

The vehicle that brings the gene of interest into the cell nucleus. Vectors are often classified as viral or nonviral. The process by which the gene of interest is introduced into a cell. The conversion of the mRNA message into a protein; takes place in the cell cytoplasm in the ribosomes. The alteration of the gene expression of a cell. The formation of mRNA from DNA genes. A gene that is added therapeutically to a cell. A process in which genes are delivered to cells in vitro and then replaced into the body or the organ of interest. A process in which the vector and gene of interest are introduced directly into the body. Deoxyribonucleic acid; a double-stranded helical molecule of which genes are made. Ribonucleic acid; a single-stranded molecule that acts as a messenger for protein production (mRNA), or as transfer RNA (tRNA) or ribosomal RNA (rRNA). The messenger RNA, which is transcribed from a DNA exon, and is then translated into protein in the cell ribosomes. Noncoding DNA in genes. The function of introns is unclear at this time. The DNA material that codes for specific gene products (usually a protein). DNA that codes for a specific protein. The organelle in the cell cytoplasm where RNA is translated into protein. A gene added to a cell. DNA segment capable of self-replication. Found in bacteria and yeast, and used to carry transgenes into cells for production of proteins. Lipid–DNA complexes used for delivery of genes to cells.

specific protein.31 Newer strategies are coming into use that lower the expression of a specific gene product through ribonucleic acid (RNA) intermediates (Figure 4–3).32 The transgenic protein can be a growth factor, an antiinflammatory cytokine, an antibiotic resistance gene, or a molecule that stimulates cell growth or gene expression.33 There are six main steps in developing an effective gene therapy (Figure 4–4). First, the physiological process to be augmented needs to be identified. For example, if enhanced meniscal healing after repair is the goal, the bar-

Additive Gene Treatment

Subtractive Gene Treatment

DNA transgene

DNA transgene

riers to successful healing (lack of blood vessel ingrowth, lack of cell proliferation, or lack of protein production) must be defined. Once the defect is identified, the second step is to define which molecules can overcome that defect. For example, if cell proliferation is the barrier to meniscal healing, then the scientist must next define the growth factors that stimulate meniscal cell proliferation. The third step is to identify the DNA sequence for the molecule of interest (e.g., the desired growth factor). The fourth step is to deliver the gene (the DNA sequence) for the molecule of

Transgene messenger RNA

Nonmessenger RNA intermediate

New protein product (novel or additive with endogenous)

ⴙ

Endogenous mRNA

Decreased protein product

ⴙ

Figure 4–3 Schematic of gene-based therapy in which RNA intermediates either enhance or inhibit production of specific proteins within the cell. Subtractive approaches are being developed that use double-stranded RNA (called RNA interference), antisense single-stranded RNA, or RNA enzymes (called ribozymes).

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interest into the cells at the desired site. The fifth step is to provide appropriate stimulus for the cells to produce the molecule of interest. The sixth step is to regulate the expression of the new molecule, and to stop its production when it is no longer needed. Use of Growth Factors to Stimulate Tissue Healing In bone, the discovery of the bone morphogenetic protein (BMP) family of growth factors has led to the use of these proteins, in particular BMP-2, to enhance bone healing.

Protein of interest identified

DNA sequence of protein determined

Gene Therapy Techniques: In Vivo Versus Ex Vivo There are two major techniques currently under development for gene therapy (Figure 4–5). The first, the indirect ex vivo method, involves removing the cells from the body, genetically modifying the cells in the laboratory, and returning them to the body with a second procedure. The second, a direct

ⴙ DNA sequence of interest

However, current applications require great amounts of the protein for any clinical effect. Therefore, new research is focusing on transfecting cells with the BMP-2 gene that can produce large amounts of the protein in situ.34 Epidermal growth factor (EGF), insulin-like growth factor (IGF-1), and transforming growth factor beta 1 (TGF-β1) have been shown to stimulate chondrocyte proliferation and proteoglycan production, and are thus under investigation for treatment of cartilage defects. IGF has also been found to have a supportive effect on physeal chondrocytes, suggesting a role for this growth factor in treatment of physeal injury. In ligaments, platelet-derived growth factor (PDGF), basic fibroblast growth factor (FGF-2), and IGF have been shown to promote cell proliferation and collagen production, and they are currently under investigation for enhancing healing of these tissues.

Virus to act as delivery mechanism into cell Ex Vivo Gene Therapy

E1. E2.

DNA sequence inserted into viral DNA

Virus and DNA sequence transfect cell target

E4. E3.

Cell cytoplasm Cell nucleus In Vivo Gene Therapy

Ribosome

I1. I2.

mRNA translated into protein of interest in ribosomes, secreted by cell

Secreted protein (i.e., growth factor)

Figure 4–4 The three intermediate steps in developing gene-based therapies: identification of the DNA sequence for the molecule of interest (e.g., the desired growth factor), transfection of the cells of interest, and transduction.

I3.

Figure 4–5 Schematic of ex vivo and in vivo gene therapy techniques. Ex vivo gene therapy involves removing cells from the body (E1) and growing them in cell culture (E2). The cells are then transfected with the gene of interest (E3), and the transduced cells are then transplanted back into the body at the site where they are needed (E4). With in vivo gene therapy the vector containing the desired gene (I1) is injected directly into the site of interest (I2), where it transfects the cells in situ and the cells begin making the protein of interest (I3).

Biology and Gene-Based Therapy

in vivo method, involves delivering the genes directly to the cells within the body. Although the in vivo approach is technically simpler to perform clinically, the ex vivo approach is thought to be safer because the addition of new genetic material takes place in a more controlled environment. Vectors Gene delivery into a cell, called transfection, can be accomplished using either viral or nonviral vectors. Once inside the cell nucleus the new DNA is transcribed into messenger RNA (mRNA) that is transported into the cytoplasm and transcribed by the ribosomes into proteins (see Figure 4–4). Nonviral vectors, such as naked DNA and plasmids, are thought to be simpler to produce, and safer than viral vectors because they do not have immunogenic potential or the toxicity associated with viruses. However, at this time, nonviral vectors also have a low transfection rate. For this reason, viral vectors are used more commonly in current experiments. These vectors are popular because the viruses already possess the machinery to insert their DNA into the cell nucleus of the host. The most commonly used viral vectors include adenovirus, adeno-associated virus, and retrovirus. To use these vectors, the pathogenic genes are removed from the virus and replaced with the gene of interest to be transfected into the cell nucleus. Current Problems The current major obstacle facing clinical use of gene therapy is safety.35 The viral vectors in current use in preclinical and clinical trials have demonstrated toxicity and side effects for the patient that may be justifiable in life-saving therapies targeted against malignancies or cystic fibrosis, but not in use for more common pediatric and adolescent knee injuries. Recently, all clinical trials using gene therapy were halted when two patients being treated for severe combined immunodeficiency defect (SCID) were using a retroviral-based gene therapy vector and developed KEY POINTS leukemia during the clinical trial.36 Potential side effects of the Gene therapy transfection of cells (with or 1. The goal of genewithout a viral vector) include based therapies is overexpression of the inserted to either induce or molecule and subsequent oversuppress a specific proliferation of cells and developgene’s expression in ment of malignancy. Certainly order to modify and these significant problems must treat a pathological make all clinicians and scientists process. regard the current use of gene 2. The current major therapy with extreme caution. Future Directions Current investigations in gene therapy are focusing on the development of safer delivery systems, both viral and nonviral. Localized delivery using geneactivated matrices (GAM) and tissue engineering techniques

obstacle facing clinical use of gene therapy is safety. 3. Current investigations in gene therapy are focusing on the development of safer delivery systems, both viral and nonviral.

39

that avoid the use of viruses and offer more targeted delivery of DNA are of great interest. Techniques that offer greater regulation of the expression of the exogenous DNA are also under investigation. In addition, more precise definitions of the physiological etiologies of the failure of musculoskeletal tissues to heal and identification of the specific factors capable of overcoming these problems are also necessary. References 1. Boden, SD, Kaplan FS: Calcium homeostasis. Orthop Clin North Am 21(1):31–42, 1990. 2. Walters MR: Newly identified actions of the vitamin D endocrine system. Endocr Rev 13(4):719–764, 1992. 3. Iannotti JP: Growth plate physiology and pathology. Orthop Clin North Am 21(1):1–17, 1990. 4. Zaleske DJ: Cartilage and bone development. Instr Course Lect 47:461–468, 1998. 5. Buckwalter JA, Mankin HJ: Articular cartilage: tissue design and chondrocyte-matrix interactions. Instr Course Lect 47:477–486, 1998. 6. Mow VC, Ateshian GA: Lubrication and wear of diarthrodial joints. In Mow VC, Hayes WC (eds): Basic Orthopaedic Biomechanics. Philadelphia: Lippincott-Raven, 1997, pp 275–315. 7. Mankin HJ: The water of articular cartilage. In Simon WH (ed): The Human Joint in Health and Disease. Philadelphia: University of Pennsylvania Press, 1978, pp 37–42. 8. Mankin HJ, Thrasher AZ: Water content and binding in normal and osteoarthritic human cartilage. J Bone Joint Surg Am 57(1):76–80, 1975. 9. Eyre DR: Collagen structure and function in articular cartilage: metabolic changes in the development of osteoarthritis. In Kuettner KE, Goldberg VM (eds): Osteoarthritic Disorders. Rosemont, Ill.: AAOS, 1995, pp 219–227. 10. Eyre DR, Wu JJ, Woods P: Cartilage-specific collagens: structural studies. In Kuettner KE, Schleyerbach R, Payron JG, Hascall VC (eds): Articular Cartilage and Osteoarthritis. New York: Raven Press, 1992, pp 191–231. 11. Bernstein J: Articular cartilage. In Bernstein J (ed): Musculoskeletal Medicine. Rosement, Ill.: American Academy of Orthopaedic Surgeons, 2003, pp 15–25. 12. Buckwalter JA, Woo SL, Goldberg VM, et al: Soft-tissue aging and musculoskeletal function. J Bone Joint Surg Am 75(10):1533–1548, 1993. 13. Roughley PJ: Articular cartilage: matrix changes with aging. In Buckwalter JA, Goldberg VM, Woo SL (eds): Musculoskeletal Soft Tissue Aging: Impact on Mobility. Rosemont, Ill.: American Academy of Orthopaedic Surgeons, 1993, pp 151–164. 14. Buckwalter JA, Mankin HJ: Articular cartilage: degeneration and osteoarthritis, repair, regeneration, and transplantation. Instr Course Lect 47:487–504, 1998. 15. Garrett WE Jr, Best TM: Anatomy, physiology and mechanics of skeletal muscle. In Buckwalter JA, Einhorn TA, Simon R (eds): Orthopaedic Basic Science: Biology and Biomechanics of the Musculoskeletal System. Rosemont, Ill.: American Academy of Orthopaedic Surgeons, 2000, 683–716. 16. Pitman, MI, Nainzadeh N, Menche D, et al: The intraoperative evaluation of the neurosensory function of the anterior cruciate ligament in humans using somatosensory evoked potentials. Arthroscopy 8(4):442–447, 1992. 17. Dorlot JM, Sidi MAB, Tremblay GM, et al: Load elongation behavior of the canine anterior cruciate ligament. J Biomech Eng 102:190–193, 1980. 18. Muller P, Dahners LE: A study of ligamentous growth. Clin Orthop Rel Res (229):274–277, 1988. 19. Woo SL, Ohland KJ, Weiss JA: Aging and sex-related changes in the biomechanical properties of the rabbit medial collateral ligament. Mech Ageing Dev 56(2):129–142, 1990. 20. Arnoczky SP, Adams M, DeHaven K, et al: Meniscus. In Woo SL, Buckwalter JA (eds): Injury and Repair of the Musculoskeletal Soft Tissues. Park Ridge, Ill.: AAOS, 1988, pp 483–537. 21. Arnoczky SP, Warren RF: The microvasculature of the meniscus and its response to injury. An experimental study in the dog. Am J Sports Med 11(3):131–141, 1983. 22. Day B, Mackenzie WG, Shim SS, Leung G: The vascular and nerve supply of the human meniscus. Arthroscopy 1(1):58–62, 1985.

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23. Andriacchi T, Sabiston P, DeHaven K, et al: Ligament: injury and repair. In Woo SL, Buckwalter JA (eds): Injury and Repair of the Musculoskeletal Soft Tissues. Park Ridge, Ill.: American Academy of Orthopaedic Surgeons, 1988, pp 103–128. 24. Arnoczky SP: Physiologic principles of ligament injuries and healing. In Scott WN (ed): Ligament and Extensor Mechanism Injuries of the Knee: Diagnosis and Treatment. St Louis: Mosby-Year Book, 1991, pp 67–81. 25. Frank C, Amiel D, Akeson WH: Healing of the medial collateral ligament of the knee. A morphological and biochemical assessment in rabbits. Acta Orthop Scand 54(6):917–923, 1983. 26. Harrold AJ: Elimination of fibrinogen from synovial joints. Ann Rheum Dis 32(1):29–34, 1973. 27. Murray MM, Martin SD, Martin TL, Spector M: Histological changes in the human anterior cruciate ligament after rupture. J Bone Joint Surg Am 82(10):1387–1397, 2000. 28. Arnoczky SP, Warren RF, Spivak JM: Meniscal repair using an exogenous fibrin clot. An experimental study in dogs. J Bone Joint Surg Am 70(8):1209–1217, 1988. 29. Murray MM, Martin SD, Spector M: Migration of cells from human anterior cruciate ligament explants into collagen-glycosaminoglycan scaffolds. J Orthop Res 18(4):557–564, 2000.

30. Murray MM, Spector M: The migration of cells from the ruptured human anterior cruciate ligament into collagen-glycosaminoglycan regeneration templates in vitro. Biomaterials 22(17):2393–2402, 2001. 31. Lieberman JR, Ghivizzani SC, Evans CH: Gene transfer approaches to the healing of bone and cartilage. Mol Ther: J Am Soc Gene Ther 6(2):141–147, 2002. 32. Caplen NJ: RNAi as a gene therapy approach. Exp Opin Biol Ther 3(4):575–586, 2003. 33. Baltzer AW, Lieberman JR: Regional gene therapy to enhance bone repair. Gene Ther 11(4):344–350, 2004. 34. Alden TD, Varady P, Kallmes DF, et al: Bone morphogenetic protein gene therapy. Spine 27(16 suppl 1):S87–S93, 2002. 35. Raper SE, Chirmule N, Lee FS, et al: Fatal systemic inflammatory response syndrome in a ornithine transcarbamylase deficient patient following adenoviral gene transfer. Mol Genet Metab 80(1–2): 148–158, 2003. 36. Williams DA, Baum C: Medicine. Gene therapy—new challenges ahead [comment]. Science 302(5644):400–401, 2003.

Chapter 5

Developmental Biology of the Knee: Embryo to Skeletal Maturity Frederic Shapiro

Development of the knee occurs by a series of cellular changes that are regional in scope. In the limb bud of the embryo the undifferentiated mesenchymal cells form initially and then undergo pattern formation and tissue differentiation from the very general to the highly specific. This mode of development is referred to as epigenetic, in which previously formed tissues direct the formation of subsequent tissues in cascade fashion. The knee region is eventually composed of the distal femur, proximal tibia and fibula, and patella; the surrounding musculature; the joint capsule, ligaments, synovial lining, cruciate ligaments, and menisci; and adjacent nerves and vessels. Histological Features of Knee Development Appendicular development moves in a wavelike fashion from the proximal part of the extremity to the distal, with upper extremity development slightly ahead of lower extremity development. The histological features of development reviewed in this section have been presented in greater detail.1–4 The bones comprising the knee are preformed as areas of mesenchymal cell condensation followed by cartilage model formation. The joints form relatively late in development, after the cartilage models of the adjacent long bones, including their epiphyses and articular cartilages, have been established. Muscle condensation also precedes joint formation, occurring around the same time as cartilage model formation. As chondrification expands toward the end of each bone, mesenchymal cells persist between the cartilage models in a region referred to as the interzone, the region that is the morphological precursor of the eventual joint. Peripherally the interzone is continuous with the perichondrium of the skeletal elements. Development of the knee joint in the human extends from

the first appearance of the joint rudiments at 11 mm crown-rump (C-R) length to the appearance of the joint cavities at 40–44 mm C-R (knee) (Streeter stages 18–23), a time period from the sixth to the ninth weeks of development. The menisci and cruciate ligaments begin formation by the eighth week of development, and by the tenth week the appearance of the joint is similar to the adult knee. Joint development can be followed histologically through four stages: (1) the homogeneous interzone of undifferentiated mesenchymal cells between the developing cartilage models of the bones, (2) the three-layered interzone with more densely packed cells representing the two developing articular surfaces of the adjacent bones and an intervening layer of more loosely packed undifferentiated cells, (3) the stage of early liquefaction of the middle layer, and (4) the stage of full separation and joint cavitation. The articular surfaces are shaped at a stage when their interzones are homogeneous with no movement between the two occurring. The final stage of joint formation is the result of a resorptive process (Figure 5–1). Several intraarticular spaces coalesce, leaving the intraarticular structures such as the menisci and cruciate ligaments in position. The fibrous capsule near the joints separates the mesenchyme (referred to as “blastema” in older literature) into two regions. One forms the perichondrium, which is partly transformed into the peripheral parts of the articular cartilage, whereas the other forms all intracapsular structures, including the cruciate ligaments, tendons, menisci, and eventually the synovium. Articular cartilage development is an integral part of knee joint formation and also develops in a staged fashion. The articular cartilage is initially shaped during epiphyseal and interzone formation. In the next (second) stage the 41

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Figure 5–1 Photomicrographs show stages of rabbit skeletal development from histological sections. Human development would appear similar. A, Part of an embryonic limb bud is shown. The apical ectodermal ridge (AER) (arrow) is shown at right. The limb bud is filled with undifferentiated mesenchymal cells. B, A developing knee region is shown from the embryo. The cartilage model of the femur is at the left and the model of the tibia is at right. The extensor mechanism is at the top middle, and the popliteal artery is at the bottom middle. The cellular region between the distal femur and proximal tibia is the interzone region where the knee joint will eventually be. C, Part of the elbow joint shows diminished cellularity of the interzone region as resorption clearing the joint space is underway. D, A newborn joint (partial) shows articular cartilage above, joint space (clear region) and articular cartilage, epiphyseal cartilage, and secondary ossification center bone below. E, Articular cartilage at skeletal maturity is shown. The darker staining material at bottom is the subchondral bone. The arrow points to the tidemark delineating the radial layer of cartilage above from the calcified layer below.

Developmental Biology of the Knee: Embryo to Skeletal Maturity

articular cartilage merges imperceptibly with the underlying epiphyseal cartilage at the distal femur and proximal tibia. The third stage occurs when the secondary ossification center of each bone has been formed and has reached its greatest relative extent in replacing epiphyseal cartilage. At this time the undersurface of the articular cartilage merges with the physis of the secondary ossification center, referred to by some as the miniplate. The final stage in the development of the articular cartilage occurs long after birth—at skeletal maturity—at the same time that the main physis of the proximal tibia or distal femur closes. At this time the innermost layer of the articular cartilage calcifies, forming the calcified layer of the articular cartilage that persists throughout life. The articular cartilage is avascular throughout all stages of its development and throughout postnatal life, in the normal state. The layers of cartilage that are not physically separable are, from superficial to deep, the tangential, transitional, radial, and calcified cartilage with the tidemark seen histologically separating the radial from the calcified layer. The calcified layer rests on the thickened subchondral bone (see Figure 5–1). The menisci, cruciate ligaments, and collateral ligaments differentiate directly from the mesenchymal cells of the interzone (the blastema).1,3,4 Differentiation of these structures occurs from the beginning in situ, at their specific anatomical locations and with their specific adult shapes. Each of these structures develops before the appearance of the synovial membrane. The embryonic menisci and cruciate ligaments are highly cellular throughout with fibrous matrices, becoming predominant during late fetal and early postnatal growth.3–6 The discoid lateral meniscus does not represent an arrest of development because the meniscal shape is always semilunar/triangular from its inception.5,6 The discoid shape is caused by repetitive trauma owing to imperfect anatomical attachments to the tibia. The major blood supply to the knee, including the epiphyseal and intraarticular components, comes from the medial and lateral superior and inferior genicular vessels, plus the middle genicular vessels, all of which originate from the popliteal artery.7 Both menisci have blood vessels across their entire extent during fetal development. The vascularity diminishes progressively after birth and is eventually confined to the peripheral 10–30% of each meniscus from skeletal maturity to old age.6–8 The perimeniscal capsular and synovial vessels originate from the medial, lateral, and middle genicular arteries and send branches into the outer parts of the menisci. The cruciate ligaments receive a rich blood supply from the synovial membranes that surround them along their entire length.9 The synovial vessels (primarily from the middle genicular artery) form a network of periligamentous vessels whose branches penetrate the ligaments to connect with the intraligamentous vessels. The bone-ligament junctions contribute little to the ligamentous blood supply. We have recently outlined the structural stages in the development of the long bones and epiphyses.1,2 The study, which was performed in the rabbit, accurately depicts the pattern in all higher vertebrates, including humans. We defined 16 stages (25 stages/substages), passing from the embryonic limb bud formation (stage 1) to calcification of the lowest zone of articular cartilage, tidemark formation, and transformation of all marrow to fat (stage 16a).

43

Gene and Molecular Features of Limb Development Enormous advances have been made over the past 20 years in defining the genes directing skeletal development from the limb bud stage onward and the molecular constituents of the tissues comprising the musculoskeletal system.10–14 Once formed, the limb buds enlarge and develop threedimensionally with specific genes directing proximal distal outgrowth, anteroposterior and dorsoventral structure differentiation, and right–left patterning. Initial formation of the limb bud from the lateral plate mesoderm is mediated by fibroblast growth factor 8 (FGF-8). Homeobox transcription factor genes (hox genes) are crucial in directing formation of the early skeleton, particularly in groups 9–13 of hoxa and hoxd clusters. A histologically discrete elevated ridge of ectodermal cells develops along the tip of the limb bud, the apical ectodermal ridge (AER). FGF-8 and FGF-4 are major mediators of AER function. The zone of polarizing activity at the posterior edge of the limb bud directs anteroposterior development mediated by the protein sonic hedgehog. The progress zone just within the AER gives cells positional information in directing proximal to distal development. Dorsoventral patterning is mediated from the dorsal nonridge ectoderm by members of the Wnt family of signaling molecules. As mesenchymal condensation occurs within the limb bud forming the early cartilage models of the bones SOX9 contributes. Indian hedgehog is active in coordinating chondrocyte proliferation and differentiation, along with parathyroid-related protein, multiple FGFs, and fibroblast growth factor receptors 1–4 (FGFR 1–4). Each stage of development has gene/molecular activities identified: Wnt 5a is expressed in the perichondrium, Wnt 5b in pre-hypertrophic chondrocytes, Wnt 4 in cells of the joint region, growth, and differentiation factors (GDF-5, GDF-6, GDF-7), and Nog at sites of joint formation; Runx2 (Cbfa 1) mediates osteoblast formation; and RANKL mediates osteoclast formation. Additional information has assessed types II, IX, X (hypertrophic zone), and XI collagen specific to cartilage, and type I collagen being the primary structural protein of bone, tendon, and ligament. Clinically Relevant Features of Knee Development Time of Appearance of Ossification Centers (Secondary Centers, Distal Femur, Proximal Tibia, Proximal Fibula; Ossification Center Patella)1 Distal Femur The first secondary ossification center to appear in human development is that of the distal femur. This is present normally at birth (full term) in 100% of boys and girls. It forms during fetal development and is an indicator of age of skeletal development using ultrasonography. The secondary center has been noted as early as 28 weeks of gestation and is present in all fetuses after 33 weeks. Proximal Tibia The proximal tibial center is the second in order of appearance after the distal femur. It is usually seen prenatally but

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develops slightly after the femur. It is present in almost 100% of boys and girls at birth (full term) and should be seen in 100% by 3 months of age. Proximal Fibula The median age of appearance of the secondary center of the proximal fibula in girls is 3 years, 1 month of age (97% by 4 years, 6 months) and in boys is 4 years, 5 months (92% by 5 years).

from 1–4 years of age, diminishing to 10% at 12 years. Some marginal irregularities at the inferior and posterior regions (seen on tunnel view radiographs) appear toward the end of the first decade and almost always remodel with growth. Proximal Tibia Irregularities are less frequently seen in the proximal tibia and are infrequently related to the articular surfaces. These too resolve with growth.

Patella The ossification center of the patella appears at age 2 years, 6 months in girls and at age 3 years, 2 months in boys. Initially it is usually multicentric. The patella develops as a cartilage model with a central ossification center forming, as in the carpal and tarsal bones. Normal Radiographic Variants of Developing Distal Femur and Proximal Tibia Secondary Ossification Centers Distal Femur There are many normal irregularities of appearance of the distal femoral secondary ossification center, which must not be mistaken for pathological processes.1 These include rough or serrated margins of the secondary ossification centers, thin bony protuberances from the margins of the secondary center, and small accessory ossification centers. They are most common in the early years of life and progressively diminish toward the end of the first decade. Uneven marginal ossification is seen in 85% of children

Radiographic Atlas of Knee Development Although the Greulich and Pyle’s Radiographic Atlas of Skeletal Development of the Hand and Wrist is widely used to calculate bone age, serial radiographs can also be used to document knee development in similar fashion.15 Although less accurate in terms of skeletal age determination, the radiographs are helpful in assessing knee formation. Physiological Bowing (Tibia Vara) Bowlegs, centered at the knee, are a common finding in many children in the first 2 years of life. The condition is referred to as physiological tibia vara. Radiographic studies in growing children have documented a femoral-tibial diaphyseal angle ranging from a mean of 15 degrees varus at birth, to neutral at 24 months, to 10 degrees valgus at 36 months, to 5–6 degrees valgus by 6 years (Figure 5–2).16 Varus angulation can be as extensive as 30–40 degrees and still correct itself spontaneously. The deformity is often worsened in appearance by intoeing due to internal tibial torsion.

Figure 5–2 Development of the tibiofemoral diaphyseal angle during growth. (From Salenius P, Vankka E: The development of the tibio-femoral angle in children. J Bone Joint Surg Am 57:259–261, 1975.)

Developmental Biology of the Knee: Embryo to Skeletal Maturity

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Figure 5–3 The four stages of tibial tubercle development. Ant, Anterior; M, metaphysis; P, physis; Post, posterior; SOC, secondary ossification center.

Tibial Tuberosity Development The proximal tibial epiphysis has a unique feature to its development involving formation of the tibial tubercle anteriorly and inferiorly. In the prenatal period there is initially a transverse proximal tibial physis only, similar to that seen in other long bones. A continuous cartilaginous segment then forms anterior and distal to the main physis.1 Ogden et al. have documented that the proximal parts of this extension are physeal in nature and the distal fibrocartilaginous.17 Formation of the tibial tuberosity can be divided into four stages: (1) the cartilaginous stage; (2) the apophyseal stage, when an ossification center forms at the distal end of the anterior tongue of cartilage; (3) the epiphyseal stage, where the proximal tibial secondary ossification center and the tibial tubercle bone center have merged into one continuous center; and (4) the bone stage, in which the growth plates at proximal tibia and tuberosity have closed (Figure 5–3).18 There is considerable variation in the ages at which these stages occur; in general, development in girls is approximately 2 years earlier than boys. The cartilaginous stage is generally present until ages 10–11 years in girls, the apophyseal stage at age 12, the epiphyseal stage at age 13, and the bony stage at age 15 in girls and age 17 in boys. Anatomy plays an integral role in relating to the pathophysiology of the Osgood-Schlatter disorder, which occurs in the apophyseal and epiphyseal stages.1 Premature tibial tubercle physeal closure rarely occurs. Weakest Points of Resistance with Trauma in the Developing Knee In the developing, skeletally immature joint the weakest regions are often (although not always) the physeal areas such that trauma that ruptures ligaments in the adult causes growth plate fracture-separations in the young. It is important to check for injuries to the distal femoral physis or the proximal tibial physis, where collateral ligament tears are suspected clinically.1 Extensor mechanism injuries often lead to tibial tubercle fractures19 rather than ligament ruptures, and cruciate stress injuries often cause anterior tibial spine fractures at the point of cruciate insertion, leaving the ligament intact.20 Time of Physeal Closure Time of physeal closure1 is less specific than time of appearance, and its clinical significance is less. Most physes have

markedly diminished their growth in the last 12–18 months before radiographic fusion. Distal Femur The median age of closure is 14 years, 9 months in girls and 16 years, 8 months in boys. Proximal Tibia The median age of closure is 14 years, 10 months in girls and 16 years, 11 months in boys. Proximal Fibula The median age of closure is 15 years, 2 months in girls and 17 years, 2 months in boys. Growth Occurring in Distal Femur and Proximal Tibia Growth Plates The tables of Anderson, Green, and Messner1,21,22 remain valuable in documenting femoral and tibial lengths and the amount of growth remaining in the distal femur and proximal tibia at time periods before skeletal maturity. References 1. Shapiro F: Pediatric Orthopedic Deformities. Basic Science, Diagnosis, and Treatment. San Diego: Academic Press/Elsevier, 2002. 2. Rivas R, Shapiro F: Structural stages in the development of the long bones and epiphyses. A study in the New Zealand white rabbit. J Bone Joint Surg Am 84:85–100, 2002. 3. McDermott L: Development of the human knee joint. Arch Surg 46:705–719, 1943. 4. Gardner E, O’Rahilly R: The early development of the knee joint in staged human embryos. J Anat 102:289–299, 1968. 5. Kaplan E: Discoid lateral meniscus of the knee joint. J Bone Joint Surg Am 39:77–87, 1957. 6. Clark C, Ogden J: Development of the menisci of the human knee joint. J Bone Joint Surg Am 65:538–547, 1983. 7. Scapinelli R: Studies on the vasculature of the human knee joint. Acta Anat 70:305–331, 1968. 8. Arnoczky S, Warren R: Microvasculature of the human meniscus. Am J Sports Med 10:90–95, 1982. 9. Arnoczky S: Anatomy of the anterior cruciate ligament. Clin Orthop Rel Res 172:19–25, 1982. 10. Capdevila J, Izpisua Belmonte JC: Patterning mechanisms controlling vertebrate limb development. Annu Rev Cell Dev Biol 17:87–132, 2001. 11. Hartmann C, Tabin CJ: Dual roles of Wnt signaling during chondrogenesis in the chicken limb. Development 127:3141–3159, 2000. 12. Johnson RL, Tabin CJ: Molecular models for vertebrate limb development. Cell 90:979–990, 1997. 13. Mariani FV, Martin GR: Deciphering skeletal patterning: clues from the limb. Nature 423:319–325, 2003.

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14. Kronenberg, HM: Developmental regulation of the growth plate. Nature 423:332–336, 2003. 15. Pyle SI, Hoerr NL: Radiographic Atlas of Skeletal Development of the Knee. Springfield, Ill.: Charles C Thomas, 1955. 16. Salenius P, Vankka E: The development of the tibio-femoral angle in children. J Bone Joint Surg Am 57: 259–261, 1975. 17. Ogden JA, Hempton RF, Southwick WO: Development of the tibial tuberosity. Anat Rec 182:431–446, 1975. 18. Ehrenborg G, Engfeldt B: The insertion of the ligamentum patellae on the tibial tuberosity: some views in connection with the OsgoodSchlatter lesion. Acta Chir Scand 121:491–499, 1961.

19. Ogden JA, Tross RB, Murphy MJ: Fractures of the tibial tuberosity in adolescents. J Bone Joint Surg Am 62:205–215, 1980. 20. Edwards PH Jr, Grana WA: Physeal fractures about the knee. J Am Acad Orthop Surg 3:63–70, 1995. 21. Anderson M, Green WT, Messner MB: Distribution of lengths of the normal femur and tibia in children from 1 to 18 years of age. J Bone Joint Surg Am 46:1197–1202, 1964. 22. Anderson M, Green WT, Messner MB: Growth and predictions of growth in the lower extremities. J Bone Joint Surg Am 45:1–14, 1963.

Chapter 6

Imaging of the Pediatric and Adolescent Knee Diego Jaramillo

This chapter reviews the imaging of the knee in children and adolescents, focusing on the manifestations of various diseases with the use of magnetic resonance imaging (MRI), which has become the dominant imaging technique in the knee joint. Normal Developmental Changes and Their Differentiation from Disease When imaging the knee it is crucial to be aware of the normal developmental appearances that can constitute pitfalls on radiographs and MRI studies. Radiography

KEY POINTS Developmental variants of the knee Radiographs 1. Distal femoral epiphyseal irregularity 2. Tibial tubercle fragmentation 3. Metaphyseal sclerosis with weight-bearing 4. Cortical defects at tendinous insertions MRI 1. Epiphyseal T2 hypointensity with weight-bearing 2. Undulation of distal central femoral physis 3. Intrameniscal vessel 4. Residual hematopoietic marrow in metaphyses

Normal irregular ossification of the epiphysis and metaphysis during childhood is often confused with disease. Irregularities of the epiphyseal ossification center of the distal femur are found in 60% of boys and 40% of girls.1 Both condyles are involved in approximately half of the cases. Irregular epiphyseal ossification in the distal femur is more common laterally, but it tends to be more severe when it occurs medially. Ossification in the tibial epiphysis is irregular in the region of the tubercle. The tubercle ossifies between 8 and 12 years of age in girls and between 9 and 14 years of age in boys. The tubercle is initially fragmented, but unlike the

irregularity seen in OsgoodSchlatter disease, there is usually no soft tissue edema. In the metaphyses of young children, the primary spongiosa can be unusually dense (Figure 6–1). The resultant metaphyseal sclerosis can resemble that seen with lead toxicity2 or bisphosphonate therapy; however, normal metaphyseal sclerosis does not affect the fibula as much as it does the tibia and femur. The metaphysis is the site of insertion of tendons and ligaments.3 At these sites, there are normally cortical defects that can simulate well-corticated lytic lesions. A particularly conspicuous cortical defect occurs in the medial aspect of the distal femoral metaphysis, at the insertion of the medial head of the gastrocnemius tendon.4,5 In older children, the avulsive femoral cortical irregularity at the insertion of the adductor magnus can show more proliferative changes and mimic an osteosarcoma.5 Magnetic Resonance Imaging MR imaging of the immature skeleton is different from that of the adult because of the abundance of hematopoietic marrow and cartilage, as well as the greater vascularization of cartilage and menisci. T2-weighted images allow differentiation between the physeal cartilage, which is of higher signal intensity, and the epiphyseal cartilage. The physis enhances with gadolinium administration; the epiphyseal cartilage contains numerous vascular canals that become apparent after contrast enhancement and are more prominent when there is inflammation in the bone or joint.6 The epiphyseal cartilage of the distal femur undergoes changes with age. At birth it is homogeneous on T2-weighted images. With walking, the weight-bearing area decreases in signal intensity (Figure 6–2).7 The posterior femoral condyles, which are the most active area of 47

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Figure 6–1 Normal metaphyseal sclerosis in a 6-year-old child. Anteroposterior radiograph shows increased density along the primary spongiosa of the metaphyses of the distal femur and proximal tibia (arrows). This is not apparent in the fibula.

Figure 6–2 A sagittal T2-weighted image of the lateral femoral condyle of a 5-year-old girl. The epiphyseal cartilage surrounds the secondary center of ossification (O). There is normal decreased signal intensity along the weight-bearing region (long arrow). There is a high-signal-intensity subperiosteal stripe (short arrow), a normal feature that disappears with age.

epiphyseal ossification during childhood, develop high signal intensity just before the conversion of cartilage into bone. The physes of the distal femur and proximal tibia close centrally. On MR images, physeal closure is seen as a loss of signal from the cartilage. Although initially the physis in early childhood is relatively flat, it becomes progressively undulated before closure.8 Transphyseal bony bridges resulting from severe injuries to the physis usually occur in areas of normal physeal undulation.9 The normal cortical irregularity at the site of the insertion of the medial head of the gastrocnemius muscle, mentioned previously, is of high signal intensity on T2-weighted images and enhances with gadolinium.4 The shape of the menisci remains constant throughout childhood and adolescence. Before puberty an intrameniscal vessel is visible on MR images as a horizontal, linear high signal in the peripheral third of the meniscus, originating from the menisco-capsular attachment.10 Unlike a tear, the vessel is always horizontal and bisects the meniscal substance; additionally, it extends to the periphery but not to the articular surface. Vessels are usually easy to differentiate from meniscal tears, which are usually vertical during childhood.11

MR imaging also allows differentiation between the normal hematopoietic marrow of the metaphysis and the fatty marrow of the epiphyseal ossification center. At birth, most of the marrow is hematopoietic, but by early adolescence the signal intensity of the majority of the marrow is similar to fat in all areas except for the metaphysis. Hematopoietic marrow contains fat and is therefore of intermediate signal intensity on T1-weighted images, typically higher in signal intensity than the adjacent muscle. On T2-weighted images, hematopoietic marrow is of intermediate to high signal intensity, being less intense than infected or tumoral marrow.12 The periosteum is clearly seen as a low signal intensity line parallel to the cortex, and before skeletal maturity there is a T2-hyperintense subperiosteal stripe (see Figure 6–2) that tends to disappear as children mature.13 Subperiosteal collections always stop at the perichondrium.6 Technical Considerations in Children For MRI (see Technical Note 6-1), children under 6 years of age require sedation, which is usually done with intravenous (IV) pentobarbital. It is best to image each extremity Text continued on p. 54

Imaging of the Pediatric and Adolescent Knee

TECHNICAL NOTE 6–1

How to Read an MRI of the Knee Charles P. Ho

Indications Magnetic resonance imaging (MRI or MR imaging) is the gold standard for optimal single imaging evaluation of the knee for internal soft tissue, as well as osseous derangement. No other imaging examination offers the unique combination of high-resolution, superb soft tissue contrast, as well as multiplanar to volumetric imaging capability ideal for demonstrating all the component structures and their possible injuries. Still, the prospect of choosing among the multitude of available imaging planes, sequences, and parameter values and reading the sometimes hundreds of images in a single MRI examination can be daunting. The user needs to develop a working knowledge and search pattern of how MR images of the knee are presented and evaluated. Technique Although a volume or slab of the knee may be queried in obtaining the MRI data, by convention the resulting information is presented as a series of two-dimensional images or slices stepped through the knee. The three-dimensional nature of the knee, with widely varying orientation and curvature of internal structures, effectively means that each structure may be best appreciated and evaluated in specific planes that differ from menisci to chondral surfaces to ligaments and tendons. Rather than facing unique images/planes for each structure that could be injured and therefore need to be evaluated, most examiners have found that using images in the three standard planes (sagittal, coronal, and axial) orthogonal to the knee provides the most practical optimal evaluation of all structures (Figures 6–3 to 6–6). All three of these planes should be used, because each is best for specific structures or parts of structures, as discussed later. As for selection of image sequence types and parameter values, new sequence types and parameters continue to evolve and be developed. I will not attempt to discuss all the sequence types already available, much less those being developed. Knee structures must be evaluated for both morphology and signal abnormalities. Thus the standard knee MRI examination should include images providing high resolution and, equally important, good signal contrast between and among the various structures, such as menisci, articular cartilage,

subchondral bone, joint fluid, and synovium. This generally means including sequences in which fluid, synovium, and edema are bright/high signal in contrast to intermediate signal articular cartilage in contrast to low signal subchondral cortical bone. So-called cartilage-specific sequences generally are gradient echo-based techniques in which cartilage is very high signal in comparison to fluid and subchondral bone. However, small chondral fissures or defects in the background of very high signal cartilage may be very difficult to appreciate, and bone and soft tissue edema may be difficult to appreciate on gradient echo sequences. I have not found cartilage-specific gradient echo sequences to be helpful and do not use them. Suppression of sometimes overwhelming background high signal of fat tissue in subcutaneous fat, fat pads/planes, and fatty marrow using various fat signal–suppression sequences may be useful for better appreciation of edematous or inflammatory change of bone and soft tissue that may otherwise be difficult to detect (see Figures 6–4 and 6–6). Tissue and Injury Signal Characteristics In general most sequences tend to be more T1-weighted, intermediate (“proton density”), or T2-weighted in their tissue signal characteristics. Fat tissue demonstrates high signal on T1-weighted images and intermediate to high signal on T2-weighted images. Fluid or edema shows low signal on T1-weighted images and high signal on T2-weighted images. Cortical bone and normal fibrous tissue or collagen such as in ligaments and tendons should be dark with little or no signal on all sequences. Muscle demonstrates low to intermediate signal on most sequences. In acute injuries, abnormal signal and morphology may be detected, with high signal edema and hemorrhage seen about the injured structures on T2-weighted images, as well as disruption of normal well-defined contours. T2-weighted fat-suppression sequences that in effect remove the background high signal of fat in soft tissue and cancellous bone marrow are particularly powerful for demonstrating high signal fluid and edema. In chronic injury there may no longer be abnormal signal edema/hemorrhage, and the observer must rely on finding abnormal morphology. Continued

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TECHNICAL NOTE 6–1

How to Read an MRI of the Knee (Continued)

Figure 6–3 Normal anatomy in a coronal PD image of a 14-year-old boy, demonstrating normal proximal (long arrow) and distal (double long arrows) lateral/fibulocollateral ligament and fibular head attachment, and normal proximal tibial and fibular physes (short arrows).

Structural Search Pattern Each specific structure of the knee may be best evaluated in one or more of the three orthogonal planes. Each structure may be evaluated in the plane most tangential to or along its length but also, and most reliably, should be assessed in shortdiameter cross-section in the plane most orthogonal to its orientation. The reader should be familiar with and use all three planes of images. The examiner must be aware of and allow for normal structures and variants that may mimic tears. Menisci: The medial and lateral menisci are best evaluated in sagittal plane images for their

anterior and posterior horns and in coronal plane for their middle/body portions. The meniscus cross-section should be low signal, well defined, smoothly marginated, and triangular. Intrasubstance peripheral high signal that does not disrupt the superior or inferior meniscal articular surface normally may be present in the immature knee and represents the still prominent peripheral vascular supply/cleft. Other normal structures often presenting as pseudotears include the popliteus hiatus of the lateral meniscus posterior horn; the lateral meniscus posterior horn attachment to the menisco-femoral ligament of Wrisberg and/or Humphrey; and the lateral meniscus anterior Continued

Imaging of the Pediatric and Adolescent Knee

TECHNICAL NOTE 6–1

How to Read an MRI of the Knee (Continued)

Figure 6–4 Prepatellar bursitis in a sagittal fat-suppressed T2-weighted image of a 14-year-old boy, revealing high signal fluid of prepatellar bursitis (short arrow). Also, note that proximal anterior cruciate ligament (ACL) (long arrow) femoral attachment cannot be evaluated adequately on sagittal images, but normal distal ACL (double long arrows) and tibial attachments are well evaluated on sagittal images.

horn attachment to the transverse intermeniscal ligament. Articular Cartilage: The articular cartilage and surfaces of the medial and lateral compartments (femoral condyles and tibial plateaus) are best evaluated in sagittal and coronal images, and both planes should be used. Small fissures or defects that may be subtle and difficult to appreciate in one plane may be more apparent and confirmed in the other plane. The patellofemoral chondral surfaces provide a challenge to evaluate because of their unique curvature, but generally they can be well assessed by using both the sagittal and the axial plane images. Hyaline cartilage should be interme-

diate in signal, with or without a zonal pattern parallel to the bone/cartilage and cartilage/synovial surfaces but otherwise homogeneous on most sequences. Focal fissures and defects should appear as bright/fluid intensity signal on T2-weighted images, with or without fat suppression. Ligaments: The collateral ligaments are best seen in length on coronal images and most reliably in cross-section on axial images. The anterior cruciate ligament (ACL) is evaluated in length on the sagittal and coronal images and in cross-section on the axial images. The proximal portion and femoral attachment of the ACL can be difficult to appreciate on the sagittal images but may be Continued

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TECHNICAL NOTE 6–1

How to Read an MRI of the Knee (Continued)

Figure 6–5 Normal anatomy in a coronal PD image of an 8-year-old girl, showing normal medial meniscus body and chondral surfaces (short arrow); normal lateral meniscus posterior horn and chondral surfaces (double short arrows); normal proximal medial collateral ligament (long arrow); and normal proximal anterior cruciate ligament (double long arrows).

reliably demonstrated on coronal and especially on axial images. The posterior cruciate ligament (PCL) is seen in length on sagittal images and most reliably in cross-section on coronal images for the proximal portion and on axial images for the distal portion, respectively. The normal organized fiber bundles of ligaments should be smooth and well defined, with little or no signal on all sequences. (The ACL may normally show intermediate synovial tissue signal between the relatively well-defined low signal anteromedial and posterolateral bundles, but the PCL anterolateral and posteromedial bundles usually are not resolved or appreciated as separate bands or portions on MR images.)

Muscles/Tendons: The patellar and distal quadriceps tendons are best seen in length on sagittal images and most reliably in cross-section on the axial images. The posteromedial pes and semimembranosus tendons and the posterolateral biceps femoris tendon may be evaluated in length on coronal images and somewhat on sagittal images, but they are most reliably seen in cross-section on axial images. The medial/lateral gastrocnemius and plantaris muscles/tendons are most usefully seen in length on the sagittal images and in cross-section on axial images. The oblique course of the popliteus muscle/tendon provides another challenge and should be evaluated on coronal and sagittal images along its length and on axial images in cross-section. Continued

Imaging of the Pediatric and Adolescent Knee

TECHNICAL NOTE 6–1

How to Read an MRI of the Knee (Continued)

Figure 6–6 Bone contusion in a sagittal fat-suppressed T2-weighted image of an 8-year-old girl, with high signal bone edema/contusion of lateral femoral condyle (short arrows) and inferior patella, possibly from transient lateral patellar dislocation. Note also the normal physes (long arrows) and lateral meniscus.

Muscles should be smoothly marginated and well defined with low to intermediate signal on all sequences. Tendons, as with ligaments, should have little to no signal on all sequences. (The distal quadriceps tendon may normally have a trilaminar appearance with intermediate signal fibro-fatty tissue among the well-defined low signal rectus femoris superficial layer, vastus medialis and lateralis intermediate layer, and vastus intermedius deep layer.) Bone: The distal femur and proximal tibia and fibula should be scrutinized on images in all three orthogonal planes. The cortical bone should be smoothly marginated with low to no signal on all

sequences. Cancellous bone of the epiphyses once ossified should have fatty marrow similar in appearance to surrounding soft tissue fat with high signal on T1 weighting and low signal on fatsuppression images. Cancellous bone of the metaphyses to diametaphyses should generally have somewhat inhomogeneous intermediate signal of hematopoietic/red marrow on most or all sequences that gradually recedes with growth to maturity but can often persist about the knee well into maturity. Bone injuries manifest as high signal, cancellous edema/hemorrhage best seen on fat-suppression images of contusions or stress reactions to focal fracture or stress fracture lines Continued

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TECHNICAL NOTE 6–1

How to Read an MRI of the Knee (Continued) disrupting cortical and cancellous bone, usually with associated surrounding soft tissue edema/ hemorrhage. Small focal fracture lines or avulsion fragments may be difficult to appreciate by MRI. Physes: The cartilaginous physes are best seen in cross-section on the sagittal and coronal images and vary in appearance as they mature to fusion. Until

separately, even when searching for disease that may be bilateral, such as a discoid meniscus. The sequences used vary with the K E Y P O I N T S anatomical structure of interest. Optimal MRI pulse Optimal differentiation of sequences cartilage from bone occurs with 1. PD: Anatomy of PD-weighted or with spoiled cartilage, menisci, gradient-recalled echo (SPGR) and ligaments images, particularly when the 2. Spoiled gradientsignal from the marrow fat is suprecalled echo: pressed.14 Optimal differentiation Anatomy of cartilage between zones of the growing only cartilage is best attained with T23. T2: Edema weighted imaging. Gadolinium4. Post-gadolinium T1: enhanced T1-weighted images Vascularity for demonstrate lesion vascularity, infection, arthritis, which is crucial when evaluating and tumors tumoral or infectious lesions.

fused, they should follow the articular cartilage in signal/appearance. Physeal injury may present as asymmetrical/focal widening or narrowing of the physis, with or without focal fracture lines, with surrounding cancellous and soft tissue edema and hemorrhage best seen on fat-suppression images in acute injury and sclerosis and possible focal fusion/bone bar formation in more chronic injury.

of the knee. These abnormalities include widening and depression of the medial physis, small and deep intrusions of cartilage into the metaphysis, and focal bone bridging (Figure 6–8).17 The lateral physis can be abnormally wide. The epiphyseal cartilage is enlarged medially, such that the loss of height of the medial epiphysis is relatively minor compared to what would be expected radiographically.18 Bridging and irregularity of the growth plate can also be seen in late-onset tibia vara.19

Congenital and Developmental Disorders Epiphyseal or Patellar Hypoplasia Patients with a congenitally short femur have absence of an intercondylar notch and absent or hypoplastic cruciate ligaments (Figure 6–7).15 In children with hereditary onychodysplasia, MRI results show a patella that is very hypoplastic and ossifies later. Epiphyseal dysplasia, such as that present in multiple epiphyseal dysplasia or spondyloepiphyseal dysplasia, results in abnormalities in the signal intensity of the cartilage, as well as irregularity, fragmentation, and decreased size of the epiphyseal ossification center. Patients with dysplasia epiphysealis hemimelica (Trevor disease) have irregularity of the contour of the ossification center at the site of the epiphyseal osteochondroma and heterogeneity of the signal intensity of the overlying epiphyseal cartilage.16 Blount Disease In Blount disease, MR images can show numerous abnormalities suggestive of excessive stress in the medial compartment

Figure 6–7 MRI of an 8-year-old child with a congenitally short femur. Sagittal PD image shows a flat contour of the femoral condyles and absence of the cruciate ligaments. The intercondylar notch was hypoplastic.

Imaging of the Pediatric and Adolescent Knee

Trauma Acute Trauma Menisci

Figure 6–8 MRI of a 5-year-old child with Blount disease. Coronal gradient-recalled echo image of the knee shows loss of signal and irregularity of the medial tibial physis (arrow). The lateral tibial physis is slightly wide. Hypertrophy and increased signal intensity of the medial meniscus are present.

Discoid Meniscus

KEY POINTS The diagnosis of a discoid Discoid meniscus meniscus on MR images is 1. Bandlike or bulbous based on increased size and lack 2. Transverse diameter of tapering of the lateral menis>15 mm cus (Figure 6–9). Unlike the 3. Extension into middle normal meniscus, which has a or medial third of transverse diameter that does joint on mid-coronal not exceed 15 mm, a discoid sections meniscus will remain bandlike 4. 75% of all complete even close to the intercondylar discoid menisci have 20 notch. The number of consecmeniscal tears utive sagittal images in which 5. MRI: Poor sensitivity the bandlike appearance is seen for subtle cases depends on the thickness of the sections. Unlike the normal meniscus that tapers beyond its outer third, a discoid meniscus in the mid-coronal image can have a bandlike or bulbous appearance extending more than the usual third of the length of the femoral–tibial articulation. There is often meniscal degeneration, seen as diffuse increase of the intrameniscal signal intensity. On MR images, tears are seen in 75% of all complete discoid menisci and in 50% of all incomplete discoid menisci.21 The sensitivity of MRI for detection of discoid menisci can be as low as 40%,22 but the specificity is higher than 90%. Occasionally a discoid meniscus can be associated with hypoplasia of the lateral femoral condyle, hypoplastic tibial spines, increased lateral joint space, high-riding fibular head, and abnormalities of the menisci or vessels.

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KEY POINTS Meniscal tears 1. Usually vertical and peripheral 2. Bucket-handle tears common ACL tears 1. Discontinuity 2. Horizontal course 3. Increased T2 signal intensity Osteochondral injuries 1. Most common lesion 2. Usually in femoral condyles 3. Associated subchondral edema

The most common types of meniscal lesions in children are the vertical tears and peripheral detachments. Unlike in adults, horizontal tears are unusual, and a transverse, linear high signal within the meniscus usually represents a normal nutrient vessel. Instances of bucket-handle tears (a vertical longitudinal disruption in which the inner fragment is displaced toward the intercondylar notch) are frequent in the older child. The reported sensitivity and specificity of MRI for evaluation of meniscal lesions in children varies widely. A report of more than 600 patients younger than 16 years of age revealed a sensitivity of 79% for the medial meniscus and 67% for the lateral meniscus,22 and specificities of 92% and 83%, respectively. A more recent but smaller study showed the following statistics for sensitivity and specificity: medial meniscus, 92% sensitivity and 87% specificity; and lateral meniscus, 93% sensitivity and 95%.23 Older studies have shown sensitivities (80–85%) and specificities (88–100%) for meniscal tears similar to that in adults.10 Ligaments The mechanism of injury that disrupts the ACL in adults tends to avulse the tibial eminence (Figure 6–10) in children with an open proximal tibial physis. If there is an ACL tear, it most commonly occurs at the tibial insertion. However, the injury also may occur at the femoral attachment or within the mid-substance. As in adults, ACL injury frequently is associated with collateral ligament and avulsions at the tibial or femoral attachment. ACL tears are seen in approximately one fourth of MRI studies done for internal derangement of the knee in children 24 Primary findings of ligamentous tear include discontinuity of the fibers (Figure 6–11), usually in the mid-substance; abnormal course; and abnormal signal intensity. These primary signs of tear are more noticeable in the sagittal plane; proton density (PD) images show the best anatomical detail of the ligament, whereas T2-weighted images show increase in signal intensity in the region of the tear. The sagittal images can sometimes be difficult to interpret. It is important to search for additional evidence of discontinuity in the coronal images, where the region of the intercondylar notch shows absence of the fascicles of the ligament. When the anterior cruciate ligament is torn, it adopts a more horizontal course, and the angle between Blumensaat’s line and the ligament exceeds 15 degrees. The axial images can show the abnormal signal intensity in the fibers or the horizontal course of the ligament. Secondary signs of ACL tear include “kissing” subchondral contusions in the region of the femoral sulcus and in the

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Figure 6–9 Bilateral discoid menisci in a 14-year-old boy, as seen in coronal PD-weighted images of the right (A) and left (B) knees. The lateral menisci (arrows) are enlarged with respect to the medial ones, which should normally appear larger. There is also increased signal intensity on both menisci. C, Sagittal PD-weighted image of the lateral right knee shows a ribbonlike appearance of the lateral meniscus, which fails to taper normally.

posterior aspect of the lateral tibial plateau, forward displacement of the tibia, redundancy of the posterior cruciate ligament, abnormal angulation of the ACL, and uncovering of the posterior horn of the lateral meniscus. In children the most sensitive primary sign is the abnormal orientation of the ligament, and the least sensitive is the discontinuity. The most sensitive secondary sign is the subchondral bruising. Nearly 80% of children with ACL tears have associated meniscal tears and 25% have associated collateral ligament injuries.25 Osteochondral Injuries Osteochondral injuries are the most common abnormalities in older children and young adolescents referred to MRI for internal knee derangement; these injuries are seen in 34% of cases. These lesions occur most commonly in the femoral condyles and usually expose the subchondral bone. They are best seen using high-resolution fast spin-echo PD images,26 or SPGR imaging. MRI can detect osteochondral injuries of the patella that may be difficult to image with conventional radiography. The “patellar sleeve fracture” refers to a cuff of cartilage that is avulsed from the patella.27 The patient typically is 9–12 years of age and has an acute hyperflexion or deceleration move-

ment that causes rapid quadriceps muscle contraction. Radiographs can be normal or show a small, avulsed fragment in the inferior pole of the patella. MRI results show a more extensive injury involving the cartilaginous tip of the patella. The radiographic appearance of a patellar sleeve fracture can be confused with a multipartite patella, but ossification abnormalities have normal overlying cartilage on MRI. Physeal Injuries MRI depicts injuries to the physis and their ensuing complications: growth arrest and KEY POINTS deformity. In the acute setting, MRI can detect subtle MRI signs of occult phyinjuries of the physis (Figure seal fracture 6–12). MRI findings of subtle 1. Increased physeal injuries include increased phythickness seal thickness, increased physeal 2. Increased physeal T2 signal, a cleft in the phyT2 signal seal cartilage, and perichondral 3. Cleft in physeal disruption. The plane of the cartilage injury through the physeal carti4. Perichondrial lage may be of prognostic signifdisruption icance because fractures that

Imaging of the Pediatric and Adolescent Knee

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Figure 6–10 Fracture of the tibial eminence in a 13-year-old boy who experienced intense pain after a fall. A coronal fatsuppressed PD-weighted image shows that an osteocartilaginous fragment of the tibial eminence (long arrow) has been avulsed at the insertion of the anterior cruciate ligament (short arrows).

course through the zone of provisional calcification have a better prognosis than those involving the juxtaepiphyseal region of the growth plate.28 Bony bridges are best demonstrated with fat-suppressed SPGR imaging, which can depict the interruption of the signal from the growth plate indicative of bony bridging.29 This sequence also allows accurate calculation of the area of physeal bridging relative to that of the entire physis and the location of the bridge, which are important when deciding whether a bony bridge can be resected (Figure 6–13). KEY POINTS Bony bridges tend to occur in the areas of maximal physeal Patellar tendon abnorundulation, which is where the malities on MRI physis closes first.8,9 acute (fracture) Chronic Trauma Patellar Tendon Abnormalities Osgood-Schlatter disease (OSD) is an abnormality resulting from repeated avulsion of the ossifying tibial tubercle. The radiological diagnosis of OSD should not rely on the bony findings but rather on the soft tissue edema surrounding the patellar tendon

1. Separation at chon dro-osseous junction (patellar sleeve, tibial tubercle fracture) Chronic (OsgoodSchlatter and SindingLarsen-Johansson lesions) 2. Peritendinous high T2 signal intensity 3. Tendinous thickening 4. Bony fragmentation at insertion site

Figure 6–11 Images of anterior cruciate ligament tear in a 15year-old boy. A, A sagittal PD-weighted image obtained at the time of the fracture shows that the fibers are not detectable and that there is high signal intensity along the intercondylar notch. B, A sagittal PD-weighted image obtained after repair of the ligament shows the ligament (arrow) in the tunnel.

and obliterating the inferior angle of Hoffa’s fat pad. Although MRI is not needed for diagnosis, evidence of OSD can be found serendipitously during the evaluation of trauma or pain. OSD results in high signal intensity on T2-

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Figure 6–12 Occult physeal fracture in a 14-year-old boy with pain in the proximal tibia after a fall. A coronal PDweighted image shows that there is increased signal intensity and widening of the proximal tibial physis. The arrow shows disruption of the perichondrium in the lateral tibial physis.

weighted images at the insertion of the patellar tendon on the tibial tubercle. There is often adjacent bone marrow edema. Like OSD, the Sinding-Larsen-Johansson (SLJ) lesion is an overuse lesion; unlike OSD, SLJ occurs at the patellar insertion of the tendon (Figure 6–14). The MRI findings resemble those of OSD, with increased T2 signal intensity at the insertion of the patellar tendon and thickening of the tendon itself. Osteochondritis Dissecans The imaging considerations with KEY POINTS osteochondritis dissecans (OCD) differ from those in the adult, Poor prognostic findbecause children with open phyings: MRI ses have a higher rate of sponta1. Discontinuity of overneous resolution of OCD as comlying articular cartipared to adults. OCD of the distal lage femur occurs most frequently in 2. Large size of the the lateral non–weight-bearing subchondral bony portion of the medial femoral fragment or condyle. The lesion often extends fragments into the intercondylar notch and 3. High T2 signal is bilateral in approximately 33% intensity surrounding of children. MRI is used to assess fragment the integrity of the overlying articular cartilage, the size of the subchondral bony fragment or fragments, and the stage of healing. MR imaging findings include irregularity or fragmentation of the subchondral bone, flattening of the cartilage surface, thickening or increased signal intensity of the overlying cartilage, subchondral necrosis, and fluid surrounding the osteochondral fragment (Figure 6–15).30 A fragment is considered stable if it is continuous with the underlying bone. A fragment is considered unstable when there is a rim of high signal between the fragment and native bone noted on T2-weighted or gradient echo images. The accuracy of MRI for staging lesions can be improved more than twofold by interpreting a high signal T2 line between the

Figure 6–13 A 13-year-old boy with post-traumatic bony bridge developing in the distal femoral physis 10 months after a distal femoral physeal fracture. A, A coronal spoiled gradient-recalled echo image of the distal femoral physis, encased by the two parallel lines, shows that the high signal intensity of the cartilage is interrupted in the central portion. B, Axial map of the physis created by a maximal intensity projection of the data from the coronal image shows a central bony bridge of low signal intensity. White arrows outline the contour of the bridge, and black arrows outline the contour of the physis.

osteochondral bone and the parent bone as a predictor of instability only when it is associated with discontinuity in the overlying cartilage on T1-weighted images.31 Ultimately the unstable fragment becomes detached, and MR images can identify loose bodies within the joint. OCD sometimes can resemble an acute osteochondral fracture, or the developmental condylar irregularities of the distal femur that occur in children ages 2–12 (Figure 6–16). Some of the developmental irregularities of ossification and OCD may be different points on a spectrum of stress-related osteochondral lesions. Infection Osteomyelitis is seen most commonly in the metaphyses of the distal femur and the proximal tibia. Many of these

Imaging of the Pediatric and Adolescent Knee

metaphyseal infections around the knee secondarily involve the physis and can result in subsequent growth disturbance. Radiographs can demonstrate deep soft tissue swelling within 48 hours of the beginning of symptoms, but this is usually subtle, and more definitive signs of bone destruction become apparent only more than 7 days later. Scintigraphy is a useful modality for evaluation of osteomyelitis, and it is particularly useful in the context of the limping young child who is unable to localize symptoms.32,33 Sonography can be useful in detecting subperiosteal abscess and deep soft tissue swelling, but it does not show the primary marrow abnormality.34 MRI is more specific than scintigraphy and is the examination of choice when a high-resolution image of the area of infection is desired. MRI can detect complications such as an abscess in the bone or under the periosteum. Because the distribution of IV gadolinium will be the same as that of most antibiotics, an area that does not enhance after gadolinium administration is likely to be an abscess that will require drainage. Hence, the author of this text uses gadolinium in all the MRI studies for evaluation of infection. 35 Osteomyelitis of the distal femoral epiphysis, although uncommon, is the most common location for epiphyseal osteomyelitis. Epiphyseal osteomyelitis can be associated with septic arthritis,36

Figure 6–14 Stress injury related to the patellar tendon in a 9-year-old girl. A sagittal T2-weighted image shows high signal intensity and fragmentation of the inferior pole of the patella consistent with a Sinding-Larsen-Johansson lesion.

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which usually results in a large effusion with marked synovial enhancement. Arthritis Synovial disorders of the knee in children are best imaged with MRI.37–39 Synovial inflamKEY POINTS mation is best depicted with T2-weighted and gadoliniumImaging signs of arthritis enhanced T1-weighted images, 1. Accelerated maturawhereas cartilage erosion is best tion on radiographs seen with PD and fat-suppressed 2. Erosions spoiled gradient echo sequences. 3. Increased thickness Whereas normal synovium is of and enhancement of low signal intensity on all the synovium sequences, inflamed synovium a. Increased postdemonstrates intermediate signal gadolinium intensity on T1-weighted and T2enhancement weighted sequences. Inflamed (MRI) synovium is of lower signal intenb. Increased flow on sity than joint fluid on T2color Doppler weighted sequences. In children (sonography)

Figure 6–15 Osteochondritis dissecans of both femoral condyles in a 10-year-old girl. A, A sagittal PD-weighted image demonstrating irregularity and flattening of the posterior aspect of the condyle (arrow). The overlying cartilage is distorted but not discontinuous.

(Continued)

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Figure 6–16 Normal irregularity of ossification of the posterior lateral femoral condyle in a 7-year-old girl. A sagittal PDweighted image shows that there is subchondral fragmentation without irregularity of the overlying cartilage, or edema of the underlying marrow.

Figure 6–15—cont’d B, There is a high signal intensity halo at the osteochondral junction on the T2-weighted image. The medial condyle showed similar, less extensive findings.

there is no normal synovial enhancement, thus significant enhancement after IV gadolinium administration indicates synovitis.40,41 The degree of enhancement and the volume of synovium seen with gadolinium-enhanced MR images are markers of inflammatory activity and can help evaluate the response to therapy.42 Sonography can be a very useful and more accessible alternative to MR imaging for followup of synovial disorders. On color Doppler sonography, synovitis is detectable as an increase in synovial thickening and increased perfusion of the synovium (Figure 6–17).43 In juvenile rheumatoid arthritis a decrease in the volume and vascularity of pannus (on MRI or sonography) implies a favorable clinical outcome.44,45

Figure 6–17 Synovitis of the suprapatellar bursa in a 5-yearold girl. Sagittal color Doppler sonography of the suprapatellar region demonstrates fluid (asterisk) within the suprapatellar bursa. There is increased flow in the synovium surrounding the fluid. The arrow points to the distal femoral physis.

Tumor Fibrous cortical defects and non-ossifying fibromas are common around the knee and are detectable on radiographs in nearly half of children during growth. They are typically metadiaphyseal, lucent, well-corticated, elongated lesions that are based on the cortex on computed tomography or MRI studies. Symptomatic lesions at risk of fracture may show perilesional edema on MR images.

Chondroblastomas around the knee are subtle radiographically and can be unsuspected in a young adolescent who presents with chronic knee pain. The appearance on MRI is characteristic (Figure 6–18). A chondroblastoma in the knee will present only in the epiphyses of the femur, tibia, or fibula. It is a well-corticated lesion that calcifies in approximately half of the cases.46 Fluid–fluid levels are

Imaging of the Pediatric and Adolescent Knee

Figure 6–18 MRI of a 15-year-old adolescent with pain in the knee. A coronal gadolinium-enhanced T1-weighted image shows a well-defined epiphyseal lesion in the posterior aspect of the lateral tibial plateau (arrow). There is extensive surrounding edema. The lesion was found to be a chondroblastoma.

common, although not as prominent as in an aneurysmal bone cyst or a telangiectatic osteosarcoma. In nearly 75% of the cases, MRI demonstrates an extensive halo of inflammation in the marrow or adjacent soft tissues.47 The perilesional inflammatory reaction can be confused with that of an infection or an osteoid osteoma. The knee is also a likely location for many of the malignant bone tumors, such as osteogenic sarcoma, Ewing’s sarcoma, and lymphoma. Although a discussion of the imaging characteristics of these tumors is beyond the scope of this chapter, it is important to mention that on occasion patients with malignant tumors can present with vague symptoms and that the tumor may be discovered serendipitously during the evaluation of knee pain. On radiographs, signs of concern for malignancy include poor definition of the margins, cortical destruction, soft tissue mass, interrupted periosteal reaction, and tumor bone formation in the soft tissues. On MRI, clearly defined margins with the adjacent marrow, large areas of necrosis, cortical destruction, subperiosteal or soft tissue mass, skip lesions and tumor extension along the cruciate ligaments should arouse suspicion of a malignant bone tumor.48 References 1. Caffey J, Madell SH, Royer C, et al: Ossification of the distal femoral epiphysis. J Bone Joint Surg Am 40:647–654, 1958.

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2. Blickman JG, Wilkinson RH, Graef JW: The radiologic “lead band” revisited. AJR Am J Roentgenol 146:245–247, 1986. 3. Keats TE, Joyce JM: Metaphyseal cortical irregularities in children: a new perspective on a multi-focal growth variant. Skeletal Radiol 12:112–118, 1984. 4. Yamazaki T, Maruoka S, Takahashi S, et al: MR findings of avulsive cortical irregularity of the distal femur. Skeletal Radiol 24:43–46, 1995. 5. Resnick D, Greenway G: Distal femoral cortical defects, irregularities, and excavations. Radiology 143:345–354, 1982. 6. Jaramillo D, Shapiro F: Growth cartilage: normal appearance, variants and abnormalities. Magn Reson Imaging Clin N Am 6:455–471, 1998. 7. Varich LJ, Laor T, Jaramillo D: Normal maturation of the distal femoral epiphyseal cartilage: age-related changes at MR imaging. Radiology 214:705–709, 2000. 8. Ecklund K, Jaramillo D: Imaging of growth disturbance in children. Radiol Clin North Am 39:823–841, 2001. 9. Ecklund K, Jaramillo D: Patterns of premature physeal arrest: MR imaging of 111 children. AJR Am J Roentgenol 178:967–972, 2002. 10. Al-Otaibi L, Siegel MJ: The pediatric knee. Magn Reson Imaging Clin N Am 6:643–660, 1998. 11. Busch MT: Meniscal injuries in children and adolescents. Clin Sports Med 9:661–680, 1990. 12. Babyn PS, Ranson M, McCarville ME: Normal bone marrow: signal characteristics and fatty conversion. Magn Reson Imaging Clin N Am 6:473–495, 1998. 13. Laor T, Chun GF, Dardzinski BJ, et al: Posterior distal femoral and proximal tibial metaphyseal stripes at MR imaging in children and young adults. Radiology 224:669–674, 2002. 14. Jaramillo D: MR imaging of musculoskeletal trauma. In: von Schulthes GK, Zollikofer ChL (eds): Musculoskeletal Diseases. Milan: Springer-Verlag. 2001, pp 209–213. 15. Laor T, Jaramillo D, Hoffer FA, et al: MR imaging in congenital lower limb deformities. Pediatr Radiol 26:381–387, 1996. 16. Peduto AJ, Frawley KJ, Bellemore MC, et al: MR imaging of dysplasia epiphysealis hemimelica: bony and soft-tissue abnormalities. AJR Am J Roentgenol 172:819–823, 1999. 17. Craig JG, van Holsbeeck M, Zaltz I. The utility of MR in assessing Blount disease. Skeletal Radiol 31:208–213, 2002. 18. Ducou le Pointe H, Mousselard H, Rudelli A, et al: Blount’s disease: magnetic resonance imaging. Pediatr Radiol 25:12–14, 1995. 19. Arai K, Haga N, Taniguchi K, et al: Magnetic resonance imaging findings and treatment outcome in late-onset tibia vara. J Pediatr Orthop 21:808–811, 2001. 20. Connolly B, Babyn PS, Wright JG, et al: Discoid meniscus in children: magnetic resonance imaging characteristics. Can Assoc Radiol J 47:347–354, 1996. 21. Araki Y, Ashikaga R, Fujii K, et al: MR imaging of meniscal tears with discoid lateral meniscus. Eur J Radiol 27:153–160, 1998. 22. Kocher MS, DiCanzio J, Zurakowski D, et al: Diagnostic performance of clinical examination and selective magnetic resonance imaging in the evaluation of intraarticular knee disorders in children and adolescents. Am J Sports Med 29:292–296, 2001. 23. Major NM, Beard LN Jr, Helms CA: Accuracy of MR imaging of the knee in adolescents. AJR Am J Roentgenol 180:17–19, 2003. 24. Oeppen RS, Connolly SA, Bencardino JT, et al: Acute chondral injury of the knee: a common but unrecognized lesion in the immature skeleton. In: Society for Pediatric Radiology Meeting. Philadelphia: 2002. 25. Lee K, Siegel MJ, Lau DM, et al: Anterior cruciate ligament tears: MR imaging-based diagnosis in a pediatric population. Radiology 213:697–704, 1999. 26. Potter HG, Linklater JM, Allen AA, et al: Magnetic resonance imaging of articular cartilage in the knee. An evaluation with use of fast-spin-echo imaging [see comments]. J Bone Joint Surg Am 80:1276–1284, 1998. 27. Bates DG, Hresko MT, Jaramillo D: Patellar sleeve fracture: demonstration with MR imaging. Radiology 193:825–827, 1994. 28. Jaramillo D, Kammen BF, Shapiro F: Cartilaginous path of physeal fracture-separations: evaluation with MR imaging—an experimental study with histologic correlation in rabbits. Radiology 215:504–511, 2000. 29. Craig JG, Cramer KE, Cody DD, et al: Premature partial closure and other deformities of the growth plate: MR imaging and three-dimensional modeling. Radiology 210:835–843, 1999.

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30. Takahara M, Ogino T, Takagi M, et al: Natural progression of osteochondritis dissecans of the humeral capitellum: initial observations. Radiology 216:207–212, 2000. 31. O’Connor MA, Palaniappan M, Khan N, et al: Osteochondritis dissecans of the knee in children. A comparison of MRI and arthroscopic findings. J Bone Joint Surg Br 84:258–262, 2002. 32. Connolly LP, Treves ST: Assessing the limping child with skeletal scintigraphy. J Nucl Med 39:1056–1061, 1998. 33. Connolly LP, Connolly SA, Drubach LA, et al: Acute hematogenous osteomyelitis of children: assessment of skeletal scintigraphybased diagnosis in the era of MRI. J Nucl Med 43:1310–1316, 2002. 34. Cardinal E, Bureau NJ, Aubin B, et al: Role of ultrasound in musculoskeletal infections. Radiol Clin North Am 39:191–201, 2001. 35. Jaramillo D, Treves ST, Kasser JR, et al: Osteomyelitis and septic arthritis in children: appropriate use of imaging to guide treatment [see comments]. AJR Am J Roentgenol 165:399–403, 1995. 36. Azouz EM, Greenspan A, Marton D: CT evaluation of primary epiphyseal bone abscesses [see comments]. Skeletal Radiol 22:17–23, 1993. 37. Johnson K, Gardner-Medwin J. Childhood arthritis: classification and radiology. Clin Radiol 57:47–58, 2002. 38. Llauger J, Palmer J, Roson N, et al: Nonseptic monoarthritis: imaging features with clinical and histopathologic correlation. Radiographics 20 Spec No:S263–278, 2000. 39. Gylys-Morin VM: MR imaging of pediatric musculoskeletal inflammatory and infectious disorders. Magn Reson Imaging Clin N Am 6:537–559, 1998.

40. Murray JG, Ridley NT, Mitchell N, et al: Juvenile chronic arthritis of the hip: value of contrast-enhanced MR imaging. Clin Radiol 51:99–102, 1996. 41. Gylys-Morin VM, Graham TB, Blebea JS, et al: Knee in early juvenile rheumatoid arthritis: MR imaging findings. Radiology 220:696–706, 2001. 42. Ostergaard M, Stoltenberg M, Henriksen O, et al: Quantitative assessment of synovial inflammation by dynamic gadolinium-enhanced magnetic resonance imaging. A study of the effect of intra-articular methylprednisolone on the rate of early synovial enhancement. Br J Rheumatol 35:50–59, 1996. 43. Doria AS, Kiss MH, Lotito AP, et al: Juvenile rheumatoid arthritis of the knee: evaluation with contrast-enhanced color Doppler ultrasound. Pediatr Radiol 31:524–531, 2001. 44. Argyropoulou MI, Fanis SL, Xenakis T, et al: The role of MRI in the evaluation of hip joint disease in clinical subtypes of juvenile idiopathic arthritis. Br J Radiol 75:229–233, 2002. 45. Sebag GH: Disorders of the hip. Magn Reson Imaging Clin N Am 6:627–641, 1998. 46. Brien EW, Mirra JM, Kerr R: Benign and malignant cartilage tumors of bone and joint: their anatomic and theoretical basis with an emphasis on radiology, pathology and clinical biology. I. The intramedullary cartilage tumors. Skeletal Radiol 26:325–353, 1997. 47. Weatherall PT, Maale GE, Mendelsohn DB, et al: Chondroblastoma: classic and confusing appearance at MR imaging. Radiology 190:467–474, 1994. 48. van der Woude HJ, Bloem JL, Hogendoorn PC: Preoperative evaluation and monitoring chemotherapy in patients with high-grade osteogenic and Ewing’s sarcoma: review of current imaging modalities. Skeletal Radiol 27:57–71, 1998.

Chapter 7

Sports Physiology and Resistance Training Avery D. Faigenbaum

Resistance training has become a popular method of conditioning for enhancing the structure and function of muscle tissue and improving sports performance. In the 1950s and 1960s, track-and-field athletes recognized the benefits of resistance training, but athletes in other sports were slow to follow. Unfounded concerns that resistance training would result in a loss of flexibility or a decrease in movement speed swayed some competitors from participating in resistance training programs. As resistance-trained athletes began to gain dominance in the sports scene, it was soon realized that resistance training was a safe and effective method of conditioning for enhancing athletic performance and reducing the injury potential in adult athletes. More recently the effectiveness of carefully prescribed and supervised resistance training programs for children and adolescents has been accepted by medical and fitness organizations.1–3 This chapter examines the potential health and performance-related benefits associated with youth resistance training. Specifically, adaptations to resistance training that are observable in healthy children and adolescents will be examined and basic guidelines for program development that are considered important for enhancing sports performance and reducing the likelihood of injury in young athletes will be discussed. This information is particularly relevant because of the growth of youth sports programs and the increasing number of children and adolescents who engage in various forms of resistance training in schools, community programs, and sports training centers. Earlier reviews on this topic have described age- and sex-associated changes in skeletal muscle during childhood and the “trainability” of children.4,5 For the purpose of this chapter, the term resistance training is broadly defined as a method of physical conditioning that involves the progressive use of a wide range of resistive loads (light manual resistance to highintensity plyometric jumps) designed to enhance or maintain muscular strength, muscular power, local muscular endurance, and proprioception (sense of position). This

term encompasses a variety of training modalities including body weight, free weights (barbells and dumbbells), weight machines, elastic tubing, and medicine balls. In this chapter the term prepubescent children refers to boys and girls before the development of secondary sex characteristics (roughly up to age 11 in girls and 13 in boys) and the term pubescent adolescents refers to girls aged 12–18 years and boys aged 14–18 years. For ease of discussion the terms youth and young athlete refer to the child and adolescent. Potential Benefits of Youth Resistance Training Misperceptions associated with youth resistance training have slowly given way to a scientific understanding of its proper use and application. Research studies indicate that appropriately prescribed and competently supervised youth resistance training programs may offer observable health and fitness value to boys and girls.3,5 In addition to increasing muscular strength, muscular power, and local muscular endurance, participation in a youth resistance training program has the potential to positively influence cardiorespiratory fitness, body composition, blood lipids, bone mineral density, and selected psychological measures.6 A growing body of evidence suggests that carefully planned youth resistance training programs may also improve selected motor performance skills, enhance sports performance, and reduce the incidence of injury in sport.3,7 Motor Skills and Sports Performance Because many sports have a significant strength or power component, it is attractive to assume that a stronger and 63

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more powerful athlete will perform better. Several studies have indeed reported significant improvements in the long jump, vertical jump, sprint speed, and agility run time after participation in a youth resistance training program.8–10 However, because a couple of studies noted significant gains in muscle strength without significant improvements in motor performance skills,11,12 it seems that the question of training specificity must be addressed when designing youth resistance training programs. As previously observed in adults,13 it appears that training adaptations in children and adolescents may not only be specific to the movement pattern but also to the velocity of movement, contraction type, and contraction force. Youth resistance training programs that include relatively fast speed movements specific to the motor performance skill may be more likely to induce improvements than are programs characterized by slow speed movements. Can training-induced gains in motor performance skills improve the sports performance of young athletes? Although anecdotal reports from parents, coaches, and young athletes suggest that resistance training enhances athletic ability, scientific evidence supporting this claim is limited because sports performance can be influenced by a number of physical, emotional, and psychosocial factors. Studies have reported favorable changes in swim performance in age-group swimmers,14 and one study noted improvements in gymnastics.15 However, other studies failed to show any significant improvement in sports performance after resistKEY POINT ance training.16 At present, limited direct and indirect evidence Carefully planned resistsuggest that youth resistance ance training programs training will not have a negative have the potential to effect on sports performance and influence positively in all likelihood will result in selected health and some degree of improvement by performance measures enhancing a young athlete’s in children and physical fitness and general welladolescents. being (Box 7–1). Injury Reduction in Young Athletes One of the most important benefits of youth resistance training may be its ability to improve the preparedness of children and adolescents for the demands of sports

Box 7–1 Potential Benefits of Resistance Training for Young Athletes Increase muscle strength Increase muscle power Increase local muscular endurance Increase bone mineral density Increase cardiorespiratory endurance Increase flexibility Improve motor skill performance Improve body composition Increase resistance to injury Enhance mental health Improve sports performance

participation, therefore decreasing the likelihood that youths drop out of sports as a result of frustration, embarrassment, failure, or injury. Although there may be many mechanisms to potentially reduce sports-related injuries in young athletes, establishing fundamental fitness abilities (including preparatory muscle conditioning) as a prophylactic health measure should not be overlooked. Scientific evidence and clinical impressions support the concept that strong muscles, tendons, and ligaments are less susceptible to injury and recover faster when injured.7,17 Although the total elimination of sports-related injuries is an unrealistic goal, reducing the incidence of sports-related injuries with resistance training is a reasonable objective. Each athlete enters a sport with a quantifiable baseline level of musculoskeletal strength. If the baseline level of strength is equal to or greater than the demands required for practice and competition, the risk of injury is reduced, and the likelihood for improved performance is enhanced. However, if the musculoskeletal strength base is inadequate or ill prepared for the demands of practice and competition, injury and decreased performance may result. A review of prospective, controlled trials examining the effects of resistance training on injury rates in young athletes is provided in Table 7–1. For more than two decades, practitioners have been interested in the prehabilitative (opposite of rehabilitative) effects of resistance training. In 1982, Hejna et al. examined the impact of resistance training on high school male and female athletes and observed that athletes who resistance trained had a lower injury rate and required less time for rehabilitation compared with their teammates who did not resistance train.18 However, details of the resistance training program are limited, and an evaluation of athletic injury pattern by body part was not reported in this study. In a more recent report involving teenage European handball players, a conditioning program that included ankle disc exercises and plyometric training significantly reduced the incidence of injury during games and practice sessions.19 Because of the increasing incidence of knee injuries in young athletes, researchers have focused on strategies to enhance dynamic knee stability by resistance training. Cahill and Griffith conducted one of the first controlled trials involving adolescents to investigate the impact of an injury reduction program on knee injuries.20 They demonstrated that a 5- to 6-week preseason conditioning program, which included resistance training, aerobic conditioning, flexibility drills, and agility exercises, significantly decreased the number of knee injuries and the severity of knee injuries in male high school football players. More recently, Hewett et al. observed that a 6-week training program that included plyometrics significantly decreased potentially dangerous landing forces by improving body mechanics and increasing hamstring muscle strength and power in female high school athletes.21 In a follow-up controlled study, 6 weeks of preseason conditioning that included plyometric training and stability drills decreased the incidence of serious knee injuries in high school female athletes, with the incidence of injury being 2.4–3.6 times higher in the untrained group versus the

Sports Physiology and Resistance Training

65

Table 7–1 Prospective Controlled Studies: Exercise Training and Injury Reduction in Young Athletes Subjects Reference

N

Heidt et al., 200023 Hewett et al., 1999

22

Wedderkopp et al., 199919 Henja et al., 198218 Cahill et al.,197820

EX=42 C=258 EX=366 C=463 C=434 EX=111 C=126 EX=232 C=29 EX=— C=—

Training Mode

Training Period

M/F

Age (yr)

Results

F

14-18

WT, PY, SCD, CV, FX

7 wk

F F M F

HS

WT, PY, FX

6 wk

16-18

PR, PY

10 ms

MF

13-19

WT, CV

≤1 yr

DEC injuries in EX vs control* DEC injuries in EX vs C

M

HS

WT, AG, CV, FX

5-6 wk

DEC injuries in EX vs C*

DEC injuries in EX vs control* DEC injuries in EX vs C(F)*

AG, Agility exercises; C, control group; CV, cardiovascular exercises; DEC, decrease; EX, exercise training group; F, female; FX, flexibility exercises; HS, high school students; M, male; ms, months; PR, proprioceptive training; PY, plyometric exercises; SCD, sport cord drills; wk, weeks; WT, weight training exercises using free weights and weight machines; yr, year; —, not reported. * Statistically significant.

trained group (depending on what sports were included in the analysis).22 In another controlled trial, female high school soccer players who participated in a 7-week preseason conditioning program that included resistance training, aerobic conditioning, speed drills, and flexibility exercises had a significantly lower incidence of injury compared with the untrained group (14.7% versus 33.7%, respectively).23 The trained teenagers also had a lower percentage (2.4%) of anterior cruciate ligament injuries compared with the untrained group (3.1%), although this finding was not statistically significant. Collectively, these data provide supporting evidence of the protective effect of resistance training and justify the use of preseason conditioning programs for young athletes. At this time, however, it is difficult to assess how much the different features of the training program contribute to the total effect. Although many factors (e.g., lower extremity malalignment, joint laxity, hormonal changes, and prior training experience) appear to be responsible for the increasing incidence of knee injuries seen in female athletes,24,25 it appears that sports-related injures in female adolescent athletes are amenable to protective strategies that include resistance training. Interestingly, most studies did not use a classic resistance training design (e.g., one set of 8–12 repetitions on 8–10 separate exercises for the major muscle groups) but typically included plyometrics and other types of conditioning as part of a multifactorial training program that targeted neuromuscular deficiencies. Although no minimal or optimal intensity or volume of training has yet been established to reduce injuries in young athletes, a training duration of at least 6 weeks seems necessary. KEY POINT Clinical evidence and practice would seem to support the use of Multifactorial presearesistance training for these purson conditioning 26 poses in children, although the programs can reduce effectiveness of this type of intersports-related injuries vention during prepubescence in young athletes. has not yet been evaluated.

Factors in Program Design Resistance training can be one of the most potent and effective methods of conditioning for children and adolescents provided that the program is carefully designed and qualified instruction is available. Although there is no minimum age for participating in a youth resistance training program, participants should have the emotional maturity to accept and follow directions and should appreciate the benefits and risks associated with this mode of exercise. If a child is ready for participation in some type of sport activity (generally at age 7 or 8), then he or she may be ready to resistance train. A preparticipation medical examination is recommended for youth with known or suspected health problems, but it is not mandatory for apparently healthy boys and girls.3 Significant health and performance benefits can be gained from properly applying resistance training principles and understanding the uniqueness of children and adolescents. A fundamental tenet of resistance training is the overload principle, which states that the neuromuscular system must be exercised at a level beyond that to which it is presently accustomed.27 Because a child with no resistance training experience will have a relatively large window of adaptation, any reasonable resistance exercise program with sufficient overload will result in large gains in muscle strength during the first few weeks of training. The rapid rate of gain typically observed during this initial adaptation period suggests that there is a dramatic increase in the neurological activation of motor units during this time.5 As training progresses, the window of adaptation begins to shrink and greater overload is needed to make continual gains. It is important that youth begin resistance at a level that is commensurate with their physical and cognitive abilities. Prescribing a program that exceeds one’s capabilities not only increases the risk of injury but also may undermine the enjoyment of the resistance training experience. Although the long-term goals of a youth and adult

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resistance training program may be the same (i.e., performance enhancement and injury reduction), the focus of youth programs should be on skill development and having fun. One of the most serious mistakes in designing a youth resistance training program is to prescribe a volume or intensity of training that exceeds a child’s capacity. Although it may be tempting to closely follow a training program described in a fitness magazine or research journal, each child must be treated as an individual and therefore the frequency, intensity, volume, and progression of training need to be carefully prescribed. Some participants with poor levels of fitness and relatively immature musculoskeletal systems may not be able to tolerate the same amount of exercise that some of their peers in the same training program can tolerate. This is where the art and science of developing a resistance training program comes into play, because the principles of training specificity and progressive overload need to be balanced with program variation to optimize gains, prevent boredom, and reduce the stress from overtraining. Before adding resistance training to a young athlete’s exercise plan, practitioners need to carefully evaluate the total exercise picture, which may include other forms of exercise (e.g., aerobic conditioning), free play, practice sessions, and several competitions per week. Because resistance training adds to the chronic repetitive stress placed on the less mature musculoskeletal system, resistance training should not simply be added to a youngster’s weekly exercise regimen, but sensibly incorporated into a multifactorial training program. In some cases young athletes may need to decrease the time they spend practicing sport skills to allow time for preparatory conditioning, because it is difficult to gain the specific benefits of resistance training without actually participating in a resistance training program. Furthermore, excessive training increases the risk of both macrotraumatic and repetitive microtraumatic injuries.28 Although no evidence indicates that resistance training programs are “riskier” than other sports and activities in which youths regularly participate,29 resistance training is a specialized method of conditioning that requires appropriate overload, gradual progression, and adequate recovery between exercise sessions. Youth resistance training programs should include KEY POINT proper instruction, correct exercise technique, a safe training Resistance training environment, and a slow but programs should be steady advancement from educaindividualized due to tion to progression to function, differences in physical because the development of and emotional maturity strength and neuromuscular peramong children and formance is very much a learned adolescents. skill (Box 7–2). Specificity of Training The principle of training specificity is one of the more important factors to keep in mind when designing resistance training programs, because the adaptations that occur in the neuromuscular system are specific to the

Box 7–2 General Plan for Developing a Youth Resistance Training Program Phase 1—Education Discover the benefits and risks associated with resistance training. Develop proper exercise technique with light loads. Understand the basic principles of overload and progression. Value the concept of a fitness workout, including warm-up and cool-down activities. Increase general strength of the major muscle groups. Phase 2—Progression Gradually increase the overload placed on the body. Perform weight-bearing exercises that require balance and stability. Monitor tolerance of exercise stress. Value rest and recovery. Phase 3—Function Continue to systematically increase training overload. Add proprioceptively challenging exercises. Incorporate sports-specific drills into the program. Periodize training to optimize gains, prevent boredom, and reduce injuries. Allow adequate recovery between training sessions.

muscle groups involved in the exercise, the type of muscle action, the movement pattern, and the velocity of contraction.27 Consequently, the more closely a resistance exercise mimics a specific sport action, the greater the carryover of strength and power to the sport action. Although conventional heavy resistance, slow velocity training on a single-joint exercise such as the knee extension will enhance one repetition maximum strength, training at higher velocities is required to optimize gains in jumping or sprinting ability.30 This does not mean that every exercise needs to be performed at a high velocity or that every training session needs to be more intense than the previous session, but over time the general stress or loading placed on the neuromuscular system must begin to match the metabolic and biomechanical characteristics of the sport activity. Therefore exercises used in a resistance training program need to be specific to the goal of the program. Although additional clinical trails are needed to determine the most effective types of resistance training for enhancing performance and reducing the incidence of injury in young athletes, current findings suggest exercise programs that include traditional resistance exercises (using free weights and weight machines) combined with plyometrics may be the best approach. General resistance exercises such as the dumbbell row, heel raise, and hamstring curl can be used to strengthen specific muscle groups. This may be particularly important for young athletes at increased risk of injury as a result of muscle imbalances between adjoining muscle groups.28 Data suggest that the increased prevalence of knee injuries in female athletes may be due, at least in part, to lower extremity muscle weakness.31 Thus general

Sports Physiology and Resistance Training

strengthening exercises, particularly hamstring exercises, should be included in the training program because strong hamstrings help to reduce anterior tibial displacement and potentially relieve anterior cruciate ligament (ACL) strain.31 In addition, because of the potential for lower back injuries in young athletes, general exercises to strengthen the abdominals and trunk extensors should be part of a resistance training program. Curl-ups, back extensions, and multidirectional exercises that involve rotational movements and diagonal patterns can be used to effectively strengthen the abdominals and lower back. Plyometric exercises are also needed to optimize performance and reduce the injury potential because these dynamic exercises duplicate joint velocity and angular movement associated with sport activity. Unlike most general resistance exercises, plyometrics train the body through dynamic exercises designed to link strength with speed of movement. This type of training typically includes hops, skips, and jumps that exploit the muscles’ cycle of lengthening and shortening to increase muscle power. Plyometric exercises start with a rapid stretch of a muscle (eccentric phase), followed by a rapid shortening of the same muscle (concentric phase). Although previously thought of as a method of conditioning reserved for adult athletes, current findings suggest that plyometric training can be safe and beneficial for youth provided the program is carefully planned.22,23 Plyometric exercises such as single leg hops and lateral jumps require more balance and stabilization than other types of resistance training.32 As such, these drills may result in more desirable changes in voluntary activation times and time to peak torque, which in turn may decrease muscle response time.33 This training adaptation may increase the ability of athletes to safely perform rapid and unexpected sport movements such as cutting and changing direction. Since noncontact ACL tears almost always occur during deceleration of the body while landing from a jump or planting a leg before cutting,25 exercises that emphasize force reduction and proprioception should be included in an injury reduction training program to train the appropriate feedback mechanisms. However, plyometric training programs need to be carefully prescribed because poor exercise technique, inappropriate progression, or inadequate recovery may result in injury. Progression to higher levels of plyometric training should be based on an athlete’s ability KEY POINT to perform a selected exercise correctly throughout the desired Resistance training range of movement. This is an adaptations are important concept to keep in specific to the type mind when training or rehabiliand intensity of tating athletes or nonathletes of training stress. any level. Periodization One of the most important developments in the design of resistance training programs has been advancements in concepts related to the periodization of training.

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Periodization generally refers to a systematic process of planned variations in the training program over time. The concept of periodization is based on Selye’s general adaptation syndrome, which proposes that after a period, adaptations to a new stimulus will no longer take place and may result in “staleness.”34 The general idea is to prioritize training goals and then develop a long-term plan that varies in volume and intensity throughout the training period. Along with a carefully developed exercise program, time for physical and mental recovery are incorporated into a periodized training plan.35 Periodically varying the training stimulus will optimize adaptations, reduce training plateaus, and decrease the likelihood of overtraining. 36 Although research studies comparing periodized and nonperiodized training protocols have not been performed in children or adolescents, training programs proven to reduce injuries in young athletes have followed KEY POINT a periodized model. For example, the 6-week conditioning The expectation that one program used by Hewett et al. training program will consisted of three phases during result in continual gains which time the young athletes is unrealistic because progressed from the technique training plateaus, borephase to the fundamental phase dom, and overuse and, finally, to the performance injuries can result. 22 phase. Restoration It is noteworthy that prospective resistance training trials that significantly reduced injuries in young athletes had a training frequency, on average, of 3 days per week. Too much recovery can initiate the detraining process, whereas a downfall of many resistance training programs for young athletes is not allowing for enough recovery between workouts (i.e., underrecovery). A reduction in performance and an increased risk of injury can result from poor programming characterized by frequent training sessions and competitions without adequate rest and recovery.37 Although observations from training studies suggest that young athletes who participate in carefully designed conditioning programs can tolerate high-intensity resistance training workouts, the key is not to “overdose” with prolonged periods of high-intensity and high-volume training sessions. It has been estimated that 10–20% of adult athletes who train intensely experience overtraining characterized by chronic decreases in performance and an impaired ability to train.38 Young athletes who train or compete year-round without adequate recovery are also at increased risk for overtraining. Even simple methods of restoration (e.g., selfmassage, sauna, contrast immersion baths, and recovery beverages) can enhance an athlete’s ability to recover from physical training and avoid injury.39,40 Providing an opportunity for physical and mental recovery should be considered an integral part of a young athlete’s resistance training program. Recovery (or rest) days need to be incorporated into the weekly training schedule and periods (weeks) of “active rest” should be part of the yearly

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training plan. The active rest period typically consists of low-intensity, low-volume resistance training or some other type of physical activity. Although the amount of restoration needed between exercise sessions may vary depending on the intensity of the training program and individual needs, adequate restoration will accelerate the adaptations to physical training and therefore reduce one’s injury potential. Because the greatest amount of delayed-onset muscle soreness results from lifting heavy loads (with eccentric muscle actions) and high-intensity plyometric jumping drills, a day of rest between workout sessions may not be adequate for all athletes. In addition, because girls mature sooner than boys, girls may be able to handle moderateto high-intensity resistance training workouts better than boys. Even though it is tempting to focus only on program design variables such as KEY POINT sets, repetitions, and exercise choice, it is important to realize Adequate rest and that what is done between exerrestoration are needed cise sessions can have a signifito fully benefit from cant impact on what is done resistance training. during exercise sessions. Preseason Conditioning There is a growing body of literature that highlights the benefits of preparatory resistance training for young athletes. Nevertheless, it seems that many youth limit their athletic participation to sports practice and competition rather than the development of fundamental fitness abilities (e.g., muscle strength, aerobic fitness, flexibility, and agility). Although some parents and coaches have argued that early sport specialization is the key to success, it now appears that participation in a variety of sports and activities is more related to later sports success than sports specialization.41 Not only does sports specialization discriminate against youth whose motor skills are not as well developed, but it may also result in acute (macrotrauma) and repetitive microtrauma or overuse injuries.42 Today, young athletes are often forced to train harder and longer to excel in sports, and in a growing number of cases it seems that their musculoskeletal system is ill prepared for the demands of sports practice and game situations. Not long ago, time spent in free play and physical chores helped to prepare the developing musculoskeletal system for sport. However, current findings suggest (1) that only approximately half of young people regularly participate in vigorous physical activity, (2) that daily enrollment in physical education classes continues to decline, and (3) that there has been a remarkable increase in the number of overweight children and adolescents in the United States.43,44 Unfit youth who participate in sports practice and competition without preparatory conditioning are an absolute set-up for injury because they lack the strength and proprioceptive skills to adequately perform sport drills. This is evidenced by the observation that most injuries to young athletes occur early in the sport season when they are less conditioned to tolerate the repetitive

stress from sports practice and competition. Participation in physical activity should not begin with competitive sports participation; rather, it should evolve out of preparatory conditioning and instructional practice sessions. During this time, young athletes at increased risk for injury because of muscle imbalances or poor muscle function can be identified and treated by physicians, trainers, and/or coaches. Additionally, athletes with a previous injury can be identified and treated so they fully regain their strength to avoid reinjury. The National Athletic Trainers’ Association (NATA) suggests that high school athletes engage in conditioning activities at least 6 weeks before the start of sport practice,45 and it seems reasonable to extend this recommendation to younger athletes as well. Other recommendations from NATA include a pre-participation physical examination, good nutritional practices, proper hydration, appropriate protective equipment, and a minimum of 15 minutes of warm-up before any game or practice. These recommendations may be particularly important for young athletes, who seem to be training harder and longer than before, yet may be consuming inadequate nutrients46 and getting insufficient amounts of sleep.47 According to some observers, the incidence of acute and overuse injuries sustained by youths could be reduced by 15–50% if young athletes were better prepared for sports practice and competition.7,28 Additionally, KEY POINT participation in a well-designed preseason conditioning program Preseason conditioning will enhance athletic performthat includes resistance ance. General preseason conditraining can help to sigtioning guidelines are outlined nificantly reduce injuries in Box 7–3. Detailed descripin youth athletes. tions of youth resistance training programs are available elsewhere.48,49

Box 7–3 Preseason Conditioning Guidelines for Young Athletes Begin conditioning at least 6 weeks before the season starts. Seek qualified instruction and supervision. Warm up before every exercise session. Develop a strength base with general resistance exercises. Incorporate neuromuscular training with plyometrics. Focus on developing proper exercise form and technique. Begin with low-intensity drills and gradually increase exercise intensity. Wear appropriate footwear, particularly when performing plyometrics. Exercise on nonconsecutive days to allow adequate recovery between workouts. If necessary, decrease sports training to allow time for preparatory conditioning. Systematically vary and progress the training program to optimize adaptations. Maximize gains by improving lifestyle habits (e.g., proper food choices and adequate sleep).

Sports Physiology and Resistance Training

Summary The benefits of youth resistance training extend far beyond an increase in muscle strength and include favorable changes in selected health and performance measures. Despite previous concerns regarding the safety and effectiveness of youth resistance training, clinical impressions and scientific evidence indicate that carefully planned resistance training programs may increase a young athlete’s resistance to injury and enhance sports performance. Although the precise mechanisms underlying the injury-reducing potential of resistance exercise have not yet been established, multifactorial training programs that include general resistance exercises and plyometric training appear to be most promising. Nevertheless, resistance training is a specialized method of conditioning that requires careful planning and qualified instruction. More research is needed to optimize training protocols designed to enhance performance and reduce the injury potential in children and adolescents. Future research should examine the mechanisms responsible for the reduced injury rates and identify the factors that may predispose young athletes to injury. Knowledge gained from research studies could reduce medical costs and have a significant impact on how practitioners prepare children and adolescents for a lifetime of physical activity and sport participation. References 1. American Academy of Pediatrics: Strength training by children and adolescents. Pediatrics 107:1470–1472, 2001. 2. American College of Sports Medicine: ACSM’s Guidelines for Exercise Testing and Prescription, 6th ed. Baltimore: Lippincott, Williams & Wilkins, 2000. 3. Faigenbaum A, Kraemer W, Cahill B, et al: Youth resistance training: position statement paper and literature review. Strength Conditioning 18:62–75, 1996. 4. Blimkie C: Age- and sex-associated variation in strength during childhood: anthropometric, morphologic, neurological, biomechanical, endocrinologic, genetic and physical activity correlates. In Gisolfi G, Lamb D (eds): Perspectives in Exercise Science and Sports. Indianapolis: Benchmark Press, 1989, pp 99–163. 5. Sale D: Strength training in children. In Gisolfi G, Lamb D (eds): Perspectives in Exercise Science and Sports Medicine. Indianapolis: Benchmark Press, 1989, pp 165–222. 6. Faigenbaum A: Strength training and children’s health. J Phys Ed Rec Dance 72:24–30, 2001. 7. Smith A, Andrish J, Micheli L: The prevention of sports injuries of children and adolescents. Med Sci Sports Exerc 25(suppl):1–7, 1993. 8. Flanagan S, Laubach L, De Marco G, et al: Effects of two different strength training modes on motor performance in children. Res Q Exerc Sport 73:340–344, 2002. 9. Lillegard W, Brown E, Wilson D, et al: Efficacy of strength training in prepubescent to early postpubescent males and females: effects of gender and maturity. Pediatr Rehabil 1:147–157, 1997. 10. Weltman A, Janney C, Rians C, et al: The effects of hydraulic resistance strength training in pre-pubertal males. Med Sci Sports Exerc 18:629–638, 1986. 11. Faigenbaum A, Westcott W, LaRosa-Loud R, et al: The effects of different resistance training protocols on muscular strength and endurance development in children. Pediatrics 104:e5, 1999. 12. Faigenbaum A, Zaichkowsky L, Westcott W, et al: The effects of a twice per week strength training program on children. Pediatr Exerc Sci 5:339–346, 1993.

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13. Sale D, MacDougall D: Specificity in strength training: a review for the coach and athlete. Can J Appl Sport Sci 6:87–92, 1981. 14. Blanksby B, Gregor J: Anthropometric, strength, and physiological changes in male and female swimmers with progressive resistance training. Austr J Sport Sci 1:3–6, 1981. 15. Queary J, Laubach L: The effects of muscular strength/endurance training. Technique 12:9–11, 1992. 16. Ford H, Puckett J: Comparative effects of prescribed weight training and basketball programs on basketball skill test scores of ninth grade boys. Percept Mot Skills 56:23–26, 1983. 17. Parkkari J, Kujala U, Kannus P: Is it possible to prevent sports injuries? Sports Med 31:985–995, 2001. 18. Hejna W, Rosenberg A, Buturusis D, et al: The prevention of sports injuries in high school students through strength training. Nat Strength Condit Assoc J 4:28–31, 1982. 19. Wedderkopp N, Kaltoft M, Lundgaard B: Prevention of injuries in young female players in European team handball: a prospective intervention study. Scand J Med Sci Sports 9:41–47, 1999. 20. Cahill B, Griffith E: Effect of preseason conditioning on the incidence and severity of high school football knee injuries. Am J Sports Med 6:180–184, 1978. 21. Hewett T, Stroupe A, Nance A, Noyes E: Plyometric training in female athletes: decreased impact forces and increased hamstring torques. Am J Sports Med 24:765–773, 1996. 22. Hewett T, Lindenfeld T, Riccobene J, et al: The effect of neuromuscular training on the incidence of knee injury in female athletes. Am J Sports Med 27:699–705, 1999. 23. Heidt R, Sweeterman L, Carlonas R, et al: Avoidance of soccer injuries with preseason conditioning. Am J Sports Med 28:659–662, 2000. 24. Brezzo R, Oliver G: ACL injuries in active girls and women. J Phys Ed Rec Dance 71:24–27, 2000. 25. Ireland M, Gaudette M, Crook S: ACL injuries in the female athlete. J Sport Rehab 6:97–110, 1997. 26. Faigenbaum A, Micheli L: Preseason conditioning for the preadolescent athlete. Ped Annals 29:156–161, 2000. 27. Pearson D, Faigenbaum A, Conley M, et al: The National Strength and Conditioning Association’s Basic Guidelines for the Resistance Training of Athletes. Strength Condition 22:14–27, 2000. 28. Micheli L: Preventing injuries in sports: what the team physician needs to know. In Micheli L, Smith A, Bachl N, et al (eds): F.I.M.S. Team Physician Manual. China: Lippincott, Williams and Wilkins, 2001, pp 12–27. 29. Guy J, Micheli L: Strength training for children and adolescents. J Am Acad Orthop Surg 9:29–36, 2001. 30. Hakkinen K: Training specific characteristics of neuromuscular performance. In Kraemer K, Hakkinen K (eds): Strength Training for Sport. Oxford: Blackwell Scientific, 2002, pp 20–36. 31. Hutson L, Wojtys E: Neuromuscular performance characteristics of elite female athletes. Am J Sports Med 24:427–436, 1996. 32. Potach D, Chu D: Plyometric training. In Baechle T, Earle R (eds): Essentials of Strength Training and Conditioning, 2nd ed. Champaign, Illinois: Human Kinetics, 2000, pp 427–470. 33. Lloyd DG: Rationale for training programs to reduce anterior cruciate ligament injuries in Australian football. J Orthop Sports Phys Ther 31:645–654, 2001. 34. Selye H: The Stress of Life. New York: McGraw-Hill, 1956. 35. Fleck S, Kraemer W: Periodization Breakthrough. New York: Advanced Research Press, 1996. 36. Fleck S: Periodized strength training: a critical review. J Strength Condition Res 13:82–89, 1999. 37. Fry A, Kraemer W: Resistance exercise overtraining and overreaching. Sports Med 23:106–129, 1997. 38. Raglin J, Barzdukas A: Overtraining in athletes: the challenge of prevention. ACSM Health Fitness J 3:27–31, 1999. 39. Siff M, Verkhoshansky Y: Supertaining. Denver: Supertraining International, 1999. 40. Yessis M, Trubo R: Secrets of Soviet Sports Fitness Training. New York: Arbor House, 1987. 41. Magill R, Anderson D: Critical periods as optimal readiness for learning sports skills. In Smoll F, Smith R (eds) Children and Youth in Sport: A Biopsychosocial Perspective. Madison, Wis.: Brown and Benchmark, 1995, pp 57–72. 42. Outerbridge A, Micheli L: Overuse injuries in the young athlete. Clin Sports Med 14:503–516, 1995.

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43. Styne D: Childhood and adolescent obesity. Prevalence and significance. Pediatr Clin North Am 48:823–854, 2001. 44. U.S. Department of Health and Human Services: Physical Activity and Health: A Report from the Surgeon General. Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, 1996. 45. National Athletic Trainers’ Association: Minimizing the risk of injury in high school athletics, 2002 (online at http://nata.org/publications/ brochures/minimizingtherisks.htm).

46. Ziegler P, Nelson J, Jonnalagadda S: Nutritional and physiological status of U.S. national figure skaters. Int J Sports Nutr 9:345–360, 1999. 47. Faigenbaum A, Mediate P, Rota D: Sleep needs of high school athletes. Strength Condition 24:18–19, 2002. 48. Bompa T: Total Training for Young Champions. Champaign, Ill.: Human Kinetics Publishers, 2000. 49. Faigenbaum A, Westcott W: Strength and Power for Young Athletes. Champaign, Ill.: Human Kinetics Publishers, 2000.

Chapter 8

Psychology of Sports Injury and Rehabilitation David Bendor

“I didn’t gain anything positive from this experience. . . There was no silver lining. . . I could have learned life’s lessons without tearing my ACL.”—Priya “I heard a ‘pop’ and I knew it was bad. . . I was a mess. . . It was a big thing that was going to change my life [forever].” —Cam

The start of the school year usually elicits moans and groans from millions of children and adolescents. Yet for those boys and girls involved in scholastic athletics, they cannot wait to lace up their soccer, football, and/or field hockey cleats and take part in practices and competitions in the cool, crisp fall air. As the winter months arrive, the cooler weather moves the competitions indoors, where hockey, basketball, and indoor track reign supreme. As the cold weather gives way to the milder spring evenings, it is time for these young athletes to head back outdoors as baseball, lacrosse, tennis, and softball games beckon. In addition to the bevy of athletic opportunities offered by the nation’s school systems, there are city and town sports leagues throughout the calendar year. In all it is estimated that 30 million children and adolescents participate in organized sports throughout the United States.1 The physiological benefits of athletic participation are well known, and their importance is underscored in this era of increasing childhood obesity. Perhaps not quite as well documented are the psychological benefits of participating in organized sports. Through sports participation these young children and adolescents acquire skills, gain understanding, and experience “life’s lessons” in ways that will serve them well throughout their lives. They learn the importance of good sportsmanship and how to win and lose gracefully. They enjoy healthy competition and learn the importance of trusting their teammates and peers. They form friendships that extend well beyond the playing fields. Clearly, the benefits of athletic participation are numerous. Unfortunately, as greater numbers of children and adolescents participate in sports, the number of sports-related injuries increases as well. According to a survey conducted

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by the Centers for Disease Control and Prevention (CDC), sports-related injuries in children and adolescents account for 2.6 million visits to the nation’s hospital emergency departments, for a cost of nearly $500 million annually.2 For persons aged 5–24 years, sports-related injuries account for nearly one fourth of the total injury visits to emergency departments.2 Boys 10–14 years of age had the highest rate of sports- and recreationrelated injuries treated in emergency departments—75.4 per 1000, compared with 15.4 per 1000 for the population overall. Males visit emergency departments twice as often as females.3 According to a 2002 study by Gotsch et al.,1 children and adolescents with basketball- and cycling-related injuries account for 900,000 visits a year—the most frequent sports-related injuries seen in emergency departments. Football- and baseball-related injuries account for 250,000 visits, while soccer injuries result in an additional 100,000. The CDC survey also found that for persons 5–24 years of age, other activities that frequently result in emergency department visits include gymnastics and cheerleading (146,000 visits), ice skating/roller skating and skateboarding (150,000 visits), and water and snow sports (100,000 visits each). More specifically, for males aged 10–19 years, football-, basketball-, and bicycle-related injuries were most common. For 10- to 19-year-old females, basketball-related injuries ranked highest.1 It should be noted that these numbers do not necessarily indicate a greater inherent danger for participating in one sport as compared to another; it may simply be that more people are participating in basketball, for example, than baseball. In comparison, injuries on the playground account for nearly 137,000 emergency department visits each year.2 Admittedly, however, the numbers of children and adolescents who are injured in sports-related activities is even higher. One must assume 71

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that many more of these injuries are not seen in emergency departments but are instead treated at home, at primary care providers’ offices, or at community health clinics.1 “I knew it was the end of athletics for a long time. If only I had just let [the opposing player] go by. If only [the coach] hadn’t put me in [the game] at that moment.”—Priya “I got angrier and angrier. . . For four months I was miserable. I was breaking things, throwing things . . . I put my fist through a window.” —Cam

KEY POINTS 1. Approximately 30 million children and adolescents participate in organized sports throughout the United States. 2. There are psychological benefits of sports participation. 3. Participating in sports leads to many injuries, ranging from serious to those that can be treated at home.

Until recently the psychological effects of sports injury and rehabilitation received very little scientific or clinical attention. Mainwaring attributes this to the lack of a sound theoretical base from which hypotheses could be generated and tested.4 In trying to conceptualize how athletes experience severe injury, psychologists have historically turned to “stage models” originally drawn from theories of death, dying, illness, and stress. In her seminal book On Death and Dying, Elisabeth Kübler-Ross describes a five-stage grief response that individuals go through when they are told that they have a terminal illness.5 Kübler-Ross identified the five stages, of grief as denial, anger, bargaining, depression, and acceptance. In the first stage, the dying individuals enter a temporary (usually) state of shock upon hearing the news. They may also deny the seriousness of their condition. This stage is typically a comparatively brief one and they next move to the stage of anger—at themselves and all those around them. In the bargaining stage, the individuals use magical thinking, wherein they attempt to postpone the inevitable death by negotiating with that which will claim their lives (e.g., “If you’ll just allow me to live to see my daughter marry”). In the fourth stage, the individuals become depressed. They have come to the realization that they have no control over the situation, that they cannot bargain their way out of the inevitable, and thus their displaced anger gives way to feelings of depression. In the final stage, dying individuals have moved into acceptance. They are able to look back at their lives with contentment and prepare themselves to take care of what needs to be done before “moving on.”5 Heil offers a model in which the athlete recovers from injury by negotiating three cycles: distress, denial, and determined coping.6 His cycle of distress is replete with many of the same components Kübler-Ross proposed in her early stages: shock, anger, bargaining, depression, isolation, guilt, humiliation, preoccupation, and helplessness. In Heil’s cycle of denial, the athlete can vacillate from experiencing a sense of disbelief to a total inability to accept the seriousness of his or her injury. Finally, the phase of determined coping is highlighted by the athlete’s eventual ability to marshal the necessary resources that will aid him or her to progress through rehabilitation.7 Mainwaring notes that there is little empirical support for the application of any of these stage models to severely

injured athletes.4 Kübler-Ross developed her model while working with terminally ill patients, and many are now questioning how effectively one can apply the same model to injured athletes.8 A study by Udry et al.7 of injured elite skiers found only minimal support for the denial stage and no support for the bargaining stage. However, there was substantial support for the anger, depression, and acceptance components of the Kübler-Ross model. The study also found support for the distress and determined coping components of Heil’s model, although little support for his denial component.7 In the past decade or so psychologists have begun openly criticizing the application of stage models to athletic injury as being too linear and too generalized4 and therefore failing to account for the individual differences among athletes. However, the more recent cognitive appraisal models attempt to do so.9 Some examples of these models include Lazarus and Folkman’s transactional model of stress, Weiss and Troxel’s psychophysiological stress model, Rose and Jevne’s “Risks Model,” and Wiese-Bjornstal and Smith’s cognitive-emotional-behavioral model.9 The prevailing assumption in models such as these is that the way in which the injured athlete appraises the injury determines his or her emotional responses and, subsequently, his or her behavioral responses. These three factors—appraisal, response, and behavior—are continually influencing one another throughout the injury process.10 The thought is that injured athletes will respond differently to their injuries and subsequent rehabilitation processes, so there is little way of predicting what those particular responses will be, in what order they will manifest, and for how long. The debilitating effects of athletic injury, while indeed varying from athlete to athlete, usually intensify in direct proportion to the severity of the injury, the prognosis for full recovery, and the significance of KEY POINTS the sport’s place in his or her life. As with most clinical popula1. There has been little tions, athletes will often respond scientific or clinical quite differently to a sports-related study of sports injury injury and the subsequent rehabiland rehabilitation, itation process. What is important although some psyis not so much recognizing what chologists have theoretical stage or phase of applied existing response to injury the athlete is in, “stage” models. but simply recognizing the emo2. Psychologists have tional responses the individual is recently criticized the presenting. Mainwaring’s research application of stage has found that the reaction to models to athletic sports injury involves “simultaneinjury for lacking ous and interrelated cognitive, empirical support and affective, behavioral, physiologiovergeneralizing. cal, and social reactions to the 3. Recent “appraisal” trauma.”4 models attempt to “I don’t like to wear skirts because of the scars. I can’t wear heels. I’ll never be 100% again.”—Priya “What did I do to deserve this? Why me? You feel like you’re letting everyone down.”—Cam

individualize injured athletes. 4. Using these models is less important than understanding the individual’s unique emotional response.

Psychology of Sports Injury and Rehabilitation

For children and adolescents in particular, issues around athletic identity and (overall) self-identity can arise after a sports injury. Athletic identity is the part of the athlete’s selfidentity that obtains validation and meaning from participation in sports participation. The amount that athletic identity contributes to the overall self-identity is directly related to the level of commitment, involvement, and meaning that the athlete derives from sports.11 From childhood through late adolescence, bonding with teammates on and off the field, experiencing healthy competition, and learning to lose and win appropriately are all important developmental milestones that are facilitated by active participation in organized sports. When an injury tears an individual away from his or her beloved sport, the effects can be crippling. The entire process of sustaining an injury and facing the prescribed rehabilitation can be quite disorienting because the athlete is thrust into a world that he or she does not recognize. Paradoxically, assistance offered by coaches, teammates, and family members with the best of intentions is often perceived negatively for drawing unwanted attention to the individuals’ ailment. The injury means the athlete is no longer able to satisfy his or her athletic needs. Athletic identity, which comprises a significant piece of the individual’s overall self-identity, is now damaged or destroyed.11 No longer assured of his or her place on the team or sure of his or her sports-based friendships, the athlete may question his or her importance, obsess over disability, become depressed, and suffer a crisis of identity. Taylor and Taylor11 point out that the traumatic experience of a sports injury can be so negative and intense that the psychological distress “not only impairs rehabilitation but also may interfere with general psychological and emotional health as well as normal daily functioning.” It is not uncommon to see elevated levels of depression, tension, and anger in injured athletes with intense rehabilitation in their futures. Additionally, Heil wrote of the cognitive distortions first identified by Aaron Beck that are prevalent in the injured athletes.6 These athletes may engage in (1) catastrophizing, in KEY POINTS which they exaggerate the severity of the injury; (2) overgeneral1. Injured athletes can ization, in which they incorface athletic identity rectly extend the impact of the and self-identity injury to aspects of playing abilissues after the ity or daily behavior not likely sports injury. to be affected; and (3) per2. The injured athlete’s sonalization, in which athletes psychological distake on undue personal responsitress can lead to bility for injury or give the injury anger, tension, and some exaggerated special meandepression. ing in relation to themselves. “The rehab was really painful. I’ve done everything I was supposed to do and it’s [the knee] still not back to normal.”—Priya “Rehab is a roller coaster. That ‘no pain, no gain’ doesn’t work. That’s the worst physical pain I ever had.”—Cam

The negative psychological impact of a sports injury must be taken into account as the athlete heads into a rehabilitation that is 75% psychological and 25% physiological.12

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Numerous studies have found that athletes approach rehabilitation with a fairly positive, problem-solving, and goal-oriented outlook.4,6,7 Yet particularly for young athletes, for whom their ability to perform effectively in their beloved sport is positively correlated to their sense of self, the emotional responses to the injury and rehabilitation must be addressed.12 This applies to athletes for whom the goal of rehabilitation is to expedite their return to the playing field, or to prepare them for a future in which athletics will not be as central. A study by Larson et al.13 in which 90% of the athletic trainers surveyed—typically the primary health care professionals treating injured athletes—reported it was “relatively important” or “very important” to treat the psychological aspect of an athletic injury additionally supports this concept. Psychologists should expect to encounter a host of mood disturbances such as frustration, irritability, anhedonia, confusion, anxiety, anger, and depression. Psychologists working with injured athletes should expect to draw on their clinical skills, demonstrating empathy, understanding, and emotional support for the individual. Trainers and physical therapists may be unsure as to whether the athletes they encounter are simply having a down day or are spiraling toward depression. According to Taylor and Taylor,11 a referral can be considered appropriate if the athlete presents with symptoms of psychological distress, the symptoms are evident outside of rehabilitation, and the symptoms persist for several days. The symptoms to be vigilant for may include depression, anger, stress, anxiety, reports of family difficulties, substance abuse, weight problems, exercise addiction, and difficulties maintaining adherence.11 Admittedly, athletes can be quite apprehensive about the usefulness of seeing a “shrink” or any other mental health provider. A psychoeducational approach discussing the significance of psychological issues that may arise in rehabilitation and the psychologist’s role in addressing those issues can help alleviate skepticism and facilitate acceptance.11 The sport psychologist can play a major role in enhancing the injured athlete’s confidence and sustaining his or her motivation throughout the rehabilitation. Taylor and Taylor11 recognize four types of confidence that have an impact on injured athletes’ recoveries: program, adherence, physical, and return to sport. They define program confidence by how strongly an athlete believes his or her prescribed rehabilitation program will help him or her fully recover. The treatment team can enhance the athlete’s program confidence by demonstrating confidence in the efficacy of the program and by increasing familiarity, predictability, and control with rehabilitation education. Adherence confidence accounts for the athlete’s belief that he or she can indeed successfully complete the rehabilitation program. The physical confidence is understood to be the confidence the athlete has in his or her body being capable of handling the demands placed upon it in rehabilitation, in training, and ultimately in competition. Finally, the returnto-sport confidence measures to what extent the athlete believes in his or her abilities to return to, meet, and/or surpass his or her previous level of performance.11 Brewer et al. outlined activities the sports psychologist can engage in with the athlete.14 Initially, the psychologist should make an assessment of the injured athlete. The results of the assessment will help inform the treatment team as to

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which psychological interventions are warranted. Second, the psychologist can serve as a conduit between the sports medicine physician and the injured athlete. The psychologist can help to ensure that the athlete understands the nature of injury and the prescribed course of rehabilitation. The psychologist can also assist in the athlete’s “coming to terms” with what lies ahead. Additionally, the sport psychologist can teach the injured athlete basic psychological skills such as relaxation training, imagery training, cognitive restructuring, and goal setting to use as tools throughout his or her upcoming ordeal. Relaxation techniques can help the athlete reduce anxiety in times when the stressors associated with injury feel overwhelming. Psychologists teach imagery training as a way for the athlete to maintain the sharpness of the mental aspects of his or her sports, thereby facilitating a speedier return to the playing field. Cognitive restructuring is taught as an efficacious means of replacing defeatist self-talk that may only contribute to psychological suffering. Finally, an experienced sport psychologist should develop a comprehensive goal-setting program that will provide direction and motivation to the injured athlete.11 Goal-setting is used to motivate the injured athlete toward achievement of rehabilitation objectives and to instill an increased sense of confidence and self-mastery.14 Motivation is a critical psychological factor that directly affects the day-to-day aspects of rehabilitation. Without proper motivation, the athlete is in danger of failing to recover as fully, psychologically and physically, as he or she might.11 Research by Granito found that it appears as though boys and girls respond similarly to injury.10 Nonetheless, sport psychologists must be aware of some existing gender differences when working with injured sports athletes. The study found that female athletes perceive their KEY POINTS coaches to be far less supportive following their injuries as com1. Psychological pared to their male counterparts. aspects of sports In addition, injured female athinjury should be letes are more concerned with treated. how their sports-related injury will 2. Trainers and physical affect their long-term overall therapists may not be health. Male athletes are often prepared to treat the more pressured by their teammates psychological to return to play, and by their aspects and should coaches to play through the be prepared to refer pain.10 Sport psychologists need to the injured athlete be attuned to these potential difto a mental health ferences and should be prepared to professional. work with the athletes’ concerns. 3. A sport psychologist “You learn how important things are and how important people are. I talked to friends about playing ball and how tough it was going to be. . . Your best friends are what get you through it. I’ll always have [their] support.”—Cam

can strengthen the injured athlete’s confidence and motivation during rehabilitation. 4. Psychologists should be aware of gender differences when treating injured athletes.

Perhaps most critical to the young athlete who is in the midst of rehabilitation is the degree to which he or she experiences social and emotional support from family, teammates, and friends. The two student athletes we interviewed—whose quotes are seen throughout this

chapter—emphasized repeatedly the importance of having good social supports in place throughout their ordeals. More than once Cam tearfully recounted the touching, steadfast support he received from teammates on his football, hockey, and lacrosse teams. Although Priya felt more removed from the basketball team after her injury (“Everyone’s life went on and I was stuck with this knee”), she nonetheless scheduled her physical therapy around her team’s games so she could attend in person and at least be around familiar and supportive faces. Both of these young athletes admitted that the rehabilitation process would have been far more grueling without the support of their family, friends, and teammates. Numerous factors (e.g., severity of injury, resilience) will influence the extent of uncertainty and loss an athlete experiences after an injury and to what degree or he she will depend on the support of others as he or she embarks on what could be a difficult rehabilitation program. The sport psychologist can assist in facilitating the social support available to the injured athlete. The role of facilitator is especially important when the novelty of the athlete’s injury begins to wear off and he or she begins to feel more forgotten and alone.15 Taylor and Taylor11 describe two general types of social support that the athlete requires during rehabilitation: emotional and technical. Emotional social support consists of listening, challenging, supporting, and sharing social reality (e.g., others with similar priorities, values, perspectives, and experiences). Technical social support comprises technical appreciation and technical challenge. Those with an intimate understanding of the rehabilitation process can acknowledge KEY POINT and appreciate when an achievement has been made and provide The athlete is helped by this type of social support. social and emotional supAdditionally, they are able to port from family, friends, challenge (or “push”) the injured and teammates. The athlete to achieve even more and sport psychologist can be creative in how he or she facilitate this support. approaches rehabilitation. Injured athletes comprise an at-risk population for which there is a need for a psychologically minded approach to both early intervention and long-term rehabilitation.6 An ideal treatment regimen consists of a multidisciplinary approach that first assesses the psychological and physiological damage incurred. After the initial assessment, the treatment team works together to design an effective program that will address the medical and psychological issues. A psychologist will be needed to address the psychological issues directly related to the actual injury, as well as those that arise thereafter, and possibly those that existed previously. Although further research is needed to more clearly define psychology’s role in the treatment process, there can be no doubt that effective recovery and rehabilitation must include psychological as well as physical interventions. References 1. Gotsch K, Annest JL, Holmgreen P, et al: Nonfatal sports- and recreationrelated injuries treated in emergency departments. MMWR Morb Mortal Wkly Rep 51:736–740, 2002. 2. Burt CW, Overpeck MD: Emergency visits for sports-related injuries. Ann Emerg Med 37:301–308, 2001.

Psychology of Sports Injury and Rehabilitation

3. Tucker ME: Nonfatal injuries. (Pediatric Briefs). Pediatr News 36:3, 2002. 4. Mainwaring LM: Restoration of self: a model for the psychological response of athletes to severe knee injuries. Can J Rehab 12:145–156, 1999. 5. Kübler-Ross E: On Death and Dying. London: MacMillan Ltd, 1969. 6. Heil J: Psychology of Sport Injury. Champaign, Ill.: Human Kinetics Publishers, 1993. 7. Udry E, Gould D, Bridges D, Beck L: Down but not out: athlete responses to season-ending injuries. J Sport Exerc Psychol 19:229–248, 1997. 8. Rose J, Jevne R: Psychosocial processes associated with athletic injuries. Sport Psychol 7:309–328, 1993. 9. Quinn AM, Fallon BJ: The changes in psychological characteristics and reactions of elite athletes from injury onset until full recovery. J Appl Sport Psychol 11:210–229, 1999.

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10. Granito VJ: Psychological response to athletic injury: gender differences. J Sport Behavior 25:243–259, 2002. 11. Taylor J, Taylor S: Psychological Approaches to Sports Injury Rehabilitation. Gaithersburg, Md.: Aspen Publishers, Inc, 1997. 12. Thompson TL, Hershman EB, Nicholas JA: Rehabilitation of the injured athlete. Pediatrician 17:262–266, 1990. 13. Larson GA, Starkey C, Zaichkowsky LD: Psychological aspects of athletic injuries as perceived by athletic trainers. Sport Psychol 10:37–47, 1996. 14. Brewer BW, Van Raalte JL, Linder DE: Role of the sport psychologist in treating injured athletes: a survey of sports medicine providers. J Appl Sport Psychol 3:183–190, 1991. 15. Ball DR: A pain in the brain: the psychology of sport and exercise injury. IDEA Health Fitness Source 20:38–47, 2002.

Chapter 9

Child and Adolescent Knee: Primary Care Perspective Pierre d’Hemecourt

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Anthony Luke

Primary care aims to encompass the comprehensive care of the patient using biological, psychological, and social models. The patient-centered approach used in primary care is different from other specialties, which may focus more on specific body systems. Some of the challenges faced by the primary care physician involve the uncertainty of the diagnosis, despite the practitioner’s efforts. The skills required of a primary care physician to identify a precise differential diagnosis include good history taking (by far the most important), followed by accurate physical examination. Evaluations are performed in various locations, such as on the playing field or in the office. Use of laboratory tests or diagnostic imaging help confirm one’s clinical suspicions. Understanding the sensitivities and specificities of the clinical tests and investigations for certain pathologies will help select the appropriate tests. Once the working diagnosis has been formulated, an effective management plan can be decided upon. Treatments and specialist referrals must be appropriate and timely depending on what pathologies the primary care physician suspects. Inevitably, healthcare professionals caring for young children will be confronted with knee pain in a musculoskeletally immature athlete. In this chapter we distinguish the patient’s complaints as (1) traumatic, (2) atraumatic, or (3) refractory in nature. Our aim with this chapter is to provide the reader with a practical, comprehensive approach to knee pain in the pediatric athlete from a primary care perspective. Readers can find more about management details in other chapters in this book. Epidemiology Sports injury rates have increased considerably over the last two decades. Sports injuries have been reported to account for 41% of all musculoskeletal injuries in 76

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Andrea Stracciolini

patients aged 5–21 years presenting to pediatric emergency departments.1 Recent investigations looking at changes in incidence over the past 15 years revealed that among patients aged 10–15, the injury risk increased from 1 in 78 for boys in 1983 to 1 in 22 in 1998. For females the increase was from 1 in 117 to 1 in 55 during the same years. The number of soccer- and rugby-related fractures increased by 52%. The main reason for these changes over time appears to result from increased organized sports participation.2 The patterns of injuries are changing in conjunction with the increase in sports participation at an early age, the growing influence of organized sports, and the continuous development of protective sports equipment. Micheli emphasizes the danger of organized sports dominance at an early age. Children may be exposed to inappropriate or excessive training by inexperienced or unqualified supervisors. This can result in sports settings that increase the risk of both overuse and acute injuries.3 Overuse or chronic injuries resulting from repetitive microtrauma are now the norm in caring for young athletes. Age and growth can determine the types of injuries encountered, especially between childhood and early adolescence. Osteochondral and chondral injuries are more frequent than meniscal and cruciate ligament problems in children younger than age 13.4 Physeal injuries are uncommon but do occur in the adolescent athlete. Although fractures of the distal femur and proximal tibia account for only 3% of overall physeal injuries, these account for the majority of bone-bridging complications and require early identification.5 With increasing demand on the lower extremities in sports, the knee becomes frequently injured. Knee injuries were seen most often in soccer.1,5 In a large series reviewing overuse injuries evaluated in an outpatient sports medicine setting, approximately a third of all injuries seen concerned the knee. The musculoskeletal disorders included patellar tendonitis, Osgood-Schlatter disease, patellar chondropathy,

Child and Adolescent Knee: Primary Care Perspective

and ligamentous sprains.6 The increasing frequency of overuse injuries emphasizes the importance of careful evaluation of malalignments predisposing young athletes to overuse injury caused by biomechanical reasons. Overuse injuries resulting from repetitive microtrauma manifest as bursitis, tendinopathy, stress fracture, chondromalacia patella, osteochondritis dissecans, and traction apophysitis and are more common in the lower extremity.7 Anterior cruciate ligament (ACL) injuries in the skeletally immature population are rising as the number of participants in contact sports grows. ACL injuries are disproportionately distributed in women participating in landing sports such as basketball and soccer.8,9 Studies looking at the incidence of injury in girls’ varsity basketball showed the largest percentage of injuries involved the ankle (31%), followed by the knee (19%). Knee injuries were by far the problems most likely to require surgery, and ACL injuries accounted for 69% of the severe knee injuries.10 Although males tend to incur a greater number of overall injuries playing soccer, the incidence of ACL injuries in female soccer players is significantly higher than for men.11 Speculation has attributed this discrepancy to hormonal influences, notch size, low hamstring–quadriceps ratio, quadriceps torque strength ratio, and KEY POINTS landing technique.12 As such, prevention of ACL injuries has 1. The total number of emphasized landing mechanics sports injuries is and muscular control. increasing. The true epidemiology of 2. The pattern of injuries acute and chronic knee injuries is changing, with more in young athletes is still an overuse knee injuries enigma because the literature is with increased repetilacking in epidemiological studtive training. ies of children’s sports injuries. 3. ACL injuries are on the Even so, keeping in mind the rise in young athletes, age, activity, and sex of the athespecially girls. lete, the data that does exist can 4. More epidemiological help us understand what injuries studies are needed. can and do occur.

anterior cruciate ligament with a torn medial collateral ligament, meniscus tear, or less KEY POINTS commonly, a dislocated patella. When the primary care provider History and physical has a clear understanding of the examination injury, some traumatic injuries 1. The distinction of traucan be managed appropriately matic versus atraumatic in the primary care setting. injury may be subtle. Alternatively, injuries that 2. Acute injury swelling inevitably require surgery and may be delayed from significant injuries to the growth the playing field. plates should be referred early. Mechanism of Injury The knee may sustain abnormal forces from hyperextension and hyperflexion in the sagittal plane. Torsion occurs in the axial plane. Varus and valgus forces involve the coronal plane. Direct blunt trauma may also be involved. These forces can be isolated or occur in combination to render specific injury patterns. ACL injuries may result from knee hyperextension with leg internal rotation or from knee flexion with leg external rotation and valgus forces.13 The athlete may describe various patterns such as a ski catching an edge on a fall, the knee buckling with landing in basketball or changing direction with the foot planted. A typical history includes an audible pop, with acute swelling that occurs within the first 12 hours. Posterior cruciate ligament (PCL) injuries are usually sustained from posteriorly directed forces on the tibia with the knee flexed.14 The mechanism for a patellar dislocation is typically a pivoting injury with femoral inversion on a planted foot. Tibial tuberosity fractures, rare though they may be, occur in the near-mature jumping athlete from large eccentric loads. Physeal injuries may be subtle with hyperextension, torsion, and axial loading (Figure 9–1).

Evaluation of Traumatic Knee Pain in the Primary Setting Using limited resources, the primary care provider is often required to evaluate the acute knee injury and determine its severity. The provider is confronted with concerns for macrotrauma to the osseous, cartilaginous, and ligamentous structures, including the growth plates. For the purposes of this text, traumatic knee pain is defined as a knee complaint related to a specific trauma or mechanism. The pain may be confused with an atraumatic injury when the traumatic event is poorly recalled. Conversely, atraumatic problems may be precipitated by minor traumatic events. The clinician must carefully investigate the mechanism of injury and the history for vague injuries and past complaints. The clinician then uses an organized examination and should understand the progression of examination findings that occur after injury. The swelling and spasm that arise with time may dramatically change the examination findings from the playing field to the office several days later. Associated injury patterns must be considered, such as a torn

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Figure 9–1 Salter-Harris classification of physeal injuries (types 1 through 5).

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Pain Focal pain may be helpful in establishing the injury. However, on the sidelines, the severity of pain may prohibit localization. Medial collateral ligament (MCL) sprains produce focal pain, whereas ACL injuries may be more diffuse. Physeal fractures may appear as a ligamentous injury. For instance, a distal femoral physeal injury may mimic an injury to the proximal MCL. Acute Swelling Acute hemarthrosis is intraarticular bleeding and associated swelling that occurs in the first day, often the first 6–8 hours of injury. This is differentiated from an effusion that may develop several days after an injury that produces synovial inflammation. The presence of an acute hemarthrosis suggests serious intraarticular pathology, including ACL tears, osteochondral fractures, tibial spine fractures, and patella dislocation.15

athlete. Compression with varus, valgus, and rotational forces may be applied with the knee in 30 degrees of flexion, which can be more sensitive in the immature athlete.16 Ligamentous laxity is evaluated with stress testing. The MCL and lateral collateral KEY POINTS ligament (LCL) are stressed with valgus and varus forces, Physical examination respectively, with the patient’s (after traumatic injury) knee flexed 20–30 degrees. The 1. Evaluate range of ACL is assessed acutely with motion. Lachman’s test and pivot shift 2. Evaluate intraarticutests. The PCL is evaluated lar fluid with ballottewith a posterior drawer test. ment of patella. ACL injury may also present 3. Evaluate with tenderness of the lateral patellofemoral joint line from a lateral meniscompartment. cus tear or anteromedial joint 4. Evaluate ligamentous tenderness from the distal ACL laxity. attachment. Imaging

Instability The sensation of instability often follows an ACL tear. However, it is not uncommon to confuse a patella dislocation or subluxation with an ACL tear, which may also produce a sensation of giving way. True ligamentous instability should be differentiated from giving way due to reflex muscle inhibition resulting from pain and causing “knee buckling.” Locking

KEY POINTS

Conversely, locking is a mechanical limitation of full extension or flexion and suggests a loose osteochondral fragment or a displaced meniscus tear. This should not be confused with pseudolocking in which the knee cannot be flexed from an extended position, which can be seen with MCL injuries.

History (after traumatic injury) Establish: 1. Mechanism of injury 2. Pain 3. Swelling 4. Instability 5. Locking

Physical Examination Examination of the acutely injured knee should proceed in an orderly pattern. Specific examination techniques have been covered in a previous chapter and will only be briefly referred to here. Range of motion should be assessed with full extension and flexion as tolerated. The knee is then evaluated for intraarticular fluid with ballottement of the patella. Palpation along the femoral and tibia physes is crucial to detect physeal fractures. A positive finding here will preclude any stress testing until these fractures have been excluded by special imaging techniques. The patellofemoral compartment is then evaluated, looking for tenderness with compression (osteochondral injury), tenderness over the medial retinaculum, and apprehension with lateralization (patella dislocation). Certain provocative maneuvers, such as a modified McMurray’s test, may elicit pain in the injured menisci. This can be difficult to elicit in the young

With a traumatic knee injury the provider must identify intraarticular versus extraarticular pathology (Table 9–1). This is determined clinically and aided with imaging. From a primary care perspective, plain radiographs are helpful in the acute traumatic event. These include the following views: an anteroposterior (AP) view, a notch view (to detect loose bone fragments and osteochondral fractures), a lateral view, and a patella axial view (Merchant or skyline to detect patella fractures and alignment). Oblique views may detect plateau fractures but are often not needed. The indications for obtaining knee radiographs include the inability to bear weight, the inability to bend the knee 90 degrees, fibular head tenderness, and patella tenderness.17 An effusion and physeal tenderness are also important. If one suspects a physeal injury, a comparison view is usually needed. Magnetic resonance imaging (MRI) is more useful and safe in this setting. With the suspicion of an intraarticular or physeal injury, MRI is helpful. However, in some situations the orthopedists may go directly to arthroscopy. Furthermore, the primary provider should recognize that some authors question MRI’s positive predictive value for a meniscal tear in the adolescent.18 In the setting of an extraarticular injury, MR images are not helpful (because they are managed conservatively), unless patella or quadriceps tendon ruptures are suspected or associated intraarticular pathology must be ruled out. Table 9–1 Traumatic Knee Injuries Intraarticular

Extraarticular

ACL/PCL

Collateral ligament injury (associated intraarticular injury) Bone and soft tissue contusion Traumatic bursitis Salter-Harris fractures (types I and II) Tendon tear

Meniscus Patella dislocation Osteochondral fracture Salter-Harris fractures (types III and IV)

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Management of Acute Knee Injuries

Patellar Fractures and Dislocations

The primary care provider may provide excellent care to the acutely injured knee once a careful analysis has eliminated the need for advanced care. The specifics of each injury, rehabilitation, and surgical management are dealt with in other sections of this text. Management details from the view of a primary care practitioner will be discussed here.

Acute pediatric fractures of the patella are uncommon, possibly because of incomplete ossification. An injury unique to the pediatric population is the patella sleeve fracture sustained with resisted extension. A distal patella osseous fragment pulls the periosteal sleeve distally, leaving the denuded patella retracted proximally. This may appear as a small distal patella avulsion and requires open reduction and internal fixation. Patella fractures may occur in later adolescence. Small, undisplaced fractures may be treated with an immobilizer, whereas a full transverse fracture may require internal fixation. Patellar dislocation is common in adolescence. It may be associated with malalignment, congenital anomalies such as patella alta, and musculoskeletal imbalance. In the acute setting, osteochondral fractures, rupture of the medial retinaculum with step off, and associated ACL injuries should be considered. These are indications for surgical intervention and require a careful examination to exclude them. In their absence, the first-time dislocation is temporarily immobilized for comfort and the patient is encouraged to do isometric quadriceps strengthening. This is followed by attention to biomechanics, including quadriceps strengthening while using a patellar tracking brace.

Physeal Injuries Distal femur Salter-Harris type II fractures are not uncommon in the adolescent athlete with hyperextension and torsional forces. A reduced fracture may be managed with an above-the-knee cast for 6–8 weeks and non–weightbearing for at least 2 weeks. Long-term monitoring is essential. Orthopedic consultation is often considered. Although rare, intraarticular fractures (Salter-Harris types III and IV) often need operative reduction and fixation.19 These may spontaneously reduce and be difficult to detect clinically. Proximal tibia physeal injuries are quite uncommon but are often intraarticular. These also require anatomical reduction. Care is needed to avoid missing neurovascular injuries. Proximal tibial tuberosity fracture is often an avulsion injury sustained with a sudden quadriceps contraction associated with jumping. This injury may be intraarticular or extraarticular. A child or adolescent with an intraarticular fracture will present with pain and hemarthrosis of the knee (Figure 9–2). This often requires internal fixation. The minimally displaced extraarticular fracture is usually treated with immobilization for 4–6 weeks. Tibial eminence fractures involve the ACL complex. The goal of treatment is a stable knee. Although these fractures have several classifications, open reduction and internal fixation should be considered if there is any instability on Lachman’s testing.

ACL and PCL Injuries ACL injuries occur with both contact and noncontact mechanisms. Although ACL injuries are predominantly a surgical problem, the primary care physician interacts in several essential roles. Certainly prevention starts at the primary care level. Particularly in the female athlete, preseason attention to hamstring strength, proprioception, and landing technique should be stressed.6 Surgical repair is the usual course for most high-demand athletes. However, rehabilitation may be appropriate in several scenarios, such as the developmentally immature athlete who has chosen to await skeletal maturity before surgical intervention. The young athlete must be willing to forego high-demand pivoting sports. If the athlete and family are unwilling to wait, physeal sparing surgeries may be considered. Another conservative situation is a partially torn ACL with no instability and a negative pivot shift. Here, early restoration of motion is followed by normalization of hamstring and quadriceps strength. The use of a functional brace is often helpful in returning to lower demand sports. In the case of a partial tear, return to pivoting sports should be delayed for 3–6 months.20 Injuries to the posterior cruciate ligament are sustained with forces directed posteriorly on the tibia with the knee in flexion. Associated injuries include the posterolateral corner and menisci. A hemarthrosis is usually absent in the isolated PCL tear. In the absence of bony avulsion, an isolated PCL tear is usually treated conservatively. Quadriceps strengthening minimizes the posterior shear of the tibia with a PCL-deficient knee. Meniscus Injuries

Figure 9–2 Salter-Harris type III fracture of the proximal tibia epiphysis.

Injuries to the meniscus are less common than in the adult. Nonetheless, they do occur and tend to be more peripheral. They may also be associated with abnormal morphology

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such as a discoid meniscus. Symptoms may include pain, swelling, and locking. Locking is manifested with intermittent or constant inability to extend the knee from a displaced meniscal fragment, which is often a bucket-handle tear. Diagnostically, MRI can be helpful but has its limitations in sensitivity and specificity in the child younger than age 12.14 The adolescent meniscus is more vascular and thus KEY POINTS more amenable to repair than Managing acute knee the adult, in which shaving is injuries usually applicable. Although The primary care most meniscus tears are surgical, provider may provide small (less than 5 mm) partial excellent care of the foltears may be managed with lowing kinds of acute activity restriction. Collateral Ligaments The MCL represents the most commonly injured ligament in the knee. It is damaged with valgus and/or external rotary forces. At the extremes of injury, they are associated with ACL, posteromedial capsule, and medial meniscus tears. Like all ligamentous tears, they may be quantified (see Technical Note 9–1). MCL sprains are almost always handled conservatively with early range of motion and strength. Isolated grades II and III sprains are stable and usually are treated with a hinged brace, along with rehabilitation. Isolated LCL sprains are not common. Conservative management is appropriate in the absence of associated injured structures, again with rehabilitation and possibly a hinged brace.

knee injuries: 1. Physeal fractures: treated with casting and immobilization, except in the case of intraarticular fractures, when operative reduction and fixation may be necessary 2. Patella sleeve fractures (unique to pediatric population): open reduction and internal fixation 3. ACL injuries: usually treated surgically 4. PCL injuries: usually treated conservatively 5. Meniscus injuries: surgery usually necessary 6. Collateral ligaments: almost always treated conservatively

Evaluation of Atraumatic Knee Pain in the Young Patient Differential Diagnosis For the purposes of this chapter, “atraumatic knee pain” is considered a knee complaint, with no specific trauma or acute mechanism of injury. Complaints often have longer duration of symptoms compared with acute problems, which usually occur days to weeks before a patient presents. However, it is not uncommon for minor traumatic events to precipitate an atraumatic syndrome, which may occur during intensive youth sports camps. Thus the initial differentiation of traumatic from atraumatic injury is not always clear. Because the differential diagnosis of atraumatic knee pain is large, it is helpful to categorize conditions by etiology. When considering the causes, the popular suggestion “when one hears hoof beats, think horses not zebras” usually holds, with common things being common. A major

concern of the primary care physician is to rule out rheumatic disease, malignancy, or other chronic pathology. This should be a priority in the decision-making process. General categories of atraumatic knee pain include mechanical, inflammatory, reactive, infectious, malignant, hematological, and referred pain. These categories are listed in Box 9–1. Box 9–1 Differential Diagnosis of Atraumatic Knee Pain Orthopedic 1. Structural Patellofemoral: patellar instability (patellar subluxation, dislocation), patellofemoral pain (lateral compression patellar syndrome) Internal derangement: meniscal injury, discoid lateral meniscus, ligament tear, plica syndrome, synovial tear, osteochondritis dissecans, osteochondral injury, synovial (osteo)chondromatosis 2. Overuse Muscle/tendon strain: hamstrings, gastrocnemius, popliteus, iliotibial band (ITB) friction syndrome, patellar tendinopathy (jumper’s knee) Bursitis: prepatellar, pes anserinus, ITB Apophysitis: Osgood-Schlatter disease, SindingLarsen-Johansson disease Stress fracture: femoral, tibial Other: hypermobility syndrome, fat pad syndrome, popliteal cyst (Baker’s cyst), fabellae syndrome, proximal tibio-fibular joint instability 3. Unidentified trauma (see Imaging Section or Table 9–1) Medical 1. Inflammatory (arthritis) a. Seropositive: JRA, systemic lupus erythematosus (SLE), juvenile dermatomyositis, scleroderma b. Seronegative: JSpA, juvenile psoriatic arthritis (JPsA), inflammatory bowel disease, Reiter syndrome c. Reactive: post-streptococcal arthritis d. Vasculitis: Henoch-Schönlein purpura e. Crystal arthropathy: pseudogout, gout f. Pigmented villonodular synovitis (PVNS) 2. Infectious a. Septic arthritis: Staphylococcus, Streptococcus, Gonococcus, others b. Brodie’s abscess c. Viral arthritis, toxic synovitis d. Lyme disease Tuberculosis, sexually transmitted disease (gonococcal, HIV) 3. Tumor a. Benign: osteoid osteoma, bone cysts, osteochondroma Malignant: leukemias, metastatic neuroblastoma, osteosarcoma, Ewing’s sarcoma, rhabdomyosarcoma 4. Hematological a. Hemophilia b. Sickle cell crisis 5. Idiopathic Refractory 1. Hip pathology 2. Spine pathology (nerve root impingement, disc, sacroiliac joint) 3. Nerve related (saphenous nerve entrapment) 4. Chronic pain syndromes (fibromyalgia, chronic fatigue syndrome) 5. Complex regional pain syndromes (reflex sympathetic dystrophy)

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Mechanical Mechanical or orthopedic structural problems are the most common pathologies. Patellofemoral pain is the most common cause of mechanical knee pain in this category. Excessive shearing and compressive forces on the surfaces of the patellofemoral joint result in pain. This is most often related to a number of biomechanical issues, including femoral anteversion, genu valgum, tibia varum, overpronation, and medial quadriceps weakness. Other mechanical problems include apophyseal injuries affecting the growth plate during the adolescent growth spurt. Common examples include Osgood-Schlatter disease (tibial tubercle apophysis) and Sinding-Larsen-Johansson syndrome (inferior pole of patella apophysis). This type of apophysitis is caused by overuse and often affects children aged 10–14 years who are involved in running and jumping sports. Athletes are affected more than the general population (21% versus 13%, respectively).21 Osteochondritis dissecans represents an injury to the articular cartilage and subchondral bone, which is often overlooked as a cause of atraumatic knee pain (Figure 9–3). Often the young athlete will give a vague history of a traumatic injury followed by a prolonged period of chronic knee pain and swelling. The majority of athletes have symptoms for as long as 8–15 months before the diagnosis is made.22 Another commonly overlooked mechanical injury is a stress fracture involving the distal femur or tibial plateaus. Inflammatory Conditions Inflammatory conditions include juvenile rheumatoid arthritis (JRA) and pediatric spondyloarthropathies (see Box 9–1). School-aged and adolescent athletes are most affected by poyarticular-onset JRA and type 2 pauciarticular arthritis.23 There is a wide spectrum of symptom severity in JRA, ranging from mild pain and swelling with minimal limitation in activity to deforming and incapacitating symptoms.23 Long-term medical treatment may be required depending on the type and severity of the arthritis. Early diagnosis and intervention are important to allow for normal growth and development. Juvenile-onset spondyloarthropathies (JSpAs) often affect males at approximately 10 years of age and occurs at an estimated rate of 2 per 100,000 in the United States24 and Canada.25 The JSpAs include the gastrointestinal-associated arthropathies, Reiter syndrome, and psoriatic arthritis. JSpA may present as an isolated arthritis, enthesitis, tendonitis, or dactylitis or as a clinical syndrome called seronegative enthesopathy and arthropathy (SEA).26 The majority of children with SEA syndromes will evolve into ankylosing spondylitis or another SpA over the subsequent decade.27 These children often will present with an asymmetric arthritis commonly involving the knee, mid-tarsal joint, and ankle.26 SpA should be suspected if there is a history of enthesitis affecting the Achilles’ tendon or insertion site of the plantar fascia to the os calcis. Infectious Etiologies Infectious conditions should always be considered when evaluating a patient with atraumatic knee pain with effusion. Septic arthritis and osteomyelitis are serious infections. A total of 5–8% of knee-pain patients have multiple joints

Figure 9–3 Osteochondritis dissecans of the medial femoral condyle.

involved.28 It usually results from an acute or subacute hematogenous source of infection but can also result from a break in the skin. Staphylococcus aureus bacteria is the most common cause.28 Neisseria gonorrhoeae is a sexually transmitted disease and is the most common cause of (polyarticular migratory) arthritis in adolescents. Infections must be ruled out in individuals with acute or chronic pain symptoms of unknown origin, especially if accompanied with symptoms of fever and malaise. Signs of acute septic arthritis are swelling, redness, heat, and pain in the affected joint. In comparison, osteomyelitis may cause constitutional symptoms without signs of joint infection. Infections must be treated immediately and may require surgical lavage, débridement and parenteral antibiotics. Reactive Arthritis Reactive arthritis can be a late complication of infection. Examples of infections causing reactive arthritis include Lyme disease, post-streptococcal arthritis, and enteric infections (Campylobacter, Clostridium difficile, Salmonella, and Shigella). Lyme disease classically presents with a history of a tick bite followed by an erythema migrans rash within days to weeks, although patients often lack the history of rash.29,30 The arthritis or arthralgia can be either monoarticular or oligoarticular and often is not painful. The knee is the most common joint affected (89%,30 90%31). Fortunately, the prognosis for children with Lyme arthritis who are treated with appropriate antibiotic treatment is excellent.31

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Malignancy and Hematological Conditions Malignancies can first present as arthritis caused by malignant cell infiltration of the structures surrounding the joint. Patients are typically ill32 and may have difficulty using the affected limb. One or many joints can be affected.32 Pathological fractures associated with benign or malignant lesions may present with sudden disability and severe pain. Osteosarcoma is often a metaphyseal lesion. Ewing’s sarcoma is more diaphyseal and is often present with fever and pain. Leukemia may cause an infiltrative process on the metaphyseal side of the growth plate. A complete blood count, erythrocyte sedimentation rate, and x-rays are often diagnostic. Hematological conditions can cause limb pain around the knee. Hemophilia most commonly manifests as joint swelling secondary to hemorrhage.33 In the adolescent age group, knee hemarthrosis is most common, followed by elbow hemarthrosis.34 Acutely, the joint may become warm, distended, and tender. Chronically, an effusion with thickening of the capsule may KEY POINTS develop with loss of range of motion as a result of erosion of Evaluation of atraumatic the cartilage, resulting in knee pain chronic arthropathy.34 Sickle 1. Rule out rheumatic cell crisis should be considered disease, malignancy, in an African-American athor other chronic lete whose pain is out of propathology. portion with what the clinical 2. General categories of findings demonstrate. When atraumatic knee pain dehydrated, the cells may include mechanical sickle, causing obstruction in (patellofemoral pain, the microvasculature, resultOsgood-Schlatter ing in bone infarcts. disease, SindingReferred Pain Referred pain must always be considered in the knee. A typical presentation of a slipped capital femoral epiphysis is medial knee pain. Sciatic pain may have skipped dermatomes and localized to the knee. History

Larsen-Johansson lesion, osteochondritis dissecans [OCD]), inflammatory (JRA, pediatric spondyloarthropathies), infections (S. aureus, septic arthritis, N. gonorrhoeae, and osteomyelitis), reactive arthritis, malignancy, hematological, and referred pain.

