The Sports Medicine Resource Manual

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

THE SPORTS MEDICINE RESOURCE MANUAL

ISBN: 978-1-4160-3197-0

Copyright ! 2008 by Saunders, an imprint of Elsevier Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Permissions may be sought directly from Elsevier’s Rights Department: phone: (+1) 215 239 3804 (US) or (+44) 1865 843830 (UK); fax: (+44) 1865 853333; e-mail: [email protected]. You may also complete your request on-line via the Elsevier website at http://www.elsevier.com/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 their own experience and knowledge of the patient, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the Editors assume any liability for any injury and/or damage to persons or property arising out of or related to any use of the material contained in this book. The Publisher

Library of Congress Cataloging-in-Publication Data Seidenberg, Peter H. The sports medicine resource manual / Peter H. Seidenberg, Anthony I. Beutler. — 1st ed. p. ; cm. Includes bibliographical references. ISBN 978-1-4160-3197-0 1. Sports medicine. 2. Sports injuries. I. Beutler, Anthony I. II. Title. [DNLM: 1. Athletic Injuries—diagnosis. 2. Athletic Injuries—therapy. 3. Physician’s Role. 4. Sports Medicine—methods. QT 261 S458s 2008] RC1210.S43 2008 617.10 027—dc22 2007041856

Acquisitions Editor: Rolla Couchman Developmental Editor: Pamela Hetherington Publishing Services Manager: Joan Sinclair Design Direction: Karen O’Keefe Owens

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Dedication We would like to thank our many teachers—those wonderful men and women who cared and took time from their busy lives to explain complex things to simple minds. This book is dedicated to our families—our parents; our children; but most of all to our patient and wonderful wives, Jen and Angie.

Contributors

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MAJ Chad Asplund, MD Sports Medicine Coordinator; Department of Family and Community Medicine; Eisenhower Army Medical Center; Fort Gordon, Georgia

Michael Cannon, MD, MS Assistant Professor; Department of Community and Family Medicine; Saint Louis University School of Medicine; St. Louis, Missouri

Michael Barron, MD Family Physician; Department of Family Medicine; Southern Illinois Healthcare Foundation; Belleville, Illinois

Dennis A. Cardone, DO Children’s Sports Center; Pediatric Orthopedics of South Florida; Fort Myers, Florida

Anthony I. Beutler, MD Chief; Injury Prevention Research Laboratory; Assistant Professor; Department of Family Medicine; Uniformed Services University of the Health Sciences; Bethesda, Maryland

Elizabeth J. Caschetta, MS, ATC Certified Athletic Trainer; Illini Sports Medicine; Belleville, Illinois

Barry P. Boden, MD Adjunct Associate Professor in Surgery; Department of Orthopaedic Surgery; F. Edward Herbert School of Medicine; Uniformed Services University of the Health Sciences; Bethesda, Maryland; Orthopaedic Surgeon; The Orthopaedic Center; Rockville, Maryland Jimmy D. Bowen, MD, FAAPMR, CSCS Assistant Professor; Departments of Surgery and Physical Medicine; Uniformed Services University of the Health Sciences; Bethesda, Maryland; Clinical Instructor; Southeast Missouri State University; Medical Director; Department of Sports Medicine; St. Francis Medical Center; Staff Psychiatrist; Orthopedic Associates of Southeast Missouri; Cape Girardeau, Missouri Lori A. Boyajian-O’Neill, DO Associate Professor and Chair; Department of Family Medicine; Kansas City University of Medicine and Biosciences; Kansas City, Missouri Fred H. Brennan, Jr, DO, FAOASM, FAAFP Director; National Capital Consortium Tri-Service Primary Care Sports Medicine Fellowship Program; Bethesda, Maryland; Assistant Team Physician; George Mason University; Fairfax, Virginia Jorge Cabrera, MD, PhD Resident; Department of Family Practice; Womack Army Medical Center; Fort Bragg, North Carolina Gregg Calhoon, ATC Athletic Trainer; Department of Physical Education; United States Naval Academy; Annapolis, Maryland

Marc A. Childress, MD Assistant Professor; Department of Family Medicine; Uniformed Services University of the Health Sciences; Bethesda, Maryland; Teaching Physician; Deparment of Family Medicine; Malcolm Grow Medical Center; Andrews Air Force Base, Maryland Raymond D. Chronister, ATC Assistant Athletic Trainer; Department of Physical Education; United States Naval Academy; Annapolis, Maryland Greg Dammann, MD Resident; Department of Orthopaedic Surgery; Tripler Army Medical Center; Honolulu, Hawaii W. Scott Deitche, MD Director of Sports Medicine; Family Medicine Residency Center; Carl R. Darnall Army Medical Center; Fort Hood, Texas Patricia A. Deuster, PhD, MPH Professor; Department of Military and Emergency Medicine; Uniformed Services University of the Health Sciences School of Medicine; Scientific Director; Consortium for Health and Human Performance; Bethesda, Maryland LTC Kevin deWeber, MD, FAAFP Director; Military Primary Care Sports Medicine Fellowship; Assistant Professor of Family Medicine; Uniformed Services University of the Health Sciences; Bethesda, Maryland Pierre A. d’Hemecourt, MD Director of Primary Care Sports Medicine; Division of Sports Medicine; Boston Children’s Hospital; Harvard Medical School; Boston, Massachusetts; Team Physician; Department of Health Services; Boston College; Chestnut Hill, Massachusetts

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David A. Djuric, MD Resident; Department of Family Medicine; Dewitt Army Community Hospital; Fort Belvoir, Virginia

Philip Ham, DO Director; Board Certified Family Practice Physician; Department of Family Practice; United States Air Force; Cannon Air Force Base, New Mexico

Timothy Dwyer, MD Senior Medical Officer; Ray Hall Branch Medical Clinic; The Basic School; Quantico, Virginia

Yuval Heled, PhD Assistant Professor; Department of Military and Emergency Medicine; Uniformed Services University of the Health Sciences School of Medicine; Bethesda, Maryland; Researcher; Heller Institute of Medical Research; Sheba Medical Center; Tel Hashomer; Ramat Gan, Israel

Adam J. Farber, MD Chief Resident; Department of Orthopaedic Surgery; Johns Hopkins Hospital; Baltimore, Maryland CPT David D. Farnsworth, MD Resident; Saint Louis University Family Medicine Residency; Cardinal Glennon Children’s Hospital; St. Louis, Missouri; Department of Family Medicine; St. Elizabeth’s Hospital; Belleville, Illinois Karl B. Fields, MD Professor and Associate Chairman; Department of Family Medicine; University of North Carolina; Director; Family Practice Residency and Sports Medicine Fellowship; Moses H. Cone Health System; Greensboro, North Carolina Scott D. Flinn, MD Clinical Professor; University of California, San Diego; Force Surgeon; Commander Naval Surface Forces; United States Navy; San Diego, California Bradley D. Fullerton, MD, FAAPMR Physical Medicine and Rehabilitation Preceptor; University of Texas Medical Branch; Galveston, Texas; Consulting Physiatrist in Ultrasound Research; Human Engineering Research Laboratory; University of Pittsburgh; Pittsburgh, Pennsylvania; Medical Director of Spasticity Clinic; Dell Children’s Hospital; Austin, Texas CPT Richard Geshel, DO Staff Physician; Department of Family Medicine; Reynolds Army Community Hospital; Fort Sill, Oklahoma

MAJ Duane R. Hennion, MD Department of Family Medicine; Uniformed Services University of the Health Sciences; Bethesda, Maryland Thomas M. Howard, MD Assistant Clinical Professor; Department of Family Medicine; Virginia Commonwealth University School of Medicine; Richmond, Virginia; Program Director; Virginia Commonwealth University; Fairfax Family Practice Sports Medicine Fellowship; Fairfax, Virginia Allyson S. Howe, MD Director of Sports Medicine; Department of Family Medicine; Malcolm Grow Medical Center; Andrews Air Force Base, Maryland Wesley R. Ibazebo, MD Resident; Department of Physical Medicine and Rehabilitation; University of North Carolina at Chapel Hill; Chapel Hill, North Carolina MAJ Christopher G. Jarvis, MD, FAAFP Senior Sports Medicine Fellow; Department of Family Medicine; Uniformed Services University of the Health Sciences; Bethesda, Maryland Shawn F. Kane, MD Family Physician; Primary Care Sports Medicine; Blanchfield Army Community Hospital; Fort Campbell, Kentucky

MAJ Rodney Gonzales, MD Family Medicine Residency Program; Martin Army Community Hospital; Fort Benning, Georgia

Brandon D. Larkin, MD Primary Care Sports Medicine Fellow; Department of Community and Family Medicine; Saint Louis University; St. Louis, Missouri

NormanW. Gill III, PT, DSc, Cert MPT, OCS, FAAOMPT Department of Orthopaedics and Rehabilitation; Walter Reed Army Medical Center; Washington, DC

LTC Jeff C. Leggitt, MD LTS US Army

EliseT. Gordon, MD Physician; Department of Family Medicine/Sports Medicine; Naval Hospital of Pensacola; Pensacola, Florida

James D. Leiber, DO Assistant Professor; Department of Family Medicine; Department of Osteopathic Principles and Practice; Lake Erie College of Osteopathic Medicine; Bradenton, Florida

Lyndon B. Gross, MD, PhD Assistant Professor; Department of Orthopedic Surgery; Saint Louis University; Active Provisional Staff; Department of Orthopedic Surgery; Des Peres Hospital; Active Provisional Staff; Department of Orthopedic Surgery; St. Joseph’s Hospital; Courtesy Staff Physician; Department of Orthopedic Surgery; Missouri Baptist Medical Center; St. Louis, Missouri

ChristopherJ. Lettieri, MD Associate Professor of Medicine; Department of Medicine; Uniformed Services University of the Health Sciences; Bethesda, Maryland; Medical Director; Sleep Disorders Clinic; Pulmonary, Critical Care, and Sleep Medicine; Walter Reed Army Medical Center; Washington, DC

Contributors

Jeffrey L. Levy, DO Director; Primary Care Sports Medicine; Family Medicine Residency Clinic; Womack Army Medical Center; Fort Bragg, North Carolina; Team Physician; Methodist College; Fayetteville, North Carolina MAJ Guy R. Majkowski, PT, DSc, OCS, FAAOMPT Director of Rehabilitation Services; Malcolm Grow Medical Center; Andrews Air Force Base, Maryland Geof D. Manzo, MS, ATC Approved Offsite Clinical Instructor; Athletic Training; McKendree College; Lebanon, Illinois; Certified Athletic Trainer; Illini Sports Medicine/Professional Therapy Services; St. Elizabeth’s Hospital; Belleville, Illinois; Head Athletic Trainer; Gateway Grizzlies Independent Minor League Baseball Club; Sauget, Illinois TimothyJ. Mazzola, MD Team Physician (Former); US Air Force Academy; United States Air Force Academy, Colorado; Chief; Pagosa Springs Sports Medicine; Pagosa Springs, Colorado Andrew T. McDonald, MD Team Physician; Primary Care and Sports Medicine; RoseHulman Institute of Technology; Sports Medicine Physician; Bone & Joint Center; AP&S Clinic; Terre Haute, Indiana MAJ Howard J. McGowan, MD Assistant Professor; Department of Family Medicine; Uniformed Services University of the Health Sciences; Bethesda, Maryland; Teaching Physician; Department of Family Medicine; Malcolm Grow Medical Center; Andrews Air Force Base, Maryland MAJ Christopher D. Meyering, DO Sports Medicine Fellow; Primary Care Sports Medicine; DeWitt Army Community Hospital; Fort Belvoir, Virginia; Sports Medicine Fellow; Tri-Service Primary Care Sports Medicine Fellowship; Uniformed Services University of the Health Sciences; Bethesda, Maryland William A. Mitchell III, MD Fellow; Primary Care Sports Medicine Fellowship; Saint Louis University; St. Louis, Missouri; Fellow; Department of Family and Community Medicine; St. Elizabeth’s Hospital; Belleville, Illinois Ryan E. Modlinski, MD Fellow; Primary Care Sports Medicine; Moses H. Cone Family Medicine Residency; Greensboro, North Carolina Sean T. Mullendore, MD Adjunct Assistant Professor; Department of Family Medicine; University of Nebraska Medical Center; Staff Family/Sports Physician; 55 MDOS/SGOPR; Ehrling Bergquist USAF Clinic; Offutt AFB; Omaha, Nebraska Daniel L. Munton, MD Staff Physician; Physical Medicine and Rehabilitation; Department of Sports Medicine; Abilene Sports Medicine and Orthopedics; Abilene, Texas

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Melissa Nebzydoski, DO Resident; Department of Family Medicine; Dewitt Army Community Hospital; Fort Belvoir, Virginia Jay E. Noffsinger, MD Professor of Pediatrics; Saint Louis University School of Medicine; Director of Medical Student Education; Pediatric Sports Medicine; Cardinal Glennon Children’s Medical Center; St. Louis, Missouri Rochelle M. Nolte, MD Sports Medicine Physician; Aviation Medical Officer; US Coast Guard; San Diego, California Francis G. O’Connor, MD, MPH Medical Director; Human Performance Lab; Military and Emergency Medicine; Associate Professor of Family Medicine; Department of Military and Emergency Medicine; Uniformed Services University of the Health Sciences; Bethesda, Maryland CPT Jessica A. Pesce, MS, PT Assistant Chief; Physical Therapy; Womack Army Medical Center; Fort Bragg, North Carolina James Phillips, MD Captain; United States Army Medical Corps; Darmstadt Health Clinic; Darmstadt, Germany Nicholas A. Piantanida, MD Assistant Professor; Department of Family Medicine; Uniformed Services University of the Health Sciences; Bethesda, Maryland; Director; Primary Care Sports Medicine; Primary Care Department; Keller Army Community Hospital; West Point, New York Scott A. Playford, MD Sports Medicine Physician; Camp Geiger Sports Medicine; Naval Hospital Camp Lejeune; Jacksonville, North Carolina MAJ Christopher M. Prior, DO, FAAFP Assistant Professor; Department of Family Practice; Uniformed Services University of the Health Sciences; Bethesda, Maryland; Director of Sports Medicine; Family Medicine; Columbine Medical Center; Family Physician; Department of Family Practice; Littleton Adventist Hospital; Littleton, Colorado; President; Rocky Mountain Sports Medicine Association; Castle Rock, Colorado Bernard Purcell, MS Manager; Injury Prevention Research Laboratory; Department of Family Medicine; Uniformed Services University of the Health Sciences; Bethesda, Maryland Scott W. Pyne, MD, FAAFP, FACSM Assistant Professor; Department of Family Medicine; Uniformed Services University of the Health Sciences; Bethesda, Maryland; Director of Health Services; Chief of the Medical Staff; Team Physician; United States Naval Academy; Naval Health Clinic Annapolis; Annapolis, Maryland

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Contributors

Ahmed A. Radwan, MD Family Medicine Attending/Sports Medicine Fellowship Staff Physician; Family Medicine/Sports Medicine; Saint Louis University; St. Louis, Missouri; Family Medicine Attending/ Sports Medicine Fellowship Staff Physician; Family Medicine/ Sports Medicine; St. Elizabeth’s Hospital; Belleville, Illinois LCDR Leslie H. Rassner, MD Assistant Professor; Department of Family Medicine; Uniformed Services University of the Health Sciences; Bethesda, Maryland; Head; Division of Sports Medicine; Department of Orthopedics; Residency Staff Physician; Department of Family Medicine; Naval Hospital Camp Lejeune; Camp Lejeune, North Carolina Jennifer Reed, MD, FAAPMR Professor; Eastern Virginia Medical School; Norfolk, Virginia; Attending Physician; Bone & Joint/Sports Medicine Institute; Naval Medical Center; Portsmouth, Virginia K. Dean Reeves, MD Clinical Associate Professor; Physical Medicine and Rehabilitation; University of Kansas Medical Center; Lawrence, Kansas; Rehabilitation Medical Director; Meadowbrook Rehabilitation Hospital; Gardner, Kansas Peter H. Seidenberg, MD, FAAFP President and Co-Founder; King Medical Care, Inc.; Bloomsburg, Pennsylvania Joel L. Shaw, MD Assistant Professor; Department of Family Medicine; Uniformed Services University of the Health Sciences; Bethesda, Maryland; Assistant Fellowship Director; Tri-Service Primary Care Sports Medicine Fellowship; Dewitt Army Community Hospital; Fort Belvoir, Virginia

Timothy L. Switaj, MD Resident; Department of Family Medicine; Dewitt Army Community Hospital; Fort Belvoir, Virginia Sean Thomas, MD Family Medicine Residency Faculty; Womack Army Medical Center; Fort Bragg, North Carolina Stephen J.Titus, MD Assistant Professor; Department of Family Medicine; Uniformed Services University of the Health Sciences; Bethesda, Maryland; Teaching Faculty; Family Medicine Residency; Malcolm Grow Medical Center; Andrews Air Force Base, Maryland GastonTopol, MD Team Physiatrist; Rosario Rugby Union; Rosario, Argentina Brian K. Unwin, MD Vice Chair for Education; Assistant Professor of Family Medicine and Geriatrics; Department of Family Medicine; Uniformed Services University of the Health Sciences School of Medicine; Faculty Physician; National Naval Medical Center; Bethesda, Maryland; Faculty Physician; Dewitt Army Community Hospital; Fort Belvoir, Virginia; Faculty Physician; Walter Reed Army Medical Center; Washington, DC Charles W.Webb, DO, FAAFP Assistant Professor; Department of Family Medicine; Oregon Health and Science University; Portland, Oregon; Director; Primary Care Sports Medicine; Department of Family Medicine; Madigan Army Medical Center; Tacoma, Washington

Mark A. Slabaugh, MD Associate Professor; Department of Surgery; Uniformed Services University of the Health Sciences; Bethesda, Maryland; Chief of Orthopaedics; Department of Orthopaedics; Malcolm Grow Medical Center; Andrews Air Force Base, Maryland

John H.Wilckens, MD Associate Professor; Orthopaedic Surgery; Johns Hopkins University School of Medicine; Attending Orthopaedic Surgeon, Chairman; Orthopaedic Surgery; Johns Hopkins Bayview Medical Center; Team Physician; Baltimore Orioles; Baltimore, Maryland; Orthopaedic Consultant; Naval Academy Athletic Association; Annapolis, Maryland

Mark B. Stephens, MD, MS Associate Professor; Family Medicine; Uniformed Services University of the Health Sciences; Bethesda, Maryland

Pamela M.Williams, MD Assistant Professor; Department of Family Medicine; Uniformed Services University of the Health Sciences; Bethesda, Maryland

Janiece N. Stewart, MD Fellow; Primary Care Sports Medicine; Saint Louis University; St. Louis, Missouri; Assistant Professor; Illini Sports Medicine; St. Elizabeth’s Hospital; Belleville, Illinois

Derek A.Woessner, MD Staff Physician; Martin Army Community Hospital; Fort Benning, Georgia

Patrick St. Pierre, MD Assistant Professor; Orthopaedic Surgery; Uniformed Services University of the Health Sciences; Bethesda, Maryland; Associate Director; Nirschl Orthopaedic Sports Medicine Fellowship; Virginia Hospital Center; Arlington, Virginia

NicoleT.Yedlinsky, MD Family Practice Physician; Department of Primary Care; BayneJones Army Community Hospital; Fort Polk, Louisiana

The views expressed in this textbook are those of the authors and should not be construed as official policy of the Department of the Air Force, the Department of the Army, the Department of the Navy, or the Department of Defense.

Foreword Francis G. O’Connor, MD, MPH

‘‘You find what you look for, and diagnose what you know.’’ —Dr. Jack Houston The late Dr. Jack Houston, founder of the Houston Sports Medicine Clinic and educator of many of today’s leaders in sports medicine, is credited with the above quote, which invites all clinicians to ‘‘think outside the box.’’ As a clinical educator, I have invoked this quote for years in an attempt to inspire primary care sports medicine fellows and family medicine residents. My goal is to remind them that they are limited only by their own imagination and that, in many respects, they are their patients’ most important risk factor. Primary care sports medicine has been a discipline practiced by primary care providers for many years. In 1988, Tucker and O’Bryan published that the great majority of physicians who were field side on Friday night in New York state for highschool football games were family physicians.1 Many of us with a little gray hair have fond memories of that first preparticipation examination in high school being performed in a busy gymnasium by the community family physician—the sports doc—who may well also have delivered us. About the same time as Tucker and O’Bryan’s study, a steady sentiment was growing in the primary care community that additional training (fellowship) in primary care sports medicine would be of great service to family physicians, internists, physical medicine and rehabilitation physicians, pediatricians, and emergency medicine physicians who were interested in gaining more expertise in this area. Sports medicine fellowships soon became quite popular and were sponsored throughout the country in academic family medicine departments, orthopedics departments, and private practice groups. The journal The Physician and Sportsmedicine became a must have, with its annual issue updating fellowships across the country.2 In April 1993, the first board examination in sports medicine, which was a certificate of added qualification, was offered to family physicians, internists, and pediatricians. At that time, a variety of fellowships were offered, there was no formal accreditation process, and physicians who could demonstrate practical experience were ‘‘grandfathered’’ into the board examination. In addition, there was a fair amount of anxiety among the growing number of primary care sports physicians because the discipline had not yet been clearly defined, and there were few if any core textbooks or published curricula.3-5 Since that time the field of primary care sports medicine has dramatically changed. Fellowships are now accredited by the Accreditation Council for Graduate Medical Education by strict criteria. An examinee who desires to sit for the Certificate of Added Qualifications examination must be a graduate of an accredited fellowship. Physiatrists will sit for the board examination in sports medicine for the first time in 2007. Hundreds of graduates abound from many fine fellowships, and they have found excellent clinical opportunities as academic leaders and private-practice clinicians. The American Medical Society of Sports Medicine was founded in 1991, with the mission being to offer a forum that fosters a collegial relationship among

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dedicated, competent, primary care sports medicine physicians as they seek to improve their individual expertise and raise, with integrity, the general level of sports medicine practice.6 In addition, the American College of Sports Medicine, which was founded in 1954, inaugurated its first family physician, William O. Roberts, MD, as College President in 2004.7 Accordingly, the written field has also changed. The discipline now has several leading journals, as well as clinical sections in other sports medicine journals. In addition to the journal literature, textbooks that were rare in 1993 abound as leaders and fellowship graduates have been quick to define the discipline. Books currently available for primary care sports medicine physicians range in scope, from definitive texts addressing defined areas to broad-based, evidence-based review texts to books devoted to exploring the idiosyncrasies of field-side coverage and monographs comprehensively detailing physical examination techniques. Missing in this picture, however, has been a definitive text that seeks to identify and describe in detail the core procedures that define the sports medicine practitioner, both in the office as well as at the field side. Peter Seidenberg and Anthony Beutler, both of whom are fellowship-trained primary care sports medicine physicians and accomplished clinical educators and researchers, recognized this missing piece. They have identified the skill set, assembled a host of talented authors, and produced a textbook that defines the integrated cognitive and procedural approach necessary to succeed as a sports medicine clinician. For those of us who have seen the birth and growth of the discipline of primary care sports medicine, we remember pivotal moments that helped to shape the specialty: board certification, accredited fellowships, the founding of the American Medical Society of Sports Medicine, the first family physician to lead the American College of Sports Medicine, and key advancements in sports medicine literature that have shaped our specialty. Just as a Strauss or Birrer text was instrumental for the first Certificate of Added Qualifications and a Mellion handbook was a necessary companion for all sports physicians attending a training room, I have no doubt that this Seidenberg/Beutler Sports Medicine Resource Manual will become a ‘‘must have’’ for every graduating family medicine resident and beginning sports medicine fellow as well as a cornerstone teaching text for their attending physicians. Returning to Dr. Houston’s quotation, Drs. Seidenberg and Beutler have been out-of-the-box thinkers, and they have truly edited a unique manuscript that will assume a fundamental position for sports medicine providers. I’m proud to have had a role in their education, and I’m sure that Dr. Houston would have admired their contribution to the field of sports medicine.

REFERENCES 1. 2. 3.

Tucker JB, O’Bryan JJ, et al: Medical coverage of high school football in New York state. Phys Sportsmed 1988;16(9):120-128. The Physician and Sportsmedicine home page (Web site). Available at www. physsportsmed.com. Accessed March 27, 2007. Strauss RB: Sports Medicine, 2nd ed. Philadelphia, WB Saunders, 1991.

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Foreword

Birrer RB: Sports Medicine for the Primary Care Physician. Philadelphia, Appleton & Lange, 1984. Mellion MB, Walsh WM, Shelton GL (eds): The Team Physician’s Handbook. Philadelphia, Hanley & Belfus, 1990.

6. American Medical Society for Sports Medicine home page (Web site). Available at www.amssm.org. Accessed March 27, 2007. 7. American College of Sports Medicine home page (Web site). Available at www.acsm. org. Accessed March 27, 2007.

Preface ‘‘You never know how big the field is, until you try and walk across it. . .’’ When we sat down to design ‘‘the one sports medicine textbook’’ for graduating family medicine residents and all sports fellows, we really did not imagine creating something 650 pages long. Sports medicine seemed a relatively simple thing, just muscles and bones and people hurting themselves. But as we tried to compile a single text describing the philosophy, examinations, treatments, procedures, and special considerations inherent in our daily practice, we soon gained a firsthand appreciation for how big the field is and how long it takes to walk across it. This is a unique text. It is largely written by primary care sports medicine physicians for primary care sports medicine physicians. The orthopedists, athletic trainers, physical therapists, and other professionals who we invited to participate were chosen because of their knowledge and also because of their proven track records in training primary care sports medicine professionals. The authors in this book are not only experts in their subject matter, but they also understand how to teach their subject matter to primary care physicians. They understand it because they do it every day. As editors, we express our sincere appreciation to these dedicated professionals who have poured their souls into these chapters. The text is organized into sections that parallel the process of sports medicine diagnosis. The opening section contains the philosophy of sports medicine: the essential duties to consider before even stepping foot on a sideline or seeing athletes in a training room. Section 2 presents the history and physical exam: how to examine and diagnose the injured athlete. After proper examination, diagnosis and treatment are presented in Section 3. In this section we have provided the basics of casting, splinting, and fracture care, as well as the treatment of traditional soft-tissue injuries. Section 4 outlines rehabilitation and bracing: the art and science of augmenting and allowing the body to heal itself. An overview of the myriad procedures and special tests in sports medicine follows in Section 5. Finally, as an overarching capstone, the appendices outline the role of exercise in maintaining health and fitness in the pediatric, pregnant, and geriatric populations.

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At the turn of the twenty-first century, evidence-based medicine is fast becoming a cliche´. However, the need to assess the evidence that underlies treatment recommendations remains critical. It is essential to understand not only what the evidence shows, but also what it does not show or what it has not shown yet. The evidence base of sports medicine can perhaps best be described as ‘‘growing.’’ Applying a mature evidence scale to the growing body of sports medicine evidence would result in having nearly all evidence rated a C or a 3. Rather than do that, we have tried to create a scale that allows for and distinguishes the small study sizes typical of the current sports medicine evidence base. This text uses the following evidence scale: Level of evidence (LOE): A—Double-blind study B—Clinical trial more than 20 subjects C—Clinical trial fewer than 20 subjects D—Series 5 or more subjects E—Anecdotal case reports Other levels of evidence (meta-analysis, consensus opinion, etc.) are noted as such in the text. The age of textbooks may be drawing to a close. With so many online sources boasting up-to-date treatment recommendations and the push to make all things digital, one might wonder how this book will compete. Long after leeches are no longer fashionable for treating patellofemoral pain (that is a joke, at least in 2007!), we hope that the well-worn pages of your Sports Medicine Resource Manual will still be a valuable physical examination review, a familiar procedure reference, and a trusted affirmation of sports medicine and team physician philosophy. So, whether you are a family medicine doctor trying to review and learn more about musculoskeletal medicine or a sports medicine fellow preparing to dive into your fast-paced fellowship, we hope you find this book valuable. It was lots of fun to create, and it was written for you. Peter H. Seidenberg, MD, FAAFP Anthony I. Beutler, MD

CHAPTER

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The Sideline Physician John H. Wilckens, MD

KEY POINTS

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Although being well-read and technically competent are key qualifications, engendering trust is the most important attribute of an effective sideline physician, and participating in the team chemistry will build that trust. The effective sideline physician must also be able to communicate well: articulating and defining the issues to the athletes, the coaches, the training staff, and the parents will provide realistic expectations that everyone understands. The primary goals of the sideline physician are to manage emergencies on the playing field and to evaluate injured athletes for return to competition. Sideline physicians should anticipate the emergencies that are unique to each particular sport. Emergency response should be planned for and rehearsed to include athletic trainers, emergency medical services personnel, event support staff, and local hospital emergency department staff. Same-day return-to-play criteria should include the consideration of the safety of the injured athlete and the other competitors, the risks and consequences of reinjury, the effectiveness of playing hurt, and the consequences that may affect ultimate healing.

INTRODUCTION Athletics (i.e., playing sports) represents an important part of our society (Figure 1.1). In its purest and simplest form, it gives participants an opportunity to compete with others and themselves and to develop cardiovascular fitness, strength, and agility, which are seen as positive factors for a productive and long life. It also teaches teamwork, encourages development of a work ethic, and prepares individuals for the hard knocks of life. However, participation in athletics also involves the risk of injury, which is greatest during actual competition, be it youth soccer or a professional sport. Because of this risk, the profession of sports medicine has evolved to make athletics as safe as possible. The ultimate sports medicine participation is as the sideline physician during games, when the risk of injury is the greatest. The sideline is a daunting place in which to practice medicine (Figure 1.2). First, the sideline physician does not have the

comforts and amenities of the ‘‘ivory tower’’ office, with its receptionists, nurses, ancillary technicians, and easily accessible diagnostic tests and imaging. Second, the sideline physician is expected to evaluate an injured athlete, make the correct diagnosis, treat the condition, and return the athlete to optimum performance, immediately if not sooner! Evaluation of the injured player often takes place without the privacy of an examination room or the option of undressing the patient: the sideline physician may have to examine, in front of 80,000 screaming spectators, an athlete who is dressed in a uniform and bulky protective equipment and who is out of breath and writhing in pain. After the diagnosis is made, the coaching staff, the fans, the athlete, and even the parents of the athlete expect the sideline physician to treat the condition and return the athlete to play. In the office, that evaluation and discussion about the return to play allows for dialog and education; there is no such luxury on the sideline. To define the roles and responsibilities of the sideline physician, this chapter offers not evidence-based medicine, but ‘‘eminencebased’’ medicine, presenting the art of sideline ‘‘physicianship’’ gleaned from years of experience working with respected team physicians, trainers, and coaches. Technically speaking, the terms team physician and sideline physician incorporate different concepts. The team physician takes care of the day-to-day medical needs of the team and is responsible for preparticipation evaluations, training rooms, scheduling referrals for medical conditions, and return-to-play timelines. However, he or she may not be on the sideline because of conflicting commitments. The sideline physician is the medical expert who is ‘‘on the scene’’ during the game. The role of the sideline physician is best fulfilled by the team physician because of the inherent knowledge of the players and related personnel and because the physician has the trust and confidence of both. However, many times the sideline physician may not have any formal connection with the team, thus making the job of caring for injured players even more difficult. No matter how competent the physician, without those relationships, the job is harder. Because the team physician and the sideline physician are most often one and the same, the terms may be used interchangeably, assuming that relationship.

REQUIREMENTS AND RESPONSIBILITIES As in clinical medicine and athletics, preparation is critical to the success of the sideline physician. In addition to having a broad

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Chapter 1

Figure 1.1

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The sideline physician

A physician (right) attends to an athlete with a dislocated finger.

knowledge of all aspects of sports medicine, the sideline physician needs to understand the specific sport within which he or she is working; to be familiar with the patterns of injuries and possible emergency conditions that are unique to that sport; and to develop a trusting, working relationship with all members of the team and its staff.

Sport-specific knowledge Understanding the sport prepares the physician for the sideline. Previous participation in that sport by the physician is helpful for but not critical to understanding the sport. Each sport has a unique constellation of injuries, and the effective sideline physician will be familiar with them. Because the sideline physician is at the scene, he or she is in a unique position to witness the injury, which provides important information for the clinical examination. However, such information offers another advantage: it permits the sideline physician to make recommendations for rules modification in an attempt to make the sport safer. The most profound advances in sports medicine are not surgical techniques but rather

injury prevention. Injury surveillance is an important responsibility of the sideline physician. Just as each sport has a unique constellation of injuries, it also has unique emergencies. The single most important responsibility of the sideline physician is to be able to identify and treat emergencies rapidly and appropriately. The knowledgeable sideline physician can anticipate and plan for such emergencies, and, more importantly, he or she can arrange for the rehearsal of such emergencies and the necessary responses. For example, the time to learn how to use a spine board or to discover that a player on an oversized backboard cannot be accommodated in a helicopter’s patient bay is not on game day. To avoid such dangerous (and embarrassing) moments, it is essential to conduct planned drills for potential emergencies. Although it is critical to rehearse and assign responsibilities to the training staff on the field, such rehearsals also need to include local emergency medical technicians, event medical staff, and local emergency department personnel. The sideline physician also needs to consider that the athletes are not the only individuals who are at risk for injury during a game. The officials represent a special group that is at risk for injury because—except for the home plate umpire in baseball—most wear no special protective equipment even though they are on the playing field. In addition, many are older and not as conditioned or as quick as the athletes they are regulating. There is also a risk of injury to the sideline participants, the coaching staff, the officiating staff, other players, injured players, photographers, media personnel, mascots, and of course to the most susceptible person: the one with his or her first sideline pass. The edges of the field of play can be a dangerous place because contact does not always end at the sideline. Of athletes crossing the perimeters of the playing field, 93% extend up to 12 feet past the boundaries, although approximately half (59%) travel less than 6 feet.1 At the collegiate and professional levels, 10% of the out-of-bounds athletes travel more than 12 feet.1 The athletes are wearing protective equipment, but the sideline personnel are not. Athletes are focused on the action, whereas sideline personnel may be distracted by taking pictures, talking on headsets, and so on. Although seasoned sideliners are usually cognizant of this extended potential injury zone, new sideline spectators and injured players may not be aware of the risks. The sideline physician can guide personnel away from a developing play. It is much easier to prevent an injury than to treat one.

Relationships

Figure 1.2 A ringside physician at the 2003 USA Boxing National Championships.

To be a good sideline physician, one has to be a good team physician. As such, one’s effectiveness is based not only on medical and sports knowledge but also on relationships with the athletic trainers, the athletes, the coaching staff, the athletes’ parents, and the team’s administrative personnel. Those relationships are best built on trust, and trust develops from establishing the fact that the sideline physician is a team player who understands the mechanics, personalities, and needs of the team; who has the athletes’ best interests at heart; who embraces and supports the mission and vision of the team; and who shares a common bond with the team. When it is clear that the team’s and the athletes’ interests are above those of the physician, then the coaches and other personnel will be more willing to accept and comply with the physician’s decisions—not only the easy ones but also the difficult ones that may affect the outcome of the competition. Many times, building this relationship means going to the training room and the athletic field on a regular basis, not just to see injured athletes, but also to understand the sport and to participate in the team effort. Athletics is all about teamwork. A great technical surgeon or a compassionate, well-read physician does not always translate to an effective team physician. A physician’s competence is, of course, respected, but he or she will not gain the team’s

Requirements and responsibilities

confidence and trust until he or she demonstrates participation in and identification with the team. Participation in the team’s chemistry will facilitate the building of that important trust. The purpose of the sideline physician in this scenario is the team’s success rather than his or her practice marketability. The most crucial relationship is the one with the athletic trainers, and the time invested in building that relationship is time well spent. These hardworking, talented providers are an important resource because they know the athletes and the coaches well. Not only during the game but also during practice and the surrounding time in the training room, they are the sideline physician’s eyes and ears. A seasoned athletic trainer is a blessing: he or she can triage and manage the injured athletes effectively, and he or she can also represent the physician to the coaching staff, translating medical terminology into coaching terminology. Alternatively, a young, inexperienced athletic trainer also can be an opportunity: the physician will need to be more hands-on with regard to the medical management of the team, but the athletic trainer will be responsive and eager to learn. Communication with the training staff is critical for the team physician, and rehearsing scenarios and practicing emergency protocols will identify opportunities to improve communication and thus the medical care provided. Much of the physician’s direct involvement depends on the quality of and the trust in the training staff. If there are deficiencies in the training staff, they need to be addressed and improved. With young staff, the physician really has to take a hands-on role during the game. A seasoned and veteran staff may relieve the physician’s anxiety somewhat, but effective communication still is required.

Team practice Visits by the physician during team practice allow for visibility and the ability to meet with all members of the team without the distraction of actual playing conditions. Getting to know the athletes and coaches in this less stressful environment can provide important clues to each athlete’s profile. For example, some athletes are very stoic, and only knowledge of that fact will permit the correct interpretation of a subtle finding as the indication of a substantial injury. Other athletes are ‘‘high maintenance’’ and require a lot of attention even with minor injuries. It is helpful to know this information before game day. Again, understanding the team is important. A team may have some positions that are deep in talent and for which the loss of one player is not critical to the team’s success. Other athletes are ‘‘franchise players,’’ and an injury that takes such a player out of the game can alter the whole team’s structure, character, and chance of success. In addition, some athletes are impact players who can play at 80% capacity and still contribute, whereas other injured players who can function at 95% capacity (e.g., a quarterback with a finger injury or turf toe) will not be able to help the team at all. Such information is gleaned only after spending time with and developing a bond of trust with the team, the trainers, and the coaches. The importance of this bond of trust between the physician and the team cannot be overemphasized. It is built and earned, and it is the means of equipbing and preparing the physician and the team for the difficult decisions that must be made on the sideline during competition.

Pregame considerations To maximize effectiveness, it is critical that the physician command and control his or her schedule to allow adequate time to cover the sporting event properly. This coverage means that the physician must end clinics, office hours, and surgery schedules well in advance of game time; he or she must not be saddled with oncall responsibilities; and he or she must have a plan in place to direct his or her office staff, colleagues, midlevel providers, and

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nurses to handle emergencies that may occur during the sporting event. The sideline physician must arrive with or before the team because his or her responsibilities begin well before the opening whistle or the first pitch. If the physician is traveling with the team, arriving with the team is easy. For home events, arriving with the team is more difficult because of potential conflicts with family and practice priorities. Getting there before the team ensures timely arrival and less hassle with traffic, parking, and credentials. In addition, since the physician’s last visit with the team, an athlete may have become ill, thus making playing status questionable; also there may be several ‘‘wait-and-see’’ injuries that need to be reevaluated. Arriving early can allow for early intervention, with improved chances for the athlete’s participation in the game; it can also permit coaches to make last-minute adjustments to their game plan and roster. In addition to caring for the ‘‘home’’ team, the sideline physician may also need to care for the visiting team, which may not have a traveling physician. This is a courteous and responsible gesture: seeing the visiting team, staff, and families also sets a precedent that may be reciprocated if the situation is reversed. If the visiting team has a physician, it is still appropriate for the home team’s physician to meet him or her early before game time to review emergency protocols and the available medical facilities. Arriving early also allows the physician to visit and meet with the stadium support staff, the referees, the umpires, and other event administrators, presenting another opportunity to establish or confirm the trust relationship. Not only is it a warm gesture, but doing so also provides an opportunity to review with the training staff emergency equipment, their location, and protocols. During the game, these individuals may require the physician’s services, services that can be facilitated by previous acquaintance. As a visiting team physician, it is important to search out the emergency medical services staff and home medical staff. Although the team may have played in a certain venue before, things can change that may have an impact on decisions on the field, such as radiology capability, the closest emergency department, and magnetic resonance imaging availability. The visiting sideline physician should become familiar with the local emergency protocols. It is wise to remember that the responsibility of being the team’s physician is applicable not only to injured players during the game but also until that player reaches home, which may include a long aircraft ride. Dealing with an ill athlete on game day requires the physician’s early presence at the field. In brief, a low-grade fever can be treated with hydration and acetaminophen. If symptoms are limited to the upper respiratory tract, the player can be allowed to warm up. If he or she feels better, the athlete can be allowed to compete. If the athlete has general malaise, body aches, gastrointestinal symptoms, and fever, then more caution about playing should be exercised. Strenuous activity can make some viral illnesses more virulent and protracted.2 It should be pointed out to the coach who insists on the sick player being available that there are serious drawbacks to this plan of action: (1) The illness is contagious and may inoculate other team members through shared water bottles, towels, and contact; (2) sick athletes are not as effective as well ones and have reduced strength, energy, and endurance; and (3) sick athletes are prone to making mistakes and incurring injury, thus increasing their downtime. This recommendation by the physician may be more palatable to the coaching staff if they have confidence and trust in that physician. Always a subject of controversy is the role of precompetition injections, particularly cortisone and ketorolac (Toradol). These injectables have a use and should be included in the team physician’s sideline medical bag, but their routine use before competition is challenged. Injury and pain are part of athletic competition: hence the role of the team physician. However, pain has some

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The sideline physician

salvific value in that it helps identify and protect an injured body part. Eliminating that pain can lead to additional injury and delayed full recovery. Cortisone is an effective anti-inflammatory drug, but it can soften and weaken the soft tissues that it contacts. Ketorolac is an injectable nonsteroidal anti-inflammatory drug and a potent analgesic. In addition to potential injection-site problems, it may mask an injury, it can affect platelet function and bleeding, and it poses a small but identifiable risk to renal function.3 This risk may be increased among athletes who are taking supplements. Each team physician must make his or her own decision about the use of injectables before and during competition. The physician must carefully weigh the risks and benefits to the patient athletes, and he or she must make a decision that he or she can defend in court and sleep with at night. Some issues to consider are, for example, what happens if a pitcher requests and receives a pregame injection, the game is then cancelled, and he is scheduled to pitch the following day? Does he receive another injection? Is it safe? Also, if such an injection is offered to one player, is it then available to all on demand? Some physicians use pregame ketorolac for athletes without any symptoms, and other physicians refuse to use it at all. There are two situations in which this author would consider using a precompetition injection: an acromioclavicular separation and a hip pointer. These two conditions can be quite painful and limit one’s ability to compete because of pain alone. Injecting the acromioclavicular joint or hip pointer with xylocaine/bupivacaine will allow an athlete to warm up without pain and see if he or she can play effectively. In the absence of a definitive sports-wide ruling on this issue, the decision about the use of injectables before or during competition is the physician’s personal preference. That decision should be made well in advance of game day, and it is important to communicate that decision clearly and specifically to athletes, coaches, and training staff. If the line is clearly drawn and communicated, the team may test it but will ultimately respect it. If the communication is not clear, then there may be an endless barrage of requests for injectable medication. The physician should take an active role in the team’s warmups so that he or she can watch and individually assess those athletes who are ill or injured. In addition to observing, the physician should not hesitate to communicate with the athlete or his or her position coach; this communication should be done not to interfere with the pregame preparation but rather to share awareness of the situation, which can build trust and confidence. In all communications with the training staff, athletes, and coaches, it is important to support the overall mission of the team. There will be risks with any decision; they should be communicated clearly, and the good coaches will understand. Just because it is safe for an injured or ill athlete to play does not mean that he or she will be effective or provide a good quality of play. No sideline physician’s preparation is complete without a thoughtfully stocked ‘‘sideline physician’s bag.’’ Recommendations are available regarding what kind of medication and equipment should be in such a bag,4 but two practical points should be taken into consideration: (1) There is no reason to stock the bag with unfamiliar medication or equipment that the physician is unable to use, and (2) the bag needs to be well organized so that the physician can find a needed item quickly and so that he or she can also direct someone else to retrieve it while he or she is attending to an athlete (see Chapter 3 for specifics regarding the physician’s bag).

Game-time position The physician exists on the sideline for two main reasons: (1) to provide medical care in the event of an emergency, and (2) to assess an athlete’s ability to return to competition after an injury.

The sideline physician should not let any other task interfere with these two priorities, and he or she should position himself or herself to be in full view of the entire playing field. Many injuries can occur away from the action, so the sideline physician should not just follow the ball. Pacing the sideline will allow one to assess players as they come off of the field. In addition, the sideline physician has a responsibility that requires great attention to detail, and he or she must not be distracted with the emotion, the drama, and the rush of competition.

MEDICAL CARE These game-position concepts frame this author’s philosophy about the participation of the sideline physician in the on-field evaluation of an injured athlete: The physician belongs on the sideline—not on the field—except for during certain specific circumstances (described later). Although this stance is controversial and may not represent what happens every weekend on television, the team physician has a limited role on the playing surface. The training staff are the first, and usually the only, responders; most calls for medical assistance on the playing field are not emergencies. The training staff should be trained to evaluate the injured athlete; the physician involved in this initial evaluation only complicates and delays the process (with a few notable exceptions, outlined later). A system that works nicely is to have the head athletic trainer and an assistant be the first responders. After the trainers are on the field, regardless of which team is involved, the sideline physician can take two to three steps onto the playing field to be in full view of the trainers on the field and to observe what is happening. The trainers will then signal if they need physician assistance. This process allows the physician to collect his or her thoughts and to anticipate the worst-case scenario on the field. Typically, during those first few seconds, the trainers will try to relieve the anxiety and agitation of the injured athlete and keep the athlete on the ground until a primary assessment can be obtained. Talking to the athlete assists with the assessment and focuses the athlete on reducing his or her agitation. Asking the athlete to move an injured extremity will provide substantial basic information.

On-field physician examinations Each downed athlete does represent a possible medical emergency, and, for these notable exceptions (possible spine injury, lower extremity dislocation, fracture—dislocation, and unstable or open fracture), the physician should rush onto the field.

Spine injury/loss of consciousness If there appears to have been a spine injury or a loss of consciousness, the physician is needed for the execution of the emergency protocol. Typically, an athlete with a spine injury lands face down, and a quick and systematic stabilized rollover is needed to assess the athlete. The physician should stabilize the neck and direct the spine management protocol as practiced. Any athlete who loses consciousness should be treated as having a spine injury until the athlete regains consciousness and a spine injury can be ruled out. It is critical in sports that require helmets and shoulder pads (e.g., gridiron football, lacrosse, hockey) that this equipment is left in place for the assessment and transportation of the potentially spine-injured athlete. Removing the helmet with the shoulder pads in place causes increased neck extension. In addition, the helmet typically has a snug fit, and it can help immobilize a sweaty head to the spine board. If an airway needs to be established, remove the facemask and leave the helmet on5 (see Chapter 5 for a full discussion of emergency procedures).

Medical care

Lower-extremity dislocation, fracture—dislocation, and unstable or open fracture The physician needs to be on the field for the initial management of lower-extremity dislocation, fracture—dislocation, and unstable or open fracture, all of which may require a gentle reduction, immobilization, or both before transport off of the playing surface. The actual reduction of a displaced fracture, dislocation, or fracture—dislocation should be attempted only by personnel who are adequately trained to do so. A simple reduction by gentle exaggeration of the deformity, followed by in-line traction and correction of the deformity, can reduce most displaced fractures and dislocations; however, an improperly performed reduction can cause more injury. If the extremity becomes cyanotic and is pulseless, a reduction maneuver is indicated, regardless of physician experience. After he or she has been splinted, the athlete should be transported off the field by vehicle (i.e., by a modified golf cart [‘‘gator’’]); these athletes are usually big and sweaty, and there are possible adverse environmental conditions that make transport by stretcher difficult, painful, and dangerous.

Injury clock Finally, if there is an injury clock (e.g., as in wrestling or lacrosse), immediate involvement of the sideline physician will save valuable time with regard to the assessment and the availability of the injured athlete.

Sideline events Nonemergencies

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respiratory distress, immediate plans should be formulated to establish a surgical airway. Other causes of stridor and respiratory distress in the downed athlete include pneumothorax (patients usually can talk but are short of breath and tachypneic), tension pneumothorax (usually manifests as a more emergent shortness of breath and deviation of the trachea; usually treated with a thoracotomy on the side away from the deviation8), and posterior sternoclavicular dislocation (characterized by stridor, shortness of breath, or difficulty swallowing9). Loose bodies lodged in the airway can be displaced with a well-executed Heimlich maneuver. Respiratory distress can also occur as a result of acute anaphylaxis from medication, food, or an insect bite; injectable epinephrine should be immediately available.10

Cardiac arrest Cardiac arrest is rare during athletic competition. However, for those competitions involving patients who are more than 30 years old, cardiac disease is the most common cause of sudden death. Among younger patients, cardiac arrest may occur from a variety of causes, including congenital anomalies and structural, vascular, or conduction defects. Many attempts have been made to screen for these conditions. The most sensitive predictors seem to be a family history of sudden death and syncope with exercise. Athletes with either of these red flags require at a minimum that the family history be evaluated and an electrocardiogram and echocardiogram be obtained.4 Drug abuse—specifically cocaine—can lead to cardiac irritability and sudden death. Another cause of cardiac arrest among young athletes is commotio cordis.11 A young athlete typically is struck with a batted baseball, a thrown lacrosse ball, or a hockey puck to induce this condition. If an automated external defibrillator is available, these patients usually can be shocked and resuscitated. Without an automated external defibrillator, cardiopulmonary resuscitation should be initiated.

For nonemergencies, the training staff’s on-field examination of an injured knee, ankle, or shoulder will be repeated on the sideline under more favorable circumstances. No physician can effectively examine an injured athlete in full uniform on the playing field while under the observation of both teams, officiating staff, tens of thousands of fans (via the JumboTron [scoreboard]), and possibly a television audience (and lawyers). To do so is to create a flawed examination with little ultimate value. In addition, the patient is usually still in extreme pain and thus cannot cooperate with a thorough examination.

Neck pain The athlete with neck pain represents a particularly urgent sideline encounter. Many times the athlete is ambulatory, has mild neck pain, and is adamant about returning to play. If the athlete has pain, cervical muscle spasm, reduced range of motion, or neurologic findings, the discussion should not focus on return to play but rather on what type of immobilization, transportation, and imaging should be done urgently.12

Emergencies

Burners and stingers The burner or stinger (i.e., transient

Fortunately, medical emergencies are very rare among young athletic individuals, but they do exist, and the sideline physician should think about each one in advance and develop a strategy for addressing the injury in accordance with sound medical judgment and the standard of care. Although specific emergencies are topics of other chapters, a short discussion is in order to frame them for the sideline physician. The management of all emergencies, whether on the sideline or in the emergency department, starts with the ABCs: airway, breathing, and circulation.6

brachial plexopathy) represents another difficult decision for the sideline physician. A thorough neck and neurologic examination should be made. Any athlete with continuing symptoms should not be allowed to return to play. If symptoms clear completely during the game, consideration can be given to return to play. Athletes and concerned parties should understand that a recurrent stinger is very common. If the athlete has had a recurrent stinger, he or she can return to play that day only if symptoms have resolved, if he or she has had fewer than three previous stingers, and if those previous symptoms resolved in less than 24 hours.13

Respiratory distress/stridor When evaluating the downed athlete, an airway needs to be established. Again, unconscious athletes should be assumed to have a spine injury, and appropriate precautions should be taken with gentle in-line traction. A jaw thrust should establish an airway. Check for tobacco, chewing gum, and broken teeth, all of which represent potential obstructions to an airway. The mouthpiece should be removed. If an airway cannot be established, the physician must insist on the early activation of the emergency medical system. Helmets should be left in place, but faceguards should be removed. Direct trauma to the laryngeal area (e.g., a direct blow to the larynx by a ball, puck, stick, or opponent) represents an acute airway emergency.7 If an athlete is unable to talk and demonstrates

Bleeding Bleeding is common in athletics and may not represent an emergency. However, as a result of blood-borne pathogens (including the human immunodeficiency virus and hepatitis), most governing athletic authorities have specific guidelines for handling the bleeding athlete.2 The sideline physician should be familiar with the recommendations set forth by the governing body of the event that is being covered. In general, the bleeding needs to be stopped and covered. Blood-soaked equipment and uniforms should be cleaned, covered, or changed to prevent possible blood-borne disease transmission. Although contracting a bloodborne disease under these conditions is a rare possibility, it represents an emotional issue.

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Infectious diseases aside, actual bleeding becomes an important issue when it occurs near the face because it may interfere with the athlete’s vision. The area around the orbit of the eye is vascular, and lacerations in this area may generate enough bleeding to make vision difficult. For example, in boxing, if an athlete cannot see, he or she cannot compete effectively or defend himself or herself adequately against the opponent. Most bleeding responds to direct pressure. If there is urgency to returning the athlete to competition, a pressure dressing should be applied. As a rule, the physician should refrain from definitive wound closure on the sideline. Most wounds require irrigation and anatomic closure, which is difficult to achieve in this setting. After the competition, when conditions in the training room or the emergency department are more conducive to definitive treatment with appropriate lighting, irrigation, local anesthetic, sutures, and equipment, lacerations can be sutured. If appropriate conditions do not exist, the injured player should be referred to a place in which those conditions are met. For wound closure, the physician should use suture material that is of sufficient strength to withstand additional trauma but that is also small enough to effect a cosmetic closure. Although Dermabond represents technology with which to close most wounds effectively and cosmetically, its ability to withstand repeat trauma is unknown, and it is difficult to apply to the sweating athlete. The physician should become familiar with its storage and handling requirements because it will not work above a certain temperature.

Head injuries Head injuries are extremely difficult to examine and monitor, and they have been the cause of many shortened athletic careers, even professional ones. These injuries affect not only athletic competition but also employment, relationships, and activities of daily living. In addition, the brain is very sensitive to reinjury. To date, there is no sideline device with which to assess and definitively treat head injuries; the Standardized Assessment of Concussion (SAC) represents an early attempt at such a device.14 However, to have worth with regard to validity, the test must be administered during the preseason, and the recorded score must be available on the sidelines. After a player is concussed, the SAC can give some insight into the brain injury. If the score is lower than baseline, it is clear evidence for keeping the athlete out of competition. Alternatively, a similar SAC score is only suggestive evidence, and it may underrepresent the injury. In this scenario, the physician’s knowledge of the athlete will provide valuable information about his or her personality, responsiveness, and mood. The more unfamiliar the physician is with the athlete, the more conservative the assessment should be. There are many criteria and classification systems for closed head injuries, and each has its own strengths and weaknesses. The sideline physician should become very familiar with one system and use it as a guide for treating closed head injuries. Decisions to play or to not play a concussed athlete should be articulated with a classification system that is appropriate for the physician’s clinical acumen. The physician should refrain from modifying, mixing, and matching classification systems. The real emergency that can occur when allowing concussed athletes to play is reinjury and the ‘‘second impact syndrome.’’ This neurologic emergency has a 50% mortality rate15 and appears to be more prevalent among young and adolescent athletes. The potential for autonomic deregulation can exist for up to 30 days after a closed head injury. In general, there are very few circumstances in which a concussed athlete should be allowed to return immediately to competition.13,16,17

Heat injury Heat injury represents a potential emergency (Figure 1.3). Usually poor play from heat injury will force the athlete to the sideline long before the risk of heat stroke. Physicians should be sensitive to the temperature and humidity. Treatment begins the

Figure 1.3 A medical team attending to a marathon participant who suffered exertional collapse.

night before with forced hydration and liberal use of salt. For heavy sweaters with a history of heat cramps, additional electrolyte solutions can be used precompetition. During competition, the liberal drinking of water and sports drinks should be encouraged. (Particular attention should be given to the officials to make sure that they are adequately hydrated.) If the athlete begins cramping, passive stretching will help break the spasm. However, after cramps start, the athlete is probably a couple of liters behind, and it will be difficult to catch up with oral hydration alone. Such athletes typically respond well to intravenous hydration (for healthy athletes, 1 or 2 L of normal saline), which is best done in the training room. Again, prevention is the best treatment: heavy sweaters should be identified, and fluids should be pushed.

RETURN-TO-PLAY DECISIONS As discussed, on-field emergencies trigger protocols that just require execution. A broken bone or a torn anterior cruciate ligament represents a severe injury, but the decision about return to play is simple. In reality, the more minor the injury, the more consuming it is for the sideline physician because a decision must be made whether or not to return the athlete to competition.

General criteria Same-day return-to-play criteria are extremely subjective, and they depend on the age and skill level of the athlete, the injury sustained, and the type of sport being played. Common sense represents an important element of this type of decision making, and the following thoughts should be taken into consideration (Figure 1.4): 1. Will clearance to play be safe for the injured athlete? Is the athlete at increased risk of injury because of his or her injury or illness? What are the risks of reinjury? What are the consequences of reinjury? 2. Will clearance to play be safe for the other competitors? Sometimes an athlete can return to competition with a splint, brace, or cast. Although doing so may protect the injured player and his or her body part, can it injure an opponent or teammate? 3. Can the athlete compete effectively? Many injuries can be treated and return to play can be safe, but the athlete is less

Return-to-play decisions

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the athlete is safe to play, then the decision to play rests with the position coach, who determines the athlete’s effectiveness. Some decisions regarding return to play are difficult. The injured athlete may be an impact player whose presence may be critical to the outcome of the competition. Again, decisions about athletes with major injuries are easy: they cannot return to play. However, with some injuries, the athlete can play, but he or she has limited effectiveness and may be exposed to a greater risk of reinjury. As best as he or she can, the sideline physician needs to spell out the risks, and preestablished trust will go a long way in this situation. Some injured players have significantly affected the outcome of a contest. However, how many more have not? How many never return to their previous level of play? A good litmus test for the sideline physician is to ask himself or herself if this athlete would be allowed to return to play if he or she were the physician’s son or daughter. Figure 1.4 A sports medicine team gathers around an athlete to discuss the plan for safe and effective return to play.

effective. A sprained ankle may be adequately taped and braced and the athlete considered for return to play, but lost agility and speed inhibit the athlete’s ability to perform. This situation may be obvious for skilled players, such as running backs, but particular concern should also be shown for those athletes whose speed and agility is not showcased, such as interior linemen. ‘‘Losing a half step’’ may not be so obvious on the sideline, but in the trenches, a loss of quickness in one player can put the whole backfield at increased risk. 4. Although the athlete can play safely while hurt, will continued play affect healing and his or her later ability to play effectively? For example, a pitcher with a high pitch count who is throwing well but with pain may win that game but pitch less effectively for the rest of the season. In addition, athletes perform at high levels of skill. Subtle changes in their performance, such as lost velocity or accuracy in pitching, may signal fatigue, be a harbinger of an impending injury, or both. The sideline physician should be aware of the context of the injury. He or she may need to inform the athletes, the coaches, and the parents about the risks and benefits of playing injured or ill. In addition, an injury that occurs at the beginning of the season may have a different solution than one that occurs during the last game of the season. As a general working guideline, some basic principles can be applied to evaluating the injured athlete and determining the appropriateness of return to play. First, the injured part should have a functional (although not necessarily full) range of motion. Second, athletes should have protective strength. Again, an injured part may seem weaker because of the injury or as a result of pain. If the patient is allowed to return to play, the strength of the injured part should be adequate enough to function and to provide protection. For lower-extremity injuries, a simple ‘‘hop test’’ will help with the decision making. After the evaluation of a strain or sprain is performed and the injury is treated, if the athlete expresses a desire to return to play, the sideline physician can ask him or her to hop or jump on the uninjured leg three times to provide an idea of the injured leg’s preinjury ability. Next, the athlete should hop three times using both legs, and the physician should watch to see if the athlete favors the injured leg; this two-leg hop also will give the athlete some gradual confidence. Then, the athlete should hop on the injured leg. If the hop on the injured leg is adequate, the player can try to assume the playing position, attempt some jogging, and then make an effort to run. If these responses are acceptable, a sideline agility test is performed. If the physician is convinced that

Specific anatomic area Ankle Ankle injuries—particularly sprains—are very common sporting injuries. In fact, when evaluating the athlete, it may be difficult to determine whether the observed laxity is acute, chronic, or acute in the presence of a chronically unstable ankle. Swelling suggests acuteness. Although some ankle sprains can be braced or taped sufficiently to allow return to competition, it is the responsibility of the sideline physician to be sure that the athlete does not have an ankle fracture. In Canada, the Ottawa criteria18 were developed to allow emergency department medical staff to triage ankle injuries and to eliminate the obtaining of unnecessary radiographs for ankle sprains without missing an ankle fracture. The Ottawa criterion for an ankle radiograph after acute injury is tenderness to palpation, specifically over the medial malleolus, the lateral malleolus, or the proximal fifth metatarsal. Tenderness over any of these regions suggests fracture and requires a radiograph. If there is no tenderness over these bony landmarks, even with substantial local soft-tissue swelling and generalized tenderness, radiography is not indicated.19 Recently, at West Point, the Ottawa criteria were validated for use during the evaluation of athletic and training injuries.20 Some ankle sprains are ‘‘bad actors’’ and may require prolonged rehabilitation before the injured player can return to play; early return to play may delay eventual healing. Athletes with ankle sprains associated with a deltoid injury or a syndesmosis injury should not immediately return to play. If the ankle has medial swelling, tenderness just below the medial malleolus, or tenderness between the distal tibia and fibula (the syndesmosis), then the ankle should be iced initially and protected with immobilization and non—weight-bearing restrictions. If an athlete sustains a minor ankle sprain and is not prophylactically braced or taped, he or she should be given an opportunity for taping, bracing, or both and evaluated for return to play. If the ankle is already taped or braced and the athlete wears a cleated shoe, the ankle and shoe can be ‘‘spatted’’ with tape over both the ankle and shoe to provide more stability. If the athlete is still symptomatic, the ankle may need to be retaped or braced before evaluation for return to play. If the decision is made to not return the athlete with an ankle sprain to competition, the ankle should be iced and elevated. This early treatment may allow for quicker recovery from this injury.

Knee Examining the knee on the field with the athlete in full gear is difficult. In addition, the athlete is typically still in too much pain for a proper examination. Transporting the patient to the sideline allows for a complete systematic evaluation of the injured and uninjured knee. From the history and mechanism of a knee injury, the sideline physician usually has a good idea of what may be injured.

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The sideline physician

It is best to examine the injured structure last. It hurts less that way, and the ‘‘bad news’’ comes last, thus keeping the athlete focused on the examination. The sideline examination represents a golden opportunity to obtain a sensitive examination. The first bout of pain from the injured structure(s) is gone, swelling has not occurred, and the adrenaline of the competition is still present. Most athletes will be comfortable with a complete examination. An hour later, the same examination would be more difficult. If the knee is stable and no injury is identified by the sideline examination, the knee should be observed for a short period (10 to 15 minutes) for swelling. If no swelling occurs, the player can try to return to play. Knee injuries are common and range from simple contusions to complete dislocations. The medial collateral ligament is commonly injured from a contact or an impact to the lateral aspect of the knee, which produces a valgus stress on that ligament. If on examination the athlete has medial collateral ligament laxity from a noncontact injury, the physician should suspect an associated anterior cruciate ligament injury. Isolated lateral collateral ligament injuries are rare; they are usually associated with a cruciate ligament injury. With lateral collateral ligament injuries, the physician should check for peroneal nerve function. The anterior cruciate ligament is commonly injured via a noncontact mechanism, with the athlete recalling a ‘‘pop.’’ The Lachman test is the most sensitive test for this injury. In addition to eliciting the amount of translation, the quality of the end point can suggest an anterior cruciate ligament injury. The posterior cruciate ligament is most commonly injured from a direct blow to a flexed knee, and it is best evaluated with a posterior drawer test. Any one of these ligamentous injuries probably precludes return to competition that day. In addition to pain and swelling, the knee is unstable, even with bracing and taping, which precludes running, pivoting, or jumping. Other acute knee injuries include a patellar dislocation, which usually occurs from a twisting maneuver with the knee straight. A dislocated patella usually self-reduces, but if it does not, the knee can be extended, and gentle lateral to medial pressure on the patella should reduce it easily. Meniscal injuries can occur with a knee ligament injury or in isolation. Athletes describe the knee as being ‘‘tweaked’’ with a contact or noncontact mechanism. These injuries have delayed swelling. Any of the above injuries precludes return to play. The knee should be packed in ice and immobilized, and the athlete should be transported to the training facility or the bench.

Shoulder The three most common traumatic shoulder injuries are clavicle fracture, acromioclavicular joint separation, and shoulder dislocation. Athletes with these injuries can usually walk off of the field. Palpating the clavicle, the acromioclavicular joint, and the shoulder under the jersey and pads can help with the preliminary diagnosis, but the shoulder is best evaluated with the jersey and equipment off. Players with a clavicle fracture should be examined for possible pneumothorax and neurovascular injury. The injured arm should be placed in a sling, and ice should be applied to the fracture site. Acromioclavicular joint separations have varying degrees of severity, but they are all painful. These injuries are also treated with ice and a sling. Most of these injuries preclude return to play, but under unusual circumstances, a grade I or II21 acromioclavicular joint separation can be injected with an anesthetic and the prominence over the acromioclavicular joint can be padded for relief in an attempt to return the athlete to play. The shoulder is the most commonly dislocated major joint. Athletes complain of having a ‘‘dead arm’’ and being unable to touch the opposite shoulder. These dislocations can be reduced with gentle traction and relaxation without medication, which is

best done in the training facility or the locker room with the athlete’s equipment off. Attempting to do this on the field or the bench is not recommended because patient relaxation is critical to a gentle reduction. Players with recurrent dislocations sometimes can self-reduce the dislocation. Pain and recurrent instability usually preclude return to play, and the shoulder should be treated with ice and a sling. Alternatively, patients with recurrent instability may have little pain; with taping, bracing, or both, an athlete with this condition can be considered for return to competition. In general, fractures anywhere, from the ankles to the fingers, are painful, and they usually preclude return to play, except under the most unusual circumstances (e.g., an offensive lineman with a metacarpal fracture that has been treated with a playing cast). The injured extremity should be iced, immobilized, and elevated. Radiographs obtained early will provide indisputable documentation and allow the player, the coach, and the physician to make the appropriate adjustments to the game plans. Abrasions should be cleaned and dressed immediately. With the emergence of community-acquired methicillin-resistant Staphylococcus aureus, this procedure becomes even more important.22 Muscle contusions and strains are very common. Hamstring and quadriceps strains are particularly annoying, and they can remove an athlete from play. A tight wrap might provide some relief and a hope of return to play, but continuing to play carries the risk of extending the muscle strain. Some physicians have advocated a local injection of an anesthetic with a corticosteroid to the area of the muscle injury after the competition; this protocol is associated with improved pain control, gait, and earlier return to play at a later time.23 Contused muscles should be stretched and, if possible, immobilized in that position overnight.20 This procedure, which reduces swelling and tightness, returns athletes to play in days instead of weeks, and it is best done on the sideline before substantial pain and swelling commence. The timely application of ice and appropriate protected immobilization on the sideline (after the player accepts that he or she cannot return to play) may facilitate quicker rehabilitation and return to function and ability later on.

