Sports-related Fractures, Dislocations and Trauma: Advanced On- and Off-field Management 3030367894, 9783030367893

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Morteza Khodaee Anna L. Waterbrook Matthew Gammons  Editors

Sports-related Fractures, Dislocations and Trauma Advanced On- and Off-field Management

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Sports-related Fractures, Dislocations and Trauma

Morteza Khodaee  •  Anna L. Waterbrook Matthew Gammons Editors

Sports-related Fractures, Dislocations and Trauma Advanced On- and Off-field Management

Editors Morteza Khodaee Department of Family Medicine and Orthopedics University of Colorado School of Medicine Denver, CO USA

Anna L. Waterbrook Department of Emergency and Sports Medicine The University of Arizona Tucson, AZ USA

Matthew Gammons Vermont Orthopedic Clinic Rutland, VT USA

ISBN 978-3-030-36789-3    ISBN 978-3-030-36790-9 (eBook) https://doi.org/10.1007/978-3-030-36790-9 © Springer Nature Switzerland AG 2020 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

I dedicate this book to my son, Arshia, who is on a path to be an incredible young gentleman; my daughter, Kimia, who is a bright star of our lives; and my beautiful wife, Atousa, who has stood by me for over 15 years, as well as to my dad, Ebrahim, who showed me the value of working hard to reach my goals, and in memory of my mom, Parvin, who taught me how to be a caring person. Without their love and support, this would not have been possible. Morteza Khodaee I dedicate this book to my family – my husband who has always been my rock and didn’t even flinch when I told him I would be working on another book while pregnant with twins and my four children who sustain me and always push me to be the best person I can be. Anna L. Waterbrook To my coeditors, Drs. Khodaee and Waterbrook, thank you for your monumental efforts that made this book possible. Thank you to my wife, Julie, and daughters, Kyra and Kelsey, who constantly inspire me to be a better person. Thanks to all those that dedicate their time to covering sports and ensuring health and safety of our athletes. Matthew Gammons

Preface

This book was first envisioned during the 25th American Medical Society for Sports Medicine (AMSSM) Annual Meeting held in Dallas, Texas, in the spring of 2016. We discussed the need for a comprehensive book in the field of Sports Traumatology. Since there is no book that covers all aspects of sports-related trauma, we wanted to have one book specific to musculoskeletal and other types of trauma encountered in different sporting activities. After contacting Springer and receiving preliminary approval, we started on listing the important topics that needed to be enclosed. With this in mind, we prepared a table of contents that was primarily oriented to the practicing clinicians who care for athletic population on the sideline or in the office. From the beginning, it was obvious that we had a huge task in front of us. There was no book to model this book after. On the one hand, we wanted to cover all aspects of sports traumatology, and, on the other hand, we wanted to focus on nonsurgical managements. Our focus was to provide as many visual aids (e.g., illustrations and radiographic images) as possible. For this, we would like to specifically thank Mr. Daniel Kolb and Mrs. Amy Brumenschenkel and other staff at Denver Health East Grand Community Clinic in Winter Park, Colorado. Today, there are unparalleled opportunities to make substantial progress in managing athletes with acute trauma. Although the wealth of information and new, powerful imaging modalities have transformed the management of sports traumatology, there are still deficiencies in evidence-based recommendations. The goal is to manage these athletes in the most efficient ways to allow them to a swift and safe return to sports. This obviously presents new challenges, as there is no consensus in many of these mostly “expert opinion” recommendations. We have been mindful of this and have asked each author to consider the best available evidence in the management of patients in each of their respective fields. Therefore, we would recommend multicenter randomized control trials to evaluate specific managements (e.g., surgical and nonsurgical) for each injury in the future. From the very beginning, a group of experts in the different areas were put together, all of them enthusiastically agreeing to participate. It is their collaboration that provides the added value to this book. It would have been impossible to complete this book without the invaluable help of Mr. Michael Griffin from Springer. We believe that we have achieved our goals and that we have come up with a comprehensive and practical text that covers initial and non-operative management of a variety of trauma in Sports Medicine. This book is a unique collection of the topics that have not been previously covered in a single book. Some of the information is difficult to find in other sources. We hope this book will help clinicians manage their athletes with acute trauma, which in the end is our real goal. If so, all the efforts will have been completely worthy. Denver, CO, USA Tucson, AZ, USA Rutland, VT, USA

Morteza Khodaee Anna L. Waterbrook Matthew Gammons

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Contents

Part I General Approach to Sports Trauma 1 Initial Evaluation, Resuscitation, and Acute Management�������������������������������������   3 Anna L. Waterbrook and Moira Davenport 2 Sports Coverage for Traveling Teams�����������������������������������������������������������������������  11 William J. Moreau and Dustin Nabhan 3 Mass Sporting Event Coverage���������������������������������������������������������������������������������  17 Andrew Pasternak and Brian J. Krabak 4 Stabilization, Immobilization, and Transportation�������������������������������������������������  25 Brenden J. Balcik and Aaron J. Monseau 5 Anesthesia and Acute Pain�����������������������������������������������������������������������������������������  35 Alexander Ebinger and Spencer Tomberg 6 Imaging �����������������������������������������������������������������������������������������������������������������������  53 Jordan S. Gold, Adam C. Zoga, and John C. Hill Part II General Synopsis of Acute Musculoskeletal Care in Sports 7 Anatomy and Physiology�������������������������������������������������������������������������������������������  71 Val Bratinov and Mark E. Lavallee 8 Fracture Types and Definitions���������������������������������������������������������������������������������  77 David Cole, Joseph Medellin, Ryan C. Wennell, and Mark E. Lavallee 9 Dislocation Types and Definitions�����������������������������������������������������������������������������  85 Katherine M. Edenfield and Jocelyn R. Gravlee 10 Musculoskeletal Healing Process�������������������������������������������������������������������������������  97 Jessica Devitt 11 Complications������������������������������������������������������������������������������������������������������������� 105 Andrew M. Wood Part III Acute Sports-Related Bones and Joints Trauma: Upper Extremity 12 Clavicle������������������������������������������������������������������������������������������������������������������������� 119 Armando F. Vidal, Mark F. Riederer, Justin H. Bartley, K. Linnea Welton, Richard Bortz, and Morteza Khodaee 13 Scapula������������������������������������������������������������������������������������������������������������������������� 143 Stephen M. Spadafore, Michelle Wolcott, and Darcy Selenke

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14 Glenohumeral Joint ��������������������������������������������������������������������������������������������������� 153 Karin VanBaak, Stephanie W. Mayer, Matthew J. Kraeutler, and Morteza Khodaee 15 Humerus����������������������������������������������������������������������������������������������������������������������� 181 Christopher D. Joyce, David Ziegler, Katherine S. Dahab, and Jonathan T. Bravman 16 Elbow Joint ����������������������������������������������������������������������������������������������������������������� 201 Jack Spittler and Adam Seidl 17 Radius and Ulna��������������������������������������������������������������������������������������������������������� 227 Emily A. Sweeney, Andrew John Maxwell Gregory, Jessica J. Wingfield, and Frank Scott 18 Carpus������������������������������������������������������������������������������������������������������������������������� 249 Kyros Ipaktchi, Omar Dimachkieh, and Sonia Chaudhry 19 Metacarpus ����������������������������������������������������������������������������������������������������������������� 265 Rebecca A. Myers, Kyle B. Nagle, and Morteza Khodaee 20 Finger��������������������������������������������������������������������������������������������������������������������������� 291 Drew Ashby, Greg Gutierrez, and Morteza Khodaee Part IV Acute Sports-Related Bones and Joints Trauma: Lower Extremity 21 Pelvis����������������������������������������������������������������������������������������������������������������������������� 319 Yuka Kobayashi, Justin E. Hellwinkel, and Morteza Khodaee 22 Hip Joint ��������������������������������������������������������������������������������������������������������������������� 341 Stephanie W. Mayer, Kimberly M. Spahn, and Rebecca Griffith 23 Femur��������������������������������������������������������������������������������������������������������������������������� 359 Lauren Oberle and Morteza Khodaee 24 Knee����������������������������������������������������������������������������������������������������������������������������� 375 Geoffrey M. Dreher, Utsav Hanspal, David M. Baxter, and Morteza Khodaee 25 Tibia and Fibula ��������������������������������������������������������������������������������������������������������� 421 William Denq 26 Ankle Joint������������������������������������������������������������������������������������������������������������������� 437 Morteza Khodaee, Matthew Gammons, and Kenneth J. Hunt 27 Tarsus��������������������������������������������������������������������������������������������������������������������������� 471 Jennifer D. Stromberg 28 Metatarsus������������������������������������������������������������������������������������������������������������������� 499 Nathaniel S. Jones, Ellen Kroin, and Adam Schiff 29 Toe ������������������������������������������������������������������������������������������������������������������������������� 523 Bryant Walrod Part V Acute Sports-Related Bones and Joints Trauma: Axial Skeletal 30 Cervical Spine������������������������������������������������������������������������������������������������������������� 537 Matthew G. Zmurko, Matthew Gammons, and Morteza Khodaee 31 Thoracic Spine������������������������������������������������������������������������������������������������������������� 561 Matthew G. Zmurko

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32 Lumbar Spine������������������������������������������������������������������������������������������������������������� 575 Catherine Mygatt Naden, Stephen Huang, and Douglas Comeau 33 Stress Fractures����������������������������������������������������������������������������������������������������������� 589 Bradley G. Changstrom Part VI Acute Soft Tissue Injuries in Sports 34 Tendons ����������������������������������������������������������������������������������������������������������������������� 595 Sagir Bera, Stephen R. Paul, and David Millward 35 Muscles������������������������������������������������������������������������������������������������������������������������� 619 Alicia Gustafson and Cory A. Newman 36 Ligaments��������������������������������������������������������������������������������������������������������������������� 631 Daphne Amanda Scott and Yvonne Chow 37 Bursa ��������������������������������������������������������������������������������������������������������������������������� 671 Morteza Khodaee 38 Nerve ��������������������������������������������������������������������������������������������������������������������������� 675 Benjamin Marshall and Rachel Brakke Holman 39 Vascular����������������������������������������������������������������������������������������������������������������������� 683 Andrew McBride, Amy M. Singer, and Holly Beach 40 Skin and Subcutaneous Tissue����������������������������������������������������������������������������������� 693 Rajwinder S. Deu and Morteza Khodaee Part VII Other Sports-Related Trauma 41 Chest Trauma ������������������������������������������������������������������������������������������������������������� 705 Jeffrey P. Feden 42 Abdominal Trauma����������������������������������������������������������������������������������������������������� 715 Jaron Santelli, Jeremiah W. Ray, and Jonathan T. Finnoff 43 Head Injury����������������������������������������������������������������������������������������������������������������� 731 Christopher Guyer and Jeremiah W. Ray 44 Facial Trauma������������������������������������������������������������������������������������������������������������� 753 Christopher Hogrefe 45 Soft Tissue Neck Injury ��������������������������������������������������������������������������������������������� 803 Allison D. Lane Part VIII Sports-Specific Injuries 46 Aquatic Sports������������������������������������������������������������������������������������������������������������� 813 Jack Spittler 47 Baseball and Softball ������������������������������������������������������������������������������������������������� 819 Andrew T. Gomez and Ashwin L. Rao 48 Basketball��������������������������������������������������������������������������������������������������������������������� 829 Deepak S. Patel and Britain O’Connor 49 Boxing�������������������������������������������������������������������������������������������������������������������������� 833 Joshua V. Okon, Christine A. Marschilok, and Adam M. Cooper

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50 Cheerleading��������������������������������������������������������������������������������������������������������������� 839 Stephanie Chu 51 CrossFit ����������������������������������������������������������������������������������������������������������������������� 843 Armando F. Vidal 52 Cycling������������������������������������������������������������������������������������������������������������������������� 847 Jonathan T. Bravman and Robin H. Dunn 53 Dance��������������������������������������������������������������������������������������������������������������������������� 853 Rajwinder S. Deu 54 Extreme Sports����������������������������������������������������������������������������������������������������������� 857 Matthew J. Kraeutler, Lior Laver, and Omer Mei-Dan 55 Field Hockey ��������������������������������������������������������������������������������������������������������������� 865 Katherine S. Dahab 56 Football ����������������������������������������������������������������������������������������������������������������������� 869 Matthew S. Leiszler, Sourav K. Poddar, and Bjorn C. Irion 57 Gymnastics������������������������������������������������������������������������������������������������������������������� 873 Stephanie Chu 58 Ice Hockey������������������������������������������������������������������������������������������������������������������� 877 Mark F. Riederer 59 Ice Skating������������������������������������������������������������������������������������������������������������������� 881 Rajwinder S. Deu 60 Lacrosse����������������������������������������������������������������������������������������������������������������������� 885 Sameer Dixit 61 Marathons������������������������������������������������������������������������������������������������������������������� 889 Brian J. Krabak and Eric T. Chen 62 Martial Arts����������������������������������������������������������������������������������������������������������������� 895 Vicki Nelson and Robert Masocol 63 Motor Sports��������������������������������������������������������������������������������������������������������������� 901 Luke Widstrom and Jodi M. Blustin 64 Racket Sports ������������������������������������������������������������������������������������������������������������� 907 Kylie Adamek and Bradley G. Changstrom 65 Rock Climbing������������������������������������������������������������������������������������������������������������� 915 Abigail Y. Wang and Sameer Dixit 66 Rowing������������������������������������������������������������������������������������������������������������������������� 921 Andrew T. Gomez and Ashwin L. Rao 67 Rugby��������������������������������������������������������������������������������������������������������������������������� 929 Darcy Selenke 68 Sailing��������������������������������������������������������������������������������������������������������������������������� 933 Jeremy D. Close and Hannah P. Leahy 69 Skiing: Alpine ������������������������������������������������������������������������������������������������������������� 937 J. Herbert Stevenson, Kimberly Sikule, and Elana Bannerman 70 Skiing: Cross-Country����������������������������������������������������������������������������������������������� 941 Kyle B. Nagle

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71 Snowboarding������������������������������������������������������������������������������������������������������������� 945 Karin VanBaak 72 Soccer��������������������������������������������������������������������������������������������������������������������������� 951 Morteza Khodaee and Seth A. Mathern 73 Track and Field����������������������������������������������������������������������������������������������������������� 955 James Thing and Volker Scheer 74 Triathlon ��������������������������������������������������������������������������������������������������������������������� 959 Brent C. Pottenger and Sameer Dixit 75 Ultramarathon and Ultra-endurance Sports����������������������������������������������������������� 965 Volker Scheer and Martin D. Hoffman 76 Volleyball��������������������������������������������������������������������������������������������������������������������� 971 Jill N. Tirabassi 77 Weightlifting ��������������������������������������������������������������������������������������������������������������� 975 Sheila E. Taylor and Mark E. Lavallee 78 Wrestling��������������������������������������������������������������������������������������������������������������������� 981 Robert Kiningham and Babak Shadgan Index������������������������������������������������������������������������������������������������������������������������������������� 985

Contributors

Kylie  Adamek, MD Department of Internal Medicine, University of Colorado School of Medicine, Denver, CO, USA Drew  Ashby, MD Department of Family Medicine, University of Colorado School of Medicine, Denver, CO, USA Brenden  J.  Balcik, MD Department of Emergency Medicine, West Virginia University School of Medicine, Morgantown, WV, USA Elana  Bannerman, MD  Department of Family Medicine, Primary Care Sports Medicine, Southern New Hampshire Medical Center, Hudson, NH, USA Justin H. Bartley, MD  Department of Orthopedic Surgery, Lovelace Hospital, Albuquerque, NM, USA David  M.  Baxter, DO Department of Sports Medicine, Healthplex Sports Medicine, Springfield, PA, USA Holly  Beach, MD  Department of Family and Community Medicine, Primary Care Sports Medicine, University of Arizona, Tucson, AZ, USA Sagir  Bera, DO, MPH, MS, ATC, CSC David Geffen School of Medicine at UCLA, Department of Family Medicine and Sports Medicine, Burbank, CA, USA Jodi M. Blustin, MD  Department of Family Medicine, North Memorial Health and University of Minnesota, Minneapolis, MN, USA Richard Bortz, MD  Winter Park Medical Center, Denver Health, Winter Park, CO, USA Val Bratinov, MD  UPMC Sports Medicine Fellowship Program, Pittsburgh, PA, USA Jonathan T. Bravman, MD  Department of Orthopedics, Division of Sports Medicine and Shoulder Surgery, University of Colorado School of Medicine, Denver, CO, USA Bradley G. Changstrom, MD  Department of Internal Medicine and Orthopedics, University of Colorado School of Medicine, Denver, CO, USA Sonia  Chaudhry Department of Pediatric Orthopaedic and Hand Surgery, University of Connecticut School of Medicine, Connecticut Children’s Medical Center, Hartford, CT, USA Eric  T.  Chen, MD Department of Physical Medicine and Rehabilitation, University of Washington, Seattle, WA, USA Yvonne  Chow, MD, MS Department of Internal Medicine, Division of Sports Medicine, Albany Medical Center, Albany, NY, USA Stephanie  Chu, DO  Department of Family Medicine and Orthopedics, Division of Sports Medicine, University of Colorado School of Medicine, Aurora, CO, USA Jeremy D. Close, MD  Department of Family and Community Medicine, Sports Medicine, Thomas Jefferson University, Philadelphia, PA, USA xv

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David Cole, MD  Department of Primary Care/Sports Medicine, One Medical, San Francisco, CA, USA Douglas  Comeau, DO, CAQSM, FAAFP Department of Family Medicine, Division of Sports Medicine, Ryan Center for Sports Medicine, Boston University, Boston, MA, USA Adam M. Cooper, MD  Department of Family and Community Medicine, Sports Medicine Section, Thomas Jefferson University Hospital, Philadelphia, PA, USA Katherine  S.  Dahab, MD  Department of Orthopedics, University of Colorado School of Medicine, Children’s Hospital Colorado, Aurora, CO, USA Moira  Davenport, MD  Department of Emergency Medicine, Allegheny General Hospital Emergency Medicine Residency, Temple University School of Medicine, Allegheny General Hospital, Pittsburgh, PA, USA William Denq, MD  Departments of Emergency Medicine and Sports Medicine, University of Arizona University of Arizona, Tucson, AZ, USA Rajwinder S. Deu, MD  Department of Orthopedic Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA Jessica Devitt, BS, MD  Department of Family Medicine, University of Colorado School of Medicine, Denver, CO, USA Omar Dimachkieh, MD  Department of Orthopaedic Surgery, UT Physicians, Houston, TX, USA Sameer  Dixit, MD Departments of Orthopaedics, Medicine, and Physical Medicine and Rehabilitation, Johns Hopkins University School of Medicine, Lutherville, MD, USA Geoffrey M. Dreher, DO  Department of Sports Medicine, Crozer-Keystone Health Network, Springfield, PA, USA Robin H. Dunn, MD  Department of Orthopedics, University of Colorado School of Medicine, Aurora, CO, USA Alexander  Ebinger, MD Department of Emergency Medicine, University of Colorado School of Medicine, Aurora, CO, USA Katherine  M.  Edenfield, MD Department of Community Health and Family Medicine, University of Florida College of Medicine, Gainesville, FL, USA Jeffrey P. Feden, MD, FACEP  Department of Emergency Medicine, Alpert Medical School of Brown University, Providence, RI, USA Jonathan T. Finnoff, DO  Department of Physical Medicine and Rehabilitation, Mayo Clinic Sports Medicine Center, Minneapolis, MN, USA Matthew  Gammons, MD Concussion Clinic, Vermont Orthopaedic Clinic, Killington Medical Clinic, Rutland Regional Medical Center, Rutland, VT, USA Jordan  S.  Gold, MD Department of Radiology, MedStar Washington Hospital Center, Washington, DC, USA Andrew T. Gomez, MD  Swedish Providence Medical Group - Mill Creek Sports Medicine, Everett, WA, USA Jocelyn R. Gravlee, MD  Department of Community Health and Family Medicine, University of Florida College of Medicine, Gainesville, FL, USA Andrew  John  Maxwell  Gregory, MD Department of Orthopedics, Vanderbilt University Medical Center, Nashville, TN, USA

Contributors

Contributors

xvii

Rebecca  Griffith, MD Department of Orthopedics, University of Colorado School of Medicine, Aurora, CO, USA Alicia Gustafson, DO  Northwest Allied Physicians, Tucson, AZ, USA Greg  Gutierrez, MD  Department of Family Medicine, University of Colorado School of Medicine, Denver Health, Winter Park Medical Center, Winter Park, CO, USA Christopher Guyer, MD, FACEP  Divisions of Emergency Medicine and of Sports Medicine, Henry Ford Health System, Detroit, MI, USA Utsav  Hanspal, MD, MPH Department of Orthopedics and Sports Medicine, Lourdes Hospital, Binghamton, NY, USA Justin E. Hellwinkel, MD, MS  Department of Orthopedic Surgery, New York Presbyterian/ Columbia University Medical Center, New York, NY, USA John C. Hill, DO  Department of Family Medicine and Orthopedics, CU Sports Medicine, University of Colorado School of Medicine, Denver, CO, USA Martin D. Hoffman, MD  VA Northern California Health Care System, Mather, CA, USA Department of Physical Medicine and Rehabilitation, University of California Davis, Sacramento, CA, USA Christopher  Hogrefe, MD, FACEP, CAQ-SM Department of Emergency Medicine, University of Iowa Hospitals and Clinics, Iowa City, IA, USA Rachel  Brakke  Holman, MD Department of Physical Medicine and Rehabilitation, University of Colorado School of Medicine, Aurora, CO, USA Stephen Huang, MD  Department of Orthopaedic Surgery, John Peter Smith Hospital Sports Medicine, Fort Worth, TX, USA Kenneth J. Hunt, MD  Department of Orthopedics, Division of Foot and Ankle, University of Colorado School of Medicine, Aurora, CO, USA Kyros  Ipaktchi, MD, FACS Department of Orthopedic Surgery, Denver Health Medical Center, Denver, CO, USA Bjorn C. Irion, MD  Western Orthopedics & Sports Medicine, Grand Junction, CO, USA Nathaniel S. Jones, MD, CAQ-SM  Department of Orthopaedic Surgery & Rehabilitation, Health Sciences Campus, Loyola University Medical Center, Maywood, IL, USA Christopher D. Joyce, MD  Department of Orthopedics, University of Colorado School of Medicine, Aurora, CO, USA Morteza  Khodaee, MD, MPH, FACSM, FAMSSM, FAAFP Department of Family Medicine and Orthopedics, University of Colorado School of Medicine, Denver, CO, USA Robert  Kiningham, MD Department of Family Medicine, University of Michigan, Ann Arbor, MI, USA Yuka  Kobayashi, DO  Department of Orthopedic Surgery, Medical College of Wisconsin, Milwaukee, WI, USA Brian  J.  Krabak, MD, MBA, FACSM Department of Rehabilitation, Orthopedics, and Sports Medicine, University of Washington and Seattle Children’s Sports Medicine, Seattle, WA, USA Matthew  J.  Kraeutler, MD Department of Orthopedics, St. Joseph’s University Medical Center, Paterson, NJ, USA

xviii

Ellen  Kroin, MD  Department of Orthopaedic Surgery, Loyola University Medical Center, Maywood, IL, USA Allison  D.  Lane, MD  Department of Emergency Medicine, University of Arizona/Banner University Medical Center, Tucson, AZ, USA Mark E. Lavallee, MD, CSCS, FACSM York Sports Medicine Fellowship Program, York, PA, USA Pennsylvania State University College of Medicine, Hershey, PA, USA USA Weightlifting, Sports Medicine Society, Colorado Springs, CO, USA International Weightlifting Federation, Budapest, Hungary York Hospital, York, PA, USA Lior  Laver  Head of the Hip Preservation and Sports Hip Service, Sports Medicine Unit, Department of Orthopaedics, Hillel Yaffe Medical Center, Hod-Hasharon, Israel Hannah  P.  Leahy, DO Department of Physical Medicine and Rehabilitation, Wellspan Health, Gettysburg, PA, USA Matthew  S.  Leiszler, MD University Health Services, University of Notre Dame, Notre Dame, IN, USA Christine  A.  Marschilok, MD  Department of Family and Community Medicine, Thomas Jefferson University, Philadelphia, PA, USA Benjamin Marshall, DO  Department of Physical Medicine and Rehabilitation, University of Colorado School of Medicine, Aurora, CO, USA Robert Masocol, MD  Department of Family Medicine, Greenville Health System/University of South Carolina School of Medicine, Greenville, SC, USA Seth A. Mathern, MD  Department of Family Medicine, University of Colorado School of Medicine, Denver, CO, USA Stephanie  W.  Mayer, MD  Department of Orthopedics, University of Colorado School of Medicine, Aurora, CO, USA Andrew McBride, MD  Department of Family Medicine, University of Colorado School of Medicine, Aurora, CO, USA Joseph Medellin, MD, MPH, MBA  Department of Sports Medicine, Henry Ford Allegiance Health, Jackson, MI, USA Omer Mei-Dan, MD  Department of Orthopedics, University of Colorado School of Medicine, Aurora, CO, USA David  Millward, MD, MS  Primary Care Sports Medicine, Campus Health Services, The University of Arizona, Tucson, AZ, USA Aaron  J.  Monseau, MD Department of Emergency Medicine, West Virginia University School of Medicine, Morgantown, WV, USA William  J.  Moreau, DC, DACBSP, FACSM Sports Medicine Division, United States Olympic Committee, Colorado Springs, CO, USA Rebecca Ann Myers, MD  Longs Peak Family and Sports Medicine, Department of Family and Sports Medicine, University of Colorado School of Medicine, Longmont, CO, USA Dustin  Nabhan, DC, DACBSP, CSCS, RMSK Sports Medicine Division, United States Olympic Committee, Colorado Springs, CO, USA

Contributors

Contributors

xix

Catherine Mygatt Naden, MD  Ryan Center for Sports Medicine, Boston University, Boston, MA, USA Kyle  B.  Nagle, MD, MPH Departments of Pediatrics, Orthopedics, and Rehabilitation, Seattle Children’s and University of Washington School of Medicine, Seattle, WA, USA Vicki  Nelson, MD, PhD Department of Family Medicine, Greenville Health System, Greenville, SC, USA Cory A. Newman, PT, DPT, OCS  Proactive Physical Therapy, Tuscon, AZ, USA Britain O’Connor, MD  Family Medicine Residency, Rush Copley Medical Center, Aurora, IL, USA Lauren  Oberle, MD Department of Family Medicine, University of Colorado School of Medicine, Denver, CO, USA Joshua  V.  Okon, MD  Department of Family and Community Medicine, Sports Medicine Section, Thomas Jefferson University, Philadelphia, PA, USA Andrew Pasternak, MD, MS  Silver Sage Sports and Fitness Lab, University of Nevada Reno School of Medicine, Reno, NV, USA Deepak  S.  Patel, MD, FAAFP, FACSM Rush Copley Sports Medicine, Rush Medical College, Yorkville, IL, USA Stephen R. Paul, MD, MA  Department of Family and Community Medicine, Campus Health Service, University of Arizona, Tucson, AZ, USA Sourav  K.  Poddar, MD Department of Family Medicine and Orthopedics, CU Sports Medicine Center, University of Colorado School of Medicine, Denver, CO, USA Brent C. Pottenger, MD, MHA  Department of Physical Medicine and Rehabilitation, Johns Hopkins University School of Medicine, Baltimore, MD, USA Ashwin  L.  Rao, MD Department of Family Medicine, University of Washington, Husky Stadium Sports Medicine Center, Seattle, WA, USA Jeremiah W. Ray, MD, FACEP, CAQSM  Department of Orthopedic Surgery, University of California at Davis Medical Center, Davis, CA, USA Mark F. Riederer, MD  Department of Orthopaedic Surgery, University of Michigan, C.S. Mott Children’s Hospital, Ann Arbor, MI, USA Jaron  Santelli, MD Department of Emergency Medicine and Orthopedics, University of Maryland Medical Center, Baltimore, MD, USA Volker  Scheer, MD, MRCGP, MECOSEP Health Science Department, Universidad a Distancia de Madrid (UDIMA), Madrid, Spain Ultra Sports Science Foundation, Pierre-Bénite, France Adam Schiff, MD  Department of Orthopaedic Surgery, Loyola University Medical Center, Maywood, IL, USA Daphne Amanda Scott, MD  Primary Sports Medicine, Hospital for Special Surgery, New York, NY, USA Frank Scott, MD  Department of Orthopedics, University of Colorado School of Medicine, Aurora, CO, USA Adam Seidl, MD  Department of Orthopedics, University of Colorado School of Medicine, UCHealth Steadman Hawkins Clinic Denver – Surgery Center, Englewood, CO, USA

xx

Darcy  Selenke, MD Department of Family Medicine, University of Colorado School of Medicine, Denver Health, Winter Park Medical Center, Winter Park, CO, USA Babak Shadgan, MD, MSc Sports Med, PhD  Department of Orthopaedics, University of British Columbia, Vancouver, BC, Canada Medical, Prevention and Anti-Doping Commission, United World Wrestling (UWW), Corsiersur-Vevey, Switzerland Kimberly Sikule, MD  Department of Family Medicine, University of Vermont, Burlington, VT, USA Amy M. Singer, DO  Department of Family Medicine, Banner UMC, Tucson, AZ, USA Stephen M. Spadafore, MD  Department of Family Medicine, University of Colorado School of Medicine, Denver, CO, USA Kimberly M. Spahn, MD  Department of Orthopaedics, Naval Medical Center San Diego, San Diego, CA, USA Jack  Spittler, MD, MS Department of Family Medicine and Orthopedics, University of Colorado School of Medicine, Denver, CO, USA J. Herbert Stevenson, MD  Department of Family Medicine, Division of Sports Medicine, University of Massachusetts Medical Center, Worcester, MA, USA Jennifer D. Stromberg, MD  Carolina Family Practice and Sports Medicine, Duke Community and Family Medicine, Cary, NC, USA Emily  A.  Sweeney, MD Department of Orthopedics, University of Colorado School of Medicine, Children’s Hospital Colorado, Aurora, CO, USA Sheila E. Taylor, DO  Christiana Care in Wilmington, University of Delaware, Delaware, USA James Thing, MBBS, BSc, MRCGP, FFSEM  Sports and Exercise Medicine, Barts Health, London, UK Jill N. Tirabassi, MD  Department of Family Medicine and Community Health, University of Massachusetts Medical Center, Worcester, MA, USA Spencer Tomberg, MD  Department of Emergency Medicine and Orthopedics, Denver Health Medical Center, Denver, CO, USA Karin  VanBaak, MD Department of Family Medicine and Orthopedics, University of Colorado School of Medicine, Aurora, CO, USA Armando F. Vidal, MD  The Steadman Clinic, Steadman Philippon Research Institute, Vail, CO, USA Bryant Walrod, MD  Department of Family Medicine, The Ohio State University, Wexner Medical Center, Columbus, OH, USA Abigail Y. Wang, BS  Department of Orthopedic Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA Anna L. Waterbrook, MD  Department of Emergency and Sports Medicine, The University of Arizona, Tucson, AZ, USA K.  Linnea  Welton, MD Department of Orthopedic Surgery, MultiCare Health System, Auburn, WA, USA Ryan C. Wennell, DO  Sports Medicine, Wellspan York Hospital, York, PA, USA Luke  Widstrom, DO  Department of Orthopedics, Essentia Health-Duluth Clinic, Duluth, MN, USA

Contributors

Contributors

xxi

Jessica J. Wingfield, MD  Department of Orthopedics, Hand Surgery, University of Colorado School of Medicine, Denver, CO, USA Michelle  Wolcott, MD Department of Orthopedics, CU Sports Medicine, University of Colorado School of Medicine, Denver, CO, USA Andrew  M.  Wood, MD  Department of Family Medicine, Denver Health Medical Center, Denver, CO, USA David Ziegler, MD  Department of Orthopedics, Denver Health Medical center, Denver, CO, USA Matthew G. Zmurko, MD  Vermont Orthopaedic Clinic, Rutland Regional Medical Center, Rutland, VT, USA Adam C. Zoga, MD, MBA  Musculoskeletal Radiology, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA, USA

Part I General Approach to Sports Trauma Anna L. Waterbrook

1

Initial Evaluation, Resuscitation, and Acute Management Anna L. Waterbrook and Moira Davenport

Key Points

• The initial sideline evaluation of an injured athlete involves rapid triage and assessment using primary and secondary survey to assess for life-threatening injuries. • Sideline management of these injuries focuses on identifying and correcting immediate life threats rather than trying to determine the precise anatomic etiology. • A high degree of suspicion is needed for many potentially life-threatening injuries: frequent reevaluations are essential and any decompensation at any time or any clinical concern warrants immediate transport to the emergency department.

One of the primary roles of the sports medicine physician is the management of acute trauma from sports. Whether it is a benign or more serious life-threatening injury, the sports medicine physician needs to be able to rapidly evaluate and triage these athletic-related injuries. As the speed and intensity with which a variety of sports are played increases, there is concern that injury rates and severity will rise proportionally. The vast majority of serious, acute injuries that are seen by sports medicine providers will be due to blunt trauma that is most commonly seen in contact/collision sports such as football, ice hockey, snowboarding, skiing, bungee jumping, and other sports characterized by rapid deceleration and/or A. L. Waterbrook (*) Department of Emergency and Sports Medicine, The University of Arizona, Tucson, AZ, USA e-mail: [email protected] M. Davenport Department of Emergency Medicine, Allegheny General Hospital Emergency Medicine Residency, Temple University School of Medicine, Allegheny General Hospital, Pittsburgh, PA, USA

high-energy impact. Despite this, there is a paucity of available sports medicine literature on how to manage acute trauma in sports. As outlined in the Team Physician Consensus Statement [1], it is imperative that sports medicine physicians be aware of the many injuries that are associated with blunt trauma and the acute sideline management of these injuries. Developing a generalized approach to the management of acute trauma in sports, whether evaluating patients on the sideline or in the office is critical. The most important element in the appropriate management of sideline trauma is early recognition and management of injuries. Advanced Trauma Life Support (ATLS) [2] is a course designed to teach physicians how to provide emergency care and stabilization for trauma patients. ATLS principles emphasize identifying and treating the greatest threat to life first and recognizing that lack of a definitive diagnosis should not impede treatment. During the primary survey, life-­threatening injuries are identified in a prioritized sequence based upon the effects these injuries will have on a patient’s physiology. Initially, it is frequently not possible to identify the specific anatomic injury. The primary survey is based upon the degree of life threat, with the most immediate threat addressed first. The mnemonic ABCDE (airway, breathing, circulation, disability, environment) defines the specific, ordered evaluations and interventions that should be followed for all patients and is based upon how quickly each injury could lead to death, e.g., loss of airway is the most immediate life threat that will lead to death before problems with breathing, circulation, or head injury. This is a very different approach than the performance of a detailed history and physical exam to develop a differential diagnosis before implementing treatment approach that is typically taught during medical training. When approaching any athlete who is found down after sustaining trauma, it is important to first quickly assess the athlete’s vital functions. This can be quickly accomplished by evaluating the athlete’s Glasgow Coma Scale (GCS) (Table  1.1), systolic blood pressure, and respiratory rate.

© Springer Nature Switzerland AG 2020 M. Khodaee et al. (eds.), Sports-related Fractures, Dislocations and Trauma, https://doi.org/10.1007/978-3-030-36790-9_1

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A. L. Waterbrook and M. Davenport

Table 1.1  Glasgow Coma Scale (GCS) 1 Does not open eyes Verbal Makes no sounds

2 Eyes open in response to painful stimuli Incomprehensible sounds

Motor Makes no movements

Nonpurposeful Decerebrate response (extensor Decorticate response posturing to painful stimuli) (flexor posturing to painful movement to painful stimuli stimuli)

Eye

3 Eyes open in response to voice Inappropriate words

A blood pressure cuff is not required to perform a rapid assessment of the patient’s blood pressure. As a general rule of thumb, if only the patient’s carotid pulse is palpable, then the systolic blood pressure is 60–70  mm Hg; if both the carotid and femoral pulses are palpable, then the systolic blood pressure is 70–80 mm Hg; and if the radial pulse is also palpable, then the systolic blood pressure is >80 mm Hg. Once the athlete’s vital functions have been assessed, then it is appropriate to move on to the primary survey. One quick way to do this is to ask the athlete his/her name, what happened/last play in game. Appropriate responses suggest normal function of vital parameters, e.g., ability to speak clearly (no airway compromise), breathing not severely compromised (air movement to produce speech), and no decreased level of consciousness (can describe what happened).

4 Eyes open spontaneously Confused, converses

5 N/A

6 N/A

Oriented, converses normally Localizes to painful stimuli

N/A

Follows commands

Fig. 1.1  Jaw thrust, chin lift technique

Airway The first priority in any trauma patient is airway management to ensure adequate oxygenation and ventilation. It is essential to know the available equipment and how to gain airway access in case of an emergency. The airway should be assessed for patency and any evidence of an airway obstruction due to acute issues such as foreign body or tracheal/laryngeal fracture. In addition, any patient with a GCS of 2–3 days post-trauma) and includes adjacent joint effusion (e.g., hemorrhage), septic and inflammatory arthritis, cellulitis, and Morel-Lavallée lesion [12, 13]. Plain radiography is only indicated if there is a concern for fracture, retention of foreign body, or concern for underlying bony abnormality (e.g., Haglund’s deformity) or calcification [1, 9, 14]. Ultrasound can be a useful modality in visualizing the enlarged bursa particularly in cases of significant soft tissue edema due to cellulitis or abrasion (Fig.  37.1d) [8, 15]. Color Doppler may help visualize inflammatory process in and around the bursa. Ultrasound can also help with needle placement for aspiration in difficult cases (e.g., smaller bursae and adjacent cellulitis or abrasion) [8, 15]. Though the presence of enhancement in MRI cannot differentiate between septic and aseptic bursitis, the absence is indicative of aseptic bursitis [8, 16, 17]. After history, physical examination, and applicable blood tests and imaging, if there is still uncertainty regarding the etiology of the bursitis, and particularly if there is a high suspicion of septic bursitis, an aspiration under sterile conditions of the bursal fluid should be performed [7, 8, 10, 13, 18–21]. A Z-track method of inserting the needle in which the skin and deeper layers are not in the same plane after needle placement helps seal the path [22]. This can be achieved by pulling the overlying skin during the needle insertion. The bursal aspiration should be performed with a large-bore needle (e.g., 18–22 gauge) prior to the administration of the first dose of antibiotics [18]. The aspirated fluid should be sent for cell count, gram stain, culture, glucose, and crystal analysis [9, 13, 14]. In general, bursal fluid that is cloudy or purulent in appearance is more likely to represent a septic bursitis. Obviously, bursal fluid appears bloody in hemorrhagic bursitis. In addition to aiding in diagnosis, bursal aspiration can improve symptoms and reduce bacterial load in septic bursitis and may be repeated daily as part of the treatment regimen if indicated [7, 8, 18]. The use of a compressive bandage after aspiration may help reduce re-­accumulation of the bursal fluid [7, 18, 23]. It seems that aspiration in patients with therapeutic INR is safe and does not significantly increases the risk of hematoma or bleeding [24].

Treatment After ruling out fractures, most acute traumatic superficial bursitis cases can be managed conservatively with ice, ele-

673 Table 37.1  SORT: key clinical recommendations Evidence Clinical recommendation rating C Bursal fluid aspiration should be performed in patients with acute large traumatic superficial bursitis [2, 3, 5, 25] Bursal fluid aspiration and culture should be performed C in patients with suspecting septic superficial bursitis [7, 13, 14, 18, 19, 21, 26–29]

vation, relative rest, and analgesics [3]. Bursal aspiration may shorten the duration of symptoms in cases of acute hemorrhagic bursitis with significant bursal enlargement and interference with daily activities (Table 37.1). It is critical to weigh the potential benefits over the potential risks of aspiration on an individual basis. If aspiration is considered, it is better to be performed in a few hours of its occurrence or after the disintegration of the coagulated bursal fluid is started a couple of weeks later [3]. Padding may decrease the risk of traumatic hemorrhagic bursitis in high-risk sports (e.g., wrestling). Padding should not limit the adjacent joint range of motion.

Return to Sports Athletes should be able to return to their sports when the affected bursitis is not interfering with their performance.

References 1. Hudson K, Delasobera BE. Bursae. In: Birrer RB, O’Connor FG, Kane SF, editors. Musculoskeletal and sports medicine for the primary care practitioner. 4th ed. Boca Raton: CRC, Taylor & Francis Group; 2016. p. 111–6. 2. Aaron DL, Patel A, Kayiaros S, Calfee R.  Four common types of bursitis: diagnosis and management. J Am Acad Orthop Surg. 2011;19(6):359–67. 3. Khodaee M.  Common superficial bursitis. Am Fam Physician. 2017;95(4):224–31. 4. Chhabra A, Cerniglia CA. Bursae, cysts and cyst-like lesions about the knee. J Am Osteopath Coll Radiol. 2013;2(4):2–13. 5. Kaiser P, Schmidle G, Raas C, Blauth M. Treatment concept for a traumatic lesion of the prepatellar bursa. Oper Orthop Traumatol. 2015;27(5):427–36. 6. Campanelli V, Piscitelli F, Verardi L, Maillard P, Sbarbati A.  Lower extremity overuse conditions affecting figure skaters during daily training. Orthop J Sports Med. 2015;3(7): 2325967115596517. 7. Baumbach SF, Lobo CM, Badyine I, Mutschler W, Kanz KG.  Prepatellar and olecranon bursitis: literature review and development of a treatment algorithm. Arch Orthop Trauma Surg. 2014;134(3):359–70. 8. Chard MD, Walker-bone K.  The elbow. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, editors. Rheumatology. 6th ed. Philadelphia: Mosby; 2015. p. 611–7. 9. Harris-Spinks C, Nabhan D, Khodaee M.  Noniatrogenic septic olecranon bursitis: report of two cases and review of the literature. Curr Sports Med Rep. 2016;15(1):33–7.

674 10. Wasserman AR, Melville LD, Birkhahn RH.  Septic bursitis: a case report and primer for the emergency clinician. J Emerg Med. 2009;37(3):269–72. 11. Wingert NC, DeMaio M, Shenenberger DW. Septic olecranon bursitis, contact dermatitis, and pneumonitis in a gas turbine engine mechanic. J Shoulder Elb Surg. 2012;21(5):e16–20. 12. Khodaee M, Deu RS, Mathern S, Bravman JT.  Morel-Lavallee lesion in sports. Curr Sports Med Rep. 2016;15(6):417–22. 13. McAfee JH, Smith DL.  Olecranon and prepatellar bursitis. Diagnosis and treatment. West J Med. 1988;149(5):607–10. 14. Reilly D, Kamineni S.  Olecranon bursitis. J Shoulder Elb Surg. 2016;25(1):158–67. 15. Blankstein A, Ganel A, Givon U, Mirovski Y, Chechick A.  Ultrasonographic findings in patients with olecranon bursitis. Ultraschall Med. 2006;27(6):568–71. 16. Bellon EM, Sacco DC, Steiger DA, Coleman PE. Magnetic resonance imaging in “housemaid’s knee” (prepatellar bursitis). Magn Reson Imaging. 1987;5(3):175–7. 17. Floemer F, Morrison WB, Bongartz G, Ledermann HP.  MRI characteristics of olecranon bursitis. AJR Am J Roentgenol. 2004;183(1):29–34. 18. Abzug JM, Chen NC, Jacoby SM. Septic olecranon bursitis. J Hand Surg Am. 2012;37(6):1252–3. 19. Laupland KB, Davies HD. Olecranon septic bursitis managed in an ambulatory setting. The Calgary home parenteral therapy program study group. Clin Invest Med. 2001;24(4):171–8.

M. Khodaee 20. Morrey BE. Bursitis. In: Morrey BE, Sanchez-Sotelo J, editors. The elbow and its disorders. 4th ed. Philadelphia: Saunders Elsevier; 2009. p. 1164–73. 21. Zimmermann B 3rd, Mikolich DJ, Ho G Jr. Septic bursitis. Semin Arthritis Rheum. 1995;24(6):391–410. 22. Pullen RL Jr. Administering medication by the Z-track method. Nursing. 2005;35(7):24. 23. McFarland EG, Gill HS, Laporte DM, Streiff M.  Miscellaneous conditions about the elbow in athletes. Clin Sports Med. 2004;23(4):743–63.. xi–xii 24. Conway R, O’Shea FD, Cunnane G, Doran MF. Safety of joint and soft tissue injections in patients on warfarin anticoagulation. Clin Rheumatol. 2013;32(12):1811–4. 25. Larson RL, Osternig LR.  Traumatic bursitis and artificial turf. J Sports Med. 1974;2(4):183–8. 26. Choudhery V. The role of diagnostic needle aspiration in olecranon bursitis. J Accid Emerg Med. 1999;16(4):282–3. 27. Sayegh ET, Strauch RJ.  Treatment of olecranon bursitis: a systematic review. Arch Orthop Trauma Surg. 2014;134(11): 1517–36. 28. Shell D, Perkins R, Cosgarea A.  Septic olecranon bursitis: recognition and treatment. J Am Board Fam Pract. 1995;8(3): 217–20. 29. Stell IM. Septic and non-septic olecranon bursitis in the accident and emergency department--an approach to management. J Accid Emerg Med. 1996;13(5):351–3.

38

Nerve Benjamin Marshall and Rachel Brakke Holman

Key Points

• Peripheral nerve injuries in sport, though common, are usually brief and self-limited • Higher-grade injuries are generally categorized into three major subtypes as detailed in Fig. 38.1. • Most injuries can be managed nonoperatively with protection/splinting and therapeutic exercise • Prognosis is highly dependent on severity of injury and can be further delineated with NCS/EMG testing • NCS/EMG testing is commonly performed at >3 weeks, 3 months, and 6 months following acute nerve injury • Return to sport decisions can be complex and are generally achieved through shared decision-making regarding the degree of functional recovery and susceptibility of nerve to reinjury during participation

Introduction and Neuroanatomy Peripheral nerve injury is a relatively common occurrence in sport and recreation though usually relatively mild; more severe injuries do occur and can result in significant disability if not recognized and managed appropriately. Knowledge of the basic structure and functional characteristics of the peripheral nervous system is essential to the diagnosis and management of nerve injury. Peripheral nerves contain an

B. Marshall (*) Department of Physical Medicine and Rehabilitation, University of Colorado School of Medicine, Aurora, CO, USA e-mail: [email protected] R. B. Holman Department of Physical Medicine and Rehabilitation, University of Colorado School of Medicine, Aurora, CO, USA e-mail: [email protected]

assortment of nerve fiber types that vary in the information they are transmitting (e.g., pain, temperature, pressure, motor signaling) and their microscopic anatomy (e.g., diameter, degree of myelination). Generally larger and more myelinated nerve fibers conduct signals faster and are more specific in functional innervation. For example, small unmyelinated C fibers transmit dull poorly localized pain signals, while large A-delta “fast” fibers transmit sharp, well-localized pain. Somatic peripheral nerves emanate from the spinal nuclei where the primary neurofunctional organization for the upper and lower extremities occurs in the brachial and lumbosacral plexuses, respectively, and then continue as singular nerves to their various target tissues. These peripheral nerves are supported externally by a connective tissue sheath, the epineurium, which encases several nerve groupings or fascicles, supported by their own perineural connective tissue and the associated vascular supply. Inside of each nerve fascicule are several individual nerve fibers insulated by an endoneurial connective tissue sheath. Each individual neural axon is supported by Schwann cells which form myelin sheaths and facilitate more rapid, saltatory conduction. This organizational hierarchy of connective tissue scaffolding plays a central role in nerve injury and regeneration.