Pain Pain is the most common presenting complaint. Details sought out in the history include location, severity, duration, radiation, and aggravating and alleviating factors. Localizing pain and activity-related pain assist in determining the source of the pain and whether it is mechanical in nature. Pain with bending and squatting is often seen with patellofemoral disorders. A runner with lateral knee pain and clicking may have iliotibial band (ITB) friction syndrome. If pain is less localized and vague in nature, the differential diagnoses turn toward medical diagnoses. A history of pain is not a useful identifier of rheumatic disease. The neg-

ative predictive value of pain as a complaint is 0.91. This tends to be higher when pain is the only presenting symptom.35 It is important to remember that pain is a subjective response and may be affected by cultural and social factors. The pain associated with tumors is variable and often consists of severe pain with weight-bearing or throbbing pain that occurs at night or at rest. A patient with osteoid osteoma presents with persistent nocturnal pain alleviated with aspirin. Swelling Another common presenting complaint is swelling. Intraarticular versus extraarticular swelling should be determined. Intraarticular swelling suggests joint pathology (e.g., loose bodies, internal derangement, ligament injuries) or a proliferative synovium, either mechanical or inflammatory in nature. When pathological processes affect or damage extraarticular structures, swelling may develop. Malignancy and infection need to be differentiated from soft tissue problems, such as bursal, tendon, and/or ligament injuries. Red Flags Constitutional symptoms including weight loss, fever, chills, nocturnal pain, and pain at rest suggest an expanding pathological lesion. Unwillingness to use the leg, a limp, and/or a gait disturbance suggest aggressive pathology such as infection, fracture, or malignancy. Another important factor is the duration of symptoms. Patients with tumors of the knee often present with a history of chronic pain for more than 6 months before diagnosis.36 Similarly, the duration for diagnosis of JRA was 5.8 months +/− 8.8 months.35 These entities should be considered in athletes with unexplained knee pain for longer than 6 weeks. KEY POINTS Training Considerations History (after traumatic

Training errors are often injury) related to mechanical knee 1. Pain: Location, severpain in younger athletes. This ity, duration, radiaincludes a sudden increase in tion, aggravating and sports activity more than 10% alleviating factors per week. Summer youth 2. Swelling: sports camps are a prime Intraarticular versus example. Athletic specializaextraarticular tion requiring repetitive 3. Be alert to red flags motion (deep knee bends, 4. Training considerajumping, and running) withtions: Sudden out a break in activity to allow increases in duration, ample tissue recovery is a comfrequency, or intenmon training error. Improper sity of exercise equipment, including poor regimen athletic surfaces and shoes to address overpronation, represents possible sources of overload forces to the knee. Most activities require proper instruction and supervision by an experienced coach; for example, proper tackling technique in football or proper weightlifting technique. It is valuable to explore details on the type and technique of training, volume (duration and frequency), and the athlete’s understanding of injury prevention practices.

Child and Adolescent Knee: Primary Care Perspective

Physical Examination Observation Reproducing the patient’s symptoms in the office can be helpful in evaluating the patient with atraumatic knee pain. Assess knee alignment looking for variants of normal, including genu valgum, genu varum, and internal and external tibial torsion. Functional tests include gait, squatting, and hopping. Gait pattern is useful in evaluating knee pain when searching for a cause. An antalgic lurching gait may suggest hip pathology. Toe walking suggests tight heel cords and, less commonly, an underlying neuromuscular disease. Knee swelling is best assessed in the suprapatellar pouch, as well as in noting loss of the medial and lateral dimples around the knee. The patellofemoral joint can be examined while the patient is in the supine position. Patella tightness is manifested by inability to elevate the lateral patella border (patellar tilt test). Conversely, patellar subluxation is noted with excessive lateralization and may elicit apprehension (apprehension test). KEY POINTS In the sitting position, the menisci, femoral osteochondral Physical Examination surfaces, and plica of the 1. Use provocative and patient are easily palpated. The helpful tests to repropatella borders and tibial duce symptoms. tubercle are also best palpated 2. Assess overall in this position. alignment. A full musculoskeletal 3. Use functional tests examination should be persuch as gait analysis, formed if inflammatory arthritis squatting, and is a concern. Pain localizing to hopping. tendon insertions may suggest 4. Observe for swelling, enthesopathy. Flexibility assessdimples, and ment can identify hypermobildeformity. ity such as in Ehler-Danlos and 5. Localize the pain. Marfan syndromes. A detailed systems review including neurological examination should be performed. Investigations in Primary Care Imaging Studies Patients with unilateral knee symptoms lasting longer than 6 weeks or having suspected bone pathology should be imaged with x-ray technology. Certain radiographic features can help identify malignant processes, including an interrupted periosteal reaction, moth-eaten destruction of bone, and poorly defined margins.37 Computed tomography is still the imaging mode of choice for fractures and bone lesions. When symptoms are vague, a bone scan is a useful study to help localize the lesion with extreme sensitivity, although it lacks specificity. A bone scan may demonstrate pathology, even before MRI results show signs of edema.38 The bone scan can identify occult bone injury (including bone bruising), osteochondral lesions, stress fractures, benign and malignant bone tumors, as well as demonstrate increased bone metabolism and activity.

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Ultrasound is a useful diagnostic tool that is safe, economical, and offers a diagnostic alternative for musculoskeletal injuries. This test is highly operator dependent. Ultrasound is useful for visualizing superficial knee structures including muscles, bursas, popliteal cysts, ligaments (MCL, LCL), and tendons (patellar and quadriceps). Magnetic resonance imagKEY POINTS ing is now a commonly used diagnostic tool in sports Imaging medicine. MRI is best used to 1. A bone scan helps to evaluate the soft tissues about localize a lesion with the knee and is useful in vague symptoms. establishing the diagnosis in 2. Ultrasound is hemophilia, arthritis,39,40 and useful but variable tumors. MRI can identify because of operator internal derangements of the dependency. knee, including intraarticular 3. MRI is an excellent pathology, erosions in cartitool for soft tissue lage and bone, and inflamed imaging. synovium. Laboratory Studies Hematological studies, specifically a complete blood count (CBC), are often obtained and can be very useful. The white blood cell count and cell type are important, especially when infection or systemic tumors are suspected. Prothrombin time (PT) or INR (standardized PT) and activated partial thromboplastin time (APTT) are used to screen for coagulopathies. Erythrocyte sedimentation rate (ESR) and C-reactive protein are acute phase-reactants that become elevated in infection, inflammatory disorders, and some malignancies. These studies are useful when following the course of infections. A normal ESR is greater or equal to 15 mm/hr in children. Rheumatological laboratory tests useful for the primary care physician include ANA testing, IgM-rheumatoid factor (IgM-RF), HLA-B27, and other immunological testing.41 A high clinical suspicion should be present before ordering these tests. A positive RF test in the absence of clinical findings has poor predictive value for rheumatic disease. HLA-B27 is only useful in confirming a pretest clinical suspicion for spondyloarthropathy. Immunoblot testing for IgG and IgM antibodies to Borrelia burgdorferi in Lyme disease is the most reliable test, often confirming a preliminary enzyme-linked immunosorbent assay test for IgG antibodies. Polymerase chain reaction testKEY POINT ing for Borrelia sequences can also be checked from samples of Laboratory studies are synovial fluid.30 False-positive useful adjuncts when serology tests are of major conevaluating for inflammacern when performed in nontory disorders and endemic areas or in patients malignancies. with nonspecific symptoms.29 Arthrocentesis Joint aspiration techniques are similar to joint injection procedures (see Technical Note 9–1). For testing purposes, the joint fluid should be divided. The fluid is analyzed for the three Cs; cell count, culture, and crys-

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TECHNICAL NOTE 9–1

Injections About the Knee Michael O’Brien

Indications The knee is subject to several different types of injections. Intraarticular knee injections are generally used to deliver corticosteroids to relieve the symptoms of an inflamed joint (e.g., osteoarthritis, gout, pseudogout). The same techniques for injection can be used to aspirate an effusion, which assists the physician in distinguishing between infectious and noninfectious causes. Another indication for intraarticular injections is to deliver viscosupplementation therapy (e.g., Hyalgan GF 20). Other injections about the knee include delivering corticosteroid to the pes anserine bursa, distal iliotibial band (ITB), or the prepatellar bursa to treat inflammation. Contraindications for corticosteroid injection include overlying soft tissue infection, coagulopathy, and the possibility of septic arthritis. Intraarticular injections should be limited to 3–4 times in a year or 10 cumulative injections. Risks include subcutaneous fat pad atrophy, crystal synovitis, and superficial skin depigmentation. Injections into tendons may result in rupture. Setup For each of these injections, strict adherence to sterile technique is paramount. The point of entry may be marked with indelible ink or indented with the tip of the needle cap after careful location of landmarks. Prep the area with an iodine agent (assuming no allergy) and then wipe with

alcohol before making any injections. The most common anesthetics used in the injection solution are 1% lidocaine (Xylocaine) or 0.25% or 0.50% bupivacaine (Marcaine). The steroids are betamethasone (Celestone) 6 mg/ml or methylprednisolone (Depo-Medrol) 40 mg/ml. Superficial anesthesia can be achieved with subcutaneous injection of an anesthetic (25-gauge needle) or by using ethyl chloride spray on the skin. Technique Intraarticular Injections: A 10- to 60-ml syringe can be used on a 1.5-inch 18- or 20-gauge needle to withdraw synovial fluid. (to confirm placement of the needle in the joint space, drain an effusion, and obtain fluid for analysis). Once you withdraw synovial fluid, leave the needle in place and replace the syringe with the solution to be injected. A hemostat may be used to hold the needle in place. Injecting the contents of the syringe should be easy with no resistance. Resistance suggests the injection is going into bone or soft tissue rather than the joint space. Typically, 1 ml of steroid with 9 ml of anesthetic is used. Lateral Approach: The lateral approach (Figure 9–4) is the method most commonly used. The patient is supine with the knee fully extended and quadriceps relaxed. Grasp the patient’s patella with your fingers and easily mobilize laterally. Draw imaginary lines along the lateral and proximal borders of the patella. Insert the needle into

Figure 9–4 The intraarticular (lateral) approach.

Continued

Child and Adolescent Knee: Primary Care Perspective

TECHNICAL NOTE 9–1

Injections About the Knee (Continued) the soft tissue between the patella and femur, just distal to the intersection point of the lines. Direct it at an angle parallel to the plane of the posterior aspect of the patella. A similar approach can be made at the medial aspect of the knee. Anterior Approach: To use the anterior approach (Figure 9–5), palpate the patellar tendon at the level of the joint with the patient sitting up and his or her leg and foot hanging over the edge of the examination table. A soft spot just lateral to the tendon can be appreciated bordered by the lateral femoral condyle, lateral tibial plateau, and the patellar tendon. The needle enters the joint space through this soft

space directed posteriorly, 30 degrees medially, and slightly superiorly (i.e., toward the intercondylar notch). A similar approach can be used starting just medial to the patellar tendon and directing the needle laterally. Iliotibial Band Instruct the patient to lie in the lateral recumbent position (unaffected side down) with the knee flexed 20–30 degrees. Along the lateral thigh, follow the course of the ITB (Figure 9–6) across the femoral condyle to its insertion at Gerdy’s tubercle (bony prominence at the anterior lateral condyle of

Figure 9–5 The intraarticular (anterior) approach.

Figure 9–6 Iliotibial band.

Continued

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TECHNICAL NOTE 9–1

Injections About the Knee (Continued) the tibia, lateral to the distal margin of the patellar tendon). Insert a 20-gauge 1-inch needle at the point of maximal tenderness perpendicular to Gerdy’s tubercle and advance to the bone. Withdraw the needle 2–3 mm before injecting the solution. Typically, use a solution of 1 ml of steroid and 4 ml of anesthetic.

Insert a 20-gauge 1-inch needle perpendicular to the tibia into the point of maximal tenderness. Gently guide the needle down to the bone and then withdraw 2–3 mm before injecting the solution. Typically, use a solution of 1 ml of steroid and 4 ml of anesthetic. Prepatellar Bursa

Pes Anserine The pes anserine bursa (Figure 9–7) is located approximately 5 cm inferior to the medial joint line and 2–3 cm medial to the tibial tubercle. It lies beneath the tendons of the sartorius, gracilis, and semitendinosus and anterior to the medial collateral ligament.

The prepatellar bursa (Figure 9–8) is located between the skin and anterior aspect of the patella. Consider aspirations and/or injections for recurrent or persistent inflammation after more conservative measures have failed. Make sure the patient is comfortable in the supine position. The knee may be slightly flexed

Figure 9–7 Pes anserine bursa.

Figure 9–8 Prepatellar bursa.

Continued

Child and Adolescent Knee: Primary Care Perspective

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TECHNICAL NOTE 9–1

Injections About the Knee (Continued) and supported to ensure a relaxed quadriceps. Advance an 18- to 20-gauge needle into the bursa from the medial or lateral side at a 45-degree angle to the plane of the patella. Drain as much fluid as possible before changing syringes and injecting the steroid solution. Typically, use 1 ml of steroid and 2–3 ml of anesthetic.

Suggested Readings

Postinjection Care Reexamine the patient in the office 15 minutes after the injection to assess improvement in symptoms while the anesthetic is acting and to monitor for any adverse effects. Caution the patient that the effects of the anesthetic will abate in a few hours. There may actually be a flare of symptoms in the first 24–48 hours, and the steroid effect peaks approximately 4 days after the injection. Instruct the patient to ice the affected area and avoid applying heat. After aspiration of the prepatellar bursa, apply a pressure dressing. In general, patients can go back to their regular activities of daily living but should avoid strenuous activities for 3–5 days.

tals. The cell count is particularly valuable because the percentage of neutrophils and the absolute cell counts for each cell type can help determine whether the effusion is inflammatory, traumatic, or infectious. As a general rule, KEY POINTS a white blood cell count less than 200 per high-powered field Arthrocentesis (HPF) is normal, 200–2000/ 1. Arthrocentesis: HPF is mechanical, and between Analyze for the three 2000 and 75,000/HPF is inflamCs: cell count, culmatory. Infectious arthritis comture, and crystals monly will have greater than 2. Etiology of effusion: 42 20,000–50,000/HPF. However, Inflammatory, trauthere is often overlap (Table matic, or infectious 9–2).

1. Cardone DA, Tallia AF: Diagnostic and therapeutic injection of the hip and knee. Am Fam Phys 67:2147–2152, 2003. 2. Kerlan RK, Glousman RE: Injections and techniques in athletic medicine. Clin Sports Med 8:541–560, 1989. 3. Mysnyk MC, Wroble RR, Foster DT, Albright JP: Prepatellar bursitis in wrestlers. Am J Sports Med 14:46–54, 1986. 4. Owen DS: Aspiration and injection of joints and soft tissues. In: Ruddy S, Harris ED Jr, Sledge CB (eds): Kelley’s Textbook of Rheumatology, 6th ed. Philadelphia: Saunders, 2001, pp 583–603. 5. Roberts WO: Knee aspiration and injection. Phys Sports Med 26:93–97, 1998. 6. Safran M, McKeag DB, Van Camp P: Manual of Sports Medicine. Philadelphia: Lippincott-Raven, 1998, pp 625–634. 7. Sutker AN, Barber FA, Jackson DW, Pagliano JW: Iliotibial band syndrome in distance runners. Sports Med 2:447–451, 1985. 8. Vangsness CT Jr: Overview of treatment options for arthritis in the active patient. Clin Sports Med 18:1–11, 1999. 9. Wen DY: Intra-articular hyaluronic acid injections for knee osteoarthritis. Am Fam Phys 62:565–570, 572, 2000.

Management of Atraumatic Knee Problems and Referral Guidelines The primary care physician’s role in implementing treatment protocols is discussed in this section. The specific treatment of atraumatic knee pathologies is discussed separately throughout the book. To properly treat athletes, sports medicine physicians should be comfortable with prescribing officebased rehabilitation, orthotics/braces, and pain medications. Nonsteroidal antiinflammatory drugs, or NSAIDs, are commonly used in the treatment of musculoskeletal injuries. The safety in prescribing, as well as the analgesic and antiinflammatory effects, make them popular medications for the sports medicine physician. They are usually prescribed orally but can be administered intramuscularly, intravenously, and topically. Side effects from prolonged

Table 9–2 Analysis of Synovial Fluid

Color Clarity Viscosity White blood cells Neutrophils

Normal

Noninflammatory

Inflammatory

Septic

Clear Transparent High 0–200 Low

Straw/yellow Transparent High 200–2000 Low

Yellow Hazy-opaque Low 2000–75,000 Medium-high

Variable Opaque Low-high > 50,000 High

From Genovese MC, van Vollenhoven RF: Aspiration and injection of joints and soft tissue. In Harris ED Jr, Genovese MC (eds): Primary Care Rheumatology. Philadelphia: WB Saunders, 2000, p 60.

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NSAID use include gastrointestinal bleeding, acute renal failure, and hypertension. There appears to be less of a role for NSAIDs and corticosteroid use when treating overuse injuries to tendons or tendinopathies than previously thought. First, the disease pathology does not significantly involve inflammation. Second, it is suggested that muscle fiber recovery and regeneration may be delayed,43,44 and bone healing may be prolonged45 when NSAIDs are used. Prostaglandin E2 (PgE2) sensitizes afferent pain fibers. PgE2 production is inhibited by antiinflammatories. Importantly, PgE2 is also involved in the production of cytokines required for tissue healing.43 Corticosteroids have the greatest antiinflammatory effect, although these effects are met with a potential increase in cell death, inhibition of collagen synthesis, and tendon atrophy leading to failure.46 Steroid injections have shown little benefit in long-term outcomes.47 NSAIDs and corticosteroids may permit improved performance because of less pain; however, they may adversely affect the necessary process for healing. Further research is needed to determine the appropriate use of NSAIDs in chronic, overuse, and acute soft tissue injuries. The treatment of JRA and pediatric spondyloarthropathies has significantly advanced in the past decade. The emphasis is on early and aggressive treatment starting with NSAIDS and advancing to disease modifying anti-rheumatic drugs and sulfasalazine. The ultimate goal is to control joint inflammation/synovitis, thus minimizing joint erosion. Mechanical pain syndromes, such as patellofemoral syndrome (PFS), are often managed conservatively with particular attention to biomechanical issues, including medial quadriceps weakness, quadriceps/hamstring muscle tightness, overpronation and patellar maltracking. Physical therapy, orthotics, and patellar tracking KEY POINTS braces are common treatment modalities. An accurate diagnosis 1. NSAIDs are a safe is the key to success in treatment. treatment option in Temporary limitation of specific the acute setting. activities and cross-training are 2. NSAIDs are less often required, although continbeneficial with uing some level of sporting activchronic/overuse ity is important in maintaining injury. peer contact when treating young 3. Steroid injections athletes. Rehabilitation often have shown little evolves around strength and benefit in long-term flexibility, while cross-training outcomes. maintains condition. This may 4. More research is include pool work, stationary needed. bike, and/or elliptical machine 5. Conservative use. However, ITB friction synmanagement for drome may be aggravated with PFS, including bicycling, because the ITB rubs bracing, orthotics, across the lateral femoral condyle. and PT is commonly In this situation the elliptical used, although accutrainer or pool work may be more rate diagnosis is key. appropriate. Knee braces can be helpful when returning the athlete to competition, whether their main effects improve proprioception or they provide structural, biomechanical changes. Patellar subluxation and lateralization are treated with a patellar tracking brace. A simple patellar tendon strap can be used with patellar

tendonitis. Hinged braces are useful with chronic collateral ligament strains. Unloading braces may be used to treat stable OCD lesions on joint weight-bearing surfaces. A functional ACL brace may assist in the treatment of chronic knee instability. Referral Patterns Patients who present acutely or have concerning “red flag” symptoms should be evaluated promptly and referred urgently to an appropriate specialist as needed. An athlete who suspects he or she might have an intraarticular infection should seek immediate emergency attention. All children with suspected inflammatory articular diseases should be referred to a rheumatologist for consultation. If symptoms are mild, a preliminary workup to identify the cause can be initiated if the primary care physician is comfortable with it. Patients with signs and symptoms of internal derangement/intraarticular pathology should be referred to an orthopedic surgeon for further evaluation, especially if the patient is having mechanical locking or has significant disability. The role of the primary care physician includes treating the athlete with structural knee problems so long as an accurate diagnosis and treatment plan has been made. The primary care KEY POINTS provider should consider orthopedic consultation for patients Referral patterns not responding to treatment or 1. Promptly refer whose diagnosis is in question. It patients with “red is also the role of the primary care flag” symptoms. physician to recognize the mental 2. Consider orthopedic stress associated with injury and consultations for disability. Patients with chronic patients not respondpain symptoms or syndromes may ing to treatment or require a pain management spewhose diagnosis is cialist’s consultation. Psychiatry questionable. and/or sports psychologists may be useful in potentiating the rehabilitation process. KEY POINTS Management of Refractory Knee Pain Syndromes Chronic Pain Syndromes Fibromyalgia syndrome (FS) is most common in midlife but may be seen at any age. Studies evaluating the prevalence of FS in children meeting the diagnostic criteria of the American College of Rheumatology found 6.2% of children studied had FS. Its prevalence in healthy children is not known, although it is felt to be common in the pediatric age group.48 Chronic fatigue syndrome (CFS) and primary juvenile fibromyalgia syndrome (PJFS)

Chronic pain syndromes 1. FS syndrome is present in children and may coexist with CFS. 2. PJFS symptoms include polymyalgias, polyarthralgias, fatigue, and sleep and school disturbances. 3. Laboratory evaluation is normal. 4. Physical examination reveals typical tender points. 5. Patients often do not respond to NSAIDs but may respond to cyclobenzaprine. 6. Reassurance is important.

Child and Adolescent Knee: Primary Care Perspective

are illnesses with a similar pattern of symptoms yet unknown etiologies. In a study that evaluated children for co-diagnoses, 30% of children with the diagnosis of CFS were found to fulfill criteria for fibromyalgia. Children who met fibromyalgia criteria had a statistically greater degree of subjective muscle pain, sleep disturbance, and neurological symptoms. Thus CFS and PJFS appear to be overlapping clinical entities.49 PJFS symptoms include polymyalgias, polyarthralgias, nonrestorative sleep, difficulty concentrating in school, and fatigue. Physical examination reveals typical tender points, absence of joint swelling, synovitis or nodules, and absence of neurological findings. Laboratory test results are normal. Diagnoses frequently confused with PJFS include juvenile chronic arthritis, “growing pains,” hysteria, and psychological problems. Patients with PJFS classically do not respond to salicylate or other antiinflammatory medication. The majority (73% in one study) respond to cyclobenzaprine.50 Reassurance is very important in treating children with this syndrome. Many parents fear that their child has a crippling disorder. Medications (especially tricyclics), moderate exercise, and proper sleep are also mainstays of therapy. Complex Regional Pain Syndromes Complex regional pain syndromes (CRPS) involve persistent pain, allodynia (pain evoked by light touch), and autonomic dysfunction. They are frequently divided into two types based on the absence or presence of an overt nerve lesion: CRPS type 1, reflex sympathetic dystrophy (RSD); and type 2, causalgia. RSD is characterized by pain and altered sensation; motor disturbance and soft tissue change; vasomotor and autonomic changes; and psychosocial disturbance. In children, RSD usually follows a relatively minor trauma of the lower extremity such as a knee sprain or fracture. Symptoms are often present for an average of 1 year before the diagnosis is made in children. The average age of onset is 12.5 years. There is a heavy female-to-male predilection, and 80% of cases involve the lower extremity.51 There also appears to be a predilection for this condition among children active in sports. In a study from Boston Children’s Hospital, the initial insult in 80% of the RSD cases seen at the Pain Service was a sports injury.52 The psychological profile of children with RSD tends to be that of high achievers and perfectionists. Psychological stressors (e.g., death of a family member, divorce, starting a new school) may worsen the pain. Reflex sympathetic dystrophy of the knee frequently does not present with the classic combination of signs and symptoms seen in the upper extremity. Pain out of proportion to the initial injury is the hallmark symptom.53 By definition there are neurosensory changes that include allodynia and hyperesthesia. Skin color changes, edema, and pain at the site of injury, proximal or distal to the site of injury, may be present. Extra hair growth and undersweating or oversweating are unusual symptoms in children. In some cases, range of motion is limited, and the child will avoid moving the extremity and guard the extremity during the examination. Diagnostic evaluation is aimed at ruling out other pathologies. Standard x-rays demonstrate patchy deminer-

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alization in the affected part, possibly due to disuse. Bone scans are more sensitive than x-rays in the early phase of the condition. Bone scans are sensitive to treatment and may therefore be used both for initial diagnosis and for monitoring response to treatment.54 The ultimate treatment goal is pain relief. Treatment for patients with RSD incorporates a multidisciplinary approach with incremental incorporation of physiotherapeutic, pharmacotherapeutic, and psychotherapeutic modalities. The most important component is a comprehensive physical therapy program.55 Initially, desensitization and overcoming fear of movement is considered important for the patient, allowing the limbs to be touched and the patient to start moving. Isometric strengthening, stress loading, and general aerobic conditioning are included in the next phase of treatment. Psychological management may be necessary throughout the treatment course. Pharmacotherapy is recommended if pain is the limiting factor for the progression of treatment, but it is considered adjunctive to therapy. KEY POINTS NSAIDs, corticosteroids, and free radical scavengers are Complex regional pain among the drugs commonly used syndrome to treat the inflammatory symp1. CRPS involves pain, toms of RSD. Tricyclic antideallodynia, and autopressants are often used to treat nomic dysfunction. neuropathic pain, as well as ion 2. It usually follows channel blocking agents such as relatively minor carbamazepine and phenytoin. trauma. The anticonvulsant gabapentin 3. It is often sports has a more favorable side effect related. profile.56 Bisphosphonates have 4. CRPS has a heavy 57 been shown to be effective. female predilection Nerve blocks are recommended commonly involving to reduce pain and facilitate physthe lower extremities. iotherapy and rehabilitation in 5. Patient profile for adults. There is a lack of scientific CRPS includes high evidence guiding the use of nerve achievers and perblocks to treat RSD in children. fectionists. Disease recurrence or failure of 6. Diagnostic evaluation conservative treatment may of CRPS is aimed at eventually lead to treatment ruling out other requiring sympathetic blockade. pathologies. Continued reassurance for 7. Treatment for CRPS is both the family and the patient is multidisciplinary, important. Children have a more including physical favorable prognosis than adults. therapy, pharmaThe recurrence rate in children is cotherapy, and psy25% and may occur in the same chotherapy. location as the original illness or 8. Family and patient in a different body part. Close reassurance is monitoring for disease recurrence important. should be maintained. References 1. Damore DT, Metzl JD, Ramundo M, et al: Patterns in childhood sports injury. Acad Emerg Med 8:458, 2001. 2. Jones SJ, Lyons RA, Sibert J, et al: Changes in sports injuries to children between 1983 and 1998: comparison of case series. J Publ Health Med 23:268–271, 2001. 3. Micheli LJ: Sports injuries in children and adolescents: questions and controversies. Clin Sport Med 14:727–745, 1995.

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4. Irha E, Vrdoljak J: Algorithm for establishing the indication for knee arthroscopy in children: a comparison of adolescent and preadolescent children. Knee Surg Sports Traumatol Arthrosc 8:99–103, 2000. 5. Peterson HA: Partial growth plate arrest and its treatment. J Ped Ortho 4:246–258, 1984. 6. Kujala UM, Kvist M, Osterman K: Knee injuries in athletes. Review of exertion injuries and retrospective study of outpatient sports clinical material. Sports Med 3:447–460, 1986. 7. BrunsW, Maffulli N: Lower limb injuries in children in sports. Clin Sports Med 9:637–662, 2000. 8. Lindenfield TN, Schmidtt DJ, Hendy MP, et al: Incidence of injury in indoor soccer. Am J Sports Med 22:364–371, 1994. 9. Iobst CA, Stanitski CL: Acute knee injuries. Clin Sports Med 19:621–635, 2000. 10. Gomez E, DeLee JC, Farney WC: Incidence of injury in Texas girls’ high school basketball. Am J Sports Med 24:684–687, 1996. 11. Bjordals JM, Arnoy F, Hannestad B, et al: Epidemiology of anterior cruciate ligament injuries in soccer. Am J Sports Med 25:341–345, 1997. 12. Hewitt TE, Stroupe AL, Nance TA, et al: Plyometric training in female athletes: decreased impact forces and increased hamstring torques. Am J Sports Med 24:765–773, 1996. 13. Nottage WM, Matsuura PA: Management of complete ACL tears in the skeletally immature patient: current concepts and review of the literature. Arthroscopy 10(5):569–573, 1994. 14. Smith AD, Tao SS: Knee injuries in young athletes. Clin Sport Med 14: 629–650, 1995. 15. Stanitski CL, Harvell JC, Fu F: Observations on acute knee hemarthrosis in children and adolescents. J Pediatr Orthop 13:506–510, 1993. 16. Stanitski C: 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. 17. Bulloch B, Neto G, Plint A, et al: Validation of the Ottawa knee rule in children: a multicenter study. Ann Emerg Med 42:48–55, 2003. 18. Kocher MS, DiCanzio J, Zurakowski D, et al: Diagnostic performance of clinical examination and selective magnetic resonance imaging in the evaluation of intraarticular knee disorders in children and adolescents. Am J Sports Med 29:292–296, 2001. 19. Zionts LE: Fractures around the knee in children. J Am Acad Orthop Surg 10:345–355, 2002. 20. Kocher MS, Micheli LJ, Zurakowski D, Luke A: Partial tears of the anterior cruciate ligament in children and adolescents. Am J Sports Med 30(5):697–703, 2002. 21. Kujala UM, Krist M, Heinonen O: Osgood Schlatter’s disease in adolescent athletes: retrospective study of incidence and duration. Am J Sports Med 13:326–341, 1985. 22. Cahill BR: Osteochondritis dissecans of the knee: treatment of juvenile and adult forms. J Am Acad Orthop Surg 3:237–247, 1995. 23. Green M: Limb and musculoskeletal pain. In: Pediatric Diagnosis: Interpretation of Symptoms and Signs in Children and Adolescents, 6th ed. Philadelphia: WB Saunders Co, 1998, p 152. 24. Bowyer S, Roettcher P: Pediatric Rheumatology Database Research Group: Pediatric Rheumatology Clinic populations in the United States: results of a 3-year survey. J Rheumatol 15:678–683, 1988. 25. Malleson PN, Fung MY, Rosengerg AM (for the Canadian Pediatric Rheumatology Association): The incidence of pediatric rheumatic diseases: results from the Canadian Pediatric Rheumatology Association Disease Registry. J Rheumatol 23:1981–1987, 1996. 26. Burgos-Vargas R, Pacheco-Tena C, Vazquez-Mellado J: Juvenile-onset spondyloarthropathies. Rheum Dis Clin North Am 17:1001–1014, 1991. 27. Cabral DA, Oen KG, Petty RE: SEA syndrome revisited: a long-term follow-up of children with a syndrome of seronegative enthesopathy and arthropathy. J Rheumatol 19:1282–1285, 1992. 28. Fisher RC, Berman S: Septic arthritis. In Berman S (ed): Pediatric Decision Making, 3rd ed. St. Louis: Mosby, 1996, p 1996. 29. Shapiro ED, Gerber MA: Lyme disease. Clin Infect Dis 31:533–542, 2000. 30. Huppertz H-I, Karch H, Suschke HJ, et al, and Pediatric Rheumatology Collaborative Group: Lyme arthritis in European children and adolescents. Arthr Rheumatol 3:361–368, 1995.

31 Gerber MA, Zemel LS, Shapiro ED: Lyme arthritis in children: clinical epidemiology and long-term outcomes. Pediatrics 102:905–908. 32. Schaller JG: Juvenile rheumatoid arthritis. Pediatr Rev 18:337–349, 1997. 33. Nuss R, Kilcoyne R, Geraghty S, et al: Magnetic resonance imaging visualization of hemorrhage into a suprapatellar pouch in a child with hemophilia. Am J Pediatr Hematol Oncol 16:183–185, 1994. 34. Montgomery RR, Gill JC, Scott JP: Hemophilia and von Willebrand disease (Chapter 44). In Nathan DG, Orkin SH (eds): Hematology of Infancy and Childhood, 5th ed. Philadelphia: WB Saunders Co, 1998, p 1634. 35. McGhee JL, Burks FN, Sheckels JL, et al: Identifying children with chronic arthritis based on chief complaints: absence of predictive value for musculoskeletal pain as an indicator of rheumatic disease in children. Pediatrics 110(2):354–359, 2002. 37. Greenspan A, Remagen W: Differential diagnosis of tumors and tumorlike lesions of bones and joints. Philadelphia: Lippincott-Raven, 1998. 38. Van der Wall H, Storey G, Frater C, et al: Importance of positioning and technical factors in anatomic localization of sporting injuries in scintigraphic imaging. Semin Nucl Med 31:17–27, 2001. 39. Ramsey SE, Cairns RA, Cabral DA, et al: Knee magnetic resonance imaging in childhood chronic monarthritis. J Rheumatol 26:2238–2243, 1999. 40. Johnson K, Wittkop B, Haigh F, et al: The early magnetic resonance imaging features of the knee in juvenile idiopathic arthritis. Clin Radiol 57:466–471, 2002. 41. Callegari PE, Williams WV, Eisenberg R: Laboratory tests in rheumatoid arthritis. J Musculoskel Med 15:5–13, 1998. 42. Genovese MC, van Vollenhoven RF: Aspiration and injection of joints and soft tissue. In Harris ED, Jr, Genovese MC (eds): Primary care rheumatology. Philadelphia, WB Saunders Co, 2000, p. 60. 43. Mishra DK, Friden J, Schmitz MC, et al: Anti-inflammatory medication after muscle injury. A treatment resulting in short-term improvement but subsequent loss of muscle function. J Bone Joint Surg Am 77:1510–1519, 1995. 44. Almekinders LC, Gilbert JA: Healing of experimental muscle strains and the effects of nonsteroidal anti-inflammatory medication. Am J Sports Med 14:303–308, 1986. 45. Friedman RJ, Acurio MT, Davis R, et al: Effects of growth factors and indomethacin on fracture healing. Trans Orthop Res Soc 17:421, 1992. 46. Khan KM, Cook JL, Bonar F, et al: Histopathology of common tendinopathies: update and implications for clinical management. Sports Med 27:393–408, 1999. 47. Newcomer KL, Laskowski ER, Idank DM, et al: Corticosteroid injection in early treatment of lateral epicondylitis. Clin J Sport Med 11:214–222, 2001. 48. Buskila D, Press J, Gedalia A, et al: Assessment of nonarticular tenderness and prevalence of fibromyalgia in children. J Rheumatol 20:368–370, 1993. 49. Bell DS, Bell KM, Cheney PR: Clinical infectious diseases. Primary juvenile fibromyalgia syndrome and chronic fatigue syndrome. Clin Infect Dis 18(suppl 1):S21–S23, 1994. 50. Romano TJ: Fibromyalgia in children; diagnosis and treatment. WV Med J 87:112–114, 1991. 51. Small E: Chronic musculoskeletal pain in young athletes. Ped Clin N Am 49:655–662, 2002. 52. Wilder RT, Berde CB, Wolohan M, et al: Reflex sympathetic dystrophy in children. Clinical characteristics and follow-up of seventy patients. J Bone Joint Surg Am 74(6):910–919, 1992. 53. Cooper DE, DeLee JC: Reflex sympathetic dystrophy of the knee. J Am Acad Orthop Surg 2:79–86, 1994. 54. Turner-Stokes L: Reflex sympathetic dystrophy-a complex regional pain syndrome. Disabil Rehabil 24:939–947, 2002. 55. Lee H, Scharff L, Sethna NF, et al: Physical therapy and cognitivebehavioral treatment for complex regional pain syndromes. J Pediatr 141:135–140, 2002. 56. Ribbers GM, Geurts AC, Henk JS: Pharmacologic treatment of complex regional pain syndrome i: a conceptual framework. Arch Phys Med Rehabil 84:141–146, 2003. 57. Kubalek I, Fain O, Paries J, et al: Treatment of reflex sympathetic dystrophy with pamidronate: 29 cases. Rheumatology 40:1394–1397, 2001.

Chapter 10

Preparticipation Physical Examination Anthony Luke

The preparticipation physical examination (PPE) is a valuable opportunity for the sports medicine practitioner to identify potential health concerns and make recommendations to the young athlete to promote safe participation in sports. In this chapter we will discuss concepts concerning the PPE, with specific emphasis on conditions requiring restriction from sports and a special focus on the knee. Organized Sports And Injuries Participation rates in sports vary substantially by age, sex, and ethnicity. Chronological age is often used to categorize child athletes for participation. However, the rate of maturity can vary remarkably for each individual.1 In one U.S. survey, approximately 70% of male students and 53% of female students reported participating on one or more sports teams in and/or outside school.2 Results of another study estimated that 36% of injuries from all causes in children 5–17 years of age are caused by sports.3 Forty-one percent of injuries in children presenting to four pediatric emergency departments were sports related.4 Injuries resulting in high school athletes missing or not completing a practice or game were reported between 22% and 39%.5,6 Purpose/Objectives of the PPE Why Do You Need to Do It? The PPE is recommended for individuals involved in a competitive or organized sport who are new to a school or a sports program. Its requirement varies by location and sport, with some states requiring yearly examinations before an athlete may participate in sports.7 The examination is ideally performed at least 6 weeks before the season begins. Athletes typically present for the PPE when they are adolescents, unless they are extremely young competitive athletes. The goals of the PPE are outlined in Box 10–1.8

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Lyle Micheli

It is important to understand that the PPE is only a part of the athlete’s ongoing care and does not eliminate his or her risk of injury in sports, including sudden death. The athlete, parents, coaches, and medical staff should not have false expectations that the PPE will rule out the possibility of significant injury or sudden death during sports activity.9 The ability to detect serious problems during the PPE is limited.10,11 Further research is needed to improve the effectiveness of the examination to establish accepted standard requirements. However, it is our opinion that the PPE is a valuable tool when performed carefully to identify, address, and anticipate specific injuries.

Relative and Absolute Contraindications to Participation One of the most difficult decisions a sports physician must make is whether to restrict an athlete from playing. Some athletes unfortunately will have medical conditions that disqualify them from participation due to an increased risk of injury. The physician must consider risks to the individual, as well as to the other competitors, in the context of the sport. Published recommendations (e.g., by the American College of Cardiology12 or by the American Academy of Pediatrics13) provide criteria for decisions to remove athletes from high-risk sports. Suggested restrictions for medical conditions of concern are outlined in Table 10–1. The most common reasons for disqualifying an athlete are cardiovascular or orthopedic problems. The rates for referral for further evaluation or treatment in adolescent PPEs have ranged from 2.1–11.9%14 in studies, while the percentage of athletes disqualified ranged from 0.2–1.3%.15 91

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Box 10–1 Objectives of the Preparticipation Physical Examination Primary Objectives 1. Screen for conditions that may be life-threatening or disabling 2. Screen for conditions that may predispose to injury or illness 3. Meet administrative requirements Secondary Objectives 1. Determine general health 2. Serve as an entry point to the healthcare system for adolescents 3. Provide opportunity to initiate discussion on healthrelated topics 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.

Counseling The preparticipation examination is an ideal time to counsel young athletes, particularly if the encounter is an isolated doctor–patient visit. This may be the only time that a young person visits a physician, making this a window of opportunity to screen for age-specific medical and social concerns and to give anticipatory advice. A thorough history or review of systems can help identify preexisting medical conditions or specific cardiovascular risk factors. During the PPE, potentially dangerous practices such as inappropriate training and improper nutrition and supplement use should also be explored. Preventative health screening should be done if the time and environment are appropriate. Investigations or follow-up should be arranged if there are concerns. Clearance for play may be delayed or restricted until important issues are addressed.

Table 10–1 Medical Conditions and Sports Participation* Condition

May Participate

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

Qualified yes Qualified yes

Cardiovascular Disease Carditis (inflammation of the heart) Explanation: Carditis may result in sudden death with exertion. Hypertension (high blood pressure) Explanation: Those with significant essential (unexplained) hypertension should avoid weight and power lifting, bodybuilding, and strength training. Those with secondary hypertension (hypertension caused by a previously identified disease) or severe essential hypertension need evaluation. The National High Blood Pressure Education Program working group3 defined significant and severe hypertension. Congenital heart disease (structural heart defects present at birth) Explanation: Those with mild forms may participate fully; those with moderate or severe forms or who have undergone surgery need evaluation. The 26th Bethesda Conference defined mild, moderate, and severe disease for common cardiac lesions. Dysrhythmia (irregular heart rhythm) Explanation: Those with symptoms (chest pain, syncope, dizziness, shortness of breath, or other symptoms of possible dysrhythmia) or evidence of mitral regurgitation (leaking) on physical examination need evaluation. All others may participate fully. Heart murmur Explanation: If the murmur is innocent (does not indicate heart disease), full participation is permitted. Otherwise, the athlete needs evaluation (see congenital heart disease and mitral valve prolapse entries). Cerebral palsy Explanation: Athlete needs evaluation. Diabetes mellitus Explanation: All sports can be played with proper attention to diet, blood glucose concentration, hydration, and insulin therapy. Blood glucose concentration should be monitored every 30 minutes during continuous exercise and 15 minutes after completion of exercise. Diarrhea Explanation: Unless disease is mild, no participation is permitted because diarrhea may increase the risk of dehydration and heat illness. See fever entry. Eating disorders Anorexia nervosa Bulimia nervosa Explanation: Patients with these disorders need medical and psychiatric assessment before participation in sports. Eyes Functionally one-eyed athlete Loss of an eye Detached retina

No Qualified yes

Qualified yes

Qualified yes

Qualified yes

Qualified yes Qualified yes

Qualified no Qualified yes

Qualified yes

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Preparticipation Physical Examination

Table 10–1 Medical Conditions and Sports Participation*—cont’d Condition Previous eye surgery or serious eye injury Explanation: A functionally one-eyed athlete has a best-corrected visual acuity of less than 20/40 in the eye with worse acuity. These athletes would suffer significant disability if the better eye were seriously injured, as would those with loss of an eye. Some athletes who previously have undergone eye surgery or had a serious eye injury may have an increased risk of injury because of weakened eye tissue. Availability of eye guards approved by the American Society for Testing and Materials, as well as other protective equipment, may allow participation in most sports, but this must be judged on an individual basis. Fever Explanation: Fever can increase cardiopulmonary effort, reduce maximum exercise capacity, make heat illness more likely, and increase orthostatic hypertension during exercise. Fever may rarely accompany myocarditis or other infections that may make exercise dangerous. Heat illness, history of Explanation: Because of the increased likelihood of recurrence, the athlete needs individual assessment to determine the presence of predisposing conditions and to arrange a prevention strategy. Hepatitis Explanation: Because of the apparent minimal risk to others, all sports may be played that the athlete’s state of health allows. In all athletes, skin lesions should be covered properly, and athletic personnel should use universal precautions when handling blood or body fluids with visible blood. Human immunodeficiency virus infection Explanation: Because of the apparent minimal risk to others, all sports may be played that the athlete’s state of health allows. In all athletes, skin lesions should be covered properly, and athletic personnel should use universal precautions when handling blood or body fluids with visible blood. Kidney, absence of one Explanation: Athlete needs individual assessment for contact, collision, and limited-contact sports. Liver, enlarged Explanation: If the liver is acutely enlarged, participation should be avoided because of risk of rupture. If the liver is chronically enlarged, individual assessment is needed before collision, contact, or limited-contact sports are played. Malignant neoplasm Explanation: Athlete needs individual assessment. Musculoskeletal disorders Explanation: Athlete needs individual assessment.

May Participate

No

Qualified yes

Yes

Yes

Qualified yes Qualified yes

Qualified yes Qualified yes

Neurological Disorders History of serious head or spine trauma, severe or repeated concussions, or craniotomy. Explanation: Athlete needs individual assessment for collision, contact, or limited-contact sports and also for noncontact sports if deficits in judgment or cognition are present. Research supports a conservative approach to management of concussion. Seizure disorder, well-controlled Explanation: Risk of seizure during participation is minimal. Seizure disorder, poorly controlled Explanation: Athlete needs individual assessment for collision, contact, or limited-contact sports. The following noncontact sports should be avoided: archery, riflery, swimming, weight or power lifting, strength training, and sports that involve heights. In these sports, occurrence of a seizure may pose a risk to self or others. Obesity Explanation: Because of the risk of heat illness, obese persons need careful acclimatization and hydration. Organ transplant recipient Explanation: Athlete needs individual assessment. Ovary, absence of one Explanation: Risk of severe injury to the remaining ovary is minimal.

Qualified yes

Yes Qualified yes

Qualified yes Qualified yes Yes

Respiratory Conditions Pulmonary compromise, including cystic fibrosis Explanation: Athlete needs individual assessment, but generally, all sports may be played if oxygenation remains satisfactory during a graded exercise test. Patients with cystic fibrosis need acclimatization and good hydration to reduce the risk of heat illness. Asthma Explanation: With proper medication and education, only athletes with the most severe asthma will need to modify their participation. Acute upper respiratory infection Explanation: Upper respiratory obstruction may affect pulmonary function. Athlete needs individual assessment for all but mild disease. See fever entry.

Qualified yes

Yes Qualified yes

Continued

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Table 10–1 Medical Conditions and Sports Participation*—cont’d Condition

May Participate

Sickle cell disease Explanation: Athlete needs individual assessment. In general, if the status of the illness permits, all but high-exertion, collision, and contact sports may be played. Overheating, dehydration, and chilling must be avoided. Sickle cell trait Explanation: It is unlikely that persons with sickle cell trait have an increased risk of sudden death or other medical problems during athletic participation, except under the most extreme conditions of heat, humidity, and possibly increased altitude.11 These persons, like all athletes, should be carefully conditioned, acclimatized, and hydrated to reduce any possible risk. Skin disorders (boils, herpes simplex, impetigo, scabies, molluscum contagiosum) Explanation: While the patient is contagious, participation in gymnastics with mats; martial arts; wrestling; or other collision, contact, or limited-contact sports is not allowed. Spleen, enlarged Explanation: A patient with an acutely enlarged spleen should avoid all sports because of risk of rupture. A patient with a chronically enlarged spleen needs individual assessment before playing collision, contact, or limited-contact sports. Testicle, undescended or absence of one Explanation: Certain sports may require a protective cup.

Qualified yes

Yes

Qualified yes Qualified yes

Yes

Reprinted from American Academy of Pediatrics, Committee on Sport Medicine and Fitness: Medical conditions affecting sports participation. Pediatrics 107:1205–1209, 2001. * This table is designed for use by medical and nonmedical personnel. The statement “Needs evaluation” means that a physician with appropriate knowledge and experience should assess the safety of a given sport for an athlete with the listed medical condition. Unless otherwise noted, this is because of variability of the severity of the disease, the risk of injury for the specific sports, or both.

Medicolegal Issues Despite even the best intentions, the clinician should be clear on the goals of the PPE (see Box 10–1). Many physical examinations are performed to meet the medicolegal requirements of an institution or school board. Consequently, sports medicine physicians should be aware of the legal ramifications of their decisions in their local area of practice. Most major sports-related organizations concur that the ultimate responsibility regarding the PPE lies with the physician (doctor of medicine or osteopathy).8 The clinician must practice to the standard of other physicians in his or her area of specialty. The physician may not be liable for missing a diagnosis, even if a problem arises, unless care deviated from accepted practice.10 Accurate and complete documentation should be performed as for any patient visit. Physicians should check with legal counsel concerning the description of law and the liabilities of providing medical care in their local area of practice. Consent from the athlete should be obtained before discussing medical information with coaches, teammates, or the media. Medical information can be written or recorded in electronic form on computers and should be protected and kept confidential. A subsequent office visit may need to be arranged with the athlete and other important participants (coaches, parents, others.) if a serious concern presents. In the event that an athlete may be disqualified, the individuals involved often do not accept these decisions easily and may not agree with the perceived risk. The athlete may appeal through the court system or seek another opinion. It is always advised to stand firm with one’s medical judgment rather than be coerced into letting an athlete compete. Safety for the health of the athletes is always paramount. Some athletes have signed exculpatory waivers16;

however, they do not legally guarantee release of the physician of all responsibility and liability.17 How Is it Carried Out? The recommended PPE has evolved from locker room assessments to detailed evaluations in the office or by stations. A recent consensus statement by prominent North American sports-related and primary care medical organizations recommended that during the preseason, prospective athletes complete a preparticipation evaluation performed by a licensed medical physician or doctor of osteopathic medicine.18 The examinations should be performed approximately 6 weeks before participation in the sport begins,19 so that the athlete may have some time to work on suggested changes. The most personal assessment is performed on an individual basis in the office. This one-on-one interaction allows for a less-hurried evaluation, facilitates individual counseling, and enhances the patient–physician relationship. With large numbers of athletes, a station-based approach maximizes time and resources, typically involving physicians, physical and athletic therapists, nurses, and/or other allied health professionals to perform parts of the history or physical examination on each athlete. This can be of great benefit because of the input of several examiners with different areas of expertise. At the elite or professional competitive levels of sport, more specialists—including dentists, ophthalmologists, and exercise physiologists—may be involved. After reviewing the literature on PPEs, the American Medical Association suggested “the identification of orthopedic problems was maximized by the station approach.”7 The preparticipation physical evaluation needs to be practical and accurate. Careful, thorough history taking and

Preparticipation Physical Examination

an efficient, effective physical examination must be carried out, because the conditions of concern are rare and difficult to detect. If a possible risk is found and other athletes are waiting, the individual in question should return at the end of the other physicals or follow up in the office, so that the problem may be explained, evaluated further, and managed properly. PPE Components History Approximately 70% of orthopedic and medical problems resulting in the disqualification of an athlete are identified by the medical history alone.7 Typically, the athlete completes a thorough screening questionnaire, which the physician then reviews. Approximately 30% of athletes are estimated to report an injury that required a physician’s treatment in the past.20,21 Previous musculoskeletal injury has been identified as the best predictor of orthopedic reinjury.22 On-line PPE Internet forms have been used to facilitate the history process.23 The advantages are that they are more accurate and efficient and the data are computerized and easily analyzed. The disadvantages remain that they are still subjective and self-reported. The physician should meet the athlete individually to inquire about any concerns reported in the questionnaire and elicit more details regarding the past medical history and previous injuries. Questions relating to conditions of particular risk in the sport in question should be asked again to the athlete during the interview, even if he or she answered negative on the questionnaire, to ensure the athlete’s response. For example, a young female gymnast should be asked specifically about possible eating disorders and menstrual irregularities. Similarly, the clinician should review cardiac symptoms in detail with a basketball player with Marfanoid features. There is a fine line with

KEY POINTS Purpose/objectives of the PPE 1. The preparticipation physical examination does not eliminate the athlete’s risk of injury in sports. 2. The most common reasons for disqualifying athletes are cardiovascular or orthopedic conditions. 3. Informed parental/guardian consent is required to perform a PPE for athletes younger than 18 years of age. 4. The PPE is an opportunity to perform preventative health screening and give anticipatory advice. 5. The physician must meet “standard of care,” for which the requirements can be facilitated by using standardized forms for the history and physical examination. 6. The physician must document each PPE carefully, as for any patient visit.

KEY POINTS How is a PPE carried out? 1. The PPE ideally should be performed 6–8 weeks before participation in the sport begins. 2. A physician typically performs the PPE during an individual office visit or by stationbased approach. 3. A physician should organize the appropriate staff, resources, and space for the number of athletes requiring physical examinations.

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some of the questions asked during the PPE, in which many athletes feel uncomfortable telling the truth. The accuracy of the athlete’s responses should be verified with the parents if possible.10,24,25 The clinician must use his or her judgment to decide whether there is enough evidence that an athlete should be withheld from participation, with follow up to explore the potential problem. Again, published recommendations can be helpful in these cases. Cardiac History The assessment for causes of sudden cardiac death is a major part of the PPE because preventing life-threatening disorders is a priority. The incidence of sudden death in high school or college athletes has been estimated from 1 in 200,00026 to 1 in 300,000.27 Hypertrophic cardiomyopathy is considered the most common cause of sudden death in young athletes in North America.24 Arrhythmogenic right ventricular dysplasia was a common cause of cardiac death in European athletes.28 Other cardiac conditions associated with fatalities include coronary artery abnormalities, myocarditis,27 rhythm and conduction abnormalities, systemic hypertension, and valvular diseases.28 The prevalence of these conditions most likely varies depending on the population in question. Hypertrophic cardiomyopathy is a particularly important cause of sudden death in AfricanAmerican athletes.24 Fortunately, there is a lower rate of sudden death in young women.29,30 The American Heart Association has made recommendations for cardiovascular preparticipation screening of young athletes (Box 10–2), which asks that history taking or the questionnaire should always include screening for cardiovascular sudden death.10,31

Box 10–2 American Heart Association Consensus Panel Recommendations for Cardiovascular Preparticipation Screening of Young Athletes Complete history taking should include (with parental verification of responses): 1. Cardiovascular symptoms: Particularly prior occurrence of exertional chest pain/discomfort; prior episodes of syncope/near-syncope; excessive, unexpected, and unexplained shortness of breath or fatigue associated with exercise 2. Past detection of a heart murmur or systemic hypertension 3. Family history of premature sudden death (younger than 50 years old) or heart disease in surviving relatives 4. Careful physical examination should include: a. Precordial auscultation in both supine/sitting and standing positions to identify heart murmurs consistent with left ventricular outflow tract obstruction b. Palpation of femoral pulses c. Stigmata of the Marfan syndrome d. Brachial artery blood pressure measurement Data from 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.

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Athletes should also be asked about the following symptoms associated with exercise: exertional chest pain/discomfort; syncope/near-syncope; and excessive, unexpected, and unexplained shortness of breath or fatigue. In addition, a history of heart murmur and systemic hypertension should be elicited. A family history of premature death, sudden or otherwise, or significant disability from cardiovascular disease in close relative(s) younger than 50 years old should be identified, especially if there was occurrence of hypertrophic cardiomyopathy, dilated cardiomyopathy, long QT syndrome, Marfan syndrome, or clinically important arrythmias.10 Another cause of cardiac death is commotio cordis, which is the sudden development of ventricular fibrillation caused by a blunt impact to the chest wall. Proper use of chest protectors for sports such as hockey and baseball (catchers) is advised to reduce the risk of this potentially fatal injury.32,33 The use of reduced impact balls for youth baseball34 younger than age 14 has also been recommended. Neurological History Head and neck injuries are the most common “traumatic” causes of serious disability. Prior concussions are recognized as a serious area of concern. The current definition of concussion is “a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces.”35 Previous guidelines have been proposed to care for recent concussions,36 although they remain controversial. They involve expert opinion regarding when a player may return to play after a minor head injury. Definitely, any athlete who still has any neurological symptoms after recent head trauma should be withheld from contact activities and investigated appropriately. Several experts recommend neuropsychological testing of athletes in contact sports in the preseason and after head injuries to check for cognitive deficits from baseline levels, which can be used to follow recovery.37,38 When considering an athlete with a history of concussions, the physician should carefully determine details of the injuries, including mechanism, frequency, and type and duration of symptoms.35 Results of studies have suggested a cumulative effect of concussion, particularly in high school athletes,39,40 although evidence regarding how many concussions are allowed before a player discontinues a sport is not yet definitive.41 A history of recurrent neurological symptoms is concerning. An athlete with recurrent seizures must have the disorder well controlled before participation in sports is considered. Cervical stenosis or instability should be ruled out in players with a history of recurrent paresthesias, pain or weakness in any extremity, which may affect their eligibility for contact sports. Referral to a neurosurgeon experienced in sports injury is recommended. Other Medical Issues The physician should screen for several common illnesses associated with sports activity. A history of coughing, wheezing, or difficulty breathing with activity may be a symptom of exercise-induced asthma. It is useful to note whether the athlete has any allergies to food, medicines, the environment, or to insect stings in order to warn the staff who supervises the sport. A rash or hives occurring with activity may suggest exercise-induced anaphylaxis. A fever

or viral illness raises suspicions about the possibility of a recent infection. Splenomegaly and myocarditis should be ruled out. Current and recent skin problems should be reported, especially in contact sports, such as wrestling, or water sports. Problems with vision and hearing can also be addressed during the PPE. The American Academy of Pediatrics and the American Academy of Ophthalmology published a joint position statement on “Protective Eyewear for Young Athletes,” which reviews specific sports and the recommendations for eye protection.42 Exertional hyperthermia is suspected to be the most common cause of noncardiovascular deaths.27 A previous history of dehydration or heat illness during sports can be an area where the physician can educate athletes, especially those participating in outdoor activities such as football and soccer. Concerns are increased about dehydration and heat stroke for athletes taking certain medications or supplements that increase metabolism, such as amphetamines, ephedra, and caffeine. Education regarding proper hydration during exercise and identification of the signs and symptoms of heat illness should be explained. Particular questions are directed toward the young female athlete. Details of the menstrual history, including the onset of menarche, the reguKEY POINTS larity of the menstrual cycle, missed cycles, last menstrual History period, and use of oral contra1. History is the most ceptives, should be discussed. useful part of the PPE There have been reports that in identifying condiamenorrhea can be as high as tions in the athlete. 66% in populations of female 2. The accuracy of the athletes.43 The practitioner must medical history can be vigilant for symptoms and be improved with signs of the female athlete triad, parental verification which is composed of disordered of the athlete’s eating, amenorrhea, and osteoanswers. porosis. 3. Cardiac symptoms Medications, Nutrition, Supplements, and Drugs The medications, supplements, and diet of an athlete can affect performance as well as pose risks.44 Supplement use is prevalent in high school athletes, with creatine use reported at 8.2% in a recent study.45 Anabolic steroid use by students has been estimated at 9%46 in high school and 2.3% in grades 5 to 7.47 Drug use including nicotine, alcohol, and illicit drugs can be explored, if the physician feels it is appropriate; the PPE could be the athlete’s only contact with a medical professional.

should be checked because hypertrophic cardiomyopathy is the most common cause of sudden death in young athletes in North America. 4. The menstrual and nutrition history should be assessed in young female athletes. 5. Anabolic steroid and supplement use is not uncommon, especially in the high school population.

Musculoskeletal History For many musculoskeletal problems, contraindications are usually relative depending on the injury and the requirements of the sport. Smith and Laskowski identified that

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musculoskeletal abnormalities were the most common abnormalities identified in the preparticipation physical examinations they performed at the Mayo Clinic.14 In their own study, they disqualified most athletes from sport, as a result of musculoskeletal conditions, and secondly by cardiac problems. They did warn of the subjectivity of the diagnosis of some musculoskeletal abnormalities. In their population of 2739 high school athletes, the knee was the second most common area of reported injury after ankle–foot injuries. Four of the athletes were restricted from participation for knee conditions, such as instability.14

a child’s ability to participate fully in his or her sport. Fortunately, these conditions are usually not contraindications to play. However, the athlete and parents should be properly counseled so that they understand the condition and the steps that can be taken (including exercise and bracing) to keep the child playing effectively.

Knee Concerns Ligament instability caused by injury to the anterior cruciate ligament (ACL) is particularly a concern for the athlete involved in contact or cutting and pivoting sports, such as football, basketball, and soccer. A young athlete with a complete ACL tear should be restricted from these sports, and surgical reconstruction of the ligament should be seriously considered. Surgical reconstruction improves the athlete’s ability to return to sports and reduces the incidences of developing a symptomatic meniscal tear and giving way symptoms during activity.48 If definitive treatment needs to be delayed because of age or surgical considerations, activities may be limited to low-impact, straight-line activities such as biking and swimming. Regarding partial ACL tears, athletes older than 15 years of age with tears greater than 50% or predominant tearing of the posterolateral bundle on scope should restrict their sports and consider reconstruction, because evidence suggests that these factors predict a worse functional outcome and increased need for reconstruction.49 Internal derangements of the joint, including injuries to the meniscus and articular surface, can affect proper joint function and make participation in certain sports dangerous because of the potential for further damage to the joint. A meniscal or cartilage injury that impairs range of motion is symptomatic, should be treated definitively, and often requires surgical attention. Athletes with a symptomatic osteochondritis dissecans (OCD) lesion should restrict activities and be referred to an orthopedic surgeon. However, asymptomatic OCD lesions present a controversial management decision. Because the OCD may progress to an unstable lesion, we recommend that an athlete with an OCD, even if asymptomatic, should be withheld from competition until cleared by a specialist who has experience with these lesions. With regard to the patellofemoral joint, athletes with recurrent patellar dislocations or refractory patellofemoral pain may have relative contraindications for cutting and pivoting sports, or for heavy jumping or running activities. Unfortunately, some athletes continue to be symptomatic with most training activities in a particular sport, despite conservative treatment, including an appropriate course of physical therapy and biomechanical corrections with orthotics, taping, and bracing. These athletes should be advised that the condition may not ultimately resolve with such measures and that they should consider participating in a less-demanding sport or seek more definitive treatment, especially if more than a third of the season is missed. During the growth spurt, overuse problems such as apophysitis (Osgood-Schlatter disease and SindingLarsen-Johansson disease) or tendinopathies can affect

Physical Examination During the PPE the clinician relies on screening test maneuvers. A specific system or joint examination should be performed if any pathology is suspected or if there is particular risk for injury in the sport the athlete participates in. We will specifically discuss the cardiac and knee screening examinations for the PPE. We refer the reader to other chapters for details on specific joint pathologies, as well as to other textbooks for the description of the examination of other organ systems.

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KEY POINTS Musculoskeletal history 1. Musculoskeletal problems are the most common injuries identified by the PPE. 2. Young athletes with ligament instability, internal derangement of the knee, patellar instability, or osteochondritis dissecans should seek appropriate evaluation with an experienced physician. 3. Athletes with signs of overuse injuries such as patellofemoral pain and/or apophysitis (Osgood-Schlatter disease, SindingLarsen-Johansson disease) should be educated on the expected course of the problem and recommendations on how to reduce/ prevent symptoms.

General Examination Body habitus, height, and weight using a calibrated scale should be noted. The body mass index can be calculated using height in meters over weight squared in kilograms (m/kg2). Physical stigmata of Marfan syndrome include tall, thin build; long fingers and arms; pectus excavatum or carinatum; scoliosis or kyphosis; and joint hypermobility. The arm span width-to-height ratio (>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.

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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

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

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.

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

References 1. Silver MD: Use of ergogenic aids by athletes. J Am Acad Orthop Surg 9:61–70, 2001. 2. Wertheim J: Jolt of reality. Sports Illustrated 98: 69–79,2003. 3. Buckley WE, Yesalis CE, Friedl KE, et al: Estimated prevalence of anabolic steroid use among high school seniors. JAMA 260:3441–3445, 1988. 4. Committee on Sports Medicine: Anabolic steroids and the adolescent athlete. Pediatrics 83:127–128, 1989. 5. Bahrke MS, Yesalis CE, Brower KJ: Anabolic-androgenic steroid abuse and performance-enhancing drugs among adolescents. Child Adolesc Psychiatr Clin N Am 7:821–838, 1998. 6. Irving LM, Wall M, Neumark-Sztainer D, et al: Steroid use among adolescents: findings from project EAT. J Adol Health 30:243–252, 2002. 7. Gaa G, Griffith E, Cahill B, et al: Prevalence of anabolic steroid use among Illinois high school students. J Athl Train 29: 216–222, 1994. 8. Stilger VG, Yesalis CE: Anabolic-androgenic steroid use among high school football players. J Community Health 24:131–145, 1999. 9. Whitehead R, Chillag S, Elliot D: Anabolic steroid use among adolescents in a rural state. J Fam Practice 35: 401–405, 1992. 10. Middleman AB, Durant RH: Anabolic steroid use and associated health risk behaviours. Sports Med 21:251–255, 1996. 11. Rickert VI, Pawlak-Morello C, Sheppard V, Jay MS: Human growth hormone: a new substance of abuse among adolescents? Clin Pediatr (Phila) 31:723–726, 1992. 12. Green GA, Uryasz FD, Petr TA, et al: NCAA study of substance use and abuse habits of college student-athletes. Clin J Sport Med 1151–56, 2001. 13. Bents RT, Tokish JM: Stimulant use among college hockey players, unpublished data, 2003. 14. Goldberg L, Bents RT, Bosworth E, et al: Anabolic steroid education and adolescents: do scare tactics work? Pediatrics 87:283–286, 1991. 15. Bents RT, Young J, Bosworth E, et al: An effective education program alters attitudes toward anabolic steroid use among adolescent athletes. Med Sci Sports Exerc 22(suppl):64, 1990. 16. Goldberg L, MacKinnon DP, Elliot DL, et al: The adolescents training and learning to avoid steroids program: preventing drug use and promoting health behaviors. Arch Pediatr Adolesc Med 154:332–338, 2000. 17. Yesalis CE, Courson SP, Wright J: History of anabolic steroid use in sport and exercise. In Yesalis CE (ed): Anabolic Steroids in Sport and Exercise. Champaign, Ill.: Human Kinetics, 1993. 18. Tanner SM, Miller DW, Alongi C: Anabolic steroid use by adolescents: prevalence, motives, and knowledge of risks. Clin J Sport Med 5:108–115, 1995. 19. Johnston LD, O’Malley PM, Bachman JG: Monitoring the future study 1998: trends in prevalence of various drugs for 8th graders and high school seniors. Rockville, Md.: National Institute on Drug Abuse, National Institutes of Health, 1998. 20. Windsor R, Dumitru D: Prevalence of anabolic steroid use by male and female adolescents. Med Sci Sports Exerc 21:494–497, 1989. 21. Terney MA, McLain LG: Use of anabolic steroids in high school students. Am J Dis Child 144:99–103, 1990. 22. Johnson MD, Jay MS, Shoup B, et al: Anabolic steroid use by male adolescents. Pediatrics 83:921–924, 1989. 23. Yesalis CE, Kennedy NK, Kopstein AN, et al: Anabolic-androgenic steroid use in the United States. JAMA 270: 1217–1221, 1993. 24. Faigenbaum AD, Zaichkowsky LD, Gardner DE, et al: Anabolic steroid use by male and female middle school students. Pediatrics 101:E6, 1998. 25. Shahidi NT: A review of the chemistry, biological action, and clinical applications of anabolic-androgenic steroids. Clin Ther 23:1355– 1390, 2001. 26. Cable NT: Anabolic-androgenic steroids; ergogenic and cardiovascular effects. In Reilly T, Orme M (eds): The Clinical Pharmacology of Sport and Exercise. Amsterdam: Exerpta Medica, 1997, pp 135–144. 27. Williams MH, Branch JD: Ergogenic aids for improved performance: In Garrett WE, Kirkendall DT (eds): Exercise and Sport Science. Philadelphia: Lippincott Williams and Wilkins, 2000, pp 373–384. 28. Miller RW: Athletes and steroids: playing a deadly game. FDA consumer HHS publication No. (FDA) 88-3170; US Government Printing Office, 1988-201-865/80014, 1988.

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29. Evans NA: Gym and tonic: a profile of 100 male steroid users. Br J Sports Med 31:54–58, 1997. 30. Crist DM, Stackpole PJ, Peake GT: Effects of androgenic-anabolic steroids on neuromuscular power and body composition. J Appl Physiol 54:366–370, 1983. 31. Friedl KE, Dettori JR, Hannan CJ Jr, et al: Comparison of the effects of a high dose of testosterone and 19-nortestosterone to a replacement dose of testosterone on strength and body composition in normal men. J Steroid Biochem Mol Biol 40:607–612, 1991. 32. Bhasin S, Storer TW, Berman N, et al: The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. N Engl J Med 335:1–7, 1996. 33. Forbes GB, Porta CR, Herr BE, et al: Sequence of changes in body composition induced by testosterone and reversal of changes after drug is stopped. JAMA 267:397–399, 1992. 34. Giorgi A, Weatherby RP, Murphy PW: Muscular strength, body composition, and health responses to the use of testosterone enanthate: a double blind study. J Sci Med Sport 2:341–355, 1999. 35. DuRant RH, Rickert VI, Ashworth CS, et al: Use of multiple drugs among adolescents who use anabolic steroids. N Engl J Med 328:922–926, 1993. 36. Yesalis CE, Bahrke MS: Anabolic-androgenic steroids. Sports Med 19:326–340, 1995. 37. Haupt HA, Rovere GD: Anabolic steroids: a review of the literature. Am J Sports Med 12:469–484, 1984. 38. Kuipers H, Wijnen JA, Hartgens F, et al: Influence of anabolic steroids on body composition, blood pressure, lipid profile, and liver functions in body builders. Int J Sports Med 12:413–418, 1991. 39. Glazer G: Atherogenic effects of anabolic steroids on serum lipid levels. A literature review. Arch Intern Med 151:1925–1933, 1991. 40. Ebenbichler CF, Sturm W, Ganzer H, et al: Flow-mediated, endothelium-dependent vasodilatation is impaired in male body builders taking anabolic-androgenic steroids. Atherosclerosis 158:483–490, 2001 41. Cooper CJ, Noakes TD, Dunne T, et al: A high prevalence of abnormal personality traits in chronic users of anabolic-androgenic steroids. Br J Sports Med 30:246–250, 1996. 42. Midgley SJ, Heather N, Davies JB: Levels of aggression among a group of anabolic-androgenic steroid users. Med Sci Law 41:309–314, 2001. 43. Melchert RB, Welder AA: Cardiovascular effects of androgenic-anabolic steroids. Med Sci Sports Exerc 27:1252–1262, 1995. 44. Hui MJ: An acute myocardial infarction occurring in an anabolic steroid user. Med Sci Sports Exerc 26:408–413,1994. 45. Yesalis CE, Vicary JR, Buckley WE: Anabolic steroid use among adolescents: a study of indications of psychological dependence. In Yesalis CE (ed): Anabolic Steroids in Sport and Exercise. Champaign, Ill.: Human Kinetics, 1993, pp 215–229. 46. Rich JD, Dickinson BP, Feller A, et al: The infectious complications of anabolic-androgenic steroid injection. Int J Sports Med 20:563–566, 1999. 47. Rich JD, Foisie CK, Towe CW, et al: Needle exchange program participation by anabolic steroid injectors, United States 1998. Drug Alcohol Depend 56:157–160, 1999. 48. Scott MJ, Scott MJ Jr: HIV infection associated with injections of anabolic steroids. JAMA 262:207–208, 1989. 49. American Academy of Pediatrics: Adolescents and anabolic steroids: a subject review. Pediatrics 99:904–908, 1997. 50. American College of Sports Medicine position statement on the use and abuse of anabolic/androgenic steroids in sports. Med Sci Sports Exerc 19:534–539, 1987. 51. National Strength and Conditioning Association position statement: Anabolic-androgenic steroid use by athletes. Strength and Conditioning 15:9, 1993. 52. Scott DM, Wagner JC, Barlow TW: Anabolic steroid use among adolescents in Nebraska schools. Am J Health-Syst Pharm 53:2068–2072, 1996. 53. Goldberg L, Elliot DL, Clarke G, et al: The adolescents training and learning to avoid steroids (ATLAS) prevention program: background and results of a model intervention. Arch Pediatr Adolesc Med 150:713–721, 1996. 54. Goldberg L, Elliot DL, Clarke G, et al: Effects of a multidimensional anabolic steroid prevention intervention: The adolescents training and learning to avoid steroids (ATLAS) prevention program. JAMA 276:1555–1562, 1996. 55. Yesalis CE, Wright J: Social alternatives. In Yesalis CE (ed): Anabolic Steroids in Sport and Exercise. Champaign, Ill.: Human Kinetics, 1993.

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56. Veronia School District 47 v Acton, 15 S Ct 2386 (1995). 57. Normand J, Lempert RO, O’Brian CP (eds): Under the influence? Drugs and the American work force. Washington, DC: National Academy Press, 1994. 58. Goldberg L, Bosworth EE, Bents RT, et al: Effect of an anabolic steroid education program on knowledge and attitudes of football players. J Adolesc Health Care 11:210–214, 1990. 59. Goldberg L, Elliot DL, Bosworth EE, et al: Boomerang effects of drug education programs. Pediatrics 88:1079, 1991. 60. Macintyre JG: Growth hormone and athletes. Sports Med 4:129–142, 1987. 61. Committee on the Judiciary, US Senate: Drug Misuse: Anabolic steroids and human growth hormone, Washington DC: General Accounting Office publication GAO1 HRD-89–109, 1989. 62. Taaffe DR, Pruitt L, Reim J, et al: Effect of recombinant human growth hormone on the muscle strength response to resistance exercise in elderly men. J Clin Endocrinol Metab 79:1361–1366, 1994. 63. Carroll PV: Treatment with growth hormone and insulin-like growth factor-I in critical illness. Best Pract Res Clin Endocrinol Metab 15:435–451, 2001. 64. Yarasheski KE: Growth hormone effects on metabolism, body composition, muscle mass, and strength. Exerc Sport Sci Rev 22:285–312, 1994. 65. Conlee RK: Amphetamine, caffeine, and cocaine. In Lamb DR, Williams MH (eds): Ergogenics: Enhancement of Performance in Exercise and Sport. Dubuque, Iowa: Brown and Benchmark, 1991, pp 285–330. 66. Chandler JV, Blair SN: The effect of amphetamines on selected physiological components related to athletic success. Med Sci Sports Exerc 12:65–69, 1980. 67. Gill ND, Shield A, Blazevich AJ, et al: Muscular and cardiorespiratory effects of pseudoephedrine in human athletes. Br J Clin Pharmacol 50:205–213, 2000. 68. Gruber AJ, Pope HG Jr: Ephedrine abuse among 36 female weightlifters. Am J Addict 7:256–261, 1998. 69. King DS, Sharp RL, Vukovich MD, et al: Effect of oral androstenedione on serum testosterone and adaptations to resistance training in young men: a randomized controlled trial. JAMA 281:2020–2028, 1999. 70. Ballantyne CS, Phillips SM, MacDonald JR, et al: The acute effects of androstenedione supplementation in healthy young males. Can J Appl Physiol 25:68–78, 2000. 71. Wallace MB, Lim J, Cutler A, et al.: Effects of dehydroepiandrosterone vs. androstenedione supplementation in men. Med Sci Sports Exerc 31:1788–1792, 1999. 72. Rasmussen BB, Volpi E, Gore DC, et al: Androstenedione does not stimulate muscle protein anablolism in young healthy men. J Clin Endocrinol Metab 85:55–59, 2000. 73. Broeder CE, Quindry J, Brittingham K, et al: The Andro Project: physiological and hormonal influences of androstenedione supplementation in men 35 to 65 years old participating in a high-intensity resistance training program. Arch Intern Med 160:3093–3104, 2000. 74. Leder BZ, Longcope C, Catlin DH, et al: Oral androstenedione administration and serum testosterone concentrations in young men. JAMA 283:779–782, 2000. 75. Brown GA, Martini ER, Roberts BS, et al: Acute hormonal response to sublingual androstenediol intake in young men. J Appl Physiol 92:142–146, 2002. 76. Brown GA, Vukovich MD, Martini ER, et al: Endocrine and lipid responses to chronic androstenediol-herbal supplementation in 30 to 58 year old men. J Am Coll Nutr 20:520–528, 2001. 77. Kraemer WJ, Volek JS: Creatine supplementation. Its role in human performance. Clin Sports Med 18:651–666, 1999. 78. Eichner ER: Ergogenic aids. Phys Sports Med 25:70–80, 1997. 79. Greenwood M, Farris J, Kreider R, et al: Creatine supplementation patterns and perceived effects in select division I collegiate athletes. Clin J Sport Med 10:191–194, 2000. 80. LaBotz M, Smith BW: Creatine supplement use in an NCAA division I athletic program. Clin J Sport Med 9:167–169, 1999.

81. Tokish JM, Hawkins RJ: Creatine in the NFL: a survey of policy, use, and practice. Unpublished data, 2001. 82. Balsom PD, Soderlund K, Ekblom B: Creatine in humans with special reference to creatine supplementation. Sports Med 18:268–280, 1994. 83. Harris RC, Soderlund K, Hultman E: Elevation of creatine in resting and exercised muscle of normal subjects by creatine supplementation. Clin Sci (Lond) 83:367–374, 1992. 84. Balsom PD, Ekbolm B, Soderlund K, et al: Creatine supplementation and dynamic high-intensity intermittent exercise. Scand J Med Sci Sports 3:143–149, 1993. 85. Kreider RB, Ferreira M, Wilson M, et al: Effects of creatine supplementation on body composition, strength, and sprint performance. Med Sci Sports Exerc 30:73–82, 1998. 86. Stone MH, Sanborn K, Smith LL, et al: Effects of in-season (5 weeks) creatine and pyruvate supplementation on anaerobic performance and body composition in American football players. Int J Sport Nutr 9:146–165, 1999. 87. Earnest CP, Snell PG, Rodriguez R, et al: The effect of creatine monohydrate ingestion on anaerobic power indices, muscular strength and body composition. Acta Physiol Scand 153:207–209, 1995. 88. Rico-Sanz J, Mendez Marco MT: Creatine enhances oxygen uptake and performance during alternating intensity exercise. Med Sci Sport Exerc 32:379–385, 2000. 89. Birch R, Noble D, Greenhaff PL: The influence of dietary creatine supplementation on performance during repeated bouts of maximal isokinetic cycling in man. Eur J Appl Physiol 69:268–276, 1994. 90. Dawson B, Cutler M, Moody A, et al: Effects of oral creatine loading on single and repeated maximal short sprints. Aust J Sci Med Sport 27:56–61, 1995. 91. Leenders NM, Lamb DR, Nelson TE: Creatine supplementation and swimming performance. Int J Sport Nutr 9:251–262, 1999. 92. Grindstaff PD, Kreider R, Bishop R, et al: Effects of creatine supplementation on repetitive sprint performance and body composition in competitive swimmers. Int J Sports Nutr 7:330–346, 1997. 93. Burke LM, Pyne DB, Telford RD: Effect of oral creatine supplementation on single-effort sprint performance in elite swimmers. Int J Sports Nutr 6:222–233, 1996. 94. Mujika I, Chatard JC, Lacoste L, et al: Creatine supplementation does not improve sprint performance in competitive swimmers. Med Sci Sports Exerc 28:1435–1441, 1996. 95. Mujika I, Padilla S, Ibanez J, et al: Creatine supplementation and sprint performance in soccer players. Med Sci Sports Exerc 32:518–525, 2000. 96. Harris RC, Viru M, Greenhaff PL, et al: The effect of oral creatine supplementation on running performance during maximal short term exercise in man. J Physiol 74:467–469, 1993. 97. Aaserud R, Gramvik P, Olsen SR, et al: Creatine supplementation delays onset of fatigue during repeated bouts of sprint running. Scand J Med Sci Sports 8:247–251, 1998. 98. Schedel JM, Terrier P, Schutz Y: The biomechanic origin of sprint performance enhancement after one-week creatine supplementation. Jpn J Physiol 50:273–276, 2000. 99. Redondo DR, Dowling EA, Graham BL, et al: The effect of oral creatine monohydrate supplementation on running velocity. Int J Sport Nutr 6:213–221, 1996. 100. Javierre C, Lizarraga MA, Ventura JL, et al: Creatine supplementation does not improve physical performance in a 150 m race. Rev Esp Fisiol 53:343–348, 1996. 101. Koshy KM, Griswold E, Schneeberger EE: Interstitial nephritis in a patient taking creatine. N Engl J Med 340:814–815, 1999. 102. Poortmans JR, Francaux M: Renal dysfunction accompanying oral creatine supplements. Lancet 352(9123):234, 1998. 103. Greenhaff P: Renal dysfunction accompanying oral creatine supplements. Lancet 352(9123):233–234, 1998.

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).

●

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 <19 years of age at the time a patient was first diagnosed. 3. “College” age group is ≥19 and <23 years of age. 4. Data from Kentucky Sports Medicine billing system, January 1, 1990 through August 11, 2003. 5. “Relative Risk” shows the ratio of percentages of females to males for each age group.

Under 15 High School College Over 23

Females

PLICA

Table 12–1 Kentucky Sports Medicine Experience

1.16 0.83 0.55 0.44 0.57

Ratio F:M 2.0 1.5 1.0 0.8

Relative Risk

510 952 480 2482 4424

Females

499 1345 756 3586 6186

Males

1009 2297 1236 6068 10610

Total

1.02 0.71 0.63 0.69 0.72

Ratio F:M

All Knee Diagnoses

1.4 1.0 0.9 1.0

Relative Risk

Special Concerns in the Female Athlete

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basketball athletes (females:males) was 6.5:1 in those younger than age 15; the ratio for high school age was 1.63:1, and college age fell to KEY POINTS 0.88:1 (Table 12–2). Of the ACL reconstructions performed 1. High-school age socin female basketball players, cer and basketball 65% were high school age and female athletes are less than 14% were younger the most vulnerable than age 15. In male basketball to ACL injury. players, 2% were performed on 2. In the 2000–2001 those younger than age 15, school year, females 40% were high school age, competing at the 17% were college age, and 41% collegiate level were older than age 23 (see numbered 157,740, Table 12–2). In soccer, ACL comprising 42% of reconstructions were performed, the total number but relative risk (female:male) of athletes. ratios were 1.9:1 in high school 3. In the 2002–2003 age players, dropping to 0.75:1 school year, high in college age players (see school female athletes Table 12–2). The true rates of numbered 2,856,358, knee injuries of pediatric and comprising 42% of adolescent ages are unknown. the total number of Funded prospective studies in this high school athletes. age group comparing the sexes 4. Girls’ basketball and sports are needed. Doculeads as the sport mentation of hours of participathat causes most tion, numbers of participants, ACL injuries in the numbers and types of surgeries, high-school and and exact diagnosis must be done college-age athlete. to determine injury rates. Growth and Development There are inherent differences between the sexes physiologically, anatomically, and psychologically. Prepubertal girls and boys have the same body composition, motor skills, strength, and endurance, and are essentially comparable in physical condition and can compete against each other in sports until between the ages of 10 and 12.7 Compared to the past, children today are heavier and taller and undergo puberty at an earlier age.7 The exception is gymnasts, who are shorter than gymnasts of 20 years ago.5 Until puberty, the

genders differ little in strength, body fat, motor skills, endurance, physical condition, and injury risk.7 The effects of estrogen on females at puberty increases their percentage of body fat and lessens lean muscle mass compared to the androgen influence on males.8 Upper body strength in females, even with training, remains 30–50% that of males, and lower extremity strength remains 70% that of males.7 Despite these differences, women show the same physiological response to training as males, with significant increases in strength, power, and endurance.9 In females, growth is essentially complete by 2 years’ postmenarche. Females reach physiological and skeletal maturity and achieve peak height velocity before males.10 The peak height velocity in females with idiopathic scoliosis by clinical measurements documents growth peak and predicts cessation of growth reliably.11 Peak height velocity occurs at a median of 6 months before menarche and 8 months before median Risser 1, and 3.5 years before median Risser 5.11 Peak limb growth occurs 6 months earlier than spinal growth.12,13 Spinal growth occurs after limb growth has ceased.14 The peak height occurs a month after menarche, with a rate of 9 cm per year. Sports training has not been shown to have any impact on height peak, height velocity, or the rate of increase in height during adolescence.11 Knee Growth Sixty-five percent of the growth of the lower extremity occurs at the knee—37% distal femoral physis and 28% proximal tibial physis.13,15,16 The appearance of the physeal plate radiographically with anteroposterior (AP), lateral, and notch views is helpful. Central physeal closure and “blurred” physis indicate skeletal knee maturity.17 Growth measurements should be repeated for each clinic visit and include growth velocity of standing height, sitting height, lower limb, and growth remaining for different segments.13 Although charts and diagrams of growth are only templates, they outline evolution of growth. Wrist films for skeletal age is a suggested method to assess skeletal maturity.18 The estimates of remaining growth at the knee in boys and girls are shown in Figure 12–319 (Carl Stanitski, personal

Table 12–2 Kentucky Sports Medicine Experience Basketball Athlete and Soccer Athlete ACL Reconstructions Kentucky Sports Medicine Data, 1990–2003 Basketball Females Age Group Under 15 (n = 24) High School (n = 149) College (n = 45) Over 23 (n = 65)

College: ≥19 and <23. High School: ≥15 and <19.

N 21 95 22 9 147

Males

Soccer Ratios F:M

Females

Males

%

N

%

N

Risk

N

%

N

14% 65% 15% 6% 100%

3 54 23 56 136

2% 40% 17% 41% 100%

7.00 1.76 0.96 0.16 1.08

6.48 1.63 0.88 0.15 1.00

6 38 9 5 58

10% 66% 16% 9% 100%

0 20 12 12 44

Ratios F:M %

0% 45% 27% 27% 100%

N

Risk

1.90 0.75 0.42 1.32

1.44 0.57 0.32 1.00

Special Concerns in the Female Athlete

117

Puberty is assessed by Tanner stages, which are reported by the athlete.20 Although Tanner 3 stage patients can be treated as adults, Tanner 1 and Tanner 2 stages require soft tissue tunnel grafts and fixation coming from the epiphyseal plate. To preserve articular cartilage and the menisci, ACL reconstruction should be performed earlier rather than later. Parents and patient should be informed of all potential risks of ACL reconstruction. Lower Extremity Alignment

Figure 12–3 The remaining growth at the knee in males and females, in centimeters, is shown in yearly average increments. (Data from Morrissy RT, Weinstein S: Lovell and Winter’s Pediatric Orthopaedics, 5th ed., Vol 1. Philadelphia: Lippincott, Williams & Wilkins, 2001, p 47.)

communication). In boys at age KEY POINTS 10, distal femoral growth is 7.5 1. Ages of growth cm and proximal tibial growth patterns and peak is 4.8 cm compared with girls, velocity of knee (4.5 cm distal femoral and 2.8 growth differ in males proximal tibia). The remaining and females. growth in centimeters is shown 2. Tanner staging and until age 14 in females and 16 radiological appearin males. A good analogy is a ance of growth plates car approaching a stop sign. about the knee are The engine is running, but the important in deciding vehicle is slowing down, such the timing, type of that the risk of an accident is graft, and fixation of less at that time remaining to ACL reconstruction. get to the stop sign. Physes 3. Peak height velocity work the same way. The physioccurs 6 months ological response and appearbefore menarche. ance of the physical plate, wide 4. Estimates of open versus partially closed, remaining growth reflects the dynamics of growth about the knee help (Carl Stanitski, personal comto counsel patients munication). on injury patterns and Most female athletes who the safety of ACL sustain an ACL tear are skeletally reconstructions. mature enough to perform bony procedures across the plate. However, in girls who are immature, the physician should know the Tanner stages.

Normal male alignment is shown in Figure 12–4, A. The hips are directly over the knees, which are over the ankles—no significant rotation. In females, rotational and valgus alignment create the forces responsible for anterior knee pain and patellar instability. Miserable malalignment syndrome is defined as excessive knee valgus, femoral anteversion, tibial external rotation, and forefoot pronation (Figure 12–4, B). This malalignment syndrome creates valgus moments at the knee, internal femoral rotation, and laterally directed patellar forces. Commonly seen in cheerleaders, gymnasts, dancers, and track athletes, miserable malalignment syndrome is evident in the swimmer pictured in Figure 12–4, C. Lower extremity alignment differences are more obvious to patient and examiner during active movements. While the patient is standing on a small step-up, ask him or her to do a simple mini-squat on one leg (Figure 12–5). The male (Figure 12–5, A) flexes KEY POINTS more at the hip and knee without rotation, keeping the hip 1. Dynamic, not static, over knee over ankle. The alignment predicts female typically acquires a more movement in sport upright posture and greater knee and knee injury valgus position. Her hip is patterns. adducted, internally rotated, and 2. Mini-squat movement the tibia is externally rotated and patterns differ in forefoot pronated. Viewed from males and females. the side, the male demonstrates a a. The male stays flat back and posteriorly rotated straighter and the position of the pelvis, while the lumbar spine is female has an anteriorly rotated flatter, resulting in pelvis position with increased knee and tibia in 21 lumbar lordosis (Figure 12–5, neutral rotation. B). This lower extremity position b. The female knee of femoral internal rotation and goes into excesadduction places the knee in the sive valgus with high-risk position predisposing to the femur interACL tears and patellofemoral nally rotated. dislocation. c. Proximally excesIt is the dynamic, not static, sive lumbar lordoanatomical measurements that sis and distally predict knee problems. It has excessive tibia been believed that females external rotation have a larger Q-angle measureand forefoot ment; however, the difference pronation create between males and females is not abnormal rotasignificant and no relationship tional forces at the between Q-angle and knee injury knee. rates has been proved. Clinical

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Figure 12–4—cont’d C, Clinical example of a collegiate swimmer from the front, showing 20 degrees genu valgum, external tibial torsion, hypoplastic VMO, heel valgus, and pes planus with forefoot pronation. This is termed miserable malalignment syndrome. (Reprinted with permission from Fu FH [ed]: Sports Injuries: Mechanisms, Prevention, Treatment. Philadelphia: Williams & Wilkins, 1994.)

measurements were recorded in a series of 50 males and 50 females. The Q-angle was 15.8 ± 4.5 degrees in females and 11.2 ± 3.0 degrees in males.22 Females have a narrower pelvis than males.22,23 The mean femoral lengths were greater by 1.5 cm in males compared to females.23 Q-angles in these two studies were slightly but not significantly greater in females compared to males. Ratios of pelvic width to femoral length may provide more injury-predictive information than absolute widths or lengths.21 Pelvic shape is determined by genetics, culture, and environment.24 Figure 12–4 Valgus and rotational forces at the knee create a higher incidence of patellofemoral disorders and ACL injuries in females. A and B, Compared with males, females have anatomical differences of increased femoral anteversion, increased Q-angle, increased genu valgum and narrower intercondylar notch, external tibial torsion, and forefoot pronation. Developmentally, females also have a less-developed thigh musculature and higher rate of vastus medialis obliquus (VMO) hypoplasia than males. (Copyright 2003 ML Ireland.)

Anterior Knee Pain Anterior knee pain is a common complaint in females. Only when the specific diagnosis is made can sport and gender injury rates be determined. The differential diagnosis categories are lengthy25 (Table 12–3) and include inflammatory (bursitis, tendinitis, arthritis), mechanical (subluxation, dislocation, patellofemoral stress syndrome, plica), and miscellaneous (other) classifications. A specific primary

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Figure 12–5 A, When instructed to do a mini-squat, the male (left) demonstrates hip over knee over ankle alignment; the female (right) demonstrates femoral adduction and internal rotation and subsequent valgus of the knee, tibial external rotation, and forefoot pronation.

Continued diagnosis should be made. An algorithm for anterior knee pain has been developed.25,26 The four categories combine clinical examination and plain radiographs. The term chondromalacia is a pathological, not clinical, diagnosis. Clinically, the use of the term patellofemoral stress syndrome (PFSS) is suggested.

Most patellofemoral disorders are best treated nonoperatively. Core strengthening including back and hip exercises is important. Avoid knee extension machines and full squats. Surgical intervention should be a last consideration for treatment of PFSS or miserable malalignment syndrome.27

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Figure 12–5—cont’d B, Seen from the side view, the female (right) has an anteriorly rotated pelvis, forward head, and forward trunk position. The male (left) has a straight upright posture with less lumbar lordosis and a more posteriorly directed pelvis. The anterior pelvis position creates lower extremity rotational compensation patterns. (Copyright 2001 ML Ireland.)

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Table 12-3

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Differential Diagnosis: Anterior Knee Pain

Mechanical

Inflammatory

Other

Repetitive Microtraumatic

Bursitis

Referred Pain

•

Patella Stability Subluxation Dislocation Tilt Rotation Malalignment Fracture Stress Bipartite Fibrous union Acute fracture • Pathologic medial plica • Patellofemoral stress syndrome • Osteochondral fracture Trochlear groove Patella • Loose bodies Cartilaginous Osteochondral • Osteochondritis dissecans Patella Trochlear groove • Skeletally immature Osgood-Schlatter’s disease Sinding-Larsen-Johansson syndrome

• •

Prepatellar Retropatellar Semimembranosus Pes anserinus

Tendinitis • Quadriceps patella • Pes anserinus • Semimembranosus • Patella tendonitis

• •

Lumbar disc herniation Others Regional Pain Syndrome (Reflex Sympathetic Dystrophy) Tumors • Benign • Malignant Pigmented Villonodular Synovitis

Neuromata/Retinacular Pain Arthritis • Osteo • Rheumatoid • Psoriatic • Others Syndromes • Reiter’s • Others

Acute Macrotraumatic Injury

•

•

Extensor mechanism disruption Quadriceps rupture Patellar tendon rupture Inferior avulsion fracture Interstitial Skeletally immature Tibial tubercle fracture Patellar fracture Transverse Displaced/nondisplaced Comminuted Status post ACL reconstruction with central third patellar tendon bone

Copyright 2003 Mary Lloyd Ireland.

Symptomatic medial plica is a real diagnosis and is common in the teenage female athlete. The thickness of the intraarticular synovial fold is best palpated in extension. The plica may become thick enough to create a snapping sensation as it moves over the medial femoral condyle with flexion. Resist the temptation for arthroscopic excision of the plica for a year. Understand the female athlete’s relationship in the family dynamics: her goals and ability/desire to comply with rehabilitation before surgery.28 Females have a higher incidence of vastus medialis obliquus (VMO) hypoplasia, and lower muscular strength than males, thus increasing the female’s risk of patellar instability.29 In the injured knee, quadriceps weakness is reflected by VMO atrophy. The VMO, with its thin fascia, reflects knee function of the entire quadriceps. A weak VMO predisposes to lateral patellar subluxation.30 The VMO hypoplasia and internal femoral rotation predisposed the runner in Figure 12–6, A, to patellar instability and anterior knee pain. As she flexes her knee, the femur further adducts

(Figure 12–6, B). With a valgus force on the patella, the train (patella) easily jumps off the track (femur), which has already been medialized. Physical examination should include open chain resistance on the tibia, watching for patellar tracking (Figure 12–7, A) The J side occurs when the patella laterally jumps at 20 degrees as a result of valgus forces, patella alta, or trochlear groove hypoplasia (Figure 12–7, B). Routine views include the following positions: standing posterior anterior (PA), lateral, femoral notch, and bilateral patellar sunrise. Attention should be paid to patella tendon length, position of the patella, and anatomy of the trochlear groove. In a study screening for patellar subluxation, only 45% of controls had normal radiographs.31 Dynamic imaging can be useful in assessing tracking abnormalities.32 Static imaging can assess articular cartilage damage and delineate anatomy of the trochlea and patella.33 Radiographic measurements include length of a patella-to-patella tendon; the ratio less than 0.8:1 is termed patella alta and greater than 0.8:1 is termed patella infera on lateral views. The basketball athlete in

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Figure 12–6 Anterior knee pain patients usually have underdeveloped musculature and malrotation of the femur and tibia. A, Although the alignment appears rather straight––no excessive genu valgum or valgus––there is significant internal rotation of the femora, indicating femoral anteversion. The patellae are pointing toward one another. B, This is accentuated when the individual gets in a flexed position: the femur goes into further adduction and internal rotation, worsening the rotation and medializing the femur, thus lateralizing the patella. (Copyright 2002 ML Ireland.)

Figure 12–7 A, A positive “J” sign is demonstrated as the patient’s patella is at 40 degrees of flexion and subluxes laterally at 20 degrees of flexion (B). Asking the patient to straighten the leg against the examiner’s resistance can demonstrate this sign of lateral patellar instability. (Copyright 2002 ML Ireland.)

Special Concerns in the Female Athlete

Figure 12–8, A and B, complained of anterior pain and swelling of her knee. Patella alta is demonstrated on AP and lateral views. The patella:patella tendon ratio is 0.5, and the Hughston patellar view shows lateral subluxation and shallow trochlear groove (Figure 12–8, C). Following a quadriceps and core strengthening program, and with the use of a neoprene sleeve with lateral pad, this patient was able to successfully return to competition. KEY POINTS Patella instability has long been thought to be a condition 1. Make a definitive that predominantly affected diagnosis in the females. However, in a review of patient who grabs her 34 the literature, Arendt et al. patella and says the found that patella dislocation and front of her knee subluxation are more common in hurts. males than females. Much of the 2. Conservative literature on patellofemoral dislomanagement of cations was dated and retrospecpatellofemoral tive. Although the surgical treatdisorders predictably ment of patella dislocations has improves anterior improved, there is currently no knee pain. 34 consensus on treatment. If 3. If the patient will not patellofemoral ligaments are do a rehabilitation injured from bony attachments, program before surarthroscopically aided repairs gery, she will not do should be considered. Lateral one after surgery. release is indicated for tight latAll involved will be eral retinaculum and is not indimiserable, including cated as a single procedure for latthe surgeon. eral patellar instability. ACL Injuries The NCAA’s Injury Surveillance System records and publishes surveys of 16% of member institutions.3 Athletic trainers complete the survey. Injury categories for the knee are collateral, ACL, meniscus, patella, patellar tendon, and other. The NCAA has recorded injury rates as numbers of injuries divided by exposure hours. Males and females similarly play soccer and basketball and, hence, injury rates can be compared. ACL rates are 3.5 times higher in women’s basketball than men’s and 2.8 times higher in soccer.35,36 Rule and competition differences do not allow comparison of gender injuries in gymnastics, ice hockey, and lacrosse. The NCAA does not record injury statistics in cheerleading. ACL injury rates in basketball games were 4.3 times greater in females compared to males and 2.4 times greater in practices. Knee injury rates in females were higher in all categories.3,35 Females who tear their ACL are generally younger than males who do. Ott et al. found in a series of ACL reconstructions that females were 5 years younger than their injured male counterparts.37 High school athletes who played soccer and/or basketball were studied for mechanism of injury, onset of swelling, and intraarticular injuries associated with ACL tears.38 Mechanisms of injury were similar in males and females—that of noncontact jumping activities. Compared to males, female soccer athletes had fewer medial meniscus tears. Female basketball players had fewer medial femoral condyle (MFC) injuries. The conclusion was that if such intraarticular injuries prove to be a significant risk factor for poor long-term outcome, women may enjoy a better prognosis after reconstruction.

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Soccer studies on injured young players give us cause for concern. In a study of indoor soccer players, females were 5.75 times more likely to sustain a serious knee injury than males.39 In Sweden, knee injuries were compared in two groups: soccer athletes younger than age 16 who play with senior teams, and those senior teams whose ages are equal to or older than age 19. Thirty-eight percent of the players had been injured before they were 16. Of these, 39% were injured while playing on senior teams. When playing on senior teams, 59% of the players younger than 16 and 44% of the players 16 years or older sustained ACL injuries during contact situations.40 It was recommended that those who were younger than 16 practice, but not play games, with the seniors. Surgical Treatment Treatment of the ACL-injured female athlete should not differ from that of the male athlete.37,41,42 The decision of graft choice—bone-patellar tendon-bone (B-PT-B), hamstring, or allograft—should be made based on surgeon and patient preference, not gender.43 Pinczewski compared the ACLreconstructed hamstrings patellar tendons of men and women. Hamstring reconstruction in females was looser at 2 years post-reconstruction but normalized by 3 years. Barrett et al.42 compared female patients undergoing bone patellar tendon and hamstring ACL reconstructions. Although failure rates were equal, short- and medium-range follow-up patients in the hamstring group did not return to pre-injury level and had an increased anterior tibial translation.44,45 More men returned to preinjury level of activities than women.45 Most gender comparisons following ACL reconstructions have been done in the adult age group. Barber-Westin et al.41 reviewed surgical outcomes in males and females after autogenous B-PT-B ACL reconstruction. Twenty-six months postoperatively there were no significant differences for complications or outcomes. Males had a higher rate of patellofemoral crepitus than females (i.e., 15% and 7%, respectively).41 Ott et al. reported the outcomes of male and females after ACL reconstruction with ipsilateral B-PT-B grafts.37 The study required a minimum 2-year follow-up. Results were an average of 5-year follow-up. Females tore their ACLs at a significantly younger age than males. Outcome instruments of the Cincinnati Scale, the ACL Quality of Life Scale, and the Tegner activity rating scale were used.46–48 There were no differences comparing gender in the ACL Quality of Life Scale. In the Tegner scale, females had a significantly higher activity level. Females showed an average of 5.7 points lower than females measured on the Cincinnati Scale. There was a trend toward lower scores in females between ages 12 and 18 and older than age 24. Following ACL reconstruction with B-PT-B, there was no difference between males and females for complaints of anterior knee pain.37 Ferrari et al.42 reported on ACL reconstruction comparing men and women with bone patellar tendon bone grafts using objective, subjective, and functional assessments with the Tegner, Lysholm, Modified Hospital Special Surgery, and Cincinnati scales. There were no differences in donor site pain, patellofemoral crepitus, stair climbing, stability, functional assessment, and rating scale scores. Men and women had similar satisfaction rates and the same knee scale scores. They concluded there was no basis for inclusion of gender as

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Figure 12–8 Routine plain radiographs include antero posterior (AP), lateral, and patellar views. Views of this left knee demonstrate patella alta. A, On the AP view the patella is significantly superolateral. B, On lateral view the measurement of the ratio of the patella to the patella tendon is 0.5, confirming patella alta. A normal ratio is 0.8. C, Hughston sunrise patellar view shows lateral patellar subluxation, which is mildly symptomatic in this basketball athlete. (Reprinted with permission from Fu FH [ed]: Sports Injuries: Mechanisms, Prevention, Treatment. Philadelphia: Williams & Wilkins, 1994.)

a determining factor regarding the decision to perform ACL reconstruction with bone-patellar tendon-bone.42 Mechanism of Injury ACL injuries typically occur rapidly, with the patient upright and with an awkward stop in anticipation of lateral movement.21 In basketball players these injuries often occur

after an awkward landing trying to land, shoot, rebound, or prevent a ball from going out of bounds. Compared to males, females tend to land more in the so-called position of no return.49 Video analysis has allowed the description of the position of no return, from which the outcome is a torn ACL.21 The basketball athlete pictured in Figure 12–9 is in a relatively upright position with less knee and hip flexion, relatively straight back, momentum forward, and excessive

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consensus as to the role of notch size and ACL injury. There are insufficient data to relate lower extremity alignment and ACL injury. There is no evidence that knee braces prevent ACL injuries. Shoe-surface friction may improve performance but increase risk of injury. This is a modifiable risk that should be studied. There is no consensus regarding the role sex hormones may play in risk of ACL injury. Hormonal intervention or modification of participation is not justified for prevention of ACL injury at this time. The trunk, hip, and pelvis may contribute to ACL injury at the knee. Neuromuscular factors are significant and may be the most important risk factor in ACL injuries in female athletes. Strong quadriceps activation with eccentric contraction is a major factor in ACL injury. Male and female athletes in the same sport may need different training and conditioning programs. Training programs that improve body control reduce ACL injury rates and may increase performance.29 Laxity and Hyperextension

Figure 12–9 The mechanism of ACL tear is captured on video. Injury to the left knee is observed from the back and left side of the athlete. She has just rebounded and stops to change direction to avoid the defending player. She lands in an upright position with less knee and hip flexion and a forward flexed lumbar spine. After the ACL fails, she falls forward and knee valgus rotation and flexion increase. She is unable to upright herself and regain pelvic control to avoid ACL injury. (Copyright 2000, ML Ireland.)

knee valgus.21 Males tend to land with more hip and knee flexion with hip over knee over ankle, with less knee valgus and less foot pronation. Landing in a safe position of greater hip and knee flexion, allowing agonist muscles to protect the ACL, is the goal (Figure 12–10). Factors Predisposing to ACL Injuries

KEY POINTS 1. In organized sports such as basketball and soccer, girls tend to sustain ACL injuries more often at a younger age. 2. The decision to perform any type of ACL reconstruction should not differ in males and females. The rate of anterior knee pain after ACL reconstruction is the same in males and females.

Why do females tear their ACLs more frequently than males? The reason is multifactorial. Three areas have been studied: neuromuscular, hormonal, and anatomical. These categories can be divided into intrinsic (not changeable), extrinsic (changeable), and combination (possibly changeable) (Table 12–4). Possible anatomical predispositions to ACL injury include notch width, pelvic size and shape, and quadriceps angle (Q-angle). In June 1999, a panel of experts on ACL injuries met in Hunt Valley, Maryland, to discuss ACL injuries in the female athlete.50 The panel evaluated risk factors and prevention strategies. The following conclusions were made. There is no

Generalized laxity and knee hyperextension are two different factors that often may coexist in females. The female athlete in Figure 12–11, A, demonstrates passive hyperextension. She underwent ACL reconstruction on the right knee, and loss of this 30-degree physiological hyperextension is shown when she is standing (Figure 12–11, B). Although laxity has been listed as an intrinsic risk for ACL injuries, SnyderMackler found no difference in laxity comparing 20 patients with ACL deficient knees, 10 who were compensators and 10 who were noncompensators.51 There is no established relationship between laxity and risk of ACL injury. Femoral Notch Notch size, notch volume, and notch width indices have been studied extensively with varying results.52–57 Regardless of gender, smaller notches have been associated with increased rate of ACL tear.52,53 The question remains: Does a smaller notch result in a smaller ACL? If so, is a smaller ACL therefore weaker and predisposed to tearing? How does the height and weight of the athlete relate to notch size and ligament size and strength? Using magnetic resonance imaging, Anderson et al.55 reported that girls had smaller ACLs and notches than boys.58 Notch assessment by plain films has been reported. Regardless of gender, a small notch-width ratio is associated with increased rate of ACL tear. Shelbourne et al.52 studied the relationship of notch width and incidence of ACL tear and found no significant differences in notch width between height groups for males and females. With height and weight as covariates, females had statistically significant smaller notches than males. Patients, both males and females, with smaller notches had an increased incidence of contralateral ACL injury. In a series of analyses of notch radiographs of 108 ACL injured and 186 normal individuals, the shape, width of femur, and notch and ratios were measured.53 Notch measurements are significantly influenced by patient position and knee flexion. Standardization of patient position by description and goniometer measurement for notch view should be done. Therefore, comparisons of notch measurement cannot be done from one clinic to another.

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Figure 12–10 This diagram shows the “position of no return.” This term refers to an awkward out-of-control landing with the leg pronated in valgus angulation, the body more upright and the leg in pronation and rotation, and the knee in valgus angulation, which places the ACL at risk of tearing. The safety position is more flexed, with the body over the legs, and more balanced. (Copyright 2002 ML Ireland.)

Table 12-4

Factors Contributing to ACL Injuries

Intrinsic

Extrinsic

Alignment Hyperextension

Strength Conditioning

Physiologic Rotatory laxity ACL size Notch size/Shape Hormonal influences Inherited skills/ Coordination

Shoes Motivation

Combined (Potentially Changeable) Proprioception Position Sense/Balance Neuromuscular Patterns Order of firing Acquired skills

Copyright 1998 Mary Lloyd Ireland.

Sex Hormones Sex hormones have effects on numerous end organs, which is most obvious during menarche. However, the influence of sex hormones (specifically estrogen) on ACL injury rates has not been proved. Researchers have reported increased rates of injuries in all phases of menses. Wojtys et al.59 reported that ACL injury rates were higher in the ovulatory phase, reported as a 4-day phase (days 10–14), and less in the follicular phase days 1–9. Repeated statistical analysis found the results were

not statistically significant but only showed a trend.60 In a second study, Wojtys et al.61 reported on 69 females with acute ACL injuries. Urinary hormone levels were obtained within 24 hours of injury, and menstrual cycle history was obtained. This study observed a significantly increased incidence of ACL injury during the ovulatory phase and fewer than expected injuries during the luteal or follicular phases.61 Arendt et al. reported less ACL injuries occurred during the ovulatory phase.36 Myklebust et al. reported higher injury rates 1 week premenses and just after menses.62 In 2000, Slauterbeck and Hardy reported higher injury rates just before and after menses.63 The cyclic phases and hormonal level measurements (blood, urine, saliva) should be standardized. History of subjects regarding oral contraceptive (OCP) use and menses must be documented. The study design must be critically reviewed by investigators with experience in hormonal research. Estrogen and relaxin receptors are present on the human ACL, as determined by histochemical analysis and bioassay.64,65 The unanswered question is: What effect does the rapidly fluctuating hormone level have on the biomechanical characteristics of the ACL? In a sheep study, Strickland et al.66 concluded that estrogen and estrogen receptor agonists at the physiological level do not lead to decreased ligament strength. Other injury patterns have not been related to cycle hormonal influences. Ankle sprains, lumbar strains, neck injuries, shoulder instability, shoulder

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Figure 12–11 Physiological laxity and joint hyperextension are common findings in the female athlete. A, In the supine position, passive extension documents the hyperextension of the knee and posterior bowing of the tibia. B, In the standing position the hyperextension of the left knee is noted. A year after ACL reconstruction of the right knee, the patient has not regained all of her hyperextension and lacks approximately 20 degrees of the hyperextension on her normal side. (Reprinted with permission from Ireland ML, Nattiv A: The female athlete, Elsevier Science, 2003.)

dislocations, and other musculoskeletal disorders do not appear to be under cyclic influence. Even though hormone receptors are present, what is the clinical significance? There are estrogen receptors on the ACL, and estrogen may effect the amount of ligament and joint laxity. Estrogen inhibits type I procollagen synthesis and proliferation of fibroblasts in vitro at physiological estradiol concentrations.64 However, the in vivo effects of estrogen and estradiol have yet to be determined. Heitz et al.67 studied knee joint laxity during the menstrual cycle in uninjured females. Hormone levels were determined by blood radioimmunoassay and knee laxity by KT-2000 arthrometry. Knee joint laxity was found to be greatest during the luteal phase; however, the sample size was small (seven participants). The question

remains: Does anterior tibial translation place the ACL at risk? There is no consensus in the scientific community as to the role hormones play in ACL injuries in female athletes.50 There is evidence to warrant continued study. No one is recommending hormonal prescription or a change in practice schedule based on phase of cycle for female athletes. Female sex hormones also affect the neuromuscular system. Sawar et al. reported increased quadriceps strength and significant slowing of muscular relaxation time during the ovulatory phase.68 Estrogen also affects the central nervous system, which may affect motor skills during different phases of the menstrual cycle.69,70 The influence of hormones on other organ systems should also be considered a factor in ACL injuries.

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Neuromuscular Differences between males and females in neuromuscular activation and muscle recruitment have been reported to contribute to ACL injury. In general, compared to males, females are more “ligament dominant” with less muscular development.71 Males are better at stiffening their knees through muscle activation. An increase in knee stiffness was 473% in males compared to 217% in females in muscle contracted states (p = .003).72 Wojtys, Huston, and coworkers have done excellent research comparing gender differences and neuromuscular performance.67,73,74 Female athletes recruit their quadriceps first, have a slower time to peak hamstring torque in the unfatigued and fatigued state, and have greater anterior tibial laxity. In a 6-week program, Wojtys et al.74 showed that females were able to improve their muscle reaction time by agility training but not with isokinetic and isotonic strengthening programs. Hewett75 showed a reduction in impact forces, increased hamstring torque, and reduced adduction/abduction movement after a plyometrics training program in females. Rozzi et al.76 showed that in healthy collegiate soccer and basketball athletes, women had greater joint laxity and longer time to detect joint motion as the knee extended. This combination of anterior tibial translation in reduced response time in an extension arc allows the quadriceps to become a more active antagonist against the agonist hamstring effect with the ACL. Chappell et al.77 compared male and female kinematics during three jumping tasks and found females to have a greater knee extension and valgus moment, increasing the peak proximal tibial anterior shear force during stop. Fatigue has also been shown to affect muscle response time and hip and knee flexion angles.73,76,78 ACL Injury Prevention Prevention programs show encouraging results for reduction of ACL injuries, moreso in females than males. Instructions give players clues and immediate feedback on safe landing positions, jump training, and sports-specific programs. Hewett et al.75 used a 6-week flexibility and plyometric training program at the high school level and reduced the rate of knee injuries signifiKEY POINTS cantly in the untrained female. Mandelbaum has reported an 1. ACL injuries are 88% reduction in rates of ACL caused by multiple tears in a 14- to 18-year-old factors. female soccer athlete group, 2. By understanding the with implementation of the injury landing pattern prevention injury in enhanced (position of no performance program.79 A monoreturn), coaches and graph that describes the current researchers can principles and programs of preimplement safe landvention of ACL injuries is availing positions—flat able.80 Although implemented back and flexed hips for ACL prevention, these proand knees. grams would be of benefit for 3. ACL prevention profemales with anterior knee pain, grams appear to be stress fractures, and other lower successful. extremity disorders.

Female Athlete Triad If you treat female athletes, you should understand the triad and definition and serious consequences. Early diagnosis is the only hope. The female athlete triad is defined as amenorrhea, disordered eating, and osteoporosis. These three components are interrelated in their etiology, pathogenesis, and health consequences.81–83 The female with the triad is at increased risk for stress fractures and recurrent injuries, but not knee injuries. The athlete at risk is prepubertal in body type, strives for perfection, wears revealing clothing and outfits for competition, and is subjectively judged.84 The true prevalence of the female athlete triad is unknown. Young athletes approaching puberty also appear to be at increased risk. If the female athlete triad is diagnosed, treatment is multidisciplinary, including a physician, a psychiatrist, a psychologist, and a nutritionist.85 Eating disorders range from anorexia nervosa, bulimia, and restrictive eating behaviors to poor nutritional habits. Athletes with disordered eating patterns are at risk for certain endocrine, skeletal, and psychiatric problems.86 Eating disorders are 10 times more prevalent in women than men. The exact prevalence in athletes is unknown and ranges from 15–62% of athletes, depending on the sport. The prevalence of eating disorders in nonathletes is estimated between 1% and 3%. There is an incidence (62–74%) of pathological weight control among college gymnasts. The incidence of anorexia is 19.0–25.7% in ballet dancers. The incidence of pathological weight control among swimmers aged 9–18 is 15.4% and nearly 70% among elite swimmers.5 The prognosis for eating disorders is dismal. In nonathletes, 50% do well and 30% struggle and relapse, and there is a 10–20% mortality rate. Many of these athletes with eating disorders continue to struggle with their weight and body image throughout their lifetime.87 The prevalence of amenorrhea in the general population is 2–6%, jumping to 3.4–66.0% in athletic populations.88 Athletic amenorrhea has a hypothalamic origin resulting in decreased ovarian hormone production and hypoestrogenemia similar to menopause.88 Although stress fractures around the knee are relatively uncommon, if diagnosed, a complete musculoskeletal and medical evaluation should be undertaken. Athletes with stress fractures often have menstrual irregularity.82,89,90 The significance of athletic amenorrhea is the observed skeletal demineralization and early osteoporosis.91 The danger is that these women are losing bone when they should be accruing it, thus never achieving peak bone mass.88 After ruling out other causes of amenorrhea, treatment of athletic amenorrhea in a woman who has been menstruating for less than 3 years is to decrease exercise intensity and improve nutrition.92 In an athlete more than 3 years postmenarche, treatment is with low-dose oral contraceptives.88 Osteoporosis is characterized by low bone mass and microarchitechtural deterioration, leading to increased skeletal fragility and risk of fracture. Women are four times more likely to develop osteoporosis than men.93 Weightbearing exercise may reduce the rate of bone loss in adult women; however, it will not produce a large increase.93 In the face of athletic amenorrhea, the positive effects of weight-bearing exercise are negated. Bone densitometry

Special Concerns in the Female Athlete

should be ordered in those athletes suspected of suffering from these serious disorders. Early diagnosis and treatment of the female athlete triad is her only hope for survival. Asking the tough questions and taking time to listen can only help her. Summary

KEY POINTS 1. Recognize the athlete with an eating disorder and female athlete triad. 2. The earlier the diagnosis of female athlete triad is made, the better chance that intervention and treatment will succeed.

Female athletes have made much progress in skill acquisition and opportunity to compete in team and individual sports. However, there are disturbing differences in the rates of ACL tears in basketball and soccer in females compared to males. The risk factors responsible for ACL injuries in females must be determined and ranked in order of importance. It has not been determined what the intervention programs are actually changing. The programs all emphasize proper landing techniques and single-leg proprioception. To continue competition in these high-risk sports, athletes (male and female) should have an ACL reconstruction performed to reduce chance of injury to the menisci and articular cartilage—the latter two are presently more difficult to treat than stabilization. A specific diagnosis should be made in the female with anterior knee pain. Arthroscopy should be considered only after failure of the rehabilitation program and understanding of patient and family dynamics. The positive benefits of being an athlete and acquiring the skills to stay healthy for life outweigh the risks of knee injury. The concern for and treatment of the female knee should not differ from that of the male knee. Keep her on the playing field and active for life!

References 1. Saperstein AL, Nicholas SJ: Pediatric and adolescent sports medicine. Ped Clin N Am 43:1013–1033, 1996. 2. National Federation of State High School Associations. www.nfhs.org 3. Powell JW, Barber-Foss KD: Injury patterns in selected high school sports: a review of the 1995-1997 seasons. J Athl Train 34(3):277–284, 1999. 4. Malina RM: Secular changes in growth, maturation and physical performance. Exerc Sport Sci Rev 6: 203–255, 1978. 5. Baum AL: Young females in the athletic arena. Child Adol Psych Clin N Am 7:745–755, 1998. 6. National Collegiate Athletic Association: NCAA Injury Surveillance System, Indianapolis, 1989–2001. 7. Greydanus DE, Patel DR: The female athlete before and beyond puberty. Ped Clin N Am 49: 553–580, 2002. 8. Marshall WA, Tanner JM: Variations in patterns of pubertal changes in girls. Arch Dis Child 44:291, 1969. 9. Sandborn CF, Jankowski CM: Physiologic considerations for women and sport. Clin Sports Med 13:315, 1994. 10. Buckler JMH: A longitudinal study of adolescent growth. London: Springer, 1990. 11. Howell FR, Mahood JK, Dickson RA: Growth beyond skeletal maturity. Spine 17:437–440, 1992. 12. DiMeglio A, Bonnel F: Le rachis en croissance. Paris: Springer, 1990. 13. Little DG, Son KM, Kat D, Herring JA: Relationship of peak height velocity to other maturity indicators in idiopathic scoliosis in girls. J Bone Joint Surg Am 82(5):685–693, 2000. 14. Wilmore JH: The application of science to sport: physiological profiles of male and female athletes. Can J Appl Sports Sci 4:103, 1979.

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15. Ireland ML: Special concerns of the female athlete. In Fu FH, Stone DA (eds): Sports Injuries Mechanisms, Prevention and Treatment. Philadelphia: Lippincott Williams and Wilkins, 1994, pp 153–187. 16. Anderson M, Green WT, Messner MB: Growth and predictions of growth in the lower extremities. J Bone Joint Surg Am 45:1–14, 1963. 17. Dimeglio A, Bonnel F: Growth and development of the knee. In: De Pablos J (ed): The Immature Knee. Biblio STM, Masson, 1998, pp 3–8. 18. Greulich WW, Pyle SI: Radiographic atlas of skeletal development of the hand and wrist, 2nd ed. Stanford, Cal.: Stanford University Press, 1959. 19. Dimeglio A: Growth in pediatric orthopaedics. J Pediatr Orthop 21(4):549–555, 2001. 20. Shelbourne KD, Patel DV, McCarroll JR: Management of anterior cruciate ligament injuries in skeletally immature adolescents. Knee Surg Sports Traumatol Arthrosc 4:68–74, 1996. 21. Ireland ML: The female ACL: why is it more prone to injury? Ortho Clin N Am 33:637–651, 2002. 22. Horton MG, Hall TL: Quadriceps femoris muscle angle: normal values and relationships with gender and selected skeletal measures. Phys Ther 69(11):897–901, 1989. 23. Livingston LA, Gahagan JC: The wider gynecoid pelvis-larger Q-angle—greater predisposition to ACL injury relationship: myth or reality? Clin Biomech 16:951–952, 2001. 24. Abitbol MM: The shapes of the female pelvis: contributing factors. J Reprod Med 41(4):242–250, 1996. 25. Kelly MA, Scuderi JR: Management of patellofemoral pain. Orthop Spec Ed 3:191–260, 1997. 26. Kelly MA: Algorithm for anterior knee pain. AAOS Instr Course Lect 47:339–343, 1998. 27. Baker MM, Juhn MS: Patellofemoral pain syndrome in the female athlete. Clin Sports Med 19:315–329, 2000. 28. Duri ZAA, Patel DV, Ainchroth PM: The immature athlete. Clin Sports Med 21:461–482, 2002. 29. Dupont JY, Guier CA: Comparison of three standard radiologic techniques for screening of patellar subluxations. Clin Sports Med 21:389–401, 2002. 30. Witonski D: Dynamic magnetic resonance imaging. Clin Sports Med 21:403–415, 2002. 31. Staebli HU, Bosshard C, Porcellini P, et al: Magnetic resonance imaging for articular cartilage: cartilage-bone mismatch. Clin Sports Med 21:417–433, 2002. 32. Hewett TE: Neuromuscular and hormonal factors associated with knee injuries in female athletes. Sports Med 29:313–327;2000. 33. Malone T, Davies G, Walsh WM: Muscular control of the patella. Clin Sports Med 21:349–362, 2002. 34. Arendt EA, Fithian DC, Cohen E: Current concepts of lateral patella subluxation. Clin Sports Med 21:499–519, 2002. 35. Ireland ML, Nattiv A: The female athlete. Philadelphia: Elsevier Science, 2002. 36. Arendt EA, Agel J, Dick R: Anterior cruciate ligament injury patterns among collegiate men and women. J Athl Train 34:86–92, 1999. 37. Ott SM, Ireland ML, Ballantyne BT, et al: Comparison of outcomes between males and females after anterior cruciate ligament reconstruction. Knee Surg Sports Traumatol Arthrosc 11:75–80, 2003. 38. Piasecki DP, Spindler KP, Warren TA, et al: Intraarticular injuries associated with anterior cruciate ligament tear: findings at ligament reconstruction in high school and recreational athletes. Am J Sports Med 31(4):601–605, 2003. 39. Lindenfeld TN, Schmitt DJ, Hendy MP, et al: Incidence of injury in indoor soccer. Am J Sports Med 22:364–371, 1994. 40. Soderman K, Pietila T, Alfredson H, Werner S: Anterior cruciate ligament injuries in young females playing soccer at senior levels. Scan J Med Sci Sports 12(2):68–68, 2002. 41. Barber-Westin SD, Noyes FR, Andrews M: A rigorous comparison between the sexes or results and complications after anterior cruciate ligament reconstruction. Am J Sport Med 25:514–526, 1997. 42. Ferrari JD, Bach BR, Bush-Joseph CA, et al: Anterior cruciate ligament reconstruction in men and women: an outcome analysis comparing gender. Arthroscopy 17(6):588–596, 2001. 43. Pinczewski LA, Deehan DJ, Salmon LJ, et al: A five-year comparison of patellar tendon versus four-strand hamstring tendon autograft for arthroscopic reconstruction of the anterior cruciate ligament. Am J Sports Med 30(4):523–536, 2002.

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44. Barrett GR, Noojin FK, Hartzog CW, Nash CR: Reconstruction of the anterior cruciate ligament in females: a comparison of hamstring versus patellar tendon autograft. Arthroscopy 18(1):46–54, 2002. 45. Noojin FK, Barrett GR, Hartzog CW, Nash CR: Clinical comparison of intraarticular anterior cruciate ligament reconstruction using autogenous semitendinosus and gracilis tendons in men versus women. Am J Sports Med 28(6):783–799, 2000. 46. Noyes FR: The Noyes knee rating system: an assessment of subjective, objective, ligamentous, and functional parameters. Cincinnati Sportsmedicine Research and Education Foundation, Cincinnati, 1990. 47. Mohtadi N: Development and validation of the quality of life outcome measure (questionnaire) for chronic anterior cruciate ligament deficiency. Am J Sports Med 26(3):350–359, 1998. 48. Tegner Y, Lysholm J: Rating systems in the evaluation of knee ligament injuries. Clin Orthop 198:43–49, 1985. 49. Ireland ML, Gaudette M, Crook S: ACL injuries in the female athlete. J Sport Rehab 6:97–110, 1997. 50. Griffin LY, Agel J, Albohm MJ, et al: Noncontact anterior cruciate ligament injuries: Risk factors and prevention strategies. J Am Acad Orthop Surg 8(3):141–150, 2000. 51. Snyder-Mackler L, Fitzgerald K, Bartolozzi AR III, Ciccotti MG: The relationship between passive joint laxity and functional outcome after anterior cruciate ligament injury. Am J Sports Med 25(2):191–195, 1997. 52. Shelbourne KD, Davis TJ, Klootwyk TE: The relationship between intercondylar notch width of the femur and the incidence of anterior cruciate ligament tears. Am J Sports Med 26(3):402–408, 1998. 53. Ireland ML, Ballantyne BT, Little K, McClay IS: A radiographic analysis of the relationship between the size and shape of the intercondylar notch and anterior cruciate ligament injury. Knee Surg, Sports Traumatol, Arthrosc 9:200–205, 2001. 54. Muneta T, Takakuda K. Yamamoto H: Intercondylar notch width and its relation to the configuration and cross-sectional area of the anterior cruciate ligament. Am J Sports Med 25(1):69–72, 1997. 55. Anderson AF, Dome DC, Tautam S, et al: Correlation of anthropometric measurements, strength, anterior cruciate ligament size, and intercondylar notch characteristics to sex differences in anterior cruciate ligament tear rates. Am J Sports Med 29(1):58–66, 2001. 56. Souryal TO, Freeman TR: Intercondylar notch size and anterior cruciate ligament injuries in athletes: a prospective study. Am J Sports Med 21(4):535–539, 1993. 57. Souryal TO, Moore HA, Evans JP: Bilaterality in anterior cruciate ligament injuries: associated intercondylar notch stenosis. Am J Sports Med 8(3):449–454, 1980. 58. Noyes FR, Mooar RA, Matthews DS, et al. The symptomatic anterior cruciate-deficient knee. I. The long-term functional disability in athletically active individuals. J Bone Joint Surg Am 65:154–162., 1983. 59. Wojtys EM, Huston LJ, Lindenfeld TN, et al: Association between the menstrual cycle and anterior cruciate ligament injuries in female athletes. Am J Sports Med 26:614– 619, 1998. 60. Wojtys EM: Letters to the editor. Am J Sports Med 28:131, 2000. 61. Wojtys EM, Huston LJ, Boyton MD, et al: The effect of the menstrual cycle on anterior cruciate ligament injuries in women as determined by hormone levels. Am J Sports Med 30:182–188, 2002. 62. Myklebust G, Machlum S, Holm I, et al: A prospective cohort study of anterior cruciate ligament injuries in elite Norwegian team handball. Scand J Med Sci Sports 8:149–153, 1998. 63. Slauterbeck JR, Hardy DM: Sex hormones and knee ligament injuries in female athletes. Am J Med Sci 322:196–199, 2001. 64. Liu SH, Al-Shaikh RA, Panossian V, et al: Estrogen affects the cellular metabolism of the anterior cruciate ligament: a potential explanation for female athletic injury. Am J Sports Med 25:704–709, 1997. 65. Dragoo JL, Lee RS, Behhaim P, et al: Relaxin receptors in the human female anterior cruciate ligament. Am J Sports Med 31(4):577–584, 2003. 66. Strickland SM, Belknap TW, Turner SA, et al: Lack of hormonal influence on mechanical properties of sheep knee ligaments. Am J Sports Med 31(2):210–215, 2003. 67. Heitz NA, Eisenman PA, Beck CL, et al: Hormonal changes throughout the menstrual cycle and increased anterior cruciate ligament laxity in females. J Athl Train 34:144–149, 1999.

68. Sawar R, Beltran NB, Rutherford OM: Changes in muscle strength, relaxation rate and fatigability during the human menstrual cycle. J Physiol 493:267–272, 1996. 69. Lebrun CM: The effect of the phase of menstrual cycle and the birth control pill in athletic performance. Clin Sports Med 13:419–441, 1994. 70. Posthuma BW, Bass MJ, Bull SB, et al: Detecting changes in functional ability in women with premenstrual syndrome. Am J Obstet Gynecol 156:275–278, 1987. 71. Andrews JR, Axe MJ. The classification of knee ligament instability. Orthop Clin N Am 16(1):69–80, 1985. 72. Wojtys EM, Ashton-Miller JA, Huston LJ: A gender-related difference in the contribution of the knee musculature to sagittal-plane shear stiffness in subjects with similar knee laxity. J Bone Joint Surg Am 84(1):10–16, 2002. 73. Wojtys EM, Wylie BB, Huston LJ: The effects of muscle fatigue on neuromuscular function and anterior tibial translation in healthy knees. Am J Sports Med 24:615–621, 1996. 74. Wojtys EM, Huston LJ, Taylor PD, et al: Neuromuscular adaptations on isokinetic, isotonic and agility training programs. Am J Sports Med 24:187–192,1996. 75. Hewett TE: Neuromuscular and hormonal factors associated with knee injuries in female athletes: strategies and intervention. Sports Med 29:313–327, 2000. 76. Rozzi SL, Lephart SM, Gear WS et al: Knee joint laxity and neuromuscular characteristics of male and female soccer and basketball players. Am J Sports Med 27:312–319, 1999. 77. Chappell JD, Yu B, Kirkendall DT, Garrett WE: A comparison of knee kinetics between male and female recreational athletes in stop-jump tasks. Am J Sports Med 30(2):261–267, 2002. 78. Nyland JA, Shapiro R, Stine RL, et al: Relationship of fatigued run and rapid stop to ground reaction forces, lower extremity kinematics and muscle activation. JOSPT 20:132–137, 1994. 79. 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, p 94. 80. Griffin LY: Prevention of Noncontact ACL Injuries. Rosemont, Ill.: American Academy of Orthopaedic Surgeons, 2001. 81. Barrow GW, Saha S: Menstrual irregularity and stress fractures in collegiate female runners. Am J Sports Med 16:209–216, 1988. 82. Lloyd T, Buchman JR, Bitzer S, et al: Interrelationships of diet, athletic activity, menstrual status and bone density in collegiate women. Am J Clin Nutr 46:681–684, 1987. 83. Matheson GO, Clement DB, McKenzie DC, et al: Stress fractures in athletes: a study of 320 cases. Am J Sports Med 15:43–58, 1987. 84. 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. 85. Otis CL, Drinkwater B, Johnson MD, et al: American College of Sports Medicine position stand. The female athlete triad. Med Sci Sports Exerc 29:i–ix, 1997. 86. Berning JR, Steen SN (eds): Sports Nutrition for the 90’s: The Health Professional’s Handbook. Gaithersburg, Md.: Aspen Publishers, 1991. 87. Nattiv A, Agostini R, Drinkwater B, et al: The female athlete triad: the interrelatedness of disordered eating, amenorrhea and osteoporosis. Clin Sports Med 13:405–418, 1994. 88. Nattiv A, Ireland ML: Special concerns of the female athlete In Safran M, McKeag DB, Van Camp S (eds): Manual of Sports Medicine. Philadelphia: Lippincott-Raven, 1998, pp 171–183. 89. Johnson MD: Disordered eating in active and athletic women. Clin Sports Med 13:355–369, 1994. 90. Arendt EA: Osteoporosis in the athletic female: amenorrhea and amenorrheic osteoporosis in the athletic female. Champaign, Ill.: Human Kinetics, 1993. 91. Gadpaille WJ, Sanborn CF, Wagner WW: Athletic amenorrhea, major affective disorders and eating disorders. Am J Psychiatr 144:939–942, 1987. 92. Marshall LA: Clinical evaluation of amenorrhea in active and athletic women. Clin Sports Med 13:371–387, 1994. 93. Snow-Harter CM: Bone health and prevention of osteoporosis in active and athletic women. Clin Sports Med 13:389–404, 1994.

Chapter 13

Physical Therapy/ Rehabilitation Michelina Cassella

Introduction The physical therapy management of knee conditions in the pediatric and adolescent patient population presents a challenge to health professionals because of the influence of growth and maturation.1 A child is not a miniature adult; therefore careful analysis of the KEY POINTS stages of growth and development must be considered in the Patient history assessment and treatment of all 1. Demographics knee conditions. 2. Current medical Comprehensive assessments diagnoses of posture, joint range of motion, 3. Previous diagnoses muscle strength, and function are 4. Past injuries with essential before initiating a knee dates rehabilitation program.2–6 Posture 5. Surgical history with deviations and muscle weakness dates and complicaand/or tightness often lead to seritions (if any) ous imbalances that can cause 6. Medications knee malalignment, an increase in 7. Chronological age pain, and a decrease in function. and bone age The goals of a successful rehabili8. Review of clinical tation program are to restore optitests, magnetic mal functional outcomes and to resonance imaging educate the patient in both health scan, bone scan, and wellness behaviors to prevent and/or radiograph future injuries. Elements of Patient Management Examination History A detailed patient history is obtained before establishing a knee rehabilitation program. Information is gathered from

9. Past and present activity level 10. Recreational versus competitive activity 11. Pain assessment at rest, night, and with activity (ageappropriate pain scale); patient’s current concerns and goals7

●

Kathleen Richards

●

Carl Gustafson

both the parent and the patient. Patient history includes the 11 categories listed in the Key Points box. Systems Review Gathering baseline information before treatment intervention is necessary to establish goals, monitor the effects of both therapeutic and conditioning exercises, and identify risks for future injury. Systems to review include cardiovascular/ pulmonary, integumentary, musculoskeletal, neuromuscular, and communication.

KEY POINTS Systems review Baseline information 1. Cardiovascular/ pulmonary 2. Integumentary 3. Musculoskeletal 4. Neuromuscular 5. Communication

Cardiovascular/Pulmonary Knowledge of normal respiratory rates, heart rates, and blood pressure for children is necessary to monitor patient response to treatment (Tables 13–1 and 13–2).3 Integumentary Assessment of the integumentary system includes skin integrity, color, trophic changes, and scar formation. Blistering, skin temperature, scar tissue pliability, texture, and sensation should be observed. Activities or movements that aggravate the incisional sight should be documented in children who have had surgery. Scar types include contracture, hypertrophic, and keloid. A contracture scar is a tightening of surrounding tissues. These scars tend to cause impaired movement. Hypertrophic scar tissue can be caused by the overproduction of connective tissue. The tissue is raised above the skin, thick, red, and itchy. Keloid formations are highly thickened areas of scar tissue. They are larger and more raised than the hypertrophic scars. This type of scarring is often genetic.4 131

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Table 13–1 Normal Respiratory Rates For Children Age

Breaths per Minute

Newborn Up to 6 years 6–10 years 10–16 years

35–55 20–30 15–25 12–20

children can understand the intent of instructions and follow directions, but they have a difficult time understanding the consequences of their actions. The adolescent understands the consequences of compliance but focuses on the here and now.12 Therefore both the approach and the instructions must consider the age of the child. Test and Measurements

Table 13–2 Normal Heart Rates and Blood Pressures for Children

Age Newborn Up to 3 years Older than 3 years

Heart Rate (bpm)

Blood Pressure (mm Hg) Systolic

Blood Pressure (mm Hg) Diastolic

120–200 100–180

60–90 75–130

30–60 45–90

70–150

90–140

50–80

Musculoskeletal Knowledge of musculoskeletal adaptation is necessary when evaluating children. The shape, length, and size of a child’s bone adapt to that of the adult, with normal compressive and shear forces applied through the bone. The knee position in the frontal plane changes from genu varum at birth to normal adult alignment by age 6 (Figure 13–1).5 There is a rapid period of longitudinal bone growth in the lower extremities during the adolescent growth spurt. As a result, limitations in muscle and joint movement may be compromised (Figure 13–2).8 Neuromuscular System The neuromuscular system includes assessment of coordination, balance, and gait. Coordination is the ability to perform movements with appropriate speed, distance, direction, rhythm, and muscle tension. When assessing children, normal development of skill acquisition must be taken into consideration so that testing is age appropriate. By age 5, the child can hop 10 times; however, a skillful hop that requires flight and distance continues to develop into early adolescence.6 Postural control or balance is a multisystem complex involving the visual, vestibular, and somatosensory systems. Postural sway with the eyes closed in a child between the ages of 7 and 10 is similar to that of the adult.9 Sutherland has described the maturing gait pattern.10 By age 7, a child achieves a mature gait pattern with the exception of step length and distance, which is directly related to the child’s shorter limb length. A thorough gait analysis should be performed to determine abnormal hip, knee, and ankle movements that may contribute to knee problems. For example, tightness of the gastrocnemius muscle can increase ankle pronation. This in turn can lead to an increase in tibial internal rotation, which results in increased patellofemoral joint forces.11 Communication Instructions to the child between ages 6 and 11 need to include outcomes of the exercise program. At this age range

Selections of the appropriate tests and measurements are necessary to establish baseline information before the development of a treatment plan.6 Thomas Test The Thomas test measures tightness in the iliopsoas muscle. Restricted flexibility in this muscle can cause increased lumbar hyperlordosis, decreased hip extension, and an increase in knee hyperextension. The test is performed passively. The patient is positioned supine with both hips and knees flexed to the chest, with the low back flat on the table. The patient holds one leg flexed to the chest. The examiner cradles the other leg and has one hand around the pelvis. The examiner’s thumb is positioned on the anterior superior iliac spine (ASIS), to determine when the pelvis begins to move anteriorly. The examiner passively lowers the leg. When the ASIS begins to move anteriorly, the test is stopped and the angle of hip flexion is measured (Figures 13–4 and 13–5).13 Straight Leg Raise

KEY POINTS Tests and measurements 1. Posture (Table 13–3) 2. Patellar alignments (Table 13–4) 3. Leg length 4. Girth 5. Patient’s chief complaint 6. Functional problems 7. Gait assessment 8. Manual muscle evaluation (Figure 13–3) 9. Joint range of motion assessment

KEY POINTS Specific tests 1. Thomas 2. Straight leg raise 3. Popliteal angle 4. Ely 5. Patellar alignment 6. Q-angle 7. Circumference 8. Leg length measurement

The straight leg raise test measures hamstring tightness. Restricted flexibility in the hamstrings will contribute to lower back, pelvis, hip, and knee malalignment. The straight leg raise test focuses on proximal hamstring tightness. The test is performed passively. The patient is positioned supine with hips and knees extended and the pelvis in a neutral position. The examiner cradles the leg with one arm and has the other hand around the pelvis. The examiner’s thumb is positioned on the ASIS. The examiner passively raises the leg, keeping the knee straight. As soon as the ASIS begins to move posteriorly, the test is stopped and the angle of hip flexion is measured (Figures 13–6 and 13–7).14 Popliteal Angle The popliteal angle also measures hamstring tightness, but it focuses on the distal hamstrings. The test is performed passively while the patient is supine. The leg to be measured

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Figure 13–1 Changes in the child’s lower extremity alignment progressing from varum to valgus as a result of compressive and shear forces during normal growth and development. (From Tachjian MO: Pediatric Orthopedics, 2nd ed, vol 2. Philadelphia: WB Saunders Company, 1990, p. 2821.)

is positioned with the hip and knee at a 90-degree angle. The contralateral hip and knee are extended. The examiner supports the thigh while slowly attempting to extend the knee. The test is stopped when there is resistance to knee extension. The popliteal angle is then measured (Figures 13–8 and 13–9).15

Ober Test The Ober test measures tightness in the iliotibial band (ITB). Restricted flexibility of the ITB often promotes lateral tracking of the patella. This malalignment of the patella can disrupt knee joint mechanics. Tightness of the ITB not

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Figure 13–2 Normal flexibility according to age level. Part (D) shows an illustration of the limitations in hamstring flexibility in children ages 11–14. This occurs as a result of rapid increase in leg length during the adolescent growth spurt. (From Kendall FP, Mcreary Kendall E: Muscle Testing and Function, 3rd ed. Baltimore: Williams and Wilkins, 1983, p 234.)

only contributes to knee pain but also can interfere with function. The test is performed passively. The patient is positioned lying on the side, with the lumbar spine in flexion. The hips and knees are flexed to the chest. The patient’s neck and trunk are also flexed. The patient holds the bottom leg to the chest while the examiner cradles the top leg, keeping the knee flexed. The examiner flexes the hip and then widely abducts and extends the hip to allow the tensor fasciae latae muscle to move over the greater trochanter. The examiner attempts to passively lower the leg to the horizontal position (Figures 13–10 and 13–11).14 Ely Test The Ely test measures tightness in the rectus femoris muscle. Restricted flexibility in this muscle can have a negative effect on patella alignment. The test is performed passively while the patient is positioned prone with the hips and knees extended. The examiner grasps the lower leg and slowly flexes the knee. The test is stopped when the hip begins to flex and the buttock begins to rise. The angle of knee flexion is measured (Figures 13–12 and 13–13).14 Patellar Alignment Patellar alignment is assessed by visual inspection and passive movement. Tests that assess patella movements are the patella glide and patella tilt.

The patellar glide test assesses lateral and medial translation of the patella. The test is performed in three positions: full knee extension, 20 degrees of knee flexion, and 45 degrees of knee flexion. Normal lateral translation is a fourth to half the width of the patella. Lateral translation greater than half the width of the patella represents laxity of the medial retinaculum, the vastus medialis oblique, and medial patellar femoral ligament. Normal medial translation is 30–40% of the patella width, or 6–10 mm. Medial translation greater than 10 mm represents hypermobility of the patella, whereas less than 6 mm represents a tight lateral retinaculum. The patellar tilt test represents tightening of the lateral retinaculum, ITB, and vastus lateralis. The test is performed with the knee in extension. The medial border is depressed while the lateral border is elevated. A patellar tilt of 0–20 is normal. A tilt less than 0 is positive for tightening.16 Q-Angle The Q-angle refers to the extensor mechanism alignment. A line is drawn from the ASIS to the middle of the patella and to the middle of the tibia tubercle. Normal angles are 15 degrees for females and 10 degrees for males. A larger Q-angle may cause the patella to track laterally with contraction of the quadriceps.17

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Table 13–3 Example of a Posture Evaluation Form Posture Evaluation Form Name________________________________ Medical Record NO.___________________________ Date of Birth_____ Sex____ Diagnosis_____________________________ Surgical Procedure/Date___________________________________________________ Precautions__________________________________________________________________________________________________________

Posterior View Head

Centered

Tilt

Shoulders

Level

Elevated

Scapulae

Level

Elevated

Spine

Aligned

Shifted

Waist folds

Symmetrical

Increased

Pelvis

Level

Elevated

Knees

Aligned

Varus

Heels

Aligned

Varus

Left

Right

Left

Right

Left

Right

Valgus

Valgus Anterior View Head

Centered

Tilt

Neck folds

Symmetrical

Increased

Breasts

Symmetrical

Prominent

Arm length

Equal

Longer

Pelvis

Level

Elevated

Knees

Aligned

Varus

Forefoot

Aligned

Valgus

Pronated Supinated Lateral View Head

Aligned

Forward

Backward

Cervical (anterior) curve

Normal

Increased

Decreased

Shoulders

Level

Forward

Backward

Scapulae

Aligned

Protracted

Retracted

Thoracic (posterior) curve

Normal

Increased

Decreased

Lumbar (anterior) curve

Normal

Increased

Decreased

Pelvis

Aligned

Anterior tilt

Posterior tilt

Adams Forward Bend Test

Left

Right

Thoracic

Negative

Rib hump

Rib hump

Lumbar

Negative

Increased muscle bulk

Increased muscle bulk

Knees

Aligned

Hyperextension

Hyperextension

Ankles

Aligned

Increased dorsiflexion

Increased dorsiflexion

Increased plantar flexion

Increased plantar flexion

Line of gravity (plumbline)

Aligned

Shifted Forward Shifted Backward

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Table 13–4 Patellar Alignment Evaluation Form Name________________________________ Medical Record NO.________________________ Date of Birth___________ Sex_____ Diagnosis_____________________________ Surgical Procedure/Date_______________________________________________________ Precautions____________________________________________________________________________________________________________

Patella Alignment

Left

Right

Comments

Patella orientation Patella mobility/glide test Patella tilt Patella tracking Leg length Apparent Real Thigh girth measurement 2′′ above patella 4′′ above patella 6′′ above patella Calf girth measurement 2′′ below patella 4′′ below patella 6′′ below patella Patient’s Chief Complaints

Functional Problems

Giving away

Catching

Edema

Pain level; indicate pain scale used

Pivoting

Night pain; y or n

Sit to stand

Stand to sit

Popping

Locking

Ambulation

Stairs

Gait assessment (describe): ________________________________________________________________________________________________________________________ ________________________________________________________________________________________________________________________ Summary/comments: ________________________________________________________________________________________________________________________ ________________________________________________________________________________________________________________________ Signature_____________________________________

Physical therapist _______________________________________________

Circumference Obtaining accurate circumference measurements of a patient’s thigh and calf before establishing an exercise program is necessary to monitor levels or changes in the amount of adipose tissue and muscle bulk during the rehabilitation program. When obtaining these measurements in children, it is recommended that the child’s limb be in a relaxed state to improve reliability (Figure 13–14).18

and femur (Figure 13–15). If there is a true leg length discrepancy, the physician may prescribe a shoe lift for the shorter limb to equal the leg lengths. If this is the case, it is important the child wear his or her shoes with the appropriate lift, for all functional activities. Performing these activities in bare feet may place undue stress on the knees. An apparent leg length discrepancy denotes malalignment of the pelvis (Figure 13–16). The use of a shoe lift for this type of discrepancy is contraindicated because it will cause a malalignment in the lower extremities.19

Leg Length Measurements Unequal leg lengths can have a negative influence on knee alignment and therefore can contribute to knee pain. There are two types of leg length discrepancies: true and apparent. A true leg length discrepancy measures the length of the tibia

Treatment Plan The physical therapy management is based on data gathered from the examination. Impairments, functional limitations,

Physical Therapy/Rehabilitation

Figure 13–3 Forms: Manual muscle evaluation and joint range of motion assessment. (Courtesy of Michelina Cassella, PT.)

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Figure 13–4 Left negative Thomas test. The lumbar spine is flat on the table, the pelvis is in a neutral position, and the thigh is in contact with the table, indicating appropriate length of the iliopsoas muscle.

Figure 13–7 Left positive straight leg raise test. The pelvis begins to move anteriorly at 60 degrees of hip flexion, indicating tightness in the hamstring muscles.

Figure 13–5 Right positive Thomas test. The lumbar spine loses contact with the table and the pelvis moves anteriorly at 30 degrees of hip flexion, indicating tightness in the iliopsoas muscle.

Figure 13–8 Left negative popliteal angle test. The hip is at a 90-degree angle, the knee at zero extension, and the ankle at neutral dorsiflexion, indicating appropriate length of the distal hamstring and gastrocnemius muscles.

Figure 13–6 Right negative straight leg raise test. The pelvis remains in a neutral position as the straight leg is passively flexed to 90 degrees, indicating appropriate length of the hamstring muscles.

and disabilities obtained from the history, systems review, and tests and measurements will serve as guides for establishing a plan of care. Treatment intervention includes any or all of the following: realistic, age appropriate, physical size, and lifestyle.

KEY POINTS Treatment intervention 1. Realistic 2. Age appropriate 3. Physical size 4. Lifestyle

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Figure 13–11 Right positive Ober test. The thigh and knee are above the horizontal position in relation to the hip joint, indicating tightness in the ITB.

Figure 13–9 Right positive popliteal angle test. The hip is at a 90-degree angle; the knee is at minus 30 degrees of extension with the ankle in neutral dorsiflexion, indicating tightness in the distal hamstring and proximal gastrocnemius muscles.

Figure 13–12 Right negative Ely test. The anterior hip remains in contact with the table with the knee in 90 degrees of flexion, indicating an appropriate length of the rectus femoris muscle.

Figure 13–10 Left negative Ober test. The thigh and knee are horizontal in relation to the hip joint, indicating normal length of the ITB. NOTE: In younger children the thigh and knee drop below the horizontal position in relation to the hip.

Therapeutic Exercise and a Home Program Teaching the patient an appropriate, realistic exercise program performed at home on a daily basis will help the patient achieve a successful, functional outcome. The exercises must be simple and age appropriate to promote both understanding and compliance. Special considerations,

Figure 13–13 Left positive Ely test. The anterior hip loses contact with the table, and the buttock begins to rise at 60 degrees of knee flexion, indicating tightness in the rectus femoris muscle.

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Figure 13–14 Thigh circumference: Measurements are taken and recorded at 2, 4, and 6 inches above the suprapatellar marker. Calf circumference: Measurements are taken and recorded at 2, 4, and 6 inches below the suprapatellar marker.

Figure 13–16 Apparent leg length is measured from the umbilicus to the medial malleolus, indicating pelvic malalignment.