CONCLUSION The first level of confidence that a team will have for the physician is in his or her technical ability. However, being a great diagnostician or an innovative surgeon will only get a foot in the door (or rather, on the sideline). Preparation is equally important to the sideline physician. An old Chinese proverb states, ‘‘The more you sweat during peacetime, the less you will bleed during war.’’ This quote is appropriate not only for the athlete and the team but also for the sideline physician. With validated knowledge and consummate preparation, the sideline physician who involves himself or herself in the team chemistry will be elevated to a whole new level of confidence and respect. That respect will provide the leverage needed to represent and articulate the medical issues of the injured athlete and the vision and mission of the team; these concepts should be one and the same. When the lines between the two become blurry, the effective sideline physician can deliver a safe, thoughtful decision, no matter how unpopular.

REFERENCES 1. 2.

Garrick JG, Collins GS, Requa RK: Out of bounds in football: player exposure to probability of collision injury. J Safety Res 1977;9(1):34-38. Wilckens JH, Glorioso JE Jr: Risk assessment and management of nonorthopaedic conditions. Section A. Viral disease. In DeLee JC, Drez D Jr, Miller MD (eds): DeLee & Drez’s Orthopaedic Sports Medicine: Principles and Practice, 2nd ed. Philadelphia, WB Saunders, 2003, pp 251-263.

References

3.

4.

5.

6.

7. 8. 9. 10. 11. 12.

Lee A, Cooper MC, Craig JC, et al: Effects of nonsteroidal anti-inflammatory drugs on postoperative renal function in adults with normal renal function. Cochrane Database Syst Rev 2004;(2):CD002765. Madden CC, Walsh WM, Mellion MB: The team physician: the preparticipation examination and on-field emergencies. In DeLee JC, Drez D Jr, Miller MD (eds): DeLee & Drez’s Orthopaedic Sports Medicine: Principles and Practice, 2nd ed. Philadelphia, WB Saunders, 2003, pp 737-768. Waninger KN, Richards JG, Pan WT, et al: An evaluation of head movement in backboard-immobilized helmeted football, lacrosse, and ice hockey players. Clin J Sport Med 2001;11(2):82-86. American College of Surgeons Committee on Trauma: Advanced Trauma Life Support Program for Doctors, 6th ed. Chicago, American College of Surgeons, 1997. Hanft K, Posternack C, Astor F, et al: Diagnosis and management of laryngeal trauma in sports. South Med J 1996;89(6):631-633. Levy AS, Bassett F, Lintner S, et al: Pulmonary barotrauma: diagnosis in American football players. Three cases in three years. Am J Sports Med 1996;24(2):227-229. Gove N, Ebraheim NA, Glass E: Posterior sternoclavicular dislocations: a review of management and complications. Am J Orthrop 2006;35(3):132-136. Gomez JE: Sideline medical emergencies in the young athlete. Pediatr Ann 2002;31(1):50-58. Link MS, Wang PJ, Maron BJ, et al: What is commotio cordis? Cardiol Rev 1999;7(5):265-269. Haight RR, Shiple BJ: Sideline evaluation of neck pain. When is it time for transport? Phys Sportsmed 2001;29(3):45-62.

13. 14. 15. 16. 17. 18. 19.

20. 21.

22.

23.

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Shah S, Luftman JP, Vigil DV: Football: sideline management of injuries. Curr Sports Med Rep 2004;3(3):146-153. McCrea M: Standardized mental status testing on the sideline after sport-related concussion. J Athl Train 2001;36(3):274-279. Cantu RC: Second-impact syndrome. Clin Sports Med 1998;17(1):37-44. Almquist J, Broshek D, Erlanger D: Assessment of mild head injuries. Athlet Ther Today 2001;6(1):13-17. Kelly JP, Rosenberg JH: The development of guidelines for the management of concussion in sports. J Head Trauma Rehabil 1998;13(2):53-65. Stiell IG, McKnight RD, Greenberg GH, et al: Implementation of the Ottawa ankle rules. JAMA 1994;271(11):827-832. Derksen RJ, Bakker FC, Geervliet PC, et al: Diagnostic accuracy and reproducibility in the interpretation of Ottawa ankle and foot rules by specialized emergency nurses. Am J Emerg Med 2005;23(6):725-729. Ryan JB, Wheeler JH, Hopkinson WJ, et al: Quadriceps contusions. West Point update. Am J Sports Med 1991;19(3):299-304. Rockwood CA Jr, Williams GR Jr, Young DC: Disorders of the acromioclavicular joint. Rockwood CA Jr, Matsen FA III, Wirth MA, et al (eds): The Shoulder, 3rd ed. Philadelphia, WB Saunders, 2004, pp 521-595. Rihn JA, Michaels MG, Harner CD: Community-acquired methicillin-resistant Staphylococcus aureus: an emerging problem in the athletic population. Am J Sports Med 2005;33(12):1924-1929. Levine WN, Bergfeld JA, Tessendorf W, et al: Intramuscular corticosteroid injection for hamstring injuries. A 13-year experience in the National Football League. Am J Sports Med 2000;28(3):297-300.

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CHAPTER

The Preparticipation Evaluation Jay E. Noffsinger, MD

KEY POINTS

will include more evidence-based medicine. Recommendations may ultimately change from guidelines to standards.

. The primary objectives of the preparticipation physical . . . .

evaluation (PPE) are to detect conditions that may be lifethreatening or disabling or that may predispose an athlete to injury or illness. The secondary objectives of the PPE include determining general health and serving as an entry point into the healthcare system for adolescents. The purpose of the PPE is to facilitate and encourage safe participation rather than to exclude athletes from participation. A comprehensive history will identify up to 75% of problems that affect athletes. Only after this history is supplemented by a careful physical examination can appropriate clearance decisions be made.

INTRODUCTION Without question, the practice of primary care sports medicine has become more and more reliant on evidence-based medicine. This textbook will be filled with examples of evidence-based medicine. Unfortunately, recommendations regarding a comprehensive preparticipation physical evaluation have been primarily based on clinical observations and ‘‘expert opinions.’’ Before 1992 there were virtually no national guidelines for a PPE for this very reason. That year representatives from many important organizations got together and published the first PPE monograph. The second edition came out in 1997, and the third was published in 2005.1 Organizations sponsoring this monograph include the American Academy of Family Physicians, the American Academy of Pediatrics, the American College of Sports Medicine, the American Medical Society for Sports Medicine, the American Orthopaedic Society for Sports Medicine, and the American Osteopathic Academy of Sports Medicine. National endorsements have come from the National Athletic Trainers Association, the Sports Physical Therapy Section of the American Physical Therapy Association, and the Special Olympics Medical Committee. This impressive list of organizations is a testament to the importance and significance of the monograph. The work of the representatives of these organizations is ongoing, and future editions of their work

GOALS AND OBJECTIVES The obvious primary objective of a well-done PPE is to detect conditions that may be life-threatening or disabling or that predispose an athlete to injury or illness. Unfortunately, cost analyses and other factors preclude the kind of evaluation that would be 100% sensitive and specific. For example, without an echocardiogram, most cases of hypertrophic cardiomyopathy will go undetected, even with a comprehensive history and physical. A final primary objective of a PPE is to meet legal and administrative requirements. For most adolescents, this PPE will be the only health maintenance visit for the year. Of course, this is not ideal, but it is reality. Therefore, secondary objectives of this evaluation are to determine general heath, to serve as an entry point into the health-care system for adolescents, and to provide an opportunity for the discussion of health and lifestyle issues.

TIMING, SETTING, AND STRUCTURE Although multiple health-care professionals may play a role in conducting the PPE, ultimate responsibility should be assigned to a physician who is a doctor of medicine or osteopathy. Different states have different regulations regarding the qualifications of practitioners. The optimal time to conduct the PPE is 6 weeks before the onset of preseason practice. This allows time to follow up on abnormalities that are discovered, but it is not so soon that new problems are likely to appear. With an estimated 7 to 8 million required PPEs occurring at the high-school level and probably an equal number at the middle-school and college levels, it may be impossible to have each evaluation performed within this timetable; however, the above principles should be considered. The monograph recommends a comprehensive PPE at entry to middle and high school, with yearly interim updates as directed by the history. The American Academy of Pediatrics recommends biannual evaluations with interval history updates. Unfortunately, state laws prevail, and most states require yearly evaluations. Other organizations that may have requirements include school districts, athletic conferences, and insurance companies.

The preparticipation physical evaluation medical history

No routine screening tests, including blood tests, are recommended currently. Rather, these tests are to be directed by findings on the PPE. Earlier recommendations included a urinalysis; this often resulted in a workup for the protein discovered and resulted in a diagnosis of benign orthostatic proteinuria after substantially alarming the athlete and parents while awaiting further tests. Ideally, the preferred setting for the PPE is the primary care physician’s office. This setting is optimal for privacy, lighting, proper instruments, familiarity with the patient (including immunization records), and ready access to appropriate referrals if necessary to follow up on identified problems. Certainly pursuing the secondary objectives of the PPE is better done in this setting. Problems include expense, availability to provide timely PPEs to all athletes, lack of direct contact with school officials (including coaches), and, unfortunately, a lack of expertise by many primary care physicians with regard to the ideal conduct of such an evaluation. A properly performed ‘‘station-method’’ PPE is an acceptable alternative. Stations may include vital signs, visual acuity assessment, fitness, flexibility, nutrition, and a physical examination that can be divided into as many stations as desired to meet the expertise of the examiners present. Advantages of this method include low expense, greater availability, likely appropriate expertise of the coordinated medical team (e.g., an orthopedist to do the musculoskeletal assessment and a cardiologist to listen to hearts), and on-site coordination with coaches and other school officials. The old ‘‘last-minute’’ locker-room method is now condemned.

THE PREPARTICIPATION PHYSICAL EVALUATION MEDICAL HISTORY It is felt that a complete history will identify 75% of the problems that affect athletes. It is important that athletes and parents complete the history together because it has been found that if each completes the form separately, there is only a 39% correlation.2 The PPE medical history form suggested by the monograph is included (Figure 2.1), and it incorporates all of the questions recommended by the American Heart Association3 (revised in 1998).4 Many states have adopted this form or use one that is very similar. Although readers of this text understand that they may be forced to use state forms that are not ideal, they are encouraged to develop their own supplementary history document to make sure that all appropriate history is obtained. Unfortunately, only about half of the United States even requires a medical history.5,6 The most common cause of nontraumatic sudden death in athletes is definitely cardiac (80% to 95%), and this is followed distantly by heat illness and then asthma. Among patients who are less than 35 years of age, any cardiac problems are usually congenital; alternatively, among those who are 35 years of age and older, arteriosclerotic cardiovascular disease predominates. The best chance of detecting hypertrophic cardiomyopathy, which is the most common congenital heart defect that causes sudden death in the United States, is the history rather than the physical. The collapse of an athlete during (rather than after) competition or a positive family history demands a comprehensive cardiologic evaluation. Participation guidelines for athletes with cardiovascular problems are covered by the 36th Bethesda Conference, which was published in 2005.7 It is known that 0.5% to 1% of all humans are born with a congenital heart defect. Approximately 1% of these defects are potentially lifethreatening, and 10% of individuals with this condition will die as a result of the problem. It can be concluded that one of these ultimately fatal defects would be present for every 200,000 PPEs. If echocardiograms were required for all PPEs, it would cost

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nearly $250,000 to detect each fatal defect or at least $18,000 for a typical sports program.8 Clearly, this is not financially feasible. In the United States, cardiologists do not recommend screening electrocardiograms because they will not rule out hypertrophic cardiomyopathy; instead, electrocardiograms often detect worrisome changes that ultimately turn out to be ‘‘athlete’s heart,’’ which is a known entity that consists of normal physiologic changes. In some countries (e.g., Italy) other heart conditions that can be detected by electrocardiograms (e.g., arrhythmogenic right ventricular dysplasia) predominate, which makes electrocardiography a sensible and inexpensive screen. The heat-illness spectrum includes heat edema, heat cramps, heat syncope, heat exhaustion, and heatstroke. Heat-illness predisposition includes a history of problems in the heat as well as a pertinent family history, and these elements of the history should be pursued. I have seen heat stroke occur in twin male athletes competing in college cross-country during successive seasons. If a prior heat illness has ever included central nervous system dysfunction, heatstroke should be assumed. Recurrences may be associated with a mortality rate of as high as 10%. In cases of exertional heatstroke the athlete may still be sweating profusely. Only in cases of classical heatstroke is the skin dry. Other predisposing factors include dehydration, old or young age, inadequate acclimatization, poor aerobic fitness, large body size with excess body fat, febrile condition, overexertion, and certain medications and supplements. Inquiries regarding sickle cell trait status should be made, and strong consideration should be given to testing those whose status is unknown. Approximately 8% of blacks and a small percentage of whites carry this trait. Although it is normally benign, under extremes of strenuous activity (particularly in the heat and at altitude), rhabdomyolysis and sudden death have occurred.9,10 Preventive measures are strongly advised, including adequate acclimatization, maintaining good hydration, avoiding diuretics, and avoiding all-out sprints or timed miles early during training. It is quite possible that the deaths of many black athletes that have been attributed to heat alone may actually be related to sickle cell trait. Most of these problems have occurred in the first 1 to 2 weeks of practice during the summer, so medical observers need to be particularly vigilant at these times. Questions about asthma may point out very poor control and lead to recommendations that will lessen the probability of serious consequences. Many athletes have very poorly controlled asthma and abuse their ‘‘rescue’’ inhalers. Other athletes with a diagnosis of exercise-induced asthma may actually have other conditions, such as paradoxical vocal cord dysfunction. Alternatively, the incidence of exercise-induced asthma is often underestimated. A detailed allergy and asthma history questionnaire was developed by the Sports Medicine Committee of the American College of Asthma, Allergy & Immunology to assist with raising awareness of exercise-induced asthma.11 Suspected cases can be confirmed by changes in peak expiratory flow rates from baseline to after exercise followed by a positive response to preventive medication, such as a short-acting b-agonist, 5 to 10 minutes before exercise. It has been said that the most common injury in sports medicine is a recurrence of a prior injury. The identification of prior injuries by the taking of a history often confirms totally inadequate rehabilitation and certainly dictates a very careful musculoskeletal examination to look for persistent problems, such as poor flexibility, strength (including core strength), proprioception, or even residual pathologic laxity of a joint. A history of concussions or repetitive ‘‘burners’’ demands a careful assessment of full recovery as well as checking for anatomic and other predispositions to recurrences that may be less benign than prior injuries. Isolated stingers are not considered to be serious, but severe or repeated injuries can lead to permanent motor or sensory sequelae. Radiologic investigation can exclude cervical spinal stenosis or degenerative disk disease.

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Chapter 2

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The preparticipation evaluation

Figure 2.1 Preparticipation physical evaluation: history form. (From the American Academy of Family Physicians, American Academy of Pediatrics, American College of Sports Medicine, et al: Preparticipation Physical Evaluation, 3rd ed. Minneapolis,The Physician and Sportsmedicine/McGraw-Hill, 2005.)

The preparticipation physical evaluation medical history

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Figure 2.2 Preparticipation physical evaluation: physical evaluation form. (From the American Academy of Family Physicians, American Academy of Pediatrics, American College of Sports Medicine, et al: Preparticipation Physical Evaluation, 3rd ed. Minneapolis,The Physician and Sportsmedicine/McGraw-Hill, 2005.)

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The preparticipation evaluation

For persistent symptoms, electrodiagnostic studies may be warranted. Prevention tools may include neck strengthening, equipment changes (including neck rolls), and reviewing tackling techniques. An athlete who reports bilateral or upper and lower extremity symptoms would never be diagnosed with a stinger, and a central cause is assumed. Transient quadriparesis should initially be handled as a catastrophic cervical spine injury. After fractures and ligamentous instability have been ruled out, further investigation is needed to exclude congenital or acquired predispositions. Even with a totally negative workup, return-to-play recommendations remain controversial and should include neurosurgical or neurologic consultation. Although there is some debate about second impact syndrome, there is no question that someone who has experienced a concussion is 4 to 6 times is more likely to have a recurrence than someone who has not.12,13 The term second impact syndrome was coined to describe massive cerebral edema with collapse and death after minor head trauma in an athlete who was still symptomatic from an earlier concussion. The theory is that autonomic dysfunction of the cerebral vessels resulted from the first injury and caused them to dilate significantly after the second impact, thus resulting in catastrophic cerebral edema. Although future studies are needed to settle the debate regarding second impact syndrome, described cases have occurred almost exclusively among very young athletes. There is also much debate regarding the classification of concussions and subsequent management decisions. International experts have recently reported their recommendations from the Second International Conference on Concussion in Sports,14 and the American College of Sports Medicine also released a consensus statement regarding concussion and the team physician.15 It is universally agreed that athletes should not be allowed to return to play until they are asymptomatic both at rest and with exertion; however, the problem is with determining what qualifies as asymptomatic. Recently developed computer-based programs to assess neuropsychological function as compared with baseline may become standard in the future as their validity is confirmed. Cumulative damage is another concern, including dementia pugilistica (punch-drunk syndrome).

THE PREPARTICIPATION PHYSICAL EVALUATION The PPE form recommended by the monograph is included here (Figure 2.2). Note that it includes follow-up questions about more sensitive issues. The physical examination can be conducted without the parents present, and it is an ideal time to explore these issues. The presence of anisocoria is noted to prevent future misinterpretation as possibly resulting from a serious head injury. Best corrected vision should be 20/40 or better, otherwise clearance considerations include appropriate protection of the good eye in many sports. I have personally seen individuals with a BB injury, a bottle-rocket injury, and a congenital cataract, and I also worked with an athlete who underwent multiple eye surgeries after a retinal detachment. Each of these individuals had almost no vision in one of their eyes, and each had been inappropriately playing contact sports for years with no protection for their good eye. Table 2.1 provides the categories of sports-related eye-injury risk to the unprotected players. Good athletic trainers may be consulted for help with designing custom protective eyewear for sports in which standards are not available, such as wrestling. Table 2.2 outlines recommended eye protectors for selected sports. Although at one point I had trouble convincing a high-school football player about the importance of placing a visor in his helmet to protect his

Table 2.1 Categories of Sports-Related Eye-Injury Risk to the Unprotected Player High Risk SMALL, FAST PROJECTILES Air rifle BB gun Paintball HARD PROJECTILES,‘‘STICKS,’’ CLOSE CONTACT Baseball/softball Basketball Cricket Fencing Hockey (field and ice) Lacrosse (men’s and women’s) Racquetball Squash INTENTIONAL INJURY Boxing Full-contact martial arts MODERATE RISK Badminton Fishing Football Golf Soccer Tennis Volleyball Water polo LOW RISK Bicycling Diving Noncontact martial arts Skiing (snow and water) Swimming Wrestling E YE SAFE Gymnastics Track and field* *Javelin and discus have a small but definite potential for injury. However, good field supervision can reduce the extremely low risk of injury to nearly negligible. Adapted with permission from Vinger PF: Phys Sportsmed 2000;28(6):49-69. In American Academy of Family Physicians, American Academy of Pediatrics, American College of Sports Medicine, et al: Preparticipation Physical Evaluation, 3rd ed. Minneapolis, The Physician and Sportsmedicine/McGraw-Hill, 2005.

good eye, it has recently become necessary to prove medical necessity for the wearing of a shaded visor because players now want them so that they can conceal the direction in which they are looking. Height, weight, and body mass index determinations allow for the addressing of both obesity and possible eating disorders. A general musculoskeletal screening examination is mandatory, and a more comprehensive examination should be performed for areas in which prior injuries have occurred. At this time, the determination of the Tanner stage is not recommended; however, for those in the middle-school age group, I think it would at least be wise to consider. For example, in a

The preparticipation physical evaluation

Table 2.2

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Recommended Eye Protectors for Selected Sports

Sport

Minimal Eye Protector

Comment

Baseball/softball (youth batter and base runner) Baseball/softball (fielder) Basketball Bicycling Boxing Fencing Field hockey (men’s and women’s)

ASTM standard F910

Face guard attached to helmet

ASTM standard F803 for baseball ASTM standard F803 for basketball Helmet plus street wear/fashion eyewear None available; not permitted in the sport Protector with neck bib ASTM standard F803 for women’s lacrosse (goalie: full face mask) Polycarbonate eye shield attached to helmet-mounted wire face mask None available; not permitted in the sport ASTM standard F513 face mask on helmet (goaltenders: ASTM standard F1587) Face mask attached to lacrosse helmet ASTM standard F803 for women’s lacrosse ASTM standard F1776 for paintball ASTM standard F803 for selected sport

ASTM specifies age ranges ASTM specifies age ranges

Football Full-contact martial arts Ice hockey Lacrosse (men’s) Lacrosse (women’s) Paintball Racket sports (badminton, tennis, paddle tennis, handball, squash, and racquetball) Soccer Street hockey Track and field Water polo/swimming Wrestling

ASTM standard F803 for selected sport ASTM standard F513 face mask on helmet Street wear with polycarbonate lenses/fashion eyewear* Swim goggles with polycarbonate lenses No standard available

Contraindicated for functionally one-eyed athletes Protectors that pass for women’s lacrosse also pass for field hockey

Contraindicated for functionally one-eyed athletes HECC-certified or CSA-certified full face shield

Should have option to wear helmet

Must be HECC or CSA certified

Custom protective eyewear can be made

*Eyewear that passes ASTM standard F803 is safer than street wear eyewear for all sports activities with impact potential. ASTM, American Society for Testing and Materials; CSA, Canadian Standards Association; HECC, Hockey Equipment Certification Council. Adapted with permission from Vinger PF: Phys Sportsmed 2000;28(6):49-69. In American Academy of Family Physicians, American Academy of Pediatrics, American College of Sports Medicine, et al: Preparticipation Physical Evaluation, 3rd ed. Minneapolis, The Physician and Sportsmedicine/McGraw-Hill, 2005.

sport like football, there is a huge difference between a Tanner-I, 210-pound overweight male and a Tanner-V athlete of the same age and weight who looks like a National Football League linebacker. An example of a general musculoskeletal screening examination as outlined in the PPE monograph is included (Figure 2.3). Unfortunately, this is one of the most common parts of the evaluation that is left out. This examination would be particularly amenable to the station method, and it could be performed by an athletic trainer, a physical therapist, or even an orthopedic surgeon. Male testicular examination allows not only for the identification of problems but also for the discussion of the importance of periodic self-examination to assist with the early detection of testicular cancer, which is the most common malignancy found in young adult males. The cardiovascular examination recommended by the American Heart Association includes checking pulses, determining blood pressure, looking for signs that are suggestive of Marfan’s syndrome, and auscultating the heart in at least two different positions to look for dynamic changes that may suggest hypertrophic cardiomyopathy (e.g., increased intensity of a systolic murmur with the Valsalva maneuver). Marfan’s syndrome is an autosomal-dominant connective tissue disease that manifests with characteristic phenotypic findings that include the following: kyphosis, high-arched palate, pectus excavatum, arachnodactyly, arm span that is greater than height, mitral valve prolapse, aortic insufficiency murmur, myopia, lenticular dislocation, a thumb sign, and a wrist sign. Screening for this disorder is recommended for men who are 6

feet tall or taller and women who are 5 feet and 10 inches tall or taller, who have two or more physical manifestations, or who have a family history of Marfan’s syndrome. The importance of identifying Marfan’s syndrome is because of the associated aortic root dilatation, which can progress to dissection and rupture with ensuing sudden death.16 Blood-pressure measurement should be accomplished using the largest appropriate cuff. The regular adult cuff is too small for many large male athletes, and it results in a false elevation of the blood-pressure measurement. The finding of elevated blood pressure for age is probably the most common abnormality found during the PPE. If decreased pulses are found in the lower extremities, blood-pressure measurements should also be taken from the legs to rule out coarctation of the aorta. Blood-pressure measurements should be repeated on at least two separate occasions to ensure that the elevation is persistent. If elevated blood pressure is confirmed, investigation for end-organ damage should follow. Table 2.3 outlines the classification of hypertension in children and adolescents, and Table 2.4 covers the classification of hypertension in adults. Specific recommendations for participation for athletes with hypertension are found in the PPE monograph and the results of the 36th Bethesda Conference.7 In general, aerobic or dynamic exercise is beneficial for hypertension, whereas high static activities may be contraindicated. It is only necessary to restrict activity while further evaluation is performed and blood-pressure control is achieved for adults with stage 2 hypertension or children with measurements that are above the 99th percentile (in whom end-organ damage is likely) or for those in whom a secondary cause is suspected.

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Chapter 2

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The preparticipation evaluation

Figure 2.3 General musculoskeletal screening examination. (From the American Academy of Family Physicians, American Academy of Pediatrics, American College of Sports Medicine, et al: Preparticipation Physical Evaluation, 3rd ed. Minneapolis,The Physician and Sportsmedicine/McGraw-Hill, 2005.)

The neurologic examination should be much more comprehensive when the history reveals prior concussions or multiple ‘‘burners’’ or ‘‘stingers,’’ as discussed previously.

DETERMINING CLEARANCE Because the goal of the PPE is to facilitate and encourage safe participation rather than to exclude athletes from participation, it is fortunate that most large studies find an ultimate disqualification rate of less than 1%. Between 3.1% and 13.9% of athletes require

further evaluation before a final clearance determination can be made. One of the largest studies on this subject, which was performed by Magnes and colleagues,17 looked at more than 10,000 athletes and resulted in a final disqualification rate of only 0.4% after an initial conditional referral rate of 10.2%. Reasons for a delay in the final clearance determination pending further investigation or referral included hypertension (38%), ophthalmologic reasons (12%), genitourinary reasons (10%), neurologic reasons (8%), infectious mononucleosis (4%), and musculoskeletal reasons (4%). The monograph-suggested clearance form is included (Figure 2.4), and clearance options include the following: (1) clearance without

Determining clearance

restriction; (2) clearance with recommendations for further evaluation or treatment; (3) no clearance for any sport; and (4) no clearance for certain sports. Decisions may be based in part on the classification of sports by contact (Table 2.5) and the classification of sports by strenuousness (Table 2.6). These tables as well as the table regarding medical conditions and sports participation (Table 2.7) come from the American Academy of Pediatrics

Table 2.3 Classification of Hypertension in Children and Adolescents Blood Pressure Classification*

Systolic and Diastolic Blood Pressure Measurementy

Normal High normal Hypertension Severe hypertension

< 90th percentile for age, sex, and height 90th-95th percentile for age, sex, and height > 95th-99th percentile for age, sex, and height > 99th percentile for age, sex, and height

*Charts for classification by age, sex, and height percentile can be found at http://www.nhlbi.nih.gov/guidelines/hypertension/child_tbl.htm. y On repeated measurement. Adapted from Update on the 1987 Task Force Report on High Blood Pressure in Children and Adolescents: Pediatrics 1996;98(1):649-658. In American Academy of Family Physicians, American Academy of Pediatrics, American College of Sports Medicine, et al: Preparticipation Physical Evaluation, 3rd ed. Minneapolis, The Physician and Sportsmedicine/McGraw-Hill, 2005.

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Committee on Sports Medicine and Fitness. As with neuropsychologic testing after concussions, with further research, future editions of the monograph will hopefully have more standards and fewer ‘‘qualified yes’’ recommendations. When the station method is used to conduct this examination, the most experienced practitioners may be at the last station, where clearance determinations are

Table 2.4

Classification of Hypertension in Adults

Blood Pressure Classification*

Systolic Blood Pressure (mm Hg)

Diastolic Blood Pressure (mm Hg)y

Normal Prehypertension Stage 1 hypertension Stage 2 hypertension

15 mm Hg >30 mm Hg >20 mm Hg

After a patient presents with CECS, it is difficult to modify all risk factors that may have contributed to the symptoms. Athletes routinely remain symptomatic unless they abstain from symptomproducing activities. However, after fasciotomy, most athletes are able to return to full sports participation by 8 to 12 weeks, when symmetric strength has returned. Numerous researchers have reported rates of 80% to 100% good to excellent results.71-73 Generally, athletes are able to return to sports participation without pain or with greatly diminished symptoms.

POPLITEAL ARTERY ENTRAPMENT SYNDROME The diagnosis of popliteal artery entrapment syndrome (PAES) should be included in the differential diagnosis of the running athlete with exertional calf and upper-leg pain.

Mechanism of injury This syndrome has classically been attributed to a congenitally abnormal relationship between the popliteal artery and the medial head of the gastrocnemius that causes intermittent arterial occlusion and subsequent claudication during exertion. However, a ‘‘functional’’ popliteal artery entrapment has been described in which no anatomic abnormalities are noted in the popliteal fossa, and entrapment has been attributed to compression from the soleus and plantaris muscles as well as to the hypertrophy of the gastrocnemius.74

Clinical features The clinical presentation of PAES involves pain and claudication, which are related to the degree of entrapment of the popliteal artery.76 Symptoms include calf pain and coolness and/or

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Lower extremity nerve entrapments 349

paresthesias of the foot that occur with exertion and that are relieved with rest. The pain is classically described as a deep ache or cramping. Physical examination at rest is often normal, and usually an exercise challenge is often required to reproduce symptoms. Popliteal, posterior tibial, and dorsalis pedis pulses should be examined before and after exercise to determine whether a reduction in pulse volume between limbs exist. The pulses should be examined with the ankle in passive dorsiflexion or active plantar flexion with the knee in extension because these positions place tension on the gastrocnemius, thereby leading to extrinsic compression of the popliteal artery.77

Diagnosis Radiographs and bone scans often produce negative results in cases of PAES, but they should be done to rule out other causes of leg pain. When PAES is suspected, MRI and magnetic resonance angiography are recommended as screening tests because a decreased flow with provocation is suggestive of PAES.78 If MRI or magnetic resonance angiography is positive for PAES, arteriography is the gold standard for the confirmation of the diagnosis.79

Treatment PAES can be managed with nonoperative and operative interventions. However, nonoperative treatment involves the avoidance of the exacerbating activities. Surgery is the preferred treatment option because PAES typically recurs with activity; it may lead to long-term arterial damage if left untreated.80

LOWER EXTREMITY NERVE ENTRAPMENTS Nerve entrapments and compression are less frequent causes of exertional leg pain. This diagnosis should be entertained in any athlete who is suspected of having exertional compartment syndrome but who has normal intracompartmental pressures. The common peroneal, superficial peroneal, and saphenous nerves are the most common nerves that are at risk for entrapment in the lower extremity.81

Mechanism of injury The common peroneal nerve leaves the popliteal fossa and winds forward around the lateral aspect of the neck of the fibula. Then, in the lateral compartment, it divides into the superficial peroneal nerve, the deep peroneal nerve, and the lateral sural cutaneous nerve. The deep peroneal nerve enters the anterior compartment, innervates all the muscles, divides into the medial and lateral branches just proximal to the ankle, and then enters the foot deep to the inferior extensor retinaculum. Its medial branch supplies sensation to the first web space. The superficial nerve innervates the lateral leg compartment and then emerges from the lateral leg compartment by penetrating the crural fascia approximately 10 to 12 cm proximal to the tip of the lateral malleolus. Trauma is a primary cause of all three forms of entrapment.82 Superficial peroneal nerve entrapment is often observed in dancers and athletes who are involved in bodybuilding, horse racing, running, soccer, and tennis. Common peroneal nerve entrapment is usually associated with repetitive exercises involving inversion and eversion, such as running and cycling. It can also be caused by external compressive sources (e.g., tight plaster casts and anterior cruciate ligament braces) as well as internal compressive sources (e.g., osteophytes and proximal tibiofibular joint ganglion cysts). Knee surgery is also a documented cause of both common peroneal and saphenous nerve entrapments.79 The saphenous nerve is most vulnerable at the medial knee, where it pierces the fascia and emerges from the

distal subsartorial canal. Causes of saph-enous neuritis include entrapment at the adductor canal, pes anserine bursitis, contusion, and postsurgical injury (Figures 27.5 and 27.6).

Clinical presentation The typical presentation of nerve entrapment consists of pain that is brought about by activity.83 With entrapment of the common peroneal nerve, the athlete may report neuropathic symptoms that extend into the dorsum of the foot and the toe web spaces. The athlete may complain of foot drop or recurrent ankle sprains. On physical examination, there may be weakness with dorsiflexion. Superficial peroneal nerve entrapment often presents with burning, superficial pain with alterations in sensation over the sinus tarsi or the dorsolateral foot that are associated with activity and relieved by rest.83 Examination may reveal percussion tenderness, a fascial defect in 60% of patients, or muscular herniation at the exit site. Deep peroneal nerve entrapment often presents with deep aching dorsal mid foot pain and paresthesias that extend into the first web space. Percussion along the course of the deep peroneal nerve may help to localize the entrapment. The athlete with saphenous nerve entrapment will complain of pain and numbness in the area of the medial knee and/or calf. There should be no motor deficits.

Diagnosis Electrodiagnostic studies should be done to determine to location of the lesion. However, these may need to be done after exercise for exertional symptoms.84

Treatment For common peroneal nerve entrapment, neuromodulatory medications and transcutaneous electrical neural stimulation (TENS) may be used for pain relief. Biomechanical interventions may be used to reduce neural tension, dorsiflexion support may be implemented, and a change in running style to avoid excessive varus/ recurvatum knee movements may be required.87 Nonoperative options include the use of NSAIDS in combination with relative rest, physical therapy for the strengthening of muscles in cases of associated weakness or recurrent ankle sprains, and the elimination of predisposing or triggering factors. Aids such as braces can be used to avoid recurrent ankle sprains. In-shoe orthotic devices may by helpful in certain instances, such as for the correction of a biomechanical malalignment in gait for patients with severe flatfoot or cavus foot. At times, the injection of steroids plus lidocaine near the site of involvement in the lower leg can reduce symptoms, and it can also serve as a diagnostic tool for confirming the zone of nerve compression. The use of antineuritic medications (e.g., gabapentin) can also be helpful for reducing and at times eliminating symptoms, particularly in cases that are associated with complex regional pain syndrome. In these cases, combination treatment with medication, physical therapy, and local and sympathetic nerve blocks may be required. Surgical decompression may be indicated for cases that are refractory to nonoperative options. This can include the release of the superficial peroneal nerve at the lateral leg for surgical decompression with partial or full fasciotomy. Some authors have also advocated fasciectomy in select cases. Neurolysis is generally not indicated because it has not been shown to improve outcome. In 1997, Styf and Morberg85 reported that 80% of their patients were free from symptoms or satisfied with their results after decompression of the superficial peroneal nerve. Three of 14 patients had local fasciectomy as well.85 Deep peroneal nerve entrapment has been successfully treated with several modalities. Nonsurgical care most importantly involves patient education to eliminate the predisposing factors.

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350 Chapter 27

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Lower leg injuries

Common peroneal nerve

Sural nerve

Lateral plantar nerve

Sural nerve

Medial plantar nerve

Flexor hallucis longus tendon Posterior tibial nerve

Flexor digitorum longus tendon Tibialis posterior tendon Plantar view left foot

Posterior views

A

Saphenous nerve

Saphenous nerve

Anterior tibial nerve (deep peroneal)

Common peroneal nerve Superficial peroneal nerve

Tibialis anterior tendon

EDL tendon EHL tendon

Superficial peroneal nerve branches Sural nerve

Anterior views

B Figure 27.5

The anatomy of the lower extremity nerves. (From Shurman DH: Anesthesiology 1976;44:348.)

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Conclusion 351

Lateral cutaneous nerve of thigh (L2-3)

Posterior cutaneous nerve of thigh (S1-2-3)

Femoral nerve (L2-3-4) Femoral nerve (L2-3-4)

Obturator (L2-3-4)

Lateral cutaneous nerve of calf (Common peroneal) (L5-S1)

Lateral cutaneous nerve of calf (Common peroneal) (L5-S1)

(Femoral) Saphenous nerve (L3-4) (Femoral) Saphenous nerve (L3-4)

(Posterior) Tibial nerve Sural nerve

Saphenous nerve Superficial peroneal nerve

Deep peroneal nerve

Medial plantar nerve

Lateral plantar nerve

Sural nerve

For example, padding of the tongue of the shoe, the elimination of shoes with laces, the use of alternative methods for lacing, and the avoidance of high-heeled shoes may be sufficient to resolve symptoms. Physical therapy is useful for strengthening the peroneal muscles for cases that are associated with weakness and for individuals with chronic ankle instability; the use of these modalities may also improve symptoms. In-shoe orthotic devices are helpful in certain instances, such as for the correction of a biomechanical malalignment in gait (e.g., for patients with severe flatfoot or cavus foot). The use of NSAIDS and antineuritic medications may be helpful as an adjunct to other treatment modalities. The injection of steroids plus lidocaine near the site of involvement can reduce symptoms in some individuals. In addition, consideration should be given to a metabolic workup to rule out thyroid dysfunction and diabetes in select individuals. Further workup may be necessary to rule out lumbar radiculopathy. Surgical options can be considered after symptoms are deemed refractory to nonoperative measures. Options include the surgical release of the deep peroneal nerve in primary and idiopathic cases to the excision of the nerve in cases of direct nerve injury as a result of previous surgery or direct trauma or in revision cases. Surgical decompression of the

Superficial peroneal nerve

Figure 27.6 The cutaneous distribution of nerves to the lower extremity. (From Bridenbaugh PO: The lower extremity: somatic blockade. In Cousins M, Bridenbaugh PO [eds]: Neural Blockade in Clinical Anesthesia and Management of Pain, 2nd ed. Philadelphia, JB Lippincott, 1988, p 425.)

nerve can provide the immediate improvement of symptoms. In 1990, Dellon84 reported about the surgical release of the deep peroneal nerve in 20 patients. With a mean follow-up time of more than 2 years, he reported excellent results in 60% of patients, good results in 20% of patients, and no improvement in 20% of patients.84 The most common presenting symptom is a vague pain on the dorsum of the foot with occasional associated numbness or weakness. Treatment options are aimed at eliminating underlying causes of entrapment. Surgical release or excision is reserved for refractory cases.

CONCLUSION Leg pain is among the most common complaints in running athletes. Although the differential diagnosis for exertional leg pain is relatively small, several diagnoses are complicated to accurately identify (e.g., exertional compartment syndrome and nerve entrapment). Careful attention to the details of the patients’ complaints and their temporal relationship to exercise will assist the physician in coming to the proper diagnosis.

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Lower leg injuries

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CHAPTER

Ankle Fractures Shawn F. Kane, MD

KEY POINTS

. The Ottawa ankle rules and the Buffalo modification of the .

. . .

Ottawa rules should be judiciously applied to adult patients with ankle trauma to decrease the total number of ankle radiographs obtained. The most important step in ankle fracture management is identifying stable verses unstable fractures. Stable fractures will have only one break in the supporting ankle ‘‘ring,’’ whereas unstable fractures will have at least two. The entire length of the fibula must be palpated when examining a patient with a suspected ankle fracture to rule out a Maisonneuve fracture. Understanding the mechanism of injury will allow the practitioner to initially focus his or her examination on a certain injury pattern to improve diagnostic accuracy and treatment. Damage to the physeal plate in pediatric patients can result in growth arrest and abnormal limb length. Pediatric patients typically do not sprain their ankles; rather, they sustain Salter—Harris I fractures of the growth plate.

reduction and fixation, and they should be referred to an orthopedic surgeon for management. Understanding the mechanism of injury will allow the practitioner to initially focus his or her examination on a certain injury pattern to improve diagnostic accuracy and treatment.

EPIDEMIOLOGY The exact incidence of ankle fractures in the general population is unknown, but it is thought to be increasing as a result of increasing longevity. Medicare data reveal that ankle fractures are the fourth most common fracture among the elderly and that women between 75 and 84 years of age had the highest age-specific incidence.5 Among patients who are less than 50 years of age, ankle fractures are more common among men than women; however, after the age of 50, ankle fractures become more common among women. Falls from a height to the ground, sports and recreational activities, and work-related activities are the leading causes of ankle fractures in the general population. Football, soccer, basketball, snowboarding, and in-line skating are some of the physical activities that involve an increased incidence of ankle fractures.6

INTRODUCTION

ANATOMY AND BIOMECHANICS

The ankle is the key focal point in the transmission of forces from the foot—ground interface up to the rest of the appendicular and axial skeleton.1 Because of its weight-bearing function and the construction of the articulation, the ankle is the most commonly injured joint among competitive and recreational athletes. The one thing that all ankle injuries—whether sprains or fractures—have in common is they result from an abnormal movement of the talus within the mortise.2 More than 75% to 85% of ankle injuries are straightforward ligamentous injuries (i.e., sprains), which are easily diagnosed and treated. The remaining injuries consist of the simple, easily managed fractures, the more complex fractures that require operative intervention, and the subtle fractures that, if missed, can result in long-term disability.3,4 The key to the successful management of ankle fractures is distinguishing between those that are stable and those that are unstable. Stable fractures can usually be conservatively managed by primary care physicians alone or in consultation with an orthopedic surgeon. Unstable fractures almost always require operative

Understanding the anatomy and biomechanics of a joint is essential to the evaluation and treatment of injuries involving that joint. There are actually two joints that are vital to the structure and function of the ankle: the talocrural joint and the subtalar joint. The subtalar joint is commonly considered part of the foot, and it will be discussed in Chapter 29. The talocrural joint is made up of the articulating surfaces of the distal tibia and fibula, which form a boxlike frame or ‘‘mortise’’ over the talar dome. The inferior surface of the distal tibia is articular and concave, and it is referred to as the tibial plafond, which means ‘‘ceiling.’’ The talus is covered almost completely by articular cartilage, and it is interposed between the tibial plafond and the calcaneous. The stability of the ankle is increased by the static stabilization provided by the ligamentous structures and the dynamic stabilization provided by the numerous muscles that cross the joint (Figure 28.1). The ankle is typically divided into medial, lateral, and syndesmotic complexes; this helps with the understanding of the mechanism of injury and of the commonly

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Anatomy and biomechanics 355

Anterior tibiofibular ligament

Deltoid ligament

Anterior talofibular ligament Posterior talofibular ligament

Calcaneofibular ligament

Anterior view

A Calcaneofibular ligament Lateral view

B Posterior inferior tibiofibular ligament Posterior inferior talofibular ligament Calcaneofibular ligament Deltoid ligament

Posterior view

C Tibiocalcaneal ligament Superficial Tibionavicular ligament deltoid Superficial tibiotalar ligament ligament

Posterior tibiotalar ligament (Deep portion of deltoid ligament) Spring ligament

Medial view

D injured structures, and it also helps physicians better devise a treatment plan7 (Table 28.1). In a neutral position, 90% of the force load is transmitted through the tibial plafond, with the remaining load being borne by the lateral talofibular articulation.8 The ankle is commonly thought of as a simple hinge joint with movement only in the sagittal (up and down) plane. Biomechanical studies have demonstrated that motion around the talocrural joint is actually very complex, with motion in the sagittal plane resulting in motion in both the axial and coronal planes. Both the talus and the plafond are wider anteriorly than posteriorly, which allows for increased bony contact and

Table 28.1

Figure 28.1 Bony and ligamentous anatomy of the ankle. A, Anterior view. B, Lateral view. C, Posterior view. D, Medial view. (From Pommering TL, Kluchursky L, Hall SL: Prim Care Clin Office Pract 2005:32;133 -161.)

stability when the ankle is dorsiflexed. The plantar flexed ankle has the least amount of bony stability, and it is therefore more vulnerable to injury. The talus both slides and rotates under the plafond when it is moved in the sagittal plane. Dorsiflexion causes the talus to externally rotate and to cause posterolateral translation, external rotation, and minimal vertical motion of the fibula. Plantar flexion results in an internal rotation of the talus relative to the tibia. In summary, fractures to the medial malleolus typically result from eversion and abduction forces that cause the lateral displacement of the joint, and lateral malleolar fractures typically result from the medial displacement caused by inversion and adduction forces.

Medial, Lateral, and Syndesmotic Complexes

Medial Complex

Lateral Complex

Syndesmotic Complex

Medial malleolus (distal tibia) Medial facet of talus Deltoid ligament: Posterior tibiotalar ligament Tibiocalcaneal ligament Tibionavicular ligament Anterior tibiotalar ligament

Lateral malleolus (distal fibula) Lateral facet of talus Lateral ligaments Anterior talofibular ligament Calcaneofibular ligament Posterior talofibular ligament

Anterior and posterior inferior tibia—fibular ligament Transverse tibiofibular ligament Tibia—fibular syndesmosis (interosseous membrane)

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The bones and ligaments of the ankle should be thought of as a ring that allows the talus to move through its normal, full range of motion under physiologic loading.9 Stable injuries are those that involve damage to one side of the ring. With stable injuries, the normal motion of the talus remains intact. With unstable injuries, more than one injury to the ring results in nonphysiologic movement of the talus and decreased joint surface contact. Stable fractures can be managed with conservative casting, whereas unstable fractures generally require operative intervention to restore stability and motion.8,9

CLASSIFICATION Classification systems were developed to provide diagnostic information and prognostic guidance for clinical decision making (Table 28.2). There are three main classification systems for ankle fractures: Lauge—Hansen, Danis—Weber, and AO, all of which attempt to accurately assess the extent of soft-tissue

Table 28.2 Fracture Classification

damage on the basis of radiographic fracture evidence. The Danis—Weber system is based on the level of the fibular fracture: inferior to the mortise, at the mortise, or superior to the mortise. The AO system is a comprehensive modification of the Danis—Weber system that is based on the presence of additional medial and posterior injuries. The Lauge—Hansen system was a landmark advancement in the classification of ankle fractures, and it remains the only system that attempts to correlate injury mechanism with observed fracture patterns (and vice versa).10 It is a two-part system: the first part denotes the position of the foot at the time of injury and the direction of the deforming force, and the second part predicts the severity of the ankle injury on the basis of damage to other associated structures. In clinical practice, none of these systems turns out to be ideal. There is poor intraobserver and interobserver reliability and reproducibility among them, and they have proven to be of limited prognostic value. However, familiarity with these systems will allow the practitioner to understand the mechanism of injury, and it will allow the referring physician to quickly convey the seriousness of the injury in simple terms.7

Ankle Fracture Classification Systems Type

Location of Fracture

Associated Injuries

Danis—Weber

A B C

Lauge—Hansen

Supination/adduction

Below ankle mortise and tibiofibular articulation At level of mortise and tibiofibular articulation Above level of mortise and tibiofibular articulation Transverse fracture of lateral malleolus

Syndesmosis likely intact Syndesmosis likely intact Syndesmosis likely disrupted (positive squeeze test) Stage 1: Tear of lateral ligaments. Stage 2: Fracture of medial malleolus

Supination/external rotation

Avulsion fracture of the lateral malleolus

Stage 1: Rupture of anterior tibia—fibular ligament Stage 2: Spiral or oblique fracture of the lateral malleolus Stage 3: Posterior tibial fracture Stage 4: Fracture of medial malleolus or torn deltoid ligament

Pronation/abduction

Medial malleolus

Stage 1: Torn deltoid ligament Stage 2: Syndesmotic disruption and posterior tibial fracture Stage 3: Oblique fracture of the fibula above mortise

Pronation/external rotation

Medial malleolus

Stage 1: Torn deltoid ligament Stage 2: Syndesmotic disruption Stage 3: Spiral fracture of the fibula above mortise Stage 4: Posterior tibial fracture

Pronation/dorsiflexion

Medial malleolus

Stage 1: Fracture of the anterior margin of the tibia Stage 2: Supramalleolar fracture of the fibula Stage 3: Transverse fracture of the posterior tibial surface

A

Fibula at or below the plafond

B

Fibula at plafond extending proximally

C

Fibula above plafond

Intact or possible medial and posterior avulsions Tibia—fibula ligaments torn; possible medial and lateral avulsions Syndesmosis always torn, deltoid ligament torn

AO

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RADIOGRAPHIC IMAGING Numerous imaging modalities—from plain radiography to computed tomography scanning to magnetic resonance imaging (MRI) to nuclear medicine—are available to aid in the diagnosis of injuries around the ankle. An appropriate physical examination and a thorough differential diagnosis will ensure that the studies obtained are both medically and financially appropriate. Plain radiographs are the most common imaging modality used for diagnosing injuries around the ankle, and they will be the primary focus of this section. The other, more advanced modalities will be discussed as required for the evaluation and diagnosis of specific injuries. The standard radiographic evaluation of the ankle consists of three views: anteroposterior, mortise, and lateral. In the present era of cost-conscious medicine, numerous studies have evaluated whether two views (anteroposterior and lateral or lateral and mortise) were as effective for identifying fractures as the traditional three views. Two views successfully identify some fractures, but the classic, three-view combination detects significantly more fractures, and it is considered the gold standard for identifying ankle fractures11 (Figure 28.2). Does every ankle injury require radiographs? There are an estimated 6 million ankle radiographs performed annually in the United States and Canada at a cost of approximately $300 million dollars. Only 15% of the radiographs demonstrate a fracture, so, to save money, resources, and time in the emergency department and to improve overall patient care, Stiell and colleagues at the

University of Ottawa in the early 1990s developed the Ottawa ankle rules (Table 28.3).11 Numerous studies have been done on the application of the Ottawa ankle rules in many settings, and each has validated and reinforced their high sensitivity and negative predicative value. The Ottawa ankle rules can decrease the number of ankle radiographs by up to 30%.13 In 1998, Leddy and colleagues recommended the Buffalo modification to the Ottawa ankle rules (i.e., pain to palpation over the crests or mid portions of the malleoli away from the ligamentous attachments) (see Table 28.3).13 They found that this modification significantly increased the specificity of diagnosing malleolar fractures (59% from 42%) without decreasing the sensitivity and that it decreased the need for ankle radiographs by 54%14 (Figure 28.3). Neither of these rules replace sound clinical judgment; rather, they augment the history and physical examination, and they help the clinician to determine the appropriateness of ankle radiographs. The application of these rules is not as clear-cut when they are applied to the immature skeleton with open epiphysial plates. The application of these rules for pediatric fractures will be discussed later in this chapter.

ADULT FRACTURES The first step in successfully managing ankle injuries is to determine whether the fracture is stable or unstable. Stable fractures, which will be discussed first, have only one break in the ring, and they can be managed conservatively by most primary care physicians (Figure 28.4). All stable adult ankle fractures are isolated to either the medial, lateral, or posterior malleolus, and, by definition,

Kager’s triangle

A C

B

Figure 28.2 Radiograph demonstrating a normal anteroposterior, mortise, and lateral view of the ankle. (From Magee DJ: Orthopedic Physical Assessment, 4th ed. Philadelphia,WB Saunders, 2002, p 823.)

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Table 28.3 Ottawa Ankle Rules and the Buffalo Modification The Ottawa Ankle Rules

The Buffalo Modification

Patient has pain over either malleolus AND Patient has tenderness to palpation over the inferior and posterior poles of either malleolus (including the distal 6 cm) AND Patient unable to bear weight (four steps taken independently) at the time of injury and at the time of evaluation

Same as the Ottawa ankle rules, except the area of malleolar tenderness to palpation is moved to over the crests or the mid portions of the malleoli, away from the ligamentous attachments

Interosseous ligament of tibiofibular syndesmosis Fibula

Medial malleolus Talus Lateral malleolus Deltoid ligament Posterior talofibular ligament

Calcaneus

they have no appreciable injury to any other structure in the ankle (i.e., the second break in the ring).

Tibia

Sustentaculum tali Interosseous talocalcanean ligament

Figure 28.4 Coronal section through the ankle demonstrating the ‘‘ring’’ that helps identify stable versus unstable fractures. (From Magee DJ: Orthopedic Physical Assessment, 4th ed. Philadelphia, WB Saunders, 2002, p 767.)

Isolated medical or lateral malleolar fractures Mechanism of injury These injuries usually result from a significant inversion (lateral malleolus), eversion (medial malleolus), or a combination of supination and external rotation (posterior malleolus). Isolated fractures of the lateral malleolus are the most common fractures of the ankle, with isolated medial or posterior fractures being less common and requiring a more thorough evaluation to not miss any associated injuries.

Posterior edge or tip of lateral malleolus

Base of fifth metatarsal

Navicular 6 cm

Risk factors No risk factors for this injury have been identified.

Clinical features The area of maximal tenderness and a history of the events surrounding the injury are usually good aids for determining which ankle structures are injured. The absence or presence of swelling is not a reliable indicator of injury severity. The amount of swelling is usually related more to the amount of elapsed time between injury and presentation than to the severity of injury. Examination soon after injury usually provides the best information because swelling has not set in to obscure physical findings. Isolated malleolar fractures are at times challenging to distinguish from severe sprains. Any time that a patient has tenderness on both the medial and lateral side of the ankle, there must be a high index of suspicion for an unstable ankle. At the same time, the clinician cannot solely focus all of his or her attention on the ankle. Because of the possibility of proximal fractures, the full length of both the tibia and the fibula must be palpated in patients with an acute ankle injury.

Diagnosis

LATERAL VIEW

6 cm

Posterior edge or tip of medial malleolus

Navicular

MEDIAL VIEW Figure 28.3 Graphic representation of the Ottawa ankle rules and the Buffalo modification. Tenderness over the shaded areas requires evaluation with an ankle series. (From Magee DJ: Orthopedic Physical Assessment, 4th ed. Philadelphia, WB Saunders, 2002, p 822.)

Isolated malleolar fractures are routinely diagnosed on plain radiographs (Figure 28.5). The fracture pattern can aid in the determination of the mechanism of injury, and it can also be helpful for categorizing the fracture as stable. Nondisplaced fractures may only be seen on one x-ray view. An avulsion or distraction force on the ankle will result in transverse fractures of the malleoli, whereas torsion of the talar dome with subsequent impact on the malleoli can cause oblique fractures.9 A vertical fracture in either malleoli increases the probability of another injury that can create an unstable ankle and thus warrants a thorough search. Stability of the ankle can be assessed by analyzing the displacement of various bones of the ankle on plain radiographs. Typically, the medial clear space, the tibiofibular clear space, the tibiofibular overlap, the talar tilt, and the talocrural angle are evaluated to determine stability. The most reliable criteria for instability is lateral talar displacement relative to the tibia, which is demonstrated by the medial clear space being larger than the superior clear space8 (Figure 28.6).

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Treatment

Figure 28.5 Stable, nondisplaced transverse fracture through the lateral malleolus. Note the fracture line. (From Eiff MP, Hatch RL, Calmbach WL [eds]: Fracture Management for Primary Care, 2nd ed. Philadelphia, WB Saunders, 1998, p 290.)

Treatment of suspected ankle fractures ideally begins on the side of the field or as soon as possible after the injury has occurred. Ankle injuries, suspected fractures, and sprains are all initially treated in the same way. The athlete will usually have to be removed from the contest and examined. If it is evident that the athlete will not return to competition, then the injured ankle should be iced, compressed, and elevated to try to reduce the impact of swelling. The patient may require crutches for ambulation immediately after the injury. If a fracture is suspected, then standard radiographs should be obtained at the earliest possible convenience. Before or after the radiographs are performed, the ankle should be placed in a bulky posterior (bulky jones) or a Uand-L—type splint. Small, nondisplaced avulsion fractures of either the lateral or medial malleolus are best treated with early mobilization (i.e., functional treatment) that is similar to that of an ankle sprain. Randomized controlled trials have shown that the functional treatment of these fractures is equally as effective whether functional braces, elastic bandages, air-casts, or hard casts are used.15 Minimally displaced fractures of the malleoli can be treated with immobilization in either a cast or a fracture boot for at least 4 to 6 weeks. The foot must be immobilized in a neutral position to minimize the risk of Achilles tendon shortening. Compliance with the fracture boot is a concern, and proper patient selection is vital to achieving a successful outcome. The amount of displacement that is acceptable to be managed nonoperatively has changed through the years. Currently, less than 3 mm of displacement of the lateral malleolus and less than 2 mm of displacement with less than 25% articular surface involvement are manageable nonoperatively.7,8 Immediate orthopedic evaluation is required if there is an open fracture, a dislocation with or without fracture that cannot be

Figure 28.6 Graphic representation of radiographic findings associated with an unstable ankle fracture. A,Tibiofibular clear space of less than 5 mm is normal. B,Tibiofibular overlap of greater than 10 mm is normal. C, Medial and superior clear spaces are normal. The medial clear space being greater than the superior clear space is a very good indicator of a displaced ankle fracture. (From Griend RV, MichelsonJD, Bone LB: J BoneJoint Surg Am 1996;78[11]:1772 -1783.)

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reduced, or evidence of persistent distal vascular compromise after reduction or splinting. Patients should be seen 2 weeks after immobilization to check on the condition of the cast and compliance. At 4 weeks, if there is radiographic evidence of fracture union and the site is nontender to palpation, then the patient may begin gradual weight bearing and ankle rehabilitation. If there is no evidence of healing or the site is still tender to palpation, then the weight bearing and rehabilitation should be delayed at least another 2 weeks. If at 6 weeks the fracture is still not clinically healed and the patient is in a cast, the cast should be removed, and a fracture boot should be used for help with walking and so that rehabilitation to decrease the amount of stiffness and atrophy can begin. After immobilization, rehabilitation should begin with range of motion and then progress to strength training. After the patient has a normal, pain-free range of motion and at least 85% strength as compared with the uninjured side, he or she may begin returning to physical activity. When the patient is back to 100% strength and when he or she can execute sport-specific motions, then he or she may return to competition. Diligent effort during rehabilitation should help patients resume physical activity as soon as is practical (Table 28.4).

Table 28.4 Management Guidelines for Isolated Stable Medial and Lateral Malleolar Fractures

Malleolar stress fractures

Follow-up interval

Stress fractures are a partial or complete bone fracture that results from the repeated application of a stress lower than the stress required to fracture the bone in a single loading. Medial and lateral malleolar stress fractures occur infrequently, with fibular stress fractures occurring more commonly. Epidemiologic studies often do not distinguish between proximal, middle, and distal (lateral malleolar) stress fractures, thereby making the exact incidence of lateral malleolar stress fractures hard to discern. Distal fibular stress fractures (within 4 to 7 cm of the tip of the lateral malleolus) occur more frequently than proximal or middle stress fractures.16 Medial malleolar stress fractures were not identified until 1975, and they account for 0.6% to 4% of all stress fractures.15 Medial malleolar stress fractures occur almost entirely among athletes (runners) and, most commonly, in the skeletally immature. Lateral malleolar stress fractures are caused by a combination of muscular forces and axial loading. Young male athletes tend to sustain stress fractures that are 5 to 6 cm proximal to the tip, whereas middle-aged females sustain the fracture 3 to 4 cm from the proximal tip. Medial malleolar fractures arise from abnormal weight transmission and torsional forces. Characteristically, these fractures present with a vertical to oblique fracture line that arises from the junction of the medial malleolus and the tibial plafond.16

Mechanism of injury The failure of bone to adequately adapt to a mechanical load experienced during physical activity is the cause of this injury. Over time, this lack of adaptation leads to the spectrum of overuse injuries, which, if not cared for, can lead to a stress fracture.

Risk factors Risk factors for this condition are listed in Table 28.5.

Clinical features A history of increased or recently changed physical activity precedes the development of symptoms. Pain, which is the primary symptom, is usually aggravated with activity and relieved with rest. It is initially hard to localize, but, as the injury progresses, it localizes to the malleolar area, and it is associated with stiffness and swelling. Patients tend to have the symptoms for a couple of days to several months before presentation. Physical examination usually reveals a normal range of motion and strength. Localized tenderness to palpation over the

AcuteTreatment Splint type and position Initial follow-up visit Patient instructions

Stirrup or posterior splint with ankle in neutral position 3 to 5 days for definitive casting No weight bearing until definitive casting; icing and elevation to minimize swelling

DefinitiveTreatment Cast or splint type and position

Length of immobilization

Healing time

Short-leg walking cast, walking cast fracture boot with ankle in neutral position Malleolar: 4 to 6 weeks Distal fibular: 6 to 8 weeks Immobilization continued for up to 8 weeks if no evidence of radiographic healing 6 to 8 weeks and possibly several months for complete radiographic healing Malleolar: 4 weeks to check radiographic healing Distal fibular: every 2 to 4 weeks Every 2 weeks after discontinuing immobilization to assess status of ankle rehabilitation

Repeat x-ray interval

Malleolar: at 4 weeks to check radiographic healing Distal fibular: at 7 to 10 days to check positioning Every 2 weeks if no healing at 4 weeks

Patient instructions

Range of motion, calf stretching. and strengthening after immobilization; full dorsiflexion and peroneal muscle strength are emphasized Unstable fractures; bimalleolar and trimalleolar fractures; posterior malleolar fractures with >25% articular involvement and >2 mm displacement; symptomatic nonunion

Indications for referral

affected malleoli is common, as is some focal pitting edema and doughy skin.17

Diagnosis Up to 70% of initial radiographs are normal, and they may not show any evidence of injury for 2 to 4 weeks after symptoms begin. Radionuclide bone scanning and MRI are the best imaging modalities to aid in the diagnosis of a stress fracture. Radionuclide scanning demonstrates increased uptake that correlates with increased bone activity. Bone scans are very sensitive, but they have a low specificity, and they can yield a false-positive rate of approximately 14%. In addition, precise anatomic location is difficult. MRI has replaced bone scanning in most areas as a result of its precise anatomic locating, its ability to differentiate between stress reactions and fractures, and its decreased radiation exposure.15

Treatment The extent of the fracture, seasonal timing, and the caliber of the athlete will aid in making the decision about whether to manage

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Table 28.5

Risk Factors for Stress Fractures

Extrinsic (Avoidable) Risk Factors

Intrinsic (Biomechanical or Unavoidable) Risk Factors

Poor training regimen Running on hard or uneven surfaces Poor footwear Inadequate nutrition Long distances (>20 miles per week) Smoking Alcohol Inhaled corticosteroid use Low level of aerobic fitness Menstrual irregularities (no menses in 6 or more months of the previous year)

History of previous stress fracture Leg-length discrepancies Tibial torsion Pes cavus/planus Narrow tibial cross section Increased hip rotation Forefoot varus Subtalar varus Tibial varum Female gender Increased age Energy imbalance

Adapted from Sherbondy PS, Sebastianelli WJ: Clin Sports Med 2006;25:129-137; Wilder RP, Sethi S: Clin Sports Med 2004;23:55-81; Wall J, Feller JF: Clin Sports Med 2006;25;781-802; Rauh MJ, Macera CA, Trone DW, et al: Med Sci Sports Exerc 2006;38(9):1571-1577.

the patient operatively or nonoperatively. All distal fibular and most medial malleolar stress fractures can be managed nonoperatively. Typical treatment involves modified rest, limited weight bearing for limping patients, and symptom-limited cross training for 3 to 8 weeks followed by a gradual return to increased levels of activity. Complete rest should be avoided. Pneumatic ankle braces, fracture boots, casts, taping, and strict activity modification all have similar results, and they all have a role in treatment, depending on the individual patient.17 Surgical intervention for radiographically detectable or displaced stress fractures in highly competitive inseason athletes is an acceptable treatment, without any significant complications.18 The primary reason for operative intervention is to return the athlete to competition as soon as 24 days after surgery. After the first stress fracture is treated, the next step is to identify and treat as many of the risk factors associated with stress fractures to try and prevent a recurrence. Even with aggressive prevention and treatment, a history of a previous stress fracture increases the risk of recurrence by to 2 to 3.5 times. Because of the complex nature of these risk factors, a multidisciplinary team approach will be most beneficial for the athlete.19

Unstable ankle fractures Unstable fractures involve two breaks in the ring, and they may require consultation with an orthopedic surgeon for proper treatment. The initial treatment is basically the same as it is for stable ankle fractures. The force required to cause an unstable fracture is usually more significant than the force that causes a stable fracture. Patients will usually be in a significant amount of pain and unable to ambulate, and they will have an ankle that appears to be abnormal. A key step in evaluating a severely injured ankle is ensuring that there has been no vascular compromise by palpating either the posterior tibial or dorsalis pedis pulses and by checking distal capillary refill. An ankle fracture with distal vascular compromise is a medical emergency that requires immediate attention. If there is no evidence of vascular compromise, the ankle should be splinted, elevated, and iced; crutches should be used for ambulation, and radiographs should be obtained as soon as is practical. It has been estimated that more than 65% of unstable ankle fractures can be managed with closed reduction to achieve satisfactory results.

Even with these acceptable results, closed reduction is generally reserved for patients with severe medical conditions that preclude their undergoing a surgical procedure. The definitive treatment of these fractures requires consultation and operative intervention by an orthopedic surgeon. If there is no vascular compromise, it is acceptable to obtain orthopedic consultation 24 to 72 hours after the injury. Open fractures and injuries with persistent neurovascular injury should be referred immediately to an orthopedic surgeon for treatment. The timing of the surgery is variable, with the amount of soft-tissue swelling, softtissue compromise and associated injuries being the main factors in the decision. Early surgical intervention commonly results in wound complications, osteomyelitis, and other issues as compared with delayed surgery. As a result, most operative interventions are done somewhere in the window of 7 to 10 days after the injury.20 The exact technique will depend on what the surgeon finds interoperatively. The techniques used are numerous and beyond the scope of this chapter, but the general concept is to restore joint integrity and to maintain as much of the articular cartilage as possible to help minimize the long-term morbidity. Rehabilitation and return to play are usually a little longer for operatively managed unstable fractures than for stable fractures. Patients with operatively reduced ankles usually should not bear weight for 6 to 8 weeks. Placing the patient in a functional brace or cast immobilization is based on a combination of surgeon preference and patient selection. There is evidence to support functional bracing in conjunction with active and passive ankle physical therapy. Patients who are functionally braced have demonstrated higher subjective and objective outcomes as compared with those who are casted.21,22 At this time, if there is evidence of bone healing, transition to a fracture boot for the next 4 to 6 weeks should occur, with a gradually decreased dependence on crutches for ambulation. After the removal of all braces or casts, the patient will have to begin a vigorous rehabilitation program to regain the range of motion and strength that were lost as a result of the injury. At this point, the rehabilitation criteria are the same as they are for an unstable fracture; it just takes longer to get to this point.

Bimalleolar and bimalleolar equivalent fractures Bimalleolar and bimalleolar equivalent fractures consist of either a fracture of the lateral and medial malleolus or a lateral malleolar fracture with complete disruption of the deltoid ligament (Figure 28.7). Injuries to the deltoid ligament are estimated to occur in 10% to 36% of ankle fractures.23 Missing an injury to the deltoid ligament and treating only the radiographically evident lateral malleolus fracture may potentially lead to complications and a less-than-satisfactory outcome.