Nerve Injury Severity Classification The most clinically useful classification system of nerve injury was first proposed in the 1940s by Dr. Herbert Seddon, a British orthopedist, and remains relatively unchanged today. It separates neural injury into three categories of increasing severity (Fig. 38.1). Neuropraxia is the least severe and represents a focal lesion to the nerve myelin sheath without damage of the underlying axon. These types of injuries represent a dysfunction in the transmission of neural depolarization, termed a conduction block, and can result in weakness or sensory loss that can last from minutes

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Fig. 38.1  Nerve injury categories

to a maximum of 3 months. These generally have an excellent prognosis for complete recovery, though they may be difficult to distinguish from more severe injury initially [11]. For example, following a “stinger”-type injury, a player may report complete upper extremity paresis that resolves in minutes to hours. Axonotmesis is the next level of severity and represents irrevocable damage to the axon in addition to its myelin sheath but without substantial damage to the supporting connective tissue scaffold (e.g., endoneurium or perineurium). This axonal discontinuity results in denervation of the target tissue with immediate clinical deficits from loss of neuronal transmission. With a focal axonal injury, unlike isolated myelin damage, the neuron will undergo Wallerian ­degeneration of the distal axonal segment starting within several days following the insult. This active degenerative process occurs to the orphaned axon may occur over a period of days to weeks. The length of this process which is mostly determined by the distance from the location of axonal injury to the target tissues. The cardinal feature of axonotmesis is the capacity for axonal regrowth. Though the axonal damage is irreparable, with the neuronal tract still in place, the axon will subsequently regrow down the intact scaffold to reinnervate its prior target. This process of regeneration, however, is notoriously slow compared to other soft tissue healing and generally occurs at a rate of 1 mm/day or approximately 1 in./month. Occasionally adjacent intact neurons can sprout additional terminal branches to innervate the orphaned tissue more rapidly. This process can occur within a few weeks but generally takes several months to form mature synapses [19].

A relatively common example of this would be axillary nerve injury following proximal humeral fractures or glenohumeral dislocations. This may significantly prolong recovery from the initial trauma from months to a year or more given the resultant deltoid weakness. The most severe category of nerve injury, neurotmesis, is notable for complete discontinuity of the axon, myelin sheath, and surrounding connective stroma. Without any substantive neural continuity, self-regeneration is not possible without surgical intervention [9]. This generally does not occur in sport without a significant concomitant injury such as peroneal nerve rupture during a severe multiligamentous knee injury.

Epidemiology and Mechanism of Injury Injury to a peripheral nerve can occur at any time during competition or practice but is rarely severe enough to cause significant debility. For example, arguably the most common injury in sport is the “stinger” or “burner” which is a traumatic upper brachial radiculoplexopathy that often results from rapid neck and shoulder distraction. This injury is common in contact sports with 50–60% of American football and rugby union athletes retrospectively acknowledging at least 1 prior episode or at an observed rate 1.5 occurrences per NCAA football team/season [3, 10]. However, fortunately, 64% of the football athletes had resolution within hours, and 8 h of hypoxemia which may occur from microvascular damage or associated compression from a hematoma or compartment syndrome [6].

Diagnosis and Imaging Diagnosis of peripheral nerve injury starts with localization of the injury along the neuroaxis. This is usually accomplished with a comprehensive history and peripheral neuromuscular exam. In most cases, seemingly similar complaints (i.e., grip weakness from ulnar mononeuropathy or lower cervical radiculopathy) can be confidently discriminated in this manner. In cases where localization is difficult or still unclear, nerve conduction studies or electromyography (EMG/NCS) may be utilized as an extension of the physical exam. EMG/NCS may better characterize the location but can also elucidate the extent of the peripheral nerve lesion. EMG/NCS is a quantitative functional neuromuscular evaluation of peripheral nerve lesions that is generally performed by a neurologist or physiatrist but is not without its limitations. Electrodiagnostic evaluation of acute peripheral nerve injury will locate a nerve injury but only if it is severe enough to significantly affect neuronal function of large sensory or motor fibers. Small caliber neuronal fibers such as sensory C-fiber injuries or dysfunction, for example, may result in substantial clinical symptoms (i.e., paresthesia, dull or achy

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pain) but is not evaluated well by EMG/NCS [19]. Furthermore, there are some electrodiagnostic limitations based on injury location. The most relevant of which is sensory neuronal injuries proximal to the dorsal root ganglion such as with radiculopathic injury due to a herniated intervertebral disc. Patients may experience significant radicular pain, paresthesia, or numbness; however, due to the injury’s location proximate to the sensory neuronal cell body, a standard electrodiagnostic evaluation may appear normal ­ unless motor neuron function is impaired [19]. Finally, the timing of electrodiagnostic testing may further limit evaluation of the nerve injury. Electrodiagnostic evaluation of axonal lesions is partly dependent on the process of Wallerian degeneration and may be of limited value until this process is completed [4]. For example, EMG/NCS testing performed immediately after an axonometric injury to the ulnar nerve can resemble a neuropraxic lesion as the ulnar nerve distal to the injury is still mostly intact and functional. However, after ~3  weeks following injury, Wallerian degeneration of the ulnar nerve distal to the lesion results in changes in the electrophysiology of the denervated muscle that may be elicited by EMG testing. EMG/NCS may be most useful to the evaluating physician in the differentiation of the neuronal injury severity. Electrodiagnostic differentiation between neuropraxia, axonotmesis, and neurotmesis is based on the functional characteristics of the nerve and innervated muscle. Neuropraxic lesions demonstrate focal slowing of nerve conduction across the lesion due to disruption of saltatory conduction from demyelination. Such slowing may be so severe that neural depolarization fails to propagate across the lesion resulting in a complete conduction block. Complete blocks may be difficult to distinguish from axonal lesions initially and partly rely on timing of evaluation, as discussed above, to convincingly discriminate the two. Axonometic injury is largely determined by the electrophysiologic response of the denervated muscle tissue. Such orphaned muscle cells spontaneously depolarize in stereotyped patterns that can be characterized with electromyography. Neurotmetic injuries demonstrate similar patterns of increased spontaneous activity of myocytes but fail to demonstrate restoration of immature motor unit action potentials, the so-called reinnervation or nascent potentials, which develop with restoration of neural continuity. Practically this suggests EMG/NCS testing is most useful ~3  weeks and 2–3  months after injury for an athlete with ongoing neurologic deficits. At 3 weeks to determine if the injury was predominantly neuropraxic or if significant axonal damage occurred and then at 3 months, to determine if the axonal injury appears to be the result of an axonometric or neurotmetic injury giving the provider a better understanding of prognosis and guiding treatment recommendations. Magnetic resonance imaging (MRI) may occasionally also play a role in diagnostic workup of an acute nerve injury.

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Generally the utility of MRI is in the analysis of associated or contributing extraneural factors such as a compressive cyst or bone fragment as well as ligament or tendinous disruption. MRI may note other features suggestive of nerve injury including increased neuronal caliber or T2 hyperintensity with loose fascicular definition, possibly with eventual neuroma formation which would suggest some degree of stroma disruption [16]. Some imaging facilities and academic centers have started to offer MR neurography to aide in the assessment of neuronal imaging. Currently there is no standard definition of what this imaging sequence entails, but it is generally composed of high-resolution T1- and a heavily fat-suppressed T2-weighted series to better visualize pathologic changes in neural tissues. Another imaging technology that is not yet readily available for clinical use but has significant potential for improving evaluation of nerve injury is MR diffusion tensor tractography (DTT). DTT is a novel imaging modality that has the potential to provide more quantitative information on axonal continuity following injury [12]. In addition to MR technologies, high-resolution ultrasound is increasingly used by physicians in the diagnosis and treatment of nerve injury [18]. Over the past decade, improvements in musculoskeletal ultrasound technology, as well as the increasing availability and affordability of commercial units, have allowed for incorporation of this technology into many sports practitioners’ clinical practice. The primary advantage of ultrasound for the imaging of nerve injury is its ability to dynamically access the nerve in real time. This is particularly useful in athletes where nerve instability, such as subluxation of the ulnar nerve at the elbow, is relatively common. High-resolution ultrasound is not without limitation as imaging of nervous tissue near bone or at increasing depth limits resolution. Ultrasound is particularly adept at the structural analysis of superficial nerves and can be used in office to further examine the peripheral nerve along the length of its anatomic course. Sonographic-­ pathoanatomic changes that occur with nerve injury will mirror the findings on MRI.  Injured nerves may appear increasingly hypoechoic with a loss of fascicular architecture and may have neuromas-in-continuity [12]. Additionally, many compressive neuropathies result in increased neural caliber relative to proximate nerve segments. As such sonographic diagnostic criteria now exist for an increasing number of neuropathies which appear complimentary to electrodiagnostic testing and have the potential to achieve similar levels of specificity and sensitivity [7].

 rognosis and General Management P Principals General management of nerve injury in an athlete relies heavily on the believed degree of injury severity as this plays a central role in the prognosis and probability of neural

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recovery. Isolated neuropraxic injuries generally experience complete recovery of prior neural function within 3 months depending on severity and segmental length of injury. The primary goal in these cases is to identify any ongoing factors, such as compressive equipment or poor sport-specific mechanics, which may be perpetuating the neuronal trauma [4]. Additionally, it is important to protect any at-risk ­structures due to the nerve dysfunction. An example of this is ankle bracing or the use of an ankle foot orthosis with peroneal nerve injuries as motor dysfunction in the ankle dorsiflexors and evertors increases risk of ankle instability and inversion sprains. Axonometric injury recovery is tied to the degree of adjacent neuronal injury. That is, if a peripheral nerve undergoes only partial axonometric injury, the neighboring intact axons may generate nodal or terminal sprouts that migrate to the denervated tissue to reestablish neuronal signaling [2]. This process is generally faster than would be allowed should these axons need to undergo the full process of Wallerian degeneration and axonal regrowth. Often electrodiagnostic evidence of recovery in these muscles is detected starting approximately 2  months following the injury, though clinically evident recovery generally takes significantly longer. If complete nerve axonal disruption occurs, whether through axonometric or neurotmetic injury, recovery is prolonged and often incomplete. If the injury is clearly a complete neurotmetic disruption, such as in open transection, urgent neurosurgery referral is needed to re-­ appose the nerve. However, most injuries of this severity in sport are closed with an unclear degree of severity despite imaging and electrodiagnostic evaluation. The clinician’s role is primarily to track the athlete’s progress closely for signs of reinnervation to attempt to better classify the degree of injury. This is typically done with serial physical exams and EMG/NCS at regular intervals starting 3  weeks post-­ injury. As stated previously, electrodiagnostic testing is more sensitive to early reinnervation in the effected muscle and, if neural continuity is found within 4–6 months, can indicate a good prognosis with ongoing conservative care [9, 19]. If no evidence of neural recovery is found on EMG/NCS within 6  months, the injury is considered to be neurotmetic, and surgical referral is warranted. In these cases, the neural injury was generally substantial enough to disrupt the supporting tissues and connective tissue architecture and not allow for axonal regeneration. The nerve will still attempt to bridge the lesion, but this usually results in a disorganized proliferation of axon, Schwann cells, and connective tissue that results in neuroma scar formation. Surgery in these cases generally consists of resection of this nonfunctional nerve proliferation and either direct or graft-based reanastomosis of the opposing nerve endings to encourage axonal regrowth. The outcome of such an intervention is partly dependent on surgical factors as well as the quality of the innervated tissue. If the target muscle is substantially replaced by fatty atrophy, a

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process that occurs after 12–24  months, reinnervation and functional recovery become much less likely. Available literature on surgical nerve repair indicates outcomes start declining at about 9 months with a more precipitous decline in outcomes after 12–15 months [9, 13]. Surgical constraints also appear to play a role as direct nerve repair tends to result in the highest degree of functional improvement with less favorable outcomes if grafting is required to maintain a tension-­free repair. In cases where nerve injury has persisted past these time points, often only function salvaging surgeries, such as tendon transfer or joint fusion, are available [9, 14].

Return to Sports The decision to allow an athlete to return to competitive sport following nerve injury can be difficult and the practitioner must balance a multitude of factors to make the best possible recommendation. Unfortunately, there is scarce empirical evidence and no formal organizational guidelines to help with the decision. Therefore, return to play criteria have mostly been guided by expert opinion. Current attempts at a classification system for return to play following nerve injury are most common among “stinger”-type injuries. No system predominates but significant similarities exist among recommendations [5, 20]. Generally, the athlete must experience complete resolution of all symptoms (including during sport-specific tasks) and have pain-free, full, cervical range of motion without the presence of significant known conditions that would predispose to recurrent injury (i.e., cervical stenosis, spondylolisthesis, etc). If the athlete does have recurrent stingers in the same season, generally more advanced workup is warranted before allowing the athlete to return. Possible specialist referral and termination of participation in collision sports, if applicable, should be considered following three or more “stinger” episodes. It is probably reasonable to extrapolate these criteria as a general guideline governing return to play for most peripheral nerve injuries. However, it is even more difficult in an athlete only experiencing partial neural recovery, as this is not an absolute contraindication to sport participation. It is primarily important that the physician ensure that presence of ongoing neurologic deficits is a result of incomplete terminal recovery and not due to significant ongoing neuronal healing. Differentiating the two is often the task of the treating physician and is accomplished by utilizing the diagnostic modalities discussed in the prior section. If there is incomplete neurologic recovery, there are several important considerations before a return to play decision can be reached. Firstly, has the athlete reached a level of functional recovery that would safely allow for sport-specific tasks? If, because of the ongoing functional deficit, the athlete cannot

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perform at a level commensurate with the demands of their sport or if the deficit would result in a higher risk of injuries to other tissues, this could preclude them from returning to sport. This determination is often made in close collaboration with the training room or physical therapy staff since subtle functional deficits may be difficult to access in the office but can result in significant relative debility in the high-demand setting of sport competition. Also, consideration of additional measures that may be taken to improve the performance or safety deficit from the impairment should help inform this determination. For example, even trace peroneal dysfunction and associated ankle eversion weakness may increase the likelihood of lateral ankle sprains. However, with ankle bracing or taping, this risk may be improved to an acceptable level to allow for a safe return to sport. Also worrisome is the potential for reinjury given a return to the environment that likely precipitated the injury. Any allowable additional protective equipment or splinting that may reduce the likelihood of recurrent injury should be recommended despite scant evidence that commonly used devices significantly reduce the risk of reinjury. The predominant example of this is the use of cervical collars or neck rolls for “stinger” prevention, which has been shown to reduce excessive cervical hyperextension but not lateral flexion in laboratory testing [8] but lack any significant analysis during competition. Similarly, a comprehensive evaluation of biomechanical factors that would have predisposed the injury should be addressed. This is seen frequently with baseball pitchers following ulnar nerve injury about the elbow. Often improved pitching mechanics can significantly reduce the vulnerability of the previously injured nerve without sacrificing performance. Although physical protection or activity modification is ideal to help facilitate a safe return to sport, occasionally avoidance of the factors that resulted in the initial injury is not feasible, and the treating physician must do their best to ensure optimal neural recovery before resumption of sport-­ specific activities.

References 1. Ali ZS, Pisapia JM, Ma TS, Zager EL, Heuer GG, Khoury V.  Ultrasonographic evaluation of peripheral nerves. World Neurosurg. 2016;85:333–9.

681 2. Boeltz T, Ireland M, Mathis K, Nicolini J, Poplavski K, Rose SJ, Wilson E, English AW. Effects of treadmill training on functional recovery following peripheral nerve injury in rats. J Neurophysiol. 2013;109(11):2645–57. 3. Cunnane M, Pratten M, Loughna S.  A retrospective study looking at the incidence of ‘stinger' injuries in professional rugby union players. Br J Sports Med. 2011;45:A19. 4. Davis G, Kline DG, Spinner RJ, Zager EL, Garberina MJ, Williams GR, McCrory P.  Clinics in neurology and neurosurgery of sport: peripheral nerve injury. Br J Sports Med. 2009;43(7):537–40. 5. Eddy D, Congeni J, Loud K. A review of spine injuries and return to play. Clin J Sport Med. 2005;15(6):453–8. 6. Feinberg JH, Nadler SF, Krivickas LS. Peripheral nerve injuries in the athlete. Sports Med. 1997;24(6):385–408. 7. Fowler JR, Munsch M, Tosti R, Hagberg WC, Imbriglia JE.  Comparison of ultrasound and electrodiagnostic testing for diagnosis of carpal tunnel syndrome: study using a validated clinical tool as the reference standard. J Bone Joint Surg Am. 2014;96(17):e148. 8. Gorden JA, Straub SJ, Swanik CB, Swanik KA. Effects of football collars on cervical hyperextension and lateral flexion. J Athl Train. 2003;38(3):209–15. 9. Grant GA, Goodkin R, Kliot M. Evaluation and surgical management of peripheral nerve problems. Neurosurgery. 1999;44:825. 10. Green J, Zuckerman SL, Dalton SL, Djoko A, Folger D, Kerr ZY. A 6-year surveillance study of "stingers" in NCAA American football. Res Sports Med. 2017;25(1):26–36. 11. Hainline BW.  Peripheral nerve injury in sports. Continuum (Minneap Minn). 2014;20(6 Sports Neurology):1605–28. 12. Kermarrec E, Demondion X, Khalil C, Le Thuc V, Boutry N, Cotten A.  Ultrasound and magnetic resonance imaging of the peripheral nerves: current techniques, promising directions, and open issues. Semin Musculoskelet Radiol. 2010;14(5):463–72. 13. Kim DH, Han K, Tiel RL, Murovic JA, Kline DG.  Surgical outcomes of 654 ulnar nerve lesions. J Neurosurg. 2003;98(5):993. 14. Kim DH, Kam AC, Chandika P, Tiel RL, Kline DG.  Surgical management and outcomes in patients with median nerve lesions. Neurosurgery. 2001;95(4):584–94. 15. Maak TG, Osei D, Delos D, Taylor S, Warren RF, Weiland AJ. Peripheral nerve injuries in sports-related surgery: presentation, evaluation, and management: AAOS exhibit selection. J Bone Joint Surg Am. 2012;94(16):e1211–0. 16. Mitchell CH, Brushart TM, Ahlawat S, Belzberg AJ, Carrino JA, Fayad LM.  MRI of sports-related peripheral nerve injuries. AJR Am J Roentgenol. 2014;203(5):1075–84. 17. Mohler LR, Hanel DP. Closed fractures complicated by peripheral nerve injury. J Am Acad Orthop Surg. 2006;14(1):32–7. 18. Omejec G, Žgur T, Podnar S.  Diagnostic accuracy of ultrasonographic and nerve conduction studies in ulnar neuropathy at the elbow. Clin Neurophysiol. 2015;126(9):1797–804. 19. Parry GJ. Electrodiagnostic studies in the evaluation of peripheral nerve and brachial plexus injuries. Neurol Clin. 1992;10(4):921. 20. Standaert CJ, Herring SA.  Expert opinion and controversies in musculoskeletal and sports medicine: stingers. Arch Phys Med Rehabil. 2009;90(3):402–6. 21. Toth C.  Peripheral nerve injuries attributable to sport and recreation. Phys Med Rehabil Clin N Am. 2009;20(1):77–100, viii.

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Vascular Andrew McBride, Amy M. Singer, and Holly Beach

Key Points

• Vascular injuries can occur in isolation or concomitantly with nerve injuries; therefore, it is important to perform a thorough history and physical examination. • In athletes, complete occlusive vascular injuries are less common than nonocclusive vascular injuries. • If a pallor-like appearance is noted, a venous obstruction is more likely than an arterial obstruction. • Cyanosis and edema are more specific signs of an arterial lesion. • Duplex ultrasonography is the diagnostic test of choice in evaluation of DVT. • Angiography is the gold standard for diagnosis of arterial disease. • Referral to vascular surgery is warranted in the setting of acute vascular compromise or refractory vascular insufficiency.

an unremarkable physical examination. Pain, pallor, pulselessness, paresthesia, and paralysis are rarely all displayed [1]. A high index of suspicion is crucial, and further provocative testing may be needed to diagnose an underlying vascular injury [2]. Specific vascular diagnostic tests can be utilized when indicated.

Vascular Clinical and Diagnostic Tests Clinical Vascular Tests There are many clinical tests which have been historically performed for peripheral vascular diseases. These tests build off the standard capillary refill assessment and peripheral pulse palpation. Unfortunately, many of these tests have poor sensitivity and specificity. A few of these tests are summarized in Table 39.1.

Ankle Brachial Index (ABI)

Introduction An athlete with a vascular injury may initially present following a traumatic injury with stereotypical symptoms including pulsatile bleeding, an expanding hematoma, cyanosis, and skin that is cool to the touch. However, it is not uncommon for them to present in the absence of trauma with A. McBride (*) Department of Family Medicine, University of Colorado School of Medicine, Aurora, CO, USA e-mail: [email protected] A. M. Singer Department of Family Medicine, Banner UMC, Tucson, AZ, USA e-mail: [email protected] H. Beach Department of Family and Community Medicine, Primary Care Sports Medicine, University of Arizona, Tucson, AZ, USA e-mail: [email protected]

ABI measures ratio of systolic pressure at the ankle (tibial artery) in comparison to the systolic pressure at the upper arm (brachial artery). Measurements are usually made preand post-exercise to assess for vascular causes of extremity pain. Patient with an ABI of 0.18 after 1 min of maximum exercise should have further arterial evaluation [1].

Angiography Angiography is the gold standard for arterial disease diagnosis [1]. A radiopaque contrast material is injected into an artery to reveal vessel abnormalities on X-ray imaging. Digital subtraction angiography is an adaptation that can permit improved visualization of blood vessels in dense soft tissue or around bone.

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Table 39.1  Summary of a few common clinical tests performed for peripheral vascular diseases Name of test Cervical quadrant test

Allen test

Adson maneuver

Roos and Wright tests

Halstead maneuver

Buerger test

Homan’s test

Anatomy assessed Vertebral artery

Description of test It is performed with the patient supine while the head and neck of the patient are passively extended and side bent laterally. The patient’s head is then passively rotated in the same direction as they are side bent and held in that position for 30 s [1] Radial and It is performed with both the radial and ulnar arteries ulnar arteries being obstructed at the same time with external pressure applied by the examiner. Return of blood flow upon release of pressure is assessed in the ulnar artery by maintaining pressure on the radial artery and releasing pressure on the ulnar artery. In a patent unobstructed artery, blood flow should return quickly (5–15 s). The test is then repeated in the same fashion but for the radial artery [1] This is a test for assessing subclavian Subclavian artery/thoracic outlet syndrome. It is artery/ thoracic outlet performed by palpating the radial pulse of the extremity of concern, while syndrome having the patient rotate his or her head toward the affected limb. The patient then actively extends their neck while their shoulder is passively extended and externally rotated. The patient then takes a deep breath with the pulse still being palpated [1] The Roos test is performed by having Thoracic patient actively abduct (90°) and outlet externally rotate (90°) his or her syndrome shoulder, while at the same time closing and opening their hands forming a fist [1]. The Wright test incorporates palpation of the radial pulse of the affected extremity [1] This test is performed with patient in Thoracic sitting or standing position. The patient outlet is then asked to retract their scapulae syndrome and depress their shoulders, while palpating the radial pulse on the affected extremity [3] It is performed with the patient laying Lower supine, and their lower extremities are extremity passively elevated at 45° of hip flexion. arterial flow The lower extremities are then monitored for skin changes or collapse of more prominent veins. The test is further confirmed by having the patient move to a seated position with his or her legs hanging down [3] The test is performed with the patient in Lower a seated or supine position with their extremity knees flexed. The patient’s distal foot is DVT then forcibly dorsiflexed at the ankle [3]

Positive findings Dizziness or nystagmus may indicate ipsilateral vertebral artery injury [1]

Sensitivity and specificity Very poor sensitivity (15 s) or absent, the artery may be occluded [1]

This test has a sensitivity of 55–70% and specificity of about 92% [4]

Diminishing or loss of pulse is concerning for occlusion or compression of the subclavian artery [1]

The sensitivity ranges from 18 to 87% with a specificity around 94% [5]

Numbness, tingling, and/or pain in the hands are considered a positive Roos test [1]. A positive Wright test includes the above or absence of a palpable radial pulse in the testing position [1]

One study suggests the Roos test has a sensitivity of 84% with a specificity of 30% [6]. The Wright test has a sensitivity of 90% and a specificity of 29% (for symptom reproduction) and sensitivity of 70% and specificity of 53% for pulse abolition [7]

Unknown Numbness, tingling, and/or pain in the hands or absence of radial pulse are considered a positive test [3]

Blanching of the foot or collapse of veins is considered a positive test. If there is a delay in return to normal skin color or filling of veins of longer than 60 s, the test is considered positive [3]

Unknown. However, patients with positive test usually have extensive peripheral vascular disease [8]

Pain in the calf can be suggestive of a DVT [3]

This test has wide ranges of sensitivity (10–50%) and poor specificity (40–90%) [3, 8]

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Advanced Imaging Angiography Computed tomography angiography (CTA) and magnetic resonance angiography (MRA) allow visualization of vascular structures and the surrounding anatomy simultaneously. Contrast is injected intravenous versus intra-arterial [1].

Duplex Ultrasonography It utilizes sound waves to produce imaging of arteries and veins. It is the method of choice for initial evaluation for DVT.

 raumatic Peripheral Arterial and Venous T Injuries Initial Management The initial evaluation of suspected vascular injury should begin with taking a focused history and a physical examination. The location of injury should be assessed for observation of the position in which the extremity is held, the presence of obvious deformity of a long bone or joint, the presence or absence of crepitus or an open wound, and the skin color compared to contralateral side along with capillary refill followed by a complete motor or sensory exam [9]. Direct pressure or a pressure dressing should be applied to the site of external bleeding if present. If these options have not controlled hemorrhage, a blood pressure cuff inflated to greater than the systolic blood pressure or a proximal tourniquet may be applied [9]. If distal pulses are not palpable or capillary refill is delayed, more severe trauma should be suspected. If Doppler ultrasound is available, it may be used to assess for distal flow [9]. If the trauma involves a long bone or joint and there is suspicion of compromised blood flow, immediate reduction and splinting or a traction device should be used [9]. Distal pulses should also be reassessed following these procedures to determine if flow is restored. Another consideration is the environment or field of play where the injury occurred. In order to best maintain an athlete’s euthermic body temperature, the athlete should be assessed in an environment avoiding extremes of temperature if able. Arterial injuries historically can have associated “hard” findings including pulsatile bleeding, loss of distal pulses, an audible bruit or palpable thrill, or an expanding or pulsatile hematoma [10]. The presence of these hard findings should lead to earlier emergent imaging and surgical evaluation [10]. Other “soft” findings include palpable yet diminished pulse compared to contralateral extremity, isolated periph-

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eral nerve injury, unexplained hypotension, history of severe hemorrhage from site of injury, or large non-pulsatile hematoma [10]. These findings help to better delineate arterial from venous injuries which have a slower rate of blood loss and are often more occult injuries. Depending on the injury setting, type, and severity, direct pressure may not be sufficient for hemostasis. Physicians and advanced practitioners must be competent in suturing techniques in order to minimize blood loss in rare, life-threatening injuries. Below we will discuss the evaluation and management of specific traumatic vascular injuries.

Axillary Artery Injury Mechanism The axillary artery can be traumatically injured in athletes with shoulder dislocations or reductions with the vessel becoming taut during shoulder abduction and external rotation [1]. The artery is then forced anteriorly against the pectoralis minor where the artery becomes damaged [1]. The artery can also be injured with repetitive forceful arm elevation and extension in overuse settings and multiple subluxations [10]. Epidemiology Injuries to axillary vasculature (artery and vein) constitutes 3–9% of all vascular injuries [11]. Male athletes appear to be at greater risk for axillary artery injury than female athletes [10]. Baseball pitchers and volleyball players appear to be the most susceptible to atraumatic axillary artery injury due to repetitive forceful arm elevation and extension [10]. This mechanism of injury leads to intimal hyperplasia and stenosis which can lead to pseudoaneurysm or aneurysm formation potentially leading to acute thromboembolism or dissection [10]. In trauma of the general population, penetrating trauma predominates, while blunt trauma leading to proximal humerus fracture, shoulder dislocation, or reduction may be more frequently seen in athletes [11]. Clinical Presentation The athlete with a suspected axillary artery injury will likely have an injury with either a fall or directed trauma onto the proximal humerus or a forced abduction and external rotation leading to anterior shoulder dislocation [12, 13]. The symptoms seen may range from arm fatigue and pain with shoulder exertion to digital pain [10]. On physical examination, the athlete may have a cool upper extremity with decreased or absent brachial, radial, or ulnar pulses [10]. If distal embolization has occurred, digital ulcerations may be seen [10].

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Diagnosis The combination of the above physical examination findings and suspicious mechanism of injury should lead to further diagnostic study. The gold standard for diagnosis of artery injury is catheter-directed angiography with chest and shoulder X-ray recommended for evaluation of bony trauma that could lead to arterial injury [10]. If occlusion of artery is suspected, elevation of arm during study should be performed if occlusion is not present with arm in neutral position [10]. Management The definitive treatment for axillary artery injury involving arterial dissection or laceration is surgical repair [10]. In cases of acute arterial thrombosis, systemic anticoagulation is the initial treatment with stenting or bypass planning depending on the arterial lesion and degree of thrombosis [10]. Complications Traumatic axillary artery injury can lead to distal extremity ischemia, necrosis, and morbidity if not diagnosed and treated appropriately. Mortality appears to occur only from concomitant injuries in multisystem trauma [14].

Brachial Artery Injury Mechanism Injury (laceration, occlusion, or thrombosis) of the brachial artery can occur with penetrating trauma, fracture of supracondylar humerus, or elbow dislocation [9]. It can also be injured in the closed reduction of a humeral fracture [9]. Epidemiology Brachial artery injuries are the most common major vascular injury in the upper extremity in the general population [11]. Case report and series data have found brachial artery injuries to occur in up to 1.7% of elbow dislocations [11]. Injuries to the elbow that can predispose to brachial artery injury make up 9% of injuries in rock climbing and bouldering [15]. Clinical Presentation Athletes with brachial artery injury may present after a fall onto outstretched hand or trauma directly to the elbow or humerus [9]. The athlete may have severe pain along with deformity of the elbow with possible pallor, mottling, or cyanosis. The radial pulse may be absent in as much as 75% of cases of brachial artery injury [11]. Diagnosis The diagnosis of brachial artery injury involves physical examination with suspicious mechanism as above.

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Absence of radial pulse should increase suspicion of brachial artery injury. Plain radiography of the elbow should be performed given the mechanism of injury along with duplex ultrasonography regardless of vascular exam [15]. CT angiography should be used to definitively diagnose the degree of arterial injury in cases based off suspicious physical exam, mechanism of injury, or abnormal duplex ultrasonography.

Management Management of brachial artery injury involves immediate splinting of extremity followed by duplex ultrasonography and angiography as described above. These arterial injuries should be surgically repaired in almost all cases due to high amputation rate with surgical ligation [11]. The median nerve should be assessed prior to repair given its proximity with the artery [11]. Complications Limb salvage rates are near 100% due to prehospital advances, improved surgical repair, and earlier administration of antibiotics [11].

 ffort Thrombosis (Paget-von Schroetter E Syndrome) Mechanism Paget-von Schroetter syndrome is a rare but serious injury involving thrombosis of the axillary or subclavian veins after trauma or intense repetitive upper extremity activity [1]. The subsequent venous compression and thrombosis which occur with compression against the first rib may be acute or chronic [10]. Epidemiology While rare in the general population, this syndrome is the most frequently encountered vascular issue in young competitive athletes [16]. The mean age at diagnosis is in the early 30s, and there appears to be a 2:1 male to female predilection [17]. This syndrome is most often seen in athletes with repetitive abduction of the shoulder, such as baseball pitchers, football players, tennis players, swimmers, and weight lifters [10]. Clinical Presentation Presenting signs and symptoms may consist of dull pain in the affected extremity along with swelling and intact pulses if compression is chronic and low grade. If acute compression has occurred, there is usually a rapid onset of symptoms such as pain, cyanosis, and non-pitting edema [2]. Pulses should remain intact unless the thrombosis is massive or collateral vasculature has not developed [1].

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Diagnosis A suspicious physical examination and history in a young active athlete with unexplained upper extremity swelling or unexplained pulmonary embolism should prompt evaluation for this syndrome [10]. Duplex ultrasonography is the diagnostic modality of choice given its ease of use and availability [1]. This study has a sensitivity of 78–100% and a specificity of 82–100% in this syndrome [18]. A hypercoagulability workup is recommended that generally includes testing for factor V Leiden, lupus anticoagulant, and proteins C and S [1]. Management Emergent thrombolysis and confirmatory venography are recommended in acute cases [1]. Temporary (about 8 weeks) anticoagulation therapy and partial venotomy is recommended to remove the stenosed portion [1]. Thoracic inlet decompression involving the costoclavicular junction is accepted as appropriate therapy to correct the underlying anatomic etiology [17]. An average of 3.5 months for return to play was found on a review [1]. Complications Pulmonary embolism can occur in up to 36% of patients [19]. There is a higher rate of recurrent DVT than the general population in these athletes [1].

Vascular Thoracic Outlet Syndrome (V-TOS) Mechanism V-TOS usually results from compressive trauma or an osseous abnormality near the thoracic inlet which can lead to stenosis or thrombosis affecting the subclavian artery (this can also affect the subclavian vein or brachial plexus, and treatment may vary depending on the type of TOS) [20]. Key structures of the thoracic outlet include the scalene triFig. 39.1  Thoracic outlet anatomy

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angle (anterior, posterior, and middle scalene), costoclavicular space, and subcoracoid/retropectoralis minor space (Fig. 39.1) [1].

Epidemiology This syndrome is commonly seen in athletes with repetitive throwing or abduction of the shoulder, such as baseball pitchers, tennis players, and weight lifters [10]. Clinical Presentation Patients may complain of numbness or exhibit pallor, digital ulceration or gangrene, weak pulses, or a reduction in arm blood pressure with positional maneuvers [20].The patient may also have unilateral scalene tenderness to palpation or bruits on auscultation (less likely) of the supraclavicular fossa [1]. Additionally, an abnormality in the first rib or clavicle may be palpated. Diagnosis Provocative testing may be helpful (e.g., Roos, Wright, and Adson maneuvers) [2]. The gold standard for venous thoracic outlet syndrome is angiography. However, if this is not available, basic cervical or chest X-ray imaging may help identify bony abnormalities of the rib or clavicle, and duplex ultrasound can be effective in assessing for compression, thrombosis, or damage to the arterial wall [20]. Management Vascular surgery evaluation and intervention may be warranted. However, nonsurgical treatment may be acceptable if there is no vascular compromise identified on imaging. If evidence of aneurysm is present, surgical repair is recommended to prevent distal embolization [20]. In most cases of chronic vascular thoracic outlet syndrome, conservative treatment is favored for 4–6 months prior to consideration of surgery [1]. This includes avoidance of overhead activities, postural reeducation, physical therapy, and pain control [1].

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Complications In the absence of a hypercoagulable state, athletes can often return to full sports activity following treatment of this syndrome [20].

Subclavian Steal Syndrome Mechanism This syndrome is the result of retrograde flow (usually down the ipsilateral vertebral artery) due to stenosis or occlusion of the subclavian artery. This can be caused by compressive trauma in the setting of high-intensity activity and/or atherosclerosis [2]. Epidemiology The prevalence of subclavian steal syndrome in the general population is reported between 0.6% and 6.4% [21]. This is most common in males (2 to 1 predilection) over the age of 50 [21]. Upper extremity exertion in athletics can lead to this steal phenomenon through increased blood flow demand [21].

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may be assessed in the office (more than 20  mmHg in affected arm) or appreciation of subclavian bruits [2].

Treatment Vascular surgery evaluation/intervention with stenting or angioplasty is the main form of treatment. In more serious cases, arterial bypass may be warranted [2].

 uadrilateral Space Syndrome and Posterior Q Humeral Circumflex Artery Injury Mechanism Quadrilateral space syndrome can be seen in conjunction with an axillary nerve entrapment and posterior humeral circumflex artery injury after blunt shoulder trauma/injury (e.g., shoulder dislocation, humeral fracture) or following surgery [22]. In this injury, pressure exerted from bony fragments, expanding hematoma, fibrous bands, or hypertrophied muscles causes occlusion of the posterior humeral circumflex artery (Fig. 39.2) [2].

Clinical Presentation The patient may present with presyncope/syncopal episodes, neurological deficits, arm weakness, paresthesia, loss of radial pulse, and claudication pain [2].

Epidemiology This rare condition occurs most commonly in athletes 20–40  years of age who participate in contact (leading to fracture or dislocation) or overhead/throwing sports such as volleyball [22].

Diagnosis Just as with thoracic outlet syndrome, provocative testing (e.g., repetitive activity on the affected extremity) may cause onset of symptoms described above. Angiography is the gold standard, but duplex US, MRA, or CTA can also be used. In addition to diagnostic testing, blood pressure discrepancy

Clinical Presentation An athlete may have signs and symptoms including pain, cramping, weakness, tingling, coolness to touch, pallor, or cyanosis of the affected extremity following mechanism of injury as described above [22]. They may have had a history of previous intermittent pain in the shoulder with activities.

Fig. 39.2  Quadrilateral space anatomy

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Forced abduction and external rotation of the shoulder may exacerbate symptoms [22].

Diagnosis The patient with any of the above presentations should be evaluated with a thorough physical examination with distal neurovascular assessment. An MRI can be used to evaluate the quadrilateral space and determine chronicity of symptoms (presence of isolated teres minor atrophy) in atraumatic cases [22]. In acute trauma, plain radiography of the s­ houlder should be performed to evaluate for compression by bony elements, and arteriography should be considered in suspected posterior humeral circumflex artery injury following trauma [22]. Distal embolization can occur with arterial thrombosis, and the presence of digital ulceration or reduced vascular flow on physical examination should prompt arteriography [23]. Management Thrombolysis or surgical thrombectomy should be considered in cases of arterial thrombosis with or without distal embolization [2]. Following this initial management, a rehabilitation program with early ROM (avoiding overhead movements) is suggested with a 6-week return to full ROM and 3–4 months before full activity can be started [23]. Complications The complications associated with this syndrome and vascular injury involve distal embolic phenomenon that can be avoided or minimized with early diagnosis and management.

 almar Arch Injury and Hypothenar Hammer P Syndrome Mechanism Palmar arch injury occurs as a result of high-impact trauma in sports such as cricket, baseball, and handball leading to ulnar arterial thrombosis or aneurysm formation [10]. Hypothenar hammer syndrome, an example of chronic palmar arch injury, can occur as a result of repetitive trauma to the hypothenar area of the hand leading to ulnar arterial damage where it overlies the hamate bone (Fig. 39.3). Epidemiology This injury tends to present in sports with repetitive and sometimes high-impact trauma to the hand. Cricket, baseball, and handball players are at risk of acute palmar arch injury [10]. Baseball players, mountain bikers, and golfers are at higher risk for hypothenar hammer syndrome [24].

Fig. 39.3  Palmar arch anatomy with an aneurysm

Clinical Presentation An athlete with palmar arch injury will likely have suffered from direct trauma from a ball or baseball/cricket bat causing direct trauma to the palmar arch [10]. The injury is usually unilateral in nature and symptoms may include pain, paresthesias, temperature sensitivity, claudication, or discoloration of fingers/fingertips [1]. Patients may also present with a pulsatile mass, splinter hemorrhages, ulcerations, or signs of gangrene [2]. Diagnosis An athlete with the above presentation and physical examination findings along with a positive Allen’s test is concerning for palmar arch and ulnar artery injury [10]. Angiography is the gold standard for diagnosis; however, CTA may be used to evaluate for hamate fracture, and MRA can be used to assess for ulnar artery trauma [2]. Management Conservative treatment is reasonable most of the time, except in cases of ischemia or ulceration where surgical intervention may be required [10]. Conservative treatment includes avoidance of provocative activities, trial of calcium channel blockers, antiplatelet agents, pentoxifylline, smoking cessation, activity modification/avoidance of repetitive activity, wearing padded gloves, and avoiding the cold [10]. Complications Complications can include digital ischemia and ulceration in cases of thrombosis or aneurysm formation [10]. A thorough

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physical examination and appropriate angiography can prevent this complication.

Acute Compartment Syndrome Mechanism Acute compartment syndrome (ACS) typically results from a fracture, severe blunt trauma from a high-energy mechanism, tendon (Fig. 11.4) or vascular injuries [25]. This trauma leads to increased intracompartmental pressure that, if untreated, leads to tissue ischemia, necrosis, and permanent disability [26]. Epidemiology The average annual incidence of ACS is estimated from 1 to 7.3 per 100,000 [25]. Men are ten times more likely to suffer ACS than women [25]. The mean age for males is 30 years while it is 44 years in females [25]. The leg and forearm are most frequently affected [25]. Over two-thirds of cases are associated with an underlying fracture [26]. This syndrome has been reported in a wide variety of sports including handball, soccer, rugby, cycling, kick boxing, karate, lacrosse, baseball, and football [1]. Clinical Presentation Patients who have suffered extremity trauma can develop swelling and pallor of the extremity. Severe disproportionate pain is also present with the later development of paresthesias and tingling. Irreversible damage may occur as early as 12 hours post-onset and pain may be absent in late ACS [25]. Diagnosis The diagnosis of ACS is clinical at this time focusing on the associated five “Ps”: pain, paresthesia, pallor, paralysis, and (high intracompartment) pressure [26]. While the “five Ps” have been described, they rarely are all present. A compartment pressure higher than 30  mmHg is indicative of compartment syndrome with a normal resting compartment pressure being accepted as 10 mmHg [26]. There are variable surgical indications, and current research is focusing on more objective methods of diagnosis. Management Initial treatment involves removal of any tight-fitting splint, cast, or clothing over the area, while the limb should be maintained at heart level. The athlete should be transported to an emergency room for close monitoring and surgical consult for possible fasciotomy (Fig. 11.4). The pressure threshold for fasciotomy is debated although a threshold of 30 mmHg (20 mmHg in hypotensive patients) is proposed by previous studies [26]. More recent research has shown the use of delta pressure (ΔP = diastolic pressure  – intracompartmental pressure) of ≤ compartmental diagnostic threshold for fasciotomy [26].

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Complications Delay in diagnosis and fascial release can lead to irreversible necrosis, deformity, and mortality. There is a reported mortality rate of 47% after acute compartment syndrome of the thigh [25].

Popliteal Artery Injury Mechanism Injury to the popliteal artery is most commonly caused by posterior knee dislocation as bone fragments directly lacerate or cause thrombosis of the artery [11]. This type of dislocation occurs during knee flexion with a posteriorly directed force onto the tibia [27]. Injury can also be caused by displaced fractures in the knee as seen with lateral tibial plateau fractures [11]. Sports injuries are often moderate energy and are less likely to lead to arterial trauma than high-energy (often involving motor vehicles) mechanisms [28]. Epidemiology Popliteal artery injury occurs in 25–33% of knee dislocations [11]. However, the injury may be clinically occult in up to 40% of cases requiring high index of suspicion in dislocation with spontaneous reduction (may occur in up to 50% of cases) and multiligament knee injuries [11]. This multiligamentous injury, which more often occurs as the result of a high-energy trauma, can be associated with multiple other traumatic injuries and can cause disruption to the neurovasculature resulting in inadequate perfusion leading to muscle and tissue necrosis within hours [28]. These traumatic injuries are more likely in contact sports such as football, soccer, and rugby [27]. Clinical Presentation Popliteal artery injury should be suspected in an athlete complaining of severe knee pain or instability following a mechanism concerning for dislocation or fracture [27]. There may be deformity of the limb, or the appearance may be more occult in cases of spontaneous reduction. The distal extremity may be cool, pale, cyanotic, and mottled and may have delayed capillary refill [28]. The “hard” findings of arterial injury as described above may be present and warrant emergent vascular imaging. Diagnosis Immediate neurovascular physical examination should be performed in cases of knee dislocation. This involves palpation of pedal pulses, sensation, and peroneal nerve testing as the peroneal nerve can be injured in up to one-third of dislocations [27]. While there is no consensus on diagnostic approach to detect popliteal artery injury following suspected knee dislocation, ABI and duplex ultrasonography are noninvasive imaging options that are often employed prior to

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angiography [11]. The gold standard of diagnosis of vascular injury is CT angiography, and most centers use this in selected cases (equivocal or suspicious noninvasive testing, mechanism of injury, or physical exam) or when “hard” findings of vascular injury are present [11].

Management Advanced Trauma Life Support protocols should be followed in patients with high-velocity injury and concomitant life-threatening injuries [28]. The initial management in athletes with lower-energy trauma is to splint the knee in extension or most comfortable position with emergent hospital transport [27]. An attempt to reduce the dislocation should be immediately performed followed by neurovascular reassessment [27]. This can be performed on the sideline, locker room, or emergency department. The above studies should be performed to assess for degree of vascular injury followed by appropriate surgical management. Complications Rapid identification of arterial injury is vital as a delay in ischemia treatment of only 8 h nearly always results in amputation [28]. Amputation rate in patients with knee dislocation and popliteal artery injury can be as high as 20% [29].

External Iliac Artery Endofibrosis (EIAE) Mechanism EIAE is a condition caused by a combination of mechanical and shear stress and results in a subsequent progressive fibrosis which ultimately can lead to stenosis. Arterial kinking alone can be a cause of EIAE. Common aggravating factor is the repetitive hip flexion endured in the setting of high blood flow to the affected area during exertion [2]. Acute on chronic conditions has been reported [30]. Epidemiology EIAE is a rare condition most commonly found in young competitive cyclists and triathletes without significant risk factors for atherosclerosis [7]. EIAE can happen among cross-country skiers, endurance runners, weight lifters, speed skaters, and rugby players. Clinical Presentation Patients can have unilateral limb pain or weakness during high-intensity activity. Swelling and paresthesias may also be noted. Worsening of symptoms may occur over the duration of activity. Diagnosis Angiography is the standard diagnostic modality. ABI, duplex US, or MRA may also be considered. Testing with

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US and ABI may be improved if completed pre- and post-exertion.