Figure 13–15 True leg length is measured from the anterior superior iliac spine to the medial malleolus, indicating discrepancies in the femur and/or tibia.

which influence the treatment plan, are chronological age, bone age, physical size, and lifestyle. An individualized exercise program will meet both the child’s physical and emotional needs. Attitude, motivation, and time availability will have a significant impact on the success of the program. Documentation of

KEY POINTS Treatment guidelines for nonsurgical conditions Assistive devices to: 1. Decrease pain 2. Promote rest and protect healing tissue

progress on a regular basis is necessary to ensure a successful outcome (Figure 13–17). Patient and parent education KEY POINTS is a key component for a successful (cont’d) outcome. Teaching the anatomy and function of the knee joint 3. Prevent further injury helps to promote compliance. 4. Protect during Showing simple illustrations activities and/or a model of the knee helps to Exercises to: demonstrate how it functions. 5. Restore full, “painDescribing how the bones are confree” range of motion nected and the role of muscles, 6. Eliminate muscle tendons, ligaments, and cartilage imbalances will help to reinforce the appropri7. Promote proper ate performance of the exercise patella alignment program. In addition, instructing and tracking the patient to keep a daily exercise 8. Increase quadriceps, log can also help to promote hamstring, adductor, patient compliance. Reviewing the and triceps surae log at each formal physical therapy strength session will give the therapist the Functional activities to: opportunity to give positive, 9. Improve balance and encouraging feedback. coordination The overall focus of the pro10. Promote program is to regain full knee motion prioception (0 degrees of knee extension; 135 11. Increase endurance degrees of knee flexion); normal 12. Return to recrequadriceps, hamstring, and triceps ational and sport surae muscle bulk and strength; activities normal proprioception; normal

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knee mechanics; endurance; and full, pain-free knee function. The key Points box suggests guidelines for nonsurgical and surgical treatment interventions. Range of motion Restoring joint range of motion may require beginning very slowly with active, assistive exercises done in a side-lying position in order to eliminate the effects of gravity. The child lies on his or her involved side with the uninvolved leg over a pillow. This is a very comfortable position that is less stressful for the child, thus instilling confidence. Using a gentle “contract/relax” exercise technique will also help to quickly regain full range of motion in the knee (Figure 13–18).20 Flexibility

KEY POINTS Treatment guidelines for surgical conditions 1. Immobilization to promote healing 2. Decrease joint effusion 3. Protective range of motion (ROM) dependent on healing constraints 4. Progressive strengthening dependent on pain level and surgical precautions 5. Progressive weightbearing 6. Achievement of functional activities including: a. Full ROM, flexibility, and muscle strength b. Normal patellar alignment, mobility, and tracking c. Joint proprioception d. Balance and coordination e. Endurance f. Return to recreational and/or athletic activities

Restricted muscle flexibility can have a detrimental effect on the overall knee rehabilitation program. In addition, restrictions and/or muscle imbalances in the quadriceps, hamstrings, tensor fascia latae, ITB, and triceps surae will not only compromise future recreational and athletic activities but may also lead to future injuries. Teaching the child how and when to stretch is the key to a successful outcome. During a growth spurt, muscle flexibility decreases and therefore it takes a greater effort to sustain optimal flexibility.21 Daily stretching exercises for the aforementioned muscles will help to maintain muscle length, especially during the growth period (Figure 13–19). Stretching is best done following a series of “warm-up” exercises. Health professionals agree that warm-up exercises increase tissue extensibility, thus making stretching exercises less stressful and more effective. However, the length of time and the type of exercises to perform are not clearly defined. A recommended guideline for warming up is to start with global gentle movements ranging in time from 3 to 30 minutes. This will help to increase the body’s core temperature. Proper warm-up exercises should promote a feeling of warmth and may cause perspiration. Strength Muscle strength, power, and endurance encompass all aspects of muscle rehabilitation. Maintaining and increasing strength in all segments of the quadriceps, hamstrings, adductors, and triceps surae muscle groups will stabilize and protect the knee joint, improve endurance and power, and decrease the risk of future injuries. Methods of providing

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optimal loading of the muscles include varying the amount of resistance, repetitions, frequency, speed, and rest intervals. Resistance training includes isometric, isokinetic, concentric, and eccentric muscle contractions. Both open and closed kinetic chain exercises are necessary to restore strength and function. Open kinetic chain (OKC) exercises are performed with the distal lower extremity segment free. A short arc quadriceps strengthening exercise is an example of an OKC. Closed kinetic chain (CKC) exercises are performed with the distal segment fixed. An example of a CKC exercise is a wall side (Figures 13–20 and 13–21). Recent studies suggest that children can participate in a properly designed and supervised resistance training program. Benefits include increased muscular strength and endurance, decreased injuries, and improved performance capacity in sports and recreational activities.22 Manual therapy Manual therapy is the application of mechanical forces to impose tensile and shear forces on contractile and noncontractile tissue.23 Mobilization of the patella to improve tilt and glide can reduce soft tissue imbalances. The child and parent must be properly instructed in these techniques. Physical agents and electrotherapy The proper use of physical agents and electrotherapy can be used to enhance and facilitate desired outcomes. Physical agents include superficial heat and cold, deep heat, and electrotherapy. These modalities can help to decrease swelling, relieve muscle spasm, increase or decrease blood flow, promote relaxation, and improve tissue extensibility. Superficial heat and cold increase or decrease tissue temperature at a depth less than 1 cm. The physiological response to heat causes vasodilatation and erythema. The application of cold causes vasoconstriction followed by vasodilatation. Both heat and cold can decrease fast and slow nerve fiber sensation.24 The main goal is to decrease pain and promote relaxation of the tissues. In addition, applying pressure with cold reduces post-traumatic swelling. Special precautions should be taken when applying heat or cold packs to children. It is essential to have a proper barrier between the skin and the hot or cold pack in order to prevent skin irritation and/or damage. Hydrotherapy is the immersion of body segments in water. This allows for an increase or decrease in superficial tissue temperature in a large body part. Most whirlpools have a turbine unit attached that allows for water aeration. The main goal of hydrotherapy is to decrease swelling, relieve joint pain and stiffness, and promote relaxation. Special precautions must be taken when placing a child in a whirlpool. The child must be positioned comfortably and safely. An adult must be present at all times during the treatment.24 Deep heat (therapeutic ultrasound) is produced by a transducer, which converts electrical energy into sound energy. Ultrasound produces a thermal effect by increasing tissue temperature 1–2 degrees at a depth of 5 cm. Nonthermal effects include cavitation and mechanical and chemical alterations.24 The main goal is to increase tissue extensibility, decrease inflammation, swelling, pain, and muscle spasm. In addition, ultrasound can help to reduce joint contractures and scar tissue. Special precautions must be taken when administering ultrasound to children with

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Figure 13–17

Progressive resistive exercise form used to record treatment progress at various intervals.

Figure 13–18 Side-lying on the involved side to facilitate gravity-eliminated knee flexion and extension.

Figure 13–19 Demonstration of an exercise to stretch the hamstring and proximal gastrocnemius muscles using a nonflexible strap around the forefoot. The hip is at a 90-degree angle, the knee at 0 degrees of extension, and the ankle at 0 degrees of dorsiflexion. NOTE: If both muscles are very tight, the strap is placed around the ankle to eliminate dorsiflexion, and the hip is positioned at a lower angle.

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Figure 13–20 The short arc quadriceps exercise is an example of an open kinetic chain (OKC) exercise. The patella is taped to promote patellar alignment. Neuromuscular electrical nerve stimulation (NMES) is applied to the vastus medialis obliquns (VMO) to provide biofeedback and stimulation; a light weight is placed around the ankle for resistance.

open physes. Although the literature suggests that low intensity ultrasound can minimally be applied, it is generally recommended that it not be used on children with open epiphyses.25 Neuromuscular electrical nerve stimulation (NMES) is electrical current applied to the skin, which activates motor units and causes an involuntary skeletal muscle contraction.26 The main goal is to provide biofeedback and muscle re-education to the involved muscles (see Figure 13–20). Special precautions must be taken when applying NMES to children. Young children may not be able to tolerate NMES because of the irritant nature of electrical stimulation. If NMES is to be used on children, it is recommended that the child observe the NMES being applied to the therapist and/or to the parent before treatment in order to alleviate fear and apprehension. NMES has been shown to enhance muscle function postoperatively.27 Iontophoresis is the transfer of topically applied active ions into the epidermis and mucous membranes of the body by direct current.28 Ions with a positive charge are introduced into the body by the positive electrode. The negative ions are introduced into the body by the negative electrode. The

Figure 13–21 The wall slide is an example of a closed kinetic chain (CKC) exercise that enhances patellar alignment and quadriceps strength. A small foam ball is placed between the lower thighs. The patient squeezes the ball to engage the adductors and VMO muscles as she slides up and down the wall while contracting the quadriceps muscle.

goals of iontophoresis include the reduction of inflammation and edema, as well as the softening of scar tissue. Precautions should be taken when applying iontophoresis to young children due to the irritating affect of the direct current. Massage is the manipulation of soft tissues by the hands. Pressure and stretching compress soft tissue and cause an increase in arterial blood and lymphatic circulation, thus promoting better muscle nutrition and relaxation.29 Massage given before performing a series of exercises will often promote a better outcome.

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Sleeves and braces The role of sleeves and bracing devices is to protect and support injured structures during the healing stages. Assistive devices can help to reduce swelling, improve proprioception, and promote proper tracking of the patella. Sleeves are usually made of elastic materials that provide compression and warmth and enhance joint proprioception. There are various types of neoprene sleeve supports, including lateral, horseshoe-shaped, and donut-shaped supports. These supports are incorporated into the sleeve to prevent lateral tracking of the patella by providing direct pressure to the patella. These devices may reduce the effects of pain inhibition in the quadriceps muscle, allowing improved knee biomechanics. Patellar taping Patellar taping is another form of support. Taping is patient specific and has been shown to reduce pain. Taping of the patella is thought to provide a long duration stretch (see Figure 13–20). Taping can correct lateral tilt, displacement, and rotation of the patella.30 The child and/or parent can be easily instructed in proper taping techniques. However, precautions should be taken with patients who have sensitive skin and/or allergic reactions. A nonallergenic liner under the tape will help to reduce skin irritation. Many tapes may contain latex and are contraindicated in patients with a latex allergy. Foot orthotics and footwear

provides constant speed and accommodating resistance with reliable and objective measurement of muscle strength, power, and endurance. Isokinetic testing of the quadriceps and hamstrings should be 80% or more when compared to the uninvolved knee (Figure 13–22). Functional tests are performance-based measurements that help to determine if the child is ready to return to recreational and sports-related activities. The hop test and agility test are two examples of functional tests. The hop test assesses function and confidence of the injured knee.31 The distance hopped is compared between the injured and uninjured leg. An average of three separate hop tests is determined. A hop index is calculated by dividing the lesser distance by the greater distance and then multiplying by 100. A hop index equal to or greater than 90% is considered normal (Figure 13–23). Agility is the ability to change direction without the loss of speed, strength, or balance.32 The short shuffle drill looks at timed directional change. The child begins at cone A. He then runs a distance of 5 yards to touch cone B and then sprints 10 yards to touch cone C, and finally returns to cone A, for a total of 20 yards. The distance is timed. As the child improves in strength, flexibility, and agility, the times should decrease. The completion of progressive activities that are recreational or sport specific are also included in functional testing. Self-assessment is the child’s ability to determine his or her readiness to return to activities. Included in the self-assessment is the child’s confidence level to perform

Foot orthotics to control excessive pronation at the subtalar joint has been shown to improve patella tracking.11 Prescribed foot orthotics should be worn for all activities. The orthotics should be evaluKEY POINTS ated at regular intervals while the child is growing. Proper footwear Treatment plan can also provide support and help 1. Joint range of motion to alleviate stresses on the foot, 2. Flexibility knee, hip, and back. Appropriate 3. Muscle strength footwear need not be expensive 4. Aerobic conditioning but should be in good repair, 5. Use of physical have a proper amount of cushion, strength and should be replaced often. 6. Massage Recommended replacement of 7. Taping footwear is every 3–4 months, 8. Orthotics and depending on the child’s growth footwear and activity. Outcomes, Discharge, and Return to Full Activity When the anticipated goals and expected outcomes have been achieved, the child is discharged from the formal knee rehabilitation program. Discharge criteria are based on analysis of the goals and outcomes. The analysis includes reevaluation, functional tests, and the child’s self-assessment. Periodic follow-up is advisable during growth and maturation. Reevaluation includes selected tests and measurements from the initial evaluation indicating the achievements of the anticipated goals. The following outcomes must be achieved: pain-free activity, no joint effusion or swelling with activity, normal knee range of motion, and normal lower extremity muscle strength. Isokinetic testing

Figure 13–22 Isokinetic testing of the quadriceps and hamstring muscles. This test provides an objective measurement to determine the child’s readiness to return to sports.

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a maintenance program stressing proper anatomical alignment, flexibility, and muscle strength is essential to prevent muscle imbalances. A proper, well-designed program will help to protect the knees and prevent future injuries. References

Figure 13–23 Patient demonstrates a hop test to assess the function in the injured leg and to promote confidence.

activities without apprehension. The child must be at an appropriate age to participate in selfassessment. Parents, coaches, athletic trainers, and health care professionals will need to guide the process of self-assessment for younger children. Summary

KEY POINTS Discharge criteria 1. Pain free 2. Normal range of motion 3. Normal muscle strength 4. No swelling or edema 5. Isokinetic testing; 80% or more when compared to uninvolved extremity 6. Balance, coordination, agility: sport specific 7. Self-assessment

In conclusion, an effective knee rehabilitation program for the pediatric and adolescent patient population must not only promote a total functional outcome for the existing problem but must also promote educating the child in healthy lifestyle changes. Instructing children in the proper care of their bodies is the responsibility of all who are involved with them: parents, health care professionals, coaches, teachers, athletic trainers, and any other responsible adult who interacts with them. Children must be made aware that their knees have to last a lifetime. A healthy lifestyle that includes

1. Cherry DB: Pediatric physical therapy: philosophy, science and techniques. Pediatr Phys Ther 3:70–75, 1991. 2. Rothstein J: Guide to physical therapy practice, 2nd ed. Phys Ther 81:9–741, 2001. 3. Gould A: Cardiopulmonary evaluation of the infant, toddler, child, and adolescent. Pediatr Phys Ther 3:9–13, 1991. 4. O’Sullivan S, Schmitz TJ: Burns. In: Physical Rehabilitation and Assessment and Treatment. Philadelphia: FA Davis Company, 1988. 5. Tachjian MO: Pediatric Orthopedics, 2nd ed. Philadelphia: WB Saunders Company, 1990. 6. Campbell SK: Physical Therapy for Children. Philadelphia: WB Saunders Company, 1994. 7. Schechter NL, Berde CB, Yaster M: Pain in Infants, Children, and Adolescents. Philadelphia: Lippincott, Williams & Wilkins, 2003. 8. Kendall FP, McCreary Kendall E: Muscle Testing and Function, 3rd Ed. Baltimore: Williams & Wilkins, 2003. 9. Shumway-Cook A, Woollacott M: The growth of stability: postural control from a development perspective. Phys Ther 17:131–147, 1985. 10. Sutherland DH, Olshen R, Cooper L, Woo SL: The development of the mature gait pattern. JBJS 52:336–353, 1980. 11. Enj J, Pieryynowski MR: Evaluation of soft foot orthotics in the treatment of patellofemoral pain syndrome. Phys Ther 73(2):62–70, 2003. 12. Patel DR: Pediatric neurodevelopment and sports participation. When are children ready to play sports? Pediatr Clin N Am 49:505–531, 2002. 13. Thomas HO: Diseases of the Hip, Knee and Ankle Joints with Their Deformities, Treated by a New and Efficient Method. Liverpool, England: T Dorr & Co, 1876. 14. Ober F: Backache. Springfield, Ill.: Charles Thomas, Publisher, 1955. 15. Starkey C, Ryan J: Orthopedic and Atheletic Injury Evaluation Handbook. Philadelphia: FA Davis, 2003. 16. Nissen CW, Cullen MC, Hewett TE, Noyes FR: Physical and arthroscopic examination of the patellofemoral joint. J Orthop Sports Phys Ther 28(5):277–285,1998. 17. Brotzman SB: Clinical Orthopaedic Rehabiliation. New York, Mosby, 1996. 18. Lohman TG, Roche AF, Martorell R: Anthropometric Standardization Reference Manual. Champaign, Ill.: Human Kinetic Books, 1988. 19. Hoppenfeld S: Physical examination of the hip and pelvis. In Hoppenfeld S (ed): Physical Examination of the Spine and Extremities. New York: Appleton-Century-Crofts, 1976. 20. Knott M, Voss D: Proprioceptive Neuromuscular Facilitation. New York: Harper and Brothers, 1956. 21. Micheli LJ: Overuse syndrome in children’s sports: the growth factor. Orthop Clin N Am 14:337–360, 1983. 22. Fleck ST, Kraemer WJ: Designing Resistance Training Programs. Champaign, Ill.: Human Kinetics, 1997. 23. Kaltenborn FM: Manual Mobilization of the Extremity Joints. Minneapolis: Orthopedic Physical Therapy Products, 1989. 24. Michlovitz SL: Thermal Agents in Rehabilitation. Philadelphia: FA Davis 1990. 25. Deforest RE, Herrick JF, Janes JM, Krusen FH: Effects of ultrasound on growing bones; experimental study. Arch Phys Med Rehabil 34:21, 1953. 26. Nelson R, Currier D: Clinical Electrotherapy. Norwalk, Connecticut: Appleton & Lange, 1991. 27. Robertson VJ, Ward AR: Vastus medialis electrical stimulation to improve lower extremity function following a lateral release. J Northup Sports Phy Ther 32:437–446, 2002. 28. Kahn J: Principles and Practice of Electrotherapy. New York: Churchill Livingstone, 1991. 29. Beard G, Wood E: Massage Principles and Techniques. Philadelphia: WB Saunders Company, 1964. 30. McConnell J: The management of chrondromalacia patellae: a longterm solution. Aust J Physiother 32:215–223, 1986. 31. Daniel D, Malcolm L, Stone ML, et al: Quantification of knee stability and function. Contemp Orthop 5(2):83–92, 1982. 32. Costello F, Kreis EJ: Sports Agility. Nashville: Taylor Sports, 1993.

Chapter 14

Operating Room Equipment and Environment Peter G. Gerbino

There has been little written regarding optimized selection and use of operating room equipment required for knee surgery. From a sports medicine perspective, one is primarily concerned about arthroscopic equipment in an outpatient surgery environment. The focus of such a discussion can be narrow, concentrating on specific tools, or broad, analyzing the entire operative experience. Tools change regularly and newer, better versions of arthroscopic cameras, optics, hand tools, and tissue ablators are on display at the annual meetings. Similarly, new sets of equipment for various procedures are unveiled on a yearly basis, incrementally improving one or more technical aspects of that particular procedure. The quality of specific tools is uniformly high. The choices are made based on individual surgeon preference. A surgeon’s comfort with the tools is what improves technique and satisfaction. Specific tools are needed for different types of arthroscopic procedures. Optimizing the entire operating room experience is of major importance. A good architect or project manager can be essential for this mission. Having state-of-the-art orthopedic or anesthesia equipment matters little if the patient arrives anxious, cold, and unhappy. The nurse’s job is more difficult when flow is not smooth or instruments are not readily available. The surgeon wants everything perfect— happy patient, scrub staff, and anesthesia staff; all instruments well maintained; and short turnover times between cases. The anesthesiologist wants well-maintained equipment and a tranquil atmosphere in the operating room. The perfect operating room environment results in happy patients, nurses, anesthesiologists, and surgeons. This further translates to happy financial managers and hospital administrators.

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The Patients’ Experience A patient and his or her family encounter five distinct situations in the course of a surgical experience. Arrival at the facility, including finding the surgery center, parking and checking in, is the first experience. The ease with which a patient can get to the correct check-in desk sets the stage for the entire process. Traffic situations, difficult parking, a maze of turns through a confusing hospital, and surly checkin staff can produce predictably anxious patients. The second situation that a patient and his or her family encounter is the waiting room. Layout of the room, amenities, lighting, and even paint colors contribute to make the experience more or less stressful.1 Many hospitals and surgery centers put minimal significance on these variables, believing that they are cosmetic only. Fortunately, many architects and healthcare consultants realize the importance of these variables and incorporate them into their designs.1 The preoperative holding area is the patient’s next experience. The Joint Commission on Accreditation of Healthcare Organizations (JCAHO) and Accreditation Association for Ambulatory Healthcare (AAAH) requirements specify size and safety requirements for surgicenters.2,3 They do not specify that minimizing noise and maximizing privacy are important to patients.4 Providing the surgical team access for preoperative counseling in a stress-free environment is mandatory. Allowing the anesthesia team access for counseling, examination, and placement of intravenous lines is also necessary. Nursing or physical therapy has to be able to teach crutch gait and prepare the patient for what is to come. The patient next moves to the operating room, which is the fourth situation in the surgical experience. Preanesthesia with amnestic agents has been shown to decrease patient anxiety and improve outcomes.5 Minimizing noise and other

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stressors can be designed into the physical layout. Temperature of the room should be considered, providing warm blankets for the patient KEY POINTS rather than constantly adjusting room temperature. Pleasant 1. Getting to the center music rather than harsh music or is the patient’s first background chatter can make experience. the patient more relaxed before 2. The check-in 6 induction. procedure should Patients’ experiences in the be pleasant. postanesthesia care unit (PACU) 3. Waiting areas should are their final memories of the be thoughtfully operation. From the patient’s designed. perspective, lack of nausea and 4. The preoperative pain are more important than area must be other factors. The family needs private. complete postoperative care 5. The operating instructions and to feel that the room should be patient’s privacy and dignity calming rather than are being maintained. The frightening. amnesic patient may not recall 6. The recovery area a high level of professionalism must address all by PACU staff, but the family patient and family will recall every detail of the concerns. experience. Nursing and OR Staff Concerns Nurses and operating room (OR) personnel have very important roles in patient satisfaction and treatment outcome. Their primary concern is patient safety. Secondary needs include patient satisfaction; proper surgical instrument selection; and the smooth, efficient running of the surgical environment. In many cases there is also a teaching function that must be provided. Patient safety encompasses everything from ensuring that patients have the proper paperwork to escorting them to their cars as they depart. Preoperative crutch training, ensuring that the correct operative site is identified and signed, and checking to see that informed consent has been obtained are routine nursing duties before bringing the patient to the operating room. Once the patient is in the operating room, the nursing duties shift to ensuring a safe transfer of the patient to the operating table, positioning the patient comfortably, assisting the anesthesiologist, and assisting the surgeon. Nursing staff members prefer warm, quiet rooms with few stimuli to alter a tranquil mood. During surgery, they want a calm surgeon who knows the surgical procedure intimately and calls for the correct instruments at the appropriate time. They want to know that the instruments have been well maintained and properly packaged after thorough cleaning. At the conclusion of the procedure, nursing continues to ensure patient safety by assisting anesthesia during extubation and overseeing patient transfer from the table to the recovery unit.7 PACU nurses pick up the patient’s care at this point. These nurses have an additional role to ensure an optimal experience for the patient. They want a smooth transition to alertness without nausea or excessive pain. They need

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detailed instructions for the patient and family to answer the myriad questions that arise once the patient returns home. Back in the operating room, the surfaces and floor need to be cleaned in preparation for the next patient. Equipment for the next procedure is brought to the room and set up. The next patient is met, along with the family, and the process repeats. Efficiency in this process results in shorter “turnover” times, defined as the time between leaving the room with one patient and arriving in the room with the next. Achieving short turnover times is not necessarily a goal of nursing and OR staff. If rapid turnover results in a shorter workday or in financial reward, times tend to be quick. If rapid turnover results in additional cases for the efficient room, with no compensation for the extra work and effort, turnover can get very slow. Unfortunately, this simple human equation is lost on many hospital administrators. Large hospitals typically have limitless caseloads, layers of workers with different jobs, and poor incentives to work efficiently. Outpatient surgery centers have better team values and can be much more efficient. Turning a section of a large hospiKEY POINTS tal into a “same-day surgery center” brings all the inefficiencies of 1. Patient safety is the large hospital, negating many nursing’s primary of the benefits of an outpatient concern. 8 surgery center. To increase effi2. Proper paperwork ciency and revenue, many sports and signing the medicine surgeons have turned to operative site have stand-alone ambulatory surgery become essential 9 centers. Companies exist whose duties in the preoperentire focus is to increase effiative setting. 10 ciency of health care entities. 3. Ensuring that In summary, nursing and surgical instruments OR staff want patient safety and are correct and in to do their jobs in a stress-free good working order environment. In the ideal surgicontinues to be an cal center, there is a stand-alone essential nursing role. building with a dedicated nurs4. Depending on the ing team motivated to get as environment, effimany operations done as safely ciency and rapid as possible. To accept anything turnover can be a less will inevitably lead to priority. decreased productivity. Anesthesia Perspective Anesthesiologists and nurse anesthetists have specific ideas about how to best run an outpatient surgery center. The American Society of Anesthesiologists publishes a text entitled Operating Room Design Manual, which gives the current recommendations for safe anesthesia in all situations. The manual discusses all facets of room size, layout, and equipment. It also discusses preoperative and PACU design, administrative areas, and lounge areas. It does not discuss efficiency, motivation, or optimal use of resources.11 Patient safety issues are codified in the JCAHO manual.2 Most of these guidelines are designed to prevent patient injury and ensure adequate antisepsis. In the outpatient setting the anesthesia team will first meet the patient in the preoperative area. An adequate history and

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physical examination requires a quiet, private examination area and enough time to complete a thorough evaluation. The surgical suite design must achieve privacy. The patient scheduling system must allow time for the evaluation. This means that the anesthesia evaluation needs to be scheduled at least 30 minutes before the planned operation start time. In healthy, young outpatients, 30 minutes is adequate for taking history, a physical examination, starting an intravenous line, and giving preoperative medicines. After the first patient of the day, subsequent patients can be evaluated while surgery is underway on the previous patient. Of course, there must be two anesthesia staff members per operating room, or at a minimum, three staff per two rooms to accomplish this. While the first anesthesiologist evaluates and provides anesthesia for the first patient, a second anesthesiologist begins evaluating the second patient. Two anesthesia staff members are necessary for rapid turnover, shortduration orthopedic cases. Other arrangements work better when the cases last longer. As in nursing, if the anesthesia professional is being paid a flat salary, there is little incentive to see more patients and get more operations done. If the anesthesia professional is being compensated by work produced or if the workday ends when the last case is finished, there is appropriate motivation to accomplish more in a shorter period. Inside the operating room, well-maintained, stateof-the-art anesthesia equipment is desired. The anesthesia technician should keep the machines re-equipped and ensure that adequate supplies are available. Because operating room time is the most valuable commodity (in most settings), starting intravenous lines, placing regional blocks, and didactic resident education should occur before entering the operating room. Likewise, KEY POINTS unless the patient awakens immediately after the case con1. The anesthesia team cludes, all patients should be needs to know about transported to the PACU while potential difficulties intubated. In the PACU the with a given patient nurses need to be comfortable as far in advance as extubating patients and providpossible. ing for immediate postextuba2. There needs to be tion care. The anesthesia profesadequate time and sional must stay with the patient privacy in the preopuntil it is safe for the nurses to erative setting to fully take charge.12 obtain a thorough If there are two anesthesia examination and professionals per operating room, history. the second person can immedi3. Operating room ately proceed to the room with anesthesia equipthe next patient. Less efficient ment must be well turnover occurs when the same maintained and anesthesia professional begins to complete. evaluate the next patient after 4. The anesthesia fully finishing with the first. team supervises In the ideal environment postanesthesia there is an anesthesia professional care. available to handle problems that 5. The anesthesia arise in the PACU and patient team and the PACU telephone calls regarding nurses manage postanesthesia complications or postoperative pain concerns. These calls can be and nausea. triaged by the nursing staff to the

surgeon or anesthesiologist, depending on the nature of the patient’s problem. Surgeon’s Concerns The sports medicine orthopedic surgeon operating in an outpatient setting has several goals. He or she desires optimal operative outcomes with maximum safety. Once those mandatory goals have been achieved, secondary objectives include a pleasant working environment and an efficient, profitable organization.13 Many individual parameters contribute to these goals. They include a well-informed patient, appropriate indications for surgery, thorough preoperative planning, and a smooth flow on the day of surgery. Most of the conditions that lead to a smooth flow of events on the day of surgery are the previously discussed parameters that lead to patient, nursing, and anesthesia satisfaction. For the surgeon’s part, once the team members have their ideal conditions, all that remains for the ideal operation is correct, state-of-the-art equipment in good repair. State-of-the-art equipment is readily available. For arthroscopy, most vendors now offer ceiling-mounted equipment racks with the latest video recording and processing equipment. Advantages of ceiling-mounted equipment purportedly include less trauma to the video equipment, faster video setup, the ability to position multiple monitors around the patient, and more rapid room turnover because cleaning is easier (Figure 14–1). These rooms are certainly a pleasure to work in, and a surgeon could undoubtedly increase productivity, but at a cost. Such a room is, of necessity, dedicated to endoscopic procedures exclusively. This is desired at some centers. At centers where multiple types of procedures are conducted in the same room, the equipment would be a severe encumbrance. This type of equipment is also expensive. If a surgery center is being built new, reinforcing the ceiling and installing the racks are much easier than retrofitting an established OR. If the extra expense cannot be covered by surgical volume, using such equipment

Figure 14–1 Artist’s rendering of a state-of-the-art endoscopic operating room using overhead installation of all surgical and anesthesia equipment. (Used with permission, ConMed Integrated Systems, Beaverton, Or. www.conmedis.com.)

Operating Room Equipment and Environment

is a poor business decision. A final disadvantage to permanent installation is that when the system malfunctions, a backup system must be brought in while the installed system continues to occupy space and cannot be repaired during surgery. There are no studies comparing one manufacturer’s equipment to another. One can discuss the relative merits of each company’s cameras, arthroscopes, shavers, and recording devices with that company’s representatives. At conKEY POINTS ference exhibits, one can 1. The surgeon wants demonstrate and handle the optimal outcomes tools. What is clear is that there with minimal are no poor systems. All are complications. excellent, and a surgeon’s past 2. A well-informed experience and specific needs patient is less anxare probably more important facious preoperatively. tors. Even price cannot be used 3. Communication with as a limiting factor. Companies nursing and anesthewill typically match or beat a sia teams prevents competitor’s bid, and all kinds of problems, anxiety, creative financing can be and inefficiency. arranged. Technical Considerations

4. Excellent equipment is the norm in the United States.

In the United States, a basic arthroscopic system would consist of 4.5-mm 30- and 70degree arthroscopic telescopes, a light source, camera, video processor, and recording/printing device(s). Additional standard equipment includes a suction shaver, radio frequency ablation/heating device, and a set of arthroscopic hand tools. A small joint 2.7-mm arthroscope is used for small knees, ankles, elbows, and wrists. A standard set of hand tools includes a probe, four to eight cutting punches, and at least one grasper. The punches typically include straight, up-biting, and left and right sidebiting forceps. Common additional punches are an extrasmall punch for tight knees, variations of the up-biter and side-biters, a back-biting punch, and biopsy punches. All power shavers use forward, reverse, and oscillate modes to accomplish the task of débridement of the various joint tissues. Suction shaver blades are sized from 3.5–5.5 mm in diameter. In addition to several degrees of aggressiveness in the jaw design, cutters that flex or come prebent are available. Round and cylindrical burrs are available for bone removal. Several companies manufacture thermal devices, including the Smith-Nephew Oratec, Mitek VAPR, and ArthroCare systems. Each uses heat to cut, ablate, contour, shrink, or cauterize tissue. Use of these devices on articular cartilage has been advocated by some, but evidence shows that a wide area of necrosis is unavoidable.14 In countries with tight health care budgets, a single telescope, light source, camera, and processor can suffice. The shaver would be accessible only when absolutely necessary, and there would be individually sterilized hand tools requested as needed. While visiting operating rooms in some of these countries, I have been impressed with what can be done with an arthroscope, probe, and a single, well-chosen basket punch.

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KEY POINTS For a common bucket-handle 1. Depending on medial meniscus tear in a young, resources, a basic healthy patient, there would be a arthroscopy set is very similar order of events in established. most sports medicine operating 2. Whether it is a rooms. Once the patient is minimal set of tools brought to the room and anesor a large allthetized, the extremity to be inclusive set, there operated on is prepared and should be uniformity draped using sterile technique. from operation to Some surgeons hang the leg off operation. the table, whereas others use a 3. Cameras, telescopes, lateral post or one of various leg and recording holders to stabilize the extremdevices are ity. Many surgeons will utilize a mandatory. pneumatic tourniquet at the 4. Basket punches and thigh, whereas others prefer not powered shavers are to use one. Some surgeons use an needed for removing arthroscopic pump for fluid contissues. trol, whereas others use a simple 5. Specific tool sets are gravity setup. used for different The choice of arthroscopic types of repairs. portals is by surgeon preference, 6. Thermal devices can but most use the anterolateral be used for ablation, portal for viewing and fluid cutting, shrinking, or inflow and the anteromedial annealing tissues. portal as the main working portal. Many additional portals have been described to access the various areas of the knee; frequently, medial and lateral tools are reversed to achieve an optimal meniscus repair. Many surgeons continue to prefer a separate proximal medial or lateral portal for fluid inflow. After a stepwise and thorough arthroscopic examination of the entire knee, a decision of whether to repair or resect the bucket-handle tear is made. If the tear is repairable, the margins are rasped to enhance healing, and the tear is repaired by one of several meniscus repair techniques. The repair is tested with the probe, and the operation is concluded. Meniscus repair technique continues to evolve. The “gold standard” remains the inside-out suture repair using vertical mattress sutures of 2-0 absorbable or nonabsorbable sutures. They are spaced 5 mm apart and tied on the posterior capsule via a separate incision. The cannulae for passing the long needles for this repair come in six configurations to achieve optimal access to the anterior, middle, and posterior regions of both menisci. Advantages to suturing are a strong, secure repair, low cost per suture, and few complications in the joint. Disadvantages include the need for a second skilled surgeon, a second incision, and increased surgical time. Other meniscus repair techniques use “all-inside” sutures, darts, arrows, screws, or staples. Most of the stiff devices, such as arrows and screws, are made from absorbable materials such as poly-L-lactic acid. Suture materials are absorbable or permanent, depending on the device. Advantages to all-inside devices include rapid placement by a single surgeon and no need for a second incision. Disadvantages include higher cost per device,

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higher failure rate than suture, possible damage to articular cartilage from prominent devices, and loose body formation when absorbable devices fail or fracture. At the end of the operation, local anesthetic is injected at the portals and into the joint for enhanced pain control. If small, the portals can be covered with adhesive strips, but larger portals are closed with suture. Sterile dressings are applied and cryotherapy is begun to complete the procedure. To protect a meniscus repair, a brace that limits range of motion is used. Weight bearing is also limited until the meniscus has healed. Summary

KEY POINTS 1. All patients are prepared and draped in a sterile manner before surgery. 2. There must be a way to stabilize the extremity to visualize the posterior horns of the menisci. 3. Two or three portals are used with gravity- or pump-fed sterile saline irrigation. 4. All knee arthroscopy includes a thorough knee examination. 5. Repairing a meniscus tear can be done by several techniques. 6. Postoperative local anesthetic helps decrease pain. 7. Rehabilitation protects the repair while restoring strength and motion.

Four individuals or groups come together to effect a successful operation: patient, nursing staff, anesthesia staff, and a surgeon. Each person or group has set needs and expectations that only sometimes overlap. Where needs conflict, problems arise. The two interrelated needs that are most prone to problems are time and money. In any surgical environment, time spent in the operating room is the most costly. If the reimbursement system is such that each procedure generates additional income, then additional procedures in that room are desirable. The additional procedures must generate additional income for nursing, anesthesia, and surgeon, as well as for the institution. In this situation, any occupation or equipment can be improved if the funds can be generated. Safeguards must be put in place to prevent patient safety from being compromised in an effort to be more productive. Conversely, in situations where not everyone benefits from increased productivity, the ideal team begins to break down. When all members of the health care team are salaried, the incentive to increase productivity must come from elsewhere. This is difficult to achieve and results in the lower surgery rates seen in U.S. military hospitals and in countries with socialized medicine. In these cases the patients receive less aggregate care because the providers are less productive. The hospital is also less efficient, which can mean more or less money is available to the institution,

depending on how the facility is funded. The ideal operating room environment in a socialized medicine system depends less on productivity and more on job satisfaction from good teamwork and good patient outcomes. Unfortunately, decreased productivity squanders operating room time, and fewer patients can receive care at a given institution. Whether increased productivity results in better care or just more care is a debate for another time. If one accepts the premise that better equipment and facilities result in better care, increased productivity becomes critical because more revenue will be generated. In this case it is mandatory to ensure that all parties benefit from increased productivity, not just the surgeon and facility. The ideal surgical environment fosters productivity that permits purchase of stateof-the-art equipment and provides revenue adequate to address needs as they arise. Common goals and motivation among all parties and a well-designed facility combine to predictably produce optimal results. References 1. Mullin M, Nash M: The second time around. When our hospital built a second outpatient center, we did the things we wished we had done the first time around. Outpatient Surg Mag: 52–60, 2003. 2. JCAHO: 2002-2003 Comprehensive Accreditation Manual for Ambulatory Care. Oakbrook Terrace, Ill.: Joint Commission on Accreditation of Healthcare Organizations, 2003. 3. Healthcare AAA: Accreditation Handbook for Ambulatory Healthcare. Skokie, Ill.: Accreditation Association for Ambulatory Healthcare, 1998. 4. Hyde R, Bryden F, Asbury A: How would patients prefer to spend the waiting time before their operations? Anaesthesia 53:192–195, 1998. 5. Williams B, DeRiso B, Figallo C, et al: Benchmarking the perioperative process. III. Effects of regional anesthesia clinical pathway techniques on process efficiency and recovery profiles in ambulatory orthopaedic surgery. J Clin Anesth 10:570–578, 1998. 6. Kain Z, Wang S, Mayes L, et al: Sensory stimuli and anxiety in children undergoing surgery: a randomized, controlled trial. Anesth Analg 92:897–903, 2001. 7. Burden N: Ambulatory Surgical Nursing. Philadelphia: AORN Inc., 2003. 8. Prybylo M, Thibeault J, Capella C, et al: Lessons learned from a hospital’s $9.9 million ASC. Outpatient Surg Mag, 2003. 9. Small N, Bert J: Office ambulatory surgery centers: creation and management. J Am Acad Orthop Surg 11:157–162, 2003. 10. MedModel. Accessed online November 28, 2005 at www.Promodel.com/ solutions/healthcare/. 11. Ehrenwerth J, Dorsh J, Dorsh S, et al: Operating Room Design Manual. Park Ridge, Ill.: American Society of Anesthesiologists, 1999. 12. Nur ASP: Standards of PeriAnesthesia Nursing Practice. Thorofare, New Jersey: American Society of PeriAnesthesia Nurses, 1998. 13. Bert J: The efficient, enjoyable, and profitable orthopedic practice. Clin Sports Med 21:321–325, 2002. 14. Edwards RB III, Lu Y, Markel MD: The basic science of thermally assisted chondroplasty. Clin Sports Med 21:619–647, 2002.

Chapter 15

Anesthesia for Surgery of the Knee Andres T. Navedo-Rivera

Anesthesia for knee surgery in the pediatric patient presents similar considerations to other pediatric patients undergoing surgery. Physicians who care for pediatric patients are familiar with the variety in patient size and level of function. Patients vary from precocious to delayed, and from rebellious to clinging. A weight lifter and a ballet dancer have very different needs and disposition. It is the task of the anesthesiologist to develop an individualized approach for the care of the patient, avoiding the simplistic one-sizefits-all approach. The plan must take into consideration not only the physical, medical, and emotional needs of the patient, but also the concerns of the parent(s) or guardian (separation anxiety occurs also in adults), as well as those of the nurse, the institution, and the surgeon.

Preoperative Evaluation For most patients the prospect of surgery presents a high level of anxiety. The avid athlete is usually more aware of the implications of his or her condition because it will affect the performance in the chosen sport or activity. The impact of the medical condition may not affect routine daily activities, but the effect on the demanding physical activities will be evident sooner. The anesthetic care begins with the preoperative evaluation. After reviewing the medical record, the anesthesiologist meets with the patient and responsible adult. From that moment the anesthesiologist starts building a trusting relationship with the patient and parent. Confirmation of the information obtained in the medical record is necessary. Discussion of the planned procedure and confirmation of the operative site is done. A review of systems, accompanied by documentation of appropriate fasting, is indicated. We establish agreement regarding allergies and current medications. Physical examination is performed and documented. Laboratory testing, when necessary, is guided by past medical history.

For post-menarche patients, or those older than age 12, a urine sample is tested to establish the absence of pregnancy. Concomitant with the medical evaluation of the patient, the preoperative encounter is aimed at reducing the stress for the patient and parent by answering questions and reducing the number of unknown factors or surprises. An anesthetic plan and probable alternatives are discussed with the patient and the parent. Most adolescents are willing to cooperate with preoperative placement of an intravenous (IV) catheter. Patients who refuse intravenous access before induction may choose to have an inhalation induction. All medications are thereafter given intravenously. Premedication Oral premedication with midazolam is commonly used.1,2 Patients who prefer an intravenous induction have the IV inserted in the company of parents or guardians in the preoperative evaluation area. IV midazolam is titrated to effect and sometimes accompanied by morphine. The nasal or rectal routes are rarely used in this population. Intraoperative Management Short Window of Cooperation In the unfamiliar setting of the operating room, anxiety again rises. Whether proceeding with a parent-present induction (PPI) or an IV induction, patients who visit the operating room for the first time may exhibit a period of calm upon entering the operating room. This window of cooperation is usually longer with older patients. The duration of this cooperation also varies with the patient’s prior surgical experiences and the effectiveness of the preoperative interventions. 151

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Anesthetic Options An anesthetic should be safe, comfortable, convenient, and efficient. If two anesthetics are equal in terms of the risks they represent for a patient, the element of patient comfort grows in importance as a deciding factor between anesthetic plans. When the safety and comfort of the patient are equally satisfied by two anesthetic plans, the patient’s convenience should cast the deciding vote. The efficiency of the system becomes a consideration after the patient’s aforementioned factors are met. General anesthesia is the most common modality in the pediatric and adolescent population. Most of our patients express no enthusiasm for a regional anesthetic, with the fear of needles being the most common objection. Although it is possible to provide a safe general, spinal, epidural, or local anesthetic block for a procedure about the knee for a young patient, the studies available compare these alternatives in the adult population. Jankowski3 compared psoas compartment block, spinal anesthesia, and general anesthesia in patients between the ages of 18 and 60. The average time to meet discharge criteria was not significantly different among the three different groups. General The induction of general anesthesia using volatile anesthetics is common practice in the pediatric population. Because of its fast action, sevoflurane is the agent of choice in most cases. “Single breath” or slow incremental concentrations of sevoflurane, with or without nitrous oxide, are commonly used.3a The IV route is used in older children or adolescents. With fast and more predictable onset of effect from medications, the IV route also has the advantage of minimizing the time that the airway is unprotected. The maintenance of general anesthesia can be accomplished by numerous methods. Whether by means of inhalation anesthetics or solely with IV medications, or a combination of these methods, the patient can safely and comfortably undergo the surgical procedures of interest. How to combine these techniques and the relative benefits of one versus another is beyond the scope of this chapter. Regional Anesthesia Techniques The use of regional anesthesia, local infiltration, or intraarticular techniques as the main anesthetic modality for the performance of knee procedures in the pediatric population is tempered by the requirement of needles in the performance of these blocks. With appropriate patient teaching and preparation and judicial use of sedation, the use of regional techniques as the main anesthetic is possible. Regional anesthesia may also be used as an adjunct to general anesthesia or be performed for the management of postoperative pain. Assessment of regional anesthesia adequacy and emotional support of the pediatric patient during the surgical procedure while the patient is conscious requires verbal communication. Language barriers sometimes make the option of regional anesthesia less attractive. Currently, only the mature and highly motivated patient chooses to have a regional anesthetic. If the

operating room team succeeds in alienating fears in young patients and their parents, the number of patients having these procedures will increase. Spinal Many of the documented benefits of spinal anesthesia in the pediatric population apply to the small number of infants who may be at risk of postoperative bradycardia, apnea, or desaturation that concurrently requires knee surgery. The most common benefit of a spinal or regional technique over general anesthesia is the diminished risk of postoperative nausea and vomiting. The notable complication of “spinal headache” or postdural puncture headache (PDPH) is greater in younger patients. Contrary to common belief, PDPH does occur in children, and no significant difference was found in the incidence of PDPH when using cutting-point or pencilpoint needles.4 Lidocaine is a local anesthetic used in many clinical situations. The use of lidocaine for spinal anesthesia has been associated with transient neurological symptoms (TNS) in patients who received lidocaine by spinal or epidural administration.5 Although few studies have examined the incidence of TNS after spinal anesthesia with lidocaine in children,6 there is abundant information in the adult patient. The incidence of TNS is not affected by the concentration of lidocaine from 0.5–2.0%.7 Other local anesthetics and medications administered neuraxially have also been shown to be associated with TNS.8–12 Epidural The epidural route is an option for the delivery of antinociceptive medications that allow surgical intervention about the knee. A benefit of this modality is the common use of an epidural catheter to continue the delivery of medications in the postoperative period. Placement of this catheter in the pediatric patient is usually done while the patient is under general anesthesia. However, with proper support it is possible to perform an epidural block, with or without catheter placement, in the conscious pediatric patient. The benefit of placing an epidural catheter is evident during long procedures or those procedures that are of unpredictable duration. With the use of short-acting local anesthetics, recovery and discharge times may be comparable to general anesthesia.13 Although similar catheters can be placed for continuous spinal or regional block, the use of epidural catheters is far more common. Intravenous Regional Anesthesia Also known as Bier block, intravenous regional anesthesia (IVRA) is a viable option for superficial procedures involving the knee. The rapid onset of anesthesia over the block area is of benefit. However, procedures lasting longer than 90 minutes, or those in which tourniquet deflation must be done before completion of the intervention, are not suitable for this technique.

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Peripheral Nerve Blocks With a combination of nerve blocks (femoral nerve, lateral femoral cutaneous nerve, sciatic nerve, and obturator nerve), it is possible to provide adequate anesthesia of the knee and the lower extremity. Single injection techniques for peripheral nerve block in knee surgery have been shown effective in the adult population.3 In the pediatric population, these blocks are used primarily to provide postoperative pain relief in combination with a general anesthetic. Intraarticular Special mention of intraarticular administration of medication is appropriate in this forum. Bupivacaine is widely used for intraarticular analgesia following knee surgery (Table 15–1). However, possible bupivacaine toxicity from this route has been reported.14 Many medications have been instilled in the intraarticular space.15–19 Clonidine and morphine have been shown to have analgesic effect when administered intraarticularly.20–22,22a The timing of administration of intraarticular morphine affects the antinociceptive effect, showing a longer duration of analgesic effect when given before surgery.23 The combination of clonidine and morphine evaluated in patients with meniscal surgery appears to offer longer analgesia than either drug alone.24 All these studies have been performed with patients older than age 18. Although similar physiology may make the clinical differences null, the magnitude of the difference has not been determined (Table 15–1). Tourniquets The use of tourniquets during knee surgery is the norm rather than the exception. It is prudent to review some of the anesthetic implications of tourniquets. The hemodynamic and metabolic effects of tourniquet inflation and deflation have Table 15–1 Maximum Recommended Doses of Local Anesthetic Agents in Children Plain Solution (mg/kg) Lidocaine Mepivacaine Bupivacaine Prilocaine Ropivacaine†

5 5 3 5–7* 2

Solution with Epinephrine (mg/kg) 10 7 3 7–9 –

From Rice LJ: Regional anesthesia and analgesia. In: Motoyama EK, Davis PJ (eds): Anesthesia for Infants and Children, 6th ed. St. Louis: Mosby-Year Book, 1996. * Not to exceed 600 mg. † Data from Rapp HJ, Molnar V, Austin S, et al: Ropivacaine in neonates and infants: a population pharmacokinetic evaluation following single caudal block. Paediatr Anaesth 14:724–732, 2004; McCann ME, Sethna NF, Mazoit JX, et al: The pharmacokinetics of epidural ropivacaine in infants and young children. Anesth Analg 93:893, 2001; Bosengerg AT, Thomas J, Lopez T, et al: Plasma concentrations of ropivacaine following a single shot caudal block of 1, 2, or 3 mg/kg in children. Acta Anaesthesiol Scand 45:1276, 2001.

Figure 15–1 Anesthesia recommendations for children must take into account the wide range of maturation levels at a given chronologic age.

been studied in adults and children.25,26 A study by Girardis25 suggests that the effects are the result of changes in cardiac output and systemic vascular resistance. The changes after deflation are dependent on ischemic time. Lynn studied the effects of tourniquets on children,26 which demonstrated increasing levels of lactate with increasing tourniquet time and with bilateral application of tourniquets. Increasing body temperature has been noted in patients with tourniquets.27,27a This may not be completely explained by a decrease in the surface area available for heat exchange. A concomitant increase in metabolism25 may contribute to this increase in temperature. The question is how one determines tourniquet inflation pressure. Does it make a difference? There is no commonly agreed-on method of determining inflation pressure.28,29 Tredwell28 proposes an individualized method of determining inflation pressure based on the measured occlusion pressure. The benefit of Tredwell’s approach will have to be contrasted with Kokki’s study, in which no difference in metabolic markers of muscle injury was found between two different tourniquet pressures.30 When looking at patients during arthroscopic knee surgery, Hirota31 showed right atrial emboli after tourniquet release. The amount of emboli was directly related to the duration of tourniquet inflation. General Remarks More patients with complex medical conditions, including congenital heart disease and debilitating pulmonary pathology, are seeking care from the sports medicine physician. These patients, similar to the high-performance individual, present unique situations and demands from the medical team. With general goals in mind, and with the collaboration of the individuals involved, a plan of medical care can be tailored to satisfy the unique needs of these patients. One size does not fit all. One size fits none (Figure 15–1). References 1. Kain ZN, Mayes LC, Bell C, et al: Premedication in the United States: a status report. Anest Analg 84:427–432, 1997. 2. Brosius KK, Bannister CF: Midazolam premedication in children: a comparison of two oral dosage formulations on sedation score and plasma midazolam levels. Anesth Analg 96:392–395, 2003.

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3. Jankowski CJ, Hebl JR, Stuart MJ, et al: A comparison of psoas compartment block and spinal and general anesthesia for outpatient knee arthroscopy. Anesth Analg 97:1003–1009, 2003. 3a. Dashfield AK, Birt DJ, Thurlow J, et al: Recovery characteristics using single-breath 8% seroflurane or propofol for induction of anaesthesia in day-case arthroscopy patients. Anaesthesia 53:1062–1066, 1998. 4. Kokki H, Heikkinen M, Turunen M, et al: Needle design does not affect the success rate of spinal anaesthesia or the incidence of postpuncture complications in children. Acta Anaesthesiol Scand 44(20): 210–213, 2000. 5. Bourlon-Figuet S, Dubousset A, Benhamou D, et al: Transient neurologic symptoms after epidural analgesia in a five-year-old child. Anesth Analg 91:856–857, 2000. 6. Kokki H, Hendolin H, Turunen M: Postdural puncture headache and transient neurologic symptoms in children after spinal anesthesia using cutting and pencil point paedriatric spinal needles. Acta Anaesthesiol Scand 42:1076–1082, 1998. 7. Pollock JE, Liu SS, Neal JM, et al: Dilution of spinal lidocaine does not alter the incidence of transient neurologic symptoms. Anesthesiology 90:445–450, 1999. 8. Bergeron L, Girard M, Drolet P, et al: Spinal procaine with and without epinephrine and its relation to transient radicular irritation. Can J Anaesth 46:846–849, 1999. 9. Sia S, Pullano C: Transient radicular irritation after spinal anaesthesia with 2% isobaric mepivacaine. Br J Anaesth 81:622–624, 1998. 10. Tarkkila P, Huhtala J, Tuominen M, et al: Transient radicular irritation after bupivacaine spinal anesthesia. Reg Anesth 21:26–29, 1996. 11. Ganapathy S, Sandhu H, Stockall C, et al: Transient neurologic symptoms (TNS) following intrathecal ropivacaine. Anesthesiology 93:1537–1539, 2000. 12. Lewis WR, Perrino AC: Transient neurological symptoms after subarachnoid meperidine. Anesth Analg 94:213–214, 2001. 13. Mulroy MF, Larkin KL, Hodgson PS, et al: A comparison of spinal, epidural, and general anesthesia for outpatient knee arthroscopy. Anesth Analg 91:860–864, 2000. 14. Liguori GA, Chimento GF, Borow L, et al: Possible bupivacaine toxicity after intraarticular injection for postarthroscopic analgesia of the knee: implication of the surgical procedure. Anesth Analg 94:1010–1013, 2002. 15. Said R, Varkel V, Grimberg B, et al: Intra-articular fentanyl (betatryl) and morphine for pain relief following arthroscopic knee surgery. J Bone Joint Surg Br 79-B(3S):343, 1997. 16. Cook TM, Nolan JP, Tuckey JP: Postarthroscopic meniscus repair analgesia with intraarticular ketorolac or morphine. Anesth Analg 84:466–467, 1997.

17. Wang JJ, Ho ST, Tang JJS, et al: Intra-articular triamcinolone, bupivacaine, triamcinolone/bupivacaine for pain control after knee arthroscopy. Acta Anaesthesiol Scand Sup 41(1):184, 1997. 18. Wrench IJ, Taylor P, Hobbs GJ: Lack of efficacy of intra-articular opioids for analgesia after day-case arthroscopy. Anaesthesia 51:920–922, 1996. 19. Elhakim M, Nafie M, Eid A, et al: Combination of intra-articular tenoxicam, lidocaine, and pethidine for outpatient knee arthroscopy. Acta Anaesthesiol Scand 43:803–808, 1999. 20. Kalso E, Tramer MR, Carroll D, et al: Pain relief from intra-articular morphine after knee surgery: a qualitative systematic review. Pain 71:127–134, 1997. 21. Gentili M, Juhel A, Bonnet F: Peripheral analgesic effect of intraarticular clonidine. Pain 64:593–596, 1996. 22. Buerkle H, Huge V, Wolfgart M, et al: Intra-articular clonidine analgesia after knee arthroscopy. Eur J Anaesthiol 17:295–299, 2000. 22a. Gupta A, Boldin L, Holstrom B, Berggren L: A systematic review of the peripheral analgesic effects of intraarticular morphine. Anesth Analg 93:761–770, 2001. 23. Reuben SS, Sklar J, El-Mansouri M: The preemptive analgesic effect of intraarticular bupivacaine and morphine after ambulatory arthroscopic knee surgery. Anesth Analg 92:923–926, 2001. 24. Joshi W, Reuben SS, Kilaru PR, et al: Postoperative analgesia for outpatient arthroscopic knee surgery with intraarticular clonidine and/or morphine. Anesth Analg 90:1102–1106, 2000. 25. Girardis M, Milesi S, Donato S, et al: The hemodynamic and metabolic effects of tourniquet application during knee surgery. Anesth Analg 91:727–731, 2000. 26. Lynn AM, Fischer T, Brandford HG, et al: Systemic responses to tourniquet release in children. Anesth Analg 65:865–872, 1986. 27. Bloch EC, Ginsberg B, Binner RA, et al: Limb tourniquets and central temperature in anesthetized children. Anesth Analg 74:486–489, 1992. 27a. Bloch EC: Hyperthermia resulting from tourniquet application in children. Annals R Coll Surg Engl 68:193–194, 1986. 28. Tredwell SJ, Wilmink M, Inkpen K, et al: Pediatric tourniquets: analysis of cuff and limb interface, current practice, and guidelines for use. J Pediatr Orthop 21:671–676, 2001. 29. Lieberman JR, Staheli LT, Dales MC: Tourniquet pressures on pediatric patients: a clinical study. Orthopedics 20:1143–1147, 1997. 30. Kokki H, Vaatainen U, Penttila I: Metabolic effects of a low-pressure tourniquet system compared with a high-pressure tourniquet system in arthroscopic anterior crucial ligament reconstruction. Acta Anaesthesiol Scand 42:418–424, 1998. 31. Hirota K, Horishi H, Kabara S, et al: The relationship between pneumatic tourniquet time and the amount of pulmonary emboli in patients undergoing knee arthroscopic surgeries. Anesth Analg 93:776–780, 2001.

Chapter 16

Patellofemoral Dysfunction Paolo Aglietti

The patella develops as a sesamoid bone within the quadriceps tendon unit. Ossification begins by approximately 2–3 years of age. Dynamic compressive forces act to modulate patellofemoral modeling and lead to a deepening of the trochlear groove and contouring of the femoral condyles. Alterations in these normal developmental forces lead to a spectrum of anatomical variation, ranging from normality to severe patellofemoral dysplasia.

●

Antonio Ciardullo

●

Pierluigi Cuomo

and of the superolateral corner are sometimes observed. An accurate radiographic examination, including axial views, may reveal the sharply irregular margins of the fragment and allow the diagnosis of recent fracture and the consequent treatment. Classification

Congenital Abnormalities Complete absence of the patella (patellar aplasia), a small patella (patellar hypoplasia), or a large patella (patella magna) have been reported in small series1,2 but are rarely encountered in clinical practice. Patellar duplication has also been reported in a few cases, usually in association with multiple epiphyseal dysplasia. The duplication may be present in the frontal plane (one patella anterior to the other), in the horizontal plane (one superior and one inferior), or in the sagittal plane (one medial and one lateral).3 The most frequent form of patellar dysplasia is patella bipartita. It usually involves the superolateral corner of the patella (bipartite patella), but it may be present at the lateral margin, at the apex,4 or at the superomedial pole. More rarely the patella may be tripartita or multipartita. The pathogenesis is probably attributable to excessive traction from the surrounding soft tissues during the critical phase of the ossification. This hypothesis agrees well with the macroscopic and histological characteristics of the junction between the two fragments, KEY POINTS which resembles pseudoarthrosis, with fibrous or cartilaginous tis1. Patella bipartite is sue filling the gap. The bipartite the most common patella is most often discovered congenital accidentally during radiographic abnormality of the examination for other pathology patellofemoral joint. of the knee. Some problems 2. Recent fracture may arise in knees that have is a differential sustained a direct blow, since diagnosis. fractures of the lateral margin

Despite numerous classifications of patellofemoral disorders, the one proposed by Merchant5 seems to be most applicable, even if it does not include the aforementioned congenital abnormalities. On the contrary, Merchant’s classification system (Box 16–1) gives, more than other systems, much importance to a group of disorders with variable expression, which can be called patellofemoral malalignment or dysplasia. These include, to a variable degree, an increased Q-angle, high-riding patella, shallow femoral sulcus, lateralized tracking of the patella, hypoplasia of the vastus medialis obliquus (VMO), increased femoral anteversion, and compensatory external tibial rotation. The most profitable way of thinking of these disorders is as a developmental dysplasia with a continuum of anatomical deficiencies. The analogies with congenital dysplasia of the hip are evident. Which of the anatomical abnormalities are genetically determined and which are adaptive changes has been disputed. From the embryological point of view, the patella has medial and lateral facets that are initially equal in size. However, by the sixth month of gestation the dimensions of the lateral patellar facets exceed those of the medial as it is found in the adult.6 The definitive adult form of the trochlea is achieved very early in fetal life.6,7 According to these data, recurrent dislocation of the patella has been described as a hereditary disease with autosomal dominant transmission.8 On the other hand, it is well known that patellar dislocation may result after multiple injections in the vastus lateralis with quadriceps fibrosis.9–11 Therefore it seems that both genetically determined and acquired forms exist and manifest themselves with lateral tracking of the patella. 155

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Chapter 16

Merchant’s Classification of Patellofemoral

I. Trauma (conditions caused by trauma in the otherwise normal knee) A. Acute trauma 1. Contusion 2. Fracture a. Patella b. Femoral trochlea c. Proximal tibial epiphysis (tubercle) 3. Dislocation (rare in the normal knee) 4. Rupture a. Quadriceps tendon b. Patellar tendon B. Repetitive trauma (overuse syndromes) 1. Patellar tendonitis (“jumper’s knee”) 2. Quadriceps tendonitis 3. Peripatellar tendonitis (e.g., anterior knee pain of the adolescent caused by hamstring contracture) 4. Prepatellar bursitis (“housemaid’s knee”) 5. Apophysitis a. Osgood-Schlatter disease b. Sinding-Larsen-Johansson disease C. Late effects of trauma 1. Post-traumatic chondromalacia patellae 2. Post-traumatic patellofemoral arthritis 3. Anterior fat pad syndrome (post-traumatic fibrosis) 4. Reflex sympathetic dystrophy of the patella 5. Patellar osseous dystrophy11 6. Acquired patella infera 7. Acquired quadriceps fibrosis II. Patellofemoral dysplasia A. Lateral patellar compression syndrome 1. Secondary chondromalacia patellae 2. Secondary patellofemoral arthritis B. Chronic subluxation of the patella 1. Secondary chondromalacia patellae 2. Secondary patellofemoral arthritis C. Recurrent dislocation of the patella 1. Associated fractures a. Osteochondral (intraarticular) b. Avulsion (extraarticular) 2. Secondary chondromalacia patellae 3. Secondary patellofemoral arthritis D. Chronic dislocation of the patella 1. Congenital 2. Acquired III. Idiopathic chondromalacia patellae IV. Osteochondritis dissecans A. Patella B. Femoral trochlea V. Synovial plicae (anatomical variant made symptomatic by acute or repetitive trauma) A. Medial patellar (“shelf”) B. Suprapatellar C. Lateral patellar

In this chapter we will focus on patellofemoral dysplasia. Other conditions not exclusive to the growing patient are addressed in other chapters.

Symptoms Pain is characteristically dull, poorly localized, and increased by stair climbing, squatting, and prolonged sitting with the knee flexed. Swelling is often reported by patients, but effusion is not frequently found at examination. Effusion becomes more common in the presence of chondromalacic changes. However, chondromalacia is rare in the child or adolescent. Catching or momentary locking are sometimes reported by the patient. These may be caused by a momentary quadriceps inhibition secondary to pain or by some cartilage irregularity that locks the smooth gliding movement of the patella during extension. Physical Examination With the patient standing, squinting of the patellae is often present. A mild varus knee may be present. The axes of the femur and tibia are parallel and connected by an oblique patellar tendon, which slopes downward and laterally (bayonet deformity). While the patient is walking, the presence of an associated pronation of the foot is checked. If pronation is present, it is corrected, and the effects on the alignment of the extensor apparatus (Q-angle) are noted. With the patient performing a half-squat and holding the position for a short time, pain is usually evoked. With the patient sitting, patella tracking is evaluated. The most frequent abnormality is a mild lateral displacement in full extension and early flexion, which reduces with further flexion. Crepitus of the patellofemoral joint is also noted during active extension against resistance and is classified as mild, moderate, or severe. Assessment of tightness of the lateral retinaculum is critical in the diagnosis of lateral patellar compression syndrome. With the patient’s knee extended, the examiner should be able to lift the lateral border of the patella until the transverse axis is tilted above the horizontal (passive patellar tilt test). With the patient’s knee at 20–30 degrees of flexion, it should be possible to push the patella medially more than a fourth of the patellar width. If these tests are positive, a tight lateral retinaculum is diagnosed. Radiographic Examination Routine anteroposterior, lateral, and axial views at 45 degrees of flexion are not very informative in knees with patellar pain and lateral patellar compression syndrome. More recently the introduction of computed tomographic (CT) scanning has offered the possibility of studying the patellofemoral joint in full extension and early flexion, (i.e., in the most informative part of the arc of motion, which cannot be explored with conventional axial views). Treatment

Patellofemoral Dysplasia Lateral Patellar Compression Syndrome The lateral patellar compression syndrome includes knees with patellar pain aggravated by flexion activities without episodes of true instability. In these knees the pathogenetic mechanism seems to involve increased lateralization forces on the patella, which remains stable in the sulcus.

An appropriate conservative treatment is based on the thorough appreciation of the mechanics of the patellofemoral joint and its disturbance, which leads to pain. Conservative treatment traditionally includes rest, quadriceps exercises, knee braces, and antiinflammatory drugs (Technical Note 16–1). A more refined rehabilitation program has been proposed by McConnell.12 It is based on a precise appreciation Text continued on p. 162

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TECHNICAL NOTE 16–1

Patellofemoral Physical Therapy Protocol Carl Gustafson

NOTE: The patellofemoral protocol should be progressed pain free. The objective is to try to minimize pain by limiting range of motion, resistance, and frequency. If any exercises cause pain, refrain from them until you talk with your physical therapist or athletic trainer (Table 16–1). Strengthening All exercises should progress to two sets of 15 repetitions. Then add resistance in the form of weights for straight leg raises, short arc lifts, long arc lifts, and leg presses. Add height in terms of step-ups.

Straight Leg Raise, Long Arc Lifts, and Adductor Lifts: (Figure 16–1, A to C) • Start with resistance of limb. • When adding weight (once you reach two sets of 15), add no greater than 3 lb per week. • Progress to as great as 10 lbs if pain free (discuss with physical therapist/athletic trainer progression to machines). • Frequency: do exercises with up to 5 lb daily (if recovered in terms of no pain or joint/muscle soreness from last workout) and 6–10 lb three times per week.

Table 16–1 Exercises for Disorders Involving the Patella Associated Diagnoses

Resistance Exercises

Lateral tracking patella

Straight leg Rectus raise

Patellofem- Adduction oral syndrome Subluxing Long arc patella quad Step-up Leg press

Stretches

Possible Contraindications Patella subluxes out of groove in terminal extension

Quad Hamstring Iliotibial band Adductor

Figure 16–1 A, Demonstration of straight leg raise.

Continued

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TECHNICAL NOTE 16–1

Patellofemoral Physical Therapy Protocol (Continued)

Figure 16–1—cont’d

B, Long arc lifts. C, Adductor lifts.

Leg Press: (Figure 16–2) • Add weight as tolerated (two sets of 15 reps; see Figure 16–2). • Do exercise one leg at a time unless it is bilateral condition. • Progress exercises to every other day until you do not recover in between workouts, then go to three times per week. Step-ups: (Figure 16–3) • Progress up to 8-inch step on a daily basis. Once you get to 8-inch step, step farther back in lunge fashion. Do only three times a week.

Stretching: (Figure 16–4) • Hold all stretches 30 seconds for three repetitions, five times per week. • Stretch daily until pain subsides, then stretch three times per week. • Quadriceps (Figure 16–4, A) • Rectus (Figure 16–4, B) • Iliotibal band (Figure 16–4, C) • Hamstring (Figure 16–4, D) • Adductors (Figure 16–4, E) • Calf (Figure 16–4, F) Continued

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TECHNICAL NOTE 16–1

Patellofemoral Physical Therapy Protocol (Continued)

Figure 16–2 Demonstration of a leg press.

Figure 16–3 Demonstration of step-ups.

Walking/Running Program Objective 1: Begin walking program three times per week and build up to 45 minutes pain free. Objective 2: Once you can tolerate walking and have 70% of strength in the unaffected limb, begin running 15–20 minutes, three times per week.

Objective 3: Once you can tolerate jogging and have 90% strength, perform agility exercises pain free, as outlined by physical therapist or athletic trainer. Then return to sports with a doctor’s recommendation.

Continued

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TECHNICAL NOTE 16–1

Patellofemoral Physical Therapy Protocol (Continued)

Figure 16–4 Stretching of quadriceps (A), rectus (B), and iliotibal band (C).

Continued

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TECHNICAL NOTE 16–1

Patellofemoral Physical Therapy Protocol (Continued)

Figure 16–4—cont’d

Stretching of hamstring (D), adductors (E), and calf (F).

Continued

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TECHNICAL NOTE 16–1

Patellofemoral Physical Therapy Protocol (Continued) Suggested Readings 1. Faigenbaum AD, Westcott WL, Loud RL, Long C: The effects of different resistance training protocols on muscular strength and endurance development in children. Pediatrics 104:1–7, 1999 2. Feigenbaum MS, Pollack ML: Strength training: rationale for current guidelines for adult fitness programs. Phys Sports Med 25(2):44–66, 1997. 3. Feigenbaum MS, Pollack ML: Prescription or resistance training for health and disease. Med Sci Sports Exerc 31(1):38–45, 1999.

of the alterations of the lower limb in the individual patient. First, muscle tightness, including the rectus femoris, iliotibial band, hamstrings, and gastrocnemius, should be identified and corrected. The patient is first taught to stretch them. This is particularly true of the tight lateral structures at the knee. Taping of the patella is used to reduce pain during the exercises and therefore enhance VMO activity. Most patients have a lateral displacement (subluxation) of the patella. This can be corrected by firm taping from the lateral aspect of the patella medially. If a tilt of the patella is also present, this can be decreased by adding a second tape from the midline of the patella medially, to lower the medial aspect of the patella and lift up the lateral border. The role of the VMO is recognized as crucial to centralizing the patella after adequate stretching of the lateral structures has been achieved. Training of the quadriceps muscle with external rotation of the femur is preferable. Most of the fibers of the VMO originate from the tendon of the adductors magnus. Therefore contraction of the adductors while performing knee extension facilitates VMO activity. Pain during exercise should be avoided because it has an inhibitory effect on muscle contraction and will result in muscle atrophy. Surgical Treatment: Lateral Retinacular Release Surgical treatment may be undertaken in those knees with persisting disabling symptoms that fail to improve after a prolonged (at least 6 months) supervised physical therapy course. In knees with pain caused by lateral patellar compression syndrome, a lateral retinacular release has been frequently performed. The sine qua non to perform a lateral retinacular release is the demonstration of a tight lateral retinaculum. The ideal candidate should show a decreased medial glide (one fourth the patellar width or less) and a decreased passive patellar tilt (the transverse axis of the patella cannot be elevated beyond the horizontal). The axial views of CT scans should show a patellar tilt with absent or mild subluxation. Lateral retinacular release can be performed with open (Figure 16–5) or arthroscopic (Figure 16–6) techniques, but the structures to be sectioned are obviously the same. They include the lateral retinaculum in its portion lateral to the

4. Lichota DK: Anterior knee pain: symptom or syndrome? Curr Womens Health Rep 3(1):81–86, 2003. 5. Metcalf JA, Roberts SO: Strength training and the immature athlete: an overview. Pediatr Nurs 19(4):325–332, 1993. 6. Thomee R, Augustsson J, Karlsson J: Patellofemoral pain syndrome: a review of current issues. Sports Med 28(4):245–262, 1999. 7. Woo SL: Injury and Repair of the Musculoskeletal Soft Tissues. American Academy of Orthopaedics, 1998.

patella and to the patellar tendon. If the surgeon feels that additional lateral release is required after sectioning the lateral retinaculum, the release should be extended in a distal direction, down to the tibial tubercle, to include the patellotibial and patellomeniscal ligaments. At the end of the procedure it should be possible to lift up the lateral border and transverse axis of the patella at least 70 degrees from the horizontal axis, and the patella should be free to glide medially over two quadrants with the knee at 30 degrees of flexion (Technical Note 16–2). Postoperative Rehabilitation The importance of starting quadriceps rehabilitation as soon as possible has been widely stressed; the success of the operation depends on the achievement of good quadriceps strength. Straight leg-raising exercises can be started as soon as the patient recovers from anesthesia. Flexion of the knee is also initiated early, and the patient is expected to reach 90 degrees of flexion by the end of the first week. Early recovery of flexion has an important role in preventing formation of scar tissue across the release, because the release opens widely in flexion. Manipulation of the patella with medial glides and lift-up of the lateral border also have a role in preventing scar formation. Patients should be made KEY POINTS aware of the necessity of a home exercise program that should be 1. Pain is the major continued indefinitely. Recurcharacteristic of rence of pain is often associated lateral patellar with low compliance with rehacompression bilitation exercises and insuffisyndrome. cient quadriceps tone. Also, it 2. A tight lateral should be pointed out that some retinaculum is exercises, including the extencommonly found. sion exercise with weights on 3. Conservative the ankle; deep knee bends; and treatment must be activities involving squatting attempted in any and jumping, overload the case. patellofemoral joint and are 4. Lateral release likely to cause relapses of sympshould be considered toms. They should be limited or if conservative avoided altogether. Finally, it treatment fails. should be remembered that,

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Figure 16–5 Lateral retinacular release can be performed with open techniques.

Figure 16–6 Lateral retinacular release can also be performed with arthroscopic techniques.

TECHNICAL NOTE 16–2

Pediatric Lateral Retinacular Release with Medial Plication Under Arthroscopic Control Jennifer L. Cook • Lyle J. Micheli

Indications Our indications for lateral release include anterior knee pain and signs and symptoms consistent with patella lateral subluxation in both male and female young athletes. These patients typically complain of a dislocating patella and have lateral patellar translation on examination. In addition, we typically perform medial plication if there is evidence of patellar tilt, either by a positive patellar tilt test or radiographic data demonstrating patellar tilt on an axial view. Setup In these patients, general anesthesia is used. A nonsterile tourniquet is applied high on the upper thigh. The patient is positioned supine. Preoperative antibiotics are administered before inflation of the tourniquet. Technique Examination Under Anesthesia: Examination usually reveals patellar subluxation and a positive patellar tilt test.

Arthroscopy: The leg is routinely prepped and draped. An Esmarch bandage is used for exsanguination. Arthroscopy is performed with a standard anterolateral viewing portal. Diagnostic arthroscopy is performed to assess patellar tracking, confirm patellar tilt in the trochlear groove, and assess for any evidence of chondral injuries associated with the extensor mechanism disorder. If there is indeed a subluxating patella, a lateral release is performed. The arthroscopic instruments are removed. A pair of curved Mayo scissors is used to identify a subcutaneous plane through the lateral arthroscopic portal proximally to the margin of the musculotendinous junction (Figure 16–7). Next, the scissors are placed through the same lateral arthroscopic portal with one limb in the subcutaneous plane just created and one limb under the lateral retinaculum. The scissors are advanced proximally until all of the lateral retinaculum has been released. This is usually approximately 5 cm. The scissors are withdrawn and the arthroscopic scope is reinserted. The cut retinaculum is viewed with the scope to ensure adequate extent of the release. The patella is then viewed to assess the mechanical effect of the release. A supramedial portal (Figure 16–8) is Continued

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TECHNICAL NOTE 16–2

Pediatric Lateral Retinacular Release with Medial Plication Under Arthroscopic Control (Continued)

Figure 16–7 Identifying a subcutaneous plane through the lateral arthroscopic portal proximally to the margin of the musculotendinous junction.

Figure 16–8 A supramedial portal is made with a puncture through the medial retinaculum.

then made with a puncture through the medial retinaculum. The ORATEC electrothermal monopolar system probe is bent 30 degrees (Figure 16–9) and then inserted through the supramedial portal. All lateral retinacular vessels are subsequently coagulated with this instrument (Figure 16–10). Hand instruments may be inserted through this portal to complete any further lateral retinacular release as needed. If there is evidence of residual patellar tilt, attention is then drawn to the medial side. The ORATEC is then used to tighten the medial retinaculum. The standard setting of

67˚C temperature and 40 watts of power is used. The electrothermal probe is drawn along the medial retinaculum in a linear fashion beginning anteriorly and extending from the superior to the inferior margin of the retinaculum. This is carried out back to the posterior margin of the patella but is not extended above the superior pole of the patella to avoid potential injury to medial retinacular vessels. The knee is irrigated and all fluid is removed. Each portal site is closed with a single, simple 3-0 nylon stitch, and 1ml/kg of a patient’s body weight of 0.25% bupivacaine with epinephrine is injected Continued

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TECHNICAL NOTE 16–2

Pediatric Lateral Retinacular Release with Medial Plication Under Arthroscopic Control (Continued)

Figure 16–9 A probe is bent 30 degrees and then inserted through the supramedial portal.

Figure 16–10 Lateral retinacular vessels are subsequently coagulated using a probe.

into the knee. A soft dressing is applied, and the tourniquet is released. Postoperative Management Postoperatively, the patients are placed into a lateral release brace. They are made partially weight-bearing for 5–7 days, and immediate straight leg-raising and quadriceps-setting exercises are begun, as well as gentle foot sliding range of motion to the knee. Patients return to the clinic in 10–14 days for suture removal and are then begun on a more

formal physical therapy program to work on range of motion and strengthening of the knee. They continue to wear their brace full time for 6 weeks and modify their athletic activity accordingly. At that point the brace is removed, and patients are advanced into their activities. Results Although lateral patellar translation can be easily addressed with lateral retinacular release alone, resulting in increased centralization of the patella, Continued

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TECHNICAL NOTE 16–2

Pediatric Lateral Retinacular Release with Medial Plication Under Arthroscopic Control (Continued) a medial retinacular capsulorrhaphy specifically addresses patellar tilt. We have noted decreased swelling with this technique and no cases of significant hemarthrosis. Furthermore, patients seem to have a lower analgesic requirement. Suggested Readings 1. Ahmad CS, Lee FY: An all-arthroscopic soft-tissue balancing technique for lateral patellar instability. Arthroscopy 17(5):555–557, 2001.

although the procedure may seem minor, rehabilitation is usually prolonged; a 3-month period before a return to recreational activities can be expected for most patients. Several authors have attempted to identify the factors that correlated with an unsatisfactory result. Micheli and Stanitski13 found that females had a worse prognosis than males and that insufficient reduction of the patella on postoperative radiographs and severe chondromalacia were associated with inferior results. Krompinger and Fulkerson14 reported less satisfactory results when the Q-angle was more than 20 degrees. Patellar Instability Patella subluxation and patella dislocation can be grouped together as patellar instability. The difference is of degree and not of nature. Subluxation is an alteration of the normal tracking of the patella, but with the patella still within the femoral sulcus. Dislocation means that the patella has been completely displaced out of the sulcus. Furthermore, the patella may show a lateralized tracking without episodes of instability (chronic subluxation of the patella). In this category are included those knees with patellar pain, where the axial view or CT scan reveal a lateral displacement (subluxation) of the patella. These knees can be interpreted as an intermediate grade of dysplasia of the extensor mechanism between lateral patellar compression syndrome and recurrent dislocation of the patella: patients complain of pain (as those affected by lateral patellar compression syndrome), but the patella shows a lateralized tracking (as in knees affected by recurrent patellar dislocation). From the clinical point of view the following situations can be encountered and will be described: acute dislocation and recurrent, habitual, and permanent dislocation of the patella.

2. Fulkerson JP: Diagnosis and treatment of patients with patellofemoral pain. Am J Sports Med 30(3):447–456, 2002. 3. Halbrecht JL: Arthroscopic patella realignment: an allinside technique. Arthroscopy 17(9):940–945, 2001. 4. Lankenner PA Jr, Micheli LJ, Clancy R, Gerbino PG: Arthroscopic percutaneous lateral patellar retinacular release. Am J Sports Med 14(4):267–269, 1986. 5. Micheli LJ, Stanitski CL: Lateral patellar retinacular release. Am J Sports Med 9(5):330–336, 1981. 6. O’Neill DB: Open lateral retinacular lengthening compared with arthroscopic release. A prospective, randomized outcome study. J Bone Joint Surg Am 79(12):1759–1769, 1997.

The patient usually presents in the emergency department and reports that during a twisting movement of the knee he or she felt a snap, the knee gave way, and he or she fell down. Sometimes, the patient may have been able to observe the patella lying on the lateral side of the knee. At this time the knee is straightened and the patella relocates in the sulcus. The rapid development of swelling is observed. Therefore it is unusual to observe the patella still in the dislocated position in the emergency department. If the patient has observed the abnormal lateral displacement of the patella, the diagnosis is straightforward. Otherwise it can be difficult. The physician is faced with a swollen and tender knee and a nonspecific history of giving way. Aspiration of the joint demonstrates hemarthrosis, and fat droplets may be present if there was an associated osteochondral fracture. Careful inquiry about the mechanism of injury will often reveal that the patient had the foot fixed on the ground, while the femur was internally rotated relative to the tibia and the quadriceps was contacted, as in the act of changing direction while running. In this position the Q-angle is increased and contraction of the quadriceps pulls the patella laterally. More rarely, a direct blow on the medial side of the knee may cause patellar dislocation in a knee with underlying malalignment. Physical Examination

Acute Dislocation of the Patella

Tenderness is easily evoked by palpation of the medial retinaculum and medial femoral epicondyle. Attempts to displace the patella laterally will be prevented by apprehension. Testing for ligamentous stability is rendered more difficult by muscle contracture, but with some patience one should be able to confirm the presence of an intact anterior cruciate ligament with a Lachman’s test. The differential diagnosis includes an anterior cruciate ligament injury and a rupture of the quadriceps or patellar tendon. The latter diagnosis can be excluded by asking the patient to do a straight leg raise.

Symptoms

Pathoanatomy and Imaging

The diagnosis of acute dislocation of the patella is applied to those knees seen after the first episode of dislocation.

Routine anteroposterior, lateral, and axial views should be obtained in every patient with a suspected diagnosis of acute

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patellar dislocation. A lateral displacement of the patella within the femoral sulcus may be evident, even if less frequently than in knees with recurrent patellar dislocation. Oblique and notch views may be necessary to exclude the presence of osteochondral fractures of the medial patellar facet or lateral femoral condyle.15,16 These are usually produced during the relocation of the dislocated patella, when the medial patellar facet strikes against the lateral femoral condyle. The conflict is increased by quadriceps contraction. The frequency of associated osteochondral fractures in knees with acute patellar dislocation has been reported to be approximately 5% (Figure 16–11).17 Failure to demonstrate osteochondral fragments on radiography does not imply that there is not any damage to the articular surface. In fact, arthroscopic examination of the knee with acute patellar dislocation has often revealed extensive cartilage injury of the patella and/or of the lateral femoral condyle. More rarely, a larger portion of the patella may be fractured during an acute dislocation. In these cases, consideration should be given to fixing the fragment rather than to excising it. Magnetic resonance imaging (MRI) can be useful to help determine both the diagnosis and the extent of injury, and a distinct pattern of some bruising is seen with patellar dislocation. NOTE: In children with open physes, the articular cartilage is also structurally a physis, with shearing injury occurring though the zone of provisional calcification. These fragments can be replaced and either sewn in place or fixed with bioabsorbable pins. This has been quite successful in our experiences. Treatment Our preferred treatment of acute patella dislocation is conservative. We recognize that the nonoperative treatment is doomed to failure with recurrence of the dislocation in probably a third of the cases, but surgery will not produce normal knees in 100% of the cases, and operative or postoperative complications may occur. Based on these observations, our preferred treatment for the first acute dislocation remains immobilization for approximately 4 weeks in an “off the shelf ” immobilizer. Quadriceps strengthening is started

Figure 16–11 The frequency of associated osteochondral fractures in knees with acute patellar dislocation has been reported to be approximately 5%.

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soon with straight leg raises, and partial weight-bearing is allowed as tolerated. By 1 month, KEY POINTS most patients will have sufficient quadriceps strength and decreased 1. Acute patellar tenderness, so that immobilization dislocation must can be discontinued. Quadriceps always be suspected strengthening is advised for in traumatic knee prolonged periods. joint effusions. There are exceptions to the 2. Accurate imaging is conservative treatment, and the mandatory to exclude most frequent is the presence of the presence of an osteochondral fragment visiosteochondral ble on the radiograph. A large fractures. fragment with underlying bone 3. In isolated acute of sufficient thickness should be patellar dislocations, fixed, but this is infrequent. conservative More often the bone is thin and treatment must does not allow a firm fixation. In be attempted. these cases arthroscopic removal is preferable. Recurrent Dislocation of the Patella Symptoms Patients who suffer from recurrent dislocation of the patella have recurrent episodes of patellar instability. The history is usually self-explanatory and sufficient to make the diagnosis. The patient is more often in the second decade of life. Several authors have reported a female predominance, but Hughston pointed out that young, athletic males are also frequently affected. The patient reports an initial episode of patellar dislocation, which was treated conservatively. After the initial episode the patient suffers one or more similar episodes of instability as a result of trivial injuries. Their severity may vary from lesser forms (with just a feeling of insecurity), to true dislocations with the patella noted on the outer aspect of the knee. Patients may learn how to avoid the dislocation; the decreased activity level beyond the twenties may also contribute to this favorable outcome. Physical Examination The presence of angular deformities (genu varum or valgum), as well as squinting of the patellae, is noted. A variety of abnormal trackings have been described. It is our experience that the most frequent finding is lateral subluxation in extension. The patella is centered in the sulcus with the knee flexed at 90 degrees but displaces laterally when it exits the sulcus. Subluxation is usually accompanied by a lateral tilt of the patella. An abnormally increased Q-angle (and a lateral placement of the tibial tuberosity) can be better appreciated with the knee at 90 degrees of flexion, because the patella relocates in the sulcus.18 Atrophy of the quadriceps and hypoplasia of the VMO can be best evaluated by asking the patient to contract the quadriceps. The bulk of the vastus medialis obliquus and its insertion on the patella should be noted.19 With the knee in extension, the mobility of the patella can be grossly estimated. This is better performed by engaging the patella in the femoral sulcus with the knee flexed

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30 degrees. The patella is alternatively pushed medially and laterally with the quadriceps relaxed. The magnitude of the displacement is measured in quadrants. A lateral displacement over two quadrants (half-width of the patella) indicates laxity of the medial structures. A medial displacement of the patella of one quadrant or less indicates tightness of the lateral structures.18 This can also be assessed by lifting up the lateral border of the patella with the knee in extension. If the transverse axis of the patella cannot be lifted over the horizontal axis, tightness of the lateral structures is again demonstrated (passive patellar tilt). Finally, the most informative test is performed—the apprehension test described by Fairbank.20 With the knee at 20–30 degrees of flexion, the patella is pushed laterally. The patient feels that the patella is going to dislocate and avoids this situation by contracting the quadriceps and displacing the hands of the examiner. The test should be performed gently. Imaging Bone abnormalities in recurrent dislocation of the patella can be studied by using traditional radiographic and CT imaging techniques. They include a high vertical position of the patella, a patella with prevalence of the lateral facet, a flat femoral sulcus, lateral subluxation and tilt of the patella, lateral placement of the tibial tuberosity, and increased femoral anteversion. Traditional axial views at 30, 45,21 or 20 degrees22 of flexion are usually sufficient to show definite abnormalities of the sulcus and patella position in knees with recurrent patella dislocation, caused by the entity of the underlying anatomical dysplasia. Nevertheless, knees with less evident malalignment of the extensor apparatus are better investigated with CT imaging or MRI, which allows visualization of the patellofemoral joint in the range from full extension to 20 degrees of flexion and avoids overlapping of bony contours. Treatment Conservative treatment should be attempted in knees with recurrent patellar instability. It is based on strengthening of quadriceps and VMO and stretching of the tight lateral structures, as previously described. The frequency of the episodes of instability may be reduced so that surgery is no longer necessary. If disabling symptoms persist, surgical treatment is indicated.

We have recently reviewed 21 knees25 with an average follow-up of 66 months (range: 22–101). Most patients (90%) had no pain or swelling at follow-up, but 1 knee (5%) had instability during sports activities and 6 knees (30%) had instability during daily living activities. Therefore only 65% of the results could be considered satisfactory. Insall’s Proximal Realignment The proximal realignment is, in fact, a rearrangement of the muscular attachments to the patella, and its purpose is to alter the line of pull of the quadriceps muscle. It is a major procedure and is indicated only after a protracted period of conservative management.26,27 Both the vastus medialis and vastus lateralis must be exposed, as well as the proximal extent of the quadriceps tendon and the insertion of the fibers from the rectus femoris. The arthrotomy is performed by an incision beginning proximally at the apex of the quadriceps tendon and placed within the tendon close to the border of the vastus medialis. The incision is continued distally to the patella and extended across the medial border of this bone, and then distally medial to the patellar ligament. A second capsular incision is made on the lateral side. The quadriceps must then be reconstructed in such a manner that the subsequent line of pull will be in a more medial direction (Figure 16–12). This is the purpose of the operative procedure and, by altering the direction of quadriceps action, patellar congruence is restored and patellar instability prevented. The first suture is placed in such a manner that the most distal part of the vastus medialis is brought laterally and distally, overlapping the upper pole of the patella and adjoining the quadriceps tendon. The amount of overlap that should be achieved depends on the preoperative laxity of the tissues. In some knees the vastus medialis will be sutured as far across as the lateral border of the patella, but the more usual amount of overlap is 10–15 mm. We reported the results of proximal realignment in 11 knees affected by recurrent patella dislocation, reviewed with a long average follow-up of 102 months. Only one case was considered unsatisfactory because of poor quadriceps rehabilitation. There were no recurrences of dislocation.

Surgical Treatment: Lateral Retinacular Release The reported percentage of satisfactory results varies from 30–100%. However, the rating systems were not uniformly stringent. We believe that any patient with persistent symptoms of instability cannot be included among satisfactory results. Dandy and Griffiths23 reported on 41 knees that underwent lateral release for recurrent dislocation. With an average follow-up of 4 years, 90% of the knees were classified as satisfactory, using the rating system of Crosby and Insall.24 However, only 44% of the patellae were stable, 24% percent were occasionally insecure, and 32% percent had had at least one redislocation. Our experience with lateral retinacular release in recurrent dislocation of the patella was not completely satisfactory.

Figure 16–12 During proximal realignment the quadriceps must be reconstructed in such a manner that the subsequent line of pull will be in a more medial direction.

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Eight of these patients (73%) were interested in sports preoperatively, and all returned to their desired sports, including soccer (2), running (3), and aerobics (3). Analysis of the Merchant axial views revealed that preoperatively the average congruence angle was 16 degrees with 80% of the knees considered abnormal. At follow-up, only one knee was still abnormal (9%), and the average congruence angle was reduced to –8 degrees. There were no signs of development of degenerative arthritis during the long period of follow-up. Arthroscopic-Assisted Procedures Arthroscopic-assisted procedures have been described in the literature.28–30 Basically they include a lateral retinacular release and plication of the medial capsule. Plication is obtained percutaneously or through short skin incisions using spinal needles, straight or curved. They are used to deliver sutures into the joint, which are then extracted and tied over the capsule. These procedures are, in fact, proximal realignments where a simple plication of the medial capsule is performed, without advancement of the VMO. This allows shortening of the medial patellofemoral ligament, which is the primary restraint to lateral displacement of the patella.31 Extension of the plication in a distal direction to the tibial tuberosity (through a short incision) may give additional support by shortening the patellomeniscal and patellotibial ligaments. Distal and Combined Realignments All the procedures in which the tibial attachment of the patellar ligament or the tibial tubercle are detached and

transferred in a medial and possibly distal direction, reducing the Q-angle and correcting the height of the patella, are classified as distal or combined realignments. Most of the techniques in use today stem from those originally described by Hauser,32 Goldthwait,33,34 and Roux.35 The procedure known as Goldthwait-Roux is an entirely soft-tissue procedure and involves a lateral release, medial plication, and longitudinal splitting of the patellar tendon with transfer of the lateral half medially.36 The Galeazzi tenodesis procedure uses the semitendinosis tendon left attached distally as a medial tether to the patella, and can be useful in the patient with an open tibial tubercle apophysis in whom tubercle osteotomy is contraindicated (Technical Note 16–3). The Hauser procedure32 consists of lateral retinacular release and transfer of the tibial tubercle medially and distally with or without medial plication. Two techniques have been widely used: the Elmsie-Trillat technique in Europe37 and the Hughston technique38 in North America. The Elmsie-Trillat operation37,39 is usually performed through a lateral parapatellar skin incision. A 4- to 6-cm fragment of bone is osteotomized, taking care to preserve the distal pedicle. The tuberosity is then displaced medially, rotating around the distal pedicle and fixed in the desired position with a screw. The Fulkerson variation emphasizes anteriorization in addition to medialization of the tibial tubercle by an oblique osteotomy (Technical Note 16–4). The Hughston operation38 involves a lateral curvilinear skin incision, which results in better cosmesis and less interruption of blood and nerve supply. A thin osteotome is inserted into the retropatellar bursa to lift the patellar tendon with a thin wafer of bone. The insertion of the patellar tendon is displaced medially and distally, as required, and fixed in place with a Stone staple. Then the VMO is Text continued on p. 176

TECHNICAL NOTE 16–3

Semitendinosus Tenodesis to the Patella for Recurrent Lateral Subluxation of the Patella Luke H. Balsamo • Peter G. Gerbino

Indications Up to 60% of acute patella dislocations become a recurrent problem. Multiple treatment options are described in the literature for this condition. These range from conservative treatment with bracing and physical therapy to early operative intervention. Many etiologies have been proposed to explain recurrent patella dislocations in children. These have included patella alta, generalized ligamentous laxity, lateral femoral condyle or patella hypoplasia, and tight lateral structures.1 Distal realignment procedures of the patellofemoral joint include soft tissue procedures and bony realignment. In the skeletally mature patient, anteriomedialization of the tibial tubercle

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has been shown to be successful.2 Soft tissue procedures are preferred in the adolescent with open physes, avoiding such complications as premature closure of the proximal tibial epiphysis with resulting recurvatum deformity, distal migration of the tibial tubercle, and traction spur formation.1 A soft tissue technique using the semitendinosus tendon as a medial checkrein as described by Galeazzi is frequently successful.1 Setup The patient is placed supine on a standard table. A nonsterile tourniquet is placed high on the thigh. A standard surgical prep is done. Continued

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Semitendinosus Tenodesis to the Patella for Recurrent Lateral Subluxation of the Patella (Continued) Technique The operative technique has changed little since 1921.3 (NOTE: We now routinely perform the Galeazzi procedure arthroscopically. We first harvest the semitendinosus graft as described, then begin an arthroscopy of the knee with a tourniquet through an anterolateral portal. The associated lateral release, if needed, can be performed under arthroscopic control, and the medial portal can be placed at the inferomedial margin of the patella to additionally serve as the inferomedial drill hole site. Only one additional portal, for the superolateral drill exit site, is then needed.) The major variation has been the use of a modern technique to harvest the semitendinosus tendon. In this technique, an incision is made over the pes anserine. Dissection is

carried down to the pes. The semitendinosus tendon is isolated as the most posterior and round of the three structures that compose the pes. During tendon isolation, the connections between the semitendinosus and the medial gastrocnemius and gracilis must be released to minimize the risk of false harvest.4 A tendon stripper is used to harvest the semitendinosus tendon and deliver it through the incision. It is important to preserve the distal attachments of the tendon to the pes anserine and tibia. An oblique hole is drilled through the patella inferomedially to superolaterally parallel to the joint surface. A small superolateral skin incision can be made to facilitate the drilling and tendon passing (Figure 16–13). The tendon is then

Figure 16–13 A hole the size of the semitendinosus tendon is drilled obliquely through the patella. Orientation is inferomedially to superolaterally and through the thickest part of the patella parallel to the joint surface.

Continued

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TECHNICAL NOTE 16–3

Semitendinosus Tenodesis to the Patella for Recurrent Lateral Subluxation of the Patella (Continued) passed through this hole. A whipstitch or use of mineral oil can be helpful at this point in aiding the tendon in its passage. After the graft is passed through the patella, the tendon is passed back through the superficial bursa. Tensioning the tendon, pull the patella medially and distally (Figure 16–14). The correct amount of tension prevents lateral subluxation without causing medial subluxation or excessive medial compression. The semitendinosus tendon is then sutured upon itself. This reinforces the medial patellotibial ligament

(MPTL), keeping the patella within the trochlea and preventing subluxation laterally. Results of recent studies have shown that the medial patellofemoral ligament (MPFL) is more instrumental than the MPTL for preventing lateral displacement of the patella.5 In a modification of the Galeazzi procedure, we pass the semitendinosus tendon through a hole inferomedially to superomedially and suture it to the medial femoral condyle. This recreates both the MPTL and the MPFL (Figure 16–15).

Figure 16–14 The semitendinosus is passed through the patella and then back across the patella through the subcutaneous bursa. After proper tensioning, the tendon is sutured to itself.

Continued

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Semitendinosus Tenodesis to the Patella for Recurrent Lateral Subluxation of the Patella (Continued)

Figure 16–15 The modified Galeazzi procedure uses a bony tunnel that both enters and exits the medial patella. This allows suture of the tendon end to the medial femoral condyle isometric point, reconstituting the MPFL, as well as the MPTL.

Typically, a lateral retinacular release is performed first. The Galeazzi procedure is performed next, ensuring that the knee has a full range of motion and the patella is not overconstrained. Preventing overconstraint and ensuring correct isometric placement on the medial femoral condyle is especially important for the modified Galeazzi procedure. The incisions are then closed in standard fashion.

Postoperative Management Some authors immobilize the knee in extension for 4–6 weeks. We prefer immediate continuous passive motion (CPM) from 0–45 degrees with protected weight-bearing for 6 weeks. A lateral release brace with a lateral bolster protects the repair. Quad sets and straight leg raises begin immediately, progressing to short-arc quads at 6 weeks and full Continued

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TECHNICAL NOTE 16–3

Semitendinosus Tenodesis to the Patella for Recurrent Lateral Subluxation of the Patella (Continued) active range of motion by 12 weeks. The patient can expect to return to full activity in 4–6 months. Results Since its initial description by Galeazzi in 1921, there have been several published reports of soft tissue realignment procedures. Most have had poor results.6 In the largest series of the Galeazzi procedure in the English-language literature, Baker reviewed 53 cases. There were good-to-excellent results in 81% of cases.1 Hall reviewed the cases of 26 knees. In his series, knees were either treated with a soft-tissue procedure alone or in combination with a Goldthwait-Roux procedure. Overall, they had 62% good-to-excellent results and 38% fair-to-poor results. The addition of the Goldthwait-Roux procedure did not affect the overall result. They concluded that the Galeazzi was a good procedure in skeletally immature patient.7 Letts had 82% good-to-excellent results in 22 children followed for more than 3 years.8 Longterm results of medial patellofemoral ligament reconstruction have not yet been published.

References 1. Baker RH, Carrol N, Dewar FG, Hall JE: The semitendinosus tenodesis for recurrent dislocations of the patella. J Bone Joint Surg Br 54(1):103–109, 1972. 2. Fulkerson J: Disorders of the Patellofemoral Joint. Baltimore: William and Wilkins, 1990. 3. Galeazzi R: Nuove Applicazioni del trapianto muscolare e tendineo (XII Congress societa Italiana di Ortopadia). Archivio di Ortopedia, 1922, p 38. 4. Brown CH, Sklar JH: Endoscopic anterior cruciate ligament reconstruction using quadrupled hamstring tendons and endobutton femoral fixation. Tech Orthop 13(3):281, 1998. 5. Schock EJ: Medial patellofemoral ligament reconstruction using a hamstring graft. Oper Tech Sports Med 9(3):169, 2001. 6. Bowker JH, Thompson Edgar B: Surgical treatment of recurrent dislocation of the patella. J Bone Joint Surg Am 46(7):1451–1461, 1964. 7. Hall JE, Micheli LJ, McManama GB Jr: Semitendinosus tenodesis for recurrent subluxation or dislocation of the patella. Clin Orthop (144):1–5, 1979. 8. Letts R, Davidson D, Beaule P: Semitendinosus tenodesis for repair of recurrent dislocation of the patella in children. J Pediatr Orthop 19(6):742–747, 1999.

TECHNICAL NOTE 16–4

Anteromedial Tibial Tuberosity Transfer for Patellofemoral Malalignment Luke H. Balsamo • Peter G. Gerbino

Indications Much patellofemoral pain can be related to patella maltracking or lateral subluxation. To correct maltracking, proximal and distal realignment procedures are required when nonoperative treatment fails. Proximal soft-tissue procedures include lateral retinaculum release with or without medial reefing. Recent interest has also focused on medial patellofemoral ligament reconstruction. Distally, bony procedures are used except in the skeletally immature. Maquet described tibial tubercle anteriorization to decrease joint reactive forces.1 Elmsie and Trillat medialized the tubercle to realign patella tracking. Fulkerson modified the Elmsie-Trillat procedure to achieve anteromedialization.2,3 This procedure uses an oblique osteotomy to transfer the tibial tubercle both

anteriorly and medially without the use of a bone graft. The procedure is indicated when abnormal contact pressures along the distal and/or lateral patella facet, as well as malalignment, are responsible for the anterior knee pain.4 Before surgery is considered, extensive physical therapy must be tried. Nonoperative treatment will be effective in most patients. Therapeutic modalities include quadriceps strengthening; quad, hamstring, and iliotibial band stretches; proprioceptive training; hip external rotator strengthening; patella taping; and orthotic devices.5 Preoperative workup should include a comprehensive history and physical. Axial radiographs can be obtained at 30 and 45 degrees of knee flexion to evaluate patellar tilt. Computed tomography for evaluation of patellofemoral alignment is more Continued

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Anteromedial Tibial Tuberosity Transfer for Patellofemoral Malalignment (Continued) accurate than plain films. Cuts are obtained at 0, 15, 30, and 45 degrees of knee flexion.2 Setup The patient is instructed to lie supine on a standard table. A nonsterile tourniquet is placed high on the thigh. A bump may be placed under the ipsilateral hip to internally rotate the lower extremity. A standard surgical prep is performed. Technique Make an incision from the mid-lateral patella to a point approximately 5 cm distal to the tibial tuberosity. Release the lateral retinaculum and invert the patella for inspection. Chondral lesions less then 1 cm in diameter are abraded to

subchondral bone. Microfracture can be performed. Resect loose flaps of articular cartilage.4 Release the proximal part of the anterior compartment sharply. Be mindful of the anterior tibial artery and peroneal nerve at this level. Continue a subperiosteal dissection until the junction of the lateral and posterior cortices are reached. Next, identify the patellar tendon distal insertion. The subperiosteal dissection should be carried out to a point approximately 7 cm distal to this insertion, leaving the insertion intact. Use a 3.2-mm drill bit and guide to drill a series of holes parallel to each other. These holes must be drilled in an anteromedial to posterolateral direction. The drill bits should exit the tibia just anterior to the posterolateral corner of the tibia. Bring the drill bits closer to the cortex as you progress distal on the tibia. This will form a tapered cut (Figure 16–16).

Figure 16–16 The osteotomy is made from an anteromedial to posterolateral direction. The cuts are angled anteriorly at the proximal end to avoid the joint and tapered distally to form a thin, bony pedicle. The patellar tendon is left attached to a large bone block.

Continued

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TECHNICAL NOTE 16–4

Anteromedial Tibial Tuberosity Transfer for Patellofemoral Malalignment (Continued) Using a flat osteotome or oscillating saw, complete the osteotomy. Take care to preserve a bony attachment distally. Once this is done, the tubercle is displaced in an anteromedial direction with the tubercle attachment as the center of rotation (Figure 16–17, A). The tubercle can be held in place with k-wires as the knee is put through a range of motion to assess tracking. A zero degree Q-angle is usually attained. The tubercle can then be affixed with two screws (Figure 16–17, B). At least one screw should engage the posterior cortex.4 A Hemovac may be used if desired, and the wound is closed in layers. No attempt is made to close the anterior or lateral compartment. Postoperative Management

therapy that includes progression to 90 degrees of flexion. A postoperative CPM device is helpful with therapy. Weight-bearing should not begin for at least 6 weeks. Progressing to full weight-bearing too soon can result in fracture of the tibia. Results Fulkerson followed 30 patients for 2 years after an anteromedial tibial tubercle transfer. He had 93% good-to-excellent results subjectively and 89% good-to-excellent results objectively. Screw removal is occasionally required becauseof patient discomfort. In these cases, knee stiffness was an uncommon problem.2

Postoperatively, patients are made non–weightbearing. They are started in immediate physical

Figure 16–17 A, Sliding the osteotomized tibial tubercle in the anteromedial direction corrects alignment of the patella and elevates the attachment, increasing the mechanical advantage and decreasing patellofemoral joint reactive forces.

Continued

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Anteromedial Tibial Tuberosity Transfer for Patellofemoral Malalignment (Continued)

Figure 16–17—cont’d B, Two 4.5-mm cortical screws hold the osteotomy in place. At least one screw should purchase both cortices. Flexing the knee before drilling through the posterior cortex lessens the chance that the neurovascular structures will be injured.

References 1. Maquet J: Advancement of the tibial tuberosity. Clin Orthop Rel Res 115:225–230, 1976. 2. Fulkerson J: Anteromedialization of the tibial tuberosity for patellofemoral malalignment. Clin Orthop Rel Res 177:176–181, 1983.

advanced in line with its fibers, usually a few millimeters, with the knee flexed at 45 degrees. The muscle is sutured to the patella with nonabsorbable sutures, and motion of the knee is checked every stitch or two. If any abnormal motion is noted, the sutures are removed and the advancement is redone. Below the VMO the capsule is closed without advancement in a side-to-side fashion. Chronic Dislocation of the Patella Chronic dislocation of the patella includes those knees with a patella permanently dislocated out of its sulcus. A difference

3. Fulkerson J: Disorders of the Patellofemoral Joint. Baltimore: William and Wilkins, 1990. 4. Fulkerson J: Diagnosis and treatment of patients with patellofemoral pain. Am J Sports Med 30:447–456, 2002. 5. Fulkerson J: Anteromedial tibial tubercle transfer without bone graft. Am J Sports Med 18:490–496, 1990.

can be made between the cases in which it is dislocated both in extension and flexion (permanent dislocation) and in those in which it dislocates each time the knee is flexed (habitual dislocation). Some clinical factors allow differentiation from the more common recurrent dislocation of the patella, which usually involve adolescents and situations in which patellar tracking shows lateral subluxation with extension and relocation in flexion. Chronic dislocation of the patella is usually detected in children in their first decade of life. The disorder can be classified as congenital or acquired; the acquired form includes those cases in which a certain

Patellofemoral Dysfunction

etiological factor has been idenKEY POINTS tified, including multiple injec1. Numerous episodes tions in the thigh of the infant of instability characor, more rarely, trauma. The terize this syndrome. condition of chronic disloca2. Careful physical tion of the patella has some examination is relationship to the contracture necessary. of the quadriceps, which also 3. CT scanning is useful affects children in their first to show underlying decade of life. trochlear groove Two cases of quadriceps abnormalities. contracture were reported by 4. Lateral release is not Fairbank and Barrett40 in idenenough. tical twins. One child was 5. Proximal, distal, or operated on, and scarring of combined realignthe vastus intermedius was ment are successful limiting flexion, with no conin most cases. tribution from the rectus, vastus medialis, or lateralis. Histological examination revealed fibrous and fat degeneration of the vastus intermedius. Gammie and co-workers41 suggested a similarity between quadriceps contracture and other congenital abnormalities, including club foot, Sprengel’s shoulder, and congenital torticollis. Some more light on the etiology of quadriceps contracture in children was shed by the works of Gunn,9 as well as Lloyd-Roberts and Thomas.11 Gunn reported on 22 patients with quadriceps contracture. In 15 of them (68%), there was a history of severe illness for which injection therapy into the thighs was almost certainly administered. Intramuscular injections seem to be a major cause of quadriceps fibrosis and contracture. In a large series of 2404 cases reported by the Japanese Ministry of Health and Welfare, 76% were postinjection, 3% were congenital, and 21% were idiopathic.42 The identification of the original cause of the disease is rendered more difficult by the fact that it may be several months after the injections before the stiffness becomes evident. In the series reported by Alvarez and co-workers43 the time interval ranged between 3 and 18 months. In five patients with chronic patellar dislocation, the condition was preceded by a period of stiffness of the knee. Green and Waugh44 described four cases of congenital lateral dislocation of the patella and emphasized the difficulties in reaching the correct diagnosis in infants. In these patients the presence of a flexion contracture should alert the physician to the possibility of a congenital lateral dislocation of the patella—once other causes, including arthrogryposis, have been excluded. In the infant the patella can be palpated with difficulty because it is very small and located on the lateral side. Radiographs are of no help because the patella is not ossified. Clinical Aspects The congenital form of chronic dislocation of the patella is rarely detected at birth because of the small dimensions of the patella, its lateral placement, and the late development of the ossific nucleus, which renders radiographs not informative in infants. As pointed out by Green and Waugh,44 the presence of a fixed flexion contracture

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should remind the physician of the possibility of a congenital lateral dislocation of the patella, once arthrogryposis has been excluded. The most frequent clinical situation is when the parents note that the child has difficulty rising from the sitting or squatting position. Even if walking and straight leg raising are possible, quadriceps power is greatly decreased. The knee at 90 degrees of flexion looks wider than the contralateral normal knee, and the medial femoral condyle can be easily palpated under the skin. If the deformity has persisted for a sufficient period, secondary deformities may develop, including valgus alignment of the knee and fixed external tibial torsion. If dislocation of the patella is prevented, knee flexion will be greatly limited by tightness of the quadriceps. The clinical picture in the acquired form is similar. There is often a history of several intramuscular injections into the thighs delivered in the first days of life, as a result of severe illness. Once again, the diagnosis can be missed until the age of 4 or 5 or even later. Some cases seem to be secondary to trauma. The patient reports that the knee was normal until the trauma dislocated the patella laterally. Afterward, lateral dislocation in flexion developed. Because the typical osseous abnormalities of a longstanding patellar dislocation (flat sulcus, small patella) are absent in some cases, it seems possible that trauma played a major role. Surgical Treatment The two goals of surgical treatment of chronic patella dislocation are (1) realignment of the patella and (2) lengthening of the contracted quadriceps. Isolated realignment of the patella may improve the tracking of the patella but fails to allow sufficient flexion. Furthermore, the efforts to improve flexion predispose to recurrence of the dislocation. Williams45 described a procedure where tight lateral bands46 are first released from the patella by means of a wide lateral release. Proximal to the patella the incision parallels the lateral border of the quadriceps tendon, thus releasing the vastus lateralis insertion from the patella and quadriceps tendon. The vastus intermedius is inspected and divided if tight. If the rectus femoris is also tight, it can be lengthened by releasing the vastus medialis from the quadriceps tendon and the rectus femoris at the musculotendinous junction. The knee is flexed, the vastus mediKEY POINTS alis and lateralis are sutured together, and the quadriceps 1. Permanent tendon is lengthened. If the dislocation of the patella still subluxates laterally, patella is present. a medial plication is added, pos2. It may be congenital sibly with advancement of the or acquired. vastus medialis or transfer of 3. Intramuscular injecthe patellar tendon or sartorius. tions may be responA similar technique has been sible for quadriceps reported by Fulkerson and contracture. 47 Hungerford, where the quadri4. Surgery is necessary ceps tendon is lengthened by in most cases. Z-plasty. See Technical Note 16–5.

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Proximal Tibiofibular Reconstruction Jennifer L. Cook • Lyle J. Micheli

Indications Our indications for performing a proximal tibiofibular reconstruction include lateral knee pain exacerbated by pressure over the fibular head with instability and recurrent snapping or popping at the fibular head in both male and female young athletes who have failed nonsurgical treatments. Clinically, this subluxation can usually be demonstrated by applying posterior pressure to its fibular head with the knee flexed at 90 degrees. Setup In these patients, general anesthesia is used. Preoperative antibiotics are given. A nonsterile tourniquet is applied high in the upper thigh. The patient is positioned supine. Technique The leg is then examined and subluxation of the fibular head demonstrated. The leg is routinely prepped and draped. An Esmarch bandage is used for exsanguination. The tourniquet is inflated to 300 mm Hg. An approximately 2-cm oblique incision is made over the pes tendon insertion on the medial aspect of the knee. The skin and subcutaneous tissues are incised. The insertion of the semitendinosus tendon is identified. The semitendinosus tendon is freed from any attachments, with careful attention paid to remove any attachments to the medial head of the gastrocnemius,

and stripped up to its musculotendinosus junction using an open tendon stripper. A whipstitch using a no. 1 Ethibond is placed in the tendinous portion of the graft, and muscle is removed from the length of the graft. The free graft is then wrapped in a saline-coated moist sponge. Next, a curvilinear incision approximately 4 cm in length is made over the proximal tibiofibular joint, with the knee in 90 degrees of flexion to protect the peroneal nerve. The skin and subcutaneous tissues are incised. The fibular head is examined to confirm subluxation. A subperiosteal exposure is used to free the proximal fibula by sweeping the periosteum posteriorly and laterally. The tibialis anterior is then released subperiosteally from the proximal lateral tibia and swept medially. The iliotibial band may be elevated and swept anteromedially off the proximal tibia as needed for better exposure. A small drill is used to place two oblique drill holes in the fibular head at 45 degrees to each other. These are connected using curved curettes. Next, two vertically arranged holes are made in the cortex of the lateral aspect of the proximal tibia and, again, are connected by curettes. A no. 5 Ethibond tape is passed through the holes drilled in the fibula and into the tibial holes in a figure-eight fashion. This maneuver reduces the fibular head. The free semitendinosus tendon is passed similarly in a figure-eight fashion through the fibula and tibia from posterior to anterior and cinched down. It is then sutured in place with no. 0 Ethibond sutures (Figure 16–18).

Figure 16–18 Illustration of drill hole placement and graft placement in the proximal tibia and fibula.

Continued

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TECHNICAL NOTE 16–5

Proximal Tibiofibular Reconstruction (Continued) The knee is kept flexed at least 30 degrees while the lateral subcutaneous tissues are closed with interrupted 2-0 Vicryl, and the skin is closed with interrupted 3-0 nylon. The medial incision is closed with interrupted 2-0 Vicryl in the subcutaneous tissues and a running 3-0 PDS to the skin. A sterile dressing is applied. The tourniquet is released and a Cryocuff is applied. Postoperative Management The patient is placed in a Bledsoe brace from 0–45 degrees and is made partially weight-bearing for 6 weeks. Immediate straight leg raising and quadriceps setting exercises are begun, as well as gentle foot sliding range of motion to the knee. The patients return to the clinic in 10–14 days for suture removal and are then begun on a more formal physical therapy program to work on range of motion and strengthening of the knee. They continue to wear their brace full-time for 6 weeks and

References 1. Bell J: Congenital absence of both patellae. J Bone Joint Surg Br 37:352, 1955. 2. Bernhang AM, Levine SA: Familiar absence of the patella. J Bone Joint Surg Am 55:1088–1090, 1973. 3. Gasco J, Del Pino JM, Gomar-Sancko F: Double patella: a case of duplication of the coronal plane. J Bone Joint Surg Br 69:602–603, 1987. 4. Sinding-Larsen C: A hitherto unknown affection of the patella in children. Acta Radiol 1:171, 1921. 5. Merchant AC: Classification of patellofemoral disorders. Arthroscopy 4(4):235–240, 1988. 6. Walmsley R: The development of the patella. J Anat 74:360–369, 1939. 7. Langer M: Uber die Entwicklung des Kniegelenkes. Z Ges Anat 89:83–101, 1929. 8. Miller GF: Familial recurrent dislocation of the patella. J Bone Joint Surg Br 60:203–204, 1978. 9. Gunn DR: Contracture of the quadriceps muscle: a discussion on the etiology and relationship to recurrent dislocation of the patella. J Bone Joint Surg Br 46:492–497, 1964. 10. Hnevkovsky O: Progressive fibrosis of the vastus intermedius muscle in children: a cause of limited knee flexion and elevation of the patella. J Bone Joint Surg Br 43:318–325, 1961. 11. Lloyd-Roberts GC, Thomas TC: The etiology of quadriceps contracture in children. J Bone Joint Surg Br 46:498–517, 1964. 12. McConnell J: The management of chondromalacia patellae: a longterm solution. Aust J Physiother 32(4):215–223, 1986. 13. Micheli LJ, Stanitski CL: Lateral retinacular release. Am J Sports Med 9:330–336, 1981. 14. Krompinger WJ, Fulkerson JP: Lateral retinacular release for intractable lateral retinacular pain. Clin Orthop 179:191–193, 1983. 15. Rosenberg NJ: Osteochondral fractures of the lateral femoral condyle. J Bone Joint Surg Am 46:1013–1026, 1964. 16. Ashtrom JP: Osteochondral fracture in the knee joint associated with hypermobility and dislocation of the patella: report of eighteen cases. J Bone Joint Surg Am 47:1491, 1965. 17. Rorabeck CH, Bobechko WP: Acute dislocation of the patella with osteochondral fracture: a review of eighteen cases. J Bone Joint Surg BR 58:237–240, 1976.

modify their athletic activity accordingly. At that point the brace is removed and they are advanced into their activities. Results Although this is a rare condition and we perform this only one to two times a year, we have had no recurrence of tibiofibular subluxation in patients who have undergone this procedure. Suggested Readings 1. Ogden JA: Subluxation and dislocation of the proximal tibiofibular joint. J Bone Joint Surg Am 56(1):145–154, 1974. 2. Sekiya JK, Kuhn JE: Instability of the proximal tibiofibular joint. J Am Acad Orthop Surg 11(2):120–128, 2003. 3. Semonian RH, Denlinger PM, Duggan RJ: Proximal tibiofibular subluxation relationship to lateral knee pain: a review of proximal tibiofibular joint pathologies. J Orthop Sports Phys Ther 21(5):248–257, 1995.

18. Kolowich PA, Paulos LE, Rosenberg TD, Farnsworth S: Lateral release of the patella: indications and contraindications. Am J Sports Med 18(4):359–365, 1990. 19. Fox TA: Dysplasia of the quadriceps mechanism. Surg Clin North Am 55:199–226, 1975. 20. Fairbank HA: Internal derangement of the knee in children. Proc Royal Soc 30:427–432, 1937. 21. Merchant AC, Mercer RL, Jacobsen RH, et al: Roentgenographic analysis of patello-femoral congruence. J Bone Joint Surg Am 56:1391–1396, 1974. 22. Laurin CA, Levesque HP, Dussault R, et al: The abnormal lateral patellofemoral angle: a diagnostic reoentgenographic sign of recurrent patellar subluxation. J Bone Joint Surg Am 60:55–60, 1978. 23. Dandy DJ, Griffiths D: Lateral release for recurrent dislocation of the patella. J Bone Joint Surg Br 71:121–125, 1989. 24. Crosby BE, Insall JN: Recurrent dislocation of the patella: relation of treatment to ostearthritis. J Bone Joint Surg Am 58:9–13, 1976. 25. Aglietti P, Buzzi R, De Biase P, Giron F: Surgical treatment of recurrent dislocation of the patella. Clin Orthop 308:8–17, 1994. 26. Insall JN, Bullough PG, Burstein AH: Proximal “tube” realignment of the patella for chondromalacia patellae. Clin Orthop 144:63–69, 1979. 27. Insall JN: Disorders of the patella. In Insall JN (ed): Surgery of the Knee. Churchill Livingstone, New York, 1984, p 191. 28. Henry JE, Pflum FA: Arthroscopic proximal patella realignment and stabilization. Arthroscopy 11(4):424–425, 1995. 29. Small NC, Glogan AI, Berezin MA: Arthroscopically assisted proximal extensor mechanism realigment of the knee. Arthroscopy 9(1):63–67, 1993. 30. Yamamoto RK: Arthroscopic repair of the medial retinaculum and capsule in acute patellar dislocations. Arthroscopy 2:125–131, 1986. 31. Conlan T, Garth WP, Lemons JE: Evaluations of the medial soft-tissue restraints of the extensor mechanism of the knee. J Bone Joint Surg Am 75:682–693, 1993. 32. Hauser EDW: Total tendon transplant for slipping patella: a new operation for recurrent dislocation of the patella. Surg Gynec Obstet 66:199–214, 1938. 33. Goldthwait JE: Dislocation of the patella. Trans Am Orthop Assoc 8:237, 1895.

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34. Goldthwait JE: Permanent dislocation of the patella: report of a case of twenty years’ duration, successfully treated by transplantation of the patella tendons with the tubercle of the tibia. Am Surg 29:62–68, 1899. 35. Roux C: Recurrent dislocation of the patella: operative treatment. Clin Orthop 144:43–44, 1979. 36. Fondren FB, Goldner JL, Bassett FH: Recurrent dislocation of the patella treated by the modified Roux-Goldthwait procedure: a prospective study of forty-seven knees. J Bone Joint Surg Am 67:993–1005, 1985. 37. Trillat A, Dejour H, Couette A: Diagnostic et traitement des subluxations recidivantes de la rotule. Rev Chir Orthop 50(6):813–824, 1964. 38. Hughston JC, Walsh WM: Proximal and distal reconstruction of the extensor mechanism for patellar subluxation. Clin Orthop 144:36, 1979. 39. Cox JS: Evaluation of the Roux-Elmsie-Trillat procedure for knee extensor realignment. Am J Sports Med 10:303–310, 1982. 40. Fairbank TJ, Barrett AM: Vastus intermedius contracture in early childhood: case report in identical twins. J Bone Joint Surg Br 43:326–334, 1961.

41. Gammie WFP, Taylor JH, Urich H: Contracture of the vastus intermedius in children: a report of two cases. J Bone Joint Surg Br 45:370–375, 1963. 42. Chin SS, Mano J, Yukawa YN, et al: Contracture of the quadriceps muscle caused by injection. Acta Orthop Belg 41:306–315, 1975. 43. Alvarez EV, Munters M, Lavine LS, et al: Quadriceps myofibrosis: a complication of intramuscular injections. J Bone Joint Surg Am 62:5–8, 1980. 44. Green JP, Waugh W: Congenital lateral dislocation of the patella. J Bone Joint Surg Br 50:285–289, 1968. 45. Williams PF: Quadriceps contracture. J Bone Joint Surg Br 50:278, 1968. 46. Jeffreys TE: Recurrent dislocation of the patella due to abnormal attachment of the iliotibial tract. J Bone Joint Surg Br 45:740–743, 1963. 47. Fulkerson JP, Hungerford DS: Patellar dislocation. In Ficat RP, Hunger Ford DS (eds): Disorders of the Patello-Femoral Joint. Baltimore: Williams & Wilkins, 1990, p 149.

Chapter 17

Tendinopathy of the Extensor Apparatus of the Knee Jason Wong

Functional Anatomy of the Extensor Mechanism of the Knee The rectus femoris, the vastus intermedius, the vastus medialis, and the vastus lateralis are connected to the patella by the quadriceps tendon. The tendon inserts on the proximal pole of the patella and continues distally as a tendinous expansion over the anterior patella to merge with the patellar tendon.1 The patellar tendon, the distal extension of the tendon of the quadriceps femoris, extends from the inferior pole of the patella to the anterior tibial tuberosity. In the adult it appears as a glistening white ribbon approximately 3 cm wide in the coronal plane and 5 mm thick in the sagittal plane. The patellar tendon receives its vascularization from the medial inferior genicular, lateral superior genicular, lateral inferior genicular, and the anterior tibial recurrent arteries,2 with the main blood supply entering just inferior to the lower pole of the patella. Nonarticular Osteochondrosis Both Osgood-Schlatter lesion (OSL) and Sinding-LarsenJohansson lesion (SLJL) are classified as “nonarticular osteochondroses.” These involve tendinous and ligamentous attachments to apophyses. In some instances, nonarticular osteochondroses can occur in response to abnormal pressure or chronic stress, which will alter the normal chondrogenesis and osteogenesis. Osgood-Schlatter Lesion OSL is a common cause of knee pain in young athletes. It causes swelling, pain, and tenderness at the anterior tibial tuberosity. It occurs mostly in boys at the time of a growth spurt during their pre-teen or teenage years. The pathophysiology of OSL is unclear, and there is no consensus on whether there are predisposing factors.

●

Nicola Maffulli

The condition probably results from the high tensile forces exerted by the quadriceps on the extensor apparatus of the knee. Histological studies suggest a traumatic etiology. Bone growth is faster than soft tissue growth, which may result in muscle–tendon tightness across the joint and loss of flexibility. When the quadriceps contracts, the forces exerted on the patellar tendon may well cause microtears at the tendon–apophysis interface at the anterior tibial tuberosity, resulting in pain. During periods of rapid growth (typically, ages 10–11 in girls and 13–14 in boys), stress from contraction of the quadriceps is transmitted through the patellar tendon onto a small portion of the partially developed tibial tuberosity.3 This may result in a partial avulsion fracture through the apophyseal ossification center. Eventually, secondary heterotopic bone formation occurs in the tendon near its insertion, producing a visible lump. Approximately 25% of patients have bilateral lesions, but the true incidence is not known. One report4 puts the prevalence of the condition in athletic adolescents at 21%, as compared with 4.5% in age-matched nonathletes. The condition has been more common in boys, although the ratio may be changing with the increased participation of girls in sports.5 The symptoms become noticeable during activities that require running, jumping, or ascending and descending stairs. OSL is more common in young athletes who play soccer or basketball or are involved in gymnastics and ballet. Normally, the symptoms wane and disappear with time, as the patellar tendon matures and the apophysis at the anterior tibial tuberosity closes. Only rarely does OSL persist beyond the growing stage. Ultrasound and magnetic resonance imaging (MRI) scans in OSL patients frequently reveal signal changes in the patellar tendon and soft tissue adjacent to the tuberosity and less frequent changes in the tuberosity itself.6,7 181

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Typically, OSL is self-limiting over a period of 12–24 months. Pain usually remits at skeletal maturity, but a small percentage of patients develop a painful ossicle that can necessitate surgical excision.8 In the long run, 24% of patients may have some limitation of activities, and 60% have discomfort with kneeling.3 Diagnosis

KEY POINTS Osgood-Schlatter lesion 1. Common cause of anterior knee pain in young athletes 2. Incidence is greater in boys than in girls 3. Occurs at time of growth spurt 4. Occasionally associated with a bony spur 5. May recur but resolves with skeletal maturity

Patients often point to the tibial tuberosity as the source of their anterior knee pain and may complain of swelling and prominence over the tuberosity. The pain generally occurs during activity and decreases with rest. Pain onset is insidious, and patients typically cannot identify an acute traumatic cause. Severity can be roughly described in terms of three grades, depending on the duration of pain (Table 17–1).9 The patient usually has full knee range of motion with no effusion or laxity and no signs of meniscal lesions. To exclude other conditions, physical examination should also include an assessment of range of motion at the hip and palpation of the inferior pole of the patella. Imaging Studies Radiographs are not normally required. Radiographs can be normal or can show irregular ossification of the tibial tuberosity, but this can be a normal variant in asymptomatic adolescents. Another possible finding is an ossicle of the distal portion of the patellar tendon (Figure 17–1). Patients with apophyseal fragmentation are more likely to have chronic symptoms than patients with normal radiographs.3 For patients who have had acute onset of pain, radiographs should be obtained to rule out an avulsion fracture of the tibial tuberosity. For patients with night pain, other non–activity-related pain, or tenderness that is not directly localized to the tibial tuberosity, radiographs should also be obtained to rule out a tumor, infection, and osteochondritis dissecans (OCD). Ultrasound and MRI scans can confirm the diagnosis of OSL but are generally unnecessary. Differential Diagnosis Other causes of anterior knee pain in athletic adolescents include Sinding-Larsen-Johansson lesion, patellofemoral syndrome, and OCD. SLJL and patellofemoral syndrome occasionally coexist with OSL in adolescents. Table 17–1 Grades of Osgood-Schlatter Lesion Severity Grade

Characteristics

1 2

Pain after activity that resolves within 24 hours Pain during and after activity that does not limit activity and resolves within 24 hours Constant pain that limits sports and daily activity

3

Figure 17–1 Lateral knee radiograph demonstrating marked ossification of the distal insertion of the patella tendon in keeping with an OSL.

SLJL presents with pain, swelling, and tenderness of the inferior patellar pole at the origin of the patellar tendon. Unlike the more obvious OSL, SLJL can be missed unless the examiner palpates the inferior patellar pole with the patient’s knee extended and the patellar tendon relaxed. Repeating the test with the knee flexed at 90 degrees should reveal decreased tenderness as the patellar tendon becomes more tense. Radiographs are usually normal but can show calcification at the inferior pole of the patella. Patellofemoral syndrome probably arises from repetitive stress of the patella on the femur, but the exact etiology is not known. Patients report chronic activity-related anterior knee pain that vaguely localizes around the patella. With the knee flexed 20–30 degrees, the patella begins to engage the trochlear groove. Pain is elicited with light manual pressure by rubbing on the patella with a side-to-side motion. OCD is a rare but serious cause of adolescent knee pain involving an abnormality of the articular cartilage and the underlying bone. Patients present with diffuse knee pain and can have loss of motion and a knee effusion. The diagnosis of OCD is usually made with radiographs because there is no reliable clinical test. The condition can lead to permanent knee damage and requires surgery. The range of motion of the hip should be assessed in any adolescent with knee pain. Limitation of, or pain with, internal rotation requires further investigations to rule out slipped upper femoral epiphysis and Perthes’ disease.

Tendinopathy of the Extensor Apparatus of the Knee

The combination of history and physical examination may suggest a need for radiography to rule out an avulsion fracture of the tibial tuberosity, a tumor, an infection, or OCD. Management The management of OSL depends on the severity of the condition. Grades 1 and 2

Grade 3

KEY POINTS Differential diagnosis of anterior knee pain in children The following conditions can give rise to anterior knee symptoms in children: 1. Acute trauma 2. Patellofemoral dysplasia 3. OSL 4. SLJL 5. Osteochondritis dissecans 6. Hip pathology

Adolescents with grade 1 or grade 2 symptoms, and their parents, only need reassurance. Patients can play sports if the pain is tolerated and resolves within 24 hours. When symptoms flare up, short-term rest from the offending activity typically eliminates pain. Prolonged total rest is not recommended, because it can lead to deconditioning and increase the chance of recurrence with return to sports. Shock-absorbent insoles in athletic shoes may decrease peak stress on the tendon and tuberosity. Icing the knee after activity may also be beneficial. Hamstring and quadriceps stretching is recommended. Neoprene knee sleeves that pad the tibial tuberosity prevent repeated contusions to the tuberosity. Nonsteroidal antiinflammatory drugs (NSAIDs) may be administered as needed, but we do not advocate their routine use. Corticosteroid injections are not recommended.

A few adolescent athletes have grade 3 OSL (constant pain that limits daily activity and sports performance). They generally do not want to wait 12–24 months for their condition to spontaneously resolve. Classically, after periods of rest they can have recurrent symptoms. Grade 3 OSL warrants more intense treatment. Rarely, a 3- to 4-week course of immobilization with a cast or brace is indicated for severe KEY POINTS recurrent OSL that resists firstline treatment. In adolescents, General management of immobilization can be required OSL and SLJL to enforce the recommendaMild to moderate tion of rest. Casting for OSL severity does not seem to alter the nat1. Short-term rest: rest, 3 ural history. ice, compression, After rest or immobiliza(RICE) therapy tion, patients can start a rehabil2. Hamstring and itation program of progressive quadriceps stretching quadriceps exercises. Bone, car3. NSAID therapy tilage, and tendons hypertrophy Severe symptoms and strengthen with gradually 4. 3–4 weeks of increasing stress (Technical immobilization with Note 17–1). cast or bracing In athletes with resistant 5. Progressive grade 3 OSL, a dual-hinged knee quadriceps brace that limits motion to exercises between 0 and 40 degrees allowed them to return to sports with immediate cessation of pain.10 Text continued on p. 189

TECHNICAL NOTE 17–1

Patellar Tendonitis Physical Therapy Protocol Carl Gustafson

NOTE: The patellar tendonitis protocol should be progressed pain free. The objective is to try to minimize pain by limiting range of motion, resist-

ance, and frequency. If any exercise causes pain, refrain from that exercise until you talk with your physical therapist or athletic trainer (Table 17–2).

Table 17–2 Exercises for Disorders Involving the Extensor Apparatus of the Knee Associated Resistance Diagnoses Exercises

Stretches

Tendonitis Jumper’s knee

Rectus Quad Hamstring

SLR Adduction LAQ or SAQ (pain-free arc) Step-up Leg press

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Possible Contraindications

Trying to progress to strengthening rehabilitation before Iliotibial band decreasing Adductor acute symptoms

SLR, Straight leg raises; LAQ, long arc quads; SAQ, short arc quads.

Continued

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Patellar Tendonitis Physical Therapy Protocol (Continued) Strengthening (Figure 17–2, A to D) All exercises should be progressed to two sets of 15 repetitions, and resistance should then be added in the form of weights for straight leg raises, short arc lifts, long arc lifts, and leg presses. Add height in terms of step-ups. Straight Leg Raise, Short Arc Lifts, Long Arc Lifts, and Adductor Lifts • Start with resistance of limb. • When adding weight (once you reach two sets of 15), add no greater than 3 lb per week. • Progress to as much as 10 lb if pain free (discuss with physical therapist/athletic trainer progression to machines).

Figure 17–2

• Frequency: do exercises with up to 5 lb daily (if recovered in terms of no pain or joint/muscle soreness from last workout), and 6–10 lb three times per week. Leg Press: (Figure 17–3) • Add weight as tolerated (two sets of 15 reps). • Do exercise one leg at a time unless you have a bilateral condition. • Progress exercises to every other day until you do not recover in between workouts then go to three times per week. Step ups: (Figure 17–4) • Progress up to 8-inch step on a daily basis. Once you get to 8-inch step, step farther back in lunge fashion. Do only three times a week.

A, Straight leg raise. B, Short arc lifts.

Continued

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TECHNICAL NOTE 17–1

Patellar Tendonitis Physical Therapy Protocol (Continued)

Figure 17–2—cont’d

C, Long arc lifts. D, Adductor lifts.

Walking/Running Program Stretching: (Figure 17–5) • Hold all stretches 30 seconds for three repetitions, five times per week. • Stretch daily until pain subsides, then stretch three times per week. • Quadriceps • Rectus • Iliotibial band • Hamstring • Adductors • Calf

Objective 1: Begin walking program three times per week and build up to 45 minutes pain free. Objective 2: Once you can tolerate walking and have 70% of strength of unaffected limb, begin running 15–20 minutes, three times per week. Objective 3: Once you can tolerate jogging and have 90% strength, perform agility exercises pain free, as outlined by the physical therapist or athletic trainer. Then return to sports with doctor’s recommendation. Continued

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TECHNICAL NOTE 17–1

Patellar Tendonitis Physical Therapy Protocol (Continued)

Figure 17–3 Demonstration of a leg press.

Figure 17–4 Demonstration of step-ups.

Figure 17–5 Stretching of quadriceps (A).

Continued

Tendinopathy of the Extensor Apparatus of the Knee

TECHNICAL NOTE 17–1

Patellar Tendonitis Physical Therapy Protocol (Continued)

Figure 17–5—cont’d

Stretching of rectus (B), iliotibial band (C), and hamstring (D).

Continued

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TECHNICAL NOTE 17–1

Patellar Tendonitis Physical Therapy Protocol (Continued)

Figure 17–5—cont’d

Stretching of adductors (E) and calf (F).

Suggested Readings 1. Almekinders LC, Vellema JH, Weinhold PS: Strain patterns in the patellar tendon and the implications for patellar tendinopathy. Knee Surg Sports Traumatol Arthrosc 10(1):2–5, 2002. 2. Basso O, Johnson DP, Amis AA: The anatomy of the patellar tendon. Knee Surg Traumatol Arthros 9(1):2–5, 2001. 3. Faigenbaum AD, Westcott WL, Loud RL, Long C: The effects of different resistance training protocols on muscular strength and endurance development in children. Pediatrics 104:1–7, 1999. 4. Feigenbaum MS, Pollack ML: Strength training: rationale for current guidelines for adult fitness programs. Phys Sports Med 25(2)44–66, 1997.

5. Feigenbaum MS, Pollack ML: Prescription or resistance training for health and disease. Med Sci Sports Exerc 31(1):38–45, 1999. 6. Khan KM, Cook JL, Taunton JE, Bonar F: Overuse tendinosis, not tendinitis. Phys Sports Med 28(4):245–262, 2000. 7. Metcalf JA, Roberts SO: Strength training and the immature athlete: an overview. Pediatr Nurs 19(4):325–332, 1993. 8. Witvrouw E, Bellemans J, Lysens R, Danneels L, Cambier D: Intrinsic risk factors for the development of patellar tendonitis in an athletic population. A two-year prospective study. Am J Sports Med 29(2):190–195, 2001. 9. Woo SL: Injury and Repair of the Musculoskeletal Soft Tissues. Park Ridge, Ill.: American Academy of Orthopaedics, 1998.

Tendinopathy of the Extensor Apparatus of the Knee

Complications and Sequelae Painful Ossicle Patients with OSL may develop a painful ossicle in the distal patellar tendon. Excision of this ossicle can be curative.8 Some authors recommend tuberosity excision or trimming in addition to ossicle excision.11 Painful Kneeling Sixty percent of patients with OSL may have painful kneeling as adults.3 Permanent Bump OSL can leave a large bump on the anterior aspect of the knee. Patients, especially girls, should be warned of this cosmetic sequela. In general, OSL is a benign condition. Mild symptoms require only patient education and activity moderation. Athletes who have severe symptoms may benefit from rest or, possibly, short-term immobilization, followed by an aggressive rehabilitation program. Sinding-Larsen-Johansson lesion Sinding-Larsen-Johansson lesion is closely related to Osgood-Schlatter lesion.12 It occurs at the opposite end of the patellar tendon, at the attachment of the patellar tendon to the patella. At the lower pole of the patella there is no apophysis involved, because the tendon attaches to the patella directly from the periosteum. If repetitive tension is applied to this site, the periosteum becomes inflamed and begins to lay down more bone to reinforce the site. The same principles of OSL management apply: ice, analgesia, and activity modifications. There are rarely complications of SLJL, and symptoms generally resolve. There is no evidence that having had either OSL or SLJL as a child predisposes to patellar or quadriceps tendinopathy as an adult. KEY POINTS Recently, apophysitis of the proximal pole of the patella has Sinding-Larsenbeen described.13 Clinical and Johansson lesion radiographic findings were similar 1. Results from either to those found in OSL and SLJL. microavulsions of the An excisional biopsy and curetpatella or stress type tage of the lesion showed granuof fractures of the lation tissue. Histopathology inferior pole revealed normal bone, no evi2. Localized point dence of cellular necrosis, and tenderness at the adequate blood supply, consistent inferior pole of the with traction-related apophysitis. patella The patient became asympto3. Usually self-limiting matic within 10 months. Patellar and Quadriceps Tendinopathy Tendinopathies of the main body of a tendon are relatively rare in children and adolescents. However, because young athletes train harder and longer and participate in sports year-round, injury patterns are changing, and overuse injuries previously seen in older individuals are now becoming more prevalent in younger individuals.14–17 Also, some sports such as soccer and American football attract early-maturing individuals, and

some athletes, although chronologically in the pediatric age group, may be fully mature biologically.18,19 To our knowledge, there are no published studies on tendinopathy of the extensor mechanism of the knee in children and adolescents, and therefore we mutate our recommendations from personal experience and the work performed in older, fully grown athletes. Pathophysiology of Tendinopathy

189

KEY POINTS Patellar tendinopathy: jumper’s knee 1. Rare in children, but on the rise 2. Characterized by mucoid degeneration of tendon 3. Caused by repeated overloading of extensor apparatus 4. Tenderness at inferior pole of patella 5. May precede patellar tendon rupture

The pathology of underlying tendinopathy has only recently been defined.20,21 This probably reflects more the confusion resulting from differences in nomenclature than a paucity of data. Macroscopically, the patellar tendon of patients with jumper’s knee contains soft, yellow-brown, and disorganized tissue, commonly labeled mucoid degeneration, and some authors have reported hyaline degeneration.22 Upon light microscopy, the pathological tendon tissue shows the presence of abnormal collagen, tenocytes, and abundant abnormal small vessel ingrowth. The amorphous and disorganized collagen bundles show degenerative and necrotic tendon tissue replacing collagen. Clefts in the collagen probably represent microscopic partial ruptures.23 The characteristic reflective polarized light appearance of normal collagen is lost, tenocytes lose their fine spindle shape, and nuclei appear more rounded.24 A major feature is the absence of inflammatory cells in excision biopsies, even at the periphery of abnormal tissue and in patients who had only had symptoms for 4 months.24 Therefore the tendons of patients suffering from patellar tendinopathy have tendinosis, a degenerative condition, instead of an inflammatory condition. Sudden repeated tensile overload may cause microtearing and fraying of tendon fibers, followed by focal degeneration, particularly at the tendon attachment to the patella.25 In patients with spontaneous patellar tendon rupture, intratendinous pathology included hypoxic degenerative change, mucoid degeneration, tendolipomatosis, and calcifying tendinopathy, or a combination of them were present even though the patients had never experienced symptoms of patellar tendinopathy.26 Therefore, symptomless tendinosis can precede acute tendon rupture.27 Nomenclature In our practice the term patellar tendinopathy encompasses the lesion associated with pain and tenderness at the lower point of the patella and lesions of the main body of the tendon.22,28 The latter are less common than the former and seem to involve the whole thickness of the tendon in the area involved, instead of mainly its posterior aspect.29 The term tendinopathy can be used to describe both acute and overuse conditions. In this way, ambiguity is prevented and terms such as tendinosis, paratendinitis, and tendinitis are reserved as pathological labels.

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Site of Patellar Tendon Overuse Lesions The “classical” site is the patella pole with well-localized tenderness. Lesions of the middle third of the tendon have been described,30 and their management may well differ from that of classical jumper’s knee.29 Over the past few years, the rate of reported cases of patellar tendinopathy seems to have increased,23 probably because athletes undergo more strenuous and prolonged periods of training and competition,31 and because of the higher awareness of both athletes and health care professionals.23,32

able to perform at a satisfactory level. In Blazina stage 3, pain is present during and after activity but is more prolonged, with progressive difficulty in performing at a satisfactory level. In Blazina stage 4 the patellar tendon is ruptured. Imaging High-resolution real-time ultrasonography (Figure 17–6) and MRI are the imaging modalities of choice in patients with patellar tendon disorders.37,38 Computed tomography has been used,39 but it does not offer any advantage over imaging methods not using ionizing radiation.

History and Physical Examination

Conservative Management

Patellar tendinopathy is most frequently located at the lower pole of the patella and is probably produced by repeated overloads on the extensor mechanism. It is more frequent in athletes whose sports involve activities requiring sudden maximal muscle–tendon unit exertion, such as in jumping. The diagnosis of patellar tendinopathy is based on patients’ subjective reports of pain related to activity levels.33 The often insidious onset usually relates to an increase in frequency or intensity of rapid, repetitive ballistic movements of the knee joint,23 with dull ache over the anterior aspect of the knee after strenuous activity. Continuing to play will exacerbate the condition and interfere with performance. Patients also commonly report pain after sitting for long periods and when ascending and descending stairs. Tissue alterations are more frequently observed close to the patellar junction than elsewhere in the tendon, probably because of the high concentration of mechanical stresses in this area. The main physical finding in jumper’s knee is tenderness at the inferior pole of the patella or in the main body of the tendon with the knee fully extended and the quadriceps relaxed. With the knee flexed to 90 degrees, thus tensioning the patellar tendon, tenderness significantly increases.34 The main differential diagnosis is with the patellofemoral syndrome, and the two conditions can coexist.

Conservative management regimens are usually based on the patient’s subjective report of pain. Treatments include correction of predisposing factors, relative or absolute rest from jumping activities or from sport, stretching, strengthening, physical therapy modalities, ice, massage, NSAIDs, and corticosteroids by injection or electrophoresis.40 We normally do not use corticosteroids, but they have recently used peritendinous injections of aprotinin.41 However, patients with an insertional tendinopathy fared less well than those with tendinopathy of the main body of the tendon. The results of conservative and operative management of patellar tendinopathy in 42 athletes were recorded.22 Of these, 26 presented with Blazina’s stage 2 and 16 with Blazina’s stage 3 conditions. All patients were initially managed conservatively with NSAIDs; physical therapy; and a progressive rehabilitation program based on isometric exercises, stretching, and eccentric exercises. After 6 months, 33 patients showed symptomatic improvement and were able to resume their sports. In the nine patients presenting with Blazina’s stage 3 disease in whom conservative measures failed, surgery was undertaken, with removal of the degenerated areas of the tendon, multiple longitudinal tenotomies, and drilling of the lower pole of the patella at the site of tendon attachment. After a mean follow-up of 4.8 years, clinical results were excellent or good in all patients. In the group treated nonoperatively, symptoms were better in the patients presenting with stage 2 disease than in those with stage 3.

Clinical Grading The reliability of the several systems of grading jumper’s knee according to the severity and timing of knee pain has not been tested.35 The systems are often incapable of discriminating between patients with KEY POINTS widely differing symptoms, and they cannot be used to grade recovBlazina grading ery. Recently, a 100-point scoring 1. Stage 1: pain after scale to assess severity of jumper’s activity, no functional knee according to symptoms and impairment 36 function has been developed, 2. Stage 2: pain during and we use it in routine clinical and after activity, no practice. functional Most clinicians use Blazina impairment 33 and colleagues’ criteria. In Bla3. Stage 3: pain during zina stage 1, pain is initially and after activity, present only after athletic particfunctional ipation with no undue functionimpairment al impairment. In Blazina stage 4. Stage 4: disruption to 2, patients experience pain durtendon ing and after activity but are still

Surgical Management Surgery is generally performed when patients have not improved after 3–6 months of conservative management. Several surgical methods for treatment of jumper’s knee are described,42 including drilling of the inferior pole of the patella, resection of the tibial attachment of the patellar tendon with realignment,43 excision of degenerated areas,44 arthroscopic débridement,45 repair of macroscopic defects,46 multiple longitudinal tenotomies,47 percutaneous needling,48 and percutaneous longitudinal tenotomy.49 We recommend removing the paratenon at the time of open surgery because the inflammatory response in that structure may cause later problems.29 Recently, arthroscopic resection of the lower pole of the patella and excision of the degenerated area of the tendon has been performed (Figure 17–7).50 Results of surgery cannot be evaluated in isolation, because a prolonged period of rehabilitation usually ensues.33 Good results may be attributable in part to the relative rest; therefore, randomized studies are needed.

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191

Figure 17–6 Transverse and longitudinal high-resolution ultrasound scans of an adolescent patient with patellar tendinopathy. Note the hypoechoic signal at the attachment of the patellar tendon on the lower pole of the patella.

Several factors confound the analysis of outcome of surgery. Surgeons differ in their diagnostic criteria, selection of cases for surgery, the actual operation performed, as well as in their postoperative protocols. Different types of surgery result in differences in the amount of bone either excised or drilled, the margin of normal tissue excised around the macroscopically degenerative tissue, the use or avoidance of longitudinal tenotomies, and the type of closure of the tendon after surgery. Intersurgeon technical ability is another major factor whose influence has never been studied. Also, the scientific methodology behind published articles on the outcome of patellar tendinopathy after surgery is poor, and the poorer the methodology, the higher the success rate.51 Obviously, improving study design would provide clinicians with a more rigorous evidence base for treating patients who have recalcitrant patellar tendinopathy. Therefore, before deciding whether to undertake surgery for the management of recalcitrant patellar tendinopathy, adequate nonoperative management should be attempted. Surgery should be considered when 6 months of modified rest and well-supervised nonoperative management fail. Stripping of the paratenon, removal of degenerated tissue, and multiple longitudinal tenotomies of the patellar tendon should be performed (Technical Note 17–2). Quadriceps Tendon

Figure 17–7 Typical bandaging of the knee in a young child following arthroscopic resection of the lower pole of the patella.

The superior strength, mechanical advantage, and better vascularity of the quadriceps tendon make quadriceps tendinopathy much less frequent than patellar tendinopathy. In adolescent athletes, avulsion injuries of the proximal patella apophysis

KEY POINTS Quadriceps tendinopathy 1. Very rare in children 2. Tenderness at superior pole of patella

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TECHNICAL NOTE 17–2

Adolescent Patellar Tendinosis: Operative Treatment John Franco • Bert Mandelbaum

Indications Our indication for operative treatment of adolescent patellar tendinosis are severe symptoms persistent for more than 3 months, pain refractory to conservative therapy, and clinical findings corroborated by changes on MRI or ultrasound. Patellar tendinosis is an overuse injury that typically affects the older adolescent athlete involved in jumping or sprinting sports such as volleyball, basketball, and soccer.1 Patellar tendinosis is distinguished from other patellar tendinopathies, such as patellar tendonitis, by the presence of intrasubstance changes demonstrated on ultrasound or MRI2,3 (Figures 17–8, A and B). Patellar tendinosis most commonly involves the proximal bone–tendon junction. The intrasubstance changes seen on MRI histologically represent areas of pseudocystic cavities filled with necrotic

tissue.4,5 Extrinsic factors such as intensity and duration of training, training surfaces, footwear, and equipment have been implicated as contributing factors to the pathogenesis of patellar tendinosis. More recent studies focus on intrinsic factors such as patellar impingement, malalignment, and muscle imbalance that may predispose a jumping athlete to patellar tendinosis.6,7 Patellar tendinosis usually resolves with prolonged conservative treatment, which in our practice focuses on quadriceps stretching; achieving quadriceps-hamstring muscle balance; ice cross-friction massage; and adjunctive modalities such as the application of ketoprofen cream, iontophoresis, and counterforce bracing. Before considering surgical intervention, it is critical to distinguish patellar tendinosis from other common causes of anterior knee pain

Figure 17–8 A and B, Patellar tendinosis is distinguished from other patellar tendinopathies, such as patellar tendonitis, by the presence of intrasubstance changes demonstrated on ultrasound or MRI.

Continued

Tendinopathy of the Extensor Apparatus of the Knee

TECHNICAL NOTE 17–2

Adolescent Patellar Tendinosis: Operative Treatment (Continued)

Figure 17–8—cont’d

in the adolescent athlete, such as SindingLarsen-Johansson disease and Osgood-Schlatter disease. Sinding-Larsen-Johansson disease, a periosteal sleeve avulsion involving the inferior pole of the patella, and Osgood-Schlatter disease, a traction enthesopathy of the tibial tuberosity apophysis, both resolve with skeletal maturity.8 We believe that skeletally mature adolescent patients with severe patellar tendinosis that is refractory to conservative therapy and verified by imaging studies are candidates for operative treatment. We feel that patellar impingement may play a significant role in the pathogenesis of patellar tendinosis and therefore include débridement of the inferior patellar pole in our arthroscopic approach to surgical treatment. Setup The patient is brought to the operating room and placed supine on the operating table. General

anesthesia is typically used. A thigh tourniquet is placed on the affected extremity.

Technique Arthroscopy: The procedure is performed arthroscopically. Before draping the extremity, 20 ml of 1% lidocaine and 0.25% bupivacaine with epinephrine are injected into the knee joint. A total of 20 ml of local anesthetic is also injected into each arthroscopic portal site, through the capsule, and into the fat pad. A standard diagnostic knee arthroscopy is performed using anteromedial and anterolateral portals and a 30-degree arthroscope. The fat pad is visualized through the anterolateral portal and débrided through the anteromedial portal with a 4.5 or 5.5 oscillating shaver. Débridement of the fat pad at the inferior pole of the patella will typically reveal a localized area of chronic inflammatory tissue at the origin of the patellar tendon Continued

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TECHNICAL NOTE 17–2

Adolescent Patellar Tendinosis: Operative Treatment (Continued) (Figure 17–9). This inflammatory tissue is débrided to expose the underlying bone tendon junction at the inferior pole of the patella. Débridement: An 18-gauge spinal needle is inserted percutaneously across the origin of the patellar tendon and into the knee joint under direct visualization with the arthroscope. Once the needle is properly placed into the central portion of the tendon, a 15 blade scalpel is used

to “cut down” on the spinal needle and establish a mid-patellar tendon portal across the diseased, necrotic tissue (Figure 17–10). The 4.5 oscillating shaver débrider is inserted through the midpatellar portal and used to débride the central diseased portion of the patellar tendon origin, as well as prominent bone at the inferior pole of the patella. Débridement is carried out medially and laterally until healthy-appearing patellar tendon tissue is visualized with the arthroscope. The shaver is removed from the mid-patellar portal

Figure 17–9 Débridement of the fat pad at the inferior pole of the patella will typically reveal a localized area of chronic inflammatory tissue at the origin of the patellar tendon.

Figure 17–10 After the needle is placed into the central portion of the tendon, a 15 blade scalpel is used to “cut down” on the spinal needle and establish a mid-patellar tendon portal across the diseased, necrotic tissue.