Mechanism of injury A pronation abduction force typically causes these fracture patterns.

Risk factors No risk factors for this condition have been identified.

Clinical features The main clinical feature of this type of fracture is tenderness to palpation over both malleoli or significant tenderness of the medial ankle ligaments in the presence of a lateral malleolar fracture. The fracture pattern will help with the identification of the mechanism that caused the injury, and it will also increase the suspicion for a possible deltoid ligament injury. Inversion injuries are associated with a vertical fracture of the medial malleolus and a transverse

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The current treatment of choice for bimalleolar equivalent fractures is the repair of the lateral component without the repair of the deltoid ligament. Surgical repair of the deltoid has not resulted in significant improvements in outcome, and it may lead to worse long-term results. Medial exploration should be undertaken only if the talus does not reduce anatomically beneath the plafond, in which case exploration to remove the incarcerated deltoid ligament is warranted.25 As with the other unstable, operatively reduced ankles, the ankle should be immobilized in the neutral position. The choice of protected weight bearing and early motion versus no weight bearing and no motion is based on surgeon and physical therapist preference because studies have not demonstrated one being better than the other.

Trimalleolar fractures A trimalleolar fracture includes the addition of a fracture to the posterior tibial plafond component or of the posterior malleolus to the bimalleolar fracture (Figure 28.8).

Mechanism of injury A high-energy rotatory supination external rotation mechanism can lead to this injury.

Risk factors Skateboarding is one of the primary risk factors for this type of injury. Figure 28.7 An unstable bimalleolar fracture that will most likely require open reduction. Note the presence of both tibia and fibula fractures. (From Eiff MP, Hatch RL, Calmbach WL [eds]: Fracture Management for Primary Care, 2nd ed. Philadelphia,WB Saunders, 1998, p 296.)

Clinical features A lateral avulsion fracture results from the pull of the posteriorinferior tibiofibular, which is also attached inferiorly to the distal fibular fragment. Less frequently, the impaction of the externally

fracture of the lateral malleolus. Eversion injuries usually have a transverse fracture of the medial malleolus and a spiral/vertical fracture of the lateral malleolus. A spiral fibular fracture that is 2 to 3 inches proximal to the mortise or a fibular fracture at the joint line should prompt a thorough evaluation of the medial structures of the ankle.1

Diagnosis Tenderness to palpation over the medial side of the ankle along with evidence of a talar shift (>4 mm of medial clear space widening) on radiographs is diagnostic for a complete deltoid ligament disruption. The diagnostic challenge is when there is tenderness medially but no evidence of talar shift on the radiographs. Gravity stress views (anteroposterior radiograph taken with the leg horizontal, medial side up, without ankle support) may be beneficial for helping to correctly identify the fracture. An increased talar tilt (>15%) or a talar shirt (>2 mm) as compared with the uninjured ankle occurs only when the superficial and deep divisions of the deltoid ligament are disrupted; this is pathognomonic for a bimalleolar equivalent fracture.8 This simple, easy-to-obtain radiograph is not difficult to interpret, and it has proven to be less problematic than MRI or ultrasound for the proper diagnosis of deltoid ligament injuries in the presence of lateral malleolar fractures.24

Treatment These injuries should be treated like the other unstable ankle fractures, and patients should be referred to an orthopedic surgeon for definitive treatment. Bimalleolar fractures are typically treated with open reduction and internal fixation. Closed reduction can provide satisfactory results in up to 65% of cases, but it is usually reserved for patients with severe medical contraindications to surgery. Surgery involves the reduction and plating of the lateral malleolus followed by the reduction and fixation of the medical malleolus.

Figure 28.8 Anteroposterior and lateral views of a trimalleolar fracture, which is by definition an unstable fracture that will require open reduction. Note the medial and lateral fractures on the anteroposterior view and the posterior malleolar fracture on the lateral view. (From Eiff MP, Hatch RL, Calmbach WL [eds]: Fracture Management for Primary Care, 2nd ed. Philadelphia, WB Saunders, 1998, pp 288 -306, 296.)

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rotating talus on the posterior lip of the tibia may result in a trimalleolar fracture.

Diagnosis Typically, plain radiographs are all that is required to diagnosis this fracture. Computed tomography scanning may also be useful for further defining the degree of damage and location of fragments.

Risk factors Syndesmotic injuries are more common among athletes who participate in contact sports that involve cutting or pivoting maneuvers. These sports include football, rugby, basketball, lacrosse, and soccer. However, syndesmotic injuries may occur in other athletes and in nonathletes as well.

Clinical features Treatment Open reduction is required for these fractures, and it is very similar to the treatment of bimalleolar fractures. Typically, the posterior malleolus portion of the fracture reduces spontaneously after treatment of the fibular fracture.8

Syndesmotic rupture of high-grade syndesmotic injury

The identification of an unstable syndesmosis is primarily based on the mechanism of injury and the associated fracture pattern. Clinically, patients with these fractures usually have supramalleolar edema, pain with passive dorsiflexion, a positive squeeze test (manual medial—lateral compression across the syndesmosis), pain during the external rotation stress test, and pain during the tibiotalar shuck (cotton) test27 (Figure 28.10).

Diagnosis

Complete syndesmotic rupture is a unique subset of ankle injuries that is thought to occur in between 1% and 10% ankle sprains. The fracture is typically fibular and at or above the level of the plafond. However, the rupture of the syndesmotic ligament results in mortise widening and a very unstable ankle. The syndesmotic ligament complex consists of the anterior and posterior inferior tibiofibular ligaments, the transverse tibiofibular ligament, and, more proximally, the interosseus membrane (Figure 28.9). The syndesmotic ligaments provide a strong restraint to external rotational forces, and they are injured when the talus is abducted or externally rotated in the mortise.26

The physical examination and history may be suggestive of this injury, although acutely the physical examination may not be that reliable as a result of pain. Radiographic findings provide additional clues regarding the identification of this injury. A tibiofibular clear space of less than 5 mm and a widening of the medial clear space of more than 4 mm are strong indicators of a syndesmotic injury.7 Plain radiographs are not always sensitive enough to aid in the diagnosis of syndesmotic injuries. For cases in which there is a high index of suspicion, either graded stress plain radiography or MRI can be used to diagnose injury to the syndesmotic complex.28 Old syndesmotic injuries can be identified by visualizing calcifications in the area of the interosseus membrane.

Mechanism of injury

Treatment

This injury typically occurs during an abrupt change in direction with internal rotation of the leg while the ankle undergoes forced pronation/external rotation, pronation/abduction, or supination/ external rotation.

Initially, high-grade syndesmotic injuries should be treated like all other unstable ankle injuries and then referred to an orthopedic surgeon for definitive treatment. The key to managing patients with a suspected syndesmotic injury is close follow-up, a high

Fibula

Interosseous membrane

Tibia

Figure 28.9 Graphic representation of the squeeze (A), external rotation (B), and cotton tests (C). The squeeze test is performed by grabbing the leg proximally and squeezing. Pain distally is a positive test.The external rotation test is performed by stabilizing the lower leg with one hand and externally rotating the ankle with the other. Pain in the syndesmotic area is a positive test. The cotton test is performed by stabilizing the leg with one had and providing alternate medial and lateral force on the talus with the other. Pain in the syndesmosis or a feeling of looseness as compared with the noninjured side is positive for a probable syndesmotic injury. (From Stephenson K, Saltzman CL, Brotzman SB. Foot and ankle injuries. In Brotzman SB,Wilk KE [eds]: Clinical Orthopedic Rehabilitation, 2nd ed. Philadelphia, Mosby, 2003, p 377.)

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Anterior view

Posterior view

Interosseous membrane

Anterior tibiofibular ligament

Interosseous ligament

Figure 28.10 The components of the distal lower extremity syndesmosis. (From Stephenson K, Saltzman CL, Brotzman SB. Foot and ankle injuries. In Brotzman SB,Wilk KE [eds]: Clinical Orthopedic Rehabilitation, 2nd ed. Philadelphia, Mosby, 2003, p 377.)

Posterior tibiofibular ligament

Inferior transverse (tibiofibular) ligament

index of suspicion, and a low referral threshold because the outcome of these injuries is much better if they are operatively treated early. The exact operative repair will be based on the fracture pattern, but it usually involves, at a minimum, a syndesmotic screw to allow those structures to heal.

Maisonneuve fracture The Maisonneuve fracture, which was first described in 1840 by a French surgeon, is a specific type of unstable ankle fracture that is characterized by a proximal fibular fracture with the associated failure of the deltoid ligament, the medial malleolus, and/or the tibiofibular syndesmosis.29 Although it is an uncommon fracture that accounts for approximately 5% of all operatively treated ankle fractures, the Maisonneuve fracture is considered one of the most unstable ankle fractures. The impaction of the talus on the fibula acts as a wedge that disrupts the anterior tibiofibular and interosseus ligaments. This rotational force exits the fibula at the site of the fibular fracture29 (Figure 28.11). Increased injury forces result in more proximal fibular fractures.

Mechanism of injury A severe pronation/external rotation of the ankle can lead to this type of fracture.

Risk factors No risk factors for this type of injury have been identified.

Clinical features This fracture presents like other medial or syndesmotic ankle injuries, with the patient complaining of pain around the ankle. Patients usually do not complain of pain in their proximal fibula until it is palpated during the examination.

Diagnosis The diagnosis of the Maisonneuve fracture may be easily overlooked; studies have demonstrated that 14% to 45% of these fractures are missed on initial presentation. The entire fibula must be palpated, and, if there is any suspicion, full-leg radiographs must be obtained. Proximal fibular tenderness with a positive ‘‘squeeze’’ test are consistent with the diagnosis, even in the absence of obvious radiographic findings.

Figure 28.11 A drawing and radiograph of a Maisonneuve fracture. (From Eiff MP, Hatch RL, Calmbach WL [eds]: Fracture Management for Primary Care, 2nd ed. Philadelphia, WB Saunders, 1998, pp 288 -306.)

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Treatment In the absence of an open fracture, the patient should be placed on crutches, put in a bulky dressing, and referred to and seen by an orthopedic surgeon in approximately 72 hours for internal fixation. Anatomic restoration of the mortise and the correction of any fibular shortening are the most important factors for determining a positive outcome. The extent and the specific damage to the syndesmosis and the medial ankle structures will dictate how they are repaired. There is usually no need to repair the proximal fibular injury, because it is enclosed in considerable muscle tissue, and there is a substantial risk of damage to the peroneal nerve when dissecting to the fracture. Patients should not bear weight, and their injuries should be immobilized in a cast for 6 to 8 weeks. At this point, they should have the syndesmotic screws removed, and they can then begin aggressive physical therapy. If there is no evidence of healing, the syndesmotic screws can be left in for 3 to 4 months, but they should be removed before weight bearing and rehabilitation because they may limit dorsiflexion and promote stiffness and pain.

Ankle dislocations Dislocations of the ankle typically occur in the presence of a fracture as a result of the mechanical efficiency of the mortise and the fact that bones are mechanically weaker than ligaments. A pure dislocation or a dislocation without a fracture is quite rare.

Mechanism of injury Dislocations of the ankle are the result of high-energy trauma, which produces a combination of plantar flexion and either forced inversion or eversion of the foot. Probably the most common circumstances that surround an ankle dislocation are a plantarflexed ankle meeting an unyielding inversion force, like that seen when a baseball or softball player slides into a base that does not break away.30 These injuries can either be open or closed, depending on the status of the overlying skin.

with a force opposite from the current location of the talus. If there is no vascular compromise and the skin is not overly stretched, then the dislocated ankle can be splinted in place, and the patient can be transported to definitive care. After the reduction of the dislocation, definitive treatment depends on whether the dislocation is associated with an unstable or a stable fracture or any open wounds. Because these injuries are uncommon, no ‘‘standard’’ treatment protocol exists; rehabilitation will be guided by associated injuries and individual response to treatment.30

Tibial plafond (pilon) fractures These are relatively uncommon fractures that constitute approximately 1% of lower-extremity fractures and 7% to 10% of tibial fractures.32

Mechanism of injury Plafond fractures can be categorized as either high- or low-energy fractures. The high-energy fractures are typically the result of a significant axial load, whereas torsion is usually the mechanism behind a low-energy fracture. High-energy fractures tend to have significant comminution and damage to the articular cartilage and a worse outcome as compared with the low-energy fractures.33

Risk factors Participation in adventure sports (e.g., parachuting, hang gliding) or high-speed motor sports is associated with the high-energy fractures, whereas skiing and rollerblading are associated with the low-energy fractures.

Clinical features

No risk factor have been identified.

The patient is typically in a significant amount of pain, and he or she will have a markedly swollen and deformed ankle. Lowenergy fractures may have a less dramatic appearance than highenergy ones, so, on the basis of the mechanism of injury, a high index of suspicion must be maintained. The worse the initial softtissue injury, the poorer the overall outcome. In addition, 20% to 25% of pilon fractures may be open, which is not unexpected when considering the energy involved in this type of injury.

Clinical features

Diagnosis

Dislocations are usually described by the dislocated position of the talus with respect to the mortise versus the normal anatomic alignment. Ankle dislocations almost always occur in conjunction with some type of fracture. Pure dislocations of the ankle (i.e., those not accompanied by fractures) do occur, although at a significantly lower rate than fractures with dislocations.31 The diagnosis of ankle dislocations is usually primarily clinical, and it is based on the appearance of the ankle and the position of the talus. Radiographs are very helpful for identifying the exact fracture pattern associated with the dislocation.

The diagnosis is usually straightforward given the presence of a deformed ankle in combination with a history of significant trauma. The neurovascular status of the extremity and the overall condition of the patient must be immediately addressed. Anteroposterior, lateral, and oblique radiographs will confirm the diagnosis, and a computed tomography scan will probably be indicated to fully assess the damage and to help with surgical planning. Because the most common mechanism of injury is a significant axial load, strong consideration should be given to obtaining lumbosacral radiographs to rule out occult injury to the spine. Although compartment syndrome is rare with these fractures, vigilance on the part of the physician is required to ensure that it does not develop.

Treatment

Treatment

The acute management of ankle dislocations requires the immediate evaluation of two things: the distal neurovascular status and the skin condition. If there is acute compromise of the distal circulation as determined by a nonpalpable dorsalis pedis or a posterior tibialis pulse, if there are significant neurologic deficits, or if the dislocated bones are stretching the overlying skin taught (commonly referred to as ‘‘tenting’’), then the situation is a medical emergency. The ankle must be reduced to return blood flow to the extremity and to save the overlying skin from pressure necrosis, which will drastically complicate this injury. The general concept of reducing a dislocated ankle is to reverse the force that caused the injury; this can usually be accomplished with distal traction in combination

Orthopedic consultation will definitely be required to treat this injury, and it should be obtained as soon as it is clinically warranted. Surgical treatments for a pilon fracture should not be conducted until the full extent of the soft-tissue damage is known. A delay of up to 10 to 14 days is justified to allow the soft-tissue damage to declare itself and to allow for late reduction while minimizing further tissue damage.34 Low-energy fractures with little or no softtissue compromise respond well to operative internal fixation. Because of the significant amount of damage, external fixation with limited internal fixation usually provides the best outcome for high-energy fractures. Prognosis for a patient with a plafond fracture is guarded until 1 year has passed since the injury.

Risk factors

Diagnosis

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The best potential for good long-term results comes with the perfect anatomic reconstruction of the joint surface and with a patient who is motivated to participate in his or her own rehabilitation.7,35

PEDIATRIC FRACTURES The skeletal system of a child significantly differs from that of an adult. These differences create unique patterns of injury and special treatment requirements for pediatric fractures. The long bones of children have many discrete areas, with the physis, the epiphysis, and the metaphysis being the most important with regard to fractures around the ankle. The physis or growth plate is the areas where bones grow longitudinally by undergoing endochondral ossification.36 Bones may have proximal and distal physes, and each may contribute differently to overall bone growth. For example, the proximal ends of the tibia and the fibula contribute 55% of overall growth, with the distal end providing the other 45%.37 Damage to the physis is reported to account for 15% to 30% of skeletal injuries in children. When unrecognized and improperly treated, up to 15% of these injuries can lead to physeal arrest; however, proper treatment of these injuries reduces the incidence of physeal arrest to 1% to 2%.38 The epiphysis is the area between the physis and the adjacent joint, and the metaphysis is the area between the physis and the mid shaft. The physis is the weak part of the bone; it is two- to five-times weaker than the surrounding ligamentous structures, and it is susceptible to shearing, bending, and tension stresses (Figure 28.12). Chapter 31 contains a more complete overview of pediatric and adolescent injuries. Foot and ankle problems in the young athlete are the second most common reason for a visit to a physician.38 In contrast with adults, ligamentous injuries to the ankle are rare among children because the ligaments are stronger than the growing bone. Children are more likely to suffer a fracture than a sprain, and any skeletally immature patient with a significant injury should have radiographs done to evaluate for the possibility of a fracture.39 The physis (or growth plate) is the weakest link in the bone— tendon—muscle chain, and it is the most commonly injured structure in the ankle of a child with open growth plates. Fracture of the distal tibia and the fibular physis is second in frequency only to fractures of the distal radius physis. Physeal ankle fractures usually occur in children who are between 9 and 14 years of age (average age: 12 years), and there is a 2:1 male predominance.9,39 Dias and Tachdjian developed a pediatric ankle fracture classification system that was modified from the adult Lauge—Hansen Joint space

Epiphysis

Metaphysis

Growth plate (physis)

Diaphysis

Figure 28.12 The anatomy of a long bone, with the different anatomic areas identified. (From Grover G: Orthopedic injuries and growing pain. In Berkowitz CD [ed]: Pediatrics: A Primary Care Approach, 2nd ed. Philadelphia, WB Saunders, 2000, p 372.)

system (Figure 28.13). However, this system has its limitations because children are notoriously unable to recall the position of the foot and the force applied to the ankle at the moment of injury.38 The Salter—Harris (SH) physeal fracture classification system (Table 28.6) is based on the location of the fracture line and the fragment in relation to the physis. (Figure 28.14). Knowledge of this system is helpful for describing fractures in the area of the physis. The Ottawa ankle rules have a sensitivity of only 83% and a specificity of only 50% for patients with an open physis; therefore, these rules should not be applied to children.39,40

Pediatric isolated fibula fractures Mechanism of injury This injury usually results from an inversion/supination injury.

Risk factors Slower running speed, decreased dorsiflexion strength, and less balance in males have been identified as risk factors for inversion injuries.39

Clinical features An SH I fracture of the distal fibula is the childhood equivalent of the lateral ankle sprain in an adult. This condition is primarily diagnosed clinically on the basis of localized tenderness and swelling over the lateral malleolus.

Diagnosis Radiographs of SH I or II fractures tend to be normal, or they may demonstrate only minimal displacement, thereby making the radiographic diagnosis difficult. As a rule of thumb, bilateral xrays should be obtained for all pediatric patients to allow for comparison with the noninjured leg. The radiographs and the clinical examination tend to be more obvious and dramatic in fractures that are SH III or greater, and bilateral x-rays are usually not required. Computed tomography scanning and MRI may be needed to fully define the extent of complex fractures.38

Treatment The initial and on-field management of a suspected ankle fracture in children is the same as it is for an adult (Rest Ice Compression Elevation). Nondisplaced SH type I and II fractures can be managed by experienced primary care physicians. Nondisplaced or minimally displaced, less than 2 mm, SH I and II fractures are best treated with a short-leg walking cast for 3 to 4 weeks.9 These patients have a low likelihood of growth arrest as long as the fracture remains nondisplaced. Patients with displaced SH II or greater fractures of the distal fibula should be referred to an orthopedic surgeon due to the high association of these fractures with tibial physeal injuries that may require internal fixation. These injuries have a higher risk of growth arrest. All other fractures around the ankle in children should be managed (or, at a minimum, comanaged) by an orthopedic surgeon because of the involvement of the growth plate and the potential for operative management that may be required to ensure the best outcome. Postfracture rehabilitation for children is the same as it is for adults, but it tends to move at a more rapid pace. Rehabilitation after immobilization should be limited by symptoms in children.

Pediatric tibial fractures Mechanism of injury This injury usually results from an eversion/pronation injury.

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Supination-inversion

Pronation-eversion external rotation

Supinationplantar-flexion

Supinationexternal rotation

Variants of supination-inversion

Figure 28.13 The Dias—Tachdjian ankle fracture classification system for skeletally immature patients. (From Chambers HG: Orthop Clin North Am 2003;34[3]:445- 459.)

Risk factors

Treatment

knee) cast with 30 degrees of knee flexion for 3 weeks followed by a short-leg walking cast for another 3 to 4 weeks. Displaced (>2 mm) SH type II and all type III, IV, and V fractures require operative intervention by an orthopedic surgeon. Patients with these fractures should not bear weight, and their fractures should be placed in a bulky compression dressing until the surgeon can be consulted. Patients with displaced SH II or greater fractures should receive follow-up radiographs every 6 months for 2 years or until Park—Harris growth arrest lines parallel to the physis appear. These lines represent transient calcification of the physeal plate during injury repair; if growth is normal, they are parallel to the physis. Angulated or tented lines are a sign of damage to the physeal plate and of the potential for growth arrest.

SH I fractures usually respond to treatment with immobilization in a short-leg walking cast for 4 weeks. SH II fractures can be treated in the same way, although another option is a long-leg (above the

Juvenile tillaux fractures

No risk factors for this injury have been identified.

Clinical features Nondisplaced SH I and II fractures of the tibia are often mistakenly treated as sprains, and then patients return for follow up because of continued pain and swelling. As with the fibular fractures, tenderness and swelling should provide clues to the diagnosis.

Diagnosis The diagnosis is similar to that of fibular fractures, although bilateral comparison films may be needed.

Table 28.6 Salter—Harris Physeal Fracture Classification System Type I

Type II

Type III Type IV Type V

A shear or slide injury; the epiphysis separates ever so slightly from the metaphysis, with the periosteal attachments surrounding the physis remaining intact; frequently seen in infants and toddlers. The fracture line extends from the physis proximally through the metaphysis; the most common Salter—Harris fracture; most commonly occurs in children who are more than 8 years of age. The fracture line extends from the physis distally through the epiphysis; an intra-articular fracture. The fracture line originates on the articular surface and travels proximally through the epiphysis, the physis, and the metaphysis. A profound compressive force that crushes the physis; the rarest Salter—Harris fracture.

A mnemonic to aid in remembering the location of a Salter—Harris fracture is based on the name SALTR: S, slide injury; A, above physis; L, lower (distal) to the physis; T, through the physis; and R, ruined (physis severely crushed).

An avulsion fracture of the lateral epiphysis by the anteroinferior tibiofibular ligament is the most common SH III fracture of the distal tibia (Figure 28.15). These fractures typically occur in teenagers close to the end of their growth as a result of the fact that the distal tibial physis closes in a medial-to-lateral fashion.9,37 A Tillaux

I

II

III

IV

V

Figure 28.14 The Salter—Harris classification of fractures.The arrows point to the physis. (From Grover G: Orthopedic injuries and growing pain. In Berkowitz CD [ed]: Pediatrics: A Primary Care Approach, 2nd ed. Philadelphia, WB Saunders, 2000, p 374.)

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Figure 28.15 A radiograph demonstrating a juvenile tillaux fracture. Note the lateral Tillaux fragment. (From Ankle fractures. In Eiff MP, Hatch RL, Calmbach WL [eds]: Fracture Management for Primary Care, 2nd ed. Philadelphia, WB Saunders, 1998, p 303.)

fracture may be minimally displaced (i.e., elbow > wrist > hand. A breakdown in force generated at any link or the inefficient transfer of force from one link to the next will result in an increased load on the next link in the chain as it tries to compensate for the weak link. The end result may be injury in the distal link. For example, if the jai alai player in Figure 33.1 has underlying

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Table 33.1

Complete Diagnosis of Plantar Fasciitis

Clinical symptom complex

Tissue overload complex Tissue injury complex Functional biomechanical deficit complex Subclinical adaptation complex Figure 33.1

Kinetic chain: jai alai player.

inflexibility in his hip or trunk rotation that interferes with the efficient transfer of force to the next link (the shoulder), he most likely will present with complaints of shoulder pain, rather than describing hip tightness (see Chapter 6 for a more complete discussion and application of the kinetic chain process).

Injury type Injury type can be categorized as either macrotrauma or microtrauma. Macrotrauma injuries are readily identified events (e.g., an anterior cruciate ligament tear). The tissue is essentially normal before the event, and it becomes abruptly abnormal after the event. Microtrauma injuries are more insidious. Over time, as a result of repetitive insult to a tissue, the integrity of the tissue is altered. Cellular repair mechanisms are disrupted, and the cells cannot produce the proper matrix required for healing. Examples include Achilles tendinitis and lateral epicondylitis.1,4,5

Method of injury presentation The method of injury presentation may be acute, chronic, or an acute exacerbation of a chronic injury.1 Acute injuries are generally the result of macrotrauma, whereas chronic injuries are typically the result of microtrauma. Acute exacerbations of chronic injuries may occur as the result of incomplete rehabilitation. It is important to note that the resolution of symptoms does not necessarily equate with normal function. For example, a subacromial injection may resolve the shoulder pain of an overhead athlete with rotator cuff impingement. However, if the athlete returns to play before addressing the biomechanical factors that contributed to the injury (i.e., poor scapular control), symptoms are likely to return at the original site or elsewhere along the kinetic chain (often in the same limb).5,6

Complete and accurate diagnosis

Table 33.1 demonstrates the application of this concept to a patient with plantar fasciitis.

Plan of treatment for the injury and return to play of the athlete When organizing a treatment plan for an athlete, it is helpful to consider rehabilitation in terms of the acute, recovery, and functional stages.

ACUTE STAGE OF REHABILITATION During the acute stage of rehabilitation (Table 33.2), attention is focused on the clinical symptoms complex and the tissue injury complex. Goals include the control of inflammation and pain, protecting the injured tissue from further damage, maintaining general strength and cardiovascular fitness, and regaining/maintaining range of motion though joint activation. Criteria for advancing to the next phase of rehabilitation include adequate tissue healing, near-normal range of motion, pain control, and tolerance for strengthening. Functional rehabilitation cannot be initiated until analgesia is effective and the control of inflammation is

Table 33.2

Acute Stage of Rehabilitation

Focus of Treatment Tools

To formulate an effective and thorough rehabilitation plan, it is useful to render a complete and accurate diagnosis by identifying and addressing the following clinical, anatomic, and mechanical complexes5,7: 1. Clinical symptoms complex: pain, swelling, and decreased range of motion 2. Tissue injury complex: the tissue that has been injured 3. Tissue overload complex: tissues that have been stressed or overloaded and that are contributing to or exacerbating the injury 4. Functional biomechanical deficit complex: physiologic and mechanical alterations such as strength imbalances or inflexibilities that affect the proper mechanics of athletic activity 5. Subclinical adaptation complex: substitution patterns that an athlete develops to compensate for the injury in an effort to maintain performance

Point tenderness over the plantar fascia insertion onto the calcaneus; symptoms worse in the morning and after running Plantar fascia and gastrocnemius Plantar fascia Gastrocnemius inflexibility and weakness; decreased ankle dorsiflexion Running on toes; decreased stride length; decreased stance phase on the affected side

Goals

Criteria for advancing to the next rehabilitation phase

Clinical Symptom Complex/Tissue Injury Complex Relative rest and/or immobilization Physical modalities Medications Manual therapy Initial exercise Surgery Control inflammation and pain Protect injured tissue from further damage Maintain general strength and cardiovascular fitness Maintain/regain range of motion Pain control Adequate tissue healing Near-normal range of motion Tolerance for strengthening

Modified from Kibler WB, Herring SL, Press JP (eds): Functional Rehabilitation of Sports and Musculoskeletal Injuries. Gaithersburg, MD, Aspen Publishers, 1998.

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accomplished.8 Biologic impairments and the physiologic losses that occur after injury begin immediately and may become substantial in a matter of days. The sooner the injured athlete can transition from the acute phase to the recovery phase, the better. Symptom relief does not mean that functional capacity has been restored. It is important to remember that the resolution of pain indicates that it is time to transition to the next phase of rehabilitation rather than for a premature return to training or competition.

RECOVERY STAGE OF REHABILITATION During the recovery stage (Table 33.3), treatment emphasis is placed on the restoration of function by addressing the tissue overload complex and the functional biomechanical deficit complex. Goals include regaining local flexibility and strength, correcting biomechanical deficits, and maintaining fitness. The recovery phase may be the longest stage of the rehabilitation process. To advance to the next phase of rehabilitation, the athlete should be free from pain; exhibiting a normal range of motion, complete tissue healing, and restored flexibility; and demonstrating strength of 75% or greater as compared with the uninjured side. Early during this phase, the recovery of joint range of motion and the restoration of flexibility receive priority. Full range of motion and joint flexibility will prepare the injured area for more dynamic training and sport-specific activity. Stretching exercises should be done after adequate warm-up. The combination of warm-up followed by stretching is more effective for improving joint range of motion than either used in isolation.9-11 The proposed benefits of improved flexibility are a reduction in risk of injury or reinjury, pain reduction, and improved athletic performance. ‘‘However, a lack of definitive research makes it difficult to make recommendations regarding an effective flexibility program.’’12 If stretching is considered to be effective, the debate then becomes what type of stretching to use. Do you begin with static stretches or ballistic stretching? Do proprioceptive neuromuscular facilitation techniques (also know as contract
relax) provide a more effective method for the restoration of flexibility? Or do dynamic range of motion and eccentric flexibility training provide additional benefits? The bottom line seems to be that after weighing economy of time, the need for intervention from the facilitator, injury protection, and the proposed improvement of athletic performance, the most commonly used

Table 33.3

Recovery Stage of Rehabilitation

Focus of Treatment Tools

Goals

Criteria for advancing to the next rehabilitation phase

Tissue Overload Complex/Functional Biomechanical Deficit Complex Manual therapy Flexibility Proprioception/neuromuscular control training Specific, progressive exercise Restoration of function Regain local flexibility and strength Address biomechanical deficits away from the site of injury Maintain general fitness Pain free Complete tissue healing Normal range of motion Good flexibility 75% or greater strength as compared with uninjured side

Modified from Kibler WB, Herring SL, Press JP (eds): Functional Rehabilitation of Sports and Musculoskeletal Injuries. Gaithersburg, MD, Aspen Publishers, 1998.

program is static stretching.12 The greatest benefits seem to be achieved when this type of stretching is used in combination with warm-up activity and as a prelude to strengthening. However, there is much controversy with regard to this topic. Definitive research will be helpful for defining the recommendations associated with flexibility training. Recovering strength is also essential because muscle weakness is a common finding in athletes with acute injuries and overuse problems. Here again it is important that functional strengthening continue even when the symptoms of the injury have abated. It is not unusual to have strength deficits proximal to the injury site (e.g., hip abductors after knee injury) and even contralateral to the injury site.13 An advancing program of isometric, concentric, eccentric, and plyometric strengthening programs should be undertaken, culminating in local and kinetically associated muscles exhibiting increased aerobic muscle endurance and anaerobic power. Progressive resistance training during the recovery phase, as described by Kraemer,14 optimally consists of 60% to 80% of the 1-repitition maximum with 3-5 sets of 8-12 repetitions each being performed 3-4 days per week. Generally during this period of rehabilitation, as the injured athlete gains strength, exercise intensity is maintained while the load increases. Strength conditioning recommendations during rehabilitation have many important variables: the selection of muscle groups, the sequence of the exercises, the combination of routines with and without equipment, and the appropriate rest activity.14

FUNCTIONAL STAGE OF REHABILITATION During the final stage of rehabilitation (Table 33.4), attention remains focused on any residual biomechanical deficits as well as on the subclinical adaptation complex. Goals include the normalization of movement patterns, strength balance, improved joint neuromuscular control, and return to athletic competition. This stage of rehabilitation ideally continues as an ongoing program to reduce the risk of future reinjury.1,4,15 The criteria for return to play include normal sports mechanics, normal strength/flexibility and range of motion, good general fitness, and the demonstration of sport-specific skills. The major goals of a well-constructed rehabilitation plan are to reduce the risk of reinjury and to reduce the risk of subsequent injuries along the kinetic chain. Consider the development of a rehabilitation plan for a female basketball player after a lateral ankle sprain. During the latter stages of the functional phase of her rehabilitation, the physician may elect to introduce a series of plyometric jumping exercises not only to reintroduce the

Table 33.4

Functional Stage of Rehabilitation

Focus of Treatment Tools

Goals

Criteria for advancing to the next rehabilitation phase

Functional Biomechanical Deficit Complex/Subclinical Adaptation Complex Power and endurance exercise (e.g., plyometrics) Sport-specific functional progression Technique/skills instruction Normalize movement patterns Return to athletic competition Reduce the risk of reinjury Normal strength and strength balance Normal sports mechanics Demonstration of sport-specific skills

Modified from Kibler WB, Herring SL, Press JP (eds): Functional Rehabilitation of Sports and Musculoskeletal Injuries. Gaithersburg, MD, Aspen Publishers, 1998.

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necessary sport-specific skills needed to challenge her ankle but also as a means of possible protection from injury elsewhere in the kinetic chain. The knee (specifically the anterior cruciate ligament) is a particularly vulnerable proximal link in the lower extremity of the female athlete. In women, neuromuscular differences appear to modify the ability to dissipate landing forces as compared with what is seen in men. Irmischer and colleagues16 observed a significant reduction in ground reaction forces during landing among women completing a 9-week, plyometric-based jumping program as compared with controls. This study demonstrates the successful use of a plyometric training program to alter landing strategies in females, which may result in a reduced risk of knee injury while landing.16

KINESIOLOGY BASICS OF SPORTS REHABILITATION A basic understanding of rehabilitation kinesiology helps the sports medicine physician to plan an appropriate rehabilitation program and to coordinate that plan with other members of the rehabilitation team (i.e., physical therapists, athletic trainers).

Types of muscle action Concentric contraction Concentric contraction occurs when the total length of the muscle shortens as tension is produced. For example, the upward phase of a biceps curl is a concentric contraction.

Eccentric contraction Eccentric contraction occurs when the total length of the muscle increases as tension is produced. For example, the lowering phase of a biceps curl constitutes an eccentric contraction. Muscles are capable of generating greater forces under eccentric conditions than under either isometric or concentric contractions.17-19 Large tensile forces are generated during sudden eccentric contractions (e.g., a linebacker coming to a rapid stop at the line of scrimmage generates large eccentric quadriceps forces). Traditional rehabilitation programs have often omitted eccentric training. Although there are no definitive studies to support eccentric training as an absolute prerequisite before returning to athletic play,19 research is emerging to support its use, particularly for the rehabilitation of microtrauma/overuse injuries. For example, Roos and colleagues20 designed a prospective randomized clinical trial to test the hypothesis that eccentric calf muscle exercises reduce pain and improve function in patients with Achilles tendinopathy. At 12 weeks, members of the group who performed eccentric exercises reported significantly less pain, and more patients in that group returned to sports participation after 12 weeks.20

Isometric contraction Isometric contraction occurs when muscle length remains relatively constant as tension is produced. For example, during a biceps curl, holding the dumbbell in a constant/static position rather than actively raising or lowering it is an example of isometric contraction.21,22 Although the forces generated during isometric contractions are potentially greater than during concentric contractions, muscles are seldom injured during this type of contraction. Isometric exercises are often used during the early phases of rehabilitating a musculotendinous injury because the intensity of contraction and the muscle length at which it contracts can be controlled.19

Closed kinetic chain During a closed kinetic chain exercise, the terminal joint is stationary, thus prohibiting free motion.2 A lower-extremity example

Figure 33.2

Closed kinetic chain: two-leg squat.

would be leg squats (Figure 33.2), and an upper-extremity example would be pushups.23 Closed kinetic chain exercises have several advantages over open-chain exercises. Rather than having muscle groups work in isolation, closed-chain exercises allow for the simultaneous activation of antagonistic muscle groups (e.g., the quads and the hamstrings during leg squats), thus promoting increased joint stability and a simulation of functional movement patterns.24 Lower-extremity closed kinetic chain exercises have often been touted as a more functional type of exercise for the rehabilitation of the lower extremity because sport-related activities are performed with the feet in fixed positions. For example, in the setting of rehabilitation after anterior cruciate ligament reconstruction, Bynum and colleagues25 performed a randomized prospective trial comparing open and closed kinetic chain rehabilitation. ‘‘The closed kinetic chain group had lower mean KT-1000 arthrometer side-to-side differences, less patellofemoral pain, was generally more satisfied with the end result, and more often thought they returned to normal daily activities and sports sooner than expected.’’ The authors thus concluded that closed kinetic chain exercises do offer some important advantages over open kinetic chain exercises during rehabilitation after anterior cruciate ligament reconstruction.25

Open kinetic chain During an open-chain kinetic exercise, the terminal link is allowed to move freely through space. Muscle groups may act in isolation with this type of exercise. For example, during an open-chain lower-extremity exercise such as knee extension, the quadriceps predominates (Figure 33.3). Both open and closed kinetic chain exercises have a role in rehabilitation. For example, rehabilitation for an overheadthrowing athlete (e.g., a baseball player) after the repair of a superior labral tear may involve closed-chain exercises to develop scapular control early during the postoperative phase, when shoulder range of motion is protected. As rehabilitation progresses toward the functional phase, open-chain exercises will be added to more closely simulate the throwing motion.

Plyometrics Plyometric exercises emphasize explosive motions (Figure 33.4). This type of exercise takes advantage of the elastic properties of connective tissue coupled with the force generated by muscle itself. A rapid prestretch (eccentric load) is followed immediately

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References 435

progressively and systematically assessed and trained before an effective return to sport-specific activities. The use of taping and orthotics and their benefits for joint proprioception should also be considered.27 (See Chapter 38 for a discussion of bracing and Chapter 37 for a discussion and primer on athletic taping.)

PSYCHOLOGIC ASPECTS OF REHABILITATION Addressing the active patient’s emotional needs is just as important as the physical recovery. An athlete may be depressed about the current injury and apprehensive about future injuries. Recognizing the psychologic and emotional needs of the injured athlete during each phase of rehabilitation will go a long way toward enhancing recovery and ensuring the enthusiastic participation of the patient.28 Framing the rehabilitation plan in a positive way by instructing the athlete regarding what he or she can do (not just what he or she cannot do) is integral to facilitating a successful outcome. Figure 33.3

Open kinetic chain: single-leg extension.

by a forceful concentric contraction.17,18 For example, high jumpers first lower their bodies toward the ground, placing a prestretch on the leg muscles; this is followed by the forceful contraction of the same muscles, which propels the athlete over the bar.19 Plyometric exercises are introduced during the functional phase of rehabilitation and are among the most sportspecific exercises performed during this stage.

Proprioception A complete rehabilitation program must not overlook the neuromuscular control that is necessary for joint control. The repair of static and dynamic constraints and the strengthening of muscles do not necessarily prepare the joint of an athlete for the sudden positional changes seen in the athletic arena. Therefore, the rehabilitative process must address the structure that contributes to the awareness of posture, movement, changes in equilibrium, and the knowledge of position, weight, and the resistance of objects related to the body.26 The joint capsule receptors, the ligament receptors, the muscle, and the tendon receptors must be appreciated and

CONCLUSION Sports rehabilitation is a dynamic program of exercise, guided evaluation and instruction, and psychologic support that is designed to prevent or reverse the deleterious functional and physiologic effects of injury. The goals of rehabilitation are best appreciated in general conceptual terms as opposed to rigid protocols. Understanding the phases of sports rehabilitation and the goals of each phase will help sports physicians to individualize programs to meet the needs of each specific athlete.

REFERENCES 1. 2. 3.

4. 5.

6. 7. 8. 9.

10. 11. 12. 13.

14. 15. 16.

Figure 33.4

Plyometrics: box jumps.

Kibler WB: A framework for sports medicine. Phys Med Rehabil Clin North Am 1994;5:1. Steindler A: Kinesiology of the Human Body Under Normal and Pathologic Conditions. Springfield, IL, Charles C. Thomas, 1955. Kibler WB: Determining the extent of the functional deficit. In Kibler WB, Herring SL, Press JM (eds): Functional Rehabilitation of Sports and Musculoskeletal Injuries. Gaithersburg, MD, Aspen Publishers, 1998, pp 16-19. Kibler WB, Herring SA: Formulating a rehabilitation program. In Griffin LY (ed): Rehabilitation of the Injured Knee, 2nd ed. St. Louis, Mosby, 1995. Herring SA, Kibler WB: A framework for rehabilitation. In Kibler WB, Herring SL, Press JM (eds): Functional Rehabilitation of Sports and Musculoskeletal Injuries. Gaithersburg, MD, Aspen Publishers, 1998, pp 1-8. Lysens, et al: The predictability of sports injuries. Sports Med 1984;1:6. Herring SA: Rehabilitation of Muscle Injuries. Medicine and Science in Sports and Exercise, vol 22. Williams & Wilkins, 1990. Frontera WR: Exercise and musculoskeletal rehabilitation. Phys Sportsmed 2003;31(12). Schwellnus M: Flexibility and joint range of motion. In Frontera WR (ed): Rehabilitation of Sports Injuries: Scientific Basis. Malden, MA, Blackwell Science, 2003, pp 232-257. Murphy DR: A critical look at static stretching: are we doing our patients harm? Chiropractic Sports Med 1994;8:59-70. Kuland DN, Tottossy M: Warm-up, strength and power. Orthop Clin North Am 1983;14:427-448. Nelson RT, Brandy WD: An update on flexibility. Strength Condition J 2005;27(1): 10-16. Urbach D, Awiszus F: Impaired ability of voluntary quadriceps activation bilaterally interferes with functional testing after knee injures: a twitch interpolation study. Int J Sports Med 2002;23(4):231-236. Kraemer WJ: Strength training basics: designing workouts to meet patients’ goals. Phys Sportsmed 2003;31(8):39-45. Kibler WB, Chandler TJ, Pace BK: Principles of rehabilitation after chronic tendon injuries. Clin Sports Med 1992;11(3):661-671. Irmischer BS, Harris C, Pfeiffer RP, et al: Effects of a knee ligament injury prevention exercise program on impact forces in women. J Strength Cond Res 2004;18(4):703-707.

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17. 18. 19.

20.

21. 22. 23.

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Komi PV (ed): Strength and Power in Sport. London, Blackwell Scientific Publications, 1992. McArdle WD, Katch FI, Katch VL. Exercise Physiology: Energy, Nutrition and Human Performance, 3rd ed. Philadelphia, Lea & Febiger, 1991. Young JL, Press JM: The physiologic basis of sports rehabilitation. In Kibler WB, Herring SL, Press JM (eds): Functional Rehabilitation of Sports and Musculoskeletal Injuries. Gaithersburg, MD, Aspen Publishers, 1998, pp 9-16. Roos EM, Engstrom M, Lagerquist A, Soderberg B: Clinical improvement after 6 weeks of eccentric exercise in patients with mid-portion Achilles tendinopathy—a randomized trial with 1-year follow-up. Scand J Med Sci Sports 2004;14(5):286-295. Kinesiology: A Scientific Basis of Human Motion, 7th ed. Philadelphia, WB Saunders, 1982. Hunter GR: Muscle physiology. In Baechle TR (ed): Essentials of Strength Training and Conditioning, 2nd ed. Champaign, IL, Human Kinetics, 2000, pp 3-15. Hillman S: Principles and techniques of open kinetic chain rehabilitation: the upper extremity. J Sports Rehabil 1994;3:319-330.

24. 25.

26.

27.

28.

Draganich LF, Jaeger RJ, Fralj AR: Coactivation of the hamstrings and quadriceps during extension of the knee. J Bone Joint Surg Am 1989;71:1075-1081. Bynum EB, Barrack RL, Alexander AH: Open versus closed chain kinetic exercises after anterior cruciate ligament reconstruction. A prospective randomized study. Am J Sports Med 1995;23(4):401-406. Harrelson GL, Leaver-Dunn D: Introduction to rehabilitation. In Andrews, Harrelson, Wilk (eds): Physical Rehabilitation of the Injured Athlete, 2nd ed. Philadelphia, WB Saunders, 1998, pp 175-217. Grossman T, Serenelli K, Mistry D: Taping and bracing. In O’Connor F, Sallis R, Wilder R, St. Pierre P (eds): Sports Medicine: Just the Facts. McGraw-Hill, pp 442-445. Brewer BW, Andersen MB, Van Raalte JL: Psychological aspects of sports injury rehabilitation: toward a biopsychosocial approach. In Mostofsky DI, Zaichkowsky LD (eds): Medical and Psychological Aspects of Sport and Exercise. Morgantown WV, Fitness Information Technology, 2002, pp 41-54.

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Practical Application of Osteopathic Manipulation in Sports Medicine Lori A. Boyajian-O’Neill, DO, and Dennis A. Cardone, DO

KEY POINTS

. The body has an inherent ability to heal and maintain or acquire

.

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.

health. Physicians seek to facilitate this inherent propensity for health through a variety of interventions, including pharmacologic, surgical, biopsychosocial, and manual therapies. Manual therapeutic techniques are applied to restore or improve function by targeting barriers to normal function.There are many specific techniques, including those that are applied to soft tissue and others that are applied to joints. Structure and function are inextricably connected; that which affects one conversely affects the other. ‘‘Normal’’ joint biomechanics vary within and among athletes even in the same sports or positions. Training alters biomechanics and neuromuscular patterns to achieve a desired level of performance.When there is injury, there is an alteration of structure and function and, thus, performance. Acute trauma, overuse injury, or abnormal anatomy that leads to abnormal biomechanics in one area will eventually adversely affect structure and function at distant sites if there is no intervention (i.e., prehabilitation or rehabilitation). Neuromusculoskeletal integrity is developed and maintained through training that optimizes function and performance. Muscle-activating patterns, which are established through training and interrupted by injury, may be reestablished through rehabilitation that includes strengthening, proprioception, and range of motion.

INTRODUCTION What is osteopathic medicine? Andrew Taylor Still, MD, who founded osteopathic medicine in 1874, was one of the first sports medicine physicians in the United States. At the American School of Osteopathy in Kirksville, Missouri, he advocated exercise as being inextricably tied to health. An anatomist by avocation, Dr. Still observed the connection between structure (anatomy) and function (physiology) in normal and pathologic states and promoted three

principles of osteopathic medicine: (1) the body is a unit; (2) structure and function are reciprocally interrelated; and (3) the body is self-healing. These tenets are the basis of osteopathic medical education and osteopathic sports medicine practice. In founding osteopathic medicine, Dr. Still put into practice his philosophy that structure and function are interconnected and thus that they affect the work and capabilities of the body (performance). The American Osteopathic Association describes osteopathic medicine as a ‘‘complete system of medical care with a philosophy that combines the needs of the patient with current practice of medicine, surgery and obstetrics and emphasizes the interrelationship between structure and function and has an appreciation of the body’s ability to heal itself.’’1 The concept of body unity means that the human being is a dynamic unit of function. Athletes use their bodies to the extreme to maximize function and achieve performance. Osteopathic sports medicine physicians apply the tenets of osteopathic medicine to assist athletes with preparing for sport, optimizing performance, and recovering from injury with the philosophy that the athlete’s structure and function are interrelated. Osteopathic sports medicine physicians use osteopathic manipulative techniques or manual techniques to improve physiologic function and/or to support homeostasis that has been altered by somatic dysfunction. The term somatic dysfunction is used in osteopathic medicine, and the American Osteopathic Association defines it as ‘‘impaired or altered function of related components of the somatic (body framework) system: skeletal, arthrodial and myofascial structures, and related vascular, lymphatic and neural elements.’’1 In osteopathic sports medicine, somatic dysfunction is treated using osteopathic manipulative techniques, pharmacotherapeutics, modalities, and surgery. Osteopathic manipulative techniques encompass a variety of techniques, including soft-tissue mobilization and manipulative techniques. This chapter focuses on the approach and application of osteopathic principles and practices to the rehabilitation of athletes, with an emphasis on osteopathic manipulation techniques.

What is osteopathic sports medicine? Osteopathic medicine is deeply rooted in the care of the athlete, whether he or she is a competitor on the playing field or a working or ‘‘industrial’’ athlete. Forrest ‘‘Phog’’ Allen, DO, won 771 basketball games at Kansas University, and he was well known to use

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manual medicine techniques in the treatment of his players. The American Osteopathic Academy of Sports Medicine defines sports medicine as the branch of the healing arts profession that uses a holistic, comprehensive approach to the prevention, diagnosis, and management of sports- and exercise-related injuries, disorders, dysfunctions, and disease processes.2

REHABILITATION PRINCIPLES OF OSTEOPATHIC SPORTS MEDICINE When structure is altered (e.g., as the result of an injury), function (or performance) is affected. Think of the athlete with a sprained ankle: ligaments (structure) are damaged, and function (performance) is adversely affected. Correspondingly, when function is altered, structure is affected. Think of a golfer who develops a new swing that causes stress at the shoulder; this may lead to acromioclavicular joint sprain, acromial spur, or other structural abnormalities. Alteration in structure or function may lead to compensatory changes through kinetic linkage, and it may cause somatic dysfunction not only locally but also at distant sites. An understanding of the kinetic chain is critical to understanding performance and osteopathic musculoskeletal pathology (somatic dysfunction). The body is a unit, and forces that affect one area will predictably evoke a series of responses in other areas of the body, including the soft tissue, the bones, and the joints. The kinetic chain requires constant feedback mechanisms to maintain homeostasis whether at rest or in dynamic states of motion. Breakdowns of the kinetic chain occur when neuromusculoskeletal systems do not function in concert. These breakdowns often occur as a result of poor muscle activation patterns that may be the result of inexperience, deconditioning, injury, or preexisting anatomic abnormalities (e.g., leg-length discrepancy, rotoscoliosis). Any interruption in the normal biomechanics of the kinetic chain predisposes the athlete to injury. Athletes demonstrate the kinetic chain of events during any sports maneuver. For example, a volleyball player who spikes a ball must first get into a crouched or ‘‘ready’’ position; explosively jump; hyperextend the lumbar spine; and severely hyperextend, abduct, and externally rotate the shoulder as he or she gets ready to strike the ball. Dynamic stabilizers keep the body balanced and aligned to complete this task. In a pathologic state, the kinetic chain is affected, and sports maneuvers or performance may be adversely affected, thus leading to injury. For example, a dysfunction of the quadriceps femoris muscle could limit jumping ability. Lumbosacral dysfunction might limit back extension. Both of these injuries, which are remote from the shoulder, could interrupt normal kinetic chain biomechanics and cause effects that are detrimental to the shoulder complex. Another example is a baseball pitcher with shoulder pain who may compensate by altering his or her delivery during the acceleration phase, thus leading to elbow pain. Understanding the kinetic chain is essential to understanding the interrelatedness of structure and function, especially during rehabilitation. The reestablishment of proprioception and neuromusculoskeletal abilities to preinjury levels is a challenge that is recognized by osteopathic sports medicine physicians and a primary goal of kinetic chain rehabilitation. The kinetic chain links one structure and function to another, and a dysfunction in any area of the kinetic chain will cause compensatory changes in the chain. If the precipitating factors are not corrected, gross trauma may occur. Recognition that the problem may not be at the obvious site of injury but rather the result of a dysfunction occurring at another part of the kinetic chain is important when developing a treatment plan.

If rehabilitation is focused only on the obvious area of injury with disregard to the entire kinetic chain, then unusual and uncompensated stress may result in further injury. Predictable patterns of fascial rotation have been described that influence or are influenced by spinal curves and that may be altered when there is somatic dysfunction of the kinetic chain. Zink and Lawson3 described predictable fascial motion preferences at transitional regions of the body as ‘‘common compensatory patterns.’’ These transitional areas are the occipitoatlantal junction, the cervicothoracic junction, the thoracolumbar junction, and the lumbosacral junction.3 Over time, the body will adapt to stress, and compensatory patterns will result. These patterns may be caused by a structural source or a functional stress. For the highly trained athlete, compensatory patterns are the result of years of training. The development of this complex of muscles—including the development and refinement of the neurologic feedback mechanisms (proprioception)—is important to the performance of the player. Symmetry is not typically the desired goal. Rather, asymmetry is the goal, and it is the result of countless hours performing a sport-specific maneuver and the development of highly complex muscle activation patterns. Think of the right-handed tennis player with relatively overdeveloped (hypertrophied) musculature of the right forearm, shoulder complex, thorax, and back. Dysfunction affecting the massive right latissimus dorsi muscle, which extends from the iliac crest to the thoracolumbar fascia to the humerus, could interrupt the kinetic chain, thereby affecting the serve of this tennis player. However, when treating this patient, it would be a mistake to assume or attempt to make the left and right latissimus muscles equal in strength or flexibility. During rehabilitation, the osteopathic sports medicine physician recognizes the somewhat predictable patterns of compensation to more effectively render an exercise/rehabilitation prescription that will address somatic dysfunction throughout the kinetic chain.

The osteopathic structural examination Osteopathic sports medicine physicians receive extensive training in recognizing injury patterns. The foundation of the evaluation of the injured athlete is the comprehensive medical and injury history and physical examination. The physical examination includes a systems-based evaluation, a traditional orthopedic examination, and an osteopathic structural examination. The osteopathic structural examination is the examination of a patient by an osteopathic physician with emphasis on the neuromusculoskeletal system, including palpatory diagnosis for somatic dysfunction and viscerosomatic/somatosomatic change within the context of total patient care. The examination is concerned with finding somatic dysfunction in all parts of the body, and it is performed with the patient in multiple positions to provide static and dynamic evaluation.1 Components of the osteopathic structural examination are described in Table 34.1.

Somatic dysfunction and barriers Osteopathic sports medicine physicians use the structural examination to recognize and treat somatic dysfunction using osteopathic manipulative techniques. The characteristics of somatic dysfunction can be described with the mnemonic STAR: Sensitivity changes, Tissue texture abnormality, and Asymmetry and alteration of the quality and quantity of Range of motion. Another mnemonic for somatic dysfunction is TART: Tissue texture abnormality, Asymmetry, Restriction of motion, and Tenderness, any one of which must be present for diagnosis (Table 34.2). Acute somatic dysfunction is the immediate or short-term impairment or altered function of related components of the

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Table 34.1 Components of the Osteopathic Structural Examination Structures Evaluated

Specific Evaluation

Pelvis and sacrum

Anterior superior iliac spine heights and distance from midline Sacral base motion Tissue texture changes Vertebral rotational motion Asymmetry Viscerosomatic reflexes Spinal curvature Fascial restrictions Sternal motion Tender points Rib motion Thoracic inlet Tissue texture changes Vertebral motion Tender points Occipitoatlantal dysfunction Atlantoaxial dysfunction Shoulder height Carrying angle at elbow Orientation of forearms and wrists Iliac crest heights Q angles Fibular head motion Tibial tubercle inversion/eversion Medial malleoli heights Achilles tendon orientation Medial arches of the foot

Lumbar and lower thoracic spine

Abdomen and abdominal diaphragm Respiratory motion and ribs Upper thoracic and cervical spines

Upper extremities

Lower extremities

Table 34.3 Physiologic Anatomic Restrictive

Barriers The end of the active range of motion The end of the passive range of motion The end of the range of motion that is less than normal

is freer; and (3) the directions in which motion is restricted.1 The point at which motion is restricted, either normally or pathologically, is called a barrier (Table 34.3). Schneider and Dvorak described physiologic and anatomic barriers to the normal range of motion in a joint and also pathologic barriers that can develop with injury.4 Anatomic barriers refer to the limit of motion imposed by anatomic structure. Clinically, this is the limit of passive range of motion. A breach of anatomic barrier will result in dislocation and/or fracture. Physiologic barriers are the limits of active range of motion. Clinically, these barriers mark the beginning of passive range of motion, which ends at the anatomic barrier. The term elastic barriers refers to the range of motion between physiologic and anatomic barriers of motion in which passive ligamentous stretching occurs before tissue disruption. A breach of elastic barriers will result in tissue disruption, as is seen in sprains. The term pathologic barriers refers to the restriction of joint motion associated with pathologic change of tissues (e.g., the impingement caused by an osteophytic acromion, which limits shoulder flexion). Restrictive barriers are functional limits that abnormally diminish the normal physiologic range of motion. Restrictive barriers are very common and include ‘‘tight muscles’’ (e.g., tight hamstrings). Athletes commonly engage the restrictive barrier and, through stretching, seek to relieve or reset this barrier to increase their range of motion. When range of motion is normalized, the athlete will engage the physiologic barrier.

Facilitation and somatic dysfunction somatic (body framework) system. Somatic dysfunction is characterized in its early stages by vasodilation, edema, tenderness, pain, and tissue contraction (e.g., an acute sprain). Somatic dysfunction is diagnosed by the history and by palpatory assessment for STAR/TART.1 Chronic somatic dysfunction is the long-term impairment or altered function of related components of the somatic (body framework) system. In contrast with acute somatic dysfunction, it is characterized by tenderness, itching, fibrosis, paresthesias, and tissue contraction. Tissue texture abnormality is a palpable change in tissue from skin to particular structures that represent any combination of the following signs: vasodilation, edema, flaccidity, hypertonicity, contracture, and fibrosis as well as the symptoms of itching, pain, tenderness, and paresthesias. Types of tissue texture abnormality include bogginess, thickening, stringiness, ropiness, firmness (hardening), increased or decreased temperature, and increased or decreased moisture.1 There are positional and motion aspects of somatic dysfunction that are best described using at least one of three parameters: (1) the position of a body part as determined by palpation and referenced to its adjacent defined structure; (2) the directions in which motion

Table 34.2

Features of Somatic Dysfunction

TART

STAR

Tissue texture changes Asymmetry Restriction of motion Tenderness

Sensitivity changes of tissues Tissue texture abnormality Asymmetry Range-of-motion abnormalities

Facilitation refers to the maintenance of a pool of neurons in a hyperexcited state or a state in which less afferent stimulation is required to elicit a neural impulse.5 A sustained or inappropriate impulse can cause somatic dysfunction through continuous sensory input (e.g., from overstretched muscles, tendons, or ligaments). The resultant prolonged muscle contraction restricts the range of motion and can cause the activation of inflammatory mediators such as bradykinins, prostaglandins, and leukotrienes, which can cause local vasodilation and tissue texture changes (TART/STAR). Reflex activity can sustain the muscle contraction and also cause adjacent muscles to contract. Viscerosomatic reflexes are observed when there is a reflexive neurologic response that results in recognized patterns of somatic or tissue changes. These reflexes involve localized visceral stimuli that produce patterns of response in segmentally related somatic structures. An example of a visceral somatic reflex is an abdominal wall muscle spasm that occurs as a result of appendicitis. Somatosomatic reflexes are localized somatic stimuli that produce patterns of reflex response in segmentally related somatic structures. These may manifest as muscle spasms, tender points (Jones6), trigger points (Travell7), and tissue temperature or texture changes. Somatosomatic reflexes may represent underlying pathology that is causing sympathetic nervous system activation or hyperactivation, which result in the clinically apparent tissue texture changes.

Tender points and trigger points Tender points are hypersensitive points in the myofascial, tendinous, and ligamentous tissues of the body that are approximately 1 cm in size and that do not have a pattern of pain radiation. Lawrence H. Jones, DO, FAAO, described tender points as a

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manifestation of somatic dysfunction and developed a system called strain and counterstrain to diagnose and treat somatic dysfunction related to tender points.6 Counterstrain is discussed later in this chapter. A myofascial trigger point is a small, hypersensitive site that, when stimulated consistently, produces a reflex mechanism that gives rise to referred pain and/or other consistent manifestations.1 Myofascial trigger responses are consistent from person to person, and so patterns of trigger-point location and radiation have been mapped. These myofascial trigger points were most extensively and systematically documented by Janet Travell, MD, and David Simons, MD.7

OSTEOPATHIC APPROACH TO THE INJURED ATHLETE History A comprehensive history of the injury, including precipitating factors and the mechanism of injury, is critical to understanding the current injury and preventing future injury. Deconditioning, poor training, and abnormal biomechanics certainly can contribute, and they may be the primary cause of acute injury. In addition, factors such as poor nutrition and the use of supplements and performance-enhancing drugs (both banned and acceptable) can contribute to injury. Knowledge of these factors forms a basis for examination and investigation. Sports medicine physicians must have an understanding of the physical demands and risks associated with specific sports and positions. An understanding of the level of competition (i.e., elite, collegiate, club, recreational, or school-based) is important for developing an approach to injury assessment, rehabilitation, and return to play. Athletes with poorly or incompletely rehabilitated injuries may be at a greater risk for the acute exacerbation of injury, chronic injury patterns, and compensatory changes that may cause injury at other, previously unaffected joints and soft tissues, as described previously. A detailed history is the basis for the comprehensive physical evaluation of the injured athlete.

Overview of osteopathic techniques The manipulative techniques used by osteopathic sports medicine physicians to treat somatic dysfunctions can be described in various manners. One way is to segregate by mode of therapy (i.e., soft tissue, mobilization, or manipulative), and another is a classification based on the method of technique (direct or indirect) relative to the barrier engaged when performing the technique. Direct techniques are those techniques in which the restrictive barrier is engaged as part of the treatment. There are many types of specific techniques under the umbrella of direct technique in which an impulse is applied across a joint. These have been developed to restore the symmetry of the movements that are associated with the vertebral or extremity joints. A well-known example of a direct technique is high-velocity/low-amplitude manipulation. Indirect techniques are those techniques in which the restrictive barrier is not engaged as part of the treatment. Rather than engaging the barrier directly (direct technique), with indirect techniques, the treatment is focused on the ‘‘normal’’ direction of motion (i.e., into the direction of freedom) rather than the direction of restriction. These techniques enhance muscle relaxation, flexibility, and the circulation of body fluids. The focus is primarily on restoring physiologic movements to altered joint mechanics. Examples of such techniques include massage, myofascial release (stretching), strain and counterstrain, muscle energy, unwinding, and indirect functional techniques. Indirect techniques do not involve the application of impulse (quick force) across a joint. Rather, the joint is gently carried repeatedly and passively through the normal range of motion. The purpose is to increase the range of motion in a joint in which the normal motion has become restricted. One example of indirect techniques is facilitated positional release, which will be described later in this chapter.

Specific osteopathic manipulative techniques The American Osteopathic Association describes more than 15 separate osteopathic manipulative techniques.1 Included in this chapter are basic descriptions of a few of the most commonly used techniques and descriptions of the application of these techniques for the treatment of athletes.

Physical examination

Muscle energy

A focused examination of the affected area as well as of areas of compensation is necessary for complete diagnosis. This would include what is traditionally thought of as an orthopedic evaluation in addition to the osteopathic structural examination. Osteopathic sports medicine physicians perform a structural examination that places emphasis on the neuromusculoskeletal system and that includes palpatory diagnosis for somatic dysfunction. Assessment for postural patterns, asymmetry, and functional kinetic chain abnormalities are also included in the examination. The examination is performed with the patient in multiple positions to provide both static and dynamic evaluation; an overview is provided in Table 34.1. The physical examination should include sport-specific maneuvers to gain information about abilities and disabilities. For example, a baseball pitcher with shoulder pain may have a primary somatic dysfunction of the ilium or thoracolumbar areas that affects the latissimus dorsi muscles, thereby causing an alteration of normal overhead throwing mechanics that leads to shoulder strain or injury. This comprehensive assessment of the injured athlete provides the information that is needed to formulate a comprehensive, holistic approach to rehabilitation. Although osteopathic sports medicine physicians use a variety of methods to treat athletes, including nonpharmacologic, pharmacologic, and surgical methods, the remainder of this chapter will focus further discussion on the use of osteopathic manipulative techniques for the treatment of athletes.

Muscle energy (ME) is a soft-tissue technique that refers to a system of treatment in which the patient voluntarily moves the body as specifically directed by the osteopathic physician. This directed patient action is from a precisely controlled position against a defined resistance.1 Fred L. Mitchell, Sr, DO, first developed this method, which seeks to increase range of motion through the relaxation of antagonistic muscles.1 The goal of ME techniques is to cause a neurophysiologic reflex that will lead to muscle relaxation. It is postulated that ME, when used directly on involved restrictions, activates the Golgi tendon organ, which relieves the muscle spasm.8 Another theory is that engaging the affected muscle in an isometric contraction causes muscular fatigue and subsequent relaxation. Active and passive joint ranges of motion are assessed in all three planes, and barriers to normal or baseline motion are observed. For example, in the spine, these ranges of motion may be flexion—extension, rotation, and side bending. In the extremities, the assessment involves flexion—extension, pronation—supination, and abduction—adduction. Upon identification of a restrictive barrier, the joint is moved to the point of the restricted barrier (engaged), and the patient is asked to move the joint away from the barrier and toward the direction of ease of movement. The patient’s force is countered by an equal opposing force by the physician, thereby causing isometric contraction of the muscle in spasm. This isometric contraction is 3 to 5 seconds in duration, and it is followed by the complete relaxation of the muscle for an additional 3 to 5 seconds;

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Table 34.4 1 2 3 4 5 6 7

Steps of Muscle Energy Technique

The physician places the joint so that restrictive barriers are engaged in all planes. The patient contracts muscles to move the joint away from the barrier and into the direction of ease of motion. The physician applies an equal counterforce for isometric contraction. The counterforce is applied for 3 to 5 seconds. The patient relaxes, and the counterforce is removed. The joint is passively moved to a new restrictive barrier. Steps 1 through 6 are repeated 3 to 5 times until the desired range of motion is achieved.

this increases the range of motion (elastic barrier) and resets the restricted barrier. The joint is then repositioned to the new barrier, and the process is repeated. The entire treatment outlined in Table 34.4 is repeated until normal or baseline range of motion is reestablished, which usually takes 3 to 6 repetitions. Think of a contracted biceps muscle that restricts elbow extension. ME would be applied by first extending the elbow to engage the restricted barrier and then having the patient contract the biceps to flex the elbow against resistance (isometric) in the manner described previously. This would activate the Golgi tendon reflex, and the biceps would relax. ME is very useful for precompetition warmup and for rehabilitation in which improved joint range of motion or muscle complex lengthening/stretching is desired. For example, the massive biceps femoris complex (hamstrings) can cause restriction to full knee extension and, when in a contracted or shortened state, be vulnerable to injury from a sudden and forceful knee extension. This somatic dysfunction of the hamstrings may render the athlete more susceptible to hamstring injury. This is typically as a result of immobilization of the knee in even slight flexion (after surgery or trauma) or simply as a result of repeated abnormal positioning. Think of the ‘‘weekend warrior’’ who sits at a desk with his or her hips and knees flexed for most of the week whose hamstrings are normally contracted and not conditioned for a weekend of sporting activity. Pregame ME can be applied to lengthen the hamstrings and increase knee extension, thereby decreasing the risk of hamstring injury or injury to associated parts of the kinetic chain.

