Sports Medicine: Study Guide and Review for Boards [2 ed.] 9781620700884, 9781617052644

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Sports Medicine

Sports Medicine Study Guide and Review for Boards Second Edition Mark A. Harrast, MD Clinical Professor, Departments of Rehabilitation Medicine, Orthopaedics and Sports Medicine Medical Director, Sports Medicine Center at Husky Stadium University of Washington Seattle, Washington

Jonathan T. Finnoff, DO, FACSM Professor, Department of Physical Medicine and Rehabilitation Mayo Clinic Rochester, Minnesota Medical Director, Sports Medicine Center Mayo Clinic Minneapolis, Minnesota

Editors

NEW YORK

Visit our website at www.demosmedical.com ISBN: 9781620700884 e-book ISBN: 9781617052644 Acquisitions Editor: Beth Barry Compositor: Exeter Premedia Services Private Ltd. Copyright © 2017 Springer Publishing Company. Demos Medical Publishing is an imprint of Springer Publishing Company, LLC. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of the publisher. Medicine is an ever-changing science. Research and clinical experience are continually expanding our knowledge, in particular our understanding of proper treatment and drug therapy. The authors, editors, and publisher have made every effort to ensure that all information in this book is in accordance with the state of knowledge at the time of production of the book. Nevertheless, the authors, editors, and publisher are not responsible for errors or omissions or for any consequences from application of the information in this book and make no warranty, expressed or implied, with respect to the contents of the publication. Every reader should examine carefully the package inserts accompanying each drug and should carefully check whether the dosage schedules mentioned therein or the contraindications stated by the manufacturer differ from the statements made in this book. Such examination is particularly important with drugs that are either rarely used or have been newly released on the market. Library of Congress Cataloging-in-Publication Data Names: Harrast, Mark A., editor. | Finnoff, Jonathan T., editor. Title: Sports medicine : study guide and review for boards / Mark A. Harrast, Jonathan T. Finnoff, editors. Other titles: Sports medicine (Harrast) Description: Second edition. | New York, NY : Demos Medical Publishing, [2016] | Includes bibliographical references and index. Identifiers: LCCN 2016020836| ISBN 9781620700884 | ISBN 9781617052644 (e-book) Subjects: | MESH: Athletic Injuries—diagnosis | Athletic Injuries—therapy | Athletic Injuries—prevention & control | Outlines Classification: LCC RD97 | NLM QT 18.2 | DDC 617.1/027—dc23 LC record available at https://lccn.loc.gov/2016020836

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Contents Contributors Preface Share Sports Medicine: Study Guide and Review for Boards, Second Edition

ix xv

I. General Topics

II.

1.

Overview of the Examination Mark A. Harrast and Jonathan T. Finnoff

3

2.

The Role of the Team Physician Katherine Louise Dec and Larry Leone Benson

5

3.

Exercise Physiology James C. Presley and Jonathan T. Finnoff

10

4.

Sports Biomechanics Erek W. Latzka and Mark A. Harrast

24

5.

Pharmacology Jeffrey L. Tanji

41

6.

Principles of Musculoskeletal Rehabilitation Sathish Rajasekaran and Mederic M. Hall

57

7.

Sports Medicine Procedures Michael Henrie, Steven Makovitch, and Stuart E. Willick

64

Health Promotion and Injury Prevention 8.

Preparticipation Examination D. Harrison Youmans and Tracy R. Ray

77

9.

Strength and Conditioning Techniques Jacob L. Sellon and Jonathan T. Finnoff

103

10.

Nutrition Susan M. Kleiner

121

11.

Exercise Prescription, Exercise Testing, and Exercise Screening Jerome T. Nichols and Kenneth R. Mautner

133

12.

Event Administration John C. Cianca

147

13.

Braces and Protective Equipment Kelli M. Kyle and Jonathan T. Finnoff

154

v

vi

CONTENTS

III. Diagnosis and Treatment of Sports Injuries and Conditions Musculoskeletal Injuries and Conditions 14.

General Concepts of Muscle and Tendon Injuries and Conditions Alfred C. Gellhorn

161

15.

Bone Injuries and Conditions Karie N. Zach and Anne Z. Hoch

171

16.

Cartilage and Joint Injuries and Conditions Brandee Waite

180

17.

Fracture and Dislocation Management Ashley M. TeKippe, Christopher A. Gee, and Stuart E. Willick

194

18.

Cervical Spine Injuries and Conditions Abby Cheng and Monica E. Rho

204

19.

Emergency Evaluation and Management of Cervical Spine Injuries Leah G. Concannon, Anthony DiGirolamo, and Mark A. Harrast

224

20.

Lumbar Spine Injuries and Conditions Rebecca A. Dutton, Byron Schneider, and David J. Kennedy

232

21.

Shoulder Injuries and Conditions Sathish Rajasekaran and Mederic M. Hall

251

22.

Elbow and Forearm Injuries and Conditions Steve J. Wisniewski

267

23.

Hand and Wrist Injuries and Conditions Joseph Michael Ihm

273

24.

Pelvis, Hip, and Thigh Injuries and Conditions Heidi Prather and Devyani Hunt

288

25.

Knee Injuries and Conditions Ashwin N. Babu and Cheri A. Blauwet

301

26.

Lower Leg Injuries and Conditions T. Joseph Malbrough and John P. Metzler

315

27. Ankle and Foot Injuries and Conditions Gerard Malanga, Ricardo Vasquez-Duarte, Michael Esrick, and Usker Naqvi 28.

Pediatric Musculoskeletal Injuries and Conditions Andrew John Maxwell Gregory

322 332

Medical, Neurological, and Psychological Conditions 29.

Environmental Illness Cara C. Prideaux and Jonathan T. Finnoff

342

30.

Exercise-Associated Collapse Daniel V. Colonno and Mark A. Harrast

351

31.

Head, Ears, Eyes, Nose, and Throat Injuries and Conditions Enoch H. Chang and Michael P. Schaefer

358

32.

Chest Trauma: Thoracic Injuries and Conditions Kristi Colbenson

368

CONTENTS

33.

Sports Cardiology Irfan M. Asif and Jonathan A. Drezner

379

34.

Sports Pulmonology Darlene R. Nelson, Brian P. Williams, and Paul D. Scanlon

398

35.

Sports Gastroenterology and Abdominal Injuries and Conditions Ashwin Rao

408

36.

Sports Nephrology and Urology Cortie J. Rolison IV, Joseph L. Mitchell, and M. Kyle Smoot

420

37.

Sports Dermatology Darryl E. Barnes and Russell A. Bergum

429

38.

Sports Hematology Irfan M. Asif and Kimberly G. Harmon

436

39.

Sports Endocrinology Darryl E. Barnes and Russell A. Bergum

445

40.

Sports Obstetrics and Gynecology Darryl E. Barnes and Russell A. Bergum

451

41.

Sports Infectious Disease David M. Siebert and John W. O’Kane Jr.

458

42. Sports Allergy and Immunology Robert J. Dimeff and Rathna Nuti

468

43. Sports Rheumatology Andrew L. Concoff

478

44.

Sports Neurology Jeffrey S. Kutcher and Sean C. Rose

486

45.

Sports Concussion and Traumatic Brain Injury Scott R. Laker and Jessica Pruente

493

46.

Neurovascular Injuries of the Upper and Lower Limbs Jason Friedrich and Venu Akuthota

501

47.

Sport Psychology Nicole Detling

519

Special Populations 48.

The Master Athlete Christopher J. Visco and Marni G. Hillinger

525

49.

The Pediatric Athlete Holly J. Benjamin and David J. Jewison

532

50.

The Female Athlete Karie N. Zach and Anne Z. Hoch

538

51. The Adaptive Athlete Lauren Rudolph and Stuart E. Willick

546

Hot Topics in Sports Medicine 52.

Regenerative Medicine in Sports Medicine Gerard Malanga and Reina Nakamura

552

vii

viii

CONTENTS

53.

Sports Ultrasound Mederic M. Hall

557

Practice Test

563

Index

613

Contributors

Venu Akuthota, MD Professor, Department of Physical Medicine and Rehabilitation, University of Colorado School of Medicine, Aurora, Colorado Irfan M. Asif, MD Assistant Professor, Fellowship Director, Department of Sports Medicine, University of Tennessee Graduate School of Medicine, Knoxville, Tennessee Ashwin N. Babu, MD Physical Medicine and Rehabilitation, Harvard Medical School, Spaulding Rehabilitation Hospital/Mass General Sports Medicine Center, Charlestown, Massachusetts Darryl E. Barnes, MD Consultant/Assistant Professor, Department of Orthopedics and Sports Medicine, Mayo Clinic Health System, Austin, Minnesota Holly J. Benjamin, MD, FAAP, FACSM Professor of Pediatrics, Orthopedic Surgery, and Rehabilitation Medicine, Director of Primary Care Sports Medicine, University of Chicago, Chicago, Illinois Larry Leone Benson, MD Clinical Director, Advanced Orthopedics/Ortho on Call, Midlothian, Virginia Russell A. Bergum, DO Physician, Orthopedics – Sports Medicine, Department of Orthopedics, Mayo Clinic Health System, Albert Lea, Minnesota Cheri A. Blauwet, MD Instructor, Physical Medicine and Rehabilitation, Harvard Medical School, Spaulding Rehabilitation Hospital/Brigham and Women’s Hospital, Charlestown, Massachusetts Enoch H. Chang, MD Department of Sports Medicine, Cleveland Clinic, Cleveland, Ohio Abby Cheng, MD Physician, Department of Physical Medicine and Rehabilitation, Rehabilitation Institute of Chicago/Northwestern University, Chicago, Illinois John C. Cianca, MD Adjunct Associate Professor of Physical Medicine and Rehabilitation, Baylor College of Medicine, Houston, Texas Kristi Colbenson, MD Assistant Program Director; Senior Associate Consultant, Departments of Emergency Medicine and Sports Medicine, Mayo Clinic, Rochester, Minnesota Daniel V. Colonno, MD Department of Neurosurgery, Kaiser Permanente, Denver, Colorado Leah G. Concannon, MD Clinical Assistant Professor, Department of Rehabilitation Medicine, University of Washington, Seattle, Washington

ix

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CONTRIBUTORS

Andrew L. Concoff, MD Medical Director, Outpatient Musculoskeletal Rehabilitation, Orthopedics and Sports Medicine, St. Jude Heritage Medical Group, Fullerton, California; Adjunct Clinical Professor, Division of Sports Medicine, Department of Family Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California Katherine Louise Dec, MD Professor, Sports Medicine Director, Department of Physical Medicine and Rehabilitation and Department of Orthopaedic Surgery, Virginia Commonwealth University, Richmond, Virginia Nicole Detling, PhD, CC-AASP Assistant Professor (Lecturer), Department of Health, Kinesiology, and Recreation, University of Utah, Salt Lake City, Utah Anthony DiGirolamo, DO Department of Rehabilitation Medicine, University of Washington, Seattle, Washington Robert J. Dimeff, MD Professor, Department of Orthopedic Surgery, Pediatrics, and Family and Community Medicine; Medical Director of Sports Medicine, University of Texas Southwestern Medical Center, Dallas, Texas Jonathan A. Drezner, MD Professor, Department of Family Medicine; Director, Sports Cardiology Center, University of Washington, Seattle, Washington Rebecca A. Dutton, MD Division of Physical Medicine and Rehabilitation, Department of Orthopaedic Surgery, Stanford University, Redwood City, California Michael Esrick, MD Physician, Combined Internal Medicine and Pediatrics, Rutgers–New Jersey Medical School, Newark, New Jersey Jonathan T. Finnoff, DO, FACSM Professor, Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, Minnesota; Medical Director, Sports Medicine Center, Mayo Clinic, Minneapolis, Minnesota Jason Friedrich, MD Assistant Professor, Department of Physical Medicine and Rehabilitation, University of Colorado School of Medicine, Aurora, Colorado Christopher A. Gee, MD Associate Professor, Division of Emergency Medicine, University of Utah, Salt Lake City, Utah Alfred C. Gellhorn, MD Medical Director, Sports Rehabilitation, Assistant Professor, Division of Rehabilitation Medicine, Weill Cornell Medical College, New York, New York Andrew John Maxwell Gregory, MD, FAAP, FACSM Associate Professor, Department of Orthopedics, Neurosurgery and Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee Mederic M. Hall, MD Clinical Associate Professor, Department of Orthopaedics and Rehabilitation, University of Iowa Sports Medicine; Department of Radiology, University of Iowa Hospitals and Clinics, Iowa City, Iowa Kimberly G. Harmon, MD Clinical Professor, University of Washington School of Medicine, Seattle, Washington Mark A. Harrast, MD Clinical Professor, Departments of Rehabilitation Medicine, Orthopaedics and Sports Medicine; Medical Director, Sports Medicine Center at Husky Stadium, University of Washington, Seattle, Washington

CONTRIBUTORS

Michael Henrie, DO Clinical Assistant Professor, Division of Physical Medicine and Rehabilitation, University of Utah, University of Utah Orthopaedic Center, Salt Lake City, Utah Marni G. Hillinger, MD Assistant Professor, Department of Physical Medicine and Rehabilitation; Director of Education, Osher Center for Integrative Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee Anne Z. Hoch, DO, FACSM Professor, Sports Medicine/Women’s Health, Department of Orthopaedic Surgery, Medical College of Wisconsin, Milwaukee, Wisconsin Devyani Hunt, MD Associate Professor, Division of Physical Medicine and Rehabilitation, Department of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, Missouri Joseph Michael Ihm, MD Attending Physician, Department of Physical Medicine and Rehabilitation, Rehabilitation Institute of Chicago; Associate Professor, Department of Physical Medicine and Rehabilitation, Northwestern University, Feinberg School of Medicine, Chicago, Illinois David J. Jewison, MD, MAT Assistant Professor and Team Physician, Department of Orthopaedic Surgery, University of Minnesota, Minneapolis, Minnesota David J. Kennedy, MD Clinical Associate Professor, Division of Physical Medicine and Rehabilitation, Department of Orthopaedic Surgery, Stanford University, Redwood City, California Susan M. Kleiner, PhD, RD, FACN, CNS, FISSN Owner, High Performance Nutrition, LLC, Mercer Island, Washington Jeffrey S. Kutcher, MD President, The Sports Neurology Clinic, Executive Director, Institute for Sports Neurology, Ann Arbor, Michigan Kelli M. Kyle, MS, PA-C, ATC Physician Assistant, Department of Orthopedic Surgery, Mayo Clinic Health System, Austin, Minnesota Scott R. Laker, MD Assistant Professor, Department of Physical Medicine and Rehabilitation, University of Colorado School of Medicine, Aurora, Colorado; Medical Director, Lone Tree Health Center, Denver, Colorado Erek W. Latzka, MD Department of Rehabilitation Medicine, University of Washington, Seattle, Washington Steven Makovitch, DO Visiting Instructor, Division of Physical Medicine and Rehabilitation, University of Utah, University of Utah Orthopaedic Center, Salt Lake City, Utah Gerard Malanga, MD Professor, Department of Physical Medicine and Rehabilitation, Rutgers–New Jersey Medical School, Newark, New Jersey; Founding Partner, New Jersey Sports Medicine and New Jersey Regenerative Institute, Cedar Knolls, New Jersey T. Joseph Malbrough, MD, MA Division of Physical Medicine and Rehabilitation, Department of Neurology, Washington University School of Medicine, St. Louis, Missouri Kenneth R. Mautner, MD Director, Primary Care Sports Medicine and Program Director Primary Care Sports Medicine Fellowship, Associate Professor of Rehabilitation Medicine, Orthopaedics, and Sports Medicine, Emory University, Emory Sports Medicine Center, Atlanta, Georgia

xi

xii

CONTRIBUTORS

John P. Metzler, MD Associate Professor of Orthopedic Surgery and Neurology, Department of Orthopedic Surgery, Washington University School of Medicine, St. Louis, Missouri Joseph L. Mitchell, MD Primary Care Sports Medicine Fellowship, UK Healthcare, Lexington, Kentucky Reina Nakamura, DO Department of Physical Medicine and Rehabilitation, Rutgers–New Jersey Medical School, Newark, New Jersey Usker Naqvi, MD, MS Department of Physical Medicine and Rehabilitation, University of Miami/ Jackson Health System, Miami, Florida Darlene R. Nelson, MD Assistant Professor of Medicine, Division of Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, Minnesota Jerome T. Nichols, MD, FAAPMR, CAQSM Department of Orthopedic Surgery and Sports Medicine, Northeast Georgia Physicians Group, Braselton, Georgia Rathna Nuti, MD Department of Family and Community Medicine, University of Texas Southwestern Medical Center, Dallas, Texas John W. O’Kane Jr., MD Professor, Departments of Family Medicine and Orthopaedics and Sports Medicine, University of Washington, Seattle, Washington Heidi Prather, DO Professor, Vice Chair, Department of Orthopaedic Surgery, Division Chief, Physical Medicine and Rehabilitation, Washington University School of Medicine, St. Louis, Missouri James C. Presley, MD Physician, Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, Minnesota Cara C. Prideaux, MD Assistant Professor, Physical Medicine and Rehabilitation/Sports Medicine, Mayo Clinic, Rochester, Minnesota Jessica Pruente, MD Department of Physical Medicine and Rehabilitation, University of Colorado School of Medicine, Aurora, Colorado Sathish Rajasekaran, MD, FRCPC Physiatrist, Sports Medicine, Kelowna Bone and Joint Health, Kelowna, British Columbia, Canada; Clinical Assistant Professor, Physical Medicine and Rehabilitation, University of British Columbia, Vancouver, British Columbia, Canada Ashwin Rao, MD Associate Professor, Department of Family Medicine—Sports Medicine Section; Program Director, Primary Care Sports Medicine Fellowship, University of Washington; Team Physician, UW Husky Athletics & Seattle Seahawks, Seattle, Washington Tracy R. Ray, MD Director, Primary Care Sports Medicine Fellowship, Duke Sports Science Institute, Durham, North Carolina Monica E. Rho, MD Assistant Professor; Director of Women’s Sports Medicine, Department of Physical Medicine and Rehabilitation, Rehabilitation Institute of Chicago/Northwestern University, Chicago, Illinois Cortie J. Rolison IV, DO Primary Care Sports Medicine Fellowship, UK Healthcare, Lexington, Kentucky

CONTRIBUTORS

Sean C. Rose, MD Director, The Sports Neurology Clinic, Ann Arbor and Southeast Michigan, Clinical Director of Research, Institute for Sports Neurology, Ann Arbor, Michigan Lauren Rudolph, MD Division of Physical Medicine and Rehabilitation, University of Utah, University of Utah Orthopaedic Center, Salt Lake City, Utah Paul D. Scanlon, MD Professor of Medicine, Division of Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, Minnesota Michael P. Schaefer, MD Director of Musculoskeletal Rehabilitation, Cleveland Clinic Foundation, Cleveland, Ohio Byron Schneider, MD Assistant Professor, Department of Physical Medicine and Rehabilitation, Vanderbilt University, Nashville, Tennessee Jacob L. Sellon, MD Program Director, Sports Medicine Fellowship, Sports Medicine Center; Assistant Professor, Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, Minnesota David M. Siebert, MD Department of Family Medicine, University of Washington, Seattle, Washington M. Kyle Smoot, MD Associate Professor, Department of Orthopaedic Surgery and Sports Medicine and Family Medicine, UK Healthcare, Lexington, Kentucky Jeffrey L. Tanji, MD Associate Medical Director, Sports Medicine, Department of Orthopedic Surgery, University of California Davis Health System, Sacramento, California Ashley M. TeKippe, MD Visiting Instructor, Division of Emergency Medicine, University of Utah, Salt Lake City, Utah Ricardo Vasquez-Duarte, MD, RMSK Advanced Neuro and Spine Institute, Miami, Florida Christopher J. Visco, MD Assistant Professor, Department of Rehabilitation and Regenerative Medicine, Columbia University School of Medicine, New York, New York Brandee Waite, MD Co-Director, Physical Medicine and Rehabilitation Sports Medicine Fellowship, Associate Professor, Department of Physical Medicine and Rehabilitation, University of California Davis School of Medicine, Sacramento, California Brian P. Williams, MD Assistant Professor of Clinical Medicine, Division of Pulmonary and Critical Care Medicine, Texas Tech University School of Medicine and Covenant Health, Lubbock, Texas Stuart E. Willick, MD Professor, Division of Physical Medicine and Rehabilitation, University of Utah, University of Utah Orthopaedic Center, Salt Lake City, Utah Steve J. Wisniewski, MD Assistant Professor, Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, Minnesota D. Harrison Youmans, MD Director, Primary Care Sports Medicine Fellowship, Orlando Health Orthopedic Institute, Orlando, Florida Karie N. Zach, MD Assistant Professor, Sports Medicine, Department of Orthopaedic Surgery, Medical College of Wisconsin, Milwaukee, Wisconsin

xiii

Preface When we conceptualized the first edition of Sports Medicine: Study Guide and Review for Boards there was a definite need for a comprehensive yet concise and easy-to-read reference and review book. Although there are now a number of excellent sports medicine books on the market, our niche is still necessary. We have received such flattering comments about the first edition, it was clear we needed to keep the format and hold our place in the sports medicine review category of thorough, yet succinct, texts. For this second edition, we have again kept true to the sports medicine board exam content outline in order to cover all topics testable on the exam. Even the length of each chapter is designed according to how much that topic is weighted on the exam. We’ve also kept the easy-to-read outline format as well as the reference lists at the end of each chapter, which can be used for more in-depth study of the topics. The general format of the original edition has also been retained, dividing the book into three primary sections: (I) General Topics; (II) Health Promotion and Injury Prevention; and (III) Diagnosis and Treatment of Sports Injuries and Conditions. The third section is divided into the following three subsections: (1) Musculoskeletal Injuries and Conditions; (2) Medical, Neurological, and Psychological Conditions; and (3) Special Populations. Besides updating every chapter, we have added a couple of new elements to the second edition. The first is an additional (fourth) subsection entitled “Hot Topics in Sports Medicine.” The material in this subsection (chapters on “Sports Ultrasound” and “Regenerative Medicine”) is not testable information on the board exam yet; however, it is certainly information pertinent to every learner and practitioner of sports medicine. The second new element is a practice test encompassing over 250 questions covering the breadth of sports medicine with an answer key including references to the appropriate chapters. This is a great addition for the reader who is studying for the board exam as well as anyone wanting to test their knowledge of sports medicine. We are very proud of the final product and believe it provides the reader with an exceptional resource covering the entire breadth of sports medicine. The book is meant to be used as a study guide for primary care sports medicine physicians (family medicine, emergency medicine, internal medicine, pediatrics, and physical medicine and rehabilitation) and orthopedic sports medicine physicians preparing to take the sports medicine board examination for initial certification or recertification. It also can serve as a sports medicine reference for other medical professionals such as athletic trainers, physical therapists, physicians in training (ie, interns, residents, and fellows), and other physicians interested in sports medicine. We, once again, would like to thank all the authors who contributed their expertise and time. Without their commitment to excellence, our hopes of enhancing this second edition and creating the best sports medicine review book on the market would have gone unrealized. We also thank our publisher, Beth Barry at Demos Medical Publishing, for her belief in our vision and continued support throughout the process. And, finally, we thank the readers of the first edition, including our own residents and fellows, whose comments and critiques have helped guide us to this second edition. Mark A. Harrast, MD Jonathan T. Finnoff, DO, FACSM xv

Share Sports Medicine: Study Guide and Review for Boards, Second Edition

I General Topics

1 Overview of the Examination Mark A. Harrast and Jonathan T. Finnoff

INTRODUCTION This chapter is aimed at those readers who are preparing for the Sports Medicine Certificate of Added Qualifications (CAQ) (or subspecialty) examination and the recertifying examination. The information presented in this section was collected in 2016 from the following American Board of Medical Specialties websites: 1. 2. 3. 4. 5.

American Board of Emergency Medicine (ABEM) (www.abem.org) American Board of Family Medicine (ABFM) (www.theabfm.org) American Board of Internal Medicine (ABIM) (www.abim.org) American Board of Pediatrics (ABP) (www.abp.org) American Board of Physical Medicine and Rehabilitation (ABPMR) (www.abpmr.org)

The ABFM administers the examination; however, the subspecialty certificates are issued by the physician’s primary board.

ELIGIBILITY FOR THE SPORTS MEDICINE CAQ EXAMINATION Applicants must meet the following requirements to take the Sports Medicine CAQ examination: 1. Board certification in one of the primary fields that participates in this examination (listed earlier) 2. Good standing with the respective board 3. Unrestricted medical license in the United States, its territories, or Canada 4. Completion of 12 months of training in an Accreditation Council for Graduate Medical Education (ACGME)–accredited Sports Medicine Fellowship program A. Before the first day of the month in which the examination will be administered (ABP), by the date of the examination (ABEM), before the end of the month in which the examination will be administered (ABFM and ABPMR), or by October 31 of the year of examination (ABIM) B. Not more than 7 years prior to taking the examination (ABP)

EXAMINATION FORMAT AND APPLICATION PROCESS The examination is a computer-based test with 200 multiple-choice questions given in two 100-question sections, each lasting 2 hours with a 15-minute break between sections. The content of this review book is based on the “outline of examination content” for the Sports Medicine CAQ examination. A link to this outline can be found on the websites of each of the primary fields that participate in Sports Medicine subspecialty certification.

3

4

I: GENERAL TOPICS

The examination is offered each year in July and November/December. Applicants must apply through their respective boards. Applications can be found on their board’s websites. Application deadlines and fees vary according to the respective board, and thus the appropriate board’s website should be reviewed for the most current information. Once you are approved to sit for the examination, you will be asked to select an examination date and location at one of the computer-based testing centers.

OTHER RESOURCES The American Medical Society of Sports Medicine (AMSSM) (www.amssm.org) offers a computerbased Fellows In Training Examination each February for current sports medicine fellows. The examination consists of 200 multiple-choice questions given over a 4-hour time period and mimics the sports medicine board examination. AMSSM also offers a recertification examination beginning in late May each year with a similar format and content to the Fellows In Training Examination. The American Academy of Physical Medicine and Rehabilitation (www.aapmr.org) also offers a downloadable written self-assessment examination in sports medicine. This is available for purchase any time of the year.

RECERTIFICATION Subspecialty certification in Sports Medicine is time limited. The certificate expires on December 31 of the 10th year after passing the primary certifying examination. Sports Medicine subspecialty maintenance of certification (MOC) requirements currently include 1. Maintaining primary board certification A. Required by ABFM, ABP, and ABEM B. Not required by ABPMR, ABIM, but must fulfill other MOC requirements outlined by the respective board 2. Holding an unrestricted medical license in the United States, its territories, or Canada 3. Passing the recertifying examination (which is currently the same as the primary certifying Sports Medicine examination). The examination must be taken in July of years 7 to 10 of the MOC cycle. In case of failure, a candidate can retake the examination in November. MOC is an evolving process; so be certain to review your primary board’s requirements at least yearly.

2 The Role of the Team Physician Katherine Louise Dec and Larry Leone Benson

I. Role of the Team Physician A. A collaborative consensus statement developed by six medical organizations suggests the following requirements for team physicians (1) 1. Provide the best medical care for athletes at all levels of participation 2. Be an MD or DO in good standing, with an unrestricted license to practice medicine 3. Possess a fundamental knowledge of on-field emergency medical care 4. Be trained in cardiopulmonary resuscitation (CPR) and automated external defibrillator use 5. Have a working knowledge of musculoskeletal injuries, psychological issues, and medical conditions in athletes 6. Understand and assist in the development and practices of sideline preparedness to promote health and safety of the athletes (2)

II. Ethics: Maintain Professionalism and Remember Primum Non Nocere; Above All, Do No Harm A. Patient autonomy: Defined as the ability of athletes/patients to make their own decisions regarding medical or surgical options. For autonomy to occur, informed consent must be present 1. Informed consent a. American Medical Association (AMA) Code of Medical Ethics notes, “The patient’s right of self-decision can be effectively exercised only if the patient possesses enough information to enable an intelligent choice” b. Requires the disclosure of diagnosis, the nature and purpose of any proposed treatment, the risks and consequences of that treatment, any reasonably feasible treatment alternatives, the risk of return to play, and the prognosis if the proposed treatment is not performed 2. The necessary conditions for legitimate informed consent as it pertains to the sideline physician are as follows a. Disclosure: All relevant information that a reasonable person in this player’s position would want to know regarding the proposed treatment, nontreatment, and alternate treatments must be explained to the player in an appropriate fashion b. Capacity: Players must have the capacity to understand this information and appreciate how it applies to them. In the legal system, this concept is known as competency c. Voluntariness: In an environment without coercion, players must voluntarily express their wishes regarding the proposed options

5

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I: GENERAL TOPICS

d. Athletes who are minors: Parents or legal guardians serve as medical decision authority (3) i. In rare circumstances, minors can make medical decisions for themselves ii. Legal status of emancipation is granted by legal statutes of the state iii. Can be legally classified as a mature minor for issues of medical decision making B. Patient confidentiality 1. Laws such as the Health Insurance Portability and Accountability Act of 1996 (HIPAA) and the Federal Educational Rights and Privacy Act (FERPA) play major roles in patient confidentiality a. If an independent physician cares for a patient in his or her private office, HIPAA rules apply i. Recommended to have an athlete’s consent to release information to coaches and other members working with the team b. However, a physician who is an employee of the team MAY disclose an athlete’s health conditions with coaches and team owners because the information may be considered as part of the athlete’s employment record and therefore would not fall under HIPAA regulations c. FERPA permits team physicians employed by a college or university student health clinic to release health information without the patient’s consent or authorization to other school officials who have an educational interest in the information d. FERPA, however, does not allow disclosure of health information to the media or other outside entities without the athlete’s signed authorization e. On-field treatment and evaluations may not fall under HIPAA if they are considered emergencies

III. Medical–Legal A. Physician responsibility 1. Fiduciary obligation of the physician a. A physician focuses exclusively on a patient’s health and on what is best for the patient’s health. Athlete–doctor relationship is a patient–physician relationship. Trust is an expected part of the relationship b. Requires a physician to give an athlete full disclosure of medical condition and risks of participation 2. Remaining an objective medical expert during treatment and return-to-play decisions 3. Ensuring safety of other participants on the playing field. For example, officials are notified if contagious skin disease is detected in a wrestling match 4. Coverage of game or practice may involve team physician or other sports medicine health professional a. Negligence related to oversight may be considered the responsibility of the team physician 5. Preparticipation physical examination (PPE) clearance determination 6. Postinjury return-to-sports decisions a. Has the athlete been evaluated by the appropriate physician? Has the athlete received adequate treatment? Were images of the injury documented (if necessary)? Has functional testing been applied before returning? Have the risks of returning been discussed with the athlete and documented? 7. Communication with other health care professionals for athlete’s health care needs 8. Knowledge of the pharmacology regarding medications their team members are prescribed. Must recognize banned drugs and follow appropriate governing bodies guidelines if therapeutic use exemption is required. The National Collegiate Athletic Association (NCAA) and the World Anti-Doping Agency (WADA) have policies and procedures in place outlined at www.ncaa.org and www.wada-ama.org, respectively

2. THE ROLE OF THE TEAM PHYSICIAN

B. Physician liability 1. Guided by tort law a. Tort = a wrong that involves a breach of civil duty owed to someone else b. A person who suffers tortuous injury is entitled to receive “damages” from the person responsible c. Medical malpractice is usually based on negligence torts that require establishment of the following i. The defendant had a duty to act ii. The defendant breached that duty iii. Harm to the plaintiff occurred due to this breach iv. The harm is measurable 2. Physicians protect themselves by practicing good medicine (ie, use published guidelines and consensus statements when able) and placing the health care needs of the athlete over all competing interests. “The physician’s judgment should be governed only by medical considerations” (4) a. Clinical practice guidelines have been allowed in evidence to establish standard of care; however, they are not conclusive to the standard of care b. Guidelines also allow reference for treatment decisions and return to play as they reduce uncertainty into the “customary practice” 3. Professional sports: Athlete–physician relationship on professional teams involves employment contracts. Physicians may have a direct contract for salary payment or an indirect financial benefit from association, name/title as team physicians, advertising, and location to help generate revenue for their practice a. If the physician is an “employee” of the professional team, those athletes on the professional team may be considered under workers’ compensation benefits and the physician is usually protected legally from being sued as they are “coemployees” b. Physicians acting in an employment contract with the professional team are recommended to disclose their relationship with the company to the athlete so the athlete understands any direct or indirect relationship with the professional team 4. The physician must educate the athlete regarding expected treatment outcomes and risks of returning to play 5. Physicians should understand their state law regarding “first responder” and “Good Samaritan” statutes a. When a patient consents to follow the care a physician has recommended and the physician has assessed and rendered an opinion on their injury, a doctor–patient relationship has been established, regardless of free care/volunteering C. PPE (*specific medical conditions covered in other chapters) 1. Assess medical history, family history, and perform a physical examination 2. Goals of PPE are a. To detect conditions that may predispose athletes to injury, illness, or death b. To detect conditions that may put other athletes at risk of illness or injury c. To meet legal and insurance requirements d. To determine general health, to counsel patients on health-related issues, and to assess fitness level for specific sport 3. PPE content may vary based on age/level of competition a. Professional athlete i. There are additional implications to consider of contracts and employment component for athlete of a professional team ii. Discuss with athlete confidentiality aspects regarding informing coaches or team management

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b. College athlete i. After first-year PPE, subsequent annual assessments should be performed to update history and examination with a focus on any new medical conditions or injuries c. Secondary schools or youth travel squads i. Confirm history information with parent/guardian or accompanying documents provided. Need parental consent ii. Clearance also relates to psychological, cognitive, and physical readiness to participate in chosen sport iii. Youth mature musculoskeletally and cognitively at different rates. This should be considered when clearing an athlete for a particular sport 4. Follow clinical practice guidelines or consensus statements by expert panels if no standard of care for clearance to participate a. Some clinical guidelines may concern certain age levels and/or level of competition; however, there are limited legal standards for preparticipation evaluation and clearance in professional athletes D. Return to play (specific conditions are covered in other chapters) 1. Physical injury or medical condition a. Utilize clinical practice guidelines in treatment and return-to-play decisions b. Understand an athlete’s practice and competition environment to prevent further injury c. Understand psychosocial aspects that may affect recovery and prevent injury in return-to-play decisions d. Engage other members of medical management team for complex issues, such as postsubstance abuse with academic and physical function implications E. Waiver of liability 1. Signed waivers (eg, exculpatory agreements) do not absolve team physicians from liability 2. Little legal framework for waiver agreements and these are viewed as unenforceable a. Assumption of risk: May be incorporated into informed consent form b. Prospective release of risk: May not be enforceable, but will undergo scrutiny and may be considered in athletes requesting release against medical advice

IV. Administrative Responsibilities A. Development of policies and procedures related to medical injuries and conditions that may affect athletes’ participation in sport 1. Understand intrinsic and extrinsic risks of sport. Identify athletes at risk. Establish prevention strategies, including athlete education, for injuries and medical conditions 2. Maintain written policies outlining communication, testing, and outside consultant referral for certain conditions a. Athletes sign a document outlining understanding of how information may be shared with team administration, coaches, and other health professionals if injury should occur. If athletes are minors, have parent or legal guardian also sign 3. Keep medical records documenting preparticipation physicals, injuries, treatments, risks of sports participation, and return-to-play decisions a. Documents medical care and establishes athlete’s awareness of injury/medical condition as well as risks of returning to sports 4. Review policies and procedures regularly. Follow state and federal guidelines and local standard of medical care when developing these policies B. Communication between appropriate school officials and rest of medical team for care of athletes’ health 1. The team physician should be the athlete’s advocate in return-to-play decisions

2. THE ROLE OF THE TEAM PHYSICIAN

2. The team physician should collaborate with outside specialists and other health care professionals, in addition to the athlete’s family, coach, and administrators as appropriate C. Policies and procedures for emergency management of athletes participating in schoolsponsored sports 1. Create a written emergency action plan that is understood by all members of athletic sports medicine team 2. Practice emergency procedures with members of athletic sports medicine team for catastrophic events and coordination with community medical systems D. Coordination of care with other health care professionals for athletes’ care 1. Meet with community agencies to provide cohesive implementation of medical care policies, such as emergency transport for catastrophic injury 2. Collaborate efforts with community and legislature to increase safety in the sports venue and to develop universal policies to prevent injury

References (1). Herring SA, Kibler WB, Putukian M, American College of Sports Medicine. Team physician consensus statement: 2013 Update. Med Sci Sports Exerc. 2013;45(8):1618–1622. (2). Herring SA, Kibler WB, Putukian M, American College of Sports Medicine. Sideline Preparedness for the Team Physician: A Consensus Statement–2012 Update. Med Sci Sports Exerc. 2012;44(12):2442–2445. (3). Committee on Bioethics, American Academy of Pediatrics. Informed consent, parental permission, and assent in pediatric practice. Pediatrics. 1995;95:314–17. (4). The American Medical Association (AMA) Code of Medical Ethics’ Opinion on Treating Athletes. Opinion 3.06 Sports Medicine. Virtual Mentor. 2014;16(7):542.

Recommended Reading 1. American Medical Association Council on Ethical and Judicial Affairs, Code of Medical Ethics: Current Opinions and Annotations, AMA, Opinion 8.08 on Informed Consent. Chicago: AMA; 2004–2005. 2. Bernstein J, Perlis C, Bartolozzi AR. Ethics in sports medicine. Clin Orthop Relat Res. 2000;378:50–60. 3. Dunn WR, George MS, Churchill L, et al. Ethics in sports medicine. Am J Sports Med. 2007;35(5):840–844. 4. Furrow BR. The problem of the sports doctor: Serving two (or is it three or four?) masters. HeinOnline. St. Louis University Law J. 2005–2006;50:165–183. 5. Howe WB. Ethical considerations in sports medicine. In: Birrer RB, et al, eds. Sports Medicine for the Primary Care Physician. 2nd ed. Boca Raton, FL: CRC Press Inc; 1994:37–39. 6. Magee JT, Almekinders LC, Taft TN. HIPAA, the team physician. Sports Med Update. 2003;4–8. 7. Matheson GO, Shultz R, Bido J, et al. Return-to-play decisions: Are they the team physician’s responsibility? Clin J Sport Med. 2011;21(1):25–30. 8. Mitten MJ. Team physicians as co-employees: A prescription that deprives professional athletes of an adequate remedy for sports medicine malpractice. HeinOnline—St. Louis University Law J. 2005–2006;50:211. 9. Pearsall AW, Kovaleski JE. Medicolegal issues affecting sports medicine practitioners. Clin Orthop Relat Res. 2005;433:50–57. 10. Stovitz SD, Satin DJ. Professionalism and ethics of the sideline physician. Curr Sports Med Rep. 2006;5:120–124. 11. Testoni D, Hornik CP, Smith B, et al. Sports medicine and ethics. Am J Bioethics. 2013;13(10):4–12.

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3 Exercise Physiology James C. Presley and Jonathan T. Finnoff

I. Muscles A. Muscle cells 1. Muscle cells = myofibers or muscle fibers a. Long, cylindrical multinucleated cells 2. Muscle cell membrane = sarcolemma 3. Muscle cell cytoplasm = sarcoplasm 4. Bundled groups of muscle cells = fascicles B. Connective tissue (Figure 3.1) 1. Endomysium = surrounds each muscle cell a. Sarcolemma is continuous with the endomysium 2. Perimysium = surrounds each fascicle 3. Epimysium = surrounds the entire muscle C. Tendons 1. Connects muscle to bone periosteum 2. Endomysium, perimysium, and epimysium all connect to the tendon D. Innervation 1. Each muscle cell is innervated by a single motor nerve, but a single nerve can innervate multiple muscle cells 2. Motor unit = single motor nerve and all the muscle cells it innervates a. All the muscle cells in a motor unit contract when they are stimulated by their motor nerve E. Myofibrils 1. Contractile apparatus of muscles 2. Composed of the myofilaments myosin (thick filament) and actin (thin filament) a. Myosin has a globular head, which can form crossbridges with actin b. Actin has a two-stranded double-helix structure c. Each actin is surrounded by three myosins d. Each myosin is surrounded by six actins 3. Sarcomere (Figure 3.1) a. Smallest contractile unit in skeletal muscle b. Z-line = end of the sarcomere i. Actin attaches to the Z-line c. M-line = center of the sarcomere i. Myosin attaches to the M-line d. A-band (dark) i. Contains myosin and actin 10

3. EXERCISE PHYSIOLOGY

Figure 3.1 Muscle anatomy including the connective tissue layers (epimysium, perimysium, endomysium), muscle organization (fascicles, muscle fibers), and contractile units (sarcomere). During muscle contraction, the H-zone and I-band decrease in size due to increased overlap of actin and myosin.

e. I-band (light) i. Contains only actin f. H-zone = in the middle of the A-band i. Contains only myosin ii. H-zone and I-band get smaller with muscle contraction F. Muscle contraction (Figure 3.1) 1. At rest a. Minimal calcium in the sarcoplasm b. Few myosin heads bound to actin c. Troponin and tropomyosin cover the actin-binding sites on the myosin head 2. During muscle contraction a. Acetylcholine released from the motor neuron binds to receptors on the muscle cell membrane b. Sarcolemma depolarizes c. Depolarization transmitted rapidly into the interior of the muscle cell via the transverse tubules (T-tubules) d. Intracellular calcium released from the sarcoplasmic reticulum e. Calcium binds to troponin, which causes a conformational change in tropomyosin, and the myosin-binding sites on the actin filament are uncovered

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Table 3.1

Characteristics of Muscle Fiber Types

Characteristic

Type I

Type IIa

Type IIx

Contraction speed

Slow

Fast

Fast

Force production

Low

Intermediate

High

Endurance

High

Intermediate/low

Low

Aerobic enzymes

High

Intermediate/low

Low

Anaerobic enzymes

Low

High

High

Fatigability

Low

Intermediate/high

High

Capillary density

High

Intermediate

Low

Fiber size

Small

Intermediate

Large

Mitochondria

High

Intermediate

Low

ATPase activity

Low

High

High

Myoglobin

High

Low

Low

Color

Red

Red

White

ATP, adenosine triphosphate.

f. Myosin head forms a crossbridge with the actin filament, flexes, then dissociates from the actin g. Myosin head recocks to its original position prior to beginning the process again h. Two adenosine triphosphate (ATP) converted into adenosine diphosphate (ADP) for muscle contraction i. One to form crossbridge with actin and flex the myosin head ii. One for dissociation of myosin from actin and to recock the myosin head G. Muscle fiber types (Table 3.1) 1. Type I (slow twitch—oxidative) 2. Type II (fast twitch—glycolytic) a. Type IIa (fast twitch—oxidative glycolytic) b. Type IIx (fast twitch—glycolytic) H. Recruitment 1. Henneman size principle a. Smaller, lower-threshold motor neurons innervate type I muscle fibers and are recruited first b. Type II fibers recruited if more force is required 2. Exception = activities of high-velocity type (ie, plyometrics) a. Type II fibers recruited first

II. Energy Systems A. Three energy systems 1. ATP-phosphocreatine a. Phosphocreatine donates its phosphate to regenerate ATP from ADP in muscle b. Catalyzed by the enzyme creatine kinase c. Main energy source for maximal exercise lasting up to 30 seconds d. Most of the phosphocreatine can be regenerated after resting 3 minutes 2. Anaerobic (glycolytic) (Figure 3.2) a. Metabolism of glucose to pyruvate via glycolysis b. No oxygen is required

3. EXERCISE PHYSIOLOGY

c. Produces two ATP if beginning with glucose, or three ATP if beginning with glycogen d. In the presence of oxygen, the end product of glycolysis (pyruvate) is metabolized via the aerobic energy system (see Section II.A.3). When pyruvate is created faster than it can be metabolized, it is reversibly converted into lactate. Pyruvate into lactate conversion is facilitated by a low-oxygen environment e. Glycolysis is the primary energy source for exercise lasting 1 to 3 minutes f. The rate-limiting step of glycolysis is catalyzed by the enzyme phosphofructokinase 3. Aerobic (oxidative) a. Occurs in the mitochondria via oxidative phosphorylation, which has two parts i. Krebs cycle (Figure 3.3a) (A) By-product is CO2 ii. Electron transport chain (Figure 3.3b) (A) By-product is H2O b. In the presence of oxygen, pyruvate is converted into acetyl coenzyme A, which is metabolized through the Krebs cycle and electron transport chain to produce 36 ATP per glucose molecule. Therefore, the net ATP produced from glycolysis and oxidative phosphorylation is 38 (beginning with glucose) or 39 (beginning with glycogen)

Figure 3.2

Glycolysis.

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Figure 3.3

(a) Krebs cycle, (b) electron transport chain.

c. Aerobic metabolism is the primary energy source for exercise lasting more than 3 minutes d. Fat is also metabolized in the mitochondria i. Triglycerides are broken down into glycerol and three free fatty acids by lipolysis ii. Free fatty acids enter the mitochondria and are converted into acetyl coenzyme A through beta-oxidation iii. Acetyl coenzyme A metabolized by the Krebs cycle and electron transport chain iv. Net ATP produced from free fatty acid metabolism is far greater than for glucose (eg, 129 ATP for one palmitic acid molecule)

III. Adaptations to Exercise A. Aerobic exercise (Table 3.2) 1. Results in an increase in a. Muscular capillary density b. Size and number of mitochondria c. Oxidative enzymes d. Fatty acid transport across the sarcolemma e. Fat metabolism f. Arterial oxygen extraction i. Increased arteriovenous oxygen concentration difference

3. EXERCISE PHYSIOLOGY

2. Owing to the increase in fat utilization, there is a relative sparing of glycogen/glucose metabolism, which results in a reduction in lactate production 3. There is no change in muscle cell lactate buffering capacity 4. Pyruvate is metabolized faster due to the increase in oxidative enzymes 5. Historically, studies have suggested that many type IIx fibers will convert to type IIa fibers after approximately 2 weeks of aerobic exercise training. Newer techniques defining muscle fiber type have emerged, suggesting this may not occur. This is a very controversial topic at the present time and research is ongoing B. Anaerobic exercise (Table 3.2) 1. Results in an increase in a. Intramuscular anaerobic enzymes such as phosphofructokinase, phosphorylase, and lactate dehydrogenase b. Oxidative enzymes (moderate increase) 2. Improves muscle cell lactate buffering capacity C. Resistance exercise 1. Causes muscle cell hypertrophy (increased muscle cell size) a. Due to an increased number of sarcomeres b. Occurs after 6 to 8 weeks of training c. Predominantly in type II muscle cells 2. Strength gains that occur prior to 6 weeks are due to neural factors including improved motor unit recruitment and repression of self-protection reflexes 3. No substantial evidence supporting hyperplasia (increased number of muscle cells) in humans due to resistance exercise 4. Fiber-type conversion from type IIx to type IIa begins after a few weeks; this is a controversial topic (see Section III.A.5)

Table 3.2

Adaptations to Aerobic and Anaerobic Exercise

Anatomic/Physiologic Adaptation

Aerobic

Anaerobic

Muscular capillary density

↑↑

−

Mitochondrial number and size

↑↑

↑

Oxidative (aerobic) enzymes

↑↑

↑

−

↑↑

Fatty acid transportation across sarcolemma

↑↑

−

Fat metabolism

↑↑

−

↓

−

↑↑

−

Lactate production

↓

↓

Lactate buffering capacity

−

↑↑

↑↑

↑−

Hypertrophy of type I muscle fibers

↑−

↑−

Hypertrophy of type II muscle fibers

−

↑

↑↑

↑

Glycolytic (anaerobic) enzymes

Glucose/glycogen metabolism Arterial oxygen extraction/arteriovenous oxygen difference

Type IIx to type IIa fiber-type conversion (controversial, see Section III.A.5)

Improved aerobic exercise performance

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5. Resistance exercises can lead to improved aerobic exercise as evidenced by the improved running economy of long-distance runners following maximal squat strength training three times weekly for 8 weeks 6. Aerobic exercise does not appear to enhance the strength benefits of resistance training alone 7. Resistance training increases a. Bone mineral density (BMD) b. Ligament and tendon strength and collagen content c. Anaerobic energy stores (glycogen, phosphocreatine, ATP) 8. Capillary and mitochondrial density decrease due to larger degree of muscular hypertrophy compared to increase in capillarization 9. High-volume, low-load resistance exercises increase a. Creatine phosphokinase b. Myokinase c. Phosphofructokinase 10. Low-volume, high-load resistance exercises cause a. Decrease in creatine phosphokinase b. No change in myokinase or phosphofructokinase 11. Lactate dehydrogenase concentrations do not change with either high-volume, lowload or low-volume, high-load resistance exercises D. Flexibility 1. Three main stretching techniques a. Static i. Muscle held in stretched position for a sustained period of time, usually 30 seconds ii. Easy to perform iii. Minimal activation of the muscle spindles iv. May lead to performance decrement when performed prior to events requiring major strength or power components b. Ballistic i. Bouncing motion is utilized to stretch the muscle ii. Activates muscle spindles causing reflex contraction of the muscle being stretched iii. As effective as static stretching BUT more painful and has a higher potential for injury c. Proprioceptive neuromuscular facilitation (PNF) i. Muscle contraction, either the agonist or antagonist, is used to facilitate the stretch through reflexes (eg, contracting the quadriceps muscle while stretching the hamstring muscle) 2. Effectiveness of stretching techniques a. PNF > static = ballistic 3. Factors that influence flexibility a. Joint range of motion is limited by the joint’s bony anatomy as well as by the muscles, fascia, tendons, and ligaments that cross the joint b. Muscle elasticity is reduced with age due to fibrocartilaginous replacement of degenerated muscle fibers, increased adhesions, and calcium deposits c. Females are more flexible than males, primarily due to pelvic structure and hormonal differences d. Physically active people tend to be more flexible than their sedentary counterparts 4. Increased flexibility from stretching due to a. Acute = musculotendinous viscoelastic properties b. Chronic = increased number of sarcomeres and increased stretching pain tolerance

3. EXERCISE PHYSIOLOGY

IV. Lactate Kinetics A. At rest and during low-intensity exercise, blood lactate levels are low and remain relatively constant B. As intensity increases, there comes a point above which lactate begins to accumulate C. If exercise intensity continues to increase, a shift takes places where anaerobic metabolism becomes the predominant energy source rather than aerobic metabolism D. This point is called the lactate or anaerobic threshold and usually occurs at 4 mmol/L of blood lactate E. In untrained individuals, the lactate threshold may reside at 50% to 60% of their maximal oxygen uptake, while in trained individuals it may be closer to 80% to 90% of their maximal oxygen uptake F. The lactate threshold is trainable G. Lactate is an energy substrate for glycolysis and does not appear to cause the “muscle burn” associated with exercise

V. Cardiovascular Response to Exercise A. As exercise intensity increases, there is a linear increase in heart rate B. Stroke volume increases initially, but then plateaus C. Early increases in cardiac output associated with exercise are due to a combination of increased heart rate and stroke volume (CO = HR × SV), whereas the increased cardiac output associated with higher-intensity exercise is nearly completely due to an increase in heart rate D. There is a linear relationship between cardiac output and maximal oxygen consumption. Therefore, cardiac output is an important determinant of aerobic exercise capacity E. During a prolonged aerobic exercise session, there is a gradual increase in heart rate and decrease in stroke volume at a given workload. This is referred to as cardiac drift and is likely due to a greater percentage of the blood being diverted to the skin for heat dissipation and a reduction in blood volume due to sweating F. During aerobic exercise, systolic blood pressure (SBP) increases proportional to exercise intensity with little effect on diastolic blood pressure (DBP). During resistance exercise, there can be extreme increases in both SBP and DBP (greater than 400/300 mmHg) especially in the setting of a Valsalva maneuver G. Long-term aerobic exercise training causes 1. Increased a. Stroke volume at rest and during maximal exercise b. Left ventricular wall thickness, internal diameter, and mass c. Blood volume i. Initially due to increased plasma volume likely due to increased antidiuretic hormone and aldosterone levels ii. Later due to increases in both plasma volume and red blood cell number (erythropoietin released from the kidneys acting on bone marrow progenitor cells) iii. Since the increase in blood volume is greater than the increase in red blood cell volume, there is a net reduction in the hematocrit referred to as a “pseudoanemia” 2. Decreased a. Resting and submaximal exercise heart rate b. SBP and DBP (see Section XII.A.1.b.) H. Long-term resistance training causes 1. Increased left ventricular wall thickness and mass 2. No change in internal left ventricular diameter

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VI. Respiratory Response to Exercise A. Initial rapid increase in ventilation, followed by a brief plateau, and another gradual rise until a steady state is reached B. During submaximal exercise, increased ventilation has a linear relationship with oxygen uptake C. Initial increase in ventilation due to increase in tidal volume 1. With increased exercise intensity, breathing rate becomes the predominant mechanism for increased ventilation

VII. Endocrine Response to Exercise A. Testosterone 1. Temporarily increases after resistance exercise a. Increase enhanced by i. Shorter rest periods (1 minute rather than 3 minutes) ii. Less intensity but higher volume (10 repetition maximum [RM] rather than 5 RM) iii. Exercise lasting longer than 20 minutes 2. Temporarily increases after anaerobic exercise 3. Lower than normal resting testosterone levels in endurance athletes B. Growth hormone 1. Increases after resistance exercise a. Increase enhanced by i. Shorter rest periods (1 minute rather than 3 minutes) ii. Less intensity but higher volume (10 RM rather than 5 RM) iii. Exercise lasting longer than 20 minutes 2. Increases after aerobic exercise C. Insulin 1. Decreases during exercise 2. Insulin sensitivity increased by exercise D. Cortisol 1. Increased after a. Resistance training b. Prolonged aerobic exercise above 70% of maximal oxygen uptake E. Aldosterone/antidiuretic hormone 1. Increased after exercise due to decreased plasma volume and increased plasma osmolarity (significant water and sodium losses with sweating) a. Restores total body water and electrolyte levels in the hours and days after acute exercise

VIII. Immune System Response to Exercise A. Low- to moderate-intensity exercise 1. Reduces infections in previously sedentary people 2. Has no effect on mucosal immunoglobulin A (IgA) concentrations B. High-intensity, prolonged exercise 1. Reduces mucosal IgA concentrations, leukocyte counts, and natural killer cell numbers for 3 to 72 hours after exercise resulting in altered immunity 2. May increase upper respiratory infections in endurance athletes

IX. Delayed-Onset Muscle Soreness (DOMS) A. Occurs following high-force, unaccustomed eccentric (and occasionally isometric in an extended position) muscle contractions

3. EXERCISE PHYSIOLOGY

B. Reason for eccentric specificity of DOMS is unknown, but the following events occur following eccentric exercise 1. Disruption of the sarcomere’s Z-lines called “Z-line streaming” 2. Sarcolemma damaged 3. Calcium is released within the cell 4. Calcium-dependent proteolytic enzymes degrade the damaged sarcomere Z-lines 5. Circulating neutrophil concentrations increase within a few hours of the injury 6. Creatine kinase leaks from the muscle cell into the circulating plasma and attracts monocytes to the area within 6 to 12 hours of the injury 7. Monocytes transform into macrophages then phagocytose damaged structures 8. Macrophages release prostaglandin PGE2, and type III and IV nerve endings are sensitized 9. Mast cells are attracted to the area and release histamine, causing tissue edema, hyperthermia, and further sensitization and mechanical compression of nociceptors 10. Monocyte/macrophage concentrations peak at approximately 48 hours after injury 11. Oxygen free radicals are also produced throughout this process causing secondary tissue damage C. Pain typically begins 6 to 12 hours after exercise, peaks 2 to 3 days after exercise, and resolves 5 to 7 days after exercise D. Symptoms treated with analgesics such as nonsteroidal anti-inflammatory drugs (NSAIDs) or acetaminophen, massage, electrical stimulation, cryotherapy, heat, and rest E. The most effective prevention measure for DOMS is the “repeated bout effect” 1. Single bout of eccentric exercise prevents the development of DOMS from the same exercise for approximately 6 weeks 2. Stretching before exercise has not been shown to decrease DOMS

X. Children A. Due to variable maturation rates, classify children by their biological rather than chronological age B. Biological age can be determined by skeletal age, sexual maturation, or physical maturity (eg, five Tanner stages) C. Muscle mass increases during maturation with 25% of a baby’s birth weight attributable to muscle versus 40% of an adult’s weight 1. Increase in muscle mass is due to hypertrophy, not hyperplasia 2. Prepuberty strength/muscle mass is similar between males and females 3. Males have a larger increase in muscle mass than females during puberty due to higher testosterone levels a. Larger increases in male muscle mass mirrored by larger increases in strength D. Females have increased estrogen levels during puberty, which causes fat deposition, secondary sex characteristic development, and widening of the hips

XI. Elderly A. Decrease in muscle 1. Strength 2. Mass a. Due to loss of muscle fibers (sarcopenia) b. Preferential loss of type II muscle fibers leads to higher percentage of type I muscle fibers 3. Function

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B. Decreased muscle mass predisposes to 1. Osteoarthritis of the knee 2. Falls 3. Osteoporotic fractures C. Endurance decreased due to 1. Decreased a. Muscle mass b. Capillary blood flow c. Oxygen uptake d. Nutritional status 2. Increased presence of chronic diseases such as a. Chronic obstructive pulmonary disease (COPD) b. Coronary artery disease (CAD) c. Congestive heart failure (CHF) D. Balance decreased due to 1. Inactivity and deconditioning 2. Chronic diseases that affect balance such as a. Peripheral vascular disease (PVD) b. Diabetes mellitus (DM) c. Parkinson’s disease d. Peripheral neuropathy 3. Poor nutrition 4. Alcoholism 5. Medications E. Flexibility decreased due to 1. Immobilization and/or a lack of regular joint movement through a full range of motion F. Physiologic changes seen with aging (Table 3.3)

Table 3.3

Physiologic Changes with Aging

System

Type of Change

Effect/Amount of Change

Cardiovascular

↓ Maximum heart rate of

10 beats/min/decade

↓ Blood vessel compliance

↑ Blood pressure 10–40 mmHg

↓ Resting stroke volume

30% by 85 years of age

↓ Maximum cardiac output

20%–30% by age 65

↓ Maximum cardiac output ↑ Residual volume

30%–50% by age 70

↓ Vital capacity

40%–50% by age 70

Metabolism

↓ Maximal oxygen uptake (VO2max)

9% per decade

Neurologic

↓ Nerve conduction velocity

1%–15% by age 60

↓ Proprioception

↑ Falls 35%–40% by age 60

Bone loss when 35–55 years old

1% per year

Bone loss when >55 years old

3%–5% per year

↓ Muscle strength

20% by age of 65

Respiratory

Musculoskeletal

↓ Flexibility

3. EXERCISE PHYSIOLOGY

G. Progressive resistance exercises 1. Increase a. Strength b. Endurance c. Submaximal aerobic capacity d. BMD 2. Decrease a. Blood pressure (BP) b. Fall risk c. Osteoarthritic knee pain d. Disability H. Aerobic exercise 1. Improves a. Efficiency (ie, reduced metabolic demands for a given activity) b. Endurance c. Oxygen uptake d. Reaction to multiple chronic diseases (see Section XII) 2. Reduces a. Resting heart rate b. Disability c. Pain I. Balance training reduces 1. Falls 2. Osteoporotic fractures J. Flexibility training improves 1. Joint range of motion 2. Muscle flexibility

XII. Patients With Chronic Disease A. Regular exercise is a beneficial adjunctive treatment of chronic diseases such as 1. Hypertension a. Fifty percent greater risk of developing hypertension in sedentary than active people b. In people with hypertension (SBP ≥ 140 and/or DBP ≥ 90), regular exercise reduces resting SBP by approximately 7.4 mmHg and DBP by 5.8 mmHg c. Moderate-intensity aerobic exercise (40%–70% of VO2max) is as effective as highintensity aerobic exercise at reducing BP d. Some reductions in SBP and DBP from resistance training i. Regular resistance training also blunts the acute elevations in BP that occur in untrained individuals who perform resistance exercises e. Small reductions in BP (2 mmHg of SBP and DBP) result in significant reductions in stroke risk (14%) and CAD (9%) f. Decreased BP probably due to reduction in sympathetic tone 2. PVD 3. Osteoarthritis 4. Claudication 5. COPD 6. Dementia 7. Pain 8. CHF 9. Syncope 10. Cerebrovascular accident 11. Deep venous thromboembolism

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12. Back pain 13. Constipation 14. DM a. Aerobic and resistance exercise decrease insulin resistance and therefore increase insulin sensitivity b. Increases GLUT4 production (a glucose-transporting protein), thus improving glucose transport in type 2 DM c. Aerobic exercises performed for 30 to 60 minutes, three to four times per week at 50% to 80% of VO2max reduces glycosylated hemoglobin levels (HbA1c) by 10% to 20% in type 2 diabetics d. Circuit-type resistance training or high-intensity progressive resistance training performed twice weekly for 3 months decreases HbA1c 8.2% to 8.8% in type 2 diabetics e. High exercise intensity is more predictive of improved glycemic control than high exercise volume f. Regular physical activity reduces mortality in athletes with type 1 or type 2 DM 15. Dyslipidemia a. Triglycerides reduced 18 to 24 hours after an acute bout of high-intensity aerobic exercise i. Shorter duration and lower intensity blunts this response b. Total cholesterol and low-density lipoprotein (LDL) have small reductions following acute exercise c. High-density lipoprotein (HDL) levels frequently increase after an acute bout of aerobic exercise d. Consistent aerobic exercise for 3 to 12 months can reduce triglyceride levels by 10% to 20% e. Reductions in LDL are approximately 5% following ≥12 weeks of aerobic exercise f. Total cholesterol does not appear to decrease with regular exercise g. Regular exercise can increase HDL levels between 4% and 25% 16. Depression a. Aerobic and resistance training decreases depressive symptoms in men and women b. Exercise appears to be as effective as psychotherapy for treating depression c. The American College of Sports Medicine’s (ACSM’s) recommendations for exercise in the treatment of depression are 20 to 60 minutes of aerobic exercise 3 to 5 days per week 17. Osteoporosis a. Physically active youth have higher peak BMD than their sedentary counterparts b. The ACSM’s position stand on exercise in the treatment of osteoporosis recommends weight-bearing endurance activities (moderate to high intensity, 30 to 60 minutes, 3 to 5 times per week), activities that involve jumping, and resistance exercise (2 to 3 times per week) c. Intake of calcium and vitamin D are important for bone health but supplementation with excessive amounts has not proven to increase BMD 18. Obesity a. Weight loss requires more caloric expenditure than intake (ie, negative caloric balance) b. Dieting alone better for weight loss than exercise alone, BUT once individuals have lost weight, they are more likely to keep it off if they participate in regular physical activity c. Regular aerobic exercise modifies multiple cardiovascular disease risk factors in obese individuals

3. EXERCISE PHYSIOLOGY

Recommended Reading 1. American College of Sports Medicine Position Stand. Physical activity and bone health. Med Sci Sports Exerc. 2004;36(11):1985–1996. 2. Anish E, Klenck, CA. Exercise as medicine: The role of exercise in treating chronic disease. In: McKeag D, Moeller JL, eds. ACSM’s Primary Care Sports Medicine. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007:107–131. 3. Baechle T, Earle RW. Essentials of Strength Training and Conditioning. 2nd ed. Champaign, IL: Human Kinetics; 2000. 4. Cheung K, Hume PA, Maxwell L. Delayed onset muscle soreness: Treatment strategies and performance factors. Sports Med. 2003;33(2):145–164. 5. Ewing GC, Bissmer B, Deschenes M, et al. American college of sports medicine position stand. quantity and quality of exercise for developing and maintaining cardiorespiratory, musculoskeletal, and neuromotor fitness in apparently healthy adults: Guidance for prescribing exercise. Med Sci Sports Exerc. 2011;43(7): 1334–1359. 6. Farrell PA, Joyner MJ, Caiozzo VJ. ACSM’s Advanced Exercise Physiology. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2012. 7. Foster C, Faber MJ, Porcari, JP. Exercise physiology and exercise testing. In: McKeag D, Moeller JL, eds. ACSM’s Primary care sports medicine. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007:29–34. 8. Frankel J, Bean JF, Frontera WR. Exercise in the elderly: Research and clinical practice. Clin Geriatr Med. 2006;22:239–256. 9. Hoffman, J. Physiological Aspects of Sport Training and Performance. 1st ed. Champaign, IL: Human Kinetics; 2002. 10. Hough D, Barry HC, Eathorne, SW. The mature athlete. In: Mellion MB, ed. Sports Medicine Secrets. 2nd ed. Philadelphia, PA: Hanley and Belfus, Inc; 1999:47–52. 11. Howatson G, van Someren KA. The prevention and treatment of exercise-induced muscle damage. Sports Med. 2008;38(6):483–503. 12. Kenney WL, Wilmore JH, Costill DL. Physiology of Sport and Exercise. 6th ed. Champaign, IL: Human Kinetics; 2015. 13. Rivera-Brown A, Frontera W. Principles of exercise physiology: Responses to acute exercise and long-term adaptations to training. PMR. 2012;4:797–804. 14. Storen O, Helgerud J, Stoa ME, Hoff J. Maximal strength training improves running economy in distance runners. Med Sci Sports Exerc. 2008;40(6):1087–1092. 15. Thigpen L. Building strength. In: Mellion MB, ed. Sports Medicine Secrets. 2nd ed. Philadelphia, PA: Hanley & Belfus, Inc; 1999.

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4 Sports Biomechanics Erek W. Latzka and Mark A. Harrast

THROWING I. Throwing as a Kinetic Chain of Motion A. Whole-body activity involving transfer of momentum from body to ball 1. Segmental transfer of energy from the ground up, with each segment’s velocity greater than the previous a. Kinetic energy initiated with the drive of stride leg b. Potential energy stored in rotation of hips and then the trunk c. These forces are then transferred distally through the shoulder girdle, elbow, forearm, and hand, before finally imparting on the ball B. The role of the trunk 1. Approximately 50% of the velocity of the pitch results from the step and body rotation (ie, from the large leg and trunk musculature) 2. The other 50% comes from the shoulder, elbow, wrist, and fingers 3. Peak velocity of a pitched ball drops to a. Eighty-four percent when forward stride is not allowed i. Stride length is generally between 85% and 100% of the pitcher’s height ii. Increased stride length improves velocity b. Sixty-four percent when lower body is restricted c. Fifty-three percent when lower body and trunk are restricted 4. Peak ball velocities in water polo are 50% that of baseball due to the lack of ground reaction force (GRF)

II. Throwing: Six Phases of the Baseball Pitch (see Figure 4.1) A. Windup 1. Begins when pitcher initiates motion 2. Continues with the “push off” a. Stride leg (contralateral to pitching arm) pushes off from behind the pitcher, moving the center of gravity (COG) of the body forward b. As the stride leg pushes off, three simultaneous movements occur i. Both arms flex forward ii. Body rotates 90° (away from home plate) iii. Stride leg continues to elevate, flexing at the hip and knee 3. Ends when removing the ball from glove. This occurs in concert with a. Maximum knee lift of stride leg b. The “balance point”: The time that the body’s COG is stable and the pitcher is positioned so that all body parts can now contribute propulsion forces to the ball 24

Windup

Early cocking

Figure 4.1

Late cocking

Acceleration

Deceleration

4. SPORTS BIOMECHANICS

Followthrough

Six phases of the baseball pitch.

B. Early cocking (stride phase) 1. Begins at the balance point, but now the COG must be lowered and accelerated toward home plate 2. As the stride leg extends toward the batter, the knee and hip of the pivot leg extend as well, propelling the body forward into the stride 3. Hips rotate forward, or “open” between 400° and 700° per second, while leaving the trunk and shoulders relatively stable or “closed,” storing elastic potential energy in the large muscles of the trunk 4. Throwing shoulder abducts, extends, and externally rotates, leaving the shoulder in a “semicocked” position 5. Ends when the stride foot contacts the ground a. Stride foot contact should be toward home plate. Excessively closed foot placement points toward third base, while excessively open foot placement points toward first base (assuming right-handed pitcher) C. Late cocking 1. Begins after stride foot makes contact with ground 2. Trunk now rotates forward toward home plate, leaving the throwing arm behind 3. Scapula retracts and upwardly rotates, allowing the shoulder to both abduct to 90° to 100° and externally rotate 4. Ends when the shoulder reaches maximum external rotation (ER) a. From 50° of ER to 175° of ER b. Allows the greatest accelerating force to the ball over the greatest possible distance c. The amount of ER correlates with the speed of the pitched ball D. Acceleration 1. Begins at maximal ER, with shoulder powerfully internally rotated by elastic forces of anterior capsule and dynamic musculature a. From 175° of ER to 90°–100° of ER at ball release 2. Very explosive phase a. Average peak angular velocity of shoulder internal rotation (IR) during the acceleration phase is approximately 7,200°/s to 9,000°/s

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3. Shoulder abduction of 90° is relatively fixed in all throwers, regardless of style; trunk lateral flexion creates the position the arm is in, relative to the vertical plane a. “Over the top” throwers i. Greater amount of contralateral lateral trunk flexion b. “Sidearm” throwers i. Less contralateral lateral trunk flexion E. Deceleration 1. After ball release 2. Decelerating IR 3. Ends when arm reaches 0° of IR F. Follow-through 1. A “passive phase” with the body merely catching up with the throwing arm 2. Arm is adducted across pitcher’s body, elbow is flexed

III. Timing Sequence of These Phases A. Preparation phase: Windup through late cocking phases take up 80% of total pitch time B. Acceleration phase: 2% of total pitch time C. Deceleration and follow-through: 18% of total pitch time

IV. Pitching Injuries and Muscle Activity According to the Phase Most injuries occur in the late cocking and deceleration phases, followed by the acceleration phase A. Windup 1. Few injuries occur in the early phases 2. Shoulder musculature is relatively inactive during windup. Indwelling electromyography shows less than 21% max volitional contraction for the rotator cuff (RC), trapezius, serratus, and deltoid 3. Most forces arise in the lower half of the body B. Early cocking (stride) 1. Scapular stabilizers (trapezius and serratus anterior) demonstrate moderate-to-high activity—to protract and upwardly rotate scapula 2. Middle deltoid generates the abduction force 3. Supraspinatus fine-tunes humeral head positioning within the glenoid 4. Static stabilizers are also active i. Inferior glenohumeral ligament limits anterior and posterior translation of the humeral head C. Late cocking 1. Maximal ER of shoulder requires multifaceted stabilization a. Internal rotators: Subscapularis, pectoralis major, and latissimus dorsi stabilize the anterior glenohumeral joint b. Biceps: Long head of the biceps limits anterior translation of the humeral head, restrains excessive ER, and alleviates strain on the inferior glenohumeral ligament c. RC: Infraspinatus and teres minor aid the deltoid in extreme ER. Supraspinatus (less active) is at a mechanical disadvantage in extreme ER i. RC is at peak activity d. Static stabilizers (glenohumeral ligaments, capsule, and labrum) are important in extremes of shoulder motion i. These ligaments increase in laxity due to the extreme range of motion (ROM) in overhead athletes

4. SPORTS BIOMECHANICS

ii. This laxity is necessary for performance; however, overstretching of these ligaments (from throwing) enhances the work of the dynamic stabilizers (RC), thus with potential injury to them 2. Common shoulder injuries a. Anterior instability i. Results from repetitive microtrauma to the anterior static and dynamic stabilizers (A) Stretching the static ligaments (B) Eccentric contractions of the dynamic musculature b. Internal (posterior superior) impingement i. The RC tendons (undersurface of the supraspinatus–infraspinatus junction) and posterior superior labrum are pinched between the greater tuberosity of the humeral head and the posterosuperior glenoid rim, resulting in posterosuperior labral tears and humeral surface tendinosis and tearing ii. Two potential mechanisms: (A) May result from anterior instability (B) May be a normal phenomenon in all shoulders noted at 90° of abduction and ER but becomes a clinical concern from repetitive motion iii. Clinical exam (A) Posterior superior shoulder pain in an apprehension position (B) May improve with scapular retraction and with the relocation test c. Type II superior labral anteroposterior (SLAP) lesion i. Instead of true anterior instability occurring with excessive ER at 90° of abduction, the arc of rotation is shifted such that ER is increased and IR is decreased equally ii. In symptomatic shoulders, this IR loss (glenohumeral internal rotation deficit [GIRD]) greatly exceeds the ER gained iii. GIRD is caused by repetitive eccentric action during deceleration, leading to hypertrophic and tight posterior musculature and posterior inferior capsular soft tissue contracture (A) Side-to-side loss of IR > 20° is consistent with shoulder impingement (B) Side-to-side loss of IR < 20° is usually tolerated well iv. Anterior capsule stretching/laxity may or may not occur v. In order to get the extreme ER range, sheer forces increase at the biceps anchor and posterior superior labrum, which eventually produces a posterior type II SLAP lesion (A) Both internal impingement and posterior SLAP lesions can result in undersurface RC fraying/tears d. Bicipital tendinopathy i. Results from repetitive trauma to the long head of the biceps tendon over the lesser tuberosity during abduction with ER 3. Common elbow injuries a. Medial tension injuries due to high valgus forces i. Little Leaguer’s elbow (A) Injury to the medial elbow in young throwing athletes (B) Includes (1) Medial epicondylitis (2) Traction apophysitis (3) Stress fracture of the medial epicondyle epiphysis ii. Ulnar collateral ligament (UCL) injury (A) During late cocking and early acceleration phases (B) Both “dropped elbow” pitching due to scapular stabilizer fatigue and sidearm pitching due to decreased lateral trunk flexion increase the stress on the UCL and also create less control of the ball (thus, pitchers should keep “elbow up”)

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D. Acceleration 1. Latissimus dorsi and pectoralis major are the primary active internal rotators 2. Subscapularis positions the humeral head in the glenoid and prevents its subluxation 3. Teres minor provides a posterior restraint to limit humeral head translation during this forceful IR a. Posterior RC (teres minor) tenderness is common in pitchers 4. Common injuries a. Subacromial impingement in older pitchers as they internally rotate and adduct the abducted arm during acceleration b. Medial tension injuries such as Little Leaguer’s elbow and UCL injuries (see preceding text) occur in the late cocking and early acceleration phases due to the high valgus forces (64 Nm) reached during these phases E. Deceleration 1. Muscle forces are eccentric, which generate the greatest tensile loads 2. To decelerate rapid IR, eccentric contraction of the posterior shoulder musculature is important, including a. Scapular stabilizers (trapezius at peak activity) b. RC external rotators (teres minor at peak activity) c. Posterior deltoid 3. To decelerate rapid elbow extension, eccentric contraction of the biceps muscle occurs a. Biceps is at peak activity 4. Common injuries a. Posterior instability i. Posterior structures are stressed as they resist glenohumeral distraction and horizontal adduction b. Isolated RC tears c. SLAP lesion i. Due to repetitive traction forces ii. Long head of the biceps eccentrically contracts to decelerate the rapidly extending elbow, which in turn places significant stress on the biceps–labral complex (particularly the anterior superior labrum) d. Bennett lesion i. An extra-articular ossification of the posterior inferior capsule arising at the insertion of the capsule onto the posterior inferior glenoid ii. Peculiar to the baseball pitcher iii. Associated with RC syndrome and/or instability iv. Etiology unclear. Potential mechanisms: (A) Subluxation and impingement of the humeral head on the posterior capsule (B) From a traction injury to the posterior inferior capsule e. Valgus extension overload (VEO) i. Impingement of the posteromedial olecranon against the medial wall of the olecranon fossa from valgus elbow stress combined with elbow extension ii. Repetitive impingement can cause olecranon osteophytes, loose bodies, and scarring iii. Pain at posteromedial olecranon during passive elbow hyperextension with valgus stress iv. Accounts for 65% of surgeries for medial elbow pain in professional baseball players F. Follow-through 1. Low-grade eccentric loading of the shoulder muscles 2. A “passive phase” where the body is merely “catching up” with the throwing arm and thus, a rare potential for injury

4. SPORTS BIOMECHANICS

V. Adaptive Changes With Repeated Throwing A. Shoulder 1. Increased ER range a. Full rotational ROM, or total arc of motion, is still the same as the contralateral shoulder, but ER is increased and IR is decreased (through various means: posterior capsule tightness, anterior instability, progressive retroversion of the humeral head, or all of the above) i. Total arc of shoulder rotation should be ≥ 180°, that is, ER + IR ≥180° ii. Pitchers at risk for impingement symptoms have a total arc ER gain) and/or a side-to-side GIRD of >20° iii. Thus, be certain to measure the full arc of motion (with the scapula stabilized to isolate glenohumeral motion) before deciding if an IR deficit is present b. May lead to anterior instability and impingement due to a shift in the glenohumeral rotation axis 2. Imbalance in shoulder rotator strength a. Normal strength ratio of IR:ER → 3:2 b. A common imbalance: Increased IR strength and decreased ER strength i. Mechanism: Repetitive concentric contraction of IRs during acceleration phase resembles plyometric training, increasing strength. In contrast, repetitive eccentric loading of ERs during deceleration can lead to chronic microtrauma and weakness B. Elbow 1. Increased valgus stress at the elbow causes a breakdown of the medial stabilizing structures—particularly during the late cocking and early acceleration phases (see sections IV.C and IV.E) a. UCL b. Joint capsule c. Medial flexor muscles 2. Elbow flexion contracture sometimes develops from hypertrophy of soft tissues and osseous structures

VI. Types of Pitches A. Determined by the spin imparted onto the ball by the hands and fingers at ball release B. Normal follow-through involves forearm pronation C. “Breaking pitches”—Forearm is relatively supinated at release and then pronates 1. “Curve ball”—Should not have much supination; the curve should come from the wrist D. USA Baseball guidelines (updated in 2015) 1. Curve balls and sliders should not be pitched until puberty has been reached (age 13–14) and bones are “more mature” a. Studies comparing curveball and fastball show no significant difference in injury rate and no significant difference between torques on the shoulder or elbow 2. Youth pitchers should not compete in baseball more than 8 months per year; during the 4 “off” months, they should not compete in other overhead arm sports (competitive swimming, javelin, etc) 3. Age-based pitch count guidelines—see Table 4.1

VII. Common Biomechanical Abnormalities in Pitching A. “Hanging” or “dropped elbow” 1. A sign of fatigue 2. Decreased shoulder abduction allows elbow to drop and thus a reduction in velocity 3. Increased risk of injury to shoulder (RC injury) and elbow (UCL injury) B. “Opening up too soon”

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Table 4.1 Age

2015 MLB and USA Baseball Age-Based Pitch Counts

Pitches per Game

Required Rest 0 days

1 day

Innings per Year

2 days

3 days

4 days

7–8

50

1–20

21–35

36–50

N/A

N/A

60

9–10

75

1–20

21–35

36–50

51–65

66+

80

11–12

85

1–20

21–35

36–50

51–65

66+

80

13–14

95

1–20

21–35

36–50

51–65

66+

100

15–16

95

1–30

31–45

46–60

61–75

76+

100

17–18

105

1–30

31–45

46–60

61–75

76+

100

Note: If a 9-year-old, who is allowed to throw a maximum of 75 pitches per game, throws 66+ pitches, then he would require 4 days of rest, but if he throws 21 to 35 pitches, then he would only require 1 day of rest. MLB, Major League Baseball.

1. Incorrect form: Rotation of shoulders toward home plate during early cocking prior to stride foot making contact with the ground a. Shoulder and hips rotating simultaneously b. Decreased trunk rotation potential energy c. Pitching shoulder will not reach maximal ER d. Increased stress on anterior shoulder, external rotators, and UCL 2. Correct form: Shoulders should remain “closed” with chest facing third base (assuming right-handed pitcher) through early cocking. Once stride foot makes contact with ground, late cocking begins and shoulders rotate toward home plate a. Hips rotate first during early cocking, followed by shoulders in late cocking

SWIMMING I. Four Competitive Strokes A. Freestyle (crawl) B. Backstroke C. Butterfly D. Breaststroke

II. Stroke Phases for A to C (Not Breaststroke) A. Entry/catch 1. Hand entry into water to the beginning of its backward movement B. Pull 1. Beginning of the hand’s backward movement to the hand’s arrival in the vertical plane of the shoulder C. Push 1. Hand’s movement from the vertical plane of the shoulder to its release from the water D. Recovery 1. Hand’s release from the water to its reentry into the water for the next stroke (ie, the aerial return of the hand)

III. Propulsive Phase: Pull and Push A. Pectoralis major and latissimus dorsi

4. SPORTS BIOMECHANICS

1. Move the arm through adduction and IR starting from a stretched position of abduction and ER B. Assistance is provided by the serratus anterior and the IR function of the subscapularis and teres major

IV. Recovery Phase A. Scapular retraction and ER 1. Rhomboids and mid-trapezius retract scapula 2. Posterior deltoid, teres minor, and infraspinatus externally rotate the shoulder B. Midrecovery 1. Hand entry preparation a. Serratus anterior and upper trapezius rotate the scapula upward for shoulder stabilization C. Body roll 1. Nearly 160° 2. Paraspinals and abdominal musculature are important contributors to body roll 3. Lack of body roll = lack of power a. Common in novice swimmers 4. Decreases form drag (see the following text) as the cross-sectional area of the body pushing through the water is decreased 5. Helps with high elbow position during recovery and thus better placement of the hand/ arm for the entry/catch

V. Drag = Water Resistance A. Form drag 1. Dependent on body position 2. The more horizontal the body is in the water, the less is the drag B. Wave drag 1. Turbulence at the water surface created by the moving swimmer 2. Can rebound from the sides or bottom of pool C. Frictional drag 1. Contact of skin and hair with water 2. Body suits (which have recently been banned from many competitions) are used to decrease frictional drag

VI. Lift Force A. Perpendicular to the drag force B. Bernoulli principle 1. Water flows around the hand during the pull and meets on the back edge of the hand, which creates a pressure known as the “lift force”

VII. “S”-Shaped Pulling Pattern A. Designed to continually find still water that is not moving in order to propel the swimmer forward B. A change in coaching technique away from the “S” pull to more of a straight through pull and sometimes somewhere in between C. Other new techniques 1. Earlier catch 2. Earlier exit (at beltline instead of at the trochanter)

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VIII. Kick Patterns A. Knees should flex only 30° to 40° in the flutter kick of the freestyle stroke B. Hip flexion should be minimal C. Two-beat flutter kick 1. One downbeat and one upbeat of each leg during the stroke cycle D. Six-beat flutter kick 1. Three downbeats and three upbeats during one arm cycle E. Whip kick in breaststroke 1. Creates a valgus stress at knee 2. Predisposes to knee injuries (ie, more knee injuries in breaststrokers) a. Medial collateral ligament sprain b. Medial plica/synovitis

IX. Common Stroke Flaws A. Body position 1. Head and shoulders are high in the water and hips/legs are lower a. Sometimes due to lack of kicking b. Decreases horizontal position c. Increases drag force B. Hand entry past midline 1. Exacerbates impingement 2. Creates side-to-side movement a. Increases form drag C. Poor body roll 1. Increased form drag 2. Predisposes to impingement 3. Bilateral breathing increases body roll 4. Ideally, swimmer should roll body 45° D. Excessively straight arm during recovery 1. Predisposes to impingement 2. Teach “high elbow” on recovery E. Striving for too much length in the stroke 1. A long stroke improves propulsion 2. But, the resultant prolonged shoulder adduction and IR may lead to hypovascularity of the supraspinatus and risk of tendinopathy, which hand paddles can exacerbate

X. General Rehabilitation (and Prehabilitation) Principles for the Swimmer A. Most shoulder pain (impingement and RC tendinopathy) in swimmers is due to dynamic muscle imbalances, weakness, and biomechanical faults (and not hard anatomical factors) B. Strengthen scapular stabilization C. Endurance training for serratus anterior and lower trap 1. During swimming, the serratus anterior has been demonstrated to function at 75% of its maximum test ability (ie, it is an overused muscle in swimming) D. Stretch external rotators and posterior capsule using the “sleeper stretch” (Figure 4.2) 1. Not the anterior capsule, which is what many swimmers do regularly (Figure 4.3) 2. This stretch is also useful for throwers to prevent GIRD E. Cervical and thoracic mobilization

4. SPORTS BIOMECHANICS

Figure 4.2

Posterior capsule shoulder stretching with a stabilized scapula (sleeper stretch).

WALKING AND RUNNING I. Walking Gait (Figure 4.4) A. Two phases 1. Stance (60%) a. Loading response (10%) i. Double-limb support occurs in the first and last 10% of stance phase b. Midstance (20%) c. Terminal stance—Propulsive portion of cycle until toe-off and swing begins (20%) d. Pre-swing/toe-off (10%) i. Double-limb support 2. Swing (40%) a. Initial swing (10%) b. Mid-swing (15%) c. Terminal swing (15%) B. Forward momentum for walking is provided by the stance leg

Figure 4.3 Anterior capsule shoulder stretching is commonly performed by swimmers but rarely needed. They should focus their stretching routine on the posterior capsule and external rotators (see Figure 4.2).

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Loading response

0%

Midstance

10%

20%

Terminal stance

30%

40%

Double support

Preswing

50%

Initial

60%

70%

80%

90%

100%

Double support Stance (60%)

Absorption

0%

Terminal swing

Mid

10%

Swing (40%)

Propulsion

20%

30%

Initial swing

40%

50%

Terminal swing

60%

70%

Double float Stance (40%)

80%

90%

100%

Double float Swing (60%)

Figure 4.4

Phases of gait.

Source: Modified from Ounpuu, S. The biomechanics of walking and running. Clin Sports Med. 1994;13(4):843–863. Copyright Elsevier 1994, used with permission.

II. Running Gait A. Two phases 1. Stance phase a. Percentage of gait cycle spent in stance phase is inversely related to speed: i. walking: 60% ii. running: 30–40% iii. sprinting: 20–30% (elite sprinters with smallest percentage of gait devoted to stance) b. Initial contact/absorption i. Lateral foot contacts the ground with the foot slightly supinated ii. Energy absorption is key here (A) Vertical GRF may reach 2.2 × body weight (bw) in running, compared to only 1.1 × bw when walking (B) Subtalar joint pronation, ankle dorsiflexion, and knee and hip flexion help to dissipate forces (C) Eccentric contractions of the proximal muscles prevent excessive hip and knee flexion and falling to the ground iii. Hip adductors provide stability (A) Adductors are active throughout the running cycle (different than walking), limiting horizontal displacement of foot strike

4. SPORTS BIOMECHANICS

c. Midstance i. Dorsiflexion maximizes and results from forward progression of the tibia while foot is on the ground ii. Supination starts the propulsive phase as the heel begins to lift off the ground d. Toe-off/propulsion 2. Swing a. Initial swing i. First float occurs in initial swing (neither foot contacts ground) b. Mid-swing c. Terminal swing i. Second float occurs in terminal swing B. Forward momentum needed for running is provided by the swinging leg and arms C. Most kinematic differences between walking and running occur in the sagittal plane of motion 1. The body lowers its COG by increasing a. Hip flexion b. Knee flexion c. Ankle dorsiflexion D. As speed increases, stance phase lessens 1. This increases the velocity and range of lower limb motion a. Serves to minimize vertical displacement 2. Energy costs increase 3. Foot contact changes as speed increases a. Walking and jogging: Heel to toe b. Running: Foot strikes with forefoot and heel simultaneously or forefoot initially followed by heel lowering to the ground i. Research suggests that even in elite distance competitions, the majority of runners actually rear-foot-strike (RFS) (see foot strike patterns in the following text) c. Sprinting: Maintains weight-bearing on the forefoot from contact to toe-off E. Foot strike patterns 1. Evolutionary hypothesis a. Running necessary for survival b. Forefoot running evolved to protect foot and reduce injury c. But cushioned soles encourage RFS both by plantar-flexing the foot and by allowing runners to heel strike comfortably 2. Biomechanics a. Forefoot strike (FFS) versus RFS i. FFS decreases GRF of impact peak and decreases joint torques (Figure 4.5) ii. FFS more efficiently converts translational into rotational energy b. Barefoot running versus shod i. Barefoot running decreases peak GRF and slows rate of loading (if done appropriately with FFS) ii. Barefoot running increases preactivation of plantar flexors iii. Barefoot running decreases torque pressures at anatomical sites prone to osteoarthritis and patellofemoral syndrome F. Angle of gait 1. Angle between the longitudinal bisection of the foot and the line of progression 2. Walking = 10° 3. Running = approaches 0° as foot strike is on the line of progression, which allows more efficient locomotion by limiting lateral deviation of the COG (ie, decreased base of support)

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I: GENERAL TOPICS

3

Active peak Impact peak

Body weight

36

2

1

Slope = rate of loading

75

Figure 4.5

150 Time (ms)

225

300

Ground reaction forces of rear foot strike running.

