Shoulder Instability in the Athlete: Management and Surgical Techniques for Optimized Return to Play [1 ed.] 2020034481, 2020034482, 9781630916640, 9781630916657, 9781630916664, 163091665X, 1630916668, 1630916641

Citation preview

Dickens • Owens

SHOULDER INSTABILITY Management and Surgical Techniques for Optimized Return to Play Shoulder Instability in the Athlete: Management and Surgical Techniques for Optimized Return to Play is a groundbreaking text that covers all aspects of care for athletes with shoulder instability—from on-the-field management and treatment to successful return to play. Edited by Drs. Jonathan F. Dickens and Brett D. Owens and featuring the expertise of internationally recognized surgeons who specialize in shoulder instability in high-level athletes, Shoulder Instability in the Athlete is a unique collaboration applicable across a variety of professional areas. This will be the premier reference for physicians, surgeons, therapists, trainers, and students involved in the care of athletes. Each chapter of Shoulder Instability in the Athlete reviews cutting-edge clinical and surgical techniques, as well as outcomes and return-to-play criteria. In-depth analysis of appropriate literature and outcomes specific to the athlete population are also presented. Important sections within the text include:

Principles for the Team Physician Anterior Instability Posterior Instability Special Topics in Instability

By focusing specifically on the unique and challenging dilemma of caring for the athlete with shoulder instability, Shoulder Instability in the Athlete will be a valuable reference for all health professionals who manage athletes.

SHOULDER INSTABILITY IN THE ATHLETE Management and Surgical Techniques for Optimized Return to Play

IN THE ATHLETE

Jonathan F. Dickens Brett D. Owens

SHOULDER INSTABILITY

IN THE ATHLETE

Management and Surgical Techniques for Optimized Return to Play SLACK Incorporated

®

®

MEDICAL/Orthopedics

https://t.me/mebooksfree

Editors

Jonathan F. Dickens, MD Chief, Sports Medicine, Walter Reed National Military Medical Center Vice Chair (Research), Department of Surgery, Uniformed Services University Associate Professor of Surgery, Uniformed Services University Adjunct Faculty, John A. Feagin Jr. Sports Medicine Fellowship, USMA Bethesda, Maryland

Brett D. Owens, MD Professor of Orthopaedic Surgery Brown University Alpert Medical School Providence, Rhode Island

SLACK Incorporated 6900 Grove Road Thorofare, NJ 08086 USA 856-848-1000 Fax: 856-848-6091 www.healio.com/books © 2021 by SLACK Incorporated

Senior Vice President: Stephanie Arasim Portnoy Vice President, Editorial: Jennifer Kilpatrick Vice President, Marketing: Mary Sasso Acquisitions Editor: Julia Dolinger Managing Editor: Allegra Tiver Creative Director: Thomas Cavallaro Cover Artist: Stacy Marek Project Editor: Dani Malady

All rights reserved. No part of this book may be reproduced, stored in a retrieval system or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without written permission from the publisher, except for brief quotations embodied in critical articles and reviews. The procedures and practices described in this publication should be implemented in a manner consistent with the professional standards set for the circumstances that apply in each specific situation. Every effort has been made to confirm the accuracy of the information presented and to correctly relate generally accepted practices. The authors, editors, and publisher cannot accept responsibility for errors or exclusions or for the outcome of the material presented herein. There is no expressed or implied warranty of this book or information imparted by it. Care has been taken to ensure that drug selection and dosages are in accordance with currently accepted/recommended practice. Off-label uses of drugs may be discussed. Due to continuing research, changes in government policy and regulations, and various effects of drug reactions and interactions, it is recommended that the reader carefully review all materials and literature provided for each drug, especially those that are new or not frequently used. Some drugs or devices in this publication have clearance for use in a restricted research setting by the Food and Drug and Administration or FDA. Each professional should determine the FDA status of any drug or device prior to use in their practice. Any review or mention of specific companies or products is not intended as an endorsement by the author or publisher. SLACK Incorporated uses a review process to evaluate submitted material. Prior to publication, educators or clinicians provide important feedback on the content that we publish. We welcome feedback on this work. Library of Congress Cataloging-in-Publication Data Names: Dickens, Jonathan F., editor. | Owens, Brett D., 1972- editor. Title: Shoulder instability in the athlete : management and surgical techniques for optimized return to play / editors, Jonathan F. Dickens, Brett D. Owens. Description: Thorofare, NJ : SLACK Incorporated, [2021] | Includes bibliographical references and index. Identifiers: LCCN 2020034481 (print) | LCCN 2020034482 (ebook) | ISBN 9781630916640 (hardcover) | ISBN 9781630916657 (epub) | ISBN 9781630916664 Subjects: MESH: Joint Instability--therapy | Shoulder | Athletes | Shoulder Injuries--therapy | Athletic Injuries--therapy Classification: LCC RD557.5 (print) | LCC RD557.5 (ebook) | NLM WE 810 | DDC 617.5/72044--dc23 LC record available at https://lccn.loc.gov/2020034481 LC ebook record available at https://lccn.loc.gov/2020034482 For permission to reprint material in another publication, contact SLACK Incorporated. Authorization to photocopy items for internal, personal, or academic use is granted by SLACK Incorporated provided that the appropriate fee is paid directly to Copyright Clearance Center. Prior to photocopying items, please contact the Copyright Clearance Center at 222 Rosewood Drive, Danvers, MA 01923 USA; phone: 978-750-8400; website: www.copyright.com; email: [email protected]

DEDICATION This book is dedicated to my family: to my wife, Amy; my children, Mary Gray and Jonathan; and my loving and supportive parents, who taught me the value of hard work, a positive attitude, and perseverance. —Jonathan F. Dickens, MD I would like to dedicate this text to my family: my wife, Julie, and children, Cassidy, Ryan, Jocelyn, and Bennett. I thank my parents and brother for helping instill a foundation of integrity and service, and my mentors in orthopedics, many of whom I am proud to have contribute to this text. Finally, I dedicate this text to my patients, whom have taught me more than can be captured in a text. —Brett D. Owens, MD

The authors would like to further dedicate this book to Dr. John A. Feagin, Jr. He was the ultimate mentor who made everyone who knew him better. We are fortunate to have had the opportunity to walk by your side for a part of this journey.

CONTENTS Dedication . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .v Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ix About the Editors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xi Contributing Authors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xiii Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xvii Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xix

Section I

Principles for the Team Physician . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

Chapter 1

Team Physician Principles for the Management of Athletes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .3 Jessica L. Brozek, MD and Bradley J. Nelson, MD

Chapter 2

Epidemiology of Shoulder Instability: Incidence, Risk Factors, and Prevention of Instability in the Athlete . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11 David J. Tennent, MD; Matthew A. Posner, MD; and Kenneth L. Cameron, PhD, MPH, ATC

Chapter 3

Evaluation of Shoulder Instability on the Field and in the Clinic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .19 Francis P. Bustos, MD; Jeremy K. Rush, MD, FAAP; and Stephen F. Brockmeier, MD

Chapter 4

Clinical Anatomy and Biomechanics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .29 David Eldringhoff, MD; Barry I. Shafer, PT, DPT, ATC; Gregory J. Adamson, MD; and Thay Q. Lee, PhD

Section II

Anterior Instability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41

Chapter 5

Management of In-Season Anterior Instability and Return-to-Play Outcomes . . . . . . . . . . . . . . . . . . . . . . . .43 Jonathan F. Dickens, MD and Maj. Michael A. Donohue, MD

Chapter 6

Decision Making in Surgical Treatment of Athletes With First-Time vs Recurrent Shoulder Instability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .55 Brian C. Lau, MD; Carolyn A. Hutyra, MMCi; and Dean C. Taylor, MD

Chapter 7

Radiographic and Advanced Imaging to Assess Anterior Glenohumeral Bone Loss . . . . . . . . . . . . . . . . . . .67 Lisa K. O’Brien, DO and Brian R. Waterman, MD

Chapter 8

Arthroscopic Anterior Shoulder Instability in the Athlete . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .79 Lauren A. Szolomayer, MD and Robert Arciero, MD

Chapter 9

Open Treatment of Anterior Instability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91 Michael J. Pagnani, MD and Jason A. Jones, MD

Chapter 10

Latarjet and Coracoid Transfer in Athletes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .103 Alexander Beletsky, BA; Ian J. Dempsey, MD, MBA; Brandon J. Manderle, MD; and Nikhil N. Verma, MD

Chapter 11

Glenoid Bone Loss Augmentation Variations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115 Matthew L. Vopat, MD; Liam A. Peebles, BA; Maj. Travis J. Dekker, MD, MC, USAF; and Matthew T. Provencher, MD, MC, USNR

Chapter 12

Arthroscopic Latarjet . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .129 Laurent LaFosse, MD; Christian Moody, MD; and Leonard Achenbach, MD

Chapter 13

Hill-Sachs Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .139 Morad Chughtai, MD; Andrew Swiergosz, MD; Linsen T. Samuel, MD, MBA; and Anthony Miniaci, MD

viii

Contents

Chapter 14

Rehabilitation of the In-Season and Postoperative Athlete . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .149 Kevin E. Wilk, PT, DPT and Lenny Macrina, MSPT, SCS, CSCS

Chapter 15

Return-to-Play Evaluation in the Postoperative Athlete for Anterior Shoulder Instability . . . . . . . . . . . . . 175 Brian Busconi, MD; Jonathon A. Hinz, DO; Benjamin J. Brill, DO; and Vickie Dills, PT, DPT, OCS, ITPT, CSAC

Section III

Posterior Instability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 185

Chapter 16

History and Examination of Posterior Instability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .187 Trey Colantonio, MD, CPT and CDR Lance LeClere, MD

Chapter 17

Imaging of Posterior Shoulder Instability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .197 Josef K. Eichinger, MD, FAOA and Joseph W. Galvin, DO, FAAOS

Chapter 18

Management of In-Season Athletes With Posterior Glenohumeral Instability . . . . . . . . . . . . . . . . . . . . . . .205 Mark Slabaugh, MD, FAAOS and Christopher Gaunder, MD

Chapter 19

Arthroscopic Management of Posterior Instability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 215 Fotios Paul Tjoumakaris, MD and James P. Bradley, MD

Chapter 20

Bone Augmentation for Posterior Instability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .221 Jaymeson R. Arthur, MD and John M. Tokish, MD

Chapter 21

Postsurgical Rehabilitation of Posterior Instability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .233 Evan W. James, MD; Kenneth M. Lin, MD; Lawrence V. Gulotta, MD; and Samuel A. Taylor, MD

Chapter 22

Return to Play Following Posterior Stabilization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .241 Tracey Didinger, MD; Jennifer Reed, NP; and Eric McCarty, MD

Section IV

Special Topics in Instability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .249

Chapter 23

Revision Arthroscopic Stabilization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .251 Craig R. Bottoni, MD and Zackary Johnson, MD

Chapter 24

Instability in the Throwing Athlete . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .265 Ashley J. Bassett, MD and Steven B. Cohen, MD

Chapter 25

Instability in the Pediatric and Adolescent Athlete . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .281 Joseph W. Galvin, DO, FAAOS and Xinning Li, MD

Chapter 26

Special Considerations for Multidirectional Instability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .291 Mark E. Cinque, MD and Geoffrey D. Abrams, MD

Chapter 27

Special Considerations for Return to Play in Collision Athletes (Hockey, Football, and Rugby) . . . . . . . .299 Bruce S. Miller, MD, MS; Asheesh Bedi, MD; and Jack W. Weick, MD

Chapter 28

Management of the Aging Athlete With the Sequelae of Shoulder Instability . . . . . . . . . . . . . . . . . . . . . . . .307 Lucca Lacheta, MD; Maj. Travis J. Dekker, MD, MC, USAF; and Peter J. Millett, MD, MSc

Financial Disclosures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 317

ACKNOWLEDGMENTS The authors would like to acknowledge the indefatigable Julia Dolinger, Kayla Whittle, Dani Malady, and Allegra Tiver. Thank you to everyone with the SLACK Incorporated team for their dedication and commitment to this project. This journey began as a concept, and with the support and guidance from SLACK has been made into a reality. We are also deeply indebted to all of the world-renowned authors who have graciously contributed their time and expertise to make this into a cogent resource of extraordinary quality. Lastly, we want to acknowledge all those whose footsteps we have followed in service to our country. There has been no better source of comradery and friendship, no finer arena in which to practice, and most of all, no better patient for which to care.

ABOUT THE EDITORS

Jonathan F. Dickens, MD is Chief of the Orthopaedic Sports Medicine and Shoulder Service at Walter Reed National Military Medical Center (WRNMMC) in Bethesda, Maryland; Vice-Chair of Research for the Uniformed Services University Department of Surgery; and Adjunct Faculty at the John A. Feagin Jr. Sports Medicine Fellowship at the US Military Academy in West Point, New York. He is an Associate Professor of Surgery at the Uniformed Services University of the Health Sciences. Dr. Dickens earned his Bachelor of Science from Davidson College in North Carolina before entering the Army. He subsequently completed medical school at Indiana University in Bloomington, followed by Orthopaedic Surgery Residency at WRNMMC. He completed his Fellowship in Sports Medicine and Arthroscopy at the John A. Feagin Jr. Sports Medicine Fellowship at West Point. Dr. Dickens is a Lieutenant Colonel in the US Army and has served as a Consultant Physician for Special Operations Task Force–Afghanistan in 2015 and Commander of the Hamid Karzi International Airport NATO Role II Hospital in Kabul, Afghanistan in 2019.

xii

About the Editors

Brett D. Owens, MD is a Board-certified orthopedic sports medicine surgeon. Dr. Owens is currently a Professor in the Department of Orthopaedic Surgery at the Brown University Alpert Medical School and practices in Providence, Rhode Island. He is a retired Colonel in the US Army and previously served as Chief of Orthopaedics and Sports Medicine at Keller Army Hospital, West Point, New York. He is currently Team Physician for Brown University Athletics and the Providence Bruins (AHL). He attended the US Military Academy and Georgetown University School of Medicine. He completed his residency at the University of Massachusetts and the John A. Feagin Jr. Sports Medicine Fellowship at West Point. He was an AOA North American Traveling Fellow as well as an AOSSM-ESSKA Traveling Fellow. Dr. Owens has published more than 250 articles in orthopedics and sports medicine. This is his fourth textbook. His research has garnered the O’Donoghue Research Award, Aircast Award, and NCAA Research Awards from the American Orthopaedic Society for Sports Medicine and the AAOS Kappa Delta Award. Dr. Owens is proud to serve as Associate Editor of the American Journal of Sports Medicine since 2012.

CONTRIBUTING AUTHORS Geoffrey D. Abrams, MD (Chapter 26) Stanford University School of Medicine Department of Orthopedic Surgery Veterans Administration–Palo Alto Health Care System Palo Alto, California

James P. Bradley, MD (Chapter 19) Clinical Professor, Orthopaedic Surgery University of Pittsburgh Medical Center Head Team Physician, Pittsburgh Steelers Pittsburgh, Pennsylvania

Leonard Achenbach, MD (Chapter 12) Department of Trauma, Hand, Plastic and Reconstructive Surgery University Hospital Wuerzburg Wuerzburg, Germany

Benjamin J. Brill, DO (Chapter 15) Orthopaedic Surgeon Longview Orthopaedic Center, LLC Leominster, Massachusetts

Gregory J. Adamson, MD (Chapter 4) Congress Medical Foundation Pasadena, California Robert Arciero, MD (Chapter 8) Professor, Orthopaedics University of Connecticut UCONN Health Farmington, Connecticut Jaymeson R. Arthur, MD (Chapter 20) Department of Orthopedics Mayo Clinic, Scottsdale Phoenix, Arizona Ashley J. Bassett, MD (Chapter 24) The Orthopedic Institute of New Jersey Sparta, New Jersey Asheesh Bedi, MD (Chapter 27) Chief, Sports Medicine Gehring Professor of Orthopedic Surgery Michigan Medicine Ann Arbor, Michigan Alexander Beletsky, BA (Chapter 10) Division of Sports Medicine Midwest Orthopaedics at Rush Rush University Medical Center Chicago, Illinois Craig R. Bottoni, MD (Chapter 23) Professor of Surgery Uniformed Services University of the Health Sciences Chief, Sports Medicine Orthopaedic Surgery Department Tripler Army Medical Center Honolulu, Hawaii

Stephen F. Brockmeier, MD (Chapter 3) Sports Medicine and Shoulder Surgery Professor of Orthopaedic Surgery University of Virginia Director, UVA Sports Medicine Fellowship Program Team Physician, UVA Athletics Charlottesville, Virginia Jessica L. Brozek, MD (Chapter 1) Orthopedic Surgeon Newton Medical Center Newton, Kansas Brian Busconi, MD (Chapter 15) Chief of Sports Medicine and Arthroscopy University of Massachusetts UMass Memorial Health Care Division of Sports Medicine Worcester, Massachusetts Francis P. Bustos, MD (Chapter 3) Department of Orthopaedic Surgery University of Virginia Charlottesville, Virginia Kenneth L. Cameron, PhD, MPH, ATC (Chapter 2) John A. Feagin Jr. Sports Medicine Fellowship Keller Army Hospital US Military Academy West Point, New York Morad Chughtai, MD (Chapter 13) Department of Orthopaedic Surgery Cleveland Clinic Cleveland, Ohio Mark E. Cinque, MD (Chapter 26) Stanford University School of Medicine Department of Orthopedic Surgery Palo Alto, California

xiv

Contributing Authors

Steven B. Cohen, MD (Chapter 24) Rothman Orthopaedic Institute Department of Orthopaedic Surgery Thomas Jefferson University Philadelphia, Pennsylvania Trey Colantonio, MD, CPT (Chapter 16) PGY-4, Research Resident Department of Orthopaedic Surgery Walter Reed National Military Medical Center Bethesda, Maryland Maj. Travis J. Dekker, MD, MC, USAF (Chapters 11 and 28) US Air Force Eglin Air Force Base, Florida Assistant Professor Uniformed Services University of the Health Sciences Bethesda, Maryland Ian J. Dempsey, MD, MBA (Chapter 10) Division of Sports Medicine Midwest Orthopaedics at Rush Rush University Medical Center Chicago, Illinois Tracey Didinger, MD (Chapter 22) LA Bone and Joint Institute Encino, California Vickie Dills, PT, DPT, OCS, ITPT, CSAC (Chapter 15) Department of Orthopedics University of Massachusetts Medical School Worcester, Massachusetts Maj. Michael A. Donohue, MD (Chapter 5) Assistant Professor of Surgery Uniformed Services University of the Health Sciences John A Feagin Jr. Sports Medicine Fellowship West Point, New York Josef K. Eichinger, MD, FAOA (Chapter 17) Sports Medicine, Shoulder and Elbow Surgery Professor of Orthopaedic Surgery Medical University of South Carolina Charleston, South Carolina David Eldringhoff, MD (Chapter 4) Congress Medical Foundation Pasadena, California Joseph W. Galvin, DO, FAAOS (Chapters 17 and 25) Assistant Professor of Surgery Uniformed Services University of the Health Sciences Department of Orthopaedic Surgery Shoulder and Elbow Surgery Madigan Army Medical Center Tacoma, Washington

Christopher Gaunder, MD (Chapter 18) Maj, USAF, MC Orthopaedic Surgeon Dayton, Ohio Lawrence V. Gulotta, MD (Chapter 21) Hospital for Special Surgery New York, New York Jonathon A. Hinz, DO (Chapter 15) Orthopaedic Surgeon Associated Orthopedists of Detroit St. Clair Shores, Michigan Carolyn A. Hutyra, MMCi (Chapter 6) Orthopaedic Surgery Duke University Durham, North Carolina Evan W. James, MD (Chapter 21) Hospital for Special Surgery New York, New York Zackary Johnson, MD (Chapter 23) Honolulu, Hawaii Jason A. Jones, MD (Chapter 9) Nashville Knee and Shoulder Center Music City Orthopaedics and Sports Medicine Nashville, Tennessee Lucca Lacheta, MD (Chapter 28) Steadman Philippon Research Institute Vail, Colorado Assistant Professor Center for Musculoskeletal Surgery Charitè—Universitaetsmedizin Berlin Berlin, Germany Laurent LaFosse, MD (Chapter 12) ALPS Surgery Institute Annecy, France Brian C. Lau, MD (Chapter 6) Duke Sport Science Institute Orthopaedic Surgery Duke University Durham, North Carolina CDR Lance LeClere, MD (Chapter 16) Sports Medicine and Shoulder Surgery Naval Health Clinic Annapolis Head Team Physician US Naval Academy Annapolis, Maryland

Contributing Authors Thay Q. Lee, PhD (Chapter 4) Congress Medical Foundation Pasadena, California Xinning Li, MD (Chapter 25) Associate Professor of Orthopaedic Surgery Department of Orthopaedic Surgery Sports Medicine and Shoulder Surgery Sports Medicine Fellowship Director Boston University School of Medicine Boston Medical Center Boston, Massachusetts Kenneth M. Lin, MD (Chapter 21) Hospital for Special Surgery New York, New York Lenny Macrina, MSPT, SCS, CSCS (Chapter 14) Physical Therapist Champion Physical Therapy and Performance Waltham, Massachusetts Brandon J. Manderle, MD (Chapter 10) Division of Sports Medicine Midwest Orthopaedics at Rush Rush University Medical Center Chicago, Illinois

Bradley J. Nelson, MD (Chapter 1) Associate Professor Department of Orthopaedic Surgery Medical Director Department of Intercollegiate Athletics University of Minnesota Team Physician, Minnesota Wild Hockey Club Minneapolis, Minnesota Lisa K. O’Brien, DO (Chapter 7) Lehigh Valley Health Network Department of Orthopaedic Surgery Scranton, Pennsylvania Michael J. Pagnani, MD (Chapter 9) Nashville Knee and Shoulder Center Music City Orthopaedics and Sports Medicine Nashville, Tennessee Liam A. Peebles, BA (Chapter 11) Tulane University School of Medicine New Orleans, Louisiana Matthew A. Posner, MD (Chapter 2) John A. Feagin Jr. Sports Medicine Fellowship Keller Army Hospital United States Military Academy West Point, New York

Eric McCarty, MD (Chapter 22) University of Colorado School of Medicine Professor, Chief of Sports Medicine and Shoulder Surgery Champions Center Boulder, Colorado

Matthew T. Provencher, MD, MC, USNR (Chapter 11) The Steadman Clinic Vail, Colorado

Bruce S. Miller, MD, MS (Chapter 27) Professor of Orthopedic Surgery Michigan Medicine Ann Arbor, Michigan

Jennifer Reed, NP (Chapter 22) CU Sports Medicine University of Colorado School of Medicine Team Provider University of Colorado–Boulder Athletics Aurora, Colorado

Peter J. Millett, MD, MSc (Chapter 28) Chief Medical Officer and Director of Shoulder Surgery Steadman Philippon Research Institute The Steadman Clinic Vail, Colorado Anthony Miniaci, MD (Chapter 13) Cleveland Clinic Sports Health Center Department of Orthopaedic Surgery Cleveland Clinic Cleveland, Ohio Christian Moody, MD (Chapter 12) Prisma Health System Department of Orthopaedic Surgery Division of Hand and Upper Extremity Greenville, South Carolina

Jeremy K. Rush, MD, FAAP (Chapter 3) Orthopaedic Sports Medicine Nemours Children’s Specialty Care Jacksonville, Florida Assistant Professor of Orthopedics Mayo Clinic College of Medicine and Science Rochester, Minnesota Linsen T. Samuel, MD, MBA (Chapter 13) Department of Orthopaedic Surgery Cleveland Clinic Cleveland, Ohio Barry I. Shafer, PT, DPT, ATC (Chapter 4) Congress Medical Foundation Pasadena, California

xv

xvi

Contributing Authors

Mark Slabaugh, MD, FAAOS (Chapter 18) Col, USAF, MC Sports Medicine Orthopaedic Surgeon Chief, Sports Medicine Service USAFA Team Physician USAFA Associate Professor of Surgery F. Edward Hébert School of Medicine Uniformed Services University of the Health Sciences Bethesda, Maryland Andrew Swiergosz, MD (Chapter 13) Department of Orthopaedic Surgery Cleveland Clinic Cleveland, Ohio Lauren A. Szolomayer, MD (Chapter 8) Excel Orthopaedic Specialists Woburn, Massachusetts Dean C. Taylor, MD (Chapter 6) Duke Sport Science Institute Orthopaedic Surgery Duke University Durham, North Carolina Samuel A. Taylor, MD (Chapter 21) Hospital for Special Surgery New York, New York David J. Tennent, MD (Chapter 2) John A. Feagin Jr. Sports Medicine Fellowship Keller Army Hospital United States Military Academy West Point, New York Fotios Paul Tjoumakaris, MD (Chapter 19) Professor, Orthopaedic Surgery Sidney Kimmel College of Medicine Thomas Jefferson University Rothman Institute Egg Harbor Township, New Jersey

John M. Tokish, MD (Chapter 20) Consultant, Orthopedic Sports Medicine Professor, Orthopedic Surgery Orthopedic Surgeon, Arizona Coyotes Director, Orthopaedic Sports Medicine Fellowship Mayo Clinic Arizona Phoenix, Arizona Nikhil N. Verma, MD (Chapter 10) Division of Sports Medicine Midwest Orthopaedics at Rush Rush University Medical Center Chicago, Illinois Matthew L. Vopat, MD (Chapter 11) University of Kansas School of Medicine–Wichita Wichita, Kansas Brian R. Waterman, MD (Chapter 7) Chief and Fellowship Director Sports Medicine Associate Professor Department of Orthopaedic Surgery School of Medicine Team Physician Wake Forest University Athletics Team Physician, Winston-Salem Dash (Chicago White Sox) Team Physician, US Ski & Snowboard Associate Editor, Arthroscopy Journal Winston-Salem, North Carolina Jack W. Weick, MD (Chapter 27) Department of Orthopaedic Surgery University of Michigan Ann Arbor, Michigan Kevin E. Wilk, PT, DPT (Chapter 14) Associate Clinical Director Champion Sports Medicine Select Medical American Sports Medicine Institute Birmingham, Alabama

PREFACE “If I have seen further it is by standing on the shoulders of giants.” —Isaac Newton c. 1675 Shoulder instability in the athlete is an important topic, often with high stakes, and filled with nuances in diagnosis, treatment, and rehabilitation. The human shoulder joint allows the greatest range of motion of any joint, making it possible for the pitcher to throw a fastball at 95 mph, the gymnast to perform a rings routine, or the linebacker to make a tackle. While the “cause” of instability can come in many forms, its presence eliminates the athlete’s foundation of trust in their shoulder, and their performance suffers. Since the first historical description of shoulder surgery, the unique complexities of shoulder instability have been an important focus. Into this context, we set out to produce a textbook focusing on the unstable shoulder in athletes. Throughout our orthopedic surgery careers, and in our exploration of shoulder instability in particular, we have been blessed by incredible mentors. It is because of these “giants” and their willingness to mentor and teach us that we have been able to assemble this textbook. We are forever grateful for the opportunity to bring together many of the world’s experts on shoulder instability with the hopes of providing clearer guidance to clinicians treating athletes. This has been a rapidly advancing field, and our hope was to document the current state of scientific knowledge in this field. Shoulder instability has been a passion for both of us, and our attempts to progressively improve the understanding of certain aspects have proven to be among the most rewarding of our careers. This book, therefore, represents a summation of our clinical, laboratory, and team physician experience. Importantly, it reflects the thoughts, accomplishments, and insights of world-renowned colleagues and mentors whose teachings have influenced all of us. We are thankful for the research teams we have worked with and the relationships we have nourished with these collaborators and colleagues. We are mostly thankful for our patients who have entrusted us with the care of their shoulders. —Brett D. Owens, MD —Jonathan F. Dickens, MD

INTRODUCTION The ambitious goal of this textbook was to assemble in one location a definitive and comprehensive guide for the treatment of shoulder instability in athletes. We are proud to have compiled an amazing list of internationally recognized authors from around the world and encompassing all aspects of care for the athlete’s injured shoulder. Our authors are surgeons and therapists, scientists and biomechanical engineers; they care for military, collegiate, and professional athletes, and have an unmatched expertise of shoulder instability. They have graciously been willing to participate in this text because of our shared passion for this worthy area of scientific pursuit. The textbook is subdivided into 4 sections for ease of consumption and each topic is uniquely constructed to address the challenges and tips to successfully treat our most demanding athletes. With in-depth analysis and expert authors, this text covers all aspects of the care of the athlete with shoulder instability, from on-the-field management, operative and nonoperative treatment, to successful return to play. Our first section is titled “Principles for the Team Physician” and details basic anatomic and biomechanical concepts that lay the foundation for the entire textbook. We review the epidemiology and also dive into the on-field management of the dislocated shoulder. The second section addresses anterior instability in athletes, reviews the unique consideration for in-season management, and addresses—in detail—the surgical management options starting with arthroscopic management and including all open stabilization indications and techniques. In the third section, we examine posterior instability, starting with initial evaluation, surgical treatment, rehabilitation, and return-to-play decision making. Lastly, we address special topics unique to the athlete’s shoulder, including throwers with instability, instability in collision athletes, and revision surgery, among others. Starting with the patient history, physical examination, and radiographic evaluation, each shoulder instability diagnosis is explored in detail. Surgical techniques are heavily emphasized with a thorough and stepwise description for all relevant procedures, interspersed with the expert’s own technical pearls. This has produced a level of detail that we hope will make this book useful not only to team physicians and providers, but to all those who care for athletes. Lastly, we are eternally indebted to our world-renowned authors who invested significant time and effort to ensure their knowledge is captured and shared in clinically useful and user-friendly text. We hope that you find Shoulder Instability in the Athlete: Management and Surgical Techniques for Optimized Return to Play a valuable aid in your care of the athlete with shoulder instability.

SECTION I Principles for the Team Physician https://t.me/mebooksfree

1 Team Physician Principles for the Management of Athletes Jessica L. Brozek, MD and Bradley J. Nelson, MD

Serving as a team physician can be a challenging but rewarding aspect of medical practice for a sports medicine physician. Although it is, at its core, no dif ferent from any other type of medicine—that is, providing expert knowledge and ser vice to improve and maintain optimal health for an individual—there are many other considerations that can complicate the ultimate achievement of that goal. When a “patient” becomes an “athlete”—or rather, an athlete becomes a patient—this is much more than a simple change in terminology. It brings with it connotations of the impact and goals of treatment, as well as the potential involvement of many other individuals who may have an investment in (and therefore affect) the decision-making process and final outcomes of treatment. The following chapter will discuss many of the nuances integral to acting as a team physician, including being prepared for many various medical scenarios, serving as leader of a diverse medical team, adhering to the ethical principles necessary to providing appropriate medical care to an athlete, and navigating the complex array of individuals involved in an athlete’s care.

BEING A TEAM PHYSICIAN A team physician’s role is more than simply the medical care of athletes. This title also inherently includes the coordination of all aspects of the medical care from each of the many multidisciplinary professionals in the medical team (to be discussed later in this chapter), oversight of emergency action plans (EAPs) and event preparedness, management of preparticipation physicals, and communication with administrators and other personnel within the athletic organization regarding medical concerns or injuries. The American Academy of

Orthopaedic Surgeons (AAOS) defines a team physician as an MD or DO with a full license to practice medicine, knowledgeable in management of on-field medical emergencies, trained in basic life support, with knowledge of musculoskeletal injuries, medical conditions, and psychological issues affecting athletes. Beyond these requirements, the AAOS recommends team physicians also have specific training in sports medicine through specialty board certification, fellowship training, research, and continuing education and a clinical practice focused on sports medicine.1 Team physicians can come from several different training backgrounds, including orthopedic surgery, family medicine, internal medicine, and pediatrics. Even within these tracks, experience in sports coverage can vary widely between residency programs. In one recent survey2 of orthopedic residents, nearly 90% of programs allow or require team/event coverage but just more than half provided training before this coverage. Only one-quarter of those without specific training had direct attending supervision. Formal training provided a statistically significantly higher level of comfort in treating sideline injuries. Many physicians will graduate training and find themselves providing care for athletic events, whether in an official or unofficial capacity; particularly in more rural or underserved settings, this is often without specific fellowship training in sports medicine. Thus, if a team physician is part of an academic institution that trains residents, part of that role may (and arguably should) include development and execution of a sideline preparation training curriculum. A certainly nonexhaustive list of topics includes education on safe spine boarding/precautions, concussion diagnosis, management of common ocular and dental injuries, triage and stabilization of medical emergencies, and a review of basic musculoskeletal physical examination.

-3-

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 3-10). © 2021 SLACK Incorporated.

4

Chapter 1

Table 1-1. American Academy of Orthopaedic Surgeons Recommendations for On-Site Supplies, Equipment, and Medication ADMINISTRATIVE

●

●

CARDIOPULMONARY

EXTREMITIES

GENERAL

Copy of athlete emergency form Copy of emergency action plan and emergency contact numbers

●

Prescription pad and pen

●

Medication log

●

Sideline concussion assessment protocol

●

Injury and illness care instruction sheets for patient

●

Airway

●

Mouth-to-mouth mask

●

Blood pressure cuff

●

Short-acting β agonist inhaler

●

Epinephrine 1:1000 in prepackaged unit

●

Stethoscope

●

Athletic tape

●

Sling

●

Crutches

●

Splints and braces

●

Elastic bandages

●

Tape cutter

●

Blanket

●

Antihistamine

●

Cotton-tip applicators

●

Antiemetic

●

Gloves (sterile/nonsterile)

●

Glucagon

●

Forceps

●

Aspirin

●

Ice

●

Cortisone

●

Oral glucose

●

Intravenous fluids and administration set and tourniquet

●

Large bore angiocatheter (14- to 16-gauge)

●

Local anesthetic, syringes, needles

●

Other medication ●

●

Topical/oral antibiotics

●

Oral fluid replacement

●

Plastic bags

●

Rectal thermometer and covers

●

Scissors

●

Sharps box and red bag

Anti-inflammatories (continued )

Although caring for an athlete is ultimately no more than caring for any patient, providing medical care at an athletic venue is inherently dif ferent from providing care in a clinic or hospital. The physician must be prepared for many potential scenarios and come equipped with supplies for such. This frequently takes the form of a medical bag. Like with definitions for the term team physician, the AAOS3 has provided recommendations for what supplies should be available when covering sports events; these are listed in Table  1-1. This is certainly not all inclusive but it does provide a basic idea of some of the medical equipment and supplies that may be required during an athletic event. Although it also does not necessarily represent what is frequently found physically within the team doctor’s bag, the availability and location of these items should ideally be known at each venue. Certain athletic events will include the presence of emergency medical personnel on site, and they can provide some of this equipment (the availability of such emergency medical services support should be included in the EAP, a topic which will be discussed later).

The team physician on the sidelines may encounter and thus must be prepared to handle medical emergencies including cardiac events (eg, hypertrophic cardiomyopathy, commotion cordis), pulmonary distress (eg, asthma, anaphylaxis, traumatic pneumothorax), heat-related injury (eg, heat stroke), and head/neck injuries (eg, subdural hematoma, spinal cord injury).4 As always in an emergency situation, the “A, B, Cs” of trauma evaluation (Airway, Breathing, Circulation) should be the initial focus, followed by a more specific secondary survey of the entire body once medical stability has been established. As leader of the team’s medical care, the team physician is ultimately responsible for the EAP. This should be a sitespecific written description completed before the season that delineates location of an automated external defibrillator and other emergency equipment, facility access for first responders, basic chain of command, and communication strategies. This EAP should be distributed to physicians, athletic trainers, safety personnel, coaches, and other administrative staff, and should also be reviewed annually.3 Examples of a basic EAP are provided in Figure 1-1.

Team Physician Principles for the Management of Athletes

5

Table 1-1. American Academy of Orthopaedic Surgeons Recommendations for On-Site Supplies, Equipment, and Medication (continued) HEAD AND NECK / NEUROLOGICAL

●

Cervical collar

●

Ocular anesthetic and antibiotics

●

Contact lens case and solution

●

Contact remover

●

Dental kit

●

Eye wash

●

Eye chart

●

SKIN

●

Dental wax

●

Mouth guard

●

Face mask removal tool

●

Cyanoacrylate glue

●

Flashlight

●

Hank’s solution

●

Mirror

●

Nasal packing material

Eye kit ●

Blue light

●

Oto-ophthalmoscope

●

Fluorescein stain strips

●

Spine board and attachments

●

Eye patch/shield

●

Tongue depressors

●

Alcohol swabs, povidone iodine swabs

●

Silver nitrate sticks

●

Benzoin

●

Skin lubricant

●

Blister care materials

●

●

Nail clippers

●

Razor and shaving cream

●

Scalpel

Although the rate of injuries during games is 3.5 times higher than those during practices, averaging 1 injury for every 2 games for National Collegiate Athletic Association athletes,5 serving as a team physician also entails medical care of the athletes outside the specific realm of competition. This often includes preparticipation physical exams (and postseason physicals, depending on level of competition) and “training room” (ie, providing on-site clinic services throughout the season). Although preparticipation physical exams are often required for athletic competition, the exact components are up for debate. A comprehensive discussion of this is beyond the scope of this chapter, but preparticipation physical exams should typically include personal and family history (with par ticular attention to any cardiac events that may prompt further screening) and physical examination.6,7 Throughout the season (and off-season) the training room can serve as a central location for athletes to receive evaluation and treatment of injuries and illnesses apart from competition days and can require the team physician to manage a wide variety of diagnoses. In one study at a National Collegiate Athletic Association institution,8 73% of initial athlete evaluations and 87% of follow-up visits were regarding musculoskeletal diagnoses, with only 4% of injuries requiring surgical management. Among the other 27% of initial visits that dealt with general medical diagnoses, the most common were for upper respiratory infection,

●

Skin stapler, suture set, butterfly bandages Wound irrigation materials ●

Sterile normal saline

●

10- to 50-cc syringe

dermatological complaints, concussions, and cardiopulmonary and gastrointestinal issues.

MULTIDIMENSIONAL MAKEUP OF THE MEDICAL TEAM Whether in the operating room or clinic, or on the sidelines or in a training room setting, a physician can rarely function alone. In serving as a team physician, the doctor will work closely with many other individuals on a multidisciplinary team, including other physicians of various subspecialties (primary care, orthopedic surgery, neurology, ophthalmology, dermatology, etc), physical therapists, athletic trainers, dietitians, sports psychologists, strength and conditioning coaches, and others (such as dentists and optometrists). Depending on the level of athletics, from amateur to professional, the resources available from each of these specialists can help to optimize an athlete’s return to play and ultimate outcome. Each will be discussed in further detail later, but we would recommend that the single most impor tant aspect of a medical team is open communication. When beginning to cover a team, the physician should establish which of these (or other) resources are present and introduce himself or herself to each of them to open that line of communication to facilitate safe, smooth, and

6

Chapter 1

Figure 1-1. Examples of an EAP. (continued)

comprehensive care of the athletes throughout the season and off-season. One of the core members of a medical team in sports medicine is the athletic trainer. The American Medical Association defines an Athletic Medicine Unit to include an allopathic or osteopathic physician director, a board certified athletic trainer, and “other necessary personnel.”9 Athletic trainers primarily focus on managing acute on-field injuries and maintaining athletes’ ability to play, whether that be returning to play after an injury or maintaining physical health on a more chronic basis. Athletic trainers are often on the sidelines of games and practice on a daily basis and therefore may have the most insight into an athlete’s individual personality, which can come into play in consideration of the athlete’s goals, ability to progress through the rehabilitation process, and return to sport. Athletic trainers often guide and supervise an athlete’s daily therapy exercises, stretching, and gradual return to practices and competition. Through this process, athletic trainers can provide invaluable insight to the rehabilitation progression. Their training also enables initial on-field assessment and stabilization of acute injuries, which can be particularly critical in settings where they are the sole members of the medical team for an athletic event. In the specific interest of this text, this can apply to reductions

of acute shoulder dislocations; however, it is always critical for team physicians to have appropriate preemptive communication and establish a good working relationship with the athletic trainers with whom they work to determine their comfort level and experience with certain common injuries, making the postinjury hand-off discussion and treatment more streamlined. Physical therapists can also be impor tant members in the medical care of an injured athlete. With training specific to the rehabilitation of injuries through a 3-year graduate degree program, they are well versed in musculoskeletal pathologies, and return to—as well as maintenance of— function from such pathologies. It is beneficial to develop relationships with therapists with whom a team physician often works, so they may become familiar with typical postoperative protocols and restrictions and feel comfortable freely discussing an athlete’s progress. This can be especially crucial because physical therapists have much more contact with the athlete through the recovery process than the physician and can therefore advise on the sport-specific functional progress the athlete has made. Increasing attention is being paid to the mental health of athletes and its effect on performance and return to play following an injury and surgery. Studies have shown that higher

Team Physician Principles for the Management of Athletes

7

Figure 1-1 (continued). Examples of an EAP.

athletic confidence and lower kinesiophobia are associated with higher return to sport,10 whereas fear of reinjury and fear of pain are common reasons for delayed or permanent inability to return to sport after anterior cruciate ligament reconstruction.11 Similar quantitative assessments of psychological readiness to return to sport have been developed for shoulder instability as well.12 Many athletes have structured their lives—and to no small extent, their identities—around their sports participation. Thus an injury, which suddenly and unexpectedly deprives them of the ability to practice and compete, can be devastating. Time spent in rehabilitation and away from a normal training environment and regimen can also isolate injured athletes from what is often their primary social group: the team. In addition to attention to this topic by physical therapists and athletic trainers on a daily basis, a trained sports psychologist can be a valuable resource throughout the recovery process and in optimizing psychological readiness to return to play. Even in healthy athletes, another facet of mental health—stress—can increase risk of injury. Nearly one-third of male and half of female athletes at the college level have reported feeling overwhelming anxiety in the last 12 months, and up to one-quarter of college

athletes may have clinically relevant depressive symptoms. Rates of eating disorders in elite female athletes can be up to 20%, and when present with amenorrhea and osteoporosis are termed the female athlete triad. In a population that often has a “work hard, party hard” mentality, athletes can also be prone to substance abuse. It is critical that team physicians be able to recognize these conditions and refer a struggling athlete for appropriate treatment. Cognitive behavioral therapy and education on stress management and coping mechanisms can all be effective when provided by a licensed sports psychologist. As an often more familiar and trusted face, the team physician can help facilitate the athlete’s involvement in and acceptance of this form of assistance, from both a standpoint of formal referral and removal of the stigma that can be associated with mental health.13 Throughout a long season of often complex schedules of training and competition, an athlete’s recovery and performance must be fueled by appropriate nutrition. This includes coordinating the timing, amount, and proportion of the intake of protein, carbohydrate, fat, and various micronutrients. Maintaining this optimal balance requires individualization based on the athlete and the sport. Registered

8

Chapter 1

dietitians can receive specialized training in sports dietetics and can serve as an impor tant asset to athletes in maximizing training and performance.14 Although a healthy body composition should be encouraged for the athlete’s overall well-being and peak performance, eating disorders unfortunately can be rampant in highly competitive athletes, and nutritionists can act as part of the medical team to provide education and support in developing healthy eating patterns.15 Strength and conditioning coaches guide athletes through a large portion of their in- and out-of-season training. The primary aspect of the strength coach’s role is safe training of the healthy athlete, and the team physician as the leader of the medical team has ultimate responsibility—either implicitly or explicitly—over the health and safety of the athletes while training.1,16 Thus, open communication is key because physicians must often advocate for the safety of the athletes if they have concerns regarding training practices. An example of this includes avoiding excessively intense preseason training, because cases of exertional rhabdomyolysis have been reported.17 A smooth transition from injury rehabilitation back to normal training is critical to the athlete’s long-term playing career, and although this is typically guided by the athletic trainer and strength coach on a functional level, restrictions must be communicated clearly between the physician and the strength coach throughout the recovery process.

ETHICAL PRINCIPLES Being a physician in any setting is more than the simple application of scientific knowledge. A doctor is expected to be caring and compassionate, personable and responsible. The 4 main tenets of ethics in medicine—beneficence, nonmaleficence, justice, autonomy—still hold true in sports medicine and team coverage. One must always seek to do what is best for the patient, cause no harm, and do what is right, all the while providing the patient with appropriate medical recommendations to allow him or her to make independent, informed decisions without unilaterally dictating care. However, in practice these principles are more than just words on a page and must be interpreted accurately in many unique scenarios, a process that becomes somewhat more complicated when caring for athletes. “Best” and “right” are at best very subjective terms. Is it best to allow an athlete to return to play sooner at the risk of further injury? Is it right to deprive an athlete of the opportunity to participate when he or she understands and accepts the potential consequences of a perhaps objectively inferior treatment plan? This concept of ambiguity is often difficult for many physicians—who spend their training answering multiple-choice questions— to accept. When players are faced with a limited time span of possible participation in their sport, the goals of treatment can change from the long term to the short term. It is a team physician’s responsibility to provide education regarding potential consequences and ramifications of medical choices.

He or she has a duty to protect the athletes—both from the athletes themselves and from others. But this is again a concept that can inherently be described only in vague subjective terms because each athlete must be cared for on an individualized basis, with each unique decision based on many factors. Some of these factors may be determined not by the athletes themselves but by others surrounding them. Nearly all patients have others who assist in their medical decision making (either overtly or subconsciously); in sports medicine this group shifts from encompassing simply family and close friends to also include coaches, teammates, agents, and others, depending on the competition level. One must recognize that all of these groups of people have varying focuses, which may or may not include the overall well-being of the athlete. Although it is becoming somewhat more common in general medical practice in the age of social media, one aspect of caring for athletes that can create difficulty and frustration for physicians is scrutiny of their decisions on a wider scale. Whereas fans and members of the media can pass judgment on an athlete’s medical care, at times without complete knowledge of the situation, team physicians often find that they are unable to defend themselves. Legally and, perhaps more impor tant, ethically, physicians are bound by the constraints of patient confidentiality to refrain from discussing the specifics of patient care. However uncomfortable it may be to remain silent, this excess scrutiny is part of the territory in being a team physician and the focus must always remain on providing the most appropriate medical care for the individual athlete that the physician is able to provide, without allowing any extraneous factors to interfere. Discussion of an athlete’s medical condition with coaches and administrators within athletic organizations is often exempt from the rules of confidentiality, either by rule or by specific written consent by the athlete. Situations that involve care of an athlete in a private clinic or hospital are bound by HIPAA (the Health Insurance Portability and Accountability Act), and thus any sharing of protected patient health information requires written consent by the patient. Professional sports organizations and collegiate athletic departments often have their athletes sign a release of information at the beginning of the season to allow open conversation with coaches and administrators to occur, or the information is considered part of the employment record and thus exempt from HIPAA.18,19 Discussing an athlete’s status and progress following an injury is necessary to anticipate timing of return to play, which is obviously a topic of great importance to coaches and other staff in the proper performance of their jobs. It is always best, however, to clarify the specifics of each par ticular team, ideally before the season starts, to avoid inadvertent breaches of confidentiality or unnecessary delays in communication when par ticular situations arise. Another aspect of navigating the ethical complexities of providing sports team coverage on the sidelines is consent. As with other medicolegal issues, we recommend that

Team Physician Principles for the Management of Athletes physicians seek out and establish the basic regulations of their par ticular location, institution, and situation. Laws regarding protection for those providing care for athletes may vary based on state, although ultimately it is impor tant from an ethical standpoint that an athlete understands any treatment, intervention, or diagnosis that occurs as it happens. For example, an acute shoulder dislocation may often be immediately reduced on the sideline prior to onset of muscle spasms (further discussion of this will occur in following chapters); however, before any attempt at reduction the physician should perform a physical exam and obtain consent (which will be discussed in further detail later), as well as perform a physical exam following reduction. All of these should be appropriately documented.7,20 In general, consent is required for any medical treatment and represents a discussion between the treating provider and the patient (or appropriate surrogate if the patient is younger than 18 years or other wise unable to provide consent) regarding the diagnosis, nature, and purpose of the treatment intervention, and expected benefits and potential risks or burdens of said treatment. The physician must also ensure that the patient or surrogate has appropriate understanding of the situation and consequences of the decisions being made, that the information is being presented appropriately for the specific patient and situation, and that the conversation is adequately documented (often via a written form that the patient or surrogate signs). In emergent situations care may be provided without informed consent, with the provider having that discussion at the first available opportunity.21 This can create a number of potentially ethically ambiguous scenarios for team physicians. The presentation of information regarding treatment options and the risks and benefits of each to the athlete should be fully inclusive and unbiased. However, one could argue that this cannot ever be truly “unbiased” because, as a human being, any physician’s viewpoint on a situation is affected by his or her previous experience with similar scenarios, as well as outside pressures (coaches, team institutions, media, etc, in the setting of sports medicine), making relaying any information to the athlete in a completely objective manner essentially impossible. It could also be suggested that “informed” consent is also an impossibility; it is unrealistic to assume that any patient will have a full and comprehensive understanding of any potential consequences of a decision based on a brief conversation with a medical professional, however impartial and skilled a communicator he or she may be. This is particularly true for athletes in an in-game setting. In the excitement of the moment it can be difficult for a player to see beyond winning the current game or match, or beyond even getting back to the current play or race. This harkens back to the concept of the team physician serving as the voice of reason and at times erring on the side of necessary paternalism overshadowing patient autonomy. Ultimately all efforts must be made, to the best of the physician’s ability, to objectively present all necessary information to the athlete or surrogate and allow him or her to make a decision, assisting as requested, and ensure that

9

decision is being made by a capable individual with reasonable understanding of the situation. One par ticular example of this could be in the area of concussion diagnosis; although the athlete may appear outwardly without injury it is medically unsafe to return him or her to play, despite the opinions and desires of the athlete, parents, or coaching staff. Another example would be an athlete who has sustained a shoulder instability event with persistent instability and weakness on examination; although the athlete may feel absolutely certain that he or she is safe to play, premature return to play may result in further injury if the athlete is unable to protect himself or herself appropriately in the game setting. This is a clinical decision that physicians must rest on their training and experience, and be firm in their decision once made.

ATHLETE-PHYSICIAN RELATIONSHIP As with all physician-patient relationships, the physicianathlete relationship must be based on trust and respect. However, the inclusion of other parties and mitigating factors (as with every thing else previously discussed in this chapter) only complicates this scenario. The physician must maintain objectivity, while also establishing the rapport necessary for the level of communication required to provide adequate medical care. This balance can often be difficult. With the amount of time often spent in covering a team, it is only natural to become invested in the success of said team, and overtly showing that enthusiasm can help to develop a connection with the players. However, this interest in the success of the team cannot be allowed to overshadow clinical decision making regarding an individual player. The player, coach, and team are (rightfully) focused solely on the team’s victory, whereas the team physician must at times be a voice of opposition when a player’s overall health is at stake. Caution must also be used in overtly showing excess enthusiasm for one team when—as is often the case—the physician may be called on to evaluate an opposing team’s player. This can create conflict and questioning of motives when the opposing athlete is ruled out of returning to play. It goes without saying that this decision must in fact be made with an appropriate level of objectivity, regardless of which jersey the player may be wearing. Ultimately, professionalism begets trust, and trust avoids unnecessary resistance to and thus delays in appropriate medical treatment.

THIRD-PARTY/AGENT CONSIDERATIONS Acting as a team physician often requires a significant amount of time, effort, and stress, at times for little quantitative compensation. A perhaps less-tangible benefit of providing a team’s medical care can be the simple fact of being known as “Team X’s doctor,” with the perception being that this position is earned by overall integrity and quality of care. Although this perception is ideally not untrue, the reality of the appointment of team physicians can be a complex and political process, often based on financial bids made by

10

Chapter 1

hospitals and health care systems to provide medical care in exchange for advertising rights. A number of professional sports leagues recognize this potential for conflict of interest and try to separate the selection of team physicians from the marketing arrangements. Physicians should make every effort to avoid letting this theoretical source of bias cloud their decision making when it comes to treating athletes, a potentially challenging goal when medical providers may be feeling pressure from the athletic institution and their own medical group to prioritize their interests over those of the athletes, with the threat of “losing” a team coverage position an overshadowing stress. In a perfect world, a team physician would be able to provide completely impartial and straightforward care that would benefit the athlete without concern for anyone or anything else, but the reality is that medicine of any kind—especially sports medicine—is not practiced in a vacuum. The best that one can do is to be aware of potential sources of bias and mitigate them as much as possible, with the best method often being through disclosure and transparency regarding financial or other types of relationships.18,22

CONCLUSION Providing medical care for an athletic team is a unique subsection of medical practice, carry ing with it many complex situations and nuances that require a physician to be dedicated both to medical practice and the institution of sports participation and competition. Athletes suffer many musculoskeletal injuries through their training and games, but a team physician must also be prepared to handle general medical ailments and medical emergencies, in addition to serving as the leader of a multidisciplinary medical team that can include athletic trainers, physical therapists, psychologists, dietitians, and others. Being a team physician requires knowledge and a strong interest in sports medicine, good communication skills, and an awareness of all the ethical complexities involved in caring for athletes. These can range from managing confidentiality and consent, to considering coaches, administrators, and other third parties whose interests may or may not coincide with the best interests of an individual athlete’s overall health. Ultimately, if one can navigate the challenges of team coverage it can be a very rewarding aspect of practice.

5.

6.

7.

8.

9.

10.

11.

12.

13.

14.

15.

16.

17.

18.

19.

REFERENCES 1.

2.

3.

4.

Herring SA, Kibler WB, Putukian M, et al. Team physician definition, qualifications, and responsibilities: a consensus statement. Rosemont, IL: American Academy of Orthopaedic Surgeons, 2013. Hodax JD, Sobel AD, DeFroda S, Chambers AB, Hulstyn MJ. Orthopaedic resident preparation and confidence in treating onfield injuries. Orthop J Sports Med. 2017;5(5):2325967117708286. doi:10.1177/2325967117708286. Herring SA, Kibler WB, Putukian M. Sideline preparedness for the team physician: a consensus statement—2012 update. Med Sci Sports Exerc. 2012;44(12):2442-2445. doi:10.1249/MSS.0b013e318275044f. Chen AW, Archbold CS, Hutchinson M, Domb BG. Sideline management of nonmusculoskeletal injuries by the orthopaedic team physician. J Am Acad Orthop Surg. 2019;27(4):e146-e155. doi:10.5435/ JAAOS-D-17-00237.

20.

21.

22.

Hootman JM, Dick R, Agel J. Epidemiology of collegiate injuries for 15 sports: summary and recommendations for injury prevention initiatives. J Athl Train. 2007;42(2):311-319. Roberts WO, Löllgen H, Matheson GO, et al; American College of Sports Medicine (ACSM); Fédération Internationale du Médicine du Sport (FIMS). Advancing the preparticipation physical evaluation: an ACSM and FIMS joint consensus statement. Clin J Sport Med. 2014;24(6):442-447. doi:10.1097/JSM.0000000000000168. Kane SM, White RA. Medical malpractice and the sports medicine clinician. Clin Orthop Relat Res. 2009;467(2):412-419. doi:10.1007/ s11999-008-0589-5. Steiner ME, Quigley DB, Wang F, Balint CR, Boland AL Jr. Team physicians in college athletics. Am J Sports Med. 2005;33(10):1545-1551. doi:10.1177/0363546505275491. American Medical Association. Policy H-470.995: Athletic (Sports) Medicine. 1998. https://www.nata.org/sites/default/files/ama_recommendation.pdf Accessed March 21, 2019. Czuppon S, Racette BA, Klein SE, Harris-Hayes M. Variables associated with return to sport following anterior cruciate ligament reconstruction: a systematic review. Br JSports Med. 2014;48(5):356-364. doi:10.1136/bjsports-2012-091786. Lentz TA, Zeppieri G Jr, George SZ, et  al. Comparison of physical impairment, functional, and psychosocial measures based on fear of reinjury/lack of confidence and return-to-sport status after ACL reconstruction. Am J Sports Med. 2014;43(2):345-353. doi:10.1177/0363546514559707. Gerometta A, Klouche S, Herman S, Lefevre N, Bohu Y. The Shoulder Instability–Return to Sport After Injury (SIRSI): a valid and reproducible scale to quantify psychological readiness to return to sport after traumatic shoulder instability. Knee Surg Sports Traumatol Arthrosc. 2018;26(1):203-211. doi:10.1007/s00167-017-4645-0. Psychological issues related to illness and injury in athletes and the team physician: a consensus statement—2016 update. Curr Sports Med Rep. 2017;16(3):189-201. doi:10.1249/JSR.0000000000000359. Thomas DT, Erdman KA, Burke LM. American College of Sports Medicine joint position statement. Nutrition and athletic performance. Med Sci Sports Exerc. 2016;48(3):543-568. doi:10.1249/ MSS.0000000000000852. Turocy PS, DePalma BF, Horswill CA, et al; National Athletic Trainers’ Association. National Athletic Trainers’ Association position statement: safe weight loss and maintenance practices in sport and exercise. J Athl Train. 2011;46(3):322-336. doi:10.4085/1062-6050-46.3.322. The team physician and strength and conditioning of athletes for sports: a consensus statement. Med Sci Sports Exerc. 2015;47(2):440445. doi:10.1249/MSS.0000000000000583. Smoot MK, Amendola A, Cramer E, et  al. A cluster of exertional rhabdomyolysis affecting a Division I football team. Clin J Sport Med. 2013;23(5):365-372. doi:10.1097/JSM.0b013e3182914fe2. Dunn WR, George MS, Churchill L, Spindler KP. Ethics in sports medicine. Am J Sports Med. 2007;35(5):840-844. doi:10.1177/0363546506295177. U.S. Department of Health and Human Ser vices, U.S. Department of Education. Joint guidance on the application of the Family Educational Rights and Privacy Act (FERPA) and the Health Insurance Portability and Accountability Act of 1996 (HIPAA) to student health records. Washington, DC: U.S. Department of Health and Human Ser vices; 2008. Skelley NW, McCormick JJ, Smith MV. In-game management of common joint dislocations. Sports Health. 2014;6(3):246-255. doi:10.1177/1941738113499721. Code of Medical Ethics Opinion 2.1.1: Informed Consent. American Medical Association. https://www.ama-assn.org/system/files/2019-06/code-of-medical-ethics-chapter-2.pdf Accessed March 21, 2019. Testoni D, Hornik CP, Smith PB, Benjamin DK Jr, McKinney RE Jr. Sports medicine and ethics. Am J Bioeth. 2013;13(10):4-12. doi:10.10 80/15265161.2013.828114.

2 Epidemiology of Shoulder Instability Incidence, Risk Factors, and Prevention of Instability in the Athlete David J. Tennent, MD; Matthew A. Posner, MD; and Kenneth L. Cameron, PhD, MPH, ATC

Acute traumatic glenohumeral joint instability, subluxations and dislocations, is a pervasive problem in young and physically active individuals.1-8 In the US population, the incidence of shoulder dislocation is approximately 23.9 per 100,000 person-years, with nearly half of the glenohumeral dislocations occurring during sporting activities and in patients between age 15 to 29 years.1 These injuries typically occur more commonly in male than female individuals at a ratio of 2.64:1 male:female.1 Similar trends in the age- and sex-based association for glenohumeral instability have been reported in Norwegian, Swedish, Canadian, Polish, and British population-based studies.3,5-9 These injuries can be particularly problematic in young, high-risk male patients because individuals with a history of a glenohumeral instability event, especially at a young age, have a substantially increased risk of subsequent recurrent events.8,10-14 These recurrent injuries can result in further damage to the soft-tissue structures of the capsule, labrum, ligaments, and rotator cuff. Furthermore, recurrent instability events can lead to progressively increasing levels of osteochondral loss from the humerus and glenoid that can result in an additional risk of future glenohumeral instability.15-18 Persistent glenohumeral joint instability also can contribute to the initiation and progression of osteoarthritis in the shoulder that can cause a substantial degree of disability, socioeconomic cost, and health care cost.19-22 Consequently, many of these injuries require surgical stabilization to definitively manage the loss of the stabilizing effects of the attenuated surrounding osseous and soft-tissue structures that can lead to persistent glenohumeral instability and eventual glenohumeral arthropathy.4,22-25 Though surgical stabilization can restore joint stability and improve function, whether

surgical repair can mitigate the long-term consequences of the initial instability event remains unclear.

INCIDENCE AND PREVALENCE OF GLENOHUMERAL INSTABILITY Multiple epidemiologic and population-based studies have evaluated the incidence of glenohumeral instability within the general population and in young, active, high-risk populations such as athletes, military ser vice members, and cadets (Table 2-1). The majority of these studies have focused on anterior glenohumeral dislocations as reported by various large database registries.1,6,7,9,11,26-30 In sum, these studies suggest that young men are at the highest risk of sustaining a traumatic glenohumeral dislocation event. These studies have shown that the nationwide incidence of glenohumeral dislocation in North American and Western European countries is between 23.1 to 56.3 cases per 100,000 person-years.1,5 In men, the incidence was reported to be between 34.9 to 40.4 cases per 100,000 person-years, and in women incidence was much lower at 11.8 to 15.5 cases per 100,000 person-years. Furthermore, these studies show that 60% to 91.3% of all dislocations occur in male patients, with a peak incidence rate in men younger than 30 years ranging between 47.8 to 204.3 cases per 100,000 person-years. Several studies have evaluated glenohumeral instability in athletes. When looking at high school–age athletes, Robinson et  al found an overall incidence rate for dislocations to be 2.15 per 10,000 athlete exposures.34 More recently, using online reporting databases, Kraeutler and colleagues found the overall incidence rate for shoulder dislocation to

- 11 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 11-18). © 2021 SLACK Incorporated.

12

Chapter 2

https://t.me/mebooksfree

Table 2-1. Epidemiologic Studies Evaluating Anterior Glenohumeral Dislocation STUDY Shah6 7

Enger

1

Zacchilli

30

Owens et al Simonet

31

5

Liavaag Leroux

3

32

Krøner

Nordqvist33 11

Kardouni

POPULATION STUDIED UK Norway US US military US Norway Canada Denmark Sweden US military

OVERALL INCIDENCE 40.4 55.0 23.9 435 8.2 56.3 23.1 17.0 23.9 31.3

PEAK AGE (INCIDENCE RATE), Y M 16-20 (80.5) NR M 20-29: (47.8) NR M 20-29 (23.4) M 20-29: (204.3) M < 20: (98.3) M 20-30 NR M 20-25

MALE INCIDENCE RATE 40.4 NR 34.9 NR 11.2 82.2 34.3 9.1 27.0 NR

FEMALE INCIDENCE RATE 15.5 NR 13.3 NR 5.0 30.9 11.8 8.0 22.0 NR

MALE, % 72.0 73.0 71.8 86.3 70.9 72.2 74.3 53.3 53.0 91.3

Abbreviations: M, median; NR, not reported; UK, United Kingdom; US, United States. Incidence rates shown as (100,000 person-year) unless other wise indicated.

be 2.04 per 100,000 athletic exposures (AEs) in high school athletes and 2.58 per 100,000 AEs in collegiate athletes.26 These rates were highest in collegiate men’s ice hockey (7.42 per 100,000 AEs), wrestling (5.05 per 100,000 AEs), lacrosse (3.59 per 100,000 AEs), football (3.29 per 100,000 AEs), and women’s basketball (3.32 per 100,000 AEs).26 Although lower, these rates were similarly high between college and high school athletics except in football, which showed a lower incidence rate in collegiate football compared to high school football (3.29 vs 6.34 per 100,000).26 This corresponds to previous studies looking at all collegiate glenohumeral instability episodes that showed the highest-risk sports consisting of football, wrestling, and hockey.35 Furthermore, these injuries most commonly occur during practices and are frequently secondary to direct contact with another player in male athletes and with an object in female athletes.35 Within the highest-risk cohort of male collegiate football players participating in the National Football League Combine, 14.9% of athletes showed magnetic resonance imaging (MRI) evidence of a labrum tear indicative of some degree of glenohumeral instability.36 These rates were highest in linemen, with 19.2% of athletes displaying labrum pathology. Furthermore, the labrum pathology was found to be nearly equally distributed between anterior (30.4%), posterior (34.7%), and combined anterior and posterior pathology (34.7%).36 Studies evaluating the incidence of glenohumeral instability in military populations have routinely demonstrated that this population is at high risk for acute traumatic and recurrent instability. When looking at the general US military population, Owens et al reported that 92.5% of glenohumeral dislocation events occurred in men, with an overall incidence rate of 169 cases per 100,000 person-years.29 Similarly, Kardouni and colleagues found an overall 10-year incidence rate of 31.3 cases per 100,000 in US Army military personnel,

with the highest risk groups in young, male soldiers.11 This incidence rate increased to 435 cases per 100,000 when looking at isolated collegiate-age men and women matriculating at the US Military Academy at West Point who sustained any instability event.30 Traumatic glenohumeral subluxations and dislocations can have a substantial negative effect on an individual’s ability to perform at a high level. Acute glenohumeral instability injuries can result in up to 8% of high school athletes being unable to return to sport during the same competitive season.34 Although the majority of these are able to return to sport during the same season, 30% of high school collision athletes require more than 10 days to return to play following an acute glenohumeral instability event.26,34,37 When compared to high school athletes, collegiate athletes have shown a longer recovery time required following an acute glenohumeral instability event, with approximately 45% of collegiate athletes requiring more than 10 days to return to sport.38 Furthermore, only 73% of collegiate contact athletes are able to return to their sport during the same season, with the vast majority of these athletes continuing to experience symptomatic instability during the same season before undergoing stabilization procedures.38 Professional athletes have shown the fastest return to sport among collision athletes; however, the sequela of acute or chronic glenohumeral instability can drastically affect the future careers of those athletes because of decreased playing time and later draft selection in those athletes participating in the National Football League Combine.39-41

CHARACTERIZATION OF INSTABILITY The overwhelming majority of glenohumeral subluxations and dislocations in the general population occur as a traumatic anterior instability injury or event.2,15,29,42 It is further

Epidemiology of Shoulder Instability: Incidence, Risk Factors, and Prevention of Instability in the Athlete impor tant to differentiate between a true glenohumeral dislocation event, which can be defined as a complete dissociation of the glenohumeral joint that often requires a reduction maneuver to restore joint congruity, and a subluxation event, in which some degree of glenohumeral articular contact remains. Subluxation episodes account for up to 85.6% of all glenohumeral instability events, and approximately 90% of all glenohumeral instability events occur secondary to an acute traumatic event.28 Furthermore, between 48% and 60% of dislocations are related to sporting activities.1,28 Although anterior instability events are most commonly reported, combined anterior and posterior labrum pathology is frequently encountered in up to 37% of cases on MRI and during arthroscopic surgery in young, active patients.36,43,44 This is critical to recognize intraoperatively to prevent treatment failures due to residual pathology and continued pathologic glenohumeral motion, because MRI can often incompletely characterize the full extent of the injury.44,45 Whereas the majority of surgically managed glenohumeral instability is primary anterior instability, recent literature has shown that up to 25% of surgically treated glenohumeral instability cases showed evidence of anterior and posterior labrum pathology that required operative intervention at the time of arthroscopy.44 Isolated posterior instability accounts for up to 17% to 19% of all glenohumeral events in some studies.2,44 Although a true posterior dislocation event requiring a manual reduction is uncommon, a subluxation event is reported in 54% of cases with symptomatic shoulder pain during activities that load the posterior labrum, such as pushups and bench-press, reported in 42% of cases.2

CONCOMITANT INJURIES Although the anterior inferior labrum is most commonly injured following a glenohumeral instability event, these injuries are often accompanied by various concomitant pathologic entities that can complicate appropriate management. Approximately 23% of patients have combined superior labrum and anterior or posterior labrum pathology when undergoing surgery.28 Furthermore, when looking at intra-articular pathology seen at the time of arthroscopy, Yiannakopoulas et  al reported that patients undergoing surgery for glenohumeral instability had an anterior labroligamentous periosteal sleeve avulsion lesion in 10.23% of cases, humeral avulsion of the glenohumeral ligament lesions (HAGL) in 1.57% of cases, and a Hill-Sachs lesion in 88.1% of cases.46 Interesting, HAGL lesions have been seen at a much higher incidence in female patients, with as many as 25% of female athletes having evidence of HAGL lesions at the time of arthroscopy.47 Concomitant rotator cuff pathology in glenohumeral instability is rare in young patients, with several small series reporting rates between 3% and 6%; however, these injuries become more common with increasing age following a traumatic dislocation event.27,48-52 Axillary nerve injury can occur in 13.5% to 48% of glenohumeral dislocation events, and this is also correlated with increased age at

13

Table 2-2. Possible Risk Factors for Glenohumeral Instability MODIFIABLE Shoulder girdle strength Activity modification Shoulder proprioception Occupation Sport participation

NONMODIFIABLE Age of primary injury Male sex Hyperlaxity Chondrolabral cleft Glenoid morphology Glenoid dysplasia Glenoid version

the time of injury.27,53,54 Articular cartilage injuries are commonly seen in approximately 18% of primary stabilization procedures and in nearly half of those individuals undergoing revision glenohumeral stabilization procedures.55 Glenoid bone loss in relation to humeral bone loss must also be carefully assessed for appropriate management because first-time and recurrent glenohumeral instability events can result in increasing levels of clinically relevant bone loss that can result in failed management.56-58

RISK FACTORS Identifying modifiable and nonmodifiable risk factors for acute traumatic glenohumeral instability is impor tant because they represent targets for injury-prevention intervention and define subpopulations at the greatest risk for injury who could benefit from injury-prevention interventions, respectively. A summary of potential risk factors for glenohumeral instability is presented in Table 2-2. Although these risk factors are not all actionable for preventive measures, understanding who is at risk for glenohumeral instability is critical for appropriate surveillance and implementing injury-prevention interventions. Furthermore, appropriate identification of those individuals with modifiable risk factors may allow preventive interventions to be most effective.

Modifiable Risk Factors Possible modifiable risk factors for glenohumeral instability can be classified into 2  categories: strength modulation and activity modification. The dynamic stabilizing effect of the rotator cuff has been investigated as a potential modifiable risk factor for glenohumeral instability with unclear results.59-61 Weak rotator cuff musculature has been associated with glenohumeral instability retrospectively; however, in a large, prospective cohort study specifically looking at external and internal rotation strength, no differences were seen between those individuals who had a subsequent glenohumeral instability event and those who did not.59,60 Consequently, although a weakened rotator cuff may result

14

Chapter 2

following a glenohumeral instability event, evidence does not support increasing rotator cuff strength as a primary prevention intervention for glenohumeral instability. Strengthening the rotator cuff following incident injury, however, may be an impor tant secondary prevention intervention in terms of mitigating recurrent instability.60 The proprioceptive and sensorimotor function of the capsulolabral soft tissues may represent a target for secondary injury–prevention interventions as well, because the mechanoreceptor activity has been found to be disrupted and subsequently restored following surgical stabilization after a glenohumeral instability event.62-64 However, it remains unclear whether sensorimotor deficits before initial injury exist in those who go on to experience an incident glenohumeral instability event in contrast to those who do not. Exercises specifically focused on improving the proprioceptive activity and dynamic stability of the glenohumeral joint may help prevent further instability events after initial injury and should be considered impor tant secondary injury–prevention interventions.64,65 Because the majority of glenohumeral instability events occur during contact sports and high-velocity activities, activity modification and avoidance of high-risk activities can greatly reduce an individual’s risk for glenohumeral instability. In par ticular, those individuals participating in contact sports and in military occupations have shown significantly higher risks for glenohumeral instability because of contact forces and/or occupational hazards. Although limiting the number of exposures to these activities may reduce the risk of glenohumeral joint instability, it is often not reasonable to modify these activities because of personal desire and/or occupational requirements. However, limiting exposure through free-time and recreational activities may be warranted.

Nonmodifiable Risk Factors Understanding the nonmodifiable risk factors for glenohumeral instability is impor tant to identify those individuals who are at a high baseline risk for glenohumeral instability. Those individuals in high-risk baseline categories should be targeted for further study and the development and evaluation of preventive strategies and counseling to reduce the risk of incident injury. The most impor tant nonmodifiable risk factors for glenohumeral instability and recurrent instability are age and sex. Multiple studies have established that male individuals younger than 30 years have the highest dislocation rates in all populations.1-8 Although much of the literature has shown that male sex is in itself a risk factor for glenohumeral instability, more recent studies have shown contrasting results in female athletes in sex-matched sports and exposures such as those seen in many contact and collision sports.35,66 Specifically, no differences were reported in collegiate soccer, basketball, softball/baseball, ice hockey, and rugby.35,66 The similarities in glenohumeral dislocation rates in these sports are likely

due to the similar exposure in these sports between the sexes compared to the general population. Anatomy has also been recognized as an impor tant nonmodifiable risk factor for glenohumeral instability. Glenoid gross anatomy, attritional bone loss, glenoid version, and coracohumeral interval distance have all been implicated in glenohumeral instability. The “inverted pear” glenoid, in which the inferior glenoid is less wide than the superior glenoid, has been shown to correlate with increasing levels of glenoid bone loss and subsequent instability.56 In a large, prospective cohort study, participants with tall, narrow glenoids were found to be at higher risk of anterior glenohumeral instability than those with short, wide glenoid morphology.42 Those patients with an anatomic chondrolabral cleft were similarly found to have 2.8 times higher risk for anterior glenohumeral instability.67 Glenoid version has also been implicated in posterior glenohumeral instability. Those patients with posterior instability were observed to have 5 degrees more retroversion than those without instability and had a 17% increased risk for posterior instability for every 1 degree of increased glenoid retroversion.68,69 Similarly, Owens et  al reported that for every 1  mm of increased coracohumeral distance, individuals were 20% more likely to sustain a glenohumeral instability event.42

Risk of Recurrence The success of nonoperative treatment of glenohumeral instability is influenced by age at the time of initial dislocation and male sex. In a recent systemic review, recurrent glenohumeral instability developed in 47% of individuals when combining all level-I studies; participants were most likely to have a recurrent event in the first year following injury, male participants were 3  times more likely to experience a recurrent episode, and those younger than 20  years were 13 times more likely to fail nonoperative treatment.13 In the general population, 55.7% of patients who experience a firsttime anterior dislocation will develop recurrent instability by 2 years.12 Furthermore, 86.7% of those individuals who experience a recurrent dislocation will sustain this by 2 years.70 In 25-year outcome data looking at nonoperative treatment of primary anterior shoulder dislocations sustained in patients age 12 to 40 years, 57% of patients sustained a recurrent anterior glenohumeral instability event with increased failure of nonoperative treatment corresponding with a younger age at the time of initial dislocation.71 Other risk factors found to be strongly correlated in a meta-analysis with recurrent anterior glenohumeral instability include hyperlaxity and a corresponding greater tuberosity fracture.14 Weaker evidence has also suggested that a bony Bankart lesion, occupation, participation in physical therapy, and nerve palsy were also risk factors for recurrent instability.14 In high-risk populations the risk of recurrence following nonoperatively treated glenohumeral instability is even higher. In the military cadet population, individuals with a prior

Epidemiology of Shoulder Instability: Incidence, Risk Factors, and Prevention of Instability in the Athlete

15

Table 2-3. Levels of Prevention and Associated Definitions LEVELS OF PREVENTION Primary prevention

Secondary prevention

Tertiary prevention

DEFINITION Primary prevention interventions are designed to prevent an injury, disease, or musculoskeletal condition from occurring in the first place. The focus is generally on policies, practices, and behaviors that mitigate initial risk. Secondary prevention initiatives attempt to recognize or identify an injury or disease at its earliest stage so that prompt and appropriate management can be initiated to mitigate the secondary effects of the injury or disease and restore function. Successful secondary prevention reduces the impact of the injury or disease in the short term and may also affect long-term outcomes. The focus is generally on emergency management and initial medical care during the acute and subacute phases. Tertiary prevention efforts focus on reducing or minimizing the long-term consequences of an injury or disease once it has occurred. The goal of tertiary prevention is to eliminate or delay the onset of complications, morbidity, and long-term disability due to the injury or disease. Most medical interventions for chronic management fall into this category. The focus is generally on long-term management and health behavior change.

history of nonoperatively treated instability were 5.6 times more likely to have a subsequent anterior glenohumeral event and 4.6 times more likely to sustain a posterior instability event. The risk of recurrent anterior glenohumeral dislocation in high-school and collegiate athletic populations is as much as 9.5 times greater than in those without a history of previous instability.72,73 When instability is further classified as a glenohumeral dislocation or subluxation, subluxationevent patients were shown to return to sport in 89% of cases during the same athletic season without surgery compared to only 26% of true glenohumeral dislocations.74 These differences between athletes and the general population are likely due to a higher exposure to an injury event without anatomic restoration of the native stabilizing anatomy.

OUTCOMES The morbidity associated with glenohumeral instability events is considerable. Most notable, glenohumeral instability is associated with the development and progression of glenohumeral post-traumatic osteoarthritis because of increased direct compression and shear injury to the chondral surfaces acutely at the time of injury and over time because of altered biomechanics.25,75-77 A substantial portion of this damage likely occurs at the time of injury; however, additional damage does occur with repeated instability events and joint incongruity without stabilization in long-term follow-up.20,25,77 Further attritional glenoid bone loss and increasing Hill-Sachs lesion size can also occur with chronic instability and as the glenohumeral instability progresses.58,77 Ultimately, the end result of glenohumeral instability can contribute to a substantial degree of disability, socioeconomic costs, and direct health care costs.19-22 Additional attention to the primary prevention and early definitive management of glenohumeral instability is required to mitigate these longterm consequences that negatively affect joint health status.

PREVENTION The prevention of glenohumeral instability is predicated on the appropriate recognition of an individual’s risk profile before the incident injury. This includes what is known about modifiable and nonmodifiable risk factors related to glenohumeral joint instability. Additional high-quality prospective research must be conducted to identify modifiable risk factors associated with injury because the majority of known risk factors to date are nonmodifiable. Furthermore, implementing preventive measures can be classified as primary, secondary, or tertiary prevention interventions (Table 2-3). Primary prevention is focused on the initial prevention of a glenohumeral instability event by targeting modifiable risk factors for intervention in high-risk populations. Unlike many other musculoskeletal injuries, such as anterior cruciate ligament injuries in the knee, these risk factors have not been fully elucidated. As a result, few primary prevention interventions or programs currently exist to reduce the risk of acute traumatic glenohumeral instability events.78 Consequently, well-designed prospective cohort studies are needed to identify the modifiable risk factors for glenohumeral instability that might serve as targets for injuryprevention interventions. These studies are needed to help clinicians understand targets for rules, policies, and actions that protect an individual from being placed in a vulnerable position. Improving these primary prevention targets would subsequently help prevent the disability associated with glenohumeral instability. Following a glenohumeral instability episode, secondary preventive measures focused on the initial management and care of the injured athlete should be undertaken to minimize the long-term morbidity of a glenohumeral instability event. This is primarily accomplished through early physical therapy focusing on shoulder strengthening, range of motion, and proprioception with return to play predicated on restoration

16

Chapter 2

of function without pain. Furthermore, bracing can be considered in the early postinjury time frame to assist with early rehabilitation; however, the data remain mixed on the efficacy of bracing to prevent recurrent glenohumeral instability events.4,79 This can often be accomplished with successful return to play within days to several weeks of the initial injury, with early surgical management reserved for highrisk individuals.77,78 In many cases of posterior glenohumeral instability, successful treatment and return to in-season play can be accomplished through conservative measures alone. However, because recurrence rates are high in athletic populations, surgical intervention is often required to minimize the long-term consequences of glenohumeral instability, including continued bone loss, the future development of osteoarthritis, and to minimize the cost of care.75 Studies have further shown that when given the objective data, individuals most often prefer primary surgical management vs nonoperative treatment because of the risk of recurrence.82 Cost analysis of operative stabilization vs nonoperative treatment also shows that arthroscopic stabilization is more costeffective than nonoperative treatment because of the risk of recurrent injury and the associated long-term sequelae, particularly in young, high-risk patient populations.83 Tertiary preventive measures focus on minimizing the long-term consequences of glenohumeral instability and optimizing quality of life. Surgical intervention focused on restoring the capsulolabral and osseous stabilizers before the development of recurrent instability should be undertaken to minimize the long-term morbidity associated with glenohumeral instability, such as osteoarthritis and recurrent instability. Avoidance of high-risk activities and activity modification may also prevent further injury to the glenohumeral joint and articular cartilage. Institution of long-term shoulder rehabilitation programs may help restore strength and proprioceptive function of the injured capsulolabral tissue. Although little research has been performed on the full long-term effects of glenohumeral instability, tertiary prevention interventions are also impor tant to minimize the morbidity of known osteoarthritic changes that occur following a glenohumeral instability event.20

CONCLUSION Although glenohumeral instability is common within the general population, the incidence of glenohumeral instability within high-risk subpopulations is much higher. These include young male individuals, young athletes engaged in contact and collision sports, and individuals engaged in occupational tasks with significant upper-extremity demands such as tactical athletes. These populations also share a number of nonmodifiable risk factors that place them at high risk for recurrent instability and subsequent glenohumeral morbidity. Despite our current understanding of these nonmodifiable risk factors, there is very little scientific evidence that has identified modifiable risk factors for glenohumeral instability that may serve as targets for

primary injury–prevention interventions. Rigorous prospective cohort studies are needed in these high-risk subpopulations to determine whether modifiable risk factors can be identified. If they are identified, subsequent clinical trials targeting these modifiable risk factors would be prudent to evaluate the efficacy and effectiveness of primary injury– prevention interventions. The majority of our current prevention efforts are focused on secondary and tertiary prevention with the goals being to eliminate recurrent instability and mitigate the long-term consequences of injury on joint health status across the life span. However, because of the impact and long-term consequences of acute traumatic glenohumeral instability injuries, primary prevention interventions are clearly needed. In high-risk subpopulations, early surgical stabilization appears to be most clinically relevant and cost-effective in managing incident glenohumeral instability events to prevent subsequent instability and bone and articular cartilage loss, and to promote overall joint health.

REFERENCES 1.

2.

3.

4.

5. 6.

7.

8.

9. 10.

11.

12.

Zacchilli MA, Owens BD. Epidemiology of shoulder dislocations presenting to emergency departments in the United States. J Bone Joint Surg Am. 2010;92(3):542-549. doi:10.2106/JBJS.I.00450. Lanzi JT Jr, Chandler PJ, Cameron KL, Bader JM, Owens BD. Epidemiology of posterior glenohumeral instability in a young athletic population. Am J Sports Med. 2017;45(14):3315-3321. doi:10.1177/0363546517725067. Leroux T, Wasserstein D, Veillette C, et  al. Epidemiology of primary anterior shoulder dislocation requiring closed reduction in Ontario, Canada. Am J Sports Med. 2014;42(2):442-450. doi:10.1177/0363546513510391. Galvin JW, Ernat JJ, Waterman BR, Stadecker MJ, Parada SA. The epidemiology and natural history of anterior shoulder instability. Curr Rev Musculoskelet Med. 2017;10(4):411-424. doi:10.1007/ s12178-017-9432-5. Liavaag S, Svenningsen S, Reikeras O, et al. The epidemiology of shoulder dislocations in Oslo. Scand J Med Sci Sports. 2011;21:e334-e340. Shah A, Judge A, Delmestri A, et al. Incidence of shoulder dislocations in the UK, 1995-2015: a population-based cohort study. BMJ Open. 2017;7:e016112. doi:10.1136/bmjopen-2017-016112. Enger M, Skjaker SA, Melhuus K, et al. Shoulder injuries from birth to old age: a 1-year prospective study of 3031 shoulder injuries in an urban population. Injury. 2018;49(7):1324-1329. doi:10.1016/j.injury .2018.05.013. Szyluk K, Jasi
ski A, Niemiec P, Mielnik M, Widuchowski W, Koczy B. Male gender and age range 20-29 years are the most important non-modifiable risk factors for recurrence after primary posttraumatic shoulder dislocation. Knee Surg Sports Traumatol Arthrosc. 2018;26(8):2454-2464. doi:10.1007/s00167-018-4924-4. Hovelius L. Incidence of shoulder dislocation in Sweden. Clin Orthop Relat Res. 1982;(166):127-131. Cameron KL, Mountcastle SB, Nelson BJ, et  al. History of shoulder instability and subsequent injury during four years of followup: a survival analysis. J Bone Joint Surg Am. 2013;95(5):439-445. doi:10.2106/JBJS.L.00252. Kardouni JR, McKinnon CJ, Seitz AL. Incidence of shoulder dislocations and the rate of recurrent instability in soldiers. Med Sci Sports Exerc. 2016;48(11):2150-2156. doi:10.1249/MSS.0000000000001011. Robinson CM, Seah M, Akhtar MA. The epidemiology, risk of recurrence, and functional outcome after an acute traumatic posterior dislocation of the shoulder. J Bone Joint Surg Am. 2011;93(17):16051613. doi:10.2106/JBJS.J.00973.

Epidemiology of Shoulder Instability: Incidence, Risk Factors, and Prevention of Instability in the Athlete 13.

14.

15.

16. 17.

18.

19.

20.

21.

22.

23.

24.

25.

26.

27.

28.

29.

Wasserstein DN, Sheth U, Colbenson K, et al. The true recurrence rate and factors predicting recurrent instability after nonsurgical management of traumatic primary anterior shoulder dislocation: a systematic review. Arthroscopy. 2016;32(12):2616-2625. doi:10.1016/j. arthro.2016.05.039. Olds M, Ellis R, Donaldson K, Parmar P, Kersten  P. Risk factors which predispose first-time traumatic anterior shoulder dislocations to recurrent instability in adults: a systematic review and meta-analysis. Br J Sports Med. 2015;49(14):913-922. doi:10.1136/ bjsports-2014-094342. Owens BD, Nelson BJ, Duffey ML, et al. Pathoanatomy of first-time, traumatic, anterior glenohumeral subluxation events. J  Bone Joint Surg Am. 2010;92(7):1605-1611. doi:10.2106/JBJS.I.00851. Brelin A, Dickens JF. Posterior shoulder instability. Sports Med Arthrosc Rev. 2017;25(3):136-143. doi:10.1097/JSA.0000000000000160. Robinson EC, Thangamani VB, Kuhn MA, Ross  G. Arthroscopic findings after traumatic shoulder instability in patients older than 35 years. Orthop J Sports Med. 2015;3(5):2325967115584318. doi:10.1177/2325967115584318. Trivedi S, Pomerantz ML, Gross D, Golijanan P, Provencher MT. Shoulder instability in the setting of bipolar (glenoid and humeral head) bone loss: the glenoid track concept. Clin Orthop Relat Res. 2014;472(8):2352-2362. doi:10.1007/s11999-014-3589-7. Virani NA, Williams CD, Clark R, Polikandriotis J, Downes KL, Frankle MA. Preparing for the bundled-payment initiative: the cost and clinical outcomes of total shoulder arthroplasty for the surgical treatment of glenohumeral arthritis at an average 4-year followup. J  Shoulder Elbow Surg. 2013;22(12):1601-1611. doi:10.1016/j. jse.2012.12.028. Ogawa K, Yoshida A, Ikegami  H. Osteoarthritis in shoulders with traumatic anterior instability: preoperative survey using radiography and computed tomography. J Shoulder Elbow Surg. 2006;15(1):23-29. doi:10.1016/j.jse.2005.05.011. Vezeridis PS, Ishmael CR, Jones KJ, Petrigliano FA. Glenohumeral dislocation arthropathy: etiology, diagnosis, and management. J  Am Acad Orthop Surg. 2019;27:227-235. doi:10.5435/ JAAOS-D-17-00056. Plath JE, Aboalata M, Seppel G, et al. Prevalence of and risk factors for dislocation arthropathy: radiological long-term outcome of arthroscopic Bankart repair in 100 shoulders at an average 13-year follow-up. Am J Sports Med. 2015;43(5):1084-1090. doi:10.1177/0363546515570621. Hovelius L, Augustini BG, Fredin H, Johansson O, Norlin R, Thorling  J. Primary anterior dislocation of the shoulder in young patients. A ten-year prospective study. J  Bone Joint Surg Am. 1996;78(11):1677-1684. doi:10.2106/00004623-199611000-00006. Bishop JA, Crall TS, Kocher MS. Operative versus nonoperative treatment after primary traumatic anterior glenohumeral dislocation: expected-value decision analysis. J  Shoulder Elbow Surg. 2011;20(7):1087-1094. doi:10.1016/j.jse.2011.01.031. Hovelius L, Saeboe M. Neer Award 2008: arthropathy after primary anterior shoulder dislocation—223 shoulders prospectively followed up for twenty-five years. J Shoulder Elbow Surg. 2009;18(3):339-347. doi:10.1016/j.jse.2008.11.004. Kraeutler MJ, Currie DW, Kerr ZY, Roos KG, McCarty EC, Comstock RD. Epidemiology of shoulder dislocations in high school and collegiate athletics in the United States: 2004/2005 through 2013/2014. Sports Health. 2018;10(1):85-91. doi:10.1177/1941738117709764. Atef A, El-Tantawy A, Gad H, Hefeda  M. Prevalence of associated injuries after anterior shoulder dislocation: a prospective study. Int Orthop. 2016;40(3):519-524. doi:10.1007/s00264-015-2862-z. Blomquist J, Solheim E, Liavaag S, Schroder CP, Espehaug B, Havelin LI. Shoulder instability surgery in Norway: the first report from a multicenter register, with 1-year follow-up. Acta Orthop. 2012;83(2):165-170. doi:10.3109/17453674.2011.641102. Owens BD, Dawson L, Burks R, Cameron KL. Incidence of shoulder dislocation in the United States military: demographic considerations from a high-risk population. J Bone Joint Surg Am. 2009;91(4):791796. doi:10.2106/JBJS.H.00514.

30.

31.

32.

33.

34.

35.

36.

37.

38.

39.

40.

41.

42.

43.

44.

45.

46.

47.

48.

17

Owens BD, Duffey ML, Nelson BJ, DeBerardino TM, Taylor DC, Mountcastle SB. The incidence and characteristics of shoulder instability at the United States Military Academy. Am J Sports Med. 2007;35(7):1168-1173. doi:10.1177/0363546506295179. Simonet WT, Melton LJ III, Cofield RH, Ilstrup DM. Incidence of anterior shoulder dislocation in Olmsted County, Minnesota. Clin Orthop Relat Res. 1984;(186):186-191. Krøner K, Lind T, Jensen  J. The epidemiology of shoulder dislocations. Arch Orthop Trauma Surg. 1989;108(5):288-290. doi:10.1007/ bf00932317. Nordqvist A, Petersson CJ. Incidence and causes of shoulder girdle injuries in an urban population. J Shoulder Elbow Surg. 1995;4(2):107112. doi:10.1016/s1058-2746(05)80063-1. Robinson TW, Corlette J, Collins CL, Comstock RD. Shoulder injuries among US high school athletes, 2005/2006-2011/2012. Pediatrics. 2014;133(2):272-279. doi:10.1542/peds.2013-2279. Owens BD, Agel J, Mountcastle SB, Cameron KL, Nelson BJ. Incidence of glenohumeral instability in collegiate athletics. Am J Sports Med. 2009;37(9):1750-1754. doi:10.1177/0363546509334591. Mannava S, Frangiamore SJ, Murphy CP, et  al. Prevalence of shoulder labral injury in collegiate football players at the National Football League Scouting Combine. Orthop J Sports Med. 2018;6(7):2325967118783982. doi:10.1177/2325967118783982. Buss DD, Lynch GP, Meyer CP, Huber SM, Freehill MQ. Nonoperative management for in-season athletes with anterior shoulder instability. Am J Sports Med. 2004;32(6):1430-1433. doi:10.1177/0363546503262069. Dickens JF, Owens BD, Cameron KL, et  al. Return to play and recurrent instability after in-season anterior shoulder instability: a prospective multicenter study. Am J Sports Med. 2014;42(12):2842-2850. doi:10.1177/0363546514553181. Murphy CP, Frangiamore SJ, Mannava S, et al. Effect of posterior glenoid labral tears at the NFL Combine on future NFL performance. Orthop J Sports Med. 2018;6(10):2325967118787464. doi:10.1177/ 2325967118787464. Murphy CP, Frangiamore SJ, Mannava S, et al. Effect of anterior glenoid labral tears and glenoid bone loss at the NFL Combine on future NFL performance. Orthop J Sports Med. 2018;6:2325967118784884. doi:10.1177/2325967118784884. Okoroha KR, Taylor KA, Marshall NE, et  al. Return to play after shoulder instability in National Football League athletes. J Shoulder Elbow Surg. 2018;27(1):17-22. doi:10.1016/j.jse.2017.07.027. Owens BD, Campbell SE, Cameron KL. Risk factors for anterior glenohumeral instability. Am J Sports Med. 2014;42(11):2591-2596. doi:10.1177/0363546514551149. Dickens JF, Kilcoyne KG, Haniuk E, Owens BD. Combined lesions of the glenoid labrum. Phys Sportsmed. 2012;40(1):102-108. doi:10.3810/psm.2012.02.1956. Song DJ, Cook JB, Krul KP, et al. High frequency of posterior and combined shoulder instability in young active patients. J  Shoulder Elbow Surg. 2015;24(2):186-190. doi:10.1016/j.jse.2014.06.053. Eisner EA, Roocroft JH, Edmonds EW. Underestimation of labral pathology in adolescents with anterior shoulder instability. J Pediatr Orthop. 2012;32(1):42-47. doi:10.1097/BPO.0b013e31823d3514. Yiannakopoulos CK, Mataragas E, Antonogiannakis E. A comparison of the spectrum of intra-articular lesions in acute and chronic anterior shoulder instability. Arthroscopy. 2007;23(9):985-990. doi:10.1016/j.arthro.2007.05.009. Patzkowski JC, Dickens JF, Cameron KL, Bokshan SL, Garcia EJ, Owens BD. Pathoanatomy of shoulder instability in collegiate female athletes. Am J Sports Med. 2019;47(8):1909-1914. doi:10.1177/0363546519850810. Hintermann B, Gächter A. Arthroscopic findings after shoulder dislocation. Am J Sports Med. 1995;23(5):545-551. doi:10.1177/ 036354659502300505.

18 49.

50.

51.

52.

53.

54.

55.

56.

57.

58.

59.

60.

61.

62.

63.

64.

65.

Chapter 2 Shin SJ, Ko YW, Lee  J. Intra-articular lesions and their relation to arthroscopic stabilization failure in young patients with firsttime and recurrent shoulder dislocations. J  Shoulder Elbow Surg. 2016;25(11):1756-1763. doi:10.1016/j.jse.2016.03.002. Kim DS, Yoon YS, Yi CH. Prevalence comparison of accompanying lesions between primary and recurrent anterior dislocation in the shoulder. Am J Sports Med. 2010;38(10):2071-2076. doi:10.1177/0363546510371607. Pevny T, Hunter RE, Freeman JR. Primary traumatic anterior shoulder dislocation in patients 40  years of age and older. Arthroscopy. 1998;14(3):289-294. doi:10.1016/s0749-8063(98)70145-8. Porcellini G, Paladini P, Campi F, Paganelli M. Shoulder instability and related rotator cuff tears: arthroscopic findings and treatment in patients aged 40 to 60  years. Arthroscopy. 2006;22(3):270-276. doi:10.1016/j.arthro.2005.12.015. Visser CP, Coene LN, Brand R, Tavy DL. The incidence of nerve injury in anterior dislocation of the shoulder and its influence on functional recovery. A prospective clinical and EMG study. J Bone Joint Surg Br. 1999;81(4):679-685. doi:10.1302/0301-620x.81b4.9005. Robinson CM, Shur N, Sharpe T, Ray A, Murray IR. Injuries associated with traumatic anterior glenohumeral dislocations. J Bone Joint Surg Am. 2012;94(1):18-26. doi:10.2106/JBJS.J.01795. Duchman KR, Hettrich CM, Glass NA, et al. The incidence of glenohumeral bone and cartilage lesions at the time of anterior shoulder stabilization surgery: a comparison of patients undergoing primary and revision surgery. Am J Sports Med. 2018;46(10):2449-2456. doi:10.1177/0363546518781331. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694. doi:10.1053/ jars.2000.17715. Dickens JF, Owens BD, Cameron KL, et al. The effect of subcritical bone loss and exposure on recurrent instability after arthroscopic Bankart repair in intercollegiate American football. Am J Sports Med. 2017;45(8):1769-1775. doi:10.1177/0363546517704184. McNeil JW, Beaulieu-Jones BR, Bernhardson AS, et al. Classification and analysis of attritional glenoid bone loss in recurrent anterior shoulder instability. Am J Sports Med. 2017;45(4):767-774. doi:10.1177/0363546516677736. Roach CJ, Cameron KL, Westrick RB, Posner MA, Owens BD. Rotator cuff weakness is not a risk factor for first-time anterior glenohumeral instability. Orthop J Sports Med. 2013;1(1):2325967113489097. doi:10.1177/2325967113489097. Edouard P, Degache F, Beguin L, et  al. Rotator cuff strength in recurrent anterior shoulder instability. J  Bone Joint Surg Am. 2011;93(8):759-765. doi:10.2106/JBJS.I.01791. Saccol MF, Zanca GG, Ejnisman B, de Mello MT, Mattiello SM. Shoulder rotator strength and torque steadiness in athletes with anterior shoulder instability or SLAP lesion. J Sci Med Sport. 2014;17(5):463-468. doi:10.1016/j.jsams.2013.10.246. Mornieux G, Hirschmüller A, Gollhofer A, Südkamp NP, Maier D. Multimodal assessment of sensorimotor shoulder function in patients with untreated anterior shoulder instability and asymptomatic handball players. J Sports Med Phys Fitness. 2018;58(4):472-479. doi:10.23736/S0022-4707.17.06874-8. Rokito AS, Birdzell MG, Cuomo F, Di Paola MJ, Zuckerman JD. Recovery of shoulder strength and proprioception after open surgery for recurrent anterior instability: a comparison of two surgical techniques. J  Shoulder Elbow Surg. 2010;19(4):564-569. doi:10.1016/j. jse.2009.09.010. Myers JB, Wassinger CA, Lephart SM. Sensorimotor contribution to shoulder stability: effect of injury and rehabilitation. Man Ther. 2006;11(3):197-201. doi:10.1016/j.math.2006.04.002. Salles JI, Velasques B, Cossich V, et al. Strength training and shoulder proprioception. J  Athl Train. 2015;50(3):277-280. doi:10.4085/ 1062-6050-49.3.84.

66.

67.

68.

69.

70.

71.

72.

73.

74.

75.

76.

77.

78.

79.

80.

81.

82.

83.

Peck KY, Johnston DA, Owens BD, Cameron KL. The incidence of injury among male and female intercollegiate rugby players. Sports Health. 2013;5(4):327-333. doi:10.1177/1941738113487165. Campbell SE, Dewitt RM, Cameron KL, et al. Posterior chondrolabral cleft: clinical significance and associations with shoulder instability. HSS J. 2014;10(3):208-212. doi:10.1007/s11420-014-9404-x. Gottschalk MB, Ghasem A, Todd D, Daruwalla J, Xerogeanes J, Karas  S. Posterior shoulder instability: does glenoid retroversion predict recurrence and contralateral instability? Arthroscopy. 2015;31(3):488-493. doi:10.1016/j.arthro.2014.10.009. Privitera DM, Siegel EJ, Miller LR, Sinz NJ, Higgins LD. Glenoid version and its relationship to glenohumeral instability and labral tears. J  Shoulder Elbow Surg. 2016;25(7):1056-1063. doi:10.1016/j. jse.2015.11.013. Robinson CM, Howes J, Murdoch H, Will E, Graham C. Functional outcome and risk of recurrent instability after primary traumatic anterior shoulder dislocation in young patients. J Bone Joint Surg Am. 2006;88(11):2326-2336. doi:10.2106/JBJS.E.01327. Hovelius L, Olofsson A, Sandström B, et al. Nonoperative treatment of primary anterior shoulder dislocation in patients forty years of age and younger. A prospective twenty-five-year follow-up. J Bone Joint Surg Am. 2008;90(5):945-952. doi:10.2106/JBJS.G.00070. Knowles SB, Marshall SW, Bowling JM, et al. A prospective study of injury incidence among North Carolina high school athletes. Am J Epidemiol. 2006;164(12):1209-1221. doi:10.1093/aje/kwj337. Van Mechelen W, Twisk J, Molendijk A, Blom B, Snel J, Kemper HC. Subject-related risk factors for sports injuries: a 1-yr prospective study in young adults. Med Sci Sports Exerc. 1996;28(9):1171-1179. doi:10.1097/00005768-199609000-00014. Shanley E, Thigpen C, Brooks J, et al. Return to sport as an outcome measure for shoulder instability: surprising findings in nonoperative management in a high school athlete population. Am J Sports Med. 2019;47(5):1062-1067. doi:10.1177/0363546519829765. Ruckstuhl H, de Bruin ED, Stussi E, Vanwanseele  B. Posttraumatic glenohumeral cartilage lesions: a systematic review. BMC Musculoskelet Disord. 2008;9:107. doi:10.1186/1471-2474-9-107. Habermeyer P, Schuller U, Wiedemann E. The intra-articular pressure of the shoulder: an experimental study on the role of the glenoid labrum in stabilizing the joint. Arthroscopy. 1992;8(2):166-172. doi:10.1016/0749-8063(92)90031-6. Habermeyer P, Gleyze P, Rickert  M. Evolution of lesions of the labrum-ligament complex in posttraumatic anterior shoulder instability: a prospective study. J  Shoulder Elbow Surg. 1999;8(1):66-74. doi:10.1016/s1058-2746(99)90058-7. Cameron KL, Mauntel TC, Owens BD. The epidemiology of glenohumeral joint instability: incidence, burden, and long-term consequences. Sports Med Arthrosc Rev. 2017;25:144-149. doi:10.1097/ JSA.0000000000000155. Jordan RW, Saithna A, Old J, MacDonald  P. Does external rotation bracing for anterior shoulder dislocation actually result in reduction of the labrum? A systematic review. Am J Sports Med. 2015;43(9):2328-2333. doi:10.1177/0363546514555661. Burns TC, Owens BD. Management of shoulder instability in inseason athletes. Phys Sportsmed. 2010;38(3):55-60. doi:10.3810/ psm.2010.10.1808. Owens BD, Dickens JF, Kilcoyne KG, Rue JP. Management of midseason traumatic anterior shoulder instability in athletes. J Am Acad Orthop Surg. 2012;20(8):518-526. doi:10.5435/JAAOS-20-08-518. Streufert B, Reed SD, Orlando LA, Taylor DC, Huber JC, Mather RC III. Understanding preferences for treatment after hypothetical first-time anterior shoulder dislocation: surveying an online panel utilizing a novel shared decision-making tool. Orthop J Sports Med. 2017;5(3):2325967117695788. doi:10.1177/2325967117695788. Crall TS, Bishop JA, Guttman D, Kocher M, Bozic K, Lubowitz JH. Cost-effectiveness analysis of primary arthroscopic stabilization versus nonoperative treatment for first-time anterior glenohumeral dislocations. Arthroscopy. 2012;28(12):1755-1765. doi:10.1016/j. arthro.2012.05.885.

3 Evaluation of Shoulder Instability on the Field and in the Clinic Francis P. Bustos, MD; Jeremy K. Rush, MD, FAAP; and Stephen F. Brockmeier, MD

Shoulder instability or dislocation is a common condition seen in athletes. The team physician should be prepared for the expeditious evaluation and management of shoulder dislocation on the field, as well as the evaluation of shoulder complaints stemming from instability in the clinic setting. In one large epidemiologic study, the male incidence rate of shoulder dislocations presenting to the emergency department was 34.90 per 100,000 person-years.1 The maximum incidence rate occurred in those between age 20 and 29 years (47.8), and 46.8% of all dislocations were in patients between age 15 and 29 years. Shah et al, using a primary care database in the United Kingdom, noted an incidence rate of 40.4 per 100,000 person-years, with a rate of 80.5 in men between age 16 and 20.2 Kerr and colleagues noted that joint dislocations represented 3.6% (n = 755) of all injuries among high school athletes, with shoulder dislocations being most common (54.9%).3 This is due to the remarkable amount of mobility of the glenohumeral joint relative to other articulations. Anatomical considerations will be discussed in the following chapter. In the clinic, shoulder instability can present in a clearer fashion, in the form of an overt dislocation event, or less overtly. Vague complaints of shoulder pain in a young athlete should alert the clinician to the potential of shoulder subluxation. In contrast to the unhurried clinic evaluation, the sideline physician may be challenged with the presentation of an acute dislocation with the expectation of providing prompt treatment in front of an audience of spectators, the team, and coaches. In lieu of radiographic confirmation, a systematic approach to assessing, obtaining reduction, and advising return to play is essential to the skillset of sideline physicians. Despite the frequency of encountering a shoulder

dislocation, there is a paucity of literature regarding onthe-field management. Nevertheless, dislocations have been directly addressed since the days of Hippocrates, and the principles practiced have been handed down by practitioners of each generation of training.

ON-THE-FIELD EVALUATION AND TREATMENT OF SHOULDER DISLOCATION History and Mechanism of Injury In caring for an athlete presenting with shoulder instability, the sideline physician must gather an initial history to determine proper management. It is estimated that 96% of dislocation events are anterior, whereas 4% are the atypical posterior dislocation. Age, hand dominance, type of sporting activity, degree of participation, dislocation history, and shoulder laxity are impor tant components of assessing instability. The mechanism of injury should be reviewed if witnessed, or perhaps video replay recordings can be referenced.4 If the physician was not able to see the injury, consulting the athletic trainer or involved athletes may yield valuable information if no confirmatory radiographs are available. Contralateral shoulder examination can provide information of baseline ligamentous laxity. Shoulder dislocation is most prevalent in football and wrestling (relative risk 2.10 and 1.99, respectively), with competition play associated with 55% of events.3 Posterior shoulder dislocation is less prevalent, and although classically seen in seizure patients, may be seen in contact athletes. Again, football players, weightlifters, and gymnasts are

- 19 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 19-28). © 2021 SLACK Incorporated.

20

Chapter 3

susceptible to a posterior force and therefore are at higher risk because these sports demand that the shoulder be in the forward elevated, internally rotated, and adducted position.10 This cohort is therefore susceptible to posterior dislocation.5

Initial Triage With an acute injury, a survey of the totality of injuries should be undertaken with airway, breathing, and circulation first addressed in accordance with advanced trauma life support protocol. It is critically impor tant to assess for cervical spine injury, and maintain appropriate precautions if spine injury is suspected. If no major injuries other than the shoulder can be identified, the focus can be narrowed and a systematic format of inspection, palpation, and passive and active range of motion specific to the shoulder should be undertaken. The physical examination on the field must include a careful and complete neurovascular exam of the suspected extremity. The clinician should pay special attention to the axillary nerve, which can be in a state of palsy following the dislocation. It is impor tant to not only examine sensation in the axillary nerve distribution but to also ensure active firing of the deltoid muscle itself. The presence of active abduction does not rule out an axillary nerve injury because athletes with even a complete axillary nerve palsy may still have some active abduction using the periscapular muscles. Brachial plexopathies can be an infrequent accompaniment to shoulder dislocation. In a prospective database study of 3633 patients with glenohumeral dislocations, Robinson et al found that 13.5% of traumatic dislocations exhibited a persistent neurological deficit following reduction.6 The shoulder will frequently be held in a position of slight abduction and internal rotation in the setting of an anterior dislocation. Palpation may reveal a prominence anterior and inferior to the normal location of the humeral head with the deltoid appearing sunken because of its absence from the glenoid. The patient experiences immediate pain from the injury aggravated by muscle spasm, which is reactionary to the loss of concavity-compressive forces that normally maintain the humeral head in the glenoid.

Considerations for Reduction on the Field, Sideline, or Locker Room The ideal reduction maneuver is one that minimizes the use of force, can be executed with minimal pain, and produces a high degree of success. Numerous techniques exist for reducing the glenohumeral joint.7 Though no single reduction maneuver has clearly been shown to be superior, Amar et  al noted in a prospective, randomized, controlled trial that the success rate and time to achieve reduction without sedation were superior for the Milch technique compared with the Stimson technique.8 Singh and colleagues demonstrated that the Milch technique was effective (96%) and led

to a shorter emergency department stay and lower cost when compared to the traction-countertraction technique.9 There is some controversy regarding prehospital reduction before radiographs. However, most sports medicine physicians will attempt reduction in patients with a witnessed, classic mechanism of injury. It cannot be overemphasized that nerve and vascular function should first be assessed before reduction attempts. Multiple attempts at reduction on the athletic field may reflect poorly on the sideline physician. A single maneuver may be attempted on field by the experienced clinician, but the athlete should be taken to the locker room or a sideline tent should the initial attempt prove unsuccessful. There is also some controversy regarding initial management in a skeletally immature athlete. Some authors advocate radiographs before reduction if possible, noting a higher incidence of associated fracture.10 Reid et al, however, noted only a 3% incidence of associated fractures in patients younger than 21 years.11 The on-the-field reduction is accomplished with longitudinal traction and gentle forward elevation. Relief of pain and apprehension is often dramatic if reduction is achieved. Should this prove unsuccessful, the athlete is quickly taken to the training tent or locker room. We then routinely use the Stimson method for reduction. If reduction remains unachievable, the athlete is promptly transferred directly to the emergency department for shoulder radiographs (anteroposterior, axillary or Velpeau view, and scapular Y views). As noted previously, myriad techniques are described in the literature, but common principles include unlocking the humerus from the lip of the glenoid, using judicious traction when necessary, and directing the humeral head back to its anatomic position. We provide a brief review of the most common reduction techniques as follows.

Milch Method A benefit of the Milch method is that it does not rely predominantly on distraction for reduction and can be performed without sedation. The technique is typically performed with the patient supine but may also work with the patient prone (Figure  3-1). The clinician stands on the athlete’s affected side and grasps the shoulder with one hand and the athlete’s wrist/forearm with the other hand. The clinician slowly moves the shoulder into abduction and external rotation while reassuring the patient. The movement is paused if the athlete has pain or increased muscle spasm. Typically, shoulder reduction occurs before the shoulder reaches 90  degrees of abduction and external rotation. The clinician can use the hand holding the shoulder to gently guide the humeral head back into place. Alkaduhimi et  al noted an overall 80% success rate in their systematic review of reduction techniques.7

Kocher Method Initially described in 1870 by Emil Theodor Kocher, a thyroid surgeon, this method is also conducted with the

Evaluation of Shoulder Instability on the Field and in the Clinic

21

Figure 3-1. Milch maneuver.

patient in supine position. The patient is positioned supine or seated with the elbow bent to 90 degrees. The athlete’s forearm should be externally rotated and the shoulder should be forward flexed. When resistance is met, the forearm should then be internally rotated until reduction is achieved. Gentle traction is maintained during the maneuver. Mechanically, this maneuver creates a lever between the humeral head and anterior glenoid. Reported complications include fracture of the neck of the humerus and pectoralis major rupture.7

Stimson Method This reduction technique involves positioning the athlete in a prone position on the edge of an examining table (Figure  3-2A). A 5- to 10-pound weight is then held by the athlete or suspended from the affected arm. This is maintained for approximately 15 to 20 minutes to provide traction to the upper extremity to fatigue the surrounding musculature and alleviate spasm. Reduction is achieved through longitudinal traction provided by gravity. When the weight is removed, the humeral head is allowed to reduce back into the glenoid fossa. Although reported reduction time is increased, the benefit of this technique is that gentle traction limits the risk of iatrogenic injury.

Scapular Manipulation This technique may be performed seated or prone, though the authors’ preference is to use this as an adjunct to the Stimson method (Figure  3-2B).7 The aim is to reorient the scapula so the glenoid can accept the dislocated humeral head. The clinician is positioned on the side of the affected shoulder and pushes the inferior angle of the scapula medially and inferiorly. This rotation promotes glenoid positioning to the inferiorly displaced humeral head.

shoulder with the patient lying supine. A sheet can be draped around the body of the athlete with an assistant on the contralateral side, prepared to pull on both sides of the sheet for countertraction. Longitudinal in-line traction is focused on the affected shoulder to reseat the humeral head. Flexing the affected elbow to 90 degrees allows the practitioner to have appropriate grip to pull traction along the axis of the humerus (approximately 45  degrees of flexion). The Hippocratic method, described as early as 460 bc, uses a similar concept. The countertraction is provided by a covered heel placed in the patient’s axilla. This technique is not as frequently used in the emergency department setting, though it may be appropriate for a swift sideline reduction. Sayegh et  al reported a 72.5% success rate with the Hippocratic maneuver in a study that compared this technique with other traction methods.12

Reduction of a Posterior Shoulder Dislocation Though comprising only 2% to 5% of all shoulder dislocations, the posterior shoulder dislocation is associated with high-energy trauma.13 This injury is associated with impaction fractures at the anteromedial humeral head and posterior glenoid. Reduction often requires “unlocking” by manipulating the shoulder into 90 degrees of flexion, adduction, and internal rotation.14 This is followed by gradual external rotation and application of an anterior guiding force to the humeral head. This should be performed gently because there is risk of fracture to the humeral head. An alternative to manipulation is to allow the shoulder to hang with traction using the Stimson method and 5- to 10-pounds of traction.

Traction-Countertraction Method and Hippocratic Method

TRANSFER TO THE EMERGENCY DEPARTMENT

The traction-countertraction technique is one of the most commonly used techniques. The success rate has been reported to be approximately 95%, though the technique requires the use of an assistant and frequently administration of sedation.7 The clinician stands on the side of the dislocated

If the attempted methods are unable to obtain reduction on the field, a direct transfer to the emergency department is warranted. Standard trauma series of shoulder films should be obtained to confirm type of dislocation and assess for concomitant fracture. Emergency department care allows

22

Chapter 3

Figure 3-2. Stimson maneuver.

for patient monitoring if intravenous sedation is desired. However, an intra-articular injection of 10 to 20  mL of 1% lidocaine has been successfully applied with a lateral approach with no significant difference in patient-reported pain and time to reduction when compared to intravenous sedation.15 A theoretical concern about intra-articular injection is infection in the shoulder, though this complication has yet to be reported. Once appropriate analgesia is obtained and X-rays have been scrutinized to rule out fracture, any of the reduction maneuvers that the practitioner is familiar with and comfortable conducting may be attempted in the emergency department.

POSTREDUCTION CARE Following reduction, the axillary nerve should be reassessed by checking sensation to the lateral deltoid and ensuring motor function in a small amount of abduction. Radiographs, including an axillary lateral or Velpeau view, are obtained to assess for glenoid of humeral head fracture and confirm a concentric reduction. Typically, patients are placed in a sling for immobilization in adduction and internal rotation for a period of 3 to 4 weeks to allow the soft tissues to heal. This is followed by judicious physical therapy to gradually reintroduce range of motion to prevent postimmobilization stiffness. Surgical management for the first-time dislocation is controversial and will be discussed in subsequent chapters. The position of immobilization has had some controversy since Itoi et  al espoused that a position of adduction and external rotation may be a position of greater stability in the setting of acute anterior dislocation.16 The rationale was to better tension the anterior soft tissues, which become stretched during dislocation. Although exciting, multiple, additional randomized controlled trials have been unable to recapitulate Itoi’s findings.17-19 Whelan and colleagues noted in a recent meta-analysis of randomized controlled trials that immobilization in external rotation was not significantly more effective in reducing the recurrence rate after primary anterior shoulder dislocation than immobilization in internal rotation.20

PHYSICAL EXAMINATION IN CLINIC The physical examination of the athlete with suspected shoulder instability is critically impor tant in developing an appropriate future treatment plan. A multitude of special tests and provocative examination maneuvers for shoulder instability exist. However, a thorough and complete physical examination begins with inspection, palpation, and range of motion and strength testing. Given the numerous available tests, the clinician must develop his or her own methodical approach to shoulder examination. Following a step-wise approach will ensure critical findings are not overlooked. Though this chapter focuses on the clinical examination of the shoulder, it is also impor tant to assess the cervical spine when evaluating any patient with shoulder complaints. Cervical spondylolysis and resultant radiculopathy or myelopathy can manifest as shoulder or arm pain. It should also be noted that cervical radiculopathy often presents in a nonstandard or nondermatomal pattern.21 Cervical range of motion should be assessed in all planes, including flexion, extension, rotation, and lateral bending. Cervical provocative tests include the Spurling test, the shoulder abduction test, Valsalva maneuver, neck distraction, and Elveys upper limb tension test.22 The most commonly used cervical provocative maneuver is the Spurling test. In this test, the clinician rotates the patient’s head toward the affected side while extending the neck and applying downward pressure to the top of the head. A positive test occurs when the athlete has a reproduction of pain. A systematic review of physical examination maneuvers found that the Spurling test using rotation and extension was the most sensitive and specific test for cervical radiculopathy, whereas axial compression alone had a low sensitivity and specificity.23 We most typically perform the seated examination maneuvers initially (inspection, palpation, range of motion, strength testing, sulcus sign, and hyperabduction sign). The patient is then placed supine and the load and shift, apprehension series, jerk test, and Kim test are performed.

Evaluation of Shoulder Instability on the Field and in the Clinic

23

Inspection

Strength

Examination of the shoulder begins with visual inspection of the shoulder girdle, including the symptomatic and asymptomatic sides. It is impor tant to preserve the patients’ modesty and place them at ease as much as possible. The provocative maneuvers performed later in the exam are potentially more accurate in the setting of a relaxed patient. Having female patients wear a tank top or a gown tied below the axilla is often helpful. Asymmetry of the deltoid, supraspinatus, and infraspinatus should be noted. Deltoid atrophy, presenting as “squaring of the shoulder,” may be secondary to axillary nerve palsy in the setting of a previous shoulder dislocation. The supraspinatus and infraspinatus are both supplied by the suprascapular nerve, which can be injured by compression or traction. Injury to the nerve at the suprascapular notch can cause atrophy of both muscles, whereas injury at the spinoglenoid notch affects only the infraspinatus muscle. Both muscles can also display atrophy in the setting of a chronic rotator cuff tear. The clinician should also assess for scapular winging, at rest as well as during active motion and during a “wall push-up.” Finally, the acromioclavicular (AC) and sternoclavicular joints should be assessed for asymmetry and deformity.

Muscle strength testing is then performed, with a focus on the rotator cuff musculature. The supraspinatus is evaluated with the supraspinatus isolation test or Jobe test. The arm is elevated 90  degrees in the scapular plane and internally rotated, and the athlete is asked to resist downward pressure. The infraspinatus is evaluated with resisted external rotation with the elbow at the side. An infraspinatus lag sign is present when the clinician passively externally rotates the arm and the athlete is unable to maintain the arm in that position. The teres minor is evaluated with the “Hornblower” test, or resisted external rotation with the arm in 90 degrees of elevation and external rotation in the scapular plane with 90 degrees of elbow flexion. The subscapularis is evaluated with the “lift-off,” “bellypress,” and “bear hug tests.” In the lift-off test, the athlete places the hand on the lumbar spine and is asked to lift it off the body. In the belly-press test, athletes place their hand on their abdomen and are asked to press posteriorly into the abdomen without flexing their wrist or moving their arm posteriorly. It is critical that the elbow remain in front of the body to accurately assess the subscapularis. In the bearhug test, the athlete places the arm in 90 degrees of forward flexion with the elbow flexed and the hand on the contralateral shoulder and is asked to maintain this position while the clinician tries to lift the hand away from the shoulder. Tokish et al demonstrated in an electromyogram study that although both the belly-press and lift-off tests were useful for assessing subscapularis strength, the belly-press test and lift-off tests provided greater challenges to the upper and lower subscapularis, respectively.24 Contrary to these results, Pennock and colleagues noted that the level of subscapularis muscle activation was similar among the bear-hug, bellypress, and lift-off tests.25

Palpation The bilateral shoulders are then palpated in entirety, focusing on tenderness, deformity, and crepitus. Tenderness at the AC joint can be seen in the setting of an AC joint injury, synovitis, or arthrosis. Likewise, tenderness, swelling, or deformity at the sternoclavicular joint is associated with sprain or instability. Rotator cuff tendinosis or partialthickness tears are associated with tenderness just anterior or lateral to the border of the acromion. Tenderness at the lateral shoulder is frequently observed with a greater tuberosity fracture or Hill-Sachs lesion associated with a dislocation event.

Range of Motion Passive and active range of motion is then assessed. Measurements should include forward flexion, abduction, external rotation in adduction and 90 degrees of abduction, and internal rotation behind the back and in 90 degrees of abduction. When assessing internal rotation behind the back, the clinician measures the most cranial vertebral segment reached. The superior scapular border is at approximately T4, the inferior scapular angle is at T7, and the iliac crest is at L4. As noted earlier, scapular winging should be assessed during active range of motion measurements. Athletes with a recent dislocation or subluxation event will often have decreases both in active and passive range of motion secondary to muscle guarding or inflammation. However, athletes with chronic instability often have normal or even increased range of motion compared to the contralateral side.

Laxity Assessment It is impor tant to distinguish “laxity” from “instability” because these 2 terms are not synonymous. Matsen et  al defined shoulder “laxity” as the ability of the humeral head to be passively translated on the glenoid fossa and “instability” as “a clinical condition in which unwanted translation of the head on the glenoid compromises the comfort and function of the shoulder.”26 Multiple physical examination tests have been described to assess shoulder laxity, including the drawer, load and shift, sulcus sign, and Gagey hyperabduction test. Gerber and Ganz described the anterior and posterior drawer tests in 1984.27 As initially described, the anterior drawer test is performed with the athlete supine and the clinician standing on the affected side. The clinician holds the brachium in 80  degrees to 120  degrees of abduction, 0 degrees to 20 degrees of forward flexion, and 0 degrees to 30 degrees of external rotation. The clinician holds the athlete’s brachium and provides an anterior directed force.

24

Chapter 3

Figure 3-3. Load and shift test.

Figure 3-4. Sulcus sign/test.

The posterior drawer test is similar to the anterior drawer with several subtle differences. The clinician holds the athlete’s wrist or forearm with one hand and places the other hand over the shoulder. The clinician’s thumb is placed anteriorly while the fingers are placed posteriorly. The clinician applies a posteriorly directed force through the humeral head. The athlete’s arm is forward flexed 20 degrees to 30 degrees and abducted 80 degrees to 120 degrees. Both drawer tests are graded similarly to the load and shift test as described below. Silliman and Hawkins initially described the load and shift test in 1991.28 The athlete is placed in the seated or supine position, though we have found the supine position allows for greater patient relaxation and also allows the table to stabilize the scapula (Figure  3-3). The athlete’s arm is placed in slight abduction, 20 degrees of forward flexion, and in neutral rotation. When performed in the seated position, the clinician stands behind the athlete’s affected shoulder and stabilizes the scapula with one hand while holding the proximal arm with the other hand. An axial load is then applied the humeral head. As the glenohumeral joint is loaded, the clinician attempts to anteriorly and posteriorly

translate the humeral head. Using the Gerber and Ganz classification, a grade I load and shift represents translation of the head to the glenoid rim, grade II is translation over the rim that spontaneously reduces, and grade III is over the rim without a spontaneous reduction.27 When using the modified Hawkins classification, grade 1 represents minimal translation of the head on the glenoid, grade II is translation of the head to the glenoid rim, and grade III is translation of the head over the glenoid rim.29 The sulcus test or sulcus sign was described by Neer and Foster in 1980.30 The test is performed with the athlete in the seated position (Figure 3-4). The arm is adducted at the side and the clinician applies an inferiorly directed force while grasping the elbow or just above the elbow. A positive test is present if the humeral head translates inferiorly and a “sulcus” appears in the subacromial region. The amount of displacement can be measured in centimeters. Grade I represents displacement of less than 1.5 cm, grade II between 1.5 and 2 cm, and grade III more than 2 cm. The test is repeated with the arm in neutral rotation and then in external rotation. Persistence of the sulcus in external rotation suggests a lesion of the rotator interval.

Evaluation of Shoulder Instability on the Field and in the Clinic

25

Figure 3-5. Hyperabduction test. A downward force is placed on the scapula as the inspected shoulder comes to abduction.

The hyperabduction test was described by Gagey and Gagey in 2001.31 This maneuver assesses laxity of the inferior glenohumeral complex. The clinician stands behind the athlete and uses one hand to stabilize the scapula (Figure 3-5). A downward or inferiorly directed force is also applied with this hand. The athlete’s affected arm is abducted until the scapular is felt to begin rotating. A positive test is abduction of more than 105 degrees before scapular rotation.

Anterior Instability Provocative Examination Maneuvers Multiple physical examination maneuvers for the assessment of shoulder instability have been described. Hegedus et al recently published an update of a 2008 systematic review and meta-analysis of shoulder physical examination tests.32 They performed statistical pooling for 3 clinical examination tests for instability: the apprehension, relocation, and surprise tests. The surprise tests demonstrated the highest sensitivity (81.8%). The apprehension test had the highest specificity (95.4%), positive likelihood ratio (17.2), and diagnostic odds ratio (53.6). Similarly, van Kampen and colleagues performed a prospective cohort study of 169 patients with shoulder complaints, 60 of whom had magnetic resonance angiography–documented shoulder instability.33 They specifically evaluated 6 physical examination maneuvers for instability, including the apprehension, relocation, release, anterior drawer, load and shift, and hyperabduction tests. The apprehension test had the highest sensitivity (98.3%), whereas the release test had the highest overall accuracy (86.4%). Like many orthopedic tests, there are multiple modifications and variations of the apprehension tests. The test can be performed in the seated position. However, placing the athlete supine allows the scapula to be stabilized by the examination table. The clinician places the affected shoulder into 90  degrees of abduction and slowly externally rotates the shoulder to 90 degrees (Figure 3-6A). A slight anteriorly

directed force can also be applied to the shoulder. Tension on the inferior glenohumeral ligament is maximized in this position. Athletes with disrupted anterior stabilizers will feel a sense of apprehension or impending dislocation, representing a positive test. When first described in 1981, Rowe and Zarins considered a positive test to be reproduction of pain or apprehension.34 Farber et al, however, noted that if that the reproduction of pain was considered a “positive” result, the sensitivity, specificity, and overall accuracy were much lower (50%, 56%, and 55%) than if considering true apprehension a positive finding.35 The relocation test can be considered a “second step” in the apprehension test (Figure 3-6B).36 If an athlete has a positive apprehension test, the clinician applies a posteriorly directed force to the humeral head. This will move a subluxed humeral head back into the correct position. A positive relocation test is relief of apprehension or guarding with this maneuver. The surprise or anterior release test is the “third step” in the apprehension test (Figure  3-6C).37 The clinician removes the posteriorly directed force and the athlete once again feels apprehension or impending dislocation.

Posterior Instability Provocative Examination Maneuvers The jerk test was initially described by Matsen and colleagues.38 The athlete lies supine on the edge of the bed and the clinician places the athlete’s arm in 90  degrees of forward flexion and maximal adduction and internal rotation (Figure  3-7). The clinician then applies a posteriorly and inferiorly directed force along the axis of the humerus. A grossly positive test may elicit subluxation. The clinician slowly abducts the arm while maintaining the posteriorly directed force and feels for a jerk or clunk as the humeral head relocates into the glenoid. The Kim test was initially described in 2005.39 While initially described in the seated position, we typically perform the Kim test in the supine position after the jerk test. The

26

Chapter 3

Figure 3-6. Anterior instability provocative maneuvers. (A) Apprehension test. (B) Relocation test. (C) Surprise test.

Figure 3-7. Jerk test.

Figure 3-8. Beighton scale for ligamentous laxity. (A) Hyperextension at elbows. (B) Thumb to volar forearm. (C) Ability to place both palms flat on the floor with knees extended.

arm is placed in 90 degrees of abduction and approximately 45 degrees of flexion. The clinician holds the athlete’s elbow and lateral aspect of the brachium and applies an axial loading force as well as an inferior and posterior force. A positive test is the sudden onset of posterior shoulder pain.

Generalized Laxity Assessment Athletes with shoulder instability will frequently have generalized ligamentous laxity. This can be assessed using the Beighton Hypermobility Score, which uses hyperextension of the small finger metacarpophalangeal joint past 90 degrees, ability to place the thumb on the volar forearm, hyperextension of the elbow joint beyond 10 degrees, hyperextension of the knee joint more than 10  degrees, and the ability to place both palms flat on the floor with the knees

extended (Figure  3-8).40 One point is given for a positive test. Generalized ligamentous laxity is most often defined as a score of 4 or greater.41 Whitehead et al, however, noted that a high proportion (34%) of individuals without shoulder instability had a Beighton score of 4 or higher and that a positive score had low sensitivity (range, 0.40 to 0.48) and low positive-predictive values (range, 0.13 to 0.31) for shoulder instability.42

CONCLUSION Sports medicine practitioners may be faced with an athlete with a dislocated shoulder during any coverage event, so a system should be in place to facilitate appropriate care to athletes. Trauma protocol followed by a focused shoulder assessment is necessary before action is taken. Our preference is to

Evaluation of Shoulder Instability on the Field and in the Clinic attempt one reduction on the field. If unsuccessful, the athlete should be taken to a controlled setting such as the training room or locker room for alternate maneuvers. Relaxation and combating muscle spasm are critical to obtaining the reduction. Once reduction is obtained, immobilization in a sling prevents early recurrence of dislocation. If the shoulder is irreducible at the sideline, the athlete may need to be referred to the emergency department for radiographic assessment. Each step provides information to the degree of instability that may portend need for surgical stabilization.

REFERENCES 1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

14.

Zacchilli MA, Owens BD. Epidemiology of shoulder dislocations presenting to emergency departments in the United States. J Bone Joint Surg Am. 2010;92(3):542-549. doi:10.2106/JBJS.I.00450. Shah A, Judge A, Delmestri A, et al. Incidence of shoulder dislocations in the UK, 1995-2015: a population-based cohort study. BMJ Open. 2017;7(11):e016112. doi:10.1136/bmjopen-2017-016112. Kerr ZY, Collins CL, Pommering TL, Fields SK, Comstock RD. Dislocation/separation injuries among US high school athletes in 9 selected sports: 2005-2009. Clin J Sport Med. 2011;21(2):101-108. doi:10.1097/JSM.0b013e31820bd1b6. Ward JP, Bradley JP. Decision making in the in-season athlete with shoulder instability. Clin Sports Med. 2013;32(4):685-696. doi:10.1016/j.csm.2013.07.005. Owens BD, Dickens JF, Kilcoyne KG, Rue JP. Management of midseason traumatic anterior shoulder instability in athletes. J Am Acad Orthop Surg. 2012;20(8):518-526. doi:10.5435/JAAOS-20-08-518. Robinson CM, Shur N, Sharpe T, Ray A, Murray IR. Injuries associated with traumatic anterior glenohumeral dislocations. J Bone Joint Surg Am. 2012;94(1):18-26. doi:10.2106/JBJS.J.01795. Alkaduhimi H, van der Linde JA, Willigenburg NW, van Deurzen DFP, van den Bekerom MPJ. A systematic comparison of the closed shoulder reduction techniques. Arch Orthop Trauma Surg. 2017;137(5):589-599. doi:10.1007/s00402-017-2648-4. Amar E, Maman E, Khashan M, Kauffman E, Rath E, Chechik  O. Milch versus Stimson technique for nonsedated reduction of anterior shoulder dislocation: a prospective randomized trial and analysis of factors affecting success. J Shoulder Elbow Surg. 2012;21(11):14431449. doi:10.1016/j.jse.2012.01.004. Singh S, Yong CK, Mariapan S. Closed reduction techniques in acute anterior shoulder dislocation: modified Milch technique compared with traction-countertraction technique. J Shoulder Elbow Surg. 2012;21(12):1706-1711. doi:10.1016/j.jse.2012.04.004. Curtis  R. Shoulder injuries in the young athlete. In: Miller MD, Thompson SR, eds. DeLee & Drez’s Orthopaedic Sports Medicine: Principles and Practice. 4th  ed. Philadelphia, PA: Elsevier; 2015:1576-1596. Reid S, Liu M, Ortega H. Anterior shoulder dislocations in pediatric patients: are routine prereduction radiographs necessary? Pediatr Emerg Care. 2013;29(1):39-42. doi:10.1097/PEC.0b013e31827b52a7. Sayegh FE, Kenanidis EI, Papavasiliou KA, Potoupnis ME, Kirkos JM, Kapetanos GA. Reduction of acute anterior dislocations: a prospective randomized study comparing a new technique with the Hippocratic and Kocher methods. J Bone Joint Surg Am. 2009;91(12):2775-2782. doi:10.2106/JBJS.H.01434. Rouleau DM, Hebert-Davies J, Robinson CM. Acute traumatic posterior shoulder dislocation. J Am Acad Orthop Surg. 2014;22(3):145152. doi:10.5435/JAAOS-22-03-145. Robinson CM, Aderinto  J. Posterior shoulder dislocations and fracture-dislocations. J  Bone Joint Surg Am. 2005;87(3):639-650. doi:10.2106/JBJS.D.02371.

15.

16.

17.

18.

19.

20.

21.

22. 23.

24.

25.

26. 27.

28. 29.

30.

31. 32.

27

Miller SL, Cleeman E, Auerbach J, Flatow EL. Comparison of intra-articular lidocaine and intravenous sedation for reduction of shoulder dislocations: a randomized, prospective study. J Bone Joint Surg Am. 2002;84-A(12):2135-2139. doi:10.2106/00004623-200212000-00002. Itoi E, Hatakeyama Y, Kido T, et al. A new method of immobilization after traumatic anterior dislocation of the shoulder: a preliminary study. J Shoulder Elbow Surg. 2003;12(5):413-415. doi:10.1016/ s1058-2746(03)00171-x. Whelan DB, Litchfield R, Wambolt E, Dainty KN; Joint Orthopaedic Initiative for National Trials of the Shoulder (JOINTS). External rotation immobilization for primary shoulder dislocation: a randomized controlled trial. Clin Orthop Relat Res. 2014;472(8):2380-2386. doi:10.1007/s11999-013-3432-6. Finestone A, Milgrom C, Radeva-Petrova DR, et al. Bracing in external rotation for traumatic anterior dislocation of the shoulder. J Bone Joint Surg Br. 2009;91(7):918-921. doi:10.1302/0301-620X.91B7.22263. Liavaag S, Brox JI, Pripp AH, Enger M, Soldal LA, Svenningsen  S. Immobilization in external rotation after primary shoulder dislocation did not reduce the risk of recurrence: a randomized controlled trial. J Bone Joint Surg Am. 2011;93(10):897-904. doi:10.2106/ JBJS.J.00416. Whelan DB, Kletke SN, Schemitsch G, Chahal J. Immobilization in external rotation versus internal rotation after primary anterior shoulder dislocation: a meta-analysis of randomized controlled trials. Am J Sports Med. 2016;44(2):521-532. doi:10.1177/0363546515585119. McAnany SJ, Rhee JM, Baird EO, et al. Observed patterns of cervical radiculopathy: how often do they differ from a standard, “Netter diagram” distribution? Spine J. 2019;19(7):1137-1142. doi:10.1016/j. spinee.2018.08.002. Iyer S, Kim HJ. Cervical radiculopathy. Curr Rev Musculoskelet Med. 2016;9(3):272-280. doi:10.1007/s12178-016-9349-4. Rubinstein SM, Pool JJ, van Tulder MW, Riphagen II, de Vet HC. A systematic review of the diagnostic accuracy of provocative tests of the neck for diagnosing cervical radiculopathy. Eur Spine  J. 2007;16(3):307-319. doi:10.1007/s00586-006-0225-6. Tokish JM, Decker MJ, Ellis HB, Torry MR, Hawkins RJ. The belly-press test for the physical examination of the subscapularis muscle: electromyographic validation and comparison to the liftoff test. J Shoulder Elbow Surg. 2003;12(5):427-430. doi:10.1016/ s1058-2746(03)00047-8. Pennock AT, Pennington WW, Torry MR, et al. The influence of arm and shoulder position on the bear-hug, belly-press, and lift-off tests: an electromyographic study. Am J Sports Med. 2011;39(11):23382346. doi:10.1177/0363546510392710. Matsen FA III, Harryman DT II, Sidles JA. Mechanics of glenohumeral instability. Clin Sports Med. 1991;10(4):783-788. Gerber C, Ganz R. Clinical assessment of instability of the shoulder. With special reference to anterior and posterior drawer tests. J Bone Joint Surg Br. 1984;66(4):551-556. Silliman JF, Hawkins RJ. Current concepts and recent advances in the athlete’s shoulder. Clin Sports Med. 1991;10(4):693-705. Hawkins RJ, Schutte JP, Janda DH, Huckell GH. Translation of the glenohumeral joint with the patient under anesthesia. J Shoulder Elbow Surg. 1996;5(4):286-292. doi:10.1016/s1058-2746(96)80055-3. Neer CS  II, Foster CR. Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. A preliminary report. J Bone Joint Surg Am. 1980;62(6):897-908. Gagey OJ, Gagey  N. The hyperabduction test. J Bone Joint Surg Br. 2001;83(1):69-74. doi:10.1302/0301-620x.83b1.10628. Hegedus EJ, Goode AP, Cook CE, et  al. Which physical examination tests provide clinicians with the most value when examining the shoulder? Update of a systematic review with meta-analysis of individual tests. Br J Sports Med. 2012;46(14):964-978. doi:10.1136/ bjsports-2012-091066.

28 33.

34. 35.

36.

37.

Chapter 3 van Kampen DA, van den Berg T, van der Woude HJ, et al. The diagnostic value of the combination of patient characteristics, history, and clinical shoulder tests for the diagnosis of rotator cuff tear. J Orthop Surg Res. 2014;9:70. doi:10.1186/s13018-014-0070-y. Rowe CR, Zarins B. Recurrent transient subluxation of the shoulder. J Bone Joint Surg Am. 1981;63(6):863-872. Farber AJ, Castillo R, Clough M, Bahk M, McFarland EG. Clinical assessment of three common tests for traumatic anterior shoulder instability. J Bone Joint Surg Am. 2006;88(7):1467-1474. doi:10.2106/ JBJS.E.00594. Jobe FW, Kvitne RS, Giangarra CE. Shoulder pain in the overhand or throwing athlete. The relationship of anterior instability and rotator cuff impingement. Orthop Rev. 1989;18(9):963-975. Abeck D, Andersson T, Grosshans E, et al. Topical application of a platelet-activating factor (PAF) antagonist in atopic dermatitis. Acta Derm Venereol. 1997;77(6):449-451. doi:10.2340/0001555577449451.

38.

39.

40.

41.

42.

Matsen FA III, Thomas SC, Rockwood CA Jr, Wirth MA. Glenohumeral instability. In: Rockwood CA Jr, Matsen FA III, eds. The Shoulder. 2nd ed. Philadelphia, PA: WB Saunders; 1998:611-754. Kim SH, Park JS, Jeong WK, Shin SK. The Kim test: a novel test for posteroinferior labral lesion of the shoulder—a comparison to the jerk test. Am J Sports Med. 2005;33(8):1188-1192. doi:10.1177/0363546504272687. Beighton P, Solomon L, Soskolne CL. Articular mobility in an African population. Ann Rheum Dis. 1973;32(5):413-418. doi:10.1136/ ard.32.5.413. Scher DL, Owens BD, Sturdivant RX, Wolf JM. Incidence of joint hypermobility syndrome in a military population: impact of gender and race. Clin Orthop Relat Res. 2010;468(7):1790-1795. doi:10.1007/ s11999-009-1182-2. Whitehead NA, Mohammed KD, Fulcher ML. Does the Beighton score correlate with specific measures of shoulder joint laxity? Orthop J Sports Med. 2018;6(5):2325967118770633. doi:10.1177/2325967118770633.

4 Clinical Anatomy and Biomechanics David Eldringhoff, MD; Barry I. Shafer, PT, DPT, ATC; Gregory J. Adamson, MD; and Thay Q. Lee, PhD

Shoulder motion is provided by several articulations, including the glenohumeral, acromioclavicular, sternoclavicular, and scapulothoracic joints. The glenohumeral joint has the greatest range of motion of any joint in the body. This unique ability is required so that the upper extremity can be positioned in space for hand function. The downside to this tremendous mobility is that it puts the glenohumeral joint at greater risk for instability. This chapter will review the clinical anatomy and biomechanics of the shoulder including the bony passive stabilizers, soft-tissue passive, and soft-tissue active stabilizers that play a role in allowing substantial range of motion while providing stability.

BONY STABILIZERS The bony passive stabilizers of the shoulder include the scapula, humeral head, and the clavicle. Specifically, the glenohumeral bony stabilizers are composed of the glenoid and the humeral head.

Glenoid The glenoid is on the lateral aspect of the scapular body and functions as a shallow socket for the glenohumeral joint. The glenoid face has been described as pear shaped because the superior aspect is narrower, from anterior to posterior, than the inferior aspect (Figures 4-1A and 4-1B). The average superior-inferior dimension of the glenoid has been reported to be 39 ± 3.7  mm and the average anterior-posterior dimension of the lower half 29 ± 3.1 mm.1 The glenoid is typically thought to be in a slight position of inclination and retroversion, which helps contribute to the

bony stability provided. In the coronal plane, the glenoid is inclined superiorly, with a mean inclination of 4.2 degrees and a range from –7 to 15.8 degrees.2 In the sagittal plane, the glenoid is retroverted 7.79 ± 4.85 degrees.3 For a surgeon, the large variation in glenoid version can become a complex challenge. Excessive retroversion has been described as a cause of posterior instability.4 An inferior tilt may lead to a higher risk for multidirectional instability (MDI) and inferior dislocations.5 Furthermore, the glenoid height-to-width ratio (glenoid index) was found to be a significant risk factor for instability. Specifically, Owens et al showed that a glenoid height-to-width ratio of greater than 1.58 (taller and thinner glenoids) had 2.64  times the risk of injury compared with those with a ratio less than 1.58.6

Humeral Head As with the glenoid, the humeral head has a wide degree of anatomical variation. The humeral head is essentially hemispherical and articulates with the glenoid cavity to form the glenohumeral joint (Figures  4-2A to 4-2C). Robertson and colleagues7 reviewed and reported on the morphology of 30 pairs of proximal humeri. They found the humeral head retroversion averaged 19 degrees with a range from 9 to 31 degrees. The head inclination, other wise known as the neck shaft angle, averaged 41 degrees with a range from 34 to 47 degrees. The radius of curvature of the humeral head averaged 23 mm with a range from 17 mm to 28 mm. The center of the humeral head is medial to the center of the longitudinal axis of the humeral shaft. This is known as the medial humeral head offset and on average it measures 7 mm with a range of 4 to 12 mm. The humeral head also has a posterior

- 29 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 29-40). © 2021 SLACK Incorporated.

30

Chapter 4

Figure 4-1. (A) View of a right scapula showing the glenoid bony anatomy. (B) Average dimensions of the pear-shaped glenoid in the superior-inferior direction and the widest anteroposterior dimension on the lower portion.1

Figure 4-2. (A) Anterior view, (B) superior view, and (C) posterior view of a right humerus showing the bony structures and muscular attachments.

head center offset with an average of 2 mm with a range from 1 to 8 mm. Just as the glenoid variation has a clinical impact, so does the humeral head variation.

Glenohumeral Joint The articulation between the glenoid and the humeral head provides minimal restraint to the shoulder because of a large humeral head and a small, shallow glenoid. This inherent instability is related to the fact that only 25% to 30% of the humeral head is in contact with the glenoid surface at any given anatomic position (Figures  4-3A and 4-3B).2,8,9 Some have compared the glenoid and humeral head to a golf ball on a tee, demonstrating the glenohumeral joint’s propensity for instability. This anatomic relationship between the humeral head and glenoid can be thought of as a ratio of the diameter of each. This is known as the glenohumeral index. It has been reported that the ratio is approximately 0.75  in the sagittal plane and 0.6 in the transverse plane.10 Glenohumeral stability was quantitatively characterized by Lippitt and Matsen11 as the stability ratio. This is the force necessary to dislocate

the humeral head from the glenoid divided by compressive force.11,12 Many factors influence the stability ratio, including the labrum, the depth of the glenoid, and the presence of any glenoid and/or chondrolabral defects.13 The clavicle and scapula are also impor tant contributors to the bony anatomy because they provide muscular attachments and contribute to the total shoulder range of motion. The following sections will review the pertinent anatomy of these impor tant bony structures.

Scapula The scapula is part of both the glenohumeral joint and the acromioclavicular joint, and is the interposed bony linkage between the humerus and the clavicle/axial skeleton.14 As with the clavicle, the scapula serves as an attachment site for many of the glenohumeral stabilizing structures. The scapula serves as the attachment site or origin for 17 dif ferent muscles (Figure 4-4A and 4-4B). The scapula allows motion along the rib cage and is not a true joint with the thorax but functions similarly to a sliding joint. It articulates with ribs 2 to 7. It has a resting-position angulation of about 10 to 20 degrees’

Clinical Anatomy and Biomechanics

31

Figure 4-3. (A) Photograph of a disarticulated right shoulder showing the mismatch in size of the glenoid and the humeral head. (B) Axial view of the glenohumeral joint showing the mismatch in amount of contact between the humeral head and the glenoid.