High-velocity/low-amplitude technique High-velocity/low-amplitude (HVLA) technique is a mobilization technique that employs a strong therapeutic impulse (high velocity) of brief duration that pushes the joint for a short distance (low amplitude) within its anatomic range of motion of a joint. HVLA is commonly known as ‘‘thrust technique.’’ The goal of HVLA is to engage and thrust through a restrictive barrier in one or more planes of motion to elicit the release of that restriction (physiologic barrier). Thrusting techniques are used to increase motion, improve function, decrease pain, and modify somatovisceral reflexes. HVLA is a passive technique and therefore the thrust is rendered completely by the physician, which can render the patient vulnerable to injury. HVLA is applied frequently to the cervical and lumbar spine, and so complications can arise in these areas as a result of operator error, anatomic anomaly, or preexisting conditions such as osteoporosis, an undiagnosed herniated disk, or fracture. Contraindications to consider when working with athletes include ligamentous laxity (acute sprains or chronic instability), suspected or diagnosed fractures, and atlantoaxial instability (often seen in Down syndrome and rheumatoid arthritis) (Table 34.5). Although demonstrated to be very safe, major complications including vertebrobasilar injury and cauda equina syndrome have

Table 34.5 Indications and Contraindications for High-Velocity/Low-Amplitude Technique Indications Decreased range of motion

Absolute Contraindications

Relative Contraindications

Suspected or known fracture Bone metastasis Osteoporosis

Acute cervical strain

Unstable joints Osteomyelitis Atlantoaxial (AA) instability

Pregnancy Postoperative condition Herniated nucleus pulposus Coagulopathy Vertebral artery ischemia

been reported. However, the risk of serious injury is quite low and reportedly in the range of 1 in 400,000 to 1 in 1,000,000.9 HVLA can be applied to the axillary and appendicular joints as well as the spine. For example, athletes who engage in overhead motion and weight lifting often experience trigger or tender points related to the spasm of the muscles of the posterior shoulder complex. The levator scapulae and rhomboid muscles can be especially affected as a result of scapular motion and thoracic spinal movement. These muscles attach at the ribs and vertebra and so motion at the costovertebral joints and functional vertebral units (two vertebrae) can be affected by muscle contraction and spasm, thereby leading to somatic dysfunction. Restrictions of the motion of vertebral units and costovertebral joints may cause pain, maintain muscle spasm, and adversely affect performance. The release of these restrictions may restore normal or baseline functioning of the shoulder complex and relieve abnormal and potentially pathologic stresses. Mobilization techniques may be enhanced when they are preceded by myofascial or ME techniques to relax the muscles.

Myofascial release Myofascial release (MFR), which was first described by Andrew Taylor Still and his early students, is a system of techniques that is directed at myofascial structures. Techniques can be described as either direct or indirect. Direct MFR techniques engage the restrictive barrier, and the tissue is then loaded with a constant force until tissue release/relaxation occurs.1 An example of this would be the very common practice of stretching myofascial tissues during warm up or rehabilitation. Indirect MFR involves gliding the dysfunctional tissues along the path of least resistance (away from the barrier) until free movement is achieved.1 MFR is generally well tolerated, and most athletes have experienced some type of MFR during their careers (i.e., stretching). MFR is often used to stretch muscles before competition and during rehabilitation. Myofascial techniques can restore range of motion and decrease pain, thus allowing for the earlier return of function. The goals of myofascial treatment include the relaxation of contracted muscles; increased circulation to an area of ischemia (often accompanying muscle spasm); increased venous and lymphatic drainage; and the stimulation of stretch reflexes in hypotonic muscles.8 Myofascial techniques are useful for interrupting the pain—muscle tension—pain cycle. Complications include increased pain, muscle spasm, and headaches (from cervical techniques).

Counterstrain Counterstrain is a system of diagnosis and treatment that considers the dysfunction to be a continuing, inappropriate strain reflex that

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is inhibited by applying a position of mild strain in the direction exactly opposite that of the reflex.1 The physiologic basis of counterstrain is based on the presumption that somatic dysfunction has a neuromuscular basis. The goals of counterstrain are to ‘‘relieve spinal or other joint pain by passively putting the joint into its position of greatest comfort’’ and to ‘‘relieve pain by reducing the continuing inappropriate proprioceptive activity.’’10 These goals are accomplished by specific, directed positioning around the point of tenderness, usually shortening the muscle in spasm by applying a strain to its antagonists; this interrupts the neurophysiologic reflex and relieves tension. Counterstrain is a very safe technique, and it is well tolerated by almost all athletes, including senior athletes in whom osteoporosis and osteoarthritis may be a concern. However, care should be taken when positioning the patient to minimize the development of conditions such as herniated disc, fracture (osteoporosis), or muscle spasm. With counterstrain, the diagnosis is made by finding tender points or areas of somatic or viscerosomatic reflexes within ligaments, muscles, or joints. These reflex points are characterized by palpable and rather superficial tissue texture changes that compromise a tense, fibrotic area approximately 1 to 2 cm in size. Tenderness at this point is greater than would be expected for the applied pressure (usually to the degree that there is blanching of the nail bed). Typically, tender points are located near the bony attachments of tendons and ligaments or in the belly of the muscles.6 There is some thought that these ‘‘Jones’ tender points’’ may be related to ‘‘Travell’s trigger points’’ and acupuncture points. However, trigger points radiate pain, which Jones’ tender points do not, and acupuncture points are more superficial and not necessarily associated with myofascial, ligamentous, or tendinous structures. Counterstrain is a passive technique that is based on positioning the area in a manner that shortens the involved muscle, thus ameliorating pain and dysfunction. When performing the technique, the physician places a finger pad over the tender point and, through joint positioning, relieves the intensity of pain at the tender point. Patients may report a decrease in pain, or the physician may note a change of tissue texture that reflects the release of the tender point. When pain is ameliorated to an acceptable degree (usually about 30%), the position is held for 90 seconds. This is the length of time that is usually required for the proprioceptive firing to decrease in frequency/amplitude and for the mechanoreceptors to reduce the stimulation of muscle contraction. At this point, the joint is slowly and deliberately moved into a neutral position by the physician without any patient effort. This lack of active patient effort during repositioning prevents the reinitiation of the inappropriate proprioceptive firing. Because counterstrain is passive and gentle, it is ideal for senior athletes, athletes recovering from surgery, and disabled athletes. Contraindications include an inflammatory process at the site of the tender point, which may be evidence of an underlying pathogenic process.

Facilitated positional release Facilitated positional release (FPR) is a system of indirect techniques developed by Stanley Schiowitz, DO, that is an enhancement of myofascial techniques.1 FPR is performed by placing the affected region in a neutral position and adding a facilitating force of compression or torsion to the tissues to induce relaxation or release of the tissues. FPR is directed toward the normalization of hypertonic muscles, both superficial and deep.8 The mechanism of FPR relates to the action of the muscle spindle gamma loop when the gain is suddenly decreased. As the spindles in the muscle become unloaded, there is a decline in the firing from the Ia fibers.11 The muscle begins to relax and subsequently lengthens. Complications of FPR are postulated to include fracture (osteoporosis) and the

Table 34.6

Categories and Types of Manipulation

Mobilization

Soft Tissue

Joint Manipulation

Articulatory

Myofascial release

High-velocity/lowamplitude technique

Facilitated positional release

Muscle energy Counterstrain

aggravation of herniated discs, although no studies have investigated the incidence of complications. FPR is performed with the use of three steps. First, the physician places the body region to be treated in neutral position (usually in the supine position). Second, compression, torsion, or a combination thereof is applied in an effort to decrease tissue tension, thus shortening the large muscle group; this position is held for 3 to 4 seconds. Finally, the treating position is released and the area is reassessed for somatic dysfunction.12

Articulatory techniques Articulatory techniques are passive methods that are designed to increase joint range of motion. These techniques include direct and indirect methods. With articulatory techniques, which are also called low-velocity/low- to moderate-amplitude techniques, the involved joint is gently assessed for full range of motion in all planes, and barriers are assessed (anatomic barriers if normal, restrictive barriers if pathologic).1 Restrictive barriers are engaged and gently moved through a series of maneuvers to increase range of motion. Low-velocity/low- to moderate-amplitude techniques are generally well tolerated by injured athletes because the techniques are passive and slow. Common indications include a decreased range of motion, especially among athletes who would benefit from a passive technique but who may not tolerate HVLA or who would not be able to participate in an active technique such as ME. To perform articulatory manipulation, the affected joint and the position at which the surrounding tissue is least taut are determined. The joint and tissue are moved into the directions of ease in all planes. The position is slightly exaggerated to increase the relaxation of the affected myofascial elements. Traction and compression are the most common forces applied to decrease tissue tension. The force and motion will commonly mobilize the joint and release the tissue to the point that there may be a sudden release as reflected by a pop, a click, or another sound. When mobilization and release occur, the forces are relaxed, and the region is brought back to a neutral position for the reassessment of the dysfunction. Articulatory techniques are very easily applied to appendicular and axial joints. An example of their use for the treatment of athletes is with the sacroiliac joint, which often develops somatic dysfunction among participants in jumping and collision sports. The sacroiliac joint is especially easily mobilized using the lower extremity as a lever to initiate motion at the joint with the athlete in the supine position. Also, athletes recovering from shoulder surgery tolerate this gentle, passive technique very well (Table 34.6).

CONCLUSION The osteopathic sports medicine physician combines the basic tenets of osteopathic medicine—the body is a unit; structure and function are reciprocally interrelated; and the body is selfhealing—with the needs of the athlete often in unique clinical settings, including in the office, on the sidelines, in a medical tent, or in a rehabilitation facility. The understanding that structure and function are interrelated and that somatic dysfunction can be a

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consequence of sports participation provides a unique perspective with regard to injury and rehabilitation. The use of manual medicine techniques to treat somatic dysfunction in an effort to restore function and enhance performance is an important aspect of osteopathic sports medicine, and it enhances traditional approaches to injury management and rehabilitation. The approaches and techniques described in this chapter are purely introductory, and they will certainly be expanded on as osteopathic sports medicine and rehabilitation medicine evolve.

REFERENCES

3. 4. 5. 6. 7. 8. 9. 10.

1.

2.

The Glossary Review Committee of the Educational Council on Osteopathic Principles: Glossary of osteopathic terminology. In AOA Yearbook and Directory of Osteopathic Physicians. Chicago, American Osteopathic Association, 2006. American Osteopathic Academy of Sports Medicine home page (Web site). Available at www.aoasm.org. Accessed December 12, 2006.

11. 12.

Zink J, Lawson W: An osteopathic structural examination and functional interpretation of the soma. Osteopathic Ann 1979;7(12):433-440. Schneider W, Dvorak J: Manual Medicine Therapy. Stuttgart, Georg Thieme Verlag, 1988. Ward R (ed): Foundations for Osteopathic Medicine, 2nd ed. Philadelphia, Lippincott Williams & Wilkins, 2003. Jones LH: Tender points. In Jones LH (ed): Strain and Counterstrain. Newark, OH, The American Academy of Osteopathy, 1988, pp 28-29. Simons DG, Travell JG: Myofascial Pain and Dysfunction: The Trigger Point Manual. Baltimore, MD, Lippincott Williams & Wilkins, 1992. DiGiovanna E, Schiowitz S: An Osteopathic Approach to Diagnosis and Treatment, 3rd ed. Philadelphia, Lippincott Williams & Wilkins, 2005. Stevinson C, Ernst E: Risks associated with spinal manipulation. Am J Med 2002;112(7):566-571. Jones LH: Strain and Counterstrain. In Jones LH (ed): Strain and Counterstrain. Newark, OH, The American Academy of Osteopathy, 1988, p 11. Carew T: The control of reflex action. In Kandel E, Schwartz J (eds): Principles of Neural Science, 2nd ed. New York, Elsevier, 1985. Savarese R, Capobianco J: OMT Review: A Comprehensive Review in Osteopathic Medicine, 3rd ed. Privately published, 2003.

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Core Stabilization Daniel L. Munton, MD; Geof D. Manzo, MS, ATC; and Elizabeth J. Caschetta, MS, ATC

KEY POINTS

. The core is comprised of groups of muscles that form the . . . .

lumbo—pelvic—hip complex. Power is generated in the core and transferred distally to the extremities. Athletes must display appropriate core strength, stability, and dynamic control to produce efficient movements. A thorough evaluation of the core must take place to evaluate possible weak links along the kinetic chain. In overhead athletes, evaluation of the scapula is an integral part of the assessment of core strength and stability.

stabilization force, and eccentric deceleration force in all three planes of movement during activity.5,6 The central nervous system plays an integral role in core stability. This system controls proprioception, which is the interpretation of sensory information and the response to position sense.7 Receptors in the skin, joints, muscles, and tendons send information to the central nervous system, which, in turn, sends appropriate information back to the muscles to provide neuromuscular control.7 In other words, core stability is the ability of the central nervous system to interpret the position of the body in space and to react accordingly. Appropriate muscle strength is needed to support the spine and to dynamically stabilize the body. With injury or a lack of training, proprioception can be altered, thus emphasizing the need for stabilization exercises.

CORE MUSCULATURE INTRODUCTION Core strength and stability are important and often overlooked aspects of athletics. Historically, rehabilitation and reconditioning programs have concentrated on the extremities. However, all power is generated in the core and transferred distally to the extremities. Therefore, neglect of the core during assessment and rehabilitation can impede an athlete’s future success. The purpose of this chapter is to explain the importance of core stability and its effect on the athlete.

CORE STRENGTH AND STABILITY DEFINED The term core refers to the lumbo—pelvic—hip complex, where the center of gravity is located.1,2 The muscles that make up this complex provide a stable base from which the extremities work. The term core strength refers to the strength and endurance of the muscles of the lumbo—pelvic—hip complex, whereas stability refers to the ability to use strength and endurance in a functional manner.3,4 Function is defined as a multiplanar movement that involves acceleration, deceleration, and stabilization.5,6 To be mechanically efficient, athletes must combine strength and stability training in their reconditioning programs. Core strength and stability together is called functional strength. Functional strength is the ability to produce concentric acceleration force, isometric

The muscles that make up the core can be divided into three groups: the abdominal muscles (Figure 35.1), the hip muscles (Figure 35.2), and the spinal muscles (Figure 35.3). The origins, insertions, and actions of these muscles are described in Tables 35.1, 35.2, and 35.3. In the overhead athlete, the scapular stabilizers (Figure 35.4) are also considered an essential core group.

THE IMPORTANCE OF CORE STABILITY IN ATHLETICS An athlete with a stable core will decrease the likelihood of injury as a result of his or her increased efficiency of movement (LOE: B).1,2,4,7-10 When the lumbo—pelvic—hip complex is stable, the peripheral muscles require less forceful contractions to produce the same amount of power.2,4,9 Adequate pelvic stability allows for the efficient transfer of power from the lower extremities to the upper extremities.7 For example, the act of throwing requires the legs and trunk to initiate movement and to transfer forces up the arm to the ball. Low back pain is a common complaint among both athletes and nonathletes.1,8 Up to 30% of college football players will miss at least one game as a result of lumbar pain.8 This pain is caused by the repeated mechanical irritation of the tissues that occupy the spine.1,2 Repeated irritation occurs as a result of the instability of

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Fifth rib

Internal intercostal External oblique muscle and aponeurosis

External intercostal

Transversus Linea alba Internal oblique Intercostal nerves

Internal oblique Rectus abdominis Superficial inguinal ring

the spine and pelvis. Therefore, core stabilization must be incorporated into a low back pain rehabilitation program.1,8

The assessment of core stability The assessment of the athlete must include all segments of the kinetic chain. Emphasis on one joint without attention to the cervical, thoracic, and lumbo—pelvic segments can lead to an incomplete picture of dysfunction. All links in the chain must have appropriate length/tension relationships for each progressive segment to be used efficiently. The evaluation of the core must include the assessment of posture, flexibility, strength, endurance, and stabilization.6 These

Inguinal canal

Figure 35.1 The abdominal core muscle group. (From Jenkins DB: Hollinshead’s Functional Anatomy of the Limbs and Back, 8th ed. Philadelphia, WB Saunders, 2002.)

components of assessment go hand in hand with determining the appropriate function of the athlete. Optimal posture is the correct alignment of each segment. Flexibility is the appropriate length of a muscle, which has a direct relationship with posture. For example, a tight psoas muscle will anteriorly rotate the pelvis, which, in turn, will increase lumbar lordosis. In addition, a tight muscle can affect the strength of other muscles. For example, the gluteus maximus will have decreased neural drive if the hip flexors are tight. This is called reciprocal inhibition.5,6 To make up for this decreased output, other muscles must compensate. Synergistic dominance will take place when synergists take over the role of the primary muscle.5,6 An example would be the hamstring dominance of hip extension when the neural drive to the gluteus

Gluteus medius

Gluteus minimus

Piriformis

Obturator internus and gemelli Obturator externus Quadratus femoris Biceps femoris

Gluteus maximus

Figure 35.2 The hip core muscle group. (From Jenkins DB: Hollinshead’s Functional Anatomy of the Limbs and Back, 8th ed. Philadelphia, WB Saunders, 2002.)

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Rectus capitis posterior minor Rectus capitis posterior major Splenius capitis

Obliquus capitis superior Obliquus capitis inferior

Semispinalis cervicis Semispinalis capitis Splenus cervicis C7 Ilicostalis cervicis

Longissimus capitis Longissimus cervicis Iliocostalis cervicis and thoracis

Longissimus cervicis Iliocostalis thoracis T6 Spinalis thoracis

Semispinalis thoracis

Longissimus thoracis

Iliocostalis lumborum

L1 Multifidi

Erector spinae

Figure 35.3 2002.)

The spinal core muscle group. (From Jenkins DB: Hollinshead’s Functional Anatomy of the Limbs and Back, 8th ed. Philadelphia, WB Saunders,

maximus is decreased. This compensation pattern leads to decreased efficiency and possible injury. Range of motion and flexibility must be assessed at the lumbo—pelvic—hip complex. The athlete must have a full range of motion at the hip to function appropriately. If the hip opens up too early during the cocking phase of throwing, all distal segments will rotate prematurely, and this may place additional stress on the anterior shoulder (LOE: E).11,12 Flexibility assessments at the hip should include the rectus femoris, the iliopsoas, the tensor fasciae latae, the hamstrings, and the piriformis. Strength should be assessed for the hip extensors, the back extensors, the abdominals, and the obliques. This can be

accomplished by manual muscle testing as described by Kendall and McCreary.13 Other authors have advocated additional testing procedures that may be more functional. Bliss4 recommends four tests for core stability: the prone bridge, the lateral bridge, torso flexor endurance, and torso extensor endurance. The athlete must hold each position with a neutral spine. Normative values in seconds are as follows: right lateral bridge, 83; left lateral bridge, 86; flexion, 34; and extension, 173 (LOE: E).4 Norms for the prone bridge have yet to be calculated, but 60 seconds seems to be ideal. Dynamic lower-extremity stabilization tests may include a single-leg stance, an overhead squat, a single-leg squat, and a step down. Inadequate lower-extremity stabilization may cause a

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Table 35.1

Abdominal Muscles of the Core

Muscle

Origin

Insertion

Action

Rectus abdominus External obliques Internal obliques

Pubic symphysis and pubic crest Inferior portion of the eighth rib

Cartilage of the fifth to seventh ribs and the xiphoid process Iliac crest and the linea alba

Iliac crest, inquinal ligament, thoracalumbar fascia

Cartilage of the last three or four ribs and the linea alba

Transverse abdominus

Iliac crest, inguinal ligament, lumbar fascia, cartilage of the inferior six ribs

Xiphoid process, linea alba, pubis

Flexion of lumbar and compression of abdomen during defecation, urination, forced exhalation, and childbirth Flexion of the lumbar vertebra when fired simultaneously; when fired unilaterally, lateral flexion and rotation Flexion of the lumbar and compression of the abdomen when fired bilaterally; lateral flexion and rotation when fired unilaterally Compression of the abdomen

Table 35.2

Hip Muscles of the Core

Muscle

Origin

Insertion

Action

Tensor fascia lata Gluteus maximus Gluteus medius and minimus Piriformis Obturator externus

Iliac crest

Lesser trochanter of the femur

Iliac crest, sacrum, coccyx Ilium

Iliotibial band, linea aspera of the femur Greater trochanter of the femur

Flexes and laterally rotates the thigh; flexes the trunk at the hip joint Extends the femur and laterally rotates the thigh Medially rotates the thigh; abduction

Anterior sacrum Inner surface of the obturator foramen, pubis, and ischium Outer surface of the obturator membrane Ischial spine

Greater trochanter of the femur Greater trochanter of the femur

Lateral rotation of the hip Lateral rotation of the hip

Greater trochanter of the femur

Lateral rotation of the hip

Greater trochanter of the femur

Lateral rotation of the hip

Ischial tuberosity

Greater trochanter of the femur

Hip stabilizer

Obturator internis Superior gemellus Inferior gemellus

Table 35.3

Back Muscles of the Core

Muscle

Origin

Insertion

Action

Quadratus laborum

Iliac crest, iliolumbar ligaments

Inferior border of the twelfth rib, transverse process of the first four lumbar vertebrae

Serratus anterior

Superior eight or nine ribs

Vertebral border and the inferior angle of the scapula

Trapezius

Nuchal line of the occipital bone and the spines of the seventh cervical and all twelve thoracic vertebra

Erector spinae Multifidus

Longitudinal axis of the back

Lateral third of the clavicle and the acromion process, medial margin of the acromion and the superior lip of spine of scapula, the tubercle at the apex of the spine of the scapula Onto the ribs, upper vertebra, and head

Extends the lumbar region when fired bilaterally; laterally flexes the lumbar region when unilaterally fired; moves the twelfth rib inferiorly during forced exhalation Abducts and rotates the scapula upward; elevates the ribs when the scapula is stabilized Elevates, adducts, depresses, and upwardly rotates the scapula, along with help to extend the head

Sacrum, ilium, transverse processes of the lumbar, thoracic, and inferior four cervical vertebra

Spinous process of a more superior vertebra

Principal extensors of the vertebra Extends the vertebral column when fired bilaterally; when fired unilaterally, laterally flexes the vertebral column and rotates the head

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Levator scapulae Ligamentum nuchae Rhomboideus minor Trapezius

Supraspinatus Spine of scapula Intraspinatus Rhomboideus major Teres minor Teres major

Serratus anterior Deltoid Latissimus dorsi

Crest of ilium

Figure 35.4

The scapular stabilizers. (From Jenkins DB: Hollinshead’s Functional Anatomy of the Limbs and Back, 8th ed. Philadelphia, WB Saunders, 2002.)

pitcher to rush through the delivery and to place increased loads on the shoulder or elbow (LOE: E).12 The scapula should be included in the core assessment of the overhead athlete. The scapula should be evaluated both statically and dynamically. Manual muscle testing can be undertaken, but it can be tedious. A scapular pinch test will decrease assessment time. The athlete should isometrically pinch the shoulder blades together and hold this position 15 to 20 seconds; burning in the periscapular area indicates weakness. Kibler14 also advocates the lateral slide test. A measurement from the inferior angle of the scapula to its associated spinous process is taken with the arm at the side, with the hands on the hips, and with the arms abducted and internally rotated at 90 degrees. A positive test is a 1.5 cm or greater difference on one side as compared with the other.14

REHABILITATION AND RECONDITIONING The rehabilitation and reconditioning program should be systematic and progressive.3-6,14-17 Training begins with the most

challenging environment that an athlete can control.6 Local muscles such as the transverse abdominus and the multifidus, however, must be activated before the global muscles of the lumbo—pelvic—hip complex. The progression is from muscle activation to dynamic stabilization.3,4 Tactile, auditory, and visual feedback may be necessary at first.3,4,17 Cues can be eliminated as the athlete masters a specific task. For example, the transverse abdominus may need several cues to fire correctly. Many athletes have difficulty firing the transverse abdominus as a result of previous concentration on the other abdominal muscles for stabilization. When an athlete masters the active contraction of the transverse abdominus, cueing can be eliminated, and more dynamic movements can take place. Progression guidelines are as follows: simple to complex, stable to unstable, static to dynamic, and single plane to multiplane.3-6,17 Flexibility is an important aspect of the core stabilization program. Flexibility training in conjunction with stability training yields results. Appropriate length/tension relationships must be maintained throughout the kinetic chain for efficient movements to take place. All muscles of the lumbo—pelvic—hip complex must be flexible and strong.

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Figure 35.5

Pelvic tilt.

CORE STABILIZATION EXERCISES Pelvic tilt progression In a study using electromyography, the following series of exercises was found to activate the abdominal muscles significantly more than abdominal hallowing exercises (LOE: B).18 The athlete is supine with the feet flat on the table. He or she should be instructed to flatten the low back onto the table and then hold it there for 5 seconds. A good verbal cue for this exercise is to instruct the athlete to pull his or her belly button back toward the spine while flattening the back. Pulling the belly button back toward the spine without tilting the pelvis is an abdominal hollowing (drawing in) exercise only. Breathing should be normal while performing the pelvic tilt (Figure 35.5). When the athlete masters the pelvic tilt, he or she may be progressed to bridging exercises. The athlete performs the pelvic tilt and then lifts his or her hips off of the table and holds them up for 5 seconds (Figure 35.6). The final progression of the supine pelvic tilt is to have the athlete extend one lower extremity during the bridge. Lower extremities should alternate with each bridge. To make this exercise

Figure 35.7

Bridge with hamstring curl on a physioball.

more difficult, the upper extremities can be alternated with the lower extremities.

Quadruped progression The athlete is positioned on his or her hands and knees and instructed to draw in the abdominal muscles. The lower extremity on one side is then extended and held for up to 5 seconds, and the extremities should be alternated. A technique that can be used to aid in the proper performance of this exercise is to place a dowel across the back, in line with the spine. The dowel should not move. When this is mastered, the dowel can be placed perpendicular to the spine, and it must then be held in a level position. The next progression is to extend both the upper and lower extremities on the same side and hold. The final progression of the quadruped exercise involves the athlete extending the opposite upper and lower extremities at the same time. A dowel can be used for this exercise as well.

Physioball exercises Seated physioball The athlete is seated on the physioball and raises one lower extremity off the ground. This exercise can be advanced by alternating the opposite upper and lower extremities.

Bridging The athlete is supine with the feet on the ball. The abdominals are drawn in, and the athlete lifts his or her hips off of the ground. Another way to perform a bridge on the physioball is to have the athlete seated on the ball and then to walk his or her legs out away from the ball. The hips should be level and must not sag. To make the bridge more difficult, one lower extremity can be extended.

Crunch A simple crunch can be performed on the physioball. The athlete starts in a supine position with the back supported on the ball. A crunch is then performed. A medicine ball can be added to provide resistance.

Wall squat Figure 35.6

Bridge.

The physioball is placed between the athlete and the wall. The athlete draws in his or her abdominal muscles and then performs a

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Figure 35.8

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Core stabilization

Walkouts.

Figure 35.10

Side-lying plank.

Gluteus medius exercises Clamshell The athlete is positioned on his or her side with the knees and hips bent. With the feet together, the athlete rotates his or her top knee up and back. The trunk should not rotate. To progress this exercise, the athlete extends his or her knee and performs a single-leg raise in abduction with slight extension.

Monster walk A resistance band is placed around the athlete’s ankles. The athlete assumes an athletic stance position and side shuffles a set distance.

Plank exercises Prone plank Figure 35.9

Prone plank.

squat to parallel. Moving the arms or adding a medicine ball can further challenge the core.

Hamstring curl An additional progression to the bridge exercise is to add a hamstring curl. The athlete is supine with his or her feet on the physioball, and he or she then performs a bridge. At the completion of the bridge, the athlete performs a hamstring curl while holding the bridge (Figure 35.7).

Push-ups Wall push-ups and standard push-ups can be progressed by using a physioball. The athlete must draw in his or her abdominals before performing the push-up.

Walkouts The athlete is prone on the physioball with his or her hands in contact with the ground. The athlete then walks forward while keeping the abdominals tight and the spine neutral. This exercise can be progressed from slow to fast (Figure 35.8).

The athlete props up on his or her forearms and toes while in the prone position. The spine should be neutral, and this position is then held for 15 seconds. The athlete can progress to 30 seconds as stabilization improves (Figure 35.9).

Side-lying plank The athlete props up on his or her forearm in the side position while drawing in the abdominals. This position is held for 15 seconds and progressed to 30 seconds as stability improves (Figure 35.10).

Medicine ball exercises Crunches Athletes can progress crunching exercises by using a medicine ball. Oblique crunches and trunk twisting maneuvers can be progressed using medicine balls as well.

Lunges With the arms outstretched and holding the medicine ball, the athlete lunges forward and twists to the side of the lunging leg. The clinician should ensure proper form. The knees should be in line with the foot, and the knees should not go past the toes. The abdominals should be tight, and the spine should be neutral. (Figure 35.11).

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Core stabilization exercises 451

Figure 35.11

Lunge with medicine ball.

Figure 35.12

Physioball Y.

Figure 35.14

Physioball 90/90 external rotation.

Figure 35.15

Push-up plus on a wobble board.

Scapular stabilization exercises Physioball Y The athlete assumes a prone position on the physioball with the chest off of the ball. The shoulder blades are drawn back and down while the upper extremities are lifted up to form a ‘‘Y.’’ The thumbs should be pointing upward (Figure 35.12).

Physioball T The athlete is positioned in a similar fashion as he or she is to perform the physioball Y. The shoulder blades are pinched together while the upper extremities are horizontally abducted with the shoulder externally rotated. The upper extremities should not go beyond parallel with the ground because this places additional stress on the anterior shoulder (Figure 35.13).

Physioball 90/90 external rotation

Figure 35.13

Physioball T.

The athlete is positioned prone on the ball as described previously. The elbows are bent at 90 degrees and then horizontally abducted to 90 degrees. The athlete then externally rotates to 90 degrees, lowers, and repeats (Figure 35.14).

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Push-up ‘‘plus’’ on the wobble board The athlete assumes a push-up position with his or her hands on the outer edge of the wobble board. The shoulder blades are protracted, and the spine is held in neutral. The athlete will hold this position for 15 seconds, and this is progressed to 30 seconds as stability improves (Figure 35.15).

peripherally, he or she may progress back to throwing. The overhead thrower should take part in an interval throwing program. Progression is from a short to a long toss and then finally off the mound. Other overhead athletes (i.e., tennis players) should follow a similar pattern of strengthening and sport-specific rehabilitation progression.

CORE STABILITY AND THE OVERHEAD ATHLETE

CONCLUSION

The role of the scapula must not be overlooked when discussing core stability in the overhead athlete. The scapula attaches to the trunk via a suction-like mechanism that is provided by the serratus anterior and the subscapularis.15 Three groups of muscles attach to the scapula.14 The first group is made up of the trapezius, the rhomboids, the levator scapulae, and the serratus anterior. The second group includes the deltoid, the biceps, and the triceps. The rotator cuff makes up the final group. The scapula serves three functions.14,15 The first function is to maintain dynamic stability. The scapula must move along with the humerus in a coordinated manner to maintain the humeral head within the glenoid. The second function is to serve as a base for muscle attachment. These muscles serve as important force couples to maintain humeral head congruity. The lower trapezius and the serratus anterior are a pivotal force couple for acromial elevation.14-16 The third function of the scapula is to provide proximalto-distal energy transfer. The scapula is the link between the legs and the trunk to the arm and hand. For the scapula to function correctly, the distal segments must be working correctly.14 Hip and spine extension are necessary for full scapular retraction.17,19 Kibler14 describes scapular retraction as a ‘‘full tank of energy’’ that is necessary for efficient force production during throwing. In addition, the muscles that control scapular movement must be strong. The serratus anterior and the lower trapezius must upwardly rotate the scapula to elevate the acromion14-16; failure to do so may lead to impingement. The serratus anterior must also protract the scapula to keep up with a rapidly internally rotating and horizontally adducting humerus during the throwing motion. The inability of the scapula to keep up with the humerus may cause injury to the posterior rotator cuff and lead to instability (LOE: B).15 The middle and lower trapezius eccentrically contract to control protraction because too much protraction can close off the subacromial space and lead to impingement.14,15 When the scapula is functioning correctly, the rotator cuff has a stable base from which to work. The rehabilitation and reconditioning of the overhead athlete should involve the mimicking of sport-specific movements.6,15-17 This can be initiated early during the process. An overhead athlete with a rotator cuff injury can begin core strengthening before rotator cuff work. Scapular stabilization should be initiated as well (see Figures 35.12 through 35.15). The rotator cuff is dependent on a stable base, and this base must be developed before isolated rotator cuff exercise (LOE: E).16,17 Closed kinetic chain exercises in low-range elevation can be initiated early as well to promote cocontraction of the rotator cuff. An athlete can do this in a standing position with an athletic stance to promote the proximal-todistal transfer of energy.16 After an athlete has developed appropriate core stability; a full, pain-free range of motion; and strength and endurance

Athletes must display appropriate core strength, stability, and dynamic control of the lumbo—pelvic—hip complex produce efficient movements. A strong core is necessary for force absorption and transfer in a proximal-to-distal fashion. A thorough evaluation of the core must take place to determine possible weak links along the chain, and these ‘‘weak links’’ must be corrected for appropriate length/tension and force couple relationships to exist. An athlete with a strong, stable core will be able to transfer energy efficiently with more power and with less stress distally. This makes for a productive, successful athlete.

REFERENCES 1. Hodges PW: Core stability exercise in chronic low back pain. Orthop Clin North Am 2003;34:245-254. 2. Arnheim DD, Prentice WE. Principles of Athletic Training, 11th ed. St. Louis, Mosby, 2003. 3. Standaert CJ, Herring SA, Pratt TW: Rehabilitation of the athlete with low back pain. Curr Sports Med Rep 2004;3:35-40. 4. Bliss LS, Teeple P: Core stability: the centerpiece of any training program. Curr Sports Med Rep 2002;4:179-183. 5. Clark MA, Russell AM: Low Back Pain: A Functional Perspective. Thousand Oaks, CA, National Academy of Sports Medicine, 2002. 6. Clark MA: Rehabilitation: core competency underlies functional rehabilitation. Biomechanics 2000;7(2):67-73. 7. Houglum PA: Therapeutic exercise for athletic injuries. In Houglum PA (ed): Athletic Training Education Series. Champaign, IL, Human Kinetics, 2001, pp 496-562. 8. Eck JC, Riley LH: Return to play after lumbar spine conditions and surgeries. Clin Sports Med 2004;13(1):367-379. 9. Allen S: Core strengthening. Gatorade Sports Science Exchange Roundtable 2002;13(1):1-4. 10. Mandelbaum BR, Silvers HJ, Watanabe DS, et al: Effectiveness of a neuromuscular and proprioceptive training program in preventing anterior cruciate ligament injuries in female athletes. Am J Sports Med 2005;33(7):1003-1009. 11. Ceasrine V, Mundorff C: Preseason screening for the overhead-throwing athlete. NATA News 2004;17(2):41-47. 12. Cappel KR: How lower extremity biomechanics affects upper body pitching. Biomechanics 1996;3(4):22-26. 13. Kendall FB, McCreary EK: Muscle Testing and Function, 4th ed. Baltimore, Md, Williams & Watkins, 1993, pp 215-226, 284–293. 14. Kibler WB: The role of the scapula in athletic shoulder function. Am J Sports Med 1998;26(2):325-337. 15. Voight ML, Thompson BC: The role of the scapula in the rehabilitation of shoulder injuries. J Athl Train 2000;35(3):364-372. 16. Wilk KE, Andrews JR: Current concepts in the rehabilitation of overhead throwing athlete. Am J Sports Med 2002;30(1):136-151. 17. McMullen J, Uhl TL: Kinetic chain approach for shoulder rehabilitation. J Athl Train 2000;35(3):329-337. 18. Drysdale CL, Earl JE, Hertel J: Surface electromyographic activity of the abdominal muscles during pelvic tilt and abdominal hallowing exercises. J Athl Train 2004;39(1):32-36. 19. Walendzak D: Rehabilitation: lower extremity theory enhances shoulder rehabilitation. Biomechanics 1998;5(10):45-51.

CHAPTER

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Physical Therapy Modalities MAJ Guy R. Majkowski, PT, DSc, OCS, FAAOMPT, and Norman W. Gill III, PT, DSC, Cert MPT, OCS, FAAOMPT

KEY POINTS

CRYOTHERAPY

.

Cryotherapy is the most commonly used modality in sports medicine. The immediate goal of cryotherapy after acute injury is purported to be the cooling of the involved tissues to control pain and to decrease blood flow to the area. The theory behind reducing blood flow to the area is to minimize the impact of secondary tissue hypoxia resulting from edema. Karunakara and colleagues determined that an ice bag applied to the forearm for a cycle of 20 minutes on, 10 minutes off, 10 minutes on, and 10 minutes off was able to reduce blood flow in the forearm/wrist (LOE: C).28 However, the authors recommended that, if decreased blood flow was the goal of therapy, treatment times of up to an hour are indicated. Cryotherapy has additional physiologic effects that are listed in Table 36.1. Despite its prominent role in the widely advocated treatment acronym PRICE (Protection, Rest, Ice, Compression and Elevation) for the early management of acute injuries, limited evidence exists to guide the clinician in recommending the best method for the application of cryotherapy. Debates continue regarding the best method of application; however, the evidence recommends crushed ice in a bag with a wet towel as being the most effective.29,30 Zemke and colleagues compared ice massage to the use of an ice bag and found no difference between methods except that the ice massage reached its lowest temperature in approximately 18 minutes as compared with an ice bag, which reached its lowest temperature after approximately 28 minutes at mean depth of 1.7 cm (LOE: C).31 The authors were unable to confirm that subcutaneous tissue variations effected the reduction in tissue temperature.31 Enwemeka and colleagues found that during a 20minute cold pack treatment, tissue temperatures at depths of more than 1 cm remained unchanged.32 However, after removing the cold pack, the researchers found that the deeper tissues conducted heat to the superficial tissue, thereby resulting in a deep tissue (3 cm deep) temperature reduction up to 40 minutes after treatment (LOE: C).32 Another research team investigated the effectiveness of commonly prescribed home treatments (a mixture of water and alcohol, gel packs, and frozen peas) as compared with an ice bag with a wet towel. Kanlayanaphotporn and colleagues validated the common practice of using an ice bag in a wet towel and also reported that a mixture of water and alcohol was superior to gel packs and frozen peas for reducing superficial skin temperatures to therapeutic levels (LOE: B).29 Although basic scientific studies conducted on knee

. . .

.

Physical therapy modalities should be used as part of a multifaceted approach to rehabilitation. The proper selection of the modality depends on the stage of healing and the goal of treatment. Within the multimodal approach, modalities have a variable and proportional contribution that is based on the nature and extent of the injury, the body area, and the tissue healing timeline. Although there is reasonable underlying scientific evidence for most modalities, there is limited evidence for clinical efficacy as a result of the heterogeneity of samples, poor research designs and methodology, and the diverse parameters available for each modality. A lack of evidence is not evidence against using a particular modality.

INTRODUCTION Physical therapy modalities play a vital role in a multimodal approach to rehabilitation, but they represent only a fraction of the total treatment options available to provide comprehensive management of the injured athlete (Figure 36.1). Although it is important that the clinician understand the general goals of each modality, it is more critical to know when to use a particular modality on the basis of the tissue healing timeline. Modalities typically serve as adjunctive treatments during the subacute or chronic phases, and they can serve as the primary treatment during the acute phase of injury. Physical therapy modalities encompass a wide range of therapeutic interventions that use various forms of energy to affect human tissue (Figure 36.2). Although alternative treatment options such as lasers, magnets, and ultraviolet lights are also referred to as ‘‘modalities,’’ this chapter addresses those modalities that are most often employed as part of sports medicine rehabilitation (see Figure 36.2). Many modalities possess a broad, basicscience evidence base for their underlying principles or mechanisms1-3; however, there is much less evidence in the applied sciences to support their clinical use. Recent attempts to validate therapeutic efficacy are limited by poor methodology, a lack of homogenous study samples, and the clinical practice of using multiple simultaneous modalities.1,3-27

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MULTIMODAL APPROACH TO REHABILITATION Bracing and Activity taping modification 5% 10% Medication 5%

Patient education 20%

Manual therapy 10%

Physical therapy modalities 20% Therapeutic exercise 30%

Figure 36.1 Typical percentage breakdown of the contribution of each therapeutic intervention to the comprehensive management of an injured athlete.

patients confirm that superficial cryotherapy with compression via a Cryocuff (Aircast, Inc, Summit, NJ) can reduce intra-articular knee temperatures up to 68C after knee arthroscopy (LOE: C)2 and after anterior cruciate ligament reconstruction (LOE: C),33 current clinical studies have been unable to demonstrate patient-oriented evidence in the form of improved clinical outcomes (LOE: B).34-36 In general, cryotherapy is relatively safe. The literature describes the possible risks of frostbite and nerve damage as the only severe complications that can directly result from this modality; therefore, caution is required in its application.37 These risks are minimized by careful screening for contraindications (see Table 36.1), supervising its application (i.e., frequently checking the area), reducing treatment duration to 20 minutes, and avoiding areas of superficial nerves (e.g., fibular head). Ultimately, insufficient evidence exists to make strong conclusions as a result of a lack of randomized controlled trials, poor methodology, and a tendency to use ice with additional interventions8,13,16,17 (Table 36.2).

Techniques and equipment Ice
Body area targeted: large body area such as the spine or the thighs; large joints such as the knee, shoulder, or ankle


Advantages: conforms to surface contours, inexpensive, and widely available
Temperatures: target tissue temperature—15 to 258C
Techniques:
Ice massage
Crushed ice in wet towel
Ice cubes in plastic bag
Frozen mixture of water and isopropyl alcohol (2:1 or 3:1 ratio)
Typical progression of sensation after application: freezing, burning, aching, and numbness
Special considerations: increased awareness of potential for superficial nerve injury (e.g., common peroneal nerve around fibular head); prevent injury by padding area or keeping ice off of the superficial nerve

Cold whirlpool bath
Body area targeted: primarily used for extremities (typically the ankle, knee, wrist, and hand)
Advantages: rapid circumferential cooling via convection; allows for range of motion and weight-bearing activities during treatment
Disadvantages: costly equipment, requires daily tank cleaning, limited portability, and restricted to aforementioned body areas
Temperatures: target water temperature at 10 to 158C (50 to 608F)
Techniques: static cooling by submerging the extremity in water versus therapeutic exercise during immersion (range-of-motion or weight-bearing exercises); optional home treatment with the patient placing either the foot or hand into an ice water bucket and performing gentle exercises as instructed by the provider; duration of treatment should be 12 to 20 minutes or until numb
Special consideration: increased awareness that digits cool more rapidly than larger joints

Gel packs
Body area targeted: large body area such as the spine or the thighs; large joints such as the knee, shoulder, or ankle
Advantages: more readily conforms to surface contours than ice cubes; reusable
Temperatures: gel packs stored at 15 to 178C (1 to 58F); tissue temperature dropped 3.788C for superficial tissue (skin) and 2.498C for deep tissue (1-cm depth) after a 20-minute application (LOE: C)32
Techniques: wet or dry cloth barrier placed between the gel pack and the skin; target treatment time of 20 minutes

Physical therapy modalities

Cryotherapy

Electrotherapy

Thermotherapy

Ice

Transcutaneous electrical nerve stimulation (TENS)

Superficial heating

Cold whirlpool Gel packs Chemical packs Vapo-coolant Cold-compression Cryokinetics

Interferential current stimulation (IFC) Neuromuscular electrical stimulation (NMES) High-volt galvanic stimulation (HVGS) Iontophoresis

Figure 36.2 therapy.

Subtypes of common modalities in physical

Over the counter (OTC) Heating wraps Moist hot pack Fluidotherapy Paraffin baths Deep heating Ultrasound Shortwave diathermy

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Cryotherapy 455

Table 36.1

Cryotherapy General Effects, Indications, and Contraindications

General Effects

Indications

Contraindications

Joint and soft-tissue stiffness

Pain

Circulatory or sensory impairments

Analgesic or sedative effect

Loss of joint motion

Cold hypersensitivity

Muscle relaxation

Muscle spasm

Cold uticaria (hives)

Reduced nerve conduction velocity

Acute inflammation

Cold-induced hemoglobinuria

Reduced motor power

Edema

Cryoglobinemia

Reduced muscle spasm

Communication impairments

Reduced blood flow

Raynaud’s syndrome

Reduced metabolic tissue demand Reduced joint proprioception

Chemical packs
Advantages: portable without external cold source; conforms to body area
Disadvantages: relatively expensive; one-time use; small size limits treatment area
Special consideration: beware of the potential for the rupture of the pack and superficial skin burns

Vapocoolant sprays (e.g., fluoromethane spray)
Body area targeted: used extensively on neck, shoulder girdle, and thigh muscles; two main uses are as a counterirritant while stretching (spray and stretch technique) and as treatment for myofascial trigger points (desensitization)
Advantages: portable without external cold source; provides immediate analgesia
Disadvantages: relatively expensive; transient effect
Techniques: apply stretch to muscle; protect eyes/nose/mouth from spray; spray in parallel lines approximately 2 inches apart;

Table 36.2

hold applicator 12 to 18 inches from target area; increase stretch as tolerated
Special consideration: use only on intact skin; avoid inhalation of spray; allow skin adequate recovery time

Cold-compression units
Body area targeted: knee, shoulder, ankle, elbow, thigh, leg/ calf, or forearm
Advantage: most units are portable with ice water maintained in an insulated container during use; can provide 360-degree cooling of a joint; avoids melting ice
Technique: joint/body part is secured in a pad/sleeve; ice water is forced into (or circulated through) a tube and into the pad/sleeve surrounding the joint or body part to provide simultaneous cooling and compression; can provide cooling from 30 minutes up to several hours (continuous circulation machines)

Summary of Evidence for Cryotherapy

Body Region

Condition

Usefulness or Effect

Evidence

Reference

Knee Wrist

Joint proprioception S/P CTR

Decreased Benefit

C B

Uchio et al, 200351 Hochberg 200152

Knee

S/P arthroscopy

Benefit

B

Lessard et al, 199753

Nonspecific

—

Benefit

SR

Swenson et al, 199637

Knee

S/P ACLR

No Benefit

B

Konrath et al, 199654

Knee

S/P ACLR

Benefit

B

Dervin et al, 199835

Knee

S/P ACLR

No Benefit

B

Edwards et al, 199634

Ankle

Soft-tissue injuries

Benefit

CR

Ogilvie-Harris and Gilbart, 199555

Lumbar

LBP

ID

SR

French et al, 200613

Elbow Elbow

DOMS DOMS Soft-tissue injuries Acute soft-tissue injuries Blood flow

No benefit No benefit Benefit ID Decreased

B C SR SR C

Yackzan et al, 198456 Paddon-Jones et al, 199757 Mac Auley, 200158 Bleakley et al, 20068 Karunakara et al, 199928

Forearm

Recommendation: The current evidence suggests the following: Protect the skin from frostbite by placing a cloth barrier between the ice and the patient. Protect superficial nerves by placing padding over the nerve or keeping ice off of these areas. Recommended crushed ice wrapped in a wet towel or a mixture of water and alcohol. The duration of treatment depends on the goal of treatment: pain control and deep tissue cooling = 20 minutes; reduce blood flow = alternating 10 minutes on and 10 minutes off for 1 hour. Evidence ratings: A, double-blind study; B, clinical trial, >20 subjects; C, clinical trial, 1 cm) Ultrasound
Heat transfer by conversion
Physics: sound waves formed by the vibration of a piezoelectric crystal are absorbed within the tissue
Body area targeted: deeper tissue and smaller areas, typically the shoulder, neck, elbow, ankle, and knee

Table 36.4


Depth of penetration: 1 to 2 cm at 3 MHz and 4 to 6 cm at 1 MHz frequencies
Power: 1.5 watts/cm2 typically used
Technique: The area is prepared and draped. Ultrasound gel (coupling agent) is applied to the sound head using small, slow, circular movements, and it is applied in an area not to exceed 4  4 inches. With continuous ultrasound, the sound head must be in motion at all times, or it will burn the tissue. Despite previously held beliefs that pulsed ultrasound does not provide a thermal effect, Gallo and colleagues found an equivalent thermal effect when comparing pulsed ultrasound (3 MHz, 1.0 watts/cm2, 50% duty cycle, 10 minutes)

Summary of Evidence for Superficial Heat

Body Region

Condition

Usefulness or Effect

Evidence

Reference

Neck

Pain

ID

CR

Wright and Sulka, 20011

Neck

Acute and chronic

ND

SR

Philadelphia Panel, 200122

Shoulder

Calcific tendinitis Capsulitis Bursitis, tendinitis Nonspecific pain

ND ID ID ID

SR

Philadelphia Panel, 200121

Lumbar

LBP Acute LBP

Benefit Benefit

SR B

French et al, 200613 Nuhr et al, 200459

Lumbar

Acute LBP Subacute LBP Chronic LBP Postsurgical LBP

ND ND ID ND

SR

Philadelphia Panel, 200124

Knee

PFS Postsurgical OA Tendinitis

ND ND ND ND

SR

Philadelphia Panel, 200123

Hamstring

Flexibility Flexibility

Benefit* No benefit

B B

Cosgray et al, 200443 Funk et al, 200141

Quadriceps

DOMS

No benefit

B

Jayaraman et al, 200460

Recommendation: Overall, there are insufficient or lacking clinical trials to establish a strong recommendation for or against superficial heat. Recent reviews indicate moderate evidence for a small, short-term decrease in pain and disability in acute and subacute patients with LBP, with an additional benefit observed from adding exercise. *Range of motion gained during treatment returned to baseline in less than 24 to 48 hours. Evidence ratings: A, double-blind study; B, clinical trial, >20 subjects; C, clinical trial, 20 subjects; C, clinical trial, 20 subjects; C, clinical trial, 300. Get a preparticipation ECG, eye exam, monofilament test for peripheral neuropathy, and creatinine level. Avoid weight-bearing activities in patients with insensitive feet (monofilament log is positive). Avoid high-intensity exercise and weight training if proliferative retinopathy is present. Eat some extra carbs prior to exercise if blood glucose < 100. Keep hydrated—early and often (2 full glasses 2 hours prior to exercise). Avoid exercise at the weather extremes. Always wear good shoes, and check your feet for blisters after exercise. Wear a diabetic bracelet or tag when exercising, or always exercise with a friend who is aware of your condition.

ECG, electrocardiogram; HRR, heart rate reserve.

The exercise prescription for diabetics should follow the general outline of mode, intensity, duration, and progression. Diabetics should start at a lower intensity (around 40% of the heart rate reserve) and progress to the recommended 50% to 70% of the heart rate reserve.51 Resistance training should also be prescribed for diabetics because it has been shown to improve insulin sensitivity to roughly the same extent as aerobic exercise.52 Weight loss is not necessary to benefit from the effects of physical activity on glucose tolerance and insulin clearance rates.20 Exercise should be avoided on days when the fasting blood glucose is greater than 250 mg/dL or when ketosis is present (Table 39.6).

The obese patient The exercise prescription for the obese should emphasize total energy expenditure and the prevention of weight gain. Although a return to ideal body weight would be optimal, regardless of weight loss, meeting the recommendations for exercise will improve the health-related benefits. Modest reductions in weight loss have been associated with significant improvements in hypertension and lipid profiles in the obese.53 Exercise improves body composition by replacing fat with muscle, especially through resistance training. To maintain weight loss, a significant amount of kilocalories must be expended per week (2500 to 2800 kcal), which generally translates into 45 to 90 minutes of moderateintensity physical activity per session.

Table 39.7

Exercise Prescription for Obesity

Maximizing Benefits

Minimizing Side Effects

Start at a intensity and duration comfortable for the patient. Manipulate intensity and duration to achieve a high total weekly energy expenditure > 2000 kcal. Exercise combined with diet control is more effective at maintaining weight loss than diet alone.

Test for diabetes and screen for cardiovascular side effects. Alternate between weight-bearing and non—weight-bearing activities. Avoid outdoor exercise during hot weather. Avoid exercise that place strain on the back (e.g., push-ups, squats, sit-ups).

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References 505

Table 39.8

Exercise Prescription for Hypertension

Maximizing Benefits

Minimizing Side Effects

A limited increase in aerobic activity has significant benefits in preventing and treating hypertension. Daily exercise can aid in optimizing control of hypertension for patients already on antihypertensives. Resistance training is a recommended secondary exercise mode with lower weights, higher repetitions, and techniques that limit Valsalva.

Avoid exercise if the resting blood pressure is > 200/110. Screen for cardiovascular disease. Beware of dehydration if on diuretics. Beware of orthostasis if on beta blockers.

should be involved in formulating an individualized exercise program. Translating these guidelines into practice may be the most effective approach to improving our nation’s health.

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4.

5.

6.

Many of the side effects of exercise for the overweight or obese patient result from the increased health risks associated with obesity. Obese patients are more likely to suffer from arthritis, cardiovascular disease, and diabetes, and they therefore may be subject to the risks of exercise with these conditions.54 In addition, obese patients have an increased risk of musculoskeletal injury, low back pain, and hyperthermia during exercise.6,55 Initially, the prescribed mode, intensity, and duration may need to begin below the recommendations for health benefits and weight loss to avoid side effects. They can then progress over the course of several weeks to achieve energy expenditure goals (Table 39.7).

The hypertensive patient The Framingham Heart Study has estimated that 75% of hypertension in men and 65% of hypertension in women is directly attributable to excess body weight.56 For patients in the prehypertensive range (systolic blood pressure, 120 to 139 mm Hg; diastolic blood pressure, 80 to 89 mm Hg), lifestyle management including an exercise prescription is the recommended initial treatment. Exercise prescriptions should follow the same general outline as the standard population, with added emphasis on a frequency of most or all days of the week to gain the benefit of acute blood pressure lowering. Exercising at intensities in the moderate range (40% to 70% of the heart rate reserve) appears to reduce blood pressure as much as exercise at higher intensities.57 Exercise should also be added to patients with a systolic blood pressure in the higher ranges (>160 mm Hg) only after medication management has been initiated. Exercise should be avoided if the resting blood pressure exceeds 220/100 mm Hg. Although resistance training should not be used as a primary exercise mode in hypertensive patients, contrary to popular belief, weight training is recommended as an adjunct exercise for these individuals. Resistance should be low, involve a great number of repetitions, and use techniques that minimize the Valsalva maneuver to maximize benefits and minimize blood pressure elevations during exercise58 (Table 39.8).

CONCLUSION Evidence-based physical activity counseling must become an integral component of routine patient care in the primary care setting to limit health risks of an increasingly sedentary population and to fully use exercise as an effective treatment for a number of chronic medical problems. Patients should be informed of the significant health benefits derived from moderate-intensity exercise and

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36.

37.

38. 39.

40.

41.

42. 43. 44.

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Pope RP, Herbert RD, Kirwan JD, Graham BJ: A randomized trial of preexercise stretching for prevention of lower-limb injury. Med Sci Sports Exerc 2000;32(2):271-277. Giri S, Thompson PD, Kiernan FJ, et al: Clinical and angiographic characteristics of exertion-related acute myocardial infarction. JAMA 1999;282(18):1731-1736. Mittleman MA, Maclure M, Tofler GH, et al: Triggering of acute myocardial infarction by heavy exertion: protection against triggering by regular exercise. N Engl J Med 1993;329(23)1677-1683. Maron BJ: Sudden death in young athletes. N Engl J Med 2003;349:1064-1075. Burke AP, Farb A, Virmar R, et al: Sports-related and non-sports-related sudden cardiac death in young adults. Am Heart J 1991;121:568-575. Devlin JT, Ruderman N: Diabetes and exercise: the risk-benefit profile revisited. In Ruderman N, Devlin JT, Schneider SH, Krisra A (eds): Handbook of Exercise in Diabetes. Alexandria, VA, American Diabetes Association, 2002. Eakin EG, Glasgow RE, Riley KM: Review of primary care-based physical activity intervention studies: effectiveness and implications for practice and future research. J Fam Pract 2000;49(2):158-168. Centers for Disease Control and Prevention: Project PACE: Physician’s Manual: Physician-Based Assessment and Counseling for Exercise. Atlanta, Centers for Disease Control and Prevention, 1992. Logsdon DN, Lazaro CM, Meier RV: The feasibility of behavioral risk reduction in primary medical care. Am J Prev Med 1989;5:249-256. Maron BJ, Zipes DP, et al: 36th Bethesda Conference eligibility recommendations for competitive athletes with cardiovascular abnormalities. J Am Coll Cardiol 2005;45:1312-1375. Henriksson J, Reitman JS: Time course of changes in human skeletal muscle succinate dehydrogenase and cytochrome oxidase activities and maximal oxygen uptake with physical activity and inactivity. Acta Physiol Scand 1977;99:91-97. Laursen PB, Jenkins DG: The scientific basis for high-intensity interval training: optimising training programmes and maximising performance in highly trained endurance athletes. Sports Med 2002;32:53-73. McArdle WD, Katch FI, Katch VL. Exercise Physiology: Energy, Nutrition, and Human Performance, 2nd ed. Philadelphia, Lea & Febiger, 1990. Noonan V, Dean E: Submaximal exercise testing: clinical application and interpretation. Phys Ther 2000;80:782-807. American College of Sports Medicine Position Stand. The recommended quantity and quality of exercise for developing and maintaining cardiorespiratory and

45. 46.

47. 48. 49. 50.

51. 52. 53.

54.

55. 56. 57. 58.

muscular fitness, and flexibility in healthy adults. Med Sci Sports Exerc 1998;30:975-991. Yates A. Compulsive Exercise and Eating Disorders: Toward an Integrated Theory of Activity. New York, Brunner/Mazel, 1991. Centers for Disease Control and Prevention: National Diabetes Fact Sheet: General Information and National Estimates on Diabetes in the United States, 2005. Atlanta, GA, US Department of Health and Human Services, Centers for Disease Control and Prevention, 2005. Mokdad AH, Bowman BA, Ford ES, et al: The continuing epidemics of obesity and diabetes in the United States. JAMA 2001;286:1195-1200. American College of Sports Medicine Position Stand. Exercise and type 2 diabetes. Med Sci Sports Exerc 2000;32(7):1345-1360. Beckman JA, Creager MA, Libby P: Diabetes and atherosclerosis: epidemiology, pathophysiology, and management. JAMA 2002;287:2570-2581. Aiello LM, Cavakkerano J, Aiello LP, et al: Retinopathy. In Ruderman NB, Devlin JT (eds): The Health Professional’s Guide to Diabetes and Exercise. Alexandria, American Diabetes Association, 1995, pp 143-152. American Diabetes Association Position Statement. Standards of medical care in diabetes—2006. Diabetes Care 2006;29:S4-S42. Ivy JL: Role of exercise training in the prevention and treatment of insulin resistance and non-insulin-dependent diabetes mellitus. Sports Med 1997;24:321-336. American College of Sports Medicine Position Stand: Appropriate intervention strategies for weight loss and prevention of weight regain for adults. Med Sci Sports Exerc 2001;33:2145-2152. Field AE, Coakley EH, Must A, et al: Impact of overweight on the risk of developing common chronic diseases during a 10-year period. Arch Intern Med 2001;161: 1581-1586. Haymes EM, McCormick RJ, Buskirk ER: Heat tolerance of exercising lean and obese prepubertal boys. J Appl Physiol 1975;39:457-461. Garrison RJ, Kanel WB, Stokes J 3rd, et al: Incidence and precursors of HTN in young adults: the Framingham Offspring Study. Prev Med 1987;16:235-251. Fagard R: Exercise characteristics and the blood pressure response to dynamic physical training. Med Sci Sports Exerc 2001;33:S484-S492. American College of Sports Medicine Position Stand: Exercise and hypertension. Med Sci Sports Exerc 2004;36:533-553.

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Cardiovascular Testing David A. Djuric, MD, and Francis G. O’Connor, MD, MPH

KEY POINTS

. Treadmill stress testing is a safe procedure when done properly, . . .

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with the risk of death during or immediately after a test estimated at less than 0.01%.1 Clinical guidelines suggest that physicians perform 50 exercise stress tests to qualify for privileges and that they perform at least 25 tests per year to maintain clinical competency.3 The Bruce protocol is the most commonly used protocol for clinical exercise testing.3 When performed on the appropriate patient and coupled with clinical information, the exercise stress test has an estimated 50% sensitivity and 90% specificity for the detection of obstructive coronary artery disease.4 There is general consensus and strong evidence that exercise testing is justified in adults with an intermediate pretest probability of disease.

INTRODUCTION Clinical exercise testing is defined as a cardiovascular stress test that uses either treadmill or bicycle exercise in conjunction with electrocardiographic and blood-pressure monitoring. The American College of Cardiology and the American Heart Association (ACC/ AHA) Task Force on Practice Guidelines (Committee on Exercise Testing) have published guidelines (most recently updated in 2002) about the performance and interpretation of clinical exercise stress testing. As with any procedure, several factors must be considered when determining the appropriateness of an exercise test and its usefulness for predicting the outcome of both symptomatic and asymptomatic patients: (1) the expertise of the professional and technical staff performing and interpreting the study; (2) the sensitivity, specificity, and accuracy of the chosen technique; (3) the cost/benefit analysis when comparing the accuracy of this technique versus a more expensive imaging test; (4) how the results of this test will affect clinical decision making; and (5) the potential benefit of patient reassurance.1 Exercise stress testing is widely used in primary care settings to assess physical fitness, determine functional capacity, diagnose cardiac disease, reassess known cardiac disease, develop an exercise prescription, and assist with cardiac rehabilitation. When clinical

exercise testing is used in an appropriate patient population, the procedure is exceptionally safe; however, myocardial infarction and death can occur in as many as 1 in 2500 tests.2 Therefore, physicians must use sound clinical judgment when referring patients for exercise testing or conducting stress testing themselves. Clinical guidelines suggest that physicians perform 50 exercise stress tests to qualify for privileges and that they perform at least 25 tests per year to maintain clinical competency3 (Box 40.1).

INDICATIONS AND CONTRAINDICATIONS Exercise testing may be used for diagnostic, prognostic, or therapeutic indications. The majority of exercise testing is used for diagnostic purposes to evaluate adults with known or suspected ischemic heart disease. The ACC/AHA Task Force on Practice Guidelines (Committee on Exercise Testing) has identified a classification system for common indications for exercise stress testing: Class I: general consensus/evidence that testing is justified Class II: divergence of opinion on utility (IIa, in favor; IIb, less evidence) Class III: agreement that testing is not warranted1 Box 40.2 outlines the current recommendations from the ACC/ AHA Task Force pertaining to the diagnosis of obstructive coronary artery disease. In this capacity, the exercise test is most useful for patients with an intermediate pretest probability of obstructive coronary artery disease based on the patient’s age, gender, and symptoms (Table 40.1). As indicated in Table 40.1, the test is most appropriate for patients who are experiencing symptoms, from the younger patient who has classic angina symptoms to middle-aged and elderly patients with atypical angina symptoms to elderly patients with seemingly noncardiac chest pain. However, testing may be helpful for evaluating asymptomatic patients who have multiple risk factors that indicate a moderate risk of an adverse cardiac event within 5 years. It may be used diagnostically for patients who are involved in high-risk occupations (e.g., pilots, police officers). Additionally, testing may be indicated for patients with sedentary lifestyles who wish to start a vigorous exercise program. It is generally not appropriate to use exercise testing as a diagnostic tool for patients with a high pretest probability of disease; however, exercise testing may be used for prognostic purposes in such cases. Although exercise testing is typically the initial diagnostic test of choice regardless of gender, it is worth

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Box 40.1: Required Equipment for Stress Testing

Box 40.2: Exercise Testing to Diagnose Obstructive Coronary Artery Disease














Class I Adult patients (including those with complete right bundle-branch block or less than 1 mm of resting ST depression) with an intermediate pretest probability of coronary artery disease on the basis of gender, age, and symptoms (specific exceptions are noted under Classes II and III)

Exercise device: treadmill or bicycle ergometer Electrocardiogram (ECG) monitor ECG recorder ECG leads ECG pads ECG paper Razor Blood-pressure cuff Stethoscope Defibrillator Resuscitative medications

Class IIa Patients with vasospastic angina

noting that, as a diagnostic tool, it has been shown to be less accurate among women as a result of a higher percentage of false-positive results (10% difference in diagnostic accuracy) (LOE: meta-analysis).1 The second most common use for exercise testing is for risk stratification and the prognosis of patients with known coronary artery disease (Box 40.3). In these patients, exercise testing is considered but one component of the evaluation. The results of the test must be used in conjunction with data collected from the clinical examination, laboratory tests, and imaging studies. The patient’s risk is determined by his or her risk factors, symptoms, functional capability, and evidence and severity of ischemic changes on the exercise test. The size of the coronary artery lesion is typically proportional to the degree of ST segment depression, the number of involved ECG leads, and the duration of depression in recovery. However, unlike the resting ECG, tracings taken during stress testing cannot localize the at-risk areas on the basis of the involved leads (LOE: B).4 The most commonly used prognostic tool is the Duke Treadmill Score (DTS), which is discussed later in this chapter. Exercise testing is additionally used for prognostic assessment in post—myocardial infarction patients (Box 40.4). Patients typically undergo a submaximal test 4 to 6 days after the myocardial infarction for prognostic assessment, activity prescription, and the evaluation of medical therapy. If not conducted at 4 to 6 days, a symptom-limited test may be performed at about 2 to 3 weeks. These tests additionally provide guidance for early cardiac

Table 40.1

Class IIb 1. Patients with a high pretest probability of coronary artery disease by age, symptoms, and gender 2. Patients with a low pretest probability of coronary artery disease by age, symptoms, and gender 3. Patients with less than 1 mm of baseline ST depression and who are taking digoxin 4. Patients with electrocardiographic criteria for left ventricular hypertrophy and less than 1 mm of baseline ST depression. Class III 1. Patients with the following baseline electrocardiogram abnormalities:
Pre-excitation (Wolff—Parkinson—White) syndrome
Electronically paced ventricular rhythm
More than 1 mm of resting ST depression
Complete left bundle-branch block 2. Patients with a documented myocardial infarction or prior coronary angiography demonstrating significant disease have an established diagnosis of coronary artery disease; however, ischemia and the subsequent risk of cardiac event can be determined by testing From Gibbons RJ, Balady GJ, Bricker JT, et al: ACC/AHA 2002 guideline update for exercise testing: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Exercise Testing). 2002. American College of Cardiology (Web site). Available at www.acc.org/clinical/ guidelines/exercise/dirindex.htm.

rehabilitation and assess the patient’s ability to perform daily activities. Finally, the exercise test is repeated at 3 to 6 weeks for a repeat prognostic assessment if the initial test was submaximal. Exercise testing can also be useful for assessing functional capacity. For the sports medicine physician, this can be an

Pretest Probability of CoronaryArtery Disease by Age, Gender, and Symptoms

Age (y)

Gender

Typical/Definite Angina Pectoris

Atypical/Probable Angina Pectoris

Nonanginal Chest Pain

Asymptomatic

30-39

Men Women Men Women Men Women Men Women

Intermediate Intermediate High Intermediate High Intermediate High High

Intermediate Very low Intermediate Low Intermediate Intermediate Intermediate Intermediate

Low Very low Intermediate Very low Intermediate Low Intermediate Intermediate

Very Very Low Very Low Very Low Low

40-49 50-59 60-69

low low low low

From Gibbons RJ, Balady GJ, Bricker JT, et al: ACC/AHA 2002 guideline update for exercise testing: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Exercise Testing). 2002. American College of Cardiology (Web site). Available at www.acc.org/clinical/guidelines/exercise/dirindex.htm. Based on Diamond GA, Forrester JS: N Engl J Med 1979;300:1350-1358.