III. Pronation A. Triplanar motion 1. Ankle dorsiflexion 2. Subtalar eversion 3. Forefoot abduction B. Effect of pronation up the kinetic chain 1. Tibial IR 2. Knee flexion and adduction (valgum) 3. Femoral IR 4. Hip flexion and adduction 5. Pelvis rotates anteriorly 6. Lumbar spine extends and laterally flexes to the same side C. Pronation phase (first half of stance phase) of gait involves mostly eccentric muscular contractions to provide joint control and shock absorption

IV. Supination A. Triplanar motion 1. Ankle plantar flexion 2. Subtalar inversion 3. Forefoot adduction B. Effects of supination up the kinetic chain 1. Tibial ER 2. Knee extension and abduction (varum) 3. Femoral ER 4. Hip extension and abduction 5. Pelvis rotates posteriorly 6. Lumbar spine extends and laterally flexes to opposite side C. Supination phase (second half of stance phase) of gait involves mostly concentric muscular contractions (particularly gluteals) to provide acceleration and propulsion

V. General Rehabilitation (and Prehabilitation) Principles for the Runner A. Core stabilization

4. SPORTS BIOMECHANICS

B. Pelvic girdle stabilization 1. Hip abductor neuromuscular reeducation and strengthening and endurance training C. Hip flexibility D. Ankle and foot flexibility to better accommodate ground reaction forces

JUMPING AND LANDING I. Noncontact Anterior Cruciate Ligament (ACL) Injury Prevention Programs Have Attempted to Influence a Variety of Noncontact ACL Injury Risk Factors A. Balance B. Flexibility C. Strength D. Jumping and landing technique

II. ACL Injuries Occur More Frequently With the Knee in Less Flexion A. Greater knee extensor loads B. Greater anterior tibial translation forces

III. Gender Differences That May Predispose Female Athletes to Noncontact ACL Injuries A. Females 1. Land more erect with less knee and hip flexion 2. Land with less hip ER and abduction 3. Increased quadriceps activation over hamstrings (less knee flexion/greater knee extension force)

IV. Teaching Appropriate Jumping/Landing Techniques Is Important in ACL Injury Prevention Programs A. Increase knee and hip flexion during landing B. Balance quadriceps to hamstring activation ratio

CYCLING I. The Key to Assessing the Injured Cyclist Is Assessing the Bike Fit and How the Rider Interacts, Statically and Dynamically, With the Bike. Static Bike Fits Are Still Quite Common, Though Many Clinicians (Who Treat Cyclists) and Coaches (Who Train Cyclists) Are Using Modern Bike Fit Technology to Assess the Rider Dynamically and How the Cyclist Interacts With the Bike (see section III) for Injury Prevention and Performance Enhancement II. Static Bike Fit A. Saddle height 1. Measured from a straight line taken from the saddle down the seat tube through the crank axis to the pedal at the bottom of downstroke 2. Appropriate height a. Knee flexion angle of 20° to 30° when the pedal is at the bottom of downstroke and foot is neutral, or b. Riders inseam length × 0.883 3. Should not have pelvic tilt when seat height is optimal a. Improves quadriceps power b. Improves core stability 4. Saddle too high

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a. Power is diminished b. Excess stress on the posterior structures i. Hamstrings, gastrocnemius, and posterior knee joint capsule c. Excessive hip extension i. Loss of pelvic and core stability ii. Pelvis rocks from side to side iii. Fatigues adductors, gluteals, spine/core, and upper body musculature 5. Saddle too low a. Power is diminished—due to suboptimal length–tension relationships of lower limb musculature b. Increased knee flexion throughout the pedal cycle i. Patellofemoral pain ii. Suprapatellar bursa loading B. Saddle fore/aft position 1. Plumb line dropped from the inferior pole of the patella should fall over the front pedal spindle (or up to 2 cm behind) when the cranks are in the horizontal position (3 o'clock position) 2. Check cleat positioning a. First metatarsal head should lie directly over the pedal axel 3. Too far forward (similar presentation as saddle too low) a. Knees are more flexed, hips more extended b. Increased patellofemoral loading c. More upright position i. Less aerodynamic ii. May need to raise the saddle height if the saddle needs to be so forward 4. Too far back a. Hamstrings and gluteals will be overlengthened i. Inhibits force production C. Saddle tilt 1. Close to level or parallel to ground 2. 10° to 15° of anterior tilt may reduce low back pain 3. Aerobar users (time trialists/triathletes) prefer a slight downward/anterior tilt to decrease perineal pressure D. Stem and handlebar height 1. Affects “reach” 2. Appropriate reach a. Pelvis is tilted forward so that the back is flat without kinks in the thoracolumbar and cervicothoracic junctions b. Shoulder girdle is not excessively protracted c. Slight elbow flexion with hand on brake hoods 3. Different-sized stems can optimize reach if the frame (top tube length) is properly fitted 4. Drop between saddle height and top of handlebars a. Usually 3 to 5 cm, but range is 0 to 8 cm b. Larger drop i. More aerodynamic ii. Only effective if the rider has the postural stability and flexibility to control the bike in this position 5. Wrists held in neutral a. Prolonged weight bearing on the ulnar aspect of an extended wrist can compress the ulnar nerve in Guyon’s canal

4. SPORTS BIOMECHANICS

III. Dynamic Fit A. Video analysis B. Wattage measure (power output) 1. Once a fit change has been made, assess the power output; if the power output improves, the change made will likely improve performance C. Heart rate 1. Heart rate (similar to power output) can be used as a performance measure to determine if a static fit change is beneficial D. Pedal torque measurement and spin analysis 1. Can help even out the pedal stroke so the rider is pulling up during the upstroke (or recovery phase) via dorsiflexion, knee flexion, and hip flexion, as well as pushing down during the downstroke (or power phase) via hip extension, knee extension, and plantarflexion

IV. Specific Injuries The upper extremities are more susceptible to traumatic injury while the lower body is more susceptible to overuse injury. A. Knee 1. Anterior knee pain a. Saddle too low or far forward b. Excessive climbing/hilly rides c. Pushing too high of a gear/low revolutions per minute d. Cranks too long 2. Medial knee pain a. Toes pointing out with cleats b. Too much pedal float c. Feet too far apart 3. Lateral knee pain a. Toes pointing in with cleats b. Too much pedal float c. Feet too narrow 4. Posterior knee pain a. Saddle too high or far back B. Ankle/foot 1. Achilles tendinopathy a. Saddle height too high (excessive stretch) b. Saddle height too low (pushing heel down excessively to generate more power) C. Spine 1. Cervical or thoracic pain a. Reach too great b. Handlebars too low 2. Lumbar pain a. Overstretched riding position (handlebars too low or too forward) b. Poor pelvic and hip mobility causing pelvic rocking, commonly seen when saddle is too high D. Neuropathy 1. Perineal: Pain, numbness, sexual dysfunction, impotence, and urinary incontinence are all symptoms of both pudendal nerve entrapment and ischemic neuropathy secondary to decreased tissue perfusion a. Saddle too high b. Saddle tilt excessive c. Saddle too narrow (not supporting the ischial tuberosities)

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2. Hand: Ulnar distribution more common than median. Usually transient neuropraxia a. Incorrect hand positioning or overly tight grip b. Prolonged riding c. Stationary biking d. Poor glove/handlebar padding

Recommended Reading 1. Barton C, Collins N, Crossley K. Clinical aspects of biomechanics and sports injuries. In: Brukner P, Khan K, eds. Clinics in Sports Medicine. McGraw-Hill, Australia; 2014:61–112. 2. Escamilla RF, Andrews JR. Shoulder muscle recruitment patterns and related biomechanics during upper extremity sports. Sports Medicine. 2009;39(7):569–590. 3. Fleisig GS, Andrews JR. Prevention of elbow injuries in youth baseball pitchers. Sports Health. 2012;4(5): 419–424. doi:10.1177/1941738112454828. 4. Kibler WB, Kuhn JE, Wilk K, et al. The disabled throwing shoulder: spectrum of pathology—10-year update. Arthroscopy: The Journal of Arthroscopic & Related Surgery. 2013;29(1):141–161. 5. Lieberman DE, Venkadesan M, Werbel WA, et al. Foot strike patterns and collision forces in habitually barefoot versus shod runners. Nature. 2010;463(7280):531–535. 6. Meuller FO, Marshall SW, Goldberg B. The learning curve: Little League® seeks to address concerns, answer questions about curveballs & overuse. University of North Carolina Department of Exercise and Sports Science; 2011. http://www.littleleague.org/Assets/forms_pubs/media/UNCStudy.pdf. 7. Nissen CW, Westwell M, Õunpuu S, et al. A biomechanical comparison of the fastball and curveball in adolescent baseball pitchers. American Journal of Sports Medicine. 2009:37(8):1492–1498. 8. “Pitch Smart” Guidelines for Youth and Adolescent Pitchers. MLB Advanced Media and USA Baseball; 2014. www.Pitchsmart.org. 9. Pollard H, Fernandez M. Spinal musculoskeletal injuries associated with swimming: A discussion of technique. ACO. 2004;12:72–80. 10. Silberman, MR. Bicycling injuries. Current Sports Medicine Reports. 2013:337–345. 11. Yu B, Lin CF, Garrett WE. Lower extremity biomechanics during the landing of a stop-jump task. Clin Biomech. 2006;21:297–305.

5 Pharmacology Jeffrey L. Tanji

I. Therapeutic Drugs A. Analgesics 1. Acetaminophen a. Mechanism of action i. Exact mechanism unclear ii. May elevate pain threshold, may affect inhibition of the nitric oxide pathway mediated by a variety of neurotransmitter receptors including N-methyl-daspartate and substance P iii. Fever reduction by inhibition of endogenous prostaglandins in the central nervous system (CNS) iv. Little to no anti-inflammatory effects b. Indications i. Excellent safety profile ii. Good initial choice (A) First-line agent for mild to moderate osteoarthritis (1) American College of Rheumatology (2) American Academy of Orthopedic Surgery (3) American Pain Society (B) First-line agent for medically complex patients (1) American Geriatric Society: Mild to moderate musculoskeletal (MSK) pain in those over 50 (2) American Heart Association: For those with cardiac conditions or risk factors (3) National Kidney Foundation: For those with underlying renal conditions iii. Temporary relief of minor aches and pains associated with the common cold, headache, toothache, muscular aches, backache, minor pain of arthritis, menstrual cramps, and for reduction of fever iv. Superior gastrointestinal (GI) safety compared to nonsteroidal anti-inflammatory drugs (NSAIDs) c. Contraindications i. Chronic alcoholics may be at risk for liver disease, but some conflicting reports ii. Reportedly safe in chronic, stable liver disease, but some conflicting evidence iii. Overdose in conjunction with taking anticonvulsants may increase risk of liver injury iv. High caffeine intake may elevate risk

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v. Recommended maximum daily dose 3,000 mg/d, narrow safety window vi. Maximum daily recommended dose higher in some European countries, but may lead to higher toxicity 2. Opioids a. Mechanism of action i. Bind opioid receptors, primarily mu, kappa, and delta ii. CNS and peripheral effects iii. Codeine conversion into morphine in liver dependent on cytochrome P-450, may not be efficacious in some populations iv. Propoxyphene adds little analgesia to acetaminophen, has been withdrawn from market in the United States, available in Australia b. Indications i. Moderate to severe pain ii. Cough (eg, codeine) iii. Diarrhea (eg, loperamide) c. Contraindications i. Hypersensitivity/allergy ii. Concern regarding combination medications (acetaminophen toxicity) iii. Dependency versus addiction iv. Increased scrutiny from Food and Drug Administration (FDA), also concern with combination medications and additional acetaminophen use leading to liver toxicity v. Drug testing may limit use (see Table 5.1) vi. Relative potency (Table 5.1) 3. Tramadol a. Mechanism of action i. Synthetic analog of codeine ii. Low affinity for opioid receptors, but primary metabolite has a high affinity for opioid receptors iii. Only partially inhibited by naloxone iv. Norepinephrine and serotonin reuptake inhibition also part of the mechanism of action v. Available as combination medication with acetaminophen b. Indications i. Moderate to severe pain

Table 5.1

Potency of Opioid Medications Relative to Morphine

Medication Dextropropoxyphene (no longer available in the United States)

Morphine Equivalent 0.025

Codeine

0.1

Demerol

0.36

Hydrocodone

0.6

Morphine

1.0

Oxycodone Fentanyl

1.5–2 75–100

5. PHARMACOLOGY

c. Precautions i. Taking tramadol and selective serotonin reuptake inhibitors can predispose to serotonin syndrome B. Antibiotics 1. Penicillin and derivatives a. Mechanism of action i. Weaken bacterial cell wall by inhibiting formation of peptidoglycan cross-links b. Little research on athletic performance c. May be overprescribed for elite athletes for nonbacterial conditions d. Many athletes fear adverse effects i. GI side effects may impair performance 2. Fluoroquinolones a. Mechanism of action i. Inhibit bacterial enzymes responsible for DNA replication and transcription b. Contraindications i. Known hypersensitivity ii. CNS conditions: epilepsy, stroke, meningitis iii. Prolonged QT syndrome iv. Children: Risk of growth plate injury, tendon rupture c. Risks i. May cause tendinopathy or spontaneous tendon rupture (particularly in the over50 age group and in patients taking corticosteroids) C. Antidiabetic agents 1. Insulin and oral medication doses may need to be adjusted during periods of exercise 2. Injection site not recommended to be at area of primary muscle use (eg, thigh for cyclist) due to increased uptake during exercise, which may lead to hypoglycemia 3. May be used as performance enhancer: Produces similar anabolic effects to insulinlike growth factor-I (IGF-I) when taken with glucose 4. Thiazolidinediones a. Mechanism of action i. Complete mechanism unclear ii. Lowers insulin resistance iii. Pioglitazone (Actos®) reduces triglycerides and increases high-density lipoprotein (HDL) iv. Rosiglitazone (Avandia®) increases HDL and slightly increases low-density lipoprotein (LDL), less interaction with oral contraceptives and erythromycin v. Generally not first-line agent b. Risks/side effects i. Upper respiratory infections and sinusitis ii. Headaches iii. Anemia iv. Fluid retention, which may lead to congestive heart failure (CHF) v. Weight gain vi. Muscle pain vii. Increased risk of fracture in women viii. Possible risk of liver damage, as seen in older thiazolidinediones 5. Sulfonylureas a. Mechanism of action

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i. Increase amount of insulin produced by the pancreas ii. Combination medications contain metformin, decrease amount of glucose produced by the liver iii. Long acting iv. Dose adjustment may be necessary to prevent hypoglycemia during competitive or training activity v. Glipizide (Glucotrol®) vi. Glyburide (DiaBeta®) vii. Glimepiride (Amaryl®) b. Risks/side effects i. Sulfa allergy cross-reactivity ii. Teratogenic, do not take while pregnant or if trying to become pregnant iii. Unsafe if liver or kidney problems, metabolized by liver, excreted via kidneys iv. Alcohol increases risk of low blood sugar v. Hyperinsulinemia may lead to increased cardiovascular disease vi. May cause weight gain 6. Meglitinides a. Mechanism of action i. Novel agents ii. Increase amount of insulin produced by pancreas, similar to sulfonylurea agents iii. Faster acting, shorter duration iv. Repaglinide (Prandin®) v. Nateglinide (Starlix®) b. Risks/side effects i. May not be safe in pregnancy ii. Similar side effects as sulfonylureas iii. May not be safe in liver or renal disease 7. Biguanides a. Mechanism of action i. Not completely understood ii. Decrease glucose production in liver iii. Increase glucose absorption in muscle iv. Decrease insulin resistance v. Metformin (Glucophage®) most commonly used antidiabetic drug in the world (A) Does not increase insulin production (B) Not associated with hypoglycemia b. Risks/side effects i. Nausea ii. Loss of appetite iii. Diarrhea iv. Increased abdominal gas v. Metallic taste vi. Rarely lactic acidosis during exercise, may limit use in athletes. Higher likelihood if liver or kidney problems exist and is associated with dehydration vii. Contraindicated in renal impairment (creatinine over 1.4) c. Increasingly used for the following indications in the United States i. Polycystic ovary syndrome ii. Nonalcoholic fatty liver disease iii. Premature puberty

5. PHARMACOLOGY

D. Antihypertensives: Joint National Committee 8 (2014) recommends the initial use of a thiazide diuretic, calcium channel blocker, angiotensin-converting enzyme (ACE) inhibitor or angiotensin II receptor blocker (ARB) in the general non-Black population or a thiazide diuretic or calcium channel blocker in the general Black population 1. ACE inhibitors a. Mechanism of action i. Inhibit ACE ii. Decrease production of angiotensin II iii. Dilation of blood vessels leads to lower blood pressure b. Indications i. Elevated blood pressure ii. CHF iii. Stroke prevention iv. Improve postmyocardial infarction survival v. Renal impairment c. Contraindications i. Not for use in pregnant individuals ii. Not for use if renal artery stenosis iii. Hypersensitivity d. Risks/side effects i. Cough ii. Increase potassium levels iii. Hypotension, dizziness iv. Headache v. Weakness vi. Rash vii. Metallic taste viii. May increase lithium levels 2. Calcium channel blockers a. Mechanism of action i. Dilate blood vessels ii. Decrease resistance to blood flow iii. Decrease cardiac oxygen requirement b. Indications i. Hypertension (HTN) ii. Angina iii. Abnormal cardiac rhythms c. Contraindications i. Verapamil and diltiazem reduce heart rate and strength of contraction, may not be best in those with CHF or in athletes ii. Amlodipine has little effect on heart rate, so poor choice if treating an arrhythmia, but good choice for athletes d. Risks/side effects i. Verapamil and diltiazem decrease elimination of many drugs by liver ii. Grapefruit juice may elevate concentrations of some calcium channel blockers iii. Common side effects include constipation, nausea, headache, rash, edema, hypotension 3. ARBs a. Mechanism of action i. Block action of angiotensin II, a potent blood vessel constrictor

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ii. Decrease blood pressure iii. Decrease cardiac work b. Indications i. HTN ii. Prevention of kidney failure in those with HTN or diabetes iii. May prevent recurrence of atrial fibrillation iv. Used when ACE inhibitors not tolerated, for example, due to cough c. Contraindications i. Pregnancy due to birth defects ii. Hypersensitivity iii. Renal artery stenosis iv. Not for use in combination with ACE inhibitors d. Risks/side effects i. Cough ii. Hyperkalemia iii. Hypotension iv. Dizziness v. Headache vi. Rash vii. Diarrhea viii. Metallic taste 4. Diuretics a. Mechanism of action i. Increase sodium chloride excretion in urine ii. Distal tubule (hydrochlorothiazide [HCTZ]) or loop segment (furosemide) is site of action b. Indications i. HTN, often initial choice in general population ii. Fluid retention c. Contraindications i. Pregnancy ii. Limited use in athletic population since it is a prohibited substance (used as a masking agent) d. Risks/side effects i. Volume depletion—May predispose to dehydration ii. Potassium imbalance iii. Decreased athletic performance iv. May contribute to cardiac events 5. Beta-blockers a. Mechanism of action i. Slow heart rate by decreasing response to sympathetic input ii. Decrease contraction of smooth muscle in peripheral arteries and airways iii. Slow resting heart rate iv. Decrease cardiac response to exercise v. Adverse affect on cardiovascular training b. Indications i. HTN ii. Tachycardia, rate control iii. Angina iv. Postmyocardial infarction drug of choice c. Contraindications i. May increase asthma symptoms

5. PHARMACOLOGY

ii. Prohibited substance for participation in several sports (shooting, archery, powerboating) due to antianxiety effects d. Risks/side effects i. Depression ii. Fatigue iii. Male impotence iv. Increased wheezing v. Nightmares vi. Impaired athlete performance E. Asthma medications 1. Anti-inflammatories (glucocorticoids) a. Mechanism of action i. Inhaled glucocorticoids upregulate gene expression of anti-inflammatory proteins, downregulate gene expression of proinflammatory proteins b. Indications i. Treatment of choice for chronic asthma ii. Second-line agent after rescue inhaler for asthma c. Contraindications i. Hypersensitivity to glucocorticoids ii. Should not be used as a rescue agent (ie, takes 1–3 weeks for effect) d. Risks/side effects i. Chronic use may lead to osteopenia/osteoporosis ii. Thrush, especially in older population iii. Hoarseness 2. Khellin derivatives—Often used in children for mild symptoms a. Derived from plant Ammi visnaga i. Bronchodilators, inhibit histamine release from mast cells ii. Cromolyn sodium (Intal®)—Indicated for those ≥2 years of age iii. Nedocromil sodium (Tilade®)—Indicated for those ≥6 years of age 3. Antileukotrienes a. Mechanism of action i. Block leukotriene-induced bronchoconstriction ii. Block leukotriene synthesis (zileuton) or receptors (zafirlukast/montelukast) iii. Decrease inflammation, rapid onset b. Indications i. Allergy and asthma symptoms c. Contraindications i. Hypersensitivity ii. Phenylketonurics should not be used, contain phenylalanine (aspartame) d. Risks/side effects i. Zileuton not approved for children, requires hepatic testing ii. Runny nose, headache, fever, stomach pain, diarrhea 4. Bronchodilators a. Mechanism of action i. Relax bronchial smooth muscle ii. Decrease mucus secretion b. Indications i. Inhaled short-acting β2-agonists (A) Main rescue medication, first-line treatment (B) Oral forms not approved by the National Collegiate Athletic Association (NCAA) or World Anti-Doping Agency (WADA) ii. Long-acting β2-agonists such as salmeterol (Serevent®)

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(A) Twelve-hour duration, not rescue/acute medication (B) Associated with increased risk of death associated with asthma c. Risks/side effects i. Oral medication (clenbuterol) banned due to anabolic effects. Not an ingredient in any FDA-approved drugs in the United States F. NSAIDs/cyclooxygenase-2 (COX-2) inhibitors 1. No evidence to suggest individual superiority for pain a. May be individual patient preference b. Dose-dependent side effects c. Lower doses may provide analgesic effect d. Higher doses have anti-inflammatory effect 2. Conventional NSAIDs block COX-1 and COX-2 a. Pain/inflammation b. Prostaglandins in GI tract c. Renal dysfunction d. Platelet inhibition 3. COX-2 specific (eg, celecoxib) a. Decreased GI toxicity b. Increased cardiovascular risks 4. COX-2 selective (eg, etodolac, meloxicam) a. Decreased GI side effects b. Unknown cardiovascular risks c. Etodolac with higher COX-2 selectivity 5. General properties a. Mechanism of action i. Block COX, reduce prostaglandins b. Indications i. Pain ii. Fever iii. Inflammation iv. Arthritis c. Contraindications i. Hypersensitivity ii. Children and adolescents recovering from viral illnesses such as chicken pox or influenza should avoid aspirin (ASA) due to the risk of Reye’s syndrome iii. Avoid ASA and conventional NSAIDs if known or high risk of GI ulcers d. Risks/side effects i. Renal disease ii. GI bleeding, ulcers iii. Headache, rash, nausea, vomiting iv. GI protective capacity of COX-2 agents mitigated by concomitant ASA use v. Animal studies suggest COX-2 may affect ligament strength, no clinically demonstrated difference in human muscle strength G. Viscosupplementation 1. Hyaluronic acid (HA) is an unbranched, high-molecular-weight polysaccharide 2. Distributed throughout the body, especially as a major component of the synovial fluid and of cartilage 3. Primary role of the HA in synovial fluid and cartilage is to maintain the viscoelastic structural and functional characteristics of the articular matrix a. Mechanisms of action i. Rheological

5. PHARMACOLOGY

(A) Immediate restoration of synovial fluid rheologic properties (ie, restoration of viscosity and elasticity) (B) Maintenance of increased rheological properties for 3 to 7 days after injection (C) Antinociceptive effect (D) Mechanical sponge or sieve (ie, assist with removal from the joint of immune complexes and inflammatory cells) ii. Biological (A) Anti-inflammatory effect (B) Effect on immune cells (C) Restoration of hyaluronate synthesis; positive feedback for endogenous hyaluronate synthesis (D) Effects on cartilage: Increased biosynthesis, decreased degradation (E) Effects on chondrocytes: Decreased apoptosis, proliferation (F) Antioxidant effect b. Indications i. Multiple brands of viscosupplementation (Synvisc®, Hyalgan®, Supartz®, Orthovisc®, Euflexxa®) ii. Differences based on molecular weight and how they are produced (eg, Euflexxa® is bacterially derived, Orthovisc® is synthetic, all of the rest are derived from rooster combs) iii. Strength gains demonstrated after viscosupplementation, due to pain relief iv. Supported by the Cochrane database (2007) for knee osteoarthritis c. Contraindications i. Known allergy ii. Allergy to poultry/eggs (except Euflexxa® and Orthovisc®) d. Risks/side effects i. Local reaction, hypersensitivity ii. Injection site pain iii. Infection iv. Bleeding H. Corticosteroids 1. Various routes—Oral, inhaled, injected, topical, iontophoresis/phonophoresis 2. Limited efficacy studies, both for acute and chronic conditions 3. Injection complications a. Fat pad atrophy and hypopigmentation most common b. Injection into tendon not recommended due to risk of tendon rupture, but paratenon injection is probably safe c. Use remains controversial 4. Systemic use is prohibited when administered orally, rectally, or by intravenous (IV) or intramuscular (IM) injection 5. Topical preparations for skin, ophthalmic (eye), otic (ear), nasal, buccal cavity (mouth), and iontophoresis or phonophoresis are permitted 6. Intra-articular and epidural injections are also permitted I. General athletic concern: photosensitivity reaction 1. Diuretics, antipsychotics, older-generation antidepressants, hypoglycemics, cardiovascular drugs, and antimalarials 2. NSAIDs, antimicrobials, antihistamines (diphenhydramine, loratadine), and estrogen/ progesterone a. Most photoactive NSAIDs are the 2-arylpropionic acid derivatives (ibuprofen, naproxen, ketoprofen)

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b. Other NSAIDs include diclofenac, piroxicam, indomethacin, sulindac, and the COX2-specific inhibitors c. Antibiotics include the tetracyclines (lower incidence with doxycycline and minocycline), the fluoroquinolones, and sulfamethoxazole d. In female athletes, combined oral contraceptive use and topical medicines such as the retinoid creams for acne

II. Performance-Enhancing (or Potentially Performance-Enhancing) Agents/Drugs A. History 1. Long history of “doping” a. Chinese Emperor Shen-Nung depicted with Ephedra b. Ancient Olympians drank herbal teas and ate mushrooms c. The late 1800s’ cycling death due to overdose 2. Gradual process of fighting against performance-enhancing drugs a. First listed banned substances by the International Olympic Committee (IOC) Medical Commission in 1967 b. Other medications added to the list, some as masking agents 3. Doping a. Original use of term controversial i. South African dialect ii. Boers religious festivity infusion: the doop iii. Amsterdam canal workers: doopen 4. Modern Olympics a. Amphetamines b. Later anabolic steroids c. Both had prior military applications B. Definition 1. Two of three affirmative to define doping a. Use of substances or methods that artificially increment performance b. Substances or methods that are harmful to athletes c. Substances or methods that are against the spirit of the games C. Structure 1. Multiple organizations involved in determining banned substances, developing rules for testing, setting punishments a. IOC i. Anti-Doping Resolution passed: 1962 ii. Banned substance list: 1967 iii. First testing: Mexico Olympics, 1968 2. WADA a. Idea developed after 1998 Tour de France i. Due to difference between governments and International Cycling Federation b. Took over many aspects of antidoping movement from the IOC after Sydney, 2000 c. WADA now based in Montreal, Canada d. The Code: Document that provides the framework for antidoping policies, rules, and regulations within sport organizations and among public authorities to harmonize antidoping policies and to insure standards 3. Many other leagues/sports perform their own antidoping efforts a. Various international sport federations b. National Football League (NFL) c. Major League Baseball (MLB) d. NCAA

5. PHARMACOLOGY

D. Categories of performance-enhancing agents 1. Any substance without approval by government health agency for human use 2. Substances prohibited at all times (in-competition and out-of-competition) a. Anabolic steroids i. Initially developed after World War II to treat emaciated prisoners of war (POWs) ii. 1954: Soviet athletes began using steroids iii. Used for strength gains, speed, endurance, healing injury (A) Applicable to nearly all sports iv. Initial control in London, 1974 v. Added to IOC banned list in 1975 (prior to the Montreal Olympiad) vi. WADA list of 2015 includes (A) Endogenous: Androstenediol, androstenedione, dehydroepiandrosterone (DHEA), epitestosterone (B) Exogenous: Bolasterone, boldenone, danazol, desoxymethyltestosterone, drostanolone, methasterone, methyl-1-testosterone, methyltestosterone, prostanozol, nandrolone, norbolethone, oxandrolone, stanozolol, tetrahydrogestrinone (THG), trenbolone, and similar substances (C) Other: Clenbuterol, selective androgen receptor modulators (SARMs), tibolone, zeranol, zilpaterol vii. Risks (A) Implicated in liver disease (B) Psychiatric effects: Mood swings, aggression (C) Overall limited data despite decades of use/abuse b. Peptide hormones, growth factors, related substances i. Erythropoiesis-stimulating agents (A) Erythropoietin (EPO) (B) Darbepoetin (dEPO) (C) Peginesatide (Hematide) (D) Continuous erythropoietin receptor activator (CERA) (E) Used by endurance athletes (F) Risks (1) Implicated in cyclist deaths due to hyperviscosity, thrombosis ii. Chorionic gonadotrophin and luteinizing hormone (males) iii. Insulins iv. Corticotrophins v. Growth hormones and growth factors (eg, IGF, platelet-derived growth factor, vascular-endothelial growth factor) c. β2-agonists i. All inhaled β2-agonists allowed ii. Salbutamol (via inhalation) has a maximum allowable urine concentration (A) Max 1,600 μg/24 h (B) Urine concentration >1,000 ng/mL presumed to be adverse analytic finding, requires proof that results are due to intended therapeutic use d. Hormone antagonists and analogs i. Aromatase inhibitors ii. Selective estrogen receptor modulators (A) Tamoxifen iii. Antiestrogen substances iv. Myostatin inhibitors e. Diuretics i. Lasix ii. HCTZ

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iii. Risks include dehydration, electrolyte disturbances, and environmental illness (eg, heat stroke) f. Masking agents i. Diuretics ii. Plasma expanders (A) Glycerol (B) Dextrose 3. Prohibited methods in-competition and out-of-competition a. Enhancement of oxygen transfer i. Blood doping (A) Includes autologous, homologous, or heterologous blood or blood products (B) Artificial enhancement of uptake, transport, or delivery of oxygen (1) Perfluorochemicals (2) Efaproxiral (RSR13) (3) Hemoglobin substitutes (4) Does not include supplemental oxygen ii. Chemical and physical manipulation (A) Tampering with samples (B) IV infusions, except those for legitimate medical reasons (C) Sequential withdrawal, manipulation, reinfusion of whole blood iii. Gene doping (A) Transfer of nucleic acids or nucleic acid sequences (B) Use of genetically modified cells (C) Use of agents that alter gene expression (1) Peroxisome proliferator–activated receptor gamma 4. Substances prohibited in-competition a. Stimulants i. Initially developed in World War II for military use ii. 1940s: Football, 1950s: other sports iii. Amphetamines have demonstrated and perceived positive effects on selfconfidence, mood, attention, aggression, and energy iv. Over-the-counter (OTC) stimulants such as phenylpropanolamine, ephedrine, and pseudoephedrine became substitutes for amphetamines in the 1970s v. Phenylpropanolamine and ephedra-containing supplements banned by the Drug Enforcement Administration (DEA), 2004 vi. Modafinil/adrafinil (A) Developed in France, only modafinil legal in the United States (B) Not picked up on urine tests for stimulants vii. Bupropion, caffeine, phenylephrine, phenylpropanolamine, pipradrol, synephrine are not considered prohibited viii. Adrenalin associated with local anesthetic injection not prohibited ix. Ephedrine/methylephedrine/pseudoephedrine prohibited in competition b. Narcotics i. Prohibited: Buprenorphine, morphine, hydromorphone, methadone, oxymorphone, fentanyl, oxycodone, others ii. Not prohibited: Codeine c. Cannabinoids i. Natural (A) Cannabis, hashish, marijuana ii. Synthetic (A) Delta-9 tetrahydrocannabinol (THC)

5. PHARMACOLOGY

iii. Cannabimimetics (A) “Spice” d. Glucocorticoids i. Prohibited oral, IV, IM, rectal 5. Sport-specific prohibition a. Alcohol >0.10 g/L i. Archery, aeronautic, automobile, karate, motorcycling, powerboating, bowling b. Beta-blockers i. Aeronautic, archery (also prohibited out-of-competition), billiards, bobsleigh, boules, bridge, curling, darts, golf, motorcycling, pentathlon (shooting), bowling, powerboating, sailing, shooting (also prohibited out-of-competition), skiing, snowboarding, wrestling 6. Other agents a. Creatine i. Nitrogenous amino acid compound produced by the liver ii. Phosphocreatine, energy store for adenosine triphosphate (ATP) in muscle iii. Discovered in the 1830s, supplement since the early 1900s iv. Mainly for short, high-intensity exercise v. Potential complications (A) Renal dysfunction (B) Liver dysfunction (C) Muscle cramping (D) Compartment syndrome 7. Nutritional supplements a. Supplies one or more nutrients purported to be missing from an athlete’s diet b. Many with unclear benefits/harm c. Rationale i. To maintain an adequate nutritional balance in terms of quality and correct quantities of specific nutrients (eg, not less than minimal but not beyond the maximum safe daily macronutrient and micronutrient requirements) ii. To minimize any deterioration in physical or mental performance caused by possible daily life- or exercise-related reduction in the physiological quantity of essential nutrients in the body iii. To improve muscle protein balance when necessary for clinical purposes (eg, aging, sarcopenia) iv. To reduce possible exercise-related, oxidative stress–linked damage (eg, antioxidants: use of vitamin C, vitamin E, and beta carotene) d. Some have banned substances. Occasionally, this is due to contamination at the manufacturing facilities e. NFL: Multiple banned companies, including General Nutrition Center, Met-Rx®, Metabolife® f. NCAA: “Ignorance is no excuse. What you don’t know can hurt your eligibility” g. Belief in supplements/ergonomic aids is driving force, without real consideration of effectiveness or risks h. Amino acids/branched chain amino acids (BCAA) E. Drug testing 1. NFL: New York, New York, USA a. Banned Substance List, Steroid Policy, and so on i. Banned Substances List NFL Players Association, Rules and Regulations 2. NCAA: Indianapolis, Indiana, USA

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a. Banned substances list i. Banned Substances List NCAA Health and Safety/Banned Drug Classes 3. WADA: Montreal, Ottawa, Canada a. Banned substances list: www.globaldro.com b. Doping testing: Urine, blood, or both c. Doping control i. In-competition: Immediately after competition d. Out-of-competition: Any time, more selective, including only anabolic agents, β2-agonists, agents with antiestrogenic activity, diuretic and masking agents, and all the banned methods. Stimulants, narcotics, and cannabis are not analyzed in this type of control e. Control during Olympics to monitor level of red blood cells i. Nonstart determination 4. WADA rulings accepted by all National Olympic Committees, IOC, Paralympic Committee, national governments, international sports federations 5. Procedural issues a. WADA: The rights of the athlete are as follows i. Check the credentials of the doping control officer for any type of control ii. Be notified in writing of a selection process iii. Be informed about the consequences of a refusal to cooperate iv. Be informed about the correct sequence of the control v. With the consent of the doping control officer, always accompanied by an escort, the athlete is entitled (A) To receive a prize (B) To do a warm-down (immediately after competition) (C) To receive medical attention (if necessary after competition) (D) To attend a press conference (E) Not to stay in the doping station, if you have other competitions that day (F) To select the equipment that will be used (G) To be observed in the passing of the urine by someone of the same gender (H) To receive a signed copy of all the documents b. The responsibilities of the athletes are as follows i. To know the norms of the WADA, National Anti-Doping Organization (NADO), the National Organizing Committee (NOC), and the international (IF) and national federations of sports ii. To inform your personal physician and your pharmacologist that you are an athlete and may be submitted to doping controls iii. To consult your NADO, NOC, or IF with anticipation of a need to use any medical treatments that are related to banned drugs in your sport iv. To complete and submit Therapeutic Use Exemption (TUE) forms, when required v. To keep an actual list of all the medications, supplements, and herbal products that you are using, to declare it in the event of a doping control vi. To be careful in the ingestion of supplements or herbal products because they may contain banned substances vii. To always bring an identification with photograph with you to show to a doping control officer in the case of a doping control viii. In an in-competition or out-of-competition doping control, to remain at all times under the sight of an escort or doping control officer until the conclusion of the control

5. PHARMACOLOGY

ix. To hydrate with previously closed nonalcoholic beverages x. To be prepared to begin a doping control process as soon as notified and be in the doping control collection room until the sample is closed xi. To ensure that all documentation is correctly made and that you receive a copy of the documentation c. Testing procedures (eg, NCAA: outlined in NCAA Drug Testing Manual) i. Athlete notified in writing by courier ii. Athlete remains in visual contact with courier, reports within 1 hour iii. Sealed beverages without caffeine or other banned substances allowed iv. Athlete selects sealed beaker v. Specimen 85 mL; if less, discarded vi. Specific gravity must be >1.005, pH between 4.5 and 7.5, otherwise discarded vii. Specimen A: 60 mL, Specimen B: 25 mL viii. Specimen prepared for shipping in the presence of athlete ix. Specimen A tested by approved laboratory x. Different lab personnel test B sample if necessary, considered final xi. Similar procedures for blood testing per WADA d. TUE i. Make possible, for therapeutic reasons, to prescribe to an athlete a restricted or prohibited substance ii. This information should be kept confidential by the Panel of Experts of the IF responsible for granting permission iii. TUE should be submitted and approved at least 21 days before a competition iv. TUE should have a period of validity. After the expiration, it can be requested again by the athlete v. Some substances included in the List of Prohibited Substances are frequently used to treat medical conditions found in the athletic population (A) Insulin for diabetes (B) Inhaled β2-agonists for asthma (C) Injectable steroids for joint problems or radiculopathies F. Future trends in doping 1. Gene manipulation a. “The non-therapeutic use of cells, genes, genetic elements, or modulation of the gene expression, having the capacity to enhance athletic performance.” (WADA website/ St. Petersburg Declaration) b. Mentioned since 2000 c. Site-specific sequence modification to affect disease versus gain-of-function expression of exogenous transgenes d. Risks i. Treatment-induced leukemia ii. Death e. Animal studies i. Peroxisomal proliferator-activated receptor delta (A) Lipid metabolism (B) Expression of slow-twitch muscle fibers f. Gene transfer vectors i. Repoxygen (A) Expresses erythropoietin gene g. Testing i. WADA prohibited since 2004 ii. Genetic markers may be used to identify perturbed physiological markers

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2. Xenon gas a. Noble gas, prefers not to react with other elements b. Boosts body’s production of HIF1α protein, may stimulate EPO production c. Official use sponsored by the Russian government in 2006 d. WADA prohibited both in-competition and out-of-competition in 2012

Recommended Reading 1. Bellamy N, Campbell J, Robinson V, et al. Viscosupplementation for the treatment of osteoarthritis of the knee. Cochrane Database Syst Rev. 2006;2:CD005321. 2. De Rose EH. Doping in athletes—An update. Clin Sports Med. 2008;27:107–130. 3. Dietary supplements in athletes. www.nutrition.gov/dietary-supplements. 4. Elers J, Pedersen L, Backer V. Asthma in elite athletes. Expert Rev Respir Med. 2011;5(3):343–351. 5. How to use GlobalDRO, USADA. www.globaldro.com. 6. James PA, Oparil S, Carter BL, et al. 2014 Evidence based guideline for the management of high blood pressure in adults: Report from the Eighth Joint National Committee (JNC8). JAMA. 2014;311(5):507–520. 7. Sachs CJ. Oral analgesics for acute nonspecific pain. Am Fam Phys. 2005;71:913–918. 8. The 2015-2016 NCAA Championship drug testing site coordinator’s manual. www.ncaa.org/health-andsafety/policy/drug-testing. 9. WADA Code: The prohibited list international standard.

6 Principles of Musculoskeletal Rehabilitation Sathish Rajasekaran and Mederic M. Hall

I. Tissue Injury and Repair Phases A. Phase I: Injury and inflammation 1. Lasts days 2. Bleeding and hemostasis 3. Inflammation a. Characteristics i. Edema ii. Pain iii. Warmth iv. Redness v. Dysfunction 4. Essential for repair 5. Short-lived in most cases a. Too much/too long = bad b. Too little/too short = bad i. Inappropriate healing can lead to chronic tendinopathy 6. Response influenced by a. Injury site and severity b. Tissue type injured c. Patient factors B. Phase II: Proliferation/fibroplasia/repair 1. Lasts for 6 to 8 weeks 2. Characterized by a. Cell proliferation (eg, fibroblasts) b. Growth factor release c. Fibroblast proliferation—Type III collagen deposition d. Formation of granulation tissue e. Neovascularization 3. Tenuous time a. Many return to play (RTP) during this time b. Appearance > function; think they are better than they are c. Risk reinjury/regression 4. Graded rehabilitation necessary a. Not based on time, but based on clinical examination and function b. Criterion based—Every person and every injury is different 5. Education a. Patient, parents, coach 6. Monitor for regression 57

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C. Phase III: Maturation/remodeling 1. Lasts for months 2. Maturation of tissue a. Type III replaced by type I collagen b. Fibers realign and remodel i. Dependent on force magnitude and direction across injured tissues c. Cellularity and vascularity decreases 3. Injured tissue never returns to normal a. Prior injury is a major factor for reinjury D. Most athletes are able to RTP at some risk 1. Many are not clinically “normal” a. Muscle imbalances b. Motion restrictions/imbalances c. Strength/endurance suboptimal/imbalanced d. Kinetic chain dysfunction e. Neuromuscular control (NMC) deficits f. Technique alterations g. Often subtle 2. Risk reinjury E. Rehabilitation 1. Identify and treat deficits 2. Monitor for trouble a. Performance problems b. Prolonged recovery c. Pain d. Swelling 3. Education 4. If regress, treat accordingly

II. Baseball Diamond Approach to Rehabilitation A. Cannot get to the next base without crossing the prior base B. Pain control → motion → strength → NMC → RTP C. Control pain and inflammation 1. PRICE a. Protect (vs. long immobilization) b. Relative rest c. Ice d. Compression (not too much) e. Elevation (above heart) 2. Medications a. Analgesics b. Acetaminophen c. Tramadol/opioids d. Anti-inflammatories i. Nonsteroidal anti-inflammatory drugs (NSAIDs) (A) Analgesic benefit (B) Anti-inflammatory benefit debatable (C) May impair healing ii. Not corticosteroids—Detrimental 3. Modalities a. Superficial heat

6. PRINCIPLES OF MUSCULOSKELETAL REHABILITATION

i. Heat transfer achieved by conduction (transfer between two bodies), convection (transfer via fluid), and conversion (conversion of electromagnetic radiation) ii. Not to be used in initial recovery (inflammatory phase) but appropriate for proliferative and maturation phases iii. Achieves penetration of 1 to 2 cm, and most often used for pain in chronic injuries (joint pain, myofascial pain, etc) iv. Contraindicated in arterial insufficiency, insensate skin, scar tissue, malignancy, edematous region, and bleeding disorders b. Deep heat i. Examples: Ultrasound (common), shortwave diathermy, and microwave diathermy ii. Ultrasound utilizes soundwaves with frequencies >20 KHz. Absorption of soundwaves occurs in all tissues (particularly at muscle–bone interface) at depths of up to 8 cm. Soundwave absorption results in heat production iii. Used for various musculoskeletal conditions affecting the joint and surrounding soft tissue (not in acute inflammatory phase) iv. Contraindicated around metal prosthesis, tumors, near central nervous system, infections, pediatric patients, pacemakers, pregnancy (close to uterus). Superficial heat contraindications also apply to deep heat c. Cold i. Achieve cold transfer through conduction and convection. Evaporation can also be employed (vaporization of liquid causing cooling of skin) ii. Can be utilized in spectrum of injuries from acute to chronic phase iii. Contraindicated in arterial insufficiency, insensate limb, and open wounds d. Electrotherapy i. Used for muscle/nerve stimulation (eg, transcutaneous electrical nerve stimulation [TENS]) and medication delivery (iontophoresis) ii. TENS used for a variety of purposes to reduce pain via the Gate Control Theory. Conventional type (high frequency, low intensity) most commonly used, but acupuncture (low frequency, high intensity) increasingly used for musculoskeletal injuries. Both types used in spectrum of injuries from acute to chronic phase iii. Iontophoresis uses an electrical current to drive charged substances (often steroid or NSAID) into a target tissue D. Restore range of motion (ROM) 1. Benefits a. Antinociceptive b. Antiedema (at right dose) i. Provides neuromuscular training ii. Prerequisite for restoration of strength/endurance iii. Promotes tissue healing iv. Mentally gratifying (function) c. Types of motion i. Passive range of motion (PROM) = patient’s joint moved by an external force ii. Active assisted range of motion (AAROM) = patient’s joint moved with a combination of own force and an external force iii. Active range of motion (AROM) = patient’s joint moved by own force iv. Resisted range of motion (RROM) = patient’s joint moved by own force against an externally applied force d. ROM prescription depends on i. Healing phase ii. Injury specifics iii. Pain control

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e. Beware PROM in acute injuries i. Increased pain ii. Increased inflammation iii. Potential damage f. General sequence of AAROM → AROM → RROM g. Control motion arc h. Control forces i. Begin in phase I j. Monitor for regression k. Types of stretching to improve ROM i. Static (A) Three to five repetitions (reps) of 30 to 60 seconds ii. Splint—Gentle, prolonged stretch iii. Proprioceptive neuromuscular facilitation (PNF) (A) Common types (1) Contract–relax agonist (2) Contract–relax antagonist (B) Possibly more efficient acute gain in ROM, some evidence to suggest better maintenance of ROM gains (C) Usually requires another person to assist iv. Ballistic—Generally not recommended due to increased risk of injury E. Strengthening 1. Remember goal of restoring adequate functional strength and endurance 2. Strength gains are specific for a. ROM b. Contraction type c. Speed d. Energy system e. Movement pattern 3. Isometric strengthening a. No intentional joint motion (but joints may still move, especially with maximal contractions) b. Muscles co-contract c. For example, 5 to 10 reps of 6 seconds d. Can start early i. Even in splint/cast e. May reduce pain, edema, and atrophy f. Role in increasing strength and mass debatable but should not be primary strengthening mode if hypertrophy is a priority g. Strength gains are angle specific (ie, ±15°). Would need to perform isometric contractions in about four to five different positions to isometrically strengthen the entire ROM arc of the elbow 4. Isotonic strengthening a. Muscles changing length against constant resistance. Speed can be varied i. Concentric—Shortening ii. Eccentric—Lengthening iii. Carryover better from eccentric to concentric than from concentric to eccentric b. Need prerequisite motion c. Issue of elastic resistance i. Nonphysiologic due to increased resistance provided by elastic band at a weak point in a muscle’s length tension curve (ie, end ROM) ii. Can be partially mitigated by positioning

6. PRINCIPLES OF MUSCULOSKELETAL REHABILITATION

d. During progression, consider percent increase in load i. Moving from 1 to 2 lb is not a large quantitative increase (eg, 1 lb) but is a 100% increase in load to that muscle ii. Common mistake in rehabilitation is too large of a jump in resistance e. Functional progressions/increased stress i. Higher resistance ii. Eccentrics iii. Higher speeds iv. Terminal motion arcs v. More reps vi. More joints f. Manipulate strength/end parameters as clinical condition (eg, healing phase) dictates, with the ultimate goal in mind 5. Isokinetic strengthening a. Variable resistance, constant speed i. Move slow, resistance reduces ii. Move faster, resistance increases b. Training benefits unclear, may not translate into better performance c. May exacerbate symptoms d. Can detect and monitor speed-specific deficits in both eccentrics and concentrics i. Research applications ii. Assists in detecting muscle imbalances, within limitations of test F. Restore NMC/proprioception/return to sports 1. NMC a. Afferent = proprioceptive b. Efferent = muscle contraction c. Coordination requires afferent input detection and processing to produce an appropriate efferent output 2. Strength does not guarantee good NMC a. Proprioceptive deficits may persist despite normal strength b. Poor movement patterns may persist despite normal strength 3. Detect deficits a. Assess balance b. Assess movement patterns c. Sport-specific scenarios 4. Training continuum for NMC a. Early—AROM, Wobble boards, foam rollers b. Later—Rhythmic stabilization, body blades c. Even later—Plyometric training i. Jumps, hops, and so on d. Throughout NMC training continuum, consider motion, speed, energy specificity e. Build movement patterns into sports-specific motions f. Graduated return to sports g. Appropriate monitoring h. Post-RTP rehabilitation

III. Principles of Rehabilitation A. During rehabilitation process, must constantly consider 1. What is needed to RTP? 2. Where are the athletes in the healing process? 3. Is there regression? 4. Can also simultaneously address pain, motion, strength/endurance, and NMC with appropriately prescribed exercises

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5. Importance of core a. Component of all phases b. Integrate throughout 6. Conditioning a. Energy system specificity b. Integrate throughout 7. Technique a. Before versus after injury b. Do not wait until you are on your way home. Assess and treat technique at all phases of rehabilitation

IV. Specialized Rehabilitation Protocols A. Tendinopathy 1. In addition to principles previously mentioned, an eccentric exercise protocol can be implemented for tendinopathy of the upper and lower limbs 2. No clear eccentric protocol exists, but generally in the lower limbs, the tendon is loaded at ≥100% of body weight, and reps of 1,260 per week for Achilles (3 sets of 15 reps with the knee flexed and with the knee straight, twice daily, 7 days a week) and 125 to 630 per week for patellar tendinopathy have been reported. In the upper limbs, the number of reps varies greatly, but resistance usually begins at 2.5 to 5 lb. Most regimens outline a daily exercise protocol. Moderate pain should be present during or after the exercise. If no pain is felt, the resistance should be increased 3. Recent literature suggest that new loading regimens (isolated concentric, heavy slow resistance, and concentric-eccentric with progression to eccentric) may provide superior results with less frequent training (not daily) B. Stress fractures 1. Nomenclature has been changed to stress injuries to recognize the continuum from bony edema to true fracture 2. Criteria for specific grade of injury should be used (if available) to prescribe the appropriate level of activity and restrictions and prognosticate estimated time for healing/ RTP. Best evidence exists for tibial stress injuries, but general principles can be applied to other locations 3. High-risk stress injuries should be identified, which may require surgical management or more aggressive nonoperative treatment and longer RTP 4. Initial treatment of stress injury begins with modification of load to allow for healing. This is guided by symptomatic complaints of pain and can range from non weight bearing in a cast to simple activity modifications. Specific location and radiographic features also factor into initial management decision 5. Typical rehabilitation progression includes gradual reintroduction of load while monitoring for return of symptoms with activity or on provocative clinical testing. Time between each phase of rehabilitation will vary, based on severity and location of injury; however, patient should remain pain-free throughout the progression 6. Resumption of loading should begin with short-duration sessions. The frequency of sessions should be increased before the duration

V. Conclusions A. Despite a paucity of data on specific rehabilitation for specific clinical problems, sufficient evidence exists to facilitate development and execution of rational rehabilitation programs B. Clinicians should consider the healing stage of the injured tissue in the context of the “baseball diamond approach” to rehabilitation, realizing the ultimate goals of pain control, restoration of motion, restoration of functional strength, and optimization of NMC

6. PRINCIPLES OF MUSCULOSKELETAL REHABILITATION

Recommended Reading 1. Clover J, Wall J. Return-to-play criteria following sports injury. Clin Sports Med. 2010;29(1);169–175. 2. Couppé C, Svensson RB, Silbernagel KG, Langberg H, Magnusson SP. Eccentric or concentric exercises for the treatment of tendinopathies? The Journal of Orthpaedic and Sports Physical Therapy. 2015;1–25. 3. Dale RB, Harrelson GL, Leaver-Dunn D. Principles of rehabilitation. In Andrews JR, Harrelson GL, Wilk KE, eds. Physical Rehabilitation of the Injured Athlete. 3rd ed. Philadelphia, PA: Saunders; 2004:157–188. 4. Kinch M, Lambart A. Principles of rehabilitation. In: Brukner P, Khan K, eds. Clinical Sports Medicine Revised. 3rd ed. Australia: McGraw-Hill; 2009:174–197. 5. Micheo WF. Concepts in sports medicine. In: Braddom RL, ed. Physical Medicine & Rehabilitation. 3rd ed. Philadelphia, PA: Saunders Elsevier; 2007:1021–1043. 6. Norris C. Healing. Sports Injuries Diagnosis and Management. 3rd ed. London: Butterworth-Heinemann; 2004:29–60.

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7 Sports Medicine Procedures Michael Henrie, Steven Makovitch, and Stuart E. Willick

BASIC PRINCIPLES I. This chapter discusses common office-based procedures performed in most sports medicine clinics II. A thorough knowledge of joint and soft-tissue anatomy is essential to successfully performing the procedures discussed in this chapter III. Physicians performing these procedures should understand the indications, contraindications, and complications of each procedure IV. Additionally, it is important to understand the different preparations and the side effects of the medications used

JOINT INJECTION AND SOFT-TISSUE INJECTIONS I. Basic Principles A. Joint and soft-tissue injections have both a diagnostic and therapeutic role B. Although evidence-based reviews of the literature have found few studies to support or refute the efficacy of these procedures, there is substantial practice-based experience that supports their use C. Prior to performing a joint or soft-tissue injection, the clinician must understand the rationale for performing these procedures and should be able to identify those patients in whom they are most likely to be beneficial D. A variety of medication combinations can be used when performing joint and soft-tissue injections (see “Common Medications Used in Joint and Soft-Tissue Injections”)

II. Indications A. Indications generally fall into one of two categories: diagnostic or therapeutic B. Diagnostic indications 1. Aspiration of synovial fluid for laboratory analysis a. Gross examination i. Blood: hemarthrosis ii. Fat: violation of subchondral bone or fracture b. Polarized microscopy i. Monosodium urate crystals (negatively birefringent): gout ii. Calcium pyrophosphate crystals (weakly positive birefringent): calcium pyrophosphate disease (CPPD) or pseudogout c. Cell count i. See Table 7.1 64

7. SPORTS MEDICINE PROCEDURES

Table 7.1

Synovial Fluid Analysis

Normal

Hemorrhagic

Noninflammatory

Inflammatory

Septic

Appearance

Transparent

Bloody

Transparent

Mildly opaque

Opaque

WBC (per mm3)

200,000

PMNs (%)

75

Total protein (g/dL)

1–2

4–6

1–3

3–5

3–5

Glucose difference vs. plasma

Nearly equal to blood

Nearly equal to blood

Nearly equal to blood

Lower than blood

Much lower than blood

PMNs, polymorphonuclear leukocytes; WBC, white blood cell.

2. Injection of contrast medium for arthrography 3. Injection of local anesthetic to confirm a presumptive diagnosis of a particular pain generator C. Therapeutic indications 1. General therapeutic indications include pain, swelling, and decreased mobility 2. Indications for soft-tissue conditions include a. Bursitis b. Tenosynovitis or tendinosis c. Trigger points d. Ganglion cysts e. Neuromas f. Nerve or tendon entrapment syndromes 3. Indications for joint conditions include a. Synovitis (commonly used in inflammatory arthritis) b. Crystalloid arthropathies c. Osteoarthritis d. Aspiration of a large joint effusion for relief of pain and stiffness D. Musculoskeletal ultrasound 1. Assists in verifying diagnosis 2. Real-time visualization of needle placement and surrounding neurovascular structures 3. Lack of radiation exposure 4. Advantages over palpation-guided injections a. Improved accuracy b. Reduced procedural pain c. Increased response rate d. Larger volume of fluid aspirated 5. Other procedures that require ultrasound imaging a. Hydrodissection b. Tenotomy E. Timing of injections 1. Generally, therapeutic injections are reserved for patients in whom physical therapy, physical modalities, nonsteroidal anti-inflammatory drugs (NSAIDs), and other analgesics have failed

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2. In some conditions such as calcific tendinopathy, an early corticosteroid injection may augment therapy by reducing pain 3. The American College of Rheumatology guidelines state: No more than four injections per year or a maximum of one injection every 3 months. These guidelines are based on expert opinion only 4. Patients who do not adequately respond to one or two injections should probably not have additional injections

III. Contraindications A. Absolute contraindications 1. Septic arthritis is a contraindication to corticosteroid injection into the involved joint, although diagnostic aspiration is allowed 2. Skin or soft-tissue infection in the target area 3. Bacteremia 4. Bacterial endocarditis 5. Joint prosthesis in the target joint (diagnostic aspiration allowed, though safest to review with arthroplasty surgeon) 6. History of severe skin reaction or anaphylaxis with any of the medications being used 7. Fracture 8. Uncooperative patient B. Relative contraindications 1. Bleeding diathesis or coagulopathy 2. Anticoagulant therapy (Note: There is no consensus on aspiration and injections in patients on anticoagulation therapy. Many practitioners safely perform soft-tissue and peripheral joint injections in these patients) 3. Joint instability 4. Poorly controlled diabetes 5. Allergy to any of the medications being injected 6. Multiple failed injections

IV. Risks and Complications A. Bleeding B. Local allergic reaction C. Local infection D. Iatrogenic septic arthritis 1. This is a rare (1/30,000–1/50,000) but serious complication 2. Always use aseptic technique when performing joint injections E. Postinjection flare of pain 1. This can occur within the first 24 or 36 hours following a corticosteroid injection and is likely related to corticosteroid crystal formation within the joint and surrounding soft tissues 2. Occurs in 1% to 6% of injections 3. It typically manifests as increased joint pain, swelling, tenderness, and warmth 4. Symptoms are self-limited 5. Patients can be treated with rest, application of ice, and anti-inflammatory medications 6. When these symptoms occur, the clinician should always consider the possibility of iatrogenic infection 7. If symptoms persist beyond 24 or 36 hours, the patient should be properly evaluated F. Fat necrosis and depigmentation of the overlying skin can occur with a corticosteroid injection

7. SPORTS MEDICINE PROCEDURES

G. Tendon rupture can occur with corticosteroid injections. Injection into a tendon should be avoided H. Traumatic injection can occur, causing direct damage to articular cartilage, local nerves, or soft-tissue structures I. Pneumothorax has been reported with thoracic trigger point injections J. Systemic complications 1. Generalized hypersensitivity reaction 2. Anaphylaxis 3. Systemic absorption of corticosteroids a. More common with water-soluble steroid preparations, higher injection dose, and injecting multiple joints b. May cause a transient hyperglycemia, particularly in diabetics c. May cause a transient increase in the white blood cell count d. May cause adrenal suppression and iatrogenic Cushing’s syndrome in HIV+ patients taking ritonavir (a protease inhibitor that inhibits the cytochrome P450 3A4 [CYP 3A4] isoenzyme)

V. Sterile Technique A. After identification of the target site, the area of skin overlying the target joint should be adequately cleansed with an appropriate antiseptic solution such as iodine-based or chlorhexidine-based soap B. Sterile technique should be used when performing these procedures C. Sterile gloves allow palpation of anatomic landmarks and the target area after skin preparation has been completed

VI. Common Supplies Used for Joint and Soft-Tissue Injections A. Povidone-iodine–based or chlorhexidine-based swabs B. Sterile gloves C. Sterile drape D. 25- to 30-gauge, 0.5- to 1-inch needle for local skin anesthesia E. 22- to 25-gauge, 1- to 1.5-inch needle for injection F. 18- to 20-gauge, 1- to 1.5-inch needle for aspiration G. 1- to 5-mL syringe for local skin anesthesia H. 1- to 10-mL syringe for medication I. 30- to 60-mL syringe for aspiration (depending on the suspected size of the joint effusion) J. Medications K. Laboratory tubes for the aspirated fluid specimen L. Bandage for puncture site

VII. Postprocedure Instructions A. There is a wide variety of clinician preferences regarding postinjection care instructions but often include the following 1. Application of ice to the injection site 2. NSAIDs may be used for postinjection discomfort 3. Strenuous exercise or strenuous activity to be avoided for several days following the injection 4. The injection site should be cleaned and a bandage should be placed over the area 5. Patients should be instructed about signs and symptoms of infection

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COMMON MEDICATIONS USED IN JOINT AND SOFT-TISSUE INJECTIONS I. Corticosteroids A. Corticosteroid preparations differ with respect to potency, concentration, duration, and solubility (see Table 7.2) 1. Less soluble preparations are likely to remain in the joint for a longer period of time 2. Evidence is lacking that efficacy differs between preparations of different potency and duration of action B. Mechanism of action 1. Suppression of inflammation occurs by several mechanisms a. Increasing synovial fluid viscosity b. Limiting capillary dilation and altering synovial permeability c. Stabilizing lysosomal membranes d. Decreasing synovial fluid complement proteins e. Preventing degranulation of granulocytes, mast cells, and macrophages f. Inhibiting the release of arachidonic acid from phospholipids, thus reducing the formation of leukotrienes, thromboxanes, prostaglandins, and prostacyclins C. Adverse reactions 1. Systemic symptoms are related to the systemic uptake of the injected corticosteroid a. Systemic uptake is related to the solubility of the corticosteroid preparation 2. Systemic side effects, if present, are generally mild and include a. Hyperglycemia b. Facial flushing and warmth c. Rash d. Headache e. Agitation and emotional lability f. Elevated blood pressure g. Transient increase in white blood cell count 3. Local side effects a. Crystalline synovitis (postinjection flare) b. Tendon rupture

Table 7.2

Common Corticosteroid Preparations Used for Intra-Articular and Soft-Tissue Injection

Agent

Trade Name

Dose Equivalent

Potency

Duration

Hydrocortisone acetate

Hydrocortone

20 mg

Low

Short

Triamcinolone acetonide

Kenalog

4 mg

Intermediate

Intermediate

Methylprednisolone acetate

Depo-Medrol

4

Intermediate

Intermediate

Betamethasone sodium phosphate

Celestone

0.6 mg

High

Long

Dexamethasone sodium phosphate

Decadron

0.75 mg

High

Long

Betamethasone sodium phosphate–betamethasone acetate

Celestone Soluspan

0.6 mg

High

Long

7. SPORTS MEDICINE PROCEDURES

II. Local Anesthetics A. Different preparations of local anesthetics are available 1. They differ primarily in onset and duration of action (see Table 7.3) 2. Most commonly, 1% lidocaine, 0.25% to 0.5% bupivacaine, 0.2% ropivacaine, or a combination of anesthetics is used. However, both in vitro and in vivo studies have demonstrated cytotoxic effects of local anesthetic drugs on articular chondrocytes. Chondrotoxicity has been shown to increase in both a time- and concentration-dependent manner with ropivacaine being the least chondrotoxic (see Table 7.4). Further research is needed to determine the exact mechanism of action and long-term effects of local anesthetics on human chrondrocytes. B. Rarely, patients exhibit signs of mild anesthetic toxicity 1. Flushing 2. Hives 3. Tinnitus 4. Anxiety 5. Chest or abdominal discomfort C. Other serious adverse reactions include 1. Seizures 2. Respiratory arrest 3. Worsening of arrhythmias 4. Heart block 5. Bradycardia

Table 7.3

Common Local Anesthetics Used for Intra-Articular and Soft-Tissue Injection

Agent

Class

Concentration

Onset (min)

Duration (h)

Max Dose (Adults)

Lidocaine

Amide

1% or 2%

1–2

1.5–2

5 mg per kg, up to 300 mg total

Prilocaine

Amide

1%

1–2

>1

700 mg per kg, up to 280 mg total

Bupivacaine

Amide

0.25% or 0.5%

5–30

2–8

2 mg per kg, up to 175 mg total

Mepivacaine

Amide

1%

3–5

1–1.5

4 mg per kg, up to 400 mg total

Ropivacaine

Amide

0.2%

1–15

2–6

3 mg per kg, up to 225 mg total

Table 7.4

Local Anesthetics and Relative Chondrotoxicity

Agent

Concentration

Chondrotoxicity

Lidocaine

2%

High

Lidocaine

1%

Medium

Bupivacaine

0.5%

Medium

Bupivacaine

0.25%

Medium

Mepivacaine

1%

Medium

Ropivacaine

0.2%

Low

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III. Hyaluronic Acid Preparations A. Several different formulations of hyaluronic acid are available under the following trade names 1. Synvisc (hylan G-F 20) 2. Orthovisc (hyaluronan) 3. Hyalgan (sodium hyaluronate) 4. Supartz (sodium hyaluronate) 5. Euflexxa (sodium hyaluronate) B. No serious reaction has been reported with use of hyaluronic acid C. Common reactions include 1. Aseptic synovitis a. Occurs 24 to 72 hours after injection at a rate of 15 mmHg

>30 mmHg

>20 mmHg

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74

Recommended Reading 1. 2. 3. 4.

Boyd AS, Benjamin HJ, Asplund C. Principles of casting and splinting. Am Fam Physician. 2009;79(1):L16–L22. Cardone DA, Tallia AF. Joint, soft tissue injection. Am Fam Physician. 2002;66(2):283–288. Egol K, Koval KJ, Zuckerman JD. Handbook of Fractures. Philadelphia, PA: Lippincott Williams & Wilkins; 2010. Malanga G, Mautner K. Atlas of Ultrasound-Guided Musculoskeletal Injections. New York, NY: McGraw Hill Professional; 2014. 5. McNabb JW. A Practical Guide to Joint & Soft Tissue Injection & Aspiration. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2010. 6. Sherman SL, Khazai RS, James CH, et al. In vitro toxicity of local anesthetics and corticosteroids on chondrocyte and synoviocyte viability and metabolism. Cartilage. 2015;6(4):233–240. 7. Stephens MB, Beutler AI, O’Connor FG. Musculoskeletal injections: A review of the evidence. Am Fam Physician. 2008;78(8):972–976.

II Health Promotion and Injury Prevention

8 Preparticipation Examination D. Harrison Youmans and Tracy R. Ray

I. Administration A. Introduction 1. Over 30 million children, adolescents, and college students are involved in organized sports in the United States 2. The development of the preparticipation physical examination (PPE) was initially driven by the American Heart Association (AHA) to decrease the risk of sudden death 3. The PPE has become the standard of care, although evidence of its effectiveness is conflicting. It fulfills legal and insurance requirements for participation in sports for many municipalities, institutions, and organizations 4. Fifty states and the District of Columbia require PPEs prior to high-school sports participation. One state allows individual school districts to set their own requirements 5. Goals of the PPE include the following a. Evaluate for the presence of medical conditions with the potential to cause lifethreatening complications during participation b. Evaluate for conditions that require a treatment plan before or during participation c. Evaluate and rehabilitate preexisting musculoskeletal injuries prior to participation d. Evaluate and treat conditions/diseases that interfere with performance e. Remove unnecessary restrictions on participation f. Advise athletes regarding appropriate sports in which to participate 6. Physician responsibilities during the PPE include a. Identifying athletes with medical conditions that increase their risk of death or significant injury and disqualify them until these conditions can be properly evaluated and treated b. Ensuring that an athlete is not excluded from participation unless there is a compelling medical reason 7. The performing physician a. AHA recommends that the PPE be performed by a physician with a background for reliably recognizing heart disease b. Must be able to accurately evaluate the musculoskeletal system c. Majority of PPEs are performed by primary care physicians (PCPs) d. Only a minority of PCPs have received formal training in sports medicine or the musculoskeletal exam B. Timing/frequency 1. Frequency of the PPE is determined by individual institutions, leagues, and governing bodies for their participants 2. The majority of high-school athletic associations require annual exams

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3. AHA recommends a history and physical be performed every 2 years, with interim follow-up in the intervening year 4. Others recommend a PPE with each new level of participation (middle school, high school, college, etc) C. Mass versus individual 1. Most PPEs occur either during individual office visits with a physician or in a station-based, mass examination setting 2. Each of these methods has advantages and disadvantages (see Table 8.1) D. Screening tests 1. General medical history a. Chronic medical conditions b. Previous hospitalizations and surgeries c. Allergies d. Medications and supplements e. Previous exclusions from athletics f. Sports-related general medical history i. Cardiovascular (CV) history ii. Musculoskeletal history iii. Seizure history iv. Respiratory symptoms or history of exercise-induced bronchospasm (EIB) v. Gastrointestinal symptoms vi. History of heat-related illness vii. Skin rashes (tinea, herpes, or methicillin-resistant Staphylococcus aureus [MRSA]) viii. Disordered eating ix. Menstrual history x. Sickle cell status 2. Physical examination a. System-based examinations are detailed in the appropriate sections within this chapter. Examination should include the following b. General appearance c. Vital signs (height, weight, blood pressure [BP], pulse) d. CV examination e. Ocular examination f. Dermatologic examination: Evaluate for infectious rashes or lesions

Table 8.1

Individual

Advantages and Disadvantages of Individual versus Mass, Station-Based PPEs Advantages

Disadvantages

More private

Less efficient

Ability to build rapport

Increased cost

Continuity of care

Lack of physician specialization

Improved opportunity for counseling Station Based

More efficient

Less private

Decreased cost

Decreased rapport with patient

Increased specialization of physicians at stations

Decreased continuity of care

Better communication between ATCs, physicians, athletes, parents, coaches

Decreased opportunity for counseling

ATC, certified athletic trainer; PPE, preparticipation physical examination.

8. PREPARTICIPATION EXAMINATION

g. Pulmonary examination h. Abdominal examination i. Genitourinary (GU) examination in males j. Musculoskeletal examination k. Evaluation for stigmata of Marfan’s syndrome 3. Laboratory testing a. General i. Laboratory testing, including complete blood count (CBC), basic metabolic panel (BMP), magnesium, phosphorous, liver function tests (LFTs), and fasting lipid panel (FLP), is not recommended as a part of routine screening PPE ii. May be ordered prior to clearing an athlete for activity if there is a compelling medical condition that requires laboratory testing for diagnosis or monitoring b. Sickle cell i. National Collegiate Athletic Association (NCAA) guidelines mandate that the sickle cell trait (SCT) status of student-athletes be known, either by history or new testing ii. Student-athletes may opt out of testing by signing a waiver iii. The U.S. military does not test recruits for SCT or disease, opting instead for universal prevention and treatment strategies iv. Not currently recommended as part of routine screening for non-NCAA athletes v. The American Society for Hematology (ASH) does not support routine screening for SCT in athletes c. Ferritin i. Many advocate for screening ferritin tests, especially in female endurance athletes, to evaluate for iron deficiency (A) Controversy exists as to whether iron replacement in nonanemic irondeficient patients may improve athletic performance d. ECG (see II. Cardiovascular in the following text) i. Evidence suggests that inclusion of ECG may increase sensitivity of the PPE for finding those at risk of sudden cardiac death (SCD) ii. The inclusion of screening ECG as part of the PPE has been a controversial topic in the United States and is the focus of ongoing research and debate iii. The International Olympic Committee (IOC), European Society of Cardiology, and several governing bodies of sports within and outside the United States advocate screening ECG iv. Not currently recommended by the AHA e. Echocardiogram i. Some propose its use as a screening tool for hypertrophic cardiomyopathy (HCM) ii. False-positive results may occur iii. Not recommended as part of routine screening PPE

II. Cardiovascular (see Chapter 33 for more details) A. Introduction 1. SCD in athletes can be caused by a diverse set of structural and electrical abnormalities of the heart 2. CV events are the leading cause of sudden death in athletes a. Estimates for risk of SCD range from 1 in 900,000 high-school athletes to 1 in 3,100 in the subpopulation of Division 1 NCAA Men’s Basketball players b. Recent reports estimate the risk of SCD in young U.S. athletes to range between 1 in 50,000 and 1 in 80,000 c. Current research objectives include attempts to better quantify the actual risk of sports-related SCD in athletes, as methodology in previous studies has varied widely

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3. The purpose of preparticipation screening, which should include a well-performed CV history and physical exam, is to detect those athletes at increased risk of SCD 4. CV history a. Question athlete regarding past history of any of the following i. Heart murmur ii. Hypertension iii. Coronary artery disease (CAD) iv. Syncope or near-syncope with exertion v. Dizziness with exertion vi. Angina vii. Palpitations viii. Disproportionate dyspnea ix. Exertional chest pain x. Kawasaki disease (consider obtaining previous medical records or new echocardiogram to rule out coronary artery aneurysm) xi. Elevated systemic BP xii. Prior restriction from sports participation xiii. Prior history of cardiac testing b. Chest pain red flags i. Occurs during exertion ii. Occurs after recent viral illness and/or fever (A) Fever is a contraindication to participation due to association with carditis iii. Associated with new murmur iv. Lack of reproducible pain on palpation c. Family history of the following i. CV disease ii. Premature or sudden death before age 50 attributable to heart disease iii. Disability from heart disease in close relative 35 years of age 2. Physical activity decreases CV mortality rates among healthy patients and those with diagnosed CAD 3. Vigorous exercise transiently increases the risk of acute myocardial infarction (MI) and SCD, especially in sedentary individuals a. Likely secondary to plaque rupture and erosion during a period of increased myocardial oxygen demand 4. Assess left ventricular (LV) function in patients with CAD diagnosed by any of the following a. Coronary angiography b. Coronary artery risk score >100 c. Evidence of inducible ischemia on stress testing d. History of prior coronary event 5. Patients should have evaluation to assess exercise capacity and possible ischemia using treadmill or bicycle exercise testing 6. Risk stratification a. Mildly increased risk: Must demonstrate all of the following i. Preserved LV systolic function at rest (ejection fraction [EF] > 50%) ii. Normal exercise tolerance for age on treadmill or bicycle exercise testing iii. Absence of exercise-induced ischemia or arrhythmia iv. Absence of hemodynamically significant coronary artery stenosis (50% or more luminal diameter narrowing) v. Successful myocardial revascularization if such procedure is performed vi. Recommendations: Can participate in low dynamic or low to moderate static sports. Should avoid intensely competitive situations b. Substantially increased risk: Present if any of the following is demonstrated i. Impaired LV systolic function at rest (EF < 50%) ii. Evidence of exercise-induced ischemia or arrhythmia iii. Hemodynamically significant coronary artery stenosis (50% or more luminal diameter narrowing) iv. Recommendations: Should be restricted to low-intensity competitive sports 7. Patients with recent MI may benefit from cardiac rehabilitation in the weeks following the myocardial injury

8. PREPARTICIPATION EXAMINATION

8. Patients should refrain from vigorous activity for a period of 4 weeks following stent placement E. Athletic heart syndrome 1. Term used to describe the physiologic adaptations of the heart to endurance training, which include increases in atrial and ventricular volume, LV wall and septal thickness, and overall cardiac mass in a heart with preserved systolic and diastolic function 2. Differentiation between athlete’s heart and other cardiac abnormalities such as HCM or dilated cardiomyopathy can be difficult, especially in males. This is particularly true when LV thickness lies within the gray zone of 13 to 15 mm. However, “athlete’s heart” shows increased wall thickness AND increased cardiac chamber volume, whereas HCM has an increased wall thickness with reduced chamber volume 3. Exercise may also increase LV wall thickness in athletes with HCM or cardiomyopathies, and a period of decreased training may partially reverse cardiac remodeling in these athletes 4. Proper differentiation from serious cardiac abnormalities is important to avoid unnecessary disqualification from sports. Tools that may be used include ECG, echocardiography, genetic testing, and serial measurements of cardiac anatomy and function F. ECG 1. Use of the ECG as a preparticipation screening tool is a highly debated topic in sports medicine currently 2. Proponents of screening ECGs cite cost-effectiveness, ease of access, and higher sensitivity rates for detecting causes of SCD with the combination of history, physical exam, and ECG compared to history and physical exam alone 3. Opponents of screening ECGs cite a high rate of false-positive exams (which can lead to unnecessary testing and disqualification from sport), low positive predictive values, overall cost, need for a large number of specially trained physicians to interpret the studies, and low prevalence of disease 4. As of its 2014 recommendations, the AHA does not advocate universal ECG screening of athletes 5. The IOC, European Society of Cardiology, and several governing bodies of sports within and outside of the United States advocate screening ECGs 6. The Summit on Electrocardiogram Interpretation in Athletes was held in February 2012, establishing the “Seattle Criteria” to develop a consensus set of guidelines for determining normal and abnormal ECG findings in athletes a. Normal ECG findings in athletes Sinus bradycardia (≥30 beats per minute [bpm]) Sinus arrhythmia Ectopic atrial rhythm Junctional escape rhythm First-degree atrioventricular (AV) block (PR interval > 200 ms) Mobitz type 1 (Wenckebach) second-degree AV block Incomplete right bundle branch block (RBBB) Isolated QRS voltage criteria for left ventricular hypertrophy (LVH) Except: QRS voltage criteria for LVH occurring with any nonvoltage criteria for LVH such as left atrial enlargement, left axis deviation, ST-segment depression, T-wave inversion, or pathological Q waves Early repolarization (ST-segment elevation, J-point elevation, J waves, or terminal QRS slurring) Convex (“domed”) ST-segment elevation combined with T-wave inversion in leads V1-V4 in Black/African athletes These findings felt to represent common physiological adaptations to regular exercise and are considered to represent normal variants in athletes No further evaluation recommended in asymptomatic athletes

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b. Abnormal ECG findings in athletes T-wave inversion >1 mm in depth in two or more leads V2-V6, II and aVF, or I and aVL (excludes III, aVR, and V1) ST-segment depression ≥0.5 mm in depth in two or more leads Pathologic Q waves >3 mm in depth or >40 ms in duration in two or more leads (except for III and aVR) Complete left bundle branch block QRS ≥120 ms, predominantly negative QRS complex in lead V1 (QS or RS), and upright monophasic R wave in leads I and V6 Intraventricular conduction delay Any QRS duration ≥140 ms Left axis deviation –30° to –90° Left atrial enlargement Prolonged P-wave duration of >120 ms in leads I or II with negative portion of the P wave ≥1 mm in depth and ≥40 ms in duration in lead V1 RV hypertrophy pattern R-V1 + S-V5 > 10.5 mm AND right axis deviation >120° Ventricular preexcitation PR interval 120 ms) Long QT interval Corrected QT interval (QTc) ≥ 470 ms (male) QTc ≥ 480 ms (female) QTc ≥ 500 ms (marked QT prolongation) Short QT interval QTc ≤ 320 ms Brugada-like ECG pattern High takeoff and downsloping ST-segment elevation followed by a negative T wave in ≥2 leads in V1-V3 Profound sinus bradycardia 140 mmHg or diastolic BP (DBP) >90 mmHg on at least two separate occasions b. Children: SBP or DBP greater than or equal to the 95th percentile for age, gender, and height

8. PREPARTICIPATION EXAMINATION

3. Aerobic exercise can be beneficial in both long- and short-term BP control, decreasing risk of death from heart disease and stroke 4. Strenuous exercise can elevate BP to dangerous levels in patients with hypertension, increasing risk of MI or stroke. Therefore, BP measurement should be a routine part of the screening PPE 5. Recommendations a. Prehypertension (120/80–139/89 mmHg): Lifestyle modification without activity restriction. Echocardiography if LVH is suspected b. Stage 1 hypertension (140/90–159/99 mmHg): Lifestyle modification without activity restriction if no evidence of end-organ damage. Monitor BP every 2 to 4 months to evaluate effect of exercise c. Stage 2 hypertension (>160/100 mmHg in adults; SBP or DBP >99th percentile + 5 mmHg in children): Patient should be restricted from activity until BP is controlled by lifestyle modification or drug therapy H. HCM 1. Most common cause of SCD in the United States, accounting for 25% to 33% 2. Estimated to affect 1:500 Americans and 1:1,000 to 1:1,500 competitive athletes 3. Diagnosis based on LV wall thickness >13 to 15 mm 4. Genetic testing can also be useful for diagnosis 5. Associated murmur is harsh, systolic, located at left or right sternal border. Murmur INCREASES in intensity with standing and during Valsalva maneuver, which decrease venous return, allowing for increased outflow tract obstruction 6. Murmur is only present in 25% of patients with HCM at rest and may increase to up to 75% with Valsalva 7. ECG is abnormal in 75% to 90% of patients with HCM. Abnormal findings can include a. Prominent Q waves b. Deep negative T waves c. Increased QRS amplitude with associated ST changes 8. Recommendations a. Asymptomatic athletes with HCM phenotype should be excluded from all but low-intensity sports b. Asymptomatic athletes with HCM genotype who are phenotypically normal should not be excluded due to lack of evidence base i. Asymptomatic athletes participating in sports should have ECG, echocardiogram, and Holter every 12 to 18 months c. Symptomatic athletes should be withheld from all sports. SCD is often the sentinel event, however I. Marfan’s syndrome 1. Inherited connective tissue disease associated with mutation of the gene for fibrillin-1 protein 2. Affects 2 to 3 patients out of 10,000 3. Major cause of mortality is due to aortic rupture or dissection due to dilation and weakness of the aortic root caused by cystic medial necrosis 4. Patients should be questioned regarding family history, genetic testing considered if family history is positive 5. Ghent criteria have been developed to aid in diagnosis (see Figure 33.2) 6. Diagnosis a. Patients with family history of Marfan’s syndrome require one major and one minor criterion from different organ systems b. Patients without family history of Marfan’s syndrome require two major criteria and one minor criterion from different organ systems

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7. Recommendations a. Patients may participate in low and moderate static/low dynamic sports if they are without the following conditions i. Aortic root dilation ii. Moderate or severe MR iii. Family history of dissection or sudden death in a relative with Marfan’s iv. Patients should have echocardiogram every 6 months to evaluate for worsening aortic root dilation v. Contact or collision sports should be avoided as these increase the risk of aortic dissection or rupture J. Murmurs 1. Precordial auscultation should be performed in supine and standing positions with and without Valsalva maneuver 2. Innocent murmurs are generally I–III/VI and systolic 3. Murmurs associated with outflow obstruction increase in intensity with maneuvers that decrease preload, such as Valsalva or moving from lying to standing a. These murmurs should prompt further evaluation with ECG and echocardiogram, and the athlete should be withheld from competition until the workup is complete 4. Still’s murmur a. Common benign murmur present in young children b. Vibratory in nature, located over apex, II–III/VI intensity c. Decreases in standing position d. Caused by blood flow into the aorta K. Syncope 1. Defined by AHA as “temporary loss of consciousness and posture . . . usually related to temporary insufficient blood flow to the brain” a. The examiner should differentiate true syncope from other symptoms such as fatigue, dizziness, and light-headedness 2. History of syncope or presyncope without a defined cause may warrant a thorough evaluation, as it may be a manifestation of a dangerous CV condition 3. Potential causes can be cardiac (structural or electrical abnormalities), neurologic (transient ischemic attack [TIA], cerebrovascular accident [CVA], seizure), vasovagal/orthostatic, or psychiatric in nature 4. History, physical examination, and clinical judgement should be used to guide further evaluation in patients who report a history of syncope a. Patients with a well-defined cause for syncope, such as vasovagal syncope during an injection or syncope occurring during an acute febrile illness, may not require further work-up b. Reassuring factors include postexertional timing; single episode; and negative family history, cardiac exam, ECG, echocardiogram, and stress testing 5. History should address stimulant use (cocaine, ephedra, etc) as potential cause 6. A thorough cardiac workup is recommended for patients whose history and physical suggest a possible underlying CV cause. Testing to be considered includes a. Twelve-lead ECG b. Echocardiogram c. Event monitor or Holter monitor d. Exercise stress test (consider performing test at the intensity of the athlete’s sport, eg, maximal intensity for a sprinter) 7. Decisions regarding clearance for play should be made based on the diagnosis made during the history, physical, and subsequent workup. In certain conditions, treatment of the underlying abnormality (eg, accessory pathway ablation for Wolff-Parkinson-White [WPW] syndrome) may make participation safer for the athlete

8. PREPARTICIPATION EXAMINATION

8. Certain cardiac arrhythmias that cause excessively fast or slow heart rates may place an athlete at increased risk for SCD or injury due to syncope/presyncope, as in diving or motorsports. These include a. Ventricular tachycardias b. Atrial flutter/fibrillation with rapid ventricular response c. WPW syndrome d. AV blocks e. Sinus node disease f. Congenital long QT syndrome g. Brugada syndrome 9. In general, patients with arrhythmias may participate in all sports if they are without underlying structural heart disease and have been treated with medications or ablation that keep their ventricular rates within normal limits for their activity

III. Neurologic A. Seizure 1. Defined as uncontrolled electrical activity of the brain, which may lead to physical convulsions, alterations in mental status, or a combination of both 2. Well-controlled seizures are not a contraindication for participation in contact or collision sports a. The physician and athlete should be aware of individual governing body restrictions on the use of antiepileptic medications 3. Poorly controlled seizures should be appropriately medically managed prior to beginning competition a. Consider referral to neurologist and/or electroencephalogram (EEG) b. Water sports (swimming, scuba, surfing, etc), shooting sports (archery, riflery), and other sports during which an alteration in consciousness could be fatal (skydiving, auto racing, etc) should be restricted in patients with poorly controlled seizures 4. Patients with history of seizures should never train for or compete in water sports without supervision B. Stingers/burners 1. Transient sensory and/or motor loss that occurs as a result of a traction injury, compression injury, or direct blow to a peripheral nerve 2. May occur at the peripheral nerve roots (most commonly C5 or C6) or at the brachial plexus 3. Symptoms include pain, paresthesias, and/or muscle weakness 4. Symptoms in more than one extremity, however brief in duration, should prompt further workup for cervical spinal cord injury 5. Duration of symptoms may vary from seconds to days 6. Workup may include cervical spine x-rays and/or MRI as well as nerve conduction studies and electromyography 7. Proposed return-to-play guidelines vary but include a. Prior to returning to play, the athlete should have complete resolution of symptoms, full cervical and affected extremity range of motion (ROM) and strength, and absence of any predisposing factors to spinal cord or peripheral nerve injury b. Indications for further workup include the following i. Recurrent stinger in the same season ii. Prolonged neurologic signs/symptoms (>1 h) c. Consider withholding athlete for remainder of season or restriction from contact sports for the following i. Third stinger in same season, with or without persistent signs/symptoms ii. Third stinger in separate seasons with persistent neurologic signs/symptoms