Management It can range from conservative management to surgical interventions. Conservative treatment mostly involves activity modification. Medical therapy with antiplatelet agents and/ or statin has not proven to be affective in treatment [2]. Surgical intervention primarily involves percutaneous transluminal balloon angioplasty. If there is only arterial kinking without stenosis, a surgical release of arterial branches to the hip flexors may be completed. More definitive treatment consists of arterial resection and vein grafting or endarterectomy and vein patch angioplasty [2].

Return to Play Return-to-play guidelines after vascular injuries in sports are variable and depend on whether conservative or surgical treatment was necessary. In most cases, relative rest and gradual return to activity should suffice with or without anticoagulation. In addition, a good sports-specific rehabilitation program is key to return to function and sports-specific activity. In cases where immediate surgical intervention is warranted, the return-to-play timeline is sports specific and may vary depending on the presence of operative or postoperative complications and the area affected.

References 1. Akuthota V, Herring S. Nerve and vascular injuries in sports medicine. J Can Chiropr Assoc. 2010;54(2):133. 2. Harrast M, Finnoff J. Sports medicine study guide and review for boards. New York: Demos Medical Publishing; 2016. 3. Côte P, Kreitz BG, Cassidy JD. TH. The validity of the extension-­ rotation test as a clinical screening procedure before neck manipulation: a secondary analysis. J Manip Physiol Ther. 1996;19(3):159–64. 4. Jarvis MA, Jarvis CL, Jones PRST.  Reliability of Allen’s test in selection of patients for radial artery harvest. Ann Thorac Surg. 2000;70:1362–5. 5. Marx RG, Bombardier CWJ.  What do we know about reliability and validity of physical examination tests used to examine the upper extremity. J Hand Surg [Am]. 1999;24(1):185–92. 6. Lee J, Laker SFM.  Thoracic outlet syndrome. PM R. 2010;2(1):64–70. 7. Gillard J, Pérez-Cousin M, Hachulla E, Remy J, Hurtevent JF, Vinckier L, Thévenon ADB. Diagnosing thoracic outlet syndrome: contribution of provocative tests, ultrasonography, electrophysiology, and helical computed tomography in 48 patients. Jt Bone Spine. 2001;68(5):416–24. 8. S M e. Evidence-based physical diagnosis. 4th ed. Philadelphia: Elsevier Saunders; 2017. p. 463–6. 9. Browner BD, Jupiter JB, AP KC, editors. Skeletal trauma: basic science, management, and reconstruction. 5th ed. Philadelphia: Elsevier Saunders; 2015.

692 10. Perlowski AA, Jaff MR. Vascular disorders in athletes. Vasc Med. 2010;15(6):469–79. 11. Marx JA, Hockberger RSWR, editors. Rosen’s emergency medicine: concepts and clinical practice. 8th ed. Philadelphia: Elsevier Saunders; 2014. 12. Proximal Humerus CSM. Fractures. Curr Rev Musculoskelet Med. 2011;4(4):214–20. 13. Cutts S, Prempeh MDS. Anterior shoulder dislocation. Ann R Coll Surg Engl. 2009;91(1):2–7. 14. Degiannis E, Levy RD, Potokar TSR.  Penetrating injuries of the axillary artery. Aust N Z J Surg. 1995;65(5):327–30. 15. Lutter C, Pfefferkorn R, Schoeffl V. Arterial damages in acute elbow dislocations: which diagnostic tests are required? BMJ Case Rep. 2016;2016:bcr2016216336. 16. Melby SJ, Vedantham S, Narra VR, Paletta GA Jr, Khoo-Summers L, Driskill MTR. Comprehensive surgical management of the competitive athlete with effort thrombosis of the subclavian vein (Paget-­ Schroetter syndrome). J Vasc Surg. 2008;47:809–20. 17. Illig KADA.  A comprehensive review of Paget-Schroetter syndrome. J Vasc Surg. 2010;51(6):1538–47. 18. Chin EE, Zimmerman PTGE.  Sonographic evaluation of upper extremity deep venous thrombosis. J Ultrasound Med. 2005;24:829–38. 19. Prandoni P, Polistena P, Bernardi E, Cogo A, Casara D, Verlato F, Angelini F, Simioni P, Signorini GP, Benedetti LGA.  Upper extremity deep vein thrombosis: risk factors, diagnosis, and complications. Arch Intern Med. 1997;157(1):57–62. 20. Mooji T, Duncan AAKS. Vascular injuries in the upper extremity in athletes. Hand Clin. 2015;31:39–52.

A. McBride et al. 21. Osiro S, Zurada A, Gielecki J, Shoja MM, Tubbs RS. LM. A review of subclavian steal syndrome with clinical correlation. Med Sci Monit. 2012;18(5):57–63. 22. Hoskins WT, Pollard HPMA.  Quadrilateral space syndrome: a case study and review of the literature. Br J Sports Med. 2005;39(2):e9. 23. Atema JJIM. Posterior circumflex humeral artery injury with distal embolisation in professional volleyball players: a discussion of three cases. Eur J Vasc Endovasc Surg. 2012;44(2):195–8. 24. Ablett CTHLA.  Hypothenar hammer syndrome: case reports and brief review. Clin Med Res. 2008;6(1):3–8. 25. Via AG, Oliva F, Spoliti MMN.  Acute compartment syndrome. Muscles Ligaments Tendons J. 2015;5(1):18–22. 26. Duckworth AD, McQueen MM. The diagnosis of acute compartment syndrome a critical analysis review. J Bone Jt Surg Rev. 2017;5(12):1–11. 27. Henrichs A.  A review of knee dislocations. J Athl Train. 2004;39(4):365–9. 28. Gray JL, Cindric M.  Management of arterial and venous injuries in the dislocated knee. Sports Med Arthrosc [Internet]. 2011;19(2):131–8. Available from: http://www.ncbi.nlm.nih.gov/ pubmed/21540710. 29. Patterson BM, Agel J, Swiontkowski MF, Mackenzie EJBM. Knee dislocations with vascular injury: outcomes in the lower extremity assessment project (LEAP) study. J Trauma. 2007;63(4):855–8. 30. Bucci F, Ottaviani NPP. Acute thrombosis of external iliac artery secondary to endofibrosis. Ann Vasc Surg. 2011;25(5):5–7.

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Key Points

• Most lacerations should be repaired within 8  h except for facial lacerations which can be repaired up to 24 h after injury. • Abrasions are superficial injuries to the skin due to friction or a scrape. • Aspiration of a Morel-Lavallée lesion has shown quicker return to play in athletes. • Methods to protect against sunburn include the use of sunscreen, avoidance of direct sunlight, and wearing protective clothing including a hat. • Refreezing must be avoided in cases of frostbite.

Introduction Skin consists of three layers: epidermis, dermis, and subcutaneous fat. The epidermis is the outer layer of skin that prevents bacteria, viruses, and other foreign substances from entering the body. It also gives skin its cosmetic appearance. The dermis is the next layer and contains nerve endings, sweat and oil glands, hair follicles, and blood vessels. It is the key layer for healing of wounds. The subcutaneous fat primarily provides protective padding and insulation. In many sports, an athlete’s skin is left unprotected and vulnerable to injury secondary to trauma, mechanical friction, pressure, and the environment. As a result, management R. S. Deu Department of Orthopedic Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA e-mail: [email protected] M. Khodaee (*) Department of Family Medicine and Orthopedics, University of Colorado School of Medicine, Denver, CO, USA e-mail: [email protected]

of skin trauma is a common occurrence for a sideline provider. Many times, this occurs during a game, making prompt diagnosis and management necessary to return the athlete to play. Specifically, a decision needs to be made on whether the wound can be treated temporarily to allow immediate return or needs definitive repair causing removal from competition.

Traumatic Lacerations Lacerations refer to full-thickness disruption of the epidermis and dermis secondary to trauma. They generally occur when exposed skin contacts an opponent or the playing surface. Various mechanisms include direct trauma (an elbow in basketball or fist in boxing), equipment (loose-fitting helmet, stick, or ball), and the ground (road or trail in bicycling) (Fig. 40.1). There are approximately 6–7 million traumatic lacerations treated in the emergency department each year [1–3]. For facial injuries, published data has shown 3–29% are due to sports participation with most injuries (60–90%) occurring in males aged 10–29 years [4]. Preparation is key and providers must ensure that their medical bag is well-­ stocked (Table 40.1). Evaluation of the athlete starts with determination of time, location, and mechanism of injury [6–8]. Time is important as the literature recommends wound closure for most injuries to be done within 8–12  h [5, 7, 8]. Facial lacerations can be closed up to 24 h after injury [5, 7, 8]. Mechanism (sharp vs blunt) and location can help predict the risk of contamination or presence of a foreign body [6–8]. In addition, the mechanism allows one to determine if there is any other associated injury such as fracture, nerve, or tendon injury. Lastly, tetanus immunization status should be confirmed. The first step in treatment is to control the bleeding which is typically performed by holding direct pressure. The pro-

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a

b

Fig. 40.1  Scalp laceration. Tree branch pierced through ski helmet causing laceration Table 40.1  Medical bag [5–7] Disposable suture kit Sterile fields/drapes Antimicrobial cleaning agents Syringes (including 60 mL for irrigation) Skin adhesive Dressings Headlamp Informed consent sheets

Suture Anesthetic Needles Skin stapler Surgical tape/strips Protective skin covering Sunscreen Aftercare instructions

vider should follow universal precautions with use of gloves and other available barriers. After hemostasis is achieved, a quick decision needs to be made regarding the urgency of treatment and whether the area can be taped or patched to allow the athlete to return. Once the athlete is ready for repair of the laceration, a local anesthetic block should be performed. Anesthetics using epinephrine can provide increased hemostasis but should not be used in areas where blood supply is limited (nose, fingers, penis, toes). Topical anesthetics may offer an effective, noninvasive approach to analgesia prior to suturing [9]. Lidocaine-epinephrine-tetracaine gel has been found to provide effective analgesia in children for treatment of simple lacerations [10, 11]. Early anesthesia will allow for more aggressive irrigation, inspection for foreign body and trauma to deeper structures, and test for nerve and tendon function (Fig. 40.2). All wounds should be considered contaminated, so irrigation is vital to decreasing the risk of infection [7]. Irrigation with normal saline (tap water if saline is not available) particularly with a protective cup is recommended.

Fig. 40.2  Partial extensor tendon rupture of the second finger in a 28-year-old female after her finger was cut by her snowboard. This could have been missed, if the adequate exploration was not performed

Several different methods have been used to close skin including sutures, surgical taping, staples, and tissue adhesives. The main goal of laceration repair is to approximate the tissue to achieve a good cosmetic result. In so doing, one

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Table 40.2  Suture selection for body region and follow-up [5, 6, 13]

Body region Scalp Face Lips

Eyelid Eyebrow Trunk

Superficial lacerations (monofilament, nonabsorbable) 5-0 or 4-0 6-0 or 5-0 5-0 (outer portion of lip/vermilion border/ skin) 4-0/3-0 mucous membranes 7-0 or 6-0 6-0 or 5-0 5-0 (low tension)

Deep lacerations (monofilament or braided, absorbable) 4-0 5-0 4-0

Not recommended 5-0 3-0 or 4-0

4-0 (high tension)

Extremities Joints Hand Foot

5-0 or 4-0 4-0 5-0, 4-0 (palms) 4-0, 3-0 (sole)

4-0 4-0 5-0 4-0

Days to removal 7 3–5

3–5 3–5 7–10 (low tension) 10–14 (high tension) 7–10 10–14 7–10 10–14

strives to provide hemostasis, prevent infection, and eliminate dead space. Suturing is the most dependable method for laceration repair. Selecting the appropriate suture material, size, and technique are critical for successful repair and cosmetic result [5]. This is dependent on the size, depth, and location of the wound along with the supplies that are available. Skin tension differs in different body regions necessitating use of various suture sizes (Table 40.2). The two main categories of suture are absorbable and nonabsorbable. Absorbable suture is used to eliminate dead space in deep wounds, while nonabsorbable suture is for skin closure. The synthetic polymers are typically used secondary to higher tensile strength, less tissue reactivity, and lower rates of infection [5, 12]. The skin can be approximated using a variety of techniques. A simple interrupted suture offers redundancy, maintaining the wound edge should one of the stitches break (Fig. 40.3). Running sutures can be performed quickly and distribute the tension evenly. It is at risk of becoming loose if one of the knots break. Subcuticular running sutures can be used in lacerations with low tension. It offers improved cosmetics but can separate if too much pressure is placed on the wound. Tapes or glues can be used to supplement this stitch [8]. Mattress sutures, vertical and horizontal, are used in areas of higher skin tension particularly when wound edges must be brought together over distance [13]. They promote skin edge eversion which limits scarring. Vertical mattress sutures are commonly used in wounds that occur on a concave surface due to the tendency of its edges to invert [13]. Horizontal mattress suture is commonly used for pulling wound edges over distance [13]. They are useful on palms and soles [8].

Surgical taping can be performed for repair of very small, superficial wounds that are not under tension. These are ideal for children as the pain is minimal. Most often, it is used after suture or staple placement as an adjunct to reinforce the repair or after suture removal to prevent dehiscence. Skin stapling can be an alternative to suturing particularly in areas where there is low tension and excellent cosmetic result is not required. It is quicker and provides less tissue reaction than suturing. It is ideal for long, linear wounds of the scalp, proximal extremities, or torso [14]. It should be avoided in facial or neck tissue, small mobile joints, wounds that are macerated or infected, or areas of large tissue loss [14]. The technique starts similarly as to suturing with anesthesia, irrigation, and exploration of the wound. It can be performed as a lone operator or with an assistant. The operator starts at one end of the wound, approximating the skin edges with forceps, lines the stapler arrow over the incision, and presses down on the trigger to engage the staple. This is repeated until the wound is closed. Typically, staples will stay in place for 8–10 days and can be removed with a staple remover. Tissue adhesives offer multiple benefits; the most important in the athletic setting is quick application allowing faster return to play. They can be used for wounds under low tension as an alternative to 5-0 or smaller suture, most commonly on the face, scalp, torso, or extremity wounds [5, 15]. Treatment with an adhesive is faster and less painful and does not require dressing changes or need to be removed. Due to these factors, it is an excellent choice for children. Studies have shown that it can be as effective as suturing in appropriate patients [16– 19]. Initial wound irrigation is still needed but the wound must be dry and bloodless prior to application. The wound edges are approximated and typically three coats of adhesive are applied. Care should be made to not get any of the adhesive into the wound as it can cause a tissue reaction and delay healing. Patients may shower immediately but should not bathe or swim for 2–3  days [5]. The adhesive typically sloughs off spontaneously within 5–10 days [3]. The wound should be kept dry and inspected daily for signs of infection (redness, swelling, warmth, tenderness, or drainage). Patients with sutures or staples may gently cleanse the area and pat dry [5]. Facial sutures should be removed in about 3–5 days, scalp and extremity wounds in 7–8 days, and 10–14 days for wounds under higher tension such as those over mobile joints, soles, palms, or back (Table 40.2) [5, 7]. Typically, adhesive strips are applied after suture removal to provide initial support while the wound continues to heal. Table 40.3 summarizes different laceration treatment options. Table  40.4 summarizes the level of evidence for key clinical recommendations for management of lacerations. Return to play is dependent on multiple factors including wound severity, type of sport, wound contamination, and risk of contamination to others [7]. The NCAA requires that in an injured athlete, bleeding must be stopped and the open

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a

b

c

d

e

f

Fig. 40.3  Good approximation of three different lacerations by sutures. A simple linear laceration (a, b), a triangular laceration (c, d), and a linear eyebrow lacreation (e, f)

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Table 40.3  Summary of laceration treatment options [3, 14, 15] Indications

Sutures Most lacerations

Contraindications Infected or heavily contaminated wounds

Advantage

Provides superior cosmetic result Excellent tensile strength Low dehiscence rate

Disadvantage

Takes longer Painful May leave suture marks Most reactive Requires removal

Staples Wounds under low tension and where excellent cosmetic result is not needed Ideal for long, linear wounds of the scalp, proximal extremities, and torso Infected or heavily contaminated wounds Facial and neck tissue Over small mobile joints (hand and foot) Wounds that are macerated or infected Fast Everts wound edges better and places less tension on edges as compared to suturing Less reactive than sutures leading to less inflammation and infection Painful Potential to provide inferior cosmetic result Leave larger puncture scars More expensive Requires removal

Adhesives Linear wounds under low tension Wounds 50% surface area or expanding Ruptured subcapsular hematoma with active bleeding Intraparenchymal hematoma > 2 cm or expanding Laceration > 3 cm parenchymal depth IV Hematoma Ruptured intraparenchymal hematoma with active bleeding Laceration Parenchymal disruption involving 25–50% of hepatic lobe V Laceration Parenchymal disruption involving > 50% of hepatic Vascular Juxtahepatic venous injuries, i.e., retrohepatic vena cava/major hepatic veins VI Vascular Hepatic avulsion The American Association for the Surgery of Trauma (AAST) presented a liver injury scale, advance one grade for multiple injuries to the same organ Table from Moore et al. [64]

ski racing and motorsports, the liver is injured as a result of high velocity forces being transmitted across the organ. As a result of these forces, lacerations can occur within the capsule and at the underlying attachment point of the parenchyma. Injuries can also occur at the intima and media of nearby arteries [1, 29, 30].

Grading of Injury Grading of liver injuries has been described by the American Association for the Surgery of Trauma (AAST) [31, 32]. The grading system of hepatic organ injury was developed to help determine intervention by injury severity. Injuries are described as grade I through grade VI where grade I is minor and grades III and above are considered severe. Grade VI is usually fatal. Luckily, the majority of injuries, ranging from 67% to 90% [31, 33], are considered minor or grades I– III. See Table 42.1.  linical Presentation and Physical Exam C The clinical presentation of athletes with closed liver injuries can vary depending on the severity of the injury. Initially, the hemodynamic stability of the athlete should be determined based on a primary and secondary survey. Athletes with severe injuries may present with hypotension and tachycardia consistent with shock. Athletes with less severe closed liver injuries will present with tenderness to

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palpation of the right upper quadrant. Peritoneal signs such as guarding, rebound tenderness, or rigidity may also be present; however, none of these are sensitive or specific for liver injury [29]. Additional physical exam findings that may suggest retroperitoneal hemorrhage or intra-abdominal hemorrhage include Grey Turner’s sign and Cullen’s sign [34]. Cullen’s sign is described as superficial edema with bruising in the subcutaneous fatty tissue around the periumbilical region [35]. Grey Turner’s sign refers to ecchymosis of the flanks and may co-occur with Cullen’s sign especially in retroperitoneal hemorrhage [36]. Both signs however are delayed findings, are indicative of a significant amount of bleeding, and will likely not be present in an initial physical exam.

Evaluation Sideline evaluation should begin with an understanding of the mechanism of trauma. A primary survey including assessment of vital signs should follow. Unstable patients should be stabilized according to ATLS guidelines [6] and the findings of the primary survey and transported without delay to the nearest emergency department with trauma capabilities (or the nearest emergency department if a trauma center is not available). Stable patients should have a more in-depth exam done looking for specific injury patterns suggestive of liver injury. Vital signs should be followed and repeated often to assess for signs of shock. Most hemorrhages of the liver occur within the first 24 h, and delayed bleeding is rare [33]. A sideline or training room FAST exam may be done to look for intraperitoneal hemorrhage. One may also see irregularities underneath the capsule of the liver suggesting hemorrhage or hematoma. Any athlete with a suspected liver injury should also be evaluated in an emergency department with trauma capabilities (or the nearest emergency department if a trauma center is not available). Laboratory tests such as liver function tests (including aspartate aminotransferase (AST) and alanine aminotransferase (ALT)), serum electrolytes, complete blood count, coagulation studies, lipase, and blood type and screen or cross depending on the stability of the individual athlete should be performed. Indications for computed tomography (CT) scan with contrast, which is the gold standard for imaging diagnosis, include a high level of suspicion, right upper quadrant tenderness, elevated AST or ALT, gross hematuria, or a declining hemoglobin or hematocrit. Hemodynamically unstable patients should not undergo a CT scan but instead evaluated with bedside eFAST or FAST and by surgery. Emergent intervention by the surgical team may be required for findings such as free fluid found on a FAST, unstable vital signs, or worsening clinical condition.

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In adults, AST values of greater than 400  IU/L or ALT values of 250 IU/L convey sensitivity and specificity of 92.9% and 100%, respectively, in the prediction of liver injuries [37]. One study done specifically in the pediatric population found that elevations in glucose and aspartate aminotransferase (AST) yielded the highest sensitivity with 75% and 65%, respectively [38, 39]; however, this same study, as well as others, notes that there is no laboratory value that is “adequately sensitive, specific or predictive so as to be clinically useful” [39]. In general, AST above 200 and ALT above 125 should prompt further evaluation either in the form of observation and repeat exam or by CT with IV contrast given the increased risk for intra-abdominal injury [40]. In athletes who have sustained a closed liver injury, providers should consider associated injuries. Up to 80% of patients with identifiable trauma to the hepatic system have at least one additional injury such as pulmonary injuries, pelvic fractures, or rib fractures [41].

Management Management of closed liver injuries depends on the severity of the injury itself as put forth by the American Association for the Surgery of Trauma guidelines (Table 42.1). Athletes presenting with hypovolemic shock or with a significant drop in their hemoglobin and hematocrit will likely require blood transfusion. The hemodynamically unstable adult athlete will likely require intervention with embolization of bleeding vessels by interventional radiology or with an emergent laparotomy by a surgeon. There is limited data available on the management of hepatic injury using embolization in children. The decision to use embolization in the pediatric population should be made in conjunction with the pediatric surgeon and interventional radiologist [42, 43]. Athletes that require surgical intervention are likely to have grade III and above injuries. Hemodynamically stable athletes are more likely to be treated nonoperatively now as there has been a paradigm shift over the past several decades. Observation of stable athletes should occur in a facility that is able to provide emergent surgical intervention if deterioration of the athlete occurs. Return to Play Currently, there are no specific guidelines in regard to return to play for athletes who have sustained closed liver injuries. If an athlete is treated operatively, then return to play should be determined in coordination with the surgeon. For the athlete that was treated nonoperatively, he or she should only be cleared for return to play once normal anatomic function of the liver has returned. Specifically, the athlete’s liver enzymes should have normalized. Serial imaging with CT scan or ultrasound is controversial and likely should not be done unless there is a specific deterioration in the athlete’s status

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[29, 33]. Protective gear, such as flak jackets or increased padding around the liver, has not been studied for its effectiveness in protecting the organ. Healing time in a closed liver injury is variable. A simple liver laceration or subscapular hematoma can heal in 2–4  months. A larger injury such as a complex laceration with vascular injury may take up to 6  months to heal [1]. Overall, resolution of the injury and return to play should be a coordinated decision between the surgeon who cared for the athlete initially, the team physician, the athlete, and his or her family.

Spleen Although the liver is the most common cause of death due to intra-abdominal blunt trauma, the spleen is the most commonly injured organ in blunt trauma sustained in sports and the organ most likely to result in intra-abdominal hemorrhage.

Anatomy This spleen is located in the left upper quadrant and lies against the left hemidiaphragm. It is protected in that area by ribs IX through XII. The spleen is connected to the curvature of the stomach by the gastrosplenic ligament and to the left kidney by the splenorenal ligament. Both of these ligaments contain blood vessels (Fig. 42.9). The blood supply for the spleen comes from the splenic artery, which enters the organ through the hilum [28]. This organ filters about 15% of the body’s blood supply every minute and is susceptible to significant bleeding with trauma [44]. The spleen also comprises about 25% of the total lymphoid mass of the body making it one of the largest lymphopoietic organs in the body [39]. In children, the spleen may not yet be covered by the rib cage, and the ribs that do cover the organ are more compliant providing less protection. Children also lack the adipose tissue and muscle tissue of adults, further contributing to the increased vulnerability to splenic injury in children [44]. Mechanism of Injury As with the liver, the spleen can be injured by either direct compressive or crush injuries or by acceleration/deceleration forces. The spleen can be more susceptible to injury in the setting of infection, pregnancy, and portal hypertension as these factors can lead to splenic enlargement. Delayed rupture and hemorrhage of the spleen is more common in adults than other organs such as the liver. The splenic capsule is able to contain bleeding rendering early signs of hemorrhage less reliable. Delayed bleeding has also been attributed to factors such as the development of pseudo-­ aneurysms, splenic abscess, or secondary tearing of the parenchyma after adherence to the omentum [1, 33]. More

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Fig. 42.9  Anatomy of the spleen

than 90% of secondary bleeds or ruptures will occur within 10 days, and the majority of the remainder will occur within 2 weeks [45, 46, 47]. Delayed rupture is rare in the pediatric population, and the majority of children with splenic injuries that require surgical intervention will usually declare themselves in the first 12 hours [47].

Grading of Injury The American Association for the Surgery of Trauma (AAST) has presented a grading system for splenic injury as identified on computed tomography (CT). This grading system helps predict the success of nonoperative management. The grading system goes from grade I for minor injuries to grade V for severe injuries. See Table 42.2.  linical Presentation and Physical Exam C An athlete with a splenic injury may present immediately after trauma or may have a delayed presentation. The athlete will likely complain of sharp left-sided pain initially, followed by dull pain. Nausea, vomiting, and the urge to defecate have also been described but are not specific for splenic injury. Kehr’s sign, referred pain to the left shoulder or proximal arm, may be present as a result of blood irritating the diaphragm and phrenic nerve. This is a delayed sign usually occurring about 30–60 minutes after the injury and so may not be present on initial evaluation [44]. On physical exam, the athletes should be evaluated for signs of hemorrhagic shock. Vitals signs may show tachycardia and hypotension; however, this may be delayed as 25% of circulating blood volume may need to be lost before hypotension occurs. The skin may be cool and clammy. The athlete will have tenderness to palpation in the left upper quadrant of the abdomen and may have Cullen’s or Grey Turner’s sign (see description in the “Liver Injury” section) if the injury is severe.

Table 42.2  Spleen injury scale [64] Grade Injury Description I Hematoma Subcapsular, nonexpanding, < 10% surface area Laceration Capsular tear, nonbleeding, < 1 cm parenchymal depth II Hematoma Subcapsular, nonexpanding, 10–50% surface area Intraparenchymal, nonexpanding, < 2 cm in diameter Laceration Capsular tear, active bleeding, 1–3 cm parenchymal depth which does not involve a trabecular vessel III Hematoma Subcapsular, > 50% surface area or expanding Ruptured subcapsular hematoma with active bleeding Intraparenchymal hematoma > 2 cm or expanding Laceration > 3 cm parenchymal depth or involving trabecular vessels IV Hematoma Ruptured intraparenchymal hematoma with active bleeding Laceration Laceration involving segmental or hilar vessels producing major devascularization (> 25% of the spleen) V Hematoma Completely shattered spleen Laceration Hilar vascular injury which devascularizes spleen The American Association for the Surgery of Trauma (AAST) has presented a grading system for splenic injury as identified on computed tomography (CT), advance one grade for multiple injuries to the same vessel Table from Moore et al. [64]

Evaluation The evaluation of a patient with a suspected splenic injury should begin on the sideline. Any athlete that sustains blunt abdominal trauma to the left upper quadrant should have a physical exam including vital signs that should be repeated frequently. As previously discussed, the splenic capsule can

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contain initial bleeding masking the severity of the injury. As part of a primary and secondary survey on the sidelines or in the training room, a FAST exam may be done to look for intraperitoneal hemorrhage. The stable patient should be monitored for changes in exam, vital signs, pain, and mentation. Even in a stable patient, if the index of suspicion is high for splenic injury, the athlete should be referred for further evaluation in an emergency department with trauma capabilities (or the nearest emergency department if a trauma center is not available). The unstable athlete should be transferred to a trauma center and managed according to ATLS guidelines. Once in the emergency department, a CT scan with contrast and laboratory testing including a complete blood count, electrolyte panel, liver function tests, lipase, possible coagulation studies, and blood type and screen should be done. Evaluation by a surgeon should also occur. In athletes that undergo CT scans, there are certain findings that are suggestive for injury. These include hemoperitoneum, hypodensities within the spleen, and a contrast blush or extravasation [45]. MRI can also be done but is not a practical choice to evaluate for splenic injuries given the length of time required for the test and the cost.

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Repeat imaging in the acute phase will be dictated by the severity of injury. For those athletes being observed, repeat imaging with CT scan is indicated if there is any clinical deterioration, in athletes with higher grade injuries with evolving neurologic injury, or if the initial injury was unclear. On average, athletes will be observed in the hospital for 1–3 days.

Return to Play Time to return to play will vary according to whether the athlete underwent observation, embolization, or splenectomy. It is common practice to restrict participation of any sport or activity that could result in trauma to the area for up to 3  months. During this time, the athlete may make gradual progression in increasing physical activity while avoiding heavy lifting or strenuous activity. As there are no clinical studies to guide return to play, a recovery plan should be discussed with the surgeon, athletes, and family if applicable.

Diaphragm Injury

The diaphragm is one of the most commonly injured organs in the abdomen. Injuries can range from very minor and very Management common, as in the case of diaphragm spasm, to very severe Splenic injuries identified on imaging will need to be evalu- and very uncommon, as in the case of diaphragm rupture. ated by a trauma surgeon for potential intervention versus Diaphragm ruptures represent less than 1% of all traumatic observation. As in all athletes with blunt abdominal trauma, injuries [51] and should be suspected in athletes presenting those who are hemodynamically unstable should be resusci- with symptoms similar to a diaphragm spasm that do not tated per ATLS guidelines with crystalloid and potentially resolve or with any significant abdominal trauma. This injury blood products and evaluated by a surgeon as soon as possi- can have life-threatening consequences and can be hard to ble. Stable athletes should undergo a CT with treatment dic- diagnose, so physicians caring for athletes must include this tated by the grade or severity of the injury. in their working differential as it can be easily missed. Surgical interventions will likely begin with spleen-­ Serious diaphragm injuries rarely occur independently. salvaging procedures like embolization. If the injury is too According to the National Trauma Database [51], at least severe or the prior has failed, a splenectomy should be per- 50% of patients with diaphragm injuries have additional formed. In the adult population, 50–70% of cases are man- injuries. aged nonoperatively [48, 49]. In children with splenic injuries, treatment course is dictated more by clinical condition than Anatomy grading of injury. If the pediatric athlete remains hemody- The diaphragm is a dome-shaped musculotendinous strucnamically stable (regardless of CT findings), he or she can be ture that separates the thoracic cavity from the abdominal observed in a hospital equipped to transition the athlete to cavity and plays a large role in respiratory mechanics. The operative management if it becomes warranted. One criterion aorta, inferior vena cava, esophagus, vagus nerve, and that is cited often for defining surgical intervention states that phrenic nerve transect the diaphragm in a horizontal plane the need to replace more than half of the athlete’s circulating (Fig. 42.10). It is composed of the costal and crural muscle blood is an indication for surgical management [50]. This can groups, which are innervated by the phrenic nerve and vagus be estimated at about greater than or equal to 20 mL/kg of nerve. The vascular supply comes from the phrenic artery packed red blood cells. Initial surgical intervention may below the diaphragm and the pericardiacophrenic arteries include embolization prior to splenectomy or other spleen- above the diaphragm [28]. salvaging procedures. Attempts to avoid a splenectomy are driven by the fact that asplenic children are at a much higher Mechanism risk of infection by encapsulated organisms and will require Any blunt force trauma to the abdomen can directly or indirectly cause injury to the diaphragm. This injury will usually additional immunizations post-procedure [45].

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Fig. 42.10  Anatomy of the diaphragm

Table 42.3  Diaphragm injury scale [65] Grade I II III IV V

Injury Contusion Laceration Laceration Laceration Laceration

Description 10 cm laceration with tissue loss 25 cm2

The American Association for the Surgery of Trauma (AAST) splenic injury grading system, advance one grade for bilateral injuries Table from Moore et al. [65]

occur after direct contact where an athlete is hit in the ­epigastrium resulting in temporary spasm of the diaphragm muscle. Injury resulting in rupture may be caused by penetrating trauma or by a direct blow that causes a sudden increase in intra-abdominal pressure that is high enough to overcome diaphragm musculature. The left diaphragm is two to three times more likely to be injured with blunt trauma, which may be due to the fact that the right side is protected by the liver or as a result of a congenital weakness on the left side [52]. A rupture of the diaphragm can result in the acute herniation of abdominal contents into the chest.

Grading of Injury Classification of diaphragm injuries has been established by the American Association for the Surgery of Trauma (AAST) which is very similar to grading for other organ injuries. And as with injury to other organs, the higher the degree of injury, the higher the associated mortality. See Table 42.3.  linical Presentation and Physical Exam C Athletes presenting with a diaphragm injury most commonly describe getting “the wind knocked out of me.” The athlete will complain of difficulty breathing until the spasm has resolved. This will usually last seconds to minutes in the set-

ting of spasm and potentially longer with rupture and herniation. The athlete may also complain of chest pain or flank pain. On physical exam, the athlete will likely have tenderness to palpation over the site of impact and may even develop ecchymosis. The provider may hear decreased breath sounds on the side of injury if a pneumothorax has occurred secondary to herniation. With severe injuries or in delayed presentations, athletes may be hemodynamically unstable and require emergent treatment.

Evaluation As with all injuries, evaluation should start with a primary and secondary survey. Given that an athlete with a diaphragm injury may complain of both shortness of breath and abdominal pain, a specific chest, pulmonary, and abdominal exam will need to be completed. If the athlete is hemodynamically unstable, he or she should be transported to the nearest trauma center (or the nearest emergency department if a trauma center is not available). In the case of herniation with pneumothorax that has progressed to tension pneumothorax, the athlete should have their chest decompressed with needle decompression as discussed in the thoracic trauma section and according to ATLS guidelines. In the case of suspected diaphragm injury, sideline or training room bedside ultrasound will not likely be helpful. There is no standardized technique, and a negative study does not rule out a diaphragm injury. If ultrasound is attempted, the diaphragm will show up as a hyperechoic structure and may be evaluated for continuity. Disruption of the continuity is associated with rupture [53, 54]. A plain film of the chest is indicated and may show elevation of the diaphragm where the injury has occurred or even herniation of abdominal contents into the chest in severe injuries. In some cases, X-rays may also be negative. If clinical suspicion is high enough, a computed tomography (CT) scan of

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the chest and abdomen should be performed; however, this also may be negative. Signs of diaphragm injury on CT include discontinuity of the diaphragm, herniation of abdominal contents into the chest, visualization of a nasogastric tube (if placed) within the chest, constriction of the bowel, or contiguous injuries from one side of the abdomen to the other (i.e., left pulmonary laceration and splenic laceration) [55]. MRI is also an option, but it is of limited utilization due to availability, cost, and time required to complete the test. Once transported to a trauma center, the athlete should have basic labs ordered including a complete blood count, complete metabolic panel including liver function tests, lipase, and possibly a type and cross or screen for blood products. A trauma surgeon should evaluate all hemodynamically unstable patients as well as all patients with a high index of suspicion for diaphragm injuries. When imaging studies have been inconclusive but injury is still suspected, more invasive procedures such as an exploratory laparotomy or laparoscopy may be required to diagnose and repair diaphragm injuries.

more significant diaphragm injury such as rupture, the athlete will need to be cleared by the surgeon who repaired the injury. Overall rates of recurrence are low, but some sources suggest that athletes should have periodic chest X-rays and pulmonary function testing after a repair. No timeline is specified [56]; however, it is generally recommended that periodic testing is only indicated if the athlete has complaints such as chest pain or shortness of breath. Return to play will be influenced by the recovery time for the laparotomy as much as the repair of the diaphragm injury itself. An average timeline of return to strenuous activity will likely be 6–8 weeks but may be further dictated by the surgeon who repaired the defect.

Management Treatment for the minor diaphragm injuries can include hip flexion and loosening of restrictive equipment or clothing to ease breathing. If symptoms resolve quickly, no additional testing is required. If symptoms persist, the athlete should be evaluated for hemodynamic stability and for more significant injuries as above. Any athlete with concern for significant injury to the chest or abdomen should be transported to the trauma center (or the nearest emergency department if a trauma center is not available) for further care. In the case of a suspected or identified diaphragm, rupture management by the surgical team will vary depending on stability, location of injury, and index of suspicion for injury severity. Hemodynamically stable athletes with negative imaging or those with small right-sided defects identified on imaging may be managed expectantly with frequent repeat exams. In unstable athletes or those with a larger injury identified on imaging, an exploratory laparoscopy or laparotomy will likely be required. Smaller diaphragm injuries will be repaired primarily by the surgeon, whereas larger injuries may require prosthetic material to close the diaphragm. Mortality in diaphragm injuries is high, around 25% [51] due to both the injury itself and the associated complications. Complications vary depending on the type of trauma (penetrating vs. blunt) but include gastrointestinal herniation, altered respiratory mechanics, diaphragm paralysis due to nerve injury, pleural fistula, and ischemic bowel.

Anatomy The abdominal wall musculature is composed of the external obliques, the internal obliques, the rectus abdominis, and the transversus muscles (Fig. 42.11). The majority of the blood supply comes from the inferior and superior epigastric arteries (Fig. 42.12). These vessels can be damaged during trauma and contribute to hematoma formation.

Return to Play In the case of a diaphragm spasm, the athlete may return to the field of play once symptoms have resolved. In the case of

Abdominal Wall Contusion Contusion of the abdominal wall musculature is another common sports-related injury. A subsequent hematoma may form especially when injuries occur to the epigastric arteries and cause bleeding within the rectus abdominis sheath.

Mechanism Injury to the abdominal wall musculature occurs as a result of either direct trauma or forceful contraction of the musculature. A contusion and hematoma may subsequently form. The rectus abdominis musculature is at a higher risk for hematoma formation given the anatomical location of the epigastric arteries.  linical Presentation and Physical Exam C In completing an assessment and physical exam of an athlete with a suspected abdominal wall contusion or hematoma, the athlete will likely complain of acute-onset pain occasionally with nausea and vomiting. If there is hematoma formation, rapid swelling in the area will occur. In the case of a rectus sheath hematoma, a mass below the umbilicus may be palpable. This injury can mimic an acute abdomen. Evaluation Any injured athlete should be screened for hemodynamic stability and injury by a primary and secondary survey. The injured area should have overlying clothing or equipment removed for full visualization. Inspection, auscultation, palpation, and percussion of the area should be done.

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Fig. 42.11  Musculature of the abdominal wall Fig. 42.12  Arterial supply on the abdominal wall

Abnormalities on exam should prompt further evaluation, and any hemodynamic instability should prompt transportation to a trauma center. Ultrasound can be used both on the sideline and in the training room to screen for hematomas of the abdominal wall. On ultrasound imaging, the area of injury will reveal a hypoechoic area. The physician can also use ultrasound to follow the injury for improvement and eventually resolution of the hematoma. Computed tomography (CT) scan can also

be used to confirm hematoma size and location and evaluate for additional injuries. Repeat CT is often not necessary.

Management Athletes with a suspected abdominal wall contusion or hematoma are unlikely to be unstable if the injury occurs independently of other injuries. However, as with any other abdominal injury, a primary and secondary survey should be performed to screen for additional injury. The hematoma can

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be monitored for progression of size by repeat physical exam and ultrasound. Movement that increases pain should be avoided initially.

be aware of possible coexisting injuries and manage the athlete accordingly. Injuries to be discussed in this section include those to the kidneys, ureters, and bladder.

Treatment Treatment of an abdominal wall contusion or hematoma initially includes ice, rest, and analgesics. Activities that include flexion or rotation of the core as well as stretching of the core should be avoided until the pain is resolved. In the case of a large hematoma, surgical evacuation and potentially ligation of the epigastric artery may be required. After the initial pain has resolved, rehabilitation should include regaining flexibility and core strength.

Kidney, Ureter, and Bladder Injuries

Anatomy The genitourinary system can be divided up into the upper and lower tracts with the upper tract consisting of the kidneys and ureters and the lower tract consisting of the bladder, urethra, and external genitalia (Fig. 42.13). The kidneys and the ureter lie within the retroperitoneal space. These organs are protected by the surrounding tissue which includes the lower ribs specifically T10 through T12, the musculature of the spine including the paraspinal musculature and the psoas muscle, and the perinephric fat. Due to the location and size of the liver, the right kidney extends lower than the left. The ureters course distally after they exit the kidney pole and enter the bladder posteriorly and inferiorly at the trigone. The bladder’s location within the pelvis varies depending on how distended it is. When it is empty, the bladder will sit along the pelvis floor, but when fully distended, it may extend to the level of the umbilicus. The peritoneal surface of the dome is the weakest point and most mobile point of the bladder.

Genitourinary injuries seldom occur in isolation and are rarely life-threatening with few exceptions. Injuries to the genitourinary system often occur in the setting of a pelvic fracture or significant abdominal trauma. Providers should

Mechanism As with all abdominal injuries in sports, the mechanisms that are most commonly associated with injury are blunt trauma and deceleration. Occasionally penetrating trauma can occur

Return to Play An athlete may return to play after an abdominal wall contusion or hematoma once he or she is able to complete functional testing. Goals should include returning to normal range of motion, preinjury strength, and preinjury flexibility. Returning an athlete to the field of play before these goals have been achieved may put him or her at risk for further injury.

Fig. 42.13  Anatomy of the genitourinary system

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although this is rare in sports. In the case of deceleration injuries seen in falls from great heights or motorsports, the athlete may sustain avulsion of renal pedicle, renal artery dissection, or avulsion of the ureter at the ureteropelvic junction. Blunt force injuries, which tend to occur in contact sports athletes or falls from lower heights, can result in a shattered kidney, bladder rupture, or injury to the external genitalia. Injuries to the lower genitourinary tract can also be caused by or in conjunction with pelvic fractures.

Table 42.6  Bladder injury scale [66]

Grading of Injury The American Association for the Surgery of Trauma Organ Injury Severity Score for the Kidney, Ureter, and Bladder [57, 58] has stratified injury according to a scale that correlates needs for surgical intervention. All of the organs listed have their own scoring scale. See Tables 42.4, 42.5, and 42.6.

The American Association for the Surgery of Trauma (AAST) Organ Injury Severity Score for the bladder, advance one grade for bilateral injuries, advance one grade if multiple lesions exist Table from Moore et al. [66]

Table 42.4  Kidney injury scale [64] Grade Injury Description I Contusion Microscopic or gross hematuria, urologic studies normal Hematoma Subcapsular, nonexpanding without parenchymal laceration II Hematoma Nonexpanding perirenal hematoma confirmed to renal retroperitoneum Laceration < 1.0 cm parenchymal depth of renal cortex without urinary extravasation III Laceration > 1.0 cm parenchymal depth of renal cortex without collecting system rupture or urinary extravasation IV Laceration Parenchymal laceration extending through renal cortex, medulla, and collecting system Vascular Main renal artery or vein injury with contained hemorrhage V Laceration Completely shattered kidney Vascular Avulsion of renal hilum which devascularizes kidney The American Association for the Surgery of Trauma (AAST) Organ Injury Severity Score for the kidney, advance one grade for bilateral injuries, advance one grade for multiple injuries to the same vessel Table from Moore et al. [64]

Table 42.5  Ureter injury scale [66] Grade Injury Description I Hematoma Contusion or hematoma without devascularization II Laceration < 50% transection III Laceration > 50% transection IV Laceration Complete transection with 2 cm devascularization V Laceration Avulsion with > 2 cm of devascularization The American Association for the Surgery of Trauma (AAST) Organ Injury Severity Score for the ureter, advance one grade for bilateral injuries, advance one grade for multiple injuries to the same vessel Table from Moore et al. [66]

Grade Injury I Hematoma Laceration II Laceration III Laceration IV V

Description Contusion, intramural hematoma Partial thickness Extraperitoneal bladder wall laceration < 2 cm Extraperitoneal (≥ 2 cm) or intraperitoneal (< 2 cm) bladder wall lacerations Laceration Intraperitoneal bladder wall laceration ≥ 2 cm Laceration Intraperitoneal or extraperitoneal bladder wall laceration extending into the bladder neck or ureteral orifice (trigone)

 linical Presentation and Physical Exam C An athlete with an injury to the genitourinary system will have complaints and a physical exam that varies by the location of the injury. In general, athletes with upper tract injuries may present with complaints of flank pain or hematuria. Athletes with lower tract injuries and specifically bladder injuries will present with complaints of suprapubic pain, gross hematuria, and difficulty or inability to void. While conducting a physical exam, the provider should be aware that injuries to the genitourinary tract rarely occur in isolation, and so a thorough physical exam should be performed. The provider should look for bruising to the flank and abdomen such as Grey Turner’s sign and Cullen’s sign. He or she may also need to perform a visual inspection of the genitals for signs of bleeding or trauma. The provider should then palpate for costovertebral angle tenderness and flank pain as well as palpate the abdomen for distention, guarding, and rebound tenderness. As ureteral injuries are often missed on initial evaluation, delayed findings include persistent flank pain, fever, and a palpable flank mass that may represent a urinoma. The pelvis should be assessed for possible fractures as two-thirds of significant bladder injuries have co-occurring pelvic fractures [59, 60]. This can be done through palpation and compression as well and evaluation of the hips. Special consideration needs to be given to pediatric athletes. Injuries to the renal system are more common in children as their kidneys are larger in comparison to their abdomen and pelvis so the surrounding organs and rib cage provide less protection. Evaluation As in previous discussions, sideline evaluation should begin with a thorough primary and secondary survey according to ATLS protocols. In the case of genitourinary injuries, complaints from athletes may be nonspecific so providers need to take into consideration the mechanism and type of trauma to have an appropriate level of suspicion for injuries to these

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organs. Vital signs should be taken and repeated looking for signs of shock. All unstable patients should be urgently transported to the nearest trauma center (or the nearest emergency department if a trauma center is not available). Any athlete with a suspected genitourinary injury should have an evaluation of his or her urine for the presence of hematuria. The quantitative measurement of hematuria can be accomplished by a chamber count or the number of red blood cells per milliliter of excreted urine, sediment count or the direct examination of a centrifuged sample, or indirect examination with a dipstick which is the simplest and least specific way to evaluate hematuria. Hematuria found by dipstick should always be confirmed by microscopic evaluation of the sediment [61]. Hematuria is then categorized into gross hematuria and microhematuria. In general, gross hematuria can be seen by the naked eye and is urine that is not clear or yellow. Although the definitions vary, microscopic hematuria can be defined as greater than or equal to three to five red blood cells (RBC) per high-powered field (hpf) [60]. Assessment for hematuria is extremely important in athletes with possible genitourinary injuries as gross hematuria is a cardinal sign of bladder injury and is reportedly present in greater than 66% [61] to 95% [30] of bladder injuries. Microhematuria will be present in almost all the remaining cases. Neither gross nor microhematuria is a sensitive marker of ureteral injuries as approximately 25% of individuals with ureteral injuries have a normal urinalysis [60]. That being said, hematuria should raise concern for genitourinary injury. In addition to urinalysis, a complete blood count and complete metabolic panel including liver function tests should be ordered. Providers may also consider lipase, blood type, and coagulation studies depending on the presentation of the athlete. The diagnostic test of choice for suspected renal injury is a CT scan with IV contrast. It is indicated in blunt abdominal trauma when gross hematuria or microhematuria with shock is present (only once the patient has been stabilized). Other indications for imaging include a fall from height, significant deceleration, or other clinical features of renal trauma (flank pain or contusion). If there is concern for injury to the collecting system, delayed CT images will be needed. The indications listed above are the same for both pediatric and adult athletes. CT scans have largely replaced intravenous pyelography for renal trauma [62, 63]. A CT cystogram with retrograde filling of the bladder is the test of choice in suspected bladder injuries [62]. Specific indications to perform this test include gross hematuria or the combination of a pelvic fracture with microhematuria. Ultrasound can be used to visualize free fluid surrounding the intraperitoneal bladder as part of the FAST exam; however, this modality cannot differentiate blood from urine.