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Box 40.3: Risk Assessment and Prognosis in Patients with Symptoms or a Prior History of Coronary Artery Disease Class I 1. Patients undergoing initial evaluation with suspected or known coronary artery disease, including those with complete right bundle-branch block or less than 1 mm of resting ST depression (specific exceptions are noted under Class IIb) 2. Patients with suspected or known coronary artery disease that has been previously evaluated and who are now presenting with a significant change in clinical status 3. Low-risk unstable angina patients 8 to 12 hours after presentation who have been free of active ischemic or heart failure symptoms 4. Intermediate-risk unstable angina patients 2 to 3 days after presentation who have been free of active ischemic or heart failure symptoms Class IIa Intermediate-risk unstable angina patients who have initial cardiac markers that are normal, a repeat electrocardiogram without significant change, cardiac markers 6 to 12 hours after the onset of symptoms that are normal, and no other evidence of ischemia during observation Class IIb 1. Patients with the following resting ECG abnormalities:





Pre-excitation (Wolff—Parkinson—White) syndrome Electronically paced ventricular rhythm 1 mm or more of resting ST depression Complete left bundle-branch block or any interventricular conduction defect with a QRS duration of more than 120 msec

2. Patients with a stable clinical course who undergo periodic monitoring to guide treatment Class III 1. Patients with a severe comorbidity that is likely to limit life expectancy and/or their candidacy for revascularization 2. High-risk unstable angina patients From Gibbons RJ, Balady GJ, Bricker JT, et al: ACC/AHA 2002 guideline update for exercise testing: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Exercise Testing). 2002. American College of Cardiology (Web site). Available at www.acc.org/clinical/ guidelines/exercise/dirindex.htm.

important tool to aid in the development of an exercise prescription or for activity counseling. These activities may include return-to-work evaluations, disability assessments, and prognosis assessments. Studies have shown that, even among patients without known coronary artery disease, low levels of aerobic fitness are an independent risk factor for all-cause and cardiovascular mortality (LOE: A).5,6 One such study showed that the highest all-cause and cardiovascular mortality was seen among men with an exercise capacity of less than 4.4 METs, whereas those who averaged greater than 9.2 METs had no deaths during the study period (LOE: A).7 A second study of 3679 men with coronary artery disease (CAD) referred for exercise testing showed that those with an exercise capacity of less than 4.9 METs had a relative risk of death of 4.1 as compared with those with a capacity of 10.7 METs during an average follow-up of 6.2 years (LOE: A).8 The National Exercise and Heart Disease Project that followed patients after

Box 40.4: After Myocardial Infarction Class I 1. Before discharge for prognostic assessment, activity prescription, evaluation of medical therapy (submaximal at about 4 to 76 days; exceptions are noted under Classes IIb and III) 2. Early after discharge for prognostic assessment, activity prescription, evaluation of medical therapy, and cardiac rehabilitation if the predischarge exercise test was not done (symptom limited, about 14 to 21 days; exceptions are noted under Classes IIb and III) 3. Late after discharge for prognostic assessment, activity prescription, evaluation of medical therapy, and cardiac rehabilitation if the early exercise test was submaximal (symptom limited, about 3 to 6 weeks; exceptions are noted under Classes IIb and III) Class IIa After discharge for activity counseling and/or exercise training as part of cardiac rehabilitation for patients who have undergone coronary revascularization Class IIb
Patients with the following ECG abnormalities:
Complete left bundle-branch block
Pre-excitation syndrome
Left ventricular hypertrophy
Digoxin therapy
More than 1 mm of resting ST-segment depression
Electronically paced ventricular rhythm
Periodic monitoring for patients who continue to participate in exercise training or cardiac rehabilitation Class III 1. Severe comorbidity that is likely to limit life expectancy and/or candidacy for revascularization 2. At any time to evaluate patients with acute myocardial infarction who have uncompensated congestive heart failure, cardiac arrhythmia, or noncardiac conditions that severely limit their ability to exercise 3. Before discharge to evaluate patients who have already been selected for or who have undergone cardiac catheterization (Although a stress test may be useful before or after catheterization to evaluate or identify ischemia in the distribution of a coronary lesion of borderline severity, stress imaging tests are recommended.) From Gibbons RJ, Balady GJ, Bricker JT, et al: ACC/AHA 2002 guideline update for exercise testing: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Exercise Testing). 2002. American College of Cardiology (Web site). Available at www.acc.org/clinical/ guidelines/exercise/dirindex.htm.

myocardial infarction showed that, for every 1 MET increase in exercise capability, there was a 10% decrease in all-cause mortality over a 19-year period, regardless of the study group.9 Further specific recommendations from the ACC/AHA Task Force are referenced in the guidelines update for exercise testing.1 The ACC/AHA guidelines outline the absolute and relative contraindications to exercise testing (Box 40.5). These guidelines are designed to ensure the safety of the patient, and they are the responsibility of the physician performing the pretest clearance.

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Box 40.5: Contraindications to Exercise Testing Absolute
Acute myocardial infarction (within 2 days)
High-risk unstable angina
Uncontrolled cardiac arrhythmias causing symptoms or hemodynamic compromise
Severe symptomatic aortic stenosis
Uncontrolled symptomatic heart failure
Acute pulmonary embolus or pulmonary infarction
Acute myocarditis or pericarditis
Acute aortic dissection Relative
Left main coronary stenosis
Moderate stenotic valvular heart disease
Electrolyte abnormalities
Severe arterial hypertension (systolic blood pressure >200 mm Hg or diastolic blood pressure >110 mm Hg)
Tachyarrhythmias or bradyarrhythmias
Hypertrophic cardiomyopathy and other forms of outflow tract obstruction
Mental or physical impairment leading to inability to exercise adequately
High-degree atrioventricular block From Gibbons RJ, Balady GJ, Bricker JT, et al: ACC/AHA 2002 guideline update for exercise testing: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Exercise Testing). 2002. American College of Cardiology (Web site). Available at www.acc.org/clinical/ guidelines/exercise/dirindex.htm.

EVALUATION Pretest procedure An overview of exercise treadmill testing is presented in Box 40.6. The reader is encouraged to reference this overview while reading the following sections detailing test performance. The physician has a number of responsibilities during exercise testing. Before the procedure, the physician is responsible for the pretest evaluation, clearance, and selection of the proper protocol. During the test, the physician must ensure proper patient preparation, perform the test, and terminate it at the appropriate time. After the test, the physician must help the patient to recover and then interpret the test results. Patient evaluation and clearance starts with a thorough history and physical that focus especially on any cardiovascular symptoms or past medical problems. This history is especially important for determining whether the patient has any contraindications for undergoing the exercise test. Chest pain symptoms must be fully elucidated and then characterized as angina, atypical angina, or atypical chest pain. The chest pain history should clarify whether the patient is experiencing unstable angina. The physician determines whether there is a history of exercise-induced syncope or presyncope or if the patient has any symptoms that are consistent with viral myocarditis, pericarditis, or unstable congestive heart failure. Any risk factors for coronary artery disease (Table 40.2) are also noted. The physician should review the results of any previous cardiac testing and discuss any problems with previous tests. Additionally, the physician should obtain a thorough medication history and discuss any orthopedic problems that may affect

ambulation or make some testing protocols difficult. It is essential to have an understanding of the patient’s exercise history and capabilities to properly select the testing protocol. Finally, the physician should ask about any significant family history of cardiac, pulmonary, or metabolic disease and about any family history of sudden death. The physician should conduct a thorough physical examination, paying special attention to any concerning findings in the patient’s history and cardiopulmonary examination. In particular, the physician should document bilateral blood pressure measurements, the pulse pressure, the carotid upstroke evaluation, carotid bruits, and simultaneous radial—femoral pulses. Cardiopulmonary auscultation should include attention to the second heart sound and a determination of the presence of any murmurs, gallops, rubs, or clicks. Murmurs that are suggestive of hypertrophic cardiomyopathy or aortic stenosis are of particular concern. The examination should exclude signs of decompensated congestive heart failure. Before administering the test, the physician must obtain informed consent from the patient. Consent forms vary among institutions; however, all must give the patient enough information to ensure that he or she understands the purpose, procedure, risks, benefits, and alternatives to the testing. The consent form should also outline the confidentiality of the patient information as described in the Health Insurance Portability and Accountability Act of 1996. Before the test, the patient is given preliminary instructions about the procedure. The patient should be instructed to eat little or no food for at least 2 to 3 hours before the test and to ensure adequate fluid intake over the day leading up to the test. To be well rested for the test, the patient should be advised to avoid strenuous exercise on the day of the test. The patient should wear loose-fitting, nonrestrictive clothing and running shoes to allow for ease of movement. If the test is performed on an outpatient basis, the patient should be asked to consider bringing someone to drive him or her from the appointment in the event that the patient is too tired to drive after the test. Specific instructions should be given regarding antihypertensive or antianginal medications. If the test is being performed for diagnostic purposes, the patient may need to taper from those medications to ensure that they do not alter the sensitivity of ischemic ECG changes. If the test is being performed for functional purposes, there is likely no need to discontinue these medications because the exercise response should mimic the responses during regular exercise. On the basis of the information obtained during the history and physical and the purpose of the test itself, an appropriate exercise protocol will be selected.

Conducting the test On arrival, the physician or technician conducts an equipment safety check to ensure that the system is in good working order. If the patient’s history was obtained before the appointment for the exercise test, the physician should again explore with the patient any changes in chest pain symptoms to ensure that any atypical chest pain has not progressed to unstable angina between the initial evaluation and the test itself. Any findings on the pretest assessment should be confirmed and reassessed. Verify that the informed consent form has been signed, and give the patient an additional opportunity to ask any questions. The patient is then given a demonstration of the equipment and shown appropriate treadmill walking. The physician discusses the indications for test termination as well (Box 40.7). The patient’s skin is prepped for ECG lead placement, which includes shaving appropriate locations and removing any lotions, oils, or dead skin cells. ECG leads are placed as shown in Figure 40.1, and the electrodes are placed in the standard positions for obtaining a routine 12-lead ECG, except the limb leads are

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Box 40.6: Exercise Treadmill Testing Procedure Pretest Checklist
Perform equipment and safety check.
Obtain informed consent.
Complete pretest history and physical examination.
Enter patient information into the exercise test system.
Prepare the skin and place the electrodes.
Connect the exercise testing monitor to the electrodes.
Secure the blood-pressure cuff on the appropriate arm.
Obtain a resting blood-pressure reading and an electrocardiogram (ECG) with the patient in a supine position.
Review the resting 12-lead ECG for any recent changes.
Obtain a blood-pressure reading and an ECG with the patient standing.
Provide instructions and demonstrate the appropriate use of the treadmill:
Instruct patient to use the handrails only for balance and to not grip them tightly.
Encourage the patient to maintain an upright position and to take long strides.
Remind the patient that his or her blood pressure will be checked during each stage.
Remind the patient to use the Borg scale.
Complete any other tests (e.g., fingerstick glucose, pulse oximetry).
Answer the patient’s final questions before beginning the testing. Conducting the Procedure
Assist the patient onto the testing equipment (i.e., treadmill or bicycle).
Provide a warmup period to ensure the patient’s comfort with the apparatus.
When the patient is comfortable, initiate the testing protocol.
Ensure continuous monitoring of the heart rate, blood pressure, and ECG as well as of symptoms.
Record the ECG during the last 15 seconds of each stage or each 2-minute period if using a ramp protocol.
Record the heart rate during the last 5 seconds of each stage or each 2-minute period if using a ramp protocol.
Record the blood pressure during the last 45 seconds of each stage or each 2-minute period if using a ramp protocol.

placed in modified locations to minimize the effects of movement. The arm leads are placed on the respective lateral front shoulders on the anterior deltoids, and the leg leads are placed on the respective upper abdominal quadrants. Alternatively, the leg leads can be placed with the right-leg electrode over the lower lumbar spine and the left-leg electrode placed directly below the umbilicus. An appropriately sized blood pressure cuff is placed firmly on the patient’s arm for obtaining serial blood pressures. Baseline measurements are now collected. The patient is instructed to lie recumbent on his or her back while a supine ECG, blood pressure, and heart rate are obtained. Next, the patient stands while an ECG, blood pressure, and heart rate are taken in this position. The patient is helped on to the treadmill and given a low-level warm up to ensure comfort on the treadmill. After the patient is












Record any symptoms as they occur. Terminate the exercise portion of the test as appropriate. Record the patient’s ECG immediately after exercise. Place the patient in a supine position while continuing monitoring. Auscultate the patient for cardiovascular changes associated with ischemia. Record an ECG at 1 minute into and every 2 minutes during recovery. Record the heart rate every minute during recovery. Record the blood pressure immediately after exercise and then every 2 minutes during recovery. Terminate the test after any ECG changes have returned to baseline and when the heart rate and blood pressure are stable.

Physician Responsibilities/Required Knowledge
Appropriate indications for exercise testing
Alternative physiologic cardiovascular tests
Appropriate contraindications, risks, and risk assessment for testing
Recognize and treat complications of exercise testing
Competence in basic and advanced cardiac life support
Various exercise protocols and the indications for each
Basic exercise physiology
Recognize and treat serious cardiac arrhythmias
Cardiovascular medications and their effects on the hemodynamic response to exercise
Principles and details of exercise testing
End points of exercise testing and indications for terminating the exercise test
Specificity, sensitivity, and diagnostic accuracy of exercise testing
How to apply Bayes’ theorem to interpret test results
Normal ECG changes in response to exercise
Conditions and circumstances that can lead to false-positive, indeterminate, or false-negative test results
Prognostic value of exercise testing
Alternative or supplementary diagnostic procedures to exercise testing and when they should be used
The concept of metabolic equivalent and the estimation of exercise intensity

comfortable, he or she is told that the protocol will now be initiated. During exercise, the patient’s blood pressure, heart rate, ECGs, and signs and symptoms are continuously monitored. The ECG is followed continuously on the monitor and recorded during the last 15 seconds of each stage or the last 15 seconds of each 2-minute time period if a ramp protocol is used. The heart rate is monitored continuously and recorded during the last 5 seconds of every minute. Blood pressure is measured and recorded during the last 45 seconds of each stage or of each 2-minute time period if using a ramp protocol. Signs and symptoms are monitored continuously and recorded when observed. In addition to this monitoring data, any adverse symptoms or abnormal ECG changes are noted. During exercise, the patient is warned of upcoming stage changes.

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Table 40.2 Coronary Artery Disease Risk Factor Thresholds Risk Factor

Defining Criteria

Positive Family history

Myocardial infarction, cardiovascular revascularization, or sudden death before 55 years of age in father or other male first-degree relative or before 65 years of age in mother or other female first-degree relative

Cigarette smoking

Current smoker or smoker who quit within the previous 6 months

Hypertension

Blood pressure more than 140/90 mm Hg or taking an antihypertensive medication

Hypercholesterolemia

Total cholesterol more than 200 mg/dL, high-density lipoprotein cholesterol less than 35 mg/dL, low-density lipoprotein cholesterol more than 130 mg/dL, or on lipid-lowering medication

Impaired fasting glucose

Fasting blood glucose more than 110 mg/ dL on at least two occasions

Obesity

Body mass index greater than 30 kg/m2 or waist girth of more than 100 cm

Sedentary lifestyle

No regular exercise or no exercise accumulating 30 minutes or more of moderate physical activity on most days of the week

Negative High serum high-density lipoprotein cholesterol

High-density lipoprotein cholesterol greater than 60 mg/dL

From American College of Sports Medicine: Guidelines for Exercise Testing and Prescription, 6th ed. Philadelphia, Lea and Febiger, 2000.

The ACC/AHA guidelines provide absolute and relative indications for terminating the exercise testing (see Box 40.7). Additionally, the test may be stopped after the patient reaches a percentage of the predicted maximal heart rate (usually 85%). However, there exists a wide spectrum with regard to maximal heart rate, and, therefore, the ‘‘target’’ heart rate may be submaximal for some patients but unobtainable for others. Thus, the committee highly recommends using symptom-limited stress testing as well as the end points outlined in Box 40.8. The absolute indications are unambiguous, whereas the relative indications do allow the physician to use clinical judgment when deciding whether to terminate the exercise portion of the test. After the completion of the exercise portion of the test, the patient is immediately placed in the supine position. This acutely increases the workload of the heart by increasing the preload, and, therefore, it may precipitate ischemic abnormalities that are not seen while the patient is upright. During this recovery phase, the ECG is continuously monitored and recorded immediately after exercise, during the last 15 seconds of the first minute of recovery, and then every 2 minutes. The heart rate is continuously monitored and recorded during the last 5 seconds of every minute. The blood pressure is measured and recorded immediately after exercise and then every 2 minutes. Again, signs and symptoms are continuously monitored and recorded as observed. Additionally, the physician auscultates the patient immediately after exercise for any abnormal heart findings, such as a new heart murmur or a third heart sound. The physician also auscultates the lungs for

Box 40.7: Indications for Terminating Exercise Testing Absolute Absolute
Drop in systolic blood pressure of >10 mm Hg from baseline blood pressure despite an increase in workload when accompanied by other evidence of ischemia
Moderate to severe angina
Increasing nervous system symptoms (e.g., ataxia, dizziness, or near syncope)
Signs of poor perfusion (cyanosis or pallor)
Technical difficulties in monitoring the electrocardiogram or the systolic blood pressure
Subject’s desire to stop
Sustained ventricular tachycardia
ST elevation of 1.0 mm in leads without diagnostic Q waves (other than in V1 or aVR) Relative
Drop in systolic blood pressure of >10 mm Hg from baseline blood pressure despite an increase in workload in the absence of other evidence of ischemia
ST or QRS changes such as excessive ST depression (>2 mm of horizontal or downsloping ST-segment depression) or marked axis shift
Arrhythmias other than sustained ventricular tachycardia, including multifocal premature ventricular contractions, triplets of premature ventricular contractions, supraventricular tachycardia, heart block, or bradyarrhythmias
Fatigue, shortness of breath, wheezing, leg cramps, or claudication
Development of bundle-branch block or interventricular conduction delay that cannot be distinguished from ventricular tachycardia
Increasing chest pain
Hypertensive response (>250 mm Hg and/or diastolic blood pressure >115 mm Hg) From Gibbons RJ, Balady GJ, Bricker JT, et al: ACC/AHA 2002 guideline update for exercise testing: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Exercise Testing). 2002. American College of Cardiology (Web site). Available at www.acc.org /clinical/ guidelines/exercise/dirindex.htm.

signs of bronchoconstriction as a possible cause of chest pain. The physician should also auscultate for new-onset rales and monitor for symptoms that are suggestive of acute-onset congestive heart failure. The recovery period with monitoring continues until the patient is stable and any ST-segment changes have returned to baseline, which usually takes 8 to 10 minutes. This completes the test, and the monitoring equipment may be removed while the test is interpreted (Box 40.9). The treadmill and bicycle ergometer protocols are compared in Figure 40.2.

INTERPRETATIONS Clinical and hemodynamic responses Interpretation of the exercise test requires the analysis and interpretation of both the electrocardiographic measurements and the nonelectrocardiographic observations related to myocardial ischemia. All of these findings contribute to the prognosis or extent of

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Right and left arm leads should be placed outwardly on the shoulders (preferentially over bone rather than muscle)

V1 and V2 are positioned in the fourth intercostal space

V4 should be placed in the fifth intercostal space on the midclavicular line

RA

LA Anterior axillary line

V1

V3 lies halfway between V2 and V4

V2 V3 V4

V5 V6 V4, V5, and V6 should be placed along a horizontal line— this line does not necessarily follow the intercostal space

RL The right leg lead (ground lead) should be placed below the umbilicus

Midaxillary line

LL

The left leg lead should be just below the umbilicus

disease. The non-ECG findings that should be evaluated include blood pressure and heart rate response, the presence or absence of symptoms, the presence or absence of dysrhythmias, aerobic capacity, and perceived exertion. By assimilating all of this information with the pretest probability, the clinician can determine the probability that the patient has coronary artery disease and the severity of the disease and thus predict the prognosis and likelihood of future adverse cardiac events. With this information, the physician can provide recommendations regarding future

Box 40.8: The Written Report
Patient’s demographics (age, gender, comorbidities)
Patient’s medications (to include whether they were taken prior to testing)
Indications for testing
Baseline heart rate, blood pressure, and any electrocardiogram abnormalities
Protocol used
Exercise time
Reason for terminating test
Heart rate response
Blood pressure response
Symptoms reported during test
Dysrhythmias or ectopy
Functional aerobic capacity (METs)
ECG changes with exercise or recovery (type, location, and in which stage)
Goal achieved: maximal versus submaximal
Presence or absence of myocardial ischemia (positive or negative test)
Duke Treadmill Score (if indicated)

Figure 40.1 Electrocardiogram lead placement. (From American Heart Association Scientific Statement: Circulation 2001;104:1694 -1740.)

management, such as deciding between revascularization and medical management. The first information provided by the patient is the presence of symptoms. Chest pain, claudication, shortness of breath, and wheezing are each important findings. Exercise-induced anginal symptoms are a component of the DTS, and they may or may not correlate with ischemic ECG changes. Typical angina with ischemic ECG changes is an indication for termination of the test.1 Other symptoms that are indicative of underlying cardiovascular disease may exist without angina or ECG changes and, thus, may presage underlying coronary artery disease. In the same manner, a patient’s appearance may be helpful in his or her assessment. Light perspiration, peripheral cyanosis, and a decrease in skin temperature may indicate poor tissue perfusion as a result of inadequate cardiac output with resulting vasoconstriction. Fatigue is a normal and expected response to exercise; however, fatigue at lower levels of exertion relates to poor exercise capacity. Fatigue can be measured using the Borg or category—ratio scale shown in Table 40.3. A Borg scale rating of more than 18 suggests that the patient has achieved maximal exercise, and values of more than 15 to 16 suggest that the anaerobic threshold has been exceeded.10

Box 40.9: Techniques and Equipment for Exercise Testing









Bruce Cornell Balke-Ware ACIP mACIP Naughton Weber Bicycle ergometry

O2 Cost Mets ml/kg/min

Bicycle ergometer

Treadmill protocols

I

3 min % grade stages at 1 Watt = 6.1 mph % gr 3.3 mph Kpm/min

Healthy, dependent on age, activity

and

56.0

15

52.5

15

49.0

14

45.5

13

42.0

12

38.5

11

IV

Limited

Symptomatic

III

Sedentary healthy

35.0

II

Balke- USAFSAM *Slow* McHenry Ware USAFSAM

10

31.5

9

28.0

8

24.5

7

21.0

6

17.5

5

14.0 10.5

4

For 70 kg body weight Kpm/min 1500

2

3.5

1

20

5.0

18

4.2

16

1350 1200 3.4

14

1050 900 750 2.5

12

600 450 300

3

7.0

5.5

150

1.7

10

1.7

5

1.7

0

Figure 40.2

ACIP

CHF

% % grade grade at at 3 mph 2 mph

1 min stages 26 25 24 23 22 21 20 19 18 17 16 15 14 13 12 11 10 9 8 7 6 5 4 3 2 1

Stanford

Cardiovascular testing

Bruce

Normal

Mets

.

Clinical status

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Functional class

mph % gr 3.3

25

mph % gr 3.3

3.3

3.3

3.3

15 2

25

2

20

2

15

2 2 0

2.0

0

15

3.1 24.0

13

3.3

18

20.0

3.0 21.0 mph % gr

3.3

15

17.5

3.0 17.5 3.4 14.0

15.0

3.0 15.0

3.3

3.0 14.0

12.5

3.0 12.5 3.0 10.5 3.0 10.0

9

10.0

17.5

3.3

6

7.5

14.0

10

5.0

10.5

5

2.5

7.0

3.0

3.0 2.0

7.0

0

3.5

2.5

2.0 2.0

3.5

2.0

0.0 1.5

0.0

1.0

0.0

2.0 2

12

0

Exercise stress testing protocols.

3

12 11

3.3

5

3.3

3.4 24.0

22.5

20

10

16

14

21

mph % gr 3.3

mph % gr

3.0

7.0

3.0

7.5

2.0 10.5

10 9 8 7 6 5 4 3 2 1

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Interpretations 515

Table 40.3 Exertion

Borg Scale for Rating Perceived

Rating of Perceived Exhaustion

New Rating Scale

6: Very, very light

0: Nothing at all

7

0.5: Very, very weak

8

1: Very weak

9: Very light

2: Weak

10

3: Moderate

11: Fairly light

4: Somewhat strong

12

5: Strong

13: Somewhat hard

6

14

7: Very strong

15: Hard

8

16

9

17: Very hard

10: Very, very strong

18

—Maximal

19: Very, very hard From American Heart Association Scientific Statement: Circulation 2001;104:16941740.

The physical examination with cardiopulmonary auscultation immediately after exercise can elucidate an exercise-induced left ventricular dysfunction through new cardiac gallops or precordial bulge. Any new murmur may also represent valvular disease or papillary muscle dysfunction, whereas new-onset rales are indicative of acute congestive heart failure. Exercise or aerobic capacity is also an important prognostic indicator. The most accurate measurement of aerobic capacity is with a direct measurement of maximal oxygen consumption. Gas analysis increases the expense when added to the stress system, and it may not be widely available for routine testing. When unavailable, the best estimate of exercise capacity is the measurement of the work effort, which is expressed in METs. Figure 40.2 shows the conversion of exercise time per protocol to METs. Studies have shown that a low exercise tolerance portends an increased risk of all-cause and cardiovascular mortality, whereas those patients with a good exercise tolerance have a lower risk of adverse cardiovascular events (LOE: A).5-9 Maximal heart rate can be predicted using a number of different equations that are based on age, with the most common being 220 minus the patient’s age (e.g., for a 35-year-old patient, 220  35 = 185 bpm). Although these equations have been validated with large study groups, there is still significant individual variability. There is a high likelihood for error when extrapolating the age-adjusted submaximal predicted maximal heart rate. Therefore, achieving the predicted maximal heart rate should not be an absolute end point or suggestive of a maximal effort. Additionally, heart rate response to exercise may be influenced by a number of factors; a rapid rise in the heart rate could be the result of deconditioning, anemia, metabolic disorders, or dehydration. A relatively slow heart rate could be attributed to training, enhanced stroke volume, or medications (e.g., b-blockers).11 Although the maximal heart rate is a highly variable factor in exercise testing, there are two significant abnormalities that should be evaluated. Chronotropic incompetence (i.e., the inability to raise heart rate above 120 bpm with exercise) is associated with the presence of heart disease and increased mortality (LOE: A).12,13

A delayed decrease in the heart rate during recovery (200 mm Hg and/or diastolic blood pressure of >110 mm Hg.

(4) the mode of exercise should be tolerated by most people.2-4 In addition, the test should be independent of the motivation or specific skill sets of the individual.1,4 Furthermore, all maximal exercise tests should begin with a warm up so that the individual has adapted to a submaximal level before moving up to maximal exercise.3 A variety of test methodologies, with these principles considered, have emerged over the years to either measure or estimate maximal aerobic power. These methodologies include continuous progressive tests with 2-minute to 3-minute stages, continuous progressive tests with less than 2-minute stages (ramp tests), continuous steady-state tests, and discontinuous progressive tests.2 Figure 41.1 provides a graphic view of these various test methodologies. Whereas steadystate protocols are always submaximal, progressive tests can be either submaximal or maximal. When submaximal tests are conducted, only an estimate of VO2max can be obtained.

Types of tests Significant efforts have been devoted to examining various exercise paradigms so that the most suitable test for achieving VO2max can be used.2,5-11 Table 41.2, which provides a comparison of different modalities, shows that treadmill running with a grade is the preferred approach to achieving VO2max.9-11 It is important to note that the magnitude of the differences across test modalities depends in part on the sport preference of the subject being tested. For example, a VO2max obtained during arm cranking approached 80% of the value obtained during arm and leg work combined, but only in a trained canoeist.5,6 Similarly, the upper range for upright cycling applies primarily to those who are trained cyclists.2,12

Treadmill tests for maximal aerobic power Exercise on a treadmill is a very common approach for measuring VO2max. As such, a variety of treadmill test protocols have been

Continuous • Progressive Maximal Submaximal • Steady state

Multistage

Ramp

Discontinuous • Progressive

Figure 41.1 Various types of exercise testing methodologies: continuous (progressive multistage), ramp, steady state, and discontinuous.

described.2-4,13-17 Some tests use a constant speed and impose incremental grade changes; these include the Balke,13 Taylor,4 and Stanford1 tests. Kyle and colleagues18 described a continuous version of the Taylor test that uses 2.5%-increment increases in grade with a constant speed. The choice of speed (6 to 8 mph) is determined from the heart rate after a 10-minute warm up. This is an excellent test that can be used with the criteria that are described later for documenting whether VO2max is achieved. Other test protocols change both grade and speed or just speed. The most commonly used test is the one described by Bruce and colleagues.3 Although the time to complete the Bruce protocol is minimal, it imposes marked increases in both speed and grade, which many people find difficult. By contrast, the original Balke protocol,1 which uses 2%-increment increases in grade coupled with 3-minute stages, takes a long time to achieve VO2max. Modified versions of both protocols can be used, depending on the population of interest. Clearly smaller-grade increments and a slow speed are preferred for older and/or deconditioned persons, whereas large work increments and high speeds may be suitable for young and highly active populations. Figure 41.2 provides a range of the relative VO2 values expected for various speeds and grades. This information can provide the tester with an estimate of

Table 41.2 Maximal Values Achieved during Various Types of Maximal Exercise Tests Types of Exercise

Percentage of Maximal Oxygen Uptake

Uphill running Horizontal running Upright cycling Supine cycling Arm cranking Cross-country skiing Step test Swimming

100% 95%-98% 90%-96% 82%-85% 62%-80% 100%-104% 97% 85%

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90

0% 2.5%

80

5.0%

Oxygen uptake (mL • kg−1 • min−1)

7.5% 70

10.0%

60

50

40

30

20

10 2

4

6

8

10

12

Speed (mph) Figure 41.2 Oxygen uptake values expected for various speeds and grades as determined by the American College of Sports Medicine’s formulas for metabolic calculations.

what to expect at a given speed and grade despite significant individual variation as a result of biomechanics, body composition, and other such characteristics.

Cycle ergometer tests for maximal aerobic power Although similar principles can be applied to cycle ergometer tests, the cycle ergometer differs from the treadmill in that work rates are weight independent, and the two primary variables are cycling rate and resistance. These factors determine the power or work per unit of time, which is expressed in watts (W). If VO2 is measured during a steady state at various cycling rates, a linear relation between a change in VO2 and the work rate is typically noted: the range of 9 to 12 mL of O2/min
1/W
1 depends on the rate of work incrementation19; Figure 41.3 depicts the relationship between W and VO2 for cycling ergometry. This relationship can be used to estimate VO2max when actual measurements are not possible, although some variability between persons will always be noted. For traditional cycle ergometer tests, a cycling rate of 50 revolutions/rotations per minute (rpm) is often used, but some subjects find this rate too slow at low resistance settings. In all cases, the person should have a warm up with either no load or a minimal load (25 W) before any progressive increase in resistance. Each progressive stage should be between 1 and 3 minutes in length, and the step increments should range between 25 and 60 W, depending on the characteristics of the population. Williams and colleagues20 recently found that adolescent boys could achieve VO2peak during only 90 seconds of a maximal intensity cycle sprint. Accordingly, a supramaximal test may present an alternative to the traditional incremental cycle exercise test to exhaustion when assessing maximal aerobic power. For a detailed description of other cycle and treadmill exercise test protocols, the reader should refer to the American College of Sports Medicine’s Guidelines for Exercise Testing and Prescription.1

Criteria for documenting the attainment of maximal aerobic power When a maximal aerobic power test is conducted, it is important to document whether a true VO2max has been achieved. Such a determination begins with an understanding of the physiologic responses to severe exercise and assessing selected parameters that have been designated as criteria for a VO2max test. The criteria allow the tester to decide whether the obtained value should be considered the VO2max or a peak VO2 (VO2peak). As noted previously, a plateau in VO2 or only a small increase in VO2 with an increase in external workload is considered the primary criterion. Secondary criterion include measures of blood (or plasma) lactate, respiratory exchange ratio (RER), heart rate, and perceived exertion.1,21,22

CRITERIA FOR MAXIMAL AEROBIC POWER A plateau in oxygen uptake A plateau in oxygen intake despite an increase in workload is considered the primary criterion for VO2max. If a plateau in VO2 is observed, VO2max has been achieved. However, this criterion is not always achieved.18,20,23-28 Various factors influence the quantification of VO2max, including between-subject variability and absolute increases in grade and speed. Meyers and colleagues29 suggested that a plateau phenomenon is not always seen with various protocols because of the sampling interval selected (e.g., breath by breath; 5-, 10-, or 15-second averages) and the magnitude of the work increments for each exercise stage. Many efforts have been undertaken to define precise criterion for attaining a plateau. In one of the early studies performed by Taylor and colleagues4 115 subjects ran at a speed of 7 mph on a given grade (0% to 12.5%) for 3 minutes; the grade was increased by

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Criteria for maximal aerobic power 523

25

5 4.2

20 3.5

3

15

2.8

2.1 10

2 1.5

1

0.9

5

0

0 50

Energy expended (kcal • min−1)

Oxygen uptake (L • min−1)

4

100

150

200

250

300

Power (watts)

2.5% until the subject could go no longer; the grade increases were typically carried out on different days or after a period of rest. With this protocol, it was shown that a 2.5%-grade increase typically resulted in a rise of approximately 300 mL/min
1 in VO2. However, at a certain point, higher levels of exercise, which were different for each person, did not elicit the 300 mL/min
1 increase. On the basis of this information, it was determined that an increase of less than 150 mL/min
1 or 2.1 mL/ kg
1/min
1 in VO2 at the next higher work rate marked a plateau. The authors of the study concluded that a grade increase was preferable to speed increases for achieving a plateau. In addition, they demonstrated that 93.9% of persons tested achieved the designated plateau.4 It is important to note that other investigators have not always found that such a high percentage of persons achieve a plateau. The percentage of adults achieving a plateau ranges from 25% of men and women26,30 to 72.5% of men.18 The numbers are similar for children, with 25%27 to 33%28 of prepubertal children achieving a plateau during treadmill exercise and cycle ergometry, respectively. For most studies, VO2peak values do not differ from VO2max values. Thus, although a plateau is not seen for many people as a result of various factors, VO2peak may be considered a valid index of VO2max. Although no consensus has been reached over the years, this criterion is still considered by many to be the gold standard or the primary criterion. Because a plateau is not consistently observed, the secondary criteria described here have evolved.

Blood lactate levels In the absence of a true plateau in VO2, a rise in blood lactate has been used to demonstrate a maximal effort.1,12 As the workload continues to rise and the person nears a maximal effort, blood lactate levels increase as a result of accelerated glycolysis, an increase in the recruitment of fast-twitch muscle fibers, a reduction in liver blood flow, and/or an elevation in plasma epinephrine concentration.1,2,12 These observations were first made by Astrand,12 who noted that, in the absence of a visible plateau, lactate values along with a subject-reported stress level could be used to document the attainment of a true VO2max.2,12

Figure 41.3 Predicted amount of oxygen consumed requirements for various power outputs (watts) on a cycle ergometer. Note that these requirements are independent of body weight.

Although identifying a standard cutoff for blood lactate levels has been difficult, the values derived from Astrand’s earliest studies suggesting a cutoff of 7.9 to 8.4 mmol/L2,12 are still accepted today. Subsequent investigators have noted that 8 mM is a reasonable criterion value.21,22,31,32 Cumming and Borysyk31 and Stachenfeld32 found that 78% of their test subjects achieved lactate levels of more than 8 mmol/L. Moreover, 8 mmol/L was the best criterion in terms of specificity and positive predictive value as compared with other secondary criteria.32 Current standards vary, but a value of 8 mmol/L or greater appears to be consistent with research studies and is well accepted by researchers in general.

Respiratory exchange ratio The respiratory quotient and the RER are both calculated as the ratio of the volume of carbon dioxide (CO2) produced to the volume of oxygen (O2) used, or VCO2/VO2. The respiratory quotient, which typically ranges between 0.7 and 1.0, is an indicator of metabolic fuel or substrate use in tissues; it must be calculated under resting or steady-state exercise conditions. A ratio of 0.7 is indicative of mixed fat use, whereas a ratio of 1.0 indicates the exclusive use of carbohydrates.33 Thus, during low-intensity, steady-state exercise, the respiratory quotient and the RER are typically between 0.80 and 0.88, when fatty acids are the primary fuel. As the intensity of the exercise increases and carbohydrates become the dominant or primary fuel, the respiratory quotient and the RER increase to between 0.9 and 1.0. Because the respiratory quotient reflects tissue substrate use, it cannot exceed 1.0. By contrast, the RER, which reflects the respiratory exchange of CO2 and O2, commonly exceeds 1.0 during strenuous exercise. During non—steady-state, strenuous exercise, the volume of CO2 production rises as a result of hyperventilation and the increased buffering of blood lactic acid derived from skeletal muscles; thus, the RER no longer reflects substrate usage but rather high ventilation rates and blood lactate levels.2,22,33 Because RER reproducibly increases during exercise, it is considered a parameter that can document maximal effort. Issekutz,33 who was the first to propose the use of RER as a criterion for VO2max, noted that it must exceed 1.15. A higher value may suggest a more accurate assessment of VO2max. The 1.15 value

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appears to be reasonable, although not all persons are able to achieve it. Studies have noted values of 1.00, 1.05, 1.10, and 1.13 as criterion for maximal performance,21,22 but, at present, no clear consensus has been reached.

Age-predicted maximal heart rate The widely recognized linear relationship between heart rate and VO2 has encouraged the use of estimated maximal heart rate as a criterion for achieving VO2max. Attaining a target percentage of the age-predicted maximal heart rate is one of the most widely recognized criterion.21,22 Unfortunately, the traditional equation used to estimate maximal heart rate (220
Age) was derived from approximately 10 different studies, and most tested subjects were less than 65 years of age.34 Additionally, the equation was never validated for adults who were more than 60 years of age, and it may underestimate maximal heart rate among older adults by more than 20 beats per minute (bpm). For this reason, the American College of Sports Medicine and others have recommended that heart rate should not be used alone but rather in conjunction with other secondary criteria.1,21,22 In 2001, Tanaka and colleages34 published a new equation for estimating agepredicted maximal heart rate (208
0.7  Age), but whether it will prove to be less variable at all ages remains to be determined.

Borg scale or rating of perceived exertion The Borg scale is the most widely used method for quantifying perceived exertion. It was designed to increase in a linear fashion as exercise intensity increased and to parallel the apparent linearity of VO2 and heart rate with workload.35,36 The original Borg scale ranges from 6 to 20, with each number anchored by a simple and understandable verbal expression. The specific numbers of the scale were intended to be a general representation of actual heart rate such that, when a person was exercising at 130 bpm, a perceived exertion of 13 should be reported. Similarly, if the perceived exertion were 19, a heart rate of around 190 would be expected. The scale was not intended to be exact but rather to be an aid in the interpretation of perceived exertion. Studies have demonstrated a good correlation between the rating of perceived exhaustion and VO2.37,38 Eston and colleagues37 obtained rating of perceived exhaustion values during a graded exercise test and reported a good correlation between heart rates and VO2 when the reported rating of perceived exhaustion was between 13 and 17. An rating of perceived exhaustion value of 17 or greater should be accepted as meeting the criterion for achieving VO2max. Since the initial scale was developed, a variant scale using 0 to 10 as the numeric ratio has been proposed. This scale, which has not been widely accepted, is suitable for examining subjective symptoms, such as breathing difficulties.35 However, the original 15-point rating of perceived exhaustion scale remains the standard for use as a criterion for VO2max. Table 41.3 provides the ratings for the original and new Borg scales.

Recommended criteria for testing The criteria for VO2max were initially established for a discontinuous treadmill test with 2.5% increases in grade. To date, the criteria for a plateau have not been redefined for other specific tests, but the 150 mL/min
1 increase continues to be used. Because the attainment of a true plateau is not an absolute prerequisite, some combination of secondary criterion may be preferable. The criteria presented in Table 41.4 are offered as a guide, and it is suggested that at least two (and preferably three) of the four secondary criteria be met. If a true plateau is noted, then this alone would be

Table 41.3 The Original and New Borg Scales for the Rating of Perceived Exertion Original Scale 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20

No exertion at all Extremely light Very light Light Somewhat hard Hard (heavy) Very hard

Ratio Scale 0 0.5 1 2 3 4 5 6 7 8 9 10 

Nothing at all Very, very weak Very weak Weak Moderate Somewhat strong Strong Very strong

Very, very strong Maximal

Extremely hard Maximal exertion

sufficient for documenting VO2max. If the criteria are not met, then the test results would be considered to reflect VO2peak.

PREDICTING MAXIMAL AEROBIC POWER Laboratory measurements are the only way to accurately quantify VO2max. Nevertheless, this procedure does pose some limitations, such as the space and equipment available, the expertise of the technician, and the health condition of the subject. These factors have led to the development of multiple ‘‘prediction’’ tests that can be conducted in clinical, commercial, and/or outdoor arenas. Current prediction tests can be divided into three types, depending on the situation: (1) maximal effort prediction tests; (2) submaximal effort prediction tests; (3) and nonexercise prediction tests. Understanding the advantages, disadvantages, and limitations of each test can be important for determining the most appropriate test to use for a given environment, a specific population, and a particular need.

Maximal prediction tests Maximal prediction tests, although designed to reduce the problems associated with ‘‘true’’ VO2max tests, do require the subject to perform a given protocol to maximal effort. Some aspect of performance is then used to predict VO2max on the basis of the values collected from a sample study. Although cycling and arm ergometry can also be used, the most common maximal prediction

Table 41.4 Criteria for Documenting a Maximal Effort Test Increase in amount of oxygen consumed is less than 150 mL/min
1 or 2.1 mL/kg
1/min
1 with a 2.5% grade increase Blood lactate 8 mM Respiratory exchange ration 1.15 Increase in heart rate to within ± 10 bpm for estimated maximal for age Borg scale rating (Perceived Exertion)  If the first criterion is not met, then at least three of the remaining four should be met.

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Predicting maximal aerobic power 525

tests involve running because the tests can be performed in a variety of ways: (1) run a required distance as quickly as possible; (2) run as far as possible within a set time; (3) perform a shuttle/ track run; or (4) run on a treadmill and use the time run during a standard maximal treadmill test. One of the best-known examples of a prediction test is the Cooper 12-minute field performance test.39 Subjects are required to run on a level surface (usually a measured track) for 12 minutes, and the distance (D = meters covered) is recorded. Cooper found that VO2max could be predicted on the basis of a regression equation with a considerable reliability (r = 0.897), and, as a result, this test has been used by many health professionals. Correlation coefficients (r) between this test and actual VO2max measures are typically around 0.87 to 0.89.39,40 The following regression equation can be used to estimated VO2max from the distance covered in 12 minutes1: VO2max ðin mL=kg
1 =min
1 Þ ¼ D  0:02233
11:3 Another commonly used walking/running test is the 1.5-mile run: subjects must complete 1.5 miles in as short a time as possible. The time (T) required to complete the distance is used to predict the VO2max of the individual. 1,40,41 Correlations between this test and actual VO2max measures range from 0.73 to 0.92.1,40,42 The equation for the 1.5-mile run (T = time) is as follows: VO2max ðin mL=kg
1 =min
1 Þ ¼ ð483=TÞ þ 3:5 Variations on the 1.5-mile run that include variables other than time have also been developed.1,42,43 For example, the Rockport 1-mile walk test uses body weight, age, gender, and heart rate.1,42,43 Fortunately, these tests yield essentially comparable values, and it is incumbent upon the tester as to which test will be easier and most feasible to conduct. Another test that has been used with children and that is useful for runners in training include the shuttle/track run test. This test involves having the individual start running at a certain speed and cover a fixed distance (20 to 400 meters) multiple times for a specified time.44-47 After each distance, the speed is increased or the time allotted to complete each shuttle is reduced. This reduction in time (or increase in speed) is continued until the subject can no longer keep pace. The speed achieved can then be used to predict the individual’s VO2max from regression formulas. Correlations between values obtained from these tests and actual measurements range from 0.83 to 0.98.44-47 The formula for estimating VO2max from the 20-meter shuttle46 (S = speed in km/h) is as follows: VO2max ðin mL=kg
1 =min
1 Þ ¼ 5:857  S
19:458 Another way to estimate VO2max is by measuring the time that a person stays on a treadmill during a standardized maximal exercise test. For each of the major maximal effort treadmill protocols, regression equations to predict VO2max from time have been developed. For example, for the Bruce protocol, regression equations with correlations between 0.86 and 0.92 have been developed for active men, sedentary men, men with coronary heart disease, and healthy adults.3,15-17 One of the more general equations for predicting VO2max from the time it takes to complete the Bruce protocol was reported by Pollack and all16 (T = time in minutes) is as follows: VO2max ðin mL=kg
1 =min
1 Þ ¼ 4:326  T
4:66 Regression equations, like that for the Bruce protocol, have also been developed with a reasonable degree of accuracy for the Balke and Ellestad protocols.3,15-17 Such equations can be

developed within any test facility from a particular standardized protocol. However, it must be remembered that prediction equations are typically specific for a population and should thus be used with caution when working with another group of individuals. Gender, age, race/ethnicity, and perceived functional ability may be important in such prediction equations. One cycle ergometry test for predicting VO2max uses maximal work rate (W), body weight (kg), and age (yr).48 This progressive test uses a constant pedal rate (60 rpm) with incremental increases in work rate (15 W/min
1) until the subject can no longer sustain 60 rpm. The equations used to predict VO2max for men and women are as follows: Men: VO2max in mL=min
1 ¼ 10:51  W þ 6:35  kg
10:49  yr þ 519:3 Women: VO2max in mL=min
1 ¼ 9:39  W þ 7:7  kg
5:88  yr þ 136:7 The above-mentioned tests are all examples of prediction tests that involve maximal effort. Each has a specific use, depending on the goals and the population of interest, but each also has the inherent problems and/or errors that come with any prediction equation.

Submaximal prediction tests Individuals who are less fit, who are just starting an exercise program, or who are recovering from medical conditions often cannot tolerate a maximal effort. In response to the need to test such populations, submaximal prediction tests have evolved. These tests, which can be either constant load, steady-state, or progressive tests, have at least four advantages over maximal exertion tests, including the following: (1) they are physically less demanding; (2) they take less time to perform; (3) they are safer to conduct; and (4) they can often be performed with large groups. However, to accomplish this, some accuracy is sacrificed. Most submaximal tests use heart rate for the estimation of VO2max. A˚strand and Ryhming49 were among the first to report a linear relationship between heart rate and VO2, and, on the basis of this relationship, they recommended the use of heart rate to predict VO2max. Thus, heart rate provides the theoretic basis behind most submaximal tests: when a subject works at submaximal levels, heart rate is used to predict a maximal performance either by extrapolation to maximal heart rate or from heart rate at a known power output. The relationship between heart rate and workload is particularly important for progressive, submaximal cycle ergometry protocols. One typical progressive protocol uses four incremental, 2-minute stages, with the initial workload based on the body weight of the subject and his or her self-reported activity level.50 For example, a 95-kg, physically active subject would complete the four-stage protocol by pedaling at 50 rpm for work rates of 50, 100, 150, and 200 W. The subject’s heart rates at each work rate are plotted, and the line of best fit is determined: the point on the line that coincides with the estimated maximal heart rate would provide an estimate of VO2max (Figure 41.4). Other progressive tests, such as those with stair steppers, treadmills, and seated rowing machines in which power outputs are known, have been used in a similar manner.51,52 Steady-state submaximal effort tests are also commonly used for the prediction of VO2max. Treadmills, track walking/running, stair steppers, cycle ergometers, bench steps, rowing machines, and squat repetitions have all been used.1,41-43,49,51,53-57 Although there are obvious differences among these tests, there are also similarities: each requires a steady-state work rate and a measure of the subject’s heart rate upon the completion of the test. From there, heart rate may either be used alone to predict VO2max from a

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200 Estimated max HR = 190 bpm

180 Estimated max HR = 170 bpm

Heart rate (bpm)

160 Max W = 220 VO2max = 3.1 L • min−1

140

120

Max W = 180 VO2max = 2.6 L • min−1

100

80 VO2 (L •

Watts 50

100

150

200

150

300

min−1)

1.5

2.1

2.8

3.5

4.2

0.9

nomogram 49,57 or in conjunction with other variables, such as age, weight, gender, and other variables from a regression equation.41-43,51,53-56One of the first nomograms for predicting VO2max from heart rate at submaximal workloads was derived by A˚strand and Ryhming from cycle, stair-stepping, and treadmill-running data.49 Although their nomogram is still used, it has been modified for use with other populations.57,58 In addition to nomograms, regression equations have been developed to predict VO2max on the basis of individuals walking/jogging on a treadmill at submaximal levels,54 stepping up and down stairs for a set time,41,53,56 jogging 1 mile on a track,42 or by using heart rate and activity counts from triaxial accelerometry.59 Swain and colleagues60 proposed a new method for estimating VO2max on the basis of VO2 reserve and heart rate at the end of a 6-minute submaximal cycle ergometry protocol that elicited 65% to 75% of heart rate reserve; the correlation between measured and predicted VO2max was 0.89. Petrella and colleagues56 described a safe and simple self-paced step test that could be conducted in a doctor’s office to predict aerobic fitness in adults who are more than 65 years of age; the correlation with VO2max was reported to be 0.93 for females and 0.91 for males. Lastly, although submaximal exercise prediction tests do serve an important role in estimating VO2max, all of them are somewhat variable with regard to their accuracy because their predictive value relies on an accurate estimate of maximal heart rate. Unfortunately, there is inherent error in estimating maximal heart rate. As noted previously, maximal heart rate can be estimated as 220
Age (as a low estimate) or 210
0.5  Age (as a higher estimate). However, despite these equations, the true maximal heart rate can still be higher or lower by as much as 20 to 30 bpm (one standard deviation: 10 to 12), depending on the subject’s age and training.1,50 Moreover, these equations assume that the decline in maximal heart rate for a given age is uniform. Clearly, an erroneous estimate of maximal heart rate can markedly affect the estimate. For example, in Figure 41.4, if the estimated maximal heart rate were 190 bpm, then the estimated VO2max

Figure 41.4 Extrapolation of maximal oxygen uptake from estimated maximal heart rate and work rate on a cycle ergometer test.

would be 3.1 L/min
1, whereas, if the true maximal heart rate were only 170 bpm, then the VO2max would be 2.6 L/min
1. If a person weighed 70 kg and the values were normalized for body weight, then the relative VO2max values would be 44.2 and 37.1 mL/kg
1/min
1, respectively, for the 190 and 170 maximal heart rates.

Nonexercise prediction tests The value of cardiorespiratory fitness as an indicator of all-cause mortality has been reported,61 and, as such, the need to estimate VO2max noninvasively has increased. Prediction equations that use nonexercise parameters such as age, body composition, gender, level of physical activity, and the subject’s perceived functional ability to walk, jog, or run given distances have emerged.62,63 The reliability of these newer nonexercise prediction tests shows promise. For example, George and colleagues63 found that a questionnaire-based regression equation predicted VO2max with a correlation of 0.85 in a sample of physically active college students. Similarly, Heil and colleagues62 developed an equation for men and women between the ages of 20 and 79 years and noted a correlation of 0.88 for the generalized equation (men and women together). The equation included percent body fat, age, gender, and an activity code derived from personal statements about activity level. Although this equation appears to be useful because of its wide age range, very few of the subjects were highly fit, and it may be best for a fairly sedentary population. Malek and colleagues developed equations to predict VO2max from age, height, weight, and exercise frequency, intensity, and duration in aerobically trained women64 and men,65 but these are population specific. Overall, nonexercise prediction tests have one distinct advantage: they can be administered without the requirements of equipment, supervision, or any inconvenience to the subject. However, as with all regression equations, generalization to a population other than the one from which it was derived remains questionable.

(

References 527

Table 41.5 NormativeValues (Percentile) for Maximal Aerobic Power for Men and Women byAge Age in Years

Poor (10)

Fair (10-30)

Average (30-70)

Good (70-90)

Excellent (90)

44

35

Men 20-29 30-39 40-49 50-59 60

REFERENCES 1. 2. 3.

4. 5. 6.

Women 20-29 30-39 40-49 50-59 60

7. 8. 9. 10. 11.



American College of Sports Medicine Aerobic Power Standards for men and women. 12. 13.

NORMATIVE AND POPULATION VALUES FOR MAXIMAL AEROBIC POWER

14.

The American College of Sports Medicine has published normative values for VO2max by age and gender so that individual values can be classified to into one of five groups: (1) poor (well below average); (2) fair (below average); (3) average; (4) good (above average); and (5) excellent (well above average)1 (Table 41.5). The importance of VO2max cannot be overemphasized with respect to health: low aerobic power or low cardiovascular fitness is associated with higher morbidity and mortality for all causes.61 Data from 1999 to 2000 and 2001 to 2002 National Health and Nutrition Examination Surveys showed that approximately 11.3% of nonHispanic whites and 22.9% of non-Hispanic blacks between 20 and 49 years of age had estimated VO2max values that were in the American College of Sports Medicine’s poor category (below 30 mL/kg
1/min
1).66 Non-Hispanic black women had the lowest VO2max values such that 30.9% were in the poor category.66 Of note is the finding that 33.6% of adolescents have poor aerobic fitness.67 Thus, despite the importance of maximal aerobic power, the distribution of estimated VO2max values from the National Health and Nutrition Examination Surveys indicates low fitness among most of the US population.

16.

CONCLUSION

15.

17.

18. 19.

20. 21. 22. 23. 24. 25.

26. 27. 28.

In summary, maximal aerobic power or VO2max is an extremely valuable measure of cardiovascular and pulmonary function, work capacity, and endurance performance. It can be directly measured using a standardized maximal treadmill or cycle ergometer protocol, or it can be predicted using a maximal or submaximal protocol or regression equation. A variety of protocols for predicting VO2max are readily available, and many are extremely easy to administer. All tests have certain advantages and limitations that should be considered by the test administrator. Care must be taken to only use a prediction equation on a population that is comparable in terms of age, gender, ethnicity, and fitness level because each prediction equation was based on results derived from a particular population and thus it may not apply to a population with different characteristics.

29. 30.

31. 32. 33. 34.

Whaley MH, Brubarker PH, Otto RM (eds): ACSM’s Guidelines for Exercise Testing and Prescription, 7th ed. Baltimore, Lippincott Williams & Wilkins, 2006. Astrand PO, Rodahl K. Textbook of Work Physiology: Physiological Bases of Exercise, 4th ed. Windsor, Canada, Human Kinetics, 2003. Bruce RA, Kusumi F, Hosmer D: Maximal oxygen intake and nomographic assessment of functional aerobic impairment in cardiovascular disease. Am Heart J 1973;85(4):546-562. Taylor HL, Buskirk E, Henschel A: Maximal oxygen intake as an objective measure of cardio-respiratory performance. J Appl Physiol 1955;8(1):73-80. Astrand PO, Saltin B: Maximal oxygen uptake and heart rate in various types of muscular activity. J Appl Physiol 1961;16:977-981. Bergh U, Kanstrup IL, Ekblom B: Maximal oxygen uptake during exercise with various combinations of arm and leg work. J Appl Physiol 1976;41(2):191-196. Brahler CJ, Blank SE: VersaClimbing elicits higher VO2max than does treadmill running or rowing ergometry. Med Sci Sports Exerc 1995;27(2):249-254. Gleser MA, Horstman DH, Mello RP: The effect on Vo2 max of adding arm work to maximal leg work. Med Sci Sports 1974;6(2):104-107. Kasch FW, Phillips WH, Ross WD, et al: A comparison of maximal oxygen uptake by treadmill and step-test procedures. J Appl Physiol 1966;21(4):1387-1388. Nagle FJ, Richie JP, Giese MD: VO2max responses in separate and combined arm and leg air-braked ergometer exercise. Med Sci Sports Exerc 1984;16(6):563-566. Secher NH, Ruberg-Larsen N, Binkhorst RA, et al: Maximal oxygen uptake during arm cranking and combined arm plus leg exercise. J Appl Physiol 1974;36(5):515-518. Astrand PO: Quantification of exercise capability and evaluation of physical capacity in man. Prog Cardiovasc Dis 1976;19(1):51-67. Balke B, Ware RW: An experimental study of physical fitness of Air Force personnel. U S Armed Forces Med J 1959;10(6):875-888. Ellestad MH, Allen W, Wan MC, et al: Maximal treadmill stress testing for cardiovascular evaluation. Circulation 1969;39(4):517-522. Froelicher VF Jr, Brammell H, Davis G, et al: A comparison of three maximal treadmill exercise protocols. J Appl Physiol 1974;36(6):720-725. Pollock ML, Bohannon RL, Cooper KH, et al: A comparative analysis of four protocols for maximal treadmill stress testing. Am Heart J 1976;92(1):39-46. Pollock ML, Foster C, Schmidt D, et al: Comparative analysis of physiologic responses to three different maximal graded exercise test protocols in healthy women. Am Heart J 1982;103(3):363-373. Kyle SB, Smoak BL, Douglass LW, et al: Variability of responses across training levels to maximal treadmill exercise. J Appl Physiol 1989;67(1):160-165. Hansen JE, Casaburi R, Cooper DM, et al: Oxygen uptake as related to work rate increment during cycle ergometer exercise. Eur J Appl Physiol Occup Physiol 1988;57(2):140-145. Williams CA, Ratel S, Armstrong N: Achievement of peak VO2 during a 90-s maximal intensity cycle sprint in adolescents. Can J Appl Physiol 2005;30(2):157-171. Duncan GE, Howley ET, Johnson BN: Applicability of VO2max criteria: discontinuous versus continuous protocols. Med Sci Sports Exerc 1997;29(2):273-278. Howley ET, Bassett DR Jr, Welch HG: Criteria for maximal oxygen uptake: review and commentary. Med Sci Sports Exerc 1995;27(9):1292-1301. Noakes TD: Maximal oxygen uptake: ‘‘classical’’ versus ‘‘contemporary’’ viewpoints: a rebuttal. Med Sci Sports Exerc 1998;30(9):1381-1398. Noakes TD: Implications of exercise testing for prediction of athletic performance: a contemporary perspective. Med Sci Sports Exerc 1988;20(4):319-330. St Clair Gibson A, Lambert MI, Hawley JA, et al: Measurement of maximal oxygen uptake from two different laboratory protocols in runners and squash players. Med Sci Sports Exerc 1999;31(8):1226-1229. Day JR, Rossiter HB, Coats EM, et al: The maximally attainable VO2 during exercise in humans: the peak vs. maximum issue. J Appl Physiol 2003;95(5):1901-1907. Gu¨rsel Y, Sonel B, Gok H, et al: The peak oxygen uptake of healthy Turkish children with reference to age and sex: a pilot study. Turk J Pediatr 2004;46(1):38-43. Rivera-Brown AM, Alvarez M, Rodriguez-Santana JR, et al: Anaerobic power and achievement of VO2 plateau in pre-pubertal boys. Int J Sports Med 2001;22(2):111-115. Myers J, Walsh D, Sullivan M, et al: Effect of sampling on variability and plateau in oxygen uptake. J Appl Physiol 1990;68(1):404-410. Fielding RA, Frontera WR, Hughes VA, et al: The reproducibility of the Bruce protocol exercise test for the determination of aerobic capacity in older women. Med Sci Sports Exerc 1997;29(8):1109-1113. Cumming GR, Borysyk LM: Criteria for maximum oxygen uptake in men over 40 in a population survey. Med Sci Sports 1972;4(1):18-22. Stachenfeld NS, Eskenazi M, Gleim GW, et al: Predictive accuracy of criteria used to assess maximal oxygen consumption. Am Heart J 1992;123(4 Pt 1):922-925. Issekutz BJ, Birkhead NC, Rodahl K: Use of respiratory quotients in assessment of aerobic work capacity. J Appl Physiol 1962;17(1):47-50. Tanaka H, Seals DR, Monahan KD, et al: Regular aerobic exercise and the age-related increase in carotid artery intima-media thickness in healthy men. J Appl Physiol 2002;92(4):1458-1464.

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35. 36. 37.

38. 39. 40. 41. 42. 43.

44.

45. 46. 47. 48. 49. 50. 51.

.

Testing for maximal aerobic power

Borg GA: Psychophysical bases of perceived exertion. Med Sci Sports Exerc 1982;14(5):377-381. Borg GA, Noble B: Perceived exertion. In Wilmore J (ed): Exercise and Sport Science Reviews. New York, Academic Press, 1974, pp 131-153. Eston RG, Davies BL, Williams JG: Use of perceived effort ratings to control exercise intensity in young healthy adults. Eur J Appl Physiol Occup Physiol 1987; 56(2):222-224. Glass SC, Knowlton RG, Becque MD: Accuracy of RPE from graded exercise to establish exercise training intensity. Med Sci Sports Exerc 1992;24(11):1303-1307. Cooper KH: A means of assessing maximal oxygen intake. Correlation between field and treadmill testing. JAMA 1968;203(3):201-204. McNaughton L, Hall P, Cooley D: Validation of several methods of estimating maximal oxygen uptake in young men. Percept Mot Skills 1998;87(2):575-584. Zwiren LD, Freedson PS, Ward A, et al: Estimation of VO2max: a comparative analysis of five exercise tests. Res Q Exerc Sport 1991;62(1):73-78. George JD, Vehrs PR, Allsen PE, et al: VO2max estimation from a submaximal 1-mile track jog for fit college-age individuals. Med Sci Sports Exerc 1993;25(3):401-406. Kline GM, Porcari JP, Hintermeister R, et al: Estimation of VO2max from a one-mile track walk, gender, age, and body weight. Med Sci Sports Exerc 1987;19(3): 253-259. Berthoin S, Pelayo P, Lensel-Corbeil G, et al: Comparison of maximal aerobic speed as assessed with laboratory and field measurements in moderately trained subjects. Int J Sports Med 1996;17(7):525-529. Leger L, Boucher R: An indirect continuous running multistage field test: the Universite de Montreal track test. Can J Appl Sport Sci 1980;5(2):77-84. Leger LA, Lambert J: A maximal multistage 20-m shuttle run test to predict VO2 max. Eur J Appl Physiol Occup Physiol 1982;49(1):1-12. Naughton LM, Cooley D, Kearney V, et al: A comparison of two different shuttle run tests for the estimation of VO2max. J Sports Med Phys Fitness 1996;36(2):85-89. Storer TW, Davis JA, Caiozzo VJ: Accurate prediction of VO2max in cycle ergometry. Med Sci Sports Exerc 1990;22(5):704-712. Astrand PO, Ryhming I: A nomogram for calculation of aerobic capacity (physical fitness) from pulse rate during sub-maximal work. J Appl Physiol 1954;7(2):218-221. Lockwood PA, Yoder JE, Deuster PA: Comparison and cross-validation of cycle ergometry estimates of VO2max. Med Sci Sports Exerc 1997;29(11):1513-1520. Holland G, Hoffman J, Vincent W: Treadmill vs. steptreadmill ergometry. Phys Sportsmed 1990;18:79-85.

52. 53. 54. 55. 56.

57. 58.

59. 60. 61. 62. 63. 64.

65. 66. 67.

Beneke R: Anaerobic threshold, individual anaerobic threshold, and maximal lactate steady state in rowing. Med Sci Sports Exerc 1995;27(6):863-867. Roy JL, Smith JF, Bishop PA, et al: Prediction of maximal VO2 from a submaximal StairMaster test in young women. J Strength Cond Res 2004;18(1):92-96. Ebbeling CB, Ward A, Puleo EM, et al: Development of a single-stage submaximal treadmill walking test. Med Sci Sports Exerc 1991;23(8):966-973. Inoue Y, Nakao M: Prediction of maximal oxygen uptake by squat test in men and women. Kobe J Med Sci 1996;42(2):119-129. Petrella RJ, Koval JJ, Cunningham DA, et al: A self-paced step test to predict aerobic fitness in older adults in the primary care clinic. J Am Geriatr Soc 2001; 49(5):632-638. Teraslinna P, Ismail AH, MacLeod DF: Nomogram by Astrand and Ryhming as a predictor of maximum oxygen intake. J Appl Physiol 1966;21(2):513-515. Macsween A: The reliability and validity of the Astrand nomogram and linear extrapolation for deriving VO2max from submaximal exercise data. J Sports Med Phys Fitness 2001;41(3):312-317. Plasqui G, Westerterp KR: Accelerometry and heart rate as a measure of physical fitness: proof of concept. Med Sci Sports Exerc 2005;37(5):872-876. Swain DP, Parrott JA, Bennett AR, et al: Validation of a new method for estimating VO2max based on VO2 reserve. Med Sci Sports Exerc 2004;36(8):1421-1426. Blair SN, Kohl HW 3rd, Paffenbarger RS Jr, et al: Physical fitness and all-cause mortality. A prospective study of healthy men and women 1989;262(17):2395-2401. Heil DP, Freedson PS, Ahlquist LE, et al: Nonexercise regression models to estimate peak oxygen consumption. Med Sci Sports Exerc 1995;27(4):599-606. George JD, Stone WJ, Burkett LN: Non-exercise VO2max estimation for physically active college students. Med Sci Sports Exerc 1997;29(3):415-423. Malek MH, Housh TJ, Berger DE, et al: A new nonexercise-based VO2(max) equation for aerobically trained females. Med Sci Sports Exerc 2004;36(10):18041810. Malek MH, Housh TJ, Berger DE, et al: A new non-exercise-based Vo(2)max prediction equation for aerobically trained men. J Strength Cond Res 2005;19(3):559-565. Duncan GE, Li SM, Zhou XH: Cardiovascular fitness among U.S. adults: NHANES 1999-2000 and 2001-2002. Med Sci Sports Exerc 2005;37(8):1324-1328. Carnethon MR, Gulati M, Greenland P: Prevalence and cardiovascular disease correlates of low cardiorespiratory fitness in adolescents and adults. JAMA 2005;294(23):2981-2988.