Continued

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Adolescent Patellar Tendinosis: Operative Treatment (Continued) and any remaining ventral, necrotic tissue is débrided under direct visualization through the portal incision. Closure: The mid-patellar portal paratenon incision is closed with 2-0 vicryl. Simple 4-0 nylon sutures are used to close skin. The knee is injected with 30 mg of ketorolac in 10 ml of 1% xylocaine solution. A sterile, soft, compressive dressing is placed over the knee, and the patient is transferred to the postoperative recovery room. The patient is discharged home on the same day, partially weight-bearing with crutches or a cane. Postoperative Management: The patient continues to ambulate with an assistive device for 5 days. Early active rehabilitation is initiated on postoperative day 1. This is a home-based program consisting of straight leg raises, isometric knee extension exercises, and gentle cycling. At 2 weeks’ postoperative the patient is transitioned into a stationary cycling program and formal physical therapy focusing on range of motion, and quadriceps/hamstring conditioning is started. Six weeks after sur-

are more common than tendinopathy of the quadriceps mechanism.52 Clinical Aspects Patients with quadriceps tendinopathy report pain at the proximal pole of the patella. The pain is insidious and often associated with a recent increase in jumping, climbing, kicking, or running. History and Physical Examination Physical examination reveals tenderness over the superior pole of the patella and discomfort with resistance to extension when the knee is in maximum flexion. Malalignment, such as femoral anteversion, increased Q-angle, and tibial torsion, should be evaluated, together with quadriceps strength and hamstring flexibility. In older individuals with quadriceps tendinopathy, degenerative changes such as calcification in the tendon or spur formation at the superior pole of the patella may be present. When extension strength is maintained, MRI may show degeneration of the posterior insertion of the tendon. Imaging Imaging techniques for evaluating the quadriceps tendon include radiography, ultrasonography, and MR imaging. MRI of normal quadriceps tendons reveals a laminated appearance with two (30%), three (56%), or four (6%) layers.53

gery the patient begins jogging a simple box course. The box perimeter and speed of movement are gradually increased. At 3 months’ postoperative, sports-specific activities are initiated and continued until there is a full return to sport. Suggested Readings 1. El-Khoury GY, Wira RL, Berbaum KS, et al: MR imaging of patellar tendonitis. Radiology 184:849–854, 1992. 2. Ferretti A, Ippolito E, Mariani P, Puddu G: Jumper’s knee. Am J Sports Med 11:58–62, 1983. 3. Fritschy D, de Guatard R: Jumper’s knee and ultrasonography. Am J Sports Med 16:637–640, 1988. 4. Krivickas LS: Anatomical factors associated with overuse sports injuries. Sports Med 24:132–146, 1997. 5. Medlar RC, Lyne ED: Sinding-Larsen-Johansson disease. J Bone Joint Surg Am 60:1113–1116, 1978. 6. Popp JE, Yu JS, Kaeding CC: Recalcitrant patellar tendonitis. Am J Sports Med 25:218–222, 1997. 7. Schmid MR, Hodler J, Cathrein P, et al: Is impingement the cause of jumper’s knee? Am J Sports Med 30:388–395, 2002. 8. Witvrouw E, Bellemans J, Lysens R, et al: Intrinsic risk factors for the development of patellar tendinitis in an athletic population. Am J Sports Med 29:190–195, 2001.

Management Nonoperative management is generally successful in the vast majority of patients with quadriceps tendinopathy. Activity modification, NSAIDs, and physical therapy should be used. Once the pain subsides, therapy should concentrate on quadriceps strengthening and increase in hamstring flexibility. Strengthening exercises should focus on eccentric training of the muscle–tendon complex.54 Eccentric training aims to KEY POINTS strengthen the tendon so that it can withstand higher stresses. Management of The program involves static tendinopathy in children stretching both before and after 1. Activity modification the exercises. Eccentric exercises (e.g., rest from jumpare performed in three sets of ing activities) 10 repetitions. As the week 2. RICE therapy progresses, the speed of contrac3. NSAIDs tions is increased. Each week, 4. Progressive the weight applied is increased rehabilitation and the cycle is repeated. Most regimes cases resolve by 2–3 weeks. Only • Quadriceps rarely is surgical intervention strengthening necessary. Indications include • Hamstring extensive tendinopathy in sympflexibility tomatic patients who have failed • Eccentric muscle a 3- to 6-month trial of nonoptraining erative management. Surgery 5. Rarely surgery should include débridement of

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degenerative, diseased tissue and promotion of healing by stimulating a vascular response either by linear tenotomy and/or needling. Partial Tendon Ruptures Partial ruptures of the quadriceps tendon are rare.55 Patients present with pain in the quadriceps tendon and weakness of knee extension. Typically, patients can participate in sports, but performance at high level is not possible. If the vastus intermedius tendon is injured, as often happens, there may be no clinically detectable deformity. Physical examination reveals weakness of extension when compared with the contralateral side. The ability to extend the knee from a flexed position does not exclude a partial quadriceps rupture. Rather, extension strength from a flexed position needs to be compared with the contralateral side. Plain radiographs are usually normal but may demonstrate degenerative calcific changes within the tendon. MRI is the best diagnostic test for identifying the location and extent of the injury. If a tear involves more than 50% of the quadriceps tendon, or if it is diagnosed late, surgical repair is recommended. With early diagnosis of a tear that involves less than 50% of the tendon, without tendon retraction, nonoperative management can be considered, with a 6- to 8-week period of brace immobilization. When the injury is chronic and the tendon retracted, surgical exploration of the partially torn tendon should be undertaken, and the tendon is then sutured to the patella through drill holes or with bone anchors. References 1. Reider B, Marshall JL, Koslin B: The anterior aspect of the knee joint. An anatomic study. J Bone Joint Surg Am 63:351–356, 1981. 2. Scapinelli R: Studies of the vasculature of the human knee joint. Acta Anat 70:305–331, 1968. 3. Krause BL, Williams JP, Catterall A: Natural history of OsgoodSchlatter disease. J Pediatr Orthop 10:65–68, 1990. 4. Kujala UM, Kvist M, Heinonen O: Osgood-Schlatter’s disease in adolescent athletes. Retrospective study of incidence and duration. Am J Sports Med 13:236–241, 1985. 5. Micheli L: Pediatric and adolescent sports medicine. In: Griffin LY (ed): Orthopaedic Knowledge Update: Sports Medicine. Rosemount, Ill.: American Academy of Orthopaedic Surgeons, 1994, pp 349–360. 6. De Flaviis L, Nessi R, Scaglione P, et al: Ultrasonic diagnosis of Osgood-Schlatter and Sinding-Larsen-Johansson diseases of the knee. Skeletal Radiol 18:193–197, 1989. 7. Rosenberg ZS, Kawelblum M, Cheung YY, et al: Osgood-Schlatter lesion: fracture or tendinitis? Scintigraphic, CT, and MR imaging features. Radiology 185:853–858, 1992. 8. Mital MA, Matza RA, Cohen J: The so-called unresolved OsgoodSchlatter lesion: a concept based on fifteen surgically treated lesions. J Bone Joint Surg Am 62:732–739, 1980. 9. Wall EJ: Osgood-Schlatter disease: practical treatment for a selflimiting condition. Phys Sports Med 26:136–140, 2003. 10. Badelon, O: Knee brace with limited range of motion for severe chronic articular cartilage and Osgood-Schlatter diseases. Pediatric Orthopaedic Society of North America, annual meeting program, 1996, p 117. 11. Flowers MJ, Bhadreshwar DR: Tibial tuberosity excision for symptomatic Osgood-Schlatter disease. J Pediatr Orthop 15:292–297, 1995. 12. Medlar RC, Lyne ED: Sinding-Larsen-Johansson disease. Its etiology and natural history. J Bone Joint Surg Am 60:1113–1116, 1978. 13. Espejo-Baena A, Urbano-Labajos V, Lopez-Arevalo R, et al: A case of apophysitis of the proximal patella. Am J Sports Med 28:583–585, 2000.

14. Micheli LJ, Klein JD: Sports injuries in children and adolescents. Br J Sports Med 25:6–9, 1991. 15. Micheli LJ: Overuse injuries in children’s sports: the growth factor. Orthop Clin North Am 14:337–360, 1983. 16. Micheli LJ, Glassman R, Klein M: The prevention of sports injuries in children. Clin Sports Med 19:821–834, 2000. 17. Roach R, Maffulli N: Childhood injuries in sport. Phys Ther Sport 4:58–66, 2003. 18. Baxter-Jones AD, Helms P, Maffulli N, et al: Growth and development of male gymnasts, swimmers, soccer and tennis players: a longitudinal study. Ann Hum Biol 22:381–394, 1995. 19. Baxter-Jones AD, Maffulli N: Intensive training in elite young female athletes. Effects of intensive training on growth and maturation are not established. Br J Sports Med 36:13–15, 2002. 20. Torstensen ET, Bray BC, Wiley JP: Patellar tendinitis: a review of current concepts and treatment. Clin J Sport Med 4:77–82, 1994. 21. King JB, Cook JL, Khan KM, et al: Patellar tendinopathy. Sports Med Arthrosc Rev 8:86–95, 2000. 22. Panni AS, Tartarone M, Maffulli N: Patellar tendinopathy in athletes. Outcome of nonoperative and operative management. Am J Sports Med 28:392–397, 2000. 23. Khan KM, Maffulli N, Coleman BD, et al: Patellar tendinopathy: some aspects of basic science and clinical management. Br J Sports Med 32:346–355, 1998. 24. Khan KM, Bonar F, Desmond PM, et al: Patellar tendinosis (jumper’s knee): findings at histopathologic examination, US, and MR imaging. Victorian Institute of Sport Tendon Study Group. Radiology 200:821–827, 1996. 25. Davies SG, Baudouin CJ, King JB, et al: Ultrasound, computed tomography and magnetic resonance imaging in patellar tendinitis. Clin Radiol 43:52–56, 1991. 26. Kannus P, Jozsa L: Histopathological changes preceding spontaneous rupture of a tendon. A controlled study of 891 patients. J Bone Joint Surg Am 73:1507–1525, 1991. 27. Waterston SW, Maffulli N, Ewen SW: Subcutaneous rupture of the Achilles tendon: basic science and some aspects of clinical practice. Br J Sports Med 31:285–298, 1997. 28. Maffulli N, Khan KM, Puddu G: Overuse tendon conditions: time to change a confusing terminology. Arthroscopy 14:840–843, 1998. 29. Maffulli N, Binfield PM, Leach WJ, et al: Surgical management of tendinopathy of the main body of the patellar tendon in athletes. Clin J Sport Med 9:58–62, 1999. 30. King JB, Perry DJ, Mourad K, et al: Lesions of the patellar ligament. J Bone Joint Surg Br 72:46–48, 1990. 31. Ferretti A, Puddu G, Mariani PP, et al: The natural history of jumper’s knee. Patellar or quadriceps tendonitis. Int Orthop 8:239–242, 1985. 32. Van der Ent A, de Beare GAJ: Jumper’s knee, results of operative therapy. Acta Orthop Scand 55:450, 1985. 33. Blazina ME, Kerlan RK, Jobe FW, et al: Jumper’s knee. Orthop Clin North Am 4:665–678, 1973. 34. King JB, Maffulli N: Personal communication, 2003. 35. Lian O, Holen KJ, Engebrestson L, et al: Relationship between symptoms of jumper’s knee and the ultrasound characteristics of the patellar tendon among high level male volleyball players. Scan J Med Sci Sports 6:291–296, 1996. 36. Visentini PJ, Khan KM, Cook JL, et al: The VISA score: an index of the severity of jumper’s knee. J Sci Med Sport 1:24–30, 1998. 37. Maffulli N, Regine R, Carrillo F, et al: Ultrasonographic scan in knee pain in athletes. Br J Sports Med 26:93–96, 1992. 38. el Khoury GY, Brandser EA, Saltzman CL: MRI of tendon injuries. Iowa Orthop J 14:65–80, 1994. 39. Mourad K, King J, Guggiana P: Computed tomography and ultrasound imaging of jumper’s knee-patellar tendinitis. Clin Radiol 39:162–165, 1988. 40. Ferretti A, Papandrea P, Conteduca F: Knee injuries in volleyball. Sports Med 10:132–138, 1990. 41. Capasso G, Testa V, Maffulli N: Aprotinin, corticosteroids and normosaline in the management of patellar tendinopathy in athletes: a prospective randomized study. Sports Exerc Inj 3:111–115, 1997. 42. Binfield PM, Maffulli N: Surgical management of common tendinopathies. Sports Exerc Inj 3:116–122, 1997. 43. Biedert R, Vogel U, Friedrichs NF: Chronic patellar tendinitis: a new surgical technique. Sports Exerc Inj 3:150–154, 1997. 44. Orava S, Osterback L, Hurme M: Surgical treatment of patellar tendon pain in athletes. Br J Sports Med 20:167–169, 1986.

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45. Coleman BD, Khan KM, Maffulli N, et al: Studies of surgical outcome after patellar tendinopathy: clinical significance of methodological deficiencies and guidelines for future studies. Victorian Institute of Sport Tendon Study Group. Scand J Med Sci Sports 10:2–11, 2000. 46. Martens M, Wouters P, Burssens A, et al: Patellar tendinitis: pathology and results of treatment. Acta Orthop Scand 53:445–450, 1982. 47. Puddu G, Cipolla M, Cerullo G, et al: Tendinitis. In: Fox JM, Del Pizzo W (eds): The patellofemoral joint. New York: McGraw-Hill, 1993. 48. Leadbetter WB, Mooar PA, Lane GJ, et al: The surgical treatment of tendinitis. Clinical rationale and biologic basis. Clin Sports Med 11:679–712, 1992. 49. Testa V, Capasso G, Maffulli N, et al: Ultrasound-guided percutaneous longitudinal tenotomy for the management of patellar tendinopathy. Med Sci Sports Exerc 31:1509–1515, 1999. 50. Coleman BD, Khan KM, Kiss ZS, et al: Open and arthroscopic patellar tenotomy for chronic patellar tendinopathy. A retrospective out-

51.

52. 53. 54. 55.

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come study. Victorian Institute of Sport Tendon Study Group. Am J Sports Med 28:183–190, 2000. Coleman BD, Khan KM, Maffulli N, et al: Studies of surgical outcome after patellar tendinopathy: clinical significance of methodological deficiencies and guidelines for future studies. Victorian Institute of Sport Tendon Study Group. Scand J Med Sci Sports 10:2–11, 2000. Schmidt DR, Henry JH: Stress injuries of the adolescent extensor mechanism. Clin Sports Med 8:343–355, 1989. Ziess J, Saddemi SR, Ebraheim NA: MR Imaging of the quadriceps tendon: normal layered configuration and its importance in cases of tendon rupture. AJR Am J Roentgenol 159:1031–1034, 1992. Fyfe I, Stanish WD: The use of eccentric training and stretching in the treatment and prevention of tendon injuries. Clin Sports Med 11:601–624, 1992. Raatikainen T, Karpakka J, Orava S: Repair of partial quadriceps tendon rupture. Observations in 28 cases. Acta Orthop Scand 65:154–156, 1994.

Chapter 18

Osgood-Schlatter Disorder and Related Extensor Mechanism Problems Angela D. Smith

Osgood-Schlatter Osgood and Schlatter1 separately described their eponymous disorder in 1903—a painful swelling at the anterior proximal tibia noted among adolescents. The disorder of the formation and growth of the proximal tibial apophysis typically occurs during the time of the ossification of this anterior and distal extension of the proximal tibial epiphysis. The disorder is generally self-limiting, requiring little treatment aside from rest from the aggravating activities and rehabilitation of flexibility and strength deficits. However, Osgood-Schlatter lesion (OSL) or disorder can disrupt a young athlete’s training. A retrospective questionnaire study of patients attending a sports clinic found that athletes with Osgood-Schlatter disorder were completely out of training for an average of 3.2 months and had to limit their training for an average of 7.3 months.2 Anatomy The tibial tuberosity growth plate is unusual. The proximal portion has the typical columnar organization and endochondral ossification, but the distal portion has a fibrocartilaginous zone with bone formed by membranous ossification.3 The tibial tuberosity secondary ossification center first ossifies near its distal extent between 7 and 9 years of age, according to Ogden’s studies of tuberosity development.4 However, an atlas based on annual radiographic studies of healthy children, 100 boys and 100 girls, shows somewhat later development. The anterior tongue of the proximal tibial epiphysis loosely caps the metaphysis by skeletal age 8.0 years (boys) and 6.3 years (girls), caps it completely approximately 1 year later, and begins to expand 198

distally by 10.0 and 7.7 years, respectively.5 The atlas indicates that the distal ossification center begins to ossify near 12.5 years in boys and 9.5 years in girls (Figure 18–1).5 Normally the two regions of ossification later coalesce into an anterior and distal apophysis, the insertion site for the patellar tendon, which applies a traction force to the tuberosity. The two ossification centers remain separated by chondroosseous tissue until an average skeletal age of 14.0 years for boys and 11.0 years for girls,5 near the time of closure of the physis. Finally, closure of the physis proceeds from proximal to distal. Even at skeletal age 16.3 years (boys) and 14.0 years (girls), when closure of the entire proximal tibial growth plate is nearly complete, a chondral “gap” is typically found at the distal tip of the apophyseal tongue.5 Pathophysiology Patients with OSL have been found to have chronological age that correlates normally with the skeletal age at the knee, so the disorder is not likely related to a systemic growth disturbance.6 Diagnostic ultrasound examination has shown that the swelling seen in the early stages of OSL is thickening of the inferior portion of the patellar tendon. There may also be an anechoic region of edema anterior to the tibial tuberosity.7 In later stages, magnetic resonance imaging (MRI) scans have shown partial avulsion of the secondary ossification center, with some of the avulsed fragments eventually forming ossicles separate from the tuberosity.8 On plain films the partially avulsed secondary ossification center often appears fragmented (Figures 18–2 and 18–3). Some cases of OSL are initiated by trauma such as a direct blow to the anterior knee. Other cases apparently result from repetitive traction of the large quadriceps muscle force concentrated on this small apophyseal region.

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Figure 18–1 MRI scan of normal tibial tubercle development in a 12-year-old girl.

Figure 18–3 Oblique view of fragmented ossifying tibial tuberosity secondary ossification center, consistent with Osgood-Schlatter disorder.

Figure 18–2 Fragmentation of the tibial tuberosity apophysis consistent with clinical symptoms of OsgoodSchlatter disorder.

A retrospective questionnaire completed by 389 Finnish students 16–21 years of age found that of those active in sports at age 13 (the most typical age for Osgood-Schlatter disorder in their population studies), 21.2% had Osgood-Schlatter symptoms, compared with 4.5% of those students who were not active in sports.2 When all physical activity hours (school, sports, and recreation) were compared, symptomatic students engaged in physical activity 10.6 hours per week on average, compared with 6.6 hours per week for the asymptomatic group. Earlier studies suggested that Osgood-Schlatter occurred much more frequently among boys than girls.10 Although many studies have included more boys than girls in their series of patients presenting for treatment, boys may not be more predisposed than girls to develop OSL or Sinding-LarsenJohansson lesion (SLJL) if the group under consideration all participate in similar sports activities. A study of young, junior elite figure skaters found that 11 of the 92 girls’ knees had OSL or SLJL compared with 9 of 88 boys’ knees, even though the boys performed more difficult jumps than the girls.11 Training time and jumping time were similar for the boys and the girls.

Epidemiology Osgood-Schlatter disorder is one of the most common epiphyseal or apophyseal injuries seen in sports clinics. One retrospective review of 2137 consecutive patients found that of 58 epiphyseal and apophyseal injuries, 34 were OSL.9

Sinding-Larsen-Johansson Disorder Sinding-Larsen-Johansson lesion (SLJL) or disorder is also a disruption of the normal ossification process, here involving the inferior pole of the patella. Medlar and Lyne believed

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the lesion to be a traction tendonitis with partial avulsion of the patellar tendon attachment to the patella and calcification of the abnormal region of the tendon.12 That remains the most accepted hypothesis. As in Osgood-Schlatter disorder, this area may become painful either from a direct blow to the area or from repetitive traction forces. Sinding-Larsen-Johansson disorder is sometimes referred to as “jumper’s knee.” However, SLJL is seen only in children with open physes. The term jumper’s knee more properly refers to patellar tendonitis, which is seen only in mature athletes involved in activities that require explosive knee extension such as jumping or kicking. Both OSL and SLJL can be considered in the spectrum of extensor mechanism problems resulting from repetitive microtrauma that also includes quadriceps tendonitis, painful proximal multipartite patella, patellar stress fracture, and patellar tendonitis. In the adolescent the developing secondary ossification centers/adjacent growth cartilage complex is more likely to fail in tension than the bone and tendon structures of the extensor mechanism. Therefore symptoms related to repetitive traction are most likely to develop at one of these centers. Nonetheless, some young athletes have tenderness and swelling of the patellar tendon and/or Hoffa’s fat pad, in addition to OSL and SLJL. Etiology and Diagnosis Heredity Osgood-Schlatter disorder occasionally runs in families. A study of young Finnish athletes with OSL found 50 patients had 53 siblings who were active in sports and 30 who were not. Of the 37 athletic siblings old enough to have potentially shown Osgood-Schlatter symptoms, 12 had OSL. However, none of the nonathletic siblings had symptoms.2

KEY POINTS 1. The tibial tuberosity begins to ossify between 7 and 10 years of age, as the anterior portion of the proximal tibial epiphysis expands distally. 2. The tuberosity normally has two segments during development: (1) the anterior tongue extending from the proximal tibial epiphysis that develops by endochondral ossification and (2) a distal ossification center that forms from fibrocartilage and undergoes membranous ossification. These two centers remain separate until the time of physeal closure. 3. Osgood-Schlatter disorders are generally related to avulsion of the apophysis or direct trauma to it. They are more common among athletic children than in inactive children.

Growth OSL and Sinding-Larsen-Johansson disorder have been associated with the adolescent growth spurt, and both may be present concurrently (Figure 18–4). This growth spurt correlates with the development of the tibial tubercle apophysis, ossification of the inferior pole of the patella, and appearance of secondary ossification centers of the patella. During this period of rapid growth, some authors have found that patella alta is generally present,13 possibly caused by a temporarily longer femur relative to the quadriceps length. However, one group actually found patella infera among patients with OSL.14 Smith and colleagues found that young athletes with OSL, SLJL, , and patellar tendonitis were more likely to have flexibility deficits in the quadriceps muscle than those without these disorders.11 Additional support for the hypothesis that excessive tension on the extensor mechanism structures causes OSL and SLJL is found among children with cerebral palsy.15 Hirano and colleagues recently performed repeated MRI scans in a longitudinal study of boys with OSL and found that the lesion was an avulsion of the secondary ossification center, peeling the secondary ossification center free from the underlying cartilage and pulling it proximally.8 When a residual separate anterior ossicle formed, it arose from the avulsed portion. Jakob and colleagues found a greater degree of patella alta among boys who had a separate ossicle than those with OSL who did not have a separate ossicle (both with greater patella alta than a control group),16 which is consistent with both the MRI findings and the plain film patella alta etiology hypothesis. Some children may be more susceptible to these traction disorders because of relative muscle inflexibility, either

KEY POINTS 1. Both OsgoodSchlatter and Sinding-LarsenJohansson disorders are included in the spectrum of extensor mechanism problems caused by excessive tension on the growing structures. 2. Sinding-LarsenJohansson disorder, more commonly found with ballistic activities such as jumping or kicking, is often associated with patellar or fat pad tenderness.

Figure 18–4 Sinding-Larsen-Johansson and OsgoodSchlatter disorders coexisting in a patient.

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from heredity or from growth. A study of athletes attending a sports medicine clinic found that 15 of 22 athletes who were diagnosed with calcaneal apophysitis—another disorder related to muscle inflexibility—later developed OSL.2 Repetitive Trauma/Overuse The majority of Osgood-Schlatter and Sinding-LarsenJohansson disorders and painful secondary ossification centers are related to repetitive microtrauma. For example, a running athlete may have recently increased the total training load by beginning to also play soccer, or a soccer player may have increased play from one team to two teams, with six practices per week. Occasionally a minor blow to the knee may cause enough pain that the child or adolescent decides to seek medical help, but these patients are often found to have swelling and slight tenderness of the corresponding region of the opposite knee, suggesting that the minor acute trauma exacerbated a preexisting, subclinical problem that was related to repetitive microtrauma. Acute Trauma Osgood-Schlatter Disorder When an adolescent falls directly on a knee or sustains a direct blow to the front of a knee, the clinician may find it difficult to differentiate the “disconnected” bone fragment of Osgood-Schlatter disorder from a tibial tubercle apophyseal fracture. The history of OSD in the past does not necessarily mean that the post-traumatic swelling is the disorder rather than a fracture. However, unstable tibial tubercle fractures are more likely to be caused by tension than compression. For example, if a running child or adolescent trips on a log and immediately feels severe pain and then falls, the x-ray finding of a wide space between the tibial metaphysis and the tubercle likely indicates a fracture (Figure 18–5). However, injuries happen so quickly that the patient is often unable to determine whether the pain occurred before the fall (a tension injury mechanism) or at the moment of impact of the knee on the ground (a direct blow or compression injury mechanism). The patient with a simple contusion superimposed on OSL can usually perform active terminal knee extension, but the patient with a fracture usually cannot. This test is not always accurate, but it seems more sensitive for fracture than the straight leg raise test. An adolescent with a minimally displaced tibial tubercle fracture may be able to accomplish a straight leg raise if the knee is locked in extension before he or she attempts to lift it. In this situation the intact patellar retinaculum across the fully extended knee allows the supine patient to lift the leg upward. Of course, if there is a large knee effusion, full extension is usually impossible. Fracture is more likely than contusion to cause a hemarthrosis, but a fracture of the distal portion of the tubercle may not cause bleeding into the joint. Both fracture and contusion can lead to a sympathetic knee effusion that develops over several hours. The tibial tubercle fragmentation seen radiographically in OSL may resemble a fracture, particularly when accompanied by marked soft tissue swelling. Comparison views

Figure 18–5 Post-traumatic Osgood-Schlatter disorder, with healing noted as ossification in the gap between the avulsed secondary ossification center and the tibial metaphysis.

may be helpful. However, if both knees had preexisting OSL, the clear space between the tubercle and the metaphysis may be widened bilaterally. An anterior “crinkle” in the cortex, forming the posterior apex of an angle with the distal portion of the tubercle pulled significantly anterior, strongly suggests fracture. If the tibial tubercle region is very tender, swollen, and ecchymotic but the x-ray shows no significant tubercle displacement, treatment for both diagnoses will be similar, so it may not be absolutely necessary to distinguish between contusion and fracture. Although these diagnoses can generally be made clinically, plain x-rays have been used to confirm the diagnosis and rule out other disorders that may also be present. (D’Ambrosia and MacDonald reported one case each of tibial tubercle osteomyelitis and arteriovenous malformation.17) More recently, diagnostic ultrasound results have shown four categories of findings: swelling of the pretibial region, fragmentation of the ossification center, insertional thickening of the patellar tendon, and excessive fluid collection in the infrapatellar bursa.18,19 These authors have suggested that ultrasound may also be used to follow the progress of the disorder, but routine follow-up imaging is not usually needed.18,19 MRI and computed tomographic (CT) scans have shown thickening of the patellar tendon consistent with tendonitis, and a distended deep infrapatellar bursa may be noted on MRI.20

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Sinding-Larsen-Johansson Disorder Pain and swelling at the junction of the patella and the patellar tendon, with an x-ray showing a small bone fragment adjacent to the inferior patella following trauma, may represent either SLJL with contusion or a sleeve fracture of the patella (Figure 18–6). The sleeve fracture may look benign radiographically, because only a tiny patellar fragment appears avulsed. However, the visible bony fragment is a tiny part of the avulsed piece of patella because much of the articular cartilage may have also been avulsed, so it is important to rule out this diagnosis. The intraarticular patellar sleeve fracture generally causes a nearly immediate hemarthrosis, as well as considerable soft tissue ecchymosis and edema from the torn patellar retinaculum. In addition, comparison lateral radiographs in extension will reveal patella alta on the involved side. In contrast, the patient who has bruised a SLJL secondary ossification center, and possibly injured the cartilage attaching it to the body of the patella, typically has only local swelling and perhaps ecchymosis. Multipartite Secondary Ossification Centers of the Patella The most common type of persistent secondary ossification center of the patella is the superolateral one. The multiple proximal ossification centers seen relatively frequently on adolescents’ knee x-rays21 apparently fuse to the body of the patella most of the time. However, during adolescence they can become painful from repetitive microtrauma. Ogden’s group suggested that some bipartite patellae might result from stress fracture of the ossifying patella.22 It is unusual for a fall or a direct blow to the knee to dislodge a proximal secondary ossification center, but a lateral or superolateral secondary ossification center may be displaced when fracture occurs through the fibrocartilage junction between the primary and secondary patellar ossification centers. Bourne and Bianco described 16 patients who required surgical intervention for painful bipartite patellae.23 Nine developed symptoms following trauma. They found that the articular cartilage was continuous across the major portion of the patella and the secondary ossification center, but they saw motion between the two pieces. They described

KEY POINTS 1. An adolescent may have inherited a predisposition to develop OsgoodSchlatter disorder, but repeated microtrauma or a macrotraumatic episode, or both, lead to most cases. These extensor mechanism disorders often occur at times of rapid longitudinal growth. 2. The secondary ossification centers of the tibial tubercle, inferior patella, and superior patella may be avulsed partially or completely, through the chondral junction between the primary and secondary ossification centers. 3. When fragmentation of a structure is noted following a traumatic event, fracture must be considered even when known OSL, SLJL, or multipartite patella has been present.

Figure 18–6 Post-traumatic painful bipartite patella.

the articular cartilage of the patellofemoral joint as normal in appearance. This differs from my experience because the secondary ossification center’s articular cartilage has generally been soft to palpation with a probe and has appeared yellow or golden-brown. Treatment Activity modification for repetitive microtrauma symptoms. Almost all children and adolescents with symptoms related to OSL, SLJL, and bipartite or multipartite patella find their symptoms are adequately controlled simply by activity modification. They can participate in some sports and fitness activities but should temporarily avoid aggravating activities such as jumping and kicking. In my experience, knee immobilization has been required only extremely rarely for

Osgood-Schlatter Disorder and Related Extensor Mechanism Problems

symptoms related to recurrent microtrauma. I have never used a cast to treat such symptoms. Knee immobilization for symptoms caused by acute trauma. When fracture has occurred through a bipartite or fragmentation region of the patella or tibial tubercle, either slightly displaced or nondisplaced, the knee should be immobilized to provide pain relief and protection from further displacement. In almost all such cases, I have used a removable knee immobilizer rather than a cast. Initial healing sufficient to allow early rehabilitation typically occurs within 2 weeks. An immobilizer without a hinge at the knee can be removed for range-of-motion exercises within the painless range. A hinged knee brace with adjustable range of motion allows a more normal gait pattern to be attained earlier by gradually increasing the amount of knee flexion allowed by the brace. Cryotherapy. Simple ice application or ice massage is one of the best ways to control symptoms related to repetitive microtrauma. An ice pack may be applied for 20 minutes as often as every hour if needed, as long as fabric such as a thin towel is placed between the ice pack and the skin. A small bag of frozen peas or corn contours well to the knee. Many athletes find ice massage to be more convenient. They fill a Styrofoam cup with water and freeze it, then remove the lip of the cup to expose approximately 1–2 cm of ice. They then apply the ice directly to the skin over the painful area, being careful to move the ice cup over the skin constantly to avoid frostbite. This procedure requires only approximately 10 minutes. The athlete is cautioned to avoid jumping, kicking, or sprinting activities while the knee is numb from the cryotherapy to decrease the likelihood of further injury during this time. Protection from blunt trauma. Knee pads made with foam or silicone viscoelastic materials decrease compressive trauma. Some athletes with OSL prefer to cut out a relief area in the padding so that with kneeling the pressure is transferred from the floor to the pad to the area surrounding the tibial tubercle, relieving the tubercle from painful pressure. The newer silicone materials can provide protection with less bulk, secured to the knee with thin fabrics or held in place by Coban wrap or foam prewrap. Medication. Symptoms may be severe enough to require the use of nonsteroidal antiinflammatory medication. An appropriate general recommendation for an athlete is that if symptoms are severe enough to require systemic medication, then further activity modification is required. Otherwise the medication masks symptoms during sports or other activities that may cause further injury. When the day’s activities have been completed, the use of systemic medication is reasonable if cryotherapy is insufficient to control symptoms. The athlete who is competing in a very important event may choose to mask symptoms with cryotherapy or medication, but he or she should be advised of the possible risks of further injury. The likelihood of sustaining serious injury such as a displaced fracture in this situation appears to be very low, but the possibility is real, particularly if the injured area is very swollen and tender in the absence of ice and medication treatment. Counseling. Young patients with OSL are generally counseled about the possibility of avulsion of the tibial tubercle. However, the literature does not provide useful guidance

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regarding the incidence of this actually occurring. A study of 14 adolescents with 15 tibial KEY POINTS tuberosity avulsion fractures found that three knees in two 1. These disorders patients had preexisting swelling typically require only of the tibial tubercle region, but activity modification none of these was symptomatic for treatment, with before the fracture occurred.24 A cryotherapy as an search of the last 40 years in the adjunct when Medline database does not find needed. Padding the any longitudinal study of patients affected area helps with OSL who later sustained tibprotect against blunt ial tubercle avulsion. A retrospectrauma. tive review of 16 type III tibial 2. Avulsion fractures tubercle fractures found that 6 of may require surgical the patients had a previous hisreduction and tory of OSL (and 2 patients had fixation if displace25 type I osteogenesis imperfecta). ment is significant. In my experience, none of the However, most of patients treated for OSL have the avulsion subsequently avulsed the tibial fractures of these tubercle. Informally surveying secondary colleagues who are considered ossification centers pediatric sports medicine experts, are incomplete, I found that their experience was and protected similar, with only very rare mobilization allows progression of one of their a young athlete to Osgood-Schlatter patients to begin rehabilitating fracture. I would estimate that the knee even as there are roughly 50–100 patients healing progresses. with Osgood-Schlatter disorder 3. The incidence of for every single patient treated complete tibial for a tibial tubercle acute avultubercle avulsion sion injury. Very few of the fracture complicating patients treated for acute avulOsgood-Schlatter sion injury indicated that they disorder seems had preexisting symptoms in that rare. region. Rehabilitation Symptom control. The first phase of treatment of these disorders includes active rest, ice, protection against direct trauma, and possibly nonsteroidal antiinflammatory medication. The specific interventions recommended are based on the severity of the pain and swelling. If the symptoms are so severe that the athlete cannot walk normally, knee immobilization can be used to allow weight-bearing that is less painful. Crutches may be useful for a few days if pain is severe, such as following acute trauma. A knee immobilizer can be removed for bathing and range-of-motion exercises. In the case of severe inflammation, ice massage is possible as well, when the knee immobilizer is removed. Also, the patient can remove the knee immobilizer to walk around the house when symptoms allow, but he or she should use it for walking longer distances, such as in school. This may decrease the severity of associated muscle atrophy by minimizing the length of time of immobilization. The length of the recommended rest period is highly variable. Therefore it is best based on the patient’s function rather than on a defined length of time. If symptoms are severe enough to require immobilization, the immobilization

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is discontinued as soon as the patient can achieve normal gait and normal range of motion. Running is not allowed until normal walking is possible. Kicking, jumping, and sports that require sudden deceleration are not allowed until normal running can be achieved. Range of motion and muscle flexibility. Unless there has been recent acute trauma, the knee joint range of motion is usually normal when the hip is flexed. In keeping with the association of patella alta and decreased quadriceps flexibility with these traction disorders, an important component of treatment is to restore normal flexibility to the quadriceps, particularly the rectus femoris. In addition, clinical experience has suggested the usefulness of ensuring normal flexibility of the hamstrings and the gastrocnemius. This is particularly important for adolescents engaged in kicking or running sports. As they try to take a full stride or do a strong kicking maneuver, if the hamstrings are excessively tight, the quadriceps may contract against a relatively fixed joint because the tight hamstrings do not allow full knee extension when the ipsilateral hip is flexed. Strength training. Adolescents with OSL or SLJL often develop associated ipsilateral quadriceps atrophy and secondary patellofemoral symptoms. Therefore it is important to incorporate strengthening exercises for the quadriceps in treatment of these disorders, particularly if quadriceps atrophy is noted. I use open chain progressive resistive exercise (PRE), straight leg raise exercises, and closed chain activities. In the closed chain activities, the concept of pressing the knees over

the toes is emphasized, rather than allowing the knees to go medial to the toes. In addition, if an athlete can pursue more advanced physical therapy instruction, functional training of the entire kinetic chain that includes improving core stability and optimizing sport-specific skills and technique is recommended (Technical Note 18–1). Surgery

KEY POINTS 1. Initial therapy is for pain control and includes activity modification, cryotherapy, and medication as needed. 2. Strength and flexibility deficits should be identified and corrected. In addition to restoration of muscle bulk alone, the dynamic function of the entire lower extremity kinetic chain should be addressed. The ability to do a partial squat with the knees directly over the toes is an important parameter to restore.

Displaced fractures. Displaced fractures should be reduced and usually require internal fixation to hold the reduction. The indications and techniques are discussed in Chapter 19. Following surgery for acute injury, rehabilitation may proceed as discussed previously. Late sequelae. Lynch and Walsh reported growth retardation leading to recurvatum deformity in the dominant kicking leg of two soccer players, ages 12 and 14.26 A few additional cases have been reported,3,27 Text continued on p. 209

TECHNICAL NOTE 18–1

Osgood-Schlatter Physical Therapy Protocol Carl Gustafson

NOTE: The Osgood-Schlatter protocol should be progressed pain free. The objective is to try to minimize pain by limiting range of motion, resistance, or frequency. If an exercise causes pain, refrain from that exercise until you talk with your physical therapist or athletic trainer (Table 18–1).

Strengthening All exercises should be progressed to two sets of 15, then add resistance in the form of weights for straight leg raises, short arc lifts, or leg presses. Add height for step-up exercises.

Table 18-1 Exercises for Osgood-Schlatter Disorders and Related Extensor Mechanism Problems Associated Diagnoses

Resistance Exercises

OsgoodStraight Schlatter leg Sindingraising LarsenShort arc Johannson quad set Step-up

Stretches Rectus femoris Hamstring Iliotibial band Adductor

Possible Contraindications Excessive knee flexion with full arc exercises may put undue stress on tibial tubercle

Continued

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TECHNICAL NOTE 18–1

Osgood-Schlatter Physical Therapy Protocol (Continued) Straight Leg Raise, Short Arc Lifts: (Figure 18–7, A and B) • Start with resistance of limb. • When adding weight (once you reach two sets of 15), add no greater than 3 lb per week. • Progress to as much as 10 lb if pain free (discuss with physical therapist/athletic trainer, progression to machines). • Frequency: do exercises with up to 5 lb daily (if recovered in terms of no pain or joint/muscle soreness from last workout), 6–10 lb three times per week.

Leg Press: (Figure 18–8) • Add weight as tolerated (2 lb at 15 repetitions). • Do exercise one leg at a time unless you have a bilateral condition. • Progress exercises to every other day until you do not recover in between workouts, then go to three times per week. Step-ups: (Figure 18–9) • Progress up to 8-inch step on a daily basis. Once you get to 8-inch step, step farther back in lunge fashion. Do only three times per week.

Figure 18–7 A, Straight leg raise. B, Short arc lifts.

Continued

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TECHNICAL NOTE 18–1

Osgood-Schlatter Physical Therapy Protocol (Continued)

Figure 18–8 Demonstration of a leg press.

Figure 18–9 Demonstration of step-ups.

Stretching: (Figure 18–10, A to F) • Hold all stretches 30 seconds for three repetitions, five times per week. • Stretch daily until pain subsides, then stretch three times per week. • Quadriceps • Rectus • Iliotibal band • Hamstring • Adductors • Calf

Walking/Running Program Objective 1: Begin walking program three times per week, build up to 45 minutes pain free. Objective 2: Once you can tolerate walking and are at 70% of strength of unaffected limb, begin running 15–20 minutes, three times per week. Objective 3: Once you can tolerate jogging and have 90% strength, perform agility exercises pain free, as outlined by the physical therapist or athletic trainer. Then return to sports with doctor’s recommendation. Continued

Osgood-Schlatter Disorder and Related Extensor Mechanism Problems

TECHNICAL NOTE 18–1

Osgood-Schlatter Physical Therapy Protocol (Continued)

Figure 18–10 Stretching of quadriceps (A), rectus (B), and iliotibial band (C).

Continued

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TECHNICAL NOTE 18–1

Osgood-Schlatter Physical Therapy Protocol (Continued)

Figure 18–10—cont’d

Stretching of hamstring (D), adductors (E), and calf (F).

Continued

Osgood-Schlatter Disorder and Related Extensor Mechanism Problems

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TECHNICAL NOTE 18–1

Osgood-Schlatter Physical Therapy Protocol (Continued) Suggested Readings 1. Faigenbaum AD, Westcott WL, Loud RL, Long C: The effects of different resistance training protocols on muscular strength and endurance development in children. Pediatrics 104:1–7, 1999. 2. Feigenbaum MS, Pollack ML: Strength training: rationale for current guidelines for adult fitness programs. Phys Sports Med 25(2):44–66, 1997.

but clinically apparent recurvatum deformity resulting from OSL is fortunately quite rare. In fact, the case reported by Zimbler does not appear to be typical of the disorder.27 The patient reported symptoms consistent with bilateral Osgood-Schlatter disorder at age 11 that resolved with conservative treatment. Three years later he was noted to hyperextend his left knee (the right had no angular deformity), and corrective osteotomy was performed at age 15. The x-rays shown in the article indicate an unusual appear-

3. Feigenbaum MS, Pollack ML: Prescription or resistance training for health and disease. Med Sci Sports Exerc 3(1):38–45, 1999. 4. Metcalf JA, Roberts SO: Strength training and the immature athlete: an overview. Pediatr Nurs 19(4):325–332, 1993. 5. Woo SL: Injury and Repair of the Musculoskeletal Soft Tissues. Park Ridge, Ill.: American Academy of Orthopaedics, 1998.

ance of both the left and right tibial tuberosities, as the tongue or apophyseal section was as long as the epiphyseal section was wide. This extremely long apophyseal growth plate appears disproportionate with respect to the width and contour of the tibia, so this was unlikely a case of typical Osgood-Schlatter disorder. An ossicle resulting from an unfused fragment in OSL may be painful with kneeling, or even with repetitive running or jumping activities (Figure 18–11). The procedure

Figure 18–11 A and B, Persistent, tender ossicles in a skeletally mature boy with Osgood-Schlatter disorder.

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most frequently recommended is simple excision of the painful ossicle, with good or excellent results reported, ranging from 80–95%.1,28–31 A study of the incidence of ossicle formation and the need for its excision followed 151 knees affected with OSL in 118 patients.32 Three patients already had a separate ossicle when they were first seen by the authors. Of the remaining 115 patients, 11 more developed an ossicle that was found at surgery to be separated from the tibial tuberosity by a bursa. In just two knees there was a fibrous tissue connection with the underlying tuberosity, but in the remaining knees the ossicle was entirely separate from the tuberosity. The ossicle was attached to the patellar tendon in all cases. Surgical excision was recommended for these patients after their pain with activity and with direct palpation of the area was not relieved following an average 3.8 years of nonoperative treatment. Surgical intervention has been recommended by several authors for persistent symptoms. Although Mital’s group recommended surgical excision in almost 10% of their patients with OSL, I have excised painful ossicles (including painful proximal or lateral patellar secondary ossification centers) fewer than five times in 15 years of pediatric sports medicine practice. In one interesting case, Osgood-Schlatter ossicle excision in a skeletally mature Olympic athlete whose sport involved both forceful jumping and repeatedly landing directly on the anterior knee was strongly recommended. Despite recurrent swelling and pain, the athlete refused surgical intervention, competed in the Olympic games, and continued with a successful professional sports career. NOTE: In the editors’ experience, if surgical treatment is initiated for painful Osgood-Schlatter ossicle, resection of the ossicle alone may not relieve symptoms. Both ossicle resection and tubercleplasty with additional reduction

of the prominent tibial tubercle is necessary to relieve symptoms (Technical Note 18–2). Because an Osgood-Schlatter patient typically is active in sports and is at risk for sports-related anterior cruciate ligament rupture, there could be concern about reconstructing the ligament through the usual tunnel and with the possibly abnormal patellar tendon if the patient had a residual ossicle. Fortunately, a series of 20 patients with OsgoodSchlatter-related ossicles anterior to the tibial tuberosity underwent patellar tendon autograft through the usual bone tunnels for anterior cruciate ligament reconstruction without problem.33 In clinical practice it seems that most patients are left with a normal or prominent tibial tuberosity that causes few, if any, symptoms. Nonetheless, Krause’s group was able to examine 62 of 120 patients diagnosed with OSL over a 10-year period, and they found persistent symptoms. After excluding 12 patients who were treated with KEY POINTS a cast, they examined the natural history of OSL in 50 patients who Sequelae of returned for follow-up at an averOsgood-Schlatter or age of 9 years after diagnosis. All Sinding-Larsenproximal tibial physes were fused Johansson disorders by that time. Only three fourths of tend to be mild and these patients reported no activity insignificant, such as limitations, and three fifths had a prominent tibial 34 pain with kneeling. However, in tuberosity. Rarely, another retrospective study of excision of an unfused 21 knees affected with OSL that ossicle may be required had imaging studies completed for persistent before and after treatment, only symptoms such as three knees had un-united ossicles, difficulty kneeling. and all three knees were asympto20 matic (see Technical Note 18–2).

TECHNICAL NOTE 18–2

Osgood-Schlatter Ossicle Resection and Tubercleplasty Jason Nielson • Lyle J. Micheli

Indications It is unknown how many children with OsgoodSchlatter disease have a residuum of a painful ossicle at the tibial tubercle resection. It is believed that adequate and early conservative intervention can reduce the incidence of ossicle resection. Nonetheless, a certain number of young athletes who have acquired OsgoodSchlatter disease in early adolescence will, after reaching full maturity, have painful ossicles at the tibial tubercle (Figure 18–12). We have successfully resected a number of ossicles over the years (Figure 18–13). Over the

course of the surgical interventions, we have made several additional observations of clinical importance. It has been our experience that it is necessary not only to resect the ossicle but also, in most instances, to perform a true tubercleplasty beneath the ossicle to minimize the potential for ongoing symptoms after resection. Setup After being given adequate general anesthesia, the patient is placed supine on the operating table with a pneumatic tourniquet placed above the Continued

Osgood-Schlatter Disorder and Related Extensor Mechanism Problems

TECHNICAL NOTE 18–2

Osgood-Schlatter Ossicle Resection and Tubercleplasty (Continued)

Figure 18–12 A lateral plain film of a 12-year-old female with a symptomatic ossicle at the tibial tubercle.

involved thigh. The entire leg, including the foot and ankle, is prepped with Betadine soap and solution and draped free. The leg is elevated, exsanguinated, and the tourniquet is elevated to the appropriate level depending on the age and size of the child or adolescent. Technique It is our custom to make a curved incision in an elongated S-type fashion with the juncture of the two vertical components just over the ossicle itself. We usually make the more proximal vertical arm lateral and the distal arm medial. The dissection is carried down through the subcutaneous tissue. The

paratenon is incised in a longitudinal fashion parallel to the fibers of the patellar tendon. Dissection is carried down to the ossicle, and then careful and meticulous dissection is carried out on the medial, lateral, proximal, and distal margins of the ossicle, with a rounded mini beaver blade. The entire ossicle is removed with exacting technique to minimize the transection of additional longitudinal fibers medial and lateral to the ossicle. After the ossicle has been removed, the dissection is carried proximal and distal, parallel to the fibers at the very center of the site of ossicle resection. This enables further exposure of the underlying tibial tubercle down to the fat pad. This often also requires some additional careful dissection Continued

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TECHNICAL NOTE 18–2

Osgood-Schlatter Ossicle Resection and Tubercleplasty (Continued)

Figure 18–13 A lateral plain film of the same patient 2 years after ossicle resection and tubercleplasty.

medial and lateral at the base of the tibial tubercle until the margins of the raised tubercle above the level of the underlying tibia have been identified. Then, using curved osteotomes ranging from 6–9 mm in width, the prominent tubercle at this site is resected and smoothed with rasps and rongeurs. At this juncture, palpation should be carried out through the split patellar tendon and superficial through the skin to be sure that there are no bony prominences or margins at the site of resection. This area is lavaged with saline, and two or three loose inverted stitches of absorbable suture are used to close the defect in the tendon. The

area is then again lavaged with normal saline, and the subcuticular tissue is closed with inverted absorbable sutures, followed by a running absorbable suture in the skin. Dry dressings are applied, the tourniquet is deflated, and the patient is placed in a frame brace with adjustable rangeof-motion hinges. Postoperative Management Postoperatively, it is necessary to maintain the patient on a partial weight-bearing crutch gait with a protective knee brace. We generally set the Continued

Osgood-Schlatter Disorder and Related Extensor Mechanism Problems

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TECHNICAL NOTE 18–2

Osgood-Schlatter Ossicle Resection and Tubercleplasty (Continued) range of motion from 0 degrees of extension to 60 degrees of flexion for the first 2 weeks. Progressive range-of-motion and strengthening exercises are then instituted. The patient is generally able to advance to a crutch-free gait at 4 weeks after the resection. We generally allow sports participation to resume at 8–12 weeks after surgery, depending on the rate of rehabilitation and restoration of normal strength and function.

Summary Osgood-Schlatter disorder, Sinding-Larsen-Johansson disorder, and bipartite or multipartite patella may cause symptoms in active children and adolescents, especially those involved in running, jumping, or kicking sports. Repeated tension on the ossifying growth cartilage is the most likely etiology. Symptoms are often first noted after relatively minor trauma such as a direct blow to the area or a fall. Fracture may occur through the cartilaginous region between the secondary ossification centers and the major part of the tibial tubercle apophysis (Osgood-Schlatter) or the patella (Sinding-Larsen-Johansson and multipartite patella). Treatment for the symptoms resulting from repeated minor trauma or for minimally displaced fractures includes rest, immobilization when appropriate, and therapeutic exercise. Significantly displaced fractures require reduction and internal fixation, followed by immobilization as appropriate and rehabilitation. The symptoms in the vast majority of active children and adolescents with these disorders are typically self-limited and rarely cause sequelae that lead the patient to seek further care for the problem as an adult. References 1. Flowers MJ, Bhadreshwar DR: Tibial tuberosity excision for symptomatic Osgood-Schlatter disease. J Pediatr Orthop 15(3):292–297, 1995. 2. Kujala UM, Kvist M, Heinonen O: Osgood-Schlatter’s disease in adolescent athletes. Retrospective study of incidence and duration. Am J Sports Med 13(4):236–241, 1985. 3. Ogden JA, Southwick WO: Osgood-Schlatter’s disease and tibial tuberosity development. Clin Orthop (116):180–189, 1976. 4. Ogden JA: Radiology of postnatal skeletal development. X. Patella and tibial tuberosity. Skeletal Radiol 11(4):246–257, 1984. 5. Pyle SI, Hoerr NL: Radiographic Atlas of Skeletal Development of the Knee, 1st ed. Springfield, Ill.: Charles C Thomas, Publisher, 1995, p 82. 6. Yashar A, Loder RT, Hensinger RN: Determination of skeletal age in children with Osgood-Schlatter disease by using radiographs of the knee. J Pediatr Orthop 15(3):298–301, 1995. 7. Lanning P, Heikkinen E: Ultrasonic features of the Osgood-Schlatter lesion. J Pediatr Orthop 11(4):538–540, 1991. 8. Hirano A, Fukubayashi T, Ishii T, et al: Magnetic resonance imaging of Osgood-Schlatter disease: the course of the disease. Skeletal Radiol 31(6):334–342, 2002. 9. Collins RC: Epiphyseal injuries in athletes. Cleveland Clin Quarterly 42(4):285–295, 1975.

Suggested Readings 1. Flowers MJ, Bhadreshwar DR: Tibial tuberosity excision for symptomatic Osgood-Schlatter’s disease. J Ped Orthop 15:292–297, 1995. 2. Mital MA, Matza RA, Cohen J: The so-called unresolved Osgood-Schlatter lesion: a concept based on fifteen surgically treated lesions. J Bone Joint Surg Am 62(5):732–739, 1980.

10. Kannus PS, Nittymaki S, Jarvinen M: Athletic overuse injuries in children. A 30-month prospective follow-up study at an outpatient sports clinic. Clin Pediatr (Phila) 27(7):333–337, 1988. 11. Smith AD, Stroud L, McQueen C: Flexibility and anterior knee pain in adolescent elite figure skaters. J Pediatr Orthop 11(1):77–82, 1991. 12. Medlar RC, Lyne ED: Sinding-Larsen-Johansson disease. Its etiology and natural history. J Bone Joint Surg Am 60(8):1113–1116, 1978. 13. Aparicio G, Abril JC, Calvo E, et al: Radiologic study of patellar height in Osgood-Schlatter disease. J Pediatr Orthop 17(1):63–66, 1997. 14. Lancourt JE, Cristini JA: Patella alta and patella infra. Their etiological role in patellar dislocation, chondromalacia, and apophysitis of the tibial tubercle. J Bone Joint Surg Am 57(8):1112–1115, 1975. 15. Rosenthal RK, Levine DB: Fragmentation of the distal pole of the patella in spastic cerebral palsy. J Bone Joint Surg Am 59(7):934–939, 1997. 16. Jakob RP, von Gumppenberg S, Engelhardt P: Does Osgood-Schlatter disease influence the position of the patella? J Bone Joint Surg Br 63B(4):579–582, 1981. 17. D’Ambrosia RD, MacDonald GL: Pitfalls in the diagnosis of OsgoodSchlatter disease. Clin Orthop (110):206–209, 1975. 18. Blankstein A, Cohen I, Heim M, et al: Ultrasonography as a diagnostic modality in Osgood-Schlatter disease. A clinical study and review of the literature. Arch Orthop Trauma Surg 121(9):536–539, 2001. 19. De Flaviis L, Nessi R, Scaglione P, et al: Ultrasonic diagnosis of Osgood-Schlatter and Sinding-Larsen-Johansson diseases of the knee. Skeletal Radiol 18(3):193–197, 1989. 20. Rosenberg ZS, Kawelblum M, Cheung YY, et al: Osgood-Schlatter lesion: fracture or tendinitis? Scintigraphic, CT, and MR imaging features. Radiology 185(3):853–858, 1992. 21. Batten J, Menelaus MB: Fragmentation of the proximal pole of the patella. Another manifestation of juvenile traction osteochondritis? J Bone Joint Surg Br 67(2):249–251, 1985. 22. Ogden JA, McCarthy SM, Jokl P: The painful bipartite patella. J Pediatr Orthop 2(3):263–269, 1982. 23. Bourne MH, Bianco AJ: Bipartite patella in the adolescent: results of surgical excision. J Pediatr Orthop 10:69–73, 1990. 24. Ogden JA, Tross RB, Murphy MJ: Fractures of the tibial tuberosity in adolescents. J Bone Joint Surg Am 62(2):205–215, 1980. 25. Wiss DA, Schilz JL, Zionts L: Type III fractures of the tibial tubercle in adolescents. J Orthop Trauma 5(4):475–479, 1991. 26. Lynch MC, Walsh HP: Tibia recurvatum as a complication of OsgoodSchlatter’s disease: a report of two cases. J Pediatr Orthop 11(4):543–544, 1991. 27. Zimbler S, Merkow S: Genu recurvatum: a possible complication after Osgood-Schlatter disease. Case report. J Bone Joint Surg Am 66(7):1129–1130, 1984. 28. Binazzi R, Felli L, Vaccari V, et al: Surgical treatment of unresolved Osgood-Schlatter lesion. Clin Orthop (289):202–204, 1993. 29. Glynn MK, Regan BF: Surgical treatment of Osgood-Schlatter’s disease. J Pediatr Orthop 3(2):216–219, 1983. 30. Hogh J, Lund B: The sequelae of Osgood-Schlatter’s disease in adults. Int Orthop 12(3):213–215, 1988.

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31. Orava S, Malinen L, Karpakka J, et al: Results of surgical treatment of unresolved Osgood-Schlatter lesion. Ann Chir Gynaecol 89(4):298–302, 2000. 32. Mital MA, Matza RA, Cohen J: The so-called unresolved OsgoodSchlatter lesion: a concept based on fifteen surgically treated lesions. J Bone Joint Surg Am 62(5):732–739, 1980.

33. McCarroll JR, Shelbourne KD, Patel DV: Anterior cruciate ligament reconstruction in athletes with an ossicle associated with OsgoodSchlatter’s disease. Arthroscopy 12(5):556–560, 1996. 34. Krause BL, Williams JP, Catterall A: Natural history of OsgoodSchlatter disease. J Pediatr Orthop 10(1):65–68, 1990.

Chapter 19

Fractures in the Growing Knee in Children and Adolescents James R. Kasser

Children and adolescents today are participating in sports and recreational activities in ever-increasing numbers and at increasing levels of intensity and physical contact.1–3 Intensive training and competition schedules, with no “off season” in order to participate in multiple sports, leave no opportunity for recovery and now seem to be the hallmark of children’s participation in sports.4 Some children even engage in the socalled extreme sports: motorized dirt biking, snowmobile racing, rock climbing, and others, resulting in an unprecedented exposure to high-impact mechanisms of injury.2,5,6 Consequently, clinicians are now seeing not only more injured children but also more severely injured children, those with sports-related injuries incurring relatively greater direct economic costs than other injuries, as a result of higher rates of hospitalization and emergency room visits.7 The growing knee has been shown to be one of the more frequently injured parts during sports and recreation in children and adolescents.2,3,8 Although many sports-related knee injuries in children are minor sprains and/or strains, fractures to the immature knee can be serious injuries requiring costly hospitalization and with potentially severe limb and life-threatening complications, including nerve injuries, compartment syndromes, and vascular compromise. Fractures to growing knees are also prone to long-term complications not seen in the adult, such as growth arrest, angular deformity, or both. These complications are related to injury to the epiphyseal growth plate. Indeed, as will be discussed, fracture-related growth problems are seen more frequently in the knee region than anywhere else in the young athlete, and serious damage in this region can have a profound effect on future longitudinal development of the lower extremity. This chapter reviews key principles of the clinical management of fractures about the growing knee, highlighting the anatomical and physiological reasons for the need for

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a different clinical approach than that seen in adult knee fractures. Knowledge of these principles and differences is essential for not only the fieldside clinician dealing with a major injury, and potentially even limb-threatening problems, but also for the treating orthopedic surgeon who needs to definitively manage and anticipate the long-term complications that can manifest even years after a fracture of the growing, pediatric knee.9 Certain fractures of the knee, such as tibial spine injuries, are reviewed in detail elsewhere in this book, and some fractures that are less likely to be sports-related are not reviewed here, such as the important “floating knee,” a high-velocity injury involving the distal femur and ipsilateral proximal tibia that is most commonly seen after motor vehicle crashes.10 Anatomy, Physiology, and Biomechanics of the Growing Knee Anatomy The distal femur’s secondary center of ossification first appears in the forming fetus at approximately 9 weeks, and at the birth of a full-term gestation, it is the only epiphyseal ossification center present.11,12 It is the last epiphysis to fuse in the adult.11 The growth plates about the knee are the largest and most rapidly growing in the human body, and this accounts for the significant growth irregularities that can occur after injury, such as arrest of longitudinal growth, abnormal angular growth, or both.12,13 In their series of distal femoral physeal fracture separations, Riseborough et al.14 reported a 56% incidence of leg length discrepancy and a 26% incidence of angular deformity. 215

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The distal femoral physis accounts for approximately 70% of the overall growth of the femoral bone and 37% of the total growth of the entire lower extremity. The proximal physis of the tibia contributes to approximately 53% of the total growth of the tibia and 25% of the overall growth of the lower extremities. These are the largest and most rapidly growing physes in humans, with distal femoral growth on the order of approximately 1 cm per year and 0.66 cm of growth per year from the proximal tibial physis.11–13,15 Rapid cellular proliferation in the epiphyseal plate of the distal femur during growth is thought to result in a local cellular paucity, resulting in the relative weakness of the physis when compared with normal surrounding bone, or even with a slower-growing physis (i.e., other than the knee) in younger children.11 This is the weakest biomechanical part of the growth plate and is most susceptible to shear forces.16 With the adolescent growth spurt and puberty, a decrease in physeal strength has been observed,17 and this may be secondary to a thinning of the ring of Ranvier, which is thought to be resistant to shear forces18 and may account for the increased incidence of physeal injuries observed at puberty. For the aforementioned reasons, ligaments are considered generally stronger than growth plates and fail under strain later than the physis. Biomechanics During the adolescent growth spurt, children are beginning to take on their approximate adult size. The combination of two large, rapidly growing (and thus weak) knee physes at the ends of the two largest (longest) mechanical lever arms in the human body—the distal femur and proximal tibia— together result in substantial mechanical forces being generated with physical exertion.19 To add to this combination of apparent biomechanical disadvantages, it is recognized that the origin and insertion of ligaments about the knee also results in concentrated forces resulting in observed fracture patterns. The medial and lateral collateral ligaments, the anterior and posterior cruciate ligaments, and capsular attachments all originate from the distal femoral epiphysis (i.e., distal to the distal femoral growth plate), making this distal femoral physis extraarticular and thus vulnerable to even more concentrated forces.11–13 Only the medial heads of the gastrocnemius and the plantaris muscles originate proximal to the distal femoral physis.20 In contrast, in the proximal tibia the collateral ligaments, the pes anserinus, and the posterior cruciate ligament (PCL) cross over the physis, insert distal to it, and protect the proximal tibial epiphyseal plate from fracture. This anatomical difference to the distal femoral epiphysis may help explain why fractures of the growing knee through the distal femur are twice as frequent as those of the proximal tibia.21 This combined anatomical and biomechanical concentration of forces on the distal femoral growth plate may help explain the evolution of a distinct, undulating pattern of four separate “mammillary” bodies with interdigitating channels. These undulations, in contrast to the relatively flatter physes seen elsewhere in the upper and lower extremities, are thought to convey some stability against

shear forces.22 At the same time, however, this complex pattern may also reduce the chances of a “clean” separation of the physis during a fracture, leaving a greater predisposition to growth arrest.14 Moreover, although the irregular anatomy may convey some stability, when it does become displaced, the complexity of the distal femoral physeal plate makes anatomical reduction technically demanding because anatomical reduction is a key feature for reducing the chance of growth arrest.23 Lombardo et al.24 and Thomson25 found that longitudinal growth or angular deformity are not so dependent on the pattern of epiphyseal separation (as defined by the Salter-Harris classification discussed later) as much as on the extent of fracture displacement. Poorest outcomes were seen in cases in which greater than 50% initial displacement was noted, and early, gentle anatomical reduction under general anesthesia was strongly recommended.24 Vascular Anatomy The vascular anatomy of the knee has an important influence on the etiologies of vascular complications after fractures in this region. The popliteal artery is relatively fixed in the popliteal fossa by the adductor magnus hiatus posterior to the distal femoral epiphysis, where it is also tethered there by the nearby geniculate arterial branches (Figure 19–1). Fracture of the distal epiphyseal growth plate with displacement can lead to stretching, kinking, transaction, or even crushing of the popliteal artery. Similarly, the popliteal artery is also adjacent to the posterior surface of the proximal tibial epiphysis, which places it at risk with any fracture-related angulation of the proximal tibial metaphysis KEY POINTS (Figure 19–2). In this area the popliteal artery is held down at 1. The growth plate three different anatomical sites: about the knee is the popliteal artery at its trifurthe largest and cation, the anterior tibial artery fastest growing in by the proximal interosseous the body; hence membrane, and the posterior disturbance can tibial artery by the fibrous arch result in significant of the soleus muscle as it comes growth off and extends distal from the abnormalities. posterior fibular head. A fracture 2. Muscle and ligathrough the proximal epiphyseal ment origins and plate of the tibia with displaceinsertions about the ment and/or angulation can lead knee protect the to a dysvascular foot, despite colproximal tibial lateral circulation. physis from fracture The tibial nerve is tethered moreso than the by the proximal interosseous distal femoral membrane and the peroneal physis. nerve by the proximal part of the 3. Postfracture growth fibula and is also considered at disturbance risk for injury. Neural structures depends more on here are believed to be less teththe displacement of ered down than the popliteal the fracture than artery and therefore may escape the Salter-Harris 26 major injury more readily. The type of epiphyseal posterior neurovascular bundle separation. sits immediately behind the dis-

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SM

LG MG

MCL LCL MIGA

LIGA

Figure 19–1 Anatomy of the posterior knee showing structures at risk. Only the popliteus muscle comes between the bone and the popliteal artery. Growth plates are indicated by thickened arrows. LCL, Lateral collateral ligament; LG, lateral gastrocnemius, LIGA, lateral inferior geniculate artery; MCL, medial collateral ligament; MG, medial gastrocnemius; MIGA, medial inferior geniculate artery; SM, Semimembranosus. (Modified with permission from Beaty JH [ed]: Rockwood and Wilkins’ Fractures in Children. Philadelphia: Lippincott, Williams & Wilkins, 2001.)

tal femur and proximal tibia and is at risk for injury by angulated fractures in this region. Fracture Classification The Salter-Harris type classification of physeal fractures has been used to describe children’s long-bone growth plate fractures for more than 40 years, and despite other classifications systems being described,27–29 the Salter-Harris system is considered the standard in the literature.23 This classification system is based on the radiographic appearance of the fracture (Figure 19–3) and indicates the extent of involvement of the joint, the epiphysis, and the physis. The higher the classification, the more likely joint incongruity or growth disturbance will occur. Its popularity as a pediatric fracture classification system lies in its simplicity and overall utility (i.e., its ability to reasonably predict prognosis of the physeal injury).

Figure 19–2 Diagram showing angulated fracture with the posterior metaphyseal fragment threatening the popliteal artery (arrow). Such fractures can automatically reduce so that the position seen in the emergency room looks much better than the maximum angulation that occurred at the time of injury. Therefore clinicians should maintain a high index of suspicion with even minimally hyperextended fractures of the proximal tibial growth plate and the distal femoral growth plate.

The knee region of the growing child, however, may be the one exception to the remarkable prognostic ability of the Salter-Harris system. For example, even with SalterHarris type II fractures of the distal femur, one can see shortening and angulation occurring in up to 40% of cases, rates usually seen for type III and IV fractures.29 In most other long-bone epiphyseal fractures seen elsewhere in the body, type II fractures do not have the same extent of growth arrest problems as the knee region.30,31 Despite these limitations, the Salter-Harris classification system is widely recognized and will be used in this chapter when describing individual fracture types. Principles of the History and Physical Examination of the Injured Immature Knee History A careful history can provide important clues as to the extent of the knee injury or other accompanying injuries, and knowledge of the precise mechanism of injury helps to anticipate potential complications, some even limb threatening, such as vascular compromise or compartment syndrome. For example, the history of a high-speed, knee-onknee injury in an ice-hockey game can suggest a severe hyperextension injury, where the distal femoral or tibial metaphyseal fracture edge can angle posteriorly, threatening injury to the popliteal artery. These fractures can automatically reduce back into a nearly anatomical position, and one

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Figure 19–3 Salter-Harris type classifications of epiphyseal fractures. Left to right: I. Type I fracture through the physis. II. Type II fracture through the physis, exiting the metaphysis. III. Type III fracture through the physis, exiting the epiphysis. IV. Type IV vertical, intraarticular fracture involving both the metaphysis and the epiphysis. V. Type V fracture representing physeal crushing.

might not suspect the potential vascular injury without knowledge of the details of mechanism by history. Any clinician accepting the care of an injured child must always keep in mind the possibility of other injuries that may be present along with the knee injury. Long bone fractures are very painful and possibly deforming, and both the patient and the physician can be distracted from other injuries. In frightened children in particular, one must ask about pain elsewhere, and the physical examination should be extensive. Very young (especially under the age of 7 years) or frightened and injured children may not be able to describe the mechanism of injury or even give an accurate localization of pain. Parents, coaches, and trainers can often give reliable accounts of the mechanism of injury and other valuable details of the injury, such as postinjury ability to weightbear, or the extent and timing of swelling about the knee. The ability to weight-bear after injury is often highly correlative with a relatively benign injury. (“Oh, but after my injury I was still able to play the second half.”) History of previous or similar knee injury is also important in the serious adolescent athlete who may have had previous reconstructive knee surgery. Physical Examination Initial inspection of the injured child’s limb is best approached in a “hands-off” fashion, with initial palpation beginning with an area unlikely to be painful (e.g., the opposite knee) in order to gain some confidence of the young patient. Visual inspection for obvious deformity of the knee region is made with posterior displacement of the proximal tibial metaphysis from a hyperextension type of injury (the most common) resulting in a concavity anterior near the level of the tibial tuberosity.13 When obvious deformity exists, any unnecessary movement of the limb is avoided until a careful neurovascular examination of the distal foot is carried out and documented. Palpation of the dorsalis pedis and posterior tibialis pulses is carried out, as well as examination of nail bed capillary refill. Comparison of pulses and capillary refill (should be exactly the same as the opposite side) with the contralateral, uninjured limb provides an instant quantitative and qualitative comparison. Notation of the relative temperature and color of the affected limb compared to the other side is also documented. Palpation of compartments is also carried out. The extent of pain with passive flexion/

extension of the toes is also noted, because this can evolve into a compartment syndrome. This first examination serves as the baseline for comparison with later pulse checks, especially when movement of a deformed leg is required for stabilization and transport. Any alteration of leg alignment should be followed by a pulse check. Changes in pain levels should also be accompanied with a pulse check. Sensory examination of the lower extremity distal nerves can help assess for injury to the common peroneal nerve or the tibial nerve. Motor function is examined with active dorsiflexion and plantar flexion of the toes and the ankle. Dorsiflexion, in particular, confirms function of the peroneal nerve, because it is prone to injury. However, many children with injured, swollen lower limbs find that dorsiflexion of their foot and/or toes causes pain and therefore they will often resist when asked to do this. On occasion, all that will be observed is a flicker of the toe or ankle dorsiflexion. Documentation of peroneal nerve function is an important preoperative examination to rule out an iatrogenic cause if the peroneal nerve does not function postoperatively. Serial examinations of pulses, nerve function, and the signs and symptoms of compartment syndrome should always be planned for, carried out, and ideally documented in any traumatic injury severe enough to cause a fracture in the knee. Vascular disruption can evolve over time with progression of intimal tears and formation of thrombi or emboli. Compartment syndrome also evolves over time, and vascular compromise and compartment syndrome can coexist.32,33 The key to evolving conditions is serial examinations, and this cannot be overly stressed. If external bleeding or obvious deformity exists, open injury of the bone or joint needs to be ruled out by a thorough and circumferential examination. The size of the external wound associated with an open bony fracture is correlated with the subsequent chance of osteomyelitis developing.34 Moreover, an open fracture near the knee joint can also risk infection of the joint itself. Removal of existing bandages or splints for a true circumferential review is essential, especially if bleeding is present. Bleeding can be associated with abrasions near the knee, and close inspection of wounds is done to determine if the dermis is penetrated. Visualizing subdermal fat indicates a breach of dermis and likely surface communication with the fracture. Air in tissue on the radiograph of a fractured leg with soft tissue injury is also suggestive of an open fracture.

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Severe pain or non–weight-bearing is usually indicative of a fracture, and no manipulation of deformity is performed until after x-rays have been taken.13 When radiographs appear normal, some authors feel it is important to prove or refute a Salter-Harris type I fracture with valgus/ varus radiographs. Children, however, seldom tolerate ligamentous laxity testing or any provocative maneuvers after an acute injury.35 Although it has been estimated that 5% of cases of fracture have a concomitant ligamentous injury,9,36,37 Stanitski38 urges that stress radiography should no longer play a major role in diagnosing type I fractures given the diagnostic accuracy from magnetic resonance imaging (MRI) studies, which will clearly delineate a fracture from a ligamentous injury. In cases in which fractures are treated operatively, clinical evaluation under anesthesia for ligamentous stability after fracture stabilization should routinely be carried out as is done in adults. When MRI is not readily available, immobilization of the injured limb and repeat radiographs 10 days to 2 weeks later will show periosteal reaction and growth plate sclerosis indicative of the recent fracture. If no bony changes are seen and the patient is asymptomatic, one can reasonably mobilize the patient, as tolerated. Hemarthrosis of the knee in children has been reviewed by Stanitski et al.,39 who found that in the preadolescent, acute hemarthrosis was either an anterior cruciate ligament (ACL) (47%) or a meniscal (47%) injury, with osteochondral fracture representing fewer injuries (13%). In adolescents as in adults, however, the majority of acute hemarthrosis cases are found to be from ACL tears (65%), followed by meniscal tears (45%), then osteochondral fractures (5%). Earlier, and in a smaller prospective series that performed arthroscopy after acute traumatic hemarthrosis, Matelic et al.40 found that 67% of children between 10 and 17 years of age had an osteochondral fracture of the lateral femoral condyle or the patella. Moreover, they found that only 36% of the preoperative films identified the osteochondral fractures, concluding arthroscopy to be a valuable tool in managing acute hemarthroses in children. Effusion of the knee with inability to weight-bear is common. Compartment syndrome is considered when pain is inappropriate to the amount of medication prescribed associated with knee region swelling. Bae et al.41 showed that one of the earliest signs of impending compartment syndrome was a request for increasing narcotic medication. Consideration of appropriate dosing per kilogram is emphasized in children and adolescence because there is a tendency to underdose children with narcotics when injured,42,43 which can add confusion in assessing a patient’s pain or painkiller needs versus an actual compartment syndrome evolving.42,43 When a patient presents with an obvious ischemic leg with lost pulses, then surgical exploration of the vessels is urgently required, and every effort must be made to expedite surgical consultation. If pulses that were absent reappear after reduction, then very close monitoring with serial examinations is required, although some authors continue to advocate arteriography routinely following the reduction to search for an intimal tear that could cause a late ischemic sequela.44,45

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The authors of this chapter do not advocate any fracture manipulations until radiographs have been obtained. Perhaps the only exception to a field-side KEY POINTS reduction of deformity that is not otherwise required for stabi1. Always establish lization or transport might be an neurovascular obvious laterally dislocated patella status early in a in the athlete with a history of patient’s assessprevious lateral patellar dislocament, especially tions. A radiograph is mandatory before any fracture following any sort of reduction of manipulations. the dislocated patella because a 2. Rule out compartfracture of the patella or the ment syndrome femoral condylar ridge near the with careful serial patellofemoral groove can be presexaminations of the ent and may require management. severely injured Many examples of delayed knee. diagnosis of hip problems that 3. Ruling out an open present as knee symptoms are fracture means reported in the literature.46,47 carefully examining Sports clinicians must also the knee circumferalways be cognizant of hip probentially, especially if lems in children and adolescents blood is found near as a cause of knee symptoms in the knee. children. Acute slipped capital 4. Stress radiographs femoral epiphysis (SCFE) can should not be done be a sports-related injury and in children to can present initially with knee assess Salter-Harris pain and is often associated with I type fracture a limitation of normal internal versus ligamentous rotation of the ipsilateral hip. injury. Often, clinical examination 5. Knee pain, if shows that the reported knee difficult to explain, symptoms are of a somewhat may be hip vague nature—for example, no pathology in real point tenderness—and this children. can be a clue to suspect the hip. Imaging of the Fractured Growing Knee Radiographic Evaluation of the Injured Child’s Knee The radiographic evaluation of the child with an injured knee begins with plain anteroposterior (AP) and lateral radiographs, which should include oblique views that can help reveal fracture lines of even minimally displaced fractures that may not be appreciated on AP and lateral views.13,48 If plain films are normal and clinical suspicion is high for fracture, the author recommend computed tomography (CT) or MRI to further evaluate the injury. Technetium bone scanning can be used but has assumed a lesser role. Initial films of injured limbs, especially in children, are often of inferior quality in that they do not truly represent AP and lateral views. Children initially x-rayed are often provisionally splinted, which obscures bony detail on the x-ray and often may be poorly medicated for pain. Radiology technicians will sometimes obtain “opportunistic” films of knees from injured children that are not rotated properly for x-rays or else moved during the film process. When the treating physician needs to decide key

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elements of management based on the x-rays (e.g., angulation, displacement, joint incongruity), then high-quality repeat films should be requested immediately with a friendly reason outlined to the radiology technician. The feeling one gets reviewing quality follow-up films 2 weeks later and that now show a fracture line with 3-mm joint incongruity not appreciated on the obscured, rotated initial films is a feeling best avoided from the beginning. Some authors48 have advocated stress films to document physeal injury that is not apparent on initial films but for which a high index of suspicion for fracture exists. This is also done to assess for possible collateral ligament injury. We agree, however, with Stanitski’s approach,38 which discourages stress films to avoid further injury to the growth plate of the distal femur, which has significant potential for physeal damage sequelae. Furthermore, it seems reasonable to avoid the possibility of entrapment of the periosteum or soft tissues, in the fracture line with such stresses. Radiographs of the opposite knee can identify type I or V fractures by demonstrating traumatic narrowing of the radiolucent physis (normally 3–5 mm up to age 10).23 When the mechanism of injury to the knee suggests subluxation or dislocation of the patella, it may be helpful to obtain a “skyline” (or “sunrise”) view of the patella,49 which is a tangential view of the patella within the patellofemoral groove in a caudal-cephalic direction with the knee in flexion. Black et al.49 found damage visible on 7 of 13 (54%) cases that had skyline views and a history of subluxation or dislocation, in contrast to 1 of 158 cases that did not. Nayak et al.50 also reported on the efficacy of skyline patellar views; however, reduced flexion of an acutely injured knee somewhat limited the quality of films taken. Efforts to identify injury in the region of the patella and the patellofemoral groove should be pursued because rates of

osteochondral fracture of the patella, or lateral femoral condyle in association with patellar fractures, have been reported as high as 40% in some series.51,52 Once identified on plain films, CT scanning can further demonstrate the fracture more precisely. CT scanning is an essential and important tool for characterizing the details of fractures, especially those involving the joint space (Salter-Harris type III and higher), and is especially helpful at quantifying the size of gaps between fragments. Moreover, the ability to reconstruct joint surfaces in various planes by CT reconstructions can determine joint incongruity step-off, a key factor in determining whether surgical intervention is required in many intraarticular fractures (Figure 19–4). CT scanning also helps one understand complex, multiplanar fracture patterns that not only help plan reduction techniques and maneuvers but also plan placement of internal fixation. Jaramillo53 recommends 1-mm thick axial cuts through the fractured areas, followed by two- and threedimensional CT reconstructions in both coronal and sagittal profiles, depending on the fracture type. Newer helical CT scans can now quickly provide extremely detailed images of fractures. Jaramillo53 found MRI to be useful in the evaluation of growth plate injuries, especially before physeal closure. MRI is especially good at demonstrating bony bridges following injuries. The use of three-dimensional fatsuppressed spoiled gradient-recalled echo (SPGR) sequence is described (all cartilage is bright). MRI can be used to confirm the presence of fracture about the knee while simultaneously allowing for evaluation of surrounding soft tissue structures54; however, the superior diagnostic utility of MRI over clinical examination has not been established, and therefore it should be used judiciously when clinic

Figure 19–4 Type IV virtually bicondylar, T-type displaced distal femoral fracture. A and B show AP and lateral views of the fracture.

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Figure 19–4—cont’d C and D show CT scanning detail of the fracture that can add sufficient detail to aid in fixation (e.g., placement of screws). The CT scan, especially in (D), demonstrates that the metaphyseal fragment on the lateral side above the physis and separate from the femoral shaft fragment is, in fact, one piece, not two or more. CT scanning thus can show tremendous detail important in identifying ideal internal fixation. E and F show internal fixation, especially lacking near the joint line but nevertheless holding the fragments together.

diagnosis is uncertain and MRI findings may alter the management of the injury.55 An arteriogram or contrast MRI can be used to detect intimal tear and/or thrombosis of blood vessels following bony injury to the vascular region.44,45

Radiographs of the hip should always be considered to rule out lesions of the hip as a cause for knee region pain, with slipped capital femoral epiphysis and avascular necrosis, both of which are known to present with knee region pain.46,47

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Toward Clinical Guidelines for Knee Injury Radiographs in Children The Ottawa Knee Rules (OKR) were developed to provide an evidence-based practice guideline indicating when radiography of the injured knee should or should not be done. Initially developed and validated KEY POINTS for adult populations, the OKR exhibited a sensitivity of 100% Oblique radiograph and suggested sparing 54% of views can show patients from unnecessary and fracture lines not seen 56 costly x-rays. The adult OKR on AP and lateral criteria include age over 55 views. years, tenderness at the head of 1. “Opportunistic” the fibula, isolated tenderness of views taken the patella, inability to flex the because of the knee 90 degrees, or inability to patient’s initial pain weight-bear both immediately should not be used and at the emergency room.56,57 for definitive A prospective study in adults management if they replicated this 100% sensitivity do not represent demonstrated in adults.57 The first true AP and lateral prospective study attempted in views. a pediatric population found 2. CT scanning, with a sensitivity of 92% (97% negareconstruction tive predictive value) with a sagittal and coronal reduction of x-rays of 49%.58 views, is most helpAlthough admitting a study limiful in determining tation based on a small sample joint incongruity size, the one missed fracture in and can help plan this children’s study left the placement of authors unable to endorse the surgical hardware. OKR for routine use in children, 3. MRI can determine but nevertheless acknowledging fractures, growth the utility of the rules. In a much plate injuries, larger, prospective multicenter and the presence validation study the OKR were and extent of found to be valid and resulted in ligamentous an absolute reduction of 31.2% of disruption. 59 knee radiographs. Specific Fractures about the Growing Knee and Their Management Physeal Fractures of the Distal Femur Epidemiology Fractures through the distal femoral physis account for less than 1% of all pediatric fractures, 1–5% of all physeal fractures, and 7–15% of lower-extremity physeal fractures.11,13,21,24,60 As uncommon as this injury may appear, however, it is unfortunately frequently associated with complications, including angular deformity, leg-length discrepancy, stiffness, and acute vascular and neurological injury*; these will be discussed in more detail in the following paragraphs. Two age-related subgroups of distal femoral physeal fractures are noted in children. Juvenile-type injuries (ages 2–10 *

References 9, 14, 24, 30, 61, 62.

years) occur most commonly after a high-energy mechanism of injury such as a motor-vehicle crash,14,24 and an adolescent-age injury group (older than 11 years) is more likely to suffer relatively low-energy injuries as seen in sports.14,24 Hyperextension is the most common precise mechanism of injury; today the most common cause of hyperextension is motor vehicle crashes (44%), followed by sports-related activities (25%).13,14,24,30 Historically, these injuries occurred following entrapment of the leg in the spokes of wheels from horse carts.63 Anatomy Salter-Harris type I fractures of the distal femur involve the separation of the distal femoral physis with no involvement of the epiphysis or metaphysis. These can present with normalappearing radiographs and even CT scans, although technetium bone scanning and MRI scans will demonstrate this fracture type. Stress maneuvers associated with radiographs or fluoroscopy to establish diagnosis are discouraged because they may do damage to the epiphyseal plate and are unnecessarily distressing to the patient, especially when alternative imaging modes are available (e.g., CT, MRI, bone scanning). When alternative imaging techniques are not readily available, immobilization for 2 weeks followed by repeat x-rays with the splint or cast off should show healing fracture sclerosis and periosteal reaction. If these are not present and the patient is comfortable and able to weight-bear, then it is unlikely for fracture to have been present. Most fractures of the distal femoral physis (54%) are Salter-Harris type II fractures (Figure 19–5).13,14,23,24 The fracture line traverses the physis and then exits obliquely across one corner of the metaphysis. The pattern of attachment of the metaphyseal fragment (the so-called HollandThurston fragment) is often a reflection of the direction of the injury force, with the metaphyseal fragment opposite the direction of force. The physis secured to this metaphyseal fragment is least susceptible to growth arrest later, because this physis is not directly injured. Type III fractures have a fracture line through the physis, then the fracture exits through the epiphysis into the joint, whereas type IV fractures traverse a metaphyseal portion, cross the epiphysis, then also exit into the joint. Type III and IV fractures often benefit from CT scanning, with sagittal or coronal reconstruction, to assess for joint incongruity. Salter-Harris type V fractures are compression-crush injuries to the physeal cartilage. These fractures can be difficult to diagnose and often present later (often 6–12 months later) as asymmetric growth in the lower extremities secondary to longitudinal growth arrest, growth angulation, or both. Radiographs suggesting type V fractures can show narrowing of the normal width of the radiolucent physis (normally 3–5 mm up to age 10 years),23 especially when compared with radiographs of the opposite normal knee. Salter-Harris type V fractures should be suspected with more severe mechanisms of injury (e.g., motor vehicle crashes or falls from a substantial height). Management of Distal Femoral Epiphyseal Fractures Nondisplaced fractures can be treated with immobilization with an above-knee cast, brace, or hip spica cast for 4–6

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Figure 19–5 A to E, A 13-year-old male hockey player with a “knee-on-knee” injury with another player, showing a Salter-Harris type II fracture of the distal femur. Neurovascular examination remained intact through serial examinations. Initial AP (A) and “opportunistic” (i.e., not a true) lateral views (B), along with an oblique view (C) showing maximum apex of deformity. The Holland-Thurston metaphyseal fragment is usually found to be on the opposite side of the direction of force at the time of fracture. D and E, View after open reduction and internal fixation with 6.5-mm cannulated screws showing an attempt to engage distal cortices with all screws.

weeks; the duration and technique depend on the age of the patient.13,22,48 Serial x-rays should be obtained weekly for at least 3 weeks to ensure no secondary displacement has occurred. Displaced type I or II fractures are reduced under general anesthetic using gentle, longitudinal traction and manipulation.13 Periosteal healing bone will usually be evident by

2 weeks following fracture. Overmanipulation can damage the growth plate. Internal fixation is usually used unless displacement is minimal and the fracture is stable. Internal fixation is also used if extreme positioning is required to maintain reduction.14,25 Some fracture patterns, such as hyperextension patterns, are more predisposed to loss of reduction and should be secured, usually with percutaneous fixation.25

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When internal fixation is indicated for displaced type I fractures, large diameter pins crossing in the metaphysis proximal to the fracture may be required to avoid rotation at the fracture site. Pins should be bent and buried beneath skin to reduce the risk of infection; they may be needed for up to 3 months; however, usually less time is required. Type II fracture fixation can make use of the metaphyseal (HollandThurston) fragment, usually two cannulated 4.0- or 6.5-mm screws inserted transversely without crossing the physis. Internal fixation for both types I and II are supplemented with an above-knee cast in slight flexion for comfort and additional stability. Weekly x-rays for at least 2 weeks ensure no loss of reduction following internal fixation. Open reduction is carried out for open fractures and for any type I or II fracture that cannot be managed by closed means. Periosteal flaps can interpose into the physeal fracture line, preventing anatomical reduction. Types III and IV fractures, if truly undisplaced and stable, are treated with immobilization with careful weekly follow-up x-rays to watch for any displacement of fragments over time.48 Treating physicians should have a low threshold for CT scanning to confirm the nondisplaced nature of any intraarticular fracture (see Figure 19–4). If the initial films showing types III and IV fractures are of poor quality, or are “opportunistic” (not true AP and lateral) films, then these films should be repeated. Furthermore, fractures that seem unstable and are likely to displace may be better secured with internal fixation to avoid late loss of reduction. When frankly displaced, types III and IV fractures generally require open reduction and internal fixation to anatomically repair joint line incongruities and the disrupted physis. Non-anatomical repair of the physis often

results in bony bars across the injured physis, leading to growth arrest and possible malalignment (Figure 19–6).13 Non–weight bearing of all fracture types is necessary until healing is complete to avoid inadvertent fracture angulation or displacement. Early range of motion in a protective brace is possible in the occasional cooperative patient. Outcomes and Complications The treating physician who manages fractures in the pediatric knee must be prepared to deal with some of the most serious potential complications seen in clinical orthopedics, including possible limb-threatening problems like vascular or neurological deficits and/or compartment syndromes. Neurovascular injury occurs in approximately 2% of cases13 and is usually caused by a hyperextension deformity in which the fracture angulation forces the sharp edge of the posterior metaphysis into the popliteal artery, which is relatively fixed proximally in the popliteal fossa by the adductor magnus behind the distal femoral epiphysis. As described earlier in the anatomy section, injury to the distal femoral physis is more prone to growth arrest. Riseborough et al.14 found that younger children, ages 2–11, with fractures exhibiting initial displacement more than half the diameter of the femoral shaft were more likely to have subsequent growth problems.24,25 Some discussion with parents of injured children of the mere possibility of a physeal arrest or alignment problems following injury can later result in fewer surprised and bewildered parents when these complications become clinically evident. Follow-up at least 6 months to 1 year after the initial fracture is required to detect irregular growth as a result of physeal injury,64 which can take the form of growth

Figure 19–6 A to F, A 14-year-old motocross racer thrown off his bike after a jump sustained a Salter-Harris type IV fracture of the distal right femur and an associated, undisplaced lateral patellar fracture. A and B show AP and lateral views of the initial fracture. The lateral patellar fracture is difficult to appreciate.

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Figure 19–6—cont’d C and D show CT scanning detail of the intraarticular fracture of the distal femur and indicate a displaced patellar fracture on D. E and F show post-internal fixation views, AP, lateral, and opportunistic oblique showing satisfactory closing of the intraarticular gap. The patellar fracture did not require internal fixation but was monitored radiographically with skyline views.

deceleration14 or growth stimulation.25 Long-standing x-rays of the hips to the ankles allow the drawing of axes to determine growth abnormalities, and once established, to determine management, if required. Leg-length discrepancy (LLD) management depends on the difference in leg lengths at the cessation of growth. Angular deformity can present challenging clinical problems that may require osteotomy or hemi-epiphysiodesis. MRI is now considered the study of choice in evaluating osseous bridges after physeal injury in which three-dimensional physeal maps can demonstrate the extent of bridging and guide management.65,66 Interestingly, Hresko and Kasser9 reported physeal growth disturbance even following nonphyseal type

fractures (i.e., fractures near but not directly involving the physis of the knee), which in their series went unrecognized until an average 22 months after the injury, when gross angular deformity became clinically evident. Adult femur fractures have been shown to be associated with ipsilateral soft tissue injuries to the knee, such as ACL, medial collateral ligament (MCL), and/or meniscal injuries.67 Buckley et al.68 found similar soft tissue injuries associated with ipsilateral femur fractures in a prospective cohort of 55 children but concluded that the incidence is probably less than in adults. Nevertheless, clinical examination of the child’s knee for signs of soft tissue injury/instability following fracture fixation should be performed.

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Physeal Fractures of the Proximal Tibia Epidemiology Fracture of the proximal tibial physis is relatively rare, representing 0.5–3.0% of all physeal injuries in children.69,70 These fractures occur approximately half as frequently as physeal fractures of the distal femur. It is believed that the presence of more soft tissue structures (ligaments, tendons) crossing the tibial physis, compared with the femoral physis, may be the reason for this, because this concentrates stresses toward the tibial metaphysis instead of the epiphysis.71 Anatomy

KEY POINTS Distal femoral physeal fractures. 1. Understand fracture planes. 2. Suspect occult fracture in pediatric knee “sprains.” 3. Smooth K-wires across the physis for 3 weeks is permissible. 4. Watch for vascular problems (best done with serial examinations). 5. Plan for minimum 1-year follow-up to assess for growth disturbance. 6. Perform MRI at 6 months to assess for growth disturbance.

Most fractures occur from a hyperextension mechanism leading to displacement of the proximal metaphysis posteriorly. This apex posterior angulation of the sharp metaphyseal fracture edge can injure the popliteal artery (see Figure 19–2). A high index of suspicion should be maintained because these fractures can automatically reduce into a less sinister position, with the vascular injury already having taken place.69 Palpation of the dorsalis pedis and posterior tibialis is neces-

sary, as is documentation of nerve function. Arteriogram or contrast MRI can be used to detect intimal tear and/ or thrombosis.44,45 The neurovascular structures are especially prone to injury with proximal tibial fractures because of anatomical tethering, as described earlier in the anatomy section of this chapter (see Figures 19–1 and 19–2).22 Proximal tibial physeal fractures are also classified according to the Salter-Harris classification. Figure 19–3 outlines the classification with type I being a separation through the growth plate without involvement of the epiphysis or the metaphysis. Type II fractures include the metaphyseal fragment, and types I and II are usually secondary to a valgus stress with the metaphyseal fragment on the lateral side (Figure 19–7).48 Type III fractures extend across the proximal tibial epiphysis and extend into the joint. Type IV fractures are vertically oriented fractures extending through the metaphysis, epiphyseal plate, and the epiphysis entering into the joint, thus making both intraarticular fractures. These are therefore more clinically important and require anatomical reduction if there is any displacement. Management of Proximal Tibial Physeal Fractures Treatment goals of proximal tibial physeal fractures include a stable, anatomical reduction with protection of the growth plate from further injury. This is followed by a period of immobilization before starting range-of-motion exercises as appropriate based on stability, fixation, fracture type, and healing. Range of motion should be started as soon as possible, but only when it is safe to proceed. As with the distal

Figure 19–7 A to E, A 5-year-old boy was snow sledding and sustained a severe hyperextension injury leading to a Salter-Harris type I fracture of the proximal tibia with marked displacement. Initial attempts at closed reduction and splinting led to increasing loss of pulses heard on Doppler. With vascular compromise and clinical compartment syndrome developing, the child was taken to the operating room for multicompartmental fasciotomies. A and B, Initial AP and lateral x-rays of the knee.

(Continued)

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Figure 19–7—cont’d C and D, Following closed reduction and posterior back-slab stabilization. E, AP film showing subsequent acceptable alignment but with early evidence of post-traumatic, peri-epiphyseal bony fusion, which will lead, in a 5-year-old, to growth arrest and possible angular deformity (F). (Case courtesy Dr. Michael B. Millis, Children’s Hospital, Boston.)

femoral physis, management of individual fractures is influenced by the Salter-Harris classification of the fracture. Nondisplaced Salter-Harris I and II fractures can be treated in a long-leg cast, usually for at least 6 weeks. Younger patients can sometimes be immobilized for shorter periods. If some reduction is required, gentle traction and reduction under general anesthesia with fluoroscopic control is recommended to minimize any further damage to the physis.

Fractures of the proximal tibial physis are often in hyperextension (i.e., apex posterior angulation), and flexion is required for reduction. However, if extensive flexion is required to maintain reduction, then there is risk of vascular impairment, and it is advised then to use smooth, transphyseal Kirschner wires as internal fixation to allow immobilization in gentle flexion only. A sizable Holland-Thurston metaphyseal fragment (Salter-Harris type II fracture) would allow fixation away from the physis using screw fixation.

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Types I and II fractures that cannot be reduced closed are reduced with open reduction and internal fixation. Occasional cases of pes anserinus interposition preventing reduction of type II fractures have been reported.72,73 Types III and IV fractures, if truly undisplaced, can be managed with cast or splint immobilization. It is recommended that high-quality x-rays or CT scanning be obtained to ensure that no joint incongruity exists; occasionally, hastily obtained opportunistic x-rays done in the emergency room through a splint may not show subtle joint incongruities that are only amenable to early anatomical reduction. Moreover, weekly radiographic follow-up is necessary to monitor for loss of reduction. Displaced types III and IV fractures require open reduction and internal fixation. Outcomes and Complications Early complications include the risk of vascular complications secondary to the proximity of the popliteal artery to the posterior aspect of the proximal tibia. The popliteal artery is tethered to this region by the anterior tibial artery, which branches into the anterior compartment of the lower leg. Reports of vascular injury in 5–7% of cases render careful and ongoing clinical scrutiny mandatory.69–74 Any suspicion of problems should lead to an arteriogram and consultation with a vascular surgeon. Delay in diagnosis and surgery for a vascular injury behind a fractured growing knee is associated with a higher rate of amputation.75 Other early complications that must be looked for are compartment syndrome, peroneal nerve palsy, and ligament and meniscal injures. Long-term prognosis for proximal tibial fractures has been described as “good” for most closed fractures.48 However, open fractures, often secondary to lawn mower type injuries (the Rang modification of the Salter-Harris classification, Salter-Harris type VI fracture), can severely damage the perichondral ring of the proximal tibial physis, leading to angular deformity in up to 28% of cases or shortening in up to 19% of injured patients.61,69,70

Physeal Fractures of the Tibial Tuberosity Epidemiology The vast majority—approximately 90%—of tibial tuberosity fractures are sports-related injuries13,76–79; however, these appear to be relatively rare injuries,69,74 occurring in the older child, between the ages of 12 and 17.76,78,79 Bohler80 considered these fractures to be secondary to “jumps with a bad landing.” Watson-Jones81 believed the mechanism of injury to be either a violent contraction of the quadriceps muscle or the sudden passive flexion of the knee against a contracted quadriceps muscle,22 resulting in avulsion of the tibial tubercle physis and propagation into the proximal tibial epiphysis.76 Essentially, these are believed to be Salter-Harris type III fractures of the proximal tibial physis.13 Tibial tuberosity fractures can also be thought of as an acute apophyseal fracture that needs to be differentiated from Osgood-Schlatter disease, or the chronic avulsion of the tubercle through the apophysis.82,83 The lack of symptoms before an acute tibial tubercle fracture usually helps differentiate the two; however, a number of authors have suggested that Osgood-Schlatter disease may predate apophyseal fractures in up to 20% of patients.78,84 Classification Ogden et al.83 modified the classification developed by Watson-Jones81 to emphasize both the intraarticular extension of the fracture proximally and the comminution involved (Figure 19–8). Type I fractures involve a small avulsed fragment of the tuberosity that is displaced proximally. Type I-A indicated incomplete separation from the metaphysis, and type I-B indicated complete separation. Type II fractures involve the entire tibial tuberosity fragment, and the fracture line does not extend into the proximal tibial epiphysis. Type II-A has no comminution, and type II-B is comminuted. Type III fractures extend proximally into the anterior tibial physis with III-A showing no comminution, and type III-B has comminuted fragments.

Figure 19–8 Tibial tubercle avulsion fracture basic classification after Ogden fracture. A, Type I fracture—crosses secondary ossification center level with posterior border of insertion of patellar ligament. B, Type II fracture separates the primary and secondary ossifications center of the proximal tibial epiphysis. C, Type III propagates into the knee joint and proximal tibial epiphysis proper. (From Ogden JA, Tross RB, Murphy MJ: Fractures of the tibial tuberosity in adolescents. J Bone Joint Surg Am 62:205–215, 1980.)

Fractures in the Growing Knee in Children and Adolescents

Physical Examination Localized swelling and palpable fragments can be found inferior to the patella, which can demonstrate, in severe cases, substantial patella alta of as much as 10 cm.13 Patients with type I fractures can usually extend their knees actively unless against resistance,81 whereas patients with types II and III cannot extend their knees. Rotation of displaced fragments can tent the skin anteriorly. Most patients with type II or III fractures will have a hemarthrosis. Imaging Quality lateral x-rays with the knee in slight internal rotation will best profile the tangent of the tibial tubercle fragment(s) to classify the fracture type. Comparative views with the contralateral normal knee can assess extent of displacement and adequacy of fracture reduction. MRI

can show extension of the undisplaced fracture line into the proximal tibial epiphysis, which can be unappreciated with plain radiographs. Management Type I fractures can be managed with a cylinder or long-leg cast immobilization in full extension for 6 weeks. Displaced type I fractures and types II and III injuries are all best managed with open reduction and internal fixation via a midline vertical incision (Technical Note 19–1). Cancellous bone screws perpendicular to the tibial tubercle and aimed posteriorly into the metaphysis offer adequate fixation unless there is severe comminution, in which case threaded K-wires and periosteal sutures may be beneficial. In type III fractures that extend proximally into the joint, the meniscus should be inspected for peripheral

TECHNICAL NOTE 19–1

Open Reduction and Internal Fixation of Tibial Tubercle Fractures Mininder S. Kocher

Tibial tubercle fractures in children and adolescents represent an avulsion fracture of the tibial tubercle apophysis. These fractures typically occur during jumping from a concentric quadriceps contraction or during landing from an eccentric quadriceps contraction. Tibial tubercle fractures are classified into three types (Figure 19–9): type I (through the tibial tubercle apophysis), type II (between the tibial tubercle apophysis and the proximal tibial epiphysis), and type III (through the proximal tibial epiphysis into the joint). The type of fracture depends on the mechanism of

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injury and the stage of development of the tibial tubercle apophysis. Tibial tubercle fractures should be distinguished from chronic apophyseal pain associated with Osgood-Schlatter lesion, although acute tibial tubercle fractures may be preceded by chronic Osgood-Schlatter lesion. Indications Nondisplaced tibial tubercle fractures are treated nonoperatively. Patients are placed in a long leg cast at 30 degrees and are maintained

Figure 19–9 Classification of tibial tubercle fractures. A, Type I (through the tibial tubercle apophysis). B, Type II (between the tibial tubercle apophysis and the proximal tibial epiphysis). C, Type III (through the proximal tibial epiphysis into the joint).

Continued

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TECHNICAL NOTE 19–1

Open Reduction and Internal Fixation of Tibial Tubercle Fractures (Continued) non–weight-bearing. The leg typically is set in a cast for 6 weeks. The patient is then mobilized with physical therapy. Eccentric quadriceps contraction is avoided until 3 months after injury. Return to sports is allowed after adequate rehabilitation 3 months after injury. Displaced tibial tubercle fractures are treated with open reduction and internal fixation. Cannulated screws are usually used. Setup Open reduction and internal fixation of displaced tibial tubercle fractures is usually performed with the patient under general anesthesia. Preoperative antibiotics are routinely given. The patient is positioned supine on a radiolucent table. Intraoperative fluoroscopy is used to confirm anatomical reduction and to assess implant length. A nonsterile tourniquet is used. A bump is placed under the knee.

The fracture can be fixed with cannulated screws. In older adolescents, 6.5- or 7.3-mm cannulated screws are routinely used. In children, smooth pins are used and removed to avoid growth disturbance. Technique A midline vertical incision is made along the medial border of the tibial tubercle. Medial and lateral flaps are elevated. There is often extensive tearing of the periosteum and patellar tendon expansion. The fracture bed is cleared of debris and interposed periosteum. For type III fractures, an arthrotomy is performed to inspect the meniscus and confirm anatomical reduction. The fracture is fixed with cannulated screws in older adolescents (Figure 19–10). After anatomical reduction, two parallel guidewires are placed through the fracture fragment and checked

Figure 19–10 Type III tibial tubercle fracture treated with open reduction and internal fixation with 7.3-mm cannulated screws in a 15-year-old male basketball player. A, Preoperative lateral radiograph. B, Postoperative lateral radiograph.

Continued

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TECHNICAL NOTE 19–1

Open Reduction and Internal Fixation of Tibial Tubercle Fractures (Continued) with fluoroscopy. These are overdrilled, and appropriate-length screws are used. Washers may be added for additional fixation strength. The posterior cortex is typically engaged. Care must be taken to avoid injury to the posterior neurovascular structures. In children with more than 3 years of growth remaining, smooth wires are used for fixation and removed later. Additionally, the periosteum and patellar tendon expansion can be closed with heavy sutures to supplement the repair. After wound closure, a long leg cast at 30 degrees is applied. Postoperative Management Patients are set in a cast for 4–6 weeks postoperatively and maintained non–weight-bearing. Patients are then mobilized in a hinged knee brace. For the first 2 weeks out of the cast, patients are allowed active flexion and passive extension. The patient may weight-bear with the brace locked in extension. After 2 weeks of rehabilitation, patients are allowed weight-bearing without locking the brace and active extension. Eccentric quadriceps contraction is avoided for 3 months after surgery. Return to sports is allowed after adequate rehabilitation and quadriceps strength, usually 4 months after surgery.

detachment, tears48 or intrafragmentary entrapment. Furthermore, anatomical reduction of the intraarticular fragment must be ensured. Outcomes and Complications Most fractures of the tibial tubercle occur toward the end of growth and therefore the risk of angular deformity, such as genu recurvatum, is minimal in general.13,85,86 Compartment syndrome following fractures of the tibial tubercle has been reported, and this is likely secondary to local damage of branches of the anterior tibial recurrent artery in the region of the tibial tubercle.87,88 Zionts 48 advocates consideration of prophylactic anterior compartment fasciotomies for any patient going to the operating room for surgical repair of the tibial tubercle.

Prognosis The prognosis is good, with most patients returning to full activity. Lack of knee flexion may occur with prolonged casting. Growth disturbance with recurvatum deformity may occur in younger children; however, the tibial tubercle fractures typically occur in patients approaching skeletal maturity. Suggested Readings 1. Bruijn JD, Sanders RJ, Hansen BRH: Ossification in the patellar tendon and patella alta following sports injuries in children. Arch Orthop Trauma Surg 112:157–158, 1993. 2. Christie MJ, Dvonch VM: Tibial tuberosity avulsion fracture in adolescents. J Pediatr Orthop 1:391–394, 1981. 3. Deliyannis SN: Avulsion of the tibial tuberosity. Injury 4: 341–344, 1973. 4. Ehrenborg G: The Osgood–Schlatter lesion: a clinical and experimental study. Acta Chir Scand Suppl 288:1–36, 1962. 5. Hand WL, Hand CR, Dunn AW: Avulsion fractures of the tibial tubercle. J Bone Joint Surg Am 53:1579–1583, 1971. 6. Kaplan EB: Avulsion fracture of proximal tibial epiphysis: case report. Bull Hosp Joint Dis 24:119–122, 1963. 7. Levi JH, Coleman CR: Fracture of the tibial tubercle. Am J Sports Med 4:254–263, 1976. 8. Ogden JA, Tross RB, Murphy MJ: Fractures of the tibial tuberosity in adolescents. J Bone Joint Surg Am 62:205–215, 1980. 9. Pape JM, Goulet JM, Hensinger RN: Compartment syndrome complicating tibial tubercle avulsion. Clin Orthop 295:201–204, 1993.

Fractures of the Immature Patella Anatomy The patella is the largest sesamoid bone in the body and lies within the extensor mechanism of the knee joint adding biomechanical advantage for power knee extension. Ossification begins centrally and extends peripherally in an irregular fashion usually beginning around the age of 3, but it may not start until age 6.89 Secondary ossification centers can exist, usually in the superolateral corner of the patella, and can persist into adulthood in up to 6% of the population.11,90 Such irregular ossification and multipartite patellae can make diagnosis of fracture confusing on plain radiographs. Careful physical examination and/or MRI can be helpful in sorting out acute injuries versus anatomical variants.

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Epidemiology

Physical Examination

Patellar fractures in children are rare, making up less than 5% of all knee injuries.91,92 This is thought to be because the patella is mostly cartilage and as such has more mobility and tissue resilience than in adults.48 Fractures of the patella are usually secondary to either a direct blow or a sudden, vigorous contraction of the extensor mechanism on a bent knee. Most are related to motor vehicle crashes, and a minority (17%) are secondary to sports.92,93 Those associated with indirect injury caused by vigorous contraction of the quadriceps muscle on a flexed knee can result in an avulsion-type injury of the inferior pole of the patella, the so-called sleeve fracture. These fractures are unique in that they involve the cartilage at the inferior pole of the patella as opposed to being mostly bone. Hunt et al.94 reviewed sleeve fractures in detail and believe they are the most common type of patellar fracture in children. They believe adolescents are more susceptible, probably related to their more likely involvement in high-intensity sports such as skateboarding.95 Hunt et al.94 emphasize the two clues suggesting sleeve type injury: a palpable gap to the lower pole of the patella associated with patella alta. Furthermore, they emphasize the difficulty of diagnosis on plain radiographs because the sleeve of cartilage remaining with the patellar tendon inferiorly may be devoid of any bone and is therefore radiotranslucent, although often some specks of subchondral bone often remain. Osteochondral fractures of the patella are discussed separately in the following paragraphs.

Physical examination shows local pain, hemarthrosis, an extension lag, and often patella alta and a palpable gap. Patella alta or a palpable gap can often be noted in the displaced patellar fracture. Active extension is painful and usually impossible against resistance. Hemarthrosis is usually present with swelling and local pain, and although aspiration of hematoma with or without infiltration with local anesthetic can be useful in alleviating pain, it is unlikely to contribute to diagnostic specificity. Management In general, the principles of management of patellar fractures seen in adults apply for children and adolescents in which displacement and disruption of the patella and the extensor mechanism requires open repair.13,48

Classification Two basic fracture patterns of the immature patella have been described96: primary osseous fractures and sleeve (avulsion) fractures. Transverse fractures through the middle of the patella are the most common; however, stellate, vertical, and oblique types of fractures can also occur.93 Classification of patellar fractures is based on anatomical location and displacement of fragments. A “sleeve” fracture95 describes a sheath of cartilage pulled off the main piece of ossified patella and usually occurs in children ages 8–12.51 Grogan and co-workers51 classified the sleeve fracture into four patterns, with the pattern depending on the direction of force acting on the patella: superior, inferior, medial, and lateral. For example, a laterally dislocating patella (from an acute medial force on the patella) can leave a small fragment with a majority of the cartilaginous sling in situ medially, and with the patellar bone and small piece of sleeve displaced laterally. Imaging Anteroposterior and lateral radiographs are able to identify fractures of the main body of the patella; however, when small flecks of bone appear adjacent to the inferior pole of the patella following an acute injury, then this can suggest a sleeve type of injury, an avulsion fracture (Figure 19–11). In uncertain clinical conditions, MRI can be used to diagnose sleeve fractures.97

Figure 19–11 Diagrammatic representation of a patellar sleeve fracture in an immature knee. The patellar tendon still holds the largely cartilaginous inferior sleeve of the patella, and this usually appears with small flecks of bone on a radiograph. The majority of the bony patella is attached superiorly to the quadriceps tendon. Such sleeve fractures require open operative repair to reconstruct the anatomy. (Diagram with permission from Beaty JH [ed]: Rockwood and Wilkins’ Fractures in Children, ed 5. Philadelphia: Lippincott, Williams & Wilkins, 2001, p 1031.)

Fractures in the Growing Knee in Children and Adolescents

Osteochondral Fractures of the Patella Osteochondral fractures of the patella are caused by either direct injury of the patella against the femur or by traumatic dislocation of the patella from its patellofemoral groove. Nietosvaara et al.52 found in 72 acute pediatric patellar dislocations that 39 cases (54%) were associated with osteochondral fractures. Half of these osteochondral fragments were avulsion fracture fragments off of the medial patella. Furthermore, 50% were loose intraarticular fragments that were detached either from the patella or the lateral femoral condyle. These femoral condylar fractures consistently came from the articular surface of the lateral condylar groove (Figure 19–12). Significant hemarthrosis accompanies osteochondral fractures, and bony fragments are usually not seen radiographically until the patella is reduced into position. Furthermore, the fragments are variably made up of both bone and cartilage, and sometimes the bone appears as a mere fleck on radiographs when, in fact, the osteochondral fragment can be quite large. Arthroscopy is used to remove fragments, although if unusually large and technically feasible, reduction and fixation may be indicated using fracture repair techniques similar to those for osteochondritis dissecans. Outcomes and Complications Avascular necrosis of the patella after transverse fracture has been described96 and is seen most often in the superior pole, where blood supply is more easily anatomically isolated. Nonphyseal Fractures of the Proximal Tibia Fractures of the proximal metaphysis of the tibia not involving the growth plate are relatively rare, and their benign appearance usually suggests they are easily managed with closed reduction techniques. However, these fractures below the growth plate have earned a reputation for the development of a valgus deformity of the proximal tibia, even following appropriate management in up to 50% of cases.23,98–100 As a result, these fractures have also earned eponymous recognition, being referred to as “Cozen’s” fracture.100 Knowledge of this potential for deformity from this fracture is welcomed when a few words of warning to the

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parents at the beginning of treatment can save literally hours of tense explanation later when the child requires a corrective osteotomy. Dislocation of the Knee Joint in Children Traumatic dislocations of the knee joint in children are rare104 and are usually caused by high-velocity sports such as snow skiing or water skiing102; however, athletic causes were second to motor vehicle injuries.101 The vigilant sports clinician who encounters severe athletic knee injury in the young athlete must maintain a thorough awareness of the possibility of a knee dislocation. Green et al.103 found 32% of patients with an acute knee dislocation had an injury to the popliteal artery, and these same authors found that the vascular injury led to amputation if the injury was not surgically addressed within 6–8 hours of injury. The limb-threatening nature of knee dislocations with its potential injury to the vascular supply to the leg must always be kept in mind. The anatomical relationship of the neurovascular structures around the knee were reviewed earlier in this chapter and must be kept in mind when dealing with fractures about the knee. The ability to examine the vascular status distal to the knee is vital in avoiding the worst possible outcome of a dislocated knee—possible amputation. The ability to serially examine the severely injured leg over time is also crucial to diagnosing a developing situation. A high index of suspicion should be maintained in the severely injured knee that exhibits multiple ligamentous injuries. Many knee dislocations are not recognized because of their ability to spontaneously reduce, and it is generally accepted26 that any knee with three or more ligaments injured should be suspected of having been dislocated and should be appropriately investigated. Whether this includes vascular angiography to document an initial tear, even in the leg that was transiently pulseless but has now recovered, is debatable but may be beyond the scope of this chapter. However, timely transport to a facility providing angiographic and vascular surgeon backup is something the physician on the field must be cognizant of because of the time factor of leg viability. Nerve damage in the dislocated knee can also lead to potential permanent disability and must be considered and avoided in the overall management of pediatric knee dislocations. References

Figure 19–12 Two diagrams of a right patella showing osteochondral fractures associated with lateral dislocation of the right patella. A, An avulsion fracture of the medial facet. B, Fracture of the lateral femoral condyle. These fractures can coexist and often are not appreciated until the patella is reduced back into the patellofemoral groove. (Diagram with permission from Beaty JH [ed]: Rockwood and Wilkins’ Fractures in Children, ed 5. Philadelphia: Lippincott, Williams & Wilkins, 2001, p 1035.)

1. Purvis JM, Burke RG: Recreational injuries in children: incidence and prevention. J Am Acad Orthop Surg 9:365–374, 2001. 2. Adirim TA, Cheng TL: Overview of injuries in the young athlete. Sports Med 33:75–81, 2003. 3. Damore DT, Metzl JD, Ramundo M, et al: Patterns in childhood sports injury. Pediatr Emerg Care 19:65–67, 2003. 4. Lord J, Winell JJ: Overuse injuries in pediatric athletes. Curr Opin Pediatr 17:43–47, 2005. 5. Parker MJ, Salter KL, Lipskie TL, Joubert GI: Pediatric injuries in organized hockey: does checking make a difference? Can J Emerg Med 3(2):2001. 6. Stanitski CL: Pediatric and adolescent sports injuries. Clin Sports Med 16:613–633, 1997.

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7. Children’s Safety Network: In A Data Book of Child and Adolescent Injury. Washington DC: National Center for Education in Maternal and Child Health, p 37. (Listernick D, Finison K, Gallagher S: The problem of sports and recreational injuries. SCIPP Reports 4:2, 1983). 8. Jones MH, Simon JE, Winell: Pediatric knee fractures. Curr Opin Pediatr 17:43–47, 2005. 9. Hresko MT, Kasser JR: Physeal arrest about the knee associated with non-physeal fractures in the lower extremity. J Bone Joint Surg Am 71:698–703, 1989. 10. Letts M, Vincent N, Gouw G: The “floating knee” in children. J Bone and Joint Surg Br 68:442–446, 1986. 11. Ogden JA: Skeletal injury in the child. Philadelphia: WB Saunders, 1990. 12. Shapiro F. Pediatric Orthopedic Deformities. Basic Science, Diagnosis, and Treatment. San Diego: Academic Press, 2001. 13. Beaty JH, Kumar A: Fractures about the knee in children. J Bone Joint Surg Am 176:1870, 1994. 14. Riseborough EJ, Barrett IR, Shapiro F: Growth disturbances following distal femoral physeal fracture-separations. J Bone Joint Surg Am 65:885–893, 1983. 15. Pritchett JW: Longitudinal growth and growth-plate activity in the lower extremity. Clin Orthop Relat Res 275:274-279, 1992. 16. Salter RB, Harris WR: Injuries involving the epiphyseal plate. J Bone Joint Surg Am 45:587–622, 1963. 17. Morscher E: Strength and morphology of growth cartilage under hormonal influence of puberty. Animal experiments and clinical study on the etiology of local growth disorders during puberty. Reconstr Surg Traumatol 10:3–104, 1968. 18. Chung SMK, Batterman SC, Brighton CT: Shear strength of the human femoral capitol epiphyseal plate. J Bone Joint Surg Am 58:94–103, 1976. 19. Heinrich SD, Finney T, D’Ambrosia RD: Bony injuries about the knee. In MacEwen GD, Kasser JR, Heinrich SD (eds): Pediatric Fractures: A Practical Approach to Assessment and Treatment. Baltimore: Williams and Wilkins, 1993, p 296. 20. Netter FH: Atlas of Human Anatomy, Plate 480. Summit, NJ: CibaGeigy Corporation, 1989. 21. Mann DC, Rajmaira S: Distribution of physeal and nonphyseal fractures in 2,650 long-bone fractures in children aged 0–16 years. J Pediatr Orthop 10:713–16, 1990. 22. Flynn JM, Skaggs D, Sponseller PD, et al: The operative management of pediatric fractures of the lower extremity. J Bone Joint Surg Am 84:2288–2300, 2002. 23. Salter RB, Best T: Pathogenesis and prevention of valgus deformity following fractures of the proximal metaphyseal region of the tibia in children. In: Proceedings of the Canadian Orthopaedic Association. J Bone Joint Surg Am 45:587–622, 1963. 24. Lombardo SJ, Harvey JP Jr: Fractures of the distal femoral epiphysis. J Bone Joint Surg Am 59:742–751, 1997. 25. Thomson JD, Stricker S, Williams MM: Fracture of the distal femoral epiphyseal plate. J Pediatr Orthop 15: 474–478, 1995. 26. Giffin JR, Briard J-L: Fractures and dislocations. In Harries M, Williams, C, Stanish WD, Micheli LJ (eds): The Oxford Textbook of Sports Medicine, ed 2. Oxford: Oxford Medical Publications, 1998, p 477. 27. Ogden JA: Skeletal growth mechanism injury patterns. J Pediatr Orthop 2:371–372, 1983. 28. Shapiro F: Developmental patterns in lower-extremity length discrepancies. J Bone J Surg Am 64:639–651, 1982. 29. Shapiro F: Epiphyseal growth plate fracture-separations: a pathophysiologic approach. Orthopaedics 5: 720–736, 1982. 30. Czitrom AA, Salter RB, Willis RB: Fractures involving the distal epiphyseal plate of the femur. Intern Orthop 4:269–277, 1981. 31. Bylander B, Aronson S, Egund N, et al: Growth disturbance after physeal injury of digital femoral and proximal tibia studied by Roentgen stereophotogrammetry. Arch Orthop Trauma Surg 98: 225–235, 1981. 32. Mubarak SJ, Hargens AR: Acute compartment syndrome. Surg Clin North Am 63:539–565, 1983. 33. Willis RB, Rorabeck CH: Treatment of compartment syndrome in children. Orthop Clin North Am 21:401–412, 1990. 34. Gustilo RB, Anderson JT: Prevention of infection in the treatment of one thousand and twenty-five open fractures of long bones. J Bone Joint Surg Am 58:453–458, 1976.

35. Song KM: Knee injuries. In Staheli L (ed): Pediatric Orthopedic Secrets, 2nd ed. Philadelphia: Hanley and Belfus, 2003, p 131. 36. Pedersen HE, Serra JB: Injury to the collateral ligaments of the knee associated with femoral shaft fractures. Clin Orthop 60:119–121, 1968. 37. Shelton ML, Neer CS, Grantham SA: Occult knee ligament ruptures associated with fractures. J Trauma 11:853–856, 1971. 38. Stanitski CL: Stress view radiographs of the skeletally immature knees. A different view. J Pediatr Orthop 24:342, 2004. 39. Stanitski CL, Harvell JC, Fu F: Observations on acute knee hemarthrosis in children and adolescents. J Pediatr Orthop 13:506, 1993. 40. Matelic TM, Aronsson DD, Boyd DW Jr, LaMont RL: Acute hemarthrosis of the knee in children. Am J Sports Med 23:668–671, 1995. 41. Bae DS, Kadiyala RK, Waters PM: Acute compartment syndrome in children: contemporary diagnosis, treatment, and outcome. J Pediatr Orthop 21(5):680–688, 2001. 42. Petrack EM, Christopher NC, Kriwinsky J: Pain management in the emergency department: patterns of analgesic utilization. Pediatrics 99:711–714, 1997. 43. Friedland LR, Kulick RM: Emergency department analgesic use in pediatric trauma victims with fractures. Ann Emerg Med 23:203–207, 1994. 44. Kendall RW, Taylor DC, Salvian AJ, O’Brien P: The role of arteriography in assessing vascular injuries associated with dislocations of the knee. J Trauma 35:875–878, 1993. 45. Trieman GS, Yellin AE, Weaver FA, et al: Examination of the patient with a knee dislocation: the case for selective arteriography. Arch Surg 127:1056–1063, 1992. 46. Matava MJ, Patton CM, Luhmann S, et al: Knee pain as the initial symptom of slipped capital femoral epiphysis: an analysis of initial presentation and treatment. J Pediatr Orthop 19:455–460, 1999. 47. Boyer DW, Mickelson MR, Ponseti IV: Slipped capital femoral epiphysis: long-term follow-up study of one-hundred and twenty-one patients. J Bone Joint Surg Am 63:85–95, 1981. 48. Zionts LE: Fractures around the knee in children. J Am Acad Orthop Surg 10:345–355, 2002. 49. Black GB, Mustapha A, Reed M, Henderson B: Usefulness of the skyline view in the assessment of acute knee trauma in children. Can Assoc Radiol J 53(2):92–94, 2002. 50. Nayak RK, Bicherstaff DR: Acute traumatic patellar dislocation: the importance of the skyline view. Injury 26:347–348, 1995. 51. Grogan DP, Carey TP, Leffers D: Avulsion fractures of the patella. J Pediatr Orthop 10:721, 1990. 52. Nietosvaara Y, Aalto K, Kallio PE: Acute patellar dislocation in children: incidence and associated osteochondral fractures. J Pediatr Orthop 14:513, 1994. 53. Jaramillo D: Imaging approaches for epiphyseal assessment. In Shapiro F: Pediatric Orthopedic Deformities: Basic Science, Diagnosis and Treatment. San Diego: Academic Press, 2001, p 147. 54. Close BJ, Strouse PJ: MR of physeal fractures of the adolescent knee. Pediatr Radiol 30:756–762, 2000. 55. Kocher MS, DiCanzio J, Zurakowski D, Micheli LJ: Diagnostic performance of clinical examination and selective magnetic resonance imaging in the evaluation of intraarticular knee disorders in children and adolescents. Am J Sports Med 29:292–296, 2001. 56. Steill IG, Greenberg GH, Wells GA, et al: Derivation of a decision rule for the use of radiography in acute knee injuries. Ann Emerg Med 26:405–412, 1995. 57. Steill IG, Greenberg GH, Wells GA, et al: Prospective validation of a decision rule for the use of radiography in acute knee injuries. JAMA 275:611–615, 1996. 58. Khine H, Dorfman DH, Avner JR: Applicability of Ottawa knee rule for knee injury in children. Pediatr Emerg Care 17:401–404, 2001. 59. Bulloch B, Neto G, Plint A, et al: Validation of the Ottawa Knee Rules in children: a multicenter trial. Ann Emerg Med 42:48–55, 2003. 60. Peterson C, Peterson H: Analysis of the incidence of injuries to the epiphyseal growth plate. J Trauma 12:275, 1972. 61. Crawford AH: Fractures about the knee in children. Orthop Clin North Am 7:639–656, 1976. 62. Ehrlich MG, Zaleske DJ, Armstrong AL: Physeal biochemistry. In Uhthoff HK, Wiley JJ (eds): Behavior of the Growth Plate. New York: Raven, 1988, pp 25–29. 63. Rang M: Children’s Fractures, ed 2. Philadelphia: Lippincott, 1983, p 279.

Fractures in the Growing Knee in Children and Adolescents

64. Ogden JA: Growth slowdown and arrest lines. J Pediatr Orthop 4:409–415, 1984. 65. Borsa JJ, Peterson HA, Ehman RL: MR imaging of physeal bars. Radiology 199:683–687, 1996. 66. Craig JG, Cramer KE, Cody DD: Premature partial closure and other deformities of the growth plate: MR imaging and three dimensional modeling. Radiology 210:835–843, 1999. 67. Dickson KF, Galland MW, Barrack RL, et al: Magnetic imaging of the knee after ipsilateral femur fracture. J Orthop Trauma 16:567–571, 2002. 68. Buckley SL, Sturm PF, Tosi LL, et al: Ligamentous instability of the knee in children sustaining fractures of the femur: a prospective study with knee examination under anesthesia. J Pediatr Orthop 16:206–209, 1996. 69. Burkhart SS, Peterson HA: Fractures of the proximal tibial eminence. J Bone Joint Surg Am 61:996–1002, 1979. 70. Neer CSI: Separation of the lower femoral epiphysis. Am J Surg 99:756, 1960. 71. Roberts JM: Operative treatment of fractures about the knee. Orthop Clin North Am 21:365–379. 1990. 72. Ciszewski WA, Buschmann WR, Rudolph CN: Irreducible fracture of the proximal tibial physis in an adolescent. Orthop Rev 18:891–893, 1989. 73. Wood KB, Bradley JP, Ward WT: Pes anserinus interposition in a proximal tibial physeal fracture. A case report. Clin Orthop 264:239–242, 1991. 74. Shelton WR, Canale ST: Fractures of the tibia through the proximal tibial epiphyseal cartilage. J Bone Joint Surg Am 61:167–173, 1979. 75. Subasi M, Cakir O, Kesemenli C, et al: Popliteal artery injuries associated with fractures and dislocations about the knee. Acta Orthop Bel 259–266, 2001. 76. Christie MJ, Dvonch VM: Tibial tuberosity avulsion fractures in adolescents. J Pediat Orthop 1:391–394, 1981. 77. Hand WL, Hand CR, Dunn AW: Avulsion fractures of the tibial tubercle. J Bone Joint Surg 53-A:465–468, 1971. 78. Levi H, Coleman CR: Fracture of the tibial tubercle. Am J Sports Med 4:254–263, 1976. 79. Mirbey J, Besancenot J, Chambers RT, et al: Avulsion fractures of the tibial tuberosity in the adolescent athlete. Risk factors, mechanism of injury, and treatment. Am J Sports Med 16 336–340, 1988. 80. Bohler L: The treatment of fractures, 5th ed. New York: Grune and Stratton, 1957. 81. Watson-Jones R: Injuries of the knee. In: Watson-Jones R (ed): Fractures and Joint Injuries, ed 4. Baltimore: Williams and Wilkins, 1955, vol. 2, pp 751–800. 82. Edwards PH, Grana WA: Physeal fractures of the knee. J Am Acad Orthop Surg 3(2):63–69, 1995.

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83. Ogden JA, Tross RB, Murphy MJ: Fractures of the tibial tuberosity in adolescents. J Bone Joint Surg Am 62:205–215, 1980. 84. Stanitski CL: Acute tibial tubercle avulsion fracture. In Stanitski CL, DeLee JC, Drez D Jr (eds): Orthopaedic Sports Medicine: Principals and Practice. Philadelphia: WB Saunders, 1994, vol. 3, pp 329–334. 85. Deliyannis S: Avulsion of the tibial tubercle: report of two cases. Injury 4:341–344, 1973. 86. Gautier E, Ziran BH, Egger B, et al: Growth disturbances after injuries of the proximal tibial epiphysis. Arch Orthop Trauma Surg 118:37–41, 1998. 87. Wiss DA, Schilz JL, Zionts L: Type III fractures of the tibial tubercle in adolescents. J Orthop Trauma 5:475–479, 1991. 88. Pape JM, Goulet JA, Hensinger RN: Compartment syndrome complicating tibial tubercle avulsion. Clin Orthop 295:201–204, 1993. 89. Ogden JA: Radiology of postnatal skeletal development. X. Patella and tibial tuberosity. Skeletal Radiol 11:246–257, 1984. 90. Green WT Jr: Painful bipartite patella. A report of three cases. Clin Orthop 110:197, 1975. 91. Belman DA, Neviaser RJ: Transverse fracture of the patella in a child. J Trauma 13:917, 1973. 92. Ray JM, Hendrix J: Incidence, mechanism of injury, and treatment of fractures of the patella in children. J Trauma 32:464, 1992. 93. Maguire JK, Canale ST: Fractures of the patella in children and adolescents. J Pediatr Orthop 13:567, 1993. 94. Hunt DM, Somashekar N: A review of sleeve fractures of the patella in children. The Knee 12:3–7, 2005. 95. Houghton GR, Ackroyd CE: Sleeve fractures of the patella in children: a report of three cases. J Bone Joint Surg Br 61:165–168, 1979. 96. Herring JA: Tachdjian’s Pediatric Orthopedics, ed 3. Philadelphia: WB Saunders, 2002, p 2336. 97. Bates DG, Hresko MT, Jaramillo D: Patellar sleeve fracture: demonstration with MR imaging. Radiology 193:825–827, 1994. 98. Visser JD, Veldhuizen AG: Valgus deformity after fracture of the proximal tibial metaphysis in childhood. Acta Orthop Scand 52:663–667, 1982. 99. Balthazar DA, Pappas AM: Acquired valgus deformity of the tibia in children. J Pediatr Orthop 4:538–541, 1984. 100. Cozen L: Fracture of the proximal portion of the tibia in children followed by valgus deformity. Surg Gynecol Obstet 97:183–198, 1953. 101. Cohn SL, Taylor WC: Vascular problems of the lower extremity in athletes. Clin Sports Med 9:449–470, 1990. 102. Frassica FJ, Sim FH, Staeheli JW: Dislocation of the knee. Clin Orthop Rel Res 263:200, 1991. 103. Green NE, Allen BL: Vascular injuries associated with dislocation of the knee. J Bone Joint Surg Am 59:236–239, 1977.

Chapter 20

Meniscal Injury in the Skeletally Immature Patient Treg D. Brown

●

J.T. Davis

Injuries to the meniscus of the knee are relatively common, prompting many athletes and “weekend warriors” to seek treatment from an orthopedic surgeon.1–3 Although this topic has been extensively reviewed in the adult literature, the incidence and prevalence of such injuries in the skeletally immature patient is not well documented. As a result, information regarding the diagnosis and treatment of pediatric meniscal injuries is comparatively limited. Traumatic meniscal injuries in children younger than age 10 are exceedingly rare.4–7 Congenital malformations such as a discoid meniscus, however, may predispose the young child to meniscal damage. As the patient progresses into adolescence, meniscal tears from twisting injuries or varus/valgus loads become increasingly prevalent. Clark and Ogden studied prenatal and postnatal cadaveric knees in an effort to determine what developmental changes occur in the menisci before skeletal maturity.8 They concluded that the vascularity and physical properties of the developing menisci might result in greater reparative potential than the menisci of either adolescents or adults. This suggests that a young, healthy meniscus is not only more resistant to injury but also more likely to heal an injury if one occurred. The number of children participating in organized athletics has grown exponentially over the past few decades. This has resulted in the once rare skeletally immature meniscal injury being seen with increasing frequency. Furthermore, there are numerous reports of these injuries occurring in conjunction with chondral injuries, tibial spine fractures, and most commonly, anterior cruciate ligament (ACL) tears.9–11 Diagnosis and proper treatment of a meniscal tear and any associated injuries are essential for good long-term functioning of the skeletally immature knee.4,6,7,12 236

Histological and Gross Anatomy The menisci are C-shaped, biconcave wedges of fibrocartilage located in the medial and lateral joint compartments of the knee. They have a thick peripheral margin that tapers centrally so that the menisci are triangular in cross-section. They are attached peripherally to the joint capsule, joined anteriorly by the transverse (intermeniscal) ligament, and anchored at the intercondylar tibial eminence (Figure 20–1). Histologically, the menisci consist of a combination of interlacing collagen, elastin, water, proteoglycans, and cells. The major cell of the meniscus is the matrixproducing fibrochondrocyte, which exists in two morphological types: the oval- or spindle-shaped cell that is found mostly in the superficial portions of the meniscus, and the polygonal, cartilage-like cell that is found in the deeper interstitium.13 The extracellular matrix (ECM) is composed primarily of water (78%), whereas most of the dry weight (60–75%) is accounted for by collagen.14–16 Type I collagen (90%) is the most abundant, but variable amounts of types II, III, V, and VI can be found.13,17,18 Although most collagen fibers are arranged in a circumferential pattern, some radial, oblique, and vertically directed fibers exist.19–21 Light and electron microscopic analyses have also revealed a three-layer model of the variable interlaced collagen framework. The superficial layer consists of fine fibrils in a meshlike network; the next innermost layer has irregularly arranged collagen fibers; and the deeper middle layer consists of more organized, coarse, large fibers oriented in a tight, parallel, circumferential direction (Figure 20–2). It is this layer that allows the meniscus to resist tensile forces and act as a load transmitter in the knee joint.22,23 Other macromolecules present in the ECM include proteoglycans, glycoproteins, and elastin. Elastin accounts for approximately 0.6% of the dry weight of the meniscus, whereas noncollagenous proteins account for another 8–13%.14

Meniscal Injury in the Skeletally Immature Patient

Transverse intermeniscal ligament

Anterior cruciate ligament

Lateral meniscus

Medial collateral ligament

Ligament of Wrisberg

Medial meniscus

Posterior cruciate ligament Figure 20–1 Anatomy of the menisci viewed from above. Note the differences in position and shape of the medial and lateral menisci. (Adapted with permission from Pagnani MJ, Warren RF, Arnoczky SP, Wickiewicz TL: Anatomy of the knee. In Nicholas JA, Hershman EB [eds]: The Lower Extremity and Spine in Sports Medicine, ed 2. St Louis: Mosby, 1995, pp 581–614.)

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the lateral meniscus and the posterior cruciate ligament (PCL). The anterior horn is attached to the anterior intercondylar fossa, 6–7 mm in front of the tibial ACL origin. The tibial attachment of the joint capsule to the medial meniscus is sometimes referred to as the tibial coronary ligament. The medial meniscus is also attached to the deep fibers of the tibial (medial) collateral ligament at its mid-portion.25 The lateral meniscus covers more of the tibial plateau than does the medial meniscus and is more circular. It is only loosely attached to the joint capsule, and unlike the medial meniscus is not attached to the collateral ligament. The posterior horn attaches posteriorly to the intercondylar eminence, in front of the posterior portion of the medial meniscus. The anterior horn attaches anteriorly to the intercondylar eminence, posterior and lateral to the tibial ACL origin. The capsular attachment of the lateral meniscus is disrupted in the posterolateral portion of the knee joint by the intraarticular popliteus tendon.24 The anterior meniscofemoral (ligament of Humphry) and posterior meniscofemoral (ligament of Wrisberg) ligaments attach the posterior horn of the lateral meniscus to the medial femoral condyle around either side of the PCL. Embryology

Superficial cells

Superficial zone

Radial tie fibers

Deep zone

Random collagen fibers Deep cells

Circumferential collagen fibers

Figure 20–2 Collagen ultrastructure and cell types in the meniscus. The illustration demonstrates the collagen fiber orientation in the surface and deep zones. The radial tie fibers are also shown. Superficial meniscal cells tend to be fibroblastic, whereas the deep cells have a rounded morphology. (Reprinted with permission from Kawamura S, Lotito K, Rodeo SA: Biomechanics and healing response of the meniscus. In Drez D, DeLee JC [eds]: Operative Techniques in Sports Medicine, Philadelphia, WB Saunders, 2003, pp 68–76.)

The medial meniscus is semicircular and its length measures approximately 3.5 cm. Its anterior-posterior dimension is wider posteriorly than anteriorly and its radius of curvature is variable.24 The posterior horn attaches to the posterior intercondylar fossa between the attachments of

There have been several excellent studies characterizing the embryological development of the knee joint and meniscus.8,26,27 The lower limb bud first appears at 4 weeks’ gestation, followed by chondrification of the femur, tibia, and fibula at 6 weeks.27 At this stage of development the knee joint is a mass of blastemal cells. The blastema initially is formed as a contiguous unit and gradually separates into the knee joint with its various structures. By 8 weeks, the end of the embryological period, the meniscocapsular ligamentous complex is well defined. The medial and lateral menisci assume their characteristic semilunar “C” shape as early as 14 weeks’ gestational age.8 At this age they are highly cellular, and the rich vascular supply extends throughout the entire substance of the fetal meniscus. This structure and composition is maintained well into the postnatal period—at which time the vascularity begins to recede in a centrifugal pattern. It has been theorized that weight-bearing and knee motion cause this progressive avascularity.8,28 In addition to the changing vascularity of the meniscus during development, the cellularity decreases, and the collagen content increases (Figure 20–3, A and B). Throughout this process the growth of the menisci continues while maintaining a constant meniscal-to-tibial articular surface ratio.8 Vascularity and Healing The meniscus has long been considered a relatively avascular structure with only tenuous peripheral blood supply.29–32 In 1936, Policard32 first described the meniscal blood supply as originating from the capsular and synovial attachments, with penetration of 10–30% of the meniscal width. Nearly 50 years later, Arnoczky and Warren

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Figure 20–3 Photomicrographs of developing menisci (hematoxylin and eosin, 50X). Note the progressive decrease in cellularity and increase in intercellular matrix with increasing maturation. A, An 80-mm fetus. B, Meniscus in a 10-year-old patient. (Reprinted with permission from Clark CR, Ogden JA: Development of the menisci of human knee joint. J Bone Joint Surg Am 65:538–547, 1983.)

reported the findings of their cadaveric study of the microvascular anatomy and histology of the medial and lateral menisci.33 They described the vascular supply to the menisci as coming from the medial, lateral, and middle genicular branches of the popliteal artery, with the majority of the supply coming from the medial and lateral genicular arteries (both superior and inferior). These vessels send branches to the peripheral capsular and synovial attachments of the meniscus where a perimeniscal capillary plexus is formed (Figure 20–4). This network of capillaries then extends in a circumferential pattern and sends radial branches into the peripheral 10–30% of the meniscal stroma (Figure 20–5, A and B). The middle genicular artery contributes primarily through a vascular synovial covering, sending terminal capillary loops for 2–3 mm into the substance of the anterior and posterior horn attachments. This is in contrast to the reflected vascular synovial tissue that covers the outer 1–3 mm of the femoral and tibial articular meniscal surface. This “synovial fringe” does not contribute vessels into the meniscal substance. The distribution of meniscal vascularity plays a large role in the injured meniscus’ ability to heal. In 1936, King reproduced meniscal tears at various locations in the canine meniscus and followed them for signs of healing. On review, he concluded that meniscal tears must communicate with the peripheral blood supply in order to heal.34 Arnoczky and Warren found a mid-substance meniscal tear to heal in 10 weeks when it communicated with the peripheral margin. However, a longitudinal tear in the avascular portion failed to heal until connected to the peripheral synovial tissue through vascular access channels.35 Several subsequent studies have further supported these findings.36,37 These reports suggest that the increased vascularity of the young

Figure 20–4 Scan of 5-mm thick frontal section of the medial compartment of the knee (Spalteholz 3X). Branching radial vessels from the perimeniscal capillary plexus (PCP) can be seen penetrating the peripheral border of the medial meniscus. F, Femur; T, tibia. (Reprinted with permission from Arnoczky SP, Warren RF: Microvasculature of the human meniscus. Am J Sports Medicine 10[2]:90–95, 1982.)

child might result in a greater potential for healing in a broader variety of meniscal injuries. However, to date there are no reports to prove this. Functions of the Meniscus The meniscus was described in the past as the “functionless remains of leg muscles”38 and was even reported as a potential graft source for ACL reconstruction.39 Our present understanding of the meniscus and its role in knee function

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Figure 20–5 Superior aspect of the medial (A) and lateral (B) meniscus following vascular perfusion with India ink and tissue clearing using a modified Spalteholz technique. Note the vascularity at the periphery of the menisci, as well as at the anterior and posterior horn attachments. The absence of peripheral vasculature at the posterior lateral corner of the lateral meniscus (arrow) represents the area of passage of the popliteal tendon. (Reprinted with permission from Arnoczky SP, Warren RF: Microvasculature of the human meniscus. Am J Sports Medicine 10[2]:90–95, 1982.)

has evolved significantly since these initial misconceptions. Today it is clear that the meniscus serves a vital role in the protection and maintenance of the articular cartilage of the knee. This is achieved through an intricate balance of load sharing, shock absorption, joint contact force reduction, increased joint conformity, stability, proprioception, and by providing nutrition to the hyaline cartilage.40–50 In 1948, Fairbank reported his observations, suggesting total meniscectomy resulted in such radiographic changes as joint space narrowing and broadening of the femoral and tibial condyles.51 Since that time, results of various clinical, laboratory, and biomechanical studies have demonstrated the predictable degenerative changes that accompany a meniscus-deficient knee.40,52,53 This degenerative process is progressive and with time will only result in further deterioration. From this concept one may extrapolate that a young athlete with a meniscus-deficient knee is at an even higher risk for the development of degenerative changes earlier in life. Compressive loads across the knee joint result in a peripheral displacement of the menisci. The displacement produces tensile forces in the circumferentially orientated, predominantly type I collagen fibers. These tensile forces are transmitted as hoop stresses across the menisci, dissipating the energy of the compressive load that is transferred to the articular cartilage and subchondral bone.54,55 Various biomechanical studies22,23,42 have supported this notion, and Ahmed et al.41 showed at least 50% of the weightbearing load at the knee joint is transmitted through the meniscus when in extension, and up to 85% of the load is transmitted when the knee is at 90 degrees of flexion.41 In addition to dispersing the forces throughout its substance,

the meniscus provides a larger surface area for the load to be distributed. In the complete or partially meniscectomized knee, the reduced contact area results in a significant increase in load per unit area across the articular cartilage.43 A complete medial meniscectomy decreases the contact area by 50%,41 and a partial meniscectomy has been shown to increase contact pressures by more than 350%.54 The meniscus has been shown to provide shock absorption during impulse loading of the knee during the gait cycle. Voloshin and Wosk45 demonstrated that the shock-absorbing capacity of normal knees is approximately 20% more than in knees that had undergone complete meniscectomy. They examined the compressive load-deformation response and concluded the viscoelastic nature of the meniscus allows attenuation of the intermittent shock waves generated with walking or running. The unique semilunar structure of the menisci increases the congruity between the femoral and tibial condyles. This results in improved joint conformity and stabilization of the knee. Levy et al.46 demonstrated the role of the meniscus as a secondary stabilizer in ACL-deficient knees. Specifically, the increased size of the posterior horn of the medial meniscus was shown to help prevent anterior translation of the tibia on the femur. In addition, the posterior horn of the medial meniscus has been shown to be the least mobile segment of either medial or lateral menisci, which may further stabilize the posteromedial knee joint.56 Joint compression acts as a pumping mechanism forcing synovial fluid out of the menisci and articular cartilage.57 Arnoczky et al. has reported that increased joint conformity may play a synergistic role in the lubrication process.47

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The meniscus has also been found to contribute to proprioception of the knee. Types I and II nerve endings found in the anterior and posterior horns have been speculated to provide joint-position sense of the knee.48,49 Whether an injury to the developing meniscus leads to permanent alterations of the knee’s proprioception is certainly of theoretical concern. Clinical Evaluation As with most orthopedic injuries, the diagnosis of meniscal tears can be made with a good history and physical examination. Patients who present with acute injuries will most often describe a twisting type of mechanism or a direct blow producing a varus or valgus moment at the knee. Patients with more chronic symptoms often give a less specific history, either because they do not recall a single traumatic event or they cannot remember the specific details of the injury. Common complaints of patients with meniscal injuries include pain, swelling, stiffness, clicking, popping, locking of the knee joint, decreased range of motion, and instability. These complaints will vary according to the duration of symptoms, the pattern of the meniscal injury or tear sustained, the presence of any associated injuries, and the patient’s level of tolerance to discomfort. Patients presenting with a “locked” knee may have a bucket-handle tear of the meniscus that has displaced into the intercondylar notch. When a child or adolescent sustains an injury, a thorough history may often be more difficult to obtain. The ability to communicate details of the injury or describe the subjective discomfort is often less developed in the younger patient. This may be compounded by the inherent fear often present at this age when visiting a doctor. Therefore it is incumbent on the physician to reassure both the anxious child and the family before proceeding with the detailed history and physical. Obtaining the history of swelling, and more specifically an effusion, after an acute injury provides the physician with valuable information. An effusion resulting from an acute injury is usually a hemarthrosis, which indicates that the injury has caused bleeding into the joint. Stanitski et al. reported 47% of preadolescents (ages 7–12) and 45% of adolescents (ages 13–18) with acute knee hemarthroses had meniscal tears.11 In addition, 47–65%, respectively, had an ACL tear and 7% had osteochondral fractures. Other studies have shown up to 23% of patients with an acute knee hemarthrosis had a patellar dislocation or subluxation.58 Therefore the differential diagnosis for an injury-related hemarthrosis in a child should include meniscal tear, ACL tear, patellar dislocation, chondral injury, or fracture.9 Patients with long-term symptoms should be asked about fevers, sweats, chills, weight loss, night pain, and general malaise to rule out more serious diagnoses. The physical examination is also of critical importance in detecting meniscal tears and any other associated injuries. As with obtaining a history, however, performing a physical examination on a younger patient may at times be challenging, requiring patience and skill. A systematic approach should be used when evaluating the injured knee. This will result in a more comprehensive and reproducible examination, which in turn leads to a more reliable diagnosis. The ini-

tial assessment should begin with observation of the patient’s gait, stance, and alignment. The presence of an effusion should be sought and distinguished from the edema seen with such common conditions as prepatellar bursitis, medial collateral ligament strain, and a soft tissue contusion. The extensor mechanism should then be evaluated, looking for complete or partial ruptures, patellar apprehension or subluxation, areas of tenderness to palpation, and quadriceps atrophy. Other common areas of injury should be examined for tenderness to palpation—femoral and tibial physes, tibial tubercle, pes anserinus insertion, collateral ligaments, and the medial and lateral joint line. Acute mid-third medial meniscus tears can closely mimic or coexist with a medial collateral ligament strain and vice versa. Therefore the integrity of the collateral ligaments should be tested with varus and valgus stress at 0 and 30 degrees of knee flexion and compared to the contralateral normal knee. The ACL and PCL should be examined using the anterior and posterior drawer tests, Lachman’s test, the pivot shift test, and the quadriceps active test if a PCL injury is suspected. It should be reiterated that the ACL needs to be critically evaluated in the case of a suspected meniscal tear in the skeletally immature patient, because there is a high rate of association between these two injuries.59,60 A comprehensive examination of the young child or adolescent athlete should also include a careful examination of the patient’s hip and spine to rule out a possible injury to one of these areas resulting in a referred pain pattern to the knee. A meniscal injury will often result in several pertinent clinical findings. Effusions have been reported to be present in 51% of knees with meniscal tears.61 Hemarthrosis and recurrent effusions may represent an acute or chronic tear, respectively. A decreased range of motion will accompany a large effusion but may also represent a displaced meniscus tear. Additional motion should not be forced because it could result in further damage to the torn meniscus. Quadriceps atrophy is also commonly associated with knee effusions and should be sought. Joint line tenderness is perhaps the most consistent finding, and efforts should be made to distinguish this from collateral ligament tenderness. Stanitski62 described his technique for diagnosing meniscus tears by physical examination in children and adolescents. In his research, he found patients with medial meniscus tears to have medial joint line tenderness with pain exacerbation upon varus and rotational (internal/ external) stress while flexing the knee 30–40 degrees. Similarly, pain with valgus and rotational stress was suggestive of a lateral meniscus tear. He reported 93% accuracy, 93% sensitivity, and 92% specificity using this technique. Posterior horn tears will often produce pain when the knee is hyperflexed. In addition, the “squat test” is a useful provocative maneuver to help distinguish patellofemoral pain from posterior meniscal pain. This test is performed by having the patient achieve a squatting position in the clinic. Patellofemoral pathology will produce anterior knee pain throughout the squatting motion, whereas posterior horn tears cause pain primarily at the nadir of the maneuver.62 Pain with hyperextension may indicate the presence of an anterior horn tear, displaced meniscus tear, or loose body. McMurray’s classic test for meniscal tears is less reliable in this age group than the reported 58% sensitivity in the adult population.62,63 Similarly, Apley’s compression/distraction

Meniscal Injury in the Skeletally Immature Patient

test with the patient prone will often reproduce pain in the anxious younger patient, regardless of the underlying diagnosis. Imaging Studies

KEY POINTS 1. The diagnosis of meniscal tears can be made with a good history and physical examination. 2. Hemarthrosis and recurrent effusions may represent an acute or chronic tear, respectively. 3. Joint line tenderness is perhaps the most consistent finding, and efforts should be made to distinguish it from collateral ligament tenderness.

A young child or adolescent with a suspected meniscus tear should undergo routine radiographic assessment including anteroposterior (AP), lateral, Merchant, and intercondylar notch views. The AP and lateral views aid in detecting a fracture and/or effusion in an acute injury. The lateral view can also demonstrate extensor mechanism pathology, such as patella baja or alta. The notch view improves visualization of loose bodies and osteochondral defects or osteochondritis dissecans. The Merchant view enables evaluation of patellar alignment and detection of loose osteochondral fragments resulting from a patella dislocation. Isolated meniscal tears may reveal an effusion but are otherwise normal. Other than direct arthroscopic visualization,64 magnetic resonance imaging (MRI) is the best diagnostic modality for detecting meniscal tears. Most reports in the literature suggest poor sensitivity and specificity when using MRI to evaluate meniscal injuries in skeletally immature patients.65–67 Initial reports found the number of false-positive MRI studies to be

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more pronounced in the pediatric population.68 These findings were attributed to the evolving vascularity in the skeletally immature meniscus. High signal changes throughout the substance of a young meniscus mimic the appearance of a meniscal tear.67 Supporting these findings, Kocher and colleagues69 reported their results using MRI in children suspected of having a meniscal injury. They found MRI to be less sensitive (61.7%) and specific (90.2%) when used in children younger than age of 12 compared to children 12–16 years of age (78.2% and 95.5%, respectively). Furthermore, Stanitski70 published a study showing a highly negative correlation between arthroscopic and MRI findings of injured knees in children and adolescents (78.5%). He suggested that MRI adds little guidance to a good clinical evaluation with regard to patient management. In spite of these reports, advances in MR imaging techniques over the past several years have improved sensitivity and specificity for detecting meniscal tears in the pediatric population (Figures 20–6, A and B). Major et al.71 correlated MRI and arthroscopic findings in adolescent knee injuries. They found 92% sensitivity and 87% specificity for detecting medial meniscus tears versus 93% and 95%, respectively, for lateral meniscus tears. Although these findings are encouraging, MRI provides limited information regarding tear size, configuration, or whether a meniscal repair will be possible. In addition, caution should be used with MRI evaluation of a possible retorn meniscus repair. Standard MRI techniques will continue to demonstrate an abnormal signal even after the tear has healed.72 As with virtually all musculoskeletal injuries, an accurate diagnosis is most often made with a thorough history and physical examination. However, diagnostic studies such as MRI often enable the physician to confirm suspicions of a

Figure 20–6 A T2-weighted, fat-suppressed MR image of an adolescent knee with a displaced bucket-handle tear of a nondiscoid, medial meniscus (confirmed at the time of arthroscopy). A, Sagittal view revealing a tear of the posterior horn of the medial meniscus. B, Coronal view demonstrating a small portion of the meniscus displaced into the intercondylar notch.

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meniscus tear and assist with preoperative planning. Although magnetic resonance imaging should not be ordered for every suspected meniscus tear in the skeletally immature patient, case-specific use by the physician can aid in patient management. Discoid Meniscus

KEY POINTS 1. Advances in MR imaging techniques over the past several years have improved sensitivity and specificity for detecting meniscal tears in the pediatric population. 2. MRI provides limited information regarding tear size, configuration, or whether a meniscal repair will be possible. 3. Caution should be used with MRI evaluation of a possible retorn meniscus repair. Standard MRI techniques will continue to demonstrate an abnormal signal even after the tear has healed.

