Prevention and Management of Common Fracture Complications [1 ed.] 9781617117121, 9781556429750

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Edited by

Michael T. Archdeacon, MD, MSE

Professor and Vice-Chairman of Orthopaedic Surgery University of Cincinnati College of Medicine Division Director for Orthopaedic Trauma Surgery University of Cincinnati Hospital Cincinnati, Ohio

Jeffrey O. Anglen, MD, FACS Professor of Orthopaedics Indiana University School of Medicine Indianapolis, Indiana

Robert F. Ostrum, MD

Director of Orthopaedic Trauma Cooper University Hospital Professor of Surgery UMDNJ-Robert Wood Johnson Medical School Camden, New Jersey

Dolfi Herscovici Jr, DO

Associate Professor of Clinical Orthopedics University of South Florida Tampa, Florida

www.slackbooks.com ISBN: 978-1-55642-975-0 Copyright © 2012 by SLACK Incorporated 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. Published by: SLACK Incorporated 6900 Grove Road Thorofare, NJ 08086 USA Telephone: 856-848-1000 Fax: 856-848-6091 www.slackbooks.com Contact SLACK Incorporated for more information about other books in this field or about the availability of our books from distributors outside the United States. Library of Congress Cataloging-in-Publication Data Prevention and management of common fracture complications / [edited by] Michael T. Archdeacon ... [et al.]. p. ; cm. Includes bibliographical references and index. Summary: “This is a quick reference guide for the prevention and treatment of common fracture complications, including the etiology of the complications, factors the surgeon can control in the operating room, and how to treat complications that arise”--Provided by publisher. ISBN 978-1-55642-975-0 (pbk.) I. Archdeacon, Michael T. [DNLM: 1. Fractures, Bone--complications--Handbooks. 2. Fractures, Bone--therapy--Handbooks. WE 39] 616.7’1--dc23

2011047134

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; web site: www.copyright.com; email: info@ copyright.com

DEDICATION This text is dedicated to all of the patients who have suffered the complications outlined in this book. Although every surgeon attempts to minimize complications, they inevitably will occur. We hope that the knowledge gained through treating these patients will ultimately improve outcomes for future patients. —Michael T. Archdeacon, MD, MSE

I dedicate this book to the fracture surgeons of the future: our fellows, residents, and students. May they avoid our mistakes, while being ever vigilant for new ways that things can go awry. Do not expect fairness, but practice it; embrace humility before it embraces you; and cultivate compassion over righteousness. —Jeffrey O. Anglen, MD, FACS

This book is dedicated to all of those patients with fractures who have allowed us to treat them and become a part of their lives and their road to recovery. It is our hope that this text will enable the orthopedic surgeon treating fracture patients to recognize, treat, and hopefully avoid the complications associated with their management. —Robert F. Ostrum, MD

This text is dedicated to the orthopedic surgeon who provides a wide spectrum of care for his or her patients. It is the hope of the editors that the information in this book will provide a little insight into the management of common and complex injuries to help decrease the complications that are a part of all of our practices. —Dolfi Herscovici Jr, DO

CONTENTS Dedication ................................................................................................................................v Acknowledgments ...................................................................................................................xi About the Editors ..................................................................................................................xiii Contributing Authors ............................................................................................................xv Preface ...................................................................................................................................xix Foreword by Berton R. Moed, MD ....................................................................................xxi

Section I

General ............................................................................................... 1

Chapter 1

Preventing Complications in Orthopedic Communication ...................3 Michael Suk, MD, JD, MPH, FACS and Eric Stiefel, MD

Chapter 2

Infection........................................................................................................ 11 Jeffrey O. Anglen, MD, FACS

Chapter 3

Deep Venous Thrombosis.......................................................................... 21 Catherine A. Humphrey, MD

Chapter 4

Fracture Complications in the Growing Skeleton ................................. 31 Christine B. Caltoum, MD

Chapter 5

Nonunion .....................................................................................................43 Jeffrey O. Anglen, MD, FACS

Chapter 6

Malunion ...................................................................................................... 53 Brady Barker, MD and Kurtis Staples, MD

Chapter 7

Arthrofibrosis/Contracture....................................................................... 67 Michael P. Rusnak, MD

Section II Upper Extremity ............................................................................. 75 Chapter 8

Complications of Clavicle Fractures ........................................................77 Janos P. Ertl, MD

Chapter 9

Complications of Proximal and Diaphyseal Humerus Fractures ....... 85 Eric S. Moghadamian, MD and Raymond D. Wright, MD

Chapter 10

Elbow Fractures........................................................................................... 99 Gregory J. Della Rocca, MD, PhD, FACS

Chapter 11

Radial and Ulnar Shaft, Monteggia, and Galeazzi Fractures ............ 111 Susan McDowell, MD and Brian H. Mullis, MD

Chapter 12

Distal Radius Fractures ............................................................................ 121 Brett D. Crist, MD, FACS and Yvonne M. Murtha, MD

Section III Pelvis and Acetabulum ............................................................... 131 Chapter 13

Open Pelvic Fracture: Infection .............................................................. 133 Marcus F. Sciadini, MD

Chapter 14

Sacral Fractures: Loss of Reduction/Failure of Fixation .................... 141 H. Claude Sagi, MD

viii

Contents

Chapter 15

Iliosacral Screw Malposition ................................................................... 151 A. Michael Harris, MD and Paul B. Gladden, MD

Chapter 16

Pelvic Ring Disruption: Malalignment ................................................. 157 Kyle F. Dickson, MD, MBA

Chapter 17

Acetabulum Fractures: Malunion .......................................................... 165 Michael Beltran, MD and Cory Collinge, MD

Chapter 18

Acetabulum Fractures: Nerve Palsy ...................................................... 171 George V. Russell, MD and Scott A. Wingerter, MD, PhD

Chapter 19

Acetabulum Fractures: Heterotopic Ossification ................................. 179 Madhav A. Karunakar, MD

Section IV Hip ................................................................................................... 189 Chapter 20

Femoral Head Fracture: Osteonecrosis and Hip Instability .............. 191 Samuel A. McArthur, MD and Walter W. Virkus, MD

Chapter 21

Femoral Neck Fracture: Nonunion ........................................................ 199 Michael T. Archdeacon, MD, MSE

Chapter 22

Intertrochanteric Fractures: Lag Screw Cut Out and Failure of Fixation ..................................................................................... 207 Brian D. Solberg, MD

Chapter 23

Intertrochanteric Fractures: Lateral Wall Fractures ............................ 213 Bradley Merk, MD and Erik Eller, MD

Chapter 24

Subtrochanteric Fracture: Varus Malalignment/Nonunion .............. 217 Robert R. L. Gray, MD and Anthony T. Sorkin, MD

Section V Femur and Tibia ........................................................................... 223 Chapter 25

Femoral Shaft Fractures: Malunion and Nonunion ............................225 Robert F. Ostrum, MD

Chapter 26

Supracondylar Femur Fractures ............................................................. 235 Michael Suk, MD, JD, MPH, FACS and Pratik Desai, MD, MS

Chapter 27

Patella Fracture: Complications .............................................................. 247 Matthew J. White, MD and Gerald J. Lang, MD

Chapter 28

Tibial Plateau Fracture: Infection, Failure of Fixation, and Instability .......................................................................................... 255 Eric D. Farrell, MD and Paul M. Lafferty, MD

Chapter 29

Tibial Shaft Fracture: Infection, Nonunion, and Malunion ............... 265 John A. Scolaro, MD and Samir Mehta, MD

Section VI Foot and Ankle ............................................................................. 279 Chapter 30

Pilon Fractures ......................................................................................... 281 Sean E. Nork, MD

Chapter 31

Ankle Fractures and Syndesmotic Injuries........................................... 289 Dolfi Herscovici Jr, DO and Julia M. Scaduto, ARNP

Contents

ix

Chapter 32

Talus ............................................................................................................ 299 Stefan Rammelt, MD, PhD and Hans Zwipp, MD, PhD

Chapter 33

Calcaneal Fractures .................................................................................. 317 James B. Carr, MD

Chapter 34

Midfoot Fractures: Lisfranc, Cuboid, Navicular .................................. 329 Clifford B. Jones, MD, FACS and Marlon O. Coulibaly, MD

Chapter 35

Metatarsal Fractures .................................................................................345 Robert Vander Griend, MD

Financial Disclosures ........................................................................................................... 351

ACKNOWLEDGMENTS I would like to acknowledge my family for their support while composing this text. The time taken to put this book together was certainly time spent away from each of them, specifically Lynne, Alyssa, Chad, Kyle, and Natalie Archdeacon. —Michael T. Archdeacon, MD, MSE

I would like to thank all the authors for their hard work and patience with our edits. Thanks to my family—Diane, Becca, Sarah, Zack, and Lexi—for their support. —Jeffrey O. Anglen, MD, FACS

I would like to thank my family for their support and understanding. A bad day for me is a bad day for them. My wife, Joan, has stood by my side through the good and bad times and has always been my biggest supporter, and I couldn’t have done any of this without her. My two boys, Sam and Zach, have been great during all of the times that I have been late and have been understanding of the demands that it takes to do this job. Finally, I would like to thank all of those health care professionals who work alongside of us during those long, often difficult days. To all of you, I say thanks for being there. —Robert F. Ostrum, MD

I would like to especially thank two people for mentoring me in the art and science of orthopedic traumatology: B. Roy Moed, MD, and the late Fred Behrens, MD. Thank you both for having the patience to answer all my questions and explain the things I did not understand. I would also like to thank my beautiful wife, Lisa, for her support and for being my sounding board, my confidante, and my de facto editor. Last, I would like to thank my four boys—Derek, Jake, Brad, and Troy—for putting up with me when I sat in my office rewriting and editing manuscripts. —Dolfi Herscovici Jr, DO

ABOUT THE EDITORS Michael T. Archdeacon, MD, MSE, is Professor and Vice-Chairman of Orthopaedic Surgery at the University of Cincinnati College of Medicine. Dr. Archdeacon is currently the Division Director for Orthopaedic Trauma Surgery and the Immediate Past Chief of Staff at the University Hospital in Cincinnati, Ohio. He has more than 10 years of experience managing complex fractures as well as the complications associated with these injuries.

Jeffrey O. Anglen, MD, FACS, is Professor of Orthopaedics at Indiana University School of Medicine. He is a former President of the Orthopaedic Trauma Association, a member of the American College of Surgeons Committee on Trauma, and Deputy Editor for Trauma of the Journal of the American Academy of Orthopaedic Surgeons. He has been dealing with the complications of fracture care (his own as well as others) since completing his fellowship in 1991, and probably before.

Robert F. Ostrum, MD, is the Director of Orthopaedic Trauma at Cooper University Hospital and a Professor of Surgery at UMDNJ-Robert Wood Johnson Medical School. He has been working in level I trauma centers for 25 years, treating fracture and trauma patients and managing their associated complications.

Dolfi Herscovici Jr, DO, is an Associate Professor of Clinical Orthopedics at the University of South Florida. He has more than 20 years of experience managing complex trauma, especially injuries and reconstructive surgery of the foot and ankle. He is currently in practice at the Florida Orthopedic Institute in Tampa, Florida.

CONTRIBUTING AUTHORS Brady Barker, MD (Chapter 6) Central Utah Clinic Provo, Utah Michael Beltran, MD (Chapter 17) CPT, MC, USA San Antonio Military Medical Center San Antonio, Texas Christine B. Caltoum, MD (Chapter 4) Assistant Professor of Clinical Pediatric Orthopedic Surgery Program Director Department of Orthopedic Surgery Indiana University School of Medicine Indianapolis, Indiana James B. Carr, MD (Chapter 33) Associate Clinical Professor Orthopedics University of South Carolina Columbia, South Carolina Cory Collinge, MD (Chapter 17) THR Harris Methodist Fort Worth Hospital Fort Worth, Texas Marlon O. Coulibaly, MD (Chapter 34) Department of Traumatology University Hospital Bergmannsheil GmbH Ruhr-University Bochum Bochum, Germany Brett D. Crist, MD, FACS (Chapter 12) Associate Professor Co-Director Orthopaedic Trauma Service Co-Director Orthopaedic Trauma Fellowship Associate Director Joint Preservation Service Department of Orthopaedic Surgery University of Missouri Columbia, Missouri

Gregory J. Della Rocca, MD, PhD, FACS (Chapter 10) Orthopaedic Trauma Service University of Missouri Columbia, Missouri Pratik Desai, MD, MS (Chapter 26) Chief Resident University of Florida Health Science Center Jacksonville, Florida Kyle F. Dickson, MD, MBA (Chapter 16) Baylor College of Medicine Houston, Texas Erik Eller, MD (Chapter 23) Feinberg School of Medicine Northwestern University Chicago, Illinois Janos P. Ertl, MD (Chapter 8) Chief, Sports Medicine Indiana University Chief, Orthopaedic Surgery Wishard Hospital Assistant Professor Department of Orthopaedic Surgery Indiana University School of Medicine Indianapolis, Indiana Eric D. Farrell, MD (Chapter 28) Assistant Professor Orthopaedic Trauma Service UCLA Department of Orthopaedic Surgery Los Angeles, California Paul B. Gladden, MD (Chapter 15) Associate Professor Clinical Orthopedics Tulane University New Orleans, Louisiana

xvi

Contributing Authors

Robert R. L. Gray, MD (Chapter 24) Assistant Professor Department of Orthopaedic Surgery University of Miami Miller School of Medicine Miami, Florida A. Michael Harris, MD (Chapter 15) Assistant Professor University of Florida Jacksonville, Florida Catherine A. Humphrey, MD (Chapter 3) Assistant Professor Department of Orthopaedics University of Rochester School of Medicine and Dentistry Rochester, New York Clifford B. Jones, MD, FACS (Chapter 34) Michigan State University College of Human Medicine Department of Surgery Orthopaedic Associates of Michigan Grand Rapids, Michigan Madhav A. Karunakar, MD (Chapter 19) Department of Orthopaedics Carolinas Medical Center Charlotte, North Carolina Paul M. Lafferty, MD (Chapter 28) Assistant Professor University of Minnesota Regions Hospital Saint Paul, Minnesota Gerald J. Lang, MD (Chapter 27) Department of Orthopedics University of Wisconsin School of Medicine and Public Health Madison, Wisconsin Samuel A. McArthur, MD (Chapter 20) Rush University Medical Center Chicago, Illinois Susan McDowell, MD (Chapter 11) Department of Orthopaedic Surgery Indiana University School of Medicine Indianapolis, Indiana

Samir Mehta, MD (Chapter 29) Orthopaedic Trauma & Fracture Service University of Pennsylvania Department of Orthopaedic Surgery Philadelphia, Pennsylvania Bradley Merk, MD (Chapter 23) Feinberg School of Medicine Northwestern University Chicago, Illinois Berton R. Moed, MD (Foreword) Professor and Chairman Department of Orthopaedic Surgery Saint Louis University School of Medicine St. Louis, Missouri Eric S. Moghadamian, MD (Chapter 9) Assistant Professor Orthopaedic Traumatology University of Kentucky Department of Orthopaedics and Sports Medicine Kentucky Clinic Lexington, Kentucky Brian H. Mullis, MD (Chapter 11) Chief, Orthopaedic Trauma Service Assistant Professor Department of Orthopaedic Surgery Indiana University School of Medicine Indianapolis, Indiana Yvonne M. Murtha, MD (Chapter 12) Advanced Orthopaedic Associates Wichita, Kansas Sean E. Nork, MD (Chapter 30) Harborview Medical Center University of Washington Department of Orthopaedic Surgery Seattle, Washington Stefan Rammelt, MD, PhD (Chapter 32) Professor Trauma and Reconstructive Surgery Carl Gustav Carus University Hospital Dresden, Germany Michael P. Rusnak, MD (Chapter 7) Orthopaedic Center of the Rockies Fort Collins, Colorado

Contributing Authors George V. Russell, MD (Chapter 18) Associate Professor Department of Orthopedic Surgery University of Mississippi School of Medicine Jackson, Mississippi

Michael Suk, MD, JD, MPH, FACS (Chapters 1, 26) Chairman Department of Orthopaedic Surgery Geisinger Health System Danville, Pennsylvania

H. Claude Sagi, MD (Chapter 14) Director of Fellowship Education and Research Orthopaedic Trauma Service Florida Orthopedic Institute Clinical Associate Professor of Orthopaedic Surgery University of South Florida Tampa, Florida

Robert Vander Griend, MD (Chapter 35) Associate Professor Division Chief Foot and Ankle University of Florida Department of Orthopaedics and Rehabilitation Gainesville, Florida

Julia M. Scaduto, ARNP (Chapter 31) Florida Orthopaedic Institute Tampa, Florida Marcus F. Sciadini, MD (Chapter 13) Associate Professor of Orthopaedics University of Maryland School of Medicine Shock Trauma Orthopaedics Baltimore, Maryland

xvii

Walter W. Virkus, MD (Chapter 20) Associate Professor Orthopaedic Surgery Residency Program Director Rush University Medical Center Cook County Hospital Chicago, Illinois Matthew J. White, MD (Chapter 27) University of Wisconsin Hospitals and Clinics Madison, Wisconsin

John A. Scolaro, MD (Chapter 29) Orthopaedic Trauma & Fracture Service University of Pennsylvania Department of Orthopaedic Surgery Philadelphia, Pennsylvania

Scott A. Wingerter, MD, PhD (Chapter 18) Department of Orthopedic Surgery University of Mississippi School of Medicine Jackson, Mississippi

Brian D. Solberg, MD (Chapter 22) LA Orthopaedic Specialists Assistant Clinical Professor Department of Orthopaedic Surgery Keck-USC School of Medicine Los Angeles, California

Raymond D. Wright, MD (Chapter 9) Orthopaedic Traumatology University of Kentucky Department of Orthopaedics and Sports Medicine Kentucky Clinic Lexington, Kentucky

Anthony T. Sorkin, MD (Chapter 24) Director, Orthopedic Trauma Rockford Orthopedic Associates Rockford, Illinois Kurtis Staples, MD (Chapter 6) Sonoran Orthopaedic Trauma Surgeons Scottsdale, Arizona Eric Stiefel, MD (Chapter 1) Division of Orthopaedic Trauma University of Florida-Shands Jacksonville, Florida

Hans Zwipp, MD, PhD (Chapter 32) Professor Trauma and Reconstructive Surgery Carl Gustav Carus University Hospital Dresden, Germany

PREFACE Prevention and Management of Common Fracture Complications was composed because every orthopedic surgeon faces complications in the management of fractures. This book offers the practicing orthopedic surgeon a quick reference for the prevention and treatment of common fracture complications, with the text focused on the etiology of the complications, the factors the surgeon controls in the operating room, and the treatment of these complications once they occur. The editors believed that a quick reference text dedicated entirely to the prevention and management of fracture complications was not readily available. Thus, the editors hope that this book will serve as a convenient and invaluable asset for the practicing orthopedic surgeon. For simplification, the book is arranged on an anatomic basis with a separate editor and contributors for each section. Each editor has specific interest and experience in his respective sections, thus providing expert overview of each topic.

FOREWORD Murphy’s Law If anything can go wrong, it will. —Attributed to Capt. Ed Murphy Air Force Project MX981, Edwards Air Force Base, 1949

O’Toole’s Commentary on Murphy’s Law Murphy was an optimist.

Any fracture surgeon who has treated a patient who subsequently developed a complication can appreciate the irony and exasperation expressed by the authors of Murphy’s Law and its many corollaries. Of course, no surgeon sets out intent on creating a complication, yet create them we do. This is not so surprising. For each and every orthopedic malady, as well as treatment course, one can find an abundant list of potential untoward events. Therefore, if we treat enough patients and/ or do enough cases, a patient with a devastating complication is bound to find us. Consequently, all practicing orthopedic surgeons providing fracture care will eventually encounter complications. Regardless of this situation, there has existed no quick reference text specifically dedicated to this aspect of trauma care. This need in the current practice of orthopedic fracture care is now fulfilled. I am honored to have been invited by Drs. Archdeacon, Anglen, Ostrum, and Herscovici to write the Foreword to this informative and well-timed textbook. Over the past decade an emphasis has been placed on techniques and procedures motivated by the desire to decrease complications and improve overall outcome. Despite the continued advances in treatment methods, complications continue to occur. Occasionally, the complication is as novel as the treatment itself. Therefore, it is extremely important that the treating physician be as well versed in the management of potential fracture complications as the traumatic event itself. In this regard, the authors of Prevention and Management of Common Fracture Complications have created a welcome addition to the armamentarium of the practicing orthopedic surgeon. —Berton R. Moed, MD Professor and Chairman Department of Orthopaedic Surgery Saint Louis University School of Medicine Saint Louis, Missouri

I

General

1 Preventing Complications in Orthopedic Communication Michael Suk, MD, JD, MPH, FACS and Eric Stiefel, MD

The physician-patient relationship exists as a dynamic partnership between two individuals that ideally serves to benefit both parties. At the core of this relationship is the concept of communication. Efforts to improve physician-patient communication have been shown to improve patient compliance and health outcomes, as well as enhance both patient and physician satisfaction.1,2 Effective communication skills have also been linked to a reduction in malpractice lawsuits.3,4 Despite the importance of communication to patient outcomes, many physicians have not developed skills in this area. Studies have shown that physician communication styles, including interrupting patients at an average of 18 seconds into their encounter and use of guided, closed-ended questions, may result in incomplete information access.5 Other studies have demonstrated that orthopedic surgeons, too, have had difficulty recognizing self-deficits in communication. In a survey conducted by the American Academy of Orthopaedic Surgeons (AAOS), 75% of surgeons surveyed believed that they communicated satisfactorily with their patients, but only 21% of patients reported satisfactory communication with their physician.6

COMMUNICATION CONCEPTS The patient-physician interaction can be conceived as being composed of several components, including initiation, exchange, education, and resolution. The initiation phase establishes a rapport and framework for the rest of the encounter. The exchange component is where data are collected and represents an important opportunity to manage the patient’s expectations with regard to outcome.7,8 Education is an important and underappreciated part of why people visit the physician. The resolution of a patient encounter sets the stage for further diagnosis or treatments (Table 1-1). 3

Archdeacon MT, Anglen JO, Ostrum RF, Herscovici D Jr, eds. Prevention and Management of Common Fracture Complications (pp 3-10). © 2012 SLACK Incorporated.

4

Chapter 1

Table 1-1

Communication Concepts COMMUNICATION CONCEPT

TIPS

Initiation

§ § §

§ §

§

§

§

Exchange

§

§

§ § §

Knock on the door of the exam room before entering. First impressions are important; physicians should dress appropriately and maintain professionalism. Introduce yourself and others who are with you, mention the role of each person in your entourage. Upon introduction, address the patient using his or her name and the appropriate courtesy title (Mr., Ms., Miss, etc). Sit. Try to recognize all parties present and remember to obtain permission prior to discussing personal medical issues when other individuals are present. Use nonverbal communication to relay interest and understanding for the patient’s concerns, and maintain eye contact. Smile. Be mindful of facial expressions. Even though you may not be looking at the patient, the patient will be looking at you. Engage the patient when reviewing electronic medical records or radiographs, and avoid turning your back to the patient without explanation. Use verbal and nonverbal techniques to demonstrate that you are actively listening to the patient, and provide structure to the patient’s thoughts by asking for clarification and summarizing the patient’s list of concerns. Make explicit statements that demonstrate empathy and understanding of the significance of what the patient is relating (eg, “That must have been very painful”). Remember to redirect the patient back to the open-ended discussion that was previously initiated. Remember to allot adequate time to examining the patient and addressing any late concerns. Apologize if you are running behind. Acknowledge how long people have been waiting. Do not rush through the visit, even if you feel pressured and the visit seems of low importance to you. (continued)

Preventing Complications in Orthopedic Communication

5

Table 1-1 (continued)

Communication Concepts COMMUNICATION CONCEPT

TIPS

Education

§

§

§

Resolution

§

§

§

When educating patients, avoid overuse of technical terminology, jargon, or abbreviations. Provide the patient with appropriate medical terminology of his or her ailment followed by a brief description of the injury in layman’s terms. Tell them what it means. Physicians take for granted the implications of their diagnoses, but patients do not have the same context. Refer patients to reliable resources, such as the AAOS patient education Web site, and be prepared to discuss any questions that may arise when the patient returns after accessing your recommended source. Provide the patient with a summary of important points, and encourage compliance with the treatment regimen and follow-up appointments. At the end of the visit, specifically ask if you have answered all of their questions. “Have I answered all of your questions?” is different from “Do you have any more questions?” Consider setting up a follow-up appointment, and appropriately document the patient’s additional concerns so that they may be addressed earlier during the next encounter.

INFORMED CONSENT The legal precedent requiring that a patient receive informed consent prior to undergoing any type of procedure, treatment, or intervention is well established in the United States. Prior to making an educated decision to undergo a procedure, the patient should be informed, in detail, regarding the risks and limitations of that procedure in order to appropriately weigh them against the benefits he or she plans to receive. While formal written documentation of informed consent is an important adjunct of communication, it should not replace the obligation to provide adequate “face time” in a private setting to answer questions and discuss expectations. In a study published in 1980, investigators analyzed surgical consent forms from five hospitals to evaluate the readability of the language. All five of the written consent forms contained language requiring a reading level consistent with upper-level undergraduate or graduate comprehension.9 In 2005, Bhattacharyya and colleagues reviewed claims from 28 lawsuits, in which informed consent was involved in the allegation of malpractice, and found that performing informed consent during the office encounter positively correlated with a successful defense.10

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Chapter 1

Rooted in the process of informed consent are the core goals of patient enlistment and education. Rather than considering the informed consent as a waiver of liability, the consenting physician should look at the process as a platform for patient education with specific endpoints in regards to the risk, benefits, realistic outcomes, and limitations of a given procedure. Similar to the verbal exchange, one should avoid exclusive use of medical terminology on the documented informed consent form.11 By performing the consent in the appropriate setting and dedicating time for discussion of concepts and concerns, the informed consent process can be used as a tool to improve physician-patient communication.

ADVERSE OUTCOMES AND MALPRACTICE The correlation between malpractice litigation and poor physician-patient communication appears to be more significant than that between malpractice litigation and the adverse event.12 Detailed analysis of plaintiff malpractice depositions has led to the identification of frequently cited “relationship issues,” which stem from poor physician communication, as the most common primary grounds for filing malpractice litigation.13 In a retrospective telephone survey to evaluate patients’ perceptions of their physician and to search for a link between malpractice suits and patients’ subjective satisfaction with care, the study grouped physicians into “no claims,” “high frequency,” and “high pay” based on the physician’s malpractice litigation history. The most frequently noted complaint directed to the high-frequency, high-pay group was “the perception that the physician would not offer information and would not listen” as well as a “lack of concern and respect for the patient.”14 In a similar analysis of highfrequency and low-frequency malpractice physicians, it was found that no-claims physicians averaged almost 4 minutes longer per encounter and were more likely to be seated during the interview.15 While the primary goal of improving communication skills should remain improvement of patient outcomes, development of rapport, and promoting patientcentered care, the implementation of evidence-based communication tools has also been shown to significantly limit a physician’s exposure to malpractice.

DISCUSSION OF COMPLICATIONS AND DISCLOSURE OF MEDICAL MISTAKES Adverse medical outcomes in orthopedic surgery exist on a spectrum of severity from disappointing but inconsequential to life threatening. In a survey conducted to evaluate the physician’s insight into the adverse outcome disclosure process, 79% of responding physicians recalled delivering bad news to patients within 4 weeks of completing the survey.16 Assuming the appropriate steps have been taken to ensure satisfactory communication throughout the treatment process, the disclosure process of suboptimal medical outcomes may proceed more efficiently; however, it may remain stressful for both the patient and provider.17 Similar to the manner in which one might plan preoperatively for a complex surgical case, the physician should prepare prior to entering into difficult discussions with patients. An adverse event, even when due to physician negligence, usually does not result in legal ramifications.18 Understand and anticipate how the patient

Preventing Complications in Orthopedic Communication

7

Table 1-2

Tips for Discussing Complications and Adverse Events §

§

§ § §

Establish the appropriate setting and timing to deliver news to the patient, and use verbal and nonverbal communication skills to relay respect and understanding for the patient’s situation. Consider individualizing the encounter by asking the patient what his or her preference may be in regards to privacy, timing, location, and level of detail. For example, some patients may desire to have a close friend or family member present during the discussion, while others may wish to be alone. Allow the patient to dictate the pace and level of detail during the disclosure process. Do not delay disclosure or attempt to mislead or cover up the nature or presence of an adverse event. Consider using a brief statement forewarning the information to follow. An opening statement, such as “I am sorry, but I have some difficult news,” may help prepare the patient for its delivery.

will respond and what information he or she may be looking for next. In a survey of patients’ family members following a traumatic death, the communicator’s attitude was the most important feature of the interaction, followed by clarity of information, respect for privacy, and ability to answer questions (Table 1-2).19 It may be beneficial to direct the discussion based on what the patient may or may not already know. In other words, ask the patient about his or her understanding of the nature of his or her medical event, educate the patient on the nature of the event and the next steps in treatment, and finally ask the patient to repeat the facts that he or she believes are most relevant to the current situation. Do not delay disclosure or attempt to mislead or cover up the nature or presence of an adverse event. In a patient-response survey conducted in 2006, 92% of patients reported that they would be more likely to file a lawsuit if they felt that the physician or hospital tried to hide an error.20

FULL DISCLOSURE In an effort to expedite closure, strengthen malpractice defense, and promote an environment of learning from mistakes, the University of Michigan Health System adopted a new policy regarding the management of adverse events and medical errors in 2001. At the root of this new policy was the concept of early, full disclosure of medical errors even under circumstances in which the disclosure could be entered into future litigation claims. Upon the first year of implementation, the savings were estimated at $2.2 million. Since implementing their unique disclosure policy, the Michigan health care system has experienced a significant reduction in malpractice lawsuits, as well as an estimated savings of 50% per case in cost of legal defense.21 Another way surgeons can acknowledge error is to apologize. In doing so, one takes responsibility while at the same time communicates regret for having caused

8

Chapter 1

harm. Apologies have the potential to decrease the risk of a medical malpractice lawsuit and mitigate malpractice settlements.22 Some states have passed “apology laws,” which allow defendants to exclude statements of sympathy or regret from being used as evidence in a malpractice case in order to encourage physicians to disclose medical errors to patients.23 Despite the fact that patients indicate they want and expect explanations and apologies after medical errors and physicians indicate they want to apologize, in practice, physicians are largely reluctant to disclose medical errors to patients, patients’ families, and even other physicians. Despite this, apologies can play an important role in resolving disputes involving medical error. Disclosure fosters an environment of education and protects the sanctity of the physician-patient relationship. As an aspect of patient-centered care, disclosure also allows the patient to participate in decisions to undergo future medical intervention and treatments. In the setting of adverse events and medical errors, it is often stated that physicians, just like patients, are human. However, we should remember that it is not the presence of error that makes us human, but rather the manner in which we contend with the consequences.

REFERENCES 1. Steward MA. Effective physician-patient communication and health outcomes: a review. Can Med Assoc J. 1995;152:1423-1433. 2. Greenfield S, Kaplan S, Ware JE. Expanding patient involvement in care: effects on patient outcomes. Ann Intern Med. 1985;102:520-528. 3. Bhattacharyya T. Evidence-based approaches to minimizing malpractice risk in orthopedic surgery. Orthopedics. 2005;28(4):378-381. 4. Levinson W, Roter D, Mullooly J, Dull V, Frankel R. Physician-patient communication. The relationship with malpractice claims among primary care physicians. JAMA. 1997;277(7):553-559. 5. Beckman H, Frankel R. The effect of physician behavior on the collection of data. Ann Intern Med. 1984;101(5):692-696. 6. Canale S. How the orthopaedist believes he is perceived by the public and how the public actually perceives the orthopaedist. Presented at the annual meeting of the American Association of Orthopaedic Surgeons, March 15-18, 2000. 7. Howell SM, Rogers SL. Method for quantifying patient expectations and early recovery after total knee arthroplasty. Orthopedics. 2009;32(12):884-890. 8. Kadzielski J, Malhotra L, Aurakowski D, Lee S, Jupiter J, Ring D. Evaluation of preoperative expectations and patient satisfaction after carpal tunnel release. J Hand Surg Am. 2008;33(10):1783-1788. 9. Grundner T. On the readability of surgical consent forms. N Engl J Med. 1980;302(16):900902. 10. Bhattacharyya T, Yeon H, Harris M. The medical-legal aspects of informed consent in orthopaedic surgery. J Bone Joint Surg Am. 2005;87(11):2395-2400. 11. Siddins M, Klinken E, Vocale L. Adequacy of consent documentation in a specialty surgical unit: time for community debate? Med J Aust. 2009;191(5):259-262. 12. Brennan TA, Leape LL, Laird N. Incidence of adverse events and negligence in hospitalized patients. Results of the Harvard Medical Practice Study I. N Engl J Med. 1996;335(26):19631967. 13. Beckman H, Markakis K, Suchman A, Frankel R. The doctor-patient relationship and malpractice. Lessons from plaintiff depositions. Arch Intern Med. 1994;154(12):1365-1370. 14. Hickson GB, Clayton EW, Entman SS, et al. Obstetricians’ prior malpractice experience and patients’ satisfaction with care. JAMA. 1994;272(20):1583-1587.

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15. Levinson W, Roter DL, Mullooly JP, Dull VT, Frankel RM. Physician-patient communication. The relationship with malpractice claims among primary care physicians. JAMA. 1997;277(7):553-559. 16. Ptacek JT, Fries EA, Eberhardt TL, Ptacek JJ. Breaking bad news to patients: physicians’ perception of the process. Support Care Cancer. 1999;7(3):113-120. 17. Ptacek JT, Eberhardt TL. Breaking bad news: a review of the literature. JAMA. 1996;276(6):496-502. 18. Localio AR, Lawthers AG, Brennan TA, et al. Relation between malpractice claims and adverse events due to negligence. Results of the Harvard Medical Practice Study III. N Engl J Med. 1991;325(4):245-251. 19. Jurkovich GJ, Pierce B, Pananen L, Rivara FP. Giving bad news: the family perspective. J Trauma. 2000;48(5):865-870. 20. Boothman RC. Apologies and a strong defense at the University of Michigan Health System. Physician Exec. 2006;32(2):7-10. 21. DerGurahian J. When sorry is enough. Study finds owning up to mistakes better approach. Mod Health. 2009;39(45):17. 22. Robbennolt JK. Apologies and medical error. Clin Orthop Relat Res. 2009;467(2):376-382. 23. Wei M. Doctors, apologies, and the law: an analysis and critique of apology laws. J Health Law. 2007;40(1):107-159.

2 Infection Jeffrey O. Anglen, MD, FACS

Infection is one of the most dreaded complications of fracture surgery. Tremendous efforts are taken to lower the risk of infection, and yet it still occurs. More than 500,000 surgical site infections (SSIs) occur in the United States every year, a rate of approximately 2.8 per 100 operations. Each orthopedic SSI results, on average, in 1 additional day of hospitalization during the initial stay, 14 additional days of hospitalization over the course of treatment, and a nearly four-fold increase in direct costs of hospitalization. An infection increases the overall cost of care by approximately 300% on average. Orthopedic patients who develop SSI have an average of twice as many hospitalizations and operations as those who do not.1 Overall, SSIs are believed to account for up to $10 billion annually in health care expenditures.2 Bacteriologic studies have suggested that the majority (approximately 80%) of SSIs originate from the patient’s endogenous flora, while only about 20% come from contamination during surgery.3 While it is likely impossible to prevent infections entirely, some measures are believed to reduce the risk of developing infection after fracture surgery (Table 2-1). These include identification of patients at high risk, careful planning of surgical timing, the use of antibiotic prophylaxis, gentle tissue handling, minimization of surgical trauma, and manipulation of certain factors in the operating room (OR) environment. For open fractures, the adequacy of the initial irrigation and débridement procedure is thought to play an important role. A variety of factors increase the risk of infection after fracture surgery. There are factors associated with the injury, the patient, the pathogen, and the surgery. Patientrelated factors that increase infection risk include age extremes (young or old), diabetes4 (including, according to recent evidence, stress-induced hyperglycemia in nondiabetic patients5), peripheral vascular disease, malnutrition, immunodeficiency 11

Archdeacon MT, Anglen JO, Ostrum RF, Herscovici D Jr, eds. Prevention and Management of Common Fracture Complications (pp 11-20). © 2012 SLACK Incorporated.

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Table 2-1

Risk Factors for Infection in Fracture Surgery RISK FACTOR Patient-related factors

Injury-related factors

Procedurerelated factors

RISK REDUCTION STRATEGY Age extremes

Appropriate operative indications, avoid operation when not necessary

Diabetes and hyperglycemia

Careful perioperative control of blood sugar

Peripheral vascular disease

Awareness, operative indications

Malnutrition

Protein and caloric supplementation, vitamins

Immunodeficiency

Avoid blood transfusion unless absolutely necessary to save life

Obesity

Awareness, alternative surgical approaches, special instruments

Smoking

Smoking cessation program

MRSA carrier

Muciporin nasal treatment and antiseptic showering? Prophylaxis with vancomycin?