CHAPTER

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Exercise-Induced Asthma Testing Rochelle M. Nolte, MD, and Christopher J. Lettieri, MD

KEY POINTS

. .

.

.

.

Self-reported symptoms are not reliable for identifying exercise-induced asthma. The International Olympic Committee Medical Commission and the United States Anti-Doping Agency require that all athletes who will use a b-agonist before competition must have objective evidence of exercise-induced asthma. Although a pharmacologic challenge such as methacholine can diagnose exercise-induced asthma in some instances, a negative test cannot definitively rule out asthma, and a physiologic bronchoprovocative test should be performed if an athlete is having symptoms. False negatives may occur if exercise-induced asthma screening is done by a physiologic challenge with inadequate exercise or environmental stress.This may lead to the need for repeat testing or for referral for methacholine challenge testing in an athlete with symptoms but with a negative test result. False positives can occur with all bronchoprovocative testing, and any diagnosis that is in doubt should be confirmed by another means.

INTRODUCTION Exercise-induced asthma (EIA) is characterized by symptoms of coughing, wheezing, shortness of breath, and/or chest tightness either during or after exercise1 (Table 42.1). EIA is also associated with airway obstruction as evidenced by a drop in forced expiratory volume in 1 second (FEV1). There are two commonly used terms: EIA and exercise-induced bronchospasm.1 In patients with underlying asthma, it is thought that the mechanism of action is an inflammatory process, and occasionally the term EIA is used to refer to an exacerbation in a patient with persistent asthma. The term exercise-induced bronchospasm is sometimes used to refer to bronchial obstruction as a result of exercise in a person who does not have persistent asthma, and the mechanism may be The views expressed in this chapter are those of the authors and are not to be interpreted as the views of the US Army, the US Coast Guard, or the US Public Health Service.

something other than an inflammatory process.1 For the purposes of this chapter, EIA will refer to both categories (Box 42.1). The overall incidence of EIA is estimated to be 12% to 15% (LOE: B).2 It is estimated that 90% of patients with asthma have EIA and that 35% to 40% of patients with allergic rhinitis have EIA. The remainder of the general population is estimated to have an incidence of EIA that ranges from 3% to 16%.2,3 The estimated prevalence of EIA in some selected populations is listed in Table 42.2. Patients with previously diagnosed persistent asthma appear to have chronic inflammatory changes that may require daily treatment with inhaled corticosteroids. Exercise may initiate a cascade of inflammatory events that leads to bronchoconstriction in patients with underlying asthma. Patients with underlying asthma can also have an exacerbation precipitated by chemical irritants (e.g., chlorine in pools, the high levels of nitrogen dioxide in ice arenas4,5). Patients with persistent asthma also seem to have more severe exacerbations than individuals who only have exercise-induced symptoms. The rare fatal asthma exacerbations associated with exercise often involve excessive mucus production and mucus plugging in patients with underlying persistent asthma.6 Patients with previously diagnosed persistent asthma may also be more prone to emotional stimuli, and they may have an exacerbation that is precipitated by competition anxiety.6 Patients who do not have persistent asthma but who only have exercise-induced symptoms appear to be more at risk of developing EIA with exposure to cold or dry air. The precise mechanism of EIA is not exactly known, but it is postulated that the high minute ventilation associated with aerobic activity may dry and cool the airways of the athletes or possibly lead to the release of mediators that cause bronchoconstriction. Another theory is that the rewarming of the airways after exercise leads to the dilatation of the small vessels that wrap around the bronchial tree and that the influx of warm blood leads to fluid exudation from the blood vessels into the submucosa of the airway wall, which leads to mediator release with subsequent bronchoconstriction. There is also some evidence that inflammation may be involved, but it does not appear to be as extensive in patients with EIA as it is in patients with chronic asthma.3 Exercise typically results in airway dilation, even among asthmatics. As such, dyspnea that occurs shortly after the onset of exercise is unlikely to result from bronchoconstriction. In individuals with an early onset of dyspnea, causes other than asthma, such as deconditioning and cardiac disease, should be considered. In susceptible individuals, exercise may result in transient

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530 Chapter 42

Table 42.1

.

Exercise-induced asthma testing

Symptoms of Exercise-Induced Asthma

Cough during or after exercise Wheezing during or after exercise Shortness of breath during or after exercise Chest tightness during or after exercise Congestion or excessive mucus production during or after exercise Excessive fatigue with training Feeling ‘‘out of shape’’ for the current level of training Chest pain or headache (atypical symptoms) Abdominal pain, cramps, or nausea (atypical symptoms)

bronchospasm and precipitate asthma symptoms. Bronchospasms typically peak 5 to 10 minutes after stopping exercise. The diagnosis should be considered for a patient with an exercise limitation who reports cough, shortness of breath, wheezing, and chest discomfort during or shortly after exercise. In May 2001, the International Olympic Committee Medical Commission (IOC-MC) held a workshop to examine asthma and the use of b-agonists. The workshop concluded the following:  At recent Olympic Games, there had been a large increase in the number of athletes who notified officials of their need to inhale a b-agonist.  Some athletes may have been misdiagnosed and may not have had EIA.  There is no scientific evidence to confirm that inhaled bagonists enhance performance in the doses that are required to inhibit EIA.

Box 42.1: Checklist Box  Take a thorough history.  Perform a thorough physical examination.  Follow up any abnormalities that are found on cardiac or pulmonary examination.  Follow up any treatment of any evidence of allergies or respiratory infections.  Perform spirometry.  If spirometry at rest is abnormal, evaluate and treat the condition as persistent asthma.  If spirometry at rest is normal, perform challenge testing.  Instruct the patient about medications to be withheld and to avoid exercise or caffeine on the day of testing.  Ensure that a portable spirometer is ready to be taken to the field, that it has an appropriate power source, and that it is set up to record and store prechallenge and (numerous) postchallenge trials  Ensure that mouthpieces are available to take to the field or that an appropriate cleaning technique can be performed.  Ensure that a nose clip is ready to be taken to the field.  Ensure that an inhaled bronchodilator is available for treating clinically significant dyspnea.  Ensure that everything that is needed for data collection is in place and working correctly. Even if it is, have a backup plan (e.g., hand copying all of the results on the display screen while you are in the field in case there is a glitch in the system when you get back to the office to download the results).

Table 42.2 Prevalence of Exercise-Induced Asthma in Selected Populations10 Patients with chronic asthma Patients with allergic rhinitis Patients without asthma or allergic rhinitis 1984 US Olympic Team 1996 US Summer Olympic Team 1998 US Winter Olympic Team Basketball players Finnish runners Figure skaters Cross-country skiers

90% 35% to 40% 3% to 16% 11% 20% 23% 12% 9% 30% to 35% 55%

 A skewed distribution of notifications of b-agonist use by sport was observed, with a higher prevalence in endurance sports.  The geographic distribution of notifications of inhaled b-agonists was markedly skewed, but it correlated well with the reported prevalence of asthma symptoms in the corresponding countries.  There is some evidence that the daily use of an inhaled b-agonist may result in tolerance to the medication.  Inhaled corticosteroids may be underused among the athletes who are notifying officials of the use of b-agonists.  Eucapnic voluntary hyperventilation (EVH) was considered to be the optimal laboratory-based challenge to confirm that an athlete has EIA.  When they are administered systemically, b-agonists do have anabolic effects.7 For the 2002 Olympic Games in Salt Lake City, Utah, and for all Olympic Games since, the IOC-MC has required objective evidence of EIA for all athletes planning to use an inhaled bagonist before competition.8 A note from a treating physician stating that the athlete has EIA is no longer acceptable because a report of symptoms has not been found to be a reliable way to make the diagnosis of EIA.1,9 The IOC-MC requires testing with either a bronchodilator test that demonstrates the reversibility of bronchoconstriction with the administration of an inhaled bronchodilator measured with spirometry or with a bronchial provocation test for athletes who only have symptoms with exercise. The acceptable bronchial provocation tests must all demonstrate a fall in FEV1. Peak expiratory flow measurements (such as those commonly obtained in primary care clinics with a peak flow meter) are unacceptable. The acceptable bronchial provocation tests include EVH, the inhalation of a hypertonic aerosol such as saline or mannitol, methacholine challenge, and an exercise challenge test, either in the laboratory or in the field.10,11 The thresholds that define a positive bronchial provocation test are arbitrarily determined. Table 42.3 lists different values that are used by various organizations to diagnose EIA. Typically, a challenge is done by measuring a baseline FEV1 and then measuring the decrease in FEV1 after the challenge. Setting the threshold for diagnosis at a lower decrement increases the sensitivity of the test but decreases the specificity. Setting the threshold for diagnosis at a higher decrement increases specificity but decreases sensitivity. Eliasson and colleagues12 evaluated the sensitivity and specificity of four techniques: indoor exercise challenge on a cycle ergometer, methacholine challenge, EVH with dry gas, and EVH with cold gas. The study looked at 20 patients without known chronic asthma who presented with symptoms of EIA. They were compared with 20 controls in the randomized crossover study. The threshold for each of the tests that yielded 100% specificity was a drop in FEV1 of 9% for indoor exercise challenge (which led to a

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Introduction 531

Table 42.3

Pulmonary Function Testing Criteria for the Diagnosis of Asthma7,12-17

American Thoracic Society

Bronchodilator Response

Exercise Testing

Methacholine Challenge

Eucapnic Voluntary Hyperventilation

12% and 200 cc improvement in FEV1 or FVC 12% improvement in FEV1

10% decrease in FEV1 after exercise 10% decrease in FEV1 after exercise 15% decrease in FEV1 after exercise None stated None stated None stated

20% decrease in FEV1 at 8 mg/mL 20% decrease in FEV1 at 4 mg/mL 20% decrease in FEV1 at 4 mg/mL None stated None stated None stated

12% decrease in FEV1 after 6 minutes of hyperpnea in dry air 10% decrease in FEV1 after 6 minutes of hyperpnea in dry air 15% decrease in FEV1 after 6 minutes of hyperpnea in dry air None stated None stated None stated

International Olympic Committee Medical Commission US Army 15% improvement in FEV1 US Air Force US Navy/Marines US Coast Guard

15% improvement in FEV1 None stated None stated

FEV1, forced expiratory volume in 1 second; FVC, forced vital capacity.

sensitivity of only 10%); 15% for methacholine challenge (which was 55% sensitive); 11% for dry gas EVH (with 50% sensitivity); and 12% for cold gas EVH (with 35% sensitivity). They determined that the indoor exercise challenge was not sensitive enough to be used to rule out EIA. For the other tests, thresholds that were thought to give the best ratio of specificity and sensitivity were 12% for methacholine challenge (95% specific and 65% sensitive); 5% for dry gas EVH (80% specific and 75% sensitive); and 5% for cold gas EVH (90% specific and 80% sensitive).12

Bronchodilator testing Bronchodilator testing is done by having the patient perform baseline spirometry (when off of caffeine and all medications that may affect the test and at least 4 hours after any physical exercise), administering an inhaled bronchodilator (e.g., a b2-agonist), and then repeating the spirometry. The reversibility of airflow obstruction is established by an increase in FEV1 or forced vital capacity (for specific levels, see the Interpretations section later in this chapter). Although a bronchodilator challenge can be used as evidence of EIA, it can give a false-negative result in some athletes. Athletes who only have symptoms after exercise may not show any increase in FEV1 after administration of a b2-agonist at rest. If an athlete who has shown no increase in FEV1 with a bronchodilator challenge is complaining of symptoms of EIA, an exercise challenge is recommended.

Methacholine challenge testing A fall in FEV1 of 20% or more from baseline is considered to be a positive methacholine challenge.7 As with the bronchodilator testing, a negative result with a methacholine challenge does not necessarily exclude EIA, and an alternate provocative test should be used if an athlete has symptoms. Although the methacholine challenge test is a commonly used bronchoprovocative test for the diagnosis of asthma, it is thought that some athletes with EIA may have a trigger that is precipitated by intense physical activity but not by a pharmacologic challenge. Although methacholine challenge testing is currently the most common airway challenge performed in the United States, it is not widely available in most primary care offices, and it may require referral to a pulmonologist or to a large clinic that has the facilities to perform full pulmonary function testing.

Eucapnic voluntary hyperventilation testing EVH is considered positive when a fall in FEV1 of 10% or more is recorded after a 6-minute period of hyperpnea in dry air.7

EVH testing requires the subject to hyperventilate dry air containing 5% carbon dioxide at room temperature for 6 minutes at a target ventilation of 30 times the subject’s FEV1.11 EVH can induce EIA symptoms in athletes by having them breathing at a ventilation rate that is equivalent to or higher than most forms of exercise.11 As with exercise, a variety of mediators are likely to be involved in the response. EVH is suggested as an alternative to exercise challenge testing. It is not as commonly performed as a methacholine challenge, and it may require referral to a large pulmonary clinic or a tertiary care medical center for testing, but the IOC-MC considers it to be the optimal laboratory-based challenge to confirm that an athlete has EIA.7

Exercise challenge testing (laboratory based) The response to an exercise challenge is considered abnormal or suggestive of EIA when there is a fall in FEV1 of 10% or more as compared with baseline during the first 30 minutes after exercise. A fall in FEV1 of 15% is considered highly suggestive and specific for EIA. Exercise challenge testing done in a laboratory usually consists of spirometry or pulmonary function testing before and after (usually immediately after and then 5, 10, 15, 20, and 30 minutes after exercise) a standard exercise protocol on either a treadmill or a cycle ergometer. Having patients do their exercise challenge test in a laboratory setting ensures that the temperature, humidity, and level of exertion can all be monitored and controlled, but there are some drawbacks. False-negative results are possible in a laboratory setting for patients who may have symptoms only at high levels of exertion during competition or intense training that cannot be simulated in the laboratory or for patients who have an environmental precipitant that is present while they are competing or training but not in the laboratory.

Exercise challenge testing (sport specific/ field based) A sport-specific exercise challenge is another option, and it can be a more sensitive tool to diagnose EIA in some athletes, especially if an environmental trigger from the training environment is contributing to their symptoms. An exercise challenge test in the field uses the same criteria for fall in FEV1 to make the diagnosis of EIA as a laboratory-based challenge test. A field-based exercise challenge is done by having the athlete perform his or her sport at the level of intensity and in the conditions in which he or she has experienced symptoms. The test is done by taking a portable spirometer to the athlete’s area of training or competition and

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having the athlete perform spirometry before competing or training and then repeating the spirometry after competition (or simulated competition). The athlete should be exercising at a level of intensity that is high enough to precipitate symptoms. Having the athlete in his or her usual training environment—whether it is an indoor pool, an ice arena, or an outdoor ski area—seems to increase the sensitivity, but conditions such as temperature or humidity outside and chlorine or nitrogen dioxide levels inside cannot always be predicted or controlled. As such, the test may need to be repeated.

EVALUATION Diagnosing EIA starts with a thorough history from the athlete regarding his or her symptoms. History taking should focus on when the athlete has symptoms and what the relationship of those symptoms is to exercise. Any symptoms that are not related to exercise should be noted (e.g., nocturnal symptoms), as should any seasonal variation. The age at which the athlete first noted symptoms is important, as is any history of any allergic symptoms, aspirin allergy, nasal polyposis, or eczema. Any specific triggers (e.g., temperature, dry air, specific indoor pools or arenas) should also be noted. A family history of asthma, atopic dermatitis, or other related problems should be asked about. When distinguishing EIA from other causes of shortness of breath while exercising, the history can be quite helpful. A lack of physical fitness may lead to shortness of breath that progresses through the exercise session but that improves with the cessation of activity. However, the symptoms of EIA generally persist after the cessation of exercise. Evaluating for risk factors of vocal cord dysfunction is important, especially in patients who appear to have EIA that is refractory to treatment. A thorough physical examination should be performed. Although the examination will usually be normal, evaluating for signs of allergies and nasal polyps as well as for cardiac or pulmonary abnormalities is important. Auscultation of the heart for murmurs, gallops, or thrills; of the glottis for an inspiratory wheeze; and of the lungs for abnormal sounds or prolonged expiration should be performed. After a thorough history and physical examination, spirometry should be performed. If spirometry at rest shows baseline obstruction, a trial of reversibility with an inhaled bronchodilator is indicated. If the pattern is reversible (and the patient is not having an acute exacerbation or trigger), then the patient has persistent asthma, and he or she should have all of his or her symptoms addressed and be evaluated for daily treatment with inhaled corticosteroids. If spirometry at rest is normal, the athlete may still have EIA, and some challenge testing should be performed (Boxes 42.2 and 42.3). For a list of tests that are commonly used to diagnose EIA in the United States, see Table 42.4. There are many portable and handheld spirometers available today. Any spirometer used should meet the standards of the American Thoracic Society. The ideal spirometer for field testing will be durable, easily transported, electrically safe, able to work at different temperatures and humidity levels, hygienic, accurate, able to hold a record of tracings until they can be downloaded and printed, and easy to use. If possible, having the athlete complete a trial of spirometry in the office before proceeding with field testing is helpful because this gives the athlete a chance to be coached and to learn how to do the spirometry correctly, and it increases the chances of having an accurate test when in the field. The patient should be instructed to withhold some medications before the exercise challenge test. Leukotriene antagonists should be withheld for 4 days. Long-acting bronchodilators,

Box 42.2: Indications for Testing for ExerciseInduced Asthma  Any typical symptoms of exercise-induced asthma  Atypical symptoms that may be related to exercise-induced asthma, such as fatigue, muscle cramps, abdominal pain, sore throat, or feeling ‘‘out of shape’’ for the current level of training and conditioning  To confirm a suspected diagnosis of exercise-induced asthma  To provide objective evidence of exercise-induced asthma before the use of a bronchodilator during competition in any event in accordance with International Olympic Committee or United States Olympic Committee guidelines  To evaluate athletes who exercise in high-risk environments (e.g., cold dry air, ice arenas, indoor pools)  To monitor the effectiveness of treatment

antihistamines, and nedocromil should be withheld for 2 days. Short-acting bronchodilators should be withheld for 8 hours. No inhaled corticosteroids or cromolyn should be used on the day of testing (some recommend withholding inhaled corticosteroids for 1 week before testing). On the day of the test, the patient should avoid caffeine, and he or she should not exercise before reporting for the testing session. The athlete should perform spirometry (with the results of the best of three trials used) before the exercise session. If the testing is being done at an actual competition, the pretest spirometry should be done before any warm up exercises are done. The athlete should proceed with his or her normal warm up routine and competition. It has been shown that an exercise session does not need to be longer than about 6 to 8 minutes to produce symptoms as long as

Box 42.3: Contraindications for Testing for Exercise-Induced Asthma              

Acute illness that may affect test results Exercise during the previous 4 hours Hemoptysis Nausea and vomiting Acute vertigo Recent pneumothorax Recent thoracic surgery Known aortic aneurysm Recent abdominal surgery Recent eye surgery Recent myocardial infarction or unstable angina Stroke within the previous 3 months Pregnancy Uncontrolled hypertension (systolic blood pressure >200 mm Hg or diastolic blood pressure >100 mm Hg)  The patient has not correctly followed instructions for withholding medications  The patient is unwilling to cooperate with testing (the test is effort dependent)

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Table 42.4 Tests Currently Used for the Diagnosis of Exercise-Induced Asthma in the United States Bronchodilator challenge testing Methacholine challenge testing Eucapnic voluntary hyperventilation Laboratory-based exercise challenge testing Sport-specific field-based exercise challenge testing

   

the exercise is done at high intensity. The exercise session should mimic the athlete’s competition environment (or the training environment, if that is where the symptoms are occurring) as closely as possible. If it is logistically possible, the exercise challenge can be done at an actual competition. In some cases, this could be an exercise session of more than an hour for some endurance events, or it may be less than a minute long for some winter sports (e.g., downhill skiing, speed skating). After the exercise session, repeat spirometry should be done at intervals 5, 10, 15, 20, and 30 minutes after exercise, with three trials performed at each interval. There are many different proposed intervals for the after-exercise testing, from every 3 minutes starting at 2 minutes after exercise to every 10 minutes for 30 minutes. Most recommended regimens involve intervals of 5 to 10 minutes for the 30 minutes after exercise. The postexercise spirometry may be discontinued if the FEV1 has hit a nadir and returned to baseline on subsequent testing. For example, if the trial at 10 minutes was 20% below baseline but the trials at 15 and 20 minutes had improved and returned to the pre-exercise baseline, then the 30-minute postexercise test can be skipped. Care should be taken to avoid having the intervals be so frequent or numerous that the athlete tires and is not capable of giving an adequate effort to produce accurate results. An inhaled bronchodilator should be available to be administered at any time to reverse clinically significant dyspnea or to treat a patient who has not recovered to within 10% of baseline by the end of the testing session.

TECHNIQUES AND EQUIPMENT  Evaluate the patient for contraindications, and review his or her medications.  Counsel the patient about the examination and what it is being used for, and ensure that the patient understands and consents to the testing.  Instruct the patient to withhold all appropriate medications and to avoid exercise and caffeine before testing.  Ensure that the patient has been adequately coached regarding how to do the spirometry and that he or she demonstrates proper technique.  Calibrate the machine according to the instructions for the particular instrument.  Enter all of the patient’s demographic data (e.g., sex, height, age) according to the instructions that accompany the spirometer.  Ask the patient if he or she would like to urinate before the test.  Provide a nose clip for the patient, and ensure that it is in place.  Have the patient take three normal tidal volume breaths.  Have the patient take a maximal inhalation.  Have the patient place the mouthpiece into his or her mouth.  Have the patient perform a forced maximal expiration by instructing the patient to blow as hard and as fast as he or she can. Coach and encourage the patient by emphatically saying

‘‘Breathe, breathe, breathe,’’ ‘‘Faster, faster, faster,’’ ‘‘Go, go, go,’’ or something similar until the forced vital curve flattens out (the test should last for at least 6 seconds) At the end of the maximal exhalation, have the patient do a maximal inhalation. Repeat this process for three trials to check the reproducibility of the results. Repeat this entire sequence at each of the postexercise testing intervals, and ensure that the results are recorded. Ensure that an inhaled bronchodilator is available to treat any clinically significant dyspnea that is precipitated by the exercise session.

INTERPRETATIONS Table 42.3 lists the diagnostic criteria of the IOC-MC, the American Thoracic Society, and the different branches of the US military for the various tests used to diagnose EIA.

Bronchodilator testing The American Thoracic Society and the IOC-MC have slightly different diagnostic criteria for diagnosing asthma when using a bronchodilator test. According to the American Thoracic Society, a patient should have symptoms that are suggestive of asthma, and he or she should have a spirometry measurement that shows obstruction at baseline that is reversible with an inhaled bronchodilator. The IOC-MC does not specify what symptoms a patient must demonstrate or that the baseline spirometry must be below normal. In other words, if an athlete has a baseline spirometry of 100% of predicted at baseline and improves to 112% of predicted after treatment with an inhaled bronchodilator, then he or she meets the IOC-MC’s established criteria for being able to use an inhaled bronchodilator before competition. A bronchial reversibility test is considered positive if there is an increase of 12% or more of the baseline FEV1 or forced vital capacity and if the increase exceeds 200 mL after that administration of an inhaled b2-agonist.7

Eucapnic voluntary hyperventilation testing The IOC-MC considers EVH to be the optimal laboratory-based challenge for confirming that an athlete has EIA. The EVH test is considered positive when a fall in FEV1 of 10% or more from baseline is recorded after a 6-minute period of hyperventilation in dry air.7

Exercise challenge testing The response to the exercise challenge is considered positive when there is a fall in FEV1 of 10% or more as compared with baseline during the first 30 minutes after exercise for either a laboratory-based or a field-based test according to the IOC-MC.7 According to the American Thoracic Society, a fall in FEV1 of 15% is more specific for EIA, but a 10% fall is a reasonable threshold for diagnosis because healthy subjects generally demonstrate an increase in FEV1 after exercise.13

Methacholine challenge testing Before a methacholine challenge test, all of the medications mentioned previously should be held. Corticosteroids in particular should be held for 1 week before testing. A methacholine challenge test is considered positive by the IOC-MC if there is a fall in FEV1 of 20% or more from baseline at a dose that is less than

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Table 42.5 Risks and Benefits of Testing for Exercise-Induced Asthma Risks

Benefits

Danger to patient if testing is done with one of the contraindications present Risk of precipitating a clinically significant asthma attack Risk of not being able to get results if all needed equipment is not present and functioning properly Risk of distracting athlete if testing is done during actual competition Risk of false-positive or falsenegative results if procedure is not properly followed Time-consuming test to do in the field

Provides proper diagnosis of exercise-induced asthma for athletes, thus permitting proper management Can help exclude exercise-induced asthma, thus preventing inappropriate prescribing of medications Provides needed documentation for athletes participating in events sanctioned by the International Olympic Committee and United States Olympic Committee who will use an inhaled bronchodilator before competition Provides a baseline against which future testing can be done when an athlete is being treated Provides results that can be used to educate the athlete about his or her condition

or equal to 2 mmol, 400 mcg (PD20); after the inhalation of a solution with a concentration that is less than or equal to 4 mg/mL (PC20); or after the inhalation of a maximum of 40 breath units when the subject is not taking inhaled corticosteroids.7 Occasionally, a patient who is taking inhaled or oral corticosteroids may be a candidate for a methacholine challenge test. For patients who have been taking inhaled steroids for at least 3 months, the PD20 should be less than or equal to 6.6 mmol, 1320 mcg, or the PC20 should be less than or equal to 13.2 mg/mL or to the inhalation of a maximum of 130 breath units to be accepted as proof of airway hyperresponsiveness, according to the IOC-MC.7

PITFALLS, COMPLICATIONS, CONTROVERSIES, RISKS, AND BENEFITS For the risks and benefits of testing for EIA, see Table 42.5.  Provocative testing may precipitate a clinically significant asthma attack. The testing physician should ensure that measures are available to treat a possible attack by having an inhaled bronchodilator available and by having the ability to provide emergency care or to call for emergency transport, if needed.  Presumptive treatment with an inhaled bronchodilator before exercise on the basis of history is still advocated by some. This may be acceptable if the following conditions are present:  The athlete has had a physical examination that excludes any cardiac or other serious causes of his or her symptoms.  The athlete has never had an attack that required emergency medical treatment.  The athlete is going to return for reevaluation to see if the symptoms do indeed improve with the use of the bronchodilator.

 The athlete has no intention of participating in any sporting event sanctioned by the IOC or the United States Olympic Committee.  The athlete has no intention of doing something in the future (e.g., applying to a military academy, entering an occupation with strict physical entrance requirements) that would be precluded by a diagnosis of asthma or the prescription of an inhaled bronchodilator. If the athlete does have contradictory intentions, spirometry should be performed to ensure that the diagnosis of asthma is correct because it may have a significant adverse effect on a young person’s future.  Evaluating for EIA by measuring peak expiratory flow rates using a peak flow meter:  This is easier for many providers because peak flow meters are more affordable than spirometers.  A peak flow meter is easier to use in the field because the athlete can be given his or her own peak flow meter and taught how to measure for a decrease in peak flow after exercise.  These meters can only be used by reliable and motivated patients because testing is extremely effort dependent. The peak expiratory flow rate is considered unreliable and insensitive for the diagnosis of asthma, and it is not recommended as a diagnostic test  This test cannot be used to confirm the diagnosis of any athlete competing in events that are sanctioned by the IOC or the United States Olympic Committee or that are monitored by the World Anti-Doping Agency or the United States AntiDoping Agency.  This test should not be used for any individual who may in the future want to do something that would be precluded by being diagnosed with asthma or being prescribed an inhaled bronchodilator, such as applying to a military academy or entering an occupation with strict physical entrance requirements. If the patient wishes to do one of these things, then spirometry should be performed to confirm that the diagnosis is correct, because the results could have significant adverse effects on a young person’s future.  Vocal cord dysfunction frequently mimics the symptoms of EIA. Patients with vocal cord dysfunction are often misdiagnosed as having EIA, which leads not only to the inappropriate use of medications (with unnecessary exposure to side effects) but also to a risk of progressing to the use of other medications with more significant side effects as the patient proves to be unresponsive to traditional treatments.  There is some controversy about the IOC-MC’s policy of requiring objective evidence of EIA because there is no scientific evidence to confirm that inhaled b2-agonists enhance performance in the doses that are required for treatment.5,6

CONCLUSION EIA can cause functional limitations for athletes. While a presumptive diagnosis can be made and short-acting bronchodilators used emprically prior to exercise, this diagnosis should be confidently established when possible. There are conditions that can mimic EIA, and patients not experiencing an expected response to therapy should be evaluated further. While there are pharmacologic and physiologic bronchoprovocative tests that are sensitive and specific for airway hyperreactivity, both false negatives and false positives can occur and the results should always be correlated with the clinical picture.

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REFERENCES 1. 2. 3. 4. 5.

6.

7.

8. 9. 10.

11.

Storms WW: Review of exercise-induced asthma. Med Sci Sports Exerc 2003;35:1464-1470. Rupp NP: Diagnosis and management of exercise-induced asthma. Phys Sportsmed 1996;24:1-9. Storms WW: Asthma associated with exercise. Immunol Allergy Clin North Am 2005;25:31-43. Pope JS, Koenig SM: Pulmonary disorders in the training room. Clin Sports Med 2005;24:541-564. Witten A, Solomon C, Abbritti E, et al: Effects of nitrogen dioxide on allergic airway responses in subjects with asthma. J Occup Environ Med 2005;47: 1250-1259. Fields KB, Reimer CD: Chapter 22: Pulmonary problems in athletes. In Fields KB, Fricker PA (eds): Medical Problems in Athletes. Malden, Massachusetts, Blackwell Science, 1997, pp 136-150. International Olympic Committee Medical and Scientific Department: Beta2 adrenoceptor agonists and the Olympic Games in Turin, 2005. E-mail address: [email protected]. Weiler JM: Why must Olympic athletes prove that they have asthma to be permitted to take inhaled beta2-agonists? J Allergy Clin Immunol 2003;111:36-37. Holzer K, Bruckner P: Screening of athletes for exercise-induced bronchoconstriction. Clin J Sport Med 2004;14:134-138. Rundell KW, Wilber RL, Szmedra L, et al: Exercise-induced asthma screening of elite athletes: field versus laboratory exercise challenge. Med Sci Sports Med 2000;32:309-320. Anderson SD, Argyros GJ, Magnussen H, Holzer K: Provocation by eucapnic voluntary hyperpnoea to identify exercise-induced bronchoconstriction. Br J Sports Med 2001;35:344-347.

12.

13. 14. 15. 16. 17.

Eliasson AH, Phillips YY, Rajagopal KR, Howard RS: Sensitivity and specificity of bronchial provocation testing: an evaluation of four techniques in exercise-induced bronchospasm. Chest 1992;102:347-355. American Thoracic Society: Lung function testing: selection of reference values and interpretative strategies. Am Rev Respir Dis 1991;144:1202-1218. Headquarters, Department of the Army: Army Regulation 40-501: Standards of Medical Fitness. May 29, 2007. Secretary of the Air Force: Air Force Instruction 48-123: Medical Examinations and Standards. 2001. Medical Department, US Navy: NAVMED p. 117: Manual of the Medical Department, US Navy. August 12, 2005. Directorate of Health and Safety, US Coast Guard: Commandant Instruction Manual 6000. IC Change 2. July 13, 2007.

OTHER READINGS Barreiro TJ, Perillo I: An approach to interpreting spirometry. Am Fam Physician 2004;69:1107-1114. Crapo RO, Casaburi R, Coates AL, et al: Guidelines for methacholine and exercise challenge testing—1999. Am J Respir Crit Care Med 2000;161:309-329. Zakynthinos SG, Koulouris NG, Roussos C: Chapter 5: Respiratory system mechanics and energetics. In Mason RJ, Murray JF (Hon), Broaddus VC, Nadel JA (Hon) (eds): Murray and Nadel’s Textbook of Respiratory Medicine, 4th ed. Philadelphia, WB Saunders, 2005, pp 87-130.

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Gait Analysis Timothy L. Switaj, MD, and Francis G. O’Connor, MD, MPH

KEY POINTS

. Videotaped observational gait analysis (VOGA) is a safe . . . .

procedure with a long history of involvement in the analysis of children with gait disorders and adults with complex neuromuscular disorders. VOGA has emerged as a useful technique for the analysis of athletes, and it can be complemented by computer software packages that permit advanced biomechanical assessments. VOGA can aid the clinician with identifying subtle biomechanical patterns that may not be present on static examination and that can lead to running injuries. VOGA can be useful not only when designing a therapeutic plan for rehabilitation or orthotic fabrication but also when assessing a therapeutic intervention. Multiple studies show that observations are moderately reliable, even for those examiners with significant experience. Computer software has helped to decrease the variability in the interpretation of data.

forces, and electromyography. Videotaped observational gait analysis (VOGA) allows for the measurement and interpretation of kinematics, movement patterns, and kinetics as well as of the forces involved in producing those movements, such as joint forces and ground reaction forces. Overall, the predominance of the literature regarding VOGA is in the setting of physical therapy and rehabilitation for patients after a stroke and for children with neuromuscular disorders such as cerebral palsy. These studies have looked at patients with gross gait abnormalities in laboratories with very sophisticated equipment rather than at patients with only slight deviations from biomechanical norms in outpatient sports medicine clinics. However, VOGA is finding an increasing role in the practical evaluation of runners and other athletes who present for runningrelated injuries or pain. As such, more evidence-based research is needed to examine the uses of this tool in the outpatient sports medicine setting. This chapter will serve to provide an overview of VOGA that includes the equipment needed, the planning of a VOGA session, and the analysis of the data obtained (Box 43.1).

INDICATIONS AND CONTRAINDICATIONS INTRODUCTION The practice of gait analysis has been around for at least a century, but only recently, with the advancement of technology, has gait analysis been practical for the office setting and the nonelite athlete. Before the advent of technology, gait analysis was performed without the assistance of computers or videography, and interpretation relied solely on the clinical experience of the observer. Multiple studies in the nonmedical literature show repeatedly that observations are moderately reliable and that heightened clinical experience increases the reliability of the examiner’s observations.1-4 Just as technology has helped to advance the practice of medicine in many other disciplines, it has substantially aided the practice of gait analysis. Gait analysis is now more reliable as computers help to make measurements and videography allows for the frame-by-frame observation of movements. It is also a more practical and affordable application in the clinical practice setting for nonelite athletes. In addition to the advantages provided by videotaping the session, computer technology aids in the interpretation of data through the complex measurements of angles,

VOGA has an ever-widening breadth of uses in modern medicine. For many years, VOGA has been used in rehabilitation clinics to aid in the development and monitoring of rehabilitation programs for people after strokes, for children with congenital muscular abnormalities, and for hosts of other patients. More recently, it has become commonly used in attempts to identify subtle patterns of kinematic or kinetic abnormalities during dynamic periods that are not visible on static examinations to diagnose, prevent, or treat running injuries. It is also commonly used for the assessment of orthotic prescriptions as well as for assessing improvement in a therapy program. The military is using VOGA more and more for the assessment and monitoring of patients after they have sustained traumatic limb amputations and now have prostheses. VOGA can also be used with the assistance of pressure monitors for the evaluation of compartment syndrome, with examiners looking for foot drop during the taping session. Contraindications are few, but they mirror those of a patient who is being considered for graded exercise testing or another treadmill evaluation. Box 43.2 gives a summary of common indications and contraindications for VOGA testing.

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Box 43.1: Videotaped Observational Gait Analysis Checklist  Identify a patient that may benefit from a videotaped observational gait analysis session.  Evaluate the patient first with a history, a physical examination, and radiographs as needed, and ensure that no contraindications exist for the patient to perform on a treadmill.  Discuss the procedure with the patient, and schedule the session.  Ensure that all equipment is available and working properly and that the room has adequate lighting.  Obtain consent from the patient for the session.  Reinterview and examine the patient before starting the session, and ask the patient about any changes since the office visit that could affect the session.  Place retroflective tape on bony landmarks.  Perform a static evaluation of the patient with and without shoes.  Perform a dynamic evaluation of the patient on a treadmill with and without shoes as per taping session protocol.  Review the tape, and record results on an available data collection form.  Interpret the data either manually or with the aid of computer software.  Identify any deficiencies that are found in the data interpretation.  Devise a therapeutic plan to resolve deficiencies and implement a plan.  Arrange for follow up and possible repeat videotaped observational gait analysis session to monitor the progress of therapy.

EVALUATION To discuss abnormalities in gait that are identified using videotaped analysis, it is essential to understand the normal biomechanics of gait during both walking and running because there are significant differences between the two.

Box 43.2: Indications and Contraindications for Videotaped Observational Gait Analysis Testing Indications  Detection of subtle dynamic abnormalities in kinematics or kinetics that are not found on static evaluation  Evaluation for compartment syndrome  Development and monitoring of physical therapy programs  Assessment of orthotics and shoe wear  Evaluation of limb prostheses after amputation Contraindications  Known significant coronary artery disease  Recent myocardial infarction  Known obstructive disease that is being medically managed  Orthopedic or other conditions with which the patient would not be able to perform on a treadmill  Respiratory conditions such as asthma or chronic obstructive pulmonary disease that may be exacerbated by exercising on a treadmill

A gait cycle occurs from the initial contact of one foot with the surface until the recontact of that foot with the surface, and it is divided into two distinct phases: the stance phase and the swing phase. During walking, the major action occurs in the stance limb. Alternatively, during running, the majority of the force is supplied by the swing arm and leg. The stance phase starts when the foot contacts the surface. The swing phase starts at the toe off of the foot that just finished the stance phase. The stance phase makes up 60% of the walking gait cycle and is divided into four subphases: loading response, midstance, terminal stance, and preswing. Each subphase accounts for approximately 15% of the total gait cycle and 25% of the stance phase during walking. Loading response begins with the initial contact of the foot with the surface, and it is a period during which both feet are on the ground, thus providing a double support to the frame. Midstance occurs when the initial-contact foot makes full contact with the surface, at which time single support occurs as the other limb enters the swing phase. Single support occurs for as long as the other limb is in the swing phase. Terminal stance is when the initial contact foot is preparing to lift off of the surface. Preswing, which is the final subphase of the stance phase, is a second period during which double support occurs. The swing phase makes up the remaining 40% of the walking gait cycle; it begins with toe off and ends with initial contact. It is subdivided into the initial swing, midswing, and terminal swing. During walking, initial swing and terminal swing each occupy about 20% of the gait cycle, and the swing phase occurs in the limb opposite the one that is in the stance phase. Although it contains both a stance and a swing phase, the running gait cycle is very different, most notably in that the stance phase only occupies 40% of the gait cycle, whereas the swing phase occupies the remaining 60%. The stance phase during running has only two subphases: absorption and propulsion. Midstance is now the point at which absorption becomes propulsion. During running, the swing phase gets divided into two subphases: initial swing and terminal swing, with midswing being the point of transition between the two. Initial swing is the first 75% of the swing phase, with terminal swing making up the remaining 25%. Instead of double support periods (of which there are two during the walking gait cycle), running contains two periods of double float during which neither limb is in contact with the surface. These periods of double float are found at the beginning and end of the swing phase of the running gait cycle. In addition to understanding the stance and swing phases of the gait cycle, one must also understand several other terms: stride length, step length, and cadence. Stride length is defined as occurring from the initial contact of one foot with the surface to the initial contact of the other foot with the surface. This is limited, and it has a maximal length as a result of a person’s leg length, height, and overall abilities. Step length is one complete gait cycle, and cadence is the number of steps that occur during a given period. Generally, cadence varies from person to person and between men and women, with women having a natural cadence of six to nine steps per minute more than men. As one runs faster, initially step length increases, and this is followed closely by an increase in cadence. As mentioned, stride length has a finite maximal length up to which point an increase in stride length correlates with increased speed; however, after attaining that maximal stride length, increases in speed only occur with increases in cadence.

Kinematics Kinematics is defined as the independent motion of joints or body segments. They occur without an outside force acting on the joint or body segment. As with the gait cycle, there are significant

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Table 43.1 Normal Range-of-Motion Values for Lower-Extremity Joints during Running Phase

Joint

Range of Motion

Foot strike to midstance

Hip Knee Ankle

Midstance to take off

Hip Knee Ankle Hip Knee Ankle Hip Knee Ankle Hip Knee Ankle

45 to 20 degrees of flexion at midstance 20 to 40 degrees of flexion by midstance 5 degrees of plantarflexion to 10 degrees dorsiflexion 20 degrees of flexion to 5 degrees of extension 40 to 15 degrees of flexion 10 to 20 degrees of dorsiflexion 5 to 20 degrees of hyperextension 15 to 5 degrees of flexion 20 to 30 degrees of plantarflexion 20 to 65 degrees of flexion 5 to 130 degrees of flexion 30 to 0 degrees of plantarflexion 65 to 40 degrees of flexion 130 to 20 degrees of flexion 0 to 5 degrees of dorsiflexion to 5 degrees of plantarflexion

Follow through

Forward swing

Foot descent

Reproduced from McPoil TG, Cornwall MW: Applied sports biomechanics in rehabilitation: running. In Zachazewski JE, MaGee DJ, Quillen WS (eds): Athletic Injuries and Rehabilitation. Philadelphia, WB Saunders, 1996, p 356.

differences in the kinematics of walking and running, and these generally manifest as increased joint range of motion (ROM) during running. The differences in joint kinematics are primarily in the sagittal plane during running, with little to no difference in joint motion within the coronal or transverse planes.5 As an athlete runs and increases speed, the hips and knees increase flexion, and this is accompanied by an increase in ankle dorsiflexion, which results in a lower center of gravity.6 Normal ROM values can be found in Table 43.1. The hip has an overall increase in ROM as one goes from walking to running, and this is manifested by an increase in flexion and a decrease in extension. During walking, the hip generally flexes about 37 degrees and extends to 6 degrees, thus giving a total ROM of 43 degrees.7 During running, the hip increases flexion to about 46 degrees, and it rarely extends beyond neutral. Maximal extension occurs at the point of take off, with maximal flexion during the terminal swing. At the same time, the pelvis begins with 8 degrees of external rotation at initial contact and converts to 8 degrees of internal rotation at take off.5 The motion of the hip in the coronal plane does not significantly change as velocity increases. The knee is similar to the hip in that the primary changes occur with sagittal ROM manifested with an increase in flexion and a decrease in extension. The knee flexes during absorption while running. The average knee ROM during walking is 60 degrees, and it increases to 63 degrees with running. Walking flexion is 64 degrees, with 8 degrees of extension; during running, flexion increases to 79 degrees, and extension increases to 16 degrees. Neutral position does not occur in the knee during walking or running. At initial contact, the knee is flexed approximately 10 degrees during walking and 35 degrees with running.6 At the midstance of running, the knee reverses motion to enter the propulsive phase. The ankle primarily goes through plantarflexion and dorsiflexion during the gait cycle. During a normal walking gait cycle, the ankle plantarflexes to 18 degrees and dorsiflexes to about 12 degrees.7 However, during running, the overall ROM of the

ankle increases to about 50 degrees, with increased hip and knee flexion limiting the amount of plantarflexion and producing rapid dorsiflexion during the propulsion phase. The joints of the foot have motion that is not as simple as that of the ankle joint. Most of the foot joints have either biplanar or triplanar motion. Pronation and supination are triplanar motions. Pronation encompasses dorsiflexion, abduction, and eversion, whereas supination involves plantarflexion, adduction, and inversion. Multiple joints in the foot have triplanar motions that include the following: subtalar, oblique midtarsal, longitudinal midtarsal, and fifth ray. The first ray is triplanar, but, instead of displaying traditional pronation and supination, it shows dorsiflexion with adduction and inversion as well as plantarflexion with abduction and eversion. The metatarsophalangeal joints are biplanar with dorsiflexion and plantarflexion accompanied by abduction and adduction to about 10 degrees. Interphalangeal joints move in a similar fashion to the metatarsophalangeal joints; however, their abduction and adduction are even more limited. A summary of the normal kinematics of joints and body segments during the walking gait cycle can be found in Figure 43.1.

Kinetics Kinetics (as opposed to kinematics) looks at the forces that cause movement. There are internal forces, such as muscular activity, and external forces, such as ground reactions. Muscle forces uniformly increase during running, with an increase in muscle activity and muscle activity duration that occurs in all muscles. Ground reactive forces are more complex and can best be measured using a force plate and by looking at shoe wear patterns during the static examination. There are three components to ground reactive forces: fore—aft, medial—lateral, and vertical. Vertical is the most significant component for the gait cycle and its resultant forces on the body. The vertical forces produced during walking are routinely 1.3 to 1.5 times the body weight, occurring in peaks during the loading response and preswing.7 With running, these forces increase to three to four times the body weight, and they are distributed through the stance phase, with a small impact force during the first 20% of stance and the rest of the force distributed throughout the remainder of the stance phase.7 Fore—aft forces can best be described as breaking and propulsion. Breaking occurs during the first half of the stance phase, whereas propulsion occurs during the last half. The maximum fore—aft forces only reach about 30% of body weight. Medial—lateral forces are very small and seemingly insignificant, with maximums of only about 10% of body weight.

The videotaped observational gait analysis session A VOGA session needs to be a systematic process that is performed in the same way with every taping session. It starts with the preparation of the equipment to ensure that all equipment is in good working order with normal functionality. After ensuring that the equipment is ready, the examiner must begin to prepare the patient for the VOGA session. The patient needs to be in the appropriate attire for exercise and to have with them their usual running shoes. The patient should be prepared with the placement of retroflective tape strips on the bony landmarks of the body as illustrated in Figure 43.2. The observation of the patient’s posture and gait when he or she enters the room can provide useful information. After this, a static assessment should be performed. Regardless of the order in which the static assessment is performed, there are certain aspects that always need to be completed. These include the

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Initial floor contact 0%

Initial floor contact

Liftoff 15%

30%

45%

60%

80%

100%

Pelvis

Femur

Internal rotation

Internal rotation

External rotation

Tibia

Ankle joint

Subtalar joint

Plantar flexion

Dorsiflexion

Plantar flexion

Dorsiflexion

Eversion

Inversion

Eversion

Unstable

Increasing stability

Unstable

Intrinsic muscles

Inactive

Increasing activity

Inactive

Pretibial muscles

Active

Inactive

Active

Calf muscles

Inactive

Active

Inactive

Transverse tarsal joint Talo-navicular joint

Floor contact reaction

Midstance

Terminal stance

Preswing

Initial swing

Stance phase

inspection of the patient’s shoes for their wear pattern, an examination of the patient’s feet and their arches, and the examination of stance both with and without the wearing of shoes. One should evaluate the spine for curvature, the pelvis and shoulders for rotation or tilt, and the legs to determine if there is an underlying leglength discrepancy. A systematic approach should be taken when inspecting the remainder of the patient’s body before the exercise portion of the examination is begun. After the static assessment is complete, the patient can step onto the treadmill to begin the gait assessment. Several protocols have been devised to yield specific lengths of videotaping each section of the body from different views; Table 43.2 describes one such protocol.8 The protocol should ensure that the entire body is imaged in both static and motion positions from the sagittal, coronal, and transverse positions. Sagittal views will provide data about pelvic tilt, hip and knee flexion/extension, and ankle dorsiflexion/plantarflexion, whereas the coronal views describe pelvic obliquity, hip abduction/adduction, knee varus/ valgus, and foot inversion/eversion. The transverse plane can be used to determine the abnormal rotation of the pelvis, femur, tibia, and feet.9 Initially, the treadmill should be set with a 0 degree inclination and at a pace that is determined by the patient to be his or her comfortable pace. This needs to be a logical, systematic, and predetermined protocol that is

Terminal swing

Swing phase

Figure 43.1 The kinematics of the normal gait cycle. (Redrawn from Mann RA, HagyJ: Am J Sports Med 1980;8[5]:345-350.)

well known to all staff involved in the session. The grade and pace may need to be adjusted with regard to the patient’s complaint. For example, if the patient notes pain only with running uphill, then one would want to tape the patient’s movements while he or she is running on a graded incline. The session should be performed first with the patient barefoot, and then the entire session should be repeated with the patient wearing his or her usual running shoes.

TECHNIQUES AND EQUIPMENT A good, reliable VOGA session starts with adequate preparation, which is always begun with ensuring that one has the appropriate equipment for the study to be performed. To start, one needs an appropriate clinical setting in which to perform VOGA. The room needs to be large enough to incorporate the treadmill, the computer equipment, a bed or examination table, the patient, the observer, and his or her necessary staff. Although rare (especially given the low exercise stress of VOGA), there is the theoretic risk of a cardiac event or fainting, and, thus, one should have a bed or examination table available and know where the nearest cardiac emergency cart is located.

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In the past, the examiner needed a camera that had frameby-frame recording and zoom features as well as a recorder to make a tape of the session and then play it back. In today’s modern world, a digital video camera encompasses all of these features in one small package. A tripod is helpful to provide a stable platform for the camera to record the patient’s movements. Ideally, the tripod should be sturdy and able to be set for a camera height of 18 inches above the ground. To perform the VOGA session, the patient must be in appropriate attire and wearing his or her usual running shoes. Retroflective tape needs to be available to mark the bony landmarks on the patient’s body. A computer is also necessary with a monitor or TV screen that is an adequate size for seeing the retroflective tape to make measurements on the basis of these markings. There are software packages available to assist with data collection and the interpretation of the session; however, they can be expensive to purchase, and training may be required to master their use. A printer is necessary so that results can be printed for ease of interpretation and for placement in the patient’s medical record. If computer software is not available to assist with interpretation, a data collection or scoring sheet is needed.

Data collection Figure 43.2 The placement of retroflective tape on bony landmarks. (From O’Connor FG, Hoke B,Torrance A: Video gait analysis. In O’Connor FB, Wilder RP [eds]: Textbook of Running Medicine. NewYork, McGraw-Hill, 2001, p 59.)

There is no specific treadmill type or model that is better than others for the performance of VOGA; however, some characteristics need to be considered during the purchase of the treadmill. It needs to be of good quality, with the ability to provide speeds of 10 to 12 miles per hour and grades of 10% to 20%. The treadmill needs to be placed in the room so that the observer is able to have a good view of the patient from all necessary angles.

Table 43.2

Taping Session Protocol

Static Posture: Head to Feet Anterior, 10 seconds Lateral, 10 seconds Posterior, 10 seconds

Data collection can be made easier with either the use of computer software or the use of a kinematic gait analysis form. Many different forms are available for use, depending on the patient being studied; the available forms may need to be tailored to the appropriate clinical setting. Retroflective tape markers placed strategically on bony landmarks of the patient’s body will allow for ease of angular measurements while watching the videotaped session (Table 43.3). It is important that one uses retroflective markers because the use of reflective markers can make it more difficult to visualize the landmarks on video replay, and this increases the likelihood of the misinterpretation of the data. The use of markers with adhesive backgrounds poses the additional difficulty of skin irritation as a result of the adhesive backings.

Table 43.3 Position

Body Part

Landmark

Lateral

Head Shoulder Elbow Wrist Hip Knee Ankle Foot Lower back Knee Lower leg

Zygomatic arch Acromion Lateral epicondyle Ulnar styloid Greater trochanter Central femoral condyle Fibular malleolus Lateral border parallel to floor Posterior sacroiliac spine Popliteal fossa Bisection of the distal third of the tibia/fibula Calcaneal bisection Anterior sacroiliac spine Midpoint Tibial tuberosity Midline of second metatarsal

Posterior View Head to feet, 30 seconds Hips to feet, 30 seconds Lower leg and rear foot Shoes on, 30 seconds Shoes off (walking), 30 seconds Shoes off (running), 30 seconds

Posterior

Lateral View Head to feet, 30 seconds Hips to feet, 30 seconds

Anterior View (Optional) Head to feet, 30 seconds Hips to feet, 30 seconds Lower leg and feet, 30 seconds Reproduced from Hoke BR, Lefever-Button SL: When the Feet Hit the Ground, Everything Changes. Level Two: Take the Next Step. Toledo, OH, American Physical Rehabilitation Network, 1994, p 75.

Retroflective Taping Landmarks

Anterior

Foot Hip Patella Lower leg Foot

Modified from Hoke BR, Lefever-Button SL: When the Feet Hit the Ground, Everything Changes. Level Two: Take the Next Step. Toledo, OH, American Physical Rehabilitation Network, 1994, p 76.

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The use of the retroflective markers allows for the easy measurements of angles between bony landmarks, but it does not allow for the evaluation of the movement of the bony structures.

INTERPRETATION Just as with the VOGA taping session, the interpretation of the data to arrive at the results of the study requires a systematic process to ensure that no abnormality is missed. To be able to identify abnormal patterns identified during the VOGA session, it is essential to understand normal motion parameters. Subtle abnormalities in displacement, rotation, and ROM can suggest causes of running problems. The patient’s head should sit straight on his or her shoulders, with no rotation or anterior or posterior displacement seen during the gait cycle. Vertical displacement should not exceed 4 cm. The earlobe should remain in line with the tip of the shoulder at all times. Torticollis, muscular weakness, and prior trauma can be suggested by the abnormal carrying of the head during the gait cycle. Leg-length discrepancies are suggested by the excessive vertical displacement of the head as a result of an early heel lift during the gait cycle. The shoulders should move in a symmetric pattern; any abnormality in this area could indicate a contralateral lower-extremity injury. Normal elbow carry for the recreational runner is 80 to 110 degrees of flexion, with excess flexion leading to wasted energy. Arm movements that cross the midline are suggestive of pelvic rotation, and they can impair forward progression while the athlete is running. The trunk must be examined not only for rotation but also for forward, backward, and lateral lean. The trunk should be neutral in a vertical position with no forward or backward lean. Forward leaning while running may indicate weak back musculature or tight hip flexors, whereas a lateral lean of more than 4 cm can indicate a leg-length discrepancy or hip abductor weakness. Excessive external rotation of the hip can be an indicator of tight hip flexors, whereas excessive internal rotation may be evident in a patient with piriformis syndrome. Normal ranges of motion for the lower-extremity joints are found in Table 43.1. The hip must be observed not only for flexion and extension but also for rotation. Hip rotation cannot be directly measured using a standard VOGA session because an overhead view would be required. However, it can be inferred from multiple other views during the session. Rotation should not exceed 8 degrees, and pelvic drop should not exceed 4 degrees. The examiner must be on the lookout for evidence of tight hip flexors, which are demonstrated by excessive external rotation at the hip as well as weak hip abductors, which could lead to iliotibial band syndrome. When looking at the knee, the most important value is the cushioning flexion range, which is a calculation performed by subtracting the position of the knee at foot strike from its position at maximum stance flexion; quadriceps weakness is suggested when this value is less than 20 to 25 degrees. Hamstring weakness can be suggested by swing phase knee flexion of less than 115 to 120 degrees. The identification of ankle plantarflexion and dorsiflexion can provide a lot of information about the gait. Marked plantarflexion at heel strike can indicate anterior tibialis weakness or, more concerning, a drop foot resulting from an exertional compartment syndrome. Gastrocsoleus inflexibility or anterior tibial impingement, which are the more likely conditions of the ankle, are suggested by limited dorsiflexion. When limited dorsiflexion is combined with early heel off, one can suspect plantar fasciitis, metatarsalgia, or hallux limitus as possible complications. Finally, during the interpretation of VOGA data, one must not neglect the foot. Two joints exist in the foot that need

consideration: the subtalar joint and the midtarsal joint. Normal foot motion through the gait cycle starts with slight subtalar supination at heel strike followed by rotation into pronation up to a maximum of 6 to 8 degrees toward the end of contact. Resupination occurs during the midstance, peaking just before toe off during propulsion. The subtalar joint pronates early during the swing phase and then hovers near neutral for the remainder of the phase. When discussing the midtarsal joint, one must talk about its position with regard to two axes: the longitudinal and the oblique. At contact, supination occurs around the longitudinal axis, with pronation around the oblique axis. During midstance, the longitudinal axis becomes progressively more pronated, whereas the oblique axis remains unchanged. Full pronation around both axes occurs at heel off, and this is followed by progressive supination around the oblique axis during propulsion, which is maximal at toe off. Early during the swing phase, the joint pronates around the oblique axis. Later during this phase, it supinates around the longitudinal axis. Subtalar motion can be measured by placing tape at the proximal calcaneus and another several centimeters distal to yield the calcaneal angle. Normal ranges are as follows: 6 degrees of inversion at foot strike; 6 to 8 degrees of eversion at maximal pronation; neutral at heel lift; and 6 to 8 degrees of inversion at toe off. Excessive pronation is defined as persistent eversion during heel off. Another parameter that can be helpful when looking at the foot is the assessment of the angle of gait. This can be assessed best using a posterior view of the feet. Excessively wide gaits (> 1.5 inches) can suggest iliotibial band syndrome. Excessive external rotation of the foot (> 7 degrees) can indicate torsional abnormalities, a weak posterior tibialis, or limited dorsiflexion, possibly from an equinus deformity. Heel whips can also be identified by observing for exaggerated rotatory twisting of the heel after heel rise. Circumduction, or the accompanying lifting of the affected extremity with rotation, can indicate weakness of the anterior tibialis, joint restriction, or weak hip flexors. If the patient does not respond to therapies that address the abnormalities found during a VOGA session, one must consider other methods of evaluation and treatment. One possibility is that of force-plate analysis of the foot and consideration for orthotics. Many different commercially available systems exist, and one must be informed about the system that is available for use.

CONCLUSION VOGA is becoming more frequently available to the sports medicine provider at the individual clinic level. This technique is not just being used on elite athletes or complicated rehabilitation patients with known gait abnormalities. If a physician is to perform VOGA, he or she must have a defined protocol for the taping session with the proper equipment and preparation. The abnormalities found during the interpretation of data from a VOGA session can provide a target for the treatment of patients with running difficulties. Subtle differences in rotation, displacement, and angles can lead to a diagnosis that may have eluded the provider without the aid of VOGA. Data interpretation needs to be systematic in its performance by trained observers, with the normal ranges for the values being measured always kept in mind. Although the reliability of VOGA is considered moderate at best, increasing technology is allowing for greater ease of data gathering and interpretation; this makes it less expensive to perform and thus an option for the recreational runner with unidentifiable abnormalities.

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REFERENCES 1.

2. 3. 4.

5. 6. 7. 8.

9.

Brunnekreef JJ, van Uden CJ, van Moorsel S, Kooloos JG: Reliability of videotaped observational gait analysis in patients with orthopedic impairments. BMC Musculoskelet Disord 2005;6:17. Eastlack ME, Arvidson J, Snyder-Mackler L, et al: Interrater reliability of videotaped observational gait-analysis assessments. Phys Ther 1991;71(6):465-472. Krebs DE, Edelstein JR, Fishman S: Reliability of observational kinematic gait analysis. Phys Ther 1985;65(7):1027-1033. Wren TA, Rethlefsen SA, Healy BS, et al: Reliability and validity of visual assessments of gait using a modified physician rating scale for crouch and foot contact. J Pediatr Orthop 2005;25(5):646-650. Ounpuu S: The biomechanics of running: a kinematic and kinetic analysis. Instr Course Lect 1990;39:305-318. Mann RA, Hagy J: Biomechanics of walking, running and sprinting. Am J Sports Med 1980;8(5):345-350. Ounpuu S: The biomechanics of walking and running. Clin Sports Med 1994;13(4):843-863. Hoke BR, Lefever-Button SL: When the Feet Hit the Ground, Everything Changes. Level Two: Take the Next Step. Toledo, OH, American Physical Rehabilitation Network, 1994. Harris GF, Wertsch JJ: Procedures for gait analysis. Arch Phys Med Rehabil 1994;75(2):216-225.

OTHER READINGS Birrer RB, Buzermanis S, Dellacorte MP, et al: Biomechanics of running. In O’Connor FG, Wilder RP (eds): Textbook of Running Medicine. New York, McGraw-Hill, 2001, p 11. Cavanagh PR, Lafortune MA. Ground reaction forces in distance running 1980; 13(5):397-406. Kopf A: Clinical gait analysis—methods, limitations and possible applications. Acta Med Austriaca 1998;25(1):27-32. Novacheck TF: Walking, running, and sprinting: a three-dimensional analysis of kinematics and kinetics. Instr Course Lect 1995;44:497-506. Thordarson DB: Running biomechanics. Clin Sports Med 1997;16(2):239-247.

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Concussion Testing and Management Scott A. Playford, MD

KEY POINTS

. .

. . .

Sport-related concussions are common and underreported. Concussions produce a complex cascade of neurotransmitter release and ion flux in the brain. This cascade results in cognitive as well as physical symptoms that may last for minutes to months. Continued reevaluation is essential. No athlete should return to play or practice while still symptomatic. Care and treatment must be individualized for each concussed athlete. There is no universal algorithm. Many sideline assessment tools and neurocognitive tests for sport-related concussion are available, but no test or screening tool replaces good clinical judgment by the physician.

INTRODUCTION Concussion is one of the most difficult problems faced by health care professionals on the sideline. It is a high-risk injury that is complicated by emotional responses and legal ramifications, but it is commonly treated using guidelines built on opinion, experience, and very little direct science. Additional challenges come from the difficulty of diagnosing a concussion, assessing symptom resolution, and relying on the individual athlete for symptom reporting. Concussion is something that the sideline physician will see and must learn to recognize and manage properly. The primary goals of correct concussion assessment and management are to identify immediate neurologic emergencies that require further intervention, prevent catastrophic outcomes, and avoid or limit cumulative injury.