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C. Traumatic brain injury (see Chapter 45 for more details) 1. Preparticipation evaluation should include questioning regarding the following a. History of concussion or injuries to the head, face, or cervical spine b. Quality and duration of symptoms and signs associated with these injuries c. Types of protective equipment used at the time of each injury and currently 2. The inclusion of neuropsychological and neuro-ophthalmologic testing as a part of the screening PPE has become increasingly common a. Proponents cite the ability to obtain objective measurements of postinjury neuropsychologic function and to compare these to preinjury baseline measurements i. May be useful for return-to-play decisions and research purposes b. Opponents cite cost and availability of the tests and limitations in the reliability of serial measurements, including false-negative tests i. Test results may vary based on environmental factors (noise, lighting, etc) and internal factors (athlete’s hydration status, motivation, illness, etc) c. These tools may be used as part of a comprehensive evaluation to aid in return-toplay and clearance decisions after a concussion 3. Decisions regarding clearance for play should be made on an individual basis for each athlete based on all available information once the athlete is without symptoms and has completed a graduated return-to-play protocol 4. Consider withholding an athlete from further contact or competition for the following a. The athlete remains symptomatic from most recent head trauma b. Severity or duration of symptoms after each head trauma is increasing c. Symptoms are occurring with mild trauma d. Academic or neuropsychological test performance has not returned to baseline 5. The PPE should be used as an opportunity to educate athletes, parents, coaches, and athletic trainers about symptoms, treatment, and prevention of concussion D. Transient quadriparesis (TQ) 1. In the United States, 10% of spinal cord injuries are estimated to occur during sports participation 2. Defined as a transient neurological episode involving sensory and/or motor function changes in two or more limbs, which may range from weakness (paresis) to paralysis (plegia) 3. Should be differentiated from stingers/burners by the involvement of more than one extremity 4. May occur as a result of cervical hyperflexion, hyperextension, or axial load 5. Most commonly occurs in collision sports, such as American football, ice hockey, wrestling 6. Rates in American football have decreased as a result of rule changes designed to prohibit axial loading due to head-down tackling (“spearing”) or leading with helmet while tackling 7. Diagnostic evaluation of the cervical spine may include the following a. X-rays, including flexion and extension views—Consider in stable patients b. CT scan—May demonstrate fracture, dislocation, or instability c. MRI—May demonstrate congenital spinal cord abnormalities, cord compression or spinal stenosis, disk herniation or osteophyte complexes, or spinal cord edema 8. Return-to-play criteria vary but may include the following Relative contraindications for return to play following TQ Healed cervical fracture Klippel-Feil fusion, single level Presence of spear tackler ’s spine Recurrent TQ Healed single-level cervical decompression and fusion without functional stenosis

8. PREPARTICIPATION EXAMINATION

Small cervical disk herniation or spondylosis without signs/symptoms of functional stenosis Absolute contraindications for return to play following TQ Persistent neurological signs/symptoms, neck pain, or limited cervical ROM MRI evidence of spinal cord defect, edema, or functional spinal stenosis Klippel-Feil fusion, multiple levels Acute cervical fracture or ligamentous disruption Cervical disk herniation, acute or chronic Arnold-Chiari malformation Basilar invagination Os odontoideum Atlanto-occipital fusion or instability Multiple-level surgical fusion

IV. Musculoskeletal A. Cervical stenosis 1. Condition in which there is narrowing of the cervical canal, with or without encroachment upon the spinal cord 2. Cervical stenosis may be defined using the following diagnostic criteria a. Functional spinal stenosis i. Imaging (MRI or CT myelogram) evaluation of the amount of cerebrospinal fluid (CSF) surrounding the spinal cord ii. Loss of CSF signal surrounding the spinal cord or indentation of the thecal sac may be present in the setting of congenital cervical stenosis, disk herniation, osteophyte complexes, or other degenerative or posttraumatic changes iii. Also defined as presence of symptoms, including pain, weakness, numbness, paresthesias, or bowel/bladder dysfunction, with normal imaging studies b. Canal measurement of 13 mm or less at level of C4 on cervical spine MRI c. Torg ratio i. Measurement used historically to define stenosis, prior to routine use of MRI ii. Ratio of canal width to vertebral body width in sagittal plane of less than 0.8 iii. No longer recommended due to increased size of vertebral bodies in athletes, which causes variability of measurements and difficulty in interpretation of results 3. Athletes with a history of bilateral paresthesias or TQ should have a cervical spine MRI to evaluate the underlying cause of symptoms 4. Return-to-play decisions should be made based on the degree of stenosis, presence or history of symptoms, and degree of contact associated with sports being considered B. Joint disorders 1. Musculoskeletal complaints are the most common ailments seen by athletic trainers and sports medicine physicians 2. Musculoskeletal history should include questions regarding the following a. Previous fractures, sprains, strains, or dislocations b. Previous use of assistive devices, prosthetics, orthotics, or physical therapy c. Signs or symptoms consistent with inflammatory arthropathies d. Any current injuries or symptoms requiring rehabilitation e. Previous imaging studies including x-rays, CT scans, or MRI 3. Musculoskeletal examination a. Introduction i. Begin with screening exam as described in the following text ii. If the athlete has a history of prior injury, perform a more detailed exam for the injured body part

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iii. An accurate diagnosis must be established before making return-to-play decisions iv. Larger institutions may include functional movement assessments b. General inspection i. Patient standing, facing the examiner ii. Evaluate symmetry of trunk and limbs c. Cervical exam i. Observe ROM in flexion, extension, rotation, and side bending ii. Important for athletes with previous history of neck injury and stingers iii. Consider exclusion from play if limited ROM, weakness, pain with movement, or radicular symptoms are present d. Shoulder exam i. Observe ROM and strength against resistance in abduction, forward flexion, internal rotation, and external rotation of the shoulders ii. Consider further evaluation if a significant side-to-side difference exists in strength or ROM e. Elbow exam i. Observe ROM and strength against resistance in flexion and extension, as well as pronation and supination of the forearm with the elbow flexed to 90° ii. Consider further evaluation if a significant side-to-side difference exists in strength or ROM f. Hand exam i. Evaluate for asymmetry and limited ROM as the patient (A) Spreads fingers in abduction (B) Makes a fist (C) Flexes fingers (D) Extends fingers g. Back exam i. Evaluate symmetry and ROM during back flexion and extension ii. Also assess symmetry of trunk and extremities facing away from the examiner iii. Inspect for scoliosis (see Section IV.D) iv. Palpate for tenderness along entire spinal column h. Leg exam i. Assess symmetry of musculature and bony prominences ii. Assess range of motion (A) Hip: Flexion, extension, internal and external rotation (B) Knee: Flexion and extension (C) Ankle: Plantar flexion, dorsiflexion, inversion, eversion iii. Inspect for edema or venous insufficiency iv. Duck walk v. Assess tibial tuberosities in adolescents (Osgood–Schlatter disease) vi. Toe raise and heel walk vii. Five hops test i. If the athlete has a history of prior injury, perform a more detailed exam of the injured body part j. An accurate diagnosis must be established before making return-to-play decisions C. The PPE should be used as a time to communicate with athletic trainers and physical therapists regarding need for further treatment and evaluation for protective devices D. Scoliosis 1. Defined as a lateral curvature of the spine greater than 10° accompanied by vertebral rotation 2. Present in 2% to 4% of children between 10 and 16 years of age

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3. Of adolescents diagnosed with scoliosis, only 10% have curves that progress and require medical intervention 4. The three main determinants of progression are a. Patient gender (more common in females) b. Future growth potential c. Curve magnitude at the time of diagnosis 5. Adam’s test a. Evaluate the patient’s back for a “rib hump” with patient flexed to 90° at the waist and arms extended forward b. Represents curves greater than 10° and should prompt radiographic evaluation 6. Surgery is considered for curves greater than 40° to 45° if the patient has potential for increased growth 7. Recommendations a. Evidence is lacking regarding risks associated with sports participation in patients with scoliosis, and the decision regarding participation should be individualized for each patient b. General guidelines exist, and are as follows i. Those with mild curves may participate without restriction ii. Those with larger curves should consider avoiding collision sports and activities that load the facet joints heavily (eg, volleyball, swimming, diving, gymnastics, etc) iii. Patients who use bracing should exercise in their brace iv. Postoperative patients should gradually increase activity in the 6 months following surgery assuming that there are no complications (A) Contact sports and activities that load the facets should be avoided (B) Noncontact endurance sports (running) should be encouraged

V. Paired Organs A. Eyes 1. Eye injuries are common in sports, and appropriate steps should be taken to minimize the risk of these injuries 2. History should address the following a. History of vision abnormalities b. Use of glasses or contacts for vision correction c. History of eye injuries, surgeries, or infections d. Use of protective eyewear 3. Visual acuity testing should be a part of the screening PPE 4. Athletes, parents, coaches, and athletic trainers should be familiar with protective eye equipment requirements for their sports 5. High-risk sports for eye injuries include those that involve projectiles, balls, sticks, bats, rackets, close contact, or intentional facial injury 6. A patient is considered functionally one-eyed if corrected visual acuity in an eye is less than 20/40 a. These athletes should be withheld from sports involving intentional injury, including boxing, full-contact martial arts, and wrestling b. These athletes should be counseled regarding risks of injury to the eyes as well as proper use of protective eye equipment, prior to being cleared for other high-risk sports 7. Patients with history of eye injury, infection, surgery, retinal detachment, or severe myopia should be evaluated and cleared for participation by an ophthalmologist 8. Patients with abnormal visual acuity at the time of the PPE should be referred to an eye-care professional for evaluation and vision correction

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B. Kidneys 1. Examination for abnormalities of the kidneys should be performed during the abdominal examination 2. Congenital or traumatic absence of a kidney does not preclude an athlete from participation 3. Individual assessment and counseling regarding risks of injury to the remaining kidney (including the potential need for transplant or dialysis) should be performed during the PPE 4. Descriptions and limitations of protective equipment should be discussed 5. Some experts believe athletes should be withheld from contact sports if the solitary kidney is multicystic, pelvic or iliac in location, or hydronephrotic 6. Consultation with a urologist or nephrologist is recommended prior to clearance for participation in patients with a solitary functioning kidney 7. Functional assessment of renal function, including serum creatinine, glomerular filtration rate, and functional kidney scans may be considered to aid in decisions regarding participation in athletes with renal abnormalities 8. The decision regarding clearance for participation should be made on an individualized basis for each athlete based on the issues discussed in the preceding text. C. Testicles 1. Testicular examination should be performed on male athletes to assess size, shape, tenderness, and presence of both testicles 2. Evaluation of inguinal canal for hernias should be performed in patients with symptoms of a hernia but is not considered mandatory in asymptomatic patients 3. Single testicle a. Congenital or traumatic absence of a testicle does not preclude an athlete from participation b. Individual assessment regarding risks of participation (including infertility) and protective equipment should be performed before participation in collision or contact sports c. A protective cup should be used if the athlete plans to participate in contact, collision, or projectile sports D. Ovaries 1. Absence of an ovary does not preclude patients from participation as risk of injury to the solitary ovary is minimal

VI. Abdominal and Pelvic A. Introduction 1. Examination of the abdomen should be performed with the patient in the supine position and should include auscultation of abdominal vessels as well as palpation of all four abdominal quadrants a. Should include evaluation for organomegaly, kidney abnormalities, gravid uterus, abdominal tenderness, and, in males, genital examination b. Pelvic examinations in females and Tanner staging are not recommended as a part of the routine PPE B. Conditions that may limit participation include 1. Infectious diarrhea a. Athletes should be withheld from competition to avoid dehydration and heat illness unless symptoms are mild and athlete is well hydrated 2. Organomegaly a. Hepatomegaly i. May be secondary to infection (hepatitis) or malignancy ii. Athletes should be withheld from competition until resolution

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iii. Athletes with chronic hepatomegaly should have individual evaluation regarding clearance to play based on sport, symptoms, and type and severity of underlying hepatic condition b. Splenomegaly i. Most commonly caused by infectious mononucleosis (A) Athletes should be withheld from competition for 28 days from onset of symptoms or date of diagnosis (see Section VII F) ii. Athletes should be withheld from competition until resolution due to risk of splenic rupture 3. Malabsorption syndromes a. Athletes require individual assessment to determine the ability to meet caloric needs to avoid nutritional deficits b. Presence of indwelling catheter or external devices for delivery of parenteral nutrition requires prevention strategy and emergency action plan in the event of damage to these devices 4. Inguinal hernia a. Patients with inguinal hernia should not be precluded from participation, although symptoms may limit performance or ability to participate b. Symptoms may include inguinal heaviness, swelling, or pain i. Symptomatic patients will often require surgical correction c. Athletes should be advised to seek care if they develop severe pain, erythema, increased swelling, nausea, or vomiting, as these may represent strangulation of the hernia

VII. Education/Prevention A. Asthma 1. Introduction a. Pulmonary disease caused by bronchial hyperreactivity and airway inflammation leading to reversible obstruction of airflow b. Symptoms may include dyspnea, wheezing, cough, or chest tightness c. Exercise-induced asthma (EIA) is used to describe exercise-induced symptoms in patients with underlying asthma d. EIB is used to describe symptoms in patients without underlying asthma, although undiagnosed asthma should be considered in athletes who show symptoms e. History questions should address the following i. Past history of asthma, wheezing, dyspnea, or chronic cough ii. Previous and current use of bronchodilators or other asthma medications iii. Previous hospitalizations or intubations for asthma exacerbations iv. Current frequency and severity of symptoms v. Presence of tobacco abuse or secondhand smoke exposure 2. Diagnosis a. Pulmonary function tests (PFTs) may be normal at rest and are therefore unreliable in the diagnosis of EIA b. PFTs performed before and after exercise may be more reliable as diagnostic tests if there is a reversible decline in forced expiratory volume in 1 second (FEV1) after exercise i. Some patients may only develop symptoms under certain environmental conditions, and therefore portable spirometry may be required to adequately diagnose EIA c. Eucapnic voluntary hyperventilation (EVH) testing is the preferred method of testing identified by the IOC i. Requires specialized equipment, therefore often used only at higher levels of competition

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ii. Six-minute protocol of hyperventilation of gas containing 21% oxygen and 5% carbon dioxide at a prescribed ventilatory rate recreates exercise conditions iii. Considered diagnostic if FEV1 decreases by 10% or more 3. Treatment a. Use of short-acting beta-agonist (SABA) bronchodilators prior to exercise may be useful in preventing symptoms b. Athletes who require bronchodilator use more than twice weekly may benefit from the addition of inhaled corticosteroids, with or without long-acting beta-agonists (LABA); mast cell stabilizers; or leukotriene inhibitors 4. Recommendations a. Athletes with well-controlled asthma should not be restricted from activities b. Athletes with poorly controlled symptoms should be evaluated for need for additional treatment c. Patients with febrile respiratory illness or acute symptoms should be withheld from competition until they are well d. Athletes, coaches, athletic trainers, and covering physicians should have inhalers available during coverage and should work together to develop an emergency action plan in the event that this treatment is inadequate to reverse symptoms B. Diabetes mellitus 1. Athletes with diabetes should be evaluated for potential complications of the disease in the same manner as any diabetic patient, including a. CV disease b. Retinopathy c. Neuropathy d. Nephropathy e. Gastroparesis 2. Athletes with well-controlled blood glucose levels and without any other contraindications should be allowed to participate in sports 3. High-risk sports for athletes with diabetes include rock climbing, skydiving, scuba, and auto sports 4. Other sports such as swimming or endurance running require proper support for the athlete, including access to insulin and food or caloric drinks 5. Athletes with retinopathy should avoid sports that are high impact or that acutely increase BP 6. Blood glucose should be monitored during exercise, and insulin dosing and caloric intake should be adjusted accordingly 7. Patients with ketosis and preexercise blood glucose greater than 250 or preexercise blood glucose greater than 300 with or without ketosis should avoid exercise C. Drugs 1. Introduction a. The PPE affords the physician an excellent opportunity for counseling patients, many of whom are in good health and may not seek health care frequently b. Adolescent athletes should be informed that discussions regarding drug and alcohol questions will be confidential 2. Prescription medications a. Athletes participating in organized team sports should provide their team physician and athletic trainer with a list of current prescription medications and drug allergies prior to participation i. Some medications should be kept on the sideline for immediate use if needed (eg, albuterol, insulin, epinephrine, etc) b. Athletes participating in individual sports should discuss medication use with their physician at the time of the PPE

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3.

4.

5.

6.

i. Consider counseling athletes with medical problems to carry a list of medications and allergies or to use one of many commercially available accessories that provide emergency contact information c. Athletes, physicians, and athletic trainers should familiarize themselves with the list of medications that may be banned by their sport’s governing bodies Alcohol a. Screening for use and abuse may be performed at the time of the PPE b. Athletes should be counseled regarding potential health problems from alcohol use as well as associated dangers such as motor vehicle accidents c. Alcohol use is banned in some sports that require fine motor control, such as archery Tobacco a. Tobacco use is the chief cause of preventable deaths in the United States each year b. Cigarette smoking is associated with increased risk of many types of cancer, chronic obstructive pulmonary disease (COPD), heart disease, and stroke c. Smokeless tobacco use is very common in young male athletes and may lead to oral or laryngeal cancers Drugs of abuse a. Screening and counseling regarding abuse of prescription drugs and street drugs may be performed during the PPE as well Supplements a. Supplement use is extremely common in the athletic population b. Athletes should provide physicians and athletic trainers with a list of supplements being used and should be counseled regarding possible adverse effects of their use c. Athletes should be counseled regarding the following information i. Supplements are not regulated by the Food and Drug Administration ii. Ingredients present in supplements and their concentrations may vary iii. Claims made by the manufacturer may not have scientific evidence to support them iv. Listed or unlisted ingredients in supplements may cause the athlete to have positive drug screens

D. Female athlete triad (see Chapter 50 for more details) 1. Introduction a. Female athletes have special concerns that should be addressed during the PPE, including increased risk relative to males for stress fractures, disordered eating, noncontact anterior cruciate ligament (ACL) injuries, and menstrual irregularities b. The female athlete triad is a constellation of symptoms caused by inadequate caloric intake that leads to decreased energy stores, causing decreased blood levels of estrogen. The triad includes the following i. Disordered eating ii. Menstrual irregularities iii. Decreased bone mineral density (BMD) 2. Disordered eating a. History questions should address the following i. History of disordered eating ii. Previous or current dietary restrictions iii. Previous or current use of diuretics, laxatives, stimulants, sweat suits, purging behavior, etc iv. Pressure from parents, coaches, athletic trainers, and so on to maintain or achieve a certain body weight v. Concerns of the athlete regarding current weight or body image b. Physical examination i. Exam should include height and weight measurements

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(A) An adult female athlete is considered underweight if her body mass index (BMI) is less than 18.5 (B) A child or adolescent female athlete is considered underweight if her BMI is less than the fifth percentile for her age ii. Exam findings associated with anorexia nervosa may include bradycardia, hypotension, lanugo hair on the skin, abdominal distension as a result of constipation from hypomotility, pallor related to anemia, or musculoskeletal abnormalities associated with decreased bone density iii. Exam findings associated with bulimia nervosa may include parotid gland hypertrophy, wear of dental enamel, and calluses on the knuckles from repeated induced vomiting 3. Menstrual irregularities a. Caloric deficit created by overtraining or caloric restriction leads to decreased estrogen levels, which can cause menstrual irregularities b. Amenorrhea is common in active females, but should be viewed as a potential sign of a serious disorder i. Primary amenorrhea is the lack of menses by age 16 ii. Secondary amenorrhea is the lack of three consecutive menstrual periods after menarche (A) Can have a number of causes, including pregnancy, some forms of contraception, or endocrine disorders iii. A thorough workup should be performed to look for the cause of amenorrhea prior to attributing it to disordered eating or overtraining c. History should address the following i. Length and frequency of menstrual periods ii. Current use of contraceptives iii. Age or presence of menarche d. Pelvic examination is not recommended as part of the PPE unless the PPE is part of a comprehensive health maintenance exam i. Patients with concerning history who may require a pelvic exam should have this scheduled with their PCP or OB/GYN at a later time 4. Decreased BMD a. Results from secondary amenorrhea and decreased estrogen levels that simulate a postmenopausal state b. History should address the following i. Presence or history of fractures or stress fractures (A) Details regarding the development of these injuries, including training regimen and diet at the time of injury, number and chronicity of injuries, and adequacy of treatment c. Physical exam should include the screening musculoskeletal exam and more thorough exam of sites of previous injuries 5. Further evaluation a. Athletes with menstrual irregularities should have a thorough workup for underlying causes, which may include urine pregnancy test, CBC, BMP, thyroid function tests, and follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels b. Athletes with disordered eating may require further workup, including CBC, BMP, iron studies, magnesium and phosphorous levels, and ECG to evaluate for heart blocks or prolonged QT intervals c. Athletes with decreased BMD may require testing of calcium and vitamin D levels, as well as monitoring with dual-energy x-ray absorptiometry (DEXA) scanning

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6. Treatment a. Treatment of the female athlete triad requires a multidisciplinary approach that should include the physician, a nutritionist, a psychologist or psychiatrist, and if applicable, the patient’s parents, coaches, and athletic trainers to an appropriate extent b. Oral contraceptive pills have not been shown to be effective in restoring BMD or preventing further decreases c. Decisions regarding clearance for sports participation should be made on an individualized basis i. Athletes should be withheld from sports if their participation puts them at risk for further injury or illness ii. In many cases, athletes may require mental health treatment prior to returning to sport iii. Activity should be resumed gradually, with monitoring to ensure that overtraining does not occur iv. Parents, coaches, and athletic trainers should be counseled that behavior intended to restrict calories or weight is likely to be detrimental to the patient’s health v. Contracts may be used with the athlete to encourage adherence with treatment recommendations and follow-up E. Injury prevention 1. Introduction a. The PPE affords the physician an excellent opportunity for counseling patients, many of whom are in good health and may not seek health care frequently b. Athletes, parents, coaches, and athletic trainers should all be aware of options and requirements for protective athletic equipment, especially as this equipment pertains to specific medical conditions present in the athlete c. Young athletes and their parents should be counseled to avoid specialization in sports at a young age, as specialization may lead to an increased rate in overuse injuries and decrease the athlete’s ability to develop balanced strength and flexibility d. Consider counseling of parents and coaches of young athletes to allow them adequate opportunity to rest, recover, and rehabilitate injuries between athletic seasons 2. ACL prevention programs a. Many programs have been developed in recent years in attempt to decrease ACL injuries i. Females are up to four times more likely than males to have an ACL injury ii. The majority of these injuries occur in noncontact situations (ie, pivoting, landing) iii. Emphasis is to place the athlete in a typical setting of injury in a controlled environment so that he or she may recognize proprioceptive cues and develop mechanisms to avoid injury b. Many authors have reported success in decreasing ACL injury rates after seasons incorporating these programs F. Infectious disease 1. HIV and hepatitis B and C a. These viral infections can be transmitted through exposure to blood of infected body fluid though open wounds, mucous membranes, or parenteral administration, sexual contact, IV drug abuse, and perinatal transmission b. The risk of transmission through sport is minimal, and the presence of these diseases alone should not preclude an athlete from sports participation c. The athlete should be evaluated for any complications from the diseases that may limit performance or place the participating athlete at risk d. Changes in the athlete’s health status warrant reevaluation for participation clearance

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2. Infectious mononucleosis a. Viral infection caused by the Epstein–Barr virus (EBV) b. Diagnosed based on serology or rapid monospot test c. Symptoms include fatigue, fever, myalgias, pharyngitis, cervical lymphadenopathy d. Symptoms may be severe enough to limit performance e. Splenomegaly occurs in the majority of patients with mononucleosis, and splenic rupture is a possible complication i. Splenic rupture is most common within the first 21 days of the illness but rarely occurs after 28 days ii. Recommendations are to withhold an athlete from competition for 3 to 4 weeks after the onset of symptoms or the time of diagnosis if the timing of symptoms is unclear iii. Serial ultrasound can be used to monitor for resolution of splenomegaly but is limited by the lack of data and consistency among spleen sizes

VIII. Special Populations A. Disabled athletes 1. “Disability” is defined by the Americans with Disabilities Act as “a physical or mental impairment that substantially limits one or more major life activities of such individual” 2. The International Paralympic Committee (IPC), a division of the IOC, is the governing body for athletic competitions for athletes with physical disabilities a. At the 2012 London Paralympics, there were 4,237 athletes competing, representing 164 countries 3. Disabled athletes are given a class score (1 [severely impaired] to 8 [minimally impaired]) based on testing of upper limb, lower limb, and trunk function a. This scoring system allows participants to compete against opponents with similar levels of functioning 4. History and physical exams should be performed in a manner similar to the general PPE with some exceptions a. Dermatologic considerations i. All wheelchair athletes should be evaluated for the presence of ischial and sacral decubitus ulcers (A) Consider withholding athletes from competition if ulcers are present until they are completely healed ii. Skin should also be evaluated for callus or ulcer formation from wheelchair propulsion and bruising, abrasions, or lacerations from blunt trauma from equipment, other wheelchairs, and so on b. Urologic considerations i. Athletes with neurologic bladder dysfunction should have the normally recommended GU examination ii. In addition, any external collection systems (catheters, etc) should be evaluated as these athletes are at increased risk for urinary tract infections c. Musculoskeletal considerations i. Wheelchair athletes should be evaluated for shoulder pain and impingement syndromes ii. Amputees should have prosthetics and orthotics evaluated for proper fit and mechanical function prior to using for athletic competition d. Neuroendocrine considerations i. Should be addressed in athletes with spinal cord injuries ii. Patients should be questioned regarding history of heat-related illness as they may have impaired thermoregulation mechanisms due to decreased ability to sweat below the level of injury

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iii. Questioning and education regarding autonomic dysreflexia should also be performed (A) Autonomic dysreflexia is a potentially life-threatening autonomic response of overstimulation from noxious stimuli (1) Occurs in patients with spinal cord injury at T6 level or above (2) Can lead to potentially fatal elevations in BP (3) Other signs and symptoms include flushing, excessive sweating above level of spinal injury, headache, nausea, bradycardia, and piloerection below the level of spinal injury (4) Can be used by athletes to gain competitive advantage in a process known as “boosting” (a) Commonly achieved by mechanically obstructing urinary catheter, ingesting large quantities of fluid to cause bladder distension, wearing tight-fitting clothes, or sitting on sharp objects (b) May also be caused by infections or skin ulcers B. Special Olympians 1. Special Olympics is a charitable organization founded in the 1960s to promote “empowerment, competence, acceptance and joy” in individuals with intellectual disabilities through athletic competition. 2. There are currently over 4.5 million Special Olympic athletes in 180 countries participating in over 30 sports 3. Due to the significant numbers of participants, sports medicine physicians and other PCPs are likely to encounter these athletes in practice and should be aware of their specific needs for proper PPE 4. History and physical exams should be performed in a manner similar to the general PPE with some exceptions a. A third party (parent, caregiver, etc) may need to be present during the PPE to provide the most accurate history possible b. Emphasis should be placed on conditions common to intellectually disabled athletes, including congenital heart disease, vision and hearing limitations, ligamentous laxity leading to joint injuries, and seizure history c. Athletes with trisomy 21 (Down syndrome) should be evaluated for asymptomatic atlanto-axial instability (AAI) prior to competition in the sports listed in the following text using lateral cervical flexion and extension views i. In children, AAI is considered to be present when the distance between the posterior aspect of the anterior arch of the atlas and the anterior aspect of the odontoid is greater than 4.5 mm ii. This testing is required prior to competing in the following sports (A) Judo, equestrian, high jump, alpine skiing, diving, snowboarding, squat lift, soccer, pentathlon, swimming (butterfly stroke or diving starts) d. Decisions regarding further evaluation (ECG, echocardiogram), specialist referrals (neurology for uncontrolled seizures, cardiology for congenital heart defects), and clearance for participation in different sports should be made in the same manner as for any other athlete C. SCT 1. Condition of inheriting one gene for sickle cell hemoglobin and one normal 2. Present in 1 of 12 African Americans and 1 in 2,000 to 1 in 10,000 white Americans 3. Intense exercise can lead to exertional sickling in those with SCT 4. Exercise provides three conditions that can account for this in combination a. Hypoxemia b. Metabolic acidosis c. Muscle hyperthermia

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5. Clinical presentation can include fatigue, muscle cramps or weakness, shortness of breath, dizziness, inability to continue with exercise, or collapse in the setting of extreme exertion 6. While exertional sickling may lead to severe metabolic complications and even death, it is a self-limited event if symptoms are treated early with rest, oxygen, cooling if necessary, and monitoring of vital signs 7. Methods to prevent exertional sickling should include the following a. Build training slowly b. Longer rest and recovery time between efforts c. Immediate cessation of activity with symptoms d. Avoidance of exercise during illness e. Adequate control of asthma if present f. Maintain adequate hydration 8. Education should be provided to athletes, athletic trainers, coaches, and medical staff regarding signs of deteriorating status in an athlete as well as an institutional emergency action plan 9. Screening for SCT is a controversial issue, with proponents on each side a. Concerns that exist regarding global screening include cost and the potential for discrimination against a sickle trait–positive athlete (eg, professional sports contracts, teammates’ views of work ethic, personal view of training efficacy) b. SCT screening has become mandatory for all NCAA athletes as of the 2010–2011 academic year c. The ASH opposes required SCT screening d. The U.S. military discontinued sickle cell screening after a 10-year prospective trial of modified training protocols, including enforced hydration and environmental monitoring, that demonstrated no deaths in 40,000 recruits with SCT i. Military sites not participating in the study had mortality rates comparable to those of the participating sites prior to the training modifications 10. Presence of SCT is not a contraindication to sports at any level D. Hematologic disorders 1. Introduction a. Patients with hematologic disorders should have individualized evaluations to determine exercise capacity and effectiveness of oxygen utilization prior to clearance for participation in sports b. Testing to consider includes i. Exercise stress test with oxygen saturation monitoring ii. Serial hematocrit assessments during the season 2. Iron deficiency anemia a. Can cause impaired performance in athletes b. Symptoms may include fatigue, dyspnea, tachycardia, or headache i. Consider CBC in patients reporting these symptoms at PPE c. Supplementation with iron should be initiated to correct anemia and is recommended for a period of 6 months to correct residual depletion of total body iron stores 3. Ferritin a. Laboratory marker representing total body iron stores b. Controversy exists as to whether a CBC and ferritin should be included as screening tests and whether iron supplementation should be initiated in athletes with nonanemic iron deficiency c. Levels below 12 ng/dL represent decreased bone marrow iron stores d. Recommendations exist for iron supplementation for ferritin levels less than 30 to 35 ng/dL to be continued for 6 months or until ferritin levels reach 50 ng/dL e. Ferrous iron products are recommended as they are better absorbed than ferric iron

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4. Hemophilia a. Inherited disorder caused by deficiency of factor VIII or IX in the clotting cascade b. Leads to spontaneous bleeding, which may be severe i. Frequent hemarthroses can lead to synovitis, joint degeneration, joint pain, limited ROM c. Risk of bleeding with physical activity varies among patients and may differ based on treatment, extent of disease, and amount of contact d. Recommendations i. Patients should be evaluated for joint injury and function prior to participation ii. Protective equipment, disease treatment, and injury rehabilitation should be maximized iii. Contact sports are not strictly contraindicated, but care should be taken in sport selection based on disease state and informed decisions by patients and parents iv. Emergency action plan should be in place to prevent and treat acute bleeds 5. Anticoagulated athletes a. Evidence-based return-to-play guidelines for those receiving anticoagulant therapy have not been established b. Multiple case reports have demonstrated successful return to prior activity levels for patients receiving short-term anticoagulation for disorders such as deep venous thrombosis (DVT) or Paget–Schroetter syndrome c. Risks must be discussed with patients regarding the dangers of contact or impact sports while on anticoagulant medications, including intracerebral hemorrhage, compartment syndrome, hemarthroses, hematomas, and so on i. Return-to-play decisions should be made on an individualized, case-by-case basis E. Cystic fibrosis 1. Disease process caused by mutation in the gene for the cystic fibrosis transmembrane conductance regulator (CFTR) protein a. Involved in the transport of chloride ions across cell membranes b. Mutation leads to fibrosis of the pancreases and abnormalities in sweat, digestive enzyme, and mucous secretions 2. Hallmark symptoms include poor weight gain and growth, presence of thick mucous secretions, cough, dyspnea, and frequent lung infections 3. Sports participation should be determined on an individual basis a. Exercise testing to determine oxygenation during exercise is recommended b. Patients should also be screened for effects of gastrointestinal malabsorption and ability to meet caloric needs for exercise 4. Medical therapy, including bronchodilators, antibiotics, and so on, should be maximized prior to participation in sports a. Consider pulmonology referral in these patients

Recommended Reading 1. Bernhardt DT, Roberts WO, eds. Preparticipation Physical Evaluation. 4th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2010. 2. Concannon LG, Harrast MA, Herring SA. Radiating upper limb pain in the contact sport athlete: an update on transient quadriparesis and stingers. Curr Sports Med Rep. 2012;11(1):28–34. 3. Drezner JA, Ackerman MJ, Anderson J, et al. Electrocardiographic interpretation in athletes: the ‘Seattle Criteria.’ Br J Sports Med. 2013;47:122–124. 4. Maron BJ, Thompson PD, Puffer JC, et al. Cardiovascular preparticipation screening of competitive athletes. A statement for health professionals from the Sudden Death Committee (clinical cardiology) and Congenital Cardiac Defects Committee (cardiovascular disease in the young), American Heart Association. Circulation. 1996;94(4):850– 856.

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5. Maron BJ, Zies DP. Bethesda Conference Report. 36th Bethesda conference: eligibility recommendations for competitive athletes with cardiovascular abnormalities. J Am Coll Cardiol. 2005;45(8):1313–1375. 6. McCrory P, Meeuwisse WH, Aubry M, et al. Consensus statement on concussion in sport: the 4th international conference on concussion in sport held in Zurich, November 2012. Br J Sports Med. 2013;47:250–258. 7. Philpott JF, Houghton K, Luke A. Physical activity recommendations for children with specific chronic health conditions: juvenile idiopathic arthritis, hemophilia, asthma, and cystic fibrosis. Clin J Sport Med. 2010;20(3):167–172. 8. Wingfield K, Matheson GO, Meeuwisse WH, et al. The preparticipation evaluation: thematic issue. Clin J Sport Med. 2004;14(3):107–187.

9 Strength and Conditioning Techniques Jacob L. Sellon and Jonathan T. Finnoff

I. Principles of Training A. General adaptation syndrome (GAS) = response to new exercise-related stress 1. Shock phase a. Several days to a few weeks b. Performance drops c. Muscle soreness and stiffness 2. Resistance phase a. Body adapts and returns to supranormal performance level i. Initially, neural adaptations ii. Later, muscular, cardiovascular, and metabolic adaptations 3. Exhaustion phase = overtraining a. Result of excessive stress b. Performance declines B. Sports specificity 1. Adaptations specific to type of exercise performed a. Neuromuscular specificity i. Motor learning due to repetition of specific movement pattern (A) Muscle action (eg, concentric, eccentric, isometric) (B) Speed of movement (C) Range of motion (ROM) (D) Muscle groups trained b. Metabolic specificity i. Energy systems (ie, adenosine triphosphate [ATP]/creatine phosphate, anaerobic lactic, aerobic) stressed during training should closely match metabolic demands of the specific sport C. Overload 1. Physiologic adaptations occur only if exercise stimulus > normal 2. Key variables are intensity and volume a. Intensity = percent of maximal functional capacity of exercise mode b. Volume = total amount of exercise performed in a period of time D. Progression 1. Training variables (eg, volume, intensity) must be periodically increased to continue improving

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E. Recovery 1. Adaptations occur during recovery, not training 2. To maximize training adaptations, optimize recovery a. Rest days, appropriate nutrition, adequate sleep, restorative techniques (eg, massage, relaxation) F. Prioritization 1. Not all fitness qualities can be optimized simultaneously 2. Develop training priorities based on athlete’s abilities and sport-specific demands G. Individuality 1. Different individuals respond differently to the same training stimulus H. Diminishing returns 1. The greatest improvements occur in individuals who are inexperienced 2. Trained individuals make much smaller gains I. Reversibility 1. If training not continued, benefits will be lost (eg, maximum oxygen uptake [VO2max] can decrease by 4% to 6% in just 2 weeks of inactivity)

II. Periodization A. Periodization = planned variation in training in a given time period 1. Developed in the 1960s by Russian physiologist Leo Matveyev 2. Concept based on GAS 3. Optimizes adaptations over long-term training while minimizing overtraining 4. Typically general physical training → sport-specific physical training B. Periodization cycles 1. Multi-year preparation (eg, 4-year Olympic cycle) 2. Macrocycle = multiple months dedicated to specific goal a. Preparation (develop fitness qualities; general → sport-specific training) b. Competition (peak performance and to maintain fitness) c. Active recovery (physical/psychological rest and injury recovery) 3. Mesocycle = typically 2 to 6 weeks focusing on same type adaptations (eg, strength, power) 4. Microcycle = typically 1 week, repeated within a mesocycle a. Deload = active rest microcycle to recover and allow supercompensation C. Periodization types 1. Linear (classical) periodization a. Gradual variation of volume and intensity over mesocycles i. Volume (high → low) ii. Intensity (low → high) b. Training focus gradually shifts from general fitness qualities (eg, endurance, strength, power) to sports-specific training c. Preferable for sports with limited number of in-season competitions and well-defined off-season 2. Nonlinear (undulating) periodization a. Acute variation of volume and intensity within microcycles/mesocycles i. Varying training stress in an attempt to maximize GAS response ii. Trains various fitness qualities simultaneously within mesocycles b. Maintains progression from general to sport-specific training, though may not be linear c. Preferable for sports that require multiple fitness qualities/skills and/or have long competitive seasons

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3. Block periodization a. Relatively short mesocycles (2- to 4-week “blocks”) focused on highly specific fitness quality/ability b. Designed for advanced athletes who require focused periods of specific training to achieve a training effect D. Linear periodization sequence 1. Preparation macrocycle a. First and longest macrocycle b. Divided into two mesocycles i. General preparation mesocycle (A) Develops anaerobic/aerobic work capacity in preparation for future highintensity, sport-specific training ii. Sport-specific preparation mesocycle (A) Develops physical capacity specific to the physiologic demands of the sport (B) Perfect sport technique c. Classically, three resistance training mesocycles in the preparation macrocycle i. Hypertrophy/endurance phase (A) Focus is increasing muscular strength, endurance, and lean body mass (B) Low to moderate loading (C) High volume, high repetition (D) Low-speed movements (E) Minimal sport-specific movements ii. Maximal strength phase (A) Focus is increasing maximal strength (B) High loading (C) Low repetition (D) Relatively low-speed movements (E) More emphasis on sport-specific movements iii. Strength/power phase (A) Focus is on power development and transfer to sport (B) Moderate to high loading (C) Low repetition (D) High-speed, sport-specific movements 2. Transition macrocycle a. Mesocycles that progressively increase resistance loads, aerobic exercise intensity, and sport technique training 3. Competition macrocycle = peaking a. Significantly tapers volume over a 2- to 3-week period b. Emphasis on maintaining high-intensity and sport-specific technique training c. Peak fitness difficult to maintain more than 2 to 3 weeks without overtraining 4. Active rest macrocycle a. Goal is physical and mental recovery from competitive season b. Injury rehabilitation/prehabilitation c. Low intensity and volume d. Unstructured, non–sports-specific recreational training

III. Resistance Training A. Definitions 1. Strength = ability to produce force 2. Hypertrophy = increase in muscle cell size due to increases in intracellular fluid and contractile protein

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3. Power = ability to produce force quickly B. Muscle strength factors 1. Muscle fiber cross-sectional area positively correlated with maximal force production 2. Expression of strength altered by muscle length, joint angle, pennation angle, and contraction velocity 3. Enhanced neural function a. Motor unit synchronization and recruitment (Henneman size principle) b. Rate coding (increased action potential frequency) c. Autogenic inhibition (protective Golgi tendon organ mechanism)—Resistance training reduces neurologic inhibition, allowing more vigorous muscle contraction C. Resistance training programming variables 1. Type of muscle action a. Concentric (muscle shortening) b. Eccentric (muscle lengthening) i. Greatest force per muscle fiber ii. Greatest stimulus for hypertrophy c. Isometric (no net change in muscle length) 2. Loading = resistance = weight lifted per repetition or set a. Intensity i. Measurement of loading ii. Often reported as a percentage of one-repetition maximum (1-RM) load b. Loading (resistance) type i. Isotonic (eg, free weights) (A) Resistance is constant and speed increases with force applied ii. Isokinetic (eg, Biodex® machine) (A) Speed is constant and resistance increases with force applied iii. Isometric (eg, plank) (A) Joint angle does not change (B) Resistance increases with force applied iv. Elastic/isodynamic (eg, band, spring) (A) Both resistance and speed are variable (B) Allows resistance in multiple planes (C) Load increased as band is stretched, causes maximum load at end ROM 3. Volume = total amount of work (~ repetitions × load) in a training session 4. Frequency = number of training sessions per week a. Whole-body versus split routines 5. Exercise selection a. Multijoint versus single-joint exercises i. Multijoint (compound) exercises (eg, squat, bench press) (A) Allow for more loading (B) Work more muscles with fewer exercises (C) Coactivation of muscles around joint promotes stability ii. Single-joint (isolation) exercises (eg, leg extension, biceps curl) (A) Technically easier (B) Allow for focus on single-joint movement (C) Less coactivation about joint → more shear force b. Closed kinetic chain (CKC) versus open kinetic chain (OKC) exercises i. CKC = distal aspect of limb is fixed (eg, squat, push-up) (A) Requires movement of proximal muscle segments, resulting in coactivation of core musculature and larger muscle groups → arguably better transfer to sport (more functional)

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6.

7.

8.

9.

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(B) Usually multijoint exercise → coactivation of muscles around joint promotes stability ii. OKC = distal aspect of limb is mobile (eg, leg extension, bench press) (A) Less core and proximal muscle coactivation → arguably less transfer to sport (B) May be single-joint (eg, leg extension) or multijoint (eg, leg press) exercises c. Bilateral (two-limb) versus unilateral (single-limb/asymmetric) exercises i. Bilateral allows for more loading ii. Unilateral (A) Asymmetry requires more core stabilization in frontal/transverse planes (B) Allows for correction of side-to-side imbalances d. Free weights versus machines i. Free weights train intramuscular and intermuscular coordination, allowing better movement specificity ii. Machines are technically easier to use and, therefore, may reduce risk of injury Exercise order a. More technically demanding exercises (eg, Olympic lifts, CKC, multijoint) should be performed before simpler exercises b. Larger muscle groups should be trained before smaller muscle groups c. Muscle strength and power are potentiated when antagonist movements paired Repetition speed a. Can be fast, moderate, or slow i. Unintentionally slow = due to high loading or fatigue ii. Intentionally slow (A) Studies have shown decreased force production Rest periods = amount of rest taken between exercises, sets, or repetitions a. Affects metabolic, hormonal, and cardiovascular responses to exercise b. More rest is required for more complex exercises (eg, Olympic lifts) Blood flow restriction = cuff or elastic wraps to occlude venous outflow from limb a. May increase muscle hypertrophy and strength with low loads (20%–40% 1-RM) b. Potential training applications i. Rehabilitation—Injury recovery, after surgery, osteoarthritis ii. Performance—Decreased training stress (eg, in-season), supplement to traditional high-load resistance training

D. American College of Sports Medicine (ACSM) recommendations for muscular strength training 1. Type of muscle action: Should include exercises with concentric, eccentric, and isometric muscle contractions 2. Loading a. Novice to intermediate: 60% to 70% 1-RM for 8 to 12 repetitions b. Advanced: Cycle loads of 80% to 100% 1-RM c. Progress loading no more than 2% to 10% between sessions 3. Volume a. Novice: One to three sets per exercise b. Intermediate to advanced: Multiple sets with systematic variation 4. Frequency a. Novice: Whole-body training 2 to 3 days per week b. Intermediate: 3 (whole body) or 4 (split routine) days per week c. Advanced: 4 to 6 days per week with option of twice per day 5. Exercise selection a. Bilateral and unilateral exercises b. Emphasis on multijoint (vs. single-joint) exercises

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c. Free weights and machines with emphasis on free weights for advanced trainees 6. Repetition speed a. Novice: Slow to moderate speed b. Intermediate: Moderate speed c. Advanced i. Include continuum of speed (slow, moderate, and fast) ii. Intent should be to maximize concentric speed 7. Rest periods a. At least 2 to 3 minutes for main (heavy load) exercises b. One to two minutes for assistance (lighter load) exercises E. ACSM recommendations for muscular hypertrophy training 1. Type of muscle action: Include concentric, eccentric, and isometric exercises 2. Loading a. Novice to intermediate: 70% to 85% 1-RM for 8 to 12 repetitions b. Advanced: Cycle loads of 70% to 100% 1-RM for 1 to 12 repetitions (majority 6–12) 3. Volume a. Novice to intermediate: One to three sets per exercise b. Advanced: Three to six sets per exercise 4. Frequency a. Novice: Whole-body training 2 to 3 days per week b. Intermediate: 3 (whole body) or 4 (split routine) days per week c. Advanced: Split routine training 4 to 6 days per week 5. Exercise selection a. Multijoint and single-joint exercises b. Free weights and machines 6. Repetition speed a. Novice and intermediate: Slow to moderate speed b. Advanced: Slow, moderate, and fast speed 7. Rest periods a. Novice to intermediate: 1 to 2 minutes b. Advanced: Variable F. ACSM recommendations for muscular power training 1. Power training should be incorporated with a concurrent strength-training program as part of a periodized plan 2. Loading a. Novice to intermediate i. Upper body: 30% to 60% 1-RM for three to six repetitions ii. Lower body: 0% to 60% 1-RM for three to six repetitions b. Advanced i. Upper body: 30% to 60% 1-RM for one to six repetitions ii. Lower body: 0% to 60% 1-RM for one to six repetitions iii. Integrate with 85% to 100% 1-RM for one to six repetitions 3. Volume a. Novice to intermediate: One to three sets per exercise b. Advanced: Three to six sets per exercise 4. Frequency a. Novice: Whole-body training 2 to 3 days per week b. Intermediate: 3 (whole body) or 4 (split routine) days per week c. Advanced: Whole-body or split routine training 4 to 5 days per week 5. Exercise selection a. Multijoint exercises (eg, jump squats, cleans, medicine ball throws)

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b. For vertical jump and long jump training i. CKC more effective than OKC resistance exercises ii. Plyometric training should be incorporated into routine 6. Repetition speed: Fast/explosive 7. Rest periods a. At least 2 to 3 minutes for main exercises b. One to two minutes for assistance exercises G. Plyometric training 1. Trains the stretch-shortening cycle (SSC) → rapid eccentric contraction followed immediately by a powerful concentric contraction 2. Developed by Russian and European coaches in the 1960s 3. Physiologic basis a. Mechanical: Stored elastic energy in musculotendinous unit b. Neurologic: Stretch reflex of eccentrically stretched muscle c. Rate (not magnitude) of eccentric stretch is key to powerful concentric contraction → effort should be made to minimize ground contact time 4. Exercise examples (easy → hard) a. Lower body i. Tuck jumps → hurdle jumps → bounding → depth jumps b. Upper body i. Medicine ball catch–throw → hand clap push-up 5. National Strength and Conditioning Association position statement on plyometric exercises a. Plyometric training can improve performance in most sports b. Plyometric training should include sport-specific exercises c. Carefully applied plyometric training programs are no more harmful than other forms of sports activity and may be necessary for safe adaptation to the rigors of explosive sports d. Only athletes who have already achieved high levels of strength through standard resistance training should engage in plyometric drills e. Athletes weighing over 220 lb should not depth-jump from >18 inches f. Plyometric drills involving a particular muscle/joint complex should not be performed on consecutive days g. Plyometric drills should not be performed when an athlete is fatigued h. Time for complete recovery should be allowed between plyometric exercise sets i. Footwear and landing surfaces used in plyometric drills must have good shockabsorbing qualities j. Thorough warm-up should be performed before beginning a plyometric training session k. Less demanding drills should be mastered prior to attempting more complex and intense drills

IV. Speed and Agility Training A. Definitions 1. Speed = distance traveled per unit time 2. Linear speed = ability to move the body in one intended direction as fast as possible 3. Multidirectional speed (MDS) = ability to produce speed in any direction or body orientation (eg, forward, backward, lateral, diagonal) 4. Agility = ability to change direction or body orientation based on rapid processing of internal or external information without significant loss of speed B. Speed training concepts

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1. Speed and agility training should be done in a rested, nonfatigued state a. Beginning of training session b. After a rest day 2. Other than speed technique training, speed drills should be done at high intensity (95%–100%) 3. Allow full recovery between sprint/drill repetitions 4. Progression of training: Technique mastery → speed → speed endurance 5. Strength training for speed a. Untrained: Speed may improve by strength training alone b. Strength trained: Further improvement in speed requires addition of high speed or power training C. Linear speed 1. Reaction time a. Reaction time and starting technique can be trained with reactive drills i. Block starts ii. Sport-specific drills with a whistle or visual cue 2. Acceleration = phase from static start to top speed a. Important component in short sprints (64% of 100-m sprint) b. Common methods of training acceleration i. Short sprints (eg, 10–30 m) ii. Resisted sprints (eg, uphill sprints, sled push/pull, bungee cord resisted) iii. Resistance training (eg, power cleans, squats) 3. Top speed = stride length × stride rate a. Stride length and rate are interdependent → optimize combination b. Stride length = distance covered with each stride i. Largely depends on height and leg length ii. Optimal stride length is 2.3 to 2.5 times leg length iii. Overstriding creates deceleration force and may lead to injury iv. Directly related to force applied into the ground v. Resisted sprints improve stride length by increasing drive phase force production (A) Light resistance (110 mmHg requires case-by-case evaluation d. Symptomatic orthostatic hypotension with >20 mmHg drop (supine to stand) e. Critical aortic stenosis f. Acute systemic illness or fever g. Uncontrolled atrial or ventricular arrhythmias h. Uncontrolled sinus tachycardia (>120 beats/min) i. Uncompensated CHF j. Unpaced, high-degree AV block k. Active pericarditis or myocarditis l. Recent embolism m. Thrombophlebitis n. Resting ST segment displacement of >2 mm o. Uncontrolled diabetes (resting blood glucose >400 mg/dL) p. Orthopedic conditions that would preclude exercise q. Certain other metabolic conditions (eg, acute thyroiditis, hypokalemia, hyperkalemia, hypovolemia) 3. Relative contraindications to participation in cardiac rehabilitation a. Tachyarrhythmias b. Bradyarrhythmias c. Moderate valvular disease d. Hypertrophic cardiomyopathy e. Left main CAD 4. Indications for cardiac stress testing prior to beginning an exercise program a. Asymptomatic persons with two or more risk factors of CAD (see Table 11.2) b. Men >45 years and women >55 years who plan to exercise >60% VO2max c. Known cardiac symptoms to assess severity and prognosis d. Post-MI for prognostic assessment e. Those involved in occupations in which cardiovascular events may affect public safety 5. When preliminary exercise testing is not feasible, pharmacologic stress testing can be beneficial

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a. Highest HR obtained with dobutamine testing may be used to guide prescribed target HR (THR) b. Other complementary methods (symptoms, Holter monitoring, ECG-telemetry, HR monitors) may be useful in determining exercise intensity 6. Exercise prescriptions in cardiovascular disease a. Intensity i. 40% to 80% of maximal heart rate reserve (HRRmax) ii. Moderate-intensity (11–16) RPE on Borg scale iii. Exercise at more vigorous intensity is associated with a 10-fold increased risk of major cardiovascular event in patients with underlying CAD iv. Should be prescribed at HR below ischemic threshold if it has been determined for the patient b. Frequency: ≥ 3 days per week c. Duration: Total duration of aerobic conditioning phase should last 20 to 60 minutes per session. This can be performed in short bouts initially of 1 to 10 minutes at a time, increasing gradually over time d. The AHA exercise recommendation for lowering BP and cholesterol is an average of 40 minutes of moderate- to vigorous-intensity aerobic activity three to four times/week 7. Progression should be over a 3- to 6-month period B. Exercise prescriptions in patients with cerebrovascular disease 1. Considerations a. Assess strength, tone, ROM b. Emphasis on exercises that do not significantly increase BP in patients with hypertensive cerebrovascular accident c. Incorporate adaptive equipment (ankle foot orthosis [AFOs], etc.) and ensure adequate skin care 2. Benefits of exercise include a. Improved mood b. Improved cardiovascular fitness c. Modification of risk factors associated with stroke (BP, hyperlipidemia)

VII. Diabetes Mellitus A. In some individuals with type 2 diabetes, adequate glycemic control can be achieved with exercise and weight reduction B. In diabetics taking insulin, response to exercise is variable in regard to glycemic control C. If under appropriate control or only slightly hyperglycemic without ketosis, exercise decreases blood glucose concentration, and a lower insulin dose may be required D. Lack of sufficient insulin prior to exercise impairs glucose transport into muscles, may lead to ketosis and worsen the hyperglycemic state 1. Adequate control prior to exercise is imperative a. Blood glucose concentration >300 mg/dL or >240 mg/dL with positive urine ketones is a relative contraindication to exercise E. Exercise-induced hypoglycemia is common 1. Hypoglycemia can result if too much insulin is present and with accelerated glucose absorption from the injection site—both can occur with exercise a. Can result during exercise or up to 4 to 6 hours after completing exercise 2. Decreasing insulin dose or increasing carbohydrate load prior to exercise can both compensate for this response 3. Insulin-dependent diabetics should consider intake of 20 to 30 g of additional carbohydrates with preexercise blood glucose of 65 C. Risk factors: (a) Age, (b) obesity, (c) prior trauma, (d) family history of OA, and (e) occupation with repetitive joint loads or high physical demands D. Primary cause of disability, impairment, and job loss in U.S. adults E. Prevalence higher in whites >65 years, women >55 years, people who are overweight, sedentary, or with 65 years, and the incidence is increasing G. Estimated annual cost = $128 billion in the United States, including $80.8 billion of direct medical costs and $47 billion of indirect costs such as job limitations/time off, activities 180

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of daily living (ADL) limitations/care giver needs, and biopsychological issues including depression, anxiety, and so on

III. Clinical Symptoms/Diagnosis A. Subjective: Joint pain, stiffness B. Objective: Limited range of motion (ROM), deformity (eg, genu valgum or genu varum at the knee), effusion C. Table 16.1: American College of Rheumatology (ACR) knee OA clinical criteria

IV. Physical Exam Findings/Tests A. Inspection: Check for malalignment, deformity, bony enlargement, asymmetry, atrophy, effusion (inflammation, if present, is usually mild and localized to the affected joint, unlike rheumatoid arthritis) B. Palpation: Tenderness to palpation at the joint margins, may also be tender over periarticular ligaments and tendons C. ROM: Crepitus with motion, limited ROM, pain or stiffness with ROM D. Strength: May or may not be impaired E. Sensation/reflexes: Should be normal unless there is a history of prior surgery, which may cause neurologic impairment F. Special tests: Compression of articular surfaces against each other/axial load with or without applied grind may cause pain

V. Imaging Studies/Lab Tests A. Radiographs: A minimum of two orthogonal views should be obtained of the joint. For knee OA, anteroposterior (AP) (weight bearing if examining the knee) and non–weightbearing lateral views are standard. Additional specific views can be obtained for each joint (eg, Merchant’s view in the knee, frog leg view in the hip, etc). Radiographic findings of OA include decreased joint space, irregular articular surfaces, osteophytes, cystic change, subchondral sclerosis (see Figure 16.1) B. Advanced imaging (MRI, CT) is not needed in cases of advanced OA, but may be of use in mild OA if there is concern for ligament, tendon, or nonarticular cartilage (meniscus, labrum) pathology C. Synovial fluid analysis is not crucial, but if conducted, should show: Viscosity—high; clarity—clear; color—straw/yellow; white blood cells (WBC)/mm3—200 to 2,000; % polymorphonuclear leukocytes (PMN)— 30 years are Outerbridge Grade III 4. Most commonly associated lesions are the medial meniscus tear (37%) and anterior cruciate ligament (ACL) injury (36%)

III. Clinical Signs and Symptoms A. Intermittent locking, recurrent effusions, crepitus, and persistent pain

IV. Physical Exam Findings/Tests A. Inspection: Normal or with effusion B. Palpation: Tenderness over articular surface or joint line C. ROM: May be impaired if loose body or free flap of cartilage blocks movement D. Strength: May or may not be impaired E. Sensation/reflexes: Normal F. Special tests: (+) McMurray’s test = meniscal tear in the knee; other maneuvers of load and shift or load and pivot type, which produce a “clunk” or sensation of instability at the joint may suggest cartilage injury

V. Imaging Studies/Lab Tests A. Plain radiographs = normal in low-grade lesions, may show defect in high-grade lesions, osteochondral lesions, or if there is a loose body B. MRI (particularly T2 proton density sequence) = 30% to 85% sensitive and 85% to 99% specific for chondral lesions C. Arthroscopy is the gold standard for detecting chondral lesions

VI. Medical Management A. Oral analgesics or NSAIDS for pain management B. Intra-articular corticosteroid injection for pain management C. Bracing for joint unloading (ie, valgus unloading knee brace)

VII. Surgical Management A. Arthroscopic debridement: Removal of loose cartilage flaps provides immediate relief of symptoms, but may not be long lasting 1. Indications: Age = any, lesion size 85 mmHg. This may require fluids and even pressors 4. Disability (ie, neurologic status) a. Level of consciousness and orientation b. Symptoms of pain, altered sensation, or motor weakness

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c. Screening exam of sensory and motor function in all limbs d. Cranial nerve exam e. If all is normal, gentle cervical spine palpation i. Abnormal/pain: Implement cervical spine precautions ii. Normal/no pain: Gentle active range of motion (AROM) with support (A) Next, AROM without support (B) If normal, the athlete may sit, and then stand (C) Full exam on sidelines/in the training room f. Any abnormality at any point requires cervical spine precautions 5. Exposure a. Cut jersey and shoulder pads to allow access to chest for auscultation 6. Even in patients with life-threatening cardiac or pulmonary collapse, cervical spine precautions should be maintained whenever possible

IV. Immediate Stabilization in Neutral Position Should Be Attained Without Traction A. Primary goal is cervical spine stabilization. A long spine board or other immobilization device should be used for transport B. Traction can cause distraction and potentially lead to further injury and is not recommended C. The person stabilizing the head/neck should direct the rescue D. Player may need to be logrolled if in prone position to allow for airway management 1. This technique requires four to five people 2. This should be done directly onto a spine board if possible to avoid moving the player twice a. Moving the spine into neutral position should cease if any of the following occur i. Movement causes increased pain ii. Increase or change in neurological symptoms iii. Airway becomes compromised iv. Resistance is encountered 3. Once the body has been secured to the spine board, the helmet should then be secured to the board as well, using foam pads for support (see Figure 19.1) a. Sand bags are no longer recommended due to excess weight 4. Tape is next used with a two-point system across the forehead and chin

Figure 19.1

Helmet secured with tape and foam pads.

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5. Arms should be kept free for easy intravenous access, but hands/thumbs should be taped together to prevent the arms from falling off the board during transport E. If the athlete is supine, the lift-and-slide technique should be used rather than logroll, as it has been shown to cause less movement at the head and cervical spine a. Previous recommendations of a six-plus-person lift have now been changed to recommend an eight-person lift (see Figure 19.2A, B, and C) F. A vacuum mattress is another alternative. This creates a custom fit and is more comfortable for the athlete, though it still requires the stabilizing force of a long spine board underneath. It can also be used with a concomitant pelvis or femur fracture.

V. Sports-Specific Equipment Considerations A. Previous recommendations have always stated that transport should occur with helmet, chin strap, and shoulder pads in place for American football and ice hockey. The National Athletic Trainers’ Association (NATA) recently released a statement, which was later amended, to recommend that protective equipment may be removed prior to transport in the appropriate situation by trained professionals 1. Face mask removal should occur first for airway access (see Section VI for description of the technique) 2. Cutting of the ties of the shoulder pads can often be performed to allow for access to the chest if needed for auscultation and CPR B. If equipment needs to be removed on the field, use the “all or nothing” principle for American football and ice hockey. The helmet and shoulder pads work together to help maintain neutral spine when they are properly fitted. At least three trained and experienced members of the medical team are required for equipment removal 1. Helmet and shoulder pads should be removed together a. Helmet removal with shoulder pads in place leads to hyperextension/lordosis of the cervical spine b. If the helmet has become dislodged, then padding should be placed under the head to maintain neutral spine until shoulder pads can be removed c. A rigid cervical collar must be placed after helmet removal. Manual in-line stabilization should be maintained until the athlete has been placed on a spine board and the head is immobilized C. Although the helmet and shoulder pads generally should not be removed until adequate stabilization has occurred after transport to the emergency department, there are certain situations (noted in Table 19.1) that require their removal on the field D. In other sports, remember that the goal is maintenance of neutral spine 1. Equipment that hinders this primary goal, or that does not assist in providing stability, should be removed by a trained professional

(A)

(B)

(C)

Figure 19.2 (A, B, C) Lift-and-slide technique (sequential pictures). Note that the rescuer who controls the head/neck is directing the rescue.

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Table 19.1

Guidelines for On-Field Equipment Removal

The following situations necessitate on-field removal of helmet and shoulder pads prior to transport 1. Helmet is not properly fitted and allows for independent movement of the head 2. The face mask cannot be removed in a reasonable period of time and is preventing airway access and control 3. Even after removal of the face mask, the helmet design is such that adequate airway control is not possible 4. Shoulder pads are preventing adequate cardiopulmonary resuscitation and require removal 5. All or none principle: Helmet and shoulder pads should be removed together in American football and ice hockey

2. Shoulder pads in lacrosse and field hockey may not be sufficient to elevate the torso to the same level as the helmeted head. In these cases, both helmet and shoulder pads may need to be removed a. A cervical collar should then be placed before transfer to a spine board

VI. Sports-Specific Equipment Removal A. Three people are recommended; one to remove equipment, one to maintain spine stabilization from the head of the patient, and one to stabilize from below as the helmet is removed (see Figures 19.5 and 19.6) B. The team physician or athletic trainer should accompany the athlete to the emergency department to ensure proper transfer of care and continued cervical spine stability during equipment removal C. Face mask 1. This is removed during the initial assessment to allow for airway access 2. Chin strap and helmet cheek pads should be left in place 3. A combined tool approach should be utilized for face mask removal a. A cordless power screwdriver is often the most efficient tool and causes the least amount of movement (see Figure 19.3)

Figure 19.3

Face mask removal with a power screwdriver.

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b. Cutting tools such as a trainer ’s angel should always be present as backup in case of screwdriver failure (see Figure 19.4) i. These have been shown to cause greater head and neck movement than utilization of the power screwdriver c. Proper maintenance and donning of equipment is key to allow its prompt removal i. Rusted or stripped screws or improperly positioned chin straps will make removal more difficult D. Helmet 1. Should be removed with the shoulder pads in American football and ice hockey. The only exception is with accidental dislodgement of the helmet at the time of the injury 2. Requires stabilization of the cervical spine from the front 3. Ear pads inside the helmet should be removed one side at a time (see Figure 19.5)

Figure 19.4 Tool options for face mask removal: a standard cutting tool and two different cordless power screwdrivers.

Figure 19.5 Ear pad removal with a tongue depressor in the emergency department. Note attention to continued cervical spine stabilization.

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4. Helmets with an air inflation system may need to be deflated prior to removal. This can be accomplished with an 18-gauge needle placed in the external ports 5. The helmet will need to be rolled forward to clear the occiput during removal (see Figure 19.6) 6. The shoulder pads should then be quickly pulled off; it is imperative that they have already been untied or cut, both anteriorly and under both arms 7. Cervical collar is put in place after helmet removal 8. Equipment may be removed before or after initial imaging of the patient in the emergency department a. Helmet and, particularly, shoulder pads make adequate visualization difficult on plain films. CT does not have this restriction b. MRI should not be the initial study of choice due to time constraints and artifact from metal within the helmet

VII. Airway Management A. Management should be left to the person with the most skill and experience. As there is no clear literature on which maneuvers cause the least amount of cervical spine movement, practitioners should use the technique with which they are most comfortable B. Jaw thrust and chin lift maneuver may be used even before face mask removal. Head tilt should be avoided to prevent further cervical spine injury C. Mouthpiece and face mask should be removed D. Pocket mask can sometimes be used even with the face mask in place 1. A bag-valve device with face mask is generally adequate for on-the-field ventilatory support E. Advanced airway management techniques produce less cervical spine movement but require the presence of trained personnel 1. Indications for definitive airway management with ventilation include apnea, inability to maintain oxygenation, high risk of aspiration, and severe closed head injuries a. Laryngeal mask airway may be safely inserted in the helmeted athlete b. Endotracheal tube (ET) is difficult to place and is often unsuccessful in the helmeted athlete c. Esophageal tracheal combitube (ETC) has been shown to be more easily and efficiently inserted in the helmeted athlete than ET

Figure 19.6

Helmet removal in the emergency department.

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VIII. Further Management Options After Transport A. High-dose methylprednisolone has been used for the initial management of spinal cord injuries, though some authors still debate its use. There is controversy over the data analysis and conclusions of the initial studies. This can be considered a treatment option rather than a treatment requirement 1. One survey demonstrated that 91% of neurosurgeons prescribe methylprednisolone after acute, nonpenetrating, traumatic spinal cord injury 2. National Acute Spinal Cord Injury Study II (NASCIS II) utilized 30 mg/kg intravenous (IV) bolus over 15 minutes, followed by a 45-minute rest, followed by 5.4 mg/kg/h for 23 hours a. This showed improvements in neurological testing scores at 6 weeks and 6 months if given within the first 8 hours from injury b. If given after 8 hours from initial injury, neurological scores were not significantly different than of those who received placebo c. Functional scores were not assessed 3. NASCIS III suggested that the NASCIS II protocol be followed if administration is started within 3 hours. In patients who received methylprednisolone within 3 to 8 hours of injury, they suggested continuation for a total of 48 hours a. The 48-hour regimen correlated with a greater risk of pneumonia and sepsis, but not greater all-cause mortality B. Hypothermia has also been used, though evidence remains sparse and is currently insufficient to justify its use. This is still considered an experimental treatment 1. Hypothermia has been shown to reduce morbidity when used in the treatment of brain injury and myocardial infarction 2. Mechanism remains unclear, but may work by slowing metabolism, decreasing oxygen requirements, and preventing the inflammatory cascade 3. Sepsis, bleeding, and arrhythmias are all possible complications 4. Rewarming can also be complicated by hypotension

Recommended Reading 1. Banerjee R, Palumbo MA, Fadale PD. Catastrophic cervical spine injuries in the collision sport athlete, part 2: principles of emergency care. Am J Sports Med. 2004;32(7):1760–1764. 2. Bell K. On-field issues of the C-spine-injured helmeted athlete. Curr Sport Med Rep. 2007;6(1):32. 3. National Athletic Trainers’ Association executive summary: appropriate prehospital management of the spine injured athlete (updated from 1998 document). Available from http://www.nata.org/sites/default/files/ Executive-Summary-Spine-Injury.pdf. Accessed September 26, 2015. Update 8/5/15 available from http:// www.nata.org/nr06242015. Accessed September 26, 2015. 4. Swartz EE, Boden BP, Courson RW, et al. National Athletic Trainers’ Association position statement: acute management of the cervical spine-injured athlete. J Athl Train. 2009;44(3):306–331. 5. Waninger KN, Swartz EE. Cervical spine injury management in the helmeted athlete. Curr Sports Med Rep. 2011;10(1):45–49.

20 Lumbar Spine Injuries and Conditions Rebecca A. Dutton, Byron Schneider, and David J. Kennedy

OVERVIEW I. Anatomy A. The lumbar spine evaluation is best approached using an anatomic model to arrive at an underlying diagnosis 1. In trauma with suspected fracture, the three-column model is used to evaluate stability in the thoracolumbar spine (see Figures 20.1 and 20.2) a. Anterior column—Anterior longitudinal ligament and anterior two-thirds of vertebral body i. Typically injured by spinal flexion b. Middle column—Posterior one-third of vertebral body to posterior longitudinal ligament i. Rarely injured in isolation, but will cause an unstable injury if accompanied by injury to the anterior or posterior columns c. Posterior column—Posterior longitudinal ligament to supraspinous ligaments i. Typically injured by spinal extension d. Spinal instability is generally implied when two or more columns are involved 2. In cases where fracture and/or spinal instability is not suspected, potential pain generators should be considered, using an anatomic model a. Bone i. Vertebral body ii. Spinous process (SP) iii. Transverse process (TP) iv. Pars interarticularis, and superior and inferior articular process v. Pedicle vi. Sacrum vii. Coccyx b. Soft tissue i. Intervertebral (IV) disk (A) Annulus fibrosus (AF)—Innervated portion of the IV disk and composed of oblique fibrocartilaginous lamellae (B) Nucleus pulposus (NP)—Poorly innervated inner core of the IV disk composed of gelatinous matrix and proinflammatory constituents ii. Ligaments (A) Anterior longitudinal ligament (B) Posterior longitudinal ligament (C) Interspinous ligaments

232

20. LUMBAR SPINE INJURIES AND CONDITIONS

Middle Posterior

Anterior

SAP Vertebral body

Pars

IV disc

* IAP SAP Lamina IAP

Figure 20.1 Anatomical columns of the lumbar spine. Bony anatomy of the lumbar spine divided into anterior, middle, and posterior columns. * Denotes the intervertebral foramen. IAP, inferior articular process; IV, intervertebral; SAP, superior articular process.

iii. Muscles (A) Lumbar paraspinals (B) Quadratus lumborum (C) Gluteal muscles (D) Piriformis c. Nerve i. Spinal nerves

Lamina SAP

*

Interlaminar space

Pars

IAP

Pedicle

*

Figure 20.2 Elements of the posterior column. Posterolateral view of the posterior column bony anatomy. * Denotes the intervertebral foramen. IAP, inferior articular process; SAP, superior articular process.

233

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3. Spinal variants a. Variants exist when there are four or six fully formed lumbar vertebrae between the ribs and fused sacrum, which may predispose to degenerative changes i. Presence of four vertebrae = sacralization of the L5 vertebra ii. Presence of six vertebrae = lumbarization of the S1 vertebra b. A unilateral or bilateral enlargement of the TP of the most caudal lumbar vertebra may articulate or fuse with the sacrum or ilium, which can predispose to L4-L5 (level above) degenerative changes, and when symptomatic is termed Bertolotti’s syndrome (common in the setting of a partially sacralized L5)

II Epidemiology and Overview of Back Pain A. Back pain affects up to 95% of people at least once during their lifetime 1. Annual incidence of 5% to 10% in the United States 2. Generally self-limited with a favorable natural history, though high recurrence rate B. Low back pain in athletes 1. Back pain is reported by ~30% of athletes; however, rates vary by sport 2. Common causes include a. Annular tears and/or IV disk herniation b. Spondylolysis (most common cause of low back pain in adolescent athletes) c. Minor fractures d. Musculoligamentous injury 3. Risk factors for low back pain in the athlete a. Prior back injury b. Anatomical considerations i. Long trunk ii. Lumbar inflexibility iii. Lower extremity inflexibility iv. Aberrant motor control c. Sports involving repetitive hyperextension, axial loading, twisting, or direct contact (eg, football, gymnastics, wrestling, rowing) C. Evaluation overview 1. Causes of low back pain vary by age (see Table 20.1) 2. History a. Red flags that warrant expedited evaluation include i. Bowel and/or bladder dysfunction ii. Saddle anesthesia iii. History of cancer or immunocompromised state iv. Unexplained weight loss (may suggest occult malignancy)

Table 20.1

Common Causes of Low Back Pain by Age

Preadolescent

Adolescent

College

Adult

Senior

Slipped capital femoral epiphysis (or other hip disorders) Malignancy

Spondylolysis Malignancy

Annular tear Intervertebral disk herniation Spondylolysis Ligament/muscle strain

Annular tear Intervertebral disk herniation Facet arthropathy Disk degeneration Lumbar spinal stenosis Mechanical low back pain

Compression fracture Facet arthropathy Disk degeneration Lumbar spinal stenosis Malignancy

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v. Fever, chills, or night sweats vi. History of violent trauma b. Yellow flags that indicate a potential poor response to basic treatment i. Maladaptive beliefs ii. Poor sleep iii. Mood disorder iv. Job dissatisfaction v. Poor social support vi. Compensation and/or litigation issues vii. Kinesiophobia 3. Physical examination a. Neuromuscular assessment may reveal the level of pathology (see Table 20.2) b. Observe for postural preference during interview i. Anterior/middle column (namely, disk) pathology is typically exacerbated by trunk flexion; patient may prefer standing or leaning backward when at rest ii. Posterior column (namely facet) pathology is typically exacerbated by trunk extension; patient may prefer sitting or leaning forward when at rest c. Kinetic chain assessment: Examine pelvis/legs for proper range of motion (ROM), strength, leg length discrepancy D. Management overview: A comprehensive, multimodal approach to include 1. Therapy programs a. Mechanical diagnosis and therapy (MDT) with focus on centralization of radicular pain b. Mobilization c. Lumbar stabilization—Can initiate in neutral, flexion, or extension based on patient tolerance d. Pelvic floor therapy to strengthen pelvic girdle musculature e. Cognitive behavioral therapy, particularly useful when yellow flags (see Section II.C.2.b) are evident 2. Pharmacologic treatment a. Anti-inflammatories i. Oral corticosteroids have been shown to be ineffective b. Opioid analgesics c. Neuromodulating agents i. Anticonvulsants (eg, gabapentin) ii. Antidepressants (eg, amitryptiline, nortryptiline, venlafaxine, duloxetine) d. Antispasmodics

Table 20.2 Muscle Action

Area of Sensory Lossa

L2

Hip flexion

Mid-anterior thigh

L3

Knee extension

Medial knee

Patellar

L4

Ankle dorsiflexion

Medial malleolus

Patellar

Dorsal aspect of third MTP

Medial hamstring

Lateral aspect of calcaneus

Achilles

S1 a

Spinal Nerve Assessment

Root

L5

a

b

Great toe extension

b

Ankle plantar flexion

Associated Reflex

Muscle action and area of sensory loss taken from ASIA Standard. Additional functional tests for myotomes include side-lying hip abduction (L5) and toe raises (S1). MTP, metatarsophalangeal. b

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i. Cyclobenzaprine—Acts centrally by blocking serotonergic pathway, ultimately inhibiting alpha-motor neurons ii. Tizanidine—Alpha 2-adrenergic agonist that increases presynaptic inhibition of motor neurons, reducing muscle spasm 3. Interventional treatment a. There are many interventional options (including injections and surgery) that may be utilized for a variety of causes of low back pain. These are discussed in the following sections based on the appropriate indication by diagnosis. E. Return to play 1. For most conditions involving the lumbar spine and not requiring immediate surgical intervention, management begins with a period of activity modification and/or relative rest, though complete bedrest is rarely indicated 2. Thereafter, a graded return protocol is often warranted a. Core strengthening exercises may commence once the patient is pain-free in daily activities and is able to perform simple strengthening exercises (eg, abdominal crunch) without pain b. Thereafter, the patient should progress through a strengthening program, building toward sport-specific activities c. An athlete should not be cleared for return to sport until pain has improved or resolved and full ROM is restored.

SPECIFIC DIAGNOSES III. Herniated NP (HNP) A. General considerations 1. More common in patients less than 50 years old a. As the NP desiccates with age, it becomes less prone to herniation 2. >90% occur at L4–L5 or L5–S1 3. Pathophysiology a. Radiculitis—Shooting pain down the lower extremity in a pattern corresponding with a specific dermatomal region i. An inflammatory process caused by the NP itself, resulting in nerve root irritation and pain b. Radiculopathy—Corresponding segmental neurologic deficits in addition to radicular pain i. Mechanical compression of the nerve roots resulting in nerve dysfunction c. The AF of the IV disk is innervated, and, accordingly, an annular tear without herniation of the NP can result in axial pain without radicular symptoms, as the spinal nerves are not involved 4. Anatomical descriptors of disk herniations a. Axially defined, relative to associated structures i. Central/paracentral—Spares the exiting nerve but may affect one or more descending nerve roots ii. Subarticular—Typically affects the nerve root that is transversing to exit at the level immediately caudal to the level of herniation but may also affect the nerve root exiting at the level of herniation iii. Foraminal—Affects the nerve root exiting at the level of herniation iv. Extraforaminal—Typically affects the exiting nerve root b. Morphologically defined i. Bulges—Involve 50% to 100% of the disk circumference and by definition are not technically herniations ii. Herniations

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(A) Protrusion—Edges of disk material in any plane are less than the edges of the base of herniation in the same plane. Can either be broad based (involving 25%–50% of disk circumference) or focal (involving 0%–25% of the disk circumference) (B) Extrusion—In at least one plane, the distance between the edges of disk material are greater than the distance between the edges of the base (C) Sequestration—Displaced disk has lost contact with the parent disk B. Diagnosis 1. History a. Pain may initially be axial but can extend down lower limb in a dermatomal pattern corresponding with affected nerve root b. May have subjective strength or sensory deficits 2. Physical exam a. Neurologic deficits corresponding with affected level (Table 20.2) b. Positive neural tractions tests i. Straight leg raise (for L4–S1 nerve roots) ii. Slump test (for L4–S1 nerve roots) iii. Femoral stretch test (for L1–L3 nerve roots) 3. Imaging a. Radiographs i. Most helpful in evaluating and ruling out pathologies other than HNP b. MRI i. HNPs are frequent incidental findings on MRI (A) Therefore, it is important to compare clinical and imaging findings (ie, whether the level and morphology of HNP correspond with the patient’s symptoms) (B) Sequestrations and extrusions are more likely than protrusions to be symptomatic 4. Electrodiagnosis for radiculopathy a. High specificity but low sensitivity i. Needle electromyography changes are demonstrated after 5 days in the paraspinal muscles but not for 2 to 3 weeks in the lower limb muscles b. Motor nerves must incur axonal damage before motor nerve conduction studies or electromyography show abnormalities C. Treatment 1. Nonoperative a. Activity modification—Absolute rest is contraindicated but avoidance of activities that exacerbate symptoms (typically lumbar flexion) may be warranted b. Physical therapy i. Classically, extension-based exercises (McKenzie approach) with the goal of centralizing radicular symptoms ii. Lumbar stabilization/strengthening to decrease mechanical stress on IV disk and vertebrae c. Oral medications—See Section II.D.2 d. Interventional procedures i. Epidural steroid injections—Primary goal is symptom relief to allow for natural recovery (A) Administration of anti-inflammatory corticosteroids directly adjacent to the inflamed spinal nerve (B) Best available evidence strongly supports use of transforaminal epidural steroid injections for radicular pain caused by HNP

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1. About 60% of patients seem to achieve at least 50% relief of pain between 1 and 2 months 2. Reduce the need for surgery and are cost-effective 2. Surgery a. For management of radicular pain, not axial pain b. Indications i. Significant or worsening neurologic deficits ii. Failure of other treatment options iii. Possibly when faster return to play is needed depending on severity of symptoms c. Most common technique is microdiscectomy of herniated disk material to decompress nerve root i. Highly successful—Estimated report 90% to 95% success rates ii. Estimates vary but approximately 10% risk of reherniation

IV. Fractures A. Compression and burst fractures 1. General considerations a. Typically caused by axial compression, with or without hyperflexion i. Compression fractures result from failure of the anterior column of the spine ii. Burst fractures represent a failure of both anterior and middle columns (A) Can have widening of pedicles and retropulsion of bone into spinal canal (B) Neurologic sequelae have been reported in up to 60% b. Most often occur at the thoracolumbar junction c. Risk factors include i. Osteoporosis ii. Advanced age iii. Social habits: Alcohol and tobacco use iv. Low body weight v. Calcium and vitamin D deficiency vi. Corticosteroid use vii. Malignancy—Most often, multiple myeloma or metastatic disease 2. Diagnosis a. Imaging i. Radiographs (A) Compression fractures appear as wedge-shaped anterior compression of the vertebral body, often of the lower thoracic or upper lumbar vertebrae (B) Burst fractures demonstrate loss of vertebral height with possible compromise of posterior elements/alignment ii. Advanced imaging (A) CT, bone scan, single photon emission computed tomography (SPECT), or MRI may increase sensitivity for compression fractures when radiographs are negative but clinical suspicion remains high (B) In instances of burst fractures, CT or MRI may be useful to evaluate for fracture or dislocation of the posterior elements as well as the integrity of the foramina and contained structures b. In patients for whom a clear mechanism of injury cannot be identified, further evaluation must be undertaken to identify an underlying cause. This includes workup for secondary causes of osteoporosis and possibly infection or malignancy if suggested by the patient’s presentation 3. Treatment a. Nonoperative management strategies include i. Activity modification

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ii. Physical therapy—Focusing on ROM and core strengthening, initially in extension bias iii. Oral medications—See Section II.D.2 iv. Bracing—With a thoracolumbosacral orthosis (TLSO) (A) May be considered as an adjuvant for compression fractures (B) Is recommended for 3 months in burst fractures that are managed nonoperatively v. Close follow-up is important to monitor for progressive deformity or changes in neurological status, which may necessitate surgical intervention b. Surgery may be considered in the following circumstances i. Greater than 50% loss of height of the anterior vertebral body ii. Greater than 25° of kyphotic deformity iii. Subluxation of the posterior facets iv. Increase in interspinous process distance v. Spinal canal compromise >50% vi. Neurologic deficits vii. Refractory pain despite an appropriate course of nonoperative care B. SP and TP fractures 1. General considerations a. Typically result from direct trauma to posterior spine i. Forced flexion with rotation may cause an SP fracture ii. Violent contraction of psoas major may cause a TP fracture b. Rarely accompanied by neurological deficits, but may have concurrent abdominal injury, such as retroperitoneal bleeding or lacerations to the spleen, liver, or kidney 2. Diagnosis a. Generally presents with well-localized pain i. Often following direct trauma or forced hip extension ii. Pain with hip flexion may suggest TP fracture b. Imaging i. Radiographs—May reveal fracture; however, relatively insensitive for TP fractures ii. CT scan to confirm diagnosis as well as evaluate concurrent fractures, soft-tissue injury, or abdominal bleeding iii. MRI is warranted only if neurologic signs are present c. For TP fractures, it is especially important to consider concomitant visceral injury i. Physical exam should include a thorough abdominal exam ii. Urinalysis for hematuria is a worthwhile screen for associated genitourinary injury iii. CT could be considered if injury to visceral/abdominal structures is suspected 3. Treatment a. Nonoperative management includes i. Activity modification ii. Cryotherapy iii. Oral medications—See Section II.D.2 iv. Physical therapy may be considered to maintain/restore core control and proper lumbar alignment b. Surgery is not indicated for isolated SP or TP fractures c. Return to play is generally considered when the athlete is pain-free with full return of ROM

V. Lumbar Strain A. General considerations 1. Injury to the lumbar intrinsic muscles, tendons, and/or ligaments

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2. While universally accepted as a common source of low back pain in the athlete, literature on the topic is sparse and its existence is even questioned by some a. Injury is believed to result from overuse, acceleration-deceleration, trauma, and/or repetitive eccentric loading b. Release of proinflammatory cytokines in response to cyclic ligamentous load has been demonstrated B. Diagnosis 1. History a. Typically presents with local paraspinal tenderness and spasm b. Pain worse with bending, twisting, and weight bearing 2. Physical exam a. Focal palpable paraspinal tenderness and spasm b. Visible swelling, edema, erythema, or bruising may be present i. Significant contusions may indicate underlying TP fracture or renal injury ii. No associated neurological deficits 3. Imaging a. Generally not indicated, but may be used to exclude other pathologies b. Should be considered for persistent symptoms (>30 days) or presence of red flags C. Treatment 1. Activity modification, but bedrest generally avoided if possible 2. Ice and/or heat; deep tissue massage 3. Physical therapy—Emphasizing lower extremity (especially hip and hamstring) flexibility, lumbar ROM, as well as lumbar stabilization

VI. Zygapophyseal (Facet) Joint Pain A. General considerations 1. Degenerative process that increases in incidence with age 2. Common cause (up to 40%) of axial low back pain 3. Anatomy and pathophysiology a. Synovial joints innervated by medial branches of dorsal rami from the two spinal nerves rostral to that level i. Most common levels affected are L4–L5 and L5–S1 b. Degeneration results in synovial inflammation and joint hypertrophy as in all other synovial joints B. Diagnosis 1. History a. Axial low back pain typically reproduced by lumbar extension and rotation b. Functionally, patient may report pain with sleeping prone, reaching overhead, or prolonged standing c. May be referred in nondermatomal distributions to flank, buttock, groin, or thigh 2. Physical exam a. No examination maneuvers are proven to be diagnostic of facet joint pain b. Facet loading maneuver (lumbar extension-rotation) commonly performed despite low sensitivity and specificity 3. Imaging a. Radiographs, MRI, and CT often show diffuse degenerative changes including facet hypertrophy and sclerosis i. Radiographic degenerative changes do not correspond with symptoms b. Bone scan/SPECT can identify active inflammation and may predict better clinical response to therapeutic injection i. Corresponding changes on MRI-T2 fat suppression imaging may also correlate with clinical response to therapeutic injection

20. LUMBAR SPINE INJURIES AND CONDITIONS

241

4. Diagnostic procedures a. Medial branch blocks (MBBs)—Most accepted/validated means of diagnosing facet joint pain is dual controlled anesthetic blocks of the corresponding medial branches C. Treatment 1. Nonoperative a. Physical therapy i. Focused on lumbar/core stabilization ii. Improve flexibility of hip flexors to reduce lumbar lordosis iii. Avoid end-range lumbar extension b. Oral medications—See Section II.D.2 c. Interventional procedures i. Intra-articular steroid injections (A) Injection of steroid into facet joints to reduce synovitis and inflammation (B) Evidence in support of the therapeutic utility of intra-articular facet steroid injections is mixed and limited (C) Those with positive findings on SPECT or MRI T2 fat suppression may respond better to facet steroid injection ii. Radiofrequency ablation (RFA) of medial branches (A) Electrothermal injury applied to the respective medial branches to block nociceptive afferent signals (B) In the general population, roughly 60% of patients can expect 80% relief and 80% of patients can expect 60% relief for up to 12 months after lumbar RFA in properly selected patients (namely, positive response to dual controlled MBBs) (1) Has not been specifically studied in athletes (C) If symptoms return, RFA is repeatable and often reinstates the relief experienced with the initial RFA

VII. Sacroiliac (SI) Joint Complex Pain A. General considerations 1. Prevalence of SI joint pain varies depending on how it is defined but it is relatively low compared to other sources of low back and buttock pain 2. Anatomy and pathophysiology a. Sacrum articulates with the ilia, distributing body weight to the pelvis b. Innervation includes L5 dorsal rami, lateral branches of sacral spinal nerves, and possibly anterior innervations to anterior joint capsule as well c. Normal SI joint function allows for small degrees of pelvic motion in multiple plains d. Pain can arise from the synovial joint itself or from the posterior sacral ligaments e. Predisposing factors to mechanical pain include leg length discrepancy, older age, prior spine surgery, and pregnancy f. Nonmechanical cause of SI pain include direct trauma and rheumatologic/inflammatory arthritis B. Diagnosis 1. History a. The clinical presentation of SI joint pain is often nonspecific, with pain reported in the buttocks (94%), low back (72%), and thigh (48%) 2. Exam a. SI joint tenderness with palpation and positive Fortin finger sign b. Pain with flexion, abduction, and external rotation (FABER) maneuver c. Hypermobility/hypomobility of SI joint on single-leg stance (Gillet’s maneuver) d. Three out of five positive provocation maneuvers increase likelihood of SI joint– mediated pain: sacral distraction, thigh thrust, Gaenslen’s maneuver, SI compression, sacral thrust

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3. Imaging a. In the absence of trauma or rheumatologic sacroiliitis, there is no correlation between pain and radiologic imaging b. In rheumatologic conditions, radiographs may show SI joint sclerosis and MRI may show subchondral edema 4. Diagnostic procedures a. Intra-articular anesthetic injections are commonly used to aid in diagnosis i. Decreased sensitivity as they fail to diagnosis posterior ligament pain ii. False-positive rates of approximately 20% C. Treatment—Nonoperative 1. Physical therapy a. If pain due to hypermobility, focus on lumbopelvic stabilization, including gluteal and pelvic floor strengthening b. If pain due to impaired mobility, focus on manipulation/mobilization of joint 2. Pelvic (SI) belt may be considered as an adjuvant 3. Interventional procedures i. Intra-articular steroid injection (A) Effective for pain management in patients with rheumatologic spondyloarthropathy (B) Effectiveness for mechanical SI joint pain less established, though recent meta-analysis suggests slightly greater than 50% of patients will get at least 50% relief for 4 to 6 weeks ii. Sacral lateral branch thermal RFA (A) Heterogeneity of available research makes it difficult to accurately assess true effectiveness (B) Considered when both conservative management and intra-articular steroid injections have failed

VIII. Scoliosis A. General considerations 1. Scoliosis is defined as abnormal lateral curvature of the spine in the coronal plane a. The degree of curvature may be characterized by the “Cobb angle” (see Figure 20.3), which is measured by the intersection of two lines drawn parallel to the superior end plate of the most tilted cephalad vertebra and to the inferior end plate of the most tilted caudal vertebra, respectively i. Scoliosis is defined by Cobb angle ≥10° ii. The direction of the curve is expressed to reflect the direction of convexity. For example, a curve that convexes to the right is termed a “right” scoliosis iii. The apex of the curve defines the level (or location) of the scoliosis (see Table 20.3) iv. Rotation often accompanies scoliosis and is graded by pedicle position in the anteroposterior (AP) radiograph or angular orientation to midline on CT b. Prevalence of scoliosis in the general population is 2% to 3% i. Prevalence of scoliotic curves >30° is 0.3% c. Subtypes and etiology i. Congenital: Results from congenital anomalies causing asymmetry of the vertebrae (eg, hemivertebrae or congenital fusion) ii. Neuromuscular: Arises secondary to underlying neurologic or musculoskeletal conditions (such as spina bifida, cerebral palsy, or muscular dystrophy) iii. Syndromic: Appears in the context of certain genetic disorders (such as Marfan syndrome and neurofibromatosis) iv. Idiopathic: No definite etiology (A) Represents the most common subtype; however, must be a diagnosis of exclusion

20. LUMBAR SPINE INJURIES AND CONDITIONS

Table 20.3

243

Defining Location of Scoliosis

Curve Apex

Level of Scoliosis

C2–C6

Cervical

C7–T1

Cervicothoracic

T2–T11

Thoracic

T12–L1

Thoracolumbar

L2–L4

Lumbar

L5 or below

Lumbosacral

a

Figure 20.3 Cobb angle. Angle a formed by perpendicular lines drawn from end plates of the maximally tilted vertebrae.