Closed fracture— Soft tissue damage

Delay surgery until soft tissue healthy, elevation in spanning external fixator, alternative approaches to avoid damaged skin, incisional VAC

Open fracture

Early antibiotics, adequate débridement, early coverage or closure, VAC or antibiotic bead pouch

Contamination

Awareness, delayed closure, VAC or antibiotic bead pouch

Duration

Good preoperative planning to prevent delays, staged procedures

Surgical trauma

Gentle tissue handling, indirect reduction, minimal incision when appropriate

OR environment

Minimize personnel changes and activity, clean scrub wear policy, mask changes every 90 minutes, UV light environment?

Infection

13

Figure 2-1. Hemorrhagic fracture blisters, as seen in this pilon fracture, are a sign of severe soft tissue injury and impairment of the ability to resist infection. Incision through this sort of skin is hazardous. The use of a temporary external fixator with pins in the tibia, calcaneus, and forefoot allows elevation with maintenance of length and alignment while waiting for soft tissue healing.

(including that resulting from blood transfusion,6 medications, or disease), obesity,7 and smoking. Injury-related factors are primarily related to the integrity of the soft tissue. Open fractures, in which there is physical disruption of the skin overlying the fracture, are at significantly higher risk for infection than closed fractures, and the risk is related to the severity of damage to the soft tissue envelope. Although the rates from different studies vary, a general estimate is that 0% to 2% of Gustilo type I open fractures will become infected, 2% to 10% of Gustilo type II, and 10% to 50% of Gustilo type III. In addition, gross contamination with soil or biologic material, arterial injury requiring repair, and delay in treatment are believed to increase the risk of infection in open fractures. The presence of significant soft tissue injury in closed fractures, as demonstrated by contusion, hematoma, fracture blisters, swelling, or degloving, may also increase the risk of infection after surgery, particularly if incisions are made through injured skin (Figure 2-1). While all surgical incisions are exposed to some microorganisms, few develop infection. The quantity of bacterial inoculation, the inherent virulence of the organism, and the growth in the hours or days after surgery are important pathogen-related factors in infection. Most SSIs result from inoculation of the patient’s endogenous normal skin flora, usually Staphylococci, during surgery. The incidence of multidrugresistant bacteria has increased significantly over the past decade; the majority of hospital-acquired infections with Staphylococci are now methicillin resistant in many hospitals and units. Different strains of methicillin-resistant Staphylococcus aureus (MRSA) are responsible for the community-acquired versions of this infection, and some isolates with reduced sensitivity to vancomycin have been reported.8 The primary procedure-related factor in the risk of infection is the duration of the operation. Excessive length of operation, defined as above the 75th percentile for that specific procedure, is one of the three components of the infection risk index used by the US Centers for Disease Control and Prevention.9 The risk of infection is proportional to the duration of surgery and roughly doubles for every elapsed hour.10

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Figure 2-2. A positive wrinkle test indicates interstitial swelling has decreased and incision is safer.

PREVENTION OF INFECTION Although all infections cannot be prevented, there are steps that can be taken to decrease the risk. In the case of surgery for closed fractures, these measures revolve around the appropriate timing of surgery, the use of antibiotic prophylaxis, and the OR environment. Closed fractures with significant swelling, contusion, ecchymosis, and blistering of the soft tissues should have surgery delayed until soft tissues have healed and recovered their ability to repel infection. This is particularly true in the situation where the necessary incision lies near or through damaged skin. While waiting for resolution of swelling, many fractured limbs can be maintained at the correct length and alignment by traction or bridging external fixation. Strict elevation of the affected extremity above the heart level helps to decrease swelling, although this should be used with caution in limbs at risk for compartment syndrome. Foot pumps or calf compression may be helpful in swelling reduction as well. The skin is ready for surgery when it is soft, mobile, not shiny, and wrinkles with light pinching (Figure 2-2). For most fractures in adults, you can wait 2 to 3 weeks before the healing advances to the point of making the surgery substantially more difficult. Antibiotic prophylaxis is indicated in fracture surgery. A single preoperative dose of broad-spectrum cephalosporin within 30 to 60 minutes of incision is as effective as multiday regimens for clean fracture surgery cases. Antibiotic prophylaxis should not continue more than 24 hours. If the procedure duration is longer than 3 hours, some evidence would suggest redosing the patient intraoperatively.11 Because most SSIs come from the patient’s own flora, patients who are MRSA carriers may benefit from decolonization of nasal and extranasal sites preoperatively, if the timing of surgery allows.12 Certain elements of the OR environment may affect the risk of intraoperative wound contamination. Such contamination occurs predominantly from airborne particles that originate from people, including lint, dust, respiratory droplets, and skin squames. Most people release 1000 to 10,000 particles per minute, of which 5% to 10% carry bacteria, although some people (“shedders”) release more than 10,000 particles per

Infection

15

minute. The number of particles in the air is proportional to the number of people in the room. Methicillin-resistant Staphylococcus epidermidis is present on particles shed by 25% to 45% of OR personnel. Exercise (activity) increases particle release. OR apparel makes a difference—clean, fresh, tightly woven scrub wear with elastic cuffs reduces particle release. In experimental settings, staff wearing used scrubs had higher particle release than those in clean scrubs and even higher than staff wearing underwear only. Studies on the use of masks and hair coverings have been equivocal in showing any protective effect on particle release. After 90 minutes of use, surgical masks are ineffective in lowering particle release. Most particles released are from the lower half of the body. Recent studies show that laminar airflow is no better and, in fact, is possibly worse than conventional air handling standards.13-15 Ultraviolet light systems are more effective than laminar airflow at preventing infection in total joint arthroplasty surgery.16 This modality has not been studied in fracture surgery. The infection risk after open fracture may be affected by some factors under the control of the surgeon. Despite classical teaching that the risk of infection is greater if surgical care of the open fracture wound is delayed beyond 6 hours, the literature does not support time to surgery as a reliable risk factor.17 Antibiotic prophylaxis is important and should be started as soon as possible. Evidence supports the use of a first-generation cephalosporin for 24 to 48 hours, but there is no good evidence of the need for gram-negative or clostridial coverage, nor for repeat courses of antibiotics during returns to the OR.18 The goal of surgical care of the open wound is creation of a clean live wound environment that can begin the healing process. Débridement should remove all foreign material and ischemic tissue. It should be done under direction of an experienced surgeon and should proceed systematically, layer by layer. Extensions of traumatic wounds are often necessary and should be performed with regard for the ultimate coverage procedures required (eg, usually longitudinal rather than transverse). Irrigation of the wound serves to remove foreign material and lower the bacterial load. Animal evidence suggests that high pressure irrigation is detrimental to healing and infection resistance, so low pressure should be used. Antibiotic irrigation solutions have not been shown to reduce infection rates compared to soap solution, which may have some advantages in wound healing.19 Adequate skeletal stability and early wound closure or coverage with healthy tissue are also important aspects of preventing infection in open fracture. Studies of open tibia fractures suggested that the use of bone morphogenetic protein 2 reduces the risk of infection, although the appropriate and cost-effective indications for use of this technology are not clear.20 When the wound is significantly contaminated, treatment is delayed, or tension-free closure cannot be performed, the use of an antibiotic bead pouch or vacuum-assisted closure (VAC) dressing will protect the wound environment between operations (Figure 2-3). The diagnosis of infection after fracture surgery may be obvious clinically when the patient presents with typical signs and symptoms: pain, fever, erythema, swelling and fluctuance, warmth, and/or purulent drainage. In more indolent cases, it should be suspected in cases of pain and delayed healing, occasionally with more subtle clinical signs, such as overlying dermatitis. The peripheral leukocyte count may be elevated, and the erythrocyte sedimentation rate usually is; the most sensitive blood test is the C-reactive protein.21 Traditional plain radiographs are often difficult to interpret, and the sensitivity for infection is low. Nuclear medicine scanning, particularly Indium-labeled

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Figure 2-3. Antibiotic bead pouch technique. Polymethylmethacrylate beads impregnated with water-soluble antibiotic are inserted in the wound after débridement and held in place with a semipermeable membrane. This prevents dessication and contamination of the wound and delivers a very high concentration of antibiotics to the local tissues.

leukocyte scans, magnetic resonance imaging, and positron emission tomography are more sensitive and should be considered.22 Cultures of deep tissue obtained from multiple sites at surgery are required to identify the causative organism and guide therapy. The goals of treatment are achievement of union and control of the infectious process. Complete eradication of all infection is often difficult, and late recurrence is common. Surgery is usually required and frequently requires a staged approach. Collections of pus must be drained and necrotic infected bone (sequestrum) removed. In most cases, implanted hardware that is required for maintenance of stability should be retained until union is achieved, although hardware that is loose or nonfunctional should be removed22 (Figure 2-4). The use of local antibiotic delivery through implantation of antibiotic-impregnated beads, rods, or spacers is a very useful technique that allows very high concentrations of drug to be achieved in local tissues without risk of systemic toxicity23 (Figures 2-4 and 2-5). Systemic antibiotics based on sensitivities of the infecting organisms should be administered, although the route of administration and duration of treatment are controversial. In some cases, consultation with an infectious disease specialist may be helpful.

Infection

A

C

B

Figure 2-4. (A) A 55-year-old man presented 6 months after open distal tibia fracture with purulent drainage, wound breakdown and exposed plate, and a nonunited tibia. (B) In the first stage, hardware was removed, the necrotic bone and other tissues were débrided, antibiotic beads were applied, intravenous antibiotics were given, and a hybrid fixator was placed for stability. (C) In the next stage of the treatment, a posterolateral iliac crest bone graft was applied with an implantable bone stimulator. The anteromedial soft tissue wound was treated with vacuum-assisted closure. Healing was achieved, and the frame was removed.

C

17

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Figure 2-5. In this 35-year-old woman who developed osteomyelitis following open reduction and internal fixation with a plate for a distal tibial shaft fracture, an antibiotic-laden polymethylmethacrylate nail was used in the intramedullary canal, in addition to intravenous antibiotics, to deliver higher concentrations of drug to infected bone.

REFERENCES 1. Whitehouse JD, Friedman D, Kirkland KB, Richardson WJ, Sexton DJ. The impact of surgical site infections following orthopaedic surgery at a community hospital and university hospital: adverse quality of life, excess length of stay and extra cost. Infect Control Hospital Epidemiol. 2002;23(4):183-189. 2. Anderson DJ, Kaye KS, Classen D, et al. Strategies to prevent surgical site infection in acute care hospitals. Infect Control Hospital Epidemiol. 2008;29(suppl 1):S51. 3. Allo MD, Tedesco M. Operating room management: operative suite considerations, infection control. Surg Clin North Am. 2006;85(6):1291-1297. 4. Soohoo NF, Krenek L, Eagan MJ, Gurbani B, Ko CY, Zingmond DS. Complication rates following open reduction and internal fixation of ankle fractures. J Bone Joint Surg Am. 2009;91(5):1042-1049. 5. Karunakar MA, Staples KS. Does stress induced hyperglycemia increase the risk of perioperative infectious complications in nondiabetic orthopaedic trauma patients? Paper #73, presented at the annual meeting of the OTA, October 10, 2009; available online at http:// www.hwbf.org/ota/am/ota09/otapa/OTA090673.htm. 6. Carson JL, Altman DG, Duff A, et al. Risk of bacterial infection associated with allogeneic blood transfusion among patient undergoing hip fracture repair. Transfusion. 1999;39(7):694-700. 7. Karunakar MA, Shah SN, Jerasek S. Body mass index as a predictor or complications after operative treatment of acetabular fractures. J Bone Joint Surg Am. 2005;87(7):1498-1502. 8. Esterhai JL, Rao N. The epidemiology of musculoskeletal infections. In: Cierny G III, McLaren AC, Wongworawat ME, eds. Orthopaedic Knowledge Update—Musculoskeletal Infection. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2009:5-7.

Infection

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9. Leong G, Wilson J, Charlett A. Duration of operation as a risk factor for surgical site infection: comparison of English and US data. J Hosp Infect. 2006;63(3):255-262. 10. Cierny G III, Rao N. Procedure-related reduction of the risk of infection. In: Cierny G III, McLaren AC, Wongworawat ME, eds. Orthopaedic Knowledge Update—Musculoskeletal Infection. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2009:46. 11. Antibiotic prophylaxis in surgery: a national guideline. National Guideline Clearinghouse, Association for Health Research and Quality (AHRQ) http://www.guideline.gov/summary/summary.aspx?doc_id=12987&nbr=6684&ss=6&xl=999. 12. Bode LGM, Kluytmans JAJW, Wertheim HFL, et al. Preventing surgical-site infections in nasal carriers of Staphylococcus aureus. N Engl J Med. 2010;362(1):9-17. 13. Babkin Y, Raveh D, Lifschitz M, et al. Incidence and risk factors for surgical infection after total knee replacement. Scand J Infect Dis. 2007;39(10):890-895. 14. Brandt C, Hott U, Sohr D, Daschner F, Gastmeier P, Ruden H. Operating room ventilation with laminar airflow shows no protective effect on the surgical site infection rate in orthopaedic and abdominal surgery. Ann Surg. 2008;248(5):695-700. 15. Miner AL, Losina E, Katz JN, Fossel AH, Platt R. Deep infection after total knee replacement: impact of laminar airflow systems and body exhaust suits in the modern operating room. Infect Control Hosp Epidemiol. 2007;28(2):222-226. 16. Ritter MA, Olberding EM, Malinzak RA. Ultraviolet lighting during orthopaedic surgery and the rate of infection. J Bone Joint Surg Am. 2007;89(9):1935-1940. 17. Crowley DJ, Kanakaris NK, Giannoudis PV. Débridement and wound closure of open fractures: the impact of the time factor on infection rates. Injury. 2007;38(8):879-889. 18. Hauser CJ, Adams CA Jr, Eachempati SR. Prophylactic antibiotic use in open fractures: an evidence-based guideline. Surgical Infection Society Guideline. Surg Infect. 2006;7(4):379405. 19. Anglen JO. A prospective, randomized comparison of antibiotic and soap solution for irrigation of open lower extremity fractures. J Bone Joint Surg. 2005;87-A(7):1415-1422. 20. Swiontkowski MF, Aro HT, Donell S, et al. Recombinant human bone morphogenetic protein-2 in open tibial fractures. A subgroup analysis of data combined from two prospective randomized studies. J Bone Joint Surg. 2006;88(6):1258-1265. 21. Anglen JO, Watson JT. Musculoskeletal infection associated with skeletal trauma. In: Stannard JP, Schmidt AH, Kregor PJ, eds. Surgical Treatment of Orthopaedic Trauma. New York, NY: Thieme Medical Publishers; 2005:21-24. 22. Berkes M, Obremskey WT, Scannell B, Ellington K, Hymes RA, Bosse M, and the Southeast Fracture Consortium. Maintenance of hardware after early postoperative infection following fracture internal fixation. J Bone Joint Surg Am. 2010;92:823-828. 23. Thonse R, Conway JD. Antibiotic cement-coated nails for the treatment of infected nonunions and segmental bone defects. J Bone Joint Surg Am. 2008;90(suppl 4):163-174.

3 Deep Venous Thrombosis Catherine A. Humphrey, MD

Deep venous thrombosis (DVT) is a widely recognized and prevalent complication of skeletal trauma. A landmark study by Geerts in 1994 revealed that the overall rate of DVT in the multiply injured patient was 58%. Eighteen percent of these patients had proximal DVT, putting them at high risk for pulmonary embolism.1 Aggressive DVT prophylaxis protocols are now considered standard care for trauma patients. In a similarly designed study published in 1996, Geerts demonstrated a reduction in overall DVT rates to 31%, with a proximal DVT rate of only 6% 2,3 when patients were treated with subcutaneous low molecular weight heparin (LMWH). Despite extensive literature on the topic, diagnosis and prevention of DVT remains a controversial topic. Methods of detection can lack sensitivity or be overly invasive. Prophylactic and treatment protocols carry significant side effects, and there is little level I evidence to support their efficacy in the trauma population.

ETIOLOGY Venous thromboembolism (VTE) is a more global term for the spectrum of disease that includes DVT and pulmonary embolus (PE). VTE was first recognized in the 16th century, but credit for the most fundamental understanding of its etiology has been given to a 19th century German physician, Rudolf Virchow. Virchow identified the concept of embolism and delineated three factors (Virchow’s triad) that underlie the pathogenesis of VTE: venous endothelial injury, activation of coagulation, and venous stasis. In the setting of skeletal trauma, venous injury occurs as a component of the initial soft tissue disruption and is propagated by ongoing skeletal instability. Venous disruption 21

Archdeacon MT, Anglen JO, Ostrum RF, Herscovici D Jr, eds. Prevention and Management of Common Fracture Complications (pp 21-30). © 2012 SLACK Incorporated.

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Figure 3-1. Risk factors for DVT. Commonly occurring risk factors in the trauma population are organized based on their contribution to Virchow’s triad of thrombosis.

causes the release of tissue factor that activates factor Xa, leading to a buildup of fibrin. In the multiply injured patient, there are many risk factors, both patient based and injury specific, that have been shown to potentiate the process of clot initiation and propagation via each component of Virchow’s triad (Figure 3-1). Several studies have shown that the effects of these risk factors in the multiply injured patient are additive.4-6 Although researchers have attempted to develop a score in order to predict those patients at the highest risk of DVT, they have thus far been unsuccessful.6 VTE can manifest in a variety of lesions that include distal or calf DVT, proximal (thigh or pelvic) DVT, and PE. Calf thromboses are often asymptomatic and, in that case, have little risk of propagation. However, distal thromboses that cause symptoms such as calf swelling or pain with calf palpation have a 25% chance of extending into the thigh when left untreated. Once DVT is noted in the thigh, the risk of embolization to the lungs increases to approximately 50%.7,8 Autopsy studies suggest that 90% of fatal PEs are associated with proximal thigh or pelvic DVT. However, PE can occur in the absence of any evidence of DVT in the extremities and vice versa. Skeletal injury is a clear risk factor of VTE. Previous studies have documented DVT in up to 80% of femur fractures and 77% of tibia fractures in the settling of multiple injuries.1 Risk of VTE is elevated even in the setting of isolated orthopedic surgery with DVT rates of 40% to 60% in patients undergoing joint arthroplasty or hip fracture surgery.9 Researchers postulate that manipulation of the skeletal system itself likely contributes to the activation of coagulation; however, the precise mechanism for this has not been described. Inherited coagulopathies also play a role in post-traumatic VTE. Approximately 6% of the White population has Factor V Leiden, an autosomal dominant trait that results in activated protein C resistance and, thus, hypercoaguability. This trait

Deep Venous Thrombosis

23

demonstrates widely variable penetrance. Simply being a gene carrier confers an indeterminate increased risk of VTE. Trauma itself induces a hypercoaguable state that is best described by assays such as thromboelastography (TEG), activated protein C, and antithrombin III.10 Older assays such as PT and PTT do not reliably demonstrate the distinct differences in dynamic clotting that occur immediately following injury. Schreiber and colleagues elucidated that hypercoaguability is most distinct at postinjury day 1 and declines by postinjury day 4, and that females demonstrate a much more distinct increase in hypercoaguability in the first 24 hours following injury.11 Many different factors impact a patient’s risk of developing symptomatic VTE. The relative weight and importance of each factor to the individual patient remains unknown. Differences in study design make direct comparison of risk difficult. Patients with skeletal injury can be divided into three large groups, each with distinct prophylaxis recommendations. Patients who have suffered systemic trauma and have even a single risk factor, such as skeletal injury, vascular injury, advanced age, or obesity, fall within the highest risk stratification. Patients who have suffered isolated hip fractures benefit from prophylaxis but are felt to be at lower risk. Finally, there is no evidence to support a treatment benefit in patients with isolated extremity injuries below the level of the knee.12

Clinical Presentation of Venous Thromboembolism Clinical diagnosis of DVT can be a challenge. Patients may complain of calf pain or increased swelling. Homan’s sign, classically ascribed to pain with dorsiflexion, which occurs in patients with calf DVT, has been shown to have poor predictive value. However, in a patient with extremity injury, these findings are almost universal and may occur on a continuum from normal post-traumatic tenderness and edema through the tense pain out of proportion to the exam, which is suggestive of compartment syndrome. Diagnosis of PE is also somewhat challenging because the clinical symptoms are vague. Unexplained shortness of breath, especially accompanied by anxiety, is a common complaint. Patients may also demonstrate hemoptysis, tachycardia, and tachypnea.

Diagnosis of Deep Venous Thrombosis An additional controversy lies in the diagnosis of DVT. Historically, contrast venography has been the gold standard. This invasive test requires injection of contrast dye into the lower extremities with subsequent radiographic verification of flow voids. It is believed to be the most sensitive test, but many of the clots identified are asymptomatic and would remain so, and venography itself entails some risk. Duplex ultrasound imaging provides a less invasive diagnostic option. An example of the images that can be obtained is seen in Figure 3-2. However, ultrasound is operator dependent, and many studies document both false-positive and false-negative results. Four level I studies support a sensitivity of 61% with a specificity of 97% (Table 3-1).13 Ultrasound can only provide imaging of the veins below the inguinal ligament and is dependent on patient comfort and the lack of bulky dressings that obscure the field of view. Magnetic resonance (MR) venography is a third option that has shown mixed results in the literature. A comparison table is included in Table 3-1. MR venography has excellent specificity and sensitivity in trials published

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Figure 3-2. Doppler ultrasound in a patient with near occlusive common femoral vein DVT. The blue represents the limited area of flow in the vein with the arrowheads indicating the limits of the vein that is occluded by clot. Doppler plot indicated no sound transmission through the bracketed area depicted. (Reprinted with permission of Susan K. Hobbs, MD, PhD.)

Table 3-1

Venous Thromboembolism in the Orthopedic Trauma Patient MODALITY

SENSITIVITY

SPECIFICITY

Contrast venography Ultrasound (color flow Doppler) Magnetic resonance venography

100% 92% to 100% 80% to 100%

100% 98% to 100% 90% to 100%

A comparison of sensitivity and specificity of the three primary modalities for imaging symptomatic DVT in the lower extremities. Contrast venography is the gold standard, and thus no comparison imaging exists to validate accuracy. Authors presume venography is 100% and use this as a basis for evaluating alternative techniques.14

primarily in the respiratory literature. However, MR venography has not shown similarly excellent results in two trials when it was employed in the setting of fracture.15,16 Diagnosis of PE is most commonly performed using a chest computed tomography. A contrast study can provide valuable information about filling defects throughout the lung field, which is both sensitive and specific to PE (Figure 3-3). An alternative in the patient who cannot tolerate a contrast load is a ventilation perfusion scan; however, the results of this study are provided as probabilities and are rarely definitive.

PREVENTION OF DEEP VENOUS THROMBOSIS VTE is a largely preventable complication that can cause morbidity and prolonged hospital stay. In recent years, at least three professional groups have provided recommendations for prevention of VTE in the trauma or orthopedic patient. Unfortunately, the recommendations are not always in accord, yielding sometimes conflicting and confusing guidelines for clinicians. The American Academy of Orthopaedic Surgeons (AAOS) released a Clinical Practice Guideline in 2009 addressing thromboprophylaxis in patients undergoing

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25

Figure 3-3. Chest CT with contrast depicts a large tubular embolus in the right main pulmonary artery. A small filling defect can also be visualized on the left. (Reprinted with permission of Susan K. Hobbs, MD, PhD.)

hip and knee arthroplasty.17 They recommend stratifying patients preoperatively based on their risk of bleeding and their risk of clotting. Based on these factors, they recommend several treatment options, including the use of aspirin for patients at standard risk of bleeding and PE. While this represents the only clinical practice guideline based on the orthopedic literature alone, it is not easily applicable to the orthopedic trauma patient because it makes the assumption that all patients will also be treated with mechanical prophylaxis and early mobilization. In the multiply injured patient, mechanical prophylaxis may be impossible due to lower extremity splints, casts, fixators, or wounds. Likewise, early mobilization is often challenging in trauma patients. The AAOS guidelines are specifically targeted at the prevention of symptomatic PE. This is one fundamental philosophical difference that separates these recommendations from those provided by the American College of Chest Physicians (ACCP) and the Eastern Association for the Surgery of Trauma (EAST), both of whom focus on the prevention of all forms of VTE, including DVT. The AAOS guidelines, because of their specific consideration of hip and knee replacement patients, emphasize that the incidence of postoperative bleeding complications exceeds the incidence of PE in the arthroplasty population. They note that the significance of those complications, including hematoma and wound breakdown leading to deep infection, were not given adequate weight in the recommendations provided by the ACCP.17

METHODS OF PROPHYLAXIS The role of mechanical prophylaxis in trauma patients has been evaluated using both calf and thigh devices as well as foot pumps. A meta-analysis looked at pooled results of five trials conducted in trauma patients. Only one of the five trials demonstrated efficacy of mechanical compression. The remaining four all demonstrated an odds ratio that included one. The conclusion of the meta-analysis was that mechanical compression alone is equivalent to no treatment.18 Both the EAST and CHEST guidelines document that mechanical prophylaxis has a historically low compliance rate.12,13

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A-V foot pumps have been recommended as an alternative because they can often be worn by patients with lower extremity injury. Unfortunately, these devices are also often inappropriately applied, and clinical trials have demonstrated mixed results with complications, including skin changes and wound problems.2,19 Intermittent pneumatic compression is often used in conjunction with a pharmacologic regimen. However, little evidence exists regarding the effectiveness of such a combination in the trauma population. Pharmacologic prophylaxis is the most effective means of DVT prevention, but carries with it a significant risk of increased bleeding, particularly in the trauma population. Both EAST and ACCP recommend the initiation of pharmacologic prophylaxis as soon as patient condition allows. In the absence of ongoing bleeding, even in the setting of chest, abdomen injury, or head injury, therapy should be started immediately.13,20 Traditional approaches to pharmacologic prophylaxis in the acute setting have used subcutaneous preparations of heparin. Low-dose unfractionated heparin (LDUH) is inexpensive, is widely used, and has demonstrated efficacy in patients with isolated hip fracture surgery and many medical conditions.21 However, LDUH has no utility in the setting of trauma. Studies have demonstrated that unfractionated heparin is inferior to LMWH and is equivalent to no treatment in meta-analysis.3,18 The preferred approach to VTE prophylaxis in the high-risk fracture patient is LMWH. Randomized trials support the use of LMWH in trauma patients. One study enrolled 344 patients with a minimum ISS of 9, of whom more than 50% sustained skeletal injury. The authors demonstrated a relative risk reduction of 58% for proximal DVT in the group who were treated with LMWH.12 Rates of bleeding complications, including transfusion requirements, were equivalent when comparing LMWH to LDUH.3,22 Therapy should be continued throughout the hospital stay. Longer term data do not exist to provide a definitive time frame for prophylaxis. Ongoing bleeding, head injuries, and spinal cord injuries can preclude the use of LMWH in the acutely injured patient. Prophylactic inferior vena cava (IVC) filters are an option in this patient population but should be placed after careful consideration. There is no evidence to suggest that they decrease the risk of PE.23 These expensive devices present short- and long-term complications, including thrombosis at the insertion site, filter breakage, and migration. Theoretically, the long-term risk of caval occlusion would be eliminated with the use of retrievable filters, but several series have demonstrated retrieval rates of only 20% to 40%.24,25 Currently, most trauma surgeons recommend restricting the use of filters to a very narrow patient population.25 Once the bleeding risk has normalized, patients who have an IVC filter should be started on a therapeutic anticoagulation protocol.

COMPLICATIONS Despite adherence to DVT prophylaxis regimens, studies demonstrate a persistent rate of DVT in the orthopedic trauma population. In a group of 312 patients, Stannard and colleagues found an 11.5% overall incidence of DVT despite the use of LMWH initiated within 36 hours of admission.15 Studies in trauma populations document persistent DVT rates of 2.5% to 30% despite prophylactic treatment. Treatment protocols are based on the location of the VTE at diagnosis. An isolated, asymptomatic DVT identified below the level of the knee is highly unlikely to cause symptomatic PE. Patients with asymptomatic, isolated calf DVT diagnosed

Deep Venous Thrombosis

27

by screening ultrasound can be treated with a repeat ultrasound in 5 to 7 days to assess for propagation. The efficacy of surveillance ultrasound as a prevention tool in itself has not been supported by the literature, however. Current recommendations include duplex ultrasound for symptomatic patients. DVT that has propagated into the thigh presents a 15% to 25% chance of symptomatic PE.26 These clots do require treatment with a therapeutic anticoagulation regimen. Patients should be placed on a therapeutic dose of either LMWH or intravenous heparin drip and should subsequently begin a course of vitamin K antagonist, such as warfarin. Patients should remain therapeutically anticoagulated for a period of 3 to 6 months. This is typically managed by a primary care physician, a hematologist, or a pharmacy dosing service. Symptomatic PE is a potentially devastating event. The rate of fatal PE in the trauma population remains at approximately 1% to 2%. Symptoms may present as mild shortness of breath or right heart strain on electrocardiogram. Unfortunately, PE can present as sudden cardiac arrest. The recognition of PE should prompt the rapid institution of intravenous heparin drip or LMWH at a therapeutic dose followed by the initiation of a vitamin K antagonist. Treatment subsequent to PE is often prolonged and may last 1 year to a lifetime based on the judgment of the patient’s internist or hematologist. Patients who require further surgery and have been diagnosed with VTE, including calf DVT, are candidates for an IVC filter. The additional risk presented by further orthopedic surgery and the attendant immobilization are an appropriate indication for a filter, with the presumption that full therapeutic pharmacologic anticoagulation will be initiated once the risk of perioperative bleeding has passed.25

SUMMARY Aggressive prophylaxis for VTE in the orthopedic trauma population has been effective at reducing rates of DVT. Continued vigilance on the part of the treating team is necessary in order to make sure that high-risk patients continue to receive prompt and appropriate therapeutic interventions. Yet, despite the institution of evidencebased prophylactic protocols, as many as 12% of orthopedic trauma patients continue to develop DVT.15 Current treatments, including LMWH, carry a documented risk of increased bleeding complications.

REFERENCES 1. Geerts WH, Code KI, Jay RM, Chen E, Szalai JP. A prospective study of venous thromboembolism after major trauma. N Engl J Med. 1994;331:1601-1606. 2. Anglen JO, Goss K, Edwards J, Huckfeldt RE. Foot pump prophylaxis for deep venous thrombosis: the rate of effective usage in trauma patients. Am J Orthop (Belle Mead NJ). 1998;27:580-582. 3. Geerts W, Jay R, Code K, et al. A comparison of low-dose haparin with low-molecularweight heparin as prophylaxis against venous thromboembolism after major trauma. N Engl J Med. 1996;335:701-707. 4. Sharma O, Oswanski M, Joseph R, et al. Venous thromboembolism in trauma patients. J Trauma Injury, Infection, and Critical Care. 1997;42:100-103. 5. Cipolle MD, Wojcik R, Seislove E, Wasser TE, Pasquale MD. The role of surveillance duplex scanning in preventing venous thromboembolism in trauma patients. J Trauma. 2002;52:453-462.

28

Chapter 3

6. Greenfield LJ, Proctor MC, Rodriguez JL, Luchette FA, Cipolle MD, Cho J. Posttrauma thromboembolism prophylaxis. J Trauma. 1997;42:100-103. 7. Moser KM, Fedullo PF, LitteJohn JK, Crawford R. Frequent asymptomatic pulmonary embolism in patients with deep venous thrombosis. JAMA. 1994;271:223-225. 8. Huisman MV, Buller HR, Cate JW, et al. Unexpected high prevalence of silent pulmonary embolism in patients with deep venous thrombosis. Chest. 1989;95:498-502. 9. Leclerc J, Gent M, Hirsh J, Geerts W, Ginsberg J. The incidence of symptomatic venous thromboembolism during and after prophylaxis with enoxaparin: a multi-institutional cohort study of patients who underwent hip or knee arthroplasty. Arch Intern Med. 1998;158:873-878. 10. Park MS, Martini WZ, Dubick MA, et al. Thromboelastography as a better indicator of hypercoagulable state after injury than prothrombin time or activated partial thromboplastin time. J Trauma. 2009;67:266-275; discussion 75-76. 11. Schreiber MA, Differding J, Thorborg P, Mayberry JC, Mullins RJ. Hypercoagulability is most prevalent early after injury and in female patients. J Trauma. 2005;58:475-480; discussion 80-81. 12. Geerts WH, Bergqvist D, Pineo GF, et al. Prevention of venous thromboembolism: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. 8th ed. Chest. 2008;133:381S-453S. 13. Rogers FB, Cipolle MD, Velmahos G, Rozycki G, Luchette FA. Practice management guidelines for the prevention of venous thromboembolism in trauma patients: the EAST practice management guidelines work group. J Trauma. 2002;53:142-164. 14. Tapson VF, Carroll BA, Davidson BL, et al. The diagnostic approach to acute venous thromboembolism. Clinical practice guideline. American Thoracic Society. Am J Respir Crit Care Med. 1999;160:1043-1066. 15. Stannard JP, Singhania AK, Lopez-Ben RR, et al. Deep-vein thrombosis in high-energy skeletal trauma despite thromboprophylaxis. J Bone Joint Surg Br. 2005;87:965-968. 16. Stover MD, Morgan SJ, Bosse MJ, et al. Prospective comparison of contrast-enhanced computed tomography versus magnetic resonance venography in the detection of occult deep pelvic vein thrombosis in patients with pelvic and acetabular fractures. J Orthop Trauma. 2002;16:613-621. 17. Johanson NA, Lachiewicz PF, Lieberman JR, et al. Prevention of symptomatic pulmonary embolism in patients undergoing total hip or knee arthroplasty. J Am Acad Orthop Surg. 2009;17:183-196. 18. Velmahos G, Kern J, Chan L, Oder D, Murray J, Shekelle P. Prevention of venous thromboembolism after injury: an evidence-based report: part I. Analysis of risk factors and evaluation of the role of vena cava filters. J Trauma. 2000;49:132-139. 19. Knudson M, Morabito D, Paiement G, Shackleford S. Use of low molecular weight heparin in preventing thromboembolism in trauma patients. J Trauma Injury, Infection, and Critical Care. 1996;41:446-459. 20. Cothren CC, Smith WR, Moore EE, Morgan SJ. Utility of once-daily dose of low-molecular-weight heparin to prevent venous thromboembolism in multisystem trauma patients. World J Surg. 2007;31:98-104. 21. Handoll HH, Farrar MJ, McBirnie J, Tytherleigh-Strong G, Milne AA, Gillespie WJ. Heparin, low molecular weight heparin and physical methods for preventing deep vein thrombosis and pulmonary embolism following surgery for hip fractures. Cochrane Database Syst Rev. 2002:CD000305. 22. Ginzburg E, Cohn SM, Lopez J, Jackowski J, Brown M, Hameed SM. Randomized clinical trial of intermittent pneumatic compression and low molecular weight heparin in trauma. Br J Surg. 2003;90:1338-1344. 23. Velmahos GC, Kern J, Chan LS, Oder D, Murray JA, Shekelle P. Prevention of venous thromboembolism after injury: an evidence-based report—part II: analysis of risk factors and evaluation of the role of vena caval filters. J Trauma. 2000;49:140-144.

Deep Venous Thrombosis

29

24. Helling TS, Kaswan S, Miller SL, Tretter JF. Practice patterns in the use of retrievable inferior vena cava filters in a trauma population: a single-center experience. J Trauma. 2009;67:1293-1296. 25. Karmy-Jones R, Jurkovich GJ, Velmahos GC, et al. Practice patterns and outcomes of retrievable vena cava filters in trauma patients: an AAST multicenter study. J Trauma. 2007;62:17-24; discussion 25. 26. Moser K, Lemoine J. Is embolic risk conditioned by localization of deep venous thrombosis? Ann Intern Med. 1981;94:439-444.

4 Fracture Complications in the Growing Skeleton Christine B. Caltoum, MD

Musculoskeletal trauma in children is common, accounting for 10% to 20% of all childhood injuries.1 Boys in the United States have a 50% risk of sustaining a fracture prior to maturity, with girls fast approaching a similar risk with increasing participation in sporting activities. However, the majority of fractures are greenstick or buckle fractures, and only 20% of fractures require reductions.2,3 In general, fractures in children heal well and quickly, and minor imperfections in diaphyseal alignment have the potential to remodel during growth. Fractures that involve the physis have a higher risk for complications. Fortunately, physeal injuries only account for 15% to 30% of all childhood fractures. They are more common in boys by a 2:1 ratio, and incidence rates increase in adolescents. Physeal fractures are most commonly seen in the upper extremities, particularly the phalanges and distal radius.4,5 Complications following physeal injuries occur in 1.8% to 5% 4,5 of these injuries. These complications include complete physeal arrest with subsequent limb length discrepancy or partial physeal arrest with ensuing angular deformity. The risk of complication is related to both the location of the injury (which physis is involved), the age of the patient, and the initial displacement of the fracture. Initial fracture management has a role in minimizing the subsequent risk of complications following physeal injuries. The physis, composed of chondrocytes in an extracellular matrix, separates the metaphysis from the epiphysis. The physeal plate is connected to both the metaphysis and epiphysis by the zone of Ranvier and the perichondrial ring of LaCroix. The perichondrial ring of LaCroix is a fibrous structure continuous with the periosteum of the metaphysis and the zone of Ranvier that surrounds and lends support to the physis. The zone of Ranvier is continuous with the physis and contributes circumferential growth to the physis. The physis itself is divided into four zones, 31

Archdeacon MT, Anglen JO, Ostrum RF, Herscovici D Jr, eds. Prevention and Management of Common Fracture Complications (pp 31-42). © 2012 SLACK Incorporated.