The discoid meniscus is a unique congenital malformation that deserves special mention. Three main types are commonly encountered: type I, complete; type II, incomplete; and type III, Wrisberg variant. Type I discoid menisci cover the entire tibial plateau, whereas a type II meniscus leaves some portion of the inner plateau uncovered. Type III menisci are distinguished by the absence of the posterior capsular attachments. Furthermore, the type III menisci tend to be more normal in appearance with only a thickened posterior horn (Figure 20–7). Watanabe and Takeda’s 1974 classification73 is most commonly used to describe discoid menisci. Neuschwander and colleagues, however, recently coined the phrase “lateral meniscal variant” to better describe the type III meniscus and its nondiscoid shape.74 The lateral meniscus tends to show more variability in size and shape during development. As a result, the formation of a congenital discoid meniscus most commonly occurs laterally. While others have written papers75–77 to

attempt to define the origin of discoid menisci, the etiology appears only partially explained. Kaplan76,77 demonstrated the discoid menisci to be a pathologic entity whose development is related to mechanical factors. This conclusion is in contrast to Smillie,75 who believed the condition was merely a persistence of the normal “meniscal disc” seen in embryological development. Clark and Ogden8 have, in essence, refuted this in their study. They showed the developing meniscus to grow at ratios corresponding to the tibial plateau and that the discoid configuration is not assumed during normal development. It was also suggested that the discoid meniscus may result from instability caused by failure of formation of the posterior meniscofemoral ligaments. The adolescent patient with a symptomatic discoid meniscus will have subjective complaints and physical findings similar to those of a patient with a developmentally normal meniscus that has torn. In contrast, young children with a discoid meniscus may notice asymptomatic “snapping” in their knee. If the discoid meniscus is subsequently injured, intermittent effusions and mechanical complaints may ensue. This is typically seen later in childhood and is usually a progressive process. The physical examination is quite similar to that seen with a torn, normally developed meniscus. Exceptions may include a more dramatic “clunk” experienced with both the McMurray maneuver and when bringing the knee into extension. This may be accompanied by an apparent shift or subluxation of the lateral compartment as an unstable type III meniscus (lateral meniscal variant) “reduces” into the knee joint.10 The presence of a visible prominence along the lateral joint line with flexion is another telltale sign. Imaging studies may be helpful in diagnosing a discoid meniscus in the young athlete. Plain radiographs are typically normal; however, a small percentage of discoid menisci will demonstrate subtle findings on close inspection. Widening of the lateral joint space, cupping of the lateral tibial plateau, squaring of the lateral femoral condyle, high fibular head, obliquity of the lateral tibial plateau

Figure 20–7 Watanabe classification of the discoid lateral meniscus. Note that type III menisci (Wrisberg variant) lack any posterior capsular attachment. Type III menisci typically have a thickened posterior horn. (Adapted with permission from Andrish JT: Meniscal injuries in children and adolescents: diagnosis and management. J Am Acad Orthop Surg 4:231–237, 1996.)

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articular surface, and hypoplasia of the lateral intercondylar spine may be clues to a diagnosis of discoid lateral meniscus (Figure 20–8).78 MRI has become more useful in the work-up of a suspected discoid meniscus. Samoto et al.79 established four criteria for diagnosing a discoid lateral meniscus by MRI: (1) meniscal width on a coronal slice of at least 15 mm, (2) meniscus-to-tibia ratio of 20%, (3) percentage coverage of the meniscus of 75%, and (4) three consecutive sagittal slices with continuity between the anterior and posterior horns (Figures 20–9, A to C). The authors reported the sensitivity between the four parameters varied between 50% and 87%, whereas the specificity ranged from 92–99%. The treatment of the discoid meniscus depends largely on the patient’s level of symptoms. Asymptomatic snapping in the young child should not be used as an indication for surgery. These patients and their families should be educated regarding the natural history of discoid menisci and the potential need for surgical intervention at a later date. Symptoms suggesting the presence of a torn discoid meniscus warrant diagnostic arthroscopy. At the time of arthroscopy, the surgeon should classify the meniscus as type I, II, or III and treat accordingly. Asymptomatic discoid menisci found incidentally at the time of arthroscopy should be left alone. Types I and II menisci require excision of the central portion of the meniscus (saucerization). This may be accomplished by excising the central, injured portion in piecemeal fashion using a variety of arthroscopic baskets and a meniscal blade (Figure 20–10). Alternatively, the tissue may be removed as one piece using a combination of arthroscopic scissors and a meniscal blade. A high index of

suspicion should be entertained for associated peripheral detachment of the discoid meniscus. Kocher and colleagues found an incidence of 28% of unstable discoid meniscus requiring repair.69 Tears extending into the red-red, redwhite zone should be repaired. Type III, or lateral meniscal

Figure 20–8 Anteroposterior radiograph demonstrating a widened lateral joint compartment (arrows). (Reprinted with permission from Stoller, DW, Cannon WD, Anderson LJ: The Knee. Magnetic Resonance Imaging in Orthopaedics and Sports Medicine. Philadelphia: Lippincott & Wilkins, 1997.)

Figure 20–9 A to C, Three consecutive MRI sagittal slices demonstrating continuity between the anterior and posterior horns of a lateral discoid meniscus. Note the increased signal within the body of the meniscus representing a horizontal cleavage tear.

(Continued)

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variant, menisci tears should be addressed in a similar fashion and then repaired to the posterior capsule using the insideout technique described in the following section. Treatment

Figure 20–9—cont’d

Posterior

or

A Anterior

B

C Figure 20–10 Surgical techniques for discoid menisci. A, Partial excision of inner, stable meniscus (saucerization). B, Partial excision and repair of unstable posterior horn. C, Partial excision of large posterior horn (lateral meniscal variant) and repair of unstable discoid meniscus. (Adapted with permission from Jordan MR: Lateral meniscus variants. Op Tech Orthop 10:234–244, 2000.)

KEY POINTS 1. Asymptomatic discoid menisci found incidentally at the time of arthroscopy should be left alone. 2. Types I and II require excision of the central portion of the meniscus (saucerization). 3. Type III, or lateral meniscal variant, menisci tears should be addressed in a similar fashion and then repaired to the posterior capsule using the inside-out technique.

Although the first meniscus repair was reported by Annandale in 1885,80 little more was written on the subject over the next 100 years. Through the work of Fairbank51 and others,40,52,53 it was shown that partial or complete excision of the meniscus often leads to the development of early degenerative arthritis. These findings spawned further research into the function of the meniscus and promoted a subsequent treatment philosophy of “meniscal preservation.” With this new awareness of the important role the meniscus plays in load sharing, articular cartilage protection, and joint stabilization, surgeons are now advocating the importance of repairing meniscal tears when possible. To this end, much effort has been directed toward the development of new indications and techniques for meniscal repair. The subsequent success of meniscal repair in the adult population has been well documented.81–87 Unfortunately, few reports exist in the literature regarding the surgical outcome of meniscal repair in the adolescent athlete.88,89 Therefore much of the treatment guidelines for the young athlete mirror those recommendations established for adults. Meniscal Repair Versus Excision Present treatment guidelines for meniscus injuries ultimately consist of four options: repair, débridement, excision, or replacement. The most notable difference among adult and adolescent recommendations is the more aggressive meniscal repair indications given for young athletes with tears in the central “avascular zone.” These treatment guidelines are directly related to the unique vascularity, histological structure, and biochemical composition of the adolescent meniscus. Each of these characteristics allows for a greater chance of healing in a young patient relative to a similar tear seen in the adult population.8,88,89 Ultimately, however, the decision to repair a meniscus should be based on several factors. Age of the patient, duration of symptoms, location and size of the tear, activity level, surgical history, and concomitant injury/instability all play a key role in determining the course of treatment. Regardless of whether the patient is a child or an adult, preservation of the meniscus should be the primary goal. Treatment guidelines for meniscus repair were initially based on the work of Arnoczky and Warren, who suggested peripheral tears within 3 mm of the meniscosynovial junction

Meniscal Injury in the Skeletally Immature Patient

had sufficient blood supply for healing.33 This area is referred to as the red-red zone. Tears in the 3- to 5-mm range were noted to have inconsistent vascularity, and this area is termed the redon-white zone. Tears occurring beyond 5 mm from the meniscosynovial junction are relatively avascular in the adult, and this region is the white-on-white zone.90 Meniscectomy

KEY POINTS 1. Tears within 3 mm of the meniscosynovial junction have sufficient blood supply for healing and are in the red-red zone. 2. A distance of 3–5 mm from the meniscosynovial junction is the red-on-white zone. 3. Tears in the whiteon-white zone (> 5mm) are relatively avascular.

A thorough evaluation of the meniscus tear should be conducted at the time of arthroscopy to determine if the meniscus is repairable. Tear configurations have been described and classified into five major patterns: vertical longitudinal, oblique (“parrot beak” and “flap”), radial, horizontal, and complex (combination of two or more). All aspects of the tear and the adjacent tissue should be probed to assess the extent and size of the tear and the quality of the surrounding meniscus. The physician should always perform a complete inspection of the entire knee joint at this time to preclude the risk of overlooking an undiagnosed ACL injury, chondral injury, chondromalacia patella, or loose body. Displaced bucket-handle tears should first be reduced into an anatomical position allowing for better visualization and inspection of the tear. Posterior horn tears may be better visualized by placing a 70-degree arthroscope through the lateral portal and into the notch between the PCL and medial femoral condyle. Tears may then be débrided through a posteromedial or posterolateral portal under direct visualization. The 70-degree scope may also be placed through KEY POINTS posterior portals to further aid the inspection of a posterior Posterior horn tears horn tear. If the tear is deemed may be better visualirreparable, a partial meniscecized by placing a tomy should be performed. 70-degree arthroscope Excision of the damaged menisthrough the lateral cus should begin with the use of portal and into the standard arthroscopic baskets notch between the removing the unstable, damPCL and medial aged tissue. An arthroscopic femoral condyle. Tears meniscal shaver should then be may then be débrided used to trim and contour the through a posteromeremaining meniscus back to a dial or posterolateral stable rim. Patients undergoing portal under direct an isolated partial meniscecvisualization. The tomy should typically begin a 70-degree scope quadriceps-strengthening promay also be placed gram on postoperative day 1 through a posterior and progress to full weightportal to further aid bearing within 3–4 days. A the inspection of a return to sporting activities can posterior horn tear. be expected within 2–3 weeks.

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Meniscal Repair Several factors should be considered before performing a meniscus repair. The tear’s location, size, configuration, and acuity will determine if a repair should be attempted. The ideal candidate for a meniscus repair is a patient with a simple, acute longitudinal tear in the red-red zone measuring approximately 15 mm in length. However, the physician and patient are seldom so fortunate. Complex, double, and even triple longitudinal tears in these regions have been found to heal following repair and should be lightly débrided and repaired using additional sutures to address each tear component.89 Tears smaller than 1 cm typically do not require repair. This is particularly true when the tear is discovered during ACL reconstruction of the injured knee. Therefore acute, stable, peripheral tears measuring smaller than 1 cm may be treated by placing the patient in a hinged knee brace (HKB) limiting range of motion to 0–60 degrees for 4 weeks (Figure 20–11). Similar tears without a concomitant ACL injury should be trephinated and then begun on a similar postoperative protocol. Trephination is a technique whereby vascular access channels are made that communicate the tear site with the peripheral blood supply. Vascular access channels have been shown in some studies to promote healing of meniscal tears, particularly those in the more avascular regions.91,92 Trephination may be performed with an 18- or 22-gauge spinal needle depending on the size of the patient and meniscus. The needle is used to puncture the meniscus from inside the tear traveling across the meniscus and into the peripheral vascular area in the capsule. Chronic tears should be rasped and trephinated, with consideration given to placing a fibrin clot at the tear site if a concomitant ACL reconstruction is not being performed.93a–94 Microfracture of the femoral notch has recently been described as an alternative method for increasing fibrin clot formation at the repair site.91,95 An HKB should once again be used, limiting range of motion to 0–60 degrees for 4 weeks. Horizontal and radial tears extending peripherally into the red-white zone are uncomKEY POINTS mon in the skeletally immature athlete but warrant repair if 1. The meniscus encountered. Similar tears contear’s location, size, fined more centrally in the configuration, and white-white zone or inner free acuity will deteredge should be débrided back to mine if a repair healthy, stable tissue. These should be tears have minimal healing attempted. potential and little biomechani2. Horizontal and cal significance. Likewise, macradial tears extenderated, complex, irreducible ing peripherally into tears involving the white-white the red-white zone zone should also be excised back are uncommon in to healthy, stable tissue. In genthe skeletally eral, however, every attempt immature athlete should be made to repair tears but warrant repair involving the red-red and redif encountered. white zone in the young athlete. Meniscal Repair Technique Currently there are three categories of arthroscopic meniscus repair: inside-out, outside-in, and all-inside.

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Meniscus tears 1 cm

Outer 2/3 (red-red and red-white zones)

Acute

() ACL reconstruction

Hinged knee brace (HKB) 0–60 degrees  4 weeks

Inner 1/3 (white-white zone)

Chronic

Excise

() ACL reconstruction

() ACL reconstruction

() ACL reconstruction

Trephinate, HKB 0–60 degrees  4 weeks

Rasp, HKB 0–60 degrees  4 weeks

Rasp, trephinate, ± microfracture, HKB 0–60 degrees  4 weeks

Figure 20–11 Nonoperative treatment algorithm for simple meniscus tears less than 1 cm in child and adolescent patients.

Arthroscopic-assisted approaches to meniscus repair have become the gold standard, whereas all-open techniques are currently indicated only for certain repairs in the multiple ligamentous-injured knees. Regardless of the technique used, it is critical to place the fixation device (suture, arrow, dart, screw, staple) in the most biomechanically sound orientation while maximizing the biological environment for healing.91–94 Proper technique, in conjunction with appropriate indications, has been shown to result in a success rate exceeding 80–90% in numerous studies.88,89,96,97 The allopen surgical approaches are similar to those used for retrieving sutures using the medial or lateral inside-out techniques, and the reader is thus referred to this section for further details. Because of the variety of existing meniscal repair techniques, a treatment algorithm has been developed based on patient age, acuity of injury, concomitant ACL injury, and the size, location, and pattern of the meniscal tear (Figures 20–11 to 20–13). It should be emphasized that although some of the third- and fourth-generation, all-inside meniscal repair devices have gained increasing popularity, there have been no long-term studies documenting their efficacy or safety when used in the young adolescent or child population. We have therefore reserved their use largely to the repair of posterior horn tears in adolescents approaching skeletal maturity. Inside-Out Technique The inside-out technique for meniscal repair was initially popularized by Henning in the early 1980s. This method remains the gold standard and enables the surgeon to address most meniscal tears, with only the extreme anterior horn tears posing any considerable difficulty (see Figure 20–12). The tear site must first be probed and evaluated for size, stability, location, and type. If the tear is deemed repairable it should be débrided of any fibrinous tissue, using a small meniscal shaver or rasp. Excoriation of the perimeniscal synovium on both the superior and inferior surfaces of the meniscus attachment peripheral to the tear site is important for chronic tears.

The inside-out technique uses 2-0 sutures with doublearmed Keith needles that are passed through zone-specific cannulas. A single-barreled cannula is preferred to ensure more exact placement of the sutures. Vertically oriented, divergent sutures have been KEY POINTS shown to provide superior fixation and should be placed 1. The inside-out approximately 4 mm apart and technique remains alternated between the superior the gold standard and inferior surfaces (Figure and enables the 20–14). The first suture pass surgeon to address should be placed 1–2 mm most meniscal peripheral and superior to the tears, with only the actual tear itself. This will allow extreme anterior a better reduction of the tear and horn tears posing prohibit any subsequent disany considerable placement. The second arm of difficulty. the same suture should then pass 2. Vertically oriented, through the central portion of divergent sutures the meniscus and across the tear. have been shown A similar technique is used for to provide superior securing the inferior surface of fixation and should the meniscus (Figure 20–15, A to be placed approxiD). Horizontal suture constructs mately 4 mm apart have been found to provide only and alternated half of the fixation strength of between the vertical sutures and should be superior and reserved for radial tears extendinferior surfaces. 98 ing into the red-white zone. 3. Posterior third Horizontal sutures in this setting meniscus tears are better able to bridge and pose some risk for reduce the tear site. Typically, a neurovascular minimum of two sutures will be injury and therefore required for most radial tears. require a posterior Posterior third meniscus approach tears pose some risk for neurovasperformed before cular injury and therefore require passage of the a posterior approach performed needles. before passage of the needles.

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Longitudinal, noncomminuted, reducible tears 1 cm

Posterior horn tears

Anterior horn tears

Inner 1/3 (white-white zone)

Excise

Outer 2/3 (red-red and red-white zones)

Inner 1/3 (white-white zone)

Outer 2/3 (red-red and red-white zones) Chronic

Acute Acute

Excise

Chronic

In child

In adolescent

Inside-out technique

All-inside technique

() ACL reconstruction

Rasp, acute protocol

Outside-in technique

() ACL reconstruction

Rasp, trephinate, acute protocol, ± microfracture

() ACL reconstruction

() ACL reconstruction

Rasp, outside-in technique

Rasp, outside-in technique, ± microfracture

Middle third tears

Outer 2/3 (red-red and red-white zones)

Acute

Inside-out or Outside-in technique

Inner 1/3 (white-white zone)

Chronic

() ACL reconstruction

Rasp, inside-out or outside-in technique

Excise

() ACL reconstruction

Rasp, inside-out or outside-in technique, ± microfracture

Figure 20–12 Treatment algorithm for simple meniscal tears greater than 1 cm in child and adolescent patients.

The posteromedial approach is performed with the knee flexed to 90 degrees while a 7-cm incision is made just anterior to the medial collateral ligament (MCL), centered at the level of the joint line (Figure 20–16, A). The infrapatellar branch of the saphenous nerve should be identified and protected. The sartorius fascia is then incised and the gracilis and semitendinosus are retracted posteriorly. Blunt dissection is performed between the medial head of the gastrocnemius muscle and the posterior capsule. A retractor should then be placed adjacent to the posterior capsule, protecting the neurovascular structures. A popliteal retractor is quite useful for this exposure; however, a pediatric speculum or sterile spoon will suffice. Needles should be identified as they exit the capsule and deflected off the retractor to prevent any neurovascular injury.

The posterolateral approach requires a 7-cm vertical incision along the posterolateral corner of the knee (Figure 20–13, B). A plane is developed between the iliotibial band and the biceps femoris. The lateral gastrocnemius muscle is identified and dissected off the posterior capsule, and a popliteal retractor inserted posterior to the joint line protects the peroneal nerve. Tear preparation and suture placement are performed in a similar manner as for the medial meniscus (Technical Note 20–1). All-Inside Technique The all-inside technique was developed to eliminate the need for a posterior incision and to simplify the repair process for posterior horn and middle-third meniscus tears (see Figure 20–12). The number of meniscal repair

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Bucket handle tears *

Acute

Figure 20–13 Treatment algorithm for bucket-handle meniscus tears in child and adolescent patients.

Chronic

Child

Adolescent

() ACL reconstruction

() ACL reconstruction

Inside-out repair

Inside-out repair, or hybrid inside-out and all inside

Rasp, acute protocol

Rasp, ± microfracture, acute protocol

* Macerated, complex, irreducible tears or complex reducible tears in white-white zone should be excised

A

B Inferior vertical divergent suture Superior vertical divergent suture

Longitudinal tear Figure 20–14 “Double-stacked” vertical suture pattern used in the repair of single longitudinal meniscal tears. A, The superior sutures are placed first to close the superior gap and to anchor the meniscus to its bed. B, The inferior sutures are then placed without displacing the tear. (Reprinted with permission from Noyes FR, Barger-Westin SD: Arthroscopic repair of meniscal tears extending into the avascular zone in patients younger than twenty years of age. Am J Sports Med 30:589–599, 2002.)

devices has increased dramatically since the introduction of the all-inside technique.99 Presently there are a variety of arrows, darts, screws, staples, and suture anchor devices available for use with this technique. The arrows are a third-generation device and are currently the most widely used implant. Studies have shown it to have pullout strength comparable to that of horizontal suture placement.99–102 A modification of the original meniscal arrow has recently been introduced with a lower profile and more contoured head. This development was made in an effort to address concerns of chondral injury that had been reported in a few cases resulting from the prominent first generation head.103–107 The effects of these design changes remain to be seen. Recommendations warning of the potential risk of neurovascular injury, cystic hematoma, and irritable subcutaneous arrow tips with inappropriate use of the 16-mm arrow (or the 13-mm arrows in smaller menisci) have further minimized the risks associated with use of this device.106,108 The meniscus arrow is a suitable option when attempting to repair an isolated, vertical tear located in the red-red or redwhite region of the posterior horn or mid-third meniscus in a young adolescent. Radial and horizontal tears are contraindicated, as are all tears in small children. Bucket-

handle tears are inherently more unstable and should be addressed using the inside-out technique (see Figure 20–13). Anterior horn tears are difficult to access using this approach, and an outside-in repair should be considered (see Figure 20–12). The RapidLoc (Ethicon, Johnson & Johnson, Somerville, New Jersey) is a fourth-generation meniscal repair device that provides good fixation and theoretically less risk of chondral injury when properly used. Although the initial experience with this product has been favorable, its recent introduction to the market has prohibited the availability of any long-term studies evaluating its use in children or young adolescents. Indications at this time are similar to those for the arrow fixation device.

KEY POINTS 1. The all-inside technique is an option when repairing an isolated, vertical tear located in the red-red or red-white region of the posterior horn or mid-third meniscus in a young adolescent. 2. Radial and horizontal tears are contraindicated, as are all tears in small children. 3. Bucket-handle tears are inherently more unstable and should be addressed using the inside-out technique.

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Figure 20–15 Inside-out repair of a bucket-handle tear. A, Displaced bucket-handle tear of a medial meniscus (see Figure 20–6). B, The tear is reduced and the first suture enters just superior to the tear site. C, The second suture enters the body of the inner portion of the meniscus. D, Multiple vertical sutures alternating between inferior and superior surfaces.

Semimembranosus

Sartorius Saphenous Biceps femoris vein

ITT

MCL Peroneal nerve Saphenous nerve

A

Gastrocnemius

B

Figure 20–16 Surgical approach for repair of the medial and lateral menisci. A, Medial. B, Lateral. (Adapted with permission from Scott WN: Arthroscopy of the Knee. Philadelphia: WB Saunders, 1990.)

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TECHNICAL NOTE 20–1

Meniscus Repair: Inside-Out and All-Inside Techniques W. Dilworth Cannon

Since Henning’s first arthroscopic meniscal repair in North America in 1980, meniscal repair using sutures remains the gold standard.1,2 The technique has become easier with the advent of precisely bent cannulas to accommodate the tibial spines and passage of long needles.3,4 The ability to place sutures alternating between superior and inferior surfaces of the meniscus is accomplished more easily with sutures than it is with most of the all-inside techniques currently available. A vertically oriented nonabsorbable suture repair is the model to which all other techniques must be compared (Figure 20–17). Long-term follow-up studies of meniscal repair are mainly limited to suture techniques because most of the newer allinside techniques have not been around long enough.

decision to perform meniscal repair, along with ACL reconstruction because of the statistically increased successful healing rate with this combined pathology compared with isolated meniscal repair.7 Tears that should be repaired include almost all vertical longitudinal tears of the posterior horns within 4 mm of the meniscosynovial junction, including displaced bucket-handle tears. The incidence of degenerative tears not amenable to repair is low in this age group compared with middle-aged and older adults. Certain radial split and oblique tears of the posterior horn of the lateral meniscus near its root origin should be repaired because the vascular supply is so rich in this area of the meniscus (Figure 20–18).

Indications

Technique of Inside-Out Suture Repair

When presented with a young adolescent with a torn meniscus, the decision to perform meniscal repair should be more easily made than in older patients. It is well documented5,6 that partial or total meniscectomy in a child will lead to poor results because of early arthritic changes. Most of these young patients will present with an ACL tear with accompanying meniscal pathology. This combination should even more influence the

When performing the classic inside-out suture repair of either the medial or lateral meniscus, it is important to make an ample posteromedial or posterolateral incision to protect the posterior neurovascular structures during needle passage and retrieval. Sutures should be tied directly against the posterior capsule. They should not entrap any additional soft tissue such as the gastrocnemius muscle bellies. A posterior retractor is essential to deflect

Figure 20–17 Ideally, sutures should be placed in a vertical orientation approximately 3–4 mm apart and should be made of nonabsorbable material.

Continued

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TECHNICAL NOTE 20–1

Meniscus Repair: Inside-Out and All-Inside Techniques (Continued) the needles for retrieval, as well as to protect posterior neurovascular structures. My favorite retractor is half of a pediatric vaginal speculum. One can also use the Henning retractor or simply a spoon. A 2- to 3-mm rasp or burr, or even a small debrider, should be used to freshen up both surfaces of the tear. This is usually accomplished through both the anterior inferior portal and the posterior portal. For placement of the sutures, I use either a malleable cannula or zone-specific cannulas to pass a nitinol needle threaded with 2-0 nonabsorbable suture

(Figure 20–19). Most suture placement for the posterior horn of the medial meniscus and all suture placement for the lateral meniscus should be done through a contralateral portal. Because it is the most difficult system to learn, I use the Henning repair system less frequently despite the fact that it provides the greatest flexibility in placement of sutures compared to other techniques. I place almost exclusively vertically oriented sutures alternating between the superior and inferior surfaces of the meniscus

Figure 20–18 Repair using pursestring sutures of a radial oblique displaced flap tear at the posterior horn origin of the lateral meniscus, a common tear pattern associated with a tear of the anterior cruciate ligament.

Figure 20–19 A nitinol needle is passed through a malleable cannula and penetrates the posterior horn of the medial meniscus. The popliteal deflector protects the neurovascular structures. (Drawing courtesy of Arthrex, Inc.)

Continued

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Meniscus Repair: Inside-Out and All-Inside Techniques (Continued) (Figure 20–20). Secure fixation and improved healing rates are directly related to the number of sutures used. I personally recommend the use of fibrin clot insertion into the tear site for all isolated meniscal repairs (Figure 20–21). For meniscus repair associated with an ACL reconstruction, I do not use fibrin clot because the incidence of successful

outcomes is significantly higher with this combined pathology.7 Results of Inside-Out Suture Repair My clinical versus anatomical healing rates are shown in Figure 20–22. Henning2 has described criteria for assessment of anatomical healing.

Figure 20–20 Vertical sutures should be alternated between superior and inferior surfaces of the meniscus.

Figure 20–21 A fibrin clot has been sutured into the tear site under the meniscus. Then the meniscus repair sutures are tied.

Continued

Meniscal Injury in the Skeletally Immature Patient

TECHNICAL NOTE 20–1

Meniscus Repair: Inside-Out and All-Inside Techniques (Continued) Menisci 100

172

134

30%

25%

90

38

80

47%

Patients (%)

70 60 50 40

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70%

30

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A

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Failed

Menisci 100

138

115

12%

8%

23

90 30% 80

Patients (%)

70 60 50

92%

88%

40

70%

30 20 10 0

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ACL and Isolated repair reconstruction 11 months F/U

B

Satisfactory

Failed

Figure 20–22 A, Meniscal repair results assessed anatomically by second-look arthroscopy or arthrogram. B, Meniscal repair results assessed clinically. Some patients have clinically successful outcomes but are anatomical failures.

Continued

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Meniscus Repair: Inside-Out and All-Inside Techniques (Continued) These criteria indicate that a number of anatomical failures, as determined by second-look arthroscopy or arthrogram, are asymptomatic and are clinical successes, at least for the short term. Successful outcomes are also related to small rim sizes and short tear lengths.4,8 Technique of All-Inside Repair The principal advantage of an all-inside technique is that it avoids posteromedial and posterolateral incisions. Tear site preparation as described for the suture technique should still be carried out. Many companies have produced allinside meniscus repair systems. First-generation systems included placement of arrows and darts across the meniscus tear site. They had a variable absorption rate, depending on their composition. If composed of 100% PLLA (poly-L lactic acid), absorption could take as long as 5 years. If composed of 70% PLLA and 30% PDLA (polymer obtained from an equivalent mixture of Dand L-lactic acid), absorption took less than 1 year. Other devices are composed of a combination of PLLA and PGA (polyglycolic acid). Device selection in children and adolescents should take into consideration device breakage and/or articular cartilage injury secondary to prominence of the implant.9–11 Early follow-up studies in adults showed that there was little difference in successful outcomes between meniscal repairs done with arrows versus sutures despite the fact that arrows were inserted only on the

superior surface of the meniscus.12 Most of the next generation techniques incorporated sutures, many of which were attached to a small implant. Even “top hat” designs (Figure 20–23) have the potential for breakage and/or cartilage damage. The composition of the “top hat” has changed from PLLA to PDS (polydioxanone) for this reason. A popular technique uses a polyacetal bar deployed behind the meniscus rim and attached to size 0 nonabsorbable suture (Figure 20–24). A second polyacetal bar loaded in tandem behind the first is then deployed, creating either a horizontal or vertical suture. A preloaded knot is then pushed and slightly countersunk below the surface of the meniscus. Because smaller knees are encountered in the pediatric age group, the surgeon should take into consideration the size of the instruments needed to introduce the fixation devices. Rehabilitation I prefer a conservative approach to rehabilitation consisting of non–weight bearing or toe touch weight bearing for 4 weeks, followed by partial to full weight bearing over the next 2 weeks. I think that this protocol is especially important when arrows or darts are used. Full range of motion should be allowed as soon as it can be accomplished, but there are surgeons who limit knee flexion to 90 degrees for the first 4 weeks. I do not allow patients to return to sports until 6 months postoperatively.

Figure 20–23 Illustration of the RapidLoc all-inside meniscal repair system showing placement of three sutures. (Courtesy of Smith and Nephew, Inc.)

Continued

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Meniscus Repair: Inside-Out and All-Inside Techniques (Continued)

Figure 20–24 Illustration of the FasT-Fix all-inside meniscal repair system showing deployment of one suture with two implants. (Courtesy of Mitek Products, Johnson and Johnson, Inc.)

Summary When a surgeon is unsure whether a meniscus repair or partial meniscectomy should be done, the surgeon should lean in the direction of performing meniscus repair in adolescents because of the poor results after partial and total meniscectomy. My preferred method, especially in a younger age group population, is to use sutures because of their proven reliability and superior holding power. Tear site preparation should be done routinely, and the use of fibrin clot for isolated meniscal repairs in ACL stable knees is highly recommended. In meniscus repairs associated with ACL reconstructions, I have obtained satisfactory outcomes in 92% of cases. Suggested Readings 1. Anderson K, Marx RG, Hannifin J, Warren RF: Chondral injury following meniscal repair with biodegradable implant. Arthroscopy 16:749–753, 2000. 2. Cannon WD: Arthroscopic meniscal repair. Am Acad Orthop Surg, monograph series, 1999.

Outside-In Technique The outside-in technique was described by Warren as a means of protecting the peroneal nerve during lateral meniscus repair.109 This technique has since evolved and is commonly used for repairing tears of the mid-third meniscus and the anterior horn. The instrumentation required is minimal, consisting of 18-gauge spinal needles, an arthroscopic grasper, and 0-Prolene (Ethicon, Johnson & Johnson, Somerville, New Jersey) sutures.

3. Cannon WD: Arthroscopic meniscal repair. In McGinty JB (ed): Operative Arthroscopy, 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 2002. 4. Cannon WD, Morgan CD: Meniscal repair. II. Arthroscopic repair techniques. J Bone Joint Surg Am 76:294–311, 1994. 5. Cannon WD, Vittori JM: The incidence of healing in arthroscopic meniscal repairs in anterior cruciate ligamentreconstructed knees vs. stable knees. Am J Sports Med 20:176–181, 1992. 6. Henning CE: Arthroscopic repair of meniscus tears. Orthopedics 6:1130–1132, 1983. 7. Hutchinson MR, Ash SA: Failure of a biodegradable meniscal arrow. Am J Sports Med 27:101–103, 1999. 8. Medlar RC, Mandiberg JJ, Lyne ED: Meniscectomies in children: report of long term results (mean, 8.3 years) of 26 children. Am J Sports Med 8:87–92, 1980. 9. Petsche TS, Selesnick H, Rochman A: Arthroscopic meniscus repair with bioabsorbable arrows. Arthroscopy 18:246–253, 2002. 10. Raber DA, Friederich NF, Hefti F: Discoid lateral meniscus in children: long-term follow-up after total meniscectomy. J Bone Joint Surg Am 80:1579–1586, 1998. 11. Ross G, Grabill J, McDevitt E: Chondral injury after meniscal repair with bioabsorbable arrows. Arthroscopy 16:754–756, 2000. 12. Scott GA, Jolly BL, Henning CE: Combined posterior incision and arthroscopic intra-articular repair of the meniscus. J Bone Joint Surg 68A:847–861, 1986.

The meniscus tear should first be prepared for repair, as described previously. While directly viewing the tear, percutaneously pass a spinal needle through the capsule and intact meniscus and then across the tear and through the displaced, inner meniscal fragment. A second needle is then placed in similar fashion and should enter the joint by passing through the intact meniscus 1–2 mm peripheral to the tear. The #0 sutures are now passed into the joint. Turning the inflow off will improve passage of the sutures into the joint. Once both sutures are inside the joint, it is

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important to grasp them simultaneously to prevent any soft tissue bridge gathering between the two sutures as they are brought out of the joint. The sutures are then tied together. A simple square knot may be tied 1–2 cm adjacent to the knot to act as a “dilator knot.” The suture end with the “dilator knot” is pulled in retrograde fashion, passing the smaller knot before the larger knot. This allows the larger knot to pass completely through the meniscocapsular complex without suture breakage occurring. The use of a dilator knot allows the meniscus to be repaired without the additional risk posed by the presKEY POINTS ence of an intraarticular suture knot abrading the adjacent artic1. The outside-in ular cartilage. A similar techtechnique is nique requires the surgeon to use commonly used for half hitches to tie the retrieved repairing tears of Prolene sutures around each the mid-third end of a single 2-0 nonabmeniscus and the sorbable braided suture. Both anterior horn. sutures and half hitch knots are 2. The use of a dilator then passed retrograde through knot allows the the meniscosynovial junction. meniscus to be A dilator knot is typically not repaired without the needed for this technique. additional risk A small skin incision is made posed by the adjacent to the sutures and dispresence of an section carried down to the exit intraarticular suture site from the capsule. The knots knot abrading the are then secured while arthroadjacent articular scopically visualizing the reduced cartilage. meniscus. Meniscal Transplant Although allograft and synthetic meniscal transplants have met with variable success in the adult population,110–115 indications for such surgeries in the skeletally immature athlete are extremely rare. These authors are unaware of the use of synthetic meniscal transplants in this young population. In contrast, meniscal allografts have been reported in certain rare, salvage-type procedures.110,112 Their use in the skeletally immature athlete, however, remains controversial and should be reserved only for select, large meniscus tears that have failed all previous attempts at repair. Postoperative Protocol The success of a meniscus repair depends heavily on the institution of a well-conceived and supervised rehabilitation program. Because of varying tear patterns, locations of tears, and methods of repair, rehabilitation protocols should be tailored to each individual patient. Unfortunately, considerable debate exists regarding the optimal postoperative course for these difficult injuries. More recent literature has supported the use of an accelerated program, encouraging early range of motion and weight-bearing.116,117 In general, the rehabilitation program should be based on the tear size, location, complexity, and whether concomitant ACL reconstruction is performed. Patients with a vertical, longitudinal meniscus tear not exceeding 2.5 cm are placed in an HKB at 0–90 degrees and

slowly progressed to full weight-bearing. Closed-kineticchain strengthening exercises are begun and increased progressively. The brace is discontinued by 6–8 weeks, and sportspecific training is initiated. A full return to sport is allowed when the patient can demonstrate a full, painless range of motion, 80% strength of the contralateral quadriceps, and no effusion. This time frame is typically 4–6 months after the time of surgery. Patients with complex tears, radial tears, and buckethandle tears (particularly chronic tears) may begin toetouch weight-bearing with a brace locked in full extension for 4–6 weeks. The brace may be removed during this time for supervised, range-of-motion exercises limiting motion from 0–60 degrees. The patient may then be progressed to full weight-bearing and full motion, discontinuing the brace at 8–10 weeks. The remainder of the rehabilitation program and return to play guidelines are similar to those outlined for the smaller meniscal tears described previously. Complications The development of new meniscal repair devices and techniques has significantly reduced the number of complications encountered in meniscal surgery. Unfortunately, complications do remain a risk and warrant further discussion. Neurovascular injury remains perhaps the most feared complication associated with meniscus repair. However, infection, deep venous thrombosis, and complex regional pain syndrome should be included in the differential diagnosis of any patient with unexplained pain after a meniscus repair. Many of the complications encountered after meniscus repair are related to the technique used: outside-in, inside-out, or all-inside. Although the various all-inside methods were designed to minimize the risk of neurovascular injury, this has yet to be proved.118,119 The most commonly reported complications reported with use of the third- and fourth-generation implants include intraarticular displacement of the device, inadequate tensioning, entrapment of extracapsular structures, and chondral injury from a protruding implant.103–105,120–123 We have not encountered such complications when using these devices in isolated posterior horn tears in adolescent and adult patients and therefore recommend limiting their use to this setting. The outside-in technique rarely has associated complications when careful attention is paid to surgical technique and local anatomy. Careful dissection and retractor placement should enable the surgeon to visualize the sutures being tied directly over the capsule, minimizing the risk of neurovascular injury. Avoiding neurovascular injury is also a major concern when performing inside-out repairs. Several authors have reported saphenous nerve injuries occurring through severance, stretch, or entrapment by knot. 97,122–124 Peroneal and vascular injuries have been reported with less frequency.122,123 Once again, most of these complications can be avoided with proper knee flexion at the time of repair and use of posterior incisions allowing protection of neurovascular structures with appropriately placed retractors.55,124,125

Meniscal Injury in the Skeletally Immature Patient

Summary Meniscal tears are being seen with increasing frequency in the young child and adolescent. Clinical suspicion and a thorough physical examination will enable the physician to make an accurate diagnosis in the majority of cases. The specificity of MRI in the diagnosis of meniscal tears continues to improve and should be considered when the diagnosis is in doubt or when warranted for preoperative planning. Most meniscal tears in the pediatric population are amenable to arthroscopic repair techniques. However, the treatment plan should be based largely on the location, size, and pattern of the tear. Regardless of the surgical technique to be used, preservation of the meniscus should be the ultimate goal. References 1. Baker BE, Peckham AC, Pupparo F, et al: Review of meniscal injury and associated sports. Am J Sports Med 13:1–4, 1985. 2. Hede A: Epidemiology of meniscal lesions in the knee: 1,215 open operations in Copenhagen 1982–1984. Acta Orthop Scand 61:435–437, 1990. 3. Nielsen AB, Yde J: Epidemiology of acute knee injuries: A prospective hospital investigation. J Trauma 31:1644–1648, 1991. 4. Bhaduri T, Glass A: Meniscectomy in children. Injury 3:176–178, 1972. 5. Ogden JA: Skeletal Injury in the Child. Philadelphia: Lea and Feniger, 1982. 6. Ritchie, DM: Meniscectomy in Children. Aust New Zealand J Surg 35:239–241, 1966. 7. Vahvanen V, Aalto K: Meniscectomy in children Acta Orthop Scand 50:791–795, 1979. 8. Clark CR, Ogden JA: Development of the menisci of the human knee joint. J Bone Joint Surg 65-A:538–547, 1983. 9. Iobst CA, Stanitski CL: Acute knee injuries. Clin Sports Med 19(4):621–635, 2000. 10. Andrish JT: Meniscal injuries in children and adolescents: diagnosis and management. J Am Acad Orthop Surg 4:231–237, 1996. 11. Stanitski CL, Harvell JC, Fu F: Observations on acute knee hemarthrosis in children and adolescents. J Ped Orthop 13:506–510, 1993. 12. Zaman M, Leonard MA: Meniscectomy in children: a study of fiftynine knees. Proceedings of the British Orthopaedic Association. J Bone Joint Surg Br 60(3):436–437, 1978. 13. Ghosh P, Taylor TKF: The knee joint meniscus—a fibrocartilage of some distinction. Clin Orthop 224:52–63, 1987. 14. McDevitt CA, Webber RJ: The ultrastructure and biochemistry of meniscal cartilage. Clin Orthop 252:8–18, 252. 15. Adams ME, Hokins DWL: The extracellular matrix of the meniscus. In: MOW VC, Arnoczky SP, Jackson DW (eds): Knee Meniscus: Basic and Clinical Foundations. New York: Raven Press, 1992, pp 15–28. 16. Eyre DR, Koob TJ, Chun LE: Biochemistry of the meniscus: unique profile of collagen types and site dependent variations in composition. Trans Orthop Res Soc 8:56, 1983. 17. Rath E, Richmond JC: The menisci: basic science and advances in treatment. Br J Sports Med 34:252–257, 2000. 18. Ghosh P, Ingman AM, Taylor TK: Variations in collagen, noncollagenous proteins, and hexosamine in menisci derived from osteoarthritic and rheumatoid knee joints. J Rheumatol 2:100–107, 1975. 19. Woo SL-Y, An KN, Arnoczky SP, et al: Anatomy, biology, and biomechanics of tendon, ligament and meniscus. In Simon SR (ed): Orthopedic Basic Science. AAOS, 1994, pp 45–88. 20. Beaupre A, Choukroun R, Guidouin R, et al: Knee menisci: correlation between microstructure and biomechanics. Clin Orthop 208: 72–75, 1986. 21. Bullough PG, Munuera L, Murphy J, et al: The strength of the menisci of the knee as it relates to their fine structure. J Bone Joint Surg Br 52:564–567, 1970. 22. Aspden RM, Yarker YE, Hukins DWL: Collagen orientations in the meniscus of the knee joint. J Anat 140:371–380, 1985. 23. Yasui K: Three-dimensional architecture of human normal menisci. J Japanese Orthop Assoc 52:391–399, 1978.

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54. Seedhom BB, Hargreaves DJ: Transmission of the load in the knee joint with special reference to the role of the menisci. II. Experimental results, discussion, and conclusions. Eng Med 8:220–228, 1979. 55. Cannon WD: Arthroscopic meniscal repair—monograph series. AAOS, 1999. 56. Vedi V, Williams A, Tennant SJ, et al: Meniscal movement. An in vivo study using dynamic MRI. J Bone Joint Surg Br 81:37–41, 1999. 57. Mow VC, Holmes MH, Lai WM: Fluid transport and mechanical properties of articular cartilage: a review. J Biomech 17:377–394, 1984. 58. Sarimo J, Rantanen J, Heikkila J, et al: Acute traumatic hemarthrosis of the knee. Is routine arthroscopic examination necessary? A study of 320 consecutive patients. Scand J Surg 91(4):361–364, 2002 59. Poehling GG, Ruch DS, Chabon SJ: The landscape of meniscal injuries. Clin Sports Med 9:539–549, 1990. 60. Duncan JB, Hunter R, Purnell M, et al: Meniscal injuries associated with acute anterior cruciate ligament tears in alpine skiers. Am J Sports Med 23:170–172, 1995. 61. Anderson AF, Lipscomb AB: Clinical diagnosis of meniscal tears. Description of a new manipulative test. Am J Sports Med 14:291–293, 1986. 62. Delee SC, Drez D: Orthopaedic Sports Medicine: Principles and Practice, ed 2. Philadelphia: Saunders, 2003. 63. Anderson AF: Clinical diagnosis of meniscal tears. Description of a new manipulative test. Am J Sports Med 14:291–293,1986. 64. Harvell JC, Fu FH, Stanitski CL: Diagnostic arthroscopy of the knee in children and adolescents. Orthopedics 12:1555–1560, 1989. 65. Boden SD, Davis DO, Dina TS, et al: A prospective and blinded investigation of magnetic resonance imaging of the knee. Clin Orthop 282:177–185, 1992. 66. Laprade RF, Burnett QM, Veenstra MA, et al: The prevalence of abnormal magnetic resonance imaging findings in asymptomatic knees— with correlation of magnetic resonance imaging to arthroscopic findings in symptomatic knees. Am J Sports Med 22:739–745, 1994. 67. Takeda Y, Ikata T, Yoshida S, et al: MRI high-signal intensity in the menisci of asymptomatic children. J Bone Joint Surg Br 80:463–467, 1998. 68. McDermott MJ, Bathgate B, Gillingham BL, et al: Correlation of MRI and arthroscopic diagnosis of knee pathology in children and adolescents. J Ped Orthop 18:675–678, 1998. 69. Kocher MS, Dicanzio J, Zurakowski D, Micheli LJ: Diagnostic performance of clinical examination and selective magnetic resonance imaging in the evaluation of intra-articular knee disorders in children and adolescents. Am J Sports Med 29(3):292–296, 2001. 70. 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. 71. Major NM, Beard LN Jr, Helms CA: Accuracy of MR imaging of the knee in adolescents. Am J Roentgenol 180(1):17–19, 2003. 72. Bronstein R, Kirk P, Hurley J: The usefulness of MRI in evaluating menisci after meniscus repair. Orthopedics 15:149–152, 1992. 73. Watanabe M, Takeda S: Arthroscopy of the knee joint. In Helfet AJ (ed): Disorders of the Knee. Philadelphia: JB Lippincott, 1974, pp 145–159. 74. Neuschwander DC, Drez D Jr, Finney TP: Lateral meniscal variant with absence of the posterior coronary ligament. J Bone Joint Surg Am 74A:1186–1190, 1992. 75. Smillie IS: Injuries of the Knee Joint, 4 ed. New York: Churchill Livingstone, 1970. 76. Kaplan EB: The embryology of the menisci of the knee joint. Bull Hosp Joint Dis 16:111–124, 1955. 77. Kaplan EB: Discoid lateral meniscus of the knee joint. Nature, mechanism, and operative treatment. J Bone Joint Surg Am 39:77–87, 1957. 78. Kim SJ, Moon SH, Shin SJ: Radiographic knee dimensions in discoid lateral meniscus: comparison with normal control. Arthroscopy 16(5):511–516, 2000. 79. Samoto N, Kozuma M, Tokuhisa T, et al: Diagnosis of discoid lateral meniscus of the knee on MR imaging. Magn Reson Imaging 20(1):59–64, 2002. 80. Annandale T: An operation for displaced semilunar cartilage. Br Med J 1:779, 1885. 81. Johnson MJ, Lucas GL, Dusek JK, et al: Isolated arthroscopic meniscal repair: a long term outcome study (more than 10 years). Am J Sports Med 27:44–49, 1999.

82. Rubman MH, Noyes FR, Barber-Westin SD: Arthroscopic repair of meniscal tears that extend into the avascular zone—a review of 198 single and complex tears. Am J Sports Med 26:87–95, 1998. 83. Eggli S, Wegmuller H, Kosina J, et al: Long-term results of arthroscopic meniscal repair. An analysis of isolated tears. Am J Sports Med 23:715–720, 1995. 84. McCarty EC, Marx RG, DeHaven KE, et al: Meniscus repair: considerations in treatment and update of clinical results. Clin Orthop 420:122–134, 2002. 85. Venkatachalam S, Godsiff SP, Harding ML: Review of the clinical results of arthroscopic meniscal repair. Knee 8:129–133, 2001. 85B. Kurzweil PR, Friedman MJ: Meniscus: resection, repair, and replacement. Arthroscopy 18:33–39, 2002. 86. Dehaven Ke, Black KP, Griffiths HJ: Open meniscus repair: technique and two and nine year results. Am J Sports Med 17:788–795, 1989. 87. Rockborn P, Gillquist J: Results of open meniscus repair. Long-term follow-up study with a matched uninjured control group. J Bone Joint Surg Br 82:494–498, 2000. 88. Mintzer CM, Richmond JL, Taylor J, et al: Meniscal repair in the young athlete. Am J Sports Med 26:630–633, 1998. 89. Noyes FR, Barber-Westin SD: Arthroscopic repair of meniscal tears extending into the avascular zone in patients younger than twenty years of age. Am J Sports Med 30:589–600, 2002. 90. Arnoczky SP, Warren RF: Microvasculature of the human meniscus. Am J Sports Med 10:90–95, 1982. 91. Zhang Z, Arnold JA, Williams T, et al: Repairs by trephination and suturing of longitudinal injuries in the avascular area of the meniscus in goats. Am J Sports Med 23(1):35–41, 1995. 92. Gershuni DH, Skyhar MJ, Danzig LA, et al: Experimental models to promote healing of tears in the avascular segment of canine knee menisci. J Bone Joint Surg Am 71:1363–1370, 1989. 93. Henning CE, Lynch MA, Yearout KM, et al: Arthroscopic meniscal repair using an exogenous fibrin clot. Clin Orthop 252:64–72, 1990. 93a. Port J, Jackson DW, Lee TQ, et al: Meniscal repair supplemented with exogenous fibrin clot and autogenous cultured marrow cells in the goat model. Am J Sports Med 24:547–555, 1996. 94. Cannon WD, Vittori JM: The incidence of healing in arthroscopic meniscal repairs in anterior cruciate ligament-reconstructed knees versus stable knees. Am J Sports Med 20(2):176–181, 1992. 95. Freedman KB, Nho SJ, Cole BJ: Marrow stimulating technique to augment meniscal repair. Arthroscopy 19(7):794–798, 2003. 96. Miller DB: Arthroscopic meniscus repair. Am J Sports Med 16:315–320, 1998. 97. Barber FA: Meniscus repair: results of an arthroscopic technique. Arthroscopy 3:25–30, 1987. 98. WV Reis, WD Cannon: Arthroscopic meniscal repair using the inside out technique. 7: 8–19, 1999. 99. Becker R, Schorder M, Starke C, et al: Biomechanical investigations of different meniscal repair implants in comparison with horizontal sutures on human meniscus. Arthroscopy 17(5):439–444, 2001. 100. Dervin GF, Downing KJ, Keene GC, et al: Failure strengths of suture versus biodegradable arrow for meniscal repair: an in vitro study. Arthroscopy 13:296–300, 1997. 101. Albrecht-Olsen P, Lind T, Kristensen G, et al: Failure strength of a new meniscus arrow repair technique: biomechanical comparison with horizontal suture. Arthroscopy 13:183–187. 102. Rankin CC, Linter DM, Noble PC, et al: A biomechanical analysis of meniscal repair techniques. Am J Sports Med 30(4):492–497, 2002. 103. Ellermann A, Siebold R, Buelow JU, et al: Clinical evaluation of meniscus repair with a bioabsorbable arrow: a 2- to 3-year follow-up study. Knee Surg Sports Traumatol Arthrosc 10:289–293, 2002. 104. Asik M, Atalar AC: Failed resorption of bioabsorbable meniscus repair devices. Knee Surg Sports Traumatol Arthrosc 10:300–304, 2002. 105. Sims WF, Simonian PT: Delayed degradation of bioabsorbable meniscal fixators. Arthroscopy 17(3):E11, 2001 106. Petsche TS, Selesnick H, Rochman A: Arthroscopic meniscal repair with bioabsorbable arrows. Arthroscopy 18:246–253, 2002. 107. Ross G, Grabill J, McDevitt E: Chondral injury after meniscal repair with bioabsorbable arrows. Arthroscopy 16:754–756,2002. 108. Jones HP, Lemos MT, Wilk RM, et al. Two-year follow-up of meniscal repair using a bioabsorbable arrow. Arthroscopy 18:64–69, 2002.

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109. Warren RF: Arthroscopic meniscus repair. Arthroscopy 1:170–172, 1985. 110. Rath E, Richmond JC, Yassir W, et al: Meniscal allograft transplantation —two to eight year results. Am J Sports Med 29:410–414, 2001. 111. Paletta GA, Manning T, Snell E, et al: The effect of allograft meniscal replacement on intra-articular contact area and pressures in the human knee—a biomechanical study. Am J Sports Med 25:692–698, 1997. 112. Wirth CJ, Peters G, Milachowski KA, et al: Long-term results of meniscal allograft transplantation. Am J Sports Med 30:174–181, 2002. 113. Hidaka C, Ibarra C, Hannafin JA, et al: Formation of vascularized meniscal tissue by combining gene therapy with tissue engineering. Tissue Eng 8(1):93–105, 2002. 114. Kobayashi M, Toguchida J, Oka M, et al: Preliminary study of polyvinyl alcohol-hydrogel (PVA-H) artificial meniscus. Biomaterials 24(4):639–647, 2003. 115. Martinek V, Usas A, Pelinkovic D, et al: Genetic engineering of meniscal allografts. Tissue Eng 8(1):107–117, 2002. 116. Barber FA: Accelerated rehabilitation for meniscus repairs. Arthroscopy 10:206–210, 1994. 117. Shelbourne KD, Patel DV, Adsit WS, Porter DA: Rehabilitation after meniscal repair. Clin Sports Med 15:595–612, 1996.

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118. Miura H, Kawamura H, Arima J, et al: A new, all-inside technique for meniscus repair. Arthroscopy 15:453–455, 1999. 119. Laprell H, Stein V, Petersen W: Arthroscopic all-inside meniscus repair using a new refixation device: a prospective study. Arthroscopy 18:387–393, 2002. 120. Miller MD, Kline AJ, Gonzalez J, et al: Pitfalls associated with fastfix meniscal repair. Arthroscopy 18:939–943, 2002. 121. Coen MJ, Caborn D, Urban W, et al: An anatomic evaluation of t-fix suture device placement for arthroscopic all-inside meniscal repair. Arthroscopy 15:275–280, 1999. 122. Committee on Complications of the Arthroscopy Association of North America: Complications in arthroscopy: the knee and other joints. Arthroscopy 2:253–258, 1986. 123. Austin KS, Sherman OH: Complications of arthroscopic meniscal repair. Am J Sports Med 21:864–868, 1993. 124. Morgan CD, Casscells SW: Arthroscopic meniscus repair: a safe approach to the posterior horns. Arthroscopy 2:3–12, 1986. 125. Edelson RH, Katchis SD, Parker RD: Complications of meniscus repair. Op Tech Sports Med 2:208–216, 1994.

Chapter 21

Discoid Meniscus Carl L. Stanitski

In 1889 in England, Young provided the first description of a discoid lateral meniscus in a cadaver dissection. He characterized it as “...the external semilunar cartilage as a complete disc.”1 Four decades later the first clinical correlation with a discoid meniscus and a snapping knee of childhood was made by Kroiss in Germany.2 Ober suggested a discoid meniscus causing a “trigger” knee.3 Discoid menisci represent a point in the spectrum of variations of meniscal morphology and stability that ranges from meniscal absence or hypoplasia to abnormally shaped menisci including ring (commonly found in birds and primates), accessory, and double-layered menisci to menisci of normal shape but with instability.4–8 Incidence and Prevalence The prevalence and incidence of discoid menisci are unknown because many are asymptomatic and noted incidentally on imaging study or at surgery.9–11 Prevalence rates are reported between 0.4% and 16.0%, depending on the population studied and the method of observation (e.g., cadaveric dissection, imaging study, or surgical cases). Higher percentages are recorded for Asian populations. A discoid meniscus of unspecified type has been reported in a 4-month–old patient.12 Male and female occurrence rates are similar. Bilaterality is estimated at 10–20%. The meniscal anomaly is almost always seen laterally. Medial discoid menisci have been reported and are quite rare.13,14 A case of ipsilateral lateral and medial discoid menisci has been recorded.13 Anatomy and Classification The initial discoid meniscal classification was proposed by Smillie in 1948 and was based on surgical observations of 29 cases.11 He postulated that discoid morphology represented an atavistic persistence of a complete fetal meniscus that failed to undergo central zone absorption. 260

In light of later information, Smillie retracted his thesis. Kaplan suggested that at no time during fetal development was the meniscus discoid shaped. He based this opinion on his findings in human and animal dissections.5,15,16 This work was later confirmed with elegant studies of human meniscal formation and development by Clark and Ogden,17 who found that although the lateral meniscus showed greater variability of morphology than the medial meniscus, at no time during prenatal or postnatal development were either menisci disc shaped. Kaplan was the first to note a deficient posterolateral tibial plateau meniscal capsular attachment and felt that the meniscus became ovoid shaped due to abnormal motion stress caused by the checkrein effects of the ligament of Wrisberg.16 A decade later, in Japan, Watanabe proposed a tripartite scheme reflecting the percentage of meniscus covering the tibial plateau and meniscal stability.8 In Watanabe’s classification, type I discoid meniscus encompasses the entire plateau, and type II covers 80% or less. Types I and II are stable. In contrast to the normal lateral meniscal 4–5 mm peripheral thickness and 12– 13-mm width, types I and II discoid meniscal thickness is 8–10 mm, and their width ranges from 10–35 mm. Watanabe’s type III classfication of discoid menisci is most commonly a normal shape, except for perhaps some increased thickness at the posterior horn. He also recognized the absence of the coronary posterior meniscotibial ligament. Like Kaplan, he felt that tethering of the meniscus by the ligament of Wrisberg produced abnormal meniscal motion in flexion and extension and, as the knee came to full extension, posterior femoral tibial space was increased and allowed the meniscus to relocate. He named this variety the Wrisberg type and included it in the discoid category despite its usually nondiscoid morphology (Figure 21–1). Neuschwander and Drez offered the term lateral meniscal variant to identify the Wrisberg type of discoid menisci and pointed out the nondiscoid shape of this variety in seven cases. In three of their patients, they were unable to document the status of meniscofemoral ligaments and their role in these cases.7

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Figure 21–1 Watanabe classification of discoid menisci. Type 1: stable, complete; type II, stable, incomplete; type III: unstable as a result of lack of posterior meniscotibial capsule. Note normal meniscal shape.

Kocher and colleagues found 28% peripheral instability on review of 128 cases of discoid menisci. A total of 47% of those with instability had instability at the anterior third of the meniscus.18 The type of meniscus was not defined. Perhaps chronic posterior instability in type III cases produces sufficient anterior tension stress to cause anterior detachment. The meniscofemoral ligaments are thickened portions of the posterior knee capsule and are present in normal knees. Their positions refer to their relationship with the posterior cruciate ligament and are anterior (Humphry) and posterior (Wrisberg), with the latter being more robust.19–22 One of them was present in 70–100% of cadaveric studies with the posterior more consistently present (90–93%) than the anterior (33–83%).23,24 Tears in stable lateral menisci with normal morphology bear no relationship to the presence or absence of meniscofemoral ligaments. None of the classification systems in popular use address the entire issue of meniscal shape, continuity, and stability or the presence of peripheral or longitudinal tears. The Watanabe system’s use must be tempered in recognition of its limitations.8 Jordan suggests a scheme that addresses some of these issues.10 Collagen arrangement in types I and II menisci is abnormal, as is collagen concentration.25 Meniscal vascularity has not been described for any of the varieties of discoid menisci. Both of these issues are important to healing potential postmeniscal repair. Clinical Presentation and Evaluation The patient may be a symptomatic with only a bulge at the outer knee noted. Symptoms are related to meniscal shape, tears, and stability. A common scenario is a 3- to 4-year-old patient whose parents notice asymptomatic snapping and a lump at the child’s lateral knee. Pain onset is usually at 8– 9 years of age and is associated with activity. Symptomatic snapping may be present at that time and seen with intermittent effusions. True mechanical complaints of locking or loss of motion are uncommon. Snapping appears to be a sign of instability, usually related to a type III meniscus or, if symptomatic, an unstable meniscal tear.9

In the asymptomatic case with a “snapping knee,” the examination is normal except for a palpable and often audible “clunk” with knee range of motion, especially in terminal extension. A lateral joint line bulge may also be palpated. In patients with symptoms, clinical evaluation often shows an antalgic gait, diminished thigh and calf muscular definition, and effusion. Focal joint line tenderness and pain exacerbation with lateral compartment loading are seen with meniscal tears. A palpable prominence along the lateral joint line is seen with knee flexion and extension. Differential diagnoses of knee snapping should include noises made by the iliotibial band at the lateral femoral tubercle and pathological plicae. Imaging Studies Routine knee radiographs are almost always normal with discoid menisci. Occasionally a widened lateral joint space is seen with types I and II discoid menisci. Similar widening of the medial compartment has been noted with discoid medial menisci. Quite rarely, tibial plateau cupping, lateral femoral condylar squaring, or decreased height of the lateral tibial eminence may be seen. Magnetic resonance imaging (MRI) criteria for a lateral discoid meniscus include continuity of the anterior and posterior horns on three or more consecutive sagittal images (“bowtie”) and a transverse diameter greater than 15 mm or more than 20% tibial width on transverse plane images.26 MR imaging may also show evidence of a meniscal tear (Figures 21–2 and 21–3). Kocher and colleagues18 found a high positive predictive value for discoid menisci with MRI (i.e., if positive, a discoid meniscus was present). However, Kocher and colleagues showed MRI to have low sensitivity for discoid menisci (i.e., a discoid meniscus could be present in spite of a negative study). Ability for MRI detection was highest with type I and diminished with type II menisci. Normomorphological Watanabe type III menisci were quite often undetected by MRI. The ligaments of Humphry and Wrisberg are often seen in coronal MRI views. Imaging of the meniscotibial capsular posterior coronary ligament (or lack thereof), on the other hand, is purely fortuitous (Figure 21–4).

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Natural History There are no significant longitudinal outcome studies of untreated discoid menisci of any type. Because many patients with types I and II discoid menisci avoid detection and are asymptomatic, or the meniscal variants are noticed as incidental findings at imaging study or surgery, the condition’s denominator is missing from the equation. It is thought that the chronic instability associated with type III discoid menisci predisposes it to injury and symptoms necessitating treatment. Types I and II may become symptomatic from tears brought on by knee hyperflexion associated with vocational-, avocational-, or cultural-based activities. The number of asymptomatic discoid menisci that convert to symptomatic ones requiring treatment remains unknown. Treatment

KEY POINTS 1. Incidence and prevalence of discoid menisci are unknown. Many asymptomatic discoid menisci are noted incidentally at surgery. 2. At no time during fetal development are menisci disc shaped. 3. Differentiation between types I and II (complete/incomplete) is based on percentage of tibial surface covered by the meniscus. Increased meniscal thickness is an associated finding for both types. 4. Type III menisci (Wrisberg) are normal shaped with an increased thickness of the posterior horn. Instability of this type is caused by absence of the posterior meniscofemoral ligament. 5. Blood supply of discoid menisci has not been studied. Abnormal collagen concentration and arrangements are seen in types I and II discoid menisci. All of these factors have implications for meniscal salvage capacity.

Symptoms of a discoid meniscus determine its treatment. Children with painless snapping from a discoid meniscus are advised to schedule follow-up visits if symptoms occur. Their activities are not limited. Patients with asymptomatic discoid menisci noted by imaging study or incidentally at surgery require no treatment. Treatment for symptomatic discoid menisci is surgical and determined by meniscal morphology, stability, and presence and characteristics of tears. In contrast to longitudinal peripheral meniscal tears seen in more than 90% of children’s meniscal injuries to morphologically normal menisci, most tears in discoid menisci are horizontal types.25,27–32 Abnormal collagen arrangement has been indicted as an etiological factor in this tear pattern in this malformed meniscus.25 Meniscal tears occur in discoid menisci from minimal trauma over an extended period and usually not from a single, acute episode. Past surgical management for all types of symptoms producing discoid menisci was total meniscectomy. With emerging understanding of the deleterious effects of loss of meniscal function leading to premature osteoarthrosis, meniscal salvage and preservation techniques have been extended to discoid meniscal pathology as well. Using a cadaveric biomechanical model, Paletta and co-workers33 showed a 45–50% loss of con-

tact area and a 235–335% rise KEY POINTS in peak contact pressures in 1. An asymptomatic knee flexion and extension after snapping knee is a complete normal lateral meniscus common presentaexcision. Whether these data can tion in patients be extrapolated to the abnormal younger than macroanatomy and micro4 years old. anatomy seen in discoid menisci 2. A snapping painful is not known, but it is a cause for knee with intermitconcern after total meniscectomy. tent effusions is Additional testimony of the seen at 8–9 years of import of load sharing in the latage and indicates eral compartment is found in an associated reports of osteochondritis dissemeniscal tear. cans (OCD) of the lateral femoral 3. Radiograph findings condyle associated with discoid are usually normal. menisci or following removal of 4. MRI findings discoid menisci.31,34–37 The relainclude a “butterfly” tionship may be associative and appearance on latnot causative, but it makes for eral views in types I interesting speculation about the and II menisci. role of repetitive microtrauma in 5. A high positive preOCD in a structurally abnormal dictive index is seen knee. with MRI, but there Meniscal salvage and preseris low sensitivity of vation techniques include menisMRI, especially with cal sculpting of stable menisci to types II and III more normal morphology (menisdiscoid menisci. coplasty), partial meniscectomy via excision of horizontal tears or repair of meniscal tears in stable menisci (with or without meniscoplasty), and stabilization of peripherally unstable menisci with or without associated tear repair (Figure 21–5).* Sculpting of type I and II stable menisci can be arthroscopically challenging procedures because of limited visualization and diminished space for instrument placement and manipulation in a child’s knee. Facility and experience with arthroscopic techniques are required. Meniscal reconfiguration is best begun with the patient’s knee in 90 degrees of flexion. As meniscal débridement progresses and visualization improves, knee extension and/or the figure-of-four positions can be used to advantage. During meniscoplasty, signs of meniscal tear and/or instability must be constantly anticipated. If a horizontal cleavage tear is seen in the nonvascularized zone, débridement of the smaller leaf is done, attempting to allow as much meniscus to remain after sculpting as possible. Various recommendations are noted in the literature concerning the amount of peripheral margin that should remain after meniscoplasty. The consensus appears to favor a 6- to 8-mm stable rim, especially at the popliteus hiatus.42 Sugawara et al.43 reported seven cases of stable type I or II discoid menisci that required secondary surgery following partial meniscal débridement for horizontal tears that extended after initial surgery. If a meniscal tear traverses to the peripheral vascularized zone, meniscal repair is done and a variety of methods can be used. Bioabsorbable nonsuture fixation devices may be too bulky and have limited purchase in the often friable meniscal tissue. I prefer to use inside-out sutures placed with zone-specific cannulae and tied outside the capsule. Capsular exposure is *

References 7, 16, 27–32, 38–41.

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Figure 21–2 Sagittal (A and B) and coronal (C) coronal MR images of a type II discoid lateral meniscus with a torn posterior horn.

Figure 21–4 A, Large free edge of a type II discoid meniscus. B, Peripheral tear (arrows) with central fragment retraction (probe). (Reprinted with permission from Drez, DeLee, Miller [eds]: Orthopaedic Sports Medicine, Elsevier Science, Philadelphia, 2003, p 1694.) Figure 21–3 MR image demonstrating the ligament of Humphry (long arrows) and posterior cruciate ligament (short arrow). (Reprinted with permission from Drez, DeLee, Miller [eds]: Orthopaedic Sports Medicine, Elsevier Science, Philadelphia, 2003, p 1694.)

Figure 21–5 A, Symptomatic type II discoid meniscus without tear. B, Post meniscoplasty. (Reprinted with permission from Drez, DeLee, Miller [eds]: Orthopaedic Sports Medicine, Elsevier Science, Philadelphia, 2003, p 1695. Courtery of Dr. James Bradley.)

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done to ensure adequate suture position and tension. If meniscal instability is at issue (e.g., type III menisci), meniscal stabilization is done using sutures placed through zone-specific cannulae with a posterolateral incision to retrieve the

sutures to aid suture placement and fixation. Protection of neural and vascular structures is mandatory and improved by knee position during suture placement and by capsular exposure for suture retrieval (Technical Note 21–1). Text continued on p. 271

TECHNICAL NOTE 21–1

Discoid Lateral Meniscus Saucerization and Repair Mininder S. Kocher

Indications Asymptomatic discoid menisci, even if found incidentally on arthroscopy, are typically observed. Children with a snapping knee without functional impairment are also typically observed. Surgery is indicated for cases of symptomatic discoid meniscus. Symptoms are often related to the type of discoid present, peripheral stability of the meniscus, and the presence or absence of an associated meniscal tear.1–17 In younger children, symptoms typically include a popping or snapping knee. In older children, symptoms typically include those of a meniscus tear: pain, swelling, catching, or locking. On physical examination the discoid meniscus may pop in the lateral compartment with hyperflexion. There may be lateral joint line tenderness, and McMurray’s maneuvers may reveal popping. Radiograph findings may show a block appearance of the lateral joint line (Figure 21–6). MRI has high specificity for discoid meniscus (Figure 21–7) but lacks sensitivity, especially for incomplete types (Watanabe type II) or normal morphological variants lacking meniscotibial ligaments (Watanabe type III).18 Historically, discoid lateral meniscus was treated with complete meniscectomy. However, the longterm results of complete meniscectomy and neartotal meniscectomy in children are poor with early degenerative changes.1,15,19–25 Thus, modern surgical treatment emphasizes meniscal preservation. Surgery consists of saucerization of the meniscus to more normal morphology and repair of the meniscus if it is unstable and detached from the capsule. In a recent study of 128 consecutive discoid lateral meniscus surgeries, we reported that 28.1% (n = 36) of discoid lateral menisci had peripheral rim instability: 47.2% (n = 17) were unstable at the anteriorthird peripheral attachment, 11.1% (n = 4) at the middle-third peripheral attachment, and 38.9% (n = 14) at the posterior-third peripheral attachment.13 Peripheral rim instability was significantly more common in complete discoid lateral menisci

(38.9% versus 18.2%; P = 0.043) and in younger patients (8.2 versus 10.7 years; P = 0.002). Thus the frequency of peripheral instability mandates a thorough and methodical assessment of meniscal stability at all peripheral attachments during the arthroscopic evaluation and treatment of discoid lateral meniscus, particularly of the anterior horn and in complete variants and in younger children. Setup Arthroscopic saucerization and repair for discoid lateral meniscus is usually performed under general anesthesia as a day surgery procedure. In children and adolescents, local anesthesia with intravenous sedation may be difficult because of lack of cooperation or disinhibition. Preoperative antibiotics are routinely given as infection prophylaxis during this procedure. I position the patient supine on the operating table. A tourniquet is applied to the upper thigh and usually used during the procedure. A lateral break-away post is used, rather than a circumferential post, because manipulation of the leg in various positions helps with exposure of the lateral compartment, and a posterolateral incision may be needed for meniscus repair. In cases of bilateral discoid meniscus in younger children (age 6 and younger), bilateral surgery is typically performed. In older children and adolescents, I prefer staged unilateral surgery because the patients can be mobilized on crutches postoperatively. In terms of equipment, a regular arthroscope is used for most cases. In the small knees of children approximately 6 years of age and younger, the small arthroscope (2.7 mm) may aid visualization, although the optics may be inferior. I use an arthroscopic fluid pump at 35 torr. Lowprofile baskets are used, which facilitate working in a small space. Straight and up-biting baskets are useful for the central portion and posterior horn of the discoid meniscus. Side-biting baskets are useful for the meniscal body portion of the discoid meniscus. Continued

Discoid Meniscus

TECHNICAL NOTE 21–1

Discoid Lateral Meniscus Saucerization and Repair (Continued)

Figure 21–6 Anteroposterior radiograph of a 10-year-old girl with discoid lateral meniscus demonstrating a block-shaped appearance of the lateral joint. (Reprinted with permission from Drez, DeLee, Miller [eds]: Orthopaedic Sports Medicine, Elsevier Science, Philadelphia, 2003, p 1695.)

Back-biting baskets and a meniscal knife are useful for the anterior horn. A small, suction-motorized shaver is necessary for shaping the meniscus after trimming with baskets. In cases of meniscus instability, I perform meniscus repair via an inside-out technique using zone-specific cannulae to pass nonabsorbable 2-0 sutures, which are retrieved via a posterolateral skin incision. Technique Examination Under Anesthesia: Popping or protrusion of the discoid lateral meniscus may be

appreciated with hyperflexion. In cases with a locked discoid lateral meniscus, there may be a lack of full knee extension. Arthroscopy: The leg is exsanguinated with an Esmarch bandage and the tourniquet elevated. A standard anterolateral viewing portal and a standard anteromedial working portal are made under arthroscopic visualization. Anteromedial portal placement can be optimized by spinal needle localization to ensure the ability to fully instrument the lateral meniscus. Routine arthroscopic examination of the knee is performed. The patellofemoral compartment, Continued

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TECHNICAL NOTE 21–1

Discoid Lateral Meniscus Saucerization and Repair (Continued)

Figure 21–7 Coronal MR image of a 10-year-old girl demonstrating complete type discoid lateral meniscus.

medial compartment, lateral compartment, and intercondylar notch are examined and probed. In young children, a large superomedial plica, large ligamentum mucosum, and fairly horizontal anterior cruciate ligament are normal variants. Diffuse synovitis may accompany discoid menisci with tears. Saucerization: Excision of the ligamentum mucosum from the top of the intercondylar notch and débridement of the fat pad and synovium in the anterolateral knee are routinely performed to facilitate complete visualization of the discoid lateral meniscus. The discoid lateral meniscus is examined to determine its morphology (complete versus incomplete), the presence and type of meniscus tear, and meniscal stability (Figure 21–8, A).

Saucerization is begun on the central portion of the discoid meniscus, with the knee in the flexed position using a straight basket (Figure 21–8, B). In the figure-four position, the remainder of the central portion and the posterior portion are excised using straight or up-biting baskets of appropriate widths. For the body portion, a side-biting basket can be useful. For the anterior portion, a back-biting basket or an arthroscopic knife (Figure 21–8, C) can be useful. After gross-shaping is performed with the arthroscopic baskets and knives, the inner rim can be more finely shaped with a small motorized shaver. The suction shaver is also useful for removal of debris from saucerization. Thinning the inner edge of the discoid meniscus is challenging because the discoid meniscus is typically block shaped. I avoid electrothermal or radiofrequency probes to Continued

Discoid Meniscus

TECHNICAL NOTE 21–1

Discoid Lateral Meniscus Saucerization and Repair (Continued)

Figure 21–8 Discoid lateral meniscus saucerization. A, Presaucerization appearance of a complete discoid lateral meniscus covering the lateral tibial plateau and extending into the intercondylar notch. B, Excision of the central portion in the flexed knee position.

(Continued) shape the meniscus because of concerns about cell death and tissue necrosis in the meniscus and adjacent articular surfaces. A 6- to 8-mm rim of lateral meniscus is usually left. The normal medial meniscus can be used as a guide. A post-saucerized meniscus that is too small may lack sufficient biomechanical shock absorption,

leading to degenerative changes. A post-saucerized meniscus that is too large may predispose to retearing. Repair: After meniscal saucerization, the meniscal rim must be thoroughly and methodically probed to evaluate for further tearing and meniscal instability. A longitudinal tear of the posterior aspect of the discoid lateral meniscus may be present. Continued

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TECHNICAL NOTE 21–1

Discoid Lateral Meniscus Saucerization and Repair (Continued)

Figure 21–8—cont’d C, Excision of anterior portion with an arthroscopic knife in the figure-four position. D, Probe within a horizontal cleavage tear of the posterior horn meniscal rim.

(Continued) Fortunately, this tear typically occurs at the 6- to 8-mm rim region and can be excised. A horizontal cleavage tear may exist in the posterior horn remnant (Figure 21–8, D). Probing the superior and inferior leaflets should be performed to assess tissue quality and stability (Figure 21–8, E). The unstable leaflet is excised (Figure 21–8, F). In cases of meniscal instability, a probe can be placed between the meniscus and the capsule, pulling the meniscus through the lateral compart-

ment. Particular attention should be paid to the anterior and posterior horns in younger children with complete discoid lateral menisci given the higher likelihood of instability.26 Meniscus repair should be performed in these cases. I perform discoid lateral meniscus repair via an inside-out technique using zone-specific cannulae to pass nonabsorbable 2-0 sutures that are retrieved via a posterolateral skin incision (Figure 21–9). In my opinion, allinside devices are usually too big for pediatric knees Continued

Discoid Meniscus

TECHNICAL NOTE 21–1

Discoid Lateral Meniscus Saucerization and Repair (Continued)

Figure 21–8—cont’d E, Probing the unstable superior flap of the horizontal cleavage tear. F, Post-saucerization appearance.

and may protrude posteriorly in proximity to neurovascular structures. Also, all-inside devices may lack the strength of repair needed for these grossly unstable discoid menisci. Finally, the majority of allinside devices are designed to repair meniscus to meniscus, not meniscus to capsule, as is necessary in these cases. A skin incision is made posterolaterally. Dissection is carried down to the posterolateral joint capsule. A retractor is placed under the lateral head of the gastrocnemius muscle. Zone-specific cannu-

lae are used to pass multiple vertical mattress 2-0 nonabsorbable sutures after careful preparation of the meniscocapsular junction with shaving and rasping. The sutures are retrieved out the posterolateral incision and tied over the capsule. Postperative Management The postoperative course depends on the age of the patient and the surgery performed. Continued

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TECHNICAL NOTE 21–1

Discoid Lateral Meniscus Saucerization and Repair (Continued)

Figure 21–9 Discoid lateral meniscus repair. Zone-specific cannulae are used to pass multiple vertical mattress 2-0 nonabsorbable sutures that are retrieved through a posterolateral incision.

For cases of saucerization alone in the older child or adolescent, a cryotherapy device is used and patients are mobilized weight-bearing as tolerated. After a course of physical therapy to regain motion, strength, and function, patients are allowed to return to sports 6–8 weeks postoperatively. For cases of saucerization and repair in the older child or adolescent, touch-down weight-bearing and a postoperative hinged knee brace allowing 0–90 degrees of flexion are used for 6 weeks postoperatively to protect the meniscus repair. Patients are then mobilized with physical therapy, returning to sports 3–4 months postoperatively. For cases of saucerization alone in the younger child, generally 6 years of age and younger, weight-bearing is allowed and no brace is used. Therapy with a physical therapist experienced with children can be helpful to regain motion and strength. For cases of saucerization and repair in the younger child, a cast is used postoperatively for 4 weeks to protect the repair. The child is then mobilized with therapy, returning to sports 3– 4 months postoperatively. Results The long-term results of total or near-total meniscectomy of discoid lateral meniscus in children are poor with early degenerative changes.1,15,19–25 The

short-term results of meniscus preservation, with saucerization and meniscal repair, are promising. However, long-term results of saucerization and repair are not known. Patients should be counseled that saucerization may produce a more normal-appearing meniscus; however, their meniscus lacks the normal meniscal ultrastructure. Thus patients may be more likely to sustain subsequent meniscal tears. In addition, altered load characteristics may lead to lateral femoral condyle chondral changes or osteochondritis dissecans. Suggested Readings 1. Aichroth PM, Patel DV, Marx CI: Congenital discoid lateral meniscus in children: a follow-up study and evolution of management. J Bone Joint Surg Br 73:932–939, 1991. 2. Aglietti P, Bertini FA, Buzzi R, et al: Arthroscopic meniscectomy for discoid lateral meniscus in children and adolescence: a ten year followup. Am J Knee Surg 12:83–87, 1999. 3. Albertsson M, Gillquist S: Discoid lateral meniscus: a report of 29 cases. Arthroscopy 4:211–214, 1998. 4. Bellier G, Dupont JY, Larrain M, et al: Lateral discoid meniscus in children. Arthroscopy 5:52–56, 1989. 5. Dickhaut SC, DeLee JC: The discoid lateral meniscus syndrome. J Bone Joint Surg Am 64:1068–1073, 1982. 6. Fleissner PR, Eilert RF: Discoid lateral meniscus. Am J Knee Surg 12:125–31, 1999. 7. Fujikawa K, Iseki F, Mikura Y: Partial resection of the discoid meniscus in the child’s knee. J Bone Joint Surg Br 63:391–395, 1981.

Continued

Discoid Meniscus

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Discoid Lateral Meniscus Saucerization and Repair (Continued) 8. Hayashi LK, Yamaga H, Ida K, et al: Arthroscopic meniscectomy for discoid lateral meniscus in children. J Bone Joint Surg Am 70:1495–1500, 1988. 9. Ikeuchi H: Arthroscopic treatment of lateral discoid meniscus: technique and long-term results. Clin Orthop 167:19–28, 1982. 10. Jordan M: Lateral meniscal variants: evaluation and treatment. J Am Acad Orthop Surg 4:191–200, 1996. 11. Jordan M, Duncan J, Bertrand S: Discoid lateral meniscus: a review. South Orthop J 2:239–253, 1993. 12. Kaplan EB: Discoid lateral meniscus of the knee joint. Bull Hosp Joint Dis 16:111–124, 1955. 13. Klingele KE, Kocher MS, Hresko MT, et al: Discoid lateral meniscus: prevalence of peripheral rim instability. J Ped Orthop 24:79–82, 2004. 14. Kocher MS, DiCanzio J, Zurakowski D, Micheli LJ: Diagnostic performance of clinical examination and selective magnetic resonance imaging in the evaluation of intraarticular knee disorders in children and adolescents. Am J Sports Med 29:292–296, 2001. 15. Kocher MS, Klingele KE, Rassman S: Meniscal injuries: normal, discoid, and cysts. Orthop Clin North Am 34:329–340, 2003. 16. 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.

Complications of surgical management of discoid menisci include iatrogenic articular injury, especially with types I and II meniscal treatment; arthrofibrosis; infection (superficial at the capsular incision and/or intraarticular); meniscal re-tear; and neural and/or vascular injury, especially to the peroneal nerve. Outcomes and Prognosis

KEY POINTS 1. Most discoid meniscal tears are horizontal types in contrast to the longitudinal ones seen in normally shaped menisci in children and adolescents. 2. Treatment options for symptomatic discoid menisci should focus on meniscal salvage, if possible. Meniscoplasty, partial meniscectomy/ débridement, and meniscal repair and stabilization are options, depending on meniscal morphology, stability, and tear patterns.

Limited long-term outcome data exist after discoid meniscal surgery. The information suffers from all the problems of retrospective analysis, including lack of definition of meniscal types and stability, a wide span of patient ages, small numbers of patients, varied surgical techniques by multiple surgeons, and short follow-up that is usually clinical and often does not include radiographic assessment. Some outcome functional rating systems are quite generous regarding excellent and

17. Manzione M, Pizzutillo PD, Peoples AB, Schweizer PA: Menisectomy in children: a long-term follow-up study. Am J Sports Med 11:111–115, 1983. 18. Medlar RC, Manidberg JJ, Lyne ED: Meniscectomies in children-report of long-term results. Am J Sports Med 8:87–92, 1980. 19. Nathan PA, Cole SC: Discoid meniscus: a clinical and pathological study. Clin Orthop 64:107–113, 1969. 20. Neuschwander DC, Drez D, Finney TP: Lateral meniscal variant with absence of posterior coronary ligament. J Bone Joint Surg Am 74:1186–1190, 1992. 21. Pellacci F, Montanari G, Prosperi P, et al: Lateral discoid meniscus: treatment and results. Arthroscopy 8:526–530, 1992. 22. Raber DA, Friederich NF, Buzzi R, et al: Discoid lateral meniscus in children: long-term follow-up after total meniscectomy. J Bone Joint Surg Am 8:1579–1586, 1998. 23. Stilli S, DiGennaro GL, Marchiodi L, et al: Arthroscopic surgery of the discoid meniscus during childhood. Chir Degli Org Mov 82:335–339, 1997. 24. Vandermeer R, Cunningham F: Arthroscopic treatment of the discoid lateral meniscus: Results of long-term followup. Arthroscopy 5:101–109, 1989. 25. Washington ER, Root L, Lierner U, et al: Discoid lateral meniscus in children—long term followup after excision. J Bone Joint Surg Am 77(9):1357–1361, 1995. 26. Woods GW, Whelan JM: Discoid meniscus. Clin Sports Med 9(3):695–706, 1990.

good results.29 Data reflect the KEY POINTS era of treatment with most cases 1. Post-meniscal treated by total and some by parexcision sequelae tial meniscectomy. include developOne is faced with meniscal ment of associated tissue to deal with that is poorly OCD (partial exciformed and biomechanically sion) and, after total at risk with questionable vascumeniscectomy, larity and healing potential. In premature knee the current arthroscopic period joint arthrosis. of meniscal salvage and pre2. Despite reported servation, outcomes may be difgood clinical results ferent, but to date there are no after total prospective, long-term results of meniscectomy at combined meniscoplasty and medium-term meniscal repair or combined follow-up, there is a meniscal repair and stabilization. disturbingly high Previous reports of outcomes incidence of radiafter total meniscectomy show ographically evident favorable clinical outcomes in degenerative the short and intermediate terms disease seen in (5–20 years).7,18,27–32,39,41 However, these patients. significant rates of radiologically apparent premature degenerative arthrosis (50–75%) despite limited clinical symptoms are cause for concern in these young adults.31,32,44 Short-term gain afforded by total discoid meniscectomy must be balanced against long-term consequences.

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References 1. Young RB: The external semilunar cartilage as a complete disc. In Cleland J, Mackey JY, Young RB (eds): Memoirs and Memoranda in Anatomy. London: Williams and Norgate, 1889, p 179. 2. Middleton DS: Congenital disc-shaped lateral meniscus with snapping knee. Br J Surg 24:246–251, 1936. 3. Ober F: Discoid cartilage: trigger knee. Surgery 6:24, 1939. 4. Arnold MP, Van Kampen A: Symptomatic ring-shaped lateral meniscus. Arthroscopy 16(8):852–854, 2000. 5. Kaplan EB: Discoid lateral meniscus of the knee joint. Bull Hosp Joint Dis 16(9):111–124, 1955. 6. Kim SJ, Lee YI, Choi, CH, et al: A partially duplicated discoid lateral meniscus. Arthroscopy 14(5):518–521, 1998. 7. Neuschwander DC, Drez D Jr, Finney TP: Lateral meniscal variant with absence of the posterior coronary ligament. J Bone Joint Surg Am 74(8):1186–1190, 1992. 8. Watanabe M, Takada S, Ikeuchi H: Atlas of Arthroscopy. Tokyo: IgakuShoin, 1969. 9. Ahn JH, Shim JS, Hwang CH, et al: Discoid lateral meniscus in children: clinical manifestations and morphology. J Pediatr Orthop 21(6):812–816, 2001. 10. Jordan MR: Lateral meniscal variants: evaluation and treatment. J Am Acad Orthop Surg 4(4):191–200, 1996. 11. Smillie I: The congenital discoid meniscus. J Bone Joint Surg Br 30:671–682, 1948. 12. Nathan PA, Cole SC: Discoid meniscus. A clinical and pathologic study. Clin Orthop 64:107–113, 1969. 13. Pinar H, Akseki D, Karaoglan O, et al: Bilateral discoid medial menisci. Arthroscopy 16(1):96–101, 2000. 14. Watson-Jones R: Specimen of internal semilunar cartilage as a complete disc. Proc Royal Acad Med 23:1588–1589, 1930. 15. Kaplan EB: The lateral menisco-femoral ligament of the knee joint. Bull Hosp Joint Dis 17:176–182, 1956. 16. Kaplan MJ: Discoid lateral meniscus of the knee joint: nature, mechanism, and operative treatment. J Bone Joint Surg Am 39:77–87, 1957. 17. Clark CR, Ogden JA: Development of the menisci of the human knee joint. Morphological changes and their potential role in childhood meniscal injury. J Bone Joint Surg Am 65(4):538–547, 1983. 18. Kocher MS, DiCanzio J, Zurakowski D, et al: Diagnostic performance of clinical examination and selective magnetic resonance imaging in the evaluation of intraarticular knee disorders in children and adolescents. Am J Sports Med 29(3):292–296, 2001. 19. Bland-Sutton J: Ligaments: their nature and morphology, ed 2. London: JK Lewis, 1897. 20. Brantigan OC: Ligaments of the knee joint: the relationship of the ligament of Humphry to the ligament of Wrisberg. J Bone Joint Surg Am 28:66–67, 1946. 21. 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. 22. Humphry GM: A treatise on the human skeleton including the joints. Cambridge-Macmillan 10(1):545–546, 1858. 23. Gupte CM, Smith A, McDermott ID, et al: Meniscofemoral ligaments revisited. Anatomical study, age correlation and clinical implications. J Bone Joint Surg Br 84(6):846–851, 2002.

24. Poynton AR, Javadpour SM, Finegan PJ, et al: The meniscofemoral ligaments of the knee. J Bone Joint Surg Br 79(2):327–330, 1997. 25. Andrish JT: Meniscal injuries in children and adolescents: diagnosis and management. J Am Acad Orthop Surg 4(5):231–237, 1996. 26. Zobel MS, Borrelo JA, Siegel MJ, et al: Pediatric knee MR imaging: pattern of injuries in the immature skeleton. Radiology 190(2): 397–401, 1994. 27. Aglietti P, Bertini FA, Buzzi R, Beraldi R: Arthroscopic meniscectomy for discoid lateral meniscus in children and adolescents: 10-year follow-up. Am J Knee Surg 12(2):83–87, 1999. 28. Hayashi LK, Yamaga H, Ida K, et al: Arthroscopic meniscectomy for discoid lateral meniscus in children. J Bone Joint Surg Am 70(10): 1495–1500, 1988. 29. Ikeuchi H: Arthroscopic treatment of the discoid lateral meniscus. Technique and long-term results. Clin Orthop (167):19–28, 1982. 30. Pellacci F, Montanari G, Prosperi P, et al: Lateral discoid meniscus: treatment and results. Arthroscopy 8(4):526–530, 1992. 31. Raber DA, Friederich NF, Hefti F: Discoid lateral meniscus in children. Long-term follow-up after total meniscectomy. J Bone Joint Surg Am 80(11):1579–1586, 1998. 32. Washington ER III, Root L, Liener UC: Discoid lateral meniscus in children. Long-term follow-up after excision. J Bone Joint Surg Am 77(9):1357–1361, 1995. 33. Paletta GA Jr, Manning T, Snell E, et al: The effect of allograft meniscal replacement on intraarticular contact area and pressures in the human knee. A biomechanical study. Am J Sports Med 25(5):692–698, 1997. 34. Irani RN Karasick D, Karasick S: A possible explanation of the pathogenesis of osteochondritis dissecans. J Pediatr Orthop 4(3):358–360, 1984. 35. Mitsuoka T, Shino K, Hamada M, et al: Osteochondritis dissecans of the lateral femoral condyle of the knee joint. Arthroscopy 15(1): 20–26, 1999. 36. Stanitski CL, Bee J: Juvenile osteochondritis dissecans of the lateral femoral condyle after lateral discoid meniscal surgery. Am J Sports Med 32(3):797–801, 2004. 37. Yoshida S, Feke GT, Ogasawara H, et al: Osteochondritis dissecans of the femoral condyle in the growth stage. Clin Orthop (346):162–170, 1998. 38. Aichroth PM, Patel DV, Marx CL: Congenital discoid lateral meniscus in children. A follow-up study and evolution of management. J Bone Joint Surg Br 73(6):932–936, 1991. 39. Fujikawa K, Iseki F, Mikura Y: Partial resection of the discoid meniscus in the child’s knee. J Bone Joint Surg Br 63(3):391–395, 1981. 40. Rosenberg TD, Paulos LE, Parker RD, et al: Discoid lateral meniscus: case report of arthroscopic attachment of a symptomatic Wrisberg-ligament type. Arthroscopy 3(4):277–282, 1987. 41. Vandermeer RD, Cunningham FK: Arthroscopic treatment of the discoid lateral meniscus: results of long-term follow-up. Arthroscopy 5(2):101–109, 1989. 42. Suzuki S: Arthroscopic surgery for discoid meniscus: a report of reoperated cases. Arthroscopy 7:115–118, 1986. 43. Sugawara O, Miyatsu M, Yamashita I, et al: Problems with repeated arthroscopic surgery in the discoid meniscus. Arthroscopy 7(1):68–71, 1991. 44. Smith CF, Van Dyk GE, Jurgutis J, et al: Cautious surgery for discoid menisci. Am J Knee Surg 12(1):25–28, 1999.

Chapter 22

Osteochondritis Dissecans of the Knee Theodore J. Ganley

Osteochondritis Dissecans of the Knee Osteochondritis dissecans (OCD) is a disorder of the subchondral bone that can secondarily affect the overlying articular cartilage and may, in some cases, lead to cartilage separation and fragmentation. In 1888, Francis König coined the phrase osteochondritis dissecans, which describes the potential of the bone–cartilage interface to separate. The prognosis of OCD depends on the status of the growth plate. The juvenile form of the disease occurs in children with open growth plates, usually between ages 5 and 15. The adult form occurs in those who have reached skeletal maturity, and is most commonly found in patients from ages 16–50. Those with greater skeletal maturity will more typically fail nonoperative treatment and have an overall worse prognosis. Males are more commonly afflicted than females, with a ratio between 2:1 and 3:1.1 The knee is the most commonly involved joint, and the lateral aspect of the medial femoral condyle is the most commonly affected site within the knee. OCD must be given sufficient medical attention in young patients, because a lesion impacts a child’s present and future activity levels and can contribute to degenerative joint disease later in life. Although some have not reported significant complications in those with juvenile OCD, Twyman et al. followed patients who had OCD as adolescents over an average of 34 years and found a 32% incidence of moderate-to-severe osteoarthritis.2 Possible causative factors for OCD include repetitive microtrauma, ischemia, genetic and endocrine factors, and anomalies of ossification. Although the term OCD refers to an inflammatory condition, the lack of inflammatory cells in histological sections of the lesions precludes this is as a primary cause. We theorize that repetitive microtrauma that leads to microfractures may cause subsequent focal ischemia and alteration of growth. As a result, the subchondral bone offers reduced support, the articular cartilage softens, and a crater may form with potential fragment separation. Mature

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articular cartilage, which does not spontaneously heal with hyaline cartilage once injured, has no significant direct blood supply, lymphatic drainage, or neural elements. KEY POINTS Clinical Presentation

1. OCD is a condition that affects the subchondral bone. 2. Repetitive trauma may contribute to subchondral changes that can secondarily lead to cartilage softening or separation. 3. Juvenile OCD has a much better prognosis than adult OCD.

Most children and adolescents with osteochondritis dissecans have a stable lesion at presentation. In this group the presenting complaints are generally nonspecific. The most commonly heard complaint is aching and activityrelated knee pain in which they localize the pain to the anterior aspect of the knee. The symptom complex overlaps with the complaints heard for other causes of anterior knee pain, such as chondromalacia patella. In both cases there may be pain when climbing hills or stairs. There is usually not a sense of knee instability. On physical examination, children and adolescents with stable OCD may walk with a mildly antalgic gait. With careful palpation over the anterior medial aspect of the knee through varying amounts of knee flexion, a point of maximum tenderness can often be found. This will correspond to the lesion, which is most commonly on the lateral aspect of the distal medial femoral condyle. In stable lesions there is usually not a knee effusion, crepitus, or much pain through a range of normal motion. Wilson’s sign3 may be helpful in diagnosing OCD. This test is performed starting with the knee flexed to 90 degrees. The tibia is then internally rotated, and the knee is extended 273

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from 90 degrees toward full extension. A positive Wilson’s test is pain at approximately 30 degrees of knee flexion. This is thought to be caused by contact of the medial tibial eminence with the osteochondritis dissecans lesion. Pain will be located over the anterior aspect of the medial femoral condyle. If the patient has been having pain for more than a few weeks, ipsilateral quadriceps atrophy may be noted. In the usual circumstance, in which the child or adolescent presents with an unstable lesion, mechanical symptoms are more pronounced. An antalgic gait is common. There is usually a knee effusion, possibly associated with crepitus as the knee is taken through a range of motion. In both stable and unstable presentations, both knees should be examined, because the condition may be bilateral. Diagnostic Studies There are several goals when taking images of children and adolescents who present with signs and symptoms that suggest an OCD lesion. Successful imaging will characterize the lesion, determine the prognosis of nonoperative management, and possibly determine the ultimate healing of the lesion. Because the success of nonoperative management has been quite unpredictable in cases of juvenile osteochondritis dissecans, many studies have sought an optimal imaging protocol to guide the surgeon and patient in determining which cases should be treated immediately with arthroscopic management and which cases will heal by nonoperative means. Technetium bone scanning, and more recently magnetic resonance imaging (MRI) and MR arthrography, have been studied, but to date there is no single imaging protocol that reliably predicts the success of nonoperative management. The initial plain radiographs should include anteroposterior and lateral views of the knee (Figure 22–1).Tunnel views are also valuable, because OCD in the typical location (the posterior lateral portion of the medial femoral condyle) may be difficult to see on an anteroposterior view. Merchant or skyline views should be added when patellar OCD is a possibility. The goal of plain radiographs is to characterize and localize the lesion, as well as to rule out other bony pathology of the knee region. In children younger than age 7, irregularities of the distal femoral epiphyseal ossification center may simulate the appearance of OCD. In older children the status of the physis (wide open, closing, or closed) should be assessed, because this has major implications in the prognosis for healing. The location of the lesion was described by Cahill and Berg.4 A general estimate of size can also be obtained from the plain films. MR imaging has become a routine part of the diagnostic evaluation of osteochondritis dissecans. Initial MRI can give an accurate estimation of the size of the lesion and the status of the cartilage in the subchondral bone (Figure 22–2, A and B). The extent of bony edema, the presence of a high signal zone beneath the fragment, and the presence of other loose bodies are also important findings on initial MRI. For more than a decade, MR imaging has been studied extensively with the hope that certain MR findings would have definitive prognostic value in determining if an OCD lesion in the skeletally immature patient will heal with

Figure 22–1 Plain radiograph revealing an OCD lesion of the lateral aspect of the medial femoral condyle.

nonoperative treatment. De Smet et al.5 described four MRI criteria on T2-weighted images: (1) A line of high signal intensity at least 5 mm in length between the OCD lesion and the underlying bone ; (2) an area of increased homogenous signal at least 5 mm in diameter beneath the lesion; (3) a focal defect of 5 mm or more in the articular surface; and (4) a high signal line traversing the subchondral plate into the lesion. Of these signs, De Smet et al. found that the high signal behind the fragment was most predictive because it was found in 72% of all unstable lesions. Pill et al.6 attempted to predict the success of nonoperative treatment using both MRI and clinical criteria. These investigators applied De Smet’s four signs and found that the high signal line was most common in patients who failed nonoperative treatment. The size of the lesion and the maturity of the patient were also very important predictors of the failure of nonoperative treatment in this study. O’Connor7 compared MRI and arthroscopic findings, focusing specifically on the prognostic value of De Smet’s high signal line behind the fragment. These authors and others believe that this high signal line can represent

Osteochondritis Dissecans of the Knee

Figure 22–2 A, MR imaging (T1-weighted image) reveals an OCD lesion of the lateral aspect of the medial femoral condyle. B, An MRI scan of the medial femoral condyle of this patient demonstrates a large OCD lesion with a defect in the overlying articular cartilage.

either healing vascular granulation tissue or articular fluid that has collected beneath the subchondral bone (implying a break in the articular surface). In this study the investigators could improve the staging accuracy from 45–85% when they interpret the high signal line on T2 as a predictor of instability only when it was accompanied by a breach in the cartilage, as seen on MRI T1 imaging.

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With several studies showing that unenhanced MRI does not have the definitive prognostic value in juvenile osteochondritis dissecans, several studies have looked at the role of gadolinium. Bohndorf 8 found intravenous (IV) gadolinium helpful by showing enhancement in the form of a gadolinium enhancement high signal line behind the fragment indicative of healing granulation tissue, and not fluid from the joint. However, Vonstein et al.9 showed no correlation between gadolinium enhancement and healing in juvenile osteochondritis dissecans. These investigators found that the lesion size was still the main determinant of healing. Kramer et al.10 looked at MR arthrography with gadolinium. Although they did not look at the prognostic value in terms of healing, they did determine that this technique could reliably show a breach in the articular cartilage. Technetium bone scans have also been evaluated in hopes that they would provide information about the biological healing capacity of an OCD lesion. Cahill and Berg4 proposed a protocol of static serial technetium bone scans every 6 weeks until evidence of healing. Litchman et al.11 found that in patients who had symptoms from OCD for more than 2 months, and who had increased blood flow quantified on technetium scans, the lesions healed spontaneously. Despite this information, serial bone scanning has not been widely adopted in the management of OCD lesions. Paletta et al.12 looked at the quantitative bone scans in a small series (12 patients) and found that increased activity predicted healing in those patients with open physis, but not in adolescents with closing physis. This is unfortunate, because it is this latter group in whom healing is more difficult to predict. Considering the results of work published to date, current diagnostic imaging recomKEY POINTS mendations for OCD include AP, lateral, and tunnel views of the 1. Factors associated involved knee at presentation. with failure of An initial MRI is often obtained nonoperative to study the lesion for its size, the treatment include status of the cartilage and the the following: larger subchondral bone, the presence size, greater of a high signal zone beneath skeletal maturity, the lesion, and the extent of surand high signal rounding bony edema, as well behind and traversas the possible presence of loose ing the cartilage of bodies or any other pathology the OCD lesion. within the knee. Smaller lesions 2. Plain radiographs with intact cartilage are much and advanced more likely to respond to nonimaging such as operative treatment, especially in MRI can be skeletally immature patients. combined with Unstable lesions, or knees with clinical information loose bodies, torn menisci, or any to help the clinician other operative intraarticular predict healing pathology, warrant initial arthropotential. scopic evaluation and treatment. Nonoperative Management Because the natural history of a stable osteochondritis dissecans lesion is generally favorable in a child with open physes, there is widespread agreement that initial nonoperative management is indicated.

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Because the failure of the cartilage surface probably follows the failure of the underlying bone, most physicians have embraced some sort of rest or immobilization protocol. Immobilization can be successfully achieved in a cast, a brace, or a standard knee immobilizer. Three options are most commonly available: a cylinder cast in slight flexion; a knee immobilizer; or a hinged, unloader-type brace. Further studies are needed to determine the optimal immobilization protocol. The nonoperative management protocol should be thought of as a three-phase program. The first phase involves immobilization of the knee for 6 weeks with partial weight-bearing. At the end of this period the child should be pain free. In the second phase (weeks 6–12), weight-bearing as tolerated is permitted without immobilization. A physical therapy protocol is initiated, emphasizing knee range of motion and low-impact quadriceps and hamstring strengthening. If the patient remains pain free, the third phase begins 3 months after diagnosis. This final phase includes close observation of the pediatric athlete as he or she begins running, jumping, and cutting sports. Such high impact and shear activities should be restricted until the child has several months of pain-free low-impact conditioning and the radiograph findings show healing. An MRI may be repeated in the third phase to assess healing. If the symptoms return, or if radiograph findings show any progression, then a repeat of immobilization can be considered. However, although immobilization alone is

often successful in juvenile OCD, it may be completely intolerable to young athletes and their parents. The art of dealing with these impatient and frustrated young athletes includes counseling on the risks and benefits of continued nonoperative treatment versus moving on to drilling or other surgical management. Operative Management The goal of treatment via nonoperative or operative means is to have a stable construct of subchondral bone, calcified tidemark, and repair cartilage. Operative treatment should be considered to attain these goals in patients with detached or unstable lesions and in those patients approaching epiphyseal closure whose lesions have been unresponsive to nonoperative management.13 We will consider surgical intervention in patients with intact OCD lesions with failure to heal after at least 6 months of nonoperative treatment. Drilling may be used to stimulate subchondral bone healing if nonoperative measures are unsuccessful in healing intact lesions. Antegrade drilling from proximal to distal through the epiphysis avoids penetration of articular cartilage, although it may be more technically challenging to obtain an accurate depth of penetration. (Technical Note 22–1). Retrograde transarticular drilling creates channels within the articular cartilage to stimulate bleeding and subsequent healing of the subchondral bone (Technical Note 22–2). This procedure is generally considered to be a Text continued on p. 285

TECHNICAL NOTE 22–1

Arthroscopically Assisted Extraarticular Drilling for Osteochondritis Dissecans of the Knee Henry G. Chambers • Scott C. Nelson

Indications Extraarticular drilling of osteochondritis dissecans lesions is indicated for lesions with intact cartilage (grade 1 as classified by Guhl).1 Those lesions showing signs of early separation (grade 2 as classified by Guhl) can be drilled as well; however, less predictable results would be expected. All patients undergo a trial of nonoperative management for at least 3 months before surgery. The basic principle of nonoperative management is a reduction of activity to a level where symptom-free activities of daily living are possible. Various authors recommend nonoperative protocols including protected weightbearing with or without immobilization for 6 months or longer.2–7 Casting may cause knee stiffness,5 and disuse atrophy has not been used at our institution. Our current recommendations include restriction from all sports activities that involve jumping, twisting, and impact loading. Activities

such as walking, bicycling, and swimming are permitted as tolerated.8 If there is no healing of the lesion, then one should consider performing an arthroscopic drilling of the lesion in an extraarticular manner. The extraarticular approach is used at our institution because the pins do not violate the joint surface, and more drill holes can be placed perpendicular to the lesion. Setup The patient is positioned supine on the operating table. The foot of the bed is removed if possible. If not, the patient is positioned so that the knees can be flexed greater than 90 degrees, and the fluoroscope can be angled under the table. A pneumatic tourniquet is applied but not routinely inflated. The arthroscopic tower and the instrument table are positioned on the contralateral side of Continued

Osteochondritis Dissecans of the Knee

TECHNICAL NOTE 22–1

Arthroscopically Assisted Extraarticular Drilling for Osteochondritis Dissecans of the Knee (Continued) the affected limb or over the top of the bed. The C-arm is brought in from the end of the bed (although it can be brought in from the side as well), and the fluoroscopy monitor is placed near the foot of the patient on the same side. Technique Preoperative prophylactic antibiotics are given. A routine diagnostic arthroscopy is performed using a three portal technique. This includes a superior outflow portal placed on the opposite side of the lesion (e.g., a superior lateral portal is used for a medial femoral condyle lesion). After introducing the arthroscope through a lateral peripatellar portal, a thorough examination of the entire knee is performed to address any meniscal, ligamentous, or other pathology. The OCD lesion is visualized to confirm intact cartilage. A blunt probe is used to assess the quality of the cartilage and check for the possibility of a loose flap. The arthroscope is

removed from the joint. The C-arm is then brought in, and an AP view of the knee is obtained with the knee in moderate extension (Figure 22–3). The C-arm may need to be tilted to visualize posterior lesions. A 0.062-mm K-wire directed toward the center of the lesion is then placed through the affected femoral condyle with a starting point just distal to the physis (Figure 22–4). The location of the lesion on preoperative lateral films is kept in mind. The typical lesion usually lies between Blumensaat’s line and the distal extension of a line drawn along the posterior cortex of the femur. The K-wire is advanced into the lesion but not through the articular cartilage (Figure 22–5). A cross-table lateral view is then obtained by rotating the C-arm (Figure 22–6). If the first K-wire is not directed into the center of the lesion, then a second wire is placed, making the necessary adjustments on the lateral view to position the pin in the center of the lesion (Figure 22–7). It is not necessary to use an aiming device such as that from the ACL set.

Figure 22–3 AP view of the knee with the knee in moderate extension.

Continued

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TECHNICAL NOTE 22–1

Arthroscopically Assisted Extraarticular Drilling for Osteochondritis Dissecans of the Knee (Continued)

Figure 22–4 A 0.062-mm K-wire directed toward the center of the lesion is placed through the affected femoral condyle with a starting point just distal to the physis.

Figure 22–5 K-wire is advanced into the lesion but not through the articular cartilage.

The wires should be advanced so that they engage the subchondral bone but do not penetrate the cartilage surface. This central K-wire is trimmed shorter to avoid impingement with subsequent wires. The “house” parallel wire guide (Synthes; Paoli, Pennsylvania) (Figure 22–8) is used to direct subsequent 0.062-mm K-wires in a circumferential fashion around the central K-wire (Figures 22–9 and

22–10). The guide is rotated in 1-mm increments to redirect the K-wire into different positions within the lesion (see Figures 22–6 and 22–7). Depending on the size of the lesion, both the inner and outer sets of holes can be used on the guide. Fluoroscopy is used as needed throughout the procedure to confirm wire position and depth. Particular attention is paid to the fluoroscopic view in which the Continued

Osteochondritis Dissecans of the Knee

TECHNICAL NOTE 22–1

Arthroscopically Assisted Extraarticular Drilling for Osteochondritis Dissecans of the Knee (Continued)

Figure 22–6 A cross-table lateral view is obtained by rotating the C-arm.

Figure 22–7 If the first K-wire is not directed into the center of the lesion, then a second wire is placed, making the necessary adjustments on the lateral view to position the pin in the center of the lesion. The “house” parallel wire guide is used to assist with sequential wire placement.

K-wire depth is closest to the articular cartilage. For lesions on the posterior aspect of the condyles, this is the lateral view, and for medial lesions the AP view may be preferable (Figures 22–11 and 22–12). Usually approximately 15–20 holes are drilled, making new skin punctures for each (Figure 22–13).

At the end of the procedure the arthroscopic portals are closed with 4-0 absorbable subcuticular suture. Bupivacaine (0.25%) and morphine (4 mg) solution is then injected intraarticularly and around the portals. Sterile dressings are applied, and an elastic wrap is placed from the toes to the thigh. Continued

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TECHNICAL NOTE 22–1

Arthroscopically Assisted Extraarticular Drilling for Osteochondritis Dissecans of the Knee (Continued)

Figure 22–8 This offset guide is used to direct subsequent 0.062-mm K-wires in a circumferential fashion around the central K-wire.

Figure 22–9 The offset guide is rotated for sequential wire placement.

Continued

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TECHNICAL NOTE 22–1

Arthroscopically Assisted Extraarticular Drilling for Osteochondritis Dissecans of the Knee (Continued)

Figure 22–10 360 degree rotation of the offset guide for sequential wire placement.

Figure 22–11 This is the lateral view for lesions on the posterior aspect of the condyles.

Continued

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TECHNICAL NOTE 22–1

Arthroscopically Assisted Extraarticular Drilling for Osteochondritis Dissecans of the Knee (Continued)

Figure 22–12 The AP view may be preferable for medial lesions.

Figure 22–13 Usually approximately 15–20 holes are drilled, making new skin punctures for each.

Postoperative Management Patients are kept touchdown weight-bearing for 6 weeks postoperatively, but they are allowed to swim 2 weeks after surgery. At 6 weeks postoperatively, AP, lateral, and tunnel x-rays of the knee are taken to assess healing. If healing is noted, progressive weight-bearing is allowed. However, if there

are no signs of radiographic healing, touchdown, weight-bearing is maintained, usually for an additional 6 weeks. Sports are avoided for at least 3 months after surgery. At 3 months postoperatively, radiographs are again taken to assess healing, and activities are advanced if the patient is pain free and healing is progressing radiographically. Continued

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TECHNICAL NOTE 22–1

Arthroscopically Assisted Extraarticular Drilling for Osteochondritis Dissecans of the Knee (Continued) Results In a preliminary study, 12 knees treated with transarticular drilling were compared with 40 knees treated with extraarticular drilling. A successful result was defined by a return to full activities with complete resolution of pain and swelling, as well as radiographic evidence of healing. Radiographic healing was evidenced by new bone formation in the preoperative lucent area surrounding the OCD lesion. By these criteria, 6 of the 12 patients drilled transarticularly healed. Healing time ranged from 3–13 months. In contrast, 37 of the 40 patients treated with extraarticular drilling went on to heal. Healing time ranged from 2–6 months. No intraoperative or postoperative complications were noted in either group.

References 1. Guhl JF: Arthroscopic treatment of osteochondritis dissecans. Clin Orthop 167:65–74, 1982. 2. Aglietti P, Buzzi R, Bassi PB, et al: Arthroscopic drilling in juvenile osteochondritis dissecans of the medial femoral condyle. Arthroscopy 10(3):286–291, 1994. 3. Cahill B: Treatment of juvenile osteochondritis dissecans and osteochondritis dissecans of the knee. Clin Sports Med 4:367–384, 1985. 4. Cain LE, Clancy WG: Treatment algorithm for osteochondral injuries of the knee. Clin Sports Med 20(2):321–342, 2001. 5. Hughston JC, Hergenroeder PT, Courtenay BG: Osteochondritis dissecans of the femoral condyles. J Bone and Joint Surg Am 66:1340–1348, 1984. 6. Kocher MS, Micheli LJ, Yaniv M, et al: Functional and radiographic outcome of juvenile osteochondritis dissecans of the knee treated with transarticular arthroscopic drilling. Am J Sports Med 29:562–566, 2001. 7. Williams JS, Bush-Joseph CA, Bach BR: Osteochondritis dissecans of the knee. Am J Knee Surg 11:221–232, 1998. 8. Glancy GL: Juvenile osteochondritis dissecans. Am J Knee Surg 12(2):120–124, 1999.

TECHNICAL NOTE 22–2

Arthroscopic Transarticular Drilling for Juvenile Osteochondritis Dissecans Lyle J. Micheli • Jennifer L. Cook

Background Osteochondritis dissecans is encountered with increased frequency in active children and adolescents. Typically, a child will complain of knee pain, particularly with activity. Mechanical symptoms such as catching or locking may be present. Radiographs of the affected knee, including AP, lateral, skyline, and notch views, may show a lesion that usually occurs in the lateral aspect of the medial femoral condyle. The extent of the lesion and whether it is an open lesion (hence not in contact with the synovial fluid) can be determined with MRI and concomitant arthrogram. Treatment depends on a multitude of factors including age of the patient, size of the lesion, location of the lesion, whether the lesion is open or closed, and whether the lesion is mechanically stable or a loose body is present. In cases where the lesion appears to be closed, we will attempt at least 6 months of conservative management involving either complete rest from sports activities or partial

immobilization with crutches in an attempt to attain healing at this site. In cases that have not attained evidence of radiographic healing with conservative management, it has been our practice, particularly with larger lesions, as well as lesions in atypical locations such as the lateral femoral condyle, trochlear patella or posterior medial central femoral condyle, to proceed with diagnostic arthroscopy. Setup: General anesthesia is used in these patients. 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: The leg is routinely prepped and draped. An Esmarch bandage is used for exsanguination. Arthroscopy is performed with a standard anterolateral viewing portal. The location of the lesion is identified based on associated preoperative radiographs and MRI. Continued

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TECHNICAL NOTE 22–2

Arthroscopic Transarticular Drilling for Juvenile Osteochondritis Dissecans (Continued) Inspection of the lesion is carried out. In cases in which it is uncertain exactly where the margins of the lesion are located, it is our practice to use fluoroscopy to help outline the position of the lesion. It is sometimes necessary to put a Kirschner wire in what is believed to be the margin of the lesion and then fluoroscoping this site. Once identified, the lesion is probed to assess size, depth, and stability. After appropriate probing of the lesion has been carried out so that the circumference is identified, and if the lesion is determined to be closed and stable, a series of transarticular drillings are performed. We generally use 0.045 smooth Kirschner wires to accomplish this. With transarticular drilling, a series of channels are developed across the necrotic subchondral bone into the marrow in an attempt to introduce clot and osteogenic cells into the dead fragment to promote healing (Figure 22–14). After the appropriate number of transarticular drillings has been carried out, we deflate the tourniquet to ensure that there is good flow from the drill sites. One of the criticisms of this transarticular technique has been that it creates an open lesion out of a closed lesion. It is our feeling that the clotting that occurs in these channels occurs very rapidly and that the open aspect of this lesion is really quite transient, perhaps in the range of only 3–5 minutes. If there are cracks or fissuring of the lesion, hence an open lesion, we proceed to debridement at the base of the lesion with reduction and screw

fixation. Any associated loose bodies are removed. Cartilage repair techniques may be needed for particularly large lesions if the fragment is unable to be reattached. Postoperative Management Postoperatively, the patient is immediately placed in a Bledsoe brace restricted to 0–30 degrees to 45 degrees range of motion. The patient is non– weight-bearing to the affected extremity with this brace immobilization. In the case of relatively confined lesions, we will immobilize and partial weight-bear these patients for 4 weeks, at which point we obtain radiographs to evaluate for evidence of early healing. In larger lesions in older children, we maintain immobilization for up to 6 weeks before obtaining radiographs postoperatively. Physical therapy is initiated at 4 weeks with discontinuation of the brace, advancement to full range of motion, and closed kinetic chain exercises. Weight-bearing is progressed over a 1-week course of time. Return to activities is permitted after 12 weeks if there is concomitant evidence of radiographic healing and resolution of symptoms. Suggested Reading 1. Kocher MS, Micheli LJ, Yaniv M, et al: Functional and radiographic outcome of juvenile osteochondritis dissecans of the knee treated with transarticular arthroscopic drilling. Am J Sports Med 29(5):562–566, 2001.

Figure 22–14 Channels are made with K-wires.

Osteochondritis Dissecans of the Knee

more technically straightforward procedure, although the channels created heal with fibrocartilage. For intact lesions of the lateral aspect of the medial femoral condyle, the arthroscopic lateral portal may be used as a working portal to allow passage of a probe for analysis and a small, smooth K-wire for treatment (Figure 22–15). Accessory portals may be used, and the knee should be flexed or extended to ensure that the K-wire is as perpendicular as possible to the articular surface. Maintaining a nearly perpendicular angle of the K-wire to the articular surfaces can help to avoid undermining the remainder of the lesion. The K-wire is passed deep enough to penetrate the subchondral bone, and the drill holes are placed several millimeters apart. The technique of transarticular drilling was performed by Anderson and colleagues14 in 17 patients, and in the skeletally immature group 18 of 20 lesions healed, whereas only 2 of 4 lesions healed in the skeletally mature group at a 2–9 year follow-up. Aglietti15 and colleagues noted healing on the AP, as well as the lateral radiographs at 4-year follow-up after transarticular drilling in 14 patients studied. Kocher et al.16 studied 23 skeletally immature patients with 30 affected knees with lesions at the lateral aspect of the medial femoral condyle. Radiographic healing was achieved in all patients at an average of 4.4 months after drilling, and there was significant improvement in the mean Lysholm score at follow-up of 3.9 years. In patients with partially unstable flap lesions, fibrous tissue frequently exists between the osteochondral flap and the underlying bone. Fixation may be performed when the fibrous tissue has been removed. If significant subchondral bone loss exists, then autologous bone graft can be packed into the crater before reduction and fixation. Unstable lesions should be fixed in place provided that there is an appropriate defect to fragment match. If there is a very small fragment and a large defect, then fixation may lead to a worse prognosis than removal and salvage procedures. Options for fixation of hinged or otherwise unstable lesions

Figure 22–15 Drilling of an intact OCD lesion, using an antegrade transarticular approach. The smooth K-wire used is perpendicular to the articular surface. The fat droplet shown indicates subchondral bone penetration from a prior drilling site.

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include pins, countersunk compression screws, and Herbert screws made of stainless steel or bioabsorbable material (Technical Note 22–3). Further options include biological fixation using repore “allograft” strips of cortical bone from the adjacent metaphysis of the tibia, and also osteochondral autograft plug fixation. The technique of using cortical strips of bone from the metaphysis of the tibia was described by Navarro and colleagues,17 and among 11 patients treated, all were able to return to strenuous activities. Although a variety of fixation devices have been developed and used with success, care should be taken to follow orthopedic principles of secure fixation, postoperative immobilization to allow adequate healing, and careful monitoring of patients to check for biomechanical symptoms postoperatively. These concepts should be followed in the use of biological fixation and bioabsorbable materials as well, because some lesions may not heal. In the event of a failed union, repetitive loading and fixation failure can occur regardless of the material used. We perform arthroscopic compression screw fixation followed by casting in a position that does not permit the patient to bear weight on the OCD lesion. The cast is placed in a position such that the screw does not articulate with the joint surface. After 6 weeks, an arthroscopic procedure is performed to remove the screw and evaluate the lesion. If the lesion is healed, the patient is advanced to a rehabilitation program. If the lesion has not healed when evaluated with a probe arthroscopically, the screw and flap are removed, and salvage procedures are performed on the remaining defect. A number of options exist for treating full-thickness OCD lesions. Arthroscopic drilling and abrasion arthroplasty using burs, as well as microfracturing using picks, serve the purpose of recruiting pluripotential cells. These are more technically simple, lower morbidity procedures, and recruited cells tend to differentiate into repair fibrocartilage (Figure 22–19). This technique may be effective in treating smaller lesions, although patients should be protected from high-impact loading for at least 9 months postoperatively. The results for larger lesions may deteriorate over time because of the stiffness and the diminished capacity of fibrocartilage to respond to sheer stress.18 Several other methods have been described to allow the treating physician to use autologous materials for biological resurfacing and fixation. A cartilaginous extracelluar matrix can also be produced using periosteum, which is transplanted with the cambium layer down into the defect. While Neidermann and colleagues19 noted 1-year successful results using periosteal transplantation for OCD, Madsen20 evaluated long-term results of this technique in OCD of the knee and found this procedure to be unsatisfactory because of continued knee pain and reoperations at 8-year followup. The technique of transplanting autologous osteochondral plugs from a nonaffected portion of the knee into the osteochondritis dissecans lesion has been described with success by Outerbridge et al.21 in a series of 10 patients with large femoral OCD lesions. Long-term effects of donor site morbidity in patients using this technique are not yet known. Peterson et al. reported on the treatment of OCD at 2–10 years using autologous chondrocyte transplantation, a technique in which chondrocytes are harvested from

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TECHNICAL NOTE 22–3

Fixation for Juvenile Osteochondritis Dissecans Lesions Bernard Cahill

Osteochondritis dissecans and juvenile osteochondritis dissecans (JOCD) are distinct entities that require different management.1 Although both conditions result from stress fractures of the subchondral bone, JOCD has a much better prognosis; treated conservatively, 50% of cases will heal, probably providing a normal knee during adult life. In contrast, OCD often is followed by the early onset of degenerative arthritis regardless of whether the patient is treated. The treatment of JOCD and OCD, whether nonoperative or operative, must be based on the principles of fracture treatment. Unfortunately, surgical correction of either of these conditions is unlikely to succeed unless the joint is perfectly restored.2 Since König’s coining of the term osteochondritis dissecans, there has been a proliferation of opinions about what to do with the unstable lesions of the femoral condyles. We can be sure that most of the physicians before König, and following him, discarded the fragments of the femoral condyles. There is no literature regarding attempts to replace the fragments into the crater. One would speculate that sutures, ivory pegs, bone pegs, and bone screws may have been used to stabilize the fragment. I have a collection of ivory and bone pegs and screws of size and tooling that could have been used, although they must have been rather useless for repair of the OCD lesion. In the 1900s, there were scattered reports of the use of bone pegs, although there was no follow-up on the results. In the 1930s, several papers were published stating that nails and metallic screws could stabilize the fragment, but again there was no follow-up with these papers. Generally, papers published on JOCD and OCD were concerned with diagnosis, etiology, and conservative treatment, not surgical repair. Preparation of the Crater It is necessary to discuss the crater in the femoral condyle in cases that are unstable. If the lesion is not properly prepared, the femoral condyle will not be restored, no matter what fixation device is implanted. Numerous authors have commented on the growth of partially detached or loose JOCD (OCD) fragments while the crater of the lesion

retains its original dimensions. This creates a fragment mismatch, which makes it difficult to perfectly fit the crater and restore joint-surface orthopticity. The fragment must be trimmed, not the crater. This is particularly difficult when the reduction is attempted arthroscopically.2 Unstable lesions that have been present for 3 months or more have detritus on both the fragment and the crater. This debris must be curetted to bleeding bone on both surfaces, to ensure healing. In hinged lesions, the “hinge” should be preserved because there is some circulation (condyle to fragment) in most of these problems. Existing Fixation Implants and Characteristics • Cannulated screws: No compression. No heads to screw. Partially threaded screws have compression. Screw head leaves indentation on the articular surface. Screw head may scuff tibial surface. Second procedure required for screw removal (Figure 22–16). • Autologous bone sticks3: Biological. No compression. May scuff tibial articular surface if they protrude. • Herbert Screws4: Variable pitch gives some compression. Second procedure is usually performed for removal (Figure 22–17). • Bioabsorbable screws: First-generation implants had complications of synovitis, osteolysis of bone surrounding implants, chronic effusions, and aseptic exudates.5 • SmartNail: A new fixation device made of SR-96L/4D PLA (self-reinforced strength 96% Levo [rotary]/4% dextro polymer.) Some limited compression. Bioabsorbable. Low profile (Figure 22–18). The Europeans have vast experience using bioabsorbable polymers in the treatment of trauma, JOCD/OCD, and sports medicine. Juutilainen et al.6 reported 1043 cases with 107 complications. There were 21 infections but no sinus formation, failure of fixation 46 patients, and 936 operations that were healed and uneventful. Rokkanen et al.7 reported 3200 operations since 1984; among them were 24 cases of OCD. All these OCD patients were operated on with bioabsorbable devices that provided 19 excellent or good results. Continued

Osteochondritis Dissecans of the Knee

TECHNICAL NOTE 22–3

Fixation for Juvenile Osteochondritis Dissecans Lesions (Continued)

Figure 22–16 Herbert screw fixation of a Ewing and Voto stage 4 lesion of the medial femoral condyle in a 15-year-old male. A, Preoperative notch radiograph. B, 6-week postoperative notch radiograph. C, 6-month postoperative notch radiograph.

Continued

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TECHNICAL NOTE 22–3

Fixation for Juvenile Osteochondritis Dissecans Lesions (Continued)

Figure 22–16—cont’d

D, 1-year postoperative notch radiograph. (Courtesy Mininder S. Kocher, MD, MPH.)

Figure 22–17 Cannulated screw fixation of a Ewing and Voto stage III lesion of the medial femoral condyle in a 14-year-old female who had undergone previous transarticular drilling. A, Preoperative sagittal MRI.

Continued

Osteochondritis Dissecans of the Knee

TECHNICAL NOTE 22–3

Fixation for Juvenile Osteochondritis Dissecans Lesions (Continued)

Figure 22–17—cont’d

B, Preoperative AP radiograph. C, 2-week postoperative AP radiograph.

Continued

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TECHNICAL NOTE 22–3

Fixation for Juvenile Osteochondritis Dissecans Lesions (Continued)

Figure 22–17—cont’d

D, 1-year postoperative AP radiograph. (Courtesy Mininder S. Kocher, MD, MPH.)

Figure 22–18 Smartnail fixation of a Ewing and Voto stage 3 lesion of the medial femoral condyle in a 13-year-old female. A, Preoperative coronal MRI.

Continued

Osteochondritis Dissecans of the Knee

TECHNICAL NOTE 22–3

Fixation for Juvenile Osteochondritis Dissecans Lesions (Continued)

Figure 22–18—cont’d B, Preoperative AP radiograph. C, 6-week postoperative AP radiograph. D, 6-month postoperative AP radiograph. (Courtesy Mininder S. Kocher, MD, MPH.)

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TECHNICAL NOTE 22–3

Fixation for Juvenile Osteochondritis Dissecans Lesions (Continued) References 1. Smillie IS: Treatment of osteochondritis dissecans: J Bone Joint Surg Am 35:26–47, 1953. 2. Cahill B: Osteochondritis dissecans of the knee: treatment of juvenile and adult forms. J Am Acad Orthop Surg 3: 237–247, 1995. 3. Navarro R, Cohen M, Filho M, et al: The arthroscopic treatment of osteochondritis dissecans of the knee with autologous bone sticks. Arthroscopy: J Arthro Rel Surg 18(8):840–844, 2002. 4. Cugat K, Garcia M, Cusco X, et al: Osteochondritis dissecans: a historical review and treatment with cannulated screws. A clinical study. Arthroscopy. 9:675–684, 1993.

5. Friederichs MG, Greis PE, Burks RT: Pitfalls associated with fixation of osteochondritis dissecans fragments using bioabsorbable screws. Arthroscopy: J Arthro Rel Surg 17(5): 542–545, 2001. 6. Juutilainen T, Hirvensalo E, Partio EK, et al: Complications in the first 1043 operations where self-reinforced poly-L-lactide implants were used solely for tissue fixation in orthopaedics and traumatology. Internat Orthop (SICOT) 26:122–125, 2002. 7. Rokkanen PU, Bostman O, Hirvensalo E, et al: Bioabsorbable fixation in orthopaedics surgery and traumatology. Elsevier, Biomaterials 21:2607–2613, 2000.

Rehabilitation

Figure 22–19 Drilling of a full-thickness OCD lesion to recruit pluripotent cells from the marrow elements.

a healthy articular cartilage surface, grown in vitro, and later injected into the defect beneath a periosteal patch. Of 48 patients treated, 7 received surgery before 18 years of age, and 35 patients had the onset of OCD as juveniles. Successful clinical results were noted in more than 90% of the patients.22 King et al.23 evaluated autologous chondrocyte transplantation for the treatment of large defects in articular cartilage of the distal femur in adolescent patients, and noted outcomes slightly better than previously reported results found in adult patients. It was theorized that this was a result of presumed superior articular substance in the adjacent regions of the knee in those without malalignment.23 In patients with significant femoral surface articular cartilage and subchondral bone defects, bone-articular surface allografts have been described, although no long-term results in skeletally immature patients are yet available.24

KEY POINTS Patients should have a rehabilitation program that combines 1. Nonoperative and, if protection of the affected articneeded, operative ular surface and underlying treatment should be subchondral bone with maintepursued until a stanance of strength and range of ble construct of motion. Straight leg raising and subchondral bone, isometric exercises can be percalcified tidemark, formed without resistance iniand repair cartilage tially, then advanced by adding exist. a few pounds per week until 2. When performing 10% of the patient’s body operative fixation weight is reached. A formal of hinged lesions, physical therapy program is the principles of instituted for 6 weeks, emphasizsecure fixation, ing flexibility training and postoperative closed kinetic chain strengthenimmobilization, ing, and functional or sportand careful specific training. Patients are postoperative kept out of running and jumping monitoring should sports, but can perform lowbe followed. impact activities such as walk3. These principles ing, submaximal biking, and should be adhered swimming within the first 3 to whether metallic, months. Patients may return to biodegradable, or running and jumping sports biological materials when healing is noted on plain are used. radiographs. Those who have undergone marrow stimulation or autologous chondrocyte implantation (ACI) are placed on a continuous passive motion (CPM) program to enhance the healing of the articular surface during the first 6 postoperative weeks. They are also protected from high-impact loading for at least 9 months. If patients return to activity before the cartilage has become firm, they will typically complain of pain with maneuvers such as squatting or jumping.

Osteochondritis Dissecans of the Knee

Summary Osteochondritis dissecans lesions therefore demand a healthy respect in patients of all ages, because untreated or inadequately treated lesions may progress from stable, intact lesions to unstable lesions with osteochondral loose bodies, chondral flap tears, and full-thickness defects. Younger patients should be given every opportunity to heal, because the prognosis deteriorates after skeletal maturity. References 1. Schenck R C Jr, Goodnight JM: Osteochondritis dissecans. J Bone Joint Surg Am 78(3):39–456, 1996. 2. Twyman RS, Desai K, Aichroth PM: Osteochondritis dissecans of the knee. A long-term study. J Bone Joint Surg Br 73(3):461–464, 1991. 3. Wilson JN: A diagnostic sign in osteochondritis dissecans of the knee. J Bone Joint Surg Am 49(3):477–480, 1967. 4. Cahill BR, Berg BG: 99m-Technetium phosphate compound joint scintigraphy in the management of juvenile osteochondritis dissecans of the femoral condyles. Am J Sports Med 11(5):329–335, 1983. 5. De Smet AA, Ilahi OA, Graf BK: Untreated osteochondritis dissecans of the femoral condyles: prediction of patient outcome using radiographic and MR findings. Skeletal Radiol 26(8):463–467, 1997. 6. Pill SG, Ganley TJ, Milam RA, et al: Role of magnetic resonance imaging and clinical criteria in predicting successful nonoperative treatment of osteochondritis dissecans in children. J Pediatr Orthop 23(1):102–108, 2003. 7. O’Connor MA, Palaniappan M, Khan N, Bruce CE: Osteochondritis dissecans of the knee in children. A comparison of MRI and arthroscopic findings. J Bone Joint Surg Br 84(2):258–262, 2002. 8. Bohndorf K: Osteochondritis (osteochondrosis) dissecans: a review and new MRI classification. Eur Radiol 8(1):103–112, 1998. 9. Vonstein DWN, Wall EJ, Laor T, et al: Juvenile osteochondritis dissecans of the knee: healing prognosis based on x-ray and gadolinium enhanced MRI. Pediatric Orthop Soc N Am, annual meeting, Amelia Island, Fla., 2003, p 79 [Abstract]. 10. Kramer J, Stiglbauer R, Engel A, et al: MR contrast arthrography (MRA) in osteochondrosis dissecans. J Comput Assist Tomogr 16(2):254–260, 1992.

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11. Litchman HM, McCullough RW, Gandsman EJ, Schatz SL: Computerized blood flow analysis for decision making in the treatment of osteochondritis dissecans. J Pediatr Orthop 8(2):208–212, 1988. 12. Paletta GA Jr, Bednarz PA, Stanitski CL, et al: The prognostic value of quantitative bone scan in knee osteochondritis dissecans. A preliminary experience. Am J Sports Med 26(1):7–14, 1998. 13. Cahill BR: Osteochondritis dissecans of the knee: treatment of juvenile and adult forms. J Am Acad Orthop Surg 3(4):237–247, 1995. 14. Anderson AF, Richards DB, Pagnani MJ, Hovis WD: Antegrade drilling for osteochondritis dissecans of the knee. Arthroscopy 13(3):319–324, 1997. 15. Aglietti P, Buzzi R, Bassi PB, Fioriti M: Arthroscopic drilling in juvenile osteochondritis dissecans of the medial femoral condyle. Arthroscopy 10(3):286–291, 1994. 16. Kocher MS, Micheli LJ, Yaniv M, et al: Functional and radiographic outcome of juvenile osteochondritis dissacans of the knee treated with transarticular arthroscopic drilling. Am J Sports Med 29(5):562–566, 2001. 17. Navarro R, Cohen M, Filho MC, da Silva RT: The arthroscopic treatment of osteochondritis dissecans of the knee with autologous bone sticks. Arthroscopy 18(8):840–844, 2002. 18. Mandelbaum BR, Browne JE, Fu F, et al: Articular cartilage lesions of the knee. Am J Sports Med 26(6):853–861, 1998. 19. Niedermann BB, Boe S, Lauritzen J, Rubak JM: Glued periosteal grafts in the knee. Acta Orthop Scand 56:457–460, 1985. 20. Madsen BL, Noer HH, Carstensen JP, Normark F: Long-term results of periosteal transplantation in osteochondritis dissecans of the knee. Orthopedics 23(3):223–226, 2000. 21. Outerbridge HKO, Outerbridge AR, Outerbridge RE: The use of a lateral patellar autologous graft for the repair of a large osteochondral defect in the knee. J Bone Joint Surg Am 77:65-72, 1995. 22. Peterson L, Minas T, Brittberg M, Lindahl A: Treatment of osteochondritis dissecans of the knee with autologous chondrocyte transplantation: results at two to ten years. J Bone Joint Surg Am 85(suppl 2):17–24, 2003. 23. King PJ, Ganley TJ, Lou JE, Gregg JR: Autologous chondrocyte transplantation for the treatment of large defects in the articular cartilage of the distal femur in adolescent patients. Am Acad Orthop Surg, annual meeting, New Orleans, LA, 2003 [Abstract]. 24. Garrett JC: Osteochondritis dissecans. Clin Sports Med 10(3): 569–593, 1991.

Chapter 23

Chondral Injuries and Osteochondral Fractures Christopher Iobst

• Mininder S. Kocher

Chondral and osteochondral injuries are being diagnosed with increasing frequency in skeletally immature patients.1 This is likely due to a combination of factors, including increased awareness of chondral injuries in general, increased participation of young children in organized sports at higher competitive levels, and improvements in magnetic resonance imaging (MRI) techniques for articular cartilage. Focal chondral and osteochondral defects of loading surfaces often cause symptoms, such as pain, swelling, clicking, and instability, and may lead to early degenerative changes.2 While chondral injuries in skeletally immature patients generally do not carry as grave a prognosis as similar injuries in skeletally mature patients, they are not inconsequential lesions. The consequences of childhood chondral injury have important long-term significance due to the age of the patients. Several treatment options involving surgical resurfacing are available to treat such defects, but the clinical outcomes of these procedures are controversial. This chapter reviews the diagnosis and management of chondral injuries and osteochondral fracture in skeletally immature patients. Chondral Injuries Chondral injuries can occur in skeletally immature patients, although the exact incidence of these injuries is unknown because they can be difficult to diagnose. One study in the adult literature, however, reports finding a chondral lesion in 63% of more than 31,000 arthroscopic procedures.3 Chondral injuries are caused by major compression and shear forces at the articular surfaces such as occurs in acute patellar dislocations. When articular cartilage is damaged locally or more extensively as a consequence of injury, its ability to dissipate the forces of articulation is compromised, which promotes further pathological changes in surrounding cartilage and neighboring bone. It is important to 294

restore these special properties of cartilage while preventing or minimizing the onset of associated pathological changes in the remainder of the joint. Natural History Little is known about the natural course of chondral defects, particularly if and when they cause clinical symptoms or radiographic signs of deterioration of the knee joint. It is known that the repair of cartilage damage may occur in the growing child but not in the adult.4 Evidence of repair has been observed in children who have had extensive joint destruction due to juvenile rheumatoid arthritis that later remitted. This repair potential is thought to exist because cartilage matrix turnover and remodeling is much more pronounced in a child as a part of the growth process. Signs and Symptoms The specific symptoms that lead clinicians to believe that an articular cartilage defect is the source of the patient’s pain can be difficult to pinpoint and are described in only a few clinical reports. Ochi et al.5 and KEY POINTS Brittberg et al.6 reported such symptoms to be locking, pain, 1. Chondral injury in the swelling, and retropatellar crepiskeletally immature tus. Peterson et al.7 described them has a repair potential as severe symptoms and pain at that is not seen in 8 rest, and Hangody et al. defined skeletally mature them as pain, pain with activity, patients. swelling, locking, or instability. It 2. The symptoms of a is difficult to determine whether chondral defect can the pain is due to the loose piece be variable but most that may be causing the locking or often include pain instability sensation or from the with activity, swelling, 9 articular cartilage defect alone. and locking. Patients with articular cartilage

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lesions may have periods of time when they are symptomatic followed by times when they are active without symptoms.9 This variation in symptoms can be particularly confusing when trying to determine when to intervene surgically. Imaging After a complete history, physical examination, and plain radiographs, if a chondral injury is suspected, then MRI is recommended to evaluate the status of the articular cartilage. Magnetic resonance imaging provides a noninvasive method for the assessment of articular cartilage abnormalities. While the initial results associated with the use of standard spin-echo pulse sequences for the detection of articular cartilage lesions were disappointing, newer MRI techniques have proven to have sensitivities of greater than 95% for the detection of focal abnormalities.10 As with all medical imaging techniques, lesion detection depends on the image contrast between abnormal and normal tissues, the signal-to-noise ratio of the image, and the spatial resolution of the imaging technique.10 Fast spin-echo (with or without fat suppression) and/or fat-suppressed (or water-selective excitation) spoiled gradient-echo image acquisitions are strongly recommended by the International Cartilage Repair Society (ICRS) as providing the most accurate assessment of the articular cartilage (Figure 23–1).10 Despite the continuing technical advances, determining the size and depth of a cartilage lesion with MRI remains challenging and depends on the status of the lesion. If a cartilage lesion is an “empty” defect with sharply defined margins and without partially attached fragments or unstable margins, MRI should be able to assess the size and depth of the lesion.10 However, MRI most often is performed before debridement of the cartilage defect, which contains partially attached fragments, thereby leading to an underestimation of the length and width of the lesion.10 In general, MRI will tend to underestimate the true size of the dimensions of a cartilage defect.10 Since most cartilage defects have irregular, ovoid shapes, it is unlikely that any one MR image will be perfectly aligned to demonstrate the maximal length or width of a lesion.10 Therefore, measurement of the distance between the margins of a defect KEY POINTS may extend over several image slice locations and will increase 1. MRI techniques are the difficulty of obtaining an now quite sensitive accurate assessment of lesion for the detection of 10 size. focal chondral As a result of these limabnormalities. Fast itations with MRI, arthroscopy spin-echo and/or still remains the gold standard fat-suppressed for identifying chondral injuries. spoiled gradientArthroscopy has the potential to echo image be both diagnostic and therapeuacquisitions are tic and can be used in situations recommended. where MRI is not available. MRI, 2. Despite advances in however, does have an advantage MRI techniques, over arthroscopy in that it proarthroscopy remains vides information regarding the the gold standard osseous extent of the lesion since for evaluation of it also directly images the subchondral injuries. chondral bone and bone marrow.

Figure 23–1 MRI imaging of acute chondral injury of the tibial plateau (A) and the trochlear groove (B).

Classification The best known arthroscopic cartilage lesion classification system was developed by Outerbridge in 1961.11 This system divides lesions into four grades (Table 23–1). However, Outerbridge grades II and III do not include a description of lesion depth, which is important information when making treatment decisions. To date, no standardized MRI classification system for articular cartilage lesions has been accepted.10 Most MRI grading methods have used a variation of the Outerbridge arthroscopic classification system to record lesion depth. The difficulty with using the Outerbridge system is that Outerbridge grade I lesions (softening) are not reliably detected with MRI. At a minimum, superficial fissuring, fibrillation, or shallow ulceration must be present before a lesion is detectable (Figure 23–2). The ICRS has developed a classification system

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Table 23–1 Outerbridge Classification System Grade

Description

0 1 2

Normal cartilage Softening and swelling of the cartilage Fragmentation and fissuring in an area 0.5 inches or less in diameter Fragmentation and fissuring in an area 0.5 inches or more in diameter Erosion of cartilage down to bone

3 4

Table 23–2 International Cartilage Repair Society Hyaline Cartilage Lesion Classification System Classification

Description

ICRS 0 (normal)

Macroscopically normal cartilage without notable defects 1a: Cartilage has intact surface but fibrillation and/or slight softening is present 1b: Same as 1a but additional superficial lacerations and fissures are found. Defects that extend deeper but involve <50% of the cartilage thickness Lesions that extend throughout >50% of the cartilage thickness 3a: Deep defects that extend through >50% of the cartilage depth but not to the calcified layer 3b: Deep defects that extend through >50% of the cartilage depth to the calcified layer 3c: Defects that extend down to but not through the subchondral bone plate 3d: Blisters Full-thickness osteochondral injuries

ICRS 1 (nearly normal)

ICRS 2 (abnormal) ICRS 3 (severely abnormal)

ICRS 4 (severely abnormal)

Management

Figure 23–2 Arthroscopic images of chondral softening with fissuring (A) and fraying (B) of the patella.

that focuses on the lesion depth and the area of damage10 (Table 23–2). The hope is that this classification will not only be diagnostic but also help direct appropriate treatment.

In clinical practice, it is unlikely that an ICRS 0 and ICRS 1 lesion will be identified because they are usually asymptomatic. In the rare instance when this level of lesion is found, no treatment is necessary. For ICRS 2, ICRS 3, or ICRS 4 lesions, however, surgical intervention is recommended. In general, the operative treatment of isolated focal chondral lesions can be divided into three basic types: debridement and stabilization of loose or worn articular cartilage, stimulation of a repair process from the subchondral bone, and repair or replacement of the damaged articular surface.9 Traditional resurfacing techniques, such as debridement, subchondral penetration, microfracture techniques (Figure 23–3), and abrasion arthroplasty, have been shown in the adult population to have limited value because of the poor biomechanical characteristics of the ingrown repair tissue.2,12 In the past 20 years, numerous investigators have developed new techniques to provide hyaline or hyalinelike repair for articular defects. These recently introduced resurfacing alternatives include periosteal and perichondral grafts, morselized autologous osteochondral mixtures, biomaterials, autologous chondrocyte transplantation, osteochondral allografts, and autologous osteochondral transplantation. The aim of these techniques is to partially or completely repair the chondral defect and decrease the risk of the development of osteoarthritic changes within the joint.9 Most of these techniques are supported by experimental data, but only autologous chondrocyte transplantation (Figure 23–4) and autologous osteochondral transplantation (Figure 23–5) have been used extensively in clinical practice2 (Technical Notes 23–1 and 23–2). Text continued on p. 307

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Figure 23–3 Microfracture technique. A full-thickness chondral defect of the medial femoral condyle (A) prepared by removing fibrous tissue and the calcified cartilage layer (B). Multiple perforations are made around the periphery and central region of the lesion (C). The tourniquet is released and pump pressure lowered to visualize bleeding from the perforations (D).

Figure 23–4 Autologous chondrocyte implantation.

Figure 23–5 Autologous osteoarticular implantation (mosaicplasty) for small chondral lesions using a single plug (A) and for large lesions with multiple plugs (B).

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TECHNICAL NOTE 23–1

Mosaicplasty for Chondral Defects of the Knee László Hangody • Gábor Ráthonyi

Joint loading surface defects of chondral and osteochondral lesions can cause clinical symptoms, such as pain, swelling, clicking, and instability, and may initiate early degenerative changes. Nonsurgical treatment is well established for low-grade superficial chondral defects, while focal full-thickness cartilage or osteochondral defects with noninflammatory pathological origin on weight-bearing surfaces may require surgical intervention. Traditional resurfacing techniques (Pridie-drilling, abrasion arthroplasty, and microfracture) provide only reparative fibrocartilage ingrowth with poor biomechanical characteristics,1–5 which has been proven inferior to hyaline or hyaline-like repair tissue covering of recently introduced new techniques. In the last two decades, several new techniques have also been developed. These new options, such as periosteum and perichondrium transplantation, tissue engineering techniques, biomaterials implantation, autologous osteochondral graft, and allograft transfers, aim to provide hyaline or hyaline-like tissue in the defective area. Most of these techniques are supported by experimental data, but only autologous chondrocyte transplantation and autologous osteochondral transplantation have been used extensively in clinical practice and tested in preclinical animal and histological studies.6–20 Successful results depend largely on proper patient selection and identification with simultaneous correction of malalignment and/or traumatic changes in affected joints.

Principles of the Procedure The advantage of mosaicplasty is congruent hyaline cartilage coverage using multiple cylindrical autologous osteochondral grafts. Although previous studies reported long-term hyaline cartilage survival of the transplanted osteochondral blocks,21–23 clinical use of single-block osteochondral transfer was limited by congruency problems and donor site availability. It was hypothesized that the use of small-sized multiple cylindrical grafts rather than a single large block graft would allow more tissue to be transplanted while preserving donor site integrity, and that the mosaic-like implanting fashion would permit progressive contouring of the new surface.24–29 Indications Initial indications were limited to relatively smalland medium-sized focal chondral and osteochondral defects of the weight-bearing surfaces of the femoral condyles and the patellofemoral joint. These indications later extended to other diarthrodial surfaces, including talar, tibial, caput, and capitulum humeri, and recently, femoral head lesions (Figures 23–6 and 23–7).30–34 Theoretical contraindications for mosaicplasty include infection, tumors, and generalized or rheumatoid arthritis because of the biochemical alterations that may occur in the involved joint’s milieu in these conditions.

Figure 23–6 Miniarthrotomy mosaicplasty on the medial femoral condyle—implantation of six pieces of 6.5 mm grafts provides ≈90% filling rate.

Continued

Chondral Injuries and Osteochondral Fractures

TECHNICAL NOTE 23–1

Mosaicplasty for Chondral Defects of the Knee (Continued)

Figure 23–7 Miniarthrotomy mosaicplasty on the lateral femoral condyle—combination of three 8.5-mm grafts and two 6.5-mm grafts provides congruent coverage.

Surgical Technique Autologous osteochondral mosaicplasty can be done as an open procedure through miniarthrotomy, or by arthroscopic method with only small alterations in the steps of different exposures. An open procedure could be required for far posterior lesions or limited knee flexion. General or regional anesthesia with tourniquet control and prophylactic antibiotics is recommended for this procedure. Preoperative consent is essential because the procedure requires weeks of limited weight bearing and an overnight stay. First, the defect is identified and cleared to good hyaline margins and the base of the defect prepared by fibrocartilage grouting, abrasion arthroplasty, or sharp curettage. Different-sized cylindrical chisels are used to harvest small-sized cylindrical osteochondral grafts (2.7, 3.5, 4.5, 6.5, and 8.5 mm in diameter) perpendicularly from the medial or lateral margin of the medial and lateral femoral condyle, superior to the sulcus terminalis. Tapping and toggling helps graft retraction. Care must be taken to push out the graft from the bony end to avoid damage to the hyaline cartilage cup. Resurfacing of chondral lesions requires only 15-mm graft length, whereas osteochondral defects call for 25-mm length to allow secure cancellous filling of bony defect. An open procedure allows graft harvest from both condyles, and arthroscopic technique provides perpendicular access mainly to the medial femoral condyle. The notch area could be used for additional graft harvesting for bigger defects.

Implantation consists of several consecutive steps (drilling, dilating, and delivering). Recipient tunnels are drilled by properly sized drill bits, then conical-shaped dilation of these holes is done, and then the harvested plugs are carefully inserted into them (Figure 23–8). A congruent surface and an 80–90% filling rate can be achieved with combinations of different graft sizes. Fibrocartilage ingrowth completes the new surface, and finally a composite cartilage surface will develop. This repair tissue consists of about 80–90% transplanted hyaline cartilage and 10–20% regenerative fibrocartilage. At the end of the procedure, full range of flexion–extension and varus–valgus stress is needed to assert graft stability. Drainage is required through a superior portal drain, and donor hole bleeding can be lessened with an elastic bandage. During the surgery, donor holes are left empty and in 8–10 weeks will be filled by cancellous bone and covered by fibrocartilage tissue. Postoperative Rehabilitation Autologous osteochondral mosaicplasty permits immediate full range of motion (ROM) but requires 2 weeks non-weight-bearing and a further 2–3 weeks partial weight-bearing (30–40 kg) period after the operation. The initial non-weight-bearing phase is recommended to prevent graft subsidence during osseous integration. Continuous passive motion (CPM) therapy could be used during this period to promote cartilage metabolism. Fibrocartilage repair Continued

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TECHNICAL NOTE 23–1

Mosaicplasty for Chondral Defects of the Knee (Continued) among implanted cylindrical plugs enhanced by partial weight-bearing further secures graft incorporation. Normal daily activity can be achieved in 8–10 weeks. High-demand sports activity should be delayed for 5–6 months. This protocol can be modified easily in accordance with established guidelines for concurrent anterior cruciate ligament reconstruction, high tibial osteotomy, meniscus reinsertion, meniscus resection, and so on. Several animal studies and subsequent clinical practice in nearly 1000 patients with knee and ankle mosaicplasty have confirmed the survival of the transplanted hyaline cartilage and fibrocartilage

filling of the donor sites located on the relatively less weight-bearing surfaces (Figure 23–9). Clinical scores, different types of imaging techniques, second-look arthroscopies, and histological examination of biopsy samples were used to evaluate the clinical outcomes and quality of the transplanted cartilage (Figure 23–10.).24–35 In 92% of patients with femoral condylar implantations, in 87% of patients with tibial resurfacement, in 74% of patients with patellar and/or trochlear mosaicplasty, and in 93% of talar procedures, clinical scores have shown goodto-excellent results. Bandi score showed minor

Figure 23–8 Arthroscopic mosaicplasty on the medial femoral condyle—step-by-step implantation of the grafts fills the defect.

Figure 23–9 Mosaicplasty on the medial talar dome—implantation of two grafts of 6.5-mm diameter by medial malleolar osteotomy approach.

Continued

Chondral Injuries and Osteochondral Fractures

TECHNICAL NOTE 23–1

Mosaicplasty for Chondral Defects of the Knee (Continued)

Figure 23–10 Mosaicplasty on the medial femoral condyle—control arthroscopy 3 years postoperative.

long-term donor site complaints in 3% of patients. Control arthroscopies in 81 of the 96 cases revealed congruent and good gliding surfaces, histologically proven survival of the transplanted hyaline cartilage, and fibrocartilage covering of the donor sites. Four deep infections and 56 painful postoperative hemarthroses complicated the 983 surgeries. Multicentric, comparative prospective evaluation of 413 arthroscopic resurfacing procedures (mosaicplasty, Pridie-drilling, abrasion arthroplasty, and microfracture cases in homogenized subgroups) demonstrated that mosaicplasty showed favorable clinical outcome in the long-term follow-up compared with the three other techniques. Durability of the early results was confirmed in intermediate-term evaluation of the femoral condylar implantations (3–6 years follow-up) and talar mosaicplasties (3–7 years follow-up).24–35 Increasingly large series with favorable outcomes in our center, supported by similar findings from other centers, showed autologous osteochondral mosaicplasty to be an alternative for small- and medium-sized focal chondral and osteochondral defects of the weight-bearing surfaces of the knee and other weight-bearing synovial joints.36–52 References 1. Newman AP: Articular cartilage repair. Am J Sport Med 26:309-324, 1998. 2. Grana WA: Healing of articular cartilage. Am J Knee Surg 13:29–32, 2000.