(B) Classified based on age at presentation: Infantile (0–3 years), juvenile (4–9 years), adolescent (≥10 years) (C) Adolescent idiopathic scoliosis (AIS) is most common, representing 80% to 85% of cases of idiopathic scoliosis B. Diagnosis 1. Important to consider signs that may indicate the presence of an underlying condition (congenital anomalies or neuromuscular disease) to account for the scoliosis a. Signs that may suggest an underlying cause include i. Rapid progression of the curve ii. Significant, functionally limiting pain iii. Associated symptoms (weakness, bowel/bladder incontinence, headache, etc.) iv. Less common curvature patterns. Right thoracic or right thoracic left lumbar double curves are typical curve patterns of idiopathic scoliosis

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b. A positive family history may favor a diagnosis of idiopathic scoliosis 2. History a. Pain does not tend to be a salient presenting symptom i. Pain, when present, often arises at the site of apex and may be proportional to severity of the curve ii. Severe pain should raise concern for nonidiopathic scoliosis 3. Physical exam a. Inspection: May reveal frank curvature of the spine or asymmetry in postural alignment (eg, side-to-side differences in the height of the shoulders and/or AIS) b. Adams forward bend test: Patient stands with feet together and legs straight, and flexes forward at the waist as if touching his or her toes. A visible thoracic or lumbar prominence on one side is suggestive of scoliosis c. Important to make note of the patient’s height, weight, and Tanner stage i. Risk for curve progression is greatest during a growth spurt 4. Imaging a. Radiographs—Standing, full-length posteroanterior (PA) and lateral views useful to assess i. Anomalies that may suggest congenital or neuromuscular causes (A) Curvature pattern (curve direction and location) (B) Degree of curvature (Cobb angle) and rotation (C) Skeletal maturity and Risser sign (1) Risser sign is a visual measure of the degree of ossification and fusion of the iliac apophysis. A lower Risser grade suggests a greater amount of remaining growth b. Serial imaging is typically performed every 4 to 6 months until skeletally mature to monitor for curve progression C. Treatment 1. Goal of treatment in scoliosis is to ensure curvature 15° between flexion and extension films b. MRI or CT may be indicated to evaluate adjacent structures if there is suspicion for other comorbid pathology or to clarify neural involvement C. Treatment—See Table 20.5 for grade-specific treatment options 1. Nonoperative management is generally appropriate for grades I and II a. Activity modification—Relative rest and elimination of aggravating activities

20. LUMBAR SPINE INJURIES AND CONDITIONS

Table 20.4

Wiltse Classification of Spondylolisthesis

Type

Name

Etiology of Spondylolisthesis

I

Dysplastic

Arises in the setting of congenital rounding of the first sacral vertebra on the superior ventral surface

II

Isthmic

Results from spondylolysis and consequent pars interarticularis separation (type IIa) or elongation (type IIb)

III

Degenerative

Occurs as the result of lumbar degenerative changes (spondylosis) leading to segmental instability

IV

Traumatic

Results from high-impact trauma and subsequent injury to the bony and ligamentous structures other than the pars interarticularis

V

Pathologic

Associated with generalized bone disease such as osteoporosis, rheumatoid arthritis, infection, or malignancy

Table 20.5

249

Grading and Treatment of Spondylolisthesis

Grade

Translation

Management

1

100%

Surgical management, most often with posterolateral fusion with decompression when indicated

† Surgical referral should be considered in an asymptomatic grade III isthmic spondylolisthesis, especially if the athlete is still growing. TLSO, thoracolumbosacral orthosis.

b. Bracing may be considered if symptoms persist despite activity modification c. Physical therapy—Focusing on lumbar and lower extremity flexibility and core stabilization d. Radiographic monitoring every 6 to 12 months may be appropriate to monitor for progression, especially during periods of rapid growth 2. Surgical intervention is considered for a. Motor weakness or evidence of cauda equina syndrome b. Persistent, refractory symptoms of an initial grade I or grade II despite an appropriate course of nonoperative care c. Symptomatic grade III spondylolisthesis d. Grade IV or grade V spondylolisthesis 3. See also Table 20.5 for grade-specific treatment options

Recommended Reading 1. Dolan AL, Ryan PJ, Arden NK, Stratton R, Wedley JR, Hamann W, et al. The value of SPECT scans in identifying back pain likely to benefit from facet joint injection. Br J Rheumatol. 1996;35(12):1269–1273.

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2. Dunn IF, Proctor MR, Day AL. Lumbar spine injuries in athletes. Neurosurg Focus. 2006;21(4):E4. 3. El-Hawary R, Chukwunyerenwa C. Update on evaluation and treatment of scoliosis. Pediatr Clin North Am. 2014;61(6):1223–1241. 4. Kim HJ, Green DW. Spondylolysis in the adolescent athlete. Curr Opin Pediatr. 2011;23(1):68–72. 5. Laslett M, Aprill CN, McDonald B, Young SB. Diagnosis of sacroiliac joint pain: validity of individual provocation tests and composites of tests. Man Ther. 2005;10(3):207–218. 6. Lawrence JP, Greene HS, Grauer JN. Back pain in athletes. J Am Acad Orthop Surg. 2006;14(13):726–735. 7. MacVicar J, King W, Landers MH, Bogduk N. The effectiveness of lumbar transforaminal injection of steroids: a comprehensive review with systematic analysis of the published data. Pain Med Malden Mass. 2013;14(1):14–28. 8. Meleger AL, Krivickas LS. Neck and back pain: musculoskeletal disorders. Neurol Clin. 2007;25(2):419–438. 9. Standaert CJ, Herring SA. Spondylolysis: a critical review. Br J Sports Med. 2000;34(6):415–422.

21 Shoulder Injuries and Conditions Sathish Rajasekaran and Mederic M. Hall

I. Anatomy A. Bony (Figure 21.1) and muscular (Figures 21.2 and 21.3) anatomy

II. Fractures A. Clavicle 1. Most injuries prior to age 23 to 25 are actually physeal injuries 2. Most fractures occur with direct blow, although they can occur with fall on outstretched arm 3. They make up 5% to 15% of all fractures, up to 50% of all shoulder fractures 4. Most midclavicular (80%), 15% distal, 5% medial 5. Examination a. Presents with pain and swelling locally, supporting the elbow with other hand. Rarely, the patient may present with an open fracture b. Tenting of the skin can be seen with middle and medial third fractures c. Neurovascular injury is most common with middle third fractures d. Distal third fractures are more difficult to diagnose clinically than middle and medial third fractures. They can be confused with acromioclavicular joint (ACJ) sprain or arthritis 6. Radiography a. Anteroposterior (AP) and AP cephalic tilt (Zanca view) as well as axillary views can best define triplanar orientation. CT will provide better detail as needed b. Shortening cannot be measured radiographically because it is a multiplanar phenomenon. Best measured clinically or with three-dimensional (3D) CT 7. Classification a. Several classification systems exist, with most identifying fractures as medial, middle, or distal third b. Each subcategory (third) is further described in terms of displaced versus nondisplaced, comminuted versus noncomminuted, and for lateral/distal fractures, whether they involve coracoclavicular ligaments (CCLs) or not. 8. Treatment a. Nonoperative: Typically sling with up to 45° elevation for 4 to 6 weeks or until bony and clinical (nontender) healing. Then gradual return to play (RTP) i. Nondisplaced/minimally displaced, defined as 100%, shortening >15 to 20 mm, flipped butterfly fragment ii. Operations include use of plate and screws or intramedullary rod. Plate and screws more commonly used but less cosmetic, risk of devascularization high, and requires second major operation to remove. Rod is harder to do, less rotational control, easier to take out, and has trend toward lower complication rate than plate fixation

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iii. Distal clavicular fractures (less common, usually in older patients) (A) Unlike midclavicle fractures, tend to be unstable due to loss of CCL support (torn or attached to distal clavicular fragment, allowing displacement of medial clavicular fragment) (B) Usually need the 45° cephalic tilt to accurately assess; CT as needed (C) Treatment is controversial. If nondisplaced, some would recommend trial of sling and close observation. If displaced, then surgery. Others feel due to high rate of instability and nonunion, these warrant early surgery. If displaced from beginning, many would operate due to difficulty obtaining and maintaining reduction (D) Most common surgical stabilization is flexible fixation with coracoclavicular screws or sutures. An added benefit to flexible over rigid fixation here is the relatively minor surgery to remove the implant B. Glenoid (see Section IV.E. Traumatic Instability) C. Humerus (see Section IV.E. Traumatic Instability)

III. Dislocation/Subluxation A. ACJ 1. Anatomy and biomechanics

*Supraspinatus

Rotator cuff

*Teres minor *Infraspinatus

Teres major

Triceps brachii *Supraspinatus *Subscapularis

* = muscles contributing to rotator cuff

Biceps brachii Shoulder muscles

Figure 21.2

Shoulder muscles.

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a. ACJ capsule and acromioclavicular ligaments (ACLs) (especially posterior) stabilize in the AP plane while CCLs stabilize in the superiorinferior plane b. 5° to 10° rotation occurs via ACJ during elevation—less than sternoclavicular joint (SCJ) c. Second most commonly dislocated joint (second to glenohumeral) 2. ACJ pain syndromes a. Include acute traumatic separation, distal clavicular osteolysis, and degenerative joint disease (DJD) b. Exam: Pain over ACJ, positive scarf sign (pain with horizontal adduction at 90° elevation), positive O’Brien test with pain localizing to ACJ. May include deformity c. Distal clavicular osteolysis—Thought to be posttraumatic, although may be microtraumatic due to repetitive overhead lifts, wide-grip bench press, and so on. Irregularity of distal clavicle with DJD. Most common in weightlifters d. Geyser sign—Periarticular ACJ cyst to full-thickness rotator cuff tear (RCT), cephalad migration of humeral head, erosion of inferior ACJ soft-tissue stabilizers, and fluid extrusion from glenohumeral joint (GHJ) into ACJ that subsequently forms periarticular cyst 3. Types of ACJ separations a. Type I—Sprain AC ligaments, joint wide, but no increase in coracoclavicular distance (CCD)

Levator scapulae Trapezius

Rhomboid major

Deltoid

Serratus anterior

Triceps brachii

Latissimus dorsi

Figure 21.3

Scapular stabilizer muscles.

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b. Type II—Tear ACL, sprain CCL. AC joint wide, slight increase in CCD (90% have Bankart lesion and most include injury to the anterior band of the IGHL. Typically need to treat both (Bankart repair and capsular plication) if surgically treated c. Most common nerve injury is axillary nerve (up to 7%); risk increased with dislocation duration and increasing age d. Relocating a dislocated shoulder i. Contraindicated if suspect neurovascular damage or humeral neck fracture, or patient has delayed (>1 week) presentation ii. Optimal technique should be quick and simple to perform, should require minimal analgesia, assistance, or force, and should be effective iii. Always do neurovascular check before/after relocation iv. Kocher ’s and Hippocratic techniques reported to have higher complication rates v. Stimson—Patient prone with weights (5–10 lb) hanging from distal forearm/ wrist; may combine with scapular manipulation, rotating scapula to relocate vi. Boss-Holzach-Matter autoreduction technique—With patient sitting with knee flexed, fingers/hands locked around knee, lean backward to self-apply traction (recommend, patient can do himself/herself, gently) vii. Cunningham technique—With patient in seated position, support affected arm with elbow flexed and shoulder adducted. Begin by massaging deltoid and other shoulder girdle muscles to facilitate relaxation. Then massage the biceps muscle as patient is instructed to shrug shoulder (scapular retraction). Reduction should occur spontaneously viii. FARES (fast, reliable, and safe)/rhythmic handshake—Patient lies supine with affected upper limb adducted, elbow extended, and thumb pointing upward. Hold patient’s hand and apply caudal traction. While applying traction, slowly abduct shoulder to 90°, while also performing vertical oscillatory movement. When shoulder abducted to 90°, externally rotate the shoulder and continue to abduct shoulder e. X-ray views for instability (regardless of etiology). Must have at least two orthogonal views, preferably three i. At least AP and axillary lateral (West Point axillary better at identifying bony Bankart). Axillary/West Point axillary will define humeral head position relative to glenoid. AP internal rotation (IR) will identify Hill-Sachs lesions, but Stryker notch view is the best view to define Hill-Sachs lesion ii. Supraspinatus outlet/scapular lateral/scapular Y view—Lateral view also shows humeral head position relative to glenoid and helps identify scapular body for fractures iii. MRI demonstrates soft-tissue and osseous abnormalities, but usually not required in acute dislocations f. Complications (worse with increasing age and duration of dislocation) i. Axillary nerve injury (see Section E.1.c)—usually resolves in 3 to 6 months. Assess deltoid and sensation on lateral shoulder ii. RCT—15% with acute dislocation if 15% if >50 years iii. Proximal humerus fracture—Up to 40% in patients over 50. Beware of nondisplaced greater tuberosity fractures

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g. Nonoperative treatment i. Immobilization likely has minimal effect on outcome ii. Early studies suggested reduced recurrence risk with external rotation (ER) bracing implemented within 24 to 48 hours, but subsequent studies have not been able to replicate these findings iii. RC and scapular stabilizer rehabilitation program iv. Risk of recurrent instability following nonoperative treatment (A) Age is #1 predictor (1) If 40, 10% h. Surgical treatment i. Primary indication is symptomatic instability, unresponsive to appropriate nonoperative management, with documented structural pathology ii. Early surgery advocated for high-intensity athletes; reduces recurrence rates. Without surgery, recurrence rates up to 95% have been reported iii. Arthroscopic equal to open techniques in skilled hands, with lower morbidity. Typically involves suturing detached labrum to glenoid, capsular plication, and rotator interval closure. Recurrence rates 5% to 15% in contact athletes iv. Common reason for surgical failure is failure to appropriately plicate the capsule v. If there is significant bony pathology, bony stabilizing procedures may need to be performed in addition to those mentioned earlier: (A) If >20% to 25% of glenoid is fractured (large bony Bankart), this needs to be fixed or supplemented with Latarjet/Bristow procedure (coracoid bone transfer to glenoid) or iliac crest bone graft (B) A large Hill-Sachs lesion (>30% humeral head) may engage the glenoid during ER and may need bone graft or osteotomy 2. Posterior—Less common a. Acute dislocation—After forward fall on outstretched arm, or after grand mal seizure or electric shock (eg, lightning strike at mass event). Arm held in significant ER, loss of anterior deltoid contour with dimple just lateral to coracoid (due to prominent coracoid) b. Chronic recurrent subluxation/dislocation—Pain/symptoms with pushing objects (eg, football lineman) c. Physical examination (PE): Posterior glide with or without sulcus sign (deficient rotator interval), scapular dyskinesis, or posterior apprehension d. Evaluation and treatment parallels anterior instability, with the following exceptions i. X-rays may demonstrate reverse bony Bankart lesion (posterior glenoid fracture) or reverse Hill-Sachs lesion (in anterior humeral head) ii. MRI, if obtained, often demonstrates reverse Bankart lesion (posterior glenoid) e. Treatment i. Typically nonoperative. Responds better than anterior dislocations. No definitive data on need or duration of immobilization ii. If surgery needed, typically perform reverse Bankart repair, capsular shift, and rotator interval closure; may be performed open or, more commonly, arthroscopically; recurrence rate 8% to 10% F. Atraumatic instability 1. Usually multidirectional, although may have symptoms primarily in one direction. May be idiopathic or acquired from repetitive use, such as in overhead athletes 2. Pain, weakness, and/or variety of symptoms with activity 3. PE: laxity in multiple directions (anterior and posterior glides, sulcus sign), possibly with apprehension (anterior and/or posterior)

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4. X-rays and MRI usually normal, but MRI may demonstrate large capsule (if gadolinium employed) or nonspecific findings (eg, tendinopathy, labral fraying). This is primarily a clinical diagnosis 5. Treatment: Rehabilitation; 80% to 90% of patients return to sport and activity without major symptoms. If surgery required, inferior capsular shift procedure usually successful (8%–10% failure rate), although with wide variability between patients in outcome G. Bracing for stability 1. Used to limit “at risk” positions. Mainly for anterior instability. May not be tolerated by athletes because of restricted motion 2. There is no hard-and-fast rule that players need to/should return to sport with a brace, although these are commonly prescribed. Must weigh benefits/risks as well as performance and compliance

V. Muscle/Tendon Injuries A. Biceps tendon, proximal 1. May be involved with RC disease. Rarely affected in isolation 2. Stabilizing structures: Rotator interval and subscapularis a. Rotator interval: Contains long head of biceps tendon, CHL, and SGHL b. Suspect rotator interval or subscapularis tear if biceps tendon unstable 3. May be affected by full spectrum of tendinopathy or tenosynovitis 4. Symptoms/PE: Anterior shoulder pain, pain with shoulder flexion, tender over bicipital groove, positive Speed’s maneuver (pain with resisted forward elevation at 90° forward elevation), positive Yergason’s maneuver (pain with resisted supination with arm at side and elbow flexed to 90°) 5. Rupture can be acute or chronic. If acute, patient may perceive a pop and develop bruising. Patients >45 often have associated RC disease. Short head of biceps remains intact. Patient will have “Popeye” sign (ie, bulging biceps muscle). Rupture results in loss of 20% supination and 8% flexion strength, with little functional compromise in most patients. Some continue to report cramping (particularly with rotation/supination) a. Radiographs usually normal. Ultrasound (US) or MRI can evaluate, depending on clinical question. US cannot evaluate intra-articular biceps or labrum b. Treatment: Most ruptures in patients over 40 treated nonoperatively. Younger patients may elect for tenodesis, but even high-level athletes have been successful without long head biceps (eg, John Elway) i. Nonoperative treatment similar to RC treatment ii. Operative intervention may include tenotomy or tenodesis if >50% tendon affected. Tenotomy used for older, less active. If 40 years old) 3. Subtypes of RC pathology a. Primary impingement syndrome—Due to structural narrowing under the anterior acromion or coracoacromial arch. Originally proposed by Neer. Thought to be uncommon in general and rare in young people i. Loose association exists between the presence of a hooked (as seen on a Neer outlet view) or laterally sloped acromion and RCT ii. Neer’s three phases of impingement (A) Stage I (acute)—Edema and hemorrhage (B) Stage II (chronic)—Scarring and fibrosis (C) Stage III (chronic)—Osteophytes, tearing b. Secondary impingement—Pain with overhead activity and RC syndrome, but with no structural compromise. Occurs due to inability to control humeral head in glenoid. Superior humeral head migration causes dynamic narrowing of coracoacromial space and RC irritation. May be due to underlying glenohumeral instability, scapulothoracic instability (leading to glenohumeral instability), or RC dysfunction (eg, tendinosis, tear, neurologic injury). Most common scenario for RC disease in young people, particularly athletes c. Posterior-superior impingement/internal impingement—Pathological contact between the undersurface of the supraspinatus–infraspinatus junction and the posterosuperior labrum. There is normal contact physiologically, but this can become pathological and produce symptoms. May cause partial articular-sided RCT and posterosuperior labral tears. Often seen in throwers during late cocking and acceleration phases of throwing (associated with glenohumeral internal rotation deficit [GIRD]) i. Present with posterosuperior shoulder pain, especially during throwing ii. Pain reproduced with anterior apprehension testing, reduced by relocation test or scapular retraction 4. History a. Insidious or traumatic. Overuse etiology common b. Deep aching pain over deltoid, acromion, deltoid insertion. Rule out ACJ disorders as this area is a common referral pattern for the ACJ. In internal impingement, pain may be more posterior c. Pain increased with activity, particularly overhead (impingement syndrome). May include night pain 5. PE a. RC atrophy or fasciculations—Suggests full-thickness, chronic tear, or suprascapular neuropathy b. Tender subacromial space c. Midrange painful arc of motion d. Pain with or without weakness i. Full can test—Emphasizes (not isolates) supraspinatus; elevation to 90° in scapular plane with arm externally rotated (preferred over empty can)

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6.

7.

8.

9.

ii. Resisted ER—Emphasizes infraspinatus and teres minor; arm at side and resist ER iii. Lift off test—Place patient’s hand on the lumbar spine, palm facing out. Lift the hand off the back and see if patient can hold position; if unable to do so, positive test and suggests subscapularis tear e. Impingement signs i. Hawkins—Arm flexed 90° in sagittal plane, elbow flexed to 90°, examiner internally rotates patient’s arm. Positive test = pain reproduction ii. Neer—Arm flexed maximally in sagittal plane, internally rotated at end range. Pain reproduction = positive test f. Neer impingement test i. Reexamine for impingement after injecting lidocaine into the subacromial space. Resolution of pain confirms external impingement Diagnostic evaluation a. X-rays—Obtain at least two orthogonal views, typically AP (ER and IR) and axillary. Outlet view may be useful to identify acromial shape and ACJ osteophytes. Evaluate for GHJ and ACJ degenerative joint disease (DJD). Os acromial—Unfused anterior acromial apophysis, seen best on axillary view, may cause impingement. Irregularities of greater tuberosity suggest RC disease, including tears. Narrowed acromiohumeral interval males B. Usually idiopathic, but may be associated with diabetes mellitus, inflammatory arthritis, trauma, prolonged immobilization, thyroid disease, stroke, myocardial infarction, or autoimmune disease. May also occur secondary to RC or other disease C. Stage 1 for the first 1 to 3 months, pain but little motion loss initially. Stage 2 months 3 to 9 with reduced pain but increased motion loss, particularly ER. Stage 3 months 9 to 15 with gradual improvement in ROM

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D. X-rays normal, but arthrogram shows significant reduction in capsule volume. Pathology thought to be due to inflammation in rotator interval > global capsule, causing capsule tightening E. During stages 1 and 2, may use modalities, analgesics/NSAIDs, and GHJ injections to reduce inflammation and pain; facilitate rehabilitation; and shorten the duration of the condition. Avoid aggressive exercise because this will exacerbate the condition F. Generally normal/near-normal function returns over a 12- to 14-month period. Patients not improved after 4 to 6 months may benefit from manipulation under anesthesia or arthroscopic lysis of adhesions. Image-guided volume distension of the GHJ and hydrodissection of the rotator interval with a corticosteroid have also been shown to be effective

VIII. Throwing Shoulder A. Understand the phases of throwing. Motion takes about 2 seconds with 75% due to windup and cocking 1. Windup 2. Early cocking 3. Late cocking—Arm abducted (AB) and ER, scapula retracted, maximal anterior shear force due to AB–ER position, and highest shoulder torque 4. Acceleration—Transition from eccentric to concentric, only one-third kinetic energy stays with ball, remainder dissipated via kinetic chain; late cocking and acceleration pathoetiologic in peel-back phenomenon associated with SLAP lesions. GHJ internally rotates at a rate of 7,000° per second 5. Deceleration—Largest joint loads, including compression equal to body weight, posterior shear 400 N, inferior shear >300 N, compression >1,000 N; traction forces during deceleration implicated as one cause of SLAP lesions 6. Follow-through B. RC (see prior discussion) 1. External impingement rare 2. Many throwers exhibit increased joint laxity and increased ROM. Laxity + overuse leads to RC dysfunction (secondary impingement) 3. Traction forces during follow-through can acutely or chronically damage RC muscles. These same traction forces may promote cumulative tensile stress to the posteriorinferior shoulder capsule, producing a Bennet lesion (see the following text) 4. Treat as previously described, surgery a consideration if failure to progress in 3 to 6 months 5. Posterosuperior/internal impingement—See prior discussion; note that condition thought to be accentuated by increased shoulder ER, anterior instability, poor scapular retraction during late cocking/acceleration, and posterior capsular tightness (GIRD) C. SLAP lesions 1. Typically type II 2. Implicated during late cocking/acceleration via peel-back phenomenon and during deceleration due to traction 3. No best test to diagnose—O’Brien, Crank, dynamic labral shear, and so on 4. Many respond to rehabilitation 5. GIRD—Note relationship of posterior shoulder tightness (loss of IR and/or horizontal adduction) to accentuation of the peel-back phenomenon and etiology of SLAP lesions; treat nonoperatively with “sleeper stretch” and, if needed, capsular release D. Bennett’s lesion—Calcification at attachment of the posterior band of the IGHL on glenoid, seen best on axillary x-rays, often an asymptomatic finding, but may be symptomatic; size

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does not correlate with symptoms; treat symptomatically, including injections; but may require surgical removal

IX. Miscellaneous Conditions A. SCJ 1. Only osseous connection of entire upper limb with rest of body. Supported by strong ligaments. Rarely injured acutely, but when injured, usually high forces involved. Costoclavicular ligaments major stabilizers during elevation and rotation 2. Osteoarthritis—May be posttraumatic, but can occur idiopathically, in postmenopausal females, and in the dominant arm a. Symptomatic treatment (eg, activity modification, NSAIDs, injections) at least 6 to 12 months prior to considering surgery b. Operation is resectional arthroplasty 3. Sepsis—Intravenous (IV) drug users, immunocompromised; likely spread hematogenously; surgical emergency; may spread into mediastinum 4. Atraumatic instability—Young, hyperlax; less common 5. Medial clavicular hyperostosis—Often as part of syndromes such as SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, osteitis) 6. Traumatic instability: Most common mechanism is indirect injury, fall onto lateral shoulder. Direction of force and arm position (flexed vs. extended) determine whether anterior or posterior dislocation. Direct injuries less common, but typically involve anterior-to-posterior force and results in posterior subluxation/dislocation a. Anterior—More common (2/3), significant pain, swelling, limited ROM b. Posterior—Less common (1/3), may suspect clinically (do not misinterpret left posterior SCJ dislocation as a right anterior SCJ dislocation); may compromise airway or adjacent vascular structures (look for venous dilatation in arm of affected side) c. Evaluation i. Radiographs should include AP and lateral of chest, but most useful is serendipity view (45° cephalic tilt centered on SCJ), which will show position of clavicle relative to manubrium ii. CT is imaging modality of choice and can be combined with CT angiography to evaluate proximity/status of great vessels iii. MRI usually unnecessary and suboptimal for bone d. Treatment i. If seen within 7 days, CR may be attempted ii. Anterior reductions usually do not remain reduced. Figure-eight brace preferred over standard sling iii. Posterior reductions should only be performed in a controlled environment, with prevascular and postvascular evaluation, with emergency medical and vascular surgery on-site. Immobilize for 6 to 10 weeks iv. If CR fails, need open reduction and stabilization. Putting wires, pins, other instruments into the area of the SCJ for stabilization is almost never the correct answer for any SCJ problem v. If chronic, anterior usually treated symptomatically for 6 to 12 months because many will improve. If not, resectional arthroplasty. Posterior usually open reduction and resectional arthroplasty. May be erosion into great vessels, which is controlled by displaced clavicle vi. In skeletally immature, more likely represents a physeal injury. Physis does not close until age 24. Eighty percent clavicle growth arises from medial clavicle, so large amount of remodeling possible. Merely observe

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B. Suprascapular neuropathy 1. Pain (posterosuperior), weakness, atrophy 2. Noncompressive a. No mass lesion. Etiology unknown, but may be traction from repetitive overhead and adduction activities. Common in volleyball players, but seen in all overhead athletes. May be minimally symptomatic b. Usually affects only the infraspinatus (possibly due to traction at spinoglenoid notch) c. Prognosis excellent with rest and rehabilitation. Many asymptomatic despite marked atrophy. Spinoglenoid notch decompression is an uncommon need d. Parsonage-Turner syndrome (neuralgic amyotrophy) should be included in the differential (see Section IX.D) 3. Compressive a. Usually paralabral ganglion cyst associated with labral tear b. May involve both supraspinatus and infraspinatus (compression at suprascapular notch) or just the infraspinatus (compression at spinoglenoid notch—more common) 4. Signs/symptoms: Posterior symptoms, atrophy, weakness > pain, and preferential affecting infraspinatus; may have labral findings 5. Evaluation: Diagnose cyst by US or MRI; MRI arthrogram better for labrum 6. Many require surgical intervention. May percutaneously drain, but recurrence risk high C. Quadrilateral space syndrome (QSS) 1. Occurs from compression or traction of the axillary nerve (neurogenic QSS) and/or posterior circumflex humeral artery (PCHA) (vascular QSS) as both pass through the quadrilateral space a. Quadrilateral space borders i. Long head of triceps ii. Humeral neck iii. Teres major iv. Teres minor 2. Most published cases are in patients 3 months): Surgical repair may be performed when anatomic reduction is possible; if anatomic reduction is not possible or osteoarthritis is present then a partial wrist arthrodesis may be performed 2. Lunotriquetral/volar intercalated segmental instability a. Much less common than scapholunate injuries and are a result of an axial load with the wrist extended and radially deviated; can also occur as a result of repetitive stress b. Ulnar-sided wrist pain that is usually worsened with activity, especially wrist movements that require rotation and ulnar deviation c. Lunotriquetral shear test—apply a dorsally directed force over the pisiform (and triquetrum) and a palmar-directed force on the lunate, with reproduction of pain with a click indicating a positive test d. Standard x-rays are usually normal; MR arthrogram may reveal a tear of the lunotriquetral interosseous ligament, but arthroscopy is necessary to assess dynamic instability and grade the instability e. Treatment consists of several weeks of immobilization ± corticosteroid injection initially; if no improvement, then surgical treatment is pursued 3. First MCP UCL (skier’s thumb, gamekeeper’s thumb) a. Mechanism of injury is hyperabduction and radial deviation of the first MCP joint b. Tenderness to palpation above the UCL, frequently at its insertion into the base of the proximal phalanx c. Need to determine presence of Stener lesion i. Occurs when the UCL detaches from the base of the proximal phalanx and is transposed dorsal to the adductor aponeurosis, thus facing proximally (Figure 23.7) ii. Visible and/or palpable mass ± gross instability is noted iii. Present in 50% to 70% of suspected cases iv. Best treated acutely with open anatomic repair but can be delayed for 3 to 4 weeks after the injury d. Plain radiographs i. Obtain AP and lateral prior to stress views to assess for fracture ii. Stress views if no fracture seen on initial films Ruptured collateral ligament

Adductor aponeurosis

Adductor aponeurosis (retracted)

Figure 23.7 Complete rupture of the ulnar collateral ligament resulting in a Stener lesion; the distal attachment has been avulsed from the bone.

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iii. Radial deviation applied with the MCP joint in extension and at 30° of flexion; if the joint opens more than 30° (or more than 15° compared to the noninjured side) with both flexion and extension views, complete rupture has occurred iv. If laxity with flexion only, then closed treatment may be adequate e. MRI and/or diagnostic ultrasound may be used to assess for extent of injury to the UCL f. Treatment i. Nonoperative for stable (clinically and radiographically) (A) Short-arm thumb spica cast for 4 weeks (B) After short-arm cast removed then removable spica splint for 2 to 4 months ii. Surgical (A) Unstable (B) Stener lesion (C) Larger displaced avulsion fractures at the base of the proximal phalanx D. Muscle/tendon injuries 1. De Quervain’s tenosynovitis (stenosing tenosynovitis of the first dorsal compartment) a. Most common tenosynovitis about the wrist in the athlete, and is a result of repetitive gliding of the APL and the EPB b. Occurs in activities requiring forceful gripping with ulnar deviation, such as golf, fly fishing, and some racquet sports c. High incidence of EPB tendon traveling in a separate compartment from the APL d. Pain is reproduced over the radial aspect of the wrist with palpation and with Finkelstein’s test (Figure 23.8)—positive when there is pain reproduced at the APL and EPB at the distal radial forearm and wrist with passive ulnar deviation of the wrist with the thumb inside a closed fist e. Treatment i. Rest and immobilization are initial treatments, with 25% to 72% experiencing resolution of symptoms ii. Corticosteroid injections are helpful for most iii. Surgical treatment is used rarely in recalcitrant cases

Figure 23.8 Finkelstein’s test: With patient actively holding the thumb in a closed fist the examiner moves the wrist into ulnar deviation. If pain is provoked over lateral wrist and/or distal forearm then this is suggestive of De Quervain’s tenosynovitis.

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2. Intersection syndrome (extensor tenosynovitis) a. Located at the crossing points of the APL and EPB with the radial wrist extensors 4 to 6 cm proximal to the radiocarpal joint/Lister’s tubercle b. Frequently seen in sports requiring repetitive wrist extension: Oarsmen, weight training, and those playing racquet sports c. Symptoms generally respond to rest, splinting, and nonsteroidal anti-inflammatory drugs (NSAIDs), with use of corticosteroid injections in recalcitrant cases 3. Jersey finger a. FDP avulsion, often at the distal phalanx; often occurs in football when a player tries to grab an opponent’s jersey while tackling, and the finger is forced into extension while the DIP is actively flexed b. Ring finger most commonly involved (75%) but any digit can be injured c. Inability to flex the DIP actively, which is tested while holding the PIP in extension; tenderness may be focal at the site of injury or as proximal as the palm since the flexor tendon sheath may retract d. Plain radiographs to assess for fractures e. MRI or diagnostic ultrasound can determine if the tendon has retracted f. Surgery is treatment of choice in acute cases and should be considered within 7 to 10 days; in chronic cases, functional impairment and pain is often minimal, so observation is preferred 4. Mallet finger (Figure 23.9) a. Results from a disruption of the terminal extensor tendon at its insertion on the distal phalanx, which occurs most often due to impact of the fingertip on a ball or another object resulting in flexion force to the DIP joint, but can occur from an extension axial force b. Common in baseball, basketball, and with football receivers c. Index finger less likely to be involved d. Inability to extend the DIP actively e. Plain radiographs should be done, with associated fractures best visualized on lateral views f. Treatment i. Splint DIP in extension (PIP can be free) for 6 weeks; then for 4 additional weeks at night ii. Surgery is considered if an associated fracture involves more than 40% of the DIP joint articular surface or if there is volar subluxation of the distal phalanx 5. Trigger finger (flexor tenosynovitis) a. Often occurs in racquet and club sports b. Nodule forms from overuse or direct pressure at the flexor tendon sheath, which leads to mechanical catching under the A1 pulley at the MCP level

Rupture

Fracture

Figure 23.9

Mallet finger: Mechanism of injury is either rupture or avulsion fracture.

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c. A corticosteroid injection into the nodule or thickened tendon sheath can improve symptoms in up to 90% of cases; modification of the racquet handle or grip may facilitate recovery 6. Boutonniere deformity (Figure 23.10) a. Rupture of the central slip of the extensor mechanism at its insertion into the base of the middle phalanx b. Results from direct trauma to the dorsum of the PIP joint, an acute flexion force at the DIP, or more commonly following a lateral volar dislocation of the PIP joint that results in injury to the central slip and collateral ligament c. Basketball players and volleyball players are the most common athletes to sustain this injury d. Inability to extend the flexed PIP joint actively, but ability to maintain the extended posture if the finger is placed there passively e. Common finger posture: PIP is flexed and DIP is extended f. Treatment i. In acute injuries, if full passive extension (ie, no flexion contracture) at PIP is present, then splint PIP in extension (DIP free) for 6 weeks ii. In chronic cases, serial casting or splinting for a longer period may be needed to correct flexion contracture iii. Surgery is indicated if associated with a displaced (>2 mm) avulsion fracture fragment E. TFCC injury 1. May be a result of acute trauma, such as from a fall on a pronated or hyperextended wrist, or from overuse or repetitive trauma (eg, in racquet sports) 2. Must be differentiated from other causes of ulnar wrist pain, such as lunotriquetral injuries and ulnar extensor tendon disorders 3. Signs/symptoms a. Pain with palpation over the hollow between the pisiform and ulnar styloid on the ulnar border of the wrist b. Pain is reproduced with lifting an object with the forearm in full supination or while pushing off the palm of the hand with the wrist extended c. The triangular fibrocartilage shear test will reproduce pain when the pisiform is pushed dorsally with the thumb while the index and middle finger translate the ulna head palmarly. 4. Diagnostic imaging a. Plain radiographs may show positive ulnar variance b. MRI with a 3 Tesla magnet or MR arthrography of the wrist approaches the diagnostic accuracy of arthroscopy, with arthroscopy still considered the gold standard in the evaluation of TFCC injuries

Figure 23.10

Boutonniere deformity.

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5. Treatment a. Neutral wrist splinting for 4 to 6 weeks b. Surgical i. Central tear (most common): debridement ii. Peripheral tear: consider repair iii. More chronic injuries and those with positive ulnar variance: ulnar shortening procedure F. Radial epiphysitis (gymnast’s wrist) 1. Seen in young gymnasts (12–14 years old) from repetitive dorsiflexion (>35 h/week of training) creating injury to the distal radial physis 2. Plain films may demonstrate radial epiphyseal widening or metaphyseal irregularity; if normal, consider bone scan or MRI to assess physis further 3. Treatment a. Modify activity b. Resist hyperextension: splint or tape c. Surgery is rarely necessary G. Nail bed injuries 1. With any of the following nail bed injuries, plain radiographs should be performed to look for fractures of the phalanx 2. Subungual hematoma—accumulating painful hematoma that can be decompressed using cautery or an 18-gauge needle 3. Simple and complex nail bed lacerations a. Simple: repaired by removing the nail plate to suture, then replacing the nail plate after repair b. Complex: often occur with a distal phalanx fracture, so both need to be addressed 4. Avulsion of the nail and complex injury with loss of nail bed: Both treated with surgical repair H. Ganglion cysts 1. Synovial cyst communicating with an associated tendon sheath or joint space, most commonly at the scapholunate space; often painless; occur at any age 2. If symptomatic, main complaint is wrist pain and decreased ROM 3. Swelling may be present but should not be relied upon to make the diagnosis 4. History of wrist trauma in 15% with a dorsal ganglion 5. Ultrasound or MRI can be used to confirm diagnosis, if necessary 6. Treatment includes observation, aspiration with corticosteroid injection, or surgical removal for persistent symptoms.

Recommended Reading 1. Chauhan A, Jacobs B, Andoga A, et al. Extensor tendon injuries in athletes. Sports Med Arthrosc Rev. 2014;22: 45–55. 2. DeLee JC, Drez D, eds. DeLee and Drez’s Orthopedic Sports Medicine: Principles and Practice. 2nd ed. Philadelphia, PA: Saunders; 2003. 3. Hile D, Hile L. The emergent evaluation and treatment of hand injuries. Emerg Med Clin N Am. 2015;33: 397–408. 4. Kirchberger MC, Unglaub F, Muhldorfer-Fodor M, et al. Update TFCC: histology and pathology, classification, examination and diagnostics. Arch Orthop Trauma Surg. 2015;135:427–437. 5. Mallee WH, Henny EP, van Dijk CN, et al. Clinical diagnostic evaluation for scaphoid fractures: a systematic review and meta-analysis. J Hand Surg Am. 2014;39(9):1683–1691. 6. McMurtry JT, Isaacs J. Extensor tendons injuries. Clin Sports Med. 2015;34:167–180. 7. Morgan WJ, Slowman LS. Acute hand and wrist injuries in athletes: evaluation and management. J Am Acad Orthop Surg. 2001;9:389–400.

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8. Padegimas EM, Ilyas AM. Distal radius fractures: emergency department evaluation and management. Orthop Clin N Am. 2015;46:259–270. 9. Rettig AC. Athletic injuries of the wrist and hand: part I: traumatic injuries of the wrist. Am J Sports Med. 2003;31:1038. 10. Rettig AC. Athletic injuries of the wrist and hand: part II: overuse injuries of the wrist and traumatic injuries to the hand. Am J Sports Med. 2004;32:262. 11. Shafel ND, Capo JT. Fractures of the digits and metacarpals: when to splint and when to repair? Sports Med Arthrosc Rev. 2014;22:2–11. 12. Slutsky DJ, Trevare J. Scapholunate and lunotriquetral Injuries: arthroscopic and open management. Sports Med Arthrosc Rev. 2014;22:12–21. 13. Wright TW, Moser MW, Sahajpal DT. Hook of hamate pull test. J Hand Surg. 2010;35A:1887–1889.

24 Pelvis, Hip, and Thigh Injuries and Conditions Heidi Prather and Devyani Hunt

I. Anatomy A. Intra-articular hip disorders include injuries to the bone cartilage ligaments and capsule of the hip. B. Extraarticular hip disorders include injuries of the bones, muscles, tendons, ligaments of the hip and pelvic girdle.

II. Epidemiology, Diagnosis, and Treatment A. Fractures 1. Femoral neck stress fractures a. Five percent of all stress fractures usually occur in adults, due to repetitive abductor muscle contraction. b. Classification: Insufficiency type (normal physiologic stress on abnormal bone) and fatigue type (excessive physiologic stress on normal bone). c. Two locations: Compression side (inferior femoral neck), tension side (superior femoral neck). d. History: Insidious onset groin or lateral hip pain, worse with weight-bearing, possible recent change in activity intensity or volume, or change in equipment/environment. e. Physical Examination (PE): Antalgic gait, pain with Patrick/FABER (hip flexion, abduction, and external rotation) test, and hip log roll (see Figure 24.1). f. Diagnosis: Anteroposterior (AP) and oblique hip radiographs, but often negative first 2 to 3 weeks after symptom onset, after which time may show periosteal reaction, fracture line, or sclerosis; three-phase bone scan (bone scan) = increased uptake at fracture site, sensitive but not specific; MRI = bone edema ± fracture line, sensitive and specific. g. Treatment: Compression side: Reduced weight-bearing to allow healing and then rehabilitation. Tension side: Often progress to displacement even with limited weightbearing, may require surgical intervention to prevent displacement. Displaced fractures require open reduction and internal fixation (ORIF). 2. Femoral shaft stress fracture a. Femoral shaft stress fractures are uncommon and make up 2.8% to 7% of all stress fractures incurred by athletes. b. History: Vague anterior thigh pain often during after training. c. PE: Hop test and fulcrum test are positive. d. Diagnostics: Radiograph of the femur, MRI, or three-phase nuclear bone scan. e. Treatment: Non-weight-bearing initially and progress to weight-bearing. Activities are gradually increased as long as symptoms do not remain.

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3. Pubic ramus stress fracture a. Occurs in the inferior rami adjacent to the pubic symphysis. b. Most commonly reported in rugby players and runners. c. History: Groin pain during and after activities. d. PE: Pain with hip adduction and internal rotation, palpation of the pubic symphysis. e. Diagnostics: AP radiographs of the pelvis with confirmation by bone scan or MRI. f. Treatment: Reduced weight-bearing with crutches or walker. Once bony healing is evident and patient is pain-free, rehabilitation includes strengthening of the pelvic girdle and return to sport or exercise specific activities. 4. Sacral stress fracture a. 1.25% of all stress fractures in runners. b. History: Insidious onset pelvic/sacral pain worse with weight-bearing activity. c. PE: Antalgic gait, pain with single leg stance/hopping. d. Diagnosis: Radiographs (AP pelvis), bone scan or MRI (see hip stress fracture section). e. Treatment: Modified weight-bearing to allow healing, then progressive rehabilitation. 5. Femoral shaft fracture a. Femoral shaft fractures occur as a result of a high-velocity trauma and are often associated with other pelvic fractures. b. Rare in sports. c. Diagnostics: Radiographs of the femur and pelvis. d. Treatment: ORIF.

(a)

(c)

(b)

Figure 24.1 Hip physical exam. (a) FABER, (b) resisted straight leg raise, (c) hip impingement test.

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e. Return to sport is often not anticipated for over a year and reduced capabilities are often expected. B. Hip dislocation 1. Orthopedic emergency (requires rapid reduction to reduce chance of avascular necrosis [AVN]); often have associated fractures, dislocations usually occur posteriorly. 2. History: Fall on hip or posteriorly directed blow to flexed knee. 3. PE: Hip pain, leg internally rotated/shortened. 4. Diagnosis: AP and lateral hip radiographs. Postreduction CT recommended to identify fractures or loose bodies. 5. Treatment: Early reduction (often requires sedation), protected weight-bearing, progressive rehabilitation program as pain resolves; surgical treatment often required for associated fractures/loose bodies. C. Muscle/Tendon Injuries 1. Hip flexor (Iliopsoas muscle–tendon complex disorders) a. The iliopsoas muscle–tendon complex consists of three muscles; the psoas major, the psoas minor, and the iliacus. b. The proximal fibers of the psoas muscles originate on the bodies of the 12th thoracic vertebrae and the lumbar vertebrae, cross into the pelvis and join with the fibers of the iliacus to make the iliopsoas tendon and insert on the lesser trochanter. c. The iliopsoas is the primary hip flexor and provides functional stability to the hip, pelvis, and spine. d. History: Anterior hip pain or groin pain that is worse with concentric or eccentric contraction of the hip flexors. Pain with sports activities that require forceful hip flexion or adduction; ambulation; and rising from a seated position. i. Runners may describe anterior groin pain when trying to lengthen their stride during speed training, or with uphill running. e. PE: Key findings include pain with palpation of the tendon during eccentric or concentric contraction, range of motion (ROM), and FABER test. f. The psoas may become dysfunctional as a result of compensating or guarding for an underlying intra-articular disorder. It is also important to examine the hip in weight-bearing during dynamic motion to further assess for abnormal motor patterns that contribute to repetitive overuse injuries. g. Diagnosis: AP and frog-leg lateral radiographs can be used to rule out underlying osseous abnormalities. An MRI or ultrasound (US) can evaluate the tendon and underlying psoas bursa for pathology. h. Treatment: See treatment for internal snapping hip syndrome, in what follows. i. Snapping hip syndrome i. The key feature for snapping hip syndrome is the audible snap heard at or around the hip joint. ii. The syndrome has been classified into three types: external, internal, and intra-articular. iii. External snapping hip is the most common type. It occurs when the gluteus maximus tendon or iliotibial band (ITB) snaps over the greater trochanter. iv. Internal snapping hip can be due to many different causes, the most common of which are a slip of iliopsoas muscle snapping back and forth under the tendon, or the iliopsoas tendon snapping over a bony prominence such as the iliopectineal prominence, anterior inferior iliac spine (AIIS), the femoral head, or the lesser trochanter. v. The snap or pop occurs as the hip moves from flexion to extension or with hip circumduction and is often associated with pain. vi. The tendon is commonly normal in appearance, but shortened in length (ie, tight). Less commonly, the tendon is thickened.

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vii. It is most likely a part of the continuum of iliopsoas chronic dysfunction. viii. The intra-articular type refers to an intra-articular source for the audible or palpable snap often associated with pain. ix. Intra-articular sources include loose bodies, synovial osteochondromatosis, labral tears, cartilage flaps, osteochondral fractures, or transient hip subluxation, which can occur in the setting of joint hypermobility. x. Diagnosis: Radiographs should be performed to assess for fracture, deformity, AVN, and osteoarthritis (OA). US can assess muscle–tendon integrity, bursitis, and dynamic snapping of the tendon. MRI can assess muscle–tendon integrity and provide basic assessment of intra-articular or bony abnormalities. xi. A diagnostic injection under image guidance (fluoroscope or US) of anesthetic into the bursa or tendon can be useful when the diagnosis remains in question. A diagnostic intra-articular injection should also be considered if an intraarticular abnormality needs to be excluded. j. Treatments i. Internal snapping hip: Reducing activities that cause the snap, require significant hip flexor contraction, or excessively stretch the tendon complex. ii. Oral or topical anti-inflammatory medications can be considered. iii. Physical therapy should focus on the iliopsoas tendon with the goal of optimizing the length and strength of the muscle–tendon complex. iv. If the athlete fails a 3-month period of conservative treatment, an image-guided lidocaine and corticosteroid injection into the psoas bursa or a peritendinous injection can be considered. Caution should be used as tendon ruptures have occurred after steroid injections. v. Surgical treatments for painful iliopsoas muscle–tendon complex disorders are used for recalcitrant cases of internal snapping and include lengthening or release of the iliopsoas tendon. A positive response to an image-guided diagnostic injection of the tendon can predict the response to surgical release. Return to full activity is generally allowed after 3 to 6 months. vi. External snapping hip: Stretch the ITB, gluteus maximus, and tensor fascia lata. Strengthen the lumbopelvic musculature with a focus on the hip abductor and external rotators. Occasionally an injection into the greater trochanteric bursa is warranted for pain relief. Surgical release of the ITB is rarely required. 2. Piriformis a. Piriformis pain is thought to be related to muscle inhibition or dysfunction while piriformis syndrome includes entrapment of the sciatic nerve. b. The diagnosis of piriformis syndrome can be confirmed with electrodiagnostic studies (electromyography [EMG]) of the sciatic nerve or image-guided piriformis injection, which provides relief of symptoms. c. Treatment includes release of myofascial restrictions, balancing of the pelvic/hip girdle muscle flexibility and strength, and neuromuscular reeducation of hip adductors, abductors, and extensors. If pain relief is incomplete, image-guided piriformis injection of steroid and or botulinum toxin may be considered. d. In rare refractory cases, surgical release of the piriformis can be considered. 3. Quadriceps contusion/strain/myositis a. Quadriceps strains (rectus femoris is the most common) occur in sports that require forceful repetitive quadriceps concentric and eccentric contraction (eg, sprinting, football, soccer). b. History: Sharp pain in the thigh followed by loss of function. c. PE: Resisted muscle activation, passive stretching, and palpation of the strained muscle all result in pain. Assess for a palpable defect. Check strength at the onset—this provides direction for further diagnostic testing and treatment.

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d. Diagnostics: When clinical examination is unclear, radiographs, US, and MRI can be used. e. Treatment: Rest, ice, compression, and elevation (RICE) are recommended initially and the quadriceps should be immobilized for grade 2 to 3 strains. Muscle activation initiated after 3 to 5 days and progress as pain and improved strength allow. f. Quadriceps contusions occur as a result of a direct blow to the quadriceps and result in muscle tear. g. Diagnostics and treatment are the same for strains with one exception: The quadriceps should be placed in flexion for 24 hours following the injury in attempts to reduce the likelihood of ossification within the muscle (ie, myositis ossificans traumatica [MOT]). h. MOT occurs in 9% to 17% of contusions and presents with painful firm area in the region of the contusion within 2 to 3 weeks. Knee flexion is often reduced and swelling continues. i. Diagnostics: Can be seen on radiographs as early as 3 weeks. US may be more sensitive than radiographs for detecting early MOT. j. Treatment: Indomethacin, stretching, ROM, and strengthening. Surgical excision can be considered for recalcitrant cases 12 to 24 months after the injury to ensure adequate time for the MOT to mature. 4. Hamstring a. Hamstring strains, incomplete, and complete tears are another source of extraarticular hip and posterior pelvic pain that can be insidious in onset or a result of trauma. b. The hamstring strain, like other muscles, likely occurs on a continuum. Overuse can occur with intramuscular strain and/or inefficiencies that result in friction at the insertion site, which leads to bursitis. The inflammation resolves and tendinopathy can develop. This can eventually lead to repetitive pain with use and even tears. c. A traumatic eccentric contraction/stretch of the hamstring beyond its physiological barrier during knee extension and/or hip flexion can result in an incomplete or complete tear. These tears occur at the myotendinous junction or insertion at the ischium and most commonly involve the biceps femoris muscle. d. Water skiers report the most hamstring injuries but sprinters, middle distance runners, and contact sports athletes are also at risk. However, the injury can occur with any sport with the mechanism as described previously. e. History: With acute tears, athletes often report feeling a “pop” and may visualize a bruise in the posterior thigh. f. PE: Localized tenderness and at times, a muscle defect can be felt on palpation with the athlete in the prone position. Pain may also be provoked with resisted knee flexion or hip extension. g. Treatment: Rest, ice, and crutch use for 3 to 5 days followed by rehabilitation to reestablish strength and flexibility of the hamstring. h. Surgical treatment: Acute traumatic tears can be surgically treated if there is no bony ischial avulsion, the tendon integrity is healthy, and the repair is completed within weeks of the initial injury. 5. Iliotibial Band a. ITB pain and dysfunction can present with proximal pain along the iliac crest and greater trochanter and distally with pain along the lateral knee just proximal and at its insertion on Gerdy’s tubercle. b. Diagnosis is based on clinical information including palpation of painful origin and insertion sites. Often the ITB is found to be tight on Ober’s test. c. Treatment includes stretching the ITB and associated muscles (ie, gluteus maximus and tensor fascia lata), and strengthening the lateral rotators and abductors of the hip.

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See the previous section regarding snapping hip and the following section regarding greater trochanteric pain. 6. Adductor a. Adductor strains are a significant cause of groin pain in athletes involved in sports that require a strong adductor muscle eccentric contraction. b. The adductor muscle group consists of six muscles in the medial thigh, which originate at various points along the pubis and insert on the medial femur. c. In the open chain activation, the primary function of this muscle group is hip adduction. In the closed chain activation, they, with the lower abdominals, stabilize the pelvis and lower extremity during the stance phase of gait. The individual muscles have secondary roles including femoral flexion and rotation. d. The adductor longus is the most commonly strained muscle due to its poor mechanical advantage and it is hypothesized that its low tendon to muscle ratio at its origin predisposes it to injury. e. History: Athletes with adductor strains present with groin pain and or medial thigh pain that is worse with activity. The onset can be acute (traumatic etiology) or insidious (overuse etiology). f. PE: Adductors are tender to palpation at the site of pathology and exhibit pain with passive stretch or activation. In traumatic cases, acute rupture or osseous avulsion should be considered. Swelling of the muscle group and weakness of hip adduction can occur. g. Diagnosis: Hip radiographs often do not confirm the diagnosis, but can identify associated bony abnormalities of the pelvis and hip such as osteitis pubis, apophyseal avulsion fractures, or pelvic or hip stress fracture. Musculoskeletal US evaluation can further visualize the tendon and bony attachment sites, muscles, ligaments, and nerves. MR can evaluate soft tissue and osseous structures of the hip. h. Treatment: Relative rest, ice, and analgesia. Rehabilitation focused on balancing muscle flexibility and strength of the adductors and other pelvic girdle muscles such as lateral hip rotators and hamstrings. i. Surgical treatment: In cases of acute, full thickness tendon tears, surgery may be considered. An open repair with suture anchors has been described with good results. D. Bursitis 1. Greater trochanteric a. Lateral hip pain has been commonly diagnosed as greater trochanteric bursitis. Current literature is beginning to refute that bursitis is the primary diagnosis. More likely, a continuum of disorders can develop and is referred to as greater trochanteric pain syndrome (GTPS). b. GTPS has been termed by some the “great mimicker” because it is often mistaken for or seen in conjunction with other sources of pain such as lumbar radiculopathy or intra-articular hip pathology. c. Studies have found GTPS to be associated with a number of other conditions, which can alter the shearing and tension forces of the hip abductors due to weakness or altered gait mechanics. d. GTPS involves the tendons and bursa of the lateral hip region including the gluteus medius (most commonly) and minimus. e. There are three main bursae in the trochanteric region: subgluteus medius, subgluteus minimus, and subgluteus maximus bursae. The subgluteus maximus bursa is considered the “greater trochanteric bursa.” Eleven other bursae have been described around the hip. f. Tears of the gluteus medius (more common) and gluteus minimus are becoming more recognized as a source of lateral hip pain. g. Lateral hip pain can also be related to intra- and extraarticular hip disorders. Intraarticular sources include labral disorders, hip deformity, and OA. Extraarticular

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sources include referred pain from the sacroiliac joint (SIJ), and hip girdle musculotendinous units. h. History: Pain when sleeping on the affected side (and, occasionally the unaffected side), climbing stairs, getting up and down from a chair, crossing the affected leg, or single leg weight-bearing on the affected limb. The pain can radiate down along the outside of the hip to the knee. i. GTPS is more common in women with approximately a 3:1 or 4:1 female-to-male predominance. It is also more common in the fourth and sixth decades of life. j. PE: Lateral hip pain with weight-bearing, resisted hip abduction, palpation over the region of the greater trochanter, and FABER test. k. Diagnosis: Imaging studies are useful to assess acute trauma and chronic repetitive overload but are not uniformly positive. Bone scan or MRI helps to rule out stress fracture. MRI and US can also be used to detect soft tissue (MRI and US) or osseous (MRI) pathology such as bursitis, tendinopathy, enthesopathy, and hip external rotator or abductor tears. 2. Iliopsoas/iliopectineal bursa a. The iliopectineal bursa (also known as the iliopsoas or psoas bursa) may become inflamed and painful as a result of hip flexor dysfunction causing friction where it crosses the anterior pelvic brim resulting in a bursitis. See the iliopsoas section for more information. 3. Ischial bursa a. The ischial bursa may become inflamed and painful as a result of direct compression or hamstring dysfunction causing friction at the site of the hamstring origin, resulting in bursitis. See the hamstring section for more information. E. Athletic Pubalgia 1. Etiology: Some describe a hyperextension injury to the rectus abdominis insertion at the pubic symphysis. Others describe an occult hernia of the posterior inguinal wall without signs of a visualized tear. 2. Gilmore’s groin is a tear in the external oblique aponeurosis and conjoint tendon. 3. Sports and exercise that require repetitive rotation of the upper leg and torso, such as ice hockey, soccer, and rugby, predispose athletes to athletic pubalgia. Repetitive trunk hyperextension and thigh hyper-abduction cause shearing at the pubic symphysis. 4. Muscle imbalances between strong proximal thigh muscles and relatively weaker abdominal muscles also pose additional risks for injury. 5. History: Insidious onset of groin pain with activity. Worsened with coughing or sneezing or explosive contractions. Pain associated with sprinting or kicking. 6. PE: Tenderness to palpation (TTP) of the superficial inguinal ring, posterior inguinal canal, pubic tubercle, or the conjoined tendon without a palpable hernia. Resisted situps, active hip adduction, or Valsalva may provoke pain. 7. Diagnosis: MRI is the recommended imaging study with good sensitivity and specificity. 8. Treatment: Surgical exploration is considered after failure of at least 6 to 8 weeks of conservative management. Both open and laparoscopic approaches are used. The surgical procedure depends on the underlying etiology. True hernias are repaired with or without the use of mesh and the athlete is allowed to return to play in 6 weeks with a laparoscopic repair and 6 months for an open repair. Other surgical procedures include repair of the adductor/rectus abdominis aponeurotic plate and adductor longus tenotomies or releases. F. Labral Injuries and Pre-Arthritic Hip Disorders 1. Intra-articular hip disorders that precede the onset of degenerative changes and include abnormalities to the acetabular labrum, articular cartilage, ligamentum teres, synovium, osseous structures, and loose bodies in the joint. 2. Acetabular labral tears.

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a. Fibrocartilage ring that surrounds the joint, seals the joint, provides stability, and aids in transferring forces away from the articular surfaces (see Figure 24.2). b. History: Labral abnormalities can cause anterior hip and groin pain in athletes. The labrum can be injured with a traumatic event but more commonly, this is due to cumulative microtrauma. Sports activities with repetitive loading, pivoting, and torsional force across the hip can damage the labrum. Symptoms include anterior hip, groin or lateral hip pain, mechanical symptoms of popping, clicking or locking, pain worsened with walking, pivoting, and impact. c. PE: Antalgic to normal gait, painful hip flexion and internal rotation, and a positive hip impingement and FABER tests (see Figure 24.1). d. Diagnosis: Radiographic assessment for fracture or deformity (see Figure 24.3). i. Suggested views include standing AP pelvis, AP hip, frog-leg lateral, Dunn, cross-table lateral, and false profile view. e. Hip labral tears commonly are associated with hip deformity. Reports include 49% to 90% of labral tears found at the time of arthroscopy are associated with bony hip deformity. f. magnetic resonance arthrograms are more specific and sensitive than plain MRI to detect labral and chondral abnormalities. Most labral tears occur in the anterior superior labrum and 15% to 20% of labral tears are not seen on magnetic resonance arthrogram. g. Image-guided intra-articular diagnostic hip injections are used to confirm pain is intra-articular and if reduction in pain is correlated with magnetic resonance arthrogram findings. h. Treatment: Options include a trial of conservative care and progression to surgery if necessary. i. Conservative treatment: Relative rest, nonsteroidal anti-inflammatory drugs (NSAIDs), and focused physical therapy to improve the femoral head motion within the joint, and biomechanics around the hip. ii. Image-guided intra-articular steroid injection considered if there is chondrosis or wearing of the articular cartilage. i. Surgical intervention should be considered after failure of a conservative trial and include: (a)

(b) Width

Hip joint capsule (cut)

Labrum Calcified cartilage Transition zone

Hip bone

Thickness

Articular hyaline cartilage

Figure 24.2 Illustration of the acetabular labrum. Cross-section of acetabular labrum. (a) labral attachment, (b) labral width and thickness. Source: From Lewis CL, Sahrmann SA. Acetabular labral tears. Phys Ther. 2006;86(1):110–121, with permission of the American Physical Therapy Association. © 2006 American Physical Therapy Association.

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(a)

(b)

(c)

(d)

Figure 24.3

X-rays of hip. (a) normal, (b) cam FAI, (c) pincer FAI, and (d) DDH.

DDH, developmental dysplasia of the hip; FAI, femoral acetabular impingement.

i. Hip arthroscopy to debride or repair the labrum. ii. Underlying osseous hip deformities should be addressed and may require an open procedure. iii. Poor prognosis is associated with a higher degree of chondrosis or articular cartilage wearing. 3. Femoral acetabular impingement (FAI). a. FAI results from morphological abnormalities of the proximal femur and/or acetabulum, which produce abnormal abutment of the acetabular rim and femoral head–neck junction. Symptomatic FAI typically occurs in young, active individuals. b. There are three categories of FAI. i. CAM impingement occurs when an abnormal femoral head–neck junction (ie, decreased femoral head–neck offset distance, “pistol grip deformity”) is driven into the acetabulum during hip flexion/internal rotation producing damage to the labrum/articular cartilage in the region of the anterosuperior rim. ii. Pincer impingement occurs when a normal femoral neck impinges against an overhanging anterosuperior acetabulum, compressing the labrum and creating circumferential microtrauma. iii. A combination of cam and pincer impingement can also occur. c. If untreated and symptomatic, FAI may lead to secondary hip OA. d. History and PE: Consistent with an intra-articular hip disorder and is associated with pain and decreased hip flexion and internal rotation ROM. e. Diagnosis: AP of the pelvis, and oblique, lateral, axial hip radiographs are essential to characterize the extent of deformity and the presence of associated OA.

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i. CAM type: Pistol grip deformity, femoral head–neck offset distance of less than 7 mm on AP or oblique radiographs, alpha angle (line from femoral head/neck junction to center of femoral head, then from center of femoral head along axis of femoral neck on axial radiograph) greater than 60°. ii. Pincer type: Protrusio acetabula (femoral head extends medial to ilioischial line on AP of pelvis), coxa profunda (acetabular fovea extends medial to ilioischial line on AP of pelvis), lateral center edge angle (line from lateral margin of acetabulum to center of femoral head, then from center of femoral head vertically to center of the cephalad portion of the femoral head on AP of pelvis) greater than 40°. f. Treatment: Trial of conservative measures is appropriate if bony deformity is mild or if OA is significant. Acetabuloplasty (for pincer-type FAI), labral repair (if torn), or femoroplasty (for cam-type FAI) is indicated for young athletes with well-maintained joint surfaces and no articular cartilage damage. Those with more advanced OA will likely require a total hip arthroplasty (THA) if conservative measures fail. 4. Developmental dysplasia of the hip (DDH). a. DDH is defined as insufficient anterolateral coverage of the femoral head due to a shallow acetabulum, superolateral inclination of the articular surface, and a lateral hip joint center (see Figure 24.3). b. The inadequate coverage of the femoral head causes excessive loading of the acetabulum and can lead to degeneration of the cartilage over time and secondary OA. c. History and PE: Findings are consistent with an intra-articular hip disorder. Excessive hip flexion, internal and external rotation ROM is common in DDH. d. Diagnosis: Radiographic analysis is essential to characterize the extent of deformity and the presence of OA. e. Treatment: Options include a trial of conservative measures depending on the severity of the deformity. Joint preservation surgeries are indicated for young athletes with well-maintained joint spaces without articular cartilage damage. G. Osteitis Pubis 1. Degenerative pubic symphyseal changes related to repetitive overload, trauma, pregnancy, rheumatologic disorders, or postinfection. More common with limited hip ROM, and sports that require repetitive forceful rotation and kicking (eg, soccer). 2. History: Insidious or acute onset of groin pain ± radiation to medial/anterior thigh or abdomen, increased with activity, relieved by rest. 3. PE: TTP over the pubic symphysis or pubic ramus, pain with passive hip internal rotation or passive or active hip adduction. 4. Diagnosis: AP pelvis radiographs = normal, widened, or narrowed pubic symphysis with bony sclerosis/cystic changes. Single leg weight-bearing radiographs may detect pelvic instability. Bone scan = increased uptake in pubic bones. MRI = bony edema in pubic bones, helps rule out other causes of pubic pain. 5. Treatment: Relative rest, SIJ belt, correction of strength/flexibility imbalances around the pelvis, occasionally pubic symphyseal corticosteroid injections. H. Avascular Necrosis (AVN) 1. AVN of the hip involves disruption of the femoral head blood supply resulting in necrosis. The hip is the most common site of AVN. 2. Etiologies: Trauma, slipped capital femoral epiphysis (SCFE), Legg–Calve–Perthes disease, corticosteroids, excessive alcohol use, blood dyscrasias, extremes in barometric pressure (deep-sea divers), femoral neck stress fractures. 3. History: Typically insidious onset of anterior hip, groin, or lateral hip pain with a painful limp or inability to bear weight. 4. PE: Consistent with an intra-articular hip disorder.

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5. Diagnosis: Radiographic evaluation with standing AP pelvis, frog-leg lateral, and crosstable lateral. Can take 3 months for x-rays to be positive, (+) crescent sign (radiolucent arc below rim of femoral head), 90% of lesions are in the anterior, superior femoral head. 6. Bone scans are sensitive but not specific. MRI has 95% sensitivity and specificity. CT is best for determining the extent of collapse and bone infarction. 7. Consider laboratory evaluation for etiology of AVN with lipid levels, proteins C and S, antithrombin III, plasminogen activator inhibitor-1. 8. Classification systems (see Table 24.1). 9. Treatment: Depends on stage, presence of subchondral collapse, articular surface involvement, and degree of arthritic change. i. Conservative treatment is considered for asymptomatic lesions, lesions prior to x-ray or MRI findings, and small lesions without articular collapse that are asymptomatic with restricted weight-bearing. Nonoperative treatment is also indicated in young patients with significant subchondral collapse and articular involvement not amenable to core decompression or free-vascularized fibular graft (FVFG) and too young to consider THA. Electromagnetic bone stimulator can be a helpful adjunct to conservative care. ii. Bisphosphonates, such as alendronate 70 mg weekly for 3 months, have been shown to improve nonoperative outcomes. Correct lipid and coagulation abnormalities if present. iii. Protected weight-bearing is essential until symptom-free, and then progress weight-bearing status and return to sport after rehabilitation for reconditioning and sport-specific training. iv. Surgical treatment with core decompression. The prognosis is improved in athletes treated earlier and with smaller lesions. Indicated when no degenerative change is seen in the hip. v. Six weeks postoperative protected weight-bearing with return to sport after rehabilitation for reconditioning and sport-specific training. vi. FVFG can be considered in early and later stages of AVN. vii. Healthy bone with intact vascular structures is harvested from the fibula and implanted into the femur after removal of the necrotic bone. viii. Osteotomy considered only for symptomatic patients without subchondral collapse. ix. Hip resurfacing or THA if athletes demonstrate significant subchondral collapse with advanced degenerative changes and other conservative measures are ineffective. I. Degenerative Joint Disease 1. The degeneration of articular cartilage of the hip with associated changes to the synovium, subchondral bone, and joint margins. 2. Primary OA is less common and due to a genetic predisposition. 3. Secondary OA has been implicated in some studies to account for 80% of cases. a. SCFE, Legg-Calve Perthes disease, trauma, FAI, DDH, labral tears, chondral injury, inflammatory arthritis, AVN, infection. 4. History: Typically insidious onset of groin pain, but can also present with anterior hip, lateral hip, and less commonly buttock pain. 5. PE: Consistent with an intra-articular process with painful and decreased hip ROM, especially internal rotation and flexion. 6. Diagnosis: Radiographic evaluation with standing AP pelvis, frog-leg lateral and cross-table lateral views demonstrates joint space narrowing, sclerosis, subchondral cysts, and osteophytes. 7. Classification systems (see Table 24.1). 8. Conservative treatment options include:

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Table 24.1

299

Classification Chart

AVN Classifications

OA Classifications

ARCO (Association Research Circulation Osseous)

Tonnis Classification

Stage 0—X-rays, MRI, bone scan normal, bone biopsy demonstrates AVN Stage I—Radiographics normal, bone scan or MRI positive Ia—30% Stage II—Radiographics show sclerosis, cystic changes, osteopenia or mottled femoral head without subchondral collapse or acetabular involvement, bone scan/MRI positive IIa—30% Stage III—Radiographics show a crescent sign, bone scan/MRI positive IIIa—4 mm depression Stage IV—Radiographs show flattened articular surface, joint space narrowing, acetabular changes, osteophytes

Grade 0—No signs of OA Grade 1—Increased sclerosis, slight narrowing of the joint space, no or slight loss of head sphericity Grade 2—Small cysts, moderate narrowing of the joint space, moderate loss of head sphericity Grade 3—Large cysts, severe narrowing or obliteration of the joint space, severe deformity of the head

Ficat Staging

Kellgren–Lawrence Classification

Stage 0—Asymptomatic hip with no radiographic changes Stage I—Slight patchy osteoporosis, subtle loss of clarity Stage IIa—Osteoporosis, sclerosis, cysts Stage III—Crescent sign indicating subchondral collapse, flattening of femoral head Stage IV—Flattened femoral head, articular surface collapse, degenerative change

Grade 0—No osteophytes, normal joint space Grade 1—Minute osteophytes, doubtful significance Grade 2—Definite osteophyte, unimpaired joint space Grade 3—Moderate diminution of joint space Grade 4—Joint space greatly impaired with sclerosis of subchondral bone

AVN, avascular necrosis; OA, osteoarthritis.

a. Relative rest with avoidance of internal rotation, end range hip flexion and pivoting. b. NSAIDs. c. Supplementation with glucosamine/chondroitin could be considered. Studies show some to no improvement in pain and functioning. d. Physical therapy for pelvic girdle muscle strengthening with special consideration to work within a pain-free ROM. e. Intra-articular, image-guided hip injections of corticosteroids have been found to transiently improve the symptoms of hip OA. f. Although not approved by the Food and Drug Administration (FDA) for the hip, intra-articular injection of viscosupplementation is another potential treatment option. 9. Surgical treatment is considered when conservative measures fail. a. Hip resurfacing or THA.

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J. Acute Compartment Syndrome of the Thigh 1. Compartment syndrome occurs when the pressure within the compartment of the thigh exceeds capillary filling pressure (12–32 mmHg). If untreated, this can lead to muscle necrosis, fibrosis, and neurologic injury. 2. Acute compartment syndrome of the thigh is usually a result of direct trauma and affects the anterior compartment, and is a surgical emergency. 3. History: Progressive pain and swelling, increasing tissue turgor, and further provocation with passive ROM. 4. Diagnosis: Intracompartmental pressure testing (>15 mmHg at rest is abnormal). 5. Early surgical consultation is imperative to minimize long-term injury.

Recommended Reading 1. Anderson K, Strickland SM, Warren R. Hip and groin injuries in athletes. Am J Sports Med. 2001;29(4):521–533. 2. Burnett RS, Della Rocca GJ, Prather H, Curry M, Maloney WJ, Clohisy JC. Clinical presentation of patients with tears of the acetabular labrum. J Bone Joint Surg Am. 2006;88(7):1448–1457. 3. Byrd JW. The role of hip arthroscopy in the athletic hip. Clin Sports Med. 2006;25(2):255–278. 4. Clohisy JC, Beaule PE, O’Malley A, Safran MR, Schoenecker P. AOA symposium hip disease in the young adult: current concepts of etiology and surgical treatment. J Bone Joint Surg Am 2008;90(10):2267–2281. 5. Clohisy JC, Carlisle JC, Beaulé PE, et al. A systematic approach to the plain radiographic evaluation of the young adult hip. J Bone Joint Surg Am. 2008;90(Suppl 4):47–66. 6. Clohisy JC, Knaus ER, Hunt DM, Lesher JM, Harris-Hayes M, Prather H. Clinical presentation of patients with symptomatic anterior hip impingement. Clin Orthop Relat Res. 2009;467(3):638–644. 7. Minnich JM, Hanks JB, Muschaweck U, Brunt LM, Diduch DR. Sports hernia: diagnosis and treatment highlighting a minimal repair surgical technique. Am J Sports Med. 2011;39(6):1341–1349. 8. Nunley RM, Prather H, Hunt D, Schoenecker PL, Clohisy JC. Clinical presentation of symptomatic acetabular dysplasia in skeletally mature patients. J Bone Joint Surg Am. 2011;93(Suppl 2):17–21. 9. Peterson L, Renström P. Groin and thigh. In: LRP Peterson, ed. Sports Injuries: Their Prevention and Treatment. London, England: Taylor & Francis; 2001:247–266. 10. Prather H, Hunt D. Hip and pelvic injuries in sports medicine. Sacroiliac Joint Problems. G. C. Philadelphia, PA: Lippincott Williams & Wilkins; 2010:200–206.

25 Knee Injuries and Conditions Ashwin N. Babu and Cheri A. Blauwet

I. Clinical Anatomy A. Joints 1. Tibiofemoral joint: Modified hinge joint a. Medial and lateral tibiofemoral compartments b. Normal range of motion (ROM): 135° of flexion, 5° to 10° of hyperextension, 10° of internal/external rotation c. Screw home mechanism: Locks the knee during terminal 20° of knee extension i. Kinetics vary, depending on open versus closed chain (A) Open chain: External rotation and anterior glide of the tibia (B) Closed chain: Internal rotation and anterior glide of the tibia ii. Unlocking of the knee is via popliteus muscle activation 2. Patellofemoral joint: Modified plane joint a. Medial stabilizers i. Dynamic—Vastus medialis obliquus (VMO) ii. Static—Medial femoral condyle, medial retinaculum, especially medial patellofemoral ligament (MPFL) b. Lateral stabilizers i. Dynamic: Vastus lateralis, iliotibial band (ITB) ii. Static: Lateral femoral condyle, lateral retinaculum c. Q angle: Formed by lines that connect the anterior superior iliac spine (ASIS) to the midpatella and the midpatella to the tibial tubercle d. Patellar loading varies and thus symptoms depend on activity i. Walking: 0.3 to 0.5 × body weight ii. Ascending stairs: 2 to 4 × body weight iii. Descending stairs: 3.5 × body weight iv. Squatting: 7 to 8 × body weight 3. Proximal tibiofibular joint: Synovial joint a. Stabilized by anterior and posterior ligaments of the fibular head B. Ligaments 1. Anterior cruciate ligament (ACL) a. Originates at the posteromedial aspect of the lateral femoral condyle and courses anteromedially to insert anterior to the intercondylar eminence b. Two bundles i. Anteromedial: Tight in flexion ii. Posterolateral: Tight in extension c. Function 301

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2.

3.

4.

5.

6.

i. Primary: Prevents anterior displacement of the tibia on the femur ii. Secondary: Limits varus/valgus stress and rotation, prevents hyperextension, assists in screw home mechanism and proprioception Posterior cruciate ligament (PCL) a. Originates at the anterolateral aspect of the medial femoral condyle, courses posterolateral to insert on the posterior surface of the tibial eminence b. Two bundles i. Anterolateral: ~65% of substance of PCL, tight in flexion ii. Posteromedial: ~35% of substance of PCL, tight in extension c. Function i. Primary: Prevents posterior displacement of tibia on femur ii. Secondary: Limits varus/valgus stress, assists in proprioception and screw home mechanism Medial collateral ligament (MCL) a. Two components i. Superficial: Originates at medial epicondyle, inserts at the proximal tibia, attaches broadly 5 to 7 cm below joint line ii. Deep: Contiguous with medial meniscus, consists of tibiomeniscal and meniscofemoral ligaments b. Primary restraint to valgus stress Lateral collateral ligament (LCL) a. Originates at lateral femoral condyle and inserts on fibular head b. Primary restraint to varus stress Ligaments of the posterolateral corner (PLC) a. Anterolateral ligament (ALL) i. Originates at the lateral femoral condyle, courses anteroinferior, inserts midway between the fibula and Gerdy’s tubercle b. Popliteofibular ligament c. Fabellofibular ligament Meniscofemoral ligament a. Courses from posterior horn of lateral meniscus to medial femoral condyle b. Anatomic variants lie either anterior (ligament of Humphrey) or posterior (ligament of Wrisberg) to PCL

C. Menisci 1. Medial meniscus a. More “C” shaped, covers 50% to 60% of medial tibial plateau b. Less excursion than lateral meniscus due to attachment of the deep component of the MCL 2. Lateral meniscus a. More “O” shaped, covers 70% to 80% of lateral tibial plateau b. More excursion than medial meniscus c. Discoid meniscus variant: Thickened, ovoid variant of the lateral meniscus where the attachment of the posterior horn is absent, predisposing to increased motion and injury 3. Vascular supply a. Outer one-third has good blood supply (red zone) and potential to heal b. Inner two-thirds have poor supply (white zone) and limited healing potential 4. Function: Load transmission, knee stability, proprioception D. Capsule 1. Composed of ligaments and tendons surrounding the knee joint 2. Lined with synovium that secretes synovial fluid

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3. Synovial plicae: Redundant folds of synovium; during fetal development, plicae are membranes that separate the knee into compartments, which typically diminish in size during the second trimester, but may resorb incompletely a. Locations: Mediopatellar (most common), suprapatellar, lateral, infrapatellar

II. Knee Injuries and Conditions A. Fractures 1. Patellar fracture a. Types i. Direct trauma (eg, fall onto patella): Often causes comminution, but typically not displaced; articular cartilage often damaged ii. Indirect trauma (eg, forceful quadriceps activation): Less likely to be comminuted but more likely displaced fragments; less damage to articular cartilage b. Imaging: Plain radiographs i. Anterior–posterior (AP) view: Difficult to visualize patella and peripheral fractures may be mistaken for bipartite patella (check bilateral films) ii. Lateral view: Often reveals comminution or displacement iii. Sunrise view: Reveals vertical fractures c. Treatment i. Nonoperative: Minimal or nondisplaced fractures with minimal disruption of articular surface, preserved extensor mechanism (A) Strict splinting in extension (B) Gradually increase flexion range as healing progresses ii. Operative: Avulsion of extensor mechanism, displaced transverse fracture d. Complications: Infection, avascular necrosis, posttraumatic arthritis of patellofemoral compartment, quadriceps weakness 2. Tibial plateau fracture a. Types i. Sports related: Often accompanied by ligamentous injury ii. Low energy/osteoporotic (A) Typically a depressed fracture iii. High energy (A) Often due to motor vehicle accidents, pattern is typically a bicondylar fracture b. Treatment i. Nonoperative if minimal displacement or depressed fracture (A) Non–weight-bearing with brace × 6 weeks ii. Operative management (A) Absolute indications: Open plateau fractures, associated compartment syndrome, associated vascular injury (B) Relative indications: Displaced bicondylar fractures, displaced medial condylar fractures, lateral fractures with joint instability 3. Segond fracture a. Features i. Small capsular avulsion fracture of the lateral tibial plateau ii. Results from abnormal varus stress to the knee combined with internal rotation of the tibia iii. Likely to be associated with ACL tear (75%–100%) and/or meniscal injury (66%–75%) iv. Can also be associated with avulsion at the fibular head or Gerdy’s tubercle b. Treatment: Typically requires surgical intervention, given concomitant injuries

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4. Stress fractures a. Types i. Patellar: High-risk stress fracture due to risk of nonunion ii. Medial tibial plateau: Commonly misdiagnosed as pes anserine bursitis b. Diagnosis should prompt evaluation for low energy availability B. Dislocation 1. Patellar dislocation: Patella displaced laterally out of the trochlear groove a. Types i. Traumatic: Often occurs with twisting or jumping, presents with hemarthrosis ii. Atraumatic: Occurs mainly in young females with generalized ligamentous laxity b. Features i. Associated with injury to medial retinaculum, particularly MPFL, which inserts onto the adductor tubercle ii. Osteochondral fracture occurs in one-third of cases iii. Usually reduced spontaneously with knee extension iv. Risk factors include shallow trochlear groove, generalized ligamentous laxity, patella alta, femoral anteversion, loose medial or tight lateral retinaculum c. Physical examination pearl i. Lateral apprehension test: Sense of apprehension with passive lateral displacement of patella in knee in extension d. Imaging i. X-rays should be obtained after reduction to evaluate for osteochondral fracture or avulsion (AP, lateral, and sunrise view) ii. Obtain MRI if concern for osteochondral defect on x-ray, persistence of symptoms, or for evaluation of medial retinaculum/ MPFL in recurrent dislocations (Figure 25.1)

Figure 25.1 T2-weighted MRI image of a knee in the axial plane in a patient with a patellar dislocation. Note the increased signal intensity over the lateral aspect of the trochlea and the medial aspect of the patella, representing a characteristic bone contusion pattern (arrows) seen in lateral patellar dislocations.

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e. Treatment i. Nonoperative: Consider knee brace/immobilizer to maintain extension in acute phase, then progress to rehabilitation program ii. Operative: For recurrent patellar dislocations or presence of an osteochondral defect 2. Knee dislocation a. Types: Described by position of the tibia relative to femur i. Anterior: Occurs in hyperextension injuries ii. Posterior: Dashboard-type injuries iii. Medial, lateral, and rotatory dislocations may also occur b. Features i. High-force injury often associated with severe multiligamentous injury, nerve injury (fibular), vascular injury (popliteal artery), fracture ii. Consider immediate arteriography to evaluate popliteal artery (medical emergency) c. Treatment i. Emergent surgical intervention: Open dislocation, popliteal artery injury, irreducible dislocations, compartment syndrome ii. Delayed intervention: Ligamentous reconstruction C. Muscle/tendon injuries 1. ITB friction syndrome a. Features i. Typically seen in athletes requiring repetitive knee motion such as running, cycling, rowing ii. Patients present with pain over lateral knee, usually absent at rest iii. Traditionally thought to be caused by friction-induced irritation of a bursa deep to the ITB as it courses over the lateral femoral epicondyle; current evidence conflicting b. Physical exam pearls i. Tenderness over ITB, commonly at insertion and 3 cm proximal to the lateral joint line ii. Ober’s test: Demonstrating ITB tightness iii. Noble’s test: Passively extend knee from 90° of flexion while palpating over the lateral femoral epicondyle; lateral knee pain reproduced at 30° of flexion c. Treatment i. Mainstay is conservative management including biomechanics evaluation, activity modification, equipment evaluation, and local anti-inflammatory modalities ii. Surgical intervention: Recalcitrant cases only, several surgical options exist 2. Patellar tendinopathy (jumper’s knee) a. Features i. Usually insidious onset in younger athletes ii. Repetitive knee flexion/extension, such as with jumping iii. Most commonly occurs at patellar insertion b. Treatment i. Nonoperative (A) Relative tendon unloading (B) Eccentric strengthening and motor control exercises (C) Correction of biomechanical factors (D) Injection therapy use debated in literature; if utilized is typically a regenerative injection ii. Operative: Often debridement of abnormal tissue, only for recalcitrant cases

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3. Popliteus tendinopathy a. Features i. Rare cause of posterolateral knee pain ii. Typically a chronic/overuse injury, exacerbated with excessive downhill walking/running b. Physical examination pearl i. Garrick’s test: Place leg in “figure four” position (crossed position) and palpate just posterior to the LCL while resisting tibial internal rotation c. Treatment: Relative rest, nonsteroidal anti-inflammatory drugs (NSAIDs), functional rehabilitation 4. Extensor mechanism injury a. Types i. Quadriceps tendon rupture (A) More common in older males (average age 60) ii. Patellar fracture (A) More common in women with osteoporosis iii. Patellar tendon rupture (A) More common in younger males (average age 40) b. Features i. In older individuals, often associated with medical comorbidities such as diabetes mellitus and atherosclerosis ii. Quadriceps and patellar tendon ruptures are often the result of a forcible contraction of the quadriceps across a flexed knee c. Treatment i. Often requires early operative repair ii. Post-op: Start early weight bearing in extension with limited ROM D. Instability/ligament injuries 1. ACL injuries a. Features i. Most common knee ligament injured in sports ii. Females two to eight times more likely than males to experience ACL injury iii. Often a noncontact injury after cutting, landing, or rapid deceleration iv. Contact injuries often result from an external force causing knee valgus v. Patients may report hearing a “pop” followed by a feeling of instability vi. Hemarthrosis/swelling occurs within hours vii. >50% of ACL injuries occur with a meniscal tear viii. “Terrible triad” is a buzzword for concomitant tears of ACL, MCL, and medial meniscus ix. ACL-injured knees are at higher risk for the development of premature osteoarthritis b. Diagnosis i. Physical examination pearls (A) May be difficult to perform complete examination in the acute phase due to pain and swelling (B) Presence of effusion (hemarthrosis) (C) Positive Lachman test (sensitivity 95%–99%) (1) Grade 1+: 0 to 5 mm displacement (2) Grade 2+: 6 to 10 mm (3) Grade 3+: >10 mm (D) Positive anterior drawer (sensitivity 22%–95%, specificity 53%–95%) (E) Positive pivot shift is pathognomonic, particularly when performed under anesthesia (sensitivity 35%–98%, specificity 98%–100%)

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ii. Imaging (A) Plain radiographs: Evaluation for bony injuries such as tibial spine avulsion, tibial plateau, or Segond fractures (B) MRI (1) Often demonstrates classic bone contusion pattern (anterior lateral femoral condyle and posterior lateral tibial plateau) (Figure 25.2) (2) Also evaluates for concomitant injuries to the meniscus, PLC, and other ligaments iii. Arthroscopic evaluation is the gold standard c. Treatment i. Acute/initial (A) Rest, ice, compression, elevation (RICE) (B) Knee immobilizer or hinged knee brace and crutches if painful or subjectively unstable (C) Early gentle knee ROM exercises (D) Exercises to prevent quadriceps inhibition/atrophy ii. Subacute/long term (A) Operative: ACL reconstruction (1) Considered in athletes playing cutting sports, with multiligamentous injury, having a repairable meniscus injury, or having functional knee instability (2) Prehabilitation is important to regain ROM and decrease swelling prior to surgery (3) Delayed surgery has decreased risk of arthrofibrosis

Figure 25.2 T2-weighted MRI image of a knee in the sagittal plane in a patient with an ACL tear. Note the increased signal intensity over the anterolateral femoral condyle and the posterolateral tibia, known as a “kissing contusion” (arrows). ACL, anterior cruciate ligament.