J. Santelli et al.

Ultrasound can also be used to evaluate the kidneys; however, there is a lack of sensitivity in the setting of trauma, and therefore it cannot be used to exclude injury [63]. X-rays do not have a role in identifying genitourinary injuries but may have a role in trauma evaluations. Fractures of the posterior ribs or spine fractures should raise the clinician’s suspicion for upper tract injuries (kidney, ureter). Any pelvic fracture seen on imaging should raise the providers’ suspicion for bladder and urethra injury in the athlete. Fractures that include the anterior arch or all four rami should increase suspicion for bladder injury. In addition, fractures of ipsilateral rami that co-occur with posterior displacement of the sacrum, sacroiliac joint, or the ilium should also raise concern for urethral injuries.

Management Treatment for blunt abdominal trauma that results in injuries to the genitourinary system depends on the type and severity of the injury according to the American Association for the Surgery of Trauma Organ Injury Severity Score [57]. Any unstable athlete should be emergently evaluated by a trauma surgeon. Athletes in whom an injury to the kidney, ureter, or bladder is identified will also need urgent evaluation and possible intervention by urology. Foley placement is advised to track urine output, except in the setting of urethral injury. Grade I and II renal injuries are usually managed nonoperatively, while grade V injuries usually require a nephrectomy. Renovascular injuries can be life-threatening and will require immediate evaluation and intervention. If such an injury is suspected, a renal arteriogram may be obtained, but this is a specialized test that may not always be available. Treatment of a renovascular injury may include operative revascularization, nephrectomy, endovascular stenting (in the case of arterial dissection), and observation [60]. Ureteral injuries may require a nephrostomy tube or possible stenting in the setting of transection by urology. Management of bladder injuries also varies by severity and location. Operative repair is often required for intraperitoneal bladder ruptures, but most retroperitoneal injuries are managed nonoperatively. In such injuries, a suprapubic catheter or Foley catheter can be placed to provide drainage of urine to keep the bladder decompressed while the injury heals [60]. In both adult athletes without gross hematuria and pediatric athletes who have microhematuria of 50  RBC/hpf or fewer who do not exhibit signs of shock, no intervention is required. These athletes should be followed by a urologist as outpatients until the microhematuria has cleared [30]. Return to Play In athletes who have no major injury identified but have simple microhematuria, return to play and return to training are

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determined by the resolution of his or her hematuria and clearance from urology. In athletes with more significant injuries, they may not return to play until they have been cleared by urology. Prior to return to play, all athletes must exhibit normal renal function and voiding. There is some literature that suggests that significant renal trauma may result in chronic hypertension. At this time, there are no specific recommendations outside of normal, routine blood pressure screening in athletes once he or she has been cleared. If the athlete is found to have persistent hypertension, appropriate treatment should occur based on the level of elevation.

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729 16. Lingawi SS, Buckley AR. Focused abdominal US in patients with trauma. Radiology. 2000;217(2):426–9. 17. McKenney KL, McKenney MG, Cohn SM, Compton R, Nunez DB, Dolich M, et  al. Hemoperitoneum score helps determine need for therapeutic laparotomy. J Trauma. 2001;50(4):650–4; discussion 4-6. 18. Miller MT, Pasquale MD, Bromberg WJ, Wasser TE, Cox J. Not so FAST. J Trauma. 2003;54(1):52–9; discussion 9-60. 19. Nural MS, Yardan T, Guven H, Baydin A, Bayrak IK, Kati C. Diagnostic value of ultrasonography in the evaluation of blunt abdominal trauma. Diagn Interv Radiol. 2005;11(1):41–4. 20. Shackford SR, Rogers FB, Osler TM, Trabulsy ME, Clauss DW, Vane DW. Focused abdominal sonogram for trauma: the learning curve of nonradiologist clinicians in detecting hemoperitoneum. J Trauma. 1999;46(4):553–62; discussion 62-4. 21. Yoshii H, Sato M, Yamamoto S, Motegi M, Okusawa S, Kitano M, et al. Usefulness and limitations of ultrasonography in the initial evaluation of blunt abdominal trauma. J Trauma. 1998;45(1): 45–50. 22. Abdulrahman Y, Musthafa S, Hakim SY, Nabir S, Qanbar A, Mahmood I, et al. Utility of extended FAST in blunt chest trauma: is it the time to be used in the ATLS algorithm? World J Surg. 2015;39(1):172–8. 23. Alrajab S, Youssef AM, Akkus NI, Caldito G.  Pleural ultrasonography versus chest radiography for the diagnosis of pneumothorax: review of the literature and meta-analysis. Crit Care. 2013;17(5):R208. 24. Alrajhi K, Woo MY, Vaillancourt C. Test characteristics of ultrasonography for the detection of pneumothorax: a systematic review and meta-analysis. Chest. 2012;141(3):703–8. 25. Wilkerson RG, Stone MB.  Sensitivity of bedside ultrasound and supine anteroposterior chest radiographs for the identification of pneumothorax after blunt trauma. Acad Emerg Med. 2010;17(1):11–7. 26. Strode C, Rubal BJ, Gerhardt RT, Bulgrin JR, Boyd SY. Wireless and satellite transmission of prehospital focused abdominal sonography for trauma. Prehosp Emerg Care. 2003;7(3):375–9. 27. Kokabi N, Shuaib W, Xing M, Harmouche E, Wilson K, Johnson JO, Khosa F.  Intra-abdominal solid organ injuries: an enhanced management algorithm. Can Assoc Radiol J. 2014;65(4):301–9. 28. Stranding S. Gray’s anatomy: the anatomical basis of clinical practice. 41st ed. New York: Elsevier Limitied; 2016. 29. Casiero D. Closed liver injuries. Clin Sports Med. 2013;32:229–38. 30. Marx J, Hockbergr R, Walls M.  Rosen’s emergency medicine. Concepts and clinical practices. 7th ed. Philadelphia: Mosby Elsevier; 2010. 31. Tinkoff G, Esposito TJ, Reed J, et al. American association for the surgery of trauma organ injury scale1: spleen, liver and kidney, validation based on the National Trauma Data Bank. J Am Coll Surg. 2008;207:646–55. 32. Parks R, Chrysos E, Diamond T. Management of liver trauma. Br J Surg. 1999;86:1121–35. 33. Rifat S, Gilvydis R. Blunt abdominal trauma in sports. Curr Sports Med Rep. 2003;2:93–7. 34. Wright WF.  Cullen Sign and Grey Turner Sign revisited. J Am Osteopath Assoc. 2016;116(6):398–401. 35. Rahbour G, Ullah M, Yassin N, Thomas G.  Cullen’s sign  case report with a review of the literature. Int J Surg Case Rep. 2012;3:143–6. 36. Chung KM, Chuanh SS. Cullen and Grey Turner signs in idiopathic perirenal hemorrhage. CMAJ. 2011;183:1221. 37. Puranik S, Hayes J, Long J, et al. Liver enzymes as a predictor of liver damage due to blunt abdominal trauma in children. South Med J. 2002;95:203–6. 38. Capraro AJ, Mooney D, Waltzman ML.  The use of routine laboratory studies as screening tools in pediatric abdominal trauma. Pediatr Emerg Care. 2006;22:480.

730 39. Wesson DE, Torrey SB, Wilwy JF. Liver spleen and pancreas injury in children with blunt abdominal trauma. Up To Date. Accessed 4 Apr 2017. Updated 25 Oct 2016. 40. Holmes JF, Sokolove PE, Brant WE, et al. Identification of children with intra-abdominal injuries after blunt trauma. Ann Emerg Med. 2002;39:500. 41. Sanchez-Bueno F, Fernandez-Carrion J, Torres-Salmeron G, et al. Changes in diagnosis and therapeutic management of hepatic trauma. A retrospective study comparing 2 series of cases in different (1997-1984 vs 2001-2008). Cir Esp. 2011;89:439–47. 42. Gross JL, Woll NL, Hanson CA, et al. Embolization for pediatric blunt splenic injury is an alternative to splenectomy when observation fails. J Trauma Acute Care Surg. 2013;75:421. 43. Kiankhooy A, Sartorelli KH, Vane DW, Bhave AD. Angiographic embolization is safe and effective therapy for blunt abdominal solid organ injuries in children. J Trauma. 2010;68:526. 44. Ralston D, Scherm M. Splenic artery avulsion in a high school football player: a case report. J Athl Train. 2004;39:201–5. 45. Maung A, Kaplan L. Management of splenic injuries in the adult trauma patient. Up To Date. Accessed 4 Apr 2017. Updated 26 Jan 2017. 46. Peitzman A, Heil B, Rivera L, Federle M, et al. Blunt splenic injuries in adults. Multi-institutional study of the Eastern Association for the surgery of trauma. J Trauma. 2000;49:177. 47. Gauer J, Gerber-Paulet S, Seiler C, Schweizer W. Twenty years of splenic preservation in trauma: lower early infection rate then splenectomy. World J Surg. 2008;32:2730. 48. Stein DM, Scalea TM.  Nonoperative management of spleen and liver injuries. J Intensive Care Med. 2006;21(5):296. 49. McIntyre LK, Schiff M, Jurkovich GJ.  Failure of nonoperative management of splenic injuries: causes and consequences. Arch Surg. 2005;140(6):563. 50. Wesson D, Filer R, Ein S, et al. Ruptured spleen- when to operate? J Pediatr Surg. 1981;16:324. 51. National Trauma Database. American college of surgeons 2000– 2004. https://ntdbdatacenter.com/. Accesses 1 Mar 2017. 52. May AK, Moore MM. Diagnosis of blunt rupture of the right hemidiaphragm by technetium scan. Am Surg. 1999;65:761. 53. Blaivas M, Brannam L, Hawkins M, et al. Bedside emergent ultrasonographic diagnosis of diaphragmatic rupture in blunt abdominal trauma. Am J Emerg Med. 2004;22:601. 54. Gangahar R, Doshi D.  FAST scan in the diagnosis of acute diaphragm rupture. Am J Emerg Med. 2010;28:387.

J. Santelli et al. 55. Williams M, Bulger EM, Collins KA.  Recognition and management of diaphragmatic injury in adults. Up To Date. Accessed 4 Apr 2016. Updated 9 July 2015. 56. Bhatt NR, McMonagle M.  Recurrence in a laparoscopically repaired traumatic diaphragmatic hernia: case report and literature review. Trauma Mon. 2016;21(1):e20421. 57. The American Association for the Surgery of Trauma. Injury scoring scale. A resource for trauma care professionals. http://www. aast.org/library/traumatools/injuryscoringscales.aspx. Accessed 6 Jun 2017. 58. Santucci R, McAninch J, Safir M, Mario L, et  al. Validation of the American Association for the Surgery of Trauma organ injury severity scale for the kidney. J Trauma. 2001;50:195–200. 59. Guttman I, Hamish AK. Blunt bladder injuries. Clin Sports Med. 2013;32:239–46. 60. Runyon M. Blunt genitourinary trauma: initial evaluation and management. Up To Date. Accessed 8 May 2017. Updated 2 Mar 2017. 61. Sutton JM.  Evaluation of hematuria in adults. JAMA. 1990;263:2475–80. 62. Morey A, Brandes S, Dugi D III, et al. Urotrauma: AUA guideline. J Urol. 2014;192:327. 63. Vaccaro J, Brody R.  CT cystography in the evaluation of major bladder trauma. Radiographics. 2000;20:1373. 64. Moore EE, Shackford SR, Pachter HL, McAninch JW, Browner BD, Champion HR, Flint LM, Gennarelli TA, Malangoni MA, Ramenofsky ML, Trafton PG. Organ injury scaling: spleen, liver, and kidney. J Trauma Acute Care Surg. 1989;29(12):1664–1666. https://journals.lww.com/jtrauma/Abstract/1989/12000/Organ_ Injury_Scaling__Spleen,_Liver,_and_Kidney.14.aspx. 65. Moore EE, Cogbill TH, Jurkovich GJ, McAninch JW, Champion HR, Genneralli TA, Malangoni MA, Shackford SR, Trafton PG, Peter G.  Organ injury scaling IV: thoracic vascular, lung, cardiac and diaphragm. J Trauma Acute Care Surg. 1994;36(3): 299–300. https://journals.lww.com/jtrauma/Citation/1994/03000/ ORGAN_INJURY_SCALING_IV__THORACIC_VASCULAR,_ LUNG.2.aspx. 66. Moore EE, Cogbill TH, Jurkovich GJ, McAninch JW, Champion HR, Gennarelli TA, Malangoni MA, Shackford SR, Trafton PG. Organ injury scaling III: chest wall, abdominal vascular, ureter, bladder, and urethra. J Trauma Acute Care Surg. 1992;33(3): 337–339. https://journals.lww.com/jtrauma/Citation/1992/09000/ O R G A N _ I N J U RY _ S C A L I N G _ I I I _ _ C H E S T _ WA L L , _ ABDOMINAL.1.aspx.

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Head Injury Christopher Guyer and Jeremiah W. Ray

Key Points

• Physicians should consider using clinical decision rules when determining the need for CT in athletes with traumatic head injuries. • There are multiple methods of diagnosing a concussion but no universally accepted standard. Neuroimaging is utilized to detect a skull fracture and/or intracranial hemorrhage but has no role in concussion diagnosis. • Return-to-play guidelines for athletes having sustained intracranial hemorrhage are based on expert opinion.

Introduction Head injury is a frequent cause of death in sport [1]. Head injuries occur as a result of athletes colliding with other players and objects. These impacts produce translational (linear) or rotational (angular) forces that lead to a variety of clinical pathology [2]. The brain is a particularly important organ because it is incapable of regeneration and transplantation is not an option. Head injuries can lead to dementia, seizure, paralysis, and death. Historically, football participation has caused the highest number of fatalities due to the number of athletes participating. Other high-risk sports include but are not limited to horseback riding, skydiving, motorcycle and car racing, gymnastics, ice hockey, boxing, martial arts, and rugby. Football is a high-profile sport and receives a significant amount of media attention C. Guyer (*) Divisions of Emergency Medicine and of Sports Medicine, Henry Ford Health System, Detroit, MI, USA e-mail: [email protected] J. W. Ray Department of Orthopedic Surgery, University of California at Davis Medical Center, Davis, CA, USA e-mail: [email protected]

and reports in medical literature. Rule changes, along with improvements in helmet technology and research into head injury biomechanics, have led to fewer catastrophic sportsrelated head injuries [3, 4]. A recent review estimates the number of catastrophic sports-­related injuries to be 0.60 per 100,000 participants per year among high school athletes [5].

Anatomy The scalp is the outermost layer of the head and has five layers: the skin, subcutaneous tissue, galea, areolar tissue, and pericranium. The scalp has a significant blood supply, and injury can result in extensive blood loss. The skull is rigid and made up of eight bones: two temporal bones, two parietal bones, the sphenoid, ethmoid, and frontal bones. In adults, expandability is limited. Cranial nerves and blood vessels enter the basilar skull (Fig. 43.1). The brain is made up of two cerebral hemispheres, the cerebellum, and the brainstem. Each hemisphere is divided into lobes: frontal, temporal, parietal, and occipital. The outermost layer covering the brain is the dura mater. Underneath this is the arachnoid mater, a thinner connective tissue layer. The innermost layer is called the pia mater. Cerebrospinal fluid is contained in the subarachnoid space that separates the arachnoid and the pia. Several subarachnoid spaces surround the brain. Within the brain are two lateral ventricles, a third ventricle, and a fourth ventricle. The ventricles communicate by several foramina (Fig. 43.2).

Spectrum of Injury Head injuries can be classified based on their anatomic location (epidural, subdural, subarachnoid, and intraparenchymal), the mechanism of injury (coup, contrecoup, linear, rotational), the distribution (focal or diffuse), and clinical presentation. Catastrophic injuries are defined by the

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a Skin

Subcutaneous tissue

Aponeurosis (galea)

Loose areolar tissue

Pericranium Frontal bone

b

Parietal bone

Sphenoid bone Ethmoid bone Temporal bone Occipital bone

Fig. 43.1  Scalp and skull anatomy Fig. 43.2  Brain anatomy

Parietal lobe Occipital lobe Frontal lobe Lateral ventricles Third ventricle

Temporal lobe

Fourth ventricle

National Center for Catastrophic Sports Injury Research as either direct (injury experienced as a result of participating in skills of the sport) or indirect (systemic failure secondary to exertion while participating in a sport). Injuries are further classified as fatal (injury causes death to the athlete), nonfatal (injury causes a permanent neurological functional disability), or serious (no permanent functional disability) [2].

Pathophysiology Factors that affect cerebral blood flow include autoregulation, cerebral perfusion pressure (CPP), mean arterial ­pressure (MAP), and intracranial pressure (ICP). Autoregulation normally regulates cerebral blood flow to achieve equilibrium between oxygen delivery and metabolism. Autoregulation

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adjusts CPP from 50 to 150 mmHg for maintenance of oxygen demands and regional blood flow. CPP < 60 mmHg is the lower limit of autoregulation. At this low of a pressure, local control of cerebral blood flow cannot be adjusted to maintain adequate flow for function. In head-­injured athletes, it is important to maintain a MAP of ≥ 80  mmHg because low blood pressure with elevated ICP results in low CPP and brain injury. The cranium is a closed space with a fixed volume. Volume changes such as bleeding increase the ICP and decrease the CPP.  The volume of the brain parenchyma, cerebrospinal fluid, and intravascular blood determines the ICP.  If one of these compartments expands, a reduction in another must occur or ICP will increase. ICP elevations can be life-threatening and can lead to a response called the Cushing reflex, a triad of hypertension, bradycardia, and respiratory irregularity [6]. Acute traumatic brain injuries can be divided into two phases: primary and secondary. In the primary phase, cellular injury occurs as a result of the force of injury. Primary injuries include contusions, hematomas, diffuse axonal injury, direct cellular damage, loss of the blood-brain barrier, disruption of neurochemical homeostasis, and loss of the electrochemical function. Injury prevention and mitigation are the only ways to reduce primary cell death. Secondary brain injury occurs as a result of the massive release of neurotransmitters, also known as the secondary neurotoxic cascade. Cytoplasmic and nuclear enzymes are activated by ionic shifts and cause mitochondrial damage. This in turn leads to cell death and necrosis. Proinflammatory cytokines and additional enzymes are released as the body tries to repair damaged cells. Secondary injury is nonselective, and extensive neuron loss can occur. Many cells will also undergo apoptosis, and this can occur even longer than a year after the initial injury [6]. Secondary insult is a clinical term used to describe conditions and circumstances that speed up neurotoxic damage and worsen outcomes. Examples include hypotension, hypoxemia, and hyperglycemia. Prevention of hypoxia and ischemia is the major treatment goal [6]. Brain edema occurs from two processes. Cytotoxic edema is caused by large ionic shifts as a result of loss of cellular membrane integrity that occurs from damage to mitochondria. Extracellular edema occurs from the breakdown of, or direct trauma to, the blood-brain barrier, ionic shifts, and changes to water exchange mechanisms. The brain swells and ICP increases in response to increased intracellular and extracellular water content. This leads to direct compression of tissues, vascular compression ischemia, herniation, and brain death.

I nitial Evaluation and Management on the Field When an athlete is “down” after sustaining a head injury, they require immediate assessment of their level of consciousness. Treatment for an unconscious athlete should fol-

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low Advanced Trauma Life Support protocols. If the athlete is facedown or on their side, they can be cautiously logrolled into a supine position while maintaining in-line stabilization of the cervical spine. Evaluation of their airway and respiratory effort is a primary concern. For athletes wearing a helmet, if airway intervention is required or there is need for respiratory support, the facemask can be removed to allow for access. The helmet should be removed if facemask removal is inadequate for airway access. A minimum of three trained rescuers is needed, and they should follow a team approach for removal of the helmet. The neck must be manually immobilized, and sequential removal of other protective gear, such as shoulder pads, should occur at the same time as helmet removal. Glasgow Coma Scale is a widely accepted and useful scoring tool for rapid assessment of trauma patients (Table 43.1). The use of this scale allows providers to communicate the condition of the patient by rating their eye, verbal, and motor responses. Injuries can be classified as severe (GCS score of 3–8), moderate (GCS score of 9–13), or mild (GCS score of 14 or 15). The next step in assessing the athlete is to perform a pupillary exam to evaluate for size and symmetry. Responses to verbal and noxious stimuli should be noted. Athletes with prolonged loss of consciousness will need to be prepared for immediate transport to a hospital with neurosurgical services. CT scanning will need to be performed to evaluate for intracranial hemorrhage. Equipment removal should be performed by those with the highest level of training. This may occur on the field in a prehospital setting or in the emergency department. In a recent statement from the National Athletic Trainers’ Association, they recommended that when appropriate, protective equipment may be removed prior to transport of the

Table 43.1  GCS score Glasgow Coma Scale Eye opening 4 Spontaneous 3 To speech 2 To pain 1 No response Verbal response 5 Alert and oriented 4 Disoriented conversation 3 Speaking but nonsensical 2 Moans or unintelligible sounds 1 No response Motor response 6 Follows commands 5 Localizes pain 4 Moves or withdraws to pain 3 Decorticate flexion 2 Decerebrate extension 1 No response

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athlete. Often the sideline sports medicine team has the most experience with equipment removal than other medical team members or hospital emergency staff [7]. If the helmet is left on, it can be taped to a rigid immobilization device. CT scanning can still be performed with a helmet, facemask, and shoulder pads in place. Brain contusion or intracerebral hematoma will usually cause headache. Neurologic deficits can also occur. These injuries may lead to a seizure. If an athlete is seizing, they can be logrolled onto their side to allow for blood and saliva to escape from the side of the mouth and the nose and to prevent the tongue from obstructing the airway. An oral airway or nasal trumpet can be placed if needed, but providers should not place objects or fingers into the athlete’s mouth as amputation can occur. Traumatic seizures will usually last 1–2 minutes. These athletes will need transportation to the hospital for further evaluation. Athletes who are awake can be evaluated on the sidelines for signs and symptoms of head injury. Providers should note level of consciousness, memory, speech, coordination, reflexes, vision, concentration, and gait. Symptoms of head injury include headache, nausea, vomiting, confusion, dizziness, photophobia, irritability, and amnesia. Athletes with symptoms should not return to play. Those with worsening headache, nausea and vomiting, or decreased level of consciousness will need to be transported to the hospital [8]. Any athlete that sustained loss of consciousness should be observed closely for worsening symptoms for at least 24 hours. Athletes with suspected skull fracture or intracranial hemorrhage will need CT scanning. CT allows for quick diagnosis of fractures and the location, type, and extent of bleeding. This modality can help with making decisions for operative intervention. Reliable clinical decision tools have been developed to assist providers in determining the need for CT scan in headinjured patients. For athletes 16  years of age and older, the Canadian CT Head Rule and New Orleans Criteria (Table 43.2) Table 43.3  PECARN pediatric head injury/trauma algorithm a Agitation, somnolence, repetitive questioning, or slow response to verbal communication b Motor vehicle crash with patient ejection, death of another passenger, or rollover; pedestrian or bicyclist without helmet struck by a motorized vehicle; falls of more than 1.5 m/5 ft; head struck by a high impact object

were developed. Prospective validation studies demonstrate 100% sensitivity and 60–76% specificity for the Canadian CT Head Rule. The New Orleans Criteria has been validated at 82–100% sensitivity and 12–26% specificity. The PECARN Pediatric Head Injury/Trauma Algorithm (Table 43.3) is useful for determining the need for CT in athletes younger than 16 years old. This algorithm has a validated sensitivity of 100% and 53–60% specificity for pediatric patients 2 years or older. Table 43.2  Canadian CT Head Rule and New Orleans Criteria Canadian CT Head Rule Can be used to clear head injury without imaging in patients with GCS of 13-15 and at least one of the following: witnessed loss of consciousness, amnesia to the head injury event, or witnessed disorientation CT of the head is indicated if any of the criteria below are present Medium-risk criteria Retrograde amnesia >30 min Dangerous mechanism of injury (pedestrian struck by motor vehicle, occupant ejected from motor vehicle, or fall from >3 feet or >5 stairs) High-risk criteria GCS score 2 hours Suspected open or depressed skull fracture Suspected basilar skull fracture Emesis ≥2 times >65 years of age If any of the following exclusion criteria are present, then the Canadian CT Head Rule does not apply: age 60 years Headache Vomiting Drug or alcohol intoxication Seizures Visible trauma above the clavicle Persistent anterograde amnesia

PECARN Pediatric Head Injury/Trauma Algorithm Age ≥2 years GCS ≤14 or signs of basilar skull fracture or signs of altered mental status*

Yes

CT recommended

No

History of loss of consciousness, vomiting, severe headache, or severe mechanism of injuryb

No CT not recommended

Yes

Observation versus CT on the basis of other clinical factors including: • Physician experience • Multiple versus isolated findings • Worsening symptoms or signs after emergency department observation • Parental preference

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Concussion

other athletes may have gradual onset of symptoms over the course of 24–48  hours. It is possible that immediately post injury, the athlete may experience some degree of headache, Mechanism of Injury in Sports head pressure, confusion, fogginess, and/or difficulty concenA concussive event results from acceleration, deceleration, trating [28]. Memory difficulties, a vacant stare, and repetior rotational forces transmitted to the brain, which do not tive questioning are common. Athletes may e­xperience necessitate direct trauma to the head [9]. This mechanism blurred vision, double vision, photophobia, balance, and induces diffuse axonal stretching, which mechanically dis- coordination difficulty. A loss of consciousness occurs in less rupts cell membranes and causes an unregulated efflux of than 10% of concussions, leaving the majority of concussions ions [10]. It is this rapid depolarization that results in the to occur without a loss of consciousness [27]. In the event of release of myriad neurotransmitters, predominately excit- head trauma, a loss of consciousness requires transient elecatory amino acids such as glutamate [11]. The Na+/K+ ATP-­ trochemical dysfunction of the reticular activating system dependent pump activates in order to reestablish proper ion caused by rotational forces exerted upon the midbrain [9]. A homeostasis but quickly depletes intracellular glucose [12, loss of consciousness was historically considered a marker of 13]. The glucose depletion leads to mitochondrial dysfunc- concussion severity but more recently was shown not to tion and inadequate oxidative metabolism, resulting in sub- strictly correlate with severity but rather point to a specific sequent anaerobic metabolism and lactate accumulation region of the brain that received the forces [29]. Minutes to [14–16]. Subsequent cerebral hypoperfusion, followed by hours after the injury, the athlete may report photophobia, hyperperfusion and edema, can occur in severe cases of trau- nausea, vomiting, and somnolence. In the hours to days after matic brain injury [17]. There have been attempts to measure the injury, the athlete may describe irritability, difficulty the force in newtons applied to the cranium to better identify sleeping, loss of appetite, fatigue, mood lability, and anxiety. high-risk events; however, accelerometers (in helmets and mouthpieces) for the assessment of concussion that report Diagnosis (Table 43.4) peak linear and rotational acceleration are not ready for clinical use and are an area of active research [18]. Table 43.4  Sport concussion signs and symptoms

Epidemiology In the United States, concussion in sports affects approximately 1.6–3.8 million athletes a year [19–21]. A concussion is also called a mild traumatic brain injury. It is important to note that although not all traumatic brain injuries are concussions, all concussions are mild traumatic brain injuries [22]. The diagnosis and management of concussion in sports is an evolving field of medicine and not without controversy. Several governing bodies have provided position statements and high-quality reviews on the topic [9, 22–27]. The American Medical Society for Sports Medicine (AMSSM) defines a concussion as “a traumatically induced transient disturbance of brain function” [22]. Various definitions for concussion exist, and to date there is no standardized objective manner for diagnosis.

Classification There is no classification system for concussions, and experts no longer grade concussions.

Clinical Presentation A significant challenge in making the diagnosis of concussion is the widely variable time of symptom onset post-­impact. Some athletes will have symptoms immediately, whereas

Signs  Loss of consciousness or moment of lying motionless on the playing surface  Balance difficulties  Gait difficulties  Motor incoordination: stumbling, slow, or labored movements  Disorientation or confusion or an inability to respond appropriately to questions  Blank or vacant look Symptoms  Headache  “Pressure in head”  Neck pain  Nausea or vomiting  Dizziness  Blurred vision  Balance problems  Sensitivity to light  Sensitivity to noise  Feeling slowed down  Feeling like “in a fog”  “Don’t feel right”  Difficulty concentrating  Difficulty remembering  Fatigue or low energy  Confusion  Drowsiness  More emotional  Irritability  Sadness  Nervous or anxious  Difficulty sleeping

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Initial Management It is imperative that if there is any concern for a concussive event, the athlete is pulled from competition immediately. Prior to concussion assessment, evaluate the athlete for the presence of adequate cardiopulmonary function and a patent airway. Next, evaluate for cervical spine injury, skull fracture, intracranial hemorrhage, and ocular globe rupture. These conditions necessitate immediate emergency medical services. Once life- and limb-threatening injuries have been excluded, proceed to your assessment for a concussion. There are multiple concussion assessment tools available, each with benefits and downsides. A well-validated and commonly utilized concussion assessment tool by sports practitioners across the world is the Sport Concussion Assessment Tool or SCAT, which is currently in its fifth edition as of 2017 [30]. The SCAT-5 can be downloaded for free from the British Journal of Sports Medicine website (http://bjsm.bmj. com/content/bjsports/early/2017/04/26/bjsports2017-097506SCAT5.full.pdf). The SCAT-5 can be utilized independently or in tandem with other sport concussion diagnostic modalities such as eye tracking, vestibular-ocular motor screen (VOMS), and neuropsychiatric testing (with or without computerized administration).

I ndications for Emergency Department Referral There are well-validated clinical decision tools to help the provider make evidence-informed decisions on whether or not imaging is clinically indicated. In children, we recommend using the PECARN [31] clinical decision rule, and for adults both the Canadian CT Head Rules and the New Orleans CT Head Rules are well validated [32]. It is important to mention that CT scans and magnetic resonance images of the brain do not diagnose concussion and are only clinically indicated when there is concern for intracranial hemorrhage (subdural hematoma, subarachnoid hemorrhage) or skull fracture. Magnetic resonance imaging (MRI), specifically, MRI diffusion tensor imaging (DTI), is a useful tool in concussion research but at this time has no clinical indication in the concussion setting [33, 34]. Any focal neurologic deficits require immediate neurological imaging. Any concern for cervical spine injury, intracranial hemorrhage, skull fracture, or ocular globe rupture mandates immediate referral for emergency services.

Follow-Up Care To date, there are no standard return-to-play algorithms. Most return-to-play strategies are based on historical ­practice patterns and not well informed by evidence. This is due to a pau-

C. Guyer and J. W. Ray Table 43.5  Graduated return-to-sport strategy Stage Light nonimpact aerobic activity such as a stationary bike for 30–45 minutes Dynamic activity such as plyometrics or weights Noncontact training drills

Full-contact practice Return to play

Goal Mild increase in heart rate

Add vestibular-ocular motor challenge Sports-specific exercise, coordination, and cognitive load Assess functional ability in full sport Play sport

city of data to guide these strategies. Table 43.5 is an example of what a return-to-play strategy might look like. Every athlete should have an individualized, graduated return protocol. The general rule is that the return to activity is gradual and an athlete may not advance to the next stage of activity until he/ she is asymptomatic at that activity load. There is some data to suggest that early nonimpact cardiovascular exercise, such as stationary cycling, improves recovery when compared to controls with strict rest [35]. Further supporting early cardiovascular activity is a growing body of observational data that prolonged activity restriction delays recovery [36].

Return to Sports As previously noted, there is no universally agreed upon return-to-sport protocol. Return-to-sport protocols are highly variable and dependent on local practice patterns. The long-­ standing cornerstone of concussion management has been rest, encompassing both physical and cognitive rests [27]. More recently, the data supporting this stance has been called into question as this practice is only supported by animal studies, two small observational studies in humans, and biochemical/physiologic theory [37]. The concept of mild physical noncontact physical activity to augment the recovery of a concussion was introduced in 2008 by Majerske et al. who advocate for prompt light cardiovascular activity, such as stationary bike [38]. In 2016, a prospective multicenter trial out of Ontario, Canada, demonstrated that early return to activity within 7 days of concussion halved the rate of post-­concussive symptoms when reexamined on day 28 [35]. Although there is broad variation in return-to-play guidelines, the general rule is that a concussed athlete is to be held from activity until asymptomatic at which point they gradually reintroduce activity [28] (Table 43.6). In the majority of concussed athletes, balance disturbances normalize by about 3  days post injury [39, 40]. Approximately 90% of athletes experience symptom resolution by post injury days 7–10 [41]. Acetaminophen is recommended for headache control if needed as there is a

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Table 43.6  Graduated return-to-academics strategy Stage Goal 1 Brain rest with no school. Some advocate for complete cognitive rest and do not allow the use of electronic devices, while others allow for these activities strictly as tolerated. The goal of this stage is to allow recovery without any symptom aggravation. This stage may require as little as a few days and a maximum of 2 weeks 2 Initiate gradual return to activity and academic work as tolerated. Begin with 15-minute reading/studying sessions a couple times a day and progress as tolerated 3 Modified school work. Return to school but with modified curriculum to accommodate needs of the patient such as a modified attendance schedule, modified curriculum, and modified environment as required by the patient 4 Full school work with minimal adjustments such as the ability to take a rest day if required or spacing out examinations as needed 5

Full school curriculum without modifications

Stage duration Advance to Stage 2 when asymptomatic or at 2 weeks regardless of symptoms

Advance to Stage 3 when asymptomatic or at 2 weeks regardless of symptoms Advance to Stage 4 when asymptomatic or at 2 weeks regardless of symptoms Advance to Stage 5 when asymptomatic or at 2 weeks regardless of symptoms Indefinite

theoretical risk of bleeding with aspirin and other nonsteroidal anti-­inflammatories [22]. The old adage of waking a concussed athlete on the first night of the concussion no longer stands. Observe a concussed athlete for 4 hours after injury, and if she/he remains with a stable neurologic examination and without increasingly severe symptoms, then that athlete may be permitted to sleep without mid-sleep evaluations [31].

Complications There is a growing body of evidence that links repetitive head trauma with chronic traumatic encephalopathy (CTE) [42, 43]. The neurobehavioral changes noted in contact sports were documented as early as the 1920s when boxers were deemed “punch drunk” and found to have increased rates of parkinsonism, dysarthria, and psychiatric disturbances [44]. There is a growing evidence to suggest that the “sloshing phenomenon” [45], in which multiple subconcussive episodes contribute to the formation of neocortical neurofibrillary tangles and tauopathy, can ultimately result in CTE [46]. The clinical presentation of CTE begins with a latent period of approximately 8 years between the last traumatic event and onset of symptoms. Athletes begin to ­manifest symptoms between the ages of 35 and 45  years (range 24–65 years) [42]. CTE has been described as “a pro-

gressive deterioration in social and cognitive functioning, mood and behavioral disorders, progressive deterioration in interpersonal relationships, violent behavior, substance abuse, headaches and/or body aches, and increasing religiosity” [47]. It is of increasing concern that this long-term sequelae of concussion may develop even in individuals where there was little, if any, evidence of significant prior history. The diagnosis of CTE is ultimately made at autopsy, but ongoing research is focused on more specific diagnostic testing to determine both such risk and more precise methods of monitoring early-phase injury as well. The concept of “second-impact syndrome” is one of the wide debates, with some arguing that this clinical entity does not exist [48]. Second-impact syndrome has also been termed “diffuse cerebral edema” and is the result of sustaining a second concussive event prior to symptom resolution of the first event. The proposed mechanism is loss of autoregulation of cerebral blood supply, which results in vascular engorgement and subsequent catastrophic cerebral edema [49]. Epidemiologically, it appears that some of the clinical presentations of “second-impact syndrome” were intracranial hemorrhages that massively expanded and caused death [50]. It is worth highlighting that the available body of literature clearly supports the fact that sustaining a second concussion shortly after an initial concussion prolongs the recovery and worsens symptom severity [51, 52].

Pediatric Considerations Younger athletes have been shown to have longer recovery times when compared to older athletes [53, 54]. It is suggested that persons with mood disorders [20], learning disabilities or ADD/ADHD [55], or migraine headaches [56] might be more susceptible to concussion as well as experience prolonged symptoms from a concussion.

Intracranial Hemorrhage Intracranial hemorrhage is the leading cause of death from sports-related head injuries. Four types of hemorrhage exist: epidural hematoma, subdural hematoma, subarachnoid hemorrhage, and intraparenchymal hemorrhage. Sideline providers should be familiar with all four types and be able to provide quick assessment for patients with suspected injuries.

Epidural Hematoma Mechanism of Injury in Sports Epidural hematomas occur when blood collects in the potential space between the skull and dura mater. The mechanism

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is direct trauma to the head when the athlete is not wearing a helmet, for example, a baseball player struck in the head by a ball. An epidural hematoma can also occur when injury is sustained to the portions of the skull not protected by a helmet. Hematomas can occur in the infratentorial and supratentorial compartments but are most common in the temporal region. Fractures of the squamous portion of the temporal bone are usually associated with laceration of the middle meningeal artery.

Epidemiology Overall, epidural hematoma is an uncommon head injury found in 1–4% of traumatic head injury patients. Observational studies have found that the mean age of patients with epidural hematoma is between 20 and 30 years of age [57]. Epidural hematomas are most often seen in the temporoparietal and temporal regions with a slight right-­ sided predominance. Bilateral epidural hematomas are seen in 2–5% of patients [58]. The majority of epidural hematomas are caused by traffic accidents, falls, and assaults with only a small number being a result of trauma sustained from participation in sports.

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C. Guyer and J. W. Ray

Clinical Presentation In classic descriptions of athletes with epidural hematomas, there is an initial loss of consciousness following the injury. This is followed by a lucid interval and subsequent deterioration. Athletes may report headache symptoms. In cases where the hematoma is rapidly expanding secondary to arterial bleeding, the patient may never regain consciousness. Abnormal pupil reaction, abnormal posturing, and focal weakness may be present on physical examination.

Diagnosis The most useful imaging modality for diagnosing epidural hematoma is a noncontrast CT of the head and brain. The CT will demonstrate a biconvex (football-shaped) mass in a focal location, usually in the temporal region. CT also allows for diagnosis of associated skull fractures. Small epidural hematomas may be missed due to volume averaging with adjacent bone. MRI and angiography are also imaging options but are used infrequently as CT is widely available (Fig. 43.3).

b

Fig. 43.3  Noncontrast head CT demonstrating (a) epidural hematoma (arrow) and (b) overlying skull fracture (arrow)

43  Head Injury

Initial Management Initial sideline management of epidural hematoma should follow ATLS protocol as outlined earlier in this chapter. Spinal injury precautions should be initiated based on the mechanism of injury and level of suspicion for injury. Athletes with initial loss of consciousness should be reexamined frequently on the sideline. Anisocoria is a sign of oculomotor nerve compression. Athletes with suspected epidural hematoma should be immediately transported to a hospital with CT capability and neurosurgeon availability.

Indications for Neurosurgery Referral All athletes with an epidural hematoma will require neurosurgical consultation. Arterial bleeding can lead to herniation within a few hours. Rapid identification and treatment is necessary. With epidural hematoma, the brain is usually spared of any direct injury, and these patients should be expected to do well. Surgical intervention is indicated if the clot is ≥ 30 cm3 or 15 mm thick, if there is ≥ 5 mm of midline shift, if focal deficits are present, or if the GCS is < 8. Surgical treatment with craniotomy and evacuation of the clot is usually effective. In patients with severe decompensation, ICP monitoring with or without hemicraniectomy may be indicated. Conservative treatment can be considered in athletes without criteria for surgical intervention and includes serial CT scanning and close neurological observation.

Follow-Up Care Athletes with epidural hematoma will require inpatient hospital management and neurosurgical consultation as indicated previously. Further care after hospitalization may include subacute rehabilitation. Athletes discharged from the hospital will need outpatient follow-up based on the interventions performed during hospitalization. This might include ambulatory clinic visits, physical therapy, and occupational therapy.

Return to Sports There is no consensus regarding return to play in athletes who have sustained an epidural hematoma. Evidence in this area is based on expert opinion. After any intracranial hemorrhage, return to collision sports is discouraged. Return to non-collision sports can be considered if recovery is complete. It has been suggested that return to sport be considered 1 year after injury in patients where neurologic recovery is complete and imaging, neurocognitive, balance, and other

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clinical measures are at baseline for the individual athlete. These decisions should be made with the treating neurosurgeon. Informed discussion must take place with the athlete and their family if they are a minor. Athletes should not be allowed to return to play if they have persistent symptoms, permanent neurologic sequelae (e.g., organic dementia, hemiplegia, homonymous hemianopsia), hydrocephalus, or symptomatic neurologic or pain-producing abnormalities about the foramen magnum [59].

Complications Complications of epidural hematomas include cerebral herniation, death, permanent neurological disability, seizures, and post-concussion syndrome.

Pediatric Considerations Clinical features in pediatric patients with epidural hematomas are similar to those in adults, including the classic description of a lucid interval. In children, skull fractures are less common because their skull is more elastic than that of adults. Providers should aim to make the diagnosis before neurologic deterioration occurs. CT is the diagnostic modality of choice in pediatric patients with head injury and signs and symptoms of an epidural hematoma. Priorities in assessment and stabilization of children with head injury are the same as in adult trauma patients. Children with epidural hematoma require emergent evaluation by a neurosurgeon. Emergent craniotomy and hematoma evacuation is required if acute epidural hematoma is present with altered mental status, signs of increased intracranial pressure, pupillary abnormalities, focal neurologic deficits, or cerebellar signs. Pediatric patients with small epidural hematomas and no neurologic deficits may be managed nonoperatively by a neurosurgeon.

Subdural Hematoma Mechanism of Injury in Sports Subdural hematoma occurs when bridging dural veins tear from sudden acceleration-deceleration of the brain parenchyma. They can also result from accumulation of blood from cortical lacerations and rupture of intraparenchymal hemorrhage into the subdural space [2]. This can occur from shearing forces or direct trauma sustained in contact sports like being tackled or tackling in football. Trauma from boxing, mixed martial arts, and rugby also can produce these injuries. Subdural hematomas can occur in noncontact sports

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where an athlete sustains head trauma, for example, a baseball player hit in the head with a bat or ball, a soccer player kicked in the head, or a cyclist thrown from a bicycle.

Epidemiology Subdural hematoma is the most frequent type of hematoma occurring from trauma sustained in football. It is also the most common fatal injury from sports participation. Studies have shown that brain injuries account for 69% of deaths related to football [60], with 86% of these being diagnosed as subdural hematoma [61].

Clinical Presentation Signs and symptoms of subdural hematoma are often delayed because veins bleed slower than arteries. Subdural hematomas can present acutely or chronically and can present with a variety of signs and symptoms. Patients with an acute subdural hematoma will typically have loss of consciousness and a poor initial neurologic examination. Those with either a small initial subdural hematoma or previously unrecognized subdural hematoma may have delayed symptoms including persistent headaches, altered mentation, blurred vision, nausea, focal weakness, and seizures. A complete list of the signs and symptoms of subdural hematoma can be found in Table 43.7.

Diagnosis The diagnosis of subdural hematoma is made using noncontrast CT scanning. Acute subdural hematomas will appear as hyperdense, crescent-shaped lesions between the calvarium and cortex. They can extend beyond the suture lines and may follow the contour of the calvarium. They may also be seen in the interhemispheric fissure. Subacute Table 43.7  Signs and symptoms of subdural hematoma History of recent head injury Loss of consciousness or fluctuating levels of consciousness Irritability Seizures Pain Loss of muscle control Altered breathing patterns Hearing loss, ringing or tinnitus Ataxia or difficulty walking Blurred vision

Numbness Headache (constant or fluctuating) Dizziness Disorientation Amnesia Weakness or lethargy Loss of appetite Personality changes Inability to speak or slurred speech Deviated gaze or abnormal movements

Fig. 43.4  Noncontrast head CT of an 18-year-old football player with right-sided subdural hematoma, effacement of the ventricles, and midline shift. (Image courtesy of Ross Mathiasen, MD)

or chronic subdural hematomas may appear isodense or hypodense. IV contrast may enhance these findings. MRI may also be a useful imaging modality. Indirect evidence may be present including midline shift, effacement of the ipsilateral cortical sulci, and compression of the ventricles. Subdural hematomas involving the posterior fossa do not cross the midline and do not extend above the tentorium (Fig. 43.4).

Initial Management Sideline management of athletes with subdural hematomas should follow ATLS protocols. Providers will need to ensure that airway, breathing, and circulation are maintained. Airway assessment should include evaluation for patency and the athlete’s ability to protect himself from aspiration of oral secretions, blood, or gastric contents. Athletes with impaired respiration may be breathing spontaneously, but tidal volumes may be low. A rapid rate of breathing may also be present and can exhaust the accessory muscles of respiration, leading to hypoventilation. Breathing should be supported with supplemental oxygen and bag valve mask ventilations. Airway support may be necessary and includes

43  Head Injury

oral or nasal airways and oral or nasotracheal intubation. Spinal injury precautions must be taken if spinal cord injury cannot be immediately excluded. Fluid resuscitation may be required to treat shock. Athletes will require evaluation for additional injuries during the secondary survey. Acute seizures may need treatment with benzodiazepines. Immediate transport to a hospital with CT scanning and neurosurgical capabilities will be necessary.

Indications for Neurosurgical Referral Any athlete with subdural hematoma will require evaluation by a neurosurgeon. Indications for surgical management include hematoma thickness ≥10 mm, midline shift ≥5 mm, if GCS score decreases two or more points between injury and hospital admission, if pupils are asymmetric or fixed and dilated, or if intracranial pressure is greater than 20 mm Hg. Surgical management usually consists of craniotomy or burr holes. Patients can be managed conservatively if GCS is greater than 9, and the hematoma is small with no mass effect seen on CT. They will require monitoring of the intracranial pressure.