Figure 4-4. (A) Posterior view and (B) anterior view of a right scapula showing the bony anatomy and muscular insertions.

anterior angulation, 30 to 45  degrees’ internal rotation in the coronal plane, and with a slight upward tilt of about 3 degrees.15 Abduction in the scapular plane, also known as Scaption, is the result of both glenohumeral and scapulothoracic motion. This has been termed scapulohumeral rhythm, by which approximately one-third of the Scaption is from the scapulothoracic motion and the other two-thirds are from the glenohumeral joint.16 The scapula is the link in proximal to distal sequencing of velocity, energy, and forces in shoulder function.17 The shoulder motion, force development, force regulation, and ligamentous tension require coupling of scapular motion and humeral motion.18 In the last 20 years, the importance of the scapula in shoulder mechanics has become a vastly discussed topic in the shoulder. Extensive work by Kibler et al14,18 and others has influenced the way we think about shoulder mechanics, kinetics, and the interplay in pathology. Scapular dyskinesis has been defined as movement of the scapula that is dysfunctional and may create a possible impairment of the overall shoulder function.19 There is now an extensive body of literature demonstrating that in the painful shoulder it is possible that scapular dyskinesis is a

major contributor to shoulder pain14,17 and therefore should be evaluated as part of the routine shoulder exam.17 Scapular dyskinesis has also been implicated as a causative factor of shoulder injuries or other pathologies.14

Acromion and Coracoid Process The acromion is the lateral-most extension of the scapula and has its medial connection to the clavicle through the acromioclavicular joint. The acromion has a somewhat triangular shape that is flattened, projects laterally, and then curves forward and upward. Its superior surface is convex and the inferior surface is concave, providing an overhang to the glenoid cavity. The acromion forms the point of attachment for the trapezius and deltoid muscles. Medially, the acromion articulates with the lateral end of the clavicle immediately behind the attachment of the coracoacromial ligament (Figure 4-5). The coracoacromial ligament, in conjunction with the acromion and the coracoid process, forms an arch over the glenohumeral joint, preventing its upward dislocation and limiting the upward rotation of the humerus. The coracoid process is an anterior projection from the scapular neck. It is known as the light house of the shoulder

32

Chapter 4

Figure 4-5. Photograph of a right shoulder showing the coracoacromial arch.

Figure 4-6. Lateral photograph showing the coracoid and head of the humerus of a right shoulder.

Figure 4-7. (A) Superior and (B) inferior view of a right clavicle showing the muscular insertion points.

because it is a vital landmark for the surgeon. It provides a medial boundary to the subacromial space and rotator interval. It serves as the attachment site for the conjoint tendon and the coracoclavicular ligaments. Coracoid impingement against the subscapularis tendon and bursa can lead to anterior shoulder pain, subscapularis degeneration, or rupture.20 The coracohumeral distance has also been implicated in shoulder instability by Owens and colleagues. They reported the coracoid location to be an independent risk factor for instability, with each millimeter increase in distance leading to a 20% increase in injury risk6 (Figure 4-6).

Humerus The humerus provides leverage for upper extremity strength and range of motion for hand positioning. The humeral head is an ellipsoidal shaped structure on the proximal end of the humerus, where it articulates with the glenoid. The proximal humerus also includes the greater and lesser tuberosities, which are bisected by the bicipital groove (see Figure  4-2). The anatomic neck is defined as the junction of the cortical bone and the articular surface. The anatomic neck is located medial to the tuberosities. The greater tuberosity is the insertion point for the supraspinatus, infraspinatus, and teres minor tendons from anterior to

posterior, respectively. The lesser tuberosity is the insertion point for the subscapularis tendon. The bicipital groove is flanked between the tuberosities and stabilizes the long head of the biceps.

Clavicle The clavicle is an S-shaped bone that functions to position the upper extremity laterally from the body axis and provides the only diarthrodial joint connection to the thorax at the sternoclavicular joint. (Figures 4-7A and 4-7B) On the lateral end of the clavicle is the acromioclavicular joint, where the clavicle articulates with the scapula. This joint is stabilized by the acromioclavicular joint capsule and the conoid and trapezoid ligaments of the coracoclavicular ligament complex. The acromioclavicular joint capsule and ligaments provide mostly horizontal (anterior-posterior) stabilization and the coracoclavicular ligaments provide mostly vertical (superiorinferior) stabilization. The clavicle facilitates shoulder elevation by allowing clavicular rotation of approximately 40 to 50 degrees throughout the shoulder range of motion.21 The clavicle also serves as the attachment site for many of the active stabilizers of the shoulder, such as the upper trapezius and deltoid muscles.

Clinical Anatomy and Biomechanics

33

Figure 4-8. (A) Photograph of a right shoulder showing the bony and soft-tissue stabilizers. (B) Softtissue stabilizers include the glenoid labrum, glenohumeral ligaments, and the glenohumeral joint capsule.

PASSIVE SOFT-TISSUE STABILIZERS The passive soft-tissue stabilizers of the shoulder include the glenoid labrum, the glenohumeral ligaments, and the glenohumeral joint capsule (Figures  4-8A and 4-8B). These soft-tissue stabilizers limit glenohumeral joint rotation and translation. The glenohumeral ligaments limit translation in a position-dependent manner. The following section will review the specific anatomy and function of these passive soft-tissue stabilizers of the shoulder.

Labrum The labrum is defined as a fibrocartilaginous tissue that surrounds the glenoid. Its function is to deepen the glenoid socket for stability. Specifically, the glenoid articular surface and labrum combine to create a socket that is approximately 9 mm deep in the superoinferior direction and 5 mm deep in the anteroposterior direction, where the labrum contributes approximately 50% of the total depth of the socket.22 It deepens the glenoid an average of 9 mm in the superior-interior plane and 5  mm in the anterior-posterior plane. The long head of the biceps tendon (LHBT) attaches intra-articularly to the supraglenoid tubercle along with the origin of the superior labrum. The labrum and biceps at this location function as a passive stabilizer of the humeral head. The labrum has been extensively studied, especially regarding shoulder instability. Often, patients who have had a traumatic dislocation of the shoulder sustain an injury to their labrum. This in turn, increases the risk of further dislocations. In a cadaveric study, the stability ratio decreases by 20% with resection of the labrum and decreases even more when chondral injury is added.13 Another cadaveric study echoed these results by removing the labrum but leaving the capsule in place. That study demonstrated an increase in laxity in the adducted position due to the labral resection.23

Glenohumeral Ligaments The glenohumeral ligaments consist of thickenings of the glenohumeral joint capsule and are typically divided into 4 dif ferent regions: superior, middle, anterior inferior, and posterior inferior (see Figures 4-8A and 4-8B). Each of these is an impor tant passive stabilizer of the shoulder. They function to prevent translation of the humeral head off the glenoid in a position-dependent manner. Capsular stretch injury without injury to the labrum also results in decreased force required for further dislocation events.24 The superior glenohumeral ligament (SGHL) originates on the superior aspect of the glenoid and coracoid process and runs to the fovea capitis just superior to the lesser tuberosity. The superior tilt of the glenoid and the SGHL both provide a passive restraint to inferior subluxation of the humeral head.25–27 The middle glenohumeral ligament (MGHL) originates just inferiorly to the SGHL on the anterior superior glenoid and runs to the anterior aspect of the anatomic neck of the humerus. The MGHL provides substantial constraint to anterior humeral head translation. It is taut in external rotation in the first 45 degrees of abduction.28 However, the MGHL has not been shown to affect anterior instability in a significant manner on its own. It was shown in a sectioning study that the MGHL alone did not result in instability but did increase the excursion of the humeral head.26 The inferior glenohumeral ligament (IGHL) is a complex that can be broken down into an anterior (AIGHL), a posterior (PIGHL), and an inferior sling that connects the two. The IGHL originates on the inferior two-thirds of the glenoid labrum and periosteum medially and runs to about 2  cm from the articular surface of the lateral humerus. It is the primary stabilizer of anterior translation of the humeral head in the apprehension (90 degrees’ abduction and 90 degrees’ external rotation) position. Functionally, in the abducted position the AIGHL is taut in external rotation and the

34

Chapter 4

Figure 4-9. Histologic photograph showing the 2 types of inferior glenohumeral ligament (IGHL) attachment on the glenoid side. (A) Labraldominant insertion where the IGHL is directly attached to the labrum. (B) Glenoid neck– dominant insertion where the IGHL is attached both to the labrum and the glenoid neck.

Coracoacromial Arch The coracoacromial arch consists of the coracoacromial ligament, acromion, and the coracoid process (see Figure  4-5). The coracoacromial ligament is considered a passive stabilizer of the glenohumeral joint. It originates from the anterolateral acromion and spans to the coracoid. There is some variation in the anatomy, with a few individuals having an accessory band.33,34 However, most have a ligament that fans out in a “V” shape from its acromial attachment to the coracoid (Figure 4-10). The coracoacromial arch provides a suspensory function that prevents anterior-inferior translation and functions as a humeral head stabilizer, providing passive restraint to the glenohumeral joint.35 Figure 4-10. Superior view schematic drawing showing bony and ligamentous anatomy of the coracoacromial arch.

PIGHL is taut in internal rotation.29 There is a positive linear correlation between the length of the AIGHL and anterior translation.30 Anatomically, there are 2 types of attachments of the IGHL on the glenoid. One is a direct, dense, collagen-fiber attachment to the labrum. The other is a dense, collagen-fiber attachment to the labrum and the front of the glenoid neck (Figures  4-9A and 4-9B).31 AIGHL and PIGHL lesions both have been implicated in the pathology of the unstable shoulder. The AIGHL is commonly injured or stretched during a traumatic anterior dislocation. One study suggested that the capsule injury is even more impor tant to the risk of subsequent dislocations than is the labrum.24 The PIGHL and capsule have been implicated in glenohumeral internal rotation deficit (GIRD). In this condition, the posterior capsule tightens in athletes and can lead to an imbalance in internal and external rotation of the effected shoulder. A cadaveric study with induced GIRD showed increased glenohumeral contact pressures, rotator cuff impingement, and posterior subluxation of the humeral head.32 These findings help reinforce the importance of sleeper stretches for the treatment of GIRD because it may help to prevent abnormal throwing kinematics.

Rotator Interval The rotator interval has a complex anatomy. It is a triangular space within the glenohumeral joint (Figure  4-11). The space starts at the coracoid process and extends laterally to the intertubercular groove. It is bounded superiorly by the supraspinatus and inferiorly by the subscapularis. This triangle has a roof superficially that is the coracohumeral ligament and a floor consisting of the SGHL as the deeper layer. The LHBT passes through this triangular space intraarticularly. The rotator interval has been studied extensively in clinical and cadaveric settings. Closure of this space has been evaluated for the treatment of MDI and release of this space for refractory adhesive capsulitis. The imbrication of the capsule over the rotator interval reduces glenohumeral joint volume and decreases translation, in all directions, for patients with MDI.36 However, there is a more anatomic strategy to effectively reducing the glenohumeral joint volume in MDI patients that includes specific sequential plication of the glenohumeral joint capsule, leaving rotator interval closure as the last step. Furthermore, it has been suggested that the closure should be performed in a position of external rotation, and any closure of this space should be performed with caution because of the risk of overtightening.37 The rotator interval can be released to help the overtightened shoulder as well. Cadaveric studies have shown that release of this triangular space is safe and that specifically releasing the coracohumeral ligament is of par ticular importance for the capsular release for adhesive capsulitis.38

Clinical Anatomy and Biomechanics

35

Figure 4-11. Schematic drawing of the rotator interval structures.

Figure 4-12. (A) Anterior view and (B) posterior view of a right shoulder showing the rotator cuff muscles.

ACTIVE SOFT-TISSUE STABILIZERS Active soft-tissue stabilizers of the shoulder play an impor tant role in shoulder biomechanics and glenohumeral stability. This has been known and studied as early as 1884.39 The rotator cuff muscles, long head of the biceps, and a variety of parascapular muscles are impor tant active soft-tissue stabilizers of the shoulder.

Rotator Cuff The rotator cuff is a group of 4 muscles (supraspinatus, infraspinatus, teres minor, and subscapularis) encapsulating the glenohumeral joint (Figures 4-12A and 4-12B). They have a dual role in which they act both as an active stabilizer of

the glenohumeral joint but also work as a mover of the joint providing shoulder motion. They provide stability via concavity compression of the humeral head in the glenoid socket throughout range of motion. The rotator cuff muscles also provide strength to the shoulder in that they are required to provide torque in multiple planes. Most biomechanical and clinical studies show that the overall shoulder motion is provided in a ratio of 2:1 glenohumeral to scapulothoracic, respectively. The rotator cuff has a substantial role in providing the glenohumeral range of motion. The supraspinatus muscle originates in the fossa superiorly to the scapular spine and it traverses laterally, over the glenohumeral joint, as its tendon inserts on the anteriorsuperior aspect of the greater tuberosity of the proximal humerus. It is more complex than a single muscle/tendon

36

Chapter 4

Figure 4-13. Photograph of a right shoulder showing the long and short head of the biceps anatomy.

unit because it has 2  distinct subregions, an anterior and a posterior.40–43 The tendon in the posterior region is slightly thinner than the more tube-like anterior portion. The tendinous portion of the anterior subregion also extends more medially from the insertion on the greater tuberosity than does the tendinous portion of the posterior subregion. Its functions are complex and include initiation of shoulder abduction and helping the deltoid. The supraspinatus also helps to facilitate some rotation to the humeral head, which has been shown both in electromyographic and cadaveric studies.44–46 It also acts with the other rotator cuff muscles to provide humeral head compression in the glenoid throughout the glenohumeral range of motion. The infraspinatus originates on the fossa inferior to the scapular spine and it traverses laterally and posteriorly, over the glenohumeral joint, as its tendon inserts on the greater tuberosity of the proximal humerus just posterior to the supraspinatus tendon. The anterior portion is overlapped by the posterior subregion of the supraspinatus. The function of the infraspinatus is to provide external rotation and elevation of the arm as well as to hold the humeral head in the glenoid cavity throughout the glenohumeral range of motion. Together the supraspinatus and infraspinatus tendons comprise the posterosuperior rotator cuff and are confluent on their lateral attachment to the greater tuberosity. Burkhart et al47 first described the terms rotator crescent and rotator cable. There is a section of thinner and thicker fibers on the articular side of the rotator cuff. The more thickened,

horseshoe-shaped section of rotator cuff, which is present in the anterior 8 to 12 mm of the supraspinatus, was coined the rotator cable. The thinner, more stress-shielded center section was coined the rotator crescent. This was then verified by multiple radiographic, anatomic, and histological studies.48–54 These regions are significant to the surgeon because studies have shown that most tears occur in the anterior portion of the supraspinatus tendon and that those tend to be larger with more fatty muscle degeneration.55,56 Several papers have described the rotator cable as the primary loadbearing structure of the supraspinatus.55,57,58 Not only is it the primary load-bearing structure, but when it is disrupted there are changes to the normal glenohumeral biomechanics.58 These effects are so pronounced that a cadaveric study showed even partial-thickness tears resulting in more than 50% of the tendon at the rotator cable was enough to increase the amount of glenohumeral translation and change the normal glenohumeral kinematics.59 The teres minor muscle originates from the dorsolateral side of the scapula just inferiorly and laterally to the infraspinatus. It traverses laterally, over the glenohumeral joint, as its tendon inserts on the inferior aspect of the greater tuberosity, which is just posterior and inferior to the infraspinatus tendon. Along with the infraspinatus, the teres minor helps to externally rotate the arm and holds the humeral head in the glenoid cavity throughout glenohumeral range of motion. The subscapularis muscle is the largest of the rotator cuff muscles and originates from the subscapular fossa on the anterior surface of the scapula. It traverses laterally over the glenohumeral joint, and its tendon insertion is on the lesser tuberosity of the proximal humerus. Its function is to internally rotate and adduct the arm and assist in humeral head compressive forces in the glenoid. The subscapularis tendon footprint has 4  distinct facets. These start just medially to the intertubercular groove and extend inferiorly and medially. The first facet accounts for about one-third of the total subscapularis footprint and is more frequently the location of tears visualized arthroscopically.60

Long Head of the Biceps Tendon The LHBT originates on the supraglenoid tubercle and exits the glenohumeral joint in the bicipital groove (Figure 4-13). It converges with the short head of the biceps just distally to the proximal musculotendinous junction. It then travels distally to the elbow joint to insert on the radial tuberosity. Like the long head of the triceps, it acts not only on the glenohumeral joint but also the ulnohumeral joint. Many studies have been completed looking at the LHBT to determine its effect on the glenohumeral joint. It has been shown to provide rotational and translational stability as well as being a humeral head depressor.61–63 In those studies the authors sequentially loaded the LHBT in a cadaver model and reported significant decreases in rotation and translation. They showed that loading the LHBT also provided a stabilizing force against translation at the ends of internal and

Clinical Anatomy and Biomechanics

37

Figure 4-14. Schematic drawing showing humerothoracic muscles, which include the deltoid, pectoralis major and minor, and the latissimus dorsi.

external rotation. They concluded that one of the functions of the LHBT is to act as a ligament, to help keep the humeral head centered on the glenoid at the end ranges of rotation. This was confirmed by another biomechanical study that showed decreased internal and external rotation with LHBT loading. They also showed that loading of LHBT shifted the humeral head apex posteriorly, which is significant in the discussion of the LHBT as an anterior restraint to humeral head subluxation.64 Yet another cadaveric study looked at the humeral head motion in a throwing athlete. They concluded that humeral head translational motion pushing against the LHBT may explain the etiology of type-II superior labrum anterior to posterior lesions in overhead athletes. This suggests that the LHBT helps as a sling to resist superior migration of the humeral head.65

Humerothoracic Muscles The humerothoracic muscles include the deltoid, pectoralis major and minor, and the latissimus dorsi. These muscles contribute significantly to shoulder function and stability and are considered the prime movers of the shoulder joint. These muscles are involved in the force couple in the superior-inferior direction (Figure 4-14). The deltoid originates on the acromion, spine of the scapula, and lateral third of the clavicle, and its insertion is on the deltoid tuberosity of the humerus. The primary function of the deltoid is abduction and forward flexion. The deltoid can be broken down into 3 areas: anterior, middle, and posterior. The anterior deltoid originates from the lateral clavicle and functions to flex and medially rotate the arm. The middle deltoid originates from the acromion and provides mostly abduction force for the arm. The posterior deltoid originates from the scapular spine and provides extension and lateral rotation force for the arm. All 3 of these sections converge distally into a single insertion on the deltoid tuberosity of the humerus. A study on glenohumeral translation showed

that the deltoid has an overall posterior translation vector on the position of the humeral head in the glenoid that can be overcome by biceps loads.66 The origin of the pectoralis major is made up of 2 portions with 1 origin on the sternum (sternal head) and the other on the medial half of clavicle (clavicular head). They insert on the lateral side of the intertubercular groove of the humerus with the clavicular head anterior to the sternal head. The pectoralis major adducts and medially rotates the humerus. A study using both a computational and cadaveric model for shoulder muscles showed that when pectoralis major activity increased, anteriorly directed forces increased. These in turn can affect the stability of the glenohumeral joint by decreasing stability.6 The origin of the pectoralis minor muscle is from the third to fifth ribs and costal cartilages, and its insertion is on the medial boarder of the coracoid process of the scapula. It provides a stabilizing function to the scapula by pulling it inferiorly and anteriorly against the thoracic wall. It is unique in that it also functions as a secondary muscle of inspiration. The latissimus dorsi muscle originates from the dorsal spine, sacrum, and the iliac crest and inserts at the floor of the intertubercular groove of the humerus. It functions in extending, adducting, and internally rotating the humerus.

Force Couples The force couple concept is essential for describing shoulder function. The definition of a force couple is 2 or more muscles acting in dif ferent directions that influence the rotation of a joint in a specific direction. If the forces are not in equilibrium, then the object will rotate in the direction of the higher force. If they are in a state of equilibrium, then the 2 forces will balance each other out and the object will not move. The glenohumeral joint has 2 major force couples: 1 in the transverse plane and 1 in the coronal plane.

38

Chapter 4

Figure 4-15. (A) The coronal plane force couple with the deltoid acting superiorly and the inferior rotator cuff (subscapularis, infraspinatus, teres minor), pectoralis major, and latissimus dorsi acting inferiorly. (B) The transverse plane force couple comprising the infraspinatus and teres minor acting posteriorly and the subscapularis acting anteriorly.

The force couple in the coronal plane involves the deltoid acting in one direction and the inferior rotator cuff muscles (infraspinatus, teres minor, and subscapularis), pectoralis major, and latissimus dorsi acting in the other direction (Figure 4-15A). This force couple functions to produce a stable glenohumeral abduction moment.67 It does so because the inferior rotator cuff muscles, pectoralis major, and latissimus dorsi provide a depressor moment and the deltoid functions in the opposite direction.68 The force couple in the transverse plan involves the subscapularis anteriorly and the infraspinatus and teres minor posteriorly (Figure  4-15B). This force couple not only provides rotational movement but allows for stability of the humeral head in an anterior-posterior direction. For example, if a subscapularis tendon repair fails it could lead to an imbalance of the force couple. There would be an inability to control the humeral head, and an overpull of the posterior muscles would give an unrestricted posterior vector on the humeral head. Mihata and colleagues69 proved this in a cadaveric study in which they simulated unbalancing of the force couples. They showed that less force from the subscapularis resulted in an increase in external rotation and posteriosuperior glenohumeral contact pressures. This not only has an effect of increasing the risk of glenohumeral arthrosis but also can lead to imbalance in the whole upper extremity.

CONCLUSION Shoulder function results from a complex interplay of bony and soft-tissue passive stabilizers and active stabilizers. Bony passive stabilizers, soft-tissue passive, and softtissue active stabilizers all play a role in allowing substantial range of motion while providing stability. The bony passive stabilizers are the scapula, including the glenoid, humerus, humeral head, and clavicle. The passive soft-tissue stabilizers include the labrum, glenohumeral ligaments, and joint capsule. These help to deepen the socket of the glenoid and help to limit translation to provide stability. The active soft-tissue stabilizers include the rotator cuff, and the humerothoracic and periscapular muscles. These

play an impor tant role in force coupling, providing a compressive force of the humeral head on the glenoid, and providing strength and range of motion while maintaining the humeral head centered on the glenoid. It is impor tant to appreciate the anatomy, biomechanics, and the complex interplay between these stabilizing systems.

REFERENCES 1.

2. 3.

4.

5.

6.

7.

8. 9. 10. 11. 12.

Iannotti JP, Gabriel JP, Schneck SL, Evans BG, Misra  S. The normal glenohumeral relationships. An anatomical study of one hundred and forty shoulders. J Bone Joint Surg Am. 1992;74(4):491-500. doi:10.2106/00004623-199274040-00004. Churchill RS, Brems JJ, Kotschi H. Glenoid size, inclination, and version: an anatomic study. J Shoulder Elbow Surg. 2001;10:327-332. Cameron KL, Tennent DJ, Sturdivant RX, et  al. Increased glenoid retroversion is associated with increased rotator cuff strength in the shoulder. Am J Sports Med. 2019;47(8):1893-1900. doi:10.1177/0363546519853591. Hurley JA, Anderson TE, Dear W, Andrish JT, Bergfeld JA, Weiker GG. Posterior shoulder instability. Surgical versus conservative results with evaluation of glenoid version. Am J Sports Med. 1992;20(4):396-400. doi:10.1177/036354659202000405. Itoi E, Motzkin NE, Morrey BF, An KN. Scapular inclination and inferior stability of the shoulder. J Shoulder Elbow Surg. 1992;1(3):131139. doi:10.1016/1058-2746(92)90090-P. Owens BD, Campbell SE, Cameron KL. Risk factors for anterior glenohumeral instability. Am J Sports Med. 2014;42(11):2591-2596. doi:10.1177/0363546514551149. Robertson DD, Yuan J, Bigliani LU, Flatow EL, Yamaguchi K. Threedimensional analysis of the proximal part of the humerus: relevance to arthroplasty. J Bone Joint Surg Am. 2000;82(11):1594-1602. doi:10.2106/00004623-200011000-00013. Bost FC, Inman VT. The pathological changes in recurrent dislocation of the shoulder. J Bone Joint Surg Am. 1942;24(3):595-613. Steindler  A. Kinesiology of the Human Body Under Normal and Pathological Conditions. Springfield, IL: Charles C. Thomas; 1955. Saha AK. Dynamic stability of the glenohumeral joint. Acta Orthop. 1971;42(6):491-505. doi:10.3109/17453677108989066. Lippitt S, Matsen F. Mechanisms of glenohumeral joint stability. Clin Orthop Rel Res. 1993;(291):20-28. Lippitt SB, Vanderhooft JE, Harris SL, Sidles JA, Harryman DT  II, Matsen FA III. Glenohumeral stability from concavity-compression: a quantitative analysis. J Shoulder Elbow Surg. 1993;2(1):27-35. doi:10.1016/S1058-2746(09)80134-1.

Clinical Anatomy and Biomechanics 13.

14.

15.

16.

17.

18.

19.

20.

21.

22. 23.

24.

25.

26. 27.

28.

29.

30.

31.

Lazarus MD, Sidles JA, Harryman DT II, Matsen FA III. Effect of a chondral-labral defect on glenoid concavity and glenohumeral stability. A cadaveric model. J Bone Joint Surg Am. 1996;78(1):94-102. doi:10.2106/00004623-199601000-00013. Kibler WB, Ludewig PM, McClure PW, Michener LA, Bak K, Sciascia AD. Clinical implications of scapular dyskinesis in shoulder injury: the 2013 consensus statement from the “scapular summit”. Br J Sports Med. 2013;47:877-885. doi:10.1136/bjsports-2013-092425. Meininger AK, Figuerres BF, Goldberg BA. Scapular winging: an update. J Am Acad Orthop Surg. 2011;19(8):453-462. doi:10.5435/ 00124635-201108000-00001. Freedman L, Munro RR. Abduction of the arm in the scapular plane: scapular and glenohumeral movements. A roentgenographic study. J Bone Joint Surg Am. 1966;48(8):1503-1510. doi:10.2106/00004623-196648080-00004. Roche SJ, Funk L, Sciascia A, Kibler WB. Scapular dyskinesis: the surgeon’s perspective. Shoulder Elbow. 2015;7(4):289-297. doi:10.1177/ 1758573215595949. Kibler WB, Uhl TL, Maddux JW, Brooks PV, Zeller B, McMullen J. Qualitative clinical evaluation of scapular dysfunction: a reliability study. J Shoulder Elbow Surg. 2002;11(6):550-556. doi:10.1067/ mse.2002.126766. Mihata T, Jun BJ, Bui CN, et  al. Effect of scapular orientation on shoulder internal impingement in a cadaveric model of the cocking phase of throwing. J Bone Joint Surg Am. 2012;94(17):1576-1583. doi:10.2106/JBJS.J.01972. Lo IK, Burkhart SS. Arthroscopic coracoplasty through the rotator interval. Arthroscopy. 2003;19(6):667-671. doi:10.1016/ S0749-8063(03)00219-6. Simovitch R, Sanders B, Ozbaydar M, Lavery K, Warner JJP. Acromioclavicular joint injuries: diagnosis and management. J Am Acad Orthop Surg. 2009;17(4):207-219. doi:10.5435/00124635-200904000-00002. Howell SM, Galinat BJ. The glenoid-labral socket. A constrained articular surface. Clin Orthop Rel Res. 1989;(243):122-125. Pouliart N, Gagey O. The effect of isolated labrum resection on shoulder stability. Knee Surg Sports Traumatol Arthrosc. 2006;14(3):301308. doi:10.1007/s00167-005-0666-1. McMahon PJ, Yang BY, Chow S, Lee TQ. Anterior shoulder dislocation increases the propensity for recurrence: a cadaveric study of the number of dislocations and type of capsulolabral lesion. J Shoulder Elbow Surg. 2013;22(8):1046-1052. doi:10.1016/j.jse.2012.11.013. Basmajian JV, Bazant FJ. Factors preventing downward dislocation of the adducted shoulder joint. An electromyographic and morphological study. J Bone Joint Surg Am. 1959;41-A:1182-1186. Schwartz E, Warren RF, O’Brien SJ, Fronek J. Posterior shoulder instability. Orthop Clin North Am. 1987;18(3):409-419. Warner JJ, Deng XH, Warren RF, Torzilli PA. Static capsuloligamentous restraints to superior-inferior translation of the glenohumeral joint. Am J Sports Med. 1992;20(6):675-685. doi:10.1177/036354659202000608. Turkel SJ, Panio MW, Marshall JL, Girgis FG. Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am. 1981;63(8):1208-1217. Jerosch J, Moersler M, Castro WHM. Über die Funktion der passiven Stabilisatoren des glenohumeralen Gelenkes - Eine Biomechanische Untersuchung [On the passive stabilizing mechanism of the glenohumeral joint—a biomechanic study]. Z Orthop Ihre Grenzgeb. 1990;128(2):206-212. doi:10.1055/s-2008-1039501. Mihata T, Lee YS, McGarry MH, Abe M, Lee TQ. Excessive humeral external rotation results in increased shoulder laxity. Am J Sports Med. 2004;32(5):1278-1285. doi:10.1177/0363546503262188. McMahon PJ, Dettling J, Sandusky MD, Tibone JE, Lee TQ. The anterior band of the inferior glenohumeral ligament. Assessment of its permanent deformation and the anatomy of its glenoid attachment. J Bone Joint Surg Br. 1999;81(3):406-413. doi:10.1302/0301-620X.81B3.9153.

32.

33.

34.

35.

36.

37.

38.

39. 40.

41.

42.

43.

44.

45.

46.

47.

48. 49.

50.

39

Mihata T, Gates J, McGarry MH, Neo M, Lee TQ. Effect of posterior shoulder tightness on internal impingement in a cadaveric model of throwing. Knee Surg Sports Traumatol Arthrosc. 2015;23(2):548-554. doi:10.1007/s00167-013-2381-7. Fealy S, April EW, Khazzam M, Armengol-Barallat J, Bigliani LU. The coracoacromial ligament: morphology and study of acromial enthesopathy. J Shoulder Elbow Surg. 2005;14(5):542-548. doi:10.1016/j. jse.2005.02.006. Holt EM, Allibone RO. Anatomic variants of the coracoacromial ligament. J Shoulder Elbow Surg. 1995;4(5):370-375. doi:10.1016/ S1058-2746(95)80021-2. Lee TQ, Black AD, Tibone JE, McMahon PJ. Release of the coracoacromial ligament can lead to glenohumeral laxity: a biomechanical study. J Shoulder Elbow Surg. 2001;10(1):68-72. doi:10.1067/ mse.2001.111138. Wolf RS, Zheng N, Iero J, Weichel D. The effects of thermal capsulorrhaphy and rotator interval closure on multidirectional laxity in the glenohumeral joint: a cadaveric biomechanical study. Arthroscopy. 2004;20(10):1044-1049. doi:10.1016/j.arthro.2004.07.001. Shafer BL, Mihata T, McGarry MH, Tibone JE, Lee TQ. Effects of capsular plication and rotator interval closure in simulated multidirectional shoulder instability. J Bone Joint Surg Am. 2008;90(1):136144. doi:10.2106/JBJS.F.00841. Tetro AM, Bauer G, Hollstien SB, Yamaguchi K. Arthroscopic release of the rotator interval and coracohumeral ligament: an anatomic study in cadavers. Arthroscopy. 2002;18(2):145-150. doi:10.1053/ jars.2002.30438. Cleland  J. Notes on raising the arm. J Anat Physiol. 1884;18(pt 3):275-278. Gagey N, Gagey O, Bastian G, Lassau JP. The fibrous frame of the supraspinatus muscle. Correlations between anatomy and MRI findings. Surg Radiol Anat. 1990;12(4):291-292. doi:10.1007/BF01623708. Roh MS, Wang VM, April EW, Pollock RG, Bigliani LU, Flatow EL. Anterior and posterior musculotendinous anatomy of the supraspinatus. J Shoulder Elbow Surg. 2000;9(6):436-440. doi:10.1067/ mse.2000.108387. Vahlensieck M, an Haack K, Schmidt HM. Two portions of the supraspinatus muscle: a new finding about the muscles macroscopy by dissection and magnetic resonance imaging. Surg Radiol Anat. 1994;16(1):101-104. doi:10.1007/BF01627931. Volk AG, Vangsness CT. An anatomic study of the supraspinatus muscle and tendon. Clin Orthop Rel Res. 2001;(384):280-285. doi:10.1097/00003086-200103000-00032. Gates JJ, Gilliland J, McGarry MH, et  al. Influence of distinct anatomic subregions of the supraspinatus on humeral rotation. J Orthop Res. 2010;28(1):12-17. doi:10.1002/jor.20947. Kronberg M, Németh G, Broström LA. Muscle activity and coordination in the normal shoulder. An electromyographic study. Clin Orthop Rel Res. 1990;(257):76-85. Reinold MM, Wilk KE, Fleisig GS, et al. Electromyographic analysis of the rotator cuff and deltoid musculature during common shoulder external rotation exercises. J Orthop Sport Phys Ther. 2004;34(7):385394. doi:10.2519/jospt.2004.34.7.385. Burkhart SS, Esch JC, Jolson RS. The rotator crescent and rotator cable: an anatomic description of the shoulder’s “suspension bridge.” Arthroscopy. 1993;9(6):611-616. doi:10.1016/ s0749-8063(05)80496-7. Clark J, Sidles JA, Matsen FA. The relationship of the glenohumeral joint capsule to the rotator cuff. Clin Orthop Rel Res. 1990;(254):29-34. Clark JM, Harryman DT II. Tendons, ligaments, and capsule of the rotator cuff. Gross and microscopic anatomy. J Bone Joint Surg Am. 1992;74(5):713-725. doi:10.2106/00004623-199274050-00010. Fallon J, Blevins FT, Vogel K, Trotter  J. Functional morphology of the supraspinatus tendon. J Orthop Res. 2002;20(5):920-926. doi:10.1016/S0736-0266(02)00032-2.

40 51.

52.

53.

54.

55.

56.

57.

58.

59.

Chapter 4 Kask K, Kolts I, Lubienski A, Russlies M, Leibecke T, Busch LC. Magnetic resonance imaging and correlative gross anatomy of the ligamentum semicirculare humeri (rotator cable). Clin Anat. 2008;21(5):420-426. doi:10.1002/ca.20639. Kolts I, Busch LC, Tomusk H, et al. Macroscopial anatomy of the socalled “rotator interval”. A cadaver study on 19 shoulder joints. Ann Anat. 2002;184(1):9-14. doi:10.1016/S0940-9602(02)80025-5. Morag Y, Jacobson JA, Lucas D, Miller B, Brigido MK, Jamadar DA. US appearance of the rotator cable with histologic correlation: preliminary results. Radiology. 2006;241(2):485-491. doi:10.1148/ radiol.2412050800. Sheah K, Bredella MA, Warner JJP, Halpern EF, Palmer WE. Transverse thickening along the articular surface of the rotator cuff consistent with the rotator cable: identification with MR arthrography and relevance in rotator cuff evaluation. AJR Am J Roentgenol. 2009;193(3):679-686. doi:10.2214/AJR.08.2285. Kim HM, Dahiya N, Teefey SA, Keener JD, Galatz LM, Yamaguchi K. Relationship of tear size and location to fatty degeneration of the rotator cuff. J Bone Joint Surg Am. 2010;92(4):829-839. doi:10.2106/ JBJS.H.01746. Namdari S, Donegan RP, Dahiya N, Galatz LM, Yamaguchi K, Keener JD. Characteristics of small to medium-sized rotator cuff tears with and without disruption of the anterior supraspinatus tendon. J  Shoulder Elbow Surg. 2014;23(1):20-27. doi:10.1016/j. jse.2013.05.015. Halder AM, O’Driscoll SW, Heers G, et al. Biomechanical comparison of effects of supraspinatus tendon detachments, tendon defects, and muscle retractions. J Bone Joint Surg Am. 2002;84(5):780-785. doi:10.2106/00004623-200205000-00013. Mesiha MM, Derwin KA, Sibole SC, Erdemir A, McCarron JA. The biomechanical relevance of anterior rotator cuff cable tears in a cadaveric shoulder model. J Bone Joint Surg Am. 2013;95(20):18171824. doi:10.2106/JBJS.L.00784. Pinkowsky GJ, ElAttrache NS, Peterson AB, Akeda M, McGarry MH, Lee TQ. Partial-thickness tears involving the rotator cable lead to abnormal glenohumeral kinematics. J  Shoulder Elbow Surg. 2017;26(7):1152-1158. doi:10.1016/j.jse.2016.12.063.

60.

61.

62.

63.

64.

65.

66.

67.

68.

69.

Yoo JC, Rhee YG, Shin SJ, et  al. Subscapularis tendon tear classification based on 3-dimensional anatomic footprint: a cadaveric and prospective clinical observational study. Arthroscopy. 2015;31(1):1928. doi:10.1016/j.arthro.2014.08.015. Saha AK, Das AK, Dutta SK. Mechanism of shoulder movements and a plea for the recognition of “zero position” of glenohumeral joint. Clin Orthop Rel Res. 1983;(173):3-10. doi:10.1097/00003086-198303000-00002. Warner JJP, McMahon PJ. The role of the long head of the biceps brachii in superior stability of the glenohumeral joint. J Bone Joint Surg Am. 1995;77(3):366-372. doi:10.2106/00004623-199503000-00006. Youm T, ElAttrache NS, Tibone JE, McGarry MH, Lee TQ. The effect of the long head of the biceps on glenohumeral kinematics. J Shoulder Elbow Surg. 2009;18(1):122-129. doi:10.1016/j.jse.2008.06.003. McGarry MH, Nguyen ML, Quigley RJ, Hanypsiak B, Gupta R, Lee TQ. The effect of long and short head biceps loading on glenohumeral joint rotational range of motion and humeral head position. Knee Surg Sports Traumatol Arthrosc. 2016;24(6):1979-1987. doi:10.1007/ s00167-014-3318-5. Grossman MG, Tibone JE, McGarry MH, Schneider DJ, Veneziani S, Lee TQ. A cadaveric model of the throwing shoulder: a possible etiology of superior labrum anterior-to-posterior lesions. J Bone Joint Surg Am. 2005;87(4):824-831. doi:10.2106/JBJS.D.01972. Lin T, Javidan P, McGarry MH, Gonzalez-Lomas G, Limpisvasti O, Lee TQ. Glenohumeral contact pressure in a simulated active compression test using cadaveric shoulders. J  Shoulder Elbow Surg. 2013;22(3):365-374. doi:10.1016/j.jse.2012.02.003. Inman VT, Saunders JB, Abbott LC. Observations of the function of the shoulder joint. 1944. Clin Orthop Rel Res. 1996;(330):3-12. doi:10.1097/00003086-199609000-00002. Halder AM, Zhao KD, O’Driscoll SW, Morrey BF, An KN. Dynamic contributions to superior shoulder stability. J Orthop Res. 2001;19(2):206-212. doi:10.1016/S0736-0266(00)00028-0. Mihata T, Gates J, McGarry MH, Lee J, Kinoshita M, Lee TQ. Effect of rotator cuff muscle imbalance on forceful internal impingement and peel-back of the superior labrum: a cadaveric study. Am J Sports Med. 2009;37(11):2222-2227. doi:10.1177/0363546509337450.

SECTION II Anterior Instability

5 Management of In-Season Anterior Instability and Return-to-Play Outcomes Jonathan F. Dickens, MD and Maj. Michael A. Donohue, MD

Glenohumeral instability in young athletes is common and may lead to prolonged absence from sports participation.1 Anterior dislocation of the glenohumeral joint most commonly occurs with the arm in a forward flexed, abducted, and externally rotated position. The broad spectrum of anterior shoulder instability in athletes ranges from complete dislocation requiring reduction to microinstability in the overhead athlete, which may be clinically harder to diagnose but equally challenging to treat.2,3 Most commonly, athletes experience traumatic shoulder subluxation events without sustaining a complete dislocation of the joint.1,4 The amount of external rotation required to place the shoulder at maximal risk has been debated. Tanaka et al5 clinically evaluated the position of maximal anterior translation in sedated patients, and found that maximal anterior translation occurred with 90 degrees of abduction, but only 26 degrees of external rotation. Most likely, there is multifactorial variability in the exact position of risk for athletes. A review of the National Collegiate Athletic Association (NCAA) Injury Surveillance System found that recorded events of shoulder instability occur at a rate of 0.12 per 1000 exposures.1 Men were more often injured compared to women. Additionally, shoulder instability events accounted for 25% of all shoulder injuries that occurred. The majority of events occurred in contact sports, namely football, hockey, and wrestling, and during contact with another player. Sustaining such an injury is not without concern for lost time from play. Almost half of the players lost more than 10 days of sports participation following a dislocation event.1 Orthopedic surgeons treating these patients can find themselves in a conundrum to recommend expeditious

return to play of the athlete, especially when the athlete is in-season. The young, in-season, contact athlete represents the most at-risk and challenging patient population to treat shoulder instability because these patients have the highest performance demands on their shoulder are the most at-risk for instability. Immediate surgical intervention at the time of the in-season instability event precludes return to play in the same season. On the other hand, nonoperative management may allow the athlete to return to an acceptable level of performance and sport, between 5 days and 4 weeks following the injury, with an in-season recurrence rate between 37% and 73%.4,6-8 Interestingly, an anonymous survey of team physicians who manage high school, collegiate, and professional athletes found that only 7% of treating orthopedic surgeons would recommend immediate in-season surgical stabilization of the athlete with a first-time dislocation.9 The management of the in-season athlete with shoulder instability is complex, and determining the optimal management requires consideration of many variables including the position and sport played, timing of the injury during the season, current level of play, expected future level of play, future risk of recurrent instability, clinical laxity, findings, glenohumeral bone loss, and ligamentous injury. Additional variables such as the type of instability event (eg, subluxation or dislocation), length and position of immobilization, as well as the use of braces have been considered as additional variables that may influence the risk of recurrence for the in-season athlete. This chapter will review the management considerations and controversies surrounding in-season anterior shoulder instability relevant to the team physician and athlete.

- 43 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 43-54). © 2021 SLACK Incorporated.

44

Chapter 5

ANATOMICAL CONSIDERATIONS FOR IN-SEASON RETURN TO PLAY There is a spectrum of injuries associated with anterior instability, and correct identification of the pathoanatomy is critical to prevent recurrence, optimize outcomes, and guide treatment. The most commonly injured structure following a shoulder dislocation is the anterior labrum (ie, Bankart lesion).10 Before routine access to magnetic resonance imaging (MRI), Taylor and Arciero evaluated first-time dislocators with either surgery or nonoperative management.11 In the surgically treated cohort, they found at the time of surgery that 97% had a Bankart tear or separation of the capsuloligamentous tissue following a single first-time dislocation. As routine use of MRI preoperatively has become standard treatment, Owens and colleagues3 similarly found 97% of first-time traumatic anterior subluxators had a Bankart lesion on MRI. Injury to the anterior labrum does not occur in isolation. The inferior glenohumeral ligament (IGHL) undergoes permanent deformation following a single dislocation that increases with repeat instability.12 Bigliani et al13 investigated the tensile strength of the IGHL in cadaveric specimens. Despite determining the ultimate tensile strength of the IGHL, a more impor tant finding from this study was significant elongation of the ligament before ultimate failure or rupture. Additionally, in a follow-up study, Ticker and colleagues14 found that the tensile strength of the IGHL decreased in the more anterior-inferior portions of the ligament. If the athlete continues to experience repeat dislocation or even subluxation events following in-season return to play, the capsuloligamentous structures are at risk for increased deformation. This information should be considered when deciding on the optimal timing (in-season vs offseason) and method of surgical stabilization (arthroscopic vs open). It also highlights the impor tant technical consideration of appropriate retensioning of the IGHL to restore shoulder stability. A bony Bankart represents a fracture of the anterior glenoid rim and can occur acutely following injury. Multiple authors have investigated both first-time and recurrent instability for glenoid morphology and bone loss properties with very similar results. Milano et al15 found that 72% of patients had presence of a bone defect in the setting of anterior instability. Similarly, Sugaya and colleageus16 used 3-dimensional computed tomography (CT) reconstruction in 100  consecutive patients with recurrent anterior instability. Ninety percent (90%) demonstrated changes in the glenoid contour. Fifty percent (50%) had a bony Bankart lesion that was identified, and 40% had glenoid erosion. This demonstrates that in the setting of recurrent shoulder instability, risk of glenoid bone loss increases. More recently, Dickens and colleagues17 analyzed a cohort of first-time shoulder dislocation events in athletes at a single institution who were followed for 4 years during the course

of their collegiate career. After sustaining only a single event, 52% of the athletes demonstrated greater than 5% bone loss, and 17% of the athletes demonstrated greater than 13.5% bone loss.17 Thirteen and a half percent bone loss is significant and will be discussed later because it has been defined as a “subcritical” amount of glenoid bone loss that may predispose patients to poorer subjective outcomes following arthroscopic stabilization surgery.18 Contact athletes were more likely than noncontact athletes to sustain a primary dislocation with concomitant bone loss. As surgeons consider athletes for return to play during the season of injury, they must evaluate for acute bony Bankart injuries and bone loss. With the exception of avulsion fragment, all acute bony Bankart fractures should exclude the athlete from return to play in season and we recommend early surgical fixation to prevent malunion. For those with early glenoid bone loss, the surgeon must consider the risk of continued glenoid erosion that occurs with recurrent instability during the season. Any amount of glenoid bone loss may place the athlete at risk for recurrent instability. Arciero et al19 performed cadaveric testing of combined lesions of the glenoid and humeral head. With as little as 2 mm of glenoid bone loss and the presence of a Hill-Sachs defect, there was an 18% to 43% decrease in load to translation. This decreased load to translation places the shoulder at risk for recurrent instability. Athletes with any measurable glenoid bone loss and a HillSachs lesion should be considered for early surgical stabilization. Additionally, athletes with greater than 10% glenoid bone loss should be withheld from competition in favor of early surgical intervention given the risk recurrent instability. Less commonly, other capsuloligamentous structures may be injured during anterior shoulder instability. A humeral avulsion of the glenohumeral ligament (HAGL) may occur from 1.5% to 9% of the time, although a recent study found a 25% occurrence in female athletes undergoing shoulder stabilization.20-22 This may indicate that the true incidence is higher than often estimated and may be a missed lesion. Ticker et  al14 reviewed the biomechanical properties of the IGHL and found that in a slow rate of strain, the IGHL more commonly failed at the humeral insertion, whereas the fibers of the IGHL were more resistant at the humeral insertion to fast rates of strain.14 In vivo, the HAGL is cited to occur either in a high-energy traumatic event or with repetitive microtrauma in the overhead athlete.23 With an HAGL lesion, there is a significant decrease in the load to translation of the glenohumeral joint.24 However, the athlete may not complain of frank instability as the primary symptom. Provencher and colleagues found that most patients’ primary complaint was related to pain rather than instability.25 In many cases the continued symptoms associated with HAGL lesions prevent return to sport in athletes; however, even when the athlete is asymptomatic we recommend early surgical intervention to facilitate surgical repair and mitigate the risk or recurrent instability. The humeral head is often injured as a contrecoup lesion (Hill-Sachs). This lesion is an impaction fracture of the

Management of In-Season Anterior Instability and Return-to-Play Outcomes

45

Figure 5-1. The glenoid track. Glenoid width * 0.83—width of missing bone compared to the size of the Hill-Sachs lesion. The strip represents a theoretical overlay of the glenoid track over the Hill-Sachs lesion and demonstrates that the track is wider than the Hill-Sachs lesion, therefore portending a better outcome following a soft-tissue– only surgery to the glenoid.

posterosuperolateral portion of humeral head adjacent to the rotator cuff insertion. The Hill-Sachs lesion occurs anywhere from 7% to 93% of the time following instability events and approaches 100% in recurrent instability.11,26 27 With continued instability, the bipolar lesions that occur at the glenoid and the humeral head can lead to continued bone loss on both sides and engagement of the Hill-Sachs lesion on the anterior glenoid as described by Burkhart and De Beer.28 A large Hill-Sachs lesion that engages may lead to failure of a Bankart repair procedure. This concept of the “engaging Hill-Sachs” lesions has now led to the concept of the glenoid track as described by Yamamoto et al29 in 2007. The glenoid track represents a comparison of the width of the Hill-Sachs lesion to 83% of the width of the glenoid minus the width of bones loss (Figure 5-1). If the Hill-Sachs lesion is wider than the glenoid track, this is considered an off-track lesion and predisposes the patient to failure of a soft-tissue–only repair of the Bankart lesion.29 In the setting of an off-track lesion, the athlete should be considered for surgical stabilization and not returned to play.

ATHLETE CONSIDERATIONS FOR IN-SEASON RETURN TO PLAY There are numerous individual and athletic participation variables that contribute to the decision making for in-season return to play, and each decision should be made using a shared decision-making model. At a minimum the following questions for the in-season athlete can help guide surgeons in their clinical decision making: 1. What is the age of the patient? When did instability first occur? Is this a primary in-season event or recurrence? Younger patients have an increased risk of recurrent instability.30 Instability occurring early in the playing season may lead the surgeon to recommend early stabilization. By contrast, near the end of the season the athlete

has a lower number of absolute exposures remaining and may wish to complete the season. Athletes with recurrent dislocation would be recommended for surgery. 2. Does the athlete play a contact, collision, or overhead sport? Is the injury in the dominant arm of an overhead athlete? These athletes are higher risk for recurrent instability with nonoperative treatment.31,32 Up to 55% of overhead athletes may not be able to return to play at their previous level following surgical stabilization.33 3. What was the position of the arm and was this a contact event? If a noncontact injury, the surgeon must elucidate the mechanism of injury. (For example, Owens et  al4 described anterior subluxation in boxers missing a punch.) 4. What is their level of play? Where in the season is the athlete and what is his or her expected level of contribution from a shared decision-making standpoint based on athlete, coach, trainer, and physician input? A thorough understanding of the patient’s history is clearly multifactorial and takes into account more than just the clinical instability event. Although axillary neuropraxia or rotator cuff atony may initially occur following injury, continued weakness must cue the examiner to consider neurologic injury or rotator cuff injury.34,35 If there is evidence of a nerve injury or rotator cuff tear, the athlete cannot return to play. In-season athletes require additional consideration of their history and indications for their potential to return to play meaningfully. Dickens et  al6 demonstrated that many athletes will attempt to return to play in-season with varying degrees of success. Contact and collision athletes experience the highest risk for continued instability when they attempt to return to play in-season. Often, though, a starting athlete at higher levels of play may be considered essential, and the surgeon must have a complete understanding of the patient’s history as well as clinical exam findings and imaging to

46

Chapter 5

Table 5-1. To Safely and Successfully Return Athletes to Sports Activity, They Should Meet the Criteria Listed at a Minimum CRITERIA Motion Strength Coordination Imaging

KEY FINDINGS Full and symmetric motion 5/5 rotator cuff strength without nerve injury Able to complete sport-specific functional skills with no pain or instability (1) < 13% to 20% glenoid bone loss (2) No bony Bankart (3) On-track Hill-Sachs lesion

make a determination of return to play while protecting the player from additional injury to the shoulder that may lead to increased bone loss.

PHYSICAL EXAMINATION A complete physical examination will serve to validate the surgeon’s diagnosis and allows him or her to identify any other associated conditions such as hyperlaxity or neurological concerns. If an athlete is being examined on the playing field and has a glenohumeral dislocation, the neurovascular status should be established both before and following reduction. In the training room the exam requires a systematic approach. We advocate the first step in examination is purely observational to determine the athlete’s range of motion in all planes and additionally to identify any scapular dyskinesis. All exams should begin by evaluating the uninjured shoulder first. Stability testing often cannot be performed in the acute period following injury. Once the athlete has regained painfree motion of the injured shoulder, this can be employed. Multiple special tests for evaluation of shoulder instability have been established—all with varying degrees of sensitivity and specificity.36 Individually, each test may be patient dependent such as a large football lineman compared to a thin runner. Therefore, using a constellation of systematic tests will confirm the suspected diagnosis. The authors routinely use the apprehension test35 with Jobe’s relocation37 and surprise test. In the setting of all 3 exam findings being positive, the positive predictive value for anterior instability is 93.6%.38 Additionally, we also advocate the use of the load shift test,39 with grading of the degree of translation as described by Hawkins et al.40 This test should be performed both during evaluation in the clinic setting, but also before surgery when the patient is under anesthetic sedation. Other tests used include the Gagey test41 to examine the IGHLs, the sulcus sign to examine to examine for capsular laxity, and

Beighton scoring for general hyperlaxity.42 Testing of rotator cuff strength, superior labrum/biceps, neurologic status, and impingement should also be performed.

IMAGING Following reduction, a complete radiographic evaluation is obtained. For the team physician, we recommend plain-film imaging either the day of injury after glenohumeral reduction, or the following days as part of an expedited workup, especially if the athlete may wish to return to play without surgery. We routinely use an instability series of plain film x-ray imaging that includes anteroposterior (AP), Grashey, Axillary Y, and West Point views. The plain-film imaging allows for evaluation of glenohumeral location, to rule out fracture, as an initial evaluation for glenoid bone loss or fracture, and to determine presence of a Hill-Sachs lesion. The study of choice for soft-tissue evaluation is MRI with or without intra-articular contrast. In general, the authors recommend early advanced axial imaging of the athlete with a first-time or recurrent in-season subluxation or dislocation event to assess for concomitant pathology and underappreciated bone loss, which more common in contact and collision athletes. We will use a standard MRI if an athlete is within approximately 10 days from a dislocation event. An MR arthrogram with intra-articular contrast is other wise used for evaluation. MRI allows for visualization of soft-tissue status for the labrum as well as for associated injuries, including rotator cuff tears and HAGL. Although not routinely used for evaluation of bone loss, the MRI can provide a gross status of glenoid and humeral head bone loss, which may lead the surgeon to obtain a CT scan. For the in-season athlete who will attempt same-season return to play criteria without surgical intervention, we do not routinely obtain a CT scan. CT is usually reserved for the athlete with bone loss and surgical intervention is planned.

TREATMENT The most common question for any athlete, trainer, and coach following a shoulder instability event in-season is what is the timeline for return to play? This can be a dilemma for all parties involved in the athlete’s care. The goal of treatment is safe return to play. Following the spectrum of treatment options that may best address the instability, whether operative or nonoperative, and appropriate rehabilitation, there is no set time criteria for return to play. Instead, rehabilitation and return to play can be multifactorial. Decision making is critical for the surgeon in guiding the patient through treatment options. By the conclusion of either treatment option, the athlete should have a pain-free shoulder with symmetric strength and no symptoms of recurrent instability during sport-specific activity. Our recommended algorithm is shown in Figure  5-2. Our recommended key criteria for return to play are noted in Table 5-1.

Management of In-Season Anterior Instability and Return-to-Play Outcomes

47

Figure 5-2. Decision-making algorithm. The flowchart demonstrates our recommended decision-making algorithm for an inseason athlete who sustains an instability event. (Abbreviations: CT, computed tomography; HAGL, humeral avulsion of the glenohumeral ligament; MRI, magnetic resonance imaging.)

Nonsurgical Management of the In-Season Athlete For the in-season athlete, nonoperative treatment represents the only potential for return to play in the same season. Many athletes therefore prefer nonoperative treatment to allow for in-season return to play; however, only suitable candidates for nonoperative treatment should be considered for in-season return to play. Nonoperative rehabilitation is a focus elsewhere in this textbook but includes a short period of immobilization for soft-tissue rest, followed by rehabilitation to regain full symmetric motion and strength of the shoulder, and finally sport-specific protocols. In one of the earliest evaluations of the natural history of shoulder instability, Wheeler et  al30 prospectively tracked West Point cadets for a minimum of 14 months following traumatic anterior shoulder dislocation events. The West Point cadet population was optimal to track because not only is the population young and active, they are required to participate in contact and collision type activities and sports in preparation for entering the military. In these young athletes, shoulder instability treated nonoperatively recurred in 92%. These patients not only experienced recurrent subluxation events, but 82% sustained recurrent dislocations.30 These high rates of recurrent instability treated nonoperatively served to bolster the findings of 2 previous studies of the natural history of shoulder instability that found rates of recurrent instability of 94% in patients younger than 20 years.43,44

One of the primary indications for nonoperative management and attempted return to play is the first time dislocator with no bone loss and imaging consistent with a Bankart lesion. Additionally, athletes who do not participate in contact sports or overhead sports likely have a better chance to return to play in the same season.4,6,30,31 The young athlete who participates in contact sports must be counseled regarding the high risk of recurrent instability with nonoperative management. Several studies have evaluated time lost from sport. The first prospective, multicenter study to assess same-season return to play in collegiate level athletes sustaining an instability event found that 73% of athletes who attempted sameseason return to sport were able to return to competition at a median of 5 days.6 Less encouraging though was that just more than one-quarter (27%) of those athletes who attempted same-season return to play were not able to rehabilitate successfully and did not return to play.6 Buss and colleagues8 were the first to report return-to-play outcomes for in-season athletes treated with an accelerated rehabilitation program. In their retrospective review, athletes were able to return to play at a mean of 10 days.8 Previous to this, several return-toplay studies that examined nonoperative treatment employed cumbersome periods of immobilization and rehabilitation lasting from 1 to 3 months.30,45 Pain associated with an instability event, especially complete dislocation of the glenohumeral joint, can be improved with a short course of immobilization. No consensus for use of immobilization or the position of immobilization exists.

48

Chapter 5

Buss et  al8 as mentioned earlier returned athletes to play at a mean of 10 days and used no immobilization in their rehabilitation protocol. Henry and Genung were among the earliest to examine use of immobilization in shoulder instability rehabilitation.46 They followed 121 patients who were immobilized for approximately 3 weeks and 59 patients who were not immobilized following injury. The rates of recurrent dislocation were similar—90% and 85%, respectively. Paterson et al47 conducted a meta-analysis of 5 level-1 studies and 1 level-2 study to determine efficacy of immobilization. They found no benefit in sling immobilization greater than 1 week, and no effect on rates of recurrence whether or not a sling was used.47 Based on these studies, we recommend a short course of immobilization as needed for pain but no longer than 3 to 5 days to facilitate early supervised motion. A significant controversy related to immobilization is the position of the arm while immobilized. Itoi and colleagues48,49 published first in a cadaveric specimen followed by an in  vivo MRI study that immobilization of the arm in a position of external rotation better reduces the anterior labrum to glenoid following shoulder dislocation and reduces rates of recurrent instability. However, several studies from other institutions attempted to reproduce these results with varying results. Additionally, concern has been raised regarding patient discomfort while immobilized in an externally rotated position. Paterson et al47 did not find a significant difference in recurrence rates based on position of immobilization in their meta-analysis, though. We do not advocate immobilization in the externally rotated position. Rather, patients should be placed into a position of comfort before beginning shoulder motion. The ultimate decision depends on surgeon preference. Outcomes following nonoperative management have historically relied on early studies that demonstrated extraordinarily high rates of recurrence in young athletes.30,45 Those studies, however, did not evaluate same-season return to play and ability to successfully complete the season without recurrence. Dickens et  al6 prospectively observed sameseason return to play in collegiate athletes treated nonoperatively. Forty-five athletes with a mean age of 20  years were included. All participated in contact sports except 2 who played baseball. Three-quarters (73%) were able to return to play at a median of 5 days. Only 12 of 45 (27%) though remained completely asymptomatic through the rest of the season. Despite the high rate of recurrent instability symptoms, 67% of those with recurrent instability were able to complete the remainder of their season. Athletes who experience dislocation as their primary instability event were at higher risk for repeat symptomatic instability.6 Buss and colleagues8 retrospectively reviewed sameseason return to play in 30 athletes. Their time to return to play as previously mentioned was a mean of 10 days. In this group, almost all were young (mean age, 16  years) contact athletes with the exception of 2—a skier and a gymnast. Seventy percent of the athletes returned to play with the use of a brace. Their return-to-play criteria though were

considered successful if the athlete returned to all or part of the same season. Reassuringly, 90% were able to return. The athletes experienced an average of 1.4 recurrent instability episodes following return to play. The majority experienced no recurrence, but some athletes experienced as many as 8 more events.8 Based on the earlier described evidence, most studies suggest there is a high risk for recurrent dislocation or instability event in the young collision or contact athlete. However, the most recent publication following return to play in young athletes may show successful return to play for high school– level athletes in season. Shanley et al50 prospectively tracked high school athletes in a single geographic region during a 4-year period. Athletes were included only if they sustained an anterior instability event in season while playing on a school-sanctioned sports team and underwent medical treatment. Two key findings from this study address nonoperative return to play through the following season, and brace wear. Ninety-seven scholastic athletes with continued sports eligibility were treated nonoperatively. Of these, 82 (85%) were able to undergo successful rehabilitation and return to sport without an instability event for at least one season. Six of the 97 (6.2%) athletes sustained a recurrent instability event during the follow-up period. The 15 athletes who failed nonoperative treatment either through failure to return to sport or recurrent instability were all contact athletes, and the majority (60%) were male football players.50 Players sustaining subluxation events were 3 times more likely to return to play than those with dislocations. The overall rate of return to play in season and with successful following-season participation is almost double that of Dickens et al,6 but similarly mirrors improved success for those with only subluxation events. Caution should be taken in applying the results of high school athletes to collegiate or higher-level athletes, for whom the level of competition and risk associated with play varies. In professional football players, return to play at the elite level can have significant effects on player longevity and team performance. Okoroha and colleagues51 hypothesized that these athletes could return to play at higher rates regardless of treatment type. They found that 92% of players treated nonoperatively were able to return to play. Players who sustained a subluxation event in season returned to play in less than 1 week, whereas those who sustained a dislocation returned to play at a mean of 3 weeks. When the authors specifically examined time of season during which the instability occurred, late-season athletes were more likely to be returned more quickly (0.5 weeks vs 3.1 weeks) than those early in the season. For those players who returned to play, recurrence occurred in 55% and at a mean of 2.5 weeks.51 This recurrence rate is similar to that published for a single National Football League team by LeClere et al52—42%. An impor tant consideration from this study must be the level of play of the athlete. Elite contact or collision athletes may have greater medical and athletic training resources available to expedite their return to play, but continue to have high rates of recurrence despite this.

Management of In-Season Anterior Instability and Return-to-Play Outcomes Overall, if an athlete meets appropriate criteria, he or she should be considered for same-season return to play. Many caveats exist, and the athlete must be counseled regarding the risks of return to play. Not only is recurrent instability a high risk, but the consequences of the continued instability’s impact on glenoid and humeral head bone loss must be factored into decision making.

ATHLETE PERFORMANCE Once players meet return to play criteria, their level of performance may not be the same as before injury or they may complain of poorer subjective outcome scores. No studies have specifically tracked subjective outcomes scores in athletes following their return to play.53 Buss et  al8 and Shanley and colleagues50 did not report subjective outcomes scores in their analyses of in-season return to play in athletes. However, data from Dickens et  al,6 Sachs and colleagues,54 and Shaha et  al18 can be extrapolated into expectations. Dickens et  al6 performed logistic regression modeling on time and likelihood to return to play using Western Ontario Shoulder Instability Index (WOSI), American Shoulder and Elbow Surgeons (ASES), Single Assessment Numeric Evaluation (SANE), and Simple Shoulder Test (SST) scores. For every point higher scored on the WOSI and SST at the time of injury, athletes were 5% and 3% more likely to return to play in season. In determining time to return to play, for every 10-point improvement in the WOSI, SST, and ASES score, athletes were able to return to play 1.3 days, 1.2 days, and 1.3 days sooner respectively than those scoring more poorly. Sachs and colleagues54 prospectively tracked patients treated at a single facility within a single, closed insurance payer system. This study included shoulder instability both of athletes and nonathletes from a full spectrum of ages (12-82  years). Impor tant in this study are their outcomes scores at time of final follow-up, which were stratified into 3 patient groups—(1) patients who had a single dislocation and did not dislocate again, (2) patients who had recurrence with nonoperative management, and (3) patients who underwent successful Bankart repair. Those who sustained only a single dislocation event with no recurrence after return to their normal activity had similar Constant, ASES, and WOSI scores as those who underwent successful Bankart repair. However, those who experienced continued instability events following their primary dislocation had significantly worse scores on all 3 tests greater than the defined minimally clinically impor tant difference for each test.54 The implications from these 2 studies suggest that improved scores on subjective testing at the time of injury and during the returnto-play period may demonstrate a player who is less likely to have recurrence with continued participation in season while deferring surgery to the off season. Shaha et al18 defined “subcritical” bone loss in an attempt to determine whether outcomes following shoulder stabilization are worse for patients who had glenoid bone loss but less

49

than 20% glenoid bone loss and thus did not undergo a bone augmenting procedure. In patients who had greater than 13.5% glenoid bone loss, there was not a statistically significant increase in recurrence; however, following stabilization, patients with subcritical bone loss had significantly worse WOSI scores that exceeded the minimally clinically important difference for WOSI scores. Based on these findings, patients can be counseled at the time of injury that if their WOSI, SST, and ASES scores are greater, they are more likely to return to play sooner; however, if imaging demonstrates glenoid bone loss greater than 13.5% and they attempt sameseason return to play, their WOSI scores may be decreased. The WOSI score is impor tant because its 21 questions specifically target disability related to use of the shoulder.55 Based on the earlier-mentioned findings, the optimal patient for in-season return to play is one who has greater subjective scoring on the WOSI test and less than 13.5% bone loss on MRI or CT imaging. The implication is 2-fold–earlier successful return to play in season, and decreased likelihood of disability or recurrence following return to play.

BRACING OPTIONS AND CONSIDERATIONS A scarcity of literature exists regarding use of a sports brace either prophylactically in the contact athlete or following an instability event to provide protection from anterior shoulder instability.56-59 Additionally, many of the data have focused on use in football players. A variety of braces exist and have the primary goal of preventing the player from placing the shoulder in a vulnerable position. The Sully brace (Figure  5-3) is a neoprene elastic brace with elastic straps that wraps the torso, affected shoulder, and affected upper arm. Using hookable elastic, the brace is designed to provide a restriction both to abduction as well as external rotation. Based on its neoprene design, it can be less restrictive than a nonelastic material to be worn by an athlete. The elasticity afforded may be better suited for an athlete who requires more overhead motion or the ability to stretch slightly beyond the limits of strap setting. With less restriction of motion, a neoprene brace or taping may provide a proprioceptive sense of stability to the athlete.59,60 These types of interventions may theoretically provide external passive positioning sense to the shoulder while causing less discomfort with wear. Additionally, there is less restriction of motion for the athlete, which may facilitate increased compliance or interest in wear. The SAWA brace (Figure 5-4) conversely is a nylon brace that is also worn across the torso, injured shoulder, and upper arm, but does not have the same elastic properties as a Sully brace. Nylon straps are used to limit abduction and external rotation. The advantage of this brace design is that it is should provide a hard stop to shoulder motion. The limitations of motion can be beneficial or detrimental depending on the sport and position played by the athlete.

50

Chapter 5

Figure 5-3. Sully brace. This brace is a neoprene elastic brace, which may provide better comfort than a more rigid nylon brace, but may not limit shoulder motion.

Figure 5-4. Sawa brace. This brace is a nylon brace that is more rigid, but also has limited evidence supporting its ability to limit athlete shoulder motion.

An analysis of the effectiveness of preset brace motion limiting abduction to 45 degrees was found to insufficiently limit collegiate football players both during active and passive testing.58 However, the brace did prevent complete abduction to 90 degrees. For a nonoverhead or nondominant-arm athlete, this can keep the shoulder from a position of maximum vulnerability. In a throwing athlete or positional player, the limitation of the dominant arm may decrease functional use of the arm and prevent full participation. Buss et  al8 placed most of their in-season athletes into a version of either of the 2  braces mentioned earlier, but

did not report outcomes following bracing and return to play. Dickens and colleagues6 performed subgroup analysis of their in-season athletes and found no protective effect of bracing to prevent recurrent instability. Additionally, Shanley et al50 found no protective benefit to brace wear in adolescent athletes with shoulder instability. Ideally, a motion-limiting brace is best used for football linemen or rugby players who already rely on limited motion of the shoulder to participate in their position, whereas the neoprene brace or taping may be more ideal for the overhead athlete. Individualized decision making based on sport

Management of In-Season Anterior Instability and Return-to-Play Outcomes played, position, and medical team comfort with application of the various braces should drive decision making.

RETURN TO PLAY CRITERIA IN-SEASON Clinical review of recommendations for in-season return to play remains varied and no consensus statement exists for decision making. A synthesis of recommendations appears in Table 5-1. A recent strength of recommendation taxonomy could find consistent high-quality data that athletes should be counseled on their high risk of recurrence only if they return to sport with nonsurgical management.7 Additionally, the literature remains limited or inconsistent for accelerated rehabilitation protocol and return to play criteria.7 Clinical criteria for clearing an athlete to return to play have focused on strength, shoulder range of motion, and pain.61 These 3 clinical criteria are not validated for protective mechanisms to prevent recurrent instability or healing but have been widely published.62 When evaluating strength, most studies vaguely report “full” or “recovered,”61 which do not objectively define specific criteria. We recommend that this is based on evaluation of the uninjured shoulder compared with rotator cuff—and deltoid-isolating maneuvers. For range of motion, similarly vague references to “full” or “complete”61 do not objectively define degrees of motion. We advocate that comparison to the contralateral shoulder in terms of forward flexion, abduction, external rotation, and abducted internal rotation must be symmetric. Finally, minimal reference to a specific pain-assessment scale exists. The athlete must be pain free with general shoulder range of motion as well as during evaluation of sport-specific maneuvers required during play.

Surgical Considerations of the In-Season Athlete The decision to pursue surgical treatment will preclude the athlete from same-season return to play given the rehabilitation course, which will last at least 6 months following surgery. Few sport seasons are amenable to this timeline. Absolute indications for surgical intervention are those with an acute glenoid fracture, significant off-track bipolar lesions, glenoid bone loss greater than 20%, and those with an HAGL lesion. Relative indications include those with glenoid bone loss greater than 10%, recurrent instability despite undergoing rehabilitation following the primary event, contact athletes, young age (< 20 years), and injuries that occur near the end of the season. Athletes in less crucial roles in their sport or with several seasons remaining of eligibility may be more inclined to pursue surgical intervention earlier with hopes of gaining a pain-free, stable shoulder. Once the decision for surgical intervention has been made, there are 3 main surgical interventions for consideration: arthroscopic repair, open repair, and osseous augmentation. Arthroscopic and open techniques focus on reapproximation of the capsulolabral complex to the glenoid and

51

restoration of the tension providing normal static restraint of the IGHL and surrounding capsule. The Hill-Sachs lesion may also be addressed arthroscopically with a remplissage procedure. Osseous augmentation procedures often address erosive glenoid bone loss; although in their introduction of the Instability Severity Index Score (ISIS), Balg and Boileau advocated a Bristow-Latarjet procedure in patients whose score was greater than 6.63 Boileau has since advocated that better subjective outcomes may be obtained by performing a Latarjet procedure in patients with an ISIS score greater than  3.64 The recommendation based on ISIS score did not include open stabilization as an option. The decision to proceed with a Latarjet procedure with limited glenoid bone loss should be approached with caution because of the high rates of complications that can be associated with the Latarjet procedure. Arthroscopic Bankart repair has become the primary procedure performed for anterior shoulder instability without bone loss. As arthroscopy became more prevalent, Wheeler et  al30 published their early results of arthroscopic Bankart repair vs nonoperative treatment of young athletes at West Point. Those treated nonoperatively sustained a very high rate of recurrent dislocation: 92%, whereas those who underwent Bankart repair only sustained recurrence in 22%. As arthroscopic techniques have progressed, rates of recurrent instability are more commonly cited to be 9% to 13%.31,65-67 Pooled data of contact athletes in a systematic review including 26 studies showed a recurrence rate of 17.8%. Once the authors controlled for surgical technique to include lateral decubitus position, a minimum of 3 anchors, and exclusion of patients with bone loss, the failure rate was found to be 7.9%.68 Risk factors associated with failure of arthroscopic repair have focused on glenoid bone loss that is not addressed at the time of surgery,28 large Hill-Sachs lesions that are off track,27 use of fewer than 3 anchors for Bankart repair,69 and patient-specific factors such as young male athletes.69 Outside these parameters, Shaha et al18 have raised concern regarding patients whose bone loss is less than 20% to 25% but greater than 13.5%. They referred to this as “subcritical” bone loss. In their study, military personnel who underwent arthroscopic Bankart repair had poorer subjective outcomes following surgery if their glenoid bone loss was greater than 13.5%.18 Dickens and colleagues70 sought to examine whether “subcritical” bone loss led to increased recurrence in a highrisk group: collegiate football players. Fifty NCAA football players underwent arthroscopic shoulder stabilization and returned to sport the following season. They were followed for a mean of 3.2 years following surgery. Among the group with bone loss less than 13.5%, there was no recurrence of instability. However, in the football players with “subcritical” bone loss, all experienced recurrent instability. A key drawback of this study was that there were only 3 athletes with subcritical bone loss identified. The combination of these findings regarding decreased subjective outcomes as well as potentially higher rates of recurrent instability raises

52

Chapter 5

the impor tant consideration for either open stabilization or bony augmentation. Though historically the mainstay of stabilization, open Bankart repair saw a large decrease in use as arthroscopic stabilization procedures were developed. Arthroscopy is considered to be less invasive and better tolerated by patients, but no study has shown earlier return-to-play rates following rehabilitation for arthroscopic or open Bankart and Latarjet. The utility of open Bankart repair cannot be understated. Uhorchak et al32 evaluated the incidence of recurrent instability specifically in contact and collision athletes following open repair. The authors followed 66 patients for a mean of approximately 4  years following surgery. Only 3% of the athletes experienced a recurrent dislocation; however, 20% had a repeat subluxation. Despite this, all patients reported excellent functions results. A follow-up study conducted in military personnel randomly assigned patients to open or arthroscopic Bankart repair.71 There was no difference in rates of recurrence of instability, and both groups showed significant improvements in subjective outcomes scores. Similar results have been found in a meta-analysis comparing open vs arthroscopic repair.72 With similar clinical results, the question of superiority arises between open and arthroscopic procedures. Purely based on recurrence in the general population, the results seem very similar. However, Virk and colleagues sought to determine whether there was a difference in time to recurrence between these procedures.65 The authors found no significant difference in rates of recurrence. They did find though that patients who underwent open repair had a statistically longer time to recurrence vs arthroscopic repair (34.2 months vs 12.6 months).65 The authors advocated that open repair may be a better procedure for contact and collision athletes to provide longer longevity of the repair during return to sport. A similar sentiment seems to exist among the ASES. A 2017 survey of ASES members found that 82% of surgeons would recommend arthroscopic repair in a noncontact athlete, but only 57% would recommend arthroscopic repair in contact and collision athletes.73 Finally, when glenoid bone loss is present bony augmentation procedures are recommended. A Latarjet procedure addresses bony defects through augmentation with a coracoid transfer and soft-tissue defect through capsular repair, and provides a sling from the conjoint tendon to improve stability.74,75 The Latarjet procedure has been advocated for contact and collision athletes because of its low rate of recurrences. In evaluating rugby players, Neyton et  al76 reported that at a minimum of 5 years’ follow-up, there was no recurrence of instability. It should be noted though that only 65% returned to play and 13% decreased their level of play. Athletes returned to rugby at a mean of 7 months. Importantly, only rugby players with recurrent instability were included. First-time dislocators were not included. More recently, Privitera et al examined the outcomes of 109 contact athletes following the Latarjet procedure in 2018.77 Eight (8) percent experienced recurrent dislocation, and 14%

had subjective instability. Only 49% of athletes returned their previous level of play, and 25% left contact sports. The Latarjet is not without complications, including graft fracture, lysis, stiffness, and nerve injury, ranging from 7% to 16% or more.78,79 Ekhtiari and colleagues attempted to quantify the learning curve for the Latarjet. They concluded that it takes surgeons 22 open Latarjet transfers to have proficiency in the procedure represented by significantly decreased operating room time, decreased rates of complications, and decreased length of hospital stay.80 A systematic review and meta-analysis performed by Cerciello et al79 found a complication rate of 16.5% with 5.6% of patients requiring revision. The Latarjet is a reliable shoulder-stabilizing procedure but can be fraught with complications if not performed properly. Additionally, once the coracoid has been transferred, further revisions if the patient develops recurrent instability are very technically demanding.

CONCLUSION Despite the variety of outcomes for athletes treated for shoulder instability, the in-season athlete requires a comprehensive and tailored decision-making approach to safely and successfully return to play. In many athletes, same-season return to play can be reasonable and attempted with the knowledge that risk for recurrent instability remains, especially in young contact athletes. Surgeons must use a constellation of physical exam, imaging, and athlete-specific factors in making a recommendation for treatment.

REFERENCES 1.

2.

3.

4.

5.

6.

7.

8.

Owens BD, Agel J, Mountcastle SB, Cameron KL, Nelson BJ. Incidence of glenohumeral instability in collegiate athletics. Am J Sports Med. 2009;37(9):1750-1754. doi:10.1177/0363546509334591. Owens BD, Dickens JF, Kilcoyne KG, Rue JP. Management of midseason traumatic anterior shoulder instability in athletes. J Am Acad Orthop Surg. 2012;20(8):518-526. doi:10.5435/JAAOS-20-08-518. Owens BD, Nelson BJ, Duffey ML, et al. Pathoanatomy of first-time, traumatic, anterior glenohumeral subluxation events. J Bone Joint Surg Am. 2010;92(7):1605-1611. doi:10.2106/JBJS.I.00851. Owens BD, Duffey ML, Nelson BJ, DeBerardino TM, Taylor DC, Mountcastle SB. The incidence and characteristics of shoulder instability at the United States Military Academy. Am J Sports Med. 2007;35(7):1168-1173. doi:10.1177/0363546506295179. Tanaka M, Koizumi K, Kakiuchi M, Hayashida K. Evaluation of dislocation position in patients with recurrent anterior shoulder dislocation. J Shoulder Elbow Surg. 2012;21(11):1588-1592. doi:10.1016/j. jse.2011.11.020. Dickens JF, Owens BD, Cameron KL, et  al. Return to play and recurrent instability after in-season anterior shoulder instability: a prospective multicenter study. Am J Sports Med. 2014;42(12):2842-2850. doi:10.1177/0363546514553181. Watson S, Allen B, Grant JA. A clinical review of return-to-play considerations after anterior shoulder dislocation. Sports Health. 2016;8(4):336-341. doi:10.1177/1941738116651956. Buss DD, Lynch GP, Meyer CP, Huber SM, Freehill MQ. Nonoperative management for in-season athletes with anterior shoulder instability. Am J Sports Med. 2004;32(6):1430-1433. doi:10.1177/0363546503262069.

Management of In-Season Anterior Instability and Return-to-Play Outcomes 9. 10. 11.

12.

13.

14.

15.

16.

17.

18.

19.

20.

21.

22.

23.

24.

25.

26.

27.

Dickens JF, Owens BD. Trends in surgical management of first time anterior shoulder instability (personal communication, 2019). Bankart ASB. Recurrent or habitual dislocation of the shoulder-joint. Br Med J. 1923;2(3285):1132-1133. doi:10.1136/bmj.2.3285.1132. Taylor DC, Arciero RA. Pathologic changes associated with shoulder dislocations. Arthroscopic and physical examination findings in first-time, traumatic anterior dislocations. Am J Sports Med. 1997;25(3):306-311. doi:10.1177/036354659702500306. Lee TQ, Dettling J, Sandusky MD, McMahon PJ. Age related biomechanical properties of the glenoid-anterior band of the inferior glenohumeral ligament-humerus complex. Clin Biomech (Bristol, Avon). 1999;14(7):471-476. doi:10.1016/s0268-0033(99)00007-8. Bigliani LU, Pollock RG, Soslowsky LJ, Flatow EL, Pawluk RJ, Mow VC. Tensile properties of the inferior glenohumeral ligament. J Orthop Res. 1992;10(2):187-197. doi:10.1002/jor.1100100205. Ticker JB, Flatow EL, Pawluk RJ, et  al. The inferior glenohumeral ligament: a correlative investigation. J Shoulder Elbow Surg. 2006;15(6):665-674. doi:10.1016/j.jse.2005.11.006. Milano G, Grasso A, Russo A, et al. Analysis of risk factors for glenoid bone defect in anterior shoulder instability. Am J Sports Med. 2011;39(9):1870-1876. doi:10.1177/0363546511411699. Sugaya H, Moriishi J, Dohi M, Kon Y, Tsuchiya A. Glenoid rim morphology in recurrent anterior glenohumeral instability. J Bone Joint Surg Am. 2003;85(5):878-884. doi:10.2106/00004623-200305000-00016. Dickens JF, Slaven SE, Cameron KL, et al. Prospective evaluation of glenoid bone loss after first-time and recurrent anterior glenohumeral instability events. Am J Sports Med. 2019;47(5):1082-1089. doi:10.1177/0363546519831286. Shaha JS, Cook JB, Song DJ, et  al. Redefining “critical” bone loss in shoulder instability: functional outcomes worsen with “subcritical” bone loss. Am J Sports Med. 2015;43(7):1719-1725. doi:10.1177/0363546515578250. Arciero RA, Parrino A, Bernhardson AS, et  al. The effect of a combined glenoid and Hill-Sachs defect on glenohumeral stability: a biomechanical cadaveric study using 3-dimensional modeling of 142 patients. Am J Sports Med. 2015;43(6):1422-1429. doi:10.1177/0363546515574677. Magee T. Prevalence of HAGL lesions and associated abnormalities on shoulder MR examination. Skeletal Radiol. 2014;43(3):307-313. doi:10.1007/s00256-013-1778-1. Bui-Mansfield LT, Taylor DC, Uhorchak JM, Tenuta JJ. Humeral avulsions of the glenohumeral ligament: imaging features and a review of the literature. AJR Am J Roentgenol. 2002;179(3):649-655. doi:10.2214/ajr.179.3.1790649. Patzkowski JC, Dickens JF, Cameron KL, Bokshan SL, Garcia EJ, Owens BD. Pathoanatomy of shoulder instability in collegiate female athletes. Am J Sports Med. 2019;47(8):1909-1914. doi:10.1177/0363546519850810. Schmiddem U, Watson A, Perriman D, Liodakis E, Page  R. Arthroscopic repair of HAGL lesions yields good clinical results, but may not allow return to former level of sport. Knee Surg Sports Traumatol Arthrosc. 2019;27(10):3246-3253. doi:10.1007/ s00167-019-05414-5. Southgate DF, Bokor DJ, Longo UG, Wallace AL, Bull AM. The effect of humeral avulsion of the glenohumeral ligaments and humeral repair site on joint laxity: a biomechanical study. Arthroscopy. 2013;29(6):990-997. doi:10.1016/j.arthro.2013.02.021. Provencher MT, McCormick F, LeClere L, et  al. Prospective evaluation of surgical treatment of humeral avulsions of the glenohumeral ligament. Am J Sports Med. 2017;45(5):1134-1140. doi:10.1177/0363546516680608. Fox JA, Sanchez A, Zajac TJ, Provencher MT. Understanding the Hill-Sachs lesion in its role in patients with recurrent anterior shoulder instability. Curr Rev Musculoskelet Med. 2017;10(4):469-479. doi:10.1007/s12178-017-9437-0. Kurokawa D, Yamamoto N, Nagamoto H, et al. The prevalence of a large Hill-Sachs lesion that needs to be treated. J Shoulder Elbow Surg. 2013;22(9):1285-1289. doi:10.1016/j.jse.2012.12.033.

28.

29.

30.

31.

32.

33.

34.

35.

36.

37.

38.

39. 40.

41. 42.

43.

44. 45.

46.

53

Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694. doi:10.1053/ jars.2000.17715. Yamamoto N, Itoi E, Abe H, et al. Contact between the glenoid and the humeral head in abduction, external rotation, and horizontal extension: a new concept of glenoid track. J  Shoulder Elbow Surg. 2007;16(5):649-656. doi:10.1016/j.jse.2006.12.012. Wheeler JH, Ryan JB, Arciero RA, Molinari RN. Arthroscopic versus nonoperative treatment of acute shoulder dislocations in young athletes. Arthroscopy. 1989;5(3):213-217. doi:10.1016/0749-8063(89)90174-6. Dickens JF, Rue JP, Cameron KL, et  al. Successful return to sport after arthroscopic shoulder stabilization versus nonoperative management in contact athletes with anterior shoulder instability: a prospective multicenter study. Am J Sports Med. 2017;45(11):2540-2546. doi:10.1177/0363546517712505. Uhorchak JM, Arciero RA, Huggard D, Taylor DC. Recurrent shoulder instability after open reconstruction in athletes involved in collision and contact sports. Am J Sports Med. 2000;28(6):794-799. doi:1 0.1177/03635465000280060501. Trinh TQ, Naimark MB, Bedi A, et al. Clinical outcomes after anterior shoulder stabilization in overhead athletes: an analysis of the MOON Shoulder Instability Consortium. Am J Sports Med. 2019;47(6):14041410. doi:10.1177/0363546519837666. Robinson CM, Shur N, Sharpe T, Ray A, Murray IR. Injuries associated with traumatic anterior glenohumeral dislocations. J Bone Joint Surg Am. 2012;94(1):18-26. doi:10.2106/JBJS.J.01795. Rowe CR. Recurrent anterior transient subluxation of the shoulder. The “dead arm” syndrome. Orthop Clin North Am. 1988;19(4):767-772. Farber AJ, Castillo R, Clough M, Bahk M, McFarland EG. Clinical assessment of three common tests for traumatic anterior shoulder instability. J Bone Joint Surg Am. 2006;88(7):1467-1474. doi:10.2106/ JBJS.E.00594. Jobe FW, Kvitne RS, Giangarra CE. Shoulder pain in the overhand or throwing athlete. The relationship of anterior instability and rotator cuff impingement. Orthop Rev. 1989;18(9):963-975. Lo IK, Nonweiler B, Woolfrey M, Litchfield R, Kirkley A. An evaluation of the apprehension, relocation, and surprise tests for anterior shoulder instability. Am J Sports Med. 2004;32(2):301-307. doi:10.1177/0095399703258690. Silliman JF, Hawkins RJ. Classification and physical diagnosis of instability of the shoulder. Clin Orthop Relat Res. 1993;291:7-19. Hawkins RJ, Schutte JP, Janda DH, Huckell GH. Translation of the glenohumeral joint with the patient under anesthesia. J Shoulder Elbow Surg. 1996;5(4):286-292. doi:10.1016/s1058-2746(96)80055-3. Gagey OJ, Gagey  N. The hyperabduction test. J Bone Joint Surg Br. 2001;83(1):69-74. doi:10.1302/0301-620x.83b1.10628. Cameron KL, Duffey ML, DeBerardino TM, Stoneman PD, Jones CJ, Owens BD. Association of generalized joint hypermobility with a history of glenohumeral joint instability. J Athl Train. 2010;45(3):253258. doi:10.4085/1062-6050-45.3.253. McLaughlin HL, MacLellan DI. Recurrent anterior dislocation of the shoulder. II. A comparative study. J Trauma. 1967;7(2):191-201. doi:10.1097/00005373-196703000-00002. Rowe CR. Acute and recurrent anterior dislocations of the shoulder. Orthop Clin North Am. 1980;11(2):253-270. Bottoni CR, Wilckens JH, DeBerardino TM, et al. A prospective, randomized evaluation of arthroscopic stabilization versus nonoperative treatment in patients with acute, traumatic, first-time shoulder dislocations. Am J Sports Med. 2002;30(4):576-580. doi:10.1177/03635 465020300041801. Henry JH, Genung JA. Natural history of glenohumeral dislocation—revisited. Am J Sports Med. 1982;10(3):135-137. doi:10.1177/036354658201000301.

54 47.

48.

49.

50.

51.

52.

53.

54.

55.

56.

57.

58.

59.

60.

61.

62.

63.

Chapter 5 Paterson WH, Throckmorton TW, Koester M, Azar FM, Kuhn JE. Position and duration of immobilization after primary anterior shoulder dislocation: a systematic review and meta-analysis of the literature. J Bone Joint Surg Am. 2010;92(18):2924-2933. doi:10.2106/ JBJS.J.00631. Itoi E, Hatakeyama Y, Urayama M, Pradhan RL, Kido T, Sato  K. Position of immobilization after dislocation of the shoulder. A cadaveric study. J Bone Joint Surg Am. 1999;81(3):385-390. Itoi E, Sashi R, Minagawa H, Shimizu T, Wakabayashi I, Sato  K. Position of immobilization after dislocation of the glenohumeral joint. A study with use of magnetic resonance imaging. J Bone Joint Surg Am. 2001;83(5):661-667. doi:10.2106/00004623-200105000-00003. Shanley E, Thigpen C, Brooks J, et al. Return to sport as an outcome measure for shoulder instability: surprising findings in nonoperative management in a high school athlete population. Am J Sports Med. 2019;47(5):1062-1067. doi:10.1177/0363546519829765. Okoroha KR, Taylor KA, Marshall NE, et  al. Return to play after shoulder instability in National Football League athletes. J Shoulder Elbow Surg. 2018;27(1):17-22. doi:10.1016/j.jse.2017.07.027. LeClere LE, Asnis PD, Griffith MH, Granito D, Berkson EM, Gill TJ. Shoulder instability in professional football players. Sports Health. 2013;5(5):455-457. doi:10.1177/1941738112472156. Zaremski JL, Galloza J, Sepulveda F, Vasilopoulos T, Micheo W, Herman DC. Recurrence and return to play after shoulder instability events in young and adolescent athletes: a systematic review and meta-analysis. Br J Sports Med. 2017;51(3):177-184. Sachs RA, Lin D, Stone ML, Paxton E, Kuney M. Can the need for future surgery for acute traumatic anterior shoulder dislocation be predicted? J Bone Joint Surg Am. 2007;89(8):1665-1674. doi:10.2106/ JBJS.F.00261. Kirkley A, Griffin S, McLintock H, Ng  L. The development and evaluation of a disease-specific quality of life measurement tool for shoulder instability. The Western Ontario Shoulder Instability Index (WOSI). Am J Sports Med. 1998;26(6):764-772. doi:10.1177/036354 65980260060501. Baker HP, Tjong VK, Dunne KF, Lindley TR, Terry MA. Evaluation of shoulder-stabilizing braces: can we prevent shoulder labrum injury in collegiate offensive linemen? Orthop J Sports Med. 2016;4(12):2325967116673356. doi:10.1177/2325967116673356. Chu JC, Kane EJ, Arnold BL, Gansneder BM. The effect of a neoprene shoulder stabilizer on active joint-reposition sense in subjects with stable and unstable shoulders. J Athl Train. 2002;37(2):141-145. Weise K, Sitler MR, Tierney R, Swanik KA. Effectiveness of glenohumeral-joint stability braces in limiting active and passive shoulder range of motion in collegiate football players. J Athl Train. 2004;39(2):151-155. Ulkar B, Kunduracioglu B, Cetin C, Guner RS. Effect of positioning and bracing on passive position sense of shoulder joint. Br J Sports Med. 2004;38(5):549-552. doi:10.1136/bjsm.2002.004275 Conti M, Garofalo R, Castagna A, Massazza G, Ceccarelli E. Dynamic brace is a good option to treat first anterior shoulder dislocation in season. Musculoskelet Surg. 2017;101(suppl 2):169-173. doi:10.1007/ s12306-017-0497-5. Ciccotti MC, Syed U, Hoffman R, Abboud JA, Ciccotti MG, Freedman KB. Return to play criteria following surgical stabilization for traumatic anterior shoulder instability: a systematic review. Arthroscopy. 2018;34(3):903-913. doi:10.1016/j.arthro.2017.08.293. Williams RJ III. Editorial commentary: reviewing the science of our unscientific criteria for return to sports after shoulder stabilization. Arthroscopy. 2018;34(3):914-916. doi:10.1016/j.arthro.2017.12.015. Balg F, Boileau P. The instability severity index score. A simple preoperative score to select patients for arthroscopic or open shoulder stabilisation. J Bone Joint Surg Br. 2007;89(11):1470-1477. doi:10.1302/0301-620X.89B11.18962.

64.

65.

66.

67.

68.

69.

70.

71.

72.

73.

74.

75.

76.

77.

78.

79.

80.

Boileau P, Lemmex DB. Editorial commentary: which patients are likely to undergo redislocation after an arthroscopic Bankart repair? Preoperative Instability Severity Index Scoring over 3 points— the game is over! Arthroscopy. 2019;35(2):367-371. doi:10.1016/j. arthro.2018.11.028. Virk MS, Manzo RL, Cote M, et  al. Comparison of time to recurrence of instability after open and arthroscopic Bankart repair techniques. Orthop J Sports Med. 2016;4(6):2325967116654114. doi:10.1177/2325967116654114. Ozturk BY, Maak TG, Fabricant P, et  al. Return to sports after arthroscopic anterior stabilization in patients aged younger than 25  years. Arthroscopy. 2013;29(12):1922-1931. doi:10.1016/j. arthro.2013.09.008. Frank RM, Saccomanno MF, McDonald LS, Moric M, Romeo AA, Provencher MT. Outcomes of arthroscopic anterior shoulder instability in the beach chair versus lateral decubitus position: a systematic review and meta-regression analysis. Arthroscopy. 2014;30(10):13491365. doi:10.1016/j.arthro.2014.05.008. Leroux TS, Saltzman BM, Meyer M, et al. The influence of evidencebased surgical indications and techniques on failure rates after arthroscopic shoulder stabilization in the contact or collision athlete with anterior shoulder instability. Am J Sports Med. 2017;45(5):12181225. doi:10.1177/0363546516663716. Brown L, Rothermel S, Joshi R, Dhawan A. Recurrent instability after arthroscopic Bankart reconstruction: a systematic review of surgical technical factors. Arthroscopy. 2017;33(11):2081-2092. doi:10.1016/j. arthro.2017.06.038. Dickens JF, Owens BD, Cameron KL, et al. The effect of subcritical bone loss and exposure on recurrent instability after arthroscopic Bankart repair in intercollegiate American football. Am J Sports Med. 2017;45(8):1769-1775. doi:10.1177/0363546517704184. Bottoni CR, Smith EL, Berkowitz MJ, Towle RB, Moore JH. Arthroscopic versus open shoulder stabilization for recurrent anterior instability: a prospective randomized clinical trial. Am J Sports Med. 2006;34(11):1730-1737. doi:10.1177/0363546506288239. Hohmann E, Tetsworth K, Glatt V. Open versus arthroscopic surgical treatment for anterior shoulder dislocation: a comparative systematic review and meta-analysis over the past 20  years. J Shoulder Elbow Surg. 2017;26(10):1873-1880. doi:10.1016/j.jse.2017.04.009. Garcia GH, Taylor SA, Fabricant PD, Dines JS. Shoulder instability management: a survey of the American Shoulder and Elbow Surgeons. Am J Orthop (Belle Mead NJ). 2016;45(3):E91-E97. Dines JS, Dodson CC, McGarry MH, Oh JH, Altchek DW, Lee TQ. Contribution of osseous and muscular stabilizing effects with the Latarjet procedure for anterior instability without glenoid bone loss. J Shoulder Elbow Surg. 2013;22(12):1689-1694. doi:10.1016/j. jse.2013.02.014. Yamamoto N, Muraki T, An KN, et  al. The stabilizing mechanism of the Latarjet procedure: a cadaveric study. J Bone Joint Surg Am. 2013;95(15):1390-1397. doi:10.2106/JBJS.L.00777. Neyton L, Young A, Dawidziak B, et al. Surgical treatment of anterior instability in rugby union players: clinical and radiographic results of the Latarjet-Patte procedure with minimum 5-year followup. J Shoulder Elbow Surg. 2012;21(12):1721-1727. doi:10.1016/j. jse.2012.01.023. Privitera DM, Sinz NJ, Miller LR, et al. Clinical outcomes following the Latarjet procedure in contact and collision athletes. J Bone Joint Surg Am. 2018;100(6):459-465. doi:10.2106/JBJS.17.00566. Frank RM, Gregory B, O’Brien M, et al. Ninety-day complications following the Latarjet procedure. J Shoulder Elbow Surg. 2019;28(1):8894. doi:10.1016/j.jse.2018.06.022. Cerciello S, Corona K, Morris BJ, Santagada DA, Maccauro  G. Early outcomes and perioperative complications of the arthroscopic Latarjet procedure: systematic review and meta-analysis. Am J Sports Med. 2019;47(9):2232-2241. doi:10.1177/0363546518783743. Ekhtiari S, Horner NS, Bedi A, Ayeni OR, Khan M. The learning curve for the Latarjet procedure: a systematic review. Orthop J Sports Med. 2018;6(7):2325967118786930. doi:10.1177/2325967118786930.

6 Decision Making in Surgical Treatment of Athletes With First-Time vs Recurrent Shoulder Instability Brian C. Lau, MD; Carolyn A. Hutyra, MMCi; and Dean C. Taylor, MD

Glenohumeral instability is one of the most common injuries in athletes.1,76 The National Collegiate Athletic Association Injury Surveillance System reported 4080  glenohumeral instability events, with an injury rate of 0.12 per 1000 exposures.1 Glenohumeral instability events in athletes are often traumatic and typically occur following a contact injury but may also occur with noncontact events. These instability events and potential reduction treatments are painful and can cause significant distress to athletes. In addition to significant discomfort, these injuries may affect immediate or long-term athletic performance. Poor selfreported outcomes have been demonstrated with diseasespecific health-related quality of life and shoulder function with recurrent dislocations.2,3 However, the motivation to resume sports participation and its timing is a major aspect for athletes seeking care. Therefore, when making treatment decisions in athletes one must understand the timing of the season, risk factors, treatment options, and likely outcomes to optimize return-to-play and function. Decision making in health care has undergone an evolution in recent decades. Historically, decision making in health care was based on experience, intuition, and largely on expert opinion. In the late 20th century, there was a push toward evidence-based and pattern-recognition models. This expanded our knowledge and allowed the growth of information, including risk factors for shoulder instability. However, it is impor tant to note that all athletes are dif ferent, not only in their risk-factor profile but also in their preferences and goals. Of late, there has been a transition in medicine to one of personalization and customization of care. In cancer treatment, this involves genetic testing and treatments based on one’s genetic profile. How do we make this transition in

glenohumeral instability? In athletes, customization of care may require consideration of peer or scholarship pressure to finish a season and continue participation in sports despite risk of recurrence of shoulder instability. This combination of personalized medical evidence, preferences, and an engaging and accessible platform are required to create rich, personalized, and efficient decisionmaking models. In the case of shoulder instability, personalized medical evidence can provide individual-level outcome probabilities for operative and nonoperative treatment. Based on specific patient factors and high-quality evidence in the literature, decision aids can appropriately model patient outcomes such as individual patient chances of recurrent dislocation, chance of primary and revision stabilization, or chance of maintaining a stable shoulder at various time points.4 Meanwhile, patient preferences provide clinicians with a systematic measurement of utility for each attribute addressed while making these risk-benefit trade-offs. The shoulder decision-making model validated by Mather et al5 and tested by Streufert and colleagues6 provided a 2-fold output. The model was designed for respondents to receive a summary of their preferences and treatment outcomes on completion of the tool, while physicians could receive the same information along with the patient’s ultimate choice of treatment (operative or nonoperative), patient activities and frequency of activities, patient concerns regarding factors such as pain and scarring, and patient desires to discuss longterm outcomes. This personalized output in a clinical setting can help clinicians differentiate between patients who are more likely to benefit from various operative or nonoperative treatments and help facilitate the conversation surrounding dif ferent management options.

- 55 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 55-65). © 2021 SLACK Incorporated.

56

Chapter 6

Figure 6-1. In-season management of traumatic shoulder instability. (Reprinted with permission from Owens BD, Dickens JF, Kilcoyne KG, Rue JP. Management of mid-season traumatic anterior shoulder instability in athletes. J Am Acad Orthop Surg. 2012;20[8]:518-526. doi:10.5435/ JAAOS-20-08-518.)

Along with advances of decision-model tools, it is critical that physicians have up-to-date knowledge of the factors that influence treatment decisions to proper counsel their athletes. In this review of decision making in surgical treatment of athletes with shoulder instability, we will review the timing of the season, risk factors, treatments and outcomes, and personalized decision-making models.

TIMING OF THE SEASON The timing of an athletic season in the consideration of management of shoulder instability is unique to athletes. The typical time range for return to sport for those who undergo nonoperative treatment is approximately 2 to 3 weeks.7-9 In comparison, the typical time range for return to sport following surgical management is typically 4 to 6 months.77,78 As such, in-season athletes typically pursue an initial course of rehabilitation, activity modification, and bracing as appropriate. A recurrent instability episode or failure of an athlete to perform sport-specific drills or at preinjury levels tends to be an indicator to pursue in-season operative management.79 Another factor in high school and collegiate athletes may be the timing in their high school or collegiate career. Freshman or sophomore athletes may benefit from earlier operative treatment to allow return to higher levels of performance for their junior and senior years. Conversely, junior

and senior athletes may prefer nonsurgical management to allow them to play during collegiate or professional scouting periods or in the final stage of their playing careers. Owens et al provided an algorithm for in-season decision making for athletes.10 Their recommendation was that in the event of an in-season acute shoulder instability event, athletes should be allowed to attempt to return to play as long as there is enough time left in the season to permit adequate rehabilitation. Their algorithm for in-season decisions is demonstrated in Figure 6-1.10

RISK FACTORS The primary focus of published literature for decision making in glenohumeral instability focuses on risk factors for recurrent instability to help stratify patients as high risk or low risk. Athletes are unique because by their nature they tend to have 2 of the major risk factors that have consistently been borne out in the literature to qualify as high-risk: young age and high-level of at-risk activities.3,11 The risks of recurrent instability events in this high-risk group have reports of up to 100%.12,13 Other risk factors to consider in athletes include sex, hand dominance, glenoid bone loss, and humeral bone loss. Understanding the role of these risk factors for recurrent instability will help during treatment decisions.

Decision Making in Surgical Treatment of Athletes With First-Time vs Recurrent Shoulder Instability

Age Young age has been identified as one of the strongest risk factors of recurrent shoulder instability14-16 (Table  6-1). Some reports demonstrate up to a 100% redislocation rate in patients younger than 30  years.15 In a meta-analysis of a systematic review of 10 studies, Olds et al17 stratified patients into 2 groups: age 15 to 40 years and older than 40 years. In patients 40 years or younger, there was a 44% recurrence rate compared to 11% in those older than 40  years.17 This was equivalent to a 13.46× increased risk in younger patients. Moreover, the study found that those younger than 30 years had an even higher risk of recurrence at 50%.17 Interestingly, when the older group of patients was stratified into those between ages 41 and 60  years vs those older than 61  years, there was no difference in occurrence rate, 11% vs 10%, respectively. Younger patients tend to be more active and engage in higher-risk activities. Therefore, it may be expected that adolescent patients would be at an even higher risk of recurrence. Robinson and Dobson18 studied patients age 15 to 20  years and identified a recurrence rate of 86.6% over 5  years. Zaremski et  al19 performed a systematic review of 17 studies and stratified adolescents into separate groups: those younger than 14  years and those older than 14  years. They identified a recurrence rate of 42.3% in those older than 14  years, and interestingly found a lower rate of recurrence in those younger than 14  years at 25%.19 It is possible that changes in a young athlete’s physical strength and capabilities during puberty may lead to greater risks. Lower recurrence rates in patients younger than 14 years may result from higher degrees of flexibility seen in younger patients or lower engagement in high-risk activities. As such, patients younger than 10 years seldom develop symptoms of shoulder instability.20 Recommendation: Primary surgical stabilization in contact or collision athletes in adolescence should be considered.

Activity Level The physical and mental benefits of sports and competition are plentiful. These include improved cardiovascular health, physical strength, and mental mood, but also grit and perseverance. Sports also may place athletes at risk for injury. Shoulder instability may develop in athletes because of traumatic contact or collisions. The sports with the highest risks include American football, rugby, and soccer but may also include martial arts, boxing, ice hockey, and wrestling.11,21 Leroux and colleagues performed a systematic review of contact or collision athletes with anterior shoulder instability.21 This study evaluated outcomes following arthroscopic surgical management of shoulder instability and identified a 17.8% failure rate in contact or collision athletes.21 This is in comparison to the general population, which has an 8.5% and 8.0% recurrence rate following arthroscopic or open shoulder stabilization, respectively.22

57

Table 6-1. Age and Rate of Recurrent Instability14-17,19 AGE GROUP, Y ≤ 10 ≤ 14 14-16 15-20 < 30 < 40 41-60 > 60

RATE OF RECURRENT INSTABILITY, % Rare 25 42.3 86.6 50 44 11 10

Overhead activities in athletics or occupation have also been identified as a risk factor for recurrence.23 Sachs et  al reported that those who worked with their arms above chest height had a 5.76× higher risk of developing recurrent instability.3 Recommendation: Contact, collision, and overhead athletes should consider operative stabilization following stabilization first-time shoulder dislocation.

Sex Male sex has also been identified as a risk factor for recurrence.16,17,21,24 It is, however, difficult to discern whether sex itself is the cause for greater recurrence or participation in more at-risk activities. American football, for example, which has some of the highest risk of shoulder instability, is primarily played by male athletes. Moreover, even in sports played by both sexes such as lacrosse and ice hockey there are differences in rules and playing style that limit the amount of contact encountered by female athletes. As such, there are conflicting reports in the literature. Hovelius et  al performed a prospective multicenter clinical study with 25  years of follow that demonstrated no significant difference in recurrence of shoulder instability with respect to sex.24 However, a systematic review demonstrated that male athletes had a 46.84% compared to a 27.22% recurrence rate compared to female athletes.17 Interestingly, however, after age 40 years there were similar rates of recurrent shoulder instability following a single traumatic shoulder dislocation: 22% and 25% in men and women, respectively.17 One explanation for these findings is that younger individuals are more likely to participate in high-risk activities. In the adolescent population, male athletes age 10 to 17  years had a 1.23× greater risk of recurrent shoulder instability compared to female athletes. The same study performed by Leroux and colleagues identified that male athletes age 15 to 17 years participating in contact or collision sports had the highest risk of recurrent dislocation.21

58

Chapter 6

Recommendation: In patients with shoulder instability, sex should be considered along with other risk factors; however, sex should not be considered alone.

Generalized Laxity Generalized laxity, as measured by Beighton score, plays an impor tant role in the incidence of shoulder instability.25-27 Patients that have greater laxity may have a higher likelihood of instability events, which may manifest as subluxations or true dislocations. As such, Owens et  al identified hyperlaxity as a risk factor for recurrent instability.25 Patients with hyperlaxity demonstrate a 2.68× likelihood of experiencing a recurrent shoulder instability compared to those without hyperlaxity. However, these patients are also more likely to cope better with these events because components of hyperlaxity may be hereditary and present since early childhood. These patients may also demonstrate components of multidirectional instability. Patients with multidirectional instability have experience poor outcomes and return to play following surgical management.28 It is impor tant to evaluate for generalized laxity and multidirectional instability because these patients may best benefit from a longer course of physical therapy.28 Recommendation: Generalized laxity and multidirectional instability should be evaluated in athletes. Patients with atraumatic multidirectional instability may benefit from an initial course of physical therapy.

Hand Dominance The rate of dislocations in relation to hand dominance has been reported with mixed findings. Lim et  al identified no statistical difference in incidence of shoulder instability but a trend toward the nondominant hand, 52.9% compared to 47.1% in the dominant hand.29 (Lim 2018) Conversely, Longo et  al30 found the opposite, with 70% of events occurring in the dominant hand vs nondominant hand. However, there is a paucity of literature on the effect of hand dominance on the natural history of recurrence and outcomes in relation to non-operative or surgical management. Hand dominance, however, may play a role in decision making in shoulder instability following a first-time dislocation to the throwing shoulder. The dominant shoulder in the throwing athletes may be more troublesome with microinstability of the shoulder, which may occur following nonoperative treatment. However, surgical treatment has a risk of loss of external rotation, which may affect an athlete’s throwing mechanics. Throwing athletes must consider whether the risks of recurrent instability or microinstability would be tolerable in their throwing shoulder in context with the risk of loss of external rotation with surgical management. In these scenarios, the work of Kavaja31 and Plath32 may offer a treatment option. These studies suggest that delaying surgery and waiting to see whether the patient develops instability symptoms after a first-time traumatic shoulder

dislocation does not lead to a less-favorable prognosis of instability, quality of life, or glenohumeral joint osteoarthritis.31,32 In throwing athletes, this would allow them to determine whether microinstability develops or whether they experience any adverse effects to their throwing mechanics. If symptoms develop, then surgical management may be warranted. Recommendation: Throwing athletes may benefit from a trial of nonoperative management following a first-time shoulder dislocation. If symptoms prevent return to the same level of activity, then a thorough discussion should occur regarding risk of loss of range of motion following surgical management.

Glenoid Bone Loss Part of the pathophysiology of anterior-inferior shoulder dislocations is impaction of the humeral head along the anterior-inferior aspect of the glenoid face.79 This may lead to a bony Bankart, which equates to a bony fracture. After a single first-time dislocation, the occurrence of glenoid rim fracture was found in 22%.33 Interestingly, several studies found that the presence of a large bony Bankart may actually afford a protective effect against recurrent instability (odds ratio, 0.51).34-36 This may result from greater reservation on the part of the physician and the athlete to rush rehabilitation and/or the result of early surgical fixation of the fracture fragment. However, more commonly bone loss is the result of repetitive microinstability or recurrent dislocations, which lead to attritional bone loss. Recent focus has been on the degree of attritional bone loss and its effect on recurrence and surgical outcomes. The widest portion of the anterior-to-posterior dimension of the glenoid is on average 25 mm. Therefore, attrition of 6 to 8  mm may represent 24% to 32% bone loss. This degree of bone loss can actually change the appearance of the glenoid as described by Burkhart et  al.37 This led to the concept of the inverted pear with the glenoid wider superiorly than inferiorly, which disrupted the arc of motion, particularly with abduction and external rotation leading to increased risk of recurrence. Similarly, Piaseck et al found that osseous defects between 9% and 15% of glenoid width (< 3-4 mm) were usually trivial, whereas defects greater than 20%j to 30% (> 6-10 mm) were significant.38 The authors described that these changes were even more impor tant in patients with high athletic demands. This led to the traditional notion that bone loss greater than 20% to 25% was considered critical bone loss leading to high clinical recurrence and surgical failure.39,40 In 2017, Shin et  al identified that even smaller amounts of bone loss may lead to poor surgical outcomes.41 In a study of 169 patients, the study identified that the critical bone loss was 17.3%. Patients with greater than 17.3% bone loss required revision surgery because of recurrence in 42.3% of patients compared to 3.7% in patients with bone loss less than 17.3% of the glenoid.41

Decision Making in Surgical Treatment of Athletes With First-Time vs Recurrent Shoulder Instability The degree of bone loss, particularly in athletes, is critical in treatment decision making. The greater the bone loss, the greater likelihood of recurrence, which should portend to a greater likelihood of surgery. Moreover, significantly higher percentage of glenoid bone loss may be better served with open vs bone block procedures. Recommendation: Glenoid bone loss should be measured in all cases. Glenoid bone loss greater than 17.3% will benefit from primary stabilization in contact and collision athletes. In athletes with larger than 25% bone loss, primary bone procedure may be considered.

Humeral Bone Loss In conjunction with glenoid bone loss from anteriorinferior dislocation of the glenohumeral joint is the development of an impaction injury in the posterior-superior aspect of the humeral head. The depression in the humeral head may engage with the glenoid and result in a recurrent instability episode. The incidence of humeral head impression has been shown to range from 70% to 100% for patients with first-time shoulder dislocations.33,42,43 Studies have shown that the presence of a humeral bone impaction or bone loss result in a 1.55× greater likelihood of a recurrent instability episode.27,36 Sekiya and colleagues sought to answer the degree of humeral bone loss that becomes clinically significant.44 In their study, biomechanical testing demonstrated humeral head lesions greater than 25% of the articular surface significantly increased the risk of recurrent instability.44 The authors’ recommendation, therefore, was to treat humeral head lesions greater than 25%.44 Although there are no comparative studies to provide a confident recommendation, treatment of isolated humeral bone loss may be targeted with a remplissage procedure, which is a capsulotenodesis of the infraspinatous tendon into the humeral defect. Lin et al performed a systematic review of remplissage procedures into defects measuring 20% to 40% of humeral volume and identified a wide range of values of return to sport ranging from 56.9% to 100% and return to previous level of sport of 41.7% to 100%.45 (Lin 2018) The authors’ recommendations were that patients with subcritical glenoid bone loss with a humeral head lesion greater than 25% should undergo a labral repair with a remplissage.45 In athletes, one must also consider that the remplissage procedure is nonanatomic and may lead to loss of motion. Depending on the sport, this loss of motion may be unacceptable. Other considerations include bone grafting of the lesion and interaction with any glenoid bony loss-glenoid track. Given the wide range of return to sport, it is difficult to determine when best to recommend a remplissage procedure, but it should be considered. Recommendation: In athletes with humeral bone loss greater than 25%, primary stabilization with or without remplissage may be considered. One must consider possible consequences of a nonanatomic procedure and loss of motion, which may affect performance in athletes.

59

Combined Bone Loss—Glenoid Track Combined bone loss is a frequently encountered scenario because glenoid bone loss incidence is 20% to 70% and humeral head bone loss ranges from 70% to 100% following instability episodes.18 Gowd et  al performed a systematic review and found that established critical glenoid bone loss values were not equally relevant in the setting of bipolar bone loss.46 In all treatment options, nonoperative and surgical, there were higher rates of recurrence in the setting of bipolar bone loss.46 Arciero et  al47 evaluated the combined biomechanical effects of bipolar lesions using 3-dimensional printing from computed tomography scans of 142 patients with varying degrees of glenoid and humeral head lesions. They defined humeral head lesions of 25% loss of humeral volume as small and lesions with loss of 50% humeral volume as medium. The study found that medium-sized humeral head impaction became clinically significant with as little as 2 mm (8%) of glenoid bone loss.47 This suggests that any humeral head lesion of greater than 50% volume would become clinically significant with any degree of glenoid bone loss. In 2007, Yamamoto and colleagues introduced the concept of glenoid track to account for the interaction of glenoid and humeral bone loss.48 The glenoid track represents the contact area of glenoid on humeral head as the arm is brought through physiologic range of motion. The glenoid track migrates from inferomedial to superolateral on the humeral head and is defined as the region from the medial margin of the rotator cuff footprint to a point 84% of the width of the native glenoid medially onto the articular surface of the humerus.48 Di Giacomo furthered the concept by identifying humeral head lesions contained within this contact area as on-track and those that had contact outside or medial to the glenoid track as off-track.49 He found that off-track lesions were more likely to engage and result in recurrent dislocation.49 Lau et al evaluated glenoid track in adolescent and adult patients and found that the greater incidence of recurrent shoulder instability in adolescents may be due in part to a higher incidence of off-track lesions compared to adults.50 (Lau 2017) Moreover, patients with 2 or more shoulder dislocations also demonstrated greater incidence of off-track lesions.50 Recommendation: Evaluation of bipolar bone loss and glenoid track should be considered in all athletes. Patients with glenoid off-track lesions may benefit from shoulder stabilization.

TREATMENTS AND OUTCOMES Several studies have investigated dif ferent treatments such as immobilization in a sling, immobilization in external rotation, and surgical treatment.2,9,51-56 These studies suggest there are several possible treatment options that may offer satisfactory outcomes. The major concern for athletes is the

60

Chapter 6

Table 6-2. Treatment Options, Recurrence Rate, Return to Play TREATMENT

RECURRENCE RATE, % Nonoperative 46-58.4 Arthroscopic repair 6.4-9.7 Open repair 3.4-8.2 Coracoid transfer 2.9-3.2

RATE OF RETURN TO PLAY, % 41.3-85 72-95.3 75-100 76.3-84.9

rate of return to sport and the level of performance upon return. See Table 6-2 for an overview of recurrence rates and return to play rates following nonoperative, arthroscopic repair, open repair, or coracoid transfer.

FIRST-TIME DISLOCATIONS Nonoperative Management Nonoperative management including joint mobilization, strengthening, endurance, neuromuscular training, and sport-specific shoulder drills can lead to satisfactory results in athletes. A recent systematic review identified no difference in rate of recurrent instability with nonoperative management related to reduction method, type of immobilization, or length of immobilization before starting physical therapy.17 Shanley and colleagues studied 101 high school athletes, and 85% of athletes treated nonoperatively compared to 72% of operated athletes returned to the same sport. Interestingly, the sex and type of sport did not influence the ability to return to sport.57

Nonoperative vs Operative Management There remains debate in the literature as to whether patients with first-time dislocations should be treated with nonoperative or surgical management, particularly in the younger patient.77,78 A meta-analysis performed by Brophy and Marx demonstrated surgical treatment was associated with a significantly lower rate of recurrent instability at 2 years of follow-up (7% vs 46%).51 At 3 to 4 years’ follow-up there was a recurrence rate of 58.4% in patients treated nonoperatively compared to 9.7% in surgical management.51 Young athletes have a return to play rate of 95.3% in patients managed operatively vs 41.3% in patients treated nonoperatively.19 Similarly, Longo et  al found that following surgical management, 87% of athletes returned to their choice sport at the same level, 4% at a lower level, 3% changed sports, and 6% did not return to sport.30 The decision for surgical management remains an individual decision based on time of the season and patient goals; however, patients may be counseled that operative

management may decrease risk of recurrence after a firsttime dislocation.

Arthroscopic Management A recent systematic review of 22 randomized controlled studies of mostly male athletes demonstrated that arthroscopic labral repair reduced risk of future shoulder dislocation (relative risk reduction of 0.15).31 The number needed to treat to prevent a redislocation at 2  years ranged from 2 to 4.7 athletes.31 Disease-specific quality-of-life measures were slightly improved with labral repair vs nonoperative management.31 Other systematic reviews performed by Handoll et al58 and Chahal and colleagues59 also demonstrated more favorable outcomes with arthroscopic surgical management. A recent study demonstrated that with modern arthroscopy techniques (lateral position and three or more anchors) the recurrence rate of shoulder instability was 7.9%.21 Lin et  al demonstrated that patients with subcritical glenoid and humeral bone loss had a rate of return to sport of 76.3% and a rate to return to previous level of sport at 75.2%.45

Open vs Arthroscopic Management Historically, collision or contact athletes were treated with open surgical stabilization with a recurrence rate as low as 3.4%.8 However, arthroscopic management has become the standard for primary shoulder stabilizations without significant bone loss. In extremely high-risk patients, one may consider open Bankart repair because there is evidence of lower dislocation rates in recurrent instability treated with open Bankart repair compared to arthroscopic repair.60,80 Additionally, glenoid rim fractures, which may be present in up to 22% of traumatic shoulder dislocations, may also benefit from open repair.33

RECURRENT INSTABILITY Factors that help in decision making in cases of recurrent instability are similar to those of first-time shoulder dislocations: age, activity level, sex, generalized laxity, hand dominance, glenoid bone loss, humeral bone loss, and glenoid track. The threshold for surgical management, however, is lower in cases of recurrent instability because athletes have already demonstrated a history of multiple dislocations, which is one of the strongest indicators of a recurrent instability episode. A level-1, prospective cohort study showed that a history of recurrent glenohumeral joint instability leads to a 5.6× greater likelihood of experiencing a subsequent instability event.61 Importantly, this was in a group of young athletic military academy cadets61 similar to an athletic population. There are higher rates and degrees of glenoid bone loss and humeral head impression in recurrent instability athletes.62-64 Clinically significant glenoid bone loss was present at an increasing rate following 2 dislocations compared to a single dislocation, 26.1% vs 8.6%.65 Patients with 2 or more

Decision Making in Surgical Treatment of Athletes With First-Time vs Recurrent Shoulder Instability dislocations demonstrated a 3.26× increased risk of clinically significant glenoid bone loss.65 There are also data to suggest that the increasing number of instability episodes increases the risk of postsurgical recurrence, as well as subsequent glenohumeral arthritis.19 Athletes with recurrent shoulder instability events benefit from operative management. The decision in treatment tends to be open or arthroscopic treatment. In the setting of subcritical bone loss, the historical approach for surgical management of contact or collision athletes was open-shoulder stabilization leading to reported reoccurrence rates as low as 3.4%.8 However, more recent data suggest that with modern arthroscopy techniques, including lateral position and 3 or more anchors, the recurrence rate is 7.9%.21 A systematic review comparing results of arthroscopic vs open repair for anterior shoulder dislocations demonstrated no significant difference in redislocation rates, return to activity, and functional outcomes between the 2 treatment options. Range of motion, however, particularly with external rotation, was marginally better following arthroscopic treatment when compared to open repair.

Glenoid and Humeral Bone Loss in Recurrent Instability Outcomes following surgical management differ in patients with glenoid and humeral bone loss. Traditional bone loss cutoffs were based on several studies that found patients with larger than 25% of glenoid bone loss had a failure rate of 67% vs 4% in those with less glenoid bone loss.37,66 These studies were further supported by cadaveric studies that showed a significant decrease in stability with glenoid defects greater than 21%.40,66 These studies supported bony augmentation procedures over isolated soft-tissue repairs in patients with more than 20% glenoid bone loss. Recent studies have suggested, however, a lower threshold for critical bone loss that should lead to bony augmentation. Shin et  al41 identified 17.3% and Arciero and colleagues47 identified that 15% glenoid bone loss led to significantly increased instability despite soft-tissue repair. It is impor tant to note that established critical bone losses are not equally relevant in the setting of bipolar bone loss.46 All repair techniques demonstrate a higher rate of recurrence in the presence of bipolar bone loss. Recommendation: The degree of bone loss should be considered when deciding on the specific type of surgical treatment (eg, arthroscopic, open, bone augmentation, remplissage, grafting of the humeral head) when treating recurrent anterior shoulder instability with associated bone loss.

Open vs Arthroscopic—Recurrent Instability There are mixed results in the literature whether open vs arthroscopic treatments are better in athletes with recurrent

61

instability. Godin and Sekiya evaluated 4 randomized controlled studies and found no significant difference in recurrence rates, return to activity, or functional outcomes between groups.67 Similarly, Brophy and Marx51 identified similar rates of recurrence using advance techniques with suture anchors in open and arthroscopic stabilizations, 8.2% and 6.4%, respectively, whereas Kavaja et  al68 evaluated 22 randomized controlled studies and found some evidence to suggest open repair was superior to arthroscopic repair. Open repair, however, led to limitations in external rotation.68 Our preferred method is to work with the patient to come up with the best treatment solution given his or her specific risk factors and preferences. In extremely high-risk environments, open surgical treatment may be appropriate following a first-time dislocation.

Primary Bony Augmentation Several authors recommend primary bone augmentation with a coracoid transfer, Latarjet procedure.69,70 Particularly in Europe, Latarjet procedures are more commonplace and used to treat primary shoulder instability independent of amount of glenoid bone loss. When used in treating first-time dislocations, the recurrent dislocation rate was 2.9%, and recurrent subluxation rate was 5.8%.71 Long-term follow-up at 10 years after primary Latarjet demonstrated a recurrence rate of 3.2% for redislocations and 6.7% for subluxations for a total rate of 8.5%. There was an 84.9% rate of return to play with 76.3% of athletes returning to the same level.72 Despite the good outcomes, however, Latarjet is a difficult procedure, particularly for those that do not perform it routinely. Complication rates have been reported to be as high as 30%, as well as reports of 7% of patients requiring unplanned reoperation.71 Complications including recurrent instability, nonunion, hardware problems, and neurovascular injury may occur. Moreover, Di Giacomo73 suggests that primary bony augmentation may be necessary only in patients with significant bone loss. Their study found that coracoid graft resorption was 40% at 1-year follow-up in patients with less than 15% glenoid bone loss, which suggests that an unloaded graft will ultimately resorb according to Wolff’s law.73 A study by Yang et  al evaluated outcomes of Latarjet procedure in the setting of bipolar bone loss and found that glenoid off-track lesions had overall recurrent instability of 15% to 17% regardless of whether glenoid bone loss was less than or greater than the threshold of critical bone loss.74

PERSONALIZED DECISION-MAKING MODELS It is critical for physicians to have an understanding of risk factors, treatment options, and outcomes to best counsel athletes during the treatment decision-making process. Equally impor tant, however, is an understanding of each athlete’s preferences. For high school–aged patients, this may

62

Chapter 6

Figure 6-2. Example of graphical representation of respondents’ preferences.

Figure 6-3. Mean importance weights, all respondents. Error bars represent 95% CI.

be their last chance for competitive sport or an opportunity to showcase their talents for a college scholarship. For college players, there may be scholarship requirements or a championship run. For professional athletes, it may be roster bonuses or contract negotiations. All of these factors should be discussed, but it is imperative that the health of the patient remain the priority. Incorporating these factors into a decision is challenging but can be supported using personalized decision-making models combining medical evidence and patient preferences. In the literature, there is a paucity of evidence of how patient preferences can be incorporated into the decisionmaking process. Although more research is being conducted on the systematic elicitation of patient preferences, the use of tools to capture objectively this information for use in the clinical context remains limited. Streufert et al6 used a novel shared decision-making tool that assessed individual preferences following a first-time anterior shoulder dislocation through a set of risk-benefit trade-off scenarios. Attributes that were evaluated for this preference-sensitive treatment decision included 1) chance of recurrent dislocation, 2) cost, 3) short-term limits on shoulder motion, 4) limits on participation in high-risk activities, and 5) duration of physical therapy. The tool then produced a graphical representation of an individual’s relative importance on these factors (Figures 6-2 and 6-3). In a clinical setting, these preferences could be reviewed with clinicians to help guide the treatment decision-making process. Personalized treatment decisions aligned with individual preferences could lead to improved communication, patient satisfaction, and outcomes. The Streufert study also reported that nearly 90% of participants

would share this graph with their physicians, indicating a desire for patients to engage in the decision-making process.6 Interestingly, Streufert and colleagues found in their study of 374 respondents that the rate of recurrence was the largest factor that predicted respondents’ subsequent decision for operative treatment.6 Informed decision-making and appropriate treatment utilization, therefore, depend on accurate dissemination of medical evidence. Equally impor tant is that this information be provided in a customized and objective manner because rates of recurrence are highly variable between patient populations. However, translating evidence into practice is limited by challenges such as the complexity of information and user uptake of information. Hutyra et al performed an analysis to evaluate how well information regarding 2-year recurrence rates and appropriate evidencebased treatments were being applied.75 The study found that physicians quoted appropriate evidence-based recurrence rate only 59% of the time.75 More impor tant, patients obtained accurate evidence-based information regarding recurrence only 29% of the time,75 indicating a clear gap in the dissemination of information. One strategy to improve and maintain up-to-date evidence-based dissemination of data is the implementation of clinical decision-support tools. In a separate study, Hutyra et  al assessed the efficacy of a preference-based decision tool in a randomized controlled trial.4 The decision-support tool provided patients up-todate evidence-based numbers of their rate of recurrence with operative and nonoperative care following shoulder dislocation based on their age, sex, and activity level. Their preferences were assessed with 8 trade-off questions. A Monte Carlo simulation of aggregated evidence provided

Decision Making in Surgical Treatment of Athletes With First-Time vs Recurrent Shoulder Instability a treatment recommendation of 1) operative treatment, 2) nonoperative treatment, or 3) either treatment, in which case either operative or nonoperative treatment would be equally effective. In the group of patients that would benefit equally from either treatment option, patient preference was the primary driver of treatment selection. The study found that participants who were in the intervention group that used the decision-support tool more closely aligned with evidence-based recommendations than those who did not use the decision-support tool, 67% vs 28%.4 Interestingly, patients who took the decision-support tool were more likely to elect surgical treatment, 43% vs 26%, compared to those in the control group. Following completion of the study, 99% of individuals said they would find a health-care decision tool with general descriptions of risks, benefits, and outcomes of treatment useful, and 97% would find a personalized report of expected risk, benefit, and outcome rates based on medical evidence useful. These findings further support the need for inclusion of personalized evidence and patient preferences in the decision-making process surrounding shoulder instability in athletes. The Mather et al model serves as the fusion of personalized medical evidence, preferences, and an engaging accessible platform and may serve as a guide to implementation of future personalized shoulder decision-making tools.5 For instance, the tool was created for noncommercial use, was meant to be readily available to the public, integrated the highest-level evidence into its construction, and was formed to be readily adaptable to the addition of new parameters. This model aimed to inform the decision-making process for shoulder interventions while increasing the understanding of potential outcomes associated with each intervention. The integration of such decision-making models for recurrent instability and other shoulder conditions are central to patient education, shared decision making, and the delivery of patient-centered care.

CONCLUSION Many factors must be considered when making treatment decisions with athletes regarding shoulder instability. The timing of the season or point in an athlete’s career may dictate treatment options. Patient factors such as age, activity level, sex, hand dominance, laxity, glenoid bone loss, and humeral bone loss are impor tant to consider. Treatment outcomes related to rate of recurrence and return to play are paramount in discussions with athletes regarding shoulder instability. Equally impor tant is consideration of patients’ preferences for or against surgery and their goals for the future. Clinical decision-making tools may serve as an efficient and convenient way to assist dissemination of knowledge to athletes. All decisions should be personalized to the athlete and the athlete’s well-being—rather than to an agent, coach, school, or franchise—as the main goal of any treatment for shoulder instability.

63

REFERENCES 1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

14. 15.

16.

Owens BD, DeBerardino TM, Nelson BJ, et al. Long-term follow-up of acute arthroscopic Bankart repair for initial anterior shoulder dislocations in young athletes. Am J Sports Med. 2009;37(4):669-673. doi:10.1177/0363546508328416. Kirkley A, Werstine R, Ratjek A, Griffin S. Prospective randomized clinical trial comparing the effectiveness of immediate arthroscopic stabilization versus immobilization and rehabilitation in first traumatic anterior dislocations of the shoulder: long-term evaluation. Arthroscopy. 2005;21(1):55-63. doi:10.1016/j.arthro.2004.09.018. Sachs RA, Lin D, Stone ML, Paxton E, Kuney M. Can the need for future surgery for acute traumatic anterior shoulder dislocation be predicted? J Bone Joint Surg Am. 2007;89(8):1665-1674. doi:10.2106/ JBJS.F.00261. Hutyra CA, Smiley S, Taylor DC, Orlanda LA, Mather RC  III. Efficacy of a preference-based decision tool on treatment decisions for a first-time anterior shoulder dislocation: a randomized controlled trial of at-risk patients. Med Decis Making. 2019;39(3):253263. doi:10.1177/0272989X19832915. Mather RC III, Orlando LA, Henderson RA, Lawrence JTR, Taylor DC. A predictive model of shoulder instability after a first-time anterior shoulder dislocation. J Shoulder Elbow Surg. 2011;20(2):259-266. doi:10.1016/j.jse.2010.10.037. Streufert B, Reed SD, Orlando LA, Taylor DC, Huber JC, Mather RC  III. Understanding preferences for treatment after hypothetical first-time anterior shoulder dislocation: surveying an online panel utilizing a novel shared decision-making tool. Orthop J Sports Med. 2017;5(3):2325967117695788. doi:10.1177/2325967117695788. Bottoni CR, Wilckens JH, DeBerardino TM, et al. A prospective, randomized evaluation of arthroscopic stabilization versus nonoperative treatment in patients with acute, traumatic, first-time shoulder dislocations. Am J Sports Med. 2002;30(4):576-580. doi:10.1177/03635 465020300041801. Pagnani MJ, Dome DC. Surgical treatment of traumatic anterior shoulder instability in American football players. J Bone Joint Surg Am. 2002;84(5):711-715. doi:10.2106/00004623-200205000-00002. Buss DD, Lynch GP, Meyer CP, Huber SM, Freehill MQ. Nonoperative management for in-season athletes with anterior shoulder instability. Am J Sports Med. 2004;32(6):1430-1433. doi:10.1177/0363546503262069. Owens BD, Dickens JF, Kilcoyne KG, Rue JP. Management of midseason traumatic anterior shoulder instability in athletes. J Am Acad Orthop Surg. 2012;20(8):518-526. doi:10.5435/JAAOS-20-08-518. Mazzocca AD, Brown FM Jr, Carreira DS, Hayden J, Romeo AA. Arthroscopic anterior shoulder stabilization of collision and contact athletes. Am J Sports Med. 2005;33(1):52-60. doi:10.1177/0363546504268037. Larrain MV, Botto GJ, Montenegro HJ, Mauas DM. Arthroscopic repair of acute traumatic anterior shoulder dislocation in young athletes. Arthroscopy. 2001;17(4):373-377. doi:10.1053/jars.2001.23226. te Slaa RL, Wijffels MP, Brand R, Marti RK. The prognosis following acute primary glenohumeral dislocation. J Bone Joint Surg Br. 2004;86(1):58-64. Ramsey ML, Getz CL, Parsons BO. What’s new in shoulder and elbow surgery. J Bone Joint Surg Am. 92:1047-1061. Marans HJ, Angel KR, Schemitsch EH, Wedge JH. The fate of traumatic anterior dislocation of the shoulder in children. J Bone Joint Surg Am. 1992;74(8):1242-1244. Porcellini G, Campi F, Pegreffi F, Castagna A, Paladini P. Predisposing factors for recurrent shoulder dislocation after arthroscopic treatment. J Bone Joint Surg Am. 2009;91(11):2537-2542. doi:10.2106/ JBJS.H.01126.

64 17.

18.

19.

20.

21.

22.

23.

24.

25.

26.

27.

28.

29. 30.

31.

32.

33.

34.

Chapter 6 Olds M, Ellis R, Donaldson K, Parmar P, Kersten  P. Risk factors which predispose first-time traumatic anterior shoulder dislocation to recurrent instability in adults: a systematic review and meta-analysis. Br J Sports Med. 2015;49(14):913-922. doi:10.1136/ bjsports-2014-094342. Robinson CM, Dobson RJ. Anterior instability of the shoulder after trauma. J Bone Joint Surg Br. 2004;86(4):469-479. doi:10.1302/0301-620x.86b4. Zaremski JL, Galloza J, Sepulveda F, Vasilopoulos T, Micheo W, Herman DC. Recurrence and return to play after shoulder instability events in young and adolescent athletes: a systematic review and meta-analysis. Br J Sports Med. 2017;51(3):177-184. doi:10.1136/ bjsports-2016-096895. Zacchili MA, Owens BD. Epidemiology of shoulder dislocations presenting to emergency departments in the United States. J Bone Joint Surg Am. 2010;92(3):542-549. doi:10.2106/JBJS.I.00450. Leroux T, Ogilvie-Harris D, Veillete C, et al. The epidemiology of primary anterior shoulder dislocations in patients aged 10 to 16 years. Am J Sports Med. 2015;43(9):2111-2117. doi:10.1177/0363546515591996. Harris JD, Gupta AK, Mall NA, et  al. Long-term outcomes after Bankart shoulder stabilization. Arthroscopy. 2013;29(5):920-933. doi:10.1016/j.arthro.2012.11.010. Balg F, Boileau P. The Instability Severity Index Score: a simple preoperative score to select patients for arthroscopic or open shoulder stabilisation. J  Bone Joint Surg Br. 2007;89(11):1470-1477. doi:10.1302/0301-620X.89B11.18962. Hovelius L, Oloffsson A, Sanstrom B, et al. Nonoperative treatment of primary anterior shoulder dislocation in patients forty years of age and younger. A prospective twenty-five-year follow up. J Bone Joint Surg Am. 2008;90(5):945-952. Owens BD, Agel J, Mountcastle SB, Cameron KL, Nelson BJ. Incidence of glenohumeral instability in collegiate athletics. Am J Sports Med. 2009;37(9):1750-1754. doi:10.1177/0363546509334591. Robinson CM, Howes J, Murdoch H, Will E, Graham C. Functional outcome and risk of recurrent instability after primary traumatic anterior shoulder dislocation in young patients. J Bone Joint Surg Am. 2006;88(11):2326-2336. doi:10.2106/JBJS.E.01327. Salomonsson B, von  Heine A, Dahlborn M, et  al. Bony Bankart is a positive predictive factor after primary shoulder dislocation. Knee Surg Sports Traumatol Arthrosc. 2009;18(10):1425-1431. doi:10.1007/ s00167-009-0998-3. Longo UG, Rissello G, Loppini M, et al. Multidirectional instability of the shoulder: a systematic review. Arthroscopy. 2015;31(12):24312443. doi:10.1016/j.arthro.2015.06.006. Lim CR, Yap C, Campbell P. Hand dominance in traumatic shoulder dislocations. JSES Open Access. 2018;2(2):137-140. Longo GU, Loppini M, Rizzello G, Romeo G, Huijsmans PE, Denaro V. Glenoid and humeral head bone loss in traumatic anterior glenohumeral instability: a systematic review. Knee Surg Sports Traumatol Arthrosc. 2014;22(2):392-414. doi:10.1007/s00167-013-2403-5. Kavaja L, Pajarinen J, Sinisaari I, et  al. Arthrosis of glenohumeral joint after arthroscopic Bankart repair: a long-term follow-up of 13  years. J  Shoulder Elbow Surg. 2012;21(3):350-355. doi:10.1016/j. jse.2011.04.023. Plath JE, Aboalata M, Seppel G, et  al. Prevalence of and risk factors for dislocation arthropathy: radiological long-term outcome of arthroscopic Bankart repair in 100  shoulders at an average 13-year follow-up. Am J Sports Med. 2015;43(5):1084–1090. doi:10.1177/0363546515570621. Taylor DC, Arciero RA. Pathologic changes associated with shoulder dislocations. Arthroscopic and physical examination findings in first-time, traumatic anterior dislocations. Am J Sports Med. 1997;25(3):306-311. doi:10.1177/036354659702500306. Vermeiren J, Handelberg PP, Casteleyn PP, Opdecam  P. The rate of recurrence of traumatic anterior dislocation of the shoulder. Int Orthop. 1993;17(6):337-341. doi:10.1007/bf00180449.

35.

36.

37.

38.

39.

40.

41.

42.

43.

44.

45.

46.

47.

48.

49.

50.

51.

Pevny T, Hunter RE, Freeman JR. Primary traumatic anterior shoulder dislocation in patients 40  years of age and older. Arthroscopy. 1998;14(3):289-294. doi:10.1016/s0749-8063(98)70145-8. Hoelen MA, Burgers AM, Rozing PM. Prognosis of primary anterior shoulder dislocation in young adults. Arch Orthop Trauma Surg. 1990;110(1):51-54. doi:10.1007/bf00431367. Burkhart SS, Danaceau SM. Articular arc length mismatch as a cause of failed Bankart repair. Arthroscopy. 2000;16(7):740-744. doi:10.1053/jars.2000.7794. Piaseck DP, Verma NN, Romeo AA, Levine WL, Bach BR Jr, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493. doi:10.5435/00124635-200908000-00002. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694. doi:10.1053/ jars.2000.17715. Itoi E, Lee SB, Berglund LJ, Berge LL, An KN. The effect of a glenoid defect on anteroinferior stability of the shoulder after Bankart repair: a cadaveric study. J Bone Joint Surg Am. 2000;82(1):35-46. doi:10.2106/00004623-200001000-00005. Shin SJ, Kim RG, Jeon YS, Kwon TH. Critical value of anterior glenoid bone loss that leads to recurrent glenohumeral instability after arthroscopic Bankart repair. Am J Sports Med. 2017;45(9):1975-1981. doi:10.1177/0363546517697963. Baker CL, Uribe JW, Whitman C. Arthroscopic evaluation of acute initial anterior shoulder dislocations. Am J Sports Med. 1990;18(1):2528. doi:10.1177/036354659001800104. Norlin R. Intraarticular pathology in acute, first-time anterior shoulder dislocation: an arthroscopic study. Arthroscopy. 1993;9(5):546549. doi:10.1016/s0749-8063(05)80402-5. Sekiya JK, Wickwire AC, Stehle JH, Debski RE. Hill-Sachs defects and repair using osteoarticular allograft transplantation: biomechanical analysis using a joint compression model. Am J Sports Med. 2009;37(12):2459-2466. doi:10.1177/0363546509341576. Liu JN, Gowd AK, Garcia GH, Cvetanovich GL, Cabarcas BC, Verma NN. Recurrence rate of instability after remplissage for treatment of traumatic anterior shoulder instability: a systematic review in treatment of subcritical glenoid bone loss. Arthroscopy. 2018;34(10):28942907.e2. Gowd AK, Liu JN, Cabarcas BC, et  al. Management of recurrent anterior shoulder instability with bipolar bone loss: a systematic review to assess critical bone loss amounts. Am J Sports Med. 2019;47(10):2484-2493. doi:10.1177/0363546518791555. Arciero RA, Parrino A, Bernhardson AS, et  al. The effect of a combined glenoid and Hill-Sachs defect on glenohumeral stability: a biomechanical cadaveric study using 3-dimensional modeling of 142 patients. Am J Sports Med. 2015;43(6):1422-1229. doi:10.1177/0363546515574677. Yamamoto N, Itoi E, Abe H, et al. Contact between the glenoid and the humeral head in abduction, external rotation, and horizontal extension: a new concept of glenoid track. J Shoulder Elbow Surg. 2007; 16: 649-656. doi:10.1016/j.jse.2006.12.012. Di Giacomo G, de Gasperis N, Costantini A, De Vita A, Beccaglia MA, Pouliart  N. Does the presence of glenoid bone loss influence coracoid bone graft osteolysis after the Latarjet procedure? A computed tomography scan study in 2 groups of patients with and without glenoid bone loss. J  Shoulder Elbow Surg. 2014;23(4):514-518. doi:10.1016/j.jse.2013.10.005. Lau BC, Conway D, Curran PF, Feeley BT, Pandya NK. Bipolar bone loss in patients with anterior shoulder dislocation: a comparison of adolescents versus adult patients. Arthroscopy. 2017;33(10):1755-1761. Brophy RH, Marx RG. The treatment of traumatic anterior instability of the shoulder: nonoperative and surgical treatment. Arthroscopy. 2009;25(3):298-304. doi:10.1016/j.arthro.2008.12.007.

Decision Making in Surgical Treatment of Athletes With First-Time vs Recurrent Shoulder Instability 52.

53.

54.

55.

56.

57.

58.

59.

60.

61.

62.

63.

64.

65.

Cheung EV, Sperling JW, Hattrup SJ, Cofield RH. Long-term outcome of anterior stabilization of the shoulder. J Shoulder Elbow Surg. 2008;17(2):265-270. doi:10.1016/j.jse.2007.06.005 Fabbriciani C, Milano G, Demontis A, Fadda S, Ziranu F, Mulas PD. Arthroscopic versus open treatment of Bankart lesion of the shoulder: a prospective randomized study. Arthroscopy. 2004;20(5):456462. doi:10.1016/j.arthro.2004.03.001. Fabre T, Abi-Chahla M, Billaud A, Geneste M, Durandeau A. Longterm results with Bankart procedure: a 26-year follow-up study of 50 cases. J  Shoulder Elbow Surg. 2010;19(2):318-323. doi:10.1016/j. jse.2009.06.010. Lenters TR, Franta AK, Wolf FM, Leopold SS, Matsen FA  III. Arthroscopic compared with open repairs for recurrent anterior shoulder instability. A systematic review and meta-analysis of the literature. J Bone Joint Surg Am. 2007;89(2):244-254. doi:10.2106/ JBJS.E.01139. Robinson CM, Jenkins PJ, White TO, Ker A, Will  E. Primary arthroscopic stabilization for a first-time anterior dislocation of the shoulder. A randomized, double-blind trial. J  Bone Joint Surg Am. 2008;90(4):708-721. doi:10.2106/JBJS.G.00679. Shanley E, Thigpen C, Brooks J, et al. Return to sport as an outcome measure for shoulder instability: surprising finding in nonoperative management in a high school athlete population. Am J Sports Med. 2019;47(5):1062-1067. doi:10.1177/0363546519829765. Handoll HH, Almaiyah MA, Rangan A. Surgical versus non-surgical treatment for acute anterior shoulder dislocation. Cochrane Database Syst Rev. 2004;(1):CD004325. doi:10.1002/14651858.CD004325. pub2. Chahal J, Marks PH, Macdonald PB, et  al. Anatomic Bankart repair compared with nonoperative treatment and/or arthroscopic lavage for first-time traumatic shoulder dislocation. Arthroscopy. 2012;28(4):565-575. doi:10.1016/j.arthro.2011.11.012. Mohtadi NG, Bitar IJ, Sasyniuk TM, Hollinshead RM, Harper WP. Arthroscopic versus open repair for traumatic anterior shoulder instability: a meta-analysis. Arthroscopy. 2005;21(6):652-658. doi:10.1016/j.arthro.2005.02.021. Cameron KL, Mountcastle SB, Nelson BJ, et  al. History of shoulder instability and subsequent injury during four years of followup: a survival analysis. J Bone Joint Surg Am. 2013;95(5):439-445. doi:10.2106/JBJS.L.00252. Bollier MJ, Arciero  R. Management of glenoid and humeral bone loss. Sports Med Arthrosc Rev. 2010;18(3):140-148. doi:10.1097/ JSA.0b013e3181e88ef9. Kim DS, Yoon YS, Yi CH. Prevalence comparison of accompanying lesions between primary and recurrent anterior dislocation in the shoulder. Am J Sports Med. 2010;38(10):2071-2076. doi:10.1177/0363546510371607. Antonio GE, Griffith JF, Yu AB, Yung PS, Chan KM, Ahuja AT. First-time shoulder dislocation: high prevalence of labral injury and age-related differences revealed by MR arthrography. J Magn Reson Imaging. 2007;26(4):983-991. doi:10.1002/jmri.21092. Rugg CM, Hettrich CM, Ortiz S, Wolf BR; MOON Shoulder Instability Group, Zhang AL. Surgical stabilization for first-time shoulder dislocators: a multicenter analysis. J  Shoulder Elbow Surg. 2018;27(4):674-685. doi:10.1016/j.jse.2017.10.041.