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Chapter 4

Figure 4-1. Salter-Harris I distal femur fracture in a 7-year-old boy.

beginning from the epiphyseal side: the resting zone or germinal zone, the proliferative zone, the zone of hypertrophy, and the zone of enchondral ossification. The zone of enchondral ossification is continuous with the metaphysis. The first two layers have abundant extracellular matrix, contributing considerable strength, especially against shear forces. The third layer, the zone of hypertrophy, has less extracellular matrix, making it weaker and vulnerable to injury. This is especially true just above the area of provisional calcification within the zone of hypertrophy. It is through this area within the hypertrophic zone that most physeal injuries occur. Therefore, when a fracture through the physis occurs, the resting and proliferative zones, which are essential to growth, remain intact with the epiphysis. As long as the blood supply is not compromised or a bony bridge does not develop, normal growth resumes. While there have been many classification systems for physeal injuries, the most universally used is the one described by Salter and Harris in 1963.6 This system divides physeal injuries into five types based on the location of the geometry of the fracture line. A Salter-Harris I injury is a transverse physeal separation contained within the zone of hypertrophy. This type of fracture is most often seen in infants. Due to the fact that the germinal zone is preserved, growth complications are rare unless there is an injury to the blood supply (Figure 4-1). Salter-Harris II injuries are composed of a fracture line that traverses through the physis but that subsequently exits through the metaphysis. The metaphyseal fragment is of varying size; it has been named Thurston Holland’s sign or fragment. The germinal layer (resting zone) of the physis remains intact and attached to the epiphyseal fragment, making the risk of growth disturbance lower. Salter-Harris II injuries are the most common type of physeal fracture (Figure 4-2).

Fracture Complications in the Growing Skeleton

33

Figure 4-2. Salter-Harris II distal femur fracture in a 13-year-old boy.

Figure 4-3. Salter-Harris III medial malleolus fracture in an 11-year-old boy.

Salter-Harris III injuries are intra-articular fractures. The fracture begins in the physis and exits into the epiphysis. These fractures begin in the zone of hypertrophy but then cross the germinal layer. They frequently require operative intervention due to the involvement at the joint level, which, as in any articular fracture, necessitates anatomic reduction (Figure 4-3).

34

Chapter 4

Figure 4-4. Salter-Harris IV medial malleolus fracture in a 14-year-old boy.

Salter-Harris IV injuries are also intra-articular fractures because the fracture line begins in the metaphysis and extends across the physis into the epiphysis. The fracture therefore crosses all zones of the physis. These fractures also require operative intervention if there is displacement at the joint level or at the level of the physis (Figure 4-4). Salter-Harris V injuries are crush injuries to the physis from a compression force. Typically, no displacement is seen on initial radiographs; rather, the injury is inferred by subsequent growth arrest. This has led authors to doubt the existence of this injury.7 This type of injury is believed to have a poor prognosis when it occurs, with almost universal growth arrest. Growth disturbance following injury to the physeal plate can result from direct injury to the germinal layer, damage to the vascularity of the physis, or to formation of a bony bar bridging from the epiphysis to the metaphysis. Damage to the epiphyseal blood supply typically leads to central arrest followed by complete shutdown of the physis. This is most often seen in widely displaced fractures. Direct injury to the germinal layer may lead to growth cessation, but permanent growth disturbance depends on the overall area of the physis that is damaged: less than 7% to 10% of the total area will not typically lead to growth arrest. Bar formation may occur when epiphyseal bone remains in contact with metaphyseal bone, such as in a Salter-Harris IV fracture with incomplete reduction. This may lead to central or peripheral lesions, with peripheral defects having the potential to lead to greater growth disturbance. Growth disturbances after physeal injuries may become apparent as early as 2 to 3 months after an injury or up to 2 years after a traumatic event, making adequate follow-up after physeal injuries important.

Fracture Complications in the Growing Skeleton

35

Equally important is not to further injure the physis during treatment. Patients should be given adequate sedation and muscle relaxation to avoid undue forces being applied to the physeal cells during reduction. Repeat reductions should also be avoided because this may produce an iatrogenic injury to the susceptible germinal layer. If open reduction is required, direct contact on the physis by instruments should be avoided. If the fracture is stable, internal fixation may not be required. If the fracture reduction cannot be maintained without internal fixation, sparing use of fixation devices that cross the physis is recommended. Smooth pins that are smaller in diameter are less likely to cause physeal arrest than larger pins or threaded pins. The number of attempts at proper positioning should also be kept to a minimum, and the devices should be removed when callous formation is seen, usually 2 to 4 weeks after reduction. Growth disturbance following physeal injury can be subdivided into complete and partial growth arrest. Complete growth arrest will result in limb length discrepancy without angular deformity. The overall amount of limb length discrepancy will depend on the age of the patient at the time of growth plate closure. This will also determine the necessity of further corrective surgery. Partial physeal arrest may not only result in limb length discrepancy but also angular deformities and/or joint incongruity. Partial physeal arrest is further subdivided into central, peripheral, and linear. A peripheral physeal arrest will cause angular deformity if enough growth remains. A central physeal arrest will cause both limb length inequality as well as joint incongruity due to the tethering effect of the central arrest. A linear bar traverses the entire physis centrally with normal physis on either side. Due to the significant deformities that partial physeal arrests may produce, it is important to recognize them early, prior to the development of significant angular deformity or joint incongruity. Patients should be followed with serial radiographs, looking particularly for Harris growth arrest lines. These lines represent areas where there has been a slowing or cessation of growth of the physis. After an injury, they can represent the health of the physis. If these lines remain transverse and parallel to the physis, they are indicators that the physis is growing symmetrically. If there is asymmetrical growth to these lines, an area of the physis may be damaged. If there is no growth, no lines will be present (Figure 4-5).8 Once growth arrest is suspected and in order to delineate the location and area of the bar, further imaging is often necessary. Computed tomography (CT) and magnetic resonance imaging (MRI) have been used. Both helical CT and MRI allow for accurate mapping of physeal bars, both peripheral and central. Both modalities allow for treatment planning and show excellent correspondence with surgical findings.9,10 MRI has become the imaging modality of choice due to the fact that there is no radiation exposure. However, sedation may be required in a young child, which may not be the case with a CT scan (Figures 4-6 and 4-7). Treatment of physeal damage depends on multiple factors: the age of the patient, which physis is affected, and the type of physeal arrest. Knowing the rate of growth of the physis involved and the age of the patient at the time of injury allows for prediction of the ultimate leg length discrepancy at skeletal maturity. Treatment options are largely based on this predicted leg length discrepancy. In the lower extremity, the proximal femoral physis has a rate of growth of 2 mm/year, the distal femur 10 mm/year, while the proximal tibia grows at a rate of 6 mm/year, and the distal tibia averages 4 mm/year. Boys continue to mature until approximately age 16, and girls mature until approximately age 14. The Green-Anderson growth remaining chart can also be used to predict ultimate leg length discrepancy.

36

Chapter 4

Figure 4-6. MRI of physeal bar.

Figure 4-5. Symmetric Harris growth arrest lines.

Figure 4-7. CT of physeal bar.

Fracture Complications in the Growing Skeleton

37

Based on the type of arrest and the ultimate discrepancy or deformity that is predicted, the options are to observe the patient, to complete a partial arrest, or to excise the bony bridge. If there will be less than 2 years of growth remaining for a slow-growing physis (eg, the distal tibia), observation may be warranted. In such a case, a complete arrest would produce a leg length discrepancy of less than 1 cm, and a partial arrest would potentially produce a minimal angular deformity. If the physeal damage has the potential to produce more than 2 cm of limb length discrepancy, surgical treatment must be considered. For partial physeal bars, the options are to complete the arrest (epiphysiodesis) to prevent an angular deformity from occurring or to excise the bony bridge. Bar excision has been shown to be successful when there is enough surrounding intact physis and growth potential remaining. The bar should not involve more than 50% of the physis, and there should be at least 2 to 2.5 years of growth remaining.11,12 Bar excision alone can be done as long as there is less than 20 degrees of angular deformity at the time of bar excision. After successful excision, minor angular deformities may correct spontaneously. For angular deformities over 20 degrees, osteotomy at the time of bar excision may be necessary. Peripheral bars can be addressed directly, while central bars are approached either through a metaphyseal window or through an osteotomy if one is necessary. Once the bar is resected, the void should be filled with either autogenous fat or Cranioplast (radiolucent methylmethacrylate), which can be anchored to the epiphysis so that it will migrate distally with growth.13 Markers are placed on either side of the resected bar to evaluate growth. Rates of growth following bar excision vary from 40% to 84%, with premature physeal closure to be expected.11,13 These patients must therefore be followed to skeletal maturity (Figure 4-8). For patients in whom bar resection is not a viable option (less than 2 to 2.5 years of growth remaining or more than 50% physeal involvement), completion of the physeal arrest through epiphysiodesis may be necessary to prevent development of an angular deformity. Consideration should be given to contralateral epiphysiodesis at the same time if more than 2 cm of limb length discrepancy will ensue (Figure 4-9). However, if there is more than 5 cm of limb length inequality predicted at the time of skeletal maturity, the patient would be a candidate for a lengthening procedure. This is especially true because, frequently, the limb length inequality is limited to one long bone (Figure 4-10).

SUMMARY Complications following physeal injuries can produce angular deformities, limb length inequalities, or a combination of the two. These may result in the need for further surgery. Fortunately, few physeal injuries result in these types of complications. Patients who sustain injuries to the physis need to be followed closely because a growth arrest may be seen as early as 2 to 3 months or as late as 1 to 2 years after the index event. Early detection can reduce the incidence or severity of angular deformity or joint incongruity, as well as allow for contralateral epiphysiodesis to minimize limb length inequality in some cases.

38

Chapter 4

A

B

C

Figure 4-8. (A) An 11-year-old girl with medial physeal bar in the proximal tibia. (B) MRI demonstrating less than 50% involvement of the physis. (C) Following resection of the peripheral bar.

Fracture Complications in the Growing Skeleton

39

A

B

C

Figure 4-9. (A) A 13.5-year-old boy with a Salter-Harris I fracture of the right distal femur. (B) Complete physeal arrest evident 3 months later. (C) Treated with contralateral epiphysiodesis due to predicted leg length discrepancy of more than 2 cm.

40

Chapter 4

A

B

C

D

Figure 4-10. (A) An 8-year-old boy who had an open Salter-Harris I fracture of the distal femur. (B) After open reduction and percutaneous pinning. (C) Complete growth arrest evident 3 months later. (D) Two years later, the patient’s right femur is 3 cm shorter with a predicted limb length discrepancy of 8 cm. The patient is a candidate for femoral lengthening.

Fracture Complications in the Growing Skeleton

41

REFERENCES 1. Landin LA. Epidemiology of children’s fractures. J Pediatric Orthop. 1997;6B:79. 2. Khosla S, Melton LJ III, Dekutoski MB, et al. Incidence of childhood distal forearm fractures over 30 years: a population-based study. JAMA. 2003;290(11):1479-1485. 3. Worlock P, Stower M. Fracture patterns in Nottingham children. J Pediatric Orthop. 1986;6B:656-660. 4. Peterson HA, Madhok R, Benson JT, Ilstrup DM, Melton LJ III. Physeal fractures: part I. Epidemiology in Olmsted County, Minnesota, 1979-1988. J Pediatric Orthop. 1994;14:423430. 5. Mizuta T, Benson WM, Foster BK, Paterson, DC, Morris LL. Statistical analysis of the incidence of physeal injuries. J Pediatric Orthop. 1987;7:518-523. 6. Salter RB, Harris WR. Injuries involving the epiphyseal plate. J Bone Joint Surg. 1963;45:587622. 7. Peterson HA, Burkhart SS. Compression injury of the epiphyseal growth plate: fact or fiction? J Pediatric Orthop. 1981;1:377-384. 8. Harris HA. Lines of arrested growth in the long bones in childhood: the correlation of histological and radiographic appearances in clinical and experimental conditions. Br J Radiol. 1931;4:561. 9. Loder RT, Swinford AE, Kuhns LR. The use of helical computed tomographic scan to assess bony physeal bridges. J Pediatric Orthop. 1997;17:356-359. 10. Craig JG, Cramer KE, Cody DD, et al. Premature partial closure and other deformities of the growth plate: MR imaging and three-dimensional modeling. Radiology. 1999;210:835843. 11. Birch JG. Surgical technique of physeal bar resection. Instr Course Lect. 1992;41:445-450. 12. Kasser JR. Physeal bar resections after growth arrest about the knee. Clin Orthop. 1990;255:68. 13. Peterson HA. Partial growth plate arrest and its treatment. J Pediatr Orthop. 1984;4:246-258.

5 Nonunion Jeffrey O. Anglen, MD, FACS

Fracture union is usually defined as pain-free function with bridging bone seen on radiographs. Nonunion exists when the fracture healing process has completely ceased prior to reconstitution of the physical and mechanical integrity of the bone. Delayed union refers to a situation in which the bone remains unhealed for longer than expected, but the healing process continues at a reduced rate. In practice, the two are difficult to separate. While various arbitrary time limits (3, 6, 9 months) have been proposed in the literature as definition of a nonunion, some fractures heal very slowly and could take over 1 year to consolidate. A practical guideline that many accept is that the absence of any radiographic progression over 3 consecutive months is evidence of nonunion and indication for consideration of treatment when the patient is symptomatic. Recent evidence suggests that delaying surgical intervention for 6 months after fracture of the tibia will reduce the need for reoperation for nonunion.1 In some cases of significant segmental bone loss, an “instant nonunion” exists, and there is no need to wait any arbitrary length of time to start treatment. The incidence of nonunion varies with fracture location. Some fracture locations, such as the femoral neck, are at high risk for nonunion, while others, such as the distal radius, rarely suffer from impaired healing. Patient factors that have been suggested to increase the risk for nonunion include diabetes, tobacco use, advanced age, malnutrition, chronic diseases, alcohol abuse, prior radiation of the bone, vasculopathy, noncompliance, and the use of certain medications (Tables 5-1 and 5-2). Injury characteristics that are associated with nonunion include open fracture with significant soft tissue injury, wide displacement of the fracture, segmental bone loss, pathologic fracture, and vascular injury.2-4 Diagnosis of nonunion involves taking a history, performing a physical exam, and appropriate use of imaging. The chief complaint is usually pain occurring when 43

Archdeacon MT, Anglen JO, Ostrum RF, Herscovici D Jr, eds. Prevention and Management of Common Fracture Complications (pp 43-52). © 2012 SLACK Incorporated.

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Chapter 5

Table 5-1

Factors Increasing the Risk for Nonunion CATEGORY

FACTOR INCREASING RISK

Patient characteristic

Fracture or injury characteristic

Treatment characteristic

§

Advanced age

§

Chronic diseases, especially diabetes and HIV infection

§

Tobacco use

§

Alcohol or substance abuse

§

Endocrine disorder, particularly hypothyroidism

§

Malnutrition

§

Prior bone radiation treatment

§

Vasculopathy

§

Medications (see Table 5-2)

§

Open fracture or soft tissue injury

§

Vascular disruption requiring repair

§

Wide displacement

§

Bone loss

§

Pathologic fracture

§

Excessive soft tissue injury or periosteal stripping during surgery

§

Excessive hardware implanted, damage to bone by reamers or drills

§

Insufficient stability provided

§

Inadequate reduction

§

Miscellaneous violation of surgical principles (eg, failure to achieve compression when required)

Table 5-2

Medications That May Impair Bone Healing CORTICOSTEROIDS § § §

Nonsteroidal anti-inflammatory drugs, such as ibuprofen, naproxen, indomethacin, and COX 2 selective inhibitors, such as celecoxib and rofecoxib Fluoroquinolone antibiotics (ciprofloxacin, levofloxacin) Anticoagulants (warfarin, heparin, and aspirin; no evidence on fondaparinux)

Nonunion

45

the bone is loaded or used. Other symptoms may be instability, abnormal motion (“extra joint”), change in hardware prominence, or progressive deformity. The differential diagnosis of pain following fracture includes the following in addition to nonunion: § Infection § Post-traumatic arthrosis § Nerve injury or neuroma § Stiffness or arthrofibrosis § Instability or malalignment § Pain due to weakness § Complex regional pain syndrome § Peri- or intra-articular hardware impingement § Unknown Plain radiographs are indicated and often are diagnostic. Two views at 90 degrees are standard, and various oblique views may be helpful. Restoration of cortical continuity is the sine qua non of a healed fracture but may be difficult to see due to overlying hardware. Radiographic changes suggesting nonunion (in addition to an obvious gap) are progressive deformity, widening fracture line with or without sclerosis of the edges, absence of bridging callus, failure of the hardware, or loosening of fixation. Stress views may be helpful in demonstrating instability at the fracture site. Tomograms or computed tomography with hardware subtraction may be helpful in identifying whether there is bridging bone. Magnetic resonance imaging and nuclear medicine bone scanning are usually not helpful, although if infection is suspected, they may be useful. Prevention of nonunion is not possible in all cases, but attention to the principles of fracture treatment will reduce the incidence. In all fracture treatment, it is important to address systemic issues that increase the risk of nonunion (ie, initiation of a smoking cessation program for nicotine addicts and elimination of nonsteroidal anti-inflammatory drug use in patients who take these medications). In fractures treated closed, the appropriate immobilization and protection to allow limb function will promote healing. For example, closed treatment of tibia fractures should avoid prolonged immobilization of the joints and restriction of weight bearing; rather, a functional approach with fracture bracing to allow joint motion, muscle exercise, and controlled loading is more successful. In fractures treated surgically, common technical errors that increase the risk of nonunion include the following: § Excessive stripping of the soft tissues and excessive exposure of the bone (Figure 5-1). Whenever possible, a minimal incision or submuscular approach to plating the diaphysis, often with a bridge plate construct, preserves vascularity and promotes healing. § Failure to achieve adequate stability (Figure 5-2). Hardware that is inadequate for the job, such as smooth K-wires in adult periarticular fractures or 1/3 tubular plates on the adult forearm, will lead to early loss of fixation and instability. Lag screws are necessary in most articular fractures. § Rigid plating with gaps or without compression of fracture lines, particularly of the tibia (Figure 5-3). If the fracture line is simple, rigid plating of the diaphysis with even small gaps without compression is hazardous.

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Figure 5-1. A 35-year-old healthy woman suffered an isolated, closed, diaphyseal humeral shaft fracture in her nondominant arm while skiing. Closed treatment with a fracture brace would likely have been successful; however, surgical treatment was performed. (A) A large anterolateral incision was performed, and an anteromedial large fragment plating was performed, placing a screw in almost every hole of a 10-hole large fragment compression plate. The procedure probably involved circumferential stripping of the bone. (B) When the bone failed to heal, the plate loosened and failed. (C) Treatment with an external fixator caused more bone damage and loss, resulting in an atrophic nonunion with a segment of substantially damaged bone. (D) Successful healing was achieved with long double-locked plating, iliac crest bone grafting, implantation of recombinant human bone morphogenetic protein 2, and an implantable bone stimulator.

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Figure 5-2. A 46-year-old woman suffered a humeral shaft fracture in addition to multiple lower extremity injuries in an automobile wreck. (A) Initial fixation with a smooth, unlocked intramedullary nail (Rush Rod [Berivon, Meridian, MI]) provided inadequate stability to allow healing and hypertrophic nonunion resulted. (B) Provision of improved stability by use of a compression plate without bone grafting allowed prompt healing within 3 months.

Reaming with dull reamers, reaming too fast, or reaming under tourniquet control can lead to excessive heat and thermal necrosis of the bone. § Failure to achieve adequate reduction, such as varus malreduction of the proximal femur, can lead to loss of fixation, displacement, and nonunion (Figure 5-4). § Too much hardware. For example, double or 90-90 plating is hazardous in many situations, although sometimes necessary. Obviously, using the appropriate amount and type of hardware, neither too much nor too little, for each individual case is key to successful healing and requires experience and judgment. When an unexplained nonunion occurs despite adequate reduction and stable fixation, work-up should include evaluation for previously undiagnosed endocrine or metabolic abnormalities, the most common of which is vitamin D deficiency.5 §

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Figure 5-3. A 63-yearold man who was status post ankle fusion suffered a fracture of the ispilateral tibia, which was treated with a locking distal tibia plate. (A) Fracture compression was not achieved, and lag screws were not used. Nonunion and fixation failure resulted. (B) Treatment with retrograde hindfoot nailing, fibular ostectomy, bone grafting, and implantable bone stimulator was successful.

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Figure 5-4. A 29-year-old man had a motorcycle accident that resulted in an ipsilateral femoral neck and shaft fracture. The shaft was stabilized with retrograde nailing and the high-angle (Pauwels 3) femoral neck fracture was stabilized with three cannulated screws. (A) The femoral neck fracture was either malreduced or displaced into varus, resulting in nonunion. (B) Valgus intertrochanteric osteotomy was performed, which resulted in restoration of the leg length and healing of the femoral neck fracture.

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Nutritional assessment and supplementation should be a routine part of nonunion treatment, with particular attention directed to protein, calcium, phosphorus, and vitamins D and C. Nonunions may be categorized by a variety of different parameters that may help guide treatment. The first is location: articular, metaphyseal, or diaphyseal. Deformity may or may not be present and should be understood in three dimensions and quantified. The presence of active infection is an important parameter. Bone loss and overlying soft tissue defects need to be addressed. The appearance of a distinct fluid-filled cavity with a lining tissue marks a synovial pseudoarthrosis. The vascularity of the bone is often indicated by the appearance on radiographs. Formation of abundant callus indicates good vascularity and characterizes a hypertrophic nonunion. These have a better prognosis and usually heal well with provision of adequate stability. The absence of callus and a “whittled” appearance to the bone ends denotes an atrophic nonunion, which will need bone grafting or some biologic stimulus in addition to stabilization. Some authors have identified an intermediate, poorly defined category called oligotrophic. Treatment of nonunion is a comprehensive undertaking that often involves several types of intervention and the need for a multidisciplinary team. In all patients, medical issues should be addressed and chronic conditions, such as diabetes, optimized. Medications that interfere with bone healing are eliminated or minimized. Malnutrition should be corrected, and the use of protein and multivitamin supplements may help to produce an overall anabolic state. In particular, vitamin D and calcium supplements are commonly used, although the evidence for their effect is not strong except in the case of defined deficiency states. Tobacco cessation programs or other substance abuse treatments are often necessary. Nonoperative treatments for nonunion include functional fracture bracing and external bone stimulation. Fracture bracing for tibial diaphyseal nonunions has been reported to be successful in more than 90% of a series of 67 patients; however, in many of them, it was preceded by fibular ostectomy.6 Electrical bone stimulation has been controversial but is widely used.7 A recent survey of OTA members revealed that more than half of the respondents had used bone stimulators for nonunion or delayed union treatment.8 Of four recent meta-analyses of the subject, three concluded that bone stimulation had a positive effect on nonunion healing, while one concluded that the evidence was not adequate to determine benefit.9-12 Although lowintensity ultrasound has been shown in prospective randomized trials to accelerate the healing of tibia and radius fractures, particularly in smokers,13 it has not been well studied for nonunion, and a recent systematic review of the topic found the evidence limited and weak.14 Surgical treatment of nonunion is a complex undertaking involving preoperative planning and requiring a number of treatment skills. Occasionally, salvage procedures such as amputation, arthroplasty, and arthrodesis are necessary. Surgical attempts to achieve union usually involve some combination of the following steps: § Removal of unstable hardware § Treatment of infection—Débridement of necrotic tissue, local and/or systemic antibiotics § Correction of deformity § Addressing bone defects—Grafting, vascularized bone transplant, transport, shortening/lengthening § Achieving stable fixation

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Biological stimulation—autogenous bone grafts, implantable chemicals or “biologics” (eg, BMP), stem cells, implantable bone stimulators § Preparation of the bone at the nonunion site by opening the intramedullary canal, and shingling, petaling, or decorticating the periosteal surface of the bone § Reconstruction of soft tissue defects § Release of contracture, mobilization of joints The treatment plan for any particular nonunion must be individualized based on an analysis of the clinical situation and the etiology of the nonunion. Some are easier than others; for example, an aseptic hypertrophic diaphyseal nonunion of a bone previously treated closed has many possible successful solutions, including bracing, bone stimulator, nailing, and plating.6,7,15,16 If nonoperative treatment is unsuccessful, the simple provision of stability with nail or plate and lag screws routinely achieves healing. At the other end of the spectrum is an infected, atrophic articular nonunion with deformity and missing bone under inadequate soft tissues. This sort of scenario often requires multiple specialties working together over a prolonged period of time in a staged approach to achieve sequential goals. §

REFERENCES 1. Bhandari M, Guyatt G, Tornetta P III, et al, for the SPRINT Investigators. Randomized trial of reamed and undreamed intramedullary nailing of tibial shaft fractures. J Bone Joint Surg Am. 2008;90:2567-2578. 2. Miranda MA, Moon MS. Treatment strategy for nonunions and malunions. In: Stannard JP, Schmidt AH, Kregor PJ, eds. Surgical Treatment of Orthopaedic Trauma. New York, NY: Theime Medical Publishers; 2007:89. 3. Anglen JO. Nonunion. Orthopaedic Knowledge Online, American Academy of Orthopaedic Surgeons, Rosemont IL, 2003. http://www5.aaos.org/oko/trauma/nonunion/pathophysiology/pathophysiology.cfm 4. Gaston MS, Simpson AHRW. Inhibition of fracture healing. J Bone Joint Surg Br. 2007;89B(12):1553-1560. 5. Brinker MR, O’Connor DP, Monla YT, Earthman TP. Metabolic and endocrine abnormalities in patients with nonunions. J Orthop Trauma. 2007;21:557-570. 6. Sarmiento A, Burkhalter WE, Latta LL. Functional bracing in the treatment of delayed union and nonunion of the tibia. International Orthopaedics. 2003;27(1):26-29. 7. Anglen JO. Enhancement of fracture healing with bone stimulator. Techniques in Orthopaedics. 2003;17(4):506-514. 8. Zura RD, Sasser B, Sabesan V, Pietrobon R, Tucker MC, Olson SA. A survey of orthopaedic traumatologists concerning the use of bone growth stimulators. J Surg Orthop Advances. 2007;16(1):1-4. 9. Akai M, Hayashi K. Effect of electrical stimulation on musculoskeletal systems: a metaanalysis of controlled clinical trials. Bioelectromagnetics. 2002;23:132-143. 10. Griffin XL, Warner F, Costa M. The role of electromagnetic stimulation in the management of nonunion of long bone fracture: what is the evidence? Injury. 2008;39:419-429. 11. Mollon B, daSilva V, Busse JW, Einhorn TA, Bhandari M. Electrical stimulation for long bone fracture healing: a meta-analysis of randomized controlled trials. J Bone Joint Surg Am. 2008;90(11):2322-2330. 12. Walker NA, Denegar CR, Preische J. Low-intensity pulsed ultrasound and pulsed electromagnetic field in the treatment of tibial fractures: a systematic review. J Athl Train. 2007;42:530-535.

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13. Cook SD, Ryaby JP, McCabe J, Frey JJ, Heckman JD, Kristiansen TK. Acceleration of tibia and distal radius fracture healing in patients who smoke. Clin Orthop. 1997;337:198-207. 14. Busse JW, Kaur J, Mollon B, et al. Low intensity pulsed ultrasonography for fractures: systematic review of randomized controlled trials. BMJ. 2009;338:b351. 15. Oh JK, Bae JH, Oh CW, Biswal S, Hur CR. Treatment of femoral and tibial diaphyseal nonunions using reamed intramedullary nailing without bone graft. Injury. 2008;39(8):952959. 16. Helfet DL, Jupiter JB, Gasser S. Indirect reduction and tension band plating of tibial nonunion. J Bone Joint Surg Am. 1992;74:1286-1297.

6 Malunion Brady Barker, MD and Kurtis Staples, MD

Malunion following fracture treatment can be defined as a deviation from the normal or preinjury shape of the bone that results in significant symptoms, decreased function, or unacceptable deformity. According to this definition, an “asymptomatic” malunion does not exist.

CLASSIFICATION While there are no widely accepted classification schemes for malunions, they can be considered based on location and deformity. They can be described as diaphyseal, metaphyseal, or intra-articular, and the resultant deformity can consist of varying degrees of angulation, rotation, translation, shortening, and/or joint incongruity. The deformity is described using the position of the distal segment relative to the proximal segment. Once the location and nature of the deformity are adequately understood, a corrective plan can then be devised.

TREATMENT OPTIONS The treatment options for malunion are observation, bracing, osteotomy, arthrodesis, arthroplasty, and amputation. The appropriate choice of treatment will depend on several factors, including the following: § Symptoms: Is the deformity causing pain, or is the complaint mainly cosmetic? Patients desiring elective malunion surgery for purely cosmetic reasons need to be counseled about the potential complications as well as the possibility

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Location: Upper extremity malunions in general are better tolerated than those in the lower extremity. Likewise, a greater deviation from normal can be tolerated more proximal in the limb compared to more distal malunion. Age: Malunions near joints in growing skeletons will often spontaneously correct. Intra-articular malunions in elderly patients, on the other hand, may best be treated with arthroplasty. Anticipated course: If left untreated, what is the expected long-term outcome? A small angular deformity in the proximal humerus may be well tolerated and may not lead to any long-term sequelae. A large angular deformity near a weight-bearing lower extremity joint may lead to altered mechanical axis, increased cartilage peak pressures, joint laxity, and ultimately arthrosis.

EVALUATION A thorough history and physical examination is required prior to undertaking treatment of any malunion. The exam should evaluate joint function, limb alignment, standing alignment, gait abnormalities, limb length discrepancy, quality of soft tissues, and overall health and motivation of the patient. Standing full-length lower extremity films allow assessment of the effects of the mechanical axis of the limb and can also be used to assess length discrepancy. If the regular anteroposterior (AP) and lateral views of the involved bone are not orthogonal to the plane of maximum angulation, the true magnitude of the deformity will not be displayed. Oblique views or computed tomography (CT) may be needed. CT cuts through the hip, knee, and ankle can quantify the amount of rotation involved and can be used as part of scanogram to better quantify limb length discrepancy.2 CT is also very helpful in planning osteotomies for intra-articular malunions.

PREVENTION The best way to deal with malunions is to prevent them from occurring. This can best be accomplished by adhering to the basic principles of closed treatment and fracture surgery.

Nonoperative Treatment Skillfully placed and molded casts are requisite. Excessive padding leads to looseness and potential displacement. Appropriate follow-up is important. In many fractures, radiographs should be checked weekly until enough callus is evident to prevent further deformity. Displacement that occurs will be identified in a timely fashion and can be treated with cast wedging or open reduction and internal fixation in a relatively simple fashion.

Preoperative Planning Planning for position, approach, reduction strategy, and implants can prevent difficulties during surgery. A formal, thorough, written, and drawn preoperative plan, including a back-up plan, will make a smooth, successful operation more likely.

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Appropriate Imaging Adequate plain films are mandatory before attempting any fracture repair. Good quality intraoperative fluoroscopy is essential for many orthopedic trauma cases. If there is any question about the adequacy of imaging, a C-arm image should be obtained after patient positioning and before prepping and draping. Although essential, fluoroscopy can be misleading at times. If plain films are obtained at the end of the procedure before the patient is awakened, necessary changes can be made without a return to the operating room. Calling for the radiographer when closing is begun will minimize delay.

CORRECTION OF MALUNION The main types of osteotomies used to correct malunions are opening and closing wedge, transverse, oblique, and dome. Closing and opening wedge osteotomies involve some shortening or lengthening, respectively. A transverse osteotomy is employed to correct a rotational deformity. Oblique osteotomies are chosen when an angular deformity predominates. Translation can also be achieved in the plane of the osteotomy. Dome osteotomies are useful when a combination of angular and rotational corrections are needed.3 Fluoroscopy is used to identify the correct plane of the oblique osteotomy. The planes are identified that provide maximum and no deformity. The plane of the osteotomy corresponds approximately to the plane of no deformity.4,5 A long oblique cut allows for a broad healing surface as well as placement of multiple lag screws. A neutralization plate then completes the fixation. A useful intraoperative technique to judge correction is to place two K-wires perpendicular to the bone, or parallel to the joint, above and below the deformity. After making the osteotomy, the deformity can be corrected using the K-wires as reference. When they are parallel, the joints are parallel as well. This should then be confirmed with radiography. Femoral distractor pins can be used in this fashion. Fixation can be performed with intramedullary (IM) nails, plate and screw constructs, or external fixators. Virtually any malunion correction can be fixed with a plate, but this fixation method is particularly useful for metaphyseal or periarticular osteotomies. Diaphyseal malunions can be internally fixed with an IM nail (Figure 6-1). In this way, the load-sharing properties of the nail can be used and early partial weight bearing allowed. External fixation may be the treatment of choice if soft tissue integrity is a concern. External fixation is also very useful when dealing with a need for lengthening or when very complex corrections are needed. The Taylor Spatial Frame (Smith & Nephew, London, England) takes advantage of a computercalculated gradual correction to achieve anatomic alignment (Figure 6-2).6

MALUNIONS OF THE PELVIS AND ACETABULUM Malunion of pelvic fractures may result from either operative or nonoperative treatment. When it occurs in the setting of operative treatment, this can be the result of inadequate reduction or deficient internal fixation. Alternatively, pelvic fractures may be treated at centers where comfort with these injuries is limited, resulting in more nonoperative management and a consequently higher rate of malunion.7 Acetabular malunion, like pelvic ring malunion, is a highly complex problem that,

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Figure 6-1. A malunited segmental tibia fracture that was corrected in a single stage and stabilized with an intramedullary nail. A and B demonstrate AP and lateral views of the malunion before correction. The distal fragment is malposition into valgus and extension (apex anterior). The degree of malrotation is demonstrated in B. However, the malunion is primarily diaphyseal, and the distal fragment is large enough to be stabilized with a nail. C and D demonstrate the alignment after hardware removal, osteotomy, and stabilization with the nail. (Reprinted with permission of Brian H. Mullis, MD.)

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Figure 6-2. Tibial malunion correction with an external fixator. A and B demonstrate AP and lateral views of a long-standing diaphyseal tibial malunion. In this case, due to concerns about soft tissue viability with one-stage correction, the decision was made to use a Taylor Spatial Frame for gradual correction. C and D demonstrate the frame in position near the end of correction of the malalignment. (Reprinted with permission of Brian H. Mullis, MD.)

like any articular malunion, may lead to arthrosis. Post-traumatic hip arthrosis due to malunion can be effectively treated through total hip arthroplasty. The most frequent findings related to pelvic ring malunion include chronic pain (especially in the sacrum),8 limb length inequality, and sitting imbalance (Figure 6-3).9,10

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Figure 6-3. (A,B) A 20-year-old woman in a motor vehicle crash with a pelvic ring that healed with malunion and broken hardware. (C,D) Three months postoperative showing healed osteotomies of the sacrum and anterior pelvic ring with improved leg length and pelvic alignment. Restored sitting balance.

The best method of preventing pelvic ring or acetabular malunion is to involve the care of a fellowship-trained pelvis and acetabular surgeon or to transfer the patient to a center where that care is available. This level of care is needed due to the complexities involved in the surgical care of these injuries.

MALUNIONS OF THE FEMUR Rotational Malunion of the Femoral Shaft The most common malunion of the long bones of the lower extremity is malrotation of the femur. Malrotation of the femur is considered to be an internal or external rotational deformity of greater than 15 degrees,11 although not all patients with this deformity will be symptomatic. This malunion is common due to difficulty in appreciating the correct rotation of this tubular bone when it is fractured. As the majority of femoral nailing occurs in a supine position, most commonly there is an internal rotation deformity of the distal segment. This occurs because the foot and

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lower leg are internally rotated in the fracture table for the procedure, perhaps due to confusion with the position of reduction for the more common intertrochanteric fracture. Furthermore, the proximal segment naturally externally rotates due to the pull of the hip muscles. In contrast, when performing the surgery in the lateral position, an external rotation deformity of the lower segment is possible from positioning and inadvertent external rotation of the foot and lower leg.12 It is imperative, therefore, to use a reliable protocol to reduce the risk of this potential malunion. Many techniques are described in the literature, including such methods as matching up fragments of the shaft or a cortical spike on the shaft and matching up the cortical width.13 Other more predictable techniques include the use of fluoroscopy to compare x-rays of the knee and hip and to ensure the average 15 to 20 degrees of anteversion of the proximal femur,14,15 or more accurately using the contralateral femur as a template. In this technique, an AP of the knee is obtained, and then without changing the C-arm settings, an AP of the hip is obtained. One can then compare the relative profile of the lesser trochanter and the profile of the proximal tibia/fibula joint and create a symmetric appearance on the injured limb, thus duplicating the appropriate rotation of the injured femur.16 Patients seem to be more able to tolerate internal rotational malunions than external rotational deformity.17 Any rotational malunion, however, may result in complaints of chronic hip, knee, or back pain and lower extremity weakness.18 The diagnosis of a rotational femoral malunion is primarily accomplished by a careful physical examination comparing the relative rotation of the hips. This can be challenging if the malalignment is not excessive. In any case, a CT scan is diagnostic and very helpful for preoperative planning.19 Treatment of a rotational malunion requires an osteotomy of the femoral shaft and can be performed either open or closed. The closed technique, most useful for a malunion previously treated with IM nailing, makes use of an IM saw. In this fashion, no further incisions are made, and a new nail can be placed after correction.20 With any technique, one needs to use some method of marking rotation and controlling the correction. A popular technique is to place K-wires or Steinmann pins in the proximal and distal segments before creating the osteotomy and then using them as a reference for the appropriate correction. The most common complications of this corrective surgery are nonunion and residual malunion. Compression of the osteotomy helps to minimize the risk of nonunion (Figure 6-4).