3. Browne JE, Branch TP: Surgical alternatives for treatment of articular cartilage lesions. J Am Acad Orthop Surg 8:180–189, 2000. 4. Sgaglione NA, Miniaci A, Gillogly SD, Carter TR: Update on advanced surgical techniques in the treatment of traumatic focal articular lesions in the knee. Arthroscopy 18: 9–32, 2002. 5. Jackson DW, Scheer MJ, Simon TM: Cartilage substitutes: overview of basic science and treatment options. J Am Acad Orthop Surg 9:37–52, 2001. 6. O’Driscoll SW, Keeley FW, Salter RB: Durability of regenerated cartilage produced by free autogenous periosteal grafts in major full-thickness defects in joint surfaces under the influence of continuous passive motion. J Bone Joint Surg Am 70:595–561, 1988. 7. Bruns J, Kersten P, Lierse W, Silberman M: Autologous rib perichondrial grafts in experimentally induced osteochondral lesions in the sheep-knee joint: morphological results. Virch Arch Pathol Anat Histopathol 421:1–12, 1992. 8. Coutts RD, Woo SL, Amiel D, et al: Rib perichondrial autografts in full-thickness articular cartilage defects in rabbits. Clin Orthop 275:263–267, 1992. 9. Ritsila VA, Santavirta S, Alhopuro S, et al: Periosteal and perichondrial grafting in reconstructive surgery. Clin Orthop 302:259, 1994. 10. Muckle DS, Minns RJ: Biological response to woven carbon fibre pads in the knee. J Bone Joint Surg Br 82:60–68, 1990. 11. Messner K, Gillquist J: Synthetic implants for the repair of osteochondral defects of the medial femoral condyle: a biomechanical and histological evaluation in the rabbit knee. Biomaterials 14:513–519, 1993. 12. Aubin PP, Cheak HK, Davis AM, Gross AE: Long-term follow up of fresh femoral osteochondral allografts for posttraumatic knee defects. Clin Orthop 391S:318–327, 2001. 13. Gross A: Fresh osteochondral allografts for posttraumatic knee defects: surgical technique. Operative Tech Orthop 7:334–339 1997. 14. Brittberg M, Lindahl A, Nilsson A, et al: Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantations. N Engl J Med 331(14):889–895 1994.

Continued

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Mosaicplasty for Chondral Defects of the Knee (Continued) 15. Minas T: Autologous chondrocyte implantation for focal chondral defects of the knee. Clin Orthop 391S:349–361, 2001. 16. Mandelbaum BR, Browne JE, Fu F, et al: Articular cartilage lesions of the knee. Am J Sports Med 26:853–861, 1998. 17. Hangody L, Feczkó P, Kemény D, et al: Autologous osteochondral mosaicplasty for the treatment of full thickness cartilage defects of the knee and ankle. Clin Orthop 391(suppl):328–337, 2001. 18. Miller RH: Osteochondral tissue transfer. Am J Knee Surg 13(1):51–62 2000. 19. Barber FA, Chow JCY: Arthroscopic osteochondral transplantation: histologic results. Arthroscopy 17:(8)832–835, 2001. 20. Christel P, Versier G, Landreau P, Djian P: Les greffes osteo-chondrales selon la technique de la mosaicplasty. Maitrise Orthop 76:1–13, 1998. 21. Campanacci M, Cervellati C, Dontiti U: Autogenous patella as replacement for a resected femoral or tibial condyle. A report of 19 cases. J Bone Joint Surg Br 67:557–563, 1985. 22. Outerbridge HK, Outerbridge AR, Outerbridge RE: The use of a lateral patellar autogenous graft for the repair of a large osteochondral defect in the knee. J Bone Joint Surg Am 77:65–72, 1995. 23. Yamashita F, Sakakida K, Suzu F, Takai S: The transplantation of an autogenic osteochondral fragment for osteochondritis dissecans of the knee. Clin Orthop 201:43–50, 1985. 24. Hangody L, Kárpáti Z: New alternative in the treatment of severe localized cartilage damages in the knee joint. Hung J Traumat Orthop 37:237–242, 1994. 25. Hangody L, Kárpáti Z, Pantó T, Kessler-Rosivall A: Treatment of localized chondral and osteochondral defects in the knee by a new autogenous osteochondral grafting technique. Hung Rev Sports Med 35:241–246, 1994. 26. Hangody L, Kárpáti Z, Tóth J, et al: Autogenous osteochondral grafting in the knees of German Shepherd dogs: radiographic and histological analysis. Hung Rev Sports Med 35:177–223, 1994. 27. Hangody L, Kish G, Kárpáti Z, et al: Autogenous osteochondral graft technique for replacing knee cartilage defects in dogs. Orthopaedics 5:175–181, 1997. 28. Bodó G, Hangody L, Szabó Z, et al: Arthroscopic autologous osteochondral mosaicplasty for the treatment of subchondral cystic lesion in the medial femoral condyle in a horse. Acta Vet Hung 48(3):343–354, 2000. 29. Bodó G, Kaposi AD, Hangody L, et al: The surgical technique and the age of the horse both influence the outcome of mosaicplasty in a cadaver equine stifle model. Acta Vet Hung 49:111–116, 2001. 30. Hangody L, Kish G, Kárpáti Z, et al: Mosaicplasty for the treatment of articular cartilage defects: application in clinical practice. Orthopaedics 21:751–758, 1998. 31. Hangody L, Kish G, Kárpáti Z, et al: Treatment of osteochondritis dissecans of talus: the use of the mosaicplasty technique. Foot and Ankle Int 18(10):628–634, 1997. 32. Hangody L, Kish G, Kárpáti Z, et al: Two to seven year results of autologous osteochondral mosaicplasty on the talus. Foot Ankle Int 22(7):552–558, 2001. 33. Hidas P, Hangody L, Csépai D, et al: Mosaikplastik—Eine neue Alternative in der Behandlung der Osteochondritis dissecans des Capitulum humeri. Arthroskopie 15:59–63, 2002. 34. Hangody L, Füles P: Autologous osteochondral mosaicplasty for the treatment of full thickness defects of weight

35.

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37. 38. 39.

40. 41.

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45. 46. 47. 48. 49. 50. 51.

52.

bearing joints—10 years experimental and clinical experiences. J Bone Joint Surg Am 85(suppl 2):25–32, 2002. Hangody L, Kish G, Kárpáti Z: Arthroscopic autogenous osteochondral mosaicplasty—a multicentric comparative prospective study. Index Traumatologie du Sport 5:3–7, 1998. Matsusue Y, Yamamuro T, Hama H: Arthroscopic multiple osteochondral transplantation to the chondral defect in the knee associated with anterior cruciate ligament disruption-case report. Arthroscopy 9:318, 1993. Bobic V: Arthroscopic osteochondral autogenous graft transplantation in anterior cruciate reconstruction: a preliminary report. Knee Surg Sports Traumatol Arthrosc 3:262, 1996. Imhoff AB, Ottl GM, Burkart A, Traub S: Autologous osteochondral transplantation on various joints. Orthopäde 28(1):33–44, 1999. Berlet GC, Mascia A, Miniaci A: Treatment of unstable osteochondritis dissecans lesions of the knee using autogenous osteochondral grafts (mosaicplasty). Arthroscopy 15(3):312–316, 1999. Solheim E: Mosaikkplastikk ved leddbruskskader i kne. Tidsskr Nor Laegeforen 27(119):4022–4025, 1999. Traub S, Imhoff AB, Öttl G: Die Technik der osteochondralen autologen Knorpeltransplantation (OATS) zum Ersatz chondraler oder osteochondraler. Defekte Osteologie 9:46–55, 2000. Ripoli PL, de Prado M, Ruiz D, Salmeron J: Transplantes osteocondrales en mosaico: estudio de los resultados mediante RMN y segunda artroscopia. Cuadernos Artroscopia 6:11–16, 2000. Attmanspacher W, Dittrich V, Stedtfeld HW: Experiences with arthroscopic therapy of chondral and osteochondral defects of the knee joint with OATS (osteochondral autograft transfer system). Zentralbl Chir 125(6):494–499, 2000. Maynou C, Mestdagh H, Beltrand E, et al: Resultats a long term de l’autogreffe osteo-cartilagineuse de voisinage dans les destructions cartilagineuses etendues du genou A propos de 5 cas. Acta Orthopaedica Belgica 64(2):193–200, 1998. Marcacci M, Kon E, Zaffagnini S, Visani A: Use of autologous grafts for reconstruction of osteochondral defects of the knee. Orthopedics 22(6):595–600, 1999. Simonian PT, Sussmann PS, Wiczkiewicz TL, et al: Contact pressures at osteochondral donor sites in the knee. Am J Sports Med 26:491–494, 1998. Duchow J, Hess T, Kohn D: Primary stability of pressfit-implanted osteochondral grafts. Am J Sports Med 28:24–27, 2000. Makino T, Fujioka H, Kurosaka M, et al: Histologic analysis of the implanted cartilage in an exact-fit osteochondral transplantation model. Arthroscopy 17:747–751, 2001. Hurtig M, Pearce S, Warren S, et al: Arthroscopic mosaic arthroplasty in the equine third carpal bone. Veterinary Surgery 30:228–239, 2001. Ahmad CS, Guiney WB, Drinkwater CJ: Evaluation of donor site intrinsic healing response in autologous osteochondral grafting of the knee. Arthroscopy 18:95–98, 2002. Assenmacher JA, Kelikian AS, Gottlob C, Kodros S: Arthroscopically assisted autologous osteochondral transplantation for osteochondral lesions of the talar dome: an MRI and clinical follow-up study. Foot Ankle Int 22(7):544–551, 2001. Matsusue Y, Kotake T, Nakagawa Y, Nakamura T: Arthroscopic osteochondral autograft transplantation for chondral lesion of the tibial plateau of the knee. Arthroscopy 17(6):653–659, 2001.

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TECHNICAL NOTE 23–2

Treatment of Articular Cartilage Lesions Using Autologous Chondrocyte Implantation Nigel Azer • Tom Minas

Articular injuries are extremely common in today’s active society. Full-thickness articular cartilage lesions secondary to work or sporting activities account for 5–10% of all acute hemarthrosis of the knee.1 A retrospective review of 31,516 patients with knee arthroscopies demonstrated a 602% overall incidence of chondral injuries.2 Symptomatic patients typically present with effusion crepitus pain and mechanical symptoms. Lesions often occur as the result of traumatic injury but may also occur as a secondary phenomenon as with osteochondritis dissecans or spontaneous osteonecrosis. Since mature articular cartilage is avascular, it is unable to regenerate or repair itself. Thus when healing is attempted by penetration of the subchondral bone plate to obtain a vascular response, the lesions are filled with biomechanically inferior fibrocartilage. Untreated, these cartilage lesions may progress to osteoarthritis, which is particularly problematic for young patients who wish to maintain a high level of activity and function.3 There are numerous treatment approaches and algorithms for the treatment of articular cartilage lesions. These approaches include (1) symptomatic treatments, such as lavage and debridement; (2) procedures that fill the defects with fibrocartilage, such as chondroplasty and microfracture; (3) procedures that fill the defects with hyaline

cartilage, such as osteochondral autografts, allografts, and autologous chondrocyte implantation; and (4) arthroplasty. The goal of surgery is to provide a durable joint with a full range of painless motion that prevents further deterioration and disability. Autologous Chondrocyte Implantation Autologous chondrocyte implantation (ACI) or autologous chondrocyte transplantation (ACT) is a technique for the treatment of articular cartilage defects in which autogenous cells are harvested, grown in culture, and then reimplanted into the patient. ACI is generally used for revision chondral surgery or large defects, or when multiple lesions require treatment.4 Autologous chondrocyte implantation should be considered in symptomatic patients with arthroscopically proven chondral defects. Grade III or IV defects on the femur, tibia, trochlea, or patella larger than 2 cm2 or defects that have failed other treatments are considered candidates for ACI (Figure 23–11). Before proceeding with ACI, axial malalignment, ligamentous laxity, or the absence of meniscus should be identified and treated appropriately with ligament reconstruction or osteotomy. Patient factors, such as smoking or pharmacological agents

Figure 23–11 Full-thickness chondral lesion on weight-bearing portion of femoral condyle. Axial malalignment and ligamentous instability should be addressed before ACI.

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Treatment of Articular Cartilage Lesions Using Autologous Chondrocyte Implantation (Continued) that interfere with cell proliferation such as NSAIDS or TNF-alpha inhibitors, should also be discontinued before surgery and during healing Technique: The technique involves two separate surgical procedures. First, the knee is examined arthroscopically. If there is an appropriate lesion, a biopsy of articular cartilage (200–300 mg) is taken from the intercondylar notch or the superior medial edge of the trochlea proximal to the sulcus terminalis (Figures 23–12 and 23–13). A cartilage

surface of 5 mm × 1 cm is typically required to acquire the necessary 200–300 mg of cartilage. The cells are then placed in a culture medium and transferred to a cell-culturing facility that meets Food and Drug Administration good laboratory practice guidelines with quality control validation for cell culturing and phenotype and viability assessment. Once an adequate numbers of cells are cultured (12 million cells per 4–6 cm2 defect), the patient undergoes an open procedure for cell implantation. The cartilage lesion is debrided back to healthy articular margins, taking care to leave

Figure 23–12 Chondral biopsy is taken from lesser weight-bearing portion of knee, usually the intercondylar notch. The cartilage biopsy is then sent for commercial cell culture.

Figure 23–13 Typical chondral biopsy site does not involve patellar–trochlear articulation.

Continued

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Treatment of Articular Cartilage Lesions Using Autologous Chondrocyte Implantation (Continued) the subchondral bone intact (Figure 23–14). A full-thickness piece of tibial periosteum that matches the size and shape of the debrided defect is harvested locally from the anteromedial aspect

of the tibia distal to the pes anserinus insertion. It is then microsutured over the articular defect with 6-0 Vicryl sutures flush with adjacent chondral borders (Figure 23–15). Fibrin sealant is applied to

Figure 23–14 Lesion is debrided back to stable articular cartilage rim for later suture. Subchondral bone should not be violated.

Figure 23–15 Periosteal flap is sutured to cartilage rim. Note that the knots are over the periosteal flap side. Fibrin sealant is then used to make a water-tight closure before injecting the cells.

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Treatment of Articular Cartilage Lesions Using Autologous Chondrocyte Implantation (Continued) ensure a watertight closure. Uncontained lesions are addressed by suturing the periosteum to bone through small drill holes. The cultured cells are then injected into the defect underneath the periosteal cover. Postoperatively patients are started on a continuous passive motion machine and follow a regimented postoperative rehabilitation protocol, which depends on the location of the lesion in the knee joint.5 Based on canine and clinical studies, three stages of tissue maturation have been identified.6 These include proliferation (weeks 0–6), transition (weeks 7–12), and maturation (week 13–2 years). During the proliferative stage, the defect is filled with soft primitive repair tissue. During the transition phase, the extracellular matrix expands and the graft becomes firmer with integration to bone and adjacent cartilage. Protected weight-bearing is required to the end of the transition period (12 weeks). By 9–18 months the tissue becomes as firm as native cartilage (Figure 23–16). Histologically this tissue resembles hyaline cartilage in 73–81% of femoral lesions.7 Advantages of this procedure include the formation of a durable hard repair tissue and the ability to treat very large defects. Ninety-six percent of patients with good clinical outcomes 2 years postoperatively continue to function a high level 10 years postoperatively.

Complications: Complications associated with ACI include arthrofibrosis, periosteal overgrowth, and graft failure (delamination). In our series, an additional operative procedure, usually arthroscopy, for complications was required in 25% of the cases. Of these, 20% were for periosteal hypertrophy and 5% for arthrofibrosis. Despite the potential occurrence of these complications, ACI remains a promising treatment in that it provides a durable joint and to date appears to prevent further deterioration and disability. Periosteal overgrowth occurs when the periosteal tissue becomes nourished by the synovial fluid and hypertrophies over the developing chondral layer. Patients usually present at 3–7 months with a new onset of catching, pain, and effusion. Most cases resolve without treatment. However, persistent symptoms may be readily treated with arthroscopic chondroplasty. Arthrofibrosis occurs in 5–10% who undergo ACI. It presents as stiffness and loss of motion early in the postoperative course. Adhesions are more prevalent in young patients who have undergone additional reconstructive surgery along with the cartilage repair. Since bands of adhesions can adhere to the graft, it is important not to perform a closed manipulation to avoid injury to the graft. These are usually treated with an arthroscopic

Figure 23–16 Second look at autologous chondrocyte implantation 16 months after implantation.

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Treatment of Articular Cartilage Lesions Using Autologous Chondrocyte Implantation (Continued) examination, lysis of adhesions, followed by extensive postoperative rehabilitation. Finally, incomplete integration of the repair tissue into the subchondral bone may lead to marginal, partial, or complete separation or “delamination” of the graft from underlying bone. Delamination occurs most commonly within the first 6 months after transplantation but may also be seen much later. This graft failure is reported to occur in 5% of the treated patients. Delamination is usually treated with arthroscopic examination and excision of the delaminated portion of the graft. The resulting defect is characterized, and a decision is made regarding whether to perform a revision ACI or to proceed with marrow stimulation technique or osteoarticular autograft. Results As of November 1999, 295 defects had been treated with ACI at our institution. These consisted of 12 simple isolated femoral condylar lesions; 86 complex lesions that include nonarthritic knees with multiple defects, patellar defects, and tibial defects; and 71 salvage procedures for patients with early osteoarthritis. The patients had a mean age of 35 years and had an average defect size of 4.3 cm2. Additional procedures, including osteotomy to improve alignment, were added as necessary in approximately one third of patients with concomitant

ICRS 2 lesions are often unstable, with partly detached fragments causing mechanical symptoms. The recommended treatment for this level of cartilage lesion is a simple debridement that involves excision of the unstable cartilage fragments back to smooth edges and leaves the base intact. For ICRS 3 or ICRS 4 lesions, the size of the lesion may direct the treatment for many patients. Osteochondral autograft transplantation is typically used for smaller lesions, and autologous chondrocyte transplantation is recommended when the lesion is large, although the definitions of small and large vary greatly.2 Theoretical and practical considerations suggest that the ideal diameter of the defect for repair with autogenous osteochondral grafting is between 1 and 4 square centimeters.2 There are, however, no studies documenting results of either of these methods in an entirely pediatric population. There are two studies in the adult literature, however, that support nonoperative management of even ICRS 2, ICRS 3, or ICRS 4 lesions. Shelbourne et al.9 reported very little difference in the postoperative clinical course after ACL repair between patients with a chondral defect and those without a chondral defect. In a similar study by Messner and Maletius,13

malalignment. At most recent follow-up, 87% reported clinical improvement.8 This compares favorably to the results previously published in the literature from our institution and elsewhere.9

References 1. Noyes FR, Bassett RW, Grood ES, et al: Arthroscopy in acute traumatic hemarthrosis of the knee. Incidence of anterior cruciate tears and other injuries. J Bone Joint Surg Am 62:687–695, 1980. 2. Curl WW, Krome J, Gordon ES, et al: Cartilage injuries: a review of 31,516 knee arthroscopies. Arthroscopy 13:456–460 1997. 3. Buckwalter JA, Mankin HJ: Articular cartilage: degeneration and osteoarthritis repair regeneration and transplantation. J Bone Joint Surg Am 79:612–632, 1997. 4. 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. 5. Minas T: Autologous chondrocyte transplantation. Op Tech Sports Med 8:144–157, 2000. 6. Minas T, Peterson L: Advanced techniques in autologous chondrocyte transplantation. Clin Sports Med 18:13–44, 1999. 7. Peterson L, Minas T, Brittberg M, et al: Two- to 9-year outcome after autologous chondrocyte transplantation of the knee. Clin Orthop 374:212–234, 2000. 8. Minas T: Autologous chondrocyte implantation for focal chondral defects of the knee. Clin Orthop 391:S349–361 2001. 9. Peterson L, Minas T, Brittberg M, et al: Two- to 9-year outcome after autologous chondrocyte transplantation of the knee Clin Orthop 374:212–234 2000.

in which 28 athletes were evaluated at 12 to 15 years after arthroscopic diagnosis of an isolated focal articular cartilage defect, 21 patients returned to their preinjury activities, and the mean Lysholm score was 92 points. Treatment of chondral injuries in the skeletally immature generally uses the same management strategies as in adults, but there are a few differences that must be taken into consideration when managing a child with this injury. First, although the surgical procedures developed to repair cartilage damage in skeletally mature patients have the same potential benefit in skeletally immature patients, there are little data in the literature to support one procedure over another in this age group. My preference is to attempt microfracture first, and then, if this is unsuccessful, to use autologous chondrocyte transplantation as a salvage procedure (Technical Note 23–3). Range of motion with protected weight bearing should be instituted immediately after surgery. Second, when operating on the skeletally immature, there are a few technical points that must be remembered that are not ordinarily issues in adults. When performing marrow stimulation techniques such as drilling or microfracture, the

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TECHNICAL NOTE 23–3

Microfracture in Chondral Defects of the Knee J. Richard Steadman • William G. Rodkey

Indications The microfracture technique in pediatric or adolescent knees is most commonly indicated for acute traumatic full-thickness loss of articular cartilage.1–4 Patients with acute chondral injuries are treated as soon as practical after the diagnosis is made. Microfracture may be performed in conjunction with treatment of ACL tears as well as meniscus injuries. We place no limitations on how large an acute lesion can be to still be considered suitable for microfracture. Setup: General anesthesia is typically the choice for these young patients. A tourniquet is not used for microfracture procedures; rather we rely on arthroscopic pump pressure to control intraarticular bleeding. The patient is positioned supine. Standard arthroscopic instruments plus special microfracture awls are used. Microfracture Technique: Using standard arthroscopic portals, we inspect all geographic areas of the knee carefully. We do all other intraarticular procedures before doing microfracture to avoid losing marrow elements during the procedure. We debride the exposed bone of all remaining unstable cartilage with a hand-held curved curette and a full radius resector. It is critical to debride all loose or marginally attached cartilage from the surrounding rim of the lesion. The calcified cartilage may have been removed with the articular cartilage at the time of the initial injury. However,

the calcified cartilage layer may remain as a cap in many lesions, and it must be removed, preferably with a curette. Removal of the calcified cartilage layer is extremely important based on animal studies completed by our group.5,6 Care should be taken to maintain the integrity of the subchondral plate by not debriding too deeply. The appearance of punctate bleeding from the subchondral bone is the indication that the calcified cartilage layer has been removed adequately. This prepared lesion, with a stable perpendicular edge of healthy wellattached viable cartilage surrounding the defect, provides a pool that helps hold the marrow clot or “super clot,” as we have termed it, as it forms (Figure 23–17). After preparation of the lesion, we use an arthroscopic awl to make multiple holes, or “microfractures,” in the exposed subchondral bone plate. We use an awl with an angle that permits the tip to be perpendicular to the bone as it is advanced, typically 30 or 45 degrees. There also is a 90-degree awl that typically is only used on the patella or other soft bone. The 90-degree awl should only be advanced manually, not with a mallet. The holes are made as close together as possible, but not so close that one breaks into another, thus damaging the subchondral plate between them. This technique usually results in microfracture holes that are approximately 3–4 mm apart. The correct depth of penetration with the microfracture awls is one that allows access to the marrow elements, typically 2–4 mm. We make microfracture holes around the

Figure 23–17 A curette (C) is used to remove damaged and unstable cartilage remnants as well as the calcified cartilage layer of a full-thickness chondral defect. Debridement is adequate when punctate bleeding of the subchondral bone is observed.

Continued

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TECHNICAL NOTE 23–3

Microfracture in Chondral Defects of the Knee (Continued) periphery of the defect first, immediately adjacent to the healthy stable cartilage rim (Figure 23–18). Then we complete the process by making the microfracture holes toward the center of the defect (Figure 23–19). In skeletally immature patients, it is essential to respect the growth plates. If a mallet is used to advance the microfracture awls, the striking pressure should be as minimal as possible. We assess the treated lesion at the conclusion of the microfracture to ensure a sufficient number of holes have been made before we reduce the arthroscopic irrigation fluid flow. After the arthroscopic irrigation fluid pump pressure is reduced, under direct visualization we are able to observe the release of marrow fat droplets and blood from the microfrac-

ture holes into the knee (Figure 23–20). We judge the quantity of marrow contents flowing into the joint to be adequate when we observe marrow emanating from all microfracture holes. Intraarticular drains should not be used1,3 because the goal is for the surgically induced marrow clot rich in marrow elements to form and to stabilize while covering the lesion.5,6 Postoperative Management The rehabilitation program after microfracture for treatment of chondral defects in the adolescent knee is crucial to optimize the results of the surgery.7,8 The rehabilitation promotes the optimal

Figure 23–18 After preparation of the lesion, the microfracture holes are started at the periphery of the defect adjacent to the stable cartilage.

Figure 23–19 After the entire periphery of the lesion has been microfractured (arrows), microfracture holes are then continued into the central portion of the defect.

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TECHNICAL NOTE 23–3

Microfracture in Chondral Defects of the Knee (Continued)

Figure 23–20 The microfracture procedure has been completed, and the holes are about 3 to 4 mm apart. Marrow elements, including blood and fat droplets, accessed by the subchondral bone microfracture can be seen coming from the microfracture holes (arrow).

physical environment for the mesenchymal stem cells to differentiate and produce new extracellular matrix that eventually matures into a durable repair tissue. The surgically induced marrow clot provides the basis for the most ideal chemical environment to complement the physical environment. After microfracture of lesions on the weightbearing surfaces of the femoral condyles, we commence immediately with a CPM machine in the recovery room. The initial range of motion typically is 30 to 70 degrees, and then it is increased as tolerated by 10 to 20 degrees until full passive range of motion is achieved. The goal is to have the patient in the CPM machine for 6–8 hours every 24 hours. We prescribe crutch-assisted touchdown weight-bearing ambulation for 6–8 weeks, depending on the size of the lesion. For patients with small lesions (<1 cm diameter), weight-bearing may be hastened by a few weeks. Patients with lesions on the femoral condyles or tibial plateaus rarely use a brace during the initial postoperative period. Patients start double-leg one-third knee bends the day after surgery.7 Because they are touchdown weight-bearing, patients place most (75–80%) of their body weight on their uninjured leg to do the exercise. They begin stationary biking without resistance and a deep water exercise program at 1–2 weeks after microfracture. Patients progress to full weight-bearing after 8 weeks and begin a more vigorous program of active motion of the knee

with elastic resistance cord exercises. Free or machine weights are not used before 16 weeks after microfracture. Depending on the clinical examination, we usually recommend that patients do not return to sports that involve pivoting, cutting, and jumping until at least 4–6 months after microfracture. All patients treated by microfracture for patellofemoral lesions must use a brace set at 0 to 20 degrees for at least 8 weeks. This brace limits compression of the regenerating surfaces of the trochlea or patella, or both. We allow passive motion with the brace removed, but otherwise the brace must be worn at all times. Patients with patellofemoral lesions are placed into a CPM machine immediately postoperatively. We carefully observe joint angles at the time of arthroscopy to determine where the defect comes into contact with the patellar facet or the trochlear groove. We avoid these areas during strength training for approximately 4 months. This avoidance allows for training in the 0- to 20-degree range immediately postoperatively because there is minimal compression of these chondral surfaces with such limited motion. Patients are allowed weight-bearing as tolerated, but it must be limited to the angles of knee flexion where the lesion is not compressed. Therefore, it is essential for patients to use a brace that prevents placing excessive shear force on the maturing marrow clot in the early postoperative period. After 8 weeks, we open the knee brace Continued

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Microfracture in Chondral Defects of the Knee (Continued) gradually before it is discontinued. When the brace is discontinued, patients are allowed to advance their strength training progressively. Results We recently published long-term follow-up results of microfracture in patients from 13 to 45 years of age.4 Patients were followed for 7 to 17 years (average 11.3 years). We observed outcomes in adolescent patients to be equal to those recorded for mature patients. Hence, we feel that microfracture is an excellent treatment for chondral lesions in young patients. References 1. Steadman JR, Rodkey WG, Rodrigo JJ: “Microfracture.” Surgical technique and rehabilitation to treat chondral defects. Clin Orthop Rel Res 391S:S362–S369, 2001.

surgeon must be cognizant of the proximity of the growth plate to prevent potential growth disturbances from inadvertent violation of the physis. Similarly, when autologous chondrocyte transplantation is attempted, it is important not to disrupt the tibial tubercle apophysis while harvesting periosteum. Another difference in the management of skeletally immature chondral injuries is that most of these procedures require a period of protected weight bearing postoperatively. This can be difficult to enforce in younger children because they may not be able to follow complex rehabilitation programs. Consequently, surgeons may need to modify their rehabilitation program to fit their patient’s capabilities. Finally, although it is generally believed that children have greater reparative abilities than adults, they also have a longer lifespan than adults. This means the implications of a fullthickness chondral injury and its repair are more important. Furthermore, the longevity of chondral resurfacing techniques is of utmost importance. It is

KEY POINTS 1. Operative treatment of chondral injuries in the skeletally immature generally uses the same management strategies as in adults. 2. There are little data in the literature to support one procedure over another in skeletally immature patients. We prefer to attempt microfracture first, and then, if this is unsuccessful, to use autologous chondrocyte transplantation as a salvage procedure. 3. When repairing chondral injuries in skeletally immature patients, it is important to avoid injuring the physis. Postoperative rehabilitation programs may have to be modified to fit the patient’s capabilities.

2. Steadman JR, Rodrigo JJ, Briggs KK, et al: Debridement and microfracture (“Pick Technique”) for full-thickness articular cartilage defects. In Insall JN, Scott WN (eds): Surgery of the Knee, 3rd ed. New York: Churchill Livingstone, 2001. 3. Steadman JR, Rodkey WG, Briggs KK: Microfracture to treat full-thickness chondral defects. J Knee Surg 15(3):170–176, 2002. 4. 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. 5. Frisbie DD, Trotter GW, Powers BE, et al: Arthroscopic subchondral bone plate microfracture technique augments healing of large osteochondral defects in the radial carpal bone and medial femoral condyle of horses. J Vet Surg 28:242–255, 1999. 6. Frisbie DD, Oxford JT, Southwood L, et al: Early events in cartilage repair after subchondral bone microfracture. Clin Orthop Rel Res 407:215–227, 2003. 7. Hagerman GR, Atkins JA, Dillman C: Rehabilitation of chondral injuries and chronic degenerative arthritis of the knee in the athlete. Oper Tech Sports Med 3:127–135, 1995. 8. Irrgang JJ, Pezzullo D: Rehabilitation following surgical procedures to address articular cartilage lesions of the knee. J Orthop Sports Phys Ther 28:232–240, 1998.

especially important to attempt to recreate an anatomical articular surface with hyaline cartilage in a young patient who will need a lifetime of use from the joint. Osteochondral Fractures Osteochondral fractures in skeletally immature patients are more common than once KEY POINTS thought. They most frequently involve the knee joint and are 1. Osteochondral typically associated with acute fractures commonly patellar dislocations. The prevaoccur after acute lence of osteochondral fractures patellar dislocations. associated with acute patella dis2. The most common 14–19 location ranges from 25–50%. locations for Matelic et al.16 found 67% of chilosteochondral dren presenting with an acute fractures are the hemarthrosis of the knee had an medial patellar facet osteochondral fracture. The most or the lateral femoral common locations for these fraccondyle. tures are the medial patellar facet 14–19 or the lateral femoral condyle. Etiology A histopathological study by Flachsmann et al20 helps to explain the occurrence of osteochondral fractures in the skeletally immature at a cellular level. They noted that in the juvenile joint, interdigitating fingers of uncalcified cartilage penetrate deep into the subchondral bone, providing a relatively strong bond between the articular cartilage and the subchondral bone. In the adult, the articular cartilage is bonded to the subchondral bone by the well-defined calcified cartilage

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layer, the cement line. When KEY POINTS shear stress is applied to the juve1. The interface nile joint, the forces are transmitbetween the articular ted into the subchondral bone by cartilage and the subthe interdigitating cartilage with chondral bone is a the resultant bending forces causzone of potential ing the open pore structure of the weakness in trabecular bone to fail. In mature adolescents, making tissue, the plane of failure occurs them vulnerable between the deep and calcified to osteochondral layers of the cartilage, the tidefracture. mark, leaving the osteochondral 2. The two primary junction undisturbed. Although mechanisms for the juvenile and adult tissue patproduction of an terns are different, they both proosteochondral vide adequate fracture toughness fracture are a direct to the osteochondral region. As blow to the knee or the tissue transitions from the a flexion-rotation juvenile to the adult pattern durinjury of the knee. ing adolescence, however, the fracture toughness is lost. The calcified cartilage layer is only partially formed, and the interdigitating cartilage fingers are progressively replaced with calcified matrix. Consequently, the interface between the articular cartilage and the subchondral bone becomes a zone of potential weakness in the joint, which may explain why osteochondral fractures are seen frequently in adolescents and young adults. There are two primary mechanisms for production of an osteochondral fracture.14-20 First, a direct blow to the knee

with a shearing force applied to either the medial or lateral femoral condyle can create an osteochondral fracture. The second mechanism involves a flexion-rotation injury of the knee in which an internal rotation force is placed on a fixed foot, usually coupled with a strong quadriceps contraction. The subsequent contact between the tibia and femur or patella and lateral femoral condyle causes the fracture. An example of this mechanism is an acute patellar dislocation. As the patella dislocates, the medial retinaculum tears, but the remaining quadriceps muscle-patellar ligament complex still applies significant compressive forces as the patella dislocates laterally and shears across the lateral femoral condyle. The medial border of the patella then temporarily becomes impacted on the prominent edge of the lateral femoral condyle before it slides back tangentially over the surface of the lateral femoral condyle due to the pull of the quadriceps. Either the dislocation or the relocation phase of this injury can cause an osteochondral fracture to the lateral femoral condyle (Figure 23–21), the medial facet of the patella (Figure 23–22), or both. Interestingly, osteochondral fractures are uncommon with chronic, recurrent subluxation or dislocation of the patella. In this situation, the laxity of the medial knee tissues and decreased compressive forces between the patella and the lateral femoral condyle prevent development of excessive shear forces. History and Physical Examination Osteochondral fractures present with severe pain, swelling, and difficulty weight-bearing. On examination, tenderness

Figure 23–21 Patellofemoral dislocation with acute osteochondral fracture of the lateral femoral condyle. A, Arthroscopic appearance of lesion. B, Gross appearance of lateral femoral condyle fragment.

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Figure 23–21—cont’d C, Arthrotomy for reattachment. D, Radiograph of fixation using cannulated screws. E, Arthroscopic appearance of healed lesion 3 months postoperatively.

to palpation over the medial femoral condyle, lateral femoral condyle, or medial patella is exhibited. The patient will usually resist attempts to flex or extend the knee and may hold the knee in 15–20 degrees of flexion for comfort. The large hemarthrosis is due to fracturing the highly vascular subchondral bone. A joint aspiration will reveal a supernatant layer of fat if allowed to stand for 15 minutes, indicating an intraarticular fracture. Late examination findings may be similar to those of a loose body with intermittent locking or catching of the knee. Imaging Radiographic visualization of the osteochondral fracture should begin with anteroposterior and lateral plain radiographs. A skyline view of the patella is mandatory if the patient has suffered an acute patellar dislocation. However, a roentgenographic diagnosis can be difficult because even a large osteochondral fragment may contain only a small

ossified portion that is visible on plain radiographs. Matelic et al.16 report that standard radiographs failed to identify the osteochondral fracture in 36% of children who had an osteochondral fracture found during arthroscopy.1 For this reason, supplemental studies, such as KEY POINTS MRI or computed tomography (CT) arthrography, may be 1. Standard radiographs necessary in cases in which there may fail to identify an is high suspicion of osteochonosteochondral fracdral fracture despite negative ture in one third of 21,22 radiographs. Arthroscopic the cases. examination can also be done as 2. If radiographs are the definitive diagnostic (and negative, but there is potentially therapeutic) test. a high suspicion of With regard to plain film findinjury, MRI, CT ings, two studies have reported arthrography, or that having a high-riding patella arthroscopy may be seems to have a protective effect necessary. against associated intraarticular

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Figure 23–22 Patellofemoral dislocation with acute osteochondral fracture of the medial patellar facet. Radiographic (A) and MRI (B) appearance of osteochondral injury. Arthroscopic appearance of osteochondral fragment (C). Gross appearance of patella through an open lateral retinacular release (D). Reapproximation of the osteochondral fragment (E) with fixation using cannulated screws (F).

(Continued)

Chondral Injuries and Osteochondral Fractures

osteochondral fractures. Patients with an Insall index >1.3 have a decreased chance of sustaining an osteochondral fracture compared with patients who have an Insall index within normal limits.21

Figure 23–22—cont’d Fixation using cannulated screws (G). Arthroscopic appearance of healed lesion 3 months postoperatively (H).

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Management The recommended management of acute osteochondral fractures of the knee is either surgical removal of the fragment or fixation of the fragment to its anatomical location.23 If the lesion is large (>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.

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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 <115 degrees. In this series, on MRI the sensitivity was 95%, and specificity was 88%. Many children will come into a referral practice with MRIs in hand or demanding them if not already done. MRIs are rarely required to determine the functional status of the ACL but are beneficial in determining the presence of meniscal or chondral damage. Care must be given to not overread age-normal meniscal vascularity, particularly in the posterior horns of the menisci.54 The authors also find MRIs to be a useful adjunct to parental and patient education. Physeal Function of the Knee In performing ACL reconstruction in the skeletally immature, what are the relative risks and potential consequences of iatrogenic physeal damage? This central question requires an appreciation of normal physeal function, mechanisms of physeal injury, nuances of surgical technique, and a review of animal and human research. The physes of the distal femur and proximal tibia are the most rapidly growing in the body. The younger the child at the time of injury, the greater the potential magnitude of angular deformity or leg length discrepancy (LLD). Initially these physes are transversely oriented and flatly discoid in shape. During development both become more undulating. This is particularly true for the distal femur, where the physis gradually develops four conical projections into the epiphyseal bone. The tibia develops a single convexity into the epiphysis of the proximal tibia. These undulations provide resistance against shear and rotational forces about the knee.55,56 This complex architecture must be kept in mind when trying to surgically avoid the physeal plates. Estimations from early work by Anderson et al.57 suggest that the distal femur physis contributes 40% to the overall lower extremity length and 70% to the femoral length. Corresponding percentages for the proximal tibia physis are 27% and 55%, respectively (Figure 24–5). However, for several reasons, these data may incorrectly estimate growth remaining about the knee. First, the data are based on a small group of New England children gathered in the 1940s. Half of the children had polio involving the contralateral leg, which may have affected their overall development. The maturation height of the children in the Anderson et al. study was 162 cm for girls and 175 cm for boys.57 This compares to modern American children of approximately 167 cm and 179 cm.58 Second, data assume that the proportion of growth out of the proximal and distal physes about the knee is constant throughout growth. Pritchett58 has shown that the relative contributions of the distal-to-proximal femur and the proximal-to-distal tibia increases significantly with age (Figure 24–6, A and B). As an example, the contribution of the distal femur to overall femoral growth increases from 55% at age 7 to 90% at age 16 for boys. The total

Figure 24–5 Relative contributions to individual bone and lower extremity growth. (From Ogden JA: Diagnostic imaging. In Ogden JA [ed]: Skeletal Injury in the Child, ed 3. New York: Springer-Verlag, 2000, pp 115–146.)

effect of this shift is kept relatively small because the effect is greatest as children approach skeletal maturity and growth velocities are slowing. Due to the cumbersome nature of chart and graph methods of predicting growth remaining, several “rule of thumb” methods have been developed. White and Stubbins59 predicted 3/8 inch yearly out of the distal femur and 2/8 inch from the proximal tibia. Menlaus60 suggested 9 mm and 6 mm yearly from the distal femur and proximal tibia. Acknowledging the relative changes from proximal and distal growth plates and utilizing a more modern cohort of children, Pritchett reported the distal femur to grow 1.3 cm per year until the last 2 years of maturity, when the rate drops to 0.65 cm per year.58 Correspondingly, the rates of the proximal tibia are 0.9 cm per year until the last 2 years of maturity, when it drops to 0.5 cm per year. Leg length discrepancy of less than or equal to 1 cm is well tolerated and often found as a normal variant. Epiphysiodesis is usually not considered until a ~3 cm LLD is projected. However, this amount of discrepancy needs to be considered during ACL reconstruction in the skeletally immature. Complete closure of the proximal tibia in the average 12-year-old boy, complete closure of the distal femur in a 13-year-old boy, or complete closure of both physes in a 14-year-old boy would result in approximately a 3-cm difference in LLD. Fortunately, the greatest concern appears to be with angular deformity rather than full LLD. This is related to the relatively small, eccentrically placed physeal insults that may result from ACL reconstruction. The posterolateral position of the femoral tunnel or over-the-top femoral groove may result in a valgus/flexion deformity of the distal femur. Damage to the anterior part of the tibial physis may result in recurvatum. Wester61 has detailed a simple method of

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Figure 24–6 Age-dependent relative contribution of proximal and distal physes to overall femoral (A) and tibial (B) growth. (From Pritchett JW: Longitudinal growth and growth-plate activity in the lower extremity. Clin Orthop 275:274–279, 1992.)

predicting worst-case scenarios for angular deformity based on gender, bone age, and physeal diameter. For example, a 14-year-old boy with 2 cm remaining of distal femoral growth, and an average-size (8-cm diameter) distal femoral physis, would sustain a 14-degree valgus deformity if the femoral physis underwent complete growth arrest at its far lateral side. The same boy sustaining a far anterior closure of the proximal tibial physes could suffer an 11-degree recurvatum.

Research on iatrogenic physeal injury suggests that physeal dysfunction is proportionate to the area of injury. Drilling less than 5% of physeal cross-sectional area has a low likelihood of causing bar formation.62,63 Perpendicular drilling involves less cross-sectional area than oblique or parallel drilling. By avoiding excessive pressure and allowing continued growth, smooth, perpendicularly oriented hardware is less problematic than threaded or angulated hardware.

Anterior Cruciate Ligament Injuries

Two canine studies64,65 have focused on the possible effects of ACL reconstruction on physeal growth about the knee. The model by Stadelmaier et al.65 involved eight immature dogs using a 5/32 transphyseal tibial tunnel (corresponding to a 9-mm tunnel in adolescents) and a transphyseal fascia lata autograft with ACL left intact. They found that placement of a soft tissue graft across the tunnels prevented bone bridge formation, which occurred with vacant tunnels. Soft tissue grafts and other inert fillers have been effective in allowing growth restoration of 80–90% after physeal bar resection. This may be effective in resections involving up to 50% of total physeal cross-sectional area.48 Even in young children, the cross-sectional area of an ACL drill tunnel is an order of magnitude smaller than this. In twelve 10-week-old beagles undergoing a highly tensioned, transphyseal ACL reconstruction, Edwards64 reported significant risk of valgus flexion deformities. There were no bone bridge formations, and deformities were felt to be due to slowed physeal growth secondary to excessive pressure across the posterolateral femoral physis. In the few cohort reports of ACL reconstruction in truly skeletally immature patients, the occurrence of significant leg length discrepancy and angular deformities have been low.66–70 However, reports by Koman71 and Kocher72 caution against a cavalier attitude. Koman described a 14-degree valgus angulation resulting after a bone–patella–tendon–bone (BPTB) ACL reconstruction in a boy who was 14 years, 4 months of age. The initial workup included no investigation of skeletal or sexual maturation. In hindsight, the child’s skeletal age at the time of surgery was ~13.2 years. Transphyseal tunnels were used, and hardware used for femoral side fixation was placed horizontally across the lateral femoral physis. Cancellous bone was packed into the femoral and tibial bone tunnels. KEY POINTS The resulting deformity necessitated a corrective osteotomy. In a 1. The distal femoral survey of the Herodicus Society and proximal tibial (an international sports medicine physes are society) and the Anterior responsible for the Cruciate Ligament Study majority of leg Group,72 15 of 140 respondents length. Their had seen a growth disturbance relative contribution from ACL reconstruction in a increases in an skeletally immature patient. Of age-proportionate these 15 reported cases, 12 were manner. on the femoral side and 3 were on 2. Although rare, the tibial side. In the 10 cases of significant angular distal femoral valgus deformity, 3 deformities have were associated with hardware been reported across the lateral physis, 3 with following ACL bone plugs of a patella tendon reconstruction in graft across the distal femoral the skeletally physis, 1 with a 12-mm femoral immature. tunnel and BPTB graft, 1 with an 3. These deformities over-the-top graft placement, and have been most 2 with lateral extraarticular tencommonly related odesis. In the two cases of LLD, to inappropriately 1 involved a 2.5-cm shortening placed fixation and and valgus deformity with the use transphyseal bone of a 12-mm BPTB graft, and the placement. other in an 11-year-old girl

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involved an overgrowth of 3 cm after transphyseal reconstruction with a 6-mm hamstring graft. There were 3 cases of genu recurvatum related to staple or suturing across the tibial physes. Assessing Skeletal Maturity Puberty is a sweeping process of change that involves alterations in cognitive ability, sexual characteristics, body composition, physiological function, and skeletal growth. There is significant variation in the onset and duration based on gender, genetic predisposition, race, and environmental conditions. On average, chronological age is an excellent predictor of developmental age, but this is not necessarily the case for any single individual. When we analyze the maturation of a young patient with an ACL insufficiency, we are really trying to determine his or her knee maturity. How much growth remains at the physes? What are the relative risks of physeal injury? A wide array of surrogates for knee maturation is available, some more specific and useful than others. Often, terms that are used, such as “wide open physes,” “postadolescent growth spurt,” “has reached parental and older sibling height,” are all relatively vague. Attention should be given to more tightly defining skeletal and sexual maturation. Skeletal Bone Age Two primary methods of determining bone age are the atlas/comparative method and the additive/scoring method. The following factors limit the reliability of bone age estimates: (1) the standardized populations of the past may not be applicable to more modern American children in improved nutritional situations and of multiple ethnic backgrounds73; (2) skeletal age estimates based on one area of the body may not reliably predict bone age at other body areas; (3) subjectivity affects both inter- and intra-rater reliability, and (4) some methods, such as Risser staging, may lack sensitivity during the critical period of early adolescent growth.74 Familiarity, ease of x-ray, and presence of multiple developing bones make hand/wrist radiographs the most commonly used to estimate skeletal bone age. The Greulich-Pyle atlas method75 is the most familiar. However, even experienced radiologists show a mean variability of 3–4 months. Cundy et al.76 reported that in 10% of patients, there was a variance of as much as 2 years. TannerWhitehouse is the most common of the additive methods utilizing hand/wrist films.77 It uses 20 specific bone landmarks about the hand and wrist to generate a standard level of maturity score, which is then converted into years and months. There is less variance and subjective error than with the atlas comparative method. Separate scores can also be based on long bones of the hands excluding the carpals. This may be more useful in estimating bone age of the knee. Bone ages obtained with this method tend to be slightly older than values obtained on the same populations utilizing the Greulich-Pyle atlas.78,79 Less commonly used methods may also be helpful in the young ACL patient. The simplified Sauvegrain80,81 method utilizes the unique skeletal maturation of the olecranon and may provide increased sensitivity for determining bone age during the high-decision age groups of 11- to 13-year-old girls and 13- to 15-year-old boys

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(Figure 24–7). Although seldom used in the United States, there are knee-specific standards available for both the atlas/comparative82 and additive/scoring methods.83 Several studies have investigated the correlations between hand/wrist and knee-generated bone ages.84–86 Average values in large populations are comparable, but select individuals’ estimated ages may vary by as much as 1.5 years. Peak growth rate during puberty occurs between 13 and 15 for boys and 11 and 13 for girls. At the conclusion of long bone growth, overall height continues to increase due to growth in the thoracolumbar spine.80 Change in leg length rather than standing height is the marker of maturation more specific to the concerns of the young ACL patient. Progressive changes in secondary sexual characteristics form the basis of the Tanner scale of maturation.87,88 The first physical sign of puberty in boys is the increase in testicular enlargement. For girls the first sign of puberty is breast budding. Secondary sexual characteristics generally develop in harmony with bone age, but there are discrepancies in 10% of children. There is a significant gender-driven difference in the relationship of skeletal and sexual maturation. For any given Tanner sexual development stage, girls are more skeletally mature than their male counterparts. In boys, peak height velocity is rarely obtained before Tanner stage IV, and 20% do not hit peak height velocity until Tanner stage V. In girls, peak height velocity occurs in Tanner stage III, preceding

Figure 24–7 Olecranon stages in the simplified Sauvegrain method. (From Dimeglio A: Growth in pediatric orthopedics. In: Morrissy RT, Weinstein SL [eds]: Lovell and Winter’s Pediatric Orthopaedics, ed 5. Philadelphia: Lippincott Williams & Wilkins, 2001, pp 33–62.)

menarche by approximately a year. Average age achievement of common markers of secondary sexual characteristics and skeletal maturation are presented in Figures 24–8 and 24–9.* Tanner stages are outlined in Table 24–1.87–90 Treatment Options and Outcomes

KEY POINTS 1. For populations, chronological age is an excellent predictor of developmental age; in most children, skeletal and sexual maturation progress concurrently. However, individuals may show significant variance from these norms. 2. Current methods of determining the growth remaining about the knee are somewhat imprecise and may be improved with olecranonbased or kneespecific methods. 3. For any given Tanner sexual development stage, girls are more skeletally mature than their male counterparts.

The most appropriate treatment for the skeletally immature athlete with ACL insufficiency depends on family and patient desires, patient maturity, level of athletic competition, presence of concurrent intraarticular pathology, functional disability, and response to previous treatment. The initial step in any treatment program is education, which should include a discussion of the skeletal maturation process, risk and potential consequences of physeal injury, consequences of cumulative meniscal and articular damage, realistic expectations of ACL reconstruction, and various operative and nonoperative options. The natural history of ACL insufficiency in the skeletally immature appears poor; however, most nonoperative programs have not been standardized or well monitored. When following a nonoperative program, a balance must be reached between environmental

Figure 24–8 Sexual and skeletal maturation milestones for average North American girls. *

References 1, 33, 80, 81, 87–92.

Anterior Cruciate Ligament Injuries

Figure 24–9 Sexual and skeletal maturation milestones for average North American boys.

demands and knee coping abilities. Circumstances that may lend themselves to initial nonoperative care include (1) strong family desire for nonoperative care, (2) truly immature Tanner stage I or II (particularly boys) patients, (3) low level of athletic demands and desires, (4) involvement in knee-friendly sports such as swimming or biking, and (5) isolated ACL injury without instability during daily activities. Nonoperative care may be viewed as “temporizing” until an adult-type reconstructive procedure may be more safely undertaken or “long-term” if well tolerated. The family and athlete must understand that an environment of recurrent instability is not an option. “Occasional” episodes of instability inevitably lead to cumulative meniscal damage. The initial goals of a nonoperative program are

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to decrease pain and swelling and to regain early quad function and a normal gait. Single plane unloaded activities, aerobic base restoration, and comprehensive lower extremity strengthening are begun as tolerated. A comprehensive, neuromuscular rehabilitation program is aimed at progressively improving knee coping mechanisms and decreasing injury risk factors. Patients are instructed to follow a long-term gym or home-based exercise program, wear a custom brace for sports activities, and apply ice after athletic activities. Sports activities should be changed to avoid high-risk injury situations but allow continued “competitive participation” in lower knee-demand sports. Circumstances lending themselves to operative intervention include (1) family desire to pursue operative intervention after full understanding of risk and benefits, (2) more mature athletes (Tanner stages IV and V girls and relatively skeletally mature Tanner IV and Tanner V boys), (2) failure of comprehensive nonoperative program, (3) concurrent meniscal or chondral injury that would benefit from operative intervention, (4) participation in high knee-demand sports, (5) unwillingness to modify high knee-demand activities, and (6) instability during daily activities. In this section, we will discuss the major operative approaches to ACL reconstruction in the skeletally immature and review the pertinent literature. Because there is no gold standard, this information is presented in detail. Hopefully, this will help readers formulate their own approach to treatment. Direct Repair Acute repair of interstitial ACL tears in the skeletally immature has met with somewhat poor results. DeLee et al.93 reported on three children less than 14 years of age who underwent primary repair of the ACL. All three patients

Table 24–1 Classification of Sex Maturity Stages Girls SMR Stage

Pubic Hair

Breasts

I II

Preadolescent Sparse, lightly pigmented, straight, medial border of labia Darker, beginning to curl, increased amount

Preadolescent Breast and papilla elevated as small mound; areolar diameter increased Breast and areola enlarged; no contour separation Areola and papilla form secondary mound Mature, nipple projects, areola part of general breast contour

III IV

Coarse, curly, abundant but amount less than in adult Adult feminine triangle, spread to medial surface of thighs

V

Boys SMR Stage

Pubic Hair

Penis

Testes

I II III IV

None Scanty, long, slightly pigmented Darker, starts to curl, small amount Resembles adult type but less in quantity; coarse, curly Adult distribution, spread to medial surface of thighs

Preadolescent Slight enlargement Longer Larger; glans and breadth increase in size Adult size

Preadolescent Enlarged scrotum, pink, texture altered Larger Larger; scrotum dark

V

Adult size

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were reported to have returned to sports activities, but two of three had recurrent giving way and grade II clinical instability. Engebertsen et al.94 reported on eight patients (mean age 15, range 13–16) operated on within the first week of injury. Postoperative immobilization was 6 weeks at 30–40 degrees of flexion, followed by active physical therapy. Although all eight regained full motion, five had significant functional instability. Failure of acute repair of the ACL may be related to loss of blood supply, lack of initial clot formation, harsh intraarticular environment, adverse biomechanical factors, or inherent inabilities in the ACL cell population to effectively regenerate.33 Bioengineering techniques aimed at improving the intraarticular healing environment may be particularly applicable to the skeletally immature where successful repair would avoid many of the potential complications of reconstructive procedures (see Chapter 5). Extraarticular Reconstruction In the adult population, extraarticular, nonanatomical reconstructions have fallen out of favor, but in the lighter, lower demand child, they may improve stability while avoiding transphyseal drill tunnels. However, transphyseal tunnels are not the only mechanism of physeal injury. Excessive compression and peripheral injury to the physis may also result in deformity. Extraarticular reconstructions may be viewed as a long-term answer or a temporary measure. These procedures may stand alone or be used in combination with acute repair or intraarticular reconstructions. Nakhostine et al.95 reported on five patients (average age 14, range 12–15, all male with “open physes,” two with chronic and three with acute anterior cruciate instability). These patients’ knees were reconstructed with an anterolateral, extraarticular procedure. At an average follow-up of 4.5 years, all subjects had returned to a pre-injury level of rugby. However, three had greater than or equal to a 3-mm sideto-side difference on KT2000 testing, and five had a +2 Lachman’s test. As expected, pivot shift was better controlled with one of four having a +1 pivot shift and the remaining four only a glide. All regained full range of motion and there were no angular deformities or LLD reported. Micheli et al.69 reported on a group of 17 prepubescent children (average age of 11, range 2–14). Eight of the ten patients who attained skeletal maturity were followed at an average postoperative length of 66 months. One of the eight had undergone reconstruction for a congenitally absent ACL at 2 years of age. Average reconstructive age for the remaining seven was 12.5 years. These patients underwent a combined intraarticular/extraarticular, physeal-sparing procedure as previously described by MacIntosh and Darby96 (Figure 24–10 and Technical Note 24–1). At follow-up, the average Lysholm score was 97.4. There was no subjective laxity, and all patients reported full return to sport activity at a time ranging from 9 to 15 months after surgery. One patient with medial meniscal repair and previous partial lateral meniscectomy had continued swelling with activity, and one patient had a 4-mm side-to-side difference at 30 pounds of testing. There were no surgery-related angular deformities or LLD. Lipscomb et al.97 reported on a group of 24 adolescent athletes (ages 12–15, 11 with “completely open physes,” 21 male and 3

Figure 24–10 Micheli variation of MacIntosh/Darby combined intra/extraarticular physeal-sparing reconstruction. (Reprinted with permission from: Rask BP, Micheli JL: The pediatric knee. In Scott WN [ed]: The knee, vol. 1, St. Louis: MosbyYear Book, 1994. Copyright Elizabeth Roselius).

female, 10 acute, 8 subacute, and 3 chronic). They combined an intraarticular, transphyseal tibial/intraepiphyseal femoral, double-stranded hamstring graft with an extraarticular Losee98 or Ellison procedure.99 At a follow-up ranging from 24–66 months, there were 16 rated as excellent, 7 as good, and 1 fair result. In one patient, the operative leg was 2 cm shorter, and in one other, the operative leg was 1.3 cm longer. There was also one valgus deformity greater than 3 degrees. Physeal-Sparing Procedures Conceptually, the next step in avoiding transphyseal drill tunneling but moving toward a more anatomically based ACL reconstruction is intraarticular, physeal-sparing procedures. This may involve total or partial physeal sparing. Total physeal sparing involves one of two approaches. First, utilization of an over-the-top procedure on the femur and an over-the-front position on the tibia. Second, the physes can be avoided by placing drill tunnels in a completely intraepiphyseal manner. The over-the-top, over-the-front position avoids any drill tunnels but compromises the insertion of the ACL at both its femoral and tibial attachments. This may lead to long-term graft laxity or potential loss of motion. Attempts to groove the graft into more anatomical locations may inadvertently damage the peripheral physes at the posterolateral femur Text continued on p. 333

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TECHNICAL NOTE 24–1

ACL Reconstruction: Physeal-Sparing Iliotibial Band Technique Lyle J. Micheli • Kevin Latz

Indication

Description of Procedure

The physeal-sparing iliotibial band (ITB) technique is indicated for preadolescents who have sustained an injury to the ACL and are experiencing instability of the knee or who have sustained an injury to both the ACL and a meniscus.

The surgery is accomplished through two incisions. Attention is initially directed toward the graft harvest. An approximately 5-cm incision is made proximal and lateral to the knee along the superior margin of the ITB extending distally to Gerdy’s tubercle (Figures 24–11). Following the skin incision, the subcutaneous tissue is injected with 0.25% Marcaine with epinephrine. The incision is then extended deeper until the ITB is visualized. The ITB is then freed of all adjacent soft tissue with a Cobb elevator for a distance of at least 20 cm. A small incision is made along the anterior margin of the ITB proximal to the femoral condyle. A Kelly clamp is then passed through this incision to the lateral intermuscular septum and out through the posterior margin of the ITB (Figure 24–12).

Setup The patient is placed supine on the surgical table with a nonsterile tourniquet around the operative leg. The tourniquet is placed as proximal as possible to avoid interference with graft harvest. An examination under anesthesia is performed to confirm the injury. The entire limb is prepped and draped circumferentially.

Figure 24–11 Skin incisions for ITB reconstruction.

Continued

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TECHNICAL NOTE 24–1

ACL Reconstruction: Physeal-Sparing Iliotibial Band Technique (Continued)

Figure 24–11—cont’d

Figure 24–12 Clamp identifying anterior and posterior borders of ITB.

Continued

Anterior Cruciate Ligament Injuries

TECHNICAL NOTE 24–1

ACL Reconstruction: Physeal-Sparing Iliotibial Band Technique (Continued) Parallel incisions at the anterior and posterior margins of the ITB are made utilizing a straight meniscotome. The incisions are carried proximally for a distance of 20 cm. The graft is transected proximally by subcutaneous dissection with scissors, a curved meniscotome or a tendon-stripping device (Figure 24–13). A #1 Ethibond suture is placed in the free segment of ITB, and traction is placed on the graft. The graft is dissected free of adjacent subcutaneous tissue and capsule distally to Gerdy’s tubercle (Figure 24–14). The graft is left attached distally. The harvested graft is then placed back

into the wound to avoid desiccation during the next portion of the procedure. The limb is then exsanguinated and the tourniquet inflated. A diagnostic arthroscopy is performed. If meniscus repair is required, it is done at this time. The remnant of the ACL is then removed. The over-the-top position of the lateral femur is cleared of soft tissue. A minimal notchplasty is performed. A 3-cm longitudinal incision is made extending from the tibial articular surface distally along the anteromedial aspect of the tibia. Care is taken

Figure 24–13 Transection of ITB graft proximally (20 cm in length).

Figure 24–14

Identification of insertion of ITB on Gerdy’s tubercle.

Continued

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TECHNICAL NOTE 24–1

ACL Reconstruction: Physeal-Sparing Iliotibial Band Technique (Continued) to avoid injury to the proximal tibial physis. A deep vertical incision is made in the periosteum distal to the physis and elevated. The periosteum is sharply incised and elevated. A trough is created in the tibial metaphysis with small gouges. A trough is then created in the tibia epiphysis with a rasp deep to the intermeniscal ligament and under the central attachment of the medial meniscus. A full-length vascular clamp is then introduced through the anteromedial portal and passed through the over-the-top position on the lateral femoral condyle. The clamp is then advanced through the previously created lateral knee incision anterior to the intramuscular septum. The Ethibond grasping suture and iliotibial graft are then placed in the clamp. The clamp is then utilized to facilitate passage of the Ethibond grasping suture and graft through the knee in an antegrade fashion. A suture retriever is then passed in the epiphyseal trough beneath the medial meniscus and used to retrieve the Ethibond grasping suture and graft. The arthroscope is reintroduced into the knee to verify correct position of the graft at the over-the-top position on the lateral femoral condyle and to ensure that the graft does not impinge on the roof of the notch with the knee in full extension. Next, attention is turned toward securing the graft. The proximal extraarticular portion of the

graft is secured initially. With the knee in 70 degrees of flexion and external rotation and moderate tension on the graft, the graft is sutured to the margin of the intramuscular septum (Figure 24–15). At the completion of this step, the patient should demonstrate a negative Lachman’s and pivot shift test. The intraarticular portion of the graft is secured with the knee in 20 degrees of flexion. The graft is pulled down into the metaphyseal trough and secured with a series of #1 Vicryl mattress sutures while applying tension on the graft. The Ethibond grasping suture is then secured to the adjacent periosteum. Closure is accomplished with interrupted Vicryl sutures and a running PDS suture. Postoperative Management The child is placed in a motion-limiting hinged knee brace and started immediately on a continuous passive motion (CPM) machine with 30–40 degrees range of motion. Range of motion is determined by the presence or absence of a concomitant meniscal repair. Physical Therapy: The child is maintained in a hinged knee brace and kept partial weight bearing for 6 weeks postoperative. Closed kinetic chain exercises are initiated approximately 6 weeks postoperative.

Figure 24–15 A, Suture of graft to intramuscular septum.

Continued

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333

TECHNICAL NOTE 24–1

ACL Reconstruction: Physeal-Sparing Iliotibial Band Technique (Continued)

Figure 24–15—cont’d

B, Position of knee during proximal fixation of graft.

Suggested Readings 1. Brief L: Anterior cruciate ligament reconstruction without drill holes. Arthroscopy 7:350–357, 1991. 2. McCarroll J, Rettig A, Shelbourne D: Anterior cruciate ligament injuries in the young athlete with open physes. Am J Sports Med 16:44–47, 1988.

or anteromedial tibia. Distally attached gracilis and semitendinosus tendons are often used for grafting. This “double” graft allows sufficient length for extraphyseal positioning but compromises cross-sectional areas. Parker et al.100 and Brief101 have reported on this technique (Figure 24–16). Parker et al.100 reported on six patients (age range 10.3 to 14.1 years, average 13.3 years). Three of the six also had primary repair of the ACL. Grooves were made at the posterolateral over-thetop position and in the anteromedial position for graft placement. On follow-up at an average of 33.2 months, Lysholm

3. Micheli LJ, Rask B, Gerberg L: Anterior cruciate ligament reconstruction in patients who are prepubescent. Clin Orthop 364:40–47, 1999.

scores were 95.2 ± 5, HHS knee score 96.6 ± 1.5. Two of the five patients had a grade I Lachman’s test, and none had a significant pivot shift. Side-to-side KT1000 values average 3.6 mm ± 1.9 mm. In all five of the follow-up patients, the operative leg was 1 cm longer than the contralateral leg. By MRI, four of the five patients had increased signal within the graft. Four of five patients were able to return to pre–level participation sports while wearing a functional brace. Brief101 reported on nine patients, average age of 17.2, two female and seven male. At 1-year postoperative, all patients had a +1

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Figure 24–16 Cross-section of over-the-front tibia and overthe-top femoral hamstring graft placement. Note graft crossing under intermeniscal ligament. (Reprinted with permission from Brief LP: Anterior cruciate ligament reconstruction without drill holes. Arthroscopy 7:350–357, 1991.)

Figure 24–17 All-epiphyseal tunneling technique as reported by Anderson.

Lachman’s test and a +1 anterior drawer. Of the five patients tested on KT1000, four of five had greater than or equal to 3mm side-to-side difference. Six of nine were satisfied with their results after a return to sport with bracing. In an intriguing approach to avoiding the physes, Anderson66 has reported an all-intra-epiphyseal approach to graft tunneling (Figure 24–17 and Technical Note 24–2). His cohort consisted of 12 patients: 10 males and 2 females, mean age 12 years 4 months. There were 3 Tanner stage I, 4 Tanner stage II, and 5 Tanner stage III individuals. Femoral and tibial tunnels were drilled over guide pins, which were placed under fluoroscopic guidance. A quadrupled hamstring graft was used with metaphyseal side fixation. Follow-up was an average of 4.1 years. IKDC subjective scores on average were 96.5 with a range of 86 to 100. KT1000 side-to-side difference was 1.5 mm with a range of 0 to 3.75, and no patients had a pivot shift. Seven patients were rated as normal and 5 as nearly normal. There were no significant angular deformities or LLD. The approach is intriguing yet technically demanding. The femoral growth plate is undulating, and the femoral origin of the ACL is quite close to the physis. Straying into the physes with a laterally based, parallel drill tunnel could result in hemiepiphysiodesis. Technical Note 24–3 details an epiphyseal reconstruction technique using staple fixation to the distal femoral epiphysis. Partial Transphyseal Procedures The next progressive step is an intraarticular, partial physeal-sparing approach (Figure 24–18). Both autografts and

Figure 24–18 Transphyseal tibia and over-the-top femoral positioning. (Reprinted by permission from Stanitski CL: Anterior cruciate ligament injury in the skeletally immature patient: Diagnosis and treatment. J Am Acad Orthop Surg 3:146–158, 1995.)

Text continued on p. 345

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TECHNICAL NOTE 24-2

ACL Reconstruction: Epiphyseal Reconstruction with Quadruple Hamstring Grafts Allen Anderson

Indications The natural history of ACL tears is worse in children than adults because children are noncompliant and have longer to live with progressive degenerative changes caused by chronic instability, recurrent injuries, and meniscal pathology. A growing body of evidence in the literature confirms that nonoperative treatment of ACL tears in skeletally immature patients has a poor outcome. The success with meniscal repair and surgical stabilization, without evidence of growth disturbance, supports a recommendation for aggressive treatment, with the use of the described technique, in patients with an ACL injury or who are in Tanner stage I and II of development. Setup A nonsterile tourniquet is applied, and the injured lower limb is placed in an arthroscopic leg holder with hip flexed 20 degrees to elevate the knee for C-arm (portable fluoroscopy) visualization in the lateral plane. The C-arm is brought in from the side of the table opposite the injured knee, and the monitor is placed at the head of the table. The tibial and femoral growth plates are visualized in both the anteroposterior and the lateral planes. When the distal part of the femur is viewed, the C-arm is adjusted so that the medial and lateral femoral condyles line up perfectly in the lateral plane. The C-arm is then rotated to visualize the extension of the tibial physis into the tibial tubercle on the lateral view of the tibia. Technique An oblique, 4-cm incision is made over the semitendinosus and gracilis tendons, which are dissected free and transected at the musculotendinous junction with use of a standard tendon stripper. The tendons are then doubled, and a #5 Ethibond suture (Ethicon, Johnson and Johnson, Somerville, NJ) is placed in the ends of the tendons with a whip-stitch. The doubled tendons are then placed under 4.5 kg (10 lb) of tension on the back table with use of the Graft Master device (Acufex, Smith & Nephew, Andover, MA). The arthroscope is inserted into the anterolateral portal, and a probe is inserted through the anteromedial

portal. Intraarticular examination is systematically performed in the usual manner. Any debris in the intercondylar notch is removed, and a minimal notchplasty is performed. If a substantial meniscal tear is found, it is repaired. With the C-arm in the lateral position, a guide wire is used to identify the site for a 2-cm lateral incision. The lateral incision is then made, the iliotibial tract is incised longitudinally, and the periosteum is stripped from a small area of the lateral femoral condyle. The C-arm is used to visualize the entry point of the guide wire in both the anteroposterior and the lateral plane. With a freehand technique, the guide wire is introduced into the femoral epiphysis with care taken to avoid the physis (Figure 24–19). Entrance of the guide wire into the intercondylar notch is then visualized arthroscopically. The guide wire should enter the joint 1 mm posterior and superior to the center of the anatomical footprint of the ACL on the femur. The femoral guide wire is left in place, and a second guide wire is inserted into the anteromedial aspect of the tibia through the epiphysis. The C-arm is used again to avoid the tibial physis (Figure 24–20). The tibial guide wire enters the joint at the level of the free edge of the lateral meniscus and in the posterior footprint of the ACL on the tibia. Tendon sizers are used to measure the diameter of the quadruple tendon graft (range from 6 to 8 mm). A tight fit is important; consequently, the smallest appropriate drill should be used to ream over the guide wires. The edge of the femoral hole is chamfered intraarticularly, and the width of the lateral femoral condyle is measured. The appropriate Endobutton continuous loop (CL) (Acufex, Smith & Nephew, Andover, MA; 2–3 cm) was chosen so that at least 2 cm of the quadruple hamstring tendon graft remains within the lateral femoral condyle. The Endobutton CL is then passed around the middle of the double tendons and is looped inside of itself to secure the tendons proximally (Figure 24–21). Alternatively, the tendons could be placed through the CL before suturing the tendon ends together. However, that would require drilling and measuring the length of the femoral hole before graft preparation. Otherwise, it would be difficult to determine the appropriate length of Endobutton CL necessary to leave 2 cm of the tendon graft within the lateral femoral condyle. Continued

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ACL Reconstruction: Epiphyseal Reconstruction with Quadruple Hamstring Grafts (Continued)

Figure 24–19 For the femoral tunnel, a guide wire is placed, under fluoroscopic assistance, from the lateral distal femoral epiphysis into the intercondylar notch. Using fluoroscopic assistance, care is taken to avoid the distal femoral physis. Using arthroscopic assistance, care is taken to properly position the guidewire in the anatomical footprint of the ACL.

Continued

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TECHNICAL NOTE 24-2

ACL Reconstruction: Epiphyseal Reconstruction with Quadruple Hamstring Grafts (Continued)

Figure 24–19—cont’d

Figure 24–20 For the tibial tunnel, a guide wire is placed, under fluoroscopic assistance, from the anteromedial aspect of the tibial epiphysis. Using fluoroscopic assistance, care is taken to avoid the proximal tibial physis. Using arthroscopic assistance, care is taken to properly position the guidewire in the anatomical footprint of the ACL.

Continued

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ACL Reconstruction: Epiphyseal Reconstruction with Quadruple Hamstring Grafts (Continued)

Figure 24–21 An Endobutton CL is passed around the middle of the double tendons and is looped inside of itself to secure the tendons proximally.

A #5 Ethibond suture is placed in one end of the Endobutton, and a guide wire is used to pass the suture from anterior to posterior up through the tibia and out the lateral femoral condyle (Figure 24–22). The Endobutton and tendons are then pulled up through the tibia and out the femoral hole with the use of the #5 suture. An Endobutton or AO washer is then placed over the Endobutton, and tension is applied to the tendons distally, pulling the Endobutton and washer to the surface of the lateral femoral condyle (Figure 24–23). The washer is necessary to anchor the graft proximally because the hole in the lateral femoral condyle is larger than the Endobutton. The knee is then extended to evaluate graft impingement on the intercondylar notch. With the knee in 10 degrees of flexion, the quadruple hamstring graft is secured distally by tying the #5 Ethibond suture over a tibial screw and post that is placed medial to the tibial tuber-

cle apophysis and distal to the proximal tibial physis (Figures 24–24 and 24–25). If the tendon graft extends through the tibial drill hole, it is also secured to the periosteum of the anterior aspect of the tibia with multiple 0 Ethibond sutures and use of figure-of-eight stitches (see Figure 24–24). The subcutaneous tissue and the skin are closed in a routine fashion, and a hinged brace is applied. Postoperative Management Patients are discharged on the day of surgery. Postoperative Rehabilitation Phase I of rehabilitation was started as soon as the patient awakened after surgery. The patient was encouraged to perform quadriceps muscle contraction and straight-leg raises. Cryotherapy Continued

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ACL Reconstruction: Epiphyseal Reconstruction with Quadruple Hamstring Grafts (Continued)

Figure 24–22 A #5 Ethibond suture is placed in one end of the Endobutton, and a guide wire is used to pass the suture through the tibial tunnel and out the lateral femoral condyle. (Copyright 2002 D. Cohn.)

was used for 5–10 minutes every hour. Range-ofmotion exercises and hamstring muscle stretches while the patient was prone were started the day after surgery. Patients who had not had a meniscal repair were allowed to walk with crutches with weight-bearing as tolerated. Those patients who had had a meniscal repair were allowed only toe-touch weight-bearing for 6 weeks. At 1 week after surgery, our goal was a range of motion of 0 degrees of extension to 90 degrees

of flexion. Phase II of rehabilitation, the strengthening phase, lasted from 2 to 11 weeks postoperatively. Active range-of-motion exercises along with patella mobilization and electrical muscle stimulation were begun. Patients progressed through the exercises at their own pace. They were fitted with a functional knee brace 2 weeks after surgery, and full weight-bearing was encouraged. Exercises, introduced into the rehabilitation program in order of increasing difficulty, included hamstring and quadriceps muscle stretching and Continued

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ACL Reconstruction: Epiphyseal Reconstruction with Quadruple Hamstring Grafts (Continued)

Figure 24–23 An AO washer is placed over the Endobutton, and tension is applied to the tendons distally, pulling the Endobutton and washer to the surface of the lateral femoral condyle. (Copyright 2002 D. Cohn.)

strengthening, proprioception exercises, functional strengthening, and strengthening exercises while in a pool. The goal was to have a full range of motion equal to that of the contralateral, normal knee at 6 weeks after surgery. Phase III of rehabilitation lasted from 12 to 20 weeks postoperatively. This phase included functional strengthening, straight-line jogging, plyometric exercises, sport cord exercises for jogging, lateral movement, and foot agility exercises. At 16 to 20 weeks postoperatively, patients were permitted to perform functional activities, including fullspeed running, while wearing the brace. They were allowed to advance to full activity, including competitive sports, 28 weeks after surgery.

Results A study was performed to evaluate the results of a transepiphyseal replacement of the anterior cruciate ligament in 12 skeletally immature patients. At a mean follow-up of 4.1 years, there was no evidence of growth disturbance, and all patients had extension of the index knee that was equal to the normal contralateral knee. The mean side-toside difference in anterior displacement was 1.5 mm as measured by the KT1000 at 134 newtons, and the mean IKDC subjective knee score was 96.5 out of 100. The preliminary results of this small series demonstrate that this surgical technique can be performed in prepubescent patients with efficacy and relative safety. Continued

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TECHNICAL NOTE 24-2

ACL Reconstruction: Epiphyseal Reconstruction with Quadruple Hamstring Grafts (Continued)

Figure 24–24 With the knee in 10 degrees of flexion, the quadruple hamstring graft is secured distally by tying the #5 Ethibond suture over a tibial screw and post that is placed medial to the tibial tubercle apophysis and distal to the proximal tibial physis. (Copyright 2002 D. Cohn.)

Figure 24–25 If the tendon graft extends through the tibial drill hole, it is also secured to the periosteum of the anterior aspect of the tibia with multiple 0 Ethibond sutures and use of figure-of-eight stitches.

Suggested Reading 1. Anderson AF: Transepiphyseal replacement of the anterior cruciate ligament in skeletally immature patients:

a preliminary report. J Bone Joint Surg Am 85:1255–1263, 2003.

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ACL Reconstruction: All-Epiphyseal Technique with Semitendinosus and Gracilis Tendons Vincenzo Guzzanti

Indications

Technique

Nonphyseal ACL reconstruction is an all-epiphyseal technique using semitendinosus and gracilis tendons placed at femoral and tibial insertion sites. The indication is ACL insufficiency in preadolescents.

Before surgery, clinical tests (Lachman’s and pivot shift) for ACL insufficiency are confirmed.

Preoperative Assessment Pretreatment clinical and radiographic growth characterization of these skeletally immature patients is the first step. These preadolescents are Tanner stage I, with a bone age of 11 years or less for girls and 12 years or less for boys, with lower extremity clinical evidence of the onset of the rapid phase of adolescent growth. Radiograph or MRI studies show fully open distal femoral and proximal tibial physes.1 Patients are submitted preoperatively to lower extremity teleoroentgenogram documenting femoral and/or tibial inequality. Bone bruise is shown preoperatively by MRI (Figure 24–26); if present, the articular cartilage condition is monitored over time. Setup General anesthesia is used, with the patient in the supine position. Standard arthroscopic and knee surgery instrumentation are used.

Arthroscopic Examination A nonsterile tourniquet is applied on the upper leg. The leg is exsanguinated with an Esmarch bandage. The tourniquet is inflated with 450 mm Hg of pressure. Under arthroscopy, intraarticular status is assessed to confirm a complete or partial ACL tear. Any associated meniscal and/or chondral lesions are observed. Treatment Meniscal injuries are treated with partial meniscectomy. Peripheral tears of menisci are treated by open suture after mini-arthrotomy. Infrequent chondral fragments are fixed with absorbable nails, while defects of cartilage are treated by mesenchymal stem cell stimulation techniques. Semitendinosus and Gracilis Harvest: A 6–8 cm transverse incision is made over the pes anserinus area of the affected knee, and then incising the fascia along the tendons. Hamstrings are isolated and dissected from the muscle–tendon junction (Figure 24–27, A), utilizing long scissors or a tendon stripper. Distally, the attachment of semitendinosus

Figure 24–26 Preoperative MRI shows a bone bruise of the lateral femoral condyle.

Continued

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TECHNICAL NOTE 24-3

ACL Reconstruction: All-Epiphyseal Technique with Semitendinosus and Gracilis Tendons (Continued)

Figure 24–27 A, Long scissors or a tendon stripper are used to isolate and dissect gracilis and semitendinosus tendons. B, The harvested tendons are sutured together with adsorbable stitches. A drill site is prepared in the distal femoral lateral epiphysis at the femoral notch. A drill hole is made in the proximal tibial epiphysis. C, Tendons are passed through the staple, then gently tensioned when the staple is positioned. D, The staple is firmly inserted into the distal femoral epiphysis below the physis. E, All tendons are sutured side to side.

and gracilis tendons is isolated, thus gaining 1–2 cm of additional length. The effective tibial insertion of tendons must not be disturbed to maintain their neurovascular supply. The harvested tendons are then sutured together with adsorbable stitches (Figure 24–27, B). The sutures are tightened in particular at the free proximal tendon ends and looped around the edges of the tendon to obtain a sufficient strength

for traction and to allow easy passage of the tendons through the tibial drill hole and around the femoral staple. ACL Preparation A mini-open arthrotomy is performed. Notchplasty is not performed. A 6-mm eccentric tunnel is drilled under fluoroscopic guidance through the Continued

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ACL Reconstruction: All-Epiphyseal Technique with Semitendinosus and Gracilis Tendons (Continued) central proximal tibial epiphysis between the physis and the articular cartilage until emergence at the tibial eminence. We prepare a drill site in the distal femoral lateral epiphysis at the femoral notch, and we create a small hole for a staple, just removing the articular cartilage and scraping 2–3 mm of subchondral bone (see Figure 24–27, B). The tendons are passed through the staple,2 then gently tensioned when the staple is placed (Figure 24–27, C). The staple is finally firmly inserted into the epiphysis below the physis (Figure 24–27, D). A small screw can reinforce the staple anchorage. We use fluoroscopy to ensure that the means of fixation does not enter the physis. With the knee in 30 degrees of flexion, the other part of the tendon is tensioned, and a suture is made to the tibial periosteum distal to the tibial tunnel. Finally, all tendons are sutured side to side (Figure 24–27, E). Graft stability is directly visualized and tested with a probe. The tourniquet is let down, and accurate hemostasis is obtained. The sutures are performed. A Cryocuff and hinged knee brace are applied. Postoperative Management A hinged knee brace is used all day for 4 weeks (except the hours dedicated to restoring motion).

A passive range-of-motion machine is used after the second week. Progressive weight bearing with crutch protection is done for the first 6 weeks postoperatively. The return to sports usually is within 6–8 months postoperatively, depending on the efficacy of progressive physical therapy.

Results The presented reconstruction method (Figure 24–28) was chosen for preadolescents with defined characteristics of growth to provide graft fixation at femoral and tibial sites without physeal risk.3 The method reported involved a technique that was modified to create a physeal sparing approach.4 Progressive incorporation of the staple into the lateral growing condyle can extend femoral bone-ligament junction. Mechanical, clinical, and radiographic assessment at follow-up at skeletal maturity of five patients demonstrated favorable and encouraging results.5 The Author thanks David Ciulla (CDU of Anatomical Design, University of Bologna, Italy) for the drawings of this surgical technique.

Figure 24–28 Postoperative anteroposterior radiograph demonstrating staple position.

Continued

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ACL Reconstruction: All-Epiphyseal Technique with Semitendinosus and Gracilis Tendons (Continued) References 1. Lo IK, Kirkley A, Fowler PJ, Miniaci A: The outcome of operatively treated anterior cruciate disruptions in the skeletally immature child. Arthroscopy 13:627–634, 1997. 2. Johnson LL: Extrasynovial conditions. In Johnson LL (ed): Arthroscopic surgery. Principles and Practice, ed 3. St. Louis: Mosby, 1986. 3. Fu FH, Bennett CH, Lattermann C, Ma CB: Current trends in anterior cruciate ligament reconstruction.

allografts have been used. The rationale of a combined overthe-top physeal-sparing femoral position and a transphyseal tibial tunnel is twofold. First, there is less growth potential in the tibia. Second, the tibial drill hole may be placed in a relatively central location, lessening the risk of angular deformity. Bisson et al.102 reported on a group of nine children, all male, ages 10–15, average age 13. Seven of the nine were available for follow-up at a mean of 39 months. Two of the nine double hamstring grafts ruptured, one at 3 years and one at 1 year, both in repeat injuries incurred in football. Of the six who had available KT1000 data, side-to-side differences for three were less than 3 mm, two were between 3 and 5 mm, and one had greater than 5-mm difference (graft failure). There were no significant LLD or angular changes. Lo et al.68 reported on five children with radiographically “wide open physes.” Their ages ranged from 8 to 14, with an average of 12.9. The children underwent ACL reconstruction, transtibial tunnel vertically oriented with a 6-mm or less tibial tunnel and an over-the-top position on the femur (Technical Notes 24–4 and 24–5). Three underwent double hamstring reconstructions, and two had quadriceps tendon reconstructions. Grafts were left attached distally. A ligament augmentation device was used in four of the five children. There was no notching around the posterolateral femur. Follow-up was an average of 7.4 years. KT1000 testing was 3 mm in one patient and less than or equal to one in the remaining four patients. Four of the five patients had returned to their previous level of activity; the fifth who had suffered patella dislocation had not. There was no significant LLD or angular deformities. Interestingly, the youngest patient was followed for 4.5 years, underwent 31 cm of longitudinal growth, and showed no progressive loss of knee stability. Andrews et al.103 reported on a group of children (average age 13.6) who underwent transtibial and over-thetop femur placement with allograft tissue, five fascia lata, and three Achilles tendons. There was also a direct repair of the ACL in all cases. Follow-up was an average of 58 months. There were six excellent, one good, and one fair result. One of the eight grafts re-ruptured at 4 years with a full return to soccer. There was one postoperative decrease

I. Biology and biomechanics of reconstruction. Am J Sports Med 277(6):821–830, 1999. 4. Stanitski CL: Anterior cruciate ligament injury in the skeletally immature patient: diagnosis and treatment. J Am Acad Orthop Surg 3:146–158, 1995. 5. Guzzanti V, Falciglia F, Stanitski CL: Physeal-spacing intraarticular anterior cruciate ligament reconstruction in preadolescents. Am J Sports Med 31(6):949–953, 2003.

in motion requiring manipulation. KT1000 revealed five grafts to have less than 3 mm and three grafts to have 3–5 mm side-to-side difference. Seven of the eight stated that they could return to jumping, cutting, and twisting activities with little or no limitations. The tibia was 1 cm short in one patient and 8 mm longer in another. In two patients the femur was short by 1 cm and 1 cm longer in another. Paletta70 presented a comparison of ACL reconstruction techniques in 14 skeletally immature patients age 10–13. The males were Tanner I, II, or III and the 3 females were all premenarchal. In all patients, the tibial tunnel was transphyseal. In 6 of the 14, the femoral limb was placed over the top, and in the remaining 8, it was transphyseal. At 2-years follow-up, after an average of 6 cm of limb growth, there were no significant LLD or angular changes. Objectively measured stability was superior for the total transphyseal tunnel group, utilizing quadrupled hamstring, versus the over-the-top femoral group, utilizing a distally attached doubled graft. In the former group, 1 of 8 had a positive pivot shift, and the mean KT 1000 values were 1.25 (range 0–3). In the latter, 4 of 6 had a positive pivot shift and the mean KT1000 values were 3.67 with a range of 1–5. Adult- Type Procedures In the skeletally immature, modifications to the typical adult ACL reconstruction may include (1) leaving only soft tissue across the physes, (2) metaphyseal side rather than aperture fixation, (3) relatively smaller tunnel size (Technical Note 24–6). Fuchs et al.67 reported on a group of 10 patients with “wide open” physes who underwent intraarticular, transphyseal ACL reconstruction through 9-mm tibial and 9-mm femoral tunnels (see Figure 24–61 on p. 370). They utilized allograft BPTB grafts. Bone plugs were fixed on the metaphyseal side with metal interference screws. Five of the 6 boys had no pigmented axillary hair, 1 had sparse, and all girls were premenarchal. At follow-up between 26–60 months, IKDC found 7 of 10 to have normal function, 2 to have nearly normal function, and 1 to have abnormal function. There were no significant angular or LLD and 9 of 10 returned to their pre-injury athletic activities. Two of 10 required removal of Text continued on p. 369

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TECHNICAL NOTE 24-4

ACL Reconstruction: Partial Transphyseal Technique Peter J. Fowler

Indications Our indication for partial transphyseal ACL reconstruction is ACL rupture in children with “wideopen” physes and significant growth remaining (Figure 24–29). We use a four-strand semitendinosus/gracilis tendon graft through a transphyseal tibial tunnel and over-the-top (OTT) femoral placement. Femoral fixation is performed with a

screw and ligament washer; tibial fixation is performed with multiple staples in a belt-buckle fashion. As shown in Figure 24–30, the position of the neoligament following OTT hamstring tendon ACL reconstruction approximates the anatomical posterior attachment site of the ACL. In theory, the risks of transphyseal techniques of ACL reconstruction in open physes are growth

Figure 24–29 Radiograph showing ACL rupture in a child with “wide-open” physes and significant growth remaining.

Continued

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TECHNICAL NOTE 24-4

ACL Reconstruction: Partial Transphyseal Technique (Continued)

Figure 24–30 The position of the neoligament following OTT hamstring tendon ACL reconstruction approximates the anatomical posterior attachment site of the ACL.

arrest and limb deformity. However, various clinical studies with average follow-ups ranging from 2.6 to 7.4 years (Table 24–2) have shown that intraarticular transphyseal ACL reconstruction can be carried out in the patient with wide-open physes with no effect on growth plate function or lower limb alignment.1–6 These findings are supported by the animal studies of Stadelmaier et al. and Seil et al.7,8 Other animal studies have suggested that there is cause for concern but indicate that the growth arrests and limb deformities observed may be associated with excessive graft tensioning and large tunnel diameters.9–11 In our view, with careful attention to technical details, intraarticular transphyseal ACL reconstruction can be safely performed in children with significant growth remaining. The theoretical risks can be minimized by the following: • More vertically oriented and centrally placed tibial tunnels • OTT femoral placement of the graft approximating the anatomical posterior

attachment site of the ACL and avoiding the femoral physeal plate • Graft fixation remote from physes • Avoidance of graft over-tensioning Technique OTT Femoral Position and OTT Exposure: A 3cm longitudinal incision is made 1.5-cm proximal to the lateral femoral epicondyle (Figure 24–31). The iliotibial band is identified and divided longitudinally in the line of its fibers. The intramuscular septum is identified and the vastus lateralis elevated anteriorly. The aperture in the intramuscular septum just proximal to Kaplan’s fibers is enlarged to allow the surgeon to insert an index finger and palpate the posterior intercondylar notch. Preparation for OTT Graft Fixation: A drill hole is made in the distal femur at least 1 cm proximal to the physis to facilitate placement of a screw with a ligament washer (Figure 24–32, A). The screw is left raised above the surrounding area for the time being (Figure 24–32, B). Continued

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ACL Reconstruction: Partial Transphyseal Technique (Continued)

Figure 24–31 A 3-cm longitudinal incision is made 1.5 cm proximal to the lateral femoral epicondyle.

Figure 24–32 A, A drill hole is made in the distal femur at least 1 cm proximal to the physis to facilitate placement of a screw with a ligament washer.

(Continued) Tibial Tunnel Setting the tibial guide at 50 degrees will ensure that the tibial tunnel is not excessively horizontal (Figure 24–33). Figure 24–34, A and B demonstrates a vertically oriented, centrally placed tibial tunnel.

When sizing the graft, it is important to keep in mind that a snug graft-to-tunnel fit will optimize biological fixation.12 To this end, as in adult reconstruction, the tibial tunnel may be undersized by 0.5 mm. Continued

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TECHNICAL NOTE 24-4

ACL Reconstruction: Partial Transphyseal Technique (Continued)

Figure 24–32—cont’d

B, The screw is temporarily left raised above the surrounding area.

Figure 24–33 Setting the tibial guide at 50 degrees ensures that the tibial tunnel is not excessively horizontal.

In Figure 24–35, the tibial tunnel has been drilled and the shaver introduced through it to demonstrate that the graft’s femoral position will be parallel and posterior to Blumensaat’s line when the knee is in extension.

Graft Fixation In Figure 24–36, the graft has been looped over the screw head and washer, which are tightened down to the femur. Note in Figure 24–37 that both proximal and distal graft fixation have been placed remote from the physes. Continued

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ACL Reconstruction: Partial Transphyseal Technique (Continued)

Figure 24–34 A, A vertically oriented, centrally placed tibial tunnel (lateral view).

Continued

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TECHNICAL NOTE 24-4

ACL Reconstruction: Partial Transphyseal Technique (Continued)

Figure 24–34—cont’d

B, A vertically oriented, centrally placed tibial tunnel (AP view).

Continued

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ACL Reconstruction: Partial Transphyseal Technique (Continued)

Figure 24–35 The tibial tunnel has been drilled and the shaver introduced through it to demonstrate that the graft’s femoral position will be parallel and posterior to Blumensaat’s line when the knee is in extension.

Figure 24–36 The graft has been looped over the screw head and washer, which are tightened down to the femur.

Continued

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ACL Reconstruction: Partial Transphyseal Technique (Continued)

Figure 24–37 Both proximal and distal graft fixation have been placed remote from the physes.

References 1. Lo Y, Kirkley A, Miniaci A, Fowler PJ: The outcome of operatively treated anterior cruciate ligament disruptions in the skeletally immature child. Arthroscopy 13(5):627-634, 1997. 2. Bisson LJ, Wickiewicz TL, Levinson M, Warren R: ACL reconstruction in children with open physes. Orthopedics 21(6):659-663, 1999. 3. Lipscomb B, Anderson K: Tears of the anterior cruciate ligament in adolescents. JBJS 68 (A):19-28, 1986. 4. Edwards TB, Grana AW: Anterior cruciate ligament reconstruction in the immature athlete: long term results of intra-articular reconstruction. Am J Knee Surg 14(4):232-237, 2001. 5. Shelbourne KD, Wiley BV: Results of transphyseal ACL reconstruction using patellar tendon autograft in skeletally immature adolescents with wide-open growth plates. Presented at 29th Annual Meeting of the American Orthopaedic Society for Sports Medicine, San Diego, July 20–23, 2003. 6. Rothrock CR, DeHaven KE, Adams MJ: Anterior cruciate ligament reconstruction in the skeletally immature athlete.

7. 8.

9. 10. 11. 12.

Presented at 29th Annual Meeting of the American Orthopaedic Society for Sports Medicine, San Diego California, July 20–23, 2003. Stadelmaier DN, Arnozcky SP, Dodds H, et al: The effect of drilling and soft tissue grafting across open growth plates. Am J Sports Med 23(431):435, 1995. Seil R, Pape D, Kohn D. ACL replacement in sheep with open physes. Presented at 29th Annual Meeting of the American Orthopaedic Society for Sports Medicine, San Diego, July 20–23, 2003. Guzzanti V, Falciglia F, Gigante A, et al: The effect of intra-articular reconstruction on the growth plates of rabbits. JBJS (B) 76:960-963, 1994. Houle J-B, Letts RM, Yang J: Effects of a tensioned tendon graft in a bone tunnel across the rabbit physis. Clin Orthop Rel Res 391:275-281, 2001. Edwards TB, Greene CC, Baratta RV, Zieske A, Willis RB: The effect of placing a tensioned graft across open growth plates. JBJS (A) 83(5):725-734, 2001. Rodeo SA, Arnozcky SP, Torzilli PA, et al: Tendon-healing in a bone tunnel. JBJS (A) 75(12):1795-1803, 1993.

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ACL Reconstruction: Physeal-Sparing Femoral and Transphyseal Tibial Technique with Quadriceps Ligament Roland P. Jakob • Matthias Jacobi

Indications Surgical treatment of ACL insufficiency in skeletally immature patients is still controversial because of the possibility of growth disturbances as a consequence of transphyseal transplant placement.1 There is concordance that a bone block crossing the epiphyseal line should be strictly avoided. Transphyseal screw placement is also contraindicated,2 but every tunnel placed through the physeal line has a small risk of consecutive growth disturbance, which is minimized when a soft tissue graft is placed in the transphyseal tunnel.3,4 Nevertheless, several authors have presented good results with the tibial and/or femoral transphyseal technique.5–7

Indication for ACL reconstruction is shown in symptomatic prepubescent patients with unsuccessful conservative treatment, because insufficient stability has a very high risk for the development of lesions like meniscal tears or cartilage lesions.8 Diagnosis is confirmed clinically and, if necessary, with an MRI (Figure 24–38). Bony avulsion of the ligament is excluded by normal radiographs in which skeletal age can also be assessed (Figure 24–39). We perform ACL reconstruction in immature patients with open physes in a femoral physealsparing and tibial transphyseal technique as shown in Figure 24–40. We use quadriceps ligament as a ligament graft. This is a modification of the technique that was described by Lipscomb and Anderson.9,10

Figure 24–38 An MRI is obtained when necessary to confirm ACL insufficiency.

Continued

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TECHNICAL NOTE 24-5

ACL Reconstruction: Physeal-Sparing Femoral and Transphyseal Tibial Technique with Quadriceps Ligament (Continued)

Figure 24–39 Tibial eminence fracture and bony avulsion of the ACL is excluded by normal radiographs.

(Continued)

Technique Examination under anesthesia includes Lachman’s and a pivot-shift test to confirm the diagnosis. Anterior drawer is quantified with the Rolimeter (Aircast). Arthroscopy: Surgery is started with arthroscopy with standard anterolateral and anteromedial portals. The diagnosis of the ACL tear is confirmed, and associated lesions are treated in the same sitting if

necessary. Meniscal lesions are sutured in an insideout technique (if possible), and chondral lesions are treated depending on the size and localization by debridement, refixation, or mosaicplasty. The ruptured ACL is resected with an arthroscopic shaver. Transplant Harvest: A quadriceps transplant is used for the ACL reconstruction. A longitudinal incision is made over the distal aspect of the quadriceps tendon. The tendon is prepared about 8 cm Continued

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ACL Reconstruction: Physeal-Sparing Femoral and Transphyseal Tibial Technique with Quadriceps Ligament (Continued)

Figure 24–39—cont’d

long and to a thickness of 8 mm (Figure 24–41). The bone block in the patella is cut with an oscillating saw in a trapezoid shape with one drill hole placed in the bone block. The transplant is anchored with a pull-out suture through the bone block and a running anchoring suture for the distal end (Figure 24–42). Ligament Insertion and Fixation: A 4–5 cm incision is made over the lateral aspect of the knee. The iliotibial tract and the lateral collateral ligament are prepared. Using a jig, a K-wire is

inserted under arthroscopic control to enter anterior to the LCL origin running below the physeal line and exiting into the posterior notch at the 10 o’clock for a right knee (Figure 24–43). The tibial approach demands a longitudinal incision medial to the tibial tuberosity tibia at the insertion of the pes anserinus tendons. A K-wire is inserted as well under arthroscopic control for the placement of the tibial tunnel (Figure 24–44). Fluorometric control shows the localization of the two K-wires (Figure 24–45) and, if necessary, the position is Continued

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TECHNICAL NOTE 24-5

ACL Reconstruction: Physeal-Sparing Femoral and Transphyseal Tibial Technique with Quadriceps Ligament (Continued)

Figure 24–40 A femoral physeal-sparing and tibial transphyseal technique can be used to perform ACL reconstruction in immature patients with open physes.

changed. The femoral and tibial tunnels are drilled to 8 mm. The graft is inserted with the bone block placed proximally (Figure 24–46), which is then impacted until it is placed next to the notch in an aperture fixation (Figure 24–47). The proximal end is sutured at its insertion

(Figure 24–48), and the distal end is sutured through the bone under 30 degrees of knee flexion. The graft is tensioned (Figure 24–49). The residual knee laxity is tested with Rolimeter (Figure 24–50) and, if necessary, the suture is retightened. Stepwise wound closure is performed. Continued

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TECHNICAL NOTE 24-5

ACL Reconstruction: Physeal-Sparing Femoral and Transphyseal Tibial Technique with Quadriceps Ligament (Continued)

Figure 24–41 After a longitudinal incision is made over the distal aspect of the quadriceps tendon, the tendon is prepared to a size of 8 cm long and 8 mm thick.

Figure 24–42 The graft is prepared with a pull-out suture through the bone block and a running anchoring suture for the distal end.

Postoperative Management We administer antibiotics for 24 hours. Partial weight bearing (10 kg) is started the second postoperative day with protection in a removable splint in 20 degrees flexion. Passive movement of the knee is started the fifth day postoperatively with the limits of 70–20–0 degrees range of motion. Radiographic controls are performed

postoperatively and at 6 weeks. After 6 weeks, complete weight bearing and range of motion is allowed. Controlled sports activity (e.g., swimming, jogging) is not started for 3 to 4 months, whereas contact sports and sports with rotation movement are not started for 6 months postoperatively, because there is an inherent tendency for secondary loosening. Continued

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TECHNICAL NOTE 24-5

ACL Reconstruction: Physeal-Sparing Femoral and Transphyseal Tibial Technique with Quadriceps Ligament (Continued)

Figure 24–43 Using a jig, a K-wire is inserted under arthroscopic control to enter anterior to the LCL origin running below the physeal line and exiting into the posterior notch at the 10 o’clock position for a right knee.

Figure 24–44 A K-wire is inserted under arthroscopic control for the placement of the tibial tunnel.

Continued

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TECHNICAL NOTE 24-5

ACL Reconstruction: Physeal-Sparing Femoral and Transphyseal Tibial Technique with Quadriceps Ligament (Continued)

Figure 24–45 Fluoroscopic control shows the localization of the two K-wires for the femoral and tibial tunnels.

Continued

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TECHNICAL NOTE 24-5

ACL Reconstruction: Physeal-Sparing Femoral and Transphyseal Tibial Technique with Quadriceps Ligament (Continued)

Figure 24–45—cont’d

Figure 24–46 The graft is inserted with the bone block placed proximally in the femur.

Continued

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TECHNICAL NOTE 24-5

ACL Reconstruction: Physeal-Sparing Femoral and Transphyseal Tibial Technique with Quadriceps Ligament (Continued)

Figure 24–47 The graft is impacted until it is placed next to the notch in an aperture fixation.

Figure 24–48 The proximal end of the graft is sutured at its insertion.

Figure 24–49 The distal end of the graft is sutured through the bone under 30 degrees of knee flexion, and the graft is tensioned.

Continued

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TECHNICAL NOTE 24-5

ACL Reconstruction: Physeal-Sparing Femoral and Transphyseal Tibial Technique with Quadriceps Ligament (Continued)

Figure 24–50 The residual knee laxity is tested with an instrumented knee laxity testing device.

References 1. Barber FA: Anterior cruciate ligament reconstruction in the skeletally immature high-performance athlete: what to do and when to do it? Arthroscopy 16:391–392, 2000. 2. Koman JD, Sanders JO: Valgus deformity after reconstruction of the anterior cruciate ligament in a skeletally immature patient. A case report. J Bone Joint Surg Am 81:711–715, 1999. 3. Edwards TB, Greene CC, Baratta RV, et al: The effect of placing a tensioned graft across open growth plates. A gross and histologic analysis. J Bone Joint Surg Am 83:725–734, 2001. 4. Stadelmaier DM, Arnoczky SP, Dodds J, Ross H: The effect of drilling and soft tissue grafting across open growth plates. A histologic study. Am J Sports Med 23:431–435, 1995. 5. Bisson LJ, Wickiewicz T, Levinson M, Warren R: ACL reconstruction in children with open physes. Orthopedics 21:659–663, 1998.

6. Attmanspacher W, Dittrich V, Stedtfeld HW: [Results on treatment of anterior cruciate ligament rupture of immature and adolescents]. Unfallchirurg 106:136–143, 2003. 7. 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. 8. McCarroll JR, Shelbourne KD, Porter DA, et al: Patellar tendon graft reconstruction for midsubstance anterior cruciate ligament rupture in junior high school athletes. An algorithm for management. Am J Sports Med 22:478–484, 1994. 9. Anderson AF: Transepiphyseal replacement of the anterior cruciate ligament in skeletally immature patients. A preliminary report. J Bone Joint Surg Am 85:1255–1263, 2003. 10. Lipscomb AB, Anderson AF: Tears of the anterior cruciate ligament in adolescents. J Bone Joint Surg Am 68:19–28, 1986.

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TECHNICAL NOTE 24-6

ACL Reconstruction: Transphyseal Technique with Autogenous Hamstring Tendons Roger V. Larson

Indications and Rationale ACL reconstruction in skeletally immature patients is reserved for those patients who have failed conservative management or those who can be expected to fail nonoperative management based upon their degree of laxity and anticipated activity level. Several studies have shown that restricting activities in this age group is often unsuccessful. Repeat injury often leads to meniscal and chondral damage that can have significant long-term negative consequences. The goal of ACL reconstruction in skeletally immature patients is to restore normal anterior laxity to the injured knee with the least risk to subsequent growth. A consideration in this age group is anatomical intraarticular reconstruction with hamstring tendon autografts through tibial and femoral transphyseal tunnels with fixation distant from the physis and with the avoidance of dissection near the physis. The

use of small centrally placed tunnels and soft tissue grafts minimizes the risk of physeal injury. By avoiding dissection near either the tibial or femoral physis and by using fixation devices distant from the physes, the risk of inadvertent influence is minimized. Setup General anesthesia is usually used in this age group. A tourniquet is used and should be placed proximally to leave as much thigh exposed as possible. A low profile thigh holder is placed over the tourniquet. Incisions: Anterolateral and anteromedial arthroscopy portals are established adjacent to the patellar tendon to facilitate access to the intercondylar notch. A vertical 1-inch skin incision is made overlying the PES insertion (Figure 24–51).

Figure 24–51 The incisions needed for this procedure include anterolateral and anteromedial arthroscopy portals adjacent to the patellar tendon. A tibial incision begins approximately 3 cm distal to the anteromedial portal and approximately 1 cm medial to the tibial tubercle. It extends 2–3 cm and allows for harvesting of the semitendinosus and gracilis tendons as well as creation of the tibial tunnel.

Continued

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TECHNICAL NOTE 24-6

ACL Reconstruction: Transphyseal Technique with Autogenous Hamstring Tendons (Continued) Graft Harvest and Preparation: The semitendinosus and gracilis tendons are isolated at their insertion into the tibia (Figure 24–52) and are sharply released. The tendons are inverted, separated, and then harvested with a tendon stripper. The grafts are then shortened to 22–24 cm in length, and muscle tissue is removed from each graft. Each end of each graft is then tagged with a #2 nonabsorbable suture utilizing a Bunnell or whip-stitch technique (Figure 24–53). The double looped grafts are then sized so that the smallest possible tunnels can be created that will allow graft passage (Figure 24–54). If desired, a soft tissue allograft such as a tibialis anterior tendon can be utilized. Joint Preparation: Diagnostic arthroscopy is next carried out, and associated pathology is treated. Debridement of the tibial stump is usually carried out, although an extensive debridement is usually not needed. It is preferable to avoid notchplasty if feasible.

Creation of Tibial and Femoral Tunnels: The tibial tunnel is created by first placing a guide pin into the center of the tibial footprint. The start point is well medial to the tibial tubercle apophysis and just proximal to the level of hamstring harvest. When the guide pin position has been fine-tuned to the optimal position, it is overdrilled with a cannulated drill to create the smallest possible tunnel that will allow passage of the grafts (Figure 24–55). Through the tibial tunnel, the femoral tunnel is created by utilizing an “over-thetop” referencing drill guide with a 3–5 mm offset to allow passage of a guide pin from high and to the back of the intercondylar notch to the anterolateral femoral cortex (Figure 24–56). Over this guide pin, a femoral socket is created with an acorn drill to a depth of 35 mm (Figure 24–57). This socket traverses the femoral physis. Tunnels placed in these positions are nearly isometric

Figure 24–52 The semitendinosus and gracilis tendons are isolated just proximal to their tibial insertion. The combined tendons are then released from the tibia, separated, and harvested with a tendon stripper.

Continued

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TECHNICAL NOTE 24-6

ACL Reconstruction: Transphyseal Technique with Autogenous Hamstring Tendons (Continued)

Figure 24–53 The tendons are cut to approximately 22–24 cm in length, and muscle tissue is removed from them. Each end of each graft is then tagged with a Bunnell or whip-stitch of #2 nonabsorbable suture.

Figure 24–54 The combined double-looped tendons are then sized so that appropriately sized tunnels can be created to tightly fit the grafts.

Figure 24–55 After the position of the tibial guide pin has been optimized, it is overdrilled with a cannulated drill.

Continued

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TECHNICAL NOTE 24-6

ACL Reconstruction: Transphyseal Technique with Autogenous Hamstring Tendons (Continued)

Figure 24–56 A femoral drill guide with a 3–5-mm offset is used to place a tibial guide pin at a position of 1 o’clock or 11 o’clock at the extreme back of the notch.

Figure 24–57 An acorn drill of predetermined diameter is used to create a socket in the femur 35 mm in depth. A passing channel for the Endobutton is then created over the guide pin.

and will allow placing a graft that will undergo minimal strain through a full range of knee motion. A passing channel is then created for the Endobutton. A continuous loop Endobutton is next selected and sized to allow 25 mm of graft penetration into the socket.

Graft Passage and Fixation: The grafts are next looped through the Endobutton loop, and passing sutures are attached to the Endobutton (Figure 24–58). The Endobutton is pulled across the joint and out to the anterolateral femoral cortex where it is “flipped.” The grafts are then tensioned and fixed to the tibial tendon by Continued

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TECHNICAL NOTE 24-6

ACL Reconstruction: Transphyseal Technique with Autogenous Hamstring Tendons (Continued) placing a low profile screw and washer around which sutures are tied. The knee is then cycled, and the tension is fine-tuned. The soft tissue washer is then advanced to directly fix the grafts, sutures, and knots (Figure 24–59). The graft is next observed arthroscopically to ensure impingement-free motion (Figure 24–60). The tourniquet is deflated and the wounds are closed. A dressing is secured with a support hose, and a cold therapy device is applied to the knee. A hinged knee brace is applied locked at 10 degrees of flexion.

Postoperative Rehabilitation Rehabilitation following this surgery is generally quite easy. The knee brace is opened to allow motion from 10 degrees to unlimited flexion at 1 week. The brace is worn for weight-bearing for 6 weeks but is removed for physical therapy and sleeping as tolerated. Full weight-bearing as tolerated is allowed, and most patients discontinue crutches by 2 weeks. Stationary bicycling is started when motion allows, and closed-chain exercises are started immediately. Activities such

Figure 24–58 The completed construct. The tape and knot shown can be replaced by a continuous-loop Endobutton of the appropriate size.

Figure 24–59 Fixation on the tibia is accomplished by placing a screw and washer at the distal ends of the grafts. After the grafts are tied snugly, their tension is fine-tuned, and the screw is then advanced, allowing the washer to directly fix the grafts as well as the sutures and knots.

Continued

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ACL Reconstruction: Transphyseal Technique with Autogenous Hamstring Tendons (Continued)

Figure 24–60 The final graft position. The position is adjacent to the PCL and has clearance with the lateral wall of the intercondylar notch. As the knee is brought into full extension, the graft should barely touch the superior notch without being impinged by it.

as recreational bicycling, swimming, and most other activities on predictable surfaces are started at 12 weeks postoperative. Running on level surfaces and resisted, open-chain terminal knee extension exercises are delayed until 6 months postoperative, and high-level jumping and pivoting sports are discouraged until 8 months postoperative.

prominent tibial side fixation. Aronowitz et al.104 presented 19 children who underwent transphyseal ACL reconstruction utilizing 9–10-mm tunnels and an Achilles tendon allograft. There were 10 girls and 9 boys, with an average bone age of ~14. At follow-up at 25 months, 16 of the 19 had returned to their pre-injury level of athletics. Lysholm score on average was 97 with a range of 94 to 100. Return to sports on average was at 7.9 months with a range of 5–12. All KT1000 side-toside differences were less than 3 mm. There were no significant LLD or angular deformities. McCarroll et al.51 reported the outcomes of 60 adolescents undergoing BPTB autograft, transphyseal adult type ACL reconstruction. Outcomes were excellent, and there were no significant LLD or angular deformities. These children were Tanner IV and V and approaching skeletal maturity. Fifty five of 60 were able to return to their previous level of sport and 3 of the 55 who returned to sports sustained a graft rupture greater than

Postoperative radiographs are usually first obtained at 12 weeks postoperative to document tunnel position and fixation devices. It is essential to continue follow-up with periodic radiographs until skeletal maturity.

2 years after reconstruction during sporting activity. In 51 of 60, KT1000 side-to-side difference was less than 3 mm; in 6 it was 4–5 mm, and in 3 of 60 it was greater than 5 mm. Graft Options The ideal graft for ACL reconstruction in the skeletally immature would reproduce the complex anatomy of the ACL, provide similar biomechanical properties, permit strong fixation without risk to the physes, rapidly incorporate, develop with the maturing knee, and have minimal donor site morbidity or graft-related complications.105,106 Obviously, the ideal graft does not yet exist. In the adult athlete, BPTB graft has been considered the gold standard but may be associated with more graft site morbidity, motion loss, and long-term extensor dysfunction. There are some specific concerns for BPTB use in the adolescent. First, it

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associated with less graft site morbidity, but care must be taken in protecting the saphenous nerve and its branches during harvest; (5) tendon-to-bone healing may require longer periods than bone-to-bone healing in BPTB grafts. The successful use of both the Achilles tendon allograft and the BPTB allograft in adolescent patients has been reported.67,103 Allograft alternatives also include anterior or posterior tibialis tendons. The benefits of allograft include lack of harvest site morbidity, a wide range of available graft sizes, a possible decrease in postoperative pain, and ease of rehabilitation. The risks of disease transmission have seemed remote, but recent, wellpublicized cases of bacterial infection following allograft use have raised a number of questions about the procurement process. There are also concerns about initial mechanical properties of treated allografts and their rates of “ligamentization.” Surgical Treatment Suggestions and Rationale

Figure 24–61 Transphyseal BPTB graft with metaphyseal side fixation. (Reprinted with permission from Fuchs R, Wheatley W, Uribe JW, et al: Intraarticular anterior cruciate ligament reconstruction using patellar tendon allograft in the skeletally immature patient. Arthroscopy 18:824–828, 2002).

may aggravate the clinical course of a patient with preexisting patellar instability or retropatellar syndrome. Second, there are concerns about patients with preexisting OsgoodSchlatter disease. McCarroll107 has reported successful use of BPTB graft after shelling out the ossicles and reinforcing the areas with suture. Conversely, Cosgarea et al.108 suggested that graft mechanical properties could be compromised by the presence of previous Osgood-Schlatter disease and suggested alternative graft sources. We commonly take the McCarroll approach in asymptomatic patients who have a small or single ossicle at the tibial tubercle. However, in patients with multiple or large ossicles, we recommend a hamstring graft. Minimizing donor site morbidity and enabling only soft tissue across the physes, hamstring autografts are also the more commonly chosen procedure in the skeletally immature population. However, there are several cautionary notes: (1) there have been higher rates of graft failure using double looped rather than quadrupled hamstrings; (2) there are suggestions that hamstring-reconstructed female athletes are at higher risk for graft laxity compared to males or to BPTB procedures.109 Reasons may include inferior fixation due to decreased bone density, decreased initial graft cross-sectional area, or increased compliance of the graft due to underlying hyperlaxity. All of these factors may also affect the immature patient; (3) possible biomechanical consequences of metaphyseal, nonaperture fixation of hamstring grafts; (4) hamstring grafts appear to be

After a full review of the available literature, we feel it is best to treat adolescents approaching maturity with adulttype surgeries. The youngest children should be treated nonoperatively, and those in the middle ages should be treated with transphyseal hamKEY POINTS string grafts, utilizing metaphyseal fixation (Tables 24–2 and 1. In reported cohorts 24–3). There is certainly room for of skeletally disagreement, which is why a full immature patients range of options and the pertinent undergoing a literature have been presented. variety of ACL However, we feel there is little reconstructive information to suggest that 6–9procedures, the mm transphyseal tunnels, filled frequency of with a soft tissue graft, are likely to significant legcause angular deformity or LLD. length discrepancy Certainly, there is little informaor angular deformity tion to suggest any higher risks is low. compared to extraarticular, extra2. Anatomical, physeal, or partial physeal-sparing intraarticular grafts procedures. Most iatrogenic deforappear safe and mities have been related to inapbiomechanically propriate placement of graft fixasuperior to most tion, excessive tunnel size, or bone extraphyseal or placement across the physes. With partial physeal this in mind, we feel it makes most procedures. sense to place the graft in an 3. Currently, hamstring anatomical position where the autografts appear biomechanical environment is to be the most most favorable. The graft can then commonly used ACL undergo appropriate ligamentizasubstitute in the tion and responsively grow with skeletally immature. the child. To improve femoral However, there are tunnel placement, we utilize an some biomechaniaccessory anterior medial tunnel cal issues that to drill the femoral tunnel, rather must be addressed than limiting femoral positioning in future research by drilling through the tibial and surgical tunnel.110 We normally utilize techniques. 111 an Endobutton on the femoral

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Table 24–2

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Surgical Treatment Methods and Results

Authors/Journal

Method

Results

Lo et al., Arthroscopy, 199768

Average F/U—7.4 years N = 5; wide-open physes Hamstring and quads–PT autografts Transepiphyseal tibia/OTT femur Average F/U—39 months N = 9; wide-open physes Hamstring autografts Transepiphyseal tibial/ OTT femur Average F/U—35 months N = 24; 11 wide-open physes ST/G + Ellison or Losee Transphyseal tibia; femoral tunnel below physes Average F/U–34 months N = 21; wide–open physes 15 hamstrings; 6 B-PT-B Transphyseal tibia/femur

4 normal; 1 nearly normal Symmetrical fusion of 4 physes (1 still open) No LLD (average height increase 17.7cm (7.6–31 cm) Mean Lysholm 99 (95-100) Average STS difference 2.8 mm (0.0–5.5) in 6 patients No LLD, angular deformity, physeal injury 16 excellent; 7 good; 1 fair Average STS difference 1.8 mm Significant growth abnormality in 1 (associated with stapling of femoral and tibial physes) No LLD No change in tibia–fibula alignment Lysholm 93/95; 19/20 back to preinjury sports Average Noyes score 95 (82-100) Average STS difference 2.1 mm (0–4 mm) No LLD Mean IKDC 89.1 (7–A; 4-B IKDC grades) STS difference 1 cm. No LLD, angular deformities

Bisson et al., Orthopedics, 1998102

Lipscomb and Anderson, J Bone Joint Surg Am, 198697

Edwards and Grana, Am J Knee Surg, 2001

Shelbourne et al., AOSSM, 2003

Average F/U—2.8 years N = 17; wide-open physes Transphyseal femoral and tibial PT allografts Average F/U—2.9 years N = 11; 10 wide-open physes Doubled ST autograft transphyseal tibial tunnel, OTT femur

Rothrock et al., AOSSM, 2003

LLD, Leg-length discrepancy; OTT, over the top.

Table 24–3

Surgical Staging Suggestions

At or Approaching Skeletal Maturity

Preadolescent

Children

Girls: Tanner IV, V Bone age ≥13 Boys: Tanner V Bone age ≥15 Adult-type surgery Bone–patella– tendon–bone: High demand Hamstring: Other

Girls: Tanner II, III Bone age ≥11 Boys: Tanner III, IV Bone age ≥ 12 Transphyseal femur and tibia Quadrupled hamstring 6-8-mm tunnels

Girls: Tanner I Bone age ≤11 Boys: Tanner I, II Bone age ≤12 Well-organized, well-monitored nonoperative care Surgery if required as noted for preadolescent or transtibial OTT femur; combine intraphyseal/ extraphyseal (see text). Aperture fixation Metaphyseal side fixation

side and post fixation on the tibia (Figure 24–62, A to D). The all-intraepiphyseal technique presented by Anderson is intriguing but carries some concern for technique-dependent physeal damage (see Figure 24–17).

Postoperative Rehabilitation Several major concepts guide rehabilitation following ACL reconstruction112–115: (1) dynamic knee function: the knee functions in a dynamic environment, and stability is dependent on numerous factors; (2) an envelope of knee function, which defines safe, responsive, and injurious ranges of loading forces on the knee joint; and (3) specific adaptations to impose demand—rehabilitation should incorporate functional, sports-related activities. Rehabilitation should promote graft protection and guided maturation, while enhancing local and central neuromuscular coordination. We have not found a “decelerated” approach necessary for anatomically placed hamstring grafts in young patients.116,117 Post-ACL Reconstruction Rehabilitation Program112–115,118 Preoperative Goals: Normalized knee function. Educate the family and patient concerning surgical intervention and expected postoperative progression. 1. Patient and family education/social preparation. 2. Decrease swelling and pain. 3. Early quad activity, regain full active and passive extension. 4. Regain normal gait. 5. Resume single plane unloaded aerobic exercise.

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Figure 24–62 A, ACL tear in a 13-year-old female. B, Femoral tunnel position utilizing accessory anteromedial portal and knee flexion of 110 degrees for drilling of femoral tunnel. C, Passage of Endobutton into femoral tunnel. D, Quadrupled intraarticular transphyseal graft.

Postoperative

Walking Phase: Weeks 2–4

Immediate Postoperative: Weeks 0–2

Goal: Maintain extension. Regain flexion. Normalized gait pattern and begin closed-chain, weight-bearing activities. 1. Maintain full extension. 2. Increase flexion as tolerated. 3. Exercise for uninvolved leg. 4. Discontinue brace use once heel toe gait is normalized and good quad control is apparent.

Goals: Reduce pain and swelling. Promote early quad function and full knee extension. 1. Decrease swelling and pain through elevation, rest, and ice. 2. Decrease pain utilizing appropriate analgesic and NSAIDs. 3. Promote early quad activity in full extension. 4. Brace locked in extension with weight bearing as tolerated with knee in locked extension. Limit walking to only that which is required. 5. Early quad activity through quad sets, straight leg raises, side leg raises, ankle pumps, and glutens sets. 6. Maintain passive extension—brace locked in extension and heel props.

Balance and Dynamic Joint Stability: Weeks 5–8 Goal: To gain controlled single and double limp support and stress dynamic contraction, functional activities. 1. Proprioceptive activities/balance activities. 2. Backwards side-to-side karaoke walking. 3. Single leg multidirectional activities. 4. Reestablish unloaded aerobic base.

Anterior Cruciate Ligament Injuries

Muscle Strengthening Phase: Weeks 9–12 Goal: To gradually increase quad, hamstring and total lower extremity muscle strength through a variety of closed and open chain exercise. Running Phase: Weeks 13–16 Goal: Resume straight running. Also include trampoline, treadmill, and outdoor straight-ahead running. Plyometric/Agility Phase: Weeks 16–24 Goals: Graduated sports-specific jumping, cutting, and plyometric activities usually progressing to gym-based program. Return to sport at ~24 weeks. Criterion for return to sport is quad hamstring strength approximately 90% of normal. Equal one-legged hop jump, vertical and horizontal. Full progression of previous functional program with no instability, swelling, or significant pain. On return to activities, patient ices knee immediately after sporting activities. 1. Custom ACL fit brace for first season return. 2. Close clinical monitoring for swelling, pain, and decreased functional abilities. Long-Term Maintenance and Injury Prevention: Weeks 24 and Beyond 1. Maintain aerobic base. 2. Lower extremity and total body maintenance strengthening. 3. Instruction and utilization of appropriate jump, land, cut, and push-off techniques. 4. Control plyometric and agility activities. NOTE: The editors’ postoperative regimen is similar. However, the authors always use three-point crutch protection until gait is symmetrical without a limp. This usually occurs 4–6 weeks postoperative. The authors do not feel that postoperative crutch use is a stigma and have observed many noncrutch–using patients postoperative, with terrible dysfunctional gaits, placing unacceptable stresses on the new, unincorporated graft. Partial ACL Tears In the course of arthroscopic examination of acute hemarthroses in skeletally immature KEY POINTS patients, a large percentage (22–65%) of ACL tears have 1. Partial ACL tears been judged to be “partial.”25,43,119 are more common An accepted definition, clinical among the importance, and treatment protoskeletally immature cols for partial ACL tears have than in adults. not been well described. The 2. Outcomes appear mechanism of injury appears the to be proportionate same as for complete tears. To to degree of injury. some degree, this diagnosis is Partial tears with driven by diagnostic arthroscopy which there is and MRI. Any ACL tear associsignificant clinical ated with positive clinical instalaxity or functional bility testing or a history of instalaxity are bility is functionally significant functionally regardless of intact substance on complete. MRI or exterior arthroscopic

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visualization.21 Poorer outcomes can be expected with tears greater than 50%, predominantly posterolateral tears, those associated with positive pivot shift, and in patients with higher activity levels.119–121 Summary Skeletally immature patients with ACL insufficiency represent a wide range of maturity levels, athletic abilities, and functional knee demands. These differences must be recognized in the treatment of individual patients, review of the literature, and in designing research. The increased recognition of ACL injuries in the young is related to increased public and professional awareness and changes in youth sports participation, which are leading to significant increases in ACL injury rates. The predisposing risk factors, underlying biomechanics, and treatment options for ACL deficiency in the skeletally immature are different from the adult population. The natural history of the ACL-deficient knee in the active adolescent athlete is often poor, with a history of recurrent instability, cumulative meniscal damage, and sports-related disability. Chronological age is an excellent predictor of sexual and skeletal maturation; however, any individual may show significant variance from the average. For any given Tanner stage, girls are on average more skeletally mature than their male counterparts. All immature patients should be appropriately screened for skeletal and sexual maturation via bone age determination and Tanner scaling. Treatment options are less controversial at the end ranges of “skeletal immaturity,” with the initial option for the youngest children being a closely monitored nonoperative program. For older adolescents, an adult-type treatment program is suitable. In the middle age range, transphyseal hamstring autografts, with relatively small tunnels and metaphyseal side fixation, appear to offer the advantages of anatomical, biomechanically sound graft placement and low risk of physeal dysfunction. The risk of significant LLD or angular deformity following ACL reconstructive surgery in the skeletally immature is low. Most iatrogenic deformities have been associated with transphyseal fixation, transphyseal bone grafting, or excessive tunnel size. If nonoperative care is chosen, it needs to be well organized and well monitored. The athlete and his or her family must understand that an environment of recurrent instability is not an option. Acute hemarthrosis in the skeletally immature represents a significant injury, is commonly associated with ACL injury, and requires aggressive diagnostic workup. References 1. Barber FA: Anterior cruciate ligament reconstruction in the skeletally immature high-performance athlete: what to do and when to do it? Arthroscopy 16:391–392, 2000. 2. Ellison AE, Berg EE: Embryology, anatomy, and function of the anterior cruciate ligament. Orthop Clin North Am 16:3–14, 1985. 3. Merida-Velasco JA, Sanchez-Montesinos I, Espin-Ferra J, et al: Development of the human knee joint ligaments. Anat Rec 248:259–268, 1997. 4. Ratajczak W: Early development of the cruciate ligaments in staged human embryos. Folia Morphol (Warsz) 59:285–290, 2000. 5. Katz MP, Grogono BJ, Soper KC: The etiology and treatment of congenital dislocation of the knee. J Bone Joint Surg Br 49:112–120, 1967.

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6. Heron D, Bonnard C, Moraine C, Toutain A: Agenesis of cruciate ligaments and menisci causing severe knee dysplasia in TAR syndrome. J Med Genet 38:E27, 2001. 7. Johansson E, Aparisi T: Congenital absence of the cruciate ligaments: a case report and review of the literature. Clin Orthop 162:108–111, 1982. 8. Johansson E, Aparisi T: Missing cruciate ligament in congenital short femur. J Bone Joint Surg Am 65:1109–1115, 1983. 9. Thomas NP, Jackson AM, Aichroth PM: Congenital absence of the anterior cruciate ligament. A common component of knee dysplasia. J Bone Joint Surg Br 67:572–575, 1985. 10. Malumed J, Hudanich R, Collins M: Congenital absence of the anterior and posterior cruciate ligaments in the presence of bilateral absent patellae. Am J Knee Surg 12:241–243, 1999. 11. Mitsuoka T, Horibe S, Hamada M: Osteochondritis dissecans of the medial femoral condyle associated with congenital hypoplasia of the lateral meniscus and anterior cruciate ligament. Arthroscopy 14:630–633, 1998. 12. Tolo VT: Congenital absence of the menisci and cruciate ligaments of the knee. A case report. J Bone Joint Surg Am 63:1022–1024, 1981. 13. Kaelin A, Hulin PH, Carlioz H: Congenital aplasia of the cruciate ligaments. A report of six cases. J Bone Joint Surg Br 68:827–828, 1986. 14. Jones DC, Moseley CF: Subluxation of the knee as a complication of femoral lengthening by the Wagner technique. J Bone Joint Surg Br 67:33–35, 1985. 15. Hoffmann FF: Abnormal femoral origin of the anterior cruciate ligament combined with a discoid lateral meniscus. Arthroscopy 13:254–256, 1997. 16. Kim SJ, Lee YT, Kim DW: Intraarticular anatomic variants associated with discoid meniscus in Koreans. Clin Orthop 356:202–207, 1998. 17. Dienst M, Burks RT, Greis PE: Anatomy and biomechanics of the anterior cruciate ligament. Orthop Clin North Am 33:605–620, 2002. 18. Smith BA, Livesay GA, Woo SL: Biology and biomechanics of the anterior cruciate ligament. Clin Sports Med 12:637–670, 1993. 19. Behr CT, Potter HG, Paletta GA, Jr: The relationship of the femoral origin of the anterior cruciate ligament and the distal femoral physeal plate in the skeletally immature knee. An anatomic study. Am J Sports Med 29:781–787, 2001. 20. Shea KG, Apel PJ, Pfeiffer RP, et al: The tibial attachment of the anterior cruciate ligament in children and adolescents: analysis of magnetic resonance imaging. Knee Surg Sports Traumatol Arthrosc 10:102–108, 2002. 21. Lintner DM, Kamaric E, Moseley JB, Noble PC: Partial tears of the anterior cruciate ligament. Are they clinically detectable? Am J Sports Med 23:111–118, 1995. 22. Liu W, Maitland ME, Bell GD: A modeling study of partial ACL injury: simulated KT-2000 arthrometer tests. J Biomech Eng 124:294–301, 2002 23. 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. 24. Kellenberger R, von Laer L: Nonosseous lesions of the anterior cruciate ligaments in childhood and adolescence. Prog Pediatr Surg 25:123–131, 1990. 25. Stanitski CL, Harvell JC, Fu F: Observations on acute knee hemarthrosis in children and adolescents. J Pediatr Orthop 13:506–510, 1993. 26. Tipton CM, Matthes RD, Martin RK: Influence of age and sex on the strength of bone-ligament junctions in knee joints of rats. J Bone Joint Surg Am 60:230–234, 1978. 27. Woo SL, Orlando CA, Gomez MA, et al: Tensile properties of the medial collateral ligament as a function of age. J Orthop Res 4:133–141, 1986. 28. Woo SL, Peterson RH, Ohland KJ, et al: The effects of strain rate on the properties of the medial collateral ligament in skeletally immature and mature rabbits: a biomechanical and histological study. J Orthop Res 8:712–721, 1990. 29. Beighton P, Solomon L, Soskolne CL: Articular mobility in an African population. Ann Rheum Dis 32:413–418, 1973. 30. Hinton RY: Pediatric anterior cruciate ligament injuries. Presented at the AAOS Advanced Session on Pediatric Orthopaedics: Current Perspectives and Techniques, La Jolla, Cal., December 3–5, 1999. 31. Souryal TO, Freeman TR: Intercondylar notch size and anterior cruciate ligament injuries in athletes. A prospective study. Am J Sports Med 21:535–539, 1993.

32. Matthews LS, Hinton RY, Burke N: Lacrosse. In Fu FH, Stone DA (eds): Sports Injuries: Mechanism, Prevention, Treatment, ed 2. Philadelphia, Lippincott Williams & Wilkins, 2001, pp 568–582. 33. National Collegiate Athletic Association: Injury Surveillance System 2001–2002, Indianapolis, NCAA, 2001. 34. Faigenbaum AD: Strength training for children and adolescents. Clin Sports Med 19:593–619, 2000. 35. Griffin LY, Agel J, Albohm MJ, et al.: Noncontact anterior cruciate ligament injuries: risk factors and prevention strategies. J Am Acad Orthop Surg 8:141–150, 2000. 36. Huston LJ, Greenfield ML, Wojtys EM: Anterior cruciate ligament injuries in the female athlete. Potential risk factors. Clin Orthop 372:50–63, 2000. 37. Arendt E, Dick R: Knee injury patterns among men and women in collegiate basketball and soccer. NCAA data and review of literature. Am J Sports Med 23:694–701, 1995. 38. Bjordal JM, Arnly F, Hannestad B, Strand T: Epidemiology of anterior cruciate ligament injuries in soccer. Am J Sports Med 25:341–345, 1997. 39. Wasilewski SA, Frankl U: Osteochondral avulsion fracture of femoral insertion of anterior cruciate ligament. Case report and review of literature. Am J Sports Med 20:224–226, 1992. 40. Janarv PM, Westblad P, Johansson C, Hirsch G: Long-term follow-up of anterior tibial spine fractures in children. J Pediatr Orthop 15:63–68, 1995. 41. McLennan JG: Lessons learned after second-look arthroscopy in type III fractures of the tibial spine. J Pediatr Orthop 15:59–62, 1995. 42. Willis RB, Blokker C, Stoll TM, et al: Long-term follow-up of anterior tibial eminence fractures. J Pediatr Orthop 13:361–364, 1993. 43. Kocher MS, DiCanzio J, Zurakowski D, Micheli LJ: Diagnostic performance of clinical examination and selective magnetic resonance imaging in the evaluation of intraarticular knee disorders in children and adolescents. Am J Sports Med 29:292–296, 2001. 44. Millett PJ, Willis AA, Warren RF: Associated injuries in pediatric and adolescent anterior cruciate ligament tears: does a delay in treatment increase the risk of meniscal tear? Arthroscopy 18:955–959, 2002. 45. Harvell JC, Jr., Fu FH, Stanitski CL: Diagnostic arthroscopy of the knee in children and adolescents. Orthopedics 12:1555–1560, 1989. 46. Matelic TM, Aronsson DD, Boyd DW, Jr., Lamont RL: Acute hemarthrosis of the knee in children. Am J Sports Med 23:668–671, 1995. 47. McDermott MJ, Bathgate B, Gillingham BL, Hennrikus WL: Correlation of MRI and arthroscopic diagnosis of knee pathology in children and adolescents. J Pediatr Orthop 18:675–678, 1998. 48. Kasser JR: Physeal bar resections after growth arrest about the knee. Clin Orthop 255:68–74, 1990. 49. Aichroth PM, Patel DV, Zorrilla P: The natural history and treatment of rupture of the anterior cruciate ligament in children and adolescents. A prospective review. J Bone Joint Surg Br 84:38–41, 2002. 50. Graf BK, Lange RH, Fujisaki CK, et al: Anterior cruciate ligament tears in skeletally immature patients: meniscal pathology at presentation and after attempted conservative treatment. Arthroscopy 8:229–233, 1992. 51. McCarroll JR, Shelbourne KD, Porter DA, et al: Patellar tendon graft reconstruction for midsubstance anterior cruciate ligament rupture in junior high school athletes. An algorithm for management. Am J Sports Med 22:478–484, 1994. 52. Mizuta H, Kubota K, Shiraishi M, et al: The conservative treatment of complete tears of the anterior cruciate ligament in skeletally immature patients. J Bone Joint Surg Br 77:890–894, 1995. 53. Lee K, Siegel MJ, Lau DM, et al: Anterior cruciate ligament tears: MR imaging-based diagnosis in a pediatric population. Radiology 213:697–704, 1999. 54. Takeda Y, Ikata T, Yoshida S, et al: MRI high-signal intensity in the menisci of asymptomatic children. J Bone Joint Surg Br 80:463–467, 1998. 55. Ogden JA: Femur. In Ogden JA (ed): Skeletal Injury in the Child, ed 3. New York: Springer-Verlag, 2000, pp 857–928. 56. Ogden JA: Tibia and fibula. In Ogden JA (ed): Skeletal Injury in the Child, ed 3. New York: Springer-Verlag, 2000, pp 990-1090. 57. Anderson M, Green WT, Messner MB: Growth and predictions of growth in the lower extremities. J Bone Joint Surg Am 45:1–14, 1963. 58. Pritchett JW: Longitudinal growth and growth-plate activity in the lower extremity. Clin Orthop 275:274–279, 1992.

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59. White JW, Stubbins SG: Growth arrest for equalizing leg lengths. J Am Med Assn 126:1146, 1944. 60. Menlaus MB: Correction of leg length discrepancy by epiphyseal arrest. J Bone Joint Surg Br 48:336–339, 1966. 61. Wester W, Canale ST, Dutkowsky JP, et al: Prediction of angular deformity and leg-length discrepancy after anterior cruciate ligament reconstruction in skeletally immature patients. J Pediatr Orthop 14:516–521, 1994. 62. Janarv PM, Wikstrom B, Hirsch G: The influence of transphyseal drilling and tendon grafting on bone growth: an experimental study in the rabbit. J Pediatr Orthop 18:149–154, 1998. 63. Makela EA, Vainionpaa S, Vihtonen K, et al: The effect of trauma to the lower femoral epiphyseal plate. An experimental study in rabbits. J Bone Joint Surg Br 70:187–191, 1988. 64. Edwards TB, Greene CC, Baratta RV, et al: The effect of placing a tensioned graft across open growth plates. A gross and histologic analysis. J Bone Joint Surg Am 83:725–734, 2001. 65. Stadelmaier DM, Arnoczky SP, Dodds J, Ross H: The effect of drilling and soft tissue grafting across open growth plates. A histologic study. Am J Sports Med 23:431–435, 1995. 66. Anderson MD: Anatomic, physeal sparing anterior cruciate ligament reconstruction in skeletally immature patients using quadruple hamstring grafts. Presented at the ACL Study Group Meeting in Big Sky, Montana, March 3–8, 2002. 67. Fuchs R, Wheatley W, Uribe JW, et al: Intraarticular anterior cruciate ligament reconstruction using patellar tendon allograft in the skeletally immature patient. Arthroscopy 18:824–828, 2002. 68. 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. 69. Micheli LJ, Rask B, Gerberg L: Anterior cruciate ligament reconstruction in patients who are prepubescent. Clin Orthop 364:40–47, 1999. 70. Paletta G: Anterior cruciate ligament reconstruction in the skeletally immature athlete: comparison of two techniques. Presented at the ACL Study Group Meeting in Big Sky, Montana, March 3–8, 2002. 71. Koman JD, Sanders JO: Valgus deformity after reconstruction of the anterior cruciate ligament in a skeletally immature patient. A case report. J Bone Joint Surg Am 81:711–715, 1999. 72. Kocher MS, Saxon HS, Hovis WD, Hawkins RJ: Management and complications of anterior cruciate ligament injuries in skeletally immature patients: survey of the Herodicus Society and The ACL Study Group. J Pediatr Orthop 22:452–457, 2002. 73. Loder RT, Estle DT, Morrison K, et al: Applicability of the Greulich and Pyle skeletal age standards to black and white children of today. Am J Dis Child 147:1329–1333, 1993. 74. Gilli G: The assessment of skeletal maturation. Horm Res 45:49–52, 1996. 75. Greulich WW, Pyle SI: Radiographic Atlas of Skeletal Development of the Hand and Wrist, ed 2. Stanford, Cal.: Stanford University Press, 1959. 76. Cundy P, Paterson D, Morris L, Foster B: Skeletal age estimation in leg length discrepancy. J Pediatr Orthop 8:513–515, 1988. 77. Tanner JM: Assessment of Skeletal maturity and Prediction of Adult Height (TW2 Method), New York: Academic Press, 1975. 78. Milner GR, Levick RK, Kay R: Assessment of bone age: a comparison of the Greulich and Pyle and the Tanner and Whitehouse methods. Clin Radiol 37:119–121, 1986. 79. Vignolo M, Milani S, DiBattista E, et al: Modified Greulich-Pyle, Tanner-Whitehouse, and Roche-Wainer-Thissen (knee) methods for skeletal age assessment in a group of Italian children and adolescents. Eur J Pediatr 149:314–317, 1990. 80. Dimeglio A: Growth in pediatric orthopedics. In Morrissy RT, Weinstein SL (eds): Lovell and Winter’s Pediatric Orthopedics, ed 5. Philadelphia: Lippincott Williams & Wilkins, 2001, pp 33–62. 81. Sauvegrain J, Nahum H, Bronstein H: Etude de la maturation osseuse du coude. Ann Radiol 5:542–550, 1962. 82. Pyle SI, Hoerr NL: A Radiographic Standard of Reference for the Growing Knee, Springfield, Ill.: Charles C Thomas Publisher, 1969. 83. Roche AF, Thissen D, Wainer H: Skeletal Maturity: The Knee Joint as a Biological Indicator. New York: Plenum Medical Book Company, 1975. 84. Aicardi G, Vignolo M, Milani S, et al: Assessment of skeletal maturity of the hand-wrist and knee: A comparison among methods. Am J Human Biol 12:610–615, 2000.

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85. Roche AF, French NY: Differences in skeletal maturity levels between the knee and hand. Am J Roentgenol Radium Ther Nucl Med 109:307–312, 1970. 86. Xi HJ, Roche AF: Differences between the hand-wrist and the knee in assigned skeletal ages. Am J Phys Anthropol 83:95–102, 1990. 87. Marshall WA, Tanner JM: Variations in pattern of pubertal changes in girls. Arch Dis Child 44:291–303, 1969. 88. Marshall WA, Tanner JM: Variations in the pattern of pubertal changes in boys. Arch Dis Child 45:13–23, 1970. 89. Needleman RD: Adolescent growth and development. In Berhman RE, Kliegman RM, Jenson HB (eds): Nelson Textbook of Pediatrics, ed 16. Philadelphia: WB Saunders, 2000, pp 52–56. 90. Tanner JM: Growth of Adolescence, ed 2. Oxford: Blackwell Scientific Publications, 1962. 91. Tanner JM, Davies PS: Clinical longitudinal standards for height and height velocity for North American children. J Pediatr 107:317–329, 1985. 92. Daniel WA, Jr.: Growth at adolescence. Clinical correlates. Semin Adolesc Med 1:15–24, 1985. 93. DeLee JC, Curtis R: Anterior cruciate ligament insufficiency in children. Clin Orthop 172:112–118, 1983. 94. Engebretsen L, Svenningsen S, Benum P: Poor results of anterior cruciate ligament repair in adolescence. Acta Orthop Scand 59:684–686, 1988. 95. Nakhostine M, Bollen SR, Cross MJ: Reconstruction of midsubstance anterior cruciate rupture in adolescents with open physes. J Pediatr Orthop 15:286–287, 1995. 96. MacIntosh DL, Darby TA: Lateral substitution reconstruction. In proceedings and reports of universities, colleges, councils and associations. J Bone Joint Surg Br 58:142, 1976. 97. Lipscomb AB, Anderson AF: Tears of the anterior cruciate ligament in adolescents. J Bone Joint Surg Am 68:19–28, 1986. 98. Losee RE, Johnson TR, Southwick WO: Anterior subluxation of the lateral tibial plateau. A diagnostic test and operative repair. J Bone Joint Surg Am 60:1015–1030, 1978. 99. Ellison AE: Distal iliotibial-band transfer for anterolateral rotatory instability of the knee. J Bone Joint Surg Am 61:330–337, 1979. 100. Parker AW, Drez D Jr, Cooper JL: Anterior cruciate ligament injuries in patients with open physes. Am J Sports Med 22:44–47, 1994. 101. Brief LP: Anterior cruciate ligament reconstruction without drill holes. Arthroscopy 7:350–357, 1991. 102. Bisson LJ, Wickiewicz T, Levinson M, Warren R: ACL reconstruction in children with open physes. Orthopedics 21:659–663, 1998. 103. 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. 104. 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. 105. Miller SL, Gladstone JN: Graft selection in anterior cruciate ligament reconstruction. Orthop Clin North Am 33:675–683, 2002. 106. Mologne TS, Friedman MJ: Graft options for ACL reconstruction. Am J Orthop 29:845–853, 2000. 107. McCarroll JR, Shelbourne KD, Patel DV: Anterior cruciate ligament reconstruction in athletes with an ossicle associated with OsgoodSchlatter’s disease. Arthroscopy 12:556–560, 1996. 108. Cosgarea AJ, Weng MS, Andrews M: Osgood-Schlatter’s disease complicating anterior cruciate ligament reconstruction. Arthroscopy 9:700–703, 1993. 109. Barrett GR, Noojin FK, Hartzog CW, Nash CR: Reconstruction of the anterior cruciate ligament in females: A comparison of hamstring versus patellar tendon autograft. Arthroscopy 18:46–54, 2002. 110. O’Donnell JB, Hinton RY: Modified endoscopic anterior cruciate ligament reconstruction: technique and rationale. Tech Orthop 13:275–280, 1998. 111. Rosenberg TD: Technique for ACL reconstruction with Acufex director drill guide and Endobutton CL. Andover, Massachusetts: Smith & Nephew, Inc, 1999. 112. Dye SF, Wojtys EM, Fu FH, et al: Factors contributing to function of the knee joint after injury or reconstruction of the anterior cruciate ligament. Instr Course Lect 48:185–198, 1999. 113. Majima T, Yasuda K, Tago H, et al: Rehabilitation after hamstring anterior cruciate ligament reconstruction. Clin Orthop 397:370–380, 2002.

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114. Risberg MA, Mork M, Jenssen HK, Holm I: Design and implementation of a neuromuscular training program following anterior cruciate ligament reconstruction. J Orthop Sports Phys Ther 31:620–631, 2001. 115. Shelbourne KD, Rask BP: Controversies with anterior cruciate ligament surgery and rehabilitation. Am J Knee Surg 11:136–143, 1998. 116. De Carlo M, Hamersly S: Decelerated rehabilitation after ACL reconstruction revisited. J Orthop Sports Phys Ther 27:238–239, 1998. 117. Hardin JA, Voight ML, Blackburn TA, et al: The effects of “decelerated” rehabilitation following anterior cruciate ligament reconstruction on a hyperelastic female adolescent: a case study. J Orthop Sports Phys Ther 26:29–34, 1997.

118. Hinton RY: Postoperative anterior cruciate ligament reconstruction, Baltimore: The Union Memorial Hospital, Rehabilitation Services, 2003. 119. Kocher MS, Micheli LJ, Zurakowski D, Luke A: Partial tears of the anterior cruciate ligament in children and adolescents. Am J Sports Med 30:697–703, 2002. 120. Buckley SL, Barrack RL, Alexander AH: The natural history of conservatively treated partial anterior cruciate ligament tears. Am J Sports Med 17:221–225, 1989. 121. Noyes FR, Bassett RW, Grood ES, Butler DL: Arthroscopy in acute traumatic hemarthrosis of the knee. Incidence of anterior cruciate tears and other injuries. J Bone Joint Surg Am 62:687–695, 757, 1980.

Chapter 25

Injury of the Medial Collateral Ligament, Posterior Cruciate Ligament, and Posterolateral Complex in Skeletally Immature Patients Kevin G. Shea

In the words of Mercer Rang,1 “Children are not small adults.” Musculoskeletal injury patterns in skeletally immature patients differ from those seen in adults. Although the mechanisms of injury may be similar, the biomechanical patterns are not identical because pediatric and adolescent skeletons differ in size, biomechanics, and physiology. Because of these factors, the clinician will see unique patterns of injury in pediatric and adolescent patients. Consideration of these differences will improve the diagnosis and treatment of injuries in the pediatric patient.1 As recently as 30 years ago, some suggested that ligamentous injuries about the knee did not occur in the skeletally immature, or were exceptionally rare.2 Historically, injuries about the knee in children were thought to consist mainly of fractures and physeal injury,1–18 although a growing body of literature supports the concept of serious ligamentous knee injury in pediatric and adolescent patients and athletes.19–27 The increase in knee injuries in skeletally immature patients may reflect several phenomena. The increased use of magnetic resonance imaging (MRI) and its ability to detect soft tissue injury may play a role,28 in addition to increased participation in sports. More children are participating in sports at younger ages, and many are training and competing yearround. Title IX legislation, designed to increase participation of female athletes in sports, appears to have been effective. It has been documented that female athletes are at a higher risk of sustaining serious ligamentous knee injury, even when skeletally immature.29 In addition to athletic injuries, trauma studies have also demonstrated ligamentous injury in skele-

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Peter J. Apel

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Ron Pfeiffer

tally immature subjects4,8,12,30 and recommend that patients be screened for ligamentous injury of the knee when fractures or effusion are present about the knee. Anatomy of the Skeletally Immature Knee and Ligaments Pediatric bone is more porous and less dense than adult bone, thus it is more flexible and less brittle (Figure 25–1).1,31–33 These different mechanical properties are evidenced by the unique fracture types seen in children, including buckle, bowing, and greenstick deformities.1 The physis has been considered the “weak link” in the pediatric knee and is more prone to injury than ligamentous structures. The epiphyseal cartilage adds unique biomechanical character to the pediatric skeleton. This tissue is more viscoelastic than bone and thus is more likely to fail in trauma situations.1,31,32,34 In many types of pediatric injuries, the epiphyseal cartilage will fail before the surrounding ligaments or osseous tissues. Examples of fractures of this type include medial epicondyle avulsion of the elbow, triplane fractures of the distal tibia, and traumatic displacement of the proximal femoral physis. These fractures are complicated by the susceptibility to growth disturbance after injury, especially when physeal fractures are involved.5,35–38 The pediatric knee has a higher percentage of cartilage than the adult knee due to the physis and nonossified regions 377

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Femoral epiphyseal plate Fibular collateral ligament

Figure 25–1 Load deformation curves, comparing the bone of a 46-year-old to a 2-year-old. (From Currey JD, Butler G: The mechanical properties of bone tissue in children. J Bone Joint Surg Am 57[6]:810–814, 1975.)

of the epiphysis, which may explain the higher incidence of physeal and apophyseal fractures in the skeletally immature knee.28,39–43 Although occasionally seen in adults, tibial eminence avulsion injuries are relatively rare compared to midsubstance anterior cruciate ligament (ACL) injury. Tibial eminence avulsion injury is commonly seen in skeletally immature patients, possibly because the epiphyseal region of the tibial plateau is composed of a relatively high percentage of cartilage compared with the adult knee.41–43 Avulsion injuries of the posterior cruciate ligament (PCL) are also seen in skeletally immature patients.41,44–48 Many studies of pediatric trauma have supported the concept that physes are weaker than ligaments and that the physeal structure is more likely to fail than ligaments, especially under conditions of high energy transfer. The weakest area of the physis is thought to be the zone of hypertrophy,28,40,49,50 although fractures can occur in other regions.16 Biomechanical studies of the physis and ligaments have shown that failure modes are related to the magnitude and rate of load application.28 Ligaments are more likely to fail at lower rates of load application, whereas physeal fractures are more likely to occur at higher rates of load application.28,51 As the child becomes older, the physis becomes stiffer and may make the incidence of ligament injury more likely than physeal injury.28,31,52–54 Most of the ligaments and capsular structures of the knee attach to the epiphysis. This anatomic configuration is probably the underlying biomechanical explanation for the higher risk of physeal injury versus ligamentous injury about the knee. With the exception of the distal medial collateral ligament (MCL), the ligaments of the knee are contained within the epiphyseal/physeal envelope, which has been described by Stanitski (Figure 25–2). The ACL originates from the epiphyseal portion of the lateral femoral condyle below the femoral physis and inserts on the epiphyseal portion of the tibia.55,56 The configurations of the lateral collateral ligament (LCL), PCL, and MCL are described later in this chapter. During torsional force application to the knee, the ligamentous and capsular tissues transfer the forces to the epiphysis, contributing to physeal injury.