66.

67.

68.

69.

70.

71.

72.

73.

74.

75.

76.

77.

78.

79.

80.

65

Greis PE, Scuderi MG, Mohr A, Bachus KN, Burks RT. Glenohumeral articular contact areas and pressures following labral and osseous injury to the anteroinferior quadrant of the glenoid. J Shoulder Elbow Surg. 2002;11(5):442-451. doi:10.1067/mse.2002.124526. Godin J, Sekiya JK. Systematic review of arthroscopic versus open repair for recurrent anterior shoulder dislocations. Sports Health. 2011;3(4):396-404. doi:10.1177/1941738111409175. Kavaja L, Lähdeoja T, Malmivaara, Paavola M. Treatment after traumatic shoulder dislocation: a systematic review with a network metaanalysis. Br J Sports Med. 2018;52:1498-1506. Blonna D, Bellato E, Caranzano F, Assom M, Rossi R, Castoldi  F. Arthroscopic Bankart repair versus open Bristow-Latarjet for shoulder instability. Am J Sports Med. 2016;44(12):3198-3205. doi:10.1177/0363546516658037. Zimmermann SM, Scheyerer MJ, Farshad M, Catanzaro S, Rahm S, Gerber  C. Long-term restoration of anterior shoulder stability: a retrospective analysis of arthroscopic Bankart repair versus open Latarjet procedure. J  Bone Joint Surg Am. 2016;98(23):1954–1961. doi:10.2106/JBJS.15.01398. Griesser MJ, Harris JD, McCoy BW, et  al. Complications and reoperations after Bristow-Latarjet shoulder stabilization: a systematic review. J Shoulder Elbow Surg. 2013;22(2):286-92. doi: 10.1016/j. jse.2012.09.009. Hurley ET, Jamal S, Zakariya AS, Montgomery C, Pauzenberger L, Mullett H. Long-term outcomes of the Latarjet procedure for anterior shoulder instability: a systematic review of studies at 10-year follow-up. J Shoulder Elbow Surg. 2019;28(2):e33-e39. doi:10.1016/j. jse.2018.08.028. Di Giacomo G, Itoi E, Burkhart SS. Evolving concept of bipolar bone loss and the Hill-Sachs lesion: from “engaging/non-engaging” lesion to “on-track/off-track” lesion. Arthroscopy. 2014;30(1):90-98. doi:10.1016/j.arthro.2013.10.004. Yang JS, Mazzocca AD, Cote MP, Edgar CM, Arciero RA. Recurrent anterior shoulder instability with combined bone loss: treatment and results with the modified Latarjet procedure. Am J Sports Med. 2016;44(4):922-932. doi:10.1177/0363546515623929. Hutyra CA, Streufert B, Politzer CS, et al. Assessing the effectiveness of evidence-based medicine in practice: a case study of first-time anterior shoulder dislocations. J Bone Joint Surg Am. 2019;101(2):e6. doi:10.2106/JBJS.17.01588. Owens BD, Duffey ML, Nelson BJ, DeBerardino TM, Taylor DC, Mountcastle SB. The incidence and characteristics of shoulder instability at the United States Military Academy. Am J Sports Med. 2007;35:1168-1173. Bishop JA, Crall TS, Kocher MS. Operative versus nonoperative treatment after primary traumatic anterior glenohumeral dislocation: expected-value decision analysis. J Shoulder Elbow Surg. 2011;20:1087-1094. Godin J, Sekiya JK. Systematic review of rehabilitation versus operative stabilization for the treatment of first-time anterior shoulder dislocations. Sports Health. 2010;2:156-165. Owens BD, Nelson BJ, Duffey ML, et al. Pathoanatomy of first-time, traumatic, anterior glenohumeral subluxation events. J Bone Joint Surg Am. 2010;92(7):1605-1611. Roberts SN, Taylor DE, Brown JN, Hayes MG, Saies A. Open and arthroscopic techniques for the treatment of traumatic anterior shoulder instability in Australian rules football players. J Shoulder Elbow Surg. 1999;8(5):403-409.

7 Radiographic and Advanced Imaging to Assess Anterior Glenohumeral Bone Loss Lisa K. O’Brien, DO and Brian R. Waterman, MD

Anterior glenohumeral instability is a common diagnosis among the athletic population, with those competing in contact sports at highest risk.1 Anterior shoulder instability covers a spectrum of injury, from subluxation to frank dislocation, and can result in varying severities of soft-tissue and bony pathology. Recognition of the involved anatomic structures through radiographic and advanced imaging is crucial for directing treatment and obtaining favorable outcomes. Increased attention is being paid to the evaluation of bone loss rather than focusing solely on soft-tissue injury because there is a high failure rate associated with soft-tissue repair alone in the face of significant glenoid width loss. Glenoid bony defects are composed of a continuum of 2 general types: fragment-type (eg, acute glenoid fracture, bony Bankart, glenolabral articular disruption) and attritional-type bone loss. Glenoid bony defects can occur in 5% to 56% of firsttime dislocators, and in upward of 90% of patients with recurrent anterior glenohumeral instability.2,3 Likewise, the Hill-Sachs lesion, or impaction fracture of the posterolateral humeral head, can occur in 65% to 88% of first-time anterior dislocators, and in up to 93% of patients with recurrent instability.2,4,5 Furthermore, glenohumeral subluxations, which comprise up to 85% of all glenohumeral instability events, are not benign and can also result in alarmingly high rates of soft-tissue and bony injury.6 Plain-film radiography can be used as a screening tool to identify patients with significant bone loss both of the glenoid and humeral head. Advanced imaging is required to better quantify the amount of bone loss. Although magnetic resonance imaging (MRI) has classically been used for soft-tissue evaluation and computed

tomography (CT) for osseous evaluation, the use of MRI for assessment of bone loss has recently gained traction thanks to advancements in its technology. Additional modalities like 3-dimensional (3D) reconstruction and imaging with intraarticular gadolinium have also been proven useful. Various measurement techniques to quantify bone loss and direct treatment algorithms have evolved in response to a previously high failure rate of arthroscopic soft-tissue repair. The development of the glenoid track concept and the on-track off-track classification system has enhanced clinical decision making in addressing bipolar bone loss, or concomitant bone loss of both the glenoid and humeral head.

PLAIN RADIOGRAPHS Imaging for the assessment of an athlete with anterior shoulder instability should be initiated with plain radiography. Orthogonal radiographs are an essential adjunct to confirming glenohumeral reduction and assessing for other abnormalities. Standard radiographs include an anteroposterior (AP) or true AP (Grashey) view, scapulolateral view (ie, scapular-Y view), and an axillary lateral view.7 Advantages of radiography include its relatively low cost, near ubiquitous access, and relative ease in obtaining. A major disadvantage is its user-dependent quality and comparatively low accuracy and reliability as to quantifying bone loss.8,9 Therefore, plain radiographs are often used primarily as a simple screening tool to detect significant deficits in glenoid and humeral head bone.

- 67 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 67-78). © 2021 SLACK Incorporated.

68

Chapter 7

Figure 7-1. (A) Anteroposterior (AP) view of the glenohumeral joint. (B) Grashey (true AP) view of the glenohumeral joint. (Copyright BRW, printed with permission.)

Anteroposterior and True Anteroposterior Views A standard AP radiograph of the shoulder is taken with the x-ray beam aiming directly perpendicular to the plane of the thorax with the arm resting in neutral. Owing to the relative position of the scapular plane angled approximately 45  degrees anterior to the thorax, the result of the AP radiograph is an oblique view of the glenohumeral joint. Therefore, overlapping of the glenoid and humeral head is seen with this view, thereby limiting certain assessments for osseous involvement (Figure 7-1A). A true AP of the shoulder, other wise known as a Grashey view, is obtained by directing the x-ray beam 45  degrees medial to lateral. With this view in a reduced shoulder, there will be no overlap between the humeral head and glenoid (Figure  7-1B). The only structure that will overlap other structures is the coracoid process. Evidence of glenohumeral overlap is indicative of either a dislocation or an inadequate radiograph. In a normal shoulder, the contour of the anteroinferior glenoid will be clearly visible. Lack of clear visualization of the anterior glenoid sclerotic contour in an other wise well-executed radiograph suggests bone loss. In one study, Jankauskas et al found the Grashey view to be specific (100%) but not sensitive (54% to 65%) for detecting glenoid bone defects.9

Scapulolateral View Other wise known as a scapular-Y, tangential lateral, or Y lateral, the scapulolateral view aims to obtain an image along the axis of the scapular spine. This view is a true lateral of the glenohumeral joint and is helpful in determining displacement of the humeral head in conjunction with orthogonal views. In the case of an anterior dislocation, the humeral head will be found anterior to the glenoid, and vice versa for posterior dislocations. This view also can provide relative assessment of the approximate humeral head and glenoid contour.

The scapulolateral view can be obtained in a variety of ways. The patient is typically positioned upright with the affected shoulder against the image receptor. The patient is rotated 45 to 60 degrees oblique (toward the image receptor) until the body of the scapula is perpendicular both to the image receptor and the x-ray beam. If tolerated, the arm can be placed behind the patient’s back to allow superimposition of the humerus over the scapula. Alternatively, the arm may be allowed to hang free or rest in a sling.

Axillary Lateral and Modified Axillary Lateral Views The axillary lateral radiograph is the most crucial view required to confirm a reduced glenohumeral joint. This view is taken with the patient either supine or upright and the arm abducted 70 to 90 degrees. In the supine position, the x-ray beam is angled toward the axilla, aiming from caudad to cephalad (vice versa for the upright position). The articulation of the humeral head and glenoid are clearly visualized with this view. An adequate image of a normal shoulder is obtained when there is visible space between the glenoid and humeral head, and the superior and inferior edges of the glenoid are superimposed.10 Static instability is easily identified if the humeral head is displaced anterior or posterior to the glenoid, or if overlapping between the 2 structures is seen. Much like the Grashey view, lack of clear visibility of the anteroinferior glenoid outline suggests bone loss, and humeral head impaction fractures may also be visualized. An alternative to the axillary lateral is the modified axillary lateral, or Velpeau view. This view can be performed in the event that abduction of the shoulder is painful or poorly tolerated by the patient. The Velpeau view is obtained with the patient’s arm maintained in adduction within a sling. The patient is positioned upright, leaning back 20 to 30 degrees, or with a 20- to 30-degree wedge placed behind the back. The x-ray beam is placed over the top of the shoulder, aiming directly vertical from superior to inferior.

Radiographic and Advanced Imaging to Assess Anterior Glenohumeral Bone Loss

69

Figure 7-2. (A) Positioning for the Bernageau view.13 (B) Positioning for the modified Bernageau view,3 other wise known as the “television watching position.”

ADDITIONAL RADIOGRAPHIC VIEWS Additional special radiographs can be obtained to clarify various bony abnormalities associated with anterior shoulder instability. These views include the West Point axillary lateral, apical oblique view, Bernageau glenoid profile view, Stryker notch view, and an AP of the shoulder with humeral internal and external rotation.7

West Point View The West Point view was initially described by surgeons at the United States Military Academy in West Point, New York.11 This view is performed to identify large glenoid defects and humeral head subluxation. The technique involves the patient lying prone with the affected shoulder abducted to 90 degrees and resting on a pad elevated 8 cm. The x-ray beam is centered at the axilla, angled 25  degrees inferiorly, and 25 degrees medially, resulting in a tangential view of the anteroinferior glenoid rim. A cadaveric study by Itoi et al revealed the West Point view to be better than the axillary lateral view at identifying glenoid bone loss.8

Apical Oblique View The apical oblique, or Garth view, is used to visualize the anteroinferior and posterosuperior glenoid, as well as the posterolateral and anterior humeral head. This view is obtained with the patient sitting upright and the hand of the affected side resting on the unaffected shoulder. The x-ray beam is angled 30 to 45 degrees from medial to lateral and 45 degrees cephalad to caudad.12

Bernageau Glenoid Profile View Developed in 1976, the Bernageau glenoid profile radiograph was introduced to obtain a true view of the anteroinferior glenoid.13 The axillary lateral view often results in superimposition of the anteroinferior rim over the anterosuperior rim, making it difficult to assess for bone loss. To perform the Bernageau glenoid profile view, the patient is positioned upright with the shoulder abducted to at least 135  degrees and the hand resting on the head. The x-ray beam is directed along the axis of the scapular plane, angled 30 degrees caudal

(Figure 7-2A). However, positioning of the shoulder for this view may not be well tolerated in patients with acute pain or severe instability. Sugaya3 developed a modified Bernageau view that allows the patient to lie in a lateral recumbent position, with the affected shoulder toward the table and the arm abducted in a resting position, known as the “television watching position” (Figure 7-2B). With the Bernageau view, a normal shoulder will reveal a well-defined anterior osseous triangle with a sharp angle, whereas anterior bone loss can result in a rounded triangle (blunted angle sign) or complete loss of the triangle (cliff sign).14 The same view of the contralateral shoulder has been recommended for comparison.15 Multiple studies have found a high rate of intraobserver and interobserver reliability compared to other plain radiographs, and it was found to have a high rate of reliability when compared to CT.15,16 The Bernageau view has also been used to identify humeral head defects.17

Stryker Notch View The Stryker notch view is used to assess for humeral head defects, particularly of the posterolateral portion, which is common with anterior glenohumeral instability. This view is especially helpful when Hill-Sachs lesions are not readily visualized on other standard orthogonal imaging. The patient is supine with the hand of the affected side resting palm down on the forehead, with the fingers facing cephalad and the elbow directed anterior. The x-ray beam is centered over the coracoid process and directed 10 degrees cephalad.

Humeral Internal and External Rotation Views An AP radiograph with the humerus internally rotated is one of the most common plain radiographs used to show impaction fractures of the posterolateral humeral head, or Hill-Sachs lesions.2 The humeral external rotation view can be included for further visualization of the proximal humerus. These views outline the profile of the greater tuberosity. In cases of large Hill-Sachs defects, anterior extension of the compression defect may be seen with this view. The patient is seated upright with the affected humerus externally rotated and the x-ray beam placed as with an AP radiograph.

70

Chapter 7

Figure 7-3. An axial fat-suppressed (FS) T2-weighted proton density (PD) fast spin- echo (FSE) sequence is the most sensitive for visualizing labral tears, labral cysts, and glenoid or humeral articular cartilage. This image reveals an obvious anterior glenolabral defect consistent with anterior glenohumeral instability. (Copyright BRW, printed with permission.)

MAGNETIC RESONANCE IMAGING MRI is a common imaging modality used for assessing anterior shoulder instability. It affords the most comprehensive visualization of soft-tissue structures and identification of pathology, with the most commonly involved structures being the anterior labrum, anterior capsule, and the anterior band of the inferior glenohumeral ligament (aIGHL).18 Owing to the small size and complexity of the structures in the shoulder, a high-resolution image is required with various 2-dimensional (2D) sequences, in-plane resolution of at least 0.5 mm, and slice thicknesses of 1 to 3 mm.19 The most commonly available MRI strength is 1.5-Tesla (T), which refers to the strength of the magnetic field. However, more institutions are acquiring 3-T (or greater) MRIs, which operate at twice the strength with a greater signal-to-noise ratio, allowing for higher-quality images. Musculoskeletal imaging protocols were developed to enhance visualization of this complex anatomy. These protocols vary by institution based on the field strength of the available MRI magnet, radiologist preference, time availability, and patient factors such as anxiety level or presence of metal implants.20 Absolute contraindications to MRI include patients with implanted devices that are not compatible with MRI such as pacemakers, spinal stimulators, and cochlear implants, patients with intraocular metallic foreign bodies, and unstable patients requiring resuscitative equipment. Relative contraindications include patients with severe claustrophobia, agitation, or movement disorders resulting in the

inability to lie still. These patients may require assistance with anxiolytics or sedation. Conventional MRI shoulder protocols consist of variable sequences in the oblique axial, coronal, and sagittal planes. It is important for these planes to be parallel to the glenohumeral joint rather than the thorax to avoid inadequate visualization from poorly cut images. Each plane is distinctively useful for evaluating dif ferent structures.20,21 The axial plane displays anterior and posterior capsulolabral anatomy, the subscapularis tendon, and the biceps-labral complex with the long head of the biceps tendon in the bicipital groove. The sagittal oblique plane affords an en face view of the glenoid articular surface, the relationship of the capsulolabral complex, acromial anatomy and its associated ligaments, and the rotator cuff tendons as they travel out to their attachment on the greater tuberosity. In the case of recurrent instability, the sagittal oblique view may reveal attritional bone loss of the anteroinferior glenoid face, resulting in a so-called “invertedpear” appearance.22 The coronal oblique plane best defines the superior labrum, anchor of the long head of the biceps, and posterosuperior rotator cuff. A patulous inferior capsule may be visualized suggesting underlying hyperlaxity, though this may be difficult to discern without the addition of intraarticular contrast. Coronal images often will underestimate the size of a bony Bankart lesion.21 Various imaging sequences are used to enhance dif ferent structures. The sequences are defined by the tissue relaxation times, or the time it takes for excited protons to either return to equilibrium (T1-weighted image) or go out of phase with each other (T2-weighted image) as it reacts to the magnetic field. T1-weighted images have the best spatial resolution and reveal subcutaneous fat and bone marrow as bright white, whereas liquids (joint fluid) and solids (cortical bone) are dark. T2-weighted images reveal fluids such as joint effusions and bone or muscle edema as bright, making them more sensitive to pathology than T1-weighted images, but with less clarity. Subsequently developed was a T2-weighted proton density (PD) fast spin-echo (FSE) sequence coupled with a fat-suppression (FS) technique, such as short T1 inversion recovery (STIR) or a fat-saturation pulse. An FS PD FSE sequence in the axial plane is most sensitive for identifying small paralabral cysts and subtle articular cartilage labral tears (Figure 7-3). FS T1-weighted images are ideal for viewing the labrum at high resolution. Additionally, various chondral mapping techniques are available when indicated, like T1 ρ and T2 mapping with post-processing and color.21 Understanding the nature of the soft-tissue injury is crucial for guiding treatment because more than one structure is typically involved. There are multiple types of anterior labral pathology that vary based on chronicity, degree of displacement, and involvement of the scapular periosteum, aIGHL, bony glenoid rim, or the glenoid articular cartilage.21 Acute bony injuries will reveal increased signal intensity in the glenoid on FS T2-weighted images with a bony fragment, whereas chronic injuries might result in bony attrition without edema or a medialized lesion that is adherent along the

Radiographic and Advanced Imaging to Assess Anterior Glenohumeral Bone Loss glenoid neck. The aIGHL is most frequently detached from its glenoid insertion in the majority of cases with primary anterior instability. However, occasionally it can detach from its humeral insertion, resulting in what is known as a humeral avulsion of the glenohumeral ligament (HAGL). These lesions often do not present alone and can easily be missed on MRI, particularly without intra-articular contrast.23 They require a high index of clinical suspicion particularly after a previously failed labral repair surgery because the instability recurrence rate with a neglected HAGL can reach 90%.24 Additionally, it is impor tant to recognize normal variants of the anterior labrum and glenohumeral ligament complex. These normal variants include a sublabral foramen, sublabral recess, and a thickened middle glenohumeral ligament (MGHL) with absent anterosuperior labrum, other wise known as a Buford complex. Though less common in younger athletes, damage to the rotator cuff can occur with higher prevalence in certain populations. This may include patients older than 40 years, contact or overhead athletes, or those with a nerve injury after dislocation.25 The most commonly involved portion of the rotator cuff is the subscapularis and posterosuperior rotator cuff. Positioning of the shoulder during the MRI procedure is crucial because internal rotation of the shoulder can result in the anterior structures appearing lax and ill defined. Conversely, extreme external rotation makes it difficult to assess the path of the biceps tendon. Ideal positioning of the shoulder is in neutral or slight external rotation.21 In some instances, positioning the shoulder in abduction and external rotation (ABER) during the MRI can help to reveal nondisplaced labral tears such as with Perthes lesions. This technique is often used in conjunction with MRA for better visualization, although it has also been described without the use of gadolinium with a sensitivity and specificity of 94% and 82%, respectively.26 The ABER position tensions the aIGHL and peels the torn labrum away from the glenoid. This view can also be useful for identifying partial-thickness rotator cuff tears. Although conventional MRI is superior for visualization of soft-tissue structures, it traditionally has not been favored for the assessment of bony pathology. Many practitioners have recommended CT imaging to characterize and quantify bone loss because CT is considered the gold standard in assessing osseous deficits. However, MRI has been gaining traction as advancing techniques have emerged. One such technique creates 3D MRI reconstructions that are similar in quality to 3D reconstructions from CT.20,27,28 The 3D reconstruction is formed from a 3D, dual-echo time, T1weighted fast low-angle shot (FLASH) sequence coupled with a fat-suppression technique known as the Dixon method. This sequencing technique creates a water-only image that is then processed using subtraction software to isolate only the osseous structures. Another sequencing technique developed to formulate a 3D image is an isotropic volumetric interpolated breath-hold examination (VIBE) with a water

71

excitation sequence using a dedicated shoulder coil and subsequent post-processing software.29 Comparison studies have shown the 3D FLASH Dixon sequence to be as accurate as CT.20,27 Quantitative measurements for quantifying glenoid bone loss have been developed for 3D MRI and are similar to techniques used for 3D CT (see further details in the section “Computed Tomography and Magnetic Resonance Imaging Measurements”).20,27,30 Recently, this sequencing technique has been used to assess osseous pathology of other joints, such as the hip in femoroacetabular impingement.31 Advantages of 3D MRI are elimination of the time, cost, and radiation required for obtaining a CT scan. Disadvantages of 3D MRI include the separate software and specialized skill set required by radiologists, which may not be feasible or readily available at some institutions.

MAGNETIC RESONANCE ARTHROGRAPHY There continues to be debate about whether intra-articular contrast enhancement is required for appropriate visualization of capsulolabral detail during MRI. Magnetic resonance arthrography (MRA) involves a diluted paramagnetic gadolinium-based contrast agent that is injected into the glenohumeral joint by a radiologist and used to outline the labrum, capsule, and rotator cuff with increased sensitivity compared with MRI.32 Saline has also been described as an alternative injection agent.33 Furthermore, a hemarthrosis in the setting of an acute injury may be sufficient alone to elucidate capsulolabral pathology. The distension afforded by the additional fluid provides improved detail of the glenohumeral ligaments, and it can place the labrum under tension so that chondrolabral separation is more apparent. In a comparison of conventional 3T MRI to MRA, one study revealed statistically significant increased sensitivity for the detection of partial-thickness rotator cuff tears, anterior labral tears, and superior labral tears with MRA.34 Subtle HAGL lesions are also more readily visible with the addition of intra-articular contrast.18 However, some authors argue that MRA is not necessary if a properly optimized MRI with high signal-to-noise and good spatial resolution is obtained.21 Notably, none of the commercially available gadoliniumbased contrast agents are approved for intra-articular use by the US Food and Drug Administration. Therefore, MRA is still considered to be an off-label procedure.35 Despite this, MRA with gadolinium is generally considered safe within the musculoskeletal radiology community. Adverse effects of MRA with gadolinium, based primarily on case reports, include local pain, reaction to the contrast, septic arthritis, synovitis or adhesive capsulitis, extra-articular placement or extravasation, improper needle placement resulting in local neurovascular injury, or poor visualization due to improper dilution.19,36-38 Most systemic adverse effects have been described from intravenous administration rather than intra-articular use; these include nephrogenic systemic fibrosis, tissue gadolinium deposition, and anaphylactoid systemic reactions.35

72

Chapter 7

Figure 7-4. (A) Oblique sagittal cut of a computed tomography (CT) of the shoulder, revealing an en face view of the glenoid with a bony Bankart lesion. (B) Three- dimensional (3D) CT reconstruction with scapulothoracic subtraction demonstrating a Hill-Sachs lesion. (C) 3D CT reconstruction with humeral subtraction demonstrating a bony Bankart lesion and an overlay of the glenoid track calculation.63 The red vertical line represents the long axis of the glenoid. The red circle is a best-fit circle representing the normal shape of the glenoid. The purple double-arrow line represents the normal width of the glenoid track, which is 83% of the best-fit circle, correlating to normal glenoid width without a bony defect. The green dotted line represents the glenoid defect (d). The blue double-arrow line represents the glenoid track incorporating the glenoid defect, which is calculated to be 83% - d. (Copyright BRW, printed with permission.)

COMPUTED TOMOGRAPHY AND 3-DIMENSIONAL RECONSTRUCTION CT with 3D reconstruction is currently considered the gold standard for identifying bony detail and quantifying bone loss in the setting of recurrent anterior shoulder instability.3 A systematic review comparing advanced imaging modalities revealed the greatest accuracy with CT and 3D reconstruction.39 CT images are formulated by multiple x-rays taken circumferentially around the body and subsequently formulated into a grayscale matrix. Denser materials, like bone, will appear brighter and clearer, whereas lessdense materials, like muscle and labral tissue, will appear darker and with less clarity. Therefore, unlike MRI, CT cannot adequately assess soft-tissue structures because of limited spatial resolution. Conventional CT shoulder protocols are obtained in the axial, coronal, and sagittal planes. The axial views can be used to help quantify the amount of glenoid bone loss or the extent of humeral head impaction. Oblique sagittal cuts are useful if aligned appropriately so that the cuts of the glenoid are seen en face (Figure 7-4). However, oblique sagittal cuts are often not included in a standard shoulder CT and must be requested. Additionally, requesting thin cuts is highly recommended for better assessment of bone loss. Originally described arthroscopically by Lo et  al,22 the inverted-pear shape can be viewed on sagittal oblique sequences with 3D reconstruction, which is indicative of 25% to 27% bone loss. Similar to 3D MRI, 3D CT requires specific software and additional steps to reconstruct the 2D image. 3D reconstruction provides better conceptualization of bony defects when compared to 2D imaging.27 Requesting humeral head subtraction is crucial for better visualization of the glenoid, and vice versa for assessing humeral head defects (Figure  7-4).

Multiple measurement techniques have been developed for the glenoid and humeral head (see further details in the section “Computed Tomography and Magnetic Resonance Imaging Measurements”). CT arthrography can be used as an alternative for patients with a contraindication to MRI.18 This imaging modality can more effectively visualize the labrum and capsule, but other soft-tissue structures such as the rotator cuff may not be readily identified with this technique. One absolute contraindication to CT is pregnancy. The most prominent disadvantages of CT with or without 3D reconstruction are cost, additional post-scan processing, and radiation exposure. More than two-thirds of radiation exposure in the United States is attributed to CT alone.40 Radiation dose–reduction protocols for musculoskeletal imaging have been implemented at some institutions with evidence of significantly decreased radiation and maintained image quality.41

GLENOID BONE LOSS MEASURING METHODS There are multiple measurement techniques that have been described to calculate glenoid bone loss using CT or MRI. These methods can best be categorized as width techniques and best-fit circle techniques (Table 7-1).39 To date, no certain method is considered the gold standard for quantifying glenoid bone loss.

Best-Fit Circle Methods Nofsinger et  al49 performed an anatomic study on 3D reconstructions of normal and abnormal glenoids and confirmed that the inferior portion of a normal glenoid is a

Radiographic and Advanced Imaging to Assess Anterior Glenohumeral Bone Loss near-perfect circle. The best-fit circle method uses either 3D reconstruction of the glenoid with humeral head subtraction or a 2D oblique sagittal view of the glenoid surface. Huijsmans and colleagues48 and Gyftopolous et  al27 found that this technique can also be performed using MRI with similar accuracy to 3D CT. A symmetric circle is drawn to best fit the inferior two-thirds of the glenoid, using the intact posteroinferior aspect of the glenoid. The percentage of anterior bone loss can then be determined by measuring and dividing the amount of bone loss by the total surface area of the circle. The measurement can also be expressed as the amount of width lost from anterior to posterior. The thresholds of the surface area calculation vs the circle width loss calculation can be different, so it is important to be aware of which calculation is being used.39 The Pico method requires CT imaging of the uninjured shoulder and uses the best-fit circle method on both the affected and the unaffected shoulders.46 The bony deficit of the affected shoulder is calculated based on a percentage of the unaffected shoulder’s best-fit circle. The Sugaya method outlines and measures a bony Bankart and compares it to the best-fit circle drawn on the ipsilateral glenoid.3 However, this method is limited only to acute injuries and cannot be used for attritional bone loss. Furthermore, Dumont et al47 devised an arc angle technique using the best-fit circle and creating an angle based on the area of anterior bone loss. An equation to calculate the surface area or a conversion chart can be used to determine the percentage of bone loss based on the size of the arc angle.

Width Measurement Methods The glenoid rim distance method uses CT to measure the distance between the bare spot of the glenoid to anterior rim (distance A) and posterior rim (distance B). These measurements are then calculated to determine the amount of anterior bone loss using the following equation: Bone loss = ([B – A]/2B) × 100%. The glenoid rim distance method has also been described arthroscopically.42 The glenoid index technique uses 2D oblique sagittal CT or 3D reconstruction of both shoulders, where the ratio of the maximum diameter of both lower two-third glenoids is compared. A glenoid index of less than 0.75 correlates to a 25% glenoid bony deficit.43 The width-length ratio measures the maximal glenoid height and width on the en face view of a normal glenoid on 2D or 3D CT and compares the measurements to the affected glenoid. The height is determined by drawing a line superiorly from a point at the posterior aspect of the coracoid base down bisecting the theoretical middle of the inferior glenoid. The width is determined by drawing a line perpendicular to the height line, at the widest portion of the inferior circle.44 Another glenoid width measurement technique by Owens and colleagues,45 referred to as the West Point Measure, uses MRI of the ipsilateral shoulder and sex-specific formulas created by a linear regression analysis of the en face glenoid

73

Table 7-1. Glenoid Bone Loss Measurement Methods WIDTH TECHNIQUES Glenoid rim distance42 Glenoid index43 Width-length ratio44 West Point measurement45

BEST-FIT CIRCLE TECHNIQUES Pico method46 Sugaya method3 Dumont arc angle method47 MRI methods27,48

Abbreviation: MRI, magnetic resonance imaging. Summary of most common glenoid bone loss measurement methods, divided into width techniques and best-fit circle techniques.

height and width of 1264 male and female shoulders. Their evaluation found significant differences between male and female glenoids, but a similar relationship between glenoid height and width. After measuring glenoid height and width on the most lateral cut of a sagittal oblique MRI, the formula to use for a male patient is Glenoid width = (1/3 height) + 15 mm. Similarly, the formula to use for a female patient is Glenoid width = (1/3 height) + 13 mm.

Comparison of Glenoid Measurement Techniques A systematic review comparing various measurement techniques for the glenoid using radiography, CT, and MRI revealed that the Pico and glenoid index methods were both the most accurate, especially when 3D reconstruction imaging was used.39 A laboratory study by Bois et al44 determined that 3D measurements demonstrated better accuracy and agreement than 2D measurements. They found that the glenoid index and width-length ratio 2D measurements consistently underestimated bone loss, which they attributed to difficulty in choosing the correct image cut and identifying 3D landmarks in a 2D plane. They did determine the Pico method to be the most reliable and accurate with 3D CT. However, Bhatia and colleagues50 found that best-fit circle methods tended to overestimate the amount of bone loss a mean of 3.9% ± 1.9%, with the greatest error occurring when the true glenoid defect width approached 20%. Moreover, Moroder et al51 noted significant alteration in measurement with any tilt of the en face glenoid view. They concluded that scapular positioning frequently can affect the result of glenoid bone loss measurement. Bakshi et  al52 compared arthroscopic estimation with surface area, Pico, ratio, and anteroposterior distance-from-bare area methods using 3D CT and found the arthroscopic methods significantly overestimated glenoid bone loss, whereas the other methods were much more accurate. A major drawback to the measurement techniques requiring CT imaging of the contralateral shoulder is the added radiation burden. Additionally, there is added cost at some institutions where both shoulders are not automatically

74

Chapter 7

included in the study. A prospective cohort by Milano et al53 compared the assessment of glenoid bone defects with and without comparison of the contralateral shoulder and found no difference in measurement outcome, indicating that comparison CT scans are not required.

HUMERAL BONE LOSS MEASURING METHODS Assessment of the Hill-Sachs lesion is highly variable and controversial, resulting in the lack of a gold-standard measurement and definitive treatment recommendations. Many authors have attempted to determine the most impor tant factor resulting in engagement of a Hill-Sachs, including size, depth, volume, orientation, and location.39,54 Measurements using radiography, CT, and MRI have been used to measure humeral bone loss, but these methods are not as well studied as with the glenoid.

Radiographic Measurements Kralinger et  al17 described the Hill-Sachs quotient technique, using a Grashey view of the shoulder with the humerus in 60 degrees of internal rotation to measure depth and width, and a Bernageau view to measure length of the Hill-Sachs. Another measurement that uses a Grashey view with humeral internal rotation calculates a ratio based on the depth of the Hill-Sachs lesion and the radius of the humeral head. Taken in sum, multiple studies have found reasonable reliability.55,56

Computed Tomography and Magnetic Resonance Imaging Measurements Kodali and colleagues57 described a method using 2D CT to measure the size of a Hill-Sachs lesion. The technique calls for a best-fit circle drawn around the humeral head in the axial, sagittal, and coronal planes. The bony defect is measured in each plane using the circle’s periphery. They found that the greatest accuracy in measurement was with the axial cuts, but still with a 14% error. Alternatively, other authors measured the Hill-Sachs lesion using only the axial cuts of CT or MRI with the largest defect.39,58,59 Stillwater et al29 described a humeral head–measurement technique using 3D osseous reformats from MRI. They isolated the humerus via scapular subtraction and used a sagittal-medial projection, resulting in an en face view of the humeral articular surface. One line was drawn parallel to the Hill-Sachs lesion to determine maximum humeral head height (A). A second line was drawn perpendicular to determine residual humeral head width (B). Assuming the humeral head is a perfect circle, they were able to calculate the percentage of humeral head bone loss via the equation [(A – B/A)*100].

THE GLENOID TRACK AND EVALUATION OF BIPOLAR BONE LOSS A large number of patients with anterior glenohumeral instability have simultaneous bone loss of the glenoid and humeral head, other wise known as a bipolar lesion.60,61 Historically, the focus has centered on glenoid bone loss for assessment and treatment of anterior instability, with humeral head impaction fractures separately considered and to a certain extent, largely neglected. Traditionally, it was thought that a humeral impaction fracture involving less than 20% of the humeral head was not clinically significant, whereas more than 40% involvement nearly always resulted in recurrent dislocations.4 There continues to be a lack of consensus on the critical size threshold of humeral head loss warranting surgical intervention. The issue with using static, isolated quantification of humeral head impaction fractures to determine treatment is that the interaction with the glenoid and other surrounding structures are ignored, making it difficult to determine its clinical significance. The earliest discussion on the interplay between the Hill-Sachs lesion and glenoid was in 2000 by Burkhart and De Beer.62 They were the first to dynamically assess the Hill-Sachs lesion arthroscopically and coined the term “engaging Hill-Sachs” if a dislocation occurred while the arm was in a position of athletic function, or in abduction and external rotation. Likewise, a Hill-Sachs lesion that did not result in dislocation while in that position was called a “non-engaging Hill-Sachs.” The phenomenon of bipolar bone loss has become a subject of controversy in more recent years. Assessment of humeral head impaction fractures and how they interact with glenoid bone loss is an additional consideration on directing humeral- and glenoid-sided treatment. The concept of the glenoid track was originally described in 2007 by Yamamoto et al60 in a cadaveric study. It is defined as the zone of contact between the glenoid and humeral head during normal range of motion. They found that with increased shoulder abduction, the glenoid contact shifted from the inferomedial to the superolateral area of the humeral head. They further defined this zone of contact by measuring the distance between the contact area to the footprint of the rotator cuff in varying degrees of abduction. They determined that the medial aspect of the glenoid track was located approximately 18.4  mm medial from the rotator cuff footprint, and was equivalent to approximately 84% of the glenoid width as the remaining portion of the glenoid width pushes against the rotator cuff attachment with increased external rotation and abduction (see Figure  7-4C). Their suspicion was that humeral head impaction fractures that extend beyond the medial margin of the glenoid track have a much higher risk of engaging. Contrary to prior classifications, this theory shows that length and depth of a Hill-Sachs lesion are not impor tant in determining engagement, but rather its location and orientation. Additionally, they determined that the

Radiographic and Advanced Imaging to Assess Anterior Glenohumeral Bone Loss width of the glenoid track was based solely on the width of the glenoid. Therefore, the risk of humeral head engagement and secondary glenohumeral dislocation is seemingly higher in the face of glenoid bone loss, particularly as the size of the glenoid track decreases. This concept was further studied by Di Giacomo and colleagues,63 who developed a radiographic and arthroscopic method of assessing bipolar lesions known as the on-track off-track method. They used the principles of the glenoid track and 3D CT for their radiographic measurements, which were validated by multiple clinical studies thereafter (see Figure  7-4C).30,64,65 Locher and colleagues64 retrospectively evaluated preoperative imaging of 100 patients who were previously managed with arthroscopic stabilization. They found a higher revision rate in patients with an off-track Hill-Sachs lesion (33%) than in patients with an on-track lesion (6%) and an odds ratio of 8.3. Gyftopolous et al30 assessed the on-track off-track method using MRI and found an overall accuracy of 84.2%. Furthermore, Shaha et al65 used MRI measurements to apply the glenoid track concept to 57 shoulders, noting a significantly higher revision rate with off-track lesions than with on-track lesions (75% vs 8%, respectively). Additionally, they determined the off-track measurement to have a higher positive predictive value than a glenoid bone loss of greater than 20% (75% vs 44%, respectively). Another study looking at the reliability and reproducibility of assessing the glenoid track found good interobserver and intraobserver agreement (94% and 96%, respectively) regarding linear bone loss of the glenoid, but higher variability and poor interobserver reliability with evaluation of Hill-Sachs lesions. Subsequently, there was found to be poor interobserver reliability with regard to on-track or off-track classification at 72%, whereas intraobserver reliability had less-variable results (80% to 90%).66 The concept of the glenoid track and supportive studies have revealed that bipolar lesions should be assessed with a critical eye rather than relying solely on concrete published thresholds because there is great variability in the pathology that results in instability. A biomechanical cadaveric study by Arciero and colleagues67 displayed the potentiation effect of combined glenoid and humeral bony deficiencies, finding that the risk of capsulolabral repair failure exists with small amounts of glenoid bone loss. They found that bony Bankart lesions as small as 2  mm can compromise a soft-tissue capsulolabral repair in the presence of a small (0.87  cm3) or medium-sized (1.47  cm3) Hill-Sachs lesion. Similarly, Gottschalk et al68 confirmed with their cadaveric study that bipolar lesions may require bony reconstruction for defect sizes smaller than what would other wise be indicated for defects in isolation.

75

Table 7-2. Risk Factors Associated With Recurrence of Instability71 Age < 20 y Competitive level of sport Contact or overhead sport type Shoulder hyperlaxity Hill-Sachs lesion visible on AP external rotation plain radiograph Loss of glenoid contour on AP plain radiograph Abbreviation: AP, anteroposterior. Risk factors associated with increased risk of recurrence following arthroscopic repair, as initially described by Balg and Boileau71 for the Instability Severity Index Score.

PUTTING IT TOGETHER: TREATMENT ALGORITHM FOR ANTERIOR GLENOHUMERAL INSTABILITY In recent years, the pendulum has swung from nonoperative management toward early surgical stabilization for athletes after a first-time anterior glenohumeral dislocation, as high failure rates and worse cost-effectiveness have been documented with conservative care alone.69,70 Despite this, there continues to be a lack of consensus on the optimal treatment strategy. A recent prospective cohort study by Dickens et al69 found the range of glenoid bone loss after a single first-time dislocation to range from 6.8% to 13.5%, which likely is contributing to the high failure rates of nonsurgical treatment. Additional factors that place a first-time dislocator at risk for continued instability include age younger than 20 years, male sex, engagement in contact or overhead sport, and evidence of hyperlaxity.18,71 Moreover, patients with these risk factors and a history of multiple dislocations have a higher risk of postoperative instability when compared to patients who undergo surgery after a single dislocation (62% vs 29%, respectively).72 For the contact or upper extremity athlete with primary or recurrent instability that has failed nonoperative management, surgical intervention is indicated. Multiple factors need to be taken into consideration when deciding the most appropriate surgical procedure. Appropriate surgical timing must also be considered for the in-season athlete.70 Proper patient selection and the recognition of glenohumeral bone loss are the most impor tant factors involved in minimizing surgical failure. Balg and Boileau developed an Instability Severity Index (ISI) based on patient factors known to increase the risk of arthroscopic surgical failure (Table 7-2).71 Points are applied based on the presence of each risk factor, and they found that patients who scored greater than 6 points were at higher risk of failing arthroscopic repair. Later studies have validated ISI to be an effective tool for preoperative

76

Chapter 7

planning, but suggest that the threshold may be even lower (> 2).73,74 Conversely, a recent study of the active military population found no correlation between ISI score and rates of instability after arthroscopic stabilization.75 Traditional recommendations proposed arthroscopic repair for glenolabral injuries with less than 20% of bone loss, whereas those with bone loss of more than 20% to 25% should be considered for an anterior glenoid bony augmentation procedure, such as a coracoid transfer (ie, modified Latarjet procedure) or other bone graft (ie, fresh distal tibial allograft, tricortical iliac crest, or distal clavicle autograft).18,60,61 However, these higher thresholds for bone loss are now being increasingly challenged. More recent research suggests that even smaller amounts of bone loss can result in continued instability and suboptimal patient-reported outcomes after arthroscopic soft-tissue repair in some populations.76,77 One study by Shin and colleagues76 quoted 17.3% as the optimal critical value of bone loss resulting in recurrent instability after arthroscopic repair. Glenoid bone loss as low as 13.5% has recently been described as a subcritical threshold for recurrent instability with soft-tissue repair in an active military population.77 Lansdown et al78 found that a flat anterior glenoid, determined by drawing a vertical line along the superior to inferior anterior glenoid on an en face view of a 3D reconstructed glenoid, correlates to 12.8 ± 3% of bony deficiency, which can be used to efficiently detect subcritical bone loss. In the absence of an acute or discreet bony Bankart fragment, the senior author (B.R.W.) uses a 15% threshold for surgical decision making with anterior glenoid loss in high-risk and/or athletic subsets. Regarding the treatment algorithm for the Hill-Sachs lesion, the concept of the glenoid track has shifted the focus more on its location and how it interacts with the glenoid rather than its absolute size. Based on the recommendations of Di Giacomo et al,63 a Hill-Sachs lesion can be left alone if it is on-track regardless of glenoid bony defect size, and the glenoid should be treated based on previously mentioned recommendations. If a Hill-Sachs lesion is off-track with a subcritical glenoid bony defect, concomitant arthroscopic Bankart repair and remplissage with infraspinatus capsulodesis are recommended for most patients. In patients with an off-track Hill-Sachs lesion and greater degrees of glenoid bone loss (> 15% to 20%), surgeons may preferentially consider a Latarjet procedure or anterior glenoid bone block reconstruction with or without remplissage based on modified calculations of the glenoid track that account for bone block augmentation.

CONCLUSION The recognition of glenohumeral bone loss in the setting of anterior instability is paramount for avoiding surgical failure. A thorough radiographic evaluation to accurately quantify the amount of bone loss, coupled with evaluation of its dynamic interplay via the glenoid track, is crucial for

guiding treatment. The development of the on-track vs offtrack classification system has proven useful with regard to addressing bipolar bone loss. Recent research is proving the classic critical threshold of 20% to 25% for treating glenoid bone loss to be inaccurate in the setting of bipolar bone loss. The technical advancements in MRI, particularly with 3D reconstruction software, are promising and continue to be refined with the hope of being able to decrease the cost, radiation, and time constraints associated with additional imaging from CT.

ACKNOWLEDGMENTS Thank you to Stephen and Dara for their assistance in photography.

REFERENCES 1.

2.

3. 4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

Owens BD, Agel J, Mountcastle SB, Cameron KL, Nelson BJ. Incidence of glenohumeral instability in collegiate athletics. Am J Sports Med. 2009;37(9):1750-1754. doi:10.1177/0363546509334591. Anakwenze O, Hsu JE, Abboud JA, Levine WN, Huffman GR. Recurrent anterior shoulder instability associated with bony defects. Orthopedics. 2011;34(7):538-544. doi:10.3928/01477447-20110526-21. Sugaya  H. Techniques to evaluate glenoid bone loss. Curr Rev Musculoskelet Med. 2014;7(1):1-5. doi:10.1007/s12178-013-9198-3. Provencher MT, Frank RM, Leclere LE, et al. The Hill-Sachs lesion: diagnosis, classification, and management. J Am Acad Orthop Surg. 2012;20(4):242-252. doi:10.5435/JAAOS-20-04-242. Trivedi S, Pomerantz ML, Gross D, Golijanan P, Provencher MT. Shoulder instability in the setting of bipolar (glenoid and humeral head) bone loss: the glenoid track concept. Clin Orthop Relat Res. 2014;472(8):2352-2362. doi:10.1007/s11999-014-3589-7. Gil JA, DeFroda S, Owens BD. Current concepts in the diagnosis and management of traumatic, anterior glenohumeral subluxations. Orthop J Sports Med. 2017;5(3):2325967117694338. doi:10.1177/2325967117694338. Jensen KL, Tirman P, Rockwood CA. Radiographic evaluation of shoulder problems. In: Matsen F, Lippitt S, eds. Rockwood and Matsen’s The Shoulder. 5th ed. Philadelphia, PA: Elsevier; 2017:135-168. Itoi E, Lee SB, Amrami KK, Wenger DE, An KN. Quantitative assessment of classic anteroinferior bony Bankart lesions by radiography and computed tomography. Am J Sports Med. 2003;31(1):112-118. do i:10.1177/03635465030310010301. Jankauskas L, Rüdiger HA, Pfirrmann CW, Jost B, Gerber C. Loss of the sclerotic line of the glenoid on anteroposterior radiographs of the shoulder: a diagnostic sign for an osseous defect of the anterior glenoid rim. J Shoulder Elbow Surg. 2010;19(1):151-156. doi:10.1016/j. jse.2009.04.013. Richards B, Riley J, Saithna A. Improving the diagnostic quality and adequacy of shoulder radiographs in a district general hospital. BMJ Qual Improv Rep. 2016;5(1). doi:10.1136/bmjquality.u209855.w3501. Rokous JR, Feagin JA, Abbott HG. Modified axillary roentgenogram: a useful adjunct in the diagnosis of recurrent instability of the shoulder. Clin Orthop Relat Res. 1972;82:84-86. Garth WP Jr, Slappey CE, Ochs CW. Roentgenographic demonstration of instability of the shoulder: the apical oblique projection. A technical note. J Bone Joint Surg Am. 1984;66(9):1450-1453. Bernageau J, Patte D, Debeyre J, Ferrane J. Value of the glenoid profile in recurrent luxations of the shoulder [article in French]. Rev Chir Orthop Reparatrice Appar Mot. 1976;62(2 suppl):142-147.

Radiographic and Advanced Imaging to Assess Anterior Glenohumeral Bone Loss 14.

15.

16.

17.

18.

19.

20.

21.

22.

23.

24.

25.

26.

27.

28.

29.

30.

31.

Edwards TB, Boulahia A, Walch  G. Radiographic analysis of bone defects in chronic anterior shoulder instability. Arthroscopy. 2003;19(7):732-739. doi:10.1016/s0749-8063(03)00684-4. Pansard E, Klouche S, Billot N, et al. Reliability and validity assessment of a glenoid bone loss measurement using the Bernageau profile view in chronic anterior shoulder instability. J  Shoulder Elbow Surg. 2013;22(9):1193-1198. doi:10.1016/j.jse.2012.12.032. Murachovsky J, Bueno RS, Nascimento LG, et al. Calculating anterior glenoid bone loss using the Bernageau profile view. Skeletal Radiol. 2012;41(10):1231-1237. doi:10.1007/s00256-012-1439-9. Kralinger FS, Golser K, Wischatta R, Wambacher M, Sperner  G. Predicting recurrence after primary anterior shoulder dislocation. Am J Sports Med. 2002;30(1):116-120. doi:10.1177/0363546502030 0010501. Streubel PN, Krych AJ, Simone JP, et al. Anterior glenohumeral instability: a pathology-based treatment strategy. J Am Acad Orthop Surg. 2014;22(5):283-294. doi:10.5435/JAAOS-22-05-283. Lejay H, Holland BA. Technical advances in musculoskeletal imaging. In: Stoller DW, ed. Magnetic Resonance Imaging in Orthopaedics and Sports Medicine. 3rd  ed. Philadelphia, PA: Lippincott Williams and Wilkins; 2007:1-28. Gottsegen CJ, Merkle AN, Bencardino JT, Gyftopolous S. Advanced MRI techniques of the shoulder joint: current applications in clinical practice. AJR Am J Roentgenol. 2017;209(3):544-551. doi:10.2214/ AJR.17.17945. Stoller DW, Wolf EM, Li AE, et al. The shoulder. In: Stoller DW, ed. Magnetic Resonance Imaging in Orthopaedics and Sports Medicine. 3rd  ed. Philadelphia, PA: Lippincott Williams and Wilkins; 2007:1131-1461. Lo IK, Parten PM, Burkhart SS. The inverted pear glenoid: an indicator of significant bone loss. Arthroscopy. 2004;20(2):169-174. doi:10.1016/j.arthro.2003.11.036. Bozzo A, Oitment C, Thornley P, et  al. Humeral avulsion of the glenohumeral ligament: indications for surgical treatment and outcomes—a systematic review. Orthop J Sports Med. 2017;5(8):2325967117723329. doi:10.1177/2325967117723329. Longo UG, Rizzello G, Ciuffreda M, et  al. Humeral avulsion of the glenohumeral ligaments: a systematic review. Arthroscopy. 2016;32(9):1868-1876. doi:10.1016/j.arthro.2016.03.009. Gombera MM, Sekiya JK. Rotator cuff tear and glenohumeral instability: a systematic review. Clin Orthop Relat Res. 2014;472(8):24482456. doi:10.1007/s11999-013-3290-2. Takubo Y, Horii M, Kurokawa M, Mikami Y, Tokunaga D, Kubo T. Magnetic resonance imaging evaluation of the inferior glenohumeral ligament: non-arthrographic imaging in abduction and external rotation. J  Shoulder Elbow Surg. 2005;14(5):511-515. doi:10.1016/j. jse.2005.02.015. Gyftopolous S, Beltran LS, Yemin A, et al. Use of 3D MR reconstructions in the evaluation of glenoid bone loss: a clinical study. Skeletal Radiol. 2014;43(2):213-218. doi:10.1007/s00256-013-1774-5. Naraghi A, White LM. Three-dimensional MRI of the musculoskeletal system. AJR Am J Roentgenol. 2012;199(3):W283-W293. doi:10.2214/AJR.12.9099. Stillwater L, Koenig J, Maycher B, Davidson M. 3D-MR vs. 3D-CT of the shoulder in patients with glenohumeral instability. Skeletal Radiol. 2017;46(3):325-331. doi:10.1007/s00256-016-2559-4. Gyftopolous S, Beltran L, Bookman J, Rokito A. MRI evaluation of bipolar bone loss using the on-track off-track method: a feasibility study. AJR Am J Roentgenol. 2015;205(4):848-852. doi:10.2214/ AJR.14.14266. Samim M, Eftekhary N, Vigdorchik JM, et  al. 3D-MRI versus 3DCT in the evaluation of osseous anatomy in femoroacetabular impingement using Dixon 3D FLASH sequence. Skeletal Radiol. 2019;48(3):429-436. doi:10.1007/s00256-018-3049-7.

32.

33.

34. 35.

36.

37. 38.

39.

40.

41.

42.

43.

44.

45.

46.

47.

48.

49.

77

Magee T, Williams D, Mani  N. Shoulder MR arthrography: which patient group benefits most? AJR Am J Roentgenol. 2004;183(4):969974. doi:10.2214/ajr.183.4.1830969. Tirman PF, Stauffer AE, Crues JV III, et  al. Saline magnetic resonance arthrography in the evaluation of glenohumeral instability. Arthroscopy. 1993;9(5):550-559. doi:10.1016/ s0749-8063(05)80403-7. Magee T. 3-T MRI of the shoulder: is MR arthrography necessary? AJR Am J Roentgenol. 2009;192(1):86-92. doi:10.2214/AJR.08.1097. Mandell JC, Cho CH. MRI safety update 2018: is contrast safe? AAOS Now. https://www.aaos.org/AAOSNow/2018/Apr/Special_Coverage /special_coverage12/. Published April  2018. Accessed March  27, 2019. Saupe N, Zanetti M, Pfirrmann CW, Wels T, Schwenke C, Hodler J. Pain and other side effects after MR arthrography: prospective evaluation in 1085 patients. Radiology. 2009;250(3):830-838. doi:10.1148/ radiol.2503080276. Busfield BT. Glenohumeral joint sepsis after magnetic resonance imaging arthrogram. Am J Orthop (Belle Mead NJ). 2012;41(6):277-278. Rajeev A, Andronic A, Mohamed A, Newby M, Chakravathy  J. Secondary frozen shoulder following septic arthritis—an unusual complication of magnetic resonance arthrogram. Int J Surg Case Rep. 2015;11:1-4. doi:10.1016/j.ijscr.2015.04.015. Saliken DJ, Bornes TD, Bouliane MJ, Sheps DM, Beaupre LA. Imaging methods for quantifying glenoid and Hill-Sachs bone loss in traumatic instability of the shoulder: a scoping review. BMC Musculoskelet Disord. 2015;16:164. doi:10.1186/s12891-015-0607-1. Kubo T, Ohno Y, Kauczor HU, Hatabu  H. Radiation dose reduction in chest CT—review of available options. Eur J Radiol. 2014;83(10):1953-1961. doi:10.1016/j.ejrad.2014.06.033. Boothe EK, Tenorio LL, Zabak EM, et al. Radiation dose reduction initiative: effect on image quality in shoulder CT imaging. Eur J Radiol. 2017;95:118-123. doi:10.1016/j.ejrad.2017.08.007. Burkhart SS, Debeer JF, Tehrany AM, Parten PM. Quantifying glenoid bone loss arthroscopically in shoulder instability. 2002;18(5):488491. doi:10.1053/jars.2002.32212. Chuang TY, Adams CR, Burkhart SS. Use of preoperative threedimensional computed tomography to quantify glenoid bone loss in shoulder instability. Arthroscopy. 2008;24(4):376-382. doi:10.1016/j. arthro.2007.10.008. Bois AJ, Fening SD, Polster J, Jones MH, Miniaci  A. Quantifying glenoid bone loss in anterior shoulder instability: reliability and accuracy of 2-dimensional and 3-dimensional computed tomography measurement techniques. Am J Sports Med. 2012;40(11):2569-2577. doi:10.1177/0363546512458247. Owens BD, Burns TC, Campbell SC, Svoboda SJ, Cameron KL. Simple method of glenoid bone loss calculation using ipsilateral magnetic resonance imaging. Am J Sports Med. 2013;41(3):622-624. doi:10.1177/0363546512472325. Magarelli N, Milano G, Sergio P, Santagada DA, Fabbriciani C, Bonomo  L. Intra-observer and interobserver reliability of the ‘pico’ computed tomography method for quantification of glenoid bone defect in anterior shoulder instability. Skeletal Radiol. 2009;38(11):1071-1075. doi:10.1007/s00256-009-0719-5. Dumont GD, Russell RD, Browne MG, Robertson WJ. Area-based determination of bone loss using the glenoid arc angle. Arthroscopy. 2012;28(7):1030-1035. doi:10.1016/j.arthro.2012.04.147. Huijsmans PE, Haen PS, Kidd M, Dhert WJ, van der Hulst VP, Willems WJ. Quantification of a glenoid defect with threedimensional computed tomography and magnetic resonance imaging: a cadaveric study. J  Shoulder Elbow Surg. 2007;16(6):803-809. doi:10.1016/j.jse.2007.02.115. Nofsinger C, Browning B, Burkhart SS, Pedowitz RA. Objective preoperative measurement of anterior glenoid bone loss: a pilot study of a computer-based method using unilateral 3-dimensional computed tomography. Arthroscopy. 2011;27(3):322-329. doi:10.1016/j. arthro.2010.09.007.

78 50.

51.

52.

53.

54.

55.

56.

57.

58.

59.

60.

61.

62.

63.

64.

Chapter 7 Bhatia S, Saigal A, Frank RM, et al. Glenoid diameter is an inaccurate method for percent glenoid bone loss quantification: analysis and techniques for improved accuracy. Arthroscopy. 2015;31(4):608-614. e1. doi:10.1016/j.arthro.2015.02.020. Moroder P, Plachel F, Huettner A, et  al. The effect of scapula tilt and best-fit circle placement when measuring glenoid bone loss in shoulder instability patients. Arthroscopy. 2018;34(2):398-404. doi:10.1016/j.arthro.2017.08.234. Bakshi NK, Patel I, Jacobson JA, Debski RE, Sekiya JK. Comparison of 3-dimensional computed tomography-based measurement of glenoid bone loss with arthroscopic defect size estimation in patients with anterior shoulder instability. Arthroscopy. 2015;31(10):18801885. doi:10.1016/j.arthro.2015.03.024. Milano G, Saccomanno MF, Magarelli N, Bonomo  L. Analysis of agreement between computer tomography measurements of glenoid bone defects in anterior shoulder instability with and without comparison with the contralateral shoulder. Am J Sports Med. 2015;43(12):2918-2926. doi:10.1177/0363546515608167. Burkhart SS, Danaceau SM. Articular arc length mismatch as a cause of failed Bankart repair. Arthroscopy. 2000;16(7):740-744. doi:10.1053/jars.2000.7794. Sommaire C, Penz C, Clavert P, Klouche S, Hardy P, Kempf JF. Recurrence after arthroscopic Bankart repair: is quantitative radiological analysis of bone loss of any predictive value? Orthop Traumatol Surg Res. 2012;98(5):514-519. doi:10.1016/j.otsr.2012.03.015. Charousset C, Beauthier V, Bellaïche L, Guillin R, Brassart N, Thomazeau H; French Arthroscopy Society. Can we improve radiological analysis of osseous lesions in chronic anterior shoulder instability? Orthop Traumatol Surg Res. 2010;96(8  suppl):S88-S93. doi:10.1016/j.otsr.2010.09.006. Kodali P, Jones MH, Polster J, Miniaci A, Fening SD. Accuracy of measurement of Hill-Sachs lesions with computed tomography. J Shoulder Elbow Surg. 2011;20(8):1328-1334. doi:10.1016/j. jse.2011.01.030. Saito H, Itoi E, Minagawa H, Yamamoto N, Tuoheti Y, Seki  N. Location of the Hill-Sachs lesion in shoulders with recurrent anterior dislocation. Arch Orthop Trauma Surg. 2009;129(10):1327-1334. doi:10.1007/s00402-009-0854-4. Salomonsson B, von Heine A, Dahlborn M, et  al. Bony Bankart is a positive predictive factor after primary shoulder dislocation. Knee Surg Sports Traumatol Arthrosc. 2010;18(10):1425-1431. doi:10.1007/ s00167-009-0998-3. Yamamoto N, Itoi E, Abe H, et al. Contact between the glenoid and the humeral head in abduction, external rotation, and horizontal extension: a new concept of glenoid track. J Shoulder Elbow Surg. 2007;16(5):649-656. doi:10.1016/j.jse.2006.12.012. Yamamoto N, Itoi  E. Osseous defects seen in patients with anterior shoulder instability. Clin Orthop Surg. 2015;7(4):425-429. doi:10.4055/cios.2015.7.4.425. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694. doi:10.1053/ jars.2000.17715. Di Giacomo G, Itoi E, Burkhart SS. Evolving concept of bipolar bone loss and the Hill-Sachs lesion: from “engaging/non-engaging” lesion to “on-track/off-track” lesion. Arthroscopy. 2014;30(1):90-98. doi:10.1016/j.arthro.2013.10.004. Locher J, Wilken F, Beitzel K, et  al. Hill-Sachs off-track lesions as risk factor for recurrence of instability after arthroscopic Bankart repair. Arthroscopy. 2016;32(10):1993-1999. doi:10.1016/j. arthro.2016.03.005.

65.

66.

67.

68.

69.

70.

71.

72.

73.

74.

75.

76.

77.

78.

Shaha JS, Cook JB, Rowles DJ, Bottoni CR, Shaha SH, Tokish JM. Clinical validation of the glenoid track concept in anterior glenohumeral instability. J Bone Joint Surg Am. 2016;98(22):1918-1923. doi:10.2106/JBJS.15.01099. Schneider AK, Hoy GA, Ek ET, et al. Interobserver and intraobserver variability of glenoid track measurements. J Shoulder Elbow Surg. 2017;26(4):573-579. doi:10.1016/j.jse.2016.09.058. Arciero RA, Parrino A, Bernhardson AS, et  al. The effect of a combined glenoid and Hill-Sachs defect on glenohumeral stability: a biomechanical cadaveric study using 3-dimensional modeling of 142 patients. Am J Sports Med. 2015;43(6):1422-1429. doi:10.1177/0363546515574677. Gottschalk LJ IV, Walia P, Patel RM, et  al. Stability of the glenohumeral joint with combined humeral head and glenoid defects: a cadaveric study. Am J Sports Med. 2016;44(4):933-940. doi:10.1177/0363546515624914. Dickens JF, Slaven SE, Cameron KL, et al. Prospective evaluation of glenoid bone loss after first-time and recurrent anterior glenohumeral instability events. Am J Sports Med. 2019;47(5):1082-1089. doi:10.1177/0363546519831286. Owens BD, Dickens JF, Kilcoyne KG, Rue JP. Management of midseason traumatic anterior shoulder instability in athletes. J Am Acad Orthop Surg. 2012;20(8):518-526. doi:10.5435/JAAOS-20-08-518. Balg F, Boileau P. The instability severity index score. A simple preoperative score to select patients for arthroscopic or open shoulder stabilisation. J Bone Joint Surg Br. 2007;89(11):1470-1477. doi:10.1302/0301-620X.89B11.18962. Marshall T, Vega J, Siqueira M, Cagle R, Gelber JD, Saluan  P. Outcomes after arthroscopic Bankart repair: patients with first-time versus recurrent dislocations. Am J Sports Med. 2017;45(8):17761782. doi:10.1177/0363546517698692. Loppini M, Delle Rose G, Borroni M, et  al. Is the Instability Severity Index Score a valid tool for predicting failure after primary arthroscopic stabilization for anterior glenohumeral instability? Arthroscopy. 2019;35(2):361-366. doi:10.1016/j.arthro.2018.09.027. Thomazeau H, Langlais T, Hardy A, et  al; French Arthroscopy Society. Long-term, prospective, multicenter study of isolated Bankart repair for a patient selection method based on the Instability Severity Index Score. Am J Sports Med. 2019;47(5):1057-1061. doi:10.1177/0363546519833920. Chan AG, Kilcoyne KG, Chan S, Dickens JF, Waterman BR. Evaluation of the Instability Severity Index score in predicting failure following arthroscopic Bankart surgery in an active military population. J Shoulder Elbow Surg. 2019;28(5):e156-e163. doi: 10.1016/j. jse.2018.11.048. Shin SJ, Kim RG, Jeon YS, Kwon TH. Critical value of anterior glenoid bone loss that leads to recurrent glenohumeral instability after arthroscopic Bankart repair. Am J Sports Med. 2017;45(9):1975-1981. doi:10.1177/0363546517697963. Shaha JS, Cook JB, Song DJ, et  al. Redefining “critical” bone loss in shoulder instability: functional outcomes worsen with “subcritical” bone loss. Am J Sports Med. 2015;43(7):1719-1725. doi:10.1177/0363546515578250. Lansdown DA, Wang K, Yanke A, Nicholson GP, Cole BJ, Verma NN. The flat anterior glenoid: a simple, clinically useful pattern to recognize sub-critical glenoid bone loss. Arthroscopy. 2019;35(6):17881793. doi:10.1016/j.arthro.2018.12.034.

8 Arthroscopic Anterior Shoulder Instability in the Athlete Lauren A. Szolomayer, MD and Robert Arciero, MD

Anterior shoulder instability and recurrent anterior shoulder dislocations are associated with limitations in sports and development of early glenohumeral arthritis.1,2 After a dislocation in young patients, instability recurrence rate has been reported to be up to 90% with nonoperative treatment.3 Many techniques exist for treatment of acute and chronic shoulder instability. Open Bankart has been the traditional approach for treatment of labral tears and instability of the shoulder. As treatment transitioned to arthroscopic techniques, the arthroscopic Bankart repair was found to significantly reduce the recurrence rate in young athletes who sustained an acute, initial anterior dislocation of the shoulder.4 Arthroscopic Bankart has increased in popularity; however, recurrence can range from 13% to 35% in reported studies.5-7 Techniques for repair are dependent on the direction and degree of instability, the patient’s desired activity, bone loss on the glenoid or humeral head, and prior surgeries. Although much of the literature has focused on recurrent instability as a key outcome, perhaps equally impor tant is the patient’s ability to return to the same level of sport or unrestricted activity. In a review of primary shoulder dislocations in West Point Cadets, the common concomitant injuries were defined including Bankart lesion in 63 out of 65 patients, type 2 superior labrum anterior and posterior tears, capsular tears, humeral avulsion of the glenohumeral ligament lesion, and 22% with a glenoid rim avulsion or “Bony Bankart.”3 The following chapter will cover the indications and contraindications for arthroscopic Bankart repair; management of soft-tissue and bony Bankart, Hill-Sachs, anterior labroligamentous periosteal sleeve avulsion (ALPSA), and glenolabral articular disruption (GLAD) lesions; outcomes;

common complications; and the senior author’s preferred technique for performing an arthroscopic Bankart repair.

INDICATIONS AND CONTRAINDICATIONS FOR BANKART REPAIR Evaluation of the athlete’s shoulder begins with a thorough history. It is impor tant to assess when and if initial traumatic dislocation occurred, the number of dislocation or subluxation events, activity level, and level of sports participation. In addition, prior treatment, if any, should be assessed, including physical therapy and surgical treatment. The evaluation and recommendations for arthroscopic treatment of Bankart also involves ruling out bone loss. Significant bone loss is rare in a first-time dislocator. If the patient’s history includes multiple dislocations, dislocation during sleep, seizure or revision surgery, or exam finding of apprehension at a low angle of abduction, all are indicators of potential bone loss both on the glenoid and humeral side. Adolescents (ages 10 to 19  years) and patients who experience multiple shoulder dislocations are both independent risk factors for development of an off-track Hill-Sachs lesion that may require addition of a remplissage accompanying the arthroscopic Bankart.8

CASE EXAMPLE A 21-year-old male college football player sustained his first dislocation in preseason and was treated with rehabilitation and a brace. He returns to practice in 7 days without apprehension signs. The initial magnetic resonance imaging

- 79 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 79-89). © 2021 SLACK Incorporated.

80

Chapter 8

Figure 8-1. Magnetic resonance imaging after a first-time dislocation with an anterior labrum tear and posterior humeral head edema.

Figure 8-2. Second magnetic resonance imaging with a 300- degree labral tear.

in Figure  8-1 shows a typical Bankart lesion that would require 2 or 3 anchors for arthroscopic repair. After undergoing a rapid return to sport, he is able to play in 5 games with 3 other subluxation events. During his sixth game he undergoes a major subluxation event (Figure  8-2). The result is a 300-degree tear that subsequently required 6 double-loaded anchors and arthroscopic repair. Figure  8-3 shows the arthroscopic images of the 300-degree labral tear after multiple instability events.

PHYSICAL EXAM A detailed description of the physical exam is provided in Chapter  3 and impor tant aspects are emphasized in

Table  8-1. The apprehension test, with the patient feeling uncomfortable or that he or she may dislocate versus just pain, should be tested in the abducted and externally rotated (ABER) position, which is generally the position of maximum instability. The load and shift may be applied in the ABER position as well, with load applied along the axis of the humerus and then translating the humerus anteriorly over the glenoid. This is graded on a scale of 0 to 3+ with no anterior translation, 1+ an anterior shift to the glenoid rim, 2+ a dislocated humerus but reduces spontaneously, and 3+ an anterior shift to dislocation, which requires manual reduction. Typically a 3+ indicates the presence of bone loss on either the humeral or glenoid side. Other tests may be applied to rule out multidirectional or posterior instability.

Arthroscopic Anterior Shoulder Instability in the Athlete

81

Figure 8-3. Arthroscopic images of a 300- degree labral tear after multiple instability events.

Table 8-1. Physical Exam Findings—Special Tests EXAM Sulcus sign

DESCRIPTION In-line traction on humerus with arm adducted Apprehension Place arm in ABER position, continue abduction Relocation sign Posteriorly directed pressure on humerus (while in apprehension position) Anterior load and Anterior translation of humerus with arm shift in ABER position Posterior load and shift

Posterior translation of humerus with arm in ABER position

POSITIVE Depression of humeral head 2 cm below acromion Discomfort or “feeling of dislocation” Discomfort relieved

INSTABILITY Multidirectional, generalized laxity Anterior

1+ to glenoid edge 2+ over glenoid edge 3+ stays dislocated

Anterior

As above

Posterior

Anterior

Abbreviation: ABER, abducted and externally rotated.

IMAGING Radiographs obtained at the initial evaluation should include a true anteroposterior (Grashey), scapular-Y, and West Point views to evaluate for bone loss. A Hill-Sachs lesion may be identified if present. Magnetic resonance imaging is indicated in all young dislocators and is the modality of choice for evaluating a labral tear. Adding contrast to the joint during imaging via magnetic resonance arthrogram can increase the sensitivity and specificity for identifying labral tears, particularly in the recurrent setting after prior repair. A computed tomography scan is indicated when bone loss is suspected based on radiographs or number and ease of dislocation events and any of the risk factors discussed earlier.

MANAGEMENT The available evidence supports operative stabilization for primary anterior shoulder dislocation in young patients participating in highly demanding physical sports.9-11 Indications for arthroscopic stabilization include a first-time dislocation in those younger than 22 years, overhead athletes, less than 15% bone loss on the glenoid, on-track bipolar defects, and

panlabral injuries. For other athletes, and those who may be in-season and unable or unwilling to take time off for surgery, it is reasonable to treat with conservative management. A shoulder stabilization brace may be donned in the acute setting immediately post-dislocation for comfort and in settings in which high-level, nonthrowing athletes require immediate return to play. Nonoperative treatment should include physical therapy for periscapular and rotator cuff strengthening and modalities as needed after a brief period of immobilization if frank dislocation has occurred.

TECHNIQUE FOR BANKART REPAIR The patient is brought to the operating room, where the anesthesia team typically places a peripheral nerve block before induction of anesthesia. This helps with postoperative pain control and decreased anesthetic requirements during the procedure. General anesthesia without complete relaxation is generally appropriate. The affected and contralateral shoulders should be examined under anesthesia before positioning. This is a critical component to evaluation of the patient to accurately characterize the direction and degree of instability while the patient is relaxed (Figure 8-4).

82

Chapter 8

Figure 8-4. Exam under anesthesia, showing anterior translation (3+ load and shift).

The authors’ preferred technique for arthroscopic stabilization is in the lateral decubitus position with a beanbag positioner and the arm in a weighted traction setup (Figures 8-5 and 8-6). This position has shown a decreased risk of instability recurrence than when performed in the beach chair position.12 This position also allows for ease with mobilization of the Bankart, re-tensioning of the inferior glenohumeral ligament (IGHL), access to the 6’oclock position on the glenoid face, and aids in addressing capsular redundancy. A weighted traction setup or arm positioner may be used, with a sterile “bump” to aid in abduction of the arm away from the body and to create increased space in the glenohumeral joint (Figure 8-7). Typically 3 to 4 portals are used (Figure  8-8). Portals will include a posterior portal marked just off the posterolateral edge of the acromion and 2  cm distal, which allows for better visualization of the anterior inferior glenoid;

8.5 mm cannulas are inserted in each portal to ease passage of instruments. Once the glenohumeral joint is entered, an anterior-superior portal is then created within the rotator interval behind the biceps tendon. This portal is created in a higher position than a standard anterior portal to allow visualization and room for a second, anterior inferior portal as a working portal, without convergence of these 2 portals. Additional percutaneous portals for anchor placement can be created if needed. A diagnostic scope is performed visualizing the glenoid and humeral cartilage surfaces, the biceps insertion, the superior labrum, which is probed, the anterior inferior labrum, presence of a humeral avulsion of the glenohumeral ligament lesion, subscapularis tendon and its insertion, and rotator cuff insertion. Posteriorly the bare spot and Hill Sachs lesion if present may be visualized prior to visualizing the posterior aspect of the axillary pouch and the posterior labrum.

Arthroscopic Anterior Shoulder Instability in the Athlete

83

Figure 8-5. Patient positioning in lateral decubitus for a right shoulder arthroscopic stabilization. Figure 8-6. Patient position in lateral decubitus with arm traction. Figure 8-7. Arthroscopy setup with “bump” in axilla to facilitate distraction and improve visualization.

84

Chapter 8

A

B

Figure 8-8. Patient positioned in the lateral decubitus position with beanbag to the left of the image. (A) The entire border of the acromion in marked out. (B) The initial posterior portal is marked at the most lateral edge of the acromion and 2 fingerbreadths inferior at the joint line. The anterior superior portal will be made just off of the anterior edge of the (C) anterior acromion and the (D) anterior inferior portal just lateral to the coracoid process, which is marked as a filled-in circle. These are placed under direct visualization.

An anterior-superior portal is placed superior to the biceps tendon to allow viewing with the arthroscope from either side (Figure 8-9A). An anterior-inferior portal may be placed percutaneously at the midgloid level, entering the capsule just superior to the subscapularis tendon (Figure 8-9B). Care should be taken to place this laterally to the coracoid process. This will be a working portal and will facilitate placement of suture anchors. Once the diagnostic scope is complete, the labrum should be mobilized along the entirety of the tear with a labral elevator, and the surface edge of the glenoid is decorticated with a rasp and arthroscopic shaver to facilitate bony healing (Figure 8-10). This can be accomplished viewing alternately from the anterosuperior and posterior portals. A small bony Bankart if encountered should similarly be freed with the labrum during the procedure. This fragment should be decorticated with the arthroscopic shaver and incorporated into repair with the redundant capsule and labrum.

Figure 8-9. (A) Anterior superior portal placement adjacent to the biceps tendon. (B) Anterior inferior portal—viewing from anterior superior portal.

An off-track Hill-Sachs lesion, if present, should be addressed first by a 1- or 2-anchor remplissage depending on the size of the lesion. Typically double- or triple-loaded suture anchors can be used. The sutures can be placed through the posterior cuff tissue and should advance the medial muscle into the defect. The sutures can then be left outside the cannula, as we recommend tying sutures after the Bankart repair is complete to allow for continued visualization and access to the glenohumeral joint. An initial anchor is typically a double-loaded suture anchor placed at the 6 o’clock position on the inferior aspect of the glenoid to facilitate capsulorrhaphy (Figures 8-11A and 8-11B). All anchors are placed on the edge of the glenoid face. A suture passer is used to pass a shuttling PDS suture through a portion of the inferior capsule and the inferior labrum and

Arthroscopic Anterior Shoulder Instability in the Athlete

A

85

A

B B

Figure 8-10. Shaver and labral elevator used to debride and decorticate the anterior inferior glenoid (A) at the side of the tear and (B) down the scapular neck. Figure 8-11. (A and B) The 6 o’clock position on left shoulder.

the anchor sutures are then passed in a simple fashion. A second pass is similarly made for horizontal mattress sutures. Capsulorrhaphy should include addressing the capsular laxity by pulling a large portion of the anteroinferior capsule into the labral repair, thereby recreating tension of the IGHL (see Figure 8-11). If there is posterior extension of the tear, this is addressed next with double-loaded anchors; these may progress up the posterior-inferior glenoid rim if needed. Typically 3 or 4 anchors are used for a typical Bankart anterior tear. Progress is made anteriorly, placing suture anchors and passing the sutures through the redundant anteroinferior capsule and the labrum and tying in a simple fashion to create a “bumper” capsulolabral tissue (Figure 8-12).

The remaining suture anchors are marched up the anterior aspect of the glenoid to the equator or 3 o’clock position, and sutures can be passed in a horizontal mattress or simple or combined fashion. If the tissue is of poor quality, additional capsular tissue should be included in the repair and simple knots tied. Figure 8-13 shows the completed repair. We recommend tying knots for fixation of suture in the Bankart repair because it confers increased ability to plicate the capsule. In addition, it allows for a combination of mattress and simple sutures, which provides more versatility and allows for a repair more similar to open. Typically it is advantageous to tie knots through the same portal through which

86

Chapter 8

Figure 8-12. Left shoulder: (A) Anchor placement and suture passage and tying, (B) a doubleloaded anchor is placed, (C) a suture passer with a monofilament suture through capsule and (D) a labrum knot tied on the outside of the tissue repeated with a second suture.

A

B

C

D

A

B

Figure 8-13. View of right shoulder anterior repair with (A) 3 suture anchors, (B) anteroinferior with tension on the inferior glenohumeral ligament, and (C) capsulolabral bumper repair extending to the 6 o’clock position. (continued)

the anchor was placed. This allows the surgeon to firmly cinch down the knot on the outer aspect of the soft-tissue capsule. Recently knotless anchors have gained increasing popularity and seem to may provide success in tight fixation

of the capsulorrhaphy, but are not the authors’ preferred technique. Occasionally an ALPSA lesion will be present with the Bankart in which the labrum and adjacent periosteum is

Arthroscopic Anterior Shoulder Instability in the Athlete

Figure 8-13 (continued). View of right shoulder anterior repair with (A) 3 suture anchors, (B) anteroinferior with tension on the inferior glenohumeral ligament, and (C) capsulolabral bumper repair extending to the 6 o’clock position.

A

A

87

B

pulled from the anterior surface of the glenoid. This often displaces the labrum further medially and down on the glenoid. It is imperative to separate this sleeve from the anteriorinferior glenoid as far medially as possible until the labrum floats at the level of the glenoid fossa. This will require significantly more work to mobilize. GLAD lesions may occur with traumatic dislocations and typically involve separation of the anteroinferior labrum with an associated cartilage defect. During repair the anchors should be placed at the most central edge of the lesion to pull the labrum and capsular plication to the level of the defect (Figure 8-14). Capsular closure is a controversial topic in Bankart repair. Some research has shown an increased risk of motion loss with capsular closure in anterior instability.13 The biomechanical data are mixed as to whether capsular closure can help in cases of anterior instability.14,15 Currently the authors reserve capsular closure for cases of multidirectional instability. The posterior portal or anterior rotator cuff interval

Figure 8-14. Right shoulder (A) glenolabral articular disruption lesion with (B) subsequent repair incorporating a cartilage defect.

may be closed in a simple fashion with use of a PDS suture and suture passer and then tied in an extracapsular position. Postoperatively the patient is typically in a sling for 4 to 6 weeks with gentle range of motion permitted. Weeks 2 to 6 focus on increasing range of motion while still protecting the repair, and then weeks 6 to 12 involve strengthening exercises. Beyond week 12, athletes may perform return-to-sport protocols with return to sport at about 4 to 6 months postoperatively depending on their sport. A detailed description of rehabilitation will be covered in another chapter.

OUTCOMES Common complications of arthroscopic Bankart include postoperative stiffness, particularly limited external rotation, and less commonly infection, deep vein thrombosis, and neurovascular injury. Recurrent instability is the most common complication.16 In a study comparing arthroscopic Bankart, open Bankart, and Latarjet-Bristow, the Latarjet-Bristow

88

Chapter 8

procedure had the highest overall complication rate (5.5%) compared with open (1.0%) and arthroscopic (0.6%) Bankart repairs.17 The reported rate of nerve injury is rare, 0.3% according to a review by Owens and colleagues of American Board of Orthopaedic Surgery data, and typically involves the axillary nerve.18 Brachial plexus palsy has also been reported; however, it is not clear whether it is due to surgical or peripheral nerve blocks.19 The rate of infection after arthroscopic Bankart is also low at 0.22%.18 Suture anchor complications are less common than previously. Inflammatory reaction, osteolysis, and chondrolysis have been reported to be associated with the use of PLLA (polyL-lactic acid) anchors, and therefore PEEK (polyetheretherketone) anchors have gained popularity.20 Post-traumatic osteoarthritis has varying reports in the literature, up to 21% at 8  years.21 Postoperative stiffness was encountered in 1.6% (5 of 302) in a series from an experienced surgeon, and all were resolved with physical therapy.19 If severe pain with stiffness occurs, the surgeon can consider injection of a corticosteroid with Toradol (ketorolac) before physical therapy. If the patient fails physical therapy, arthroscopic lysis of adhesions (vs manipulation) can be performed. Surgeons have been able to achieve improved outcomes from arthroscopic Bankart repair after diligent application of evidence-based indications and techniques, with recurrence rates as low as 8% as reported by Leroux et al.22 In this study, authors operated typically on patients with few episodes of dislocation/instability, thus ensuring good tissue and no bone loss, and used a minimum of 3 anchors and in the lateral decubitus position. Patients with bone loss, poor capsulolabral tissue, collision athletes, or hyperlaxity may be better served with an alternate procedure such as the open Bankart or Latarjet. Boileau and colleagues23 showed that bone loss and capsular laxity were risk factors for recurrence with a more than 25% glenoid defect resulting in a 75% recurrence rate. Other authors have identified risk factors for recurrence including an inverted pear-shape glenoid and engaging HillSachs lesion.24 Recurrence will be discussed in more detail in a subsequent chapter. Evidence has shown that patients who undergo arthroscopic Bankart repair have higher rates of return to sport than those who underwent Latarjet, likely driven by patient selection, number of dislocations, and bone loss. Overall, return to sport pooled from a systematic review showed 97.5% with an average return to sport of 5.9 months.25 At least one study of outcome after a 25-year radiographic follow-up showed that the rate of arthropathy was significantly improved in patients who did not experience recurrence after primary dislocation, 40% versus 18% if they did not experience recurrence.1

CONCLUSION Arthroscopic Bankart is the most commonly used technique for treatment of athletes with anterior shoulder

instability, including first-time dislocators. A detailed history and physical exam will aid in determining which patients will benefit from arthroscopic treatment and help to identify those patients with bone loss who may require additional workup and would be better served with Latarjet procedure. Our preferred technique is to place the patient in the lateral decubitus position, which allows for better visualization, improved access to the inferior glenoid, and better ability to re-tension the IGHL. The rate of recurrent anterior instability can be reduced by early intervention with patients who have dislocated, identifying patients who are at higher risk for recurrence, and performing meticulous repair of the labrum with attention to restoration of capsular tension. Effective return-to-sport protocols can get patients back to their desired level of athletic performance.

REFERENCES 1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

11.

Hovelius L, Saeboe M. Neer Award 2008: arthropathy after primary anterior shoulder dislocation—223 shoulders prospectively followed up for twenty-five years. J Shoulder Elbow Surg. 2009;18(3):339-347. doi:10.1016/j.jse.2008.11.004. Galvin JW, Ernat JJ, Waterman BR, Stadecker MJ, Parada SA. The epidemiology and natural history of anterior shoulder instability. Curr Rev Musculoskelet Med. 2017;10(4):411-424. doi:10.1007/ s12178-017-9432-5. Taylor DC, Arciero RA. Pathologic changes associated with shoulder dislocations. Arthroscopic and physical examination findings in first-time, traumatic anterior dislocations. Am J Sports Med. 1997;25(3):306-311. doi:10.1177/036354659702500306. Arciero RA, Wheeler JH, Ryan JB, McBride JT. Arthroscopic Bankart repair versus nonoperative treatment for acute, initial anterior shoulder dislocations. Am J Sports Med. 1994;22(5):589-594. doi:10.1177/036354659402200504. van der Linde JA, van Kampen DA, Terwee CB, Dijksman LM, Kleinjan G, Willems WJ. Long-term results after arthroscopic shoulder stabilization using suture anchors: an 8- to 10-year follow-up. Am J Sports Med. 2011;39(11):2396-2403. doi:10.1177/0363546511415657. Castagna A, Delle Rose G, Borroni M, et al. Arthroscopic stabilization of the shoulder in adolescent athletes participating in overhead or contact sports. Arthroscopy. 2012;28(3):309-315. doi:10.1016/j. arthro.2011.08.302. Porcellini G, Campi F, Pegreffi F, Castagna A, Paladini P. Predisposing factors for recurrent shoulder dislocation after arthroscopic treatment. J Bone Joint Surg Am. 2009;91(11):2537-2542. doi:10.2106/ JBJS.H.01126. Lau BC, Conway D, Curran PF, Feeley BT, Pandya NK. Bipolar bone loss in patients with anterior shoulder dislocation: a comparison of adolescents versus adult patients. Arthroscopy. 2017;33(10):17551761. doi:10.1016/j.arthro.2017.04.004. Longo UG, Loppini M, Rizzello G, Ciuffreda M, Maffulli N, Denaro V. Management of primary acute anterior shoulder dislocation: systematic review and quantitative synthesis of the literature. Arthroscopy. 2014;30(4):506-522. doi:10.1016/j.arthro.2014.01.003. Godin J, Sekiya JK. Systematic review of rehabilitation versus operative stabilization for the treatment of first-time anterior shoulder dislocations. Sports Health. 2010;2(2):156-165. doi:10.1177/1941738109359507. Gonçalves Arliani G, da Costa Astur D, Cohen C, et  al. Surgical versus nonsurgical treatment in first traumatic anterior dislocation of the shoulder in athletes. Open Access J Sports Med. 2011;2:19-24. doi:10.2147/OAJSM.S17378.

Arthroscopic Anterior Shoulder Instability in the Athlete 12.

13.

14.

15.

16.

17.

18.

Frank RM, Saccomanno MF, McDonald LS, Moric M, Romeo AA, Provencher MT. Outcomes of arthroscopic anterior shoulder instability in the beach chair versus lateral decubitus position: a systematic review and meta-regression analysis. Arthroscopy. 2014;30(10):13491365. doi:10.1016/j.arthro.2014.05.008. Provencher MT, Dewing CB, Bell SJ, et al. An analysis of the rotator interval in patients with anterior, posterior, and multidirectional shoulder instability. Arthroscopy. 2008;24(8):921-929. doi:10.1016/j. arthro.2008.03.005. Mologne TS, Zhao K, Hongo M, Romeo AA, An KN, Provencher MT. The addition of rotator interval closure after arthroscopic repair of either anterior or posterior shoulder instability: effect on glenohumeral translation and range of motion. Am J Sports Med. 2008;36(6):1123-1131. doi:10.1177/0363546508314391. Provencher MT, Mologne TS, Hongo M, Zhao K, Tasto JP, An KN. Arthroscopic versus open rotator interval closure: biomechanical evaluation of stability and motion. Arthroscopy. 2007;23(6):583-592. doi:10.1016/j.arthro.2007.01.010. Matsuki K, Sugaya H. Complications after arthroscopic labral repair for shoulder instability. Curr Rev Musculoskelet Med. 2015;8(1):5358. doi:10.1007/s12178-014-9248-5. Bokshan SL, DeFroda SF, Owens BD. Comparison of 30-day morbidity and mortality after arthroscopic Bankart, open Bankart, and LatarjetBristow procedures: a review of 2864 cases. Orthop J Sports Med. 2017;5(7):2325967117713163. doi:10.1177/2325967117713163. Owens BD, Harrast JJ, Hurwitz SR, Thompson TL, Wolf JM. Surgical trends in Bankart repair: an analysis of data from the American Board of Orthopaedic Surgery certification examination. Am J Sports Med. 2011;39(9):1865-1869. doi:10.1177/0363546511406869.

19.

20.

21.

22.

23.

24.

25.

89

Ahmed I, Ashton F, Robinson CM. Arthroscopic Bankart repair and capsular shift for recurrent anterior shoulder instability: functional outcomes and identification of risk factors for recurrence. J Bone Joint Surg Am. 2012;94(14):1308-1315. doi:10.2106/JBJS.J.01983. Haneveld H, Hug K, Diederichs G, Scheibel M, Gerhardt  C. Arthroscopic double-row repair of the rotator cuff: a comparison of bio-absorbable and non-resorbable anchors regarding osseous reaction. Knee Surg Sports Traumatol Arthrosc. 2013;21(7):1647-1654. doi:10.1007/s00167-013-2510-3. Franceschi F, Papalia R, Del Buono A, Vasta S, Maffulli N, Denaro V. Glenohumeral osteoarthritis after arthroscopic Bankart repair for anterior instability. Am J Sports Med. 2011;39(8):1653-1659. doi:10.1177/0363546511404207. Leroux TS, Saltzman BM, Meyer M, et al. The influence of evidencebased surgical indications and techniques on failure rates after arthroscopic shoulder stabilization in the contact or collision athlete with anterior shoulder instability. Am J Sports Med. 2017;45(5):12181225. doi:10.1177/0363546516663716. Boileau P, Villalba M, Héry JY, Balg F, Ahrens P, Neyton L. Risk factors for recurrence of shoulder instability after arthroscopic Bankart repair. J  Bone Joint Surg Am. 2006;88(8):1755-1763. doi:10.2106/ JBJS.E.00817. Burkhart SS, Debeer JF, Tehrany AM, Parten PM. Quantifying glenoid bone loss arthroscopically in shoulder instability. Arthroscopy. 2002;18(5):488-491. doi:10.1053/jars.2002.32212. Abdul-Rassoul H, Galvin JW, Curry EJ, Simon J, Li  X. Return to sport after surgical treatment for anterior shoulder instability: a systematic review. Am J Sports Med. 2019;47(6):1507-1515. doi:10.1177/0363546518780934.

9 Open Treatment of Anterior Instability Michael J. Pagnani, MD and Jason A. Jones, MD

Open stabilization techniques have had a long history of effectiveness in reducing anterior shoulder instability. The results of such procedures have been almost uniformly excellent, with postoperative recurrence rates generally reported between 0% and 5% in nonselected populations.1-8 Yet, owing largely to the popularity of arthroscopic methods of stabilization,9 open capsular repairs have been largely neglected in the training of younger orthopedic surgeons. Although arthroscopic repairs have advantages (including smaller incisions, less trauma to the subscapularis tendon, less perioperative pain, easier rehabilitation, and more predictable return of motion), they have been plagued by unacceptably high recurrence rates in high-risk groups such as contact athletes, patients with capsular laxity, and those with bone loss of the humeral head or glenoid fossa.10-19 Balg and Boileau10 devised an Instability Severity Index Score that recommended that arthroscopic methods of stabilization be avoided in most of these high-risk patients. It is now commonly recommended that such at-risk patients be treated with a boneaugmentation technique such as the Latarjet procedure. In our opinion, such an algorithm is essentially going from “point A to point C.” These guidelines ignore “point B”— open capsular repair.

RATIONALE FOR OPEN CAPSULAR REPAIR The hope that the results of “modern” techniques for arthroscopic stabilization for anterior shoulder instability would approximate those reported for open capsular repair has not been realized; recurrence rates for arthroscopic

repair have been shown in recent meta-analyses to continue to exceed the historical rates for open stabilization.20,21 Hohmann et  al, in a recent systematic review, noted that results reported in the literature for arthroscopic stabilization between 2005 and 2015 had not improved statistically when compared to results reported between 1995 and 2004.21 Alkaduhimi and colleagues,20 in another systematic review published in 2016, concluded, “Despite advances in surgical techniques and devices during the last 20  years, . . . the recurrence rate for arthroscopic shoulder stabilization has only marginally decreased.” These higher failure rates have persisted despite careful patient selection by which many arthroscopic studies exclude high-risk groups such as contact athletes, patients with bony defects of the humeral head and glenoid, and patients with capsular laxity.11,15,22-24 The preponderance of highly selected patients in reports of the results of arthroscopic stabilization makes comparison with the outcomes of open stabilization without such exclusions problematic. In addition, the dearth of case series on the results of open stabilization from experienced surgeons at leading centers of shoulder surgery over the past 20  years does not permit adequate assessment of “modern” open techniques for such comparisons. However, in this era of evidence-based medicine, no fewer than 7 separate meta-analyses have concluded that the results of open stabilization have been superior to those of arthroscopic stabilization.15,20,21,25-28 In fact, Hohmann et al21 found a 37% higher risk of recurrent instability with arthroscopic techniques compared to open methods. Open stabilization has several advantages over arthroscopic repair that may well explain the differences in recurrence rates: 1) Open methods allow the surgeon to completely

- 91 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 91-101). © 2021 SLACK Incorporated.

92

Chapter 9

free the capsule from the subscapularis tendon to precisely tension the capsule without adherence to the subscapularis; 2) the rotator interval can be better visualized and tensioned via an open technique; open rotator interval closure does not have the same effect on shoulder translation or rotation as arthroscopic closure29,30; 3) the thickness of the capsule can be doubled by overlapping the capsule during open repair; 4) the arm can be optimally positioned for open repair; 5) open techniques allow for repair of the capsule and labrum with knots tied extra-articularly, eliminating concern about suture impingement on the articular surfaces of the shoulder.

INDICATIONS The general indications for surgical treatment of recurrent anterior shoulder instability are highly subjective. They include a desire of the patient to avoid recurrent episodes of instability (including the necessity of reporting to the emergency room on a frequent basis to have the shoulder reduced), problems with recurrent pain, an inability to perform certain activities because of apprehension regarding the shoulder, and the desire to improve athletic performance with improved shoulder stability. Failure of a thorough trial of nonoperative treatment is also an indication for surgical treatment. Indications for open stabilization over arthroscopic stabilization include 1) participation in a contact or collision sport, 2) male patients younger than 20 years with instability, 3) small to moderate bony defects of the humeral head or glenoid, 4) humeral avulsion of the glenohumeral ligaments, 5) failed arthroscopic repair, and 6) atraumatic instability. Essentially patients with an Instability Severity Index Score of 6 or greater (in which arthroscopic methods have a reported failure rate of 70%),10 are candidates for open capsular repair. In our practice, such patients represent approximately 80% of the patients who fail conservative treatment and require surgical treatment for anterior instability. We will consider 2 of these indications in the following sections.

Contact Athletes The results of arthroscopic stabilization in contact athletes have been generally disappointing, with failures rates ranging from 14% to 60%.12,14-16,19,20,24 Recently, a report from the Hospital for Special Surgery revealed a 26% recurrence rate after arthroscopic repair.19 Contemporary systematic reviews have noted an 18% failure rate in contact/collision athletes15 and an 8 times greater absolute risk for recurrence in collision athletes compared to other patients after arthroscopic repair.20 Okoroha and colleagues31 reported a 26% recurrence rate in National Football League players after operative repair. In contrast, our series of open stabilization in 58 American football players yielded a 3% recurrence rate, with 2 athletes sustaining postoperative subluxation and no postoperative dislocations.4

Bony Defects of Humeral Head/Glenoid High recurrence rates have been reported after arthroscopic Bankart repair in patients with bony defects of the glenoid and humeral head.11,12 Burkhart and De Beer12 reported that contact athletes who had an “engaging” Hill-Sachs lesion or “inverted pear” glenoid had a recurrence rate of 89%. Their subdivision of Hill-Sachs lesions into “engaging” and “nonengaging” types is commonly used in contemporary lectures on shoulder instability to determine the risk of postoperative instability after arthroscopic repair. More recently, the description of “on-track” and “off-track” lesions has come into common usage. The use of these terms (and the impression of high rates of failure after operative treatment) has been erroneously assigned to open capsular repair as well. In fact, a review of the published results of traditional open capsular repair in the face of bony deficiency consistently reveals outcomes that have been more than acceptable. Rowe et al,5 in their historic 1978 end-result study of open Bankart repairs, found that postoperative recurrence actually decreased, from 3.5% to 2%, in patients with defects of the glenoid rim. Bigliani and colleagues32 reported a 12% recurrence rate after open capsular shift in patients with glenoid bone loss. Rowe et  al5 found only a slight increase in recurrence after open Bankart repair in patients with moderate or severe HillSachs lesions (5% vs 3.5%). Gill et al1,2 found a recurrence rate of 6% in the presence of a large Hill-Sachs lesion. We have assessed recurrence rates with a contemporary method of open anterior stabilization without bony augmentation in patients in our practice with defects of the glenoid and/or humeral head.3 The overall recurrence rate was 2% (2/103), with one patient having a postoperative dislocation and the other experiencing subluxation. There were no recurrences in the 14 patients with glenoid rim deficiency. Patients with engaging Hill-Sachs lesions had a 4% recurrence (1/28), but this was not statistically significant. One of the 9 patients (11%) with large defects of the humeral head had a recurrence—again, not statistically significant. These results suggest that very large bony defects of the humeral head may be more problematic for open capsular repairs than glenoid defects. Overall, however, the results in patients with bony defects are comparable to those reported for bone-block procedures such as the Latarjet. The resurgence of interest in bone-block procedures such as the Latarjet has, in our opinion, significant pitfalls. The popularity of bony augmentation procedures of this type, which were largely abandoned in North America until relatively recently, raises several concerns: 1) unless performed in a modified form, they do not address capsular laxity or capsulolabral separation, 2) there is a high risk of complications from hardware loosening or nonunion, 3) revision surgery is difficult, and 4) there is a high incidence of postoperative arthrosis. Although there is little doubt that such procedures are effective at restoring stability, complication rates after the Latarjet can be extremely high. In an observational review of patients referred to our office for

Open Treatment of Anterior Instability continued shoulder dysfunction after a Latarjet procedure at another institution,33 we noted that 21 of 27 patients had a nonunion of the transferred coracoid. Nineteen of the 21 also had screw breakage. (The fact that only 5 of the 21 patients with coracoid nonunion had instability complaints leads one to wonder what clinical role, if any, the bone block actually plays in restoring stability.) More than half the patients had radiographic evidence of osteoarthritis, and nerve injuries occurred in 6 patients with 2 axillary nerve injuries causing permanent disability. In addition, 3 patients had biceps pain and asymmetry and 1 had subscapularis insufficiency. Although this was a selected population that sought our assistance after problems with the procedure, it is clear that significant complications are not uncommon—especially when the Latarjet is performed by surgeons who are inexperienced with the technique. In another study,3 we concluded that large defects of the humeral head and/or glenoid are uncommon—even in a tertiary referral shoulder practice with a large percentage of contact athletes. In a 6-year period, we encountered only 9 patients with large (> 4  cm long and 0.5  cm deep) humeral head defects and only 4 with large (> 20% of the glenoid diameter) defects of the glenoid. Based on the low rates of recurrence, motion loss that was equal to or better than that reported for bone-block procedures, and the seemingly self-evident premise that the complication rate of capsular repair alone should be lower than that of capsular repair combined with bone augmentation, it appears that bone-block or grafting procedures are not necessary in the majority of patients with bony defects of the glenoid and/or humeral head if they are treated with contemporary techniques of open stabilization.

CONTRAINDICATIONS Contraindications to the open technique include voluntary instability and concomitant psychological disease. Large Hill-Sachs lesions or glenoid lesions may (in our opinion, rarely) require supplemental bone grafting to compensate for the defects.34 In our practice, such procedures are generally reserved for patients who have failed an attempt an attempt at open capsular repair—an uncommon situation. We prefer to use arthroscopic methods of stabilization in athletes whose primary focus is throwing and in other overhead athletes who cannot accept any restrictions in postoperative motion. If an arthroscopic method is used in an overhead athlete, we strongly encourage the surgeon to have a frank discussion with the athlete and his or her family about the high risk of recurrent instability should the athlete return to contact sports. We subtly encourage the multisport athlete to prioritize the importance of his or her various athletic pursuits. If a contact sport is the priority, we recommend an open repair. In such a case, we do not hesitate to delay operative intervention until the postseason if the athlete has infrequent episodes of instability and can continue to play at a level that he or she finds acceptable. On the other hand, if an

93

overhead sport is deemed to be primary, we encourage early arthroscopic repair. In the unusual case that an open method is used in this group (ie, after failed arthroscopic repair in an athlete who continues to prioritize an overhead sport), we use the technique described by Jobe and colleagues35 in which the subscapularis tendon is split rather than detached.

PATHOANATOMY OF ANTERIOR INSTABILITY The shoulder has the greatest range of motion of any joint in the human body. Because bony restraints to motion are minimal, the surrounding soft tissue maintains the humeral head on the glenoid—yet the shoulder capsule is large, loose, and redundant. There are 3 main ligaments in the anterior capsule that help prevent subluxation or dislocation. These ligaments are known as the superior glenohumeral ligament (SGHL), the middle glenohumeral ligament (MGHL), and the inferior glenohumeral ligament complex (IGHLC). Damage to the IGHLC, which supports the inferior part of the shoulder capsule like a hammock, is related to most cases of anterior instability. The Bankart lesion, involving detachment of the IGHLC insertion on the glenoid, is the most common pathologic lesion associated with traumatic anterior instability. Defects or injuries to the SGHL and MGHL may also contribute to instability.36

GOALS The primary goals of the surgical treatment of shoulder instability should be to restore stability and to provide the patient with near-full, pain-free motion. Older techniques of open shoulder stabilization tended to limit shoulder range of motion in exchange for providing stability. Limiting shoulder motion often led to osteoarthritis; we now understand that it is probably more impor tant to preserve motion than it is to stabilize the shoulder. As a result, any method of open stabilization should be designed to provide close to full range of motion of the shoulder as well as stability.

PREOPERATIVE CONSIDERATIONS History The diagnosis of an anterior shoulder dislocation is usually obvious. The patient typically gives a history of a traumatic injury in which the shoulder “popped out” and had to be reduced. Often, the arm is positioned in abduction and external rotation at the time of the episode. In some cases, however, dislocation can occur with no history of significant trauma. These latter patients are frequently noted to have generalized ligamentous laxity and multidirectional instability and are less likely to demonstrate a Bankart lesion. Such patients typically have enlargement of the rotator interval and loose capsular tissue.

94

Chapter 9

The diagnosis of anterior subluxation can be more subtle. The chief complaint may be a sense of movement, pain, or clicking with certain activities. Pain, rather than instability, may be the predominant complaint. The pain commonly localizes to the bicipital groove area and to the infraspinatus fossa, possibility because of compensatory overload of the dynamic stabilizers of the shoulder.

Physical Examination Apprehension tests are designed to induce anxiety and protective muscular contraction as the shoulder is brought into a position of instability. The anterior apprehension test is performed with the arm abducted and externally rotated. As the examiner progressively increases the degree of external rotation, the patient develops apprehension that the shoulder will “slip out.” This test is uniformly positive in patients with anterior instability. During the relocation test, the examiner’s hand is placed over the anterior shoulder of the supine patient. A posteriorly directed force is applied with the hand to prevent anterior translation of the humeral head. The shoulder is then abducted and externally rotated as it is in the apprehension test. A positive result is obtained when this anterior pressure allows increased external rotation and diminishes associated pain and apprehension. The relocation test seems to be more reliable in overhead athletes and may not be positive in all cases of anterior instability. The belly press and lift off tests should also be performed to confirm the integrity of the subscapularis tendon.

Imaging Routine radiographic examination of the unstable includes an anteroposterior (AP) view (deviated 30 to 45 degrees from the sagittal plane to parallel the glenohumeral joint), a trans-scapular (Y) view, and an axillary view. West Point and Stryker Notch views are helpful in demonstrating bony lesions of the humeral head and glenoid. Magnetic resonance imaging (MRI) is useful to determine whether a Bankart lesion is present and also to assess patients for evidence of concomitant rotator cuff or superior labral pathology. The accuracy of MRI in determining labral pathology is, in our experience, increased with arthrography. Because of the possibility of concomitant rotator cuff injury, MRI should always be considered in older patients with instability—especially if strength and motion are slow to recover after a traumatic episode. Computed tomography (CT) scans may be indicated if bony deficiency is suspected on plain films. However, the surgeon should be cautioned that that CT tends to overestimate the size of larger glenoid lesions and that CT measurement of smaller lesions is not superior to arthroscopic measurement. These phenomena have been previously noted by others.37,38

TIMING OF OPEN SURGICAL REPAIR As mentioned earlier, we do not hesitate to delay open surgical treatment of anterior instability until an athlete completes his or her competitive season. Although there is increasing evidence that the results of arthroscopic stabilization are less satisfactory when surgery is delayed or after multiple recurrences,39,40 delaying open repair has had no such negative impact on recurrence rates in our experience.

SURGICAL TECHNIQUE Our basic procedure for the open surgical treatment of recurrent anterior instability is a modification of the Bankart procedure and involves repair of the anterior capsule and labrum to the glenoid. In most cases, the capsular ligaments are stretched as well as detached, and the procedure is also designed to remove any abnormal laxity.

Anesthesia The procedure is performed after preoperative placement of an interscalene block and an inter-scalene catheter for postoperative analgesia. In most cases, the block is supplemented with general laryngeal mask airway anesthesia. In properly selected patients, the procedure may be performed using regional anesthesia alone.

Arthroscopic Examination We routinely perform a complete arthroscopic examination before proceeding with the open procedure. The patient is placed in the beach-chair position with the head elevated to 60  degrees. Before elevation of the head, an armboard is attached to the operative side of the table and folded sheets are taped to the armboard. The armboard is then rotated against the side of the table to provide arthroscopic access to the shoulder until conversion to the open procedure. A mechanical arm holder is used to control shoulder position during arthroscopy. The shoulder is examined through standard anterior and posterior arthroscopic portals. Supplementary portals are created if indicated based on the findings of labral or rotator cuff pathology. Any loose bodies are removed during arthroscopy. When superior or (less commonly) posterior labral tears accompany anterior instability, they are repaired arthroscopically because access to these parts of the labrum is not possible with an open anterior approach. Similarly, supraspinatus or infraspinatus pathology is addressed with arthroscopic treatment before the open procedure. When sizable Hill-Sachs lesions are noted in patients at high risk for recurrent instability, we now commonly perform arthroscopic “remplissage” to cover the defect prior to the open repair.41 In addition, the arthroscopic examination is helpful in determining the specific anterior pathology prior to the open repair.

Open Treatment of Anterior Instability

95

Figure 9-1. Incision along the anterior axillary crease.

Conversion to Open Procedure and Positioning After completion of the arthroscopic examination and treatment, the posterior and accessory portals are closed. The arm is detached from the mechanical arm holder. The head of the operating table is lowered to 15 degrees of elevation, and the previously placed armboard is rotated from the table so the upper extremity can abducted 45 degrees on an armboard. The folded sheets, which had been taped to the armboard, are placed beneath the elbow. The sheets maintain the arm in the coronal plane of the thorax and minimize extension of the shoulder. The surgeon initially stands in the axilla. Two assistants are used. The first assistant’s primary responsibilities are to control arm position and to keep the humeral head reduced during the capsular repair. The first assistant alternates position with the surgeon. When the surgeon is in the axilla, the first assistant stands lateral to the arm. When the surgeon moves to the lateral aspect of the arm, the first assistant shifts to the axilla. The first assistant also holds the humeral head retractor when it is in position. The second assistant stands on the opposite side of the table and holds the medial (glenoid) retractors.

OPEN SURGICAL TECHNIQUE An anterior deltopectoral approach to the shoulder is used. The anterior arthroscopic portal is incorporated into the skin incision. The skin is incised along the anterior axillary crease (Figure  9-1) in a longitudinal fashion along Langer’s lines. When the incision is placed in the anterior axillary crease, the cosmetic result is usually quite satisfactory. The incision is lateral to the coracoid process. The deltopectoral interval

Figure 9-2. Placement of self-retaining retractors.

is identified, the cephalic vein is retracted laterally, and the interval is developed. The clavipectoral fascia is then incised at the lateral border of the conjoined tendon near its coracoid attachment, and the coracoacromial ligament is divided to facilitate exposure of the superior aspect of the capsule and, particularly, the rotator interval area. Two self-retaining retractors are then placed in the wound (Figure 9-2). Placement of these retractors frees the assistants to aid in arm position and shoulder reduction. At this point, the surgeon shifts position from the axilla and stands lateral to the arm. The bicipital groove and the lesser tuberosity are identified. A vertical tenotomy of the subscapularis tendon is performed with electrocautery approximately 1  cm medial to insertion on the lesser tuberosity. The medial portion of the tendon is tagged with heavy No. 1 nonabsorbable braided polyester (Ethibond, Ethicon, Inc) sutures placed in a modified Kessler fashion. The interval between the anterior aspect of the capsule and the subscapularis tendon is then carefully developed with a combination of blunt and sharp dissection. Care is taken to undermine the subscapularis without completely detaching it superiorly and inferiorly. (Preservation of the superior and inferior attachments is believed to largely eliminate the small risk of postoperative subscapularis rupture.) In our opinion, splitting the subscapularis42 (as opposed to tenotomizing it) has 2  significant disadvantages: 1) it is difficult to assess the rotator interval without tenotomy, and a significant rotator interval defect can easily be missed,

96

Chapter 9

Figure 9-3. Horizontal capsulotomy. (Reprinted with permission from and copyrighted by Delilah Cohn.)

and 2) because some capsular attachments to the subscapularis remain when the tendon is split, it is more difficult to eliminate excess capsular laxity when performing an open repair. We believe these factors explain higher postoperative recurrence rates in series that feature routine splitting of the subscapularis.43 (In our practice, the subscapularis split is reserved for rare cases of revision stabilization in throwing and overhead athletes—we prefer early arthroscopic repair as the primary surgical treatment in throwing and overhead athletes. With the subscapularis split, the muscle and tendon are incised with an electrocautery and the split is developed using blunt dissection with a periosteal elevator. The elevator is swept superiorly and inferiorly to free the capsule from the subscapularis muscle. Dissection is then continued medially in the same fashion. Laterally, sharp dissection with a scalpel is necessary to free the capsule from the firmly attached portion of the tendon.) After separation of the anterior capsule from the subscapularis, the laxity and quality of the capsule are assessed. If there is a lesion in the rotator interval, it is closed at this point with No.  1 nonabsorbable braided polyester (Ethibond) sutures. A horizontal capsulotomy is then performed (Figure 9-3), and a ring (Fukuda) retractor is placed intra-articularly. The anterior glenoid neck is explored for evidence of a Bankart lesion. The joint is then irrigated to remove any residual loose bodies. If a Bankart lesion is noted, the capsulolabral separation at the anteroinferior glenoid neck is extended medially with

Figure 9-4. The inferior capsular flap is used to repair a Bankart lesion. (Reprinted with permission from and copyrighted by Delilah Cohn.)

an elevator or knife to allow placement of a retractor along the glenoid neck. The glenoid neck is then roughened with an osteotome or motorized burr to provide a bleeding surface. Two or 3 suture anchors are placed in the anteroinferior glenoid neck near, but not on, the articular margin of the glenoid. The inferior capsular flap is mobilized slightly medially and superiorly. The inferior flap is reattached to the anterior aspect of the glenoid to repair the Bankart lesion using horizontal mattress sutures arising from the suture anchors (Figure  9-4). The arm is placed in 45 degrees of abduction and 45 degrees of external rotation and the humeral head is maintained in reduction as the sutures are tied. The goal is not to reduce external rotation but to eliminate excess capsular volume and to restore the competency of the IGHLC at its glenoid insertion. After repair of the Bankart lesion (or in the absence of a Bankart lesion), an anterior capsulorrhaphy is performed to eliminate excess capsular laxity. The arm is maintained in 45 degrees of abduction and 45 degrees of external rotation, and the superior and inferior capsular flaps are reapproximated with forceps. The shoulder is held in a reduced position. If there is no overlap of the capsular flaps, the superior flap is attached to the superior margin of the inferior flap. If the flaps can be overlapped, the capsule is shifted to eliminate excess capsular volume. If 5 mm or less of overlap is present (the most common occurrence), capsular laxity is eliminated by pulling the superior flap over the inferior flap using horizontal mattress sutures derived from the same anchors that were used to repair the inferior flap (Figure  9-5). The sutures are tied a second time after placement through the superior flap. The overlapped superior flap is then fixed

Open Treatment of Anterior Instability

Figure 9-5. Sutures are passed a second time through the superior capsular flap to double the thickness of the repair and to eliminate excess capsular laxity. (Reprinted with permission from and copyrighted by Delilah Cohn.)

to the underlying inferior flap with absorbable sutures to double the capsular thickness With more than 5 mm of capsular overlap, the capsulotomy is extended in a vertical direction near its lateral insertion on the humeral neck, and a lateral “T-plasty” capsular shift is performed (Figure 9-6). The inferolateral capsular flap of the lateral T-plasty is shifted superolaterally and the superolateral flap is moved over the inferior flap in an inferolateral direction. After the capsule has been addressed satisfactorily, the subscapularis is reapproximated, but not shortened, with nonabsorbable suture. The deltopectoral interval is closed with absorbable suture. Routine wound closure is then performed.

POSTOPERATIVE CONSIDERATIONS

97

Figure 9-6. Lateral T-plasty capsular shift in cases with pronounced capsular laxity. (Reprinted with permission from and copyrighted by Delilah Cohn.)

impor tant to note that the patients in most series of open Bankart repairs were not carefully selected. Patients with bone loss and/or excess capsular laxity and athletes who participated in contact athletes were often included in these series. The outcomes of open stabilization in contact athletes and in patients with bone loss appear to be superior to those reported in similar populations with arthroscopic techniques.1-5,8,13-16,32

Range of Motion Motion loss with current open techniques is also acceptable. In our experience,4 84% of patients regained all or nearly all of their motion. No patient lost more than 15 degrees of external rotation when compared with the contralateral side.

TIMING OF RETURN TO PLAY

Rehabilitation Our standard rehabilitation protocol is described in Table 9-1.

RESULTS Recurrence As mentioned earlier, the published recurrence rates after open stabilization for anterior instability have generally been low, ranging from 0% to 5% in most series.1-8 It is

In a recent systematic review of 29 series of open Bankart repairs, Stone and Pearsall44 found that noncontact athletes were allowed to return to play (RTP) between 12 and 16 weeks. In our opinion, this seems overly aggressive. In contrast, the same authors44 found that contact athletes were allowed to RTP at an average of 23.2 weeks (5.3 months). Okoroha et  al noted that professional football players did not RTP until an average of 9 months after surgical treatment.31 Such a delay is likely due to the long off-season in professional football. Our policy, if an athlete has completed

98

Chapter 9

Table 9-1. Postoperative Rehabilitation Protocol Weeks 0 to 4 Perform pendulums, elbow ROM. Weeks 4 to 8 Perform passive and AAROM and limit external rotation to 45 degrees. Perform deltoid isometrics with arm at low abduction levels. When 140 degrees of active forward flexion is obtained, begin TheraBands (Performance Health): IR/ER cuff strengthening with arm at side. Perform scapular rehabilitation: stability exercises, isometrics, scapular pinch, scapular shrug. Perform closed-chain exercises: hand in contact with wall or ball. Perform specific scapular maneuvers: elevation, depression, retraction, protraction. Correct strength or flexibility deficit in trunk, back, and hip. Weeks 8 to 12 Limit external rotation to 45 degrees. Continue IR/ER strengthening with bands. If no impingement or cuff symptoms, may slowly increase abduction with time. Perform scapular elevation with thumbs up (“full can”), prone horizontal abduction in ER to 100 degrees of abduction, prone horizontal abduction in neutral, and prone rowing. Do not use empty cans!!! Perform scapular rotator strengthening: press ups, shrugs, open-can exercise, and body blade. Perform manual resistance scapular stabilization drills. Weeks 12 to 16 Work on regaining terminal external rotation. Perform side-lying dumbbell or tubing: ER at neutral and 90 degrees abduction, and IR at neutral and 90 degrees abduction. Perform diagonal pattern extension and diagonal pattern flexion. Perform reciprocal isometric contractions for IR/ER muscles. Facilitate agonist-antagonist co-contraction to restore balance to force couples. Perform dynamic stabilization: PNF patterns with rhythmic stabilization, rhythmic stabilization throwing Plyoball (www. donchu.com) against wall, and push-ups onto a ball. Perform Plyometrics: 2-handed drills: chest pass, overhead soccer throw, and side-to-side throws. Progress to 1-handed drills. Perform endurance drills: wall dribbling with Plyoball, wall arm circles, upper body cycle, and low-weight and highrepetition isotonic weights. > Week 16 Perform conventional weight training, orient for return to sport. Assess ER to IR ratio (ideal > 66%). Perform fatigue testing. If indicated, obtain abduction harness. Abbreviations: AAROM, active assisted range of motion; ER, external rotation; IR, internal rotation; PNF, proprioceptive neuromuscular facilitation; ROM, range of motion.

rehabilitation in a dedicated fashion and has achieved the goals of the terminal phases of therapy, has been to allow RTP as early as 4.5 months when in season, although we prefer to wait 6 months if there is not a pressing need to return

to competition. It is our belief that returning at 4.5 months carries with it a slight increase in the risk of recurrence and that there is little advantage to waiting beyond 6 months in a properly rehabilitated patient.

Open Treatment of Anterior Instability

Return to Play RTP rates can be affected both by physical and psychological factors. Some of the nonmusculoskeletal issues that can prevent athlete from returning to his or her previous level of performance include fear of recurrence that exceeds the desire to return, fear of another operation and an additional lengthy period of rehabilitation, performance anxiety, and change in sport priority—particularly when an athlete sustains an injury in a less-favored activity. Surgical treatment of shoulder instability has been shown to improve an athlete’s ability to return to his or her sport. In a recent meta-analysis, Zaremski et al40 reported an RTP rate of 41% in adolescent athletes who were treated nonoperatively for instability compared to RTP rates of 95% in athletes treated with early surgical intervention and 77% in patients treated with a delayed operation. Memon and colleagues45 assessed RTP rates after arthroscopic Bankart repair and found that only 53% of athletes were able to return to their previous levels of competition. They also reported that competitive athletes returned to preinjury levels only 71% of the time. Aboalata et al34 found that only 49% of patients returned to preinjury levels after arthroscopic stabilization. In a systematic review, Ialenti et  al reported that 71% of patients treated surgically returned to preinjury performance.37 We find these RTP rates unacceptable in the treatment of the elite athlete—these figure indicates that, at best, only 3 of every 4 athletes treated for shoulder instability are able to return to their sport at the same level. It is impor tant to note that RTP is not the same thing as RTP without recurrent instability—recurrence affects performance and the level to which an athlete is able to return. It is highly unlikely that athletes with recurrent instability will be able to return to their previous level performance. With the high recurrence rates reported for arthroscopic stabilization in high-demand patients and the low RTP rates described earlier in series reported primarily after arthroscopic repair, it is our fervent hope that readers of this chapter will agree and consider the technique described in this chapter. There has been a paucity of high-quality studies in recent years on the results of open capsular repair from major centers of shoulder surgery. Ialenti et  al37 found only 3 studies of open Bankart repair to include in their systematic review, and Abdul-Roussel and colleagues46 were able to find only 4 such studies. These papers reported overall RTP rates of 66% and 85%, respectively, after open Bankart. The latter study indicated that 86% of athletes were able to return to their previous levels of competition after the procedure. In our series of open stabilization in American football players, 52 of 58 athletes (89%) returned to their previous level of sport.4 Of the 6 players who did not return, only 1 discontinued because of recurrent instability and 5 stopped participation for reasons unrelated to their shoulder.

99

COMPLICATIONS Recurrent instability is the greatest concern after any stabilization procedure. In 3 large series analyzing failures of open capsular repair (from Harvard, Columbia, and the Hospital for Special Surgery), unaddressed excess capsular laxity was determined to be the primary reason for failure in each series. On the other hand, bony deficiency was not considered a common cause of failure.7,47,48 The risk of subscapularis insufficiency is often discussed as a major risk of open stabilization. This concern appears to be somewhat overstated. Prior to the publication of 2 papers that created alarm about the risk of subscapularis rupture after open anterior stabilization,49,50 such an occurrence was a reportable case.5,51 In addition, in one of the series,49 only one patient had documented subscapularis insufficiency by MRI. In the other,50 no complete ruptures were noted on MRI; instead, a degree of atrophy was noted in the superior portion of the tendon that was largely compensated for by hypertrophy of the inferior portion. Clinical insufficiency of the subscapularis after open stabilization is exceedingly rare. (We have had no instances after primary stabilization in our practice over more than 25  years.) Two analyses of shoulder strength after open vs arthroscopic stabilization have determined that there were no differences between open and arthroscopic groups at 1 year after surgery.18,52 Other than recurrence instability, subcutaneous hematoma formation is the most common complication in our experience (1.5% of our cases). If a hematoma forms, it may be observed as long as the wound is not draining. When the hematoma causes persistent wound drainage, surgical evacuation is recommended. We have seen little evidence of “postcapsulorrhaphy” arthropathy in our patients, some of whom we have followed for more than 25 years. It is our impression that the prevalence of shoulder arthropathy in this group does not exceed that of the general population.

CONCLUSION As orthopedic surgeons and team physicians, we need to “do better” for the patients and athletes under our care. The high recurrence rates reported for arthroscopic stabilization have led to an increase in bone-block procedures. Such bone-block procedures seem unnecessary except in unusual circumstances. They are plagued by high complication rates, and assignment of an impor tant clinical function to the bone-block itself should be subject to skepticism. There is an intermediate option between arthroscopic stabilization and the Latarjet procedure that consistently yields excellent results even in high-risk populations—open capsular repair.

100

Chapter 9

REFERENCES 1.

2.

3.

4.

5. 6. 7.

8.

9.

10.

11.

12.

13.

14.

15.

16.

17.

18.

Gill TJ, Micheli LJ, Gebhard F, Binder C. Bankart repair for anterior instability of the shoulder. Long-term outcome. J Bone Joint Surg Am. 1997;79(6):850-857. doi:10.2106/00004623-199706000-00008. Gill TJ, Zarins B. Open repairs for the treatment of anterior instability. Am J Sport Med. 2003;31(1):142-153. doi:10.1177/03635465030 310011001. Pagnani MJ. Open capsular repair without bone block of anterior instability in patients with and without bony defects of the glenoid and/or humeral head. Am J Sports Med. 2008;36(9):1805-1812. doi:10.1177/0363546508316284. Pagnani MJ, Dome DC. Surgical treatment of traumatic anterior shoulder instability in American football players. J Bone Joint Surg. 2002;84(5):711-715. doi:10.2106/00004623-200205000-00002. Rowe CR, Patel D, Southmayd WW. The Bankart procedure: a longterm end-result study. J Bone Joint Surg Am. 1978;60(1):1-16. Rowe CR, Zarins B. Recurrent transient subluxation of the shoulder. J Bone Joint Surg Am. 1981;63(6):863-872. Rowe CR, Zarins B, Ciullo JV. Recurrent anterior dislocation of the shoulder after surgical repair. Apparent causes of failure and treatment. J Bone Joint Surg Am. 1984;66(2):159-168. Wirth MA, Blatter G, Rockwood CA Jr. The capsular imbrication procedure for recurrent anterior instability of the shoulder. J Bone Joint Surg Am. 1996;78(2):246-260. doi:10.2106/00004623-199602000-00012. Owens BD, Harrast JJ, Hurwitz SR, Thompson TL, Wolf JM. Surgical trends in Bankart repair: an analysis of data from the American Board of Orthopaedic Surgery certification examination. Am J Sports Med. 2011;39(9):1865-1869. doi:10.1177/0363546511406869. Baig F, Boileau  P. The Instability Severity Index Score. A simple pre-operative score to select patients for arthroscopic or open shoulder stabilization. J Bone Joint Surg Br. 2007;89(11):1470-1477. doi:10.1302/0301-620X.89B11.18962. Boileau P, Villalba M, Héry JY, Balg F, Ahrens P, Neyton L. Risk factors for recurrence of anterior instability after arthroscopic Bankart repair. J Bone Joint Surg Am. 2006;88(8):1755-1763. doi:10.2106/ JBJS.E.00817. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694. doi:10.1053/ jars.2000.17715. Cole BJ, L’Insalata J, Irrgang J, Warner JJ. Comparison of arthroscopic and open anterior shoulder stabilization. A two to sixyear follow-up study. J Bone Joint Surg Am. 2000;82(8):1108-1114,. doi:10.2106/00004623-200008000-00007. Hubbell JD, Ahmad S, Bezenoff LS, Fond J, Pettrone FA. Comparison of shoulder stabilization using arthroscopic transglenoid sutures versus open capsulolabral repairs: a 5-year minimum follow-up. Am J Sports Med. 2004;32(3):650-654. doi:10.1177/0095399703258747. Leroux TS, Saltzman BM, Meyer M, et al. The influence of evidencebased surgical indications and techniques on failure rates after arthroscopic shoulder stabilization in the contact or collision athlete with anterior shoulder instability. Am J Sports Med. 2017;45(5):12181225. doi:10.1177/0363546516663716. Mazzocca AD, Brown FM Jr, Carreira DS, Hayden J, Romeo AA. Arthroscopic anterior shoulder stabilization of collision and contact athletes. Am J Sports Med. 2005;33(1):52-60. doi:10.1177/0363546504268037. Mologne TS, Provencher MT, Menzel KA, Vachon TA, Dewing CB. Arthroscopic stabilization in patients with an inverted pear glenoid: results in patients with bone loss of the anterior glenoid. Am J Sports Med. 2007;5(8):1276-1283. doi:10.1177/0363546507300262. Rhee YG, Lim CT, Cho NS. Muscle strength after anterior shoulder stabilization: arthroscopic versus open Bankart repair. Am J Sports Med. 2007;35(11):1859-1864. doi:10.1177/0363546507304329.

19.

20.

21.

22.

23.

24.

25.

26.

27.

28.

29.

30.

31.

32.

33.

34.

Voos JE, Livermore RW, Feeley BT, et  al; HSS Sports Medicine Ser vice. Prospective evaluation of arthroscopic Bankart repairs for anterior instability. Am J Sports Med. 2010;38(2):302-307. doi:10.1177/0363546509348049. Alkaduhimi H, van der Linde JA, Willigenberg NW, Paulino Pereira, NR, van Deurzen DF, van den Bekerom MP. Redislocation risk after an arthroscopic Bankart procedure in collision athletes: a systematic review. J Shoulder Elbow Surg. 2016;25(9):1549-1558. doi:10.1016/j. jse.2016.05.002. Hohmann E, Tetsworth K, Glatt V. Open versus arthroscopic surgical treatment for anterior shoulder dislocation: a comparative systematic review and meta-analysis over the past 20  years. J Shoulder Elbow Surg. 2017;26(10):1873-1880. doi:10.1016/j.jse.2017.04.009. Arce G, Arcuri F, Ferro D, Pereira E. Is selective arthroscopic revision beneficial for treating recurrent anterior shoulder instability? Clin Orthop Relat Res. 2012;470(4):965-967. doi:10.1007/ s11999-011-2001-0. Bartl C, Schumann K, Paul J, Vogt S, Imhoff AB. Arthroscopic capsulolabral revision repair for recurrent anterior shoulder instability. Am J Sports Med. 2011;39(3):511-518. doi:10.1177/0363546510388909. Rhee YG, Ha IH, Cho NS. Anterior shoulder stabilization in collision athletes. Am J Sports Med. 2006;34(6):979-985. doi:10.1177/0363546505283267. Freedman KB, Smith AP, Romeo AA, Cole BJ, Bach BR  Jr. Open Bankart repair versus arthroscopic repair with transglenoid sutures or bioabsorbable tacks for recurrent anterior instability of the shoulder: a meta-analysis. Am J Sports Med. 2004;32(6):1520–1527. doi:10.1177/0363546504265188. Lenters TR, Franta AK, Wolf FM, Leopold SS, Matsen FA  III. Arthroscopic compared with open repairs for recurrent anterior shoulder instability. A systematic review and meta-analysis of the literature. J Bone Joint Surg Am. 2007;89(2):244-254. doi:10.2106/ JBJS.E.01139. Mohtadi NG, Bitar IJ, Sasyniuk TM, Hollinshead RM, Harper WP. Arthroscopic versus open repair for traumatic anterior shoulder instability: a meta-analysis. Arthroscopy. 2005;21(6):652-658. doi:10.1016/j.arthro.2005.02.021. Wang L, Liu Y, Su X, Liu S. A meta-analysis of arthroscopic versus open repair for treatment of Bankart lesions in the shoulder. Med Sci Monit. 2015;21:3028-3035. doi:10.12659/MSM.894346. Mologne TS, Zhao K, Hongo M, Romeo AA, An KN, Provencher MT. The addition of rotator interval closure after arthroscopic repair of either anterior or posterior shoulder instability: effect on glenohumeral translation and range of motion. Am J Sports Med. 2008;36(6):1123-1131. doi:10.1177/0363546508314391. Plausinis D, Bravman JT, Heywood C, Kummer FJ, Kwon YW, Jazrawi LM. Arthroscopic rotator interval closure: effect of sutures on glenohumeral motion and anterior-posterior translation. Am J Sports Med. 2006;34:1656-1661. doi:10.1177/0363546506289881. Okoroha KR, Taylor KA, Marshall NE, et  al. Return to play after shoulder instability in National Football League athletes. J Shoulder Elbow Surg. 2018;27(1):17-22. doi:10.1016/j.jse.2017.07.027. Bigliani LU, Newton PM, Steinmann SP, Connor PM, McIlveen SJ. Glenoid rim lesions associated with recurrent anterior dislocation of the shoulder. Am J Sports Med. 1998;26(1):41-45. doi:10.1177/03635 465980260012301. Pagnani, MJ, Hill JE. Complications of the Latarjet procedure. Paper presented at: Closed Meeting, American Shoulder and Elbow Surgeons (ASES) 2013 Annual Meeting; October  12-15, 2013; Las Vegas, NV. Aboalata M, Plath JE, Seppel G, Juretzko J, Vogt S, Imhoff AB. Results of arthroscopic Bankart repair for anterior-inferior shoulder instability at 13-year follow-up. Am J Sports Med. 2016;45(4):782-787. doi:10.1177/0363546516675145.

Open Treatment of Anterior Instability 35.

36.

37.

38.

39.

40.

41.

42.

43.

Jobe FW, Giangarra CE, Kvitne RS, Glousman RE. Anterior capsulolabral reconstruction of the shoulder in athletes in overhand sports. Am J Sports Med. 1991;19(5):428-434. doi:10.1177/036354659101900502. Pagnani MJ, Warren RF. Stabilizers of the glenohumeral joint. J Shoulder Elbow Surg. 1994;3(3):173-190. doi:10.1016/ S1058-2746(09)80098-0. Ialenti MN, Mulvihill JD, Feinstein M, Zhang AL, Feeley BT. Return to play following shoulder stabilization: a systematic review and meta-analysis. Orthop J Sports Med. 2017;5(9):2325967117726055. doi:10.1177/2325967117726055. Sugaya H, Moriishi J, Dohi M, Kon Y, Tsuchiya A. Glenoid rim morphology in recurrent anterior glenohumeral instability. J Bone Joint Surg Am. 2003;85(5):878-884. doi:10.2106/00004623-200305000-00016. Owens BD, Cameron KL, Peck KY, et al. Arthroscopic versus open stabilization for anterior shoulder subluxations. Orthop J Sports Med. 2015;3(1):2325967115571084. doi:10.1177/2325967115571084. Zaremski JL, Galloza J, Sepulveda F, Vasilopoulos T, Micheo W, Herman DC. Recurrence and return to play after shoulder instability events in young and adolescent athletes: a systematic review and meta-analysis. Br J Sports Med. 2017;51(3):177-184. doi:10.1136/ bjsports-2016-096895. Wolf EM, Wilk RM, Richmond JC. Arthroscopic Bankart repair using suture anchors. Oper Techn Orthop. 1991;1(2):184-191. doi:10.1016/ S1048-6666(05)80030-8. Itoi E, Lee S-B, Amrami NN, Wender DE, An KN. Quantitative assessment of classic anteroinferior bony Bankart lesions by radiography and computed tomography. Am J Sports Med. 2003;31(1):112118. doi:10.1177/03635465030310010301. Mohtadi NG, Chan DS, Hollinshead RM, et al. A randomized clinical trial comparing open and arthroscopic stabilization for recurrent traumatic anterior shoulder instability: two-year follow-up with disease-specific quality-of-life outcomes. J Bone Joint Surg Am. 2014;96(5):353-360. doi:10.2106/JBJS.L.01656.

44.

45.

46.

47.

48.

49.

50.

51.

52.

101

Stone GP, Pearsall AW IV. Return to play after open Bankart repair: a systematic review. Orthop J Sport Med. 2014;2(2):2325967114522960. doi:10.1177/2325967114522960. Memon M, Kay J, Cadet ER, Shahsavar S, Simunovic N, Ayeni OR. Return to sport following arthroscopic Bankart repair: a systematic review. J Shoulder Elbow Surg. 2018;27(7):1342-1347. doi:10.1016/j. jse.2018.02.044. Abdul-Rassoul H, Galvin JW, Curry EJ, Simon J, Li  X. Return to sport after surgical treatment for anterior shoulder instability: a systematic review. Am J Sports Med. 2019;47(6):1507-1515. doi:10.1177/0363546518780934. Levine WN, Arroyo JS, Pollock RG, Flatow EL, Bigliani LU. Open revision stabilization surgery for recurrent anterior glenohumeral instability. Am J Sports Med. 2000;28(2):156-160. doi:10.1177/0363 5465000280020401. Zabinski SJ, Callaway GH, Cohen S, Warren RF. Revision shoulder stabilization: 2- to 10-year results. J  Shoulder Elbow Surg. 1999;8(1):58-65. doi:10.1016/s1058-2746(99)90057-5. Sachs RA, Williams B, Stone ML, Paxton L, Kuney  M. Open Bankart repair: correlation of results with postoperative subscapularis function. Am J Sports Med. 2005;33(10):1458-1462. doi:10.1177/0363546505275350. Scheibel M, Tsynman A, Magosch P, Schroeder RJ, Habermeyer P. Postoperative subscapularis muscle insufficiency after primary and revision open shoulder stabilization. Am J Sports Med. 2006;34(10):1586-1593. doi:10.1177/0363546506288852. Greis PE, Dean M, Hawkins RJ. Subscapularis tendon disruption after Bankart reconstruction for anterior instability. J Shoulder Elbow Surg. 1996;5(3):219-222. doi:10.1016/s1058-2746(05)80010-2. Hiemstra LA, Sasyniuk TM, Mohtadi NG, Fick GH. Shoulder strength after open versus arthroscopic stabilization. Am J Sports Med. 2008;36(5):861-867. doi:10.1177/0363546508314429.

10 Latarjet and Coracoid Transfer in Athletes Alexander Beletsky, BA; Ian J. Dempsey, MD, MBA; Brandon J. Manderle, MD; and Nikhil N. Verma, MD

Anterior shoulder instability includes a broad range of physical findings, ranging from seemingly benign subluxations to complete dislocation of the humeral head from the glenohumeral joint. Of those presenting with primary anterior instability, as many as 40% to more than 95% go on to develop recurrent instability depending on the targeted patient population.1-4 Recurrent instability further destabilizes the shoulder because of weakening of critical capsuloligamentous structures.5 Repeated translation of the humeral head over the glenoid rim can lead to bony lesions to the glenoid, bony Bankart of bone atrition6,7 as well as the humeral head (ie, Hill-Sachs lesion).8,9 Surgical intervention is often turned to as a means of decreasing the risk of recurrent dislocation, preventing progression of glenoid and humeral bone loss, and maintaining appropriate quality of life.9,10 Surgical procedures for the treatment of anterior shoulder instability include both open and arthroscopic soft-tissue procedures such as the Bankart repair. When bone involvement is present, several surgical options are available. In situations with minimal glenoid bone involvement, an open or arthroscopic Bankart repair incorporating any bone fragment may be performed. Large degrees of glenoid bone involvement lends itself to bony procedures like the Latarjet, Bristow, iliac crest bone graft, and distal tibial allograft (DTA).11-14 Additionally, the use of an iliac crest bone graft or DTA is often reserved for revision scenarios.9,15 Hill-Sachs lesions can also play a major role in recurrent anterior shoulder instability.16 Soft-tissue procedures like remplissage or bony procedures like bulk allograft transplant may be necessary to address humeral head bone loss.17,18 The majority of patients with recurrent anterior instability exhibit a bony Bankart lesion or glenoid rim irregularities, but may also exhibit “bipolar bone

loss” in the scenario of bony changes to both the glenoid and humeral head.8,19,20 Although traditionally bone loss thresholds surpassing 20% have been linked to increased risk of failure with soft-tissue repair,21,22 new literature has suggested that “subcritical” glenoid bone loss may also pose heightened risks of recurrent instability.23-25 As a result, bony techniques are receiving increased consideration, particularly in cases of recurrent instability and even primary instability in patients with significant bone loss.26,27

EVALUATION AND INDICATIONS Initial Evaluation and Diagnostic Steps Clinical assessment begins with a thorough patient history, physical examination, and appropriate imaging. During the initial history taking, one must identify the mechanism of injury (subluxation vs dislocation) with specific discussion on how the shoulder was reduced if a dislocation occurred (eg, self-reduction, on-field reduction, need for emergency department evaluation, and sedation). Other key features include the frequency of dislocation and/or subluxation events, history of hyperlaxity, and sport-specific factors (eg, collision sports, swimming, overhead athletes). Physical examination should include inspection, palpation, and the assessment of a patient’s range of motion (ROM) (ie, flexion, extension, abduction, internal rotation, external rotation), strength, and neurovascular status to exclude neurological sequelae common in shoulder dislocation (ie, axillary nerve palsy, brachial plexus palsy). Provocative testing should be used to assess for the presence of specific patterns of instability (ie, anterior, posterior, multidirectional). Anterior and

- 103 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 103-113). © 2021 SLACK Incorporated.

104

Chapter 10

Figure 10-1. Glenoid bone loss calculation. Glenoid bone loss is measured by dividing the true glenoid diameter with any possible glenoid bone loss considered, from the diameter of a perfect circle fit of the glenoid prior to any bone loss. Accuracy may be maximized by using the contralateral shoulder as an estimate of the perfect circle fit of the glenoid, especially if it lacks glenoid bone loss.

posterior instability can be assessed using a combination of the sulcus sign on arm traction and the load-shift test.28 The relocation test is particularly useful in the diagnosis of anterior instability, given a positive predictive value of 98% and a specificity of 99%.29 Other clinical tests, such as the hyperabduction test, Kim test, and jerk test, can assess for inferior and posterior instability.30,31 Imaging evaluation is particularly critical in the evaluation of acute instability, in that anatomic reduction is confirmed on radiographs. Impor tant views to obtain include true anterior-posterior (Grashey), axillary, and scapular-lateral views. These images are critical in establishing humeral head alignment and aid in the diagnosis of any related fractures. Computed tomography (CT) is the optimal imaging modality for assessment of the role of glenoid bone loss in management. The preferred methodology for optimal glenoid bone loss measurement is the use of thin-slice CT imaging with 3-dimensional (3D) reconstruction, allowing for subtraction of the humeral head to provide an en face view of the glenoid. Magnetic resonance imaging (MRI) has an impor tant role in the evaluation of possible soft-tissue injury, including the evaluation of capsulolabral structures of the shoulder. MRI may also be used to calculate bone loss; however, correlations between modalities ranged from 0.39 to 0.64 depending on the dimension of interest.32-34 After gathering this important information, the provider and athlete should discuss the athlete’s functional expectations as it relates to return to future play.

Bone Loss: Glenoid, Humeral Head, or Bipolar? The importance of assessing bone loss cannot be overlooked both in the primary and recurrent anterior shoulder instability patient. The presence of specific bony defects can in some cases signal the need for urgent surgical

intervention (eg, bony Bankart lesion in acute instability).35 When using the aforementioned imaging techniques (eg, 3D CT) to evaluate for bone loss, it is critical to evaluate for bony changes both to the glenoid and humeral head. Bipolar bone loss has traditionally been evaluated using the concept of “engaging or nonengaging” humeral head lesions that rely on the identification of impor tant risk factors for failure after arthroscopic Bankart repair (ie, “inverted-pear” glenoid, a Hill-Sachs lesion that engages the glenoid in abduction and external rotation).36 More recently, Itoi et  al used 3D CT to define the contact zone between the glenoid and humeral head as a “track.” An “on-track” is a nonengaging Hill-Sachs lesion that occurs when the medial margin of a Hill-Sachs lesion falls onto the glenoid rim so the bony support exists medially. An “off-track” or engaging lesion on the other hand occurs when the edge of the Hill-Sachs lesion is more medial than that of the glenoid track, so no bony support exists.37,38 The methodology to determine the on-track or off-track nature of a Hill-Sachs lesion in the presence of glenoid bone loss begins with the use of 3D-CT with bone reconstruction to model the glenoid and humeral head. Glenoid bony defect size may be assessed using various methods, such glenoid length,39 width-to-length ratio,22 glenoid index,40 and the defect area.19 The method preferred at our institution involves the glenoid index, using the sagittal view on CT to superimpose a circle encapsulating the glenoid circumference (Figure  10-1). If CT of the contralateral shoulder is available, it may be used as a reference point for estimation of the total glenoid width. Other wise, we estimate a perfect circle fit of the glenoid on the operative side and measure the total circle diameter and defect diameter. Dividing the defect diameter by the total circle diameter yields the estimated percentage of glenoid bone loss. Eighty-three percent of the total glenoid width minus the defect size is calculated.41 The medial rotator cuff attachment margin is estimated on the humeral head, and the previous measurement is used to mark the medial glenoid track edge with the presence of a

Latarjet and Coracoid Transfer in Athletes

105

Figure 10-2. Determining glenoid track and on/ off track lesions. The figure depicts the process by which to determine glenoid track. Begin by measuring the width of anterior glenoid bone loss (d), subtracting this from 0.83 times the total diameter D to estimate width of the glenoid track (GT). Next, calculate the Hill-Sachs (HS) width and width between the end of the HS and rotator cuff insertion, the sum of which is known as the Hill-Sachs Index (HSI). If the HSI is greater than the GT, the lesion if off-track and engaging, and if the HSI is less than the GT, the lesion is on-track and nonengaging.

glenoid defect. If the Hill-Sachs lesion extends beyond the estimated medial edge, the lesion is considered to be offtrack 37 (Figure 10-2).