DEFINITION A good measure of the level of controversy for an injury or condition is the difficulty involved with defining it. In 1966, the Committee of Head Injury Nomenclature of the Congress of Neurological Surgeons developed a consensus definition of concussion as ‘‘a clinical syndrome characterized by immediate and transient post traumatic impairment of neural function The views expressed in this chapter are those of the author and do not necessarily reflect the official policy or position of the Department of the Navy, the Department of Defense, or the US Government.

due to brainstem involvement.’’1 Over the years, the definition and features continued to be debated and modified. The First International Symposium on Concussion in Sports convened in Vienna, Austria, in November 2001 and proposed a much more thorough definition.2 The group defined a sports concussion as a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces. Several common features that incorporate clinical, pathologic and biomechanical injury constructs that may be utilized in defining the nature of a concussive head injury include: 1. Concussion may be caused either by a direct blow to the head, face, neck, or elsewhere on the body with an ‘‘impulsive’’ force transmitted to the head. 2. Concussion typically results in the rapid onset of shortlived impairment of neurologic function that resolves spontaneously. 3. Concussion may result in neuropathological changes but the acute clinical symptoms largely reflect a functional disturbance rather than structural injury. 4. Concussion results in a graded set of clinical syndromes that may or may not involve loss of consciousness. Resolution of the clinical and cognitive symptoms typically follows a sequential course. 5. Concussion is typically associated with grossly normal structural neuroimaging studies. In November 2004, the Second International Conference on Concussion in Sport met in Prague, Czech Republic, and, after review, recommended no changes to the previous definition from the Vienna conference but did add a note that ‘‘in some cases postconcussive symptoms may be prolonged or persistent.’’3 To add to the confusion, the term mild traumatic brain injury is being used more in recent literature. This term is derived from the assessment of a head injury based on the Glasgow Coma Scale. The Glasgow Coma Scale assesses the individual in the areas of postinjury eye response, verbal response, and motor response and assigns a score from 3 to 15, with 3 being the worst and 15 being the best. A score of 13 to 15 is considered ‘‘mild brain injury.’’4

INCIDENCE Determining the true incidence of concussion has been a challenge for a number of reasons. The two most common sources of data are from surveys and emergency department visits. Surveys

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tend to underestimate the number of concussions as a result of recall bias and a lack of education about concussion signs and symptoms. Emergency department data have varied widely partly because of the lack of consensus about the definitions of concussion and mild traumatic brain injury. In addition, statistics from emergency departments will not effectively represent the true occurrence of athletic head injury, because the vast majority of sports concussions do not get seen in the emergency department. Various sports governing bodies have begun to monitor the rate of concussions and to establish reporting systems such as the National Collegiate Athletic Association Injury Surveillance System, which provides a more accurate source of sports-related data but still tends to underestimate the incidence when selfreporting is relied on. Surveys of high school sports shows that the majority of injuries occur among football players. One group collected data from 10 different high school sports over the 1995 to 1997 season and documented 23,566 reportable injuries in 75,298 player seasons (i.e., one person on one team in one season).5 Of the sports monitored, football had the highest rate, with 34.6% of players being injured or a case rate of 8.1 per 1000 athlete exposures (i.e., one athlete participating in one game or practice). Although numbers of concussions were not specifically listed, 13.3% of the football injuries were classified as head, neck, or spine trauma, and 10.3% were labeled as ‘‘neurotrauma.’’5 A secondary analysis of data regarding emergency department visits in the National Hospital Ambulatory Medical Care Survey for the period of 1998 to 2000 showed that, out of 70,900 emergency department visits, 878 (1.23%) were for mild traumatic brain injury.6 On the basis of this information, the authors estimated the national number of emergency department visits for mild traumatic brain injury to be approximately 1,350,000 or 503.1 per 100,000. On the basis of survey and surveillance data, the number of traumatic brain injuries in the United States from sports-related activities has been estimated at 300,000 annually.7 One study of high school athletes estimated the annual rate of concussion to be 17.15 per 100,000 or 0.17 per 1000 athlete exposures.8 Many believe this to be a significant underestimation, so another group studied 1532 high school football players and administered a confidential survey. At the end of the season, 15.3% of the players reported sustaining a concussion during that season, but only 47.3% of those injured said that they reported it.9 Data from the National Collegiate Athletic Association Injury Surveillance System show a much higher estimate at the collegiate level. National Collegiate Athletic Association data from 2004 to 2005 show the rate of concussion to be 1.24 per 1000 athlete exposures for soccer.10 Data from the system for football show the rate to be 0.44 per 1000 for practices11 and 3.91 per 1000 athlete exposures for games.12 A group compared the Injury Surveillance System data with an Internet-based collection technique and still suggests an underestimation. For 2001 to 2002, the Injury Surveillance System showed the concussion rate for games to be 2.64 per 1000 and the total for both games and practices to be 0.49 per 1000, but the Internet-based data showed a game rate of 5.56 per 1000 and a total of 0.74 per 1000.13 The Athletic Injury Monitoring System collected data about injuries in American football in high school and college during the 1997 and 1998 seasons. They found a total of 595 reported concussions (273 high school and 322 college), which accounted for 10% of the total injuries reported.14 They extrapolated that, with an estimated 1.08 million participants in organized football in the United States, there would be approximately 43,000 footballrelated concussions annually in the nation. From their survey, the rates of concussion (practice and games) were 0.56 per 1000 athlete exposures for high school and 0.58 per 1000 athlete exposures for college.14

PATHOPHYSIOLOGY Despite the long time that the clinical syndrome of concussion has been recognized and the amount of research that has been performed, the pathophysiologic basis of concussion is still largely a mystery. The majority of concussions are minor and result in full recovery in a short period of time, so most concussed athletes do not present to medical centers for imaging or other testing. As a result, most human studies on traumatic brain injury have involved more severe head injury rather than minor trauma from athletic participation. Although this may give some insight into the postinjury cascade that takes place, it is unclear how it translates to sports concussions. More prospective studies have been done in recent years, but usually with only small numbers and often with conflicting results. Creating models for experimental concussion presents more of a problem. Ethical considerations prohibit human testing, so animal models have been the primary source of knowledge about the early and late effects of concussion. Although this provides important information and new directions for research, there are a number of limitations. Aside from the differences in the structure and anatomy that changes the way animals handle head trauma as compared with humans, the ability to interpret amnesia and other cognitive changes in animals is poor at best. With that being said, animal studies have provided researchers with a much better understanding of the cellular and biochemical changes that take place after traumatic brain injury. In recent years, with the development of cerebral microdialysis, researchers have been able to make the jump from animal models to direct observation in the human brain.15 Traumatic brain injury is caused by either static or dynamic loads (the head is either fixed or free to move). Forces applied to the brain can be categorized as compressive, tensile, or shearing. Compressive forces are usually the best tolerated, whereas shearing forces are the least tolerated.16 Concussion usually results from an acceleration—deceleration force that is applied to the moving brain. This creates a shearing force or a distortion of the vascular and neural elements of the brain. In animal models, rotational forces (particularly in the coronal plane) are more often implicated.17 Increased intracranial pressure has not been correlated with concussion.17 On the cellular level, there has been a better elucidation of posttraumatic events. After the traumatic event, there is a large release of excitatory amino acids acting as neurotransmitters. Of these excitatory amino acids, glutamate has been the most studied, and it is thought to be the major player.18,19 When glutamate reacts with specific receptors on neural tissue, sodium—potassium pumps are activated, thereby causing an influx of sodium, chloride, and calcium, which leads to cellular swelling and damage.18,20 Along with the glutamate release, there is a large extracellular increase in potassium that likely adds to electrophysiologic alterations.18,21,22 With the neurotransmitter and ion flux, cellular metabolism also appears to be affected. Animal models have shown a brief period of increased metabolism and hyperglycolysis followed by a longer-lasting metabolic depression with hypoglycolysis.18,19,23-25 Because the increase in metabolism is accompanied by a decrease in cerebral blood flow, there is an accumulation of lactic acid. Human studies, although having small numbers, suggest that traumatic brain injury in humans also produces focal alterations in the blood—brain barrier,26 and they confirm an initial increase in glucose metabolism that is followed by a more prolonged depression.19,27,28 These changes in ion concentrations and cellular metabolism represent cellular changes that, although still ongoing, put the brain at a relatively increased risk for further injury with repeated trauma. As a result, further research is being done to more clearly define the sequence and timeline of the injury

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Table 44.1

Common Signs and Symptoms of Concussion

Signs

Symptoms

           

   

Loss of consciousness or impaired conscious state Vacant stare or glassy eyes Appears dazed or confused Slow to answer questions or follow instructions Easily distracted, poor concentration, unable to focus Disorientation to game, score, or opposing team Inappropriate playing behavior (e.g., running in the wrong direction) Slurred or incoherent speech Lack of coordination or clumsiness Significantly decreased playing ability Inappropriate emotional reactions (e.g., laughing or crying) Memory deficits (e.g., forgets plays, unable to recall three out of three words or objects)  Vomiting  Changes in personality or typical behavior  Convulsive movements or motor phenomena (e.g., tonic posturing)

cascade and to attempt to correlate the pathophysiologic changes with the clinical symptoms. This will allow clinicians to more effectively develop guidelines for a safe return to play. Another area of great interest and increasing research is the identification of useful serum biochemical markers (biomarkers) that are specific to brain injury. Biomarkers have been used for many years for other conditions, such as the measurement of creatine kinase and troponin for cardiac muscle injury. A number of biomarkers for neural injury have been investigated, but the one that has shown the most promise so far is S100B. It is the major low-affinity calcium-binding protein in astrocytes, and it is released with astrocyte injury and death.29 S100B release is immediate and short lived, so delayed testing in patients with minor head trauma may not be useful. Small studies have shown an increase in serum S100B levels in individuals suffering a mild traumatic brain injury as compared with healthy controls30 and a correlation of serum S100B levels with the degree of injury and the time to recovery.29,31-33 Unfortunately, as many small studies have also shown a poor correlation between measured serum S100B and symptom severity or persistence.34,35 To add to the confusion, a group measured serum S100B levels in 61 teenage amateur soccer players after 55 minutes of controlled heading and found a small increase as compared with other exercising players without heading,36 thereby raising the question of normal cutoffs for exertion versus injury.

FEATURES The identification of a concussed player is often difficult. Although a loss of consciousness is usually readily apparent, as previously stated, this is often not present. In other cases of concussion, the diagnosis is made on the basis of the report of symptoms by the player or the observation of abnormalities or deficits by teammates, coaches, or medical staff. Some features of concussion are easy to observe, such as stumbling, slurred speech, or vomiting. Other features, such as an impairment in memory or concentration, may not be as obvious unless specifically tested for. Amnesia is usually described as anterograde or retrograde. Anterograde amnesia, which is often called short-term memory loss, involves intact memory up to the event but difficulty with maintaining new memories after the concussive event. Retrograde amnesia involves the inability to remember events

         

Headache or pressure in the head Nausea Dizziness or balance problems Visual problems (e.g., seeing stars or flashing lights, double or fuzzy vision) Sensitivity to light or noise Feeling ‘‘dinged,’’ ‘‘foggy,’’ ‘‘dazed,’’ or lightheaded Feeling slowed down or fatigued Hearing problems (e.g., ringing in the ears) Depressed mood or anxiety Irritability or low frustration tolerance Sleep disturbances Feeling more emotional Lack of attention or concentration difficulty Memory problems

that occurred before the concussive injury. Table 44.1 lists the common signs and symptoms of a concussed athlete.3,37,38

GRADING Grading or categorizing concussions on the basis of severity is another source of controversy. Many grading scales have been proposed over the years, with variable acceptance. Unfortunately, the grading scales are primarily based on expert opinion and little evidence. The three most commonly accepted and quoted grading scales are those of Cantu (developed in 1986, revised in 2001),39 those of the Colorado Medical Society,40 and the American Academy of Neurologists guidelines.38 Table 44.2 summarizes the scales and compares their similarities and differences. One primary difference that can be seen when comparing these scales is the relative importance of the loss of consciousness. For many years, physicians have believed and perpetuated the idea that a loss of consciousness indicated a more severe injury to the brain and thus a worse outcome. There have also been studies that support this assumption, although they often have very small numbers of participants.41 More recently, additional studies have been done that suggest that it is posttraumatic amnesia rather than loss of consciousness that is a marker for more significant injury or prolonged recovery.42-44 This is reflected in Cantu’s revisions in 2001, in which he differentiated between brief and prolonged loss of consciousness. In 2004, during the International Conference on Concussion in Sport in Prague, this issue was discussed, and the consensus opinion was that loss of consciousness as a symptom would not necessarily classify an injury as being more severe.3 This decision was in agreement with the conclusion from Vienna in 2001, which stated that injury grading scales should be abandoned and instead combined measures of recovery developed to determine injury severity or prognosis and to guide return to play decisions on an individual basis.2,3 The members proposed a new classification scheme for management purposes that distinguished concussion as either simple or complex.3

Simple concussion The athlete suffers an injury that resolves without complication over a period of 7 to 10 days. Other than limiting play or training

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Table 44.2

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Common Concussion Grading Systems

Concussion Grade

Cantu (2001 Revision)

Colorado Medical Society (1991)

American Academy of Neurologists (1997)

Grade 1 (mild)

No LOC PTA or postconcussion signs and symptoms that clear in less than 30 minutes

Transient mental confusion No PTA No LOC

Grade 2 (moderate)

LOC lasting 1 minute or PTA lasting >24 hours or Postconcussion signs and symptoms lasting >7 days

No LOC Confusion with PTA

No LOC Transient confusion Symptoms or abnormalities clear in 15 minutes Any LOC, either brief (seconds) or prolonged (minutes)

Grade 3 (severe)

Any LOC, however brief

LOC, loss of consciousness; PTA, posttraumatic amnesia.

while symptomatic, the athlete requires no other intervention and has no long-term sequelae.

Complex concussion The athlete suffers persistent symptoms, including a return of symptoms with exertion. A concussion is also considered to be complex if the athlete exhibits specific sequelae, such as a prolonged loss of consciousness (> 1 minute), concussive convulsions, or prolonged cognitive impairment after the injury. Athletes with multiple concussions or those who have repeat concussions with progressively less force may also be included in this group. These athletes may have additional management considerations, and they may require a more thorough workup.

MANAGEMENT Preparation As with any potentially serious injury, concussion occurrence should be considered and planned for before the sporting event. Emergency action plans and procedures should be in place and reviewed with the medical and training staff ahead of time. Special equipment such as a backboard and straps for spinal immobilization should be inspected, and practice drills should be done so that everyone is familiar with the equipment. Emergency transport procedures should also be considered and disseminated.

Standardized testing When the Quality Standards Subcommittee of the American Academy of Neurology met in 1996 and published its practice parameters for the management of concussions in 1997, the panel of experts presented a recommendation for future research to develop ‘‘a valid, standardized, systematic sideline evaluation designed for the immediate assessment of concussion in athletes.’’38 In response to the challenge, later in 1996, the Standard Assessment of Concussion was developed and tested. The goal was to design an evaluation tool to be used on the sideline by athletic trainers and similar personnel for the immediate assessment of athletes who were suspected of having a concussion.45 The test was designed to be sensitive and specific enough for sports concussion but also easy to learn and quick to administer. Another potential obstacle came from the practice effect exhibited when a test was repeated on the same athlete. The practice or learning effect occurs when an athlete’s test performance improves with repeated exposures to the same test. The developers of the Standard Assessment of Concussion created three forms

of the examination to allow for repeated assessment of the same player while limiting the practice effect.45 A number of other checklists and evaluation tools have been developed, with variable acceptance and use. In 2004, the Prague conference set out to improve on the available tests by combining eight different existing tools (including the Standard Assessment of Concussion) into one new standardized tool called the Sport Concussion Assessment Tool3 (Figure 44.1 and Box 44.1). An additional complication with the development and use of sideline assessment tools has been the establishment of standard scores and norms. Because these tests are used across the spectrum of ages and economic and educational levels, it is impossible to present a set of normative data for use as standard comparison. As a result, high-risk athletes should be tested with whatever standardized tool is chosen before the start of the season. An individual baseline can then be established for each athlete and used for comparison when the athlete is retested after an injury. Choosing a tool with alternate forms will reduce the likelihood of practice effect.

On-field evaluation Immediate evaluation is similar to any other emergency and should first involve the assessment of the airway, breathing, and circulation. The level of consciousness of the injured athlete should next be assessed. If the athlete is unconscious or unable to respond appropriately or cooperate with the examination, cervical spine precautions should be taken. If he or she is complaining about any neck pain or shows any focal neurologic deficits in the extremities, the neck should be immobilized and the protocol for cervical spine injury followed. In this event, the helmet should not be removed, and the athlete should be strapped onto a backboard with the pads and helmet in place. The goal of the on-field evaluation is to quickly differentiate between neurologic emergencies that require transport for further workup or stabilization and less-severe injuries that can be evaluated on the sideline.

Sideline evaluation On the sideline, the physician should get a more detailed history and perform a more complete examination. The physician should try to delineate the mechanism of injury and identify symptoms such as a history of loss of consciousness or the presence of posttraumatic amnesia (PTA). The examination should look for focal neurologic deficits as well as any alteration in cognitive functions, such as memory, attention span, concentration, or speed of information processing. The athlete should not be left alone, and he or she should be reassessed at regular intervals because many concussed athletes will have a delayed onset of signs and symptoms.

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This tool represents a standardized method of evaluating people after concussion in sport. This tool has been produced as part of the Summary and Agreement Statement of the Second International Symposium on Concussion in Sport, Prague 2004.

The SCAT Card (Sport Concussion Assessment Tool) Athlete Information What is a concussion? A concussion is a disturbance in the function of the brain caused by a direct or indirect force to the head. It results in a variety of symptoms (like those listed below) and may, or may not, involve memory problems or loss of consciousness.

Sport concussion is defined as a complex pathopsychological process affecting the brain, induced by traumatic biomechanical forces. Several common features that incorporate clinical, pathological, and biomechanical injury constructs that may be utilized in defining the nature of a concussive head injury include: 1. Concussion may be caused either by a direct blow to the head, face, neck, or elsewhere on the body with an “impulsive” force transmitted to the head. 2. Concussion typically results in the rapid onset of short-lived impairment of neurological function that resolves spontaneously. 3. Concussion may result in neuropathological changes, but the acute clinical symptoms largely reflect a functional disturbance rather than structural injury. 4. Concussion results in a graded set of clinical syndromes that may or may not involve loss of consciousness. Resolution of the clinical and cognitive sypmtoms typically follows a sequential course. 5. Concussion is typically associated with grossly normal structural neuroimaging studies. Postconcussion Symptoms Ask athletes to score themselves based on how they feel now. It is recognized that a low score may be normal for some athletes, but clinical judgment should be exercised to determine if a change in symptoms has occurred following the suspected concussion event. It should be recognized that the reporting of symptoms may not be entirely reliable. This may be due to the effects of a concussion or because the athlete’s passionate desire to return to competition outweighs the natural inclination to give an honest response. If possible, ask someone who knows the athlete well about changes in affect, personality, behavior, etc. Remember, concussion should be suspected in the presence of ANY ONE or more of the following: • Symptoms (such as headache), or • Signs (such as loss of consciousness), or • Memory problems. Any athlete with a suspected concussion should be monitored for deterioration (ie, should not be left alone) and should not drive a motor vehicle. For more information see the “Summary and Agreement Statement of the Second International Symposium on Concussion in Sport” in: Clinical Journal of Sport Medicine 2005;15(2):48–55 British Journal of Sports Medicine 2005;39(4):196–204 Neurosurgery 2005, in press The Physician and Sportsmedicine 2005;33(4):29–44 This tool may be copied for distribution to teams, groups, and organizations.

Figure 44.1

How do you feel? You should score yourself on the following symptoms, based on how you feel now. Postconcussion Symptom Scale Headache “Pressure in head” Neck pain Balance problems or dizzy Nausea or vomiting Vision problems Hearing problems/ringing “Don’t feel right” Feeling “dinged” or “dazed” Confusion Feeling slowed down Feeling like “in a fog” Drowsiness Fatigue or low energy More emotional than usual Irritability Difficulty concentrating Difficulty remembering

None 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1

2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2

Moderate 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3

4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4

Severe 5 6 5 6 5 6 5 6 5 6 5 6 5 6 5 6 5 6 5 6 5 6 5 6 5 6 5 6 5 6 5 6 5 6 5 6

1 1 1 1 1 1 1

2 2 2 2 2 2 2

3 3 3 3 3 3 3

4 4 4 4 4 4 4

5 5 5 5 5 5 5

(Follow-up symptoms only) Sadness Nervous or anxious Trouble falling asleep Sleeping more than usual Sensitivity to light Sensitivity to noise Other:

0 0 0 0 0 0 0

6 6 6 6 6 6 6

What should I do? Any athlete suspected of having a concussion should be removed from play, and then seek medical evaluation. Signs to watch for: Problems could arise over the first 24–48 hours. You should not be left alone and must go to a hospital at once if you: • Have a headache that gets worse • Are very drowsy or can’t be awakened (woken up) • Can’t recognize people or places • Have repeated vomiting • Behave unusually or seem confused; are very irritable • Have seizures (arms and legs jerk uncontrollably) • Are unsteady on your feet; have slurred speech. Remember, it is better to be safe. Consult your doctor after a suspected concussion. What can I expect? Concussion typically results in the rapid onset of short-lived impairment that resolves spontaneously over time. You can expect that you will be told to rest until you are fully recovered (that means resting your body and your mind). Then, your doctor will likely advise that you go through a gradual increase in exercise over several days (or longer) before returning to sport.

The Sport Concussion Assessment Tool.

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The SCAT Card (Sport Concussion Assessment Tool) Medical Evaluation Name: _________________________ Sport/Team: _____________________

Instructions: This side of the card is for the use of medical doctors, physical therapists, or athletic trainers. In order to maximize the information gathered from the card, it is strongly suggested that all athletes participating in contact sports complete a baseline evaluation prior to the beginning of their competitive season. This card is a suggested guide only for sport concussion and is not meant to assess more severe forms of brain injury. Please give a COPY of this card to athletes for their information and to guide follow-up assessment.

Date: _________ Mouth guard? Y

1) SIGNS Was there loss of consciousness or unresponsiveness? Was there seizure or convulsive activity? Was there a balance problem/unsteadiness?

Y Y Y

N N N N

Signs: Assess for each of these items and circle Y (yes) or N (no)

2) MEMORY Modified Maddocks questions (check correct)

Memory: If needed, questions can be modified to make them specific to the sport (eg, “period” versus “half”).

At what venue are we? __; Which half is it? __; Who scored last? __ What team did we play last? __; Did we win last game? __ 3) SYMPTOM SCORE Total number of positive symptoms (from reverse side of the card) = ___ 4) COGNITIVE ASSESSMENT 5 word recall

Immediate

(Examples)

Word 1______________ Word 2______________ Word 3______________ Word 4______________ Word 5______________

cat pen shoe book car

Delayed

(after concentration tasks)

__ __ __ __ __

__ __ __ __ __

Months in reverse order: Jun-May-Apr-Mar-Feb-Jan-Dec-Nov-Oct-Sep-Aug-Jul (circle incorrect) or Digits backward (check correct) 5-2-8 3-9-1 ____ 6-2-9-4 4-3-7-1 ____ 8-3-2-7-9 1-4-9-3-6 ____ 7-3-9-1-4-2 5-1-8-4-6-8 ____ Ask delayed 5-word recall now 5) NEUROLOGICAL SCREENING Pass Fail ____ ____ Speech ____ ____ Eye motion and pupils ____ ____ Pronator drift ____ ____ Gait assessment Any neurological screening abnormality necessitates formal neurological or hospital assessment 6) RETURN TO PLAY Athletes should not be returned to play the same day of injury. When returning athletes to play, they should follow a stepwise symptom-limited program, with stages of progression. For example: 1. Rest until asymptomatic (physical and mental rest) 2. Light aerobic exercise (eg, stationary cycling) 3. Sport-specific exercise 4. Non-contact training drills (start light resistance training) 5. Full contact training after medical clearance 6. Return to competition (game play) There should be approximately 24 hours (or longer) for each stage, and the athlete should return to stage 1 if symptoms recur. Resistance training should only be added in the later stages. Medical clearance should be given before return to play.

Figure 44.1

Cognitive Assessment: Select any 5 words (an example is given). Avoid choosing related words such as “dark” and “moon,” which can be recalled by means of word association. Read each word at a rate of one word per second. The athlete should not be informed of the delayed testing of memory (to be done after the reverse months and/or digits). Choose a different set of words each time you perform a follow-up exam with the same candidate. Ask the athlete to recite the months of the year in reverse order, starting with a random month. Do no start with December or January. Circle any months not recited in the correct sequence. For digits backward, if correct, go to the next string length. If incorrect, read trial 2. Stop after incorrect on both trials. Neurological Screening: Trained medical personnel must administer this examination. These individuals might include medical doctors, physical therapists, or athletic trainers. Speech should be assessed for fluency and lack of slurring. Eye motion should reveal no diplopia in any of the 4 planes of movement (vertical, horizontal, and both diagonal planes). The pronator drift is performed by asking patients to hold both arms in front of them, palms up, with eyes closed. A positive test is pronating the forearm, dropping the arm, or drifting away from midline. For gait assessment, ask the patient to walk away from you, turn, and walk back. Return to Play: A structured, graded exertion protocol should be developed and individualized on the basis of sport, age, and the concussion history of the athlete. Exercise or training should be commenced only after the athlete is clearly asymptomatic with physical and cognitive rest. Final decision for clearance to return to competition should ideally be made by a medical doctor. For more information see the “Summary and Agreement Statement of the Second International Symposium on Concussion in Sport” in: Clinical Journal of Sport Medicine 2005;15(2):48–55 British Journal of Sports Medicine 2005;39(4):196–204 Neurosurgery 2005, in press The Physician and Sportsmedicine 2005; 33(4):29–44

Continued

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Box 44.1: Concussion Testing Checklist      

Check the preseason cognitive testing scores. Use sideline testing to look for a change from baseline. Repeat testing after recovery. Consider more in-depth neuropsychologic testing. Use testing with multiple versions to avoid practice effect. Correlate testing with an examination; never allow a symptomatic athlete to return to play.  Remember to check the airway, breathing, and circulation and to consider cervical spine precautions.

The American Academy of Neurology summary statement recommends repeat examinations every 5 minutes.38 As with the initial on-field examination, the primary goal is to identify neurologic emergencies that require additional medical evaluation or intervention. If the athlete is showing persistent symptoms, worsening symptoms, focal neurologic deficits, or an alteration in level of consciousness, he or she should be transported for further evaluation. Intracranial hemorrhage is the leading cause of death from athletic head injury, and athletes with an epidural hematoma often will have a lucid period before the hematoma reaches a fatal size over 30 to 60 minutes.16

After the event Appropriate counseling after the competition is essential. The athlete should be educated about his or her condition and its implications. Intracranial hemorrhage from an epidural hematoma, a subdural hematoma, a subarachnoid hemorrhage, or an intracerebral hematoma may have a delayed onset, and coaches, roommates, or parents need to be instructed about signs and symptoms to watch for. Warning signs and an emergency plan should be reviewed with the athlete and anyone who will be caring for or staying with the injured athlete (e.g., parents). Follow-up plans should also be discussed and arranged. The athlete should be instructed about complete rest, which may include mental rest as well (e.g., no homework, classes, or tests).

Imaging Because concussions are generally not associated with any structural abnormalities, neuroimaging is usually not required. A number of imaging modalities are available, including computed tomography scanning, magnetic resonance imaging, functional magnetic resonance imaging, positron emission tomography, single-photon emission computed tomography, electroencephalography, and evoked potentials. They are indicated on the basis of symptoms or examination findings.3,46

NEUROPSYCHOLOGIC TESTING Because the return-to-play decision continues to be an area of disagreement and controversy, efforts have been made to establish more objective, scientifically based decisions regarding when it is safe to allow a player to resume practice and play. As previously discussed, it is universally accepted that no injured athlete should return to play while still symptomatic, but, because most postconcussive symptoms are subjective and rely on the athlete’s report, reliability is questionable. Neuropsychologic testing has been examined as the potential objective solution to the provider’s

dilemma. This type of testing has been used for many years by neuropsychologists to detect and quantify residual effects after traumatic brain injury. There are more than 20 different batteries of tests that measure various aspects of cognitive function, including concentration, motor dexterity, information processing, visual memory, verbal memory, executive function, and brain stem function.47 Traditionally, neuropsychologists test psychologic functioning and some sensory and motor functioning as well. Because the testing is time consuming and expensive and because it requires interpretation by a neuropsychologist, it has had limited usefulness in the sports setting. Recently the neurocognitive portions of the testing have been modified and grouped to be more useful for the patient with a sports concussion, and its use has grown to include the National Football League, the National Hockey League, and increasing numbers of colleges, universities, and high schools.47 Tests have shown various abnormalities in the concussed athlete, including those involving maintaining and distributing attention, alterations in balance and stability, information processing, reaction times, verbal learning, and memory (LOE: D).47-51 These findings may be present despite the absence of subjective complaints by the athlete. Gait stability studies have shown that concussed athletes may learn to compensate for altered stability and show no deficits on gait testing. If the individual is challenged with a second task, such as one involving memory or concentration while undergoing gait testing, the instability will be unmasked (LOE: D).48,52 As with sideline concussion assessment tools, to optimize the use of neuropsychologic testing, the athlete must be tested before the start of the season to establish an individual baseline for future comparison. Computers have opened new doors for neuropsychologic testing. Recently, more companies have developed commercial computer-based and Internet-based testing tools. For a fee, schools or teams can purchase program software or access to Internetbased programs. Each athlete completes a brief computerized test before the start of the season to establish a neurocognitive baseline, and this information is then stored in a computer database. If a head injury occurs, the injured player repeats the test, and the physician receives an automated report back from the program or the company comparing the preinjury and postinjury performances. The goal is to simply determine if there has been a change from baseline functioning rather than to produce data that require complex interpretation, so reports are often a simple ‘‘yes’’ or ‘‘no.’’ Companies currently marketing programs include CogState (CogState Ltd, Victoria, Australia), Headminder (Headminder Inc, New York City), and ImPACT (University of Pittsburgh Medical Center Sports Medicine Concussion Program). The programs are all designed to be administered with little training because the athletes are self-guided through the computerized test. The systems also include randomization to help reduce the practice effect from repeated use on the same athlete.52 The tests have not been compared head to head, so when choosing one of the products, the physician and athletic staff should consider the reliability of the testing, the validation that the tests detect subtle changes from sports-related concussions, and the clinical utility in the setting in which the test will be used. Although the companies developing the software have put out some data regarding reliability and validity, studies are ongoing.53 Computerized neuropsychologic testing shows promise, but it is too early to call its use the standard of care; nothing replaces good clinical judgment by a physician. In its position statement regarding the management of sportsrelated concussions, the National Athletic Trainers’ Association proposes that neuropsychologic testing offers a good adjunct to the clinical assessment of a concussed athlete but that it should not be used as the only means to determine the return to play. The Association discusses the potential benefits of the commercial computerized programs, but it makes no formal recommendation

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regarding their use. It is recommended that some sort of baseline neurocognitive testing should be done before the start of the season.54 The Prague consensus also discusses the potential benefits of neuropsychologic testing, but it cautions that, in the symptomatic concussed athlete, testing ‘‘adds nothing to the return-toplay decisions and it may contaminate the testing process by allowing for practice effects to confound the results.’’3

COMPLICATIONS Second-impact syndrome Second-impact syndrome (SIS) occurs when an athlete who sustains a head injury (e.g., a concussion or a cerebral contusion) sustains a second head injury before the symptoms of the first one have fully cleared. The second injury is often minor or incidental, and the result is the rapid development of increased intracranial pressure from vascular engorgement and edema; this syndrome carries a mortality rate of approximately 50%.16 In the United States, most reports of SIS have been in football players, but it has also been noted in hockey players and boxers.55 It is most commonly described as occurring among adolescents males (between 14 and 16 years of age), and it is almost unheard of among adults.55,56 SIS was first described in 1973,57 and the term second-impact syndrome was first used to describe the condition in 1984.58 The syndrome is believed to be related to the loss of the autoregulation of cerebral blood flow that results in vascular engorgement and a rapid increase in intracranial pressure, which is similar to the malignant brain edema found in children after a traumatic head injury.16,55,59 More recent evidence suggests that cytotoxic or cellular edema, which is related to the postconcussive altered membrane permeability and ion transport, is also a significant contributor to the condition.60-62 As a result of the high morbidity and mortality rates, SIS has received a lot of attention over the years, and it has provided the major impetus for the development of accurate athlete-assessment tools and return-to-play guidelines. Many experts question the existence of SIS as a separate and discrete syndrome as opposed to a variant of the malignant brain edema of children. Some researchers have reviewed published cases of SIS using strict diagnostic criteria and failed to find convincing evidence of either an initial head injury or a repeat blow.56,63 Clearly this has many implications, and research is ongoing.

Repeat concussions It has been commonly presumed and taught over the years that athletes who suffer a concussion are at an increased risk of repeat concussion in the future, but evidence has been lacking. More recent studies have attempted to determine if this is in fact true and if so, to quantify the risk. One study looking at data from high school and college football players over two consecutive seasons recorded 572 concussions. They found that, among high school players who had a history of concussion, 18% sustained another concussion as compared with only 3% of players with no history. In the college athletes, 16% of players with a history of concussion suffered a repeat concussion as compared with only 3% of those with no such history. The calculated relative risk showed that concussion was 5.8 times more likely among individuals with a history of concussion (LOE: D).64 Another study of college football players examining 184 concussed athletes found that those athletes with a history of three or more concussions during the previous 7 years were three times more likely to sustain another concussion (LOE: D).65 One big question that still remains unanswered is whether the increased risk of repeat concussion is actually the result of pathoanatomic changes that lead to an increase in susceptibility. Alternatively, the higher risk may be related to

behavioral components such as more aggressive play, poor athletic technique, or less supervision.

Cumulative effects Another source of conflicting opinion is the long-term effects of concussion and the cumulative effects of repeated concussions. As with other aspects of concussion, results of studies have not been consistent. One study compared children with brain injuries with children with orthopedic injuries over an average of 4 years and found an increased incidence of cognitive and behavioral problems in those children who had severe traumatic brain injury as compared with the strictly orthopedic group. The authors failed to show a statistical difference between the moderate traumatic brain injury group and the group without brain injury, which raises questions about whether this would be a concern in athletic head injuries.66 With regard to repetitive concussions, some studies failed to show a significant cumulative effect (LOE: D).67-69 The majority of research, however, suggests that concussed athletes who have a history of concussion are more symptomatic and require more time to recover (LOE: D).65,70-76 One study of high school athletes identified four markers of concussion severity as positive loss of consciousness, retrograde amnesia, anterograde amnesia, and confusion. They found that athletes with a history of three or more concussions were more than nine times more likely to exhibit three or four of the abnormal markers when they sustained a subsequent concussion (LOE: D).76 Chronic traumatic brain injury has long been described in boxing as dementia pugilistica, traumatic encephalopathy, or ‘‘punch drunk’’ syndrome. Severity has been linked to the length of the boxer’s career, and it ranges from affective changes and psychiatric disturbances to a permanent decrease in cognitive function and Parkinson-like symptoms.74,77 Chronic traumatic brain injury is being described more in other sports as well, including soccer and football.74 A survey of 2552 retired professional football players found that those with a history of three or more concussions had a fivefold greater prevalence of being diagnosed with mild cognitive impairment as compared with those with no history of concussion (LOE: D).75 An area of growing interest with regard to long-term outcomes is that of apolipoprotein E, a gene with three primary alleles. The e-4 allele has been linked to poor neurocognitive outcomes after various types of brain injury. Studies of professional boxers with chronic traumatic brain injury have shown that those with the most severe impairments are more likely to have the apolipoprotein E e-4 allele.78 Other studies have linked the apolipoprotein E e-4 genotype to poorer recovery after traumatic brain injury.79 A study of mild traumatic brain injury suggested that the presence of the apolipoprotein E e-4 allele might be associated with worse initial presentation but failed to show any relation to recovery rate or prolonged symptoms.80 There was also no association with the presence of the apolipoprotein E e-4 genotype and diffuse brain edema in children.81 The link with athletic concussions is still being studied. The implication of being able to predict which athletes are at risk for long-term cognitive impairment is enticing but not yet a reality.

Postconcussive syndrome Postconcussive syndrome criteria are described in the Diagnostic and Statistical Manual of Mental Disorders, 4th edition, of the American Psychiatry Association. The syndrome is characterized by persistent headache, an inability to concentrate, irritability, fatigue, vertigo, emotional lability, and disturbances in gait, sleep, and vision.82,83 It usually follows a more severe concussion (a loss of consciousness of less than 5 minutes or prolonged posttraumatic

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amnesia), but the time to onset and the course is not well defined or universally agreed upon.82

TREATMENT The treatment of concussion is another area with little supporting research. The standard approach has been complete rest until all symptoms resolve. If impairments in cognition, memory, or concentration are present, the concussed athlete may also require mental rest as well. For high school and college students, this may require consultation with coaches, teachers, and/or guidance counselors. One study compared 6 days of bed rest with routine exertional avoidance and found some improvement in subjective dizziness immediately after the concussion but otherwise no effect on the recovery curve or the development of prolonged symptoms (LOE: B).84 Pharmacologic intervention has not proven to be useful for the treatment of concussion. Several options have been studied, including corticosteroids, antioxidants, glutamate receptor antagonists, and calcium-channel antagonists, but unfortunately no agent has been found to alter the course of mild traumatic brain injury.85 Antidepressants may be useful for treating prolonged postconcussive symptoms such as depression or affective changes.

Return to play As with the grading of concussions, this is an area of disagreement and variation. One unifying theme that should always apply is that no concussed athlete should ever resume play while still symptomatic. As previously discussed, the presence of symptoms reflects

Table 44.3

ongoing alterations of the neural cells and tissue and represents a period of vulnerability for further injury. All decisions related to return to play should involve a physician and should be individualized for the athlete in question. For mild concussions, many experts agree that it is safe to return to play on the same day as the injury. The athlete’s history of concussions should be taken into consideration. Cantu, the American Academy of Neurologists, and the Colorado Medical Society all agree that an athlete who suffers a mild concussion and who is asymptomatic may resume play, but they caution that the athlete should be monitored for 15 to 20 minutes first because symptoms may have a delayed onset.38-40 If the injured athlete is asymptomatic after an adequate period of observation, he or she should have an exertional challenge (e.g., push-ups or running on the sideline) before being allowed to return to play. If symptoms return with exertion, the player should remain out. Table 44.3 shows additional recommendations that are based on the three previously discussed grading scales.38-40 Initially, 1 week was chosen as an arbitrary timeline on the basis of experience and practice. Researchers have since attempted to more accurately determine the recovery curve. Studies of college and professional athletes have shown that the majority of concussed athletes have a resolution of symptoms and return to baseline in 3 to 7 days (LOE: D).69,70,86 Concussed high school athletes have shown a trend toward longer recovery times (LOE: D).44,86 Studies involving neuropsychologic testing have raised more questions, with some showing resolution in 5 to 10 days but others showing persistent alterations in several measurements up to 14 days out among both high school and college athletes, despite the resolution of subjective complaints by the players (LOE: D).47,68,87

Return-to-Play Guidelines by Concussion Grading System

Concussion Grade

Number of Concussion Suffered

Grade 1 (mild)

First

Grade 1 (mild)

Second

Grade 1 (mild)

Third

Grade 2 (moderate)

First

Grade 2 (moderate)

Second

American Academy of Neurologists

Cantu

Colorado Medical Society

Return to play after 1 symptom-free week End season if computed tomography scanning or magnetic resonance imaging abnormal Return to play in 2 weeks after 1 symptom-free week

Remove from contest May return to same contest or practice if symptom free for at least 20 minutes

Remove from contest May return to play if symptom free within 15 minutes

May not return to contest or practice May return after 1 symptom-free week

May not return to contest or practice May return to play after 1 symptom-free week

End season May return to play next season if no symptoms Return to play after 1 symptom-free week

End season May return to play in 3 months if without symptoms May not return to contest or practice May return to play after 1 symptomfree week

May not return for a minimum of 1 month May return to play then if symptom free for 1 week Consider ending season

Consider ending season May return in 1 month if symptom free

May not return to contest or practice May return to play after 1 full symptom-free week Computed tomography scanning or magnetic resonance imaging recommended if symptoms or signs persist May not return to contest or practice May return to play after at least 2 symptom-free weeks End season if any computed tomography scanning or magnetic resonance imaging abnormalities Continued

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Table 44.3 Concussion Grade

.

Concussion testing and management

Return-to-Play Guidelines by Concussion Grading Systemçcont’d Number of Concussion Suffered

Grade 2 (moderate)

Third

Grade 3 (severe)

First

Grade 3 (severe)

Second

Grade 3 (severe)

Third

Cantu

Colorado Medical Society

End season May return to play next season if without symptoms May not return to play for a minimum of 1 month May return to play then after 1 symptom-free week

End season May return to play next season if without symptoms May not return to contest or practice Transport to hospital for evaluation May return to play in 1 month after 2 symptom-free weeks

End season May return to play next season if no symptoms

End season May return to play next season if no symptoms

Recent expert consensus statements recommend a more individualized approach and suggest a stepwise progression with the return to play as shown in Table 44.4.3,88 With this approach, the athlete should proceed to the next level as long as he or she is asymptomatic. However, if any symptoms return, the athlete will drop back to the previous asymptomatic level and try to advance again in 24 hours. For mild concussions, this process will normally take 1 week to complete (1 to 2 days at each level), but it should be tailored for the individual athlete.

Table 44.4 Prague Conference Recommendations for Return to Play after Concussion Level

Action

1

No activity, complete rest Once asymptomatic, proceed to step 2 Light aerobic exercise such as walking or stationary cycling No resistance training Sport-specific exercise Progressive addition of resistance training at steps 3 or 4 Noncontact training drills Full-contact training after medical clearance Game play

2 3 4 5 6

American Academy of Neurologists

May not return to contest or practice Transport to hospital if unconscious or in the presence of neurologic abnormality Computed tomography scanning or magnetic resonance imaging recommended if posttraumatic symptoms or signs persist If loss of consciousness is brief (seconds), may return to play in 1 week if no symptoms or signs If loss of consciousness is prolonged (minutes), return to play after 2 symptom-free weeks May not return to contest or practice May return to play after a minimum of 1 symptom-free month End season if any computed tomography scanning or magnetic resonance imaging abnormalities

End season Strongly discourage any return to contact or collision sports

CONTROVERSIES  Most recommendations regarding concussion management have been based on expert opinion and little clinical research.  Presentation and symptom resolution after a concussion are highly variable and difficult to predict. Postconcussive amnesia may be more indicative of significant injury than loss of consciousness.  Subtle neurochemical changes in the brain after a concussion may put the injured athlete at an increased risk for more severe injury, including death from SIS.  Historically, neuropsychologic testing has been used to assess for changes and deficits after more severe central nervous system insults, such as stroke or Alzheimer’s dementia. Studies are ongoing to determine whether these tests are sensitive enough to detect the often subtle changes associated with sports-related concussion.  Computerized neuropsychologic testing is quick and easy, but the increased accessibility may lead to its use in lieu of proper assessment and disposition by a physician.

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Yoshino A, Hovda DA, Kawamata T, et al: Dynamic changes in local cerebral glucose utilization following cerebral conclusion in rats: evidence of a hyper- and subsequent hypometabolic state. Brain Res 1991;561(1):106-119. Richards HK, Simac S, Piechnik S: Uncoupling of cerebral blood flow and metabolism after cerebral contusion in the rat. J Cereb Blood Flow Metab 2001;21(7): 779-781. Korn A, Golan H, Melamed I, et al: Focal cortical dysfunction and blood-brain barrier disruption in patients with Postconcussion syndrome. J Clin Neurophysiol 2005;22(1):1-9. Bergsneider M, Hovda DA, Shalmon E, et al: Cerebral hyperglycolysis following severe traumatic brain injury in humans: a positron emission tomography study. J Neurosurg 1997;86(2):241-251. Hovda DA, Lee SM, Smith ML, et al: The neurochemical and metabolic cascade following brain injury: moving from animal models to man. J Neurotrauma 1995;12(5):903-906. 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Collins MW, Lovell MR, Mckeag DB: Current issues in managing sports-related concussion. JAMA 1999;282(24):2283-2285. Practice parameter: the management of concussion in sports (summary statement). Report of the Quality Standards Subcommittee. Neurology 1997;48(3):581-585. Cantu RC: Posttraumatic retrograde and anterograde amnesia: pathophysiology and implications in grading and safe return to play. J Athl Train 2001;36(3):244-248. Report of the Sports Medicine Committee: Guidelines for the Management of Concussion in Sports. Denver, Colorado, Colorado Medical Society, 1990 (revised May 1991). McCrea M, Kelly JP, Randolph C, et al: Immediate neurocognitive effects of concussion. Neurosurgery 2002;50(5):1032-1040. Lovell MR, Iverson GL, Collins MW, et al: Does loss of consciousness predict neuropsychological decrements after concussion?. Clin J Sport Med 1999;9(4):193-198. Collins MW, Iverson GL, Lovell MR, et al: On-field predictors of neuropsychological and symptom deficit following sports-related concussion. Clin J Sport Med 2003; 13(4):222-229. Lovell MR, Collins MW, Iverson GL, et al: Recovery from mild concussion in high school athletes. J Neurosurg 2003;98(2):296-301. McCrea M, Kelly JP, Kluge J, et al: Standardized assessment of concussion in football players. Neurology 1997;48(3):586-588. Johnston KM, McCrory P, Mohtadi NG, et al: Evidence-based review of sport-related concussion: clinical science. Clin J Sport Med 2001;11(3):150-159. Grindel SH, Lovell MR, Collins MW: The assessment of sport-related concussion: the evidence behind neuropsychological testing and management. Clin J Sport Med 2001;11(3):134-143. van Donkelaar P, Osternig L, Chou LS: Attentional and biomechanical deficits interact after mild traumatic brain injury. Exerc Sport Sci Rev 2006;34(2):77-82. Collins MW, Fields M, Lovell MR, et al: Relationship between postconcussion headache and neuropsychological test performance in high school athletes. Am J Sports Med 2003;31(2):168-173. Gosselin N, Theriault M, Leclerc S, et al: Neurophysiological anomalies in symptomatic and asymptomatic concussed athletes. Neurosurgery 2006;58(6):1151-1161. Collie A, Makdissi M, Maruff P, et al: Cognition in the days following concussion: comparison of symptomatic versus asymptomatic athletes. J Neurol Neurosurg Psychiatry 2006;77(2):241-245. Parker TM, Osternig LR, Van Donkelaar P, et al: Gait stability following concussion. Med Sci Sports Exerc 2006;38(6):1032-1040. Randolph C, McCrea M, Barr WB: Is neuropsychological testing useful in the management of sport-related concussion? J Athl Train 2005;40(3):139-152. Guskiewicz KM, Bruce SL, Cantu RC, et al: National Athletic Trainers’ Association position statement: management of sport-related concussion. J Athl Train 2004;39(3):280-297. Cantu RC: Recurrent athletic head injury: risks and when to retire. Clin Sports Med 2003;22(3):593-;603, x. McCrory P: Does second impact syndrome exist? Clin J Sport Med 2001;11(3): 144-149. Scheider RC. Head and neck injuries in football: mechanisms, treatment, and prevention. Baltimore, Williams & Wilkins, 1973, pp 35-43. Saunders RL, Harbaugh RE: The second impact in catastrophic contact-sports head trauma. JAMA 1984;252(4):538-539. Bruce DA, Alavi A, Bilaniuk L, et al: Diffuse cerebral swelling following head injuries in children: the syndrome of "malignant brain edema." J Neurosurg 1981;54(2):170-178. Marmarou A, Fatouros PP, Barzo P, etal: Contribution of edema and cerebral blood volume to traumatic brain swelling in head-injured patients. J Neurosurg 2000;93(2):183-193. Erratum in J Neurosurg 2001;94(2):349. Barzo P, Marmarou A, Fatouros P, et al: Cerebral edema and changes of cerebral blood volume in patients with head injuries. Orv Hetil 2002;143(27):1625-1634. Unterberg AW, Stover J, Kress B, et al: Edema and brain trauma. Neuroscience 2004;129(4):1021-1029. McCrory PR, Berkovic SF: Second impact syndrome. Neurology 1998;50(3):677-683. Zemper ED: Two-year prospective study of relative risk of a second cerebral concussion. Am J Phys Med Rehabil 2003;82(9):653-659.

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Guskiewicz KM, McCrea M, Marshall SW, et al: Cumulative effects associated with recurrent concussion in collegiate football players: the NCAA Concussion Study. JAMA 2003;290(19):2549-2555. Yeates KO, Armstrong K, Janusz J, et al: Long-term attention problems in children with traumatic brain injury. J Am Acad Child Adolesc Psychiatry 2005;44(6):574-584. Iverson GL, Brooks BL, Lovell MR, et al: No cumulative effects for one or two previous concussions. Br J Sports Med 2006;40(1):72-75. Macciocchi SN, Barth JT, Littlefield L, et al: Multiple concussions and neuropsychological functioning in collegiate football players. J Athl Train 2001;36(3):303-306. Pellman EJ, Lovell MR, Viano DC, et al: Concussion in professional football: neuropsychological testing—part 6. Neurosurgery 2004;55(6):1290-1303. McCrea M, Guskiewicz KM, Marshall SW, et al: Acute effects and recovery time following concussion in collegiate football players: the NCAA Concussion Study. JAMA 2003;290(19):2556-2563. Wall SE, Williams WH, Cartwright-Hatton S, et al: Neuropsychological dysfunction following repeat concussions in jockeys. J Neurol Neurosurg Psychiatry 2006; 77(4):518-520. Moser RS, Schatz P, Jorda BD: Prolonged effects of concussion in high school athletes. Neurosurgery 2005;57(2):300-306. Iverson GL, Gaetz M, Lovell MR, et al: Cumulative effects of concussion in amateur athletes. Brain Inj 2004;18(5):433-443. Rabadi MH, Jordan BD: The cumulative effect of repetitive concussion in sports. Clin J Sport Med 2001;11(3):194-198. Guskiewicz KM, Marshall SW, Bailes J, et al: Association between recurrent concussion and late-life cognitive impairment in retired professional football players. Neurosurgery 2005;57(4):719-726. Collins MW, Lovell MR, Iverson GL, et al: Cumulative effects of concussion in high school athletes. Neurosurgery 2002;51(5):1175-1179. Guterman A, Smith RW: Neurological sequelae of boxing. Sports Med 1987; 4(3):194-210.

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Running Shoes: Assessment and Selection Charles W. Webb, DO, FAAFP, and Marc A. Childress, MD

Equipment and apparel have become inseparable aspects of modern athletics. In some cases, these items may be critical to the sport, but, in far more situations, these products are designed to augment and protect athletes during the course of their endeavors. This is certainly the case with running shoes. Although the human body is perfectly capable of running and jogging without shoes, nearly all runners today elect to use shoes for a variety of reasons, including protection from the running surface, the prevention of injury, or the improvement of performance. As opposed to the barefooted competitors of ancient times, runners today face a dizzying array of options for sportspecific footwear. Additionally, it is difficult to find objective and useful information to guide runners in their decision-making process. For any physician who cares for both active and prospective runners, it can be very helpful to have a good basic knowledge of available products and to know how to counsel patients with regard to the selection of appropriate footwear. This chapter is designed to provide a background on the design and function of running shoes and a framework for creating a helpful running shoe prescription.

products, which are highly linked to sponsored events and athletes. Additionally, each company is extremely aggressive in attempting to convince runners that their proprietary components provide superior performance. A close inspection of marketing techniques and published information will reveal a paucity of objective information for the making of these distinctions. From a business perspective, this makes perfect sense. Consider the analogy of competing medications within the same class. Rarely will patients and physicians be provided with the results of head-to-head trials because these trials are either never attempted or simply never published as a result of a lack of overwhelming evidence. Additionally, in an unregulated industry (in contrast with the US Food and Drug Administration approval processes), there is often no interest in pursuing these types of investigations because there is no enforced accountability or need to prove efficacy. With footwear, this is made all the more interesting by the dynamics of fashion and sports culture. It is often impossible to gauge function from a simple visual inspection. Shoes that are innovative and well designed may be bland and appear rather simple, whereas poorly made shoes can easily be flashy and attractive. This can make the process of assessing shoes more difficult for patients and physicians alike. Runners are often extremely loyal to a certain brand. This can be the case for providers as well, especially if they have a background in running. Care must be taken to maintain some objectivity when making recommendations to patients regarding footwear choices. The running culture is full of anecdotal advice that covers training regimens, nutrition, apparel, and footwear. In an attempt to be a consistent and unbiased source of advice to patients, physicians need to be cognizant of the lack of clinical information and outcome data for many of the factors that will be discussed here. Despite these concerns, there are some tenets that have gained universal acceptance in the market (if not in the clinical world). Although research continues in the field of biomechanics and in the relationship of materials and technology to footwear, the industry currently works within the framework that is described below.

BUSINESS AND INDUSTRY CONCERNS

RUNNING SHOE ANATOMY

Like so many aspects of medicine, footwear is big business. Shoe manufacturers spend billions of dollars annually to market their

Running shoe components can be discussed in three basic segments. From top to bottom, these are as follows (Figure 45.1):

KEY POINTS

. Try on more than one shoe. . Briefly jog in each shoe (with the agreement of the salesperson, . .

of course). Purchase running shoes that are a half-size larger than your street shoes; make sure that there is at least a thumb’s width of space between your longest toe and the end of the shoe. Never purchase a shoe if it does not feel perfect the moment that you put it on: there is no ‘‘break-in’’ period for running shoes.

INTRODUCTION

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Running shoes: Assessment and selection

Table 45.1 A Sample of Various Midsole Technologies on the Market Today

Upper

Outsole

Device

Manufacturer Description

Air DMX Adiprene Hydroflow GRID ARC Wave N-ergy

Nike Reebok Adidas Brooks Saucony Avia Mizuno New Balance

Inert gas encapsulated in a polyurethane shell Communicating air chambers Proprietary ethylene vinyl acetate Encapsulated gel fluid Cartridge of synthetic strings under tension Plastic arch Plastic series of arches Varied pressure chambers

Midsole Figure 45.1

Basic figure of a running shoe.

Outsole: A rubber or composite layer that comes in contact with the running surface. Midsole: A foam layer that provides cushioning and support. It can also contain extra support or cushioning devices. Upper: The part of the shoe that secures the foot to the shoe and that provides additional support. This is the layer that contains the laces and the tongue of the shoe. Outsoles are typically constructed of one of two rubber compounds: blown rubber and carbon rubber. Blown rubber is lighter and it offers a subtle benefit in cushioning, but it is less durable. Carbon rubber is slightly heavier and denser and thus more durable. Heavier runners (> 180 pounds) or runners who are maintaining higher mileage (> 30 miles) may benefit from a carbon rubber outsole, whereas most others will not compromise the integrity of the shoe with the more typical blown-rubber outsole. Many manufacturers are experimenting with other composite materials for outsoles, such as clear polymers, integrated midsole ethylene vinyl acetate polymers, and molded plastic frames. Most of these options will still include a rubber compound at the contact surface. Flexibility can be enhanced or diminished by outsole design. Flex grooves, separate outsole plates, and other methods to maintain the natural flex point at the ball of the foot will often be incorporated. Many of these measures will have little effect,1 but, in some situations (e.g., excessive heel flare, which is common in trail shoes), they may increase the velocity of pronation and exacerbate instability injuries.2 Midsole design varies widely among manufacturers, and this is often where the marketed cushioning options will be found. Although there is a profound lack of data to this effect, there appears to be no clear difference in injury prevention among the proprietary methods of cushioning. These include air pads, encapsulated gels, lower-density ethylene vinyl acetate pads, arched plastic plates, silicone honeycomb pads, suspension fibers, and others. Some of these substances will offer a subjective difference in the sense of cushioning, but there is little evidence to support a clinical difference. Although impact dispersion may not be clearly affected by these inserts, there is a demonstrable difference in the durability of the midsole when various devices are used. Foam rubber products such as ethylene vinyl acetate are quickly susceptible to compression and loss of memory.3 The addition of air, gel, or plastic devices can prolong the cushioning life span of the midsole by virtue of higher material memory. The variety of these devices is remarkable, and often manufacturers will incorporate numerous named compounds or devices into the same shoe (Table 45.1). Most manufacturers will also use the midsole to incorporate various stability devices, most of which are designed to help bolster support on the medial aspect of the shoe. There are a few

examples on the market of shoes that truly attempt to compensate for underpronators. Because underpronating feet tend to be high arched and rigid, they benefit less from addition lateral stability and more from appropriate cushioning. For medial stability devices (which are often referred to as medial posts), most shoes will use a higher-density form of the midsole material. This is often denoted by a darker color (usually varying shades of gray). This is not a universal rule, but it is often helpful for locating shoes with extra medial support. Some shoes that are designed for those with more excessive stability needs will incorporate a semirigid thermoplastic polyurethane device into the medial portion of the midsole, thus further minimizing the amount of allowable pronation. Various manufacturers have also used a midsole cutout under the junction of the midfoot and the hindfoot junction. This serves to reduce weight as well as (in theory) to allow the foot to flex and roll in a more natural pattern. There is little objective evidence to suggest that this is helpful in the area of injury prevention. Some will place thermoplastic polyurethane devices here to control the amount of this motion between the hindfoot and the forefoot. Flexibility at the forefoot has long been touted as critical to a natural and efficient gait, although it is questionable whether the flexion of the forefoot is affected to any significant degree by the midsole as opposed to the natural degree of flexibility of the foot itself.4 Upper design is often driven by the stylistic emphasis of the shoe, but there are some important functional factors as well. Around the heel, the shoe will have a ‘‘heel counter’’ that serves to cradle the heel and to hold the heel firmly to the rest of the shoe (most times there is a very slight angle into the foot to prevent slippage). The heel counter stiffness varies with the overall stability of the shoe, and it can range from nearly fixed in some motioncontrol shoes to crushable in some racing flats. Ensure that the heel counter does not create friction at either of the malleoli or at the Achilles tendon because these are common areas of complaint in poor-fitting running shoes. The counter should not come in contact with the malleoli in running shoes (as opposed to other athletic footwear, which may envelope the ankle in an attempt to provide additional support). The vamp, which is the middle portion of the upper that the laces are tied into, should be comfortable and flexible. The tongue should line up over the highest point of the foot, and it should feel very well cushioned. If the foot feels constricted around this area during standing, then the shoe is either too narrow or the laces are too tight. The toe box is the area between the vamp and the front portion of the shoe. This should allow enough room laterally for the foot to feel flat and relaxed, and it should be long enough for an additional thumb’s width of space from the tip of the longest toe to the end of the shoe when standing straight (see the sizing tips discussed later in this chapter). Another component to consider is the insole (or sock liner), which is most often a removable piece. This piece is designed to

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Use of the running shoe prescription 557

provide a smooth and soft contour for the sole of the foot. Most insoles will include a porous foam material with a fabric overlay. This portion of the shoe can have a significant impact in the non—weight-bearing or standing comfort of a shoe. However, the cushion provided by this layer has little impact relative to the forces that are encountered during running. This is one of the best reasons to ‘‘test jog’’ in a shoe before purchase because the degree of comfort when running can be significantly different than the comfort noted when sitting or standing.

LASTING Each manufacturer uses a proprietary model of a human foot to build the shoe around. This template, or ‘‘last,’’ varies per brand and even from model to model within certain companies. Factors such as heel and forefoot width, arch placement, and shoe curvature will be affected by the last that is used in the construction of each particular shoe. This accounts for the large variety of fits encountered by different models and brands. Additionally, each shoe will follow a predetermined shape along the contact area of the shoe; this is designed to complement the normal amount of curve seen in the footprint of the human foot. When advertised, shoes will often be grouped into one of three categories: curved, semi-curved, and straight. Typically, curved lasts are more flexible and better matched to high-arched (pes cavus) feet. Semi-curved shoes are the most common, following the natural curvature of the most common foot type. Straight lasted shoes are designed as exactly that, with a reduction in the amount of curvature and often better accommodating those with significant pes planus; these runners may have greater needs for support and motion control. Certain brands have used unique lasting to cater to certain specific foot types, offering shoes that are designed to fit female runners, narrow feet, flatter or wider feet, and so on (Figure 45.2). The term last also applies to the manner in which the upper is secured to the midsole. Shoes will generally be constructed in one of three fashions: board lasted, slip lasted, and combination lasted. Board lasted shoes have an insole board that runs the length of the shoe, with attachments to the upper at the sides. Slip lasting involves a circumferential wrap of the upper in a moccasin (or ‘‘slipper’’) style that adheres more directly to the midsole.

Combination lasted shoes are typically slip lasted in the forefoot, with an insole board in the hindfoot and midfoot. Board lasting is more commonly used in shoes that are designed for motion control because the process offers greater stability and less flexibility. Likewise, slip lasting is used in highly flexible shoes that cater to higher-arched runners. Combination lasted shoes are designed to match runners who desire the fit benefits of slip lasting but who may require the added stability of the board lasting. The differences in the type of lasting are usually easily visible on removal of the insole (Figure 45.3). Because information about each model’s construction is often not readily available to the public or clinicians, it is critically important that the patient try on multiple brands and models within those brands. Even within the appropriate genre of running shoe (e.g., cushion, stability, motion control), a shoe constructed for a differently shaped foot can create problems ranging from minor discomfort to increased slippage and friction to more significant injury. The combination of design and materials in each of the portions of the shoe described previously make for a unique fit and feel for each available shoe on the market. The degree of difference depends in great part on the foot and the gait type of the runner. These are the factors that can be helpful when recommending certain features in the hopes that injuries can be reduced.

USE OF THE RUNNING SHOE PRESCRIPTION Although there is a decent amount of information regarding the kinematic effects of some of the design features discussed previously,5 there remains a gap between this body of information and its application to shoes that are available on the market.

Board lasted

Slip lasted

Combination lasted

Straight-lasted shoe

A Figure 45.2 lasted (B).

Curved-lasted shoe

B Examples of shoes that are straight lasted (A) and curve

Figure 45.3 Schematic views of shoes that are board lasted, slip lasted, and combination lasted.

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In addition, there is often significant disagreement in these studies on the basis of the method of testing. For the most part, the biomechanical studies do not publish data regarding commercially available shoes or shoe components, and it can be difficult to translate the results of these studies into appropriate recommendations for branded shoes on the market. As a result, physicians have fewer resources available to make evidence-based suggestions regarding footwear. Thus, it has been found that the best practical suggestions are made on the basis of design divisions in the industry. When making a recommendation or even a prescription, it is suggested that certain patient characteristics be evaluated to best match with the various types of running shoes on the market. The following segment of this chapter describes a stepwise patient assessment for a running shoe prescription. This form guides recommendations on the basis of easily identified genres and factors that are available from major shoe companies. An example form is included. The goals of this form and this discussion are to equip patients with both the information and the vocabulary that will help guide them to the most appropriate shoe. A helpful prescription should include recommendations that could be easily understood by both the patient and the supplier. Runners are increasingly seeking information from the Internet, and many retailers have incorporated helpful questionnaires that guide runners to matching shoes.6 Although there is certainly no recognized format for such a prescription, the listed items can be helpful for both runners and salespeople (Table 45.2).

Table 45.2

Running Shoe Prescription

Patient Name: _________________________ Height: _____ Weight: _____ Average weekly miles: _____ Average pace (if known): _____ Orthotics: Y/N

Standing Foot Analysis Resting ankle ____ Neutral ____ Pronated ____ Supinated With heel raise ____ Neutral ____ Pronated ____ Supinated

Circle One

Background information The initial questions listed relate to the durability needed from the shoe. Heavier runners (> 180 lbs) may benefit from more durable midsole (polyurethane) and outsole (carbon rubber) materials. The same may also be said for higher mileage runners (> 20 to 30 miles/week). However, keep in mind that the use of these denser materials in lighter runners may decrease the amount of cushioning, even if only in a subjective way. It is important to ask about orthotic use, even if the patient is using over-the-counter products. This may help highlight certain features that would be beneficial in the shoes. Runners who use prescription orthotic products need to have them available when they are trying on new shoes because many shoes are not well designed to accommodate the additional width and height of many orthotics. It is also not uncommon to see runners who use over-the-counter orthotic devices that may or may not be helpful. There is a considerable amount of discussion regarding the efficacy of these inserts.7

A

B

C

Foot-Strike Analysis (Preferably jogging/running gait rather than walking gait) (If performed, please note the method of analysis [i.e., treadmill, flat ground, examination of previous footwear].) Method: _________________________ _____ Heel strike _____ Midfoot strike _____ Forefoot strike

Recommendations (Check one from each category)

Foot analysis The next section involves having the patient stand with his or her back to you and his or her heels at eye level (it is recommended that the examiner be lowered rather than having the patient elevated). The typical heel will usually be in slight pronation (hindfoot valgus) and then swing into a more varus position upon rising onto the toes. Heels that remain in valgus upon rising will most likely need medial support, but they may also need evaluation for the root of their hindfoot rigidity (e.g., previous injury, coalition). Heels that start and remain in varus are usually high-arched rigid feet, and good shoes for these feet will need to maximize cushioning. The images seen on the prescription form represent a relief of the standing foot. They can be obtained in a variety of ways, including simple visualization (and possibly tracing the contact area) or having the patient wet his or her feet in a basin and then stand on an absorbent surface (e.g., a brown paper bag, a dark towel, a Chux pad) to see the area of weight-bearing contact. The basic spectrum involves pes planus (flatfeet) through pes

_____ Normal/stability (This is for most neutral runners with normal arches, and it incorporates a moderate amount of support in combination with good cushioning.) _____ Motion control (This is for lower-arched runners who may roll toward the inside of their feet while running; it also incorporates good cushioning.) _____ Cushion (This is for higher-arched runners with more rigid feet who may stay on the outside of their feet while running.) _____ Normal durability (This is for low to mid mileage runners who are light to normal build for their weight.) _____ Extra durability (This is for heavier runners or those who run more miles.) _____ Heel striker _____ Midfoot striker _____ Forefoot striker  Examples of arches of human foot. A, Normal. The forefoot and heel are connected by a curved band that is about 2 inches wide. B, Flat. A large impression or a very little arch. C, High. The forefoot and heel are connected by a very narrow strip.

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cavus (high-arched feet). It is important to remember that, contrary to the belief of many patients, high-arched feet do not provide more cushioning to the body. In fact, these feet are often rigid and inflexible. Thus, patients with high arches typically will be less likely to overpronate, and they may in some cases underpronate (supinate). As mentioned previously, few shoes target underpronation specifically, but the emphasis should be on maximizing cushioning. Most shoes that target these runners will be labeled as cushion shoes. By contrast, the flatfooted arch often allows for sufficient cushioning, so shoes can help control the amount of pronation that these feet tend to exhibit; these shoes are usually described as motion-control shoes. For those with feet that would appear to fall in the middle of the spectrum, the bulk of the market is targeted at providing a comfortable mix of stability and cushioning; these will often be described as stability shoes.

Gait assessment Gait assessment is the next segment of the prescription. Although much is made of pronation and supination (underpronation) in runners, it is important to remember that these are normal motions of the natural gait. The difference between an athlete with a neutral gait and one that might benefit from correction is sometimes subtle, and it depends in great part on whether the natural gait is causing pain or injury. Upon foot strike, the heel is typically the first to make contact at the lateral aspect. This is important to evaluate for runners who may make contact at the midfoot or the forefoot because this can affect the need for support and cushioning. In ideal circumstances, this part of the evaluation would be performed on a dedicated treadmill with computer and video equipment to assess the moment-by-moment strike and roll of the foot. However, for the vast majority of clinic situations, this is nowhere near reality. If time and facilities allow, having the patient run on a regular treadmill can allow for similar visualization. However, without the aid of slow-motion cameras, it is difficult to visualize each of the components of the stride. For more details about gait analysis, see Chapter 43. Another way of assessing the gait is through an examination of the patient’s last pair of running shoes. It is far preferable to have a pair of shoes that have been primarily for running because the gait is often quite different from that seen when walking and running. However, this is often not possible, especially if patients are seeking an initial recommendation. The normal gait cycle includes foot strike at the lateral aspect of the heel. Upon impact, the heel will undergo pronation as the body moves forward over the foot. As the leg arcs forward, the weight of the body is transferred through the midfoot, by which time the foot has undergone a mild amount of supination, thus distributing the weight more evenly over the ball of the foot. Through flexion at the metatarsophalangeal joints, the foot rolls up onto the toes, and it is again pushed into the air. This cycle is repeated with every stride. This is where the examination of the previous footwear can be very helpful. By evaluating the wear patterns, one can estimate the average distribution of force in the shoe over time. For example, most shoes will wear first over the lateral heel. As discussed previously, this is consistent with the neutral gait. However, if there is a significant amount of tread wear and midsole breakdown on the medial side of the heel, this may suggest overpronation. As the physician looks further forward on the shoe, he or she should see that, by the ball of the foot, the wear pattern is fairly even. Again, excessive wear to the inside is consistent with overpronation. Likewise, a wear pattern that started normally in the lateral heel and that continued laterally into the ball of the foot suggests underpronation. Look at the toe to see that wear is fairly even, often

focused at the longest toe. Having the old shoes can also allow for a brief examination for some of the other items emphasized in this chapter. Separation of the midsole from the upper in the ball of the foot suggests that the shoe may have been too narrow. Stressed or broken seams at the toes can be an indicator that the patient needs a larger size. With all of this information, it is helpful to make simple recommendations that are understandable to both the patient and the salesperson. Time rarely allows for a full explanation of each part of the evaluation, so it can be helpful to include on the prescription a brief explanation of why the recommendations are being made.

GENERAL TIPS Sizing Be sure to recommend that your patients try shoes that are one half to one full size larger than their street shoes. Also recommend that the shoes be tried on either at the end of the day or soon after running or exercise. Feet swell during exercise, and the repeated impact of the running stride can slightly stretch the feet lengthwise. Shoes that are too small can lead to toenail damage, and they can severely impair the foot’s ability to attenuate shock throughout the natural arc of the foot. Shoes that are too narrow can lead to blisters and to forefoot and toe pain, and they can limit the natural flex points at the metatarsophalangeal joints. Allow at least a thumb’s width of space between the end of the longest toe (not always the great toe) and the front end of the shoe. In addition, if the ball of the foot feels constricted, look at wider shoes or other brands.