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(4) Surgery does not appear to prevent the development of osteoarthritis (5) Postoperative rehabilitation program lasts 6 to 9 months prior to full return to play (B) Nonoperative: Aggressive rehabilitation program (1) Can be considered in sedentary patients, athletes participating in noncutting sports (eg, cycling), those without significant instability (2) Hamstring strengthening to aid ACL in its role in preventing anterior tibial translation (3) Patient should by followed regularly to assess for knee instability or symptomatic meniscus injury (4) Bracing for ACL-deficient athletes, though commonly used, is controversial 2. PCL injuries a. Features i. Less common than ACL injuries ii. Majority associated with injury to other structures, need to evaluate PLC when PCL injury is suspected iii. Typically from an impact to anterior tibia with knee flexion (eg, dashboard injury), less commonly from knee hyperextension iv. Often presents with minimal swelling and poorly defined posterior knee pain b. Physical examination pearls i. Posterior drawer test (A) Grade 1+: 0 to 5 mm displacement (B) Grade 2+: 6 to 10 mm (C) Grade 3+: >10 mm ii. Positive quadriceps activation test (sensitivity 54%–98%, specificity 97%–100%): (A) Patient is supine with knee flexed to 90°, foot stabilized by examiner, then asked to slide foot gently down the table (B) In a PCL-deficient knee, quadriceps contraction results in anterior shift of tibia ≥2 mm iii. Reverse Lachman’s test iv. Posterior sag sign (quadriceps spasm may cause false-negative) c. Imaging i. Plain radiographs (A) Usually negative in isolated PCL injuries (B) Can evaluate for concomitant avulsion injury of the tibial insertion ii. MRI (A) Useful to diagnose PCL injury and evaluate for associated ligamentous injuries iii. Arthroscopic evaluation is gold standard d. Treatment i. Acute/initial (A) RICE (B) Early ROM exercises (C) Consider knee brace (in full extension)/crutches × 1 to 2 weeks if significant functional limitation ii. Subacute/long term (A) Functional rehabilitation, especially quadriceps strengthening to help support PCL’s role in preventing posterior tibial translation (B) Surgical reconstruction for PCL rarely required, but useful if there is persistent instability or other surgically repairable injuries

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3. MCL injuries a. Features i. Caused by impact to lateral knee causing valgus stress, especially with foot planted in knee flexion ii. Concomitant ACL injuries can be seen with cutting, rotational movements b. Diagnosis i. Physical examination pearls (A) Tenderness along course of MCL (B) Valgus stress test: Performed with knee flexed to 30° (1) Grade 1: Pain but no laxity (2) Grade 2: Some laxity but clear end point (3) Grade 3: Complete disruption of ligament with gaping of medial joint line without end point (C) Valgus stress test should also be performed with knee in full extension; if laxity or gapping, a concomitant ACL, PCL, or PLC injury may be present (D) Minimal effusion in isolated injury given MCL is extraarticular ii. Imaging (A) X-ray usually normal: AP and lateral views can rule out associated bony injury (epiphyseal fracture) (1) Pellegrini-Stieda sign (Figure 25.3): Typically asymptomatic, posttraumatic ossification of the MCL near its origin at the medial femoral condyle can be seen in those with a history of MCL injury (B) MRI: Usually obtained if there are other suspected injuries c. Treatment i. RICE in acute phase ii. Consider hinged knee brace × 4 to 6 weeks iii. Early gentle knee ROM exercises (within 1–2 weeks) iv. Gradual advance to higher-level activities as tolerated (next 1–4 weeks) v. Isolated MCL injuries rarely require surgery unless tibial-sided avulsion is present, for which acute surgical repair is indicated 4. LCL injuries a. Features i. Typically the result of an acute varus stress ii. Rarely injured in isolation b. Physical examination pearls i. Positive varus stress test, performed at 30° of knee flexion (grading system is the same as for MCL, noted in the preceding text) (A) Varus stress test should also be perFigure 25.3 Tunnel radioformed with knee in full extension; if graph of the knee with findings laxity or gapping, a concomitant ACL, of a Pellegrini-Stieda sign, indiPCL, or PLC injury may be present cating a history of MCL injury. ii. Evaluate for associated fibular nerve MCL, medial collateral ligament. injury

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c. Treatment i. RICE ii. Early knee ROM exercises iii. Functional rehabilitation iv. Surgical intervention typically depends upon concomitant injuries 5. PLC injuries a. Features i. Injury to the PLC may be associated with severe injury to other structures (especially PCL or ACL) ii. Untreated PLC injuries are a major source of failure for ACL reconstructions b. Physical examination pearls i. Dial test (Figure 25.4): Assess external rotation (ER) of the tibia compared to the contralateral side at 30° and 90° of knee flexion (A) Increased external rotation at 30°, but not 90°, indicates isolated PLC injury (B) Increased external rotation at both angles suggests injury to both the PLC structures and the PCL c. Imaging i. MRI is needed to determine the specific structures involved d. Treatment: If injury is associated with cruciate ligament tear, surgical intervention is typically warranted E. Anterior knee pain 1. Plica syndrome a. Features i. Most synovial plicae are asymptomatic; however, may progress to be painful, inflamed, and eventually hypertrophic ii. Mediopatellar plica is most commonly involved b. Physical examination pearl: Taut band of tissue that reproduces concordant pain with palpation c. Imaging: Plain radiographs or MRI to rule out more common sources of anterior pain d. Treatment i. RICE, NSAIDs; consider steroid injection ii. Functional rehabilitation

Figure 25.4 The dial test. In the left panel, the examiner passively externally rotates the tibia on the femur at 30° of knee flexion. In the right panel, the examiner repeats the maneuver at 90° of knee flexion. Note the increased external rotation of the right knee with 30° of knee flexion but not at 90° of knee flexion, suggesting an isolated posterolateral corner injury.

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iii. Arthroscopic removal is reserved for recalcitrant cases and may have a high rate of failure 2. Fat pad impingement (Hoffa’s syndrome) a. Features i. Hoffa’s fat pad, located deep to the patellar tendon, can become inflamed/swollen due to direct trauma, hyperextension, or chronic irritation ii. When inflamed, it may impinge between the inferior pole of the patella and femoral condyle iii. Causes anterior/inferior knee pain worsened with knee extension iv. Commonly irritated by transitioning from sit to stand (A) Contrast with patellofemoral pain, which is more symptomatic with prolonged sitting in knee flexion b. Physical examination pearls i. May have genu recurvatum ii. Positive Hoffa’s test (A) Patient lies supine with knee flexed, and examiner presses both thumbs along the sides of the patellar tendon, just distal to the patella (B) Pain/apprehension with active knee extension is considered positive c. Treatment i. RICE ii. Patellar taping iii. Surgical removal of fat pad in recalcitrant cases 3. Patellofemoral syndrome a. Features i. Anterior knee pain in region of patella ii. Typically insidious onset, often bilateral, worse with prolonged sitting (positive “theater sign”) or activities that load the patellofemoral joint (see Section I.A.2, patellofemoral joint: modified plane joint) iii. Likely combination of poor patellar tracking/malalignment within femoral groove as well as peripatellar synovial irritation iv. May be associated with patellar hypermobility/subluxation v. Chondromalacia patellae: Degeneration of the patellar cartilage, often associated with patellofemoral syndrome, particularly in aging athletes b. Risk factors: Consider the entire kinetic chain i. Proximal factors: Femoral anteversion, weak hip abductors and external rotators, tight hip flexors, tight ITB ii. Local factors: Patella alta/baja, increased Q angle, genu valgum, weak quadriceps, hypermobile patella, tight hamstrings, tight quadriceps iii. Distal factors: Increased subtalar pronation, tibial external rotation, weak foot intrinsics, tight gastrocnemius/soleus c. Physical examination pearls i. Important to evaluate kinetic chain assessing for proximal hip strength, femoral rotational control, dynamic knee stability, ankle and foot mechanics (Figure 25.5) ii. Evaluate patellar position both statically and dynamically (A) J sign: Lateral translation of the patella at terminal extension, with medial motion during early flexion iii. Positive patellofemoral grind/compression test d. Imaging: Can be used to assess for intra-articular pathology, bipartite patella, patellar malalignment e. Treatment i. RICE, activity modification

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ii. Rehabilitation program, focusing on risk factors listed in Subsection b in the preceding text iii. Taping: Based upon position of the patella in relation to the femur (A) Need to evaluate tilt, glide, and rotation iv. Bracing: Patellar tracking brace provides firm lateral support to facilitate medial glide of the patella in flexion; should be used only after athlete’s own intrinsic strength is optimized v. Orthotics: Consider correction of overpronation vi. Surgical interventions such as lateral release or tibial osteotomy rarely indicated F. Meniscal pathology 1. Medial and lateral meniscus tears a. Features of medial meniscus injury i. More common than lateral meniscus injury ii. Often a history of cutting activity, tibial rotation with knee flexion during weight bearing (eg, soccer, football) Figure 25.5 A patient with hip iii. Commonly associated with ACL abductor and external rotator injury weakness (ie, poor proximal conb. Features of lateral meniscus injury trol) performing a single-leg squat. i. Injury after squatting, full flexion with Note the contralateral pelvic tilt as rotation (eg, wrestling) well as femoral adduction/interii. Discoid meniscus variation can be nal rotation with resultant valgus cause of lateral knee pain in a young moment at the knee, highlighted athlete by the lines. c. Features common to medial and lateral meniscus injuries i. Present with mechanical symptoms: Painful clicking, popping, catching ii. Degenerative tears typically occur at >40 years old, minimal trauma d. Physical examination pearls i. Effusion ± restricted ROM ii. Pain with squatting iii. Joint line tenderness iv. Provocative maneuvers (A) McMurray test: Audible and palpable click is considered a positive test, although more often it produces pain only (B) Apley grind: Tenderness with flexion, rotation, and axial compression (C) Bounce home test: Pain with terminal extension (D) Thessaly test: Pain with rotation on a partially flexed knee e. Imaging i. Plain radiographs evaluate for degenerative changes, loose bodies ii. MRI: Grading system used for meniscal signal intensity (A) Grade 1: Small focal area of hyperintensity, no extension to the articular surface

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(B) Grade 2: Linear area of hyperintensity, no extension to articular surface (C) Grade 3: Hyperintensity extends to at least one articular surface, is referred to as definite meniscal tear f. Treatment i. Nonoperative for those with minor tears and without significant functional disability ii. Surgical intervention: For those with functional limitation not responding to conservative management or with large tears causing mechanical symptoms (A) Attempt to maximize preservation of meniscus (B) Inner two-thirds poorly vascularized, may require removal of damaged tissue (ie, partial meniscectomy) (C) Outer one-third can often be repaired G. Degenerative joint disease 1. Osteoarthritis a. Features i. Medial compartment most commonly affected ii. Involvement of lateral, patellofemoral, or a combination of all compartments possible iii. Osteoarthritis present in a relatively young patient is often due to history of joint trauma/acute ligamentous injury b. Imaging i. Plain radiographs: Weight bearing films, sunrise view to evaluate patellofemoral compartment (A) Hallmarks: Joint space narrowing, subchondral cysts, sclerosis, marginal osteophytes or spoking of the tibial spines c. Treatment i. Conservative management (A) Activity modification (B) Weight loss (C) Rehabilitation (quadriceps and gluteal strengthening) (D) Unloader bracing (limited evidence) (E) Assistive devices (cane in contralateral hand) (F) Heel wedge (lateral wedge to offload medial compartment) (G) Oral medications (acetaminophen/NSAIDs) ii. Intra-articular injections (A) Steroid injection commonly used (B) Other options include viscosupplementation and regenerative injections, although evidence remains limited iii. Operative management: Knee arthroplasty (A) Indications: Failure of nonsurgical management, significant functional limitations, notable radiographic degenerative changes H. Bursitis 1. General principles a. Bursae typically provide an interface between bony surfaces and ligaments or tendons in areas of friction b. Acute traumatic injury, infection or systemic disease, abnormal biomechanics, or chronic overuse can cause bursitis/irritation of bursa c. Examination typically demonstrates focal tenderness and swelling i. Warmth or erythema may indicate infection d. Treatment typically consists of RICE, NSAIDs, and occasionally aspiration with corticosteroid injection if noninfectious

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2. Prepatellar bursitis (housemaid’s knee) a. Due to trauma or chronic irritation from extensive kneeling b. May have urate crystals due to gout 3. Pes anserine bursitis a. Difficult to differentiate between bursal pathology and tendon insertional pathology of the sartorius, gracilis, or semitendinosus 4. MCL bursitis (Voshell’s bursitis) a. Located between superficial and deep portions of MCL

Recommended Reading 1. Beynnon BD, Vacek PM, Newell MK, et al. The effects of level of competition, sport, and sex on the incidence of first-time noncontact anterior cruciate ligament injury. Am J Sports Med. 2014;42(8):1806–1812. 2. Garner MR, Gausden E, Berkes MB, Nguyen JT, Lorich DG. Extensor mechanism injuries of the knee: demographic characteristics and comorbidities from a review of 726 patient records. J Bone Joint Surg Am. 2015;97(19):1592–1596. 3. Katz JN, Brophy RH, Chaisson CE, et al. Surgery versus physical therapy for a meniscal tear and osteoarthritis. N Engl J Med. 2013;368(18):1675–1684. 4. Mallee WH, Weel H, van Dijk CN, van Tulder MW, Kerkhoffs GM, Lin CW. Surgical versus conservative treatment for high-risk stress fractures of the lower leg (anterior tibial cortex, navicular and fifth metatarsal base): a systematic review. Br J Sports Med. 2015;49(6):370–376. 5. McAlindon TE, Bannuru RR, Sullivan MC, et al. OARSI guidelines for the non-surgical management of knee osteoarthritis. Osteoarthritis Cartilage. 2014;22(3):363–388. 6. Pomajzl R, Maerz T, Shams C, Guettler J, Bicos J. A review of the anterolateral ligament of the knee: current knowledge regarding its incidence, anatomy, biomechanics, and surgical dissection. Arthroscopy. 2015;31(3):583–591. 7. Powers CM. The influence of abnormal hip mechanics on knee injury: a biomechanical perspective. J Orthop Sports Phys Ther. 2010;40(2):42–51. 8. Sihvonen R, Paavola M, Malmivaara A, et al. Arthroscopic partial meniscectomy versus sham surgery for a degenerative meniscal tear. N Engl J Med. 2013;369(26):2515–2524. 9. Strauss EJ, Kim S, Calcei JG, Park D. Iliotibial band syndrome: evaluation and management. J Am Acad Orthop Surg. 2011;19(12):728–736. 10. Wijdicks CA, Griffith CJ, Johansen S, Engebretsen L, LaPrade RF. Injuries to the medial collateral ligament and associated medial structures of the knee. J Bone Joint Surg Am. 2010;92(5):1266–1280.

26 Lower Leg Injuries and Conditions T. Joseph Malbrough and John P. Metzler

I. Anatomy A. Four fascial compartments (Figure 26.1) 1. Anterior compartment a. Muscles: extensor hallucis longus, extensor digitorum longus, peroneus tertius, anterior tibialis b. Deep peroneal nerve 2. Lateral compartment a. Muscles: peroneus longus and brevis b. Superficial peroneal nerve 3. Deep posterior compartment a. Muscles: flexor hallucis longus, flexor digitorum longus, posterior tibialis b. Posterior tibial nerve 4. Superficial posterior compartment a. Muscles: gastrocnemius, soleus b. Sural nerve B. Proximal tibiofibular joint 1. Diarthrodial joint 2. Communicates with the knee in 10% of adults 3. Stabilized by the tibiofibular ligaments, biceps femoris tendon, and lateral collateral ligament 4. Functions to diminish torsional stresses at the ankle joint

II. Fractures: Tibia A. Epidemiology 1. Uncommon injury in athletes 2. High incidence of major complications: Associated soft-tissue injuries, compartment syndrome, delayed union, malunion, or nonunion 3. Mechanism: Contact during a tackle or a collision B. Diagnosis 1. Tender at fracture site 2. Evaluate for neurovascular, knee, or ankle injuries 3. Radiographs—Anteroposterior, lateral, oblique C. Treatment 1. Nondisplaced: Immobilization (splint, then cast) 2. Displaced: Closed reduction and casting versus open reduction and internal fixation (ORIF) or intramedullary nail 315

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Anterior compartment: Tibialis anterior m. Tibia

Extensor digitorum longus m. Extensor hallucis longus m.

Deep posterior compartment:

Lateral compartment: Peroneus brevis m. Peroneus longus m.

Flexor digitorum longus m. Tibialis posterior m. Flexor hallucis longus m.

Fibula

Superficial posterior compartment:

{

Soleus muscle

Figure 26.1

Gastrocnemius m.

Four fascial compartments.

Source: From Brown E, Kelly, M. Sports Medicine: A Comprehensive Approach. Chapter 24, p. 389. Elsevier/ Mosby; 2005.

III. Fracture: Fibula A. Mechanism: direct blow to the lateral leg B. Maisonneuve fracture (Figure 26.2) 1. Fracture of proximal fibula 2. Mechanism: ankle eversion/external rotation causing medial malleolar fracture or deltoid ligament injury, anterior–inferior tibiofibular ligament sprain (ie, high ankle sprain), and syndesmotic membrane injury C. Diagnosis 1. Tender proximal fibula 2. Radiographs—Anteroposterior, lateral, oblique of fibula D. Treatment 1. Nondisplaced with insignificant associated injury: Short leg walking cast or walking boot for 6 to 8 weeks 2. Displaced or with significant associated injury: Non-weight-bearing cast immobilization or surgical treatment with percutaneous screws to reapproximate syndesmosis

IV. Stress Fractures: Tibia A. Epidemiology 1. Medial tibia (compression side): Most common stress fracture site in athletes. Highest incidence is in runners 2. Anterior tibia (tension side): Usually seen in repetitive jumping athletes B. Diagnosis 1. Insidious onset of pain, worse with activity, better with rest

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2. Recent history of change in training volume or surface 3. Localized pain with palpation over a confined area 4. Radiographs (Figure 26.3): Anteroposterior, lateral, oblique. Often normal in first 2 to 3 weeks, later show periosteal reaction or fracture line 5. Bone scan: High sensitivity, poor specificity 6. MRI: Highly sensitive and specific. See fracture line surrounded by edema 7. Treatment a. Medial tibial stress fracture: Relative rest (ie, avoid painful activities), avoid nonsteroidal anti-inflammatory drugs (NSAIDs), core/lower extremity strengthening, gradual return to activity as pain resolves b. Anterior tibial stress fracture: High risk of delayed union or nonunion, athlete should be non-weight-bearing and placed in a cast. Bone grafting or intramedullary tibial nailing is indicated when closed treatments are unsuccessful or to facilitate quicker return to sport C. Fibula 1. Usually seen in distance runners in distal one-third of the fibula 2. Diagnosis and treatment similar to medial tibial stress fracture

V. Instability/Dislocation: Fibular Head A. Injury to the proximal tibiofibular joint is uncommon and can occur in isolation or with associated trauma B. Diagnosis 1. Usually a traumatic onset with a “popping sensation”

(a)

(b)

Figure 26.2

Maisonneuve fracture.

Source: From Eiff MP, Hatch R, Calmbach W. Fracture Management for Primary Care. Chapter 13, p. 201, W.B. Saunders Company; 1998.

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2. Tender over the fibular head, more mobile than contralateral fibula, may lack full knee extension 3. Classification (Figure 26.4) a. Subluxation i. Seen with underlying connective tissue disorder and generalized hypermobility b. Anterolateral dislocation i. Most common type ii. Seen with sliding as the athlete falls on an inverted and plantar flexed foot with the knee flexed and the leg adducted c. Posterior medial dislocation i. Caused by direct trauma or twisting motion ii. Concomitant injuries may include the peroneal nerve or lateral collateral ligament d. Superior dislocation i. Extremely rare ii. Usually associated with severe trauma to the lower extremity 4. Radiographs: Leg in internal rotation will maximize the distance between the lateral tibia and fibula. Compare with contralateral extremity 5. Treatment a. Acute injuries—Closed reduction and 3 weeks of immobilization b. Chronic instability—Often requires ligamentous reconstruction

VI. Muscle/Tendon Injury: Gastrocnemius Tear A. Medial head tears (“tennis leg”) more common than lateral due to larger size and more oblique fiber orientation of the medial head B. Diagnosis 1. Middle-aged recreational athlete who experiences a sharp, acute pain in the posterior calf during activity 2. Pain and tenderness at the musculotendinous junction with swelling and ecchymosis that may track distally to the ankle

Figure 26.3

Stress fracture of the anterior tibia in a 16-year-old female.

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3. MRI or ultrasound can be used to confirm diagnosis C. Treatment 1. Rest, ice, compression, elevation 2. Ultrasound-guided aspiration can be considered if there is significant fluid collection 3. Stretching and strengthening with sports-specific activities as symptoms allow

VII. Medial Tibial Stress Syndrome A. Repetitive traction of the muscular attachments to the periosteum creates a periostitis B. Most commonly seen in runners. Presents bilaterally in 50% of cases C. Diagnosis 1. History: Aching pain over tibial shaft, worse with exertion but athlete may be able to “run through the pain,” better with rest, recent change in training volume/intensity, early in athletic season 2. Physical exam: Diffuse medial tibial tenderness, often elicited with resisted plantar flexion a. Evaluate for biomechanical abnormalities and muscle imbalances 3. Imaging a. Radiographs: Usually normal, but may show periosteal or cortical thickening b. MRI or bone scan: Can differentiate from stress fracture i. Bone scan—Longitudinal/linear uptake on delayed images (versus a localized uptake seen on all three phases with a stress fracture)

(a)

(b)

SUBLUXATION

(c)

ANTEROLATERAL

(d)

POSTEROMEDIAL

Figure 26.4

SUPERIOR

Classification of tibiofibular joint dislocation.

Source: From Ogden JA. Subluxation and dislocation of the proximal tibiofibular joint. J Bone Joint Surg Am. 1974; 56:145–154; p. 146. Used with permission.

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D. Treatment 1. Relative rest with appropriate cross-training, correction of biomechanical deficits, arch supports in athletes with overpronation, correction of training errors

VIII. Acute Compartment Syndrome A. Increased pressure in a fascial compartment causing impaired tissue perfusion, ischemic pain, and tissue necrosis if not urgently treated B. Diagnosis 1. Suspect with persistent or progressive severe pain after fracture or soft-tissue injury 2. Paresthesia, weakness of affected compartments 3. Late findings can include pulselessness and pallor 4. Compartmental pressure testing a. Not necessary if clinical picture is unequivocal b. Diagnosis = intracompartmental pressure > 30 mmHg C. Treatment—Emergency surgical decompression via fasciotomy

IX. Chronic Exertional Compartment Syndrome A. Recurrent episodes of reversible ischemia due to transient elevations in intracompartmental pressure due to activity, which subsides with rest or cessation of activity B. Runners most commonly affected C. Diagnosis 1. History: Tight, cramping leg pain in a specific leg compartment (see anatomy section) that occurs with exercise at a predictable intensity and duration and is relieved with rest. Paresthesias and weakness may occur due to nerve compression 2. Physical exam and radiologic studies are normal 3. Diagnosis confirmed when pre- and postexercise compartment pressure testing demonstrates one of the following: a. Pre-exercise ≥ 15 mmHg b. 1 minute postexercise ≥30 mmHg c. 5 minute postexercise ≥20 mmHg D. Treatment 1. Cessation or alteration of symptom-inducing activity 2. Cross-training with nonaggravating activity 3. If the symptoms are isolated to the anterior compartment, try changing the running technique from a rearfoot initial contact to a mid or forefoot initial contact pattern 4. Botulinum toxin injections have demonstrated short-term symptom relief and decreased intracompartmental pressures 5. If the athlete is unwilling to change or alter the level of activity then surgical referral for fasciotomy is appropriate

X. Popliteal Artery Entrapment A. Can be due to congenital or functional 1. Congenital = deviation of the popliteal artery or development of the medial/lateral gastrocnemius leading to entrapment by the medial or lateral gastrocnemius or the popliteus muscle 2. Functional = compression by normal calf musculature without any congenital abnormality B. Diagnosis 1. Most common in athletic males under the age of 40 2. History: claudication symptoms in the leg and foot (unilateral or bilateral)

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3. Physical exam may demonstrate decreased posterior tibial or dorsalis pedis artery pulses with provocative maneuvers (ie, passive ankle dorsiflexion with knee in extension or active ankle plantar flexion with knee in extension). Popliteal bruit may be present 4. Diagnostic Tests: ultrasound, MR arteriogram, or CT arteriogram with provocative maneuvers provides definitive diagnosis a. Most common finding is medial displacement and compression of the popliteal artery beneath the origin of the medial gastrocnemius C. Treatment—Surgical release and, if necessary, vascular reconstruction

Recommended Reading 1. Eiff MP, Hatch R, Calmbach WL. Fracture Management for Primary Care. Philadelphia, PA: Saunders; 1998:283. 2. Garrett WE Jr, Kirkendall DT, Squire DL, eds. Principles and Practice of Orthopaedic Sports Medicine. Philadelphia, PA: Lippincott Williams & Wilkins; 2000:1062. 3. Gill CS, Halstead ME, Matava MJ. Chronic exertional compartment syndrome of the leg in athletes: evaluation and management. Phys Sportsmed. 2010;38(2):126–132. 4. Harrast MA, Colonno D. Stress fractures in runners. Clin Sports Med. 2010;29(3):399–416. 5. O’Connor FG, Robert N, Robert W. Textbook of Running Medicine. New York, NY: McGraw-Hill, Medical Publishing Division; 2001:696. 6. Pedowitz RA, Hargens AR, Mubarak SJ, Gershuni DH. Modified criteria for the objective diagnosis of chronic compartment syndrome of the leg. Am J Sports Med. 1990;18(1):35–40. 7. Scuderi GR, McCann PD. Sports Medicine: A Comprehensive Approach. 2nd ed. Philadelphia, PA: MosbyElsevier; 2005:782. 8. Sinha S, Houghton J, Holt PJ, Thompson MM, Loftus IM, Hinchliffe RJ. Popliteal entrapment syndrome. J Vasc Surg. 2012;55:252–262. 9. 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. 10. Tucker AK. Chronic exertional compartment syndrome of the leg. Curr Rev Musculoskelet Med. 2010;3(1–4): 32–37.

27 Ankle and Foot Injuries and Conditions Gerard Malanga, Ricardo Vasquez-Duarte, Michael Esrick, and Usker Naqvi

I. Relevant Anatomy A. Bones: Tibia, fibula, tarsals (eg, calcaneus, talus), metatarsals, phalanges B. Ligaments: Anterior inferior tibiofibular (AITFL), deltoid, anterior talofibular (ATFL), calcaneofibular (CFL), posterior talofibular (PTFL), calcaneonavicular (spring ligament) C. Joints: Ankle, subtalar, mid-tarsal, tarsal–metatarsal (Lisfranc), metatarsophalangeal (MTP), proximal interphalangeal (PIP), distal interphalangeal (DIP) D. Tendons: Anterior: tibialis anterior, extensor hallucis longus (EHL), extensor digitorum longus (EDL); posteromedial: tibialis posterior, flexor digitorum longus (FDL), flexor hallucis longus (FHL); posterior: Achilles, plantaris; posterolateral: peroneus longus, peroneus brevis; plantar: foot intrinsic muscles E. Nerves: Tibial nerve, medial and lateral plantar nerves, deep and superficial peroneal nerves, sural nerve, saphenous nerve F. Blood vessels: Posterior tibial artery, dorsalis pedis artery

II. Fractures A. Ankle 1. Classification system a. Danis–Weber: Based solely on fibula and location of fracture (fx) in relationship to ankle mortise i. Type A—fibular fx below ankle mortise ii. Type B—fibular fx at the level of ankle mortise iii. Type C—fibular fx above the ankle mortise 2. Diagnosis a. Radiographs: Anteroposterior (AP), lateral, mortise view 3. Treatment a. Type A: If avulsion fx of fibula is nondisplaced or minimally displaced, and if there is no medial lesion (by exam and x-ray), then apply a walking cast until fibula has healed (usually 6–8 weeks) b. Patients with possible unstable injury (Danis–Weber classification types B and C) or those with bimalleolar fx’s should be referred to an orthopedist B. Talus 1. 1% of foot fx’s 2. fx sites: Neck (most common), talar dome, posterior process, lateral process (snowboard fx) 322

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3. Diagnosis: a. Radiographs: AP, lateral, mortise views of ankle b. CT if fx suspected but x-rays normal 4. Treatment: a. Nondisplaced: Cast immobilization × 6 to 8 weeks b. Displaced: Open reduction and internal fixation (ORIF) C. Calcaneus 1. Mechanism: Axial load with/without plantar or dorsiflexion 2. Diagnosis: a. Radiographs: AP, lateral, mortise, 45° oblique b. CT if high index of suspicion but negative radiograph 3. Treatment a. Nondisplaced: Cast immobilization and non-weight-bearing (NWB) × 6 to 8 weeks b. Displaced: ORIF D. Metatarsals 1. Common fx sites: Diaphysis (traumatic or stress fx), base of fifth (Jones fx or avulsion fx) 2. Diagnosis: a. Radiographs: AP, lateral, oblique b. MRI if stress fx suspected and x-ray normal 3. Treatment a. Nondisplaced: Walking boot or postoperative shoe × 6 to 8 weeks, Jones fx requires cast and NWB × 8 to 12 weeks versus surgical treatment (possible faster recovery) b. Displaced: ORIF E. Phalanges 1. Common: 8% to 9% of fx’s involve the toes 2. Diagnosis: AP, lateral, oblique radiographs 3. Treatment: Nondisplaced: walking boot/postoperative shoe × 3 to 4 weeks, then buddy tape for 4 to 6 additional weeks F. Os trigonum 1. Accessory ossicle formed by lack of fusion of the posterior talar process 2. Present in 10% of population 3. Causes posterior ankle pain with ankle plantar flexion 4. Diagnosis: AP, lateral radiographs 5. Treatment: Relative rest, occasionally a steroid injection, surgical excision if nonoperative treatments ineffective G. Stress fx’s 1. 0.7% to 20% of all sports injuries, most common in running athletes and female athletes 2. History: Progressive pain with activity, training errors, female athlete triad, history of stress fx’s 3. Physical examination (PE): Localized tenderness and swelling, (+) hop test, (+) pain with tuning fork 4. Diagnosis: a. Radiographs: Usually negative within 2 to 3 weeks of symptom onset, usually positive (fx or periosteal reaction) 6 weeks after symptom onset b. Bone scan: Sensitive, not specific. (+) 2 to 8 days after symptom onset c. MRI—Sensitive and specific. Graded as follows: i. Grade 1—abnormal short tau inversion recovery (STIR) ii. Grade 2—abnormal T2 iii. Grade 3—abnormal T1 iv. Grade 4—fx line on T1

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5. Treatment a. Relative rest, avoid nonsteroidal anti-inflammatory drugs (NSAIDs), correct biomechanics, change shoes every 300 to 500 miles, strengthen legs/core, possibly use orthotics 6. Complicated versus uncomplicated stress fx’s a. Complicated: Anterior tibial cortex, navicular (may require CT to define fx), proximal fifth metatarsal, proximal second metatarsal, sesamoids b. Uncomplicated: Fibular, medial tibia, calcaneus, distal metatarsal diaphysis

III. Dislocations A. Ankle dislocations (tib/fib and talus) 1. Frequently have associated fx’s 2. Direction: Posterior (most common), anterior, lateral, superior 3. Treatment: Surgical repair of capsular/ligamentous tears and fx’s B. Interphalangeal dislocation 1. Mechanism: Hyperflexion or hyperextension 2. Dorsal PIP joint dislocation most common 3. Diagnosis: AP, lateral, oblique radiographs 4. Treatment: Reduction, splint immobilization × 3 weeks, then buddy tape × 3 to 6 additional weeks

IV. Tendinopathy: Usually Degenerative (-osis) Rather Than Inflammatory (-itis) A. Achilles tendinopathy 1. Athletes (24% lifetime incidence) > nonathletes, incidence 7:100,000 general population, men > women, most common site = 2 to 6 cm above insertion (watershed zone/poor vascular supply) 2. History: Insidious onset, pain with activity, relieved with rest, occasional edema/crepitus 3. PE: Tenderness to palpation (TTP) at tendinopathy site, ± edema 4. Diagnosis: Usually clinical, but can be confirmed with ultrasound (US) or MRI 5. Treatment: Activity modification, correct training errors/biomechanical deficits, heel lift, glyceryl trinitrate (nitroglycerin) patch, eccentric strengthening program. Investigational treatments: percutaneous needle tenotomy, autologous blood injections, platelet-rich plasma (PRP) injections, percutaneous ultrasonic tendon debridement, and so on. Surgery if nonoperative treatment fails B. Tibialis posterior tendinopathy 1. Inverts the subtalar joint, stabilizes the hind foot and arch 2. More common in middle-aged/older individuals, can cause pes planus 3. History: Insidious or acute onset posteromedial ankle pain, acute or gradual development of flat foot deformity, sometimes associated with underlying inflammatory condition 4. PE: Tender posterior/inferior to medial malleolus, ± edema, pes planus, calcaneal valgus, too many toes sign (see > 2 toes from behind), unable to perform single-leg heel raise 5. Diagnosis: AP, lateral, mortise view radiographs to identify arthrosis, MRI or US to evaluate posterior tibialis tendon 6. Treatment: Rule out inflammatory condition, protection/rest/ice/compression/elevation (PRICE) principles, rigid orthosis to control pronation, medial heel flare, firm heel counter, eccentric exercises. Walking boot for severe cases. Surgery if nonoperative treatment fails C. Peroneal tendinopathy and subluxation/dislocation 1. Usually insidious, but can be traumatic 2. History: Posterolateral ankle pain (insidious or acute/posttraumatic), snap/pop (tendon subluxation/dislocation), ± edema, ankle instability, pain increases with forceful ankle plantar flexion or walking on uneven surface

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3. PE: Posterolateral ankle edema, ± ecchymosis (posttraumatic), tenderness posterior/ inferior to lateral malleolus, click/pain with active ankle range of motion (ROM) (tendon subluxation/dislocation), pain with resisted ankle plantar flexion/eversion, tendon subluxation/dislocation with ankle eversion–plantar flexion to ankle eversion–dorsiflexion against resistance 4. Diagnosis: AP, lateral, mortise view radiographs to evaluate for osseous abnormality; MRI to evaluate for tendinopathy; US to evaluate for tendinopathy or tendon instability (dynamic imaging) 5. Treatment a. Tendinopathy: PRICE, heel lift, eccentric exercises. US-guided injection in refractory cases. Surgery if nonoperative treatment fails b. Tendon subluxation: Immobilization in walking boot/cast with heel lift. NWB × 2 weeks, weight-bearing as tolerated (WBAT) × 4 weeks, then reestablish ROM, strength, proprioception. Nonoperative treatment frequently fails. Surgical treatment can be performed before nonoperative treatment or after nonoperative treatment fails D. Plantar fasciopathy 1. Men = women, bilateral in up to one-third of cases, chronic > acute 2. History: Insidious onset of sharp, medial, or inferior heel pain; most severe with first step out of bed in the morning or after a period of inactivity, lessens with gradually increased activity, worsens toward end of day with increased duration of weight-bearing activity, often associated with a recent increase in intensity of walking or running regimen, change in footwear, exercise on different surface 3. PE: Localized area of maximal tenderness over the anteromedial aspect of the plantar heel surface, gastroc–soleus tightness 4. Diagnosis: Radiographs to rule out other causes of heel pain (eg, stress fx, osseous lesion), bone scan to rule out stress fx, MRI or US to evaluate plantar fascia (abnormal: >5 mm thick) 5. Treatment: 80% will resolve within 1 year regardless of treatment, conservative treatment within 6 weeks hastens recovery, PRICE, stretch gastroc–soleus complex and plantar fascia, strengthen foot intrinsics and ankle support muscles, NSAIDs for pain control, night splint, orthotics, or arch taping, proper footwear (runners should replace shoes every 300–500 miles), corticosteroid or possibly PRP injection (palpation or US-guided), extracorporeal shock wave therapy (ECSWT). Surgery if refractory to nonoperative treatment × 6 months E. Tibialis anterior tendinopathy 1. Primary dorsiflexor of the foot; also adducts and supinates the foot 2. Due to overuse of ankle dorsiflexors (eg, downhill running, over-striding), excessive pronation, restricted ankle ROM, athletes who wear a fixed boot (eg, skiers, skaters), excessive tightness of strapping or shoelaces over area of tendon (eg, runners, “weekend” athletes who do not maintain a consistent level of training), sports requiring abrupt change in direction 3. History: Anteromedial ankle pain, edema, stiffness, increased with activity, especially running or walking down hills 4. PE: Localized tenderness, swelling, occasional crepitus along tendon, pain with resisted dorsiflexion 5. Diagnosis: MRI or US can be used to confirm diagnosis and exclude tendon rupture 6. Treatment: Eccentric strengthening, soft-tissue therapy, ankle mobilization, correction of biomechanical errors, orthotics, correct shoe wear (soft heel), mobilization of ankle joint, US-guided injections for refractory cases F. Flexor hallucis longus tendinopathy 1. Assists with plantar flexion of ankle

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2. Due to overuse, large or medially positioned os trigonum, posterior ankle impingement (ballet dancer’s tendinosis due to en pointe position) or trauma; wearing large shoes 3. History: Posteromedial ankle pain with radiation along medial arch, worse on toe-off or forefoot weight-bearing, may report snap/pop or triggering 4. PE: TTP over posteromedial ankle or under sustentaculum tali at medial longitudinal foot arch, aggravated with resisted first toe flexion or passive first toe and ankle dorsiflexion 5. Diagnosis: AP lateral, mortise view ankle radiographs, and lateral view with foot in full equinus (fully plantar-flexed and inverted) to rule out bony abnormalities; MRI or US to diagnose tendon abnormalities 6. Treatment: PRICE, occasional walking boot progressing to rigid shoe insert, avoid en pointe temporarily, tape first MTP joint to restrict dorsiflexion, US-guided corticosteroid injection in refractory cases. Surgery if nonoperative treatment fails—may need to excise os trigonum.

V. Tendon Tear A. Achilles 1. Peak age 30 to 40 years old, male > female, usually 2 to 6 cm above insertion (decreased blood supply/watershed zone), left > right, usually have underlying tendinopathy (sometimes asymptomatic), 80% occur during recreational “stop–go” sports (eg, basketball), type O blood, fluoroquinolone exposure, anabolic–androgenic steroid use, corticosteroid exposure (oral or injected), obesity 2. History: Sudden sharp pain with/without “pop” during “stop–go” sport, reported as “someone hit me with a bat in the back of my leg,” unable to bear weight 3. PE: Ecchymosis, edema, palpable defect, (+) Thompson test (no plantar flexion of ankle when calf squeezed) 4. Diagnosis: MRI or US 5. Treatment: a. Surgical for active/young athlete b. Some literature suggests nonoperative treatment with dynamic splinting may be as good as surgery in active individuals, particularly if torn ends of tendon approximate with passive ankle plantar flexion

VI. Ligament Injury/Instability A. Lateral ankle sprain 1. Most common sports injury, accounts for 14% to 21% of all sports injuries, most common injury presenting to emergency room (ER) or primary care office: 25,000 occur daily; estimated 1.5 million ER visits annually in the United States, 85% of ankle injuries are ankle sprains. Eighty-five percent of ankle sprains are lateral ankle sprains, most commonly occurs in basketball, volleyball, soccer, football (ie, sports that require rapid direction changes) 2. Mechanism of injury: Inversion of plantar-flexed foot 3. Most commonly injured ligaments: ATFL > CFL > PTFL 4. History: Inversion ankle injury, “giving way,” lateral ankle pain, possible “pop” at time of injury, ecchymosis, edema; usually able to bear weight immediately after injury with subsequent increase in pain and swelling later 5. PE: Lateral ankle ecchymosis, edema, restricted ROM, TTP over injured ligament (usually ATFL), no bony tenderness, poor proprioception (if able to bear weight), (+) ankle anterior drawer test (assesses ATFL—more laxity when pulling ankle anteriorly relative to tibia), (+) talar tilt (assesses CFL—increased inversion with inversion ankle stress) 6. Diagnosis: Radiographs of ankle or foot if (+) Ottawa ankle or foot rules, respectively (Ottawa ankle rules: TTP over posterior aspect of distal 6 cm of tibia or fibula or distal tip of medial or lateral malleolus, or inability to walk four steps immediately after injury

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and in the emergency department; Ottawa foot rules: TTP over base of fifth metatarsal, navicular bone, or inability to walk four steps immediately after the injury and in the emergency department). CT scan for occult fx’s. MRI for occult fx’s, osteochondritis dissecans (OCD), chondral injury, or soft-tissue injury 7. Treatment: PRICE (including crutches until the patient can walk without a limp), over the counter (OTC) analgesics, active range of motion (AROM), isometric progressing to isotonic strengthening, proprioceptive exercises when able to bear weight, ankle bracing or taping during normal ambulation until ankle feels stable, then just with sports for 6 to 12 months; functional exercises prior to return to sport B. Medial ankle sprain 1. Due to eversion injury, injures deltoid ligament, isolated medial ankle sprain very uncommon due to deltoid ligament strength, often have associated medial malleolar fx 2. History: Anteromedial ankle pain, ecchymosis, and edema following eversion ankle injury 3. PE: TTP over injured ligament 4. Diagnosis: Radiographs indicated if (+) Ottawa ankle or foot rules; other diagnostic studies as discussed previously 5. Treatment: Same as lateral ankle sprain, but may take longer to return to play C. Syndesmotic sprain (AITFL sprain, also known as a “high ankle sprain”) 1. Usually due to ankle dorsiflexion and external rotation. Ten percent of all ankle sprains. Most common in collision sports. May also involve posterior inferior tibiofibular ligament or syndesmotic membrane. Can lead to Maisonneuve fx (fx of proximal fibula) 2. History: Anterior ankle pain after the aforementioned mechanism 3. PE: TTP over AITFL (be sure to palpate proximal fibula to evaluate for Maisonneuve fx), (+) squeeze test (syndesmotic pain with tibiofibular compression in the mid-leg), (+) external rotation stress test (syndesmotic pain with external rotation of the ankle in a neutral dorsiflexion/plantar flexion position) 4. Diagnosis: Radiographs of entire tibia and fibular, and AP, lateral, and mortise views of the ankle. Ideally should be weight-bearing. A (+) mortise view for a syndesmotic injury would be indicated by any of the following: tibiofibular clear space of >5 mm (same measurement for AP view), tibiofibular overlap of 3 mm anterior excursion), talar tilt (positive if >15° side-to-side difference). MRI can identify osseous and soft-tissue lesions contributing to ankle instability 6. Treatment: Ankle muscle strengthening, proprioceptive exercises, taping, bracing, orthotics, heel wedge (lateral for lateral ankle instability, medial for medial ankle instability). Surgical intervention considered if nonoperative treatment fails E. Lisfranc joint injury 1. Sprain of the Lisfranc ligament (connects lateral aspect of medial cuneiform with medial aspect of second metatarsal base) of the tarsal–metatarsal joint 2. Two mechanisms a. Direct: Crush injury b. Indirect: Longitudinal force sustained while foot plantar-flexed and slightly rotated (eg, opponent roles onto plantar aspect of plantar-flexed foot of football linemen causing hyperplantar flexion) 3. History: Mechanism discussed previously, mid-foot pain aggravated by weight-bearing (particularly when weight-bearing through forefoot), severity of injury often underestimated at time of injury. Suspect if pain persists >5 days 4. PE: TTP over dorsal mid-foot, ± edema, pain with combined eversion and abduction of forefoot, pain with passive pronation/supination of tarsometatarsal joint 5. Diagnosis: AP, 30° oblique, and lateral weight-bearing radiographs of foot. Positive x-rays = displacement >2 mm between first and second metatarsal bases. “Fleck sign” = avulsion fx near base of the second metatarsal or medial cuneiform in AP view. Medial cortex of second metatarsal base should line up with medial border of intermediate cuneiform on AP x-ray. Medial cortex of fourth metatarsal base should line up with medial border of cuboid on 30° oblique x-ray. Dorsal cortex of first metatarsal and medial cuneiform should line up on lateral weight-bearing x-ray. MRI: more sensitive than x-ray for ligament injury. CT scan may demonstrate small avulsion fx 6. Nunley and Vertullo grading system a. Stage 1 i. Able to bear weight but cannot return to play ii. Local point tenderness over medial aspect of first tarsal-metatarsal (TMT) joint iii. No radiographic diastasis between first and second metatarsals on AP weightbearing x-ray and no medial longitudinal arch on weight-bearing lateral x-ray b. Stage 2 i. Similar physical findings to Stage 1 ii. Diastasis 2 to 5 mm (normal = 1–2 mm) between first and second metatarsals on AP weight-bearing x-ray but no collapse of arch on weight-bearing lateral x-ray c. Stage 3 i. Diastasis 2 to 5 mm between first and second metatarsals on AP weight-bearing x-ray and collapse of medial longitudinal arch on weight-bearing lateral x-ray evidenced by displacement of dorsal cortical line between first metatarsal and medial cuneiform

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7. Treatment a. Stage 1: NWB cast or cast boot immobilization × 2 weeks. Repeat x-ray at 2 weeks to rule out diastasis. If follow-up x-ray shows stability and patient is nontender, then can begin weight-bearing and progressive functional rehabilitation program of foot and ankle with orthotic to provide arch support. If nondisplaced but still tender at 2 weeks, transition to walking boot/cast × 4 weeks, then begin progressive functional rehabilitation program with orthotic to provide arch support b. Stage 2 or 3: Surgical treatment with ORIF F. First metatarsophalangeal joint sprain (“turf toe”) 1. Hyperextension injury to first MTP joint causing damage to plantar plate, joint capsule, and first MTP joint ligaments. Risks include playing on artificial turf, pes planus, poor ankle dorsiflexion ROM, poor first MTP joint extension ROM, flexible shoes 2. History: Hyperextension injury to first MTP causing pain with weight-bearing and great toe movement. Ecchymosis and edema are often present 3. PE: Plantar (and occasionally dorsal) first MTP joint tenderness, first MTP joint effusion, pain with passive and active first MTP ROM, decreased first MTP joint ROM 4. Diagnosis: Radiographs usually unremarkable, but may show small plantar avulsion fx of MTP capsule. MRI may demonstrate soft-tissue injuries to capsule, ligaments, or plantar plate 5. Treatment: WBAT in postoperative shoe, rest, ice, compression, elevation, taping. As pain resolves, gradually work on reestablishing first MTP joint ROM. Transition from postoperative shoe to running shoe with carbon fiber insert and Morton’s extension to decrease first MTP joint dorsiflexion. Often takes 3 to 6 weeks to recover. Can be complicated by the development of hallux rigidus

VII. Bursitis A. Retro-Achilles (subcutaneous calcaneal) 1. Located posterior to Achilles tendon 2. Caused by excessive friction posterior to insertion of Achilles tendon on calcaneus. Seen in athletes who wear heel tabs, shoes that are too tight or too large, stiff boots (ie, ice skates, cricket), Haglund deformity (bony prominence at the posterosuperior aspect of the calcaneus) 3. History: Posterior heel pain aggravated by direct pressure, weight-bearing activity and at the beginning of activity (ie, warm-up phenomenon). May cause limp. ± edema (“pump bump”) 4. PE: TTP retro-Achilles region, ± edema 5. Diagnosis: Radiographs may demonstrate a Haglund deformity, Achilles calcific enthesopathy, or stress fx. MRI and US can demonstrate bursitis 6. Treatment: Ice, reduce pressure (ie, widen/press out heel of shoe), doughnut pad around area, heel cup to raise area over heel counter, NSAIDs, iontophoresis. Occasionally corticosteroid injections are warranted, but be aware of tendon rupture risk. Surgical treatment for Haglund deformity can be considered if nonoperative treatment fails B. Retrocalcaneal (subtendinous) 1. Located between the Achilles tendon and calcaneus 2. Predisposing factors: Training errors, tight Achilles tendon, Haglund deformity, Achilles enthesopathy, underlying seronegative spondyloarthropathy 3. History: Posterior heel pain, ± edema, aggravated by weight-bearing activity (particularly when weight-bearing on forefoot), may report limp 4. PE: ± limp, TTP between calcaneus and Achilles tendon, possible “pump bump” 5. Diagnosis: Radiographs usually normal but may reveal evidence of enthesopathy (eg, enthesophytes) or Haglund deformity. MRI or US can demonstrate the bursopathy

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6. Treatment: Ice, reduce pressure on area (eg, stretch calf, wear shoes that do not press on area), modify training/activities, heel lift, NSAIDs, and iontophoresis. Occasionally a walking boot is beneficial. May consider corticosteroid injection if unresponsive to other treatments, but beware of increased tendon rupture risk. Surgical treatment of Haglund deformity if nonoperative treatment fails

VIII. Osteochondritis Dissecans (OCD) A. Talus 1. Up to 50% of ankle sprains result in OCD but these can also appear without a history of trauma 2. Usually affects articular surface or subchondral bone of talar dome 3. Often attributed to direct trauma to chondral surface or poor vascular supply to injured cartilage 4. Typically seen in males between 20 and 30 years of age 5. History: Ankle pain worse with prolonged weight-bearing; locking, catching, giving way; typically 4 to 5 weeks after ankle injury 6. PE: Persistent effusion, decreased ROM, medial or lateral talar tenderness with ankle plantar-flexed, ankle instability 7. Diagnosis: Radiographs can be normal in 50% of cases but are important for ruling out fx 8. MRI may show bone marrow edema and a cystic lesion (dark on T1) and is useful for measuring the size and location of the lesion and likelihood for healing 9. Treatment: NWB and immobilization with progression to weight-bearing and full ROM over 12 to 16 weeks. Refractory cases should undergo surgery, typically arthroscopic debridement with bone marrow stimulation

Recommended Reading 1. Alfredson H, Cook J. A treatment algorithm for managing Achilles tendinopathy: new treatment options. Br J Sports Med. 2007;41:211–216. 2. Bennell KL, Malcom SA, Thomas SA, et al. Risk factors for stress fractures in track and field athletes. A twelve-month prospective study. Am J Sports Med. 1996;24(6):810–818. 3. Bruckner P, Khan K. Clinical Sports Medicine. Rev. 3rd ed. New York, NY: McGraw-Hill Companies; 2010. 4. Buchbinder R. Plantar fasciosis. N Engl J Med. 2004;350:2159–2166. 5. Dyck D, Boyajian-O’Neill L. Plantar fasciosis. Clin J Sport Med. 2004;14:305–309. 6. Fredericson M, Jennings F, Beaulieu C, Metheson GO. Stress fractures in athletes. Top Magn Reson Imaging. 2006;17(5):309–325. 7. Fu FH, Stone DA. Sports Injuries: Mechanisms, Prevention, and Treatment. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001 8. Gudemann SD, Eisele SA, Heidt RS Jr, Colosimo AJ, Stroupe AL. Treatment of plantar fasciitis by iontophoresis of 0.4% dexamethasone: a randomized, double-blind placebo controlled study. Am J Sports Med. 1997;25(3):312–316. 9. Hoch AZ. Dx, Mx, Rx of sports-related injuries and conditions: lower leg/ankle/foot. AAPM&R Sports Medicine Board Examination Review Course Self Study Material. pp. 315–331. 10. Jensen SL, Andresen BK, Mencke S, Nielsen PT. Epidemiology of ankle fractures. A prospective population-based study of 212 cases in Aalborg, Denmark. Acta Orthop Scand. 1998;69(1):48–50. 11. Judith FB. The foot and ankle. In: Greene W, eds. Netter’s Orthopaedics; 2006:428–453. 12. Kader D, Sazena A, Movin T, Maffulli N. Achilles tendinopathy: some aspects of basic and clinical management. Br J Sports Med. 2002;36:239–249. 13. Kelsey JL, Bachrach LK, Procter-Gray E, et al. Risk factors for stress fractures among young female crosscountry runners. Med Sci Sports Exercise. 2007;39(9):1457–1463. 14. Lake C, Trexler G, Barringer W. Posterior tibial tendon dysfunction: a review of pain and activity level of twenty-one patients. J Prosth Ortho. 1999;11(1):2–5. 15. Maughan K. Ankle sprain. UpToDate Online. May 2010.

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16. Miller MD, Thompson SR. Articular Cartilage Injuries. In: DeLee & Drez’s Orthopaedic Sports Medicine. 4th ed. Philadelphia, PA: Elsevier Saunders; 2015:1428–1441. 17. Premkumar A, Perry MB, Dwyer AJ, et al. Sonography and MR imaging of posterior tibial tendinopathy. AJR Am J Roentgenol. 2002;178:223–32. 18. Renstrom PA, Konradsen L. Ankle ligament injuires. Br J Sports Med. 1997;31:11–20. 19. Roth J, Tayler W, Whalen J. Peroneal tendon subluxation: the other lateral ankle injury. Br J Sports Med. 2010;44:1047–1053. 20. Savage-Elliott I, Ross KA, Smyth NA, Murawski CD, Kennedy JG. Osteochondral lesions of the talus: a current concepts review and evidence-based treatment paradigm. Foot Ankle Spec, 2014;7(5):414–422. 21. Sherman KP. The foot in sport. Br J Sports Med. 1999;33:6–13. 22. Sorosky B, Press J, Plastaras C, Rittenber J. The practical management of Achilles tendinopathy. Clin J Sport Med. 2004;14:40–44.

28 Pediatric Musculoskeletal Injuries and Conditions Andrew John Maxwell Gregory

I. Fractures A. Plastic deformation—bending of bone without fracture propagation 1. Ulna/fibula most common B. Buckle (torus)—compression failure of cortex/periosteum (very common) 1. Metaphyseal/diaphyseal junction C. Greenstick—tension failure causing single cortex separation and buckling opposite D. Complete—fracture propagates through both cortices 1. Spiral—rotational, low velocity, associated with child abuse 2. Oblique—diagonal to diaphyseal bone, unstable 3. Transverse—three-point bending E. Epiphyseal fractures—fractures that involve the physis (growth plate) at the end of long bones 1. Distal radius is most common 2. Potential for deformity—angular, limb length discrepancy or joint incongruity 3. Salter–Harris (SH) classification (see Figure 28.1) a. SH I—through the physis only (x-ray normal or widened physis), growth disruption is unusual, treatment is generally cast immobilization b. SH II—through the metaphysis and the physis, most common, growth disruption is unusual, treatment is generally cast immobilization c. SH III—through the epiphysis and the physis, intra-articular, anatomic reduction required d. SH IV—through the metaphysis and epiphysis, intra-articular, anatomic reduction required e. SH V—crush injury to the physis, difficult to recognize as initial films will appear similar to SH I, high risk of growth disturbance, often diagnosed retrospectively after growth arrest is obvious F. Slipped capital femoral epiphysis—SH I of the femoral head 1. Boys aged 13, girls aged 11, African American (AA), obese 2. Bilateral 30% to 40% 3. Endocrine disorders should be screened for 4. Groin, thigh, or knee pain and limp 5. Loss of internal rotation with flexion 6. AP and frog-leg pelvis x-rays—widening of the physis, posteromedial displacement of the epiphysis 332

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Figure 28.1

333

Illustration of the Salter–Harris classification schema.

a. Klein’s line—line drawn along the superior femoral neck should intersect with the femoral head (see Figure 28.2) 7. Immediate non-weight-bearing 8. Prompt referral for open reduction and internal fixation (ORIF)

II. Apophyseal/Epiphyseal Avulsion Fractures Traction injury of the bony attachment of the tendon or ligament from its origin/insertion; general treatment is conservative; however, marked displacement may indicate surgical management A. Shoulder 1. Coracoid—origin of short head of the biceps and coracobrachialis a. Adolescents b. Fall c. Anterior pain, pop d. Anterior tenderness e. Rest, sling, ice B. Elbow 1. Medial epicondyle—humeral origin of the ulnar collateral ligament and wrist flexor tendons a. School-age children b. Fall, throwing c. Medial pain, pop, swelling d. Medial tenderness, pain with valgus stress e. X-ray—displacement of medial epicondyle

Figure 28.2

Slipped capital femoral epiphysis on the left noted by an abnormal Klein’s line.

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f. Long-arm splint/cast, surgery for significant displacement (>5 mm) C. Wrist/Hand 1. Proximal phalanx (PP) of the thumb—insertion of the ulnar collateral ligament a. Adolescents b. Fall c. Pain, swelling d. Tenderness ulnar side of the base of the PP, pain with valgus stress e. X-ray—SH III fracture f. Thumb spica splint/cast 2. Middle and distal phalanges (MP, DP)—insertion of the flexor and extensor tendons or collateral ligaments (see Figure 28.3) a. Adolescents b. “Jammed finger” c. Pain, swelling d. Tenderness at the base of the MP, DP e. Pain with varus/valgus stress, flexor/extensor tendon testing f. X-ray—SH III fracture g. Flexion splint for volar plate avulsion, extension splint for extensor tendon avulsion, ice, acetaminophen, tape for collateral injuries D. Spine 1. Superior/inferior endplate—attachment of the annulus fibrosus of the intervertebral disc (limbus vertebrae) a. Adolescents b. Olympic weight lifting (squats) c. Pain with sitting, bending d. Decreased forward flexion with pain, positive straight leg raise e. X-ray, CT, MRI—displacement of endplates f. Rest, avoid flexion, extension exercises E. Pelvis and hip 1. Iliac crest—origin of the iliotibial (IT) band/tensor fascia lata (TFL) (palpable) 2. Anterior superior iliac spine (ASIS)—origin of the sartorius (palpable) 3. Anterior inferior iliac spine (AIIS)—origin of the rectus femoris just superior to the acetabulum (not palpable) 4. Ischial tuberosity—pelvic origin of the adductors and hamstrings (palpable) 5. Greater trochanter—femoral insertion of the gluteus medius (palpable) 6. Lesser trochanter—femoral insertion of the iliopsoas (not palpable) 7. General a. Adolescents b. Painful pop with sprinting, kicking, or doing the splits c. Tenderness over the apophysis d. X-ray—widening of the apophysis e. Rest, crutches, stretching, ice, acetaminophen F. Knee 1. Superior pole patella—patellar insertion of the quadriceps tendon 2. Inferior pole patella—patellar origin of the patellar tendon 3. Tibial tubercle—tibial insertion of the patellar tendon 4. General a. Adolescents b. Painful pop with jumping or landing c. Tenderness over the patella or tibial tubercle

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Figure 28.3 Distal phalanx epiphyseal avulsion fracture.

d. X-ray—widening of the apophysis, ossicle e. Knee immobilizer, rest, crutches, ice, acetaminophen G. Foot 1. Base of the fifth metatarsal—insertion of the fibularis brevis tendon a. Adolescents b. Inversion injury with pop c. Swelling, pain on the lateral foot d. Tenderness at the base of the fifth metatarsal e. X-ray—widening of the apophysis f. Walking boot, ankle brace, ice, acetaminophen

III. Apophysitis/Epiphysitis—Overuse Injury to the Apophysis or Epiphysis A. Little league shoulder 1. Humeral head epiphysis—insertion of rotator cuff musculature a. Age 8 to 15 years b. Pitchers, catchers c. Shoulder pain with throwing d. Tenderness of the proximal humerus e. X-rays—normal or lateral widening of epiphysis, sclerosis, cystic changes f. Rest from throwing until pain-free, ice, acetaminophen, rehabilitation to correct biomechanical faults that may predispose to injury g. Adhere to age-based pitch counts when returning to pitching (see Chapter 4, Table 4.1)

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B. Little league elbow 1. Medial epicondyle apophysis—humeral origin of the ulnar collateral ligament a. Age 8 to 15 years b. Pitchers, catchers c. Medial elbow pain with throwing d. Tenderness of the medial epicondyle e. X-rays—normal or widening of apophysis, ossicle f. Rest from throwing until pain-free, ice, acetaminophen, rehabilitation to correct biomechanical faults that may predispose to injury g. Adhere to age-based pitch counts when returning to pitching (see Chapter 4, Table 4.1) C. Gymnast’s wrist 1. Distal radial epiphysis—compression from weight-bearing on the arms a. Age 8 to 15 years b. Gymnasts, cheerleaders c. Wrist pain with tumbling d. Tenderness of the distal radius e. X-rays—normal or closing of epiphysis, shortening of the radius (positive ulnar variance) f. Rest from tumbling until pain-free, ice, acetaminophen, rehabilitation, wrist braces D. Pelvis 1. Iliac crest—origin of the IT band/TFL 2. ASIS—origin of the sartorius 3. AIIS—origin of the rectus femoris just superior to the acetabulum 4. Ischial tuberosity—pelvic origin of the adductors and hamstrings a. General i. Adolescents ii. Hip/groin pain with activity iii. Tenderness over the apophysis iv. X-rays—normal or widening of apophysis v. Rest from activity until pain-free, ice, acetaminophen, stretching E. Sinding-Larsen–Johansson disease 1. Superior pole patella—patellar insertion of the quadriceps tendon 2. Inferior pole patella—patellar origin of the patellar tendon a. Adolescents, typically during periods of rapid growth b. Anterior knee pain with activity c. Tenderness of the apophysis d. X-rays—normal or widening of the apophysis e. Rest from activity until pain-free, ice, acetaminophen, stretching, Cho-Pat strap, reassurance F. Osgood–Schlatter disease (see Figure 28.4) 1. Tibial tuberosity—tibial insertion of the patellar tendon a. Adolescents, typically during periods of rapid growth b. Anterior knee pain with activity c. Tenderness of the apophysis d. X-rays—normal or widening of apophysis, ossicle e. Rest from activity until pain-free, ice, acetaminophen, stretching, Cho-Pat strap, reassurance G. Sever’s disease 1. Posterior calcaneus—insertion of the Achilles tendon a. School-age children

28. PEDIATRIC MUSCULOSKELETAL INJURIES AND CONDITIONS

Figure 28.4

b. c. d. e. f.

337

Osgood–Schlatter disease with ossicle-A.

Soccer, baseball Heel pain with activity Tenderness of the posterior calcaneus X-rays—normal open apophysis, often multipartite Rest from activity until pain-free, ice, acetaminophen, calf stretching, heel cups, walking boot for severe cases

H. Iselin’s disease 1. Base of the fifth metatarsal—insertion of the fibularis brevis tendon 2. Adolescents 3. Lateral foot pain with activity 4. Tenderness at the base of the fifth metatarsal, supination 5. X-rays—normal or widening of apophysis 6. Rest from activity until pain-free, ice, acetaminophen, stretching, lateral heel wedge, walking boot for severe cases.

IV. Osteochondritis Dissecans (OCD) Subchondral bone and cartilage fragment that loses its blood supply due to trauma or vascular insult, most commonly seen in elbow, knee, and ankle, second decade A. General 1. Tends to heal well in the skeletally immature 2. Surgery for unstable lesions or skeletally mature 3. MRI classification (Berndt and Harty)—stable (attached fragment) versus unstable (detached fragment) a. Stage I—subchondral compression, cartilage still attached, edema and signal changes seen on MRI (stable) b. Stage II—partially detached with breach in articular cartilage, fluid leaking under articular cartilage (low signal rim underneath fragment indicating fibrous attachment) (stable)

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c. Stage III—completely detached fragment but still in crater with a breach in articular cartilage but with high signal on MRI underneath fragment and subchondral bone (unstable) d. Stage IV—completely detached fragment loose in joint (loose body) (unstable) B. Elbow 1. Capitellum—compression from valgus stress from throwing or tumbling a. Adolescents b. Pain, swelling with activity c. Effusion, lateral tenderness, loss of motion d. X-rays—sclerosis, fragmentation, collapse e. Rest from activity, physical therapy for stable lesions f. Surgery—removal of loose bodies C. Knee (see Figure 28.5) 1. Femoral condyles (medial 80%; lateral 15%), patella (5%), trochlea a. Male adolescents b. Pain, swelling with activity c. Effusion, joint line tenderness d. Tunnel view x-ray—Semilunar lucency, fragmentation e. Rest, physical therapy, unloader brace for stable lesions f. Surgery for unstable lesions D. Ankle 1. Talar dome a. Pain, swelling with activity, associated with ankle sprain b. Effusion, joint line tenderness c. AP x-ray—semilunar lucency, fragmentation, typically in the superomedial corner of talar dome d. Rest, physical therapy e. Surgery for unstable lesions

V. Osteonecrosis—Avascular Necrosis of the Apophyseal Center A. Elbow 1. Panner’s disease—capitellum a. Children under age 10; throwing, gymnastics b. Good prognosis c. Lateral elbow pain d. X-rays—sclerosis, fragmentation, collapse e. Self-limited process, thus conservative management is warranted: rest, range of motion B. Wrist/Hand 1. Kienbock’s disease—carpal lunate a. Men aged 20 to 40 b. X-rays—increased density, fragmentation, collapse c. Tenderness to palpation of the lunate d. Osteoarthritis develops e. Treatment with a cast or splint initially, surgery for bone grafting, osteotomy, excision or fusion if chronic/recalcitrant C. Spine 1. Scheuermann’s disease—vertebral superior or inferior endplates: a. Male adolescents b. Poor posture, barrel chest, mid-back pain c. Rigid kyphosis

28. PEDIATRIC MUSCULOSKELETAL INJURIES AND CONDITIONS

Figure 28.5 right knee.

339

Large osteochondritis dissecans lesion of the lateral femoral condyle of the

d. Diagnosis via x-ray—three adjacent vertebrae with 5° of anterior wedging, kyphosis of 45°, Schmorl’s nodes, irregular endplates e. Treatment—physical therapy, extension exercises, brace, surgery for severe deformity D. Hip 1. Legg–Calve–Perthes disease—femoral head a. Boys aged 4 to 8 b. 90% unilateral c. Limp with groin, thigh, or knee pain d. Limited hip abduction e. AP and frog-leg pelvis x-rays—sclerosis, fragmentation, crescent sign f. Osteoarthritis can develop, especially if more than 10 years old g. Better prognosis for those less than 10 years h. Physical therapy for range of motion maintenance, crutches or walker with decreased weight-bearing to limit femoral head deformity i. Abduction brace E. Knee 1. Blount’s disease (tibia varum)—medial tibial epiphysis a. Adolescent—obese, AA b. Infantile—unilateral, distinguish from physiologic varus c. Genu varus (bow leg) d. Lateral thrust with gait e. X-rays—beaking of the proximal medial tibia, metaphyseal–diaphyseal angle less than 80 degrees f. Weight loss, bracing (effective in infantile form) g. Surgery—osteotomy F. Foot/Ankle 1. Freiberg’s infraction—second or third metatarsal (see Figure 28.6)

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Figure 28.6

Freiberg’s infraction of the second metatarsal head.

Adolescent females Tenderness at the metatarsal head X-rays—flattening of the metatarsal head If diagnosis is early, conservative management often successful: orthotic (metatarsal cutout, graphite shank), relative rest e. Surgery—debridement, loose body removal 2. Kohler’s disease—tarsal navicular a. Children aged 4 to 8 b. Arch pain and limp c. Tenderness over the medial navicular d. X-rays—sclerosis, collapse, fragmentation e. Walking boot, short leg cast a. b. c. d.

Recommended Reading 1. Bracker MD, ed. The 5-Minute Sports Medicine Consult. 2nd ed. Philadelphia, PA: Wolters Kluwer; 2011: 596–597. 2. Green MD, Swiontkowski MD, eds. Skeletal Trauma in Children. 3rd ed. Philadelphia, PA: Saunders; 2003. 3. Harris SS, Anderson SJ, eds. Care of the Young Athlete, Harris. 2nd ed. Elk Grove Village, IL: American Academy of Pediatrics; 2010:315–321. 4. Kibler B, ed. Orthopaedic Knowledge Update, Sports Medicine. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2009:389–431.

28. PEDIATRIC MUSCULOSKELETAL INJURIES AND CONDITIONS

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5. Metzl MD, ed. Sports Medicine in the Pediatric Office. Elk Grove Village, IL: American Academy of Pediatrics; 2008. 6. Micheli MD, eds. The Sports Medicine Bible for Young Athletes. Naperville, IL: Sourcebooks, Inc.; 2001. 7. Snider RK, ed. Essentials of Musculoskeletal Care. Rosemont, IL: American Academy of Orthopaedic Surgeons; 1999.

MEDICAL, NEUROLOGICAL, AND PSYCHOLOGICAL CONDITIONS

29 Environmental Illness Cara C. Prideaux and Jonathan T. Finnoff

I. Heat Illness A. Thermoregulation = balance between heat production and dissipation 1. Metabolism: Contributes to heat production, greater with exercise than rest 2. Radiation = exchange of heat via electromagnetic waves (ie, no direct contact between objects) a. Heat gain in partially clothed athlete > fully clothed athlete b. Heat absorption in pigmented skin > nonpigmented skin 3. Convection = heat transfer between the body and circulating medium (air, water) a. Greater rate of medium movement (eg, wind) → more rapid heat exchange b. High thermal conductivity → more rapid heat transfer (eg, water > air) 4. Conduction = transfer of heat between warmer and cooler objects via direct contact 5. Evaporation: Sweat vaporization → heat loss a. 580 kcal of heat is lost per liter of evaporated sweat b. Evaporation is the primary mechanism for heat dissipation if ambient temperature >68°F or with vigorous exercise c. High humidity, lack of wind → reduced sweat vaporization d. Wearing hat and coat → impaired evaporative cooling B. Body temperature regulated by preoptic area of hypothalamus 1. Exercise → blood flow decreased to viscera and skin, increased to exercising muscles 2. Rise in core temperature >38°C detected by hypothalamus → activation of efferent fibers of autonomic nervous system → cutaneous vasodilation and increased rate of sweating → heat loss C. Risk factors predisposing to heat-related injury 1. Hot, humid, no clouds, no wind; males > females; improper clothing; acute illness (fever, upper respiratory infection [URI], gastrointestinal [GI]); poor fitness; lack of acclimatization; dehydration; heavier weight, shorter height, higher body mass index; extremes of age; cardiovascular disease; skin injury; previous heat-related illness; sickle cell trait sleep deprivation 2. Medications: diuretics, beta-blockers, anticholinergics, alcohol, phenothiazines, butyrophenones, benztropine, ephedra, amphetamines, cocaine, ecstasy D. Heat-related disorders 1. Miliaria rubra (heat rash—a pruritic papulovesicular rash) a. Due to occluded sweat glands on skin covered by clothing b. Treatment: Good hygiene; cooling and drying the skin 2. Heat edema a. Dependent edema in athletes undergoing heat acclimatization 342

29. ENVIRONMENTAL ILLNESS

3.

4.

5.

6.

7.

8.

343

b. Due to increased plasma volume associated with acclimatization c. Treatment: Elevation of the extremity; resolves with acclimatization Sunburn a. Predominantly caused by ultraviolet B (UV B) rays b. Risk factor for heat illness (reduced heat transfer in sunburned skin) c. Prevention: Cover skin with clothing or sunscreen Heat tetany—Carpopedal spasms a. Due to compensatory hyperventilation from acute heat exposure b. Treatment: Remove athlete from heat, breathe in a paper bag Heat cramps—Muscle cramps in large muscle groups a. Due to heat exposure and electrolyte loss in sweat b. Treatment: Rest, prolonged static stretching of muscle group, rehydration, electrolyte replacement, cooling c. Intravenous (IV) normal saline if severe. IV benzodiazepines administered as the last option Heat syncope—Orthostasis a. Due to peripheral vasodilation and venous pooling b. Treatment: Elevate legs, rehydrate, cool Heat exhaustion a. Profuse sweating, headache, nausea, weakness, malaise, mild mental status changes, inability to continue exercise. No end-organ damage b. Core (ie, rectal) temperature 2% weight loss during activity

Table 29.1

Modifications or Cancellations of Athletic Events Based on WBGT

WBGT (°F)

WBGT (°C)

Continuous Activity and Competition

≤50

≤10

50.1–65

Training and Noncontinuous Activity Nonacclimatized

Acclimatized

Safe

Normal activity

Normal activity

10.1–18.3

Generally safe

Normal activity

Normal activity

65.1–72

18.4–22.2

Risk of EHS rises; monitor high-risk individuals closely

Increase rest:work ratio

Normal activity

72.1–78

22.3–25.6

Risk for all competitors increased

Increase rest: work ratio, decrease total duration

Normal. Monitor fluids

78.1–82

25.7–27.8

Risk for unfit, nonacclimatized individuals is high

Increase rest: work ratio, decrease duration and intensity

Normal. Monitor fluids

82.1–86

27.9–30

Cancel level for EHS risk

Increase rest: work ratio, decrease duration and intensity, watch atrisk individuals closely

Plan intense or prolonged exercise with discretion. Watch at-risk individuals closely

86.1–90

30.1–32.2

Cancel or stop practice or competition

Limit intense exercise and heat exposure. Monitor for signs and symptoms of heat illness

≥90.1

≥32.3

Cancel exercise

Cancel exercise

ACSM, American College of Sports Medicine; EHS, exertional heatstroke; WBGT, wet bulb globe temperature.

29. ENVIRONMENTAL ILLNESS

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d. Fluid: 20 to 30 mEq/L sodium, 2 to 5 mEq/L potassium, 6% to 8% carbohydrate e. IV fluids: severe dehydration >7% body weight loss, cannot rehydrate orally 3. Pre-exercise/during exercise cooling: cold water or air; drink cold fluids. Improves exercise tolerance/performance in heat stress environment G. Quantification of environmental heat stress: Wet bulb globe temperature (WBGT) 1. Takes into account humidity (Tw), solar radiation (Tg), and heat (Td) using the following equation: WBGT = 0.7Tw + 0.2Tg + 0.1Td 2. Table 29.1 shows the American College of Sports Medicine (ACSM) recommendations for exercise in a heat-stressed environment utilizing the WBGT (1).

II. Cold Illness A. Body temperature regulated by preoptic area of hypothalamus 1. Body temperature males; amenorrheic > eumenorrheic women C. Hypothermia 1. Core body temperature ≤35°C (95°F) (rectal thermometer) 2. Mild hypothermia: core temperature 35°C to 32°C a. Ataxia, dysarthria, apathy are often present b. Athlete will shiver and skin will be pale and cool 3. Moderately severe hypothermia: core temperature 32°C to –28°C a. Core temperature 250 mg/dL with ketones or >300 mg/dL b. May participate in short duration events (180 mmHg (eg, weightlifting, isometrics), inverted exercises due to increased intra-ocular pressure, scuba diving, or jarring exercises (eg, plyometrics) b. Peripheral neuropathy/peripheral vascular disease = avoid activities that may traumatize the feet (eg, running)

II. Menstrual Disorders in Athletes A. Athletes have greater risks for menstrual disorders than nonathletes B. Amenorrhea incidence ~50% in athletes compared to 3% to 5% of the general population (primarily gymnast, endurance athletes, ballet dancers, ice skaters) 1. Primary amenorrhea = no menses by age 16 2. Secondary amenorrhea = menses stop for >6 months after they have menstruated C. Athletes at risk = exercise intensely, lower body fat, abnormality in nutritional status (disordered eating), late menarche, and/or a history of menstrual irregularity D. Exercise alone does not cause amenorrhea and may improve dysmenorrhea E. Diagnosis necessary in all athletes presenting with menstrual abnormalities 1. History and physical examination a. Galactorrhea i. Can be due to hyperprolactinemia from medication use or a pituitary tumor ii. Medications that produce hyperprolactinemia (A) Amphetamines (B) Cannabis (C) Cardiovascular drugs (atenolol, verapamil) (D) H2 blockers (E) Herbal therapies (fennel, fenugreek seed) (F) Psychotropic drugs (selective serotonin reuptake inhibitors, tricyclic antidepressants, buspirone) (G) Neurologic drugs (valproic acid, sumatriptan) iii. Test prolactin level. Hyperprolactinemia is associated with 20% of amenorrhea cases in the general population (A) If prolactin is 100 ng/mL, probably due to a pituitary adenoma iv. MRI or CT of brain looking for pituitary adenoma b. Atrophic vaginal changes/dryness (hypoestrogenic state) c. Anatomical abnormalities associated with outlet obstruction i. Asherman’s syndrome (hysteroscopy) ii. Congenital absence of the vagina and uterus iii. Imperforate hymen iv. Uterine and cervical defects

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III: DIAGNOSIS AND TREATMENT OF SPORTS INJURIES AND CONDITIONS

2. 3.

4.

5.

6.

7.

8. 9.

d. Weight loss e. Hirsutism (polycystic ovarian syndrome) f. Virilization i. Suggests adrenal or ovarian neoplasm g. Visual field defect i. Suggests pituitary adenoma h. Short stature, sexual infantilism, and webbed neck = Turner’s syndrome Pregnancy assessment a. Most common cause of secondary amenorrhea in childbearing-age women Thyroid-stimulating hormone (TSH) a. If abnormal then complete thyroid cascade panel (T3, T4, free T4). Hypothyroidism is rarely a cause of amenorrhea Progestin challenge test a. Differentiate those with estrogen deficiency from those with normal or high estrogen levels b. Medroxyprogesterone acetate 10 mg by mouth once per day for 5 to 7 days or norethindrone 5 mg PO once daily for 7 to 10 days will produce bleeding within 1 week of the final dose in those with normal estrogen levels and anovulation is the expected cause of amenorrhea. Those who do not bleed likely have estrogen deficiency, but outflow tract obstruction is possible Estrogen–progestin challenge test a. Differentiates those with outflow tract obstruction and estrogen deficiency b. Estrogen given for 21 to 25 days c. Progestin given for the final 5 to 7 days to motivate withdrawal bleeding d. No bleeding = outflow obstruction e. Bleeding = estrogen deficiency (further investigation required) Gonadotropin levels a. Follicle-stimulating hormone (FSH) > 40 mIU/mL—primary ovarian failure (POF) or menopause b. Both FSH and luteinizing hormone (LH) elevated = POF c. LH:FSH ratio > 2:1 = polycystic ovarian syndrome d. Low levels of LH and FSH = prepubertal state or hypothalamic and pituitary dysfunction (ie, female athlete triad, anorexia nervosa) Androgen testing a. Investigate those with acne, hirsutism, and virilization b. Testosterone levels >200 ng/dL probably due to ovarian source. Workup for neoplasm c. Didehydroepiandrosterone (DHEAS) >7 mg/dL probably due to an adrenal source. Workup for neoplasm Karyotyping (POF before age 30 or evidence of Turner’s syndrome) In those with amenorrhea >6 months, a bone density screen is advised

F. Management 1. Four main causes of amenorrhea a. Hyperprolactinemic, hypogonadotropic, hypergonadotropic, normogonadotropic i. Hypogonadotropic is related to athletic causes of amenorrhea 2. Treatment for hypogonadotropic amenorrhea a. Gain body mass and maintain intensity of exercise b. Maintain body mass and decrease intensity of exercise i. Address eating disorder if present (dietary/psychological counseling) ii. Take time off (2 months) or decrease training (intensity/duration/frequency) by 10% iii. Oral contraception for bone protection from loss until normal menses returns

39. SPORTS ENDOCRINOLOGY

449

(A) Avoid in patients who smoke, have hypertension, or history of migraine headaches iv. Calcium supplement 1.5 g/day and vitamin D 800 IU/day v. Antiresorptive therapy in those with osteoporosis who are not of childbearing age. Avoid in those of childbearing age due to teratogenicity

III. Osteoporosis/Osteopenia A. Diagnosis 1. Dual-energy x-ray absorptiometry (DEXA) a. T-score of ≤–2.5 = osteoporosis b. T-score between –1.0 and –2.5 = osteopenia B. May be seen in athletes with large energy deficit (energy availability of 100,000 mm3). Gram stain generally positive for Gram-positive infection. Blood cultures positive in about 50% of cases.

III. Treatment A. IV antibiotics: 1. Vancomycin for Gram-positive stain or empiric treatment pending culture results. 2. Vancomycin and third-generation cephalosporin if Gram-negative more likely based on presenting history. 3. Depending on the organism and severity of infection, IV treatment is recommended for about 2 weeks followed by an additional 2 weeks of pathogen-specific oral antibiotics. B. Joint drainage is generally recommended, although studies comparing treatment with and without drainage and comparing methods of drainage (needle aspiration, arthroscopic lavage, open lavage) are lacking.

SEXUALLY TRANSMITTED INFECTIONS I. Epidemiology A. In the United States, the average age of first intercourse is 16 (and earlier in certain populations). Athletes are potentially at greater risk for sexually transmitted diseases (STDs) than the general population. B. Studies with adolescent athletes are mixed; some suggest female athletes are at lower risk for STDs and pregnancy than their nonathlete counterparts, but other studies suggest increased sexual activity and an increased number of sexual partners in athletes. The social environment in certain high-profile professional sports is associated with high numbers of sexual partners. C. Common STDs include gonorrhea, chlamydia, trichomoniasis, genital warts (primarily HPV types 6 and 11) or cervical dysplasia/carcinoma (primarily HPV types 16, 18, 52), and herpes (herpes simplex virus 2 [HSV 2] >1 for genital lesions). D. Adolescents engaging in early intercourse (age < 16) are at particularly high risk for chlamydia and HPV, with studies reporting infection rates above 30%. The highest reported rates of chlamydia are in 15- to 19-year-old females. E. Less common STDs include hepatitis B and C, HIV, and syphilis.

II. Diagnosis A. Symptoms vary with the common infections. Common manifestations of STDs include vaginal or urethral discharge, warts, ulcerations, and, in women, pelvic inflammatory disease (PID). B. Gonorrhea, trichomoniasis, and chlamydia are the most common sexually transmitted causes of discharge. Males are most likely to have symptomatic urethral discharge. Women may have vaginal discharge but are more likely than men to have asymptomatic infection. Chlamydia is often asymptomatic in women, but 10% of women infected will develop PID if untreated. Because of the high incidence of asymptomatic infection, the CDC recommends annual screening for gonorrhea and chlamydia in all sexually active females aged 24 and under.

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III: DIAGNOSIS AND TREATMENT OF SPORTS INJURIES AND CONDITIONS

1. Diagnostic testing: a. Trichomoniasis is diagnosed by identifying organisms on wet mount. b. Gonorrhea in males can be identified by Gram stain and culture of discharge. This technique is less sensitive in females. c. Currently, the most sensitive and specific testing for gonorrhea and chlamydia is nucleic acid amplification. Test can be performed on a urine sample or oral, vaginal, or rectal swab. Vaginal swab is considered the optimal test by the CDC. Providerand patient-administered vaginal swabs are considered equivalent in sensitivity and specificity. C. HSV is the most common cause of genital ulceration. Primary infection presents with prodromal itching and pain followed by the development of painful vesicles that often spontaneously rupture, resulting in ulcers. Local lymphadenopathy and dysuria are common. Systemic symptoms, including fever and myalgia, occur over half the time. Lesions spontaneously resolve, but viral reactivation causes clinical recurrence, often with fewer vesicles recurring at the same site. Systemic symptoms are uncommon with recurrence, and recurring lesions may be asymptomatic. 1. Diagnostic testing includes viral culture of vesicle fluid during outbreak. PCR of the fluid is more sensitive. HSV serology can be used for diagnosis in patients without active lesions. D. HPV causes genital warts, and oncogenic HPV strains cause cervical and anogenital neoplasia. Genital warts appear as flat, smooth, or verrucous papules on the external genitalia, anus, or cervix. Cervical infection is generally asymptomatic until presentation with advanced cervical cancer. Asymptomatic infection is identified through regular cervical Pap testing, with HPV DNA testing playing a role in secondary testing and screening. Screening recommendations include Pap smears every 3 years for women aged 21 to 29. In women 30 years of age or older, Pap smear with HPV cotesting every 5 years is the preferred method; cotesting should not be used in women under age 30. The CDC states that in women who have never had any type of sexual encounter, it can be reasonable to delay Pap testing past age 21 on a patient-to-patient basis; however, major groups (The American Congress of Obstetricians and Gynecologists [ACOG], U.S. Preventive Services Task Force [USPSTF]) recommend initiation of screening at age 21 regardless of sexual history. All major groups recommend against screening earlier than age 21, regardless of age of first sexual encounter or other behaviors.

III. Treatment A. Chlamydia is treated with azithromycin 1 g po as a single dose or doxycycline 100 mg po bid for 7 days. Gonorrhea is treated with cefixime 400 mg po single dose or ceftriaxone 250 mg intramuscular. The infections often coexist, and combination treatment is recommended unless infection with one is ruled out at the time of documentation of the other infection. Partners should be treated, and intercourse should be avoided for 1 week after completion of treatment. B. Trichomoniasis is treated with tinidazole or metronidazole 2 g po as a single dose. Topical metronidazole recurrence rates are 50%, possibly from urethral reinfection. C. HSV infection cannot be cured. Barrier contraceptives can decrease the likelihood of transmission and infection. 1. For primary infection, antiviral treatment within 72 hours of onset can decrease length and severity of symptoms. Acyclovir 400 mg tid for 7 to 10 days or a comparable regimen of another antiviral medication is recommended. 2. Recurring infection is treated with acyclovir 800 mg tid for 2 days started immediately at first sign of recurrence. 3. Acyclovir 400 mg bid can be used as suppressive therapy in those with more frequent recurrences, and suppressive therapy can decrease the risk of transmission.