Management Options Nonoperative management may be favored in patients with primary instability without signs of Bankart lesions on MRI, although previous studies have demonstrated that up to 97% of athletes with anterior shoulder instability present with either a labral lesion or damage to supporting ligaments.42 A Sullivan brace may be used in athletes to permit completion of the season of play, although the benefit of delaying management must be weighed against the risk of redislocation and further injury. Surgical management most often applies to the athlete suffering recurrent instability with the goal of further injury prevention, maintenance of appropriate neurovascular status, and re-establishing confidence in shoulder function. Two distinct classes of surgical interventions include soft-tissue operations and bony procedures. The primary soft-tissue repair technique is the arthroscopic Bankart repair, often performed using suture anchors placed along the inferior glenoid rim.43-45 Bony procedures include the Latarjet, Bristow, iliac crest bone graft, and DTA, each of which harvest various bony grafts and transfer them to the anterior glenoid to provide a bony block to future anterior dislocation.12-14,46,47 Risk factors of failure following primary arthroscopic shoulder stabilization include the following: male sex,48 age younger than 20  years,48 3 or more preoperative dislocations,48 3 or fewer suture anchors,49 and beachchair positioning.50,51 Significant glenoid or humeral head bone loss is the most well-established risk factor across the literature. Significant glenoid bone loss is classically defined as an inverted-pear glenoid configuration or more than 20% glenoid bone loss, and significant humeral head bone loss defined as an engaging off-track Hill-Sachs lesion.8,14,37,49 Greis and colleagues showed that as bone is lost from the anterior glenoid, the contact area of the glenoid decreases significantly, thus resulting in increased contact pressure in the anteroinferior quadrant.52 Biomechanical studies have

set the stage for re-examination of the benefit of bony procedures at lesser degrees of “subcritical” bone loss. Jeon et al demonstrated comparable outcomes between Bankart repair and the Latarjet in those with glenoid bone loss levels of 15% to 20%,53 and Shaha and colleagues demonstrated the need to redefine the “critical” bone loss threshold given bone loss of more than 13.5% leading to decreased patient-reported outcome scores postoperatively.24 All relevant risk factors should be balanced with an athlete’s expectations for return to sport (RTS) success and time. A recent meta-analysis suggested that patients undergoing Bankart repair have the greatest rates of return to preinjury sport levels compared to the Latarjet, respectively (91.5% vs 69.0%).54 Accordingly, soft-tissue fixation with arthroscopic Bankart repair is the most common first line of treatment in the athlete with low to intermediate risk factors of surgical failure. When decision making is unclear, an Instability Severity Index Score can be used to better predict the risk of failure after arthroscopic Bankart repair based on age, involvement in competitive sport, and hyperlaxity, among other variables.55

Bony Surgical Intervention for Anterior Instability: Latarjet The Latarjet, also known as the Latarjet-Bristow procedure, has been established as a reliable treatment option for individuals with recurrent anterior shoulder instability.56-58 In the context of recent studies suggesting increased failure rates with even “subcritical” levels of bone loss as low as 13.5%, interest in the use of the Latarjet is increasing.24,56 The premise of this surgical technique is the transfer of the coracoid process from its natural position in the anterior shoulder to the anterior edge of the glenoid where the bony defect resides. Transfer of the coracoid in this fashion presents a possible “triple effect” of mechanisms bringing stability to the glenohumeral joint, including (a) the “sling effect,” in which the subscapularis and/or conjoint tendon increase dynamic stabilizing forces on the glenohumeral joint58,59; (b) the “bone-block effect,” in which the transferred bony

106

Chapter 10

fragment provides a hard stop preventing full dislocation of the humeral head59-61; and (c) the “Bankart” effect in which repair of the capsulolabral complex or coracoacromial ligament (CA) provides additional stability to the labrum.26 The Latarjet offers superior results with respect to instability event recurrence, perceived apprehension, and patient satisfaction when compared to soft-tissue repair.57,58 Recurrent instability rates are in the single digits after Latarjet and have been reported to exceed 20% after soft-tissue repair for recurrent instability.57,62

Indications and Contraindications for Latarjet The 2 primary indications for Latarjet include (1) recurrent anterior instability in the context of failed primary soft-tissue fixation, and (2) primary surgical intervention for anterior instability in the context of “significant” bone loss.63 Previously, absolute thresholds for significant bone loss (ie, > 20%) have been replaced with more nuanced views that even subcritical bone loss (13.5% to 20%) may predispose patients to failure after soft-tissue repair.8,19,24,25,56 Accordingly, providers must synthesize this structural information with known risk factors based on patient history (ie, young age, male sex, previous surgery on operative shoulder, hyperlaxity) to appropriately educate the patient to make an informed medical decision. Specific contraindications to the Latarjet procedure include (1) recurrent anterior instability associated with a massive irreparable rotator cuff tear, (2) primary traumatic dislocation in the presence of glenoid rim fracture requiring open reduction and internal fixation of the rim fracture, (3) patients suffering from uncontrolled seizure activity despite adequate medical intervention, and (4) unstable painful shoulders with high suspicion of “microinstability,” a relatively new clinical entity defined by any pathological laxity leading to abnormal shoulder mechanisms without frank instability.26,64,65 Athletes warrant special consideration with respect to surgical options for anterior shoulder instability. Glenohumeral instability accounts for nearly 1  in 4 shoulder injuries suffered by American collegiate athletes.66 Specific athletic populations have demonstrated a predisposition toward recurrence of anterior shoulder instability, including collision sports such as rugby and football. Collision sport athletes (eg, rugby, football, hockey) have demonstrated recurrence rates ranging from 14.7% to 28.6% after soft-tissue stabilization when compared to contact sport athletes (eg, field hockey, soccer, basketball, wrestling), who have demonstrated recurrence rates of 0.0% and 14.7%, respectively.67,68 Consequently, there may be value in having a lower threshold for pursuing bony procedures in collision athletes with the hope of minimizing the risk of recurrent dislocation and the need for potential revision surgery.36 These benefits must be weighed against the possible disadvantages, including decreased RTS rates reported for the Latarjet when compared to Bankart repair.54 Further study is required to more definitively

identify differences in the rates and time to RTS in athletes based on competitive status (recreational vs competitive) and by sport (collision, contact, noncontact).

SURGICAL TECHNIQUE FOR LATARJET This section details the technique used to perform a mini– open Latarjet as practiced by the senior author. Impor tant technical variations are detailed with respect to approach, treatment of the subscapularis, optimal coracoid technique (eg, standard, articular congruity), optimal positioning on the anterior glenoid, and capsular management.

Anesthesia, Patient Positioning and Diagnostic Arthroscopy Patients undergoing the Latarjet receive general anesthetic agents often in conjunction with regional anesthesia (commonly an interscalane block) to provide appropriate intraoperative analgesia and full muscle relaxation. Adjunctive interscalene nerve blocks demonstrated reduce postoperative pain and postoperative analgesic requirements in open-shoulder surgery patients, in addition to increasing patient satisfaction more broadly in those undergoing shoulder surgery.69,70 The mini–open technique described in this section seeks to use a standard deltopectoral incision while limiting incision size. Once the patient is appropriately anesthetized, an exam under anesthesia is performed to confirm previous exam findings characteristic of shoulder instability. Diagnostic shoulder arthroscopy using a standard 2-portal approach is performed with the patient in a beach-chair position sitting upright at approximately 90 degrees.71,72 Appropriate positioning of the patient aligns the medial border of the scapula with the lateral edge of the bed to allow for full scapular retraction, external rotation, and abduction. This is particularly impor tant during the harvesting of the coracoid graft, when the arm is externally rotated and abducted for appropriate visualization. The patient is repositioned for the Latarjet by lowering the head of the bed to a 20- to 30-degree incline and placing the arm into an externally rotated and abducted position. It is impor tant to note that the Latarjet is being performed arthroscopically with more frequency, although the literature demonstrates a significant learning curve and consequent risk of inappropriate graft placement and possible redislocation.73-77

Deltopectoral Approach, Coracoid Exposure, and Coracoid Osteotomy A 5 cm deltopectoral incision is made approximating the medial and inferior edge of the deltoid following Langer’s lines in line with the coracoid. Careful attention is paid to mobilize the cephalic vein laterally opening the deltopectoral interval. The subscapularis is identified. Retractors are strategically placed to avoid structural damage to adjacent

Latarjet and Coracoid Transfer in Athletes

107

Figure 10-3. Coracoid osteotomy.

neurovascular structures. The conjoint tendon is identified and tracked proximally to the coracoid tip. Retractors are then repositioned to have full visualization of the superior, inferior, medial, and lateral surfaces of the coracoid. Laterally, the CA ligament is dissected and released with a 1-cm stump, which is impor tant for later closure. The coracohumeral ligament is also released just deep enough to reach the CA ligament because this tissue can prevent appropriate mobilization of the coracoid after osteotomy. Medially, the insertion of the pectoralis minor is identified and released off the coracoid in a subperiosteal fashion. Once mobilized appropriately, the anterior aspect of the coracoid process can be appropriately palpated to approximate the extent of the osteotomy (Figure 10-3). A Bovie cautery may be used to identify the top of the coracoid and the proposed osteotomy site. At this time the coracoclavicular ligaments should be palpated at the base of the coracoid to ensure they are not disrupted during the osteotomy. The osteotomy site is marked 2 to 3 cm proximally to the anterior coracoid edge. A coracoid retractor is placed medially. The osteotomy is performed using a 90-degree saw cutting from medial to lateral. The osteotomy is completed using an osteotome. The Bovie cautery is used to free the coracoid from any remaining medial soft tissue. Keep in mind during dissection that the musculocutaneous nerve lies approximately 5 cm distal to the coracoid.

Coracoid Graft Preparation With the coracoid graft freed, a coracoid holder is used to prepare the graft. The inferior aspect of the graft is flattened and decorticated to aid in bony fusion. A coracoid

drill guide is attached to determine appropriate spacing of the 2 drill holes. Two holes are drilled through the coracoid process from inferior to superior and marked with the Bovie cautery. The offset guide is placed in either hole to determine the appropriate offset to the articular surface. This also determines which offset guide that will be used later for fixation. The depth of the coracoid is also measured using a depth gauge. It is impor tant to note that the standard Latarjet technique fixes the inferior coracoid surface onto the anterior glenoid (the technique described here), with the lateral edge of the graft lying in plane with glenoid articular surface. This is in contrast to the congruent arc modification, in which the medial surface is fixed onto the anterior glenoid with the inferior edge of the graft lying in place with the glenoid articular surface.46 Neither technique has been appropriately compared with respect to RTS or outcomes in athletes. Cadaveric studies have suggested that the congruent arc technique allows the bone graft to more closely match the native glenoid curvature and gives an overall wider graft, but it also requires fixation through the thinnest portion of the glenoid which may predispose the graft to intraoperative fracture (Figure 10-4).78

Glenoid Exposure, Subscapularis Treatment, and Coracoid Fixation With the coracoid bone graft prepared appropriately, a horizontal split of the subscapularis in the middle of the tendon (50-yard line) in line with its fibers is preferred. The angle of the horizontal split is typically 20 degrees cephalad. This is particularly impor tant in athletic patients hoping

108

Chapter 10

Figure 10-4. Coracoid graft preparation and offset guide.

to preserve strength with respect to internal rotation and adduction. Other treatment strategies for the subscapularis include partial tenotomy and an L-shaped incision; however, these techniques are largely inappropriate in the athletic patient because of concern for subscapularis atrophy and reduced strength of internal rotation when compared to the horizontal split technique described.79,80 After the subscapularis is split and retracted, the capsule is identified and dissected away from the subscapularis. A horizontal incision is made sharply through the capsule to expose the anterior glenoid. A Fukuda retractor is placed to move the humeral head laterally. An anterior glenoid retractor is placed exposing the capsule. A Bovie is used to “T” open the capsule for anterior glenoid exposure. The superior and inferior leaflets of the capsule are tagged at this time for retraction and later closure. With the anterior surface of the glenoid appropriately exposed, the anterior surface is debrided and decorticated to establish an interface for the coracoid graft. Although the optimal position for graft placement on the anterior glenoid is still under debate, general consensus exists that a position between 2 o’clock and 5 o’clock is preferred. The senior author favors a 3  o’clock position based on clinical experience.81 Using the aforementioned offset guide, the inferior drill hole is drilled by angling away from the joint line and drilling bicortically. This can be completed without the coracoid graft in place because we know the appropriate offset. The glenoid drill hole is measured and this value is added to the previously measured depth of the coracoid graft to get the screw length. The screw typically measures from 32 to 38  mm. The screw and washer is started in the graft, a guidewire is placed through the screw and through the glenoid drill hole, and the graft is provisionally reduced. This is not yet finally tightened to allow appropriate rotation of the graft relative to the glenoid articular surface to the

appropriate offset. The superior screw is then drilled through the graft in a similar orientation to the inferior screw. This is measured and placed with a washer. The screws are tightened sequentially, compressing the graft against the anterior glenoid surface. It is critical to be meticulous when checking for articular congruity because any level of overhang can compromise function by altering shoulder biomechanics.82 Any remaining overhang may be corrected using a burr.

Capsular Management Capsular management may involve one of several various techniques. A vertical capsular incision allows for the remnant CA ligament to be included in the capsular closure, where it may be plicated to the lateral side of the capsule. A horizontal capsular split may be partially closed on itself laterally but then incorporated into the CA ligament remnant. The senior author places a double-loaded anchor deep toward the coracoid graft between the superior and inferior screws. Either simple or horizontal mattress sutures are passed in the inferior and superior leaflets separately. Depending on the graft size, the superior leaflet may not be repairable. It is preferred that the inferior leaflet be repaired to avoid inferior instability. Laterally to the anchor the subscapularis and capsule are closed together using figure-of-8 sutures and tensioned at 30  degrees of external rotation, avoiding overtensioning the anterior capsule. Although there are a limited amount of biomechanical studies examining the role of capsular management in maintaining stability of the glenohumeral joint through various ROMs, a study by Itoigawa et al demonstrated superior outcomes with respect to external rotation both at 0 and 60 degrees of abduction in cadaveric shoulders treated with coracoid-based capsular fixation.83 However, a similarly designed biomechanical study by Kleiner and colleagues suggested that capsular

Latarjet and Coracoid Transfer in Athletes repair provides no additional stability, but does restrict external rotation both in the scapular and coronal planes.84 Thus, the literature suggests a possible advantage of capsular closure along the coracoid process in making the coracoid block extra-articular and decreasing subsequent rates of osteoarthritis on long-term follow-up.85,86 However, no studies have compared the biomechanical value of various fixation techniques to one another (eg, suture anchor vs screw vs suture alone), or determined whether the changes observed in shoulder biomechanics translate to clinical significance.85

REHABILITATION, OUTCOMES, AND RETURN TO PLAY Postoperative Rehabilitation Rehabilitation of the athlete after Latarjet plays an important role in expedient RTS. Initial rehabilitation relies on the use of a sling and abduction pillow immobilization to allow appropriate bony healing early in the postoperative process. During the immobilization period, passive range of motion (ROM) at the elbow, wrist, and hand is allowed in the immediate postoperative period to prevent muscular atrophy. Pain can be mitigated with cryotherapy and nonsteroidal anti-inflammatory agents. Passive ROM begins approximately 10 days postoperatively with passive external rotation to 30 degrees, passive forward flexion to 120  degrees, and passive internal rotation to 30 degrees. Pendulum exercises may be started, with periscapular stretches and abduction against gravity. At 4 weeks’ time, sling and abduction pillow immobilization is discontinued and the patient is advanced to full ROM as tolerated. Full passive ROM is expected to be achieved between 6 and 8 weeks, and full active ROM is generally achieved between 8 and 10 weeks. Exercises used to promote the development of full active ROM include submaximal isometrics, isometric deltoid exercises, scapular stabilization, serratus punches, and isotonic resistance. Athletes tend to achieve full active ROM at earlier time points and progress rapidly to the functional phase of rehabilitation, where the goal is further strengthening. Strengthening exercises begin between 8 and 12 weeks after surgery, including resistance exercises, closed-chain exercises, light biceps curls, and free weights. As strength and confidence in the shoulder is developed, the patient may be transitioned to push-ups, band exercises, medicine ball exercises, Plyometrics, and bench press. A CT scan is also obtained at 16 weeks to evaluate for appropriate bony fusion. If full bony union is demonstrated, the patient may return to full unrestricted activities. RTS requires clearance from a provider with clear demonstration of full passive and active ROM, no complaints of pain or instability, and demonstration of appropriate strength and control through various rotator cuff and scapular motions. Many athletes complete sport-specific rehabilitation programs in which the shoulder is rehabilitated with the focus on the development of muscular endurance and improved strength (eg, golf swing, baseball pitch). Other impor tant

109

considerations in athletes include balancing proprioceptive inputs, building core strengthening, and protecting the shoulder postoperatively. A wobble or slide board can be used to help the athlete develop further comfort with balancing. The wearing of a shoulder brace is encouraged for athletes in collision and contact sports, although not required.87

Athlete Return to Sport and Play and Outcomes Numerous studies have examined the rate at which athletes RTS after Latarjet.88-94 Rates of RTS have ranged from 65% to 96.4% across studies. However, it is impor tant to note that the study reporting a return rate of 65% was in a cohort of rugby players, with only one player who did not RTS stating that it was because of shoulder limitations.89 Across RTS studies in Latarjet coracoid surgery, return to preinjury levels of sport are slightly lower than overall RTS rates, ranging from 48% to 71%.88-93 It is impor tant to note that rates of recurrent shoulder instability are low across these studies (0% to 5%), whereas studies examining recurrent instability in Bankart repair have been reported to be as high as 20%.95,96 The single-digit dislocation rates after Latarjet are an important distinguishing feature from Bankart repair, which has classically been associated with double-digit recurrence rates (ie, as high as 67%).57,58,62 More current research has complicated RTS expectations after Latarjet based on the type of sport and the competition level.91,93,94 A study by Kee et al examined RTS after Latarjet both in collision and noncollision athletes, reporting a large discrepancy between overall RTS rates (96.4%) and return to preinjury level of sport (16.1%).94 Furthermore, noncollision athletes were more likely to return to the same level of sport than collision athletes (29.6% vs 3.4%).94 A study by Privitera and colleagues91 also examined RTS in contact and collision athletes, reporting 49% return to preoperative sport levels and an overall RTS rate of 89%. Lastly, a study by Baverel et al recently examined RTS between competitive and recreational athletes, reporting that 100% of competitive athletes returned to the same or higher performance level, and 69.4% of recreational athletes accomplished comparable performance levels. Accordingly, the Latarjet procedure demonstrates favorable RTS rates and may be considered in patients with primary shoulder instability if the patient is deemed to be at high risk of redislocation (eg, collision or contact sport).93

Complications More general outcomes after Latarjet have suggested overall satisfaction rates of 94.8%, with good to excellent outcomes reported by 86.0% of patients across studies.97 Nonetheless, complications are not uncommon and have been reported to occur at an overall rate of 15%, based on a recent systematic review.98 These complications are most commonly transient neurologic injury, infection,

110

Chapter 10

hardware-related complication, dislocation, subluxation, and reoperation.99,100 Meticulous surgical technique is impor tant in avoiding nerve injury to the suprascapular, axillary, or musculocutaneous nerves, as well as vascular injury to the anterior circumflex humeral artery. Nonetheless, neurovascular injury has been reported to occur at a rate of 1.4% across open and arthroscopic techniques.77 Infection has been reported to carry an incidence rate of up to 6% with full resolution after appropriate irrigation and debridement.101 Graft fracture has also been reported, although fracture risk can be minimized by (a) ensuring there is a proper bony bridge in between screw placement sites (~ 9  mm) and (b) avoidance of excessive screw tightening. Graft positioning has also been well reported in influencing the propensity toward postoperative complications.59,102 Placing the graft too high can predispose to recurrent instability, whereas placing the graft too low can predispose to nonunion.103 It is impor tant to ensure appropriate glenoid exposure and visualization of articular congruity prior to initiation of surgical closure. Other common postoperative complications include hematoma, swelling, neuropraxias, or plexopathy. Hematoma and postoperative swelling are more common after the arthroscopic approach, with hematoma commonly due to rebleeding and postoperative swelling tending to subside within 1 week.104 Musculocutaneous and suprascapular neuropraxias are well documented in the literature, albeit rare following the Latarjet.105,106 A high number of brachial plexus lesions have previously been reported, although these are thought to be due to differences in approach and surgical technique in comparison to the modern-day open Latarjet.81 Other long-term complications that warrant discussion with patients include nonunion, osteolysis, instability, and arthritis, although the clinical significance of nonunion and osteolysis is debatable.77,107

CONCLUSION Latarjet, whether performed using an open or arthroscopic approach, is a bony stabilization procedure of par ticular value to contact (eg, basketball, soccer) and collision (eg, wrestling, football, rugby) sport athletes that may place dynamic forces on the shoulder predisposing to recurrent instability after soft-tissue repair. Athletes may warrant specific considerations with respect to counseling, bone loss thresholds, surgical technique (eg, subscapularis treatment, coracoid graft positioning), and postoperative rehabilitation. Surgical decision making in the athlete must also highlight recurrence rates, given that recurrent instability after Bankart repair has been reported to be as high as 20% to 67% in comparison to the Latarjet (< 5%).77,81,98 Treatment of the subscapularis is another particularly impor tant consideration in athletes. Partial tenotomy and L-shaped incisions are associated with reduced internal rotation strength and subscapularis atrophy.79,80 A horizontal-split technique is preferred to maintain the abduction and internal rotation

capacity of this tendon. Lastly, postoperative rehabilitation protocols should use CT imaging to determine the state of bony union prior to allowing release to full activity. Sportspecific rehabilitation programs are encouraged to address the sport and position-specific needs that an athlete may have and enhance strength through par ticular compound motions. RTS outcome studies have suggested that the rate of RTS after Latarjet may increase as surgeons gain increased familiarity with the surgical technique. More recent studies suggest RTS rates broadly exceed 80%, with decreased rates in recreational athletes (69.4%) when compared to competitive athletes (100%).93 All in all, special considerations with respect to preoperative, intraoperative surgical technique, and postoperative treatment must be acknowledged when caring for the athlete with anterior shoulder instability, making Latarjet a particularly intriguing surgical option in this patient population. The Latarjet is a surgical procedure aimed at prevention of recurrent anterior shoulder instability that is most commonly performed in patients with glenoid bone loss. Appropriate identification of risk factors for surgical failure with soft-tissue techniques, quantification of bone loss with CT or MRI, and an understanding of an athlete’s desired return to function are critical in informing shared decision making. Optimal surgical technique for the athlete seeking maximal preservation of function includes horizontal splitting of the subscapularis and meticulous graft positioning to avoid malpositioning or fracture. Postoperative rehabilitation should be focused on a step-wise progression through ROM goals, with plans for a sport-specific rehabilitation program to address athlete-specific needs. Outcome studies after Latarjet have demonstrated favorable results, with RTS rates ranging from 65% to 96.4%, and more recent studies supporting rates exceeding 80%. Compared to soft-tissue and other bony surgical interventions for anterior shoulder instability, the Latarjet most notably offers decreased recurrent instability rates (< 5%), warranting appropriate consideration for collision and contact athletes in par ticular.

REFERENCES 1.

2.

3.

4.

Olds M, Ellis R, Donaldson K, Parmar P, Kersten  P. Risk factors which predispose first-time traumatic anterior shoulder dislocations to recurrent instability in adults: a systematic review and meta-analysis. Br J Sports Med. 2015;49(14):913-922. doi:10.1136/ bjsports-2014-094342. Sofu H, Gürsu S, Koçkara N, Öner A, Issın A, Çamurcu Y. Recurrent anterior shoulder instability: review of the literature and current concepts. World J Clin Cases. 2014;2(11):676-682. doi:10.12998/wjcc. v2.i11.676. Leroux T, Wasserstein D, Veillette C, et  al. Epidemiology of primary anterior shoulder dislocation requiring closed reduction in Ontario, Canada. Am J Sports Med. 2014;42(2):442-450. doi:10.1177/0363546513510391. Roberts SB, Beattie N, McNiven ND, Robinson CM. The natural history of primary anterior dislocation of the glenohumeral joint in adolescence. Bone Joint  J. 2015;97-B(4):520-526. doi:10.1302/0301-620X.97B4.34989.

Latarjet and Coracoid Transfer in Athletes 5.

6.

7.

8.

9.

10.

11.

12.

13.

14.

15.

16.

17.

18.

19.

20.

21.

22.

Owens BD, Nelson BJ, Duffey ML, et al. Pathoanatomy of first-time, traumatic, anterior glenohumeral subluxation events. J Bone Joint Surg Am. 2010;92(7):1605-1611. doi:10.2106/JBJS.I.00851. Godin JA, Altintas B, Horan MP, et al. Midterm results of the bony Bankart bridge technique for the treatment of bony Bankart lesions. Am J Sports Med. 2019;47(1):158-164. doi:10.1177/0363546518808495. Skupi
ski J, Piechota MZ, Wawrzynek W, Maczuch J, Babi
ska A. The bony Bankart lesion: how to measure the glenoid bone loss. Pol J Radiol. 2017;82:58-63. doi:10.12659/PJR.898566. Piasecki DP, Verma NN, Romeo AA, Levine WN, Bach BR Jr, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493. doi:10.5435/00124635-200908000-00002. Haber DB, Sanchez A, Sanchez G, Ferrari MB, Ferdousian S, Provencher MT. Bipolar bone loss of the shoulder joint due to recurrent instability: use of fresh osteochondral distal tibia and humeral head allografts. Arthrosc Tech. 2017;6(3):e893-e899. doi:10.1016/j. eats.2017.02.022 Hovelius L, Olofsson A, Sandström B, et al. Nonoperative treatment of primary anterior shoulder dislocation in patients forty years of age and younger. A prospective twenty-five-year follow-up. J Bone Joint Surg Am. 2008;90(5):945-952. doi:10.2106/JBJS.G.00070. Giles JW, Degen RM, Johnson JA, Athwal GS. The Bristow and Latarjet procedures: why these techniques should not be considered synonymous. J Bone Joint Surg Am. 2014;96(16):1340-1348. doi:10.2106/JBJS.M.00627. Dauzère F, Faraud A, Lebon J, Faruch M, Mansat P, Bonnevialle N. Is the Latarjet procedure risky? Analysis of complications and learning curve. Knee Surg Sports Traumatol Arthrosc. 2016;24(2):557-563. doi:10.1007/s00167-015-3900-5. Ekhtiari S, Horner NS, Bedi A, Ayeni OR, Khan  M. The learning curve for the Latarjet procedure: a systematic review. Orthop J Sports Med. 2018;6(7):2325967118786930. doi:10.1177/2325967118786930 Lo IK, Parten PM, Burkhart SS. The inverted pear glenoid: an indicator of significant glenoid bone loss. Arthroscopy. 2004;20(2):169-174. doi:10.1016/j.arthro.2003.11.036. Fortun CM, Wong I, Burns JP. Arthroscopic iliac crest bone grafting to the anterior glenoid. Arthrosc Tech. 2016;5(4):e907-e912. doi:10.1016/j.eats.2016.04.011. Fox JA, Sanchez A, Zajac TJ, Provencher MT. Understanding the Hill-Sachs Lesion in its role in patients with recurrent anterior shoulder instability. Curr Rev Musculoskelet Med. 2017;10(4):469-479. doi:10.1007/s12178-017-9437-0. Boileau P, McClelland WB Jr, O’Shea K, et  al. Arthroscopic HillSachs remplissage with Bankart repair: strategy and technique. JBJS Essent Surg Tech. 2014;4(1):e4. doi:10.2106/JBJS.ST.M.00033. SH, Cha JR, Lee CC, Hwang IY, Choe CG, Kim MS. The influence of arthroscopic remplissage for engaging Hill-Sachs lesions combined with Bankart repair on redislocation and shoulder function compared with Bankart repair alone. Clin Orthop Surg. 2016;8(4):428436. doi:10.4055/cios.2016.8.4.428. H, Moriishi J, Dohi M, Kon Y, Tsuchiya A. Glenoid rim morphology in recurrent anterior glenohumeral instability. J Bone Joint Surg Am. 2003;85(5):878-884. doi:10.2106/00004623-200305000-00016. Nakagawa S, Ozaki R, Take Y, Iuchi R, Mae T. Relationship between glenoid defects and Hill-Sachs lesions in shoulders with traumatic anterior instability. Am J Sports Med. 2015;43(11):2763-2773. doi:10.1177/0363546515597668. Yamamoto N, Muraki T, Sperling JW, et  al. Stabilizing mechanism in bone-grafting of a large glenoid defect. J Bone Joint Surg Am. 2010;92(11):2059-2066. doi:10.2106/JBJS.I.00261. Itoi E, Lee SB, Berglund LJ, Berge LL, An KN. The effect of a glenoid defect on anteroinferior stability of the shoulder after Bankart repair: a cadaveric study. J Bone Joint Surg Am. 2000;82(1):35-46. doi:10.2106/00004623-200001000-00005.

23.

24.

25.

26.

27.

28.

29.

30. 31.

32.

33.

34.

35.

36.

37.

38. 39.

40.

111

Rabinowitz J, Friedman R, Eichinger JK. Management of glenoid bone loss with anterior shoulder instability: indications and outcomes. Curr Rev Musculoskelet Med. 2017;10(4):452-462. doi:10.1007/s12178-017-9439-y. Shaha JS, Cook JB, Song DJ, et  al. Redefining “critical” bone loss in shoulder instability: functional outcomes worsen with “subcritical” bone loss. Am J Sports Med. 2015;43(7):1719-1725. doi:10.1177/0363546515578250. Dickens JF, Owens BD, Cameron KL, et al. The effect of subcritical bone loss and exposure on recurrent instability after arthroscopic Bankart repair in intercollegiate American Football. Am J Sports Med. 2017;45(8):1769-1775. doi:10.1177/0363546517704184. Domos P, Lunini E, Walch  G. Contraindications and complications of the Latarjet procedure. Shoulder Elbow. 2018;10(1):15-24. doi:10.1177/1758573217728716. Rossi LA, Bertona A, Tanoira I, Maignon GD, Bongiovanni SL, Ranalletta  M. Comparison between modified Latarjet performed as a primary or revision procedure in competitive athletes: a comparative study of 100 patients with a minimum 2-year follow-up. Orthop J Sports Med. 2018;6(12):2325967118817233. doi:10.1177/2325967118817233. Knesek M, Skendzel JG, Dines JS, Altchek DW, Allen AA, Bedi  A. Diagnosis and management of superior labral anterior posterior tears in throwing athletes. Am J Sports Med. 2013;41(2):444-460. doi:10.1177/0363546512466067. Lo IK, Nonweiler B, Woolfrey M, Litchfield R, Kirkley A. An evaluation of the apprehension, relocation, and surprise tests for anterior shoulder instability. Am J Sports Med. 2004;32(2):301-307. doi:10.1177/0095399703258690. Gagey OJ, Gagey  N. The hyperabduction test. J Bone Joint Surg Br. 2001;83(1):69-74. doi:10.1302/0301-620x.83b1.10628. McFarland EG, Kim TK, Savino RM. Clinical assessment of three common tests for superior labral anterior-posterior lesions. Am J Sports Med. 2002;30(6):810-815. doi:10.1177/03635465020300061001. Friedman LG, Ulloa SA, Braun DT, Saad HA, Jones MH, Miniaci AA. Glenoid bone loss measurement in recurrent shoulder dislocation: assessment of measurement agreement between CT and MRI. Orthop J Sports Med. 2014;2(9):2325967114549541. doi:10.1177/2325967114549541. Stecco A, Guenzi E, Cascone T, et al. MRI can assess glenoid bone loss after shoulder luxation: inter- and intra-individual comparison with CT. Radiol Med. 2013;118(8):1335-1343. doi:10.1007/ s11547-013-0927-x. Stillwater L, Koenig J, Maycher B, Davidson M. 3D-MR vs. 3D-CT of the shoulder in patients with glenohumeral instability. Skeletal Radiol. 2017;46(3):325-331. doi:10.1007/s00256-016-2559-4. Murray IR, Ahmed I, White NJ, Robinson CM. Traumatic anterior shoulder instability in the athlete. Scand J Med Sci Sports. 2012;23(4):387-405. doi:10.1111/j.1600-0838.2012.01494.x. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694. doi:10.1053/ jars.2000.17715. Di Giacomo G, Itoi E, Burkhart SS. Evolving concept of bipolar bone loss and the Hill-Sachs lesion: from “engaging/non-engaging” lesion to “on-track/off-track” lesion. Arthroscopy. 2014;30(1):90-98. doi:10.1016/j.arthro.2013.10.004. Itoi E. ‘On-track’ and ‘off-track’ shoulder lesions. EFORT Open Rev. 2017;2(8):343-351. doi:10.1302/2058-5241.2.170007. Gerber C, Nyffeler RW. Classification of glenohumeral joint instability. Clin Orthop Relat Res. 2002;(400):65-76. doi:10.1097/00003086-200207000-00009. Chuang TY, Adams CR, Burkhart SS. Use of preoperative threedimensional computed tomography to quantify glenoid bone loss in shoulder instability. Arthroscopy. 2008;24(4):376-382. doi:10.1016/j. arthro.2007.10.008.

112 41.

42.

43.

44.

45.

46.

47.

48.

49.

50.

51.

52.

53.

54.

55.

56.

Chapter 10 Yamamoto N, Itoi E, Abe H, et al. Contact between the glenoid and the humeral head in abduction, external rotation, and horizontal extension: a new concept of glenoid track. J  Shoulder Elbow Surg. 2007;16(5):649-656. doi:10.1016/j.jse.2006.12.012. Taylor DC, Arciero RA. Pathologic changes associated with shoulder dislocations. Arthroscopic and physical examination findings in first-time, traumatic anterior dislocations. Am J Sports Med. 1997;25(3):306-311. doi:10.1177/036354659702500306. Castagna A, Markopoulos N, Conti M, Delle Rose G, Papadakou E, Garofalo R. Arthroscopic Bankart suture-anchor repair: radiological and clinical outcome at minimum 10 years of follow-up. Am J Sports Med. 2010;38(10):2012-2016. doi:10.1177/0363546510372614. Hendawi T, Milchteim C, Ostrander  R. Bankart repair using modern arthroscopic technique. Arthrosc Tech. 2017;6(3):e863-e870. doi:10.1016/j.eats.2017.02.019. Brown M, Wallace A, Lachlan A, Alexander  S. Arthroscopic soft tissue procedures for anterior shoulder instability. Open Orthop  J. 2017;11(suppl 6):979-988. doi:10.2174/1874325001711010979. McHale KJ, Sanchez G, Lavery KP, et al. Latarjet technique for treatment of anterior shoulder instability with glenoid bone loss. Arthrosc Tech. 2017;6(3):e791-e799. doi:10.1016/j.eats.2017.02.009. Amar E, Konstantinidis G, Coady C, Wong IH. Arthroscopic treatment of shoulder instability with glenoid bone loss using distal tibial allograft augmentation: safety profile and short-term radiological outcomes. Orthop J Sports Med. 2018;6(5):2325967118774507. doi:10.1177/2325967118774507. Wasserstein D, Dwyer T, Veillette C, et  al. Predictors of dislocation and revision after shoulder stabilization in Ontario, Canada, from 2003 to 2008. Am J Sports Med. 2013;41(9):2034-2040. doi:10.1177/0363546513492952. Boileau P, Villalba M, Héry JY, Balg F, Ahrens P, Neyton L. Risk factors for recurrence of shoulder instability after arthroscopic Bankart repair. J Bone Joint Surg Am. 2006;88(8):1755-1763. doi:10.2106/ JBJS.E.00817. Frank RM, Saccomanno MF, McDonald LS, Moric M, Romeo AA, Provencher MT. Outcomes of arthroscopic anterior shoulder instability in the beach chair versus lateral decubitus position: a systematic review and meta-regression analysis. Arthroscopy. 2014;30(10):1349-1365. Balg F, Boileau  P. The Instability Severity Index Score. A simple pre-operative score to select patients for arthroscopic or open shoulder stabilisation. J Bone Joint Surg Br. 2007;89(11):1470-1477. doi:10.1302/0301-620X.89B11.18962. Greis PE, Scuderi MG, Mohr A, Bachus KN, Burks RT. Glenohumeral articular contact areas and pressures following labral and osseous injury to the anteroinferior quadrant of the glenoid. J Shoulder Elbow Surg. 2002;11(5):442-451. doi:10.1067/mse.2002.124526. Jeon YS, Jeong HY, Lee DK, Rhee YG. Borderline glenoid bone defect in anterior shoulder instability: Latarjet procedure versus Bankart repair. Am J Sports Med. 2018;46(9):2170-2176. doi:10.1177/0363546518776978. Abdul-Rassoul H, Galvin JW, Curry EJ, Simon J, Li  X. Return to sport after surgical treatment for anterior shoulder instability: a systematic review. Am J Sports Med. 2019;47(6):1507-1515. doi:10.1177/0363546518780934. Leroux TS, Saltzman BM, Meyer M, et al. The influence of evidencebased surgical indications and techniques on failure rates after arthroscopic shoulder stabilization in the contact or collision athlete with anterior shoulder instability. Am J Sports Med. 2017;45(5):12181225. doi:10.1177/0363546516663716. Freehill MT, Srikumaran U, Archer KR, McFarland EG, Petersen SA. The Latarjet coracoid process transfer procedure: alterations in the neurovascular structures. J Shoulder Elbow Surg. 2013;22(5):695-700. doi:10.1016/j.jse.2012.06.003.

57.

58.

59.

60. 61.

62.

63.

64.

65.

66.

67.

68.

69.

70.

71.

72. 73.

74.

Zimmermann SM, Scheyerer MJ, Farshad M, Catanzaro S, Rahm S, Gerber  C. Long-term restoration of anterior shoulder stability: a retrospective analysis of arthroscopic bankart repair versus open Latarjet procedure. J Bone Joint Surg Am. 2016;98(23):1954-1961. doi:10.2106/JBJS.15.01398. Burkhart SS, De Beer JF, Barth JR, Cresswell T, Roberts C, Richards DP. Results of modified Latarjet reconstruction in patients with anteroinferior instability and significant bone loss. Arthroscopy. 2007;23(10):1033-1041. doi:10.1016/j.arthro.2007.08.009. Allain J, Goutallier D, Glorion  C. Long-term results of the Latarjet procedure for the treatment of anterior instability of the shoulder. J Bone Joint Surg Am. 1998;80(6):841-852. doi:10.2106/00004623-199806000-00008. Weaver JK, Derkash RS. Don’t forget the Bristow-Latarjet procedure. Clin Orthop Relat Res. 1994;(308):102-110. Yamamoto N, Muraki T, An KN, et  al. The stabilizing mechanism of the Latarjet procedure: a cadaveric study. J Bone Joint Surg Am. 2013;95(15):1390-1397. doi:10.2106/JBJS.L.00777. Owens BD, DeBerardino TM, Nelson BJ, et al. Long-term follow-up of acute arthroscopic Bankart repair for initial anterior shoulder dislocations in young athletes. Am J Sports Med. 2009;37(4):669-673. doi:10.1177/0363546508328416. Chen AL, Hunt SA, Hawkins RJ, Zuckerman JD. Management of bone loss associated with recurrent anterior glenohumeral instability. Am J Sports Med. 2005;33(6):912-925. doi:10.1177/0363546505277074. Chambers L, Altchek DW. Microinstability and internal impingement in overhead athletes. Clin Sports Med. 2013;32(4):697-707. doi:10.1016/j.csm.2013.07.006. Castagna A, Nordenson U, Garofalo R, Karlsson  J. Minor shoulder instability. Arthroscopy. 2007;23(2):211-215. doi:10.1016/j. arthro.2006.11.025. Owens BD, Agel J, Mountcastle SB, Cameron KL, Nelson BJ. Incidence of glenohumeral instability in collegiate athletics. Am J Sports Med. 2009;37(9):1750-1754. doi:10.1177/0363546509334591. Ranalletta M, Rossi LA, Alonso Hidalgo I, et  al. Arthroscopic stabilization after a first-time dislocation: collision versus contact athletes. Orthop J Sports Med. 2017;5(9):2325967117729321. doi:10.1177/2325967117729321. Saper MG, Milchteim C, Zondervan RL, Andrews JR, Ostrander RV III. Outcomes after arthroscopic Bankart repair in adolescent athletes participating in collision and contact sports. Orthop J Sports Med. 2017;5(3):2325967117697950. doi:10.1177/2325967117697950. Baskan S, Cankaya D, Unal H, et  al. Comparison of continuous interscalene block and subacromial infusion of local anesthetic for postoperative analgesia after open shoulder surgery. J Orthop Surg (Hong Kong). 2017;25(1):2309499016684093. doi:10.1177/2309499016684093. Hughes MS, Matava MJ, Wright RW, Brophy RH, Smith MV. Interscalene brachial plexus block for arthroscopic shoulder surgery: a systematic review. J Bone Joint Surg Am. 2013;95(14):1318-1324. doi:10.2106/JBJS.L.01116. Paxton ES, Backus J, Keener J, Brophy RH. Shoulder arthroscopy: basic principles of positioning, anesthesia, and portal anatomy. J Am Acad Orthop Surg. 2013;21(6):332-342. doi:10.5435/ JAAOS-21-06-332. Farmer KW, Wright TW. Shoulder arthroscopy: the basics. J Hand Surg Am. 2015;40(4):817-821. doi:10.1016/j.jhsa.2015.01.002. Valenti P, Maroun C, Wagner E, Werthel JD. Arthroscopic Latarjet procedure combined with Bankart repair: a technique using 2 cortical buttons and specific glenoid and coracoid guides. Arthrosc Tech. 2018;7(4):e313-e320. doi:10.1016/j.eats.2017.09.009. Lafosse L, Lejeune E, Bouchard A, Kakuda C, Gobezie R, Kochhar T. The arthroscopic Latarjet procedure for the treatment of anterior shoulder instability. Arthroscopy. 2007;23(11):1242.e1-e5. doi:10.1016/j.arthro.2007.06.008.

Latarjet and Coracoid Transfer in Athletes 75.

76.

77.

78.

79.

80.

81.

82.

83.

84.

85.

86.

87.

88.

89.

90.

He  Z. The arthroscopic Latarjet procedure: effective and safe. Ann Transl Med. 2015;3(suppl  1):S25. doi:10.3978/j. issn.2305-5839.2015.03.28. Hurley ET, Lim Fat D, Farrington SK, Mullett  H. Open versus arthroscopic Latarjet procedure for anterior shoulder instability: a systematic review and meta-analysis. Am J Sports Med. 2019;47(5):12481253. doi:10.1177/0363546518759540. Griesser MJ, Harris JD, McCoy BW, et  al. Complications and reoperations after Bristow-Latarjet shoulder stabilization: a systematic review. J Shoulder Elbow Surg. 2013;22(2):286-292. doi:10.1016/j. jse.2012.09.009. Noonan B, Hollister SJ, Sekiya JK, Bedi  A. Comparison of reconstructive procedures for glenoid bone loss associated with recurrent anterior shoulder instability. J Shoulder Elbow Surg. 2014;23(8):11131119. doi:10.1016/j.jse.2013.11.011. Paladini P, Merolla G, De Santis E, Campi F, Porcellini  G. Longterm subscapularis strength assessment after Bristow-Latarjet procedure: isometric study. J Shoulder Elbow Surg. 2012;21(1):42-47. doi:10.1016/j.jse.2011.03.027. Ersen A, Birisik F, Ozben H, et al. Latarjet procedure using subscapularis split approach offers better rotational endurance than partial tenotomy for anterior shoulder instability. Knee Surg Sports Traumatol Arthrosc. 2018;26(1):88-93. doi:10.1007/s00167-017-4480-3. Gupta A, Delaney R, Petkin K, Lafosse  L. Complications of the Latarjet procedure. Curr Rev Musculoskelet Med. 2015;8(1):59-66. doi:10.1007/s12178-015-9258-y. Ghodadra N, Gupta A, Romeo AA, et  al. Normalization of glenohumeral articular contact pressures after Latarjet or iliac crest bonegrafting. J Bone Joint Surg Am. 2010;92(6):1478-1489. doi:10.2106/ JBJS.I.00220. Itoigawa Y, Hooke AW, Sperling JW, et al. Repairing the capsule to the transferred coracoid preserves external rotation in the modified Latarjet procedure. J Bone Joint Surg Am. 2016;98(17):1484-1489. doi:10.2106/JBJS.15.01069. Kleiner MT, Payne WB, McGarry MH, Tibone JE, Lee TQ. Biomechanical comparison of the Latarjet procedure with and without capsular repair. Clin Orthop Surg. 2016;8(1):84-91. doi:10.4055/ cios.2016.8.1.84. Zumstein MA, Raniga S. The role of capsular repair in Latarjet procedures: commentary on an article by Yoshiaki Itoigawa, MD, PhD, et al.: “Repairing the capsule to the transferred coracoid preserves external rotation in the modified Latarjet procedure.” J Bone Joint Surg Am. 2016;98(17):e75. doi:10.2106/JBJS.16.00686. Bouju Y, Gadéa F, Stanovici J, Moubarak H, Favard L. Shoulder stabilization by modified Latarjet-Patte procedure: results at a minimum 10  years’ follow-up, and role in the prevention of osteoarthritis. Orthop Traumatol Surg Res. 2014;100(4  suppl):S213-S218. doi:10.1016/j.otsr.2014.03.010. Conti M, Garofalo R, Castagna A, Massazza G, Ceccarelli E. Dynamic brace is a good option to treat first anterior shoulder dislocation in season. Musculoskelet Surg. 2017;101(suppl 2):169-173. doi:10.1007/ s12306-017-0497-5. Blonna D, Bellato E, Caranzano F, Assom M, Rossi R, Castoldi  F. Arthroscopic Bankart repair versus open Bristow-Latarjet for shoulder instability: a matched-pair multicenter study focused on return to sport. Am J Sports Med. 2016;44(12):3198-3205. doi:10.1177/0363546516658037. Cerciello S, Edwards TB, Walch G. Chronic anterior glenohumeral instability in soccer players: results for a series of 28 shoulders treated with the Latarjet procedure. J Orthop Traumatol. 2012;13(4):197202. doi:10.1007/s10195-012-0201-3. Neyton L, Young A, Dawidziak B, et al. Surgical treatment of anterior instability in rugby union players: clinical and radiographic results of the Latarjet-Patte procedure with minimum 5-year followup. J Shoulder Elbow Surg. 2012;21(12):1721-1727. doi:10.1016/j. jse.2012.01.023.

91.

92.

93.

94.

95.

96.

97.

98.

99.

100.

101.

102.

103.

104.

105.

106.

107.

113

Privitera DM, Sinz NJ, Miller LR, et al. Clinical outcomes following the Latarjet procedure in contact and collision athletes. J Bone Joint Surg Am. 2018;100(6):459-465. doi:10.2106/JBJS.17.00566. Beranger JS, Klouche S, Bauer T, Demoures T, Hardy  P. Anterior shoulder stabilization by Bristow-Latarjet procedure in athletes: return-to-sport and functional outcomes at minimum 2-year followup. Eur J Orthop Surg Traumatol. 2016;26(3):277-282. doi:10.1007/ s00590-016-1751-5. Baverel L, Colle PE, Saffarini M, Anthony Odri G, Barth  J. Open Latarjet procedures produce better outcomes in competitive athletes compared with recreational athletes: a clinical comparative study of 106 athletes aged under 30 years. Am J Sports Med. 2018;46(6):14081415. doi:10.1177/0363546518759730. Kee YM, Kim JY, Kim HJ, Lim CT, Rhee YG. Return to sports after the Latarjet procedure: high return level of non-collision athletes. Knee Surg Sports Traumatol Arthrosc. 2018;26(3):919-925. doi:10.1007/ s00167-017-4775-4. Castagna A, Delle Rose G, Borroni M, et al. Arthroscopic stabilization of the shoulder in adolescent athletes participating in overhead or contact sports. Arthroscopy. 2012;28(3):309-315. doi:10.1016/j. arthro.2011.08.302. Rhee YG, Ha JH, Cho NS. Anterior shoulder stabilization in collision athletes: arthroscopic versus open Bankart repair. Am J Sports Med. 2006;34(6):979-985. doi:10.1177/0363546505283267. Hurley ET, Jamal MS, Ali ZS, Montgomery C, Pauzenberger L, Mullett  H. Long-term outcomes of the Latarjet procedure for anterior shoulder instability: a systematic review of studies at 10-year follow-up. J Shoulder Elbow Surg. 2019;28(2):e33-e39. doi:10.1016/j. jse.2018.08.028. Longo UG, Loppini M, Rizzello G, et al. Remplissage, humeral osteochondral grafts, weber osteotomy, and shoulder arthroplasty for the management of humeral bone defects in shoulder instability: systematic review and quantitative synthesis of the literature. Arthroscopy. 2014;30(12):1650-1666. doi:10.1016/j.arthro.2014.06.010. Gartsman GM, Waggenspack WN Jr, O’Connor DP, Elkousy HA, Edwards TB. Immediate and early complications of the open Latarjet procedure: a retrospective review of a large consecutive case series. J Shoulder Elbow Surg. 2017;26(1):68-72. doi:10.1016/j. jse.2016.05.029. Yang JS, Mazzocca AD, Cote MP, Edgar CM, Arciero RA. Recurrent anterior shoulder instability with combined bone loss: treatment and results with the modified Latarjet procedure. Am J Sports Med. 2016;44(4):922-932. doi:10.1177/0363546515623929. Shah AA, Butler RB, Romanowski J, Goel D, Karadagli D, Warner JJ. Short-term complications of the Latarjet procedure. J Bone Joint Surg Am. 2012;94(6):495-501. doi:10.2106/JBJS.J.01830. Hovelius L, Korner L, Lundberg B, et al. The coracoid transfer for recurrent dislocation of the shoulder. Technical aspects of the BristowLatarjet procedure. J Bone Joint Surg Am. 1983;65(7):926-934. Weppe F, Magnussen RA, Lustig S, Demey G, Neyret P, Servien  E. A biomechanical evaluation of bicortical metal screw fixation versus absorbable interference screw fixation after coracoid transfer for anterior shoulder instability. Arthroscopy. 2011;27(10):1358-1363. doi:10.1016/j.arthro.2011.03.074. Verma NN. Editorial commentary: arthroscopic Latarjet: is it ready for prime time? Arthroscopy. 2019;35(4):1062-1063. doi:10.1016/j. arthro.2019.01.015. Bach BR Jr, O’Brien SJ, Warren RF, Leighton M. An unusual neurological complication of the Bristow procedure. A case report. J Bone Joint Surg Am. 1988;70(3):458-460. Maquieira GJ, Gerber C, Schneeberger AG. Suprascapular nerve palsy after the Latarjet procedure. J Shoulder Elbow Surg. 2007;16(2):e13e15. doi:10.1016/j.jse.2006.04.001. Di Giacomo G, Costantini A, de Gasperis N, et  al. Coracoid graft osteolysis after the Latarjet procedure for anteroinferior shoulder instability: a computed tomography scan study of twenty-six patients. J Shoulder Elbow Surg. 2011;20(6):989-995. doi:10.1016/j. jse.2010.11.016.

11 Glenoid Bone Loss Augmentation Variations Matthew L. Vopat, MD; Liam A. Peebles, BA; Maj. Travis J. Dekker, MD, MC, USAF; and Matthew T. Provencher, MD, MC, USNR

As the osseous architecture of the glenohumeral joint allows for a large arc of motion as well as rotation, it is inherently predisposed to an elevated risk of instability. The incidence of glenohumeral instability events has been estimated to be 0.08 per 1000 person-years in the general US population, and is significantly greater in active, contact/collision sport, and military populations.1-5 Moreover, recent reports in the literature suggest that military personnel specifically are at a 20 times greater risk of experiencing shoulder instability compared to the general US population in the form of either subluxation or dislocation.3,6 It has been found that these patients are commonly younger athletes who are highly active because this population is at the greatest risk of recurrent instability; furthermore, their risk of recurrent instability increases directly with patient activity level.4,5 It is impor tant to identify the specific patient populations that are at risk for not only primary events of instability but recurrent instability as well, as numerous clinical studies have reported a significant correlation between the rate of recurrence following surgical treatment and the presence and severity of glenoid bone loss (GBL).7-10 In cases of recurrent glenohumeral instability, numerous studies have cited occurrence rates of bony glenoid injury ranging from 36% to 93.7% because higher rates of bone loss are associated with a greater number of instability events.11-14 Furthermore, it has been reported that patients with as little as 13.5% GBL experience worse functional outcomes following primary surgical stabilization procedures.15,16 In attempts to mitigate this risk of recurrent instability through the restoration of natural glenohumeral joint anatomy and function, numerous types of osseous grafts and bonyaugmentation procedures have been proposed, including

1) the iliac crest bone graft (ICBG), 2) the distal tibia allograft (DTA), and 3) the distal clavicular allograft. Although the Latarjet procedure, which uses a coracoid autograft, has long been considered to be the gold standard for anterior shoulder stabilization in the setting of significant GBL, these more recent bone grafting options have demonstrated early success in avoiding some of the potential complications commonly seen following a Latarjet and providing excellent clinical outcomes in highly active and athletic populations.

PREOPERATIVE ASSESSMENT OF INSTABILITY AND BONE LOSS Physical Examination Although recurrent anterior instability commonly results from a Bankart tear of the glenoid labrum, in cases of recurrent subluxation or dislocation patients will frequently present with bony defects of the glenoid. Following initial traumatic dislocation or subluxation of the shoulder, the static capsulolabral restraints of the joint may be compromised due to the presence of a glenoid rim fracture or attritional bone loss, making recurrent instability more likely in the future. The accurate assessment of these potential osseous defects given a patient’s history and physical exam findings in a clinical setting is critical to the overall success of a surgeon’s treatment algorithm. An in-depth understanding of the clinical factors that contribute to anterior glenohumeral instability such as age, sex, level activity, and events of recurrent instability may also help the surgeon accurately predict

- 115 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 115-127). © 2021 SLACK Incorporated.

116

Chapter 11

and diagnose the presence of such osseous deficiencies of the glenoid prior to imaging. In patients who present after sustaining contact or collision injuries, namely if the arm was axially loaded and abducted 70  degrees or more with extension of 30  degrees or more, the diagnosis of GBL may be suspected if further supported by physical exam findings.17,18 These patients are commonly younger and highly active athletes because this population is at the greatest risk of recurrent instability, which has been found to increase directly with patient activity level.4,5 In patients that have a history and physical examination indicative of potential GBL, it is commonly noted that they will also report a longer duration of instability symptoms, experience a progressive ease in subluxation or dislocation of the glenohumeral joint as well as a mechanical “clunk” on manipulation of the symptomatic shoulder. Prior treatments, whether operative or nonoperative, and their respective outcomes should be assessed along with previous operative reports and imaging studies to clearly delineate the initial pattern of injury and adequacy of proposed treatment for the patient’s pathology. These crucial pieces of information extracted from a patient’s history provide a basis from which a surgeon can tailor their physical exam of both the patient’s defective and contralateral shoulders. During the physical examination, it is crucial that both shoulders be inspected to identify abnormal physical deformity, prior surgical scarring, scapular dyskinesia, and/or potential atrophy of the rotator cuff on the pathologic shoulder vs the contralateral shoulder.9,18 This comparison can also aid in quantifying the direction and magnitude of glenohumeral laxity by performing physical manipulations of the shoulder such as the Jobe relocation test,19 Gagey hyperabduction sign,20 apprehension sign,21 and sulcus sign.22 Along with the aforementioned tests to assess glenohumeral laxity, the primary physical examination should also incorporate a careful neurovascular evaluation of the entire upper extremity, testing of active and passive shoulder motion, assessment of rotator cuff strength, and provocative labral signs. In the presence of mild to severe anterior GBL, patients will typically demonstrate a positive apprehension test in 90 degrees of shoulder abduction (AB) and 90 degrees of external rotation, and may also exhibit significant anterior or inferior translation of the of the humeral head over the glenoid rim. Physical findings of this nature may be indicative of GBL that is compromising glenohumeral stability and should be further investigated with diagnostic imaging.

DIAGNOSTIC IMAGING MODALITIES Two-Dimensional and 3-Dimensional Computed Tomography Numerous methodologies for quantifying the extent and severity of GBL have been proposed in the literature. These techniques are most commonly derived from either surface

area- or diameter-based measurement methods. The methodology of measuring GBL stems from the notion that the inferior aspect of the glenoid in the en-face view has a similar shape and curvature to a true circle, from which the degree of bone loss can be calculated by measuring the total surface area of bone loss or comparing the ratio of measurements taken to a healthy, contralateral shoulder.11,23 Although there is a lack of consensus and heterogeneity in reporting persists in the literature, this section describes these measurement techniques and their clinical implications. The percentage of GBL can be calculated with the use of surface area techniques, which require measuring the area of the superimposed circle not occupied by the glenoid surface and dividing this area by the total area of the best-fit circle.24 Sugaya et al23 first described the “circle method” to determine percentage of bone loss area, which was further expanded on by Baudi and colleagues25 and referred to as the ‘Pico’ method. This method involves superimposing a circle with a horizontal diameter from 3  o’clock to 9  o’clock on the inferior part of the healthy glenoid, and the circle area is measured, most commonly in millimeters squared. That same circle is then transferred to the contralateral, defective glenoid and the area of bone loss outlined, allowing surgeons to calculate percent total bone loss. Recent studies have found that quantification of GBL using bilateral computed tomography (CT) scans, such as the Glenoid Index, produce the most accurate assessment of GBL. This method consists of comparing the ratio of the measured widths of the injured glenoid to the healthy glenoid.26 In a clinical study, Altan et  al27 reported no statistically significant differences between Glenoid Index calculations and the surface area–based measurement technique in patients with more than 6% GBL. It was noted that, although insignificant, as the amount of bone loss increased, the differences in measurements increased as well.27 However, a unilateral affected shoulder CT is the senior author’s preferred method because it exposes the patient to far less radiation and maintains high accuracy. It has been reported that the location of the glenoid defect is also a fundamental variable in the overall accuracy of bone loss quantification for linear measurement techniques.28 This is primarily because linear measurements are hindered in their ability to represent defects outside the anteroposterior (AP) plane. This results in a significant underestimation of defects that are located in the anteroinferior portion of the glenoid. This was highlighted in a study conducted by Provencher et  al,17 who reported that diameter-based measurements are the most inaccurate when the defect is located anteroinferiorly at a 45-degree angle relative to the long axis of the glenoid. Recent studies that have employed 3-dimensional (3D) CT imaging have called into question the use of diameterbased measurements as a whole. This is primarily because these measurements have been reported to significantly overestimate GBL, which has the potential to misguide a surgeon’s treatment algorithm.24 In regards to the best-fit circle

Glenoid Bone Loss Augmentation Variations

117

technique, it has been proposed that its inaccuracy arise from the use of incorrect geometric formulas that more closely applies to calculating the area of a square, rather than a circle.29 In a study by Bhatia and colleagues,29 these inaccuracies were most prominent in bony defects that range between 15% and 25%. Therefore, these studies have suggested that unnecessary bony augmentation may be performed because of the overestimation of bone loss that appears to exceed the critical threshold of 20% to 21% for recurrent instability.29-31

Magnetic Resonance Imaging The primary benefits of using magnetic resonance imaging (MRI) to diagnose and quantify GBL include its ability to evaluate both soft-tissue and bony pathologies concurrently and the avoidance of a patient’s exposure to excessive radiation.32 However, scapular tilt and difficult visualization of the glenoid rim in the presence of soft tissue have been reported to be innate factors that limit the accuracy of MRI in the assessment of GBL.33 These inherent limitations lead to inaccurate measurements because of the difficulty of obtaining a true en face slice of the glenoid as well as in determining the exact edge of the glenoid rim, which is critical when quantifying bone loss via width-length methods. Although inconsistency in the literature persists regarding whether MRI is a viable substitute for CT, previous studies have reported that MRI does not produce significantly different measurements when comparing the 2 modalities.33,34 Gyftopoulos et  al33 concluded that MRI measurements can be as equally accurate to those produced via 3D CT with small margins of error when using the best-fit circle method. Similarly, Huijsmans and colleagues34 reported minimal, insignificant differences in accuracy using the best-fit circle method. Although other studies have reported high accuracy and strong correlations between MRI and 3D CT measurements,35,36 MRI has ultimately proved to be less sensitive and less reliable than 3D CT.37 Overall, 2-dimensional measurements such as the width-length ratio may be less reliable than surface area measurements because of the disadvantages described previously.38 Therefore, when using MRI to preoperatively assess GBL, surface area measurements such as the Pico method or other best fit-circle techniques are suggested to be more clinically applicable.32,34

Radiographic Assessment Because routine plain radiographs are commonplace in the first steps of patient diagnostic workup, the assessment for bony lesions of the glenoid with this modality may be favorable to clinicians because it offers an efficient, low-cost, and low-radiation diagnostic alternative to other aforementioned imaging modalities.39 Although numerous studies have advocated for the use of plain radiographs for these reasons, diagnostic sensitivity, specificity, and accuracy can be drastically influenced by patient positioning.30 When discussing optimal patient positioning for plain radiographs,

Figure 11-1. The patient is positioned in the reclined beach- chair position and a small bump or towels are placed under the medial border of the scapula. In this case, the patient’s arm is supported by an arm holder at the side of the operative table.

the axillary view, West Point View, true AP radiographs, and the Bernageau view have been recommended. Of these methods, recent studies have reported the Bernageau view to be the most accurate and reliable when referenced to 3D CT imaging,30,39,40 although using this method makes it difficult to evaluate inferior bony lesions.30 However, true AP radiographs may still provide utility in determining whether there is a loss of contour, or disruption of the sclerotic line, along the anteroinferior glenoid rim. The West Point view has demonstrated potential efficacy in identifying bone loss, but may not be sufficiently accurate in clinical settings to ultimately guide operative decision making.30

BONE GRAFTING VARIATIONS FOR GLENOID BONE LOSS Patient Positioning for Open-Shoulder Stabilization After induction of anesthesia with use of an interscalene regional nerve block when possible, the patient is placed into a beach-chair position with 30 degrees of head elevation (Figure 11-1). A small bump or towels are placed under the medial border of the scapula to prevent anterior and internal rotation. The arm can be placed into an armholder of choice or remain free for manipulation with the use of a padded Mayo stand for resting the extremity.67

Standard Deltopectoral Approach for Bone Grafting Procedures A standard Bankart-type incision with a No.  10 scalpel is made from the tip of the coracoid toward the axillary fold

118

Chapter 11

measuring 8 to 10 cm in length. The deltopectoral interval is identified and the cephalic vein is mobilized and protected laterally.41 Deep blunt dissection occurs followed by the identification of the short head of the biceps muscle belly adjacent to the conjoint tendon. A Gelpi or Weitlaner retractor is used to expose the fascia overlying the conjoint tendon, which when identified is then incised, and the lateral aspect of the conjoint tendon is retracted medially with a Kolbel retractor placed beneath the deltoid laterally. A Fukuda retractor is placed just behind the glenoid to retract the humeral head and deltoid laterally. The subscapularis insertion is identified and cleared of adhesions. The junction between the superior two-thirds and inferior one-third is identified and, using this junction, a sharp incision is made in line with the fibers of the subscapularis, taking care to not go medially to the coracoid to prevent iatrogenic nerve injury. However, in revision settings, the quality of subscapularis tissue may make this impossible and instead the subscapularis tendon may be taken down. If this is done, then the subscapularis tendon is tagged with a 2 Fiberwire Suture (Arthrex) for ease of later identification and repair. After clearance of the subscapularis off of the glenohumeral capsule, a medial T-shaped capsulotomy is used for glenohumeral joint exposure with a No. 15 scalpel. The capsule is then elevated off the glenoid neck sharply in a medial and subperiosteal fashion. In the revision setting, hardware, scar tissue, and prior implants are removed with the use of a rongeur and elevators of choice. While remaining perpendicular to the face of the glenoid, the anterior glenoid neck and rim are prepared with a high-speed burr to create a uniform bed of bleeding bone to complete the preparation of the recipient site. One should also evaluate the humeral head for an engaging Hill-Sachs lesion; this can be identified with the prior diagnostic arthroscopy.41

Debates continue about the quantity and setting of GBL that should lead a surgeon to perform a bone augmentation procedure in the setting of anterior shoulder instability. Most recently, Shaha et  al defined bone loss of 13.5% as being a critical number to identify because it leads to unacceptable clinical results and thus would require a bone augmentation procedure.15 Traditionally, biomechanical models and clinical studies have identified the normal cutoff of performing a soft-tissue only repair to a bony augmentation procedure at 20% to 25%.7,9,10,17,31,53-55 Furthermore, the concept of the glenoid track has revolutionized treatment because it aids the surgeon in identifying Hill-Sachs lesions that will engage based on location alone and not necessarily size of either the GBL or the Hill-Sachs lesion. The on-track, off-track concept uses a mathematical equation based on the size and location of the Hill-Sachs lesion and compares it to the amount of remaining glenoid bone stock. If the lesion is “off-track,” the patient has an engaging lesion that will portent to worse outcomes if soft-tissue–only repairs are performed.56,57 At present, the senior author uses tricortical or bicortical ICBG in patients requiring a revision technique procedure (ie, after a failed Latarjet) or those that have extensive attritional bone loss exceeding 30%. Preoperative workup is similar to that of a Latarjet in that patients should demonstrate anterior instability and apprehension on physical exam. Preoperative imaging should consist of standard shoulder radiographs (AP/Grashey/scapular Y/axillary lateral) along with advanced imaging of a 3D CT scan to quantify GBL (Figure  11-2). The senior author uses the en  face view of the reformatted CT and uses the circle method to quantify GBL.23,25

Iliac Crest Bone Graft

Operative Technique

Use of bone graft for anterior glenoid bone augmentation to extend the arc and effective articulation with the humeral head has occurred for more than a century. Although Eden42 and Hybbinette43 originally described augmentation with distal tibia, both authors almost immediately switched to the use of the iliac crest autograft (ICBG). The original procedure describes the use of bicortical iliac crest graft but more modern approaches have used tricortical iliac crest.44,45 The iliac crest remains a main source of autograft because of its ease in harvest, more than ample amounts of graft that would be necessary for augmentation, as well as flexibility to give both tricortical and bicortical graft that can be used per surgeon preference. Multiple variations exist, from implant free J-bone graft to bicortical screws to more recent descriptions of cortical suspensory devices.46-52 The iliac crest is most often used in revision procedures but can be used as a primary procedure in the setting of large anterior GBL defects where the Latarjet coracoid transfer would be insufficient (> 30% GBL). This section discusses surgical indications, a variety of ICBG glenoid augmentation techniques, and the associated outcomes to date.

Both open and arthroscopic techniques have been described in the setting of anterior glenoid bone augmentation for anterior shoulder instability with associated bone loss. Arthroscopic techniques have been described with purported benefits that the procedure is completely subscapularis sparing, with smaller incisions along with ease of access to the ICBG harvest site. Pitfalls include that with all new arthroscopic techniques, that there is a steep learning curve, possible increased risk of neuropraxia to the musculocutaneous nerve and axillary nerve, and possible graft harvest site complications.47,49,50,52 Fortun and colleagues47 describe their arthroscopic technique that places the ICBG in an extraarticular fashion along with being able to perform a large capsular shift. Furthermore, they advocate the routine use of a 70-degree arthroscope to facilitate complete visualization of the anterior glenoid rim and neck. Giannakos et al used a double-barreled cannula through a low anterior “J portal” to aid in ease of passage and bicortical graft fixation.48 Authors have also used both screw fixation with bicortical purchase through the glenoid as well as bicortical suspensory devices

Indications and Contraindications

Glenoid Bone Loss Augmentation Variations

119

Figure 11-2. (A) An iliac crest autograft may be used to reconstruct the anterior aspect of the native glenoid in cases of extensive attritional bone loss, with the figure demonstrating approximately 45% glenoid bone loss on preoperative 3- dimentional computed tomography (3D CT). (B) Postoperative 3D CT scan following bony augmentation with a tricortical iliac crest autograft, which successfully extended the glenoid-humeral interface to a near native state.

in an arthroscopic fashion to provide firm and reliable iliac crest cortical abutment.49 The open technique for ICBG for anterior glenoid deficiency has also been described with benefits of direct visualization of the graft/glenoid interface but known technical challenges in revision exposure after failed Latarjet.45,51 The senior author uses the open technique and exposure in the setting of ICBG for anterior GBL.

Iliac Crest Bone Graft Harvest Starting 2  cm posteriorly to the anterior superior iliac spine, a 5-cm curvilinear incision is made sharply with a No. 10 blade along the iliac crest. A plane between the tensor fascia lata and the external abdominal obliques is created with the use of electrocautery, ensuring the insertion of the abductors remain intact. After complete exposure of the superior iliac crest, blunt retractors are placed on the inner and outer table of the crest to facilitate full exposure for graft harvest. The dimensions of the graft are measured and marked with electrocautery (typically 3 cm long by 2 cm wide). Using a small 1 cm oscillating saw followed by the use of small straight and curved osteotomes, the graft harvesting is completed. The inner table is contoured to approximate the correct contour of the native glenoid, which will eventually articulate with the native humeral head.

Graft Fixation After contouring and shaping has been completed, two 4.0 mm cannulated screws with suture washers initially positioned with appropriately sized K-wires are placed for graft fixation (Figure 11-3). The goal for screw trajectory is to be within 10 degrees of parallel to the face of the glenoid with the screws as far medially on the graft as possible to avoid articulation with the native humeral head. Small adjustments and recontouring of the graft/glenoid interface can occur to ensure a perfectly smooth transition from glenoid to the graft with the use of a small burr. The humeral head retractor is

Figure 11-3. Following appropriate contouring of the harvested iliac crest autograft, K-wires are used to initially position and affix the graft. These are then removed and two 4.0-mm cannulated screws with suture washers are inserted for final graft fixation and capsular reconstruction with the attached sutures.

removed and articulation along with stability is retested at this time. The high-strength sutures from the washers are then used to repair the capsulolabral ligamentous complex back to the edge of the graft. The lateral limbs of the capsule can often not be repaired in the setting of revision procedures or chronic bone loss. The lateral subscapularis can effectively extend the lateral capsule by fixing the capsule to the undersurface of the subscapularis with the humerus in 30 degrees of external rotation.45 The procedure is then completed with a dermis closure of 2-0 Vicryl followed by a running resorbable 3-0 monofilament suture. The incision is dressed and placed into an immobilizer.

120

Chapter 11

Postoperative Rehabilitation Shoulder pendulum exercises are the first allowable movement that occurs after the first week. Supervised formal physical therapy is started after week 4 along with arm use for routine daily activities. Serial imaging is performed to verify graft healing, which aids in the advancement to active and passive assisted-motion protocols. Water therapy can begin after 6  weeks and formal strength training after 3 months. Recreational noncontact sports can begin after month 4 with full clearance to all sporting activities (contact/ professional) at 8 months.

Clinical Outcomes and Return to Play Biomechanical models have validated the use of ICBG to extend the glenoid-humerus interface in the setting of anterior GBL. With concerns about long-term development of osteoarthritis (OA) in the setting of ICBG as the bone graft of choice for glenoid augmentation,58-60 it is of the utmost importance that the graft be flush with the anterior glenoid. Ghodadra and colleagues61 showed that peak pressures of a flush iliac crest graft returns contact pressures to 116% of normal. However, the placement of proud graft peak pressures increases to that of 250% in the anteroinferior quadrant and 200% of normal in the posterosuperior glenoid, placing the shoulder at significant risk of developing OA. The inner table ICBG demonstrates restoration of the glenoid depth but does not restore the coronal radius of curvature in comparison to the congruent arc Latarjet.62 Furthermore, ICBG has been shown to have excellent restoration of glenoid surface area as well as axial radius of curvature.63 Willemot et  al63 also brings attention to the placement of ICBG and how it affects peak force required for recurrent instability—ideally, the graft should be placed between 50% and 75% below the equator to optimize the biomechanical stability of the graft. In summary, the biomechanical studies have shown ICBG to be an excellent choice in the setting of revision bone augmentation procedures as well those requiring more than 30% bone loss augmentation. Clinical outcome studies are currently limited to case series and retrospective cohort studies. Results are generally positive, with good results seen at 2-year minimum follow-up (2-17  years) with good to excellent outcomes ranging from 68% to 78% of patients who undergo ICBG for revision anterior glenoid bone augmentation procedures.45,46,64,65 Lunn and colleagues64 reported that at a mean follow-up of 6.8  years, 79% (27/34 patients) reported good to excellent outcomes, with 68% of patients in this cohort able to return to presurgery sporting activity levels. Furthermore, 11.8% (4/34) of patients reported failure after revision with reporting of a subsequent dislocation after ICBG for anterior glenoid bone augmentation.48,64 Mascarenhas et  al51 reported statistically significant improvement across all clinical outcome score domains of the American Shoulder and Elbow Surgeons evaluation, Simple Shoulder Test, and Western Ontario Shoulder

Instability Index (WOSI) at an average 16-month follow-up. Furthermore, all patients exhibited a negative apprehension/ relocation test and full shoulder strength at final follow-up. These findings were corroborated at a mean 8-year follow-up by Moroder et al, with improvement in WOSI scores, Rowe score, and a pain level of 0.5/10 with only a 3% redislocation rate.46 Overall, ICBG as a choice for alternative bone augmentation procedures provides consistent and reliable results with improvement in clinical outcome scores as well as the ability for the majority of patients to return to preinjury activities despite their complex pathology. The most commonly reported complications reported after ICBG include recurrence of instability but also the development of OA. Lunn et al.64 reported an incidence of the development of OA in 29% (10 of 34) of patients after ICBG, with 6 of 34 patients (10%) being rated as moderate or severe. In the largest case series to date with use of ICBG for anterior GBL, Moroder and colleagues46 reported no arthropathy in 26% (9 of 35) of patients, mild in 63% (22 of 35), and moderate to severe in 11% (4 of 35). Nonunion is a risk of any bone augmentation procedure and has been reported to occur approximately 20% of the time.51 Giannakos et al48 reported a nonunion rate of 22% (4 of 18) that directly correlated with their outcomes and unsatisfactory result. Another rare complication was reported by Steffen and Hertel, with 1 of 40 patients (2.5%) developing subscapularis insufficiency after an open procedure with ICBG.65 Overall, although ICBG does not prevent the onset of radiographic signs of OA, the majority of patients are asymptomatic and are able to return to activities.

Distal Tibia Allograft For patients with glenoid bone deficiency in the setting of recurrent anterior shoulder instability, Latarjet procedures have become the favored treatment in recent years. However, even with the successful outcomes that the Latarjet reconstruction and even the ICBG have both produced, there is growing concern about development of early symptomatic glenohumeral arthritis. This is likely due to the nonanatomic reconstruction of the anterior osseous profile of the glenoid and to the graft reabsorption.66,67 In contrast, the use of the DTA is becoming a more popular option for severe cases of GBL because of its dense, weight-bearing osseous tissue source that has great conformity, as well as the additional benefit of a cartilaginous surface to correct chondral deficiencies.41 Even so, inferior coracoid autograft and DTA have both been found to have a similar radius to the native glenoid.68,69 However, Bhatia el  al70 found that DTA may allow greater joint congruity and may have a lower peak force at 60 degrees of AB, and AB and external rotation position compared to the coracoid autograft used in the Latarjet procedure. This may justify the need for a graft with these superior biomechanical properties such as DTA, which has a cartilaginous tissue articular layer with a similar radius of curvature to the native glenoid, to help provide greater

Glenoid Bone Loss Augmentation Variations

121

functional outcomes for these patients suffering from anterior shoulder instability with severe GBL. This section discusses surgical indications, insight on operative techniques, and the associated outcomes up to date on DTA glenoid augmentation.

Indications and Contraindications Preoperative workup is similar to that of a patient who would undergo a Latarjet procedure in that patients should demonstrate signs of anterior instability and apprehension on physical exam. Preoperative imaging should consist of standard shoulder radiographs (AP/Grashey/scapular-Y/ axillary lateral) along with advanced imaging of a 3D CT scan to quantify GBL. The senior author uses the en face view of the reformatted CT and uses the circle method to quantify GBL.23,25 Traditionally, the GBL of 20% to 25% has been indication for bony reconstruction.7,18,71 However, this critical GBL value continues to be debated. For instance, Shaha and colleagues15 showed that soft-tissue repair alone was insufficient fixation for patients with at least 13.5% GBL and that this amount of bone loss should be used to indicate a bony augmentation reconstruction. The Latarjet reconstruction has become one of the gold standards for this bony reconstruction. Unfortunately, in cases for which Latarjet procedure has failed and there needs to be a revision because of persistent instability and/or osteolysis of the old coracoid autograft, the senior author would indicate that a DTA could be a valuable treatment option. Also, another indication for DTA by the senior author is for primary or revision anterior shoulder instability cases for which there is severe GBL (> 30%), in which coracoid autograft from a Latarjet procedure would be insufficient.72 Even though the DTA is an excellent graft option, it should be noted that DTA has a high cost and can be difficult to acquire in areas outside the United States. Initial results have demonstrated that the DTA undergoes minimal lysis at nearly 4-year follow-up66 and provides patient outcomes comparable to those following a Latarjet procedure.73 However, further studies are required to determine the development or worsening, or lack thereof, of postoperative glenohumeral OA because this has been a complication commonly associated with the Latarjet procedure.

Operative Technique Allograft Preparation Preparation of the allograft is performed on the back table. The anterior glenoid bone graft is harvested from the lateral one-third of the fresh DTA and cut to size to the dimensions of the glenoid defect. The graft should be constantly irrigated with saline while it is being cut to prevent damage from thermoneurosis. Then, two 4.0 drill holes are drilled in the prepared graft while using the graft holder as a guide. Next, for approximately 5 minutes, a pulsatile lavage is used to irrigate the graft to remove all marrow elements

Figure 11-4. Preoperative planning with CT imaging will provide crucial information regarding the approximate dimensions of the graft necessary to restore the bony anatomy. By use of the distal tibia allograft workstation, the graft is irrigated with saline solution and cut sequentially into the appropriate dimensions.

before graft fixation. Additionally, after the pulse lavage, the graft can be soaked in a combination of autologousconditioned plasma and platelet-rich plasma through use of a double-syringe system (Greylege Technologies). Prior to this step, 60 cm3 of peripheral blood is collected from the patient and applied to centrifugation for approximately 10 minutes to heterogeneously divide the blood.41 A cutting jig may also be used that allows for the precise sizing of the allograft from an average of 17 to 23 mm superior to inferior, 7 to 10 mm anterior to posterior, and also at 5-degree, 10-degree, and 15-degree angles (Figure 11-4).

Graft Fixation The allograft is then positioned to the anterior glenoid rim with 2 K-wires placed in a bicortical fashion to the posterior aspect of the glenoid. If needed a third K-wire may be used to aid in this fixation to the glenoid. Next, these K-wires are then measured for the screw size (sizes are usually between 32 to 36 mm in length). By providing a lag screw by technique

122

Chapter 11

Figure 11-5. Following adequate preparation of the bony glenoid interface, the distal tibia allograft is affixed with two 3.75-mm noncannulated, fully threaded interference screws. The surgeon should confirm a smooth transition between the cartilage surface of the glenoid to that of the allograft.

compression, a cannulated drill is used over the K-wires to subsequently drill through the previously drilled 4.0  mm holes in the allograft and into the near cortex of the native glenoid. K-wires are then removed, and two 3.75  mm noncannulated fully threaded interference screws with suture washers are inserted (Arthex). After graft fixation, it should be thoroughly assessed that the allograft cartilage is flush with the cartilage surface of the native glenoid (Figure 11-5). After this has been confirmed, the anterior-inferior capsule is repaired using the sutures from the suture washers. In revision cases, the subscapularis is then identified through a No. 2 Fiberwire suture (Arthrex) tag stitch and is repaired with multiple suture anchors by a double-row technique. Finally, the procedure is then completed with a dermis closure of 2-0 Vicryl followed by a running resorbable 3-0 monofilament suture. The incision is dressed and placed into an UltraSling.[41]

Postoperative Rehabilitation Postoperatively, the patient is placed in an UltraSling for 4 to 6 weeks. The rehabilitation is divided into 6 phases.41 In the first phase (first 2 weeks), there is no activation of the

biceps. Aerobic exercises, stationary bike, and walking on a level surface are achieved for 30 minutes. Passive range of motion (PROM) should be performed 4 times per week and should reach the goals of the following: 120 degrees of forward flexion (FF), 120 degrees of motion in the scapular plane (SC), 30 degrees of external rotation (ER) at the side and AB to 90 degrees. The patient is allowed to perform active wrist and elbow range of motion in this phase. Once patients achieve phase-1 PROM goals, then they proceed to the second phase (weeks 2-4). The aerobic exercises progress to 45 to 60 minutes. The patient’s PROM goals are now 150 degrees of FF, 150 degrees of motion in the SC, 45 degrees of ER at the side and AB to 90  degrees. The patient also starts isometric exercises for extension, ER, internal rotation and AB. After phase-2 goals are achieved, the use of the UltraSling is discontinued. The patient then proceeds to the third phase (weeks 6-12), which consists of the PROM goals progressing to 160 degrees of FF, 160 of motion in SC, 45 degrees of ER at the side, and AB to 140 degrees. Deltoid isometric exercises start at 4 weeks. For the fourth phase, an inclined treadmill is integrated and active assisted range of motion is progressed to active range of motion and increases in internal and external exercises are performed. From weeks 12 to 16, the goal of this phase is to restore strength. This is achieved by external and internal rotation at 90 degrees with cable, push-up, and Plyometric exercises. The final phase is started after all these goals are met, which usually takes more than 16 weeks. The patient can then start swimming, military press, and lat pulldown exercises. The patient may also start throwing but is progressed from short to long distances. The return to full activity is achieved on an individual basis and per the patient’s goals.41

Clinical Outcomes and Return to Play The early literature on this new DTA reconstruction technique has shown favorable outcomes for the short-term follow-up. Provencher et al66 evaluated 27 male patients who had recurrent anterior shoulder instability, with an average GBL of 23.7 ± 67% (range, 15.9% to 35.2%) that was treated with DTA reconstruction. In their results, they found significant improvement from preoperative to postoperative in functional outcome scores with American Shoulder and Elbow Society Score (63 to 91, P < .01), WOSI (46% to 11% of normal, P < .01), and single numeral assessment evaluation score (50 to 90.5, P < .01) at an average 45-month followup. There were no cases of recurrent instability within this cohort. They were also able to evaluate 25 of these patients with a postoperative CT at an average 1.4-year follow-up. In their findings, they found that the allograft had an 89% healing rate and an allograft lysis of only 3%. Furthermore, they found that allografts with angles less than 15  degrees were found to have a greater change of healing and graft incorporation. These results show the importance of optimal allograft placement for superior bony incorporation with the native glenoid.

Glenoid Bone Loss Augmentation Variations When comparing to more traditional bony augmentation such as Latarjet reconstruction, Frank and colleagues73 found that patients undergoing DTA reconstruction had significantly greater GBL defects, with values of 22.4 ± 10.3% vs 28.6 ± 7.4%, respectively. However, even though patients undergoing Latarjet reconstruction had less-severe GBL, only the Simple Shoulder Test (P = .011) had a significantly superior functional outcome. No significant difference was found with the American Shoulder and Elbow Surgeons, WOSI, or Single Assessment Numeric Evaluation. There was still an overall 10% complication rate, with 5% in the Latarjet treatment group vs 5% in the DTA treatment group. Thus, the overall reoperation rate was 6% (3% from each group). The overall recurrence of instability rate was 1%, and this was one patient who had a traumatic fall 16 months after the DTA reconstruction. From the authors’ results, they concluded that DTA reconstruction can provide similar outcomes to Latarjet reconstruction. Overall, the early literature for DTA reconstruction for patients with recurrent anterior shoulder instability has been favorable for the short-term follow-up for functional outcomes, minimal osteolysis of graft, and recurrent instability. However, longer-term follow-up and future studies are needed to evaluate return to sport and/or activity for patients undergoing DTA reconstruction.

Distal Clavicular Allograft Tokish et  al74 were the first to describe using the distal clavicle autograft (DCA) as a bony augment in cases of recurrent anterior shoulder instability with associated GBL. Since then, the DCA has gained interest because of potential advances of being an osteochondral autograft with articular cartilage surface similar to the glenoid cartilage. It also is a corticocancellous graft that can provide a broad healing surface to allow secure fixation to the native glenoid.74 In contrast to Latarjet reconstruction and ICBG, which do not provide articular cartilage, there is a growing concern about development of early symptomatic glenohumeral arthritis associated with these graft chooses.66,67 Also, because DCA is an osteochondral autograft, this graft option is more favorable economically, has greater availability, lacks antigenicity, has decreased infection risk, and possibility greater healing potential as compared to the DTA. There is still little known about the clinical outcomes for DCA augmentation for recurrent anterior shoulder instability with GBL. However, this section will provide insight in potential indications/contraindications, operative technique, postoperative rehabilitation, and the literature supporting DCA.

Indications and Contraindications Similarly as described in other sections of this chapter, the preoperative workup is the same as that of a patient who would undergo a Latarjet procedure in that patients should demonstrate signs of anterior instability and apprehension

123

on physical exam. Preoperative imaging should consist of standard shoulder radiographs (AP/Grashey/scapular-Y/axillary lateral) along with advanced imaging of a 3D CT scan to quantify GBL. The senior author uses the en face view of the reformatted CT and uses the circle method to quantify GBL.23,25 Also, a surgeon should always access the shoulder AP radiograph to evaluate for AC joint arthritis, for which this can be an relative contradiction because of the loss of articular cartilage that a DCA can provide.74 As recently discussed, 20% to 25% GBL has been the traditional critical value for bony augmentation for patients with anterior instability.7,18,71 However, Shaha and colleagues15 most recently showed that 13.5% GBL cannot be acceptably repaired with soft-tissue repair alone and needs additional bony augmentation fixation. Even though there has been no clinical evidence to support the amount of GBL DCA can successfully repair, it has been suggested that 15% to 30% of GBL can be successfully treated by DCA. One needs to keep in mind, however, when harvesting the DCA not to resect more than 1.5  cm of the distal clavicle because of risk of providing instability to the acromioclavicular (AC) joint.75,76 This theoretically provides a limitation on the amount of GBL that a DCA can successfully correct. However, a cadaver study by Kwapisz et al79 did find that a 1-cm resected DCA can restore up to 44% of the native glenoid diameter. Thus, more clinical studies are needed to define the exact amount of GBL that can be successfully corrected by DCA. It has also been suggested that using DCA in contrast to the Latarjet procedure in young patients may help preserve the native tissue and prevent injury to axillary and musculocutaneous nerves.77 Whereas the DCA can provide the benefit of not distorting the normal anatomy, it does happen with the Latarjet procedure. This is especially concerning if a revision is needed in the future.78 Also, DCA provides the same benefit as the DTA and ICBG, for which it can used in cases of posterior instability with associated posterior GBL.78 It also should be noted that, in certain regions where DTA is not routinely available, DCA can be another viable option to be used for bony glenoid augmentation fixation. Even with all these potential benefits of DCA, Choate and colleagues78 posed some potential limitations to DCA in that it does not address anterior capsular structures that can be a part of the complex instability. In cases of collagenopathies, such as Ehlers-Danlos, patients with previous thermal capsulorrhaphy, or multiply operated-on patients, Choate et  al recommend evaluating alternative techniques to address these concerns.

Operative Technique Tokish et al74 were the first to describe arthroscopic DCA augmentation fixation for GBL in the setting of shoulder instability. This is achieved first by performing a diagnostic arthroscopy to evaluate for other pathologies and measure the exact amount of GBL by a 3 mm graduated probe. Then, after determining the accurate GBL, the DCA is harvested

124

Chapter 11

Figure 11-6. (A) The distal clavicular autograft is harvested with an oscillating saw and (B) sized to match the glenoid defect based on preoperative templating.

in a similar fashion as a Mumford open distal clavicle excision (Figure  11-6). The DCA is then fixed to the glenoid arthroscopy with either 2 cannulated, titanium 3.75  mm screws (Arthrex) or two 3.0 mm BioCompostite SutureTaks (Arthrex). Native labrum is then fixed on top of the bone augmentation fixation.74

Postoperative Rehabilitation Postoperatively these patients are placed in a neutral rotation sling for 6 weeks, but they are allowed to perform pendulum exercises immediately.74,78 PROM is started at 3 weeks, with the goal of obtaining full range of motion at 8 weeks. Imaging is then evaluated at the 8-week follow-up to determine whether the graft has incorporated. If the DCA has incorporated to the native glenoid, then active range of motion is begun. Strength training does not start until 4 months postoperatively. The patient is evaluated at 6 months to determine whether he or she can return to full activity. Final radiographs are also taken at this time to ensure the graft has incorporated.74,78

Clinical Outcomes and Return to Play Clinical research is currently lacking for DCA. However, there have been recent biomechanical and cadaver studies that have evaluated DCA for GBL in shoulder instability.79,80 Petersen and colleagues80 biomechanically compared the

contact area and pressure between a cadaver corocoid graft used in a Latarjet procedure and DCA in dif ferent glenohumeral joint positions. They found that DCA had the lowest mean pressure in all testing positions and lowest contact area in all humeral head positions. However, this was not found to be statistically significant. Thus, they concluded that DCA is comparable to the coracoid bone graft both in glenohumeral contact area and pressures in restoring GBL.80 Similarly, the cadaver study by Kwapisz et al79 also compared the DCA to the coracoid graft; however, they evaluated the amount of native glenoid radius that was restored between these 2 grafts. They found that DCA significantly restored a greater amount of the native glenoid at 44% vs 33% of the native glenoid restored with the coracoid. This study does in put into question the upper limit of GBL that the DCA can restore, but one must also consider staying within 1.5 cm of harvested DCA to avoid AC joint instability.75,76 Hence, more clinical studies are needed to help quantify the exact amount of GBL DCA can restore. In addition, this study also evaluated the articular cartilage thickness between the glenohumeral joint and DCA. The authors found that in all the specimens the DCA was 1.5 mm thinner than the glenohumeral joint. However, when excluding the clavicle specimens with OA, the DCA was only 1 mm thinner, further justifying the benefit of DCA in restoring a similar articular surface to the native glenoid.79 DCA is the first osteochondral autograft used for GBL in patients with shoulder instability, and this can provide the same DTA benefits of restoring a articular cartilage surface to the native glenoid; without additional cost, possible unavailability, and increased infection risk that can be seen with DTA.74 Furthermore, even with the potential benefits of DCA, the literature is in need of clinical studies to help define possible complications, functional outcomes, time to return to sport, and long-term prognosis for patients suffering from anterior shoulder instability with associated GBL who are treated with DCA.

CONCLUSION When electing operative management to restore glenohumeral joint stability in the shoulder, patient-specific factors along with assessment of bone loss with advanced imaging should be taken into account to best tailor a treatment algorithm to the patient’s unique pathologies. The optimal surgical procedure will aim to minimize the risk of further shoulder instability events. In the setting of extensive GBL, the DTA and the iliac crest or distal clavicular autografts have all been demonstrated to be effective in restoring the osseous architecture of the glenoid and overall joint stability with promising patient outcomes. Moving forward, further clinical studies are needed for these bony-augmentation procedures to help better define potential complications, functional outcomes, and rates of return to sport following surgery.

Glenoid Bone Loss Augmentation Variations

REFERENCES 1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

14.

15.

16.

17.

Porcellini G, Campi F, Pegreffi F, Castagna A, Paladini P. Predisposing factors for recurrent shoulder dislocation after arthroscopic treatment. J Bone Joint Surg Am. 2009;91(11):2537-2542. doi:10.2106/ JBJS.H.01126. Hovelius L, Augustini BG, Fredin H, Johansson O, Norlin R, Thorling  J. Primary anterior dislocation of the shoulder in young patients. A ten-year prospective study. J Bone Joint Surg Am. 1996;78(11):1677-1684. doi:10.2106/00004623-199611000-00006. Owens BD, Duffey ML, Nelson BJ, DeBerardino TM, Taylor DC, Mountcastle SB. The incidence and characteristics of shoulder instability at the United States Military Academy. Am J Sports Med. 2007;35(7):1168-1173. doi:10.1177/0363546506295179. Pagnani MJ, Dome DC. Surgical treatment of traumatic anterior shoulder instability in American football players. J Bone Joint Surg Am. 2002;84(5):711-715. doi:10.2106/00004623-200205000-00002. Buckup J, Welsch F, Gramlich Y, et  al. Back to sports after arthroscopic revision Bankart repair. Orthop J Sports Med. 2018;6(2):2325967118755452. doi:10.1177/2325967118755452. Owens BD, Dawson L, Burks R, Cameron KL. Incidence of shoulder dislocation in the United States military: demographic considerations from a high-risk population. J Bone Joint Surg Am. 2009;91(4):791796. doi:10.2106/JBJS.H.00514. Boileau P, Villalba M, Héry JY, Balg F, Ahrens P, Neyton L. Risk factors for recurrence of shoulder instability after arthroscopic Bankart repair. J Bone Joint Surg Am. 2006;88(8):1755-1763. doi:10.2106/ JBJS.E.00817. Balg F, Boileau  P. The Instability Severity Index Score. A simple pre-operative score to select patients for arthroscopic or open shoulder stabilisation. J Bone Joint Surg Br. 2007;89(11):1470-1477. doi:10.1302/0301-620X.89B11.18962. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694. doi:10.1053/ jars.2000.17715. Lo IK, Parten PM, Burkhart SS. The inverted pear glenoid: an indicator of significant glenoid bone loss. Arthroscopy. 2004;20(2):169-174. doi:10.1016/j.arthro.2003.11.036. Griffith JF, Antonio GE, Tong CW, Ming CK. Anterior shoulder dislocation: quantification of glenoid bone loss with CT. AJR Am J Roentgenol. 2003;180(5):1423-1430. doi:10.2214/ajr.180.5.1801423. Guity MR, Akhlaghpour S, Yousefian R. Determination of prevalence of glenoid bony lesions after recurrent anterior shoulder dislocation using the 3-D CT scan. Med J Islam Repub Iran. 2014;28:20. Carrazzone OL, Tamaoki MJ, Ambra LF, Neto NA, Matsumoto MH, Belloti JC. Prevalence of lesions associated with traumatic recurrent shoulder dislocation. Rev Bras Ortop. 2011;46(3):281-287. doi:10.1016/S2255-4971(15)30196-8. Edwards TB, Boulahia A, Walch  G. Radiographic analysis of bone defects in chronic anterior shoulder instability. Arthroscopy. 2003;19(7):732-739. doi:10.1016/s0749-8063(03)00684-4. Shaha JS, Cook JB, Song DJ, et  al. Redefining “critical” bone loss in shoulder instability: functional outcomes worsen with “subcritical” bone loss. Am J Sports Med. 2015;43(7):1719-1725. doi:10.1177/0363546515578250. Dickens JF, Owens BD, Cameron KL, et al. The effect of subcritical bone loss and exposure on recurrent instability after arthroscopic Bankart repair in intercollegiate American football. Am J Sports Med. 2017;45(8):1769-1775. doi:10.1177/0363546517704184. Provencher MT, Bhatia S, Ghodadra NS, et  al. Recurrent shoulder instability: current concepts for evaluation and management of glenoid bone loss. J Bone Joint Surg Am. 2010;92(suppl 2):133-151. doi:10.2106/JBJS.J.00906.

18.

19.

20. 21. 22.

23.

24.

25. 26.

27.

28.

29.

30.

31.

32.

33.

34.

35.

36.

125

Piasecki DP, Verma NN, Romeo AA, Levine WN, Bach BR Jr, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493. doi:10.5435/00124635-200908000-00002. Jobe FW, Kvitne RS, Giangarra CE. Shoulder pain in the overhand or throwing athlete. The relationship of anterior instability and rotator cuff impingement. Orthop Rev. 1989;18(9):963-975. Gagey OJ, Gagey  N. The hyperabduction test. J Bone Joint Surg Br. 2001;83(1):69-74. doi:10.1302/0301-620x.83b1.10628. Magee DJ. Orthopedic Physical Examination. 2nd  ed. Philadelphia, PA: WB Saunders; 1992. Neer CS  II, Foster CR. Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. A preliminary report. J Bone Joint Surg Am. 1980;62(6):897-908. Sugaya H, Moriishi J, Dohi M, Kon Y, Tsuchiya A. Glenoid rim morphology in recurrent anterior glenohumeral instability. J Bone Joint Surg Am. 2003;85(5):878-884. doi:10.2106/00004623-200305000-00016. Bakshi NK, Cibulas GA, Sekiya JK, Bedi  A. A clinical comparison of linear- and surface area-based methods of measuring glenoid bone loss. Am J Sports Med. 2018;46(10):2472-2477. doi:10.1177/0363546518783724. Baudi P, Righi P, Bolognesi D, et  al. How to identify and calculate glenoid bone deficit. Chir Organi Mov. 2005;90(2):145-152. Chuang TY, Adams CR, Burkhart SS. Use of preoperative threedimensional computed tomography to quantify glenoid bone loss in shoulder instability. Arthroscopy. 2008;24(4):376-382. doi:10.1016/j. arthro.2007.10.008. Altan E, Ozbaydar MU, Tonbul M, Yalcin  L. Comparison of two different measurement methods to determine glenoid bone defects: area or width? J Shoulder Elbow Surg. 2014;23(8):1215-1222. doi:10.1016/j.jse.2013.11.029. Saito H, Itoi E, Sugaya H, Minagawa H, Yamamoto N, Tuoheti  Y. Location of the glenoid defect in shoulders with recurrent anterior dislocation. Am J Sports Med. 2005;33(6):889-893. doi:10.1177/0363546504271521. Bhatia S, Saigal A, Frank RM, et al. Glenoid diameter is an inaccurate method for percent glenoid bone loss quantification: analysis and techniques for improved accuracy. Arthroscopy. 2015;31(4):608-614. e1. doi:10.1016/j.arthro.2015.02.020. Itoi E, Lee SB, Amrami KK, Wenger DE, An KN. Quantitative assessment of classic anteroinferior bony Bankart lesions by radiography and computed tomography. Am J Sports Med. 2003;31(1):112-118. do i:10.1177/03635465030310010301. Yamamoto N, Itoi E, Abe H, et al. Effect of an anterior glenoid defect on anterior shoulder stability: a cadaveric study. Am J Sports Med. 2009;37(5):949-954. doi:10.1177/0363546508330139. Martins e Souza P, Brandão BL, Brown E, Motta G, Monteiro M, Marchiori  E. Recurrent anterior glenohumeral instability: the quantification of glenoid bone loss using magnetic resonance imaging. Skeletal Radiol. 2014;43(8):1085-1092. doi:10.1007/ s00256-014-1894-6. Gyftopoulos S, Hasan S, Bencardino J, et al. Diagnostic accuracy of MRI in the measurement of glenoid bone loss. AJR Am J Roentgenol. 2012;199(4):873-878. doi:10.2214/AJR.11.7639. Huijsmans PE, Haen PS, Kidd M, Dhert WJ, van der Hulst VP, Willems WJ. Quantification of a glenoid defect with threedimensional computed tomography and magnetic resonance imaging: a cadaveric study. J Shoulder Elbow Surg. 2007;16(6):803-809. doi:10.1016/j.jse.2007.02.115. Tian CY, Shang Y, Zheng ZZ. Glenoid bone lesions: comparison between 3D VIBE images in MR arthrography and nonarthrographic MSCT. J  Magn Reson Imaging. 2012;36(1):231-236. doi:10.1002/ jmri.23622. Lee RK, Griffith JF, Tong MM, Sharma N, Yung  P. Glenoid bone loss: assessment with MR imaging. Radiology. 2013;267(2):496-502. doi:10.1148/radiol.12121681.

126 37.

38.

39.

40.

41.

42.

43.

44.

45.

46.

47.

48.

49.

50.

51.

52.

53.

Chapter 11 Moroder P, Plachel F, Huettner A, et  al. The effect of scapula tilt and best-fit circle placement when measuring glenoid bone loss in shoulder instability patients. Arthroscopy. 2018;34(2):398-404. doi:10.1016/j.arthro.2017.08.234. Saliken DJ, Bornes TD, Bouliane MJ, Sheps DM, Beaupre LA. Imaging methods for quantifying glenoid and Hill-Sachs bone loss in traumatic instability of the shoulder: a scoping review. BMC Musculoskelet Disord. 2015;16:164. doi:10.1186/s12891-015-0607-1. Pansard E, Klouche S, Billot N, et al. Reliability and validity assessment of a glenoid bone loss measurement using the Bernageau profile view in chronic anterior shoulder instability. J Shoulder Elbow Surg. 2013;22(9):1193-1198. doi:10.1016/j.jse.2012.12.032. Murachovsky J, Bueno RS, Nascimento LG, et al. Calculating anterior glenoid bone loss using the Bernageau profile view. Skeletal Radiol. 2012;41(10):1231-1237. doi:10.1007/s00256-012-1439-9. Sanchez A, Ferrari MB, Akamefula RA, Frank RM, Sanchez G, Provencher MT. Anatomical glenoid reconstruction using fresh osteochondral distal tibia allograft after failed Latarjet procedure. Arthrosc Tech. 2017;6(2):e477-e482. doi:10.1016/j.eats.2016.11.003. Eden  R. Zur Operation der habituellen Schulterluxation unter Mitteilung eines neues Verfahrens bei Abriss am inneren Pfamnnenrande. Dtsch Ztsch Chir. 1918;144:269. doi:10.1007/ BF02803861. Hybbinette S. De la transplantation d’un fragment osseux pour remedier aux luxations recidivantes de l’epaule; constations et resultats. Acta Chir Scand. 1932;71:411-445. Lynch JR, Clinton JM, Dewing CB, Warme WJ, Matsen FA  III. Treatment of osseous defects associated with anterior shoulder instability. J Shoulder Elbow Surg. 2009;18(2):317-328. doi:10.1016/j. jse.2008.10.013. Warner JJ, Gill TJ, O’Hollerhan J D, Pathare N, Millett PJ. Anatomical glenoid reconstruction for recurrent anterior glenohumeral instability with glenoid deficiency using an autogenous tricortical iliac crest bone graft. Am J Sports Med. 2006;34(2):205-212. doi:10.1177/0363546505281798. Moroder P, Plachel F, Becker J, et al. Clinical and radiological longterm results after implant-free, autologous, iliac crest bone graft procedure for the treatment of anterior shoulder instability. Am J Sports Med. 2018;46(12):2975-2980. doi:10.1177/0363546518795165. Fortun CM, Wong I, Burns JP. Arthroscopic Iliac Crest Bone Grafting to the Anterior Glenoid. Arthrosc Tech. 2016;5(4):e907e912. doi:10.1016/j.eats.2016.04.011. Giannakos A, Vezeridis PS, Schwartz DG, Jany R, Lafosse  L. Allarthroscopic revision Eden-Hybinette procedure for failed instability surgery: technique and preliminary results. Arthroscopy. 2017;33(1):39-48. doi:10.1016/j.arthro.2016.05.021. Kalogrianitis S, Tsouparopoulos  V. Arthroscopic iliac crest bone block for reconstruction of the glenoid: a fixation technique using an adjustable-length loop cortical suspensory fixation device. Arthrosc Tech. 2016;5(6):e1197-e1202. doi:10.1016/j.eats.2016.07.007. Kraus N, Amphansap T, Gerhardt C, Scheibel M. Arthroscopic anatomic glenoid reconstruction using an autologous iliac crest bone grafting technique. J Shoulder Elbow Surg. 2014;23(11):1700-1708. doi:10.1016/j.jse.2014.03.004. Mascarenhas R, Raleigh E, McRae S, Leiter J, Saltzman B, MacDonald PB. Iliac crest allograft glenoid reconstruction for recurrent anterior shoulder instability in athletes: surgical technique and results. Int J Shoulder Surg. 2014;8(4):127-132. doi:10.4103/0973-6042.145269. Scheibel M, Kraus N, Diederichs G, Haas NP. Arthroscopic reconstruction of chronic anteroinferior glenoid defect using an autologous tricortical iliac crest bone grafting technique. Arch Orthop Trauma Surg. 2008;128(11):1295-1300. doi:10.1007/s00402-007-0509-2. Itoi E, Lee SB, Berglund LJ, Berge LL, An KN. The effect of a glenoid defect on anteroinferior stability of the shoulder after Bankart repair: a cadaveric study. J Bone Joint Surg Am. 2000;82(1):35-46. doi:10.2106/00004623-200001000-00005.

54.

55.

56.

57.

58.

59.

60.

61.

62.

63.

64.

65.

66.

67.

68.

69.

Bigliani LU, Newton PM, Steinmann SP, Connor PM, McLlveen SJ. Glenoid rim lesions associated with recurrent anterior dislocation of the shoulder. Am J Sports Med. 1998;26(1):41-45. doi:10.1177/03635 465980260012301. Mologne TS, Provencher MT, Menzel KA, Vachon TA, Dewing CB. Arthroscopic stabilization in patients with an inverted pear glenoid: results in patients with bone loss of the anterior glenoid. Am J Sports Med. 2007;35(8):1276-1283. doi:10.1177/0363546507300262. Yamamoto N, Itoi E, Abe H, et al. Contact between the glenoid and the humeral head in abduction, external rotation, and horizontal extension: a new concept of glenoid track. J  Shoulder Elbow Surg. 2007;16(5):649-656. doi:10.1016/j.jse.2006.12.012. Shaha JS, Cook JB, Rowles DJ, Bottoni CR, Shaha SH, Tokish JM. Clinical validation of the glenoid track concept in anterior glenohumeral instability. J Bone Joint Surg Am. 2016;98(22):1918-1923. doi:10.2106/JBJS.15.01099. Brox JI, Finnanger AM, Merckoll E, Lereim P. Satisfactory long-term results after Eden-Hybbinette-Alvik operation for recurrent anterior dislocation of the shoulder: 6-20 years’ follow-up of 52 patients. Acta Orthop Scand. 2003;74(2):180-185. doi:10.1080/00016470310013923. Wildner M, Wimmer B, Reichelt  A. Osteoarthritis after the EdenHybbinette-Lange procedure for anterior dislocation of the shoulder. A 15 year follow up. Int Orthop. 1994;18(5):280-283. doi:10.1007/ bf00180226. Zuckerman JD, Matsen FA  III. Complications about the glenohumeral joint related to the use of screws and staples. J Bone Joint Surg Am. 1984;66(2):175-180. Ghodadra N, Gupta A, Romeo AA, et  al. Normalization of glenohumeral articular contact pressures after Latarjet or iliac crest bonegrafting. J Bone Joint Surg Am. 2010;92(6):1478-1489. doi:10.2106/ JBJS.I.00220. Noonan B, Hollister SJ, Sekiya JK, Bedi  A. Comparison of reconstructive procedures for glenoid bone loss associated with recurrent anterior shoulder instability. J Shoulder Elbow Surg. 2014;23(8):11131119. doi:10.1016/j.jse.2013.11.011. Willemot LB, Akbari-Shandiz M, Sanchez-Sotelo J, Zhao K, Verborgt  O. Restoration of articular geometry using current graft options for large glenoid bone defects in anterior shoulder instability. Arthroscopy. 2017;33(9):1661-1669. doi:10.1016/j. arthro.2017.04.002. Lunn JV, Castellano-Rosa J, Walch G. Recurrent anterior dislocation after the Latarjet procedure: outcome after revision using a modified Eden-Hybinette operation. J  Shoulder Elbow Surg. 2008;17(5):744750. doi:10.1016/j.jse.2008.03.002. Steffen V, Hertel R. Rim reconstruction with autogenous iliac crest for anterior glenoid deficiency: forty-three instability cases followed for 5-19 years. J Shoulder Elbow Surg. 2013;22(4):550-559. doi:10.1016/j. jse.2012.05.038. Provencher MT, Frank RM, Golijanin P, et  al. Distal tibia allograft glenoid reconstruction in recurrent anterior shoulder instability: clinical and radiographic outcomes. Arthroscopy. 2017;33(5):891897. doi:10.1016/j.arthro.2016.09.029. Di Giacomo G, Costantini A, de Gasperis N, et  al. Coracoid graft osteolysis after the Latarjet procedure for anteroinferior shoulder instability: a computed tomography scan study of twenty-six patients. J Shoulder Elbow Surg. 2011;20(6):989-995. doi:10.1016/j. jse.2010.11.016. Dehaan A, Munch J, Durkan M, Yoo J, Crawford D. Reconstruction of a bony Bankart lesion: best fit based on radius of curvature. Am J Sports Med. 2013;41(5):1140-1145. doi:10.1177/0363546513478578. Rios D, Jansson KS, Martetschläger F, Boykin RE, Millett PJ, Wijdicks CA. Normal curvature of glenoid surface can be restored when performing an inlay osteochondral allograft: an anatomic computed tomographic comparison. Knee Surg Sports Traumatol Arthrosc. 2014;22(2):442-447. doi:10.1007/s00167-013-2391-5.

Glenoid Bone Loss Augmentation Variations 70.

71.

72.

73.

74.

75.

Bhatia S, Van Thiel GS, Gupta D, et al. Comparison of glenohumeral contact pressures and contact areas after glenoid reconstruction with Latarjet or distal tibial osteochondral allografts. Am J Sports Med. 2013;41(8):1900-1908. doi:10.1177/0363546513490646. Bhatia S, Ghodadra NS, Romeo AA, et al. The importance of the recognition and treatment of glenoid bone loss in an athletic population. Sports Health. 2011;3(5):435-440. doi:10.1177/1941738111414126. Provencher MT, Ghodadra N, LeClere L, Solomon DJ, Romeo AA. Anatomic osteochondral glenoid reconstruction for recurrent glenohumeral instability with glenoid deficiency using a distal tibia allograft. Arthroscopy. 2009;25(4):446-452. doi:10.1016/j. arthro.2008.10.017. Frank RM, Romeo AA, Richardson C, et  al. Outcomes of Latarjet versus distal tibia allograft for anterior shoulder instability repair: a matched cohort analysis. Am J Sports Med. 2018;46(5):1030-1038. doi:10.1177/0363546517744203. Tokish JM, Fitzpatrick K, Cook JB, Mallon WJ. Arthroscopic distal clavicular autograft for treating shoulder instability with glenoid bone loss. Arthrosc Tech. 2014;3(4):e475-e481. doi:10.1016/j. eats.2014.05.006. Novak PJ, Bach BR Jr, Romeo AA, Hager CA. Surgical resection of the distal clavicle. J  Shoulder Elbow Surg. 1995;4(1 pt 1):35-40. doi:10.1016/s1058-2746(10)80006-0.

76.

77.

78.

79.

80.

127

Harris RI, Vu DH, Sonnabend DH, Goldberg JA, Walsh WR. Anatomic variance of the coracoclavicular ligaments. J Shoulder Elbow Surg. 2001;10(6):585-588. doi:10.1067/mse.2001.118480. Delaney RA, Freehill MT, Janfaza DR, Vlassakov KV, Higgins LD, Warner JJ. 2014 Neer Award Paper: neuromonitoring the Latarjet procedure. J Shoulder Elbow Surg. 2014;23(10):1473-1480. doi:10.1016/j.jse.2014.04.003. Choate SW, Kwapisz A, Tokish JM. Distal clavicle autograft—I would like to use my own osteochondral graft please. Ann Joint. 2017;2(77). doi:10.21037/aoj.2017.10.12. Kwapisz A, Fitzpatrick K, Cook JB, Athwal GS, Tokish JM. Distal clavicular osteochondral autograft augmentation for glenoid bone loss: a comparison of radius of restoration versus Latarjet graft. Am J Sports Med. 2018;46(5):1046-1052. doi:10.1177/0363546517749915. Petersen SA, Bernard JA, Langdale ER, Belkoff SM. Autologous distal clavicle versus autologous coracoid bone grafts for restoration of anterior-inferior glenoid bone loss: a biomechanical comparison. J Shoulder Elbow Surg. 2016;25(6):960-966. doi:10.1016/j. jse.2015.10.023.

12 Arthroscopic Latarjet Laurent LaFosse, MD; Christian Moody, MD; and Leonard Achenbach, MD

Shoulder anterior instability may present with dif ferent symptoms: shoulder dislocation, subluxation, or simple pain. As soon as the shoulder dislocates, the inferior glenohumeral ligament (IGHL) can be damaged along with labral detachment and a potential bony lesion. These problems when combined commonly lead to recurrent instability. In cases of isolated labrum detachment, arthroscopic reattachment provides excellent results, but in our experience as soon as the IGHL is involved during a dislocation, long-term results of soft-tissue reattachment are poor. Management of shoulder instability in young collision athletes with soft tissue stability alone remains problematic with high revision and recurrent dislocation rates.1,2 A variety of open and arthroscopic treatment methods exist and are described in this textbook. Our preferred technique not only for athletes but for patients with recurrent anterior instability, instability secondary to any bony Bankart lesions, off-track lesions including bipolar lesions, and those with humeral avulsions of the glenohumeral ligament (HAGL) is that of an arthroscopic Latarjet. The arthroscopic Latarjet has several advantages over the traditional open Latarjet procedure described in 1954.3 These advantages include better visualization of the entire joint, which allows for optimum graft placement as well as management of concomitant lesions of the posterior and superior labrum. In addition, direct visualization of the axillary nerve and surrounding hypervascular tissue allows for reducing the change of a neurovascular injury.4,5 The Latarjet procedure is successful in stabilizing the shoulder through several key mechanisms. First, the coracoid transfer provides static stability by increasing the glenoid surface area, which results in a greater articular arc, thus preventing a Hill-Sachs lesion from engaging the anterior rim.

Second, the conjoint tendon serves as a dynamic reinforcement of the inferior capsule providing a “hammock” effect, particularly when the shoulder is in its most vulnerable position of abduction, external rotation. Last, the intersection between the split subscapularis tendon and the conjoint tendon provides further dynamic tension to the inferior portion of the subscapularis tendon, again with the most tension during the position of highest vulnerability.4,5 Further details describing all pathology and mechanisms of stabilization will be described in the following text. Our technique has evolved since we first published on the arthroscopic Latarjet in 2007.4 It is impor tant to note that this procedure should be reserved for surgeons with extensive arthroscopy expertise. We recommend becoming familiar with the anterior shoulder compartment, including the subcoracoid space when possible during routine arthroscopic procedures. Then, in a laboratory setting use a cadaver to perform the full procedure for the first time, and multiple times if possible. Finally, asking a local mentor to assist in the live setting can provide tips and troubleshooting assistance that is second to none.

THE ANTERIOR SHOULDER INSTABILITY LESION “Anterior instability of the shoulder” is commonly used to include all symptoms of pathological anteroinferior displacement of the glenohumeral joint. However, with our expanded knowledge of the shoulder, it is critical to be more precise. One must describe the direct correlation between the severity of the symptoms and the location of the lesion.

- 129 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 129-137). © 2021 SLACK Incorporated.

130

Chapter 12

According the severity of the symptoms, 3 major groups of patients have been defined by the French Arthroscopic Society: 1. Group I (56%): Dislocation (at least one full dislocation that needs a reduction by a person other than the patient) 2. Group II (26%): Subluxation (shoulder never fully dislocates, but the patient has a sensation of shoulder instability confirmed by physical exam) 3. Group III (18%): Unstable painful shoulder (the patient complains of shoulder pain and the surgeon determines the origin is an issue of instability such as labral detachment) Further subdifferentiation includes the following: Soft-tissue lesions range from a simple Bankart lesion to more complicated capsulolabral lesions like the anterior labroligamentous periosteal sleeve avulsion, complicated ruptures of the labrum (Detrisac II and IV), or humeral avulsion of HAGLs. In the most frequent cases of instability with dislocation (group I) concerning only soft tissues, the humeral displacement is anterior, medial, and inferior. The IGHL is always involved and most of the time, the soft tissue is badly damaged (ligament stretch or tear; humeral detachment: HAGL lesion). In addition to ligament damage, the labral ring is frequently torn, thus causing a loss of concentric forces of the intact ring that are critical to the healing process. Associated bone lesions are created on both the humeral and glenoid side at the moment of the dislocation. These lesions are the Hill-Sachs lesion, at the level of the posterior humerus, and the Bankart/glenoid rim fractures with permanent loss of glenoid bone, which can further impair the remaining stability. Four of 5 patients who have anterior shoulder instability have a “bipolar lesion,” which is defined as having both a Hill-Sachs and glenoid bone lesion.6 Itoi described the contact zone between the glenoid and humeral head as the “glenoid track.” Based on the location of the HillSachs lesion, it will either engage the glenoid and dislocate (off-track lesion) or avoid engagement and remain reduced (on-track lesion).6

WHY A CORACOID TRANSFER? Operative Bankart repair, both open and arthroscopic, has demonstrated excellent results when used for isolated soft tissue Bankart lesions. However, in cases of unrecognized soft-tissue injury, for example, humeral avulsion of HAGL lesions, complex labral disruptions, irreparable soft-tissue damage, and in cases of bony deficiency, this technique may not be sufficient to stabilize the shoulder. For young patients (age < 20  years), overhead athletes, and those involved in contact sports, soft-tissue repair alone should be avoided. In 2006, Boileau highlighted several reasons for failure of the Bankart procedure for anterior instability.1 The most impor tant risk factors identified were bone loss on the glenoid or humeral sides and inferior ligament hyperlaxity. This

is often a result of stretching from the initial dislocation. A combination of these abnormalities can result in up to a 75% recurrence of instability after soft-tissue repair.1,7 It seems clear that a simple Bankart repair, which reduces the labrum back on to the glenoid, cannot be expected to return soft-tissue stability to the shoulder when the HAGLs are torn or attenuated. Further to this point, where there is glenoid bone loss or an engaging Hill-Sachs lesion, a softtissue repair does not lengthen the glenoid articular arc, which is necessary to prevent future engagement and recurrent symptoms. In these situations another approach must be adopted. The initial description of Bristow procedure was a simple translation into the subscapularis muscle of the conjoint tendon by sawing the bony chip of the distal part of the coracoid. The modified Bristow by Helfet8 uses a larger fragment of the coracoid tip which is fixed to the anterior glenoid neck with a single screw..

Latarjet The Latarjet procedure is fixing half of the coracoid in a flat position using the advantage of congruence between the curvature of the anterior glenoid and the coracoid fragment. A larger-size bone block allows for double screw fixation with rotational stability and better compression as well as restoration of the area of glenoid bone loss. The ligamentoplasty effect is created by crossing the conjoint tendon over the inferior part of the subscapularis tendon, which is slightly reoriented in an inferior and posterior direction.4 This creates a dynamic tension applied to the inferior capsule and subscapularis especially in external rotation and therefore reinforces the anterior restraint. By augmenting the glenoid bony contour, engagement of a Hill-Sachs lesion is prevented. At present, the subscapularis muscle is split horizontally between the upper two-thirds and lower one-third and not superiorly detached with an L-like incision as described initially.

Autologous Bone and Iliac Crest Grafting Alternatives such as autologous bone or iliac crest grafting have been routinely performed using open techniques with success and are indicated as a salvage surgery in cases of hardware failure, recurrent dislocation, or nonunion.

Isolated Transfer of the Conjoint Tendon The isolated transfer of the conjoint tendon to the glenoid neck over the subscapularis tendon has been described to replace the sling of the torn HAGLs, but this does not address the inferior ligament weakness and/or glenoid bone loss.

Arthroscopic Latarjet The Latarjet or modified Bristow procedure are successful because they combine a bony procedure with a ligamentoplasty by the conjoint tendon transfer through the subscapularis muscle. Biomechanical studies from Itoi proved that bony reconstruction restores 100% of a native glenoid, and that association of bony reconstruction and conjoint tendon fixation provides 130% stability of a native shoulder. Capsule reconstruction on top of Latarjet does not affect the result.9

WHY AN ARTHROSCOPIC LATARJET? Advantages over open Latarjet include the following: 1. Placement of the bone graft is more accurate under arthroscopic control. Several views can be afforded by the arthroscopic technique that not only improve graft placement but will reduce the chances of overhang and impingement. 2. Unlike open surgery, arthroscopic surgery allows for the treatment of concomitant pathologies such as superior labrum anterior and posterior tears and posterior labral lesions. 3. Double instabilities can be treated during the same surgical procedure using both anterior and posterior bone blocks when employing arthroscopic methods. This is not possible through a single open approach. 4. Even though the strength of the bone block fixation allows early mobilization, the risk of adhesions and shoulder stiffness is higher with an open technique over arthroscopy. 5. If during an intended Bankart repair the tissue is determined to not be repairable, then an arthroscopic Latarjet offers an alternative solution to traditional open surgery and potentially having to reposition the patient. 6. As in other joints, arthroscopy offers the advantages of less postoperative pain, earlier mobility, quicker rehabilitation, and faster return to sport. 7. Improved cosmetic result for the patients with an arthroscopic technique. Drawbacks of arthroscopic Latarjet include the following: 1. There is a high level of difficulty during many steps of the procedure.

131

INDICATIONS FOR ARTHROSCOPIC LATARJET Once a detailed history, clinical examination and radiological investigations are performed, an intra operative assessment of the ligamentous stability can determine the appropriate operation. The following scenarios will provide examples of dif ferent surgical indications.

Glenoid Bone Loss Many authors have reported failure of soft-tissue repair due to glenoid bone loss.10 The mechanical consequences of the anteroinferior glenoid erosion has been proven by biomechanics studies and assessed by dif ferent x-ray, computed tomography (CT) scan techniques, and arthroscopic visualization (inverted pear).11 In some cases, the bony fragment can be replaced and arthroscopically repaired by anchors and sutures. However, this is always smaller than the original glenoid and is not as strong and supportive as a bony block. This is a common cause for recurrent instability and can manifest as a bony Bankart lesion or a true fracture of the anterior or inferior glenoid rim. Standard anteroposterior x-rays may show a fracture or a more subtle loss of contour of the anteroinferior glenoid rim. A decrease in the apparent density of the inferior glenoid line often signifies an erosion of the glenoid rim between 3 and 6 o’clock. An axillary view or better, a Bernageau view may show flattening of this area of the glenoid when bone loss has occurred.12 In summary, assessment of the degree of bone loss can be made through a variety of methods including plain radiographs, specific MRI sequences, CT scan with 3D volume rendering, arthroscopic assessment and measurement.13 CT reconstructions provide more robust static measurements than those afforded by the arthroscopic view. Arthroscopically, the distance from the glenoid rim as measured from the bare spot can assist the surgeon in identifying an inverted-pear glenoid, confirming substantial bone loss and the likely failure of an isolated soft-tissue repair. Even when the bony fragment is present, replacing it is not always sufficient to restore the bony glenoid articular arc because of the difficulties in the healing of this necrotic bone. In these cases a bone reconstruction as performed by the Latarjet procedure should be considered.

2. There are risks linked to swelling. 3. Potential malpositioning of the graft and of the screws may be caused by the difficulties of scapula positioning. 4. There are neurologic and vascular risks. 5. Arthroscopic Latarjet is not possible if operating conditions are not optimum, which is highly dependent on a perfect fit with the anesthesiology team. It is impor tant to keep in mind that conversion from arthroscopic to open Latarjet is possible at any stage.

Humeral Bone Loss The location and the depth of the Hill-Sachs lesion vary with each case: sometimes small and superficial, sometimes deep, extended, and exceptionally, double. Its location and depth is responsible for persistent instability, even in cases of well-done Bankart repair. Its precise assessment is difficult but can be approached by simple x-ray in internal rotation and 2-dimensional or 3-dimensional CT scan. Remplissage of the infraspinatus tendon has been described with satisfactory results but external rotation is limited and long-term results have not been reported.

132

Chapter 12 but our results with this technique have been disappointing because of the stiffness after repair. Furthermore, in patients with multiple dislocations, the intrinsic structure of the HAGLs is usually deranged, although this may not be evident macroscopically. Simply repairing this damaged tissue to the glenoid does not restore stability to the shoulder. This has been likened to rehanging a baggy or incompetent hammock. A final situation is that of the labral tear, often in association with an HAGL lesion. In this situation, the ring of the labrum is disrupted and the strength of a repair will be unable to match that of an intact labral ring. In these situations, there is a need for a ligamentoplasty and accompanying bone block. A complete dislocation, according to our experience, as it is correlated to an inferior ligament detachment, is a bad prognostic factor for ligament injury. Multiple complete dislocations causes even further damage to the soft-tissues structures.

Figure 12-1. Portals.

Revision of Bankart Repair

The location and size of the Hill-Sachs lesion determines whether the articular arc is reduced and whether this will engage on the glenoid. A dynamic arthroscopy with the shoulder in abduction and external rotation will demonstrate whether the lesion is engaging even within an athletic overhead range of movement. A bone block procedure here will increase the arc of the anterior glenoid, thereby increasing the degree of external rotation that can be achieved before the Hill-Sachs lesion approaches the glenoid rim. We believe that by enlarging the glenoid articular arc with a bone graft, there is no increased joint contact pressure during external rotation. A remplissage, however, can lead to a decrease in external rotation and may give rise to increased contact forces on the articular cartilage during external rotation.

After an open or arthroscopic Bankart repair, success is often measured by the absence of recurrent dislocations. In some cases, the joint is not sufficiently stabilized but it does allow function for a more sedentary lifestyle without overt symptoms of instability. This can in part explain the excellent results seen in series with short follow-ups. After 5 to 7  years, we find this par ticular group of patients can go on to develop instability and/or arthritis. In these cases the initial operation was considered successful although the pathological lesion was never truly corrected and the glenoid subsequently becomes increasingly eroded. Again, these patients can be successfully managed with a bone block ligamentoplasty.

Combination of Glenoid and Humeral Bone Loss

There are some patients who participate in high-risk sports (climbing, football, rugby) or work (carpentry) or have a high risk of recurrence due to the intensity and action or their activity (throwers). The Latarjet procedure provides a strong stabilization mechanism and fast recovery time for these individuals.

As stated previously, the “bipolar lesion” is responsible for many cases of recurrent instability. This combination of 2 lesions usually occurs with varying degrees of severity for each individual lesion. These can be assessed before the procedure by exam, plain radiographs, and CT scan. It is critical to look for both lesions during the arthroscopy exploration under dynamic visualization.

Irreparable Soft-Tissue Damage/ Complex Soft-Tissue Injury The HAGL lesion is sometime possible to diagnose by magnetic resonance imaging or CT arthrography, but in most cases it is discovered during the arthroscopy. Dif ferent techniques of humeral reattachment by suture and anchor are possible depending on the location of the detachment,

Specific Patients

TECHNIQUE FOR ARTHROSCOPIC LATARJET The arthroscopic Latarjet technique can be divided into 5 steps. These include joint evaluation and exposure, harvesting of the coracoid process (CP), subscapularis split, coracoid transfer, and finally fixation of the CP. Patient positioning is beach chair, and the use of an armholder helps to manage the arm and with scapula positioning. We use 7 portals (Figure 12-1): 1. Portal A: standard posterior 2. E: Anterolateral to access the rotator interval (RI)

Arthroscopic Latarjet 3. D: Anterolateral at the level of the anterolateral corner of the acromion 4. I: Aligned with the CP above the axillary fold 5. J: Between the I and D portal, parallel to the subscapularis fibers 6. M: The most medial and anterior portal through the pectoralis major aligned with the glenoid surface 7. H: Anterosuperior portal above the coracoid

Step 1: Joint Evaluation and Exposure The intra-articular approach commences through the standard A posterior portal. By means of the anterolateral E portal—which is established using an outside-in technique—a probe is introduced through the RI. With the probe, a diagnostic arthroscopic exam including a dynamic stability assessment is performed, specifically looking for bony glenoid lesions, humeral defects, and soft-tissue lesions, such as a HAGL. Opening of the RI exposes both sides of the subscapularis and preparation of the glenoid neck. The glenohumeral joint is opened at the upper border of subscapularis and the anteroinferior labrum and medial glenohumeral ligament are detached between 2 and 5 o’clock to expose the glenoid neck. This can be performed using electrocautery. The intended graft site is exposed and the capsule between the glenoid neck and subscapularis is split. Remove the pathological anterior capsule and bony Bankart, if necessary. To provide a healthy base for graft healing, the glenoid neck is abraded with the burr. Both sides of the subscapularis tendon are then exposed, with par ticular attention to the articular side of subscapularis. These releases are necessary to facilitate the transfer of the coracoid graft. If case of any further intraarticular pathology, it should be addressed at this stage, for example, a posterior labral repair. The intra-articular preparation is now completed. Coracoid soft-tissue preparation includes the following: A long spinal needle is inserted parallel to the upper part of the subscapularis tendon to ensure best positioning of the D portal. The instruments are then used in this D portal. Remove the end of the bursa under the coracoid and expose the conjoint tendons down to the level of the pectoralis major. Behind the conjoint tendon exists a medial tissue barrier that separates the brachial plexus from the subcoracoid bursa. This is gently dissected to reveal the single nerves, such as the axillary nerve. It is impor tant to visualize this nerve and appreciate its location when it comes to splitting the subscapularis muscle and placing the graft. Any further soft-tissue attachments to the coracoid in the bursa are released to free the coracoid for its later transfer. The coracoacromial ligament should be located at its coracoid insertion site and subsequently detached. Attention must be paid to coagulate the terminal branch of the acromiothoracic artery. The anterior aspect of the conjoint tendon is liberated from the deltoid fascia. The inferior limit of

133

this release should be the pectoralis major tendon. Splitting the deltoid fascia anterior of the CP facilitates visualization. The scope is now moved from the posterior A portal to the lateral D portal. Split the adhesions between the conjoint tendons and the pectoralis minor (PM). The PM tendon on the medial border of the coracoid is now released, taking care to keep the electrocautery on bone during this step. Finalize the preparation of the CP by completely debriding its superior part from any soft tissue. With this dissection completed and having an awareness of the position of the nerves, we can proceed with the knowledge that every thing lateral to the conjoint tendon is safe.

Step 2: Harvesting the Coracoid To prepare the anterior portals, establish the I, J, and M portals. Using an outside-in technique, the I portal is placed above the axillary fold, aligned with the CP. Manipulation of the needle used to perform this portal should anticipate visualizing the 4 sides of the coracoid when the scope is introduced through this I portal. The J  portal is placed midway on an arc between the I and the D portals. It gives a more head-on view of the coracoid, whereas the D portal gives a better lateral view. Two perpendicular views are necessary to ensure optimum coracoid preparation. The M portal is the most medial. It should be aligned with the glenoid surface and should provide for management of the coracoid fixation parallel to the glenoid. Despite its very medial location, this portal is not dangerous as long as the pectoralis minor is not penetrated. Once this muscle is detached, the plexus is in line with the M portal and close attention should be paid with use of this portal. PM detachment includes the following: once the scope is introduced in the I portal, the electrocautery is introduced into the M portal and the upper and lower part of the PM are located. It is difficult but crucial to separate the PM from the conjoint tendon. The electrocautery should remain superficial and the split should be managed with great care until the musculocutaneous nerve is located. The PM is then totally detached from the CP. The plexus can be visualized at that stage, but it is not necessary to dissect the plexus. At this point the scope is in the J portal and the electrocautery is in the I portal. To define the H portal, place an arthroscopic switching stick in the D portal and elevate the space above the coracoid (like using a retractor in open surgery). We like to place the other end through the plastic fluid collection bag on the drapes to keep this “retractor” in the same position as long as it is needed there. Locate the coracoid’s midpoint again with a long spine needle perpendicular to the axis. This will serve to guide the position of the coracoid drill guide. Once satisfied, make a superior incision for the H portal. To drill the coracoid and inserting the anterior top hat, place the 15-degree coracoid drill guide flush on top of the CP. It is impor tant to regularly change the viewing angle of

134

Chapter 12

Figure 12-3. Coracoid osteotomy.

Figure 12-2. Coracoid guide.

Figure 12-4. Subscapularis split.

the scope by rotation to ensure mediolateral alignment of the now inserted coracoid drill guide. Place the guide over the junction of the lateral two-thirds and medial one-third of the coracoid. Use the 7-mm distance device—included in the new drill guides (DePuy-Synthes)—to ensure proper alignment to the lateral aspect of the CP (Figure 12-2). Drill the α hole (inferior and distal) with a K-wire. It is impor tant while doing this to visualize under the coracoid to verify that the direction of the K-wires are perpendicular to the superior surface of the coracoid and to avoid penetrating too deeply into the brachial plexus. Locate the final position of the beta hole relative to the axis. Rotationally align the coracoid drill guide and then drill the β (proximal) K-wire. Remove the drill guide, leave the K-wires, and check the wire positions. Overdrill both holes with the coracoid step drill. To ensure drilling is bicortical, place a clamp at the end of the K-wire while drilling. When the clamp (and thus the wire) begin rotating, the second cortex has been passed. Remove the clamp and the drill but keep the K-wires.

The drill holes are now tapped to prepare for the top hat and glenoid screws. The posterior β K-wire is removed. The anterior top hat is now inserted in the anterior α drill hole and the K-wire is removed. Once the coracoid is prepared we are now ready to make the coracoid osteotomy through the H portal. First, the osteotome is placed on the medial most proximal aspect just anterior to the coracoclavicular ligaments. Here, osteotomy of the medial quarter of the coracoid is performed. The same is performed on the lateral aspect. Then, in a third step, a controlled complete osteotomy is performed by placing the osteotome in the line connecting the 2 previous osteotomies (Figure 12-3). At this stage, there is often fascia that maintains the coracoid superiorly. It is necessary to release this fascia, paying attention to preserve the axillary nerve just behind.

Step 3: Subscapularis Split Determine the level of the subscapularis split. Remove any remaining bursa at the anterior face of the tendon and muscle by introducing the shaver in the J portal. Hemostasis by the electrocautery introduced in the M portal is managed at the same time. Locate the 3 sisters (1 artery and 2 veins) and the axillary nerve running along the muscle to avoid neurovascular injury. Determine the upper two-thirds and lower onethird of the subscapularis muscle-tendon unit. The subscapularis split is shown in Figure 12-4. The arm is placed in external rotation without causing anterior translation of the humeral head. Create the split by using electrocautery. The split is completed down to the glenoid neck in the line of fibers of the subscapularis, extending from the lateral insertion of the subscapularis on the lesser tuberosity, passing medially close to the axillary nerve. Expert tip: Start medially by the axillary nerve, and moving lateral in line with the fibers of the muscle, use a switching stick to elevate the upper edge of the split muscle to provide countertension while moving to the deeper layers of muscle.

Arthroscopic Latarjet

135

Figure 12-5. Coracoid preparation.

A probe is introduced through the A portal and can be used to keep the subscapularis window open.

Step 4: Preparation of Glenoid Bed and Graft Trimming The shoulder is manipulated with the armholder in a slight internal rotation with scapula retropulsion to decrease the subscapularis tension and to facilitate the screw orientation. Use this chance to view the anterior glenoid neck and ensure that the surface is flat and ready to accept the CP graft. Additional bony abrasion with a burr can be performed by introducing the burr in the M portal for this task. Next, insert the 15-degree coracoid process guide (CPG) through the M portal and through the subscapularis split onto the previously prepared anterior glenoid. The guide should be placed from 3 to 5 o’clock and flush with the glenoid. Put the CPG into the correct orientation, with the hole pointing inferiorly. Correct distance of the 2  drill holes to the glenoid surface ensures correct alignment of the coracoid graft with the glenoid surface. Identifying the correct distance of the K-wire drill holes is supported by introducing a 7-mm probe—the same distance as the drill holes on the CP from the lateral border of the CP—through the A portal and locating the correct drill hole insertion distance. Insert a glenoid K-wire through the Alpha portal of the CPG and drill across the glenoid. These wires will emerge through the skin of the posterior shoulder, at which stage a clamp is placed on them. The handle of the cannula must be pushed medially to obtain a minimum angulation between the K-wires and the glenoid surface. Expert tip: Good orientation of the K-wire represents approximately 2 to 3 cm more medial to the A portal. Overdrill the glenoid K-wire with the cannulated glenoid 3.2 drill bicortically from posterior. Remove the drill. Insert the cannulated measurement device from posterior until resistance of the cortex is felt. Remove the K-wire. Visualize and make note of the depth of the glenoid using the measurement device to determine screw lengths for fixation of the CP.

Graft trimming is shown in Figure 12-5. Move the scope to the J portal. Detach the CPG and thread the free CP onto the CPG (M portal). Secure it to the CPG by manually screwing the coracoid positioning cannula into the top hat. The freshly harvested graft is mobilized and all remaining adhesions of the pectoralis minor and the medial fascia are removed. Par ticular attention must be paid to avoid the musculocutaneous nerve while this is performed. The mobile CP usually has a medial spike arising from its base that must be trimmed to permit good bony contact with the glenoid. To stabilize the coracoid while the burr is introduced through the D portal, a K-wire is introduced into the α coracoid screw hole and then into the cannulated measurement device that remains in the glenoid bone. This K-wire will ensure that the coracoid does not move during its preparation and protect the plexus, which is in close proximity. To achieve this, the scope is held by the assistant, and using a 2-handed technique, and the graft is controlled on the cannula with one hand and trimmed with the burr (D-portal) with the other. The graft is now ready for transfer and fixation to the glenoid.

Step 5: Coracoid Transfer and Coracoid Fixation Manipulate the CP on the coracoid positioning cannula to the glenoid neck along the K-wire. This is made easier by elevating the subscapularis split with the switching stick. Pass the graft horizontally through the subscapularis, then turn 90 degrees for its desired position on the glenoid. This position should not be prominent compared to the glenoid surface but flush with the subchondral bone. Once the graft is placed on the glenoid neck in the desired position, then fixation with screws is undertaken. As a last step, one screw is passed into each predrilled hole. The length of the screws was previously determined by the measurement device. The screws are inserted and alternately tightened to reduce the graft using compression onto the glenoid neck. The K-wires can then be removed posteriorly.

136

Chapter 12

Figure 12-6. Coracoid fixation, final view.

Figure 12-7. Postoperative 3D CT scan.

Final checks are performed by revisiting the graft and screw position graft through the D and J portals (Figure 12-6) and any final trimming can be performed at this stage with the burr. Any prominence of the graft thereafter can be burred flush to the glenoid. After skin closure, the patient is placed on a slight resting abduction pillow. Postoperative x-rays should confirm that the graft is properly fixed. Only 3-dimensional CT can accurately assess the graft positioning (Figure  12-7). We usually follow-up with the patient at 6 weeks and 3 months postoperatively.

Recurrent instability is uncommon but is a difficult problem to manage; however, arthroscopic revision bone grafting with an iliac crest graft (Eden-Hybbinette) has resulted in good outcomes with restored stability.14 During this revision operation, care should be taken because of its proximity to the neurovascular structures of the upper limb.

MANAGEMENT OF COMPLICATIONS Perioperative complications are essentially coracoid breakage and neurovascular injury. When encountering excessive arthroscopic difficulties (uncontrolled bleeding, excessive swelling, difficulties for screw positioning) these conditions should lead to an open conversion to perform the best possible Latarjet. Early postoperative complications are extremely rare, but it is impor tant to control and monitor swelling. Hematomas, though rare, need to be closely watched to detect any sign of possible vascular injury. Graft nonunion occurs rarely, and this complication has decreased with the use of the top hat washer. The top hat allows greater compression to be applied to the graft. When compression is accomplished, successful union usually occurs within 6 weeks. Longer-term graft resorption, however, has been a more common problem, leading to uncovering of the screw heads anteriorly. This has resulted in pain and tendon impingement in some patients that later resolved with arthroscopic removal of the screws.

REHABILITATION AND RETURN-TO-PLAY CONSIDERATIONS The initial strength of the bone fixation with 2 screws allows for early rehabilitation. Postoperative immobilization will depend on postoperative pain tolerance. Patients remain in a sling until they feel pain free. The sling can be removed at a maximum of 2 weeks and free passive and active assisted mobilization is initiated. This management protocol has to be adapted to the profile of the patient and possible additional intraoperative procedures, such as superior labrum anterior and posterior or posterior Bankart repair. Rehabilitation should gradually progress from closed- to open-chain exercises. Open-chain exercises should progress from basic rotator cuff training to full throwing capacity, focusing on internal and external rotational strength and explosive capacity. Scapular rehabilitation and kinetic chain exercises are obligatory. For high-risk (throwing) and collision sports, we recommend patients not resume these activities before 3 months. For throwers, special attention should be given to the eccentric strength of the external rotators, being the most impor tant decelerator mechanism for the glenohumeral joint during throwing. The Latarjet technique is thus beneficial for throwers as early external strength training can be initiated.

Arthroscopic Latarjet

RESULTS During a symposium at the French Arthroscopic Society meeting in December 2015, we analyzed a multicentric study of open and arthroscopic Latarjet performed by the 10 members of the symposium. We prospectively analyzed and compared complications, clinical and radiological results, positioning, and evolution of the graft by postoperative CT scans on a series of 390 patients. No significant difference was found between open and arthroscopic Latarjet. Both techniques provide excellent and good results with low complication rates. We also evaluated perioperative arthroscopic difficulties and found that the highest difficulties involved visualization, subscapularis split, and screw positioning. Complication rates in open and arthroscopic Latarjet range from 5%15 to 30%.16 In the largest arthroscopic Latarjet series, 1555 patients were evaluated retrospectively and found to have a 4.2% overall complication rate and 0.2% neurologic complication rate.17

CONCLUSION Anterior shoulder instability is a common problem facing practicing shoulder surgeons for which the operative treatment options have expanded considerably in the past 20 years. Arthroscopy has led to the improved diagnosis of previously unrecognized soft-tissue lesions underlying many cases of instability. In combination with radiological investigations, arthroscopy has also improved the awareness of bony lesions of both the glenoid and humeral head and their contribution to shoulder instability. The arthroscopic Latarjet technique is our preferred treatment option, especially for lesions with significant bone loss and for athletes involved in contact sports or throwing. The ability of a surgeon to visualize the shoulder from dif ferent angles via various portals is crucial to the outcome of the surgery. We strongly recommend starting with the open technique and once it becomes reliable, to proceed arthroscopically and convert to the open technique if necessary. This allows progressively improving the skills of arthroscopic steps and facing difficulties with reliable solutions.

REFERENCES 1.

Boileau P, Villalba M, Héry JY, Balg F, Ahrens P, Neyton L. Risk factors for recurrence of shoulder instability after arthroscopic Bankart repair. J  Bone Joint Surg Am. 2006;88(8):1755-1763. doi:10.2106/ JBJS.E.00817.

2.

3. 4.

5. 6. 7.

8.

9. 10.

11.

12.

13.

14.

15.

16.

17.

137

Walch G, Boileau P, Levigne C, Mandrino A, Neyret P, Donell  S. Arthroscopic stabilization for recurrent anterior shoulder dislocation: results of 59 cases. Arthroscopy. 1995;11(2):173-179. doi:10.1016/0749-8063(95)90063-2. Latarjet  M. Treatment of recurrent dislocation of the shoulder [article in French]. Lyon Chir. 1954;49(8):994-997. Lafosse L, Lejeune E, Bouchard A, Kakuda C, Gobezie R, Kochhar  T. The arthroscopic Latarjet procedure for the treatment of anterior shoulder instability. Arthroscopy. 2007;23(11)1242.e1-e5. doi:10.1016/j.arthro.2007.06.008. Ravenscroft M, Odak S. Arthroscopic Latarjet: tips for success. Oper Tech Sports Med. 2019;27(2):69-76. doi:10.1053/j.otsm.2019.03.004. Itoi E. ‘On-track’ and ‘off-track’ shoulder lesions. EFORT Open Rev. 2017;2(8):343-351. doi:10.1302/2058-5241.2.170007. Gill TJ, Micheli LJ, Gebhard F, Binder C. Bankart repair for anterior instability of the shoulder. Long-term outcome. J Bone Joint Surg Am. 1997;79(6);850-857. doi:10.2106/00004623-199706000-00008. Griesser MJ, Harris JD, McCoy BW, et  al. Complications and reoperations after Bristow- Latarjet shoulder stabilization: a systematic review. J Shoulder Elbow Surg. 2013;22(2):286-292. doi:10.1016/j. jse.2012.09.009. Helfet AJ. Coracoid transplantation for recurring dislocation of the shoulder. J Bone Joint Surg Br. 1958;40-B(2):198-202. Yamamoto N, Muraki T, Sperling JW, et  al. Stabilizing mechanism in bone grafting of a large glenoid defect. J Bone Joint Surg Am. 2010;92(1):2059-2066. doi:10.2106/JBJS.I.00261. Burkhart S, De Beer J, Tehrany A, Parten PM. Quantifying glenoid bone loss arthroscopically in shoulder instability. Arthroscopy. 2002;18(5):488-491. doi:10.1053/jars.2002.32212. Burkhart S, De Beer J. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;88(8):677-694. doi:10.1053/jars.2000.17715. Wellmann M, Petersen W, Zantop T, et al. Open shoulder repair of osseous glenoid defects: biomechanical effectiveness of the Latarjet procedure versus a contoured structural bone graft. Am J Sports Med. 2009;37(1):87-94. doi:10.1177/0363546508326714. Bernageau J, Patte D, Debeyre J, Ferrane J. Value of the glenoid profile in recurrent luxations of the shoulder [article in French]. Rev Chir Orthop Reparatrice Appar Mot. 1976;62(2 suppl):142-147. Giannakos A, Vezeridis PS, Schwartz DG, Jany R, Lafosse  L. Allarthroscopic revision Eden-Hybinette procedure for failed instability surgery: technique and preliminary results. Arthroscopy. 2017;33(1):39-48. doi:10.1016/j.arthro.2016.05.021. Gartsman G, Waggenspack WN Jr, O’Connor DP, Elkousy HA, Edwards TB. Immediate and early complications of the open Latarjet procedure: a retrospective review of a large consecutive case series. J  Shoulder Elbow Surg. 2017;26(1):68-72. doi:10.1016/j. jse.2016.05.029. Lafosse L, Leuzinger J, Brzoska R, et al; French Arthroscopy Society. Complications of arthroscopic Latarjet: a multicenter study of 1555 cases. J Shoulder Elbow Surg. 2017;26(5):e148. doi:0.1016/j. jse.2016.12.007.