Follow-Up Care As with epidural hematoma, athletes with a subdural hematoma require inpatient hospital management and neurosurgical consultation. Aftercare may include subacute rehabilitation, outpatient follow-up visits, physical therapy, and occupational therapy.

Return to Sports Similar to epidural hematoma and any intracranial hemorrhage, return to contact sports after resolution of subdural hematoma is discouraged. No level I evidence exists to guide decisions. Current return-to-play recommendations are based on expert opinion. Athletes might consider return to play in noncontact sports after 1 year. This time is suggested to allow for reabsorption of the hematoma. Confirmation of resolution of subdural hematoma will need to be documented on repeat imaging, and the brain must be re-expanded to fill the subdural space with no residual hygroma.

Complications Complications of subdural hematoma include cerebral herniation, death, persistent post-concussive symptoms (memory

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loss, dizziness, headache, anxiety, difficulty concentrating), seizures, and neurologic deficits.

Pediatric Considerations Shaken baby syndrome and subdural hematoma in very young children are beyond the scope of this discussion. Child athletes with subdural hematomas usually have a history of major head trauma. Predisposing factors may be present but are less frequent. These include bleeding tendency, cerebral atrophy, and arachnoid cyst. Subdural hematoma should be considered in adolescent athletes with neurologic deterioration following head injury. Anisocoria, hemiparesis, and hemiplegia are all lateralizing neurologic signs and indicate cranial nerve compression or brainstem compression and signify progression to cerebral herniation. Initial assessment and management of these patients follows that for adult trauma patients. Pediatric patients with GCS ≤ 12 require emergent neurosurgical evaluation, and those with GCS ≤ 8 will require ICP monitoring. As with epidural hematoma, CT is the imaging modality of choice. No definitive criteria exist for surgical decision-making in pediatric patients with subdural hematoma. Surgical evacuation is performed in most children with acute subdural hematoma, neurologic deficit, and midline shift seen on CT. Comatose patients with severe edema and signs of infarct are poor candidates for surgical intervention. This contrasts with the management approach of epidural hematoma. Pediatric patients with subdural hematoma should be managed in a facility with advanced imaging and neurosurgical capabilities. Initial neurologic status is the best predictor of outcome regardless of age or injury mechanism.

Subarachnoid Hemorrhage Mechanism of Injury in Sports Traumatic subarachnoid hemorrhage is the result of disruption of the parenchyma and subarachnoid vessels. In subarachnoid hemorrhage, bleeding is confined to the cerebrospinal fluid space between the pia mater and the arachnoid membranes. These injuries can occur spontaneously from rupture of an aneurysm or arteriovenous malformation or from trauma sustained while participating in sports. Additional causes include cavernous angiomas, mycotic aneurysms, neoplasms, and blood dyscrasias. Subarachnoid hemorrhage has been reported from participation in swimming, diving, gymnastics, golf, weight training, and other sports [62]. The increase in risk of subarachnoid hemorrhage with physical activity or sports participation is thought

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to be due to activation of the sympathetic nervous system, with increased heart rate and blood pressure and/or Valsalva maneuvers.

Epidemiology Current literature suggests that subarachnoid hemorrhages occur in association with physical activity in up to 58% of cases. Only 2.1% of these cases occurred in athletes participating in sport. The majority of athletes with subarachnoid hemorrhage are male. Aneurysms were found in one-third of athletes with subarachnoid hemorrhage [62].

Clinical Presentation Athletes with traumatic subarachnoid hemorrhage can present with sentinel headache, photophobia, and meningeal signs. Classically, the headache is described as the worst headache of their life. There may be a lucid period after the injury. Other symptoms include altered mental status, nausea and vomiting, and seizure. Physical exam may reveal signs of cranial nerve palsy, hypertension, retinal hemorrhages, papilledema, and motor deficits. Neurologic deterioration may be rapid, even to the point of death.

Diagnosis CT scanning is the imaging modality of choice in detecting traumatic subarachnoid hemorrhage (Figs.  43.5 and 43.6). Some subarachnoid hemorrhages may be missed on delayed CT, but typically in the setting of traumatic injury, CT is obtained immediately following the injury. CT scanning within 6 hours after injury or onset of headache is typically sensitive (93–100% in the first 24 hours) for diagnosing subarachnoid hemorrhage. If suspicion is high for subarachnoid hemorrhage, cognitively intact patients may require lumbar puncture to exclude aneurysm or arteriovenous malformation-related subarachnoid hemorrhage. CT angiography is the test of choice for detecting aneurysms. Providers may also consider the use of magnetic resonance angiography, but this test is limited by technical considerations in unstable patients [63].

Initial Management As with other types of intracranial hemorrhage, the initial management of athletes with subarachnoid hemorrhage should follow ATLS protocols. In an unconscious athlete, the primary evaluation will focus on assessment of airway,

Fig. 43.5  Noncontrast head CT showing acute subarachnoid hemorrhage involving the right frontal and temporoparietal lobes (arrow) in addition to a large left posterior parietal scalp hematoma (arrowhead). (Image courtesy of Brent Griffith, MD)

breathing, and circulation. As with any unconscious athlete, cervical spine instability should be assumed, and their spine should be immobilized. If airway, breathing, and circulation have been adequately secured, a secondary survey can begin which includes evaluation of the head, maxillofacial structures, cervical spine and neck, chest, abdomen, genitourinary system, musculoskeletal system, and neurologic system. Unconscious athletes will require immediate transport to a hospital where CT scanning and neurosurgical services are available. If the patient is awake and cooperative, knowing the athlete’s neuropsychological baseline is important for short- and long-term management of their head injury. Physical examination includes neurological, musculoskeletal and spine, maxillofacial, and ophthalmologic exams. Athletes will need to be observed for signs of neurologic deterioration. If intracranial hemorrhage is suspected, athletes must be transferred for imaging with CT and further evaluation.

Indications for Neurosurgeon Referral Neurosurgical consultation will be necessary for any athlete with subarachnoid hemorrhage. Athletes with a GCS score from 13 to 15 can typically be managed conserva-

43  Head Injury

a

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b

Fig. 43.6  Noncontrast head CT demonstrating (a) a depressed skull fracture involving the right parietal bone near the vertex (axial, bone window) and (b) associated hemorrhagic parenchymal contusion (coronal, brain window)

tively. They will require monitoring with follow-up CT scanning to ensure that bleeding is resolving. They will also require observation of blood pressure and possible intracranial pressure monitoring. Surgical management is rarely necessary in isolated traumatic subarachnoid hemorrhage. If an underlying aneurysm is found, it will often require treatment.

Complications

Follow-Up Care

Pediatric Considerations

Athletes who have sustained subarachnoid hemorrhage will require further outpatient care after hospital discharge. This may include subacute rehabilitation and outpatient physical and occupational therapy.

Aneurysms are uncommon in children and adolescents. Subarachnoid hemorrhage usually occurs secondary to arteriovenous malformation. Risk factors that may be present in the pediatric population include polycystic kidney disease, Marfan syndrome, Ehlers-Danlos syndrome, and coarctation of the aorta. In children, the reported incidence of subarachnoid hemorrhage is 0.18–2/100,000.

Return to Sports Return to contact sports is contraindicated in athletes who have sustained spontaneous subarachnoid hemorrhage from any cause. Return to contact sports is also contraindicated in any athlete who requires operative intervention of their intracranial hemorrhage. No evidence-based guidelines exist, and return-to-play decisions are typically based on expert opinion. As with other types of intracranial hemorrhage, return to noncontact sports could be considered in athletes with subarachnoid hemorrhage 1 year after injury if they have complete recovery, have returned to baseline, have normal neuroimaging, and have no vascular abnormalities or coagulopathy.

Complications of subarachnoid hemorrhage include vasospasm, rebleeding, thromboembolism, cerebral infarction, cerebral edema, hydrocephalus, intracranial hypertension, electrolyte abnormalities, respiratory failure, myocardial dysfunction, and sepsis.

I ntracerebral Hemorrhage (Brain Contusions) Mechanism of Injury in Sports Traumatic intracerebral hemorrhage in athletes can result from sudden acceleration and deceleration of the orbitofrontal lobes and temporal poles along the skull base as well as from direct head trauma sustained during sports participation. Bleeding occurs directly into the brain parenchyma, typically from rupture of a torn artery. Bleeding can also

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occur from rupture of congenital vascular lesions like aneurysms or arteriovenous malformations. Traumatic intracerebral hemorrhages will typically expand over time.

Clinical Presentation Athletes with intracerebral hemorrhage will often have stroke-like symptoms. They may not have a lucid interval, and their presentation can progress rapidly and lead to death. Intraparenchymal hemorrhage may have been unavoidable in cases where a congenital abnormality exists. Additional signs and symptoms of intracerebral hemorrhage include decreased mental status, nausea and vomiting, headache, seizures, and a focal or evolving neurological exam. See Table  43.8 for common focal neurological findings. Signs of increased intracranial pressure or herniation include lethargy, hypertension, papilledema, emesis, and the Cushing reflex (bradycardia, decreased respiratory rate, and hypertension).

Diagnosis The imaging modality of choice for diagnosing intracerebral hemorrhage is a noncontrast CT of the head and brain. A positive test will often reveal hyperdense areas that are well demarcated. They are usually located at the frontal, tempoTable 43.8  Focal neurological findings in intracerebral hemorrhage Structure Putamen

Findings Contralateral hemiparesis, sensory loss, conjugate gaze paresis Homonymous hemianopia Aphasia, neglect, apraxia Thalamus Contralateral sensory loss, hemiparesis, conjugate gaze paresis Homonymous hemianopia Miosis, aphasia, confusion Lobar Contralateral hemiparesis, sensory loss, conjugate gaze paresis Homonymous hemianopia Abulia, aphasia, neglect, apraxia Caudate Contralateral hemiparesis, conjugate gaze paresis nucleus Confusion Brainstem Quadraparesis, facial weakness Decreased level of consciousness Gaze paresis, ocular bobbing Miosis, autonomic instability Cerebellum Truncal ataxia Ipsilateral facial weakness, sensory loss Gaze paresis, skew deviation Miosis Decreased level of consciousness

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ral, and occipital poles. Surrounding edema and mass effect may be present with midline shift and herniation. Serial CT scanning in the first 48 hours is usually required as hemorrhagic transformation can occur.

Initial Management Initial treatment of athletes with intracerebral hemorrhage is consistent with the other types of hemorrhage previously discussed. In unconscious athletes, the focus should be on evaluating and securing the athlete’s airway, breathing, and circulation while maintaining spinal immobilization precautions until spinal injury can be safely excluded. Following the primary survey, a secondary survey can be completed, and the athlete can be transferred to a facility with CT scanning and neurosurgical capabilities. Awake athletes with head injuries will require neurological, ophthalmologic, maxillofacial, musculoskeletal, and spine exams as appropriate based on their injury. If intracerebral hemorrhage is suspected, the athlete will require transfer to an appropriate facility where CT imaging can be performed and neurosurgical consultation is available.

Indications for Neurosurgical Referral Any athlete with intracerebral hemorrhage will require admission to the hospital and consultation with a neurosurgeon. Operative management should be considered if neurologic deterioration is caused by the contusion, if the contusion volume is ≥ 50  cm3, with frontal and temporal contusion volume ≥ 20 cm3, in those with ≥ 5 mm of midline shift or effaced basal cisterns, and if the GCS score is 6–8 [57, 59].

Follow-Up Care Similar to previously described types of hemorrhage, follow­up care after hospitalization for intracerebral hemorrhage is based on the type of interventions required and the deficits sustained as a result of the injury. Rehabilitation in subacute and ambulatory settings may be required.

Return to Sports Athletes with intracerebral hemorrhage should be discouraged from returning to contact sports. Return to noncontact sports can be considered after 1 year if recovery is complete. If return to sports is contemplated, imaging studies should be normal. Physical exam, neurocognitive testing, and balance

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testing should be at the athlete’s baseline. Contraindications to return to play include persistent edema or hemorrhage. Return to noncontact sports after craniotomy can be considered in athletes who have returned to baseline as above and if CT demonstrates complete bony union and MRI shows no underlying brain or meningeal injury.

Complications Athletes with intracerebral hemorrhage are at risk of hematoma expansion, perihematomal edema with increased intracranial pressure, intraventricular extension of hemorrhage with hydrocephalus, seizures, venous thrombotic events, hyperglycemia, hypertension, fever, and infections [64].

Pediatric Considerations In the pediatric population, intracerebral hemorrhage can be caused by trauma, vascular malformations, hematologic causes like thrombocytopenia, platelet dysfunction, hemophilia, congenital and acquired coagulopathies, hemoglobinopathies, cancer, moyamoya disease, and cryptogenic causes. Similarly to adults, pediatric patients can present with symptoms of nausea and vomiting, focal or generalized seizure, focal neurologic deficits, neck pain, and altered level of consciousness. Initial evaluation follows that for adults neuroimaging with CT or MRI is required for diagnosis. MRI is a preferred imaging modality in stable patients because of the lack of radiation and better resolution. CT should be performed if the patient is unstable or if obtaining MRI might delay the diagnosis. Management is similar to adults with initial evaluation focusing on stabilization of the athlete and treating elevated intracranial pressure if present with close monitoring for herniation. Neurosurgery consultation is required, and hematology consultation may be necessary if hematologic abnormalities are suspected.

Posttraumatic Seizure Mechanism of Injury in Sports Seizures can occur as a result of sports-related head trauma and can manifest as early seizures or late seizures. The exact pathophysiology of early seizures and concussive convulsions is unknown. The current theory suggests that rapid, nondiscriminatory release of excitatory neurotransmitters occurs at the time of impact, followed by spreading depression [65]. This is thought to result in loss of cortical inhibition and transient functional decerebration.

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Posttraumatic seizures are thought to occur as a result of pathological changes and include reactive gliosis, axon retraction balls, Wallerian degeneration, microglial scar formation, and cystic white matter lesions. Changes to intrinsic membrane properties of pyramidal neurons and enhanced N-methyl-D-aspartate synaptic conductances are also thought to cause posttraumatic seizures. Hippocampal injury may also be a contributor. In patients with brain contusion or cortical laceration, iron is released as a result of breakdown of hemoglobin. Iron may increase intracellular calcium oscillation and free radical formation. This results in excitotoxic damage, neuronal death, and glial scarring, leading to epileptiform activity [66].

Epidemiology Up to 1 in 70 patients with concussion will experience a concussive convulsion after impact. Early posttraumatic seizures occur in 6–10% of individuals with head injury and in up to 20% in those with depressed skull fractures and intracerebral hematomas. Status epilepticus can develop in about 10% of patients with acute head injury. Focal motor status epilepticus is more common with subdural hematomas and depressed skull fractures. The incidence of posttraumatic epilepsy at 10  years is approximately 2%. This risk is correlated with severity of the injury. Patients are considered to be at higher risk if they have early seizures, intracranial hemorrhage, cerebral contusion, or depressed skull fracture. Seizures begin within 2 years for the majority of patients with traumatic brain injury.

Classification Posttraumatic seizures are classified based on the time of their occurrence following injury. Seizures occurring within seconds after injury were previously called impact seizures but are now referred to as concussive convulsions to better describe the non-epileptic nature of these events. Early posttraumatic seizures occur within 1 week of head trauma. Similar to concussive convulsions, early seizures are not thought to represent epilepsy. Posttraumatic epilepsy occurs more than 1  week after head injury. These occur as the result of more permanent structural and physiologic changes to the brain.

Clinical Presentation Concussive convulsion will present with immediate tonic activity, followed by a clonic or myoclonic phase, and can last up to several minutes. If present, a postictal state is very

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brief. Early posttraumatic seizures typically occur during the first 24 hours. The majority of these are generalized tonic-­ clonic. Seizures that occur later are more likely to be focal in onset, and more than half of those occurring after the first day are simple partial (pure motor) or focal with secondary generalization. The majority of early posttraumatic seizures occurring in the first 24  hours are generalized tonic-clonic. Focal-onset seizures occur more often after the first day with more than half being either simple partial (pure motor) seizures or focal with secondary generalization. In posttraumatic epilepsy, the seizures are not typically secondarily generalized. A smaller number are simple or complex. About one in ten patients with an acute head injury will develop status epilepticus. Focal motor status epilepticus is seen most often in those with subdural hematoma or depressed skull fracture.

Diagnosis The diagnosis of concussive convulsion is made clinically based on the athlete’s presentation, and neuroimaging is not required. A noncontrast head CT is required in athletes with early posttraumatic seizures. MRI and EEG are not required during the acute phase of head injury. Evaluation of athletes with posttraumatic seizure should follow that for any patient with first-time seizure. In patients with known traumatic brain injury within the last 2  years, diagnostic testing may be limited to neuroimaging, serum chemistries, and toxicology screen. If the patient is febrile and has other findings on exam or if the seizure is not consistent with the site of previous brain injury, further diagnostic evaluation may be required.

Initial Management For athletes who sustain a concussive convulsion, immediate treatment includes supportive care and airway protection. No correlation has been shown with these injuries and abnormal imaging with CT and MRI.  Athletes with early posttraumatic seizure will require imaging with a head CT.  Treatment with antiepileptic drugs may be required if an athlete has significant risk factors such as a depressed skull fracture, intracerebral hematoma, or penetrating head injury and can reduce the incidence of early seizures in these patients. Treatment may also be required if there is concern for risk of status epilepticus or aggravating a systemic injury. Recurrent seizures can also increase cerebral blood flow and increase intracranial pressure.

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Treatment is typically started during hospitalization and withdrawn within the first few weeks. Anticonvulsant treatment is recommended for athletes who have a late seizure. The risk of recurrence is up to 86% in untreated individuals [67]. Prophylactic treatment for posttraumatic epilepsy is not routinely recommended.

I ndications for Neurology or Neurosurgical Referral Neurology consultation should be considered for confirmation of the diagnosis in athletes with early or late posttraumatic seizures and for assistance with antiepileptic medication management in athletes with posttraumatic seizures. Neurosurgical consultation will be necessary if the athlete has a depressed skull fracture, intracerebral hematoma, or penetrating head injury.

Follow-Up Care Athletes with concussive convulsion will not require treatment with anticonvulsant therapy. Those patients started on antiepileptic treatment will require regular outpatient follow-­up for monitoring their seizure frequency, neurologic status and medication, observation for development of adverse medication effects, and measurement of drug levels.

Return to Sports Concussive convulsions are considered benign and by themselves will not prevent an athlete from returning to play. If an underlying skull fracture or intracranial hemorrhage precipitated the onset of seizure, return-to-play decisions would be based on the underlying injury. For athletes with recently diagnosed early or late posttraumatic seizures, return to sports may need to be delayed until treatment and control of seizures is established. Sports-­specific restrictions are outlined in Table 43.9. Participation in high-risk sports is not typically recommended for athletes with a seizure disorder. Helmet use is recommended for athletes participating in sports like cycling, equestrian sports, football, skateboarding, and skiing. A partner should be present for equestrian sports, ice skating, rollerblading, skateboarding, and boating. If an athlete with a seizure disorder is participating in sports that involve water, a lifeguard should be present and aware that the athlete has epilepsy. Activities should not be performed in the ocean or

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Table 43.9  Risk stratification for sports participation in athletes with seizures High risk

Moderate risk

Low or no risk

Contact sports with no known risk

Bungee jumping Gymnastics Hang gliding Motor sports Mountain and rock climbing Scuba diving Sky diving Surfing Cycling Equestrian sports Ice skating Rollerblading Skateboarding Sailing/canoeing Swimming Water skiing/wakeboarding/ wakesurfing Aerobics Bowling Cross-country running or skiing Dancing Field hockey Golf Hiking Track Baseball Football Basketball Soccer

in water where visibility is limited. Athletes should also wear a life jacket if appropriate [8].

Complications Athletes with concussive convulsion rarely have significant complications. Those with early posttraumatic seizures and posttraumatic epilepsy may be at risk for aspiration pneumonia if food or saliva is inhaled during a seizure episode, injuries that occur during a fall (fall, contusion, tongue biting, dislocation, fracture, etc.). Athletes can also experience side effects from using anticonvulsant medications.

Pediatric Considerations Children under 7 years of age are more likely to have early posttraumatic seizures when compared to adolescents or adults. Early seizures and depressed skull fractures are risk factors for late posttraumatic seizures [68].

Skull Fracture Mechanism of Injury in Sports Skull fractures result from direct trauma. This occurs in contact sports and in sports with a high risk of collision or other trauma to the head.

Epidemiology Sports-specific epidemiologic data on skull fractures is lacking. Simple linear fractures are the most common. Sports with the highest distribution of reported skull fractures include baseball, skateboarding, soccer, skiing and snowboarding, horseback riding, golf, street hockey, football, rollerblading and roller hockey, and skating [69]. In the general population, skull fractures are reported to occur between 2% and 20% of all cases of head trauma with an incidence of 35–45/100,000 people annually. Skull fractures occur most commonly between the ages of 20 and 50 years. Males are affected more predominantly than females. Falls are the most common mechanism and account for up to 35% of cases [70].

Fracture Classification Skull fractures are classified by location (skull convexity or basilar), pattern (linear, depressed, or comminuted), and if they are open or closed. Linear fractures are the most common type and involve a single full-thickness fracture line. They account for 60–90% of skull fractures. Intracranial injury occurs in 15–30% of these patients [71]. If there is no associated intracranial injury, they are considered isolated. Comminuted fractures occur when the bone is broken into multiple pieces. The evaluation and management of simple comminuted skull fractures follows that of linear fractures. A depressed fracture is one where a palpable bony abnormality is present. The risk of intracranial injury is up to 30%. Depressed fractures have a higher risk than linear fractures of dural tear and brain laceration. They also carry a higher risk of posttraumatic seizure. Basilar skull fractures commonly involve the temporal bone, external auditory canal, and the tympanic membrane. Fractures are considered as open if they communicate with the skin, sinuses, or middle ear. Open fractures, depressed fractures, fractures that involve a sinus, and those that are associated with pneumocephalus are all considered complicated fractures.

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Clinical Presentation The mechanism of injury is particularly important when considering a diagnosis of skull fracture. Aside from localized pain, other high-risk features to be aware of include loss of consciousness, seizure, amnesia, persistent headache, vomiting, and changes in behavior or confusion. Patients may present with signs of intracranial injury, such as altered mental status with GCS  5 mm or if there is associated dural tear, pneumocephalus, underlying hematoma, or gross contamination. All patients with basilar skull fractures will require admission and neurosurgery consultation. Skull fractures caused by penetrating injuries are considered open fractures and require consultation with a neurosurgeon.

Follow-Up Care Athletes with skull fractures will require outpatient follow­up based on the type of injury and any associated injuries such as intracranial hemorrhage or concussion. For other types of fractures, the type of follow-up care is based on management and interventions required during hospitalization and associated injuries.

Return to Sports No evidence-based guidelines exist for return to play. The majority of skull fractures heal within 3–6 months. Athletes with simple linear fractures can return to exercise as soon as symptoms allow. Return to high-risk sports can be considered at 12 weeks if CT demonstrates fracture union. Athletes with comminuted fractures, basilar skull fractures, and those requiring surgical treatment may consider return to play after fracture union is demonstrated. This may take 6 months or longer. Special consideration should be given for return to play when there are other associated injuries including intracranial hemorrhage.

Complications Complications from skull fractures include cerebrospinal fluid leak, intracranial hemorrhage, venous sinus stenosis or thrombosis, meningitis, cranial nerve deficits, motor deficits, posttraumatic seizure, and postsurgical anosmia [70].

Pediatric Considerations Signs and symptoms of skull fractures in the pediatric population are similar to those in adults. History may include traumatic injury, loss of consciousness, and localized pain and swelling. Physical examination features include soft tissue swelling of the scalp, hematoma, palpable fracture, skull defect, crepitus, and signs of basilar skull fracture (e.g., raccoon eyes, Battle’s sign, hemotympanum, cerebrospinal fluid rhinorrhea, or otorrhea). As in adult patients,

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pediatric patients will need to be evaluated for traumatic brain injury. CT is the imaging modality of choice. Pediatric patients with depressed skull fractures, basilar skull fractures, and linear skull fractures with greater than 3 mm of separation will all require evaluation by a neurosurgeon with pediatric expertise. If basilar skull fracture is present with CSF leakage, evaluation by a pediatric otolaryngologist is also required. Pediatric patients with no neurological findings and isolated linear skull fractures with no depression and narrow margins (< 3  mm separation) or isolated basilar skull fractures who have an otherwise normal CT can be treated conservatively without neurosurgical consultation [72].

Soft Tissue Injuries Soft tissue injuries of the scalp are not uncommon from head trauma sustained during sports participation. High-risk sports include boxing, martial arts, and baseball. The use of a helmet is effective at reducing the risk of soft tissue injury to the head. Abrasions of the scalp are common in sports. Local wound care is usually all that is necessary for treatment. Athlete can be instructed on keeping the wound clean, using antibiotic ointment to prevent infection, and covering the wound prior to participation. Scalp lacerations can cause significant blood loss. Immediate management should focus on hemostasis and can often be achieved with direct pressure with sterile gauze pads and compression. If this is not effective, infiltration of lidocaine with epinephrine can be performed, and bleeding vessels can be clamped or ligated. Wounds should be explored for fractures and lacerations of the galea. Typically, anesthesia can be provided with local infiltration or by performing a scalp block. Copious irrigation can be performed with a high-pressure irrigation device. Debridement should be performed conservatively. Caution should be taken to ensure that hair is not buried in the wound. Superficial wounds can be closed using nonabsorbable sutures or staples. Large or gaping wounds can be closed using a two-layer technique, with absorbable sutures used subcutaneously for approximation of the galea. Avulsed tissue from the scalp can usually be reimplanted because of the scalp’s excellent blood supply. Risk of infection and scalp wounds is low but is increased in multilayer closures. Scalp hematomas can occur as a result of direct contact. Patients should be evaluated for underlying skull fracture or intracranial hemorrhage. Localized hematoma can be treated conservatively. Initial management includes cold therapy and compression. Aspiration and incision and drainage are not normally required (Table 43.10).

749 Table 43.10  SORT: key clinical recommendations Clinical recommendation The need for neuroimaging in a head-injured athlete should be determined by using clinical decision rules Concussion is a clinical diagnosis; there are no objective diagnostic criterion for concussion It is common for concussed athletes to remain asymptomatic or minimally symptomatic in the initial 24 hours post injury 90% of athletes with concussion are asymptomatic by day 10 post injury; however, it is still considered normal to have symptoms for up to 28 days Return to collision sports is discouraged after any intracranial hemorrhage Return to non-collision sports can be considered after intracranial hemorrhage if recovery is complete Participation in high-risk sports is not typically recommended for athletes with a seizure disorder Athletes with simple linear skull fractures can return to exercise as soon as symptoms allow

Evidence rating A C C

C

C C C C

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43  Head Injury 55. Collins MW, Grindel SH, Lovell MR, et al. Relationship between concussion and neuropsychological performance in college football players. JAMA. 1999;282:964–70. 56. Kinart CM, Cuppett MM, Berg K.  Prevalence of migraines in NCAA division I male and female basketball players. National Collegiate Athletic Association. Headache. 2002;42:620–9. 57. Bullock M, Chesnut R, Ghajar J, Gordon D, Hartl R, Newell D, et al. Surgical management of depressed cranial fractures. Neurosurgery. 2006;58(Supplement):S2–56–60. 58. Bracker M. 5-minute sports medicine consult. 1st ed. Philadelphia: Wolters Kluwer Health; 2015. 59. Cantu R.  Head injuries in sport. Br J Sports Med. 1996;30(4): 289–96. 60. Cantu R, Mueller F. Brain injury-related fatalities in American football, 1945–1999. Neurosurgery. 2003;52(4):846–53. 61. Miele V, Norwig J, Bailes J.  Sideline and ringside evaluation for brain and spinal injuries. Neurosurg Focus. 2006;21(4):1–11. 62. Sousa Nanji L, Melo T, Canhão P, Fonseca A, Ferro J. Subarachnoid haemorrhage and sports. Cerebrovasc Dis Extra. 2015;5(3): 146–51. 63. Dubosh N, Bellolio M, Rabinstein A, Edlow J. Sensitivity of early brain computed tomography to exclude aneurysmal subarachnoid hemorrhage. Stroke. 2016;47(3):750–5. https://doi.org/10.1161/ STROKEAHA.115.011386.

751 64. Balami J, Buchan A. Complications of intracerebral haemorrhage. Lancet Neurol. 2012;11(1):101–18. 65. Ban V, Botros J, Madden C, Batjer H. Neurosurgical emergencies in sports neurology. Curr Pain Headache Rep. 2016;20(9):55. 66. Evans RW. In: Pedley TA, Eichler AF, editors. Post-traumatic seizures and epilepsy. Waltham: Up To Date; 2017. 67. Haltiner AM, Temkin NR, Dikmen SS. Risk of seizure recurrence after the first late posttraumatic seizure. Arch Phys Med Rehabil. 1997;78(8):835–40. 68. Asikainen I, Kaste M, Sarna S.  Early and late posttraumatic seizures in traumatic brain injury rehabilitation patients: brain injury factors causing late seizures and influence of seizures on long-term outcome. Epilepsia. 1999;40(5):584–9. 69. MacIsaac Z, Berhane H, Cray J, Zuckerbraun N, Losee J, Grunwaldt L.  Nonfatal sport-related craniofacial fractures. Plast Reconstr Surg. 2013;131(6):1339–47. 70. Skull fractures  - Summary  - Best practice  - English [Internet]. Bestpractice.bmj.com. 2017 [cited 28 Mar 2017]. Available from: http://bestpractice.bmj.com/best-practice/monograph/398.html. 71. Shane S, Fuchs S. Skull fractures in infants and predictors of associated intracranial injury. Pediatr Emerg Care. 1997;13(3):198–203. 72. Caviness AC. In: Bachur RG, Wiley II JF, editors. Skull fractures in children: clinical manifestations, diagnosis, and management. Waltham: Up To Date; 2017.

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Facial Trauma Christopher Hogrefe

Key Points

• Up to 42% of facial fractures are secondary to sports injuries (Fig. 44.1) [1]. • There is a high rate of associated injuries with facial fractures. Be certain to assess for concomitant injuries, particularly airway, intracranial, and cervical spine trauma. • The size of the fracture does not always portend the treatment. Readily apparent orbital fractures may not necessitate an operative intervention, while subtle mandibular fractures may require surgical fixation. • Protective equipment (e.g., face shields, mouthguards, etc.) can help reduce the risk of these injuries in addition to safeguarding a healing fracture.

Facial Fractures and Dislocations Introduction Over the years the advent and advancement of protective equipment (e.g., helmets, visors, glasses, etc.) have helped to decrease the incidence of facial fractures [2]. However, increased involvement in sports with higher risk for injury and/or more contact has diminished some of the progress in this regard [3]. In the United States, baseball and softball have been associated with the highest incidence of facial fractures (44.3%). Throwing, catching, and hitting a ball have been correlated with these injuries (34.1%), while collisions are the next most common etiology (24.5%) [4]. On the other hand, in countries like Italy, Chile, and Germany, soccer accounts for the highest frequency of sports-related C. Hogrefe (*) Department of Emergency Medicine, University of Iowa Hospitals and Clinics, Iowa City, IA, USA e-mail: [email protected]

Fig. 44.1  A maxillofacial CT 3-D reconstruction of a mixed martial arts fighter with multiple facial fractures following a knee to the head Table 44.1  Incidence of sports-related facial fractures∗ [9] Facial bone Nasal Orbital Maxillary Mandibular Zygomatic Naso-orbitoethmoid

Incidence (%) 35.9 33.5 12.6 7.2 4.2 1.2

∗

Skull fractures represented 30.5% of overall fractures in this study

facial fractures (up to 59.2%) [5]. Regardless, it appears that adolescents and young adults are at the greatest risk for such fractures [6]. The facial bone anatomy is complex and contains at least 14 bones (not including the frontal bone). The frequency with which these bones fracture varies, but Table  44.1 provides insight into the relative incidence of certain facial bone frac-

© Springer Nature Switzerland AG 2020 M. Khodaee et al. (eds.), Sports-related Fractures, Dislocations and Trauma, https://doi.org/10.1007/978-3-030-36790-9_44

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tures [7]. Some of the pertinent nuances to the bony anatomy are discussed in the sections that follow. In general, it is worth noting that the amount of force needed to fracture a facial bone is quite significant (30 grams of force for the nose and up to 200 grams of force for the superior orbital rim) [3]. The design of the face serves many purposes, including to protect the intracranial contents by functioning as a crumple zone and dispersing forces across the facial bones. Additionally, due to the rich vascularity of the face, edema and ecchymosis often promptly follow these injuries, complicating the physical examination. Consequently, it is important that the sports medicine physician has a high index of suspicion for these fractures and other accompanying injuries.

Orbital Fractures Athletic competition can precipitate direct trauma to the orbital rim and orbital walls, resulting in fractures to any of the associated bones. The orbit itself consists of seven bones: frontal, sphenoid, maxilla, palatine, zygomatic, ethmoid, and lacrimal bones (Fig. 44.2). The medial and inferior orbital walls are the most frequently affected, which often result in “blow-out” fractures. In fact, the posteromedial portion of the orbital floor and the lamina papyracea of the medial wall are the weakest components of the orbit. It is important to note that orbital fractures can result in concomitant ocular injuries as well.

 echanism of Injury in Sports M There are generally thought to be two broad mechanisms by which orbital fractures transpire. A direct blow to the orbital rim can cause one type of fracture, such as when a baseball or tennis ball collides with the orbital rim. Conversely, direct trauma to the eye itself, for instance, by an (in)advertent fist or elbow, can precipitate an orbital “blow-out” fracture. There is another, less common injury pattern referred to as a Fig. 44.2  The bones comprising the orbit

“blow-in” fracture, which can occur if fracture fragments are displaced into the orbital space, often secondary to trauma to the frontal and/or maxillary bones [8].

Epidemiology It is reported that roughly one-third of orbital fractures transpire in sport. The actual number of cases that this represents is not known [9]. “Blow-out” fractures are the most common type of orbital fractures, with only 5% of these injuries occurring bilaterally [10]. Clinical Presentation First and foremost, patients should have normal (or baseline) visual acuity. If this is not the case, it should significantly raise one’s suspicion for ocular injury. Roughly 25% of orbital fractures involve the globe, with “blow-out” fractures carrying an associated ocular injury rate of up to 40% [11]. Especially noteworthy, 5–10% of “blow-out” fractures result in a ruptured globe [12]. One should assess for bony tenderness, swelling, and/or ecchymosis. Enophthalmos (depression of the globe due to orbital fat sinking through an orbital fracture) may be appreciated. Periorbital emphysema can be present, attributed to communication with either the ethmoid or maxillary sinus. Impaired ocular mobility may be seen as well due to entrapment of the extraocular muscles within the fracture fragments. For instance, if the medial rectus is entrapped, there will be a defect with lateral gaze (Fig. 44.3). Athletes may also note decreased sensation in the upper lip region due to an injury to the infraorbital nerve. Diagnosis While the physical examination can certainly provide evidence to suggest an orbital fracture, further confirmation in the form of imaging is warranted. Plain films of the orbits (including Waters view or exaggerated Waters view) should primarily be considered if there is no accessibility to further

Frontal bone Supraorbital notch

Sphenoid

Ethmoid Optic canal

Nasal bone

Superior orbital fissure

Lacrimal bone

Zygomatic bone

Nasolacrimal canal (fossa)

Zygomaticofacial foramen Inferior orbital fissure

Infraorbital groove

Maxilla Infraorbital foramen

Palatine bone

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Fig. 44.3  A patient with a right medial orbital fracture causing medial rectus entrapment and a lateral gaze defect (i.e. decreased abduction of the right eye) (Image from Joseph and Glavas [114])

advanced imaging. A CT scan of the orbits is the preferred imaging modality. Thin-sliced (1.5  mm) helical scans are recommended, although axial and coronal CT scans can suffice [11]. The sensitivity of an orbital CT scan is between 79% and 96% [8]. Ultrasound and MRI are of limited utility, and ultrasound in particular should be avoided if there is suspicion for a concomitant globe rupture.

Initial Management The most important initial management step in the treatment of orbital fractures is to assess for physical examination findings that should prompt an immediate Emergency Department, Ophthalmology, and/or Facial Trauma evaluation (see below under the section “Indications for Referral”). Otherwise, the current recommendations for treatment include the aggressive use of cold packs or ice for the first 48  hours [13]. Sneezing with one’s mouth open, the avoidance of nose blowing, and refraining from coughing or other Valsalva maneuvers should be recommended. Sleeping with the head of the bed elevated has been advocated as well. Provide the athlete with nasal decongestants and pain control. The utilization of prophylactic antibiotics is debated; however, it is generally recommended if there is communication of the fracture with a sinus [14]. Amoxicillin-clavulanate and azithromycin are considered appropriate selections in this context with the duration of treatment lasting 10–14 days. Indications for Referral An immediate evaluation is warranted if there is concern for a ruptured globe, concomitant facial fracture, visual changes, or impaired ocular motion. If these entities have been ruled out on physical examination, athletes can be further evaluated (including the procurement of imaging) 1–2 days after the initial injury. Follow-up Care If a fracture is diagnosed, follow-up with an Ophthalmologist and an Otolaryngologist/Facial Surgeon is warranted within

Fig. 44.4  A protective face mask for use after an orbital fracture

1 week. The timing of such follow-up is designed to allow for the swelling to resolve, which may further improve the athlete’s symptoms. Keep in mind that only approximately 15% of patients will require a surgical intervention [15]. Typical reasons for a surgical intervention include persistent diplopia, impaired ocular movement, and/or significant enophthalmos.

Return to Sports In the setting of an isolated orbital fracture, return to noncontact sports typically occurs in approximately 2 weeks. In contact sports the return is closer to 4–6 weeks [8]. If there is an associated ocular injury or surgery is pursued, the return will be longer and is dependent upon the extent of the ocular injury and/or complexity of the surgical intervention. Regardless, proper eye protection is recommended upon an athlete’s return, generally for up to 8 weeks after the injury [4] (Fig. 44.4). Complications There are several potential complications associated with orbital fractures. The more common complications include sinusitis, permanent extraocular movement restriction, orbital infection, and/or enophthalmos. Depending upon the severity of the injury, athletes can suffer permanent vision loss and/or cosmetic defects, particularly if there is a delay in treatment [16]. Pediatric Considerations While orbital wall fractures can occur in children, they are less common, especially under the ages of 6 or 7. The bones are more malleable, allowing them to bow or bend more prior to fracturing. This can, however, increase the risk for ocular entrapment. Recall that given the lack of pneumatization of the paranasal sinuses in younger athletes, the orbital floor is

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not as weak in children as it is in adults. With that said, orbital roof fractures are slightly more common in this age group and associated neurologic involvement can follow.

Mandibular Fractures Given its prominence on the face and lack of surrounding support, the mandible is a common site of fractures in sports. There is some variability in the literature as to the most common sites of fracture within the mandible. Broadly speaking, the condyle, angle, and the body of the mandible are the most common fracture sites (typically in that order), followed by the molar and mental regions, respectively (Fig. 44.5). It is estimated that 20–40% of patients with mandible fractures will have another injury. Thus, the sideline physician should be ever mindful of the ABCs of patient stabilization and advanced cardiac life support (ACLS) protocols.

 echanism of Injury in Sports M Mandibular fractures in the setting of sports are most commonly found in contact sports (e.g., boxing, wrestling, and football), although sports account for only 4% of all such fractures [17]. They are typically the result of direct trauma to the mandible, which is a ring structure (similar to the pelvis). Thus, contralateral fractures occur with some frequency and should be considered. It is not uncommon for these fractures to be associated with concomitant intracranial and/or cervical spine injuries. Epidemiology Among all of the facial fractures, mandibular fractures are the third most common (trailing only nasal and zygomatic fractures). The incidence of these injuries peaks between the ages of 16 and 20 years old [8]. Sport-specific mandibular fractures do not appear to show a gender predilection,

although in the overall population young males have a higher prevalence of such injuries [2, 18].

Clinical Presentation Athletes with mandible fractures often report pain exacerbated by jaw movement, dysphagia, and/or an abnormal bite in the setting of a traumatic episode. On physical examination, one should be certain to thoroughly inspect the jaw. In addition to a visible step-off and/or facial asymmetry, mandible fractures can be associated with lacerations, particularly under the chin. A valuable clinical test is the tongue blade bite test, which is performed by inserting a tongue depressor into the patient’s mouth between the maxillary and mandibular teeth. The patient should bite down on the depressor, and the physician should then twist the blade. If the tongue depressor can be broken without causing the ­athlete pain, the test is considered negative. This test has been shown to have a sensitivity of 88.5% with a specificity of 95% for identifying mandible fractures (with roughly the same utility in isolated pediatric patients) [19]. Additional valuable physical examination findings commonly associated with mandible fractures are noted in Table 44.2. Diagnosis As opposed to some of its facial fracture counterparts, plain films can be quite useful in diagnosing mandible fractures. An orthopantomogram (or Panorex) is generally the view of choice, facilitating both a diagnosis in addition to surgical planning when necessary (Fig. 44.6). In athletes where there Table 44.2  Clinical findings associated with mandible fractures [3] Loose, fractured, or missing teeth Trismus (mouth opening 21 mmHg) more than 30% of the time in the setting of a hyphema [42]. Diagnosis The physical examination is generally sufficient for making the diagnosis of a hyphema, and this can often be accomplished on the sideline or in the training room. Laboratory testing is generally not required in the absence of a suspected coagulation disorder. However, if the mechanism of injury does not seem significant enough to result in a hyphema, consideration should be given to pursuing further testing. Underlying (and/or undiagnosed) diabetes mellitus, clotting disorders, and/or tumors should be considered in these instances. Imaging (including orbital CT scans and/or an ultrasound) is typically reserved for the investigation of another associated injury. Initial Management Once a hyphema is diagnosed, a rigid shield should be applied to the eye. Ideally, the shield should contain holes to allow for the patient to determine if visual change/loss develops. Athletes should be advised to minimize the movement

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of the eye as much as possible. The avoidance of coughing, sneezing, and/or other straining should be encouraged. The patient’s head should be kept elevated, optimally to approximately 30° to 45°, which will help to keep the blood in the inferior-most portion of the anterior chamber. Avoid the administration of NSAIDs, and do not allow the patient to eat and/or drink anything (in case a surgical intervention is deemed necessary). Athletes should then be referred for immediate Ophthalmologic evaluation (e.g., in an Emergency Department or Ophthalmology Clinic).

Indications for Referral The current recommendations for immediate evaluation include anything greater than a grade I hyphema and/or a patient with increased intraocular pressure. The assessment of intraocular pressure may not always be feasible on the sideline or in the training room. Thus, in the presence of a hyphema with an unknown pressure, immediate evaluation is recommended. Any concern for a concomitant injury (e.g., globe rupture, orbital fracture, retinal detachment, retrobulbar hematoma, etc.) should warrant an immediate evaluation as well. Follow-up Care Grade I hyphemas are generally managed as an outpatient. However, it should be noted that the intraocular pressure is typically more important than the grading in determining whether or not a patient is admitted to the hospital. Roughly 5% of all hyphemas will require a surgical intervention [8]. Ophthalmology should help to guide the follow-up as a component of the athlete’s Emergency Department evaluation. Repeat slit-lamp evaluation for the first 3 days after the diagnosis is the norm with the subsequent duration of treatment contingent on the improvement (or lack thereof) in bleeding and/or intraocular pressure.

Fig. 44.16  Corneal staining due to a hyphema (Image courtesy of EyeRounds.org – University of Iowa)

grade III or grade IV hyphemas) [42]. Lastly, corneal staining can occur as a result of a hyphema. The corneal stroma becomes opacified, affecting vision in larger hyphemas (Fig.  44.16). While this can be permanent, it will often resolve in months to years. However, it clears peripherally first, leaving the impact on vision remaining until toward the end of the healing process. Risk factors for this complication include persistent hyphemas and those associated with intraocular pressures >25 mmHg.

Pediatric Considerations Pediatric patients are at a particularly high risk for rebleeding. Also keep in mind that the accuracy of the physical examination may be decreased in young children, which may alter one’s threshold for evaluation in an Emergency Department and/or Ophthalmology Clinic. It is typically recommended that children younger than 7 years old be admitted, as they are at a higher risk of developing amblyopia [12]. Corneal staining in children increases the risk of amblyopia and can result in permanent vision loss.

Return to Sports A return to sports should not transpire until the athlete is cleared by an Ophthalmologist, typically after the hyphema resolves. For a grade I hyphema, resolution can occur in 4–5 days. However, larger hyphemas may take longer. Ultimately, the athlete must be comfortable with his/her visual acuity. Additionally, adequate eye protection should be worn moving forward in all sports at risk for eye injuries.

Retinal Detachment/Tear

Complications A significant complication of a hyphema is rebleeding, which typically occurs between 2 and 5 days after the initial injury. This can arise in up to 18% of patients [43]. Generally, the higher the grade of hyphema or the greater the initial intraocular pressure, the higher the risk of rebleeding. This secondary hyphema is often more significant than the initial injury. Visual acuity loss also increases as the severity of the hyphema increases (20/50 vision or worse in 50–75% of

The retina is responsible for converting photons into neural impulses that travel to the visual cortex. This structure can be detached or torn, leading to a surgical emergency (Fig. 44.17). While there are three types of retinal detachments, rhegmatogenous retinal detachments (RRD) are the most relevant to the care of athletes as they tend to result from direct trauma to the eye. Tractional retinal detachments (TRD) can occur with penetrating injury. The third type (exudate retinal detachments) are less germane to athletes.

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C. Hogrefe Table 44.6 Key components of the sideline ocular physical examination Visual acuity (monocular and binocular) Anterior chamber evaluation (with a penlight) External exam (including eyelid eversion)

Visual field confrontation Extraocular movement Funduscopic examination (Fig. 44.17)

Fig. 44.17  A retinal tear (purple arrow) and a retinal detachment (gray arrow) via funduscopic evaluation

 echanism of Injury in Sports M Virtually any sport carries with it the risk of experiencing a retinal detachment. Collisions, inherent in the sport or incidental, can result in trauma to the eye and thus a retinal detachment or tear. With that said, it should be noted that an RRD is the most common type of retinal detachment/tear, and the majority of these are spontaneous. Additionally, there has been a reported link to oral fluoroquinolone use [44]. Epidemiology Overall, the incidence of retinal detachments/tears increases with age. There is also a slight predilection for males over females (approximately 3:2). However, it is unclear whether these epidemiologic characteristics apply to sports-related retinal injuries in the same manner as they do the general population. Athletes with Marfan syndrome are at an increased risk for an RRD, while sickle cell retinopathy can lead to a TRD. Clinical Presentation While some athletes may have a traumatic mechanism of injury, retinal detachments and tears can occur spontaneously as well. The most common symptom reported by patients is the presence of flashers (a response to traction) or floaters (condensation in the vitreous gel that produces shadows) [45]. Visual defects may be present, and remember that a superior visual field injury results in an inferior visual field defect. The evaluating team physician can use this information to better guide the funduscopic examination. Athletes may also report the sudden, complete loss of vision. A thorough eye examination is essential, the components of which are noted in Table 44.6.