41. SPORTS INFECTIOUS DISEASE

465

D. HPV infection is not treated directly. Treatment is directed at preventing and managing the sequelae of HPV infection. Additionally, HPV infection may clear spontaneously in a large percentage of cases. 1. Warts can be destroyed or excised but may recur, and infection can be transmitted in the absence of visible warts. 2. Imiquimod is a topical immunomodulator approved in the treatment of anogenital warts. 3. Two vaccines against HPV are available: Quadrivalent Gardasil (HPV 6, 11, 16, 18) covers the most common cause of genital warts (HPV 6, 11) and cervical cancer (HPV 16, 18). Cervarix is bivalent, covering HPV 16 and 18. The vaccines are given in three doses and are most effective if administered prior to HPV exposure. The HPV vaccine is generally recommended for both girls and boys starting at age 11.

UPPER RESPIRATORY TRACT INFECTION I. Epidemiology A. Caused by picornaviruses: rhino, echo, coxsackie. B. Generally spread via hand-to-hand or hand-to-face secretions. They are less commonly via aerosolized droplets. C. The incubation period is 2 to 3 days, and symptoms typically last 4 to 10 days. D. Exercise appears to influence susceptibility to URI. Moderate exercise may be protective, while heavy exercise may increase susceptibility to infection. 1. High-mileage runners are twice as likely to report URI symptoms compared to lower mileage runners, and studies have reported a sixfold increase in URI symptoms after running a marathon. 2. Mechanism of susceptibility is likely a combination of increased cortisol and decreased IgM, salivary IgA, and natural killer cells brought about by high-intensity training.

II. Diagnosis A. Diagnosis is made clinically, and diagnostic testing should be reserved for symptom severity out of the ordinary, symptoms more specific for differential diagnosis listed next, or symptoms that fail to resolve in typical time course. B. Typical symptoms include congestion with secretions often becoming purulent, cough, sore throat, low-grade fever, and headache/sinus pressure. C. Common differential includes allergic rhinitis, acute bronchitis, pneumonia, bacterial sinusitis, acute otitis media, strep pharyngitis, and Infectious Mononucleosis.

III. Treatment A. Antipyretics, analgesics, decongestants, and antihistamines are all effective for symptom management. Decongestants are banned by some sports governing bodies. B. Antibiotics do not shorten illness course or provide relief for URI or bronchitis and should be discouraged to avoid fostering the development of antibiotic resistance. C. Athletes with significant fatigue, high fever, and systemic symptoms (ie, symptoms below the neck) should restrict training until improving (see sections on febrile illness and mononucleosis).

METHICILLIN-RESISTANT STAPHYLOCOCCUS AUREUS I. Epidemiology A. MRSA was identified in the 1960s as a nosocomial infection. Currently, it is the most commonly community-acquired skin infection in the United States.

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III: DIAGNOSIS AND TREATMENT OF SPORTS INJURIES AND CONDITIONS

B. When first identified, hospital-acquired MRSA primarily consisted of two distinct types, and community-acquired MRSA represented a third type. Additional types have been described, and infection with the different types is no longer limited to one setting or the other. C. Methicillin resistance is defined by an oxacillin minimum inhibitory concentration (MIC) 4 mcg/mL or greater. MRSA is resistant to all beta-lactam antibiotics, and certain types have developed rapid resistance to other antibiotics, quinolones being a prime example. D. MRSA outbreaks have been reported in athletic settings, and athletes, specifically football players, are classified as an at-risk group. One large outbreak on a college football team was extensively investigated by the local health department, and shared towel use was suspected in the transmission of infection. MRSA has also been cultured from surfaces and athletic equipment in the setting of outbreaks.

II. Diagnosis A. In athletes, MRSA is most likely to present as a skin infection, most often an abscess. Other skin manifestations include cellulitis, necrotizing fasciitis, and wound infections. MRSA can also cause osteomyelitis, ear and urinary tract infection, pneumonia, endocarditis, and sepsis. B. Typical skin infections are painful, presenting with erythema, induration, and frequently an abscess that may drain pus. The initial lesion is often mistaken for a spider bite. The course varies from indolent to rapidly progressive in some individuals.

III. Treatment A. Recommendations vary for empiric treatment of soft-tissue infection. Some recommend initial coverage with cephalosporin or dicloxacillin pending culture. Others feel the prevalence of MRSA warrants empiric treatment with MRSA-active antibiotics, and local infection patterns should guide this decision. B. The first-line oral treatments for MRSA are not as effective against group A strep, so double coverage for MRSA and group A strep is recommended by some authorities pending culture results. C. Athletes, coaches, and athletic training staff need to be aware of early signs of infection. Often, incision and drainage (I&D) provide adequate treatment, and some authorities recommend I&D without antibiotics for isolated abscess less than 5 cm in healthy individuals. Some recommend culture with sensitivities for all abscesses, while others reserve culture for lesions that do not respond to initial I&D or those appearing more serious. D. Traditional oral antibiotics that are generally effective for MRSA include trimethoprim– sulfamethoxazole (Bactrim DS) 2 tabs bid, clindamycin 300 to 450 mg Q 6 to 8 hours, or minocycline or doxycycline 100 mg bid. A 7- to 10-day course is recommended. E. Infections not responding to these regimes or more serious infections should be treated with vancomycin IV (15–20 mg/kg every 12 hours). Linezolid is a second-line oral and IV drug with activity against strep and MRSA. There are reports of patients with MRSA developing linezolid resistance rapidly, and potential toxicities require regular monitoring. Thrombocytopenia is a common adverse effect of linezolid. F. Athletic settings should incorporate MRSA prevention strategies including: 1. Athlete and staff education regarding the appearance of MRSA infection. 2. Athlete education regarding bathing with bactericidal soap after every training session. 3. Cleaning and covering any cuts or breaks in the skin. 4. The use of universal precautions. 5. Regular cleaning of surfaces and shared equipment with antimicrobial agent effective against MRSA. 6. Avoid sharing of towels and other personal hygiene items.

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Recommended Reading 1. Bacon RM, Kugeler KJ, Griffith KS, Mead PS. Lyme disease—United States, 2003–2005. MMWR Weekly. 2007;56(23):573–576. 2. Becker JA, Smith JA. Return to play after infectious mononucleosis. Sports Health. 2014;6(3):232–238. 3. Gutierrez RL, Decker CF. Blood-borne infections and the athlete. Dis Mon. 2010;56:436–442. 4. King OS. Infectious disease and boxing. Clin Sports Med. 2009;28;545–560. 5. Kordi R, Wallace WA. Blood borne infections in sport: risks of transmission, methods of prevention, and recommendations for hepatitis B vaccination. Br J Sports Med. 2004;38:678–684. 6. Luke A, d’Hemecourt P. Prevention of infectious diseases in athletes. Clin Sports Med. 2007;26:321–344. 7. Neiman DC. Exercise, upper respiratory tract infection, and the immune system. Med Sci Sports Exerc. 1994;26(2):128–139.

42 Sports Allergy and Immunology Robert J. Dimeff and Rathna Nuti

I. Immunizations A. The sports medicine physician may be the only medical doctor to attend to an athlete. This relationship allows for an opportunity to promote primary preventative care with respect to immunizations. B. Immunizations involve administration of inactivated or live, attenuated viruses to provide immunity 1. Adverse effect occur most commonly with live, attenuated viruses a. Local pain, hypersensitivity reaction to vaccine constituents 2. Conditions commonly misperceived as contraindications to vaccines: a. Acute illness with or without fever b. Current antimicrobial therapy c. Mild or moderate local reaction to previous vaccine d. Recent exposure to infectious disease e. Allergies f. Family history of adverse event C. The sports medicine physician should consider the following: 1. Routine health maintenance 2. Catch-up immunizations for those who fall behind or start late 3. High-risk groups—immunocompromised, chronic cardiovascular or pulmonary disease, asplenia, sickle cell, diabetes mellitus, cirrhosis, and age over 65 4. Close contact or recent potential exposure to infected individual 5. Influenza vaccine is recommended for all persons older than 6 months of age 6. Travel planned to endemic area a. Ideally should plan several months in advance b. Centers for Disease Control and Prevention (CDC) website provides information on recommended vaccines for travel (wwwnc.cdc.gov/travel) D. CDC vaccination schedule (Tables 42.1–42.3)

II. Anaphylaxis A. Severe, acute, potentially life-threatening systemic reaction resulting from the degranulation of mast cells and basophils B. Prevalence estimated from 0.05 to 2% in the general population C. Asthma, allergic rhinitis (AR), and atopy are risk factors for anaphylaxis D. Signs and symptoms: 468

42. SPORTS ALLERGY AND IMMUNOLOGY

Table 42.1

Birth

Recommended Immunization Schedule for Persons Aged 0–6 Years (United States, 2015)

1 2 4 6 12 15 18 19–23 2–3 Month Months Months Months Months Months Months Months Years

Hep B

469

Hep B

4–6 Years

Hep B

Rota

Rota

Rota

DTaP

DTaP

DTaP

Hib

Hib

Hib

Hib

PCV

PCV

PCV

PCV

IPV

IPV

DTaP

DTaP

IPV

IPV Influenza (yearly)

MMR

MMR

Varicella

Varicella Hep A (two doses)

DTaP, diphtheria, tetanus, and pertussis; Hep A, Hepatitis A; Hep B, Hepatitis B; Hib, haemophilus influenzae type B; IPV, inactivated polio vaccine; MMR, measles, mumps, and rubella; PCV, pneumococcal conjugate vaccine; Rota, rotavirus.

Table 42.2 7–10 Years Tdap (catch-up)

MCV4 (high-risk)

Recommended Immunization Schedule for Persons Aged 7–18 Years (United States, 2015) 11–12 Years

13–18 Years

Tdap

Tdap (catch-up)

HPV (three doses)

HPV (catch-up)

MCV4

MCV4 (catch-up)

Booster at age 16 years

Influenza (yearly) Pneumococcal (high-risk) Hep A (catch-up and high-risk) Hep B (catch-up) IPV (catch-up) MMR (catch-up) Varicella (catch-up) Hep A, Hepatitis A; Hep B, Hepatitis B; HPV, human papillomavirus; IPV, inactivated polio vaccine; MCV4, meningococcal conjugate vaccine; MMR, measles, mumps, and rubella; Tdap, adult tetanus, diphtheria, and pertussis.

1. Sensation of tingling or warmth, flushing, generalized pruritus, urticarial lesions typically 1 to 2 cm in diameter or angioedema 2. Respiratory symptoms such as wheezing, cough, chest tightness, stridor, swelling of the mouth or airway, and respiratory distress 3. Gastrointestinal (GI) symptoms such as vomiting, cramping, or diarrhea

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III: DIAGNOSIS AND TREATMENT OF SPORTS INJURIES AND CONDITIONS

Table 42.3 Age Group → Vaccine ↓

Recommended Vaccines for Persons Aged 19 years and Older (United States, 2015)

19–21 Years

22–26 Years

27–49 Years

50–59 Years

60–64 Years

≥65 Years

Influenza

One dose annually

Td/Tdap

Substitute one time dose of Tdap for Td booster, then boost with Td every 10 years

Varicella

Two doses

HPV

Three doses for females Three doses males if high-risk

Zoster

One dose

MMR

One or two doses

PCV13

High-risk

One time dose

PPSV23

One or two doses if high-risk

One dose

Meningococcal

One or more doses if high-risk

Hepatitis A

Two doses if high-risk

Hepatitis B

Three doses if high-risk

Hib

One or three doses if high-risk

Hib, haemophilus influenzae type B; HPV, human papillomavirus; MMR, measles, mumps, and rubella; PCV13, pneumococcal conjugate vaccine; PPSV23, pneumococcal polysaccharide vaccine; Tdap, adult tetanus, diphtheria, and pertussis.

4. Pale, diaphoresis, palpitations, chest pain, arrhythmias, hypotension 5. Presyncope, syncope, headache, feeling of impending doom, unconsciousness 6. Late phase or “biphasic” reactions due to slow-releasing substances a. Symptoms appear to resolve but return in 1 to 72 hours (mean of 10 hours) and can be more severe b. Occur in up to 25% of cases of fatal or near fatal anaphylaxis E. Causes 1. Food is the most common cause of anaphylaxis a. Accounts for 30% of fatal cases b. Most commonly implicated—peanuts, tree nuts, seafood, wheat, soy, egg 2. Drugs (penicillin), biological agents, or radiographic contrast 3. Nonsteroidal anti-inflammatory drugs (NSAIDs) and aspirin (second most common drug causing anaphylaxis) 4. Insect bites or stings 5. Natural rubber latex a. High-risk groups for reaction to latex: health care workers, workers with occupational exposure to latex, and children with spina bifida and genitourinary abnormalities 6. Seminal fluid 7. Allergen immunotherapy 8. Exercise 9. Idiopathic

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F. Pathophysiology 1. Generally thought to be IgE-mediated type 1 hypersensitivity reaction, but may also be IgE-independent, IgG-dependent, or nonimmunologically mediated 2. Exposure to allergen or other factors that activate mast cells and basophils 3. Degranulation and release of vasoactive mediators such as histamine 4. Production of prostaglandins, leukotrienes, platelet activating factor (PAF), cytokines (eg, tumor necrosis factor [TNF]), chemokines G. Diagnosis 1. Thorough history from patient, witnesses of event, and family members a. Characteristics of symptoms during event b. All medications and food consumed 4 to 6 hours prior to episode c. Activities 4 to 6 hours prior to episode (sexual activity, exercise) d. Any preceding bite or sting e. Medical history (asthma, atopy, AR) f. Family medical history (asthma, atopy, AR) 2. Skin prick testing is more sensitive than in vitro specific IgE testing a. History may be so conclusive of a specific agent that no additional testing is needed b. Testing for a specific agent or potential allergen may not be available or may have a low predictive value c. Must consider the risk of having a severe reaction during skin testing versus the potential benefits of testing 3. Challenge testing may be appropriate but must be performed under controlled circumstances with appropriate rescue treatment available 4. Laboratory studies that may be helpful in diagnosing anaphylaxis a. Serum tryptase i. Level peaks in first 1 to 1.5 hours after onset of symptoms and persists for 5 to 6 hours ii. Should be drawn in first 1 to 2 hours after onset of symptoms iii. May not be elevated in anaphylaxis due to food iv. Elevated tryptase when asymptomatic may indicate mastocytosis b. Plasma histamine i. Levels begin to increase 5 to 10 minutes after onset of symptoms and remain elevated for 30 to 60 minutes ii. Less helpful if not drawn within an hour after the onset of symptoms H. Treatment of anaphylaxis 1. Acute management a. Assess airway, breathing, circulation, and consciousness (unconsciousness may reflect hypoxia) b. Epinephrine 1:1000 dilution (1 mg/ml) 0.2 to 0.5 ml (0.01 mg/kg in children with maximum dosage 0.3 mg) intramuscular (IM) into lateral aspect of thigh; may repeat every 5 minutes. If patient is taking beta-blockers, consider intravenous (IV) glucagon c. Place patient recumbent and elevate legs d. Supplemental oxygen e. May require large volumes of IV colloid or crystalloid fluid f. Consider inhaled beta-2-agonists (eg, albuterol metered dose inhaler [MDI] 2–6 puffs or nebulized 2.5–5 mg, repeated doses as necessary) g. Histamine-1 (H1) antagonist such as diphenhydramine IV or IM 25 to 50 mg in adults and 1 to 2 mg/kg in children, hydroxyzine, or other H1 antagonists h. Histamine-2 (H2) antagonist such as ranitidine IV or IM 50 mg in adults and 12.5 to 50 mg (1 mg/kg) in children or cimetidine 4 mg/kg in adults (no dosage studied in children)

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i. Combination of H1 and H2 antagonists is superior to H1 antagonist alone ii. Should not be given in lieu of epinephrine iii. Glucocorticoids have the potential to prevent recurrent or protracted anaphylaxis (A) No conclusive evidence for prevention of biphasic reaction 2. Prevention/lifestyle modification a. Identify cause if possible b. Immunotherapy/desensitization therapy c. Patient education i. Avoidance of known or suspected triggers ii. Medical alert bracelet iii. Epinephrine autoinjector (Epi-Pen) availability and teaching

III. Exercise-Induced Anaphylaxis (EIAn) A. Specific form of anaphylaxis in which exercise is the only trigger B. Can occur during vigorous exercise such as jogging, tennis, soccer, football, dancing, aerobics, or may occur with light activity such as brisk walking or yard work C. May be isolated or recurrent 1. Most patients experience fewer and less severe attacks over time 2. Episodes are unpredictable and occur sporadically even in the face of regular exercise D. Fifty percent of patients with EIAn have personal or family history of atopy E. Cotriggers 1. Often required for symptoms to occur 2. In absence of exercise, cotriggers do not cause any symptoms 3. NSAID/aspirin ingestion preceding exercise by hours to a day has been associated with EIAn 4. Alcohol ingestion 4 to 6 hours prior to exercise 5. Menstruation 6. Pollen exposure in pollen-sensitive individual 7. Extremes of temperature F. Food-dependent, exercise-induced anaphylaxis (FDEIAn) 1. Ingestion of specific food or a meal consumed within 4 to 6 hours of exercise leads to symptoms 2. Ingestion of food alone does not cause symptoms 3. Most common food implicated is wheat, specifically water-insoluble gliadins, other grains, and nuts a. Other foods: shellfish, vegetables (celery), fruits, vegetables, seeds, legumes, various meats, cow’s milk, and eggs G. Variant-type exercise-induced anaphylaxis (VTEIAn) 1. About 10% of cases 2. Combination of features of EIAn and cholinergic urticaria (CU) a. Punctate (2–4 mm) urticaria as seen in CU and can progress to complete vascular collapse as seen in EIAn 3. Precipitated only by exercise and not by passive warming H. Symptoms 1. Feeling of warmth, flushing, fatigue, malaise, pruritus, and urticaria a. May progress to angioedema, respiratory distress and laryngoedema, GI symptoms, hypotension, and cardiovascular collapse 2. Headache that can persist for several days 3. Symptoms frequently abate over several hours with cessation of exercise I. Pathophysiology of EIAn

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1. Not well understood, likely mast cell mediated 2. Exact mechanism leading to mast cell activation has not been elucidated J. Diagnosis 1. Thorough clinical history, including detailed dietary recall and medications to identify any cotriggers 2. Skin or in vitro allergen testing 3. Exercise treadmill testing 4. Food challenge with exercise treadmill testing K. Differential diagnosis 1. Exercise-induced asthma, CU, exercise-associated gastroesophageal reflux, arrhythmias 2. CU can usually be differentiated by smaller 1 to 3 mm punctuate wheals and symptoms can be elicited by passively increasing body temperature L. Treatment of EIAn 1. Immediate cessation of exercise at onset of symptoms 2. Acute treatment as in anaphylaxis of any cause 3. Patient education/lifestyle modification a. Avoid exercise 4 to 6 hours after eating b. Avoid foods known to trigger FDEIAn c. Avoid aspirin and other NSAIDs before exercise d. Refrain from exercise around menses e. May need to avoid exercise on warm/humid days or reduce intensity f. Epinephrine availability at all times and proper training on use g. Exercise with a partner who is aware of medical condition and epinephrine use h. Cease exercise immediately at first signs or symptoms i. Impending anaphylactic reaction may abate spontaneously ii. Seek immediate medical assistance if symptoms occur M. Prophylactic medications 1. Controversial, not effective in majority of patients with EIAn 2. Small subset of patients may benefit from daily use of antihistamine 3. H1 antagonists can be used to treat dermatologic symptoms a. Hydroxyzine 25 to 50 mg four times daily b. Other nonsedating H1 antagonists (cetirizine, loratadine, fexofenadine) may have similar effects and should not impair athletic performance c. H2 antagonists (famotidine, ranitidine) can be added for refractory symptoms 4. Cromolyn, a mast cell stabilizer that prevents degranulation and release of plasma histamine and other inflammatory mediators, has had inconclusive results in prophylactic treatment of EIAn 5. Other medications such as leukotriene-modifying agents (montelukast, zafirlukast, zileuton) to date have not been studied for the management of EIAn

IV. Urticaria A. Circumscribed, raised, erythematous evanescent areas of edema involving superficial portion of dermis 1. Usually highly pruritic and arises suddenly 2. Rarely persists more than 24 to 48 hours 3. Acutely affects 20% of the population B. Angioedema occurs when edematous process extends into the deep dermis and/or subcutaneous and submucosal layers 1. Commonly affects face, neck, and part of extremity 2. Can be painful but usually not pruritic 3. Can persist for 72 hours

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4. Adults more likely to experience angioedema with urticaria C. Classification 1. Acute urticaria less than 6 weeks duration a. Causes include drugs, foods, viral upper respiratory tract infections 2. Chronic urticaria greater than 6 weeks duration a. Causes include autoimmune, idiopathic, physical (eg, pressure, cold, solar), infections, paraneoplastic, enzymatic defects (hereditary angioedema) D. Physical urticaria 1. Dermographism a. Exaggerated response in which stroking of the skin produces an initial red line followed by broadening erythema and formation of a linear wheal 2. Cold urticaria/angioedema a. Occurs within minutes of exposure to changes in ambient temperature or direct contact with cold objects or air b. Can be associated with headache, hypotension, syncope, wheezing, shortness of breath, palpitations, GI symptoms c. Affects inside of the mouth and tongue in 25% of patients d. Wheal elicited after application of ice is diagnostic (cold contact test) e. Can be lethal if hypotension and syncope occur when entire body is cooled (eg, swimming) f. Can be associated with infectious diseases (syphilis, measles, hepatitis, HIV, and mononucleosis) g. Frequently associated with CU h. Cyproheptadine is drug of choice for cold-induced urticaria 3. Cholinergic urticaria a. Develops after increase in core body temperature of 0.5°C to 1.5°C or 0.9°F to 2.7°F b. During exercise, warm bath, stress, emotions, spicy foods, staying in a heated environment c. Predominately in 20- to 30-year-old patients d. Associated with increased prevalence of atopy e. Pruritic, punctate wheals often surrounded by erythematous halo f. Lesions can become confluent and angioedema may develop g. Typically begins on neck and upper trunk but may spread to entire body h. Can be associated with systemic symptoms but rarely with vascular collapse/ shock i. Lesions usually resolve within 20 minutes, multiple lesions may persist for hours j. Diagnosis i. Intradermal injection of methacholine produces a nonfollicular distribution of characteristic wheals in one-third of patients k. Frequently also have cold-induced urticaria 4. Solar urticaria a. Erythema, wheals, pruritus, and occasionally angioedema occur within minutes after exposure to sun or artificial light sources b. Can be associated with systemic symptoms c. Usually occurs in the third decade of life d. Diagnosis i. Irradiation with ultraviolet (UV) solar stimulator or visible light produces characteristic wheals 5. Aquagenic urticaria a. Contact with water produces wheals 6. Delayed-pressure urticaria

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a. Lesions are typically deep, painful swellings that develop 4 to 8 hours after applied pressure b. Frequently involve buttocks, palms, soles 7. Contact urticaria a. Eruption appears within minutes of exposure b. Most commonly nonimmunologically mediated c. IgE-mediated, may be associated with systemic symptoms d. Most frequent allergen = latex, cross-reactivity frequently seen (banana, avocado, kiwi) e. High-risk groups for reaction to latex: health care workers, workers with occupational exposure to latex, and children with spina bifida and genitourinary abnormalities f. Associated manifestations include AR, conjunctivitis, and respiratory symptoms g. Rarely associated with shock h. Diagnosis with skin prick testing or IgE-specific in vitro assays when indicated E. Treatment 1. General management a. Avoidance of identified triggers b. Treatment of any coexisting infections 2. Pharmacotherapy (see Table 42.4).

Table 42.4

Medications to Treat Urticaria

H1 blocking antihistamines

Nonsedating: Loratadine Cetirizine Desloratadine Levocetirizine Fexofenadine

First-line treatment for acute and chronic urticaria Start with nonsedating antihistamines Treat 4–6 weeks, then may try tapering off

H1 blocking antihistamines

Sedating: Diphenhydramine Hydroxyzine Doxepin Cyproheptadine

Added if symptoms uncontrolled after 1–2 weeks of nonsedating H1 blocker Anticholinergic side effects—dry mouth, urinary retention, cognitive impairment Sedative effect is variable and medication should be taken before bedtime Avoid alcohol, hypnotics, opioids, and mood-elevating drugs Doxepin is a tricyclic antidepressive with H1 and H2 antagonist Cyproheptadine beneficial for cold-induced urticaria

H2 antagonists

Ranitidine Cimetidine

Can be added to H1 blocker to achieve better control

Corticosteroids

Prednisone Dexamethasone

Short course can be helpful in reducing duration of symptoms if severe episode. Refer to specialists if unable to stop because of recurrence of urticaria

Leukotriene receptor antagonist

Montelukast Zafirlukast

Second-line treatment Efficacy not well established (continued)

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Table 42.4

Medications to Treat Urticaria (continued)

Immunomodulatory Cyclosporine agents/antiMethotrexate inflammatory agents Hydroxychloroquine Dapsone Sulfasalazine Cyclophosphamide Omalizumab Tacrolimus Sirolimus Mycophenolate

Significant potential side effects Should be monitored by specialist Sulfasalazine may be beneficial in delayed-pressure urticaria

V. Allergic Rhinitis A. Caused by allergen-induced inflammation of the nasal mucosa B. Affects 10% to 20% of the population C. Signs and symptoms 1. Watery rhinorrhea; sneezing; itching of nose, throat, or eyes; nasal congestion; mouth breathing; snoring; nasal voice; sniffing; postnasal drainage; and occasionally cough 2. Systemic symptoms can include headache, fatigue, decreased concentration, reduced productivity, sleep disturbance 3. Can have negative effect on quality of life and impair athletic performance D. Diagnosis 1. Not necessary to identify exact offending allergen 2. Time of year and circumstances of symptoms can provide clues 3. Nasal smear with more than 4% eosinophilia may be suggestive 4. Specific IgE in vitro assays such as radioallergosorbent testing or skin prick testing can help identify specific allergen E. Treatment 1. Allergy avoidance/limit exposure: avoid peak pollen times (5 a.m.–10 a.m.), keep air conditioning on during pollen seasons 2. Antihistamines a. Oral: second- or third-generation H1 blocking antihistamines (cetirizine, loratadine, fexofenadine) have little sedation and less anticholinergic side effects b. Intranasal: azelastine is a fast-acting spray good for acute allergy management without adverse effects of sedation c. Pseudoephedrine should only be used when nasal congestion is present 3. Intranasal corticosteroids (INSs) a. INS (beclomethasone dipropionate, flunisolide, budesonide) should be used as firstline therapy b. Onset of action as soon as 12 hours and can be taken on an as-needed basis c. Do not compromise eligibility to participate in sports d. Few side effects other than local irritation 4. Oral leukotriene receptor antagonists (LTRAs) a. LTRAs (montelukast, zafirlukast) improve symptoms 5. Intranasal decongestants a. Oxymetazoline (long-acting alpha-1 and 2a-agonist) b. Phenylephrine (alpha-1-agonist)

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c. Very effective for treatment of nasal obstruction d. Risk of rebound vasodilation and rhinitis medicamentosa with prolonged use 6. Oral decongestants a. Pseudoephedrine (alpha- and beta-agonist properties) b. More systemic side effects, longer acting than topical c. May require a therapeutic use exemption for use during competition season

Recommended Reading 1. Beaudouin E, Renaudin JM, Morisset M, Codreanu F, Kanny G, Moneret-Vautrin DA. Food-dependent exercise-induced anaphylaxis: update and current data. Eur Ann Aller Clin Immunol. 2006;38(2):45–51. 2. Bennett J. Anaphylaxis attributed to exercise: considerations for sports medicine specialists. Phys Sportsmed. 2015;43(1):1–12. 3. Dice J. Physical urticaria. Immunol Aller Clin North Am. 2004;24(2):225–246. 4. Feldweg A. Exercise-induced anaphylaxis. Immunol Allergy Clin North Am. 2015;35(2):261–275. 5. Frigas E, Park M. Acute urticaria and angioedema: diagnostic and treatment considerations. Am J Clin Dermatol. 2009;10(4):239–250. 6. Hosey R, Carek P, Goo A. Exercise-induced anaphylaxis and urticaria. Am Fam Physician. 2001;64(8): 1367–1372. 7. Lieberman P, Nicklas R, Oppenheimer J, Kemp S, Lang D. The diagnosis and management of anaphylaxis practice parameter: 2010 update. J Aller Clin Immunol. 2010;126(3):477–480.e1–42. 8. MacKnight J, Mistry D. Allergic disorders in the athlete. Clin Sports Med. 2005;24(3):507–523. 9. Mahr T, Sheth K. Update on allergic rhinitis. Pediatr Rev. 2005;26(8):284–289. 10. Robson-Ansley P, Toit G. Pathophysiology, diagnosis and management of exercise-induced anaphylaxis. Curr Opin Aller Clin Immunol. 2010;10(4):312–317. 11. Schwartz L, Delgado L, Bonini S, et al. Exercise-induced hypersensitivity syndromes in recreational and competitive athletes: a PRACTALL consensus report (what the general practitioner should know about sports and allergy). Allergy. 2008;63(8):953–961.

43 Sports Rheumatology Andrew L. Concoff

I. General A. Arthritis ranks among the most common causes of disability in the United States, and affected persons have a substantially lower health-related quality of life B. Patients typically require ongoing management including: 1. Activity modification 2. Rehabilitation to correct biomechanical deficits 3. Appropriate use of braces and assistive devices 4. Medical therapy to decrease inflammation and slow joint destruction (eg, diseasemodifying antirheumatic drugs [DMARDs] and/or biologic agents) C. Achieving “remission” is the main goal of arthritis treatment: 1. Defined as the absence of disease activity 2. Lifelong medication is typically required to maintain remission a. Achieving a “cure” for arthritis, defined as the absence of disease activity despite discontinuing all medications, is not typically achievable D. Increased risk of premature cardiovascular disease recognized with nearly all forms of arthritis: 1. Aggressive monitoring and treatment of cardiovascular risk factors is vital to comprehensive care 2. Increase in activity and exercise (aerobic and weight resistance) recommended during periods of remission 3. More aggressive exercise may yield symptomatic improvements but risks more rapid progression of permanent structural joint damage

II. Rheumatoid Arthritis (RA) A. Prevalence 1. Affects nearly 1% of adults over 35 years in the United States 2. Nearly twice as common in females 3. Currently, a decline in the incidence of the disease B. Pathogenesis 1. Joint destruction begins with inflammatory cell invasion 2. A vicious cycle of inflammatory cell invasion and irregular synovial tissue overgrowth 3. Synovial inflammation becomes chronic as destructive synovitis called pannus 4. In seropositive individuals, inflammatory burden can also affect other organs and organ systems leading to systemic complications C. Physical findings

478

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1. Patients commonly present with joint swelling, pain, and morning stiffness for more than 30 minutes 2. One should consider workup in patient with even a single joint with unexplained synovitis 3. Joints of the wrist and hand often involved a. Metacarpophalangeal (MCP) b. Proximal interphalangeal (PIP) c. NOT distal interphalangeal (DIP) (30 min) iii. Worse with rest relieved with activity b. Enthesitis (inflammation at attachment site of tendon, ligament, and joint capsule to bone) i. Achilles tendon insertion ii. Plantar fascia calcaneal insertion c. Uveitis (anterior) 3. Diagnosis a. Positive Schober test (less than 5 cm increase with forward flexion) (see Figure 43.1) b. Negative RF c. Elevation of acute-phase reactants (ESR and CRP) d. Imaging i. Bilateral sacroiliitis seen on radiographs and/or MRI—also seen in enteropathic arthritis (A) Colonoscopy to differentiate AS versus enteropathic arthritis (1) Biopsies in enteropathic arthritis reveal Crohn’s disease or ulcerative colitis ii. Vertebral syndesmophytes causing squaring of the vertebral bodies, “bamboo spine” seen on radiograph in late stage of the disease 4. Treatments for AS a. NSAIDs (first line) b. TNF-alpha inhibitors (second-line treatment for most patients) i. Etanercept ii. Infliximab c. Sulfasalazine—treats peripheral joints only, not effective for spinal involvement d. Methotrexate (less effective than in RA) e. Intra-articular steroid injections f. Physical therapy and home exercise programs 5. AS and exercise

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Figure 43.1 Schober test: A mark is made over the spinous process of L5 (at the level of the superior iliac crest). A second mark is made 5 cm below the first mark, and a third mark is made 10 cm above the first mark. The patient is then asked to perform maximal forward flexion. The test is positive if the distance between the second and third marks (15 cm while standing) does not increase by at least 5 cm (20 cm between second and third marks with forward flexion). Photos courtesy of Natalie M. Mason.

a. Flexibility training (focusing on thoracic extension and hip flexor stretching) and extension-biased core strengthening with mild-to-moderate exercise within limits of ROM and disease activity b. Aerobic exercise with full expansion of breathing muscles, which helps maintain chest expansion c. Swimming preferred as it avoids high impact to the spine, though may be difficult to side-breathe secondary to stiffness d. Avoid contact sports due to risk of fracture e. Can participate in carefully chosen aerobic sports when disease inactive E. Reactive arthritis 1. Prevalence and pathogenesis a. 0.1% of U.S. population b. Triggered by an extraarticular infection i. Gastrointestinal (Shigella, Salmonella, Yersinia, Campylobacter) ii. Genitourinary (Chlamydia, Ureaplasma) 2. Presentation a. Classic triad of reactive arthritis i. Conjunctivitis (cannot see) ii. Urethritis (cannot pee) iii. Arthritis (cannot climb a tree) b. Arthritis begins 1 to 4 weeks following infection c. Asymmetric arthritis (more common in lower extremities) d. Back pain 3. Diagnosis a. Primarily a clinical diagnosis b. Elevated ESR and/or CRP that returns to normal with resolution of inflammation c. Bacterial cultures from the throat, stool, or urogenital tract occasionally identify the causative organism 4. Treatment a. NSAIDs b. Sulfasalazine for chronic symptoms c. Intra-articular steroid injections d. Antibiotics are controversial 5. Prognosis a. Frequently self-limited (resolves in 3 months to a year) b. Fifteen to thirty percent develop chronic arthritis

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F. Psoriatic arthritis 1. Presentation a. Occurs in 10% of those with psoriasis b. Skin manifestations typically precede the arthritis in 90% c. Asymmetric arthritis commonly found in distal joints (eg, DIP) d. Uveitis (anterior) e. Severity of arthritis does not necessarily correlate with severity of skin manifestations 2. Diagnosis a. Presence of psoriatic lesions on the skin or nail dystrophy b. Elevated ESR and/or CRP c. Radiographic evidence of erosive arthritis, commonly seen at the DIP joints 3. Treatment a. Joint therapies i. Sulfasalazine: first line, particularly with milder disease ii. TNF antagonists: second line (depending on severity) iii. Intra-articular steroid injections (may be less responsive than RA) iv. Utility of methotrexate has been questioned b. Skin-directed therapies i. Ultraviolet (UV) light therapy ii. Topical corticosteroids iii. Topical retinoids 4. Exercise for reactive arthritis and psoriatic arthritis a. Same protocols as OA i. Maintaining ROM ii. Avoiding impact to joint when synovitis/effusion present iii. Strength training to stabilize joints.

Recommended Reading 1. Aletaha D, Neogi T, Silma AJ, et al. 2010 rheumatoid arthritis classification criteria. Arthritis Rheum. 2010;62(9):2569–2581. 2. Clark BM. Rheumatology: physical and occupational therapy in the management of arthritis. CMAJ. 2000;163(8):999–1005. 3. Clinical Update in Musculoskeletal Medicine. Rheumatology update: new approaches to diagnosis and treatment. J Musculoskeletal Med. 2005;22(12):650, 653–654. 4. Gill JM, Quisel AM, Rocca PV, Walters DT. Diagnosis of systemic lupus erythematous. Am Fam Physician. 2003;68(11):2179–2186. 5. Kataria RK, Brent LH. Spondyloarthropathies. Am Fam Physician. 2004;69(12):2853–2860. 6. Keysor JJ, Currey SS, Callahan LF. Behavioral aspects of arthritis and rheumatic disease self-management. Dis Manage Health Outcomes. 2001;9(2):89–98. 7. Labowitz RJ, Challman J, Palmeri S. Aerobic exercise in the management of rheumatic diseases. Del Med J. 1988;60(11):659–662. 8. Lavallee ME. Connective tissue and rheumatologic conditions in sports. In: O’Grady E, ed. Netter ’s Sports Medicine: The Team Physician’s Handbook. Philadelphia, PA: Saunders; 2010:285–295. 9. Minor MA. Physical activity and management of arthritis. Ann Behav Med. 1990;13:117–124. 10. Rindfleisch JA, Muller D. Diagnosis and management of rheumatoid arthritis. Am Fam Physician. 2005;72(6):1037–1047, 1049–1050. 11. Speed CA. Sports and exercise medicine and rheumatology. Rheumatology (Oxford). 2005;44(2):143–144. 12. United States Bone and Joint Decade. The Burden of Musculoskeletal Diseases in the United States. 2008:71–96.

44 Sports Neurology Jeffrey S. Kutcher and Sean C. Rose

SEIZURE DISORDERS I. Seizure A. Transient occurrence of signs or symptoms due to abnormal excessive or synchronous neuronal activity in the brain B. Usually self-limited, lasting 1 to 2 minutes. Status epilepticus = symptoms lasting more than 5 minutes or multiple seizures without return to baseline neurologic function C. Followed by a “postictal” state of decreased cerebral activity D. Can be induced by pre-existing intrinsic brain pathology or from acute provocation 1. Common provocations include metabolic derangements, substance use, and head trauma 2. Provoked seizures are not necessarily associated with epilepsy E. Classification 1. Focal (formerly called “partial”)—involving a particular region of cortex a. Without impairment of consciousness or awareness (formerly called “simple partial”) i. Motor signs ii. Somatosensory or special sensory signs iii. Autonomic signs iv. Psychic symptoms (ie, déjà vu) b. With impairment of consciousness or awareness (formerly called “complex partial”) i. Typically a transient state of confusion ii. May involve automatic behavior (automatisms) c. Evolving to a bilateral, convulsive seizure (formerly called “secondarily generalized”) 2. Generalized—involving both hemispheres of the brain synchronously a. Absence—lapse in consciousness b. Myoclonic—brief, sudden, bilateral, synchronous muscle jerk(s) c. Tonic—increase in tone, rigidity d. Clonic—rapidly alternating muscular contraction and relaxation e. Tonic–clonic (generalized tonic–clonic [GTC])—period of tonic posturing followed by clonic activity

II. Epilepsy A. Chronic condition of recurrent unprovoked seizures 1. Genetic—epilepsy is the direct result of a known or presumed genetic defect in which seizures are the core symptom of the disorder 2. Structural/metabolic—a separate structural or metabolic condition increases risk of developing epilepsy (eg, stroke, trauma, infection) 486

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3. Unknown cause B. Epidemiology 1. Prevalence in the United States is 5–10/1000 2. Incidence in the United States is approximately 50/100,000 3. Bimodal age of presentation with diagnoses made more commonly in the pediatric and geriatric populations C. Diagnosis 1. If possible, try to determine from the history the presence or absence of signs that support the diagnosis of seizure a. Increased muscle tone during the event b. Witnessed convulsive movements c. Postictal state of confusion, especially if lasting longer than 1 hour d. Oral trauma from tonic jaw contraction e. Enuresis or encopresis 2. Consider possible nonseizure causes of the event a. Syncope i. May be preceded by “presyncopal” symptoms (diaphoresis, dizziness, loss of hearing or vision, pallor) ii. Typically eyes are closed and muscle tone is decreased iii. Loss of consciousness is typically less than 30 seconds iv. Minimal postevent confusion v. Convulsive syncope: syncope followed immediately by tonic or clonic movements (usually 10 days) 6. Gender a. Females have higher rates than males 7. Younger age a. Children and adolescents have longer recovery times than adults. Limited data exist regarding athletes under 10 years of age 8. Personal or family history of attention-deficit disorder, headache disorder, migraines, psychiatric disease, learning disability

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9. Medications a. Psychoactive medications b. Anticoagulants 10. Style of play a. Aggressive, dangerous play b. Poor technique 11. Level of play (adult professional, adult amateur, college, high school, junior, peewee) 12. Sport of choice 13. Apolipoprotein E (ApoE) polymorphisms are associated with increased brain injury risk. ApoE testing has not been integrated into clinical practice to date and does not need to be routinely discussed with concussed athletes K. Return to play (RTP) 1. Same-day RTP a. No same-day RTP for athletes more than 18 years old or collegiate athletes b. Consideration can be given to a professional athlete returning to play if symptoms resolve before the end of that competition c. If covering an event, be up to date on your league’s policy regarding same-day RTP and have a plan for athlete disposition 2. RTP determination a. RTP is a medically supervised, stepwise approach to returning to full competition b. RTP is a medical decision c. All RTP is individualized d. Athletes should be asymptomatic before considering RTP e. Consensus agreement suggests at least a 5-day protocol. An athlete should be asymptomatic for 24 hours before proceeding to the next step (see Table 45.1) i. This outline is not comprehensive; some athletes may take weeks to months before being able to fully return to competition ii. The risk for repeat concussion is limited but increases once the potential for contact resumes iii. Other nonorganic factors should be considered when returning athletes to full contact. These include fear of repeat injury, concern about future disability, and performance anxiety

Table 45.1

Return-to-Play Protocol

Functional Task

Goal

Step One

Rest until asymptomatic

Symptom management and recovery

Step Two

Light aerobic exercise (eg, walking, stationary bike, elliptical trainer)

Increase heart rate

Step Three

Sport-specific exercise (eg, shoot around drills, soccer juggling, baseball long toss)

Adding motion and coordination, increased aerobic challenge

Step Four

Noncontact training drills (eg, running drills, cutting drills, pass patterns)

Coordination, cognitive challenge, increased aerobic challenge

Step Five

Full-contact practice

Assess readiness for play, return to full-speed participation

Step Six

Return to competition

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III: DIAGNOSIS AND TREATMENT OF SPORTS INJURIES AND CONDITIONS

iv. Athletes who have been sidelined for prolonged periods must regain their cardiovascular fitness, strength, and flexibility to prevent other injuries once they return 3. Subdural and epidural hematomas and RTP a. Expert opinion differs but does suggest a 12-month period of rest before return to sport b. The hematoma needs to be completely resolved, with no residual hygroma. In the presence of intraparenchymal injury, the athlete should likely not return to play c. In subarachnoid hemorrhage it is recommended that athletes not return to contact or collision sports d. Intrinsic risk factors must be explored (coagulopathy, arteriovenous malformation, aneurysm, etc) e. Return to contact sports after burr hole or craniotomy is considered on an individual basis. Full bony healing must be achieved, typically taking at least 12 months f. In general, RTP after subdural hematoma (SDH), epidural hematoma (EDH), and/ or craniotomy requires normalization of imaging, full bony healing, and return to neurological and functional baseline including NP testing. Athletes should be cleared by neurosurgery, neuropsychologist, and sports medicine physician 4. Consider retirement from collision or contact sports in the setting of a. Multiple concussions b. Increasing severity and duration of symptoms with successive concussions c. Decreasing impacts leading to concussion d. Fixed NP testing abnormalities

III. Second-Impact Syndrome Catastrophic brain swelling resulting from a second trauma while the patient is still symptomatic from a previous concussion. The second trauma is typically much smaller than the first and results in rapid neurologic deterioration and cerebral herniation; within minutes the athlete is in a comatose state A. Pathophysiology is thought to be due to cerebral dysautoregulation, posttraumatic catecholamine release, and hyperemia and vascular engorgement B. Extraordinarily rare, true incidence and prevalence are not known but at least 17 autopsy-confirmed cases exist in the literature, though a larger number of similar “unconfirmed” cases have been reported C. More commonly seen in adolescents, but has been reported in college-age athletes D. While the mechanism of injury does not include mass effect by intracranial bleeding, several case studies report the presence of small subdural hematomas E. Second-impact syndrome (SIS) has a high mortality and morbidity rate. In the rare event of complete neurologic recovery after SIS, this would be a contraindication to RTP

IV. Long-Term Sequelae of Multiple Concussions A. Cognitive impairment and executive function impairments have been found on NP testing when athletes with a history of multiple concussions are compared to nonconcussed controls B. Headache disorders C. Decreased perceived health-related quality of life measures D. Psychiatric: athletes with multiple concussions may be at increased risk of depression E. Dementia pugilistica: dementia associated with retired professional boxers

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V. Chronic Traumatic Encephalopathy (CTE) A. Currently diagnosed upon autopsy and microscopic evaluation of brain tissue. Impossible to premorbidly differentiate from other dementias prior to autopsy and evaluation for tau protein deposition patterns. Increasing numbers of professional athletes are donating their brain tissue to evaluate for CTE B. True incidence unknown but at least 110 cases have been reported to date C. Pathologic findings: distinguished from other tauopathies by the predominant involvement of the superficial cortical layers, the distribution patterns in the frontal and temporal cortices, and the accumulation of tau-immunoreactive astrocytes as well as: 1. Atrophy of cerebral hemispheres, medial temporal lobe, thalamus, mammillary bodies, and brainstem 2. Ventricular dilatation 3. Widespread deposition of tau-immunoreactive neurofibrillary tangles, astrocytic tangles, and neuritis throughout the brain D. Clinical syndrome associated with subconcussive blows rather than multiple frank concussions 1. Insidious and progressive cognitive decline, confusion, disorientation, and behavioral changes 2. Physically, patients may present with parkinsonian features (shuffling gait, masked facies, and tremor) 3. Psychotic features, homicidality, suicidality, and parasuicidality

VI. Concussion Prevention A. Rule changes to prevent head-to-head contact, dangerous play, and enforcing rules that support fair play and unnecessary violence have proven helpful B. Use of padded goal posts in soccer and field-goal markers in football C. There is no convincing evidence that new helmet technology, custom mandibular orthoses, face shields, or protective headgear prevent concussions D. While heading in soccer is the most common activity associated with concussion, there is no consensus on banning this in youth sport E. Helmets in alpine sports, cycling, equestrian, bull riding, football, and motorsports help prevent moderate and severe traumatic brain injury (TBI) with skull fractures

Recommended Reading 1. Barkhoudarian G, Hovda DA, Giza CC. The molecular pathophysiology of concussive brain injury. Clin Sports Med. 2010;30:34–48. 2. Benson BW, Hamilton GM, Meeuwisse WH, et al. Is protective equipment useful in preventing concussion? A systematic review of the literature. Br J Sports Med. 2009;43(suppl 1):i56. 3. Cantu RC, Gean AD. Second-impact syndrome and a small subdural hematoma: an uncommon catastrophic result of repetitive head injury with a characteristic imaging appearance. J Neurotrauma. 2010;27:1557. 4. Davis G, Marion DW, Le Roux P, et al. Clinics in neurology and neurosurgery—extradural and subdural haematoma. Br J Sports Med. 2010;44:1139. 5. Dick RW. Is there a gender difference in concussion incidence and outcomes? Br J Sports Med. 2009;43 (suppl 1):i46. 6. Difiori JP, Giza CC. New techniques in concussion imaging. Curr Sports Med Rep. 2010;9:35. 7. Guskiewicz KM, Mihalik JP. Biomechanics of sport concussion: quest for the elusive injury threshold. Exerc Sport Sci Rev. 2011;39:4. 8. McCrory P, Meeuwisse W, Johnston K, et al. Consensus statement on concussion in sport: The 3rd International Conference on Concussion in Sport held in Zurich, November 2008. Br J Sports Med. 2009;43(suppl 1):i76–i84.

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9. McKee AC, Cantu RC, Nowinski CJ, et al. Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury. J Neuropathol Exp Neurol. 2009;68:709. 10. Nowak LA, Smith GG, Reyes PF. Dementia in a retired world boxing champion: case report and literature review. Clin Neuropathol. 2009;28:275. 11. Tierney RT, Mansell JL, Higgins M, et al. Apolipoprotein E genotype and concussion in college athletes. Clin J Sport Med. 2010;20:464. 12. Wetjen NM, Pichelmann MA, Atkinson JL. Second impact syndrome: concussion and second injury brain complications. J Am Coll Surg. 2010;211:553.

46 Neurovascular Injuries of the Upper and Lower Limbs Jason Friedrich and Venu Akuthota

I. Principles of Nerve Injury Evaluation and Management A. Peripheral nerve anatomy 1. Includes afferent sensory and efferent motor pathways 2. Sensory pathway = cutaneous receptors → sensory axons → pure sensory or mixed nerves → nerve plexus (eg, brachial plexus, lumbosacral plexus) → cell bodies in the dorsal root ganglion → dorsal roots synapse in the dorsolateral spinal cord 3. Motor pathway = anterior horn cell (spinal cord) → spinal nerves, subsequently dividing into ventral and dorsal rami. Ventral rami → nerve plexus → peripheral motor nerve → neuromuscular junction → muscle fibers 4. Motor unit = an alpha motor neuron, its axon, neuromuscular junction, and all the muscle fibers it innervates 5. Support structures a. Fascicle = bundle of axons running together b. Endoneurium = connective tissue surrounding axons within a fascicle c. Perineurium = connective tissue surrounding each fascicle d. Epineurium = connective tissue binding fascicles into a nerve trunk e. Myelin = axon insulation (from Schwann cells) i. Myelinated fibers conduct rapidly by way of saltatory (“jumping”) conduction; depolarization occurs only at interspersed nodes of Ranvier 6. Nerve fiber types: classical (and modern) classifications a. Ia (A-alpha) = motor, muscles/muscle spindles b. Ib (A-alpha) = motor, Golgi tendon organs c. II (A-beta) = sensory, pressure/touch d. III (A-delta) = sensory, pain/temperature/touch e. IV (C) = pain and other receptors B. Pathophysiology of peripheral nerve injury 1. Seddon classification a. Neurapraxia = partial injury affecting the myelin, but intact axon. Conduction block occurs b. Axonotmesis = interruption of axons and myelin sheath, but intact nerve stroma. Wallerian degeneration occurs c. Neurotmesis = complete disruption of the axon and enveloping nerve sheath. Regeneration without surgical intervention is not possible

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2. Mixed axonal and myelin injury a. Most athletic nerve injuries produce a neurapraxic lesion (injury to myelin) and also often display axonal involvement b. Electrodiagnostic (EDX) testing can help classify nerve injuries as primarily axonal, demyelinating, or mixed type C. Mechanisms of athletic nerve injury (can be acute or chronic) 1. Compression (pressure) a. Causes motor and/or sensory deficits b. Secondary effects of chronic compression can also include nerve edema, hemorrhage, and neural fibrosis 2. Ischemia (hypoxia) a. Rarely the sole cause of athletic nerve injury b. Important secondary cause of nerve injury in situations of sustained compression or compartment syndrome c. Rapidly reversible physiologic block of conduction = rapid restoration of nerve conduction with reperfusion (if less than 6 hours of ischemia) d. Causes pain and paresthesias 3. Traction (stretch, angulation) a. Most nerves can stretch 10% to 20% without significant damage b. Nerves can adapt to slow chronic stretch better than acute tension c. Examples of athletic nerve stretch injuries i. 15% of all grade II and III lateral ankle sprains have damage to the peroneal/ fibular nerve on EDX studies ii. Burner or stinger = acute tension on the superior trunk (C5 and C6) of the brachial plexus, with contralateral deviation of the neck and ipsilateral shoulder depression 4. Laceration a. Rare traumatic event in sports b. Immediate surgical repair of nerve may reduce neuronal loss D. Evaluation of athletic nerve injury 1. History: clearly define symptom perception and time course a. Neuropathic pain = pain originating from nervous system b. Paresthesia = any abnormal sensation on the skin c. Dysesthesia = unpleasant abnormal sensation d. Numbness = lacking sensation 2. Neurologic examination a. Strength = manual muscle testing and functional strength testing b. Reflexes = abnormalities rarely seen in athletic peripheral nerve injuries, except in cases of radiculopathy and significant motor nerve injury c. Sensation = fine touch/vibration/proprioception (dorsal column/medial lemniscus pathway) and pain/temperature (anterolateral pathway) d. Provocative maneuvers i. Neural tension tests (numerous variations exist) (A) Upper-limb tension testing (ULTT) (see Figure 46.1) (B) Straight-leg raise (C) Sit-slump test (D) Femoral stretch test ii. Direct nerve compression or percussion 3. EDX testing a. Evaluates the physiology and function of a nerve, which can complement structural abnormalities found on imaging b. Localizes and characterizes nerve injury

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Figure 46.1 Upper-limb tension test, with median nerve bias. Positioning includes shoulder abduction with scapular depression; increasing elbow extension, forearm supination, wrist and finger extension; and cervical spine contralateral flexion.

c. Can differentiate neurapraxia from axonotmesis (important for prognosis) d. Consists of nerve conduction studies (NCS) and needle electromyography (nEMG) e. NCS = evaluate motor and sensory nerves and provide data about the integrity of the myelin and the number of functioning axons f. EMG = evaluates the motor unit (lower motor neuron pathway), but not the sensory pathway, and assesses for muscle denervation from axonal injury 4. Imaging a. Magnetic resonance neurography (MRN) = specific MRI sequences for optimal visualization of peripheral nerves i. T1 sequences can delineate anatomic context of nerve, its fascicular nature, and epineural fat plane ii. On T2 sequences, normal nerves appear uniform in size, intermediate in signal, and often slightly hyperintense compared to adjacent muscle iii. Enlargement and/or hyperintense T2 signal in a nerve are abnormal findings (see Figure 46.2) iv. Allows visualization of space-occupying lesions compressing the nerve v. Can complement EDX findings for localization of nerve injury vi. MR signal patterns in muscle can identify acute and chronic denervation (A) Acute denervation = increased T2 short tau inversion recovery (STIR) signal (B) Chronic denervation = decreased volume/fatty infiltration on T1 b. Musculoskeletal ultrasound (MSK US) i. Focal peripheral nerve entrapments can often be visualized by ultrasound ii. In longitudinal view, normal peripheral nerves have a fascicular appearance with hypoechoic fascicles surrounded by hyperechoic connective tissue iii. In transverse view, normal nerves display a honeycomb or speckled appearance (see Figure 46.3) iv. Nerve injury is characterized by increased nerve caliber, loss of fascicular pattern, and decreased echogenicity v. Hypoechoic swelling of a nerve can be seen just proximal to the site of nerve compression vi. Transducer pressure on the nerve can elicit symptoms c. Diffusion Tensor Tractography (DTT)

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(a)

(b)

Figure 46.2 MR neurogram of left ulnar nerve demonstrating well-circumscribed T2 hyperintense lesion intimately associated with the ulnar nerve, consistent with a schwannoma (arrows). (a) Axial view. (b) Coronal view. Courtesy of Dr Colin Strickland, University of Colorado. i. EDX studies, MRN, and MSK US are all unable to differentiate different types of axonotmesis, especially when some portion of the nerve remains in continuity ii. DTT is an emerging MRI technology allowing small bundles of nerve fibers to be tracked and regeneration visualized, which may become important for more rapid prognosis and prediction of surgical need in severe nerve injuries E. Management of athletic nerve injury 1. Nerve recovery a. Capacity for regeneration persists for at least 1 year (but survival of neuron not ensured after severe injury) b. Order of recovery in mixed lesions

Figure 46.3 Axial (or transverse) ultrasound image of volar wrist, including median nerve (arrow). Courtesy of Dr John Hill, University of Colorado.

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i. Resolution of conduction block ii. Distal axon sprouting of spared axons iii. Muscle fiber hypertrophy iv. Redistribution of sensory function v. Axonal regeneration of injured axons c. Timeline for nerve recovery i. Ischemia-producing conduction block: reversal is rapid, often minutes to hours ii. Compression-induced conduction block (neurapraxia): recovery over several months iii. Axonal injury (axonotmesis): axon regrowth 1 mm/day, 1 cm/week, 1 inch/ month (A) Denervated muscle fibers are viable for only 18 to 24 months after injury (B) Excessive scar tissue, neuroma, or injury to neural tubes reduces the potential for functional regeneration d. General monitoring guidelines for closed nerve trauma i. Reasonable to observe for 4 to 6 weeks. If no or partial recovery, then EDX testing +/- MRI or MSK US depending on location. If nerve in continuity, then recheck clinical progress and EDX testing at 12 weeks. If recovery evident, then continue rehabilitation. If no recovery and no reinnervation seen, then surgical exploration at 3 to 6 months. 2. Nonoperative treatment a. Rehabilitation i. Activity modification = a period of relative rest (including temporary avoidance of the aggravating activity) and an emphasis on cross-training ii. Bracing may be necessary for protection of joints, tendons, and ligaments iii. Pads may be useful over hypersensitive regions iv. Kinetic chain rehabilitation (A) Formulate biomechanical diagnosis that led to the nerve injury (B) Evaluate entire kinetic chain for proximal deficits that predispose to more distal injury (C) Correct biomechanical faults within the kinetic chain, optimizing flexibility, endurance, strength, and power (D) Strengthening through closed kinetic chain training is emphasized to restore coordination, proprioception, and functional sequential muscle activation patterns (E) Careful adaptive strengthening of compensatory muscles may help maintain function while a nerve recovers v. Neuromobilization = nerve glides (often akin to flossing) and nerve mobilization (avoiding end range) may help with nerve healing, nerve pain, and reduction of nerve scarring b. Nonpharmacologic pain relief = considerations include ice, heat, transcutaneous electrical nerve stimulation (TENS), acupuncture c. Medications i. Minimal efficacy data for medication use for athletic peripheral nerve injuries ii. Initial considerations for symptom control include topical lidocaine gel or patches, nonsteroidal anti-inflammatory gel/patches/oral agents, acetaminophen, low dose tricyclics, or anticonvulsants d. Injections = rarely indicated for peripheral nerve injury i. Exception = corticosteroid injection for carpal tunnel syndrome 3. Surgery a. Open or endoscopic surgical release and/or decompression may be indicated for severe or refractory peripheral nerve entrapments

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b. Traumatic nerve lacerations may be treated by direct repair or grafting c. Salvage procedures, including muscle transfers, may be necessary for restoration of basic function in setting of severe chronic nerve injury and weakness 4. Emerging treatments: biologics a. Use of growth factors, platelet-rich plasma, and stem cells for the promotion of nerve recovery or to maintain growth-permissive environment remains under investigation 5. Return to play a. The best determination for return to play remains the athlete’s functional performance in simulated sports activities b. EDX or imaging studies may lag behind clinical recovery

II. Peripheral Nerve Entrapments and Injuries Upper-Limb Nerve Injuries A. Neurogenic thoracic outlet syndrome (N-TOS) 1. Neurovascular entrapment syndrome of the upper limb, separated into N-TOS and vascular thoracic outlet syndrome (V-TOS) depending on which components of the neurovascular bundle are thought to be entrapped (see also the following section on V-TOS) 2. N-TOS is a controversial diagnosis 3. Definitive (true) N-TOS = objective neurological deficit (most often lower trunk, C8–T1 roots) a. Very rare (~1/1 million cases of N-TOS) b. Often requires surgery 4. Disputed N-TOS = no objective neurological deficit (pain predominates) a. More common and more controversial b. Generally managed conservatively 5. Three potential sites of compression of neurologic structures a. Scalene triangle (most common) b. Costoclavicular space c. Retropectoralis minor space 6. Common etiology = anatomic variant + cumulative trauma (ie, repetitive overhead motion) a. Anatomic variants i. Cervical rib (6-month history of disordered eating, oligomenorrhea, or amenorrhea • EKG—prolonged QT interval may be seen in severe eating disorders • Pelvic ultrasound—evaluate for polycystic ovarian syndrome • CT of adrenal glands (rule out adrenal adenoma, adrenal hyperplasia) • MRI brain—evaluate for pituitary source

DEXA, dual-energy x-ray absorptiometry.

2. Screen for the Triad—during preparticipation physical examination, annual physical examination by primary care physician, clinic appointment for other sports-related injuries 3. Promote healthy eating and exercise habits

III. Exercise During Pregnancy A. Moderate aerobic and strength training poses no increased risk on the mother or fetus in uncomplicated pregnancies 1. The American Congress of Obstetricians and Gynecologists (ACOG) recommends moderate exercise for 30 minutes on most, if not all, days of the week B. Benefits of exercise 1. Decreases risk of preeclampsia 2. May prevent gestational diabetes

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3. Women have more favorable subjective outcomes C. Women who exercise before and during pregnancy have decreased risk of pregnancyrelated low back and pelvic pain D. Contraindications to aerobic exercise and when to stop activity—Tables 50.3–50.5

Table 50.3

The American Congress of Obstetricians and Gynecologists (ACOG) Committee Opinion No. 267

Absolute Contraindications to Aerobic Exercise During Pregnancy Hemodynamically significant heart disease Restrictive lung disease Incompetent cervix/cerclage Multiple gestation at risk for premature labor Persistent second- or third-trimester bleeding Premature labor during the current pregnancy Ruptured membranes Placenta previa after 26 weeks of gestation Preeclampsia/pregnancy-induced hypertension Source: From Exercise During Pregnancy and the Postpartum Period. Used with permission. © American College of Obstetricians and Gynecologists, 2002, Committee Opinion No. 267.

Table 50.4

The American Congress of Obstetricians and Gynecologists (ACOG) Committee Opinion No. 267

Relative Contraindications to Aerobic Exercise During Pregnancy Severe anemia Unevaluated maternal cardiac arrhythmia Chronic bronchitis Poorly controlled type 1 diabetes Extreme morbid obesity Extreme underweight (BMI < 12) History of extremely sedentary lifestyle Intrauterine growth restriction in current pregnancy Poorly controlled hypertension Orthopedic limitations Poorly controlled seizure disorder Poorly controlled hyperthyroidism Heavy smoker BMI, body mass index. Source: From Exercise During Pregnancy and the Postpartum Period. Used with permission. © American College of Obstetricians and Gynecologists, 2002, Committee Opinion No. 267.

50. THE FEMALE ATHLETE

Table 50.5

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The American Congress of Obstetricians and Gynecologists (ACOG) Committee Opinion No. 267

Warning Signs to Terminate Exercise While Pregnant Vaginal bleeding Dyspnea prior to exertion Dizziness Headache Chest pain Muscle weakness Calf pain or swelling (rule out thrombophlebitis) Preterm labor Decreased fetal movement Amniotic fluid leakage Source: From Exercise During Pregnancy and the Postpartum Period. Used with permission. © American College of Obstetricians and Gynecologists, 2002, Committee Opinion No. 267.

E. Avoid elevated temperature in the first trimester—persistent elevated temperature in the first trimester (time of neural tube closure and organogenesis) has been linked to birth defects 1. Wear loose-fitting, well-ventilated clothing 2. Moderate intensity—use “talk test”: if unable to maintain a conversation, intensity may be too high. F. Sports to avoid 1. Scuba diving—fetus at increased risk for decompression sickness 2. Sports with high risk of falling or abdominal trauma

Recommended Reading 1. Benjaminse A, Gokeler A, Fleisig G, Sell T, Otten B. What is the true evidence for the gender-related differences during plant and cut maneuvers? A systematic review. Knee Surg Sport Tr A. 2011;19(1):42–54. 2. DeSouza MJ, Nattiv A, Joy E, et al. 2014 Female athlete triad coalition consensus statement on treatment and return to play of the female athlete triad. Br J Sports Med. 2014;48:289–309. 3. Dugan SA. Sports-related knee injuries in female athletes: what gives? Am J Phys Med Rehabil. 2005;84:122–130. 4. Hewett TE, Zazulak BT, Myer GD, Ford KR. A review of electromyographic activation levels, timing differences, and increased anterior cruciate ligament injury incidence in female athletes. Br J Sports Med. 2005;39:347–350. 5. Hoch AZ, Pajewske NM, Moraske L, et al. Prevalence of the female athlete triad in high school athletes and sedentary students. Clin J Sport Med. 2009;19(5):421–428. 6. Lynch SL, Hoch AZ. The female runner: gender specifics. Clin Sport Med. 2010;29(3):477–498. 7. Micheo W, Hernandez L, Seda C. Evaluation, management, rehabilitation, and prevention of anterior cruciate ligament injury: current concepts. PMR. 2010;2(10):935–944. 8. Nattiv A, Loucks AB, Manore MM, Sanborn CF, Sundgot-Borgen J, Warren MP. American college of sports medicine position stand. The female athlete triad. Med Sci Sports Exerc. 2007;39(10):1867–1882.

51 The Adaptive Athlete Lauren Rudolph and Stuart E. Willick

I. Overview of Musculoskeletal Injuries in Adaptive Sports A. Background 1. There is a relative lack of published literature on injuries occurring in athletes with impairments as compared to able-bodied athletes 2. Much of the epidemiology has involved retrospective surveys using athlete self-report data 3. However, more recent reports are more comprehensive and capture exposure data with injury surveillance studies 4. Overall injury rates are similar for athletes with and without physical impairment but show sport-specific variation 5. Injury patterns with regard to type and location of injury differ by sport and impairment 6. Understanding the complex classification system of Paralympic sports is helpful when reviewing the available literature a. For example, the 2010 Vancouver Winter Games consisted of 5 sporting categories (alpine skiing, biathlon, cross-country skiing, ice hockey, wheelchair curling) subdivided into 64 medal events based on sport (eg, alpine skiing includes downhill, slalom, super-G), impairment type (eg, downhill is divided into sitting, standing, and visually impaired groups), and sport class (based on specific details related to the athlete’s impairment) as well as sex (male, female) 7. Injuries carry greater functional consequences for the athlete with an impairment B. Brief literature review 1. Wheelchair athletes versus ambulatory athletes: wheelchair athletes primarily experience upper-limb injury while ambulatory athletes (amputee, visually impaired, and cerebral palsy) more often experience lower-limb injury 2. Amputees: athletes with upper-limb deficiencies tend to have more cervical and thoracic spine injuries compared with athletes with lower-limb deficiencies who have more lumbar spine injuries 3. Acute versus chronic injury rates are about the same 4. Atlanta Summer Paralympic Games 1996 a. Athletes with lower-limb deficiencies or with visual impairments sustained more ankle injuries than athletes with other impairments b. Incidence of shoulder pain in wheelchair users was estimated as 30% to 70% 5. Salt Lake City Winter Paralympic Games 2002 a. Nine percent of all athletes sustained an injury; most common diagnoses: sprains (32%), fractures (21%), and strains and lacerations (14% each) b. Of all injuries, 77% were due to an acute traumatic etiology

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6. 7.

8.

9.

547

c. Injury rates were highest in sledge hockey (14%) and alpine skiing (12%), and lowest in Nordic skiing (2%) Torino Winter Paralympic Games 2006 a. Injuries were reported in 8% of all athletes Vancouver Winter Paralympic Games 2010 a. Injuries were reported in at least 11% of all athletes b. Sports with high risk of injury included ice sledge hockey and alpine skiing; sports with low risk of injury included Nordic skiing and wheelchair curling London Summer Paralympic Games 2012 a. Overall injury incidence rate was 12.7 injuries per 1,000 athlete days b. Male versus female injury rates were similar c. Older athletes had higher injury rates compared to younger athletes Prevalence of osteoarthritis (OA) in amputees a. Lower-limb amputees have increased prevalence of OA in the contralateral knee, compared with able-bodied persons b. It is not known if sports participation increases this risk

C. Injury prevention 1. For wheelchair athletes, prescribe a training program directed at strengthening the available trunk muscles, rotator cuff, and scapular stabilizer muscles 2. Provide wheelchair accessible weight machines or modify free weight program 3. Encourage a stretching program individualized to the athlete, considering the sport and the physical impairment 4. Include proprioception and balance exercises 5. Do not overtrain with one type of exercise; use cross-training programs 6. Considerations should also include proper equipment, nutrition, and technique

MEDICAL ISSUES UNIQUE TO THE ADAPTIVE ATHLETE I. Autonomic Dysreflexia (AD) A. Definition/pathophysiology 1. Occurs in spinal cord injury (SCI), typically at or above the level of T6 2. In the absence of cortical regulation, any noxious stimuli below the level of the spinal lesion can result in abnormal sympathetic discharge a. Sympathetic surge may cause life-threatening hypertension b. Brain detects hypertensive crisis via intact baroreceptors in the neck c. A compensatory vagal/parasympathetic response decreases heart rate, cardiac output, and blood pressure (BP) d. Vasodilation results from intact parasympathetic nerves above the level of injury causing intracranial vasodilation, which evokes headache e. Lowered cardiac output is not sufficient to offset the sympathetic surge below the injury level and hypertension persists B. Signs and symptoms include: headache, hypertension, bradycardia, blurred vision, nasal congestion, anxiety, piloerection, flushing, and diaphoresis above the level of injury C. Treatment 1. Remove the inciting noxious stimulus. Etiologies may include: distended bladder, distended or impacted bowel, urinary tract infection, tight clothing, hemorrhoids, gallstones, skin breakdown (including ulcers, blisters, sunburn), acute trauma, deep venous thrombosis 2. Sit the athlete up to cause an orthostatic drop in BP

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3. Treat hypertension a. Nitropaste to skin is fast-acting and can be wiped off when symptoms resolve or hypotension ensues b. Oral/intravenous (IV) antihypertensives with rapid onset, short duration may be used D. Boosting 1. Prohibited form of intentional induction of AD to improve sports performance 2. Athletes use techniques to produce “controlled” sympathetic surge via purposeful, self-induced AD with noxious stimulus, including: a. Clamping urinary catheter b. Tightening leg straps c. Sticking themselves with sharp objects in an insensate location 3. Boosting presents a serious health risk to the athlete 4. Boosting is cheating and is prohibited in sports competition 5. Athletes are subject to disqualification and long-term sanctions

II. Orthostatic Hypotension A. Definition/pathophysiology 1. Athletes with SCI may have sympathetic/parasympathetic neuroregulatory impairment resulting in venous pooling in dependent areas 2. Evoked by position changes, sitting up suddenly, or during intensive sport competition B. Signs and symptoms, including lightheadedness, dizziness, nausea, tachycardia, and syncope, can occur if not corrected C. Treatment 1. Maintain appropriate hydration, nutrition, and salt balance/supplementation 2. Lower-limb compression stockings decrease peripheral vascular pooling 3. Abdominal binders promote venous return 4. Place athlete supine or in Trendelenburg position for severe episodes 5. IV fluids and sympathomimetic agents may be used for BP support only in emergency instances as these interventions are included on the prohibited list of the World AntiDoping Agency (WADA)

III. Thermoregulation A. Pathophysiology in SCI 1. Impaired vasomotor control secondary to impaired autonomic function 2. Lack of muscle mass below the level of the SCI lesion 3. Decreased input to hypothalamic thermoregulatory centers 4. Impaired sweating mechanism below the level of the lesion results in less surface area available for cooling via evaporation 5. Unable to generate sufficient body heat or “shiver” response below the level of the lesion 6. Diminished or absent sensation impairs awareness of cold or damp limbs B. Prevention and treatment 1. Educate swimmers and cold weather athletes on hypothermia and frostbite 2. Educate endurance and warm weather athletes on hyperthermia 3. Avoid dehydration with appropriate fluid repletion 4. In hot conditions, athletes should wear lightweight, breathable clothing; cooling systems may also be necessary 5. In cold conditions, athletes should wear layered, breathable clothing 6. In cold conditions, athletes with impaired sensation can consult their sensate teammates regarding the presence of cold or numb limbs

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IV. Skin Breakdown A. Pathophysiology 1. Pressure to insensate, paralyzed locations causes local tissue ischemia 2. Every pressure sore seen on the skin should be regarded as serious because of the probable damage below the skin surface, hidden from the examiner B. At-risk populations 1. Athletes with SCI can get pressure ulcers if they have poor compliance with pressure relief techniques and with prolonged sitting for travel or in race chairs 2. Athletes with severe spasticity are prone to skin breakdown in locations where high muscle tone or contractures cause persistent skin friction 3. Amputees are prone to skin issues at the stump site or areas of increased pressure between skin and prosthesis including: ulcers, abrasions, verrucous hyperplasia (choke syndrome), blisters, contact dermatitis, hyperhidrosis, folliculitis, fungal infections C. Diagnosis of pressure ulcers 1. Press on the red, pink, or darkened area with your finger; skin should blanch 2. Remove pressure and the area should return to red, pink, or darkened color within a few seconds, indicating good blood flow 3. If the area stays white, then blood flow is impaired and damage has begun 4. Darkly pigmented skin may not display visible blanching even when healthy D. Staging of pressure ulcers 1. Stage I: skin is intact but appears red, discolored, hardened, and nonblanchable; high risk for further breakdown 2. Stage II: epidermis is broken, exposed, creating a shallow open bed 3. Stage III: open wound extends beyond dermis to the adipose tissue layer; signs of necrosis and infection may be present 4. Stage IV: wound extends to muscle and bone with probability of infection E. Prevention and treatment 1. Proper wheelchair positioning and cushion support 2. Correct fit of adaptive equipment and prosthetics 3. Compliance with pressure reliefs 4. Reduce skin moisture by wearing absorbent fabric; hyperhidrosis can be controlled with antiperspirants 5. The athlete must: a. Stay off the area and remove all pressure b. Keep the area clean and dry c. Eat adequate calories high in protein, vitamins (especially A and C), and minerals (especially iron and zinc) d. Maintain adequate hydration e. Find and remove inciting factors f. Inspect the area at least twice a day

V. Peripheral Nerve Injuries A. Traumatic neuroma 1. Definition/pathophysiology a. Hyperplasia of nerve fibers and their supporting tissues at the distal end of a transected nerve b. Athletes with amputations are at risk of developing neuromas at their stump site c. Pressure on the neuroma can cause pain and paresthesias 2. Diagnosis is usually clinical, supplemented by ultrasonography or MRI 3. Treatment

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a. b. c. d. e. f. g.

Socket modifications to relieve pressure on the neuroma Topical capsaicin cream or lidocaine patch Acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs) Corticosteroid injection Neuropathic agents such as gabapentin or pregabalin Percutaneous ablation with alcohol injection or radiofrequency energy Surgical resection is considered last as neuroma may reoccur

B. Peripheral nerve entrapment syndromes 1. Athletes who use wheelchairs or crutches are at increased risk for development of upperlimb peripheral neuropathies including: a. Median neuropathy at the wrist b. Ulnar neuropathy at the wrist within Guyon’s canal c. Ulnar neuropathy at the elbow within the cubital tunnel d. Brachial plexopathies and other proximal nerve injuries at the shoulder 2. Athletes with below-knee amputations are at risk for fibular neuropathy at the fibular head due to improper prosthetic fit 3. Proper padding and equipment fit is key to prevention 4. Treatment a. Resting wrist splint to keep wrist in neutral position for ulnar or median neuropathy at the wrist b. NSAIDs c. Corticosteroid injections d. Surgical intervention for athletes who fail conservative management.

VI. Osteoporosis A. Athletes with SCI at extremely high risk; also seen in athletes with polio and neuromuscular diseases B. Pathophysiology 1. Non-weight-bearing causes disuse demineralization 2. Imbalanced osteoblastic and osteoclastic activity occurs 3. Low bone density occurs predominantly in pelvis and lower limbs, which are chronically non-weight-bearing and denervated 4. Increased fracture risk with even relatively minor trauma 5. Parathyroid dysfunction can be seen in chronic SCI C. Diagnostic imaging to evaluate bone mineral density 1. Dual-energy x-ray absorptiometry a. Most commonly used method because of its high precision b. Report includes measurements of the spine and hip c. T-score is the standard deviation of the athlete’s bone density compared with an individual at peak bone mass d. Osteoporosis is defined as a T-score of −2.5 or less D. Prevention with calcium, vitamin D, and/or bisphosphonates for SCI athletes E. Treatment 1. Early weight-bearing with assisted standing if possible 2. Mechanical-loading exercises to the lower extremities 3. Calcium, vitamin D, and bisphosphonates F. Fracture management 1. Athletes with sensory loss may not report pain after a fracture 2. Maintain high index of suspicion in setting of osteopenia or osteoporosis even with minimal trauma or normal x-rays

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3. Nondisplaced fractures can be missed on x-rays in setting of low bone density 4. MRI or CT imaging may be warranted to fully assess possible bone injury

Recommended Reading 1. Bernardi M, Castellano V, Ferrara MS, Sbriccoli P, Sera F, Marchetti M. Muscle pain in athletes with locomotor disability. Med Sci Sports Exercise. 2003;35(2):199–206. 2. Dec KL, Sparrow KJ, McKeag DB. The physically-challenged athlete: medical issues and assessment. Sports Med. 2000;29(4):245–258. 3. Ferrara MS, Peterson CL. Injuries to athletes with disabilities: identifying injury patterns. Sports Med. 2000;30(2):137–143. 4. Klenck C, Gebke K. Practical management: common medical problems in disabled athletes. Clinl J Sport Med. 2007;17(1):55–60. 5. WADA: The most current list of restricted medications. www.globaldro.com. 6. Webborn N, Willick S, Reeser JC. Injuries among disabled athletes during the 2002 Winter Paralympic Games. Med Sci Sports Exerc. 2006;38:811–815. 7. Willick S, Webborn N. Sport medicine. In: Vanlandewijck YC, Thompson WR, eds. The Paralympic Athlete. 1st ed. West Sussex, UK: Blackwell Publishing Ltd; 2011:76–90. 8. Willick SE, Webborn N, Emery C, et al. The epidemiology of injuries at the London 2012 Paralympic Games. Br J Sports Med. 2013;47:426–432.

HOT TOPICS IN SPORTS MEDICINE

52 Regenerative Medicine in Sports Medicine Gerard Malanga and Reina Nakamura

INTRODUCTION I. Conventional Management of Soft-Tissue Sports Injuries A. PRICE principle (protection, rest, ice, compression, elevation) 1. Initial therapy. 2. Postulated to minimize bleeding, ease pain, and swelling. 3. Clinical use is based on strong evidence from experimental studies. There are currently no randomized-controlled clinical trials. B. Nonsteroidal anti-inflammatory drugs (NSAIDs/Analgesics) 1. Frequently prescribed for acute, postacute, and chronic injuries from repetitive trauma. 2. Primarily treats pain and inflammation. 3. Cyclooxygenase enzyme (COX-1/COX-2) antagonist. a. COX-1 is present in multiple tissues as part of normal function. b. COX-2 is specific to injury and inflammation. NSAIDS are prescribed to treat sports injuries due to their ability to block COX-2. c. Decrease eicosanoids. d. Gastrointestinal, cardiovascular, renal, and metabolic side effects. e. A short course of NSAIDS has a limited capacity in treating soft-tissue sports injuries, without being harmful. C. Injectable corticosteroids 1. Commonly used anti-inflammatory. 2. Inhibits cyclooxygenase isoforms and lipoxygenase; that is, enzymes that mediate inflammation and chemotaxis. 3. Cutaneous, vascular, and endocrine side effects.

II. Evidence Challenges Routine Use Evidence challenges routine use of anti-inflammatory medications and corticosteroids, especially for treatment of tendinopathy. A. Corticosteroids 1. Meta-analysis on the response of tendons to corticosteroid therapy. a. Lateral epicondylalgia—short-term pain relief with corticosteroids (up to 3 months), but worse function and pain in intermediate (13+ weeks) and long term (>1 year). b. Rotator cuff—uncertain results short term, no difference with placebo intermediate and long term. c. Patellar tendon—less pain short term. d. Achilles tendon—no change in pain short term.

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2. Randomized placebo-controlled trial, lateral epicondylalgia. a. Those treated with corticosteroids had better outcome at 4 weeks, albeit worse compared to placebo long term (26 weeks, 1 year).

III. Tendinopathy A. Tendinosis/tendinopathy better characterizes the pathological process than tendonitis. 1. Histology—absence of inflammatory cells, haphazard/poor cellular organization, neovascularization. 2. An overuse injury resulting from degeneration rather than inflammation. 3. Pain mediators—lactic acid, glutamate, substance P among others. B. Stages of healing (tendons, muscle, ligament) 1. Inflammatory phase—(days after injury) inflammation and chemotaxis, clean up necrotic tissue, synthesize type III collagen. 2. Proliferative phase—(weeks) lay down more type III collagen, produce proteoglycans. 3. Remodeling—(6 weeks to 1 year) lay down type I collagen, generation of scar.

IV. Successful Return to Sport Program A. Control initial postinjury symptoms with PRICE and NSAIDs as needed (first 7–10 days). B. Start rehabilitation with a focus on restoring normal and symmetric range of motion, muscle strength, and proprioception in conjunction with an individualized return-to-play protocol. C. The utility of NSAIDs and corticosteroids in most postacute injuries is uncertain. 1. May restrict response to healing by hindering physiology. 2. The long-term risks of injectable corticosteroids may outweigh short-term benefit.

REGENERATIVE TREATMENTS I. Prolotherapy (Regenerative Injection Therapy [RIT]) A. Use of an irritant to achieve healing. B. Irritating or chemotactic agent elicits the inflammatory cascade resulting in fibroblast proliferation and collagen formation. 1. Irritants—hyperosmolar dextrose, zinc sulfate, glycerin, phenol, guaiacol, pumic acid. 2. Chemotactic agent—sodium morrhuate. C. Protocol is not yet standardized. D. Preclinical trials 1. Possible utility for tendinopathy. 2. Increase in tendon strength and cross-sectional area. 3. Indeterminate evidence for ligamentous injury. E. Human trials 1. Literature possibly supporting use in groin pain, Achilles tendinopathy, plantar fasciitis, and lateral epicondylalgia. 2. Lateral epicondylalgia—better pain and isometric contraction strength compared to saline injection 16 weeks later. 3. Achilles tendinopathy—study comparing eccentric loading exercises, prolotherapy, or combined treatment showed overall better pain scores compared to baseline in prolotherapy at 6 weeks and combined treatment group at 12 weeks. No overall difference between groups found at 12 months. 4. Evidence is lacking in high quality trials regarding use of prolotherapy to treat sports injuries.

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II. Autologous Blood Injection A. Injecting autologous venous blood into the injured tissue to provoke a healing response. B. Humoral and cellular intermediaries in blood initiate the inflammatory cascade and subsequent healing. 1. Use is described in lateral epicondylalgia, plantar fasciitis, and patellar tendinopathy. 2. Evidence is lacking in high quality trials regarding use of ABI to treat sports injuries.

III. Platelet-Rich Plasma (PRP) A. Generally describes plasma consisting of platelet density above baseline. Minimum concentration to obtain healing is felt to be 1 million cells/microliter/5 mL plasma. B. Platelets release growth factors and cytokines from alpha, dense, and lysosomal granules, in addition to mitochondria, which regulate physiologic healing and repair. C. Alpha granules contain multiple key growth factors including insulin-like growth factor (IGF-I/III), transforming growth factor beta (TGFβ), platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF), and basic fibroblast growth factor (bFGF). 1. IGF-I stimulates fibroblast chemotaxis and proliferation, mostly during inflammatory and proliferative phases of healing. 2. TGFβ has multiple functions including mesenchymal stem cell (MSC) stimulation and specialization, collagen synthesis, neovascularization, chemotaxis of endothelial cells, and regulation of mitosis. TGFβ also plays a role in fibrosis of skeletal muscle, ultimately leading to scar formation. 3. PDGF stimulates other growth factors, and modifies tissue during the process of healing. 4. VEGF primarily mediates angiogenesis. 5. bFGF regulates neovascularization, multiplication/chemotaxis of inflammatory cells resulting in formation of type III collagen. D. PRP and muscle 1. Clinical application for muscle strain is uncertain at this time, since the literature is primarily based on case reports and preclinical studies. Note the presence of TGFβ in PRP may impede muscle healing due to profibrotic effects. E. PRP and tendons 1. Variable clinical utility. Some tendons seem to respond better than others. a. Rotator cuff tendon i. The utility of direct application of PRP following arthroscopic rotator cuff repair to augment healing is uncertain. Research concerning direct treatment with PRP is inconclusive, although with some promising results. b. Patellar tendon i. Improved pain, function, and personal opinion of health were shown in a case series. More rigorous studies are needed to draw conclusions. c. Achilles tendon i. There may be a role in augmenting surgical repair of tendon rupture; however, a randomized placebo-controlled trial showed no concrete evidence on the benefits of PRP over placebo. d. Lateral epicondylalgia i. Level I evidence in favor of using PRP.

IV. Tenotomy A. An option for patients with refractory tendinopathy who are not responsive to conventional and conservative management. B. Percutaneous needle tenotomy is used in isolation and with the regenerative injections discussed earlier. Needling, and thus creating bleeding in, tendinopathic tissue is thought to stimulate the cascade of events inducing a healing response in refractory tendinopathy.

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1. Evidence is lacking in high quality trials regarding the use of needle tenotomy with and without ABI and PRP to treat sports injuries. 2. In some positive studies it is difficult to determine what ultimately contributed to the positive healing response: tenotomy alone, the regenerative injectate (ABI, PRP), or the combination. C. Ultrasound guided percutaneous fasciotomy and surgical tenotomy using the TX1 system (Tenex Health, Lake Forest, California) has been found to be safe and effective in treating chronic, refractory lateral and medial epicondylosis in several case series. 1. Ultrasound used to target precise areas of tendon degeneration. 2. An oscillating 18-gauge hollow needle is used to emulsify and remove tendinopathic tissue. The surrounding cannula provides continuous inflow of fluid, allowing debris to be removed through the hollow needle tip. 3. Lateral epicondylopathy: significantly improved pain and function starting at 6 weeks postprocedure, which was sustained for up to 1 year. Most benefit seen in the first 3 months after treatment. 4. An alternative to open surgical techniques, without exposure to risks of surgery.

V. Mesenchymal Stem Cell Therapy A. Multipotent, nonhematopoietic adult stem cells that are present in blood, bone marrow, adipose, and synovium. MSCs become specialized cells of mesenchymal lineage, which comprise bone, bone marrow stroma, cartilage, adipose, tendons, skeletal muscle, and other types of soft tissue. 1. MSC are not embryonic or induced pluripotent stem cells and are likely a better source for the treatment of orthopedic injury given they differentiate into bone, cartilage, tendon, and muscle 2. Normal function: a. Direct differentiation—replacement units for expired cells. b. Trophic effects—secrete a broad spectrum of growth factors and cytokines that affect cells locally. 3. Unclear which function predominates in treating orthopedic injuries: paracrine/immunomodulatory/trophic effects versus direct differentiation into and regeneration of the injured tissue. B. Although limited, the literature supports the use of bone marrow derived MSCs to treat various orthopedic injuries more so than other sources. C. Evidence is limited to bench research and preclinical studies. Some human studies have been published, although limited to case reports/series or cohort studies. 1. ACL regeneration with collagen I scaffold and MSC in rats Complete ACL transection was repaired with suture alone (n = 6), suture with type I collagen scaffold (n = 8), or suture with type I collagen scaffold and MSCs (n = 6). Thirtythree percent of rats treated with MSCs showed complete regeneration of ACL. There was no regeneration seen in the other two groups. 2. Medial femoral condyle lesion in a Judo player Chondral defect of 20 × 30 mm. Arthroscopic evaluation after treatment showed filling of previously seen defect, with near-resolution of lesion on imaging. Significant improvement of symptoms 7 months after treatment, with full return to sport. 3. Partial medial meniscectomy, with and without osteoarthritis Randomized, double blind controlled trial of candidates for partial meniscectomy. MSC injected 7 to 10 days after meniscectomy. Some knees with MSC injections showed evidence of meniscal regeneration. There was a clinically meaningful improvement in pain scores with MSC injection in those with osteoarthritis over those without at 1 and 2 years. D. For a more detailed discussion on the topic of stem cell therapy for sports injuries, in addition to the subjects discussed in this chapter, refer to Malanga and Nakamura (2014) (7).