13 Hill-Sachs Management Morad Chughtai, MD; Andrew Swiergosz, MD; Linsen T. Samuel, MD, MBA; and Anthony Miniaci, MD

Hill-Sachs lesions refer to bone defects resulting from posterolateral humeral head impaction against the anterior rim of the glenoid in an anterior shoulder dislocation event (Figures  13-1 and 13-2). The management of these in the athlete depends mainly on the size of the lesion and whether it is an engaging one. Although most of these lesions are small and may not necessarily be significant, when surgically addressed this is mostly indirectly performed by addressing instability at the glenoid; for example, a Bankart repair or glenoid reconstruction, which is discussed in another chapter. For the purposes of this chapter, we will specifically discuss surgical management options and techniques for bone defects of the humeral head for optimized return to play in the athlete. Multiple techniques have been described to address symptomatic engaging Hill-Sachs lesions. Historical techniques such as rotational osteotomies are no longer or rarely used, and these techniques are associated with complications and have been largely replaced by more successful techniques.1-5 Open anterior procedures, such as a capsulorrhaphy or east-west plication, are performed to offer some stability by shifting the glenoid track medially and superiorly, which in turn limits external rotation, thereby inhibiting the humeral head defect from engaging.2,3 However, these techniques that do not use bony manipulation or augmentation may not be sufficient in the settings of large humeral head defects. Additionally, range-of-motion loss in the athlete may prevent return to play and possibly cause late arthrosis.6 For the purposes of this chapter, we will discuss the following current surgical options to address humeral head defects in shoulder instability for the athlete: 1) remplissage, 2) humeral head augmentation with autograft or allograft

bone, and 3) prosthetic humeral head augmentation. Other options that are experimental or salvage procedures without enough evidence for the “athlete” that will be briefly discussed are 4) humeroplasty and 5) arthroplasty.

SURGICAL OPTIONS Remplissage Technique Remplissage is a French term that translates to “filling” or “to fill.” In terms of shoulder surgery, it describes filling the humeral head defect with tendon and capsule. By doing this, it converts the defect from intra-articular to extra-articular, thereby preventing the defect from engaging with the anterior glenoid rim, effectively turning the defect into an extraarticular defect with soft-tissue coverage to prevent engagement with the anterior glenoid rim. The procedure was originally reported by Connolly as an open procedure that involved filling the defect with transfer of the infraspinatus tendon in conjunction with a portion of greater tuberosity.7 Eventually, an all-arthroscopic technique was published by Wolf and Pollack,8 who performed a posterior capsulodesis and infraspinatus tenodesis into the humeral head defect in conjunction with standard Bankart repair (Figures  13-3 and 13-4). This is typically recommended when there is less than 25% of anterior glenoid bone loss; larger glenoid loss would require bony glenoid augmentation procedure such as the Bristow-Latarjet9 (Figures 13-5 and 13-6). Koo et al10 described using a double-pulley technique in which 2 anchors were used to insert the infraspinatus tendon into the defect,

- 139 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 139-147). © 2021 SLACK Incorporated.

140

Chapter 13

Figure 13-1. Hill-Sachs defect. Figure 13-2. Hill-Sachs defect.

Figure 13-3. Anterior glenoid bone defect (Bankart lesion). Figure 13-4. Hill-Sachs defect (arthroscopic view).

anatomic and tissue-preserving construct (Figure  13-7). Elkinson et al11 studied the biomechanical effect of dif ferent anchor positions when performing remplissage technique in a cadaveric model. They demonstrated that among the various models, medial suture passage through the infraspinatus muscle belly consistently had the greatest mean restriction of range of motion and highest stiffness value.

Outcome

Figure 13-5. Exposure for conjoined tendon and coracoid for BristolLatarjet technique.

thus allowing for sutures to be tied over rather than through the tendon on the muscle belly, which in turn was a more

Although there have been concerns about the nonanatomic nature and probable loss of motion and subsequent revision surgery, clinical outcomes have been relatively successful (Table 13-1). Several reports of the procedure reported a 7% (2 of 24) incidence of recurrent instability with maintained range of motion in all planes at 2-year follow-up.4 Zhu et al12 reported on 49 consecutive patients who underwent remplissage, and at a minimum of 2-year follow-up, they found that patients had a mean increase of 8 degrees of forward elevation and only a mean loss of 1.9 degrees of external rotation. On the basis of rheumatic review of 7 studies (levels II, III,

Hill-Sachs Management

Figure 13-6. Transferred coracoid for Bristol-Latarjet technique.

141

Figure 13-7. Sutures remplissage for Hill-Sachs lesion.

Table 13-1. Examples of Studies Evaluating Remplissage Outcomes REFERENCE

NO. OF APPLICATION PATIENTS OR SHOULDERS 567 patients Examine clinical outcomes and (570 shoulders) biomechanical data supporting use of remplissage procedure.

RESULTS OR FINDINGS

694 patients

Report outcomes after arthroscopic remplissage in patients with anterior shoulder instability and subcritical glenoid bone loss, specifically regarding recurrence of instability, return to sport, and changes in range of motion.

Recurrence rate of instability, 0% to 20%. Change in external rotation in 90 degrees of abduction –11.3 to –1.0 degrees, and change in external rotation with arm fully adducted, –8.0 to +4.5 degrees. Overall rate of return to sport, 56.9% to 100% after remplissage. Arthroscopic remplissage + BR had reduced odds of recurrent instability developing, 0.07 to 0.88, when compared with isolated BR.

Camus 146 patients et al, 201817

Compare BR + remplissage to isolated BR for management of anterior shoulder instability with engaging Hill-Sachs lesion.

Recurrent dislocation occurred in 14.8% (11/74) of isolated BR and in 1.4% (1/72) of BR + remplissage procedure. Difference was significantly dif ferent (RR = 4.52, 95% CI [1.04 to 19.6], P = .04), with approximately 4.5-fold higher risk of redislocation after isolated BR.

Rashid et al, 201618

Assess outcomes and complica- Mean redislocation rate 4.2 ± 3.9% (range, 0% to 15%) and tions of arthroscopic remplissage mean recurrent instability rate 3.2 ± 3.8% (range, 0% to for anterior shoulder instability. 15%). Posterosuperior shoulder pain and stiffness were only complications described.

Lazarides et al, 201915

Liu et al, 201816

207 patients

5.8% of shoulders (33/570) displayed recurrent instability after arthroscopic remplissage. Of shoulders with recurrent instability, 42.4% (14/33) underwent further surgical management. In all studies evaluating preoperative and postoperative patient-reported outcomes, arthroscopic remplissage procedure improved patient-reported outcomes a statistically significant amount postoperatively.

(continued )

142

Chapter 13

Table 13-1. Examples of Studies Evaluating Remplissage Outcomes (continued) REFERENCE

APPLICATION

RESULTS OR FINDINGS

Examine outcomes of remplissage procedure for treatment of anterior glenohumeral instability of shoulder with humeral head defect.

Rowe score of 36.1 preoperatively compared with 87.6 postoperatively (P < .001). In studies with motion measurements, shoulder motion was not affected postoperatively (P > .05); mean forward elevation changed from 165.7 degrees preoperatively to 170.3 degrees postoperatively, and mean external rotation changed from 57.2 to 54.6 degrees. Nine of 167 shoulders experienced episode of recurrent glenohumeral instability (overall recurrence rate, 5.4%).

McCabe 30 patients et al, 201420 (31 shoulders)

Evaluate outcomes of primary vs revision arthroscopic remplissage for shoulder instability with primary bone loss.

Prior instability surgery had failed in 11 patients, and they underwent capsulolabral reconstruction and remplissage (“revision surgery”). Failure rate in revision cases (36%) significantly higher than failure rate in primary surgery cases (0%) (P = .01). Failure resulted from trauma in all 4 patients, and none required further surgery. Mean ASES score for all patients improved from 50 preoperatively to 91 postoperatively (P < .001), with no significant postoperative difference between primary and revision patients (P = .13).

Longo 769 shoulders et al, 201421

Evaluate clinical outcomes, rate of recurrence, complications, and range of movement after remplissage, Weber osteotomy, humeral allograft reconstruction, shoulder arthroplasty, and hemiarthroplasty in patients with anterior or posterior shoulder instability associated with humeral bone loss.

Shoulder arthroplasty procedures had highest rate of postoperative recurrence and lowest scores for postoperative clinical outcomes. Combination of remplissage and Bankart procedures was associated with lower rate of recurrence when compared with BR alone (odds ratio, 0.05; 95% CI, 0.01 to 0.25; P = .001).

Buza et al, 201419

NO. OF PATIENTS OR SHOULDERS 167 patients

Abbreviations: ASES, American Shoulder and Elbow Surgeons; BR, Bankart repair; RR, relative risk.

and IV) of combined arthroscopic remplissage with Bankart repair, the pooled recurrent dislocation was 3.4%. At a mean 26-month follow-up,13 the investigators concluded there was no clinically significant loss of range of motion after remplissage. Furthermore, in 4 of the 7 studies postoperative imaging showed high rates of healing and tissue filling at the infraspinatus tenodesis. Similarly, a magnetic resonance imaging investigation of 11 patients at an average follow-up of 18  months found evidence of tendon incorporation into humeral head defect as early as 8 months.14 Boileau et  al22 reported on 47 patients who underwent arthroscopic remplissage: There was a mean loss (SD) of 8  degrees (± 7  degrees) of external rotation and 9  degrees (± 7 degrees) abduction, which was not functionally limiting. However, of 41 of the 47 patients who participated in athletics before surgery, 37 (90%) returned to sport with 28 (68%) returning to the same level of sport, including overhead sports, at a mean follow-up of 2 years.

Humeral Head Augmentation With Autograft or Allograft Bone Technique Owing to the Hill-Sachs lesion that is created during the dislocation mechanism, techniques have been reported to restore the resulting bone loss with a goal of restoring the articular arc. This has been reportedly used in young patients who meet the surgical indications.23 There are 2 types of allograft reconstructions: size-matched bulk graft and osteochondral plug transfer (see Figures 13-6 and 13-7). Having a size- and side-matched osteoarticular humeral head allograft is essential for optimal recreation of the radius of curvature of the humeral head (± 2  mm) (Figure  13-8). The graft is preferably one that is fresh-frozen and cryopreserved.24 Using a deltopectoral approach and capsulotomy for exposure and inspection allows for addressing abnormalities at the anteroinferior capsulolabral and glenoid complex.

Hill-Sachs Management

143

Figure 13-9. Hill-Sachs allograft reconstruction complete.

Figure 13-8. Proximal humeral allograft size and side matched.

Figure 13-11. Allograft reconstruction for anterior glenoid defect.

Figure 13-10. Allograft in position on Hill-Sachs lesion.

Once this is achieved, the Hill-Sachs lesion is shaped in a chevron fashion and the matching allograft is then cut to fit the site of the humeral head osteotomy. The allograft is then secured with a lag technique using countersunk screws (Figures  13-9 through 13-11). Some techniques have been described in the literature describing osteochondral plug transfer; however, reports are scarce.25,26

Outcome Miniaci et  al23,27 reviewed 18 patients who failed previous attempts at surgical stabilization and underwent this procedure using 18 irradiated allografts . There were no episodes of recurrent instability and 16 of 18 (89%) patients returned to work, with a mean Constant score of 79, as well as decreased Western Ontario Shoulder Instability Index

scores indicating better quality of life with a mean follow-up of 50 months (range, 24 to 96 months). However, complications included radiographic evidence of partial graft collapse in 2 of 18  patients, early evidence of osteoarthritis in 3 patients (marginal osteophytes), and 1 mild subluxation (posterior).23,27 Furthermore, 2 patients required reoperation within 2 years to remove irritable screws. In a another study, Diklic et al28 performed this technique in 13 patients with fresh-frozen femoral head allograft reconstructions for Hill-Sachs lesions with sizes between 25% and 50% of the humeral head. At a mean follow-up of 54 months, the mean Constant score was 87. Twelve of 13 patients were reported to have shoulder stability. However, one patient did develop evidence of osteonecrosis. Overall, more long-term and higher-quality research is needed with allograft reconstructions but may be limited because of the narrow indications and required technical expertise. The technique of osteochondral plug transfer into the base of a humeral defect, although reports are scarce, has produced good results after 12  months of follow-up.25,26 At present, these techniques may not be the best way to optimize an athlete who wants to return to play; however, this may be considered if more conventional measures fail.

144

Chapter 13

Figure 13-13. Hill-Sachs defect filled with hemicap. Figure 13-12. Prosthetic humeral head augmentation.

Prosthetic Humeral Head Augmentation Technique Prosthetic partial surface implants are another option to consider. This technique is accomplished using an implant that is a round, cap-like, cobalt-chrome articular component that serves to fill the Hill-Sachs defect. This technique is similar to that of allograft reconstruction in its advantage of not having the potential complications of disease transmission, nonunion, and graft resorption24,29 (Figure 13-12). However, the use of prosthetic components comes with its own set of potential adverse reactions including hardware loosening and glenoid wear.

Outcomes Table  13-2 demonstrates examples of studies of prosthetic humeral head augmentation. Several early case series described success with this procedure with or without glenoid bone procedures depending on associated glenoid bone loss.23,27,30,31 These series demonstrated no recurrence rates, no hardware complications, and no early evidence of glenoid wear associated with the metal implant.23,27,31 In 2009, Raiss and colleagues32 performed uncemented resurfacing arthroplasty in 10 patients with chronic locked anterior shoulder dislocations with large Hill-Sachs defects. At a mean followup of 24 months, the patients’ Constant score improved from 20 to 61 points preoperatively to postoperatively (P < .007). However, there were 2  reoperations required because one patient had a dislocation and the other developed glenoid erosion. Postoperative imaging evaluation of the humeral head centered on the glenoid in 9 of the 10 cases, and there were no signs of loosening determined. Scalise and colleagues38 recommend sufficient quantity and quality of bone in the epiphyseal portion of the humerus

to allow stable fixation of the implant and suggest caution for its use in patients with severe Hill-Sachs lesions associated with chronic locked dislocations depending on bone quality. However, in terms of athletically active patients and with regards to return to sport, Bessette et  al33 retrospectively reviewed a cohort of 16 patients with recurrent or locked shoulder instability who underwent partial prosthetic humeral head resurfacing for Hill-Sachs lesion (Figure 13-13). At a mean follow-up of 36 months, there were no reported repeat dislocations. In addition, 81% of patients returned to their full preinjury activity level. The cohort’s Penn Shoulder Score improved by 36 points, asserting the potential effectiveness of partial humeral head resurfacing for offering stability in the athletic patient.

Humeroplasty Humeroplasty, or humeral head disimpaction, is another potential option but has very few clinical data to support its use. This technique has been described being performed open, or more frequently percutaneously, and involves using kyphoplasty balloon (Kyphon) or a tamp to disimpact the humeral head lesion. Stachowicz et  al39 performed percutaneous balloon humeroplasties in 18 cadaveric shoulder HillSachs defects and were able to restore 99.3% of the volume of the initial defect. Kazel and colleagues40 also performed humeroplasties with tamps in cadaveric humeri and were able to restore the lesions from −1755 mm3 to −50 mm3.41

Arthroplasty Complete humeral head resurfacing or isolated humeral head arthroplasty (hemiarthroplasty) can be considered for patients with large Hill-Sachs defects greater than 40% of the articular surface.42 In younger or more active patients, or the athlete, hemiarthroplasty or total shoulder arthroplasty should be used

Hill-Sachs Management

145

Table 13-2. Studies Evaluating Outcomes of Partial Resurfacing REFERENCE Bessette et al, 201733

NO. OF PATIENTS 21 patients

Ranalletta et al, 9 patients 201934

Ingoe et al, 201835

RESULTS OR FINDINGS

Evaluate cohort of patients with large Hill-Sachs and reverse Hill-Sachs lesions whose treatment included filling of humeral head defects with HemiCAP implants. Hypothesis: treatment, including use of this implant, would successfully prevent recurrent instability and improve patient-reported outcomes.

Follow-up of cohort of patients treated with partial resurfacing and its success at preventing recurrent instability, with low rate of complications and satisfactory outcomes for motion and activity levels.

Report short-term results and complications of partial humeral head resurfacing (HemiCAP) in patients treated by avascular necrosis.

Patients had significant improvement in functional scores and mobility between preoperative and last follow-up control. Constant score improved from 35 to 79 points (P < .001), ASES score improved from 31 to 76 points (P < .001), forward flexion and external rotation improved from 101 to 150 degrees (P < .001), and from 24 to 45 degrees (P < .001), respectively.

87 global caps, Survival analysis of Global HemiCAP 75 patients resurfacing implanted by multiple surgeons with up to 10 years’ follow-up.

Ramhamadany and Modi, 201636

Visco et al, 201137

APPLICATION

Survival at year 7 with component exchange as end point was 80% (95% CI = 93 to 65) and survival with reoperation for any reason as end point was 62% (95% CI = 82 to 50).

Review of current methods for manage- Addressed current concepts in identifying and ment of recurrent anterior glenohumer- treating such patients using best current evial joint instability with bone loss. dence available. Current literature is limited, and further high-level evidence studies are needed to further investigate benefit of dif ferent surgical strategies, particularly in area of combined humeral and glenoid bone loss. 10 patients

Presented surgical technique for All patients said they were satisfied with results HemiCAP-Arthrosurface system and from surgical treatment. Mean UCLA score: 30 evaluated its results for treating primary points; mean analog pain score: 2 points. and/or secondary shoulder osteoarthrosis.

Abbreviations: ASES, American Shoulder and Elbow Surgeons; UCLA, University of California at Los Angeles.

with caution, and partial-head resurfacing can be successful even with this much bone loss.23,27,31 The likelihood of revision increases secondary to glenoid erosion, and component wear and loosening ultimately may ensue.43 Pritchett and Clark42 reported their outcomes of hemiarthroplasty and total-shoulder arthroplasty in 7 patients with significant Hill-Sachs and chronic dislocations. The mean patient age was 55 years (range, 36 to 67 years) and mean follow-up was 2 years. Five of the 7 patients had good results and there were no recurrent dislocations. Overall, these procedures should be reserved for older or less-active patients with defects involving greater than 40% of the articular surface and/or significant degeneration of articular cartilage. For the young athlete returning to play, the inevitable wear and tear of components, subsequently revisions, and consequences thereof should be emphasized.

CONCLUSION Hill-Sachs lesions, or humeral head defects resulting from shoulder dislocations, are often initially surgically managed indirectly by addressing instability at the glenoid consisting of a Bankart repair or glenoid bone reconstruction depending on the pathology. With regards to addressing these lesions directly on the humeral side, these are managed based on the size of the lesion, patient characteristics, and goals of care. We recommend initially opting for more conservative surgical options such as the remplissage procedure for smaller defects no greater than 20% of the humeral head diameter because there is well-documented literature with a reliable result. Patients with large bone defects greater than 20% likely require some attention to filling of the defects with a bone

146

Chapter 13

graft or partial arthroplasty. Failure to address humeral head pathology this large continues to place significant stress on the anterior glenoid soft-tissue and bone repairs and could be associated with a higher failure rate.44 Partial resurfacing with prosthetics has demonstrated promise and provides stability with reasonable results in terms of stability and function. When all else fails, arthroplasty can be considered. In younger, more-active patients, an anatomic resurfacing or hemiarthroplasty can be considered. However, in patients with glenoid wear, a total arthroplasty may be necessary.

REFERENCES 1. 2.

3.

4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

14.

Rowe CR, Patel D, Southmayd WW. The Bankart procedure: a longterm end-result study. J Bone Joint Surg Am. 1978;60(1):1-16. Burkhart SS, Danaceau SM. Articular arc length mismatch as a cause of failed Bankart repair. Arthroscopy. 2000;16(7):740-744. doi:10.1053/jars.2000.7794. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694. doi:10.1053/ jars.2000.17715. Purchase RJ, Wolf EM, Hobgood ER, Pollock ME, Smalley CC. Hill-Sachs “remplissage”: an arthroscopic solution for the engaging Hill-Sachs lesion. Arthroscopy. 2008;24(6):723-726. doi:10.1016/j. arthro.2008.03.015. Weber BG, Simpson LA, Hardegger F. Rotational humeral osteotomy for recurrent anterior dislocation of the shoulder associated with a large Hill-Sachs lesion. J Bone Joint Surg Am. 1984;66(9):1443-1450. Bigliani LU, Weinstein DM, Glasgow MT, Pollock RG, Flatow EL. Glenohumeral arthroplasty for arthritis after instability surgery. J Shoulder Elb Surg. 1995;4(2):87-94. doi:10.1016/ s1058-2746(05)80060-6. Connolly JF. Humeral head defects associated with shoulder dislocation: their diagnostic and surgical significance. AAOS Instr Course Lect. 1972;21:42-54. Wolf EM, Pollack ME. Hill-Sachs “remplissage”: an arthroscopic solution for the engaging Hill-Sachs lesion (SS-32). Arthroscopy. 2004;20(suppl 1):e14-e15. doi:10.1016/j.arthro.2004.02.033. Sekiya JK, Wickwire AC, Stehle JH, Debski RE. Hill-Sachs defects and repair using osteoarticular allograft transplantation. Am J Sports Med. 2009;37(12):2459-2466. doi:10.1177/0363546509341576. Koo SS, Burkhart SS, Ochoa  E. Arthroscopic double-pulley remplissage technique for engaging Hill-Sachs lesions in anterior shoulder instability repairs. Arthroscopy. 2009;25(11):1343-1348. doi:10.1016/j.arthro.2009.06.011. Elkinson I, Giles JW, Boons HW, et  al. The shoulder remplissage procedure for Hill-Sachs defects: does technique matter? J Shoulder Elbow Surg. 2013;22(6):835-841. doi:10.1016/j.jse.2012.08.015. Zhu YM, Lu Y, Zhang J, Shen JW, Jiang CY. Arthroscopic Bankart repair combined with remplissage technique for the treatment of anterior shoulder instability with engaging Hill-Sachs lesion. Am J Sports Med. 2011;39(8):1640-1648. doi:10.1177/0363546511400018. Leroux T, Bhatti A, Khoshbin A, et al. Combined arthroscopic Bankart repair and remplissage for recurrent shoulder instability. Arthroscopy. 2013;29(10):1693-1701. doi:10.1016/j.arthro.2013.06.007. Park MJ, Garcia G, Malhotra A, Major N, Tjoumakaris FP, Kelly JD IV. The evaluation of arthroscopic remplissage by high-resolution magnetic resonance imaging. Am J Sports Med. 2012;40(10):23312336. doi:10.1177/0363546512456974.

15.

16.

17.

18.

19.

20.

21.

22.

23.

24.

25.

26.

27.

28.

29.

30.

31.

Lazarides AL, Duchman KR, Ledbetter L, Riboh JC, Garrigues GE. Arthroscopic remplissage for anterior shoulder instability: a systematic review of clinical and biomechanical studies. Arthroscopy. 2019;35:617-628. doi:10.1016/j.arthro.2018.09.029. Liu JN, Gowd AK, Garcia GH, Cvetanovich GL, Cabarcas BC, Verma NN. Recurrence rate of instability after remplissage for treatment of traumatic anterior shoulder instability: a systematic review in treatment of subcritical glenoid bone loss. Arthroscopy. 2018;34:28942907.e2. doi:10.1016/j.arthro.2018.05.031. Camus D, Domos P, Berard E, Toulemonde J, Mansat P, Bonnevialle N. Isolated arthroscopic Bankart repair vs. Bankart repair with “remplissage” for anterior shoulder instability with engaging Hill-Sachs lesion: a meta-analysis. Orthop Traumatol Surg Res. 2018;104(6):803809. doi:10.1016/j.otsr.2018.05.011. Rashid MS, Crichton J, Butt U, Akimau PI, Charalambous CP. Arthroscopic “remplissage” for shoulder instability: a systematic review. Knee Surg Sport Traumatol Arthrosc. 2016;24(2):578-584. doi:10.1007/s00167-014-2881-0. Buza JA, Iyengar JJ, Anakwenze OA, Ahmad CS, Levine WN. Arthroscopic Hill-Sachs remplissage. J Bone Joint Surgery Am. 2014;96:549-555. doi:10.2106/JBJS.L.01760. McCabe MP, Weinberg D, Field LD, O’Brien MJ, Hobgood ER, Savoie FH. Primary versus revision arthroscopic reconstruction with remplissage for shoulder instability with moderate bone loss. Arthroscopy. 2014;30:444-450. doi:10.1016/j.arthro.2013.12.015. Longo UG, Loppini M, Rizzello G, et al. Remplissage, humeral osteochondral grafts, Weber osteotomy, and shoulder arthroplasty for the management of humeral bone defects in shoulder instability: systematic review and quantitative synthesis of the literature. Arthroscopy. 2014;30(12):1650-1666. doi:10.1016/j.arthro.2014.06.010. Boileau P, O’Shea K, Vargas P, Pinedo M, Old J, Zumstein  M. Anatomical and functional results after arthroscopic Hill-Sachs remplissage. J Bone Joint Surgery Am. 2012;94(7):618-626. doi:10.2106/ JBJS.K.00101. Miniaci A, Martineau PA. Humeral head bony deficiency (large HillSachs). In: El Attrache NS, ed. Surgical Techniques in Sports Medicine. Philadelphia, PA: Lippincott Williams & Wilkins; 2006. Miniaci A, Mascia AT, Salonen DC, Becker EJ. Magnetic resonance imaging of the shoulder in asymptomatic professional baseball pitchers. Am J Sports Med. 2002;30(1):66-73. doi:10.1177/036354650203 00012501. Chapovsky F, Kelly JD IV. Osteochondral allograft transplantation for treatment of glenohumeral instability. Arthroscopy. 2005;21(8):1007. doi:10.1016/j.arthro.2005.04.005. Kropf EJ, Sekiya JK. Osteoarticular allograft transplantation for large humeral head defects in glenohumeral instability. Arthroscopy. 2007;23(3):322.e1-e5. doi:10.1016/j.arthro.2006.07.032. Miniaci A, Gish MW. Management of anterior glenohumeral instability associated with large Hill-Sachs defects. Tech Shoulder Elb Surg. 2004;5(3):170-175. doi:10.1097/01.bte.0000137216.70574.ba. Diklic ID, Ganic ZD, Blagojevic ZD, Nho SJ, Romeo AA. Treatment of locked chronic posterior dislocation of the shoulder by reconstruction of the defect in the humeral head with an allograft. J Bone Joint Surg Br. 2010;92(1):71-76. doi:10.1302/0301-620X.92B1.22142. Armitage MS, Faber KJ, Drosdowech DS, Litchfield RB, Athwal GS. Humeral head bone defects: remplissage, allograft, and arthroplasty. Orthop Clin North Am. 2010;41(3):417-425. doi:10.1016/j. ocl.2010.03.004. Moros C, Ahmad CS. Partial humeral head resurfacing and Latarjet coracoid transfer for treatment of recurrent anterior glenohumeral instability. Orthopedics. 2009;32(8). doi:10.3928/01477447-20090624-21. Grondin P, Leith J. Case series: combined large Hill-Sachs and bony Bankart lesions treated by Latarjet and partial humeral head resurfacing: a report of 2 cases. Can J Surg. 2009;52(3):249-254.

Hill-Sachs Management 32.

33.

34.

35.

36.

37.

Raiss P, Aldinger PR, Kasten P, Rickert M, Loew M. Humeral head resurfacing for fixed anterior glenohumeral dislocation. Int Orthop. 2009;33(2):451-456. doi:10.1007/s00264-007-0487-6. Bessette MC, Frisch NC, Kodali P, Jones MH, Miniaci  A. Partial resurfacing for humeral head defects associated with recurrent shoulder instability. Orthopedics. 2017;40:e996-e1003. doi:10.3928/01477447-20171012-01. Ranalletta M, Bertona A, Tanoira I, Rossi LA, Bongiovanni S, Maignón GD. Resultados de la artroplastia parcial de superficie para el tratamiento de pacientes con necrosis ósea avascular del húmero proximal [Results of partial resurfacing of humeral head in patients with avascular necrosis]. Rev Esp Cir Ortop Traumatol. 2019;63(1):29-34. doi:10.1016/j.recot.2018.08.001. Ingoe H, Holland P, Tindall E, Liow R, McVie JL, Rangan A. Sevenyear survival analysis of the Global® CAP® (Conservative Anatomic Prosthesis) shoulder resurfacing. Shoulder Elbow. 2018;10(2):87-92. doi:10.1177/1758573217704818. Ramhamadany E, Modi CS. Current concepts in the management of recurrent anterior gleno-humeral joint instability with bone loss. World J Orthop. 2016;7(6):343-354. doi:10.5312/wjo.v7.i6.343. Visco A, Vieira LAG, Gonçalves FB, et  al. Surface arthroplasty for treating primary and/or secondary shoulder osteoarthrosis by means of the Hemicap-Arthrosurface® system. Rev Bras Ortop. 2011;46(3):288-292. doi:10.1016/S2255-4971(15)30197-X.

38.

39.

40.

41.

42. 43.

44.

147

Scalise JJ, Miniaci A, Iannotti JP. Resurfacing arthroplasty of the humerus: indications, surgical technique, and clinical results. Tech Shoulder Elb Surg. 2007;8(3):152-160 Stachowicz RZ, Romanowski JR, Wissman R, Kenter  K. Percutaneous balloon humeroplasty for Hill-Sachs lesions: a novel technique. J Shoulder Elbow Surg. 2013;22(9):e7-e13. doi:10.1016/j. jse.2012.12.035. Kazel MD, Sekiya JK, Greene JA, Bruker CT. Percutaneous correction (humeroplasty) of humeral head defects (Hill-Sachs) associated with anterior shoulder instability: a cadaveric study. Arthroscopy. 2005;21:1473-1478. doi:10.1016/j.arthro.2005.09.004. Ratner D, Backes J, Tokish JM. Arthroscopic reduction and balloon humeroplasty in the treatment of acute Hill-Sachs lesions. Arthrosc Tech. 2016;5:e1327-e1232. doi:10.1016/j.eats.2016.08.007. Pritchett JW, Clark JM. Prosthetic replacement for chronic unreduced dislocations of the shoulder. Clin Orthop Relat Res. 1987;(216):89-93. Denard PJ, Raiss P, Sowa B, Walch  G. Mid- to long-term followup of total shoulder arthroplasty using a keeled glenoid in young adults with primary glenohumeral arthritis. J  Shoulder Elbow Surg. 2013;22(7):894-900. doi:10.1016/j.jse.2012.09.016. Gottschalk LJ, Walia P, Patel RM, et al. Stability of the glenohumeral joint with combined humeral head and glenoid defects. Am J Sports Med. 2016;44:933-940. doi:10.1177/0363546515624914.

14 Rehabilitation of the In-Season and Postoperative Athlete Kevin E. Wilk, PT, DPT and Lenny Macrina, MSPT, SCS, CSCS

Shoulder instability is a common pathology seen in athletes and in active individuals. The glenohumeral joint is the most commonly dislocated major joint in the human body. This is probably due to the inherent laxity and tremendous range of motion (ROM) exhibited by individuals along with the large amounts of stress applied to the shoulder joint. Thus, the glenohumeral joint is inherently unstable in many individuals. Mannava et  al1 reported 15% of all players reporting to the National Football League Combine exhibited labral tears. Brophy et al2,3 stated it was the fourth most common procedure seen at the Combine. Furthermore, it is the fourth most common procedure performed in college football players.4 Following injury or surgery, we believe appropriate welldesigned rehabilitation is essential to a successful outcome. The rehabilitation must be based on numerous factors (we will discuss those later), but perhaps the most impor tant factor is a team approach to the rehabilitation program. The physician and the physical therapist must communicate regarding the type of surgery performed, concomitant procedures or lesions, and the surgeon’s overall impression regarding the rate of progression based on tissue quality, bone quality, etc. The specific factors will be discussed in this chapter. In this chapter we will discuss the postoperative rehabilitation guidelines following specific surgical procedures such as Bankart repairs, Latarjet procedures, and remplissage procedure. In addition, we will discuss our return-to-play criteria for patients returning to sports and higher-level functional activities.

REHABILITATION FACTORS There are 9 key factors that should be considered when designing a rehabilitation program for a patient with shoulder instability (Table  14-1). We will briefly discuss these factors and their significance to the rehabilitation program.

Onset of Pathology The first factor to consider in the rehabilitation of a patient with shoulder instability is the onset of the pathology. Shoulder instability may result from an acute event, a traumatic event, or from chronic recurrent episodes. The goal of the rehabilitation program may vary greatly based on the onset and mechanism of injury. Following a traumatic subluxation or dislocation, the patient typically presents with significant tissue trauma, pain, muscle guarding, and apprehension. The first-time dislocation episode is generally more painful than recurrent episodes. Conversely, a patient presenting with atraumatic or chronic instability often presents with a history of repetitive injuries and symptomatic complaints. Often the patient does not complain of a single instability episode but rather a feeling of shoulder laxity or an inability to perform specific tasks.

Degree of Instability The second factor is the degree of instability present in the patient and its effect on his or her function. Varying degrees of shoulder instability exist such as a subtle subluxation to gross (uncontrollable) instability.

- 149 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 149-174). © 2021 SLACK Incorporated.

150

Chapter 14

Table 14-1. Nine Key Factors to Consider in the Rehabilitation of the Unstable Shoulder 1. Onset of pathology 2. Degree of instability: subluxation vs dislocation 3. Frequency of dislocation: chronic vs acute 4. Direction of instability: anterior, posterior, multidirectional 5. Concomitant pathologies 6. End-range neuromuscular control 7. Premorbid activity level 8. Age of the patient 9. Desired activity level

The term subluxation refers to the complete separation of the articular surfaces with spontaneous reduction. Conversely, a dislocation is a complete separation of the articular surfaces and requires a specific movement or manual reduction to relocate the joint. This will result in underlying capsular tissue trauma. Thus, with shoulder dislocations the degree of trauma to the glenohumeral joint’s bone and soft tissue is much more extensive. Speer et  al5 has reported that for a shoulder dislocation to occur, a Bankart lesion must be present. Furthermore, soft-tissue trauma must be present on both sides of the glenohumeral joint capsule. Thus, an acute traumatic dislocation, the anterior capsule may be avulsed off the glenoid (Bankart lesion) and the posterior capsule may be stretched, allowing the humeral head to dislocate. This has been referred to as the “circle stability concept” as described by Warren et al.6

Frequency The next factor to influence the rehabilitation program is the frequency of dislocation or subluxation. The primary traumatic dislocation is most often treated conservatively with immobilization in a sling and early controlled passive ROM (PROM) exercises, especially with first-time dislocations. The incidence of recurrent dislocation ranges from 17% to 96% with a mean of 67% in patient populations between ages 21 and 30  years.7-18 Therefore, the rehabilitation program should progress cautiously in young, athletic individuals. It should be noted that Hovelius et al26-29 has demonstrated that the rate of recurrent dislocations is based on the patient’s age and is not affected by the length of postinjury immobilization. Individuals between ages 19 and 29 years are the most likely to experience multiple episodes of instability. Hovelius et al10,19-21 noted patients in their 20s exhibited a recurrence

rate of 60% whereas patients in their 30s to 40s had less than a 20% recurrence rate. In adolescents, the recurrence rate is as high as 92%22 and 100% with an open physes.23 Chronic subluxations, as seen in the atraumatic, unstable shoulder, may be treated more aggressively because of the lack of acute tissue damage, less muscular guarding, and inflammation. Caution is placed on avoiding excessive stretching of the joint capsule through aggressive ROM activities. The goal is to return the patient’s ROM, enhance strength, proprioception, dynamic stability, and neuromuscular control. This is especially true in the specific points of motion or direction that results in instability complaints.

Direction of Instability The fourth factor is the direction of instability present. The 3 most common forms include anterior, posterior, and multidirectional. Anterior instability is the most common traumatic type of instability seen in the general orthopedic population. It has been reported that this type of instability represents approximately 90% to 95% of all traumatic shoulder instabilities.15 However, the incidence of posterior instability appears to be dependent on the patient population.24 For example, in professional or collegiate football, the incidence of posterior shoulder instability appears higher than the general population. This is especially true in linemen because of the pushing methods employed during the blocking motion. Mair et  al25 reported on 9 athletes with posterior instability, 8 of 9 of whom were linemen and 7 of whom were offensive linemen. Often, these patients require surgery, as Mair and colleagues25 also reported 75% required surgical stabilization. Kaplan and colleagues4 reported in a study of collegiate football players with shoulder instability that 78% required surgical stabilization. Overhead athletes undergoing a posterior labral repair are less likely to return to their preinjury levels of sport compared with contact athletes or the overall athletic population.26 Multidirectional instability (MDI) can be identified as shoulder instability in more than one plane of motion. Patients with MDI often have a congenital predisposition and exhibit ligamentous laxity due to excessive collagen elasticity of the capsule. Furthermore, Rodeo et al27 reported that this type of patient exhibits a greater concentration of elastin compared to collagen and also smaller-diameter collagen fibrils. The authors consider an inferior displacement of greater than 8 to 10  mm during the sulcus maneuver (Figure 14-1) with the arm adducted to the side as significant hypermobility, thus suggesting significant congenital laxity.28 Owing to the atraumatic mechanism and lack of acute tissue damage, ROM is often normal to excessive. Patients with recurrent shoulder instability due to MDI generally have weakness in the rotator cuff, deltoid, and scapular stabilizers with poor dynamic stabilization and inadequate static stabilizers.

Rehabilitation of the In-Season and Postoperative Athlete

151

Premorbid Tissue Status The fifth factor involves considering other tissues that may have been affected and the premorbid status of the tissue. Disruption of the anterior capsulolabral complex from the glenoid commonly occurs during a traumatic injury resulting in an anterior Bankart lesion. Often osseous lesions may be present, such as a concomitant Hill-Sachs lesion caused by an impaction of the posterolateral aspect of the humeral head as it compresses against the anterior glenoid rim during relocation. This has been reported in up to 80% of dislocations.29-31 Conversely, a reverse Hill-Sachs lesion may be present on the anterior aspect of the humeral head due to a posterior dislocation.32 Also, glenoid bone loss of approximately 20% to 25% after a dislocation is considered significant and may contribute to long-term instability episodes for the patient. Recent studies show that not even 15% to 17% glenoid bone loss may be a critical level, as well.33-35 Occasionally, a bone bruise may be present in individuals who have sustained a shoulder dislocation thereby restricting upper extremity weight-bearing activities early on in the rehabilitation process. In rare cases of extreme trauma, the brachial plexus may become involved as well.36 Burkhart and De Beer37 reported some patients exhibited a bony defect or inverted-pear–shaped glenoid resulting in recurrent instability if not accurately identified or properly treated. Other common injuries in the unstable shoulder may involve the superior labrum (SLAP lesion) such as a type V SLAP lesion characterized by a Bankart lesion of the anterior capsule extending into the anterior superior labrum.38 Injuries to the rotator cuff may also be observed and significantly affect the rehabilitation progression and long-term function of the patient. These concomitant lesions will affect the rehabilitation significantly to protect the healing tissue.

Neuromuscular Control The sixth factor to consider is the patient’s level of neuromuscular control, particularly at end range. Neuromuscular control may be defined as the efferent, or motor output in reaction to an afferent, or sensory input.13,28 The afferent input is the ability to detect the glenohumeral joint position and motion in space with resultant efferent response by the dynamic stabilizers as they blend with the joint capsule to assist in stabilization of the humeral head. Injury with resultant insufficient neuromuscular control could result in deleterious effects to the patient. As a result, the humeral head may not center itself within the glenoid, thereby compromising the surrounding static stabilizers. The patient with poor neuromuscular control may exhibit excessive humeral head migration with the potential for injury, an inflammatory response, and reflexive inhibition of the dynamic stabilizers. Several authors have reported that neuromuscular control of the glenohumeral joint may be negatively affected by joint instability. Lephart et  al13 compared the ability to detect passive motion and the ability to reproduce joint positions

Figure 14-1. Sulcus maneuver to assess inferior capsular laxity.

in normal, unstable, and surgically repaired shoulders. The authors reported a significant decrease in proprioception and kinesthesia in the shoulders with instability when compared both to normal shoulders and shoulders undergoing surgical stabilization procedures. Smith and Brunolli39 reported a significant decrease in proprioception following a shoulder dislocation. Blasier and colleagues40 reported that individuals with significant capsular laxity exhibited a decrease in proprioception compared to patients with normal laxity. Zuckerman et  al41 noted that proprioception is affected by the patient’s age, with older patients exhibiting diminished more proprioception than a comparably younger population. Thus, the patient presenting with traumatic or acquired instability may present with poor proprioception and neuromuscular control.

Arm Dominance The seventh factor to consider in the nonoperative rehabilitation of the unstable shoulder is the arm dominance and the desired activity level of the patient. If the patient frequently performs an overhead motion or sporting activities such as a tennis, volleyball, or a throwing sport, then the rehabilitation program should include sport-specific dynamic stabilization exercises, neuromuscular control drills, and Plyometric exercises in the overhead position once full, pain-free ROM, and adequate strength has been achieved. Patients whose functional demands involve below-shoulder– level activities will follow a progressive exercise program to return full ROM and strength. The success rates of patients returning to overhead sports after a traumatic dislocation of their dominant arm are extremely low.42,43 Arm dominance can also significantly influence the successful outcome. The recurrence rates of instabilities vary based on age, activity level, and arm dominance. In athletes involved in collision sports, the recurrence rates have been reported between 86% and 94%.8,44-47

152

Chapter 14

Patient Age The next factor is the age of the patient. Younger patients (ages 17 to 24  years) tend to exhibit a lesion dif ferent from older patients (older than 40  years). Younger patients usually exhibit a Bankart lesion, and some may even exhibit a humeral avulsion of the glenohumeral ligament lesion. Conversely, older patients may exhibit an anterior labral periosteal avulsion lesion.48 The patient’s age is a significant prognostic factor for recurrent instability and generally a very impor tant consideration for treatment.

Patient Goals The ninth, and maybe the most critical factor, is the activity level and type of activities the patient desires to return to once full ROM and strength are obtained. Patients who desire to return to strenuous and aggressive activities, especially overhead or involving contact sports, should undergo surgical repair if a capsulolabral lesion is present. In contrast, inactive patients or patients with low-risk activities may be able to be treated successfully without surgery.

NONOPERATIVE REHABILITATION GUIDELINES Patients may be classified into 2 common forms of shoulder instability: traumatic and atraumatic. Specific guidelines to consider in the rehabilitation of each patient population will be outlined. A 4-phase rehabilitation program will be discussed for traumatic shoulder instability, followed by an overview of variations and key rehabilitation principles for atraumatic (congenital) laxity.

Traumatic Shoulder Instability Phase I, Acute Phase Following a first-time traumatic shoulder dislocation or subluxation, the patient often presents in considerable pain, muscle spasm, and an acute inflammatory response. Patients usually self-limit their motion by guarding the injured extremity in an internally rotated and adducted position against the side of their body to protect the injured shoulder. The goals of the acute phase are to 1) diminish pain, inflammation, and muscle-guarding; 2) promote and protect healing soft tissues; 3) prevent the negative effects of immobilization; 4) reestablish baseline dynamic joint stability; and 5) prevent further damage to the glenohumeral joint capsule (Table 14-2). We allow immediate limited and controlled motion following a traumatic dislocation in some patients (ages 18 to 28  years) but immobilize patients ages 29 to 45  years. However, motion is restricted so as not to cause further tissue attenuation. A short period of immobilization in a sling

to control pain and to allow scar tissue to form for enhanced stability may be necessary for 7 to 14 days although no longterm benefits regarding recurrence rates and immobilization have been made in patients ages 17 to 29 years.10,49 Individuals older than 29 years are usually immobilized for 2 to 4 weeks to allow scarring of the injured capsule. The ideal position in which to immobilize the glenohumeral has traditionally been in internal rotation with the arm close to the body. Potential complications with immobilization may include a decrease in joint proprioception, muscle disuse and atrophy, and a loss of ROM in specific age groups. Therefore, prolonged use of immobilization following a traumatic dislocation may not be recommended in all patients. PROM is initiated in a restricted and protected range based on the patient’s symptoms. Early motion is intended to promote healing, enhance collagen organization, stimulate joint mechanoreceptors, and aid in decreasing the patient’s pain through neuromuscular modulation.17,50-52 Pain-free active-assisted ROM (AAROM) exercises such as pendulums and external/internal rotation at 45 degrees of abduction using an L-bar (Breg Corp) may also be initiated. PROM exercises are also performed in a pain-free arc of motion. In addition, passive/active joint positioning is also performed in a restricted motion. Modalities such as ice, low-level laser, or transcutaneous electrical nerve stimulation may also be beneficial to decrease pain, inflammation, and muscle guarding. Strengthening exercises are initially performed through submaximal, pain-free isometric contractions to initiate muscle recruitment and retard muscle atrophy. Electrical stimulation of the posterior cuff musculature may also be incorporated to enhance this muscle-fiber–recruitment process early on in the rehabilitation process and also in the next phase when the patient initiates isotonic strengthening activities (Figure 14-2). Reinold et al53 stated that the use of electrical stimulation may improve force production of the rotator cuff, particularly the external rotators, immediately after an acute injury. Dynamic stabilization exercises are also performed to reestablish dynamic joint stability. The patient maintains a static position as the rehabilitation specialist performs manual rhythmic stabilization drills to facilitate muscular co-contractions. These manual rhythmic stabilization drills are performed for the shoulder internal and external rotators in the scapular plane at 30  degrees of abduction and are performed at pain-free angles that do not compromise the healing capsule. Rhythmic stabilizations for flexion and extension may also be performed with the shoulder at 100  degrees of flexion and 10  degrees of horizontal abduction. Strengthening exercises are also performed for the scapular retractors and depressors to reposition the scapula in its proper position. Scapula strengthening is critical for successful rehabilitation. Closed kinetic-chain exercises such as weight-shifting on a ball are performed to produce a co-contraction of the surrounding glenohumeral musculature and to facilitate joint

Rehabilitation of the In-Season and Postoperative Athlete

153

Table 14-2. Traumatic Dislocation Protocol Nonoperative rehabilitation for traumatic dislocation of the shoulder The program will vary in length for each individual depending on several factors: 1. Severity and onset of symptoms 2. Degree of instability symptoms 3. Direction of instability 4. Concomitant pathologies 5. Age and activity level of patient 6. Arm dominance 7. Desired goals and activities I. Phase I, acute motion phase Goals: Protect healing capsular structures Reestablish nonpainful ROM Decrease pain, inflammation, and muscular spasms Retard muscular atrophy/establish voluntary muscle activity Reestablish dynamic stability Improve proprioception **During the early rehabilitation program, caution must be applied in placing the capsule under stress until dynamic joint stability is restored. It is impor tant to refrain from activities in extreme ROM early in the rehabilitation process. Decrease pain/inflammation Sling or ER brace for comfort and depending on age of patient (physician’s preference) • Therapeutic modalities (ice, TENS, etc) • NSAIDs • Gentle joint mobilizations (grades I to II) for pain neuromodulation *Do not stretch injured capsule. ROM exercises • Gentle ROM only, no stretching • Pendulums • Rope and pulley Elevation in scapular plane to tolerance • Active-assisted ROM L-bar to tolerance Flexion IR with arm in scapular plane at 30 degrees of ABD ER with arm in scapular plane at 30 degrees of ABD - Motion is performed in nonpainful arc of motion only* **Do not push into ER or horizontal ABD with anterior instability.** **Avoid excessive IR or horizontal ADD with posterior instability.** • Strengthening/PRN exercises • Isometrics (performed with arm at side) Flexion ABD Extension IR (multiangles) (continued )

154

Chapter 14

Table 14-2. Traumatic Dislocation Protocol (continued) ER (multiangles) Biceps Scapular retract/protract, elevate/depress (seated manual resist) *E-stim may be used to ER during isometrics • Rhythmic stabilizations ER/IR in scapular plane (pain-free multiangles) Flex/Ext in scapular plane(pain-free angles, multiangles) • Weight shifts, standing hands on table (CKC exercises) (anterior instability only) • Proprioception training drills, -active joint reproduction proprioceptive drills (ER, IR, flex) II. Phase II, intermediate phase Goals: Regain and improve muscular strength Normalize arthrokinematics Enhance proprioception and kinesthesia Enhance dynamic stabilization Improve neuromuscular control of shoulder complex Criteria to progress to phase II 1. Nearly full to full passive ROM (ER may be still limited) 2. Minimal pain or tenderness 3. “Good” MMT of IR, ER, flexion, and ABD 4. Baseline proprioception and dynamic stability • Progress ROM activities at 90 degrees of ABD to tolerance (pain-free) • Initiate isotonic strengthening • Emphasis on ER and scapular strengthening ER/IR Tubing Scaption raises (full can) Abduction to 90 degrees Sidelying external rotation to 45 degrees Standing ER with tubing with manual resistance Hand on ball against wall resistance stabilization Prone extension to neutral Prone horizontal ADD Prone rowing Lower and middle trapezius Sidelying neuromuscular exercise drills Push-ups onto table Seated manual scapular resistance Biceps curls Triceps pushdowns E-stim may be used to ER during exercises. • Improve neuromuscular control of shoulder complex Initiation of PNF (continued )

Rehabilitation of the In-Season and Postoperative Athlete

155

Table 14-2. Traumatic Dislocation Protocol (continued) Rhythmic stabilization drills ER/IR at 90 degrees abduction (limit degree of ER) Flexion/extension/horizontal at 100 degrees flexion, 10 degrees horizontal ABD Progress to mid- and end-ROM Progress OKC program PNF Manual resistance ER (supine → sidelying → eccentrics, prone row ER/IR tubing with stabilization Progress CKC exercises with rhythmic stabilizations Wall stabilization on ball Hand on wall, wall circles for rotator cuff endurance Hand on wall, side-to-side motion for scapular muscles and deltoid Static holds in push-up position on ball Push-ups on tilt board Core Abdominal strengthening Trunk strengthening/low back Gluteal strengthening • Continue use of modalities (as needed) Ice, electrotherapy modalities III. Phase III, advanced strengthening phase Goals: Improve strength/power/endurance Improve neuromuscular control Enhance dynamic stabilizations Prepare patient/athlete for activity Criteria to progress to phase III 1. Full nonpainful range of motion 2. No palpable tenderness 3. Continued progression of resistive exercises 4. Good: normal muscle strength, dynamic stability, neuromuscular control • Continue use of modalities (as needed) • Continue isotonic strengthening (progress resistance) Continue thrower’s ten Progress to end-range stabilization drills Progress to full ROM strengthening Progress to bench press in restricted ROM (restrict horizontal abduction ROM) Progress to flat and incline chest press (weighted) restrict motion Program to seated rowing and lateral pull-down (in front) in restricted ROM • Emphasize PNF • Manual D2 with rhythmic stabilization at 45, 90, and 145 degrees • Advanced neuromuscular control drills (for athletes) Ball flips on table (continued )

156

Chapter 14

Table 14-2. Traumatic Dislocation Protocol (continued) ER tubing at 90-degree ABD with manual resistance and rhythmic stabilization at end range Push-ups on ball/rocker board with rhythmic stabilizations Manual scapular neuromuscular control drills Initiate perturbation activities (ER with exercise tubing with end-range rhythmic stab) Endurance training Timed bouts of exercises: 30 to 60 seconds Increase number of repetitions (sets of 15 to 20 repetitions) Multiple bouts throughout day (3×) Initiate Plyometric training 2-handed drills: Chest-pass throw Side-to-side throw Overhead soccer throw Progress to 1-handed drills: 90/90 baseball throws Wall dribbles 90/90 baseball throws against wall **Continue to avoid excessive stress on joint capsule.** IV. Phase IV, return to activity phase Goals: Maintain optimal level of strength/power/endurance Progressively increase activity level to prepare patient/athlete for full functional return to activity/sport Criteria to progress to phase IV 1. Full ROM 2. No pain or palpable tenderness 3. Satisfactory isokinetic test 4. Satisfactory clinical exam • Continue all exercises as in phase III • Progress isotonic strengthening exercises • Resume normal lifting program (Physician will determine) • Initiate interval sport program (as appropriate) • Continue modalities: ice, e-stim, etc (as needed) • Consider GH joint stabilizing brace for contact sports Follow-up • Isokinetic test (ER/IR and ABD/ADD) • Progress interval program • Maintenance of exercise program Abbreviations: ABD, abduction; ADD, adduction; CKC, closed-kinetic chain; ER, external rotation; e-stim, electrical stimulation; GH, glenohumeral; IR, internal rotation; MMT, manual muscle testing; NSAIDs, nonsteroidal anti-inflammatory drugs; OKC, open-kinetic chain; PNF, proprioceptive neuromuscular facilitation; ROM, range of motion; TENS, transcutaneous electrical nerve stimulation.

mechanoreceptors to enhance proprioception. Weight shifts are usually able to be performed immediately following the injury unless posterior instability or an articular cartilage lesion (bone bruise) is present.

Phase II, Intermediate Phase During the intermediate phase, the program emphasizes regaining full ROM along with progressing strengthening exercises of the rotator cuff, reestablishing the muscular

Rehabilitation of the In-Season and Postoperative Athlete

157

Figure 14-3. Sidelying manual external rotation while the clinician imparts rhythmic stabilization drills at end range.

Figure 14-2. Electrical stimulation to the posterior rotator cuff during exercise activity to improve muscle fiber recruitment and contraction.

balance of the glenohumeral joint, scapular stabilizers, and surrounding shoulder muscles. Before the patient enters phase II certain criteria must be met, including diminishing pain and inflammation, satisfactory static stability, and adequate neuromuscular control. To achieve the desired goals of this phase, PROM is performed to the patient’s tolerance with the goal of attaining nearly full ROM. AAROM exercises using a rope and pulley along with flexion and external/internal rotation exercises at 90 degrees of abduction using an L-bar may be progressed to tolerance without stressing the involved tissues. External rotation at 90 degrees of abduction is generally limited to 65 to 70 degrees to avoid overstressing the healing anterior capsuloligamentous structures for approximately 4 to 8 weeks but eventually increasing to full ROM as the patient tolerates. Isotonic strengthening exercises are also initiated during this phase. Emphasis is placed on increasing the strength of the internal and external rotators and scapular muscles to maximize dynamic stability. The ultimate goal of the strengthening phase is to reestablish muscular balance following the injury. Kibler et al12 noted that scapular position and strength deficits have been shown to contribute to glenohumeral joint instability. Exercises initially include external and internal rotation with exercise tubing at 0 degrees of abduction along with sidelying external rotation and prone rowing. During the latter part of this phase, exercises are progressed to include the “Progressive isotonic strengthening program” (Table  14-3) to emphasize rotator cuff and

Figure 14-4. Manual rhythmic stabilization drills: external rotation/ internal rotation rhythmic stabilization in neutral rotation to promote a co- contraction and improve dynamic stability.

scapulothoracic muscle strength (Figure 14-3). Manual resistive exercises such as sidelying external rotation and prone rowing may also prove beneficial by having the clinician vary the resistance throughout the ROM. Incorporating manual concentric and eccentric manual exercises and rhythmic stabilization drills at end range to enhance neuromuscular control and dynamic stability is also recommended (Figure 14-4). Closed kinetic-chain exercises are progressed to include hand on the wall stabilization drills in the plane of the scapular at shoulder height as the patient tolerates (Figure  14-5). Push-ups are performed first with hands on a table then progressed to a push-up on a ball or unstable surface while the rehabilitation specialist performs rhythmic stabilizations to

158

Chapter 14

Table 14-3. Progressive Isotonic Strengthening Program This program is designed to exercise the major muscles of the shoulder joint. The program’s goal is to be an organized and concise exercise program. In addition, all exercises included are specific to improve strength, power, and endurance of the shoulder complex musculature. 1. Diagonal pattern D2 flexion: Gripping tubing handle in hand of involved arm, begin with arm out from side 45 degrees and palm facing backward. After turning palm forward, proceed to flex elbow and bring arm up and over involved shoulder. Turn palm down and reverse to take arm to starting position. Perform _____ sets of _____ repetitions _____ times daily.

2. (A) External rotation at 0 degrees of abduction: Stand with involved elbow fixed at side, elbow at 90 degrees and involved arm across front of body. Grip tubing handle while the other end of tubing is fixed. Pull out arm, keeping elbow at side. Return tubing slowly and controlled. Perform _____ sets of _____ repetitions _____ times daily.

2. (B) Internal rotation at 0 degrees of abduction: Stand with elbow at side fixed at 90 degrees and shoulder rotated out. Grip tubing handle while other end of tubing is fixed. Pull arm across body keeping elbow at side. Return tubing slowly and controlled. Perform _____ sets of _____ repetitions _____ times daily. 3. Shoulder abduction to 90 degrees: Stand with arm at side, elbow straight, and palm against side. Raise arm to the side, palm down, until arm reaches 90 degrees (shoulder level). Perform _____ sets of _____ repetitions _____ times daily.

4. Scaption, external rotation: Stand with elbow straight and thumb up. Raise arm to shoulder level at 30-degree angle in front of body. Do not go above shoulder height. Hold 2 seconds and lower slowly. Perform _____ sets of _____ repetitions _____ times daily.

5. Sidelying external rotation: Lie on uninvolved side, with involved arm at side of body and elbow bent to 90 degrees. Keeping the elbow of involved arm fixed to side, raise arm. Hold 2 seconds and lower slowly. Perform _____ sets of _____ repetitions _____ times daily.

(continued )

Rehabilitation of the In-Season and Postoperative Athlete

159

Table 14-3. Progressive Isotonic Strengthening Program (continued) 6. (A) Prone horizontal abduction (neutral): Lie on table, face down, with involved arm hanging straight to the floor, and palm facing down. Raise arm out to the side, parallel to the floor. Hold 2 seconds and lower slowly. Perform _____ sets of _____ repetitions _____ times daily. 6. (B) Prone horizontal abduction (full ER, 100 degrees ABD): Lie on table face down, with involved arm hanging straight to the floor, and thumb rotated up (hitchhiker). Raise arm out to the side with arm slightly in front of shoulder, parallel to the floor. Hold 2 seconds and lower slowly. Perform _____ sets of _____ repetitions _____ times daily. 6. (C) Prone rowing: Lie on your stomach with your involved arm hanging over the side of the table, dumbbell in hand and elbow straight. Slowly raise arm, bending elbow, and bring dumbbell as high as possible. Hold at the top for 2 seconds, then slowly lower. Perform _____ sets of _____ repetitions _____ times daily. 6. (D) Prone rowing into external rotation: Lie on your stomach with your involved arm hanging over the side of the table, dumbbell in hand and elbow straight. Slowly raise arm, bending elbow, up to the level of the table. Pause 1 second. Then rotate shoulder upward until dumbbell is even with the table, keeping elbow at 90 degrees. Hold at the top for 2 seconds, then slowly lower, taking 2 to 3 seconds. Perform _____ sets of _____ repetitions _____ times daily. 7. Press-ups: Seated on a chair or table, place both hands firmly on the sides of the chair or table, palm down and fingers pointed outward. Hands should be placed equal with shoulders. Slowly push downward through the hands to elevate your body. Hold the elevated position for 2 seconds and lower body slowly. Perform _____ sets of _____ repetitions _____ times daily. 8. (A) Seated rowing: While seated in a chair, grip the handles of a cable pulley or of tubing fixed in front of you with your elbows in at your side. Pull elbows back, until in line with your trunk, squeezing shoulder blades together. Slowly return to starting position. Perform _____ sets of _____ repetitions _____ times daily. 8. (B) Seated machine bench press (restricted motion): While in the seated position, grip the handles of the machine and extend the elbows straight forward, pause then return back to the starting position. Avoid extending beyond the plane of the body to avoid excessive capsular stress. Perform _____ sets of _____ repetitions _____ times daily. (continued )

160

Chapter 14

Table 14-3. Progressive Isotonic Strengthening Program (continued) 8. (C) Latissimus dorsi pull-down (restricted motion): Sit at a lat pulldown machine and grip the bar just wider than shoulder width. Recline the upper body back approximately 45 degrees, pull bar to chest, then return to starting position. Do not allow the elbows to go beyond the plane of the body while pulling the bar to the chest. Also, avoid extending the elbows completely when returning to the starting position. Perform _____ sets of ______ repetitions ______ times daily. 9. Push-ups: Start in the down position with arms in a comfortable position. Place hands no more than shoulder width apart. Push up as high as possible, rolling shoulders forward after elbows are straight. Start with a push-up into wall. Gradually progress to table top and eventually to floor as tolerable. Perform _____ sets of _____ repetitions _____ times daily. 10. (A) Elbow flexion: Standing with arm against side and palm facing inward, bend elbow upward turning palm up as you progress. Hold 2 seconds and lower slowly. Perform _____ sets of _____ repetitions _____ times daily.

10. (B) Elbow extension (abduction): Raise involved arm overhead. Provide support at elbow from uninvolved hand. Straighten arm overhead. Hold 2 seconds and lower slowly. Perform _____ sets of _____ repetitions _____ times daily.

11. (A) Wrist extension: Supporting the forearm and with palm facing downward, raise weight in hand as far as possible. Hold 2 seconds and lower slowly. Perform _____ sets of _____ repetitions _____ times daily.

11. (B) Wrist flexion: Supporting the forearm and with palm facing upward, lower a weight in hand as far as possible and then curl it up as high as possible. Hold for 2 seconds and lower slowly. Perform _____ sets of _____ repetitions _____ times daily. (continued )

Rehabilitation of the In-Season and Postoperative Athlete

161

Table 14-3. Progressive Isotonic Strengthening Program (continued) 11. (C) Supination: Forearm should be supported on table with wrist in neutral position. Using a weight or hammer, roll wrist taking palm up. Hold for a 2-count and return to starting position. Perform _____ sets of _____ repetitions _____ times daily. 11. (D) Pronation: Forearm should be supported on table with wrist in neutral position. Using a weight or hammer, roll wrist taking palm down. Hold for a 2-count and return to starting position. Perform _____ sets of _____ repetitions _____ times daily. Abbreviation: ABD, abduction.

Figure 14-5. Wall stabilization drill: hand on the ball in the plane of the scapula while rhythmic stabilization drills are performed.

the involved and uninvolved upper extremity along with the trunk to integrate dynamic stability and core strengthening (tilt board, ball, etc) (Figure 14-6). Caution should be taken while performing closed kinetic-chain exercises in patients with posterior instability for 6 to 8 weeks to allow for adequate tissue healing and strength gains. Furthermore, patients with significant scapular winging should perform push-ups with a plus54 until adequate scapular strength is accomplished. Core stabilization drills should also be performed to enhance scapular control. Additionally, strengthening exercises may be advanced in regards to resistance, repetitions, and sets as the patient improves. End range rhythmic stabilization drills with the arm at 0 degrees of adduction or at 45 degrees of abduction are also performed. We refer to these exercises as perturbation drills. Exercises such as tubing with manual resistance and end-range rhythmic stabilization drills are also performed (Figure 14-7). The goal of these exercise drills is to improve proprioception and neuromuscular control at end range. Often these exercises are performed seated on a stability ball to recruit core, hip, and scapular muscles as the patient attempts to maintain good stability and posture.

Figure 14-6. Rhythmic stabilization drill: push-ups on an unstable surface (tilt board) to challenge patient’s neuromuscular control and improve dynamic stabilization.

Figure 14-7. External rotation with tubing while the therapist applies a manual resistance throughout ROM.

162

Chapter 14

Figure 14-8. Two-handed overhead Plyometric throw into a Plyoback (Exertools, Inc).

Phase III, Advanced Strengthening In the advanced strengthening phase, the focus is on improving strength, dynamic stability, and neuromuscular control near end range through a series of progressive strengthening exercises for a gradual return to the patient’s activity. Criteria to enter this phase include 1) minimal pain and tenderness, 2) full ROM, 3) symmetrical capsular mobility, 4) good (at least 4 out of 5 manual muscle test) strength, endurance, and dynamic stability of the scapulothoracic and upper extremity musculature. Muscle fatigue has also been associated with a decrease in neuromuscular control. Carpenter and colleagues55 observed the ability to detect passive motion of shoulders positioned at 90 degrees of abduction and 90 degrees of external rotation. The investigators reported a decrease in both the detection of external and internal rotation movement following an isokinetic fatigue protocol. Thus, exercises designed to enhance endurance in the upper extremity such as low resistance and

high repetitions (20 to 30 repetitions per set) are incorporated during this phase. Also, exercise sets using time may be incorporated, such as 30-second or 60-second exercise bouts. These exercises may include tubing external and internal rotation, Plyoball wall dribbling, and submaximal manual resistance drills. Aggressive upper body strengthening through the continuation of a progressive isotonic resistance program is recommended. A gradual increase in resistance as well as a progression to a more functional position by performing tubing exercises at 90 degrees of abduction to strengthen the external and internal rotators is also recommended. Additionally, more aggressive isotonic strengthening exercises such as bench press, seated row and latissimus pulldowns may be incorporated in a protected ROM during this phase. Additionally, the Advanced Throwers Ten may be used at this phase to help build strength and endurance in the shoulder girdle region.56 During bench press and seated rows, the patient is instructed to not extend the upper extremities beyond the plane of the body during the descending phase to minimize stress on the shoulder capsule. Also, during this phase the patient continues to perform rhythmic stabilization drills with the rehabilitation specialist and gradually progresses to a position of apprehension using tubing at 90 degrees of abduction with end range rhythmic stabilization drills to enhance dynamic stability. A patient wishing to return to athletic participation may be instructed to perform Plyometric exercises for the upper extremity. These activities are incorporated to regain any remaining functional ROM as well as improving neuromuscular control, and to train the extremity to produce and dissipate forces. Initially, 2-handed drills close to the body such as chest pass, side-to-side, and overhead soccer throws (Figure  14-8) using a 3- to 5-pound medicine ball may be performed to enhance dynamic stabilization of the glenohumeral joint. Exercises are initiated with 2 hand drills close to the center of gravity and gradually progress to longer lever arms away from the patient’s body. Drills are progressed to challenge the dynamic stabilizers of the shoulder. The clinician should regularly monitor for excessive pain as the athlete progresses through this phase. After approximately 2 weeks of pain-free 2-handed drills, the athlete progresses to 1-handed Plyometric drills using a small medicine ball (1 to 2 pounds) while throwing into a PlyoBack. PlyoBall wall dribbles in the 90/90 position (Figure  14-9) to improve overhead muscle endurance may also be incorporated.

Phase IV, Return-to-Activity Phase In the return-to-activity phase, the goal is to increase, gradually and progressively, the functional demands on the shoulder for the patient to return to unrestricted sports or daily activities. Other goals of this phase are to maintain the patient’s muscular strength and endurance, dynamic stability, and functional ROM. The criteria to progress to this phase include 1) full functional ROM, 2) adequate static stability, 3)

Rehabilitation of the In-Season and Postoperative Athlete

163

Figure 14-9. Wall dribbles with a 2-pound Plyoball in the 90/90 position for shoulder muscle endurance.

satisfactory muscular strength and endurance, 4) adequate dynamic stability, and 5) a satisfactory clinical exam. The general orthopedic patient continues to perform a maintenance program to improve strength, dynamic stability, and neuromuscular control as well as maintaining full, functional, and pain-free ROM. The athlete continues to perform aggressive strengthening exercises such as Plyometrics, proprioceptive neuromuscular facilitation (PNF) drills, and isotonic strengthening. In addition, the athlete may begin functional sport activities through an interval return-tosport program. These activities are designed to gradually return motion, function, and confidence in the upper extremity by progressing through graduated sport-specific activities.57-59 These interval sport programs are set up to minimize the chance of reinjury while training the patient for the demands of each individual sport. Each program should be individualized based on the patient’s injury, skill level, and goals. The duration of each program is based on several factors, including the extent of the injury, the sport, and level of play along with the time of season. The athlete is allowed to return to unrestricted sports activities after completion of an appropriately designed rehabilitation program and a successful clinical exam including full ROM and strength, along with adequate dynamic stability and neuromuscular control. We routinely perform a combination of isokinetic testing for our overhead athletes, which we refer to as the Thrower’s Series.60,61 Criteria to begin an interval sport program include an external rotation/internal rotation strength ratio of 66% to 76% or higher at 180  degrees per

Figure 14-10. DonJoy shoulder stabilizer brace used during sports activities to prevent excessive shoulder ROM.

second and an external rotation to abduction ratio of 67% to 75% or higher at 180 degrees per second.60,61 Patients returning to contact sports such as hockey, football, and rugby may be required to wear a shoulder stability brace (DonJoy) for the initiation of the sport return (Figure 14-10).

NONOPERATIVE REHABILITATION FOR ATRAUMATIC SHOULDER INSTABILITY Rehabilitation of the patient with congenital shoulder instability poses a significant challenge for the rehabilitation specialist. The patient typically presents with a history of several episodes of instability that has limited him or her from performing certain tasks. This may include daily work tasks as well as recreational or sports activities. This type of instability may arise from several factors, including excessive capsular redundancy and capsular laxity, poor osseous configuration such as a flattened glenoid fossa, or weakness in the glenohumeral and scapular musculature resulting in poor neuromuscular control. Any of these factors, individually or in combination, may contribute to pathological glenohumeral instability. The focus of the rehabilitation program for the patient with atraumatic instability is to improve proprioception, dynamic stability, neuromuscular control, to increase muscle tone, and to optimize scapular position and muscle strength

164

Chapter 14

Table 14-4. Atraumatic Instability Protocol Nonoperative rehabilitation for atraumatic instability This multiphase program is designed to allow patients/athletes to return to their previous functional level as quickly and safely as possible. Each phase will vary in length for each individual depending on the severity of injury, ROM/strength deficits, and the required activity demands of the patient. Phase I, acute phase Goals: Decrease pain/inflammation Reestablish functional ROM Establish voluntary muscular activation Reestablish muscular balance Improve proprioception Decrease pain/inflammation Therapeutic modalities (ice, electrotherapy, etc) NSAIDS Gentle joint mobilizations (grades 1 and II) for neuromodulation of pain ROM Gentle ROM exercises, no stretching Pendulum exercises Rope and pulley Elevation to 90 degrees, progressing to 145 to 150 degrees of flexion L-Bar Flexion to 90 degrees, progressing to full ROM Internal rotation with arm in scapular plane at 45 degrees abduction External rotation with arm in scapular plane at 45 degrees abduction Progressing arm to 90 degrees abduction ■

■

■

■

■

■

■

■

■

■

■

■

■

■

(continued ) to gradually return the patient to functional activities without limitations. As previously mentioned, the early phase of rehabilitation involves reducing shoulder pain and muscular inhibition while abstaining from activities that cause apprehension to the patient. Shoulder muscle activation has been shown to differ in patients with congenital laxity vs in a normal, stable shoulder.62-67 Normal force coupling that exists to dynamically stabilize the glenohumeral joint is altered, resulting in excessive humeral head migration and a feeling of subluxation by the patient. Burkhead and Rockwood42 found that an exercise program was effective in the management of 80% of atraumatic instability. Misamore et  al68 reported improved results in 28 of 59 patients in a long-term follow-up study of atraumatic, athletic patients. The rehabilitation program (Table  14-4) for the patient with atraumatic instability involves slowly regaining motion without excessive stress to the involved tissues. The patient often presents with excessive ROM, therefore PROM activities are not the focus of the rehabilitation program. Special attention is placed to avoid positions, movements, or stretches to the involved tissues that may place the shoulder in an

unstable position. Modalities such as cryotherapy, iontophoresis, low-level laser, or transcutaneous electrical nerve stimulation may be used to minimize pain and inflammation. The reduction of shoulder pain may also be accomplished through gentle motion activities to neuromodulate pain, nonsteroidal anti-inflammatory drugs prescribed by the physician, and abstaining from painful arcs of active and PROM. The primary focus of the early phase of the rehabilitation program is to minimize any further muscle atrophy and reflexive inhibition resulting from disuse, repeated subluxation episodes, and pain. Exercises are focused on creating dynamic stability, improved scapular position, enhance proprioception, and increase muscle tone throughout the body. Isometric contraction exercises may be performed for the glenohumeral muscles, particularly the rotator cuff. Rhythmic stabilization drills may also be performed to facilitate a muscular co-contraction/coactivation to improve neuromuscular control and enhance the sensitivity of the afferent mechanoreceptors.13 The goal is to create a more efficient agonist/antagonist co-contraction to improve force coupling and joint stability during active movements.

Rehabilitation of the In-Season and Postoperative Athlete

165

Table 14-4. Atraumatic Instability Protocol (continued) Strengthening Exercises Isometrics (performed with arm at side) Flexion Abduction Extension External rotation at 0 degrees abduction Internal rotation at 0 degrees abduction Biceps Scapular isometrics Retraction/protraction Elevation/depression Weight shifts with arm in scapular plane (closed-chain exercises) Rhythmic stabilizations (supine position) External/internal rotation at 30 degrees abduction Flexion/extension at 45 and 90 degrees flexion Note: It is impor tant to refrain from activities and motion in extreme ROM early in the rehabilitation process to minimize stress on the joint capsule. Proprioception/Kinesthesia Active joint reposition drills for ER/IR Phase II, intermediate phase Goals: Normalize arthrokinematics of shoulder complex Regain and improve muscular strength of glenohumeral and scapular muscle Improve neuromuscular control of shoulder complex Enhance proprioception and kinesthesia Criteria to progress to phase II: - Full functional ROM - Minimal pain or tenderness - “Good” MMT Initiate Isotonic Strengthening Internal rotation (sidelying dumbbell) External rotation (sidelying dumbbell) Scaption to 90 degrees Abduction to 90 degrees Prone horizontal abduction Prone rows Prone extensions Biceps Lower trapezius strengthening Initiate eccentric (surgical tubing) exercises at 0 degrees abduction Internal rotation External rotation ■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

(continued )

166

Chapter 14

Table 14-4. Atraumatic Instability Protocol (continued) Improve neuromuscular control of shoulder complex Rhythmic stabilization drills at inner, mid-, and outer ROM (ER/IR, and Flex/Ext) Initiate proprioceptive neuromuscular facilitation Scapulothoracic musculature Glenohumeral musculature Open kinetic chain at beginning and mid ranges of motion PNF Manual resistance External rotation Begin in supine position progress to sidelying Prone rows ER/IR tubing with rhythmic stabilization Closed kinetic chain Wall stabilization drills Initiated in scapular plane Progress to stabilization onto ball Weight shifts had on ball Initiate core stabilization drills Abdominal Erect spine Gluteal strengthening Continue use of modalities (as needed) Ice, electrotherapy Phase III, advanced strengthening phase Goals: Enhance dynamic stabilization Improve strength/endurance Improve neuromuscular control Prepare patient for activity Criteria to progress to Phase III - Full nonpainful ROM - No pain or tenderness - Continued progression of resistive exercises - Good to normal muscle strength Continue use of modalities (as needed) Continue isotonic strengthening (PREs) Fundamental shoulder exercises II Continue eccentric strengthening Emphasize PNF exercises (D2 pattern) with rhythmic stabilization hold Continue to progress neuromuscular control drills Open kinetic chain PNF and manual resistance exercises at outer ranges of motion ■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

(continued )

Rehabilitation of the In-Season and Postoperative Athlete

167

Table 14-4. Atraumatic Instability Protocol (continued) Closed kinetic chain Push-ups with rhythmic stabilization Progress to unsteady surface Medicine ball Rocker board Push-ups with stabilization onto ball Wall stabilization drills onto ball Program scapular neuromuscular control training Sidelying manual drills Progress to rhythmic stabilization and movements (quadrant) Emphasize endurance training Time bouts of exercise 30 to 60 s Increase number of repetitions Multiple boots bouts during day (2×/d) Phase IV, return to activity phase Goals: Maintain level of strength/power/endurance Progress activity level to prepare patient/athlete for full functional return to activity/sport Criteria to progress to phase IV - Full nonpainful ROM - No pain or tenderness - Satisfactory isokinetic test - Satisfactory clinical exam Continue all exercises as in phase III Initiate interval sport program (if appropriate) Patient education Continue exercise of fundamental shoulder exercise II ■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

■

Abbreviations: ER, external rotation; IR, internal rotation; MMT, manual muscle testing; NSAIDs, nonsteroidal anti-inflammatory drugs; PNF, proprioceptive neuromuscular facilitation; PRE, progressive resistive exercises; ROM, range of motion.

The authors of this paper believe that exercises such as rhythmic stabilization drills and closed kinetic-chain exercises to promote a co-contraction and an improvement in proprioception are beneficial for this patient population. Axial compression exercises are progressed from standing weight shifts on a table top to including the quadruped and tripod positions; however, this should be avoided if posterior instability is present. Rhythmic stabilizations of the involved extremity as well as at the core and trunk may be applied during these closed kinetic-chain drills to further challenge the patient’s dynamic stability and neuromuscular control. Unstable surfaces such as tilt boards, foam, large exercise balls, and the Biodex stability system (Biodex Corp) may be incorporated to further challenge the patient’s dynamic stability while in the closed chain position to further promote a coactivation or co-contraction of the surrounding musculature (Figure 14-11).

Figure 14-11. Axial compression drill: weight shifts on an unstable surface (Plyoball) while clinician performs rhythmic stabilizations to patient’s involved shoulder and trunk.

168

Chapter 14

Figure 14-12. Isotonics exercise (tubing external rotation and internal rotation) performed in a seated position on a stability ball to promote dynamic stabilization.

Figure 14-13. Dynamic stabilization drills performed on a stability ball with one foot on floor and with a sustained hold of a dumbbell to improve shoulder muscle activity.

Patients with congenital laxity often present with significant rotator cuff and scapular strength deficits, particularly the external rotators, scapular retractors, and scapular depressors. A progressive isotonic strengthening program may be initiated to improve rotator cuff and scapular musculature strength, endurance, and dynamic stability. Proper scapula stability and movement is vital for asymptomatic function. Scapula strengthening will improve proximal stability and therefore enable distal segment mobility during the patient’s functional tasks. These exercises may include external rotation at 0 degrees of abduction, sidelying external rotation, standing external rotation at 90 degrees of abduction, prone external rotation, prone rowing, prone extension, and prone horizontal abduction at 100 degrees with external rotation. Other scapular training exercises commonly incorporated include supine serratus punches and a dynamic hug for serratus anterior strengthening. Bilateral external rotation with scapular retraction and table press downs with scapular retraction may also be performed to strengthen the lower trapezius. Neuromuscular control drills are performed for the scapular musculature by having the rehabilitation specialist manually resist scapula movements. The goal of these drills is to enhance strength and endurance and also improve scapula proprioception. The function of neuromuscular control system must not be overlooked in this patient population. Functional exercise drills that include positions of instability to induce a reflexive muscular response28,69,70 may protect against future injury or recurring episodes of instability. Active joint repositioning tasks, PNF, and Plyometric exercises may be beneficial as well to evoke a neuromuscular response. We encourage exercises to be performed on a stability ball. By performing these exercises on an unstable surface, these drills will increase the demands on the glenohumeral and scapular muscles. Often these exercises are performed on a stability ball with one foot

on the floor and the opposite arm using a sustained hold with a dumbbell (Figures 14-12 and 14-13). Once sufficient strength of the scapular stabilizers and posterior cuff has been achieved, the patient is encouraged to use the shoulder only in the most stable positions—those in the plane of the scapular during humeral elevation. Activities that promote a feeling of joint instability with or without subluxation or dislocation should be avoided. Only when coordination and confidence are achieved through progressive strengthening should the patient attempt activities in an intrinsically unstable position. Bracing of the glenohumeral joint for return to sports activities may also be necessary to provide immobilization or controlled ROM to protect against further injury. The primary focus of the rehabilitation program for the congenitally unstable shoulder patient is to enhance strength and balance in the rotator cuff, improve scapular position and core stability, along with improved proprioception and neuromuscular control. Once symptoms have subsided and sufficient strength has been achieved, the patient may resume normal shoulder function, which may include sports activities.

POSTOPERATIVE REHABILITATION FOR SHOULDER INSTABILITY Rehabilitation Following Anterior Bankart Repair Rehabilitation following arthroscopic Bankart repair involves gradually restoring glenohumeral PROM while respecting the constraints of the healing tissues. Many authors advocate postoperative immobilization for 4 to 6

Rehabilitation of the In-Season and Postoperative Athlete weeks and a guarded-motion program. Wickiewicz and colleagues71 suggested 4 weeks of immobilization followed by AAROM and PROM exercises from week 4 and full motion by approximately 8 to 10 weeks. Various authors suggested several time frames for immobilization.72 Some authors suggested 3 weeks of immobilization,44,73 others 4 weeks, and others 6 weeks after arthroscopic stabilization. Grana and colleagues73 noted that some patients may not comply with long periods of strict immobilization because of the minimal pain and less operative morbidity following the arthroscopic approach. These patients may return to some activities prematurely. The rehabilitation program is divided into 4 specific phases. The first phase is considered the maximal protection phase or restricted-motion phase. Immediately after surgery, the patient’s shoulder is placed in an abduction brace; this brace is used consistently for the first 2 to 4  weeks and is worn during sleep for 4 to 6 weeks after surgery. During the first 2 weeks, the patient is allowed to perform AAROM and PROM exercises. The active-assisted motion is restricted to 60 degrees of forward flexion, 45 degrees of internal rotation, and 5 to 10 degrees of external rotation with the arm placed in 45 degrees of abduction. Additionally, PROM is performed for shoulder flexion to a maximum of 90 degrees and internal rotation and external rotation, with the arm at 45  degrees of abduction. These ranges are strictly enforced to prevent potentially deleterious forces on the anteroinferior aspect of the glenohumeral capsule where the surgical procedure has been performed. During this phase, the patient also performs submaximal and subpainful isometrics for the shoulder musculature. Additionally, cryotherapy and other modalities may be used to reduce postoperative pain and inflammation. At 3 to 4 weeks, ROM is increased but restricted—PROM and AAROM flexion is allowed to 90 degrees, while external rotation ROM is limited to 20 to 30 degrees. In addition, the patient will perform light strengthening exercises such as rhythmic stabilization exercises for the external rotation/ internal rotation muscles and submaximal isometrics for all the shoulder musculature, both to restore dynamic joint stability. At week 4, the sling is usually discontinued; this is based on the clinical assessment of the stability of the joint and the patient’s response to surgery and pain level. Occasionally, the patient is encouraged to continue use of the abduction pillow while sleeping to restrict excessive uncontrolled shoulder motions and positioning. At this time, AAROM and PROM exercises are continued gradually to improve abduction and external rotation, as well as flexion and internal rotation. During the first 6 weeks, we restrict motion to prevent overloading or overstressing the repaired capsule. Furthermore, we attempt to gradually restore motion, which helps to prevent the negative effects of immobilization and assists in collagen formation and organization. During these first 6 weeks, care must be taken by the clinician not to overstress the healing tissue and the soft-tissue fixation.

169

At approximately week 6 after the surgery, the goal is to gradually restore motion and initiate light isotonic strengthening of the rotator cuff and scapula stabilizers. The external rotation/internal rotation stretching and motion exercises are performed at 45 degrees of abduction, which produces a mild stretch on the inferior capsule (during external rotation motion). The patient is encouraged to gradually improve shoulder flexion, progressing to approximately 140 degrees. Also at this time, we will allow the patient to begin light resistance isotonic strengthening exercises. The external rotation/internal rotation muscles are exercised by using exercise tubing. Additionally, a light weight (1 to 2 pounds) can be used to perform abduction to 90  degrees, flexion to 90 degrees, and scapular musculature strengthening such as prone rowing and prone extension. Phase II, the moderate protection phase, begins at week 6 and progresses to week 14. The goals of this phase are to 1) gradually restore full, nonpainful ROM, 2) preserve the integrity of the surgical repair, 3) restore muscular strength and endurance, and 4) allow some functional activities. During this phase, all motions gradually progress. Shoulder flexion and abduction progress to 180  degrees. Shoulder internal rotation and external rotation motion exercises are performed at 90 degrees of abduction, and at 7 to 8 weeks, the patient should have 75 to 80 degrees of external rotation and full internal rotation (70 to 75 degrees). At weeks 9 to 10, we expect full ROM; external rotation should be approximately 85 to 90 degrees. At week 12, we begin to aggressively stretch the thrower’s shoulder past 90  degrees or external rotation with the goal of 115 to 125  degrees of external rotation. All strengthening exercises gradually progress with the goal of improving rotator cuff and scapular strength, restoring muscular balance, and enhancing dynamic stabilization of the glenohumeral joint complex. The patient is not allowed to perform isotonic exercises on weight-lifting equipment such as the bench press or pullovers. Phase III is the minimal-protection phase, extending from weeks 14 through 22. The goals of this phase are to 1) establish or maintain full ROM, 2) improve strength and endurance, and 3) initiate functional activities gradually. At approximately 14 to 16 weeks, activities such as light swimming exercises at 90 degrees of abduction, Plyometrics, and golf swings are permitted. An interval throwing program or other interval sports programs may be initiated at weeks 16 to 18 if the criteria have been met by the patient. The advanced strengthening phase extends from weeks 22 through 26. This phase is characterized by aggressive strengthening exercises such as Plyometrics, PNF drills, isotonic strengthening, and functional sports activities. In the overhead-throwing athlete, throwing from the pitching mound may be initiated. Contact sports may also be permitted during this period. Competitive throwing is usually not permitted until 7 to 9 months after surgery.

170

Chapter 14

Rehabilitation Following Posterior Labral Repair and/or Stabilization The rehabilitation program following posterior shoulder stabilization and/or posterior labrum repair is more conservative than following an anterior stabilization procedure. The rehabilitation program following posterior stabilization surgery is much slower with more restrictions and precautions. The most significant differences are the type of postoperative brace used, length of time in the postoperative brace, shoulder motion restrictions, and length of recovery time before returning to sports. Following surgery, the patient is placed into a shoulderimmobilizer brace with the arm positioned in either neutral rotation or slight external rotation to minimize tension on the posterior capsule. The postoperative shoulder immobilizer is worn for 6 weeks, and the patient is instructed to wear the brace all day and sleep in the brace as well. The only time the brace is not worn is when the patient is performing exercises and showering. We allow early but restricted PROM exercises immediately following surgery. We initiate PROM with the shoulder abducted to 45 degrees and internal rotation is performed to neutral and external rotation to approximately 20 to 25 degrees. PROM for shoulder flexion is to 90 degrees in the scapular plane. We also perform isometrics, rhythmic stabilization exercises for the scapula and rotator cuff muscles. All of the strengthening exercises are performed at a pain-free level and with the shoulder in neutral rotation. During the first 8 weeks of recovery, the focus is to gradually increase the patient’s PROM without causing excessive and unwanted posterior shoulder laxity, while gradually enhancing the patient’s strength and dynamic stabilization. During this time frame, we restrict excessive shoulder internal rotation, horizontal adduction beyond neutral for 8 weeks, and no pushing motions for 8 to 12 weeks. By weeks 10 to 12 postoperatively, the patient should exhibit nearly full PROM, usually 90 degrees of ER at 90 degrees of abduction, flexion to 165 to 170 degrees, and internal rotation at 90 degrees of abduction to approximately 45 to 50  degrees. During this phase, the patient is instructed to perform rotator cuff—and scapula-strengthening exercises as described earlier to improve neuromuscular control exercises to enhance dynamic stabilization. During weeks 12 to 26, the strengthening and dynamic stabilization exercises are increased. Additionally, isotonic strengthening exercises such as seated rowing are initiated (week 10), seated chest press (weeks 14 to 16), and 2-handed Plyometrics at weeks 12 to 16. A gradual return to sportspecific drills is initiated when patients fulfill specific criteria, and it also depends on the sport and position they are returning to. For overhead athletes, the gradual return to sports would be initiated at 6 to 7 months postoperatively with a return to competition at approximately 9 months. For athletes involved in contact sports, the return to competition is approximately 7 to 9 months, but depends on the position

that they play. Football linemen usually return at 7 to 9 months following surgery. Several authors have reported excellent results following arthroscopic shoulder stabilization surgery. Provencher et  al74 reported on 33 consecutive patients with a follow-up of 39 months; 83% exhibited a stable shoulder. Savoie and colleagues75 reported on 131 patients with an average followup of 28 months; 97% were stable. Lenart et al76 reported on 34  consecutive patients following arthroscopic repair; 94% exhibited a stable shoulder at 36 months.

Rehabilitation Following Anterior Laterjet Procedure The Laterjet procedure was developed in France and has been recently popularized by Dr Laurent Lafosse to treat chronic shoulder instability.77-79 This procedure is sometimes performed when the repair of the labrum in the shoulder is not possible. Indications for this procedure are a shoulder dislocation associated with a glenoid bone fracture, a large Hill-Sachs lesion, or an engaging Hill-Sachs lesion with continued instability and loss of function. Also, the patient may have had a previous shoulder reconstruction, labral repair, or stabilization surgery with continued shoulder instability. Immediately postoperatively, the patient presents to rehabilitation with the arm in an abduction pillow. The rehabilitation specialist should gradually restore PROM for the first 8  weeks. Owing to the nature of the surgery, early postoperative therapy must protect the subscapularis and the developing bony merging of the coracoid process. Therefore, external rotation PROM at 30 degrees of abduction is limited to 20 to 30 degrees for the first 2 to 4 weeks. Slowly reestablishing full external rotation PROM by 8 to 10 weeks after the surgery will enable good healing while not compromising the integrity of the muscle. Strengthening of the surrounding shoulder musculature may be initiated with submaximal and pain-free isometrics. Internal rotation strengthening should be limited for the first 6 weeks to allow adequate healing to occur. Light isotonic strengthening as mentioned in previous sections may be initiated 6 to 8 weeks postoperatively. Again, the goals are to improve strength, dynamic stability, and neuromuscular control before returning to a sport-specific training program approximately 16 weeks after surgery. Excellent results have been reported throughout the literature for return to sports, including contact-type sports with very few complications.77,80,81

REHABILITATION FOLLOWING STABILIZATION PROCEDURES Capsular Shift or Plication Surgical management for patients with MDI often consists of reducing the excessive capsular volume that surrounds

Rehabilitation of the In-Season and Postoperative Athlete the glenohumeral joint to provide improved static stability. In this par ticular group of patients, a positive sulcus sign reveals an abundance of inferior humeral translation due to an excessive rotator interval and inferior capsule. Ultimately the goal is to restore normal joint biomechanics and arthrokinematics, which will allow the patient to return to normal function without further onset of instability episodes. This surgical procedure remains to be a viable option to return the patient to his or her prior level of function with good to excellent results expected.82,83 Immediately postoperatively, the primary goal is to protect the healing tissues through the use of an immobilizer or abduction pillow for at least 6 weeks. The rehabilitation specialist may apply controlled stresses through gentle PROM and AAROM to 90 to 100 degrees of elevation for the first 4 to 6 weeks. Gentle isometric strengthening activities are also initiated to prevent atrophy of the surrounding musculature. Six weeks after surgery, PROM and AAROM are progressed until full motion is achieved by approximately 10 to 12 weeks. Special consideration should be made to avoid stretching of the tissue, which may result in excessive humeral translation and poor outcomes. The slow ROM progression is critical to achieve good long-term outcomes. An isotonic strengthening program for the rotator cuff and scapula stabilizers may commence to improve dynamic stability and neuromuscular control as described in previous sections. There should be a concerted effort to improve proprioception and correct postural abnormalities in this subpopulation of unstable shoulders. These simple corrections are vital to regaining full function without further episodes of instability.

RETURN-TO-PLAY OBJECTIVE CRITERIA It has been recently reported by several investigators that by establishing and having a patient fulfill specific objective criteria following anterior cruciate ligament reconstruction the reinjury rate substantially reduces. Grindem et al84 reported an 84% reduction in reinjuries when specific criteria are fulfilled. We believe this to be true at the glenohumeral joint following shoulder dislocation and/or surgery. We have established a 5-step assessment to reduce reinjury rates following shoulder stabilization: 1. ROM assessment (passive and active) 2. Stability testing 3. Strength assessment 4. Special testing (SLAP, biceps tests, scapula dyskinesis test) 5. Functional testing We routinely perform 5 functional tests for athletes returning to sports following shoulder stabilization. These tests include the unilateral chest press, push-up test, Davies The Closed Kinetic Chain Upper Extremity Stability Test (CKCUEST), unilateral ball drop test, and the upper quarter Y balance test.

171

Ball Drop Test The ball drop test has been developed to evaluate endurance, willingness to move quickly and dynamic stability. It is performed in the prone position with the arm abducted at 90  degrees with the elbow extended, using a 2-pound–weighted ball with the testing arm completely off the plinth as a measure of dynamic stability of the shoulder. The test is performed for a bout of 30 seconds counting the number of releases and catches and then compared involved to uninvolved side for a performance percentage. A satisfactory score is 110% or greater on the dominant extremity based on the number of catches compared to the nondominant. Scoring is based on clinical data collection as well as the authors’ clinical experience.

Push-Up Test A push-up test is performed as a measure of muscular endurance of the upper body and shoulder complex. The test is performed in a standard push-up position measuring the number of correct form push-ups an athlete can perform down to one-fist distance of the floor in 60  seconds. Two bouts of the test are performed, with the first bout serving as a warm-up. There is an expectation that the athlete will able to perform a greater number of push-ups during the second bout of the examination.

Closed Kinetic-Chain Upper Extremity Stability Test The Closed Kinetic Chain Upper Extremity Stability Test (CKCUEST) is administered as a measure of upper quarter stability, agility and power.85-88 The test is performed in a push-up position with the hands placed 36 inches apart on strips of athletic tape. The person reaches with alternating hands across the body to touch the piece of tape under the opposing hand. The number of cross-body touches performed in 15 seconds is recorded, followed by a 45-second rest, 3 sets, and the number of touches is averaged.

One-Repetition Maximum Bench Press Test A one-repetition maximum (1RM) bench press is used as an assessment of upper extremity strength.89 The test is evaluated for symmetrical performance without compensation, lag, or substitution. If available, preinjury 1RM maximum lift scores are used as a comparison to assist in determination of functional strength.

Unilateral Maximum Chest Press Test A unilateral maximum (1RM) chest press test can be used by the clinician using a chest press isotonic weight machine.

172

Chapter 14

The senior author of this manuscript (K.E.W.) has used this test on athletic patients with the goal being 80% or greater on the involved side compared to the uninvolved side. Although a clinically useful test, there are no data or research to validate this test method.

Upper Quadrant Y-Balance Test The Upper Quadrant Y-Balance Test, a test similar to the Lower Quadrant Y-Balance Test except for the upper quadrant, was first published by Westrick et al90 as an assessment of upper quarter closed kinetic-chain performance in the rehabilitation setting. The test involves maintaining sustained unilateral stance with one upper extremity while the other reaches out in a smooth and controlled manner in the medial, superolateral, and inferolateral directions. The average distance reached based on 3  trials is then recorded. Westrick et  al90 and Gorman and colleagues91 have demonstrated good test-retest (intraclass correlation coefficient: 0.91, 0.92, and 0.80 to 0.99, respectively) and interrater reliability (intraclass correlation coefficient: 1.00) as well as the establishment of normative data for active adults and young adults. Taylor et  al92 have also documented normative data for male and female collegiate athletes.

5.

6. 7.

8. 9.

10.

11. 12. 13.

14. 15.

CONCLUSION

16.

The glenohumeral joint is an inherently unstable joint that relies on the interaction of the dynamic and static stabilizers to maintain stability. Disruption of this interplay or poor development of any of these factors may result in instability, pain, and a loss of function. Rehabilitation will vary based on the type of instability present and the key principles described. A comprehensive program designed to establish full ROM, balance capsular mobility, along with maximizing muscular strength, endurance, proprioception, dynamic stability, and neuromuscular control is essential. A functional approach to rehabilitation using movement patterns and sport-specific positions along with an interval sport program will allow a gradual return to athletics. The focus of the program should minimize the risk of recurrence and ensure that the patient can safely return to functional activities.

17.

REFERENCES 1.

2.

3.

4.

Mannava S, Frangiamore SJ, Murphy CP, et  al. Prevalence of shoulder labral injury in collegiate football players at the National Football League Scouting Combine. Orthop J Sports Med. 2018;6(7):2325967118783982. Brophy RH, Barnes R, Rodeo SA, Warren RF. Prevalence of musculoskeletal disorders at the NFL Combine—trends from 1987 to 2000. Med Sci Sports Exerc. 2007;39(1):22-27. Brophy RH, Chehab EL, Barnes RP, Lyman S, Rodeo SA, Warren RF. Predictive value of orthopedic evaluation and injury history at the NFL Combine. Med Sci Sports Exerc. 2008;40(8):1368-1372. Kaplan LD, Flanigan DC, Norwig J, Jost P, Bradley J. Prevalence and variance of shoulder injuries in elite collegiate football players. Am J Sports Med. 2005;33(8):1142-1146.

18. 19.

20.

21.

22.

23.

24. 25. 26.

27.

28.

Speer KP, Deng X, Borrero S, Torzilli PA, Altchek DA, Warren RF. Biomechanical evaluation of a simulated Bankart lesion. J Bone Joint Surg Am. 1994;76(12):1819-1826. Warren RF, Kornblatt IB, Marchand R. Static factors affecting posterior shoulder instability. Orthop Trans. 1984;8:89-93. Aronen JG, Regan K. Decreasing the incidence of recurrence of first time anterior shoulder dislocations with rehabilitation. Am J Sports Med. 1984;12(4):283-291. Henry JH, Genung JA. Natural history of glenohumeral dislocation— revisited. Am J Sports Med. 1982;10(3):135-137. Hoelen MA, Burgers AM, Rozing PM. Prognosis of primary anterior shoulder dislocation in young adults. Arch Orthop Trauma Surg. 1990;110(1):51-54. Hovelius L, Augustini BG, Fredin H, Johansson O, Norlin R, Thorling  J. Primary anterior dislocation of the shoulder in young patients. A ten-year prospective study. J  Bone Joint Surg Am. 1996;78(11):1677-1684. Kazar B, Relovszky E. Prognosis of primary dislocation of the shoulder. Acta Orthop Scand. 1969;40(2):216-224. Kibler WB. The role of the scapula in athletic shoulder function. Am J Sports Med. 1998;26(2):325-337. Lephart SM, Warner JP, Borsa PA, Fu FH. Proprioception of the shoulder joint in healthy, unstable, and surgically repaired shoulders. J Shoulder Elbow Surg. 1994;3(6):371-380. doi:10.1016/ S1058-2746(09)80022-0. McLaughlin HL, MacLellan DI. Recurrent anterior dislocation of the shoulder. II. A comparative study. J Trauma. 1967;7(2):191-201. Rowe CR. Prognosis in dislocations of the shoulder. J Bone Joint Surg Am. 1956;38(5):957-977. Simonet WT, Cofield RH. Prognosis in anterior shoulder dislocation. Am J Sports Med. 1984;12(1):19-24. Tipton CM, Matthes RD, Maynard JA, Carey RA. The influence of physical activity on ligaments and tendons. Med Sci Sports. 1975;7(3):165-175. Yoneda B, Welsh RP, MacIntosh DL. Conservative treatment of shoulder dislocation in young males. J Bone Joint Surg Br. 1982;64:254-255. Hovelius  L. Anterior dislocation of the shoulder in teen-agers and young adults. Five-year prognosis. J  Bone Joint Surg Am. 1987;69(3):393-399. Hovelius L, Eriksson K, Fredin H, et al. Recurrences after initial dislocation of the shoulder. Results of a prospective study of treatment. J Bone Joint Surg Am. 1983;65(3):343-349. Hovelius L, Nilsson JA, Nordqvist A. Increased mortality after anterior shoulder dislocation: 255 patients aged 12-40 years followed for 25 years. Acta Orthop. 2007;78(6):822-826. Postacchini F, Gumina S, Cinotti G. Anterior shoulder dislocation in adolescents. J Shoulder Elbow Surg. 2000;9(6):470-474. doi:10.1067/ mse.2000.108385. Marans HJ, Angel KR, Schemitsch EH, Wedge JH. The fate of traumatic anterior dislocation of the shoulder in children. J Bone Joint Surg Am. 1992;74(8):1242-1244. Antosh IJ, Tokish JM, Owens BD. Posterior shoulder instability. Sports Health. 2016;8(6):520-526. Mair SD, Zarzour RH, Speer KP. Posterior labral injury in contact athletes. Am J Sports Med. 1998;26(6):753-758. DeLong JM, Jiang K, Bradley JP. Posterior instability of the shoulder: a systematic review and meta-analysis of clinical outcomes. Am J Sports Med. 2015;43(7):1805-1817. Rodeo SA, Suzuki K, Yamauchi M, Bhargava M, Warren RF. Analysis of collagen and elastic fibers in shoulder capsule in patients with shoulder instability. Am J Sports Med. 1998;26(5):634-643. Wilk KE, Arrigo CA, Andrews  JR. Current concepts: the stabilizing structures of the glenohumeral joint. J Orthop Sports Phys Ther. 1997;25(6):364-379.

Rehabilitation of the In-Season and Postoperative Athlete 29. 30.

31. 32.

33.

34.

35.

36.

37.

38.

39. 40.

41.

42.

43. 44.

45.

46.

47.

48.

49.

Caspari RB, Geissler WB. Arthroscopic manifestations of shoulder subluxation and dislocation. Clin Orthop Relat Res. 1993(291):54-66. Goubier JN, Duranthon LD, Vandenbussche E, Kakkar R, Augereau  B. Anterior dislocation of the shoulder with rotator cuff injury and brachial plexus palsy: a case report. J Shoulder Elbow Surg. 2004;13(3):362-363. O’Brien SJ, Warren RF, Schwartz  E. Anterior shoulder instability. Orthop Clin North Am. 1987;18(3):395-408. Beltran J, Rosenberg ZS, Chandnani VP, Cuomo F, Beltran S, Rokito A. Glenohumeral instability: evaluation with MR arthrography. Radiographics. 1997;17(3):657-673. Warner JJ, Flatbow EL. Anatomy and biomechanics. In: Bigliani LU, ed. The Unstable Shoulder. Rosemont, IL: American Academy of Orthopaedic Surgeons; 1996. Shaha JS, Cook JB, Song DJ, et al. Redefining “critical” bone loss in shoulder instability: functional outcomes worsen with “subcritical” bone loss. Am J Sports Med. 2015;43(7):1719-1725. Shin SJ, Jun BJ, Koh YW, McGarry MH, Lee TQ. Estimation of anterior glenoid bone loss area using the ratio of bone defect length to the distance from posterior glenoid rim to the centre of the glenoid. Knee Surg Sports Traumatol Arthrosc. 2018;26(1):48-55. Shin SJ, Koh YW, Bui C, et al. What is the critical value of glenoid bone loss at which soft tissue Bankart repair does not restore glenohumeral translation, restricts range of motion, and leads to abnormal humeral head position? Am J Sports Med. 2016;44(11):2784-2791. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging HillSachs lesion. Arthroscopy. 2000;16(7):677-694. Maffet MW, Gartsman GM, Moseley  B. Superior labrum-biceps tendon complex lesions of the shoulder. Am J Sports Med. 1995;23(1):93-98. Smith RL, Brunolli  J. Shoulder kinesthesia after anterior glenohumeral joint dislocation. Phys Ther. 1989;69(2):106-112. Blasier RB, Carpenter JE, Huston LJ. Shoulder proprioception. Effect of joint laxity, joint position, and direction of motion. Orthop Rev. 1994;23(1):45-50. Zuckerman JD, Gallagher MA, Lehman C, Kraushaar BS, Choueka J. Normal shoulder proprioception and the effect of lidocaine injection. J Shoulder Elbow Surg. 1999;8(1):11-16. doi:10.1016/ s1058-2746(99)90047-2. Burkhead WZ Jr, Rockwood CA  Jr. Treatment of instability of the shoulder with an exercise program. J Bone Joint Surg Am. 1992;74(6):890-896. Thorsness R, Alland JA, McCulloch CB, Romeo A. Return to play after shoulder surgery in throwers. Clin Sports Med. 2016;35(4):563-575. Arciero RA, Wheeler JH, Ryan JB, McBride JT. Arthroscopic Bankart repair versus nonoperative treatment for acute, initial anterior shoulder dislocations. Am J Sports Med. 1994;22(5):589-594. Larrain MV, Botto GJ, Montenegro HJ, Mauas DM. Arthroscopic repair of acute traumatic anterior shoulder dislocation in young athletes. Arthroscopy. 2001;17(4):373-377. Watson S, Allen B, Grant JA. A clinical review of return-to-play considerations after anterior shoulder dislocation. Sports Health. 2016;8(4):336-341. Wheeler JH, Ryan JB, Arciero RA, Molinari RN. Arthroscopic versus nonoperative treatment of acute shoulder dislocations in young athletes. Arthroscopy. 1989;5(3):213-217. Yoneda  M. Neviaser’s contribution to the treatment of ALPSA lesions. J Bone Joint Surg Am. 2001;83(4):621-622. doi:10.2106/00004623-200104000-00027. Kiviluoto O, Pasila M, Jaroma H, Sundholm  A. Immobilization after primary dislocation of the shoulder. Acta Orthop Scand. 1980;51(6):915-919. doi:10.3109/17453678008990894.

50.

51.

52.

53.

54.

55.

56.

57. 58.

59. 60.

61.

62.

63.

64.

65. 66.

67.

68.

69. 70.

173

Dehne E, Torp RP. Treatment of joint injuries by immediate mobilization. Based upon the spinal adaptation concept. Clin Orthop Relat Res. 1971;77:218-232. Haggmark T, Eriksson E, Jansson  E. Muscle fiber type changes in human skeletal muscle after injuries and immobilization. Orthopedics. 1986;9(2):181-185. Salter RB, Hamilton HW, Wedge JH, et al. Clinical application of basic research on continuous passive motion for disorders and injuries of synovial joints: a preliminary report of a feasibility study. J Orthop Res. 1984;1(3):325-342. Reinold MM, Macrina LC, Wilk KE, Dugas JR, Cain EL, Andrews JR. The effect of neuromuscular electrical stimulation of the infraspinatus on shoulder external rotation force production after rotator cuff repair surgery. Am J Sports Med. 2008;36(12):2317-2321. Decker MJ, Hintermeister RA, Faber KJ, Hawkins RJ. Serratus anterior muscle activity during selected rehabilitation exercises. Am J Sports Med. 1999;27(6):784-791. doi:10.1177/036354659902700616 01. Carpenter JE, Blasier RB, Pellizzon GG. The effects of muscle fatigue on shoulder joint position sense. Am J Sports Med. 1998;26(2):262-265. Wilk KE, Yenchak AJ, Arrigo CA, Andrews  JR. The Advanced Throwers Ten exercise program: a new exercise series for enhanced dynamic shoulder control in the overhead throwing athlete. Phys Sportsmed. 2011;39(4):90-97. doi:10.3810/psm.2011.11.1943. Ellenbecker TS, Mattalino AJ. The Elbow in Sport: Injury, Treatment, and Rehabilitation. Champaign, IL: Human Kinetics; 1997. Reinold MM, Wilk KE, Reed J, Crenshaw K, Andrews  JR. Interval sport programs: guidelines for baseball, tennis, and golf. J Orthop Sports Phys Ther. 2002;32(6):293-298. Wilk KE, Reinold MM, Andrews JR. Postoperative treatment principles in the throwing athlete. Sports Med Arthrosc Rev. 2001;9(1):69-95. Wilk KE, Andrews JR, Arrigo CA. The abductor and adductor strength characteristics of professional baseball pitchers. Am J Sports Med. 1995;23(6):778. doi:10.1177/036354659502300627. Wilk KE, Andrews JR, Arrigo CA, Keirns MA, Erber DJ. The strength characteristics of internal and external rotator muscles in professional baseball pitchers. Am J Sports Med. 1993;21(1):61-66. Barden JM, Balyk R, Raso VJ, Moreau M, Bagnall  K. Atypical shoulder muscle activation in multidirectional instability. Clin Neurophysiol. 2005;116(8):1846-1857. Kronberg M, Broström LA, Németh G. Differences in shoulder muscle activity between patients with generalized joint laxity and normal controls. Clin Orthop Relat Res. 1991;(269):181-192. Kronberg M, Németh G, Broström LA. Muscle activity and coordination in the normal shoulder. An electromyographic study. Clin Orthop Relat Res. 1990;(257):76-85. Morris AD, Kemp GJ, Frostick SP. Shoulder electromyography in multidirectional instability. J Shoulder Elbow Surg. 2004;13(1):24-29. Myers JB, Ju YY, Hwang JH, McMahon PJ, Rodosky MW, Lephart SM. Reflexive muscle activation alterations in shoulders with anterior glenohumeral instability. Am J Sports Med. 2004;32(4):1013-1021. von Eisenhart-Rothe RM, Jäger A, Englmeier KH, Vogl TJ, Graichen H. Relevance of arm position and muscle activity on threedimensional glenohumeral translation in patients with traumatic and atraumatic shoulder instability. Am J Sports Med. 2002;30(4):514522. doi:10.1177/03635465020300041101. Misamore GW, Sallay PI, Didelot W. A longitudinal study of patients with multidirectional instability of the shoulder with seven- to tenyear follow-up. J Shoulder Elbow Surg. 2005;14(5):466-470. Wilk KE, Arrigo C. Current concepts in the rehabilitation of the athletic shoulder. J Orthop Sports Phys Ther. 1993;18(1):365-378. Wilk KE, Voight ML, Keirns MA, Gambetta V, Andrews JR, Dillman CJ. Stretch-shortening drills for the upper extremities: theory and clinical application. J Orthop Sports Phys Ther. 1993;17(5):225-239.

174 71. 72. 73. 74.

75.

76.

77. 78.

79.

80.

81.

82.

Chapter 14 Wickiewicz TL, Pagnani MJ, Kennedy  K. Rehabilitation of the unstable shoulder. Sports Med Arthrosc Rev. 1993;1:227-235. DeFroda SF, Mehta N, Owens BD. Physical therapy protocols for arthroscopic Bankart repair. Sports Health. 2018;10(3):250-258. Grana WA, Buckley PD, Yates CK. Arthroscopic Bankart suture repair. Am J Sports Med. 1993;21(3):348-353. Provencher MT, Bell SJ, Menzel KA, Mologne TS. Arthroscopic treatment of posterior shoulder instability: results in 33 patients. Am J Sports Med. 2005;33(10):1463-1471. Savoie FH  III, Holt MS, Field LD, Ramsey  JR. Arthroscopic management of posterior instability: evolution of technique and results. Arthroscopy. 2008;24(4):389-396. Lenart BA, Sherman SL, Mall NA, Gochanour E, Twigg SL, Nicholson GP. Arthroscopic repair for posterior shoulder instability. Arthroscopy. 2012;28(10):1337-1343. Lafosse L, Boyle S. Arthroscopic Latarjet procedure. J Shoulder Elbow Surg. 2010;19(2 suppl):2-12. doi:10.1016/j.jse.2009.12.010. Lafosse L, Boyle S, Gutierrez-Aramberri M, Shah A, Meller  R. Arthroscopic Latarjet procedure. Orthop Clin North Am. 2010;41(3):393-405. doi:10.1016/j.ocl.2010.02.004. Lafosse L, Lejeune E, Bouchard A, Kakuda C, Gobezie R, Kochhar T. The arthroscopic Latarjet procedure for the treatment of anterior shoulder instability. Arthroscopy. 2007;23(11):1242 e1241-1245. Schmid SL, Farshad M, Catanzaro S, Gerber  C. The Latarjet procedure for the treatment of recurrence of anterior instability of the shoulder after operative repair: a retrospective case series of fortynine consecutive patients. J Bone Joint Surg Am. 2012;94(11):e75. Schroder DT, Provencher MT, Mologne TS, Muldoon MP, Cox JS. The modified Bristow procedure for anterior shoulder instability: 26-year outcomes in Naval Academy midshipmen. Am J Sports Med. 2006;34(5):778-786. Jacobson ME, Riggenbach M, Wooldridge AN, Bishop JY. Open capsular shift and arthroscopic capsular plication for treatment of multidirectional instability. Arthroscopy. 2012;28(7):1010-1017.

83.

84.

85.

86.

87.

88.

89.

90.

91.

92.

Pollock RG, Owens JM, Flatow EL, Bigliani LU. Operative results of the inferior capsular shift procedure for multidirectional instability of the shoulder. J Bone Joint Surg Am. 2000;82(7):919-928. Grindem H, Snyder-Mackler L, Moksnes H, Engebretsen L, Risberg MA. Simple decision rules can reduce reinjury risk by 84% after ACL reconstruction: the Delaware-Oslo ACL cohort study. Br J Sports Med. 2016;50(13):804-808. doi:10.1136/bjsports-2016-096031. Goldbeck TG, Davies GJ. Test-retest reliability of the Closed Kinetic Chain Upper Extremity Stability Test: a clinical field test. J Sport Rehabil. 2000;9(1):35-46. doi:10.1123/jsr.9.1.35. Pontillo M, Spinelli BA, Sennett BJ. Prediction of in-season shoulder injury from preseason testing in division I collegiate football players. Sports Health. 2014;6(6):497-503. doi:10.1177/1941738114523239. Roush JR, Kitamura J, Waits MC. Reference values for the Closed Kinetic Chain Upper Extremity Stability Test (CKCUEST) for collegiate baseball players. N Am J Sports Phys Ther. 2007;2(3):159-163. Tjong VK, Devitt BM, Murnaghan ML, Ogilvie-Harris DJ, Theodoropoulos JS. A qualitative investigation of return to sport after arthroscopic Bankart repair: beyond stability. Am J Sports Med. 2015;43(8):2005-2011. doi:10.1177/0363546515590222. Seo DI, Kim E, Fahs CA, et  al. Reliability of the one-repetition maximum test based on muscle group and gender. J Sports Sci Med. 2012;11(2):221-225. Westrick RB, Miller JM, Carow SD, Gerber JP. Exploration of the Y-Balance Test for assessment of upper quarter closed kinetic chain performance. Int J Sports Phys Ther. 2012;7(2):139-147. Gorman PP, Butler RJ, Plisky PJ, Kiesel KB. Upper Quarter Y Balance Test: reliability and performance comparison between genders in active adults. J Strength Cond Res. 2012;26(11):3043-3048. doi:10.1519/ JSC.0b013e3182472fdb. Taylor JB, Wright AA, Smoliga JM, DePew JT, Hegedus EJ. Upperextremity physical-performance tests in college athletes. J Sport Rehabil. 2016;25(2):146-154. doi:10-1123/jsr.2014-0296.

15 Return-to-Play Evaluation in the Postoperative Athlete for Anterior Shoulder Instability Brian Busconi, MD; Jonathon A. Hinz, DO; Benjamin J. Brill, DO; and Vickie Dills, PT, DPT, OCS, ITPT, CSAC

Shoulder instability in the competitive athlete, because of a multitude of factors, can be challenging to treat. In 2018, the MOON Shoulder Instability Cohort confirmed previously associated risk factors of shoulder instability, which include male sex, contact sports, age younger than 30 years, and anterior instability.1 The study further noted a significant risk for recurrence in the younger than 25-year-old age group. In a 25-year follow-up study, Hovelius found that the recurrence rate of shoulder instability was approximately 50% in 12- to 25-year-old study participants.2 A number of additional studies have corroborated this number, with some studies finding the number to be substantially higher.3 Data gathered from these studies provide improved ability to predict recurrence rates of shoulder instability, thus improving management in the athletic population. Management of athletes presenting with shoulder instability can consist of nonoperative treatment or surgical intervention, including arthroscopic and open stabilization procedures. In this chapter we will be focusing on the return to play evaluation in the postoperative athlete.

BODY Anatomy Anatomic consideration for shoulder instability includes both active stabilizers and passive restraints (Table  15-1).4 Turkel et al in 1981 first described stabilization of the anterior shoulder at 0, 45, and 90 degrees of abduction.5 In this study, the investigators described the role of the subscapularis at 0 degrees, the middle glenohumeral ligament and subscapularis at 45 degrees, and the importance of the inferior glenohumeral

ligament at 90 degrees of abduction (Figure  15-1). Another passive restraint addressed during shoulder instability surgery is the glenoid labrum. Biomechanically the glenoid labrum, when disrupted, can cause reduction in stability of 10% to 15%.33 This information has provided the basis of continued study of capsular and labral importance in shoulder instability and has been instrumental in guiding decisions in regards to surgical procedures for shoulder instability. Dynamic stability through the rotator cuff (RTC) was studied by Lee and colleagues, who introduced the dynamic stability index. The dynamic stability index takes into account compression as well as shear forces on the shoulder.6 Lee’s study concluded that the anterior (subscapularis) and posterior RTC (infraspinatus and teres minor) produce a significant amount of glenohumeral stability at the end range of motion (ROM), which is the position of instability. Bigliani et  al reports that congruency of the articular surfaces through midrange motion along with the dynamic stabilization of the RTC are the primary mode of stabilization.7 When there is a rotational force added, which creates increased translation, such as in the position of anterior dislocation, there is a significant relevance of the glenohumeral ligaments, particularly the inferior glenohumeral ligament.7 The complexity of structures and function in the shoulder complex demonstrates the significance of the intricate balance between the active stabilizers and passive restraints throughout shoulder ROM. The reestablishment of anterior instability of the glenohumeral joint through a surgical approach will restore static restraints of shoulder instability. However, recognizing the importance of dynamic stabilization supports the critical need for proper rehabilitation postoperatively.

- 175 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 175-183). © 2021 SLACK Incorporated.

176

Chapter 15

Table 15-1. Dynamic Stabilizers and Passive Restraints of the Shoulder DYNAMIC STABILIZERS Deltoid Rotator cuff Biceps

PASSIVE RESTRAINTS Articular surface Bony architecture Labrum Capsular structures Ligamentous structures

Based on the crucial balance of stability and restraint, no matter which surgical procedure restores the static stabilizers, a proper rehabilitative program to restore the dynamic function to the shoulder complex is imperative for optimal outcomes.

TREATMENT The decision-making process for an athlete with shoulder instability is multifactorial. The patient can be preseason, in-season, or postseason. They can be a first-time dislocator or plagued with chronic instability. The pathology of the instability itself can be soft-tissue or bone related. This multifactorial picture can complicate the treatment process. In 2012 Owens and colleagues created a treatment algorithm for in-season instability. The pathway begins with imaging, both plain-film and magnetic resonance imaging. Next, the primary pathology is determined, bone or soft tissue. If the pathology is primarily bony (bone defect > 25%) surgery is indicated. If the pathology is primarily soft tissue, the next decision is made based on history and physical exam. If recurrent instability is the primary problem, surgery is discussed as the primary option; if it is an initial instability event, a course of rehabilitation including sport-specific training is discussed. In this scenario if the patient is able to return to sport, further decisions can be made after the season. With any type of recurrent instability surgery is proposed8 (Figure 15-2).

Nonoperative Current nonoperative treatment consists of a period of immobilization followed by physical therapy and ultimately, return to play. The goals of nonoperative treatment are very similar to that of surgical management: the restoration of ROM, strength, and stability of the shoulder. In the current literature return to play following nonoperative treatment has mixed results. Recently, Shanley et al published results in the high school athletic population that 85% of patients with nonoperatively treated episodes of anterior shoulder instability were able to return for their subsequent season and a 6.2% recurrence rate.9 This is in stark contrast to 2 previously

Figure 15-1. Labeled anatomy of the glenohumeral joint visualized arthroscopically through the posterior portal.

published studies that showed 80% recurrence of instability and 60% recurrence of instability.3,10 The wide disparity in results can be from a multitude of factors and should not dismiss nonoperative treatment. First, when looking at the return-to-sport literature, desired outcomes of the study need to be evaluated. Some studies may have an end point of return to play, whereas another may have an end point of recurrence of stability. Using this published data in conjunction with the desires of the patient, the patient, physician, and therapy staff work together to accomplish the patient’s goals.

Operative Traditionally data regarding recurrence rates for instability after arthroscopic repair have been approximately 10% to 12%,3,11 and open repair procedures typically produce a recurrence rate of approximately 3% to 5%.12-14 Petrera and colleagues published a meta-analysis that looked at arthroscopic procedures using only suture anchors vs the traditional open Bankart procedure and found no statistical difference in recurrences between the 2  procedures (6% vs 6.7%).15 They discussed that previous arthroscopic data used a mix of prior surgical techniques and did not represent current fixation, which may have contributed to statistical differences. Return-to-play data for shoulder instability in National Collegiate Athletic Association football players published in 2017 had 168 arthroscopic procedures, with those who just had anterior procedures seeing an 82.4% return to sport.16 Bone augmentation procedures have been traditionally reserved for patients with bony insufficiency. This is important to consider whenever treating shoulder instability, especially with poor outcomes being associated with more than 25% bone loss and even as little as less than 13% bone

Return-to-Play Evaluation in the Postoperative Athlete for Anterior Shoulder Instability

177

Figure 15-2. Proposed algorithm used for in-season shoulder instability. (Abbreviations: AP, anteroposterior; MRI, magnetic resonance imaging; ROM, range of motion.) (Reprinted with permission from Owens BD, Dickens JF, Kilcoyne KG, et al. Management of mid-season traumatic anterior shoulder instability in athletes. J Am Acad Orthop Surg. 2012;20[8]:518-526. doi:10.5435/JAAOS-20-08-518.)

loss being associated with worse outcomes.17,18 In this setting publications on return-to-sport rates have been published as 65% in rugby players and 96.4% in combined collision and noncollision sports.19,20

POSTOPERATIVE REHABILITATION Most postoperative rehabilitation protocols follow very similar principles that include return to normal ROM and flexibility as well as restoration of strength, all of which are pain free.21 An impor tant aspect of return to play for the competitive athlete is functional rehabilitation, whose principles include restoring proprioceptive capacity and neuromuscular control of the shoulder joint after injury.22 Arthroscopic stabilization procedures require a slower progression of rehabilitation.21,23,24 The patient is usually protected for 4 for 6 weeks in a sling while initially working

on passive and active-assisted ROM. This protected phase is impor tant for initial healing of the soft tissues and has been proven impor tant for postoperative instability.25 Phases of rehabilitation then progress in approximately 4- to 6-week intervals to improve ROM, then strengthening, and finally functional rehabilitation and sport-specific activities. The goal for return to sport at full participation usually falls between months 7 and 9. Open stabilization procedures such as capsular shift as well as Latarjet procedures can have a slightly accelerated time frame of rehabilitation.24 ROM as well as strengthening exercises are performed slightly earlier than in an arthroscopic repair program with anticipation of return to sport at the 6-month mark. This again is predicated on functional rehabilitation as well as sport-specific activities symptom free.

178

Chapter 15

The role of functional rehabilitation involves recreating the sensory motor pathways involved with proprioception. During rehabilitation, Myers and Oyama describe the 4 facets of functional rehabilitation: awareness of proprioception, dynamic stabilization restoration, preparatory and reactive muscle facilitation, and finally replication of functional activities.22 Each of these facets is completed at dif ferent stages during rehabilitation. Awareness of proprioception is started with initial ROM, dynamic stabilization restoration involves reestablishing muscular force couple contraction, reactive muscle facilitation begins the process of muscle activation with unexpected forces, and finally replication of functional activities return the patient to athletic activities within a controlled environment. The senior author presents his current postoperative rehabilitation treatment course for arthroscopic Bankart repairs in Table  15-2. This includes the functional testing used in the return-to-play phase of treatment. The rehabilitation protocol is divided into phases I through V. Each phase has its own goals as well as expected outcomes. Phase I starts immediately postoperatively and is a protection phase. Goals include protecting the repair and limiting the negative effects of immobilization. This phase begins with passive and active-assisted ROM. The second half of phase I begins scapular stabilization, strengthening, and the beginning of proprioceptive training. In phase II there is increased emphasis on returning to normal ROM, proprioception, and core stabilization. Phase III is the initiation of strength and power, and stretching becomes more aggressive. A sport interval training program is integrated with functional exercises, which begin the process of sport-specific proprioceptive training. Phase IV represents the advance strengthening phase in which goals are returning to preinjury levels of strength, mobility, and endurance. Functional testing also begins during this phase outlined in Table 15-2. Phase V is return to sport. Passing appropriate criteria and functional testing, the athlete returns to unrestricted sporting activity and continues with a strengthening program.

Criteria for Progression to Functional Testing Phase to Access Return to Play • Full, pain-free shoulder ROM without substitutional patterns • No shoulder instability • Pain-free exercises • Proper scapular posture with rest and dynamic scapular control with ROM and strengthening exercises • Muscular strength of 75% to 80% of contralateral side • Satisfactory scores on shoulder activity scores

Functional Tests 1. Trunk Stability Push-Up: Tests the ability to stabilize the spine and hips in a sagittal plane with closed kinetic chain (CKC) activity during upper body symmetrical pushing motions. A variety of sports require trunk stabilization while applying symmetrical forces between the upper and lower extremities 2. Closed Kinetic Chain Upper Extremity Stability Test: Measures speed, agility, and power. Along with the number of repetitions counted over a 15-second trial, the athlete should be monitored for instability with movement, thoracic kyphosis, scapular winging, lumbar lordosis, and pelvic rotation. 3. Upper Extremity Y Balance Test (Figure 15-3): Dynamic test to maximally challenge the mobility and stability of the upper extremity, shoulder complex, and trunk. Combines scapular stability and mobility, thoracic rotation, and core stability. 4. Posterior Shoulder Endurance Test: Test to assess scapular muscle endurance. 5. One-Arm Hop Test: Dynamic performance test to compare the injured upper extremity to the contralateral upper extremity.

FUNCTIONAL TESTING

6. Long Arm Plank Ball Tap: Assesses joint stability, endurance, and proprioception.

An athlete’s ability to return to sport determined by objective measures of strength and ROM do not demonstrate the ability to perform sport-related skills effectively, efficiently, and confidently. Performance-based testing is essential in evaluating movement deficits and dysfunction for identification of increased predisposition for injury. Functional tests measure the relationship between injured and uninjured side, determining “normal” and “abnormal” performance. It is impor tant to recognize that following injury and surgical intervention, the athlete’s activity level will decrease. The effect can be global, affecting not only the postoperative extremity but involving the athlete’s overall strength, stability, and endurance.

7. Plank Weight Stacking (Figure 15-4): Assesses dynamic stability of the core and scapula. Assesses right vs left stability and proprioception. 8. Overhead Band Reach: Assesses the athlete’s ability to maintain scapular and core stability while reaching in various directions. Demonstrates functional RTC activity throughout various ROMs. Athletes must maintain proper scapulothoracic alignment while avoiding upper trapezius dominance, trunk lean, and pelvic tilt/lumbar lordosis.

Return-to-Play Evaluation in the Postoperative Athlete for Anterior Shoulder Instability

179

Table 15-2. Rehabilitation Protocol for Postoperative Anterior Shoulder Instability Initiate stretching trap/levator and Lat PHASE I: IMMEDIATE POSTOPERATIVE Side lying ER/IR at Week 6 Goals Scapular strengthening Protect repair Deltoid/supraspinatus/serratus strengthening Prevent negatives of immobilization Continue rhythmic stabilization Promote dynamic stability/proprioception Bodyblade 1 hand/2 hand in neutral grip Diminish pain and inflammation No stretching PHASE II: INTERMEDIATE PHASE No active external rotation/abduction or extension Goals Weeks 1 to 2 Gradually restore full ROM Sling Preserve integrity of repair Sleep in immobilizer Restore muscular strength and balance Elbow/hand ROM Enhance neuromuscular control Passive/gentle AAROM Weeks 7 to 9 Flexion 70 degrees Week 1 Gradual advance ROM Flexion 90 degrees Week 2 Flexion 160 degrees Scapular plane elevation 60 degrees Abduction in the scapular plane 160 degrees Ext/Int rotation with 30 degrees of abduction (P/AA) Initiate Ext/Int rotation at 90 degrees of abduction Ext rotation 10 degrees Ext/Int rotation in 60 degrees of abduction in Int rotation 45 degrees scap. plane Scapular retraction Ext rotation 70 degrees Weeks 3 to 4 Int rotation 75 degrees Discontinue sling Isotonic strengthening Passive/AAROM Supine serratus press Flexion 90 degrees Periscapular stabilization Elevation in scaptation 90 degrees Proprioceptive facilitation Ext/Int rotation in 45 degrees of abduction in Wall push-ups scap. plane PlyoBall on wall Ext rotation 20 degrees BodyBlade progression Int rotation 60 degrees Rhythmic stabilization Proprioceptive training Core stabilization Ball stabilization Weeks 10 to 13 Standing wobble board Progress strengthening exercises Treadmill UE walking Seated row, biceps curl, prone Ts and Ys, sidelyCore stabilization ing ER Scapular stabilization/strengthening Advance isotonic strengthening Weeks 5 to 6 Advance stretching exercises Progress from AAROM to AROM Standing ER stretch Flexion 140 degrees PlyoBall diagonal patterns, ball catching Ext/Int rotation in 45 degrees abduction in scap. Progress to regular push-up plane Ext 50° Int 60° ●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

(continued )

180

Chapter 15

Table 15-2. Rehabilitation Protocol for Postoperative Anterior Shoulder Instability (continued) PHASE III: MINIMAL PROTECTION PHASE Goals Maintain full ROM Improve muscular control, strength, power and endurance Initiate functional activities Core stabilization and conditioning Phase III Criteria Full, painless ROM Satisfactory stability Muscular strength No pain or tenderness Weeks 15 to 18 Continue stretching Continue core strengthening Continue shoulder strengthening Functional exercise and restricted sport activities Initiate sport interval program Week 16 Weeks 18 to 21 Advance interval sport program

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

PHASE IV: ADVANCE TO STRENGTHENING PHASE Goals Maintain full ROM Improve strength, power, and endurance Advance functional activities Phase IV criteria Full, painless ROM Satisfactory stability Muscular strength 80% contralateral side No pain or tenderness Weeks 22 to 26 Continue flexibility exercises Continue isotonic strengthening Neuromuscular control drills Plyometrics Advance interval sport program ●

●

●

●

●

●

●

●

●

●

Pass functional testing Trunk stability push-up 3 reps with control Closed Kinetic Chain Extremity Stability Test 21 touches, 15 s Upper extremity Y balance 3 consecutive progressions ●

PHASE V: RETURN-TO-SPORT PHASE Goals Enhance strength, power, and endurance Pass all functional testing Maintain mobility Phase V criteria Full, painless ROM Satisfactory static stability Muscular strength 80% contralateral side No pain or tenderness Weeks 26 to 32 Advance sport activity to unrestricted participation Pass functional testing Continue stretching and strengthening Posterior shoulder endurance 85% of contralateral arm One-arm hop test 5 repetitions Long arm plank ball tap 10 bidirectional taps with body control Plank weight stacking 4 × 1 pound Overhand band reach Maintain stability ●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

●

Abbreviations: AAROM, active assisted range of motion; AROM, active range of motion; ER, external rotation; Ext, external; Int, internal; IR, internal rotation; P/AA, passive/active assisted; ROM, range of motion; UE, upper extremity.

TRUNK STABILITY PUSHUP The athlete begins in the prone position. The male position is thumbs at the forehead; the female position is thumbs

at the chin. The athlete maintains knees in full extension, ankles neutral, and feet remain perpendicular to the floor. The athlete performs one pushup while maintaining this position. The test is performed a maximum of 3 attempts.

Return-to-Play Evaluation in the Postoperative Athlete for Anterior Shoulder Instability

181

Figure 15-3. Patient demonstrating Upper Extremity Y Balance Test.

Poor performance is demonstrated by inability to stabilize the core. In addition, compromised upper extremity strength and/or poor scapular stability as well as limited hip or spinal mobility results in poor performance of this test.

CLOSED KINETIC CHAIN UPPER EXTREMITY STABILITY TEST The male athlete is in the prone plank position; the female athlete is in the modified kneeling pushup position. Athletes are timed for 15 seconds as they alternate periods of single upper limb support to touch 1 of 2 lines place 36 inches apart. The athlete performs a warm-up trial followed by 3 test trials with a rest period of 45 seconds between trials. The score is the average of number of times the patient touches the line in 15 seconds. A score of less than 21 indicates the athlete is at risk for future injury.

UPPER EXTREMITY Y BALANCE Measure the right upper extremity length: The athlete is in standing with shoulder at 90 degrees of abduction. Measure from the spinous process of C7 to the distal tip of the third digit to the nearest half centimeter. The athlete assumes the starting position with the testing hand on a stable surface and the thumb adducted while being aligned behind the starting line. Performance of the test consists of the athlete reaching in the 3 reach directions (medial, superolateral, inferolateral) with the free hand while maintaining a push-up position with remaining feet shoulder width apart. Testing order: right medial, right inferorlateral, right superolateral, left medial left inferolateral, left superolateral. The trial should be discarded and repeated if: • The athlete fails to maintain unilateral stance surface. • The athlete fails to return the reach hand to the starting position under control. • The athlete lifts either foot off the floor.

Figure 15-4. Patient demonstrating Plank Weight Stacking.

Record the distance (1/2  cm) from the lateral support hand to the most distal portion of the reaching hand. This process is repeated until 3 trials in each direction on each hand are performed. The maximum reach distances are divided by the patient’s upper extremity length to normalize each reach distance. The composite reach distance is calculated by averaging the greatest trial in each of the 3 normalized reach distances for an analysis of overall performance on the test. There should not be a greater than 4-cm right and left reach distance in the anterior, posterolateral, and posteromedial directions.26,27

POSTERIOR SHOULDER ENDURANCE TEST Positioned on a plinth in prone, the athlete holds a weight equal to 2% of his or her body weight (rounded to the nearest half pound). Starting with the arm perpendicular to the floor, the athlete horizontally abducts the arm to 90 degrees at a cadence of 30 beats per minute. Repetitions are performed until the participant is fatigued, indicated by one of the following conditions: • Inability to hold the arm at the top of the arc for the required duration (1 second) • Compensation with elevation of the entire upper torso • The athlete reports an inability to continue

ONE-ARM HOP TEST The athlete assumes a one-arm push-up position with back flat, feet and shoulders apart, and weight-bearing upper extremity positioned perpendicular to the floor.

182

Chapter 15

The athlete places the non–weight-bearing hand on the posterior aspect of the low back. The athlete uses the weight-bearing arm to hop onto the step and lands on the rubber portion of the step with the entire hand. The patient then uses the weight-bearing arm to hop off of the step and return the hand to the start position next to the step. This is repeated 5 times as quickly as possible. An acceptable trial is defined as a test in which the athlete fully hopped onto the rubber portion of the step, did not use the other hand, did not touch down with a knee, and kept the back flat and the feet in the same position. On average, the nondominant upper-extremity performance times were 4.4% slower than the dominant upperextremity performance times; however, this difference was not statistically significant.28

LONG ARM PLANK BALL TAP The athlete is in a long arm plank position. The athlete alternately taps an 8-pound medicine ball from one hand to the other. The test is timed for 15 seconds. The athlete should maintain scapular stability and a neutral spine.

PLANK WEIGHT STACKING The athlete is in the high plank position. Switch five 10pound plates from one side to the other. Assess the ability of the athlete to perform the following: • Maintain a stable, neutral spine with equal weightbearing lower extremities • Maintain proper scapular congruency on the thoracic spine

OVERHAND BAND REACH The athlete stands facing the wall, anchoring a resistance band at chest level with the nontest upper extremity. The other end of the band is gripped in the test hand. The athlete slowly flexes the test extremity to 180 degrees then returns to shoulder height. This action is repeated with the test extremity to 45  degrees and to 90  degrees horizontal abduction. Repeat for 10 repetitions. Both sides should be tested. Assess the scapular and RTC function of the active extremity in each direction. The anchoring shoulder should be assessed for consistent scapular stability and endurance.

PSYCHOLOGICAL BARRIERS INHIBITING RETURN TO PLAY Evidence supports that successful return to sport is not only dependent on physical readiness but is also contingent on an athlete’s psychological readiness. Many return-tosport rehabilitation protocols provide guidelines for resolving physical deficits and dysfunction but do not address the fears of reinjury. Psychological barriers inhibiting athletes return to play at preinjury levels of sport include pain catastrophizing, kinesiophobia, fear avoidance, and confidence deficits. These psychological factors can lead to attentional distractions and affect the athlete’s performance.29 • Pain catastrophizing: magnification the threat value of pain • Kinesiophobia: fear that movement will cause pain or injury • Fear avoidance/fear or reinjury • Confidence deficient Potential interventions can include patient education; graded exposure to activity; setting progressive, obtainable goals; and relaxation techniques/anxiety management. Self-report questionnaires can be reliable in assessing the athletes of fear of reinjury. There are several questionnaires available to track and assess fear of injury to determine psychological appropriateness for return to sport. It is suggested that these surveys be conducted at intervals because typically an athlete’s fear of return to sport is elevated at baseline, decreases during rehabilitation, and increases as clearance to return to sport is granted.31 The Tampa Scale for Kinesiophobia-11 (TSK-11) has demonstrated reliability in measurement of fear of movement and injury. The authors recommends administering this scale on day 1, at week 16, and on return to play. A low score of 16 or less is suggested for clearance to return to sport.30

CONCLUSION Return to sport after surgical intervention for anterior shoulder instability is possible at a high rate with proper surgical considerations and a judicious postoperative rehabilitation plan. The goals of postoperative rehabilitation for shoulder instability include painless ROM, return of strength, and restoration of stability. A key feature in the rehabilitation process is the functional training restoring proprioceptive feedback, which is critical for the athlete’s ability to return to sport. Through the dif ferent phases of rehabilitation, each of these concerns is addressed with the ultimate goal of return to sport.

Return-to-Play Evaluation in the Postoperative Athlete for Anterior Shoulder Instability

REFERENCES 1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

14.

15.

16.

Kraeutler M, McCarty E, Belk J, et  al. Descriptive epidemiology of the MOON Shoulder Instability Cohort. Am J Sports Med. 2018;46(5):1064-1069. Hovelius L, Olofsson A, Sandström B, et al. Nonoperative treatment of primary anterior shoulder dislocation in patients forty years of age and younger. J Bone Joint Surg Am. 2008;90(5):945-952. doi: 10.2106/ JBJS.G.00070. Arciero RA, Wheeler JH, Ryan JB, McBride JT. Arthroscopic Bankart repair versus nonoperative treatment for acute, initial anterior shoulder dislocations. Am J Sports Med. 1994;22(5):589-594. doi:10.1177/036354659402200504. Abboud JA, Soslowsky LJ. Interplay of the static and dynamic restraints in glenohumeral instability. Clin Orthop Relat Res. 2002;400:48-57. doi:10.1097/00003086-200207000-00007. Turkel SJ, Panio MW, Marshall JL, Girgis FG. Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J  Bone Joint Surg. 1981;63(8):1208-1217. doi:10.2106/00004623-198163080-00002. Lee S, Kim K, O’Driscoll SW, Morrey BF, An K. Dynamic glenohumeral stability provided by the rotator cuff muscles in the mid-range and end-range of motion. J Bone Joint Surg Am. 2000;82(6):849-857. doi:10.2106/00004623-200006000-00012. Bigliani LU, Kelkar R, Flatow EL, Pollock RG, Mow VC. Glenohumeral stability. Clin Orthop Relat Res. 1996;330:13-30. doi:10.1097/00003086-199609000-00003. Owens BD, Dickens JF, Kilcoyne KG, et  al. Management of midseason traumatic anterior shoulder instability in athletes. J Am Acad Orthop Surg. 2012;20(8):518-526. doi:10.5435/JAAOS-20-08-518. Shanley E, Thigpen C, Brooks J, et al. Return to sport as an outcome measure for shoulder instability: surprising findings in nonoperative management in a high school athlete population. Am J Sports Med. 2019;47(5):1062-1067. doi:10.1177/0363546519829765. Dickens JF, Rue J, Cameron KL, et al. Successful return to sport after arthroscopic shoulder stabilization versus nonoperative management in contact athletes with anterior shoulder instability: a prospective multicenter study. Am J Sports Med.2017;45(11):2540-2546. doi:10.1177/0363546517712505. Bottoni CR, Wilckens JH, DeBerardino TM, et al. A prospective, randomized evaluation of arthroscopic stabilization versus nonoperative treatment in patients with acute, traumatic, first-time shoulder dislocations. Am J Sports Med.2002;30(4):576-580. doi:10.1177/036354 65020300041801. Uhorchak JM, Arciero RA, Huggard D, Taylor DC. Recurrent shoulder instability after open reconstruction in athletes involved in collision and contact sports. Am J Sports Med. 2000;28(6):794-799. doi:1 0.1177/03635465000280060501 Rowe CR, Zarins B, Ciullo JV: Recurrent anterior dislocation of the shoulder after surgical repair. Apparent causes of failure and treatment. J Bone Joint Surg Am. 1984;66(2):159-168. Hovelius L, Augustini BG, Fredin H, Johansson O, Norlin R, Thorling  J. Primary anterior dislocation of the shoulder in young patients. A ten-year prospective study. J  Bone Joint Surg Am. 1996;78(11):1677-1684. doi:10.2106/00004623-199611000-00006. Petrera M, Patella V, Patella S, Theodoropoulos J. A meta-analysis of open versus arthroscopic Bankart repair using suture anchors. Knee Surg Sports Traumatol Arthrosc. 2010;18(12):1742-1747. doi:10.1007/ s00167-010-1093-5. Robins RJ, Daruwalla JH, Gamradt SC, McCarty EC, Dragoo JL, Hancock RE. Return to play after shoulder instability surgery in National Collegiate Athletic Association Division I intercollegiate football athletes. Am J Sports Med. 2017;45(10):2329-2335. doi:10.1177/0363546517705635.

17.

18.

19.

20.

21.

22.

23.

24.

25.

26.

27.

28.

29.

30.

31.

32.

183

Shaha JS, Cook JB, Song DJ, et  al. Redefining “critical” bone loss in shoulder instability. Am J Sports Med. 2015;43(7):1719-1725. doi:10.1177/0363546515578250. Boileau P, Villalba M, Hery JY, Balg F, Ahrens P, Neyton L. Risk factors for recurrence of shoulder instability after arthroscopic Bankart repair. J Bone Joint Surg Am. 2006;88(8):1755-1763. Neyton L, Young A, Dawidziak B, et al. Surgical treatment of anterior instability in rugby union players: clinical and radiographic results of the Latarjet-Patte procedure with minimum 5-year followup. J  Shoulder Elbow Surg. 2012;21(12):1721-1727. doi:10.1016/j. jse.2012.01.023. Kee Y, Kim J, Kim H, Lim C, Rhee  Y. Return to sports after the Latarjet procedure: high return level of non-collision athletes. Knee Surg Sports Traumatol Arthrosc. 2017;26(3):919-925. Gaunt BW, Shaffer MA, Sauers EL, Michener LA, McCluskey GM, Thigpen CA; American Society of Shoulder and Elbow Therapists. The American Society of Shoulder and Elbow Therapists’ consensus rehabilitation guideline for arthroscopic anterior capsulolabral repair of the shoulder. J Orthop Sports Phys Ther. 2010;40(3):155-168. doi:10.2519/jospt.2010.3186. Myers JB, Oyama  S. Sensorimotor training for shoulder injury. Athl Train Sports Health Care. 2009;1(5):199-208. doi:10.3928/ 19425864-20090611-01. Blackburn TA, Guido JA  Jr. Rehabilitation after ligamentous and labral surgery of the shoulder: guiding concepts. J  Athl Train. 2000;35(3):373-381. Andrews JR, Harrelson GL, Wilk KE. Shoulder rehabilitation. In: Physical Rehabilitation of the Injured Athlete. 4th ed. Philadelphia, PA: Elsevier Saunders; 2012:190-231. Grana WA, Buckley PD, Yates CK. Arthroscopic Bankart suture repair. Am J Sports Med. 1993;21(3):348-353. doi:10.1177/036354659302100304. Gorman P, Butler RJ, Plisky PJ, Kiesel KB. Upper Quarter Y Balance Test: reliability and performance comparison between genders in active adults. J Strength Cond Res. 2012;26(11):3043-3048. doi:10.1519/ JSC.0b013e3182472fdb. Westrick RB, Miller JM, Carow SD, Parry Gerber  J. Exploration of the Y-Balance Test for assessment of upper quarter closed kinetic chain performance. Int J Sports Phys Ther. 2012;7(2):139-147. Falsone SA, Gross MT, Guskiewicz KM, Schneider RA. one-arm hop test: reliability and effects of arm dominance. J  Orthop Sports Phys Ther. 2002;32(3):98-103. doi:10.2519/jospt.2002.32.3.98. Hsu CJ, Meierbachtol A, George SZ, Chmielewski TL. Fear of reinjury in athletes. Sports Health. 2016;9(2):162-167. doi:10.1177/1941738116666813. Tkachuk GA, Harris CA. Psychometric properties of the Tampa Scale for Kinesiophobia-11 (TSK-11). J  Pain. 2012;13(10):970-977. doi:10.1016/j.jpain.2012.07.001. Olds MK, Ellis R, Parmar P, Kersten  P. Who will redislocate his/her shoulder? Predicting recurrent instability following a first traumatic anterior shoulder dislocation. BMJ Open Sport Exerc Med. 2019;5(1):e000447. 2019;5(1):e000447. doi:10.1136/ bmjsem-2018-000447. Klemt C, Nolte D, Grigoriadis G, Di Federico E, Reilly P, Bull AMJ. The contribution of the glenoid labrum to glenohumeral stability under physiological joint loading using finite element analysis. Comput Methods Biomed Biomedical Engin. 2017;20(15):1613-1622. doi:10.1080/10255842.2017.1399262.