Tibial collateral ligament

Lateral capsular ligament Medial capsular ligament

Fibular epiphyseal plate

Tibial epiphyseal plate

Figure 25–2 Knee ligament anatomy in the skeletally immature. The anterior cruciate ligament, posterior cruciate ligament, lateral collateral ligament, and posterolateral complex are contained within the “physeal envelope” of the knee. The medial collateral ligament extends below the tibial physis and attaches to the tibial metaphysis. (From Delee JC: Ligamentous injury of the knee. In Staniski CL, Delee JC, Drez DJ Jr. [eds]: Pediatric and Adolescent Sports Medicine. Philadelphia: WB Saunders, 1994, pp 406–432.)

tant. Lachman’s test excursions may be easier to detect and quantify compared with adult patients. Specialized pediatric equipment, such as a KT1000 Junior, may be helpful for these exams. Although serious injuries are rare, especially in smaller children, physeal and ligamentous injury should be considered. In addition, physeal anatomy and location of symptoms need to be carefully examined to distinguish between physeal and ligamentous injuries. Treating pediatric and adolescent patients is more forgiving than treating adults in some respects. Younger patients tend to heal more quickly than adults and have a lower risk of arthrofibrosis. Younger patients may require a shorter period of immobilization because of rapid healing. Adolescents and older patients with serious knee injury are usually mobilized as soon as possible to reduce the risk of arthrofibrosis. In the authors’ experience, arthrofibrosis tends to respond better to nonoperative measures in children than adults. For this reason, the treating physician may observe young patients longer before considering surgical intervention in the stiff knee. In cases of severely ankylosed knees, Cole et al.57 described a successful approach for restoration of function in children. For cases in which manipulation is considered, caution is warranted because a physeal injury could occur. Diagnostic Imaging

Principles of Examination and Treatment of the Pediatric and Adolescent Knee Principles of examination for the pediatric knee are similar to those used for adults. The pediatric exam may be easier because of the smaller knee and very distinct ligamentous endpoints. In some children, there is increased laxity; therefore, comparison with the contralateral knee is impor-

Diagnostic imaging is useful for serious knee injuries in young patients. Plain radiographs can identify osseous injury, although they are inadequate for the evaluation of an acutely injured knee with a hemarthrosis.58,59 If a physeal injury is suspected, stress views under anesthesia may be helpful (Figure 25–3). Both stress and nonstress radiographs should be examined closely for evidence of

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Figure 25–3 Stress radiograph view. This demonstrates medial “laxity” of the knee associated with a physeal fracture, not on medial collateral ligament injury. (From Delee JC: Ligamentous injury of the knee. In Stanitski CI, Delee JC, Drez DJ, Jr. [eds]: Pediatric and Adolescent Sports Medicine. Philadelphia: WB Saunders, 1994.)

capsular avulsion, opening of the physis, or tibial spine avulsions.9 MRI may be useful in place of stress testing for differentiating physeal versus ligamentous injury.5,60,61 MRI has been assessed for evaluation of the knee in children, demonstrating the effectiveness of this modality,5,60,61 although imaging in children under the age of 5–7 years may be limited due to the small size of the knee.60–62 The indications for MRI in children are still being established, although many clinicians rely upon MRI for diagnosis.63 MRI is a very sensitive tool for the evaluation of physeal, osseous, and ligamentous structures,5,18,64–67 but interpretation of meniscal tissue can be problematic.62,67 Kocher et al.63 and others62,68,69 have questioned the effectiveness and necessity of the MRI for the routine evaluation of knee injury in children, although imaging studies may help identify occult18 and ligamentous67 injuries.

KEY POINTS 1. Pediatric bone is more flexible than adult bone, and the physis is the “weakest link.” Ligaments are more likely to fail at lower rates of load application, whereas physeal fractures are more likely to occur at higher rates of load application. 2. Principles of examination for the pediatric knee are similar to those used for adults, and treatment in this population may be more forgiving. 3. Plain radiographs are useful for evaluating osseous injury, although MRI may also be useful for suspected physeal or ligamentous injury.

The Medial Collateral Ligament Anatomy and Biomechanics The medial aspect of the knee has been well defined through anatomic studies. Three distinct layers have been described.28,70–73 These structures act as a complex sleeve of tissues that is both a dynamic and static stabilizer of the knee (Figures 25–4 and 25–5). The static structures include the superficial medial collateral ligament, the posterior oblique ligament, and deep medial collateral ligament.71 The dynamic structures include the vastus medialis and the semimembranosus muscles.74 The first layer of the medial aspect of the knee is the fascial plane investing the sartorius and its insertion. The second layer includes the superficial MCL, originating from the medial femoral epicondyle, anterior to the adductor tubercle and below the distal femoral physis (Figure 25–4). Unlike other ligaments of the knee, the insertion of the MCL is distal to the tibial physis (Figures 25–2 and 25–6). The MCL extends 5–7 cm below the articular surface of the tibia, crossing the physis and attaching over a relatively broad area. The insertion of the MCL is located on the periostium, and it is covered by the pes anserine attachment externally.28,75 In the third and deepest layer of the medial knee, the MCL is a continuation of the joint capsule. This structure is intimately associated with the medial meniscus; thus injuries to this layer of the MCL are often associated with medial meniscal injury. The posterior oblique ligament is a continuation and thickening of the deep posterior capsule of the knee (Figure 25–5).76

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Figure 25–4 Superficial medial knee anatomy. (From Indelicato PA: Isolated medial collateral ligament injuries in the knee. J Am Acad Orthop Surg 3[1]:9–14, 1995.)

Figure 25–6 Magnetic resonance imaging of knee showing the MCL and tibial physis. The MCL insertion extends below the epiphysis, attaching to the tibial metaphysis.

Figure 25–5 Deep medial knee anatomy. (From Indelicato PA: Isolated medial collateral ligament injuries in the knee. J Am Acad Orthop Surg 3[1]:9–14, 1995.)

The MCL is the primary static knee stabilizer for valgus stress,70,72 with both the deep and superficial MCL contributing resistance.75,77 The posterior oblique ligament works in concert with the superficial MCL as a medial stabilizer. The MCL and posterior oblique ligament also resist external rotation of the tibia.70,72,74 The posterior fibers of the MCL/ posterior oblique complex tighten as the knee extends (Figure 25–7). The ACL also plays a role in resisting valgus

Figure 25–7 In extension, the posterior fibers of the medial ligament complex are relatively tight. In flexion, the tension in the fibers decreases. (From Linton RC, Indelicato PA: Medial ligament injuries. In Drez DJ Jr. [ed]: Orthopaedic Sports Medicine. Philadelphia: WB Saunders, 1994, p 1263.)

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

forces about the knee78 and works in concert with the MCL to provide stability.75 Evaluation and Treatment of MCL Injury There have been relatively few descriptions of MCL injury in skeletally immature athletes. These injuries are rare in young athletes with wide-open growth plates, but they do occur (Figure 25–8). MCL injury is probably more common in adolescents as they approach skeletal maturity.79 The possibility of a physeal fracture always needs to be considered in these pediatric and adolescent patients, especially those with open physes.5 Fractures can occur through the distal femoral physeal scar and may mimic an MCL injury. In addition, MCL injury can also occur with epiphyseal fractures4 or with an avulsion-type injury.28 Bradley et al.39 described a series of pediatric patients with serious knee injury and reported a small number of MCL injuries. In 40 pediatric patients (≤16 years old) with hemarthrosis, Eiskjaer et al.80 identified two isolated ruptures of the MCL. The history of the acute injury is an important factor for evaluation of MCL injuries. Injury to the MCL most often occurs as a result of a valgus stress but may also be seen from an external rotation of the knee. In many sports-related cases, these injuries involve contact with another athlete. This mechanism of injury is very common in American football

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and soccer, although it can be seen with any contact sport. As a general rule, younger and more skeletally immature patients have a higher risk of sustaining a physeal fracture, whereas older and more skeletally mature adolescents have a higher probability of soft-tissue MCL injury. The physical examination is important for distinguishing an MCL injury from a physeal fracture. For most isolated MCL injuries, an effusion, if present, is likely to be small. Palpation of the medial aspect of the knee is important to localize the area of injury and to determine if there is physeal involvement. Tenderness may be localized to the region of the MCL, including the femoral, joint-line, or tibial regions. If MCL injury is suspected, the knee should be subjected to valgus stress testing at full extension and at 30 degrees of flexion. In cases of isolated MCL injury, the knee will be stable to stress at full extension because of the integrity of the posteromedial capsular structures and the cruciate ligaments. If laxity is demonstrated in full extension, a more serious soft-tissue injury or physeal fracture needs to be considered. In these cases, the patient can be evaluated under anesthesia or by MRI. In flexion, the posteromedial capsular structures are relaxed, allowing for isolated evaluation of the MCL. The degree of laxity should be quantified and compared to the uninjured knee. Laxity of the medial knee should be graded by using the criteria in Table 25–1.79 Grade I and II ligament tears will usually have definite endpoints, whereas a type III injury may not. If a large effusion is present, evaluation for a more serious knee injury will need to be performed. If pain is not localized to the region of the MCL, or if the pain and swelling are significant, then a physeal fracture should be considered. If a fracture is suspected, any manipulation of the knee should be done under anesthesia. An alternative to an exam under anesthesia is MRI.5,60,61 In most cases of a nondisplaced physeal fracture, the use of a cylinder cast for 3–4 weeks is appropriate, although use of internal fixation is necessary in some cases with significant instability.81 To reduce the risk of physeal arrest after physeal injury, anatomic alignment is important. Because the literature on MCL injury in pediatric and adolescent athletes is limited, the adult literature provides guidance for management of these injuries in young athletes. The management of MCL injury in the adult patient has evolved in the last 30 years. Kennedy9 described a surgical procedure for MCL reconstruction in young athletes in the late 1970s, although limited clinical information was available for follow-up evaluation. Bradley et al.39 gathered data over 15 years and described six children, aged 6–11 years, who underwent operative repair of the MCL following traumatic rupture. Patients were treated with open

Table 25–1 Grades for Measuring the Laxity of the Medial Knee Grade Figure 25–8 MRI of a medial collateral ligament injury in a 9-year-old with wide-open physes. The MRI shows significant edema around the medial capsular structures of the knee.

I II III

Amount of Opening (mm) 0–5 5–10 >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

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

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.

Continued

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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.

Continued

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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.

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

72. Warren LA, Marshall JL, Girgis F: The prime static stabilizer of the medical side of the knee. J Bone Joint Surg Am 56(4):665–674, 1974. 73. Warren LF, Marshall JL: The supporting structures and layers on the medial side of the knee: an anatomical analysis. J Bone Joint Surg Am 61(1):56–62, 1979. 74. Muller W: The Knee: Form, Function, and Ligament Reconstruction. New York: Springer-Verlag, 1983. 75. Linton RC, Indelicato PA: Medial ligament injuries. In Drez DJ Jr. (ed): Orthopaedic Sports Medicine. Philadelphia: WB Sanders, 1994, pp 1261–1274. 76. 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. 77. Kennedy JC, Fowler PJ: Medial and anterior instability of the knee. An anatomical and clinical study using stress machines. J Bone Joint Surg Am 53(7):1257–1270, 1971. 78. Inoue M, McGurk-Burleson E, Hollis JM, et al: Treatment of the medial collateral ligament injury. I: The importance of anterior cruciate ligament on the varus-valgus knee laxity. Am J Sports Med 15(1):15–21, 1987. 79. Miller MD, Cooper D, Warner JJ: Review of sportsmedicine and arthroscopy. New York: WB Saunders, 1995. 80. Eiskjaer S, Larsen ST, Schmidt MB: The significance of hemarthrosis of the knee in children. Arch Orthop Trauma Surg 107(2):96–98, 1988. 81. Edwards PH Jr., Grana WA: Physeal fractures about the knee. J Am Acad Orthop Surg 3(2):63–69, 1995. 82. Joseph KN, Fogrund H: Traumatic rupture of the medial ligament of the knee in a four-year-old boy. J Bone Joint Surg Am 60(3):402–403, 1978. 83. Hughston JC, Barrett GR: Acute anteromedial rotatory instability. Long-term results of surgical repair. J Bone Joint Surg Am 65(2):145–153, 1983. 84. O’Donoghue DH: An analysis of end results of surgical treatment of major injuries to the ligaments of the knee. J Bone Joint Surg 37A(1):1–13, 1955. 85. Ellsasser JC, Reynolds FC, Omohundro JR: The non-operative treatment of collateral ligament injuries of the knee in professional football players. An analysis of seventy-four injuries treated nonoperatively and twenty-four injuries treated surgically. J Bone Joint Surg Am 56(6):1185–1190, 1974. 86. Fetto JF, Marshall JL: Medial collateral ligament injuries of the knee: a rationale for treatment. Clin Orthop (132):206–218, 1978. 87. Indelicato PA: Non-operative treatment of complete tears of the medial collateral ligament of the knee. J Bone Joint Surg Am 65(3):323–329, 1983. 88. Indelicato PA, Hermansdorfer J, Huegel M: Nonoperative management of complete tears of the medial collateral ligament of the knee in intercollegiate football players. Clin Orthop 256:174–177, 1990. 89. Kannus P, Jarvinen M: Knee ligament injuries in adolescents. Eight year follow-up of conservative management. J Bone Joint Surg Br 70(5):772–776, 1988. 90. Indelicato PA: Nonoperative management of complete tears of the medial collateral ligament. Orthop Rev 18(9):947–952, 1989. 91. Reider B: Medial collateral ligament injuries in athletes. Sports Med 21(2):147–156, 1996. 92. Reider B, Sathy MR, Talkington J, et al: Treatment of isolated medial collateral ligament injuries in athletes with early functional rehabilitation. A five-year follow-up study. Am J Sports Med 22(4):470–477, 1994. 93. Jones RE, Henley MB, Francis P: Nonoperative management of isolated grade III collateral ligament injury in high school football players. Clin Orthop 213:137–140, 1986. 94. Lundberg M, Messner K: Long-term prognosis of isolated partial medial collateral ligament ruptures. A ten-year clinical and radiographic evaluation of a prospectively observed group of patients. Am J Sports Med 24(2):160–163, 1996. 95. Kannus P: Long-term results of conservatively treated medial collateral ligament injuries of the knee joint. Clin Orthop 226:103–112, 1988. 96. Woo SL, Vogrin TM, Abramowitch SD: Healing and repair of ligament injuries in the knee. J Am Acad Orthop Surg 8(6):364–372, 2000. 97. Derscheid GL, Garrick JG: Medial collateral ligament injuries in football. Nonoperative management of grade I and grade II sprains. Am J Sports Med 9(6):365–368, 1981. 98. Hastings DE: The non-operative management of collateral ligament injuries of the knee joint. Clin Orthop 147:22–28, 1980.

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122. Wadia FD, Pimple M, Gajjar SM, et al: An anatomic study of the popliteofibular ligament. Int Orthop 27(3):172–174, 2003. 123. Jakob RP, Hassler H, Staeubli HU: Observations on rotatory instability of the lateral compartment of the knee. Experimental studies on the functional anatomy and the pathomechanism of the true and the reversed pivot shift sign. Acta Orthop Scand Suppl 191:1–32, 1981. 124. Shahane SA, Ibbotson C, Strachan R, et al: The popliteofibular ligament. An anatomical study of the posterolateral corner of the knee. J Bone Joint Surg Br 81(4):636–642, 1999. 125. Veltri DM, Warren RF: Operative treatment of posterolateral instability of the knee. Clin Sports Med 13(3):615–627, 1994. 126. Watanabe Y, Moriya H, Takahashi K, et al: Functional anatomy of the posterolateral structures of the knee. Arthroscopy 9(1):57–62, 1993. 127. Maynard MJ, Deng X, Wickiewicz TL, et al: The popliteofibular ligament. Rediscovery of a key element in posterolateral stability. Am J Sports Med 24(3):311–316, 1996. 128. Chen FS, Rokito AS, Pitman MI: Acute and chronic posterolateral rotatory instability of the knee. J Am Acad Orthop Surg 8(2):97–110, 2000. 129. Gollehon DL, Torzilli PA, Warren RF: The role of the posterolateral and cruciate ligaments in the stability of the human knee. A biomechanical study. J Bone Joint Surg Am 69(2):233–242, 1987. 130. Harner CD, Hoher J: Evaluation and treatment of posterior cruciate ligament injuries. Am J Sports Med 26(3):471–482, 1998. 131. Seering WP, Piziali RL, Nagel DA, et al: The function of the primary ligaments of the knee in varus-valgus and axial rotation. J Biomech 13(9):785–794, 1980. 132. Hughston JC: The importance of the posterior oblique ligament in repairs of acute tears of the medial ligaments in knees with and without an associated rupture of the anterior cruciate ligament. Results of long-term follow-up. J Bone Joint Surg Am 76(9):1328–1344, 1994. 133. Hughston JC, Andrews JR, Cross MJ, et al: Classification of knee ligament instabilities. Part I. The medial compartment and cruciate ligaments. J Bone Joint Surg Am 58(2):159–172, 1976. 134. LaPrade RF, Terry GC, Montgomery RD, et al: Winner of the Albert Trillat Young Investigator Award. The effects of aggressive notchplasty on the normal knee in dogs. Am J Sports Med 26(2):193–200, 1998. 135. Veltri DM, Warren RF: Posterolateral instability of the knee. Instr Course Lect 44:441–453, 1995. 136. Veltri DM, Warren RF: Anatomy, biomechanics, and physical findings in posterolateral knee instability. Clin Sports Med 13(3):599–614, 1994. 137. Bergstrom R, Gillquist J, Lysholm J, et al: Arthroscopy of the knee in children. J Pediatr Orthop 4(5):542–545, 1984. 138. Cooper DE, Warren RF, Warner JJ: The posterior cruciate ligament and posterolateral structures of the knee: anatomy, function, and patterns for injury. Instr Course Lect: 249–270, 1991. 139. Veltri DM, Warren RF: Isolated and Combined Posterior Cruciate Ligament Injuries. J Am Acad Orthop Surg 1(2):67–75, 1993. 140. Havranek P: Proximal fibular physeal injury. J Pediatr Orthop B 5(2):115–118, 1996. 141. Baker CL, Jr., Norwood LA, Hughston JC: Acute combined posterior cruciate and posterolateral instability of the knee. Am J Sports Med 12(3):204–208, 1984. 142. DeLee JC, Riley MB, Rockwood CA Jr.: Acute posterolateral rotatory instability of the knee. Am J Sports Med 11(4):199–207, 1983. 143. Hughston JC, Norwood LA Jr.: The posterolateral drawer test and external rotational recurvatum test for posterolateral rotatory instability of the knee. Clin Orthop 147:82–87, 1980. 144. Kannus P: Nonoperative treatment of grade II and III sprains of the lateral ligament compartment of the knee. Am J Sports Med 17(1):83–88, 1989. 145. Chen CH, Chen WJ, Shih CH: Lateral collateral ligament reconstruction using quadriceps tendon-patellar bone autograft with bioscrew fixation. Arthroscopy 17(5):551–554, 2001. 146. Latimer HA, Tibone JE, ElAttrache NS, et al: Reconstruction of the lateral collateral ligament of the knee with patellar tendon allograft. Report of a new technique in combined ligament injuries [see comments]. Am J Sports Med 26(5):656–662, 1998. 147. Veltri DM, Deng XH, Torzilli PA, et al: The role of the cruciate and posterolateral ligaments in stability of the knee. A biomechanical study. Am J Sports Med 23(4):436–443, 1995. 148. Baker CL, Jr., Norwood LA, Hughston JC: Acute posterolateral rotatory instability of the knee. J Bone Joint Surg Am 65(5):614–618, 1983.

149. Hughston JC, Jacobson KE: Chronic posterolateral rotatory instability of the knee. J Bone Joint Surg Am 67(3):351–359, 1985. 150. Noyes FR: PCL and posterolateral complex injuries. Overview. Am J Knee Surg 9(4):171, 1996. 151. Noyes FR, Barber-Westin SD: Surgical restoration to treat chronic deficiency of the posterolateral complex and cruciate ligaments of the knee joint. Am J Sports Med 24(4):415–426, 1996. 152. Saddler SC, Noyes FR, Grood ES, et al: Posterior cruciate ligament anatomy and length-tension behavior of PCL surface fibers. Am J Knee Surg 9(4):194–199, 1996. 153. Latimer HA, Tibone JE, ElAttrache NS, et al: Reconstruction of the lateral collateral ligament of the knee with patellar tendon allograft. Report of a new technique in combined ligament injuries. Am J Sports Med 26(5):656–662, 1998. 154. Noyes FR, Barber-Westin SD: The treatment of acute combined ruptures of the anterior cruciate and medial ligaments of the knee. Am J Sports Med 23(4):380–389, 1995. 155. Lill H, Glasmacher S, Korner J, et al: Arthroscopic-assisted simultaneous reconstruction of the posterior cruciate ligament and the lateral collateral ligament using hamstrings and absorbable screws. Arthroscopy 17(8):892–897, 2001. 156. Shea KG, Apel PJ, Pfeiffer RP: Anterior cruciate ligament injury in paediatric and adolescent patients: a review of basic science and clinical research. Sports Med 33(6):455–471, 2003. 157. Kocher MS, Saxon HS, Hovis WD, et al: Management and complications of anterior cruciate ligament injuries in skeletally immature patients: survey of the Herodicus Society and The ACL Study Group. J Pediatr Orthop 22(4):452–457, 2002. 158. Koman JD, Sanders JO: Valgus deformity after reconstruction of the anterior cruciate ligament in a skeletally immature patient. A case report. J Bone Joint Surg Am 81(5):711–715, 1999. 159. Morgan CD, Kalman VR, Grawl DM: The anatomic origin of the posterior cruciate ligament: where is it? Reference landmarks for PCL reconstruction. Arthroscopy 13(3):325–331, 1997. 160. The knee: ligaments. In Herring JA (ed): Tachdjian’s Pediatric Orthopaedics. Philadelphia: WB Saunders, 2002, p 2356. 161. Harner CD, Livesay GA, Kashiwaguchi S, et al: Comparative study of the size and shape of human anterior and posterior cruciate ligaments. J Orthop Res 13(3):429–434, 1995. 162. Covey DC, Sapega AA: Anatomy and function of the posterior cruciate ligament. Clin Sports Med 13(3):509–518, 1994. 163. Ogata K, McCarthy JA: Measurements of length and tension patterns during reconstruction of the posterior cruciate ligament. Am J Sports Med 20(3):351–355, 1992. 164. Racanelli JA, Drez D, Jr.: Posterior cruciate ligament tibial attachment anatomy and radiographic landmarks for tibial tunnel placement in PCL reconstruction. Arthroscopy 10(5):546–549, 1994. 165. Van Dommelen BA, Fowler PJ: Anatomy of the posterior cruciate ligament. A review. Am J Sports Med 17(1):24–29, 1989. 166. Greis PE, Georgescu HI, Fu FH, et al: Particle-induced synthesis of collagenase by synovial fibroblasts: an immunocytochemical study. J Orthop Res 12(2):286–293, 1994. 167. Ahmad CS, Cohen ZA, Levine WN, et al: Codominance of the individual posterior cruciate ligament bundles. An analysis of bundle lengths and orientation. Am J Sports Med 31(2):221–225, 2003. 168. Covey DC, Sapega AA, Sherman GM: Testing for isometry during reconstruction of the posterior cruciate ligament. Anatomic and biomechanical considerations. Am J Sports Med 24(6):740–746, 1996. 169. Butler DL, Noyes FR, Grood ES: Ligamentous restraints to anteriorposterior drawer in the human knee. A biomechanical study. J Bone Joint Surg Am 62(2):259–270, 1980. 170. Delee JC, Bergfeld J, Drez DJ, Jr., et al: The posterior cruciate ligament. In Delee JC, Drez DJ Jr. (eds): Orthopaedic Sports Medicine. Philadelphia: WB Saunders, 1994, pp 1374–1400. 171. Clancy WG Jr., Shelbourne KD, Zoellner GB, et al: Treatment of knee joint instability secondary to rupture of the posterior cruciate ligament. Report of a new procedure. J Bone Joint Surg Am 65(3):310–322, 1983. 172. Fowler PJ, Messieh SS: Isolated posterior cruciate ligament injuries in athletes. Am J Sports Med 15(6):553–557, 1987. 173. Kennedy JC, Hawkins RJ, Willis RB, et al: Tension studies of human knee ligaments. Yield point, ultimate failure, and disruption of the cruciate and tibial collateral ligaments. J Bone Joint Surg Am 58(3):350–355, 1976.

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174. MacDonald PB, Black B, Old J, et al: Posterior cruciate ligament injury and posterolateral instability in a 6-year-old child: a case report. Am J Sports Med 31(1):135–136, 2003. 175. Torisu T: Avulsion fracture of the tibial attachment of the posterior cruciate ligament. Indications and results of delayed repair. Clin Orthop 143:107–114, 1979. 176. Itokazu M, Yamane T, Shoen S: Incomplete avulsion of the femoral attachment of the posterior cruciate ligament with an osteochondral fragment in a twelve-year-old boy. Arch Orthop Trauma Surg 110(1):55–57, 1990. 177. Mayer PJ, Micheli LJ: Avulsion of the femoral attachment of the posterior cruciate ligament in an eleven-year-old boy. Case report. J Bone Joint Surg Am 61(3):431–432, 1979. 178. Suprock MD, Rogers VP: Posterior cruciate avulsion. Orthopedics 13(6):659–662, 1990. 179. Parolie JM, Bergfeld JA: Long-term results of nonoperative treatment of isolated posterior cruciate ligament injuries in the athlete. Am J Sports Med 14(1):35–38, 1986. 180. Torg JS, Barton TM, Pavlov H, et al: Natural history of the posterior cruciate ligament-deficient knee. Clin Orthop 246:208–216, 1989. 181. Boynton MD, Tietjens BR: Long-term followup of the untreated isolated posterior cruciate ligament-deficient knee. Am J Sports Med 24(3):306–310, 1996. 182. Dandy DJ, Pusey RJ: The long-term results of unrepaired tears of the posterior cruciate ligament. J Bone Joint Surg Br 64(1):92–94, 1982. 183. Geissler WB, Whipple TL: Intraarticular abnormalities in association with posterior cruciate ligament injuries. Am J Sports Med 21(6):846–849, 1993. 184. Keller PM, Shelbourne KD, McCarroll JR, et al: Nonoperatively treated isolated posterior cruciate ligament injuries. Am J Sports Med 21(1):132–136, 1993. 185. 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(3):276–283, 1999.

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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.

Tibial Eminence Fractures

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.

Tibial Eminence Fractures

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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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

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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 (<2 years of age).

Figure 27–7 The quadriceps is lengthened via a V–Y advancement. The vastus medialis and vastus lateralis are reattached. (Reprinted with permission from Morrissy RT, Weinstein SL: Atlas of Pediatric Orthopaedic Surgery. Philadelphia: Lippincott Williams & Wilkins, 2001, p 632.)

Continued

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TECHNICAL NOTE 27–1

Quadricepsplasty for Congenital Knee Dislocation (Continued) References 1. Curtis BH, Fisher RL: Congenital hyperextension with anterior subluxation of the knee. J Bone Joint Surg Am 51:255–269, 1969. 2. Austwick DH, Dandy DJ: Early operation for congenital subluxation of the knee. J Pediatr Orthop 3:85, 1983. 3. Johnson EJ, Audell R, Oppenheim WL: Congenital dislocation of the knee. J Ped Orthop 7:194–200, 1987.

Outcome Excellent results are seen in those children without coexisting disorders and in those who respond to early and nonoperative treatment.9,26 A positive response to nonoperative treatment results in increased knee flexion and infrequent instability or future deformity in comparison to those knees requiring open reduction and quadricepsplasty.4,7 Outcomes can be somewhat skewed, however, because the majority of knees requiring open reduction are the severe Grade III knees, often with underlying disorders such as Larsen’s syndrome or arthrogryposis. Multiple retrospective reviews have identified several residual problems seen in this population of patients. Extensor weakness, or a lag up to 30 degrees, has been reported after open reduction and quadriceps lengthening.10,25 Others claim that the amount of so-called normal quadriceps muscle, regardless of treatment, has no effect on long-term outcome.26 Recurrent hyperextension is rare, but progressive valgus instability and angulation is commonly reported.10,26 In a retrospective review of 19 patients, Ooishi et al.10 reported a 50% incidence of valgus deformity due to anterior displacement of the medial ligamentous structures and hamstring insertions. Such deformity was treated with posteroinferior transfer of the pes anserinus and posterior transposition of the MCL tibial insertion. A retrospective review of 15 congenital knee dislocations by Curtis and Fisher26 described a valgus deformity requiring osteotomy 7 years after open reduction. One patient required arthrodesis 3 years after reduction for pain and instability.26 Recurrent knee instability can be related to either ACL hypoplasia or absence or from severe valgus deformity and loss of medial constraint. The review by Ko et al.9 of 24 knees described four knees with residual laxity, one of which had developed a significant valgus deformity. In addition, an iatrogenic tibia fracture occurring with manipulation has been reported.28 Congenital Absence of the Cruciate Ligaments Congenital absence of the ACL was first reported by Katz et al.,8 who proposed that aplasia of the cruciate ligaments led to congenital knee dislocation. They identified four patients with congenital knee dislocation and associated

4. Katz MP, Grogono BJ, Soper KC: The etiology and treatment of congenital dislocation of the knee. J Bone Joint Surg Br 49:112–120, 1967. 5. Morrissey RM: Surgical repair of irreducible congenital dislocation of the knee. In Morissy RT, Weinstein, SL: Atlas of Pediatric Orthopaedic Surgery, 3rd edition. Philadelphia: Lippincott Williams & Wilkins, 2001.

absence of the ACL, two of whom also showed no PCL. Although refuted by some to be the true cause of congenital knee dislocation, such an association between cruciate aplasia, congenital knee dislocation, and associated disorders such as Larsen’s syndrome is now well documented.8,14,27,30 Congenital absence of the ACL as an isolated entity has been described, but it is exceedingly rare.31 Most reports signify a high association with other lower extremity deformity and knee disorders. Congenital leg-length discrepancy, such as congenital short femur and fibular or tibial hemimelia, often presents with associated absence of the cruciate ligaments.32–36 Resulting instability becomes a significant issue if lengthening procedures are performed. Posterior tibiofemoral subluxation and dislocation have been reported secondary to femoral lengthening in patients with absent cruciate ligament.35 Other associated lower extremity disorders reported include patellar aplasia or instability, congenital absence of menisci, congenital ring meniscus, discoid lateral meniscus, developmental hip dysplasia, tarsal coalition, and clubfeet.37–40 Congenital thrombocytopenia/absent radius (TAR) syndrome has also been reported to include an absence of cruciate ligaments.39,41 Patients with congenital absence of the ACL or both cruciate ligaments usually present because of the primary associated condition, often without complaints of instability. Thomas et al. reported 10 patients with congenital ACL-deficient knees. Five patients were unstable clinically, but none had activity restrictions in a knee brace. Three of these patients had an attenuated or absent PCL as well. Although all patients required some form of surgery, no ligamentous reconstruction was needed to correct anteroposterior laxity.38 Kaelin et al.35 presented six cases of congenital leg-length discrepancy and associated cruciate deficiency. Two patients presented with significant retropatellar knee pain secondary to chondromalacia, and two patients presented with pain secondary to buckethandle medial meniscus tears. Nonetheless, no patients complained of knee instability. Radiographic findings include hypoplasia of a V-shaped intercondylar notch with decreased width and height of the notch seen on the anteroposterior film. Flattening of the medial and lateral tibial spines occurs, producing a rounded appearance to the shallow eminence. An associated valgus deformity of the knee may also be seen with hypoplasia of the lateral femoral condyle or, if menisci

Congenital Knee Deformities

are absent, a convex proximal tibia with an associated saddleshaped, concave distal femur.33,39 On physical exam, patients will show a positive anterior and/or posterior drawer, with at least a Grade III Lachman’s maneuver. Associated varus/valgus laxity is common. Anterior subluxation of the tibia with the knee in extension can also be seen.5,24,38 Assessment of gait, function, leg-length discrepancy, and limb alignment should coincide with a comprehensive physical examination. The natural history of congenital absence of the cruciate ligaments is unknown. Patients often present with many confounding medical issues and associated pathology, making it difficult to determine the true long-term outcome. It is not known if congenital ACL deficiency behaves similarly to traumatic ACL deficiency. Some reports suggest it may indeed, with a higher risk for subsequent meniscal injury.35 However, treatment should remain conservative despite clinical instability as long as the child or adolescent remains asymptomatic without activity restrictions. Bracing may be required. If significant valgus deformity exists, osteotomy may be indicated. Congenital Tibiofemoral Subluxation/Congenital Snapping Knee

KEY POINTS 1. Congenital dislocation of the knee is commonly associated with other musculoskeletal disorders such as developmental hip dysplasia, clubfoot, congenital radial head dislocation, and scoliosis. It is often a manifestation of such syndromes as Larsen’s syndrome, Down syndrome, and arthrogryposis. 2. The primary pathology within congenital dislocation of the knee is shortened and fibrotic quadriceps. 3. Treatment should begin early with conservative treatment consisting of serial manipulations, bracing, and/or casting. Operative open reduction is required if conservative treatment fails. Varying levels of surgery are required, depending on the classification of disease, degree of contracture, and other frequent confounding medical issues or associated hip pathology. 4. Children who respond to nonsurgical treatment seem to have an excellent outcome. Residual instability, extensor weakness, and genu valgum are frequent problems encountered by patients requiring open reduction.

“Congenital snapping knee” is a rare form of congenital knee instability caused by habitual anterior subluxation of the tibia during knee extension. Curtis and Fisher5 first reported this condition in five patients, all of whom showed signs of skeletal dysplasia and positive family history. Ferris and Jackson24 described a similar condition in four patients with congenital syndromes such as Larsen’s syndrome, CatelManzke syndrome, and congenital short tibia. Congenital tibiofemoral subluxation shares many of the same clinical features and associated disorders as congenital knee dislocation, yet it remains a distinct diagnosis.

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ACL deficiency is an imporKEY POINT tant component of this condi5,24 1. Congenital absence tion. Congenital absence or of the anterior crucihypoplasia of the ACL allows ate ligament is rarely anterior subluxation of the tibia an isolated entity. to occur with knee extension as 2. Common associated the biceps femoris and iliotibial disorders include band become active subluxating congenital leg-length forces lying anterior to the knee discrepancy (conaxis. This causes a sudden visible genital short femur, and often audible snap at the tibial/fibular knee. Reduction occurs spontahemimelia/amelia), neously at approximately 30 discoid meniscus, degrees of flexion, producing congenital patellar another dramatic snap. Children instability, developmay walk with a flexed knee to mental hip dysplasia, avoid subluxation or with a stifftarsal coalition, and knee gait, locking the knee in clubfoot. extension to prevent reduction. Unlike congenital knee dislocation, however, knee flexion is unlimited and is not restricted by quadriceps fibrosis. Marked recurvatum or hyperextension is not seen. In older children, fixed deformity and lack of spontaneous or passive reduction may result from altered distal femur or proximal tibia morphology. Radiographs taken with knee extension may demonstrate anterior tibiofemoral subluxation. Features consistent with congenital ACL deficiency may be present, including blunted tibial spines and a short and narrow intercondylar notch. In children near skeletal maturity, dysplasia of the distal femur and proximal tibial articular surfaces is seen; flattening of the anterior femoral condyles accompanies an increased posterior tibial slope. Significant valgus deformity may also be present. Conservative treatment in the form of prolonged immobilization or splinting has not been shown to prevent long-term subluxation.5,24 Based on intraoperative findings, Curtis and Fisher5 advocated release of the iliotibial band, sectioning of the distal intermuscular septum, and transfer of the distal biceps femoris insertion to the vastus lateralis. No patients had recurrence of subluxation. Ferris and Jackson24 suggested early operative intervention to prevent fixed deformity or dysplastic changes. They performed an extraarticular, iliotibial band tenodesis—passing a strip of IT band behind the lateral collateral ligament, behind the knee, and attaching it medially to the rectus femoris tendon. This reconstruction technique for anterolateral instability prevented snapping but not the abnormal anterior glide. In addition, one patient required corrective osteotomy for severe valgus deformity. In patients with congenital ACL deficiency and marked instability or subluxation, early stabilization is suggested. Physeal-sparing procedures may improve clinical symptoms and prevent dysmorphology of the tibiofemoral articulation. Congenital Absence of the Menisci Isolated congenital absence of the menisci has not been reported. Like many congenital knee deformities, multiple anomalies are usually present. Kaelin et al.35 presented a patient with congenital leg-length discrepancy, aplasia of the

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cruciate ligaments, and absence of the medial and lateral menisci. Tolo39 reported a patient with congenital thrombocytopenia, radial club hands, and bilateral knee instability. Arthrography at age 5 years suggested absence of both the cruciates and menisci, confirmed with arthrotomy at age 8 years. Natural history for congenital absence of the menisci is unknown and depends largely on the associated conditions of the patient and the dysplasia within the knee. Reconstructive efforts are limited.

KEY POINTS 1. Congenital tibiofemoral subluxation is a distinct condition caused by absence or hypoplasia of the anterior cruciate ligament. 2. Long-term anterior subluxation leads to fixed deformity and dysmorphic changes to the distal femur and proximal tibial articulation.

Congenital Dislocation of the Patella/ Habitual Dislocation of the Patella Congenital and habitual patellar dislocations are rare clinical findings. Congenital dislocation of the patella was first described by Singer in 1856.42 Goldthwait43 was the first to report in the English literature on the surgical treatment of this condition. In addition, Conn44 was the first to report on treatment in a child, describing the surgical correction of a 16-month-old with a fixed lateral patellar dislocation. Although considered a spectrum of disease related to the recurrent patellar instability often seen in healthy children and adolescents, congenital and habitual dislocation of the patella have now become understood as two distinct entities. Nevertheless, clinical findings and treatment principles all lie within a spectrum of pathology that is most severe in congenital or “persistent” dislocation of the patella. Etiology The cause of congenital patellar dislocation is unknown. Stanisavljevic et al.42 believed it was due to failure of the quadriceps-containing myotome to undergo internal rotation—an event normally occurring within the first prenatal trimester. This results in a laterally displaced and shortened extensor mechanism of the knee. Anatomic dissections reported by Ghanem et al.45 agreed with this theory, with congenital patellar dislocation due to early malrotation rather than dislocation of a previously located patella. Theories related to trauma have also been suggested. Gao et al. report46 that, of 35 patients with either congenital or habitual dislocation, nine had previous intramuscular quadriceps injections. They felt that intrauterine or neonatal trauma produced an infarct of the quadriceps, leading to its fibrosis, contracture, and subsequent laterally displacing force upon the patella. A genetic etiology is supported by the many associated syndromes and clinical findings seen in accordance with congenital dislocation of the patella. Associated conditions include Larsen’s syndrome, arthrogryposis, myelomeningocele, Down syndrome, nail-patella syndrome, Rubinstein-Taybi syndrome, Beckwith-Wiedemann syndrome, diastrophic dysplasia, chondroosteodystrophy, Hecht syndrome, proximal femoral focal deficiency, congenital short femur, and Ellis

van Creveld syndrome. In addition, DDH and foot abnormalities such as clubfoot, congenital vertical talus, and calcaneovalgus foot have commonly been reported. Several reports have identified a positive family history.47,48 Mumford48 discussed a 25-year-old with bilateral, congenital patellar dislocations and six maternal relatives with the same condition.48 Unilateral dislocation is most common, but bilateral disease has been reported.49–52 Classification Two distinct clinical syndromes exist, both of which lead to dysfunction and disability during childhood. Congenital dislocation of the patella, or so-called persistent lateral dislocation of the patella, presents in early infancy with a fixed lateral displacement of the patella. The patella is unable to be reduced within the intercondylar groove. This must be differentiated from habitual dislocation of the patella, or “obligatory” patellar dislocation, which often presents later in childhood and is characterized by spontaneous reduction of the patella with flexion and extension of the knee. Clinical Features Conn44 described four criteria for a congenital patellar dislocation: (1) permanent or fixed lateral dislocation, (2) lack of active knee extension, (3) unimpaired passive knee extension, and (4) absence of the patella from intertrochlear fossa. Frequently associated with a generalized syndrome, congenital patellar dislocation produces a significant flexion contracture and functional disability. Children are often evaluated for a delay in walking or an abnormal gait. Often the clinical picture is confusing and may mimic a neuromuscular etiology. On physical exam, the patella is displaced laterally and cannot be reduced. A hypoplastic patella, however, may be difficult to palpate in the young child. Significant flexion deformity accompanies a lack of active knee extension. Valgus deformity may coexist.53 Pain is often the presenting complaint in older children.50 Habitual patellar dislocation usually presents as an isolated entity later in childhood, long after the child has begun walking. Normal range of knee motion and little functional disability exist. The child will often present with complaints of instability—a sensation produced by lateral patellar dislocation with knee extension and relocation with knee flexion (Figure 27–8). If the patella is held reduced, the knee cannot be flexed. Pain is not usually present unless the deformity becomes fixed. Radiographic Findings Normal patellar ossification occurs between 3–4 years of age. Radiographs in children before patellar ossification may not be helpful in confirming clinical suspicion of patellar dislocation. Plain radiographs may show a decreased quadriceps soft-tissue shadow, but no patella will be seen. Difficulty in palpating a hypoplastic patella in the infant compounds this dilemma. Ultrasound can be used to locate the patella and confirm the diagnosis. Bar-On et al.54 reported the use of ultrasound in diagnosis of a congenital left patella

Congenital Knee Deformities

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Box 27–1 Pathology of congenital or habitual dislocation of the patella42,45,46,52,53 1. Quadriceps contracture—involves primarily vastus lateralis and iliotibial band 2. Anterolateral malrotation/displacement of extensor mechanism 3. Lateral capsular contracture and medial capsular laxity 4. Atrophic vastus medialis and overdistension of medial retinaculum 5. Hypoplastic, flat patella without central ridge 6. Shallow or absent intercondylar groove 7. External rotation of tibia with posterolateral rotatory displacement 8. Lateral displacement of tibial tubercle 9. Lateral insertion of patellar tendon 10. Neoarticulation between patella and lateral femoral condyle 11. Valgus knee deformity

Figure 27–8 Clinical photograph of habitual dislocation of the patella.

dislocation in a newborn female. Similarly, Walker et al.55 presented two cases of ultrasound diagnosis in 3-month-old and 1-year-old infants. Plain radiographs are more helpful in the older patient with a “sunrise” view, showing lateral patellar dislocation and often a shallow and poorly formed intercondylar groove. The patella will appear small and flat, without a patellar ridge. The distal femur may appear rounded and smooth with low lateral condylar height. Posteromedial tibial sloping may be seen, secondary to rotatory dislocation of the tibia. Genu valgum often is seen as well. In longstanding disease, degenerative changes develop. MRI or computed tomography (CT) is seldom indicated but can be helpful in evaluating for associated knee pathology or ligamentous insufficiency.

thin medial capsule and retinaculum are drawn over and often adherent to the underlying femoral condyles. The suprapatellar pouch is obliterated, and overall joint volume is decreased. Such pathology produces a shortened and anterolaterally displaced extensor mechanism, which in the face of a knee flexion contracture will produce knee flexion and external rotation rather than extension. This contributes not only to the flexion and valgus deformity seen with congenital patellar dislocation, but also to the accompanying posterolateral, rotatory displacement of the tibia. Osseous abnormalities include a hypoplastic patella that lacks a central ridge and normal height. Articular cartilage may be thin. Development of the intercondylar groove depends on the presence of an articulating patella and normal extensor function. Therefore, the trochlear notch may be shallow or absent, depending on a fixed or reducible deformity. In addition, the tibial tubercle is displaced laterally, as is the insertion of the patellar tendon. This accentuates excessive external tibial torsion. Increased femoral anteversion may also contribute to deformity. Intraarticular abnormalities have been described, including discoid meniscus, fat-pad hypertrophy, and cruciate absence or hypoplasia.42,56 Treatment

Pathology Dysplasia of the patellofemoral joint is considered abnormal development of the entire anterior knee structure. Both softtissue and osseous abnormalities produce what should be thought of as a dislocation of the entire extensor mechanism, not just an isolated dislocation of the patella. This produces a wide spectrum of severity, with persistent dislocation often more severe than habitual. Cadaver and surgical dissections have documented many common findings seen in both congenital and habitual patellar dislocations (Box 27–1). Contracture of a hypertrophic vastus lateralis produces a lateral soft-tissue constriction, which is worsened by a thick, tubular iliotibial band often inserting behind the posterior border of the patella or the outer aspect of the lateral femoral condyle rather than Gerdy’s tubercle. The patella is tethered to the lateral intermuscular septum. An underdeveloped vastus medialis muscle group is seen as well, and a

The natural history of congenital patellar dislocation is not well documented. In children, progressive valgus deformity and knee flexion contracture produce limited ambulatory ability. A weakened extensor mechanism contributes to functional limitations. Some children may be tolerant of a fixed patellar dislocation but most will show progressive pain, weakness, and loss of function.42,50–53,57,58 Multiple reports of degenerative knee arthrosis secondary to a fixed lateral patellar dislocation exist.51,59,60 In those with habitual patellar dislocation, instability becomes a functional issue later in childhood. Pain presents with the development of fixed displacement or early arthrosis. Any delay in treatment enhances the potential for worsening contracture, weakness, and functional limitation. Severity of the deformity may indeed be related to the length of time the deformity remains uncorrected. Nonoperative treatment is seldom indicated in the young

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and symptomatic child. Closed reduction, of the patella in a true congenital dislocation is not feasible, and bracing regimens are merely temporary means of delaying definitive treatment. Serial casting may be helpful, however, in improving some of the flexion contracture before surgical correction. With early diagnosis, surgical correction to centralize the extensor mechanism is indicated.47,49,56,61 Delay in the treatment of congenital patellar dislocation may not only diminish the surgical results, but may also make surgical correction less predictable and more technically difficult.47,49,56,58 Surgical realignment is preferred within the first 6 months to 1 year of life because early reduction improves trochlear development and decreases patellofemoral dysplasia. Operative treatment may be delayed in those with habitual dislocation until symptoms or functional limitations dictate correction. The primary objective of surgery is to centralize the extensor mechanism, and reconstruction must be individualized based on the severity of pathology present. Multiple techniques have reported satisfactory results. Release of tight lateral structures, advancement or plication of medial structures, and realignment of the patella and patellar tendon forms the basis of all techniques. We prefer a modification of Stanisavljevic et al.’s technique,42 similar to that described by Gordon and Schoenoecker.50 A long midline or anterolateral incision runs from approximately the middle one third of the thigh to approximately 2–3 cm distal and medial to the tibial tubercle. The entire extensor mechanism is exposed. An extensive lateral release of both the lateral retinaculum and capsule runs along the lateral border of the patellar tendon up to the vastus lateralis, which must be stripped off the intermuscular septum. The iliotibial band is released in line with the skin incision, with the addition of several horizontal cuts if needed. Passive relocation of the patella into the intercondylar groove should be obtainable. Release of the quadriceps off the underlying femur allows medial rotation of the extensor mechanism. Evidence for both extraperiosteal and subperiosteal stripping can be found.53,62 The medial retinaculum is often adherent to the underlying femoral condyles and must be mobilized. Release of the retinaculum off the middle one third of the patella has been described.42,49 Medial plication may utilize the retinaculum by advancement and suture to the lateral border of the patella. More commonly performed, however, is a vastus medialis obliquus (VMO) advancement.50,62 The distal extent of the VMO tendon is incised along the proximal and medial patellar insertion. A small cuff of vastus medialis tissue is deliberately left to allow suturing to the patella. Careful distal and lateral advancement prevents overcorrection and medial subluxation of the patella. Exploration of the knee joint for intraarticular pathology is also carried out. If unable to obtain near full flexion after reduction of the extensor mechanism, incorporation of a rectus lengthening is indicated. A V–Y quadricepsplasty is most commonly used. Rarely, continued knee contracture will require hamstring lengthening or posterior capsular release.49 The presence of a proximal tibial physis prevents any type of tubercle transfer to be done in the skeletally immature patient. Lateral displacement of the patellar tendon

insertion is corrected by transferring the lateral one half of the tendon medially. After splitting the tendon at its midline and carefully detaching the lateral 50% of its insertion, the lateral half is run beneath the medial half of the tendon and sutured to adjacent periosteum and tissue.43 Distal advancement should be avoided. In older children, transfer of the semitendinosus or so-called Galeazzi tenodesis provides greater medial reinforcement to the realignment and should be added.46 In skeletally mature adolescents, tibial tubercle transfers may be performed. Following an extensive lateral release and relocation of the patella, a large soft-tissue defect remains laterally. A free fascia lata graft or excised portion of the medial capsule may be used to close this gap.42,44,50 Other authors do not advocate its closure.46,49,62. Postoperatively, the patient is placed in a cylinder cast for 4–6 weeks before any range of motion, with weight bearing as tolerated. Many other techniques have been described. Langenskiold et al.53 proposed adding a complete patellar tendon transfer, detaching the tendon at its cartilaginous insertion, passing it through a horizontal split in the medial retinaculum, and securing it distal to the proximal, medial tibial physis. With an average follow-up of over 13 years, all 12 patients (18 knees) had satisfactory results; only two knees had residual extensor lag.53 Beals and Buehler63 recently reported on four patients with chromosomal abnormalities, patellar dislocations with unsuccessful soft-tissue realignments, and no femoral sulcus. Creation of a patellar groove was performed with a gouge to the anterior distal femur. No patient had recurrence of dislocation at a 2–10-year follow-up. Outcome Results of extensor realignment for congenital and habitual patellar dislocation are generally satisfactory. Outcome is determined by the presence of recurrent instability, range of motion, and extensor function or strength. Gao et al.46 reported 35 patients (41 knees) treated surgically with individualized soft-tissue realignments. At an average 5-year follow-up, approximately 88% satisfactory results were seen with no extensor lag, full range of knee motion, and no degenerative changes. Gordon and Schoenecker50 presented 10 patients (13 knees) with a mean 5-year follow-up. All patients reported increased activity tolerance, and the average extensor lag improved from approximately 15 degrees preoperatively to about 2 degrees postoperatively. With careful soft-tissue balancing, patellar stability can be restored. Although surgical results are not as good as those after traumatic, recurrent patellar dislocations, satisfactory results are usually seen. Early reduction is beneficial for trochlear development, and long-term quadriceps weakness is seldom seen.46 Congenital Hypoplasia of the Patella Isolated, congenital hypoplasia of the patella is an uncommon disorder transmitted in an autosomal-dominant mode.64,65 More commonly, patellar hypoplasia manifests as part of an associated dysplasia or syndrome. Such disorders

Congenital Knee Deformities

include nail-patella syndrome, “small patella” syndrome, trisomy 8, Coffin-Siris syndrome, and Kushokwin syndrome.66 Nail-patella syndrome (also called osteo-onychodysplasia or onycho-osteodysplasia) was first described by Chatelain in 1820.67 Its incidence is reportedly 1–4.5 per million live births, and it is transmitted by autosomaldominant inheritance with a linkage to the ABO blood group locus of chromosome 9.68–71 Four common characteristic findings define nail-patella syndrome: hypoplasia or absence of the patella (Figure 27–9), dysplasia of the fingernails (Figure 27–10), radial head dysplasia or dislocation (Figure 27–11), and iliac horns (Figure 27–12). Fingernail involvement is seen in nearly all patients and lessens in the more ulnar-sided rays, being most severe in the thumb. Absent, split, bifid, or ridged nails are seen. Toenails are rarely involved. Absent or poorly formed dorsal skin creases affect the metacarpal-phalangeal and interphalangeal joints. Radial head dislocation accompanies dysplasia or hypoplasia of the capitellum and lateral condyle. In addition, asymptomatic bony projections of the posterior ileum, so-called iliac horns, are seen on x-ray and are pathognomonic for nail-patella syndrome. The patella is hypoplastic, irregular in shape or absent, often lying more distally within the anterior knee. Commonly, patellar instability is seen, with habitual lateral dislocation and a hypoplastic lateral femoral condyle. Treatment principles are similar to those discussed earlier for congenital and habitual patellar dislocations. Clinical manifestations are variable in frequency and severity, even among family members.72 Other common clinical findings include multiple foot deformities (clubfoot, congenital vertical talus, metatarsus adductus, pes planus, calcaneovalgus), shoulder dysplasia (glenoid, acromial, and scapular hypoplasia,

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KEY POINTS 1. True congenital dislocation of the patella is a fixed, lateral displacement of an irreducible patella. It presents early in childhood with a knee flexion contracture and lack of active knee extension. If untreated, long-term functional disability, pain, and deformity often result. 2. Habitual dislocation of the patella presents later in childhood. This entity is characterized by spontaneous reduction of the laterally displaced patella at varying degrees of flexion/extension arc. Early symptoms relate to instability rather than pain or functional loss. Long-term outcome is related to early patellofemoral arthrosis. 3. Common pathologic findings include a shortened and laterally displaced extensor mechanism, osseous hypoplasia of the patella and trochlear notch, obliteration of the suprapatellar pouch with underdeveloped medial retinacular and vastus medialis structure, and lateral displacement of the patellar tendon and tibial tubercle. 4. Operative treatment entails centralizing the extensor mechanism via numerous described techniques. Long-term results are generally satisfactory.

Figure 27–9 Congenital absence of the patellae associated with nail-patella syndrome.

Figure 27–10 Fingernail dysplasia associated with nail-patella syndrome.

clavicular horns), scoliosis, and DDH.68,73–75 Nephropathy secondary to long-standing proteinuria ultimately affects mortality more so than any musculoskeletal problem. “Small patella” syndrome (also called ischia-patellar dysplasia or coxo-podo-patellar syndrome) is a newly recognized dysplasia with diagnostic features in the pelvis and knees.66 First recognized as a disorder separate from nail-patella syndrome by Scott and Taor,76 it can be familial or sporadic in presentation. Pelvic manifestations include absent or delayed ossification of the ischium and/or pubis, an elongated femoral neck, coxa vara/valga, and a hypoplastic lesser trochanter. Patellar hypoplasia or deficient KEY POINT patellar ossification are also seen. In addition, multiple foot anomNail-patella syndrome alies have been reported, includis defined by hypoplaing an increased space between sia or absence of the the first and second toes, brachypatella, fingernail dactyly, tarsal coalition, pes dysplasia, radial head planus, and clubfeet. dislocation, and the Small patella syndrome is presence of iliac benign and much less severe than horns. nail-patella syndrome because no

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References

Figure 27–11 Radial head dislocation associated with nailpatella syndrome.

Figure 27–12 Iliac horns associated with nail-patella syndrome.

renal involvement occurs. Other reported features unique to small patella syndrome are hypotonia, macrocephaly, cleft palate, hand asymmetry, and a delayed bone age. Patients may have elbow deformity, but nail dysplasia and iliac horns are not seen.

1. Charif P, Reichelderfer TE: Genu recurvatum congenitum in the newborn: its incidence, course, treatment, prognosis. Clin Pediatr 4:587–594, 1965. 2. Jacobsen K, Vopalecky F: Congenital dislocation of the knee. Acta Orthop Scand 56:1–7, 1985. 3. Shattock SG: Genu Recurvatum in a foetus at term. Trans Pathol Soc Lond 42:280, 1891. 4. Bensahel H, Dal Monte A, Hjelmstedt A, et al: Congenital dislocation of the knee. J Ped Orthop 9:174–177, 1989. 5. Curtis BH, Fisher BL: Heritable congenital tibiofemoral subluxation: clinical features and surgical treatment. J Bone Joint Surg 52A:1104–1114, 1970. 6. Ferris BD, Aichroth P: The treatment of congenital knee dislocation: A review of nineteen knees. Clin Orthop 216:135–140, 1987. 7. Johnson E, Andell R, Oppenheim WL: Congenital dislocation of the knee. J Ped Orthop 7:194–200, 1987. 8. Katz MP, Grogono JS, Soper KC: The etiology and treatment of congenital dislocation of the knee. J Bone Joint Surg 49B:112–120, 1967. 9. Ko JY, Shih CH, Wenger DR: Congenital dislocation of the knee. J Ped Orthop 19:252–259, 1999. 10. Ooishi T, Sugioka Y, Matsumoto S, et al: Congenital dislocation of the knee: its pathologic features and treatment. Clin Orthop Rel Res 287:187–192, 1993. 11. Provenzano F: Congenital dislocation of the knee. N Engl J Med 236:360, 1947. 12. McFarlane AL: A report on four cases of congenital genu recurvatum occurring in one family. Br J Surg 34:388, 1947. 13. Haga N, Nakamura S, Sakaguchi R, et al: Congenital dislocation of the knee reduced spontaneously or with minimal treatment. J Ped Orthop 17:59–62, 1997. 14. Niebauer J, King D: Congenital dislocation of the knee. J Bone Joint Surg 42:207–225, 1960. 15. Middleton DS: The pathology of genu recurvatum. Br J Surg 22:696, 1935. 16. Uhthoff HK, Ogata S: Early intrauterine presence of congenital dislocation of the knee. J Ped Orthop 14:254–257, 1994. 17. Ahmadi B, Shahriaree H, Silver CM: Severe congenital genu recurvatum. J Bone Joint Surg 61A:622–623, 1979. 18. Gilbert RJ, Larsen LJ, Ashley K, et al: Open reduction with patellar tendon elongation for congenital dislocation of the knee. J Bone Joint Surg 57A:133, 1975. 19. Stern MB: Congenital dislocation of the knee. J Bone Joint Surg 50A:1054, 1968. 20. Carlson DH, O’Conner J: Congenital dislocation of the knee. Am J Roentgenol 127:465–468, 1976. 21. Finder JG: Congenital hyperextension of the knee. J Bone Joint Surg 46B:783, 1964. 22. Roy DR, Crawford AH: Percutaneous quadriceps recession: A technique for management of congenital hyperextension deformity of the knee in the neonate. J Ped Orthop 9:717–719, 1989. 23. Elchalal U, Ben Itzhak I, Ben-Meir G, et al: Antenatal diagnosis of congenital dislocation of the knee: a case report. Am J Perinatol 10:194–196, 1993. 24. Ferris BD, Jackson AM: Congenital snapping knee: habitual anterior subluxation of the tibia in extension. J Bone Joint Surg 72B:453–456, 1990. 25. Bell, MJ, Atkins RM, Sharrard WJ: Irreducible congenital dislocation of the bone. J Bone J Surg 69B:403–406, 1987. 26. Curtis BH, Fisher BL: Congenital hyperextension with anterior subluxation of the knee: surgical treatment and long-term observations. J Bone Joint Surg 51A:255–269, 1969. 27. Austwick DH, Dandy DJ: Early operation for congenital subluxation of the knee. J Ped Orthop 3:85–87, 1983. 28. Nogi J, MacEwen GD: Congenital dislocation of the knee. J Ped Orthop 2:509–513, 1982. 29. Insall JN, Scott WN: Surgery of the Knee, 3rd edition. New York, Churchill-Livingstone, 2001. 30. Ferrone JD: Congenital deformities about the knee. Orthop Clinics NA 7:323–330, 1976. 31. Barrett GR, Tomasin JD: Bilateral congenital absence of the anterior cruciate ligament. Orthopaedics 11:431–434, 1988. 32. Cuervo M, Albinana J, Cebrian J, et al: Congenital hypoplasia of the fibula: clinical manifestations. J Ped Orthop B 5:35–38, 1996.

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33. Johansson E, Aparisi T: Congenital absence of the cruciate ligaments: A case report and review of the literature. Clin Orthop Rel Res 162:108–111, 1982. 34. Johansson E, Aparisi T: Missing cruciate ligament in congenital short femur. J Bone Joint Surg 65A:1109–1115, 1983. 35. Kaelin A, Hulin PH, Carlioz H: Congenital aplasia of the cruciate ligaments: a report of six cases. J Bone Joint Surg 68B:827–828, 1986. 36. Torode IP, Gillespie R: Anteroposterior instability of the knee: a sign of congenital limb deficiency. J Ped Orthop 3:467–470, 1983. 37. Malumed J, Hudanich R, Collins M: Congenital absence of the anterior and posterior cruciate ligaments in the presence of bilateral absent patellae. Am J Knee Surg 12:241–243, 1999. 38. Thomas NP, Jackson AM, Aichroth PM: Congenital absence of the anterior cruciate ligament: a common component of knee dysplasia. J Bone Joint Surg 67B:572–575, 1985. 39. Tolo VT: Congenital absence of the menisci and cruciate ligaments of the knee, a case report. J Bone Joint Surg 63A:1022–1024, 1981. 40. Noble J: Congenital absence of the anterior cruciate ligament associated with a ring meniscus. J Bone Joint Surg 57A:1165–1166, 1975. 41. Schoenecker PL, Cohn AK, Sedgwick WG, et al: Dysplasia of the knee joint in association with the thrombocytopenia absent radius (TAR) syndrome. Orthop Trans 5:404–405, 1981. 42. Stanisavljevic S, Zemenick G, Miller D: Congenital, irreducible, permanent lateral dislocation of the patella. Clin Orthop 116:190–199, 1976. 43. Goldthwait JE: Slipping or recurrent dislocation of the patella with the report of eleven cases. Boston Med Surg J 150:160, 1904. 44. Conn HR: A new method of operative reduction for congenital luxation of the patella. J Bone Joint Surg 7:370, 1925. 45. Ghanem I, Wattincourt L, Seringe R: Congenital dislocation of the patella, Part I: pathologic anatomy. J Ped Orthop 20:812–816, 2000. 46. Gao GX, Lee EH, Bose K: Surgical management of congenital and habitual dislocation of the patella. J Ped Orthop 10:255–260, 1990. 47. Green JP, Waugh W: Congenital lateral dislocation of the patella. J Bone Joint Surg 50B:285–289, 1968. 48. Mumford EB: Congenital dislocation of the patella: case report with a history of four generations. J Bone Joint Surg 29:1083, 1947. 49. Ghanem I, Wattincourt L, Seringe R: Congenital dislocation of the patella, Part II: orthopaedic management. J Ped Orthop 20:817–822, 2000. 50. Gordon JE, Schoenecker PL: Surgical treatment of congenital dislocation of the patella. J Ped Orthop 19:260–264, 1999. 51. Marmor L: Total knee arthroplasty in a patient with congenital dislocation of the patella. Clin Orthop 226:129–133, 1988. 52. McCall RE, Lessenberry HB: Bilateral congenital dislocations of the patella. J Ped Orthop 7:100–102, 1987. 53. Langenskiold AL, Ritsila V: Congenital dislocation of the patella and its operative treatment. J Ped Orthop 12:315–323, 1992. 54. Bar-On E, Howard CB, Porat S: The use of ultrasound in the diagnosis of atypical pathology in the unossified skeleton. J Ped Orthop 15:817–820, 1995. 55. Walker J, Rang M, Daneman A: Ultrasonography of the unossified patella in young children. J Ped Orthop 11:100–102, 1991.

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56. Jones RDS, Fisher RL, Curtis BH: Congenital dislocation of the patella. Clin Orthop 119:177–183, 1976. 57. Dugdale TW, Renshaw TS: Instability of the patellofemoral joint in Down syndrome. J Bone Joint Surg 68A:405–413, 1986. 58. Zeier FG, Dissanayke C: Congenital dislocation of the patella. Clin Orthop 148:140–146, 1980. 59. Marumo K, Fujii K, Tanaka T, et al: Surgical management of congenital permanent dislocation of the patella in nail patella syndrome by Stanisavljevic procedure. J Orthop Sci 4:446–449, 1999. 60. Takehino T: Neglected congenital permanent dislocation of the patella: a case report. Clin Orthop 155:136–401, 1981. 61. Eilert RE: Congenital dislocation of the patella. Clin Orthop 389:22–29, 2001. 62. Drennan, JC: Congenital dislocation of the knee and patella. Inst Course Lect 42:517–524, 1993. 63. Beals RK, Buehler K: Treatment of patellofemoral instability in childhood with creation of a femoral sulcus. J Ped Orthop 17:516–519, 1997. 64. Bernhang AM, Levine SA: Familial absence of the patella. J Bone Joint Surg 55A:1088–1090, 1973. 65. St. Braun H: Familial aplasia or hypoplasia of the patella. Clin Genet 13:350–352, 1978. 66. Azouz EM, Kozlowski K: Small patella syndrome: a bone dysplasia to recognize and differentiate from the nail-patella syndrome. Pediatr Radiol 27:432–435, 1997. 67. Duncan JG, Souter WA: Hereditary onycho-osteodysplasia, the nailpatella syndrome. J Bone Joint Surg 45B:242–258, 1963. 68. Guidera KJ, Satterwhite Y, Odgen JA, et al: Nail patella syndrome: a review of 44 orthopaedic patients. J Ped Orthop 11:737–742, 1991. 69. Wynne-Davis R, Hall C, Apley AG: Atlas of Skeletal Dysplasias. Edinburgh, Churchill Livingstone, 1985. 70. Duthie RB, Hecht F: The inheritance and development of the nailpatella syndrome. J Bone Joint Surg 45B:259, 1963. 71. Renwick JH, Lawler SD: Genetic linkage between the ABO and nailpatella loci. Ann Hum Genet 19:312–331, 1965. 72. Beals RK, Eckhardt AL: Hereditary onycho-osteodysplasia (nail patella syndrome). A Report of nine kindreds. J Bone Joint Surg 51A:505–516, 1969. 73. Hogh J, Macnical JF: Foot deformities associated with onychoosteodysplasia: a familial study and a review of associated features. Int Orthop 9:135–138, 1985. 74. Sweeney E, Fryer A, Mountford R, et al: Nail patella syndrome: a review of the phenotype aided by developmental biology. J Med Genet 40:153–162, 2003. 75. Yarali HN, Erden GA, Karaaslan F, et al: Clavicular horn: another bony projection in nail patella syndrome. Pediatr Radiol 25:549–550, 1995. 76. Scott JE, Taor WS: The “small patella” syndrome. J Bone Joint Surg 61B:172–175, 1979. 77. Messina D, Meister K, Montgomery WJ: Bilateral congenital absence of the patellar tendon. Am J Knee Surg 10:23–25, 1997.

Chapter 28

Angular Deformity About the Knee in Children Deborah Stanitski

Coronal plane angular abnormality about the knee is extremely common in children.1 Genu varum and genu valgum are normal physiological developments and are age dependent. In general, radiographs are neither helpful nor appropriate unless an abnormality is suspected. Symmetrical genu varum is expected up to 24 months of age, followed by symmetrical genu valgum until familial norms are generally reached by age 7 years.2 Even at this point, “normal” should not be expected because some familial differences may exist, which are usually revealed in an accurate history. Surgery for persistent, unresolving deformity is probably indicated if angulation exceeds 10–15 degrees.3 In general, radiographs (long, supine, or standing radiographs with patellae anterior) may be warranted if the child is asymmetrical (and rotational differences have been corrected), has short stature, has disproportionate body segments, or is overweight or underweight for his or her age. Radiographs may also be warranted if there is a peculiar dietary history (for example, hypervitaminosis or single foods). It is very important to get not only an accurate patient history, but also an accurate family history. This can often help with the diagnosis even before examination of radiographs (when indicated). Also, anyone in varus tends to bear weight on the outer side of the foot, whereas those that are valgus tend to bear weight on the inner surface of the foot. The appearance of someone with genu valgum, because of the orientation of the feet and pronation, is that of one with “flat feet.” As with most orthopedic conditions, there are congenital and acquired varus and valgus abnormalities. The skeletal dysplasias may cause angular abnormalities about the knee. Diagnosis at birth may not occur in mild cases or even in things such as achondroplasia, which may not have obvious cranial or facial abnormalities. Birth length may be normal. It should be remembered that 90% of achondroplasia in children is caused by spontaneous mutations. The first 436

clue to a skeletal dysplasia may be short stature and unresolving varus. This occurs in hypochondroplasia, which tends to be a milder form of achondroplasia.4 Birth length in these patients may be normal, and the first clue to their diagnosis may be unresolving varus in a 2.5-year-old with short stature (Figures 28–1 and 28–2). The chondrometaphyseal dysplasias, particularly Schmid type, may be the cause of genu varum or genu valgum (Figures 28–3 and 28–4). Usually correction of these deformities remains permanent, and recurrence is an exception.5 Other dysplasias commonly associated with knee angular deformities are the valgus associated with Morquio’s disease and Ellis-van Creveld syndrome, as well as more rare etiologies such as pseudoachondroplasia (Figure 28–5).6 Osteogenesis imperfecta may produce any deformity.7 Although this condition is genetic, whether the child is born with a deformity depends most often on the severity of the condition (Sillence type III). Although distal femoral and/or proximal tibial deformities occur, diaphyseal rather than metaphyseal deformity is the rule (Figure 28–6). Varus or valgus deformity may occur in X-linked hypophosphatemic rickets (Figure 28–7) and dietary rickets (Figure 28–8).8 A careful dietary history can help separate the two diagnoses; serum calcium, phosphorus, alkaline phosphatase, and vitamin D (25-hydroxyvitamin D and 1,25-dihydroxyvitamin D) abnormalities usually clinch the diagnosis. Urine values may be helpful as well as serum blood urea nitrogen and creatinine. Medical management may be lifelong in hypophosphatemic rickets. Early diagnosis and medical treatment can eliminate deformity or improve it in the growing child. In the absence of spontaneous correction, osteotomy—with the patient in good medical control— usually has a rewarding outcome. Renal disease is another common cause of bony deformity (Figure 28–9) and requires management of the underlying cause. Orthopedic reconstruction of these patients requires appropriate medical input and is often challenging.9

Angular Deformity About the Knee in Children

Figure 28–1 An adolescent patient with hypochondroplasia. Clinical photo with dressing after staple removal.

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Heath and Staheli2 and other authors have defined the limits of “normal.” There are children, however, whose valgus does not resolve despite a normal family history, normal growth plates on standard radiographs (Figure 28–10), and normal metabolic profiles. They often are referred because of cosmetic concerns. Depending on the patient’s age, growth remaining, and deformity severity, stapling or hemiepiphysiodesis may be considered instead of osteotomy. Stapling requires patient and family compliance and an understanding that close follow-up is essential or overcorrection is a distinct possibility. Proximal tibial metaphyseal fractures (Cozen’s fractures) may result in unilateral genu valgum.10 The reasons for this are unclear and may be due to lack of proper reduction, periosteum in the fracture site, or asymmetrical medial tibial overgrowth. It is clear, however, that if deformity is mild, it will most often spontaneously resolve over several years. Osteotomy too early can lead to recurrent deformity despite initial correction. In the event of a proximal tibial metaphyseal fracture in a 2- to 8-year-old child, parents must be warned of this potential outcome. Measurement of the degree of angulation of the proximal tibia requires a nearly extended knees, and this position should be remembered

Figure 28–2 Photograph (A) and radiograph (B) of an adolescent patient with hypochondroplasia and tibia vara.

Figure 28–3 A patient with chondrometaphyseal dysplasia (Schmid type) and valgus.

Figure 28–5 Radiograph of a patient with pseudoachondroplasia. Staples are in place from a previous surgery to prevent varus.

Figure 28–4 Clinical picture of a patient with chondrometaphyseal dysplasia (Schmid type) and varus deformity.

Figure 28–6 A, Patient with osteogenesis imperfecta demonstrating clinical diaphyseal deformity.

(Continued)

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when placing the child in a cast and for follow-up examination. The long-term clinical and radiographic results of operative correction are not superior to observation and parental reassurance.11 Partial growth arrest due to fracture, infection, or physeal bar is not uncommon in North America. Any deformity may be produced depending on the location of the bar (e.g., medial versus lateral, distal femoral versus proximal tibial). The first problem is bar identification, followed by assessment of the bar. Whether it should be resected depends on its location (peripheral or central), growth remaining, and extent of the bar. In general, 2 or more years of remaining growth are necessary to make resection a worthwhile venture, leading to deformity correction secondary to

Figure 28–6—cont’d B, Patient with osteogenesis imperfecta demonstrating radiographic diaphyseal deformity.

Figure 28–7 Two patients with X-linked hypophosphatemic rickets. A, “Windswept” deformity. B, Bilateral varus.

Figure 28–8 A patient with dietary rickets. A, Radiograph before treatment. B, This radiograph demonstrates physeal healing.

Figure 28–9 Photograph (A) and radiograph (B) of a patient with severe valgus deformity secondary to renal disease.

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Figure 28–10 Photograph (A) and radiograph (B) of a patient with severe idiopathic valgus. The patient had normal physes and laboratory results.

continued growth. Resection of growth arrests that are more peripheral and/or excessively large (greater than 30%) are often unsuccessful in restoring anatomical alignment to the extremity and may require growth arrest of the remainder of the physis as well as osteotomy. Percutaneous epiphysiodesis is an easy and reliable procedure. Osteotomy with internal or external fixation has its pros and cons. The difficulty with osteotomy and internal fixation is that correction is permanent. Changing angulation, if deemed necessary by postoperative assessment, requires another operative procedure. External fixation has its cons because, although it is adjustable, the individual must wear a contraption, and there are always pin sites to worry about. Pin-tract infections are a relatively common postoperative complication. If treated aggressively and early with oral antibiotics on an outpatient basis, they will often resolve, rather than leading to abscess formation or bone involvement requiring intravenous antibiotics and/or surgery. A problem that has a wide spectrum of ages of onset is tibia vara or Blount’s disease, a progressive proximal tibial varus and rotational deformity of unknown etiology. In 1922 in Austria, Erlacher12 reported a 2.5-year-old child with an isolated unilateral 30-degree proximal tibial deformity.

In the United States in the same year, McCurdy reported the first bilateral case of tibia vara. In 1928 and 1929, Langenskiold in Finland and Lewis, Ritter, and Sloane in the United States reported cases of tibia vara. In 1930, Lulsdorf 13,14 reported 23 cases in Germany and 7 years later, Blount15 reported on his review of Lulsdorf’s cases and added 13 new cases from his own personal experience and named the condition “osteochondrosis deformans tibia” or “tibia vara.” In North America, the condition became referred to as Blount’s disease because of his involvement in its description and classification. In portions of Europe, it is called Erlacher-Blount’s disease. The etiology of this condition is unknown but is thought to be a combination of biological and mechanical factors causing progressive medial tibial physeal growth retardation and/or arrest. Despite earlier investigators who thought that it might be an inflammatory condition similar to Legg-Calve-Perthes disease, Blount15 insisted, based on biopsy evidence, that it was not an inflammatory sequel but rather due to some growth abnormality of the metaphysis, physis, and epiphysis. Langenskiold theorized that the deformity was a response to abnormal ossification of the medial tibia from an obese child’s weight bearing on a varus knee in early childhood.

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Mechanical factors are KEY POINTS attractive hypotheses for Blount’s 1. Physiological genu disease etiological agents in bilatvarum is symmetrieral clinical varus deformity in cal and seen up to overweight children.16,17 Analysis 24–25 months of age of tibial mechanical loads has when it gradually been performed by Fine and converts to symmetElman using gait-load analysis rical physiological studies. Cook et al.18 assessed the genu valgum. load distribution in the proximal 2. Familial norms of tibia during single-leg stance in genu valgum are 2- and 5-year-olds by finite elereached by the age ment analysis. In 2-year-olds, of 7 years. 20 degrees of varus resulted in 3. Asymmetrical genu forces that would cause medial varum or valgum physeal arrest.18 In 5-year-olds, 10 requires additional degrees of varus caused borderline evaluation. forces, and the obese child 4. Children with excesexceeded the force limit that sive genu varum or could cause growth modification. valgum (i.e., outside In a clever clinical model, Davids established norms) et al.19 used three-dimensional need assessment of gait analysis to assess kinetic proheight and weight files in normal subjects fitted relative to their with appliances to produce a “fat peers. Family history thigh” gait, a condition commay be positive for monly seen with tibia vara in dysplastic or metathose who are obese. The applibolic disorders. ance increased the normal thigh 5. Renal and X-linked radius by 175% in six otherwise hypophosphatemic normal-weight individuals. These rickets require authors hypothesized that the medical managegait alteration due to massive ment for metabolic thigh girth led to increased control before and medial tibial loading, which after osteotomy. would result in a progressive varus deformity. The data of Davids et al. from these studies confirmed that gait deviations with increased stance phase knee varus increased stance rotation and increased swing-phase circumduction. A free-body analysis model of proximal tibial loading based on the gait study showed inhibitory medial pressures generated by body weights over the 95th percentile for age. This scenario is commonly seen in patients with Blount’s disease, often unilaterally in patients with adolescent Blount’s disease. In this gait analysis model, Davids et al.19 support the role of obesity or fat thighs in the production of dynamic gait alterations, hostile to the medial tibial physis. This study also supports the fact that pre-existing knee malalignment (varus) is unnecessary for the development of late-onset tibia vara. Despite these data on the adverse effects of obesity, weight alone and its mechanical effects cannot account for the entire story, because unilateral disease is often seen in older patients, and bilateral disease is commonly asymmetrical. There have been attempts to define etiology based on histological analysis of the medial physeal tissue.16 The etiology issues in this method are similar to ones questioned by mechanical factors. The question that arises is whether the changes are secondary to the deformity or the cause of it. Blount’s histopathological specimen from a 3-year-old girl’s

bilateral disease revealed bending of the bony trabeculae that pushed the periosteum outward, causing it to arch over the bone and the cartilage. Other authors report the common findings of cellular and matrix disorganization and misalignment within the metaphysis, physis, and epiphysis.15 Findings were also seen laterally but were of a lesser extent than those found medially. Endochondral ossification was retarded or ceased medially. The immature unossified chondroepiphyseal cartilage can respond favorably with normalized growth if the unfavorable mechanical forces are changed, because no intraarticular abnormality or deformity is found in the early stages of the disease. Normal intraarticular alignment of unossified cartilage has been demonstrated by magnetic resonance imaging (MRI) and arthrographic evidence in cases of infantile and early juvenile tibia vara by Stanitski et al.20 With continued growth and unaltered mechanics, a stage is reached whereby the chondroepiphyseal complex changes become irreversible with progressive varus deformity and sagittal involvement posteriorly. Continued forces lead to physeal bar formation and medial growth arrest, with true intraarticular deformity in the advanced case. As a result of growth retardation, limb length inequality may be associated with tibia vara. Clinical classification by the age of onset of disease was initially proposed by Blount,15 who suggested use of the terms “infantile” and “adolescent.” According to Blount, the infantile type is seen in children 1–3 years of age, whereas the adolescent variety is seen after age 12. He felt that the infantile group represents a lack of the expected normal resolution of infantile genu varum with pathological progression of the existing varus due to a primary epiphyseal defect. The adolescent type, he noted, occurred in previously normal children, and he felt that trauma was indicted as a cause and possibly chronic infection. This classification system has persisted and, commonly the adolescent form is referred to as the “late onset” variety Thompson and Carter21 suggested a juvenile category to indicate the onset of disease between ages 4 and 10 years (Figure 28–11) in a group whose clinical presentation and course act midway between the infantile and the adolescent forms. Radiographic classification depends on the magnitude of the deformity and evidence of progressive changes of the medial proximal tibia. Significant difficulty occurs in differentiation between normal physiological genu varum and early onset tibia vara in children under 2 years of age and, occasionally, older children if changes are not obvious radiographically. In 1952, Langenskiold13 reported on the progressive radiographic changes seen in 23 cases of tibia vara reviewed in Finland. The changes of proximal tibial morphology were represented by six stages of sequelae of altered medial proximal tibial physeal growth (Figure 28–12). Early stages included medial metaphyseal beaking and fragmentation of the metaphysis and the epiphysis (stages 1 and 2). Stages 3 and 4 showed increased deformity and development of a step off within the medial tibial physis. Progressive medial physeal closure is seen in Stages 5 and 6. Interobserver and intraobserver differences reflect the difficulty with precise determination of the staging in early disease, especially stages 2 and 3. Similar problems are seen in distinguishing physiological genu varum from early pathological tibia vara

Angular Deformity About the Knee in Children

Figure 28–11 Photograph (A), radiographs (B), and intraoperative arthrogram (C) of a patient with juvenile Blount’s disease.

stage 1. Documentation of true deformity of infantile tibia vara requires repeated observation of serial radiographs during growth. Definitive diagnosis is not usually made on a single radiograph in a very young child with mild genu varum. The infantile form (Figure 28–13) of tibia vara starts with a proximal tibia in some degree of physiological varus that does not go through the usual spontaneous reversal of the varus to physiological valgus. Progression of varus may occur, leading to the development of secondary radiographic

Figure 28–12 Langenskiold classification of infantile Blount’s Disease Types 1–6.

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Figure 28–13 Radiograph of infantile bilateral Blount’s disease.

changes of true pathological tibia vara of varying severities. Differentiation at the initial visit between the physiological and pathological process may be difficult if it is bilateral and symmetrical. Pathological tibia vara generally becomes evident between ages 2 and 5 years.22,23 Pathological infantile tibia vara begins between ages 20 and 24 months as a painless varus deformity, often bilateral (50–75%), in an otherwise healthy child. Usually the child is obese and has begun walking at an early age.24 It is more commonly seen in girls and, in North America, among African-Americans. If bilateral, the deformity is commonly of different magnitudes. The child’s height and weight should be plotted on a normative graph for age. Gait is observed for abnormal lateral knee thrust, which is often found in older children (30–36 months). Leg length inequality at this age is rare. Davids and associates found the “cover-up test” useful to differentiate physiological from pathological genu varum.19 This test’s validity has not been reproduced yet by other centers. My personal experience finds this test difficult to reproduce in chubby toddlers. Medial-lateral knee laxity should be assessed and side-to-side comparisons noted. Pathological bowing is almost always passively uncorrectable. Radiographic assessment depends on the patient’s age and his or her ability to cooperate. Because of internal tibial torsion, one should be careful to mark the patellae and have anteroposterior (AP) lower extremity radiographs taken with the patellae directly anterior to adequately assess the deformity. This should be done in the young child in the supine position because it is often difficult to obtain standing radiographs in this age group. To avoid effects of rotation on angulation, great effort is needed to make sure limb rotation is controlled and symmetrical because children often tend to walk and stand internally rotated. Internal rotation may occur through the knee or distal to the knee, and the thigh-foot axis may be normal. In addition to assessing lower extremity alignment, epiphyseal and physeal development and deformity should be evaluated to rule out dysplastic, endocrine, or metabolic causes of the deformity. Lateral radiographs are performed to

assess whether the child has tibia procurvatum. The metaphyseal-diaphyseal angle originally described by Drennan is useful in assessing pathological versus physiological bowing (Figure 28–14).25,26 There has been discussion as to whether one should use the mid-axis of the tibia, the lateral border of the tibia, or the fibula as the reference line to assess the metaphyseal-diaphyseal angle. It is currently generally agreed that children with metaphyseal-diaphyseal angle (MDA) of 11–16 degrees require observation, and those with an MDA greater than 16 degrees are likely to develop pathological tibia vara. The optimal way of documenting pathological tibia vara is by serial radiographic assessments that show progressive deformity with concomitant medial tibial changes. There is some controversy over whether the metaphyseal–diaphyseal or the tibia–femoral angle is more sensitive in detecting true deformity. MRI or computed tomography (CT) are other imaging modalities that may be useful to assess intraarticular pathology in children (e.g., a proximal medial physeal growth arrest).27 Focal fibrocartilaginous dysplasia is a rare cause of proximal tibial varus.28 This condition is generally seen from ages 1–2 years and may be associated with proximal tibial

Figure 28–14 Metaphyseal-diaphyseal angle. (Reprinted with permission from 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.)

Angular Deformity About the Knee in Children

metaphyseal (not physeal or epiphyseal) varus deformity. Radiographs are usually diagnostic. Frank discussions are needed with the patient’s family about the uncertainty of differentiating physiological bow legs from pathological tibia vara, with emphasis on the need for follow-up assessment and caution against unnecessary treatment. Once the diagnosis of pathological infantile Blount’s disease is made, treatment depends on the magnitude of the deformity and the patient’s age. Bracing has been advocated for children younger than 3 years old with Langenskiold Stages 1 or 2 disease.29,30 Generally, a KAFO with an antivarus vector is used. It is more useful during daytime weight-bearing activities than at night because it seems logical that the orthosis will exert its greatest mechanical impact during daytime weight-bearing activity, despite accelerated growth rates during nighttime. Compliance with orthotic management may be difficult because the child can remove the device. In addition, frequent adjustments are necessary in the growing child. Finally, effective brace fitting may be difficult in the small child with large thighs. If a child is older than 3 years and has a progressive deformity with Langenskiold stage 2 or greater disease, bracing is usually ineffective, and surgical intervention may be indicated in this group.31 In the past, outcomes were fraught with complications, including wound breakdown, loss of fixation, recurrent deformity, neurological and vascular injury, and inadequate correction. Greene reported a 50% complication rate for surgical treatment in 1993.24 It is essential to evaluate these children for a physeal bar before institution of any surgical treatment because, if there is a bar, recurrence is the norm rather than the exception. Recent improved fixation methods, atraumatic osteotomy, and awareness of neurological and vascular compromise, as well as compartment syndrome, have significantly improved outcomes. Surgical options vary depending on the patient’s age and size, degree of deformity, physeal status, and presence or absence of limb-length inequality. The most common procedure in straightforward cases is osteotomy of the tibia and fibula. Proximal metaphyseal tibial osteotomy is done to reestablish the mechanical axis and to unload the medial proximal tibial chondroepiphysis to allow restoration of growth in the involved segment. The osteotomy is done taking care to avoid the tibial tubercle and proximal tibial physis. Some debate exists about the need for prophylactic fasciotomy of the anterior compartment or decompression of the peroneal nerve. In a study by Young et al.,32 compartment pressures were measured following traditional tibial osteotomy and external fixation for 48 hours after surgery. Compartment pressures never exceeded 30 mm Hg. In my experience, prophylactic fasciotomy—even when the osteotomy is done in a more traditional fashion—is not required. I prefer to perform the fibular osteotomy in the distal third, approximately 5–6 cm above the syndesmosis, to avoid complications with the ankle joint. In this location, the fibula is readily accessible without the need for significant muscle stripping or special concern for the course of the peroneal nerve. The tibial osteotomy may be done by a variety of methods. Chevron, dome, and oblique plane osteotomies have been described in attempts to pro-

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vide stability postoperatively.33–35 A transverse osteotomy using a subperiosteal Gigli saw produces a very controlled, atraumatic complete cut that heals rapidly because of the intact periosteal cuff, large metaphyseal bone surface, and minimal cortical disruption.36 The distal tibial segment is translated medially to maintain mechanical axis alignment. Maintenance of alignment in the past has been a significant problem because of difficulty with fixation and casting methods. Newer methods of fixation allow precise alignment, including outpatient alignment and adjustment (using external fixation) where appropriate long-leg alignment radiographs can be obtained.37–39 This is in contrast to the “best guess” intraoperative method using a Bovie cord or K-wire reference points. Deformity correction may be done acutely or gradually, depending on the fixation method chosen. Acute correction osteotomy may be fixed with K-wires or screws with adjunctive cast management for 5–6 weeks in a young child. The difficulty with this is that one cannot obtain good long-leg radiographs in the operating room. External fixation with either ring or cantilever fixators allows modularity and gradual correction. It provides secure fixation with access to compartment and distal neurovascular evaluation. In contrast to a long-leg cast, which is often difficult to apply on a short, fat limb, it also allows postoperative long-leg radiographic assessment. Fixator choice is based on surgeon and patient preference. In general, if complex correction is required, circular fixation may be preferable, whereas one can easily use cantilever-type fixators for most corrections. Use of a fixator allows rapid return to functional use of the limb, including weight-bearing as well as knee and ankle motion, in contrast to cast immobilization. Lateral staple epiphysiodesis in this age group has been suggested in the early stages. Recurrences of deformity and need for repeat surgery are possible, and strict patient compliance is necessary if one uses this technique.40 If this method is chosen, it must be assumed that the medial tibial physis has the potential to fully normalize its growth in the face of continued (temporary) hostile compressive forces during gait because of a persistent deformity and increased body weight. The need for physeal bar resection is uncommon in the infantile age group, except those with greater than stage 3 disease.27 This patient subgroup should be evaluated with MRI or CT imaging to determine the location and magnitude of the physeal arrest preoperatively. The bar, if it exists, is almost always in a peripheral posterior medial position. Bar excision can be attempted if the bar is not more than 30% of the physeal area in a very young patient, which is a rare situation. Proximal tibial osteotomy is often combined with bar excision to correct alignment and reduce compressive forces on the medial tibial physis. Long-term results of this combination surgery have not been reported. In severe deformity with a physeal arrest in an older child, tibial osteotomy combined with lateral physeal arrest is recommended to avoid recurrent deformity. One may need to combine this with leg lengthening as an adjunctive procedure. Assessment of subsequent limb length is done following the usual guidelines. These children need to be followed until they are close to maturity to ensure limb-length equalization.

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Inconsistency in Blount’s classification of infantile and adolescent tibia vara led to initiation of an intermediate group, termed juvenile tibia vara. Thompson and Carter21 proposed a juvenile class with a clinical onset between 4 and 10 years of age, with adolescent reserved for those 11 years of age or older. Debate exists as to whether the juvenile form represents a sequel of unrecognized mild infantile disease or whether it is a separate entity. The juvenile group (Figure 28–15) shares similarities and differences with the infantile type in clinical and radiographic presentations. Juvenile tibia vara has about 50% bilaterality, more male involvement, and often presents with pain (not deformity) as the major complaint. True internal rotation deformity, as evidenced by a medially directed thigh foot axis, is minimal, and limb-length inequality is usually minor. As with the infantile type, in North America it is more common in African-Americans, and marked obesity is the rule in affected patients. Clinical examination shows a significant lateral knee thrust during gait, and relative lateral collateral ligament laxity may be present. Knee stability is normal in other planes. Tenderness may be seen at the medial physis and along the lateral collateral ligament. The presence of a knee effusion suggests associated intraarticular pathology. Imaging studies in the juvenile group should include standing

Figure 28–15 A 9-year-old patient with unilateral juvenile Blount’s disease.

long-leg films (with the patellae directed anteriorly) to assess alignment, including distal femoral alignment and boneage radiographs to determine skeletal maturity. Lateral limb radiographs are used as in the infantile type to assess proximal tibial procurvatum. Long-leg films are useful to determine sites and magnitude of deformity as well as potential limb length inequality. If there is any question about physeal or intraarticular status, MRI and/or CT studies should be done. MRI may also be useful to determine the meniscal status, with the caveat of the high frequency of false-positive readings for meniscal pathology in this age group.41 Treatment in this group is surgical. Accurate preoperative clinical and radiographic evaluations of skeletal maturity are mandatory for any proposed surgical intervention. Some authors recommend lateral staple hemiepiphysiodesis, although the previously mentioned concerns about this method are the same. The limits of angular deformity appropriate for correction by this technique in this group are not defined. Proximal tibial and distal fibular osteotomy and the principles just outlined are the usual treatment to provide normalization of the mechanical axis of the limb. Medial translation of the distal tibial segment must be done to restore the mechanical axis alignment. Distal femoral osteotomy may also be required to eliminate distal femoral valgus or varus deformity. The femoral deformity, if it exists, is usually no more than 10 or 12 degrees and may be done acutely using external or internal fixation (Figure 28–16). If femoral osteotomy is done from a valgus to a varus direction, a transverse tenotomy of the fascia lata is done to eliminate a valgus vector. Excision of a physeal bar with concomitant tibial and fibular osteotomies may be considered in this age group, but there are limited data about outcomes following this combination of procedures. Proximal lateral tibial epiphysiodesis is often combined with the osteotomy to prevent recurrence, especially in cases with major deformity, large physeal arrest, and limited growth potential. If epiphysiodesis is needed and major growth remains, provision for management of the limb-length inequality is made. This may include concomitant lengthening of the extremity. Depending on the age of the child, one may also consider epiphysiodesis of the contralateral proximal tibia. In the uncommon situation of severe Stage 5 or 6 disease and established intraarticular incongruity, medial epiphyseal elevation osteotomy (Figure 28–17) with proximal tibial valgus and rotational osteotomy and fibular osteotomy may be necessary. This will produce joint congruity, improve weight-bearing, and eliminate the posterior medial slide of the femoral condyles on the tibia, as well as completion of the proximal tibial-physeal closure.42 Attention to possible progressive limb-length inequality is mandatory. Patients and their families should be alerted to the possible need for later surgery to provide limb-length equalization at or near maturity. Adolescent or “late-onset” tibia vara, unlike infantile tibia vara, is more often unilateral than bilateral (Figure 28–18). It is initially discovered as adolescents go through their growth spurt and develop progressive deformity. Occasionally, afflicted individuals complain of two different sorts of pain. One type of pain is sharp, medial at the affected physis. The other type of pain is lateral, due to pressure and stretching of the lateral collateral ligament, and

Angular Deformity About the Knee in Children

Figure 28–16 A, A patient with femoral and tibial deformity. B, The deformity is not obvious from clinical appearance.

Figure 28–17 Schematic drawing of an intraepiphyseal elevating osteotomy.

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Figure 28–18 Photograph (A) and radiograph (B) of an adolescent patient with tibial deformity.

it is described as dull and aching. Both pain types are present only on weight-bearing. Like the infantile and juvenile types, the patient with late-onset tibia vara in North America is too heavy for his or her height and is often African-American. Boys are more commonly affected than girls. In my personal series of more than 70 adolescent Blount’s cases, the average male and female were 180% and 220% above their ideal body weight, respectively. Although body habitus, race, and age parallel those seen with slipped capital femoral epiphysis, it is highly unusual (in my significant experience with both conditions) to see the two occur simultaneously. Hip examination is routinely done in these patients, followed by radiographs when the hip exam is abnormal. I only found a silent simultaneous slip in one patient and a symptomatic sequential slipped epiphysis in another patient. Limb-length inequality, usually less than 2 cm, is a rule and may simply be the result of the deformity. It certainly does not play a large role in the disorder or in its treatment in these almost skeletally mature patients. Deformity magnitude is usually limited to 20 degrees, but the femur must be carefully assessed because distal femoral varus or valgus may coexist.43 Clinical examination usually reveals a very large patient with an antalgic, laterally thrusting gait.44 Knee

stability is normal in the AP plane but may be lax in the medial-lateral plane. Tenderness may be present at the medial physis on direct palpation or along the fibular collateral ligament. The former KEY POINTS is usually point tenderness. It may not be possible, because of 1. Blount’s disease is the large size of the limb, to classified as infandetermine whether there is tile (age 2–3 years), femoral deformity. Only overall juvenile (age 4–10 limb realignment may be evaluyears), or adolesated, which will be varus. Knee cent (age >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.

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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.

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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 <16 years Arthritis defined as joint swelling/effusion or two of the following: Decreased range of joint motion Tenderness/pain on joint motion Increased warmth in one or more joints Symptoms persistent for at least 6 weeks duration Other forms of arthritis must be excluded JRA onset subtypes Systemic-onset JRA: Persistent intermittent fever (daily intermittent temperatures to ≥103˚F) with or without rash or other organ involvement. Pauciarticular-onset JRA: Arthritis in four or fewer joints during the first 6 months of disease. Children with systemic onset JRA are excluded from this category. Polyarticular-onset JRA: Arthritis in five or more joints during the first 6 months of disease. Children with systemic onset JRA are excluded from this category. Modified from JRA Criteria Subcommittee of the Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association: Current proposed revision of the JRA criteria. Arthritis Rheum 20(Suppl):195–199, 1977.

children.1 Although there are likely geographic, genetic, and environmental factors that result in true variations,2 several factors likely contribute to reported differences, making interpretation of epidemiological studies difficult. First among these is the fact that no gold standard exists for the diagnosis of arthritis; children treated for systemic JRA for decades subsequently may be diagnosed with vasculitis or Crohn’s disease. Even standards for diagnosing arthritis are not uniform. Typically, rheumatologists in the Americas use the diagnostic criteria set forth by the ACR in 1977, whereas investigators and clinicians in Europe generally follow the criteria established by the European League Against Rheumatism in 1978.2a Among the major differences are the duration of symptoms necessary to make the diagnosis (6 weeks in New York, 12 weeks in London) and whether conditions should be distinguished on the basis of patterns of arthritis and enthesitis.

Systemic-onset JRA (soJRA), also known as Still disease, accounts for approximately 10% of JRA cases. This form of JRA is most similar to an infection, with prominent systemic features and equal numbers of boys and girls affected. Most characteristic is a hectic fever spiking to 39–41˚C that occurs once (quotidian) or twice (double quotidian) per day. A salmon-pink, maculopapular rash is another hallmark of soJRA, typically appearing during fever peaks. Other physical examination findings in soJRA may include significant lymphadenopathy, hepatosplenomegaly, and pericarditis. Pathology The synovium is the target organ of the autoimmune process in JRA. Infiltration by plasma cells and lymphocytes leads to pannus formation, exuberant fibrin deposition, and increased production of synovial fluid.3 General vascularity of the synovium is increased, and inflammatory cells migrate, particularly to perivascular areas. In growing children, the hyaline cartilage layer is more substantial than in adults, one of the factors contributing to the delayed erosive and destructive changes in JRA compared to adult rheumatoid arthritis. Nonetheless, chronic changes may develop after only a few months of joint inflammation, including bony cysts, degradation of cartiKEY POINTS lage, and joint-space narrowing.4 In growing children, inflamma1. Chronic arthritis is tory changes may spread beyond one of the most the joint, leading to periarticular common illnesses periostitis and bony overgrowth of childhood, affectat the epiphyses. Older children, ing 70,000 girls and on the other hand, may develop 30,000 boys in the premature fusion of the epiphyses United States. and cessation of growth. As in 2. Arthritis is marked adults, severe arthritis may cause by lymphocytic bony sclerosis or even fibrous inflammation of the ankylosis. Although uncommon, synovium and rice bodies have also been perivascular areas. 5 reported in JRA. Physical Examination of the Arthritic Knee

Clinical Course There are three types of juvenile rheumatoid arthritis, defined by the number of joints involved and the presence or absence of associated systemic features. The subtype of JRA is defined by the disease pattern during the first 6 months of illness. Approximately 50% of cases are classified as pauciarticular JRA, involving fewer than five joints. This form of JRA is three times more common in girls than in boys, and it carries the highest risk of associated uveitis, particularly if the child is ANA-positive. Approximately 40% of cases are classified as polyarticular JRA. This form of the disease most closely mimics adult rheumatoid arthritis. Children with polyarticular JRA— 80% of whom are girls—are likely to go on to have active arthritis into adulthood. The presence of a positive rheumatoid factor is a marker of particularly severe disease, but unlike adult RA, it is insufficiently sensitive or specific to be helpful in confirming the diagnosis.

Signs of inflammation are the hallmark of arthritis (Figure 30–1). Warmth and swelling are most characteristic, whereas overlying erythema is more characteristic of septic arthritis. The child may report that he is uncomfortable, but this is more commonly described as stiffness than as pain. In fact, at least 20% of children with juvenile arthritis never complain of pain, and a recent study from Oklahoma found that only 13 of 226 children referred to a rheumatology clinic with joint pain actually had arthritis.6 The knee may exhibit a ballotable effusion, meaning that applying pressure directly to the patella forces it downward, displacing synovial fluid and bouncing it against the femur. The characteristic springiness is not noted when fluid does not intervene between patella and femur, as in healthy children. The joint may also be swollen from synovial proliferation, which has a boggier consistency than the free fluid of a joint effusion. Careful examination of an inflamed knee may also allow estimation of the duration of the arthritis. Synovitis is char-

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

Figure 30–1 Bilateral knee arthritis due to juvenile rheumatoid arthritis. Six months of arthritis have resulted in both acute and chronic changes. Knee swelling with loss of bony landmarks, as well as atrophy of vastus medialis muscles and mild overgrowth of medial femoral condyles, are demonstrated.

acterized by increased blood flow, typically more pronounced in the medial compartment of the knee as a result of mechanical factors. Hyperemia leads to increased delivery of nutrients and accelerated growth. Initially, this may be seen as prominence of the medial femoral condyle, and later as genu valgus. Ultimately the leg with the inflamed knee grows more rapidly and a leg-length discrepancy develops. The lower leg may bow in order to compensate for the greater length of the upper leg. At the same time, the knee loses extension and develops a flexion contracture, with resultant atrophy of the vastus medialis and wasting of the quadriceps muscle. Laboratory Studies Laboratory studies may be helpful in excluding infectious and proliferative causes of a swollen knee, but they cannot confirm a diagnosis of arthritis. A child may have JRA even if all laboratory studies are normal. Even when laboratory studies support a diagnosis of JRA, they are nonspecific and must be interpreted within the context the patient’s clinical presentation. Ultimately, a diagnosis of JRA rests on history and physical examination. The laboratory studies that are most characteristic of JRA are those that reflect systemic inflammation. These include elevated erythrocyte sedimentation rate, C-reactive protein, or platelet count. In general, the elevation of acute phase reactants is proportional to the number of joints involved. In a case of monoarticular arthritis of the knee, therefore, normal laboratory studies are the rule. Leukocytosis may be present in JRA, particularly in children with systemic- onset JRA, and a mild to moderate anemia may also be seen in the setting of chronic inflammation. The antinuclear antibody (ANA) is usually measured when a child is being evaluated for possible JRA. This is rarely helpful diagnostically, although an ANA at a titer of a 1:1024 or higher is suggestive of an autoimmune condition. At lower titers, positive ANAs are quite nonspecific, seen in conditions characterized by disordered immune regulation and recognition of self-antigens, but also in numerous

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other infectious and inflammatory conditions, including viral illnesses. Thus, up to 2% of children have a positive ANA at any time, typically of low titer, and most are healthy. On the other hand, a positive ANA in a child with known arthritis is a marker for an increased risk of developing anterior uveitis. One of the most overused tests in children with a swollen joint is the rheumatoid factor (RF). This is an autoantibody directed against the Fc portion of the immunoglobulin (Ig) G molecule; however, unlike adult RA, in which 80% of cases are associated with a positive RF, this test is rarely positive in children. Only 2% of more than 400 children seen at a rheumatology clinic in Philadelphia had a positive RF, and many of these were considered to be false-positives.7 The only setting in which a RF is helpful in children is in the case of polyarticular JRA; those with a positive RF are more likely to have a severe, erosive arthritis, warranting more aggressive management. Even in such a case, however, the test is nonspecific, and children may have a positive RF in infections and other conditions associated with circulating immune complexes. Radiographic Studies Radiographic studies are essential for evaluating children with musculoskeletal pathology. They may be particularly helpful in confirming a clinical impression of arthritis by excluding other causes of joint pathology and by showing the characteristic changes caused by disease progression. Plain films are usually the first imaging modality utilized for evaluating a child with a swollen knee. They are generally normal during the initial stages of arthritis, or a child may have nonspecific findings such as soft-tissue swelling, joint effusion, periarticular osteopenia, or periosteal new bone formation.8 Radiographs also may help rule out fractures or foreign bodies. In longer-standing arthritis, more severe changes become evident on plain radiographs (Figure 30–2).9 Joint space narrowing reflects cartilage destruction, and it may be accompanied by other signs of inflammatory damage, including bony erosions and subchondral cysts. Epiphyseal maturation may be accelerated during active disease, leading to asymmetrical growth, so bilateral films comparing structures on the uninvolved side may be particularly helpful. Later signs of inadequately controlled arthritis—including bony ankylosis, subluxations, epiphyseal fractures, and avascular necrosis— are fortunately rare today because of the more effective medications available for treating children with arthritis. Plain radiographs provide limited information on the soft tissues of joints, inherently restricting their utility in the evaluation of synovitis or arthritis. Accordingly, other imaging modalities may be preferable, particularly for detecting and assessing early disease. Magnetic resonance imaging (MRI) is able to demonstrate cartilage thinning, meniscal changes, joint effusions, and popliteal cysts.10 The sensitivity of MRI increases significantly when performed with gadolinium enhancement. Following intravenous administration, gadolinium accumulates quickly in tissues with increased vascularity, including inflamed synovium.11 Synovial enhancement and hypertrophy, joint effusions, meniscal hypoplasia, cartilage thinning and loss, and bone-marrow

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Figure 30–2 Progression of radiographic changes due to juvenile rheumatoid arthritis of the right knee. A, Anteroposterior images obtained at presentation when patient was 5 years of age, demonstrating minimal overgrowth of the medial femoral condyle, as well as accelerated maturation of the epiphyses. B, Same patient at 12 years of age. Medial overgrowth and disordered epiphyseal maturation have progressed. Joint-space narrowing due to cartilage destruction is now also evident. C, By 19 years of age, permanent changes in the morphology of the structures of the right knee are evident, including significant joint space narrowing. The knee images are included as part of a scanogram, which documents a 2.5-cm leg-length discrepancy as well.

signal enhancement all may be demonstrated in this manner. In one study that assessed the value of gadolinium enhancement in MRI images of knees affected with JRA, pannus was detected in 14 of 24 knees in noncontrast MRI, whereas gadolinium-enhanced images revealed the presence of pannus in 23 of the same 24 knees.12 Even when pannus was detected, the extent of involvement was underestimated on the noncontrast images. Also striking was the degree to which unenhanced images underestimated the degree of articular cartilage

loss; the images obtained without contrast found cartilage to be intact in 20 of 24 knees, whereas gadolinium-enhanced images found intact cartilage in only 3 of the same 24 knees. In addition to offering better definition of the extent of active disease, MRI may be a tool to assess response to therapy.13 Its utility is limited primarily by its cost and by the need to sedate young children to prevent movement artifact. Ultrasonography (USG) is another imaging modality that may be used to assess arthritic joints. In the hands of

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

experienced operators, ultrasound may be useful for detecting joint effusions; popliteal cysts; lymph nodes; and to some degree, changes on articular cartilage. MRI is superior to USG for detecting the extent of pannus formation, as well as damage to cartilage and menisci.14 USG is far less expensive, however, and images may be acquired rapidly, avoiding the need for sedation or anesthesia in children who cannot remain still. Treatment

KEY POINTS 1. Arthritis is a clinical diagnosis, typically manifested by joint swelling and stiffness, but only rarely causing pain. 2. No laboratory or radiographic findings are pathognomonic for juvenile arthritis, although evidence of systemic inflammation, immune activation, and thinning of cartilage are all consistent with the diagnosis.

Treatment of inflammatory joint disease has advanced significantly in the last decade.15 Joint changes due to synovitis are gradual but inexorable. The rapidity with which they develop varies with the severity of the arthritis. Accordingly, the goal of therapy is to completely prevent joint damage by halting inflammation. This is particularly important in a growing child, in whom inflammation may result in permanent derangements in joint development and function.16 On the other hand, growing children are also far better able to heal damage to cartilage and bone if the arthritis is completely suppressed, increasing the incentive for adequate disease control. The argument for aggressively and rapidly controlling joint inflammation in JRA is further bolstered by evidence that the longer an autoimmune condition persists, the more it tends to become resistant to therapy.17 Therapies for arthritis may be divided into those that are largely symptomatic, relieving symptoms but not preventing joint damage, and disease-modifying drugs that alter the biology of the process. Although symptomatic relief may be necessary depending on a child’s level of discomfort, disease control is essential for preventing chronic joint changes due to ongoing inflammation. Nonsteroidal Antiinflammatory Drugs First-line agents for the symptomatic relief of pain in JRA are nonsteroidal antiinflammatory drugs (NSAIDs). Although dozens of medications in the category are available, only a handful have received approval from the U.S. Food and Drug Administration for use in children. Aspirin is the prototype of this category of medications, although it has generally fallen out of favor in pediatrics due to concern about Reye syndrome and its very brief serum half-life. Ibuprofen is available over-the-counter as a suspension, so it is often prescribed by primary care physicians. Antiinflammatory doses are 10 mg/kg three or four times daily, with the caveat that the medication must be given every 6 hours to achieve maximal antiinflammatory effect. Use of naproxen avoids this issue since its long half-life allows twice-daily dosing (10 mg/kg every 12 hours). Although all NSAIDs carry potential gastrointestinal, hepatic, and renal toxicities, naproxen has an additional predilection for causing pseudoporphyria, especially in fair children. Because up

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to 12% of children develop this potentially scarring photosensitive eruption, patients should be diligent about using sunscreen while they are taking naproxen. Intraarticular Corticosteroid Intraarticular (IA) corticosteroid injection is an accepted therapeutical option, particularly in children with pauciarticular JRA. This intervention is most often used when patients have had an incomplete response to NSAID therapy. Ideally, IA corticosteroids avoid the need for systemic medications to treat a localized inflammatory process. It may also be employed as an adjunct to more advanced therapies in children with particularly resistant synovitis in one or two joints.18 Delivery of corticosteroid directly into the affected knee almost always results in some degree of improvement in swelling and pain. Efficacy in achieving full and lasting remission, however, varies greatly. Reported remission rates 6–12 months postinjection are 22–77%; remission rates 2 years postinjection are 16.7–55%.19,20 A significant degree of this variability may reflect differences in study designs and patient populations of the published series. In addition, early disease may respond better to IA corticosteroid than long-established synovitis, and efficacy may differ between patterns of JRA, with systemic onset JRA prone to earlier relapse following corticosteroid injection.21 Patients with psoriatic arthritis and spondyloarthropathy may have a lower response rate compared to JRA patients. Results also vary based on choice of corticosteroid preparation, with less soluble agents generally resulting in the most durable responses. Thus, triamcinolone hexacetonide is the agent of choice for local treatment of JRA, and triamcinolone acetonide offers a reasonable alternative. Other options, including methylprednisolone acetate and hydrocortisone acetate, are less effective in providing long-term relief of synovitis after intraarticular administration. Potential side effects if IA corticosteroid include subcutaneous atrophy at the site of injection if steroid extravasates into the cutaneous tissue. There is the possibility of joint infection, although with sterile technique this risk is small (0.002% in adults, no reported cases in children). There is limited systemic absorption after an intraarticular injection, but generalized side effects are far less than those following parenteral or oral administration of corticosteroids. IA steroids are generally very well tolerated, with no evidence of cartilage damage on MRI up to 13 months postinjection. As with all pediatric therapies, small children may require conscious sedation or general anesthesia to lie still for the procedure, so risks of sedation must be taken into account when considering this approach. Advanced Therapies The disease-modifying antirheumatic drugs (DMARDs; Table 30–3) derive their name from the fact that, unlike NSAIDs, they slow the progression of bony erosions in arthritis.22 In general, this class of medications is quite effective in childhood inflammatory joint disease as well, altering the arthritis without causing significant immunosuppression. Although different chemically, one feature they have in common is that their clinical benefits manifest themselves slowly, over weeks to months. A patient who stops a DMARD before finishing 3 months of therapy has not really given the drug a chance.

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Table 30–3

Chapter 30

Advanced Therapies for Inflammatory Arthritis

Drug

Recommended Monitoring

Mechanism of Action

Dose

Principal Toxicities

1. Block folate metabolism and purine synthesis 2. Increase adenosine levels (antiinflammatory mediator) Block lysosome antigen processing

0.5 mg/kg weekly PO/SQ/IV, escalate as tolerated

Hepatitis, nausea, oral ulcers, bone marrow suppression, pneumonitis (rare in children)

LFTs q4–8wks, periodic CBCs; folate can limit GI and hematologic toxicity

<7.0 mg/kg/d PO, max 400 mg daily, divided QD-BID Escalate slowly to 40-70 mg/kg/d PO divided BID-TID, max 3 g/d

Retinopathy, diarrhea, nausea, rash, agranulocytosis Rash, nausea, leukopenia, hepatitis, headache/CNS, Stevens-Johnson syndrome

Ophthalmologic exam q6 mo, CBC, LFTs q 3-6 mos CBC + LFTs q month initially, then periodically

Disease-Modifying Antirheumatic Agents Methotrexate

Hydroxychloroquine Sulfasalazine

Increase adenosine levels

Biologic Response Modifiers Etanercept

TNF receptor fusion protein; blocks TNF-α and lymphotoxin

Infliximab

Humanized monoclonal antibody against TNF-α

Adalimumab

Human monoclonal antibody against TNF-α

0.4mg/kg SQ twice Injection site reactions, weekly, or 0.8 mg/kg infections, weekly, max 50 mg/wk cytopenias, autoimmune diseases 3-10 mg/kg IV q4-8 wk Infections (especially reactivation TB), multiple sclerosislike illness Adult: 40 mg SQ Injection site reactions, q2 weeks infections

Methotrexate (MTX) is the most commonly used DMARD in JRA. Since its addition to the JRA armamentarium in the 1980s, MTX has dramatically improved both short- and long-term outcomes. As with most antirheumatic drugs, the mechanism of action of MTX is unknown. It is a potent inhibitor of dihydrofolate reductase, but at therapeutic doses its effects on adenosine metabolism are more likely to be primary.23 Methotrexate is given weekly, either by mouth or parenterally (typically via subcutaneous or intramuscular injection). It is common for patients and their families to notice improvement within 4 weeks of starting therapy, but peak effects may be delayed for up to 12 weeks. Despite its development as a chemotherapeutic agent, MTX is remarkably safe and well tolerated for treating arthritis, likely because doses are 500- to 1000-fold lower than those used in malignancies. Furthermore, its convenient onceweekly dosing tends to promote compliance. Liver toxicity is the major potential side effect, of greatest concern in those who drink alcoholic beverages. Less serious gastrointestinal adverse effects, especially nausea and mucositis, may be dose limiting, although they generally respond to folic acid supplementation or leucovorin rescue. In addition, methotrexate is a potent teratogen, necessitating careful discussion of contraception with adolescent patients. Overall, however, longterm toxicity continues to be rare, even after use in hundreds of thousands of children over several decades. The oldest DMARD is sulfasalazine, formulated in the 1930s as the first designer drug for the treatment of arthritis from the only two antirheumatic compounds then avail-

CBC periodically; sole biologic approved by FDA for children CBC periodically; use with low-dose MTX to inhibit antibodies against drug CBC periodically

able—aspirin and an antibiotic. Although cumulative toxicity is minimal, up to 1 in 1000 patients treated with this sulfa drug develops a hypersensitivity reaction, and 1 in 40,000 develops full-blown Stevens-Johnson syndrome. Other toxicity includes leukopenia, abdominal pain, headaches, fatigue, and (rarely) seizures. Despite this, the medication is quite effective in pauciarthritis or mild polyarthritis, and it has synergistic effects when used with methotrexate. It may take up to 8 weeks to demonstrate significant benefit, but this may be an acceptable time frame in children with mild disease. It must be avoided in systemic-onset JRA, where it is associated with up to a 20% incidence of severe hepatotoxicity (macrophage activation syndrome). Recommended monitoring of children receiving sulfasalazine includes periodic checks of blood counts and liver function tests, more frequently at the start of therapy. Antimalarial medications, of which the most prominent is hydroxychloroquine (Plaquenil), were noted serendipitously to have beneficial effects on arthritis and other autoimmune diseases. A controlled trial in JRA did not demonstrate benefit from hydroxychloroquine, possibly because subjects were not stratified by disease subtype or severity.24 Nonetheless, the agent appears to be useful in mild cases of arthritis, often in conjunction with methotrexate. Hydroxychloroquine is generally well tolerated, but it may cause rash, gastrointestinal upset, myopathy, or agranulocytosis, among other side effects. The major toxicity is eye disease (maculopathy), but this is extremely rare as long as doses are kept below 7 mg/kg/day. Ophthalmological screening every

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

6 months allows the medication to be discontinued before irreversible changes occur in those rare children who do develop ocular complications of hydroxychloroquine. Biological Response Modifiers An exciting new frontier in antirheumatic therapy is specific targeting of proinflammatory immune mediators central to the pathogenesis of arthritis. These agents have been called “biologics” because they are engineered biotechnologically rather than chemically. Although very effective, they are extremely expensive, generally over $10,000 per patient per year. The first molecules to be targeted by commercially available agents have been the cytokines tumor necrosis factor alpha (TNF-α) and interleukin-1. Agents directed against specific cells and cell-surface receptors that orchestrate the autoimmune attack on joints are currently being evaluated. Etanercept, a fusion protein composed of a modified receptor for TNF-α, was the first biological agent studied in children. In a double-blind, randomized, placebo-controlled trial, twice-weekly injections of etanercept benefited 74% of children with methotrexate-resistant JRA.25 An increased risk of infection is one of the potential side effects of etanercept. There is evidence in early adult rheumatoid arthritis that etanercept slows radiographic progression of disease. Formal studies of the other TNF inhibitors in the JRA population, including infliximab and adalimumab, are ongoing. To date, risks and benefits of these agents appear to be similar. They differ mainly in their frequency (biweekly to monthly) and method of administration (intramuscularly, subcutaneously, or intravenously). Adjunct Therapies In addition to medications directed against the underlying synovial inflammation, children with JRA generally require physical therapy to regain full strength and function. Arthritis of the knee causes pain as a result of stretching of the joint capsule by synovial fluid. A position of about 30 degrees flexion provides the maximum volume and therefore the minimum capsular stretching, so children prefer moderate flexion when they have knee synovitis; full flexion or extension are most painful. The vastus medialis muscle provides the final 5 degrees of extension, and this is the first to atrophy when splinting of the knee due to synovitis leads to a joint contracture. Aquatic therapy in a heated pool is particularly helpful early in the course, because it allows for effective therapy without requiring impact on the inflamed joint. Patients are transitioned to land therapy as the knee improves. Nighttime splinting and serial casting are sometimes used in severe flexion contractures to maximize extension. In the setting of significant leg-length discrepancies, children may require shoe lifts. Rarely, surgical correction of flexion deformities or leg-length discrepancies may be necessary, although these generally resolve spontaneously provided that sufficient potential for growth remains at the time that the synovitis is controlled. Outcomes For many years pediatricians reassured families (and themselves) by promising that most children outgrow their arthritis. In fact, the truth is nearly opposite this false hope.

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Most children with arthritis continue to have active disease well into adulthood.26 Using Kaplan-Meier survival curves, remission rates are 38% for systemic onset JRA, 54% for pauciarticular JRA, and 15% for polyarticular disease at 10 years. Furthermore, even patients who do achieve full remissions may have disease flares after several years of health. Clearly, aggressive, long-term follow-up and management are essential for this treatable but incurable disease. In fact, giving up the vain expectation that a child with juvenile arthritis will spontaneously improve has resulted in significant improvements in outcomes over the past 30 years. In the 1970s, the percentage of polyarticular JRA patients with at least some difficulty caring for themselves (i.e., Steinbrocker Class III or KEY POINTS IV) was estimated at 15–20%; in the 1990s, this percentage was 1. Children with JRA reported at 5–12%. For systemic who are treated JRA, the 1970s found 22–40% early and aggresin Class III or IV; in 2000, there sively have the best were reports of 19% and 29%. prognosis. Quantifying disability in a child 2. Although NSAIDs with a single swollen knee is parmay be used for the ticularly difficult, but similar short-term control improvements appear to be of symptoms, use of occurring in pauciarthritis. DMARDs or biologic Thus, Class III and IV rates of response modifiers 8–14% were reported in the to completely con1970s, whereas no patients were trol articular inflamreported to be in Class III or IV mation is most likely 27 in 1984. This is encouraging to prevent chronic but certainly not adequate; joint damage from milder disabilities still greatly arthritis.27 affect a child’s daily life. Lyme Disease Lyme disease (LD) is the most common vector-borne illness reported in the United States. It is caused by the spirochete Borrelia burgdorferi, which is transmitted to mammals by the Ixodes species of ticks. In the life cycle of B. burgdorferi, humans are incidental hosts. Cutaneous manifestations of LD have been recognized in Europe since 1883, and neurological manifestations have been appreciated since 1922. However, the modern history of LD—particularly its association with arthritis—began in Old Lyme, Connecticut, when an unusual clustering of arthritis was reported to the Connecticut State Department of Health in 1975. Since implementation of surveillance by the Centers for Disease Control and Prevention (CDC) in 1982, the number of reported cases of LD has risen steadily. In 2000, 17,730 cases were reported to the CDC (incidence 6.3/100,000), an 8% increase from 1999 (16,273 cases).28 Hidden within the national statistics are significant regional and demographical differences in the incidence of LD. As many as 95% of cases occur in 12 states in the northeast, mid-Atlantic, and north-central regions (Connecticut, Rhode Island, New Jersey, New York, Delaware, Pennsylvania, Massachusetts, Maryland, Wisconsin, Minnesota, New Hampshire, and Vermont). In all areas, children aged 5–9 years have the highest attack rate (9.3/100,000), followed by adults aged 50–59 years (8.2/100,000).

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Clinical manifestations of LD vary by the stage of the infection. Acute LD is characterized by the pathognomonic rash, erythema migrans (formerly erythema chronicum migrans). The typical erythematous ring with central clearing (“bull’s-eye”) starts at the site of the tick bite, usually by the end of the first week following the bite. Patients with early LD also may have regional lymphadenopathy and nonspecific flu-like constitutional symptoms. By the time a child develops arthritis related to LD, the infection has progressed from acute or localized to disseminated disease. Arthritis is the most common late manifestation of LD, occurring in more than 50% of untreated patients. Lyme arthritis predominantly affects large joints, particularly the knee in approximately 90% of cases.29 Other joints less commonly affected include hips, ankles, shoulders, elbows, and wrists; it is uncommon for the small joints of the hands and feet to be involved. Joints affected by Lyme arthritis may be massively swollen but are rarely erythematous or particularly painful. Arthritis may occur as early as 1 month or as late as 12 months after the initial infection. Lyme arthritis may follow one of several different patterns, the most characteristic being intermittent episodes of joint swelling lasting 1–2 weeks interspersed between asymptomatic periods. Approximately one third of children with Lyme arthritis, however, present with a clinical picture mimicking acute septic arthritis, including fever, local erythema, and high white blood cell counts in the synovial fluid.30 An additional 10% of children will present with a chronic pattern of joint involvement indistinguishable from pauciarticular JRA (Figure 30–3). Less than 5% of Lyme arthritis in children is polyarticular in nature, and a similarly low percentage of patients present with a migratory course.31 The leukocyte counts in synovial fluid analysis of Lyme arthritis can vary between 2000 and 100,000 cells/mm3, with higher cell counts typically seen in the pseudoseptic form. Neutrophils generally predominate, although Lyme arthritis may also exhibit a significant number of eosinophils in the synovial fluid. The synovial pathology of Lyme arthritis is

Figure 30–3 Acute Lyme arthritis. A 6-year-old boy presented with an acute monoarthritis and underwent arthroscopic debridement. The entire right lower extremity (including the thigh, knee, and lower leg) remains swollen following the procedure.

similar to that of JRA, with villous hypertrophy, synovial cell hyperplasia, and inflammatory cell infiltration. Pannus formation and erosive cartilage changes are also reported. Imaging is usually nonspecific with evidence of soft-tissue swelling. MRI demonstrates synovitis; inflammation of surrounding soft tissues may be more diffuse than is seen typically in other causes of inflammatory arthritis (Figure 30–4). Between 5% and 10% of children with Lyme arthritis develop recurrent or persistent synovitis, even after receiving adequate antimicrobial treatment. Diagnosis For CDC reporting purposes, the case definition of LD is an illness consisting of either physician-diagnosed erythema migrans >5 cm in diameter or at least one manifestation of disseminated disease (involvement of the musculoskeletal, neurologic, or cardiac system), plus laboratory confirmation of infection.32 Because most people do not make an antibody response during the first month after a tick bite, early LD is typically a clinical diagnosis. Nonetheless, if there is strong clinical suspicion of acute LD, comparison of acute and convalescent sera may be helpful. The CDC currently recommends a two-tiered testing approach for serological confirmation of Lyme disease. The first level of testing is an antibody screen using an enzyme immunoassay or immunofluorescent assay. If the antibody screen is negative, no further testing is generally required;

Figure 30–4 MRI findings in acute Lyme disease. Oblique sagittal T2 image with fat suppression was acquired after administration of 5 ml of gadolinium to the child shown in Figure 30–3. There is a moderate joint effusion with synovial hypertrophy and enhancement. The effusion extends into the posterior joint capsule with mild bowing of the anterior cruciate ligament. Inflammatory changes are also seen within Hoffa’s infrapatellar fat pad. Prepatellar and infrapatellar fatpad edema as well as enhancement within the interstices of the quadriceps tendon are also shown. (Courtesy of Kirsten Ecklund, MD.)

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

despite much concern among lay people, so-called seronegative Lyme disease is extremely rare and seldom warrants consideration. In disseminated or late LD in particular, patients typically have serological evidence of an antiBorrelia antibody response. Viral illnesses and autoimmune conditions may result in false-positive antibody screens, so positive Lyme titers should be followed up by a confirmatory immunoblot assay. The IgM immunoblot is considered positive if at least two or three significant bands are present; the IgG immunoblot is considered positive if at least five of 10 significant bands are detected. It should be noted that approximately one third of children with Lyme arthritis have a low-titer positive ANA, which can increase difficulty in distinguishing between LD and JRA. Therefore, if a child with arthritis has both a positive ANA and positive Lyme serologies, the approach should be to treat for Lyme arthritis first, and to consider alternative diagnoses only after the child has received adeKEY POINTS quate antibiotic therapy. Treatment The mainstay of treatment for LD is antibiotics, the route and duration of which are determined by the stage and severity of disease (Table 30–4).33 Lyme arthritis is a late manifestation of Borrelia infestation, so treatment for disseminated disease is recommended. Antibiotics are generally given by the oral route first (doxycycline in children 8 years of age or older, amoxicillin in those younger). If arthritis persists, intravenous therapy is usually indicated. NSAIDs may be helpful adjunct agents, whereas physical therapy is often essential for helping children regain full strength and mobility

Table 30–4

1. Lyme disease affects approximately 20,000 people annually in the United States. 2. Diagnosis of Lyme disease requires a characteristic manifestation of disseminated disease, such as monoarthritis, with confirmatory serological evidence of borrelial infection. 3. Antibiotic treatment results in a complete cure of Lyme arthritis in 95–98% of cases.

Treatment for Lyme Arthritis Treatment

Initial diagnosis Age ≥8 years Age <8 years Persistent/ recurrent

Doxycycline 100 mg po BID for 28 days Amoxicillin 25-50 mg/kg/d PO divided BID, (maximum 2 g/d) for 28 days Ceftriaxone 75-100 mg/kg IV/IM qday (maximum 2g/day) for 14-28 days Penicillin 300,000 U/kg/d IV divided q4hr (maximum 20 million U/day) for 14-28 days For patients who are allergic to penicillin, cefuroxime axetil and erythromycin are alternative options.

Modified from American Academy of Pediatrics, Lyme disease. In Red Book: 2003 Report of the Committee on Infectious Diseases. 26th edition. Pickering LK (ed). Elk Grove Village, IL: American Academy of Pediatrics, 2003: 411.

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following Lyme arthritis. The infrequent cases in which arthritis persists, even after adequate antibiotic therapy, appear to have a self-perpetuating autoimmune process similar to JRA and other chronic arthritides. Therapeutically, the goal is the same as for treatment of JRA: complete resolution of the arthritis, resumption of full and normal function, and prevention of chronic joint changes. In general, the prognosis for adequately treated Lyme arthritis in children is excellent.34 Summary Chronic arthritis (JRA) is now the most common rheumatic disease of children in the developed world, having replaced acute rheumatic fever during the past 20 years. It occurs in all races and ethnic groups, and in the United States alone may affect as many as 100,000 children.35 Whether caused by Lyme disease, rubella infection, or undefined genetic and environmental factors, the major goal of therapy of childhood arthritis is to help the children and their families maintain as normal a life as possible. Because most children with arthritis are referred first to orthopedists, recognition of inflammatory joint disease best treated medically, not surgically, is essential. Expeditious and accurate diagnosis allows the synovitis to be treated before chronic joint damage occurs. Whether this involves appropriate antibiotics for Lyme arthritis, disease modifying agents for JRA, or novel biological response modifiers for recalcitrant joint inflammation, few if any children should suffer chronic consequences of arthritis. Emotional support, including the information that most children with this disease recover with minimal residual problems, adds reassurance to this prescription. Although high-impact activities must be avoided, participation in normal activities, including competitive sports, further reaffirms the message that a child with arthritis is not “abnormal.” Working with pediatric rheumatologists, physiatrists, physical therapists, and parents, pediatric orthopedic surgeons can help ensure the continued joint health of children with arthritis. References 1. Manners PJ, Bower C: Worldwide prevalence of juvenile arthritis— Why does it vary so much? J Rheumatol 29:1520–1530, 2002. 2. Falcini F, Cimaz R: Juvenile rheumatoid arthritis. Curr Opin Rheumatol 12:415–419, 2000. 2a. Hofer M, Southwood TR: Classification of childhood arthritis. Best Pract Res 16:379–396, 2002. 3. Bywaters EGL: Pathologic aspects of juvenile chronic polyarthritis. Arthritis Rheum 20:271–276, 1977. 4. Wynne-Roberts CR, Anderson CH, Turano AM, et al: Light- and electron-microscopic findings of juvenile rheumatoid arthritis synovium: comparison with normal juvenile synovium. Sem Arthritis Rheum 7:287–302, 1978. 5. Chung C, Coley BD, Martin LC: Rice bodies in juvenile rheumatoid arthritis. AJR:698–700, 1998. 6. McGhee JL, Burks FN, Sheckels JL, et al: Identifying children with chronic arthritis based on chief complaints: absence of predictive value for musculoskeletal pain as an indicator of rheumatic disease in children. Pediatrics 110:354–359, 2002. 7. Eichenfield AH, Athreya BH, Doughty RA, et al: Utility of rheumatoid factor in the diagnosis of juvenile rheumatoid arthritis. Pediatrics 78:480–484, 1986. 8. Cassidy J, Martel W: Juvenile rheumatoid arthritis: clinicoradiologic correlations. Arthritis Rheum 20:207–211, 1977.

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9. Martel W, Holt JF, Cassidy JT: Roentgenologic manifestations of juvenile rheumatoid arthritis. Am J Roentgenol 88:400–423, 1962. 10. Johnson K, Wittkop B, Haigh F, et al: The early magnetic resonance imaging features of the knee in juvenile idiopathic arthritis. Clin Radiol 57:466–471, 2002. 11. Gylys-Morin VM, Graham TB, Blebea JS, et al: Knee in early juvenile rheumatoid arthritis: MR imaging findings. Radiology 220:696–706, 2001. 12. Herve-Somma CMP, Sebag GH, Prieur AM, et al: Juvenile rheumatoid arthritis of the knee: MR evaluation with Gd-DOTA. Radiology 182:93–98, 1992. 13. Eich GF, Halle F, Hodler J, et al: Juvenile chronic arthritis: imaging of the knees and hips before and after intraarticular steroid injection. Ped Radiol 24:558–563, 1994. 14. El-Miedany YM, Housny IH, Mansour HM, et al: Ultrasound versus MRI in the evaluation of juvenile idiopathic arthritis of the knee. Joint Bone Spine 68:222–230, 2001. 15. Murray KJ: Advanced therapy for juvenile arthritis. Best Pract Res Cl Rh 16:361–378, 2002. 16. Ilowite NT: Current treatment of juvenile rheumatoid arthritis. Pediatrics 109:109–115, 2002. 17. Turvey SE, Sundel RP: Autoimmune diseases. In Leung DYM, Sampson HA, Geha RS, Szefler SJ (eds): Pediatric Allergy: Principles and Practice. St. Louis: Mosby, 2003, pp 159–169. 18. Sherry DD, Stein LD Reed AM, et al: Prevention of leg length discrepancy in young children with pauciarticular juvenile rheumatoid arthritis by treatment with intraarticular steroids. Arthritis Rheum 42:2330–2334, 1999. 19. Huppertz HI, Tschammler A, Horwitz AE, et al: Intraarticular corticosteroids for chronic arthritis in children: Efficacy and effects on cartilage and growth. J Pediatr 127:317–321, 1995. 20. Cleary AG, Murphy HD, Davidson JE: Intra-articular corticosteroid injections in juvenile idiopathic arthritis. Arch Dis Child 89:192–196, 2003. 21. Dent PB, Walker N: Intra-articular corticosteroids in the treatment of juvenile rheumatoid arthritis. Curr Opin Rheumatol 10:475–480, 1998.

22. Fleischmann R: Safety and efficacy of disease-modifying antirheumatic agents in rheumatoid arthritis and juvenile rheumatoid arthritis. Expert Opin Drug Safety 2:347–365, 2003. 23. Chan ES, Cronstein BN: Molecular action of methotrexate in inflammatory diseases. Arthritis Res 4:266–273, 2002. 24. Brewer EJ, Kuzmina N, Alekseev L: Penicillamine and hydroxychloroquine in the treatment of severe juvenile rheumatoid arthritis. Results of the U.S.A.–U.S.S.R. double-blind placebo-controlled trial. N Engl J Med 314:1269-1276, 1986. 25. Lovell DJ, Giannini EH, Reiff A, et al: Etanercept in children with polyarticular juvenile rheumatoid arthritis. Pediatric Rheumatology Collaborative Study Group. New Engl J Med 342:763–769, 2000. 26. Fantini F, Gerloni V, Gattinara M, et al: Remission in juvenile chronic arthritis: A cohort study of 683 consecutive cases with a mean 10 year followup. J Rheumatol 30:579–584, 2003. 27. Oen K: Long-term outcomes and predictors of outcomes for patients with juvenile idiopathic arthritis. Best Pract Res Cl Rh 16:347–360, 2002. 28. Orloski KA, Hayes EB, Campbell GL, et al: Surveillance for Lyme disease-United States, 1992-1998. MMWR 49:1–11, 2000. 29. Athreya BH, Rose CD: Lyme disease. Curr Prob Ped 26:189–207, 1996. 30. Willis AA, Widmann RF, Flynn JM, et al: Lyme arthritis presenting as acute septic arthritis in children. J Ped Orthoped 23:114–118, 2003. 31. Gerber MA, Zemel LS, Shapiro ED: Lyme arthritis in children: Clinical epidemiology and long-term outcomes. Pediatrics 102:905–908, 1998. 32. Centers for Disease Control: Recommendations for test performance and interpretation from the Second National Conference on Serologic Diagnosis of Lyme Disease. MMWR 44:590–591, 1995. 33. American Academy of Pediatrics: Lyme disease (Borrelia burgdorferi). 2000 Red Book: Report of the Committee on Infectious Diseases. Elk Grove Village, Ill.: American Academy of Pediatrics, 2000, pp 374–379. 34. Wang TJ, Sangha O, Phillips CB, et al: Outcomes of children treated for lyme disease. J Rheumatol 25:2249–2253, 1998. 35. Gare BA: Juvenile arthritis—who gets it, where and when? A review of current data on incidence and prevalence. Clin Exp Rheumatol 17:367–374, 1999.

Chapter 31

Complex Regional Pain Syndrome and Other Forms of Neuropathic Pain in Children and Adolescents Charles B. Berde

Neuropathic pain conditions are those associated with injury, dysfunction, or altered excitability of portions of the peripheral, central, or autonomic nervous system.1 Implied in this definition is that the painful sensation is not nociceptive; that is, pain persists independent of ongoing tissue injury or inflammation. In this chapter, we review (1) biological bases of persistent neuropathic pain, (2) clinical diagnostic evaluation of patients with neuropathic pain, (3) general approaches to treatment, (4) epidemiology, and (5) clinical features of common neuropathic pain conditions in childhood. Nociceptive pain refers to pain associated with acute tissue injury or acute inflammation. Nociceptive pain is an expected result of tissue injury. It is associated with normal neural transmission, well-localized, and usually resolves with healing. Conversely, when the somatosensory system is damaged, sensory loss—a negative symptom—may be accompanied by unexpected positive sensations and either spontaneous or evoked pain. Animal studies and human psychophysical and functional magnetic resonance imaging (fMRI) studies indicate that different forms of neuropathic pain may reflect different patterns of plasticity and altered excitability in peripheral nerve, dorsal root ganglia, autonomic fibers, spinal cord, or the brain. Chronic nociceptive stimulation of the peripheral and central nervous system, as occurs with chronic infection, arthritis, and chemical irritation of peripheral tissues, may also ultimately produce sustained pain and altered excitability in the peripheral and central nervous systems with some features in common with neuropathic injury. Common clinical characteristics of neuropathic pain disorders are summarized in Box 31–1.

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Senthilkumar Sadhasivam

Common clinical sensory features of neuropathic pain are cutaneous hypesthesia; hyperalgesia (lowered sensory threshold) to noxious, thermal, and mechanical stimuli; allodynia (when a normally nonnoxious stimulus, such as light touch, produces pain); and hyperpathia (summation of stimuli ultimately reduce threshold and intensify response). Associated features may include neurogenic inflammation, autonomic dysregulation, and motor phenomena such as dystonia and weakness. Failure to understand that neuropathic pain may persist despite healing of a site of surgery or trauma has commonly led clinicians to falsely diagnose malingering or somatoform disorders. In general, invoking psychogenic causation of pain should be based on positive evidence, not solely on the basis of exclusion of ongoing tissue injury or inflammation. Psychological factors more commonly influence how patients cope with pain and how much pain impacts on their functioning; psychogenic causation is relatively less common. Nociceptive pains are often protective in the sense that they may protect the subject from further damage to tissues. In the absence of nociceptive sensation, patients might walk too soon after a fracture or a sprain, for example. In contrast, neuropathic pain rarely serves to keep the subject from harm because it involves erroneous generation and transmission of information. The pain is just as “real” as the pain of fractures and sprains, so it is a challenge to clinicians to convince patients and their parents that it is generally not injurious to move or bear weight on an extremity with 473

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Box 31–1 Common Features of Neuropathic Pain Conditions Pain descriptors Burning, electrical, stabbing, shooting Spontaneous pain as well as evoked pain Sensory disturbances Allodynia, hyperpathia/hyperalgesia Dysesthesias, paresthesias Focal sensory deficits in some or all modalities Hypersensitivity to cold Motor findings Spasms, dystonia, tremor Fasciculations, weakness, atrophy Autonomic disturbances Cyanosis, erythema, mottling Increased sweating, swelling Poor capillary refill

neuropathic pain because of the difference between protective and nonprotective pain. Mechanisms

KEY POINTS 1. Neuropathic pain refers to pain due to abnormal excitability in nerves. 2. Neuropathic pain is often characterized by allodynia, paresthesias, and sensory changes. It is often nonprotective and may persist despite healing of the original injury.

The mechanisms that generate or perpetuate neuropathic pain are varied and complex. Injuries to peripheral nerves may involve crush, transection, compression, demyelination, axonal degeneration, inflammation, ischemia, or a variety of other processes. For a detailed discussion of the pathophysiology of damaged nerve, see Devor.2 The loci of increased excitability following peripheral nerve transection, for example, may include several levels in the nervous system, including axon sprouts or neuroma at the cut end of the nerve, the dorsal root ganglion cell bodies, cell bodies in the spinal dorsal horn, or a variety of more rostral sites in the central nervous system. The pathophysiological mechanisms associated with chronic inflammatory (nociceptive) and neuropathic pain are now being elucidated through basic science at a molecular level. This new understanding is just starting to produce novel clinical therapies, targeting cloned ion channel proteins, neurotrophins3 and their receptor sites, cytokines and other inflammatory mediators of hyperalgesia,4 and specific opioid receptor subtypes. Central sensitization is the pathophysiological hallmark of neuropathic pain. It is defined by a variety of nociceptive mechanisms involving molecules, receptors, and neural networks that produce neuronal plasticity, a neuronal reorganization within the central nervous system following peripheral tissue damage or nerve injury.5 Central sensitization can be initiated by sustained C-fiber discharge projecting to the superficial layers of the dorsal horn. These nociceptive fibers produce slow excitatory postsynaptic potentials that, when summated, induce “wind-up” in central pain projection neurons. C-fiber noci-

ceptor discharge is increased by both inflammatory and neuropathic processes. Soft-tissue injury releases algesic molecules (bradykinins, ATP, hydrogen ions) and induces cytokines and prostanoids. Soft-tissue and neural injury increase local production and retrograde transport of nerve growth factors (tumor necrosis factor alpha, nerve growth factor, leukemia inhibitory factor), which alter dorsal root ganglion (DRG) and dorsal horn function, and ion channel induction and expression. Other mechanisms that induce central neural changes include ectopic firing of DRG cells and neurites, proliferation of DRG satellite cells, phenotypic change of afferent A-beta fibers and DRG cells with changes in gene expression of sodium channels and neuropeptides in the nociceptive terminals and DRG. Within the dorsal horn, sustained C-fiber input decreases the magnesium blockade of the activity-dependent N-methyl D-aspartate (NMDA) receptor in association with increased intracellular calcium influx. Calcium-dependent second messenger cascades perpetuate central pain transmission neuron activity. A-delta fiber activation depresses analgesic, inhibitory, gamma aminobutyric acid (GABA), and glycinergic interneurons in lamina II. Recent animal studies suggest a plausible mechanism for allodynia (pain evoked by light touch). When peripheral nerves are partially injured, there is sprouting of new neurites not only distally at the site of injury, but also at the proximal terminals of sensory fibers in the spinal dorsal horn. A-beta fibers that are activated by light touch send new projections, which synapse on cell bodies in the superficial laminae I and II of the dorsal horn. Laminae I and II cell bodies normally receive most of their inputs from C-fibers and A-delta fibers involved in pain transmission. These cell bodies give rise to axons that travel rostrally in the anterolateral spinothalamic tract, a primary afferent pain transmission pathway in the spinal cord. Through this pathway, there is now a means after nerve injury whereby light touch can evoke transmission in A-beta fibers, which (through these new spinal synaptic connections) can produce afferent activity in spinal ascending pain pathways. Chronic pain in animal models can also be mediated via death of inhibitory interneurons in lamina II in the dorsal horn, increasing central pain transmission and limiting pharmacological efficacy. Concurrent with central sensitization, gene expression of ion channels and neuropeptides is altered at nociceptive terminals and the DRG. Immediate early genes regulating opioid receptor classes and peptides are also altered. This complex array of pain mechanisms following focal injury, made more complicated following multifocal and variable injury, may explain the comparatively poor success with medication management and regional nerve blockade in chronic pain states.6 Although central sensitization is commonly associated with persistently increased peripheral afferent activity, particularly in C-fibers, it is sometimes (but not always) dynamically maintained by ongoing peripheral hyperexcitability.7 An essential and potent descending analgesic system originates in the midbrain periaqueductal gray.8 This pathway is densely populated with endogenous opioids, opioid receptors, and analgesic biogenic amines (norepinephrine and serotonin). It projects to the rostral ventromedial medulla and spinal dorsal horn. It is modulated by input

Complex Regional Pain Syndrome and Other Forms of Neuropathic Pain in Children and Adolescents

from the prefrontal and insular cortex, cingulate cortex and amygdala, hypothalamus, reticular formation, and locus ceruleus. The rostral ventromedial medulla has two major neuronal populations—on-cells and off-cells—both projecting to laminae I, II, and V of the spinal cord. On-cells are inhibited and off-cells are activated by morphine.9 Offcells contribute to constitutive descending facilitation of responsiveness to pain. Much of the mechanistic KEY POINTS study of neuropathic pain has initially focused on periph1. Neuropathic pain eral, spinal, and brainstem may involve a combimechanism, in part because of nation of peripheral, the ability to study identified autonomic, spinal, groups of neurons in animal and supraspinal models using electrophysiologmechanisms. ical and immunohistochemical 2. Future research may techniques. It is apparent, better clarify the however, that nerve injury also roles of multiple sites generates plastic changes in in generation and 10 higher brain structures, perpetuation of neuincluding thalamus and priropathic pain and mary sensory cortex, but also a may guide improved variety of brain regions therapies, both pharinvolved in emotion and macological and attention. Recent work using nonpharmacological. 11,12 fMRI, positron-emission tomography,13 and magnetic source imaging has documented some of these changes; examples will be described next. Diagnostic Approach Careful history and physical examination is essential to diagnostic evaluation. Classically, adults with neuropathic pains often describe their pain as burning, shooting, or electrical. Children may provide similar descriptors, but we have been impressed with the wide variety of descriptors used. The history should include a detailed description of the inciting event or injury when present. Along with a history of the presenting complaint, a broad-based assessment of the impact of the pain on individual and family functioning is important. Neurological examination should be thorough and systematic. It is important to establish the overall integrity of neurological functioning by evaluation of motor, sensory, cerebellar, cranial nerve, reflex, cognitive, and emotional functioning. Although the clinician may regard the causes of pain as obvious from the history, thorough examination is mandatory to avoid missing uncommon but severe conditions, including malignancies and degenerative disorders. Commonly, evaluation for strength may be limited by pain, and careful and repeated evaluation may be needed to distinguish true deficits from limitations due to pain. Sensory examination should establish dermatomal deficits and abnormalities in distinct sensory modalities, including light touch, pinprick, temperature sense, and proprioception. The term hyperalgesia is used to mean an increased sensitivity to pain (a left-shifted stimulus-response curve). Allodynia, as noted previously, refers to normally innocuous stimuli (such as light stroking of the skin) pro-

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voking intense pain. Allodynia is an extremely significant clinical sign supporting the diagnosis of neuropathic pain. Although marked sensitivity to touch may be associated with conditions that injure the skin directly (e.g., obvious burns), allodynia in the absence of severe skin pathology generally implies disordered sensory processing. Deep-tissue pathology affecting bones, joints, and muscles cannot account for allodynia. A considerable percentage of children with complex regional pain syndromes (see below) exhibit mechanical allodynia and hyperalgesia to cold in a distribution that crosses peripheral portions of several dermatomes and instead involves a “stocking” or “glove” distribution of the affected limb. In these cases, a nondermatomal distribution does not imply psychogenic pain, somatization, or conversion disorder. Conversely, some patients with truly psychogenic conditions may have distress with light touch that can be mistaken for true allodynia. The sensory exam may be quantified with formal quantitative sensory testing (QST)14,15 using a computer-assisted device that measures subjective sensory thresholds to detection of cool and warm sensation, minimally painful hot and cold sensation, and vibration. A-delta fibers respond to cool stimuli, pinprick, and cool/heat pain. C-fibers respond to heat stimuli and cool/heat pain. A-beta fibers respond to vibration and touch stimuli. QST may be useful to confirm impressions from clinical examination suggestive of sensory fiber dysfunction (numbness, allodynia, hyperalgesia, summation). It is particularly useful in pediatric practice because it is noninvasive and painless, thus eliminating the need for sedation. Nerve conduction studies (NCS) measure the amplitude and velocity of compound action potentials in myelinated large- and medium-sized nerve fibers. Conduction velocities are generally abnormal in hereditary sensorymotor neuropathies and severe, nonselective nerve injury. However, they may be unaffected in small fiber neuropathies because with standard recording techniques, the amplitudes of compound action potentials from A-delta and C-fibers are undetectably small relative to the amplitudes from A-beta fibers. A normal NCS does not exclude the diagnosis of neuropathy or neuropathic pain. Nerve conduction studies are generally performed in conjunction with electromyographic studies (EMGs), which detect potentials in muscle. EMGs are useful for objective demonstration of dysfunction arising in muscle, at the neuromuscular junction, or due to denervation injury. Sedation may be required for NCS/EMGs in some children, due to pain or anxiety associated with electrical stimulation. Appropriate choices with mild effect on baseline nerve conduction include benzodiazepines, nitrous oxide, and barbiturates. Other diagnostic testing for selected patients with suspected neuropathy may include somatosensory-evoked potentials; local and systemic autonomic evaluation, including laser Doppler fleximetry to assess capillary flow in affected limbs with sympathetic dysfunction16; tilt-table testing for orthostatic intolerance; cardiac R–R interval variability; and quantitative measurement of sudomotor function. If the history and exam suggest metabolic or toxic neuropathy, then specific studies may be obtained for toxins (e.g., heavy metals), metabolic abnormalities (e.g., vitamin

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B12 deficiency, thyroid dysfunction, storage diseases), or other biochemical abnormalities. Extremity pain with neuropathic features and Raynaud’s phenomenon may be an early finding in some children with vasculopathies; rheumatological consultation is advisable if clinical evaluation is suggestive of these disorders. Epidemiology

KEY POINTS 1. History and physical exam are the best guides to diagnosis of neuropathic pain. 2. Additional specific tests should be guided by the particular clinical setting. 3. Allodynia, in the absence of skin pathology, should alert the clinician to the possibility of neuropathic pain.

The incidence of neuropathic pain in adults is estimated between 0.6% and 1.4% (based on a U.S. population of 270 million) and includes the following, in order of most frequent to least frequent diagnoses: diabetic neuropathy, postherpetic neuralgia, cancerassociated causalgia and reflex sympathetic dystrophy (CRPS I and II), spinal cord injury, phantom pain, multiple sclerosis, stroke, HIV-associated peripheral nerve disease (Guillain-Barré, lead and other toxic neuropathies, vasculitis), and trigeminal neuralgia. Other mixed disorders, such as low back pain with a neuropathic component due to arachnoiditis, would increase these estimates substantially. Several forms of recurrent pain are common among children, including recurrent headaches, limb pain, and abdominal pain. These complaints are generally episodic, with painful episodes alternating with pain-free periods in a child who is otherwise medically well and growing appropriately. In contrast, chronic or persistent daily pain is relatively less common in children. A recent review of the epidemiology of chronic and recurrent pain in children17 presents the following prevaKEY POINTS lence data for several chronic or recurrent painful disorders: 1. Neuropathic pain arthritis, 3–460/100,000; sickleoverall is more comcell disease, 28–120/100,000; mon in adults than limb pain, 4.2–33.6%; knee pain, in children. 3.9–18.5%; recurrent abdominal Disorders such as pain, 6–15%; nonmigraine diabetic neuropathy, headache, 6.3–29%. postherpetic neuralIn contrast, the incidence gia, and trigeminal and prevalence of neuropathic neuralgia are quite pain conditions in children and rare in children. adolescents is unknown because 2. Post-traumatic population-based epidemiologiperipheral neurocal studies are largely unavailpathic pain is able. Several conditions that are commonly seen by common in adults—such as diapediatric orthopedic betic peripheral neuropathy, surgeons and is a trigeminal neuralgia, postcommon cause of herpetic neuralgia, and stroke— referral to our pediare quite rare among children. atric pain clinic, At the Pain Clinic at although relatively Boston Children’s Hospital, rarely seen by any painful disorders with a neuroindividual general pathic component comprise pediatrician. more than 30% of outpatient

referrals. Among these patients, the more common neuropathic conditions include posttraumatic and postsurgical peripheral neuropathic pains, complex regional pain syndromes types 1 and 2 (see below), and neuropathic pain due to tumor involvement of the peripheral or central nervous system. Metabolic and toxic neuropathies, neurodegenerative disorders, and pain following central nervous system injury are all seen, but with a lower frequency than the previous group of conditions. It is hoped that, in the future, large-scale population-based epidemiological studies of neuropathic pain will be conducted. General Considerations for Treatment of Neuropathic Pain The management of neuropathic pain may be frustrating for patients and their caregivers. Much of the treatment involves trial and error, titration of medications as limited by side effects, and weighing of risks and benefits. Because of these difficulties, it becomes especially important to develop a solid therapeutic alliance with patients and their parents. Functional rehabilitaKEY POINTS tion with return to school or work and palliation are often the 1. Different therapies treatment goals. In some condifor neuropathic pain tions, pain will resolve with work for different healing over periods of weeks patients; and months; in others, longapproaches should term pain persists despite a range be individualized. of interventions, and the goal 2. Functional rehabilibecomes amelioration rather tation is as importhan cure. tant a goal as relief Psychological/CognitiveBehavioral Treatments for Neuropathic Pain Many patients with neuropathic pain, in our experience, benefit from relaxation training, biofeedback training, and structured counseling regarding coping strategies and stress management. Supportive individual or family counseling has provided great benefit to many patients. School avoidance, depression, alexithymia, anxiety, and family dysfunction are common and require active intervention. Some patients or their parents have a concept of illness or impairment that may be roughly summarized as “stay out of school until you are all better.” Although this may be appropriate for brief febrile illnesses, it generally counterproductive for most forms of chronic pain, and this pattern of belief can amplify or perpetuate a disabled condition. It is in most

of pain. 3. Most children with neuropathic pain improve with a noninvasive regimen that emphasizes functional rehabilitation. 4. Cognitivebehavioral interventions should be considered more widely; they have demonstrated efficacy for a range of chronic pain conditions in adults and children. 5. There is a need for additional controlled clinical trials to evaluate safety, efficacy, and cost-to-benefit ratios for a variety of treatments of neuropathic pain, both in adults and in children.