Proximal Femoral Malunions Due to the tremendous forces about the hip, fractures of the proximal femur (femoral neck and pertrochanteric fractures) are prone to malunion if inadequately reduced or stabilized. The most common malunion in this anatomic region is varus malunion. This is generally the result of a poor reduction or a reduction without bony apposition and support.21 In these scenarios, the muscle forces and gait cycle lead to varus collapse with retroversion. Frequently, this situation results in a nonunion rather than malunion; however, the treatment principles are the same. Two treatment options are available to correct this deformity: valgus osteotomy and prosthetic replacement.

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Figure 6-4. (A,B) Injury x-rays of femur fracture. (C,D) Postoperative x-rays after intramedullary nail. (E,F) CT images showing internal rotation deformity distally. (Reprinted with permission of Brian Miller, MD.)

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Figure 6-4 (continued). (G,H) Postoperative x-rays after osteotomy and exchange intramedullary nail. (Reprinted with permission of Brian Miller, MD.)

Distal Femoral Malunion Prior to the availability of locking plates, distal femoral varus malunion was more common.22 This malunion would necessitate an osteotomy and bone grafting and was generally treated with the use of the 95-degree angled-blade plate. Locking plate technology has been revolutionary in treating distal femur fractures and has significantly reduced the incidence of malunion.23,24 Other distal femoral malunions still occur as a result of missed fractures, such as the Hoffa fracture25 (coronal plane fracture of a femoral condyle) or from a malreduction during retrograde femoral nailing. The prevalence of CT scans in trauma and careful attention to reduction prior to reaming and nailing can reduce the risk of these malunions. Intra-articular malunion generally results in a poor outcome, resulting in a need for arthroplasty or arthrodesis. If identified early on, an intra-articular osteotomy is possible.

MALUNIONS OF THE TIBIA Proximal Tibial Malunion Both locking plate fixation and novel nailing techniques have lessened the incidence of this problem. A common malunion of the proximal tibia in fractures treated with nails is that of valgus and flexion.26 Nailing the proximal tibia fracture with the knee flexed results in malreduction due to pull of the patellar tendon on the proximal fractured segment. Patients with this malunion are unable to gain full extension of their leg and have a resultant limp. Furthermore, it causes a shift in the mechanical axis of the limb and overloads the lateral joint space of the knee or the ankle joint, which can result in early arthrosis.

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The best treatment is prevention. Malreduction can be avoided with the use of blocking screws,27 the correct starting point, a femoral distractor, or unicortical plates. Nailing a tibia in extension with a transarticular approach can also aid in the prevention of this deformity.28 Correction requires osteotomy. If the deformity is in the upper diaphysis, correction can be achieved via an oblique osteotomy, as described earlier, in which the three-dimensional deformity can be corrected via a single cut. If the proximal segment is very small, one may consider using a thin-wire frame such as an Ilizarov or Taylor Spatial Frame for this correction. Other techniques, such as a nail or locking plate, are acceptable treatment options as well. The most feared complications of treatment of these malunions are compartment syndrome and nerve injury. Overcorrection from a valgus position or overlengthening can precipitate either of these problems.

Tibial Shaft Malunion IM nailing of tibial shaft fractures has eliminated the majority of diaphyseal malunions of the tibia. However, tibia fractures are still treated with external fixation or inattentive casting, and malunion may result. The amount of deformity that leads to knee or ankle arthritis is uncertain.29,30 An intact fibula may result in a varus alignment and malunion.31 Close follow-up during cast or fixator treatment is necessary in order to recognize and prevent a varus malunion. If malunion occurs, treatment necessitates an osteotomy, usually followed by internal fixation with a plate or nail. The main complication of such treatment is nonunion.

Distal Tibial and Ankle Malunion The lower portion of the tibia, including the plafond, is susceptible to malunion in a similar fashion to the proximal tibia. This may occur with IM nailing of a distal tibial fracture due to lack of cortical contact of the nail in the distal metaphysis. Inadequate reduction while reaming leads to malpositioning of the nail and malunion with healing. Blocking screws can be used to keep the nail in a central location32 within the distal tibia. This malunion can be caught prior to leaving the operating room by intraoperative plain film x-rays of the entire length of the bone. Fluoroscopic images may be subject to misinterpretation, although generally the central position of the nail is a reliable indicator. Intra-articular malunions, whether associated with a plafond injury or a simple ankle fracture, can result in ankle arthritis. As little as 1 mm of translation of the talus under the tibial plafond changes the contact pressures by greater than 40%.33 Osteotomies to correct these intra-articular malunions have modest results, and, in many situations, patients are better served by arthrodesis or arthroplasty.

MALUNIONS OF THE FOOT The most well known of the tarsal malunions is the varus malunion of the talar neck.34 This is nearly always a direct result of comminution of the neck, which prevents anatomic and stable reduction. Varus malunion of the talus results in a gait

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pattern in which the foot is internally rotated, and subsequently there is increased weight-bearing pressure on the lateral border of the foot.35 This can lead to adjacent joint arthrosis (especially the subtalar joint) and can result in chronic pain and deformity.36 Recommendations to prevent these problems include a two-incision approach, bone graft if necessary, and the use of plates, especially medially. As good radiographs of the talus can be challenging to obtain, the two-incision open approach can help prevent malreduction and malunion. Unfortunately, malunions of the talus are often only identified after these late manifestations have already presented, and treatment is limited to shoe wear modifications or arthrodesis. Another common malunion of the foot occurs following calcaneus fractures. This is often the result of nonoperative treatment. Frequent complaints include increased heel width, subfibular impingement, tibiotalar impingement, varus deformity of the hindfoot, peroneal tendon dysfunction, and subtalar arthrosis.37 Similar to the talar neck malunions, malunions of the calcaneus result in significant mechanical changes in adjacent joints and alterations in gait. In some patients, shoe modifications may help. The surgical treatment of this challenging problem requires a customized approach to the specific patient’s symptoms. It may include a lateral wall ostectomy, peroneal tenolysis, subtalar arthrodesis, or calcaneal osteotomy.38

REFERENCES 1. Probe RA. Lower extremity angular malunion: evaluation and surgical correction. J Am Acad Ortho Surg. 2003;11(5):302-311. 2. Carey RP, de Campo JF, Menelaus MB. Measurement of leg length by computerized tomographic scanography: brief report. J Bone Joint Surg Br. 1987;69:846-847. 3. Paley D. Principles of deformity correction. In: Browner BD, Jupiter JB, Levine AM, Trafton PG, eds. Skeletal Trauma. Philadelphia, PA: Saunders; 2003:2519-2576. 4. Sanders R, Anglen JO, Mark JB. Oblique osteotomy for the correction of tibial malunion. J Bone Joint Surg Am. 1995;77:240-246. 5. Marti RK. Malunion. In: Redi TP, Buckley RE, Moran CG, eds. AO Principles of Fracture Management. New York, NY: Thieme; 2007:482-503. 6. Feldman DS, Shin SS, Madan S, Koval KJ. Correction of tibial malunion and nonunion with six-axis analysis of deformity correction using the Taylor Spatial Frame. J Ortho Trauma. 2003;17(8):549-554. 7. Olson SA, Pollak AN. Assessment of pelvic ring stability after injury: indications for surgical stabilization. Clin Orthop Relat Res. 1996;329:15-27. 8. Cole JD, Blum DA, Ansel LJ. Outcome after fixation of unstable posterior pelvic ring injuries. Clin Orthop Relat Res. 1996;329:160-179. 9. Van den Bosch EW, Van der Kleyn R, Hogervorst M, Van Vugt AB. Functional outcome of internal fixation for pelvic ring fractures. J Trauma. 1999;47:365-371. 10. Matta JM, Dickson KF, Markovich GD. Surgical treatment of pelvic nonunions and malunions. Clin Orthop Relat Res. 1996;329:199-206. 11. Jaarsma RL, Pakvis DF, Verdonschot N, Biert J, Van Kapmen A. Rotational malalignment after intramedullary nailing of femoral fractures. J Orthop Trauma. 2004;18:403-409. 12. Ricci WM, Bellabarba C, Lewis R. Angular malalignment after intramedullary nailing of femoral shaft fractures. J Orthop Trauma. 2001;15:90-95. 13. Langer JS, Gardner MJ, Ricci WM. The cortical step sign as a tool for assessing and correcting rotational deformity in femoral shaft fractures. J Ortho Trauma. 2010;24:82-88.

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14. Krettek C, Miclau T, Grun O. Intraoperative control of axes, rotation and length in femoral and tibial fractures. Injury. 1998;29:C29-C39. 15. Tornetta P, Ritz G, Kantor A. Femoral torsion after interlocked nailing of unstable femoral fractures. J Trauma. 1995;38:213-219. 16. Jaarsma RL, Pakvis DM, Verdonschot N. Avoiding rotational malalignment after fractures of the femur by using the profile of the lesser trochanter: an in vitro study. Arch Orthop Trauma Surg. 2005;125:184-187. 17. Jaarsma RL, Pakvis DFM, Verdonschot N, Biert J, Van Kampen A. Rotational malalignment after intramedullary nailing of femoral fractures. J Orthop Trauma. 2004;18:403-409. 18. Gugenheim JJ, Probe RA, Brinker MR. The effects of femoral shaft malrotation on lower extremity anatomy. J Orthop Trauma. 2004;18:658-664. 19. Dugdale TW, Degnan GG, Turen CH. The use of computed tomographic scan to assess femoral malrotation after intramedullary nailing. A case report. Clin Orthop Relat Res. 1992;279:258-263. 20. Winquist RA. Closed intramedullary osteotomies of the femur. Clin Orthop Relat Res. 1986;212:155-164. 21. Archdeacon MT, Cannada LK, Herscovici D, Ostrom RF, Anglen JO. Prevention of complications after treatment of proximal femoral fractures. Instr Course Lect. 2009;58:13-19. 22. Schatzker J. Fractures of the distal femur revisited. Clin Orthop Relat Res. 1998;347:43-56. 23. Weight M, Collinge C. Early results of the less invasive stabilization system for mechanically unstable fractures of the distal femur (AO/OTA types A2, A3, C2 and C3). J Orthop Trauma. 2004;18:503-508. 24. Kregor PJ, Stannard JA, Zlowodzki M, Cole PA. Treatment of distal femur fractures using the less invasive stabilization system: surgical experience and early clinical results in 103 fractures. J Orthop Trauma. 2004;18:509-520. 25. Nork SE, Segina DN, Aflatoon K, et al. The association between supracondylar-intercondylar distal femoral fractures and coronal plane fractures. J Bone Joint Surg Am. 2005;87:564-569. 26. Lindvall E, Sanders R, Dipasquale T, Herscovici D, Haidukewych G, Sagi C. Intramedullary nailing versus percutaneous locked plating of extra-articular proximal tibial fractures: comparison of 56 cases. J Orthop Trauma. 2009;23:485-492. 27. Ricci WM, O’Boyle M, Borrelli J, Bellabarba C, Sanders R. Fractures of the proximal third of the tibial shaft treated with intramedullary nails and blocking screws. J Orthop Trauma. 2008;22:S39-S45. 28. Morandi M, Banka T, Gaiarsa GP, et al. Intramedullary nailing of tibial fractures: review of surgical techniques and description of a percutaneous lateral suprapatellar approach. Orthopedics. 2010;22:172-179. 29. Puno RM, Vaughan JJ, Stetten ML, Johnson JR. Long-term effects of tibial angular malunion on the knee and ankle joints. J Orthop Trauma. 1991;5:247-254. 30. Mckellop HA, Llinas A, Sarmiento A, Luck V. Effects of tibial malalignment on the knee and ankle. Orthop Clin North Am. 1994;25:415-423. 31. Tietz CC, Carter DR, Frankel VH. Problems associated with tibial fractures with intact fibulae. J Bone Joint Surg Am. 1980;62:770-776. 32. Bedi A, Le TT, Karunakar MA. Surgical treatment of nonarticular distal tibia fractures. J Am Acad Ortho Surg. 2006;14:406-416. 33. Ramsey PL, Hamilton W. Changes in tibiotalar area of contact caused by lateral talar shift. J Bone Joint Surg Am. 1976;58:356-357. 34. Canale ST. Fractures of the neck of the talus. Orthopedics. 1990;13:1105-1115. 35. Sangeorzan BJ, Wagner UA, Harrington RM, Tencer AF. Contact characteristics of the subtalar joint: the effect of talar neck misalignment. J Orthop Res. 1992;10:544-551.

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36. Daniels TR, Smith JW, Ross TI. Varus malalignment of the talar neck: its effect on the position of the foot and on subtalar motion. J Bone Joint Surg Am. 1996;78:1559-1567. 37. Reddy V, Fukuda T, Ptaszek AJ. Calcaneus malunion and nonunion. Foot Ankle Clin. 2007;12:125-135. 38. Clare MP, Lee WE, Sanders RW. Intermediate to long-term results of a treatment protocol for calcaneal fracture malunions. J Bone Joint Surg Am. 2005;87:963-973.

7 Arthrofibrosis/Contracture Michael P. Rusnak, MD

Loss of joint range of motion (ROM) following orthopedic trauma is a significant factor in the outcome and satisfaction of patients. This problem is often overlooked in the treatment of the trauma patient. Loss of joint motion after fracture may be caused by malreduction, hardware impingement, weakness, heterotopic ossification (HO), or arthrofibrosis. There is very little in the literature on the etiology, prevention, and management of arthrofibrosis and other causes of stiffness.

ETIOLOGICAL FACTORS Arthrofibrosis is best defined as restricted motion of a joint caused by dense, proliferative scar formation, in which adhesions can progressively spread to further limit motion. This thickening and contracture of the periarticular structures leads to a decrease in joint volume and capsular compliance so that motion is limited in all planes. The underlying pathophysiology is related to an exaggerated synovial and inflammatory response leading to a proliferation of fibroblastic cells. These cells produce elevated levels of type VI collagen and extracellular proteins.1 TGF-␤ is felt to play an important role in the regulation of this process.2 As this heightened response continues, scar tissue is deposited around the joint and within the muscles, with eventual contraction of the tissues. Some believe that specific alpha-smooth muscle actin-containing fibroblastic cells play a role in this contraction.3 A possible genetic predisposition to development of excessive scar was found in a study on anterior cruciate ligament (ACL) reconstruction and arthrofibrosis.4 The etiology of the clinical symptoms is multifactorial and involves the genetic potential for hyperresponse as well as the specific situation. For example, articular incongruity from malreduction 67

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Figure 7-1. AP radiograph of the knee in a 40-year-old male following a head-on motor vehicle accident at 80 mph. Despite details of the history, the significant comminution, severe displacement, and wide involvement of the tibial plateau give valuable information into the energy imparted on the knee joint. This patient went on to temporary external fixator followed by definitive open reduction and internal fixation and meniscal repair. The patient’s final outcome was good to excellent with 0 to 120 degrees range of motion following manipulation under anesthesia and lysis of adhesion at 5 months postoperative.

or insufficient fixation will lead to pain, inflammation, and possibly a mechanical block. Pain and inflammation will lead to an extended period of immobility and a delay in postoperative rehabilitation, both of which will lead to disuse, muscle atrophy, and loss of motion. Prolonged immobilization causes scarring between tissue planes from the development of abnormal cross-links between collagen fibers, which decrease their extensibility.5 Limited joint motion begins a vicious cycle of softening and degeneration of hyaline cartilage, leading to more inflammation and pain. An obvious, but often overlooked, source of inflammation includes infection. Infection leads to intra-articular inflammatory mediators resulting in direct scar formation, damage to articular cartilage, and an exaggerated pain response. Other intraarticular conditions may impair joint rehabilitation. Articular cartilage lesions were found in 79% to 90% of ankles examined arthroscopically after an ankle fracture.6,7 A missed rotator cuff or meniscus tear will lead to pain and disuse, causing muscle atrophy and restricted active motion. A neglected knee effusion will limit motion by inhibiting the function of the quadriceps muscle, leading to atrophy, weakness, and flexion contracture.8 One way to predict the development of these problems is by assessment of injury severity (Figure 7-1). Significant energy imparted to a joint and the periarticular tissues leads to more damage and a larger inflammatory response. This has been studied in regard to the development of HO around acetabular fractures, another cause of joint stiffness.9 HO occurs when pluripotent mesenchymal cells differentiate into osteoprogenitor cells following some sort of trauma. There are several clinical scenarios related to the development of HO, including head trauma, elbow fracture/dislocations, thermal wounds, and extensile posterior approaches to acetabular fracture fixation. Direct trauma is the most common cause of HO around

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the elbow, with rates as high as 89% when there is concomitant neural axis trauma.10 Awareness of patients at risk for this condition may help in the prevention of HO, as there are prophylactic regimens as discussed below.

PREVENTION: CONTROL OF PAIN AND INFLAMMATION There are three keys to preventing postfracture loss of motion. The first two are controlling pain and inflammation, and the third is early rehabilitation. The fundamental goals of fracture surgery include anatomic joint reduction and stable fixation to allow early motion. In addition, rest, ice, compression, and elevation (RICE) to manage pain and minimize swelling are important principles. The importance of adequate and effective pain medication is frequently underestimated, or shortened due to concerns about misuse, but it is essential to facilitate early motion. In fractures treated nonoperatively, immediate mobilization is not only safe, but has been found to be more effective than prolonged immobilization in restoring physical capability and performance of an injured extremity.11 Pain control can be accomplished through various methods. These include traditional modalities, such as medications, local or regional injections, relative immobilization, and physical treatments such as ultrasound and electrical stimulation, as well as nontraditional methods like acupuncture and manipulations. Many of these techniques are felt to increase circulation, decrease inflammation, and promote tissue healing. A joint injection can be both therapeutic and diagnostic. For example, in the work-up of post-traumatic adhesive capsulitis of the shoulder, a subacromial injection will reveal the true active motion once the pain inhibition is eliminated. This will help differentiate whether pain or soft tissue adhesions are the culprit of a “non-outlet” impingement.12 The source of pain can also be misleading, as is the case with complex regional pain syndrome (CRPS), formerly known as reflex sympathetic dystrophy. If left untreated, CRPS inhibits effective patient participation in proper postoperative rehabilitation and potentiates that vicious cycle of pain, inflammation, and weakness leading to stiffness. A recent study showed the potential advantages of adequate postoperative pain control in fracture care.13 In this study, patients undergoing ankle fracture fixation with spinal anesthesia experienced less pain and had better function in the early postoperative period. One preventative measure well established in the literature on ACL surgery is the timing of the operation. It has been shown that ACL reconstruction done within 1 week of injury had a statistically significant increased risk of arthrofibrosis compared to those done after 3 weeks.14 Delay may not always be possible in the treatment of fractures, but a factor that is under the control of the surgeon is the surgical insult to the tissues. Minimally invasive techniques and temporizing external fixators are tools that can be used to limit ongoing tissue damage, inflammation, and swelling.

PREVENTION: EARLY REHABILITATION A primary objective of musculoskeletal rehabilitation is to restore function through muscle strength, balance, and flexibility. Postoperative rehabilitation is pivotal in returning individuals to their preinjury level of function, through restoring ROM of key joints. It has been established that the functional ROM of an elbow is 30 to 130 degrees (extension-flexion) and 50 degrees pronation/50 degrees supination.15 The arc of active flexion in the knee needed for activities of daily living is

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10 to 120 degrees.16 Dorsiflexion at the ankle of at least 10 degrees is required of the stance limb during the gait cycle to prevent knee hyperextension and an abnormal gait, both leading to increased energy requirements.17 Early ROM exercise is essential to restoration of joint mobility and is beneficial to the cartilage.18 For example, postoperative treatment of ankle fracture patients with a brace and early motion resulted in earlier return to work than use of a cast.19 However, early motion alone does not always mean better results, and there may be some risks. A separate study found an increased incidence of superficial wound infections in postoperative ankle fracture patients who were randomized to early mobilization in a brace compared with patients immobilized in a cast for 6 weeks.20 A study of 60 patients with isolated distal radius fractures treated with a volar locking plate were assigned to early motion (average of 8 days) or late motion (average of 49 days). No difference was found at 3 and 6 months postoperatively with regard to motion, pain, DASH scores, grip strength, or radiographic parameters.21 The appropriate timing and extent of postoperative rehabilitation requires experience and attention of the surgeon.

PREVENTION: HETEROTOPIC OSSIFICATION The prevention of HO deserves a special section because it does not fall under the typical preventative rehabilitation care of controlling pain and inflammation. There is no completely effective or well-accepted regimen. Radiation therapy has proved effective in the prevention of HO at the hip.22-24 Indomethacin has also been shown to be equally as effective as radiation in the prevention of HO following surgical treatment of acetabular fractures through a posterior or extensile approach.25 Indomethacin works by interrupting the synthesis of prostaglandin E2 (PGE2) and inhibits the differentiation of precursor cells into osteoblasts. It must be started within 24 hours and is typically given as 25 mg orally three times daily for 6 weeks. Radiation therapy is typically a single dose of 800 cGy and is administered within 72 hours. Once the HO process begins, it is questionable whether any preventative method is available to improve the outcome.23,26,27 Treatment of established symptomatic HO requires surgical excision, a procedure with significant risks of bleeding, infection, and nerve or vessel injury.

COMPLICATION MANAGEMENT: ARTHROFIBROSIS The initial management of arthrofibrosis is physical therapy, control of pain and inflammation, and occasionally manipulation under anesthesia. If these conservative measures fail and no progress is made by 3 months after surgery, then more aggressive surgical steps should be initiated. In the knee, arthroscopic lysis of adhesions with manipulation under anesthesia is the procedure of choice when limitation of motion is nonprogressive and primarily due to a discrete intra-articular lesion.28 Adhesions are resected under direct visualization, and intra-articular structures are evaluated. This procedure is better for gaining flexion than extension,29 perhaps due to the fact that adhesions causing loss of extension are likely to be posterior and difficult to access. The ideal time frame for intervention is 3 to 9 months after surgery.30-32 Success is less likely after 1 year of restricted motion.30,33,34 Open quadricepsplasty is a more aggressive approach used for refractory extension contractures of the knee. This classical procedure, described by Judet and Thompson, includes excision of the

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vastus intermedius with or without lengthening of the rectus femoris. To reduce the high rate of complications associated with these procedures, a recent study described a minimally invasive quadricepsplasty combined with arthroscopic lysis of adhesions.35 This procedure led to comparable results, with an average flexion gain of 88 degrees. There is recent evidence to support arthroscopic release of refractory frozen shoulder, whether it is idiopathic, postfracture, or post-traumatic.36-38 A patient with limitation of external rotation to less than 60% of the contralateral shoulder should be considered for surgical lysis to avoid the development of arthritis from eccentric contact, especially if supervised physical therapy shows no improvement after a period of 3 to 4 months.12 The first line of offense in elbow stiffness is graduated active-assisted stretching supervised with a physical therapist. This is most successful in the first 2 months. If this fails, dynamic and/or static splinting is the next step. A dynamic hinged elbow splint with spring or rubber band tension is useful for flexion deficits, but often is not well tolerated. A static, progressive (turnbuckle) splint is tolerated better by most patients and has shown good results.39 This method of splinting has also shown good results in the wrist and knee.40,41 A manipulation under anesthesia is not useful in the elbow joint, as it can cause tearing of soft tissue, worsen swelling and inflammation, as well as articular cartilage delamination or damage.42 A motivated patient with no improvement after 3 to 6 months of conservative treatment should be managed operatively. The options include soft tissue releases along with removal of bony impingement, limited bony arthroplasties (Outerbridge-Kashiwagi ulnohumeral arthroplasty), or total elbow arthroplasty. The current state of the articular cartilage should be considered in selection of the procedure. A young patient with healthy cartilage should be managed with a limited soft tissue release and excision of osteophytes. The more common bone spurs located at the tip of the olecranon and coronoid can be excised arthroscopically. A continuous passive motion (CPM) machine may be used in the initial postoperative period after manipulation of any joint, but active motion is preferred. It is generally more difficult to treat established contractures with CPM machines because they lack the mechanical advantage or power to affect end-range mobility.42 Again, prevention of pain and inflammation is very important during rehabilitation. A continuous epidural anesthesia infusion is beneficial in the initial postoperative period following manipulation or surgical release, especially if CRPS is an underlying issue or if pain played a significant part in the development of stiffness. If impingement or painful hardware may be the underlying culprit of loss of motion, hardware removal should be considered. Improvement in pain and function can be expected with minimal risk.43 Delay of removal until after fracture healing may be an option if the restriction of motion is not critical.

COMPLICATION MANAGEMENT: HETEROTOPIC OSSIFICATION If prevention fails and there is severe limitation of ROM or ankylosis, then surgical excision of HO is indicated. The timing of excision is controversial, but waiting until the bone “matures” has been recommended. The reduction of bone scan activity or return to normal alkaline phosphatase levels have been seen as evidence of bone maturity; however, these may take many months. A significant delay may be harmful by allowing scar formation, muscle contracture, and cartilage erosion; however, early

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excision carries the risk of recurrence. A typical time frame in the hip is approximately 6 months.44 There is evidence to support excision as early as 3 months in the elbow followed by radiation therapy.45 Following excision, perioperative radiation within 48 hours of surgery with a single dose of 700 to 800 cGy has been shown to reduce the recurrence.46

SUMMARY The development of a stiff joint after fracture is a frustrating and difficult problem with significant clinical implications. Anatomic joint alignment with sufficient fixation to allow early motion is the initial goal of the orthopedic traumatologist. Adequate control of pain and inflammation is often underappreciated but is essential for allowing early postoperative motion and early return to function.

REFERENCES 1. Zeichen J, van Griensven M, Albers I, Lobenhoffer P, Bosch U. Immunohistochemical localization of collagen VI in arthrofibrosis. Arch Orthop Trauma Surg. 1999;119:315-318. 2. Border WA, Noble NA. Transforming growth factor beta in tissue fibrosis. N Engl J Med. 1994;331:1286-1292. 3. Unterhauser FN, Bosch U, Zeichen J, Weiler A. Alpha-smooth muscle actin containing contractile fibroblastic cells in human knee arthrofibrosis tissue. Winner of the AGADonJoy Award 2003. Arch Orthop Trauma Surg. 2004;124:585-591. 4. Skutek M, Elsner HA, Slateva K, et al. Screening for arthrofibrosis after anterior cruciate ligament reconstruction: analysis of association with human leukocyte antigen. Arthroscopy. 2004;20:469-473. 5. Salter RB. The biologic concept of continuous passive motion of synovial joints. The first 18 years of basic research and its clinical application. Clin Orthop. 1989;242:12-25. 6. Thomas B, Yeo JM, Slater GL. Chronic pain after ankle fracture: an arthroscopic assessment case series. Foot Ankle Int. 2005;26:1012-1016. 7. Hintermann B, Regazzoni P, Lampert C, Stutz G, Gachter A. Arthroscopic findings in acute fractures of the ankle. J Bone Joint Surg Br. 2000;82:345-351. 8. DeAndrade JR, Grant C, Dixon AS. Joint distension and reflex muscle inhibition in the knee. J Bone Joint Surg. 1963;47-A:313-322. 9. Ghalambor N, Matta JM, Bernstein L. Heterotopic ossification following operative treatment of acetabular fractures. An analysis of risk factors. Clin Orthop. 1994;305:96-105. 10. Garland DE, O’Hollaren RM. Fractures and dislocations about the elbow in the headinjured adult. Clin Orthop. 1982;168:38-41. 11. Lefevre-Colau MM, Babinet A, Fayad F, et al. Immediate mobilization compared with conventional immobilization for the impacted nonoperatively treated proximal humeral fracture. A randomized controlled trial. J Bone Joint Surg Am. 2007;89:2582-2590. 12. Warner JJ. Frozen shoulder: diagnosis and management. J Am Acad Orthop Surg. 1997;5:130140. 13. Jordan C, Davidovitch RI, Walsh M, Tejwani N, Rosenberg A, Egol K. Spinal anesthesia mediates improved early function and pain relief following surgical repair of ankle fractures. J Bone Joint Surg Am. 2010;92:368-374. 14. Shelbourne KD, Wilckens JH, Mollabashy A, DeCarlo M. Arthrofibrosis in acute anterior cruciate ligament reconstruction: the effect of timing of reconstruction and rehabilitation. Am J Sports Med. 1991;19:332-336.

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15. Morrey BF, Askew LJ, Chao EY. A biomechanical study of normal functional elbow motion. J Bone Joint Surg Am. 1981;63:872-877. 16. Magit D, Wolff A, Sutton K, Medvecky MJ. Arthrofibrosis of the knee. J Am Acad Orthop Surg. 2007;15:682-694. 17. Esquenazi A, Talaty M. Physical medicine and rehabilitation: the complete approach. In: Grabois M, Garrison SJ, Hart KA, Lehmkuhl LD, eds. Normal and Pathological Gait Analysis. New York, NY: Blackwell Science; 2000:242-262. 18. Gebhard JS, Kabo JM, Meals RA. Passive motion: the dose effects on joint stiffness, muscle mass, bone density, and regional swelling. A study in an experimental model following intra-articular injury. J Bone Joint Surg Am. 1993;75:1636-1647. 19. Egol KA, Dolan R, Koval KJ. Functional outcome of surgery for fractures of the ankle. A prospective, randomised comparison of management in a cast or a functional brace. J Bone Joint Surg Br. 2000;82:246-249. 20. Lehtonen H, Järvinen T, Honkonen S, Nyman M, Vihtonen K, Järvinen M. Use of a cast compared with a functional ankle brace after operative treatment of an ankle fracture: a prospective, randomized study. J Bone Joint Surg Am. 2003;85:205-211. 21. Lozano-Calderón SA, Souer S, Mudgal C, Jupiter JB, Ring D. Wrist mobilization following volar plate fixation of fractures of the distal part of the radius. J Bone Joint Surg Am. 2008;90:1297-1304. 22. Ayers DC, Evarts C, Parkinson JR. The prevention of heterotopic ossification in highrisk patients by low-dose radiation therapy after total hip arthroplasty. J Bone Joint Surg. 1986;68-A:1423-1430. 23. Ayers DC, Pellegrini VD Jr, Evarts C. Prevention of heterotopic ossification in high-risk patients by radiation therapy. Clin Orthop. 1991;263:87-93. 24. Coventry MB, Scanlon PW. The use of radiation to discourage ectopic bone. A nine-year study in surgery about the hip. J Bone Joint Surg. 1981;63-A:201-208. 25. Burd TA, Lowry KJ, Anglen JO. Indomethacin compared with localized irradiation for the prevention of heterotopic ossification following surgical treatment of acetabular fractures. J Bone Joint Surg. 2001;83-A:1783-1788. 26. Garland DE. A clinical perspective on common forms of acquired heterotopic ossification. Clin Orthop. 1991;263:13-29. 27. Jupiter JB. Heterotopic ossification about the elbow. In: Instructional Course Lectures, The American Academy of Orthopaedic Surgeons. Park Ridge, IL: American Academy of Orthopaedic Surgeons; 1991;40:41-44. 28. Lindenfeld TN, Wojtys EM, Husain A. Operative treatment of arthrofibrosis of the knee. In: Instructional Course Lectures, The American Academy of Orthopaedic Surgeons. J Bone Joint Surg Am. 1999;81:1772-1784. 29. Sprague NF III. Motion-limiting arthrofibrosis of the knee: the role of arthroscopic management. Clin Sports Med. 1987;6:537-549. 30. Achalandabaso J, Albillos J. Stiffness of the knee—mixed arthroscopic and subcutaneous technique: results of 67 cases. Arthroscopy. 1993;9:685-690. 31. Christel P, Herman S, Benoit S, Bornet D, Witvoët J. A comparison of arthroscopic arthrolysis and manipulation of the knee under anaesthesia in the treatment of post-operative stiffness of the knee. French J Orthop Surg. 1988;2:348-355. 32. Cosgarea AJ, DeHaven KE, Lovelock JE. The surgical treatment of arthrofibrosis of the knee. Am J Sports Med. 1994;22:184-191. 33. Barber-Westin SD, Noyes FR, Andrews M. A rigorous comparison between the sexes of results and complications after anterior cruciate ligament reconstruction. Am J Sports Med. 1997;25:514-526. 34. Akeson WH, Woo SL, Amiel D, Coutts RD, Daniel D. The connective tissue response to immobility: biochemical changes in periarticular connective tissue of the immobilized rabbit knee. Clin Orthop. 1973;93:356-362.

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35. Wang JH, Zhao JZ, He YH. A new treatment strategy for severe arthrofibrosis of the knee. A review of twenty-two cases. J Bone Joint Surg Am. 2006;88:1245-1250. 36. Pollock RG, Duralde XA, Flatow EL, Bigliani LU. The use of arthroscopy in the treatment of resistant frozen shoulder. Clin Orthop. 1994;304:30-36. 37. Warner JJ, Allen A, Marks PH, Wong P. Arthroscopic release for chronic, refractory adhesive capsulitis of the shoulder. J Bone Joint Surg Am. 1996;78:1808-1816. 38. Holloway GB, Schenk T, Williams G, Ramsey M, Iannotti J. Arthroscopic capsular release for the treatment of refractory postoperative or post-fracture shoulder stiffness. J Bone Joint Surg Am. 2001;83-A:1682-1687. 39. Green DP, McCoy H. Turnbuckle orthotic correction of elbow-flexion contractures after acute injuries. J Bone Joint Surg Am. 1979;61:1092-1095. 40. McGrath MS, Ulrich SD, Bonutti PM, Smith JM, Seyler TM, Mont MA. Evaluation of static progressive stretch for the treatment of wrist stiffness. J Hand Surg Am. 2008;33(9):14981504. 41. Bonutti PM, McGrath MS, Ulrich SD, McKenzie SA, Seyler TM, Mont MA. Static progressive stretch for the treatment of knee stiffness. Knee. 2008;15(4):272-276. 42. Bruno R, Lee M, Strauch RJ, Rosenwasser MP. Posttraumatic elbow stiffness: evaluation and management. J Am Acad Orthop Surg. 2002;10:106-116. 43. Minkowitz RB, Bhadsavle S, Walsh M, Egol KA. Removal of painful orthopaedic implants after fracture union. J Bone Joint Surg Am. 2007;89:1906-1912. 44. Cipriano CA, Pill SG, Keenan MA. Review article: heterotopic ossification following traumatic brain injury and spinal cord injury. J Am Acad Orthop Surg. 2009;17:689-697. 45. Mcauliffe JA, Wolfson AH. Early excision of heterotopic ossification about the elbow followed by radiation therapy. J Bone Joint Surg Am. 1997;79-A:749-755. 46. Poggi MM, Thomas BE, Johnstone PA. Excision and radiotherapy for heterotopic ossification of the elbow. Orthopedics. 1999;22:1059-1061.

II

Upper Extremity

8 Complications of Clavicle Fractures Janos P. Ertl, MD

Fractures of the clavicle account for 2.6% to 4% of all fractures and account for 35% of fractures about the shoulder girdle.1-3 Although commonly treated closed, surgical treatment has been increasingly used for clavicle fracture in recent years. The most common complications of both open and closed treatment are nonunion, malunion, and cosmetic dissatisfaction. Surgical treatment carries the additional risks of infection, vascular injury, hemo/pneumothorax, neurologic injury to the brachial plexus, hardware complaints or migration, and dysesthesia or cutaneous numbness. Less common late complications include ulnar neuropathy, acromioclavicular joint arthritis, and refracture.4

NONUNION Multiple comprehensive, prospective studies have clearly shown the nonunion rate in nonoperative treatment of clavicle fracture to be up to 21%, exponentially higher than previously reported,5 and a 2.4% incidence after surgical treatment.6,7 Nonunion risk factors include mechanism of injury (high velocity versus low velocity), open fracture, fracture displacement, comminution, distal clavicle fracture, increasing age, refracture, failed internal fixation, soft tissue injury, and female gender. Paradoxically, the risk of nonunion was highest in elderly female patients with a diaphyseal fracture. However, most clavicle fractures are encountered in the young male population and therefore result in the highest incidence of nonunion. Some have suggested that lateral end clavicle fractures seem to be particularly at risk, and in some small case series, the rate was reported to be between 18% and 40%. A larger prospective study of 263 lateral end fractures demonstrated a nonunion rate of 11.5%.3,7 77

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Table 8-1

Risk Factors RISK FACTORS FOR NONUNION FOLLOWING NONOPERATIVE TREATMENT1-3 Age Gender Comminution Displacement Severity of trauma Lateral end fracture

Associated with osteoporosis Greater in females Results in less stability >2 cm, soft tissue interposition Amount of energy transferred, devascularization Displacement due to the weight of the arm and inability to immobilize

RISK FACTORS FOR NONUNION FOLLOWING OPERATIVE TREATMENT8 Unstable fixation Excessive soft tissue stripping

Weak implant or inadequate fixation8 Devascularization

Anatomic studies have demonstrated the main blood supply to the middle third of the clavicle is periosteal. This supply stems from the two branches of the thoracoacromial trunk that penetrate the pectoralis major muscle and the deltoid muscle. Fractures with significant displacement will result in double vascular compromise with disruption of the periosteal blood supply located between the muscles, insertions, and the arterial supply from the suprascapular artery. On the basis of these anatomical studies, it has been suggested that bone grafting is appropriate when surgical treatment of acute displaced clavicular fractures or nonunions cannot preserve the periosteal blood supply. Bone grafting, vascularized or not, must be as long as necessary to bridge the nonvascularized part of the bone.9 Some series suggest that supplementary autologous bone grafting is commonly used and may shorten the time to union.3 Patient selection for surgical treatment may be the most important strategy for reducing the risk of nonunion—displacement, comminution, female gender, and age may be taken into account (Table 8-1). Robinson reviewed 1000 clavicle fractures and showed that displaced (100% translation of fracture fragments) midshaft fractures were 18.5 times more likely to result in delayed or nonunion as compared with undisplaced fractures. In addition, in cases of conservative management, current treatment of choice for displaced midshaft fractures of the clavicle is a simple sling for comfort, followed by early range of motion exercise as pain diminishes.5 Most patients are advised to begin “out of sling” activities after 3 weeks, and at the 6-week point, a rehabilitation schedule is carried out, depending on the status of fracture healing.10-12 The period required for stabilization of fractures of the middle shaft of the clavicle is 2 weeks for the newborn, 3 weeks for children, 4 to 6 weeks for adolescents, and 6 weeks for adults, but there has not been clinical evidence for these guidelines.3 There appears to be no consensus on the optimal duration of immobilization, and recommendations are made between 2 and 6 weeks. There has been no recognized association between nonunion and length of sling wear.2 Radiologically confirmed healing appears much later when compared with clinically assessed healing and can take 12 weeks.