SECTION III Posterior Instability

16 History and Examination of Posterior Instability Trey Colantonio, MD, CPT and CDR Lance LeClere, MD

Isolated posterior glenohumeral instability is often a challenging diagnosis with significant performance implications in athletes. Overhead and contact athletes are particularly at risk for posterior instability, and shoulder instability is one of the most common injuries in high-level athletes.1,2 Often the primary presenting symptom is generalized shoulder pain, and the patient may have been referred with a diagnosis other than shoulder instability.3,4 This is an impor tant distinction from anterior instability, which most often presents with a chief complaint of instability, whereas posterior instability most commonly presents with a chief complaint of pain. Posterior instability is the result of abnormal posterior translation of the humeral head on the glenoid and may occur as a result of traumatic dislocation, recurrent posterior subluxation, or as pain due to microinstability and repetitive microtrauma. Although less common than anterior instability, with reported incidence ranging from 2% to 10% of glenohumeral instability,2,4-7 posterior instability is observed more frequently in athletes and in young, active populations.4,5,8 Contact athletes subject to blunt force trauma to the glenohumeral joint as well as overhead athletes exposed to repetitive microtrauma are at higher risk for developing posterior instability.5,9 Additionally, posterior instability and lesions of the posterior glenoid labrum may be present in patients with combined anterior instability.10,11 As such, a thorough history and physical examination must be conducted in combination with advanced imaging to adequately diagnose posterior glenohumeral instability. Recurrent posterior instability presents a challenging injury and often leads to decreased athletic performance; however, if treated appropriately, patients can have excellent results and return to play.1 This chapter will outline the anatomic and biomechanical considerations,

historical findings, and physical examination of the athlete with posterior glenohumeral instability.

ANATOMY, BIOMECHANICS, AND PATHOANATOMY An appreciation of the anatomic elements of glenohumeral stability is essential to the diagnosis and management of posterior glenohumeral instability. Stability of the glenohumeral joint is conferred through a combination of static and dynamic stabilizers that act in concert to maintain the proper relationship of the humeral head and glenoid at rest and during motion. Injury, anatomical variation, or dysfunction of one or various elements of glenohumeral stability can lead to instability of the joint.

Static Stabilizers The primary static stabilizers of the glenohumeral joint are the bony anatomy and capsulolabral ligamentous structures.12-17 The osseous morphology of the glenoid and humerus are critical components of static glenohumeral stability. The glenoid concavity forms the articular surface of the joint and has a normal retroversion of 4 to 7 degrees18,19 or 1 ± 3 degrees when controlled for scapular orientation.20 Increased glenoid retroversion has been shown to predispose patients to posterior instability.9,20,21 In a prospective study of 714 young athletes, Owens et al found a mean retroversion of 7.7 degrees in noninjured participants compared to 17.6 degrees in those with posterior instability. They also found a 17% increased risk of subsequent posterior instability with each 1-degree

- 187 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 187-195). © 2021 SLACK Incorporated.

188

Chapter 16

increase in glenoid retroversion.9 Additionally, Bradley and colleagues examined magnetic resonance imaging of patients undergoing arthroscopic posterior labrum repair and found that these patients had increased glenoid and chondrolabral retroversion when compared to a control group.22 Despite several studies demonstrating increased glenoid retroversion as a risk factor for posterior instability, this area remains a contentious topic and other authors have shown that humeral subluxation may not be increased in the setting of increased retroversion.23 In addition to the orientation of the glenoid, the concavity has a significant role in posterior stability of the glenohumeral joint. A congenital deficiency of the glenoid rim or concavity is commonly referred to as glenoid dysplasia.24 In a cadaveric study, Inui et  al demonstrated that a deficiency of the glenoid concavity, or a flat glenoid, particularly in the inferior glenoid, led to posterior instability.25 Edelson similarly described posteroinferior hypoplasia defined as a “dropping away” of the flat plateau of the posterior glenoid. Edelson incidentally discovered posteroinferior hypoplasia in 20% to 35% of cadaveric scapulae examined, and this was found to be present in 75% of patients with multidirectional instability (MDI) in the prospective portion of the study.26 The incidence of hypoplasia is unknown and may often be an incidental finding on imaging studies. Hypoplasia likely results from a failure of the inferior glenoid to develop and may often be bilateral. Common associated findings include cartilage and labral compensatory thickening in the posterior inferior glenoid and abnormal humeral head and neck development. Weishaupt and colleagues studied computed tomography (CT) arthrograms of a series of patients with recurrent posterior instability and defined 2 types of dysplastic glenoids: a rounded “lazy J form” or a “delta form” with a triangular osseous deficiency.27 Harper et al went on to classify glenoid dysplasia on magnetic resonance arthrogram (MRA) from mild to severe based on the appearance of the posterior glenoid rim on axial imaging and also noted that patients with severe glenoid dysplasia often have hypertrophy of the posterior labrum.24,28 In addition to congenital variations of glenoid morphology, acquired posterior glenoid bone deficiency can affect posterior stability of the glenohumeral joint. Bone loss from posterior instability can range from attritional wear due to repetitive microtrauma to a large osteochondral fracture from acute trauma.4 Bone loss may also be seen in the form of a reverse bony Bankart lesion, in which a displaced posterior labrum tear leads to a fracture off the posterior glenoid. The amount of bone loss is known to affect recurrent anterior stability, and the success of surgical management and posterior glenoid bone loss has become an area of recent research interest. Hines et al retrospectively reviewed a cohort of patients who received surgical treatment for isolated posterior instability and found a mean posterior bone loss of 7.3%, with 22% of patients having more than 13.5% bone loss. They found no significant difference in reoperation rates or outcome scores;

however, patients with more than 13.5% bone loss were less likely to return to military active duty.29 A biomechanical study by Nacca and colleagues demonstrated that posterior glenoid osseous defects greater than 20% of the glenoid predisposed cadaveric shoulders to recurrent instability after reverse Bankart repair.30 Orientation and morphology of the humerus also play an impor tant role in static glenohumeral stability. The humeral head has a normal retroversion of 25 to 35 degrees with an inclination of 130 degrees to the humeral shaft.20,31 Increased humeral head retroversion is associated with an increased baseline external rotation and decreased internal rotation, and as such may predispose patients to posterior instability due to the easier force vector when the arm is held in a flexed, adducted, and internally rotated position.32 Additionally, a traumatic posterior instability event may generate an osteochondral impaction fracture, or reverse Hill-Sachs lesion (RHSL), of the humeral head. Similarly to humeral bone loss in anterior instability, a large RHSL with concomitant posterior glenoid bone loss can predispose the glenohumeral joint to recurrent instability due to engagement on the glenoid.33-35 The glenoid labrum increases the concavity-compression mechanism of the humeral head in the glenoid and increases the depth of humeral articulation.12,36,37 The labrum is a wedge-shaped, fibrous structure that serves as an anchor for capsuloligamentous structures and reduces glenohumeral translation.37,38 Because the posterior labrum is only loosely attached to the surrounding capsule with less ligamentous reinforcement,39-41 it contributes less stability to humeral translation than does the anterior labrum. Nevertheless, the increase in glenoid depth is a significant contributor to chondrolabral containment. Labral height combined with glenoid retroversion are critical to the concept of chondrolabral containment, and patients with recurrent posterior instability have been shown to have a loss of chondrolabral containment.38 Lesions of the labrum can develop after acute trauma or repetitive microtrauma. A reverse Bankart lesion is most commonly seen in the setting of acute trauma and consists of a complete detachment of the posterior labrum from the glenoid. Separation of the labrum from the posterior glenoid leads to a loss of labral height and predisposes patients to recurrent instability. These lesions have uniformly good outcomes with surgical treatment, and restoration of labral height is a key component in prevention of recurrent instability.7,42,43 Depending on the force vector of the trauma and the displacement of the labral tear, a bony avulsion from the glenoid, commonly known as a reverse bony Bankart lesion, may occur. In a biomechanical study,44 a posterior inferior Bankart lesion generated an increase in posterior translation by 83%. Additionally, a posterior labrocapsular periosteal sleeve avulsion may occur in which the periosteum of the posterior glenoid separates from the bone and remains attached to the posterior capsule and detached posterior labrum.45 Repetitive microtrauma most commonly leads to

History and Examination of Posterior Instability a partial tear of the posterior labrum known as a Kim lesion. This occurs when an accumulation of shearing forces due to persistent subluxation or repetitive microtrauma lead to a loss of chondrolabral containment with subsequent development of posterior labral marginal cracks or partial avulsions of the glenoid labrum.46 The capsular ligaments of the glenohumeral joint contribute significantly to posterior stability. Unlike the robust composition of the anterior capsule, the posterior capsule is relatively thin and biomechanically inferior to the anterior capsule.41 The posterior band of the inferior glenohumeral ligament (PIGHL) is an impor tant component of the posterior capsule. The PIGHL inserts at the 7 to 9 o’clock position on the glenoid and is the most impor tant ligament in the posterior loading position with the arm held in internal rotation and forward flexion. This arm position places the PIGHL in an anterior-posterior orientation under tension and is commonly implicated in blocking injuries in football linemen.4,47 If the posterior capsule and PIGHL are stretched beyond the initial resting length, posterior glenohumeral instability may develop.12,13,48 The posterior capsule has been shown to have an increased cross-sectional area in patients with MDI and posterior instability as compared to those with anterior instability.49 This finding suggests that less energy may be required to disrupt the posterior capsule and may partially explain why repetitive microtrauma is a common cause of posterior instability. A posterior, or reverse, humeral avulsion of the glenohumeral ligaments (RHAGL) is a rare injury that most commonly occurs in concert with additional chondrolabral pathology and may predispose patients to recurrent instability.46,50 A RHAGL is rarely seen in isolation and usually occurs as a result of hyperabduction with the arm in maximal external rotation. Additionally, RHAGL lesions have been shown to be more common in female athletes in studies of patients with instability.51 The presence of a RHAGL has been shown to generate an increase in posterior and inferior translation by 43% in the jerk position.44 The middle glenohumeral ligament (MGHL) and superior glenohumeral ligament also contribute to posterior stability. The MGHL augments the PIGHL and stabilizes the joint against posterior translation during midrange abduction, and the superior glenohumeral ligament augments the PIGHL in shoulder adduction, forward flexion, and internal rotation.4,52-54 Although controversial, the rotator interval is postulated to provide static stabilization against posterior instability via the “circle concept.”55 This theory states that posterior instability must be accompanied by damage to anterior capsuloligamentous structures. The rotator interval has been shown to play a role in prevention of inferior and posterior translation with the arm in forward flexion.32 The coracohumeral ligament within the rotator interval capsule provides stability against inferior translation in external rotation. The circle concept remains controversial, and rotator interval repair during arthroscopic treatment of posterior instability has been challenged in cadaveric studies.56,57

189

Dynamic Stabilizers The rotator cuff muscles13,14,58,59 and the long head of the biceps tendon37,47 provide dynamic stability to the glenohumeral joint during normal active motion. The subscapularis muscle is the primary dynamic stabilizer in preventing posterior translation12,13,47; however, all the rotator cuff muscles have an impor tant role in maintaining concavitycompression of the glenohumeral joint.12,47,60 The supraspinatus muscle provides dynamic inferior stability,47 whereas the infraspinatus and teres minor provide posterior compression.14,61 The long head of the biceps tendon also provides some dynamic resistance against inferior translation.62 Scapular mechanics also provide stability to the glenohumeral joint. Orientation of the scapula during motion affects the orientation of the glenoid on the humerus during motion, and poor scapular mechanics may predispose patients to instability. An increase in scapular internal rotation and medial scapular winging has been shown to be present in patients with glenohumeral instability. Additionally, reduced scapular upward rotation is believed to be detrimental to maintaining inferior glenohumeral stability.63

CLASSIFICATION Patients with posterior instability can present in a variety of circumstances because of the varying etiology of their symptoms. Posterior instability can be classified by the direction, degree, mechanism, and volition of instability. Posterior instability may arise as the result of acute trauma or repetitive microtrauma, or less commonly may be atraumatic. Patients with an acute trauma can recall a specific injury and subluxation or dislocation event that may result in recurrent instability. Repetitive microtrauma, the most common mechanism of recurrent posterior instability, results from the culmination of posteriorly directed force vectors with the arm in forward flexion, internal rotation, and adduction. The classic example of this mechanism is the football lineman with recurrent posterior subluxations when blocking. Patients with posterior instability without a history of trauma should be evaluated for an underlying collagen disorder or an abnormality of glenohumeral static stabilizers. Posterior instability is most commonly unidirectional but may occur in the setting of bidirectional instability or MDI.4,49 In the evaluation of posterior instability, attention must be given to the volitional nature of the instability. Involuntary instability most often results in recurrent subluxations as a result of acute or repetitive trauma. Volitional instability occurs when a patient can generate a posterior subluxation or dislocation at will. There are 2 types of volitional instability: voluntary positional and voluntary muscular.40,64,65 Patients with voluntary muscular instability typically have an underlying muscular imbalance that allows for willful subluxation or dislocation independent of arm position and are considered poor surgical candidates.4 Patients with voluntary

190

Chapter 16

positional instability are able to generate a subluxation or dislocation event in a certain arm position, typically flexion and adduction, and generally avoid provocative positions. Patients with voluntary positional instability should not necessarily be excluded from surgical management.4,64,66

HISTORY Obtaining a thorough history is essential when evaluating an athlete with suspected recurrent posterior glenohumeral instability because these patients often present with vague generalized symptoms or confounding injuries. This aty pical presentation poses a clinical challenge and determining instability because the nature of these symptoms may lead to a delay in diagnosis.9 Athletes may present in the setting of an acute trauma and recall a specific injury with the arm in an at-risk position for posterior instability; however, athletes more commonly present with recurrent symptoms as a result of repetitive microtrauma. Patients with recurrent instability most frequently present with generalized pain or pain deep in the posterior aspect of the shoulder rather than frank instability.4,5,64 This pain is often accompanied by a decline in performance or strength.67,68 This weakness is most often pronounced with the arm in the forward-flexed, adducted, and internally rotated provocative position for exercises such as bench press or push-ups.4 Throwing or overhead athletes may describe pain that occurs later during activity because of muscle fatigue of the dynamic stabilizers.65,69 Patients may also report mechanical symptoms such as crepitation or clicking sensations with the arm in provocative positions that may be associated with the unstable reverse Bankart lesions, chondral lesions, or loose bodies.32,69 Athletes participating in sports that place high demand on the shoulder, such as football, rugby, wrestling, volleyball, swimming, weightlifting, climbing, and paddling, are particularly at risk.4,5 Additionally, athletes participating a higher levels of sport have been shown to be at increased risk for posterior instability when compared to recreational athletes.5 In an analysis of shoulder injuries at the National Football League Combine, Kaplan et al found a history of a shoulder injury in 50% of participants, with recurrent posterior instability accounting for 4% of these injuries.70 In contact athletes such as football linemen, symptoms are reproduced with a posteriorly directed load in the common blocking position of forward flexion and internal rotation. Throwing athletes or golfers often describe symptoms in the follow-through phase of throwing or swing.65 In racket sports symptoms often occur with a backhand stroke. Swimmers typically report symptoms during the pull-through phase of swimming, and butterfly swimmers are particularly predisposed to posterior instability.65,69 In a young athlete presenting with vague shoulder complaints, posterior instability must be ruled out to avoid potential delayed or missed diagnosis.

PHYSICAL EXAMINATION A complete physical examination is essential to proper diagnosis of posterior glenohumeral instability, particularly because of the often vague and nonspecific nature of the presenting symptoms. Additionally, careful attention must be paid to signs of generalized hyperlaxity and volitional shoulder subluxation or dislocation because these may be indicative of MDI rather than pathologic posterior instability. Both shoulders should be examined for any signs of obvious dislocation, asymmetry, abnormal motion, muscle atrophy, or swelling. In the setting of an acute traumatic posterior dislocation event, the shoulder is often fixed in internal rotation with a block to external rotation as well as a posterior axillary fullness and prominent coracoid process.71 Acute posterior dislocations are often missed or delayed in diagnosis in up to 79% of patients; however, this incidence decreases significantly if adequate radiographs and physical examination are performed.71 Scapular motion should be examined and any dyskinesis should be noted. Range of motion is most commonly normal, but an increase in external rotation and slight loss of internal rotation is occasionally seen in patients with posterior instability.4,32,72 Several provocative maneuvers are particularly useful in diagnosing recurrent posterior instability. Although each has been demonstrated to be useful in detecting patients with recurrent posterior instability,73 the combination of provocative tests is essential to making the diagnosis. The Kim test,74 jerk test,47 load and shift test,75 and posterior stress test48 are all commonly performed to assess the degree of posterior instability. The Kim test is performed with the patient seated and the arm in 90 degrees of forward flexion and internal rotation. The examiner grasps the patient’s elbow with one hand and uses the other to grasp the lateral aspect of the patient’s proximal arm or places the hand on the scapula to provide scapular stabilization. A posterior translational force is applied and pain is indicative of a positive Kim test regardless of a palpable click or clunk.74 The downward pressure applied while performing the Kim test displaces the humeral head inferiorly and the axial load compresses the inferior portion of the posterior labrum. As such, pain elicited when performing this maneuver is highly sensitive for a posteroinferior labrum lesion.74 The jerk test is performed with the patient in the standing or seated position. The examiner stands next to the affected shoulder and grasps the elbow in one hand and the distal clavicle and scapular spine in the other. The arm is placed in a flexed, abducted, and internally rotated position and a posterior force is applied to the flexed elbow while an anterior force is applied to the shoulder girdle (Figure  16-1). In patients with posterior instability, this will result in a posterior dislocation or subluxation of the glenohumeral joint. The jerk test is positive when a sudden jerk associated with pain occurs as the subluxated humeral head translates out of the glenoid fossa and glides over the torn posterior labrum with

History and Examination of Posterior Instability adduction of the shoulder.4,74 With use of the thumb placed on the posterior glenohumeral joint as the hand stabilizes the scapula, a palpatory shift can usually be felt. A “reverse” jerk test can also be performed, and at times is more easily felt than a conventional jerk test. In the “reverse” jerk test, the arm is adducted 90 degrees, forward-flexed 90 degrees, and internally rotated. As the shoulder is taken from adduction to abduction, the reduction of the humeral head into the glenoid fossa can be felt with the thumb of the hand stabilizing the scapula. A combination of a positive Kim test and jerk test has been shown to have a 97% sensitivity for posterior instability.74 The load and shift test is performed with the patient seated or in the lateral decubitus position. The arm is positioned at approximately 20 degrees of forward elevation and abduction to achieve 45 to 60  degrees in the scapular plane. The examiner grasps the humeral head and gently compresses the head into the glenoid. An anterior and posterior stress is applied to grade the degree of translation of the humeral head. A modified load and shift test may be performed with the patient positioned in supine and the affected shoulder at the edge of the examination table. The examiner grasps the elbow and proximal arm and positions the humerus in the scapular plane. The humeral head is compressed into the glenoid and anterior and posterior forces are applied to grade the degree of translation. A grade 0 load and shift describes minimal translation of the humeral head. Grade 1 describes the humeral head translating to the glenoid rim. Grade 2 describes humeral head translation over the glenoid rim that spontaneously reduces. Grade 3 describes humeral head dislocation that does not spontaneously reduce. It is critical to examine the contralateral shoulder because a grade-2 or -2+ load and shift may be physiologic in young athletes.15 Additionally, excessive inferior translation observed with the load and shift test is often associated with posterior subluxation but may also indicate bidirectional instability or MDI.39 The posterior stress test is performed with the patient seated or supine. The examiner grasps the arm at the elbow and, if performed in the seated position, uses the other hand to stabilize the medial border of the scapula. The arm is flexed to 90 degrees, adducted, and internally rotated. A posterior force is applied to the arm to axially load the humerus against the posterior glenoid. The posterior stress test is positive if a posterior subluxation or dislocation occurs with reproduction of the patient’s pain or apprehension. Patients with suspected posterior glenohumeral instability should be examined for bidirectional instability or MDI. Excessive inferior translation of the humerus on the glenoid is often associated with posterior instability.65,76 The sulcus test is performed with the patient seated and the arm in a neutral position. The examiner grasps the patient’s elbow and applies downward traction while observing the interval between the greater tuberosity and the acromion. If a depression is observed, this may be indicative of inferior instability. A sulcus sign greater than 2  cm is highly suggestive of MDI. If the sulcus does not reduce when the arm is brought

191

Figure 16-1. The jerk test is performed with the patient’s shoulder in a forward-flexed and internally rotated position. The examiner places a hand on the elbow and the opposite hand on the scapula. Placing the thumb on the posterior glenohumeral joint can improve tactile sense of subluxation/dislocation during the maneuver. With a posteriorly directed force, the arm is taken from abduction or neutral position into adduction. A posterior subluxation or dislocation is indicative of a positive jerk test.

into external rotation, it can be considered pathologic with a defect in the rotator interval.65 The Gagey test is also useful in determining insufficiency of the IGHL. The examiner stands on the side of the affected extremity and with one hand grasps the elbow and stabilizes the scapula with the other. The arm is held in neutral rotation and abducted. The test is considered positive if passive abduction of greater than 105 degrees is achieved. In the setting of posterior instability, the Gagey test may be useful for determining the presence of a RHAGL or HAGL lesion.65,78 A positive finding may also be indicative of inferior or MDI. Patients should also be examined for generalized signs of hyperlaxity using the criteria established by Beighton et al.78

IMAGING Imaging evaluation of patients with posterior instability begins with plain radiographs. A standard anteroposterior, Grashey, scapular-Y, and axillary view of the shoulder should be obtained. Radiographs are typically normal; however, the axillary or Velpeau view is useful in evaluating the morphology of the glenoid and humeral head. Occasionally an RHSL may be seen, indicating a prior posterior dislocation or subluxation. Additionally, the axillary view provides information regarding glenoid version, dysplasia, and the station of the humerus on the glenoid.4,32 In the event of an acute posterior dislocation, attention should be paid to the anteroposterior and lateral radiographs to assess for fixed internal rotation or the “lightbulb sign,” in which the internally rotated humeral head appears smooth. A Grashey view may also show the “trough line” sign, indicative of medial humeral head impaction or potentially medial migration of

192

Chapter 16

Figure 16-2. Left shoulder radiographs. (A) Grashey view demonstrating the “trough line” sign. (B) Axillary view demonstration a posterior dislocation with a reverse Hill-Sachs lesion.

Figure 16-3. Left shoulder, magnetic resonance arthrogram, protondensity axial image demonstrating a posterior labral tear (arrow).

the humeral head.71 A reverse bony Bankart lesion may also occasionally be evident on plain radiographs (Figure 16-2). CT is particularly useful in evaluating bony structures in patients with posterior instability. CT can be used to assess glenoid version and dysplasia. Additionally, 3-dimensional reconstructed images can be used to determine the extent of glenoid bone loss. Patients with significant glenoid bone loss may be indicated for a primary bony stabilization procedure because biomechanical studies have shown that patients with more than 20% posterior bone loss are predisposed to failure of arthroscopic stabilization.30 MRA is the study of choice when evaluating capsulolabral pathology in patients with recurrent posterior instability (Figure 16-3). MRA is essential for evaluating the soft tissues surrounding the glenohumeral joint and allows surgeons to characterize soft-tissue pathology to guide treatment. CT

Figure 16-4. Arthroscopic image of a right shoulder in the lateral position viewed from the posterior portal. Note the reverse Hill-Sachs lesion in the central aspect of the humeral head articular surface.

and magnetic resonance imaging/MRA both are valuable in assessing posterior bone loss and RHSLs, which occur anteriorly or centrally (Figure 16-4) on the humeral head and can result in more articular cartilage damage than conventional Hill-Sachs lesions from anterior instability. Patients with posterior instability have been shown to have an increased posterior capsular volume on MRA as a result of posterior humeral head translation stretching the weak posterior capsule.49 Lesions of the posterior capsulolabral structures, such as a reverse Bankart lesion or a RHAGL, are best visualized on MRA (Figure 16-5). Additionally, MRA is the most optimal study to visualize a Kim lesion or an incomplete avulsion of the posterior labrum. A Kim lesion appears as a marginal crack of the labrum and can be classified according to the criteria described by Kim and colleagues4,46 (Figure  16-6).

History and Examination of Posterior Instability

Figure 16-5. Left shoulder, MRA, proton- density axial image demonstrating a typical Kim lesion, with signal between the glenoid and posterior labrum. The tear does not span the entire attachment of the labrum to the glenoid, but rather is a partial tear or crack on MRA (arrow).

The 4 types of Kim lesions are as follows: type I, incomplete detachment; type II, incomplete and concealed avulsion (Kim lesion); type III, chondrolabral erosion; and type IV, flap tear. Kim lesions and other labral pathology are often significant pain generators resulting from acute or repetitive microtrauma, and their recognition is essential because patients with labral injury typically have successful outcomes from surgical intervention.7,22,67,69 (Table 16-1).

CONCLUSION Posterior glenohumeral instability is a challenging diagnosis because of the often vague presenting symptoms and relative infrequency of the condition when compared to anterior instability and other shoulder injuries in athletes. In overhead and contact athletes presenting with generalized shoulder pain, clinicians should maintain a high degree of suspicion for posterior instability. Although acute traumatic subluxation or dislocation may occur, the most frequent cause of posterior instability is recurrent microtrauma due to repetitive shearing forces of a posteriorly loaded glenohumeral joint with the arm in a forward-flexed, adducted, and internally rotated position. Additionally, an appreciation of the various static and dynamic stabilizers of the shoulder against posterior translation is essential for understanding the pathoanatomy and surgical options when addressing posterior instability. Provocative physical examination maneuvers, particularly the Kim and jerk tests, should be employed when athletes present with vague shoulder complaints and are highly sensitive for posterior instability. Posterior glenohumeral instability is increasingly recognized as a cause of

193

Figure 16-6. Left shoulder, magnetic resonance arthrogram, proton density coronal image demonstrating the typical appearance of a reverse humeral avulsion of the glenohumeral ligament lesion. The arthrogram dye is seen extending along the medial aspect of the humeral head because of the lack of capsular attachment of the glenohumeral ligament on the humerus (arrow).

Table 16-1. Kim Classification of Posterior Labrum Tears Type I

Incomplete detachment

Type II

Incomplete tear and concealed avulsion (Kim lesion)

Type III

Chondrolabral erosion

Type IV

Flap tear

shoulder pain in athletes that may lead to decreased performance, and specific historical keys and physical examination findings are essential to making the diagnosis.

REFERENCES 1.

2.

3.

Robins RJ, Daruwalla JH, Gamradt SC, McCarty EC, Dragoo JL, Hancock RE. Return to play after shoulder instability surgery in National Collegiate Athletic Association Division  I intercollegiate football athletes. Am J Sports Med. 2017;45(10):2329-2335. doi:10.1177/0363546517705635. Cameron KL, Mauntel TC, BD Owens. The epidemiology of glenohumeral joint instability: incidence, burden, and long-term consequences. Sports Med Arthrosc Rev. 2017;25(3):144-149. doi:10.1097/ JSA.0000000000000155. Neer CS  II. Involuntary inferior and multidirectional instability of the shoulder: etiology, recognition, and treatment. Instr Course Lect. 1985;34:232-238.

194 4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

14.

15.

16.

17.

18.

19.

20.

21.

22.

Chapter 16 Provencher MT, LeClere LE, King S, et  al. Posterior instability of the shoulder: diagnosis and management. Am J Sports Med. 2011;39(4):874-886. doi:10.1177/0363546510384232. Lanzi JT, Chandler PJ, Cameron KL, Bader JM, Owens BD. Epidemiology of posterior glenohumeral instability in a young athletic population. Am J Sports Med. 2017;45(14):3315-3321. doi:10.1177/0363546517725067. Owens M, Duffey ML, Nelson BJ, DeBerardino TM, Taylor DC, Mountcastle SB. The incidence and characteristics of shoulder instability at the United States Military Academy. Am J Sports Med. 2007;35(7):1168-1173. doi:10.1177/0363546506295179. Bottoni CR, Franks BR, Moore JH, DeBerardino TM, Taylor DC, Arciero RA. Operative stabilization of posterior shoulder instability. Am J Sports Med. 2005;33(7):996-1002. doi:10.1177/0363546504271509. Tannenbaum EP, Sekiya JK. Posterior shoulder instability in the contact athlete. Clin Sports Med. 2013;32(4):781-796. doi:10.1016/j. csm.2013.07.011. Owens BD, Campbell SE, Cameron KL. Risk factors for posterior shoulder instability in young athletes. Am J Sports Med. 2013;41(11):2645-2649. doi:10.1177/0363546513501508. Dickens JF, Kilcoyne KG, Haniuk E, Owens BD. Combined lesions of the glenoid labrum. Phys Sportsmed. 2012;40(1):102-108. doi:10.3810/psm.2012.02.1956. Song DJ, Cook JB, Krul KP, et al. High frequency of posterior and combined shoulder instability in young active patients. J  Shoulder Elbow Surg. 2015;24(2):186-190. doi:10.1016/j.jse.2014.06.053. Matsen FA  III. The biomechanics of glenohumeral stability. J  Bone Joint Surg Am. 2002;84(3):495-496. doi:10.2106/00004623-200203000-00033. Turkel SJ, Panio MW, Marshall JL, Girgis FG. Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J  Bone Joint Surg Am. 1981;63(8):1208-1217. Ovesen J, Nielsen  S. Posterior instability of the shoulder. A cadaver study. Acta Orthop Scand. 1986;57(5):436-439. doi:10.3109/17453678609014766. Lintner S, Levy A, Kenter K, Speer KP. Glenohumeral translation in the asymptomatic athlete’s shoulder and its relationship to other clinically measurable anthropometric variables. Am J Sports Med. 1996;24(6):716-720. doi:10.1177/036354659602400603. O’Connell PW, Nuber GW, Mileski RA, Lautenschlager  E. The contribution of the glenohumeral ligaments to anterior stability of the shoulder joint. Am J Sports Med. 1990;18(6):579-584. doi:10.1177/036354659001800604. Ovesen J, Nielsen  S. Stability of the shoulder joint. Cadaver study of stabilizing structures. Acta Orthop Scand. 1985;56(2):149-151. doi:10.3109/17453678508994342. Antosh IJ, Tokish JM, Owens BD. Posterior shoulder instability: current surgical management. Sports Health. 2016;8(6):620-626. doi:10.1177/1941738116672446. Randelli M, Gambrioli P. Glenohumeral osteometry by computed tomography in normal and unstable shoulders. Clin Orthop Relat Res. 1986;(208):151-156. Matsumura N, Ogawa K, Kobayashi S, et  al. Morphologic features of humeral head and glenoid version in the normal glenohumeral joint. J  Shoulder Elbow Surg. 2014;23(11):1724-1730. doi:10.1016/j. jse.2014.02.020. Brewer BJ, Wubben RC, Carrera GF. Excessive retroversion of the glenoid cavity. A cause of non-traumatic posterior instability of the shoulder. J Bone Joint Surg Am. 1986;68(5):724-731. Bradley JP, Baker CL  III, Kline AJ, Armfield DR, Chhabra  A. Arthroscopic capsulolabral reconstruction for posterior instability of the shoulder: a prospective study of 100 shoulders. Am J Sports Med. 2006;34(7):1061-1071. doi:10.1177/0363546505285585.

23.

24.

25.

26. 27.

28.

29.

30.

31.

32.

33.

34.

35.

36.

37. 38.

39.

40. 41.

Parada SA, Eichinger JK, Dumont GD, et al. Comparison of glenoid version and posterior humeral subluxation in patients with and without posterior shoulder instability. Arthroscopy. 2017;33(2):254-260. doi:10.1016/j.arthro.2016.06.023. Eichinger JK, Galvin JW, Grassbaugh JA, Parada SA, Li X. Glenoid dysplasia: pathophysiology, diagnosis, and management. J Bone Joint Surg Am. 2016;98(11):958-968. doi:10.2106/JBJS.15.00916. Inui H, Sugamoto K, Miyamoto T, et  al. Glenoid shape in atraumatic posterior instability of the shoulder. Clin Orthop Relat Res. 2002;(403):87-92. doi:10.1097/00003086-200210000-00014. Edelson  J. Localized glenoid hypoplasia. Clin Orthop Relat Res. 1995;(321):189-195. Weishaupt D, Zanetti M, Nyffeler RW, Gerber C, Hodler J. Posterior glenoid rim deficiency in recurrent (atraumatic) posterior shoulder instability. Skeletal Radiol. 2000;29(4):204-210. doi:10.1007/ s002560050594. Harper KW, et al. Glenoid dysplasia: incidence and association with posterior labral tears as evaluated by MRI. AJR Am J Roentgenol. 2004;182(4):59. Hines A, Cook JB, Shaha JS, et  al. Glenoid bone loss in posterior shoulder instability: prevalence and outcomes in arthroscopic treatment. Am J Sports Med. 2018;46(5):1053-1057. doi:10.1177/0363546517750628. Nacca C, Gil JA, Badida R, Crisco JJ, Owens BD. Critical glenoid bone loss in posterior shoulder instability. Am J Sports Med. 2018;46(5):1058-1063. doi:10.1177/0363546518758015. Bäcker HC, Galle SE, Maniglio M, Rosenwasser MP. Biomechanics of posterior shoulder instability—current knowledge and literature review. World J Orthop. 2018;9(11):245-254. doi:10.5312/wjo. v9.i11.245. Frank, RM, Romeo AA, Provencher MT. Posterior glenohumeral instability: evidence-based treatment. J  Am Acad Orthop Surg. 2017;25(9):610-623. doi:10.5435/JAAOS-D-15-00631. Moroder P, Plachel F, Tauber M, et al. Risk of engagement of bipolar bone defects in posterior shoulder instability. Am J Sports Med. 2017;45(12):2835-2839. doi:10.1177/0363546517714456. Longo UG, Rizzello G, Locher J, et  al. Bone loss in patients with posterior gleno-humeral instability: a systematic review. Knee Surg Sports Traumatol Arthrosc. 2016;24(2):612-617. doi:10.1007/ s00167-014-3161-8. Skendzel JG, Sekiya JK. Diagnosis and management of humeral head bone loss in shoulder instability. Am J Sports Med. 2012;40(11):26332644. doi:10.1177/0363546512437314. Lazarus MD, Sidles JA, Harryman DT II, Matsen FA III. Effect of a chondral-labral defect on glenoid concavity and glenohumeral stability. A cadaveric model. J Bone Joint Surg Am. 1996;78(1):94-102. doi:10.2106/00004623-199601000-00013. Lippitt S, Matsen F. Mechanisms of glenohumeral joint stability. Clin Orthop Relat Res. 1993;(291):20-28. Kim S, Noh KC, Park JS, Ryu BD, Oh I. Loss of chondrolabral containment of the glenohumeral joint in atraumatic posteroinferior multidirectional instability. J Bone Joint Surg Am. 2005;87(1):92-98. doi:10.2106/JBJS.C.01448. Hawkins RJ, Janda DH. Posterior instability of the glenohumeral joint. A technique of repair. Am J Sports Med. 1996;24(3):275-278. doi:10.1177/036354659602400305 Hawkins RJ, McCormack RG. Posterior shoulder instability. Orthopedics. 1988;11(1):101-107. Bey MJ, Hunter SA, Kilambi N, Butler DL, Lindenfeld TN. Structural and mechanical properties of the glenohumeral joint posterior capsule. J  Shoulder Elbow Surg. 2005;14(2):201-206. doi:10.1016/j. jse.2004.06.016.

History and Examination of Posterior Instability 42.

43.

44.

45.

46.

47.

48. 49.

50.

51.

52.

53.

54.

55.

56.

57.

58.

59.

Park JY, Lee SJ, Lhee SH, Oh JH. Change in labrum height after arthroscopic Bankart repair: correlation with preoperative tissue quality and clinical outcome. J  Shoulder Elbow Surg. 2012;21(12):17121720. doi:10.1016/j.jse.2012.04.009. Bradley JP, McClincy MP, Arner JW, Tejwani SG. Arthroscopic capsulolabral reconstruction for posterior instability of the shoulder: a prospective study of 200 shoulders. Am J Sports Med. 2013;41(9):20052014. doi:10.1177/0363546513493599. Wellmann M, Blasig H, Bobrowitsch E, et al. The biomechanical effect of specific labral and capsular lesions on posterior shoulder instability. Arch Orthop Trauma Surg. 2011;131(3):421-427. doi:10.1007/ s00402-010-1232-y. Yu JS, Ashman CJ, Jones G. The POLPSA lesion: MR imaging findings with arthroscopic correlation in patients with posterior instability. Skeletal Radiol. 2002;31(7):396-399. doi:10.1007/s00256-002-0513-0. Kim SH, Ha KI, Yoo JC, Noh KC. Kim’s lesion: an incomplete and concealed avulsion of the posteroinferior labrum in posterior or multidirectional posteroinferior instability of the shoulder. Arthroscopy. 2004;20(7):712-720. doi:10.1016/j.arthro.2004.06.012. Blasier R, Soslowsky LJ, Malicky DM, Palmer ML. Posterior glenohumeral subluxation: active and passive stabilization in a biomechanical model. J Bone Joint Surg Am. 1997;79(3):433-440. Pollock RG, Bigliani LU. Recurrent posterior shoulder instability. Diagnosis and treatment. Clin Orthop Rel Res. 1993;(291):85-96. Dewing C, McCormick F, Bell SJ, et  al. An analysis of capsular area in patients with anterior, posterior, and multidirectional shoulder instability. Am J Sports Med. 2008;36(3):515-522. doi:10.1177/0363546507311603. Rebolledo BJ, et  al. Posterior humeral avulsion of the glenohumeral ligament and associated injuries: assessment using magnetic resonance imaging. Am J Sports Med. 2015;43(12):2913-2917. doi:10.1177/0363546515606427. Provencher MT, McCormick F, LeClere L, et  al. Prospective evaluation of surgical treatment of humeral avulsions of the glenohumeral ligament. Am J Sports Med. 2017;45(5):1134-1140. doi: 10.1177/0363546516680608. O’Brien SJ, Neves MC, Arnoczky SP, et al. The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med. 1990;18(5):449-456. doi:10.1177/036354659001800501. Bigliani LU, Kelkar R, Flatow EL, Pollock RG, Mow VC. Glenohumeral stability. Biomechanical properties of passive and active stabilizers. Clin Orthop Relat Res. 1996;(330):13-30. Bradley JP, Tejwani SG. Arthroscopic management of posterior instability. Orthop Clin North Am. 2010;41(3):339-356. doi:10.1016/j. ocl.2010.02.002. Harryman DT II, Sidles JA, Clark JM, McQuade KJ, Gibb TD, Matsen FA III. Translation of the humeral head on the glenoid with passive glenohumeral motion. J Bone Joint Surg Am. 1990;72(9):1334-1343. Provencher MT, Mologne TS, Hongo M, Zhao K, Tasto JP, An KN. Arthroscopic versus open rotator interval closure: biomechanical evaluation of stability and motion. Arthroscopy. 2007;23(6):583-592. doi:10.1016/j.arthro.2007.01.010. Provencher MT, Dewing CB, Bell SJ, et al. An analysis of the rotator interval in patients with anterior, posterior, and multidirectional shoulder instability. Arthroscopy. 2008;24(8):921-929. doi:10.1016/j. arthro.2008.03.005. Ovesen J, Nielsen  S. Anterior and posterior shoulder instability. A cadaver study. Acta Orthop Scand. 1986;57(4):324-327. doi:10.3109/17453678608994402. Saha  A. Mechanics of elevation of glenohumeral joint. Its application in rehabilitation of flail shoulder in upper brachial plexus injuries and poliomyelitis and in replacement of the upper humerus by prosthesis. Acta Orthop Scand. 1973;44(5):668-678. doi:10.3109/17453677308989106.

60.

61.

62.

63.

64.

65.

66.

67.

68. 69.

70.

71.

72. 73.

74.

75.

76.

77. 78.

195

McIntyre LF, Caspari RB, Savoie FH  III. The arthroscopic treatment of posterior shoulder instability: two-year results of a multiple suture technique. Arthroscopy. 1997;13(4):426-432. doi:10.1016/ s0749-8063(97)90119-5. Matsen FA  III, Chebli C, Lippitt S; American Academy of Orthopaedic Surgeons. Principles for the evaluation and management of shoulder instability. J Bone Joint Surg Am. 2006;88(3):648659. doi:10.2106/00004623-200603000-00026. Soslowsky LJ, Malicky DM, Blasier RB. Active and passive factors in inferior glenohumeral stabilization: a biomechanical model. J  Shoulder Elbow Surg. 1997;6(4):371-379. doi:10.1016/ s1058-2746(97)90005-7. Ludewig PM, Reynolds JF. The association of scapular kinematics and glenohumeral joint pathologies. J  Orthop Sports Phys Ther. 2009;39(2):90-104. doi:10.2519/jospt.2009.2808. Hawkins RJ, Koppert G, Johnston  G. Recurrent posterior instability (subluxation) of the shoulder. J  Bone Joint Surg Am. 1984;66(2):169-174. Millett PJ, Clavert P, Hatch GF  III, Warner JJ. Recurrent posterior shoulder instability. J  Am Acad Orthop Surg. 2006;14(8):464-476. doi:10.5435/00124635-200608000-00004. Abrams JS. Arthroscopic repair of posterior instability and reverse humeral glenohumeral ligament avulsion lesions. Orthop Clin North Am. 2003;34(4):475-483. doi:10.1016/s0030-5898(03)00090-7. Kim S, Ha KI, Park JH, et al. Arthroscopic posterior labral repair and capsular shift for traumatic unidirectional recurrent posterior subluxation of the shoulder. J Bone Joint Surg Am. 2003;85(8):1479-1487. doi:10.2106/00004623-200308000-00008. Robinson CM, Aderinto J. Recurrent posterior shoulder instability. J Bone Joint Surg Am. 2005;87(4):883-892. doi:10.2106/JBJS.D.02906. Bradley JP, Forsythe B, Mascarenhas R. Arthroscopic management of posterior shoulder instability: diagnosis, indications, and technique. Clin Sports Med. 2008;27(4):649-670. doi:10.1016/j.csm.2008.06.001. Kaplan LD, Flanigan DC, Norwig J, Jost P, Bradley J. Prevalence and variance of shoulder injuries in elite collegiate football players. Am J Sports Med. 2005;33(8):1142-1146. doi:10.1177/0363546505274718. Rouleau DM, Hebert-Davies J, Robinson CM. Acute traumatic posterior shoulder dislocation. J Am Acad Orthop Surg. 2014;22(3):145152. doi:10.5435/JAAOS-22-03-145. Fronek J, Warren RF, Bowen M. Posterior subluxation of the glenohumeral joint. J Bone Joint Surg Am. 1989;71(2):205-216. Owens BD, Duffey ML, Deberardino TM, Cameron KL. Physical examination findings in young athletes correlate with history of shoulder instability. Orthopedics. 2011;34(6):460-464. doi:10.3928/01477447-20110427-21. Kim S, Park JS, Jeong WK, Shin SK. The Kim test: a novel test for posteroinferior labral lesion of the shoulder—a comparison to the jerk test. Am J Sports Med. 2005;33(8):1188-1192. doi:10.1177/0363546504272687. Gerber C, Ganz R. Clinical assessment of instability of the shoulder. With special reference to anterior and posterior drawer tests. J Bone Joint Surg Br. 1984;66(4):551-556. Hawkins RH. Glenoid osteotomy for recurrent posterior subluxation of the shoulder: assessment by computed axial tomography. J Shoulder Elbow Surg. 1996;5(5):393-400. doi:10.1016/s1058-2746(96)80071-1. Hawkins R, Belle R. Posterior instability of the shoulder. Instr Course Lect. 1989;38:211-215. Beighton P, De Paepe A, Steinmann B, Tsipouras P, Wenstrup RJ. Ehlers-Danlos syndromes: revised nosology, Villefranche, 1997. Ehlers-Danlos National Foundation (USA) and Ehlers-Danlos Support Group (UK). Am J Med Genetics. 1998;77(1):31-37. doi:10 .1002/(sici)1096-8628(19980428)77:13.0.co;2-o.

17 Imaging of Posterior Shoulder Instability Josef K. Eichinger, MD, FAOA and Joseph W. Galvin, DO, FAAOS

Posterior shoulder instability is becoming increasingly recognized in young, athletic populations, especially in the military.1-3 Compared to anterior shoulder instability, posterior instability can be more challenging to diagnose both clinically and radiographically. Patients often do not experience frank posterior dislocation events such as that with anterior shoulder instability and more commonly develop attritional lesions. As a result posterior shoulder instability may present with vague shoulder pain, and a clinical examination is less demonstrative than anterior shoulder instability and may therefore be more difficult to diagnose. Imaging studies therefore are an impor tant adjunct to the diagnosis and treatment of posterior shoulder instability. However, imaging studies do not always demonstrate obvious pathologic findings and thus a nuanced approach to the interpretation of x-rays, computed tomography (CT), and magnetic resonance imaging (MRI) is necessary to elucidate and identify subtle findings that can enable the clinician to make the correct diagnosis. In this chapter we will review imaging findings of posterior instability on standard radiographs, CT scan, MRI, and magnetic resonance arthrogram (MRA), and 3-dimensional (3D) reconstruction CT and 3D MRI, which assist in the diagnosis and treatment of symptomatic posterior shoulder instability.

X-RAYS Plain radiographs in patients with posterior shoulder instability are an impor tant and critical adjunct to making the diagnosis of posterior shoulder instability. Biplanar radiographs should always be obtained when evaluating patients with suspected shoulder instability. An anteroposterior (AP)

Grashey image (also known as a “true AP” view because the beam is oriented perpendicular to the scapula, which is oriented 30 degrees anterior to the coronal plane) (Figure 17-1) along with an axillary x-ray (Figure 17-2), are the minimum radiographs that should be obtained. Although x-ray findings are typically normal, they must be scrutinized to avoid errors of diagnosis such as missed posterior dislocations. Diagnosis of a locked posterior humeral dislocation can be avoided by recognizing on the AP Grashey radiograph the presence of the “lightbulb sign” (Figure 17-3A), which is the humeral head taking on a rounded appearance similar to the shape of a lightbulb because of fixed internal rotation secondary to a posterior glenohumeral dislocation.4 In addition to recognizing the lightbulb sign on an AP Grashey radiograph, an axillary x-ray will confirm the diagnosis of a locked posterior dislocation (Figure 17-3B). In addition to aiding in the recognition of a locked posterior dislocation, the axillary radiograph is necessary to a complete an orthogonal radiographic analysis. If the patient is unable to abduct the arm, then a Velpeau view is an alternate orthogonal radiograph (Figure 17-4). The axillary radiograph is also helpful in the traumatic scenario for identifying a posterior glenoid rim fracture or a reverse Hill-Sachs lesion. X-rays also demonstrate evidence of glenoid dysplasia (increased retroversion and hypoplasia), arthritic changes, and posterior humeral head subluxation or decentering of the humeral head. Other radiographic lesions that may be associated with posterior labral pathology and instability include the Bennett lesion, which is an extra-articular posterior ossification of the posterior inferior glenoid. Bennett lesions are more commonly found in overhead athletes, typically baseball players, and can be visualized on axillary radiographs.5 The development

- 197 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 197-204). © 2021 SLACK Incorporated.

198

Chapter 17

A

Figure 17-1. True anteroposterior or Grashey x-ray.

B

Figure 17-2. Axillary x-ray. Figure 17-3. (A) Lightbulb sign demonstrating rounded appearance of the humeral head with a posterior glenohumeral dislocation. (B) Axillary radiograph of locked posterior glenohumeral dislocation.

Figure 17-4. Velpeau axillary x-ray.

of this lesion is hypothesized to be secondary to either traction of the posterior band inferior glenohumeral ligament during the throwing deceleration phase, or impingement in the cocking phase.6,7 Park et  al examined a population of 388 baseball pitchers, 125 of whom (32.2%) had Bennett lesions. When comparing the 2 groups, they found that 12% of patients in the Bennett group had a posterior labral tear on MRI, whereas only 6.8% of patients in the non-Bennett group had a documented posterior labral tear, although the results were not statistically significant.8 Therefore, although Bennett lesions are typically not associated with posterior shoulder instability, it is impor tant to recognize these lesions because they can be associated with posterior labral tears.

Imaging of Posterior Shoulder Instability

199

Additionally, a recent study by Meyer et  al9 highlighted the importance of x-rays in evaluation of posterior shoulder instability. The authors found that specific acromial morphology on scapular-Y x-rays is significantly associated with the direction of glenohumeral instability. In shoulders with posterior instability, the acromion is situated higher and is oriented more horizontally in the sagittal plane than in normal shoulders and those with anterior instability. Future larger studies are needed to confirm these findings.

COMPUTED TOMOGRAPHY SCAN Following plain radiographs, a CT scan is another useful imaging modality to evaluate the bony morphology of the glenoid including retroversion, glenoid dysplasia, and glenoid bone loss (GBL), and to further characterize the size and location of a reverse Hill-Sachs lesion. A CT scan is typically performed to evaluate posterior bone loss due to either a reverse bony Bankart lesion or attritional bone loss, and to assess degree of retroversion and glenoid dysplasia, and is performed in revision scenarios. Also, it allows preoperative planning if a posterior bone block procedure is planned. Glenoid retroversion has been shown to be a risk factor for posterior shoulder instability.3 In a prospective study of 714 West Point cadets who were followed for 4 years, 46 shoulders had a documented glenohumeral instability event, 7 of which (10%) were posterior instability. Glenoid retroversion was significantly associated with the development of posterior shoulder instability (P < .001). Similarly, Bradley and colleagues found that in a cohort of 100 shoulders that underwent arthroscopic capsulolabral repair, patients with posterior instability had significantly greater chondrolabral injury and osseous retroversion in comparison with controls.10 The measurement of glenoid retroversion on 2-dimensional CT scan is performed by using Friedman’s method, which has been validated and accepted (Figure  17-5).11 It is generally accepted that normal glenoid version is between 4 to 7 degrees of retroversion. Although increased glenoid retroversion is a risk factor for posterior shoulder instability, there is little evidence to support the claim that increasing glenoid retroversion is associated with worse outcomes following posterior labral repair.12 Hurley et al found that patients with symptomatic posterior instability and glenoid retroversion of greater than 9 degrees had higher recurrence rates after open soft-tissue procedures.13 Conversely, Bigliani and colleagues performed CT scans for 16 of 35 shoulders prior to an open posterior capsular shift and found the average retroversion was –6 degrees.14 Their surgical cohort had an 80% success rate but they did not attribute their failures to osseous anatomy. Mauro et  al found increased retroversion in a cohort of 118 patients who were operatively treated for posterior instability in comparison with a group of normal controls, but the authors did not attribute retroversion as a risk factor for failure. They did find that smaller glenoid width was a risk factor for failure.12

Figure 17-5. Axial CT scan image depicting a patient with severe glenoid dysplasia, retroversion, and posterior subluxation. Measurement of Friedman’s angle and posterior humeral head subluxation (yellow lines depict Friedman’s angle; red line depicts percentage of posterior humeral head subluxation).

Glenoid Dysplasia and Hypoplasia Severe glenoid dysplasia or hypoplasia is a rare condition due to either brachial plexus birth palsy or a developmental abnormality with lack of stimulation of the inferior glenoid ossification center. These terms are interchangeable because there is underdevelopment of the posterior inferior aspect of the glenoid. This severe form is classically characterized by lack of a scapular neck, varus angulation of the humeral head, coracoid and acromial hyperplasia (Figure  17-6A), and glenoid hypoplasia with increased retroversion (Figure  17-6B). With increased advancements in CT and MRI, more subtle forms of glenoid dysplasia have been recognized. Edelson was the first to define the incidence of subtle forms of glenoid dysplasia by studying scapular specimens from several museum collections.15 Posteroinferior hypoplasia was defined as a “dropping away” of the normally flat plateau of the posterior part of the glenoid beginning 1.2 cm caudad to the scapular spine (Figure 17-7). Glenoid dysplasia/hypoplasia occurred in 19% to 35% of specimens.15,16 Additionally, several studies have identified that subtle posteroinferior glenoid deficiency and hypoplasia are significantly associated with posterior labral tears and symptomatic posterior shoulder instability.17-19 Weishaupt et al18 used CT arthrograms to determine the incidence and severity of glenoid dysplasia in a population of patients with atraumatic posterior shoulder instability. They developed a classification system in which

200

Chapter 17

A

Figure 17-7. The qualitative descriptions of glenoid dysplasia as developed by Edelson5 and Weishaupt et al.18 “Pointed” glenoid on axial imaging sequences is a normal-appearing glenoid without dysplasia, a “lazy J” has a rounded appearance of the posterior inferior glenoid, and a “delta” glenoid is a triangular osseous deficiency. (Adapted from Weishaupt D, Zanetti M, Nyffeler RW, Gerber C, Hodler J. Posterior glenoid rim deficiency in recurrent [atraumatic] posterior shoulder instability. Skeletal Radiol. 2000;29[4]:204-210. doi:10.1007/s002560050594.)

B

Figure 17-8. Axillary T1-weighted magnetic resonance imaging scan showing glenoid dysplasia with combined lesions of an enlarged posterior aspect of the labrum (blue arrow), retroversion, posterior humeral head subluxation, and posterior-inferior glenoid hypoplasia (orange star). Figure 17-6. (A) Anteroposterior radiograph of severe glenoid dysplasia showing hypoplasia of the glenoid neck (blue arrow) and coracoid enlargement (orange star). (B) Axillary radiograph demonstrating severe glenoid dysplasia with hypoplasia of the posterior glenoid and severe retroversion.

a “pointed” glenoid on axial imaging sequences is a normalappearing glenoid without dysplasia, a “lazy J” has a rounded appearance of the posterior inferior glenoid, and a “delta” glenoid is a triangular osseous deficiency. These are depicted in Figure  17-7. Harper and colleagues17 similarly developed a classification scheme with normal, mild, moderate, and severe glenoid dysplasia. Also, although better visualized on MRA imaging, a hypertrophied posterior glenoid labrum is evident in patients with glenoid dysplasia (Figure  17-8).

Despite multiple studies documenting a clear significant association between subtle glenoid dysplasia and posterior labral tears with associated posterior shoulder instability, there is little evidence demonstrating an association with worse outcomes following surgical intervention. Galvin et al performed a retrospective comparative outcomes analysis of 37 patients, mean age 28 years, who underwent arthroscopic posterior labral repair for symptomatic posterior shoulder instability with a mean follow-up of 3.1  years. Comparison between 18  patients with glenoid dysplasia and 19 patients without dysplasia revealed no significant difference in outcomes between the 2 groups.20

Imaging of Posterior Shoulder Instability CT scan axial cuts are also useful for evaluation of posterior humeral head subluxation, which is a measure of the position of the humeral head on the glenoid. Although no studies have correlated posterior humeral head subluxation with symptomatic posterior shoulder instability, there is evidence associating static posterior subluxation with retroversion and development of arthritis.21,22 Although 2-dimensional CT scans are helpful in identifying bony abnormalities, their accuracy in determining bone loss is limited and may overestimate or underestimate bone loss depending on how the patient lies in the CT gantry and how the axial images are formatted.23 CT scan with 3D reconstructions are therefore more accurate and useful for evaluating and calculating glenoid and humeral bone loss. Nacca and colleagues in a cadaveric study demonstrated that critical bone loss for posterior shoulder instability is 20% of the width of the glenoid articular surface.24 Multiple validated methods exist for calculation of GBL on 3D CT scan, including the linear measurement percentage method and a new effective technique, the circle line method.25 We prefer to use the circle line method because it has been shown to be reliable and easy to perform. First, select the best en face view of the glenoid on a 3D CT scan with humeral head subtraction. Next, create a best-fit circle of the inferior twothirds of the glenoid. Then, measure a line of bone loss that encompasses a straight line connecting only 2 points on the circle (chord). Finally, measure a line perpendicular to the line of bone loss to measure the diameter of the circle. A Microsoft Excel worksheet can be used to calculate the algebraic geometry to provide the percentage of bone loss. The linear measurement percentage method involves viewing an en  face view of the glenoid on a sagittal oblique CT image. A best-fit circle is drawn to fit the inferior two-thirds of the glenoid. The distance from the bare spot to the posterior glenoid rim is measured (A), followed by the measurement from the bare spot to the anterior glenoid rim (B). The percentage of posterior bone loss is calculated by the equation: (B − A/2 × B) × 100%. Lastly, a CT arthrogram is an effective tool to characterize capsulolabral pathology and a validated method of identifying clinically relevant lesions, and is helpful in the scenario in which an MRI may not be available.

MAGNETIC RESONANCE IMAGING/ MAGNETIC RESONANCE ARTHROGRAM Whereas MRI can identify cartilage and labral pathology, an MRA allows for a more comprehensive assessment of the suspected unstable shoulder and we recommend an MRA study for all suspected posterior labral pathology. The MRA increases the diagnostic accuracy and the ability to identify labral tears, capsular injuries such as tears, stretching, and avulsion patterns. The axillary sequences are commonly used to identify capsulolabral pathology, but both the coronal and axillary sequences can assist in identifying specific

201

Figure 17-9. Coronal T2 MRA sequence demonstrating posterior-inferior capsular stretch lesion (blue arrow), and axillary neurovascular structures (red arrow).

features of an injury pattern, which is extremely helpful for surgical planning and having awareness of the nature of the injury. Identification of a stretched or elongated capsule will allow for the recognition that a capsular plication may be necessary (Figure  17-9). Accurate identification of subtle capsular lesions may require manual adjustment of the “brightness” to visualize posterior humeral avulsion of the glenohumeral ligament (HAGL), also known as reverse HAGL (Figures 17-10A and 17-10B).26 Extravasation of contrast below the axillary neurovascular bundle is indicative of a HAGL lesion (Figure 17-11). MRA allows assessment of the “patulous” or enlarged capsular area. Recent research has sought to define the subjective assessment of an enlarged capsule. Dewing et  al examined the capsular area on MRA in a shoulder instability cohort and found that posterior and multidirectional instability patients had significantly larger capsular area measurements.26 Galvin and colleagues determined that the diagnosis of posterior shoulder instability was greater than 90% specific for a clinically symptomatic posterior labral tear when any of the following are present on MRA: axial posterior capsular area greater than 300  mm2, a sagittal linear capsular measurement greater than 12 mm, or a linear capsular length of 14 mm present on an axillary MRI sequence (Figure 17-12).19 MRA is also helpful in diagnosing a Kim lesion or chondrolabral separation that may not other wise be identified without contrast resolution (Figure  17-13).28,29 The chondrolabral separation is defined as a marginal crack and a superficial tear at the chondrolabral junction without complete detachment of the labrum. Kim et al28,29 noted that probing this lesion reveals detachment of the inner portion of the labrum from the medial surface of the glenoid. Lastly,

202

Chapter 17

A

Figure 17-11. Posterior humeral avulsion of the glenohumeral ligament (HAGL): sagittal T1 MRA sequence demonstrating the posterior HAGL. The figure is oriented with the posterior on the right side of the image and the posterior acromion is annotated with an orange star. Contrast extravasation down the posterior aspect of the humerus (blue arrow) inferior to the axillary neurovascular structures (yellow arrow) can be visualized.

B

Figure 17-10. (A) Axillary T1 MRA sequence demonstrating posterior humeral avulsion of the glenohumeral ligament (HAGL). Biceps are denoted with a green arrow and free edge of the posterior HAGL lesion (blue arrow). (B) Arthroscopic axillary pouch view of the lesion in (A) while viewing from a standard posterior arthroscopy portal.

not only does an MRA allow a thorough evaluation of the labrum, capsule, and posterior capsular volume, it also provides an assessment of the articular cartilage and the possible glenolabral articular disruption lesion.30

THREE-DIMENSIONAL MAGNETIC RESONANCE IMAGING Recently, there has been investigation into the role of 3D MRI in the evaluation of GBL.31 Currently 3D CT with

Figure 17-12. Axial MRA sequence with the axial linear capsular measurement equal to line “a” minus line “b.” This measurement quantifies the posterior capsular distention, which is commonly referred to as a patulous posterior capsule.

humeral head subtraction is commonly employed to evaluate GBL. Vopat and colleagues31 examined 8 shoulders with clinical instability both with 3D CT and 3D MRI and evaluated GBL and glenoid bone surface area. They concluded that

Imaging of Posterior Shoulder Instability

203

3D MRI of the glenoid is nearly identical to 3D CT scans for measurement of glenoid bone surface area and GBL, making 3D MRI a reliable, radiation-free alternative to a CT scan for a preoperative shoulder evaluation of glenoid pathology.

CONCLUSION Compared to anterior instability, posterior shoulder instability can be more challenging to diagnose clinically as well as radiographically. Therefore, it is essential for clinicians to combine a thorough history, physical examination, and review of appropriate imaging studies to successfully diagnose and treat symptomatic posterior shoulder instability. Orthogonal radiographs (AP and axillary lateral) are the appropriate initial imaging modality and can identify obvious findings indicating a diagnosis of posterior shoulder instability, including posterior glenoid rim fractures, reverse Hill-Sachs lesions, retroversion, and glenoid dysplasia. Recent evidence suggests that posterior acromial morphology identified on scapular-Y x-rays may assist in the diagnosis of posterior instability. CT arthrograms, MRI, and MRA are useful adjuncts for evaluating for labral tears, capsular tears, and avulsions (ie, reverse HAGL), and for assessing and identifying pathologic increased capsular volume. Finally, 3D reconstruction CT and 3D MRI are the imaging modalities of choice to define the location and severity of GBL, and these have impor tant implications for future surgical treatment.

REFERENCES 1.

2.

3.

4.

5. 6.

7.

8.

9.

Blomquist J, Solheim E, Liavaag S, Schroder CP, Espehaug B, Havelin LI. Shoulder instability surgery in Norway: the first report from a multicenter register, with 1-year follow-up. Acta Orthop. 2012;83(2):165-170. doi:10.3109/17453674.2011.641102. Song DJ, Cook JB, Krul KP, et al. High frequency of posterior and combined shoulder instability in young active patients. J Shoulder Elbow Surg. 2015;24(2):186-190. doi:10.1016/j.jse.2014.06.053. Owens BD, Campbell SE, Cameron KL. Risk factors for posterior shoulder instability in young athletes. Am J Sports Med. 2013;41(11):2645-2649. doi:10.1177/0363546513501508. Wolfson AB, Hendey GW, Ling LJ, Rosen CL, Schaider JJ, Sharieff GQ, eds. Harwood-Nuss’ Clinical Practice of Emergency Medicine. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2012. Bennett GE. Elbow and shoulder lesions of baseball players. Am J Surg. 1959;98:484-492. doi:10.1016/0002-9610(59)90542-2. Lombardo SJ, Jobe FW, Kerlan RK, Carter VS, Shields CL  Jr. Posterior shoulder lesions in throwing athletes. Am J Sports Med. 1977;5(3):106-110. doi:10.1177/036354657700500302. Ferrari JD, Ferrari DA, Coumas J, Pappas AM. Posterior ossification of the shoulder: the Bennett lesion. Etiology, diagnosis, and treatment. Am J Sports Med. 1994;22(2):171-175; discussion 175-176. doi:10.1177/036354659402200204. Park JY, Noh YM, Chung SW, et al. Bennett lesions in baseball players detected by magnetic resonance imaging: assessment of association factors. J Shoulder Elbow Surg. 2016;25(5):730-738. doi:10.1016/j. jse.2015.11.062. Meyer DC, Ernstbrunner E, Boyce G, Imam MA, Nashar RE, Gerber  C. Posterior acromial morphology is significantly associated with posterior shoulder instability. J  Bone Joint Surg Am. 2019;101(14):1253-1260. doi:10.2106/JBJS.18.00541.

Figure 17-13. Kim lesion: axial MRA image demonstrating a Kim lesion (blue arrow) and measurements for retroversion (yellow lines) and posterior humeral head subluxation (red line).

10.

11.

12.

13.

14.

15.

16.

17.

18.

Bradley JP, Baker CL  III, Kline AJ, Armfield DR, Chhabra  A. Arthroscopic capsulolabral reconstruction for posterior instability of the shoulder: a prospective study of 100 shoulders. Am J Sports Med. 2006;34(7):1061-1071. doi:10.1177/0363546505285585. Friedman RJ, Hawthorne KB, Genez BM. The use of computerized tomography in the measurement of glenoid version. J Bone Joint Surg Am. 1992;74(7):1032-1037. Mauro CS, McClincy MP, Bradley JP. Effect of glenoid version and width on outcomes of arthroscopic posterior shoulder stabilization. Am J Sports Med. 2016;44(4):941-947. doi:10.1177/0363546516631738. Hurley JA, Anderson TE, Dear W, Andrish JT, Bergfeld JA, Weiker GG. Posterior shoulder instability. Surgical versus conservative results with evaluation of glenoid version. Am J Sports Med. 1992;20(4):396-400. doi:10.1177/036354659202000405. Bigliani LU, Pollock RG, McIlveen SJ, Endrizzi DP, Flatow EL. Shift of the posteroinferior aspect of the capsule for recurrent posterior glenohumeral instability. J Bone Joint Surg Am. 1995;77(7):1011-1020. doi:10.2106/00004623-199507000-00006. Edelson JG. Localized glenoid hypoplasia. An anatomic variation of possible clinical significance. Clin Orthop Relat Res. 1995;(321):189-195. Eichinger JK, Galvin JW, Grassbaugh JA, Parada SA, Li X. Glenoid dysplasia: pathophysiology, diagnosis, and management. J Bone Joint Surg Am. 2016;98(11):958-968. doi:10.2106/JBJS.15.00916. Harper KW, Helms CA, Haystead CM, Higgins LD. Glenoid dysplasia: incidence and association with posterior labral tears as evaluated on MRI. AJR Am J Roentgenol. 2005;184(3):984-988. doi:10.2214/ ajr.184.3.01840984. Weishaupt D, Zanetti M, Nyffeler RW, Gerber C, Hodler J. Posterior glenoid rim deficiency in recurrent (atraumatic) posterior shoulder instability. Skeletal Radiol. 2000;29(4):204-210. doi:10.1007/ s002560050594.

204 19.

20.

21.

22.

23.

24.

Chapter 17 Galvin JW, Parada SA, Li X, Eichinger JK. Critical findings on magnetic resonance arthrograms in posterior shoulder instability compared with an age-matched controlled cohort. Am J Sports Med. 2016;44(12):3222-3229. doi:10.1177/0363546516660076. Galvin JW, Morte DR, Grassbaugh JA, Parada SA, Burns SH, Eichinger JK. Arthroscopic treatment of posterior shoulder instability in patients with and without glenoid dysplasia: a comparative outcomes analysis. J  Shoulder Elbow Surg. 2017;26(12):2103-2109. doi:10.1016/j.jse.2017.05.033. Parada SA, Eichinger JK, Dumont GD, et al. Comparison of glenoid version and posterior humeral subluxation in patients with and without posterior shoulder instability. Arthroscopy. 2017;33(2):254-260. doi:10.1016/j.arthro.2016.06.023. Walch G, Ascani C, Boulahia A, Nové-Josserand L, Edwards TB. Static posterior subluxation of the humeral head: an unrecognized entity responsible for glenohumeral osteoarthritis in the young adult. J Shoulder Elbow Surg. 2002;11(4):309-314. doi:10.1067/ mse.2002.124547. Gross DJ, Golijanin P, Dumont GD, et  al. The effect of sagittal rotation of the glenoid on axial glenoid width and glenoid version in computed tomography scan imaging. J  Shoulder Elbow Surg. 2016;25(1):61-68. doi:10.1016/j.jse.2015.06.017. Nacca C, Gil JA, Badida R, Crisco JJ, Owens BD. Critical glenoid bone loss in posterior shoulder instability. Am J Sports Med. 2018;46(5):1058-1063. doi:10.1177/0363546518758015.

25.

26.

27.

28.

29.

30.

31.

Parada SA, Eichinger JK, Dumont GD, et  al. Accuracy and reliability of a simple calculation for measuring glenoid bone loss on 3-dimensional computed tomography scans. Arthroscopy. 2018;34(1):84-92. doi:10.1016/j.arthro.2017.07.032. Shah AA, Butler RB, Fowler R, Higgins LD. Posterior capsular rupture causing posterior shoulder instability: a case report. Arthroscopy. 2011;27(9):1304-1307. doi:10.1016/j.arthro.2011.04.005. Dewing CB, McCormick F, Bell SJ, et  al. An analysis of capsular area in patients with anterior, posterior, and multidirectional shoulder instability. Am J Sports Med. 2008;36(3):515-522. doi:10.1177/0363546507311603. Kim SH, Noh KC, Park JS, Ryu BD, Oh I. Loss of chondrolabral containment of the glenohumeral joint in atraumatic posteroinferior multidirectional instability. J Bone Joint Surg Am. 2005;87(1):92-98. doi:10.2106/JBJS.C.01448. Kim SH, Ha KI, Yoo JC, Noh KC. Kim’s lesion: an incomplete and concealed avulsion of the posteroinferior labrum in posterior or multidirectional posteroinferior instability of the shoulder. Arthroscopy. 2004;20(7):712-720. doi:10.1016/j.arthro.2004.06.012. Shah N, Tung GA. Imaging signs of posterior glenohumeral instability. AJR Am J Roentgenol. 2009;192(3):730-735. doi:10.2214/ AJR.07.3849. Vopat BG, Cai W, Torriani M, et  al. Measurement of glenoid bone loss with 3-dimensional magnetic resonance imaging: a matched computed tomography analysis. Arthroscopy. 2018;34(12):31413147. doi:10.1016/j.arthro.2018.06.050.

18 Management of In-Season Athletes With Posterior Glenohumeral Instability Mark Slabaugh, MD, FAAOS and Christopher Gaunder, MD

The treatment of athletes who have been diagnosed with posterior instability in season is difficult because there is little literature regarding the most optimal treatment algorithm and best outcomes for these athletes. Variables such as timing of the injury, sport and position played, patient motivation, and the natural history of the disease all play a role in helping determine the best treatment for athletes in season with posterior instability. Surgical treatment in season will remove the athlete from the playing field but has the advantage of reducing the risk of recurrence. Rehabilitation and/ or bracing might facilitate returning to play within the same season but there is a risk of continued pain and/or instability. A team-based approach working with the team’s athletic trainer, physical therapist, and/or strength coach can help the team physician and athlete make an informed decision about how best to treat this pathology in season.

EPIDEMIOLOGY AND PATHOANATOMY Although less common than anterior instability, posterior instability poses a challenge to the orthopedic surgeon when diagnosing and treating in-season athletes. Posterior glenohumeral instability has become an increasingly recognized problem and cause of significant shoulder pain and dysfunction. It represents around 10% to 20% of all shoulder instability events in athletes and can be seen at a much higher percentage in collegiate athletes and military populations secondary to their fitness requirements.1,2 Longitudinal cohort studies have demonstrated that male intercollegiate athletes are among the highest-risk patient population to sustain injuries that will ultimately lead to posterior shoulder

instability needing surgical intervention.3 Male injury rates have been shown to be almost 9 times that of women in one longitudinal study looking at this specific injury.4 Whereas injury rates at a military academy for men have been shown to be 4.67 per 1000 person-years, in women it is only 2.04 per 1000 person-years.5 Sports with the highest incident rate of posterior instability are wrestling, football, gymnastics, and rugby in men, with basketball and rugby having the highest incident rate in women.5 Although the anatomic structures that make up the posterior aspect of the shoulder are well understood, there still remains questions as to whether it is the bony anatomy, softtissue laxity, or combination of both that could predispose to recurrent instability events. Glenoid retroversion has been questioned as a possible cause of posterior shoulder instability and is therefore an increasingly discussed topic because of its implications when it comes to addressing this problem surgically.5 It is thought that retroversion of the glenoid more than 10 degrees is a risk factor for posterior instability. Patients in one study were found to be 6  times more likely to have recurrent posterior instability with glenoid retroversion, and just 1-degree increased retroversion increases one’s risk of posterior instability 17%.6 It is currently unknown how much soft-tissue laxity contributes to isolated posterior pathology; however, it is well known that underlying elements of soft-tissue laxity can lead to injury of the posterior labrum.7,8 Static structures such as the glenoid labrum and posterior capsule have been shown to increase the depth of the glenoid, help with compression of the joint, contain the shoulder joint, and prevent shoulder subluxation posteriorly especially in adduction and internal rotation.9

- 205 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 205-214). © 2021 SLACK Incorporated.

206

Chapter 18

PRESENTATION OF IN-SEASON POSTERIOR INSTABILITY Unlike anterior instability in the athlete, the mechanism of injury can vary greatly depending on sport, position played, and level of competition. Frank traumatic dislocations, repetitive trauma, and ligamentous laxity make up the spectrum that these athletes can present with. Athletes who present with a frank dislocation in season are easily recognized because the injury is acute and the athlete will have an internally rotated and adducted shoulder with a history of a posterior directed force in a susceptible sport.10,11 Repetitive trauma with a posterior directed force is typically the culprit in sports such as weightlifting or football (interior linemen) and can lead to tearing of the labrum and capsule posteriorly. Ligamentous laxity is common in overhead athletes such as swimmers, volleyball players, and athletes who rely on increased range of motion of the shoulder to perform well in their sport leading to stretching out of the static stabilizers of the shoulder. These varying causes of posterior instability can make the diagnosis extremely difficult for sports medicine physicians, especially in athletes who wish to remain on the field of play.12 It has been noted that the most common cause of posterior instability is recurrent subluxation, and typically athletes present with pain rather than complaints of instability.12,13 Therefore, sports medicine physicians should have a high clinical suspicion when athletes present with posterior shoulder pain during competition or during practice. This is especially true in athletes who have frequent adducted, internal rotation with posterior directed forces as part of their sport. Moreover, subtle worsening in athletic performance or decreased endurance strength over a period of time especially in overhead athletes should make the clinician suspicious of posterior instability in an athlete.14 Athletes can also present with mechanical symptoms when describing posterior instability. Subtle clicking and popping throughout a range of motion may be described as the humeral head shears over the posteriorly torn labrum. Although less common, an athlete may describe frank instability or may be able to voluntarily dislocate the shoulder posteriorly on examination. Identifying at-risk athletes, who place posteriorly directed loads onto the shoulder, particularly swimmers, pitchers, weight lifters, and football players, will help physicians have a high index of suspicion for this entity. Additionally, attention should also be paid to athletes who as part of their sport are required to lift heavily, especially bench press or overhead lifting. Even batters with their lead shoulder are at risk of posterior shoulder instability.15,16 It is also well known that posterior shoulder instability is commonly found in conjunction with other shoulder conditions such as a superior labral tear, anterior labral tear, or capsular tears such as a reverse humeral avulsion of the glenoid ligaments. Therefore, because of the vague and varying presentation clinicians,

should consider posterior instability in any athlete with the insidious onset of shoulder pain.

PHYSICAL EXAMINATION To confirm the diagnosis, a complete physical evaluation of the athlete must be performed. The examination on the sideline during competition should be the same as in the office. Often this is difficult because sports that have a higher prevalence of posterior instability are typically those for which removal of protective equipment is required. Therefore, a player with a suspected posterior instability event should be removed from competition and taken to the training room where a detailed examination can be performed. This includes taking the helmet, pads, and shirt off. Evaluation of the affected shoulder should be performed comparing to the nonaffected side. If a posterior dislocation is suspected when an athlete is holding the arm in an adducted internally rotated position, the physician should palpate the shoulder for any changes in shoulder contour or depressions. Range of motion in patients with a posterior dislocation is very painful and significantly limited, especially external rotation. In these patients a reduction maneuver is attempted as quickly as possible after the dislocation to facilitate the ease of the reduction. We prefer to have the athlete lie in the prone position with the arm slightly off the table. Traction on the shoulder is coupled with pressure on the posterior aspect of the shoulder with external rotation and adduction. A clunk will be felt as the humerus reduces into the glenoid. Provocative exam maneuvers can be used to help delineate the subtleties of posterior glenohumeral instability. These tests help the provider identify painful sources that can lead to the posterior instability and eliminate other shoulder pathology. There are 4 routine tests that we use for the diagnosis of posterior instability, all of which are a variation of one another (Table  18-1).17-19 The diagnosis of posterior instability becomes much more sensitive when 2 or more of these exams are positive.17 These provocative tests during a game can be used to determine the extent of the injury and also help the physician to determine whether return to play is appropriate. Therefore, removing the patient from the game into the training room is key so a detailed examination can be performed. We have found that the push-pull test is especially helpful in determining return to play. If athletes have minimal pain with this test, they typically can be returned to play during the same competition. We typically like to simulate the forces they would experience in the game (ie, blocking) with the trainer in functional testing as well to determine whether they can safely be returned to play. If a patient can complete a voluntary jerk test, this is a more ominous indication of more significant pathology. If this maneuver is painful, then return to play is contraindicated. When posterior instability is suspected, imaging studies are indicated. This is especially true in patients with a

Management of In-Season Athletes With Posterior Glenohumeral Instability

207

Table 18-1. Physical Examination Tests for Posterior Instability 1. Jerk test: The patient sits upright with the arm forward elevated 90 degrees and internally rotated with an applied axial/posterior load to the humerus. Positive exam findings would include a clunk (dislocation) or pain often with another clunk (reduction) when the arm is brought back to abduction. 2. Kim test: The patient is seated with the arm in 90 degrees of abduction. While holding the patient’s elbow, the arm is elevated 45 degrees, simultaneously applying a downward posterior force on the arm. Positive exam findings would include pain or clunk. 3. Posterior load and shift test: The patient’s arm is placed in flexion, abduction and internal rotation with a posteriorly directed force. Positive exam findings would include pain or more translation than the contralateral side. 4. Push-pull test: Patient is lying supine with the shoulder in 90 degrees of abduction. The shoulder is posteriorly loaded. Positive findings would be pain or subluxation of the humeral head posteriorly or significant difference in the amount of translation when compared to the contralateral side (Figure 18-1).

Figure 18-1. Push-pull examination for posterior instability. The examiner’s hand is placed on the shaft of the humerus and a posterior directed force is placed on the glenohumeral joint. If the patient has pain with this maneuver, it is positive for posterior instability.

Figure 18-2. Magnetic resonance arthrogram showing a posterior labral tear in a football player with an associated chondral loose body. A loose body is a contraindication for return to play until surgically corrected.

suspected posterior dislocation. In athletes with an acute unreduced dislocation, we typically do not order x-rays to confirm the diagnosis because the physical exam findings are pronounced. However, we do order radiographs directly after the reduction to confirm the reduction. A true anteroposterior (Grashey view), scapular-Y, and axillary views should be obtained in all patients. The axillary view is impor tant to visualize a posterior dislocation, subluxation, or evidence of posterior glenoid bone loss or a posterior glenoid fracture. Magnetic resonance imaging (MRI) is also indicated in all athletes in season to evaluate the posterior soft tissue of the shoulder, including the labrum and posterior capsule. MR arthrogram is warranted in every patient with posterior instability unless there has been a recent traumatic dislocation where a traumatic effusion would be expected (Figure 18-2). We order an MRI in all patients with suspected posterior instability within a week of their instability event to ensure there are no contraindications to return to play (Table  18-2). In addition to posterior labral tears or posterior soft-tissue redundancy, several par ticular findings on MRI may be concerning for posterior instability. A reverse Hill-Sachs injury to the anterior humeral head secondary to subluxation or frank dislocation may be seen. There have also been descriptions of a posterior reverse humeral avulsion of the glenohumeral ligament.17,20 The MRI should also be scrutinized for any additional intra-articular findings because concomitant pathology is very frequent with posterior shoulder instability.

208

Chapter 18

Table 18-2. Contraindications to Nonoperative Treatment ●

●

●

●

●

●

●

●

●

Loose body Chondral defect or GLAD lesion Bony reverse Bankart or bone loss greater than 10% Large reverse Hill-Sachs lesion Reverse HAGL lesion Labral tear greater than 270 degrees of circumference of glenoid Gross instability on clinical examination (grade 3) Recurrent symptoms (pain or instability event) Failure of nonoperative treatment

Abbreviations: GLAD, glenoid labral articular defect; HAGL, humeral avulsion of the glenohumeral ligament.

DETERMINATION OF TREATMENT FOR IN-SEASON ATHLETES WITH POSTERIOR INSTABILITY The decision on how to best treat posterior instability in athletes in season is multifactorial and is best made with input from the entire medical team in conjunction with the athlete. Besides the team physician, the athletic trainer and the strength and conditioning coach will have keen insights and input and often know the athlete much better than the team physician. A team-based approach is key to the success of treating these athletes nonoperatively if this is the decision of the in-season athlete. Special consideration is warranted for patients with acute posterior instability during competition. During a game when a patient comes onto the sideline with complaints and mechanism consistent with a posterior instability event, the examination findings are key to determining whether the athlete can return to play in the same game. Those patients with full range of motion with protective equipment removed and minimal pain with a push-pull maneuver can be safely returned to play that same game. These patients typically have decreased strength right after the instability event; however, their strength quickly returns to normal and is painless within minutes and therefore can be safely returned to the game. Thus, we keep the athletes in the training room for serial examinations to determine return-to-play ability. We have found that if athletes have not had any improvement in their strength or push-pull within 10 minutes, then they should be kept from same-day competition. Radiographs are obtained that day or the next both in patients who return to play and those who do not return. In the office, when an athlete has a history and clinical examination combined with MRI findings of posterior instability and he or she is in season, the entire medical team

confers to ensure that all parties are on the same page so that the athlete doesn’t receive conflicting information. The team physician can then counsel athletes and their family about the risks and the benefits of continuing to play with posterior instability or having surgery to treat their pathology. A typical discussion includes the risk and benefits of operative and nonoperative treatment of this injury so the athlete can make an informed decision that is best for himself or herself, the team, and their future aspirations. The athlete is counseled that the current thinking would indicate that there is a lower risk of redislocation, continued pain, and further injury to the labrum over the long-term with operative treatment.13,21-23 Our initial findings (unpublished data) have indicated that approximately 70% of patients can be returned to sport the same season but more than two-thirds elect surgery at the end of the season. The athlete is also counseled that it is unknown how much damage could take place if he or she is allowed to play through the season and then opts for surgery at the end of the season. With the current literature, it is unclear whether treating posterior instability nonoperatively in season could lead to further damage to the labrum over the course of one season. However, it has been well documented that patients with posterior instability (chronic and acute) can be successfully treated operatively with a labral reconstruction.13,22 Therefore, immediate risks with nonoperative treatment are not currently as well elucidated as with anterior instability.24-26 With this discussion, the athlete is counseled that there are some benefits to waiting over pursuing operative intervention in some cases. There have been certain studies that have shown that patients can return to sport with nonoperative treatment. Several authors have advocated that physical therapy is effective in treating posterior instability and thus surgery can be avoided in a certain subset of patients.14,27,28 In a study of 19 consecutive patients, therapy was able to allow all patients to return to their respective sport but no Tegner level was mentioned and thus it is unknown whether they returned to the same level of play or just returned to sport.27 In a nonrandomized trial comparing nonoperative rehabilitation with operative stabilization for posterior instability, one study found that both groups had significantly better outcomes at 1 year after diagnosis and treatment even though the operative group fared better than the rehabilitation group. However, in this study the patients who were treated nonoperatively were younger and had more clinical laxity, making the comparison of results between groups difficult.28 Additionally, there was no mention about return to sport in either group. Most authors recommend treating posterior instability nonoperatively for a period of 3 to 6 months to determine whether patients can become pain free and more functional with a physical therapy-based regimen.9,12 When consenting patients about their risk of recurrent symptoms, it is impor tant to note that there is no study that has looked at posterior instability in athletes in season. There are a few studies that have indirectly looked at an athlete’s ability to return to sport with nonoperative treatment. In a

Management of In-Season Athletes With Posterior Glenohumeral Instability study looking at the effect of posterior labral tears on the playing time in National Football League (NFL) athletes, the authors found that 78 of 221 athletes at the NFL Combine with posterior labral tears were treated nonoperatively. 29 However, it is unknown when these athletes sustained their injury and how long they had been playing with their posterior instability. Though, this study did note there was no difference in playing time between those treated nonoperatively and those treated surgically in their first season in the NFL, indicating there is a role for conservative treatment in the appropriately selected patients. One could surmise that athletes could be treated at least for one season without a compromise in playing time. There are several factors to consider when contemplating treating athletes nonoperatively. The first consideration is the type of sport and the position that the athlete plays. Contact sports such as American football, in which athletes are exposed to significant posterior forces on the glenohumeral joint, make nonoperative treatment more difficult. Positions such as linemen, who are taught to keep their hands in close to their chest, are at much higher risk for failure of a course of nonoperative treatment because their blocking creates a posterior stress in the shoulder with relative internal rotation while trying to shed a blocker. In fact, the NFL study mentioned earlier has shown that the number of snaps linemen participate in during their second NFL season is significantly less both in offensive and defensive linemen with known posterior instability who were treated nonoperatively vs surgically.29 We consider athletes who compete in football, hockey, gymnastics, power lifting, and boxing to be more at risk for recurrent symptoms solely based on the sport they play. The second consideration to understand when educating athletes is the imaging or MRI findings. Those patients with a small Kim lesion and no evidence of patulous capsule are treated much differently from those with a glenoid labral articular defect lesion and a loose body. In fact, there are several key findings on MRI that would make nonoperative treatment of the in-season athlete less desirable. We consider the following findings on imaging to be contraindications to nonoperative treatment in season: loose body, chondral defects/glenoid labral articular defect lesions, bony reverse Bankart, or bone loss greater than 10%, large engaging reverse Hill-Sachs, reverse humeral avulsion of the glenohumeral ligament lesion, and labral tears that are greater than 270  degrees of the circumference of the glenoid (see Table 18-2). The last consideration for recommending nonoperative treatment is the severity of the injury. Athletes with posterior instability typically present with repetitive trauma and not one frank dislocation. It has been our experience that these patients with posterior instability typically present with pain and not frank instability, as other authors have found as well.30 We have found that the in-season rehabilitation is much quicker than for anterior instability. In a study of inseason bracing for anterior instability, the average time away

209

from sport was approximately 10 days for anterior instability.31 In our experience athletes treated nonoperatively with posterior instability typically recover within a week. For those athletes who have a frank dislocation, we are much more conservative and they need more time to recover, typically 2 to 4 weeks. The timing of the injury also plays a part in how we consent the athletes and their families. Those athletes who are injured at the beginning of the season or during the preseason are much more likely to return to competition than those who injure themselves during the last part of the season. Therefore, the time left during the season can help counsel athletes whether they will be able to return to play in season with posterior instability. Additionally, where an athlete is in terms of schooling can help determine the recommendation to continue playing vs immediate surgical intervention. Seniors in their last year of eligibility are much more apt to consider nonoperative treatment in season vs a freshman with several years of eligibility left. With all these considerations in mind, we feel that most athletes can be treated nonoperatively and we offer the following treatment algorithm to all of our athletes who still have more than 2 weeks of competition left in their season. For those who are at the end of their season, we typically do not offer this because the likelihood of getting them back to meaningful competition is less likely. We feel the risk of a subsequent in-season instability event is low and therefore the risk of further chondral, labral, or bone damage is likewise low. However, we admit that this is based on level V data in our own experience at a Division I program. Therefore, we are currently conducting a prospective study to determine whether our hypothesis is correct. Our preliminary findings are that approximately two-thirds of athletes can be treated with in-season physical therapy and returned to sport safely (ie, no further instability episodes) until the end of the season when the status of their shoulder can be readdressed and surgery can be performed if necessary. Our treatment algorithm is shown in Figure 18-3.

NONOPERATIVE TREATMENT For those athletes who desire to be treated nonoperatively and return to their sport in-season, a 4-phase therapy program is developed for the athlete with progression through the phases as soon as the athlete is able to complete each phase with no symptoms.32 The first phase, or acute phase, is begun right after the instability episode and focuses on reducing the inflammation from the traumatic subluxation or dislocation. The goals of this phase are to decrease pain, gain range of motion, and institute some simple strengthening exercises within the athlete’s tolerance. Initially, the therapist or trainer will initiate range-of-motion exercises with restrictions based on the athlete’s symptoms. If needed, passive range-of-motion exercises are instituted but the goal is to quickly move into active assisted or active range of motion for neuromuscular

210

Chapter 18

Figure 18-3. Treatment algorithm for athletes who present with posterior labral tear/instability in-season.

modulation to begin. As symptoms allow, isometric exercises are begun with focus on the internal and external rotators of the shoulder in addition to the deltoid. Initially, submaximal stimulation of these muscles is begun and then progressed as symptoms allow. Furthermore, modalities such as ice, laser therapy, and transcutaneous electrical nerve stimulation are used to facilitate pain control in this acute phase. We typically do not recommend any immobilization of the joint during this acute phase. The second phase typically begins as soon as the athlete has pain-free, full passive range of motion of the shoulder and active motion up to 90 degrees of forward elevation. The goals of this phase are to achieve full pain-free active range of motion in all planes and dynamic glenohumeral control. To facilitate progression and healing of the injury, isotonic exercises are begun and focus on rotator cuff strengthening of the supraspinatus and infraspinatus. Scapular control is especially critical for the rehabilitation in this phase, and scapular stabilization exercises are instituted. Dynamic joint stabilization exercises are begun in this phase as the athlete begins to tolerate more perturbations in the shoulder. Exercises such as push-ups on a wall are progressed to a gentle incline.

The third phase is a strengthening phase. Progression to this phase is begun as soon as the athlete has full, pain-free active range of motion, good scapular control, and no pain with light resistive rotator cuff exercises. High repetition and low resistive exercises are instituted at the beginning of this phase to enhance neuromuscular control of the joint. As the athlete’s symptoms allow, increasing resistance is added to allow the shoulder to regain full strength and dynamic control. Several functional exercises are added that are specific to the athlete’s sport to test whether the athlete is ready to progress to the next phase of the rehabilitation. When lifting exercises commence, free weights are used to avoid overcompensation with the nonaffected extremity. Shorter arcs of motion with weights are encouraged to avoid terminal extension or forward flexion where the joint forces are highest. The last phase of therapy is return to sport with further functional exercises that mimic what the athlete will see in his or her sport. Athletes are advanced to this phase of their therapy once they have full active range of motion with resistance therapy, normal strength, and no pain with posterior instability provocative testing. Therapeutic exercises include further increases in strength training. An interval

Management of In-Season Athletes With Posterior Glenohumeral Instability return-to-sport program that is sport specific is begun and the athlete is gradually reintroduced into practices with functional drills as his or her symptoms dictate. Once patients are fully able to perform their sport of choice pain free, they are allowed to return to unrestricted competition under close supervision of their athletic trainer. Progression through these 4 phases of therapy is typically faster with posterior instability than with anterior instability because posterior instability is typically a microtraumatic event with more subluxation episodes than anterior instability, which typically involves a traumatic dislocation with a required reduction causing much more joint inflammation.31 We have typically found that athletes can progress through these phases in approximately 7 days unless there was a true posterior dislocation requiring reduction. Athletes do not necessarily have to begin their therapy in the first phase; they can begin in any of the phases based on their symptoms. In fact, most athletes with posterior instability will begin in phase 2 progressing quickly to phase 3. Once patients have returned to their sport, they continue to work on dynamic stabilization exercises to ensure that they maintain dynamic control of their shoulder to avoid subluxation of the joint during practice or competition. For those patients in sports that allow brace wear such as football, a brace is recommended for the rest of the season. This brace attempts to restrict cross-arm adduction and to a lesser extent internal rotation. We recommend using a type of brace that has an adjustable system of buckles or snaps/ grommets to individualize the amount of restricted motion. These types of braces can be customized to tighten posteriorly to help limit the excursion of the shoulder in positions of vulnerability (Figure  18-4). Bracing has been shown to decrease humeral head translation both during adduction and internal rotation and thus can help decrease the risk of posterior translation.33 However, there has been no study on bracing in posterior instability patients to determine whether it can help return patients to their competitive field in-season as there has been with anterior instability.34 Yet, if the athlete can tolerate the brace, then it is recommended to help reduce shoulder translation during competition.

IN-SEASON OPERATIVE TREATMENT For those patients who have any of the clinical exam or radiographic findings in Table 18-2, surgical stabilization is recommended. Because the rehabilitation period typically is approximately 5 to 6 months after posterior labral repair, we recommend surgical repair for the athlete as soon as possible. The surgical technique is described in detail in Chapter 19; therefore, the following is a brief synopsis of our surgical technique for posterior labral repair. Typically, patients are given an interscalene block with general anesthesia. After intubation, all patients are examined under anesthesia to confirm the diagnosis. In most patients, 2+ posterior instability will be found during this examination with negative anterior instability unless combined instability is suspected.

211

Figure 18-4. Example of a brace that restricts internal rotation and adduction in an American football player. This brace can be tightened to further restrict these motions based upon player comfort and position.

The patient is then placed in the lateral decubitus position. When placing the posterior portal in the soft spot of the shoulder, this incision is typically placed 5 mm more lateral than a typical portal to enter the joint lateral to the joint line. Two portals are placed anteriorly, one just off the superolateral edge of the acromion and the other just lateral to the coracoid above the subscapularis. A portal (percutaneous or cannulated) is then placed at the 5 or 7 o’clock position, typically 4 cm off the posterolateral edge of the acromion. This portal is very effective for placement of the anchors because it provides a more direct approach to the posterior glenoid to avoid skiving into the glenoid cartilage during drilling. After a diagnostic examination, a liberator from the superolateral portal is used to free the labrum off the glenoid in the torn portions of the posterior labrum. Typically, liberation approximately 1 hour anterior on the clock face is needed to free the labrum so the tissue can be advanced laterally and superiorly creating a sling effect and a larger bumper posteriorly. Burring and rasping is performed to prepare the glenoid to stimulate bleeding and thus healing of the repair. After labral preparation, at least 3 anchors are placed sequentially from inferior to posterior about 1 hour away from each other.35 We typically start at the 5:30 position (left shoulder) with the first anchor and proceed superiorly with each subsequent anchor. Either simple or horizontal mattress sutures are placed and then tied off the glenoid on the labral capsular side (Figure  18-5). These steps are then repeated for each anchor until about the 1:30 position (left shoulder). We then

212

Chapter 18 any weight-training activities that place a posterior directed force on the humerus should be avoided until at least 5 to 6 months. Rehabilitation should encourage much work to be performed within the scapular plane. Introducing sportsspecific activity begins at the 3- to 6-month time frame depending on the sport.

COMPLICATIONS

Figure 18-5. Arthroscopic picture of a posterior labral repair in a right shoulder with the labrum advanced to cover the glenoid labral articular defect lesion.

release traction and perform a posterior drawer test with the arm in the adducted internally rotated position to ensure that the humeral head will not translate more than 50%. If there is superior or anterior labral pathology, these locations are then addressed after the posterior labral repair.

POSTOPERATIVE REHABILITATION After the shoulder has been stabilized surgically, the shoulder should be immobilized in a sling and abduction pillow for 6 weeks with the goal of maintaining neutral rotation. Some advocate that the shoulder be placed in external rotation in the immediate postoperative period to avoid tension on the repaired posterior capsule.20 During the first 3 weeks postoperatively, pendulum exercises, active scapular retraction, and protraction exercises, and wrist and elbow range of motion are initiated. Around 3 weeks from surgery, passive range of motion is begun and advanced to 90 degrees at 6 weeks. At this same time, isometric exercises are initiated in the neutral shoulder position. Athletes should be instructed to avoid internal rotation with the shoulder in a flexed position. At 6 weeks sling use is discontinued. From 6 to 10 weeks, active range of motion with terminal stretching is initiated. Active range of motion is permitted in all planes with progressive stretching of internal and external rotation. The goal of full active range of motion should be achieved by 12 weeks. Once full range of motion is achieved, strengthening can be initiated. These strength exercises should start with light seated rows and shoulder shrugs along with lifting exercises with the arm at the side. Attention should be paid to avoid overhead weight-lifting activities as well as any weight-training exercises with the arm locked in a forward position. Exercises such as military press, wide grip bench, or

For those patients with posterior instability who are treated nonoperatively in season, the most worrisome complication is another instability event during practice or competition that might reinjure the labrum and lead to further instability episodes. As in anterior instability, one would expect further subluxations or dislocations would put the patient at even more risk of further instability. However, although one study has shown that there is progressive bone loss in anterior instability, there is no study that shows this is the case in athletes with posterior instability even though this would make intuitive sense.26 In a military academy study, more than three-quarters of the cadet athletes required surgery at some point during their athletic career because continued pain or instability with athletics.5 However, this study did not indicate what criteria were used for recommending surgical stabilization or when surgery was recommended. Additionally, no mention was made about what the risk of recurrent instability was after the initial instability episode. In an epidemiologic study, an even higher likelihood of patients requiring surgery (87.5%) at 5  years from injury was noted; however, no data were given for when or why surgery was recommended.4 This study did note that surgical treatment rates increased over the past 20  years, which raises interesting questions regarding what has led to this trend of operative over nonoperative treatment. Is this due to better surgical fixation methods for this type of injury or are patients with posterior instability not functioning as well with this clinical entity as previously thought? Because pain is typically the most common presenting symptom with posterior instability, continued pain after nonoperative treatment with activities that load the posterior labrum might make rehabilitation difficult, especially in athletes. Returning to lifting, especially with bench press or overhead lifting, could be difficult with a posterior labral tear and could compromise athletes’ strength and thus their ability to perform in their respective sport. Thus, if an athlete is struggling to return because of pain, then surgical repair is recommended. In the absence of pain, return to play following an isolated subluxation or dislocation has been variable in the literature. One study of 19 consecutive patients showed a 100% return to sport with conservative treatment; however, the level of sport was not reported and no other cohort was examined in this study for comparison.27 In an NFL observational study, Murphy et  al on the other hand showed only slightly more than 34% of NFL athletes could be treated nonoperatively and still compete.29 As mentioned earlier, in military college athletes 23% with a posterior labral

Management of In-Season Athletes With Posterior Glenohumeral Instability tear were able to be treated conservatively.5 Unfortunately, neither of these studies mentioned any criteria that led to the successful return to sport with nonoperative treatment. Both were epidemiologic studies and thus no conclusion can be made regarding which athletes could be treated in season with nonoperative means. One complication that is unique to labral tears is cyst formation over time if the labral tear enlarges and allows synovial fluid egress. Spinoglenoid notch cysts typically are most commonly associated with superior labral anterior to posterior tears; however, in a radiographic study it was shown that cyst formation had equal prevalence both in superior labral anterior to posterior and posterior labral tears.36 However, it is unknown which patients are more predisposed to cyst formation and what risk factors may contribute to this pathology. There is no literature about this risk with nonoperative treatment. The risks of operative treatment of posterior instability have been much more thoroughly documented in the literature. As with nonoperative treatment, the biggest concern is recurrent instability in patients with this type of tear. In a study of 200 consecutive cases, 94% of patients had a stable shoulder at an average of 3  years after surgery. Similarly, Savoie et  al found a 97% success rate for surgical repair of posterior labral repairs.37 In regards to return to play, the largest study on posterior labral repairs showed more than 90% return to play with 64% returning to their previous level of play.22 Likewise, in a study of 28 patients with posterior labral tears and arthroscopic repair, there was more than 93% return to sport with 82% of those returning to the same level of play with no symptoms.38 In elite rugby players, the return to play was 100% with a posterior labral repair, showing that even contact athletes have a high successful return to sport.39 There have been significant improvements in other highlevel contact athletes, with 93% of NFL athletes returning to play after surgical stabilization of posterior labral tears, of which 79% returned at the same level of play.23 Improved pain relief with surgical intervention has been shown to be significant. However, patients with repairs still can report pain after surgery at medium-term follow-up. For example, pain on the visual analog scale averaged 1.6  in one study and 0.38  in another with ranges from 0 to 9.22,38 However, no mention in these studies was made of the percentage of patients who were pain free after surgery. Thus, surgery presents a good way to stabilize the shoulder but pain relief can be variable. Other complications such as arthrofibrosis or nerve injuries are very rare, and only a few case reports exist documenting their occurrence in this patient population.40

213

no contraindications to nonoperative treatment, once the patient is asymptomatic and has full range of motion with normalized strength and no symptoms with posterior stability examination, he or she may successfully be returned to competition. If a patient has any recurrent symptoms of instability or pain with competition, then surgical repair is indicated. Additionally, if any of the examination or radiographic findings as indicated in Table 18-2 are identified in the work-up, then surgical repair is also indicated. It has been our experience that more than two-thirds of athletes can be treated nonoperatively during the season with no recurrence of symptoms during competition. At the end of the season, athletes are then counseled and operative intervention is recommended to allow time for rehabilitation during the off-season.

REFERENCES 1.

2.

3.

4.

5.

6.

7. 8.

9.

10.

11. 12.

CONCLUSION

13.

In appropriately selected athletes with in-season posterior labral tears, treatment should consist of an organized rehabilitation program progressing the athlete as his or her shoulder symptoms improve with time. In patients who have

14.

Song DJ, Cook JB, Krul KP, et al. High frequency of posterior and combined shoulder instability in young active patients. J Shoulder Elbow Surg. 2015;24(2):186-190. doi:10.1016/j.jse.2014.06.053. Owens BD, Duffey ML, Nelson BJ, DeBerardino TM, Taylor DC, Mountcastle SB. The incidence and characteristics of shoulder instability at the United States Military Academy. Am J Sports Med. 2007;35(7):1168-1173. doi:10.1177/0363546506295179. Provencher MT, LeClere LE, King S, et  al. Posterior instability of the shoulder: diagnosis and management. Am J Sports Med. 2011;39(4):874-886. doi:10.1177/0363546510384232. Woodmass JM, Lee J, Wu IT, et  al. Incidence of posterior shoulder instability and trends in surgical reconstruction: a 22-year population-based study. J Shoulder Elbow Surg. 2019;28(4):611-616. doi:10.1016/j.jse.2018.08.046. Lanzi JT Jr, Chandler PJ, Cameron KL, Bader JM, Owens BD. Epidemiology of posterior glenohumeral instability in a young athletic population. Am J Sports Med. 2017;45(14):3315-3321. doi:10.1177/0363546517725067. Owens BD, Campbell SE, Cameron KL. Risk factors for posterior shoulder instability in young athletes. Am J Sports Med. 2013;41(11):2645-2649. doi:10.1177/0363546513501508. Fronek J, Warren RF, Bowen M. Posterior subluxation of the glenohumeral joint. J Bone Joint Surg Am. 1989;71(2):205-216. Galvin JW, Parada SA, Li X, Eichinger JK. Critical findings on magnetic resonance arthrograms in posterior shoulder instability compared with an age-matched controlled cohort. Am J Sports Med. 2016;44(12):3222-3229. doi:10.1177/0363546516660076. Frank RM, Romeo AA, Provencher MT. Posterior glenohumeral instability: evidence-based treatment. J Am Acad Orthop Surg. 2017;25(9):610-623. doi:10.5435/JAAOS-D-15-00631. Rouleau DM, Hebert-Davies J, Robinson CM. Acute traumatic posterior shoulder dislocation. J Am Acad Orthop Surg. 2014;22(3):145152. doi:10.5435/JAAOS-22-03-145. Brelin A, Dickens JF. Posterior shoulder instability. Sports Med Arthrosc Rev. 2017;25(3):136-143. doi:10.1097/JSA.0000000000000160. Antosh IJ, Tokish JM, Owens BD. Posterior shoulder instability. Sports Health. 2016;8(6):520-526. doi:10.1177/1941738116672446. Bradley JP, Baker CL  III, Kline AJ, Armfield DR, Chhabra  A. Arthroscopic capsulolabral reconstruction for posterior instability of the shoulder: a prospective study of 100 shoulders. Am J Sports Med. 2006;34(7):1061-1071. doi:10.1177/0363546505285585. Pollock RG, Bigliani LU. Recurrent posterior shoulder instability. Diagnosis and treatment. Clin Orthop Relat Res. 1993;(291) (291):85-96.

214 15.

16.

17.

18.

19.

20.

21.

22.

23.

24.

25.

26.

27.

Chapter 18 Kang RW, Mahony GT, Harris TC, Dines JS. Posterior instability caused by batter’s shoulder. Clin Sports Med. 2013;32(4):797-802. doi:10.1016/j.csm.2013.07.012. Wanich T, Dines J, Dines D, Gambardella RA, Yocum LA. ‘Batter’s shoulder’: can athletes return to play at the same level after operative treatment? Clin Orthop Relat Res. 2012;470(6):1565-1570. doi:10.1007/s11999-012-2264-0. Kim SH, Park JS, Jeong WK, Shin SK. The Kim test: a novel test for posteroinferior labral lesion of the shoulder—a comparison to the jerk test. Am J Sports Med. 2005;33(8):1188-1192. doi:10.1177/0363546504272687. Munro W, Healy R. The validity and accuracy of clinical tests used to detect labral pathology of the shoulder—a systematic review. Man Ther. 2009;14(2):119-130. doi:10.1016/j.math.2008.08.008. Owen JM, Boulter T, Walton M, Funk L, Mackenzie TA. Reinterpretation of O’Brien test in posterior labral tears of the shoulder. Int J Shoulder Surg. 2015;9(1):6-8. doi:10.4103/0973-6042.150216. Campbell SE, Dewitt RM, Cameron KL, Thompson AK, Owens BD. Posterior chondrolabral cleft: clinical significance and associations with shoulder instability. HSS J. 2014;10(3):208-212. doi:10.1007/ s11420-014-9404-x. Radkowski CA, Chhabra A, Baker CL  III, Tejwani SG, Bradley JP. Arthroscopic capsulolabral repair for posterior shoulder instability in throwing athletes compared with nonthrowing athletes. Am J Sports Med. 2008;36(4):693-699. doi:10.1177/0363546508314426. Bradley JP, McClincy MP, Arner JW, Tejwani SG. Arthroscopic capsulolabral reconstruction for posterior instability of the shoulder: a prospective study of 200 shoulders. Am J Sports Med. 2013;41(9):20052014. doi:10.1177/0363546513493599. Arner JW, McClincy MP, Bradley JP. Arthroscopic stabilization of posterior shoulder instability is successful in American football players. Arthroscopy. 2015;31(8):1466-1471. doi:10.1016/j. arthro.2015.02.022. Kim DS, Yoon YS, Yi CH. Prevalence comparison of accompanying lesions between primary and recurrent anterior dislocation in the shoulder. Am J Sports Med. 2010;38(10):2071-2076. doi:10.1177/0363546510371607. Porcellini G, Campi F, Pegreffi F, Castagna A, Paladini P. Predisposing factors for recurrent shoulder dislocation after arthroscopic treatment. J Bone Joint Surg Am. 2009;91(11):2537-2542. doi:10.2106/ JBJS.H.01126. Habermeyer P, Gleyze P, Rickert  M. Evolution of lesions of the labrum-ligament complex in posttraumatic anterior shoulder instability: a prospective study. J Shoulder Elbow Surg. 1999;8(1):66-74. doi:10.1016/s1058-2746(99)90058-7. Blacknall J, Mackie A, Wallace WA. Patient-reported outcomes following a physiotherapy rehabilitation programme for atraumatic posterior shoulder subluxation. Shoulder Elbow. 2014;6(2):137-141. doi:10.1177/1758573213517218.

28.

29.

30.

31.

32.

33.

34.

35.

36.

37.

38.

39.

40.

Cruz-Ferreira E, Abadie P, Godenèche A, Mansat P, Clavert P, Flurin P; French Arthroscopy Society. Posterior shoulder instability: prospective non-randomised comparison of operative and non-operative treatment in 51 patients. Orthop Traumatol Surg Res. 2017;103(8S):S185-S188. doi:10.1016/j.otsr.2017.08.004. Murphy CP, Frangiamore SJ, Mannava S, et  al. Effect of posterior glenoid labral tears at the NFL combine on future NFL performance. Orthop J Sports Med. 2018;6(10):2325967118787464. doi:10.1177/2325967118787464. DeLong JM, Bradley JP. Posterior shoulder instability in the athletic population: variations in assessment, clinical outcomes, and return to sport. World J Orthop. 2015;6(11):927-934. doi:10.5312/wjo. v6.i11.927. Buss DD, Lynch GP, Meyer CP, Huber SM, Freehill MQ. Nonoperative management for in-season athletes with anterior shoulder instability. Am J Sports Med. 2004;32(6):1430-1433. doi:10.1177/0363546503262069. Wilk KE, Macrina LC. Nonoperative and postoperative rehabilitation for glenohumeral instability. Clin Sports Med. 2013;32(4):865-914. doi:10.1016/j.csm.2013.07.017. Dellabiancia F, Parel I, Filippi MV, Porcellini G, Merolla  G. Glenohumeral and scapulohumeral kinematic analysis of patients with traumatic anterior instability wearing a shoulder brace: a prospective laboratory study. Musculoskelet Surg. 2017;101(suppl 2):159167. doi:10.1007/s12306-017-0494-8. Conti M, Garofalo R, Castagna A, Massazza G, Ceccarelli E. Dynamic brace is a good option to treat first anterior shoulder dislocation in season. Musculoskelet Surg. 2017;101(suppl 2):169-173. doi:10.1007/ s12306-017-0497-5. Bradley JP, Arner JW, Jayakumar S, Vyas D. Risk factors and outcomes of revision arthroscopic posterior shoulder capsulolabral repair. Am J Sports Med. 2018;46(10):2457-2465. doi:10.1177/0363546518785893. Tirman PF, Feller JF, Janzen DL, Peterfy CG, Bergman AG. Association of glenoid labral cysts with labral tears and glenohumeral instability: radiologic findings and clinical significance. Radiology. 1994;190(3):653-658. doi:10.1148/radiology.190.3.8115605. Savoie FH  III, Holt MS, Field LD, Ramsey  JR. Arthroscopic management of posterior instability: Evolution of technique and results. Arthroscopy. 2008;24(4):389-396. doi:10.1016/j.arthro.2007.11.004. Pennington WT, Sytsma MA, Gibbons DJ, et  al. Arthroscopic posterior labral repair in athletes: Outcome analysis at 2-year follow-up. Arthroscopy. 2010;26(9):1162-1171. doi:10.1016/j. arthro.2010.01.006. Badge R, Tambe A, Funk L. Arthroscopic isolated posterior labral repair in rugby players. Int J Shoulder Surg. 2009;3(1):4-7. doi:10.4103/ 0973-6042.50875. Matsuki K, Sugaya H. Complications after arthroscopic labral repair for shoulder instability. Curr Rev Musculoskelet Med. 2015;8(1):5358. doi:10.1007/s12178-014-9248-5.

19 Arthroscopic Management of Posterior Instability Fotios Paul Tjoumakaris, MD and James P. Bradley, MD

In recent years, posterior shoulder instability has become a recognized cause of shoulder pain and disability, particularly in overhead athletes. Although less common than anterior shoulder instability, posterior instability of the shoulder can be just as disabling and cause athletes to miss games or have reduced sports performance. Anterior instability typically presents to the clinician with a dislocation event, whereas posterior shoulder instability presenting complaints are often more vague (pain, loss of strength, etc). More commonly, patients presenting with symptoms likely suffer from recurrent posterior subluxation (RPS), and not necessarily frank glenohumeral instability. With a detailed history, physical examination, and appropriate imaging, the diagnosis is often easily made. With the emergence of advanced imaging techniques, such as magnetic resonance arthrogram (MRA), a clear picture of the pathology necessary to treat is evident. Management of associated pathology, such as capsular laxity, may often be necessary in many patients, making an accurate diagnosis and patient specific considerations impor tant (sport of play, position, etc). In years past, open shoulder stabilization of posterior shoulder instability was the gold standard; however, many patients treated under this paradigm continued to report symptoms. Higher-level athletes were often unable to return to their previous level of competition, necessitating a more effective treatment strategy. For this reason, arthroscopic techniques were developed and have continued to advance over the past 3 decades. An arthroscopic approach allows for a more detailed assessment of joint status, the ability to treat associated pathology, and an enhanced ability for both capsular and labrum repair. The results of arthroscopic treatment have outpaced those of open techniques and continue

to evolve. The following chapter will outline and describe the arthroscopic management of posterior shoulder instability.

INDICATIONS Whether a patient presents after an initial dislocation event, or with symptoms consistent with RPS, an initial trial of nonoperative management is typically attempted. Those patients who fail treatment with nonoperative management (activity modification, physical therapy, nonsteroidal antiinflammatory medication, etc) and demonstrate imaging findings consistent with the diagnosis of posterior shoulder instability are surgical candidates. Additionally, those patients who qualify for surgery must also be cooperative and willing to engage in an extensive postoperative rehabilitation program. The majority of patients are candidates for arthroscopic repair; however, patients with capsular deficiency (from prior surgery) or who have significant bone abnormalities (glenoid retroversion, large reverse HillSachs lesion) may be candidates for an open technique (allograft capsular reconstruction, glenoid wedge osteotomy, McLaughlin technique).

PREOPERATIVE ASSESSMENT Patient History and Examination The diagnosis of dislocation may have been missed after an initial evaluation. This often occurs after a fall on an outstretched hand in the position of adduction, slight forward flexion and internal rotation. Patients can often dislocate posterior after a seizure or an electrocution accident. Patients

- 215 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 215-220). © 2021 SLACK Incorporated.

216

Chapter 19 head and anterior glenoid pathology that is often found in anterior glenohumeral instability. Computed tomography (CT) is often obtained when there has been a dislocation event or when significant osseous pathology is suspected. MRA of the shoulder is generally considered the gold standard and is helpful for detecting posterior labrum detachment as well as concealed labral tears (Kim lesion). A Kim lesion is an incomplete avulsion of the posterior-inferior labrum that is hidden by an intact superficial component. The MRA is also checked for posterior chondral erosion, paralabral cysts, and concomitant pathology of the superior and anterior labrum, biceps tendon, and the rotator cuff musculature (Figure 19-1).

OPERATIVE TECHNIQUE Figure 19-1. Axial T2-weighted magnetic resonance arthrogram demonstrating a posterior labrum tear.

will report pain with any attempted range of motion and will often hold the arm at the side in a position of internal rotation. The majority of patients will often present with symptoms of RPS. This will often be the result of repetitive microtrauma to the posterior capsule and/or labrum. Athletes may report deep seated or posterior shoulder pain. They may report difficulty with overhead throwing or a loss of velocity. In some instances, patients may report clicking in the shoulder or a “clunk” when the arm is moved from adduction to an abducted position. Patients who present with a posterior glenohumeral dislocation will have a “locked” shoulder that is resting at the side in maximum internal rotation. The patient is often unable to have the arm externally rotated secondary to the entrapment of the lesser tuberosity on the posterior glenoid rim. Labrum provocative testing such as O’Brien’s test and the Mayo shear test may be positive. Specific posterior labrum tests such as the Kim test or “jerk” test may be present, and a posterior apprehension sign with load and shift testing may also help to rule in the diagnosis when positive. Pain or instability is classically elicited with the arm in the posterior apprehension position (flexion, adduction, and internal rotation).

Imaging (X-Rays and Magnetic Resonance Imaging/Computed Tomography) Radiographs are often initially ordered and reviewed for glenohumeral dislocation. In rare instances, glenoid dysplasia or reverse Hill-Sachs lesions may be present on screening radiographs (Grashey AP, Y-view, axillary). Additional views (Stryker notch, West Point) can be obtained as well; however, these views are often better at evaluating posterior humeral

The overall goal of posterior instability repair is to tailor the surgical technique to the individual needs and demands of the patient. Patients who present after a singular or multiple dislocation episodes (macroinstability) without bone defects will likely require posterior labrum repair in addition to capsular plication to prevent recurrence. Patients with microinstability (RPS) or those who are likely to return to overhead throwing are more likely to benefit from isolated posterior labrum repair without an extensive capsular plication to optimize their return to sport and specifically, throwing. Those patients who present with a multidirectional instability picture will likely require a combination of techniques around the shoulder to restore normal glenohumeral biomechanics.

Examination Under Anesthesia Patients undergoing arthroscopic posterior labrum repair typically receive general anesthesia (for muscle relaxation) with or without interscalene nerve block for postoperative analgesia. While the patient is under anesthesia and in the supine position, range of motion is first checked for symmetry to the contralateral extremity. A load and shift test is then performed on the operative extremity and once again compared to the opposite shoulder. It is not uncommon for the humeral head to be displaced posteriorly over the glenoid rim rather easily; however, on release of posterior directed pressure, the humeral head should once again reduce into the glenoid socket. Any abnormal motion, clicking, grinding, or gross subluxation could indicate labrum pathology, or a glenoid or humeral head defect.

Patient Positioning Our preferred patient positioning for arthroscopic posterior labrum repair is the lateral decubitus position. Although the beach chair position can be used, the lateral decubitus position lends itself naturally to excellent visualization of the posterior labrum, glenoid, and capsule. The arm is placed in an abducted position of 45 degrees with 20 degrees of

Arthroscopic Management of Posterior Instability

217

forward flexion (this can be flexed more during placement of the most inferior anchor for better access and visualization). Ten to 15 pounds of longitudinal traction is usually applied for slight joint distraction and to maintain this abducted and forward-flexed posture of the shoulder. Additionally, the axilla should be kept free or padded to prevent neuropraxia on the down extremity. A peroneal pad is also placed on the lower extremity that the patient is resting on. The bed is typically angled 45 degrees away from anesthesia and the visualization tower is placed across the surgical field and at eye level to the surgeon for 360-degree viewing. A wide preparation is then performed to make sure that easy access to the shoulder both anteriorly and posteriorly can be achieved.

Portal Placement The acromion, coracoid process, and acromioclavicular joint are palpated and denoted prior to incision with a marking pen. The posterior portal to the shoulder is typically in line with the lateral edge of the acromion (slightly lateral to a traditional posterior portal). This portal is typically made 2 to 3 fingerbreadths below the acromion. This portal placement allows for tangential access to the posterior glenoid rim for future anchor placement if necessary (or if a single posterior portal technique is preferred). The joint is insufflated with 20 to 30 cc of normal saline from this portal prior to the stab incision. The anterior portal is placed next in an “inside-out” fashion in the rotator interval with a trajectory that is diagonal from the coracoid process to the anterolateral edge of the acromion. After portal placement, a 6- to 7-mm clear cannula can be placed anteriorly using a traditional dilation technique.

Diagnostic Arthroscopy A 30-degree arthroscope is traditionally used and viewing is first undertaken from the posterior portal. Concomitant pathology such as superior labrum tears, anterior labrum tears, subscapularis tendon tears, undersurface rotator cuff tears (internal impingement), and chondral injury are evaluated. The biceps tendon is also critically evaluated by inspecting the biceps root, labrum just posterior to the biceps root, and the degree of pathology once the tendon is pulled into the joint from the anterior portal. Any synovitis or tendon damage should be assessed and the need for biceps tenodesis is critically evaluated. The posterior labrum is then evaluated in its entirety through the posterior portal from the inferior aspect by the axillary recess to just posterior to the biceps attachment. An arthroscopic probe from the anterior portal can be used to evaluate detachment of the labrum (Figure 19-2). Superficial debridement of the labrum is first undertaken with a 4.5-mm full radius shaver to remove free edge fraying to gain better visualization of the labrum. Following the diagnostic arthroscopy, working cannulas are then placed into both the anterior and posterior portal. Both portals are dilated to 8  mm and 8.25-mm cannulas

Figure 19-2. Arthroscopic view from the anterior viewing portal. A probe is being used from the posterior working portal to displace a confirmed posterior labrum tear.

are placed both anteriorly and posteriorly. This size cannula allows for easy trespass of most commercially available suture-passing devices. The arthroscope is then placed into the anterior cannula for easy visualization of the posterior labrum, glenoid, and capsule. A 70-degree arthroscope will allow slightly better visualization of the posterior and inferior capsule and is very helpful for visualization for the most inferior anchor placement along the glenoid rim. Switching between the 30- and 70-degree arthroscope throughout the procedure is encouraged to obtain the optimum field of view during the repair.

Labrum and Glenoid Preparation Once the diagnosis of a posterior labrum tear has been confirmed, work is immediately begun to prepare the labrum and glenoid for repair. First and foremost, the labrum must be adequately released from the glenoid neck and then mobilized adequately to restore tension in the posterior band of the inferior glenohumeral ligament. An arthroscopic periosteal elevator is used to elevate the labrum in similar fashion to performing a Bankart repair anteriorly. The labrum is released from any scar tissue and mobilized until the underside of the capsule and glenoid rim is visualized. Care is taken during labrum mobilization to not go too far beyond the medial border of the glenoid to prevent neurovascular injury. Having a good trajectory through the posterior portal is critical to ensure careful labrum elevation and mobilization without creating a rip or tear in the labrum (labrum transection). If this trajectory is challenging, an accessory lateral portal can be established, or, the labrum can be elevated from the anterior portal while the arthroscope is placed in the posterior portal for visualization. Paralabral cysts, if

218

Chapter 19

Figure 19-3. Arthroscopic view from the anterior viewing portal. An arthroscopic shaver is used to debride the edge of the labrum and glenoid articular margin. Note the chondral defect at the labral/chondral junction.

present on preoperative imaging, can be decompressed during labrum mobilization; however, they often resorb once successful labrum healing is achieved if left untreated. Once the labrum has been adequately mobilized and dissected free of soft tissue, the attention is turned to the glenoid rim. The glenoid is first evaluated for any rim fractures or bone loss. Once the glenoid edge is established, a hooded burr is used to debride the edge of the glenoid and remove any soft tissue that may be remaining. Care must be taken to ensure that the labrum is protected during this process. The posterior labrum and capsule can be attenuated and is vulnerable to iatrogenic injury during this portion of the repair. Once the burr has created a fresh edge, a shaver is once again introduced to remove any remaining soft tissue (Figure 19-3). The glenoid preparation is completed with an arthroscopic rasp to create a fresh, bleeding surface conducive to soft-tissue healing.

Suture Passing and Labrum Repair Once the labrum and glenoid have both been adequately prepared, the “repair” portion of the procedure can commence. Fixation of the labrum to the glenoid rim is typically achieved with suture anchors drilled through an accessory posterior-lateral portal. In recent years, our primary fixation method has evolved to a knotless anchor system. Knotless anchors minimize the risk of knot impingement against the posterior-superior rotator cuff and also minimize the risk of chondral damage from knot abrasion. One added advantage of a knotless repair is the noticeable decrease in operative time secondary to less knot-tying during surgery. As mentioned previously, depending on the demands and pathology of each patient, the labrum repair may differ. Patients who

Figure 19-4. Arthroscopic view from the anterior working portal in a traditional, knot-based repair. A suture hook can be seen penetrating the labrum and delivering a monofilament suture into the joint to use as a shut tle for the anchor-based suture in this repair construct.

engage in overhead throwing sports and who present with symptoms of RPS without macroinstability will likely benefit from a primary labrum repair without capsular plication or advancement. Patients with macroinstability of the shoulder (dislocation history) and those who participate in highdemand contact sports may require labral repair with plication (anchor-based with the repair) of the posterior capsule (ie, offensive linemen). Establishment of an accessory posterior portal can be helpful for inferior anchor placement. This is performed in similar fashion to creating the posterior working portal, with the benefit of direct arthroscopic visualization from the anterior viewing portal. The accessory posterior portal is created so a 45-degree tangential trajectory is achieved to the glenoid. A spinal needle is used to facilitate portal placement. This portal is usually 2  cm distal and lateral to the posterior portal, which had been previously created. Once this portal is created, a 5-mm cannula is introduced using a traditional outside-in technique. Care must be taken during portal placement to prevent iatrogenic injury to the axillary nerve as it courses in close proximity to this portal. Anchors are typically placed from the 6 o’ clock position to the 11 o’ clock position along the glenoid face (for a right shoulder). The anchors are placed sequentially along the glenoid face in an inferior to superior direction after suture passage. Next, a curved suture hook or other suture-passing device is loaded with a 0 monofilament suture and passed through the posterior working cannula while the arthroscope is in the anterior cannula (Figure 19-4). When performing a capsular plication, a bite of capsulolabral tissue just inferior and lateral to the desired anchor location is preferred (other wise, just lateral around the labrum will suffice when less plication is desired). The suture is then delivered into the joint while

Arthroscopic Management of Posterior Instability

Figure 19-5. Arthroscopic view of the posterior labrum repair. The suture has been passed and threaded through the anchor, which is tensioned and ready to be implanted into the pilot drill hole. Note the osteochondral injury of the posterior humeral head (just off field of view).

holding the passing device against the edge of the glenoid. The suture-passing device is then taken from the joint, and a suture retriever is used to retrieve the delivered portion of the monofilament suture. A loop of SutureTape (Arthrex) is then placed in a knot in the monofilament suture to create a “cinch” stitch similar to how a luggage tag works. This type of stitch provides secure fixation around the labrum without compromising the integrity of the labrum tissue. This loop of SutureTape is then delivered into the joint via the monofilament shuttle, through/around the labrum, and once again out the posterior working cannula. The tails of the SutureTapeTM are then delivered through the loop outside the cannula (after the monofilament shuttle is removed) and the SutureTape is “cinched” down around the labrum. If the tissue is of poor quality, a knot pusher can be used to reduce the knot to the labrum and capsule. This creates 2.6 mm of SutureTape because the suture is doubled over, providing added fixation of the labrum. Once the suture has been passed, a pilot hole is drilled slightly on the face of the glenoid in the desired anchor location through the accessory posterior portal. The SutureTape is then retrieved through the accessory posterior portal and threaded through the knotless anchor (2.4-mm biocomposite PushLock anchors (Arthrex). The anchor is then slid down the suture tails with slight tension on the limbs of the suture (Figure  19-5). The anchor is then impacted into place within the pilot hole as the labrum and capsule are reduced to the glenoid margin. The anchor is then gently unscrewed, and the tails of the suture are cut flush against the glenoid, leaving very little suture material in the joint. Additional anchors are then placed in identical fashion in the 8 o’clock to the 11 o’clock position. As one moves up the posterior glenoid, it may be easier to convert to drilling through the posterior working portal because this may provide a better trajectory and prevent skiving across the glenoid surface. The repair is completed when the inferior and superior margins of the tear have been anatomically restored to

219

Figure 19-6. Arthroscopic view of the finalized posterior labrum repair using a knotless technique and “cinch” stitch suture configuration.

the glenoid articular margin with minimal gapping between anchor points (Figure 19-6).

Associated Procedures (Remplissage/ Capsular Closure/Interval Closure) For the majority of patients, the repair concludes with the aforementioned steps. For patients who have macroinstability, it may be necessary to augment the traditional posterior labrum repair with a remplissage technique, posterior capsular closure, or rotator interval closure. Remplissage, from the French word “to fill,” is traditionally used for the treatment of engaging Hill Sachs lesions in anterior glenohumeral instability. For patients with posterior shoulder instability, there may be a reverse Hill-Sachs lesion that engages with internal rotation and is just medial to the lesser tuberosity. Dynamic assessment of this lesion is necessary and if engagement of the lesion is encountered, placing an anchor in the defect and suturing the subscapularis to the anterior reverse Hill-Sachs lesion for a tenodesis effect can prevent engagement and subsequent dislocation. Although remplissage may infrequently be required, many patients may require closure of the posterior capsulotomy. Typically, a No.-1 polydiaxanone (PDS) suture (Ethicon) is used for posterior portal closure. This is achieved by retracting the posterior working cannula just posterior the capsulotomy. A suture passer is then used to pierce the capsule adjacent to the portal and introduce the PDS suture into the joint. A penetrating grasper is then used to pierce the capsule on the opposite side of the cannula and retrieve the PDS suture through the cannula. A sliding, locking knot is then used to tie the suture external to the capsule in a “blind” fashion to secure the capsular closure. This same technique can also be used anteriorly for patients with rotator interval laxity on clinical examination (sulcus sign that does not diminish with external rotation) to secure the rotator interval and prevent posterior laxity during adduction and internal rotation.

220

Chapter 19

REHABILITATION Following surgery, patients are placed in a well-padded abduction sling orthosis for 6  weeks. During this initial phase, wrist and elbow active range of motion is initiated. Passive range of motion exercises of the shoulder is allowed, with the exception of internal rotation and adduction. At 6 weeks, active assisted range of motion progressing to full active motion is initiated and the sling is discontinued. This phase of rehabilitation continues until 10 to 12  weeks, at which point strengthening is begun. Strengthening consists of periscapular strengthening and rotator cuff strengthening. Overhead-throwing athletes are also encouraged to begin working on trunk/core and lower body exercises in preparation for a throwing program. The throwing athlete typically begins a throwing program at 6 months; however, it may take a year or more to achieve peak performance. Patients should have at least 80% of strength and near normal range of motion before returning to full activities and athletics.

OUTCOMES/RESULTS The results of arthroscopic posterior shoulder instability repair have advanced considerably over the past several decades. Although traditional open techniques were successful at preventing recurrence of dislocation events, they more than likely contributed to worsening osteoarthritis and demonstrated inferior outcomes in athletic populations. With the advent of modern arthroscopic techniques, success rates range from 85% to 95% even in the most demanding and athletic patient populations. Recent studies have also demonstrated equal rates of success in the pediatric population

using similar fixation techniques. As rehabilitation programs become even further refined and more specific criteria are established for return to play, it is likely that we will continue to see improvements in outcomes.

REFERENCES 1.

2.

3.

4.

5.

6.

7.

8.

Bottoni CR, Franks BR, Moore JH, DeBerardino TM, Taylor DC, Arciero RA. Operative stabilization and anterior capsular plication for recurrent posterior glenohumeral instability. Am J Sports Med. 2005;33(7):996-1002. doi:10.1177/0363546504271509. Bradley JP, Baker CL  III, Kline AJ, Armfield DR.  Chhabra  A. Arthroscopic capsulolabral reconstruction for posterior instability of the shoulder: a prospective study of 100 shoulders. Am J Sports Med. 2006;34(7):1061-1071. doi:10.1177/0363546505285585. Bradley JP, McClincy MP, Arner JW, Tejwani SG. Arthroscopic capsulolabral reconstruction for posterior instability of the shoulder: a prospective study of 200 shoulders. Am J Sports Med. 2013;41(9):20052014. doi:10.1177/0363546513493599. Hawkins RJ, Koppert G, Johnston  G. Recurrent posterior instability (subluxation) of the shoulder. J Bone Joint Surg Am. 1984;66(2):169-174. Kim SH, Park JS, Jeong WK, Shin SK. The Kim test: a novel test for posteroinferior labral lesion of the shoulder—a comparison to the jerk test. Am J Sports Med. 2005;33(8):1188-1192. doi:10.1177/0363546504272687. McClincy MP, Arner JW, Thurber L, Bradley JP. Arthroscopic capsulolabral reconstruction for posterior shoulder instability is successful in adolescent athletes. J Pediatr Orthop. Published online June  30, 2018. doi:10.1097/BPO.0000000000001210. Tibone J, Ting  A. Capsulorrhaphy with a staple for recurrent posterior subluxation of the shoulder. J Bone Joint Surg Am. 1990;72(7):999-1002. Tjoumakaris FP, Bradley JP. The rationale for an arthroscopic approach to shoulder stabilization. Arthroscopy. 2011;27(10):14221433. doi:10.1016/j.arthro.2011.06.006.

20 Bone Augmentation for Posterior Instability Jaymeson R. Arthur, MD and John M. Tokish, MD

EPIDEMIOLOGY, BACKGROUND, AND RISK FACTORS Compared to anterior shoulder instability, posterior instability is rare and classically has accounted for approximately 2% to 10% of all cases of shoulder instability.1,2 Most epidemiologic studies on shoulder instability, however, have mainly reported on acute dislocations and do not account for the more subtle forms of posterior instability such as recurrent subluxation. This is especially true in young, athletic populations.3-7 For example, Lanzi et al7 studied posterior instability in the United States Military Academy and found posterior instability to comprise 17.9% of the total injuries. Similarly, Song et al8 evaluated 231 patients at a single military institution being treated operatively for instability and found that 24% of all surgically treated instabilities had isolated posterior pathologic findings, with an additional 19% treated for combined instability. These studies highlight that the incidence of posterior instability is likely under-reported, especially in younger active populations. Nonetheless, advances in magnetic resonance imaging (MRI) and arthroscopy continue to improve our awareness and understanding of this clinical entity.9 Bony defects following posterior shoulder instability include the reverse Hill-Sachs lesion, the reverse bony Bankart lesion, and attritional posterior bone loss. The reverse Hill-Sachs lesion (Figure 20-1) is an impression fracture of the anteromedial humeral head and is associated with locked and difficult-to-reduce dislocations. Alternatively, fracture of the posteroinferior rim of the glenoid is referred to as the reverse bony Bankart lesion (Figure 20-2). Although

the incidence of bony defects following posterior instability is not well defined by large, epidemiologic studies, several case series have reported their findings. Bradley and colleagues6 in their large prospective series found that 66% of patients with traumatic instability had reverse Hill-Sachs lesions. Longo et  al10 performed a systematic review on several of these case series and found that, of the 328 shoulders analyzed, 9% of cases of posterior instability had a bony glenoid defect, 39% had humeral head defects, and 2% of cases had combined defects. Although capsulolabral derangement in isolation more commonly presents in the more subtle forms recurrent instability such as recurrent subluxation, bony defects typically occur in the higher-energy forms of posterior instability.11-13 Bony defects from both the humeral and glenoid can predispose patients to recurrent dislocation by altering the glenohumeral congruity and by altering the function of the static glenohumeral stabilizers.14 Further, these injuries often do not present in isolation and a combination of bony and softtissue injuries are often present together.5,15-17 Rouleau and Hebert-Davies16 conducted a systematic review of more than 100 articles focusing on the incidence of associated injury in posterior dislocation. They found that 65% of dislocations had associated injuries, with fracture being most common (34% of cases) followed by reverse Hill-Sachs lesions (29%). In the younger, military population, Bottoni et al5 found that 97% of shoulders operated on in their series for traumatic posterior instability had reverse Bankart lesions, posterior rim fracture, or rim calcification. Several risk factors for posterior instability have been identified. Classically, posterior instability has been associated with epilepsy, ethanol use, and electrocution, termed

- 221 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 221-232). © 2021 SLACK Incorporated.

222

Chapter 20

A

A

B B

Figure 20-1. Reverse Hill-Sachs lesion. (A) Axial computed tomography scan of left shoulder showing the anteromedial humeral head defect of approximately 40%. (B) Arthroscopic visualization of anteromedial humeral head impression defect following an acute, traumatic posterior shoulder dislocation.

the 3 E’s. In fact, bilateral posterior dislocations without associated trauma is considered essentially pathognomonic for seizure.18,19 This is thought to occur because of the stronger contraction of the shoulder internal rotators (primarily the pectoralis major and latissimus dorsi) overpowering the weaker external rotators. This muscle imbalance leads to superior posterior displacement of the humeral head relative the glenoid and subsequent posterior dislocation.20,21 Despite these classically described “3 E’s,” Robinson and colleagues22 found that traumatic accidents (fall from height and motor vehicle accidents) accounted for the majority of posterior shoulder dislocations (67%), whereas seizure and electrocution were less common (31% and 1.7%, respectively).

Figure 20-2. Reverse bony Bankart lesion. (A) Axial T2-weighted magnetic resonance imaging of right glenohumeral joint with clearly visualized fracture (red arrow) through the posterior aspect of the glenoid. (B) Three- dimensional reconstruction of right scapula further demonstrating significant posterior bone loss. (C) Arthroscopic visualization of glenoid face showing severe bone loss posteriorly with associated softtissue Bankart lesion as well.

Several authors have shown that anatomical factors, such as glenoid hypoplasia,11 posterior glenoid rim deficiency,23,24 and glenoid retroversion6,25-27 can contribute to posterior instability. For example, in their series, Hurley et al25 showed that the average glenoid retroversion in patients with posterior instability was –10 degrees vs –4 degrees in the control group. Brewer et al27 defined excessive retroversion as more than –7  degrees of retroversion and Owens et  al26 showed

Bone Augmentation for Posterior Instability that for every 1 degree of increased retroversion, there was a 17% increased risk of subsequent posterior instability in their young, military population. In athletic populations experiencing recurrent posterior instability, common etiologies include a fall onto the outstretched hand,5 blocking linemen in American football,28 weight lifting, rugby, and climbing.29 Posterior instability has even been described in baseball players’ leading shoulder during batting30 and in rifle shooting.31 Unfortunately, recurrent instability is common in these patient populations as well. Robinson et al22 retrospectively reviewed 120 cases of posterior dislocation and found as many as 18% of patients experienced recurrent instability at 1  year. They found risk factors for recurrent instability included age younger than 40 years, dislocation during seizure, and large reverse HillSachs lesion (> 1.5 cm3).

CLASSIFICATION SYSTEMS Although no single classification system has been widely adopted, several descriptive terms have been used to describe shoulder instability and dislocations. These include the direction of instability (anterior, posterior, inferior, multidirectional), etiology (atraumatic vs traumatic), presence and size of the bony defects, and chronicity (acute, chronic, recurrent).21,32,33 Further, it is impor tant to delineate the simple dislocations from the more complex, fracture-dislocations.

HISTORY It is critical to recognize that there are many forms of posterior instability that range from the obvious acute, traumatic posterior dislocations all the way to the more subtle forms of recurrent posterior subluxation.13,21 Overall, studies have shown that posterior dislocations are more frequently clinically missed, with up to a 50% delay in diagnosis.3 Further, many patients with posterior instability may be initially misdiagnosed or referred for other diagnoses.34 Millet et al35 found that in athletic patients the most common presenting complaint is pain, and the authors noted that this may often draw attention away from the clinical suspicion of instability. In the setting of acute fracture in the elderly patient, dislocations can also be commonly missed.36 Therefore, a combination of a detailed history, accurate physical examination, and proper imaging is essential for correct diagnosis. A detailed history begins with questions regarding the onset, severity, and progression of any symptoms. Often, patients will describe an acute traumatic event such as a fall onto an outstretched hand, a blow to the arm during a sporting event, or a motor vehicle accident. Inquiring about the position of the arm/shoulder and the direction of applied force may give the clinician invaluable information leading to the diagnosis, because a fall on an outstretched arm, or in a position of flexion and horizontal adduction, may be indicative of a posterior event.

223

These higher-energy mechanisms should increase the clinician’s suspicion for bony abnormalities. Even in the absence of a high-energy mechanism, a history of manual shoulder reduction should also cue the clinician that bony pathology may be present. When bony defects are present, a patient may often describe a sense of locking or grinding, especially with a reverse Hill-Sachs lesion.35,37 With increasing bone loss due to recurrence, patients may report lower energy necessary to result in a recurrence, dislocations in nonprovocative positions, and episodes may happen during sleep. When seizure is the root cause of posterior instability, a detailed history of seizure frequency and antiseizure medication compliance is useful. Of note, these patients are at high risk of developing locked posterior dislocations with subsequent humeral head lesions.20 In the post-seizure setting, it may be difficult to obtain any history from the patient but collateral information from the family, friends, or emergency medical personnel is often helpful. Lastly, it should be noted that many posteriorly unstable patients can reproduce their sensation on exam “voluntarily.” This voluntary reproduction should be differentiated between voluntarily positional and muscular, because the latter may best be avoided surgically.35,38

PHYSICAL EVALUATION In the setting of posterior shoulder instability in general, the clinical evaluation begins with a thorough inspection, palpation, range-of-motion testing, strength testing, and various special tests. The involved shoulder should be carefully compared to the contralateral shoulder in all these aspects. Often, the patient will present with tenderness to palpation along the posterior glenohumeral joint line.35 In the setting of acute dislocation, the patient will typically present with the shoulder internally rotated, with prominent coracoid and axillary fullness.37,39 If significant humeral head deformity is present (ie, reverse Hill-Sachs lesion), this bone defect may engage the posterior aspect of the glenoid leading to a mechanical block to external rotation.39 The basic physical examination starts with testing the shoulder in the vulnerable positions of flexion, adduction, and internal rotation. Axial load can elicit pain posteriorly and instability can often be detected even with this simple maneuver, especially when bony defects are present. In this at-risk position, when axial load is applied to the shoulder, the soft-tissue restraints, mainly the posterior band of the inferior glenohumeral ligament and the posterior capsulolabral complex, cannot sufficiently resist the force and posterior dislocation occurs.21,35 Several provocative tests for posterior instability have also been described. These include the jerk test, posterior load and shift test, and push-pull testing. The jerk test40 is described in Figure 20-3. This maneuver specifically tests the posteroinferior labrum by forcefully impinging the humeral head over the diseased posteroinferior labrum causing pain.

224

Chapter 20

A

B

Figure 20-3. Jerk test. (A) The affected shoulder is placed in forward flexion to 90 degrees with the elbow bent and slightly internally rotated. (B) Examiner then axially loads the glenohumeral joint with a posteriorly directed force while stabilizing the scapula (this causes the shoulder to sublux posteriorly). (C) The arm is then horizontally abducted and a palpable and/or painful click is felt signifying reduction of the glenohumeral joint. Reproduction of the pain and/or the palpable relocation of the joint is considered a positive test.

C

Not only is this test useful for diagnostic purposes but it also has prognostic value in that it helps predict which patients are more likely to fail nonoperative treatment.41 The posterior load and shift test40 is performed by placing the patient in a supine position with the affected arm in neutral rotation with 40 to 60 degrees of abduction and forward flexion. Axial force is applied along the axis of the humerus with one hand while the other hand places a posteriorly directed force on the proximal humerus. The amount of glenoid translation is noted and more than 50% translation is considered a positive test. The push-pull test40 is performed by placing the patient in the supine position with the arm in 90 degrees of abduction and neutral rotation. The examiner then grasps the wrist and “pulls” with one hand in line with the axis of the arm. Using the other hand, the shoulder is “pushed” posteriorly with one hand and the other hand is then placed on the proximal humerus. While pulling with the hand holding the wrist, the examiner simultaneously pushes the proximal humerus posteriorly with the other hand. The test is positive

when the maneuver reproduces the patient’s pain/symptoms (Figure 20-4). In these tests, if a shoulder remains out, it is indicative of bone loss.

IMAGING AND SURGICAL DECISION MAKING Standard imaging begins with anteroposterior, axillary, and scapular-Y radiographs to ensure orthogonal views of the joint are obtained.22,37,39 If the patient is not able to achieve adequate abduction, the Velpeau view,42 with the patient leaning backward 20 to 30  degrees with the beam directed from cranial to caudal centered on the glenohumeral joint, can be used. The classic “lightbulb sign” or “half-moon sign” will often be present on anteroposterior radiographs.43 Nonetheless, the axillary view has been shown to be most sensitive for the detection of posterior instability on plain radiographs.44,45

Bone Augmentation for Posterior Instability

A

225

B

Figure 20-4. Push-pull test. (A) Placing the patient in the supine position with arm in 90 degrees abduction and neutral rotation. (B) The examiner then grasps the wrist and “pulls” with one hand in line with the axis of the arm. Using the other hand, “push” the shoulder posteriorly with one hand and then place the other hand on the proximal humerus. While pulling with the hand holding the wrist, the examiner simultaneously pushes the proximal humerus posteriorly with the other hand. The test is positive when the maneuver reproduces the patient’s pain/symptoms.