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Recommended Reading 1. Coombes BK, Bisset L, Vicenzino B. Efficacy and safety of corticosteroid injections and other injections for management of tendinopathy: a systematic review of randomised controlled trials. Lancet. 2010;376: 1751–1767. 2. DeChellis DM, Cortazzo MH. Regenerative medicine in the field of pain medicine: prolotherapy, platelet-rich plasma therapy, and stem cell therapy: theory and evidence. YTRAP. 2011;15(2):74–80. doi:10.1053/ j.trap.2011.05.002. 3. Foster TE, Puskas BL, Mandelbaum BR, Gerhardt MB, Rodeo SA. Platelet-rich plasma: from basic science to clinical applications. Am J Sports Med. 2009;37(11):2259–2272. doi:10.1177/0363546509349921. 4. Jarvinen TAH. Muscle injuries: biology and treatment. Am J Sports Med. 2005;33(5):745–764. doi:10.1177/ 0363546505274714. 5. Koh JSB, Mohan PC, Howe TS, et al. Fasciotomy and surgical tenotomy for recalcitrant lateral elbow tendinopathy: early clinical experience with a novel device for minimally invasive percutaneous microresection. Am J Sports Med. 2013;41(3):636–644. doi:10.1177/0363546512470625. 6. Lee KS, Wilson JJ, Rabago DP, Baer GS, Jacobson JA, Borrero CG. Musculoskeletal applications of platelet-rich plasma: fad or future? AJR Am J Roentgenol. 2011;196(3):628-636. doi:10.2214/AJR.10.5975. 7. Malanga G, Nakamura R. The role of regenerative medicine in the treatment of sports injuries. Phys Med Rehabil Clin N Am. 2014;25(4):881–895. doi:10.1016/j.pmr.2014.06.007. 8. Sharma P, Maffulli N. Tendon injury and tendinopathy: healing and repair. J Bone Joint Surg Am. 2005;87(1): 187–202.

53 Sports Ultrasound Mederic M. Hall

I. Ultrasound Basics A. Physics 1. Electric voltage converted to sound waves by reverse piezoelectric effect 2. Sound wave requires medium (eg, water, acoustic coupling gel, etc) to pass through 3. Sound waves reflected at tissue boundaries 4. Acoustic impedance a. Acoustic impedance = media density × propagation speed b. Similar acoustic impedance = less reflection c. Greater difference in acoustic impedance = more reflection 5. Angle at which sound wave strikes a tissue interface = angle of incidence a. Perpendicular incidence i. Sound wave traveling perpendicular to boundary between media ii. Maximizes amount of echoes reflected back to transducer iii. Ideal b. Oblique incidence i. Sound wave not traveling perpendicular to boundary between media ii. Some echoes reflected away from transducer iii. Can result in artifact of anisotropy 6. Returning sound waves detected by transducer and converted to volts via piezoelectric effect 7. Volts assigned color on gray scale and location on screen to produce image B. Terminology 1. Anechoic—black (ie, no reflection) 2. Hypoechoic—dark relative to surrounding structures (ie, less reflection) 3. Isoechoic—same shade of gray as another structure 4. Hyperechoic – bright/light gray relative to surrounding structures (ie, high reflection) C. Transducers 1. Frequency a. Higher frequency—better resolution, but lower penetration i. Good for imaging superficial structures b. Lower frequency—lower resolution, but better penetration i. Good for imaging deep structures 2. Linear array—sound waves exit perpendicular to flat transducer surface. Minimizes anisotropy. Recommended for superficial structures and diagnostic imaging. Limitation = smaller field of view

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3. Curvilinear array—sound waves exit in fan shape from the curved transducer surface. Provides larger field of view, but increases risk of anisotropy. Recommended for imaging deep structures or guiding procedures requiring steep angles D. Artifacts 1. Anisotropy—common artifact in musculoskeletal (MSK) imaging. Occurs when sound waves strike structure at oblique angle of incidence. Sound waves reflect away from the transducer = artifactual hypoechoic/anechoic appearance. Risk of false positive. Effects tendons > ligaments > nerves 2. Posterior acoustic shadowing—hypo/anechoic region deep to area of high reflectivity or high attenuation. Commonly seen deep to bone/calcium. Also seen deep to scar tissue and normal fibrous septae 3. Edge shadowing—refraction artifact secondary to velocity change deep to curved interface. Seen at edges (eg, torn tendon, normal A1 pulley) 4. Posterior acoustic enhancement/increased through transmission—hyperechoic region deep to area of low attenuation. Commonly seen deep to fluid collections 5. Reverberation—multiple internal reflections from highly reflective surface casting a “dirty” shadow below the object as opposed to “clean” shadow of bone. Commonly seen with metal (orthopedic hardware, needles, etc). For needles, looks like multiple needles located deep and in parallel to the original needle

II. Diagnostic Sports Ultrasound A. Musculoskeletal 1. Tendon—typically imaged best with high frequency, linear array transducer. Exceptions are select deep tendons in patients of large body habitus (iliopsoas, gluteals, etc) a. Normal sonographic appearance—hyperechoic tightly packed linear echoes in fibrillar pattern on long axis. Stippled clustered dots in “broom end” appearance on short axis b. Pathology i. Tendinosis—thickening/swelling, hypoechogenicity, heterogeneity with loss of usual fibrillar echotexture. May also see calcifications, intra/peritendinous hyperemia on power or color Doppler imaging (neovascularity) ii. Tear (A) Partial—well-defined, focal defect in tendon confirmed in two planes. Often occurs in “critical zones” of specific tendons related to hypovascularity, biomechanical factors, and repetitive trauma (B) Full thickness—tear extends from deep to superficial surface, but may not involve full width of tendon (1) Complete—full thickness and full width tear with retraction of torn tendon fibers. Appears as a gap in the tendon or complete absence of tendon (C) Calcific tendinopathy—calcium hydroxyapatite deposition within tendon. Appearance is hyperechoic with variable amounts of posterior acoustic shadowing dependent on type/phase of calcification. Symptoms typically related to mass effect/impingement or inflammatory response in resorptive phase. May be asymptomatic c. Pearls and pitfalls i. Anisotropy—can mimic tendinosis or tear. Common finding, especially in rotator cuff ii. Edge shadowing useful in identifying torn tendon ends iii. Dynamic imaging helpful when complete tear suspected iv. Neovascularity—clinical significance is controversial

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2. Muscle a. Normal sonographic appearance—hypoechoic muscle fibers/fascicles with hyperechoic septa of peri- and epimysium forming a pennate pattern on long axis, and Van Gogh “starry night” pattern in short axis i. Pathology—focal disruption of normal fiber structure. May appreciate focal defect. Hemorrhage → hematoma → scar. Strain—more common in muscle crossing two joints ii. Contusion—typically involves deep fibers next to bone. Myositis ossificans appears as hyperechoic linear calcific density within zone of muscle injury. Seen earlier on ultrasound than x-ray 3. Ligament—identify bony landmarks and then align transducer with ligament. Long axis imaging most useful a. Normal sonographic appearance—hyperechoic fibrillar pattern (less compact than tendon). May appear hypoechoic dependent on surrounding tissue. Less susceptible to anisotropy than ligament b. Pathology i. Grade I—swollen and hypoechoic without fiber disruption or laxity on dynamic stress imaging ii. Grade II—partial tear/evidence of fiber disruption. May have some laxity on dynamic stress imaging, but end point appreciated iii. Grade III—complete tear. Dynamic stress imaging demonstrates laxity and absence of bridging fibers 4. Nerve—short axis imaging most useful. High frequency transducers allows for detailed evaluation a. Normal sonographic appearance—hypoechoic nerve fascicles and hyperechoic intraand extraneural epineurium. “Honeycomb” appearance on short axis. Fascicular appearance on long axis. Minimal anisotropy. Typically adjacent to vessels b. Pathology—swelling and hypoechogenicity. Often with loss of normal fascicular pattern. May demonstrate focal swelling proximal to entrapment site or focal narrowing (“notch sign”) at entrapment site. Dynamic testing may demonstrate subluxation/ dislocation or hypomobility 5. Bone—evaluation limited to superficial portion due to inability of ultrasound waves to pass through bone a. Normal sonographic appearance—smooth, linear, hyperechoic b. Pathology i. Fracture = disruption of smooth cortical surface. Periosteal thickening in stress injury. Hypoechoic hematoma at fracture site. Hyperemia common. Pain on sonopalpation ii. Stress fracture/reaction = periosteal thickening with (fracture) or without (reaction) cortical discontinuity 6. Cartilage a. Normal sonographic appearance i. Hyaline cartilage—hypo/anechoic. Noncompressible (distinguish from fluid collection). Uniform thickness ii. Fibrocartilage—hyperechoic or mixed echogenicity with uniform echotexture (“salt and pepper”) b. Pathology—limited evaluation due to intra-articular location. Loss of uniformity in hyaline cartilage. Focal hypoechoic defect in fibrocartilage. Secondary signs may be helpful (parameniscal cyst, joint effusion, etc)

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7. Vessels a. Normal sonographic appearance—hypo- or anechoic tubular structures i. Arteries—pulsatile, thicker walls, less compressible ii. Veins—thinner walled, easily compressible, nonpulsatile b. Pathology—often requires formal vascular study outside of typical sports ultrasound. Focal enlargement → aneurysm. Noncompressible → thromboembolism B. Nonmusculoskeletal—role in sports ultrasound continues to be defined 1. Chest/Abdominal trauma i. Focused assessment with sonography for trauma (FAST)—goal is identifying free fluid (blood) in peritoneum. Four views: (a) hepatorenal recess (Morison’s pouch), (b) splenorenal recess, (c) bladder, and (d) pericardial. Any anechoic fluid identified is considered positive exam. Low sensitivity (does not exclude injury). High specificity. Potential to shorten time for more definitive care ii. Solid organ injury—liver, spleen, and kidney. Low sensitivity. Any positive finding requires urgent referral. Laceration → hypo- to anechoic fluid collection perpendicular to organ capsule. Contusion → inhomogeneous hypoechoic fluid collection iii. Pneumothorax—sensitivity and specificity better than chest x-ray. Criteria for diagnosis: (a) absence of lung sliding (identification = 100% negative predictive value), (b) disappearance of “B-lines” (visualization = 100% negative predictive value), and (c) M-mode transition from “sandy beach” in normal lung to “barcode” in pneumothorax 2. Cardiology—multiple potential uses. Identification of pericardial effusion/tamponade. Evaluation of central venous volume status (inferior vena cava [IVC] collapse). Limited echocardiography may also be beneficial for identifying athletes at risk for sudden cardiac death during the preparticipation physical examination 3. Ocular trauma—evaluate posterior chamber trauma (retinal and vitreous detachments). Anterior chamber difficult to assess. Normal posterior chamber is anechoic. Any echogenic material suggestive of injury and requires immediate referral

III. Interventional Sports Ultrasound A. Injections 1. Ultrasound-guided injections (USGIs) are more accurate than landmark-guided injections (LMGIs) a. SORT evidence rating A b. Site and practitioner specific variability 2. USGIs are more efficacious than LMGIs a. SORT evidence rating B b. Study limitations: lack of specific target and diagnosis; inherent limitations related to corticosteroids (predominance of available literature) c. Potential to reduce complications d. Importance of diagnostic injections 3. USGIs are more cost-effective than LMGIs a. SORT evidence rating B b. Small number of studies B. Advanced procedures 1. Examples: tenotomies, fascial releases for chronic exertional compartment syndrome, carpal tunnel releases, trigger finger releases, nerve hydrodissections, regenerative medicine techniques 2. USG key to safe and effective performance 3. New techniques and devices being introduced 4. Potential to augment, improve, or replace current surgical techniques

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Recommended Reading 1. Berkoff DJ, English J, Theodoro D. Sports medicine ultrasound (US) beyond the musculoskeletal system: use in the abdomen, solid organs, lung, heart and eye. Br J Sports Med. 2015;49(3):161–165. 2. Finnoff JT, Berkoff D, Brennan F, et al. American medical society for sports medicine recommended sports ultrasound curriculum for sports medicine fellowships. Br J Sports Med. 2015;49(3):145–150. 3. Finnoff JT, Hall MM, Adams E, Berkoff D, Concoff AL, Dexter W, Smith J. American Medical Society for Sports Medicine (AMSSM) position statement: interventional musculoskeletal ultrasound in sports medicine. Br J Sports Med. 2015;49(3):145–150. 4. Hoffman DF, Adams E, Bianchi S. Ultrasonography of fractures in sports medicine. Br J Sports Med. 2015;49(3):152–160. 5. Smith J, Finnoff JT. Diagnostic and interventional musculoskeletal ultrasound: Part 2. Clinical applications. PMR. 2009;1(2):162–177. 6. Smith J, Finnoff JT. Diagnostic and interventional musculoskeletal ultrasound: Part 1. Fundamentals. PMR. 2009;1(1):64–75. 7. Yim ES, Basilico F, Corrado G. Early screening for cardiovascular abnormalities with preparticipation echocardiography: Utility of focused physician-operated echocardiography in preparticipation screening of athletes. J Ultrasound Med, 2014;33(2):307–313.

Practice Test

QUESTIONS 1. A 16-year-old football player presents to clinic the same day after a fall on an outstretched hand in practice. Tenderness is noted in the area of the right snuffbox. Imaging is negative for fracture. What is the most appropriate management at this time? A. B. C. D.

Ice, ACE wrap, and rest with return to play as tolerated Short arm thumb spica splint with follow-up in 1 week in order to reimage Short arm thumb spica cast with follow-up in 4 weeks Short arm thumb spica splint with follow-up in 4 weeks

2. Regarding the structure of normal tendon, which is true? A. The tendon’s vascular and lymphatic supply is contained in the loose connective tissue sheath of the endotenon B. Collagen type III makes up approximately 80% of the dry weight of tendon C. Water accounts for approximately 70% of tendon mass D. The osseotendinous junction is the weakest part of the muscle/tendon unit E. The majority of the blood flow to the tendon midportion arises from vessels originating at the myotendinous junction 3. A 32-year-old recreational basketball player comes to your office with a chief complaint of right posterolateral knee pain. He is unclear about the exact mechanism, but he believes he may have twisted and hyperextended his knee during a game 3 days ago. During your physical examination, you note a knee effusion and guarding to passive range of motion. You decide to perform a dial test, and you note 15° more of tibial external rotation of the right knee compared to the left when at 30° of flexion but symmetric external rotation when the knee is held at 90° of flexion. This physical exam finding suggests which pathology or combination of pathologies? A. B. C. D.

Posterior cruciate ligament (PCL) injury only Posterolateral corner (PLC) injury only Neither PCL nor PLC injury Both PCL and PLC injury

4. This fracture pattern involves only compression failure of cortex/periosteum at the metaphyseal/diaphyseal junction: A. B. C. D. E.

Plastic deformation Physeal fracture Complete fracture Buckle fracture Greenstick fracture

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5. After sustaining trauma to the anterior, lateral shoulder, a collegiate rugby player presents with chest pain, shortness of breath, right arm paresthesias, and cramping. He holds his head tilted to the right side and has pain near the right sternal border. His neurovascular exam is normal. The best management for this patient is: A. Assume this is an anterior sternoclavicular joint dislocation; hold from play and follow up with orthopedics after completion of the game B. Assume this is a posterior sternoclavicular joint dislocation; hold from play and follow up with orthopedics after completion of the game C. Assume this is a posterior sternoclavicular joint dislocation; perform emergent reduction on the sideline D. Assume this is a posterior sternoclavicular joint dislocation; transfer to the nearest emergency department for intraoperative reduction 6. A 27-year-old female presents to your office for evaluation of leg pain. She reports pain predominantly over the anteromedial portion of her leg from about mid-tibia extending slightly distally. She began training for a half marathon 6 weeks ago. Her pain is most severe when she starts running but eases once she warms up. Her most likely diagnosis is? A. B. C. D.

Compartment syndrome Medial tibial stress syndrome Tibial stress fracture Popliteal artery entrapment

7. The two most important factors in the treatment of exertional heat stroke in a preseason football athlete are: A. B. C. D.

Early core temperature assessment and early transportation to emergency facility Initiation of rapid cooling measures and intravenous fluid administration Early core temperature assessment and initiation of rapid cooling measures Appropriate off-season conditioning program and maintaining body mass index within normal limits

8. Which of the following is not a feature of periodization? A. B. C. D. E.

Microcycles are commonly 1 week Increased training volume leading up to competition Transitions from general to specific training Decreases risk of overtraining Linear periodization is designed for sports with a small number of in-season competitions and a well-defined off-season

9. A 16-year-old male wrestler presents to the training room for evaluation of auricular swelling, pain, and erythema that began the previous evening during a wrestling match. The swelling and pain have progressively worsened. What is your treatment plan? A. Ice, nonsteroidal anti-inflammatory drugs (NSAIDs), and gentle compression for 10 to 14 days B. Referral to dermatology for biopsy of suspected cancerous lesion C. Referral to ear, nose, and throat (ENT) for possible excision and grafting D. Needle aspiration of auricular hematoma and external compression for 7 to 10 days E. Cephalexin 500 mg 4 times a day for 7 days

PRACTICE TEST

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10. Which one of these is NOT a requirement of the team physician? A. B. C. D.

Possess knowledge of on-field emergency care at sporting events Be an MD or DO, with an unrestricted license Be advanced cardiovascular life support (ACLS) certified Have a fundamental knowledge of musculoskeletal injuries

11. A 35-year-old male presents to the clinic with right knee pain 5 days after running a 10K race. The right knee is swollen and warm to the touch. He denies any fevers, chills, or other systemic symptoms. He does mention he was with friends over the weekend at a college reunion party. Indomethacin has provided great relief for a similar episode in the past. You aspirate the knee and send the fluid to the lab for analysis. What would you expect to find on synovial fluid analysis and what is the appropriate treatment at this time? A. Synovial fluid: Cloudy appearance with 5,000 white blood cells (WBCs) per mm3. Treatment: initiation of allopurinol B. Synovial fluid: Opaque appearance with 100,000 WBCs per mm3. Treatment: initiation of indomethacin C. Synovial fluid: Cloudy appearance with 5,000 WBCs per mm3. Treatment: initiation of indomethacin D. Synovial fluid: Cloudy appearance with 100,000 WBCs per mm3. Treatment: intra-articular corticosteroid injection 12. Tendons elongate under load, with properties of elongation determined by the stress–strain curve. Which statement about stress and strain is correct? A. The linear region of the stress–strain curve represents the area in which maximal stress is required to produce additional tendon elongation B. The elastic limit occurs at 10% strain, after which there is rupture of the tendon C. Tendon crimp is straightened at 5% tendon strain D. The linear region of the stress–strain curve represents the area where the cross-links between tendon fibrils are separated during application of stress 13. A 23-year-old female runner presents to your clinic with diffuse right anterior knee pain. Her symptoms worsen at the end of a run and are associated with aching the following day. The pain is worse with going up/down stairs. Her physical exam of the right knee is notable for no effusion, tenderness to palpation over the medial patellar facet, negative patellar apprehension, and contralateral pelvic drop with right genu valgum in single-leg stance. Quadriceps testing reveals 5-/5 strength on the right, with some guarding noted. During side-lying examination, right gluteus medius strength is 4-/5. She asked a friend about this problem, who told her that she should strengthen her quadriceps. How would you counsel her? A. Her friend was correct—Quadriceps strengthening should be the main component of her rehabilitation protocol B. Her friend was incorrect—Quadriceps strengthening is not important for her rehabilitation protocol C. While quadriceps strengthening is important, the main focus of her rehabilitation protocol should be to focus on core strength and lumbo-pelvic stabilization, specifically addressing her gluteus medius weakness D. While quadriceps strengthening is important, the main focus of her rehabilitation protocol should be to utilize modalities such as ultrasound and massage to decrease her pain

566

PRACTICE TEST

14. This epiphyseal fracture pattern involves a fracture through the epiphysis and into the physis: A. B. C. D. E.

Salter–Harris I Salter–Harris II Salter–Harris III Salter–Harris IV Salter–Harris V

15. All of the following are energy systems except A. B. C. D.

Aerobic (oxidative) Anaerobic (glycolytic) Mitochondrial ATP-phosphocreatine

16. Which of the following is NOT the correct listing of anatomical structures for the associated fascial compartment? A. Anterior compartment: extensor hallucis longus, extensor digitorum longus, peroneus tertius, anterior tibialis B. Lateral compartment: peroneus longus, peroneus brevis, superficial peroneal nerve C. Deep posterior compartment: flexor hallucis longus, flexor digitorum longus, posterior tibialis, deep peroneal nerve D. Superficial posterior compartment: gastrocnemius, soleus 17. An 18-year-old weightlifter presents to your training room complaining of a red eye after weightlifting. He is not complaining of pain, visual disturbance, photophobia, tearing, or blepharospasm. Physical examination is negative except for bright redness of the sclera on the lateral side of the iris, without anisocoria or swelling. The next step in management is: A. B. C. D.

Immediate referral to ophthalmologist Lateral canthotomy and cantholysis Reassurance and artificial tears prn Cycloplegic agent and antibiotic ointment

18. Which of the following contractions provides the greatest stimulus for muscle hypertrophy at a given load? A. B. C. D. E.

Eccentric Concentric Isometric Isokinetic Plyometric

19. A high-school lacrosse player was struck in the anterior chest by a ball. He describes pain, and then collapses pulseless on the ground. Which is the best management for this patient? A. Two minutes of chest compressions followed by a rhythm check, and if warranted, synchronized cardioversion B. Immediate defibrillation C. Two minutes of chest compressions followed by a rhythm check and if warranted, defibrillation D. Immediate synchronized cardioversion

PRACTICE TEST

567

20. Who does NOT have legal authority to make medical decisions for an athlete who is a minor? A. B. C. D.

The parent The legal guardian The athlete The student assistant athletic trainer

21. A 23-year-old recreational male runner presents with ongoing complaints of achy, burning pain in both legs that occurs when he runs for greater than 10 minutes. The pain forces him to stop running and symptoms usually completely resolve within a 1/2 hour. Which of the following compartment pressure testing results confirms your clinical suspicion of chronic exertional compartment syndrome of the anterior compartment of the leg? A. B. C. D.

A 5-minute postexercise pressure of 18 mmHg tested in the tibialis anterior A 1-minute postexercise pressure of 31 mmHg tested in the peroneus longus A 1-minute postexercise pressure of 34 mmHg tested in the tibialis anterior A 5-minute postexercise pressure of 30 mmHg tested in the gastrocnemius

22. Tendon healing tends to follow a stereotypical pattern, proceeding through inflammatory, proliferative, and remodeling phases. Which statement is true regarding normal tendon healing? A. The proliferative phase of healing begins at approximately 6 weeks after injury B. The synthesis of type II collagen peaks during the proliferative phase and lasts several months C. Type III collagen is produced primarily during the remodeling phase D. Type I collagen has fewer cross-links than type III collagen, accounting for the decreased strength of tendons during the proliferative phase E. Glycosaminoglycan content remains high during the proliferative phase, which results in mildly swollen tendon substance 23. What is the relationship between experiencing an anterior cruciate ligament (ACL) tear and osteoarthritis of the knee? A. B. C. D.

History of an ACL tear does not impact one’s risk of developing knee osteoarthritis History of an ACL tear increases one’s risk of developing knee osteoarthritis History of an ACL tear decreases one’s risk of developing knee osteoarthritis The injury status of the ACL has no effect on osteoarthritis in the knee

24. This is a common physical exam finding in a hip with a slipped capital femoral epiphysis: A. B. C. D. E.

Swelling Deformity Leg length discrepancy Loss of internal rotation with hip flexion Pain to palpation

25. The muscle fiber with both fast twitch and endurance characteristics is A. B. C. D.

Type Ia Type Ix Type IIa Type IIx

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PRACTICE TEST

26. A patient presents to your office with complaints of claudication-like symptoms in his right calf when he plays soccer. His ankle brachial index (ABI) is noted to be diminished on the right compared with the asymptomatic side. You suspect he has popliteal artery entrapment. Which is the most likely anatomical finding causing his symptoms? A. The popliteal artery passing below the popliteus muscle or fibrous bands B. The medial head of the gastrocnemius attaching laterally to the medial femoral condyle C. Presence of an accessory slip of gastrocnemius branching from the medial head of the gastrocnemius D. Displacement of the popliteal artery medial to and beneath the medial head of the gastrocnemius 27. The antihypertensive medication least likely to affect training for an endurance athlete A. B. C. D.

Beta-blocker Diuretic Angiotensin-converting enzyme inhibitor Calcium channel blocker

28. Which of the following is not true about endurance training? A. American College of Sports Medicine (ACSM) recommends a frequency of 3 to 5 days per week B. High-intensity interval training can simultaneously improve maximum oxygen uptake (VO2max) and anaerobic endurance C. Lactate threshold is a strong predictor of endurance performance D. Improves oxidative capacity in type 1 but not type 2 muscle fibers 29. A 16-year-old lacrosse player is struck with a ball and is complaining of tooth pain. She has no other complaints and physical examination is negative except for her teeth. You examine her teeth and find an intrusion displacement of the right incisor with angulation of approximately 45 degrees. There is no step-off deformity of the maxilla nor malocclusion. What is true about this condition? A. B. C. D.

The physician should reposition the tooth on the sideline and splint it for 2 weeks This form of displacement has the worst prognosis for tooth survival With immediate realignment and proper oral hygiene, the patient should recover fully The patient is able to return to play with a mouthguard and dental follow-up

30. The necessary conditions for legitimate informed consent include A. B. C. D. E.

Disclosure Benevolence Voluntariness All of the above A and C

31. A 57-year-old active female skier presents with left-sided groin pain. She has a positive hip scour maneuver that reproduces her pain. Imaging shows mild osteophytes around the hip joint and mild subchondral sclerosis of the acetabulum with a preserved joint space. What is the most appropriate anesthetic to use in combination with a corticosteroid for intra-articular injection? A. 2% lidocaine B. 1% lidocaine

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569

C. 0.5% bupivacaine D. 0.2% ropivacaine 32. Which tissue is the most commonly involved in sports injury? A. B. C. D. E.

Bone Muscle Tendon Nerve Ligament

33. A football player presents to your clinic with history, physical examination, and imaging findings consistent with an isolated, grade II medial collateral ligament (MCL) sprain. Which of the following most likely represents the best course of management? A. Return to play the following week with a hinged knee brace B. Hinged knee brace, physical therapy, and a return to play protocol taking roughly 4 to 6 weeks C. Hinged knee brace, physical therapy, and a return to play protocol taking roughly 4 to 6 months D. Surgical reconstruction of the MCL 34. An avulsion fracture of the anterior inferior iliac spine involves the origin of what muscle? A. B. C. D. E.

Sartorius Rectus femoris Tensor fascia lata Gluteus medius Iliopsoas

35. All of the following are physiologic adaptations to aerobic conditioning except A. B. C. D.

Increased ventricular wall thickness and decreased internal diameter Larger stroke volume Lower-end diastolic volume Lower resting heart rate

36. You are treating an elite collegiate level distance runner who reports developing tightness and cramping in his right leg during workouts at race pace. He also occasionally feels tingling in his foot as the workout continues. Pre- and postexercise compartment pressure testing is consistent with a diagnosis of chronic exertional compartment syndrome. He states he is hoping to qualify for the Olympic trials during his spring season 6 months from now. What is the best recommendation for treatment? A. B. C. D.

Evaluate and change his shoes to increase the cushioning Decrease his running distance during training Referral for fasciotomy Retire from competition as he risks development of critical limb ischemia with continued running

37. The use of viscosupplementation is supported by the Cochrane medical database (2007) for the treatment of knee osteoarthritis A. True B. False

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PRACTICE TEST

38. To enhance athletic performance by living at altitude, the optimal elevation is A. B. C. D. E.

2,000 to 3000 m 3,000 to 4,000 m 4,000 to 5,000 m 5,000 to 6,000 m 6,000 to 7,000 m

39. A 12-year-old softball player presents with a mild nose bleed, which seems to resolve within minutes. On examination, you find that he has blood draining down the back of his throat, but is not complaining of coughing or problems breathing. After ruling out a fracture, what is an appropriate next step? A. A Foley catheter can be used to achieve temporary hemostasis prior to transport to the hospital B. The nose can be packed with a nasal tampon and monitored C. The patient should be instructed to lean forward while pinching his nose D. The patient may return to play since he no longer has bleeding from the nostrils 40. Medical malpractice is usually based on negligence and requires establishment of which of the following? A. B. C. D.

The defendant had a duty to act A catastrophic injury occurred The patient did not sign a waiver The defendant was not ACLS certified

41. A 28-year-old male presents with right hand pain after a fight during a hockey game. Imaging shows a nondisplaced fracture of the fifth metacarpal neck. The appropriate initial management should include A. Buddy taping of the fourth and fifth digits as it is a nondisplaced fracture B. Ulnar gutter splint with the wrist in 30° of extension, metacarpophalangeal (MCP) joints in 70° to 90° of flexion, and the proximal interphalangeal (PIP) and distal interphalangeal (DIP) joints in 5° to 10° of flexion C. Ulnar gutter splint with the wrist in 30° of extension, MCP joints in 10° of flexion, and the PIP and DIP joints in 5° to 10° of flexion D. Ulnar gutter splint with the wrist neutral, MCP joints in 70° to 90° of flexion, and the PIP and DIP joints in 5° to 10° of flexion 42. Myositis ossificans traumatica (MOT) may develop after a muscle contusion. Which statement about MOT is correct? A. Ultrasound cannot differentiate between a cystic and solid lesion B. The etiology of MOT involves the action of cytokine bone morphogenic protein 2 (BMP-2) and transforming growth factor (TGF) that act on vascular endothelial cells to cause transformation of endothelial cells to mesenchymal stem cells that undergo additional transformation to osteoblasts C. Calcification is apparent by 7 to 10 days after injury in typical MOT D. Aspiration of large fluctuant hematomas will not reduce the risk of developing MOT E. Surgical excision of MOT should be considered before 3 months to reduce the risk of local recurrence

PRACTICE TEST

571

43. A 17-year-old female soccer player presents to your clinic with lateral knee pain after experiencing a noncontact injury during a game. Physical examination reveals significant swelling, positive Lachman’s test, positive anterior drawer test, and positive pivot shift test. X-rays taken in the office do not show any osseous abnormality. The patient and her parents ask if an MRI is necessary. Which is the best reply? A. B. C. D.

An MRI is not necessary because the diagnosis is clear from the examination An MRI is necessary because the diagnosis is unclear from the examination An MRI is helpful to rule out other, concomitant intra-articular knee injuries A musculoskeletal ultrasound examination is the next best test

44. All of the following are names of common traction apophysitis except: A. B. C. D. E.

Sever ’s Osgood-Schlatter Sinding-Larson–Johansson Iselin’s Kohler ’s

45. Increased blood volume results in a A. B. C. D.

Decreased ability to dissipate heat Pseudoanemia Lower blood pressure Increased heart rate

46. A 20-year-old female collegiate basketball player presents with a 1-week history of progressive anterior leg pain. On exam she has focal tenderness over the anterior tibia. You obtain plain x-rays of her tibia and fibula, which are normal. The next test you order is? A. B. C. D.

MRI of the lower leg CT of the lower leg Immediate compartment pressure testing Exertional compartment pressure testing

47. The World Anti-Doping Agency (WADA) code was created primarily to accomplish the following: A. Unify drug-testing protocols among the National Basketball Association (NBA), Major League Baseball (MLB), and the National Football League (NFL) B. For use on approved laboratory to test and screen athletes for performance-enhancing drugs (PEDs) C. Streamline and coordinate antidrug policies across many government and sport agencies D. Supervise the drug testing and surveillance for the International Olympic Committee (IOC) 48. Which of the following is not true regarding stretching exercise? A. To improve flexibility, proprioceptive neuromuscular facilitation (PNF) stretching is more effective than static stretching B. Preactivity stretching does not appear to reduce injury risk C. To improve flexibility, ACSM recommends holding stretches 10 to 30 seconds for two to four repetitions D. Sprint performance may be impaired by static stretching E. The Golgi tendon organ activation associated with ballistic stretching is counterproductive

572

PRACTICE TEST

49. A 26-year-old professional football player was struck in the throat by an opposing player in a high-velocity collision. He complains of severe laryngeal pain and has vocal tone changes (hoarseness). After 5 minutes of observation you also notice mild subcutaneous emphysema but no stridor nor respiratory distress. Which of the following measures should be taken? A. Immediate intubation on the sideline B. Close observation and transport to the nearest emergency department for possible laryngoscopy C. Return to play once pain starts to improve D. Withhold from play, apply ice, and instruct on vocal rest until follow-up in clinic or training room 50. “Good Samaritan” statutes in your state A. B. C. D.

Will travel with you wherever you travel with your team Are only applicable if you provide care to an unknown person Do not travel across state lines regardless of your role with the team Are federal statutes

51. A collegiate football player has three episodes of hemoptysis with associated shortness of breath after sustaining a forceful blow to the anterior chest after a tackle. He is held from play and transferred to the local emergency department where chest x-ray (CXR) is read as normal. He continues to describe pain and shortness of breath. He is tachypneic and hypoxic. Which of the following describes the best course of action? A. CXR has a low sensitivity in the acute phase of this injury; obtain another CXR in 24 to 28 hours for better visualization B. CXR has a low sensitivity in the acute phase of this injury; obtain a bone scan immediately for diagnosis C. Perform inspiratory and expiratory CXRs, and if they are normal assume this is a small pneumothorax and treat conservatively D. CXR has a low sensitivity in the acute phase of this injury; obtain a CXR in 3 to 4 weeks for better visualization 52. Which of the following is an absolute indication to proceed with imaging after blunt trauma to evaluate for renal trauma in adults? A. B. C. D. E.

Microscopic hematuria only, otherwise stable patient Flank tenderness Microscopic hematuria with hypotension Low speed collision History of solitary kidney

53. A 20-year-old male college football player presents for evaluation of a painful furuncle on his right anterior thigh. It is erythematous, with scant purulent discharge present, and a honey-crusted appearance at the center. It measures 1 cm in diameter with no signs of surrounding cellulitis. He is afebrile and reports no fever, chills, or sweats. He has no other skin lesions and has no prior history of furuncles or cellulitis. Appropriate initial treatment would be: A. Incision and drainage B. Immediately begin twice a day whirlpool treatments in the training room C. Intravenous (IV) vancomycin q6h

PRACTICE TEST

573

D. Nasal mupirocin tid for 3 to 5 days, and nasal cultures of all teammates E. Bactrim DS bid for 7 days 54. Most sports-related concussions resolve in: A. B. C. D.

2 months 1 month 7–10 days 1 day

55. Increased muscle strength between 2 and 4 weeks after initiating exercise is due to A. B. C. D.

Muscle hypertrophy Muscle hyperplasia Increased mitochondrial density Improved neuromuscular coordination

56. Based on the “Seattle Criteria,” which of the following ECG findings do NOT require further evaluation prior to giving an asymptomatic athlete clearance to participate? A. B. C. D. E.

ST segment elevation in leads V1–V3 RSR pattern in lead V1 with QRS duration of 90 ms Corrected QT interval (QTc) of 490 msec in a male athlete Sinus rhythm with a rate of 28 beats per minute Two premature ventricular contractions during a 10-second tracing

57. The following category of drugs is prohibited at all times by WADA A. B. C. D.

Beta-blockers Alcohol Cannabinoids Diuretics agents

58. A 10-year-old soccer player complains of nose pain after colliding with another player. She had no loss of consciousness nor headache but examination is remarkable for moderate nasal deformity. There is crepitation with gentle manipulation of the nose but she can only tolerate gentle examination. Management should include: A. B. C. D.

Immediate relocation on the sidelines Ice and analgesics, with follow-up in clinic within 2 to 3 days Transport to the emergency department for urgent relocation Observation and relocation after 2 weeks if deformity persists

59. A 28-year-old recreational female runner presents with complaints of diffuse erythema, warmth, and pruritus affecting her arms, chest, and back that occur during exercise. Occasionally she can get lightheaded during these attacks, but has not lost consciousness. She has not started any new medications, and has no history of asthma, diabetes, or recent infection. Your diagnose her with: A. B. C. D. E.

Solar urticaria Drug-induced photodermatitis Exercise-induced urticaria Raynaud’s disease Dermatographia

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PRACTICE TEST

60. Which of the following is not true regarding iron-deficiency anemia (IDA) in athletes? A. Women are at higher risk of developing IDA than men B. In the initial stage of IDA, serum iron concentrations are low while the ferritin and hemoglobin levels are normal C. Footstrike hemolysis is a known cause of IDA D. Inadequate calorie consumption and menstrual losses are common causes in female athletes Preamble for Q61–66: A 14-year-old high-school pitcher presents with chronic medial elbow pain, recently exacerbated after participation in an All Star Tournament, in which he threw 60 pitches on day 1 and 100 pitches on day 5. In the last year, he has pitched approximately 90 innings. His coach, a former professional pitcher, has routinely encouraged him to throw curve balls in games and perform the sleeper stretch each night before bed. On exam, he is tender to palpation at his medial epicondyle and has increased pain with valgus force at the elbow. 61. Which phases of the pitching cycle are responsible for his injury? A. B. C. D. E.

Windup and early cocking Late cocking and acceleration Deceleration and follow-through Acceleration and deceleration Early cocking and late cocking

62. Which USA Baseball guideline has the athlete (and his coach) violated? A. B. C. D.

He did not have sufficient rest between games He exceeded the maximum innings pitched per year He exceeded the pitch per game maximum He used breaking ball pitches, such as the curve ball and slider

63. Which of the following interventions would be most appropriate to prevent the same injury in the future? A. B. C. D.

Performing the sleeper stretch daily Restricting the use of the curve ball Strengthening the dynamic internal rotators of the shoulder Improving endurance of the shoulder abductors

64. The sleeper stretch is a useful tool to prevent injury in pitchers. Which biomechanical changes does it help prevent? A. B. C. D.

Increased internal rotation (IR), increased external rotation (ER) Decreased IR, decreased ER Increased IR, decreased ER Decreased IR, increased ER

65. These changes in internal and external rotation are primarily a product of which phase of the pitching cycle? A. B. C. D. E. F.

Windup Early cocking (stride) Late cocking Acceleration Deceleration Follow-through

PRACTICE TEST

575

66. If the pitcher were to ignore his coach’s advice to perform the sleeper stretch, which injuries would he be at increased risk for? A. B. C. D. E.

Little Leaguer’s elbow and ulnar collateral ligament (UCL) injury Type II superior labral anteroposterior (SLAP) tear and biceps tendonitis Anterior instability and rotator cuff (RC) tear Posterior instability and RC tear Bennet lesion and valgus extension overload

67. According to the Arthritis Foundation and many expert panels, the first-line pharmacologic agent to treat osteoarthritis is the following: A. B. C. D. E.

Ibuprofen Acetaminophen/hydrocodone Acetaminophen Naproxen Diclofenac

68. The medical director ’s primary role on the day of a mass participation sporting event is that of A. B. C. D.

Caregiver Crisis manager Educator Race spokesperson

69. Which ligament is most commonly injured during an inversion ankle sprain? A. B. C. D. E.

Anterior tibiofibular ligament Anterior talofibular ligament Calcaneofibular ligament Posterior talofibular ligament Posterior tibiofibular ligament

70. _______________ has the greatest impact on training, performance, and recovery A. B. C. D.

Energy consumption Hydration Recovery nutrition Vitamin deficiency

71. A collegiate rower comes to your clinic describing chest pain that has been progressive over the past 3 weeks. She localizes the pain to the posterolateral ribs. She describes the pain is worse when she breathes deeply. Which of the following is most likely to reveal the diagnosis? A. Draw a D-dimer laboratory test, and if negative perform a CT angiography for pulmonary embolism B. Perform a chest x-ray and if negative, obtain a ventilation perfusion scan for spontaneous pneumothorax C. Perform a chest x-ray and if negative, obtain a technetium bone scan D. Perform a chest x-ray and if negative, obtain a dedicated sternal lateral view 72. All of the following are standard knee brace classifications EXCEPT A. B. C. D.

Rehabilitative Active Prophylactic Patellofemoral

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PRACTICE TEST

73. You are treating a football athlete for exertional rhabdomyolysis developed during preseason workouts. The goal urine output for this patient should be: A. B. C. D. E.

1 cc/kg/hr At least 200 cc/hr At least 500 cc/hr No more than 100 cc/hr Does not matter as this is not an important marker to track

74. A 21-year-old college male wrestler presents for evaluation of recurrent tinea corporis, generally affecting his arms and legs. He is wondering if there is something he can take to prevent future infections. He currently has no visible lesions. What prophylactic treatment do you recommend? A. B. C. D. E.

Daily showers with Head-n-Shoulders shampoo. Fluconazole 100 mg po once a week Vitamin C 1000 mg po daily Tetracycline 250 mg po tid Valacyclovir 500 to 1000 mg po daily

75. A mixed martial arts competitor describes chest pain and shortness of breath after his competition. His “rib-springing” test is positive and he suggests it feels like his unhealed rib fractures, but he appears to be in considerable distress. You obtain a chest x-ray that reveals as shown in the following figure. What is the best management?

A. B. C. D.

Supportive treatment with oxygen and close monitoring Needle decompression into the second intercostal space, mid-clavicular line Transfer to the nearest emergency department Intubation for airway protection

76. Which of the following findings on a screening preparticipation examination (PPE) does NOT require further evaluation prior to giving an athlete clearance to participate? A. Family history of myocardial infarction in a grandfather at age 67 B. Personal history of syncope while running a 5k C. Personal history of numbness and weakness in both arms after a tackle in a high-school football game D. Family history of death while sleeping of athlete’s mother at age 43 E. Personal history of palpitations while lifting weights

PRACTICE TEST

577

77. How much body weight should be used for an eccentric exercise protocol in the rehabilitation of an Achilles or patellar tendinopathy? A. B. C. D.

≥100% ≥75% ≥50% ≥25%

78. The main goals of medical coverage of a mass participation event are to A. Ensure the safety of the medical team B. Monitor for undue stress to the community’s emergency management system C. Ensure the safety of participants and event workers and protect the community from being unduly stressed by casualties from the event D. Provide care for all situations and conditions 79. Which of the following is a complex lower extremity stress fracture? A. B. C. D. E.

Calcaneal Medial tibial cortex Anterior tibial cortex Distal metatarsal diaphysis None of the above

80. To fuel serious training, consume A. B. C. D.

5 g branched chain amino acids prior to exercise 3 to 6 mg/kg caffeine during exercise 1.0 to 1.5 g carbohydrate/kg for each hour of serious exercise A very low-carbohydrate, high-fat diet

81. Sickle cell trait, which has been shown to be a cause of sudden death in the exercising athlete, has a incidence in the African American population of what? A. B. C. D. E.

1:6 1:12 1:100 1:500 1:1,000

82. An example of an extremely high-risk sport for eye injuries is A. B. C. D.

Mixed martial arts Basketball Football Swimming

83. A baseball athlete presents to the emergency room where you are moonlighting. He was fielding the ball when the short hopper bounced, missed his glove, and hit him in the groin. He denies use of a protective cup. Your exam shows a young male in discomfort from pain. His scrotum is tender to palpation, swollen, and ecchymotic. There is no blood at the urethral meatus. What is your next step in management? A. B. C. D. E.

Rule out urethral injury, and then place Foley catheter Obtain a scrotal ultrasound as it is fast, reliable, and noninvasive STAT (immediate) CT scan to assess the testicular parenchyma Emergent surgical evaluation in the operating room (OR) Ice and elevate with frequent examinations to monitor for resolution of symptoms

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PRACTICE TEST

84. A 17-year-old female cross-country runner presents with the chief complaint of lack of menses. She reports that she never has had a menstrual period. Although her parents are concerned and insisted that she come in for evaluation, she is not worried about the condition and actually finds the situation quite convenient as it has not affected her training and event participation. She has not been sexually active and denies recreational drug use. What is your initial diagnosis? A. B. C. D. E.

Female athlete triad Primary amenorrhea Asherman’s syndrome Turner ’s syndrome Secondary amenorrhea

85. Loss of consciousness occurs in ______ percent of athletes. A. B. C. D. E.

100% 75% 50% 25% 10%

86. All of the following are likely advantages of performing PPE screenings in a mass, station-based format, as opposed to a private, office-based format, EXCEPT for A. B. C. D.

Increased specialization of providers at each station Increased efficiency Decreased cost per athlete Increased opportunity for preventive counseling

87. In connection with the rehabilitation of stress fractures, which statement is correct for duration and frequency of loading exercises? A. Begin with short-duration loading exercises and gradually increase exercise frequency before duration B. Begin with short-duration loading exercises and gradually increase exercise duration before frequency C. Begin with short-duration loading exercises and only increase the duration D. Begin with short-duration loading exercises and only increase the frequency 88. Which of the following statements best describes automated electronic defibrillators (AEDs)? A. B. C. D.

AEDS can be critical to treating sudden cardiac arrest Bike medic teams are ideal for deploying AEDs Deploying AEDs at the finish line and on the course is recommended All of the above are true

89. Which of the following is not considered part of the Ottawa ankle rules? A. Tenderness to palpation (TTP) over the posterior aspect of distal 6 cm of the tibia B. TTP over the posterior aspect of the distal tip of the medial malleolus C. TTP over the posterior calcaneus

PRACTICE TEST

579

D. Inability to walk four steps immediately after injury E. Inability to walk four steps in the emergency room 90. During luteal phase of the menstrual cycle, female athletes A. B. C. D.

Use reduced levels of carbohydrate during rest and moderate-intensity exercise Use increased levels of carbohydrate during rest and moderate-intensity exercise Use reduced levels of protein during rest and moderate-intensity exercise Use increased levels of fluids during rest and moderate-intensity exercise

Preamble for Q91–94: A 40-year-old female triathlete who is training for an upcoming competition presents with multiple chief complaints and questions regarding improving her performance. She reports that she often sees swimmers on TV stretching their pectoralis muscles and chest and that she has been frequently repeating those motions to improve her range of motion (ROM). Despite this precaution, she has started to have superior right shoulder pain during freestyle stroke, at the entry phase of her hand into the water. She also reports chronic anterior knee pain that is exacerbated during cycling and continues while running. A friend encouraged her to transition from a regular running shoe to a minimalist shoe to alleviate her knee pain but this has not made a difference. 91. Which of these findings would be the most UNLIKELY on examination? A. B. C. D. E.

Positive Neer ’s Scapular dyskinesis Decreased shoulder ER Rotator cuff weakness Painful arc

92. Which modification to her stroke would improve her symptoms? A. B. C. D. E.

Move hand entry point past midline Change from unilateral breathing to bilateral breathing Lowering her elbow (straightening her arm) during recovery phase Increasing the length of her stroke Decreasing kick rate and intensity of kick pattern

93. Examination of her knee is likely to reveal A. B. C. D. E.

Medial joint line tenderness Q angle 200 mmHg and/or a diastolic BP of >110 mmHg) at rest

121. Which of the following is true concerning iron-deficiency anemia? A. B. C. D.

Males and females are affected equally Chronic illness, menstruation, and malnourishment are risk factors Pseudoanemia is another name for iron-deficiency anemia in the athletic population Ferritin levels remain normal until the late stages of iron-deficiency anemia

122. Chest protectors A. B. C. D.

Reduce the incidence of commotio cordis Should be required for all ball sports in the world Are currently required for baseball and softball in the United States Are typically used in sports where chest trauma can occur

123. A 13-year-old boy presents to your sports medicine clinic with a 2-month history of right hip pain. There is no history of injury. His pain is worse with activity and at night. His mom reports intermittent fevers. X-rays of the pelvis and hip reveal a lesion in the pelvis, with onionskin layering. Labs are remarkable for an elevated erythrocyte sedimentation rate (ESR). The most likely diagnosis is A. B. C. D.

Giant cell tumor Ewing’s sarcoma Chondrosarcoma Osteosarcoma

124. A 20-year-old football player sustains a transverse process fracture. When is return to play permissible? A. Once the athlete achieves full, pain-free range of motion B. Following 3 months of nonoperative care including activity modification and bracing

PRACTICE TEST

585

C. When fracture healing is confirmed radiographically D. After consultation with a spine surgeon 125. A 40-year-old right-handed female presents for evaluation of right wrist pain stemming from a minor fall at home that morning. She states that she was kneeling on the floor of her kitchen wiping up some spilled milk, and slipped and fell as she tried to stand up, landing on her right outstretched hand. X-rays of the right wrist show a nondisplaced transverse distal radius fracture. The injury seems out of proportion to the mechanism of injury, which prompts you to: Order wrist MRI arthrogram, looking for a triangular fibrocartilage complex (TFCC) tear Contact the county social services office to investigate suspected domestic abuse Order a dual-energy x-ray absorptiometry (DEXA) scan to assess for suspected osteoporosis Order an MRI with/without contrast for suspected pathologic fracture secondary to metastatic cancer E. Order a bone survey for suspected Padgett’s disease A. B. C. D.

126. Athletes should be sent for emergency department evaluation in the setting of: A. B. C. D. E.

Dizziness Loss of consciousness 20 mmHg drop (supine to stand) Heart transplant Coronary artery bypass graft End-stage renal disease Pacemaker insertion

141. Which of the following statements is not true regarding injuries seen in Paralympic athletes? A. The injury patterns seen in Paralympic athletes are identical to the injury patterns seen in Olympic athletes B. Injury patterns seen in Paralympic athletes are specific to each sport and each type of impairment C. The International Paralympic Committee prospectively studies Paralympic injuries in order to help medical personnel better understand and treat Paralympic athletes D. The International Paralympic Committee prospectively studies Paralympic injuries in order to guide the implementation of safety interventions E. An injury sustained by an athlete with an impairment may have a greater functional consequence for the athlete compared with an identical injury sustained by an athlete without an impairment 142. Which of the following is associated with an increased risk of overuse injuries in youth athletes? A. B. C. D. E.

Use of appropriately sized equipment Five days a week of single sport participation Eleven months a year of single sport participation Supervised training Workload limits

143. A 52-year-old female present to your clinic with a 6-month history of fatigue and chronic musculoskeletal pain. Lab results include a vitamin D level of 18 ng/mL. What statement below is incorrect? A. One would expect the patient’s parathyroid hormone (PTH) level to be low B. Vitamin D stimulates intestinal absorption of calcium and phosphate C. With low vitamin D levels, often need to replace 50,000 international units (IU) per week × 6 to 8 weeks D. Reassurance for the patient, this is a normal level for a postmenopausal female 144. All of the following are indications for surgical referral in patients with spondylolysis EXCEPT A. B. C. D.

Neurologic deficits Chronic, terminal-stage defects Spinal instability Refractory, debilitating pain

145. Which of the following is not typically associated with the female athlete triad? A. B. C. D. E.

Low energy availability with or without an eating disorder Obsessive or perfectionist personality trait/characteristics Hypogonadotropic amenorrhea Low bone mineral density Hyperprolactinemic amenorrhea

PRACTICE TEST

589

146. You are the team physician of a collegiate football team. Just prior to practice in mid-August, you assess the wet bulb globe temperature and obtain a reading of 64°F. Which of the following would you recommend? A. Normal activity for acclimatized and unacclimatized individuals B. Increased rest:work ratio for unacclimatized individuals and normal activity for acclimatized individuals C. Increased rest:work ratio for unacclimatized individuals and acclimatized individuals D. Cancel practice for unacclimatized individuals and limit intense exercise and monitor for signs and symptoms of heat illness in acclimatized individuals 147. Women are at a higher risk of anterior cruciate ligament (ACL) injury than men. Which statement below is incorrect in regard to one of the proposed mechanisms for this risk? A. B. C. D.

Women have a smaller femoral intercondylar notch size Women have increased quadriceps activation Women are more likely to rupture their ACL with a contact injury Women have a thinner mid-substance size of the ACL

148. What acute headache medication is recommended as first-line therapy prior to physical exertion for patients with primary exercise headache? A. B. C. D. E.

Acetaminophen Ibuprofen Oxycodone Gabapentin Indomethacin

149. The most appropriate initial treatment for knee osteoarthritis is: A. B. C. D. E.

Oral nonsteroidal anti-inflammatory drugs (NSAIDs) Neutraceuticals including glucosamine and chondroitin sulfates Intra-articular corticosteroid injection Topical NSAIDs Nonpharmacologic interventions including weight loss and exercise

150. Which of the following is most true regarding strength training in the pediatric population? A. Strength training in the pediatric population is discouraged as it can stunt growth B. Repetitive use of maximal weight in children younger than Tanner Stage 5 is recommended C. Overload should first be achieved with increased resistance, followed by an increase in repetitions D. Resistance exercises should not be performed to the point of severe muscle fatigue E. Strength training with weights is the only recommended resistance training in pediatric athletes

590

PRACTICE TEST

151. A 20-year-old female gymnastics athlete presents with complaints for evaluation of an upper respiratory infection (URI). Her symptoms have been present for the past week. She states that the cough has been keeping her up at night so she has not been sleeping well, and she has increased her coffee intake to help with daytime drowsiness. She also reports a history of urinary leakage during coughing, sneezing, and her floor routine. In addition to her URI, you diagnose her with stress urinary incontinence (SUI). What would be one of the first treatments that you would recommend for her SUI? A. B. C. D. E.

Have her fitted with a vaginal pessary Provide informational handouts and instruction on Kegel exercises Increase coffee intake to 3 to 5 cups a day OB/GYN referral for a sling procedure Bladder BOTOX injections

152. Which one of the following is the least appropriate reason to have a child regularly participate in organized sports? A. B. C. D. E.

To have fun Socialization Develop self-confidence Improve physical fitness To win against his or her peers

153. A 13-year-old boy is in a clinic for a 6-week history of anterior left knee pain. Pain is worse after playing soccer and basketball. There is no history of injury. X-rays of the left knee are negative for a bone lesion. A. B. C. D.

Recommend left knee brace and crutches for NWB status × 4 weeks Physical therapy and avoidance of activities for 6 weeks Physical therapy, activity as tolerated, and follow-up if not improving MRI of the left knee and orthopedic consultation for surgical management

154. A 35-year-old pregnant female presents to your clinic and has questions about exercise. This is her first pregnancy. She has no significant past medical history and no complications in her pregnancy. Absolute contraindications to exercise during pregnancy include everything in the following except: A. B. C. D.

Incompetent cervix Restrictive lung disease Preeclampsia Anemia

155. The normal sonographic appearance of tendon can be described as: A. B. C. D.

Fascicular “Broom end” with tightly packed stippled dots Honeycomb Pennate

156. When the ambient temperature is above 68°F, the primary mechanism for heat loss is: A. B. C. D.

Radiation Convection Conduction Evaporation

PRACTICE TEST

591

157. Absolute contraindications to continuation of an exercise program in a 30-year-old, 28-week pregnant athlete include all of the following except: A. B. C. D. E.

Incompetent cervix or current cerclage Poorly controlled hypertension Restrictive lung disease Placenta previa Premature labor during the current pregnancy

158. A scuba diver develops a headache during a dive. With resurfacing, the headache worsens. What treatment is recommended? A. B. C. D. E.

Ibuprofen Oxygen administration Sumatriptan Morphine Acetaminophen

159. Which of the following is TRUE regarding the relationship between systemic lupus erythematosus and exercise? A. Avoidance of sun exposure is critical to reduce risk of cutaneous and systemic flares among athletes with systemic lupus erythematosus B. Patients with systemic lupus erythematosus are encouraged to continue exercise during fevers, when feeling otherwise well, given the anti-inflammatory benefits of exercise C. The prevalence of atherosclerotic coronary artery disease among those with systemic lupus is no different than among age-matched cohorts without systemic lupus D. The cause of microscopic hematuria among runners with systemic lupus erythematosus can be assumed to be march hemoglobinuria (sports hemolysis) unless proven otherwise E. Echocardiography is unnecessary for clearance of athletes with systemic lupus erythematosus unless they are of northern Italian descent 160. Your patient, a 32-year-old male with type I diabetes mellitus and a BMI of 42 with no other significant past medical or family history and an otherwise normal examination, presents to you requesting your expert recommendations prior to initiating an exercise program. Which of the following would you tell this individual? A. Precede unplanned exercise with 10 to 15 g of carbohydrates 1 hour prior to exercise B. Insulin doses prior to and following exercise should be increased to compensate for hyperglycemia induced by exercise C. Hypoglycemic episodes only occur within the first 60 to 90 minutes after exercise D. Avoid exercise during periods of peak insulin activity E. Carbohydrate-rich snacks following exercise should be avoided to prevent rebound hyperglycemia 161. A 16-year-old runner complains of fatigue at the end of her practice. On further questioning, she has only had 1 menstrual cycle in the past 6 months. Her past medical history is significant for menstrual cycles starting at age 13, and a tibial stress fracture during the past season. Her pregnancy test is negative. Which statement is correct? A. She has a diagnosis of primary amenorrhea B. Obtain lab work including complete blood count (CBC) and thyroid-stimulating hormone (TSH) C. Consult with psychiatry D. She has luteal phase dysfunction

592

PRACTICE TEST

162. Which of the following is true regarding physiologic effects of exercise in youth athletes? A. Speed, power, and mass are lower in children due to lower levels of circulating androgens B. Healthy, well-nourished children are at increased risk for impaired growth and maturation if they regularly engage in prolonged, high-intensity exercise C. Strength gains are greatest in adolescent males at the beginning of their adolescent growth spurt D. Both anaerobic and aerobic performances reach maximal levels by early adolescence 163. The track-and-field coach from the local high school has called you in regard to helping out his team stay healthy for the upcoming season. What statement below is incorrect in regard to risk factors for stress fractures? A. Female runners who have not had a menstrual cycle for 3 months are not at an increased risk B. There is a correlation with leg length discrepancy and lower extremity stress fractures C. Athletes with excessive pronation or supination while running are at an increased risk D. A rapid increase in intense training correlates with increased incidence of stress fractures 164. Which of the following is not a maternal benefit of exercise during pregnancy? A. B. C. D. E.

Improved mood Decreased weight gain Decreased edema Improved gestation diabetes control Increased orientation and response to stimuli postpartum

165. In which of the following scenarios can an athlete be cleared to return to play to football without any further workup? A. Third stinger in a season. No residual symptoms or neurologic deficits B. First episode of cervical cord neurapraxia that lasted 20 minutes. The athlete wants to return to play the same game C. First episode of transient quadriparesis that lasted 10 hours. No residual symptoms or neurologic deficits. No functional cervical stenosis on MRI imaging D. Cervical muscle sprain with persistent limitation in neck range of motion, but fracture, ligamentous instability, and other more serious injuries have been ruled out 166. What is the number one predictor of recurrence of glenohumeral dislocation after first dislocation? A. B. C. D.

Age Type or relocation procedure used Use of external rotation brace Activity level

167. An athlete collapses after crossing the finish line at a marathon. You perform a rapid assessment. The patient is lethargic, flushed, and sweating. Vital signs are: respiratory rate 20, heart rate 110, blood pressure 95/60, rectal temperature 104.5°F. Serum sodium is 138 and glucose is 96. The most important treatment at this time is: A. B. C. D.

Encourage the patient to begin oral rehydration with an electrolyte containing broth Place the athlete in a supine position with legs elevated Rapidly cool the athlete by submerging him or her in a tub of ice water Administer 100 ml of hypertonic saline intravenously over 10 minutes

PRACTICE TEST

593

168. A healthy 16-year-old male football player is practicing outside in the heat when he develops dizziness, diaphoresis, and pallor. He then loses consciousness and has 15 seconds of stiffening and rhythmic jerking of all four extremities. What is the most likely diagnosis? A. B. C. D. E.

Generalized tonic–clonic seizure Heat exhaustion Convulsive syncope Heat stroke Absence seizure

169. A female competitive cyclist presents for evaluation of pubic and pelvic pain after being involved in a crash on her bicycle with another cyclist. In addition to minor superficial abrasions on her right shoulder and forearm, she reports that she sustained direct trauma to her pelvis on her bicycle frame top tube, has moderate pain with all lower extremity activities, and mild pain with urination. She was wearing a helmet and denies any head trauma. On physical examination, she has tenderness to palpation at the pubic symphysis, a superficial abrasion and swelling of the external urethra, and swelling and hematoma formation of the right labia majora. What would your initial evaluation and treatment plan include? A. B. C. D. E.

Pelvic x-ray to assess for a possible pubic ramus fracture Sexually transmitted disease screen for suspected sexual assault Bladder catheter insertion CT scan of the head Emergent incision and drainage of the right labia majora hematoma

170. A Schober test that demonstrates a 1.5 cm increase following forward flexion is suggestive of which of the following: A. B. C. D. E.

Systemic lupus erythematosus Rheumatoid arthritis Lumbar spondylolisthesis Ankylosing spondylitis Normal lumbar spine flexion range of motion

171. Which of the following is not a primary antecedent of performance anxiety? A. B. C. D.

Fear of physical harm Fear of failure Fear of negative affective evaluation Situation ambiguity

172. The primary restraint to valgus stress of the elbow between 30 and 120° degrees of flexion is the? A. B. C. D.

Lateral ulnar collateral ligament Anterior bundle of the ulnar collateral ligament Posterior bundle of the ulnar collateral ligament Transverse oblique bundle of the ulnar collateral ligament

173. Considerations for exercise regimens post knee and hip arthroplasty include: Considering the stress across the bone–implant interface Balancing too much versus too little physical activity Recommending not taking up a new, high-impact sport That there are no definite guidelines regarding exercise regimens post total knee and hip arthroplasty E. All of the above A. B. C. D.

594

PRACTICE TEST

174. Exercise-induced urticaria is associated with all of the following conditions except: A. B. C. D. E.

Swimming in cold water Exercise-induced anaphylaxis Exposure to ultraviolet (UV) radiation Community-acquired methicillin-resistant Staphylococcus aureus (MRSA) Swimming in warm water

175. Which of the following cervical fractures is stable? A. B. C. D.

Compression fracture Extension teardrop fracture Type II odontoid fracture (through base of dens) Hangman’s fracture (bilateral C2 pars fracture) with C2 facet dislocation

176. Which is not a border of the quadrilateral space? A. B. C. D.

Long head of triceps Humeral shaft Teres minor Teres major

177. A cross-country ski racer presents to the medical tent complaining of being cold. The athlete is able to answer your questions appropriately, but does display some dysarthria. He or she is shivering and skin is pale and cool. Blood pressure is 98/70, respiratory rate is 18, and heart rate is 80. You diagnose the athlete with mild hypothermia. All of the following are appropriate treatments except: A. B. C. D.

Giving the athlete warm fluids to drink Administering warm, intravenous saline Removing the athlete’s damp cloths Wrapping the athlete with a warm blanket

178. Physiologic changes and adaptations that occur in the pregnant athlete include which of the following? A. B. C. D. E.

Decreased minute ventilation Decreased stroke volume in the second trimester Decreased respiratory rate Decreased skin vasodilation Decrease in insulin resistance

179. A 20-year-old female collegiate soccer player with no significant medical history has a 30-second generalized tonic–clonic seizure immediately after sustaining a concussion. A head CT in the emergency room is normal. The next day in clinic, she is recovering from her concussion as expected but asks about her risk of future unprovoked seizures. What is the best response? A. Reassurance that her risk of future seizures is not significantly increased B. Explain that her risk of seizures is approximately twice normal, and let her decide if she wants to start a daily antiepileptic medication C. Explain that her risk of seizures is high, and recommend that she start a daily antiepileptic medication D. Order a routine electroencephalogram (EEG) and brain MRI to assess future seizure risk E. Recommend that she retire from playing soccer and all other contact sports

PRACTICE TEST

595

180. A 23-year-old male runner presents with a 3-month history of right knee swelling. He denies trauma to the affected area. He reports 45 minutes of morning stiffness in his fingers and wrists despite 800 mg ibuprofen three times daily. His physical examination is notable for mild metacarpophalangeal joint and proximal interphalangeal joint tenderness without synovitis. Examination of the right knee reveals a moderate-to-large effusion and mild, diffuse tenderness. Lachman and McMurray tests are negative. Knee radiographs are normal. Aspiration of the knee reveals a white blood cell count of 14,000 with 60% lymphocytes. Gram stain and cultures are negative. An MRI of the right knee reveals moderate synovitis with no chondral, ligamentous, or meniscal pathology. What is the most appropriate next step for this patient? A. Begin methotrexate 10 mg per week and folic acid 1 mg per day B. Repeat MRI of the right knee with gadolinium contrast to rule out occult cartilage damage C. Order blood tests including rheumatoid factor and cyclic citrullinated peptide (CCP) antibody for laboratory evidence of inflammatory arthritis D. Discontinue ibuprofen, begin naproxen 500 mg twice daily E. Admit the patient for urgent arthroscopic irrigation and intravenous antibiotics 181. A 21-year-old collegiate football athlete presents with abdominal pain following a “big hit.” He was tackled at the waist but reports that the opposing tackler ’s helmet struck his abdomen with force in the process. On physical exam, you observe an uncomfortable appearing male who is most comfortable in a bent forward position. His pulse is 120 and palpation of the abdomen reveals diffuse tenderness, greatest in the left upper quadrant, with guarding. All of the following should be on your differential diagnosis except: A. B. C. D. E.

Abdominal wall contusion Rib contusion/fracture Rectus hematoma Splenic laceration Ruptured appendix

182. What nerve travels between the two heads of the pronator teres muscle? A. B. C. D.

Median nerve Ulnar nerve Radial nerve Musculocutaneous nerve

183. In older athletes with congestive heart failure, exercise will: A. B. C. D.

Decrease VO2max and increase systolic blood pressure Decrease VO2max and systolic blood pressure Increase VO2max and systolic blood pressure Increase VO2max and decrease systolic blood pressure

184. A 19-year female cross-country runner presents with recurrent sinus congestion, headache, cough, and watery eyes during the fall season. Initial treatment should be: A. B. C. D. E.

Inhaled beta-agonist (albuterol) half-hour before exercise Leukotriene receptor antagonist (montelukast) Intranasal corticosteroids (beclomethasone dipropionate) Ephedrine Long-acting alpha-1 and 2a-agonist (oxymetazoline)

596

PRACTICE TEST

185. In which of the following scenarios can an athlete be cleared to play? A. B. C. D.

Healed C4–C7 surgical fusion Healed teardrop fracture that had required halo stabilization but no surgery Atlanto-occipital Klippel-Feil anomaly Healed clay-shoveler ’s (C7 spinous process) fracture

186. Which type of acromioclavicular joint separation has evidence for conservative and surgical treatment? A. B. C. D.

Type II Type III Type IV Type V

187. A 42-year-old woman presents to your clinic to discuss diving. She is planning on going scuba diving while on a trip to the Caribbean. All of the following are true about scuba diving except: A. B. C. D.

The most common area for barotrauma is the middle ear. Chronic obstructive pulmonary disease is a contraindication to scuba diving. Athletes should wait 6 hours after a dive before flying on an airplane. Pruritus and an urticarial rash are examples of type I decompression illness.

188. The initial treatment of benign exercise-associated collapse includes all of the following except: A. B. C. D.

Placing athlete in supine position and elevating legs and pelvis relative to head Oral rehydration Observing mental status and monitoring heart rate and blood pressure for 15 to 30 min Intravenous fluid administration

189. Cognitive behavioral therapy (CBT) is indicated as a viable treatment for which of the following? A. B. C. D.

Anorexia nervosa Bulimia nervosa Performance anxiety All of the above

190. Regarding osteoarthritis in the elderly, which of the following is true? A. It is the most common cause of pain and disability B. Shearing injuries can result in microtears in the cartilage C. Treatment can include analgesics, physical therapy, unloader braces, activity modification, and surgical interventions D. All of the above 191. A successful rehabilitation program to manage an abdominal contusion includes all of the following components except: A. B. C. D. E.

Avoidance of offending and aggravating activities Pain control with anti-inflammatory medications and cryotherapy Isometric strengthening protocol Eccentric strengthening protocol Functional moment screen to identify risk factors

PRACTICE TEST

597

192. All of the following radial head fractures need surgery except? A. B. C. D.

Fracture with displacement Comminuted fracture Fracture with depression or angulation Nondisplaced fracture

193. Which of the following is the best determination for return to play after an athletic nerve injury? A. B. C. D. E.

Improvement of T2 signal in and around the nerve on MRI Return of normal nerve echogenicity on ultrasound Reinnervation changes seen on needle electromyography (EMG) Resolution of conduction block on nerve conduction study Near normal strength on clinical testing and good performance on sport-specific functional testing

194. All collegiate athletes should be vaccinated against all the following except: A. B. C. D. E.

Hepatitis B Measles, mumps, and rubella Meningococcal Rotavirus Tetanus

195. Which of the following is NOT true about cervical stenosis? A. The best way to assess for functional cervical stenosis is with MRI B. Functional cervical stenosis does not increase an athlete’s risk of neurological damage after cervical spine (C-spine) trauma if the stenosis has not been symptomatic C. Cervical stenosis is part of the diagnostic criteria for spear tackler ’s spine D. The presence of functional cervical stenosis impacts the return-to-play recommendation for an athlete who sustained an episode of transient quadriparesis that fully resolved 196. What is the most common type of clavicle fracture? A. B. C. D.

Medial Midclavicular Distal Spiral

197. An athlete who is mentally struggling with recovering from injury yet does not show signs of significant mental health issues should be referred to: A. B. C. D.

Clinical sport psychologist Educational sport psychology specialist Psychiatrist No referral necessary

198. Before intravenous fluid administration in a case of exercise-associated collapse, which laboratory value should be confirmed? A. B. C. D. E.

CRP Ca Na BUN K

598

PRACTICE TEST

199. You are covering a high-school football game when one of the players goes in for a tackle with his head down and does not immediately get up. You suspect an acute cervical spine injury. Which of the following pieces of equipment should always be removed while you await emergency transport? A. B. C. D.

Face mask Helmet Helmet and shoulder pads Remove no equipment

200. According to the American College of Rheumatology guidelines, all of the following are criteria for knee osteoarthritis EXCEPT A. B. C. D.

Age older than 50 years Morning stiffness for 45 minutes or longer Crepitus with knee motion Bony enlargement

201. Ischemic colitis in the athletic setting is most commonly seen in: A. B. C. D. E.

Endurance runners Individuals engaged in intensive weight training programs Individuals involved in Olympic weight training (cross fit) programs Soccer athletes Mountain climbers

202. The most common direction of an elbow dislocation is? A. B. C. D.

Medial Lateral Posterior Anterior

203. A 30-year-old female elite cyclist has been training for a long-distance race and has been hampered by pain in her anterior thigh and lack of power when climbing hills. She has no symptoms at rest. She has had a normal lumbar and hip MRI. Her physical exam is normal. Which of the following is the most likely diagnosis? A. B. C. D. E.

Lumbar radiculopathy Occult femoral neck stress fracture Femoral vein thrombosis External iliac artery endofibrosis Popliteal artery entrapment syndrome

204. All of the following are risk factors for anaphylaxis except: A. B. C. D. E.

Asthma Nonsteroidal anti-inflammatory drugs (NSAIDs) Atopy Cold water exposure Migraine and vascular headaches

205. The shaft of a long bone is called the A. Physis B. Metaphysis C. Epiphysis

PRACTICE TEST

599

D. Diaphysis E. Cortex 206. Which of the following is TRUE regarding safety in football? A. Spearing is allowed but discouraged by football regulatory organizations B. Cowboy collars have been proven to decrease the risk of stingers/burners C. A National Football League (NFL) player with mild, stable weakness after treatment for a cervical radiculopathy may not return to play D. Head-up, shoulder-first technique is the proper way to initiate a tackle or block 207. Which method of glenohumeral relocation has shown to have a higher rate of complications? A. B. C. D.

Kocher Stimson Cunningham FARES (fast, reliable, and safe)

208. The single greatest factor affecting survival for out-of-hospital cardiac arrest is: A. B. C. D.

Time interval from arrest to defibrillation Prescreening of athlete prior to athletic participation Proximity to nearest hospital Experience of level of medical responders

209. You are covering a high-school football game when one of the players goes in for a tackle with his head down and does not immediately get up. You suspect an acute cervical spine injury. The athlete is complaining of severe neck pain and some altered sensation in his arms. His helmet screws are rusted and cannot be removed, and the trainer ’s angel cannot be found. You are unable to remove the face mask. Which of the following should occur next? A. B. C. D.

Remove no equipment Remove the shoulder pads Remove the helmet Remove the helmet and shoulder pads

210. Four months after a grade II ankle sprain, a collegiate track athlete complains of persistent throbbing ankle pain with plyometric exercises. The most likely diagnosis is A. B. C. D.

Osteoarthritis Chronic ligament injury Osteochondral defect Pseudogout

211. A 21-year-old college female sprinter with a history of asthma presents with symptoms of chest tightness and wheezing during workouts despite being on high dose inhaled corticosteroids. She reports getting very little relief from her albuterol inhaler. She is under a lot of pressure as the conference championships are approaching and she feels like she is letting her team down. On physical exam you note that her lungs are clear to auscultation. You suspect that she may have a component of vocal cord dysfunction contributing to her symptoms. Which one of the following tests would you order next? A. B. C. D.

Chest x-ray Methacholine challenge test Video laryngoscopy CT scan of the head and neck

600

PRACTICE TEST

212. The tendon most commonly involved in lateral epicondylosis is? A. B. C. D.

Extensor digitorum Extensor carpi radialis longus Extensor carpi radialis brevis Brachioradialis

213. Abdominal stabilizers include the: A. B. C. D. E.

Internal oblique and rectus abdominis External oblique and transversus abdominis Internal oblique and transversus abdominis Serratus anterior and lumbricals Obturator internus and the piriformis

214. There has been a skin infection outbreak in the locker room. One of your athletes needed to have a fairly large abscess drained, and cultures isolated methicillin-resistant Staphylococcus aureus (MRSA). If needed, what oral antibiotic would be inappropriate to prescribe to treat an MRSA skin infection? A. B. C. D. E.

Trimethoprim–sulfamethoxazole Doxycycline Clindamycin Cephalexin All of the above would be appropriate to treat MRSA

215. The term for repetitive overuse and stress of a bone leading to microfracture is A. B. C. D. E.

Open fracture Torus fracture Pathologic fracture Greenstick fracture Stress fracture

216. A preparticipation physical was performed on a collegiate athlete. The ECG computer reading suggests an ion channel disorder. Which of the following cardiac diseases is not an ion channel disorder? A. B. C. D.

Catecholaminergic polymorphic ventricular tachycardia Long QT syndrome LV noncompaction Brugada syndrome

217. The most sensitive and specific test to determine the presence of avascular necrosis (AVN) in the hip is: A. B. C. D.

Radiograph Bone scan CT scan MRI

218. All of the following are known risk factors for heat exhaustion except: A. B. C. D. E.

Exertion at or near maximum Dehydration Exercise at sea level Inadequate conditioning Not acclimatized to heat

PRACTICE TEST

601

219. You are covering a collegiate baseball game when the pitcher is hit in the head by a batted ball and collapses, landing on his side. When you arrive at the mound, he is unconscious. Which of the following is your initial step in management? A. B. C. D.

Immediately roll the athlete onto his back to better maintain his airway Initiate cervical spine precautions Logroll the athlete with the help of the coach and athletic trainer Take out your smelling salts to quickly revive the athlete

220. Which of the following medications is indicated for the maintenance of chronic gout? A. B. C. D.

Allopurinol Folic acid Indomethacin Colchicine

221. A golfer comes to see you for thumb pain on the radial aspect, which began after he was on vacation the past week, where he played golf 3 days in a row. On exam, he has tenderness to palpation and swelling over the radial aspect of the wrist and just proximal to this. Which of the following are the tendons involved in this condition? A. B. C. D.

Abductor pollicis brevis and extensor pollicis longus Abductor pollicis longus and extensor pollicis brevis Abductor pollicis brevis and extensor pollicis brevis Abductor pollicis longus and extensor pollicis longus

222. An 18-year-old male is playing football. He is tackled on the field and after the play is noted not to be moving. You are the physician on the sideline and are called to evaluate him. You note that he is unconscious but has a pulse and is breathing. You note that his breathing is shallow and he is intermittently apneic and you suspect airway compromise. Which of the following should you do first? A. B. C. D.

Insert an endotracheal tube via direct laryngoscopy Perform a jaw thrust Begin cardiopulmonary resuscitation (CPR) Perform a head tilt and jaw lift

223. The liver performs all of the following functions except: A. B. C. D. E. F. G. H.

Glycogen synthesis Micturition Plasma protein synthesis Drug detoxification Gluconeogenesis Insulin storage B and F B, E, and F

224. You are in your college training room. After evaluation of her knee injury, one of your athletes, a 19-year-old freshman, asks you when she should get her first Pap smear and how often she should repeat them. She tells you she has been sexually active for about 2 years. What do you recommend? A. She should get her first Pap smear at age 21, regardless of when she became sexually active, and repeat it every 3 years B. She should get her first Pap smear now, as more than 1 year has elapsed since she first became sexually active, and repeat it every 3 years

602

PRACTICE TEST

C. She should get her first Pap smear at age 20, or about 3 years after she became sexually active, and repeat it annually D. She should get her first Pap smear at age 21 with HPV cotesting and repeat this every 5 years, regardless of when she became sexually active E. She should get her first Pap smear at age 21 or 3 years after she became sexually active, whichever comes first, and repeat it every 3 years. 225. Which of the following fracture/dislocation scenarios require(s) emergent or urgent surgical referral? A. A patient with a midshaft femur fracture and difficulty breathing with decreasing oxygen saturations B. A patient with a widely displaced, intra-articular, bicondylar tibial plateau fracture C. A patient with a suspected knee dislocation and impaired sensation and pulses in the foot and ankle D. A patient with two displaced rib fractures and a 24% pneumothorax E. All of the above 226. A 30-year-old male marathon runner presents with a 3-week history of progressive fatigue and exercise intolerance after a flu-like illness. His evaluation leads you to make the diagnosis of viral myocarditis. The most common virus implicated in myocarditis is: A. B. C. D.

Echovirus Adenovirus Influenza Coxsackie B

227. Why is it important to obtain a pelvis and lateral frog-leg and/or Dunn view radiograph of the athlete suspected to have an acetabular labral tear? A. Radiographs are not needed because the labral tear is visualized on magnetic resonance arthrogram. B. Radiographs are the best imaging study to describe femoral neck stress fractures that can occur simultaneously with labral tears. C. Most acetabular labral tears occur in the setting of bony hip deformity, which is best measured at the time of presentation on radiographs. D. Labral tears are depicted by calcification in the superior labrum always visualized on radiographs. 228. The most important factor in the development of exercise-associated hyponatremia is: A. B. C. D. E.

Overconsumption of hypotonic fluids during prolonged exercise Level of conditioning prior to competition Athlete experience Race day temperature below 60°F Atmospheric pressure

229. An athlete is violently tackled in a football game and loses consciousness. The athlete regains consciousness and complains of significant neck pain. You have initiated cervical spine precautions. Which of the following describes the best management approach? A. B. C. D.

Immediately logroll the athlete with the assistance of the coach and athletic trainer Immediately logroll the athlete with a total of four to five people Logroll the athlete directly onto a spine board with four to five people Logroll the athlete directly onto a spine board using cervical traction

PRACTICE TEST

603

230. Keinbock’s disease is avascular necrosis (AVN) of which structure? A. B. C. D.

Femoral head Capitellum Metatarsal head Lunate

231. You are covering the urgent care clinic in a ski town. A 30-year-old female comes in complaining of pain at the ulnar aspect of her thumb around the metacarpophalangeal joint. She says her pain began when her ski pole caught in the snow and pulled on her thumb. On exam, she is tender over the ulnar aspect of the metacarpophalangeal joint, where there is also swelling. Compared to the other side there is laxity with valgus stress. You obtain plain films with stress views since no fracture is seen on initial images. She is more likely to have a Stener lesion if the affected thumb opens more than how many degrees compared to the unaffected side? A. B. C. D.

5° 10° 15° Stener lesion can be present with no difference in laxity between sides

232. A 59-year-old male runner has developed a gradually worsening productive cough over the past 3 to 4 years. He is a former smoker (30 pack-years) but quit 10 years earlier and took up running 1 year ago after being told he had heart disease. He now also has developed occasional wheezing since he started running. Given his respiratory symptoms, he is wondering if it is safe for him to exercise. Which of the following would be the most appropriate counsel for the patient? A. He most likely has chronic obstructive pulmonary disease (COPD) given his smoking history and symptoms. If so, he should continue to exercise given its importance in maintaining quality of life in patients with COPD. B. He most likely has asthma given his history and symptoms. He should stop exercising until his asthma is under control. C. He most likely has COPD given his smoking history and symptoms. Exercise has not been shown to improve quality of life in patients with COPD. D. He most likely has asthma given his history and symptoms. He should continue to exercise but would benefit from visiting with an allergist. 233. A 25-year-old shot-putter presents with acute right upper arm pain and hand swelling after a hard strength workout. His distal radial pulse is intact, but you still order an emergent duplex ultrasound. Your clinical suspicion is confirmed. What can you tell him about his prognosis for returning to sport posttreatment? A. B. C. D. E.

About 90% of athletes return to sport at an average of 5 months It takes 2 years to recover from treatment Few athletes are able to ever return to previous level of competition If he needs surgery, then he will not be able to throw a shot put again He will probably need lifelong anticoagulation and should not do any contact sports

234. Exercise-induced anaphylaxis: A. B. C. D. E.

Is due to phagocytosis of antigens released during exercise Is due to mast cell degranulation Is nonfatal even if left untreated Occurs predictably based on exercise intensity in affected individuals Is rarely associated with seafood allergies

604

PRACTICE TEST

235. You are evaluating a patient with an acute, displaced midshaft tibia fracture. The patient has the following symptoms and signs: significant swelling in the midleg, severe pain in the leg and also in the distal foot and ankle, a cool foot, diminished posterior tibial and dorsal pedis pulses, severe pain when you wiggle the patient’s great toe, and the leg feeling firm to palpation. The best next step is Advise rest, ice, compression, and elevation of the extremity Provide conscious sedation for pain control Emergent orthopedic consultation for closed reduction of the fracture Emergent compartment pressure testing and orthopedic consultation for consideration of emergent fasciotomy E. Elective preexercise and postexercise compartment pressure testing to rule out chronic exertional compartment syndrome A. B. C. D.

236. You are the team physician of a college soccer team. One of your athletes was diagnosed with infectious mononucleosis (IM) recently by his primary care physician after complaining of classic symptoms. Blood work showed an atypical lymphocytosis of greater than 10% atypical lymphocytes and a positive heterophile antibody test. Which statement below best describes when it is safe for the athlete to return to training? A. He or she can return to training after a minimum of 6 weeks since initial diagnosis, there are no longer complaints of significant fatigue, and an abdominal ultrasound demonstrates normal spleen size B. He or she can return to training after a minimum of 3 to 4 weeks, his or her spleen is not palpable on physical exam, and systemic symptoms are improving and not limiting the necessary exercise intensity of playing soccer C. He or she can return to training as soon as systemic symptoms are resolving and no sooner than 2 weeks after diagnosis. No routine spleen examination or imaging is needed for soccer athletes D. He or she can return to training after being afebrile for 48 hours, no longer has abdominal pain, and no longer feels fatigue that would limit his or her play on the field E. He or she can return to training after a minimum of 1 to 2 weeks, systemic symptoms are improving, and an abdominal ultrasound has ruled out splenomegaly 237. The mechanism for the development of athletic pubalgia is: A. B. C. D.

Repetitive hip flexion and abduction Overload to the hip adductors with a rectus abdominis hernia Hyperextension of the rectus abdominis or hernia of the posterior inguinal wall Hyperflexion of the lower abdominal muscles or an inguinal hernia

238. Which of the following is not considered a high-risk group for sudden cardiac death in the National Collegiate Athletic Association (NCAA) population? A. B. C. D.

Swimming Basketball players Males African Americans

239. You are covering a collegiate football game. You watch as an athlete drops his head as he goes in for a tackle and hits helmet to helmet. He gets up after a few seconds and walks over to you, complaining of some mild numbness and tingling in both hands. He has had stingers before and is unconcerned and wants to go back in. What do you do next? A. Evaluate for possible concussion B. Initiate cervical spine precautions

PRACTICE TEST

605

C. Assess for neck range of motion D. Test the athlete’s upper extremity strength 240. The preferred imaging study to evaluate suspected advanced osteoarthritis is A. B. C. D.

X-ray Ultrasound MRI Dual-energy x-ray absorptiometry (DEXA) scan

241. You are covering a high school wrestling match and see one of the athletes thrown to the ground, landing on an extended wrist. He comes to you immediately because of wrist pain. On exam, pain is reproduced with the scaphoid shift test. You see him the next day and obtain plain films of both wrists, with anteroposterior (AP) and pronated clenched fist views. A gap between the scaphoid and lunate bones of more than how many millimeters suggests that scapholunate/ dorsal intercalated segmental instability is more likely to be present? A. B. C. D.

0 mm 1 mm 2 mm 3 mm

242. Which of the following statements regarding exercise-induced bronchospasm (EIB) is true? A. B. C. D.

EIB only occurs in people with asthma Summer sport athletes are at a higher risk for EIB EIB has no association with environmental factors The most common symptoms of EIB include cough, poor performance given level of conditioning, and decreased participation

243. In the older athlete: A. There will be increased tissue stiffness, increased fatty infiltration in muscles, and a decrease in performance over age 75 B. There will be decreased tissue stiffness, increased fatty infiltration in muscles, and a decrease in performance over age 75 C. There will be decreased tissue stiffness, decreased fatty infiltration in muscles, and a decrease in performance over age 75 D. There will be increased tissue stiffness, decreased fatty infiltration in muscles, and a decrease in performance over age 75 244. Which of the following is not a risk factor for exertional heat illness in children? A. B. C. D. E.

Diuretics Hot humid environments Scheduled recovery time between bouts of exertion Deconditioning Chronic disease

245. The most commonly dislocated joint in adults is the A. B. C. D. E.

Glenohumeral joint Femoroacetabular joint Facet joint Scapulothoracic joint Lisfranc joint

606

PRACTICE TEST

246. You are seeing an 18-year-old lacrosse player who sustained a shoulder dislocation 1 week ago, which was successfully reduced in the emergency department. He is in a sling. Your neurovascular exam identifies some numbness over the lateral aspect of his affected shoulder. What is the most likely explanation for this finding? A. B. C. D. E.

Thoracic outlet syndrome C6 radiculopathy Axillary nerve injury Posterior cord of brachial plexus injury Tear of the deltoid muscle

247. It is important to treat a quadriceps contusion within the first 24 hours of the injury because: A. The optimal time for muscle repair is within the first 24 hours. B. Placing quadriceps in flexion during the first 24 hours reduces the risk of the development of myositis ossificans. C. Quadriceps strains and contusions can heal only if aggressive range of motion is initiated soon after the injury. D. If treatment is not completed in the first 24 hours, surgical repair of the muscle is often needed. 248. Which of the following is not a typical indicator of poor psychological adjustment to injury? A. B. C. D.