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In patients treated surgically, prevention of nonunion involves following good principles of internal fixation: minimization of soft tissue stripping, anatomic reduction with lag screws when possible, selection of adequate implants, and bone grafting in the face of extensive comminution or bone loss. Ideally, a 3.5-mm dynamic compression plate or plate of similar strength should be used, and the length should be at least three screw holes on each side when possible. Semitubular plates are not as rigid and should not be used.13 Reconstruction plates are more easily contoured and have been used with success; however, they account for several failures in obtaining union.13 Precontoured plates of suitable thickness offer the advantage of ease of placement without manipulation of the plate. Locked plates are not necessary for the acute plating of nonosteoporotic clavicular fractures. There is no significant advantage over conventional plating, and the cost is higher. In osteopenia or with short fragments at the lateral end, locking fixation is advantageous (Table 8-2). Nonunion is usually associated with complaints of pain and is diagnosed by plain radiographs showing hardware or fixation failure, displacement, and discontinuity. Infection should be ruled out. If the clavicle cannot be visualized due to hardware, computed tomography may be helpful. However, not all clavicle nonunions are symptomatic, particularly those at the lateral end. Treatment of a symptomatic nonunion following conservative treatment involves internal fixation with plating and lag screws when possible. If there is atrophy of the bone ends, absorption, or bone loss, cancellous grafting is helpful. In cases of significant shortening, cortical or corticocancellous grafts from the iliac crest or fibula can re-establish correct length.12 The intramedullary canal on both sides of the nonunion should be drilled and opened during treatment. Nonunion treatment following previous surgery is more complicated and usually involves hardware removal, evaluation for infection, and grafting. The use of a temporary spacer of antibioticladen polymethylmethacrylate can be useful to form a Masquelet membrane for subsequent cancellous grafting.14 Treatment of a symptomatic nonunion of the lateral clavicle may include excision of the lateral end of the clavicle or fracture fixation with or without bone graft. Excision is usually preferred if the lateral fragment is small and the coracoclavicular ligaments are intact, whereas fixation is used when there is a larger fragment, with good bone stock, and there is a reasonable chance of the procedure successfully promoting union. Fixation options include locking plates, the hook plate,15,16 and transarticular pin fixation across the acromioclavicular joint, which is removed after healing. Transacromial rigid fixation has only anecdotal support, and it is felt that rigid transacromial fixation has a high rate of loosening and fatigue.17 The hook plate has been used with some success for displaced lateral end clavicular fractures, but there are concerns that the plate may induce shoulder stiffness and osteoarthritis of the acromioclavicular joint.16 There is also a risk of skin slough and infection. Improper positioning of the hook may lead to inadequate fixation. Osteolysis has been noted around the hole for the hook as shoulder movement increases, and most surgeons advise routine plate removal as early as 3 months after implantation or after fracture union, which necessitates a second operation. The results of nonunion treatment have been assessed only in small numbers of patients, in studies mainly focusing on the treatment of midshaft nonunions.18

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Table 8-2

Implant Options for Clavicle Fixation IMPLANT

CRITICAL FACTORS1,2,3,5,6,8,11,15

Semitubular plate

Too weak to maintain sufficient stability

Reconstruction plate, 3.5 mm

Easily contoured; however, may not be strong enough to maintain stability

LCDCP, 3.5 mm

Provide sufficient stability, six cortices on either side of fracture, difficult to contour

Precontoured plates, 3.5 mm

Ease of application, must be sufficiently thick, do not require contouring

Locked plate

Reserved for osteoporotic bone, small lateral fragments

Hook plate

Used in distal fractures, however, bulky and cause shoulder pain necessitating planned removal

Intramedullary implant

More cosmetic, less rigid, may migrate

Ex-Fix

Rarely used, less rigid, if used then for infected nonunion

Bone graft

When shortening is present, tricortical segment of iliac crest

MALUNION All displaced clavicle fractures that are treated nonoperatively heal with some alteration of bone shape secondary to angulation or shortening, but often with few or no symptoms.19,20 A prospective study examining the risk factors for long-term functional problems found that, although comminution, initial displacement, and increasing age were predictive of symptomatic malunion, the degree of shortening was not.21 However, in a retrospective study, McKee noted that fractures with more than 2 cm of shortening (average 2.9 cm) have a tendency to be associated with decreased abduction strength and greater patient dissatisfaction.20,22 A significant number of patients with malunited fractures have ongoing symptomatology with orthopedic, neurologic, and functional cosmetic deficits in a characteristic pattern; it would appear that clavicular malunion is a distinct clinical entity.5 Prevention of clavicular malunion involves patient assessment and consideration of surgery for those at risk for symptomatic malunion. Careful follow-up of conservatively treated patients may identify problems early. There is no role for “figure of eight” bracing in conservative management, as it has not been shown to prevent malunion. Malunion after surgical treatment is a result of malreduction. The risk may be reduced through preoperative planning using the contralateral side and intraoperative imaging with portable plain films prior to leaving the operating room.6 Treatment of a clavicle malunion consists of surgical correction to restore length, angular deformity, and rotation of the clavicle. A corrective osteotomy and plate

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fixation can improve function in patients in whom symptomatic malunion has produced neurovascular compression, discomfort and weakness with use of the shoulder, or cosmetic deformity.19,20 The corrective osteotomy may be supplemented with cancellous bone grafting or an intercalary bone graft. When difficulty in determining the length of the malunited clavicle is anticipated, a preoperative radiographic image of both clavicles is helpful. Treatment of symptomatic malunions/delayed unions up to 63 months postinjury has resulted in improvement of the function of the upper extremity, decreased pain, and increased patient satisfaction, equivalent to treatment of acute fractures.23

NEUROVASCULAR INJURY The main potential intraoperative complication is injury to the subclavian artery or vein at the time of fracture mobilization or from drill penetration. The risk of this complication is very low, but it may necessitate vascular or cardiothoracic surgical intervention. Prevention involves the use of fresh, sharp drill bits and careful attention to gentle technique while drilling. Plate position may play a role. The plate usually is placed on the tension side of the bone—for the clavicle, the anterosuperior position. Biomechanically, this position provides the best stability.24 However, clinically successful treatment with anteroinferior placement also has been described.25 The anteroinferior position, although less favorable biomechanically, allows for drilling in a direction away from the subclavian vessels and lung.

HEMO/PNEUMOTHORAX Injury to the lung may be a result of the injury or, very rarely, of surgical treatment. The risk of this associated finding is substantially higher in the case of open clavicle fracture. Based on a retrospective review from a busy trauma center, open clavicle fractures are unlikely to occur in isolation and represent an early clinically identifiable sign that should warn the caregiver of the potential for associated, lifethreatening injuries.26 In particular, the 50% rate of pneumothorax in this population greatly exceeds the 3% rate as previously reported associated with clavicle fractures. All of the pneumothoraces were recognized as part of the initial trauma evaluation and were treated with thoracostomy tubes.

HARDWARE COMPLAINTS The most common hardware issue with clavicle fractures is prominence of plates or screws placed superiorly, where the clavicle is quite subcutaneous under sensitive skin, and where it may be irritated by backpack or clothing straps or during carrying of burdens on the shoulder. Anteroinferior placement of plates may reduce the risk of this problem. The treatment is removal of the hardware after the fracture is healed, which may be difficult to ascertain. Premature removal may lead to refracture. Another common hardware problem is migration of smooth wires or pins used for fixation. Such implants can migrate an incredible distance through the body, ending up in such concerning places as the spinal canal, the heart, the lungs, and the abdomen.27 Prevention involves avoiding the use of smooth pins or wires, and if they

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must be used, careful follow-up radiographs and planned removal are essential. If a pin, wire, or screw is missing from a follow-up radiograph, one cannot assume that it was extruded from the body, but rather must initiate a radiographic search. The use of the hook plate allows fixation of lateral fractures or nonunions, particularly associated with acromioclavicular joint injury or dislocation. However, because of the hardware in the subacromial space, these plates should be removed routinely after healing. Most surgeons advise routine plate removal at 3 months after implantation, which necessitates a second operation.16 The timing of plate removal is critical, as early removal may result in nonunion or refracture due to instability at the fracture site, whereas delayed removal can lead to shoulder stiffness or even fracture medial to the plate.3 In a retrospective review of 44 patients, Renger and colleagues removed all 44 implants after consolidation at a mean of 8.4 months (2 to 33 months) postoperatively.15

NERVE INJURY/SCAR PROBLEMS Complaints about painful scars, dysesthesia, or numbness of the skin of the anterior chest wall are common and often result from injury or division of the supraclavicular nerves during surgical exposure. These nerves should be sought and preserved, if possible. It is useful to warn patients about the possibility of some numbness before surgery, as part of the informed consent. A newly described surgical incision alternative is to incise the inferior skin after pulling it up over the fracture site.28 As this mobile skin is released, the incision will fall 1 to 2 cm below the clavicle and prevent the wound from being directly in contact with the plate. The aim is to improve cosmesis and prevent wound complications.

REFERENCES 1. Postacchini F, Gumina S, De Santis P, Albo F. Epidemiology of clavicle fractures. J Shoulder Elbow Surg. 2002;11:452-456. 2. Jeray K. Acute midshaft clavicle fractures. J Am Acad Orthop Surg. 2007;15(7):26A. 3. Khan LAK, Bradnock TJ, Scott C, Robinson CM. Fractures of the clavicle. J Bone Joint Surg Am. 2009;91:447-460. 4. Kitsis CK, Marino AJ, Krikler SJ, Birch R. Late complications following clavicular fractures and their operative management. Injury. 2003;34:69-74. 5. McKee MD. Clavicle fractures in 2010: sling/swathe or open reduction and internal fixation? Orthop Clin N Am. 2010;41:225-231. 6. Zlowodzki M, Zelle BA, Cole PA, Jeray K, McKee MD. Treatment of midshaft clavicle fractures: systematic review of 2144 fractures. J Ortho Trauma. 2005;19(7):504-507. 7. Robinson CM, Court-Brown CM, McQueen MM, Wakefield AE. Estimating the risk of nonunion following nonoperative treatment of a clavicular fracture. J Bone Joint Surg Am. 2004;86:1359-1365. 8. Chen CH, Chen JC, Wang C, Tien YC, Chang JK, Hung SH. Semitubular plates for acutely displaced midclavicular fractures: a retrospective study of 111 patients followed for 2.5 to 6 years. J Ortho Trauma. 2008;22:463-466. 9. Havet E, Duparc F, Tobenas-Dujardin AC, Muller JM, Delas B, Fréger P. Vascular anatomical basis of clavicular non-union. Surg Radiol Anat. 2008;30(1):23-28. Epub 2007 Nov 24. 10. Kulshrestha V, Roy T, Audige L. Displaced midshaft clavicle fractures: a prospective cohort study. J Ortho Trauma. 2011;25(1):31-38.

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11. Simpson NS, Jupiter JB. Clavicular nonunion and malunion: evaluation and surgical management. J Am Acad Ortho Surg. 1996;4(1):1-8. 12. Jupiter JB, Leffert RD. Non-union of the clavicle. Associated complications and surgical management. J Bone Joint Surg Am. 1987;69:753-760. 13. Böstman O, Manninen M, Pihlajamaki H. Complications of plate fixation in fresh displaced midclavicular fractures. J Trauma. 1997;43:778-783. 14. Masquelet AC, Begue T. The concept of induced membrane for reconstruction of long bone defects. Orthop Clin North Am. 2010;41(1):27-37. 15. Renger RJ, Roukema GR, Reurings JC, Raams PM, Font J, Verleisdonk EJ. The clavicle Hook plate for Neer type II lateral clavicle fractures. J Ortho Trauma. 2009;23(8):570-574. 16. Flinkkilä T, Ristiniemi J, Lakovaara M, Hyvönen P, Leppilahti J. Hook-plate fixation of unstable lateral clavicle fractures. A report on 63 patients. Acta Orthopaedica. 2006;77(4):644-649. 17. Bucholz RW, Court-Brown C, Heckman JD. Rockwood & Green’s Fractures in Adults. Philadelphia, PA: Lippincott Williams & Wilkins; 2009. 18. Der Tavitian J, Davison JN, Dias JJ. Clavicular fracture non-union surgical outcome and complications. Injury. 2002;33:135-143. 19. Edelson JG. The bony anatomy of clavicular malunions. J Shoulder Elbow Surg. 2003;12:173178. 20. McKee MD, Wild LM, Schemitsch EH. Midshaft malunions of the clavicle. Surgical technique. J Bone Joint Surg Am. 2004;86(suppl 1):37-43. 21. Nowak J, Holgersson M, Larsson S. Can we predict long-term sequelae after fractures of the clavicle based on initial findings? A prospective study with nine to ten years of followup. J Shoulder Elbow Surg. 2004;13:479-486. 22. McKee MD, Wild LM, Schemitsch EH. Midshaft malunions of the clavicle. J Bone Joint Surg Am. 2003;85-A(5):790-797. 23. Potter JM, Jones C, Wild LM, Schemitsch EH, McKee MD. Does delay matter? The restoration of objectively measured shoulder strength and patient-oriented outcome after immediate fixation versus delayed reconstruction of displaced midshaft fractures of the clavicle. J Shoulder Elbow Surg. 2007;16:514-518. 24. Iannotti MR, Crosby LA, Stafford P, Grayson G, Goulet R. Effects of plate location and selection on the stability of midshaft clavicle osteotomies: a biomechanical study. J Shoulder Elbow Surg. 2002;11:457-462. 25. Kloen P, Sorkin AT, Rubel IF, Helfet DL. Anterioinferior plating of mid shaft clavicular nonunions. J Ortho Trauma. 2002;16:425-430. 26. Taitsman LA, Nork SE, Coles CP, Barei DP, Agel J. Open clavicle fractures and associated injuries. J Ortho Trauma. 2006;20(6):396-399. 27. Lyons FA, Rockwood CA. Migration of pin used in operations on the shoulder. J Bone Joint Surg Am. 1980;68:434-440. 28. Coupe BD, Wimhurst JA, Indar R, Calder DA, Patel AD. A new approach for plate fixation of midshaft clavicular fractures. Injury. 2005;36:1166-1167.

9 Complications of Proximal and Diaphyseal Humerus Fractures Eric S. Moghadamian, MD and Raymond D. Wright, MD

PROXIMAL HUMERUS Fractures of the proximal portion of the humerus are a common injury and an increasing problem in the elderly osteoporotic patient. While multiple treatment strategies exist for this injury, treatment can be complicated by loss of fixation (regardless of the method chosen) due to the poor bone quality and extensive comminution often encountered. In addition, impingement and avascular necrosis of the humeral head can occur after internal fixation.

Etiological Factors of Loss of Fixation and Avascular Necrosis Selecting the optimal treatment strategy for each patient is the first step in minimizing complications in proximal humerus fractures. The minimally displaced and somewhat stable nature of up to 75% of these fractures makes them amenable to nonoperative treatment, especially in the elderly.1,2 However, complex or displaced fractures may warrant operative treatment in order to maintain shoulder mobility.3 Endoprosthesis, either hemi- or total shoulder arthroplasty, may be considered in patients with severe osteoporosis, a highly comminuted or head-splitting fracture, or those with pre-existing degenerative joint disease (DJD) of the shoulder.4 Anatomical reconstruction of the proximal humerus is technically demanding, and failure of fixation may result in nonunion.5 Loss of fixation after surgical treatment has been reported in up to 14% of operative cases.6,7 Loss of tuberosity fixation may occur when arthroplasty is employed if sutures are not solidly placed into the rotator cuff tendons. Furthermore, 85

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Table 9-1

Risk Factors for Proximal Humeral Fracture Complications COMPLICATION

RISK FACTORS

Aseptic necrosis

Metaphyseal head extension with medial hinge displacement, four-part fractures, head-splitting fractures

Subacromial impingement

Lateral implant positioned cranial to the greater tuberosity; failure of fixation of greater tuberosity with resultant cranial displacement

Failure of fixation

Use of nonlocking implants, osteoporotic bone, failure to restore medial calcar support

Glenohumeral screw penetration

Settling of comminuted fracture, placement of screws that are too close to subchondral bone of humeral head, inadequate intraoperative visualization

the cancellous bone of the proximal humerus does not provide for strong screw purchase; therefore, conventional (nonlocking) plates frequently demonstrate screw loosening in the proximal segment. Intramedullary nails also may provide suboptimal fixation in the proximal segment due to the paucity of fixation points. Percutaneous, terminally threaded wire fixation may result in displacement of the wire into the thorax or adjacent neurovascular structures, as well as catastrophic fixation failure if too few or poorly positioned wires are employed.8 Locking plate fixation has become the most popular method of operative treatment for proximal humerus fractures.9 The advent of locked plating, although an improvement, is not a panacea and has introduced a new method of fixation failure.8 Aseptic necrosis, subacromial impingement, screw penetration into the humeral head, and loss of fixation in the proximal segment are among the most common complications related to plate and screw fixation of proximal humerus fractures (Table 9-1).9,10

Prevention: Surgical Techniques and Reduction Successful open treatment of proximal humerus fractures requires anatomic restoration of the relationship between the humeral head, shaft, and tuberosities. Preoperative radiographs should include anteroposterior (AP), scapular-Y, and axillary lateral views. This procedure can be performed in the beach chair position or with the patient positioned supine on a radiolucent table. Intraoperative fluoroscopy with visualization in two planes is essential to assess reduction and implant position.

Implant-Related Complications: Failure of Fixation, Subacromial Impingement, Screw Penetration Loss of fixation in the proximal humerus may be in the humeral head or the humeral shaft. Connor and colleagues detailed 349 cases in which 13% had fixation failure.6 He identified fixation failure as most commonly due to loosening of the fixation in the humeral head. In addition to nonlocking screw constructs, blade plate fixation has resulted in a high complication rate.11

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Table 9-2

Prevention: Proximal Humeral Fixation Strategies FIXATION CHALLENGE

CRITICAL FACTORS

Fracture of tuberosity

Suture fixation through rotator cuff; may aid in reduction and can be definitive fixation as sutures are passed through the plate

Osteoporosis

Locking implants; intramedullary fibular strut graft

Medial cortical comminution

Caudal screws within locking implant; intramedullary fibular strut graft

Figure 9-1. Proper plate application. Note the caudal screws directed into the humeral head. The lateral plate is positioned caudal to the superior extent of the greater tuberosity. The screws are inserted 5 to 10 mm short of the subchondral bone.

The surgeon applying locking plates must adhere to principles as these implants are applied.12,13 As with any locking plate, reduction must precede fixation because screws through the plate cannot be used to reduce the fracture. Placing the plate in a direct lateral position more effectively allows multiplanar fixation in the humeral head with multiple locking screws. The plate must be applied caudal to the proximal extent of the greater tuberosity to avoid subacromial impingement. Placement of heavy suture in the rotator cuff and threading the suture through the peripheral plate holes may augment tuberosity fixation and prevent displacement (Table 9-2).14 Gardner demonstrated that re-establishment of the medial-inferior cortex buttress function either by bony contact or by inferomedial screw placement prevented varus collapse of the humeral head segment (Figure 9-1).15 In the case of severe osteoporosis or a high degree of comminution of the inferomedial portion of the humeral head, an intramedullary fibular strut graft may be employed to help restore stability (see Table 9-2 and Figure 9-2).16

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A

B

Figure 9-2. (A) Preoperative studies demonstrated a highly comminuted proximal humerus fracture in a patient with osteoporotic bone. (B) The postoperative radiograph demonstrates anatomic restoration of the fracture with an intramedullary fibular strut graft. (Reprinted with permission of Michael J. Gardner, MD.)

Screw penetration into the glenohumeral joint is a potential complication of locking proximal humeral plate application. This may lead to glenoid cartilage destruction and resultant degenerative disease. Owsley demonstrated cutout of screws in 43% of patients older than age 60 and cautioned against open reduction and internal fixation (ORIF) in patients with advanced age and a thin rim of bone in the humeral head for fixation.8 It has been suggested to hand thread the screws directed into the head in order to allow for tactile appreciation for the screw length to avoid intraoperative screw perforation into the glenohumeral joint. Also, a smooth peg system (as opposed to screws) had been recommended for the theoretical decreased damage to the glenoid if late penetration occurs.17 Ricchetti recommends inserting screws that are 5 to 10 mm short of the subchondral bone in order to avoid intraoperative screw penetration and late penetration that may come with fracture settling.14

Avascular Necrosis Perfusion to the humeral head is principally from the arcuate and anterior humeral circumflex arteries. However, these arteries may be disrupted in low energy or simple fracture patterns with the implication that posterior humeral circumflex perfusion may be adequate for humeral head perfusion.12 Predictive factors for humeral head ischemia have been investigated by Hertel and colleagues.18 In perfusion studies, they determined that extension of the humeral head fracture into the metaphysis of less than 8 mm was a positive predictor of ischemia. Additionally, a greater than 2-mm disruption of the medial hinge was predictive of ischemia. A combination of metaphyseal head extension of less than 8 mm with a greater than 2-mm disruption of the medial hinge led to a 97% positive predictive value of ischemia in the humeral head.18

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The arcuate artery travels cranially just lateral to the groove of the biceps tendon and then enters the humeral head within the groove.10 Theoretically, avoiding dissection in this area could decrease the risk of iatrogenic osteonecrosis of the proximal humerus.

Rehabilitation Factors Postoperative passive motion may begin immediately as long as stable fixation is achieved. The patient should be encouraged to engage in active motion of the ipsilateral elbow and wrist as well. The passive shoulder motion is initiated with the intent to avoid frozen shoulder (adhesion formation).14 Ricchetti recommends passive assist and active exercises at 6 weeks and the commencement of resistance exercises at 10 to 12 weeks postoperatively.14 Resistance exercises performed before adequate healing is present may lead to loss of fixation.

Complication Management: Salvage Procedures The complication of aseptic necrosis of the proximal humerus has a significance that continues to be debated. In one study with 10-year follow-up, 37% of patients treated operatively developed osteonecrosis. However, 77% of the patients with osteonecrosis had good or excellent functional outcomes.19 Symptomatic treatment, including nonsteroidal anti-inflammatory drugs, activity restriction, and physical therapy, is the cornerstone for managing this complication. In patients who fail nonoperative treatment, treatment with core decompression has consistently demonstrated improved function in patients who have aseptic necrosis without collapse.20 Arthroscopy may be used for débridement of loose bodies and osteochondral flaps and may be used in addition to core decompression. Arthroplasty and resurfacing is reserved for patients with severe degenerative disease of the glenohumeral joint. Multiple factors must be taken into consideration when failure of fixation occurs, including patient age, activity level, medical comorbidities, and reason for fixation failure. Revision fixation can be considered as long as there is sufficient bone available for fixation and minimal or no degeneration of the glenohumeral joint. The use of locking plates and bone augmentation, for example with allograft struts, is usually necessary. In the case of severe comminution of the humeral head segment with degenerative disease of the glenohumeral joint, treatment with arthroplasty may be considered.

HUMERAL DIAPHYSIS Diaphyseal fractures of the humerus are relatively common, representing approximately 1% of all fractures.21 Common complications include nonunion and radial nerve palsy. Fortunately, humeral nonunion is a rare occurrence, with reported union rates between 94% and 98% with both closed22-24 and operative management.25-28

Etiological Factors of Nonunion Certain fracture patterns and patient characteristics may lead to problems with healing (Table 9-3). For example, transverse fractures that remain distracted or spiral/ oblique fractures involving the mid or proximal third of the diaphysis are thought to be at increased risk for nonunion.29-31 In addition, patients with pre-existing shoulder

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Table 9-3

Risk Factors for Humeral Shaft Nonunion After Nonoperative Treatment FACTOR

IMPLICATION/RESULT

Fracture distraction

Potential soft tissue interposition at fracture site, instability

Proximal third oblique/ spiral fracture

Continual pull of deltoid may distract fracture and prevent healing Possible increased risk for soft tissue interposition

Pre-existing shoulder or elbow pathology

Arthrosis or ankylosis of adjacent joints Increased motion at the fracture site predisposes patients to nonunion

Brachial plexus palsy

Absence of active muscle contractions and hydraulic effect required for maintaining alignment and compression of fracture

or elbow pathology32 or brachial plexus injuries are at increased risk for nonunion with nonoperative management. Bone loss in open fracture may create an “instant nonunion.” For those patients treated surgically, nonunion or failure of fixation is often secondary to technical errors by the treating surgeon; however, host factors such as occult infection, malnutrition, and endocrinopathies must also be ruled out (Table 9-4).

Prevention: Nonoperative Techniques Humeral shaft fractures amenable to nonoperative treatment are best treated with functional bracing, rather than casting. After a short period (~1 week ) of initial immobilization in a coaptation splint or hanging arm cast to allow for pain control, patients should be transitioned to a prefabricated fracture brace. Early active and passive elbow extension and flexion as well as pendulum exercises of the shoulder are an essential part of the treatment. Radiographs are typically obtained weekly to ensure appropriate reduction is maintained and progressive healing is exhibited. If acceptable reduction cannot be maintained or no evidence of clinical or radiographic healing is noted by 8 to 10 weeks, then operative treatment should be considered.33

Prevention: Operative Technique and Implant Selection While multiple forms of surgical treatment of humeral shaft fractures have been described, open reduction and plate osteosynthesis of the humerus remain the standard against which all other forms of fixation should be compared. This can be performed via a variety of approaches including the anterior (or anterolateral), posterior, direct lateral, or direct medial, with the anterior and posterior most commonly chosen. The anterior approach is most often selected for fractures involving the proximal and middle thirds of the humerus. The posterior approach provides excellent

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Table 9-4

Risk Factors for Humeral Shaft Nonunion After Surgical Treatment FACTOR

IMPLICATION/RESULT

Inadequate reduction

Lack of compression leading to instability Distraction at fracture site

Improper plate size (small fragment)

Diminished resistance to axial and torsional loads Increased risk of plate or screw failure

Inadequate screw number

Increased risk of screw pullout Higher risk of fixation failure

Compromised host

Malnutrition or undiagnosed endocrinopathy34

visualization of the middle and distal third of the humerus, as well as varying portions of the proximal third of the humerus depending on the deep surgical plane used.

Prevention: Implant Selection and Application Regardless of the surgical approach elected for plate fixation, the principles of fixation remain the same. In simple fractures amenable to direct reduction, either lag screw fixation with plate neutralization or compression plating is used to achieve interfragmentary compression. In more comminuted fractures, indirect reduction and bridge plating may be more appropriate because direct reduction and fixation may violate the soft tissues to such an extent that would preclude healing (Figure 9-3). Typically, a 4.5-mm plate should be selected. Although narrow 4.5- or 3.5-mm plates may be necessary in smaller individuals with narrow humeri, a broad 4.5-mm plate may be considered, as this implant is biomechanically superior to its smaller counterparts, and the staggered screw hole options theoretically prevent longitudinal fracturing of the humerus.35 In nonpathologic bone, most authors recommend at least three or four bicortical screws both proximal and distal to the main fracture line. A more practical recommendation would be three bicortical screws proximal and distal to any lag screw fixation in neutralization plates and four bicortical screws proximal as well as distally when using a compression plating technique. The length of the plate is more important than the number of screws, and every screw hole in the plate is not necessarily filled. When using a bridge plating technique, relative stability rather than absolute stability is the goal. With this type of construct, the size, length, and number of screws necessary for stable fixation has yet to be determined, although most authors promote the use of longer plates (10 to 12 holes) with screw fixation more remote from the fracture site to allow for a more flexible construct with a longer working length in order to achieve this state of relative stability (Figure 9-4).36

Nonunion Management Nonunion can occur following both nonoperative and operative treatment. The first step in appropriately managing this problem is to rule out or address possible correctable host factors that may have contributed to a nonunion, such as occult

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Figure 9-3. A comminuted midshaft humerus. This fracture is best suited for indirect reduction and bridge plating of the comminuted segment because direct interfragmentary reduction and fixation would likely result in complete devitalization of the comminuted fragments.

Figure 9-4. Bridge plate fixation of previous fracture from Figure 9-3 via an anterior approach resulted in radiographic union and an excellent clinical outcome.

A

B

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infection, endocrinopathy, or nicotine dependence. Once these potential confounders have been addressed and corrected, surgical management can proceed. The successful treatment of nonunions of the humerus is largely dependent upon establishing mechanical stability and/or appropriate biology at the nonunion site. Although multiple surgical tactics have been used to address nonunions of the humerus, open reduction and internal fixation by plating has consistently yielded good results. In cases of simple hypertrophic nonunion, especially after failed closed treatment, mechanical stabilization via open reduction and internal fixation alone is usually sufficient, but in oligotrophic and atrophic nonunions, augmentation of the nonunion site biology should be considered as well. Traditionally, this has been accomplished with autogenous bone grafting, but recent literature has suggested that stimulation of the nonunion site biology with demineralized bone matrix in lieu of autogenous bone graft may occasionally be effective with potentially less donor site morbidity.37 There have not been good comparative studies of these two strategies, and traditional bone grafting is the gold standard technique. Nonunion after previous operative treatment represents a more difficult problem. Preoperatively, erythrocyte sedimentation rate and C-reactive protein should be measured to evaluate for occult infection. If infection is identified, all indwelling implants should be removed and the causative organism treated with appropriate intravenous antibiotics until resolution. The addition of an antibiotic cement spacer or cement nail can also provide local antibiotic delivery as well as temporary stabilization and maintenance of the soft tissues. In the absence of infection or after resolution of a preexisting infection, proper treatment should include adequate débridement of the nonunion site to healthy viable bone and reopening of the medullary canals of the proximal and distal fragments to enhance vascularization of the nonunion site, followed by stable compression plating or wave plating and the addition of autogenous bone graft (Figures 9-5 and 9-6). In the presence of necrotic bone ends, bone shortening can be performed if necessary, although shortening more than 2 cm may lead to residual triceps weakness.38 In more severe situations where adequate débridement results in a larger segmental defect, cancellous autografting has been successful, although vascularized fibular bone graft may be necessary if cancellous grafting fails.

Etiological Factors of Radial Nerve Palsy Because the radial nerve lies in such close proximity to bone in the area of the spiral groove of the humerus, radial nerve palsies occur in approximately 12% of humeral shaft fractures. These palsies occur more frequently in association with factures of the middle and distal third of the humerus. Most palsies occur as a result of the initial injury and are usually due to contusion or stretching of the nerve at the time of injury. However, secondary palsies, which occur during the course of closed or open treatment, may also occur. Fortunately, approximately 90% of these palsies, whether primary or secondary, will ultimately recover.39,40

Prevention: Radial Nerve Palsies Unfortunately, because most radial nerve palsies are primary in nature, these are unpreventable. When they do occur, it is imperative for the treating physician to perform and document a detailed physical exam prior to initiating treatment. Secondary palsies will also occur despite appropriate nonoperative or operative care. However, if open treatment is selected, identification and protection of the radial

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Figure 9-5. A 34-year-old morbidly obese, vitamin D-deficient woman status post two failed surgical procedures with small fragment implants with recalcitrant infected nonunion.

Figure 9-6. Successful treatment of the same patient with removal of all pre-existing implants, débridement of the nonunion site back to healthy viable bone, culture-specific antibiotics, and placement of an antibiotic cement spacer followed by delayed shortening, compression plating, and wave plating and the addition of autogenous bone graft after resolution of infection.

nerve is paramount. When a posterior approach with a triceps split is chosen, the radial nerve and profunda brachii artery are best identified proximally between the confluence of the long and lateral heads of the triceps (Figure 9-7). If a medial reflection of the triceps is performed, the lateral or posterior brachial cutaneous nerve is identified laterally to the triceps (Figure 9-8) and traced proximally to the radial nerve proper. The lateral intermuscular septum is then released approximately 3 cm over the course of the radial nerve to allow for medial mobilization of the nerve with the triceps to prevent excess traction on the nerve during retraction of the triceps mass.41 With an anterior approach, radial nerve dissection and mobilization is not mandatory during exposure for more proximal fractures; however, distal exposure and plating of the anterior humerus does put the radial nerve at risk because it courses around the distal humerus between the brachialis and brachoradialis. Radial nerve identification and protection is recommended in these instances. Finally, after fixation, the location of the radial nerve relative to any implant should be well documented in the operative note to allow for easier identification and possible prevention of a secondary palsy if a subsequent procedure is required (Figure 9-9).

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Figure 9-7. Identification and mobilization of the radial nerve via the interval between the long and lateral heads of the triceps.

Figure 9-8. Lateral brachial cutaneous nerve exiting the lateral aspect of the triceps.

Figure 9-9. The position (directly overlying proximal holes 2 and 3) of the radial nerve after reduction and plate application should be documented in the operative record.

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COMPLICATION MANAGEMENT Primary Radial Nerve Palsy In most complete primary nerve palsies, expectant nonsurgical management is indicated. A repairable nerve is rarely found at exploration, and early exploration has not been shown to improve overall recovery rates in these patients.39,42 During this period of expectant management, early passive wrist and finger range of motion is encouraged to prevent contractures, and dynamic radial nerve palsy splints can be used. Electromyography and nerve conduction velocity tests should be obtained at approximately 4 weeks postinjury and then serially thereafter to determine the extent of radial nerve injury and to monitor for electrophysiological signs of recovery. If clinical signs of recovery are exhibited, observation should be continued; however, if no clinical or electrophysiological signs of recovery are exhibited after 4 to 6 months, surgical exploration is warranted.39 If nerve exploration is not elected or fails, tendon transfers remain a viable alternative. Radial nerve palsy associated with an open humerus fracture is an indication for immediate exploration at the time of irrigation and débridement and operative fixation due to an increased likelihood of transection. Exploration in this setting will allow for diagnostic and potentially prognostic information to direct further treatment. However, because the zone of injury extends beyond the area of the transection in these high-energy injuries, primary neurorrhaphy is likely to be unsuccessful, and thus is not recommended. In this setting, delayed resection of the injured segment and nerve grafting43 or tendon transfers will likely result in more predictable outcomes. Similarly, a humeral shaft fracture with an associated radial nerve palsy that otherwise meets indications for operative treatment may warrant exploration of the nerve if a posterior approach is selected. Although this may provide additional diagnostic and prognostic information, the overall recovery rate is likely to be unchanged, and the routine use of this approach should be weighed against the potential disadvantages of further nerve injury or devascularization, especially if the fracture may be more easily or safely treated from another approach.

Secondary Radial Nerve Palsy Secondary radial nerve palsies were once considered an indication for early exploration due to concerns for iatrogenic nerve entrapment or transection, especially in the typical Holstein Lewis fracture pattern. However, more recent literature suggests recovery rates in this subset of patients is equal to that of patients with primary radial nerve palsies; therefore, like patients with primary radial nerve palsies, initial observation and expectant management is now recommended.44

REFERENCES 1. Court-Brown CM, Garg A, McQueen MM. The translated two-part fracture of the proximal humerus. Epidemiology and outcome in the older patient. J Bone Joint Surg Br. 2001;83(6):799-804. 2. Iannotti JP, Ramsey ML, Williams GR Jr, Warner JJ. Nonprosthetic management of proximal humeral fractures. Instr Course Lect. 2004;53:403-416. 3. Reid JS. Fractures of the proximal humerus. Curr Opin Ortho. 2003;14(4):269-280.