Complex Regional Pain Syndrome and Other Forms of Neuropathic Pain in Children and Adolescents

cases helpful to encourage continued full participation in school and other activities whenever possible. As noted above, the view of neuropathic pain as nonprotective pain is crucial. Physical Therapy for Neuropathic Pain Cutaneous desensitization and transcutaneous electrical nerve stimulation (TENS) may be symptomatically helpful for patients with allodynia. Aerobic exercise training, strength training, and postural exercises may restore function in patients who have become deconditioned due to their painful condition. Physical therapy also appears to have a primary “cycle-breaking” role in patients with complex regional pain syndromes,18–20 as outlined next. Drug Therapy for Neuropathic Pain Most of the pharmacological treatment of neuropathic pain in children and adolescents is based on extrapolation from adult studies. In selected conditions, several classes of drugs including antidepressants, anticonvulsants, local anesthetic-like drugs, and opioids have shown varying degrees of effectiveness in the treatment of a number of neuropathic conditions in adults. Pediatric prescribing for neuropathic pain is largely based on limited case reports or case series. For antidepressants and anticonvulsants, there are more extensive pediatric safety and pharmacokinetic data from clinical trials of their use for treatment of nonpainful conditions such as depression, epilepsy, or enuresis. For most drugs used in the treatment of neuropathic pain, slow titration is recommended to minimize development of side effects and to detect adverse reactions when they are mild rather than severe. Children and parents need proper anticipatory guidance regarding assessment of central and peripheral side effects, and they should recognize that a tradeoff between moderate analgesia and some side effects is often necessary. A side effect such as sedation may be more or less desirable for an individual patient. For example, the side effect of sedation may be harmful to a patient unable to focus during school but may be helpful to a patient unable to fall asleep at night. Tricyclic antidepressants Tricyclics are among the oldest and best-established analgesics for a number of neuropathic pain conditions,21 including diabetic neuropathy,22 postherpetic neuralgia,23 and central poststroke pain. Prospective controlled studies have shown effectiveness both in reducing pain intensity and in improving related measures of well-being (i.e., sleep quality, work attendance, mood) in several neuropathic conditions in adults.21 Studies in adults have found effectiveness with a range of tricyclics that have predominant actions on both serotonin and norepinephrine reuptake.24,25 In most cases, our preference is to start first with nortriptyline because of a suggestion of slightly less bothersome anticholinergic side effects than with amitriptyline. For selected patients who are oversedated with very small doses of nortriptyline,

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desipramine may be considered as an alternative. Titration is based on both the patient’s analgesic response and on the occurrence of side effects. The dosing scheme listed here refers to ambulatory outpatients. For occasional inpatients with severe neuropathic pain such as from spinal metastases due to cancer, a more rapid titration scheme may be used. In a small number of children treated with tricyclics (especially desipramine) for depression, behavioral disorders, or enuresis, there have been case reports of sudden death attributed to rhythm disturbances. It has not been established whether these children had an underlying predisposition to arrhythmias, such as abnormal conduction pathways or abnormal excitability, and epidemiological studies would suggest that the overall risk of sudden death is quite low.26,27 Before initiating a tricyclic, a careful history should be elicited for suggestive symptoms, such as palpitations or presyncope. It is generally recommended to obtain an electrocardiogram before initiating a tricyclic and again if there is dose escalation to a full antidepressant therapeutic range. Cardiovascular effects of tricyclics in therapeutic doses in children are overall fairly mild.28 Tricyclics should be used with extreme caution among patients with preexisting rhythm disturbances or among patients with cardiomyopathies, including those due to Adriamycin. Common side effects of tricyclics include sedation, dry mouth, orthostatic hypotension, constipation, urinary retention, and tachycardia. If tricyclics are to be discontinued, tapering over 1–2 weeks is recommended to avoid symptoms such as irritability and bothersome, vivid dreaming at nighttime, due to rapid eye movement rebound. Other Antidepressants In general, data supporting other classes of antidepressants in the treatment of neuropathic pain are much less robust than for tricyclics. There have been occasional positive trials for selective serotonin reuptake inhibitors (SSRIs), such as paroxetine,29 but negative results have been more common. Nevertheless, they can be considered for trials for individual patients and for treatment of associated depressed mood, anxiety, and sleep disturbance. In general, SSRIs are preferable to benzodiazepines in the long-term treatment of anxiety. A range of other agents such as bupropion, venlafaxine, and nefazodone have been used, but in general, they have insufficient data to recommend them as first-line analgesics for patients with neuropathic pain. For patients with occasional apparent visceral neuropathic pain due to motility disorders, SSRIs or a tetracyclic such as trazodone may be beneficial because these drugs have much less of the anticholinergic constipating effects of tricyclics. Anticonvulsants Anticonvulsants are first-line agents for many forms of neuropathic pain.30 Earlier studies in adults showed some effectiveness of phenytoin, carbamazepine, clonazepam, and valproic acid in clinical trials. In recent years, gabapentin has emerged as the most widely prescribed anticonvulsant for neuropathic pain because of its effectiveness,31,32 a comparatively low side effect profile, and a very low frequency of severe adverse reactions. In particular, gabapentin lacks most

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of the hematological, hepatic, dermatological, immunological, periodontal, and maxillofacial complications of some of the older agents listed above. Gabapentin is also commonly used in the treatment of anxiety and mood disorders, although the evidence does not support efficacy for these indications. As with the use of anticonvulsants in treatment of epilepsy, sudden discontinuation should be avoided.33 Pediatric experience with gabapentin is extensive for its use in epilepsy, but it is largely confined to case reports or very small case series in the treatment of pain in children.34,35 Dosing of gabapentin must be individualized. Recommendations vary widely for a titration scheme. Gabapentin is generally well tolerated. Patients occasionally report a wide range of mood or behavioral changes. Carbamazepine, valproic acid, and clonazepam are also commonly used for management of neuropathic pain in adults. Carbamazepine, valproic acid, and phenytoin all require monitoring for their individual spectra of hematological, hepatic, pancreatic, or dermatological36 toxicities. Phenytoin and valproic acid have the unique advantage in the setting of severe neuropathic pain (e.g., a “cancer pain emergency”) that one can rapidly (within 1–2 hours) achieve therapeutic effect by an intravenous-loading procedure identical to that used for treatment of status epilepticus. There is little experience available with a similar rapid-loading procedure for most oral agents such as gabapentin. Second-Line Anticonvulsants: Pregabalin, Topiramate, and Lamotrigine Pregabalin, topiramate, and lamotrigine are being used increasingly for adults with neuropathic pain who have not responded to other agents. Pediatric experience is largely confined to the treatment of refractory epilepsy. The mechanisms of these agents overlap and involve voltage-gated ion channels, glutamate release, excitatory amino acid receptors (including both NMDA receptors and adenosine monophosphate acid [AMPA] receptors), GABA receptors, and glycine receptors. Lamotrigine limits repetitive firing of sodium channels and inhibits neurotransmitter release (glutamate, aspartate, GABA, and acetylcholine). Therapeutic range is 300–500 mg/day. A potentially serious side effect is Stevens-Johnson reaction or toxic epidermal necrolysis. This adverse effect is most likely in patients under 6 years of age, receiving multiple antiepileptic drugs, with developmental delay, and with a history of hypersensitivity. Topiramate inhibits voltage-gated sodium and calcium channels, AMPA-subtype glutamate receptors, and carbonic anhydrase. The therapeutic dosage range is 50–400 mg/day. Adverse reactions include dizziness, somnolence, mild cognitive impairment (including confusion and difficulty with word finding), and renal calculi. Weight loss is a potential side effect, although this is used for therapeutic benefit in patients with neurological or psychological disorders who are significantly overweight. Local Anesthetic-Like Drugs Lidocaine and its oral analogues, including mexiletine, show evidence of effectiveness for several types of neuro-

pathic pain.37 In many centers, an intravenous lidocaine infusion38 is used to predict response to either oral mexiletine or to chronic subcutaneous39 lidocaine infusion. The predictive value of the lidocaine test is imperfect. Several initial case series described fairly rapid infusion of large doses, which were likely to have transiently produced plasma concentrations in excess of 5–10 μg/ml. A positive analgesic response, in our opinion, is much more specific and predictive of future effectiveness if analgesia can be achieved either by a brief infusion of 2 mg/kg over 20 minutes or by a targeted, computer-controlled infusion set to achieve plasma concentrations of 2–4 μg/ml. Mexiletine dosing is very commonly limited by the occurrence of gastrointestinal side effects.40 Lidocaine infusions are used most commonly in our practice for inpatients with refractory pains due to cancer.39 Opioids The effectiveness of opioids for neuropathic pain has been a subject of considerable controversy. It was common clinical teaching that opioids were ineffective for neuropathic pain. This view was supported in some degree by a study by Arner et al.41 using a fixed dose of morphine in patients classified by clinical exam as having “nociceptive,” “neuropathic,” or “idiopathic” pain conditions. Other studies suggest modifying this view and report that a considerable percentage of adult patients with neuropathic pain due to cancer,42 phantom limb,43 postherpetic neuralgia44 and other causes may find good analgesic benefit with tolerable side effects. Long-term use of systemic or spinal opioids for CRPS is reported in a number of small case series, but controlled trials were not identified. Even fewer data are available regarding the use of opioids for neuropathic pain in children. In children with advanced cancer, neuropathic pain is associated with a requirement for much larger opioid dosing than nociceptive pain.45 For chronic noncancer pain, there is little consensus. Our practice is to be cautious regarding longterm use of opioids in children and adolescents. In general, it is preferred to optimize nonopioid pharmacological interventions and a range of nonpharmacological interventions in most cases. Opioids are tried on a shortterm basis immediately before physical therapy for a subgroup of children who cannot tolerate limb mobilization without them. In some cases, they are helpful; in others, they are not. Regional Anesthetic Approaches for Neuropathic Pain In adults with some forms of neuropathic pain (especially CRPS), either selective sympathetic blockade46 or combined sympathetic-somatic blockade (e.g., via an epidural block47) can reduce pain and facilitate mobilization. Regional anesthetic approaches can be useful for selected children as well. In our opinion, these approaches should be used not in isolation but as part of a multimodal approach that combines physical rehabilitation, cognitivebehavioral interventions, and a strategy to facilitate return to work or school. Because most children and many ado-

Complex Regional Pain Syndrome and Other Forms of Neuropathic Pain in Children and Adolescents

lescents are fearful of needle procedures, we generally employ deep sedation or brief general anesthesia to facilitate block placement. It is often more practical to place an epidural catheter and then use it via a continuous infusion for a period of 4–7 days. Spinal Cord Stimulation A variety of electrodes placed in the epidural space, either percutaneously or via laminotomy, can be used to produce analgesia by delivering electrical stimulation to the spinal cord. Although traditionally labeled as “dorsal column stimulation,” it is not determined which specific tracts or cell bodies are the predominant sites of action. Spinal cord stimulation has been used for a variety of forms of neuropathic pain, “failed back syndrome,” inoperable angina pectoris, and inoperable peripheral vascular disease. Spinal cord stimulation has been used for CRPS in a number of uncontrolled case series, and in one randomized controlled (unblended) trial in adults48; a systematic review identified methodology problems in the majority of uncontrolled case series.49 In the single randomized trial, there was a modest reduction in pain scores, a significant improvement in health-related quality-of-life scores, and, in the authors’ words, “no clinically important improvement in functional status.” It has some theoretical advantages: absence of sedating side effects as with many drug therapies and avoidance of the irreversibility associated with neurodestructive sympathectomy. Conversely, technical problems are common, including infection and longer-term failure of analgesia due to movement of electrodes, epidural fibrosis, or changing location of pain-generating neurons. Sympathectomy Resection of sympathetic ganglia has been a treatment for CRPS for more than 80 years. Alternatives to open operative approaches include use of minimally invasive surgery, chemical sympathectomy using phenol and other agents, and use of radiofrequency probes to destroy the nerves. Although this approach has many advocates,50 systematic reviews51 and other outcome studies suggest lack of evidence for efficacy, a substantial complication rate, and a substantial failure rate in providing either long-term analgesia or functional improvement. Our approach is to discourage neurodestructive interventions, including sympathectomy, in almost all cases of pediatric CRPS. Because up to 25% of children and adolescents will eventually develop involvement in a second extremity, the potential morbidity of bilateral lumbar sympathectomy (in terms of long-term effects on circulatory reflexes, urinary control, and sexual function) are additional factors discouraging use of this approach. Moreover, because the overwhelming majority of children and adolescents at long-term follow up will have excellent reduction in pain and improvement in functional status using a rehabilitative approach and selective use of medications or nerve blocks, sympathectomy seems not to be worth the potential morbidity for almost all children and adolescents.

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Acupuncture and Other Complementary Therapies for Neuropathic Pain Acupuncture and other complementary therapies are being used with increasing regularity for children as well as adults with neuropathic pain. The safety of acupuncture appears well established, and children in general exhibit surprisingly little distress over the procedure52 if it is explained and demonstrated in an appropriate manner. Because of its low risk and side-effect profile, acupuncture can be considered for patients who do not improve with a range of other treatments. Conversely, the status of evidence for effectiveness of acupuncture in controlled trials for a range of pain conditions is comparatively weak.53,54 Design of clinical trials for acupuncture is difficult; there is considerable disagreement regarding best scientific and ethical practices for inclusion of sham, placebo, or untreated control groups. Expectation of benefit has a substantial impact on effectiveness.55 Cost, availability of services, and the requirement for repeated visits can be practical limitations to acupuncture for many patients. Herbal medications are widely used by children as well as adults.56 It is important for clinicians to ask patients and their parents about the use of these formulations, because many have significant interactions with prescribed medications. The status of evidence regarding herbal treatments for pain is weak. Lack of standardization of formulations is an ongoing concern. In addition, some herbal medications, such as St. John’s wort, may activate specific cytochrome p450-linked enzyme systems, altering metabolism of other drugs. Dietary intake of vitamins, minerals, and protein is extremely variable among children and adolescents. Whether subtle nutritional deficiencies contribute to delayed healing following nerve injury is also a matter of dispute. In two adult trials, one randomized prospective57 and the other with historical controls,58 early supplementation with vitamin C following a wrist fracture was associated with a reduced frequency of CRPS compared to a control group.

Neuropathic Pain Syndromes Pain After Amputation Amputation necessarily involves sectioning of major nerve trunks. Patients experience nociceptive pain shortly after the surgery. Nociceptive stump pain may persist due to a variety of causes, including wound breakdown, superficial or deep-tissue infection, or mechanical pain due to pressure from a poorly-fitting prosthesis. Stump pain may also have neuropathic characteristics including allodynia, autonomic changes, and dysesthesias. The indications for exploration of a stump and for “burying a neuroma” are controversial. Phantom phenomena refer to pain and other sensations experienced by the patient as if they are occurring in the missing distal extremity. The term phantom limb pain was apparently introduced by S. Weir Mitchell during the American Civil War.59 Phantom limb sensations are variable. The limb may be perceived to be present, often in a foreshortened, plastic, and distorted position. Over time, approximately 1–6 months, the sensations may be less anatomic and more

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transient, kinesthetic, and paresthetic. The phantom may be felt to telescope into the stump and eventually fade away. Functional MRI has recently provided a fascinating window into the biological traces (tissue oxygen consumption/ ratio of oxyhemoglobin to deoxyhemoglobin) of cortical reorganization underlying these phenomena.11,43,60 Patients with phantom pain show a change in the somatotopic map of the parietal cortex. Cortical regions that previously were activated via stimulation of the missing limb part subsequently become activated by stimulation of adjacent body regions. In the case of upper extremity amputation, stimulation of the face may activate parietal cortex previously mapped to the distal upper extremity. Phantom pain, as with phantom sensations, may vary in intensity, localization, frequency, and duration. It is not restricted to limbs, possibly occurring after the removal of any body part. For example, phantom breast sensation is well described following mastectomy. Prevalence estimates in the adult literature vary widely,61 but more recent prospective studies suggest that roughly half of amputees will experience moderate to severe phantom pain.62 Several case series of pediatric amputees have been reported in recent years; these have described some of the clinical characteristics of children with phantom pain. Krane and Heller63 retrospectively surveyed a cohort of children ages 5–19 years who had undergone amputation over a 10-year period. In their series, 100% of patients reported phantom sensations. Although the majority of subjects reported phantom pain, less than 40% had this documented in the medical record, suggesting that there was underrecognition of the problem by medical and nursing staff. Among those with preoperative pain, 75% experienced phantom pain. Wilkins et al.64 reported on a retrospective survey of 42 pediatric patients with a missing limb secondary to congenital anomalies, surgery, or trauma. Phantom pain was reported in 29% of the total sample, 3.7% of the congenital group, and 48.5% of the surgical/posttraumatic group. Smith and Thompson65 retrospectively reviewed 75 pediatric patients with amputations, 67 cancer-related and 8 trauma-associated. Phantom limb pain was reported in 48% of patients with cancer-related amputations in comparison with 12% of patients with trauma-associated amputations. “Among patients with cancer, phantom limb pain was experienced by 74% who were exposed to chemotherapy before or at the time of amputation, 44% who received chemotherapy after amputation, and 12% who never received chemotherapy.”65 Patients with trauma-related amputation and those who did not receive chemotherapy reported phantom pain at a mean of 6 days postsurgery. In all, 76% of patients with cancer and exposure to chemotherapy reported phantom pain within 72 hours postsurgery. Prevention and treatment of phantom pain has received some recent study. Early and active use of a functional prosthesis appears to reduce the persistence and severity of phantom pain. The benefits appear to be related to use of the prosthesis in functional activities,60 not the mere presence of an artificial appendage, because patients who used nonfunctioning prostheses were more likely to experience phantom pain.66 Ramachandran et al.67 have described a novel approach to treatment of phantom pain in which a vertical mirror is

positioned so that movement of the contralateral (intact) limb is seen by the patient as if it were in the expected position of the amputated limb. This approach is fascinating. In view of its safety and simplicity, it should be considered more widely for these patients. Drug therapy for phantom pain has received limited study. Despite the common view that opioids are ineffective, Huse et al.43 recently reported on a controlled prospective trial of sustained release oral morphine for adults with phantom pain. They showed both a significant analgesic response and a significant effect in reversing amputation-induced cortical reorganization, based on magnetic source imaging. A prospective trial by Panerai et al.25 included patients with phantom pain along with other diagnoses collectively labeled as “central pain.” This study showed effectiveness of tricyclic antidepressants, especially clomipramine, compared with placebo. Case reports and small case series have reported some effectiveness of anticonvulsants, including clonazepam and gabapentin. Rusy and colleagues35 treated seven children and adolescents with gabapentin with relief of pain in six patients at approximately 1-year follow-up. Because of the widely reported association of preamputation pain with subsequent phantom pain, several investigators have examined whether regional anesthesia via peripheral perineural, plexus, epidural, or subarachnoid routes might reduce the incidence, severity, or persistence of phantom pain. Results have been somewhat inconsistent. A series by Bach et al.68 showed a substantial reduction in phantom pain at 6 months following intensive preoperative, intraoperative, and postoperative epidural infusions of opioids and local anesthetics. Similar results were reported by Jahangiri et al.69 Other studies have yielded mixed results. Nikolajsen et al.70,71 compared groups of patients receiving preoperative, intraoperative, and postoperative epidural bupivacaine-morphine infusions with control subKEY POINTS jects that received epidural saline preoperatively and intra1. Amputation can operatively, and epidural bupivaproduce both neucaine-morphine postoperatively. ropathic stump pain In their studies, there was no and phantom pain in difference between groups on some children. 71 QST measures in the stump 2. Aggressive treatat 1 week and at 6 months, nor ment of pain around was there a difference in the the time of amputaincidence or severity of stump tion may reduce the 70 pain or phantom pain. A study frequency of proby Lambert et al.72 compared longed pain. epidural analgesia to a peri3. Early return to use of neural infusion of bupivacaine. the limb with a funcPostoperative analgesia was sigtional prosthesis nificantly better in the epidural may reduce the fregroup, although there were no quency of prolonged differences in the incidence of pain. The benefits of phantom pain at 6 and 12 early limb use may months. relate to prevention It has been speculated that or reversal of some the differences in findings in difforms of “cortical ferent studies relate to differrewiring” that ences in patient population, occurs after duration of infusions, drug selecamputation. tion for infusions, placebo effects

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that are better controlled in some studies than others, or other factors. It is possible that increased understanding of the essential generators of central hyperexcitability (preoperative, intraoperative, and postoperative factors) will lead to more effective approaches to preemptive or preventive treatments for phantom pain and other forms of postsurgical neuropathic pain.73 Because the immediate pain of amputation can be quite severe, we continue to make use of epidural infusions in our practice and try to achieve very dense degrees of afferent blockade before the onset of surgery. Plexus Injuries and Other Plexopathies Adults who suffer major stretch or avulsion injuries of the brachial plexus frequently experience prolonged neuropathic pain, which may be difficult to treat. Traumatic plexopathies may occur in adolescents following motorcycle or bicycle accidents. Additional deafferentation syndromes resulting in central pain include spinal cord injury (congenital and posttraumatic) and nerve root avulsion. Brachial plexus injury at the time of delivery due to shoulder dystocia is not uncommon in obstetrical practice. A large epidemiological study from Sweden reports an incidence of 4.6/1000 live births.74 Neonatal brachial plexus traction injury presents with a variable spectrum of motor and sensory deficits. The majority of infants show spontaneous recovery of function over the first 6 months of life, with no apparent signs of distress or guarding with touch or limb movement suggestive of neuropathic pain. A subgroup of infants, probably less than 5%, appear to experience guarding or distress with touch or movement of the limb. In rare cases, infants may manifest self-injurious behavior, such as biting their insensate hand. KEY POINTS This may be a possible human correlate of autotomy, the self1. Brachial plexus mutilating behavior observed in injuries are the animals following partial and most common form focal nerve injury. of nerve injury in Fortunately, the neonatal infancy. Most of presentation is rarely complithese infants do not cated by pain,75 but limitations appear to experiof pain assessment in this popuence chronic pain. lation may falsely reassure inves2. Infants occasionally tigators. A study from Riyadh, show signs of selfSaudi Arabia76 reviewed 127 mutilation and pain consecutive cases of obstetrical behaviors, particubrachial plexus injury and found larly a number of six cases (4.7%) with clinical months following evidence of self-mutilation. nerve dissection McCann et al. (manuscript or nerve-grafting in preparation) reviewed the procedures. medical records of 281 infants and young children with neonatal brachial plexus injury cared for in our center in Boston by orthopedic surgeons and neurosurgeons with a specialized interest in pediatric reconstructive surgery. Seven cases were identified with evidence for self-mutilation and, in some cases, distress with touch or physical therapy. Interestingly, in six of the seven cases, self-mutilation began only after surgical reconstructive procedures, and more commonly with

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nerve dissection and nerve grafting procedures than with tendon transfer or osteotomy procedures. Complex Regional Pain Syndromes (Reflex Sympathetic Dystrophy and Causalgia) Complex regional pain syndromes types 1 and 2 refer to conditions in which there is pain in an arm or leg with neuropathic pain and sensory characteristics (e.g. spontaneous and evoked pain, burning, allodynia, hyperalgesia, dysesthesia, paresthesias) along with neurovascular abnormalities including coldness, mottling, abnormal sweating, poor capillary refill, or nonarticular swelling. CRPS1/RSD refers to this constellation of findings in patients with no demonstrable injury to a particular peripheral nerve. CRPS2/causalgia refers to this group of findings occurring in association with signs and symptoms of partial or complete peripheral nerve injury, with a well-defined area of sensory abnormalities. The terms CRPS1 and CRPS2 were developed by a consensus conference with at least a partial aim of relying on clinical features and avoiding presumptions regarding specific mechanisms or treatment responses in diagnosis.77 The diagnostic criteria from this consensus group may have some drawbacks, including relatively poor specificity,78,79 and some clinicians object to the choice of the term CRPS, which they regard as too vague to be helpful. Table 31–1 shows the major differences between adult and pediatric complex regional pain syndromes, a major and common cause for neuropathic pain.80 Figure 31–1 shows the lower extremities of two patients, one with comparatively mild involvement and one with long-standing severe involvement. The terms sympathetically maintained pain (SMP) and sympathetically independent pain (SIP) were introduced by Roberts. SMP is relieved (at least temporarily) by selective sympathetic blockade, whereas SIP is not. The positive effect of sympathetic block, at least in the early stages of the disorder, is important. These terms have been criticized on several grounds: (1) patients with SIP may also show clear signs of sympathetic dysfunction, (2) most approaches to selective sympathetic blockade have the potential for falsepositive and false-negative interpretations, (3) the same patient may change from SMP to SIP over time, (4) some patients who fail to respond to selective sympathetic blockade will have useful therapeutic responses to combined sympathetic and somatic blockade, and (5) different responses to a therapy do not prove different underlying mechanisms. In pediatrics, the emphasis on confirming SMP versus SIP seems less crucial for diagnosis than for adults, in part because of the high percentage of children who will show excellent recovery using a regimen that combines physical therapy (PT) and cognitive-behavioral treatment (CBT)18,19,81,82 and will thereby never receive or require sympathetic blockade (see Table 31–1). CRPS was regarded as rare in children until several case series were reported in the 1970s and 1980s.18,81 It is probable that this was due to underrecognition of this group of disorders. For example, in our series from 1991,82 the median time from onset of symptoms to seeking medical attention was 2 weeks; the median time to a diagnosis of

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Table 31–1

Comparison of Causalgia and Reflex Sympathetic Dystrophy in Adults and Children Adult CRPS

Child CRPS

Sex ratio

Adults have a more even sex ratio

Spontaneous pain Spread of symptoms

Common Adult patients do not exhibit much spread of signs and symptoms from one extremity to the other Upper extremity commonly involved

Pediatric CRPS affects females about five times as often as males Common Children more frequently have the signs and symptoms spread from one extremity to another Marked lower extremity predominance (5.3:1) Most patients Psychiatric pathology not well documented. Possible increased tendency to reflex sympathetic dystrophy with psychosocial stressors Children can have recurrent episodes after apparent complete resolution, with and without any inciting injury More favorable Resolution often possible with physical therapy, transcutaneous electrical nerve stimulation, and cognitive and behavioral pain management techniques Place catheter, run continuous infusion as inpatient

Site Mechanical allodynia Psychological aspects

Most patients Psychiatric pathology not well documented

Recurrence Prognosis Treatment Strategy

Not as favorable a prognosis as children Early sympathetic block strongly advocated

Technique for sympathetic block

Multiple outpatient “single shot” blocks

Figure 31–1 The spectrum of clinical findings in children and adolescents with causalgia and reflex sympathetic dystrophy. A, The majority of patients are diagnosed with comparatively mild autonomic and trophic changes, largely on the basis of persistent pain, allodynia, and avoidance of weight-bearing. B, If untreated, or if the patient refuses to bear weight for prolonged periods of time, the findings can progress to include severe swelling, muscle atrophy, osteopenia, joint contractures, and altered hair and nail growth. Even with prolonged involvement and severe limb dysfunction, as in the case of the patient in B, an intensive rehabilitation program can produce good improvement in limb function and weight-bearing and reduction in pain and hypersensitivity in a majority of cases.

Complex Regional Pain Syndrome and Other Forms of Neuropathic Pain in Children and Adolescents

RSD/CRPS/causalgia was 11 months. Our impression is that over the past 10 years, clinicians have become much more aware of this group of diagnoses, and the majority of children are now being diagnosed much earlier after the onset of signs and symptoms. CRPS in children and adolescents has a unique set of epidemiological features. These disorders are very rare before age 6 years. Onset of symptoms occurs more frequently around age 10–12 years, and new-onset cases continue to be frequent throughout adolescence and young adulthood. Pediatric CRPS is predominantly a condition of lower extremities (roughly 6–8:1 compared with upper extremities), and girls are affected at least six times as often as boys. These features are different from CRPS in adults, where the sex ratio is less marked, and upper and lower extremity cases occur with roughly equal frequency. The majority of published case series on CRPS in children have been retrospective. Our group in Boston completed two prospective randomized controlled trials for treatment of CRPS in children: (1) a prospective “rehabilitative” trial of PT and CBT for the treatment of CRPS in children and adolescents and (2) a prospective trial of sympathetic blockade in children and adolescents with CRPS. The study also included a standardized assessment profile Box 31–2 Rehabilitative Treatment Trial for Pediatric Causalgia and Reflex Sympathetic Dystrophy Design 6-week randomized comparison between Group A (PT 3 times weekly + CBT once weekly) versus Group B (PT once weekly + CBT once weekly) Measures Pain, gait, stair climbing, psychological inventories, regional and systemic autonomic signs and symptoms, QST Detailed assessment by observers blinded to group performed at: 1. Enrollment 2. Short-term (after 6 weeks) 3. Long-term (6-12 months) 4. End-of-study telephone follow-up assessments of pain and functional status Outcomes 28 patients completed protocol At enrollment, all required assistive devices (wheelchair, crutches, cast boots) Psychological scores within normal ranges for age Normal cardiovascular autonomic regulation despite prevalent regional signs and systemic autonomic symptoms Neurological exams showed 18 cases with CRPS1, 10 with CRPS2 QST abnormalities were common and varied CRPS1 most commonly showed cold hyperalgesia CRPS2 most commonly showed vibration hypoesthesia VAS spontaneous pain scores (median) improved in both groups Group A: pre, 6.3; short-term, 0; long-term, 0 Group B: pre, 6.7; short-term, 1.4; long-term, 1.8 Gait and stair climbing function scores improved in both groups No between-group differences in pain or motor function scores 42% experienced at least one recurrent episode At end-of-study, none of the patients required assistive devices

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that included pain measures, quantitative gait measures, a structured neurological examination, autonomic measurements, psychological measures, and QST. Findings of the PT/CBT trial are summarized in Box 31–2. Overall, there was excellent improvement in both pain scores and measures of gait and stair-climbing impairment. All patients were ambulating without assistive devices by the end of the 6-week study protocol. A cohort of patients with persistent pain and limb dysfunction after treatment with PT and CBT underwent a prospective controlled trial of lumbar sympathetic blockade, using combined infusions via lumbar epidural and lumbar paravertebral sympathetic indwelling catheters. In the majority of cases, the decision to perform blockade was made based on persistent pain, rather than on persistent inability to bear weight or tolerate PT. The initial dosing of the lumbar sympathetic catheter was performed using a double-blind, double-dummy comparison of intravenous saline plus lumbar sympathetic lidocaine versus intravenous lidocaine plus lumbar sympathetic saline. Patients then received an intensive 1-week inpatient treatment program that utilized open-label continuous infusions of local anesthetics via either epidural or lumbar sympathetic catheters, along with PT, CBT, and a therapeutic milieu. Blinded administration showed lumbar sympathetic administration of lidocaine was more effective than placeboplus-intravenous lidocaine, and the majority of patients with persistent pain and dysfunction on admission showed good improvements over the course of a 1-week hospitalization. A small subgroup of patients showed good improvement of limb function, but little or no improvement in their pain score during this treatment regimen. Even among this more refractory subgroup, reductions in pain scores were shown over subsequent weeks and months, with a diverse spectrum of other individualized treatment trials. Several response patterns to nerve blockade have been noted in CRPS patients. A subgroup of patients exhibits both of the following two anomalous responses: (1) a marked right shift in epidural or spinal local anesthetic dose response curves, such that doses much larger than normal are required to produce clinical signs of sensory, motor, and sympathetic blockade; and (2) even with apparently very dense sensory, motor, and sympathetic blockade of the lower body (including lack of response to tetanic stimulation), pain is undiminished. Medications that have been used for pediatric CRPS include antidepressants, anticonvulsants, local anestheticlike drugs, calcitonin, corticosteroids, and opioids. Responses to each of these are quite variable. Individual patients have had excellent analgesic responses to gabapentin, nortriptyline, and prednisone; others have not. Experience with a series of pediatric patients with CRPS at St. Gorans’s Children’s Hospital in Stockholm (abstract presentation, International Symposium on Pediatric Pain, London, June 2001) found that amitriptyline produced a high frequency of side effects and little evidence for effectiveness. From 1985–2001, over 650 pediatric patients with CRPS have been evaluated and cared for at Boston Children’s Hospital. Over this time period, we referred only one patient for operative sympathectomy and two for phenol chemical

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sympathectomy (based on circulatory insufficiency, rather than for pain relief). A small number of patients (less than eight, based on available records) have either self-referred for operative, chemical, or radiofrequency sympathectomy or have had sympathectomy before referral. One patient with causalgia following limb-sparing resection of an osteosarcoma of the femur chose above-the-knee amputation and a prosthesis for both pain and functional improvement following removal of two infected bone allografts and multiple reconstructive procedures. No other patients with CRPS have received limb amputation at our center in Boston. Approximately one or two patients annually receive temporary trials of either spinal cord stimulation or peripheral nerve stimulation for CRPS; an additional one to two patients with other diagnoses KEY POINTS receive spinal cord stimulation trials or implantation annually. 1. RSD/CRPS is not Implantable spinal opioid infurare among children sions for pediatric CRPS have and adolescents. been tried for only a few patients 2. RSD/CRPS occurs at our center over this 16-year more often in girls time period; they are used more than boys, is rare frequently for patients with maligbefore age 8 years, nancies and for patients with and occurs predomspasticity of cerebral origin. inantly in the lower Based on experience in cenextremities. ters worldwide, including that 3. The prognosis for summarized above, we believe pediatric RSD/CRPS that it is absolutely critical to is much better than reassure patients and families that that for adults, and CRPS in the overwhelming most children majority of children and adolesrespond to a regicents should not be regarded as a men that emphasizes diagnosis that implies long-term active PT and return pain and/or disability. Because to weight-bearing. the experience in the adult literature appears so much less optimistic, it is common for families to come to physicians with a very worried and pessimistic attitude. A systematic Internet search for sites related to pediatric CRPS or RSD (Dr. Oscar Arenas, personal communication) revealed a high preponderance of very pessimistic impressions regarding prognosis and the potential for long-term disability. Reassurance, avoidance of catastrophizing, and development of a positive rehabilitative outlook is an essential aspect of the treatment approach. Neuropathic Pain as a Secondary Component of Other Disorders It is worth noting that many acute and chronic pain conditions not generally regarded as neuropathic can result in secondary nerve dysfunction and may have clinical features, underlying peripheral and central mechanisms, and responses to drug therapy that resemble the better-recognized neuropathic disorders. For example, scleroderma and mixedconnective tissue disease are properly regarded as collagen vascular disorders, with autoimmune and vasculopathic processes as primary sources of pathology, leading initially to nociceptive pain due to joint inflammation and ischemia of distal extremities. However, repetitive or ongoing ischemia of

the vasa nervorum can lead to ischemic peripheral neuropathy, whereas fibrosis of the connective tissues enveloping the brachial plexus can cause a painful plexopathy. In many of these patients, drug therapies used traditionally for neuropathic pain, such as tricyclics and anticonvulsants, may be effective. In a similar fashion, although burn injury can produce active nociceptive pain, this form of injury is also a potent and sustained sensitizer of primary cutaneous nociceptive afferents. Third-degree burns, which destroy dermal terminals of sensory fibers, produce a multifocal neural trauma, leading to central sensitization. Chronic neuropathic pain, as well as eschars and contractures, may limit functional rehabilitation in the recovery period. Conclusions Neuropathic pain conditions are a comparatively common source of persistent pain among children referred to tertiary centers. Much of the treatment is currently extrapolated from that for similar disorders in adults, although agerelated biological differences may be relevant to disease mechanisms, natural history, and responses to treatment. Prospective clinical trials, in most cases involving multiple pediatric centers, are needed to better define the pathophysiology, epidemiology, and optimal treatments for pediatric neuropathic pain disorders. References 1. Bennet G: Neuropathic pain: an overview. In Borsook D (ed): Molecular Neurobiology of Pain. Seattle: IASP Press, 1997, pp 109–113. 2. Devor M: The pathophysiology and anatomy of damaged nerve. In Wall W, Melzack R (eds): Textbook of Pain. Edinburgh: Churchill Livingston, 1984, pp 49–64. 3. McArthur JC, Yiannoutsos C, Simpson DM, et al: A phase II trial of nerve growth factor for sensory neuropathy associated with HIV infection. AIDS Clinical Trials Group Team 291. Neurology 54:1080–1088, 2000. 4. Watkins LR, Goehler LE, Relton J, et al: Mechanisms of tumor necrosis factor-alpha (TNF-alpha) hyperalgesia. Brain Res 692:244–250, 1995. 5. Woolf CJ, Salter MW: Neuronal plasticity: increasing the gain in pain. Science 288:1765–1769, 2000. 6. Schwartzman RJ, Grothusen J, Kiefer TR, et al: Neuropathic central pain: epidemiology, etiology, and treatment options. Arch Neurol 58:1547–1550, 2001. 7. Gracely RH, Lynch SA, Bennett GJ: Painful neuropathy: altered central processing maintained dynamically by peripheral input. Pain 51:175–194, 1992. 8. Fields HL: Pain modulation: expectation, opioid analgesia and virtual pain. Prog Brain Res 122:245–253, 2000. 9. Heinricher MM, Schouten JC, Jobst EE: Activation of brainstem N-methyl-D-aspartate receptors is required for the analgesic actions of morphine given systemically. Pain 92:129–138, 2001. 10. Flor H: The functional organization of the brain in chronic pain. Prog Brain Res 129:313–322, 2000. 11. Borsook D, Becerra L, Fishman S, et al: Acute plasticity in the human somatosensory cortex following amputation. Neuroreport 9:1013–1017, 1998. 12. Hofbauer RK, Rainville P, Duncan GH, et al: Cortical representation of the sensory dimension of pain. J Neurophysiol 86:402–411, 2001. 13. Rainville P, Duncan GH, Price DD, et al: Pain affect encoded in human anterior cingulate but not somatosensory cortex. Science 277:968–971, 1997. 14. Yarnitsky D, Sprecher E, Zaslansky R, et al: Heat pain thresholds: normative data and repeatability. Pain 60:329–332, 1995. 15. Meier PM, Berde CB, DiCanzio J, et al: Quantitative assessment of cutaneous thermal and vibration sensation and thermal pain detection

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16.

17. 18. 19. 20. 21. 22. 23. 24. 25.

26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. 37. 38. 39. 40.

thresholds in healthy children and adolescents. Muscle Nerve 24:1339–1345, 2001. Irazuzta JE, Berde CB, Sethna NF: Laser Doppler measurements of skin blood flow before, during, and after lumbar sympathetic blockade in children and young adults with reflex sympathetic dystrophy syndrome. J Clin Monitor 8:16–19, 1992. McGrath P: Chronic pain in children. In Crombie IK, Croft PR, Linton SJ, et al (eds): Epidemiology of Pain. Seattle: IASP Press, 1999, pp 81–102. Bernstein BH, Singsen BH, Kent JT, et al: Reflex neurovascular dystrophy in childhood. J Pediatr 93:211–215, 1978. Sherry DD, Wallace CA, Kelley C, et al: Short- and long-term outcomes of children with complex regional pain syndrome type I treated with exercise therapy. Clin J Pain 15:218–223, 1999. Lee BH, Scharff L, Sethna NF, et al: Physical therapy and cognitivebehavioral treatment for complex regional pain syndromes. J Pediatr 141:135–140, 2002. McQuay HJ, Tramer M, Nye BA, et al: A systematic review of antidepressants in neuropathic pain. Pain 68:217–227, 1996. Max MB, Culnane M, Schafer SC, et al: Amitriptyline relieves diabetic neuropathy pain in patients with normal or depressed mood. Neurology 37:589–596, 1987. Bowsher D: The effects of pre-emptive treatment of postherpetic neuralgia with amitriptyline: a randomized, double-blind, placebocontrolled trial. J Pain Symptom Manag 13:327–331, 1997. Max MB, Lynch SA, Muir J, et al: Effects of desipramine, amitriptyline, and fluoxetine on pain in diabetic neuropathy. New Engl J Med 326:1250–1256, 1992. Panerai AE, Monza G, Movilia P, et al: A randomized, within-patient, cross-over, placebo-controlled trial on the efficacy and tolerability of the tricyclic antidepressants chlorimipramine and nortriptyline in central pain [comment]. Acta Neurologica Scandinavica 82:34–38, 1990. Varley CK: Sudden death related to selected tricyclic antidepressants in children: epidemiology, mechanisms and clinical implications. Paediatr Drugs 3:613–627, 2001. Biederman J, Thisted RA, Greenhill LL, Ryan ND: Estimation of the association between desipramine and the risk for sudden death in 5- to 14-year-old children. J Clin Psychiatr 56:87–93, 1995. Wilens TE, Biederman J, Baldessarini RJ, et al: Cardiovascular effects of therapeutic doses of tricyclic antidepressants in children and adolescents. J Am Acad Child Psy 35:1491–1501, 1996. Sindrup SH, Gram LF, Brosen K, et al: The selective serotonin reuptake inhibitor paroxetine is effective in the treatment of diabetic neuropathy symptoms. Pain 42:135–144, 1990. Ross EL: The evolving role of antiepileptic drugs in treating neuropathic pain. Neurology 55:S41–S46, 2000. Backonja MM: Gabapentin monotherapy for the symptomatic treatment of painful neuropathy: a multicenter, double-blind, placebo-controlled trial in patients with diabetes mellitus. Epilepsia 40:S57–S59, 1999. Rowbotham M, Harden N, Stacey B, et al: Gabapentin for the treatment of postherpetic neuralgia: a randomized controlled trial. JAMA 280:1837–1842, 1998. Cora-Locatelli G, Greenberg BD, Martin JD, et al: Rebound psychiatric and physical symptoms after gabapentin discontinuation. J Clinical Psychiatr 59:131, 1998. McGraw T, Kosek P: Erythromelalgia pain managed with gabapentin. Anesthesiology 86:988–990, 1997. Rusy LM, Troshynski TJ, Weisman SJ: Gabapentin in phantom limb pain management in children and young adults: report of seven cases. J Pain Symptom Manag 21:78–82, 2001. Tennis P, Stern RS: Risk of serious cutaneous disorders after initiation of use of phenytoin, carbamazepine, or sodium valproate: a record linkage study. Neurology 49:542–546, 1997. Kalso E, Tramer MR, McQuay HJ, Moore RA: Systemic localanaesthetic-type drugs in chronic pain: a systematic review. Eur J Pain 2:3–14, 1998. Galer BS, Harle J, Rowbotham MC: Response to intravenous lidocaine infusion predicts subsequent response to oral mexiletine: a prospective study. J Pain Symptom Manag 12:161–167, 1996. Brose WG, Cousins MJ: Subcutaneous lidocaine for treatment of neuropathic cancer pain. Pain 45:145–148, 1991. Wallace MS, Magnuson S, Ridgeway B: Efficacy of oral mexiletine for neuropathic pain with allodynia: a double-blind, placebo-controlled, crossover study. Region Anesth Pain Med 25:459–467, 2000.

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41. Arner S, Meyerson BA: Lack of analgesic effect of opioids on neuropathic and idiopathic forms of pain. Pain 33:11–23, 1988. 42. Portenoy RK, Foley KM, Inturrisi CE: The nature of opioid responsiveness and its implications for neuropathic pain: new hypotheses derived from studies of opioid infusions. Pain 43:273–286, 1990. 43. Huse E, Larbig W, Flor H, Birbaumer N: The effect of opioids on phantom limb pain and cortical reorganization. Pain 90:47–55, 2001. 44. Rowbotham MC, Reisner-Keller LA, Fields HL: Both intravenous lidocaine and morphine reduce the pain of postherpetic neuralgia. Neurology 41:1024–1028, 1991. 45. Collins JJ, Grier HE, Kinney HC, Berde CB: Control of severe pain in children with terminal malignancy. J Pediatr 126:653–657, 1995. 46. Hord AH, Rooks MD, Stephens BO, et al: Intravenous regional bretylium and lidocaine for treatment of reflex sympathetic dystrophy: a randomized, double-blind study. Anesth Analg 74:818–821, 1992. 47. Cooper DE, DeLee JC, Ramamurthy S: Reflex sympathetic dystrophy of the knee. Treatment using continuous epidural anesthesia. J Bone Joint Surg Am 71:365–369, 1989. 48. Kemler MA, Barendse GA, van Kleef M, et al: Spinal cord stimulation in patients with chronic reflex sympathetic dystrophy. New Engl J Med 343:618–624, 2000. 49. Grabow TS, Tella PK, Raja SN: Spinal cord stimulation for complex regional pain syndrome: an evidence-based medicine review of the literature. Clin J Pain 19:371–383, 2003. 50. Schwartzman RJ, Liu JE, Smullens SN, et al: Long-term outcome following sympathectomy for complex regional pain syndrome type 1 (RSD). J Neurologic Sci 150:149–152, 1997. 51. Mailis A, Furlan A: Sympathectomy for neuropathic pain. Cochrane Database Systematic Rev 2003: CD002918. 52. Kemper KJ, Sarah R, Silver-Highfield E, et al: On pins and needles? Pediatric pain patients’ experience with acupuncture. Pediatrics 105:941–947, 2000. 53. Smith LA, Oldman AD, McQuay HJ, et al: Teasing apart quality and validity in systematic reviews: an example from acupuncture trials in chronic neck and back pain. Pain 86:119–132, 2000. 54. Moore RA, McQuay HJ, Oldman AD, et al: BMA approves acupuncture. BMA report is wrong. BMJ 321:1220–1221, 2000. 55. Kalauokalani D, Cherkin DC, Sherman KJ, et al: Lessons from a trial of acupuncture and massage for low back pain: patient expectations and treatment effects. Spine 26:1418–1424, 2001. 56. Gardiner P, Kemper KJ: Herbs in pediatric and adolescent medicine. Pediatr Rev 21:44–57, 2000. 57. Zollinger PE, Tuinebreijer WE, Kreis RW, et al: Effect of vitamin C on frequency of reflex sympathetic dystrophy in wrist fractures: a randomised trial. Lancet 354:2025–2028, 1999. 58. Cazeneuve JF, Leborgne JM, Kermad K, et al: Vitamin C and prevention of reflex sympathetic dystrophy following surgical management of distal radius fractures. Acta Orthopaedica Belgica 68:481–484, 2002. 59. Mitchell SW, Morehouse CR, Keen WW: Gunshot wounds and other injuries of the nerves. Philadelphia: JB Lippincott, 1864. 60. Lotze M, Grodd W, Birbaumer N, et al: Does use of a myoelectric prosthesis prevent cortical reorganization and phantom limb pain? Nature Neurosci 2:501–502, 1999. 61. Kalauokalani D, Loeser JD: Phantom limb in pain. In Crombie IK, Croft PR, Linton SJ, et al (eds): Epidemiology of Pain. Seattle: IASP Press, 1999, pp 143–153. 62. Kooijman CM, Dijkstra PU, Geertzen JH, et al: Phantom pain and phantom sensations in upper limb amputees: an epidemiological study. Pain 87:33–41, 2000. 63. Krane EJ, Heller LB: The prevalence of phantom sensation and pain in pediatric amputees. J Pain Symptom Manag 10:21–29, 1995. 64. Wilkins KL, McGrath PJ, Finley GA, et al: Phantom limb sensations and phantom limb pain in child and adolescent amputees. Pain 78:7–12, 1998. 65. Smith J, Thompson JM: Phantom limb pain and chemotherapy in pediatric amputees. Mayo Clinic Proc 70:357–364, 1995. 66. Weiss T, Miltner WH, Adler T, et al: Decrease in phantom limb pain associated with prosthesis-induced increased use of an amputation stump in humans. Neuroscience Lett 272:131–134, 1999. 67. Ramachandran VS, Rogers-Ramachandran D: Synaesthesia in phantom limbs induced with mirrors. Proc Royal Soc Lond B 263:377–386, 1996.

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68. Bach S, Noreng MF, Tjellden NU: Phantom limb pain in amputees during the first 12 months following limb amputation, after preoperative lumbar epidural blockade. Pain 33:297–301, 1988. 69. Jahangiri M, Jayatunga AP, Bradley JW, et al: Prevention of phantom pain after major lower limb amputation by epidural infusion of diamorphine, clonidine and bupivacaine. Ann Royal Coll Surg Engl 76:324–326, 1994. 70. Nikolajsen L, Ilkjaer S, Christensen JH, et al: Randomised trial of epidural bupivacaine and morphine in prevention of stump and phantom pain in lower-limb amputation. Lancet 350:1353–1357, 1997. 71. Nikolajsen L, Ilkjaer S, Jensen TS: Effect of preoperative extradural bupivacaine and morphine on stump sensation in lower limb amputees. BJA 81:348–354, 1998. 72. Lambert A, Dashfield A, Cosgrove C, et al: Randomized prospective study comparing preoperative epidural and intraoperative perineural analgesia for the prevention of postoperative stump and phantom limb pain following major amputation. Region Anesthes Pain Med 26:316–321, 2001. 73. Kissin I: Preemptive analgesia. Why its effect is not always obvious. Anesthesiology 84:1015–1019, 1996. 74. Hoeksma AF, Wolf H, Oei SL: Obstetrical brachial plexus injuries: incidence, natural course and shoulder contracture. Clin Rehab 14:523–526, 2000.

75. Rossitch E Jr, Oakes WJ, Ovelmen-Levitt J, et al: Self-mutilation following brachial plexus injury sustained at birth. Pain 50:209–211, 1992. 76. Al-Qattan MM: Self-mutilation in children with obstetric brachial plexus palsy. J Hand Surg Br 24:547–549, 1999. 77. Stanton-Hicks M, Janig W, Hassenbusch S, et al: Reflex sympathetic dystrophy: changing concepts and taxonomy. Pain 63:127–133, 1995. 78. Harden RN, Bruehl S, Galer BS, et al: Complex regional pain syndrome: are the IASP diagnostic criteria valid and sufficiently comprehensive? Pain 83:211–219, 1999. 79. Bruehl S, Harden RN, Galer BS, et al: External validation of IASP diagnostic criteria for complex regional pain syndrome and proposed research diagnostic criteria. International Association for the Study of Pain. Pain 81:147–154, 1999. 80. Wilder RT: Reflex sympathetic dystrophy in children and adolescents: differences from adults. In Hicks-Stanton M, Janig W (eds): Reflex Sympathetic Dystrophy: A Reappraisal. Progress in Pain Research and Management. Seattle: IASP Press, 1996, p 67. 81. Dietz FR, Mathews KD, Montgomery WJ: Reflex sympathetic dystrophy in children. Clin Orthopaed Rel Res 225–231, 1990. 82. Wilder RT, Berde CB, Wolohan M, et al: Reflex sympathetic dystrophy in children. Clinical characteristics and follow-up of seventy patients. J Bone Joint Surg Am 74:910–919, 1992.

Chapter 32

Pediatric Musculoskeletal Tumors About the Knee Mark C. Gebhardt

Neoplasms occurring about the knee can present with a variety of signs and symptoms, which may mimic the more common traumatic or sports-induced injuries seen by those caring for young athletes. Although relatively rare, a delay in diagnosis can have significant implications for the life and limb of the patient and cause confusion in establishing the true diagnosis for the physician. To make matters worse, the vast majority of patients presenting with knee pain and a tumor have an associated history of a traumatic or sports injury. For that reason, knowledge about the types of neoplasms that occur about the knee is important. The old adage—if one doesn’t know about a diagnosis, one won’t make it—applies to these lesions. Approximately 1000 new cases of malignant musculoskeletal tumors are diagnosed annually in the United States in the pediatric population, making up approximately 10% of childhood cancers. The most common of these are osteosarcoma, rhabdomyosarcoma, and Ewing’s sarcoma. Although overall survival rates from these diseases are improving, there remains much that needs to be understood about these conditions. The improvement in survival rates is due to improvement in chemotherapeutic regimens, better diagnostic modalities, and a better understanding of the biology of these specific disorders.1 The incidence of osteosarcoma is approximately 5–6 per 1 million children under the age of 15. There is a peak incidence of occurrence during the adolescent growth spurt. A predilection for race has not been identified, but osteosarcoma is slightly more common in boys than in girls.2 There is no known cause, but there is a documented association between osteosarcoma and exposure to ionizing radiation.3 Osteosarcoma can occur in Paget’s disease, enchondromatosis, hereditary multiple exostoses, and fibrous dysplasia. It is also frequently seen as a second cancer in patients with hereditary retinoblastoma, a condition related to loss of a tumor suppressor gene Rb.4 In a review of 1649 patients with osteosarcoma, 508 were in the distal femur, 248 in the proximal tibia, 38 in

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proximal fibula, and 1 in the patella. These cases together constituted 48% of cases in this study, making the knee by far the most common joint around which these tumors are found.5 The predilection of osteosarcoma and infection for the knee is thought to relate to the rate of growth at these sites (so-called Phemister Law). Dallas Phemister noted the correlation between the growth of long bones such as the femur and the tendency of pathological processes such as infection or neoplasia to occur there. It was surmised that the rate of occurrence of pathological processes was highest in the fastest-growing end of the longest bones of the skeleton. Correspondingly, the distal femur and proximal tibia— which contribute approximately 40% and 30%, respectively, of the growth of the lower extremity in normal individuals—are the most common sites for many of the bony and soft-tissue lesions seen in the developing child. Benign bone tumors are not uncommon in children, and the true incidence is unknown because many of these lesions may never come to medical attention. Of the benign lesions that are discovered, many never require further treatment after radiographic diagnosis. The most common of these conditions will be discussed. Benign soft tissue tumors about the knee can be grouped into true benign neoplasms and neoplastic simulators. Examples of true benign neoplasms include hemangiomas, vascular malformations, lipomas, neurofibromas, lymphangiomas, and schwannomas. Masses about the knee that simulate neoplasms share the characteristic of a waxing and waning course, or resolution over time. These include juxtaarticular cysts such as Baker’s cysts, meniscal cysts, and proximal tibiofibular cysts. The synovium itself is an uncommon place for neoplasms to arise in childhood, but pigmented villonodular synovitis and synovial hemangioma do occur. These processes 487

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present as painful swelling of the knee and may be associated with a soft-tissue mass. They are often responsible for mechanical symptoms or knee effusions. These processes may be detected incidentally or intentionally on arthroscopic examination. Classically, pigmented villonodular synovitis is associated with recurrent, atraumatic hemarthroses. Presentation

KEY POINTS 1. A variety of benign and malignant conditions occur about the knee in the pediatric population. It is important to have an understanding of these lesions so they will be considered when a patient presents with knee pain. 2. Tumors about the knee may come to attention with an independent traumatic or sporting injury, which may confuse or delay diagnosis. 3. Survival rates in malignant tumors of the extremities are improving, largely due to advances in chemotherapy. 4. Pathological intraarticular processes are rare in childhood, but they do occur.

Patients with tumors about the knee present with a variety of complaints that may initially be attributed to injuries or other causes. A careful history and understanding of the character of the pain can often lead to the diagnosis. The most common presenting symptom is pain. An investigation of the nature and quality of pain may give clues to the nature of the lesion. In general, malignant lesions are associated with pain at rest or at night, whereas benign lesions are often painful with activity. Worsening pain in a patient with a mass increasing in size is highly suggestive of a malignancy. A patient suspected of having a sprain or other sporting injury who does not improve after 6 weeks of conservative therapy requires further evaluation with at least a radiograph to exclude a tumor. Presentation with pathological fracture in the absence of significant pain suggests a process of longer duration. This may suggest a slower, more benign process. On occasion, benign lesions are found incidentally on radiographic evaluation of the affected limb for another reason such as a sports injury. Careful physical examination is critical in patients suspected of having a musculoskeletal tumor. The contralateral limb provides an important control for the examination. The examination begins with careful inspection of the affected knee. The presence of a mass may be identifiable even without palpation by apparent fullness of one limb compared to the other. Due to its superficial location, the bony and ligamentous anatomy of the knee is readily palpable in most cases with the knee placed in the appropriate position. Location of any masses should be noted with respect to the surrounding anatomical landmarks. A palpable mass is a critical finding on examination and should be carefully noted in terms of size and characteristics. Range of motion of the knee may be affected not only by intraarticular lesions, but also by distal femoral and proximal tibial lesions. Knee effusions should be noted because they may be indicative of intraarticular neoplasm.

Evaluation Plain radiographs remain the primary modality for imaging of musculoskeletal tumors. In many cases, a specific diagnosis is made on the basis of plain x-ray alone. Careful evaluation of plain radiographs usually allows the construction of a differential diagnosis based on appearance of the lesion in the bone, the reaction of the host bone, and other characteristics such as location within the bone, the type of bone destruction, and the presence or absence of mineralization within the lesion. Soft-tissue masses are usually better visualized with magnetic resonance imaging (MRI). In some cases, computed tomographic scanning may be helpful in evaluating the extent of cortical involvement or in assessing for risk of pathological fracture. Radionuclide total body bone scintigraphy and computed tomography (CT) of the chest are important studies for evaluation of potential metastatic disease. Based on imaging studies, a decision is made regarding the necessity for biopsy to establish the diagnosis. In many cases of benign lesions, a biopsy is not needed. When in doubt, a needle or open biopsy is necessary to confirm diagnosis or rule out malignancy. Pitfalls Knee pain is a common presenting complaint of many musculoskeletal conditions and is not necessarily restricted to knee pathology. Disorders of the hip may often refer pain to the knee and should be considered in any child presenting with knee pain or a limp. Conditions such as a slipped capital femoral epiphysis; hip sepsis; or proximal femoral, pelvic, or spine tumors may all present with knee pain as the only or primary symptom. This is important to consider in any case in which expected pathology at the knee is not found. In these cases, careful hip and spine examination and imaging is warranted. Recent developments have improved the ease, speed, and efficiency of arthroscopy of the knee. Sports-related injuries in children and adults are increasingly managed with arthroscopic examination and treatment. Otherwise asymptomatic tumors of the knee, however, may also be brought to the attention of the physician following a sports injury or other trauma. Recent reports have described tumors about the knee initially misdiagnosed and treated as sports injuries.6,7 In a recent series of 25 tumors about the knee originally misdiagnosed as sports injuries, 15 had arthroscopic procedures that affected the ultimate oncological treatment.8 Initial poor-quality radiographs and a presumed original diagnosis despite persistent symptoms were the most frequent causes of an erroneous diagnosis. In most cases of persistent symptoms in this series, MRI was not obtained to confirm the diagnosis. In cases of presumed sports injury with questionable diagnosis or persistent symptoms despite conservative management, further imaging with MRI and bone scan is warranted to exclude neoplasms, infections, and inflammatory disorders. Intraarticular procedures such as arthroscopy in these cases may result in extension of the tumor and contamination of adjacent uninvolved tissues, leading to the need for a more extensive surgical resection, or even amputation, at the time definitive treatment.

Pediatric Musculoskeletal Tumors About the Knee

Biopsy of a known lesion, if performed inappropriately, can also lead to the need for a more extensive surgical resection than otherwise necessary. Biopsy should preferably be performed by the oncological surgeon, who can take into consideration future surgical procedures. Biopsy tracts are considered contaminated with tumor and must be excised with the lesion at the time of resection. Biopsies are therefore planned along the lines of incision for the ensuing surgery. Upon discovery of a soft-tissue or bony lesion in the pediatric extremity, referral to an oncological surgeon is appropriate before biopsy or definitive diagnosis. Benign Lesions Simple Cysts

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KEY POINTS 1. Patients suspected of sprain or other minor injury who do not improve with conservative therapy after 6 weeks should undergo a screening evaluation for tumor, usually with plain radiographs. 2. Plain radiographs are the primary imaging modality for musculoskeletal tumors. 3. In cases of suspected traumatic injury with unclear diagnosis, MRI and bone scan are warranted before undertaking an operative procedure such as arthroscopy. 4. Hip and spine pathology must be considered in any patient with knee pain or limp and absence of knee findings. 5. Inappropriately performed biopsy of a lesion may necessitate more extensive surgical resection than otherwise necessary.

Simple cysts of bone are most commonly solitary lesions. These lesions are usually found between 4–10 years of age and have a 2:1 male predominance. Around the knee, these lesions are found in the metaphyseal regions of the femur and tibia. Nearly 70% of these lesions, however, are found in the proximal humerus and proximal femur.9 A unicameral cyst is a simple cyst composed of a single chamber (Figure 32–1). The cysts can be classified as active or latent based on proximity to the growth plate.10 Since the growth plate tends to grow away from the cyst as the child matures, authors have defined cysts as active if the cyst is located less than 0.5 cm from the growth plate and believe that active cysts are more likely to continue to enlarge. Latent cysts (more than 0.5 cm from the growth plate) also have some remaining growth potential, leading to the occasional phenomenon of recurrence after adequate treatment in the adolescent patient. Once skeletal maturity is achieved, the cysts usually heal and fill in with bone. At this point there is less risk of recurrence or progression. Simple bone cysts erode the surrounding cortex, yet cause little reactive bone formation. They may thin the cortex sufficiently to induce fracture, often leading to formation of multiple bony septae and a thickened cortical wall. Unicameral bone cysts are not true cysts because they are not lined by epithelium and lack basement membranes; rather, they are lined with thin fibrovascular tissue.11 The contained fluid is straw-colored and has the biochemical characteristics of extracellular fluid.

Figure 32–1 A 7-year-old boy presents with knee pain. Imaging of the knee is negative. Further workup reveals a unicameral bone cyst in the proximal femur.

Simple cysts may be diagnosed following fracture and complaint of pain or may be incidental findings. Pain from a cyst may be the result of microscopic fractures through the thinned cortex. Cysts located adjacent to the growth plate may lead to premature physeal closure.12 Spontaneous resolution of simple cysts is the rule, although it may take several years and does not usually occur until skeletal maturity.13 On occasion, cysts will heal following pathological fracture, but this is the exception rather than the rule. Treatment options vary and include modalities such as corticosteroid injection, autologous bone marrow injection, multiple drilling and drainage, and open curettage and bone grafting. The decision to treat is based on the likelihood of adverse occurrence such as pathological fracture or growth arrest and associated deformity. In the weight-bearing lower extremity, the threshold for treatment is lower than for a similar lesion in the upper extremity. Aneurysmal Bone Cyst Aneurysmal bone cysts are the second type of bone cysts that occur in childhood. The lesions are usually metaphyseal but, unlike simple bone cysts, they have no gender predilection and are seen most commonly in patients between the ages of 5–20 years. The most common sites are the femur and tibia. These lesions can occasionally be found to cross the physis. These cysts may be primary or a secondary response to a preexisting lesion. For example, up to 35% of these lesions are found in association with other lesions such as nonossifying fibromas, fibromyxomas, fibrous dysplasia, chondroblastomas, giant cell tumors, simple bone cysts, telangiectatic osteosarcomas, chondrosarcomas, or metastatic lesions.14,15 As such, it is critical to perform a through investigation and obtain adequate tissue at the time of operation to allow accurate diagnosis. On pathological evaluation, aneurysmal bone cysts contain soft, reddish-brown, spongy tissue that is filled with dark-red blood or organized blood clots. Presenting symptoms include pain, tenderness, and swelling, with a duration of weeks to months. Radiographically, these lesions are classically described as

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expansile lesions that are contained by a thin wall of cortex and periosteal new bone formation. These are eccentric lesions, which distinguish them from simple bone cysts, and are metaphyseal when occurring in long bones (Figure 32–2). Once diagnosed, treatment of aneurysmal bone cysts is usually recommended because spontaneous resolution is unusual, and the diagnosis is frequently in question. Traditional treatment is curettage and bone grafting of the lesion. A recurrence rate of up to 20–40% has been reported with this method of treatment.16 Further adjunctive therapy (such as cementation, cryotherapy, embolization, and radiation therapy) has been used with various levels of success. Radiotherapy is reserved for recurrent lesions in sites difficult to treat surgically, such as the spine.17 Embolization or sclerotherapy is now generally preferable to radiation to avoid the risk of secondary neoplasm later in life. Osteochondroma Solitary osteochondroma is the most common benign tumor of bone. These lesions are characterized by an osseous projection covered by a cartilage cap. These lesions are commonly found in the metaphyses of the distal femur and proximal tibia. These locations, in addition to the proximal humerus, account for 50% of osteochodromas.18 The lesion is metaphyseal, arising probably as an outcropping from the physis. The etiology of the lesion is believed to be either a defect in the perichondral ring of the physis causing an ectopic area of cartilage, which subsequently undergoes enchondral ossification, or a misdirected growth of a portion of the growth plate with lateral projections causing the development of eccentric cartilage-capped prominences.19 These lesions do not have any known genetic component, as opposed to the autosomaldominant pattern found in the hereditary exostoses. The lesions can be defined as sessile or pedunculated and have a thick cartilaginous cap of 1–3 mm or even thicker in the younger patient. The cap is usually covered with perichondrium, and the cortical bone shares a cortex with the underlying host bone. Histologically, the cartilaginous cap is normal hyaline cartilage, which undergoes normal

Figure 32–2 Radiograph of a 14-year-old girl presenting with a painful swollen knee. An aneurysmal bone cyst is found in the proximal tibia.

enchondral ossification as the lesion grows. The likelihood of malignant degeneration is exceedingly low, although rarely chondrosarcomas do arise in osteochondromas in patients with hereditary multiple osteochondromatosis (Figure 32–3).20 Clinically, osteochondromas present as a painless protrusion or bump on the affected extremity. The most common age of presentation is between 10 and 20 years. They are also often found as incidental radiographic findings. Other clinical signs and symptoms include angulation of the involved bone, reduced joint motion, impingement on neighboring soft tissues, or rarely fracture of the osteochondroma. Bursa formation over the lesion may be present and cause symptoms. In the proximal tibia or lateral distal femur, the pes tendons or iliotibial band, respectively, can be irritated or cause snapping as they move over the bony prominence.21 These factors may be responsible for pain at the site of the lesion. Treatment of osteochondromas is usually reserved for symptomatic cases. Pain may develop if the lesion is repeatedly traumatized, if a painful bursa develops over the lesion, or if the pedunculated stalk fractures. Occasionally cosmesis is a concern. If excision is undertaken, it is important to avoid injury to the adjacent growth plate and to completely excise the cartilaginous cap and perichondrium.22 Malignant degeneration of osteochondroma to chondrosarcoma is rare. Current estimations suggest that this

Figure 32–3 Osteochondromas. This 10-year-old boy presented with multiple masses around his knee.

Pediatric Musculoskeletal Tumors About the Knee

occurs in about 0.25% of cases.9 This transformation is in adult life and is usually heralded by pain and growth of the lesion after a period of quiescence following maturity. MRI is useful in identifying potentially malignant lesions, by defining the extent of the lesion into surrounding soft tissues. Bone scans have not been found to be useful in this regard.23 Fibrous Dysplasia

KEY POINTS 1. Simple cysts do resolve spontaneously, and the decision to treat is based on the likelihood of fracture. 2. Aneurysmal bone cysts may be secondary to other potentially malignant conditions, so accurate tissue diagnosis is critical. Spontaneous resolution is uncommon; therefore, treatment is recommended. 3. Solitary osteochondromas are the result of normal endochondral ossification in an abnormal location. Treatment is symptomatic, and malignant degeneration is rare.

Fibrous dysplasia has been classically described as a benign nonfamilial disorder characterized by the presence of expanding intramedullary fibro-osseous tissues in one or more bones.24 The disorder occurs more frequently in females and occurs in monostotic (affecting only one bone) and polyostotic (affecting multiple bones) forms. The polyostotic form is more severe and usually affects one side of the body more severely than the other. A special subset of the polyostotic form is found in conjunction with precocious puberty and café-au-lait spots and other endocrinopathies, referred to as the McCuneAlbright syndrome.25 It is thought that fibrous dysplasia is a result of failure of maturation of woven bone to lamellar bone. Although the exact etiology is unknown, it has been demonstrated that mutation of a specific G protein involved in the development of bone is found in patients with McCune-Albright syndrome.26 Clinical manifestations of fibrous dysplasia are usually mild in the monostotic form. The superficial location of the tibia may lead to pain and swelling at the site of a lesion. Femoral lesions may lead to pain and a limp and may result in referred pain to the knee. On radiographs, fibrous dysplasia is typically described as having a “ground glass” appearance, with expansion and thinning of the cortex. The lesion may be surrounded by denser reactive bone. The lesions invariably demonstrate increased uptake on bone scans, in keeping with the fact that they are bone-producing lesions. Fibrous dysplasia lesions may be confused with cysts of bone or enchondromas. Surgical treatment is indicated in weight-bearing bones when the lesions are symptomatic and appear at risk for fracture, have fractured, or are causing unacceptable deformity, usually related to repetitive microfractures. Recurrence is frequent following curettage and bone grafting, and the graft is often resorbed and replaced by dysplastic bone over time.27 Therefore, if the size and location is such that fracture is a concern, prophylactic fixation with a plate or a rod is recommended. Nonoperative management of fractures in a cast often leads to healing in a young child, but repetitive fractures may require internal fixation for treatment.

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Malignant degeneration rarely occurs in these lesions but carries a poor prognosis. There is an association between radiation therapy and malignant degeneration.28 There are no current medical regimens that have proven to be consistently useful. Enchondroma Intramedullary cartilaginous islands are known as enchondromas and are common benign tumors. They are usually noticed in the second decade but may present at any age. Radiographically, there is a medullary radiolucency with punctuate calcification and sharp margins. Enchondromas do not usually have a rim of reactive bone surrounding the lesion, but individual lobules of cartilage may have bony reaction around them, giving the appearance of rings and arcs on radiographs. There may be an associated expansion of bone if the lesion is located near the cortex. These are usually asymptomatic lesions unless there has been a pathological fracture. The majority of these lesions present in the upper extremity, with up to 50% in the hand, but they are also seen in the distal femur and proximal tibia. There are conditions of multiple enchondromas known as Ollier disease and Maffucci syndrome. These are uncommon, nonhereditary conditions in which multiple enchondromatous lesions are seen and may be associated (in the case of Maffucci syndrome) with multiple soft-tissue hemangiomas. In the multiple enchondromatoses, the femur and tibia are commonly involved, usually more prominently on one side of the body. The lesions often extend from the physis into the metaphysis, causing angular deformity, leg-length discrepancy, failure to tubularize, and clubbing. They give the appearance of gauge marks or sled tracks in the metaphysis of the bone. Epiphyses may be involved as well. There is a risk of malignant degeneration in the multiple enchondromatoses, with conversion to chondrosarcoma. In Ollier disease, this incidence is about 25–30% by age 40 years.29,30 The risk in Maffucci syndrome is equivalent or higher.31 Increased localized growth of a lesion associated with pain suggests malignancy. The biggest challenge of enchondromas is to distinguish them from chondrosarcomas. This is seldom an issue in the child or teenager, but pain in association with a cartilage tumor in the adult is worrisome. If there is radiolucency around a calcified cartilage tumor, thickening of the cortex, scalloping of the endosteal bone, or soft-tissue mass, chondrosarcoma is likely.9 The difficulty is when the patient has pain in the shoulder or knee, and an enchondroma is encountered. It may be very difficult to discern if the pain is coming from the lesion, or more likely, from other sources. Initial treatment is with observation unless there is structural weakening of the bone or risk of pathological fracture, in which case curettage and bone grafting may be undertaken. In the multiple enchondromatoses, biopsy should be performed if there is increased growth of a particular lesion associated with pain. Periodic scanning for abdominal or brain malignancies is also indicated. Additionally, treatment of deformity caused by these lesions may need to be considered, such as osteotomy for angular deformity of an affected limb.

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Chondroblastoma Chondroblastoma is a benign cellular cartilage tumor that usually occurs in the epiphyses of long bones. It is found primarily in patients between the ages of 10 and 20 years. The tumor was described by E.A. Codman in 1931 and has hence acquired the name “Codman Tumor.”32 The most common locations are the epiphyses of the distal femur, proximal tibia, and proximal humerus. In adults, flat bones or ribs may be involved. Local pain and tenderness are the usual presenting symptoms, rarely associated with joint symptoms such as limited range of motion. Tumors at the knee are often associated with a limp. Muscle wasting may also be present in the area of the tumor. Because the pain is often mild to moderate in severity, the lesion may be present for several months to years before diagnosis. At other times, the pain may be quite intense and inflammatory in nature, keeping the patient awake at night and mimicking the symptoms of an osteoid osteoma. Although the lesion is located in an epiphysis or an apophysis, it may cross an open physis to involve the metaphysis. Radiographically, chondroblastoma presents as a radiolucent lesion of the epiphysis of a long

bone (Figure 32–4). There is a radiodense rim around the lesion with variable amounts of stippled calcification within the lesion. On MRI, the adjacent bone marrow and soft tissue show signal abnormality consistent with edema, which may at times mimic a soft-tissue mass.33 Differential diagnosis includes giant cell tumor of bone, chondromyxoid fibroma, Langerhans cell histiocytosis, aneurysmal bone cyst, or malignant lesions such as clear cell chondrosarcoma or chondroblastic osteosarcoma. Histologically, the lesion is composed of sheets of chondroblasts interspersed with multinuclear giant cells. True cartilage is seldom seen, but islands of chondroid matrix are seen. There are areas of calcifications arranged around chondroblasts, giving a “chicken wire” type of appearance. There may also be larger masses of amorphous calcification.34 Treatment of chondroblastoma is primarily by curettage and bone grafting. Complete excision is the priority over preservation of the physis, but because these lesions appear near the end of skeletal maturity, growth disturbances are unusual. Occasionally, local recurrence or pathological fracture may require repeat curettage; wide margin resection and reconstruction with allograft, prosthesis, or arthrodesis is seldom indicated.

Figure 32–4 A, A 12-year-old girl with a chondroblastoma of the proximal tibia. Note the epiphyseal location. B and C, Computed tomography scan of the chondroblastoma shown in (A).

(Continued)

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Osteoid Osteoma

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KEY POINTS Osteoid osteoma is a solitary 1. Treatment of fibrous painful bony lesion that occurs dysplasia lesions in children and young adults often requires hardbetween the ages of 5 and 30 ware fixation, even years. They may occur in virtuin the pediatric popally any bone, but they have the ulation. The disorder highest incidence in the proxmay be associated imal femur, followed by the with endocrine proximal tibia. There is a 2:1 abnormalities. male-to-female predominance.36 2. Syndromes of multiThe clinical features are ple enchondromas variable, but in general patients (Maffucci syndrome present with a sharp, boring pain, or Ollier disease) worse at night, that is typically carry a risk of relieved or alleviated by aspirin malignancy. or other nonsteroidal antiinflam3. Chondroblastoma is matory drugs (NSAIDs). Osteoid an epiphyseal lesion osteomas of the spine may presand, although benign, ent with symptoms similar to it may have assoradiculopathy or demonstrate an ciated “benign pul37 irritative scoliosis. Patients may monary metastases.” present with limpness and muscle atrophy. Direct tenderness over the site is common, but erythema and swelling are usually not found unless the lesion is in a superficial location. The characteristic lesion is a small, intracortical, round lucency called a nidus 1.0–2.0 cm in size, surrounded by a dense radiodense reactive rim (Figure 32–5). Computed tomography is the best imaging modality for detecting these lesions, but technicium-99 bone scans may be useful in diagnosis as well, because the nidus appears as an intense focal abnormality on bone scan.38 Radiographic differential diagnosis includes stress fracture, osteomyelitis, or Brodie’s abscess. The natural history is usually that the symptoms resolve over time, but this may take several years.

Figure 32–4—cont’d D and E, Magnetic resonance imaging of the chondroblastoma shown in (A).

Although chondroblastomas are benign lesions, “benign pulmonary metastases” are rarely seen in conjunction with a bony lesion.35 Although these pulmonary lesions generally prove to be histologically benign implants of chondroblastoma, surgical resection is recommended.

Figure 32–5 Computed tomography scan of an osteoid osteoma.

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Histologically, the tissue is composed of sheets of woven bone rimmed by osteoblasts in a fibrovascular stroma. The tissue is red and granular. Cartilage is not present. Numerous nonmyelinated axons in or around the nidus are thought by some observers to be responsible for the pain. Medical management with nonsteroidal antiinflammatory medications and salicylates may help avoid surgery but are most often required for several years, leading most patients to seek alternative treatment. Surgical excision or curettage was commonplace as the mainstay of treatment, but recently radiofrequency ablation via a percutaneous approach is the preferred method of treatment because of its success and low morbidity.39 Alternative techniques such as CT-guided trephination are also employed. Postoperatively, pain relief is immediate, complete, and dramatic if the lesion is completely removed or ablated. Recurrence is uncommon.

radiolucent lesions with a “moth-eaten” appearance are seen. The adjacent cortex may show some periosteal elevation or new bone formation with surrounding sclerosis. Grossly, lesions are composed of a soft, reddish-brown material, which is a mix of eosinophils, plasma cells, histiocytes, and Langerhans cells. Histologically, the cytological characteristics of Langerhans cells are an indented or folded nucleus with a crisp nuclear membrane, abundant pale eosinophilic cytoplasm with “Birbeck granules” or a finely stippled chromatin pattern. Solitary lesions with the risk of fracture are treated with curettage and bone grafting. Otherwise, observation of a biopsy-proven lesion is reasonable, given a generally benign course and a small chance of spontaneous remission. Steroid injection is an alternative. The systemic varieties of HandSchüller-Christian disease and Letterer-Siwe disease may respond to chemotherapeutic or corticosteroid treatments.42

Osteoblastoma Osteoblastoma is a rarer lesion than osteoid osteoma, occurring in patients from 10–25 years of KEY POINTS age. There is a 2:1 male-to-female predilection.40 The pattern of pain 1. The hallmark of may be similar to osteoma but is osteoid osteoma is not necessarily so. The associated sharp pain that is pain is less likely to be relieved by worse at night, NSAIDs. Osteoblastomas occur relieved by NSAIDS. primarily in the long bones of the Radiofrequency upper and lower extremities and ablation has the spine. Spinal lesions may presbecome the preent with scoliosis or neurological ferred treatment in deficit from nerve root compresmost cases. sion. Osteoblastoma is histologi2. Osteoblastoma is cally similar to osteoid osteoma similar to osteoid but is larger in size, often 2.0 cm or osteoma histologi41 more. As opposed to osteoid cally but is rarer, osteomas, these lesions are usually usually intramedullary. Treatment is with intramedullary, and curettage and grafting, or en bloc has a higher recurexcision with a small margin. rence rate after There is a recurrence rate of about treatment. 10–20%.

Fibrous Defects: Nonossifying Fibroma and Focal Cortical Defects Fibrous defects in bone are common in childhood and are often diagnosed incidentally. These lesions are usually in the metaphysis of the distal femur and proximal tibia. Incidence is equal in males and females, and the peak age is 10–20 years. Nonossifying fibromas appear near the physis and appear to migrate away from the physis as bone growth proceeds. The lesions are expansile and sharply marginated with scalloped edges and a multiloculated appearance (Figure 32–6). They are often eccentrically located in the bone. Histological examination reveals soft, friable yellow tissue with hemosiderin pigment. Cellular makeup includes spindle cells in a storiform pattern interspersed with regions of histiocytic cells and giant cells scattered throughout in irregular clusters.43 Observation of these lesions is usually adequate, because the natural history is of spontaneous regression over time. Pathological fracture may occur, which may be adequately managed with closed treatment. Occasionally, nonossifying fibromas may be painful. In these instances, curettage and bone grafting are reasonable treatment and have a low recurrence rate. Large lesions (>50% of bone diameter) are at higher risk

Histiocytosis X Langerhans cell, histiocytosis, or histiocytosis X is a disease process with solitary- or multiple-skeletal cystic lesions. The lesions are found in patients less than 20 years old in two thirds of cases, with the majority presenting in those aged 5–10 years. Patients present with pain, swelling, and fevers; laboratory evaluation may show an elevated erythrocyte sedimentation rate.9 Systemic symptoms are usually seen in conjunction with defined multisystem disease processes known as Hand-Schüller-Christian disease or Letterer-Siwe disease. The most commonly affected areas are the skull and femur. The lesions are usually intramedullary and diaphyseal. However, the radiographic appearance is highly variable and may mimic other skeletal lesions. The distinction between these lesions and Ewing’s sarcoma or osteomyelitis may be particularly difficult based on radiographic criteria alone. In general, well-defined

Figure 32–6 Nonossifying fibroma of the distal femur.

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for pathological fracture and therefore may also be prophylactically treated with open curettage and bone grafting.44 Focal cortical defects are lesions usually found on the medial posterior supracondylar ridge of the femur 1–2 cm above the epiphyseal plate with no associated clinical symptoms. There is a 3:1 male predominance, and one third of the lesions are bilateral. These KEY POINTS lesions are usually managed with observation alone given the low 1. Histiocytosis X is risk of pathological fracture. Chondromyxoid fibroma Similar in appearance to a fibroma or aneurysmal bone cyst, this is an eccentric metaphyseal lesion with sharp sclerotic, scalloped margins. Pain and tenderness are the most common presenting complaint. There is a slight male predominance, and the age range is primarily in the first three decades of life. The proximal tibia and distal femur are the most common sites

associated with multisystem disease. Bone lesions may require treatment if there is a risk of fracture. 2. Fibrous defects are relatively common and spontaneously regress. Observation is usually adequate. 3. Chondromyxoid fibroma is treated with curettage and bone grafting.

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of involvement.45 Microscopically, the tumor is bluish gray and grossly resembles hyaline cartilage. The tumor cells are spindled and stellate and may have bizarre-appearing nuclei. Treatment is curettage and bone grafting. They are reported to have the highest recurrence rate of all of the benign cartilage tumors, but complete curettage or marginal excisions are usually successful. Intraarticular Conditions Pigmented Villonodular Synovitis Pigmented villonodular synovitis (PVNS) is a monoarticular synovitis that occurs primarily in young to middle-aged adults. The knee is the affected joint in about 80% of cases. Recurrent atraumatic hemarthroses and mechanical symptoms are the presenting complaints. The synovium undergoes a proliferative villous nodular thickening. Histological evaluation of affected synovium reveals hemosiderin- and lipid-laden macrophages. These tightly packed histiocytes fill the tissue. Radiographically, there are lucencies on either side of the joint that may appear aggressive. MRI reveals scattered areas of very low signal intensity that represent hypertrophied synovium or fibrous components of the lesion (Figure 32–7). Treatment is total synovectomy. A combined

Figure 32–7 Pigmented villonodular synovitis. A, X-ray. B, Magnetic resonance imaging. C, Intraoperative view.

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approach may be used with arthroscopic anterior and open posterior synovectomy. Recurrence is not uncommon and may require repeat synovectomy.46,47 Synovial Chondromatosis

KEY POINTS

This entity is a rare benign metaplasia of the intimal layer of the synovial membrane characterized by multiple foci of cartilaginous nodules. There is a 2:1 male predominance, and young to middle-aged adults are affected. The process is monoarticular, and mechanical symptoms are reported from the affected joint. There is some suggestion that trauma may be an etiological factor, and cytological studies suggest a clonal nature to the cartilaginous proliferations.48 Radiographs show soft-tissue masses within the joint with varying degrees of calcification. In long-standing cases, there may be some associated joint arthropathy with bony erosion. The treatment is total synovectomy, either open or arthroscopic, with removal of loose bodies.49 Reconstructive arthroplasty may be necessary in cases of significant joint destruction.

1. PVNS is suspected with recurrent atraumatic hemarthroses. Total synovectomy is the treatment. Recurrence is common. The knee is most commonly affected. 2. Synovial chondromatosis may be associated with joint erosion and requires total synovectomy and removal of loose bodies. 3. Total synovectomy for PVNS or synovial chondromatosis may be undertaken with a combined arthroscopic anterior and open posterior approach.

The lesions however, can enter the joint by direct extension along ligamentous or capsular planes.53 The physis is only penetrated during later stages of the disease.54 Radiographically, the lesion is a tumor in the metaphysis of a long bone with radiolucent and/or radiodense features (Figure 32–8). The lesion appears aggressively, with poorly

Malignant Lesions Osteosarcoma Osteosarcoma is the most common malignant bone tumor in adolescents and children. The classic form is a bone-forming tumor of the medullary cavity of the metaphysis of a long bone. Several variants exist: parosteal and periosteal tumors, which are cortical lesions, and telangiectatic tumors, which are highly vascular aneurysmal tumors. Features of classic osteosarcoma include a tender, palpable mass on examination. Symptoms of pain, swelling, and mass are often present for weeks to months before presentation. A limp may be present. The patient usually does not demonstrate systemic symptoms at the time of presentation because severe systemic illness from pulmonary metastases is a late finding. Pathological fracture through a lesion is a relatively uncommon presenting feature. There is an equal distribution between males and females, and most patients are in the 10- to 20-year age range.50 The tumor has been described in every bone of the body but is relatively uncommon in the hands and feet. Disease may be multifocal, and skip lesions may be present. There is a predilection for the areas around the knee joint, with up to 50% located in this region in some series.51 In general, lesions do not penetrate the articular surface unless there has been a fracture into the joint.52 Fascial planes may present somewhat of a barrier to spreading of the tumor.

Figure 32–8 A, Osteosarcoma of the tibia with associated pathological fracture. B, Magnetic resonance imaging of the osteosarcoma lesion shown in (A).

Pediatric Musculoskeletal Tumors About the Knee

definable margins and soft-tissue extension. Periosteal new bone formation and a Codman’s triangle are often seen on x-ray. The central portion of the tumor may appear more heavily mineralized than marginal areas. On pathological examination, there is a hypercellular stroma with malignantappearing osteoblasts that produce an osteoid matrix. Spindle cells are seen with abundant mitotic figures. The parosteal variety occurs in an older age group and shows a high preference for the distal femur; it usually has a broad attachment to the cortex. The cortex appears thickened and deformed. There may be a cartilaginous cap. Knee joint motion may be limited. On occasion, the tumor may encircle the entire bone. On pathological examination, the tumor appears to be lower grade than the classic variety.55 The periosteal variety is often diaphyseal and has a particular preference for the tibia. It has the same age predilection as classic osteosarcoma. This is a surface lesion with an uninvolved medullary cavity. There is often abundant chondroid matrix with spiculated mineralization.56 The telangiectatic variety is a metaphyseal, purely radiolucent lesion with hemorrhagic tissue. Often these tumors appear as aneurysmal bone cysts. Treatment of osteosarcoma begins with accurate staging of the patient’s disease to include a chest CT and a bone scan. Approximately 10–20% of patients will have metastatic disease at the time of presentation, usually in the lung or in another bone. The mainstays of treatment are chemotherapy and surgical resection. Amputation is the KEY POINTS gold standard of surgical treatment, but limb-salvage procedures 1. Significant improvehave become quite successful in ments in survival appropriate cases. Limb salvage rates have been may be considered if there is no due primarily to local or distant progression of disrecent advances in ease with chemotherapy, and if the chemotherapy. related neurovascular bundles are 2. Limb-salvage techfree of tumor. A 5- to 10-mm niques are improvsurgical margin of normal tissue ing, and may be is required. In boys younger than considered in cases 12 years or girls younger than in which neurovas10 years with lesions about the cular bundles are knee, limb-length discrepancies free of disease and resulting from surgical resection chemotherapy is and ensuing contralateral growth effective. can be of major concern. Some 3. Amputation is the surgeons use expandable prosthegold standard and ses in these young children. In a may result in excelyoung child with a distal femoral lent functional lesion, amputation would lead to a outcome in the pedishort lever arm for a prosthesis, atric population. which becomes relatively shorter 4. In very young chilover time. In these cases, a sucdren, continued cessful alternative to transfemoral growth is a signifiamputation is the rotationplasty cant concern, and 57 procedure. special procedures The difficult nature of this such as rotationdisease, and the potentially displasty or an figuring surgical treatment expandable prosmodalities that are necessary to thesis may need to treat it, makes emotional and be considered. psychological support a critical

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aspect of treatment for these patients. Treatment in a cancer center specializing in children, visits with other patients with similar procedures, visits with physical therapists and prosthetists, and other supportive measures are invaluable in the treatment of these patients. Ewing’s Sarcoma Ewing’s sarcoma is part of a family of tumors derived from primitive round cells that share a common chromosomal translocation, (t11;22). The family of tumors is referred to as primitive neuroectodermal tumors.9 The tumor originally described by James Ewing in 1921 represents a poorly differentiated member of this family of tumors. It is the second most common malignant primary bone tumor in children, usually affecting 10- to 20-year-olds. If a diagnosis of Ewing’s sarcoma is given to a patient outside this age group, the diagnosis should be called into question. In these cases, the following pathologically similar-appearing tumors are more common: neuroblastoma (5 years or younger), lymphoma (30 years or older), myeloma (50 years or older). There is a slight male preference, and the tumor is rarely found in Asian or black populations. The lesions are more frequently found in the pelvis and lower extremity and are usually diaphyseal.58 There is no known preference for the knee region. Clinical findings include local pain and swelling and a tender local mass. Joint stiffness and limp may be present. Pathological fracture is a common presenting feature. Similar to osteosarcoma, patients are generally not systemically ill at the time of presentation. Radiologically, the lesion demonstrates a permeative appearance and can be either radiolucent or radiodense. There is evidence of periosteal new bone formation, and a Codman triangle is often seen. There may be enlargement of the bone, with laminations of bone known as “onion skinning.” Areas of bone appear mottled, and there is often evidence of an associated soft-tissue mass. MRI is useful in determining the extent of the lesion, with T1-weighted series best demonstrating marrow involvement and T2-weighted series demonstrating the soft-tissue mass (Figure 32–9). CT scanning may be useful for demonstrating the amount of cortical destruction.59

Figure 32–9 Ewing’s sarcoma of the fibula in a 14-year-old girl.

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On pathological examination, the lesion is found to arise in the marrow spaces of the involved bone and is a whitish-grey soft-tissue mass. Necrotic and hemorrhagic areas are found, and neoplastic tissue destroys and replaces normal bone. There is usually an associated soft-tissue mass, which extends beyond the bony boundary of the lesion. The necrotic areas of the tumor and its whitish appearance at the time of surgery may often lead to a misinterpretation as pus. Osteomyelitis is thus one of the differential diagnoses in these cases, and care must be taken to avoid misdiagnosis. Histologically, the tumor is composed of sheets of small polyhedral or round cells with pale cytoplasm and illdefined boundaries. There are uniform round nuclei. Glycogen stores are seen, which distinguishes the lesion from lymphoma on histological examination. Some signs of neural differentiation may be seen, such as S100-staining and neuron-specific enolase staining.60 The genetic basis of Ewing’s sarcoma has been a topic of intense investigation, because a common chromosomal translocation is found in these tumors. Most commonly this is a (t11;22) translocation, but (t21;22), t(7;22), and others have been described. The EWS gene is found at the locus on chromosome 22, encoding a DNA transcription factor. Fusion of this gene to the gene found on chromosome 11, 21, 7, or others encoding a DNA-binding protein is responsible for the transformation of the host cell line.61 Initial workup of the patient with Ewing’s sarcoma includes chest CT, bone scan, and bone-marrow biopsy to evaluate for metastatic disease. Metastatic disease at presentation is found in about 25% of cases. The prognosis for these patients is poor.62 Treatment is with multiagent chemotherapy, radiation therapy, and surgery. Radiation therapy carries an associated risk of secondary malignancy.63 Surgery for Ewing’s sarcoma begins with biopsy. Biopsy should be performed open, with special attention paid to avoiding generation of cortical defects. Large cortical defects in combination with radiation increase the risk for pathological fracture. Local resection of tumors has the KEY POINTS significant benefit of reducing the dosages of radiation necessary, 1. Prognosis for and thereby reducing risk of secpatients with ondary malignancy. Amputation metastatic disease at is a surgical option, especially in presentation is poor. cases of pathological fractures or 2. Multiagent bulky tumors with poor response chemotherapy, radito chemotherapy. In very young ation, and surgery patients with tumors about the are used in combiknee, chemotherapy, radiation, nation for treatment. and surgery can all contribute to 3. The genetic basis of growth arrest of the affected limb Ewing’s sarcoma is and result in leg-length discrepbecoming increasancy. In these cases, amputation ingly elucidated. is a reasonable consideration.

commonly affects Caucasian children than black or Asian children.65 Rhabdomyosarcomas are also one of the tumors found in patients with the Li-Fraumeni syndrome, the multiple-malignancy condition that occurs as a result of a defect in the tumor suppressor gene p53.66 Rhabdomyosarcoma represents more than one half of all soft-tissue tumors in children. The cause is not known, and the tumor can occur at any site. The usual presentation is a painful or painless mass. The mass is often deep, so redness, swelling, and warmth are usually undetectable. There are no systemic signs at this common stage of presentation. However, regional lymph nodes may be positive at the time of presentation. There are several pathological subtypes with differing prognoses. There include embryonal, botryoid, alveolar, and pleomorphic. The embryonal form is most common in children; up to one half of the tumors found in the extremities of children are of this subtype. The remainder are alveolar or undifferentiated. The alveolar subtype has a poorer prognosis and is more commonly associated with positive lymph-node disease at the time of presentation. Imaging of the lesion is best done with MRI to define the soft-tissue mass (Figure 32–10). Bone scan, chest CT, and bone-marrow aspiration are performed to stage the disease and evaluate for metastases. Histologically, the tissue is composed of large cells with an eosinophilic cytoplasm with few distinct defining characteristics. Muscle striations may be seen. Diagnosis is confirmed by immunohistochemical staining, which confirms the presence of muscle-specific actin, myosin, desmin, myoglobin, z-protein, MyoD, and vimentin. Genetic studies suggest that a loss of heterozygosity at chromosome 15 may be important to the development of the tumor. The alveolar form has a (t2:13), or more rarely t(1;13), translocation.67 The treatment consists of chemotherapy, and in most cases, radiation therapy before or after complete surgical resection. Amputation is a reasonable option, particularly

Rhabdomyosarcoma Rhabdomyosarcoma occurs in about 4–7 patients per 1 million under 15 years of age, for a total of about 250 new cases annually in the United States.64 Approximately two thirds of these patients are under 10 years of age. There is a slightly higher incidence in boys than in girls. The condition more

Figure 32–10 Rhabdomyosarcoma is seen in the thigh of this 10-year-old boy presenting with knee pain.

Pediatric Musculoskeletal Tumors About the Knee

in younger children. In general, extremity lesions have a poorer prognosis than lesions at other sites. Overall, the 5-year survival rate for a child with an extremity rhabdomyosarcoma is 74%. If metastatic disease is present at the time of diagnosis, this falls to 20–30%.72 There is no known predilection for the knee region. Summary

KEY POINTS 1. Rhabdomyosarcoma occurs in young children, with two thirds of cases occurring in patients under 10 years of age. 2. Extremity lesions have a poorer prognosis than other sites. 3. Treatment is chemotherapy and radiation in addition to surgery.

Musculoskeletal tumors, although considered rare overall, have a predilection for the knee region in the pediatric population. The basic principles of careful history and physical examination, detailed laboratory and imaging evaluation, and knowledge of the characteristics of the tumor are critical for appropriate management and care of patients with these conditions. Caution should be employed in any case of knee pain with unclear etiology, and the differential diagnosis in these patients should include the possibility of tumor at the hip, spine, or knee until adequate evidence is found to the contrary. Early referral to an oncological specialist is warranted in the management of patients with these conditions. References 1. Carola AS, Arndt MD, Crist WM: Common musculoskeletal tumors of childhood and adolescence. N Engl J Med 341:342–352, 1999. 2. Link MP, Gebhardt MC, Meyer PA: Osteosarcoma. In Pizzo PA, Poplack DG (eds): Principles and Practice of Pediatric Oncology. 4th ed. Philadelphia: Lippincott-Raven, 2003. 3. Tucker MA, D’Angio GJ, Boice JD, et al: Bone sarcomas linked to radiotherapy and chemotherapy in children. N Engl J Med 317:588–593, 1997. 4. Schmike RN, Lowman JT, Cowan AB: Retinoblastoma and osteogenic sarcoma in children. Cancer 34:2077–2079, 1974. 5. Unni KK: Dahlin’s Bone Tumors: General Aspects and Data on 11,080 cases. 5th ed. Philadelphia: Lippincott-Raven, 1996. 6. Joyce MJ, Mankin HJ: Caveat arthoscopos: Extra-articular lesions of bone simulating intra-articular pathology of the knee. J Bone Joint Surg Am 65:289–292, 1983. 7. Lewis MM, Reilly JF: Sports tumors. Am J Sports Med 15:362–365, 1987. 8. Muscolo DL, Ayerza MA, Makino A, et al: Tumors about the knee misdiagnosed as athletic injuries. J Bone Joint Surg Am 85:1209–1214, 2003. 9. Herring JA: Benign musculoskeletal tumors. In Herring JA (ed): Tachdjian’s Pediatric Orthopaedics, 3rd ed. Philadelphia: Saunders, 2002, pp 152–166. 10. Neer CS, Francis KC, Johnston AD: Current concepts in the treatment of solitary unicameral bone cyst. Clin Orthop 97:40–51, 1973. 11. Hecht AC, Gebhardt MC: Diagnosis and treatment of unicameral and aneurysmal bone cysts in children. Curr Opin Pediatr 10:87–94, 1998. 12. Campanacci M, Capanna R, Picci P: Unicameral and aneurysmal bone cysts. Clin Orthop 204:25–36, 1986. 13. Cohen J: Unicameral bone cysts. Ortho Clin N Amer 8:715–736, 1972. 14. Levy WM, Miller AS, Bonakdarpour A, et al: Aneurysmal bone cyst secondary to other osseous lesions: report of 57 cases. Am J Clin Pathol 63:1–8, 1975. 15. Kransdorf MJ, Sweet DE: Aneurysmal bone cyst: concept, controversy, clinical presentation, and imaging. Am J Roentgenol 164:573–580, 1995. 16. Marcove RC, Sheth DS, Takemoto S, et al: The treatment of aneurysmal bone cyst. Clin Orthop 311:157–163, 1995. 17. Papagelopoulos PJ, Currier BL, Shaughnessy WJ, et al: Aneurysmal Bone cyst of the spine: management and outcome. Spine 23:621–628, 1998.

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51. Unni KK: Dahlin’s Bone Tumors: General Aspects and Data on 11,080 Cases. 5th ed. Philadelphia: Lippincott-Raven, 1996. 52. Schima W, Amman G, Stiglbauer R, et al: Preoperative staging of osteosarcoma: efficacy of MR imaging in detecting joint involvement. Am J Roentgenol 163:1171–1175, 1994. 53. Simon MA, Hecht JD: Invasion of joints by primary bone sarcoma in adults. Cancer 50:1649–1655, 1982. 54. Enneking WF, Kagan A: Transepiphyseal extension of osteosarcoma: incidence, mechanism and implications. Cancer 41:1526–1537, 1978. 55. Unni KK, Dahlin DC, Beabout JW, et al: Parosteal osteogenic sarcoma. Cancer 37:2466–2475, 1976. 56. Unni KK, Dahlin DC, Beabout JW: Periosteal osteogenic sarcoma. Cancer 37:2476–2485, 1976. 57. Camissa FP Jr, Glasser DB, Otis JC, et al: The Van Nes tibial rotationplasty: a functionally viable reconstructive procedure in children who have a tumor of the distal end of the femur. J Bone Joint Surg Am 72:1541–1547, 1990. 58. Kissane JM, Askin FB, Foulkes M, et al: Ewing’s sarcoma of bone: clinicopathologic aspects of 303 cases form the Intergroup Ewing’s Sarcoma Study. Hum Pathol 14:773–779, 1983. 59. Eggli KD, Quiogue T, Moser RP, Jr: Ewing’s Sarcoma. Radiol Clin North Am 31:325–337, 1993. 60. Perlman EJ, Dickman PS, Askin FB, et al: Ewing’s Sarcoma-routine diagnostic utilization of MIC2 analysis. Hum Pathol 25:304–307, 1994.

61. Delattre O, Zucman J, Melot T, et al: The Ewing’s family of tumors— a subgroup of small round cell tumors defined by specific chimeric transcripts. N Engl J Med 331:294–299, 1994. 62. Grier HE: The Ewing’s family of tumors: Ewing’s sarcoma and primitive neuroectodermal tumors. Pediatr Clin North Am 44:991–1004, 1997. 63. Tucker MA, D’Angio GJ, Boice JD, Jr, et al: Bone sarcomas linked to radiotherapy and chemotherapy in children. N Engl J Med 317:588–593, 1987. 64. Wexler LH, Crist WH, Helman LJ: Rhabdomyosarcoma and the undifferentiated sarcomas. In Pizzo PA, Poplack DG (eds): Principles and Practice of Pediatric Oncology. 4th ed. Philadelphia: LippincottRaven, 2003, pp 769–794. 65. Stiller CA, McKinney PA, Bunch KJ, et al: Childhood cancer and ethnic groups in Britain: A United Kingdom Children’s Cancer Study Group (UKCCSG) study. Br J Cancer 64:543–548, 1991. 66. Li FP, Fraumeni JF Jr: Prospective study of a family cancer syndrome. JAMA 247:2692–2694, 1982. 67. Pappo AS, Shapiro DN, Crist WM, et al: Biology and therapy of pediatric rhabdomyosarcoma. J Clin Oncol 13:2123–2139, 1995. 68. Carola AS, Arndt MD, Crist WM: Common musculoskeletal tumors of childhood and adolescence. N Engl J Med 341:342–352, 1999.

Index Page numbers followed by the letter b refer to boxes; those followed by the letter f refer to figures, and those followed by the letter t refer to tables.

A AAS. See Androgenic anabolic steroids Abscesses, androgenic anabolic steroid use and, 107 ACI. See Autologous chondrocyte implantation ACL. See Anterior cruciate ligament Activated partial thromboplastin time (APTT), 83 Active retaining test, 23, 25, 25f Acupuncture, for neuropathic pain, 479 Acute hematogenous osteomyelitis (AHO) complications of, 458 diagnosis of, 452–454 bone scan, 454, 454f computed tomography, 454 history, 452 magnetic resonance imaging, 454 physical examination, 452 radiographs, 453, 453f ultrasound, 453–454 differential diagnosis of, 456 bone infarction, 457 Henoch-Schönlein purpura, 457 juvenile rheumatoid arthritis, 456 Lyme disease, 456 rheumatic fever, 456 trauma, 456–457 tumor, 457 epidemiology of, 451 laboratory studies, 454–455 organisms, 455–456 Hemophilus influenzae, 455 Kingellia kingae, 456 Neisseria gonorrhoeae, 456 Salmonella, 456 Staphylococcus aureus, 455 Streptococci, 455 pathophysiology of, 451–452 subacute, 458 treatment of, 457–458 Adalimumab, 468t Adenosine triphosphate (ATP), 110 Adolescents Training and Learning to Avoid Steroids (ATLAS) program, 105 AHO. See Acute hematogenous osteomyelitis Alpine sports injuries, 4t, 5–6 American Heart Association, cardiovascular preparticipation screening and, 95–96, 95b Amphetamines, 109 Amputation, neuropathic pain and, 479–481 Androgenic anabolic steroids (AAS), 105–108 associated behaviors of, 106–107 basic science of, 106 decrease usage of, 107–108 first use of, 106 intervention of usage of, 107–108 motivation of usage of, 107 performance studies, 106 risk factors and, 107 side effects of, 106–107

Androstenedione, 109 Anesthesia, surgery of knee and intraoperative evaluation, 151 options of, 152–153 epidural, 153 general, 152 intraarticular, 153, 153t intravenous regional, 152 peripheral nerve blocks, 153 regional techniques, 152 spinal, 153 tourniquets, 153 premedication, 151 preoperative evaluation in, 151 Aneurysmal bone cyst, 489–490, 490f Anterior cruciate ligament (ACL) anatomy of, 318–319, 319f biomechanics, 319–320, 319f congenital deformity of, 317–318, 318f direct repair of, 327–328 embryology of, 317 extraarticular reconstruction, 328, 328f injury of, 2–3, 20 diagnosis of, 322–323 epidemiology of, 320 female athlete, 123–128 factors predisposing to, 125 femoral notch, 125 hyperextension, 125 injury mechanism, 124–125, 125f, 126f laxity, 125 neuromuscular, 128 prevention of, 128 sex hormones, 126–127 surgical treatment, 123–124 frequency in, 77 management of, 79 natural history of, 321–322 patterns of, 321 preparticipation physical examination and, 98 risk factors for, 320 magnetic resonance imaging and, 51–52 physeal-sparing procedures, 328, 333–334, 345, 369 adult-type, 345, 369 graft options, 369–371, 371t, 372f partial transphyseal, 334, 345 postoperative rehabilitation for, 371 physical function of, 323–325, 323f reconstruction epiphyseal, with quadruple hamstring grafts indications for, 335 postoperative management of, 338 postoperative rehabilitation for, 338–340 results of, 340 setup for, 335 technique of, 335, 336–341f, 338 partial transphyseal technique graft fixation, 349, 352–353f indications for, 346–347, 346f, 347f technique of, 347, 348–349f tibial tunnel, 348–349, 349–352f

Anterior cruciate ligament (ACL) (Continued) physeal-sparing femoral and transphyseal tibial technique, with quadriceps ligament indications for, 354–357f postoperative management of, 358 technique of, 355–357, 358–363f rehabilitation program for partial tears, 373 postoperative, 372–373 preoperative, 371 with semitendinous and gracilis tendons arthroscopic examination, 342 indications for, 342 postoperative management of, 344 preoperative assessment of, 342, 342f preparation for, 343–344 results of, 344, 344f setup for, 342 technique of, 342 treatment for, 342–342, 343f transphyseal technique, with autogenous hamstring tendons indications for, 364 postoperative rehabilitation for, 368–369 rationale for, 364 setup for, 364–368, 364–369f skeletal maturity assessment, 325–326, 326f, 327f, 327t tears of, female athlete, 113, 116 treatment options, 326–327 Anteromedial tibial tuberosity, for patellofemoral malalignment indications for, 173–174 postoperative management of, 175 results of, 175 setup for, 174 technique of, 174–175, 174–176f Anticonvulsants, for neuropathic pain, 477–478 Apical ectodermal ridge (AER), 43 Apley compression test, 19 APTT. See Activated partial thromboplastin time Arthritis. See also Septic arthritis imaging and, 59–60, 60f juvenile rheumatoid, 80b, 81, 456 clinical course of, 464 diagnosis of, 463, 464b epidemiology of, 463 laboratory studies, 465 outcomes of, 469 pathology of, 464 physical examination of, 464–465, 465f presentation of, 463, 464b radiographic studies of, 465–467, 466f treatment of, 467–469 adjunct therapies, 469 biological response modifiers, 468t, 469 disease-modifying antirheumatic drugs, 467–469, 468t intraarticular corticosteroids, 467 nonsteroidal antiinflammatory drugs for, 467 reactive, 81

501

502

Index

Arthrocentesis, primary care investigations and, 83, 87, 87t Articular cartilage development of, 41–42 gene-based therapy, 36–39, 37f, 37t, 38f histologic zones of, 34–35, 34f injury of, healing response to, 36 ligaments, 35–36 magnetic resonance imaging of, 51 meniscus, 36 musculotendinous unit of, 35 Athlete amphetamines, 109 androgenic anabolic steroid use in, 105–108 androstenedione, 109 creatine, 109–110 Dexedrine, 109 female anterior cruciate ligament injuries, 123–128 factors predisposing to, 125 femoral notch, 125 hyperextension, 125 injury mechanism, 124–125, 125f, 126f laxity, 125 neuromuscular, 128 prevention of, 128 sex hormones, 126–127 surgical treatment, 123–124 anterior cruciate ligament tears and, 113, 116 anterior knee pain, 118–119, 121, 121t, 123 college sports, 114f development of, 116–118 growth of, 116–118, 117f lower extremity alignment, 117–118, 118–120f sports participation, 114f triad, 128–129 human growth hormone, 108–109 injuries of, 4t, 5 pseudoephedrine, 109 ATLAS. See Adolescents Training and Learning to Avoid Steroids program ATP. See Adenosine triphosphate Autologous bone sticks, 286 Autologous chondrocyte implantation (ACI), 303–307, 303f complications, 306–307 results of, 307 technique, 304–306, 304f, 305f, 306f

B Ball sports injuries, 6 Basketball injuries, 4–5, 4t Bioabsorbable screws, 286 Blount’s disease, 441, 442, 443f, 444f, 446f BMP. See Bone morphogenetic protein Bone morphogenetic protein (BMP), 38 Bones deformity, 436, 440f fractures of, 33–34 immature, anatomy of, 377–378, 378f magnetic resonance imaging of, 53–54 mechanical role of, 33 metabolic function of, 33 remodeling of, 33 Borrelia burgdorferi, 456–469 Bowlegs, 44, 44f, 444f

C Calcified cartilage, 35 Cannulated screws, 286, 287–290f Cardiovascular disease, sports participation and, 92–93 Causalgia, 481–484, 482f, 482t, 483b management of, 89 CBC. See Complete blood count CFS. See Chronic fatigue syndrome Child abuse injuries, 6 Chondri defects of microfracture in indications for, 308–309, 308–310f postoperative management of, 309–311 results of, 311 mosaicplasty for indications of, 298, 298f, 299f postoperative rehabilitation of, 299–301, 300f, 301f procedure principles of, 298 surgical technique of, 299, 300f injuries of classification of, 295–296, 296f, 296t imaging of, 295, 295f management of, 296, 297f, 307, 311 natural history of, 294 signs of, 294–295 symptoms of, 294–295 Chondroblastoma, 492–493f imaging and, 60 Chondromalacia patellae (CMP), 10 Chondrometaphyseal dysplasia (Schmid type), 436, 438f Chondromyxoid fibroma, 495 Chronic fatigue syndrome (CFS), 89–90 Chronic pain syndromes, 88–89 CKC. See Closed kinetic chain exercise Closed kinetic chain (CKC) exercise, 143f CMP. See Chondromalacia patellae Collateral ligament(s), 35–36 injury of, management of, 80 lateral anatomy of, 384–385, 385–386f biomechanics of, 384–385, 385–386f injury to, 20 clinical examination of, 386–388, 388f incidence of, 385–386 mechanism of, 385–386 treatment of, 388, 392 magnetic resonance imaging of, 51–52 medial anatomy of, 379–381, 380f biomechanics of, 379–381, 380f injury of, 20 evaluation of, 381–384, 381f, 381t treatment of, 381–384, 381f, 381t sprain, rehabilitation program, 382–383–383f Complete blood count (CBC), 83 Complex regional pain syndrome (CRPS), 89, 481–484, 482f, 482t, 483b Congenital deformities cruciate ligaments, absence of, 428–429 dislocation classification of, 421–422, 423f clinical features of, 422, 423f etiology of, 421, 422f outcome of, 428 of patella classification of, 430 clinical features of, 430, 431f etiology of, 430

Congenital deformities (Continued) of patella (Continued) outcome of, 432 pathology of, 431, 431b radiographic findings of, 430–431 treatment of, 431–432 pathology of, 423–424 quadriceplasty for postoperative management of, 427 results of, 427 technique of, 425–427, 425–427f radiographic findings, 422–423, 423f treatment of, 424 hypoplasia, of patella, 432–434, 433f, 434f menisci, absence of, 429–430 snapping knee, 429 tibiofemoral subluxation, 429 Coxo-podo-patellar syndrome, 433 Cozen’s fractures, 437 Creatine, 109–110 basic science of, 110 performance studies of, 110 side effects of, 110 CRPS. See Complex regional pain syndrome Cruciate ligament(s), 35–36 absence of, 428–429 posterior anatomy of, 392–393, 393f biomechanics of, 393 evaluation of, 394, 394t incidence of, 394 management of, 394, 394t natural history of, 394 repair and reconstruction of indications for, 389–390, 389–391f postoperative management of, 391–392 setup for, 390 technique of, 391 treatment of, 394–395 Cycling injuries, 4t, 5 Cysts aneurysmal bone, 489–490, 490f simple, 489, 489f

D Deoxyribonucleic acid (DNA), 36–39, 37f, 37t, 38f Dexedrine, 109 Diagnostic and Statistical Manual of Mental Disorders (DSM3-R), 107 Dianabol (methandrostenolone), 106 Dietary rickets, 436, 440f Discoid menisci, 242–24f, 242–244 anatomy of, 260–261 classification of, 260–261, 261f evaluation of, 261 imaging studies of, 261, 263f incidence of, 260 natural history of, 262 outcome of, 271 presentation of, 261 prevalence of, 260 prognosis of, 271 saucerization and repair of indications for, 264, 265f, 266f postoperative management of, 269–270 results of, 270 setup for, 264–265 technique of, 265–269, 267–270f treatment of, 262–264, 263f, 271

Index

Dislocation classification of, 421–422, 423f clinical features of, 422, 423f etiology of, 421, 422f outcome of, 428 of patella chronic, 176–177 clinical aspects of, 177 surgical treatment of, 177 imaging of, 166–167, 167f pathoanatomy of, 166–167 physical examination of, 166 recurrent imaging of, 168 Insall’s proximal realignment, 168–169, 168f lateral retinacular release, 168 physical examination of, 167–168 symptoms of, 167 treatment of, 168 symptoms of, 166 treatment of, 167 pathology of, 423–424 quadriceplasty for postoperative management of, 427 results of, 427 technique of, 425–427, 425–427f radiographic findings, 422–423, 423f treatment of, 424 DNA. See Deoxyribonucleic acid Down syndrome, 28 DSM3-R. See Diagnostic and Statistical Manual of Mental Disorders

E ECM. See Extracellular matrix EGF. See Epidural growth factor Ehlers-Danlos syndrome, 16 Electrotherapy, 141, 143 Ellis-van Crevald syndrome, 436 Ely test, 134, 139f Embryology, of knee growth plates, 28 ligaments, 30–31, 30f menisci, 29–30 patellofemoral mechanism, 28–29, 29f tibial tubercle, 31–32 Enchondroma, 491 Epidural anesthesia, 153 Epidural growth factor (EGF), 38 Erythrocyte sedimentation rate (ESR), 83 ESR. See Eerythrocyte sedimentation rate Etanercept, 468t Ewing’s sarcoma, 497–498, 497f imaging and, 61 Exertional hyperthermia, 96 Extensor mechanism, functional anatomy of, 181 Extraarticular tissues, injury to, healing response to, 36 Extracellular matrix (ECM), 236

F Femur deformity of, 447f distal fractures of anatomy of, 222, 223f complications of, 224–225 epidemiology of, 222 management of, 222–224

Femur (Continued) distal (Continued) fractures of (Continued) outcome of, 224–225 growth plates, 45 ossification center appearance in, 43, 44 physeal closure time, 45 FGF-2. See Fibroblast growth factor Fibroblast growth factor (FGF-2), 38 Fibroblast growth factor 8 (FGF-8), 43 Fibrochondrocyte, 29 Fibromyalgia syndrome (FS), 89 Fibrous dysplasia, 491 Fibula, proximal ossification center appearance in, 44 physeal closure time, 45 Flow-mediated dilatation (FMD), 107 FMD. See Flow-mediated dilatation Focal fibrocartilaginous dysplasia, 444–445 Football injuries, 4, 4t Fractures, 33–34 classification of, 217, 218f osteochondral etiology of, 311–312, 312–315f history and physical examination of, 312–313 imaging of, 313, 315 management of, 315–316, 315f of patella anatomy of, 232 classification of, 232 complications of, 233 epidemiology of, 232 imaging of, 232, 232f management of, 79, 233 osteochondral, 233, 233f outcomes of, 233 physical examination of, 233 physeal of distal femur anatomy of, 222, 223f complications of, 224–225 epidemiology of, 222 management of, 222–224 outcome of, 224–225 of proximal tibia anatomy of, 217f, 226–227f complications of, 228 epidemiology of, 226 management of, 226–228 outcome of, 228 of tibial tuberosity classification of, 228, 228f complications of, 231 epidemiology of, 228 imaging of, 229 management of, 229–231 outcome of, 231 physical examination of, 229 tibial tubercle, open reduction internal fixation of, 229f indications for, 229–230 postoperative management of, 230–231 prognosis of, 231 setup for, 230 technique of, 230, 230f tibial tuberosity, 228–231, 228f FS. See Fibromyalgia syndrome

G Gallazzi procedure, 172, 173 GAM. See Gene-activated matrices

503

Gene-activated matrices (GAM), 39 Gene-based therapy, articular cartilage and, 36–39, 37f, 37t, 38f growth factors, 38 vectors, 39 in vivo versus ex vivo, 38–39 Genu valgum, 15 Growing knee anatomy of, 215–216 vascular, 216, 217f biomechanics of, 216 fractures of classification of, 217, 218f of distal femur anatomy of, 222, 223f complications of, 224–225 epidemiology of, 222 management of, 222–224 outcome of, 224–225 nonphyseal, 233 of proximal tibia anatomy of, 217f, 226–227f complications of, 228 epidemiology of, 226 management of, 226–228 outcome of, 228 of tibial tuberosity classification of, 228, 228f complications of, 231 epidemiology of, 228 imaging of, 229 management of, 229–231 outcome of, 231 physical examination of, 229 imaging of clinical guidelines, 222 radiographic evaluation of, 219–221, 220–221f injury of history, 217–218 physical examination, 218–219 joint dislocation, 233

H Hand-Schüller-Christian disease, 494 HD. See High-density lipoprotein Heat/cold therapy, 141 Hemarthrosis, 82 Hemophilia, 82 Hemophilus influenzae, 455 Henoch-Schönlein purpura, 457 Hepatitis B, androgenic anabolic steroid use and, 107 Hepatitis C, androgenic anabolic steroid use and, 107 Herbert Screws, 286, 288–290f HGH. See Human growth hormone High-density lipoprotein (HDL), 107 Histiocytosis X, 494 Histology, of knee development, 41–43, 42f History, of pediatric knee, 14 HIV. See Human immunodeficiency virus Homoeobox transcription factor genes (hox genes), 43 Hughston posteromedial drawer sign, 383f Human growth hormone (hGH), 108–109 Human immunodeficiency virus (HIV), androgenic anabolic steroid use and, 107 Hydrotherapy, 141 Hydroxychloroquine, 468t Hypochondroplasia, 436, 436f, 437f

504

Index

I Idiopathic valgus, 437, 441f IGF-1. See Insulin-like growth factor Iliotibial band (ITB) injection of, 85–86, 86f Ober test and, 133–134, 139f Iliotibial band (ITB) friction syndrome, 82 Imaging, of knee arthritis, 59–60, 60f Blount disease, 54, 55f chondri, 295, 295f chondroblastoma, 60 clinical guidelines, 222 congenital disorders, 54–55 developmental disorders, 54–55 developmental variants in magnetic resonance imaging, 47–48, 48f radiography, 47, 48f discoid meniscus, 55, 56f, 261, 263f epiphyseal hypoplasia, 54, 54f Ewing’s sarcoma, 61 fractures osteochondral, 313, 315 of patella, 232, 232f physeal, of tibial tuberosity, 229 infection, 58–59 ligaments, 55–56, 57f lymphoma, 61 meniscus, 55, 241–242, 241f Osgood-Schlatter disease, 182, 182f osteochondral fractures, 313, 315 injuries, 56 osteogenic sarcoma, 61 osteomyelitis, 58–59 patella dislocation of, 166–167, 167f recurrent, 168 fractures, 232, 232f lesion sites, 190, 191f patellar hypoplasia, 54, 54f primary care investigations and, 83 quadriceps, 190, 191f, 195 radiographic evaluation of, 219–221, 220–221f technical considerations, 48, 54 tendinopathy, 190, 191f tibial tuberosity, 229 trauma, 55–58, 78, 83 acute ligaments, 55–56, 57f menisci, 55 osteochondral injury, 56 physeal injuries, 56–57, 58f chronic osteochondritis dissecans, 58, 59–60f patellar tendon abnormalities, 57–58, 59f tumor, 60–61, 61f Infections acute hematogenous osteomyelitis complications of, 458 diagnosis of, 452–454 bone scan, 454, 454f computed tomography, 454 history, 452 magnetic resonance imaging, 454 physical examination, 452 radiographs, 453, 453f ultrasound, 453–454 differential diagnosis of, 456 bone infarction, 457 Henoch-Schönlein purpura, 457 juvenile rheumatoid arthritis, 456

Infections (Continued) acute hematogenous osteomyelitis (Continued) differential diagnosis of (Continued) Lyme disease, 456 rheumatic fever, 456 trauma, 456–457 tumor, 457 epidemiology of, 451 laboratory studies, 454–455 organisms, 455–456 Hemophilus influenzae, 455 Kingellia kingae, 456 Neisseria gonorrhoeae, 456 Salmonella, 456 Staphylococcus aureus, 455 Streptococci, 455 pathophysiology of, 451–452 subacute, 458 treatment of, 457–458 imaging and, 58–59 neonatal, 458 of prepatellar bursa, 458 Infliximab, 468t Injections, of knee after care of, 87 iliotibial band, 85–86, 86f indications for, 84 pes anserine, 86, 86f prepatellar bursa, 86–87, 86f setup for, 84 technique of, 84–85, 84f, 85f Injuries activities of, 4–6 alpine sports, 5–6 athletics, 4t, 5 ball sports, 6 basketball, 4–5, 4t child abuse, 6 cycling, 4t, 5 football, 4, 4t road traffic accidents, 6 roller sports, 4t, 5 soccer, 4t, 5 trampoline-related, 6 age and, 2–3, 2f of anterior cruciate ligament, 2–3, 20 diagnosis of, 322–323 epidemiology of, 320 female athlete, 123–128 frequency in, 77 management of, 79 natural history of, 321–322 patterns of, 321 preparticipation physical examination and, 98 risk factors for, 320 characteristics of, 6–7, 6t, 7t, 8t of chondri classification of, 295–296, 296f, 296t imaging of, 295, 295f management of, 296, 297f, 307, 311 natural history of, 294 signs of, 294–295 symptoms of, 294–295 epidemiology of, 76–77 fractures, 7t, 8, 9t, 10, 400–402 gender and, 2–3, 3f incidence of, 2, 2f, 3f of lateral collateral ligament, 20 clinical examination of, 386–388, 388f incidence of, 385–386 mechanism of, 385–386 treatment of, 388, 392

Injuries (Continued) of medial collateral ligament, injury of, 20 evaluation of, 381–384, 381f, 381t treatment of, 381–384, 381f, 381t of meniscus, 8, 79–80 osteochondral, 56 outcome of, 11 patterns of, 76 physeal, 79–80 plexus, 481 prevention of, 11 resistance training and reduction of, 64–65, 65t risk factors, 3–4 extrinsic, 4 intrinsic, 4 soft tissue, 7, 7t ligament, 7, 7t muscle, 7 tendon, 7, 7t sports-related, 1 tissue, 36 Insall’s proximal realignment, 168–169 Insulin-like growth factor (IGF-1), 38 Intraarticular anesthesia, 153, 153t Intraarticular corticosteroids, for juvenile rheumatoid arthritis, 467 Intraarticular tissues, injury to, healing response to, 36 Intraepiphyseal elevating osteotomy, 447f Intravenous regional anesthesia (IVRA), 152 Ischia-patellar dysplasia, 433 ITB. See Iliotibial band IVRA. See Intravenous regional anesthesia

J JOCD. See Juvenile osteochondritis dissecans Joint range of motion assessment form, 139f Joints, development of, 41 JRA. See Juvenile rheumatoid arthritis JSpAs. See Juvenile-onset spondyloarthropathies Juvenile osteochondritis dissecans (JOCD) arthroscopic transarticular drilling for background of, 283, 284f postoperative management of, 284 fixation for crater preparation, 286 existing fixation implants, 286, 287–293f Juvenile rheumatoid arthritis (JRA), 80b, 81, 456 clinical course of, 464 diagnosis of, 456, 463, 464b epidemiology of, 463 laboratory studies, 465 outcomes of, 469 pathology of, 464 physical examination of, 464–465, 465f presentation of, 463, 464b radiographic studies of, 465–467, 466f treatment of, 467–469 adjunct therapies, 469 biological response modifiers, 468t, 469 disease-modifying antirheumatic drugs, 467–469, 468t intraarticular corticosteroids, 467 nonsteroidal antiinflammatory drugs for, 467 Juvenile-onset spondyloarthropathies (JSpAs), 81

K Kentucky Sports Medicine (KSM), 115t, 116t Kingellia kingae, 456

Index

KSM. See Kentucky Sports Medicine Kübler-Ross Elisabeth, 72

L Laboratory studies, primary care investigations and, 83 Lachman’s test, 20 Lamina splendens, 34 Lamotrigine, for neuropathic pain, 478 Langenkiold classification, 442, 443f Langerhans cell. See Histiocytosis X Larsen’s syndrome, 16, 28 Lateral collateral ligament (LCL) anatomy of, 384–385, 385–386f biomechanics of, 384–385, 385–386f injury to, 20 clinical examination of, 386–388, 388f incidence of, 385–386 mechanism of, 385–386 treatment of, 388, 392 Lateral patellar compression syndrome lateral retinacular release, 162, 163f physical examination of, 156 postoperative rehabilitation, 162, 166 radiographic examination of, 156 symptoms of, 156 treatment of, 156, 162 Lateral retinacular release, with medial plication under arthroscopic control indications for, 163 postoperative management of, 165 results of, 165–166 setup for, 163 technique of, 163–165, 164f, 165f Lazarus and Folkman’s transactional model of stress, 72 LCL. See Lateral collateral ligament LD. See Lyme disease Leg length measurements, 136, 140f Legg-Calvé-Perthes disease, 15, 441 Lemaire, Marcel, 21 Letterer-Siwe disease, 494 Lidocaine, for neuropathic pain, 478 Li-Fraumeni syndrome, 498 Ligament(s), 35–36. See also Anterior cruciate ligament collateral, 35–36 injury of, management of, 80 magnetic resonance imaging of, 51–52 collateral, lateral anatomy of, 384–385, 385–386f biomechanics of, 384–385, 385–386f injury to, 20 clinical examination of, 386–388, 388f incidence of, 385–386 mechanism of, 385–386 treatment of, 388, 392 collateral, medial anatomy of, 379–381, 380f biomechanics of, 379–381, 380f injury of evaluation of, 381–384, 381f, 381t treatment of, 381–384, 381f, 381t injury to, 20 sprain, rehabilitation program, 382–383–383f cruciate, 35–36 absence of, 428–429 cruciate, posterior anatomy of, 392–393, 393f biomechanics of, 393 evaluation of, 394, 394t

Ligament(s) (Continued) cruciate, posterior (Continued) incidence of, 394 management of, 394, 394t natural history of, 394 repair and reconstruction of indications for, 389–390, 389–391f postoperative management of, 391–392 setup for, 390 technique of, 391 treatment of, 394–395 immature, anatomy of, 377–378, 378f Ligament of Humphry, 237, 261 Ligament of Wrisberg, 237, 261 Limbs, development of, 43 Liorzou’s “Losee II test.” See Twist-out test Losee’s test, for subluxation, 22–23, 24f Lyme disease (LD), 456, 470f diagnosis of, 470–471 treatment of, 471, 471t Lymphoma, imaging and, 61

M MacIntosh test, 22, 22f Magnetic resonance imaging (MRI) developmental variants in, 47–48, 48f reading of, 49–54 indications, 49 injury signal characteristics, 49 structural search pattern, 50–54 articular cartilage, 51 bone, 53–54 ligaments, 51–52 menisci, 50–51 muscles, 52–53 physis, 54 tendons, 52–53 technique, 49, 50f, 51f, 52f tissue characteristics, 49 septic arthritis, 454 of traumatic knee pain, 78 Malignancies, traumatic knee pain and, 82 Manual muscle evaluation form, 137f Marfan syndrome, 16 Massage, 143 McGwire, Mark, 109 McKeever classification system, 404f MCL. See Medial collateral ligament McMurray’s test, 17–18, 19f, 20f Mechanical pain syndrome, management of, 88 Medial collateral ligament (MCL) anatomy of, 379–381, 380f biomechanics of, 379–381, 380f injury of evaluation of, 381–384, 381f, 381t treatment of, 381–384, 381f, 381t injury to, 20 sprain, rehabilitation program, 382–383–383f Menisci, 36 absence of, 429–430 anatomy of, 237–238, 238f clinical evaluation of, 240–241 complication of, 256 discoid, 242–24f, 242–244 anatomy of, 260–261 classification of, 260–261, 261f evaluation of, 261 imaging studies of, 55, 56f, 261, 263f incidence of, 260 natural history of, 262 outcome of, 271

505

Menisci (Continued) discoid (Continued) presentation of, 261 prevalence of, 260 prognosis of, 271 saucerization and repair of indications for, 264, 265f, 266f postoperative management of, 269–270 results of, 270 setup for, 264–265 technique of, 265–269, 267–270f treatment of, 262–264, 263f, 271 embryology of, 237, 238f functions of, 238–240 healing of, 237–238 imaging studies of, 241–242, 241f injury of, 8 management of, 79–80 magnetic resonance imaging of, 50–51 meniscectomy, 245 pathology, 17–20, 19f, 20f postoperative protocol, 256 repair of, 245, 246f indications for, 250, 251f technique, 245–248, 250f, 255–256 all-inside, 247–248, 247f, 248f, 254, 254f, 255f inside-out, 246–247, 247–249f, 250–254, 252f, 253f, 257f outside in, 255–256 rehabilitation after, 254 repair versus excision of, 244–248, 255–256 transplant, 256 treatment of, 244 vascularity of, 237–238, 238f, 239f Merchant’s classification system, 155–156, 156b Methandrostenolone (Dianabol), 106 Methotrexate, 468t Monoarthritis, 462–463, 462t Morquio’s disease, 436 Mosaicplasty, for chondri indications of, 298, 298f, 299f postoperative rehabilitation of, 299–301, 300f, 301f procedure principles of, 298 surgical technique of, 299, 300f MRI. See Magnetic resonance imaging Muscles, magnetic resonance imaging of, 52–53 Musculotendinous unit, of articular cartilage, 35

N Nail-patella syndrome, 16, 28 NATA. See National Athletic Trainer’s Association National Athletic Trainer’s Association (NATA), 68 National Health Interview Survey (NHIS), 2 NCS. See Nerve conduction studies NEISS. See United States National Electronic Injury Surveillance System Neisseria gonorrhoeae, 81, 456 Neonatal, infections, 458 Nerve conduction studies (NCS), 475 Neurologic disorders, sports participation and, 93 Neuromuscular electrical nerve stimulation (NMES), 143, 143f

506

Index

Neuropathic pain acupuncture, 479 amputation and, 479–481 anesthetic approach to, 478 diagnostic approach to, 475–476 epidemiology of, 476 features of, 474b mechanisms of, 474–475 spinal cord stimulation, 479 sympathectomy, 479 therapy drug, 477–478 anticonvulsants, 477–478 lamotrigine, 478 lidocaine, 478 opioids, 478 pregabalin, 478 serotonin reuptake inhibitors, 477 topiramate, 478 tricyclic antidepressants, 477 physical, 477 treatment of, 476 psychological/cognitive, 476 NHIS. See National Health Interview Survey NMES. See Neuromuscular electrical nerve stimulation Nonarticular osteochondrosis Osgood-Schlatter lesion, 181–189 Sinding-Larsen-Johansson lesion, 181 Nonossifying fibroma, 494–495, 494f Nonsteroidal antiinflammatory drugs (NSAIDs) for juvenile rheumatoid arthritis, 467 musculoskeletal injuries and, 87–88 NSAIDs. See Nonsteroidal antiinflammatory drugs

O Ober test, 133–134, 139f OCD. See Osteochondritis dissecans OKR. See Ottawa Knee Rules Open reduction internal fixation, of tibial tubercle fractures, 229f indications for, 229–230 postoperative management of, 230–231 prognosis of, 231 setup for, 230 technique of, 230, 230f Operating room anesthesia perspective, 147–148 patient’s experience in, 146–147 staff concerns, 147 surgeon’s concern, 148–150, 148f surgical technique in, 149–150 technical considerations in, 149 Operating Room Design Manual, 147 Opioids, for neuropathic pain, 478 Organisms, 455–456 Hemophilus influenzae, 455 Kingellia kingae, 456 Neisseria gonorrhoeae, 456 Salmonella, 456 Staphylococcus aureus, 455 Streptococci, 455 Orthotics, 144 OSD. See Osgood-Schlatter disease Osgood-Schlatter disease (OSD), 10–11, 15, 16, 31, 35, 45, 47, 57–58, 181–189 acute trauma, 201–201f anatomy of, 198–199f complications of painful kneeling, 189

Osgood-Schlatter disease (Continued) complications of (Continued) painful ossicle, 189 permanent bump, 189 diagnosis of, 182, 182t differential diagnosis, 182–183 epidemiology of, 199 growth, 200–201, 200f imaging studies of, 182, 182f management of, 183 ossicle resection/tubercleplasty indications for, 210, 211f, 212f postoperative management of, 212–213 setup for, 210–211 technique of, 211–212 pathophysiology of, 198, 199f physical therapy protocol for, 204t strengthening, 204–206, 205–208f walking/running program, 206 PPE of, 98 Osgood-Schlatter lesion. See Osgood-Schlatter disease OSL. See Osgood-Schlatter disease Osteoblastoma, 494 Osteochondral fractures etiology of, 311–312, 312–315f history and physical examination of, 312–313 imaging of, 313, 315 management of, 315–316, 315f Osteochondritis dissecans (OCD), 10, 58, 59–60f, 81f clinical presentation of, 273–274 diagnostic studies of, 274–275, 274f, 275f juvenile arthroscopic transarticular drilling for background of, 283, 284f postoperative management of, 284 fixation for crater preparation, 286 existing fixation implants, 286, 287–293f management of arthroscopically assisted extraarticular drilling for indications for, 276 postoperative management of, 282 results of, 283 setup for, 276–277 technique of, 277–281, 277–282f nonoperative, 275–276 operative, 275–276, 285, 292 rehabilitation, 292 preparticipation physical examination and, 98 Osteochondroma, 490–491, 490f Osteogenesis imperfecta, 436, 438–439f Osteogenic sarcoma, imaging and, 61 Osteoid osteoma, 493–494, 493f Osteomalacia, 33, 34f Osteomyelitis. See Acute hematogenous osteomyelitis Osteoporosis, 33, 34f Osteosarcoma, 496–497, 496f Ottawa Knee Rules (OKR), 222

P Pain. See also Neuropathic pain anterior knee, 118–119, 121, 121t, 123 complex regional pain syndrome, 89, 481–484, 482f, 482t, 483b Osgood-Schlatter disease, 189 patellofemoral joint, 16, 16t

Pain. See also Neuropathic pain (Continued) rheumatology, knee complaints and, 461–462 sympathetically independent, 481 sympathetically maintained, 481 traumatic knee differential diagnosis of, 80, 80b evaluation of, 77–78 acute swelling, 78 injury mechanism, 77, 77f instability, 78 locking, 78 pain, 78 hematological conditions in, 82 history of pain, 82 red flags, 82 swelling, 82 training considerations, 82 imaging of, 78 infectious etiologies of, 81 inflammatory conditions in, 81 malignancy in, 82 management of, 79–80 chronic pain syndromes, 88–89 collateral ligaments, 80 complex regional pain syndromes, 89 physeal injuries, 79–80 referral guidelines, 87–88 mechanical/orthopedic structural problems, 81, 81f physical examination of, 78 observation, 83 primary care investigations arthrocentesis, 83, 87, 87t imaging studies, 83 laboratory studies, 83 reactive arthritis, 81 referral patterns, 88 referred pain, 82 Palmer, Ivar, 21 Passive retaining test, 23, 24f Patella alignment of, 134 congenital abnormalities of, 155 dislocation of chronic, 176–177 clinical aspects of, 177 surgical treatment of, 177 classification of, 430 clinical features of, 430, 431f etiology of, 430 imaging of, 166–167, 167f management of, 79 outcome of, 432 pathoanatomy of, 166–167 pathology of, 431, 431b physical examination of, 166 radiographic findings of, 430–431 recurrent imaging of, 168 Insall’s proximal realignment, 168–169, 168f lateral retinacular release, 168 physical examination of, 167–168 symptoms of, 167 treatment of, 168 symptoms of, 166 treatment of, 167, 431–432 fracture of anatomy of, 232 classification of, 232 complications of, 233 epidemiology of, 232

Index

Patella (Continued) fracture of (Continued) imaging of, 232, 232f management of, 79, 233 osteochondral, 233, 233f outcomes of, 233 physical examination of, 233 hypoplasia of, 432–434, 433f, 434f Merchant’s classification system, 155–156, 156b ossification centers of appearance in, 44 rehabilitation, 203–204 surgery, 204, 209–210, 209f treatment of, 202–203 tendinopathy lesion sites clinical grading, 190 history and physical examination, 190 imaging, 190, 191f management of, 190–191, 191f nomenclature, 189 pathopysiology of, 189 tendon, abnormalities of, 57–58–, 59f Patella magna, 155 Patellar alignment evaluation form, 136t Patellar aplasia, 155 Patellar hypoplasia, 155 Patellar taping, 143f, 144 Patellar tendinosis indications for, 192–193, 192–193f setup for, 193 technique of, 193–195 Patellar tendonitis, physical therapy protocol for, 183t strengthening, 184–185, 184–185f, 186–188f walking/running program, 185 Patellofemoral dysplasia arthroscopic-assisted procedures, 169 lateral patellar compression syndrome lateral retinacular release, 162, 163f physical examination of, 156 postoperative rehabilitation, 162, 166 radiographic examination of, 156 symptoms of, 156 treatment of, 156, 162 patellar dislocation chronic, 176–177 clinical aspects of, 177 surgical treatment of, 177 imaging of, 166–167, 167f pathoanatomy of, 166–167 physical examination of, 166 recurrent imaging of, 168 Insall’s proximal realignment, 168–169, 168f lateral retinacular release, 168 physical examination of, 167–168 symptoms of, 167 treatment of, 168 symptoms of, 166 treatment of, 167 patellar instability, 166 physical therapy protocol strengthening, 157–158–157–158f, 159f, 160–161f walking/running program, 159 realignments, 169, 176 Patellofemoral joint instability of, 16–17, 17f, 18f, 19f maltracking, 17f mechanism of, 28–29, 29f pain of, 16, 16f

PCL. See Posterior cruciate ligament PCU. See Postanesthesia care unit PDGF. See Platelet-derived growth factor Pediatric spondyloarthropathies, 80b, 81 PEE. See Preparticipation physical examination Peripheral nerve blocks, 153 Pes anserine, injection of, 86, 86f PGEZ. See Prostaglandin EZ Physeal injury of management of, 79–80 Salter-Harris classification of, 77f magnetic resonance imaging of, 54 Physeal-sparing iliotibial band technique indication for, 329 postoperative management of, 332 procedure description, 329–332, 329f, 330–333f setup for, 329 Physeal-sparing procedures, of anterior cruciate ligament, 328, 333–334, 345, 369 adult-type, 345, 369 graft options, 369–371, 371t, 372f partial transphyseal, 334, 345 postoperative rehabilitation for, 371 Physical examination, of pediatric knee apprehension test, 15, 15f gait analysis, 15 of joint line, 15, 15f ligamentous injuries, 20, 25 of ligamentous structures, 14–15 meniscal pathology, 17–20, 19f, 20f overuse of, 15–16 patellofemoral instability, 16–17, 17f, 18f, 19f patellofemoral pain, 16, 16f range of motion, 15 stress testing, 15 Physical therapy discharge after, 144–145 full activity after, 144–145 functional tests, 144f hop test, 145 isokinetic testing, 144 outcome of, 144–145 patient management examination cardiovascular/pulmonary, 131, 132t communication, 132 history, 131 integumentary, 131 musculoskeletal, 132, 133f, 134f neuromuscular system, 132 systems review, 131 tests/measurements, 132–136 circumference, 136, 140f Ely test, 134, 139f joint range of motion assessment form, 139f leg length measurements, 136, 140f manual muscle evaluation form, 137f Ober test, 133–134, 139f patellar alignment, 134 patellar alignment evaluation form, 136t popliteal angle, 132–133, 138f, 139f posture evaluation form, 135t Q-angle, 134 straight leg raise, 132, 138f Thomas test, 132, 138f treatment plan, 136, 138–144 closed kinetic chain exercise, 143f deep heat (therapeutic ultrasound), 141, 143 electrotherapy, 141, 143 flexibility, 141, 142f

507

Physical therapy (Continued) patient management (Continued) treatment plan (Continued) heat/cold, 141 home program, 139–141, 142f hydrotherapy, 141 iontophoresis, 143 manual therapy, 141 massage, 143 neuromuscular electrical nerve stimulation, 143, 143f orthotics, 144 patellar taping, 143f, 144 physical agents, 141, 143 range of motion, 141, 142f sleeves/braces, 144 strength, 141, 143f therapeutic exercise, 139–141, 142f self-assessment, 144–145 Physiological tibia vara, 4f, 44 Pigmented villonodular synovitis (PVNS), 495–496, 495f Pivot shift, examination of, 21–25 active retaining test, 23, 25, 25f Losee’s test for subluxation, 22–23, 24f MacIntosh test, 22, 22f passive retaining test, 23, 24f twist-out test, 22, 23f PJFS. See Primary juvenile fibromyalgia syndrome Platelet-derived growth factor (PDGF), 38 Plexus, injury of, 481 Plica patellofemoral, pain and, 16f PMNs. See Polymorphonuclear leukocytes Polyarthritis, 463 Polymorphonuclear leukocytes (PMNs), 451 Popliteal angle, measurement of, 132–133, 138f, 139f Postanesthesia care unit (PCU), 147, 148 Posterior cruciate ligament (PCL) anatomy of, 392–393, 393f biomechanics of, 393 evaluation of, 394, 394t incidence of, 394 injury of, 20 management of, 79 mechanism of, 77 magnetic resonance imaging and, 51–52 management of, 394, 394t natural history of, 394 repair and reconstruction of indications for, 389–390, 389–391f postoperative management of, 391–392 setup for, 390 technique of, 391 treatment of, 394–395 Posterior cruciate ligament laxity grading system, 394t Posture evaluation form, 135t Pregabalin, for neuropathic pain, 478 Preparticipation physical examination (PPE) anterior cruciate ligament and, 98 cardiovascular, 95b, 97–98 components of, 95–97 history, 95–96 cardiac, 95–96, 95b drugs, 96 knee concerns, 97 medications, 96 musculoskeletal, 96–97 neurological, 96 nutrition, 96 supplements, 96 follow up braces, 102

508

Index

Preparticipation physical examination (PPE) (Continued) follow up (Continued) equipment, 102 investigations, 100 orthotics, 102 proprioceptor, 100–101 protection, 102 training recommendations, 100 general, 97 knee, 98–100 alignment, 98–99f, 98–100 ankle, 100 flexibility, 100, 101 hip, 100 patellofemoral joint, 100 limitations, 102 Osgood-Schlatter disease and, 98 osteochondritis dissecans and, 98 process of, 94–95 purpose/objectives of, 91–94 counseling, 92 medicolegal issues, 92b, 94 participation, 91, 92–94t Sinding-Larsen-Johansson and, 98 Prepatellar bursa infection of, 458 injection of, 86–87, 86f Primary juvenile fibromyalgia syndrome (PJFS), 89–90 Prostaglandin EZ (PGEZ), 451 Prothrombin time (PT), 83 Proximal tibiofibula, reconstruction of indications for, 178 postoperative management of, 179 results of, 179 setup for, 178 technique of, 178–179, 178f Pseudoachondroplasia, 436, 438f Pseudoephedrine, 109 PT. See Prothrombin time PVNS. See Pigmented villonodular synovitis

Radiography, developmental variants in, 47, 48f RapidLoc, 248 Reactive arthritis, 81 Reflex sympathetic dystrophy (RSD), 481–484, 482f, 482t, 483b management of, 89 Rehabilitation. See Physical therapy Renal disease, bone deformity and, 436, 440f Resistance training benefits of, 63–65, 64b injury reduction, 64–65, 65t motor skills, 63–64 sports performance, 63–64 program design, 65–68, 66b periodization, 67 preseason conditioning, 68, 68b restoration, 67–68 specificity of, 65–67 Respiratory conditions, sports participation and, 93–94 Rhabdomyosarcoma, 498–499, 498f Rheumatic fever, 456 Rheumatologic laboratory studies, 83 Rheumatology, knee complaints and, 461, 462t differential diagnosis of, 462 bony pain, 462 mechanical derangement, 462 neuropathic pain, 462 inflammatory pain, 461–462 joint involvement pattern, 462–463 monoarthritis, 462–463, 462t polyarthritis, 463 Ribonucleic acid (RNA), 37, 37f, 106 Rickets, 33 dietary, 436, 440f x-linked hypophosphatemia, 436, 439f RNA. See Ribonucleic acid Road traffic accidents, knee injuries from, 6 Roller sports injuries, 4t, 5 Rose and Jevne’s “Risk Model,” 72 RSD. See Reflex sympathetic dystrophy

Q

S

Q-angle, 134 QST. See Quantitative sensory testing Quadriceplasty, for dislocation postoperative management of, 427 results of, 427 technique of, 425–427, 425–427f Quadriceps, tendinopathy lesion sites clinical grading, 190 history and physical examination, 190 imaging, 190, 191f management of, 190–191, 191f nomenclature, 189 pathopysiology of, 189 Quadriceps tendon, 191, 195–196 clinical aspects of, 195 history and physical examination of, 195 imaging of, 195 management of, 195–196 partial rupture of, 196 Quantitative sensory testing (QST), 475

Salmonella, 456 Salter-Harris classification, 77f, 79, 217, 218f SCFE. See Slipped capital femoral epiphysis SCI. See Severe combined immunodeficiency defect Screws bioabsorbable, 286 cannulated, 286, 287–290f Herbert, 286, 288–290f SEA. See Seronegative enthesopathy and arthropathy Semitendinous tenodesis, for recurrent lateral subluxation of patella indications for, 169 postoperative management of, 172–173 results of, 173 setup for, 169 technique of, 170–172, 170f, 171f, 172f Septic arthritis complications of, 458 diagnosis of, 452–454 bone scan, 454, 454f computed tomography, 454 history, 452 magnetic resonance imaging, 454 physical examination, 452 radiographs, 453, 453f ultrasound, 453–454

R Radial zone, 34 Radiographic Atlas of Skeletal Development of the Hand and Wrist, 44

Septic arthritis (Continued) differential diagnosis of, 456 bone infarction, 457 Henoch-Schönlein purpura, 457 juvenile rheumatoid arthritis, 456 Lyme disease, 456 rheumatic fever, 456 trauma, 456–457 tumor, 457 epidemiology of, 451 laboratory studies, 454–455 organisms, 455–456 Hemophilus influenzae, 455 Kingellia kingae, 456 Neisseria gonorrhoeae, 456 Salmonella, 456 Staphylococcus aureus, 455 Streptococci, 455 pathophysiology of, 451–452 treatment of, 457–458 Seronegative enthesopathy and arthropathy (SEA), 81 Serotonin reuptake inhibitors (SSRIs), for neuropathic pain, 477 Severe combined immunodeficiency defect (SCID), 39 Sex Maturity Stages, classification of, 327t Sharpey’s fibers, 35 Sickle cell crisis, 82 Sillence type III, 436 Sinding-Larsen-Johansson lesion (SLJL) acute trauma, 202, 202f diagnosis of, 200–201 disease, 15 etiology of, 200–201 growth, 200–201, 200f heredity, 200 lesion, 58, 59f nonarticular osteochondrosis, 181 preparticipation physical examination and, 98 repetitive trauma/overuse, 201 SIP. See Sympathetically independent pain Skiing injuries, 4t, 5–6 Slingshot effect, of patella, 25f Slipped capital femoral epiphysis (SCFE), 15, 33, 219 SLJI. See Sinding-Larsen-Johansson lesion Small patella syndrome, 433 SmartNail, 286, 290–291f SMP. See Sympathetically maintained pain Snapping knee, 261, 429 Snow boarding injuries, 4t, 5–6 Soccer injuries, 4t, 5 SPGR. See Spoiled gradient-recalled echo Spinal anesthesia, 153 Spinal cord stimulation, for neuropathic pain, 479 Spoiled gradient-recalled echo (SPGR), 220 Spondyloarthropathies juvenile-onset, 81 pediatric, 80b, 81 Sports injuries, 4–6 ball, 6 cost of, 71 psychological effects of, 72–74 participation rates of, 91 Sports-related (SR) knee injuries, 1 SSRIs. See Serotonin reuptake inhibitors Staphylococcus aureus, 81, 455 Step-off grading system, 394t Straight leg raise, 132, 138f Streptococci, 455

Index

Sulfasalazine, 468t Superficial zone, 34 Sympathectomy, for neuropathic pain, 479 Sympathetically independent pain (SIP), 481 Sympathetically maintained pain (SMP), 481 Synovial chondromatosis, 496 Synovial fluid, analysis of, 87t Synovitis, 59–60, 60f

T TE. See Testosterone enanthate Tendinopathies lesion sites clinical grading, 190 history and physical examination, 190 imaging, 190, 191f management of conservative, 190 surgical, 190–191, 191f nomenclature, 189 pathopysiology of, 189 Tendons, magnetic resonance imaging of, 52–53 TENS. See Transcutaneous electrical nerve stimulation Testosterone enanthate (TE), 106 TGF-β1. See Transforming growth factor beta 1 Therapeutic ultrasound, 141, 143 Thomas test, 132, 138f Tibia deformity of, 447f, 448f proximal fractures of anatomy of, 217f, 226–227f complications of, 228 epidemiology of, 226 management of, 226–228 outcome of, 228 growth plates, 45 ossification center appearance in, 43–44 physeal closure time, 45 Tibial eminence, fracture of approach to, 413 arthrofibrosis, 418 complications of, 417 diagnosis of, 400 growth arrest, 417 injury mechanism, 400–402 classification of, 401, 401f treatment of, 401–402 malunion, 418 range of motion loss, 418 residual laxity, 418 screw fixation, 413, 416

Tibial eminence, fracture of (Continued) techniques for preferred, 413–417f surgical, 402–403, 402–403f, 407, 413 suture, 416–417 Tibial spine fractures, arthroscopic reduction and internal fixation of epiphyseal cannulated screws background of, 403, 404f physical examination in, 403–404 postoperative management of, 406–407 results of, 407 setup for, 404 technique of, 404–406, 405–406f with sutures indications for, 408 postoperative management of, 411 results of, 411 setup for, 408 technique of, 408–410, 408–412f Tibial tubercle fractures, open reduction internal fixation of, 229f indications for, 229–230 postoperative management of, 230–231 prognosis of, 231 setup for, 230 technique of, 230, 230f Tibial tuberosity development of, 45, 45f fractures of classification of, 228, 228f complications of, 231 epidemiology of, 228 imaging of, 229 management of, 229–231 outcome of, 231 physical examination of, 229 Tibiofemoral subluxation, 429 Tissues, injury to, healing response to, 36 Topiramate, for neuropathic pain, 478 Tourniquets, anesthesia and, 153 Track-and-field injuries, 4t, 5 Trampoline-related injuries, 6 Transcutaneous electrical nerve stimulation (TENS), 477 Transforming growth factor beta 1 (TGF-β1), 38 Transitional zone, 34 Transplant, menisci, 256 Trauma infections diagnosis, 456–457 weakest points of resistance with, 45 Trevor disease, 54 Tricyclic antidepressants, for neuropathic pain, 477

509

Tumors, 457 benign aneurysmal bone cyst, 489–490, 490f chondroblastoma, 492–493f chondromyxoid fibroma, 495 enchondroma, 491 fibrous dysplasia, 491 focal cortical defects, 494–495 histiocytosis X, 494 nonossifying fibroma, 494–495, 494f osteoblastoma, 494 osteochondroma, 490–491, 490f osteoid osteoma, 493–494, 493f simple cysts, 489, 489f evaluation of, 488 imaging and, 60–61, 61f intraarticular conditions pigmented villonodular synovitis, 495–496, 495f synovial chondromatosis, 496 malignant Ewing’s sarcoma, 497–498, 497f osteosarcoma, 496–497, 496f rhabdomyosarcoma, 498–499, 498f pitfalls of, 488–489 presentation of, 488 Twist-out test, 22, 23f

U United States National Electronic Injury Surveillance System (NEISS), 2 US Consumer Product Safety Commission (USCPSC), 2 USCPSC. See US Consumer Product Safety Commission

W Watanabe classification, 261f Weiss and Troxel’s psychophysiological stress model, 72 Wiese-Bjornstal and Smith’s cognitiveemotional-behavioral model, 72 Windswept deformity, 439f

X X-linked hypophosphatemia rickets, 436, 439f