Although plain radiographs can show bony deformity when large enough, further advanced imaging with computed tomography (CT) scan and MRI are often required for more detailed characterization. Several studies have shown that CT is most useful for defining humeral head and glenoid defects,46-48 whereas MRI is especially useful for detecting concomitant capsulolabral injury.11,49 Often, a CT scan paired with MRI can ensure the most accurate diagnosis and that all injuries are accounted for. Because the size of the bony defect often directs management, the clinician should be familiar with how to accurately measure bone loss. With respect to the humerus, previously surgeons simply estimated the percentage of affected humeral articular surface seen on the CT scan. Most of the previous literature has focused around measuring anterior bone loss. However, Hines et al17 evaluated posterior glenoid bone loss and proposed a standardized method for measuring it. Using a best-fit circle technique, the size, location, and depth of the defect can be assessed. These authors found that 69% of patients undergoing surgery for posterior instability had some measurable bone loss, and 22% of patients had greater than subcritical bone loss (13.5% or more). Although critical glenoid bone loss in anterior instability has been studied at length,50,51 it is less clear what constitutes critical bone loss for posterior instability. And although many authors agree that the larger the bony defect, the higher likelihood of recurrent instability; there is no consensus on the exact size of the defect that requires the surgeon to address the bony defect directly. Nacca and colleagues52 conducted a cadaveric study in which the posterior glenoid was sectioned to varying degrees in conjunction with reverse Bankart repair. They found that bony defects greater than 20% of the posterior glenoid width

remained unstable after isolated reverse Bankart repair. Bryce et  al53 conducted a similar cadaveric study in which they assessed humeral head translation on 3-dimensional CT with respect to the scapula at each humerus position after removing the posterior glenoid in 5-degree increments. They found that posterior humeral head translation was significantly increased after only 5 degrees of posterior glenoid bone loss. In both of these cadaveric studies, however, bone was sectioned directly from the posterior glenoid in the cranial-caudal axis and, as we know, most often clinically the reverse Bankart lesion tends to occur in the posteroinferior aspect of the glenoid.11 In perhaps the most clinically relevant investigation, Hines and colleagues17 conducted a retrospective review of 43 consecutive patients at a single military institution who underwent arthroscopic isolated stabilization of the posterior labrum. They found 69% of their patients had measurable bone loss and 22% of patients had greater than the previously described 13.5% glenoid bone loss. Although these patients were statistically less likely to return to full duty, the authors found reoperation rates, complications, and patient-reported outcomes to be no dif ferent based on the size of the lesion. As opposed to the anterior shoulder instability counterpart, this suggests that bony defects in posterior instability can be well treated with standard arthroscopic techniques without bone augmentation. The critical threshold for bony stabilization or augmentation for humeral defects is even less studied. Backer and Warren54 found that reverse Hill-Sachs lesions greater than 30% of the articular surface can lead to instability. Longo et  al10 conducted a systematic review looking at trends in surgical techniques for humeral bone loss. They analyzed 19 articles and found that when there was less than 25%

226

Chapter 20

humeral head bone loss, this was most commonly managed with posterior capsular repair (50%), closed reduction (47%), or arthroscopically repaired (3%). If the humeral head bone loss was between 25% and 50%, this was primarily managed with open reconstruction with bone grafting (67%), with the subscapularis tendon transfer technique second at 33% of cases. If the humeral head bone loss was greater than 50%, arthroplasty was most commonly employed. They also showed that 91% of patients were able to return to sport when managed with distal tibia allograft, arthroscopic bone block augmentation, and arthroscopic repair. In the end, bony defects in posterior shoulder instability remain a difficult challenge to treat for orthopedic surgeons. Because of the wide range of pathology, many dif ferent techniques have been developed to address these problems. Furthermore, many of the data that currently exist consist of small case reports and case series. Although new techniques, including more advanced arthroscopic techniques, are being developed, future research must continue to be developed to improve outcomes following posterior shoulder instability with bony defects.

TREATMENT Reduction of Acute Dislocation Before discussing nonsurgical and surgical treatment, the clinician should first be aware of how to perform closed reduction of the posteriorly dislocated shoulder. To begin, forceful reduction should be avoided because it can lead to humeral head fracture and subsequently osteonecrosis. In-line traction has been shown to be successful in 33% of posterior dislocations.22 Open reduction can be performed through a deltopectoral approach. Reduction can be accomplished after opening the rotator interval and gently levering the head back into place. If this is unsuccessful, a formal arthrotomy is required.

Nonsurgical Management Because of the wide spectrum of disease severity, there exist many therapeutic options for the treatment of posterior shoulder instability, including nonsurgical and surgical options. Nonsurgical treatment is typically the first-line treatment, provided the joint is not resting in a subluxed or dislocated position, and the goal of the reduced shoulder after posterior instability event is to increase the dynamic stability of the glenohumeral joint through strengthening the rotator cuff and periscapular muscles,55 especially the external rotators, posterior deltoid, and scapular stabilizers, which are often deficient in posterior instability.56 After 3 to 6 months, patients who have persistent shoulder pain, dysfunction, and instability who fail the above conservative management may be considered for surgery. Once reduced or in the case of the athletic patient with recurrent posterior subluxation, physical therapy is

encouraged to optimize dynamic stabilization.55 In these populations, appropriate strengthening and proprioceptive programs have been shown to diminish pain and improve stability in approximately two-thirds of patients with posterior and multidirectional instability.55,56 Nonoperative management is less successful in patients with a history of traumatic events, with a roughly 16% success rate compared to 70% to 80% in atraumatic counterparts.55

Surgical Management To achieve successful surgical management of glenohumeral instability, the surgeon must be able to accurately identify and address what factors are causing the instability. Furthermore, the instability must be attributable to mechanical factors that can be corrected with surgery.57 The surgical procedures for the treatment of bone defects can be divided broadly between treatment of humeral lesions and glenoid lesions. Although this chapter focuses on the management of bony defects, it cannot be understated that few bony lesions exist in isolation. Therefore, it is critical for the surgeon to evaluate which soft-tissue structures are deficient and address these properly at the same time as the bony defect is addressed. Patient age, severity of injury, pattern of instability (isolated posterior instability vs multidirectional instability), and functional demands of the patient also play a vital role in surgeon decision making and should be considered carefully. Further, although bony defects have often been an indication for open procedures, the indications for arthroscopic techniques that address these bony defects are expanding as surgical technique and our understanding of the pathoanatomy increases.57

HUMERAL DEFECTS For small humeral defects (< 20% to 25% of articular surface), an arthroscopic Connelly or “reverse remplissage” has been advocated.58,59 Duey and Burkhart60 described an arthroscopic technique for addressing small to medium reverse Hill-Sachs lesions in which the middle glenohumeral ligament is sutured into the defect, turning it into and extraarticular defect and preventing it from engaging the posterior glenoid. For medium humeral defects (25% to 40% of articular surface), the McLaughlin technique and the modified McLaughlin technique have been advocated. In 1952, McLaughlin described the transfer of the subscapularis tendon as a means of treating reverse Hill-Sachs lesions after posterior dislocations. Via the deltopectoral approach, the humeral bone defect is approached and the surface of the bone is freshened until underlying vascular bone is exposed. The subscapularis is then reattached to the humerus in the depths of the defect by mattress sutures passed through drill holes in the bone.39 Hawkins and colleagues46 later described a modification to this technique whereby an osteotomy of the lesser tuberosity was performed and the osteotomized bone

Bone Augmentation for Posterior Instability was transposed into the defect. Arthroscopic techniques for this procedure have been subsequently developed as well.61,62 Disimpaction and autogenous vs allogenic bone grafting of the humeral head defect have also been used to treat these medium defects.21,59,63,64 These techniques are indicated when the underlying bony is not significantly osteoporotic or deformed, and when there is not significant arthritis already present. This is especially useful when the injury is treated promptly, within 2 weeks of the injury.63 Partial prosthetic humeral head resurfacing has also been reported and has been shown to be effective in preventing recurrent dislocations for patients with significant reverse Hill-Sachs lesions.65 In older patients with large humeral head defects (> 40% to50% of articular surface), both hemiarthroplasty and arthroplasty have been advocated.21,46,57,59 No studies to our knowledge have directly compared the 2 techniques directly to each other; however, the presence of underlying arthritis before the injury may be a solid indication for total shoulder arthroplasty as first-line treatment in this situation.46,66 Rotational osteotomy of proximal humerus has also been described.67,68 This technique simply attempts to shift the bony defect away from the position where it engages with the glenoid, thus reducing instability. However, this is a technically challenging operation and has increased risk of disruption to the humeral head blood supply; therefore. it is not widely used.21,43

Figure 20-5. The distal clavicle autograft for the treatment of posterior glenoid defects.

A summary and list of the various treatment options for bone augmentation in posterior instability are included in Table 20-1.

GLENOID DEFECTS To begin, glenoid dysplasia and retroversion can contribute significantly to posterior instability. Although there is no consensus as to how much retroversion is acceptable, the posterior glenoid opening wedge osteotomy can be a viable option in cases of severe dysplasia and retroversion. Some authors consider 15  degrees to be excessive retroversion,9 and studies have shown that retroversion greater than 15 degrees may lead to increased rates of failure of soft-tissue repair if the retroversion is not simultaneously addressed.69 Nonetheless, there are limited studies assessing patient outcomes with this approach that have helped better define the cutoff for this procedure. Posterior bone block and osteoarticular augments can also be used in the setting of glenoid dysplasia and retroversion. Reverse bony Bankart lesions often heal with a medialized posterior fragment. If the fragment is large enough, it may be elevated and incorporated into a standard posterior Bankart repair. If the bone is attritional or deficient, options to address this defect include the use of posterior bone block procedures. Several dif ferent techniques have been described to accomplish this, including using iliac crest autograft,70,71 acromion autograft,72,73 distal tibial allograft,74 and distal clavicle autograft (Figure 20-5).75 Further, arthroscopic techniques have been developed to address bony glenoid deficiencies and have the advantage of avoiding the extensive open approach.76

227

CONCLUSION Bone defects in the setting of posterior shoulder instability can significantly complicate treatment and outcomes. With the advent of MRI and arthroscopy, an increased appreciation for these defects has emerged. Treatment of these defects depends on their location on the humeral head, glenoid or both, and their size. Smaller defects can be treated with soft-tissue advancements or incorporation of bone if present. Larger defects require consideration of grafting or replacement. Outcomes can be promising with the proper application of these techniques, but there is much work to be done to further our understanding of the optimal treatments in this pathology.

REFERENCES 1.

2.

3. 4.

Simonet WT, Melton LJ  III, Cofield RH, Ilstrup DM. Incidence of anterior shoulder dislocation in Olmsted County, Minnesota. Clin Orthop Relat Res. 1984;(186):186-191. Krøner K, Lind T, Jensen  J. The epidemiology of shoulder dislocations. Arch Orthop Trauma Surg. 1989;108(5):288-290. doi:10.1007/ bf00932317. Hawkins RJ, Belle RM. Posterior instability of the shoulder. Instr Course Lect. 1989;38:211-215. Kim SH, Ha KI, Park JH, et al. Arthroscopic posterior labral repair and capsular shift for traumatic unidirectional recurrent posterior subluxation of the shoulder. J Bone Joint Surg Am. 2003;85(8):14791487 (). doi:10.2106/00004623-200308000-00008.

5 (7 shoulders)

4

NA

J Orthop Trauma. 1995

J Bone Joint Surg Am. 1996

Arch Orthop Trauma Surg. 2009

Finkelstein et al77

Gerber and Lambert63

Charalambous et al78

NA

MEAN F/U, MO

Modification to McLaughlin procedure: subscapularis tendon is not divided, instead is plicated directly into defect

Allograft reconstruction in humeral head defects > 40% of joint surface

Lesser tuberosity transfer

NA

68

60

Multiple treatment approaches, 66 including closed reduction alone, subscapularis tendon transfer, transfer of lesser tuberosity with attached subscapularis, hemiarthroplasty, and total shoulder arthroplasty

Closed reduction, humeral head hemiarthroplasty, and transposition of subscapularis insertion into reverse Hill-Sachs lesion

NO. OF PATIENTS APPROACH/TYPE OF REPAIR

J Bone Joint 22 Surg Am. 1952

JOURNAL/ YEAR

Hawkins et al46 J Bone Joint 40 Surg Am. 1987 (41 shoulders)

HUMERUS McLaughlin39

AUTHOR

Case report of patient treated successfully with this technique

Described open approach for addressing humeral head defects > 40% of articular surface. Used humeral head allogenic bone contoured to fit defect to restore sphericity of humeral head. In 3 patients, graft was secured with lag screw and in 1 patient, graft was press-fit into defect alone. All shoulders, at minimum of 5 y, remained free of dislocation; 3 of 4 patients reported little to no pain with no or minimal functional deficits. Authors emphasize importance of quality underlying host bone for success with this technique

Early report of clinical outcomes of modified McLaughlin procedure with lesser tuberosity transfer. In all patients, defect compromised 25% to 40% of humeral head. Authors found slightly reduced internal rotation compared to contralateral shoulder in unilateral cases but no cases of recurrent dislocation at 5-year F/U

As part of treatment options, authors modified original McLaughlin technique by also transferring lesser tuberosity into humeral defect. They found for those treated with subscapularis transfer alone, 4 of 9 shoulders were successfully treated. In 4 patients who underwent subscapularis + lesser tuberosity transfer, all 4 were successfully treated

Original technique article for remplissage technique used for posterior dislocations. Authors note most impor tant aspect of care is arriving at proper diagnosis. He found patients whose injuries are detected sooner and treated properly, regardless of treatment, have more favorable outcomes overall

MAIN FINDINGS/OUTCOMES

Table 20-1. Proposed Techniques and Treatments for Bony Augmentation in Posterior Shoulder Instability Including Management of Humeral and Glenoid Defects

228 Chapter 20

Smith et al76

Modified arthroscopic McLaughlin procedure

NA

13

Orthop Traumatol Surg Res. 2009

Arthrosc Tech. NA 2012

11

8

Knee Surg 21 Sports Traumatol Arthrosc. 2007

Acta Orthop Scand. 1995

Arthroscopic posterior shoulder stabilization with iliac bone graft and capsular repair

Open iliac posterior bone block

Open iliac posterior bone block

open iliac posterior bone block

Open glenoid osteotomy with iliac bone grafting

NA

216

34

72

108

Orthop 83 retrospective, Capsulolabral reconstruction in isola- 58 retrospective, Traumatol 18 prospective tion or in combination with capsular 13 prospective Surg Res. 2017 shift, labral repair, closure of the rotator interval, and/or notch remplissage

Meuffels et al81 J Bone Joint Surg Br. 2010

Barbier et al70

GLENOID Bessems and Vegter71 Servien et al80

Andrieu et al79

Martetschläger Knee Surg NA et al61 Sports Traumatol Arthrosc. 2013

(continued )

Authors describe all-arthroscopic technique using iliac crest autograft and capsular plication. Graft is fixated with two 3.5-mm cannulated screws. In addition to commonly described advantages of arthroscopic surgery (minimally invasive, quicker recovery, faster return to lay, and cosmesis), proposed advantages: precise arthroscopic visualization to ensure accurate graft placement and ability to address other concomitant posterior pathology

Mean postoperative scores: Rowe 60, WOSI 60%; 4 with recurrent instability

4 of 7 returned to play but at lower level; all patients considered themselves cured but 5 not pain free; postoperative scores: Constant 96.3, Walch-Duplay 90

15 of 21 patients returned to preinjury level of play; mean postoperative scores: Constant 93.3, WalchDuplay 85.6; 3 with recurrent instability

Rowe and Zarins scores indicated 12 patients with excellent outcomes and 1 case with good outcomes

35% failure in retrospective group, 22% failure in prospective group, yet 92% of all patients returned to work and 80% of athletes returned to preinjury level of sport. 85% of patients were satisfied or very satisfied after surgery. Authors noted older patients, those with an unclassified clinical form of dislocation, and those who underwent an isolated procedure were more likely to fail

Technique article describes arthroscopic means of reproducing McLaughlin procedure: subscapularis tendon is not detached and double-mattress suture with wide footprint tenodesed into defect

Bone Augmentation for Posterior Instability 229

Arthrosc Tech. 15 2013

J Shoulder Elbow Surg. 2013

Arthrosc Tech. NA 2014

Boileau et al82

Schwartz et al83

Tokish et al75

Posterior bone block

Distal tibial allograft

Arthroscopic technique article describing distal tibial allograft. Distal tibial plafond with intact articular surface is harvested and contoured to defect, then secured via lag screws

MAIN FINDINGS/OUTCOMES

NA

20.5

Technique article describes distal clavicle osteochondral autograft for bony augmentation: ~2 cm of distal clavicle is resected and sculpted to fit defect. Graft can then be secured with lag-screw technique or with suture anchors. Advantages of this technique: graft readily available, inexpensive, minimal donor site morbidity, can be used for anterior and posterior glenoid defects

16 of 18 patients returned to sport; mean postoperative scores: Rowe 82.1, Walch-Duplay 82.9; 1 with recurrent instability

5 patients Technique article describes iliac crest bone graft fixwith > 1 y F/U ated with suture anchors for augmentation of glenoid (average, 18 mo) defect. No patients with recurrent instability at an average of 18 mo postoperatively. Rowe score was 87 points in this group and Walch-Duplay scores were 89 points on average. Also used CT scan to evaluate position of graft postoperatively; found excellent reproducibility with 14 of 15 grafts properly positioned.

NA

MEAN F/U, MO

Abbreviations: CT, computed tomography; F/U, follow-up; NA, not available; WOSI, Western Ontario Shoulder Instability index.

Arthroscopic distal clavicle autograft

18 (19 shoulders) Arthroscopic iliac posterior bone block

Arthrosc Tech. NA 2013

Gupta et al74

NO. OF PATIENTS APPROACH/TYPE OF REPAIR

JOURNAL/ YEAR

AUTHOR

Table 20-1. Proposed Techniques and Treatments for Bony Augmentation in Posterior Shoulder Instability Including Management of Humeral and Glenoid Defects (continued)

230 Chapter 20

Bone Augmentation for Posterior Instability 5.

6.

7.

8.

9.

10.

11. 12.

13. 14.

15.

16.

17.

18.

19. 20. 21. 22.

23.

24.

Bottoni CR, Franks BR, Moore JH, DeBerardino TM, Taylor DC, Arciero RA. Operative stabilization of posterior shoulder instability. Am J Sports Med. 2005;33(7):996-1002. doi:10.1177/0363546504271509. Bradley JP, Baker CL  III, Kline AJ, Armfield DR, Chhabra  A. Arthroscopic capsulolabral reconstruction for posterior instability of the shoulder: a prospective study of 100 shoulders. Am J Sports Med. 2006;34(7):1061-1071. doi: :10.1177/0363546505285585. Lanzi JT Jr, Chandler PJ, Cameron KL, Bader JM, Owens BD. Epidemiology of posterior glenohumeral instability in a young athletic population. Am J Sports Med. 2017;45(14):3315-3321. doi:10.1177/0363546517725067. Song DJ, Cook JB, Krul KP, et al. High frequency of posterior and combined shoulder instability in young active patients. J. Shoulder Elbow Surg. 2015;24(2):186-190. doi:10.1016/j.jse.2014.06.053. Antosh IJ, Tokish JM, Owens BD. Posterior shoulder instability: current surgical management. Sports Health. 2016;8(6):520-526. doi:10.1177/1941738116672446. Longo UG, Rizzello G, Locher J, et  al. Bone loss in patients with posterior gleno-humeral instability: a systematic review. Knee Surg Sports Traumatol Arthrosc. 2016;24(2):612-617. doi:10.1007/ s00167-014-3161-8. Shah N, Tung GA. Imaging signs of posterior glenohumeral instability. AJR Am J Roentgenol. 2009;192:730-735. Chen L, Keefe D, Park J, Resnick  D. Posterior bony humeral avulsion of glenohumeral ligament with reverse bony Bankart lesion. J  Shoulder Elbow Surg. 2009;18(3):e45-e49. doi:10.1016/j. jse.2008.09.014. Robinson C, Aderinto  J. Recurrent posterior shoulder instability. J Bone Joint Surg Am. 2005;87(4):883-892. doi:10.2106/JBJS.D.02906 Van Tongel A, Karelse A, Berghs B, Verdonk R, De Wilde  L. Posterior shoulder instability: current concepts review. Knee Surg Sports Traumatol Arthrosc. 2011;19(9):1547-1553. doi:10.1007/ s00167-010-1293-z. Tannenbaum EP, Sekiya JK. Posterior shoulder instability in the contact athlete. Clin Sports Med. 2013;32(4):781-796. doi:10.1016/j. csm.2013.07.011. Rouleau D, Hebert-Davies J. Incidence of associated injury in posterior shoulder dislocation. J Orthop Trauma. 2012;26(4):246-251. doi:10.1097/BOT.0b013e3182243909. Hines A, Cook JB, Shaha JS, et  al. Glenoid bone loss in posterior shoulder instability: prevalence and outcomes in arthroscopic treatment. Am J Sports Med. 2018;46(5):1053-1057. doi:10.1177/0363546517750628. Shaw JL. Bilateral posterior fracture-dislocation of the shoulder and other trauma caused by convulsive seizures. J Bone Joint Surg Am. 1971;53(7):1437-1440. Brown RJ. Bilateral dislocation of the shoulders. Injury. 1984;15:267-273. Goudie EB, Murray IR, Robinson CM. Instability of the shoulder following seizures. J Bone Joint Surg Br. 2012;94:721-728. Robinson C, Aderinto J. Posterior shoulder dislocations and fracturedislocations. J Bone Joint Surg. 2005;87:639-650. Robinson C, Seah M, Akhtar  M. The epidemiology, risk of recurrence, and functional outcome after an acute traumatic posterior dislocation of the shoulder. J Bone Joint Surg Am. 2011;93(17):16051613. doi:10.2106/JBJS.J.00973. Edelson JG. Localized glenoid hypoplasia. An anatomic variation of possible clinical significance. Clin Orthop Relat Res. 1995;(321):189-195. Weishaupt D, Zanetti M, Nyffeler RW, Gerber C, Hodler J. Posterior glenoid rim deficiency in recurrent (atraumatic) posterior shoulder instability. Skeletal Radiol. 2000;29(4):204-210. doi:10.1007/ s002560050594.

25.

26.

27.

28.

29.

30.

31. 32. 33.

34.

35.

36.

37.

38.

39. 40.

41.

42.

43.

44. 45. 46. 47.

231

Hurley JA, Anderson TE, Dear W, Andrish JT, Bergfeld JA, Weiker GG. Posterior shoulder instability. Surgical versus conservative results with evaluation of glenoid version. Am J Sports Med. 1992;20(4):396-400. doi:10.1177/036354659202000405. Owens BD, Campbell SE, Cameron KL. Risk factors for posterior shoulder instability in young athletes. Am J Sports Med. 2013;41(11):2645-2649. doi:10.1177/0363546513501508. Brewer BJ, Wubben RC, Carrera GF. Excessive retroversion of the glenoid cavity. A cause of non-traumatic posterior instability of the shoulder. J Bone Joint Surg Am. 1986;68(5):724-731. Williams RJ, Strickland S, Cohen M, Altchek DW, Warren RF. Arthroscopic repair for traumatic posterior shoulder instability. Am J Sports Med. 2003;31:203-209. Provencher MT, LeClere LE, King S, et  al. Posterior instability of the shoulder: diagnosis and management. Am J Sports Med. 2011;39(4):874-886. doi:10.1177/0363546510384232. Kang RW, Mahony GT, Harris TC, Dines JS. Posterior instability caused by batter’s shoulder. Clin Sports Med. 2013;32(4):797-802. doi:10.1016/j.csm.2013.07.012. Cho JH, Chung NS, Song HK, Lee DH. Recurrent posterior shoulder instability after rifle shooting. Orthopedics. 2012;35:e1677-1679. Detenbeck LC. Posterior dislocations of the shoulder. J  Trauma. 1972;12(3):183-192. doi:10.1097/00005373-197203000-00001. Heller KD, Forst J, Forst R, Cohen  B. Posterior dislocation of the shoulder: recommendations for a classification. Arch Orthop Trauma Surg. 1994;113:228-231. Neer CS  II. Involuntary inferior and multidirectional instability of the shoulder: etiology, recognition, and treatment. Instr Course Lect. 1985;34:232-238. Millett PJ, Clavert P Hatch GF  III, Warner JJ. Recurrent posterior shoulder instability. J  Am Acad Orthop Surg. 2006;14(8):464-476. doi:10.5435/00124635-200608000-00004. Schulz TJ, Jacobs B, Patterson RL  Jr. Unrecognized dislocations of the shoulder. J  Trauma Acute Care Surg. 1969;9(12):1009-1023. doi:10.1097/00005373-196912000-00005. Kowalsky MS, Levine WN. Traumatic posterior glenohumeral dislocation: classification, pathoanatomy, diagnosis, and treatment. Orthop Clin North Am. 2008;39:519-533. Fuchs B, Jost B, Gerber  C. Posterior-inferior capsular shift for the treatment of recurrent, voluntary posterior subluxation of the shoulder. J Bone Joint Surg Am. 2000;82:16-25. McLaughlin HL. Posterior dislocation of the shoulder. J Bone Joint Surg Am. 1952;24A(3):584-590. Krishnan SG, Hawkins RJ, Warren RF, eds. The Shoulder and the Overhead Athlete. 1st  ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2004. Kim SH, Park JC, Park JS, Oh I. Painful jerk test: a predictor of success in nonoperative treatment of posteroinferior instability of the shoulder. Am J Sports Med. 2004;32:1849-1855. Bloom MH and Obata WG. Diagnosis of posterior dislocation of the shoulder with use of Velpeau axillary and angle-up roentgenographic Views. J Bone Joint Surg Am. 1967;49(5):943-949. Walch G, Boileau P, Martin B, Dejour  H. Unreduced posterior luxations and fractures-luxations of the shoulder. Apropos of 30 cases [article in French]. Rev Chir Orthop Reparatrice Appar Mot. 1990;76(8):546-558. Richardson JB, Ramsay A, Davidson JK, Kelly IG. Radiographs in shoulder trauma. J Bone Joint Surg Br. 1988;70:457-460. Perron AD, Jones RL. Posterior shoulder dislocation: avoiding a missed diagnosis. Am J Emerg Med. 2000;18:189-191. Hawkins RJ, Neer CS  II, Pianta RM, Mendoza  F. Locked posterior dislocation of the shoulder. J Bone Joint Surg Am. 1987;69(1):9-18. Wadlington,VR, Hendrix RW, Rogers LF. Computed tomography of posterior fracture-dislocations of the shoulder: case reports. J Trauma. 1992;32:113-115.

232 48.

49.

50.

51.

52.

53.

54.

55. 56. 57.

58.

59.

60.

61.

62.

63.

64.

65.

66.

Chapter 20 Griffith JF, Yung PS, Antonio GE, Tsang PH, Ahuja AT, Chan KM. CT compared with arthroscopy in quantifying glenoid bone loss. AJR Am J Roentgenol. 2007;189(6):1490-1493. doi:10.2214/AJR.07.2473. Harish S, Nagar A, Moro J, Pugh D, Rebello R, O’Neill  J. Imaging findings in posterior instability of the shoulder. Skeletal Radiol. 2008;37(8):693-707. doi:10.1007/s00256-008-0487-7. Itoi E, Lee SB, Berglund LJ, Berge LL, An KN. The effect of a glenoid defect on anteroinferior stability of the shoulder after Bankart repair: a cadaveric study. J Bone Joint Surg Am. 2000;82:35-46. Saito H, Itoi E, Sugaya H, Minagawa H, Yamamoto N, Tuoheti  Y. Location of the glenoid defect in shoulders with recurrent anterior dislocation. Am J Sports Med. 2005;33(6):889-893. doi:10.1177/0363546504271521. Nacca C, Gil JA, Badida R, Crisco JJ, Owens BD. Critical glenoid bone loss in posterior shoulder instability. Am J Sports Med. 2018;46(5):1058-1063. doi:10.1177/0363546518758015. Bryce CD, Davison AC, Okita N, Lewis GS, Sharkey NA, Armstrong AD. A biomechanical study of posterior glenoid bone loss and humeral head translation. J Shoulder Elbow Surg. 2010;19(7):994-1002. doi:10.1016/j.jse.2010.04.010. Backer M, Warren RF. Glenohumeral instability in adults. In: DeLee JC, Drez DJ, Miller MD, eds. DeLee and Drez’s Orthopaedic Sports Medicine: Principles and Practice. 2nd ed. Philadelphia, PA: Saunders; 2003: 1020-1034. Burkhead W, Rockwood C. Treatment of instability of the shoulder with an exercise program. J Bone Joint Surg. 1992;74:890-896. Fronek J, Warren R, Bowen M. Posterior subluxation of the glenohumeral joint. J Bone Joint Surg Am. 1989;71(2):205-216. Matsen FA, Chebli C, Lippitt S; American Academy of Orthopaedic Surgeons. Principles for the evaluation and management of shoulder instability. J Bone Joint Surg Am. 2006;88:648-659. Purchase RJ, Wolf EM, Hobgood ER, Pollock ME, Smalley CC. Hill-Sachs “remplissage”: an arthroscopic solution for the engaging Hill-Sachs lesion. Arthroscopy. 2008;24(6):723-726. doi:10.1016/j. arthro.2008.03.015. Longo UG, et al. Remplissage, humeral osteochondral grafts, Weber osteotomy, and shoulder arthroplasty for the management of humeral bone defects in shoulder instability: systematic review and quantitative synthesis of the literature. Arthroscopy. 2014;30(12):1650-1666. doi:10.1016/j.arthro.2014.06.010. Duey RE, Burkhart SS. Arthroscopic treatment of a reverse HillSachs lesion. Arthrosc Tech. 2013;2(2):e155-e159.doi:10.1016/j. eats.2013.01.007. Martetschläger F, Padalecki JR, Millett PJ. Modified arthroscopic McLaughlin procedure for treatment of posterior instability of the shoulder with an associated reverse Hill-Sachs lesion. Knee Surg Sports Traumatol Arthrosc. 2013;21(7):1642-1646. doi:10.1007/ s00167-012-2237-6. Luedke C, Tolan SJ, Tokish JM. Arthroscopic repair of posterior bony Bankart Lesion and Subscapularis Remplissage. Arthrosc Tech. 2017;6:e689-e694. Gerber C, Lambert S. Allograft reconstruction of segmental defects of the humeral head for the treatment of chronic locked posterior dislocation of the shoulder. J  Bone Joint Surg Am. 1996;78(3):376382. doi:10.2106/00004623-199603000-00008. Begin M, Gagey O, Soubeyrand  M. Acute bilateral posterior dislocation of the shoulder: One-stage reconstruction of both humeral heads with cancellous autograft and cartilage preservation. Chir Main. 2012;31(1):34-37. doi:10.1016/j.main.2012.01.002. Bessette MC, Frisch NC, Kodali P, Jones MH, Miniaci A. Partial resurfacing for humeral head defects associated with recurrent shoulder instability. Orthopedics. 2017;40:e996-e1003. Cheng SL, Mackay MB, Richards RR. Treatment of locked posterior fracture-dislocations of the shoulder by total shoulder arthroplasty. J. Shoulder Elbow Surg. 1997;6:11-17.

67.

68.

69.

70.

71.

72.

73.

74.

75.

76.

77.

78.

79.

80.

81.

82.

83.

Ponce BA, Millett PJ, Warner JJP. Management of posterior glenohumeral instability with large humeral head defects. Tech Shoulder Elb Surg. 2004;5(3):146-156. doi:10.1097/01.bte.0000130603.30293.3c. Keppler P, Holz U, Thielemann FW, Meinig  R. Locked posterior dislocation of the shoulder: treatment using rotational osteotomy of the humerus. J  Orthop Trauma. 1994;8(4):286-292. doi:10.1097/00005131-199408000-00003. Owens BD, Tucker CJ, Zacchilli  M. Surgical management of posterior shoulder instability. Curr Orthop Pract. 2011;22(6):474-482. doi:10.1097/BCO.0b013e318232d7ca. Barbier O, Ollat D, Marchaland JP, Versier G. Iliac bone-block autograft for posterior shoulder instability. Orthop Traumatol Surg Res. 2009;95(2):100-107. doi:10.1016/j.otsr.2008.09.008. Bessems JH, Vegter J. Glenoplasty for recurrent posterior shoulder instability. Good results in 13 cases followed for 1-16 years. Acta Orthop Scand. 1995;66(6):535-537. doi:10.3109/17453679509002310. Arciero RA, Mazzocca AD. Posterior acromial bone block augmentation for the treatment of posterior glenoid bone loss associated with recurrent posterior shoulder instability. Tech Shoulder Elb Surg. 2006;7:210-217. Kouvalchouk JF, Coudert X, Watin Augouard L, Da Silva Rosa R, Paszkowski A. Treatment of posterior instability of the shoulder joint using an acromial stop with a pediculated deltoid flap [article in French]. Rev Chir Orthop Reparatrice Appar Mot. 1993;79(8):661-665. Gupta AK, Chalmers PN, Klosterman E, Harris JD, Provencher MT, Romeo AA. Arthroscopic distal tibial allograft augmentation for posterior shoulder instability with glenoid bone loss. Arthrosc Tech. 2013;2(4):e405-e411. doi:10.1016/j.eats.2013.06.009. Tokish JM, Fitzpatrick K, Cook JB, Mallon  W.J. Arthroscopic distal clavicular autograft for treating shoulder instability with glenoid bone loss. Arthrosc Tech. 2014;3(4):e475-e481. doi:10.1016/j. eats.2014.05.006. Smith T, Goede F, Struck M, Wellmann  M. Arthroscopic posterior shoulder stabilization with an iliac bone graft and capsular repair: a novel technique. Arthrosc Tech. 2012;1(2):e181-e185. doi:10.1016/j. eats.2012.07.003. Finkelstein JA, Waddell JP, O’Driscoll SW, Vincent  G. Acute posterior fracture dislocations of the shoulder treated with the Neer modification of the McLaughlin procedure. J Orthop Trauma. 1995;9(3):190-193. Charalambous CP, Gullett TK, Ravenscroft MJ. A modification of the McLaughlin procedure for persistent posterior shoulder instability: technical note. Arch Orthop Trauma Surg. 2009;129(6):753-755. doi:10.1007/s00402-008-0721-8. Andrieu K, Barth J, Saffarini M, Clavert P, Godenèche A, Mansat P; French Arthroscopy Society. Outcomes of capsulolabral reconstruction for posterior shoulder instability. Orthop Traumatol Surg Res. 2017;103(8S):S189-S192. doi:10.1016/j.otsr.2017.08.002. Servien E, Walch G, Cortes ZE, Edwards TB, O’Connor DP. Posterior bone block procedure for posterior shoulder instability. Knee Surg Sports Traumatol Arthrosc. 2007;15(9):1130-1136. doi:10.1007/ s00167-007-0316-x. Meuffels DE, Schuit H, van Biezen FC, Reijman M, Verhaar JA. The posterior bone block procedure in posterior shoulder instability: a long-term follow-up study. J Bone Joint Surg Br. 2010;92(5):651-655. doi:10.1302/0301-620X.92B5.23529. Boileau P, Hardy MB, McClelland WB, Thélu CE, Schwartz DG. Arthroscopic posterior bone block procedure: a new technique using suture anchor fixation. Arthrosc Tech. 2013;2(4):e473-e477. doi:10.1016/j.eats.2013.07.004. Schwartz DG, Goebel S, Piper K, Kordasiewicz B, Boyle S, Lafosse L. Arthroscopic posterior bone block augmentation in posterior shoulder instability. J Shoulder Elbow Surg. 2013;22(8):1092-1101. doi:10.1016/j.jse.2012.09.011.

21 Postsurgical Rehabilitation of Posterior Instability Evan W. James, MD; Kenneth M. Lin, MD; Lawrence V. Gulotta, MD; and Samuel A. Taylor, MD

Posterior shoulder instability is relatively rare compared to anterior or multidirectional instability, accounting for just 2% to 5% of unstable shoulders.1-3 Posterior instability can result from an acute, traumatic posterior dislocation event, such as following a motor vehicle accident with the arm in the forward-flexed adducted position, or from repetitive microtrauma, such as the posteriorly directed forces experienced by a football lineman. Posterior subluxation of the humeral head relative to the glenoid often results in tearing of the posterior labrum from the posterior glenoid rim and attenuation of the glenohumeral capsule.4 The labrum is a rim of fibrocartilage surrounding the glenoid that functions to increase congruency of the glenohumeral joint, thereby providing improved stability to the shoulder. When a posterior labral tear occurs, there is glenohumeral incongruency and relative laxity of the posterior glenohumeral capsule leading to instability to the glenohumeral joint when a posteriorly directed force is exerted on the upper extremity. Treatment options are initially nonsurgical and include physical therapy focused on dynamic stabilization exercises. When conservative approaches prove insufficient, then operative shoulder stabilization is indicated followed by a phase-specific rehabilitation program. Although many first-time posterior dislocators may initially try nonoperative management, a high percentage of these patients eventually require surgical stabilization. A recent study by Woodmass et  al, which evaluated 143 patients with posterior shoulder instability from 1994 to 2015, included 79 patients initially managed nonoperatively.5 Of the nonoperatively managed patients, 46% converted to surgery between 1 and 10  years after the diagnosis, and 70% of patients converted to surgery by final follow-up.

Posterior shoulder stabilization is typically performed arthroscopically using suture anchors to stabilize the posterior labrum on the glenoid rim with or without capsular plication (Figure  21-1).6,7 Postoperative immobilization occurs in neutral rotation. After surgery, a rehabilitation program under the direction of the treating surgeon and an experienced physical therapist is critical to achieving an excellent outcome. The purpose of this chapter is to review postsurgical rehabilitation guidelines following posterior shoulder stabilization, including bracing, adjunctive treatments, phase-specific rehabilitation protocols, and return-to-play guidelines. The protocol outlined in this chapter was developed in cooperation with the Hospital for Special Surgery Department of Rehabilitation with minor modifications and has been used with great success among the authors of this chapter.8

PHASE-SPECIFIC REHABILITATION PROTOCOL The primary goal of rehabilitation following posterior shoulder stabilization is to reestablish stability of the glenohumeral joint. This is accomplished by restoring normal shoulder strength, flexibility, range of motion, and scapulohumeral rhythm, with the ultimate goal of returning to sports and other activities. We follow a general progression through a phase-based approach reviewed below, which includes phase I (immediate postoperative), phase II (protected range of motion), phase III (range of motion normalization and neuromuscular re-education), phase IV (normalization of strength, flexibility, and scapulohumeral rhythm), phase V (return to play), and phase VI (maintenance).

- 233 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 233-240). © 2021 SLACK Incorporated.

234

Chapter 21

Figure 21-1. Arthroscopic images from a 16-year- old male baseball pitcher with posterior shoulder instability. Arthroscopic images viewed from an anterior superior portal show: (A) a posterior labrum torn off the posterior glenoid rim with redundant posterior capsule, (B) mobilization of the torn labrum with a labral elevator, (C) debridement of the posterior glenoid rim, and (D) the final repair using a knotless suture anchor construct.

Phase I (Weeks 0 to 2)

Phase II (Weeks 2 to 4)

The immediate postoperative period typically consists of the first 2 weeks after surgery. During this phase, emphasis is placed on pain control and protecting the surgical repair. Patients are required to wear a shoulder immobilizer, or “gunslinger” shoulder brace, in neutral rotation at all times except when performing approved home exercises (Figure  21-2). Patients must remain non-weight–bearing on the operative extremity and avoid internal rotation. Patients should be educated on how to safely don and doff their sling, as well as how to perform activities of daily living such as bathing and dressing while abiding by range of motion limitations. The immobilizer should be positioned in the scapular plane with the arm in neutral internal and external rotation, which avoids excessive strain on the posterior capsule and surgical repair. Full supported range of motion of the elbow, wrist, and digits is encouraged to avoid stiffness and aid in edema reduction. Formal physical therapy is typically not employed during this immediate postoperative phase. Adjunctive treatments including cryotherapy, oral analgesics, and oral anti-inflammatory medications are recommended on an as-needed basis.

Some clinicians wish to begin formal physical therapy 2 weeks postoperatively, whereas others may wish to abstain until week 4 postoperatively. In either case, the focus during this time is to initiate early controlled range of motion without compromising the integrity of the surgical repair (Table 21-1). Emphasis is placed on minimizing pain, swelling, and inflammation while continuing to protect the surgical repair. Active-assisted range of motion may be used during this phase in which the patient uses the unaffected extremity to control the operative extremity through the desired range of motion. Active-assisted forward flexion is performed in the scapular plane with the patient in the supine position to mitigate the effects of gravity and assist in scapular stabilization while the operative extremity is fully extended at the elbow. The shoulder is then forward flexed in a controlled fashion while supported by the unaffected extremity to a maximum of 90  degrees. Active-assisted external rotation is performed with the elbow flexed at 90  degrees while the unaffected extremity guides the operative extremity into external rotation. Cane-assisted active-assisted motion may be used to guide the operative extremity through the desired arc of motion. Pain, however, should be closely monitored and excessive stretching beyond the desired range of motion

Postsurgical Rehabilitation of Posterior Instability

235

Figure 21-2. A “gunslinger” brace with an abduction pillow in neutral rotation as viewed in the (A) anterior, (B) lateral, and (C) oblique planes is recommended during the first 4 weeks after surgery.

Table 21-1. Phase I (Postoperative Weeks 2 to 4) Goals

Protect surgical repair Minimize pain, swelling, and inflammation Achieve AAROM forward elevation in scapular plane to 90 degrees Achieve AAROM external rotation to 30 degrees Initiate home exercise program

Precautions

Shoulder immobilizer at all times when not performing rehabilitation exercises Limit cross-body adduction to neutral Limit internal rotation to neutral

Exercises

AAROM forward elevation in scapular plane to 90 degrees AAROM external rotation to 30 degrees Sidelying scapular mobility and stability Deltoid isometrics in neutral (submaximal effort) Rotator cuff isometrics in neutral (submaximal effort) AROM wrist, elbow, digits Gripping exercises

Adjunctive treatments

Modalities as needed

Criteria to advance to next phase

Adequate pain control and minimal inflammation Achieve external rotation to 30 degrees

Abbreviations: AAROM, active assisted range of motion; AROM, active range of motion.

must be avoided. Elbow, wrist, and digit range of motion is encouraged through a full arc of motion. Gripping exercises using a stress ball or therapy putty may also be used for distal motion in the operative extremity. In addition to range-of-motion exercises, isometric exercises with submaximal effort may also initiated during this phase. Scapular isometrics are performed with the patient lying on his or her unaffected side. Rotator cuff isometrics are performed in a seated or standing position with the shoulder in neutral rotation. Isometrics are performed both for internal and external rotation. Again, activities that produce pain should be avoided because this is often indicative of excessive strain on the posterior capsule. A shoulder immobilizer should be continued at all times except when performing rehabilitation exercises. Horizontal

cross-body adduction and internal rotation are limited to neutral to avoid excessive stretch on the posterior capsule. Adjunctive treatments including cryotherapy, electrical stimulation, oral analgesics, and oral anti-inflammatory medications may again be used on an as-needed basis. Finally, the surgeon and physical therapist should work together to provide a home-based exercise program with clearly delineated exercises and precautions to perform outside formal physical therapy.

Phase III (Weeks 4 to 6) The goal of phase III is to improve shoulder range of motion and neuromuscular activation with isometric exercises (Table  21-2). Patients may discontinue the shoulder

236

Chapter 21

Table 21-2. Phase II (Postoperative Weeks 4 to 6) Goals

Protect the surgical repair Achieve AAROM forward elevation in scapular plane to 90 degrees Achieve internal rotation to 45 degrees Initiate rotator cuff strengthening Progress home exercise program Discontinue shoulder immobilizer

Precautions

Protect against excessive stretch on the posterior capsule Protect surgical repair during activities of daily living Limit cross-body adduction to neutral Limit internal rotation to 45 degrees

Exercises

AAROM forward elevation in scapular plane to 90 degrees AAROM external rotation to 30 degrees Modified closed chain scapular strengthening for posterior capsule Deltoid isometrics in neutral (submaximal effort) Rotator cuff isometrics in internal and external rotation (submaximal effort)

Adjunctive treatments

Modalities as needed

Criteria to advance to next phase

Adequate pain control and minimal inflammation Achieve 4/5 strength for internal and external rotation Achieve forward elevation in the scapular plane to 90 degrees

Abbreviation: AAROM, active assisted range of motion.

immobilizer beginning at postoperative week 4. Active assisted motion is performed in the scapular plane to a maximum of 90 degrees of forward flexion and 30 degrees of external rotation. Internal rotation is gradually advanced in this phase from neutral to 45 degrees. Cross-body horizontal adduction is limited to neutral. Abduction with external rotation to 30 degrees is initiated, which off-loads stress on the posterior capsule when performing scapular-stabilization exercises. Rotator cuff isometrics in internal and external rotation and deltoid isometrics should be performed with submaximal effort. Scapular stabilization should be advanced to include modified closed-chain exercises in the scapular plane. By strengthening the periscapular musculature during this phase, a solid foundation is created at the scapulothoracic level, which will support gains in active shoulder range of motion and shoulder strengthening later in the program. Closed-chain exercises in the scapular plane improve glenohumeral congruency without exerting excessive stress on the posterior labrum and capsule. At this stage patients must demonstrate adequate progress toward achieving the earlier stated range-of-motion parameters. Failure to demonstrate adequate improvement in range of motion is concerning for a stiff shoulder, which could portend a poor long-term outcome. In these instances, patients may require additional sessions with a physical therapist to accelerate improvements. Patients who struggle

during this phase may also use aquatic therapy, using the buoyancy of water to improve range of motion in a controlled fashion.9 We find aqua therapy to be a particularly useful tool to safely regain motion. Compliance with the home exercise program should also be assessed. Conversely, range of motion that easily progresses beyond these limits is also concerning for excessive joint laxity, which can lead to recurrent instability. These patients may require an extended period of immobilization or a revised exercise program. An open channel of communication among the patient, surgeon, and physical therapist is essential to address these concerns on an ad hoc basis.

Phase IV (Weeks 6 to 12) The goal of phase IV is to achieve normal shoulder range of motion, strength, flexibility, and scapulohumeral rhythm while continuing to protect the surgical repair (Table 21-3). This is accomplished by continuing to build on the exercises and rehabilitation principles used in the earlier phases. Patients should continue to avoid excessive passive stretching of the posterior join capsule and exercises that result in excessive inflammation of the rotator cuff. The volume and intensity of exercises should be titrated gradually to avoid compromising the repair. The patient should continue active assisted range-ofmotion exercises in internal rotation, external rotation, and

Postsurgical Rehabilitation of Posterior Instability

237

Table 21-3. Phase III (Postoperative Weeks 6 to 12) Goals

Protect surgical repair Achieve full range of motion Achieve normal scapulohumeral rhythm Restore full scapula and shoulder strength Restore full scapula and shoulder flexibility Progress home exercise program

Precautions

Avoid excessive passive stretching of posterior capsule Avoid rotator cuff inflammation

Exercises

AAROM internal rotation, external rotation, and forward elevation Internal and external rotation with rolled towel under axilla Scapula strengthening program Humeral head stabilization program Proprioceptive neuromuscular facilitation exercises when strength is full Isokinetic training Latissimus strengthening Upper extremity endurance exercises

Adjunctive treatments

Modalities as needed

Criteria to advance to next phase

Complete resolution of pain Full strength, flexibility, and range of motion Normal glenohumeral rhythm through full range of motion

Abbreviation: AAROM, active assisted range of motion.

forward flexion. Modified internal and external rotation using a rolled towel placed under the axilla is recommended to improve congruency of the glenohumeral joint in the scapular plane and optimize the length-tension orientation of the shoulder musculature.10,11 Resistance bands in internal and external rotation may be added. These are typically performed with the patient standing while holding a resistance band secured to the wall. Scapular-strengthening exercises to build a strong scapulothoracic foundation for higherintensity exercises later in the program are a significant focus of this phase. Scapular-strengthening exercises include standing weighted shoulder shrugs, seated weighted rows, and supine weighted serratus punches. Finally, latissimus dorsi strengthening is initiated in the plane of the scapula with the patient standing while holding a resistance band secured to the wall. Once full 5/5 muscular strength has been achieved, the patient may begin active range of motion in the plane of the scapula and proprioceptive neuromuscular facilitation exercises. Endurance training may also be started using an upper body ergometer. For aerobic exercise, patients are permitted to use a recumbent stationary bike, but are not allowed to use a standard stationary bike because arms on the handlebars generate a posteriorly directed force on the glenohumeral joint and thus stresses the surgical repair. Criteria to advance to the final phase include complete resolution of pain, as well

as normal strength, flexibility, and range of motion, and glenohumeral rhythm.

Phase V (Weeks 12 to 18) The goal of phase V is to transition patients back to their desired sports and activities (Table 21-4). A running program may be initiated to rebuild overall endurance, and patients are now permitted to use a standard stationary bicycle. The physical therapist should work with each patient to create a personalized program to meet future functional demands. As stresses on the operative extremity increase, it is impor tant to avoid exercises and sport-specific tasks that produce pain. Training volume and intensity should be increased gradually. Flexibility exercises, isokinetic training, and endurance training should be continued and progressed as tolerated. However, excessive stretching of the posterior capsule should continue to be avoided. Rotator cuff strengthening may be performed with the shoulder in 90 degrees of abduction and 90 degrees of external rotation. This is especially impor tant for throwing athletes, who require power in the overhead position. Once full painless strength and flexibility is achieved through a full arc of motion, a sport-specific Plyometrics program may be initiated. Plyometric exercises should be tailored to match functional demands of each individual

238

Chapter 21

Table 21-4. Phase IV (Postoperative Weeks 12 to 18) Goals

Achieve normal neuromuscular coordination Initiate sport-specific activity program Internal and external rotation isokinetic strength ≥ to other side External rotation:internal rotation strength ratio > 66% Establish independent sport-specific program

Precautions

Avoid pain with increasing sport-specific training program Avoid overtraining

Exercises

Eccentric upper-extremity strengthening Internal and external strengthening at 90/90 position Continue flexibility exercises Continue isokinetic training Continue endurance training Initiate sport-specific activity program Core and lower-extremity strengthening Begin Plyometrics with emphasis on sport-specific movements

Adjunctive treatments

Modalities as needed

Criteria to advance to next phase

Pain-free participation in sport-specific activities Isokinetic strength equal to contralateral upper extremity External rotation:internal rotation strength ratio > 66% Independent sport-specific program established

patient. Plyometrics below 90  degrees of forward flexion are typically started first, and later progressed to overhead exercises. For example, plyometric chest passes should be completed prior to progressing overhead Plyometrics. Again, volume and intensity should be increased gradually. If the patient reports sharp pain or feeling of instability, the surgeon must be notified, exercises modified, and return to a prior phase of the program may be required. Finally, it is also impor tant to identify other deficiencies in muscular strength and endurance. For example, deficiencies in lower-extremity and core strength, neuromuscular control, and side-to-side imbalances can alter mechanics during throwing in an overhead athlete. Additional strengthening, flexibility, and coordination exercises may be added during this phase of the program to address deficiencies before returning to higher-level activities. After successfully completing the previously described program, the patient, surgeon, and physical therapist should convene to evaluate readiness for return to play. A self-directed strength and flexibility regimen should be continued after returning to play to avoid reinjury.

Phase VI (Weeks 18+) The goal of phase VI—the final phase of rehabilitation— is to establish a maintenance program to prevent reinjury. After patients have demonstrated adequate range of motion,

strength, and muscular endurance to participate in sport, they should be instructed on a home exercise program focused on maintenance of the attained dynamic stability. Exercises should be provided that can be performed independently or incorporated into their sport-specific training program. From this point forward, reevaluation by the treating surgeon and physical therapist may proceed on an as-needed basis to address any new symptoms or patient concerns.

RETURN TO PLAY GUIDELINES There are no widely accepted guidelines for return to sport following posterior shoulder dislocation; rather, each patient is handled on a case-by-case basis, because dif ferent sports have dif ferent demands on the shoulder and require dif ferent functional range of motion and levels of impact. Typically, athletes may begin returning to sport between 5 and 8 months postoperatively under controlled conditions. Before returning to the previous level of play the patient must achieve full range of motion without pain, and should regain at least 80% of strength compared to the contralateral shoulder, which usually occurs around 6 to 9 months after surgery in the case of posterior stabilization.12 Rates of return to sport and return to prior level of play are lower for posterior instability than anterior instability patients, and higher for contact athletes than throwing athletes.13,14 A large prospective study by Radkowski and

Postsurgical Rehabilitation of Posterior Instability colleagues showed that despite similar pain, stability, function, range of motion, strength, and American Shoulder and Elbow Surgeons scores, nonthrowing athletes were able to return to their previous level of play at a higher rate than throwing athletes (71% vs 55% at 27 months) after posterior stabilization.15 A recent meta-analysis by DeLong et  al showed that among all athletes, return to sport at any level of play was 91.81%, whereas return to preinjury level was 67.40%.14 Among contact athletes, return to any level of play was 89.33%, whereas return to preinjury level was 71.91%, compared to 83.87% and 58.06% in overhead or throwing athletes following surgical stabilization. In the future, a greater understanding of the biomechanics and pathoanatomy, as well as more precise functional shoulder outcome measures in throwing athletes, will be necessary. Athletes hoping to return to overhead or throwing sports should be counseled appropriately.

SPORT-SPECIFIC TASKS Once adequate motion and strength have been achieved, return to sport is dependent on the patient’s functional or sport-specific goals. Despite varying pathology at the time of surgery and varying demands of sports such as throwing, golf, tennis, or swimming, the theme is similar for each— introduce an interval training program to gradually increase activity, strength, and muscular endurance to allow effective and protected motion.16 It is impor tant that the rehabilitation program not only incorporate specific exercises that mimic the sport or activity, but do so at an appropriate dosage or volume that gradually resembles competition demands.17 For example, a 3-phase interval throwing program can be initiated at 4 months postoperatively for throwing athletes, with progression based on throwing pain free at a specified distance.18 The first phase is flat ground throwing, focusing on mechanics and strengthening. The second phase consists of throwing off the mound, starting with fastballs only at 50%, 75%, and 100% effort, followed by initiating throwing breaking balls and progressing in a similar fashion. Following the second phase, if the athlete remains pain free after simulated innings for 2 weeks, he or she may return to game play. Once an athlete returns to game play, it is imperative to monitor for recurrent pain and instability, which may require further evaluation from a physician.

CONCLUSION Postoperative rehabilitation following arthroscopic posterior stabilization follows a periodized phase-based approach with each subsequent phase building on gains from prior phases. The immediate postoperative period is dedicated to protecting the surgical repair, minimizing inflammation, and improving pain. As the patient transitions to the next rehabilitation phase, the goal is to initiate early controlled range of motion without compromising the integrity of the surgical repair. The third phase focuses on continuing

239

to improve shoulder range of motion and neuromuscular activation with isometric exercises. After meeting criteria to progress, the patient transitions to the fourth phase in which normal shoulder range of motion, strength, flexibility, and scapulohumeral rhythm are achieved. The fifth phase is dedicated to meeting the functional demands of return to sports and activities, and includes Plyometric exercises and sport-specific drills. Return-to-play criteria should be individualized to each patient. After returning to sports and activities, patients turn to the sixth and final phase focused on diligent maintenance of a shoulder strength and flexibility program to prevent recurrence.

REFERENCES 1.

2.

3. 4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

14.

Mair SD, Zarzour RH, Speer KP. Posterior labral injury in contact athletes. Am J Sports Med. 1998;26(6):753-758. doi:10.1177/036354 65980260060301. Robinson CM, Seah M, Akhtar MA. The epidemiology, risk of recurrence, and functional outcome after an acute traumatic posterior dislocation of the shoulder. J Bone Joint Surg Am. 2011;93(17):16051613. doi:10.2106/JBJS.J.00973. Schwartz E, Warren RF, O’Brien SJ, Fronek J. Posterior shoulder instability. Orthop Clin North Am. 1987;18(3):409-419. Ockert B, Braunstein V, Sprecher CM, Shinohara Y, Milz  S. Fibrocartilage in various regions of the human glenoid labrum. An immunohistochemical study on human cadavers. Knee Surg Sports Traumatol Arthrosc. 2012;20(6):1036-1041. doi:10.1007/ s00167-011-1686-7. Woodmass JM, Lee J, Johnson NR, et  al. Nonoperative management of posterior shoulder instability: an assessment of survival and predictors for conversion to surgery at 1 to 10  years after diagnosis. Arthroscopy. 2019;35(7):1964-1970. doi:10.1016/j. arthro.2019.01.056. Bradley JP, Forsythe B, Mascarenhas R. Arthroscopic management of posterior shoulder instability: diagnosis, indications, and technique. Clin Sports Med. 2008;27(4):649-670. doi:10.1016/j.csm.2008.06.001. Bradley JP, McClincy MP, Arner JW, Tejwani SG. Arthroscopic capsulolabral reconstruction for posterior instability of the shoulder: a prospective study of 200 shoulders. Am J Sports Med. 2013;41(9):20052014. doi:10.1177/0363546513493599. Levinson  M. Posterior stabilization surgery. In Cioppa-Mosca J, Cahill JB, Young Tucker C, eds. Postsurgical Rehabilitation Guidelines for the Orthopedic Clinician. St. Louis, MO: Mosby Elsevier; 2006. Speer KP, Cavanaugh JT, Warren RF, Day L, Wickiewicz TL. A role for hydrotherapy in shoulder rehabilitation. Am J Sports Med. 1993;21(6):850-853. doi:10.1177/036354659302100616. Graichen H, Stammberger T, Bonel H, Karl-Hans Englmeier, Reiser M, Eckstein  F. Glenohumeral translation during active and passive elevation of the shoulder—a 3D open-MRI study. J  Biomech. 2000;33(5):609-613. doi:10.1016/s0021-9290(99)00209-2. Saha AK. The classic. Mechanism of shoulder movements and a plea for the recognition of “zero position” of glenohumeral joint. Clin Orthop Relat Res. 1983;(173):3-10. Tannenbaum EP, Sekiya JK. Posterior shoulder instability in the contact athlete. Clin Sports Med. 2013;32(4):781-796. doi:10.1016/j. csm.2013.07.011. DeLong JM, Bradley JP. Posterior shoulder instability in the athletic population: variations in assessment, clinical outcomes, and return to sport. World J Orthop. 2015;6(11):927-934. doi:10.5312/wjo. v6.i11.927. DeLong JM, Jiang K, Bradley JP. Posterior instability of the shoulder: a systematic review and meta-analysis of clinical outcomes. Am J Sports Med. 2015;43(7):1805-1817. doi:10.1177/0363546515577622.

240 15.

16.

Chapter 21 Radkowski CA, Chhabra A, Baker CL  III, Tejwani SG, Bradley JP. Arthroscopic capsulolabral repair for posterior shoulder instability in throwing athletes compared with nonthrowing athletes. Am J Sports Med. 2008;36(4):693-699. doi:10.1177/0363546508314426. Reinold MM, Wilk KE, Reed J, Crenshaw K, Andrews JR. Interval sport programs: guidelines for baseball, tennis, and golf. J Orthop Sports Phys Ther. 2002;32(6):293-298. doi:10.2519/jospt.2002.32.6.293.

17.

18.

Watson L, Balster S, Warby SA, Sadi J, Hoy G, Pizzari T. A comprehensive rehabilitation program for posterior instability of the shoulder. J Hand Ther. 2017;30(2):182-192. doi:10.1016/j.jht.2017.05.007. Chang ES, Greco NJ, McClincy MP, Bradley JP. Posterior shoulder instability in overhead athletes. Orthop Clin North Am. 2016;47(1):179187. doi:10.1016/j.ocl.2015.08.026.

22 Return to Play Following Posterior Stabilization Tracey Didinger, MD; Jennifer Reed, NP; and Eric McCarty, MD

Posterior shoulder instability, in comparison to anterior instability, is relatively uncommon. Posterior instability represents 2% to 10% of shoulder instability.1-3 Hawkins emphasized the difference between recurrent posterior dislocations and subluxations.4 Athletes often sustain traumatic posterior shoulder dislocations as a result of a direct blow to the anterior shoulder with the arm flexed, adducted, and internally rotated. Athletes may also have generalized ligamentous laxity which contributes to repetitive microtrauma causing recurrent posterior subluxations (RPS). RPS can be seen in overhead athletes, swimmers, weightlifters, football lineman, tennis players, and others.5,6 Along with performing a thorough history and physical exam, physicians should maintain a high index of suspicion when evaluating patients for posterior instability. Patients often report pain with the shoulder in provocative positions including forward flexion, adduction, and internal rotation.7 As shown by Pollock and Bigliani,8 two-thirds of athletes who ultimately required surgery presented with symptoms using their shoulder outside of sport, particularly when above shoulder height. Ultimately it is impor tant to understand the athlete’s sport, position, future goals, and requirements when considering his or her post-surgical rehabilitation and return to play. Greater details of treatment for posterior instability was discussed in Chapters 19 and 20; however, numerous authors recommend a trial of conservative management for nontraumatic posterior instability.4 This includes at least 6 months of physical therapy focusing on shoulder range of motion (ROM) and increasing the strength and control of the dynamic shoulder stabilizers.9 Surgical intervention is often

required particularly in athletes that sustained a traumatic posterior dislocation. This chapter will focus on a series of phases in the rehabilitation following posterior stabilization with the goal of return to play, keeping in mind these phases should not be approached strictly sequentially as there is overlap throughout. The importance of a team approach among the surgeon, athlete, and physical therapist cannot be overemphasized. Throughout the initial phases of recovery there is an intricate balance between immobilization to allow the repair to heal and mobility to prevent stiffness and muscle shutdown. Rehabilitation progresses over approximately six to nine months to include increasing ROM, strengthening, and ultimately sport-specific programs. Goals for an athlete should mirror an ability to first gain sport-specific skills and ability to perform, followed by practice in controlled situations, and finally return to play in competition.

POSTERIOR STABILIZATION REHABILITATION Phase I: 0 to 2 Weeks The initial goals following surgery include healing of the incisions, managing pain and inflammation, protecting the repaired structures, and minimizing the effects of immobilization. Following arthroscopic or open posterior stabilization patients should be placed in a sling using an abduction pillow in neutral or slight external rotation (ER) (Figures 22-1A and 22-1B). The purpose of ER is to limit tension and protect

- 241 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 241-247). © 2021 SLACK Incorporated.

242

Chapter 22

A

B

Figures 22-1. (A and B) Example of an arm in sling in neutral to slight external rotation.

the posterior structures. Patients may remove the sling for showering and exercises, other wise they are to remain in the sling 24 hours a day. The need for compliance with sling wear should be emphasized, particularly when sleeping. Initial pain control is often provided by a regional block placed before surgery. Patients should be counseled appropriately regarding when the block will typically wear off so they can adequately control their pain beforehand with the use of oral narcotics and anti-inflammatories. The use of cryotherapy (Figure 22-2) throughout recovery, particularly in the first 7 to 10 days, is impor tant for inflammation and pain control. Advise patients to always keep a layer of protection between the skin and ice to prevent thermal injury. Transcutaneous electrical nerve stimulation should also be used for pain and inflammation in the acute postoperative period as well as throughout recovery. Pain control is important because it can interfere with muscle firing and scapular kinetics.10 Weaning off narcotics in the first 7 to 10  days is strongly encouraged, as patients will often complain of the negative effects of narcotics, such as lightheadedness, constipation, and nausea, with more prolonged usage. As previously mentioned, during phase I there is a delicate balance between protecting the repaired tissue with immobilization and early ROM to avoid the negative effects of prolonged immobilization. As discussed by McCarty et al,11

gentle early ROM will also help with preventing muscle atrophy, increase tissue circulation, promote healing, and decrease inflammation. There is no restriction on elbow, wrist, and hand ROM exercises that can be performed while a sling. Passive ROM of the shoulder can be performed with the following precautions, 0 degrees of internal rotation (IR), 20 degrees ER and humeral elevation in the scapular plane below 90 degrees. For the first 2 weeks, patients should perform supported Codman pendulum exercises (Figure  22-3) to help maintain passive motion of the glenohumeral joint. Shoulder ROM should be performed either sitting or standing because scapular mobility is restricted when supine. Passive ROM can also be performed by a physical therapist. While wearing the sling, patients can begin light cardiovascular exercise. This will help patients mentally because they feel limited in many activities following surgery, as well as promote increased blood flow for healing, improve sleep, and help maintain their overall health. Patients can walk on a treadmill or flat surface or ride a stationary recumbent bike during this phase.

Phase II: 2 to 6 Weeks The goals of phase II include continued immobilization to allow healing of the repair, while minimizing the negative

Return to Play Following Posterior Stabilization

243

Figure 22-3. Supported Codman passive range of motion. Instruct patients to fully relax muscles around the glenohumeral joint and allow gravity and movement of the trunk to create passive motion of the arm. Figure 22-2. Cryotherapy should be used throughout recovery and particularly in the first 7 to 10 days to help with inflammation.

effects of immobilization, progressive increase in passive and active assisted ROM, and to begin restoring proper scapulohumeral and scapulothoracic mechanics. Patients should continue wearing a sling for 6 weeks. Depending on surgeon preference, patients may start to sleep without a sling at 5 weeks. As previously mentioned, a sling can be removed for showering and daily exercises. During phase II of recovery patients should be off all narcotic pain medication. Patients should continue to use antiinflammatories, cryotherapy, and transcutaneous electrical nerve stimulation as needed. Shoulder ROM will continue to increase throughout phase 2 with use of unsupported Codman and table slides. Passive ROM should remain within the following precautions, and attention should be placed on appropriate scapular motion. Patients will progressively increase passive and active assisted forward flexion from 90 to 120 degrees and passive/active assisted abduction to 90  degrees, and scapular plane elevation to 120 degrees by week 4 and 140  degrees at week 6. Patients should avoid combined abduction and IR, as well as horizontal adduction to avoid placing stress on the posterior

structures. Various techniques including manual manipulation, pulleys, and wands can be used to obtain ROM. During this phase, an emphasis should be placed on restoring proper scapulohumeral and scapulothoracic mechanics. Patients should avoid compensatory scapular motion and work on scapular elevation, protraction, retraction, depression, and upward rotation. These exercises can be performed with the shoulder in the sling and out of the sling. Submaximal effort isometric exercises are started at 2 weeks; however, ER should be avoided. Patients will continue to exercise on a stationary (recumbent or upright) bike or walk, while wearing their sling, for a cardiovascular workout.

Phase III: 6 to 12 Weeks The goal of phase III is to have full painless passive and active ROM by 12 weeks and reestablish normal glenohumeral and scapulothoracic mechanics. Patients can discontinue the use of their sling. This can be achieved immediately at 6 weeks or with a gradual wean at 6 to 7 weeks. Often it is best to encourage patients to wear the sling for protection when in large crowds or traveling from 6 to 8 weeks postoperatively. This is particularly impor tant for

244

Chapter 22

A

B

Figure 22-4. (A and B) Wall push-ups begin at 10 to 12 weeks postoperatively and progress sequentially throughout the remainder of the rehabilitation.

the high school athlete, who might be around a lot of people in busy hallways at school. During phase III, patients have unlimited passive/active assisted forward flexion. Active motion in all planes can begin but keep less than passive limits. Continue with table and wall slides, use of pulley, and wand exercises to gradually increase ROM. Beginning at week 6, patients can begin resisted isometrics; however, no ER is allowed. Progressive resistance exercises (PREs) are begun as well, with no IR/ER. The patient may continue with scapula-stabilizing exercises, including protraction and retraction. By week 8, patients may increase passive/active assisted IR to 30 degrees with the arm at the side and passive/active assisted IR at 45 degrees of abduction to 30 degrees. Continue to progress with active motion and increase resistance with exercise to include therabands. At 10 weeks, patients have unlimited passive and active IR. PREs with IR/ER are also begun. At 10 to 12 weeks, patients can begin wall pushups (Figures 22-4A and 22-4B). During phase III, add an upper-body ergometer (UBE) without resistance within pain-free ROM. Patients can

continue to ride on a stationary bike or walk on a treadmill. As phase  III progresses, use of an elliptical is acceptable if pain free. After 8 to 10 weeks, jogging is allowed. In addition to increasing ROM, continued focus during phase III should be on the scapulohumeral and scapulothoracic muscles, which include the middle and lower trapezius, serratus anterior, rhomboid, and rotator cuff muscles.

Phase IV: 12 to 20 Weeks By phase IV, patients should have full painless passive and active ROM. If lacking, focus should be placed both on manual therapy and stretching to achieve desired ROM. A mildly tight shoulder at 12 weeks is acceptable and no reason for concern. IR stretching, including sleeper stretches, can be initiated. The goals for phase IV include improved strength, power, endurance, and neuromuscular control. There is increasing focus on strengthening during phase IV in preparation for sport-specific exercises. PREs include bicep curls, triceps extension, prone rows, lat pulldowns, and rotator cuff strengthening in neutral and 90 degrees abduction. Continue with a gradual increase in resistance and

Return to Play Following Posterior Stabilization functional movement patterns. A gradual push-up progression from a wall push-up, to incline push-up on a table, to incline push-up on a box, and ultimately to standard pushups is continued. Progression depends on proper pain-free technique at each stage. Continue to pay attention to proper scapulothoracic mechanics during all exercises. Continue with the UBE, adding resistance and duration. Patients can also transition from sitting to standing while using the UBE. Patients may start increasing lower-extremity exercises in preparation for return to sport. This includes hopping, jumping, and agility drills. As phase IV progresses and patient’s strength and endurance increases, begin to tailor exercises for the athletic demands that will be placed on the patient’s shoulder as he or she returns to sport. Attention should be paid to total body movement patterns that will optimize the neuromuscular training and endurance for the shoulder. For example, patients may need to change the stability of their base support from 2 legged to a single leg stance depending on their sport-specific needs. In preparation for sport-specific training, isokinetic training may start at 4 to 5 months with the goal for isokinetic testing between 5 to 6 months. Isokinetic testing will provide objective feedback that can then be addressed by the patient and therapist as rehabilitation continues to progress.12

Phase V: Beyond 20 Weeks Phase V is the transition to sport-specific exercises with the ultimate goal of unrestricted return to play. It is necessary for the shoulder to demonstrate power, dynamic stability, and endurance before an athlete can return to unrestricted level of play. As McCarty et  al11 previously published, the “ideal” criteria for return to play is little/no pain, patient subjectivity, near normal ROM, near normal strength, normal functional ability, and normal sports-specific skills. Also, it is impor tant to consider the athletes’ level of confidence in their shoulder. The Western Ontario Shoulder Instability Index evaluates the physical and psychological components of a patient’s recovery.13 The subjective scoring is a valid indicator of shoulder stability in general orthopedic patients or collision athletes. Several tests have also been developed to evaluate athletes and their readiness to return to sport. Ball drop test (Figure  22-5): This was developed by Wilk14 to evaluate endurance, willingness to move quickly, and dynamic stability. The test is performed in the prone position using a 2-pound weighted ball with the arm being tested completely off the plinth. For 30 seconds the number of catches and releases is counted and then the involved and uninvolved sides are compared for a performance percentage. A satisfactory score is 110% or greater on the dominant extremity. Push-up test: This test is a measure of muscular endurance of the upper body and shoulder complex. The number of correct form push-ups an athlete can perform, using standard

245

Figure 22-5. Ball drop test is used as a measure of endurance, willingness to move quickly, and dynamic stability.

push-up position, down to one fist distance off the floor in 60 seconds is measured. Two rounds of the test are performed with 1 minute of rest in between. There is an expectation that the athlete will be able to perform a greater number of pushups during the second bout of the examination.15 Closed Kinetic Chain Upper Extremity Stability Test (CKCEUST) (Figures  22-6A and 22-6B): The CKCUEST is a measure of upper quarter stability, agility, and power. The patient is in a push-up position with the hands 36 inches apart on strips of athletic tape. The patient reaches with alternating hands across the body to touch the piece of tape under the opposing hand. The number of cross-body touches in 15 seconds is recorded.16 A total of 21 cross-body touches is needed to “pass” this test. One repetition maximum bench press test: This test is used as an assessment of upper extremity strength. The test evaluates for symmetrical performance without compensation, lag, or substitution. Functional strength can be determined if pre-injury one repetition maximum lift scores are available.17 The desired goal is 75% of the previous one repetition maximum that had been accomplished before injury. Unilateral pulling assessment: Using a cable machine, a standing pull-back is performed for 20 repetitions with each arm to assess efficiency and imbalances during pulling movements. Movement is evaluated for undesired compensation, along with side-to-side comparison.18 Unilateral pushing assessment: This test also assesses movement efficiency and imbalances during a pushing activity. Using a cable machine, 20 repetitions are performed with

246

Chapter 22

A

B

Figure 22-6. (A and B) Closed Kinetic Chain Upper Extremity Stability Test is a measure of upper quarter stability, agility, and power.

each arm. The amount of weight the athlete can use for test and the presence of undesired movement compensations is evaluated.18 Wilk et  al14 previously discussed the sequence of performance, practice, and play for the athlete. Performance is a part of shoulder instability rehabilitation. Performance training includes sport-specific drills that should mirror activity demands of the sport. Athletes should demonstrate an ability to perform progressively more challenging sportspecific drills asymptomatically while maintaining shoulder stability. Next, an athlete begins practicing in a controlled environment. Practice should be progressive with increasing time, intensity, and repetitions. Once an athlete obtains maximal intensity and effort, participation in a practice game or scrimmage would be appropriate. Once successfully accomplishing the first 2 steps, the athlete returns to play. A suggested timeline for a few sports will follow. For throwing athletes, light overhead toss can begin at 6 months and progress to a gradual throwing program at 7 months. Athletes may return to unrestricted throwing when they are able to throw at full speed for 2 weeks without discomfort.19 Swimmers begin with freestyle or breaststroke initially at 6 to 7 months, and typically resume butterfly and backstroke at 9 months. With tennis, athletes should begin with lowintensity overhead hits at 6 to 7 months and progress to forceful overhead strokes at 8 to 9 months. Lastly, contact athletes typically return at 6 months as long as the athlete demonstrates full painless ROM, strength, power, and endurance. A harness for return to play is not typically used, but it might be used occasionally on a case-by-case basis if the athlete wants to use one when first starting back.

ROLE OF MEDICAL TEAM AND ATHLETE RELATIONSHIP IN RECOVERY The importance of the role of the physician and his or her communication with the athlete and the physical therapist and athletic trainer should not be underestimated. It is critical during the injury and postoperative period that there be frequent visits of the athlete with the physician to ensure that the athlete is progressing appropriately and to titrate the progress as needed. Sometimes more aggressive therapy is needed and sometimes the athlete is doing too much and needs to be slowed down. Frequent communication with the physical therapist and athletic trainer will help in this process. Additionally, the process of surgery and rehabilitation is most frequently very challenging emotionally for the athlete. Depression can occur, and the athlete needs to be constantly encouraged and supported through the months of recovery. It is essential that everyone involved in the care of the athlete stay positive and help the athlete through this time.

CONCLUSION In summary, the importance of a team approach between the surgeon, athlete, and physical therapist and athletic trainer cannot be overemphasized when discussing return to sport following posterior shoulder stabilization. A progression through the complete rehabilitation protocol is essential for athletes to regain their ROM, strength, power, and endurance necessary to return to high level of play.

Return to Play Following Posterior Stabilization

REFERENCES 1.

2. 3.

4. 5.

6.

7. 8. 9.

10.

Antoniou J, Duckworth DT, Harryman DT II. Capsulolabral augmentation for the management of posteroinferior instability of the shoulder. J Bone Joint Surg Am. 2000;82(9):1220-1230. doi:10.2106/00004623-200009000-00002. McLaughlin HL. Posterior dislocation of the shoulder. J Bone Joint Surg Am. 1952;34(3):584-590. Bottoni CR, Franks BR, Moore JH, DeBerardino TM, Taylor DC, Arciero RA. Operative stabilization of posterior shoulder instability. Am J Sports Med. 2005;33(7):996-1002. doi:10.1177/0363546504271509. Hawkins RJ, Koppert G, Johnston  G. Recurrent posterior instability (subluxation) of the shoulder. J Bone Joint Surg Am. 1984;66:169. Bradley JP, Baker CL  III, Kline AJ, Armfield DR, Chhabra  A. Arthroscopic capsulolabral reconstruction for posterior instability of the shoulder: a prospective study of 100 shoulders. Am J Sports Med. 2006;34(7):1061-1071. doi:10.1177/0363546505285585. Mair SD, Zarzour RH, Speer KP. Posterior labral injury in contact athletes. Am J Sports Med. 1998;26(6):753-758. doi:10.1177/036354 65980260060301. Tibone JE, Bradley JP. The treatment of posterior subluxation in athletes. Clin Orthop Relat Res. 1993;(291): 124-137. Pollock RG, Bigliani LU. Recurrent posterior shoulder instability. Diagnosis and treatment. Clin Orthop Relat Res. 1993;(291):85-96. Hurley JA, Anderson TE, Dear W, Andrish JT, Bergfeld JA, Weiker GG. Posterior shoulder instability: surgical versus conservative results with evaluation of glenoid version. Am J Sports Med. 1992;20(4): 396-400. doi:10.1177/036354659202000405. Hallström E, Kärrholm J. Shoulder rhythm in patients with impingement and in controls. Acta Orthop 2009;80(4):456-464. doi:10.3109/17453670903153543.

11.

12.

13.

14.

15.

16.

17.

18. 19.

247

McCarty EC, Ritchie P, Gill HS, McFarland EG. Shoulder instability: return to play. Clin Sports Med. 2004;23(3):335-351, vii-viii. doi:10.1016/j.csm.2004.02.004. Ellenbecker TS, Davies GJ. The application of isokinetics in testing and rehabilitation of the shoulder complex. J Athl Train 2000;35(3):338-350. Kirkley A, Griffin S, McLintock H, Ng  L. The development and evaluation of a disease-specific quality of life measurement tool for shoulder instability. The Western Ontario Shoulder Instability Index (WOSI). Am J Sports Med. 1998;26(6):764-772. doi:10.1177/036354 65980260060501. Wilk KE, Arrigo CA, Bagwell MS. Shoulder instability rehabilitation and return to sport. In: Arciero, Cordasco, Provencher. Shoulder and Elbow Injuries in Athletes: Prevention, Treatment, and Return to Sport. Philadelphia: Elsevier; 2018:178-201. Department of the Army. Army Regulation 350-1, Army Training and Leader Development, Washington, DC: Headquarters, Section VI, Army Training Programs, 1-24. Army Phys Fitness Train. December 2009; 10-13. Tucci HT, Martins J, Sposito Gde C, Camarini PM, de Oliveira AS. Closed Kinetic Chain Upper Extremity Stability test (CKCUES test): a reliability study in persons with and without shoulder impingement syndrome. BMC Musculoskelet Disord. 2014;15:1. doi:10.1186/1471-2474-15-1. Seo DI, Kim E, Fahs CA, et  al. Reliability of the one-repetition maximum test based on muscle group and gender. J Sports Sci Med. 2012;11(2):221-225. Clark MA, Sutton BG, Lucett SC. NASM Essentials of Personal Fitness Training. 4th ed. Burlington, MA: Jones and Bartlett Learning; 2014. Radkowski CA, Chhabra A, Baker CL  III, Tejwani SG, Bradley JP. Arthroscopic capsulolabral repair for posterior shoulder instability in throwing athletes compared with nonthrowing athletes. Am J Sports Med. 2008;36(4):693-699. doi:10.1177/0363546508314426.

SECTION IV Special Topics in Instability

23 Revision Arthroscopic Stabilization Craig R. Bottoni, MD and Zackary Johnson, MD

The successful arthroscopic treatment of shoulder instability remains a challenge in the young athlete, most notably in those who participate in contact or overhead sports. The wide range of motion in the shoulder allows an athlete to perform many incredible feats, but it also comes at a cost. This freedom of motion can make the shoulder prone to instability, which can be disabling to the athlete. Traditionally, instability was treated using an open technique allowing for direct visualization and suture fixation of the disrupted labrum (Figure  23-1). With the introduction of arthroscopy, the standard of care for the treatment of anterior glenohumeral instability slowly transitioned to arthroscopic stabilization. Although the improvement in arthroscopic techniques has resulted in equivalency to traditional open techniques, recurrent glenohumeral instability does occur. The question of what may contribute to the failure of the primary arthroscopic procedure and subsequently, what are the options that should be considered prior to proceeding with a revision stabilization, are the focus of this chapter. A patient who presents following a failed arthroscopic stabilization presents a challenging problem requiring thoughtful evaluation. Considerable debate exists about how to manage a failed arthroscopic shoulder stabilization. More conventional belief advised surgical treatment via an open stabilization for a failed arthroscopic stabilization. This advice has recently been challenged, and more surgeons are considering a repeat arthroscopic technique for a patient who has had a failed arthroscopic stabilization. Revision arthroscopic stabilization has a higher failure rate than primary repair, but this can be mitigated by evaluation and planning as well as proper technique. Understanding the cause of a failed stabilization is key to the revision. There are

multiple reasons for failure, and each may contribute to the overall process. This chapter will review the potential etiologies of failure, recommend how to properly evaluate a failed stabilization, and then suggest options when an arthroscopic revision surgery may be indicated.

ARTHROSCOPY AND BANKART Recurrent anterior glenohumeral instability has always been a significant problem for the athlete, especially in sports requiring overhead movements. Traditionally, instability was addressed through an open operative procedure. This slowly changed in the 1990s, when shoulder arthroscopy became more popular. Initially, arthroscopic stabilization of recurrent anterior shoulder instability resulted in much higher failure rates than what had been reported following open techniques. Most likely the higher failure rates were due to limited understanding of the pathoanatomy of the shoulder following a dislocation, limited availability of arthroscopic equipment, and minimal experience in the techniques used to perform arthroscopic Bankart repairs. When arthroscopic techniques were first attempted, only nonanatomical repairs were performed. Walch et al1 reported on the Morgan transglenoid suture arthroscopic technique in 1995 (Figure 23-2). In their series, they had a 49% rate of poor results with the same number reporting recurrent dislocation or subluxation. Grana similarly reported a recurrence rate of 44% with the transglenoid suture technique.2 In comparison to the generally accepted success rate of greater than 90% following open procedures at the time, many authors strongly opined against arthroscopic stabilization.1 Other arthroscopic techniques employed to address anterior instability had disappointing

- 251 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 251-263). © 2021 SLACK Incorporated.

252

Chapter 23

Figure 23-2. Early arthroscopic stabilization technique using transglenoid sutures. Figure 23-1. Open Bankart repair using deltopectoral approach, which was traditionally standard of care for instability.

and unacceptably high failure rates. Lane reported on a 33% recurrent instability rate using the arthroscopic staple capsulorrhaphy in 1993, and noted significant complications with this procedure.3 As arthroscopic techniques evolved and implants, primarily suture anchors, improved over time, the arthroscopic stabilization soon became the standard of care. Multiple studies since then have found the arthroscopic Bankart to have outcomes equivalent to that of open techniques. Tjoumakaris and colleagues retrospectively compared open and arthroscopic techniques in 2006 and found equivalent patient-reported outcome scores and recurrent instability.4 Bottoni et  al looked prospectively at open vs arthroscopic stabilization and found equivalent failure rates and noted an increased loss of shoulder motion in the open group.5 Improved outcomes with arthroscopic techniques were likely due to a better understanding of the pathoanatomy associated with recurrent anterior shoulder instability, improved arthroscopic equipment allowing better visualization of the shoulder joint, and greater surgeon experience in treating this condition. Despite the advancements in arthroscopy and the benefits conferred, recurrent shoulder instability can still result following arthroscopic stabilization. The reported recurrence rate for an arthroscopic Bankart is 10% to 15% when using modern suture anchor techniques. However, specific cohorts of patients have been identified that had higher rates of failure following arthroscopic stabilization. Specifically, overhead athletes, contact athletes, those with bone loss of the humerus and/or glenoid, patients with generalized ligamentous laxity, and younger patients were all groups or findings reported to be associated with significantly higher failure rates following arthroscopic techniques employed to address their anterior shoulder instability. Despite the growing

popularity of arthroscopy and improving results in primary instability, open operative techniques were usually recommended for failed arthroscopic stabilization procedures. Nevertheless, revision arthroscopic techniques have been reported with good results. In 2009, Boileau et al looked at a series of 22 patients who underwent a revision arthroscopic procedure after previous failed open stabilization and found an 85% rate of good or excellent results.6 Barnes and colleagues evaluated 18 shoulders that underwent a revision arthroscopic procedure after a failed open or arthroscopic stabilization and found 94% remained stable at a mean follow-up of 38 months.7 A crucial factor to success in a revision shoulder stabilization is understanding why the original surgery may have failed. Carefully evaluating the probable etiology for the recurrent instability and then formulating a plan to address those issues are the keys to success. Sir Winston Churchill said, “Those who fail to learn from the past are doomed to repeat it.” This is also true of the revision arthroscopic stabilization. Understanding the reasons why an arthroscopic stabilization has failed is the first step, followed by a plan to address the new or previously unrecognized pathology. Boileau et al evaluated the factors contributing to failure of arthroscopic stabilizations. In their study of 91 consecutive arthroscopic stabilizations, they found a relatively typical rate of failure at 15%. Of these they found the strongest risk factors for failure were bone loss either on the glenoid or humeral side followed by the number of anchors used in fixation, which suggests a less than optimal original technique.8 Other factors implicated in the failure of shoulder stabilization are other soft-tissue injuries that were not addressed such as an anterior labroligamentous periosteal sleeve avulsion (ALPSA), glenolabral articular disruption (GLAD), a humeral avulsion of the glenohumeral ligament (HAGL) lesion, or unrecognized posterior instability.

Revision Arthroscopic Stabilization

253

Figure 23-3. Arthroscopic view of significant glenoid bone loss from a bony Bankart.

GLENOID BONE LOSS Over the past decade the importance of glenohumeral bone loss in the glenoid and/or humerus has been cited as a potential etiology for failure of arthroscopic stabilization. Glenoid bone loss can occur for a variety of reasons, but is due to a single traumatic glenohumeral dislocation or respective injuries. The initial glenohumeral dislocation can often result in a bony avulsion from the anteroinferior glenoid along with the attached labrum, known as a bony Bankart (Figure  23-3). The size of this avulsion can vary, but in all cases the result is a more narrowed glenoid tract on which the humerus articulates. Bone loss can also occur because of repetitive episodes of instability. These recurrent subluxations can erode glenoid bone over time, also resulting in a narrowed glenoid tract. Evaluating the glenoid and any bone loss is essential to planning a revision arthroscopic Bankart because it can affect technique in the revision, change the arthroscopic procedure, or disqualify the patient from an arthroscopic revision procedure. The identification of and subsequent quantification of the amount of glenoid bone loss remain a challenge. The best imaging modality and the technique to quantify glenoid bone loss remain controversial.

Imaging Evaluation of glenoid bone loss can be accomplished through a variety of means. Traditional 3-view shoulder radiographs may raise suspicion of bone loss, but typically do not allow for any quantification of the amount of glenoid bone missing. Garth et al described the apical oblique view.9 This view is obtained by having the patient seated with the uninjured shoulder angled 45 degrees away from the cassette,

Figure 23-4. West Point view showing glenoid bone loss.

thus putting the beam parallel to the articular surface of the glenoid and the normally anteverted shoulder. The beam is also angled 45 degrees from cephalad to caudal. When performed correctly, the coracoid should appear as a ring. The authors demonstrated the ability to see larger bony Bankart lesions as well as Hill-Sachs lesions better than standard 3-view radiographs, but smaller attritional bony defects were not well visualized. The West Point view, originally described by Rokous and colleagues, is a modified axillary view10 (Figure  23-4). The patient is positioned prone with the affected shoulder bumped approximately 3 inches off the table. The arm is abducted 90 degrees with the forearm hanging off the table. The beam is directed down 25 degrees from the horizontal and 25 degrees medially, again attempting to parallel the glenoid articular surface. Finally, the Didiée view is performed by again having the patient lie prone with the affected arm abducted and the hand on the patient’s back resting on the iliac crest. The beam is directed at a 45-degree angle from lateral to medial.11 The authors found this to be an effective view for evaluating a bony Bankart but not a Hill-Sachs lesion. Again, although these views can be useful and clue a provider in to the presence of glenoid bone loss, quantifying the size of the lesion requires advanced imaging. They also can be technically difficult to obtain, especially in patients with abnormal glenoid version (Table 23-1). Computed tomography (CT), especially with computerrendered 3-dimensional (3D) reconstruction, has become the gold standard for evaluating and quantifying glenoid bone loss. Two-dimensional CT can also be limited in accurately quantifying glenoid bone loss because of variability in shoulder anatomy, most notably glenoid version, which will require adjustment of the imaging orientation. CT imaging

254

Chapter 23

Table 23-1. Specialized Radiograph Views for Visualizing Bone Loss VIEW Apical oblique view

TECHNIQUE Patient seated upright. Shoulder angled 45 degrees away from cassette and beam 45 degrees cephalad to caudal.

USES Glenoid bone loss Hill-Sachs lesion Glenoid bone loss Hill-Sachs lesion

West Point view

Patient prone with shoulder bumped 3 inches with arm hanging off table at 90 degrees of abduction. Beam angled 25 degrees down from horizontal and 25 degrees medial.

Didiée view

Patient prone with hand of on patient’s back resting on iliac crest. Beam angled 45 degrees lateral to medial.

Glenoid bone loss

Stryker Notch view

Patient supine with hand on top of head. Beam directed 10 degrees cephalad.

Hill-Sachs lesion

Radiographs may be used for detection but not for quantification.

Table 23-2. Methods for Calculating Bone Loss Using Computed Tomography METHOD Superimposed circle method Pico method Ratio method Distance from bare area method

Surface area method Bankart length method

DESCRIPTION Best-fit circle of injured and uninjured shoulder superimposed and area compared to determine % of bone loss. Uninjured shoulder best-fit circle (A) superimposed on injured shoulder to determine defect size. Calculated as % of bone loss (D/A × 100%). Measure radius of best-fit circle (R) and the distance from center to anterior lesion (d). Use ratio d/R to determine % of bone loss based on author’s table. Measure distance from bare area to anterior lesion (A) and from bare area to posterior glenoid (B). % bone loss = ([B − A]/2B) × 100. Best-fit circle of injured shoulder only. Use digital measuring means to determine % of bone loss. Best-fit circle drawn on injured shoulder. Radius of circle (R), length of osseous lesion measured (x). If x > R, then dislocation resistance is < 70% of uninjured shoulder.

Three-dimensional reconstructions are best for measurements when available.

of the glenoid, and subsequently the accurate quantification of bone loss, depends on the proper orientation of the patient’s shoulder and specifically, the glenoid in the CT gantry. This is solely operator dependent, and slight misalignment will dramatically change the bone loss determination. The CT images can be reconstructed via software to allow for a 3D visualization of the glenoid. Three-dimensional CT provides the best technique for evaluation of bone loss because it allows for humeral subtraction and an isolated image of the glenoid. In a patient who has failed an initial arthroscopic stabilization and bone loss is suspected, a CT should be obtained, if possible, with 3D reconstructions, to properly evaluate bone loss prior to consideration of a revision stabilization (Table 23-2; Figure 23-5). There have been several techniques described for quantifying glenoid bone loss using CT with 3D reconstruction.12 Most techniques rely on the assumption that the inferior two-thirds of the glenoid creates a true circle with the bare spot roughly in the center.13 Chuang and colleagues described the superimposed circle method and the Pico

method respectively, both of which rely on imaging of the contralateral shoulder and on comparing the area of fitted circles to the injured and uninjured glenoid to calculate glenoid bone loss14 (Figure 23-6). These methods can expose the patient to additional radiation because of the need to image the other shoulder. Other methods such as the ratio method described by Barchilon and the anteroposterior distance from bare area method described by Sugaya rely on distance rather than area.15 Both methods rely on the assumption that the bare spot can be roughly approximated on imaging by locating the intersection of a line drawn down the long axis of the glenoid and a line drawn horizontally through the widest point of the glenoid. The ratio method calculates bone loss by dividing the distance from the bare spot to the anterior lesion by the radius of the best-fit circle centered on the bare spot. The distance from the bare spot method is performed by measuring the distance from the bare spot to the posterior edge of the glenoid and distance from the bare spot to the anterior lesion and using these to calculate the percentage of bone loss. The surface area method as

Revision Arthroscopic Stabilization

255

Figure 23-6. Best fit circle of lower 2/3 of the glenoid demonstrating bone loss. Figure 23-5. Bony Bankart noted on axial cuts of a shoulder CT. (Reprinted with permission from Kyong Su Min, MD.)

described by Sugaya et al15 uses digital software to measure the area of the best-fit glenoid circle and the area of the defect to calculate the percentage of bone loss. Alternatively, Gerber and Nyffeler found that if one measured the length of the osseous Bankart lesion and found it to be greater than the radius of the best-fit circle, the glenoid will have 70% or less of its original resistance to dislocation.16

Classification and Treatment Because glenoid bone loss is a common explanation for failure of arthroscopic stabilization, it should be evaluated and, if present, quantified prior to any revision surgery to consider all options, but techniques have also been described to measure bone loss arthroscopically. This can be useful in confirming a surgical plan intraoperatively. To measure bone loss during shoulder arthroscopy, a graduated probe is inserted from the posterior portal and used to measure from the bare spot to the anterior edge of the glenoid, and then to the posterior aspect of the glenoid. Assuming the bare spot is in the center of the glenoid, bone loss can then be calculated. Bone loss will be overestimated if more inferior to the horizontal axis of the inferior two-thirds of the glenoid, but this is uncommon. Also, some authors have suggested that the bare spot is typically slightly anterior to the true center of the glenoid or, at times, not present at all. Barcia and colleagues evaluated the glenoid bare spot and found that the bare spot was visible only 48% of the time and centered only 37% of the time17 (Figure 23-7). Therefore, this technique although confirmatory, is not recommended to make treatment decisions.

Once the amount of bone loss has been quantified, the next step is determining the appropriate procedure to address the recurrent instability. “Critical” glenoid bone loss thresholds have been reported, but the cutoff where a bone augmentation procedure is recommended is still unclear. Traditionally, 20% to 25% bone loss has been used as a threshold for arthroscopic stabilization. Burkhart et  al described the inverted-pear morphology of the glenoid, which he later specified to represent an average of 28% bone loss, had 67% recurrence rate after arthroscopic anterior stabilization.18,19 Conversely, Porcellini and colleagues found that 92% of patients with bone loss of 25% or less who underwent arthroscopic stabilization demonstrated a stable shoulder at 2-year follow-up.20 It should be noted, however, that this study looked at acute injuries. A lower threshold of glenoid bone loss may be necessary in recurrent shoulder instability because they have already demonstrated failure. Shaha et al reexamined critical bone loss and failure rates in terms of outcomes as opposed to recurrent instability. They found that bone loss between 13.5% to 20%% led to worse patient-reported outcomes.21 Provencher et  al suggested an algorithm in their review article in 2010, that 0% to 15% bone loss may be treated arthroscopically.12 If a small avulsion fragment of the glenoid, called a bony Bankart lesion, is present and unaddressed, it may be another source of failure. Even in small bony lesions, incorporation of the fragment in the repair, if possible, can help with healing especially in the revision setting (Figures 23-8A and 23-8B). However, in the acute injury, bone fragments are often easier to mobilize and fixate to the native glenoid. In revisions, the quality and size of the remaining bone fragment is variable. Careful preoperative evaluation of the fragment itself is impor tant. If

256

Chapter 23

A

A

B

B

Figure 23-7. Arthroscopic view of the glenoid bare spot.

a large bony fragment is present that is either malunited or has a fibrous union, it must be ascertained whether it can be mobilized and incorporated into the repair. Should this be the case, careful arthroscopic preparation of the fragment should be performed to ensure a bony union when this is incorporated into the repair. In the revision setting, however, bone loss can often be attritional. Any remaining bony fragment may either be malunited so it cannot be mobilized or may have undergone significant resorption. In this case, a bone augmentation procedure may be indicated. Patients with bone loss greater than 25% will most likely require a bone augmentation procedure. Traditionally, this has been performed through an open deltopectoral approach using a coracoid transfer (Bristow or Latarjet) or an autograft iliac crest. Recently there have been some authors who have reported on an arthroscopic coracoid transfer. The arthroscopic Latarjet was originally described by Lafosse

Figure 23-8. (A) Anchor placement on the face of the glenoid to incorporate bone lesion into Bankart repair. (B) Bony fragment of Bankart lesion reapproximated at the glenoid rim using suture anchors. (Reprinted with permission from Kyong Su Min, MD.)

et  al and demonstrated promising results22 (Figure  23-9). In their study, 91% of patients reported their outcome as excellent and average return to sport was approximately 10 weeks. Benefits of the arthroscopic Latarjet include the ability to provide bony augmentation through a minimally invasive technique and the ability to easily visualize the glenoid surface, which allows for proper alignment of the graft. Early arthrosis or graft lysis can occur in the improperly placed graft. Lafosse and colleagues found that 80% of their arthroscopically placed grafts were flush with the glenoid. Although the benefits are apparent, this procedure is very technically challenging and should be reserved for only the very skilled arthroscopist.

Revision Arthroscopic Stabilization

257

A

Figure 23-9. Metal subtraction CT demonstrating placement of coracoid at the anterior glenoid (Latarjet) for treatment of glenoid bone loss.

HILL-SACHS LESION Another location for bone loss following an anterior glenohumeral dislocation is the compression fracture of the posterolateral humeral head, which occurs when the humerus impacts the relatively harder anteroinferior glenoid. This finding was originally described by Hill and Sachs in 1940.23 This can be another location of bone loss present in acute or chronic shoulder instability that can contribute to failure of an initial operative stabilization. Despite the HillSachs lesion being present in most cases of recurrent instability, it can remain unrecognized and therefore, unaddressed. Yiannakopoulos et  al, in an arthroscopic study, found a Hill-Sachs lesion in 93% of patients with chronic instability.24

B

Imaging Hill-Sachs lesions can be easily missed on the routine 3-view shoulder radiograph, but as described earlier these can be better viewed using specialized radiographs such as the apical oblique view or West Point axillary lateral view. In addition, a Stryker notch view is used to best visualize a Hill-Sachs lesion by internally rotating the humerus, thus bringing the lesion into plane with the beam.25 Advanced imaging is typically required to better identify and quantify the lesion. The Hill-Sachs lesion is readily identified on magnetic resonance imaging (MRI), but the optimal imaging for quantifying the lesion is via CT with 3D reconstructions (Figures  23-10A and 23-10B). The presence of a Hill-Sachs lesion in addition to any glenoid bone loss may be the primary etiology for recurrent instability following a failed attempt at operative stabilization as the humeral defect more easily engages the narrowed tract of the glenoid (see Table 23-1).

Figure 23-10. (A) Sagittal CT cuts demonstrating Hill-Sachs lesion. (B) CT 3D reconstruction demonstrating bipolar bone loss including large Hill-Sachs.

Classification and Treatment Traditionally, the recommendation to treat a Hill Sachs lesion was based off the size of the humeral head defect, specifically those lesions of less than 20% never requiring treatment and those with more than 40% requiring intervention. The middle ground has been the subject of debate. More recently the track concept, whereby the Hill-Sachs lesion and

258

Chapter 23

Table 23-3. Burkhart Method for Determining On-Track vs Off-Track Lesion26 1. Using 3D CT, measure diameter of glenoid (D) 2. Measure width of bone loss (d) 3. Glenoid track width (GT) = 0.83 D − d 4. HS interval (HSI) = HS lesion (HA) + bone bridge 5. If HSI > GT then the HS is off-track (engaging) Abbreviations: 3D, 3-dimensional; CT, computed tomography; HS, Hill-Sachs. All measurements are in millimeters.

glenoid bone loss are evaluated, has played a more significant role in the decision to treat a Hill-Sachs lesion. This concept, which has been championed by Burkhart, describes a lesion as lying within the medial margin of the glenoid track and thus nonengaging (on-track), or medial to the glenoid margin and thus engaging (off-track).26 Off-track lesions are often also associated with significant glenoid bone defects and larger Hill-Sachs lesions, termed bipolar bone loss. This can be determined with the technique described by Burkhart using 3D CT (Table 23-3). Kurokawa and colleagues, in a CT study of 100 unstable shoulders, found that 7% of Hill-Sachs lesions were engaging. Of these, 3 were large lesions, and the remaining 4 were narrow and medial.27 With this in mind, irrespective of its size, an off-track lesion will likely require intervention, especially in the revision scenario. Practically all Hill-Sachs lesions are engaged at the time of their creation. The impor tant clinical question is whether they continue to engage with functional shoulder range of motion after the initial shoulder stabilization was performed. If they do engage, and recurrent instability occurs, this may need to be the primary focus of the revision surgery. Off-track Hill-Sachs lesions can be addressed with softtissue procedures, bony procedures, or a combination of both. The Latarjet procedure, which increases the contact surface area on the glenoid for the humerus, has been described not only to address glenoid bone loss but also to treat large Hill-Sachs lesions. By increasing the size of the glenoid track, it now moves the Hill-Sachs from being an off-track lesion to being an on-track lesion. The possibility of a revision in an unstable shoulder through an arthroscopic Latarjet was discussed previously. Another arthroscopic revision option for an engaging Hill-Sachs lesion is a revision arthroscopic Bankart with a concomitant remplissage procedure. Remplissage is a French term that translates to “filling in,” which describes the concept of this technique. The procedure, originally described as an open procedure by Connolly in 1972, is commonly performed arthroscopically.23 The idea behind a remplissage is that by filling the lesion with the tendon of the infraspinatus, it converts an intraarticular lesion into one that is extra-articular. A variety

Figure 23-11. Arthroscopic remplissage anchor placement, which will advance the posterior capsule and infraspinatus into defect.

of techniques have been described for the remplissage, which all involve a posterior capsulodesis with advancement of the infraspinatus tendon into the defect in a similar fashion as a rotator cuff repair.28,29 A suture anchor or 2 are inserted percutaneously into the Hill-Sachs lesion. The sutures are identified in the subacromial space. They are then used to pull the tendon of the infraspinatus into the humeral defect, thus precluding engagement of the humeral lesion by the glenoid with abduction and external rotation (Figure 23-11). Good results of arthroscopic remplissage have been reported in the literature with regard to stability and recurrence rate. One concern often cited as a consequence of this procedure is decreased internal or external rotation when the posterior structures are advanced medially. Merolla et al reported on 61 patients who underwent an arthroscopic remplissage and demonstrated only one patient with recurrent instability at an average follow-up of 39.5 months.30 The authors did demonstrate a significant decrease in external and internal rotation compared to the unaffected side but this did not appear to affect quality of life. Degen et al performed a biomechanical comparison on cadaveric models of remplissage vs Latarjet for engaging Hill-Sachs and found similar rates of stability.31 Similarly, Cho and colleagues retrospectively evaluated 2 groups of patients who underwent either a remplissage or Latarjet for large engaging Hill-Sachs and found no significant difference in stability, with a 5.4% and 5.7% recurrence rate, respectively.32 The authors found similar rates of loss of external rotation between the groups, but found higher complication rates in the Latarjet group. When a large humeral head defect is present (> 40%) or significant bipolar bone loss is appreciated, open bony procedures such as humeral head allograft augmentation with or without an open Latarjet may be necessary. Thus, it is impor tant that appropriate preoperative imaging be obtained

Revision Arthroscopic Stabilization

259

and the patient be properly counseled before undergoing a revision procedure.

SOFT-TISSUE INJURIES Many soft-tissue injuries about the shoulder have been implicated in the failure of stabilization procedures. This is especially true if the additional pathology is not recognized or addressed initially. When evaluating a failed stabilization, it is impor tant to review original imaging for any missed pathology, as well as obtain a new MRI. In revision planning it is impor tant to closely scrutinize the MRI for possible etiologies of failure.

ANTERIOR LABROLIGAMENTOUS PERIOSTEAL SLEEVE AVULSION The ALPSA was initially described by Neviaser as a shoulder soft-tissue injury in which the labrum has torn off its insertion and healed in a medialized position on the glenoid neck.33 The ALPSA lesion, often identified in cases of recurrent instability, results in a loss of the labrum bumper effect and resultant capsular laxity. The presence of an ALPSA lesion has been previously shown to increase the risk of recurrence after stabilization. Ozbaydar et  al compared their results of arthroscopic stabilization of a typical Bankart lesion with those shoulders that had an ALPSA lesion. They found higher failures in those shoulders noted to have ALPSA lesions. They noted recurrence rates of 7.4% in arthroscopic stabilization of Bankart repairs and 19.2% in those repairs with an ALPSA.34 Although the ALPSA lesion can usually be identified by preoperative MRI, an ALPSA may also be unexpectedly encountered intraoperatively (Figure 23-12). The actual reason for higher rates of recurrence associated with an ALPSA is unknown but may be due to a failure to recognize this variant or properly address it intraoperatively. Repair of the ALPSA requires aggressive mobilization of the labrum from the glenoid neck and separation of the capsule from the underlying subscapularis to anatomically reduce the labrum, reproduce the bumper effect, and re-tension the capsule. This is especially true in the revision setting. Incorrect medial glenoid anchor placement in the index procedure can also produce an iatrogenic ALPSA lesion and result in recurrent instability. When performing a revision stabilization, it is impor tant to place suture anchors 1 to 2 mm on the glenoid articular surface to ensure the bumper is recreated, thus lowering the risk of further recurrence.35

GLENOID LABRAL ARTICULAR DISRUPTION LESION The GLAD lesion has been implicated in an increased rate of recurrence after initial stabilization. The lesion was

Figure 23-12. Arthroscopic image demonstrating an anterior labroligamentous periosteal sleeve avulsion (ALPSA).

also described by Neviaser in 1993. This is a loss of articular cartilage at the interface between the bony glenoid the injured labrum.36 The lesions can at times be identified on preoperative MRI but may be noted at the time of surgery. The GLAD lesion has been theorized to increase the chance of recurrent instability in a much similar way as glenoid bone loss, by disrupting the normal glenoid track. Pogorzelski et  al evaluated 72  patients who were more than 2  years out following an arthroscopic repair of traumatic glenohumeral instability. Of the several factors they evaluated, the presence of a GLAD lesion was the only significant factor predisposing to failure.37 Addressing a GLAD lesion surgically and the results thereof are not well described in the literature. In the revision setting, one approach to address this lesion is to fix the labrum over the GLAD lesion. By pulling the labrum and capsule over the surface of the glenoid, thus filling the articular defect and restoring the glenoid track, the chance of recurrence may be decreased. These lesions, if unaddressed, may also be a source of postoperative pain as the humerus articulates with the exposed glenoid bone of the GLAD lesion.

HUMERAL AVULSION OF THE GLENOHUMERAL LIGAMENT Another source of potential instability in the primary or revision setting is the HAGL. Wolf first coined the phrase in 1995, but it had previously been recognized in small case series and reports.38 It is traditionally described as an avulsion of the anterior inferior glenohumeral ligament from the humeral neck. Although almost all HAGL lesions occur in conjunction with a Bankart lesion, studies have shown that a HAGL is present in 7% to 9% cases of primary shoulder

260

Chapter 23

Figure 23-13. Radiograph demonstrated bony avulsion associated with a humeral avulsion of the glenohumeral ligament (HAGL).

instability.39 Bokor and colleagues reported retrospectively on a group of 547  shoulders and found 41 (7.5%) HAGL lesions. Of those, they noted that 6 HAGL lesions were found at the time of revision procedures.40 The surgeon performing a revision must have a high index of suspicion for a HAGL lesion because it can be another reason for failure of the index stabilization. Occasionally, plain radiographs can demonstrate an avulsion fracture of the medial anatomic neck of the humerus where the capsule inserts, coined a bony HAGL, or BHAGL (Figure  23-13). On magnetic resonance arthrogram, the HAGL will produce the typical “J” sign as the contrast tracks distally on the humerus through the defect in the capsule. Even if a HAGL is not identified on preoperative imaging, the surgeon must be vigilant during the initial diagnostic arthroscopy and evaluate the humeral insertion of the capsule closely for an unrecognized HAGL lesion. If there is a high degree of suspicion, a 70-degree arthroscope may be used to better visualize the anteroinferior humerus. Repair of a HAGL requires access to the axillary pouch and creation of a posterior inferior portal. There is inherent danger to the axillary nerve in the creation of this inferior portal and during repair of the HAGL. Reports on arthroscopic HAGL repair are limited mostly to small case series. Fritz et  al reported on a series of 3 patients who underwent arthroscopic HAGL repair and found them to have no recurrent instability at an average 16-month follow-up.41 Owing to the technical difficulty of the arthroscopic repair and danger to the axillary nerve, many opt for an open repair, which has also demonstrated good results.

Figure 23-14. Axial MRI demonstrating a posterior labral tear and instability.

POSTERIOR INSTABILITY Posterior shoulder instability can be an easily misdiagnosed in the athlete. The symptoms of posterior shoulder instability can be subtle and often present only as pain. Previous studies have reported an incidence of posterior shoulder instability to range from 2% to 10% of all cases of instability.42 The incidence has recently been shown to be much higher than previously reported in specific patient populations. Certain patients are especially susceptible, such as athletes and members of the military. This is especially true for athletes who undergo repetitive posterior stress such as football linemen or weightlifters. Song and colleagues reviewed posterior and combined instability among the military population and found that 24% of their instability population had isolated posterior instability and 18% had combined instability, rates much higher than has historically been reported43 (Figure 23-14). Diagnosis of posterior instability can be a challenge because the chief complaint is often pain and not frank instability, and a single inciting posterior dislocation event is less common. Physical examination can also be difficult because a shoulder that is chronically subluxated posteriorly that reduces into the glenoid can be mistaken for anterior instability. In the setting of recurrent instability after an operative stabilization, it is impor tant to have a high index of suspicion for missed posterior or bidirectional instability. This is especially impor tant because performing an anterior repair in the setting of posterior instability can worsen posterior symptoms. Magnetic resonance arthrogram is the gold standard for diagnosing labral pathology. As with other

Revision Arthroscopic Stabilization soft-tissue pathology in the revision setting, it may not be recognized preoperatively. The provider must be prepared to address this pathology intraoperatively. When addressing posterior or bidirectional instability, the surgeon should pay careful attention to balancing the shoulder to ensure it is centralized in the glenoid. Historical outcomes of posterior stabilization have been generally poor, especially following open techniques. More recently, arthroscopic techniques have demonstrated better outcomes. Savoie et al demonstrated no recurrent instability in 97% shoulders that underwent posterior stabilization. In the same study, they also noted that a reverse Bankart lesion was found in only 51% of these shoulders, and that posterior capsule laxity was a more common finding.44 Bottoni and colleagues also found satisfactory patient-reported outcomes in his retrospective review of 19  arthroscopic posterior shoulder stabilizations.45 Thus, in the revision setting, the surgeon should have a low threshold for a posterior labral repair and/or capsulorrhaphy.

PATIENT AND SURGEON FACTORS There are several factors in the literature with regard to the patient or the surgeon that can contribute to an increased risk of failure of the arthroscopic primary stabilization. In the revision setting, these must be considered and, if present, addressed to increase the chance of success in an arthroscopic revision. Balg and Boileau described a scoring system to predict failure following arthroscopic stabilization that they coined the Instability Severity Index Score.46 The score incorporates elements of the patient and the injury itself, including age at surgery, degree of sports participation, type of sport, shoulder hyperlaxity, and glenoid/humeral bone loss. Bone loss has been covered previously. In the setting of revision stabilization in the athlete, the surgeon must be aware of patients’ expectations, including their return to overhead sports participation and their acceptance of the time needed for rehabilitation to minimize the chance of recurrence. Although smoking has been very well documented in as a risk factor for failure in rotator cuff surgery, it is still debatable in stabilization procedures.47 Park et  al evaluated failure of superior labrum repairs and found a significant correlation between smoking and failure of the procedure.48 Provencher and colleagues performed a similar evaluation, however, but did not find a significant correlation.49 In the revision setting, it is probably best to encourage smoking cessation prior to revision procedures. Surgeon-related factors must also be evaluated prior to revision surgery. There are several technical aspects of the index stabilization that may contribute to recurrent instability. Anchor position, hardware loosening or overt failure, inadequate tissue tensioning, and poor knot tying can lead to failure. When preparing for the revision procedure, it is difficult to evaluate whether the index surgeon tensioned the soft tissue appropriately or whether the knots failed. However, anchor position, cystic changes in the glenoid, and the number of anchors used can usually be evaluated by MRI or CT.

261

In preparation for operative treatment of recurrent instability, the surgeon must determine whether there is adequate bone stock to place more anchors in the correct positions. Anchors are generally placed inferior to the equator, and the lowest anchors are necessary to treat inferior instability. In addition to their location, the number of anchors has been shown to be impor tant. Kim and colleagues found a significantly higher rate of arthroscopic failure when fewer than 3 anchors were used.50 Boileau et al also found that they had higher recurrence rates with fewer than 4 anchors.8 In the revision setting, the surgeon must carefully plan anchor placement to ensure secure fixation and elimination of capsular redundancy to mitigate the risk of recurrence.

CONCLUSION Revision arthroscopic stabilization surgery can be very challenging even for the very skilled arthroscopist. Keys for success in revision surgery are careful evaluation and planning to maximize the chances for success. Reasons for recurrent instability include bone loss, unrecognized soft-tissue pathology, and patient/surgeon factors that must be identified and addressed before and at the time of the revision arthroscopic stabilization.

REFERENCES 1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

Walch G, Boileau P, Levigne C, Mandrino A, Neyret P, Donell  S. Arthroscopic stabilization for recurrent anterior shoulder dislocation: results of 59 cases. Arthroscopy. 1995;11(2):173-179. doi:10.1016/0749-8063(95)90063-2. Grana WA, Buckley PD, Yates CK. Arthroscopic Bankart suture repair. Am J Sports Med. 1993;21(3):348-353. doi:10.1177/036354659302100304. Lane JG, Sachs RA, Riehl B. Arthroscopic staple capsulorrhaphy: a long-term follow-up. Arthroscopy. 1993;9(2):190-194. doi:10.1016/ s0749-8063(05)80373-1. Tjoumakaris FP, Abboud JA, Hasan SA, Ramsey ML, Williams GR. Arthroscopic and open Bankart repairs provide similar outcomes. Clin Orthop Relat Res. 2006;446:227-232. doi:10.1097/01. blo.0000205883.73705.19. Bottoni CR, Smith EL, Berkowitz MJ, Towle RB, Moore JH. Arthroscopic versus open shoulder stabilization for recurrent anterior instability: a prospective randomized clinical trial. Am J Sports Med. 2006;34(11):1730-1737. doi:10.1177/0363546506288239. Boileau P, Richou J, Lisai A, Chuinard C, Bicknell RT. The role of arthroscopy in revision of failed open anterior stabilization of the shoulder. Arthroscopy. 2009;25(10):1075-1084. doi:10.1016/j. arthro.2009.04.073. Barnes CJ, Getelman MH, Snyder SJ. Results of arthroscopic revision anterior shoulder reconstruction. Am J Sports Med. 2009;37(4):715719. doi:10.1177/0363546508328411. Boileau P, Villalba M, Héry JY, Balg F, Ahrens P, Neyton L. Risk factors for recurrence of shoulder instability after arthroscopic Bankart repair. J Bone Joint Surg Am. 2006;88(8):1755-1763. doi:10.2106/ JBJS.E.00817. Garth WP Jr, Slappey CE, Ochs CW. Roentgenographic demonstration of instability of the shoulder: the apical oblique projection. J Bone Joint Surg Am. 1984;66(9):1450-1453. Rokous J, Feagin J, Abbott H. Modified axillary roentgenogram. Clin Orthop Relat Res. 1972;82:84-86.

262 11.

12.

13.

14.

15.

16. 17.

18.

19.

20.

21.

22.

23.

24.

25.

26.

27.

28.

29.

Chapter 23 Pavlov H, Warren RF, Weiss CB Jr, Dines DM. The roentgenographic evaluation of anterior shoulder instability. Clin Orthop Relat Res. 2006;(194):153-158. doi:10.1097/00003086-198504000-00020. Provencher MT, Bhatia S, Ghodadra NS, et  al. Recurrent shoulder instability: current concepts for evaluation and management of glenoid bone loss. J Bone Joint Surg Am. 2010;92(suppl 2):133-151. doi:10.2106/JBJS.J.00906. Huysmans PE, Haen PS, Kidd M, Dhert WJ, Willems JW. The shape of the inferior part of the glenoid: a cadaveric study. J Shoulder Elbow Surg. 2006;15(6):759-763. doi:10.1016/j.jse.2005.09.001. Chuang TY, Adams CR, Burkhart SS. Use of preoperative threedimensional computed tomography to quantify glenoid bone loss in shoulder instability. Arthroscopy. 2008;24(4):376-382. doi:10.1016/j. arthro.2007.10.008. Sugaya H, Kon Y, Tsuchiya A. Arthroscopic repair of glenoid fractures using suture anchors. Arthroscopy. 2005;21(5):635. doi:10.1016/j. arthro.2005.02.006. Gerber C, Nyffeler R. Classification of glenohumeral joint instability. Clin Orthop Relat Res. 2002;400:65-76. Barcia AM, Rowles DJ, Bottoni CR, Dekker TJ, Tokish JM. Glenoid bare area: arthroscopic characterization and its implications on measurement of bone loss. Arthroscopy. 2013;29(10):1671-1675. doi:10.1016/j.arthro.2013.06.019. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy. 2000;16(7):677-694. doi:10.1053/ jars.2000.17715. Lo IKY, Parten PM, Burkhart SS. The inverted pear glenoid: an indicator of significant glenoid bone loss. Arthroscopy. 2004;20(2):169174. doi:10.1016/j.arthro.2003.11.036. Porcellini G, Campi F, Paladini  P. Arthroscopic approach to acute bony Bankart lesion. Arthroscopy. 2002;18(7):764-769. doi:10.1053/ jars.2002.35266. Shaha JS, Cook JB, Song DJ, et  al. Redefining “critical” bone loss in shoulder instability. Am J Sports Med. 2015;43(7):1719-1725. doi:10.1177/0363546515578250. Lafosse L, Bongiorno V, Schwartz DG. Arthroscopic latarjet procedure. In: Milano G, Grasso A, eds. Shoulder Arthroscopy: Principles and Practice. London: Springer-Verlag; 2014. doi:10.1007/978-1-4471-5427-3_37. Provencher MT, Frank RM, LeClere LE, et al. The Hill-Sachs lesion: diagnosis, classification, and management. J Am Acad Orthop Surg. 2012;20(4):242-252. doi:10.5435/JAAOS-20-04-242. Yiannakopoulos CK, Mataragas E, Antonogiannakis E. A comparison of the spectrum of intra-articular lesions in acute and chronic anterior shoulder instability. Arthroscopy. 2007;23(9):985-990. doi:10.1016/j.arthro.2007.05.009. Hall RH, Booth CH, Isaac F. Dislocations of the shoulder with special reference to accompanying small fractures. J Bone Joint Surg Am. 1959;41-A(3):489-494. Di Giacomo G, Itoi E, Burkhart SS. Evolving concept of bipolar bone loss and the hill-sachs lesion: From “engaging/non-engaging” lesion to “on-track/off-track” lesion. Arthroscopy. 2014;30(1):90-98. doi:10.1016/j.arthro.2013.10.004. Kurokawa D, Yamamoto N, Nagamoto H, et al. The prevalence of a large Hill-Sachs lesion that needs to be treated. J Shoulder Elbow Surg. 2013;22(9):1285-1289. doi:10.1016/j.jse.2012.12.033. Purchase RJ, Wolf EM, Hobgood ER, Pollock ME, Smalley CC. Hill-Sachs “remplissage”: an arthroscopic solution for the engaging Hill-Sachs lesion. Arthroscopy. 2008;24(6):723-726. doi:10.1016/j. arthro.2008.03.015. Koo SS, Burkhart SS, Ochoa  E. Arthroscopic double-pulley remplissage technique for engaging Hill-Sachs lesions in anterior shoulder instability repairs. Arthroscopy. 2009;25(11):1343-1348. doi:10.1016/j.arthro.2009.06.011.

30.

31.

32.

33.

34.

35.

36. 37.

38.

39.

40.

41.

42.

43.

44.

45.

46.

Merolla G, Paladini P, di Napoli G, Campi F, Porcellini G. Outcomes of arthroscopic Hill-Sachs remplissage and anterior Bankart Repair: a retrospective controlled study including ultrasound evaluation of posterior capsulotenodesis and infraspinatus strength assessment. Am J Sports Med. 2015;43(2):407-414. doi:10.1177/0363546514559706. Degen RM, Giles JW, Johnson JA, Athwal GS. Remplissage versus Latarjet for engaging Hill-Sachs defects without substantial glenoid bone loss: a biomechanical comparison. Clin Orthop Rel Res. 2014;472(8):2363-2371. doi:10.1007/s11999-013-3436-2. Cho NS, Yoo JH, Rhee YG. Management of an engaging Hill-Sachs lesion: arthroscopic remplissage with Bankart repair versus Latarjet procedure. Knee Surg Sport Traumatol Arthrosc. 2016;24(12):37933800. doi:10.1007/s00167-015-3666-9. Neviaser TJ. The anterior labroligamentous periosteal sleeve avulsion lesion: a cause of anterior instability of the shoulder. Arthroscopy. 1993;9(1):17-21. doi:10.1016/S0749-8063(05)80338-X. Ozbaydar M, Elhassan B, Diller D, Massimini D, Higgins LD, Warner JJ. Results of arthroscopic capsulolabral repair: Bankart lesion versus anterior labroligamentous periosteal sleeve avulsion lesion. Arthroscopy. 2008;24(11):1277-1283. doi:10.1016/j. arthro.2008.01.017. Bedi A, Ryu RK. Revision arthroscopic Bankart repair. Sports Med Arthrosc Rev. 2010;18(3):130-139. doi:10.1097/ JSA.0b013e3181ec8484. Neviaser TJ. The GLAD lesion: another cause of anterior shoulder pain. Arthroscopy. 1993;9(1):22-23. doi:10.1016/S0749-8063(05)80339-1. Pogorzelski J, Fritz EM, Horan MP, Katthagen JC, Provencher MT, Millett PJ. Failure following arthroscopic Bankart repair for traumatic anteroinferior instability of the shoulder: is a glenoid labral articular disruption (GLAD) lesion a risk factor for recurrent instability? J Shoulder Elbow Surg. 2018;27(8):e235-e242. doi:10.1016/j. jse.2018.02.055. Wolf EM, Cheng JC, Dickson K. Humeral avulsion of glenohumeral ligaments as a cause of anterior shoulder instability. Arthroscopy. 1995;11(5):600-607. doi:10.1016/0749-8063(95)90139-6. Bozzo A, Oitment C, Thornley P, et  al. Humeral avulsion of the glenohumeral ligament: Indications for surgical treatment and outcomes—a systematic review. Orthop J Sport Med. 2017;5(8):2325967117723329. doi:10.1177/2325967117723329. Bokor DJ, Conboy VB, Olson  C. Anterior instability of the glenohumeral joint with humeral avulsion of the glenohumeral ligament. A review of 41 cases. J Bone Joint Surg Br. 1999;81(1):93-96. doi:10.1302/0301-620x.81b1.9111. Fritz EM, Pogorzelski J, Hussain ZB, Godin JA, Millett PJ. Arthroscopic repair of humeral avulsion of the glenohumeral ligament lesion. Arthrosc Tech. 2017;6(4):e1195-e1200. doi:10.1016/j. eats.2017.04.008. Provencher MT, LeClere LE, King S, et  al. Posterior instability of the shoulder: diagnosis and management. Am J Sports Med. 2011;39(4):874-886. doi:10.1177/0363546510384232. Song DJ, Cook JB, Krul KP, et al. High frequency of posterior and combined shoulder instability in young active patients. J Shoulder Elbow Surg. 2015;24(2):186-190. doi:10.1016/j.jse.2014.06.053. Savoie FH  III, Holt MS, Field LD, Ramsey  JR. Arthroscopic management of posterior instability: evolution of technique and results. Arthroscopy. 2008;24(4):389-396. doi:10.1016/j.arthro.2007.11.004. Bottoni CR, Franks BR, Moore JH, DeBerardino TM, Taylor DC, Arciero RA. Operative stabilization of posterior shoulder instability. Am J Sports Med. 2005;33(7):996-1002. doi:10.1177/0363546504271509. Balg F, Boileau P. The Instability Severity Index Score: a simple preoperative score to select patients for arthroscopic or open shoulder stabilisation. J Bone Joint Surg Br. 2007;89(11):1470-1477. doi:10.1302/0301-620X.89B11.18962.

Revision Arthroscopic Stabilization 47.

48.

Santiago-Torres J, Flanigan DC, Butler RB, Bishop JY. The effect of smoking on rotator cuff and glenoid labrum surgery: a systematic review. Am J Sports Med. 2015;43(3):745-751. doi:10.1177/0363546514533776. Park MJ, Hsu JE, Harper C, Sennett BJ, Huffman GR. Poly-L/Dlactic acid anchors are associated with reoperation and failure of SLAP repairs. Arthroscopy. 2011;27(10):1335-1340. doi:10.1016/j. arthro.2011.06.021.

49.

50.

263

Provencher MT, McCormick F, McIntire S, Dewing C, Solomon D. A prospective analysis of 179 type 2 superior labrum anterior and posterior repairs. Am J Sports Med. 2013;41(4):880-886. doi:10.1177/0363546513477363. Kim SH, Ha KI, Kim SH. Bankart repair in traumatic anterior shoulder instability: open versus arthroscopic technique. Arthroscopy. 2002;18(7):755-763. doi:10.1053/jars.2002.31701.

24 Instability in the Throwing Athlete Ashley J. Bassett, MD and Steven B. Cohen, MD

ANATOMY AND BIOMECHANICS The glenohumeral joint is a highly specialized, multiaxial ball-and-socket articulation that yields the greatest joint range of motion in the human body at the expense of skeletal stability. The humeral head is a spherical structure roughly 3 times larger than the glenoid cavity of the scapula. Only 25% to 30% of the head articulates with the shallow glenoid fossa at any given time.1 The scarcity of bony constraint and minimal articular surface contact allow for sizable arcs of shoulder motion but also predisposes to instability. Glenohumeral stability is instead provided by a combination of static soft tissue structures and dynamic restraints.

Static Restraints Static stability is conferred by the glenohumeral geometry, adhesion-cohesion forces mediated by the synovial fluid, glenohumeral capsule, coracoacromial arch, glenoid labrum, and the glenohumeral ligaments. The glenoid fossa has on average approximately 7 degrees of retroversion and 5 degrees of superior tilt relative to the scapular spine, contributing inferior stability to the articulation.2 Synovial fluid stabilizes the glenohumeral joint through the process of adhesion cohesion, where molecular attraction of the synovial fluid to itself, termed cohesion, and to the joint surfaces, termed adhesion, holds the 2 joint surfaces together. An intact glenohumeral capsuloligamentous complex fully seals the joint space, containing the synovial fluid and maintaining negative intra-articular pressure to further add to overall joint stability.

The coracoacromial arch confers anterosuperior stability and is formed by the coracoid, coracoacromial ligament, acromioclavicular joint and clavicle. The glenoid labrum is a fibrocartilaginous structure circumferentially attached to the glenoid rim that is integral to glenohumeral stability. The labrum increases the anteroposterior dimension of the glenoid and deepens the glenoid cavity approximately 50%, expanding the articular surface contact area for the humeral head.2 It also creates a vacuum seal around the glenohumeral articulation and is essential for the concavity compression mechanism of stability generated by the rotator cuff musculature.3 Additionally, the glenoid labrum provides a mechanical bumper to humeral head translation and serves as an attachment point for the glenohumeral ligaments. Once thought to be mere capsular thickening, the glenohumeral ligaments have been increasingly recognized as vital to the static stability of the shoulder joint. The superior glenohumeral ligament (SGHL) originates on the anterosuperior labrum and inserts just superior to the lesser tuberosity. The coracohumeral ligament (CHL) is closely associated with the SGHL and spans from the lateral surface of the coracoid to the greater and lesser tuberosities, crossing the bicipital groove. The SGHL and CHL are both found within the rotator interval, a triangular-shaped area demarcated superiorly by the anterior edge of the supraspinatus, inferiorly by the superior border of the subscapularis and laterally by the coracoid base. The 2 ligaments work in concert to limit inferior translation and external rotation of the adducted shoulder. The anatomy of the middle glenohumeral ligament (MGHL) is quite variable and may be absent in up to 30% of shoulders.4 Most commonly it originates on the anterior labrum near the SGHL and inserts onto the lesser tuberosity. The

- 265 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 265-279). © 2021 SLACK Incorporated.

266

Chapter 24

Figure 24-1. Phases of the throwing cycle.

MGHL restrains anterior translation of the humeral head with the shoulder in 45 to 60 degrees of shoulder abduction. The inferior glenohumeral ligament (IGHL) arises from the anteroinferior labrum and inserts just inferior to the MGHL. The IGHL is the strongest of the glenohumeral ligaments and is composed of an anterior band, a posterior band, and the axillary pouch. The anterior IGHL (AIGHL) restrains anterior and inferior translation of the humeral head with the shoulder in 90  degrees of abduction and external rotation. The posterior IGHL (PIGHL) limits posterior and inferior translation of the humeral head with the shoulder in 90  degrees of abduction and internal rotation. With the shoulder in neutral rotation and 90 degrees of abduction, the axillary band restrains inferior translation of the humeral head.5

Dynamic Restraints The dynamic stabilizers of the glenohumeral joint include the rotator cuff complex, deltoid, long head of biceps, and the scapular stabilizing muscles. Stability is achieved through a combination of joint concavity-compression, coordinated muscle contraction with balancing of coupled forces, and glenohumeral ligament dynamization through direct attachment to the rotator cuff.6 The rotator cuff complex provides a medially directed force, centering and compressing the humeral head against the glenoid and maintaining the humeral head in a depressed position. During shoulder motion, the synergistic action of the rotator cuff and deltoid muscles maintain balanced force couples in both the coronal and axial planes. Coordinated contraction of the supraspinatus balances the superiorly directed force generated by the deltoid. The posterior rotator cuff, the infraspinatus, and teres minor, are balanced in the transverse plane by the subscapularis anteriorly. The long head of biceps tendon is thought to depress the humeral head during shoulder abduction, providing further superior stability.7 The trapezius, latissimus dorsi, serratus anterior, rhomboids, and levator scapulae muscles work to stabilize the

scapula during shoulder motion and thereby increase dynamic stability of the glenohumeral joint. Coordinated contraction of the shoulder girdle musculature is essential for synchronous movement between the scapula and the humerus, termed scapulohumeral rhythm. During shoulder elevation, contraction of the trapezius and serratus anterior rotate the scapula upward while counteracting the downward rotational force generated by the deltoid and rotator cuff complex. The serratus anterior also posteriorly tilts the scapula, directly approximating the scapula to the thorax and constructing a more stable base for shoulder motion. The rhomboids and levator scapulae muscles work synergistically to prevent excessive lateral scapular translation by the upper serratus anterior.8 The periscapular muscles work in concert to produce efficient shoulder motion and further stabilize the glenohumeral joint during range of motion.

Biomechanics of Pitching Overhead athletes, particularly pitchers, experience significant and repetitive torsional, distractive. and compressive forces at the glenohumeral joint. The sequential phases of an overhead baseball pitch have been well defined and are characterized by synchronous activation of select muscle groups within a kinetic chain. Energy is transmitted from the lower extremities, through the pelvis and trunk, to the upper extremity, and ultimately distally to the hand to power ball release, the so-called kinetic chain.9 The 6 phases of the throwing motion are windup, early cocking or stride, late cocking, acceleration, deceleration, and follow through (Figure 24-1).10 The windup phase begins with initial movement of the lead leg and ends when the lead leg reaches maximum knee height, in a position termed the balance point. The center of gravity is over the back leg to allow efficient generation of maximum momentum once forward motion is initiated. Upper extremity muscle activity and risk of injury are both low in this phase compared to the remainder of the pitching motion.11

Instability in the Throwing Athlete The early cocking or stride phase spans begins at the point of maximum lead knee height and ends when the lead foot contact with the pitching mound. Proper positioning of the lower extremities, pelvis, and trunk is crucial for efficient transfer of energy from the lower extremities to the upper extremity. The lead foot should be directed toward home plate or slightly “closed” toward third base to optimize pelvic rotation and energy transfer. Excessively closed lead foot placement can limit pelvic and hip rotation, whereas an excessively open lead foot position can cause premature pelvic rotation, both of which result in less energy transferred to the arm and loss of momentum. The upper extremity must subsequently generate more velocity, increasing the stress on the anterior shoulder and medial elbow and predisposing to injury. At the shoulder, serratus anterior, middle trapezius, rhomboids, and levator scapulae muscles position the scapula in upward rotation and retraction to provide a stable glenoid for humeral head rotation. The deltoid is active early in the stride phase to aid in abduction of the shoulder. The supraspinatus, infraspinatus, and teres minor become active later in the phase to initiate shoulder external rotation.11 The late cocking phase begins with lead foot contact and ends at the point of maximum external rotation of the throwing shoulder. The upper torso continues to rotate, building angular and rotational velocity, as the pelvis reaches maximum rotation. The trunk begins a derotational pattern back toward the lead leg. The trapezius, rhomboids, and levator scapulae muscles retract and rotate the scapula upward to ensure sufficient subacromial space to accommodate hyperabduction of the humeral head without impingement. The infraspinatus and teres minor generate significant humeral external rotation. The supraspinatus is the least active of the rotator cuff complex in this phase and is thought to mainly function to provide glenohumeral compression and humeral head depression, thereby resisting the distraction forces at the shoulder caused by the torque of the rapidly rotating upper torso. As the shoulder reaches maximum external rotation, the subscapularis, pectoralis major, and latissimus dorsi eccentrically contract to terminate external rotation and stabilize the anterior shoulder. The acceleration phase begins at the point of maximum shoulder external rotation and ends at ball release. The trunk continues to rotate toward the lead leg and tilt forward, generating angular momentum that is transmitted to the upper extremity. The serratus anterior protracts the scapula to maintain a stable base as the anterior deltoid and pectoralis major horizontally adduct the humerus to bring the throwing arm anterior to the torso. The anterior shoulder musculature—the subscapularis, pectoralis major, and latissimus dorsi—shift from eccentric contraction to maximum concentric contraction, resulting in high-velocity internal rotation of the humerus. The posterior shoulder muscles—the infraspinatus, teres minor, and posterior deltoid—shift from concentric contraction to eccentric contraction to counteract the enormous force generated as the arm is adducted and internally rotated during this phase.

267

The deceleration phase begins at ball release and ends at the point of maximum humeral internal rotation, horizontal adduction to 35  degrees, and maximum elbow extension.12 This is the most violent phase of the throwing cycle, characterized by excessive glenohumeral distraction with large posterior and inferior shear forces and extreme eccentric loading of the rotator cuff to resist joint distraction and anterior humeral head translation. The trapezius, serratus anterior, and rhomboid muscles work to decelerate the shoulder girdle and stabilize the scapula. Eccentric contraction of the biceps and brachialis muscles decelerates the rapidly extending elbow and pronates the forearm. The follow-through phase proceeds until forward motion ceases and the pitcher returns to the fielding position. There is minimal muscle activity and joint forces during this phase, lessening the risk of injury. Maximum torque forces at the glenohumeral joint occur during the late cocking, early acceleration, and deceleration stages. Repetitive excessive torque stress can ultimately result in adaptive structural changes of the glenohumeral joint, as well as the development of true glenohumeral pathology including labral tears, rotator cuff injury, and capsular trauma.

Adaptive Changes of the Glenohumeral Joint Adaptive anatomic and nonpathologic changes of the glenohumeral joint are often seen in throwing athletes as a result of the repetitive stresses associated with the overhead throwing cycle. It is crucial to recognize these osseous and soft tissue irregularities and differentiate them from true pathology that may warrant intervention. Common osseous adaptations seen in throwing athletes include increased proximal humerus retroversion, increased glenoid retroversion, cystic changes in the posterolateral humeral head, and sclerosis of the posterosuperior glenoid rim. Soft tissue changes include attenuation of the AIGHL and anterior capsule, thickening of the PIGHL and posterior capsule, and alteration in scapular position and motion and overall upper extremity kinematics.13 Bony and soft tissue adaptations both have been postulated to contribute to the altered arc of shoulder motion seen in throwing athletes. The proximal humerus originates as a retroverted structure in utero and progressively derotates through childhood and adolescence until approximately age 16 years.14 The proximal humeral physis is most resistant to tensile forces and least resistant to torsional forces.15 In the skeletally immature overhead throwing athlete, repetitive rotatory forces at the proximal humeral growth plate can limit the natural physiologic derotation and lead to increased proximal humerus retroversion at skeletal maturity. Whereas the average adult has less than a 5-degree difference in mean retroversion between the dominant and nondominant arm, throwing athletes demonstrate a significant greater difference in mean retroversion between the dominant throwing arm and

268

Chapter 24

nondominant arm.16,17 Collegiate and professional throwers demonstrate greater than 10  degrees of increased retroversion in the dominant shoulder compared to the nondominant arm, as well as increased glenoid retroversion. These osseous changes are associated with a greater arc of shoulder external rotation and greater total arc of shoulder motion, thought to enhance performance and potentially decrease risk of shoulder injury. By positioning the glenohumeral joint in greater baseline external rotation, humeral and glenoid retroversion is thought to decrease the strain on the anterior capsuloligamentous structures and maximize the rotational torque generated during the throwing cycle.18,19 Structural changes of the joint capsule and glenohumeral ligaments are also seen in throwing athletes and contribute to alteration in glenohumeral motion. The posterior capsule of the dominant shoulder demonstrates increased thickness and decreased tissue elasticity compared to the nondominant shoulder in overhead-throwing athletes.20,21 This soft tissue adaptation develops in response to excessive and repetitive tensile stresses experienced by the posterior capsuloligamentous complex. In the deceleration phase of the throwing cycle, the posterior rotator cuff and posterior glenohumeral capsule counteract the extreme joint distraction forces generated during the acceleration phase. Recurrent tensile forces and microtrauma concentrated at the posteroinferior capsule and PIGHL may ultimately trigger a fibroblastic healing response with increased collagen production, capsular hypertrophy, and loss of tissue compliance.22 Tightening of the posterior capsule is thought to protect the shoulder by better mitigating the distractive forces at the glenohumeral joint during deceleration. Posterior capsule tightness also shifts the humeral head center of rotation posteriorly and superiorly, which can lead to anterior pseudolaxity by detensioning the anteroinferior capsuloligamentous structures.13 Anterior pseudolaxity without subluxation should not be mistaken for be true pathologic anteroinferior capsular attenuation with resultant anterior laxity. Many of the structural adaptations of the glenohumeral joint observed in the throwing athlete are nonpathologic and may in fact serve to increase shoulder range of motion and enhance athletic performance. Increased shoulder motion has been correlated with greater arm cocking and ball velocity in elite pitchers.23 However, as with any adaptive response, too much compensation along the spectrum of structural change can disrupt the delicate balance of the glenohumeral joint mechanics and progress to shoulder injury.

PATHOPHYSIOLOGY Glenohumeral instability comprises a spectrum of pathology ranging from subtle subluxation episodes to frank dislocation. Instability may arise from an acute traumatic event, repetitive microtrauma to the shoulder, or generalized ligamentous laxity. Shoulder instability may be further categorized as unidirectional, including anterior or posterior instability, or multidirectional. Instability in the overhead

throwing athlete is a unique entity and has been described as subtle instability or pathologic acquired laxity resulting from repetitive microtrauma to the glenohumeral joint and capsuloligamentous complex.24,25 In overhead-throwing sports, the shoulder is very susceptible to injury due to substantial forces concentrated at the glenohumeral joint during the pitching cycle. With continued high-intensity throwing, the repetitive stress eventually exceeds the tensile strength and repair capabilities of the static joint restraints and progressive damage occurs. The capsule and glenohumeral ligaments are progressively attenuated, allowing for subtle subluxation of the glenohumeral joint. The dynamic joint stabilizers initially compensate for this microinstability by increasing muscle activity during shoulder motion; however, in the setting of continued activity, the dynamic stabilizers eventually fatigue. As the compensatory mechanisms wane, glenohumeral instability worsens and subluxation events become more frequent. Recurrent humeral head subluxation results in damage to the labrum, glenoid rim, and humeral head, as well as impingement of the rotator cuff. Ultimately, a combination of capsular laxity, labral detachment, osseous defects of the humeral head or glenoid, and rotator cuff pathology contribute to progressive shoulder pain and dysfunction.

Anterior Glenohumeral Instability In the late cocking and early acceleration phases of the throwing cycle, the glenohumeral joint is subject to a tremendous external rotational torque with significant shear forces applied to the anteroinferior capsuloligamentous complex. Over time, the repetitive insult leads to gradual tensile failure and attenuation of the anterior capsule with a subtle increase in glenohumeral translation.26 Increased activity of the posterior deltoid and rotator cuff complex compensates for the mild glenohumeral instability, but with continued overhead throwing the dynamic stabilizers gradually fatigue. Without the support of the surrounding musculature, the anteroinferior capsular tissue experiences increased loads and eventually fails. Although progressive stretching and redundancy of the anterior capsule is most often the mechanism of anterior instability, isolated tears of the anterior capsule and humeral avulsion of the glenohumeral ligament have also been reported in professional baseball players with anterior microinstability.27,28 Excessive anterior translation of the humeral head during the late cocking and early acceleration phases results in tearing of the anterior and anteroinferior labrum (Bankart lesion) with further loss of glenohumeral stability. As the humeral head subluxates anteriorly, it contacts the coracoacromial arch and can lead to subacromial impingement and rotator cuff tendinitis. The undersurface of the posterior rotator cuff complex may also impinge on the posterosuperior border of the glenoid rim during excessive anterior humeral head translation with development of partial articular-sided rotator cuff tears (internal impingement).

Instability in the Throwing Athlete

Posterior Glenohumeral Instability Osseous morphology of the glenoid and proximal humerus contributes to the static stability of the glenohumeral joint, and altered anatomy has been linked to the development of posterior instability.29 Humeral head and glenoid retroversion, glenoid hypoplasia, posterior glenoid bone loss—acutely traumatic or attritional—and reverse Hill Sachs lesions of the proximal humerus are all associated with recurrent posterior glenohumeral instability. Increased retroversion of the humeral head and glenoid is a bony adaptation seen in overhead throwers and facilitates the supraphysiologic range of shoulder motion in these athletes. It is also thought to predispose throwers to posterior instability by generating an easier vector of posterior subluxation of the humeral head on the glenoid.30 The soft tissue stabilizers, the posterior capsuloligamentous complex and glenoid labrum, are particularly at risk for injury in 2 specific phases of the throwing cycle: late cocking and deceleration. During the late cocking phase, the arm is held in hyperabduction and maximum external rotation. Hyperangulation of the humerus in this position can result in internal impingement of the rotator cuff against the posterior glenoid and labrum. With repetitive throwing, degeneration and tearing of the posterior labrum may occur and contribute to loss of static glenohumeral stability. In the deceleration phase, the posterior rotator cuff and capsuloligamentous complex is subject to extreme tensile forces as the humerus continues to violently adduct, flex, and internally rotate following ball release. Repetitive eccentric stress can ultimately precipitate tensile failure of the posterior supraspinatus or anterior infraspinatus along the bursal surface of the rotator cuff. Diminished rotator cuff function in this phase leads to even greater tensile forces being transmitted to the posterior capsule and PIGHL. Recurrent microtrauma to the posterior capsuloligamentous complex may result in gradual attenuation and capsular laxity.31

Glenohumeral Internal Rotation Deficit Repetitive tensile strain applied to the posterior capsule and ligamentous structures may conversely trigger a fibrotic healing response and capsular hypertrophy with loss of soft tissue compliance and limitation of shoulder motion. Glenohumeral internal rotation deficit (GIRD) is a change in rotational motion of the shoulder joint characterized by increased external rotation with a corresponding loss of interval rotation of greater than 25  degrees compared to the nonthrowing shoulder.32 Development of posteroinferior capsular contracture is thought to be the predominant underlying etiology of GIRD. Takenaga et al used ultrasound to measure the thickness and elasticity of the posterior capsule in 45 collegiate pitchers with the diagnosis of GIRD. The mean stiffness and thickness of the posteroinferior capsule was significantly greater in the throwing shoulder compared to the nonthrowing shoulder.21 Osseous anatomy may also

269

contribute to the development of GIRD.33 A study by Noonan and colleagues demonstrated that pitchers with GIRD had a mean side-to-side difference in humeral retroversion of 19.5  degrees compared with the nondominant shoulder, whereas those without GIRD had only a 12.3-degree side-toside difference in retroversion.34 The pathologic alteration of shoulder motion seen in throwers with GIRD results from stretching of the anterior soft tissues that resist external rotation—the coracohumeral ligament, rotator interval, and anterior capsuloligamentous complex—and contracture of the posterior soft tissues—the PIGHL, posterior capsule, pectoralis minor, and short head of the biceps—with subsequent posterior shift of the glenohumeral center of rotation.35 Excessive external rotation strains the biceps anchor, which can ultimately “peel back” under tension, culminating in injury to the superior and posterior labrum. Owing to the posterior shift of the humeral head center of rotation, impingement of the rotator cuff between the greater tuberosity of the humerus and the posterosuperior glenoid can occur, resulting in articular-sided partial rotator cuff tears (internal impingement).