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4. Anglen JO, Archdeacon MT, Cannada LK, Herscovici D Jr. Avoiding complications in the treatment of humeral fractures. J Bone Joint Surg Am. 2008;90(7):1580-1589. 5. Micic ID, Kim KC, Shin DJ, et al. Analysis of early failure of the locking compression plate in osteoporotic proximal humerus fractures. J Orthop Sci. 2009;14(5):596-601. 6. Connor PM, Flatow EL. Complications of internal fixation of proximal humeral fractures. Instr Course Lect. 1997;46:25-37. 7. Hessman MH, Blum J, Kuchle R, Hofmann A, Rommens PM. Internal fixation of proximal humeral fractures: current concepts. Eur J Trauma Emerg Surg. 2003;29(5):253-261. 8. Owsley KC, Gorczyca JT. Fracture displacement and screw cutout after open reduction and locked plate fixation of proximal humeral fractures [corrected]. J Bone Joint Surg Am. 2008;90(2):233-240. 9. Ring D. Current concepts in plate and screw fixation of osteoporotic proximal humerus fractures. Injury. 2007;38(suppl 3):S59-S68. 10. Norris T, Green A. Proximal humeral fractures and glenohumeral dislocations. In: Browner B, Jupiter J, Levine A, Trafton P, eds. Skeletal Trauma. 3rd ed. Philadelphia, PA: Saunders; 2003:1512-1624. 11. Meier RA, Messmer P, Regazzoni P, Rothfischer W, Gross T. Unexpected high complication rate following internal fixation of unstable proximal humerus fractures with an angled blade plate. J Orthop Trauma. 2006;20(4):253-260. 12. Nho SJ, Brophy RH, Barker JU, Cornell CN, MacGillivray JD. Innovations in the management of displaced proximal humerus fractures. J Am Acad Orthop Surg. 2007;15(1):12-26. 13. Rose PS, Adams CR, Torchia ME, Jacofsky DJ, Haidukewych GG, Steinmann SP. Locking plate fixation for proximal humeral fractures: initial results with a new implant. J Shoulder Elbow Surg. 2007;16(2):202-207. 14. Ricchetti ET, DeMola PM, Roman D, Abboud JA. The use of precontoured humeral locking plates in the management of displaced proximal humerus fracture. J Am Acad Orthop Surg. 2009;17(9):582-590. 15. Gardner MJ, Weil Y, Barker JU, Kelly BT, Helfet DL, Lorich DG. The importance of medial support in locked plating of proximal humerus fractures. J Orthop Trauma. 2007;21(3):185191. 16. Gardner MJ, Boraiah S, Helfet DL, Lorich DG. Indirect medial reduction and strut support of proximal humerus fractures using an endosteal implant. J Orthop Trauma. 2008;22(3):195-200. 17. Badman BL, Mighell M. Fixed-angle locked plating of two-, three-, and four-part proximal humerus fractures. J Am Acad Orthop Surg. 2008;16(5):294-302. 18. Hertel R, Hempfing A, Stiehler M, Leunig M. Predictors of humeral head ischemia after intracapsular fracture of the proximal humerus. J Shoulder Elbow Surg. 2004;13(4):427-433. 19. Wijgman AJ, Roolker W, Patt TW, Raaymakers EL, Marti RK. Open reduction and internal fixation of three and four-part fractures of the proximal part of the humerus. J Bone Joint Surg Am. 2002;84-A(11):1919-1925. 20. Harreld KL, Marker DR, Wiesler ER, Shafiq B, Mont MA. Osteonecrosis of the humeral head. J Am Acad Orthop Surg. 2009;17(6):345-355. 21. Court-Brown CM, Aitken SA, Forward D, O’Toole RV III. The epidemiology of fractures. In: Bucholz RW, Heckman JD, Court-Brown CM, Tornetta P III, McQueen M, Ricci WM, eds. Rockwood and Green’s Fractures in Adults. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009. 22. Sarmiento A, Kinman PB, Galvin EG, Schmitt RH, Phillips JG. Functional bracing of fractures of the shaft of the humerus. J Bone Joint Surg Am. 1977;59(5):596-601. 23. Sarmiento A, Horowitch A, Aboulafia A, Vangsness CT Jr. Functional bracing for comminuted extra-articular fractures of the distal third of the humerus. J Bone Joint Surg Br. 1990;72(2):283-287.

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24. Sarmiento A, Zagorski JB, Zych GA, Latta LL, Capps CA. Functional bracing for the treatment of fractures of the humeral diaphysis. J Bone Joint Surg Am. 2000;82(4):478-486. 25. Crates J, Whittle AP. Antegrade interlocking nailing of acute humeral shaft fractures. Clin Orthop Relat Res. 1998;350:40-50. 26. Habernek H, Orthner E. A locking nail for fractures of the humerus. J Bone Joint Surg Br. 1991;73(4):651-653. 27. McCormack RG, Brien D, Buckley RE, McKee MD, Powell J, Schemitsch EH. Fixation of fractures of the shaft of the humerus by dynamic compression plate or intramedullary nail. A prospective, randomised trial. J Bone Joint Surg Br. 2000;82(3):336-339. 28. McKee MD, Seiler JG, Jupiter JB. The application of the limited contact dynamic compression plate in the upper extremity: an analysis of 114 consecutive cases. Injury. 1995;26(10):661-666. 29. Foster RJ, Dixon GL Jr, Bach AW, Appleyard RW, Green TM. Internal fixation of fractures and non-unions of the humeral shaft. Indications and results in a multi-center study. J Bone Joint Surg Am. 1985;67(6):857-864. 30. Ring D, Chin K, Taghinia AH, Jupiter JB. Nonunion after functional brace treatment of diaphyseal humerus fractures. J Trauma. 2007;62(5):1157-1158. 31. Rutgers M, Ring D. Treatment of diaphyseal fractures of the humerus using a functional brace. J Orthop Trauma. 2006;20(9):597-601. 32. Pugh DM, McKee MD. Advances in the management of humeral nonunion. J Am Acad Orthop Surg. 2003;11(1):48-59. 33. Brinker MR, O’Connor DP, Monla YT, Earthman TP. Metabolic and endocrine abnormalities in patients with nonunions. J Orthop Trauma. 2007;21(8):557-570. 34. Foulk DA, Szabo RM. Diaphyseal humerus fractures: natural history and occurrence of nonunion. Orthopedics. 1995;18(4):333-335. 35. Muller ME, Allgower M, Schneider R, Willenegger H. Manual of Internal Fixation. 3rd ed. New York, NY: Springer-Verlag; 1991. 36. Ziran BH, Belangero W, Livani B, Pesantez R. Percutaneous plating of the humerus with locked plating: technique and case report. J Trauma. 2007;63(1):205-210. 37. Hierholzer C, Sama D, Toro JB, Peterson M, Helfet DL. Plate fixation of ununited humeral shaft fractures: effect of type of bone graft on healing. J Bone Joint Surg Am. 2006;88(7):14421447. 38. Hughes RE, Schneeberger AG, An KN, Morrey BF, O’Driscoll SW. Reduction of triceps muscle force after shortening of the distal humerus: a computational model. J Shoulder Elbow Surg. 1997;6(5):444-448. 39. Shao YC, Harwood P, Grotz MR, Limb D, Giannoudis PV. Radial nerve palsy associated with fractures of the shaft of the humerus: a systematic review. J Bone Joint Surg Br. 2005;87(12):1647-1652. 40. Pollock FH, Drake D, Bovill EG, Day L, Trafton PG. Treatment of radial neuropathy associated with fractures of the humerus. J Bone Joint Surg Am. 1981;63(2):239-243. 41. Gerwin M, Hotchkiss RN, Weiland AJ. Alternative operative exposures of the posterior aspect of the humeral diaphysis with reference to the radial nerve. J Bone Joint Surg Am. 1996;78(11):1690-1695. 42. Ring D, Chin K, Jupiter JB. Radial nerve palsy associated with high-energy humeral shaft fractures. J Hand Surg Am. 2004;29(1):144-147. 43. Lee YH, Chung MS, Gong HS, Chung JY, Park JH, Baek GH. Sural nerve autografts for high radial nerve injury with nine centimeter or greater defects. J Hand Surg Am. 2008;33(1):83-86. 44. Shah A, Jebson PJ. Current treatment of radial nerve palsy following fracture of the humeral shaft. J Hand Surg Am. 2008;33(8):1433-1434.

10 Elbow Fractures Gregory J. Della Rocca, MD, PhD, FACS

Fractures and fracture-dislocations about the elbow are difficult injuries to treat due to the complex anatomy and biomechanics, the proximity of neurovascular structures, and frequently limited bone for fixation. Elbow fractures in the elderly present an increased challenge due to frequent comminution and osteopenia. However, even straightforward fractures, such as noncomminuted transverse olecranon fractures, require meticulous surgical care to avoid postoperative complications. The most common postoperative problems affecting fractures about the elbow include nonunion, elbow stiffness, instability, arthrosis, and neurological injury. The risk of these complications can be reduced by observing proper surgical techniques, obtaining and maintaining an anatomical reduction, using stable implants that are positioned safely, and ensuring proper rehabilitation.

PREVENTION: SURGICAL TECHNIQUES/REDUCTION Anatomical reduction of fracture fragments restores both proper joint alignment and the shape of the articular surface, prevents instability of the elbow joint, provides substantial fracture stability (thereby minimizing the work of fixation implants), and allows for early range of motion (ROM) exercises, important for avoiding postoperative stiffness. Occasionally, anatomical reduction cannot be achieved due to loss of bone or severe comminution. Even if anatomical reduction to the diaphysis is not possible, precise articular reduction and then stabilization of the articular segment to the shaft can be a reasonable treatment method if strong and durable implants are used. Consideration may be given to shortening of the humeral metaphysis in order to provide a stable surface for reduction of the articular segment to the diaphysis.1 99

Archdeacon MT, Anglen JO, Ostrum RF, Herscovici D Jr, eds. Prevention and Management of Common Fracture Complications (pp 99-110). © 2012 SLACK Incorporated.

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Figure 10-1. (A) Lateral radiograph of right elbow in a patient who underwent open reduction and internal fixation of a comminuted right distal humerus fracture using a right olecranon osteotomy. The patient was noted to have extensive bone loss during the index procedure, and an accurate reduction of the distal humerus was not obtained. This radiograph reveals chronic fracture of the proximal ulna at the distal extent of the proximal ulna plate, along with heterotopic bone formation along the anterior aspect of the distal humerus. The ulna fracture occurred at the location of the most distal screw in the olecranon plate; it was taken out, and allograft was placed at the fracture site without further stabilization. (B) AP radiograph of same elbow, revealing loss of distal humeral fixation with unacceptable alignment of the distal humeral articular surface.

Also, for elderly patients in whom inability to obtain secure fixation is anticipated (those with poor bone stock, highly comminuted fractures, and/or extremely distal fractures), elbow arthroplasty may be an option.2 Failure to obtain a stable reduction often results in loss of fixation, deformity, and nonunion (Figure 10-1). Recognition of injury patterns is important when planning surgical reconstruction. Good plain radiographs are important for accurate assessment. Specialized views (eg, radiocapitellar, traction) may add to the surgeon’s understanding of the injury complex. Computed tomography (CT) is used by some practitioners, ostensibly for a more accurate view of comminution and of small fractures, but some surgeons question the utility of information gained from CT images of the fractured and dislocated elbow. As an example of how specific injury patterns may dictate surgical approach, transolecranon fracture-dislocations of the elbow with associated radial head fractures may be repaired through an extensile posterior approach to the elbow for treatment of the proximal ulna fracture, elevation of wide cutaneous flaps, and exploitation of the Kocher interval to access the radial head fracture. This injury pattern often is associated with intact elbow ligaments.3 If the lateral collateral ligament is intact, it is important not to dissect posterior to the anterior border of the anconeus muscle using this lateral approach in order to avoid injury to the ligament and concomitant destabilization of the elbow (Figure 10-2).4

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Figure 10-2. Lateral collateral ligament complex as seen during surgical dissection of the elbow via the Kocher (anconeus) approach. The course of the lateral collateral ligament is depicted by the black line. It is important not to dissect posterior to the anterior border of the ligament in order to prevent destabilization of the elbow.

It is tempting to reconstruct fracture-dislocations of the elbow that include small coronoid fractures without performing fixation of the coronoid fracture. However, it has been shown that failure to reduce and stabilize the coronoid fracture is associated with postoperative instability and redislocation.5-7 Often, a perfectly anatomical reduction of the coronoid fracture fragment(s) is not possible. However, fixation may still be important, because restoration of the anterior elbow capsular attachment may be the most important aspect of the coronoid repair in re-establishing ulnohumeral stability.7 Resection of the radial head in the setting of highly comminuted radial head fractures is occasionally indicated. Small articular fragments are difficult to reduce and hold securely, both to each other and to the radial neck. However, radial head resection should be approached with caution in the traumatized elbow.8 The radial head is an important secondary restraint for elbow stability, and in the absence of the primary restraints (coronoid process, medial collateral ligament, and lateral ulnar collateral ligament), the radial head is vital for maintaining a reduced elbow joint.9,10 Extensive damage to the interosseous membrane of the forearm associated with radial head fractures (the Essex-Lopresti lesion) also requires preservation or replacement of the radial head; resection results in proximal migration of the radial shaft with concomitant distal radioulnar joint incongruence and dysfunction of the wrist and forearm.11-14 If a radial head fracture is unreconstructable in the face of an unstable elbow (such as the “terrible triad”), then replacement is preferable to excision to avoid early problems with instability of the elbow or forearm. Ulnar nerve injury during repair of distal humerus fractures is avoided via careful surgical dissection with mobilization of the nerve. The nerve should be mobilized from its hiatus in the medial intermuscular septum of the brachium distally to the first motor branch to the flexor carpi ulnaris muscle. The nerve then can be retracted medially or laterally as necessary for reduction of distal humerus fractures and for application of implants to the medial aspect of the distal humerus. Care should be taken when applying transarticular screws from lateral to medial across the distal humerus because the tips of these screws (or drill bits used in preparation of screw tracts) can injure the ulnar nerve. Transposition of the ulnar nerve has been recommended15 but is not always done after fixation of distal humerus fractures.16,17

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Patients should be warned preoperatively that transient ulnar nerve-related sensorimotor changes are not unusual after ORIF of distal humerus fractures due to the extensive neurolysis and intermittent traction used during the repair. Few data are available regarding the investigation of postoperative ulnar nerve palsies after fixation of distal humerus fractures; many seem to resolve on their own. A recent study of iatrogenic ulnar nerve palsies after percutaneous fixation of supracondylar humerus fractures in children demonstrated complete nerve recovery in 25 patients by 7 months. Nerve conduction studies and electromyography were used 6 and 12 weeks postoperatively, and no nerves were explored. Electrical investigation of postoperative ulnar nerve palsies may best be delayed until at least 6 weeks postoperatively, and routine exploration of the nerve in the postoperative period is not recommended until at least 7 months after surgical fixation.18 How these results apply to the adult patient population is unknown. The posterior interosseous nerve (PIN) is at risk of injury where it lays closely apposed to the radial neck. Pronation of the forearm during treatment of radial head and neck fractures helps to keep the PIN clear of the surgical dissection. Careful dissection in a subperiosteal fashion around the radial neck (ie, no dissection into the soft tissues surrounding the radial neck) can also be helpful in avoiding injury to the PIN. The anterior interosseous nerve (AIN) is also at risk of injury with certain fixation procedures; there have been reported instances of AIN injury from prominent wires after fixation of olecranon fractures using tension band techniques.19 Careful wire placement during tension banding of olecranon fractures can help avoid this unusual complication.

PREVENTION: IMPLANT SELECTION AND APPLICATION A common problem with fixation of distal humerus fractures has been early implant failure with resultant nonunion. Use of stronger implants has reduced this problem. Most often, at least one plate of strength comparable to a compression plate is used, in conjunction with another contourable (reconstruction) plate. Thin plates, such as 1/3 tubular plates, are not strong enough to endure the torsional forces to which the distal humerus is subjected.1 Although precontoured and locking plates are currently available, there is no evidence of superior outcomes using these implants, nor that the use of locking plate technology allows unicolumnar fixation. A long-standing principle of stable fixation of the distal humerus is to plate both the medial and lateral columns. Configuration of distal humerus plates, whether it is the traditional 90-90 configuration or a 180-degree medial-lateral configuration, seems to be of relatively less importance. The 180-degree medial-lateral plate configuration has been shown in the laboratory to be biomechanically superior to the 90-90 configuration, although this has not been proven clinically.20 The Mayo Clinic has had high degrees of success with 180-degree medial-lateral plating techniques for comminuted distal humerus fractures.1 If bone loss has occurred at the articular surface of the distal humerus, care must be taken during reduction to avoid overreduction of the joint surface. A common error entails placing a lag screw across the condyles of the distal humerus when bone loss at the articular surface is present. This mistake leads to overcompression and narrowing of the articular surface, which leads to an incongruity of the ulnohumeral or radiocapitellar articulations (or both). This can create problems with postoperative stiffness and early arthrosis. Avoidance of compression across articular surfaces with bone loss, by using positioning screws instead of lag screws or through placement of bone graft to occupy the area of bone loss, may help prevent this problem.

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Isolated radial head fractures with good bone stock and large fragments can be reconstructed, but there are hazards that should be avoided. First, prominent implants must avoid the 250-degree articular zone of the radial head (where it articulates with the lesser sigmoid notch of the ulna) so that forearm rotation is not compromised.4 Any implants placed within the proximal radioulnar joint articulation should be countersunk beneath the articular surface to prevent impingement. Second, implants cannot be overly bulky, and implants that are too thin can lead to problems with secure fixation. An accurate and anatomical reduction of radial neck involvement can provide a degree of stability that relieves the implant of some of the work it must perform in holding the fracture reduced. Because the adult elbow is intolerant of immobilization after injury and stiffness rapidly develops, secure fixation of any fractures about the elbow is imperative to allow for early unrestricted motion. Radial head replacement should be considered after elbow trauma when an unreconstructible radial head fracture has occurred. Radial head replacement, however, has a number of pitfalls that must be avoided. First, using an appropriately sized radial head implant is vital. A radial head prosthesis of larger diameter than the native radial head will produce tightness in the proximal radioulnar joint, possible subluxation of the radiocapitellar joint, and problems with forearm mechanics. A radial head prosthesis that is too thick will “overstuff” the radiocapitellar joint, leading to difficulty with elbow motion, forearm rotation, and capitellar wear.21,22 A common mistake is to size thickness of the radial head prosthesis to the thickest portion of the resected radial head; this will result in overstuffing of the radiocapitellar joint unless the radial neck is properly prepared by further resection of bone. After implantation of the radial head prosthesis, evaluation of congruity of the ulnohumeral joint on the anteroposterior (AP) fluoroscopic radiograph may be helpful, but radiographic incongruity of the joint may be a normal anatomical variant and may not indicate that the radial head prosthesis is too large.23 Contralateral elbow films may be helpful. Finally, radial head prosthetic design must be considered. Many “anatomical” radial head prosthesis designs are available. Use of this type of radial head prosthesis requires exacting technique, as these prostheses are often not perfectly round at the articulation with the ulna. Cementation or bony ingrowth for radial head prostheses does not seem to be necessary.24 The prosthesis simply acts as a spacer, and stable placement of the radial head prosthesis in an improper position can cause problems with the ulnar or capitellar articulations. Implants used for fixation of proximal ulna fractures include tension band wires, medullary screws, plate-and-screw constructs, and medullary nails. Not all fractures are adequately treated with all implant choices. For example, medullary screws may cause displacement of olecranon fractures if not placed in an eccentric fashion, taking the proximal ulnar bow into consideration. Also, tension band wiring is generally not recommended for proximal ulna fractures that extend distal to the coronoid process. When using a tension band wiring technique or plate-and-screw technique, care must be taken to avoid overpenetration of the anterior cortex of the ulna with wire or screw tips. If they are directed toward the radius, they may obstruct forearm rotation. Some prominence of wire or screw tips that appears safe on certain fluoroscopic images may belie the possibility that the bicipital tuberosity of the radius may impinge on the implants with forearm rotation. Also, there is the possibility of injury to anterior neurovascular structures (including the AIN) with prominent anterior proximal ulnar fixation implants.19 Nonunion of either an olecranon fracture or an olecranon osteotomy can occur after failure to achieve compression across the fracture line.25 Transverse olecranon

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osteotomies may exhibit difficulties with union, and chevron-type osteotomies may be of benefit for accurate reduction and compression.26,27 Use of either a medullary screw and dorsal wire or a dorsal plate is associated with good results after olecranon osteotomy.28 If a single medullary compression screw is used, the surgeon must verify proper placement and seating of the screw. A straight screw placed into the curved proximal ulna can induce a varus or valgus deformity if not accomplished carefully. Also, the medullary canal of the ulna is very narrow. Use of a 6.5-mm screw, for instance, may yield a false sense of strong screw compression and “bite” as the threads of the screw engage the dense cortical bone of the ulnar diaphysis, despite the possibility that the head of the screw has yet to engage the olecranon fracture fragment. Good lateral fluoroscopic imaging is necessary to verify complete seating of the screw head on bone. An alternative method of fixation for olecranon fractures or osteotomies is with contoured plates; this has been shown to be highly successful and associated with low risk of nonunion.29 In the setting of olecranon fracture associated with bone loss, compression across the joint surface should be avoided in order to reduce the likelihood of incongruence with the distal humerus articular surface.

COMPLICATION MANAGEMENT: SALVAGE PROCEDURES Despite the most meticulous surgical and postoperative care, some patients will invariably develop complications related to their elbow injuries. A functional ROM of the elbow is generally accepted to be 30 to 130 degrees at the ulnohumeral joint and 50 degrees each of pronation and supination.30,31 Stiffness (failure to achieve these ROM parameters postinjury) can occasionally be treated with closed manipulation under anesthesia, followed by an aggressive active ROM protocol.32 However, care must be exercised to avoid iatrogenic fracture during closed manipulation, and there is concern both that this mode of treatment is not routinely successful and that it may lead to formation of heterotopic ossification.31,33 Continuous passive motion is occasionally used, although a recent study has questioned its utility and demonstrated a lack of improvement in 1-year outcomes.34 Failure of closed manipulation prompts surgical capsular release. This can be accomplished through the Kocher approach to the elbow (either via a lateral incision or through an extensile posterior incision), with elevation of anterior and posterior capsules from the distal humerus and resection of tissue within the coronoid and olecranon fossae. Release of the posterior band of the medial collateral ligament can improve flexion of the elbow if the capsular release seems insufficient35; this can be accomplished through a medial approach or an extensile posterior approach. In the setting of stiffness associated with an overstuffed radiocapitellar joint after radial head replacement, downsizing of the radial head prosthesis at the time of contracture release may be beneficial for restoration of motion (Figure 10-3). Open release of the stiff elbow, with or without excision of heterotopic bone, may place the ulnar nerve at risk of traction injury that results from restoration of a near-normal elbow motion arc. This may be an important consideration for those patients with extension contractures prior to release. Transposition of the ulnar nerve is advocated by some authors to prevent ulnar neuritis after elbow release.36 Heterotopic bone formation is addressed through open surgical excision and release (Figure 10-4). CT scanning may be helpful to delineate the location of the ulnar nerve relative to the mass of heterotopic bone; occasionally, it is found within the bone mass. It is desirable to wait until the heterotopic bone mass has fully matured,

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Figure 10-3. (A) Lateral and AP radiographs of the left elbow in a patient with severe difficulties moving elbow and rotating forearm after undergoing open repair of a “terrible triad” fracture-dislocation. The radial head prosthesis appears too large. (B) Postoperative lateral and AP radiographs of the same elbow after open capsular release and downsizing of radial head prosthesis. Intraoperatively, the patient was noted to have wear of the capitellar articular surface. His elbow flexion-extension arc was 12 to 138 degrees, and forearm pronationsupination arc was 73 to 85 degrees at final follow-up. .

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Figure 10-4. (A) Lateral and AP radiographs of a nearly ankylosed right elbow after open reduction and internal fixation of a highly comminuted, intra-articular left distal humerus fracture using a left olecranon osteotomy. The fracture and osteotomy are healed. (B) Postoperative lateral and AP radiographs of the same elbow after excision of heterotopic ossification, capsular release, and partial implant removal. The patient regained an elbow flexion-extension arc of 20 to 135 degrees at final follow-up.

as assessed via plain radiographs, prior to excision in order to minimize risk of recurrence.37,38 However, estimates of bone maturity on plain radiographs are very difficult and may be unreliable. Excision of heterotopic bone is often accompanied by a single dose of 600 to 1000 cGy external beam radiation either before or within 72 hours

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after the surgical procedure or by a 6-week regimen of oral indomethacin, in order to minimize recurrence of bone formation. Of note, indomethacin use for prophylaxis against heterotopic ossification has been shown to increase the nonunion rate in long bone fractures as compared to external beam radiation prophylaxis.39 Nonunion of fractures of the distal humerus can be a difficult problem. It seems often to result from inadequate fixation, and revision surgery for nonunions that are related to instability is often successful using bicolumnar, rigid plate-and-screw fixation.40,41 Olecranon osteotomy may be required for adequate exposure of the articular surface of the nonunited distal humerus fracture.27 Salvage of the distal humerus fracture nonunion with use of elbow arthroplasty is also possible, but, in the highdemand younger patient, this may be contraindicated.42,43 Implant prominence, particularly around the olecranon, may be the most common complaint after elbow fracture fixation and is easily treated with implant removal. Prominence of implants can be problematic, as even obese patients have humeral condyles and olecranon processes closely apposed to the skin. Implant removal should be postponed until after fracture healing, if at all possible. Occasionally, a short period of protected weight bearing after implant removal may be worthwhile to minimize the risk of refracture through prior screw holes; patients should be warned in advance that fracture is a risk after removal of implants. Radiocapitellar arthrosis in the setting of malunited or nonunited fractures of the radial head or neck, or in the setting of radial head arthroplasty, can be treated successfully with late excision of the radial head or radial head prosthesis.44,45 Longterm results of radial head excision are unknown and may include attritional wrist or distal radioulnar joint problems, but short-term results of late radial head resection are good. Late post-traumatic instability of the elbow (which, paradoxically, can be associated with elbow stiffness) is a difficult entity to treat. Surgical reconstruction of this problem often includes soft tissue releases and application of a hinged external fixator device, allowing for elbow motion during the recovery phase.46,47 Distraction hinged external fixation, occasionally with interposition arthroplasty, has been used successfully for late post-traumatic elbow instability or contracture in some series.48-50 Symptomatic elbow arthrosis can be treated with elbow arthroplasty. Unconstrained, semiconstrained, and constrained prostheses are available from multiple manufacturers. Hemiarthroplasty of the distal humerus has also been proposed but is not approved by the US Food and Drug Administration for use in the United States.

SUMMARY Fractures and fracture-dislocations about the adult elbow are difficult to treat and rehabilitate. Aside from routine complications that can occur in all postoperative patients, such as infection, bleeding, and nerve injury, the post-traumatic elbow is also subject to postoperative stiffness, instability, and arthrosis. Meticulous surgical technique, use of strong and stable implants, and aggressive early rehabilitation can avoid some of the most common complications of surgical elbow reconstruction. Salvage procedures can be difficult for the post-traumatic elbow. Avoidance of complications represents the best way to achieve satisfactory outcomes for adults with complex elbow trauma.

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REFERENCES 1. O’Driscoll SW. Optimizing stability in distal humeral fracture fixation. J Shoulder Elbow Surg. 2005;14(suppl 1):186S-194S. 2. Frankle MA, Herscovici D Jr, DiPawquale TG, Vasey MB, Sanders RW. A comparison of open reduction and internal fixation and primary total elbow arthroplasty in the treatment of intraarticular distal humerus fractures in women older than age 65. J Orthop Trauma. 2003;17:473-480. 3. Ring D, Jupiter JB, Sanders RW, Mast J, Simpson NS. Transolecranon fracture-dislocation of the elbow. J Orthop Trauma. 1997;11:545-550. 4. Hotchkiss RN. Displaced fractures of the radial head: internal fixation or excision. J Am Acad Orthop Surg. 1997;5:1-10. 5. Ring D, Jupiter JB, Zilberfarb J. Posterior dislocation of the elbow with fractures of the coronoid and radial head. J Bone Joint Surg Am. 2002;84:547-551. 6. Pugh DM, Wild LM, Schemitsch EH, King GJW, McKee MD. Standard surgical protocol to treat elbow dislocations with radial head and coronoid fractures. J Bone Joint Surg Am. 2004;86:1122-1130. 7. Doornberg JN, Ring D. Coronoid fracture patterns. J Hand Surg Am. 2006;31:45-52. 8. O’Driscoll SW, Jupiter JB, Cohen M, Ring D, McKee MD. Difficult elbow fractures: pearls and pitfalls. Instr Course Lect. 2003;52:113-134. 9. Deutch SR, Jensen SL, Tyrdal S, Olsen BS, Sneppen O. Elbow joint stability following experimental osteoligamentous injury and reconstruction. J Shoulder Elbow Surg. 2003;12:466-471. 10. Egol KA, Immerman I, Paksima N, Tejwani N, Koval KJ. Fracture-dislocation of the elbow: functional outcome following treatment with a standardized protocol. Bull NYU Hosp Jt Dis. 2007;65:263-270. 11. Edwards GS Jr, Jupiter JB. Radial head fractures with acute distal radioulnar dislocation: Essex-Lopresti revisited. Clin Orthop. 1988;234:61-69. 12. Ruch DS, Chang DS, Koman LA. Reconstruction of longitudinal stability of the forearm after disruption of interosseous ligament and radial head excision (Essex-Lopresti lesion). J South Orthop Assoc. 1999;8:47-52. 13. Van Riet RP, Morrey BF. Documentation of associated injuries occurring with radial head fracture. Clin Orthop. 2008;466:130-134. 14. Pike JM, Athwal GS, Faber KJ, King GJW. Radial head fractures—an update. J Hand Surg Am. 2009;34:557-565. 15. Wang KC, Shih HN, Hsu KY, Shih CH. Intercondylar fractures of the distal humerus: routine anterior subcutaneous transposition of the ulnar nerve in a posterior operative approach. J Trauma. 1994;36:770-773. 16. McKee MD, Wilson TL, Winston L, Schemitsch EH, Richards RR. Functional outcome after surgical treatment of intra-articular distal humeral fractures through a posterior approach. J Bone Joint Surg Am. 2000;82:1701-1707. 17. Doornberg JN, van Duijn PJ, Linzel D, et al. Surgical treatment of intra-articular fractures of the distal part of the humerus: functional outcome after twelve to thirty years. J Bone Joint Surg Am. 2007;89:1524-1532. 18. Kalenderer O, Reisoglu A, Surer L, Agus H. How should one treat iatrogenic ulnar injury after closed reduction and percutaneous pinning of paediatric supracondylar humeral fractures? Injury. 2008;39:463-466. 19. Parker JR, Conroy J, Campbell DA. Anterior interosseus nerve injury following tension band wiring of the olecranon. Injury. 2005;36:1252-1253. 20. Stoffel K, Cunneen S, Morgan R, Nicholls R, Stachowiak G. Comparative stability of perpendicular versus parallel double-locking plating systems in osteoporotic comminuted distal humerus fractures. J Orthop Res. 2008;26:778-784.

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21. Birkedal JP, Deal DN, Ruch DS. Loss of flexion after radial head replacement. J Shoulder Elbow Surg. 2004;13:208-218. 22. Doornberg JN, Linzel DS, Zurakowski D, Ring D. Reference points for radial head prosthesis size. J Hand Surg Am. 2006;31:53-57. 23. Rowland AS, Athwal GS, MacDermid JC, King GJ. Lateral ulnohumeral joint space widening is not diagnostic of radial head arthroplasty overstuffing. J Hand Surg Am. 2007;32:637641. 24. Doornberg JN, Parisien R, Duijn PJ, Ring D. Radial head arthroplasty with a modular metal spacer to treat acute traumatic elbow instability. J Bone Joint Surg Am. 2007;89:10751080. 25. Ring D, Gulotta L, Roy A, Jupiter JB. Concomitant nonunion of the distal humerus and olecranon. J South Orthop Assoc. 2003;12:27-31. 26. Gainor BJ, Moussa F, Schott T. Healing rate of transverse osteotomies of the olecranon used in reconstruction of distal humerus fractures. J South Orthop Assoc. 1995;4:263-268. 27. Ring D, Gulotta L, Chin K, Jupiter JB. Olecranon osteotomy for exposure of fractures and nonunions of the distal humerus. J Orthop Trauma. 2004;18:446-449. 28. Coles CP, Barei DP, Nork SE, Taitsman LA, Hanel DP, Henley MB. The olecranon osteotomy: a six-year experience in the treatment of intraarticular fractures of the distal humerus. J Orthop Trauma. 2006;20:164-171. 29. Hewins EA, Gofton WT, Dubberly J, MacDermid JC, Faber KJ, King GJ. Plate fixation of olecranon osteotomies. J Orthop Trauma. 2007;21:58-62. 30. Morrey BF, Askew LJ, Chao EY. A biomechanical study of normal functional elbow motion. J Bone Joint Surg Am. 1981;63:872-877. 31. Lindenhovius ALC, Jupiter JB. The posttraumatic stiff elbow: a review of the literature. J Hand Surg Am. 2007;32:1605-1623. 32. Duke JB, Tessler RH, Dell PC. Manipulation of the stiff elbow with patient under anesthesia. J Hand Surg Am. 1991;16:19-24. 33. Michelsson JE, Rauschning W. Pathogenesis of experimental heterotopic bone formation following temporary forcible exercising of immobilized limbs. Clin Orthop. 1983;176:265272. 34. Lindenhovius AL, van de Luijtgaarden K, Ring D, Jupiter J. Open elbow contracture release: postoperative management with and without continuous passive motion. J Hand Surg Am. 2009;34:858-865. 35. Ruch DS, Shen J, Chloros GD, Krings E, Papadonikolakis A. Release of the medial collateral ligament to improve flexion in post-traumatic elbow stiffness. J Bone Joint Surg Br. 2008;90:614-618. 36. Cohen MS, Hastings H II. Post-traumatic contracture of the elbow: operative release using a lateral collateral ligament sparing approach. J Bone Joint Surg Br. 1998;80:805-812. 37. McAuliffe JA, Wolfson AH. Early excision of heterotopic ossification about the elbow followed by radiation therapy. J Bone Joint Surg Am. 1997;79:749-755. 38. Viola RW, Hanel DP. Early “simple” release of posttraumatic elbow contracture associated with heterotopic ossification. J Hand Surg Am. 1999;24:370-380. 39. Burd TA, Hughes MS, Anglen JO. Heterotopic ossification prophylaxis with indomethacin increases the risk of long-bone nonunion. J Bone Joint Surg Br. 2003;85:700-705. 40. McKee M, Jupiter J, Toh CL, Wilson L, Colton C, Karras KK. Reconstruction after malunion and nonunion of intra-articular fractures of the distal humerus: methods and results in 13 adults. J Bone Joint Surg Br. 1994;76:614-621. 41. Ali A, Douglas H, Stanley D. Revision surgery for nonunion after early failure of fixation of fractures of the distal humerus. J Bone Joint Surg Br. 2005;87:1107-1110. 42. LaPorte DM, Murphy MS, Moore JR. Distal humerus nonunion after failed internal fixation: reconstruction with total elbow arthroplasty. Am J Orthop. 2008;37:531-534.

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43. Cil A, Veillette CJ, Sanchez-Sotelo J, Morrey BF. Linked elbow replacement: a salvage procedure for distal humeral nonunion. J Bone Joint Surg Am. 2008;90:1939-1950. 44. Herbertsson P, Josefsson PO, Hasserius R, Karlsson C, Besjakov J, Karlsson M. Uncomplicated Mason type-II and III fractures of the radial head and neck in adults. A long-term follow-up study. J Bone Joint Surg Am. 2004;86:569-574. 45. Shore BJ, Mozzon JB, MacDermid JC, Faber KJ, King GJ. Chronic posttraumatic elbow disorders treated with metallic radial head arthroplasty. J Bone Joint Surg Am. 2008;90:271280. 46. McKee MD, Bowden SH, King GJ, et al. Management of recurrent, complex instability of the elbow with a hinged external fixator. J Bone Joint Surg Br. 1998;80:1031-1036. 47. Ring D, Hannouche D, Jupiter JB. Surgical treatment of persistent dislocation or subluxation of the ulnohumeral joint after fracture-dislocation of the elbow. J Hand Surg Am. 2004;29:470-480. 48. Morrey BF. Post-traumatic contracture of the elbow: operative treatment, including distraction arthroplasty. J Bone Joint Surg Am. 1990;72:601-618. 49. Cheng SL, Morrey BF. Treatment of the mobile, painful arthritic elbow by distraction interposition arthroplasty. J Bone Joint Surg Am. 2000;82:233-238. 50. Ruch DS, Triepel CR. Hinged elbow fixation for recurrent instability following fracture dislocation. Injury. 2001;32(suppl 4):SD70-SD80.

11 Radial and Ulnar Shaft, Monteggia, and Galeazzi Fractures Susan McDowell, MD and Brian H. Mullis, MD

Radius and ulna fractures represent a wide spectrum of injuries ranging from low to high energy. The forearm operates as a single unit composed of six independent relationships: ulnohumeral, radiocapitellar, proximal and distal radioulnar, radiocarpal, and the interosseous membrane (IOM). Fractures can involve one or both bones; when a single bone is involved, there may be an associated joint injury. Well-recognized patterns include the Monteggia fracture, which is an ulna fracture with proximal radioulnar joint (PRUJ) dislocation, and the Galeazzi fracture, which is a radius fracture with distal radioulnar joint (DRUJ) dislocation. The Galeazzi has also been called the Piedmont fracture and the “fracture of necessity.” Common complications include the following: undiagnosed concomitant injury to the wrist or elbow, nonunion or malunion with pain and limitation of motion, synostosis, forearm compartment syndrome, and refracture.