Lacing Recommend that patients try various heights of lacing. Rarely do all of the uppermost eyelets need to be used. These recommendations apply to those individuals with heel slippage that results from very narrow hindfeet. If shoes are laced excessively high or tightly, pain along the anterior ankle joint may result, sometimes with distal nerve irritation (i.e., ‘‘lace bite’’). There are a variety of lacing styles available for different foot types; these will not be covered here, but they can be found on the Internet. Keep in mind that these are not universal solutions. There is little objective evidence that these are helpful, but there is no harm in experimenting as long as the foot is secure.

In-store tips It is imperative that patients try on more than one shoe before making a purchase. Recommend that patients try different brands and different models. There is no shoe that will cater appropriately to every runner, especially in the area of fit. If the shoe does not feel great immediately and feel better than all of the other options, then it is not the right shoe. Please emphasize this point of the immediate sensation. Unlike other footwear, there is no break-in period for running shoes. If there are any points of stiffness, pressure, or friction, then these will likely only worsen. Encourage patients to be as extensive when testing the shoe as the salesperson will allow. Some stores will allow and even encourage short jogs in or around the store before purchasing. Regarding price, there are a few tips worth remembering. The most expensive shoe is not necessarily the best shoe. Although the prices of shoes have increased as a whole, a 1988 study suggested that there was no appreciable difference in injury avoidance between shoes that cost less than $25 and those that cost more than $40.8 The numbers used are likely to be less relevant today, but the premise remains.

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Many patients will be tempted to shop for running footwear through the Internet or catalogs. Many of these Web sites and sales resources are great sources of information for guiding runners to the appropriate shoes; however, it must be emphasized that the only time when it is appropriate to purchase a pair of shoes without trying them on is if the shoe is identical in model and size to a pair in which the athlete has already successfully run. Shoes from the same brand and even the same model in a different generation can have a significantly different fit, road feel, and level of flexibility.

Shoe life span Most shoes are designed to offer adequate protection through 300 to 500 miles.9 This depends again on the makeup of the shoe and the weight of the runner. In lower-mileage runners, these distances may not be reached within 6 months. The effective life of some of the cushioning materials can also deteriorate over time, regardless of use. For this reason, recommend a mileage cutoff or roughly 6 months of time, whichever comes first. Other signs that shoes may need to be replaced are the ability to sense small rocks and seams in the road through the sole of the shoe as well as a stinging or slapping sensation when the forefoot of the shoe hits the ground. Shoe life can also be affected by weather conditions. Moisture and cold temperatures have both been implicated in a reduced life span.10

SPECIAL CONSIDERATIONS Older runners Although the natural heel pad is excellent for providing a significant amount of shock attenuation, it is known to atrophy and lose elasticity with age.11 Additionally, the normal human gait cycle is well suited to absorb additional shock through the degree of flexion in the feet and legs. Older (approximately 60 years old) and younger (approximately 20 to 30 years old) subjects are biomechanically different in the way that they run.12 For example, older runners use shorter steps at a higher frequency and display smaller knee ranges of motion, higher vertical impact speeds, higher peak impact forces, and higher initial loading rates than younger runners. These findings demonstrate that the older runner may be less able to compensate for the repeated stresses of distance running, and this may even explain the higher incidence of overuse injuries in this population.13 Accordingly, cushioning becomes a more important consideration when prescribing running shoes for older runners.

Female runners Many shoe companies have become sensitive to the athletic needs of women and are promoting footwear that has a narrower fit

for women. The female foot has a narrower Achilles tendon, a narrower heel in relation to the forefoot, and a foot that is narrower in general than the male counterpart. Women have been historically noted to have larger Q angles than men,14 although this may be over estimated.15 Women have the following differences from men while running: the impact in their vertical ground force reaction; peak tibial acceleration; maximal pronation; peak pronation velocity; and peak pressures and peak pressure rates.16 In the recent past, women’s shoes were based on a scaled-down version of lasts derived from the male foot anatomy. However, more manufacturers are now producing shoes solely for women that are designed with the previously mentioned factors having been addressed.

REFERENCES 1. Stacoff A, Reinschmidt C, Nigg BM, et al: Effects of shoe sole construction on skeletal motion during running. Med Sci Sports Exerc 2001;33(2):311-319. 2. Nigg BM, Morlock M: The influence of lateral heel flare of running shoes on pronation and impact forces. Med Sci Sports Exerc 1987;19(3):294-302. 3. Verdejo R, Mills NJ: Heel-shoe interactions and the durability of EVA foam runningshoe midsoles. J Biomech 2004;37(9):1379-1386. 4. Oleson M, Adler D, Goldsmith P: A comparison of forefoot stiffness in running and running shoe bending stiffness. J Biomech 2005;38(9):1886-1894. 5. Frederick EC: Kinematically mediated effects of sport shoe design: a review. J Sports Sci 1986;4(3):169-184. 6. www.roadrunnersports.com 7. Nigg BM, Stergiou P, Cole G: Effect of shoe inserts on kinematics, center of pressure, and leg joint moments during running. Med Sci Sports Exerc 2003;35(2):314-319. 8. Gardner LI Jr, Dziados JE, Jones BH, et al: Prevention of lower extremity stress fractures: a controlled trial of a shock absorbent insole. Am J Public Health 1988 Dec;78(12):1563-1567. 9. Cook SD, Kester MA, Brunet ME, Haddad RJ Jr: Biomechanics of running shoe performance. Clin Sports Med 1985;4(4):619-626. 10. Dib MY, Smith J, Bernhardt KA, et al: Effect of environmental temperature on shock absorption properties of running shoes. Clin J Sport Med 2005;15(3):172-176. 11. Hsu TC, Wang CL, Tsai WC, et al: Comparison of the mechanical properties of the heel pad between young and elderly adults. Arch Phys Med Rehabil 1998;79(9): 1101-1104. 12. Bus SA: Ground reaction forces and kinematics in distance running in older-aged men. Med Sci Sport Exerc 2003;35:1167-1175. 13. Egermann M, Brocai D, Lill CA, Schmitt H: Analysis of injuries in long-distance triathletes. Int J Sports Med 2003;24(4):271-276. 14. Tillman MD, Bauer JA, Cauraugh JH, Trimble MH: Differences in lower extremity alignment between males and females. Potential predisposing factors for knee injury. J Sports Med Phys Fitness 2005;45(3):355-359. 15. Grelsamer RP, Dubey A, Weinstein CH: Men and women have similar Q angles: a clinical and trigonometric evaluation. J Bone Joint Surg Br 2005;87(11): 1498-1501. 16. Henning EM: Gender differences for running in athletic footwear. In Hennig E, Stacoff A (eds): Proceedings of the 5th Symposium on Footwear Biomechanics. Zurich, Switzerland, 2001, p 44.

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Compartment SyndromeTesting Brandon D. Larkin, MD, and Janiece N. Stewart, MD

KEY POINTS

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Compartment syndrome is a common cause of exertional leg pain in athletes, and clinical diagnosis alone is unreliable. Successful compartment pressure testing requires a thorough knowledge of anatomy. The Pedowitz criteria are the generally accepted guidelines for the diagnosis of chronic exertional compartment syndrome. However, debate exists regarding the accuracy of the currently used diagnostic criteria. Numerous alternative noninvasive investigative methods (e.g., magnetic resonance imaging, bone scanning, nearinfrared spectroscopy, and technetium- 99m methoxyisobutyl isonitrile perfusion imaging) have been studied and shown to have variable diagnostic values.

INTRODUCTION Chronic leg pain in athletes is a common complaint that is often difficult to diagnose because several distinct pathologic processes may present with similar characteristics. Although the range of potential diagnoses is wide, medial tibial stress syndrome, stress fracture, chronic exertional compartment syndrome (CECS), nerve entrapment, and popliteal artery entrapment syndrome are the most common causes of exercise-related leg pain in athletes1 (Table 46.1). Several studies have investigated the prevalence of individual diagnoses to explain exercise-related lower leg pain, and the findings are somewhat contradictory on the basis of the patient populations studied. A retrospective review of 150 athletes with chronic leg pain found that CECS was the most prevalent condition, with an incidence of 33%; this was followed by stress fractures in 25% and medial tibial stress syndrome in 13% (LOE: D).2 Another study of 98 patients with recurrent anterior leg pain caused by either sports or trauma noted a 42% incidence of medial tibial stress syndrome, a 27% incidence of CECS, and a 13% incidence of peroneal nerve entrapment (LOE: D).3 Regardless of distribution, a thorough knowledge of the anatomy and biomechanics of the lower extremities is necessary to successfully determine the most likely cause in a specific case and to develop an efficient, appropriate diagnostic plan and treat-ment regimen.

CECS is a common cause of exercise-induced lower leg pain in athletes. With this condition, pain is the result of elevated intramuscular pressure within an anatomic compartment. Four individual compartments exist in the lower leg: the anterior compartment, the lateral compartment, the superficial posterior compartment, and the deep posterior compartment. Housed within each of these compartments are muscles, nerves, and blood vessels, which are enclosed by fibrous fascia. During activity, muscle size may increase by 20%, thereby causing a compression of the components of the compartment if the surrounding fascia is of limited compliance.4 This in turn leads to symptoms of pain and numbness in the area of the affected musculature or distally as a result of nerve compression.

Pathophysiology The pathophysiology of CECS is not well understood. In normal athletes, intracompartmental pressure may rise threefold- to fourfold during exercise, but it rapidly returns to normal within a few minutes.5 In athletes with CECS, however, there is a higher increase in pressure for a longer duration. Four factors have been identified that may, in combination, contribute to this difference: (1) an inelastic nature of the fascial sheath; (2) an increased skeletal muscle volume as a result of blood flow and edema; (3) muscle hypertrophy during exercise; and (4) gait-related dynamic contraction factors.6 The combination of these factors causes a transient rise in compartment pressure that eventually compromising the microcirculatory status. As blood flow decreases below the level that is needed to meet metabolic demands, tissue ischemia results, and the athlete experiences symptoms of pain, numbness, and weakness.7

EVALUATION History The hallmark of CECS is its reproducibility. The classic presentation involves recurrent leg cramping, burning, or aching pain and tightness during exercise over a specific component of the leg at a predictable point of activity, increasing in severity if that activity persists and resolving within minutes of the cessation of exercise. A longer period of rest is required for the complete resolution of a pain episode. CECS is most commonly associated with overuse injury in well-conditioned athletes, particularly runners.8 Prolonged periods of rest do not result in a lack of pain when

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Compartment syndrome testing

Differential Diagnosis for Chronic Exertional Compartment Syndrome

Diagnosis

Presentation

Diagnostic Studies

Stress fracture

Localized tenderness over the tibia; pain with bending stress Pain on resisted plantarflexion and inversion along the posteromedial aspect of the tibia Tingling or numbness in a specific nerve distribution Pain and coolness after excessive dorsiflexion and plantarflexion Sensory deficits; weakness

Plain x-ray, magnetic resonance imaging, bone scanning

Medial tibial stress syndrome Peripheral nerve entrapment Popliteal artery entrapment syndrome Radiculopathy

activity later ensues,9 so athletes may actually completely stop their participation in the provocative sports. Pain is usually constant and unrelated to ground contact. Approximately 75% to 95% of patients present with bilateral symptoms (LOE: B).10 Nonsteroidal antiinflammatory medications are thought to be largely ineffective.8 Pain associated with the anterior and lateral compartments is typically described as occurring over the anterolateral aspect of the shin, with occasional radiation to the anterior ankle and the dorsum of the foot. Pain in the mid and upper calf is usually referred to the superficial posterior compartment, where deep posterior compartment pain lies over the medial shin or the distal calf, often spreading to the medial arch of the foot.9 Numbness, tingling, and weakness may also occur, and these may be the only presenting complaints, which indicate the involvement of the affected compartment’s resident nerve. The athlete often notes a feeling of altered foot strike while running as a result of the transient weakness of the affected nerve’s musculature.11

Physical examination Another hallmark of CECS is a lack of physical signs at rest.9 There may be a palpable firmness and/or fascial muscle herniation in the affected compartment, but little else is usually evident. Therefore, all patients with historic features that are indicative of CECS should undergo an exercise challenge test followed by a postexercise examination.7 Ideally, the actual provoking activity (i.e., running, rollerblading, elliptical machine) should be performed during this testing. After the reproduction of the discomfort, the athlete should be assessed for tenderness, tightness, or swelling over the affected compartment. A full vascular and neurologic examination should be performed that includes sensation to light touch and strength testing. Abnormal neurologic findings may clue the examiner in as to the identity of the affected nerve and, therefore, the compartment involved.9 Anterior compartment involvement after exercise may display weakness of dorsiflexion or toe extension, paresthesias over the dorsum of the foot, numbness in the first web space, or even transient or persistent foot drop.12 Sensory changes over the anterolateral aspect of the leg and weakness of ankle inversion may indicate lateral compartment involvement. Superficial posterior compartment symptomatology includes dorsolateral foot sensory deficits and weakness of plantar flexion, and deep posterior compartment involvement may lead to plantar foot paresthesias and weakness of toe flexion and ankle inversion.7 The patient should have normal dorsalis pedis and posterior tibialis pulses after exercise challenge testing. If these are decreased from baseline, a vascular cause such as popliteal artery entrapment should be considered.7 Despite a history that is suggestive of CECS, no physical examination finding can firmly establish the diagnosis. Numerous other causes can result in similar symptoms. A false-positive rate of 74% on the basis of clinical examination has been reported (LOE: D).3 Therefore, diagnosis that is based only on clinical presentation

Bone scanning, magnetic resonance imaging Electromyelogram, nerve conduction study Arteriogram Electromyelogram, central nervous system evaluation

increases the risk of misdiagnosis, delayed diagnosis, and inappropriate therapy.13 Most studies emphasize the need for intramuscular pressure measurement during the diagnostic process. Targeted testing can be performed on the basis of the history if the clinical presentation indicates the involvement of a specific compartment. A vague location of symptoms may necessitate the testing of all four compartments of the leg (Table 46.2).

TECHNIQUES AND EQUIPMENT Testing strategies Compartment pressure testing is an invasive procedure. Successful and uncomplicated performance of this test requires a thorough knowledge of the anatomy of the compartments to be entered to avoid contact with vital neurovascular structures. Two types of intracompartmental pressure measurement strategies have been used. Dynamic testing makes use of a slit catheter inserted into the compartment before exercise and attached to the athlete’s leg. Using this technique, the examiner is able to continuously monitor pressure changes during exercise and to correlate symptoms with objective data.6 However, dynamic testing is not without problems. Catheter placement in the compartment is difficult to maintain during exercise. Also, the attachment of the apparatus to the patient may restrict the natural gait. In addition, dynamic testing does not allow the athlete to run on his or her usual training

Table 46.2 Indication and Contraindications for Compartment Pressure Testing Indications

Contraindications

Clinical evidence of chronic exertional compartment syndrome:  Recurrent exercise-induced leg discomfort that increases with continued exercise and resolves with rest  Tight, cramping, or squeezing ache over a specific compartment area  Numbness, tingling, or weakness of the leg or foot Exercise challenge testing provoking signs of chronic exertional compartment syndrome:  Firmness or tenderness to palpation of an anatomic compartment of the leg  Weakness in an anatomic nerve distribution  Loss of sensation to light touch in an anatomic nerve distribution

History of a bleeding disorder or anticoagulation Rash or infection of the overlying skin

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surface because it may only be performed on a treadmill, and it does not allow for the simultaneous testing of multiple compartments. Many have found the results of the dynamic measurement technique to be inconsistent and difficult to interpret because values vary substantially from patient to patient (LOE: B).14 Static compartment pressure testing is currently the most common technique employed for the determination of pathology. Static pressure measurements are obtained via a needlestick both before and after exercise. This technique allows the athlete to move freely during activity and affords some degree of freedom to accurately reconstruct actual training conditions and location. In addition, several compartments on both legs can be measured, which is often necessary if the clinical presentation is vague. However, this method does require two to three needlesticks per compartment tested.

Equipment Numerous apparatuses have been used to measure compartment pressures in both static and dynamic testing. Techniques employed include a needle manometer, a slit catheter, a wick catheter, continuous infusion, and a solid-state transducer intracompartmental catheter.6,15 A commonly used device is the Stryker Intracompartmental Pressure Monitor (Stryker Corporation, Kalamazoo, Mich) (Figure 46.1). It is a battery-operated, handheld, digital fluid pressure monitor that has been found to be more accurate and easier to use than the needle manometer.16 It is compatible with both static and dynamic testing. Its convenience and, more importantly, its reproducibility between examiners make it an appropriate tool for the busy clinical office setting.7,17

Anatomy As mentioned previously, a thorough understanding of the anatomy of the compartment to be studied is imperative for safe and effective compartment pressure testing. The leg contains four anatomically distinct compartments, each bound by bone and fascia

Figure 46.1 Stryker handheld compartment pressure monitor. (From Canale ST [ed]: Campbell’s Operative Orthopaedics, 10th ed. St. Louis, Mosby, 2003.)

and each containing a major nerve (Figure 46.2). The anterior compartment contains muscles that are used to extend the toes and to dorsiflex the ankle. It contains the extensor hallucis longus, the extensor digitorum longus, the peroneus tertius, and the anterior tibialis muscles as well as the deep peroneal nerve. The blood supply is from the anterior tibial artery. The lateral compartment houses the muscles that are responsible for the eversion of the foot: the peroneus longus and brevis. It also contains the superficial peroneal nerve as well as branches of the peroneal artery. The plantarflexors of the foot—the gastrocnemius, the soleus, and the plantaris—are contained in the superficial posterior compartment along with the sural nerve. The deep posterior compartment contains the muscles of toe flexion, ankle plantarflexion, and ankle inversion, which are the flexor hallucis longus, the flexor digitorum longus, and the posterior tibialis muscles. The posterior tibial nerve and the posterior tibial artery are also located within the deep posterior compartment.

Anterior compartment:

Figure 46.2 Axial anatomy of the lower extremity. m., muscle. (Redrawn from Scuderi, McCann [eds]: Sports Medicine: A Comprehensive Approach. Philadelphia, Mosby, 2005.)

Tibialis anterior m. Tibia

Extensor digitorum longus m. Extensor hallucis longus m.

Deep posterior compartment: Lateral compartment:

Flexor digitorum longus m. Tibialis posterior m.

Peroneus brevis m. Peroneus longus m.

Flexor hallucis longus m.

Fibula

Superficial posterior compartment:

Soleus muscle

Gastrocnemius m.

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Compartment syndrome testing

Although all compartments can be affected and often are affected in combination, most studies have found the distribution of pathology to be relatively consistent. Anterior compartment syndrome is the most common (45%), followed by the deep posterior compartment (40%), the lateral compartment (10%), and the superficial posterior compartment (5%).18 Some describe a separate and distinct fifth compartment that is encompassed by the fascia surrounding the posterior tibialis muscle and that may be important in CECS.11 However, recent studies have called into question the consistency of this anatomic finding, describing it alternatively as a subcompartment that is only occasionally demonstrable in cadaveric investigation. Regardless of its classification, the area may display a separate increase in intramuscular pressure, and it should likely be an important target of surgical treatment (LOE: E).19

The procedure (Box 46.1) 1. Obtain written informed consent from the patient after explaining the risks and benefits of the procedure. 2. The Stryker pressure monitor is a reusable device that requires a disposable set of accessories that are packaged together. This set should include a sterile 18-gauge needle, a diaphragm chamber, and a syringe filled with 3 mL of normal saline. Additional equipment includes sterile gloves, alcohol swabs, gauze, Betadine solution, a 25-gauge needle and syringe for the instillation of local anesthesia, and 1% xylocaine without epinephrine. Bupivacaine 0.5% solution should also be used for local anesthesia if the patient’s

3. 4. 5.

6.

7.

8.

9.

10.

Box 46.1: Checklist of Procedure  Obtain written informed consent after discussing risks and benefits with the patient.  Gather and assemble equipment.  Position the patient supine with the knees extended and the ankles in a vertical position.  Sterilize the overlying skin.  Anesthetize the skin and the subcutaneous tissue.  Prepare the Stryker monitor by instilling saline to fill the diaphragm and needle.  Power on the monitor, and zero the unit.  Orient the device at a 90-degree angle to the skin, and zero the device again.  Insert the needle through the skin, the subcutaneous tissue, and the fascia and into the compartment.  Instill a small amount of saline, and wait for the monitor to equilibrate.  Record the measurement, and remove the needle.  Repeat the procedure in all compartments that are suspicious for involvement.  Cover the needle sites with bandages.  Have the patient exercise until symptoms occur and until the point at which he or she would normally discontinue exercise as a result of pain.  Repeat the procedure in all involved compartments at 1 minute and 5 minutes after exercise.  Dispose of the needles in a biohazard container.  Advise the patient about postprocedure care.

11.

symptoms require an extended period of time to occur to avoid repeated injections of the shorter-acting anesthetic.7 Have the patient lie relaxed in the supine position with the knees extended and the ankle in a vertical position. Identify the desired compartments, and sterilize the overlying skin with alcohol and Betadine. Anesthetize the column of tissue between the skin and fascia with 1 to 3 mL of 1% lidocaine without epinephrine, taking care to avoid penetration through the fascia and into the compartment. Prepare the Stryker monitor for insertion by connecting the provided disposable syringe, the sterile needle, and the diaphragm transducer (see Figure 46.1). Press the syringe to fill the diaphragm and needle until a drop of saline is expressed from the needle tip and no air bubbles are visible in the diaphragm. Power on the monitor, and depress the ‘‘zero’’ button to clear the unit. Orient the device at a 90-degree angle to the skin to be entered. Immediately before inserting the needle into the extremity, zero the device again, ensuring that the angle of entry is maintained as the ‘‘zero’’ button is depressed. Insert the needle at 90 degrees into the anesthetized skin, through the subcutaneous tissue and fascia, and into the compartment. There is a palpable ‘‘pop’’ as the fascia is breached. Approaches for individual compartments are described later in this chapter. After the needle has entered the compartment, instill a small amount of saline to ensure a solid column of fluid. Allow a few moments for the monitor to equilibrate. Record the measurement, and remove the needle. To approach the anterior compartment, palpate the tibialis anterior just lateral to the anterior tibial border, and insert the needle at the level of the mid third of the tibia (Figure 46.3). Just above the interosseous membrane sits the neurovascular bundle, which contains the deep peroneal nerve, the anterior tibial artery, and the veins and which should be avoided. To approach the lateral compartment, palpate the muscle bellies of the peroneus longus and brevis at the same midtibial level as the anterior approach (Figure 46.4). Needle insertion should be at the midpoint between the head of the fibula and the lateral malleolus. The intramuscular septum between the anterior and lateral compartments is usually apparent with deep palpation from the anterior tibia laterally. The angle of entry into the lateral compartment is typically parallel with the examination table.

Figure 46.3

Anterior approach.

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16. Compartment pressures should be measured again at 1 minute after exercise or as soon as possible after the onset of symptoms. The procedure should be repeated 5 minutes into the rest period (LOE: B).14 Entry into each compartment should use the same needle holes that were used during pre-exercise testing. 17. Dispose of the needles in a biohazard container. 18. Advise the patient about postprocedure care. Bleeding, signs of infection, or neurologic complaints should signal a need to return for evaluation and treatment.

INTERPRETATION

Figure 46.4

Lateral approach.

12. To approach the superficial posterior compartment, palpate the muscle bellies of the gastrocnemius and the soleus. Approach this compartment from the medial side just posterior to the medial border of the tibia, avoiding the small saphenous vein and the medial and lateral sural cutaneous nerves (Figure 46.5). It is helpful to flip the monitor so that the display faces the examiner during this approach. 13. To approach the deep posterior compartment, continue advancing the needle after completing testing of the superficial compartment, closely approximating the posterior aspect of the tibia. A second ‘‘pop’’ is felt when the deep compartment is entered. A vascular bundle containing the peroneal artery and veins lies medial to the posterior border of the fibula. A neurovascular bundle with the tibial nerve, the posterior tibial artery, and veins lies in the posterior aspect of the compartment behind the tibialis posterior muscle. 14. Cover the needle sites with bandages. 15. Have the patient perform the provocative activity until typical symptoms are fully reproduced,20 usually to the point at which the athlete would normally discontinue exercise as a result of pain. It is important to use provocative activities that are as similar to the pain-provoking exercise as possible (LOE: E).21

Figure 46.5

Superficial and deep posterior approach.

Findings that are consistent with the diagnosis of CECS are an elevated resting compartment pressure obtained before exercise, a marked elevation of postexertion pressure, and/or a delayed return to normal pressure several minutes into the rest period. The most commonly accepted criteria for the accurate diagnosis of CECS were described by Pedowitz and colleagues.13 One or more of the following criteria must be met in addition to an appropriate history and physical examination (LOE-B):  Pre-exercise compartment pressure of 15 mm Hg or more  1-minute postexercise compartment pressure of 30 mm Hg or more  5-minute postexercise compartment pressure of 20 mm Hg or more There is a fair amount of controversy regarding the most accurate threshold for the diagnosis of CECS. Although the Pedowitz criteria are generally considered to be the standard scale, several studies have used differing or additional criteria. Reports of normal values for resting intracompartmental pressure even vary as a result of such variables as operator experience, the catheter type, the volume of the instilled fluid, the position of the leg and foot of the subject, the type of exercise performed, and the timing of the measurement. Although Pedowitz and colleagues consider a pressure of less than 15 mm Hg to be normal in a resting compartment, other authors have found that a measurement of less than 10 mm Hg may be a more accurate normal value at rest.20 The same study proposed that levels of greater than 20 mm Hg at 1 minute and greater than 20 mm Hg at 5 minutes and an intracompartmental pressure normalization time of greater than 15 minutes are adequate criteria, with the latter being the most reliable for diagnosing CECS in adolescent athletes (LOE: B). Several authors agree that delayed pressure normalization time may be the most appropriate indicator of pathology.14 If symptoms are fully reproduced during provocative exercise testing, the subjective relief of pain by the athlete—and, thus, the return of the compartment pressure to normal (LOE: D)22—has been found to occur after a period of 20 minutes of rest.20 Therefore, the measurement of compartment pressure at 15 minutes after exercise would seem to be appropriate if findings at 5 minutes after exercise are equivocal.1 Although the Pedowitz criteria are, for the most part, commonly agreed on, they are based on a comparison with 210 normal anterior muscle compartments that were tested during the study’s data collection. With CECS of the posterior compartment, there is considerably more disagreement about the proper cutoff values.9 However, most clinicians use the same criteria for the anterior compartment and other compartments.23 Because of the variability in the interpretation of the results of compartment pressure testing, positive pressure tests alone are insufficient to make the diagnosis and should never replace a thorough history and physical examination.

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Other diagnostic modalities Because results of compartment pressure testing are interpreted differently and objective criteria are the focus of continuing debate, the search for other diagnostic methods is vigorous, especially for a noninvasive modality. Other tools that have been employed include the triple-phase bone scan, magnetic resonance imaging (MRI), near-infrared spectroscopy, and technetium-99m methoxyisobutyl isonitrile perfusion imaging. Bone scanning may show decreased radionuclide uptake in or near the affected area, thereby supporting the diagnosis of decreased blood flow and thus elevated intracompartmental pressure. The characteristic pattern also displays increased tracer concentration superior and inferior to the abnormality.15 MRI may be useful for the diagnosis of CECS as a result of its sensitivity to changes in water distribution in skeletal muscle. If tissue edema is involved in pressure elevation in individual compartments, postexercise MRI may be able to detect the increased water content (LOE: C).24 Although MRI is sensitive, its specificity remains questionable because it may display findings that are similar to those of metabolic rhabdomyolysis, muscle lesions, or even changes in normal muscle caused by exercise.24 Studies question the diagnostic value of MRI with regard to its ability to consistently confirm CECS (LOE: D).25 Nevertheless, if the limitations of these modalities are taken into account, bone scanning and MRI offer diagnostic alternatives for the athlete who is hesitant to consent to the more invasive compartment pressure testing procedure. Near-infrared spectroscopy is an indirect, noninvasive method of investigating CECS in which the degree of the deoxygenation of muscle tissue as a result of exercise can be measured. It is based on the discovery of ischemia caused by increased intracompartmental pressure that causes an increased extraction of oxygen from arterial blood by muscle, thereby resulting in decreased venous oxyhemoglobin content. The tissue oxygen saturation is thought to reflect the oxygen saturation of venous blood because most of the blood content of tissue is in the venous compartment. Recent studies have shown that patients with the clinical complaints and elevated compartment pressures that are typical of CECS show a larger decrease in tissue oxygen saturation on near-infrared spectroscopy and a longer period of recovery to normal levels than do healthy controls (LOE: C).26 In addition, spectroscopy approaches the sensitivity of intracompartmental pressure testing for diagnosis (LOE: D).25 However, because it depends on light absorption through tissue to measure muscle oxygenation, near-infrared spectroscopy is limited in its usefulness for very dark-skinned athletes.26 Technetium-99m methoxyisobutyl isonitrile perfusion testing evaluates the uptake of a radiolabeled intravenous solution by peripheral muscles. Uptake is determined by blood flow and inhibited by hypoxia, thus making it useful for detecting muscle ischemia. Case reports exist that illustrate a visually apparent decrease in its concentration in muscles that are contained in compartments with elevated pressures after exercise as compared with imaging at rest (LOE: E).27 Technetium-99m methoxyisobutyl isonitrile imaging requires the visual interpretation of concentration within the compartment, and its results were not found to be identical to invasive compartment pressure testing. Further study is needed to determine its place in the diagnosis of CECS.

UPPER EXTREMITY COMPARTMENT SYNDROME Although CECS in the lower extremity is well described in the literature, there is a relative dearth of discussion regarding its involvement in the upper extremity. A likely reason for this is the rarity of the condition among athletes. When it does occur, its typical

Box 46.2: Pitfalls Errors in Measurement7  Calibration of the monitor at an inconsistent angle on repeat testing  Inconsistency of knee and ankle joint positioning on repeat testing  Application of external pressure on the compartment while stabilizing the extremity Errors in Diagnosis  Unnecessary surgical procedure that may lead to further complications  Recurrence of pain after a ‘‘curative’’ surgical procedure

presentation is tightness and pain in the forearm (not related to trauma) that occurs during a steady increase in activity. As is seen in lower extremity compartment syndrome, pain relents within minutes of the cessation of the exercise. Dyesthesias and weakness may also occur in the distal extremity. Affected athletes include those with repetitive arm motion, including tennis players,28 weight-lifters,29 and motorcyclists.30 Because of its rarity, the diagnosis of CECS in the upper extremities is often delayed. Physical examination findings may include the swelling and palpable tenderness of the affected musculature after exercise. These findings may be elicited during the examination after repetitive resisted range-of-motion exercises of the elbow, wrist, and/or fingers.28 Numerous techniques for compartment pressure testing of the upper extremity have been described. The insertion of a catheter into the individual compartments of the forearm has been used for the measurement of compartment pressures before, during, and 15 to 30 minutes after repetitive exercise to the point at which symptoms recur (LOE: E).30 Others instruct the patient to perform maximal isometric contractions of the affected muscle group for 5 seconds; recording compartmental pressures during this effort and again shortly after exercise ceases to determine whether an immediate return to baseline has occurred (LOE: E).28 Although there is no consensus regarding the best method for the measurement of upper extremity compartment pressure, there is also none concerning which values are to be considered diagnostic.31 It has been suggested that a resting pressure of greater than 15 mm Hg or a 5-minute postexercise pressure of greater than 25 mm Hg is pathologic (LOE: E).29 Others suggest that the period of greater than 15 minutes for the recovery of pressure to the baseline level after exercise is more indicative (LOE: E).32 They point out that resting baseline pressures are often quite variable and intensely technique dependent and that they therefore should not be used as diagnostic criteria. As with lower-extremity CECS, clinical factors are most important for diagnosis. However, objective studies do provide supportive data and thus should be used when appropriate (Boxes 46.2, 46.3, 46.4, and 46.5).

Box 46.3: Complications  Postprocedure bruising, swelling, and pain  Neurologic sequelae from nerve injury  Bleeding from damage to local vasculature

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11.

Box 46.4: Controversies  Timing of postexercise testing  Accurate diagnostic criteria  Dynamic versus static testing

12. 13.

14.

15.

Box 46.5: Risks and Benefits

16.

Risks

17.

   

18.

Infection Scarring at the site of the injection Damage to the surrounding neurovascular structures Reaction to the local anesthesia

19. 20. 21.

Benefits  Accurate diagnosis  Avoidance of an unnecessary surgical procedure

22.

23.

REFERENCES 1. 2. 3. 4.

5.

6.

7. 8. 9. 10.

Edwards PH, Wright ML, Hartman JF: A practical approach for the differential diagnosis of chronic leg pain in the athlete. Am J Sports Med 2005;33(8):1241-1249. Clanton TO, Solcher BW: Chronic leg pain in the athlete. Clin Sports Med 1994;13(4):743-759. Styf J: Diagnosis of exercise-induced pain in the anterior aspect of the lower leg. Am J Sports Med 1988;16(2):165-169. Touliopolous S, Hershman EB: Lower leg pain. Diagnosis and treatment of compartment syndromes and other pain syndromes of the leg. Sports Med 1999;27(3):193-204. Walker WC: Lower leg pain. In Lillegard WA, Butcher JD, Rucker KS (eds): Handbook of Sports Medicine: A Symptom-Oriented Approach, 2nd ed. Boston, ButterworthHeinemann, 1999, p 251. McDermott AG, Marble AE, Yabsley RH, et al: Monitoring dynamic anterior compartment pressures during exercise. A new technique using the STIC catheter. Am J Sports Med 1982;10(2):83-89. Glorioso JE, Wilckens JH: Exertional leg pain. In O’Connor FG, Wilder RP (eds): Textbook of Running Medicine. New York, McGraw-Hill, 2001, p 95. Turnipseed W, Detmer DE, Girdley F: Chronic compartment syndrome. An unusual cause for claudication. Ann Surg 1989;210(4):557-562. Blackman PG: A review of chronic exertional compartment syndrome in the lower leg. Med Sci Sports Exerc 2000;32(3 Suppl):S4-S10. Kiuru MJ, Mantysaari MJ, Pihlajamaki HK, et al: Evaluation of stress-related anterior lower leg pain with magnetic resonance imaging and intracompartmental pressure measurement. Mil Med 2003;168(1):48-52.

24.

25.

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29. 30.

31.

32.

Dammann GG, Albertson KS: Surgical considerations in the leg. In O’Connor FG, Sallis RE, Wilder RP, et al (eds): Sports Medicine: Just the Facts. New York, McGraw-Hill, 2005, p 373. Detmer DE, Sharpe K, Sufit RL, et al: Chronic compartment syndrome: diagnosis, management, and outcomes. Am J Sports Med 1985;13(3):162-170. Pedowitz RA, Hargens AR, Mubarak SJ, et al: Modified criteria for the objective diagnosis of chronic compartment syndrome of the leg. Am J Sports Med 1990;18(1):3540. Rorabeck CH, Bourne RB, Fowler PJ, et al: The role of tissue pressure measurement in diagnosing chronic anterior compartment syndrome. Am J Sports Med 1988;16(2):143-146. Wilder RP, Sethi S: Overuse injuries: tendinopathies, stress fractures, compartment syndrome, and shin splints. Clin Sports Med 2004;23(1):55-81. Awbrey BJ, Sienkiewicz PS, Mankin HJ: Chronic exercise-induced compartment pressure elevation measured with a miniaturized fluid pressure monitor. A laboratory and clinical study. Am J Sports Med 1988;16(6):610-615. Hutchinson M, Ireland M: Chronic exertional compartment syndrome—gauging pressure. Phys Sportsmed 1999;27;101. Edwards P, Myerson M: Exertional compartment syndrome of the leg: steps for expedient return to activity. Phys Sportsmed 1996;24;31-37. Hislop M, Tierney P, Murray P, et al: Chronic exertional compartment syndrome: the controversial "fifth" compartment of the leg. Am J Sports Med 2003;31(5):770-776. Garcia-Mata S, Hidalgo-Ovejero A, Martinez-Grande M: Chronic exertional compartment syndrome of the legs in adolescents. J Pediatr Orthop 2001;21(3):328-334. Padhiar N, King JB: Exercise induced leg pain-chronic compartment syndrome. Is the increase in intra-compartment pressure exercise specific? Br J Sports Med 1996;30(4):360-362. Styf J, Korner L, Suurkula M: Intramuscular pressure and muscle blood flow during exercise in chronic compartment syndrome. J Bone Joint Surg Br 1987;69(2):301305. Tzortziou V, Maffulli N, Padhiar N: Diagnosis and management of chronic exertional compartment syndrome (CECS) in the United Kingdom. Clin J Sport Med 2006;16(3):209-213. Eskelin MK, Lotjonen JM, Mantysaari MJ: Chronic exertional compartment syndrome: MR imaging at 0.1 T compared with tissue pressure measurement. Radiology 1998;206(2):333-337. van den Brand JG, Nelson T, Verleisdonk EJ, et al: The diagnostic value of intracompartmental pressure measurement, magnetic resonance imaging, and near-infrared spectroscopy in chronic exertional compartment syndrome: a prospective study in 50 patients. Am J Sports Med 2005;33(5):699-704. Mohler LR, Styf JR, Pedowitz RA, et al: Intramuscular deoxygenation during exercise in patients who have chronic anterior compartment syndrome of the leg. J Bone Joint Surg Am 1997;79(6):844-849. Owens S, Edwards P, Miles K, et al: Chronic compartment syndrome affecting the lower limb: MIBI perfusion imaging as an alternative to pressure monitoring: two case reports. Br J Sports Med 1999;33(1):49-51. Berlemann U, al-Momani Z, Hertel R: Exercise-induced compartment syndrome in the flexor-pronator muscle group. A case report and pressure measurements in volunteers. Am J Sports Med 1998;26(3):439-441. Hider SL, Hilton RC, Hutchinson C: Chronic exertional compartment syndrome as a cause of bilateral forearm pain. Arthritis Rheum. 2002;46(8):2245-2246. Goubier JN, Saillant G: Chronic compartment syndrome of the forearm in competitive motor cyclists: a report of two cases. Br J Sports Med 2003;37(5):452-453; discussion 453-454. Kumar PR, Jenkins JP, Hodgson SP: Bilateral chronic exertional compartment syndrome of the dorsal part of the forearm: the role of magnetic resonance imaging in diagnosis: a case report. J Bone Joint Surg Am 2003;85-A(8):1557-1559. Garcia Mata S, Hidalgo Ovejero A, Martinez Grande M: Bilateral, chronic exertional compartment syndrome of the forearm in two brothers. Clin J Sport Med 1999;9(2):91-99.

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Electrodiagnostic Testing Jimmy D. Bowen, MD, FAAPMR, CSCS

KEY POINTS

. . .

. .

A careful history and physical examination of the patient is not replaced but rather is complemented by electrodiagnostic testing. The electrodiagnostic evaluation is a continuation and an extension of the clinical investigation. Electrodiagnostic evaluation allows for the clinical use of nerves and the probing of muscles to localize lesions that are demonstrated by the weaknesses, sensory losses, and reflex changes of the physical examination. Electrodiagnostic evaluation helps to determine the type and chronology of an abnormality. Like the clinical examination, the electrodiagnostic evaluation is dependent on the evaluator.

INTRODUCTION ‘‘Since the measuring device has been constructed by the observer ð we have to remember that what we observe is not nature itself, but nature exposed to our method of questioning.’’ —Werner Karl Heisenberg1 A 16-year-old high school football strong safety reports to your office with his second stinger in the last month (Figure 47.1). Four weeks before the visit, he was making a chop tackle, hitting the running back with his right shoulder, when he noted that his neck bent laterally to the left. He had an immediate lancinating pain down his right arm, and he was unable to raise his arm. He became weak in that arm, and the athletic trainer held him out for 2 weeks, until his strength returned to normal. During his second game after returning, he dove in in front of a running back to make a tackle. His head hit the running back’s thigh, and his head and neck went into lateral flexion and extension to the right. He again experienced immediate lancinating pain and an inability to raise his arm. He reports to your office with improving aching right proximal arm pain. On clinical examination, he is weak in the external rotators of the shoulder, the deltoid, the biceps, the supinator, and the radial wrist extensors. He has no sensory deficit.

The above description is of a stinger or burner, which is a very common injury in football. In fact, it may have affected as many as 65% of college football players at one time or another.2 Much controversy exists regarding this pinch
stretch injury of the cervical C5-C6 nerve roots or of the more distal upper trunk brachial plexopathy. Is this player’s injury proximal at the nerve root level or more distal at the upper trunk? What is the prognosis for the return of strength and return to play? An electrodiagnostic examination (EDX) may be the definitive test for answering these questions for this athlete and his parents.3

THE ELECTRODIAGNOSTIC EXAMINATION EDX is not the ‘‘black box’’ from which the physiatrist or neurologist4 produces magical explanations for some mysterious neurologic or muscle ailment, although at times it may seem that way. EDX can be a great tool for evaluating athletes with neuromuscular problems. This chapter will provide the sports medicine specialist with a basis for requesting and understanding the EDX. To appropriately refer a patient for EDX, it is important to understand the when, why, and how to facilitate the most productive consultation for the patient. To understand the basic concepts associated with the EDX, it is important to understand the basics of nerve, muscle, and neuromuscular junction physiology as well as the anatomy and examination of the neurologic and musculoskeletal systems. From this information, an understanding of the application of the EDX and its components is achievable. In almost every article, chapter, or textbook about electrodiagnosis, two statements are consistently observed:  A careful history and physical examination of the patient is not replaced but rather is complemented by EDX.  The EDX is a continuation and an extension of the clinical investigation. The EDX allows for the clinical use of nerves and muscles to localize lesions that have been demonstrated by the weaknesses, sensory losses, and reflex changes found during a physical examination. It also can help with the determination of the type and chronology of an abnormality. Like the clinical examination, the EDX is dependent on the evaluator.3,4 If the evaluator is skilled and confident with localizing neuromuscular lesions on the clinical examination, is there any additional useful information gained by requesting EDX? If the

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What to know about neuroanatomy and physiology 569

Figure 47.1 Right brachioplexus superimposed on athlete with a history of a stinger.

evaluator is less skilled or confident with the examination, he or she may not be able to frame requests and questions in anatomic terms and therefore may not get the information desired. In these cases, it may be advisable for the patient to be referred to a physiatrist, a neurologist, or a nonphysician practitioner for a clinical evaluation before any request for EDX4,5 (Box 47.1).

Indications for electrodiagnostic testing Press and Young6 gave some useful generalizations for the indications for EDX: (1) to establish or confirm a clinical diagnosis; (2) to localize nerve lesions; (3) to determine the extent and chronicity of nerve injury; (4) to use the information obtained for anatomic study correlation; and (5) to provide information that will be useful when making decisions about return to play and prognosis, remembering that the best indication of return to play is the athlete’s functional ability in reproducible sport-specific activities.7

Box 47.1: The Electrodiagnostic Evaluation The electrodiagnostic evaluation should include the following:         

A history A physical examination Directed nerve conduction studies Complementary needle electrode examination A table of results A written summary of the results with evaluator interpretation A discussion of potential causes of the impairment A written direction for further evaluation The prognosis regarding any impairment recognized

Limitations of electrodiagnostic testing EDX does not replace a competent history and physical examination.3,8-10 If the mechanism of injury, the time course of the injury, the history of the athlete, and the physical examination are sensitive and specific when correlated to the present injury, then the diagnosis may be unequivocal and the EDX may be of little or no additional value. If the diagnosis is equivocal, however, EDX can substantially alter, confirm, and clarify it.11 Because of the changes that occur after an injury to the nervous system, the timing of the EDX is essential for providing the best information about the injury. Because of the changes that occur pathophysiologically after a nerve injury, it may become necessary to use serial studies to fully evaluate the degree and prognosis of the injury. In addition, there are some relative contraindications to EDX, including open wounds in the area being tested and a pending muscle biopsy. The use of pacemakers or defibrillators and patients with coagulopathy, lymphedema, or anasarca would pose relative contraindications to the use of EDX,12 although these patients would rarely present in as members of the athletic patient population.

WHAT TO KNOW ABOUT NEUROANATOMY AND PHYSIOLOGY In simplistic terms, the typical EDX investigates problems that are associated with the physiology and function of the peripheral nervous system.13 The nerves of the peripheral nervous system are essentially insulated bundles of wires that are bound together and insulated inside a cable that can transmit electricity in any direction that the cable runs. The sensory system of the peripheral nervous system receives an electrical impulse and transmits this electrical ‘‘message’’ to the central nervous system for modulation and interpretation. The motor system takes an impulse—action potential—from the central nervous system, directing it to the neuromuscular junction, where the message is transformed to an electrochemical transmission across the junction. Upon receipt at the muscle, the message is transmitted

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Axon

Myelin sheath Schwann cell cytoplasm Schwann cell nucleus Node of Ranvier

A

Unmyelinated axons Schwann cell nucleus Schwann cell cytoplasm

B Figure 47.2 Myelination. A, A myelinated axon demonstrating the circumferential wrapping of the myelin sheath insulating the nerve along its length (except for the node of Ranvier). There is one Schwann cell per internode.B, One Schwann cell may provide a modicum of myelination for multiple axons inunmyelinated nerves. (From Dumitru D, AmatoA, Zwarts M: Electrodiagnostic Medicine, 2nd ed.Philadelphia,Hanley & Belfus, 2002,p 15.)

through ionic changes, thus causing depolarization, propagation of the action potential, and eventual muscle action. Within each nerve, there may be sensory fibers (afferent), motor fibers (efferent), or both. Fibers (axons) differ with regard to their activity, size, and amount of insulation (myelin) (igure 47.2). The axons are analogous to the wires in our previous description. Nutrition for the axon and the removal of wastes are provided by movement within the axon cellular material (axoplasm), which is

known as axoplasmic flow. The nutrition center for a sensory nerve is the dorsal root ganglion, which is located at or distal to the neuroforamina of the spine. The nutrition center for the motor unit and motor nerve is in the ventral spinal cord at the alpha motor neuron. The larger the axon, the faster electrical transmission occurs. The myelin of the axon is maintained by Schwann cells. Myelin provides for the salutatory propagation of the electrical impulse at the nodes of Ranvier, significantly increasing the velocity of transmission of the electrical impulse. The EDX primarily tests the large myelinated axons that make up the nerves of the peripheral nervous system.

Types of nerve injury According to Seddon, nerve injuries can be divided into three classes: neuropraxia, axonotmesis, and neurotmesis13,14 (Table 47.1). Neuropraxia represents a failure of nerve conduction (usually reversible) that is caused by metabolic or microstructural abnormalities without disruption of the axon. It in essence represents an injury to the myelin. If it is severe, salutatory conduction is disrupted, and a conduction block occurs. If it is less than severe, a focal slowing of conduction may occur, as seen in focal nerve entrapments such as carpal tunnel syndrome. Axonotmesis represents an injury to the myelin and the axon with the preservation of the nerve supportive connective tissue (endoneurium), which results in axonal degeneration (Wallerian) distal to the injury. A common example is a stinger, which that may represent a fifth-level or sixth-level cervical radicular injury or a proximal upper trunk brachial plexus injury. Neurotmesis is the partial or complete transection of the nerve that causes discontinuity of the myelin and the axons proximally and distally and that leads to distal Wallerian degeneration of the nerve.

COMPONENTS OF THE ELECTRODIAGNOSTIC EXAMINATION The EDX should consist of a history, a physical examination, directed nerve conduction studies, complementary needle electrode examination, a table of results, a written summary of the results with evaluator interpretation, a discussion of the potential causes of the impairment, a written direction for further evaluation, and, finally, the prognosis regarding any impairment recognized. The integration of these components provides a meaningful diagnostic conclusion. This is what the physician is requesting and what the athlete or patient is purchasing. A solid understanding of the process helps the physician to better enlighten and educate the athlete regarding what to

Table 47.1

Nerve Pathophysiology and Classification

Type

Pathology

Electrodiagnostic Examination Changes

Recovery

Neuropraxia

Local myelin injury; primarily large fibers; axonal continuity; no Wallerian degeneration

Weeks to months

Axonotmesis

Disruption of axonalcontinuity with Wallerian degeneration; endoneurium may be intact

Neurotmesis

Disruption of entire nerve

Conduction velocity slowing across segment; distal latency prolonged across segment; loss of amplitude across segment; preservation of amplitude distal; needle examination normal Loss of amplitude proximal and distal; needle examination with spontaneous activity; needle examination with abnormal motor units No response proximal or distal; needle examination with spontaneous activity; needle exam without recruitable motor units

Months to years; axonal regeneration required for recovery; prognosis dependent on intact endoneurium Surgical modification of nerve ends required; prognosis guarded and dependent on the nature of the injury and local factors

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Principles of nerve conduction studies 571

expect during the evaluation. The evaluation is at worst painful and at best mildly uncomfortable, depending on the cooperation of the patient and the skill of the electrodiagnostician.15 The testing is also relatively expensive in terms of time and money. Therefore, getting the most out of the examination is important. The EDX is divided into two complementary portions: the nerve conduction studies and the electromyography. The nerve conduction studies involve exciting the nerves electrically with externally applied safe pulses over various points along a nerve and measuring the obtained responses. This type of testing evaluates the large myelinated axons found within a nerve. The electromyography evaluation represents an electrophysiologic assessment of the motor unit.16 Electromyography involves recording the electrical activity of a muscle at rest and during activity by inserting needle electrodes into multiple areas of a muscle and recording the electrical activity of a small number of fibers of a single motor unit with each pass or needle advancement. A motor unit represents the anatomic unit of the anterior horn cell (alpha motor neuron), its axon, the neuromuscular junction, and all of the muscle fibers innervated by the axon (Figure 47.3). The motor unit is influenced by inputs from the brain and the spinal cord (upper motor neuron) as well as afferent inputs from the periphery, such as position sensors in joints, Golgi tendon organs, and muscle spindles. The result is the ability of the muscles to have the various contraction patterns that are necessary for functional activity that is under the control of the central nervous system.16

PRINCIPLES OF NERVE CONDUCTION STUDIES Nerve conduction studies evaluate the fastest 20% of the fibers, and the aim is to investigate and document focal abnormalities in the length of a mixed, motor, or sensory nerve. During this evaluation, the following questions are given attention:  Is the fastest conduction velocity normal?  Is the summated action potential response measured under the recording electrodes of normal size and shape?  Does the response seen alter in size, shape, or duration when evaluating the response using different stimulation points?

laboratory determinations.12 Clinically it is useful to study the motor and sensory functions of the peripheral nerves separately. However, most peripheral nerves are mixed nerves. Fortunately, at their distal ends, all mixed nerves form discrete motor and sensory branches, which can be studied separately.12-14,17

Specific techniques Motor conduction studies evaluate the motor nerve or the motor portion of a compound nerve by electrically stimulating a proximal portion of the nerve and recording a summated voltage response from the stimulated muscle fiber action potentials through the use of recording electrodes placed over the belly (motor end point) of a specific muscle that is innervated by the nerve. The voltage response recorded is known as a compound muscle action potential (CMAP). This CMAP is the digital summation of near synchronous muscle action potentials recorded from a common area of muscle. This summated action potential is achieved by sequentially elevating the voltage or current used to stimulate a nerve to a supramaximal level such that all possible stimulation is achieved as demonstrated by no change in the CMAP (i.e., it does not get any larger). The criteria measured from a CMAP are the latency, the amplitude, and the duration (Figure 47.4). The latency represents the onset of the summated response after the stimulus. The amplitude is measured by the change from the baseline to the peak of the action potential. The duration represents the time from the action potential’s deflection from the baseline until its return to the baseline. The stimulus is usually done at a distal and proximal point along a nerve. The more proximal stimulus produces a similarlooking action potential (amplitude and shape) if the nerve is normal, except the latency should be greater from the proximal point. By measuring the distance between the two stimulation points, the conduction velocity of the fastest axons can be determined. The technique is usually orthodromic, which means that the stimulus and the recording are in the normal direction of propagation of a motor response. Sensory conduction studies demonstrate a sensory nerve action potential from supramaximally stimulating sensory fibers and

Normal values for the nerve conduction studies are age matched and temperature controlled from published studies or specific

Myelin sheath

Type II fiber

Type I fiber

Amplitude

Type II motor neuron

* *

*

Phases Turns

Baseline

Satellite

*

Initial Rise portion time

Type I motor neuron

*

*Terminal portion

Spike duration Total duration Axon

Figure 47.3 Two motor units (type I and type II fibers). Note that the fibers from one motor unit are interspersed with those from another motor unit. (From Dumitru D, Amato A, Zwarts M: Electrodiagnostic Medicine, 2nd ed. Philadelphia, Hanley & Belfus, 2002, p 267.)

Figure 47.4 Motor unit action potential morphology. A schematic representation of a single motor unit action potential with the various subcomponents delineated. (From Dumitru D, Amato A, Zwarts M: Electrodiagnostic Medicine, 2nd ed. Philadelphia, Hanley & Belfus, 2002, p 43.)

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Electrodiagnostic testing

recording the results more distally along a nerve’s path. This may be done orthodromically or antidromically. The term antidromically refers to the stimulus being proximal and the recording distal for a sensory nerve, which is the opposite of the normal sensory propagation. It has to be remembered that, when a nerve is stimulated through the stimulating electrodes, the propagation of electricity is in both directions along the nerve path.13 Again, the amplitude, latency, duration, and conduction velocity can be observed, recorded, calculated, and compared with known normals. The responses of F waves are used to evaluate the most proximal portions of a motor nerve axon, which cannot be accessed in a normal motor nerve conduction studies. When the motor nerve action is stimulated, the propagation is in both directions, thus giving rise to the CMAP distally and causing the alpha motor neuron and the axon hillock to be depolarized proximally. The proximal stimulus propagation gives rise to different axon populations backfiring and sending a variable late response that is recorded at the same distal electrodes that measured the CMAP. This late response is most reliable if 10 to 20 firings are recorded and the minimal reproducible latency is measured.12,13 Because of the great length of transmission, a small focal change may not be appreciated. However, in patients with conditions such as Guillain
Barre´ syndrome (acute inflammatory demyelinating polyradicular neuropathy), in whom the proximal portions of the nerve are affected by demyelination, the F-wave response may be the testing of choice.

Nerve conduction study results Nerve conduction studies provide pathophysiologic information that evaluates the length of a nerve. The pathology of a peripheral nerve affects the axons or myelin either exclusively, predominately, or in combination. During the evaluation of the nerve action potentials of the motor or sensory nerves if there is axon loss, a reduction in the CMAP or sensory nerve action potential amplitude may be seen when stimulating across and distal to the injury site. For the CMAP, this represents fewer functioning motor axons connected to muscle fibers. The latency and conduction velocity remain relatively normal unless the largest axons are affected. The timing of testing becomes important after an axonal injury, because the distal portions of the axon will be normal for days until Wallerian degeneration occurs. Demyelination causing a slowing or blocking of conduction will prolong the latency of the action potential and slow the conduction velocity when stimulation occurs across the demyelination site. The amplitude may also be affected when stimulation occurs across the site, but it may be normal distal to the demyelination site.9 Stimulation proximal or distal to an area of neurotmesis demonstrates no action potential after Wallerian degeneration occurs.

Electromyography (needle examination) The needle examination makes use of a needle electrode that is inserted into a muscle to evaluate the lower motor neuron pathway.13,18 However, it does not evaluate the sensory pathway. Conventional needles record from a radius of about 1 mm; within this radius may be 100 muscle fibers. A motor unit may have hundreds of motor fibers associated with it throughout a muscle. Within the 1 mm, the needle may ‘‘see’’ four to six fibers of a single motor unit. An electromyographer becomes skilled at interpreting the appearance of the muscle activity as well as the sound of the activity. The muscle is evaluated both at rest, when it is normally silent, and during voluntary muscle activity. If there is spontaneous activity in a resting muscle, it may represent a lesion or a disease process that affects the axons of the motor unit or the muscle itself.

The types of spontaneous activity are fibrillation potentials, positive sharp waves, fasciculations, complex repetitive discharges, and myotonic and myokymic discharges. With the activation of the muscle, motor units can be analyzed to evaluate and distinguish between neuropathic and myopathic processes. The motor units are evaluated for size (amplitude and duration), complexity (phases), and recruitment. The patient is asked to minimally activate a muscle, which should result in a few recorded motor units. The early recruited waveforms are usually small and have a frequency of 6 to 10 Hz, which is represented by consistent spikes or discharges. As the activity increases, other motor units are recruited. Spontaneous activity normally begins to occur in muscle that has been denervated. Within 2 to 3 weeks after the activity of the axon is reduced or eliminated, the muscle fibers associated with the motor unit become supersensitive, producing acetylcholine receptors over the whole muscle fiber and not just the neuromuscular junction. The effect is to render the muscle fiber supersensitive to acetylcholine, which results in spontaneous discharges. It is detected with the electromyography electrode as a muscle fiber fibrillation or positive sharp wave. These are graded by the number of different fibrillations (the density of the fibers affected) and by the persistence throughout the muscle from a scale of 0 to 4+.19 Complex repetitive discharges represent the ephaptic transmission (time-linked cross talk) of a stereotyped group of single-fiber potentials that begin and end abruptly and that have a constant frequency between 1 and 100 Hz. They occur predominately in neuropathic disease. Fasciculations arise from the discharge of a single motor unit occurring at irregular intervals.20 They may be visible (if superficial) at the skin. The fasciculations may resemble a voluntary muscle potential, except they are not under voluntary control. Fasciculations may be benign or associated with motor neuron disease, radiculopathy, and neuropathy. Myotonic discharges are seen with myotonic dystrophies and channelopathies. They vary in frequency and size, but they characteristically sound like a dive bomber or a two-cycle motorcycle. Myokymia is a regular or irregular discharge of groups of motor units that produce a ‘‘flickering’’ in muscle and that may be seen in the face of individuals with demyelinating disease such as multiple sclerosis or tumors of the brain stem. The pattern and recruitment of voluntary muscle action potentials helps distinguish myopathy from neuropathy and acute neuropathy from chronic neuropathy. Reduced recruitment is usually distinguished by the presence of large motor units firing at high rates before the next motor unit is recruited. This represents the presence of motor units that have reinnervated through the branching of nerves, which usually represents neurogenic injury. Early recruitment represents small fibers that are typically noted at a low frequency before the next fiber is recruited, and, with minimal voluntary activity, many fibers are recruited. In effect, small ineffective fibers require more fibers firing earlier to generate force. This usually represents a primary muscle disease. By isolating a single motor unit on a display, amplitude, duration, and number of phases can be measured. With primary muscle disease, the motor unit potentials will be small and of short duration. With an axonotmetic injury to the nerve, there is Wallerian degeneration. Intact axons will sprout collaterals, thus reinnervating areas of muscle that had been denervated. Early during reinnervation, the motor unit potentials may show increased complexity and increased duration as a result of the difference in axonal maturity. As the collateral sprouts mature and become more organized, the complexity (or phases) is reduced and the motor unit potentials will become large in amplitude and duration, thus demonstrating the increased amount of muscle fibers that are activated through the collateral sprouting of one axon. By combining the presence of spontaneous activity and the appearance of motor unit potentials, acute, subacute, and chronic denervation and reinnervation may be distinguished.

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7.

CONCLUSION The use of an EDX as an adjunct for the care of an athlete may produce a reliable tool for evaluating pathology within the neuromuscular system. To get the most out of an EDX study, it is important to realize the examiner-dependent nature of the clinical examination, to provide referral-directed questions, and to develop effective communication with the patient about the prognosis. Understanding the examination of the neuromuscular system, the pathophysiology of the nerve injury or the neuromuscular disease, and the components of a requested EDX will make a physician a more complete sports medicine specialist.

8. 9. 10. 11.

12. 13. 14.

REFERENCES

15. 16.

1. Heisenberg WK: Physics and Philosophy. Copenhagen, George Allen and Unwin, 1958. 2. Torg JS: Cervical spine injuries in the adult. In DeLee JC, Drez D Jr, Miller MD (eds): DeLee & Drez’s Orthopaedic Sports Medicine: Principles and Practice, 2nd ed. Philadelphia, WB Saunders, 2003, pp 797-799. 3. Fuller G: How to get the most out of nerve conduction studies and electromyography. J Neurol Neurosurg Psychiatry 2005;76(suppl II):ii41-ii46. 4. Dillingham TR, Pezzin LE, Rice JB: Electrodiagnostic services in the United States. Muscle Nerve 2004;29(1):198-204. 5. Spielholz NI: Electrodiagnostic services in the United States. Muscle Nerve 2004;30(4):510-511. 6. Press JM, Young JL : Electrodiagnostic evaluation of spine problems. In Gonzalez EG, Materson RS (eds): The Nonsurgical Management of Acute Low Back Pain. New York, Demos Vermande, 1997, pp 191.

17. 18. 19. 20.

Feinberg JH: Burners and stingers. Phys Med Rehabil Clin North Am 2000;11(4): 771-783. Hogan CJ, Degnan GC: An orthopedic surgeon’s guide to interpreting electromyography. Am J Orthop Oct 2001;30(10):745-750. Dillingham TR: Electrodiagnostic approach to patients with suspected radiculopathy. Phys Med Rehabil Clin N Am 2002;13(3):567-588. Dillingham TR: Electrodiagnostic approach to patients with weakness. Phys Med Rehabil Clin N Am 2003;14(2):163-184. Haig AJ, Tzeng H-M, Lebreck DM: The value of electrodiagnostic consultation for the patient with upper extremity nerve complaints: a prospective comparison with the history and physical examination. Arch Phys Med Rehabil 1999;80:1273-1281. Mallik A, Weir AI: Nerve conduction studies: essentials and pitfalls in practice. J Neurol Neurosurg Psychiatry 2005;76(suppl II):ii23-ii31. Dumitru D, Amato AA, Zwarts MJ: Electrodiagnostic Medicine, 2nd ed. Philadelphia, Hanley and Belfus, 2002. Akunthota V, Tobey J: Electrodiagnostic testing. In O’Connor F, Sallis R, Wilder R, St. Pierre P, (eds): Sports Medicine: Just the Facts. McGraw-Hill, 2004, pp 111-117. Strommen JA, Daube JR: Determinants of pain in needle electromyography. Clin Neurophysiol 2001;112(8):1414-1418. Barkhaus PE, Nandedkar SD: EMG evaluation of the motor unit: the electrophysiologic biopsy. http://emedicine.com/neuro/topic610.htm. Accessed January 2005. Robinson LR, Stolp-Smith KA: Paresthesias and focal weakness: the diagnosis of nerve entrapment. In AAEM Annual Assembly. Vancouver, BC, Johnson Printing, 1999. Mills KR: The basics of electromyography. J Neurol Neurosurg Psychiatry 2005;76(suppl II):ii32-ii35. Kraft GH: Fibrillation potential amplitude and muscle atrophy following peripheral nerve injury. Muscle Nerve 1990;13:814-821. Layzer RB: The origin of muscle fasciculations and cramps. Muscle Nerve 1994;17(4):1243-1249.

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Therapeutic and Diagnostic Injections and Aspirations Thomas M. Howard, MD, and LCDR Leslie H. Rassner, MD

KEY POINTS

. . . . .

Injections and aspirations can be valuable diagnostic and therapeutic tools in the management of musculoskeletal complaints. There is mixed evidence to support and refute the value and accuracy of various musculoskeletal injections. Before being given any injection, the patient must give informed consent regarding the potential benefits, risks, and alternatives to the procedure. The provider should have adequate familiarity with the anatomic landmarks and procedure technique before attempting a musculoskeletal injection. Pertinent radiographs should be ordered and reviewed before performing a musculoskeletal injection.

INTRODUCTION Musculoskeletal injections can be very satisfying procedures for both providers and patients. Injections may be diagnostic, therapeutic, or both. The management of musculoskeletal injury should always begin with a pathoanatomic diagnosis. The next steps in treating injury include controlling inflammation, promoting healing, increasing fitness, controlling abuse, and returning to activity.1 Since the 1950s, intra-articular, peritendinous, and bursal steroid injections have been used for a variety of musculoskeletal disorders, targeting their anti-inflammatory effects to specific areas.2 The decreased pain associated with a successful injection can allow the completion of rehabilitative therapy, which promotes healing, increases fitness, and ultimately results in the successful return to activity.

The views expressed in this chapter are those of the authors and do not necessarily reflect the official policy or position of the Department of the Navy, the Department of Defense, or the US Government.

Despite the ubiquitous use of steroid injections, the perception of therapeutic efficacy and safety varies widely and among patients and practitioners.3 The original publications of the rheumatologic pioneers of steroid injections relied on retrospective, uncontrolled, nonblinded case series of their clinical experience.4 As experience and research designs progressed, questions of side effects, cartilage damage, and risks versus benefits arose. Studies have contradicted original reports of the efficacy of many common musculoskeletal injections.3,5,6 Additionally, the literature continues to vary with regard to medications used, injection techniques, whether steroid placement is confirmed objectively, outcome measures, and the length of follow up, thus making meta-analysis difficult.5,7,8 During the past decade, the accuracy of the techniques themselves has been called into question by radiographic surveillance for correct injection placement, with experienced providers rating between 37% and 70% accuracy for intra-articular injections.9,10 Simultaneously, studies are correlating pain relief with the accuracy of the injection placement.9 This brings into question the significance of previous, well-designed, prospective, controlled, and blinded studies that lacked radiographic confirmation of medication placement.6 In summation, concerns about injection accuracy and efficacy highlight the importance of proper training in injection techniques and the thorough counseling of each patient with regard to the risks, benefits, and alternatives of these procedures.

INDICATIONS Musculoskeletal aspirations and injections can be both diagnostic and therapeutic. Aspirations allow for the diagnostic evaluation of synovial fluid using gross appearance and laboratory analysis (Table 48.1). Joint aspirations of tense effusions are also therapeutic, relieving pain and returning a functional range of motion. Steroid injections of the joints and soft tissue can reduce the pain of various rheumatologic diseases and musculoskeletal injuries and allow for the completion of physical therapy.6 The shortterm benefit of intra-articular corticosteroids for the treatment of knee osteoarthritis is well established (LOE: B).7 For the treatment of rheumatoid arthritis, intra-articular triamcinolone has been shown to relieve pain in the injected joint for at least 6 months in 50% of patients (LOE: B).11,12 In a study of patients

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Table 48.1

Synovial Fluid Analysis

Classification (with Examples)

Appearance

White Blood Cells per
L

Polymorphonuclear Leukocytes (%)

Crystals

Normal

Clear to straw-colored