Dwelling on minor physical complaints Rapid mood swings Apathy Decreased body weight

249. Which of the following statements about athlete susceptibility to upper respiratory infections is true? A. Moderate exercise does not affect an athlete’s susceptibility to upper respiratory infections B. Heavy exercise tends to protect against upper respiratory infections through via decreased cortisol levels and increased IgM levels C. Heavy exercise does not affect an athlete’s susceptibility to upper respiratory infections D. Moderate exercise may be somewhat protective against upper respiratory infections E. Moderate exercise tends to increase an athlete’s susceptibility to upper respiratory infections through upregulation of cortisol and downregulation of IgM and salivary IgA 250. Recent studies have shown that the overall incidence of sudden cardiac death in National Collegiate Athletic Association (NCAA) athletes is approximately? A. B. C. D. E.

1:20,000 1:50,000 1:100,000 1:200,000 1:300,000

251. You are covering a high school basketball game and see an athlete shake her hand after attempting to catch a ball that was thrown to her quickly by a nearby teammate. You evaluate her on the bench and there is swelling and tenderness to palpation at the proximal interphalangeal joint of the index finger. There is also a visible deformity of the finger at that joint, suggesting that a dislocation may have occurred. A dislocation of this joint is most likely to be directed in which direction? A. Dorsal B. Volar

PRACTICE TEST

607

C. Medial D. Lateral 252. Which of the following athletes most likely has asthma? A. 12-year-old male baseball player with 2 weeks of cough after a recent upper respiratory infection B. 19-year-old female runner who complains of wheezing and chest tightness, when running during the fall cross-country season, that resolve after she switches to indoor treadmill workouts in the winter C. 22-year-old male swimmer who recently has been having difficulty finishing his 2-hour daily workouts secondary to fatigue D. 55-year-old male golfer who complains of chronic cough and productive sputum for the past 2 years 253. All of the following are physiologic changes that occur in the older athlete except? A. B. C. D. E.

Decreased maximal heart rate Increased risk of sudden death with exercise Decreased vital capacity Increased cardiac output Decreased vessel compliance

254. A 29-year-old female presents to your clinic. She is 22 weeks pregnant, and has a vacation planned to Mexico in 2 weeks. This is her second pregnancy, and there have been no complications with this pregnancy, or her first pregnancy. She is an avid scuba diver, and is hoping to participate in a dive on her trip. Which statement below is correct for recommendations? A. B. C. D.

Okay to scuba dive, to shallow depth of 25 meters Okay to scuba dive, no limit on depth No scuba dive, okay to snorkel Cancel trip

255. Which of the following is true regarding growth in preadolescents and adolescents? A. Growth spurts in girls occur most frequently between the ages of 12 and 16 years B. Growth spurts in boys occur most frequently between the ages of 14 and 18 years C. Large physiologic differences are seen between girls and boys in preadolescent growth phases D. Girls develop two-thirds of the amount of muscle and twice as much body fat as boys by adolescence 256. Which of the following describes neurapraxia? A. B. C. D. E.

Partial axonal injury with denervation of the affected muscles Complete disruption of the axon and nerve sheath Injury to the nerve myelin, which affects conductivity, but the axon remains intact Interruption of the axon and myelin sheath, but intact nerve stroma Nerve inflammation

257. It is important to determine the location of a femoral neck stress fracture in an athlete because: A. Tension-sided stress fractures frequently progress to displacement and may require surgical intervention for appropriate healing. B. Compression-sided stress fractures frequently progress to displacement and may require surgical intervention for appropriate healing.

608

PRACTICE TEST

C. The location of the stress fracture determines if the bone health of the athlete should be assessed. D. No treatment is needed for compression-sided stress fractures in healthy athletes. 258. A 15-year-old male wrestler presents with the following: significant weight loss, fatigue, and inability to maintain previous levels of performance. He was told by his coach 2 months ago to cut weight so that he could compete in a different weight class. He has since been restricting caloric intake and exercising independently outside of practice. He has an intense fear of gaining weight and thinks he looks fat when he looks in the mirror. His body mass index (BMI) is 17.5 kg/m2. What is the diagnosis? A. B. C. D.

Anorexia nervosa Bulimia nervosa Performance anxiety Burnout

259. You are a team physician for a semiprofessional football team. Over the course of preparticipation evaluations, you become aware that three of your athletes carry blood-borne infections: one each with HIV, hepatitis B, and hepatitis C. All are asymptomatic, and after counseling, you clear each to play. Which athlete carries the greatest risk of transferring their infection to a teammate or competitor based on documented transmissions? A. B. C. D. E.

The athlete with HIV The athlete with hepatitis C The athlete with hepatitis B The athletes with hepatitis B and HIV carry similar risks There have never been documented cases of transmission of any of these viruses between teammates or competitors

260. You are asked by your high-school trainer to see a ninth grade football player after he collapsed at the end of practice over the weekend. You examine him in the high-school training room on Monday because he “can’t get a ride to the office.” He states that this has never happened to him before, it was very hot that day, and he had not eaten anything all day before practice. He denies any funny heart beats and does not know his family history. He feels completely normal now. You review his preparticipation exam (PPE) done by an outside facility, which states that he had an uncle who drowned at 27 on his mother ’s side, he had been raised by his mother so there is no family history from his father ’s side, and his cardiac exam was unremarkable. On your physical exam he has a II/VI holosystolic murmur heard best at the left sternal boarder. The murmur improves when he is supine and gets worse when you ask him to “bear down.” You call his mother to inquire about the uncle who drowned and about the father ’s family history. She is unavailable and the athlete is anxious to get to practice so he does not miss anything. You next step is? A. B. C. D.

Allow him to go to practice, but make him noncontact until he is able to get an EKG Fully restrict him, order an EKG, and pursue his family history Clear him to return to play, but order an echocardiogram Clear him to return to play, as this was a response to the heat and lack of food, but make it very clear to him that he has to eat before practice and take water breaks when he gets thirsty

PRACTICE TEST

609

261. You are covering a college football game and you see the running back tackled while falling on an outstretched arm with the wrist extended. While he gets up quickly after the tackle, he is grabbing the wrist that hit the ground and comes to you on the sideline for an evaluation. On exam, he is tender at the anatomic snuff box and has pain with longitudinal compression of the thumb. You are concerned he has a fracture. A fracture at which part of this bone is more likely to lead to avascular necrosis: A. B. C. D.

Proximal pole Distal pole Waist Anterior pole

610

PRACTICE TEST

ANSWERS 1. B (Chapter 7)

42. C (Chapter 14)

83. B (Chapter 36)

2. C (Chapter 14)

43. C (Chapter 25)

84. B (Chapter 39)

3. B (Chapter 25)

44. E (Chapter 28)

85. E (Chapter 45)

4. D (Chapter 28)

45. B (Chapter 3)

86. D (Chapter 8)

5. D (Chapter 32)

46. A (Chapter 26)

87. A (Chapter 6)

6. B (Chapter 26)

47. C (Chapter 5)

88. D (Chapter 12)

7. C (Chapter 31)

48. E (Chapter 9)

89. C (Chapter 27)

8. B (Chapter 9)

49. B (Chapter 31)

90. A (Chapter 10)

9. D (Chapter 37)

50. C (Chapter 2)

91. C (Chapter 4)

10. C (Chapter 2)

51. A (Chapter 32)

92. B (Chapter 4)

11. C (Chapter 7)

52. C (Chapter 36)

93. E (Chapter 4)

12. A (Chapter 14)

53. A (Chapter 37)

94. A (Chapter 4)

13. C (Chapter 25)

54. C (Chapter 45)

95. D (Chapter 36)

14. C (Chapter 28)

55. D (Chapter 3)

96. A (Chapter 8)

15. C (Chapter 3)

56. B (Chapter 8)

97. D (Chapter 6)

16. C (Chapter 26)

57. D (Chapter 5)

98. B (Chapter 12)

17. B (Chapter 31)

58. C (Chapter 30)

99. B (Chapter 27)

18. A (Chapter 9)

59. C (Chapter 37)

100. D (Chapter 10)

19. B (Chapter 32)

60. B (Chapter 38)

101. B (Chapter 37)

20. D (Chapter 2)

61. B (Chapter 4)

102. B (Chapter 13)

21. C (Chapter 7)

62. C (Chapter 4)

103. D (Chapter 20)

22. E (Chapter 14)

63. D (Chapter 4)

104. C (Chapter 36)

23. B (Chapter 25)

64. D (Chapter 4)

105. D (Chapter 38)

24. D (Chapter 28)

65. E (Chapter 4)

106. E (Chapter 51)

25. C (Chapter 3)

66. B (Chapter 4)

107. A (Chapter 6)

26. D (Chapter 26)

67. C (Chapter 5)

108. C (Chapter 12)

27. C (Chapter 5)

68. B (Chapter 12)

109. D (Chapter 27)

28. D (Chapter 9)

69. B (Chapter 27)

110. B (Chapter 10)

29. A (Chapter 31)

70. B (Chapter 10)

111. D (Chapter 38)

30. E (Chapter 2)

71. C (Chapter 32)

112. D (Chapter 13)

31. D (Chapter 7)

72. B (Chapter 13)

113. D (Chapter 20)

32. B (Chapter 14)

73. B (Chapter 36)

114. D (Chapter 39)

33. B (Chapter 25)

74. B (Chapter 37)

115. B (Chapter 45)

34. B (Chapter 28)

75. B (Chapter 32)

116. C (Chapter 53)

35. A (Chapter 3)

76. A (Chapter 8)

117. D (Chapter 6)

36. C (Chapter 26)

77. A (Chapter 6)

118. D (Chapter 51)

37. A (Chapter 5)

78. C (Chapter 12)

119. D (Chapter 8)

38. A (Chapter 9)

79. C (Chapter 27)

120. D (Chapter 11)

39. B (Chapter 31)

80. C (Chapter 10)

121. B (Chapter 38)

40. A (Chapter 2)

81. B (Chapter 38)

122. D (Chapter 13)

41. B (Chapter 7)

82. A (Chapter 13)

123. B (Chapter 15)

PRACTICE TEST

124. A (Chapter 20)

166. A (Chapter 21)

208. A (Chapter 30)

125. C (Chapter 39)

167. C (Chapter 29)

209. D (Chapter 19)

126. C (Chapter 45)

168. C (Chapter 44)

210. C (Chapter 16)

127. C (Chapter 50)

169. A (Chapter 40)

211. C (Chapter 34)

128. B (Chapter 53)

170. D (Chapter 43)

212. C (Chapter 22)

129. C (Chapter 51)

171. C (Chapter 47)

213. C (Chapter 35)

130. C (Chapter 11)

172. B (Chapter 22)

214. D (Chapter 41)

131. E (Chapter 51)

173. E (Chapter 48)

215. E (Chapter 17)

132. A (Chapter 53)

174. D (Chapter 42)

216. C (Chapter 33)

133. C (Chapter 15)

175. A (Chapter 18)

217. D (Chapter 24)

134. C (Chapter 20)

176. B (Chapter 21)

218. C (Chapter 30)

135. D (Chapter 39)

177. B (Chapter 29)

219. B (Chapter 19)

136. A (Chapter 45)

178. D (Chapter 40)

220. A (Chapter 16)

137. D (Chapter 53)

179. A (Chapter 44)

221. B (Chapter 23)

138. C (Chapter 44)

180. C (Chapter 43)

222. B (Chapter 34)

139. D (Chapter 43)

181. E (Chapter 35)

223. G (Chapter 35)

140. A (Chapter 11)

182. A (Chapter 22)

224. A (Chapter 41)

141. A (Chapter 51)

183. C (Chapter 48)

225. E (Chapter 17)

142. C (Chapter 49)

184. C (Chapter 42)

226. D (Chapter 33)

143. A (Chapter 15)

185. D (Chapter 18)

227. C (Chapter 24)

144. B (Chapter 20)

186. B (Chapter 21)

228. A (Chapter 30)

145. E (Chapter 39)

187. C (Chapter 29)

229. C (Chapter 19)

146. A (Chapter 29)

188. D (Chapter 30)

230. D (Chapter 16)

147. C (Chapter 50)

189. D (Chapter 47)

231. C (Chapter 23)

148. E (Chapter 44)

190. D (Chapter 48)

232. A (Chapter 34)

149. E (Chapter 43)

191. E (Chapter 35)

233. A (Chapter 46)

150. D (Chapter 11)

192. D (Chapter 22)

234. B (Chapter 42)

151. B (Chapter 40)

193. E (Chapter 46)

235. D (Chapter 17)

152. E (Chapter 49)

194. D (Chapter 42)

236. B (Chapter 41)

153. C (Chapter 15)

195. B (Chapter 18)

237. C (Chapter 24)

154. D (Chapter 50)

196. B (Chapter 21)

238. A (Chapter 33)

155. B (Chapter 53)

197. B (Chapter 47)

239. B (Chapter 19)

156. D (Chapter 29)

198. C (Chapter 30)

240. A (Chapter 16)

157. D (Chapter 40)

199. A (Chapter 19)

241. D (Chapter 23)

158. B (Chapter 44)

200. B (Chapter 16)

242. D (Chapter 34)

159. A (Chapter 43)

201. A (Chapter 35)

243. A (Chapter 48)

160. D (Chapter 11)

202. C (Chapter 22)

244. C (Chapter 49)

161. B (Chapter 50)

203. D (Chapter 46)

245. A (Chapter 17)

162. A (Chapter 49)

204. E (Chapter 42)

246. C (Chapter 46)

163. A (Chapter 15)

205. D (Chapter 17)

247. B (Chapter 24)

164. E (Chapter 40)

206. D (Chapter 18)

248. D (Chapter 47)

165. C (Chapter 18)

207. A (Chapter 21)

249. D (Chapter 41)

611

612

PRACTICE TEST

250. B (Chapter 33)

254. C (Chapter 50)

258. A (Chapter 47)

251. A (Chapter 23)

255. D (Chapter 49)

259. C (Chapter 41)

252. B (Chapter 34)

256. C (Chapter 46)

260. B (Chapter 33)

253. D (Chapter 48)

257. A (Chapter 24)

261. A (Chapter 23)

Index

AAI. See ankle arm index; atlanto-axial instability abdomen musculature, 408 preparticipation examination, 92–93 abdominal injuries pain (see exercise-related transient abdominal pain) rectus hematoma, 413–414 strains and contusions, 414–415 ABI. See ankle brachial index abrasions, 360, 429 abrasive conjunctivitis, 363 absence seizure, 486 acetabular labral tears, 294–296 acetaminophen, 41–42 Achilles paratenon, 161 tendinopathy, 163–164, 324 tendon tear, 326 ACL. See anterior cruciate ligament acne mechanica, 429 acromioclavicular joint (ACJ) dislocation, 254–255 actin, 10 active assisted range of motion (AAROM), 59 active rest macrocycle, 105 acute mountain sickness (AMS), 347–348 Adam’s test, 91 adaptive athlete autonomic dysreflexia, 547–548 musculoskeletal injuries, 546–547 orthostatic hypotension, 548 osteoporosis, 550–551 peripheral nerve injuries, 549–550 skin breakdown, 549 thermoregulation, 548 adductor strain, 293 adhesive capsulitis, 261–262 Adson maneuver, 516 advanced cardiac life support (ACLS), 403 aerobic exercise cardiovascular response, 17 cortisol, 18 depression, 22 DM, 22

dyslipidemia, 22 elderly, 21 growth hormone, 18 hypertension, 21 obesity, 22 pregnancy, 453–454 aging on injuries, 527 on performance, 525–527 airplane headache, 490 airway compromise, 402–403 alcohol, 95 aldosterone/antidiuretic hormone, exercise, 18 allergic conjunctivitis, 363 allergic rhinitis, 476–477 allergy and immunology allergic rhinitis, 476–477 anaphylaxis, 468–472 exercise-induced anaphylaxis, 472–473 immunizations, 468, 469 urticaria, 473–476 alpha-thalassemia, 442 altitude illness acute mountain sickness, 347–348 high-altitude cerebral edema, 348 high-altitude pulmonary edema, 348 hypoxia, 347 altitude training, 114–115 American Association for the Surgery of Trauma (AAST) Organ Injury Scale scores for the kidney, 427 American College of Sports Medicine (ACSM) recommendations muscular hypertrophy training, 108 muscular power training, 108–109 muscular strength training, 107–108 American Congress of Obstetricians and Gynecologists (ACOG) Committee Opinion No. 267, 544–545 AMS. See acute mountain sickness anabolic steroids, 51 anaerobic exercise adaptations to, 15 testosterone, 18 613

614

INDEX

analgesics acetaminophen, 41–42 opioids, 42 tramadol, 42–43 anaphylaxis, 468–472 androgen testing, 448 anemia foot-strike hemolysis, 438–439 iron-deficiency anemia, 436–438 sports/dilutional anemia, 438 anesthesia in fracture management, 196–197 angioedema, 473, 474 angiotensin-converting enzyme (ACE) inhibitors, 45, 392 angiotensin receptor blockers (ARBs), 45–46, 392 angulated fracture, 173 anisotropy, ultrasound, 558 ankle, anatomy, 322 ankle and foot injuries Achilles tendinopathy, 324 bursitis, 329–330 calcaneus fracture, 323 chronic ankle instability, 327–328 dislocations, 324 first metatarsophalangeal joint sprain, 329 flexor hallucis longus tendinopathy, 325–326 fractures, 322–324 interphalangeal dislocation, 324 ligament injury/instability, 326–329 Lisfranc joint injury, 328–329 medial ankle sprain, 327 metatarsals fractures, 323 Nunley and Vertullo grading system, 328 osteochondritis dissecans, 330, 338 osteonecrosis, 339–340 os trigonum fractures, 323 peroneal tendinopathy, 324–325 phalangeal fracture, 323 plantar fasciopathy, 325 syndesmotic sprain, 327 talus fracture, 322–323 tendinopathy, 324–326 tendon tears, 326 ankle arm index (AAI), 514 ankle brachial index (ABI), 514 ankylosing spondylitis (AS) diagnosis, 483, 484 exercise, 483–484 presentation, 483 prevalence, 483 treatments, 483 annular fissure, 213 anomalous origin coronary artery, 382 anorexia nervosa, 520 anterior atlanto-axial ligament, 204 anterior capsule shoulder stretching, 33 anterior cruciate ligament (ACL), 301–302

injuries, 306–308, 538–539 injury prevention programs, 37 anterior instability, 27 anterior knee pain fat pad impingement (Hoffa’s syndrome), 311 patellofemoral syndrome, 311–312 plica syndrome, 310–311 anterior longitudinal ligament (ALL), 206 antibiotics, 43, 402 anticoagulated athletes, 101 antidiabetic agents biguanides, 44 insulin and oral medication, 43 meglitinides, 44 sulfonylureas, 43–44 thiazolidinediones, 43 antihypertensives ACE inhibitors, 45 ARBs, 45–46 beta-blockers, 46–47 calcium channel blockers, 45 diuretics, 46 anti-inflammatories, 47 antileukotrienes, 47 anxiety control, 521 aortic dissection, 377 aortic stenosis (AS), 81, 383 apophyseal/epiphyseal avulsion fractures elbow, 333–334 foot, 335 knee, 334–335 pelvis and hip, 334 shoulder, 333 spine, 334 wrist/hand, 334 apophysitis/epiphysitis gymnast’s wrist, 336 Iselin’s disease, 337 little league elbow, 335–336 little league shoulder, 335 Osgood–Schlatter disease, 336, 337 pelvis, 336 Sever’s disease, 336–337 Sinding–Larsen–Johansson disease, 336 arrhythmogenic right ventricular cardiomyopathy, 381 arrhythmogenic right ventricular dysplasia (ARVD), 81–82 arteriosclerotic coronary artery disease diagnosis, 389 epidemiology, 388 physical exam, 388–389 preparticipation screening, 82–83 symptoms, 388 arthrocentesis, 187 arthroscopic debridement chondral lesions, 184

INDEX

knee OA, 183 AS. See ankylosing spondylitis asthma acute exacerbations, 399 diagnosis, 93–94, 398 exercise-induced, 399 history, 93 medications, 47–48 pathogenesis, 398 pediatric athlete, 537 recommendations, 94 symptoms, 93 treatment, 94, 399 athletic heart syndrome, 83, 389–390 athletic pubalgia, 294 atlanto-axial instability (AAI), 99 atlanto-axial instability from Down syndrome, 219–220 atrial fibrillation athletic participation, 395 diagnostic tests, 394 physical exam, 394 risk factors, 393 symptoms, 394 treatment, 394–395 auricular hematoma, 362, 429 autologous blood injection (ABI), 554 autonomic dysfunction, 118 autonomic dysreflexia (AD), 99, 547–548 autopsy-negative sudden unexplained death, 385 avascular necrosis (AVN), 297–298 definition/pathology, 188 epidemiology, 188–189 imaging studies/lab tests, 189–190 medical management, 190 physical exam findings/tests, 189 signs and symptoms, 189 surgical management, 190–191 axillary nerve injury, 508–509 axonotmesis, 501 azithromycin, 407 B1. See thiamin B2. See riboflavin B3. See niacin B6. See pyridoxine back pain causes, 234 history, 234–235 incidence, 234 interventional treatment, 236 pharmacologic treatment, 235 physical examination, 235 return to play, 236 risk factors, 234 therapy programs, 235 bacterial conjunctivitis, 363

Balance Error Scoring System (BESS), 495 balance training, 21 ballistic stretching, 116 barotrauma, 349 basic life support (BLS), 403 Battle’s sign, 360 bayonet fracture, 173 bee stings, 356–357 Bennett fracture, 278 Bennett lesion, 28, 262–263 Berndt and Harty Scale, 186 Bernoulli principle, 31 beta-alanine (BA), 129 beta-blockers, 46–47, 53, 392–393 beta-carotene, 129 beta-hydroxy-beta-methylbutyrate (HMB), 129–130 beta-thalassemia, 442 biceps tendon, 258 bicipital tendinopathy, 27 Bier block, 197 biguanides, 44 biotin, 128 black heel (talon noir), 429 bleeding disorders, 443 blood-borne pathogens hepatitis B and C, 459 HIV, 458–459 Blount’s disease, 339 BLS. See basic life support blunt cerebrovascular injuries (BCVIs), 220–221 blunt trauma orbital, 363–364 renal, 426 scrotum, 424 bone cellular biology, 172 composition, 194 health, 526 matrix, 171 mineral metabolism, 172 nerve, 559 remodeling, 172 resorption, 172 tumors, 178–179 types of, 171–172 bony Bankart, 261 Borg scale, 134 Boss-Holzach-Matter autoreduction technique, 256 Boutonniere deformity, 285 boxer’s fracture, 278 boxing gloves, 158 braces. See also cast; protective equipment; sling knee, 154 Milwaukee, 244 scoliosis treatment, 244 shoulder stability, 258 spondylolysis treatment, 248

615

616

INDEX

brachial neuritis. See Parsonage–Turner syndrome breast cancer, 378 breast contusion, 378 bronchial asthma, 138 bronchodilators, 47–48 chronic obstructive pulmonary disease, 406–407 cystic fibrosis, 402 Brugada syndrome, 386 buckle fractures, 332 buddy taping, 71 bulimia nervosa, 520 burning hands syndrome, 210 burnout, 523 bursitis, 293–294 ankle and foot, 329–330 knee, 313–314 burst fractures, 238–239, 370 CAD. See coronary artery disease caffeine, 130 calcaneus fractures, 323 calcific tendinopathy, 558 calcitonin, 172 calcium channel blockers, 45, 392 calcium pyrophosphate dihydrate (CPPD), 187 callus, 429 cancellous bone, 171–172 cancer, exercise prescription, 143–144 cannabinoids, 52–53 capitellum, 338 capsular ligament, 206 capsule, knee, 302–303 capsuloligamentous structures, 255 cardiac MRI arrhythmogenic right ventricular cardiomyopathy, 381 athletic heart syndrome, 390 HCM, 381 cardiac rehabilitation contraindications, 140 indications, 140 cardiac tamponade, 376–377 cardiology athletic heart syndrome, 389–390 congenital/structural cardiac disease, 380–385 heart disease, acquired, 387–389 hypertension, 390–393 primary electrical disease, 385–387 sudden cardiac death, 379–380 supraventricular arrhythmias, 393–395 cardiopulmonary disease, 528–529 cardiopulmonary resuscitation (CPR), 396 cardiorespiratory endurance ACSM recommendations for, 113 frequency, 113 intensity and duration, 112–113 mode, 112

cardiovascular preparticipation screening arrhythmogenic right ventricular dysplasia, 81–82 arteriosclerotic CAD, 82–83 athletic heart syndrome, 83 chest pain red flags, 80 CV history, 80 ECG, 83–84 family history, 80 HCM, 85 hypertension, 84–85 Marfan’s syndrome, 85–86 murmurs, 86 physical examination, 80 sudden cardiac death, 79–80 syncope, 86–87 valvular disease, 80–81 carpal tunnel syndrome, 511 carpopedal spasms, 343 cartilage, 200 ultrasound, 559 cartilage and joint injuries acute ligament injuries, 191–192 avascular necrosis, 188–191 chondral lesions, 183–185 chondrocalcinosis, 187–188 chronic ligament injuries, 192–193 osteoarthritis, 180–183 osteochondral lesions, 185–187 casting casts, 72–73 complications, 71 fracture reduction, 197 indications, 71 principles of, 70 catecholaminergic polymorphic ventricular tachycardia (CPVT), 386 cauliflower ear. See auricular hematoma cell based therapy, 185 cerebral palsy, 138 Certificate of Added Qualifications (CAQ) examination, 3–4 cervical cord neurapraxia (CCN), 210–211 cervical spine intervertebral disks, 204 joints, 204 kinesiology, 206–207 ligaments, 204–206 muscles, 206 spinal canal, 204 spinal nerve roots, 204, 205 vertebral bodies, 204 cervical spine injuries airway management, 230 cervical cord neurapraxia, 210–211 cervical stenosis, 212–213 congenital anomalies, 219–220 disk pathology, 213–214

INDEX

emergency action plan, 224–225 fractures, 215–217 immediate stabilization, 226–227 initial assessment, 225–226 mechanism of, 224 on-field evaluation, 225 radiculitis/radiculopathy, 214–215 safety considerations, 222 spear tackler’s spine, 215 sports-specific equipments, 227–230 sprains and strains, 218–219 stingers and burners, 209–210 transient quadriparesis, 210–211 vascular injuries, 220–221 whiplash, 219 cervical stenosis, 89, 212–213 chafing, 429 chemoprophylaxis, 462 chest protectors, 157 chest/thoracic pain, 368 chest trauma breast injuries, 378 chest/thoracic pain, 369 dislocations/subluxation/inflammation, 372–373 fractures, 369–372 heart and great vessels, 376–377 penetrating trauma, 377–378 pulmonary conditions, 373–376 chest wall, 368 chest x-ray (CXR) aortic dissection, 377 pericardial effusion and cardiac tamponade, 377 pneumomediastinum, 374 pulmonary contusion, 375 pulmonary embolism, 375 chilblains, 346–347 chlamydia, 463, 464 chlorotrichosis, 430 choline, 128 chondral lesions definition/pathology, 183–184 epidemiology, 184 imaging studies/lab tests, 184 medical management, 184 Outerbridge classification, 184 physical exam findings/tests, 184 signs and symptoms, 184 surgical management, 184–185 chondrocalcinosis definition/pathology, 187 epidemiology, 187 imaging studies/lab tests, 187–188 medical management, 188 physical exam findings/tests, 187 prevention, 188 signs and symptoms, 187 surgical management, 188

chondrosarcoma, 178 chronic ankle instability, 327–328 chronic exertional compartment syndrome, 320 chronic obstructive pulmonary disease (COPD) airflow obstruction, 405 chronic asthma, 405 chronic bronchitis, 405 clinical features, 405 diagnostic studies, 405–406 emphysema, 405 epidemiology, 405 exercise, 528–529 exercise-related issues, 407 physical examination, 405 sports-related issues, 404 treatment, 406–407 chronic traumatic encephalopathy (CTE), 499 clavicle fracture, 251–253 clear cell sarcoma, 170 clonic seizure, 486 coagulopathy, 442–443 coaptation splint, 72 Cobb angle, 243 cognitive behavioral therapy (CBT) depression, 519 eating disorders, 520 cold illness body temperature, 345 chilblains, 346–347 frostbite, 346 hypothermia, 345–346 trench, 347 comminuted fracture, 173 commotio cordis, 376 commotio retinae, 366 compartment syndrome, 199 compartment syndrome, acute, 272, 320 competition macrocycle, 105 complex regional pain syndrome (CRPS) definition and pathophysiology, 490 diagnosis, 491 epidemiology, 490–491 treatment, 491 compression fracture, 173, 238–239, 370–371 computed tomography (CT) scan pulmonary contusion, 375 spondylolysis, 247 stress fracture, 176 concussion biomarkers, 496 biomechanics, 494 chronic traumatic encephalopathy, 499 definition, 493 diagnosis, 495 epidemiology, 493–494 helmets, 156–157 imaging, 495–496

617

618

INDEX

concussion (Cont.) intrinsic and extrinsic factors, 496–497 long-term sequelae, 498 neuropsychological testing, 496 pathophysiology, 494 prevention, 499 return to play (RTP), 497–498 second-impact syndrome, 498 sideline management, 494–495 symptoms, 494 conditioning and training techniques altitude training, 114–115 diminishing returns, 104 endurance training, 111–114 flexibility training, 115–117 general adaptation syndrome (GAS), 103 individuality, 104 overload, 103 overtraining, 117–119 periodization, 104–105 prioritization, 104 progression, 103 recovery, 104 resistance (see resistance training) reversibility, 104 speed and agility training, 109–111 sports specificity, 103 congenital/structural cardiac disease anomalous origin coronary artery, 382 aortic stenosis, 383 arrhythmogenic right ventricular cardiomyopathy, 381 dilated cardiomyopathy (DCM), 381–382 hypertrophic cardiomyopathy (HCM), 380–381 LV noncompaction, 382 Marfan’s syndrome, 382–384 mitral valve prolapse, 383, 385 congestive heart failure, 528 conjunctivitis, 363 contact dermatitis, 430 contusion abdomen, 414–415 breast, 378 liver, 411–412 pulmonary, 374–375 soft-tissue, 360 spleen, 412–413 convulsive syncope, 487 corn (clavus), 429 corneal abrasion, 363, 364 coronary artery disease (CAD), 388–389 cortical bone, 171 corticosteroids, 49, 68, 172, 552–553 cortisol, exercise, 18 costochondritis, 372–373 costovertebral subluxation, 372 creatine (Cr), 53, 130

crush trauma, 424 Cunningham technique, 256 cycling dynamic fit, 39 injuries, 39–40 static bike fit, 37–38 cyclobenzaprine, 235 cyclooxygenase enzyme (COX-1/COX-2) antagonist, 552 cystic fibrosis (CF), 101, 138 epidemiology, 401 frequency, 401 pathophysiology, 402 symptoms, 401–402 treatment, 402 decompression illness, 348–349 decongestants, allergic rhinitis, 476–477 deep heat, 59 deep-venous thrombosis (DVT), 101, 375. See also effort thrombosis degenerative joint disease (DJD), 298–299 degenerative spinal stenosis, 245–246 degenerative tendinopathy, 163 dehydration, 121–122 delayed-onset muscle soreness (DOMS), 18–19 delayed union fracture, 195 Denis’s three-column model, 370 dental injury lip lacerations, 367 tooth avulsion, 366 tooth displacement, 366 tooth fractures, 366 depression, 22, 519–520 De Quervain’s tenosynovitis, 283 dermatology environmental-induced injuries, 430–432 herpes gladiatorum, 433 impetigo/folliculitis/furunculosis, 432–433 mechanical injuries, 429–430 molluscum contagiosum, 433 scabies, 432 seabather’s eruption, 432 skin lacerations, 434 swimmer’s ear, 432 swimmer’s itch, 432 tinea corporis (gladiatorum)/pedis, 433–434 warts, 433 desmoid tumor, 170 developmental dysplasia of the hip (DDH), 297 diabetes mellitus (DM), 22, 138, 529 diagnosis, 445 exercise benefits, 446 exercise prescription and testing, 141–142 exercise risk, 446 hyperglycemia, 445 management, 446–447

INDEX

physiology of exercise, 445–446 preparticipation screening, 94 treatments, 445 type 1 and 2, 445 diaphysis fractures, 173 lesions, 179 diarrhea, 418–419 dilated cardiomyopathy (DCM), 381–382 dilutional anemia, 438 direct testicular injury, 424–425 discogenic pain, 213 disease-modifying antirheumatic drugs (DMARDs), 479–480 disk pathology, 213–214 dislocations ankle and foot, 324 chest trauma, 372–373 elbow, 269 emergencies, 202 hand and wrist injuries, 279–281 indications for referral, 201–202 interphalangeal, 324 knee, 305 lower leg, 317–318 mandible, 361–362 patellar, 304–305 principles, 200 reduction techniques, 201 testicle, 425 disordered eating, 520 displaced fracture, 173 distal biceps rupture, 270 distal interphalangeal (DIP) joint dislocation, 281 distal radial epiphysis, 336 distal radial ulnar joint (DRUJ), 273 dislocation, 279–280 distracted fracture, 173 diuretics, 46, 51 doping, 50 doping pharmacology acetaminophen, 41–42 angiotensin receptor blockers, 45–46 antibiotics, 43 antidiabetic agents, 43–44 antihypertensives, 45–47 anti-inflammatories, 47 antileukotrienes, 47 biguanides, 44 bronchodilators, 47–48 calcium channel blockers, 45 corticosteroids, 49 diuretics, 46 fluoroquinolones, 43 khellin derivatives, 47 meglitinides, 44 sulfonylureas, 43–44

thiazolidinediones, 43 tramadol, 42–43 dorsal extension block splint, 71 double sugar-tong splint, 72 drug testing, 53–55 dynamic restraints, 200 dynamic stretching, 116 dyslipidemia, exercise, 22 ear injury, 362 eating disorders, 520 pediatric athlete, 537 eccentric resistance training, 116 echocardiogram, 79 aortic stenosis, 383 arrhythmogenic right ventricular cardiomyopathy, 381 hypertrophic cardiomyopathy, 381 Marfan’s syndrome, 383 mitral valve prolapse, 383 myocarditis, 387 edge shadowing, ultrasound, 558 educational sport psychology specialists, 521 effort thrombosis, 515 elastic/isodynamic loading, 106 elbow acute compartment syndrome, 272 apophysitis/epiphysitis, 335–336 avulsion fractures, 333–334 bones, 267 dislocation, 269 instability/ligament injury, 269–270 ligaments, 267 muscles, 267 muscle/tendon injury, 270–271 nerves, 268 olecranon bursitis, 271 olecranon fracture, 268–269 osteochondritis dissecans, 338 osteonecrosis, 338 pads, 157 radial head fracture, 268 radius/ulna midshaft fracture, 269 supracondylar fracture, 268 tendinopathy, 164 valgus extension overload, 270 electrocardiogram (ECG), 79 aortic stenosis, 383 arteriosclerotic coronary artery disease, 389 athletic heart syndrome, 389 Brugada syndrome, 386 hypertrophic cardiomyopathy, 381 long QT syndrome, 385 myocarditis, 387 pulmonary embolism, 375 screening and interpretation, 395 short QT syndrome, 385

619

620

INDEX

electrodiagnostic testing (EDX testing), 502–503 electron transport chain, 13, 14 electrotherapy, 59 endocrinology diabetes mellitus, 445–447 female athlete triad, 449–450 menstrual disorders, 447–449 osteoporosis/osteopenia, 449 endurance training ACSM recommendations, 113–114 definitions, 111 factors, 111–112 programming variables, 112–113 energy systems aerobic (oxidative), 13–14 anaerobic (glycolytic), 12–13 ATP-phosphocreatine, 12 environmental illness altitude illness, 347–348 barotrauma, 349 cold illness, 345–347 decompression illness, 348–349 heat illness, 342–345 nitrogen narcosis, 349 enzyme-linked immunosorbent assay (ELISA) screen, 458 epidermal hyperplasia, 429 epididymis/spermatic cord hematoma, 424 epiphysis fractures, 173 lesions, 178 epistaxis, 362–363 Epstein–Barr virus (EBV), 461 erythema migrans (EM) rash, 460 essential amino acids (EAA), 130–131 estrogen–progestin challenge test, 448 eucapnic voluntary hyperventilation (EVH) testing, 93–94 event administration, 147–153 Ewing’s sarcoma, 178 exercise-associated collapse (EAC) anaphylaxis, 356–357 benign exercise-associated collapse, 351 cardiac arrest, 352 emergency evaluation, 351 exercise-associated hyponatremia, 355–356 heat-related illness, 353–354 hypoglycemia, 355 hypothermia, 354–355 postural hypotension, 351–352 prevention, 441–442 sickle cell trait, 357 exercise-associated GI symptoms, 410 exercise-associated hyponatremia (EAH), 355–356 exercise-induced anaphylaxis (EIA), 357, 472–473 exercise-induced bronchospasm (EIB)

diagnosis, 400 epidemiology, 399–400 pathogenesis, 400 symptoms, 399 testing, 400–401 treatment, 401 exercise-induced urticaria, 431 exercise physiology aerobic exercise, 14–15 anaerobic exercise, 15 cardiovascular response, 17 children, 19 chronic diseases, 21–22 delayed-onset muscle soreness, 18–19 elderly, 19–21 endocrine response, 18 energy systems, 12–14 flexibility, 16 immune system response, 18 lactate kinetics, 17 muscles, 10–12 resistance exercise, 15–16 respiratory response, 18 exercise prescription and testing cancer athletes, 143–144 cardiovascular/cerebrovascular disease, 140–141 diabetes mellitus, 141–142 fibromyalgia, 142–143 geriatric athlete, 139 HIV athletes, 143 lactate (anaerobic) threshold, 137 medical clearance/screening, 135–136 osteoarthritis athletes, 144 osteoporosis athletes, 144 pediatric athlete, 137–139 principles, 133–135 pulmonary disease athlete, 144–145 VO2max, 136–137 weight control exercise, 145 exercise-related transient abdominal pain (ETAP) diagnosis and treatment, 410–411 history, 410 incidence, 410 physical exam, 410 exertional heat illness (EHI), 534 exertional heatstroke (EHS), 343, 353–354 exertional rhabdomyolysis complications, 421 diagnosis, 420 pathophysiology, 420 risk and confounding factors, 420 treatment, 420–421 exhaustion phase, GAS, 103 external compression headache, 490 external iliac artery endofibrosis (EIAE), 515 extrusion, 237

INDEX

eye preparticipation screening, 91 structure, 358, 359 eye injury commotio retinae, 366 conjunctivitis, 363 corneal abrasion, 363, 364 foreign body, 363 hyphema, 364–365 lid lacerations, 365–366 orbital blunt trauma, 364 periorbital hematoma, 364 retinal detachment, 365 retinal hemorrhage, 366 retrobulbar hemorrhage, 366 ruptured globe, 365 scleral laceration, 365 subconjunctival hemorrhage, 364 traumatic iritis, 366 vitreous hemorrhage, 365 FABER’s test, 289 face nerves, 358–359 shields, 154 trigeminal nerve, 359 vascular anatomy, 359 facial nerve, 358–359 facial structures, 358 failed healing response theory, 163 fat pad impingement (Hoffa’s syndrome), 311 fats, 125–126 febrile illness, 460 Federal Educational Rights and Privacy Act (FERPA), 6 female athlete. See also female athlete triad anterior cruciate ligament injuries, 538–539 female athlete triad, 449–450 decreased BMD, 96 disordered eating, 95–96 evaluation, 96, 542, 543 low BMD, 540–541 low energy availability, 539–540 menstrual dysfunction, 540 menstrual irregularities, 96 outcomes and future risk, 542 prevalence, 541 prevention, 542–543 return to play, 542 treatment, 97, 541–542 femoral acetabular impingement (FAI), 296–297 femoral condyles, 338 femoral neck stress fracture, 288 femoral shaft fracture, 289–290 ferritin, 79, 100 fibromyalgia (FM), 142–143

fibula fracture, 316, 317 fibular nerve injuries, 512–513 Finkelstein’s test, 283 first metatarsophalangeal joint sprain, 329 flexibility training ACSM recommendations, 116 ankylosing spondylitis (AS), 484 elderly, 21 factors, 115–116 muscle soreness, 117 preactivity stretching, 117 programming variables, 116 regular stretching, 117 stretching and injury prevention, 117 warm-up, 116–117 flexor hallucis longus tendinopathy, 325–326 fluid replacement beverage, 122 dehydration, 121–122 hyperhydration, 122 hyponatremia, 122–123 volume recommendation, 122 fluoroquinolones, 43 focused assessment with sonography for trauma (FAST), 560 food-dependent, exercise-induced anaphylaxis (FDEIA), 357, 472 foot apophyseal/epiphyseal avulsion fractures, 335 osteonecrosis, 339–340 football gloves, 157 helmets, 155–156 padding, 157 foot-strike hemolysis, 422, 438–439 forefoot strike (FFS), 35 foreign body, 363 Fothergill sign, 414 fracture acute, 173 angulated, 173 ankle, 322 avulsion, 333–335 bayonet, 173 Bennett, 278 boxer’s fracture, 278 buckle (torus), 332 burst fractures, 238–239 calcaneus, 323 clavicle, 251–253 closed, 173 comminuted, 173 complete, 332 complications, 195 displaced, 173 distracted, 173

621

622

INDEX

fracture (Cont.) epiphyseal, 332 fractures, 322–324 greenstick, 332 healing, 173–175 metatarsals, 323 os trigonum, 323 patellar, 303 phalanges, 323 plastic deformation, 332 radiologic description, 195–196 rib fracture, 369–370 Segond, 303 slipped capital femoral epiphysis, 332–333 sternal fracture, 370 stress (see stress fracture) stress fx’s, 323–324 talus, 322–323 thoracic vertebrae, 370–371 tibial plateau, 303 fracture healing, 173–175 factors affecting, 174–175, 194–195 inflammatory stage, 173, 194 remodeling stage, 174, 194 repair stage, 173–174, 194 fracture management compartment syndrome, 199 indications for referral, 198 nerve injury, 199 open fractures, 198 principles of, 194–195 reduction techniques, 196–198 skin tenting, 199 soft-tissue damage, 199–200 vascular compromise, 198–199 Freiberg’s disease, 188 Freiberg’s infraction, 177, 339–340 friction blister, 430 Froment sign, 510 frontal sinus fracture, 360–361 frostbite, 346, 431 functional changes, aging, 526 gait phases in running, 34–36 phases in walking, 33–34 galactorrhea, 447 gall bladder, 409 gamekeeper’s thumb, 282–283 ganglion cysts, 286 GAS. See general adaptation syndrome gastric bleeding, 436 gastrocnemius tear, 318–319 gastroenterology. See also abdominal injuries abdominal musculature, 408 gall bladder, 409 large intestine, 409–410

liver, 408–409 pancreas, 410 small intestine, 409 spleen, 409 gastroesophageal reflux disease (GERD), 417–418 gastrointestinal (GI) bleeding, 416–417 gene doping, 52 gene manipulation, 55 general adaptation syndrome (GAS), 103 generalized tonic–clonic (GTC) seizure, 486 genetics, tendinopathy, 164 GERD. See gastroesophageal reflux disease geyser sign, 254 giant cell tumors, 178 Gilmore’s groin, 294 GIRD. See glenohumeral internal rotation deficit glenohumeral internal rotation deficit (GIRD), 27 glenohumeral joint (GHJ) dislocation, 255–257 gloves, 157–158 glucocorticoids, 47, 53, 399 glycolysis, 12–13 goggles/glasses, 154–155 golfer’s nails, 430 gonadotropin, 448 gonorrhea, 464 greater trochanteric pain syndrome (GTPS), 293–294 green hair. See chlorotrichosis greenstick fracture, 173, 196 growth factors, 51 growth hormone, exercise, 18 GTPS. See greater trochanteric pain syndrome gymnast’s wrist, 286, 336 HACE. See high-altitude cerebral edema Halstead (costoclavicular) maneuver, 516 hamate hook fracture, 275–277 hamstring strains, 292 hand and wrist apophyseal/epiphyseal avulsion fractures, 334 carpal tunnel, 274, 275 distal radial ulnar joint, 273 osteonecrosis, 338 triangular fibrocartilage complex, 273 ulnar variance, 273 hand and wrist injuries dislocations, 279–281 distal radius fracture, 275 distal ulna fracture, 275 ganglion cysts, 286 hamate hook fracture, 275–277 instability, 281–283 metacarpal fractures, 277–278 muscle/tendon injuries, 283–285 nail bed injuries, 286 phalangeal fracture, 278–279 radial epiphysitis (gymnast’s wrist), 286 scaphoid fracture, 275–276

INDEX

TFCC injury, 285–286 volar plate fracture, 279 handlebar palsy. See ulnar neuropathy HAPE. See high-altitude pulmonary edema headache airplane headache, 490 diving headache, 490 external compression headache, 490 high-altitude headache, 490 posttraumatic, 489 primary exercise headache, 488–489 Health Insurance Portability and Accountability Act of 1996 (HIPAA), 6 heart disease, acquired arteriosclerotic coronary artery disease, 388–389 commotio cordis, 388 myocarditis, 387–388 heat acclimatization, 344 heat exhaustion, 353 heat illness body temperature, 342 exertional heatstroke, 343 exhaustion, 343 heat cramps, 343 heat edema, 342–343 heat tetany, 343 miliaria rubra, 342 prevention of, 344–345 return to sport, 343–344 risk factors, 342 sunburn, 343 syncope, 343 thermoregulation, 342 helmets certification, 155 concussions, 156–157 football, 155–156 hockey, 156 lacrosse, 156 hematocele, 424 hematologic disorders bleeding disorders, 443 coagulopathy, 442–443 “foot-strike” hemolysis, 438–439 iron-deficiency anemia, 436–438 iron deficiency without anemia, 439 sickle cell disease, 439 sickle cell trait, 439–442 sports/dilutional anemia, 438 thalassemia, 442 hematoma block, 197 hematuria, 421, 441 hemoglobinuria, 421–422 hemophilia, 101, 138, 443 hemothorax, 374 hepatitis B virus (HBV), 459 hepatitis C virus (HCV), 459

hepatomegaly, 92–93 herniated nucleus pulposis (HNP) anatomical descriptors, 236 diagnosis, 237 morphologically defined, 236–237 pathophysiology, 236 treatment, 237–238 herniation disk pathology, 213 herpes gladiatorum, 433 Hgb solubility test, 441 high-altitude cerebral edema (HACE), 348 high-altitude headache, 490 high-altitude pulmonary edema (HAPE), 348 highly active antiretroviral therapy (HAART), 458–459 hip apophyseal/epiphyseal avulsion fractures, 334 AVN, 188 impingement test, 289 osteonecrosis, 339 hockey gloves, 157 helmets, 156 padding, 157 Hoffa’s syndrome, 311 hormone antagonists and analogs, 51 housemaid’s knee, 314 human immunodeficiency virus (HIV) diagnosis, 458 epidemiology, 458 exercise prescription and testing, 143 treatment, 458–459 human papillomavirus (HPV), 464, 465 humeral head epiphysis, 335 hyaluronic acid (HA), 48, 70 hydroxychloroquine, 482 hyperhydration, 122 hypertension classification, 390 diagnosis, 391 exercise, 21 lab evaluation, 391 participation in sports, 393 pathophysiology, 390–391 pediatric athlete, 537 physical exam, 391 preparticipation screening, 84–85 risk factors, 391 symptoms, 391 treatment, 392–393 hyperthermia, 452 hypertrophic cardiomyopathy (HCM) diagnostic tests, 381 epidemiology, 380 physical exam, 380–381 symptoms, 380 hyphema, 364–365 hypoglycemia, 355

623

624

INDEX

hyponatremia, 122–123 hyposthenuria, 441 hypothenar hammer syndrome, 516–517 hypothermia, 354–355 assessment/treatment, 346 mild, 345 moderately severe, 345 risk factors, 345 severe, 346 hypoxia, 164–165, 347 hypoxic training. See altitude training iatrogenic septic arthritis, 66 ICSs. See inhaled corticosteroids identity awareness, 522 iliopsoas/iliopectineal bursa, 294 iliopsoas muscle–tendon complex disorders, 290–291 iliotibial band (ITB) friction syndrome, 305 iliotibial band pain, 292–293 IM. See infectious mononucleosis immune deficiency, overtraining, 118 immunizations, 462 impetigo/folliculitis/furunculosis, 432–433 impingement, tendinopathy, 164 infectious disease HBV and HCV, 459 HIV, 458–459 immunizations, 462 infectious mononucleosis, 461 influenza, 462 Lyme disease, 460–461 MRSA, 465–466 septic joints, 462–463 sexually transmitted infections, 463–465 upper respiratory tract infection, 460, 465 infectious mononucleosis (IM), 98, 461 inflammation, tendinopathy, 164 influenza, 462 informed consent, 5 ingrown toe nail (onychocryptosis), 430 inguinal hernia, 93 inhaled corticosteroids (ICSs) asthma, 399 chronic obstructive pulmonary disease, 407 cystic fibrosis, 402 exercise-induced bronchospasm (EIB), 401 insulin, 18, 43 insulin pumps, 446–447 intellectual and developmental disability, 138–139 intermittent hypoxic exposure, 115 internal (posterior–superior) impingement, 27 interphalangeal dislocation, 324 intersection syndrome (extensor tenosynovitis), 283–284 interspinous ligament, 206 intertransverse ligament, 206 interval training, 113

intervertebral disks, 204 intra-articular fracture, 173 intranasal corticosteroids (INSs), 476 intravenous (IV) iron, 437 iron, 129 liquid iron, 437 iron-deficiency anemia, 100 epidemiology, 436 etiology, 436–437 laboratory values, 437 physical exam, 436 presentation, 436 treatment, 437–438 ischemic colitis, 415–416 ischial bursa, 294 Iselin disease, 177–178, 337 isokinetic strengthening, 61 isometric strengthening, 60 isotonic strengthening, 60 Jersey finger, 284 jogger’s nipples, 430 joint cervical spine, 204 composition, 200 knee, 301 joint and soft-tissue injections contraindications, 66 corticosteroids, 68 diagnostic indications, 64–65 hyaluronic acid preparations, 70 local anesthetics, 69 musculoskeletal ultrasound, 65 postprocedure instructions, 67 principles, 64 risks and complications, 66–67 sterile technique, 67 supplies used for, 67 therapeutic indications, 65 timing of, 65–66 joint capsule, 200 joint disorders back and leg exam, 90 cervical exam, 90 elbow and hand exam, 90 general inspection, 90 musculoskeletal history, 89 screening exam, 90 shoulder exam, 90 jumper’s knee, 305 jumping, 37 Karvonen formula, 11 khellin derivatives, 47 kidney AAST Organ Injury Scale scores, 427 preparticipation screening, 92

INDEX

Kienbock’s disease, 189, 338 Klippel–Feil syndrome, 220 knee anterior knee pain, 310–312 avulsion fractures, 334–335 bursitis, 313–314 capsule, 302–303 degenerative joint disease, 313 dislocation, 304–305 fractures, 303–304 instability/ligament injuries, 306–310 joints, 301 ligaments, 301–302 meniscal pathology, 312–313 menisci, 302 muscle/tendon injuries, 305–306 osteoarthritis clinical criteria, 181 osteochondritis dissecans, 338, 339 osteonecrosis, 339 knee dislocations, 202 kneepads, 157 knee pain, cycling, 39 Kocher’s and Hippocratic techniques, 256 Kohler’s disease, 340 Krebs cycle, 13, 14 labial trauma, 456 labral tears adhesive capsulitis, 261–262 shoulder injuries, 261 throwing shoulder, 262–263 lacerations facial nerve, 359 lid, 365–366 lip, 367 liver, 411–412 scleral, 365 skin, 434 soft-tissue, 360 spleen, 412–413 lace-up ankle brace, 154 lacrosse gloves, 158 helmets, 156 padding, 157 lactate kinetics, 17 landing, 37 landmark-guided injections (LMGIs), 560 large intestine, 409–410 laryngeal injury, 367 lateral collateral ligament (LCL) injuries, 309–310 lateral epicondylopathy, 271 lateral ulnar collateral ligament (LUCL) injury, 270 Le Fort type facial fractures, 361 Legg–Calve–Perthes disease, 339 leukotriene modifiers asthma, 399

exercise-induced bronchospasm (EIB), 401 leukotriene receptor antagonists (LTRAs), 476 Lhermitte’s sign, 208 lid lacerations, 365–366 lift-and-slide technique, 227 ligament injury/instability ACL injuries, 306–308 acute, 191–192 chronic, 192–193 chronic ankle instability, 327–328 first metatarsophalangeal joint sprain, 329 lateral ankle sprain, 326–327 LCL injuries, 309–310 Lisfranc joint injury, 328–329 MCL injuries, 309 medial ankle sprain, 327 PCL injuries, 308 PLC injuries, 310 syndesmotic sprain, 327 ligament injuries, acute definition/pathology, 191 epidemiology, 191 imaging studies/lab tests, 191–192 medical management, 192 physical exam findings/tests, 191 prevention, 192 signs and symptoms, 191 surgical management, 192 ligaments cervical spine, 204–206 knee, 301–302 ultrasound, 559 ligamentum flavum, 206 Lisfranc joint injury, 328–329 Little Leaguer’s elbow, 27, 177 liver anatomy, 408–409 function, 409 laceration and contusion, 411–412 local anesthetics, 69 local nerve blocks, 197 long-acting inhaled beta-2 agonists (LABAs) asthma, 399 exercise-induced bronchospasm (EIB), 401 long-acting muscarinic antagonist (LAMA), 406–407 long arm cast, 73 long arm posterior splint, 72 long QT syndrome (LQTS), 385 long thoracic nerve injury, 508 lower leg injuries acute compartment syndrome, 320 chronic exertional compartment syndrome, 320 fibula fracture, 316, 317 instability/dislocation, 317–318 medial tibial stress syndrome, 319–320 muscle/tendon injury, 318–319 popliteal artery entrapment, 320–321

625

626

INDEX

lower leg injuries (Cont.) stress fractures, 316–317 tibial fracture, 315 lower-limb nerve injuries fibular nerve injuries, 512–513 meralgia paresthetica, 512 Morton’s interdigital neuroma, 513–514 obturator nerve injury, 512 saphenous nerve injury, 512 tarsal tunnel syndrome, 513 LQTS. See long QT syndrome lumbarization of the S1 vertebra, 234 lumbar pain, 39 lumbar spine bony anatomy, 232, 233 nerve, 233 soft tissue, 232–233 spinal variants, 234 lumbar spine injuries. See also back pain; cervical spine injuries; radiculopathy degenerative spinal stenosis, 245–246 fractures, 238–239 herniated nucleus pulposis, 236–238 low back pain, 234–236 lumbar strain, 239–240 sacroiliac (SI) joint complex pain, 241–242 scoliosis, 242–245 spondylolisthesis, 248–249 spondylolysis, 246–248 zygapophyseal (facet) joint pain, 240–241 lumbar strain, 239–240 lunate and perilunate dislocation, 280 lung, 368 lunotriquetral/volar intercalated segmental instability, 282 Lyme disease, 460–461 lymphedema, 378 macrocycle, 104 magnetic resonance imaging (MRI) avascular necrosis (AVN) of the hip, 189–190 herniated nucleus pulposis, 237 spondylolysis, 247 stress fracture, 176, 177 maintenance of certification (MOC), 4 Maisonneuve fracture, 316, 317 major depressive disorder (MDD), 519–520 malabsorption syndromes, 93 mallet finger, 71, 284 malunion fracture, 195 mandible fractures and dislocations, 361–362 march hemolysis, 422 Marfan’s syndrome, 85–86, 382–383 masking agents, 52 master athlete age effect on injuries, 527 age impact on performance, 525–527

exercise status post-joint arthroplasty, 529–530 exercise with chronic disease, 527–529 maximal steady-state training, 112–113 MDD. See major depressive disorder medial ankle sprain, 327 medial collateral ligament (MCL), 302 medial epicondyle apophysis, 336 medial epicondylopathy, 271 medial tension injuries, 27 medial tibial stress syndrome, 319–320 median nerve, 268 mediastinum, 368 meglitinides, 44 menisci, 302 meniscofemoral ligament, 302 menstrual disorders amenorrhea, 447, 448 androgen testing, 448 estrogen–progestin challenge test, 448 gonadotropin levels, 448 history and physical examination, 447–448 pregnancy assessment, 448 progestin challenge test, 448 thyroid-stimulating hormone, 448 meralgia paresthetica, 512 mesenchymal stem cell therapy, 555 metabolic changes, 526–527 metabolic specificity, 103 metacarpal fractures, 277–278 metacarpophalangeal joint dislocation, 280 metaphysis, fracture, 173 metatarsals fractures, 323 methicillin-resistant Staphylococcus aureus (MRSA), 465–466 microfracture, chondral lesions, 185 migraine headache, 487 miliaria rubra, 342 mitral valve prolapse (MVP), 81, 383, 385 molluscum contagiosum, 433 mood disturbance, overtraining, 118 Morton’s interdigital neuroma, 513–514 mosaicplasty, chondral lesions, 185 MOT. See myositis ossificans traumatica motility disorders, 418–419 murmurs, 86 muscle action type, 106 cervical spine, 206 compartment pressure testing, 73 contraction, 11–12 elbow, 267 exercise physiology, 10–12 fiber types, 12 shoulder, 253, 254 strength factors, 106 ultrasound, 559

INDEX

muscle injuries elbow, 270–271 hand and wrist injuries, 283–285 knee, 305–306 lower leg, 318–319 myositis ossificans traumatica, 168–169 pelvis, hip, and thigh injuries, 290–293 shoulder injuries, 258–261 strains, 167–168 muscular dystrophy, 139 muscular endurance training, 113–114 musculoskeletal preparticipation screening cervical stenosis, 89 joint disorders, 89–90 scoliosis, 90–91 musculoskeletal rehabilitation baseball diamond approach, 58–61 principles of, 61–62 stress fractures, 62 tendinopathy, 62 tissue injury and repair phases, 57–58 MVP. See mitral valve prolapse myocarditis complications, 388 diagnosis, 387 epidemiology, 387 physical exam, 387 symptoms, 387 treatment, 387–388 myoclonic seizure, 486 myofibrils, 10–11 myoglobinuria, 422 myositis ossificans traumatica (MOT), 168–169 nail bed injuries, 286 narcotics, 52 nasal fractures, 361 neck distraction test, 208 fracture, 278 injury, 367 pain, 207–209 structures, 358 needle decompression, 373 nephrolithiasis, 423 nephrology and urology AAST Organ Injury Scale scores for kidney, 427 exertional rhabdomyolysis, 420–421 hematuria, 421 hemoglobinuria, 421–422 myoglobinuria, 422 nephrolithiasis, 423 proteinuria, 422–423 pudendal nerve injury, 423–424 renal trauma, 426–428 scrotal trauma, 424–425 testicular torsion, 425–426

nerve injury, athletic evaluation, 502–504 injections, 505 mechanisms, 502 medications, 505 nerve recovery, 504–505 nonpharmacologic pain relief, 505 rehabilitation, 505 return to play, 506 surgery, 505–506 nerve injuries of limbs. See also vascular injuries of limbs carpal tunnel syndrome, 511 magnetic resonance neurogram, 504 Morton’s interdigital neuroma, 513–514 neurogenic thoracic outlet syndrome, 506–511 Parsonage–Turner syndrome, 507 pronator syndrome, 511 radial nerve injuries, 509 Seddon classification, 501 tarsal tunnel syndrome, 513 ulnar neuropathy, 509–511 neuralgic amyotrophy, 265–266 neural tendinopathy, 165 neurapraxia, 501 neurodynamic (dural tension) tests, 208 neuroendocrine dysfunction, overtraining, 118 neurogenic thoracic outlet syndrome (N-TOS), 506–507 neurologic preparticipation screening seizure, 87 stingers/burners, 87 transient quadriparesis (TQ), 88–89 traumatic brain injury, 88 neurology complex regional pain syndrome, 490–491 epilepsy, 486–488 headache, 488–490 seizure, 486 neuromuscular specificity, 103 neuropathy, cycling, 39–40 neurotmesis, 501 niacin, 128 nitrogen narcosis, 349 Noble’s test, 305 nondisplaced fracture, 173 nonsteroidal anti-inflammatory drugs (NSAIDs), 48, 165–166, 183, 552 nonunion fracture, 195 nose injury, 362–363 NSAIDs. See nonsteroidal anti-inflammatory drugs nuchal ligament, 206 Nunley and Vertullo grading system, 328 nutrition carbohydrates, 123–124 fats, 125–126

627

628

INDEX

nutrition (Cont.) fluid replacement, 121–123 metabolism, 126–127 pediatric athlete, 535 principles of, 121 protein, 124–125 supplements, 129–131 vitamins/minerals, 127–129 weight management, 131–132 OA. See osteoarthritis Ober’s test, 305 obesity exercise, 22 pediatric athlete, 139 oblique fracture, 173 obstetrics and gynecology exercise recommendations, 453–455 fetal health, 452 labial trauma, 456 lactation considerations, 453 musculoskeletal factors, 453 pelvic floor dysfunction, 455–456 obturator nerve injury, 512 OCD. See osteochondritis dissecans 2-octylcyanoacrylate (Dermabond), 434 ocular trauma, 560 olecranon bursitis, 271 open fractures, 173, 196 opioids, 42 optimal exercise prescription, 133–135 orbital blowout fracture, 361 orbital blunt trauma, 364 Organ Injury Severity Scale, 427 organomegaly, 92–93 orthostasis, 343 orthostatic hypotension, 548 Osgood–Schlatter disease, 177, 336, 337 osteitis pubis, 297 osteoarthritis (OA) clinical symptoms/diagnosis, 181 definition/pathology, 180 diagnosis, 481 epidemiology, 180–181 exercise, 481, 527–528 exercise prescription and testing, 144 imaging studies/lab tests, 181–182 knee, 313 medical management, 182–183 pathogenesis, 480–481 physical exam findings, 181 physical findings, 481 prevalence, 480 surgical management, 183 treatment, 481 weight loss, 481 osteoblasts, 172

osteochondral autologous transplantation (OAT) procedure, 185 osteochondritis dissecans (OCD) clinical signs and symptoms, 185 definition/pathology, 185 epidemiology, 185 imaging studies, 185–186 medical management, 186 pediatrics, 337–338 physical exam findings/tests, 185 surgical management, 187 talus, 330 osteochondrosis in children, 177–178 overuse syndromes, 177 treatment, 178 osteoclasts, 172 osteocytes, 172 osteon, 171 osteonecrosis elbow, 338 foot/ankle, 339–340 hip, 339 knee, 339 spine, 338–339 wrist/hand, 338 osteopenia, 449 osteophytes, 180 osteoporosis, 449 adaptive athlete, 550–551 exercise, 22 exercise prescription and testing, 144 ovaries, preparticipation screening, 92 overload, 103 overtraining autonomic dysfunction, 118 biochemical alterations, 119 immune deficiency, 118 medical evaluation, 119 mood disturbance, 118 neuroendocrine dysfunction, 118 performance decrement, 118 risk factors, 117–118 treatment, 119 Owen equation, 132 oxygen therapy, 373 padding, 157 Paget–von Schroetter syndrome, 514, 515 paired organs preparticipation examination eyes, 91 kidney, 92 ovaries, 92 testicles, 92 pancreas, 410 Panner’s disease, 338 pantothenic acid, 128

INDEX

parathyroid hormone (PTH), 172 paroxysmal dyskinesias, 487 Parsonage–Turner syndrome, 265–266, 507 passive range of motion (PROM), 59 patellar fracture, 303 patellar tendinopathy, 164, 305 patellofemoral joint, 301 pathologic fracture, 173, 196 PCL. See posterior cruciate ligament pediatric athlete age-appropriate physical activity, 535 bronchial asthma, 138 cerebral palsy, 138 CF and diabetes mellitus, 138 clinical exercise testing, 138 definition and issues, 532 exercise prescription, 138 fitness testing, 137 growth and development, 532–533 health benefits, 532 hemophilia, 138 intellectual and developmental disability, 138–139 medical conditions, 537 muscular dystrophy, 139 obesity, 139 physical activity impact, 535–536 physiological differences, 533–535 rehabilitation, 536–537 rheumatoid arthritis, 139 risk of injury, 536 spina bifida, 139 sports participation, 532 strength and resistance training, 536 pediatric musculoskeletal injuries apophysitis/epiphysitis, 335–337 avulsion fractures, 333–335 fractures, 332–333 osteochondritis dissecans, 337–338 osteonecrosis, 338–340 pelvic floor dysfunction, 455–456 pelvis apophysitis/epiphysitis, 336 avulsion fractures, 334 preparticipation examination, 92–93 pelvis, hip, and thigh injuries acute compartment syndrome, 300 anatomy, 288 athletic pubalgia, 294 avascular necrosis, 297–298 bursitis, 293–294 degenerative joint disease, 298–299 dislocation, 290 femoral neck stress fracture, 288 femoral shaft fracture, 289–290 femoral shaft stress fracture, 288 labral injuries and pre-arthritic hip disorders, 294–297

muscle/tendon injuries, 290–293 osteitis pubis, 297 pubic ramus stress fracture, 289 sacral stress fracture, 289 penetrating trauma, 377–378 penicillin and derivatives, 43 peptic ulcer disease (PUD), 417–418 peptide hormones, 51 performance-enhancing agents alcohol, 53 anabolic steroids, 51 beta-blockers, 53 β2-agonists, 51 cannabinoids, 52–53 chemical and physical manipulation, 52 creatine, 53 diuretics, 51 drug testing, 53–55 enhancement of oxygen transfer, 52 gene doping, 52 gene manipulation, 55 glucocorticoids, 53 growth factors, 51 history, 50 hormone antagonists and analogs, 51 masking agents, 52 narcotics, 52 nutritional supplements, 53 peptide hormones, 51 stimulants, 52 structure, 50 xenon gas, 55–56 periarticular ACJ cyst, 254 pericardial effusion, 376–377 pericarditis, 376 periodization block periodization, 105 cycles, 104 linear (classical) periodization, 104 linear periodization sequence, 105 nonlinear (undulating) periodization, 104 periorbital hematoma, 364 peripheral nerve entrapment syndromes, 549–550 peripheral nerve injury adaptive athlete, 549–550 pathophysiology, 501–502 peripheral vascular disease, 529 pernio (chilblains), 431 peroneal tendinopathy, 324–325 pes anserine bursitis, 314 petechiae, 429 PFTs. See pulmonary function tests phalangeal fracture, 278–279, 323 pharmacotherapy complex regional pain syndrome, 491 posttraumatic headache, 489 primary exercise headache, 489

629

630

INDEX

photodermatitis, 431 photoinjury (sunburn), 430–431 physiologic anemia, 438 physiologic changes, aging, 20 piezogenic papules, 430 PINS. See posterior interosseous nerve syndrome piriformis pain, 291 plantar fasciopathy, 325 platelet-rich plasma (PRP), 554 plica syndrome, 310–311 PLL. See posterior longitudinal ligament plyometric training, 109 pneumomediastinum, 373–374 pneumothorax, 373, 560 polycarbonate shields, 154 polymerase chain reaction (PCR), 458 popliteal artery entrapment, 320–321, 517–518 popliteus tendinopathy, 306 posterior acoustic enhancement, ultrasound, 558 posterior acoustic shadowing, ultrasound, 558 posterior ankle splint, 72 posterior atlantoaxial ligament, 206 posterior capsule shoulder stretching, 33 posterior cruciate ligament (PCL), 302 posterior interosseous nerve syndrome (PINS), 509 posterior longitudinal ligament (PLL), 206 postrace anemia, 437 posttraumatic conjunctivitis, 363 posttraumatic headache, 489 PPE. See preparticipation physical examination preactivity stretching, 117 prednisone, 482 pregnancy cardiorespiratory factors, 451 cardiovascular factors, 451–452 energy balance factors, 452 exercise, 543–545 exercise recommendations, 453–455 fetal benefits of exercise, 451 fetal health, 452 labial trauma, 456 lactation considerations, 453 maternal benefits of exercise, 451 menstrual disorders, 448 musculoskeletal factors, 453 pelvic floor dysfunction, 455–456 thermoregulatory factors, 452 premature delivery, 452 preparticipation physical examination (PPE), 7–8 abdominal and pelvic, 92–93 alcohol, 95 asthma, 93–94 cardiovascular (see cardiovascular preparticipation screening) cystic fibrosis, 101 development, 77 diabetes mellitus, 94

disabled athletes, 98–99 drugs of abuse, 95 eyes, 91 female athlete triad, 95–97 general medical history, 78 goals of, 77 hematologic disorders, 100–101 infectious disease, 97–98 injury prevention, 97 kidneys, 92 laboratory testing, 79 mass vs. individual, 78 musculoskeletal preparticipation screening, 89–91 neurologic preparticipation screening, 87–89 ovaries, 92 performing physician, 77 physical examination, 78–79 physician responsibilities, 77 prescription medications, 94–95 sickle cell trait, 99–100 special olympians, 99 supplements, 95 testicles, 92 timing/frequency, 77–78 tobacco, 95 prepatellar bursitis, 314 PRICE. See protection, rest, ice, compression, and elevation primary electrical disease autopsy-negative sudden unexplained death, 385 Brugada syndrome, 386 catecholaminergic polymorphic ventricular tachycardia (CPVT), 386 long QT syndrome (LQTS), 385 short QT syndrome, 385–386 WPW syndrome, 386–387 primary spontaneous pneumothorax (PSP), 373 progestin challenge test, 448 PROM. See passive range of motion pronator syndrome, 511 proprioceptive neuromuscular facilitation (PNF), 16, 116 protection, rest, ice, compression, and elevation (PRICE), 552 protective equipment. See also braces braces, 154 breakaway bases, 158 eye protection, 154–155 gloves, 157–158 helmets, 155–157 padding, 157 protein nitrogen balance, 124–125 quality, 124, 125 requirements, 124 proteinuria, 422–423 protrusion, 236

INDEX

proximal interphalangeal (PIP) joint dislocation, 280–281 proximal radial nerve entrapment, 509 proximal tibiofibular joint, 301 PRP. See platelet-rich plasma pseudoanemia, 438 pseudogout, 187–188 psoriatic arthritis, 485 PSP. See primary spontaneous pneumothorax psychology burnout, 523 clinical sport psychologists, 521 coping with injury, 522–523 depression, 519–520 eating disorders/disordered eating, 520 educational sport psychology specialists, 521 field-specific certification, 521 performance anxiety, 522 performance enhancement, 521–522 PTH. See parathyroid hormone pubic ramus stress fracture, 289 PUD. See peptic ulcer disease pudendal nerve injury, 423–424 pudendal neuropathy, 424 pulmonary contusion, 374–375 pulmonary disease athlete, 144–145 pulmonary embolism, 375–376 pulmonary function tests (PFTs), 93 pulmonology acute airway compromise, 402–403 asthma, 398–399 chronic obstructive pulmonary disease, 404–407 cystic fibrosis, 401–402 exercise-induced bronchospasm (EIB), 399–401 vocal cord dysfunction, 403–404 pyridoxine (B6), 127 quadriceps contusion/strain/myositis, 291–292 quadrilateral space syndrome (QSS), 265, 509, 515 neurogenic, 264–265 vascular, 265 RA. See rheumatoid arthritis radial epiphysitis (gymnast’s wrist), 286 radial gutter splint, 71 radial nerve, 268 injuries, 509 radial tunnel syndrome, 509 radiculitis, 214–215, 236 radiculopathy, 214–215, 236 rapidly reversible physiologic block of conduction, 502 reactive arthritis, 484 reactive tendinopathy, 162 rear-foot-strike (RFS), 35 rectus hematoma, 413–414 rectus sheath, 408

regenerative injection therapy (RIT), 553 regenerative treatments autologous blood injection (ABI), 554 mesenchymal stem cell therapy, 555 platelet-rich plasma, 554 prolotherapy, 553 tenotomy, 554–555 renal trauma, 426–428 resistance exercise cardiovascular response, 17 cortisol, 18 depression, 22 DM, 22 elderly, 21 growth hormone, 18 hypertension, 21 testosterone, 18 resistance phase, GAS, 103 resistance training ACSM recommendations, 107–109 blood flow restriction, 107 definitions, 105–106 exercise order, 107 exercise selection, 106–107 frequency, 106 loading, 106 muscle action type, 106 muscle strength factors, 106 plyometric training, 109 repetition speed, 107 rest periods, 107 volume, 106 resisted straight leg raise, 289 resting metabolic rate (RMR), 131–132 retinal detachment, 365 retinal hemorrhage, 366 retro-Achilles bursitis, 329 retrobulbar hemorrhage, 366 retrocalcaneal bursitis, 329–330 return to play (RTP) atlanto-axial instability from Down syndrome, 220 BCVI, 221 cervical cord neurapraxia, 211 cervical stenosis, 213 concussion, 497–499 disk pathology, 214 Klippel–Feil syndrome, 220 low back pain, 236 PRICE and NSAIDs, 553 radiculitis/radiculopathy, 214–215 sprains and strains, 219 stingers and burners, 210 subdural and epidural hematomas, 498 transient quadriparesis, 211 whiplash, 219 reverberation, ultrasound, 558 RFS. See rear-foot-strike

631

632

INDEX

rhabdomyolysis, 440 rhabdomyoma, 170 rhabdomyosarcoma, 170 rheumatoid arthritis (RA) diagnostic guidelines, 479 exercise, 480 pathogenesis, 478 pediatric athlete, 139 physical findings, 478–479 prevalence, 478 prognosis, 480 treatment, 479–480 rheumatology osteoarthritis, 480–481 rheumatoid arthritis, 478–480 spondyloarthropathies, 483–485 systemic lupus erythematosus, 481–483 rib fracture, 369–370 riboflavin (B2), 127 RIT. See regenerative injection therapy RMR. See resting metabolic rate roflumilast, 407 Rolando fracture, 278 Roos test, 516 RTP. See return to play running gait angle of gait, 35 foot strike patterns, 35 forward momentum, 35 kinematic differences, 35 midstance, 34–35 pronation, 36 rear foot strike, 35, 36 rehabilitation, 36–37 stance phase, 34 supination, 36 swing, 35 ruptured globe, 365 sacralization of the L5 vertebra, 234 sacral stress fracture, 289 sacroiliac (SI) joint complex pain, 241–242 Salter–Harris classification schema, 332, 333 saphenous nerve injury, 512 sarcomere, 10–11 sarcopenia, 526 SCA. See sudden cardiac arrest scabies, 432 scapholunate/dorsal intercalated segmental instability, 281–282 SCAT3. See Sport Concussion Assessment Tool 3 SCD. See sickle cell disease; sudden cardiac death SCFE. See slipped capital femoral epiphysis Scheuermann’s disease, 338–339 Schober test, 483, 484 scleral laceration, 365 scoliosis, 90–91, 242–245

adolescent idiopathic scoliosis (AIS), 243 scrotal trauma, 424–425 SCT. See sickle cell trait seabather’s eruption, 432 secondary spontaneous pneumothorax (SSP), 373 Seddon classification, 501 segmental fracture, 173 Segond fracture, 303 seizure disorders epilepsy, 486–488 seizure, 486 selective serotonin reuptake inhibitors (SSRIs), 519 septal hematoma, 363 septic joints, 462–463 sequestration, 237 Sever’s disease, 177, 336–337 sexually transmitted infections diagnosis, 463–464 epidemiology, 463 treatment, 464–465 shaft fracture, 278 shock phase, GAS, 103 short arm cast, 73 short leg cast, 73 short QT syndrome, 385–386 shoulder anatomy, 252 apophyseal/epiphyseal avulsion fractures, 333 apophysitis/epiphysitis, 335 muscles, 253, 254 shoulder injuries ACJ dislocation, 254–255 adhesive capsulitis, 261–262 atraumatic instability, 257–258 bracing for stability, 258 clavicle fracture, 251–253 dislocation/subluxation, 253–255 glenoid fracture, 253 humerus fracture, 253 labral tears, 261 muscle/tendon injuries, 258–261 neuralgic amyotrophy, 265–266 quadrilateral space syndrome, 264–265 SCJ, 263 suprascapular neuropathy, 264 traumatic instability, 256–257 sickle cell, 79 sickle cell disease (SCD), 439 sickle cell trait (SCT), 99–100 epidemiology, 440 etiology, 439 exertional death, 441 exertional heat stroke, 440–441 hematuria, 441 hyposthenuria, 441 laboratory evaluation, 441 prevention, 441–442

INDEX

rhabdomyolysis, 440 splenic infarction, 441 sickle prep test, 441 Sinding–Larsen–Johansson disease, 336 single photon emission computed tomography (SPECT), 176, 247 single sugar-tong splint, 72 skeletal injury frontal sinus fracture, 360–361 Le Fort type facial fractures, 361 mandible fractures and dislocations, 361–362 nasal fractures, 361 orbital blowout fracture, 361 skull fractures, 360 tripod fracture, 360 zygomatic fractures, 360 skier’s thumb, 282–283 skin age-related changes, 526 breakdown, 549 lacerations, 434 tenting, 199 SLE. See systemic lupus erythematosus sleep behaviors, 487 sling, 201 slipped capital femoral epiphysis (SCFE), 188 slipping-rib syndrome, 372 small intestine, 409 snapping hip syndrome, 290–291 soft-tissue injury, 360 soft-tissue sarcoma, 170 soft-tissue tumors muscle tumors, 170 tendon and tendon sheath tumors, 169–170 solar urticaria, 431, 474 solitary kidney, 428 spear tackler’s spine, 215 SPECT. See single photon emission computed tomography speed and agility training, 109–111 spina bifida, 139 spinal nerve roots, 204, 205 spinal stenosis exercise, 528 spine avulsion fractures, 334 osteonecrosis, 338–339 spinous process (SP) fracture, 239, 371 spiral fracture, 173 spirometry, 405–406 spleen anatomy, 409 function, 409 laceration and contusion, 412–413 splenic infarction, 441 splenomegaly, 93 splinting

complications, 71 fracture reduction, 197–198 indications, 70 principles of, 70 splints, 71–72 spondyloarthropathies ankylosing spondylitis, 483–484 psoriatic arthritis, 485 reactive arthritis, 484 spondylolisthesis, 248–249 spondylolysis, 246–248 Sport Concussion Assessment Tool 3 (SCAT3), 495 sports anemia, 438 sports biomechanics cycling, 37–40 jumping and landing, 37 running gait, 34–36 swimming, 30–33 throwing, 24–30 walking gait, 33–34 sports specificity, 103 Spurling’s neck compression test, 208 SSP. See secondary spontaneous pneumothorax SSRIs. See selective serotonin reuptake inhibitors static bike fit, 37–38 static restraints, 200 static stretching, 116 sternoclavicular joint, 372 steroid injection, 166 Still’s murmur, 86 stimulants, 52 stingers and burners definition, 209 diagnosis, 209–210 epidemiology, 209 mechanisms of injury, 209 preparticipation screening, 87 RTP guidelines, 210 treatment, 210 stirrup splints, 72 stress fracture, 62, 196, 304, 371–372 etiology, 174 incidence, 174 location, 174–175 management, 176–177 physical examination, 174 presentation, 174 radiological grading, 176, 177 risk factors, 174 stress urinary incontinence (SUI), 456 striae distensae (stretch marks), 430 subclavian steal syndrome, 517 subconjunctival hemorrhage, 364 sudden cardiac arrest (SCA), 396–397 sudden cardiac death (SCD) causes of, 379, 380 definition, 379

633

634

INDEX

sudden cardiac death (SCD) (Cont.) ECG screening, 380 gender and race, 379 incidence, 379 preparticipation screening, 379 sports, 379 symptoms, 379 SUI. See stress urinary incontinence sulfonylureas, 43–44 sunburn, 343 superficial heat, 58–59 superior labral anteroposterior (SLAP) lesion, 27 suprascapular nerve injury, 507–508 supraventricular arrhythmias, 393–395 swimmer’s ear, 432 swimmer’s itch, 432 swimming ankylosing spondylitis (AS), 484 competitive strokes, 30 drag, 31 kick patterns, 32 lift force, 31 propulsive phase, 30–31 recovery phase, 31 rehabilitation, 32–33 “S”-shaped pulling pattern, 31 stroke flaws, 32 syncope epilepsy, 487 preparticipation screening, 86–87 syndesmotic sprain, 327 synovectomy, 188 synovial fluid, 65, 180, 181 systemic lupus erythematosus (SLE) exercise, 482–483 presentation and diagnosis, 481–482 prevalence, 481 prognosis, 482 treatments, 482 talar dome, 338 talk test, 11 talon noir, 429 talus fracture, 322–323 Tanner stages of pubertal development, 533 tarsal tunnel syndrome, 513 team physicians administrative responsibilities, 8–9 liability, 7 patient autonomy, 5–6 patient confidentiality, 6 postinjury return-to play, 8 preparticipation physical examination, 7–8 requirements for, 5 responsibility, 6 waiver of liability, 8 tendinopathy, 62, 553 Achilles, 163–164, 324

age, 164 continuum theory, 162–163 definition, 161 elbow, 164 enthesis, 165 exercise, 165 extrinsic factors, 164 failed healing response theory, 163 flexor hallucis longus, 325–326 gender, 164 genetics, 164 hypoxia, 164–165 impingement, 164 inflammation, 164 mechanical load, 164 neural, 165 oral medications, 165–166 pain, 165 patellar, 164 peroneal, 324–325 plantar fasciopathy, 325 rotator cuff, 164 steroid injection, 166 systemic diseases, 164 tendon healing, 165 tendon rupture, 166–167 tenotomy, 166 tibialis anterior, 325 tibialis posterior, 324 topical nitroglycerin, 166 tendinosis, 558 tendon biomechanics, 161–162 clear cell sarcoma, 170 dysrepair, 162–163 structure, 161 ultrasound, 558 tendon sheath fibroma, 170 giant cell tumors, 169–170 tenotomy, 554–555 tension pneumothorax, 373 testicle rupture, 424–425 testicular torsion, 425–426 testosterone, exercise, 18 thalassemia, 442 theophylline, 407 therapeutic drugs analgesics, 41–43 antibiotics, 43 antidiabetic agents, 43–44 antihypertensives, 44–47 asthma medications, 47–48 corticosteroids, 49 NSAIDs/cyclooxygenase-2 inhibitors, 48 photosensitivity reaction, 49–50 viscosupplementation, 48–49 thermoregulation, 548

INDEX

thiamin (B1), 127 thiazide diuretics, 393 thiazolidinediones, 43 thoracic spine, 368 throwing adaptive changes, 29 baseball pitch, 25–28 biomechanical abnormalities in pitching, 29–30 as a kinetic chain of motion, 24 types of pitches, 29, 30 throwing shoulder, 262–263 thumb metacarpal fractures, 278 thumb spica splint, 71–72 thyroid hormone, 172 thyroid-stimulating hormone (TSH), 448 tibial fracture, 315 tibialis anterior tendinopathy, 325 tibialis posterior tendinopathy, 324 tibial plateau fracture, 303 tibia stress fractures, 316–317 tibiofemoral joint, 301 tick-borne disease, 460 Tietze’s syndrome, 372 tinea corporis (gladiatorum)/pedis, 433–434 tissue adhesives, 434 tissue changes, 525–526 tizanidine, 235 tonic seizure, 486 Torg ratio, 89 tort law, 7 torus fracture, 173, 196 trabeculae, 171 trabecular bone, 171–172 traction dislocation management, 201 fracture reduction, 197 tramadol, 42–43, 183 transient quadriparesis (TQ), 88–89, 210–211 transition macrocycle, 105 transverse ligament, 206 transverse process (TP) fractures, 239 traumatic brain injury (TBI), 88 traumatic iritis, 366 traumatic neuroma, 549–550 trench foot, 347 triangular fibrocartilage complex (TFCC), 273 triceps tendinopathy, 271 trichomoniasis, 463–464 trigeminal nerve, 359 trigger finger (flexor tenosynovitis), 284–285 tripod fracture, 360 Turf toe, 329 tympanic membrane rupture, 362 ulnar collateral ligament (UCL) injury, 27, 269–270 ulnar gutter splint, 71 ulnar nerve, 268 ulnar neuropathy

elbow, 509–510 wrist, 510–511 ultrasound artifacts, 558 bone, 559 cardiology, 560 cartilage, 559 chest/abdominal trauma, 560 injections, 560 ligament, 559 muscle, 559 musculoskeletal, 558 nerve, 559 ocular trauma, 560 physics, 557 pulmonary embolism, 375 terminology, 557 transducers, 557–558 vessels, 560 ultrasound-guided injections (USGIs), 560 uncovertebral joints, 204 upper-limb nerve injuries axillary nerve injury, 508–509 carpal tunnel syndrome, 511 long thoracic nerve injury, 508 Parsonage–Turner syndrome, 507 pronator syndrome, 511 radial nerve injuries, 509 suprascapular nerve injury, 507–508 ulnar neuropathy, 509–511 upper limb tension testing (ULTT), 502, 503 upper respiratory tract infection (URI), 460, 465 urge urinary incontinence (UUI), 456 urine markers hematuria, 421 hemoglobinuria, 421–422 myoglobinuria, 422 proteinuria, 422–423 urticaria acute, 474 acquired cold, 431 angioedema, 473–474 aquagenic, 431, 474 cholinergic, 474 chronic, 474 cold, 474 contact, 475 delayed-pressure, 475 dermographism, 474 solar, 474 treatment, 475–476 valgus extension overload (VEO), 28 valvular disease, 80–81 variant-type exercise-induced anaphylaxis (VTEIAn), 472 vascular injuries of limbs athletic vascular injury, 514–515

635

636

INDEX

vascular injuries of limbs (Cont.) effort thrombosis, 515 external iliac artery endofibrosis, 515 hypothenar hammer syndrome, 516–517 popliteal artery entrapment, 517–518 quadrilateral space syndrome, 515 subclavian steal syndrome, 517 vascular thoracic outlet syndrome, 515–516 vascular thoracic outlet syndrome, 515–516 ventricular fibrillation, 346 vertebral bodies, 204 viral conjunctivitis, 363 viscosupplementation, 48–49 vitamin A, 129 vitamin C, 128 vitamin D, 129, 172 vitamin E, 128 vitreous hemorrhage, 365 vocal cord dysfunction clinical presentation, 403–404 definition, 403 diagnostic studies, 404 etiology, 404 treatment, 404 volar/dorsal forearm splint, 72 Volkmann canals, 171 von Willebrand’s disease, 443 Voshell’s bursitis, 314 walking gait, 33–34

warm-up, 116–117 warts, 433 Watson’s sign, 281 wave drag, 31 weight control exercise, 145 weight management, 131–132 wet bulb globe temperature (WBGT), 345 whey protein, 130 whiplash, 219 Wolff–Parkinson–White (WPW) syndrome, 386–387 Wolff’s law, 172 woven bone, 171 Wright test, 516 wrist avulsion fractures, 334 guards, 157 injuries (see hand and wrist injuries) osteonecrosis, 338 xenon gas, 55–56 xerosis, 431 x-ray hemothorax, 374 pneumothorax, 373, 374 sternoclavicular joint, 372 zygapophyseal (facet) joint, 204 pain, 240–241 zygomatic fractures, 360