ETIOLOGICAL FACTORS Many complications result from “missed” diagnoses (ie, the long bone fracture is seen, but a more subtle injury at the wrist or elbow may be overlooked) (Table 11-1). This may result from inadequate radiographs, which do not include the joints above and below. A high-energy mechanism increases the risk for compartment syndrome, synostoses, and missed joint injuries. Comminution and bone loss increase the risk for nonunion or early fixation failure due to instability. Injuries that have a significant soft tissue component seem to be at higher risk for developing synostosis, as well as head and spinal cord injury patients.

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Table 11-1

Risk Factors for Complications in Forearm Fractures COMPLICATION

RISK FACTORS

Malunion

Unacceptable alignment after reduction: length, angulation, radial bow Proximal fractures

Nonunion

Inadequate reduction (gaps) Unstable fixation Open fractures Infection

Synostosis

Single operative approach for fixation High-energy mechanism Large soft tissue injury Bone graft over interosseous membrane Screws protruding into interosseus space Head/spinal cord injury Radial head fracture/Monteggia variant

Compartment syndrome

High-energy injury Crush injury Open fracture

Refracture

High-energy or open fracture Excessively rigid fixation (eg, 4.5-mm plates) Failure to achieve good compression and reduction initially Early hardware removal Persistent radiolucency at fracture site Unprotected fall after hardware removal

Undiagnosed concomitant injury

Inadequate radiographs Proximal one-third ulna fracture Distal one-third radius fracture

PREVENTION: CLINICAL EVALUATION AND SURGICAL TECHNIQUES/REDUCTION Forearm Compartment Syndrome Compartment syndrome should be ruled out in every fracture of the forearm. High-energy injuries, crush injuries, and open injuries are at significant risk for developing elevated compartment pressures. The awake patient is assessed via palpation of the compartment, looking for pain with passive stretch of the compartment and following the patient’s pain control and course. Obtunded patients present a more difficult problem and often require diagnosis with the assistance of an intracompartmental pressure monitor. Early stabilization may help to prevent development of compartment syndrome by preventing further soft tissue injury. Delayed fixation

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A

B

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Figure 11-1. Radius and ulnar shaft fractures. This patient suffered a closed both-bone forearm fracture after being struck by a motor vehicle while crossing a street. He also suffered a closed head injury, requiring emergent craniotomy. Note in both A (AP) and B (lateral), the entire forearm and both elbow and wrist can be seen.

may allow the soft tissue to swell in a shortened position, leading to increased pressure when length of the compartment is restored. Although the initial injury itself can lead to limb-threatening intracompartmental edema, diligent monitoring of soft tissue status throughout the treatment phase is mandatory to enable early diagnosis of compartment syndrome and prevent permanent damage. After open reduction and internal fixation (ORIF) procedures in a swollen forearm, it may be difficult to close the incisions. It may be prudent to leave the wounds open and covered with a negative pressure dressing, use elevation for a few days, and then return to the operating room (OR) for closure.

Undiagnosed Concomitant Injury Radiographic imaging should consist of an anteroposterior and lateral view of the forearm showing both the elbow and wrist. Dedicated views of the wrist or elbow should be obtained if there is clinical suspicion of joint involvement (Figure 11-1). Subtle subluxation of the PRUJ or DRUJ may be easily overlooked on a long view of the forearm. Poor outcomes of both the Monteggia and Galeazzi fractures and their variants are associated closely with unrecognized derangement of the DRUJ or PRUJ.1-3 The physician must especially have a critical eye when assessing “single bone” forearm injuries to ensure the joints are not involved (Figure 11-2). Elbow instability after a Monteggia fracture is another source of poor outcome after surgery. Generally, restoration of anatomic ulnar length and alignment will reduce the radial head; however, in dislocations with marked displacement, ulnar collateral ligament injuries can occur, causing postfixation posterolateral rotatory instability.1

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Figure 11-2. Galeazzi fracture. (A) AP radiograph of a distal forearm showing a radial shaft fracture. Clinical exam showed significant wrist pain and tenderness. Note the subtle shortening of the radius and reduction of radial inclination. Intraoperative exam confirmed the diagnosis of DRUJ instability. (B) Postoperative films show the appropriate length restored and the DRUJ stabilized.

A

B

The joints should be examined clinically and radiographically at the time of presentation for signs of injury. This should be repeated in the OR after fixation of the fracture to assess the reduction and recheck for subtle instability. Preoperative assessment of the contralateral wrist and elbow with radiographs, range of motion (ROM), and PRUJ/DRUJ exams will provide a context for evaluation of the injured limb. When joint injury is identified, stable reduction must be achieved and verified in the OR by evaluating the joint during a full range of pronation and supination. If the DRUJ is unstable at any point in the arc after anatomic reduction and rigid fixation of the radius, the joint should be examined in supination. If the DRUJ is stable in that position, it can be immobilized in a long arm cast with the forearm supinated. The cast is exchanged for a hinged brace holding the forearm in supination for 4 to 6 weeks. If unstable in supination, the DRUJ should be pinned in a reduced position with two smooth K-wires (2 mm in diameter) placed from the ulna to the radius and protected with a supination cast and/or brace for a similar period. Similarly, reduction and stability of the radiocapitellar joint must be achieved and verified when treating Monteggia injuries. If the joint is not stably reduced after reduction and fixation of the ulna fracture, re-evaluate the reduction. If it is anatomic, the radial head may be buttonholed through the capsule, and this requires open reduction through a separate incision.

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Figure 11-3. Synostosis. This is a 2-month follow-up x-ray for the same patient pictured in Figure 11-1. Despite two separate approaches and early stabilization, this patient developed a synostosis between the radius and ulna.

Malunions and Nonunions Successful treatment of fractures of the radius and ulna requires restoration of the anatomic relationships of the forearm. In children, this is often obtained via closed reduction, using the intact periosteal hinge. Maintenance of the reduction obtained is aided by the minimization of cast padding and careful molding of the cast or splint by using three-point fixation molding techniques. The quality of the final outcome is reliant upon the initial reduction and subsequent maintenance of the reduction. Therefore, these fractures should be followed closely with radiographs to permit subsequent intervention, if necessary, in order to prevent malunion.4 Surgery is the treatment of choice for adults due to the high frequency of malunion and poor function following closed treatment. The exception may be isolated diaphyseal fractures of the ulna (“nightstick” fractures), which can be treated with casting or bracing in many cases. The surgeon must obtain correct length, angulation, and rotation for both bones, and the natural bow should be restored to the radius.5 A preoperative plan drawn using the contralateral extremity is helpful for most fracture patterns and will help avoid malreductions.

Synostosis Unfortunately, the surgeon cannot change the circumstances of the injury that may increase the risk for synostosis (Figure 11-3). Errors in surgical technique can be avoided, and this is the surgeon’s role in prevention. Two separate approaches should be used for fixation of fractures involving both bones of the forearm. The Henry or

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Thompson approach to the radius is commonly used in conjunction with a subcutaneous approach between the extensor and flexor carpi ulnaris for the ulna. This prevents excessive soft tissue stripping across the IOM and hematoma formation that could contribute to cross union. Early splinting and definitive, rigid fixation should be used whenever possible to minimize further soft tissue injury. An effort should be made to minimize trauma to the interosseous space. This means screw lengths should be carefully measured, and bone graft should not stray from its intended area of use.6,7

PREVENTION: IMPLANT SELECTION AND APPLICATION In adults, the most rigid construct possible is desired in the fixation of forearm fractures.8 Malunions, nonunions, and hardware failures have been noted historically in those fractures treated by K-wires, thin plate stock, short plate length, and intramedullary techniques.8,9 The ideal fixation construct takes into account the soft tissue envelope, degree of comminution of the bone of interest, and medical condition of the patient. Standard implant choice is a small fragment nonlocking compression plate in adults. Traditional teaching is to maximize rigidity of the construct via longer plate fixation with at least three bicortical screws on each side of the fracture. Stern and Drury found a nonunion rate four times higher (17% versus 4%) in forearm bones plated with four or fewer screws compared to those plated with five or more screws.10 These authors noted that Lane had observed in 1912 that “The longer the plate and the greater the number of screws, the more secure is the hold of the plate...” Some recent literature has focused on plate length rather than the number of screws, supporting “minimal screw fixation” (four cortices on each side) with emphasis on maximizing the working length of the plate.11,12

Refracture After Hardware Removal Refracture of the radius or ulna after hardware removal has been reported to occur in 4% to 25% of cases.13 Most of the series of refractures include patients who have been fixed with large-fragment (4.5 mm) compression plates, which are excessively rigid and may result in osteopenia in underlying bone. Other risk factors for refracture include high-energy or open fracture, failure to achieve adequate initial compression or reduction, and persistent radiolucency at the fracture site.13 Hardware should not routinely be removed from adults due to the elevated risk of refracture; however, hardware removal is an option if the patient is significantly symptomatic from hardware prominence.14 If hardware is to be removed electively, at least 1 year should be allowed for fracture healing prior to undergoing removal in the adult. Routine removal of hardware in children remains controversial, but recent research supports removal, especially if a less rigid construct was used.15 In children, hardware removal can be performed as early as 6 months and can become quite difficult to perform after 1 year due to bone growth over the implant. Protection of the forearm in a splint has been shown to offer some prevention of refracture following hardware removal. In the event one or both of the forearm bones refracture, treatment is tailored to the degree of displacement and angulation. There has been some success with treating stable, nondisplaced fractures with nonoperative management. When operative intervention is required, repeat ORIF with rigid plate fixation is used in adults (Table 11-2).16

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Table 11-2

Implants for Forearm Fracture Fixation IMPLANT

CRITICAL FACTOR

Small fragment, nonlocking compression plate

Neutralization, compression, or bridge plate Anatomic reduction with absolute stability when possible Adequate plate length above and below for rigid construct Pelvic reconstruction and one-third tubular plates should not be used

Flexible nail

Used primarily in pediatric fractures Increased potential for malunion or nonunion in adults

Static interlocked intramedullary nail

Alternative in adults Better option when soft tissue compromise is an issue

External fixation

Useful for staged procedures, such as in open fractures Pins in ulna are preferred Change to more definitive fixation as early as possible (to prevent pin tract infection)

COMPLICATION MANAGEMENT: SALVAGE PROCEDURES Nonunions Analysis of the type of nonunion is important for determining the approach to address the problem. Fractures treated with intramedullary or less rigid fixation tend to demonstrate hypertrophic nonunions. The radiographs of these nonunions display abundant callus with a lack of bridging bone. Because the appropriate biology is present at the fracture site for healing, as evidenced by the body’s callus response, these fractures can be treated by exchange of the previous fixation choice in favor of a more rigid plate and screw construct.17 Injuries in which segmental defects fail to unite despite bone grafting and plate fixation may require complex procedures such as vascularized intercalary grafts. These patients should be referred to an upper extremity or trauma specialist. Atrophic nonunions (Figure 11-4) may be treated by removal of hardware, nonunion takedown, and insertion of bone graft. Choice of graft is dependent on the size of the gap and the surgeon’s estimate of the biology present at the fracture site. Cancellous bone graft from the iliac crest is an option for large defects with poor biology; in smaller defects, local bone from the distal radius or humerus can be used. Regardless, care should be taken to not place bone graft over the IOM to prevent synostosis.17

Malunions It is difficult to regain perfect function after malunion correction due to derangement and scarring of the DRUJ, PRUJ, or IOM; therefore, the emphasis should be on prevention.17 Malunions should be addressed when there is a significant loss of ROM, unstable DRUJ, or unacceptable cosmetic deformity.18 We have learned that

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Figure 11-4. Monteggia fracture and atrophic nonunion. This polytrauma patient underwent open reduction and internal fixation of this Monteggia fracturedislocation. (A) Initial films show a Monteggia fracture. Note how on this single view the elbow injury could be missed if not suspected. Dedicated elbow films (not shown) revealed radial head dislocation. (B) Initial postoperative films show a wellbalanced plate with long working length and three bicortical screws on either side of the fracture. However, the fracture site shows a slight gap and lack of compression. (C) Atrophic nonunion of the fracture developed, with loosening of the hardware. (D) Revision surgery used both autologous bone graft and bone morphogenic protein-7 to achieve the union. These films show the 1-year follow-up.

A

B

C

D

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20 degrees of angulation in any direction significantly affects pronation/supination.19 Osteotomies are needed for correction of malunions. Shortening alters the joint mechanics of both the DRUJ and PRUJ.17 Impingement caused by alteration of the width of the IOM due to angular malunion can be a difficult problem as it can also lead to a secondary IOM contracture, which cannot be treated by osteotomy alone. For segmental defects, more advanced salvage techniques may be needed.

Synostosis There is no consensus as to the treatment for radioulnar synostoses. Various treatment methods have been attempted with mixed success. Resection of the heterotopic bone is always involved. This is done with careful technique to avoid injury to nearby nerves and blood vessels. Jupiter and Ring reported results after treatment of 18 proximal radioulnar synostoses and divided them into three anatomic types, based on the level of the cross union.20 Timing of surgery has almost universally been after union of the fractures and when the bone formation between the radius and ulna has reached a steady state as seen on serial radiographs7,21; however, Jupiter and Ring correlated earlier resection with better results. Whether to use interpositional grafts of fat, muscle, fascia lata, or postoperative radiation therapy remains controversial.1,22 Postoperative rehabilitation includes splinting for soft tissue rest and a scripted therapeutic return to motion.21

SUMMARY The more common complications of forearm fracture include compartment syndrome, loss of function at elbow or wrist due to missed or undertreated joint injury, malunion or nonunion, refracture, and synostosis. High-energy injury, open fracture, and/or crushing mechanism raise the risk of all complications. Surgeons can reduce the risk of these complications by careful evaluation of the patient with good-quality radiographs including wrist and elbow; careful surgical technique employing good reduction, compression, and stable fixation with adequate length 3.5-mm compression plates; and avoiding hardware removal when possible.

REFERENCES 1. Ring D, Jupiter JB, Simpson NS. Monteggia fractures in adults. J Bone Joint Surg Am. 1998;80:1733-1744. 2. Mikic Z. Galeazzi fracture-dislocations. J Bone Joint Surg Am. 1975;57:1071-1080. 3. Reckling F. Unstable fracture-dislocations of the forearm (Monteggia and Galeazzi lesions). J Bone Joint Surg Am. 1982;64:857-863. 4. Younger AS, Tredwell SJ, Mackenzie WG. Factors affecting fracture position at cast removal after pediatric forearm fracture. J Pediatr Orthop. 1997;17(3):332-336. 5. Schemitsch EH, Richards RR. The effect of malunion on functional outcome after plate fixation of fractures of both bones of the forearm in adults. J Bone Joint Surg Am. 1992;74:1068-1078. 6. Bauer G, Arand M, Mutschler W. Post-traumatic radioulnar synostosis after forearm fracture osteosynthesis. Arch Orthop Trauma Surg. 1991;110:142-145.

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7. Vince KG, Miller JE. Cross-union complicating fracture of the forearm. Part I: adults. J Bone Joint Surg Am. 1987;69:640-653. 8. Anderson LD, Sisk D, Tooms RE, Park WI 3rd. Compression-plate fixation in acute diaphyseal fractures of the radius and ulna. J Bone Joint Surg Am. 1975;57:287-297. 9. Burwell HN, Charnley AD. Treatment of forearm fractures in adults with particular reference to plate fixation. J Bone Joint Surg. 1964;46B(3):404-425. 10. Stern PJ, Drury WJ. Complications of plate fixation of forearm fractures. Clin Orthop 1983;175:25-29. 11. Crow BD, Mundis G, Anglen JO. Clinical results of minimal screw plate fixation of forearm fractures. Am J Orthop. 2007;36(9):477-480. 12. Lindvall EM, Sagi HC. Selective screw placement in forearm compression plating: results of 75 consecutive fractures stabilized with 4 corices of screw fixation on either side of the fracture. J Orthop Trauma. 2006;20(3):157-162. 13. Deluca PA, Lindsey RW, Ruwe PA. Refracture of bones of the forearm after the removal of compression plates. J Bone Joint Surg Am. 1988;70:1372-1376. 14. Langkamer VG, Ackroyd CE. Removal of forearm plates. J Bone Joint Surg Br. 1990;72B:601-604. 15. Kim WY, Zenios M, Kumar A, Abdulkadir U. The removal of forearm plates in children. Injury. 2005;36:1427-1430. 16. Deluca PA, Lindsey RW, Ruwe PA. Refracture of bones of the forearm after the removal of compression plates. J Bone Joint Surg Am. 1988;70:1372-1376. 17. Jupiter JB, Fernandez DL, Levin LS, Wysocki RW. Reconstruction of posttraumatic disorders of the forearm. J Bone Joint Surg Am. 2009;91:2730-2739. 18. Trousdale RT, Linscheid RL. Operative treatment of malunited fractures of the forearm. J Bone Joint Surg Am. 1995;77:894-902. 19. Matthews LS, Kaufer H, Garver DF, Sonstegard DA. The effect on supination-pronation of angular malalignment of fractures of both bones of the forearm. J Bone Joint Surg Am. 1982;64:14-17. 20. Jupiter JB, Ring D. Operative treatment of post-traumatic proximal radioulnar synostosis. J Bone Joint Surg Am. 1998;80:248-257. 21. Hanel DP, Pfaeffle HJ, Ayalla A. Management of posttraumatic metadiaphyseal radioulnar synostosis. Hand Clin. 2007;23:227-234. 22. Cullen JP, Pellegrini VD Jr, Miller RJ, Jones JA. Treatment of traumatic radioulnar synostosis by excision and postoperative low-dose irradiation. J Hand Surg. 1994;19A:394-401.

12 Distal Radius Fractures Brett D. Crist, MD, FACS and Yvonne M. Murtha, MD

Distal radius fractures are among the most common fractures encountered by an orthopedic surgeon. The complications associated with distal radius fractures treated nonoperatively include malunion, arthritis, carpal tunnel syndrome, complex regional pain syndrome (CRPS), and wrist or finger stiffness. Following operative management, the same complications can occur, with the addition of infection, iatrogenic nerve injury, and tendon injury or late rupture. Nonunion is very rare in distal radius fractures, as is deep or incisional infection. Pin site infection or irritation is common after percutaneous or external fixation but is usually transient and easily treated with oral antibiotics and local wound care. Complications are more commonly associated with high-energy injuries with complex fracture patterns or patients with poor bone quality. Malunion typically results from inadequate initial reduction or unstable fixation. Patient factors associated with malunion include age greater than 80 years, dependent patients, and patients with osteopenia or osteoporosis.1 Injury factors associated with fracture instability and malunion include initial dorsal or volar angulation more than 20 degrees, radial inclination less than 10 degrees, radial shortening greater than 5 mm, ulnar variance greater than 2 mm difference from the uninjured side, articular displacement more than 2 mm, volar or dorsal shear-type fractures where the carpus is displaced with the distal fragment, high-energy injuries in young/active patients, and inadequate closed reduction or redisplacement after closed reduction including residual dorsal angulation more than 5 degrees.1-4 Radiocarpal arthritis may be caused by articular injury, malreduction, or damage due to improper hardware position. Carpal tunnel syndrome is more common in fractures with comminution and significant dorsal displacement.4 It can result from swelling or bleeding in the carpal canal or immobilization in a position of excessive wrist flexion.5 CRPS (formerly 121

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“reflex sympathetic dystrophy” [RSD]) occurs more frequently in women, elderly patients, and those patients with psychological predisposition.5 CRPS is also associated with increased fracture severity, closed management with tight-fitting casts, and external fixation with excessive joint distraction. Complaints of pain in the cast are predictive for development of CRPS and should not be ignored. Nerve injury, most commonly the median nerve, can result from direct trauma from the injury, during surgical exposure for volar plating, or from placement of pins, wires, or screws. Similarly, tendon injury can result from direct surgical trauma or can occur late due to chronic hardware impingement.

PREVENTION: SURGICAL TECHNIQUES/REDUCTION As with all fractures, adequate radiographs are required and should include PA, lateral, and oblique wrist radiographs. If there is articular comminution, a wrist computed tomography (CT) scan with reconstructions should be considered. The fracture reduction goals include restoring the articular congruity to within 2 mm, radial inclination to approximately 22 degrees, volar tilt to 11 degrees, and ulnar variance equal to the uninjured side.4 Malunion occurs after both operative and nonoperative management of distal radius fractures and is problematic when it affects function, resulting in pain, arthrosis, loss of motion, or weakness.1 Although it has been shown that age greater than 80 years is a risk factor for malunion,1 elderly patients with lower functional demands tend to tolerate deformity6 and have similar function to cohorts undergoing operative fixation (Figure 12-1).7 Using the uninjured distal radius as a template for fracture reduction is helpful to ensure appropriate fracture reduction when significant comminution is present. The best way to avoid malunion is to achieve fracture reduction goals as stated previously and to understand which fractures are more likely to have fracture displacement when undergoing closed management.2-4 In patients undergoing closed treatment who are at risk for loss of reduction, radiographs should be obtained at least weekly for the first month in order to avoid missing early displacement. The volar flexor carpi radialis surgical approach is commonly used to address distal radius fractures due to better articular visualization and reduced risk of late extensor tendon rupture, compared to the dorsal approach. However, extensor tendons are still at risk from excessively long screws through a volar plate. Use of the dorsal surgical approach between the third and fourth extensor compartments should still be considered as either a primary or an accessory incision to obtain an anatomic reduction and minimize soft tissue stripping, especially when there is dorsal lunate facet fragment displacement or a dorsal Barton’s fragment (Figure 12-2). Anatomic fracture reduction (Figure 12-3) should be the goal, whether obtained by open or closed means, especially for the articular surface. However, remember that some low-demand patients will have no complaints with even substantial deformity (see Figure 12-1). If there is significant metaphyseal comminution, bridging fixation techniques may be required, with the goal of restoring overall length, alignment, and rotation. Occasionally, when significant articular comminution is present, anatomic reduction may not be possible, and bridge-type fixation can be used to restore general alignment. Provisional or definitive K-wire fixation is an important adjunct for maintaining reduction obtained by closed or open means. Loss of fixation or late fracture displacement may occur after operative or nonoperative management. The risk of lost reduction in a cast is reduced by avoiding

Distal Radius Fractures

A

B

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Figure 12-1. (A,B) Distal radius malunion in an elderly woman with excellent function. (C) Full supination is demonstrated.

C

Figure 12-2. Dorsal approach to the distal radius. Distal is toward the bottom of the picture. The extensor pollicis longus tendon crosses the plate distally.

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Figure 12-3. Fluoroscopic AP view showing anatomic open reduction and internal fixation achieved in an intra-articular distal radius fracture with a volar locking plate.

excessive padding, curving and flattening the forearm segment to provide threepoint fixation, and wrapping the cast snugly. Loss of fixation after surgery may occur in the osteopenic patient, and it is believed that the risk of this problem is reduced by the use of locking plate fixation in the elderly.8 Obtaining the best possible reduction will help reduce the risk of fixation loss with both conservative and surgical treatment.

Median Nerve Injury and Acute Carpal Tunnel Syndrome Median nerve symptoms that either begin or worsen after closed reduction have been associated with multiple closed reduction attempts and positioning the wrist in flexion 20 degrees or more to maintain the reduction.5,9 This would also hold true for wrist position when using external fixation or percutaneous pinning and casting, and so avoiding this position may lower the risk. When using a volar surgical approach to the distal radius, the median nerve can be injured during the surgical dissection if the approach is too ulnar due to mistaking the palmaris longus tendon for the flexor carpi radialis tendon (Figure 12-4). One should also avoid excessive or prolonged retraction of the volar wrist contents, particularly with the wrist distracted. When using dorsal implants that are volarly directed, such as percutaneous K-wires, nonbridging external fixator, or dorsal plates, care should be taken to avoid excessive penetration of the volar cortex.

Stiffness Loss of wrist or finger motion that occurs after distal radius fracture is associated with prolonged immobilization, soft tissue scarring, and malreduction. Stable fixation in the correct alignment and early rehabilitation, often under the direction of an occupational or physical therapist, will help to reduce the incidence. Missed instability of the distal radioulnar joint (DRUJ) also leads to limited supination and pronation.

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Figure 12-4. Volar flexor carpi radialis approach. Scissors are pointing to the median nerve. Notice the proximity to the flexor carpi radialis tendon being retracted.

Chronic Regional Pain Syndrome CRPS results in chronic pain, limited motion, and significant functional loss. Complaints of pain after cast placement or significant pain complaints after operative management are predictive of subsequent CRPS and should alert the physician to the possibility of its development.5 Level I evidence suggests that vitamin C helps to prevent CRPS in patients with distal radius fractures.10

PREVENTION: IMPLANT SELECTION AND APPLICATION Malunion With percutaneous K-wire fixation, loss of fixation can be minimized by using the intrafocal pinning technique (Kapandji pinning), supplementing with calcium phosphate for metaphyseal comminution, and adding a bridging external fixator— especially when comminution is present in elderly patients.3,5,11 Using hydroxyapatite-coated pins or increasing the number of pins helps minimize the risk of external fixator pin loosening.3 If there is enough intact distal fragment to allow for external fixator pin placement, nonbridging external fixation alone has been shown to maintain volar tilt and carpal alignment better than bridging external fixation.12 Although indications for operative management of distal radius fractures are controversial,13 using fixed-angle or locking plates volarly or dorsally has been shown to be biomechanically and clinically superior at maintaining reduction when compared to conventional plates, particularly when small articular fragments, comminution, and osteoporotic bone are encountered.3 When there is an intra-articular volar shear component, ensuring that the volar lunate facet is captured with volar plate distal screw fixation minimizes the risk of postoperative displacement.14 In fractures with significant metadiaphyseal comminution, temporary joint-spanning (distraction plating) dorsal plating in addition to anatomic articular reduction may be an alternative to bridge plating or external fixation.15

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Figure 12-5. An elevated true lateral intraoperative fluoroscopic view showing the reduction achieved and that the screws are extra-articular.

Stiffness To avoid loss of motion associated with operative management, specific techniques can be used. When a bridging external fixator is used, once the reduction is obtained and K-wire fixation is complete, joint distraction should be released and the wrist placed in a neutral position, and the external fixator should be tightened in order to minimize the risk of CRPS development.16

Nerve, Tendon, or Joint Injury To minimize the risk of nerve or tendon tethering or injury, formal surgical dissection should be done prior to K-wire placement. After wire or external fixator pin placement, full passive finger and thumb motion should be performed to identify any signs of motion limitation. Tendon irritation leading to synovitis and eventual rupture has been associated with plate application dorsally and volarly, as well as overpenetration of screws through the opposite cortex. The risk of this complication may be reduced by using lower profile implants, applying the implant in a more proximal location, and verifying screw or peg length fluoroscopically after implantation. If dorsal plating is necessary, it may be prudent to plan for early hardware removal after the fracture is healed to reduce the risk of late tendon rupture. Intra-articular hardware can affect motion, and fluoroscopic views should verify that the periarticular implants are extra-articular. This requires evaluating the elevated lateral view, in which the fluoroscope beam is aligned with the radial inclination of the distal articular surface on the lateral view by elevating and pronating the wrist until a true articular lateral is obtained (Figure 12-5). To avoid missing an injury or malreducing the DRUJ, both clinical and fluoroscopic evaluation of the joint should be done using the opposite extremity as a reference for normal.

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Figure 12-6. Preoperative plan showing corrective osteotomy for a volar and radially deviated malunion.

20-degree deformity 5-mm ulnar positive 60-degree deformity Supine position Tourniquet Volar exposure: HWR and CTR Dorsal exposure: Osteotomy with Hall saw Fashion and insert graft Two hole ½ tubular plate dorsal Right angle T-plate volar (or vice versa?) 0.7 cm

0.4 1.5 cm cm

0.4 cm

Graft dimensions 2.5 1.2 0.5

1.0 2.5 cm cm Right angle T plate with one hole cut off

2.5

COMPLICATION MANAGEMENT: SALVAGE PROCEDURES Malunion A corrective distal radial osteotomy is the mainstay of reconstructive procedures to restore normal wrist anatomy. Standard radiographs and CT scan (if there is articular involvement) should be done to evaluate the deformity, and preoperative planning is required (Figure 12-6). Indications for consideration of corrective radial osteotomy includes a patient with clinical symptoms and more than 10 degrees of dorsal tilt, more than 25 degrees of volar tilt, radial inclination of 12 degrees or less, and 2- to 5-mm of shortening.4 Whether the osteotomy is approached dorsally or volarly is determined by the type of angulation and whether an opening or closing wedge osteotomy is desired. Alternative approaches in low-demand patients include an ulnar shortening osteotomy or excisional ulnar arthroplasty.4 If there is persistent pain and degenerative articular changes, wrist fusion is also a consideration. If loss of fixation or late fracture displacement is encountered prior to fracture malunion and reoperation is being considered, it should not be delayed.17 Additional surgical approaches to obtain fracture reduction and supplemental fixation may be required, depending upon the circumstances. For example, if plate fixation is used and loss of fixation occurs proximally in the radial shaft, simply using a longer implant may prove successful. If articular fixation is lost or fracture displacement occurs, open reduction of the articular surface should be performed. Bridging

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external fixation may also be used in addition to plating to help maintain reduction. Auto- or allograft bone graft or synthetic bone void filler may be required to address metaphyseal bone loss. Infection should always be ruled out as a cause of failure.

Carpal Tunnel Syndrome Compression of the median nerve after fracture is an emergent condition and should be treated promptly to reduce the risk of permanent damage. The first step is to position the wrist in neutral, loosen the splint, elevate, and re-evaluate. Carpal tunnel symptoms that are initially present after the injury may improve after closed reduction and avoiding the flexed position for maintaining the reduction. If symptoms are severe or progressive after closed reduction, an emergent carpal tunnel release should be performed to minimize risk of permanent neurological deficits.5 If mild carpal tunnel symptoms persist after closed or open reduction, early carpal tunnel release should be performed to maximize chances of improvement.

Stiffness and Complex Regional Pain Syndrome If loss of motion is encountered postinjury or postoperatively, occupational or physical therapy should be used as an initial treatment method. Dynamic and staticprogressive splinting may be incorporated. If implant malposition or prominence is suspected as a contributor, early hardware removal or revision should be performed. If fracture malreduction is identified, revision surgery should be performed. If CRPS is identified, early management is important, and surgery should be avoided if possible. A multidisciplinary approach including medication, occupational/physical therapy, and, potentially, regional anesthetic blocks is important. If patients are suspected to be at risk for CRPS preoperatively, a prophylactic course of vitamin C has been shown to be helpful.10 Lastly, if nonoperative methods fail to improve loss of motion, open or arthroscopic contractural release may be considered.18,19

SUMMARY The incidence of distal radius fractures will increase as the population ages and the incidence of osteoporosis increases. Operative management of distal radius fractures has become more popular as implant selection and operative techniques have advanced. Complications associated with distal radius fractures can be minimized by the following: § Appropriate patient selection § Identifying radiographic signs of fracture instability and patient factors that increase complication risk § Obtaining an anatomical reduction Using newer operative techniques like open reduction and internal fixation with volar fixed-angle plates when indicated § Using supplemental fixation techniques when necessary § Paying close attention to details, such as making sure normal motion is achievable intraoperatively. If complications do occur, it is often important to address them early, such as performing a carpal tunnel release in a patient with progressive or persistent carpal tunnel symptoms. §

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REFERENCES 1. Mackenney PJ, McQueen MM, Elton R. Prediction of instability in distal radial fractures. J Bone Joint Surg Am. 2006;88(9):1944-1951. 2. Leone J, Bhandari M, Adili A, McKenzie S, Moro JK, Dunlop RB. Predictors of early and late instability following conservative treatment of extra-articular distal radius fractures. Arch Orthop Trauma Surg. 2004;124(1):38-41. 3. Liporace FA, Adams MR, Capo JT, Koval KJ. Distal radius fractures. J Orthop Trauma. 2009;23(10):739-748. 4. Friedman SL, ed. Distal Radius Fractures. 1st ed. Chicago, IL: American Academy of Orthopaedic Surgeons; 2005. 5. Turner RG, Faber KJ, Athwal GS. Complications of distal radius fractures. Orthop Clin North Am. 2007;38(2):217-228, vi. 6. Young BT, Rayan GM. Outcome following nonoperative treatment of displaced distal radius fractures in low-demand patients older than 60 years. J Hand Surg Am. 2000;25(1):19-28. 7. Arora R, Gabl M, Gschwentner M, Deml C, Krappinger D, Lutz M. A comparative study of clinical and radiologic outcomes of unstable colles type distal radius fractures in patients older than 70 years: nonoperative treatment versus volar locking plating. J Orthop Trauma. 2009;23(4):237-242. 8. Orbay JL, Fernandez DL. Volar fixed-angle plate fixation for unstable distal radius fractures in the elderly patient. J Hand Surg Am. 2004;29(1):96-102. 9. Gelberman RH, Szabo RM, Mortensen WW. Carpal tunnel pressures and wrist position in patients with Colles’ fractures. J Trauma. 1984;24(8):747-749. 10. Shah AS, Verma MK, Jebson PJ. Use of oral vitamin C after fractures of the distal radius. J Hand Surg Am. 2009;34(9):1736-1738. 11. Trumble TE, Wagner W, Hanel DP, Vedder NB, Gilbert M. Intrafocal (Kapandji) pinning of distal radius fractures with and without external fixation. J Hand Surg Am. 1998;23(3):381394. 12. McQueen MM. Redisplaced unstable fractures of the distal radius. A randomised, prospective study of bridging versus non-bridging external fixation. J Bone Joint Surg Br. 1998;80(4):665-669. 13. Koval KJ, Harrast JJ, Anglen JO, Weinstein JN. Fractures of the distal part of the radius. The evolution of practice over time. Where’s the evidence? J Bone Joint Surg Am. 2008;90(9):1855-1861. 14. Harness NG, Jupiter JB, Orbay JL, Raskin KB, Fernandez DL. Loss of fixation of the volar lunate facet fragment in fractures of the distal part of the radius. J Bone Joint Surg Am. 2004;86-A(9):1900-1908. 15. Ruch DS, Ginn TA, Yang CC, Smith BP, Rushing J, Hanel DP. Use of a distraction plate for distal radial fractures with metaphyseal and diaphyseal comminution. J Bone Joint Surg Am. 2005;87(5):945-954. 16. Combalia A. Over-distraction of the radio-carpal and mid-carpal joints with external fixation of comminuted distal radial fractures. J Hand Surg Br. 1995;20(4):566-567. 17. Jupiter JB, Ring D. A comparison of early and late reconstruction of malunited fractures of the distal end of the radius. J Bone Joint Surg Am. 1996;78(5):739-748. 18. Watson HK, ed. Stiff Joints. New York, NY: Churchill Livingston; 1988. 19. Verhellen R, Bain GI. Arthroscopic technical note capsular release for contracture of the wrist: a new technique. Arthroscopy: The Journal of Arthroscopic and Related Surgery. 2000;16(1):106-110.

III

Pelvis and Acetabulum

13 Open Pelvic Fracture Infection Marcus F. Sciadini, MD

Infections associated with open pelvic fractures reflect the complex nature of these injuries and the typically high-energy mechanisms of causation. Patients have often sustained severe injuries to multiple organ systems including closed head injuries, pulmonary injury, and hollow viscous or other intra-abdominal trauma.1 Significant blood loss requiring massive transfusion is frequently associated with the pelvic ring injury, and the most common type of wound in the perineal region is in direct proximity to fecal material. All of these factors combine to put the open pelvic fracture at substantial risk for infection and other complications, and the resulting mortality rate is high.2 Figure 13-1 is a radiograph demonstrating a widely displaced APC-3 pelvic fracture with associated subtrochanteric femoral shaft fracture. The patient was a 16-year-old boy involved in a tubing accident in which he was pulled into a dock at high speed.

PREVENTION: SURGICAL PRIORITIES, STRATEGY, AND TECHNIQUE Avoidance of infection among numerous other potentially devastating complications associated with open pelvic fractures presents a challenge that must be met with emergent, aggressive, and multidisciplinary treatment. General protocols for the management of these injuries are in place at most level I trauma centers. The first priority is to recognize the severity of the injury and the likely association of lifethreatening conditions. Immediate application of a pelvic binder is appropriate to decrease the pelvic volume, tamponade ongoing bleeding, and diminish soft tissue damage by providing provisional bony stability. 133

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Figure 13-1. AP pelvis radiograph demonstrating complex pelvic fracture and left subtrochanteric femur fracture. The patient also sustained a right open tibial shaft fracture.

Figure 13-2. (A) AP pelvis radiograph demonstrating good reduction after application of pelvic binder. (B) Clinical photo demonstrating use of sheet to achieve provisional reduction and fixation.

A

B

Figure 13-2A is a radiograph demonstrating provisional reduction obtained with placement of pelvic binder. Sheets may also be employed, as illustrated in Figure 13-2B.

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A

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Figure 13-3. (A) Intraoperative photo after initial débridement showing massive perineal wound. Significant stripping and dead space extended up to the anterior sacrum and bilateral sacroiliac joints. (B) AP pelvis radiograph demonstrating placement of initial anterior pelvic external fixator and damagecontrol external fixation of femur.