Fig. 44.18 An ocular ultrasound of a retinal detachment (purple arrow); note the lens at the top of the image

Diagnosis The diagnosis of a retinal detachment and/or tear is most commonly made on physical examination. A dilated exam in the hands of an Ophthalmologist is the best manner by which to confirm the diagnosis. While further advanced imaging (e.g., an orbital CT scan) is not a component of the evaluation (barring a suspected associated injury), ultrasound can be useful in making the diagnosis (Fig. 44.18). Studies suggest that emergency physicians can detect retinal detachments using bedside ultrasound with 97% sensitivity and 92% specificity [46]. Initial Management No immediate sideline management of retinal detachment or tears is necessary. They require prompt evaluation by an Ophthalmologist. Indications for Referral Any time a team physician suspects or diagnoses a retinal detachment or tear, a prompt Ophthalmology evaluation should be pursued. Of note, involvement of macula-sparing

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tears or detachments is fixed immediately. However, not all detachments or tears will necessitate such a prompt surgical intervention. The nuances of that decision are likely beyond the scope of the team physician.

Follow-up Care Rhegmatogenous retinal detachments (RRDs) typically involve the macula and are generally repaired within 3–7 days. The traction retinal detachments (TRDs) are often corrected 1–2 weeks after the injury. Meanwhile, the final category, or exudative retinal detachments (ERDs), tend to resolve on their own. Team physicians need not to be able to detect the specifics of each retinal detachment subcategory on physical examination, but it is important to consider the timeline of the associated injury moving forward. Return to Sports As with several other ocular injuries, the return to sport following a retinal detachment is variable. The athlete must be comfortable with his/her visual acuity and receive clearance from the treating Ophthalmologist. Eye protection in the future should be strongly encouraged, if not required. Complications The most noteworthy complication of a retinal detachment or tear is long-term, permanent vision loss. There are potential complications following a repair as well, including vitreous hemorrhage and/or cataracts, although they are of lesser immediate concern in the setting of this injury.

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soccer athletes [47]. These injuries are due to the traumatic (or chemical in some instances) removal of the superficial epithelial layer overlying the cornea. Corneal ulcers occur when the injuries are more severe and deeper or when infection sets in, leading to penetration of the thicker Bowman’s layer (Fig.  44.19). Since the cornea has one of the highest densities of nerve endings in the body, these injuries are often quite painful [48].

 echanism of Injury in Sports M Collision sports and those that involve projectiles (e.g., balls) present the greatest risk for corneal abrasions or ulcers. A mechanism as seemingly innocuous as a poke to the eye can result in this painful injury. Commonly offending sports include wrestling, martial arts, boxing, basketball, and soccer. Epidemiology There is a relative lack of data on the incidence of corneal abrasions and/or ulcers secondary to sport. However, it has been reported that it is the second most common type of eye injury broadly in this context (after soft tissue injuries) [8]. Athletes who wear contact lenses are at a higher risk, particularly if they wear soft lenses. Additionally, it should be noted that protective eyewear markedly reduces the risk of such injuries.

Clinical Presentation Prominent features of a corneal abrasion include pain immediately after the insult, a foreign body sensation, photophobia, and/or tearing. Athletes who typically wear contact lenses may report that the associated pain is improved when wearing the lenses, as this may serve as a bandage (although Corneal Abrasion/Ulcer it should not be used as such in treatment). The physical examination of the eye should include the maneuvers highCorneal abrasions are among the most common sports-­ lighted in Table  44.6. Of particular importance, the team related ocular injuries, which can progress to corneal ulcers physician should be sure to thoroughly inspect both the if they do not heal or are improperly treated. For instance, upper and lower eyelids, including eyelid eversion. Retained 10% of ocular injuries in the National Basketball Association foreign bodies can become trapped, particularly in the upper (NBA) are due to corneal abrasions, while they account for eyelid. Failure to appreciate this finding will result in greater than 20% of ball-related ocular injuries in amateur repeated and likely persistent corneal epithelial defects, Fig. 44.19  A corneal abrasion (purple arrow) without fluorescein staining is noted on the left; a deeper corneal ulcer (gray arrow) is illustrated on the right, highlighted by its white, scaly appearance (Images courtesy of EyeRounds.org – University of Iowa)

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Fig. 44.20  Technique for everting the upper eyelid in search of foreign bodies, in this case revealing a small pustule (purple arrow)

Fig. 44.21  A corneal abrasion visualized with fluorescein staining (left) and with such staining under a cobalt blue light or Woods lamp (middle; both images courtesy of EyeRounds.org – University of Iowa);

the “ice rink sign” (right) can occur when repeated, linear abrasions result from a foreign body retained under the eyelid. The fluorescein-­ uptake lines can mimic the lines on a hockey rink

which may lead to a corneal ulcer. One can assess the undersurface of the upper eyelid by utilizing a cotton-tipped applicator (Fig.  44.20). Ask the athlete to look downward and then grasp the patient’s eyelashes and upper lid in one hand, applying gentle traction down and out away from the patient. Next, insert the cotton-tipped applicator just superior to the globe at the tarsal plate. By moving the eyelashes and upper eyelid margin toward the superior orbital rim, the team physician can successfully evert the eyelid and assess for the presence of foreign bodies. Eversion of the lower eyelid can be achieved with simple, gentle downward traction. In the absence of concern for a ruptured globe, the intraocular pressure should be noted. Lastly, a fluorescein examination should be completed. Strips of fluorescein (or fluorescein-containing anesthetic drops) should be included in a team physician’s ophthalmologic toolkit and utilized in conjunction with a blacklight flashlight (at minimal cost) or the cobalt filter on an ophthalmoscope. Fluorescein demarcates the borders of a corneal abrasion and/or identifies other ongoing disease processes (e.g., herpes keratitis). In the setting of a retained foreign body under the eyelid, one might

appreciate fluorescein uptake in linear lines, referred to as the “ice rink sign” (Fig. 44.21).

Diagnosis The diagnosis of a corneal abrasion and/or ulcer is clinical. Further advanced imaging (e.g., an orbital CT scan or an ultrasound) should be entertained if there is concern for an associated orbital fracture, a retained foreign body, and/or other associated injury. Initial Management Uncomplicated, small corneal abrasions secondary to trauma can be managed safely by a team physician without immediate Ophthalmologic consultation. Treatment entails prophylactic topical antibiotics, with ointment theoretically superior to drops given its stronger lubricating properties [49]. Erythromycin ointment is a sound choice, typically prescribed four times per day for 1 day longer than the patient’s symptoms persist (roughly 3–5 days) [49]. For patients who insist upon drops, sulfacetamide, polymyxin/trimethoprim, ciprofloxacin, and ofloxacin are reasonable. In the case of

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contact lens wears, the antibiotic selected should cover for Pseudomonas such as ciprofloxacin, ofloxacin, and gentamicin. In addition, athletes should be instructed not to wear contact lenses during the course of treatment. Otherwise, avoid preparations containing steroids given the risk of delayed healing. Pain control for these athletes is an important component of management. Oral NSAIDs are a reasonable option, and topical ophthalmic NSAIDs (e.g., ketorolac or diclofenac) are acceptable as well. Topical preparations do not appear to adversely impact healing, although they may be painful to apply and/or expensive [50]. There is also evidence that in the setting of small corneal abrasions, topical tetracaine can be utilized for up to 24 hours without adverse outcomes [51]. Patching may help to alleviate pain, but this is primarily reserved for large abrasions and in conjunction with an Ophthalmology consultation [35]. Lastly, eye protective strategies for the athlete with a corneal abrasion are recommended. Participating in eye rest (e.g., avoiding activities that can result straining of the eye such as computer use), wearing sunglasses, and avoiding rubbing or direct contact with the eye will help to ensure healing in a timely fashion.

Indications for Referral The presence of concomitant injuries (e.g., hyphema, orbital fracture, ruptured globe, etc.) necessitates an immediate referral to an Ophthalmologist (or an Emergency Department with the ability to consult with such a specialist). Additional indications to seek prompt further evaluation and treatment are provided in Table 44.7. Recurrent corneal abrasions warrant an outpatient referral as well to identify any potential underlying etiologies (e.g., recurrent erosion syndrome). Follow-up Care Corneal abrasions generally heal quickly, with smaller injuries resolving in 24–48 hours. These abrasions do not require follow-up unless the associated symptoms persist for more than 3–4 days. It is wise for the team physician to follow-up with the athlete in this window to ensure complete resolution of symptoms. Athletes with large abrasions (>50% of the corneal surface area) or those that wear contact lenses should be reassessed daily until their symptoms have resolved and reepithelialization has occurred, typically within 1 week. Table 44.7  Indications for immediate ophthalmologic referral in corneal abrasions Large epithelial defects Herpes keratitis (dendritic fluorescein stain pattern) Presence of a rust ring

Corneal ulcers Intraocular foreign body concern Concomitant ocular infection

Return to Sports The athlete can return to sport as soon as his/her visual acuity returns to baseline and the associated pain is controlled. This will commonly take at least 1–2 days for smaller abrasions and up to a week for more substantial injuries. Athletes should not utilize a topical anesthetic in an attempt to expedite a return to sport. Complications A concerning complication associated with corneal abrasions is the development of a corneal ulcer. Often the result of a subsequent viral or bacterial infection, corneal ulcers penetrate deeper through the layers of the cornea. Scar formation can subsequently occur, and permanent vision loss may also result. There is a phenomenon known as recurrent erosion as well, which may not be related to another ­traumatic insult. This entity may require debridement of the corneal tissue. Pediatric Considerations When selecting a type of antibiotic for the prophylactic treatment of corneal abrasions, remember that the drops are more irritating than the ointment. The latter is generally better tolerated in the pediatric population. In children, if there is persistent drainage or an unwillingness to keep the eye open 24 hours after the injury, an Ophthalmology consult should be pursued.

Ear Trauma

Key Points

• Delays in identifying or adequately evacuating an auricular hematoma can result in permanent disfigurement (Fig. 44.22). • There are several methods for properly and sufficiently draining an auricular hematoma; a sideline physician should be comfortable with at least one such method. • Tympanic membrane injuries may result in significant pain and temporary hearing loss. • A tympanic membrane rupture should raise one’s suspicion for a temporal bone fracture as well.

Introduction The ear is an extremely complex structure that can be divided into the external, middle, and inner ear. The pinna and external auditory canal comprise the external ear, whereas the middle ear serves as the home of the tympanic membrane, malleus, incus, and stapes. This middle ear machinery subse-

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Fig. 44.22 Wrestling, particularly without the use of headgear, can result in significant and potentially permanent ear trauma

quently propagates vibrations to the inner ear to produce sound. The inner ear itself is composed of the cochlea and labyrinth. A disruption of any of these components can detrimentally impact one’s hearing. This section will focus on noteworthy sports injuries involving the external and middle ear, as a timely diagnosis of these conditions will help to reduce the risk of potential permanent cosmetic deformities and/or hearing loss.

Auricular Hematomas An auricular hematoma is a collection of blood in the subperichondrial space of the external ear (Fig.  44.23). These almost exclusively occur on the anterior surface of the pinna [52]. If untreated, this can result in pressure necrosis within the cartilage of the ear as the accumulating blood prevents nutrient delivery to the cartilage. When combined with neocartilage formation and fibrosis, permanent disfigurement can occur. It is critical that these injuries be identified promptly and treated adequately via drainage and occasionally incision.

 echanism of Injury in Sports M Auricular hematomas are typically the result of direct, blunt trauma and/or friction/shearing to the ear. This causes bleeding between the perichondrium and elastic cartilage of the ear. Contact sports are typically implicated

Epidermis Dermis Perichondrium Cartilage Subcutaneous tissue

Fig. 44.23  The layers of the external ear presented in cross section

in this injury, including wrestling, mixed martial arts, judo, boxing, and rugby.

Epidemiology Overall, the exact prevalence is unknown given a lack of historical recording. However, these injuries are much more prev-

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alent in young males due to their increased participation in the aforementioned sports, particularly wrestling. Regardless, they do affect both genders. In one study, collegiate wrestlers who wore headgear (26%) were less likely to suffer an auricular hematoma compared to those that did not (52%). Overall, wearing properly fitting headgear consistently can decrease the incidence of this condition by 50% [53]. Improperly fitted headgear, however, may not prevent this injury.

Diagnosis A careful physical examination is generally all that is needed to facilitate the prompt diagnosis of an auricular hematoma. Ultrasound can be helpful in differentiating an acute on chronic hematoma from a chronic cartilage deformity. No further laboratory testing and/or imaging will prove beneficial in the diagnosis of this condition for the majority of athletes.

Clinical Presentation The diagnosis of an auricular hematoma is made based on clinical history and physical examination. Often, a history of direct trauma to the auricle is noted, but this is not always the case. Athletes will frequently note a painful ear, and hearing loss may also be reported. The lack of headgear use should raise one’s suspicion for such a condition. Additionally, athletes with chronic cartilage deformities, often referred to as “cauliflower ear”, can still develop an acute auricular hematoma. The sideline provider should be able to discern the difference and be prepared to intervene on the fluctuant, tender, ecchymotic acute injury while avoiding aspirating or incising the chronic malady (Fig. 44.24). If there is any question about the acuteness of the injury, assessing the contralateral ear for contour and/or tactile differences may be beneficial. The athlete’s external auditory canal and tympanic membrane should be thoroughly evaluated as well.

Initial Management Management of an auricular hematoma should be within the skillset of a team physician. Care should be taken to perform this procedure in as sterile a fashion as possible to avoid complications such as chondritis, perichondritis, and/or an abscess formation. Betadine and/or chlorhexidine should be utilized to help prevent these conditions. The administration of anesthesia constitutes the next step, and it can be achieved through either a local injection or a ring block, either option employing lidocaine or bupivacaine. The ring block provides anesthesia to the entire ear and may facilitate a procedure that is better tolerated for the patient. As shown in Fig. 44.25, anesthetic is injected both superior to the attachment of the helix to the scalp both anteriorly and posteriorly (addressing the auriculotemporal nerve) and inferior to the ear anteriorly and posteriorly (anesthetizing the greater auricular nerve). Remember that the facial nerve courses

Fig. 44.24  The more fluctuant, tender, acute auricular hematoma (left; image courtesy of Otolaryngology Houston; www.ghorayeb.com) versus the firm, non-tender “cauliflower ear” (right; image courtesy of Skidmore K, Hatcher JD. Cauliflower ear. StatPearls. 2018 Dec 9)

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Fig. 44.26  The incisional landmarks for an auricular hematoma drainage; note the superior incision along the curve of the anterior pinna with a potential incision site along the conchal bowl inferiorly (if necessary)

Fig. 44.25  The approach for a ring block of the ear; note that the injection should be administered behind the auricle

through this territory (anterior and inferior to the tragus); accordingly, paresis of this nerve may occur. The inclusion of epinephrine with the anesthetic for certain anatomic sites (including the ear) continues to be a somewhat contentious topic. It has been argued in the literature that no cases of vasoconstrictor-induced tissue necrosis have been reported since commercial lidocaine with epinephrine was introduced in 1948 [54]. As such, it is most likely safe to use lidocaine with epinephrine in this context, particularly if implementing a ring block.

The technical manner in which the remainder of the procedure is approached depends on both the size of the auricular hematoma and the timing of presentation. If the hematoma is 2 cm) or those that present after more than 2 days, an incisional approach is recommended. With an 11-blade scalpel, a superficial, curvilinear incision should be made along the natural curve of the anterior pinna. This may require two incisions, with the other in the conchal bowl [52] (Fig.  44.26). The hematoma can then be evacuated with gentle pressure, and thorough irrigation should then follow. Finally, pressure dressings should be applied. The second component of the successful treatment of an auricular hematoma involves an adequate pressure dressing. For hematomas treated via needle aspiration, one should place gauze around the ear, which can be achieved by cutting out the center of the gauze and draping it around the ear.

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Pseudomonas. This is also the preferred prophylactic antibiotic in this setting for athletes under the age of 18.

Indications for Referral This is a condition that is within the scope of a sideline physician. However, auricular hematomas greater than 1  week old may contain granulation tissue and warrant a Plastic Surgery or Otolaryngology referral [57]. Also, if concern for a post-decompression cosmetic deformity or other complication exists, a referral is indicated to improve the cosmetic outcome. Follow-up Care These patients should be re-evaluated daily for the first 3–5 days to assess for evidence of reaccumulation of the hematoma, pressure necrosis, and/or infection. If sutures were placed as a component of the compressive dressing, they should be removed within approximately 7 days.

Fig. 44.27  A pressure dressing applied after an auricular hematoma needle aspiration (Image courtesy of Michelle Lin, MD; aliem.com)

Petroleum gauze, saline-soaked cotton balls, or plaster surrounded in padding should then be molded to the inner contours of the auricle (Fig. 44.27). Sterile gauze is then placed over the entire ear, and a head dressing (often with Kerlix gauze) is applied over the top of the ear and around the head to keep the entire dressing in place. The post-procedural dressing for auricular hematomas requiring an incision is a bit more complex. It is appropriate to use absorbable or non-absorbable sutures to reapproximate the incision edges, leaving a small, dependent area open to drain. However, it is often more advantageous to apply bolsters. Petroleum gauze or dental rolls on either side of the ear are sutured into place via through-and-through non-absorbable suture (e.g., 3-0 or 4-0 nylon). Care should be taken to ensure that the sutures are tight enough to prevent reaccumulation but not too tight to cause tissue necrosis. The sutures are typically left in place for 5–7 days. If a conchal bowl incision is also made, the area can be packed with petroleum gauze. Antibiotic prophylaxis is advised following this procedure, although the supporting evidence for this practice is not robust. Historically, coverage of Pseudomonas has been recommended for 7–10 days. The first-line treatment in those older than 18 has been a fluoroquinolone. However, given the increased risk of tendon damage with this class of antibiotics, fluoroquinolones may be suboptimal in athletes. Amoxicillin-clavulanate is a reasonable choice to cover against skin flora infection despite its lack of efficacy against

Return to Sports There is some debate as to the proper return to sport for athletes following the treatment of an auricular hematoma. Some have argued for no activity that places the ear at risk for additional trauma until it is healed, which can occur as soon as 7 days [56, 58]. Others contend that athletes should be allowed to participate in full activity with a compressive dressing and proper ear protection [59]. The ultimate decision should be made in consultation with the athlete (and parents when appropriate) after discussing the potential complications of returning to sport before complete healing has transpired. Regardless of the timing of the return to sport, athletes should be strongly encouraged to wear protective headgear moving forward. Complications As previously referenced, permanent cosmetic deformity can occur with these injuries. This condition, often referred to as “cauliflower ear”, can develop as new cartilage is formed that is associated with scarring and tissue necrosis. Risks for this complication include failure to promptly recognize and treat an auricular hematoma, insufficient drainage, repeated need for aspiration, and a premature or early return to sport [60]. Additional potential complications include an infection of the auricular cartilage, referred to as chondritis or perichondritis. Subsequent abscesses can also develop in the aftermath of an auricular hematoma.

Tympanic Membrane Ruptures The sudden onset of ear pain in conjunction with decreased hearing in an athlete can be disconcerting to both the ath-

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Fig. 44.28  A direct blow to the ear can result in a tympanic membrane rupture

lete and the sideline physician. A rupture of the tympanic membrane can account for this precise scenario and can be skillfully treated in most cases by a sideline physician. The tympanic membrane is responsible for conductive hearing, amplifying sound by a factor of 17; thus, damage to it may be readily apparent clinically [61]. While the majority of these injuries heal well without complication, a sideline physician should always consider other significant concomitant injuries, particularly a temporal bone fracture.

Table 44.8  The signs/symptoms of tympanic membrane rupture Mild pain Purulent/bloody drainage Vertigo Nausea

Partial hearing loss Tinnitus Otorrhea Vomiting

 echanism of Injury in Sports M Tympanic membrane ruptures can occur secondary to a variety of mechanisms. Barotrauma is one such mechanism of injury, which can result from scuba diving or mountain climbing. Trauma to the side of the head, such as in boxing (Fig.  44.28), can rupture the tympanic membrane as well. While a less frequent occurrence in sports, direct trauma to the membrane could lead to its compromise. An underlying otitis media should be considered as a contributing component in the setting of an athlete’s tympanic membrane rupture as well. Epidemiology There is no epidemiological data regarding the incidence or prevalence of tympanic membrane ruptures in athletes specifically. In fact, it has not been well studied in the general population either, although estimates of traumatic tympanic membrane perforations suggest a rate of 6.8 cases per 1000 individuals [62]. Clinical Presentation There are a constellation of signs and symptoms that should raise a team physician’s suspicion for a tympanic membrane perforation (Table  44.8). Recall that infection remains a leading cause of tympanic membrane rupture, and thus assessing for infectious symptoms is advised. If the patient

Fig. 44.29  A central tympanic membrane perforation (Image courtesy of Sean Flanagan, MBBS, FRACS)

notes significant pain and/or complete hearing loss, the pursuit of additional, more significant injuries should be initiated. A complete otic physical examination is essential to make this diagnosis. Direct visualization of the tympanic membrane with an otoscope will often reveal the perforation (Fig. 44.29). One can also use insufflation if there is doubt. The tympanic membrane should not move if ruptured or perforated. Also, if one holds pressure on the tragus, nystagmus or vertigo may ensue [8]. Called the fistula sign, this occurs due to the transmission of pressure through the middle ear into the labyrinthine fistula. The team physician should also

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be sure to check the hearing in both ears. On a related note, Weber testing may also be of some utility. By placing a tuning fork on the frontal bone, hearing should be louder in the injured ear (suggesting a conductive hearing impairment). Conversely, if the hearing is louder in the unaffected ear, there may be an otic nerve injury. Lastly, one should palpate the bones surrounding the ear, particularly the temporal bone, to assess for tenderness suggestive of a concomitant injury.

Diagnosis Properly diagnosing a ruptured tympanic membrane generally only requires a thorough physical examination. If there is concern for a temporal bone fracture, a temporal bone CT scan should be secured. Initial Management Isolated, uncomplicated tympanic membrane ruptures can be treated effectively in the training room and/or office. The vast majority of these injuries heal without complication or further intervention, with 68% resolved within 1 month and 94% healed at the 3-month mark [8]. Athletes should be counseled to keep the auditory canal dry to minimize the risk of infection. Otic antibiotic drops are recommended, with ofloxacin being a reasonable choice. Otic preparations of fluoroquinolones carry a substantially lower risk to tendons than systemic therapies [63]. An appropriate treatment regimen consists of four to five drops in the affected ear twice daily for 1–2  weeks. However, the evidence supporting the use of prophylactic antibiotics for tympanic membrane perforations is limited. One study did suggest that ofloxacin drops shortened the closure time and improved the closure rate of such injuries but did not affect hearing improvement or the rate of middle ear infections [64]. Indications for Referral While most tympanic membrane ruptures can be handled without referral, it is important to recognize which signs and/ or symptoms warrant an immediate evaluation by a specialist. Patients with marked or complete hearing loss and/or facial/otic nerve involvement should be seen by an Otolaryngologist promptly. Concern for a basilar skull fracture (e.g., ecchymosis over the mastoid (i.e., Battle’s sign), raccoon eyes, cerebrospinal fluid rhinorrhea) warrants an evaluation by both an Otolaryngologist and a Neurosurgeon. Additionally, patients with significant vertigo should be evaluated by an Otolaryngologist. Follow-up Care Athletes should follow up with an Otolaryngologist approximately 2 weeks after the initial injury to ensure that the tympanic membrane is healing and no other sequelae have developed.

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Return to Sports Barring a concomitant injury (e.g., a temporal bone fracture or otic nerve injury), athletes can return to sport once their pain is adequately controlled. In water-based sports, care should be taken to protect the injury as it heals (e.g. ear plugs). If there is question regarding a return to sport, one should seek an Otolaryngology evaluation to help guide this decision. Complications Tympanic membrane ruptures can result in persistent defects, which may need to be patched (e.g., paper patch, fat plug, or surgical tympanoplasty). Otherwise, as the membrane heals patients may develop a cholesteatoma, which is why the involvement of an Otolaryngologist in follow-up is advisable. Pediatric Considerations Since otitis media is more common in younger age groups, a team physician should give additional consideration to this condition as a contributing factor in the pediatric athlete. If suspicion for otitis media is present, oral antibiotics may also be appropriate.

Nasal Trauma Key Points

• Nasal trauma can result in significant injuries or compromise to the airway of an athlete; a sideline physician must be prepared to maintain a patient’s airway first and foremost (Fig. 44.30). • Proper treatment of a nasal fracture may also necessitate the management of epistaxis and/or a septal hematoma. • The majority of epistaxis originates anteriorly from Kiesselbach’s plexus; targeting interventions at this region often yields the highest rate of success.

Fig. 44.30  Nasal trauma is a common occurrence in sport

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Introduction Anatomically, the nose is comprised of the nasal process of the frontal bone along with the frontal process of the maxilla, ethmoid, vomer, palatine, and nasal bones (Fig. 44.31). The blood supply within the nose is worth noting based on the location of the vessels. The anterior and posterior ethmoidal arteries, a terminal branch of the sphenopalatine artery, a portion of the greater palatine artery, and the septal branch of the superior labial artery converge to form Kiesselbach’s plexus along the anteroinferior septum. Meanwhile, the posterior aspect of the nasal septum is primarily supplied by the sphenopalatine artery. Finally, the nose also consists of several cartilaginous components, including the nasal septum and the lateral cartilage (the lower end of which supports the tip of the nose).

Nasal Fractures As the most prominent facial structure, the nose is the most commonly fractured structure in the adult face and the third most fractured bone overall [65]. The majority of these fractures occur in the lower half of the nasal region since these bones are thinner and broader. Given the frequency of these fractures, athletes may have sustained previous fractures, making it more difficult to discern if a new fracture is present and/or the extent of a new fracture.

 echanism of Injury in Sports M Participation in virtually any sport carries with it a risk of a nasal fracture. Studies have suggested that the incidence of such injuries is actually higher in limited contact team sports (e.g., baseball and softball). One report revealed that only 13.2% of nasal fractures occurred in football. There is also a higher rate of such fractures in organized competition as opposed to recreational play [66].

Ethmoid

Epidemiology Young males are the most likely to suffer nasal fractures, with the peak incidence occurring in the 20s to 30s. While these fractures are rare in children younger than 5 years old, they do increase with age. This has been attributed to increasing participation in competitive and high-speed sports [67]. One study noted that while patients 17  years of age or younger accounted for 42% of all nasal fractures, this same age demographic accounted for 61% of sports-related nasal fractures [68]. Fracture Classification Strictly speaking, there is no specific nasal fracture classification system. However, it is worth noting the type of fracture patterns associated with the velocity and direction of injury. Low-velocity injuries (e.g., an elbow to the nose) generally result in a simple fracture pattern. However, injuries at high velocities, such as from a hockey puck, are more likely to result in complex or comminuted fracture patterns and other concomitant injuries (e.g., intracranial and/or cervical spine pathology). Blows to the lateral aspect of the nose tend to be the most common, and they can result in displaced fractures. Trauma to the anterior nose may lead to nasal obstruction. Lastly, an injury originating along the inferior nose may cause septal cartilage and/or nasal tip damage. Clinical Presentation The best time to evaluate a nasal fracture is within the first few hours of the injury prior to the onset of edema. Regardless, after such an injury athletes may report some degree of nasal airway obstruction. Visual deformities are almost always apparent (Fig. 44.32). This may include periorbital swelling and/or ecchymosis. Patients may have associated epistaxis and/or a septal hematoma. These conditions should be addressed first and are discussed later in this chapter.

Nasal bone

Septal cartilage

Vomer

Greater alar cartilage Palatine Maxilla

Fig. 44.31  The bony anatomy of the nose (Image courtesy of Oliver Jones; The TeachMeSeries)

Fig. 44.32  A nasal bone fracture in a rugby player

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There are several noteworthy physical examination pearls for the sideline physician to consider. Be sure to evaluate both nasal passages, paying particularly close attention for bulging septal hematomas and/or septal dislocations. A lighted nasal speculum can be very useful for this evaluation. Palpation of all of the nasal bones for deformity and/or crepitance is a must. The team physician should also be certain to palpate the remainder of the face, including the dentition, to assess for concomitant injuries. Finally, in the presence of clear drainage from the nose, one should ensure that this is not cerebrospinal fluid. The athlete may report a postnasal drip or the taste of something sweet in the mouth. A ring or halo test can prove useful in this regard by taking a sample of the fluid and placing it on filter paper or even a pillow case. If the fluid separates leaving blood at the center and clear fluid surrounding it in a halo pattern, one should be concerned for a cerebrospinal fluid leak (Fig. 44.33).

Diagnosis Routine imaging, including plain radiography, is usually not necessary to make the diagnosis of a nasal bone fracture (Fig.  44.34). This has been investigated in the Emergency Department, where such imaging did not significantly impact either the diagnosis or management of nasal trauma [69]. If imaging is pursued, ultrasound is a reasonable option as well, having been shown to have an accuracy rate of 100% (compared to 92% for CT) [70]. CT scans should still be considered if there is concern for complex nasal fractures and/or other associated facial fractures.

Fig. 44.33  Halo sign concerning for a cerebrospinal fluid leak due to a cribriform plate fracture (Image courtesy of Vishwas Kulkarni)

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Initial Management In the setting of an acute nasal fracture, the sideline physician must first address a septal hematoma and/or epistaxis, if present. The management of those entities is discussed in other sections of this chapter. Attention can then be turned to the fracture(s). The goal of the intervention is to establish an acceptable appearance to the premorbid location, to achieve bilateral nasal airway patency, and to prevent intranasal stenosis or septal perforation [71]. This can be done immediately on the sideline or in the training room if significant edema has not developed. However, it is acceptable to attempt a reduction 3–5 days after the injury once the athlete’s edema has improved or resolved. Prior to embarking upon a closed reduction, it is wise to advise the athlete that the procedure can be aborted at any time in lieu of a re-examination in several days [67]. Patients should also be apprised of the potential outcomes of the reduction. One study reports that even after an immediate closed reduction, the incidence of nasal deformities requiring subsequent surgical intervention ranges from 14% to 50% [72]. This study is juxtaposed by a report that 91% of patients were satisfied with their closed nasal fracture reduction at 3 months, 87% at 3 years, and only 3% proceeded to

Fig. 44.34  Plain radiography illustrating a nasal fracture in a collegiate wrestler (Image courtesy of Morteza Khodaee, MD, MPH)

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a surgical intervention. Overall, long-term patient satisfaction with this procedure is thought to be between 70% and 90% [67]. Thus, while there is still a risk of a future surgical intervention, a closed reduction is an appropriate procedure to perform. If pursued, closed reduction of a nasal fracture should be preceded with the application of anesthetic. There are various methods for providing this pain relief, including topical cocaine (unlikely to be available on the sideline for most providers), 1% lidocaine with epinephrine, a hematoma block with 1% lidocaine with epinephrine, and/or bilateral infraorbital nerve blocks. Once adequate anesthesia has been achieved, the provider should place the palmar surface of his or her thumb against the lateralized segment of the nasal bone with the remaining fingers extending past the zygomatic process. Broad and gentle pressure is then applied to the bony step-off until movement of the nasal bone is achieved into the desired position (Fig.  44.35). While an audible or palpable click may be appreciated, this is not always the case. It should be noted that this approach may fail if the fragment segments overlap or the necessary reduction requires lateralization of a fracture fragment [67]. Regardless of whether a reduction was attempted, successful, or unsuccessful, patients should be advised to keep the head and nose elevated as much as possible to reduce edema in the nasal region. Regular icing may also help in this regard. Nasal decongestants should also be recommended. Prophylactic antibiotics are also advised, with amoxicillin-­ clavulanate appropriate for a duration of 7 days. However, this recommendation is based more on expert opinion rather than quality studies assessing their efficacy or benefit in this context.

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Indications for Referral There are several indications for immediate referral in athletes who have sustained nasal fractures. First, if there is a delay in presentation greater than 2 weeks, fibrous connective tissue may have developed, making a closed reduction very difficult [73]. Any evidence of concomitant facial fractures warrants a referral as well, particularly those involving the orbit. If the team physician encounters a septal hematoma that cannot be treated in the training room, an inability to achieve hemostasis, and/or an athlete with difficulty breathing, prompt evaluation in an Emergency Department should be sought. Additionally, if there is concern for a cerebrospinal fluid leak, an immediate referral to an Otolaryngologist and/ or an Emergency Department is indicated. Follow-up Care Athletes with nasal fractures should be evaluated by an Otolaryngologist between 3 and 7 days of the initial injury. Sufficient time should have elapsed to allow for a significant amount of edema resolution. The Otolaryngologist will be able to assess the efficacy of the initial closed reduction attempt (if performed), entertain a closed reduction attempt at that time, or discuss the possibility of an open reduction if deemed necessary. Return to Sports Athletes with uncomplicated fractures may be able to return to sport approximately 2 weeks following the injury if they are engaged in noncontact sports. Typically, these fractures heal within 3 weeks in adults, at which time a full return to sport can be considered [74]. If a surgical intervention is required, a decision on a timeline for a return should be made in conjunction with the treating Otolaryngologist. Regardless, it should be strongly encouraged that the athlete utilizes adequate facial protection for several weeks upon resuming participation (Fig. 44.4). Complications Persistent cosmetic deformities can result from nasal fractures, which can be mitigated with proper follow-up. One such deformity is referred to as saddle nose, which is typically due to a loss of nasal height when the nasal bridge collapses. Other potential complications include septal deviation, compromised nasal passage patency, and the subsequent development of a septal hematoma. Another particularly important potential complication is meningitis. If an athlete has an associated fracture of the cribriform plate, he or she is at risk for such an infection. Thus, it is imperative that the sideline physician carefully evaluate for evidence of a cerebrospinal fluid leak.

Fig. 44.35  Technique for a closed reduction of a nasal bone fracture

Pediatric Considerations In general, the pediatric nose is more malleable and less prone to comminution given its high cartilaginous content. With that

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said, edema can develop very quickly in children. This confluence of factors can make the diagnosis of nasal fractures more difficult in this demographic. Regardless, the indications for a closed reduction of a nasal fracture in children are essentially no different than those in the adult population [75].

Septal Hematoma A septal hematoma is a collection of blood in the space between the septal cartilage and the perichondrium (Fig.  44.36). The net result is a separation of the cartilage from its source of nutrients (i.e., the perichondrium). These injuries typically occur with a blow to the cartilaginous inferior portion of the nose. They can occur both unilaterally and bilaterally. If the condition is not identified and treated, avascular necrosis can occur in as little as 3 days [76].

 echanism of Injury in Sports M Septal hematomas typically result from a direct blow to the nose (e.g., facial contact with the mat in wrestling, being struck in the face by a ground ball in softball, a field hockey stick to the face). Epidemiology The overall incidence of septal hematomas is rare, although the exact incidence is unknown. Given the potential devastating consequences of missing this condition, it should be considered in all athletes who sustain nasal trauma. Clinical Presentation Aside from noting recent direct trauma to the nose, athletes with a septal hematoma may report significant pain (poten-

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tially also due to a concomitant fracture), difficulty breathing through the nose, and swelling. Epistaxis may be experienced by some athletes as well. On physical examination, an external nasal deformity may or may not be present. Once it is clear that the patient’s airway is protected, be certain to palpate the nasal and facial bones to assess for fractures. Assuming none are identified, the athlete should then evacuate the nasal passages (i.e., blow his/her nose). This helps to clear the field of blood, including clotted blood that may masquerade as a septal hematoma. Visual inspection (with a lighted speculum, if available) will reveal asymmetric bulging of the nasal mucosal fold. Widening of the septum can be an early indication of a developing septal hematoma. The classic appearance of a septal hematoma is a bluish-red mass, although fresh injuries may not possess such discoloration. Tenderness and fluctuance of this mass are often present. In the event that the injury is more proximal, a cotton-tipped applicator can be used to assess for tenderness and/or fluctuance.

Diagnosis No laboratory testing and/or imaging is necessary to arrive at this diagnosis; physical examination is generally sufficient. Initial Management A team physician should be prepared to treat a septal hematoma, whether it be in the training room or the office. Once identified, a nasal decongestant (e.g., 0.05% oxymetazoline) should be instilled into the nasal passages. Local anesthetic can then be administered; 1% lidocaine with 1:100,000 epinephrine is an appropriate choice for both anesthesia and vasoconstriction2 [67]. Aspiration with an 18- or 22-gauge needle is recommended first to confirm the presence of a blood and thus a septal hematoma. This should be attempted in the most fluctuant aspect. Once verified, a 15-blade scalpel can be utilized to make an incision in the most fluctuant portion of the hematoma, taking care not to penetrating too deep and damage the underlying cartilage (Fig.  44.37). A hemostat can then be utilized to open the incision slightly, if needed. Copious irrigation with saline is advised; an 18-gauge angiocatheter can prove to be valuable for this aspect of the procedure. Some advocate for the placement of a wick or drain, but this is generally unnecessary unless there is suspicion for a septal abscess [77]. In the context of bilateral septal hematomas, the incisions should be offset to avoid the potential of a through-and-through perforation. Subsequent anterior packing of the bilateral passages is advised for 2–4 days [78]. As previously stated, there have been no reports of vasoconstrictorinduced tissue necrosis attributed to lidocaine with epinephrine since 1948. We contend that this is a safe medication in the nose (among other anatomic sites), which is also supported by Marston et al. [67].

2 

Fig. 44.36 Bilateral nasal septal hematomas (Image courtesy of Handler and Myer [116])

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C. Hogrefe Table 44.9  Potential complications of septal hematomas Complication Septal abscess Septal necrosis Cavernous sinus thrombosis Sinusitis Saddle deformity Hematoma reaccumulation

Clinical Presentation Tenderness at the nasal tip; pain out of proportion to exam Tenderness at the nasal tip; pain out of proportion to exam Lethargy; focal neurologic abnormalities (e.g., a lateral gaze palsy) Facial pain; nasal obstruction; purulent drainage Visual loss of nasal bridge height (Fig. 44.38) Increased pain and pressure within the nose

Fig. 44.37  The approach for incising a septal hematoma (Image courtesy of AO Foundation)

Following the successful drainage of a septal hematoma, antibiotic prophylaxis is recommended, particularly with the placement of anterior nasal packing [67]. A 7-day course of amoxicillin-clavulanate or clindamycin is acceptable. It is important to counsel the athlete that reaccumulation of the hematoma can occur. Thus, increasing pain, swelling, and/or difficulty breathing should prompt an immediate re-evaluation.

Indications for Referral The initial indications for referral include an inability to control any associated bleeding, significant coexisting facial fractures, and/or difficulty breathing. The recurrence of a septal hematoma also warrants a prompt referral to an Otolaryngologist. Follow-up Care All patients with a septal hematoma should be evaluated by an Otolaryngologist in approximately 3 days. This appointment is beneficial to assess for a potential failed drainage attempt, reaccumulation of the hematoma, development of an abscess, presence of another infection, and/or evidence of another complication. Return to Sports In the absence of other associated injuries (or complications), the athlete can return to play once the nasal packing is removed and there are no difficulties with nasal breathing. Upon resuming participation, it should be strongly encouraged that the athlete utilizes adequate facial protection for several weeks (Fig. 44.4). Complications Untreated or suboptimally treated septal hematomas can lead to a myriad of potentially devastating complications. These conditions and their associated clinical findings are presented in Table 44.9.

Fig. 44.38  A saddle nose deformity featuring decreased height of the nasal bridge

Pediatric Considerations The nasal septum in pediatric patients serves as a growth center for the nose. Failure to recognize and treat septal hematomas properly can restrict further nasal development. Similar to nasal fracture treatment, the indications for the treatment of pediatric septal hematomas mirror the indications for adults. Children should be followed for 12–18  months following septal hematoma treatment to ensure that there are no significant cartilaginous changes and/or cosmetic defects [78].

Epistaxis With a rich mucosal blood supply, the nose is primed to bleed. Common causes include digital exploration, low humidity, foreign bodies, genetic conditions (e.g., hereditary hemorrhagic telangiectasia), and of course trauma.

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Epistaxis can be severe, prolonged, and difficult to control. Nasal bleeding is typically described as either anterior or posterior. Kiesselbach’s plexus, a confluence of vessels in the anterior septum, is the origin of 90% of all epistaxis cases [79]. Posterior epistaxis stems from the posterolateral branches of the sphenopalatine artery primarily, but the carotid artery can be the source as well. Such bleeds can become serious enough to warrant an inpatient admission.

 echanism of Injury in Sports M Epistaxis can occur in virtually any sport. As suggested previously, the environmental conditions may be sufficient to result in bleeding from the nares. Additionally, the prospect of a fall onto the nose, contact with an opponent or teammate, or direct trauma with a ball, stick, bat, or other projectile can result in nasal bleeding that necessitates a medical intervention. Epidemiology Epistaxis is a very common problem, with estimates suggesting that it affects up to 60% of the population [80]. However, only 10% of the population will present for a medical evaluation. The true incidence of this entity is unknown since many individuals do not seek medical attention. Similarly, there is minimal data on the incidence of epistaxis in athletes. In the population at large, epistaxis is most common in those under the age of 10 and over the age of 50. Clinical Presentation Athletes with epistaxis will report blood from one or both nares. Blood down the posterior oropharynx may be reported as well, particularly in the setting of posterior epistaxis. This may result in nausea. In traumatic scenarios patients may note significant swelling and/or ecchymosis. The epistaxis itself is typically not painful; however, pain may result from a concomitant septal hematoma, nasal fracture, and/or other facial fracture. Additionally, a sideline physician should inquire about recent medication use such as aspirin or other NSAIDs. Before direct nasal inspection, we recommend an initial attempt at tamponade. The athlete should grasp the nasal septum just below the nasal bridge with the thumb and index finger (Fig.  44.39). Enough pressure should be applied to blanch the finger tips, and the pressure should be maintained consecutively for 10–15  minutes. It may be worthwhile to have the patient lean forward slightly as well to minimize the swallowing of blood. Other tips of the trade include the application of a cold compress to the nasal bridge to aid in achieving hemostasis. If the epistaxis persists after this intervention, ensure that all clots are evacuated from the nose. This can be accomplished with suction or gentle blowing of the nose. Direct

Fig. 44.39  Positioning for anterior epistaxis tamponade

visual inspection of the nasal passages should then commence and is crucial in identifying and addressing the source of bleeding. Properly positioning the patient in an upright, sniffing position will help to facilitate an optimal view. The use of a lighted nasal speculum (if available) and application of a vasoconstrictor such as oxymetazoline can be beneficial as well. In fact, in one study showed that the use of oxymetazoline resolved epistaxis in 65% of patients in the Emergency Department [81]. The team physician should evaluate Kiesselbach’s plexus first, looking for bleeding, ulceration, and/or erosion. If no source of bleeding is appreciated, one should be concerned for a posterior source.

Diagnosis Epistaxis is a clinical diagnosis; imaging in the setting of epistaxis is not typically needed. Even in the setting of a traumatic event, only suspected complex nasal fractures warrant further advanced imaging (e.g., a maxillofacial CT). Depending upon the severity of the bleeding, patients may warrant laboratory testing to assess for anemia and/ or coagulation abnormalities. However, these tests are generally to assess for the severity of the epistaxis or a contributing etiology rather than making the diagnosis itself.

782 Fig. 44.40  An algorithm for managing anterior epistaxis

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Chemical Cautery (Silver Nitrate) • Start peripherally and move centrally • Apply for < 10 seconds • Avoid cauterizing both sides of the nasal septum to prevent perforation

• Useful for aggressive bleeding or those involving larger vessels • Apply anestheia to the bilateal nares • Ineffective on overtly bloody surfaces

Anterior Nasal Packing

• Petroleum gauze • Nasal tampon (e.g. Merocel) • Inflatable carboxymethylcellulose (e.g. Rhino Rocket)

• Select one of the following materials for nasal packing • Should be left in for 1 to 5 days

• Absorbable/Degradable cellulose (Surgicel) or gelatin (Gelfoam)

Initial Management The first steps in managing epistaxis as described above serve as a precursor to the visual inspection of the nares. If the source of bleeding is directly visualized and the aforementioned interventions are not successful, one should proceed in a stepwise fashion to control the bleeding. Figure  44.40 provides an outline for treatment moving forward. There are a few nuances to nasal packing that are worth noting. The application of petroleum gauze can be technically difficult. However, when similar gauze (in one study bismuth subnitrate and iodoform paste-impregnated gauze, which is akin to Xeroform) was compared to nasal tampons, there appeared to be no difference in the efficacy of controlling epistaxis [82]. If a nasal tampon is used, it should be coated in a topical antibiotic, such as bacitracin. When using an inflatable balloon-style catheter (e.g., a Rhino Rocket), soak the catheter in sterile water; do not use saline, apply lubricants, or utilize topical antibiotics. These substances may impair the cellulose coating on the balloon. While studies on this type of balloon catheter have not shown them to be superior to nasal packing, they do appear to insert easier and are less uncomfortable for patients [83]. The use of systemic antibiotics following anterior nasal packing is a topic of debate. While it may be common practice for Otolaryngologists to do so, there is not sufficient evidence to suggest that it is necessary, particularly to prevent toxic shock syndrome. This decision should be made on an individual basis and depends upon the patient’s perceived risk of infection (e.g., diabetes mellitus). If prescribed, amoxicillin-­ clavulanate or a second-generation cephalosporin are appropriate choices for as long as the packing remains in place. If the epistaxis cannot be controlled with the aforementioned measures, the patient may require a more aggressive

Electric Cautery

• Prophylactic oral antibiotics should be considered on an individual basis

intervention (e.g., embolization or surgical ligation). Conversely, the bleeding may be posterior, in which case other interventions should be entertained. There are commercial available products that can aid in this endeavor (e.g., Epistat and Brighton balloon). However, these may not be readily available to the team physician given the relative rarity of their utilization. More commonly available is a Foley catheter, which can be utilized to tamponade a posterior nasal bleed. Once the nasal passage is anesthetized (topical lidocaine is adequate), a 10–14-French Foley catheter should be coated with a petroleum-free lubricant (to avoid balloon degradation). The catheter can then be advanced along the floor of the nose until it is seen in the posterior oropharynx. The balloon should then be filled with 5–7  mL of sterile water and retracted gently until it lodges in the posterior oropharynx. At that juncture the balloon should be completely filled with an additional 5 mL of sterile water. The tube is then clamped in place (using something such as an umbilical clamp, for instance) with sufficient surrounding padding at the anterior tip of the nose to prevent pressure necrosis (Fig.  44.41). Many clinicians will also pack the anterior nasal passage at this point as well to avoid blood pooling anteriorly. Other options for posterior packing exist (e.g., cotton packing), although they are more complex and carry additional significant risks. Unlike its anterior counterpart, antibiotics are typically prescribed for posterior nasal packing. Given that these patients should be evaluated by an Otolaryngologist and/or Emergency Department provider, initiation of the antibiotic regimen can be reserved until that time.