Scapular Dyskinesis Asynchrony of scapulothoracic motion and alterations both in static and dynamic scapular positioning has been associated with glenohumeral instability.36 Scapular dyskinesis arises from dysfunction of the periscapular muscles due to fatigue, trauma, or nerve injury. The resulting muscular imbalance can alter the normal scapulohumeral rhythm during the overhead-throwing motion. Specifically, patients with shoulder instability have exhibited excessive protraction and delayed retraction with shoulder elevation, linked to decreased activity in the lower trapezius and serratus anterior muscles.37 During the normal overhead-throwing motion, the scapula must retract in the cocking phases to keep the glenoid centered under the humerus. Failure of the scapula to retract appropriately results in hyperangulation of the humerus to achieve maximum external rotation with increased stress transmitted to the anterior capsuloligamentous complex.38 Loss of normal scapulohumeral motion also results in altered throwing mechanics and inefficient transfer of energy from the trunk to the arm with loss of ball velocity. Athletes may subsequently increase the work of the shoulder to compensate for lost velocity, which further increases strain on the glenohumeral stabilizers.

CLINICAL EVALUATION History A thorough history and physical examination is critical when evaluating a throwing athlete for glenohumeral instability. Very few throwing athletes will report overt symptoms of instability; rather, diminished performance and shoulder pain are often the primary complaints.39 Concerns

270

Chapter 24

related to performance include loss of pitching velocity, loss of command of the pitch, and change in pitching mechanics. The onset, timing, and location of shoulder pain, as well as exacerbating and relieving factors, should be carefully determined. Most throwing athletes with instability cannot recall a par ticular inciting event or acute trauma to the shoulder. They often detail a gradual onset of intermittent deep shoulder pain that is reproduced by certain arm positions or in specific phases of the throwing cycle. Anterior shoulder pain in the late cocking phase, with the arm in an abducted and externally rotated position, can be indicative of anterior capsuloligamentous pathology. Posterior shoulder pain in the deceleration and follow-through phases, with the arm in an adducted, flexed, and internally rotated position, is more suggestive of injury of the posterior capsule and labrum. It is common for these athletes to report more than one location of pain that occurs in dif ferent phases of the throwing cycle, related to concomitant pathology such as subacromial impingement or rotator cuff/biceps tendinitis. Rotator cuff pathology is common in throwing athletes and is often characterized by night pain. Patients should be questioned about mechanical symptoms, such as grinding, clicking, or catching because these are associated with labral tears. Though less common, instability-related symptoms can be described as a feeling of the arm going dead or a frank sensation of the shoulder slipping out. Lastly, details about past treatment should be obtained, including prior shoulder immobilization, physical therapy and modalities, injections to the shoulder girdle, or surgical intervention.

Physical Examination Examination begins with careful inspection of the bilateral upper extremities and shoulder girdles, taking note of overall posture and symmetry. It is normal for the dominant extremity of a throwing athlete to have greater muscular development than the contralateral nondominant extremity.40 The deltoid, supraspinatus, and infraspinatus muscles are evaluated for atrophy. Atrophy of the supraspinatus and/ or infraspinatus musculature suggests chronic rotator cuff dysfunction or suprascapular nerve injury. The static and dynamic positioning of the scapula is assessed for scapular dyskinesis and compared to the contralateral shoulder girdle. Resting scapular drooping or scapular winging with active elevation may be due to periscapular muscle fatigue or intra-articular pathology and should be noted. Shoulder landmarks should be palpated for tenderness, including the acromioclavicular joint, coracoid process, biceps tendon, greater tuberosity, posterior cuff, and capsule. Tenderness to palpation of the anterior joint line is often found in patients with anterior glenohumeral instability but is a nonspecific finding also seen in patients with impingement syndrome. Palpation of the posterior glenohumeral joint elicits tenderness in approximately 60% of patients with posterior instability.41

Shoulder range of motion should be assessed in the sitting position, as well as in the supine position to stabilize the scapula and eliminate scapulothoracic contribution to glenohumeral motion. Forward elevation in the scapular plane, and internal and external rotation at 0  degrees and 90 degrees of shoulder abduction are recorded and compared to the contralateral shoulder. Throwing athletes frequently exhibit increased shoulder external rotation with an associated loss of internal rotation in their dominant shoulder. This alteration in glenohumeral rotation is often due to adaptive nonpathologic changes of the glenohumeral anatomy and is associated with a preserved total arc of shoulder motion that is symmetric to the contralateral shoulder. Loss of the total arc of shoulder rotation, specifically in the setting of internal rotation deficit, is a common finding in the evaluation of an injured throwing athlete. Strength testing should include specific evaluation of the rotator cuff musculature and periscapular stabilizers. The pinch test can be used to assess scapular retraction strength.42 Inability to hold an isometric pinch of the scapula for 15 seconds indicates periscapular weakness. Shoulder ligamentous stability is tested in the anterior, posterior, and inferior directions using a number of specialized examination maneuvers summarized in Table  24-1. Stability tests are performed on the bilateral shoulders. Increased laxity is expected in the dominant shoulder of a throwing athlete compared to the nondominant shoulder. Therefore, it is impor tant to note whether distinct subluxation of the humeral head can be produced and if these provocative maneuvers reproduce the patient’s symptoms. Anterior shoulder instability is best evaluated with the patient in the supine position. The anterior apprehension, Jobe relocation, and anterior release tests can be used to assess for symptoms related to anterior instability, including a sensation of instability or anterior shoulder pain. Most throwers with subtle anterior instability will endorse anterior shoulder pain but no frank apprehension during these provocative maneuvers. The Jobe relocation test has high sensitivity and specificity if apprehension is the primary symptom; however, the diagnostic accuracy of this exam maneuver is poor if pain alone is evaluated.43 Reproduction of symptoms with the anterior release test is 90% sensitive for the diagnosis of occult anterior glenohumeral instability.44 The anterior drawer, posterior drawer, and load-and-shift tests are all used to measure translation of the humeral head and grade laxity using the modified Hawkins scale. Grade 1+ indicates increased translation to the glenoid rim but no subluxation, grade 2+ indicates subluxation of the humeral head over the glenoid rim, and grade 3+ indicates dislocation of the humeral head over the glenoid rim that does not spontaneously reduce.45 Throwing athletes are expected to have grade 1+ anterior laxity, and grade 2+ posterior laxity is not uncommon. Anterior laxity of grade 2+ or greater is usually suggestive of a pathologic condition. Recurrence of symptoms during these stress maneuvers, including pain

Instability in the Throwing Athlete

271

Table 24-1. Shoulder Instability Examination Tests TEST

DESCRIPTION

PERTINENT FINDINGS Anterior Instability

Anterior apprehension Jobe relocation

●

●

●

●

●

Anterior release

●

●

●

Anterior drawer

●

●

Load and shift

●

●

●

Patient is supine with the arm in 90 degrees of abduction and 90 degrees of elbow flexion Examiner then rotates the arm from neutral to 90 degrees of ER Continuation of Anterior Apprehension test

●

●

●

Patient is supine with arm in 90 degrees of abduction and 90 degrees of ER

Sensation of apprehension and resistance to further ER are classic positive findings Patients with subtle instability may endorse pain anteriorly without apprehension Relief of symptoms, apprehension and/or pain, with a posteriorly directed stabilizing force applied to anterior HH signifying positive test result

Examiner then applies a posteriorly directed pressure to anterior HH Continuation of the Jobe relocation test

●

Patient is supine with arm in 90 degrees of abduction and 90 degrees of ER, with a posteriorly directed pressure applied to the anterior HH

Positive test characterized by recurrence of symptoms, apprehension and/or pain, with sudden release of posteriorly directed force

Examiner then suddenly releases pressure from anterior HH Patient supine with arm in 80 to 120 degrees of abduction, 0 to 20 degrees of flexion and 0 to 30 degrees of ER Examiner then applies anteriorly directed force to HH Patient supine with arm in 20 degrees of abduction and 20 degrees of flexion to center HH in glenoid fossa

●

Grade 1: increased HH translation to glenoid rim

●

Grade 2: HH subluxation over glenoid rim

●

Grade 3: HH dislocation over glenoid rim

●

Same grading system as Drawer tests

Examiner then applies anterior and posterior force to HH Maneuver examines both anterior and posterior stability Posterior Instability

Posterior drawer

●

●

Jerk

●

●

Kim

●

●

Patient supine with arm in 80 to 120 degrees abduction and 20 to 30 degrees of flexion Arm is then internally rotated and flexed to 80 degrees as a posteriorly directed force is applied to HH Patient seated upright with arm in 90 degrees of abduction and 90 degrees of IR

●

●

●

Examiner then applies an axial load and horizontally adducts arm Patient seated upright with arm in 90 degrees of abduction The arm then axially loaded and diagonally elevated to 45 degrees while applying a posteriorly and inferiorly directed force to upper arm

●

Same grading system as anterior drawer and load and shift tests Apprehension and/or pain also considered positive findings Sharp pain in posterior shoulder with or without a clunk signifies a posterior labrum tear Sharp pain in posterior shoulder with or without a clunk signifies a posteroinferior labrum tear

(continued )

272

Chapter 24

Table 24-1. Shoulder Instability Examination Tests (continued) TEST

DESCRIPTION

PERTINENT FINDINGS Inferior instability

Sulcus

Gagey or hyperabduction

●

Patient seated upright with arm resting at the side

●

Examiner then applies downward traction to arm

●

●

●

Patient seated upright with a downward force applied to scapula Examiner then passively abducts arm

Sulcus is a depression between lateral acromion edge and HH, graded by size in centimeters

●

Grade 1: < 1 cm

●

Grade 2: 1 cm to 3 cm

●

Grade 3: > 3 cm

●

Abduction > 105 degrees or apprehension limiting passive abduction are positive findings

Abbreviations: ER, external rotation; HH, humeral head; IR, internal rotation.

and/or apprehension, is also considered a positive finding for anterior or posterior instability.46 Additionally, the jerk test and the Kim test both load the posterior labrum and can be used to assess specifically for posterior labral pathology and posterior instability.47 The jerk test has been shown to be more accurate for direct posterior labral tears, whereas the Kim test is better at identifying posteroinferior labral tears.48 Inferior instability is evaluated by assessing presence of the sulcus sign as well as the Gagey or hyperabduction test. Throwing athletes normally exhibit a 1+ to 2+ sulcus sign, characterized by a sulcus measuring 1 to 3 cm. A grade 3+ sulcus sign, greater than 3 cm, is associated with pathologic instability.49 Greater than 105  degrees of passive abduction or the presence of apprehension limiting passive abduction during the Gagey test is considered positive for laxity of the inferior glenohumeral ligament.50 Coexistent pathology of the rotator cuff, superior labrum, and biceps tendon can be evaluated with additional provocative tests. Rotator cuff tendinitis and subacromial impingement can be assessed with the Neer impingement test and Hawkins impingement test. Numerous examination maneuvers have been described for the identification of superior labrum anterior to posterior (SLAP) tears, including the O’Brien active compression test, crank test, anterior slide test, biceps load test, modified dynamic labral shear test, labral tension test, resisted supination external rotation test, and the forced shoulder abduction and elbow flexion test. Of these maneuvers, the modified dynamic labral shear test was found to be the best screening tool for SLAP tears and consistently demonstrated high sensitivity and low negative likelihood ratio.46 Biceps tendon pathology can be confirmed by the Speed test, Yergason test, and upper cuff test, all of which have high specificity and positive likelihood ratio.46

Imaging Studies Radiologic evaluation begins with obtaining plain radiographs of the involved shoulder in several planes—true

anteroposterior (AP) views in neutral, external, and internal rotation; a lateral outlet view; an axillary view; and a Stryker notch view. In cases of traumatic glenohumeral instability a Hill-Sachs lesion may be seen on the Stryker notch view or on the AP view in internal rotation. Bony Bankart lesions of the glenoid may be seen on the axillary view. In the overheadthrowing athlete with glenohumeral microinstability, radiographs will rarely be diagnostic. A Bennett lesion, a focal ossification at the posteroinferior glenoid seen in throwing athletes, may be present on the axillary view. Magnetic resonance imaging (MRI) allows enhanced evaluation of the glenohumeral joint including the capsuloligamentous complex, labrum, rotator cuff, articular cartilage, and the osseous anatomy. In an overhead-throwing athlete, MRI may show thickening of the posterior capsule, cystic changes in the posterior glenoid and posterolateral tuberosity, posterior glenoid osteophyte formation, and/or calcification of the posterior labrum (Figure 24-2). Magnetic resonance arthrogram (MRA) with intra-articular injection of gadolinium allows for controlled distention of the glenohumeral capsule and better definition of the anatomy of the labrum. It is considered the gold standard for evaluation of capsulolabral injuries and has a sensitivity for detection of anterior and posterior labral tears ranging from 90% to 95%.51 SLAP tears and partial tears of the rotator cuff may also be seen.

NONOPERATIVE MANAGEMENT The initial treatment of symptomatic glenohumeral instability in the vast majority of overhead-throwing athletes should be nonsurgical. Conservative management focuses on dynamic stability, enhancing proprioception, and improving neuromuscular coordination of the kinetic chain. A multiphase progressive and sequential rehabilitation program has been advocated for the nonoperative treatment of shoulder injury in the overhead-throwing athlete.52

Instability in the Throwing Athlete Phase I is the acute phase of rehabilitation and focuses on reduction of pain and inflammation and normalization of range of motion deficits. Pain relief is achieved through combination of activity modification, nonsteroidal antiinflammatory medications, and various modalities including cryotherapy, iontophoresis, phonophoresis, electrical stimulation, massage therapy, neuromuscular facilitation, and rhythmic stabilization exercises. Exercises focus on improving range of motion and flexibility of the shoulder girdle musculature. The sleeper stretch and the cross-body adduction stretch improve flexibility of the posterior shoulder soft tissues and increased shoulder internal rotation. The sleeper stretch is performed by having the patient lie in the lateral decubitus position on the affected side with the shoulder in 90 degrees of forward flexion and internally rotating the shoulder. The cross-body adduction stretch is performed by having the patient stand against a wall to prevent the scapula from rotating and using the other arm to pull the involved arm across the body. The unilateral corner stretch and supine manual stretch are effective for lengthening the pectoralis minor. The unilateral corner stretch is performed with the shoulder in 90 degrees of abduction and elbow in 90 degrees of flexion. The volar aspect of the forearm is place on a doorframe and the trunk is rotated away from the side being stretched. The supine manual stretch is also performed with the arm in the 90-degree/90-degree position. The patient lies supine with a towel roll along the upper thoracic spine and the therapist applies a posteriorly directed force to the coracoid process.35 Once the patient exhibits minimal pain and normalized shoulder range of motion, he or she may progress to the second phase. Phase II is the intermediate phase and introduces strengthening exercises that aim to restore muscular balance and enhance dynamic stability of the shoulder while maintaining flexibility. Exercises include full isotonic strengthening of the rotator cuff and periscapular muscles and neuromuscular control drills. Lower extremity strengthening and core-stabilization activities are also performed in the intermediate phase. Criteria to advance to the next phase include full pain-free shoulder range of motion, full rotator cuff and scapular strength, and neuromuscular control, and no pain or apprehension on provocative examination maneuvers that originally produced symptoms. Phase III is the advanced strengthening phase and includes aggressive upper extremity strengthening and endurance exercises, sport-specific neuromuscular control drills, introduction of Plyometric training and an initial interval throwing program. Plyometric exercises are characterized by a rapid transition from eccentric to concentric contraction and facilitate recruitment of muscle fibers. National Collegiate Athletic Association Division I baseball players who participated in a shoulder conditioning program with high-load plyometric training had significantly increased throwing velocity compared to players without Plyometric training.53 Phase IV is the return-to-activity phase and involves an advanced interval throwing program and a high-repetition

273

Figure 24-2. T2 magnetic resonance imaging showing a posterior glenoid osteophyte with surrounding edema (red arrow) and calcification of the posterior labrum consistent with a Bennett lesion.

low-resistance strength and neuromuscular maintenance program. The athlete is advanced to position-specific throwing. Pitchers beginning a mound throwing program, whereas positional players progress through a long-toss program and positional drills. Throwing and long-tossing is encouraged to lengths that are comfortable for the athlete without altering mechanics. Use of weighted balls for throwing rehabilitation is generally discouraged. The goal of this rehabilitation protocol is to return to full throwing velocity over the course of 6 to 12 weeks. Lack of improvement after 3 months of rehabilitation or an inability to return to competitive play within 6 months constitutes a failure of nonoperative management and should prompt discussion of operative treatment options.35

OPERATIVE MANAGEMENT Indications and Contraindications The indications for surgical treatment of glenohumeral instability in the overhead-throwing athlete are persistent shoulder pain, symptoms of instability or shoulder dysfunction with physical examination, and/or imaging findings consistent with capsulolabral pathology that has failed a trial of structured rehabilitation and renders the patient unable to return to his or her desired level of play. Presence of certain associated injuries, including full-thickness rotator cuff tears or large osseous defects of the glenoid or humeral head (> 25%), are indications for early surgical intervention. Contraindications for surgical treatment include voluntary nonpositional shoulder instability and patients who are

274

Chapter 24

unable or unwilling to comply with the postoperative rehabilitation protocol. Glenoid hypoplasia and glenoid retroversion greater than 15  degrees are relative contraindications specifically for isolated capsular shift.

Surgical Techniques Selection of the optimal surgical technique should be individualized to address the anatomic cause and direction of glenohumeral instability. A patient with recurrent shoulder dislocations after a traumatic event with glenoid bone loss noted on imaging may benefit most from a bony stabilization procedure, such as glenoid reconstruction with coracoid autograft transfer or distal tibia allograft. Conversely, shoulder instability in the overhead-throwing athlete is more often related to repetitive microtrauma to the glenohumeral joint with subsequent soft tissue attenuation and development of pathologic capsuloligamentous laxity. Various capsulorraphy techniques have been described to address this subtle glenohumeral instability by reducing capsular redundancy and capsular volume. Open capsular shift was the gold standard for surgical treatment of pathologic capsuloligamentous laxity with symptomatic glenohumeral instability for more than 30  years. Cadaveric biomechanical studies have suggested that open capsular shift results in significantly greater capsular volume reduction compared to arthroscopic capsular plication.54 Failure to correct capsular redundancy has been identified as a cause of failure and recurrent instability following glenohumeral stabilization surgery, highlighting the importance of capsular volume reduction55; however, the precise amount of volume reduction required to eliminate shoulder instability remains unclear. Steady advancements in the field of arthroscopy over the past decades have made arthroscopic management of pathologic capsular redundancy and glenohumeral instability a viable and less invasive treatment option. Another biomechanical study found that arthroscopic capsular plication reduced glenohumeral translation comparable to that of open capsular shift but resulted in less restriction of external rotation, which may be particularly advantageous in overhead throwing athletes.56 Additional advantages of arthroscopic treatment include decreased morbidity, avoidance of subscapularis detachment anteriorly and deltoid detachment posteriorly, intra-articular visual confirmation of decreased capsular laxity, ability to address both anteroinferior and posteroinferior capsular redundancy in a single approach, capacity to evaluate and treat other intraarticular pathology, small incision, shorter operative time, less blood loss, and ability to undergo early rehabilitation.57 Arthroscopic thermal capsulorraphy was a surgical technique proposed to address the capsular redundancy associated with shoulder instability. Application of thermal energy to the capsuloligamentous tissues by a radiofrequency device stimulated collagen denaturation and capsular shrinkage with subsequent reduced capsular volume and decreased

glenohumeral laxity. Though short-term results appeared excellent, with 93% of athletes returning to overhead activities, mid- and long-term follow-up showed significant deterioration of results and recurrent instability requiring revision surgery. Results of revision surgery were quite poor, with only half of the patients achieving a satisfactory outcome. Other reported complications include glenohumeral chondrolysis and thermal axillary nerve injury with transient dysesthesias.58

Examination Under Anesthesia Surgical stabilization of the shoulder is performed under general anesthesia, with or without a regional interscalene nerve block. Prior to positioning, the shoulder is examined under anesthesia in the supine position. The range of motion, grade of preoperative capsuloligamentous laxity, and direction of occult instability is noted. Following examination of the shoulder, the patient is placed in the beach chair position or lateral decubitus position, depending on surgeon preference.

Diagnostic Arthroscopy A diagnostic arthroscopy of the shoulder can be performed prior to both open and arthroscopic capsulorraphy procedures and allows for complete evaluation of the glenohumeral joint and identification of any concomitant pathology. A standard posterior portal is placed approximately 2 to 3 cm inferior and 1 to 2 cm medial to the posterolateral corner of the acromion. A standard anterior superior portal is established using an inside-out or outside-in technique and is placed just lateral to the coracoid process entering the joint through the rotator interval. A diagnostic arthroscopy is performed with systematic evaluation of the articular cartilage, glenoid labrum, glenohumeral capsule and ligaments, long head of biceps tendon, axillary pouch, and the rotator cuff tendons. A patulous capsule and positive drive-through sign, defined as the ability to pass the arthroscope easily between the humeral head and the glenoid at the level of the AIGHL, are often found. The presence of a positive drive-through sign is associated with shoulder laxity and is highly sensitive, but not specific, for shoulder instability.59 The glenoid labrum is circumferentially probed to identify any detached labral tears requiring repair. The posterior labrum is best viewed from the anterior portal and commonly shows fraying in overhead-throwing athletes. The glenohumeral ligaments are inspected next. The SGHL blends with the glenohumeral capsule and often cannot be seen as a distinct structure. The MGHL can be visualized draped over the subscapularis tendon. The AIGHL attaches to the anterior inferior labrum and is often attenuated and redundant in throwers with glenohumeral instability. The undersurface of the rotator cuff is evaluated for articular-sided tears. If a partial articular rotator cuff tear is found, the tear should be tagged with a monofilament

Instability in the Throwing Athlete

275

Figure 24-3. Arthroscopic capsulolabral plication with suture anchors.

suture for later evaluation of the bursal surface in subacromial space. Partial rotator cuff tears and labral fraying are debrided. After thoroughly assessing the glenohumeral joint, the arthroscope is then placed in the subacromial space from the posterior portal to evaluate the bursal surface of the rotator cuff and undersurface of the acromion. Subacromial bursitis can be arthroscopically debrided. Additional portal placement depends on the intraarticular pathology found on diagnostic arthroscopy and the planned surgical approach. If no additional pathology is noted and an open procedure is planned, the arthroscope can be removed and the surgeon may proceed with open capsular shift.

Open Anterior Capsular Shift The deltopectoral approach is used to access the anterior glenohumeral joint. The deltoid is retracted laterally and the pectoralis major and conjoint tendon are retracted medially to expose the subscapularis. The subscapularis tendon can be split horizontally in the lower third or transected vertically at the insertion onto the lesser tuberosity laterally. A horizontal split is thought to minimize risk of postoperative shortening of the subscapularis and consequent loss of external rotation compared to vertical transection.60 The subscapularis is then dissected off the capsule and retracted to expose the anterior glenohumeral capsule. The capsule is incised and the glenoid labrum is carefully inspected. If a displaced labral tear is present, it can be anatomically repaired to the glenoid using nonabsorbable suture through drill holes or suture anchors. Multiple variations of the capsular shift technique have been proposed, including T-shaped capsulotomies based laterally61 or medially49 and linear capsulotomies fashioned horizontally62 or vertically.63 In 1980, Neer and Foster61 were the first to describe the open anteroinferior capsular shift with a laterally-based T-shaped capsulotomy between the MGHL and AIGHL. With the arm held in 45 degrees of abduction and 45  degrees of external rotation, the inferior capsular flap is shifted superolaterally and the superior flap is reinforced over the inferior flap. In 1991, Altchek et al modified the T-plasty to be based medially at the glenoid rather than laterally at the humerus, to facilitate concomitant Bankart repair.49 Biomechanical comparisons of the dif ferent shift

techniques have shown that the laterally based capsular shift results in the greatest reduction of capsular volume and demonstrated less limitation of shoulder external rotation compared to medially based capsular shift.54,64

Open Posterior Capsular Shift The Rockwood approach to the posterior glenohumeral joint is used.65 The posterior deltoid is split along the posterolateral raphe down to the level of the teres minor. Further dissection distally is avoided to prevent injury to the axillary nerve inferiorly. If necessary, the deltoid can be partially detached from the scapular spine for improved visualization and repaired at the end of the case. The interner vous plane between the infraspinatus (suprascapular nerve) and teres minor (axillary nerve) is developed and retracted to expose the posterior glenohumeral capsule. A laterally based T-shaped capsulotomy is made and the posterior glenoid labrum is inspected. If a displaced labral tear is present, it can be anatomically repaired to the glenoid using nonabsorbable suture through drill holes or suture anchors. With the arm held in 10 to 15 degrees of abduction, 5 to 10 degrees of external rotation, and neutral flexion-extension, the superior flap is shifted inferiorly and attached laterally to the humerus. The inferior flap is then shifted superiorly to obliterate the inferior pouch and reinforce the repair.66

Arthroscopic Capsular Plication Arthroscopic capsular reconstruction can be accomplished using a variety of fixation techniques, including suture-only plication, suture anchor plication, or a combination of suture anchor plication with additional free plication sutures (Figure  24-3). Biomechanical analysis has shown suture-only capsule-to-labrum fixation has an ultimate load to failure similar to that of suture anchor capsule-to-labrum fixation.67 Suture anchor plication is most often used in the presence of a detached labral tear, deficient labrum, or significant capsular laxity. With the exception of accessory portal placement, the operative technique for anterior68 and posterior69,70 capsulolabral reconstruction is similar and is summarized as follows.

276

Chapter 24

The redundant capsule is gently abraded using a motorized synovial shaver or arthroscopic rasp to remove the synovial layer and help stimulate a healing response, taking care to avoid capsular penetration. After the capsule is prepared, suture-anchor plication is performed using a curved or angled suture passer. The passer device penetrates the attenuated capsule roughly 1  cm from the glenoid rim,31,71 aiming to capture approximately 20% of the capsule.68 The capsule is then advanced superiorly and medially and the suture passer re-enters the capsulolabral tissue, exiting at the glenoid rim between the annular labral fibers and the articular cartilage. A nonabsorbable suture is shuttled through the capsulolabral tissue and anchored to the glenoid using a standard arthroscopic knotless or knot-tying technique. Suture anchor plication is performed in a similar manner using either bioabsorbable or polyetheretherketone anchors placed at the glenoid margin. In the presence of a detached labral tear, an arthroscopic soft tissue elevator is used to mobilize the torn labrum. The glenoid bed is then prepared with a combination of an arthroscopic rasp and motorized shaver to a bleeding surface. Suture anchor plication in the absence of a labral tear can be performed with or without glenoid bed preparation. Some surgeons describe elevation of the labrum and bone bed preparation similar to that of a labral repair,71 whereas others proceed with suture anchor placement at the glenoid margin without disruption of the glenoid-labral junction.68 Capsulolabral plication proceeds from inferior to superior to best facilitate visualization as the inferior capsule shifts superiorly and capsular volume is sequentially decreased. Capsular laxity is reassessed after each suture is tied and the need for additional plication is determined. Regardless of the capsulorraphy technique chosen, defining the appropriate magnitude of capsular plication is critical to the success of this procedure. Capsular volume reduction is critical for achieving glenohumeral stability and failure to address pathologic capsular redundancy has been implicated as a cause of recurrent instability.49,55 Conversely, overly aggressive capsular plications can result in loss of glenohumeral motion, specifically external rotation, which can significantly affect the ability of an overhead-throwing athlete to return to his or her prior level by affecting throwing velocity. Jones and colleagues described tightening the anteroinferior capsule until the intraoperative drive-through sign was no longer present.68 Others propose a 5- to 10-degree reduction of external rotation with the shoulder held in 90  degrees of abduction as a goal for adequate anterior stabilization.72 Ninety degrees of external rotation should still be possible to ensure enough sport-specific capsular laxity to return to normal throwing.39 Bradley et  al69 and McClincy and colleagues31 evaluated the degree of humeral head translation with intraoperative stress maneuvers to determine adequate posterior glenohumeral stability. Pathologic laxity should be eliminated and the humeral head should not be able to translate beyond the glenoid rim (grade 1+ or less).

Postoperative Management Postoperatively, the patient is placed in an abduction sling that immobilizes the shoulder in approximately 30 degrees of abduction for 4 to 6 weeks. Cryotherapy is used for pain and edema control. Active range of motion of the elbow, wrist, and digits in encouraged on the first postoperative day. The sling is discontinued at 4 to 6 weeks and gentle passive and active assisted range of motion exercises are initiated. The patient typically progresses to full active range of motion at 6 to 10 weeks postoperatively, followed by strengthening exercises of the rotator cuff, posterior deltoid, and periscapular muscles. At 4 months, all throwing athletes begin a regimented throwing program with close monitoring of their throwing speed and distance. Postoperative rehabilitation generally follows the same multiphase structured program detailed in the “Nonoperative Treatment” section.

OUTCOMES Successful results have been reported both with open and arthroscopic capsulorraphy techniques. Following open anterior capsular shift, 68% to 92% of overhead athletes were able to return to preinjury competition.49,60,73 Rubenstein et  al reported that 33 of 36 baseball players (92%) were able to return to their prior level of play after open anterior capsular shift, 20 of whom were professional players. There were no episodes of recurrent instability and at final follow-up, no patients exhibited pain or apprehension with provocative shoulder instability maneuvers.60 Though there has been a growing trend toward arthroscopic management of glenohumeral instability, outcomes after arthroscopic anterior capsular plication for microtraumatic capsular laxity in throwers remain quite limited. At the present time, Jones et al68 completed the only study documenting clinical results after arthroscopic anterior capsulolabral plication for anterior instability related to isolated capsular redundancy in overhead-throwing athletes. In their analysis, 18 of 20 athletes (90%) were able to return to overhead sports, with 17 (85%) returning at their preinjury level of play. Postoperative glenohumeral range of motion was symmetric to the contralateral uninvolved shoulder. Open posterior capsular shift for posterior glenohumeral instability has unfortunately not demonstrated the same level of clinical success as open anterior capsulorraphy. Hawkins and Janda reported that although 13 of 14 patients were satisfied postoperatively and there was no recurrence of posterior instability, 4 (29%) were disabled from activities of daily living, 6 (43%) experienced shoulder fatigue at work, and 4 (29%) were unable to return to recreational sports.74 Bigliani et al found 28 of 35 patients (80%) who underwent open posterior capsular shift for recurrent posterior glenohumeral instability reported good to excellent results. Of the 7 patients (20%) who reported unsatisfactory results, 6 had a history of prior ipsilateral surgical stabilization that failed.

Instability in the Throwing Athlete Four shoulders (11%) experienced recurrent instability. A successful outcome was achieved in 23 of the 24 shoulders (96%) without prior shoulder stabilization surgery.66 No study has specifically investigated the clinical outcomes of open posterior capsular shift in overhead-throwing athletes. Conversely, several clinical studies have reported the effectiveness of arthroscopic posterior capsular plication for posterior shoulder instability in athletes.31,69-71 Bradley et  al performed arthroscopic posterior capsulolabral plication in 200  athletes and reported that 180 (90%) were able to return to sport with 127 (64%) able to return at the same level of play. Patients demonstrated significant improvement in stability, pain, and function scores. With regards to fixation, patients who underwent suture anchor plication showed significantly greater improvement in American Shoulder and Elbow Surgeons scores (ASES) and a higher rate of return to play compared to patients with suture-only plication. Only 56 athletes (28%) in this study were throwers, including pitchers and quarterbacks.69 Radkowski and colleagues71 and McClincy et  al31 investigated the outcomes of arthroscopic posterior capsulolabral reconstruction in throwing athletes compared to nonthrowing athletes and conclude that despite equivalent clinical outcomes postoperatively, overhead throwers were significantly less likely to return to their preinjury level of play compared to nonthrowing athletes. There were no significant differences noted between the groups with regards to postoperative pain, strength, range of motion, stability, function, or ASES scores in both studies. Clinical failure was defined as postoperative subjective instability and ranged from 7%31 to 10%.71 Seventy-one percent of nonthrowing athletes were able to return to the same level of sport31,71 compared to only 55%71 to 60%31 of throwing athletes. Pitchers demonstrated the poorest return-to-play rates of all throwing athletes, with only 50% returning to their preinjury level of play, despite having clinical outcome scores equivalent to other throwers.31 Throwing athletes who underwent suture anchor plication exhibited a 10-fold increased likelihood of returning to play compared to sutureonly plication, whereas nonthrowing athletes showed no variability by fixation technique.31

performance. Examination is notable for increased glenohumeral translation over the glenoid rim with anterior/posterior drawer and load-and-shift maneuvers with concomitant reproduction of symptoms. Initial management begins with structured therapeutic rehabilitation. If surgical intervention is required, open and arthroscopic capsular plication techniques have demonstrated resolution of pain, improved stability, and return to athletic activities. Throwing athletes have demonstrated inferior rates of return to preinjury level of play after arthroscopic posterior capsulolabral plication compared to nonthrowing athletes, despite equivalent successful clinical outcome measures. Arthroscopic capsulolabral plication with suture anchor fixation, compared to suture-only fixation, has been postulated to increase the likelihood of return to full play in throwing athletes.

REFERENCES 1. 2. 3.

4.

5.

6. 7.

8. 9.

10.

CONCLUSION Glenohumeral instability in the throwing athlete results from repetitive microtrauma to the capsuloligamentous complex, particularly during the late cocking and deceleration phases of the overhead-throwing cycle. Anatomic adaptations of the glenohumeral joint and soft tissue structures are common and must be distinguished from true glenohumeral pathology. Repetitive stresses in the setting of continued high-intensity throwing may eventually exceed the tensile strength of the capsuloligamentous complex, with progressive attenuation of the static joint restraints and development of pathologic capsular laxity. Primarily complaints are activity-related shoulder pain and diminished athletic

277

11. 12.

13. 14. 15. 16.

Soslowsky LJ, Flatow EL, Bigliani LU, Mow VC. Articular geometry of the glenohumeral joint. Clin Orthop Relat Res. 1992;(285):181-190. Howell SM, Galinat BJ. The glenoid-labral socket: a constrained articular surface. Clin Orthop Relat Res. 1989;(243):122-125. Halder AM, Kuhl SG, Zobitz ME, Larson D, An KN. Effects of the glenoid labrum and glenohumeral abduction on stability of the shoulder joint through concavity-compression: an in  vitro study. J Bone Joint Surg Am. 2001;83(7):1062-1069. DePalma AF, Gallery G, Bennett GA. Variational anatomy and degenerative lesions of the shoulder joint. In Blount WP, Banks SW, eds. American Academy of Orthopaedic Surgeons: Instructional Course Lectures. Chicago, IL: American Academy of Orthopaedic Surgeons; 1949;6:255-281. O’Connell PW, Nuber GW, Mileski RA, Lautenschlager E. The contribution of the glenohumeral ligaments to anterior stability of the shoulder joint. Am J Sports Med. 1990;18(6):579-584. Levine WN, Flatow EL. The pathophysiology of shoulder instability. Am J Sports Med. 2000;28(6):910-917. Youm T, ElAttrache NS, Tibone JE, McGarry MH, Lee TQ. The effect of the long head of the biceps on glenohumeral kinematics. J Shoulder Elbow Surg. 2009;18(1):122-129. Paine R, Voight ML. The role of the scapula. Int J Sports Phys Ther. 2013;8(5):617-629. Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology. Part I: pathoanatomy and biomechanics. Arthroscopy. 2003;19(4):404-420. Seroyer ST, Nho SJ, Bach BR, Bush-Joseph CA, Nicholson GP, Romeo AA. The kinetic chain in overhand pitching: its potential role for performance enhancement and injury prevention. Sports Health. 2010;2(2):135-146. Calabrese GJ. Pitching mechanics, revisited. Int J Sports Phys Ther. 2013;8(5):652-660. Meister K. Injuries to the shoulder in the throwing athlete: Part one: biomechanics/pathophysiology/classification of injury. Am J Sports Med. 2000;28(2):265-275. Gelber JD, Soloff L, Schickendantz MS. The thrower’s shoulder. J Am Acad Orthop Surg. 2018;26(6):204-213. Edelson G. The development of humeral head retroversion. J Shoulder Elbow Surg 2000;9(4):316-318. Caine D. Physeal injuries in children’s and youth sports: reasons for concern? Br J Sports Med. 2006;40(9):749-760. Kronberg M, Broström LA, Söderlund V. Retroversion of the humeral head in the normal shoulder and its relationship to the normal range of motion. Clin Orthop Relat Res. 1990;253:113-117.

278 17.

18.

19.

20.

21.

22.

23.

24.

25.

26.

27.

28.

29.

30.

31.

32.

33.

34.

35.

Chapter 24 Levine WN, Brandon ML, Shubin Stein BE, Gardner TR, Bigliani LU, Ahmad CS. Shoulder adaptive changes in youth baseball players. J Shoulder Elbow Surg. 2006;15(5):562-566. Reagan KM, Meister K, Horodyski MB, Werner DW, Carruthers C, Wilk K. Humeral retroversion and its relationship to glenohumeral rotation in the shoulder of college baseball players. Am J Sports Med. 2002;30(3):354-360. Crockett HC, Gross LB, Wilk KE, et al. Osseous adaptation and range of motion at the glenohumeral joint in professional baseball pitchers. Am J Sports Med. 2002;30(1):20-26. Thomas SJ, Swanik CB, Kaminski TW, et  al. Humeral retroversion and its association with posterior capsule thickness in collegiate baseball players. J Shoulder Elbow Surg. 2012;21(7):910-916. Takenaga T, Sugimoto K, Goto H, et al. Posterior shoulder capsules are thicker and stiffer in the throwing shoulders of healthy college baseball players: a quantitative assessment using shear-wave ultrasound elastography. Am J Sports Med. 2015;43(12):2935-2942. doi:10.1177/0363546515608476. Thomas SJ, Swanik CB, Higginson JS, et  al. Neuromuscular and stiffness adaptations in Division I collegiate baseball players. J Electromyogr Kinesiol. 2013;23(1):102-109. Ellenbecker TS, Roetert EP, Bailie DS, Davies GJ, Brown SW. Glenohumeral joint total rotation range of motion in elite tennis players and baseball pitchers. Med Sci Sports Exerc. 2002;34(12):2052-2056. Jobe FW, Kvitne RS, Giangarra CE. Shoulder pain in the overhand or throwing athlete. The relationship of anterior instability and rotator cuff impingement. Orthop Rev. 1989;18(9):963-975. Ryu RKN, Dunbar WH, Kuhn JE, McFarland EG, Chronopoulos E, Kim TK. Comprehensive evaluation and treatment of the shoulder in the throwing athlete. Arthroscopy. 2002;18:70-89. Mihata T, McGarry MH, Neo M, Ohue M, Lee TQ. Effect of anterior capsular laxity on horizontal abduction and forceful internal impingement in a cadaveric model of the throwing shoulder. Am J Sports Med. 2015;43(7):1758-1763. Gulotta LV, Lobatto D, Delos D, Coleman SH, Altchek DW. Anterior shoulder capsular tears in professional baseball players. J Shoulder Elbow Surg. 2014;23(8):e173-e178. Chang EY, Hoenecke HR, Fronek J, Huang BK, Chung CB. Humeral avulsions of the inferior glenohumeral ligament complex involving the axillary pouch in professional baseball players. Skeletal Radiol. 2014;43(1):35-41. Inui H, Sugamoto K, Miyamoto T, et  al. Glenoid shape in atraumatic posterior instability of the shoulder. Clin Orthop Relat Res. 2002;403:87-92. Frank RM, Romeo AA, Provencher MT. Posterior glenohumeral instability: evidence-based treatment. J Am Acad Orthop Surg. 2017;25(9):610-623. McClincy MP, Arner JW, Bradley JP. Posterior shoulder instability in throwing athletes: a case-matched comparison of throwers and nonthrowers. Arthroscopy. 2015;31:1041-1051. Kibler WB, Sciascia A, Thomas SJ. Glenohumeral internal rotation deficit: pathogenesis and response to acute throwing. Sports Med Arthrosc. 2012;20(1):34-38. Hibberd EE, Oyama S, Myers JB. Increase in humeral retrotorsion accounts for age-related increase in glenohumeral internal rotation deficit in youth and adolescent baseball players. Am J Sports Med. 2014;42(4):851-858. Noonan TJ, Shanley E, Bailey LB, et  al. Professional pitchers with glenohumeral internal rotation deficit (GIRD) display greater humeral retrotorsion than pitchers without GIRD. Am J Sports Med. 2015;43(6):1448-1454. Braun S, Kokmeyer D, Millett PJ. Shoulder injuries in the throwing athlete. J Bone Joint Surg. 2009;91(4):966-978.

36.

37.

38.

39. 40. 41. 42. 43. 44. 45.

46.

47.

48.

49.

50.

51.

52.

53.

54.

55. 56.

Warner JJ, Micheli LJ, Arslanian LE, Kennedy J, Kennedy  R. Scapulothoracic motion in normal shoulders and shoulders with glenohumeral instability and impingement syndrome. A study using Moiré topographic analysis. Clin Orthop Relat Res. 1992;285:191-199. Matias R, Pascoal AG. The unstable shoulder in arm elevation: a three-dimensional and electromyographic study in subjects with glenohumeral instability. Clin Biomech. 2006;21:S52-S58. McMahon PJ, Jobe FW, Pink MM, Brault JR, Perry J. Comparative electromyographic analysis of shoulder muscles during planar motions: anterior glenohumeral instability versus normal. J Shoulder Elbow Surg. 1996;5:118-123. Altchek DW, Dines DM. Shoulder injuries in the throwing athlete. J Am Acad Orthop Surg. 1995;3(3):159-165. King JW, Brelsford HJ, Tullos HS. Analysis of the pitching arm of the professional baseball pitcher. Clin Orthop. 1969;67:116-123. Pollock RG, Bigliani LU. Glenohumeral instability: evaluation and treatment. J Am Acad Orthop Surg. 1993;1(1):24-32. Kibler WB. The role of the scapula in athletic shoulder function. Am J Sports Med. 1998;26:325-337. Speer KP, Hannafin JA, Altchek DW, Warren RF. An evaluation of the shoulder relocation test. Am J Sports Med. 1994;22(2):177-183. Gross ML, DiStefano MC. Anterior release test. A new test for occult shoulder instability. Clin Orthop Relat Res. 1997;339:105-108. McFarland EG, Kim TK, Park HB, Neira CA, Gutierrez MI. The effect of variation in definition on the diagnosis of multidirectional instability of the shoulder. J Bone Joint Surg Am. 2003;85:2138-2144. Hippensteel KJ, Brophy R, Smith MV, Wright RW. Comprehensive review of provocative and instability physical examination tests of the shoulder. J Am Acad Orthop Surg. 2019;27(11):395-404. doi:10.5435/ JAAOS-D-17-00637. Kim SH, Park JS, Jeong WK, Shin SK. The Kim test: a novel test for posteroinferior labral lesion of the shoulder—a comparison to the jerk test. Am J Sports Med. 2005;33:1188-1192. DeFroda SF, Goyal D, Patel N, Gupta N, Mulcahey MK. Shoulder instability in the overhead athlete. Curr Sports Med Rep. 2018;17(9):308-314. Altchek DW, Warren RF, Skyhar M, Ortiz G. T-plasty modification of the Bankart procedure for multidirectional instability of the anterior and inferior types. J Bone Joint Surg Am. 1991;73(1):105-112. Gagey OJ, Gagey N. The hyperabduction test: an assessment of the laxity of the inferior glenohumeral ligament. J Bone Joint Surg Br. 2001;83(1):69-74. Ajuied A, McGarvey CP, Harb Z, Smith CC, Houghton RP, Corbett SA. Diagnosis of glenoid labral tears using 3-tesla MRI vs. 3-tesla MRA: a systematic review and meta-analysis. Arch Orthop Trauma Surg. 2018;138(5):699-709. Wilk KE, Meister K, Andrews  JR. Current concepts in the rehabilitation of the overhead throwing athlete. Am J Sports Med. 2002;30(1):136-151. Carter AB, Kaminski TW, Douex AT Jr, Knight CA, Richards JG. Effects of high volume upper extremity plyometric training on throwing velocity and functional strength ratios of the shoulder rotators in collegiate baseball players. J Strength Cond Res. 2007;21:208-215. Cohen SB, Wiley W, Goradia VK, Pearson S, Miller MD. Anterior capsulorrhaphy: an in vitro comparison of volume reduction— arthroscopic plication versus open capsular shift. Arthroscopy. 2005;21(6):659-664. Lazarus MD, Harryman DT II. Complications of open anterior stabilization of the shoulder. J Am Acad Orthop Surg. 2000;8:122-132. Alberta FG, ElAttrache NS, Mihata T, McGarry MH, Tibone JE, Lee TQ. Arthroscopic anteroinferior suture plication resulting in decreased glenohumeral translation and external rotation: study of a cadaver model. J Bone Joint Surg Am. 2006;88(1):179-187.

Instability in the Throwing Athlete 57. 58.

59.

60.

61.

62.

63.

64.

65.

Gaskill TR, Millett PJ. Management of multidirectional instability of the shoulder. J Am Acad Orthop Surg. 2011;19(12):758-767. D’Alessandro DF, Bradley JP, Fleischli JE, Connor PM. Prospective evaluation of thermal capsulorrhaphy for shoulder instability: indications and results, two to five year follow-up. Am J Sports Med. 2004;32:21-33. McFarland EG, Neira CA, Gutierrez MI, Cosgarea AJ, Magee  M. Clinical significance of the arthroscopic drive-through sign in shoulder surgery. Arthroscopy. 2001;17(1):38-43. Rubenstein DL, Jobe FW, Glousman RE, Kvitne RS, Pink M, Giangarra CE. Anterior capsulolabral reconstruction of the shoulder in athletes. J Shoulder Elbow Surg. 1992;1(5):229-237. Neer CS II, Foster CR. Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. J Bone Joint Surg Am. 1980;62:897-908. Ahmad CS, Freehill MQ, Blaine TA, Levine WN, Bigliani LU. Anteromedial capsular redundancy and labral deficiency in shoulder instability. Am J Sports Med. 2003;31:247-252. Wirth MA, Blatter G, Rockwood CA  Jr. The capsular imbrication procedure of recurrent anterior instability of the shoulder. J Bone Joint Surg Am. 1996;78:246-259. Deutsch A, Barber JE, Davy DT, Victoroff BN. Anterior-inferior capsular shift of the shoulder: a biomechanical comparison of glenoidbased versus humeral-based shift strategies. J  Shoulder Elbow Surg. 2001;10(4):340-352. Wirth MA, Butters KP, Rockwood JC. The posterior deltoid-splitting approach to the shoulder. Clin Orthop Relat Res. 1993;(296):92-98.

66.

67.

68.

69.

70.

71.

72.

73.

74.

279

Bigliani LU, Pollock RG, McIlveen SJ, Endrizzi DP, Flatow EL. Shift of the posteroinferior aspect of the capsule for recurrent posterior glenohumeral instability. J Bone Joint Surg. 1995;77(7):1011-1020. Provencher MT, Verma N, Obopilwe E, et al. A biomechanical analysis of capsular plication versus anchor repair of the shoulder: can the labrum be used as a suture anchor? Arthroscopy. 2008;24(2):210-216. Jones KJ, Kahlenberg CA, Dodson CC, Nam D, Williams RJ, Altchek DW. Arthroscopic capsular plication for microtraumatic anterior shoulder instability in overhead athletes. Am J Sports Med. 2012;40(9):2009-2014. Bradley JP, McClincy MP, Arner JW, Tejwani SG. Arthroscopic capsulolabral reconstruction for posterior instability of the shoulder: a prospective study of 200 shoulders. Am J Sports Med. 2013;41(9):2005-2014. Savoie FH III, Holt MS, Field LD, Ramsey  JR. Arthroscopic management of posterior instability: evolution of technique and results. Arthroscopy. 2008;24:389-396. Radkowski CA, Chhabra A, Baker CL III, Tejwani SG, Bradley JP. Arthroscopic capsulolabral repair for posterior shoulder instability in throwing athletes compared with nonthrowing athletes. Am J Sports Med. 2008;36(4):693-699. Levitz CL, Dugas J, Andrews  JR. The use of arthroscopic thermal capsulorrhaphy to treat internal impingement in baseball players. Arthroscopy. 2001;17:573-577. Jobe FW, Giangarra CE, Kvitne RS, Glousman RE. Anterior capsulolabral reconstruction of the shoulder in athletes in overhand sports. Am J Sports Med. 1991;19(5):428-434. Hawkins RJ, Janda DH. Posterior instability of the glenohumeral joint. A technique of repair. J Shoulder Elbow Surg. 1996;5:275-278.

25 Instability in the Pediatric and Adolescent Athlete Joseph W. Galvin, DO, FAAOS and Xinning Li, MD

Instability in the pediatric and adolescent athlete is predominantly anterior in direction and secondary to trauma. Posterior and multidirectional instability (MDI) are less commonly involved in this population. With an increase in adolescent participation in contact sports, there has been a resultant rise in pediatric sports injuries.1 Also, single-sport focus and year-round sport participation have likely contributed to the high rate of anterior shoulder instability.2 Studies have shown high recurrence rates following nonoperative treatment of anterior shoulder instability in adolescent skeletally mature athletes.3 Therefore, surgical treatment is indicated in these adolescent athletes to stabilize the shoulder and prevent further damage both to the soft tissue and cartilage due to high rates of recurrent instability. However, in the skeletally immature athlete, those typically younger than 13 years, recent studies have shown lower rates of recurrent instability; therefore, nonoperative treatment is the most appropriate initial management in this population.2,4 Leroux et al2 examined the epidemiology of anterior shoulder instability and found that the rate of closed reduction (primary or recurrent) for the 10- to 13-year age group is considerably lower than for 14- to 16-year-old patients, and therefore these skeletally immature individual should be treated conservatively. These results are similar to the findings of Li et  al4 after performing a comprehensive review of the literature on this topic. Furthermore, posterior instability and MDI are becoming increasingly recognized in adolescent populations. The initial treatment for both of these conditions is nonoperative with dedicated physical therapy. In this chapter we will review epidemiology, natural history of shoulder instability in pediatric and adolescent patients, and indications for nonsurgical and surgical management.

Additionally, we will review the special considerations both for arthroscopic and open stabilization of the pediatric and adolescent athlete, surgical techniques, rehabilitation, and outcomes.

EPIDEMIOLOGY There is a high incidence of anterior shoulder instability among young men and boys in the United States. Zacchilli and Owens5 queried the National Electronic Injury Surveillance System, which is composed of a probability sample of all injuries presenting to US emergency departments from 2002 to 2006. A total of 8940 dislocations were identified over this time period with an overall incidence rate of 23.9 dislocations per 100,000 person-years. The maximum incidence rate occurred in individuals between ages 20 and 29 years, with age and male sex identified as risk factors for a dislocation event. Leroux et  al2 found that the person-time incidence rate of anterior shoulder instability in 10- to 16-year-olds in Canada between April  2002 and September  2010 was 20.1 dislocations per 100,000 person-years, with the highest incidence rate reported in male patients age 16 years (164.4 dislocations per 100,000 person-years) and lowest incidence rate in female patients age 10 years (1.3 dislocations per 100,000 person-years). The differences in the person-time incidence rates reported are likely secondary to the increase in youth sports participation, particularly contact and collision sports among adolescent male patients.6,7 Furthermore, only 2% of dislocations occurred in patients younger than 10  years.5,8 Postacchini and colleagues9 also found the incidence of shoulder dislocations in patients 13  years or younger to be very rare, with only 3  patients (0.38%) out of 780 patients

- 281 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 281-289). © 2021 SLACK Incorporated.

282

Chapter 25

with anterior shoulder instability treated in their institution in a 4-year time period.

NATURAL HISTORY The natural history of anterior shoulder instability and the risk of recurrence are highly variable and are based on age and skeletal maturity. Based on the available literature, skeletally immature individuals, typically those younger than 13  years, have a lower recurrence rate than skeletally mature (age 14 years and older) adolescents. Cordischi et al10 prospectively followed 14 skeletally immature patients (age 10.9 to 13.1 years) who sustained an initial traumatic anterior glenohumeral dislocation and were treated nonoperatively. At final follow-up of mean 5.6  years, 3 (21%) patients sustained a recurrent shoulder dislocation that required surgical stabilization. Similarly, Lampert et  al11 conducted a retrospective review of 54 patients (age range, 4 to 18 years) who sustained an anterior shoulder dislocation. Patients younger than 14  years (mean, 11.2  years) had no recurrent instability, whereas those 14  years or older (mean, 15.8  years) had a 69% recurrent dislocation rate. In contrast, other studies have shown higher recurrence rates in skeletally immature patients, ranging from 53% to 100%.12,13 Deitch et  al14 performed a retrospective cohort study of 32 patients, age 11 to 18  years, following a traumatic anterior shoulder dislocation. Recurrent instability occurred in 24 of 32  patients (75%). In skeletally immature patients the recurrence rate was 53%, compared to 80% in skeletally mature children.13 Furthermore, in the largest population-based epidemiologic study of anterior shoulder dislocation in patients age 10 to 16 years, Leroux et al2 found a correlation between age and recurrent dislocation requiring a second closed reduction. Of the 2066 patients who required primary closed reduction, the highest rate of recurrence was seen among patients age 16 years (42.3%) and the lowest in patients age 10 to 12 years (17.4%). Postacchini and colleagues9 also reported a similar recurrence (92%) and a mean number of 7 redislocations in patients age 14 to 17 years compared to 33% recurrence with only 1  redislocation in patients age 13 or younger. Despite variable results in the literature regarding recurrent instability, initial management of a first-time dislocation in a skeletally immature patient should be nonsurgical.8 Management of anterior shoulder instability in adolescents with closed physes is entirely dif ferent. The published recurrence rate is consistently much higher in this population, which may be related to increased contact or collision sports participation in this age group, and some authors have hypothesized that the differences in anatomy may play a role in the recurrence rate with less elasticity of the anterior inferior glenohumeral ligament in adult patients than in the skeletally immature patient. A recent prospective study evaluated the natural history of nonoperatively treated anterior shoulder dislocations in adolescents with closed physes at a single institution.3 The authors prospectively followed 133 adolescent patients (mean age, 16.3  years; range, 13 to

18) after a first-time anterior glenohumeral dislocation. The majority of patients (102, 76.7%) had a recurrent dislocation. The incidence of recurrent shoulder instability was 59%, 38%, 21%, and 7% at 1-, 2-, 5-, and 10-year follow-up, respectively. This mirrors similar redislocation incidences seen in long-term natural history studies in the adult patient population.15,16

CLINICAL AND RADIOGRAPHIC EVALUATION It is essential to separate shoulder instability in the adolescent patient population as either atraumatic or traumatic in etiology. Patients with atraumatic onset of shoulder instability will typically present with multidirectional symptoms that will need to be evaluated for ligamentous laxity (Beighton scores), scapular thoracic kinematics, and possible connective tissue disease. Patients with traumatic locked shoulder dislocation often present with an obvious deformity, pain, and limitation in shoulder range of motion. Physical examination including range of motion testing, signs of ligamentous laxity, apprehension/relocation, load and shift, posterior jerk test, and careful neurovascular examination are essential in the initial evaluation of these adolescent athletes. Plain radiographs are the initial imaging obtained if a shoulder dislocation is suspected. Orthogonal views are paramount and typically include anteroposterior view, axillary view, and occasionally scapular-Y view. The axillary view is essential following shoulder reduction to confirm that the humeral head is centered on the glenoid. Although magnetic resonance imaging (MRI) scans are typically not necessary or practical in the acute setting, MRI does provide specific details regarding concomitant soft-tissue injuries following a shoulder dislocation. The status of the labral tissue and presence of an injury (ie, bony or soft-tissue Bankart lesion), as well as whether the patient has an open or closed physis, may affect treatment decision making following a shoulder dislocation (Figures  25-1A and 25-1B). Additionally, in adolescent athletes with recurrent instability and attritional glenoid bone loss, a computed tomography (CT) scan is essential to evaluate the amount of bone loss that may affect surgical indications. Please see the chapter on physical examination and radiographic evaluation for more in-depth details related to each clinical examination finding as well as the key radiographic images for adolescent athletes who present with shoulder instability.

NONSURGICAL TREATMENT The initial management of shoulder instability in skeletally immature individuals is nonsurgical, as discussed earlier. In the adolescent skeletally mature patient population with a first-time dislocation, the decision on whether to undergo surgery should be established through a shared decisionmaking process (Figure 25-2). Regardless, most patients are

Instability in the Pediatric and Adolescent Athlete

283

Figure 25-1. (A) Anteroposterior radiographic view of the right shoulder shows open physis (star) and bone loss in the anterior inferior glenoid after shoulder dislocation in a skeletally immature patient. (B) Magnetic resonance image in the abduction external rotation view shows anterior inferior labral tear (Bankart lesion, yellow arrow) in a skeletally immature patient with open physis (star). (Reprinted with permission from Brett D. Owens, MD.)

Figure 25-2. Algorithm for the management of shoulder instability in the adolescent and skeletally immature patient population. (Adapted from Li X, Ma R, Nielsen NM, Gulotta LV, Dines JS, Owens BD. Management of shoulder instability in the skeletally immature patient. J Am Acad Orthop Surg. 2013;21[9]:529-537.)

typically treated with a brief period (less than 3 weeks) of immobilization for pain reduction and comfort. However, there is a paucity of evidence to guide decision making on the need for post-reduction immobilization following a first-time anterior shoulder dislocation. Henry and Genung17 studied 121 first-time anterior shoulder dislocators and found that the rate of recurrent instability for those immobilized in a sling post-reduction was 90% vs 85% among those who were not immobilized. Additionally, no studies have found that immobilization for greater than 1 week has any effect on recurrence rate.18 Post-reduction external rotation (ER) immobilization acutely after injury has also been a topic of controversy in the nonoperative management of first-time anterior shoulder dislocators. Initial imaging and cadaveric studies demonstrated

anatomic reduction of the anterior inferior labral tear to the glenoid in the externally rotated (ER) position by the muscle belly of the subscapularis, as opposed to the internal rotation (IR) position. An early preliminary study in 2003 by Itoi et al19 demonstrated a lower recurrence rate in patients treated with ER immobilization (ER: 0% vs IR: 30%) at a mean follow up of 1.3  years. However, more recent literature has not shown a significant difference in outcomes when comparing ER to IR immobilization. Paterson and colleagues18 conducted a systematic review and meta-analysis and found no statistically significant difference in recurrent instability between ER and IR immobilization. Similarly, Whelan et al20 performed a meta-analysis of 6 randomized controlled trials and also found no significant difference between arm position (ER vs IR) for post-reduction immobilization. Therefore,

284

Chapter 25

the decision for ER immobilization must be made based on a shared decision-making model with patients and their parents, given the increased cost of an ER immobilizer and the potential difficulty with patient compliance in the adolescent patient population.

ROLE OF PHYSICAL THERAPY In skeletally immature patients, initial treatment should be nonoperative with a physical therapy program. Physical therapy should focus on strengthening and improved proprioceptive control of the dynamic stabilizers of the shoulder, including the rotator cuff and scapulothoracic stabilizers. There is limited evidence to support the role for physical therapy in skeletally immature or mature adolescents. In the college athlete population, Dickens et  al21 prospectively followed West Point cadets (mean age, 20.7; SD 1.63  years) who were in-season athletes (skeletally mature) and treated with an accelerated rehabilitation protocol after a firsttime shoulder dislocation. In their protocol, no patient was immobilized after the injury and a supervised physical therapy protocol was started the day after the injury. This consisted of regaining shoulder range of motion and rotator cuff strengthening with light weight. Once symmetric range of motion was achieved, then periscapular and resistance exercises were initiated. If the player was asymptomatic with all rehabilitative exercises, had symmetric and full strength, was able to perform sport-specific exercises, and had no pain or limitations, he or she was cleared for sports participation. Although 73% of patients were able to return to sport during the season, only 27% were able to finish the season without recurrent instability. Gaballah et  al22 evaluated a 6-week physical therapy rehabilitation protocol consisting of elastic bands and resistive exercise to improve joint strength and shoulder range of motion in 12 patients with acute primary anterior shoulder instability. They found there was no difference in range of motion and strength between the injured side compared to the uninjured contralateral side at final follow-up. However, compliance remains a challenge when recommending an extensive physical therapy protocol and exercise program in this patient population. There is a high prevalence of low adherence to treatment during the adolescent years, which will increase morbidity and contribute to poorer outcomes with nonoperative management. There are many dif ferent factors that affect adherence, including developmental stage, emotional state, socioeconomic factors, and family dynamics. It is impor tant to evaluate for adherence to physical therapy on a regular basis in this patient population.23

SURGICAL MANAGEMENT Numerous studies have evaluated the outcome both of skeletally immature and mature adolescents following surgical treatment. This is a distinctively dif ferent population

from the older young adult population (age 20 to 35 years). A number of studies have established the results of operative vs nonoperative treatment in this older population.24-27 The results have demonstrated a significant benefit to arthroscopic stabilization in reducing the risk of recurrent instability as compared to nonoperative treatment. We have summarized the results of studies examining the outcomes and recurrence rates of operative vs nonoperative treatment of anterior shoulder instability in adolescents (Table 25-1) as well as proposed an algorithm both for conservative and surgical management in this patient population (see Figure 25-2). We included studies comparing both nonoperative treatment to arthroscopic and open stabilization procedures for anterior shoulder instability. Gigis et al28 performed a prospective cohort study of adolescent patients (ages 15 to 18 years) after a first-time anterior glenohumeral dislocation. A conservative treatment group (27 patients) and an arthroscopic stabilization group (38 patients) were identified and followed for 36 months. The recurrence rate for the conservative treatment group was 19 of 27 (70.3%), and 5 of 38 (13.1%) for the operative group. The authors concluded that nonoperative treatment of adolescent patients (age 15 to 18  years) resulted in an unacceptably high rate of recurrent instability compared to arthroscopic Bankart repair. Similarly, Jones and colleagues29 performed a retrospective review of adolescent patients (mean age, 15.4  years; range, 11 to 18 years) who underwent arthroscopic Bankart repair, with a mean follow-up of 25.2 months. The authors had an overall 15.6% recurrent instability rate. Furthermore, there is a paucity of literature examining the role of the Latarjet procedure in the management of recurrent anterior shoulder instability in a pediatric population. Khan et al30 conducted a retrospective cohort study of 49 patients who underwent treatment for recurrent anterior shoulder instability at a mean age of 15.9 years (range, 13 to 16 years). All patients had open physes on radiographs at the time of injury. Approximately half the cohort underwent nonoperative treatment and the other half underwent an open Latarjet procedure. The recurrence rate for the nonoperative and operative group was 52% and 7%, respectively. This study further confirmed that with short- to mid-term follow-up, operative treatment of anterior shoulder instability in the adolescent patient results in lower recurrence rates as compared to nonoperative treatment. Additionally, Blackman et al31 reported the results of revision anterior shoulder stabilization surgery in adolescent athletes (ages 14 to 18 years) in a retrospective study. Of the 90 patients undergoing primary shoulder stabilization, 15 (17%) failed and underwent revision stabilization surgery. With an average follow-up of 5.5  years, 5 revision patients (33%) had recurrent instability requiring another revision surgery. Although the authors were unable to identify specific risk factors for failure after revision surgery, they concluded that adolescent patients who fail primary stabilization also have a high failure rate following revision surgery with mid-term follow-up.

Instability in the Pediatric and Adolescent Athlete

285

Table 25-1. Nonoperative and Operative Outcomes for Shoulder Instability in the Adolescent Athlete STUDY Wagner et al13

NO. OF PATIENTS 9 (10 shoulders)

MEAN AGE, Y 12 to 16

TREATMENT Nonoperative

11

< 14

Nonoperative

Postacchini et al

28

12 to 17

Nonoperative

Lampert et al11

54

14.5

Nonoperative (40), operative (14)

Deitch et al14

32

11 to 18

Nonoperative

Roberts et al3

133

16.3 (13 to 18)

Nonoperative

Cordischi et al10

14

10.9 to 13.1

Nonoperative (sling, no weight-bearing 4 weeks)

Gigis et al28

65 (38 operative; 27 conservative)

16.7 (15 to 18)

Nonoperative: immobili- Nonoperative, 70.3% recurrence; zation and rehabilitation; Operative, 13.1% recurrence operative: arthroscopic stabilization

Khan et al30

49/80 (63.8% follow-up), all skeletally immature

15.9 (13 to 16)

Nonoperative vs Latarjet procedure

Nonoperative, 52% recurrence rate. Operative, 7% recurrence rate. Nonoperative 92% operative returned to same level of activity vs 52% for nonoperative

Jones et al29

30

15.4 (11 to 18)

Operative: arthroscopic Bankart repair

15.6% recurrence rate

Blackman et al31

90

16.6 (14 to 18)

Operative: arthroscopic Bankart repair (72), open Bankart repair (18)

17% recurrence rate

Marans et al12 9

POSTERIOR INSTABILITY Although less common than anterior shoulder instability, posterior shoulder instability is becoming increasingly recognized in young athletic populations.32 Many times, symptomatic posterior shoulder instability is more difficult to diagnose because patients present with vague shoulder pain and less frequently describe symptoms consistent with instability. Furthermore, a posterior labral tear may not be clearly evident on advanced imaging studies. Radiographic variables such as increased glenoid retroversion, glenoid dysplasia, and increased posterior capsular area have been shown to be significantly associated with posterior shoulder instability and can assist in diagnosis.33 Recently, McClincy et  al34 performed a retrospective review of prospectively collected

RECURRENCE RATE/OUTCOME 67% recurrence rate (age ≤ 13 y) 8 of 10 shoulders (80%) recurrence rate 100% recurrence rate 33% recurrence rate (1 of 3), (age ≤ 13 y) 92% recurrence rate (age 14 to 17 y) Nonoperative: 0% recurrence rate (age < 14 y); 96.4% recurrence rate (age ≥ 14 y) 24 of 32 (75%) recurrence rate. This led 16 patients to undergo operative stabilization 102 patients (76.7%) had a recurrent dislocation. Incidence of recurrent shoulder instability was 59, 38, 21, and 7% at 1-, 2-, 5-, and 10-year follow-up 21% recurrence rate

data and identified 68 athletes (82 shoulders) with isolated unidirectional posterior shoulder instability who underwent arthroscopic posterior capsulolabral reconstruction with a mean follow-up of 36 months. The average age of the cohort was 17.2  years (range, 14 to 19  years). The mean American Shoulder and Elbow Surgeons (ASES) score significantly improved from 48.6 to 85.7 (P < .001) after surgery. Overall, 89% of athletes were able to return to competition, with 71% returning to their preinjury level of play. Additionally, 8.5% of adolescent patients had either pain or instability and underwent a revision surgery. The only other study examining the outcomes of arthroscopic posterior labral repair in adolescents is by Wooten et al,35 who retrospectively reviewed 22 patients (25  shoulders) who underwent arthroscopic posterior capsulolabral reconstruction for unidirectional

286

Chapter 25

recurrent posterior shoulder instability. The mean age of patients was 17 years and the mean follow-up was 63 months. Twenty-three of 25 shoulders (92%) were stable at final follow-up and 67% of patients returned to sport. Two shoulders continued to have episodes of traumatic recurrent posterior shoulder instability. Male patients, contact athletes, and those with a traumatic etiology had significantly improved postoperative ASES scores.

MULTIDIRECTIONAL INSTABILITY Multidirectional shoulder instability is defined as shoulder instability in 2 or more directions. This occurs in patients with multidirectional hyperlaxity. Typically, this is atraumatic in nature, bilateral, and seen in young athletic patient populations. The hallmark of treatment for this condition is nonsurgical, with physical therapy and activity modification, to focus on strengthening and improving proprioception of the dynamic stabilizers of the shoulder, rotator cuff, and scapulothoracic musculature. Clinicians must also conduct a thorough history and physical exam and to assess for generalized joint hypermobility and laxity and also consider the presence of connective tissue disorders such as Ehlers-Danlos syndrome. The Beighton-Horan criteria are most commonly used for this assessment: small finger dorsiflexion of the metacarpophalangeal joint to greater than 90 degrees (one point for each side (left/right), oppose thumb to the volar aspect of the forearm (one point for each side), hyperextend elbow at least 10 degrees (one point for each side), hyperextend knee at least 10  degrees (one point for each side), and place both hands flat on the floor with knees extended (one point). A score of greater than or equal to 4 indicates generalized hypermobility.36 Cameron et  al37 performed a crosssectional cohort study examining 1311 cadets entering the United States Military Academy at West Point. The authors found 11 cadets (1.5%) had generalized hypermobility as determined by the Beighton score (≥ 4). Logistic regression demonstrated a significant association between generalized hypermobility and a history of glenohumeral instability. The natural history of nonoperative treatment for shoulder MDI has been well established. Misamore et al38 performed a prospective longitudinal study to determine the long-term outcomes of MDI treated with rehabilitation. Fifty-seven patients were evaluated after undergoing nonoperative treatment of shoulder MDI, and the mean follow-up was 8 years. During this follow-up period, 36 patients (mean age, 16 years) completed rehabilitation and 21 patients underwent surgery for MDI. Of the 36 who underwent nonoperative treatment, 23 (63.8%) patients rated their shoulder as good or excellent for pain, and 17 (47%) were good or excellent with regards to instability. According to the modified Rowe grading scale, 5 of 36 patients (14%) had excellent results, and 12 had good results (33%). The remaining 19 patients (53%) were rated as having poor results. Only 8 patients (22%) reported their shoulders were free of all pain and instability. The authors concluded that young patients with MDI in this small cohort

had a relatively poor response to nonsurgical management in the long term. Despite evidence indicating poor long-term results in young adolescent patients with MDI treated nonoperatively, the initial management should be nonsurgical with dedicated physical therapy for at least 6 months. Operative treatment of MDI is indicated in adolescents after failure of at least 6 months of physical therapy. Additionally, a key component of nonoperative treatment is activity modification and cessation of sporting activity because many patients will continue to play through injuries and exacerbate the problem. Although there are no exclusively pediatric cohorts from which to draw surgical outcomes, there are a number of studies evaluating surgical treatment with open and arthroscopic management of MDI in young athletic populations. Neer and Foster39 were the first to describe MDI and in their preliminary report they evaluated 36 patients (40 shoulders) following an open inferior capsular shift for the treatment of this condition. Thirtynine of 40 shoulders (98%) had no recurrent instability, and 17 shoulders were followed for more than 2  years. More recently, authors have reported satisfactory outcomes with arthroscopic treatment of MDI, which is accomplished with anterior, inferior, and posterior capsular shift using suture anchors. Kim et  al40 analyzed the results of arthroscopic treatment of MDI in 31 patients. At a mean follow-up of 51 months, 30 patients (97%) had a stable shoulder. Additionally, Baker and colleagues41 performed a retrospective analysis of 40 patients (43 shoulders; mean age, 19.1  years) with MDI who were treated arthroscopically and were evaluated at a mean of 33.5 months postoperatively. The mean ASES score postoperatively was 91.4 of 100. The mean postoperative Western Ontario Shoulder Instability score was 91.1 of 100. Ninety-one percent of patients had full or satisfactory range of motion, 98% had normal or slightly decreased strength, and 86% were able to return to their sport with little or no limitation. Therefore, if young patients continue to have symptomatic instability after an extended course of dedicated activity modification and physical therapy, operative treatment with open or arthroscopic capsular shift is effective in restoring stability and allowing for return to activity.

SURGICAL TECHNIQUE The principles of operative treatment for pediatric instability are similar to that of adults. For symptomatic anterior shoulder instability, repair of the pathologic anterior inferior labral and/or capsular injury (Bankart lesion) is paramount to restoring stability (Figures 25-3A to 25-3D). Care must be taken in preoperative imaging and at the time of arthroscopy to evaluate not only for a Bankart lesion, but the rare intracapsular rupture and humeral avulsion of the glenohumeral ligament in addition to the status of the proximal humeral physis (open or closed). Patients who present with posterior labral tears on MRI and with persistent pain despite a course of therapy will benefit from arthroscopic posterior labral repair (Figures  25-4A to 25-4D). Additionally,

Instability in the Pediatric and Adolescent Athlete

Figure 25-3. A 16-year- old male lacrosse player with recurrent anterior shoulder instability. (A) Anterior inferior labral tear is seen arthroscopically (arrows). (B) Arthroscopic radiofrequency device (CoVator) is used to release the anterior inferior labrum so the muscle belly of the subscapularis is visualized (star). (C) A metal labral passer is used to shut tle the labral tape (Arthrex) across the tear. (D) Final repair with 3 labral tapes and knotless fixation.

adolescent patients with an unreconstructable bony Bankart or attritional anterior inferior bone loss are indicated for the Latarjet procedure (Figures 25-5A to 25-5D). There is limited evidence on the outcomes of Latarjet in adolescent patients. Khan et al30 conducted a retrospective review of 26 patients (mean age, 15.9 years; SD 0.7) who were 16 years or younger, had open proximal humeral physes, and who underwent an open Latarjet procedure. All patients had at least 3 proven glenohumeral dislocations and failed a course of physiotherapy. The authors found that 92% of post-surgical patients returned to preinjury activity level, and they concluded that younger age and skeletal immaturity (open physis) are not contraindications to a Latarjet procedure. Controversy does exist on the indications for Latarjet in these skeletally immature and mature adolescents, and future large prospective studies are needed to determine outcome and complications. Furthermore, there is no minimal age limit on surgical indications, but most if not all patients reported in the literature are 13  years or older. It is generally agreed that adolescents have an indication for Latarjet in the setting of critical glenoid bone loss, bipolar bone loss, prior failed arthroscopic stabilization procedure, or a skeletally mature contact/collision athlete with subcritical bone loss. This list of indications is not all encompassing, and ultimately the decision to proceed with Latarjet should be a shared decision-making process among the patient, parents, and surgeon with a thorough discussion of the risks and potential complications of surgery.

287

Figure 25-4. (A) A 17-year- old high school football lineman with posterior labral tear. (B) Metal passer is used to shut tle labral tape (Arthrex) across the posterior labrum. (C) A 2.9-mm drill guide is used to assist in the drilling for the push lock anchor (Arthrex). (D) Final arthroscopic knotless posterior labral repair performed with 4-anchor fixation.

Figure 25-5. (A) A 16-year- old high school football player with chronic anterior shoulder instability and anterior inferior glenoid rim fracture. (B) Computed tomography with 3- dimensional reconstruction of the glenoid face shows more than 15% of anterior glenoid bone loss. (C and D) An open Latarjet procedure was performed with 2 partially threaded screws given the amount of bone loss and chronic bony Bankart lesion.

288

Chapter 25

REHABILITATION Postoperative physical therapy for arthroscopic and open stabilization procedures should begin with a protection phase during which patients remain in a sling for 4 to 6 weeks. Immediately following surgery, patients are allowed elbow, wrist, and finger range of motion to prevent stiffness. An ER immobilizer is used for patients following posterior labral repair for 4 to 6 weeks; however, a standard sling in IR is sufficient following surgery for anterior shoulder instability to keep the arm in IR. Passive and active range of motion of the shoulder in all planes is started at the 4- to 6-week mark following arthroscopic anterior and posterior shoulder stabilization procedures, with strengthening beginning at 8 weeks postoperatively. Sport-specific training can begin at 3 to 4 months postoperatively. Generally, patients are able to return to sport 5 to 6 months following surgery. For pediatric patients who undergo an open Latarjet procedure, the rehabilitation protocol is slightly dif ferent. Patients are allowed to perform pendulum exercises immediately following surgery. At 2 weeks postoperatively, they can begin passive range of motion, with active range of motion starting at 4 weeks. Gentle strengthening is started at 8 weeks, and then a CT scan is recommended at 4 to 6 months to confirm bony union of the coracoid to the anterior glenoid. Once healing is achieved and confirmed by CT scan, the patient is allowed to gradually return to sporting activities. Rehabilitation after arthroscopic capsular shift procedures for MDI is similar; however, it is progressed more slowly to allow for sufficient healing.

CONCLUSION Instability in the pediatric and adolescent athlete is predominantly anterior in direction and secondary to trauma. It is imperative that clinicians perform a thorough history, physical exam, and review of appropriate imaging to identify those rare patients with posterior and MDI. Owing to lower recurrence rates, the initial management of a first-time anterior glenohumeral dislocation in skeletally immature patients (typically younger than 13 years) should be conservative. The management of skeletally mature adolescent patients with a first-time anterior shoulder dislocation should be based on a thorough discussion and shared decision-making process with the patient and parents regarding the risk of recurrent instability both with nonoperative and operative treatment. Arthroscopic Bankart repair and the Latarjet procedure are both effective surgical methods for achieving stability in adolescent patients, and indications for these procedures are based on a number of variables, including age, glenoid and humeral bone loss, contact or collision athletic status, history of prior failed arthroscopic procedure, and surgeon experience. Future prospective studies are needed to determine the optimal treatment in this young patient population.

REFERENCES 1.

2.

3.

4.

5.

6. 7.

8.

9.

10.

11.

12.

13.

14.

15.

16.

17.

18.

Smucny M, Kolmodin J, Saluan  P. Shoulder and elbow injuries in the adolescent athlete. Sports Med Arthrosc Rev. 2016;24(4):188-194. doi:10.1097/JSA.0000000000000131. Leroux T, Ogilvie-Harris D, Veillette C, et  al. The epidemiology of primary anterior shoulder dislocations in patients aged 10 to 16  years. Am J Sports Med. 2015;43(9):2111-2117. doi:10.1177/0363546515591996. Roberts SB, Beattie N, McNiven ND, Robinson CM. The natural history of primary anterior dislocation of the glenohumeral joint in adolescence. Bone Joint  J. 2015;97-B(4):520-526. doi:10.1302/0301-620X.97B4.34989. Li X, Ma R, Nielsen NM, Gulotta LV, Dines JS, Owens BD. Management of shoulder instability in the skeletally immature patient. J Am Acad Orthop Surg. 2013;21(9):529-537. doi:10.5435/ JAAOS-21-09-529. Zacchilli MA, Owens BD. Epidemiology of shoulder dislocations presenting to emergency departments in the United States. J Bone Joint Surg Am. 2010;92(3):542-549. doi:10.2106/JBJS.I.00450. Bishop JY, Flatow EL. Pediatric shoulder trauma. Clin Orthop Relat Res. 2005(432):41-48. doi:10.1097/01.blo.0000156005.01503.43 20% to 25% of the glenoid or an engaging Hill-Sachs defect), studies using fewer than 3 suture anchors, and studies with stabilization not performed with lateral decubitus positioning, they found the failure rate declined to 7.9%. This suggests that arthroscopic stabilization is a reasonable option for collision athletes when used in the correct patient population and when appropriate surgical technique is used. Though this failure rate is still relatively high, when considering open stabilization techniques may still have a recurrence rate ranging anywhere between 3.4% and 30%,38,39 the historical suggestion that all collision athletes with glenohumeral instability should be managed with open stabilization is questioned.

Bone Augmentation Procedures As discussed in the “Preoperative Considerations” section earlier, preoperative evaluation of glenoid bone loss is crucial to selection of the appropriate surgical intervention. There is no clearly defined number in terms of percentage of glenoid bone loss in which a bone augmentation procedure should be performed. It is typically recommended to have a lower threshold in terms of bone loss in collision athletes to perform a bone augmentation procedure. The Latarjet procedure has had successful results in terms of return to play and prevention of recurrent instability events in collision athletes.35,42 Though the Latarjet has been described for athletes with minimal or no glenoid bony deficiency, its superiority for these patients over arthroscopic intervention in terms of return to play or recurrence is questioned. Blonna and colleagues compared arthroscopic stabilization vs Latarjet procedure in athletes with less than 20% glenoid bone loss found a greater return-to-sport rate in the arthroscopic population (90% vs 83%), improved postoperative ROM, and subjective perception of the shoulder.43 Though there were more recurrent instability events in the arthroscopic group, this was not statistically significant. Results in collision athletes were not substratified in this study.

Posterior Instability Surgical Considerations Though posterior shoulder instability is less common than anterior instability, collision athletes are at risk for traumatic posterior instability. In collision athletes, these can be managed with surgical intervention. Though there are limited data, there are several reports of success with arthroscopic surgical stabilization for collision athletes. Typically, this involves posterior capsulolabral reconstruction with plication sutures and/or suture anchors. Arner et  al reported on 56 American football players with unidirectional posterior shoulder instability treated with arthroscopic repair.44 Ninety-three percent of these collision athletes returned to sport with excellent or good results in 96.5% of patients.

A series of 11 rugby players with posterior instability who underwent arthroscopic repair showed all athletes returning to play within 3 to 6 months postoperatively.45

POSTOPERATIVE PROTOCOL Arthroscopic Repair Postoperatively, patients are immobilized in a shoulder immobilizer in internal rotation. The patient is typically immobilized for up to 4 weeks except for removal for therapy and home elbow, wrist, and hand exercises to prevent stiffness. Pendulum exercises with slight forward lean can begin at postoperative day 1. Passive ROM exercises progressing slowly to active assist ROM exercises may begin in the first week postoperatively. Both passive and active motion are limited to 90 degrees of forward elevation, 20  degrees of external rotation, internal rotation to the abdomen, and 45 degrees of abduction. Cross-body adduction is avoided until at least 6 weeks postoperatively. Strengthening exercises are slowly progressed starting with isometric exercises in the first week postoperatively. Progressive resistive exercises begin around 4 weeks postoperatively. Full active ROM should be achieved by 6 to 8  weeks postoperatively. Typically, sportsspecific rehabilitation begins at around 3  months. Patients are typically allowed to return to sport participation at 5 to 6 months postoperatively if they are pain free and strength/ function is near that of the contralateral shoulder. For collision athletes, this is taken in a stepwise fashion starting with noncontact drills and progressively increasing the amount of participation until they are back to normal activities. Any increased pain or feelings of instability during this return to play should be taken with extreme caution given the high risk collision athletes have of recurrence.

Bone Augmentation Procedures Postoperative rehabilitation after bone augmentation procedures such as the Latarjet procedure is similar to rehabilitation protocols of soft-tissue anterior instability stabilization operations. Early, no active ROM (AROM) is allowed and the focus is on protecting the surgical repair and restoring passive ROM. The patient is immobilized in an immobilizer at all times, except for hygiene, for the first 3 to 4 weeks postoperatively. From weeks 4 to 9, there is gradual restoration of active ROM. Weeks 10 to 15 begin the strengthening phase, during which the goal is to normalize strength, endurance, and neuromuscular control of the operative shoulder. Any collision drills must still be avoided at this time. From weeks 16 to 20 (about 4 to 5 months postoperatively), the patient can begin to return to full activities. The collision athlete can begin a stepwise return to play if he or she has no complaints of pain or instability, adequate ROM of the shoulder for the sport, and full strength required for the activity required.

Special Considerations for Return to Play in Collision Athletes (Hockey, Football, and Rugby)

305

RECURRENCE

CONCLUSION

As discussed previously, Balg and Boileau’s ISIS score has been used as a means to identify patients at high risk for recurrent anterior shoulder instability after surgical stabilization.37 Involvement in contact sports had a major influence on the ISIS score and, subsequently, resulted in the recommendation for open stabilization procedures in many of these athletes. However, more recently, authors have suggested that arthroscopic stabilization can still be used successfully with low rates of recurrence in collision athletes when appropriate surgical technique is used.33 Regardless, recurrence of instability can be devastating for the collision athlete. Frequently, recurrent shoulder instability events may result in increased glenoid bone loss whether this is from traumatic bone loss or attritional cause.46 The subchondral bone damage that results from recurrent instability can alter both the mechanical and biological bone tissue properties, which places the glenohumeral joint at risk for early degenerative changes.47,48 In the setting of recurrent glenohumeral instability in the collision athlete, the patient should undergo evaluation similar to after an initial instability event. Careful history and physical exam can provide insight as to whether there was a traumatic event or if there is increased sensation of apprehension in the joint. Imaging evaluation is similar as well. A computed tomography scan is valuable in a repeat instability event in the collision athlete given the risk of glenoid bone loss. Typically, surgical intervention is recommended for collision athletes with recurrent instability. As with a primary instability event, if the athlete is in-season and desires to finish the season, an accelerated rehabilitation protocol can be used to allow the athlete to return to play in 1 to 2 weeks with delayed surgical intervention for the off season. However, any evidence of gross instability or significant bone loss places the athlete at significant risk if he or she were to undergo delayed surgical intervention. Therefore, careful discussion with the patient about the risks of recurrent instability with delayed surgical fixation is essential. With recurrent instability, the surgeon should consider a lower threshold for performing open Bankart or bone augmentation procedures. Previous episodes of instability place the patient at increased risk of repeat instability events.36 Therefore, bone augmentation procedures should be considered with any significant glenoid bone loss. Postoperative rehabilitation and return to play are typically similar to that of athletes treated surgically for a firsttime shoulder instability event. Return to play is usually initiated at around 5 to 6 months postoperatively if the athlete has no complaints of pain or instability, adequate ROM of the shoulder for the sport, and full strength required for the activity required. Again, for collision athletes, this should be performed in a stepwise fashion beginning with noncontact participation and slowly progressing to full return to play. Any increased pain or sensation of instability should be a marker to slow the pace of returning to participation and warrants clinical evaluation.

Glenohumeral instability is a common injury in collision athletes. After an instability event, careful clinical evaluation is necessary to help define the best treatment strategy to allow for return to play in these athletes. Though modern surgical and rehabilitation techniques have significantly improved the rate at which these athletes can return to play with no limitations, there is still risk for recurrence in collision athletes. Continued study and advancement is necessary to optimize the treatment and timing of return to play for collision athletes with glenohumeral instability.

REFERENCES 1.

2.

3.

4.

5.

6.

7.

8.

9. 10.

11.

12.

13.

14.

Owens BD, Agel J, Mountcastle SB, Cameron KL, Nelson BJ. Incidence of glenohumeral instability in collegiate athletics. Am J Sports Med. 2009;37(9):1750-1754. doi:10.1177/0363546509334591. Hootman JM, Dick R, Agel J. Epidemiology of collegiate injuries for 15 sports: summary and recommendations for injury prevention initiatives. J Athl Train. 2007;42(2):311-319. Headey J, Brooks JHM, Kemp SPT. The epidemiology of shoulder injuries in English professional rugby union. Am J Sports Med. 2007;35(9):1537-1543. doi:10.1177/0363546507300691. Kerr ZY, Collins CL, Pommering TL, Fields SK, Comstock RD. Dislocation/separation injuries among US high school athletes in 9 selected sports: 2005-2009. Clin J Sport Med. 2011;21(2):101-108. doi:10.1097/JSM.0b013e31820bd1b6. Dickens JF, Owens BD, Cameron KL, et  al. Return to play and recurrent instability after in-season anterior shoulder instability: a prospective multicenter study. Am J Sports Med. 2014;42(12):2842-2850. doi:10.1177/0363546514553181. Sachs RA, Lin D, Stone ML, Paxton E, Kuney M. Can the need for future surgery for acute traumatic anterior shoulder dislocation be predicted? J Bone Joint Surg Am. 2007;89(8):1665-1674. doi:10.2106/ JBJS.F.00261. Wheeler JH, Ryan JB, Arciero RA, Molinari RN. Arthroscopic versus nonoperative treatment of acute shoulder dislocations in young athletes. Arthroscopy. 1989;5(3):213-217. Aronen JG, Regan K. Decreasing the incidence of recurrence of first time anterior shoulder dislocations with rehabilitation. Am J Sports Med. 1984;12(4):283-291. doi:10.1177/036354658401200408. Bankart AS. Recurrent or habitual dislocation of the shoulder-joint. Br Med J. 1923;2(3285):1132-1133. Fabbriciani C, Milano G, Demontis A, Fadda S, Ziranu F, Mulas PD. Arthroscopic versus open treatment of Bankart lesion of the shoulder: a prospective randomized study. Arthroscopy. 2004;20(5):456462. doi:10.1016/j.arthro.2004.03.001. Bottoni CR, Smith EL, Berkowitz MJ, Towle RB, Moore JH. Arthroscopic versus open shoulder stabilization for recurrent anterior instability: a prospective randomized clinical trial. Am J Sports Med. 2006;34(11):1730-1737. doi:10.1177/0363546506288239. Boileau P, Mercier N, Roussanne Y, Thélu CÉ, Old  J. Arthroscopic Bankart-Bristow-Latarjet procedure: the development and early results of a safe and reproducible technique. Arthroscopy. 2010;26(11):1434-1450. doi:10.1016/j.arthro.2010.07.011. Hintermann B, Gächter A. Arthroscopic findings after shoulder dislocation. Am J Sports Med. 1995;23(5):545-551. doi:10.1177/036354659502300505. Owens BD, Nelson BJ, Duffey ML, et al. Pathoanatomy of first-time, traumatic, anterior glenohumeral subluxation events. J Bone Joint Surg Am. 2010;92(7):1605-1611. doi:10.2106/JBJS.I.00851.

306 15.

16.

17.

18.

19.

20.

21.

22.

23.

24.

25.

26.

27.

28.

29.

30.

31.

32.

Chapter 27 Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging HillSachs lesion. Arthroscopy. 2000;16(7):677-694. Piasecki DP, Verma NN, Romeo AA, Levine WN, Bach BR, Provencher MT. Glenoid bone deficiency in recurrent anterior shoulder instability: diagnosis and management. J Am Acad Orthop Surg. 2009;17(8):482-493. Spatschil A, Landsiedl F, Anderl W, et  al. Posttraumatic anteriorinferior instability of the shoulder: arthroscopic findings and clinical correlations. Arch Orthop Trauma Surg. 2006;126(4):217-222. doi:10.1007/s00402-005-0006-4. Kurokawa D, Yamamoto N, Nagamoto H, et al. The prevalence of a large Hill-Sachs lesion that needs to be treated. J Shoulder Elbow Surg. 2013;22(9):1285-1289. doi:10.1016/j.jse.2012.12.033. Mattern O, Funk L, Walton MJ. Anterior shoulder instability in collision and contact athletes. Journal of Arthroscopy and Joint Surgery. 2018;5(2):99-106. doi:10.1016/j.jajs.2018.05.010. Farber AJ, Castillo R, Clough M, Bahk M, McFarland EG. Clinical assessment of three common tests for traumatic anterior shoulder instability. J Bone Joint Surg Am. 2006;88(7):1467-1474. doi:10.2106/ JBJS.E.00594. Kim SH, Park JS, Jeong WK, Shin SK. The Kim test: a novel test for posteroinferior labral lesion of the shoulder—a comparison to the jerk test. Am J Sports Med. 2005;33(8):1188-1192. doi:10.1177/0363546504272687. Buss DD, Lynch GP, Meyer CP, Huber SM, Freehill MQ. Nonoperative management for in-season athletes with anterior shoulder instability. Am J Sports Med. 2004;32(6):1430-1433. doi:10.1177/0363546503262069. Itoi E, Sashi R, Minagawa H, Shimizu T, Wakabayashi I, Sato  K. Position of immobilization after dislocation of the glenohumeral joint. A study with use of magnetic resonance imaging. J Bone Joint Surg Am. 2001;83-A(5):661-667. Itoi E, Hatakeyama Y, Sato T, et  al. Immobilization in external rotation after shoulder dislocation reduces the risk of recurrence. A randomized controlled trial. J Bone Joint Surg Am. 2007;89(10):21242131. doi:10.2106/JBJS.F.00654. Liavaag S, Brox JI, Pripp AH, Enger M, Soldal LA, Svenningsen  S. Immobilization in external rotation after primary shoulder dislocation did not reduce the risk of recurrence: a randomized controlled trial. J Bone Joint Surg Am. 2011;93(10):897-904. doi:10.2106/ JBJS.J.00416. Burns TC, Owens BD. Management of shoulder instability in inseason athletes. Phys Sportsmed. 2010;38(3):55-60. doi:10.3810/ psm.2010.10.1808. Owens BD, Dickens JF, Kilcoyne KG, Rue J-PH. Management of midseason traumatic anterior shoulder instability in athletes. J Am Acad Orthop Surg. 2012;20(8):518-526. doi:10.5435/JAAOS-20-08-518. Brophy RH, Marx RG. The treatment of traumatic anterior instability of the shoulder: nonoperative and surgical treatment. Arthroscopy. 2009;25(3):298-304. doi:10.1016/j.arthro.2008.12.007. Dickens JF, Rue JP, Cameron KL, et  al. Successful return to sport after arthroscopic shoulder stabilization versus nonoperative management in contact athletes with anterior shoulder instability: a prospective multicenter study. Am J Sports Med. 2017;45(11):2540-2546. doi:10.1177/0363546517712505. Cho NS, Hwang JC, Rhee YG. Arthroscopic stabilization in anterior shoulder instability: collision athletes versus noncollision athletes. Arthroscopy. 2006;22(9):947-953. doi:10.1016/j.arthro.2006.05.015. Yamamoto N, Kijima H, Nagamoto H, et al. Outcome of Bankart repair in contact versus non-contact athletes. Orthop Traumatol Surg Res. 2015;101(4):415-419. doi:10.1016/j.otsr.2015.03.008. Nakagawa S, Ozaki R, Take Y, Iuchi R, Mae T. Relationship between glenoid defects and Hill-Sachs lesions in shoulders with traumatic anterior instability. Am J Sports Med. 2015;43(11):2763-2773. doi:10.1177/0363546515597668.

33.

34.

35.

36.

37.

38.

39.

40.

41.

42.

43.

44.

45.

46.

47.

48.

Leroux TS, Saltzman BM, Meyer M, et al. The influence of evidencebased surgical indications and techniques on failure rates after arthroscopic shoulder stabilization in the contact or collision athlete with anterior shoulder instability. Am J Sports Med. 2017;45(5):12181225. doi:10.1177/0363546516663716 Bhatia S, Ghodadra NS, Romeo AA, et al. The importance of the recognition and treatment of glenoid bone loss in an athletic population. Sports Health. 2011;3(5):435-440. doi:10.1177/1941738111414126. Neyton L, Young A, Dawidziak B, et al. Surgical treatment of anterior instability in rugby union players: clinical and radiographic results of the Latarjet-Patte procedure with minimum 5-year followup. J Shoulder Elbow Surg. 2012;21(12):1721-1727. doi:10.1016/j. jse.2012.01.023. Balg F, Boileau  P. The Instability Severity Index Score. A simple pre-operative score to select patients for arthroscopic or open shoulder stabilisation. J Bone Joint Surg Br. 2007;89(11):1470-1477. doi:10.1302/0301-620X.89B11.18962. Boileau P, Villalba M, Héry J-Y, Balg F, Ahrens P, Neyton  L. Risk factors for recurrence of shoulder instability after arthroscopic Bankart repair. J  Bone Joint Surg Am. 2006;88(8):1755-1763. doi:10.2106/JBJS.E.00817. Pagnani MJ, Dome DC. Surgical treatment of traumatic anterior shoulder instability in American football players. J Bone Joint Surg Am. 2002;84-A(5):711-715. Roberts SN, Taylor DE, Brown JN, Hayes MG, Saies A. Open and arthroscopic techniques for the treatment of traumatic anterior shoulder instability in Australian rules football players. J Shoulder Elbow Surg. 1999;8(5):403-409. Flinkkilä T, Hyvönen P, Ohtonen P, Leppilahti  J. Arthroscopic Bankart repair: results and risk factors of recurrence of instability. Knee Surg Sports Traumatol Arthrosc. 2010;18(12):1752-1758. doi:10.1007/s00167-010-1105-5. Frank RM, Saccomanno MF, McDonald LS, Moric M, Romeo AA, Provencher MT. Outcomes of arthroscopic anterior shoulder instability in the beach chair versus lateral decubitus position: a systematic review and meta-regression analysis. Arthroscopy. 2014;30(10):13491365. doi:10.1016/j.arthro.2014.05.008. Privitera DM, Sinz NJ, Miller LR, et al. Clinical outcomes following the Latarjet procedure in contact and collision athletes. J Bone Joint Surg Am. 2018;100(6):459-465. doi:10.2106/JBJS.17.00566. Blonna D, Bellato E, Caranzano F, Assom M, Rossi R, Castoldi  F. Arthroscopic Bankart repair versus open Bristow-Latarjet for shoulder instability: a matched-pair multicenter study focused on return to sport. Am J Sports Med. 2016;44(12):3198-3205. doi:10.1177/0363546516658037. Arner JW, McClincy MP, Bradley JP. Arthroscopic stabilization of posterior shoulder instability is successful in American football players. Arthroscopy. 2015;31(8):1466-1471. doi:10.1016/j. arthro.2015.02.022. Badge R, Tambe A, Funk  L. Arthroscopic isolated posterior labral repair in rugby players. Int J Shoulder Surg. 2009;3(1):4-7. doi:10.4103/0973-6042.50875. Donohue MA, Mauntel TC, Dickens JF. Recurrent shoulder instability after primary Bankart repair. Sports Med Arthrosc Rev. 2017;25(3):123-130. doi:10.1097/JSA.0000000000000159. Leyh M, Seitz A, Dürselen L, et al. Subchondral bone influences chondrogenic differentiation and collagen production of human bone marrow-derived mesenchymal stem cells and articular chondrocytes. Arthritis Res Ther. 2014;16(5):453. doi:10.1186/s13075-014-0453-9. Ramme AJ, Lendhey M, Raya JG, Kirsch T, Kennedy OD. A novel rat model for subchondral microdamage in acute knee injury: a potential mechanism in post-traumatic osteoarthritis. Osteoarthr Cartil. 2016;24(10):1776-1785. doi:10.1016/j.joca.2016.05.017.

28 Management of the Aging Athlete With the Sequelae of Shoulder Instability Lucca Lacheta, MD; Maj. Travis J. Dekker, MD, MC, USAF; and Peter J. Millett, MD, MSc

Treatment of the aging athlete with early glenohumeral osteoarthritis (GHOA) and as a sequelae of shoulder instability is challenging because shoulder arthroplasty may not be the treatment of choice in this population. The increased risk of GHOA of the shoulder joint in patients with shoulder instability has been well documented1,2 (Figure 28-1). The cause of these degenerative changes remains unclear. The trauma of shoulder luxation itself certainly plays a significant role in the initial injury to the articular cartilage. This theory is supported by the fact that even in those who undergo successful nonoperative treatment GHOA still develops in about 50% of cases.2 Unfortunately, neither open nor arthroscopic operative techniques have been able to prevent the development of GHOA completely.1,3,4 Although the majority of patients show only minor pathological changes, the overall incidence in long-term studies is around 60% to 80%.1,3,4 Age at the time of the first dislocation and at the time of operative stabilization, the number of dislocations before surgical intervention, and the number of anchors used have been shown to be risk factors.1 Historically, nonanatomic procedures with tightening of the subscapularis tendon to limit external rotation by transecting then overlapping the medial and lateral segments (Putti-Platt) or by moving the insertion point more laterally and distally (Magnuson-Stack) were shown to result in an increased rate of GHOA.5,6 In the setting of coracoid transfer procedures, recent long-term analysis with follow-up greater than 10 years has shown posttraumatic GHOA occurring in up to 38% of patients.7 Older age, high-demand sports, and lateral positioning of the transferred coracoid in relation to the glenoid rim promotes the development of GHOA.7-10 Avoidance of overtightening the capsule tissue during initial surgical treatment, correct hardware placement, and maybe

new-generation anchor materials (all-suture soft anchors) can help to reduce or even avoid the risk of development of GHOA. Furthermore, an early stabilization after first-time dislocation and technically correct and well-performed surgery with no iatrogenic injuries may prevent the development of GHOA. When it comes to early or even end-stage GHOA, various treatment options have been described that will be summarized in this chapter focusing on the management of the aging athlete with glenohumeral instability sequelae.

SUBSCAPULARIS LENGTHENING Many historical surgical procedures have been associated with the development of GHOA (eg, Putti-Platt, MagnusonStack) with stiffness and tightness of the glenohumeral joint. Hawkins and Angelo reported on a series of patients who after undergoing a Putti-Platt procedure developed painful GHOA at 13.2  years after surgery.6 Provencher termed this condition capsulorrhaphy arthropathy to describe GHOA developed because of excessive soft-tissue tightening.11 Historically, subscapularis tendon lengthening was one treatment option for those patients to increase external rotation that was first described by Neer et  al,12 by dissecting the subscapularis tendon free and lengthening by a coronal-plane z-plasty. Nicholson and colleagues reported their technique of subscapularis lengthening in shoulder arthroplasty with outcomes in 27 patients.13 External rotation improved to 48 degrees postoperatively with more than half the patients reporting a decrease in subscapularis function. Owing to poor functional results, therefore, this procedure is not usually recommended and serves as a salvage procedure alone.13,14

- 307 -

Dickens JF, Owens BD, eds. Shoulder Instability in the Athlete: Techniques for Optimized Return to Play (pp 307-315). © 2021 SLACK Incorporated.

308

Chapter 28

Figure 28-1. Postoperative anteroposterior radiograph of a right shoulder with severe post-instability glenohumeral osteoarthritis after surgical stabilization.

COMPREHENSIVE ARTHROSCOPIC MANAGEMENT PROCEDURE FOR EARLY GLENOHUMERAL OSTEOARTHRITIS Joint-preserving arthroscopic management options for degenerative joint disease in young patients have been used to address dif ferent pain generators that are involved in the pathoanatomy related to GHOA to reduce pain, improve shoulder function, and to delay or even avoid the need for total joint replacement. Key considerations of this comprehensive approach to mitigating GHOA include addressing all the various factors that can cause pain and limit function. The pathologic adaptive changes seen with glenohumeral arthritis are the following: capsular contracture, loose bodies, biceps tenosynovitis, inferior humeral osteophyte formation with axillary nerve compression, subcoracoid impingement, and subacromial spurs. Arthroscopically, the surgeon can perform debridement, chondroplasty, synovectomy, loose body removal, capsular release, subacromial decompression with acromioplasty, subcoracoid decompression with coracoidplasty, humeral osteoplasty, axillary nerve decompression, and biceps tenodesis. The goal of these procedures is to treat mechanical and inflammatory causes of pain and to improve functional limitations. Although data are still emerging, clinical studies report that the comprehensive arthroscopic approach to GHOA improves function and reduces pain in short- and mid-term follow-up periods.

The goal of various arthroscopic management techniques is to treat potential causes of pain and address functional limitations associated with GHOA. Initially, arthroscopic management consisted of intra-articular debridement of the glenohumeral joint alone with resection of synovitis and loose bodies. The rationale behind arthroscopic debridement is to simply remove possible sources of mechanical irritation, creating a less painful environment for the patient’s shoulder.15,16 Additionally, capsular release was added to the arthroscopic management to increase the effect of restoring shoulder function and range of motion,17 which leads both to pain relief and increase in patient satisfaction. Another well-known source of pain addressed arthroscopically in the osteoarthritic shoulder is pathology associated with the long head of the biceps tendon. Biceps pathologies such as tendinitis, hourglass deformity, or pulley lesions warrant a tenotomy with or without later tenodesis.18-22 The senior author has combined several previous arthroscopic techniques used to treat GHOA with a number of additional key procedures23—the so-called comprehensive arthroscopic management (CAM) procedure. A detailed technique description has previously been published23 An impor tant point and source of pain are inferior humeral head osteophytes, also described as the goat’s beard deformity, which are frequently seen in patients with advanced GHOA (Figure  28-2). Owing to its proximity to the axillary nerve, frequent impingement of the osteophytes on the nerve can result in pain and dysfunction of the teres minor with observed fatty infiltration.24 In clinical practice, inferior humeral head osteophytes are addressed when they are large and when pain in the axillary nerve distribution exists. The use of preoperative and postoperative electromyography may be of use in the future. To address the inferior humeral osteophytes, an accessory posteroinferior portal is established to facilitate resection. To confirm the amount of osteophyte resection intraoperatively fluoroscopy is used (Figure 28-3). In case of nerve impingement symptoms, the inferior capsule is opened to access the axillary nerve for neurolysis (Figure 28-4). Clinical signs for nerve impingement can be muscle weakness or atrophy, seen on the preoperative magnetic resonance imaging (MRI), or it can be visualized arthroscopically. Additional arthroscopic shoulder procedures can be added as indicated. If clinical signs of subacromial impingement are present, with positive provocative testing, increased subacromial spurs on radiographs according to the Bigliani classification, or increased bursal inflammation on MRI, a subacromial decompression is performed (Figure  28-5). If patients present with anterior shoulder pain during internal rotation and arthroscopic findings of fraying or tearing of the upper border of the subscapularis tendon as a sign for anterior subcoracoid impingement, a subcoracoid decompression can be performed; there are also loose bodies frequently present in the subcoracoid space (Figure  28-6). Radiographically, a coracohumeral distance of less than 8 mm (in women) or less

Management of the Aging Athlete With the Sequelae of Shoulder Instability

309

Figure 28-2. (A) Left shoulder: arthroscopic view via the posterior standard portal visualizing the inferior humeral osteophyte (*). (B) Humeral resection arthroplasty via an accessory inferior posterolateral portal by the use of an oscillating shaver. (C) Final result (#) of the humeral osteophyte resection arthroplasty.

Figure 28-3. (A) Left shoulder: preoperative anterior-posterior radiograph showing a large extending inferior humeral osteophyte (arrows). (B) Left shoulder: intraoperative fluoroscopy of the same patient confirming total resection of the inferior humeral osteophyte with restoring of the gothic arch.

Figure 28-4. (A) Left shoulder: arthroscopic view via the posterior standard portal with a hooked electrocautery device coming through an accessory inferior posterolateral portal to perform an inferior capsular release (*) and (B) additional neurolysis of the underlying axillary nerve.

than 10 mm (in men) with associated symptoms may warrant arthroscopic treatment.25,26 In cases of focal chondral defects, microfracture is performed to stimulate the subchondral bone for fibrocartilage stimulation. This step should be performed last during the CAM procedure to avoid washing out the nascent clot with arthroscopic fluid.27 Subpectoral biceps tenodesis is performed in most cases at the end of the case. Even though little to no differences are observed in clinical outcome between tenodesis and tenotomy of the long head of the biceps tendon, many surgeons and patients prefer tenodesis because it is associated with higher patient satisfaction and fewer cosmetic problems.21 The senior author’s preferred technique of biceps tenodesis is a subpectoral biceps tenodesis with interference screw fixation below the bicipital groove, with resection of the tenosynovitis and frayed proximal part of the biceps tendon.28

The goal of these arthroscopic procedures is to address all mechanical causes of pain and functional impairment associated with GHOA. Although each individual procedure has shown clinical benefits, the purpose of combining these techniques is to achieve a synergetic effect in pain relief and to restore function so joint arthroplasty can be delayed or in some cases even avoided. Previous literature has demonstrated inconsistent improvement in patient satisfaction as well as postoperative motion after primarily addressing GHOA with arthroscopic procedures.16,17,29 When focusing on chondral defects, Kerr and McCarty15 have shown that patients treated with arthroscopic glenohumeral debridement, microfracture, and biceps tenotomy had no differences in clinical outcome depending on the grade of lesion; however, they reported favorable outcomes in patients with unipolar defects when compared to patients with bipolar chondral

310

Chapter 28

Figure 28-6. (A) Left shoulder: arthroscopic view via the posterior standard portal visualizing a large loose body in the subcoracoid space. (B) Arthroscopically removed loose bodies on the back table (ex vivo). Figure 28-5. Arthroscopic view via the posterior standard portal into the subacromial space in a left shoulder: subacromial decompression of the inferior acromion of approximately 5 mm by the use of an oscillating shaver (half shaver width).

defects. Furthermore, patients with less-advanced GHOA at time of arthroscopic management may improve more with arthroscopic intervention. Furthermore, Millett et  al have noted an association between inferior humeral head osteophytes and teres minor fatty infiltration in 91 patients who were retrospectively reviewed.24 A correlation between size of the inferior humeral head osteophytes and the grade of fatty infiltration in the teres minor, with larger osteophytes associated with more fat infiltration, was observed. Patients presenting with anterior shoulder pain and osteoarthritis may have long head of the biceps tendon pathology with tenosynovitis, pulley lesions with an unstable tendon, and fraying. The gold standard to address these pathologies in patients with GHOA is either tenodesis or tenotomy of the tendon. Both procedures improve patient outcomes postoperatively.30 However, a greater rate of distalization of the muscle belly—so-called “Popeye” deformity—when tenotomy is performed has been reported. Some patients do complain of subjective and functional differences between tenodesis and tenotomy; therefore, in young athletes with early GHOA, we prefer biceps tenodesis because of concerns about cramping and cosmesis following tenotomy. Some studies suggest that patients undergoing tenotomy will have fatigue, discomfort, and slightly reduced elbow supination strength when compared to tenodesis.31,32 Millett and colleagues reported the surgical outcomes of 30 shoulders with symptomatic GHOA in young, active patients with advanced shoulder GHOA.33 Of those 30 shoulders, 24 were still functioning at final follow-up, whereas 6 progressed to arthroplasty at a mean of 1.9 years. They found that patients with a joint space on radiographs of less than 2  mm were more likely to undergo shoulder arthroplasty. For shoulders that did not fail, the minimum follow-up was 2  years and the mean follow-up was 2.6  years. The

overall improvement in this patient cohort in the American Shoulder and Elbow Surgeons (ASES) score was from 58 points to 83 points. The postoperative patient satisfaction was a median of 9. The authors presented a survivorship rate of 92% at 1 year and 85% at 2  years postoperatively. In the most recent study performed by Mitchell et  al,34 49 shoulders that underwent a CAM procedure were evaluated with a minimum follow-up of 5  years. The mean age at time of surgery was 52 years in this patient population. All patients were recreational athletes with 7 former collegiate or professional athletes. Thirty-seven of the 49 survived 5  years or longer. Twelve out of 49 shoulders (26%) progressed to a total shoulder arthroplasty at a mean of 2.6 years postoperatively. In this cohort, the authors found a survivorship rate of 76% at 5 years. The mean ASES score was stable over time at 85 points at final follow-up for those shoulders that did not fail. Patient satisfaction was also stable over time with a median of 9 of possible 10 points. An analysis of preoperative factors that predicted failure of treatment showed that patients who failed had significantly less joint space than those who succeeded (1.3  mm vs 2.6  mm). Higher Kellgren-Lawrence grades for GHOA and age older than 50 years were also associated with failure. Shoulders with Walch type B2 and type C glenoid deformities were also significantly more likely to fail than glenoid types A1, A2, and B1.

INTERPOSITION ARTHROPLASTY/ BIORESURFACING Hemiarthroplasty has been widely used with younger patients while avoiding the risks of glenoid implant loosening and polyethylene wear. Nevertheless, mid- and long-term studies have shown that even in patients who were initially pain free, recurrent symptoms with loss of motion and pain caused by progression of glenoid erosion occur over time.35-37 Interposition arthroplasty is a chosen biologic graft, secured to the glenoid surface, with or without a prosthetic

Management of the Aging Athlete With the Sequelae of Shoulder Instability

311

Figure 28-7. Surgical decision-making algorithm in the aging athlete with post instability osteoarthritis.

hemiarthroplasty to treat young patients with advanced GHOA. The goal of interposition arthroplasty is to delay or even avoid a total shoulder arthroplasty and the associated complications seen in young and high-demand patients: early wear and loosening of the glenoid component. The use of various grafts has been reported for bioresurfacing the glenoid. Autografts included the anterior capsule of the glenohumeral joint, and fascia lata from the thigh. Allograft options included the lateral meniscus, Achilles tendon, and acellular human allograft. Ideally, the graft material should be durable enough to withstand the compressive and shear forces exerted at the glenoid joint surface. The clinical results for interposition arthroplasty are quite variable, owing partially to the variety of grafts and techniques used. There is some evidence suggesting that interposition arthroplasty with securely fixed Achilles tendon or lateral meniscus graft may improve pain and function in the young patient with GHOA and may actually allow to return to premorbid activities; however, the current evidence of bioresurfacing is challenging to interpret. Although some studies reported favorable clinical outcomes,37-39 these results have not been confirmed by other investigators.40-42.

ARTHROPLASTY—ANATOMIC AND REVERSE Despite promising results with joint-preserving procedures, when GHOA becomes end stage, total shoulder arthroplasty (TSA) or even reverse total shoulder arthroplasty (RTSA) may be a necessary surgical solution, even

in young patients, to provide pain relief, restore range of motion, and improve function.43 To date, no clear consensus recommendations exist to guide surgeons in the decision-making process as to when to perform TSA in young and active patients. Figure 28-7 is intended to help in this decision-making process. TSA in athletes remains challenging because of concerns of implant longevity caused by higher activity levels and participation in sports events but also because of patient expectations.44 Henn and colleagues showed in their multivariable analysis that younger age was the only independent predictor of greater expectations.45 A patient’s desire to return to sport activities following TSA historically conflicted with the surgeon’s recommendation, which limited patients to low-demand activities to avoid failure. Several studies have surveyed shoulder surgeons about activities they allow after TSA and have found that most surgeons advise their patients to avoid contact or overhead sports.46,47 Reasons for these restrictions included rotator cuff tears after TSA, glenoid loosening, and general concerns of implant failure. The senior author in contrast has not placed specific restrictions on patients after TSA. In a study performed by Mannava et  al, patients who had undergone TSA showed excellent postoperative improvement in clinical outcome scores, satisfaction, and, more impor tant, high rates of return to athletic activities.43 Despite the expected decreases in activity levels with the progression of GHOA, in the series by Mannava et  al, 94% of patients successfully returned to recreational sporting activities. This study showed that return to recreational sports can be achieved at participation levels equal to preoperative levels. However, athletes in some overhead

312

Chapter 28

sports, such as tennis or swimming—sports that place more demand on the shoulder—are less likely to return to the same level of sport. At a mean follow-up of 4 years, the complication rate was 9%; one patient was revised because of glenoid loosening and 4  patients were converted to RTSA because of rotator cuff insufficiency over time. These findings suggest TSA offers both reliable and consistent outcomes in the active patient providing improvement in range of motion as well as a decrease in pain.43 In cases of end-stage rotator cuff tear arthropathy, an irreparable subscapularis tear (as may be present after open soft-tissue stabilization or Latarjet procedures) or in those who have unmanageable persistent glenohumeral instability (eg, multidirectional instability) reverse shoulder arthroplasty (RTSA) is a helpful option. Though historically used in the elderly population, greater biomechanical knowledge and heightened technical expertise have expanded the indications for RTSA to younger populations. In this patient demographic, significant increases in outcomes and range of motion have been reported, but high complication rates still remain.48,49 In terms of return to sports, Bulhoff and colleagues showed in patients treated with RTSA for cuff tear arthropathy a participation-in-sports rate prior to surgery of 71%.50 The return-to-sports rate was reliable with 67% after RTSA. Similar results were presented by Matthews et  al, with a return to recreational activities and sport in 67% in RTSA in patients younger than 65  years.51 The authors found significantly inferior outcome scores (mean postoperative ASES score of 71) in patients younger than 65 years when compared to patients older than 70  years (mean postoperative ASES score of 79). Ernstbrunner et al showed there was no deterioration in subjective and functional improvements at 10 years after RTSA in patients younger than 60 years. However, the authors concluded that RTSA in younger patients is associated with a substantial complication rate and that complications compromised the ultimate subjective and objective outcomes of their study.49 In summary, TSA and RTSA are viable treatment options with predictable clinical outcome for a selected patient population.

TREATMENT DECISION MAKING The initial management of GHOA in the athlete in some cases may consist of nonsurgical treatment options such as cross-training and lifestyle modifications, pain medication, physical therapy, and, if preferred, intra-articular injections of corticosteroid or viscosupplementation.34,52-54 However, if mechanical problems such as loose bodies are the source of pain that will not respond to nonoperative measures or nonoperative treatment fails, surgical options such as arthroscopic debridement, biological interposition arthroplasty, hemi- and total shoulder arthroplasty may become necessary. Arthroscopic debridement with additional procedures such as capsular release is a reasonable approach for mild to moderate GHOA. Owing to release of the tight

capsule, this option may help to decrease joint contact forces and improve joint function by restoring range of motion. However, studies have shown that the beneficial effect may be short lived; furthermore, failure rates have been reported to be up to 30%, particularly with bipolar disease.15,17 Establishing realistic expectations through extensive counseling sessions both with patients and the people supporting them throughout their episode of care is essential. The timing and treatment options should be communicated carefully with the patient. The ultimate treatment selection must be individualized for each patient, with consideration of the patient’s age, demands, degree of GHOA, the remaining joint space, and glenoid morphology as defined by Walch et al.34,53,55 A Markov decision-making model reported that the arthroscopic approach to GHOA was the preferred treatment option for patients younger than 45  years, whereas total shoulder arthroplasty was preferred for patients older than 66 years.56 Furthermore, in 2 studies Mitchell and colleagues demonstrated that patient age older than 50 years was a risk factor for early failure of a joint-preserving, arthroscopic approach.34,53 The Kellgren-Lawrence grading system of GHOA has been shown to be a good predictor for survivorship of arthroscopic management of GHOA. More advanced states of GHOA (Kellgren-Lawrence grade IV) with greater degrees of jointspace narrowing were associated with earlier conversions to total joint replacement and worse clinical outcomes after arthroscopic management in the series by Mitchell et  al of patients who underwent the CAM procedure.53 Furthermore, preoperative joint space of less than 2  mm on true anteroposterior radiographs, bipolar cartilage defects, posterior subluxation of the humeral head, and more severe glenoid deformities (Walch type B2 and C) were also associated with earlier failures of arthroscopic treatment (Table 28-1).55 Patients undergo routinely advanced radiological evaluation by plain radiographs, as well as MRI or computed tomography in our practice. Arthroscopic management may be contraindicated when there is superior escape of the humeral head with or without acetabularization with rotator cuff tear and any instances of an active inflammatory arthritis. Arthroplasty of the glenohumeral joint is a reasonable alternative in cases for which arthroscopic management is contraindicated and may be preferable when there is joint incongruity or a large irreparable rotator cuff tear. A treatment decision-making algorithm for arthroscopic management vs total shoulder arthroplasty is illustrated in Figure 28-7.

CONCLUSION Surgical management of the aging athlete with instability sequelae remains challenging. The best approach is prevention. We strongly believe that early surgical intervention and carefully performed stabilization procedures will reduce the incidence of posttraumatic and postsurgical GHOA. When

Management of the Aging Athlete With the Sequelae of Shoulder Instability

313

Table 28-1. Indications and Contraindications for Arthroscopic Management of Glenohumeral Osteoarthritis INDICATIONS Advanced symptomatic OA ●

●

Young (< 50 y)

●

Active patients

CONTRAINDICATIONS Mild OA ●

●

●

Desire for joint preservation

●

Failed nonsurgical treatment

RELATIVE CONTRAINDICATIONS Joint space < 2 mm

●

●

●

Nonsurgical treatment not yet attempted Incongruous joint space and severe glenoid deformity Inflammatory arthritis

●

Severely limited range of motion (especially IR)

●

Large osteophytes

●

Bipolar chondral defects

●

Low critical shoulder angle

●

Kellgren-Lawrence grade III or IV

●

Walch B2 or C glenoid

Abbreviations: IR, internal rotation; OA, osteoarthritis.

GHOA does occur as a sequela of instability or instability surgery, it is impor tant to determine the cause and to identify the pathoanatomy. Arthroscopic procedures to treat early GHOA in these mostly young, active, and high-demanding patients are emerging and evolving. Arthroscopic management has several advantages over total shoulder replacement with promising short- and mid-term outcomes. Arthroplasty remains a reliable option in those with more advanced osteoarthritis. Fortunately, with advances both in technique and technology, arthroplasty can be used in active patients with reliable return to desired activities. Because most of the studies that examine arthroscopic interventions and arthroplasty in the setting of GHOA are case series with small patient numbers and relatively short follow-up intervals, there is an opportunity to perform higher-level prospective studies to evaluate long-term outcomes and the durability of these procedures.

7.

8.

9.

10.

11. 12.

REFERENCES 1.

2.

3.

4.

5.

6.

Plath JE, Aboalata M, Seppel G, et  al. Prevalence of and risk factors for dislocation arthropathy: radiological long-term outcome of arthroscopic Bankart repair in 100  shoulders at an average 13-year follow-up. Am J Sports Med. 2015;43(5):1084-1090. doi:10.1177/0363546515570621. Hovelius L, Saeboe M. Neer Award 2008: arthropathy after primary anterior shoulder dislocation—223 shoulders prospectively followed up for twenty-five years. J Shoulder Elbow Surg. 2009;18(3):339-347. doi:10.1016/j.jse.2008.11.004. Berendes T, Mathijssen N, Verburg H, Kraan G. The open-modified Bankart procedure: long-term follow-up ‘a 16-26-year follow-up study’. Arch Orthop Trauma Surg. 2018;138(5):597-603. doi:10.1007/ s00402-017-2866-9. Fabre T, Abi-Chahla ML, Billaud A, Geneste M, Durandeau A. Longterm results with Bankart procedure: a 26-year follow-up study of 50 cases. J Shoulder Elbow Surg. 2010;19(2):318-323. doi:10.1016/j. jse.2009.06.010. Millett PJ, Clavert P, Warner JJ. Open operative treatment for anterior shoulder instability: when and why? J Bone Joint Surg Am. 2005;87(2):419-432. doi:10.2106/JBJS.D.01921. Hawkins RJ, Angelo RL. Glenohumeral osteoarthrosis. A late complication of the Putti-Platt repair. J Bone Joint Surg Am. 1990;72(8):1193-1197.

13.

14.

15.

16.

17.

18. 19.

Hurley ET, Jamal MS, Ali ZS, Montgomery C, Pauzenberger L, Mullett  H. Long-term outcomes of the Latarjet procedure for anterior shoulder instability: a systematic review of studies at 10-year follow-up. J Shoulder Elbow Surg. 2019;28(2):e33-e39. doi:10.1016/j. jse.2018.08.028. Mizuno N, Denard PJ, Raiss P, Melis B, Walch  G. Long-term results of the Latarjet procedure for anterior instability of the shoulder. J Shoulder Elbow Surg. 2014;23(11):1691-1699. doi:10.1016/j. jse.2014.02.015. Lädermann A, Lubbeke A, Stern R, Cunningham G, Bellotti V, Gazielly DF. Risk factors for dislocation arthropathy after Latarjet procedure: a long-term study. Int Orthop. 2013;37(6):1093-1098. doi:10.1007/s00264-013-1848-y. Gordins V, Hovelius L, Sandström B, Rahme H, Bergstrom U. Risk of arthropathy after the Bristow-Latarjet repair: a radiologic and clinical thirty-three to thirty-five years of follow-up of thirty-one shoulders. J Shoulder Elbow Surg. 2015;24(5):691-699. doi:10.1016/j. jse.2014.09.021. Provencher MT, Barker JU, Strauss EJ, et al. Glenohumeral arthritis in the young adult. Instr Course Lect. 2011;60:137-153. Neer CS II, Watson KC, Stanton FJ. Recent experience in total shoulder replacement. J Bone Joint Surg Am. 1982;64(3):319-337. Nicholson GP, Twigg S, Blatz B, Sturonas-Brown B, Wilson  J. Subscapularis lengthening in shoulder arthroplasty. J Shoulder Elbow Surg. 2010;19(3):427-433. doi:10.1016/j.jse.2009.05.017. Kruit AS, Choukairi F, Mishra A, Gaffey A, Jester A. Subscapularis Z-lengthening in children with brachial plexus birth palsy loses efficiency at mid-term follow-up: a retrospective cohort study. Int Orthop. 2016;40(4):783-790. doi:10.1007/s00264-015-3062-6. Kerr BJ, McCarty EC. Outcome of arthroscopic débridement is worse for patients with glenohumeral arthritis of both sides of the joint. Clin Orthop Relat Res. 2008;466(3):634-638. doi:10.1007/ s11999-007-0088-0. Weinstein DM, Bucchieri JS, Pollock RG, Flatow EL, Bigliani LU. Arthroscopic debridement of the shoulder for osteoarthritis. Arthroscopy. 2000;16(5):471-476. doi:10.1053/jars.2000.5042. Richards DP, Burkhart SS. Arthroscopic debridement and capsular release for glenohumeral osteoarthritis. Arthroscopy. 2007;23(9):10191022. doi:10.1016/j.arthro.2006.11.016. Braun S, Horan MP, Elser F, Millett PJ. Lesions of the biceps pulley. Am J Sports Med. 2011;39(4):790-795. doi:10.1177/0363546510393942. Pogorzelski J, Horan MP, Hussain ZB, Vap A, Fritz EM, Millett PJ. Subpectoral biceps tenodesis for treatment of isolated type II SLAP lesions in a young and active population. Arthroscopy. 2018;34(2):371376. doi:10.1016/j.arthro.2017.07.021.

314 20.

21.

22.

23.

24.

25.

26.

27.

28.

29.

30.

31.

32.

33.

34.

Chapter 28 Katthagen JC, Vap AR, Tahal DS, Horan MP, Millett PJ. Arthroscopic repair of isolated partial- and full-thickness upper third subscapularis tendon tears: minimum 2-year outcomes after single-anchor repair and biceps tenodesis. Arthroscopy. 2017;33(7):1286-1293. doi:10.1016/j.arthro.2017.01.027. Tahal DS, Katthagen JC, Vap AR, Horan MP, Millett PJ. Subpectoral biceps tenodesis for tenosynovitis of the long head of the biceps in active patients younger than 45 years old. Arthroscopy. 2017;33(6):11241130. doi:10.1016/j.arthro.2016.10.013. Vap AR, Katthagen JC, Tahal DS, et  al. Isolated biceps reflection pulley tears treated with subpectoral biceps tenodesis: minimum 2year outcomes. Arthroscopy. 2017;33(10):1788-1794. doi:10.1016/j. arthro.2017.04.021. Mook WR, Petri M, Greenspoon JA, Millett PJ. The comprehensive arthroscopic management procedure for treatment of glenohumeral osteoarthritis. Arthrosc Tech. 2015;4(5):e435-e441. doi:10.1016/j. eats.2015.04.003. Millett PJ, Schoenahl JY, Allen MJ, Motta T, Gaskill TR. An association between the inferior humeral head osteophyte and teres minor fatty infiltration: evidence for axillary nerve entrapment in glenohumeral osteoarthritis. J Shoulder Elbow Surg. 2013;22(2):215-221. doi:10.1016/j.jse.2012.05.030. Lo IK, Burkhart SS. Arthroscopic coracoplasty through the rotator interval. Arthroscopy. 2003;19(6):667-671. doi:10.1016/ s0749-8063(03)00219-6. Brunkhorst JP, Giphart JE, LaPrade RF, Millett PJ. Coracohumeral distances and correlation to arm rotation: an in vivo 3-dimensional biplane fluoroscopy study. Orthop J Sports Med. 2013;1:2325967113496059. Millett PJ, Huffard BH, Horan MP, Hawkins RJ, Steadman  JR. Outcomes of full-thickness articular cartilage injuries of the shoulder treated with microfracture. Arthroscopy. 2009;25(8):856-863. doi:10.1016/j.arthro.2009.02.009. Altintas B, Pitta R, Fritz EM, Higgins B, Millett PJ. Technique for type IV SLAP lesion repair. Arthrosc Tech. 2018;7(4):e337-e342. doi:10.1016/j.eats.2017.10.004. Cameron BD, Galatz LM, Ramsey ML, Williams GR, Iannotti JP. Non-prosthetic management of grade IV osteochondral lesions of the glenohumeral joint. J Shoulder Elbow Surg. 2002;11(1):25-32. doi:10.1067/mse.2002.120143. Slenker NR, Lawson K, Ciccotti MG, Dodson CC, Cohen SB. Biceps tenotomy versus tenodesis: clinical outcomes. Arthroscopy. 2012;28(4):576-582. doi:10.1016/j.arthro.2011.10.017. Kelly AM, Drakos MC, Fealy S, Taylor SA, O’Brien SJ. Arthroscopic release of the long head of the biceps tendon: functional outcome and clinical results. Am J Sports Med. 2005;33(2):208-213. doi:10.1177/0363546504269555. Wittstein JR, Queen R, Abbey A, Toth A, Moorman CT III. Isokinetic strength, endurance, and subjective outcomes after biceps tenotomy versus tenodesis: a postoperative study. Am J Sports Med. 2011;39(4):857-865. doi:10.1177/0363546510387512. Millett PJ, Horan MP, Pennock AT, Rios  D. Comprehensive arthroscopic management (CAM) procedure: clinical results of a jointpreserving arthroscopic treatment for young, active patients with advanced shoulder osteoarthritis. Arthroscopy. 2013;29(3):440-448. doi:10.1016/j.arthro.2012.10.028. Mitchell JJ, Horan MP, Greenspoon JA, Menge TJ, Tahal DS, Millett PJ. Survivorship and patient-reported outcomes after comprehensive arthroscopic management of glenohumeral osteoarthritis: minimum 5-year follow-up. Am J Sports Med. 2016;44(12):3206-3213. doi:10.1177/0363546516656372.

35.

36.

37.

38.

39.

40.

41.

42.

43.

44.

45.

46.

47.

48.

49.

50.

Sperling JW, Cofield RH, Rowland CM. Minimum fifteen-year follow-up of Neer hemiarthroplasty and total shoulder arthroplasty in patients aged fifty years or younger. J Shoulder Elbow Surg. 2004;13(6):604-613. doi:10.1016/S1058274604001296. Smith RG, Sperling JW, Cofield RH, Hattrup SJ, Schleck CD. Shoulder hemiarthroplasty for steroid-associated osteonecrosis. J Shoulder Elbow Surg. 2008;17(5):685-688. doi:10.1016/j.jse.2008.01.149. Krishnan SG, Nowinski RJ, Harrison D, Burkhead WZ. Humeral hemiarthroplasty with biologic resurfacing of the glenoid for glenohumeral arthritis. Two to fifteen-year outcomes. J Bone Joint Surg Am. 2007;89(4):727-734. doi:10.2106/JBJS.E.01291. Bois AJ, Whitney IJ, Somerson JS, Wirth MA. Humeral head arthroplasty and meniscal allograft resurfacing of the glenoid: a concise follow-up of a previous report and survivorship analysis. J Bone Joint Surg Am. 2015;97(19):1571-1577. doi:10.2106/JBJS.N.01079. Wirth MA. Humeral head arthroplasty and meniscal allograft resurfacing of the glenoid. J Bone Joint Surg Am. 2009;91(5):1109-1119. doi:10.2106/JBJS.H.00677. Elhassan B, Ozbaydar M, Diller D, Higgins LD, Warner JJ. Soft-tissue resurfacing of the glenoid in the treatment of glenohumeral arthritis in active patients less than fifty years old. J Bone Joint Surg Am. 2009;91(2):419-424. doi:10.2106/JBJS.H.00318. Strauss EJ, Verma NN, Salata MJ, et al. The high failure rate of biologic resurfacing of the glenoid in young patients with glenohumeral arthritis. J Shoulder Elbow Surg. 2014;23(3):409-419. doi:10.1016/j. jse.2013.06.001. Nicholson GP, Goldstein JL, Romeo AA, et al. Lateral meniscus allograft biologic glenoid arthroplasty in total shoulder arthroplasty for young shoulders with degenerative joint disease. J Shoulder Elbow Surg. 2007;16(5 suppl):S261-S266. doi:10.1016/j.jse.2007.03.003. Mannava S, Horan MP, Frangiamore SJ, et  al. Return to recreational sporting activities following total shoulder arthroplasty. Orthop J Sports Med. 2018;6(7):2325967118782672. doi:10.1177/2325967118782672. Schumann K, Flury MP, Schwyzer HK, Simmen BR, Drerup S, Goldhahn  J. Sports activity after anatomical total shoulder arthroplasty. Am J Sports Med. 2010;38(10):2097-2105. doi:10.1177/0363546510371368. Henn RF III, Ghomrawi H, Rutledge JR, Mazumdar M, Mancuso CA, Marx RG. Preoperative patient expectations of total shoulder arthroplasty. J Bone Joint Surg Am. 2011;93(22):2110-2115. doi:10.2106/ JBJS.J.01114. Magnussen RA, Mallon WJ, Willems WJ, Moorman CT  III. Longterm activity restrictions after shoulder arthroplasty: an international survey of experienced shoulder surgeons. J Shoulder Elbow Surg. 2011;20(2):281-289. doi:10.1016/j.jse.2010.07.021. Golant A, Christoforou D, Zuckerman JD, Kwon YW. Return to sports after shoulder arthroplasty: a survey of surgeons’ preferences. J Shoulder Elbow Surg. 2012;21(4):554-560. doi:10.1016/j. jse.2010.11.021. Ek ET, Neukom L, Catanzaro S, Gerber  C. Reverse total shoulder arthroplasty for massive irreparable rotator cuff tears in patients younger than 65 years old: results after five to fifteen years. J Shoulder Elbow Surg. 2013;22:1199-1208. doi:10.1016/j.jse.2012.11.016. Ernstbrunner L, Suter A, Catanzaro S, Rahm S, Gerber  C. Reverse total shoulder arthroplasty for massive, irreparable rotator cuff tears before the age of 60 years: long-term results. J Bone Joint Surg Am. 2017;99(20):1721-1729. doi:10.2106/JBJS.17.00095. Bülhoff M, Sowa B, Bruckner T, Zeifang F, Raiss  P. Activity levels after reverse shoulder arthroplasty. Arch Orthop Trauma Surg. 2016;136(9):1189-1193. doi:10.1007/s00402-016-2494-9.

Management of the Aging Athlete With the Sequelae of Shoulder Instability 51.

52.

53.

Matthews CJ, Wright TW, Farmer KW, Struk AM, Vasilopoulos T, King JJ. Outcomes of primary reverse total shoulder arthroplasty in patients younger than 65 years old. J Hand Surg Am. 2019;44(2):104111. doi:10.1016/j.jhsa.2018.11.008. Cole BJ, Yanke A, Provencher MT. Nonarthroplasty alternatives for the treatment of glenohumeral arthritis. J Shoulder Elbow Surg. 2007;16(5 suppl):S231-S240. doi:10.1016/j.jse.2007.03.011. Mitchell JJ, Warner BT, Horan MP, et al. Comprehensive arthroscopic management of glenohumeral osteoarthritis: preoperative factors predictive of treatment failure. Am J Sports Med. 2017;45(4):794-802. doi:10.1177/0363546516668823.

54.

55.

56.

315

Denard PJ, Wirth MA, Orfaly RM. Management of glenohumeral arthritis in the young adult. J Bone Joint Surg Am. 2011;93(9):885-892. doi:10.2106/JBJS.J.00960. Walch G, Badet R, Boulahia A, Khoury  A. Morphologic study of the glenoid in primary glenohumeral osteoarthritis. J Arthroplasty. 1999;14(6):756-760. doi:10.1016/s0883-5403(99)90232-2. Spiegl UJ, Faucett SC, Horan MP, Warth RJ, Millett PJ. The role of arthroscopy in the management of glenohumeral osteoarthritis: a Markov decision model. Arthroscopy. 2014;30(11):1392-1399. doi:10.1016/j.arthro.2014.06.011.

FINANCIAL DISCLOSURES Department of Defense The views presented in the book are those of the individual authors and do not necessarily represent the views of the Department of Defense, its Components, or the US Government.

Authors Dr. Geoffrey D. Abrams has no financial or proprietary interest in the materials presented herein. Dr. Leonard Achenbach has no financial or proprietary interest in the materials presented herein. Dr. Gregory J. Adamson receives financial or material support and research support from Arthrex, Inc. Dr. Robert Arciero receives institutional educational and research funding from Arthrex, Inc; receives institutional educational and research funding from Don-Joy; and is a consultant for Biorez, Inc. Dr. Jaymeson R. Arthur has no financial or proprietary interest in the materials presented herein. Dr. Ashley J. Bassett has no financial or proprietary interest in the materials presented herein. Dr. Asheesh Bedi is a consultant for and receives royalties from Arthrex, Inc. Alexander Beletsky has no financial or proprietary interest in the materials presented herein. Dr. Craig R. Bottoni has no financial or proprietary interest in the materials presented herein. Dr. James P. Bradley is on the board for the American Orthopaedic Society for Sports Medicine and receives royalties from Arthrex, Inc. Dr. Benjamin J. Brill has no financial or proprietary interest in the materials presented herein. Dr. Stephen  F. Brockmeier has relationships with Arthrex, Exactech, Zimmer Biomet, WorkForce Rx, and Springer Publishing. Dr. Jessica L. Brozek has no financial or proprietary interest in the materials presented herein. Dr. Brian Busconi has relationships with COI, Arthrex, and Mitek. Dr. Francis P. Bustos has no financial or proprietary interest in the materials presented herein. Dr. Kenneth L. Cameron receives a nominal amount of royalties from Springer and has no other disclosures related to his chapter. Dr. Morad Chughtai has no financial or proprietary interest in the materials presented herein. Dr. Mark E. Cinque has no financial or proprietary interest in the materials presented herein. Dr. Steven B. Cohen has no financial or proprietary interest in the materials presented herein. Dr. Trey Colantonio has no financial or proprietary interest in the materials presented herein. Dr. Maj. Travis J. Dekker has no financial or proprietary interest in the materials presented herein. Dr. Ian J. Dempsey has no financial or proprietary interest in the materials presented herein. Dr. Jonathan F. Dickens has no financial or proprietary interest in the materials presented herein. Dr. Tracey Didinger has no financial or proprietary interest in the materials presented herein. Dr. Vickie Dills has not disclosed any relevant financial relationships. Dr. Maj. Michael A. Donohue has no financial or proprietary interest in the materials presented herein. Dr. Josef K. Eichinger has no financial or proprietary interest in the materials presented herein. Dr. David Eldringhoff has no financial or proprietary interest in the materials presented herein. Dr. Joseph W. Galvin is a consultant for FH Ortho. He has no conflict of interest pertaining to this topic. Dr. Christopher Gaunder has no financial or proprietary interest in the materials presented herein. - 317 -

318

Financial Disclosures

Dr. Lawrence V. Gulotta receives royalties, consulting, and speaking for Exactech, Inc; receives royalties from ZimmerBiomet, Inc; and is a consultant for Mitek. Dr. Jonathon A. Hinz has no financial or proprietary interest in the materials presented herein. Carolyn A. Hutyra has no financial or proprietary interest in the materials presented herein. Dr. Evan W. James has no financial or proprietary interest in the materials presented herein. Dr. Zackary Johnson has no financial or proprietary interest in the materials presented herein. Dr. Jason A. Jones has no financial or proprietary interest in the materials presented herein. Dr. Lucca Lacheta has no financial or proprietary interest in the materials presented herein. Dr. Laurent LaFosse has no financial or proprietary interest in the materials presented herein. Dr. Brian C. Lau receives research and education support from Arthrex and Wright Medical. Dr. CDR Lance LeClere has no financial or proprietary interest in the materials presented herein. Dr. Thay Q. Lee discloses the following: American Orthopaedic Society for Sports Medicine: board or committee member; American Shoulder and Elbow Surgeons: board or committee member; Arthrex, Inc: paid consultant, research support; Clinics in Orthopaedic Surgery: editorial or governing board; CONMED Linvatec: IP royalties; Coracoid Solutions: stock or stock options; Journal of Shoulder and Elbow Surgery: editorial or governing board, publishing royalties, financial or material support; Smith & Nephew: IP royalties; Stryker: IP royalties; Subchondral Solutions: stock or stock options. Dr. Xinning Li is a consultant, IP, and receives royalties from FH Ortho; is on the editorial board for AJSM and Orthopedic Reviews; and is Associate CME Editor for JBJS. Dr. Kenneth M. Lin has no financial or proprietary interest in the materials presented herein. Lenny Macrina has no financial or proprietary interest in the materials presented herein. Dr. Brandon J. Manderle has no financial or proprietary interest in the materials presented herein. Dr. Eric McCarty is a consultant for and receives royalties from Zimmer Biomet. He receives Fellowship support from Ossur, Smith & Nephew, Arthrex, Mitek, Breg, and DJO and is on the Board of AOSSM. Dr. Bruce S. Miller is a consultant: for Arthrex Inc and is a consultant and receives royalties from FH Orthopedics. Dr. Peter J. Millett discloses that he receives royalties and consultant payments from Arthrex, Inc, Medbridge, and Springer Publishing, which is not related to the subject of this work. He is a paid consultant for Arthrex (exceeding $500.00/year) and he receives royalties from Arthrex for surgical devices not related to this paper. Dr. Millett has stock in VuMedi and received research support the Steadman Philippon Research Institute (a 501(c)(3) nonprofit institution supported financially by private donations and corporate support from the following entities: Smith & Nephew, Inc, Arthrex, Inc, Siemens, Ossur Americas, Inc). Dr. Anthony Miniaci discloses the following: American Orthopaedic Society for Sports Medicine: board or committee member; American Shoulder and Elbow Surgeons: board or committee member; Arthroscopy Association of North America: board or committee member; Arthrosurface: IP royalties, other financial or material support, paid consultant, paid presenter or speaker, research support, stock or stock options; DePuy, a Johnson & Johnson Company: stock or stock Options; International Society of Arthroscopy, Knee Surgery, and Orthopaedic Sports Medicine: board or committee member; Medtronic: stock or stock options; Stryker: other financial or material support, stock or stock options; Trice: paid consultant, stock or stock options; Wolters Kluwer Health—Lippincott Williams & Wilkins: editorial or governing board, publishing royalties, financial or material support; Zimmer: stock or stock options. Dr. Christian Moody has no financial or proprietary interest in the materials presented herein. Dr. Bradley J. Nelson is a consultant for Marrow Access Technologies. There is no potential conflict of interest with his chapter. Dr. Lisa K. O’Brien has no financial or proprietary interest in the materials presented herein. Dr. Brett D. Owens is a consultant for Mitek, Vericel, and Conmed; receives royalties from Conmed; and owns stock in Vivorte. Dr. Michael J. Pagnani has no financial or proprietary interest in the materials presented herein. Liam A. Peebles has no financial or proprietary interest in the materials presented herein.

Financial Disclosures

319

Dr. Matthew A. Posner has no financial or proprietary interest in the materials presented herein. Dr. Matthew  T. Provencher discloses the following: AAOS: board or committee member; AANA: board or committee member; AOSSM: board or committee member; ASES: board or committee member; Arthrex, Inc: IP royalties, paid consultant; Arthroscopy: editorial or governing board; Arthrosurface: honorarium; ISAKOS: board or committee member; Joint Restoration Foundation (Allosource): paid consultant; Knee: editorial or governing board; Orthopedics: editorial or governing board; San Diego Shoulder Institute: board or committee member; SLACK Inc: editorial or governing board, publishing royalties, material or financial support; Society of Military Orthopaedic Surgeons: board or committee member; Patent numbers 9226743, 20150164498, 20150150594, and 20110040339. Research activities supported by Steadman Philippon Research Institute and Vail Health. Jennifer Reed has no financial or proprietary interest in the materials presented herein. Dr. Jeremy K. Rush has no financial or proprietary interest in the materials presented herein. Dr. Linsen T. Samuel has no financial or proprietary interest in the materials presented herein. Dr. Barry I. Shafer has no financial or proprietary interest in the materials presented herein. Dr. Mark Slabaugh has no financial or proprietary interest in the materials presented herein. Dr. Andrew Swiergosz has no financial or proprietary interest in the materials presented herein. Dr. Lauren A. Szolomayer has no financial or proprietary interest in the materials presented herein. Dr. Dean C. Taylor receives research and education support from Arthrex, Breg, DJOrtho, Histogenics, and Smith & Nephew. He is a paid consultant for Mitek and receives IP royalties from Depuy. Dr. Samuel A. Taylor receives royalties, consulting, and speaking from DJO. Dr. David J. Tennent has no financial or proprietary interest in the materials presented herein. Dr. Fotios Paul Tjoumakaris has no financial or proprietary interest in the materials presented herein. Dr. John M. Tokish is a consultant and receives royalties, fellowship, and research support from Arthrex; is a consultant and receives fellowship support from Depuy-Mitek; and is Associate Editor of Journal of Shoulder and Elbow Surgery. Dr. Nikhil N. Verma has served as a paid consultant and received research support from Arthrex, Inc, and has received intellectual property royalties and research support from Smith & Nephew. Dr. Matthew L. Vopat has no financial or proprietary interest in the materials presented herein. Dr. Brian R. Waterman discloses the following: AAOS: board or committee member; American Orthopaedic Society for Sports Medicine: board or committee member; Arthrex, Inc: research support; Arthroscopy: editorial or governing board, publishing royalties, financial or material support; Arthroscopy Association of North America: board or committee member; Elsevier: publishing royalties, financial or material support; FH Ortho: paid consultant; Kaliber AI: stock or stock options, unpaid consultant; Sparta Science: unpaid consultant; Vericel: paid presenter or speaker; Vivorte: stock or stock options. Dr. Jack W. Weick has no financial or proprietary interest in the materials presented herein. Dr. Kevin E. Wilk has no financial or proprietary interest in the materials presented herein.