Indications for Referral The indications for an emergent referral to an Otolaryngologist or an Emergency Department include anterior epistaxis that

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tally exploring the nares, and minimizing heavy lifting. Nasal saline washes and water-soluble ointments can assist in promoting healing of the nasal mucosa. When nasal packing is required, the overall complication rate is said to be approximately 3% [84]. Toxic shock syndrome is a reported complication, and its risk is greatest with retention of the nasal packing for more than 72 hours. Other potential complications include septal hematomas, abscesses, pressure necrosis, sinusitis, and/or acute airway obstruction due to dislodging of the nasal packing.

Pediatric Considerations Chemical and electric cautery are still appropriate means for controlling epistaxis in younger patients if pressure tamponade is unsuccessful. Both work well if the patient remains calm. In this demographic, if nasal packing is needed (anterior or posterior), the threshold for consulting an ­ Otolaryngologist is lower. Additionally, if needed, nasal balloon catheters are suitable for use in pediatrics athletes, although they may not be as well tolerated in this age group. Fig. 44.41  Proper Foley catheter placement for posterior epistaxis

cannot be controlled and posterior epistaxis (controlled or otherwise, as even if controlled it may only be a temporizing measure prior to a surgical intervention). Athletes with atraumatic recurrent epistaxis also warrant a nonemergent referral to assess for a possible underlying etiology (e.g., tumor).

Follow-up Care If the epistaxis is controlled with digital tamponade or cautery, follow-up with the team physician in 1–2 days is advisable to ensure that there is no persistent bleeding, infection, and/or other associated complications. If anterior packing is utilized, follow-up with an Otolaryngologist is reasonable within 24–48 hours. Athletes who are treated with posterior nasal packing will require emergent evaluation by an Otolaryngologist, who should assist in guiding the athlete’s follow-up timeline depending upon the extent of intervention and/or the presence of complications.

Dental Trauma Key Points

• There is a high rate of associated injuries in the context of dental trauma; team physicians should be cognizant of other entities such as concussions, mandible fractures, temporomandibular joint injuries, and/or lacerations (particularly of the lip) (Fig. 44.42). • The Ellis classification can aid a sideline physician in assessing an athlete’s need for immediate dental intervention and appropriateness for return to play. • Tooth fracture fragments or avulsed teeth that cannot be successfully replanted should be placed in a preservation liquid such as a balanced salt solution, milk, contact solution, or sterile saline. • Dental fractures that do not involve the pulp can be evaluated by a Dentist or Oral Surgeon in 24–48 hours. More significant fractures necessitate an immediate referral for definitive treatment. • Mouthguards are an extremely effective means for reducing the incidence of dental trauma and should be encouraged for athletes in high-risk sports where it is not mandatory (e.g., basketball and soccer).

Return to Sports In the case of isolated anterior epistaxis, once the athlete’s bleeding is controlled, he or she may be cleared for return to sport. If packing is left in place, the athlete must be able to comfortably breathe and perform without restrictions and/or limitations. Patients requiring packing for posterior epistaxis should not be cleared for participation until the packing is removed and the cessation of bleeding is verified.

Introduction

Complications Recurrent epistaxis is a complication that can be somewhat mitigated by avoiding blowing one’s nose, refraining from digi-

Sport-related activities find themselves among the most common causes of dental trauma. It has been estimated that an athlete has a 10% chance of suffering such an injury each

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season and between a 33% and 56% chance of encountering dental trauma during his or her career [85]. From an anatomical perspective, the tooth can be divided into the root and the crown, with the former below the gingival line and the latter visible above it (Fig. 44.43). The layers of the crown (from external to internal) contain the enamel (white, or at least it is supposed to be) and dentin (yellow). These layers cannot regenerate themselves [86]. The nerves of the tooth reside in the next layer, which is the pulp. As for the root, it rests in alveolar bone and is attached by the periodontal ligament. Preserving this ligament is critical to successfully replanting an avulsed tooth (a topic that is discussed later) [87].

Fig. 44.42  Direct trauma to the face, especially by high-velocity projectiles, can result in significant dental injuries

 echanism of Injury in Sports M Direct blows to the teeth are the primary cause of dental trauma in sport. This can occur in virtually any sport, ranging from mechanisms such as falls onto the face to contact with projectiles (e.g., sticks, bats, balls, or pucks) to encounters with the anatomy of another participant. It has been reported that such injuries occur more frequently in organized sports, but this could be a function of underreporting in nonorga-

Fig. 44.43  The anatomy of a tooth

Enamel

Crown

Gingiva (gum) Dentine Pulp chamber Cementum Root canal containing pulp tissue (also called pulp canal)

Periodontal ligament

Root

Accessory canal Apical foramen

Alveolar bone

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nized sporting endeavors [8]. Outdoor sports that occur in warmer times of the year show a higher incidence of such injuries as well [88]. With regard to specific sports, the use (and mandatory implementation in some sports) of mouthguards has significantly affected the context in which dental trauma transpires. For instance, at one point the prevalence of dental injuries in football and rugby was 54% [89]. However, it is now reported that basketball and soccer players are at significantly higher risk for such injuries compared to football players [90]. Mouthguards (ranging from stock mouthguards to “boil and bite” mouthguards all the way to custom-fit mouthguards from a dental professional) have been extremely beneficial in this regard, preventing more than 200,000 dental injuries a year [29]. The National Federation of State High School Associations (NFHS) mandates that mouthguards be used in football, field hockey, ice hockey, lacrosse, and wrestling (for wrestlers with braces) [91]. The American Dental Association (ADA) has recommended the use of mouthguards in numerous (or even most) sports, both in practice and competition, as outlined in Table 44.10 [92].

Epidemiology Males are typically more impacted by dental trauma than females by a rate of approximately three to one, although this could be skewed based on relative rates of exposure. Overall, 25% of the population between 6 years old and 50 years old have reported dental trauma, with the rate even slightly higher in children [8]. Studies have cited that 31% of such trauma is secondary to sports injuries [93]. Anatomically based epidemiological facts worth noting include that most dental injuries involve a single tooth (with 80% occurring in one of the four maxillary incisor teeth); the left side is more commonly affected than the right side; and there is a high incidence of recurrence [94].

Dental Fractures Dental fractures are a relatively common occurrence in sport. However, not all such injuries require emergent intervention, and the athlete can return to participation immediately in cerTable 44.10  ADA recommendations for sports in which mouthguards should be used [92] Acrobatics Field hockey Handball Martial arts Rugby Skiing Squash Water polo

Basketball Football Ice hockey Racquetball Shot putting Skydiving Surfing Weightlifting

Boxing Gymnastics Lacrosse Roller hockey Skateboarding Soccer Volleyball Wrestling

tain cases. An astute sideline physician will always consider the location of the fractured tooth fragment, as it can be embedded in the surrounding soft tissue (e.g., the lip), aspirated, or even lodged within another participant.

Fracture Classification The Ellis classification system is utilized to describe the severity of dental fractures and helps guide their management (Fig. 44.44 and Table 44.11, with the relative frequency (%) of dental fractures noted in parentheses)3 [8]. Clinical Presentation The majority of athletes will report a traumatic event involving the head, neck, and/or face. It can be useful to inquire about the direction of force associated with the injury, as it may aid the sideline physician in locating missing tooth fragments and/or identifying other associated injuries. Aside from the historical pearl of trauma to the face, athletes will also typically note pain (although Ellis I fractures may go largely unnoticed initially). Sometimes the associated pain may be appreciated after the consumption of a hot or cold liquid or with mastication. Bleeding may be present, raising the suspicion for a concomitant oral laceration (e.g., gingiva, lip, tongue, etc.). Similarly, the athlete may have pain elsewhere in the face, including the ear, temporomandibular joint, and/or neck. The savvy team physician should also assess for the presence of concussion-related symptoms. Physical Examination As with all facial trauma, the sideline physician should first ensure that the athlete is protecting his or her airway and breathing appropriately. Once these potential issues have been evaluated, verify that the athlete’s circulation is intact. Next, the skull, cervical spine, and other facial structures (i.e., eyes, ears, and nose) should be inspected. Prior to proceeding to the dental examination, one should perform an extraoral assessment. As detailed previously in this chapter, be sure to palpate the mandible, maxilla, zygoma, temporomandibular joint, and mastoid bones. Any identified lacerations should be thoroughly inspected for foreign bodies (e.g., dirt, sand, tooth fragments) and removed, if found. At that juncture one can proceed to the intraoral evaluation. Visual inspection is paramount, with care taken to first account for any missing teeth (with dental avulsion, or Ellis V injury, management discussed later in this chapter). Some dental texts have extended the Ellis classification through Ellis IX injuries. This further delineation of dental trauma past an Ellis V is beyond the scope of this chapter, and such injuries should warrant immediate evaluation by a Dentist or Oral Surgeon. 3 

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Class I

Class II

Class III

Class IV

Class V

Fig. 44.44  The Ellis classification system for dental fractures

Table 44.11  The Ellis classification system for dental fractures Ellis Grade I II III IV V

Description of the Injury Enamel only; rough or chipped tooth (15.8%) Enamel and dentin; painful with exposure to the air, cold liquids, and/or palpation (39.9%) Enamel, dentin, and pulp; red-pink pulp will be exposed (25.7%) (Fig. 44.45) The entire tooth and root; the extent of root involvement impacts outcomes (18.5%) An avulsion of the tooth (Fig. 44.45; discussed later in this chapter)

Fig. 44.45  A dental fracture involving tooth #9 (Ellis III) and a dental avulsion of tooth #8 (Ellis V)

Careful inspection of the affected tooth or teeth provides significant insight into the grading of the dental fracture. Gently wiping the affected tooth may reveal a spot of blood, indicative of an Ellis III injury. Be sure to assess the buccal mucosa, gingival tissue, tongue, and the frenulum for damage. Any lacerations should be probed for foreign bodies as well. Then, palpate the alveolar bone for potential fractures. Having the athlete bite down may result in malocclusion. Lastly, evaluate the mobility of the teeth. Patients with malalignment and/or excessive mobility are more likely to have underlying fractures (alveolar and/or root), and further imaging is warranted. The tongue blade bite test, as discussed previously in this chapter, can aid in the identification of associated fractures as well.

Diagnosis Some have argued that not all dental fractures are visible on physical examination, and thus any tooth trauma warrants imaging [29]. While a low index of suspicion is certainly prudent, routine referral (emergent or otherwise) for imaging of Ellis I and Ellis II fractures is not necessary. However, there is a role for further imaging when attempting to distinguish between an Ellis III and an Ellis IV injury. Clinically this is relevant because while both are dental emergencies, the nature of the intervention performed by a dental professional may vary. Occlusal plain radiography (intraoral radiographs similar to those secured in a Dentist’s office) is the imaging of choice, which will likely necessitate an evaluation by a Dentist or an Oral Surgeon. Such imaging may not be accessible for all team physicians, but some may possess the ability to secure this radiography. Of note, two periapical views at different angles are often required to identify a root fracture [8]. Lateral, anterior views can also prove to be beneficial in this setting. Keep in mind that similar to bony fractures, dental fractures may not be evident initially on imaging. If concern for a root fracture persists, repeat imaging may be sought 1–2 days after the traumatic event. Otherwise, additional imaging decisions are predicated on the concern for concomitant injuries. For instance, an athlete with a missing tooth segment and dyspnea may warrant a chest radiograph to search for a potentially aspirated fragment. Even when an Ellis III or Ellis IV dental fracture is not suspected, an orthopantomogram may be secured to determine if a tooth fragment is lodged in the surrounding soft tissue. Lastly, in the setting of significant facial trauma with associated dental injuries, an orthopantomogram or maxillofacial CT may be indicated to evaluate for a mandibular fracture, for example. Initial Management The initial management of dental fractures depends upon the extent of injury, as detailed below. Regardless of the extent of injury, significant attention should be placed on

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Fig. 44.46  Some tooth preservation options for dental fracture fragments and avulsions

locating the fracture fragment(s). Remember that the section of tooth could be expelled, lodged in the athlete’s soft tissues or that of an opponent, or even aspirated. If located, the fragment should be placed in a balanced salt solution (e.g., Hank’s Balanced Salt Solution), milk, contact solution, or a commercially available tooth preservation system (Fig. 44.46). • Ellis I: If only the enamel is involved, the athlete can continue to participate in sports if desired and his or her pain is controlled. In the event that the tooth fragment is found, it can be reattached up to 48 hours later. • Ellis II: This injury does not necessarily require a removal from activity either. If the patient can tolerate the discomfort of the exposed dentin and the edges of the tooth do not present a risk to the athlete or others, continued participation in sport is reasonable [29]. Treatment should be pursued within 1–2 days. Of note, there may be an increased risk of bacterial infection the longer the dentin is exposed. • Ellis III: Athletes should be removed from sport and promptly evaluated by a Dentist or Oral Surgeon, preferably within 3 hours. No immediate treatment on the sideline or in the office is necessary. Minimal exposure of the pulp may allow for direct capping, although a root canal may be necessary for more extensive injuries. • Ellis IV: The tooth component should be handled as little as possible and promptly placed in a preservation solution. Gentle pressure to the fracture site can be applied (e.g., with sterile gauze held in place by the athlete biting down lightly) to prevent further movement of the remaining tooth. No further immediate on-site management is advised, and the athlete should be referred for definitive management.

• Ellis V: These injuries amount to dental avulsions; the overall management of this condition is discussed later in the chapter.

Indications for Referral Ellis I and Ellis II fractures should be evaluated by a Dentist within 48  hours. Ellis III or greater fractures warrant an immediate referral for further dental evaluation and treatment. As indicated above, some dental injuries may require a root canal. In certain more severe cases, dental extraction may be required with subsequent replacement using a dental implant. Follow-up Care Virtually all athletes with dental fractures should be advised to follow up with a Dentist or Oral Surgeon. This may amount to nothing more than an initial follow-up visit 24–48  hours after the incident. In other contexts, patients may need a root canal 1–2 weeks after the trauma. On the far end of the spectrum, an Ellis IV fracture involving the root may require up to 2–3 months of immobilization and subsequent follow-up for up to 2 years [8]. Additional management of these injuries includes making sure that the athlete’s tetanus status is current. Flossing should be avoided until the injury is fully healed, but general oral hygiene is otherwise essential. A soft diet may be necessary to avoid exacerbating the patient’s pain. And after such an injury it is important for the team physician to ensure that the athlete has an adequate mouthguard, which may require a new mold/fitting.

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Return to Sports Athletes can safely be allowed to resume sporting participation as soon as their pain is controlled in the setting of Ellis I and Ellis II fractures. The return to sport after the management of more significant dental fractures is variable and should be made in conjunction with the consulting Dentist or Oral Surgeon. The use of a mouthguard is highly encouraged moving forward to decrease the risk of reinjury. Complications Dental fracture complications can occur despite optimal management. These complications range from permanent cosmetic deformities to complete loss of the affected tooth. Bacterial infections can develop when exposure of dentin and/or the root occurs. As such, prophylactic antibiotics (e.g., penicillin VK or clindamycin) are recommended when pulp is exposed [95]. In general, the longer the delay to definitive treatment, the poorer the outcome, whether cosmetic or functional. Pediatric Considerations The Ellis classification system can still be utilized in the setting of pediatric dental fractures even though the injury may involve primary teeth rather than permanent teeth. The incidence of certain classes of injuries does differ. For instance, the more severe root fractures are less common in primary teeth [96]. Management of these injuries may differ with care taken to avoid damaging the underlying permanent tooth. For this reason, primary teeth should generally not be replanted. Otherwise, the overall management of these injuries is roughly the same as in adults; however, one should consider consultation with a pediatric dental specialist if a referral is necessary.

Dental Avulsions Defined as a complete traumatic displacement of a tooth from the alveolar socket, dental avulsions are also referred to as Ellis V fractures. They require prompt identification and treatment by the sideline physician.

Clinical Presentation Direct trauma to the head and/or face generally precedes this injury. Given the force often required to create these injuries, athletes may have altered consciousness (raising a team physician’s concern for an intracranial hemorrhage or concussion), marked facial pain, and/or brisk bleeding from the oropharynx. Otherwise, dental avulsions should be suspected when an athlete presents a seemingly intact tooth to the medical staff or there is an absent tooth on intraoral examination. When the athlete reports such an

C. Hogrefe

injury but cannot find the tooth, it is important to locate the potentially avulsed tooth, evaluating the surrounding playing surface, the athlete’s soft tissues, and even considering aspiration.

Physical Examination The physical examination for dental avulsions should commence as was previously described in the “Dental Fractures” section of this chapter. After the integrity of the patient’s airway, breathing, and circulation are confirmed, the team physician should assess for damage to the other facial structures and/or facial bones. The intraoral examination is also as noted above. The primary difference will be the finding of a dental socket devoid of tooth contents. Diagnosis Identifying a dental avulsion is generally accomplished on a clinical basis alone. However, further advanced imaging (e.g., an orthopantomogram or a maxillofacial CT) may be warranted if a retained tooth fragment, alveolar fracture, and/ or other facial fracture is suspected. Also keep in mind that a missing tooth could be found in other anatomic areas, including the nasal cavity (by penetration equating to an intrusion dental luxation, which is discussed later in this chapter) or the chest (via aspiration). If there is concern for such an occurrence, the requisite imaging should be pursued. Initial Management If the athlete is noted to have altered mental status or cannot protect his or her airway, one should not attempt to replant the avulsed tooth. In those instances, the tooth should be placed in a preservation solution until it can be safely replaced (Fig. 44.46). Barring such a contraindication, the sideline physician can and should make an effort to return the tooth to its proper location. Studies suggest that the time out of the socket can impact the success of replantation, with 66% of teeth replanted within 1 hour functionally normal and radiographically healed at 5  years [97]. Research has shown that replantation within 5 minutes produces the best results [98]. The tooth should be rinsed in water or saline but not wiped or scrubbed. Try to handle the tooth primarily by the crown to prevent disturbing the root structures. Reinsertion of the tooth is straightforward, but care should be taken to minimize disruption of the socket. Often there is a “click” when the tooth is successfully replaced [99]. Hold the tooth directly in place for 5  minutes. This freshly replaced tooth will require further stabilization (e.g., splinting) by a Dentist or Oral Surgeon. In the event that the tooth cannot be successfully replanted, it should be protected in one of the aforementioned solutions or even between the patient’s gingiva and buccal mucosa until securing definitive treatment.

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Indications for Referral All patients with dental avulsions should be immediately referred to either a Dentist’s office or an Emergency Department with the requisite capabilities to successfully replant and/or splint such injuries. Follow-up Care The vast majority of dental avulsions necessitate splinting, which will require follow-up care (Fig. 44.47). The duration of splinting can be variable with 1–2 weeks being relatively common. Similar to dental fractures, a soft diet may help to decrease the athlete’s pain with mastication. Prophylactic antibiotics are often prescribed (e.g. penicillin VK or clindamycin). General hygiene is otherwise highly encouraged to decrease the risk of subsequent infection following a dental avulsion. Return to Sports The athlete’s return to sport will be contingent upon the recommendations of the Dentist or Oral Surgeon assisting in the provision of care. Participation should not be considered until the patient’s splinting is removed and the tooth is deemed stable (typically 2 weeks or longer depending upon the severity of injury). As expected, a well-fit molded mouthguard should be utilized upon the patient’s return. One should avoid mouthguards that can be displaced upon impact, which includes the over-the-counter variety [29]. Complications Delays in replanting dental avulsions can make subsequent attempts to relocate the affected tooth more difficult if coagulation or blood clotting occurs in the socket. The nature of the injury itself can lead to a root canal, loss of the tooth, and/or a surrounding infection. Pediatric Considerations When a primary tooth is avulsed, it generally should not be replanted. Doing so may damage the underlying development of the permanent teeth.

Fig. 44.47  Splinting of a dental avulsion involing tooth #21 with a fracture involving tooth #11 (Image courtesy of Rls, CC BY-SA 3.0. Savas et al. [117])

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Dental Luxations Blunt trauma to the teeth may not result in fractures or avulsions but rather varying degrees of loosening of the tooth itself. Sometimes referred to as subluxations or luxations, these dental injuries occur in sports, and a well-trained team physician should be able to deftly treat them and recognize when further evaluation with a dental specialist is indicated.

Injury Classification Typically, these injuries involve the maxillary incisors, although they can involve any tooth. With that said, there are several terms that are utilized to further delineate the traumatic events that fall within the realm of subluxations or luxations [29]. • Concussion: This trauma results in pain to the touch of the affected tooth, but there is no loosening or visual displacement. Root fractures can still occur, however, and should be considered by the astute sideline physician. • Subluxation: Limited mobility of the tooth is the hallmark of this condition. Visible displacement may not be appreciated, although bleeding from the gingiva can be seen. • Lateral luxation: This description can be a bit misleading because it encompasses lateral or anterior/posterior displacement of the affected tooth (Fig.  44.48). It is often accompanied by a fracture of the alveolar plate, and the tooth is usually firmly situated in the socket. • Extrusive luxation: These injuries are apparent by a partial displacement of the injured tooth as it protrudes outward from the tooth socket. • Intrusive luxation: A tooth that is relocated through the floor of the tooth socket falls into this category. For the most part, an associated fracture of the alveolar socket should be considered. These are the most severe injuries within luxations.

Fig. 44.48  A lateral luxation of tooth #9 (Image courtesy of Arikan and Sari [118])

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Clinical Presentation Similar to its dental injury cousins (e.g., dental fractures and dental avulsions), luxations are the result of direct trauma to the head and/or face. This force may be directly to the anterior aspect of the teeth or the result of contact with the distal most ends of the teeth. These traumatic events are almost always associated with pain at or near the affected tooth. However, as noted above, the athlete may not report laxity of the tooth. Patients may describe an abnormal bite or an unusual sensation with mastication. Physical Examination The physical examination for dental luxations mirrors that for its dental predecessors. After the athlete is stabilized with regard to his or her airway, breathing, and circulation, care should be taken to assess for associated facial fractures. Once those etiologies have been ruled out and/or addressed, a thorough intraoral evaluation should be completed. The presence of tooth laxity is an important feature to note. Athletes may have concomitant dental fractures (e.g., an Ellis III fracture) with a luxation. Diagnosis A thorough physical examination is generally all that is required to identify a dental luxation. As with other dental trauma, additional advanced imaging is indicated if there is concern for a facial fracture or concomitant injury. An immediate orthopantomogram or maxillofacial CT is not necessary for all isolated dental luxations (e.g., concussions or subluxations). However, subsequent imaging may be obtained in follow-up to evaluate for a possible root fracture and/or to ensure that the tooth is seated properly in the socket [29]. Athletes with more significant luxations (i.e., lateral, extrusions, or intrusions) may benefit from such advanced imaging, which will likely be at the discretion of the consulting dental specialist. Also remember that intrusion injuries can violate the nasal cavity, which may necessitate imaging. Initial Management Once the athlete’s airway, breathing, and circulation are confirmed to be intact and other associated potential injuries have been evaluated for and/or treated, the team physician should turn toward managing and stabilizing the dental luxation. It is likely beyond the scope of the sideline physician to splint injured teeth in the training room or office. With that said, not all of these injuries require immediate intervention. For instance, a tooth concussion, likely resulting in pain but no tooth laxity, will not need any emergent dental management. In the setting of a tooth subluxation, there again may be no need for immediate intervention. The sideline physician should assess the

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patient’s degree of tooth laxity. If the tooth is deemed to be at an increased risk for falling out or the sport itself presents a significant risk for such an occurrence or additional injury (e.g., boxing, mixed martial arts, and wrestling), the athlete should be withheld from participation until the tooth is stabilized [29]. Lateral, extrusion, and intrusion luxations should be immediately managed by relocating the tooth to its natural position without exerting excessive force. For extrusions and intrusions, this may require anterior or posterior manipulation in addition to a force aimed at positioning the tooth within its socket. Such interventions can help to preserve the tooth and decrease the risk of subsequent complications, which are discussed below. It should be noted that with lateral luxations, the tooth can be wedged in a fractured alveolar plate. In these cases the tooth may be extremely difficult to manipulate. Local anesthesia (e.g., a local dental block or an inferior alveolar nerve block) may be necessary to facilitate such a reduction. Regardless, the next management step for these athletes is to seek an immediate dental consultation.

Indications for Referral It is advisable that all dental luxation injuries be evaluated by a Dentist or Oral Surgeon, but the timing of this referral varies. As previously suggested, dental concussions and minor subluxations can be seen within the next 24–48 hours. If the team physician deems a dental subluxation to be at high risk to fall out, a more prompt (i.e., same day) evaluation is appropriate. All lateral, extrusion, and intrusion luxation injuries should be immediately referred to a Dentist or Oral Surgeon. The affected tooth may require prompt splinting (or potentially a surgical intervention) in order to optimize the chances of saving the injured tooth and limit the risk of sequelae. Follow-up Care As indicated above, dental luxations should be evaluated by a Dentist or an Oral Surgeon, with continued follow-up at the discretion of the treating subspecialist. The most significant of these injuries may require follow-up for up to 1 year. With that said, there are a couple of other considerations to keep in mind. A soft diet should be recommended for these athletes until they are able to eat without pain. Antibiotics are generally recommended for all lateral, extrusion, and intrusion luxations. Similarly, if there is bleeding from the base of a subluxed tooth, antibiotics are advised. The argument here is that damage to the periodontal ligament can allow for the spread of bacteria and subsequent infection [29]. Penicillin and clindamycin are appropriate selections in this context, and a typical course lasts for approximately 10 days. Additionally, an antibiotic

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mouthwash may be beneficial to further prevent the spread of infection.

Return to Sports Athletes with dental concussions and minor subluxations can return to sport as soon as the associated pain is controlled, if so desired by the athlete. They should return to sport with a mouthguard to further protect the affected tooth (or teeth). More substantial subluxations and lateral, extrusion, and intrusion luxations will require an immediate dental evaluation. Splinting of the injury tooth is likely to ensue, and the return to sport in most cases should not occur until the splinting is removed. In the event of a splinted subluxed tooth, one can consider a return while the splint is in place if a mouthguard is worn. This mouthguard should be molded to fit around the existing splint [29]. Regarding the duration of splinting of subluxations, it may be kept in place for 2–3 weeks. However, if multiple teeth are involved in an extrusion injury, the splinting may persist for up to 6–8 weeks. Regardless, upon clearance for a return to sport (made in conjunction with the dental specialist, team physician, athlete, and parents when appropriate), a new, freshly molded protective mouthguard for the athlete should be utilized. Complications There are several noteworthy complications that may arise following luxations, even if they are treated promptly and effectively. These complications include darkened teeth (due to pulp death), dental abscesses, loss of surrounding bone, and/or root resorption [29]. If the dental luxation is missed or not relocated promptly, the tooth can actually fuse with the surrounding bone, making it extremely difficult to relocate. Ensuring prompt follow-up with a dental specialist can help to correct and/ or limit these issues. Pediatric Considerations The primary consideration for pediatric athletes with dental luxations is to assess whether the permanent teeth are affected. Radiographs will prove to be valuable in this regard. For extrusion injuries (generally with >3  mm of extrusion), the tooth may be extracted altogether [96]. It is imperative that a prompt dental evaluation be pursued to avoid sequelae to the underlying permanent teeth. Minor intrusion injuries and lateral luxations may either re-erupt or reposition themselves on their own, but this should not spare the athlete from the aforementioned dental evaluation [100]. And as an additional aside, pulp death (and thus darkening of the injured tooth) is less common in pediatric patients compared to adults. This is due to the open apex of the tooth, which allows the pulp to revascularize [29].

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Facial Lacerations Key Points

• The primary tenants of facial laceration care include evaluating for concomitant injuries (and treating them first when necessary), irrigating the wound, inspecting for foreign bodies, and performing a skilled primary closure (when indicated). • The optimal repair of facial lacerations, both in terms of cosmetic outcome and patient comfort, involves the use of adequate anesthesia, including regional nerve blocks when appropriate. • The most important aspect of a lip laceration repair involves the meticulous reapproximation of the vermillion border. • It is imperative to note the types of eyelid lacerations that warrant immediate subspecialty referral, including those that are full thickness, involve the tear drainage system, or those with orbital fat prolapse. • Auricular and nasal lacerations necessitate that each anatomical layer be closed or reapproximated individually. • Most tongue and intraoral lacerations will heal well and rapidly without any further intervention.

Introduction Facial lacerations in sports come in numerous shapes, sizes, and complexities, ranging from an apparently simple laceration after being struck by the rogue cleat of an opponent all the way to a gaping, deep injury to the forehead during pugilistic activity (Fig.  44.49). With that said, even seemingly minor injuries should be taken seriously and thoroughly evaluated given the complexity of the underlying facial structures. Additionally, facial injuries carry the heightened emphasis on an optimal cosmetic outcome along with an ideal functional result. In short, a well-prepared team physician should be capable of addressing facial lacerations in their various forms, keenly recognizing when subspecialty assistance is necessary.

 echanism of Injury in Sports M Lacerations in sport are common and can occur in virtually any sport. Blunt trauma from another participant or direct contact with a projectile may result in such an injury. Also, some rather unique mechanisms of injury can precipitate a facial laceration, such as from the blades of an ice skate, fishhooks, the edges of skis, and even environmental features (e.g., rocks).

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C. Hogrefe

Fig. 44.50  Proper irrigation of a facial laceration in a mountain biker (Image courtesy of Morteza Khodaee, MD)

Fig. 44.49  A significant forehead laceration in boxer

Epidemiology The true incidence of facial lacerations in sport is a very difficult figure to accurately identify. Some injuries may be initially deemed “minor” thus avoiding further evaluation and treatment. Consequently, they are unlikely to be reported and captured in an epidemiologic study. Conversely, formal assessments on the topic have produced widely variable results. For instance, in the 2004 Olympics, 14 of the 19 injuries (occurring in team sports only for the purposes of this study) involving the head and neck were lacerations [101]. Meanwhile, another study assessing the injuries of a Swedish hockey team over 3 seasons found a total of 95 injuries, with 29 of the cases (31%) diagnosed as facial lacerations [102]. Overall, facial lacerations appear to be a relatively common occurrence in sport. Clinical Presentation The clinical presentation of facial lacerations is typically straightforward. Direct trauma to the face is the norm, and the mechanism of injury is most often penetrating (e.g., from an opponent’s fingernail or the blade of an ice hockey skate). With that said, blunt trauma can also result in these lacerations, such as from a mixed martial arts gloved–hand blow to the eyebrow region. Bleeding is frequently present, and the rich vascularity of the facial structures means that the bleeding may be brisk. Pain may or may not be associated with these injuries. Diagnosis Lacerations to the face and its structures (e.g., ears, nose, lips, and intraoral surfaces) rarely require further imaging.

Considerations for imaging include the need to evaluate for retained foreign bodies and/or to assess for concomitant fractures (e.g., mandible fractures). Depending upon the concern, plain radiography, maxillofacial CT scans, or an ultrasound can be utilized, if needed.

Initial Management One of the first and most important steps in caring for all lacerations entails thoroughly irrigating the injured tissue (Fig. 44.50). Tap water is safe and effective for this purpose if sterile saline is not available. Exploration for foreign bodies should then occur. Additionally, nonviable tissue should be removed in order to ensure proper reapproximation of the wound edges. Consideration should then be given as to whether a repair is necessary at all as opposed to allowing the wound to heal by secondary intention. Of note, it is considered safe and appropriate for facial lacerations to be closed within 24–48  hours with proper cleansing [103]. Other considerations that might steer a provider toward allowing a wound to heal by secondary intention include associated open fractures, heavily contaminated wounds, and those that involve human bites [104]. If the wound is deemed appropriate for a repair by the team physician, he or she should contemplate the optimal type of material to utilize for the repair, whether it be skin adhesive, Steri-Strips, superficial sutures, or deep, absorbable sutures in conjunction with superficial sutures. There are a couple of other associated issues that also should be addressed in the context of facial lacerations. The team physician should ensure that every athlete’s tetanus status is current. The routine use of prophylactic antibiotics is not necessary (aside from bite wounds) and is made on an individual basis. A prolonged time to presentation (>24 hours) is one such indication for the administration of antibiotics. General post-procedure wound care instructions should highlight daily gentle cleaning of the wound with soap and water. Topical antibiotic ointment (e.g., bacitracin/polymyxin) should be applied one to two times daily. Athletes

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should be advised to avoid submerging the affected area in water until the wound edges are healed, typically once the sutures are removed.

Indications for Referral Overall, if the team physician is not comfortable with the complexity of the facial laceration a referral should be sought immediately. Similarly, if there is concern for a suboptimal cosmetic outcome, an evaluation by a Plastic Surgeon is appropriate. Otherwise, lacerations that cause nerve injury or those that result in bleeding that cannot be controlled warrant prompt evaluation in an Emergency Department with a possible Plastic Surgery consultation to follow. Follow-up Care Typically, sutures placed in the facial structures should be removed within 5–7 days. This can be done in the training room or the office barring any complications. It is important to note that scar formation can occur for up to 1 year after the repair (and up to several years in children) [105]. Thus, athletes should be encouraged to keep the lacerations covered during that interval, whether that be with a hat, protective garment, or sunscreen. Return to Sports Once the laceration is repaired with any associated bleeding and/or pain controlled, athletes are safe to resume full activity without restrictions. Pediatric Considerations Broadly speaking, the repair of facial lacerations in younger patients may require sedation in order to achieve optimal closure and wound reapproximation. If the patient is not able to remain calm and still for the repair with local anesthesia or a regional block of the affected area, a referral to a specialist and/or an Emergency Department may be necessary to facilitate wound closure. Further discussion of the unique considerations for specific lacerations of facial structures is discussed below. The general tenants of facial laceration care as described above apply unless otherwise noted.

Eyelid Lacerations Eyelid lacerations can appear visually complex and perhaps even intimidating (Fig. 44.51). The relatively small amount of territory contains several layers of tissue and important associated structures. Technically, the eyelid itself is the skin that overlies the orbicularis muscle. Just beneath this muscular layer is a fibrous sheet of tissue that comprises the orbital septum. Toward the posterior aspect sits orbital fat separating the orbital septum from the levator muscle, which func-

Fig. 44.51  A complex, full-thickness upper eyelid laceration that should not be repaired by a team physician (Image courtesy of EyeRounds.org – University of Iowa)

tions to retract the eyelid. Lastly, the conjunctiva coats the inner aspect of the eyelid and makes direct contact with the surface of the eye. There are several other important structures around the eyelids that the astute team physician should recall. The lacrimal system is key among them. Along the medial aspect of the eyelid both superiorly and inferiorly rest puncta. Tears pass through these structures in canaliculi, which converge to form a canaliculus that in turn drains into the lacrimal sac. This entity sits just lateral to the nose and empties into the nasolacrimal duct. Recognizing these structures is critical to creating a plan for repairing eyelid lacerations, as damage to any of them warrants a referral to a subspecialist.

Initial Management Before a team physician entertains an eyelid repair in the training room or office, he or she should thoroughly assess the athlete for other ocular injuries. An open globe injury is chief among these concerns, and if sufficient suspicion is present a referral for immediate evaluation should be pursued. Other entities associated with eyelid lacerations include hyphemas, corneal abrasions, and foreign bodies. Most of these conditions are discussed elsewhere in this chapter. Some of these conditions may also warrant a CT scan of the orbits (e.g., to confirm a ruptured globe or to assess for the presence of a foreign body). Having addressed these concerns, one can then focus on repairing simple eyelid lacerations. Size matters, and these injuries are no different. Horizontal lacerations along the skin lines do not require primary closure if they involve 24 hours old and there is a risk of infection. Upon embarking on the procedure, selecting the anesthesia plan may be slightly different than for other facial

C. Hogrefe

Fig. 44.54  The vermillion border (black line) is the most critical landmark in repairing lip lacerations

lacerations. Direct infiltration of the lip should be avoided as it will distort the tissue and affect the cosmesis of the repair. Thus, the adept team physician will select between the infraorbital nerve block (Fig. 44.52) for upper lip lacerations and the mental nerve block for lower lip injuries (Fig.  44.56, which is discussed in detail later in this chapter). After thorough irrigation, debridement of the lip should be kept to a minimum. Removing such tissue can distort the original architecture of the lip and affect the cosmetic outcome. The presence of a large amount of devitalized tissue warrants consultation with a Plastic Surgeon, Otolaryngologist, or Oral Maxillofacial Surgeon. The vermillion border (the demarcation between the lip and the surrounding facial skin) is the landmark of critical importance for lip lacerations (Fig.  44.54). The vermillion tissue is either wet (inner portion of the lip when the mouth is closed) or dry (the outer, visible portion when the lips are closed). Superficial dry vermillion lip lacerations are straightforward. They should be closed with 5-0 or 6-0 chromic or fast-absorbing chromic gut suture. Simple interrupted sutures will suffice for this repair. As for superficial wet vermillion lacerations, a majority of them do not require closure. However, if such a laceration is >2 cm, has a gaping defect, or persistently bleeds it should be closed with absorbable 5-0 or 6-0 chromic gut. It is best to bury these sutures to avoid irritating the gums, mucosa, and/ or tongue. The most technically difficult lip laceration repair is the one that traverses the vermillion border. The first stitch in this repair is the most important. 6-0 non-absorbable suture should precisely reapproximate the vermillion border. Once this suture is in place, the remainder of the laceration can be closed with simple interrupted sutures. Non-absorbable 5-0 or 6-0 suture is preferred for this endeavor. If there is a con-

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cern about access to follow-up, 6-0 fast-absorbing chromic gut suture could be utilized in stead. Through-and-through lacerations of the lip warrant special consideration as well. Before the repair commences, traumatized minor salivary glands should be excised to prevent the formation of a mucocele. The vermillion border should then be approximated with a single 6-0 non-­ absorbable suture as described above. Then, the deep fibrofatty junction should be closed with 4-0 or 5-0 absorbable suture. Next, re-irrigate the wound from the external aspect. If the orbicularis oris muscle is involved it should be closed with 5-0 absorbable suture. At that point the wet and dry vermillion borders should be reapproximated as detailed previously. The remaining skin beyond the vermillion border can then be closed with 5-0 or 6-0 nonabsorbable suture. Again, 6-0 fast-absorbing gut could be used for this step, particularly if follow-up is a concern. Antibiotic prophylaxis is the next issue to consider in managing these wounds. The risk of wound infection following a laceration in or around the lip has been cited to be up to 27% [112]. The literature, however, is mixed on whether or not empiric antibiotics are beneficial. The totality of the evidence suggests that when significant mucosal involvement is present (i.e., the wet vermillion border), prophylactic antibiotics are appropriate (e.g., amoxicillin or clindamycin) [111]. Following the laceration repair, patients should apply topical antibiotic (e.g., bacitracin) to the laceration twice per day. A soft diet is advised for 2–3 days with water rinsing performed after food consumption. It is advisable to avoid spicy and/or salty foods until the wound is healed. Also, these patients should refrain from using straws to avoid compromising the repair.

Indications for Referral Plastic Surgery, Otolaryngology, or Oral Maxillofacial consultation should be considered in the context of crush wounds or a significant loss of tissue (especially those involving the upper lip), avulsion or luxation dental injuries, and/or associated facial fractures (e.g., Le Fort or mandible fractures).

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Pediatric Considerations As a general rule, 6-0 suture should be utilized for the repair of pediatric lip lacerations whenever possible. Due to the significant cosmetic and functional repercussions of this procedure, one’s threshold for referring the anxious or uncooperative pediatric athlete for procedural sedation should be lowered.

Tongue Lacerations The only muscle in the body attached at one end (barring injury), the tongue is extremely vascularized. As such, significant hemorrhage may result, which can impair one’s ability to repair the laceration (when needed) and also lead to hypovolemia or even shock. Hemostasis is the name of the game with tongue lacerations, as the muscle generally heals well and cosmesis is a secondary concern (if at all).

Initial Management Many tongue lacerations will not require any intervention. Particularly in adolescents, adequate healing will often transpire without a primary repair; treatment consists of a soft diet and dilute peroxide mouth rinses over several days. Indications for a suture repair are noted in Table 44.14. When indicated (Fig. 44.55), adequate repair of the laceration requires sufficient anesthesia, which can be particuTable 44.14  Indications for primary closure of tongue lacerations Lacerations >1–2 cm in length Through-and-through lacerations Large flaps or gaps in the tongue (Fig. 44.55) Lacerations with significant hemorrhage Bisection of the tongue

Follow-up Care Reassessment of the laceration repair should be performed by the team physician in 48–72  hours to ensure adequate healing. When non-absorbable sutures are placed, they can be removed in 3–5 days. Any absorbable sutures that persist beyond 5 days can also be extracted as well. Complications As previously suggested, suboptimal lip laceration repairs may result in cosmetically unacceptable outcomes and/or affect one’s speech. Significant scar development may occur in addition to localized infection and/or abscess formation.

Fig. 44.55  A tongue laceration with a gap that warrants primary closure

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larly difficult in very young patients. Consider the use of lidocaine-soaked gauze applied to the tongue for 5 minutes. One may also utilize 1% lidocaine with epinephrine to both anesthetize the tongue and help control the bleeding. Alternatively, an inferior alveolar nerve block (potentially bilaterally) can be effective in anesthetizing the tongue. Once sufficient analgesia is achieved, sutures can then be placed in an interrupted fashion. If possible, it is recommended to wrap the distal aspect of the tongue in gauze and maintain traction to facilitate an optimal repair. It is generally recommended that 4-0 absorbable sutures be utilized. Such sutures can become untied, and consequently burying the knots is advisable. When feasible, closure of all three layers of the tongue should be attempted (i.e., the inferior mucosa, muscle, and superior mucosa). However, closing the muscle layer of the tongue is generally sufficient to control the bleeding, and the mucosal layers will heal rapidly even if not completely reapproximated. For through-and-through lacerations, one should consider closing the top half of the tongue separately from the bottom half. Cosmesis is not generally a concern in the setting of tongue lacerations. While most lacerations will be due to human bites (by technicality), the risk of infection is low. Prophylactic antibiotics are not typically necessary, but in cases where they are deemed appropriate (e.g., contaminated wounds and associated fractures), amoxicillin-clavulanate is an appropriate choice. Dual therapy with trimethoprim-sulfamethoxazole and clindamycin in penicillin-allergic athletes is a reasonable option. Three to five days of treatment is considered sufficient. Post-repair instructions should highlight the maintenance of good oral hygiene to reduce the risk of infection, a soft diet for a couple of days to facilitate rapid healing, and the use of ice chips or popsicles (any flavor) to reduce the associated tongue edema.

Indications for Referral In the event that the laceration complexity is beyond the skillset of the team physician or the patient’s comfort level will not tolerate the repair (i.e., procedural sedation is needed), an immediate referral to an Emergency Department should be sought.

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additional complication. If they are not buried the knots can loosen and potentially compromise the repair.

Intraoral Lacerations Perhaps surprisingly, the majority of intraoral lacerations are the result of blunt trauma. However, traumatic causes exist (e.g., tooth bites), as do external mechanisms (e.g., an opponent’s finger). Due to the robust vascular supply, these lacerations heal quickly, and a majority of them will not require any intervention. Many of those that do necessitate an intervention can be addressed by the capable sideline physician. With that said, there are a couple of nuances of these injuries that warrant subspecialist evaluation and treatment.

Initial Management Care should be taken to assess for concomitant injuries. Be certain to ensure that the airway is intact and protected. Dental injuries (e.g., avulsion, luxation ) should be treated in advance of addressing any lacerations that are appreciated. Recognizing which intraoral lacerations require primary care closure is obviously critical in managing these injuries. Typically, if the wound is wide enough to collect food particles, is greater than 2 cm in length, or there is a flap of tissue that can interfere with mastication, a primary closure is recommended. In those cases, local or regional anesthesia should then be considered. Lidocaine or bupivacaine, either with or without epinephrine, is appropriate for such anesthesia. If one elects to proceed with a regional nerve block, several options are available to a provider depending upon the location of the intraoral laceration. An infraorbital nerve block (Fig. 44.52), mental nerve block (Fig. 44.56), and an inferior alveolar nerve block are all viable options. Once sufficiently numb, one may proceed with the necessary repair.

Follow-up Care Re-evaluation of the laceration repair is recommended within the first 48 hours to assess the wound healing and/or for complications. If dental injuries are noted, follow-up with a Dentist is advised within 24 hours of the injury. In the event that non-absorbable sutures are utilized, these should be removed approximately 5–7 days after placement. Complications Complications of tongue lacerations are rare but include localized infections. Suture knots can pose one potential

Fig. 44.56  Illustration of the proper placement of a mental nerve block

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Absorbable suture is the preferred choice for these lacerations, for instance 4-0 or 5-0 chromic gut. For gaping buccal mucosa and gingival lacerations in need of primary closure, one should place deep, buried, interrupted sutures in the submucosal tissue. These can then be followed by additional interrupted sutures in the mucosal surface. It is prudent to use as few sutures as possible to avoid irritation with chewing or tongue movement. For lacerations that feature gingival avulsions, further dissection of the tissue may be needed to facilitate the repair. If there is insufficient mucosal space to allow for passage of the suture, one can guide the needle between two nearby teeth, creating a flossing-type suture. The suture is then passed around a tooth and back through the avulsed tissue, with the knot overlying the lacerated tissue (Fig.  44.57) [104]. Post-procedural recommendations are similar to those provided for lip lacerations. These include a soft diet for 2–3 days and mouth rinsing with water following eating. Athletes should try to avoid spicy and/or salty foods until the wound is healed. Lastly, it is advisable to refrain from using straws; negative pressure can lead to ecchymosis and/or bleeding from the wound. In the setting of gaping wounds, antibiotic prophylaxis (e.g., amoxicillin or clindamycin) is recommended [113].

Indications for Referral Crush wounds and those with large defects should be evaluated by an Oral Surgeon or a Plastic Surgeon. Injuries that involve the salivary glands, parotid duct, and/or submandibular duct should be sent for immediate evaluation by such a subspecialist. As with other facial lacerations, when concomitant facial fractures are present that require a subspecialist evaluation, the athlete should be promptly referred. Such additional injuries include dental avulsions or luxations. Follow-up Care Most patients will not require any further follow-up (so long as absorbable suture is used), as these wounds heal rapidly. Any patients with risk factors for delayed wound healing

Fig. 44.57  A gingival avulsion laceration status post-primary closure

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(e.g., diabetes mellitus) should have the repair re-evaluated in 48–72 hours.

Complications Intraoral lacerations in isolation are not fraught with significant complications. Local infection and abscess formation are the primary complications for which a team physician should be vigilant.

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44  Facial Trauma 64. Lou Z, Lou Z, Tang Y, Xiao J. The effect of ofloxacin otic drops on the regeneration of human traumatic tympanic membrane perforations. Clin Otolaryngol. 2016;41(5):564–70. 65. Higuera S, Lee EI, Cole P, Hollier LH, Stal S. Nasal trauma and the deviated nose. Plast Reconstr Surg. 2007;120:64S–75S. 66. Cannon CR, Cannon R, Young K, Replogle W, Stringer S, Gasson E. Characteristics of nasal injuries incurred during sports activities: analysis of 91 patients. Ear Nose Throat J. 2011;90(8):E8–E12. 67. Marston AP, O’Brien EK, Hamilton GS. Nasal injuries in sports. Clin Sports Med. 2017;36:337–53. 68. Perkins S, Dayan S, Sklarew E, Hamilton M, Bussell G. The incidence of sports-related facial trauma in children. Ear Nose Throat J. 2000;79(8):632–8. 69. Logan M, O’Driscoll K, Masterson J.  The utility of nasal bone radiographs in nasal trauma. Clin Radiol. 1994;49(3):192–4. 70. Min H, Jang G, Hyun S, Jong S, Seong J, Sang H, Hae K. Comparison of high-resolution ultrasonography and computed tomography in the diagnosis of nasal fractures. J Ultrasound Med. 2009;28(6):717–23. 71. Bailey BJ. Head and neck surgery: otolaryngology. Philadelphia: Lippincott, Williams, and Wilkins; 2001. 72. Rohrich R, Adams W.  Nasal fracture management: minimizing secondary nasal deformities. Plast Reconstr Surg. 2000;106:266. 73. Cummings CW.  Cummings otolaryngology head and neck surgery. 4th ed. Philadelphia: Elsevier Mosby; 2005. 74. Haraldson SJ.  Nasal fracture follow-up. Medscape, 15 Dec 2016. [Online]. Available: http://emedicine.medscape.com/ article/84829-followup. 75. Lawrence R. Pediatric septoplasty: a review of the literature. Int J Pediatr Otorhinolaryngol. 2012;76(8):1078–81. 76. Fry H.  The pathology and treatment of haematoma of the nasal septum. Br J Plast Surg. 1969;22(4):331–5. 77. Perkins SW, Dayan SH. Management of nasal trauma. Aesthetic Plast Surg. 2002;26(Suppl 1):3. 78. Savage RR, Valvich C.  Hematoma of the nasal septum. Pediatr Rev. 2006;27:478–9. 79. Alvi A, Joyner-Triplett N. Acute epistaxis: how to spot the source and stop the flow. Postgrad Med. 1996;99(5):83. 80. Kucik CJ, Clenney T.  Management of epistaxis. Am Fam Physician. 2005;71(2):305. 81. Krempl GA, Noorily AD. Use of oxymetazoline in the management of epistaxis. Ann Otol Rhinol Laryngol. 1995;104(9 (Part 1)):704. 82. Corbridge R, Djazaeri B, Hellier W, Hadley J. A prospective randomized controlled trial comparing the use of Merocel nasal tampons and BIPP in the control of acute epistaxis. Clin Otolaryngol Allied Sci. 1995;20:305. 83. Badran K, Malik TH, Belloso A, Timms MS.  Randomized controlled trial comparing Merocel and Rapid Rhino packing in the management of anterior epistaxis. Clin Otolaryngol. 2005;30(4):333–7. 84. Pollice PA, Yoder MG.  Epistaxis: a retrospective review of hospitalized patients. Otolaryngol Head Neck Surg. 1997; 117(1):49. 85. Glassman M.  The first line of defense. N Y State Dent J. 1995;61(7):48–50. 86. Seidenberg PH, Beutler AI. The sports medicine resource manual. Philadelphia: Saunders Elsevier; 2008. p. 253–71. 87. Ranalli DN.  Dental injuries in sports. Curr Sports Med. 2005;4(1):12–7. 88. Ranalli DN.  Sports dentistry and dental traumatology. Dent Traumatol. 2002;18:231–6. 89. Kummamoto DP, Maeda Y. A literature review of sports-related orofacial trauma. Gen Dent. 2004;52(3):270–80. 90. Flanders RA, Bhat M. The incidence of orofacial injuries in sports: a pilot study in Illinois. J Am Dent Assoc. 2005;126(4):491–6.

801 91. N. F. o. S. H. S. A. (NFHS). Position statement and recommendations for mouthguard use in sports. 2014. [Online]. Available: https://www.nfhs.org/media/1014750/mouthguard-nfhs-smacposition-statement-october-2014.pdf. Accessed 2017. 92. N. C. Hospital. Mouthguards in sports: a necessary piece of equipment. 2017. [Online]. Available: http://www.nationwidechildrens. org/mouth-guards-in-sports-a-necessary-piece-of-equipment. 93. Gassner R, Tuli T, Hachl O, Rudisch A, Ulmer H.  Craniomaxillofacial trauma: a 10 year review of 9,543 cases with 21,067 injuries. J Craniomaxillofac Surg. 2003;31(1):51–61. 94. Andreasen J.  Etiology and pathogenesis of traumatic dental injuries. A clinical study of 1,298 cases. Eur J Oral Sci. 1970;78(1–4):329–42. 95. Mark DG, Granquist EJ.  Are prophylactic oral antibiotics indicated for the treatment of intraoral wounds? Ann Emerg Med. 2008;52(4):368–72. 96. McTigue DJ.  Evaluation and management of dental injuries in children. UpToDate, 11 Aug 2016. [Online]. Available: www. uptodate.com. 97. Schatz J, Hausherr C, Joho J. A retrospective clinical and radiologic study of teeth re-implanted following traumatic avulsion. Endod Dent Traumatol. 1995;11(5):235. 98. Kenny DJ, Barrett EJ, Casas MJ.  Avulsions and intrusions: the controversial displacement injuries. J Can Dent Assoc. 2003;69(5):308–13. 99. Mayersak RJ. Initial evaluation and management of facial trauma in adults. UpToDate, 7 Nov 2016. [Online]. Available: www.uptodate.com. 100. Keels MA. Management of dental trauma in a primary care setting. Pediatrics. 2014;133(2):e466. 101. Junge A, Langevoort G, Pipe A, Peytavin A, Wong F, Mountjoy M, Beltrami G, Terrell R, Holzgraefe M, Charles R, Dvorak J.  Injuries in team sport tournaments during the 2004 olympic games. Am J Sports Med. 2006;34(4):565–76. 102. Lorentzon R, Werdren H, Pietila T. Incidence, nature, and causes of ice hockey injuries: a three-year prospective study of a Swedish elite ice hockey team. Am J Sports Med. 1988;16(4):392–6. 103. Hollander JE, Singer AJ.  Laceration management. Ann Emerg Med. 1999;34(3):356. 104. Armstrong B. Lacerations of the mouth. Emerg Med Clin North Am. 2000;18(3):471. 105. Semer NB. Practical plastic surgery for nonsurgeons. Philadelphia: Hanley & Belfus, Inc.; 2001. 106. Brown DJ, Jaffe JE, Henson JK.  Advanced laceration management. Emerg Med Clin North Am. 2007;25(1):83. 107. Handschel J, Depprich R, Dirksen D, Runte C, Zimmermann A, Kubler N. A prospective comparison of octyl-2-cyanoacrylate and suture in standardized facial wounds. Int J Oral Maxillofac Surg. 2006;35(4):318–23. 108. Fisher CG, Kacica MA, Bennett NM.  Risk factors for cartilage infections of the ear. Am J Prev Med. 2005;29(3):204. 109. Malloy KM, Hollander JE. Assessment and management of auricle (ear) lacerations. UpToDate, 7 Nov 2016. [Online]. Available: www.uptodate.com. 110. Hollander JE, Camacho M. Assessment and management of facial lacerations. UpToDate, 18 Nov 2015. [Online]. Available: www. uptodate.com. 111. Hollander JE, Weinberger Conlon LN.  Assessment and management of lip lacerations. UpToDate, 1 June 2016. [Online]. Available: www.uptodate.com. 112. Abubaker AO.  Use of prophylactic antibiotics in preventing infection of traumatic injuries. Oral Maxillofac Surg Clin. 2009;21(2):259–64. 113. Hollander JE, Weinberger Conlon LN. Assessment and management of intra-oral lacerations. UpToDate, 29 Sept 2016. [Online]. Available: www.uptodate.com.

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Soft Tissue Neck Injury

45

Allison D. Lane

Key Points

• Cervical strain is the most common soft tissue neck injury. • Soft tissue neck injuries in sports are most common in contact sports and with high-velocity trauma. • Be aware of the potential for injury to vessels, digestive tract, and airway that require emergent evaluation and treatment. • In cases of penetrating injury with retained foreign body, stabilize the object, and DO NOT remove it. • Follow your ABCDs for initial management.

Introduction In sports, blunt neck trauma is much more common than penetrating trauma. The most common soft tissue neck injury in sports is a cervical strain. In most cases, this is usually a benign and self-limiting condition. However, there are other much less common injuries, which, if not recognized and treated appropriately, may cause significant morbidity or mortality. All soft tissue neck injuries occur more frequently in contact sports and with high-velocity trauma.

Anatomy Neck Borders • Posterior – spine • Anterior – larynx/trachea A. D. Lane (*) Department of Emergency Medicine, University of Arizona/Banner University Medical Center, Tucson, AZ, USA e-mail: [email protected]

• Superior – head • Inferior – chest

Neck Zones (Table 45.1 and Fig. 45.1) • Zone I – thoracic inlet to cricoid cartilage • Zone II – cricoid cartilage to angle of mandible • Zone III – angle of mandible to skull base Neck Contents • Musculoskeletal – vertebral bodies; cervical muscles, tendons, ligaments; clavicles; first and second ribs; hyoid bone • Neural – spinal cord, cervical roots of phrenic nerve and brachial plexus, recurrent laryngeal nerve, cranial nerves IX–XII, stellate ganglion • Vascular – carotids, vertebral arteries, vertebral vein, brachiocephalic vein, jugular veins • Visceral – thoracic duct, esophagus and pharynx, larynx and trachea • Glandular – thyroid, parathyroid, submandibular • Fascia – superficial and deep cervical fascia [1, 2].

Table 45.1  Zones of the neck for penetrating trauma Location Zone 1 Thoracic inlet to cricoid cartilage

Contents Mediastinal structures, thoracic duct, proximal carotid artery, vertebral/ subclavian artery, trachea, lung, esophagus Zone 2 Cricoid cartilage Carotid/vertebral artery, larynx, trachea, esophagus, jugular vein, vagus, and to angle of recurrent laryngeal nerves mandible Distal carotid artery, vertebral artery, Zone 3 Angle of mandible to skull distal jugular vein, salivary/parotid glands, CN 9–12 base

© Springer Nature Switzerland AG 2020 M. Khodaee et al. (eds.), Sports-related Fractures, Dislocations and Trauma, https://doi.org/10.1007/978-3-030-36790-9_45

803

804 Fig. 45.1  Neck zones (Illustrated by Dr. Yvonne Chow)

A. D. Lane

Parotid gland

Zone 3

Jugular vein Carotid artery

Zone 2

Esophagus Larynx Lung

Zone 1

Subclavian vessels Vagus nerve Recurrent laryngeal nerve

Blunt Neck Trauma Cervical Strain Mechanism of Injury • This is most commonly a stretch injury to the muscle fibers (strain) and/or ligament (sprain) from a traction-­ type injury or forceful contraction against resistance and most commonly occurs at the musculotendinous junction. • Cervical sprain and strain often occur in combination, in addition to a contusion from a direct blow to the soft tissues [3, 4]. Classification • Injury may be either acute or chronic. –– Chronic may include repetitive stress injury or abnormal strained posture. • Injury may also be high velocity or low velocity. –– Low velocity may vary from acute to chronic in presentation [4].  linical Presentation: Signs and Symptoms C • Presentation may vary from acute to chronic. • Pain can range from mild to severe. • Radicular pain can occur in all types of cervical spine injuries including strain. • Those with voluntary movement of the neck are less likely to have more significant injury. • Edema of cervical tissues without pitting is common. They may be boggy to tight. There may be mild warmth over involved tissues. • Limited range of motion due to muscle spasm is likely and does not necessarily reflect severity of injury. • In those with radicular symptoms, consider performing the Spurling maneuver to assist in differentiating nerve impingement from arthritic or disc herniation rather than muscular

or ligamentous strain. Reproduction of radicular symptoms with this maneuver suggests more than just strain [4].

Diagnosis • The most important issue is to differentiate cervical strain from a more serious injury. • Evaluation of the mechanism of injury may provide clues to the relative risk of strain versus other injury [4]. • Imaging to determine more serious injury may include x-ray (AP/lateral/odontoid views), CT, and/or MRI. Initial Management • Consider placement of a cervical collar if more than cervical strain is considered, if high-risk patient or mechanism, and according to protocols. • History and physical have been shown effective in guiding the need for imaging using NEXUS criteria or the Canadian c-spine rule [4]. • NEXUS criteria • The NEXUS criteria for c-spine is a well-validated clinical decision rule used to assist in safely ruling out cervical spine injuries without the need to obtain radiographic studies. • Initial validation studies showed a sensitivity of 99.6% for clinically significant cervical spine injuries (majority of subsequent studies showing 90-100% sensitivity) and a sensitivity of 99.0% for all cervical spine injuries. • There is no age cutoff, though use caution when applying the criteria to patients over 65 years of age, as sensitivity may be as low as 66-84% [5]. • The National Emergency X-Radiography Utilization Study (NEXUS) Low-Risk Criteria (NLC) state cervical spine radiography is indicated for patients with trauma unless they meet all the following criteria: –– No posterior midline cervical spine tenderness –– No evidence of intoxication –– A normal level of alertness

45  Soft Tissue Neck Injury

• •

•

• •

• • •

• • • • • •

•

–– No focal neurologic deficit –– No painful distracting injuries Canadian c-spine rule. The Canadian c-spine rule is also well validated. It performs as well or better than NEXUS in terms of sensitivity, but is more complex. It is highly sensitive for cervical spine injury, with a majority of studies showing 99-100%. It is easiest to use with a smartphone app or digital reference. Exclusion criteria: –– Non-trauma patients –– GCS < 15 –– Unstable vital signs –– Age 20 mmHg. • Fasciotomy is the definitive treatment though is rarely needed [12, 23]. • If exertional compartment is sustained, rhabdomyolysis may occur; rhabdomyolysis has also been documented in elite rowers as a result of rigorous exertion as well [24, 25].

Hook of Hamate Fracture • Hook of hamate fractures are rare but may occur in rowers given their extensive contact with the oar. • Athletes usually report pain over the hypothenar eminence and hamate hook. • Pain may be elicited with resisted flexion of the fourth and fifth fingers. • Plain radiography often provides inadequate visualization and CT is typically required for diagnosis. • Acute non-displaced fractures can be managed with cast immobilization, while displaced or non-united fractures generally require surgical intervention. • Complications of hook of hamate fracture include ulnar neuritis, flexor tendon irritation and rupture, ulnar artery thrombosis, and symptomatic nonunion [26].

66 Rowing

Triangular Fibrocartilage Complex Injury • Triangular fibrocartilage complex (TFCC) injuries occur from repetitive load bearing and rotational stresses. • The TFCC stabilizes the distal radioulnar joint (DRUJ) and also functions as a load absorber of the wrist. • Ulnar-sided wrist pain in the rower with associated tenderness in the foveal area with occasional clicks and pops may be found on physical examination. • Plain radiography should include a PA zero view rotation (with the shoulder abducted 90° and elbow flexed 90°), clenched fist pronation PA view, and contralateral views to assess ulnar variance, which may affect treatment decision if ulnocarpal abutment is suspected. • MRI (occasionally an MR arthrogram) may provide better visualization and aid in diagnosis. • Unstable DRUJs or stable symptomatic DRUJs may require surgical intervention [26].

Scapholunate Dissociation • Scapholunate dissociation or instability may be the cause of pain in the dorsoradial aspect of the wrist in a rower as a result of a tear to the scapholunate ligament. • Athletes may present with a “click” or “pain” in the dorsoradial region of the wrist that may be exacerbated on resisted second finger extension. • The classic clinical examination for scapholunate instability is the scaphoid shift test, which elicits a pain and/or a click. • Examination may also yield generalized ligamentous laxity. • Fluoroscopy or advanced imaging with CT or MR arthrogram may be necessary for diagnosis. Arthroscopy can confirm the diagnosis. • Surgical intervention is indicated for high-grade scapholunate ligament tears, while lower grade tears may be managed with splinting and PT [27, 28].

Neuropathology in Rowing • Nerve entrapments occur in rowers and range from digital nerve compression in the fingers, carpal tunnel syndrome, or sciatica in the lower extremity. • Digital nerve compression may be related to a tight grip with pressure localized to the neurovascular bundle. Equipment modification can alleviate symptoms.

925

• Carpal tunnel syndrome may also relate to a tight grip combined with repetitive wrist movements during feathering and squaring. Technique modification, loosening the grip, equipment changes, in addition to routine management usually alleviate symptoms. • Radial and ulnar neuropathies may also occur in rowers given the repetitive motion of the upper extremities. • Sciatica may occur as a result of an improperly fitted seat that places pressure on the sciatic nerve. Many seats have holes to accommodate the ischial tuberosities, and an improper fit may contribute to symptoms, especially in women given their wide pelvis [1, 29].

Parsonage–Turner Syndrome • Although the pathophysiology is not entirely understood, a rower who presents with acute onset upper extremity pain lasting for several days to weeks, followed by weakness and muscle atrophy may be suffering from Parsonage– Turner syndrome, also known as acute brachial neuritis. • Autoimmune, genetic, infectious, and mechanical processes have been implicated the pathophysiology. • Symptoms vary widely and may include pain, paresthesias, and sensory disturbances. • Pain is usually localized to the shoulder and often radiates into the arm or neck and aggravated by movement of the shoulder; symptoms are often unilateral, but bilateral pain followed by unilateral motor symptoms has been reported. • Muscle weakness typically begins days to weeks after the onset of pain and often worsens after the pain subsides. • EMG findings are often nondiagnostic and may provide more information 4–6 weeks after onset of symptoms. • Imaging may be useful in ruling out other disorders, including a Pancoast tumor (plain radiography) or nerve root compression with MRI. • Laboratory studies are generally not helpful in diagnosis. • Treatment requires a multidisciplinary approach including pharmacologic therapy with oral corticosteroids and opioids or NSAIDs in addition to physical therapy; surgery may be required for cases refractory to conservative therapy [30].

Quadrilateral Space Syndrome (QSS) • The quadrilateral space (QS) is bound superiorly by the teres minor or scapulohumeral capsule, inferiorly by the teres major and latissimus dorsi, laterally by the surgical neck of the humerus, and medially by the long head of the triceps.

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• QSS develops from injury to the axillary nerve or to the posterior circumflex humeral artery (PCHA) as they pass through the quadrilateral space. • Rowers are at risk given their repetitive shoulder movements. • Neurogenic QSS, or nQSS, causes non-dermatomal neuropathic pain, numbness, and weakness that radiates down the arm. The etiology is likely the result of fibrous bands or space-occupying lesions. • Vascular QSS, or vQSS, may result in thrombosis, microembolism, macroembolism, digital or hand ischemia, or signs/symptoms of acute ischemia. The etiology is likely related to repetitive mechanical injury to the PCHA as it passes through the QS. • Evaluation includes CT angiography, MR angiography, ultrasound, EMG, or digital subtraction angiography (DSA). • nQSS should be treated conservatively initially with NSAIDs and PT.  Definitive treatment involves surgical neurolysis and QS decompression. • vQSS treatment involves PCHA ligation with or without surgical thromboembolectomy and/or thrombolysis to prevent distal embolization. Anticoagulation should be considered for 3 months [31].

Thoracic Outlet Syndrome (TOS) • Thoracic outlet syndrome occurs when the neurovascular (brachial plexus, subclavian artery or vein) bundle passing through the thoracic outlet is compressed. Repetitive upper extremity movements may predispose those already at risk to develop TOS. • The thoracic outlet is the opening created by the first rib, the clavicle, the subclavius muscle, and costoclavicular ligament, and the anterior scalene. • Etiologies include trauma, repetitive stress, or postural abnormalities. • Those with an accessory rib or hypertrophied musculature in this region may be particular risk. • Neurogenic symptoms include pain, paresthesias, weakness; vascular symptoms suggest compression of the subclavian artery or vein. • Plain films may exclude an accessory rib; MRI/MRA are more useful in locating the neurovascular bundle and/or the presence of stenosis. • NSAIDs and opioids have been used for pain management, while corticosteroid injections may be diagnostic and therapeutic. • Surgery may be indicated for athletes with refractory symptoms [32].

A. T. Gomez and A. L. Rao

Dermatoses in Rowing • Handles should be cleaned so as not to expose open blisters to infection or spread infection to other athletes [1, 3, 12, 33]. • Repetitive trauma to wet, macerated, or traumatized hands may increase risk of inoculation with the papilloma virus, causing hand warts in crew athletes from boat oar handles [34]. • About 20 of 80 (25%) ofcrew members in one cohort reported they developed warts since beginning varsity crew, highlighting the importance of appropriate hygiene [34]. • Superficial abrasions at the MCP or PIP joints may occur in scullers resulting from impact from the opposing oar handle (known as “Sculler’s knuckles”) [1, 3, 12]. • “Slide bites” are abrasions that occur on the posterior lower leg resulting from contact between the skin and the track; protective layering with socks or tape prevent this common injury; these lesions should be monitored for infection [1, 3, 12]. • Abrasions from an improperly fitted seat are common and vary from irritation to ulcerations from repetitive chafing; management includes monitoring for infection, changing the seat, using a foam pad, and usage of petrolatum jelly [1, 3, 12]. • “Rower’s rump” has been described and may develop from repetitive frictional contact of the buttocks resulting in lichen simplex chronicus. Avoidance of friction, topical corticosteroids, or tar preparations are used for therapy [35]. • Any open lesions while rowing should be monitored, and proper hygiene should be encouraged to prevent the spread of infectious disease through skin breaks. • Sun protection is always encouraged. In one cohort, 44% of crew athletes never used sunscreen. Application of sunscreen is doubly important given the risk of exposure from sunlight reflected from the water [12, 36]. • Layering and a wind barrier may be necessary during colder months [12].

Trauma • “Catching a crab” involves inadvertent contact between the water and oar at the incorrect phase of the stroke. • This contact between the oar and the water typically causes the oar handle to abruptly move toward the rower often resulting in injuries related to impact. In certain instances, rowers can be ejected.

66 Rowing

• Contact injuries related to contact with the oar handle may include contusions, concussions, and superficial skin injuries [13]. • An ejected rower may suffer consequences of cold-water exposure or other infectious exposures depending on the circumstances. • If trauma occurs resulting in concussion, evaluate the athlete with a standardized approach.

 xercise-Associated Collapse (EAC), Syncope, E Sudden Cardiac Death • Rowing performance is associated with both aerobic and anaerobic capacity, resulting in unique hemodynamic alterations during exercise. • Blood pressures as high as 200 mmHg at the catch phase results from high cardiac output, while working against high systemic vascular resistance [37]. • Despite this, there is no evidence that rowers are at increased risk for sudden cardiac death relative to athletes in other sports. • Given the large number of competitors at rowing events, there is a possibility of EAC, syncope, or sudden cardiac death. • Management protocols for EAC, syncope, or sudden cardiac death pose unique logistical challenges [38]. • As AED use is contraindicated on the water, the medical team should have an emergency action plan prepared to rescue collapsed rowers and get them rapidly to shore. • Furthermore, an athlete that collapses while on the water is at risk of falling overboard, altering boat mechanics, or possibly causing capsize [2].

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Coverage of Rowing Events • Team physicians should familiarize themselves with common musculoskeletal injuries that occur among rowers, especially those that occur at the lower back, shoulder, and upper extremity. • Dermatopathology is common, and sideline medical personnel should be prepared to care for a variety of skin conditions. • Though more obscure, neurologic and vascular pathologies occur. • Emergency action plan (EAP) should be developed for possible traumatic events. • EAP consensus for traumatic events, EAC, syncope, cold-­ water immersion, and sudden cardiac arrest in rowing are in their early stages of development. In general, an athlete should be removed from the water if immersed and assessed quickly. Harbor patrol may be required for more significant emergencies. • Personal flotation devices should be available for all rowers.

Return to Play • As most injuries in rowing involve overuse, rehabilitation must focus on appropriate form (biomechanics) and rowing mechanics to avoid future injury. • Only athletes that are completely pain free from rib stress fractures may return to rowing. • Appropriate attention to skin conditions is required in order to prevent further deterioration, complications of infection, or spreading of infectious organisms to other athletes. • Although less prevalent, awareness of possible neurologic and vascular injuries expedites appropriate diagnosis, management, and return to play.

Cold-Water Immersion • Flotation devices must be easily available for all rowers. • Priority for rescue should be given to smaller and leaner individuals in cold-water rescue scenarios. • After triage, athletes with the most severe hypothermia should be attended to first. • In potential cold-water rescue situations, heating devices should be available, including heating pads/packs and forced air warming devices. • Cardiopulmonary bypass, if available, should be initiated for hypothermic patients in asystole or ventricular fibrillation [39].

References 1. Perron AD. Crew. In: O’Connor FG, editor. ACSM’s sports medicine: a comprehensive review. Philadelphia: USA Wolters Kluwer; 2012. p. 593–5. 2. Karlson KA. Rowing: sport-specific concerns for the team physician. Curr Sports Med Rep. 2012;11(5):257–61. 3. Rumball JS, Lebrun CM, Di Ciacca SR, Orlando K. Rowing injuries. Sports Med. 2005;35(6):537–55. 4. Hosea TM, Hannafin JA.  Rowing injuries. Sports Health. 2012;4(3):236–45. 5. Baugh CM, Kerr ZY. High school rowing injuries: National Athletic Treatment, Injury and Outcomes Network (NATION). J Athl Train. 2016;51(4):317–20.

928 6. Smoljanovic T, Bojanic I, Hannafin JA, Hren D, Delimar D, Pecina M. Traumatic and overuse injuries among international elite junior rowers. Am J Sports Med. 2009;37(6):1193–9. 7. Verrall G, Darcey A.  Lower back injuries in rowing national level compared to international level rowers. Asian J Sports Med. 2014;5(4):e24293. 8. Wilson F, Gissane C, Gormley J, Simms C. A 12-month prospective cohort study of injury in international rowers. Br J Sports Med. 2010;44(3):207–14. 9. Hickey GJ, Fricker PA, McDonald WA. Injuries to elite rowers over a 10-yr period. Med Sci Sports Exerc. 1997;29(12):1567–72. 10. Teitz CC, O’Kane J, Lind BK, Hannafin JA. Back pain in intercollegiate rowers. Am J Sports Med. 2002;30(5):674–9. 11. O’Kane JW, Teitz CC, Lind BK. Effect of preexisting back pain on the incidence and severity of back pain in intercollegiate rowers. Am J Sports Med. 2003;31(1):80–2. 12. Thornton JS, Vinther A, Wilson F, Lebrun CM, Wilkinson M, Di Ciacca SR, et al. Rowing injuries: an updated review. Sports Med. 2016; 13. McNally E, Wilson D, Seiler S.  Rowing injuries. Semin Musculoskelet Radiol. 2005;9(4):379–96. 14. Roston AT, Wilkinson M, Forster BB. Imaging of rib stress fractures in elite rowers: the promise of ultrasound? Br J Sports Med. 2017; 15. McDonnell LK, Hume PA, Nolte V.  Rib stress fractures among rowers: definition, epidemiology, mechanisms, risk factors and effectiveness of injury prevention strategies. Sports Med. 2011;41(11):883–901. 16. Karlson KA. Rib stress fractures in elite rowers. A case series and proposed mechanism. Am J Sports Med. 1998;26(4):516–9. 17. Vinther A, Thornton JS. Management of rib pain in rowers: emerging issues. Br J Sports Med. 2016;50(3):141–2. 18. Christiansen E, Kanstrup IL. Increased risk of stress fractures of the ribs in elite rowers. Scand J Med Sci Sports. 1997;7(1):49–52. 19. Brukner P, Khan K. Stress fracture of the neck of the seventh and eighth ribs: a case report. Clin J Sport Med. 1996;6(3):204–6. 20. Wilson F, McGregor A, Milne C, Waddell R, Trease L, Edgar M, et  al. Mythbusters in rowing medicine and physiotherapy: nine experts tackle five clinical conundrums. Br J Sports Med. 2014;48(21):1525–8. 21. DeFroda SF, Nacca C, Waryasz GR, Owens BD.  Diagnosis and Management of Distal Clavicle Osteolysis. Orthopedics. 2016:1–6. 22. Hanlon DP, Luellen JR. Intersection syndrome: a case report and review of the literature. J Emerg Med. 1999;17(6):969–71. 23. Harrison JW, Thomas P, Aster A, Wilkes G, Hayton MJ. Chronic exertional compartment syndrome of the forearm in elite rowers: a technique for mini-open fasciotomy and a report of six cases. Hand (N Y). 2013;8(4):450–3.

A. T. Gomez and A. L. Rao 24. Keltz E, Khan FY, Mann G.  Rhabdomyolysis. The role of diagnostic and prognostic factors. Muscles Ligaments Tendons J. 2013;3(4):303–12. 25. Hansen KN, Bjerre-Knudsen J, Brodthagen U, Jordal R, Paulev PE. Muscle cell leakage due to long distance training. Eur J Appl Physiol Occup Physiol. 1982;48(2):177–88. 26. Henderson CJ, Kobayashi KM. Ulnar-sided wrist pain in the athlete. Orthop Clin North Am. 2016;47(4):789–98. 27. Chennagiri RJ, Lindau TR. Assessment of scapholunate instability and review of evidence for management in the absence of arthritis. J Hand Surg Eur Vol. 2013;38(7):727–38. 28. Cassidy CR.  L. K. fractures and dislocations of the carpus. In: Browner BDJ, B J, Krettek C, Anderson PA, editors. Skeletal trauma: basic science, management, and reconstruction. 5th ed. Philadelphia: Elsevier, Saunders; 2015. p. 1217–62.e7. 29. Karlson KA.  Rowing injuries: identifying and treating muscu loskeletal and nonmusculoskeletal conditions. Phys Sportsmed. 2000;28(4):40–50. 30. Smith CC, Bevelaqua AC.  Challenging pain syndromes: Parsonage-Turner syndrome. Phys Med Rehabil Clin N Am. 2014;25(2):265–77. 31. Brown SA, Doolittle DA, Bohanon CJ, Jayaraj A, Naidu SG, Huettl EA, et al. Quadrilateral space syndrome: the Mayo Clinic experience with a new classification system and case series. Mayo Clin Proc. 2015;90(3):382–94. 32. Twaij H, Rolls A, Sinisi M, Weiler R. Thoracic outlet syndromes in sport: a practical review in the face of limited evidence – unusual pain presentation in an athlete. Br J Sports Med. 2013;47(17):1080–4. 33. Knapik JJ, Reynolds KL, Duplantis KL, Jones BH.  Friction blisters. Pathophysiology, prevention and treatment. Sports Med. 1995;20(3):136–47. 34. Roach MC, Chretien JH. Common hand warts in athletes: association with trauma to the hand. J Am Coll Heal. 1995;44(3):125–6. 35. Tomecki KJ, Mikesell JF.  Rower’s rump. J Am Acad Dermatol. 1987;16(4):890–1. 36. Wysong A, Gladstone H, Kim D, Lingala B, Copeland J, Tang JY.  Sunscreen use in NCAA collegiate athletes: identifying targets for intervention and barriers to use. Prev Med. 2012;55(5):493–6. 37. Whyte G, Stephens N, Budgett R, Sharma S, Shave RE, McKenna WJ. Exercise induced neurally mediated syncope in an elite rower: a treatment dilemma. Br J Sports Med. 2004;38(1):84–5. 38. Asplund CA, O’Connor FG, Noakes TD. Exercise-associated collapse: an evidence-based review and primer for clinicians. Br J Sports Med. 2011;45(14):1157–62. 39. Giesbrecht GG, Hayward JS.  Problems and complications with cold-water rescue. Wilderness Environ Med. 2006;17(1):26–30.

67

Rugby Darcy Selenke

Key Points

• Rugby is a contact sport centered around the movement of an oval ball down a field to a goal line. • It is a high-velocity game, and no specific protective gear is worn. • Most injuries are associated with tackling. • Lower limb injuries occur more often than other body parts. • Most available injury data comes from Rugby Union at the professional level. • Concussions are a common injury.

Introduction Rugby is a contact sport involving an oval ball that evolved from the Greek and Roman games that involved kicking an air-filled ball. It was developed in England in the 1800s. It is the precursor to Canadian and American Gridiron Football. There are two forms of the game, Rugby Union and Rugby League. They differ in rules concerning how possession is maintained or given up. Rugby Union has scrum, mauls, and rucks, but Rugby League does not. Both games use passing of the ball, tackling and kicking of the football to maintain possession of the ball and score. Scoring requires that the ball cross a goal line at opposing ends of the field of play. There are a few unique play formations in rugby. These include mauls, rucks, and scrums. A maul is when the ball carrier joins with teammates to push the ball down the field, and the opposing team members also join together to oppose the other team (Fig. 67.1). A ruck is when the ball carrier is D. Selenke (*) Department of Family Medicine, University of Colorado School of Medicine, Denver Health, Winter Park Medical Center, Winter Park, CO, USA e-mail: [email protected]

tackled and places the ball on the ground, and then his teammates defend the ball by pushing away the defensive players. A scrum is when the opposing teams line up pushing against each other to take possession of the ball after a penalty that stopped play. Players are divided into back row and front row positions. In the back row are a flanker, an eighthman, and two locks. The front row consists of hookers and props. The flanker’s job is to tackle the opposition and try to steal the ball. The eighthman is a utilitarian position that can move the ball out of the scrum, carry the ball, and provide extra force in the scrum. Locks are usually the tallest players, provide force from behind to the front line during the scrum, and are targeted to catch the ball during a line out. Hookers are in the middle of the front row during a scrum, locked arm and arm with the props, and try to hook the ball toward the line with their foot or disrupt the other team’s attempt at getting the ball in the scrum. Hookers often carry the ball upfield during open play. Props are the force on the front line and provide stability during the scrum. During a line-out, the props support the jumpers that are trying to get high enough to acquire the ball. Most games are played on grass or turf. There is not specific protective gear worn except optional mouthguards and scrum caps (that protect ears).

Injury Epidemiology Injury patterns and incidents vary across different studies, gender and levels of rugby play and include head to toe injuries. The most comprehensive injury data at the professional level is the England Professional Rugby Injury Surveillance Project (EPRIS) [1]. The latest published data is from the 2015 to 2016 season. The overall incident of injuries has slowly declined from 100/1000  h played to 62/1000 since 2002. The severity of injury has also decreased. This is thought to be the result of formal concussion recognition programs, introduction of a new

© Springer Nature Switzerland AG 2020 M. Khodaee et al. (eds.), Sports-related Fractures, Dislocations and Trauma, https://doi.org/10.1007/978-3-030-36790-9_67

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Fig. 67.1  Maul. (Reprinted with permission from iStock#535116333)

scrum engagement sequence and changes in the line out process of bringing the ball back into play after it has gone out of bounds. During play, the causes of injury observed in the EPRIS study are as follows: tackling (45%), collision (15%), running (9%), ruck (8%), scrum (4%), maul (3%), line out (2%), and unknown (10%) [1]. The most common cause of injury is during tackling at all levels of rugby. The EPRIS findings show that the ball carrier suffers the injury at a slightly higher rate that the tackler [1]. The distribution of injuries during tackling for the ball carrier is concussion (20%), MCL injury (7%), ACL injury (7%), and ankle syndesmosis sprain (4%) [1]. Injuries of the tackler are concussion (47%), ACJ injury (7%), cervical spine stinger/burner (3%), and elbow hyperextension (2%) [1]. Tackles from the side caused the highest injury rate. Increasing tackling technique proficiency has been shown to lower injury rates [2–5]. Concussion rates have increased over the past 20 years, and it is unclear if that is a result of purely a higher rate of injury, improved reporting, or better recognition of concussion. The latter reasons are the most probable. Concussion rates vary across studies from 3% to 17% of all injuries and have become the most common rugby injury. Concussions

occur from head to head, head to body, and head to ground mechanisms. In 2015, World Rugby adopted the head injury assessment into law, making it a standard in on field concussion recognition and management [6]. These measures dictate that any player with a suspected head injury sit out at least 10 minutes and receive a side-line assessment. Any player with confirmed concussion signs or symptoms cannot return to play for at least 6 days, and further cognitive assessment such at the SCAT tool needs to be implemented in their return to play treatment plan. Adolescent concussion rates range from 0.2 to 6.9 per 1000 player hours for rugby union and 4.6–14.7 per 1000 player hours for rugby league [7]. In general, just over half of injuries in rugby are closed soft tissue injuries [8]. Injuries are divided among capsular/ ligament sprains or tears (20–34%), muscle/tendon strains or tears (20–29%), open wounds (12–27%), bruises/hematomas (10–22%), fractures (4–14%), and lastly concussion (3–25%) [8]. Hamstring injuries are the most commonly seen and highest risk soft tissue injury. Acromioclavicular joint, ankle lateral ligament, ACL, and calf injuries are also quite common. Dislocations of the shoulder and finger occur at lower rates, but require immediate sideline management. Clavicle fractures are the most common type of fracture [8].

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Spinal cord injuries are a very small portion of rugby injuries. Most commonly, cervical cord neurapraxia (cervical “stinger”) occur with direct axial load to the top of the head. These are self-limited events that do not lead to persistent neurologic symptoms. Acute spinal cord injuries with permanent neurological sequelae and traumatic brain injury was reported as 4.25/100,000 players by a study in South Africa from 2008 to 2011 [9]. In the lumbar region, violent collisions with or without existing disk herniation can lead to paraplegia. The recent changes in rules regarding how a player enters the scrum have decreased serious spinal injuries [9]. Injuries to the torso occur frequently and must be accurately assessed. The rate of thoracic injuries is 8.3/1000 player hours [10]. Rib, clavicle, and scapular fractures can be associated with significant vascular and internal organ injury. Players with shortness of breath, thoracic bony tenderness, signs of internal organ damage, or persistent pain need to be kept out of the game and referred to a higher level of medical assessment and care. These injuries often require x-ray and CT scan evaluation to understand the full breadth of injury [10]. Injury rates are similar forward and back. However, it is a common belief that the seriousness of injuries is higher for forwards. This is thought to be due to higher rates of high-­ velocity collisions. The specific data on injuries by position is varied and inconclusive [8]. In adolescent rugby, higher weight and higher levels of competition were associated with higher rates of injury [11]. Concussions lead to the most time out of play [11]. The most common sites of injury are head/face, clavicle/shoulder, and knee. This was followed closely by ankle injuries [11]. There is limited data available in terms of women’s rugby injuries. Overall women rugby players have a lower injury rate than men. The most common injury in women’s rugby is knee followed by ankle injuries [12]. Concussion rates are also lower for women players as opposed to men [12]. Preparation for sideline providers should be the same for both sexes and all age groups. Programs such as Boksmart, a youth injury prevention program in South Africa, have been shown to lower injury rates [2]. There has been no definitive evidence showing a difference in injury rates or patterns when comparing play on turf versus grass [13]. Highest rate of injury occurs in the second and fourth quarters [13].

What Is Unique About Rugby Injuries? • The high physical velocity and high level of contact of the game lends itself to all types of traumatic athletic mechanisms. • No protective equipment is required. • Higher skill/proficiency of tackling leads to lower injury rates.

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 hat Do the Physicians Need to Know While W Covering a Rugby Game on the Sideline? • Be prepared to evaluate and treat the lower extremity, shoulder, and finger injuries, skin wounds, and blunt chest trauma. • Know how to reduce shoulder and finger dislocations. • Know how to assess extent of blunt chest trauma. • Be aware of concussion assessment and return to play protocols. • Be equipped to clean, dress, and possibly repair skin wounds.

General Rule About Return to Play • General concussion protocol should be applied. • Players with joint injuries that require dislocation reduction cannot return to play until further evaluation. • Players with complete ligamentous ruptures cannot return to play. • Players with finger and mild soft tissue injuries can be taped or splinted for return to play. • Athletes with neck stingers may return to play after all neck pain and neurologic symptoms have resolved. • Any blunt chest trauma resulting in shortness of breath, persistent pain, or bony tenderness requires further evaluation, and the player should not return to play.

References 1. England Professional Rugby Injury Surveillance Project, 2015–2016 Season Report. Accessed on December 16, 2017. Available at: http://www.englandrugby.com/mm/Document/ General/General/01/32/25/17/1516_PRISP_Annual_Report_ FINAL(withcontentspage)_English.pdf. 2. Brown JC, Gardner-Lubbe S, Lambert MI, van Mechelen W, Verhagen E. Coach-directed education is associated with injuryprevention behaviour in players: an ecological cross-sectional study. Br J Sports Med. 2018;52(15):989–93. 3. Brown JC, Gardner-Lubbe S, Lambert MI, Van Mechelen W, Verhagen E.  The BokSmart intervention programme is associated with improvements in injury prevention behaviours of rugby union players: an ecological cross-sectional study. Inj Prev. 2015;21(3):173–8. 4. Burger N, Lambert MI, Viljoen W, Brown JC, Readhead C, Hendricks S. Tackle technique and tackle-related injuries in high-­ level South African Rugby Union under-18 players: real-match video analysis. Br J Sports Med. 2016;50(15):932–8. 5. Burger N, Lambert MI, Viljoen W, Brown JC, Readhead C, den Hollander S, Hendricks S.  Mechanisms and factors associated with tackle-related injuries in South African Youth Rugby Union Players. Am J Sports Med. 2017;45(2):278–85. 6. World Rugby Concussion Guidance. Accessed on December 16, 2017. Available at: http://playerwelfare.worldrugby. org/?documentid=158.

932 7. Kirkwood G, Parekh N, Ofori-Asenso R, Pollock AM. Concussion in youth rugby union and rugby league: a systematic review. Br J Sports Med. 2015;49(8):506–10. 8. Kaux J, Julia M, Delvaux F, Croisier J, Forthomme B, Monnot D, Chupin M, Crielaard J, Le Goff C, Durez P, Ernst P, Guns S, Laly A. Epidemiological review of injuries in rugby union. Sports. 2015;3:21–9. 9. Brown JC, Lambert MI, Verhagen E, Readhead C, van Mechelen W, Viljoen W. The incidence of rugby-related catastrophic injuries (including cardiac events) in South Africa from 2008 to 2011: a cohort study. BMJ Open. 2013;3(2). pii: e002475. 10. Hayashi D, Roemer FW, Kohler R, Guermazi A, Gebers C, De Villiers R. Thoracic injuries in professional rugby players: mecha-

D. Selenke nisms of injury and imaging characteristics. Br J Sports Med. 2014 Jul;48(14):1097–101. 11. Archbold HA, Rankin AT, Webb M, Nicholas R, Eames NW, Wilson RK, Henderson LA, Heyes GJ, Bleakley CM. RISUS study: Rugby injury surveillance in Ulster Schools. Br J Sports Med. 2017 Apr;51(7):600–6. 12. Taylor AE, Fuller CW, Molloy MG. Injury surveillance during the 2010 IRB Women’s Rugby World Cup. Br J Sports Med. 2011 Dec;45(15):1243–5. 13. Fuller CW, Brooks JH, Cancea RJ, Hall J, Kemp SP. Contact events in rugby union and their propensity to cause injury. Br J Sports Med. 2007 Dec;41(12):862–7; discussion 867

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Sailing Jeremy D. Close and Hannah P. Leahy

Table 68.1  Types of sailing crafts

Key Points

• Highly variable injuries exist, given the type of craft, the position of the crew member, and the weather or environmental conditions. • Sailors are at risk of both acute injury and chronic overuse injury. • Low back injuries are common in sailing. • Heavy weather is the most significant risk factor for acute injury during sailing. • Bowman are at the highest risk of acute injury and subject to the most physiologic stress such as hyperthermia or dehydration. • Most injuries are related to trip or fall events and can be in part avoided by proper communication and equipment.

Introduction Sailing has been done for thousands of years as a means of traveling. It was first widely recognized as a sport in 1851 with the start of America’s Cup competition. It was included in Olympic competitions as early as 1896. It has become a very popular sport over the last 20 years due to increases in sponsorship, commercialization, and media attention [1]. It requires great technical skill as well as physical and mental endurance to compete in sailing races. The environ-

J. D. Close (*) Department of Family and Community Medicine, Sports Medicine, Thomas Jefferson University, Philadelphia, PA, USA e-mail: [email protected] H. P. Leahy Department of Physical Medicine and Rehabilitation, Wellspan Health, Gettysburg, PA, USA

Keelboat (Fig. 68.1) >2 crew members Weighted keel provides stability

Dinghy (Fig. 68.2) 1–2 crew members Body mass of crew provides stability

mental conditions are a large variable that sailors must face, which can greatly impact their risk of injury. There are two types of competitive sailing crafts, keelboats and dinghies (Table  68.1). Keelboats are typically larger than dinghies. They tend to be more stable due to the weighted keel (Fig. 68.1). Dinghy racing is done in relatively small boats. This type of boat relies upon a motion called hiking, which is a technique that uses body weight to keep the boat upright (Fig.  68.2). This motion requires a lot of leverage and strength.

Injury Epidemiology The most common injuries in sailing are sprains, lacerations, contusions, and fractures. The most common mechanism of injury is trip/fall and getting caught in the lines (Table 68.2). Injuries are typically related to sail change or crossing over the centerline while tacking (Table  68.3). Rates of injury have varied in the literature from 0.42 per 1000 h to 2.2 per 1000 h [1, 3]. The location and type of injury varies based on experience of the sailor, boat type, boat position, and weather conditions. Inclement weather has been found to contribute to 23% of injuries [1].

Sailor Experience Inexperienced or recreational sailors tend to injure their hands or head more frequently, whereas more experienced sailors tend to suffer from chronic strains, sprains, or tendinopathies [1]. In a study of beginner dinghy sailors, not

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Fig. 68.1  A dinghy boat. (Reprinted with permission from iStock – photo ID:479579196)

Fig. 68.2  A keelboat. (Reprinted with permission from iStock – photo ID:475069301)

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Boat Position

Table 68.2  Mechanism of injury (by boat type) Mechanism of injury Trip/fall Caught in lines Hit by object Winch Fall overboard N/A Other

Keelboat (%) 30 22 21 8 2 7 10

Dinghy (%) 19 12 21 0 4 6 38

Adapted from Nathanson et al. [2]

Table 68.3  Activity associated with acute injury during sailing Activity Sail change Crossing centerline during tack Tailing Grinding Walking Steering Hiking Climbing mast Trapeze N/A Other

Keelboat (%) 18 17 10 9 8 8 5 1 0 5 18

Dinghy (%) 3 14