B

Adequate resuscitation with intravenous fluids and blood products to obtain hemodynamic stability should be followed by emergent operative treatment to address life-threatening nonorthopedic injuries, obtain additional provisional pelvic fixation, and perform a thorough débridement of the perineal wound. Perhaps most importantly, diverting colostomy should be performed at the time of this initial surgical treatment. Associated orthopedic injuries, such as the subtrochanteric femur fracture present in the illustrative case, should be temporized with external fixation using the principles of damage-control orthopedics.3 Figure 13-3 shows a massive perineal wound following initial surgical débridement. Exploratory laparotomy with diverting colostomy was performed first, followed by external fixation of the pelvis and associated long-bone fractures. Application of a pelvic external fixator prior to placing the patient in lithotomy position for débridement of the perineal wound minimizes additional displacement of the pelvis and ongoing soft tissue injury. If the patient remains hemodynamically

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Figure 13-4. AP pelvis radiograph showing definitive fixation of subtrochanteric femur fracture.

unstable following adequate resuscitation and initial surgical treatment, pelvic angiography should be considered, although it may be associated with an increased incidence of tissue necrosis and complications associated with definitive pelvic surgery.4 Surgical débridement should be aggressive and should include sharp excision of all devitalized and contaminated bone and soft tissue followed by pulsed lavage. Rectal tears need to be recognized and addressed by the general surgical team. Adequate débridement usually results in a massive dead space and soft tissue defect. Negative pressure wound therapy has been advocated.5 However, a reasonable alternative is to initially treat these wounds with open packing using Clorpactin (oxychlorosene)dampened gauze rolls. The complexity and deep interstices of these open perineal wounds make adequate negative pressure drainage difficult if not impossible in the early stages, and obtaining an airtight seal is likewise challenging. The patient should be returned to the operating room on 12- to 48-hour intervals until an adequate surgical wound has been obtained with dead space control. Associated orthopedic injuries may be definitively addressed during these repeat trips to the operating room. Figure 13-4 is an anteroposterior (AP) pelvic radiograph demonstrating definitive fixation of subtrochanteric femur fracture. When appropriate, transition to vacuum-assisted wound dressings may be employed and frequency of débridements decreased. For female patients with pelvic ring injuries and evidence of vaginal bleeding, gynecologic exam is warranted to rule out an open fracture through the vaginal wall.6 If present, the bone should be delivered into the vagina, débrided, irrigated, and reduced before repairing the vaginal laceration. Perineal wounds may eventually be treated by delayed primary closure, splitthickness skin grafting, rotational, advancement, or free-flap coverage depending upon the extent and nature of the wound. If adequate anterior pelvic ring reduction and stability can be maintained with external fixation, this may be the preferred means of fixation in open injuries with open or percutaneous fixation of the posterior ring as indicated. However, when internal fixation of the anterior ring is necessary, it should be delayed until definitive soft tissue coverage has been achieved. These procedures are often performed in conjunction with one another, as the improved reduction and fixation obtained with internal fixation is also protective of the soft tissue repair.

Open Pelvic Fracture: Infection

Figure 13-5. (A) AP pelvis radiograph demonstrating definitive anterior and posterior pelvic fixation performed at time of definitive soft tissue coverage. (B,C) Five-year follow-up radiographs demonstrating healed subtrochanteric femur and pelvic ring fractures.

A

B

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C

Figure 13-5 shows open reduction and internal fixation of symphysis performed through open perineal wound at time of gracilis musculocutaneous advancement flap and healed subtrochanteric femur and pelvic ring fractures at 5 years postinjury.

COMPLICATION MANAGEMENT: TREATMENT OF DEEP PELVIC INFECTION If deep pelvic infection develops, general principles of treating orthopedic infections apply. A high index of suspicion and early diagnosis can lead to effective treatment and eradication of the infection. Increasing pain, erythema, wound drainage, and fever are clinical signs that should be thoroughly investigated with appropriate laboratory and imaging studies. Plain radiographic findings of hardware loosening or failure may indicate an underlying infection, and computed tomography scans can be helpful in identifying the presence of a pelvic abscess. Early and aggressive surgical débridement is indicated in cases of documented infection. Functioning hardware may be retained as maintenance of bony stability facilitates management of

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Figure 13-6. AP pelvis radiograph of different case in which partial internal hemipelvectomy was necessary to treat osteomyelitis following open pelvic ring injury.

the infection. However, if hardware loosening or failure is present, implants should be removed, and alternative fixation employed. Hardware removal may also be required if serial débridements fail to clear the clinical signs of infection. Placement of antibiotic-impregnated methylmethacrylate beads during serial débridements may be helpful in delivering locally high doses of antimicrobial agents without systemic side effects, and use of negative-pressure wound therapy is also a valuable adjunct. Infectious disease consultation and pathogen-specific long-term antibiotic therapy is essential. In most cases, eventual removal of hardware after bony and ligamentous healing is complete should be planned to ensure eradication of deep infection. Failure to recognize, adequately treat, and control deep pelvic infection can lead to a catastrophic outcome, including death from sepsis or massive bone loss and resultant loss of function. In rare cases, hemipelvectomy may be required to control sepsis in complex open pelvic ring injuries. Figure 13-6 is an AP pelvic radiograph of a different case in which hemipelvectomy was required to treat osteomyelitis.

SUMMARY Infection after open pelvic fractures is a common complication due to multiple factors, including the high-energy mechanism of injury, associated nonorthopedic injuries, high transfusion requirements, and fecal wound contamination (Table 13-1). Avoidance requires an aggressive, emergent, and multidisciplinary approach to address resuscitation, life-threatening associated injuries, wound débridement, pelvic stabilization, and fecal diversion. Early definitive fixation and soft tissue coverage once a healthy wound bed has been achieved enhances the chances for a favorable outcome. Early diagnosis and aggressive surgical and medical treatment are essential for successful management when infection does occur.

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Risk Factors for Infection in Open Pelvic Fractures RISK FACTOR

IMPLICATION/RESULT

Multiply injured patient

High transfusion requirements, at risk for systemic infection and multisystem organ failure

Perineal wound

Direct contamination by fecal material

Delayed stabilization of pelvic injury

Ongoing soft tissue injury due to pelvic instability

Delayed diversion of fecal material

Ongoing contamination of wound and/or fracture with fecal material

Failure to diagnose open fracture through vaginal wall

No surgical débridement of open fracture or repair of vaginal wall

Refractory hemodynamic instability requiring angiography

Potential for increased tissue necrosis and infection

REFERENCES 1. Burgess AR, Eastridge BJ, Young JW, et al. Pelvic ring disruptions: effective classification system and treatment protocols. J Trauma. 1990;30:848-856. 2. Duchesne JC, Bharmal HM, Dini AA, et al. Open-book pelvic fractures with perineal open wounds: a significant morbid combination. Am Surg. 2009;75(12):1227-1233. 3. Scalea TM, Boswell SA, Scott JD, Mitchell KA, Kramer ME, Pollak AN. External fixation as a bridge to intramedullary nailing for patients with multiple injuries and with femur fractures: damage control orthopedics. J Trauma. 2000;48:613-621. 4. Yasumura K, Ikegami K, Kamohara T, Hohara Y. High incidence of ischemic necrosis of the gluteal muscle after transcatheter angiographic embolization for severe pelvic fracture. J Trauma. 2005;58(5):985-990. 5. Labler A, Trentz O. The use of vacuum assisted closure (VACTM) in soft tissue injuries after high energy pelvic trauma. Langenbecks Arch Surg. 2007;392(5):601-609. 6. Niemi TA, Norton LW. Vaginal injuries in patients with pelvic fractures. J Trauma. 1985;25(6):547-551.

14 Sacral Fractures Loss of Reduction/Failure of Fixation H. Claude Sagi, MD

Many complications such as neurological and visceral injury related to the magnitude of the pelvic fracture and mechanism itself are largely unavoidable. However, sacral fracture reduction and fixation can be a complex undertaking in a patient with marginal physiological status and, therefore, can result in a number of potentially significant complications that can impact the ultimate functional outcome of the patient. Reduction and fixation complications associated with the treatment of sacral fractures can best be divided into the pre-, peri-, and postoperative periods (Table 14-1).

PREOPERATIVE COMPLICATIONS: THE MISSED INJURY It is important to recognize and remember that any ring structure with disruption in one area must, by virtue of “ring mechanics,” have at least one other point of disruption. Therefore, any patient with a seemingly insignificant ramus fracture should be scrutinized with further imaging to disclose other injuries to the pelvic ring. Young patients with good bone quality should have computed tomographic (CT) scanning performed to further evaluate the pelvic ring, and elderly patients may require magnetic resonance imaging (MRI) or even nuclear bone scans to disclose occult insufficiency fractures of the sacrum (Figure 14-1). Another frequently missed injury is the U-shaped sacral fracture (spinal-pelvic dissociation). This injury is not classically considered a pelvic injury because the ring is itself in continuity through the sacroiliac joints and pubic symphysis. U-shaped sacral fractures are best defined as bilateral sacral alar fractures connected by a transverse fracture line. They tend to occur through or in close proximity to the vestigial disc spaces of the sacrum. Because both alae are disrupted, the path for force transmission 141

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Table 14-1

Risk Factors for Sacral Fracture Loss of Reduction/Failure of Fixation PERIOD

COMPLICATION

Preoperative

Missed injury (insufficiency and U-shaped fractures)

Perioperative

Inability to reduce vertical displacement Inability to reduce sagittal and axial plane rotation

Postoperative

Malunion and loss of reduction Nonunion

Figure 14-1. Bone scan and plain radiographs of an occult sacral fracture in (A) young and (B) elderly patients.

B

A

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Figure 14-2. Diagram showing fracture lines for U-shaped sacral fractures.

from the sciatic buttress to the spine is no longer in continuity—the spine has been disconnected from the pelvis (Figure 14-2). Radiographically, this injury needs to be suspected in two situations: 1) when the anteroposterior (AP) pelvic radiograph shows an inlet view of the proximal sacrum, and 2) when “nondisplaced” bilateral alar fractures are noted on the axial CT scan. A lateral pelvic radiograph or sagittal CT reconstruction is imperative in disclosing spinal pelvic dissociation and will often reveal substantial displacement and kyphosis that is not at all apparent on standard imaging. Displaced kyphotic fractures with canal compromise and cauda equina syndrome can go completely undetected if this additional imaging is not obtained (Figure 14-3).

PERIOPERATIVE COMPLICATIONS Inability to Achieve Reduction: Vertical Sacral Fractures Completely unstable vertical sacral fractures have a tendency to displace in a cephalad direction with sagittal plane flexion and axial plane external rotation. In widely displaced fractures, reduction can at times be very difficult, if not impossible. A sick patient in the intensive care unit who will not be able to withstand the operation to stabilize his or her pelvis can, over 1 or 2 weeks, develop significant proximal migration and pelvic deformity that becomes increasingly difficult to reduce as time passes. Therefore, when the patient comes to the hospital post-trauma, it is imperative that he or she be placed into longitudinal balanced skeletal traction as soon as possible. Pelvic binders help to control venous bleeding, improve external rotation and abduction deformity, and give some element of pain control to the patient. Properly applied over the trochanters, the binder can be in place for days as long as proper skin care is continued, and the binder is gently released to examine for the development of pressure sores.

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Figure 14-3. (A) Axial and (B) sagittal CT images of spinal pelvic dissociation.

A

B

Intraoperatively, traction, again, is the key element needed to achieve reduction. In patients with significant displacement, longitudinal skeletal traction helps to reduce not just cephalad displacement but also the sagittal plane flexion-rotation deformity because the hip joint is anterior to the posterior pelvic ring. Traction will often perform the bulk of reduction that only then needs to be fine-tuned with reduction clamps to close fracture gaps. Frequently, sufficient traction is unable to be applied because the patient starts to slide down the bed. A perineal post is not effective in this situation because the ischial tuberosity abuts the post and prevents further caudal translation of the hemipelvis, impairing reduction. To overcome this, the patient’s uninjured hemipelvis can be secured to the table using a table-skeletal fixation set-up with pins placed into the ilium and/or femur to hold the patient in place and prevent tilting of the pelvis while forceful traction is applied. For preventing iatrogenic sciatic nerve injury, it is important to keep the patient’s knee flexed to relax the lumbosacral plexus. It is also important to ensure that, during positioning, the pelvis hangs freely so that the patient is not resting on the anterior superior iliac spine, which may impair the surgeon’s ability to manipulate the pelvis (Figure 14-4). Finally, if satisfactory reduction of the sacral fracture is achieved but the anterior ring has not come into alignment (often residual flexion deformity with some external rotation), then the patient should be turned into the supine position, and the anterior ring reduced and stabilized with a reconstruction plate or ramus screw.

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Figure 14-4. Prone positioning and table-skeletal fixation with traction for sacral fracture surgery and hemipelvic stabilization.

B

Inability to Achieve Reduction: U-Shaped Sacral Fractures These fractures often present impacted and kyphotic. Because this is not a pelvic ring injury, longitudinal skeletal traction does not aid in reduction, and the fracture needs to be disimpacted and reduced directly. The patient should be positioned prone with the pelvis hanging freely to give a hyperextension moment to the pelvis and hips. After sacral laminectomy, decompression, and mobilization of the thecal sac, bilateral spinal pelvic constructs are placed into the pedicles of L4/L5 and the ilium. Distraction along the connecting rods will help to disimpact the upper sacral segment, which can then be manipulated into a less kyphotic position. Once this occurs, it is important to relax the distraction along the rods to allow the fracture to re-impact itself and gain some inherent stability. The spinal-pelvic construct is then locked down to maintain this position and restore a posterior tension band until healing of the fracture occurs (Figures 14-5 and 14-6).

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Figure 14-5. Sacral laminectomy for exposure of the thecal sac.

Figure 14-6. Bilateral spinal-pelvic construct with reduction of sacral kyphosis.

POSTOPERATIVE COMPLICATIONS Loss of Sacral Reduction With Malunion Sacral malunion may result in leg length inequality, sitting imbalance, dyspareunia, and chronic pain. For these reasons, unstable sacral fractures need to be treated aggressively and stabilized with adequate fixation to prevent loss of reduction (Figure 14-7).

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Figure 14-7. Pelvic malunion secondary to untreated sacral fracture.

Figure 14-8. Failed iliosacral screw for sacral fracture with loss of reduction.

The most common reason for loss of reduction with malunion is inadequate fixation for a comminuted, vertically unstable sacral fracture. Apart from the type of fixation, anatomic reductions and close apposition of fracture surfaces with closure of fracture gaps is imperative in helping to maintain stability across the fracture and preventing loss of reduction. However, in some instances of comminution and highenergy fractures, reduction of the fracture does not provide any inherent stability to the construct, and the surgeon must rely on the fixation to maintain the reduction. While iliosacral screws have become the workhorse for posterior pelvic fixation, they must be used with caution in the comminuted, vertically unstable sacral fracture. Inability to achieve maximal compression and interdigitation across fracture surfaces increases the chances of failure of fixation for this technique. Placing multiple sacroiliac screws or trans-sacral screws gaining purchase in the contralateral ilium augmented with anterior fixation can help to mitigate this complication in some cases (Figure 14-8).

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Figure 14-9. Comminuted sacral fracture with a vertical shear component.

Figure 14-10. Spinal-pelvic construct for a comminuted sacral fracture.

With severe degrees of comminution and disruption of the L5/S1 facet joint, consideration should be given to a spinal pelvic construct that bypasses the sacral fracture and more effectively resists the deforming vertical shear forces on the hemipelvis (Figures 14-9 and 14-10).

Sacral Fracture Nonunion With the sacrum being a vascular bony structure, nonunion is infrequent. The primary etiological factor resulting in sacral fracture nonunion is failure to close any residual fracture gap. Because the sacrum does not tend to heal with abundant callus, it does not bridge the fracture gap effectively, even with rigid fixation. Therefore, it is critical in the treatment of sacral injuries that any fracture gap be closed and minimized with either reduction clamps or lag screw techniques. In the case of application of spinal pelvic fixation constructs, it is important to close the fracture gap with the iliosacral screw prior to locking down the spinal pelvic fixation (Figure 14-11).

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Figure 14-11. Sacral nonunion secondary to residual fracture gap at the time of fixation.

SUMMARY Sacral fractures are complex injuries that involve both the spinal-pelvic junction and the pelvic ring. Variable bony healing, poor bone quality, and neurological structures and injuries add to the complexity of treating these injuries successfully. The treating surgeon must take into account all of these factors to prevent the myriad serious complications that can result from inattention to details and anatomy. Taking the time to accurately interpret preoperative injury films for the involved structures and anatomical variations, as well as obtaining anatomic reductions and safely placing solid fixation, will help to avoid these complications.

BIBLIOGRAPHY Beaulé PE, Antoniades J, Matta JM. Trans-sacral fixation for failed posterior fixation of the pelvic ring. Arch Orthop Trauma Surg. 2006;126(1):49-52. Epub 2005 Nov 26. Denis F, Davis S, Compfort T. Sacral fractures, an important problem. Retrospective analysis of 236 cases. Clin Orthop. 1988;227:67-81. Gorczyca JT, Varga E, Woodside T, Hearn T, Powell J, Tile M. The strength of ilio-sacral lag screws and trans-iliac bars in the fixation of vertically unstable pelvic injuries with sacral fractures. Injury. 1996;27(8):561-564. Griffin DR, Starr AJ, Reinert CM, Jones AL, Whitlock S. Vertically unstable pelvic fractures fixed with percutaneous ilio-sacral screws: does posterior injury pattern predict fixation failure? J Orthop Trauma. 2003;17(6):399-405. Hak DJ, Olson SA, Matta JM. Diagnosis and management of closed internal degloving injuries associated with pelvic and acetabular fractures: the Morel-Lavallée lesion. J Trauma. 1997;42(6):1046-1051. Matta JM, Yerasimides JG. Table-skeletal fixation as an adjunct to pelvic ring reduction. J Orthop Trauma. 2007;21(9):647-656. Nork SE, Jones CB, Harding SP, Mirza SK, Routt ML Jr. Percutaneous stabilization of U-shaped sacral fractures using ilio-sacral screws: technique and early results. J Orthop Trauma. 2001;15(4):238-246.

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Pohlemann T, Angst M, Schneider E, Ganz R, Tscherne H. Fixation of transforaminal sacrum fractures: a biomechanical study. J Orthop Trauma. 1993;7(2):107-117. Reilly MC, Bono CM, Litkouhi B, Sirkin M, Behrens FF. The effect of sacral fracture malreduction on the safe placement of ilio-sacral screws. J Orthop Trauma. 2003;17(2):88-94. Sagi HC. Technical aspects and recommended treatment algorithms in triangular osteosynthesis and spinopelvic fixation for vertical shear transforaminal sacral fractures. J Orthop Trauma. 2009;23(5):354-360. Sagi HC, Militano U, Caron T, Lindvall E. A comprehensive analysis with minimum one-year follow-up of vertically unstable trans-foraminal sacral fractures treated with spinal-pelvic fixation. J Orthop Trauma. 2009;23(5):313-319; discussion 319-321. Schildhauer TA, Bellabarba C, Nork SE, Barei DP, Routt ML Jr, Chapman JR. Decompression and lumbo-pelvic fixation for sacral fracture-dislocations with spino-pelvic dissociation. J Orthop Trauma. 2006;20(7):447-457. Schildhauer TA, Josten C, Muhr G. Triangular osteosynthesis of vertically unstable sacrum fractures: a new concept allowing early weight-bearing. J Orthop Trauma. 1998;12(5):307314. Schildhauer TA, Ledoux WR, Chapman JR, Henley MB, Tencer AF, Routt ML Jr. Triangular osteosynthesis and ilio-sacral screw fixation for unstable sacral fractures: a cadaveric and biomechanical evaluation under cyclic loads. J Orthop Trauma. 2003;17(1):22-31. Simonian PT, Routt ML, Harrington RM, Tencer AF. Internal fixation of the transforaminal sacral fracture. Clin Orthop. 1996;323:202-209. Tseng S, Tornetta P 3rd. Percutaneous management of Morel-Lavallee lesions. J Bone Joint Surg Am. 2006;88(1):92-96. Van Zwienen CM, van den Bosch EW, Snijders CJ, Kleinrensink GJ, van Vugt AB. Biomechanical comparison of sacroiliac screw techniques for unstable pelvic ring fractures. J Orthop Trauma. 2004;18(9):589-595.

15 Iliosacral Screw Malposition A. Michael Harris, MD and Paul B. Gladden, MD

Iliosacral screws are commonly used for fixation of posterior pelvic ring fractures and dislocations. The placement of an iliosacral screw is demanding and is associated with a potential risk of iatrogenic injury to the surrounding neurovascular structures.1-3 Complex anatomy and variable sacral morphology make accurate placement of iliosacral screws a challenge. There have been reports of malpositioned screws with serious consequences.1 In an attempt to decrease the risk associated with screw placement, some authors have recommended neurodiagnostic monitoring using computed tomography (CT) and image-guided techniques (Table 15-1).4-7 Safe placement of iliosacral screws requires a thorough understanding of the anatomy of the posterior pelvic ring and intense preoperative planning through the use of high-quality radiographs and CT scans. Quality imaging and skill with interpretation of these studies are mandatory. Included in radiographic preparation must be an anteroposterior (AP) pelvis, inlet and outlet views, a lateral sacral image, and a pelvic CT. Intraoperative fluoroscopy that allows for clear visualization of osseous landmarks must be obtained in order to be successful with this procedure. Adequate training and experience is necessary to safely insert iliosacral screws because the safe corridor for placement can be fairly small. In some patients, such as those with a dysmorphic sacrum, this safe corridor is even smaller and may preclude the placement of an iliosacral screw.1,8 The placement of an iliosacral screw is made more difficult if an anatomic reduction has not been achieved. Achieving an anatomic reduction through the use of the screw requires an intimate understanding of the normal anatomy of the pelvis, the deforming forces of the injury, and the placement and ability of the implant. Malreductions alter the posterior pelvic ring anatomy and obscure the radiographic 151

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Table 15-1

Risk Factors for Iliosacral Screw Malposition SURGEON-RELATED FACTORS

PATIENT-RELATED FACTORS

TECHNIQUE-RELATED FACTORS

Poor preoperative planning

Sacral dysmorphism

Poor-quality fluoroscopic imaging

Lack of understanding of the anatomy

Morbid obesity

Incorrect screw trajectory

Malreduction

Bowel gas/contrast

Incorrect screw length

landmarks needed for safe placement of the screw. Furthermore, the already-narrow safe zone for insertion is functionally narrowed further by a malreduction.8 Another factor that contributes to the surgeon’s ability to place an iliosacral screw safely is patient body habitus. Adequate fluoroscopic imaging can be extremely difficult in the morbidly obese patient. The ability to obtain an inlet and outlet view of the posterior pelvic ring may not be possible due to a large abdominal panniculus and a lateral sacral image because of thigh and buttock girth. If imaging is obtainable, fluoroscopic detail may be lost secondary to the excessively large soft tissue masses. Additionally, intra-abdominal bowel gas or contrast may completely obstruct visualization and preclude fixation. If adequate fluoroscopic visualization cannot be obtained, an alternative method of fixation should be employed. With a command of the anatomy and confidence in imaging obtained, insertion of a cannulated screw can be quite routine. However, the screw starting point, length, and trajectory all contribute to the ability to place the implant safely. Underestimating the level of skill and risk associated with this procedure can increase the potential for surgical error and patient injury.

PREVENTION: OPERATIVE TECHNIQUE Iliosacral screw insertions can be performed with the patient in the supine or prone position using either an open or percutaneous technique. In either position, adequate high-quality triplanar (anterior-posterior, oblique [inlet and outlet], and lateral) imaging should be obtained to prevent iatrogenic complications. These images should be performed prior to prepping and draping to ensure they can be adequately obtained. A radiolucent table without a central base will allow for the image intensifier to rotate fully, providing the appropriate imaging. The image intensifier should be positioned opposite the injured hemipelvis. Caudal and cephalad angulations for the inlet and outlet images should be noted on preoperative fluoroscopy to ensure reproduction of desired images during the procedure. It cannot be overemphasized that the ability to obtain these views preoperatively and reproduce them intraoperatively is dependent on a highly skilled radiology technologist and quality fluoroscopic equipment.

Iliosacral Screw Malposition

A

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B

Figure 15-1. (A,B) An axial pelvic CT scan of a poorly positioned iliosacral screw going from the ilium, exiting anterior to the sacral alar region, and re-entering the upper sacral vertebral body.

Reduction of the posterior pelvic ring injury can be performed by a number of different methods. Open reductions are performed when closed methods will not achieve the desired goal of an anatomic reduction. Early surgical intervention provides the best opportunity to achieve an anatomic reduction with closed methods. After an anatomic reduction has been achieved, the appropriate starting point is identified. The insertion site for iliosacral screws lies along the posterior ilium between the greater sciatic notch and the iliac crest. Many surgeons prefer the tactile feedback of an oscillating drill, while others use a threaded guide pin. The guide pin can be gently pushed through bone while on reverse or malleted in to aid in one’s ability to feel if the wire remains contained within the bone. This extraosseous feeling should be brief as the drill/wire exits the medial wall of the innominate bone, crosses the joint, and contacts the lateral wall of the sacrum. This technique can limit the “in-out-in” screw malposition (Figure 15-1). The ideal screw trajectory is more horizontal for the fixation of sacral fractures than for fixation of a sacroiliac joint disruption. This allows for fixation more perpendicular to the obliquity of the sacral fracture or for a sacroiliac joint disruption, respectively, when using a lag technique. The drill or guide wire is advanced from the ilium across the sacroiliac joint and into the sacrum until it is located superolateral to the foramen of the S1 nerve root as seen on the pelvic outlet image (Figure 15-2). A lateral sacral image is now obtained to ensure appropriate positioning of the wire. It is imperative to superimpose the greater sciatic notches and iliac cortical densities to ensure an accurate lateral image. This image validates that the drill/wire is positioned caudally to the iliac cortical densities and anterior to the S1 foramen. An image where the sciatic notches and iliac cortical densities are not aligned will misrepresent where the safe corridor lies (Figure 15-3). Once accurate placement has been confirmed, the wire is advanced into the sacral body. The inlet view should have the S1 body superimposed on the S2 body, demonstrating that the wire/drill remains contained within the bone (Figure 15-4). Inaccurate interpretation of these images can result in iatrogenic neurovascular injury secondary to screw misplacement

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Figure 15-2. A fluoroscopic true outlet view of the pelvis demonstrating the appropriate position of the guide wires cephalad to the S1 foramen.

Figure 15-3. A lateral sacral fluoroscopic image that demonstrates the iliac cortical densities; however, the sciatic foramina are not perfectly superimposed.

Figure 15-4. A fluoroscopic inlet view demonstrating the superimposition of the anterior cortical body of S1 on S2 and the appropriate positioning of the guide wires.

violating the sacral foramina (Figure 15-5). Typically, partially threaded screws are used for sacroiliac disruptions and fully threaded screws for sacral fractures to prevent overcompression of neural foramina. Ensuring that iliosacral screws placed perpendicular to the sacroiliac joint do not go beyond midline prevents breaching the contralateral sacral alar area, potentially compromising adjacent neurovascular structures.

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Figure 15-5. An axial pelvic CT scan of a poorly positioned iliosacral screw traversing the sacral foramen.

Loss of fixation can occur in patients who have highly unstable injury patterns of the posterior pelvic ring. A trans-sacral screw can be placed for sacral fractures that are comminuted and provide resistance to vertical migration. Furthermore, an iliosacral screw placed in S2 sacral body can provide additional stability. The insertion of an S2 screw is a much more technically demanding procedure, as the safe zone for insertion is significantly narrowed relative to the S1 corridor.9

COMPLICATION MANAGEMENT: SALVAGE PROCEDURES A malpositioned iliosacral screw can not only cause an iatrogenic injury, but also can create or accentuate pelvic deformity. An additional complication of this procedure may include loss of fixation. The salvage of an errant or ineffective iliosacral screw includes direct exposure of the area through an anterior or posterior approach. Access to the sacroiliac joint through an anterior (lateral window of the ilioinguinal) approach is a safe and effective way to reach anterior portions of the sacral ala and sacroiliac joint. The iliosacral screw can be removed via this approach, and the sacroiliac joint (or sacral fracture) can be reduced and an alternative form of fixation performed after reduction is achieved. This allows for direct inspection of the sacroiliac joint and placement of a properly placed screw or plate fixation. Reduction and plating or proper screw placement may be undertaken through a posterior approach as well. Additionally, decompression of the sacral foramina can be achieved via this approach. Care must be taken to protect the soft tissues in this area because they see regular pressure. If plating is done, the plate should be tunneled through and not over the ilium. During the approach, care must also be taken not to devitalize the muscles overlying the posterior pelvic ring.

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SUMMARY Iliosacral screw placement can be deleterious and detrimental if done incorrectly. Complications of iliosacral screw fixation can be surgeon related, patient related, and/or technique related. A number of methods have been described to prevent screw malposition and iatrogenic injury; however, paramount to successful placement of the iliosacral screw is the understanding of the anatomy of the posterior pelvic ring. Placement of iliosacral screws should only be done by someone familiar with pelvic anatomy and interpretation of pelvic images. A complete understanding will not only allow for the proper path to be chosen, but also an understanding of the patient who is a poor candidate for the procedure.

REFERENCES 1. Routt MLC, Simonian PT, Mills WJ. Iliosacral screw fixation: early complications of the percutaneous technique. J Orthop Trauma. 1997;11:584-589. 2. Sagi HC, Lindvall EM. Inadvertent intraforaminal iliosacral screw placement despite apparent appropriate positioning on intraoperative fluoroscopy. J Orthop Trauma. 2005;19:130-133. 3. Altman DT, Jones CB, Routt ML Jr. Superior gluteal artery injury during iliosacral screw placement. J Orthop Trauma. 1999;13:220-227. 4. Moed BR, Ahmad BK, Craig JG, et al. Intraoperative monitoring with stimulus-evoked electromyography during placement of iliosacral screws. An initial clinical study. J Bone Joint Surg Am. 1998;80:537-546. 5. Tonetti J, Carrat L, Lavallee S, et al. Percutaneous iliosacral screw placement using image guided techniques. Clin Orthop Relat Res. 1998;354:103-110. 6. Gardner MJ, Farrell ED, Nork SE, et al. Percutaneous placement of iliosacral screws without electrodiagnostic monitoring. J Trauma-Injury Infect Crit Care. 2009;66:1411-1415. 7. Ziran BH, Smith WR, Towers J, et al. Iliosacral screw fixation of the posterior pelvic ring using local anaesthesia and computerised tomography. J Bone Joint Surg Br. 2003;85-B:411418. 8. Reilly MC, Bono CM, Litkouhi B, et al. The effect of sacral fracture malreduction on the safe placement of iliosacral screws. J Orthop Trauma. 2003;17:88-94. 9. Moed BR, Fissel BA, Jasey G. Percutaneous transiliac pelvic fracture fixation: cadaver feasibility study and preliminary clinical results. J Trauma. 2007;62(2):357-364.

16 Pelvic Ring Disruption Malalignment Kyle F. Dickson, MD, MBA

Optimal initial care can reduce the occurrence of pelvic ring malreductions; however, nonunions and malunions may still occur.1-4 Tile5 estimated a 5% incidence of residual severe deformity in major disruptions of the pelvic ring. However, nonoperative management of vertically unstable pelvic ring injuries can lead to malunion and/or nonunion in 55% to 75% of cases.4,6 The factors that lead to malreduction of pelvic ring disruptions include injury factors, surgeon factors, and patient factors. Pelvic malunions often present with pain posteriorly,7 but can also present with neurologic, gynecologic, or urologic problems. Additional presentations include imbalance during sitting, lying, or standing (Table 16-1).

PREVENTION: SURGICAL TECHNIQUES/REDUCTION The key for the orthopedic surgeon to prevent pelvic malunions is to understand the deformity, anatomically reduce the pelvis, and then adequately stabilize to the pelvis to prevent loss of reduction. The most common deformities include cephalad and posterior translation and internal rotation of the hemipelvis.3,8-11 Despite the limited bony stability of the pelvis, once operative reduction and fixation occurs, having the pelvis anatomically reduced significantly increases the stability of the construct12 (Figure 16-1). Furthermore, malreduced fractures may make safe iliosacral screw fixation impossible. In classifying pelvic injuries, the most significant information to the orthopedic surgeon is 1) where the pelvis is broken, 2) the stability of the fracture, and 3) the actual deformity that is occurring in the pelvis. The specific location of the injury is easily defined during the radiographic evaluation (anteroposterior [AP], inlet, outlet, and computed tomography [CT] scan of the pelvis). 157

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Table 16-1

Risk Factors for Pelvic Malunion FACTOR

IMPLICATION/RESULT

Injury factors

Posterior disruption of the pelvis

Surgeon factors

Failure to understand the deformity of the pelvic disruption Failure to obtain anatomical reduction at surgery

Patient factors

Healing of the pelvic malreduction prior to operative intervention (patient instability, soft tissue injuries, infections, etc) Failure of fixation after anatomical reduction of pelvic disruption (patient noncompliance, etc)

Figure 16-1. An inlet view of the pelvis with the spine removed showing the inherent instability of the bony architect if the sacroiliac ligaments were disrupted.

Defining the stability of the pelvis is more complex. Stability is defined as the ability of the pelvic ring to withstand physiologic forces without abnormal deformation. The stability of the pelvis is determined both by physical exam and radiographic evaluation. An anterior superior iliac spine (ASIS) compression test and iliac wing compression test should be performed. Radiographic signs of instability include sacroiliac displacement of greater than 5 mm in any plane. Also, a posterior fracture (ilium or sacral) fracture gap may signify instability. Using the combination of radiographs and physical exam, the surgeon can determine whether the pelvis is stable. The most critical analysis of the injury prior to fixation is the actual deformity of the pelvic ring. Only by defining the deformity can the surgeon plan the appropriate reduction maneuvers. Unfortunately, the complexity of the pelvis makes analysis of the deformity quite difficult. It is helpful to think of the deformity on an X, Y, and Z axis1,3,9 (Figure 16-2). Each axis has a translational deformity as well as a rotational deformity, including X-axis diastasis or impaction with flexion-extension, Y-axis cephalad-caudad translation with internal-external rotation, and Z-axis anterior-posterior translation with abduction-adduction. Radiographic landmarks are essential in planning and assessing reduction. Cephalad translation can be assessed with a transverse

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Figure 16-2. A pelvis with the three axes superimposed. Each axis has a translational deformity and a rotational deformity: X axis Translation Impaction-diastasis Rotation Flexion-extension Y axis

Translation Rotation

Cephalad-caudad Internal-external rotation

Z axis

Translation Rotation

Anterior-posterior Abduction-adduction

line parallel to the cephalad border of the sacrum followed by perpendicular lines measuring the dome height (leg length discrepancy) and ischial height (sitting imbalance), while rotational deformities are only accurately assessed with a true AP of the sacrum (Figure 16-3). Reduction of the sacroiliac joint or the posterior pelvic injury is critical prior to fixation. Closed reduction and percutaneous fixation can often be achieved within the first 48 hours of injury using table traction, external fixators, the femoral distractor, and/or half pins as joy sticks.13 Definitive fixation of posterior pelvic injury often uses iliosacral lag screws. Anterior sacral iliac plating and transiliac bars or plating are also options. If closed reduction fails to obtain an anatomical reduction and/or if more than 48 hours have passed since the injury occurred, open reduction and internal fixation of the posterior pelvic injury may be indicated.

PREVENTION: IMPLANT SELECTION AND APPLICATION In general, in completely unstable pelvic injuries, the posterior hemipelvis requires reduction prior to the anterior pelvis as even a few millimeters of rotation anteriorly can translate into significant malalignment posteriorly. Reduction of the symphysis is often accomplished using a Weber clamp through an anterior pelvic approach. Alternatively, a Jungbluth clamp can reduce the symphysis and assist with the sacroiliac reduction as well.

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Figure 16-3. Demonstration of the method of linear measurement of deformity using the (A) AP radiograph of the pelvis obtained before the application of an external fixator in a 26-year-old pedestrian struck by a motor vehicle and (B) a corresponding line drawing. First, a line (unlabeled horizontal line in these figures) is drawn parallel to the X axis (as defined in Figure 16-2). Often, the remaining bilaterally intact sacral foramina can be used as guides to draw this line. Next, lines are drawn perpendicular to this first line, ending at the acetabular roof of the uninjured (X) and injured (X1) hemipelves, as well as the distal aspect of the ischium (Y and Y1, uninjured and injured sides, respectively). Comparing X to X1 provides a measure of leg length, and comparing Y to Y1 provides a measure of sitting (ischial) imbalance. The width of the ischium (Z and Z1, uninjured and injured sides, respectively) increases as internal rotation of the hemipelvis increases.

A

B

With the patient prone, open reduction of the posterior ring injury (sacroiliac joint) is facilitated with an angled Matta clamp placed through the sciatic notch with one prong on the sacral ala or midline sacrum and the other on the outer iliac wing (Figure 16-4).14 This helps reduce external rotation deformities as well as diastasis of the posterior pelvic injury. Additionally, a Weber clamp is placed from the posterior superior iliac spine (PSIS) to the sacral spinous process and reduces cephalad displacement and internal rotation deformities of the hemipelvis. The key to reduction is with a combination of clamps that create the reduction vector for anatomical reduction. Often, subtle manipulation of clamp placement will correct the deformity. Once anatomical reduction is achieved on the inlet, outlet, AP, and lateral views, iliosacral screws are the main form of posterior fixation. Posterior tension band plating can be performed as well using a 14- to 16-hole recon plate placed at the superior portion of the sciatic notch below the PSIS. These tension band plates are used in cases of significant comminution of the sacrum and/or severe osteoporosis and are often used as an adjunct to iliosacral screws.

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Figure 16-4. Reduction clamp placement on sacroiliac joint displacement.

Posterior crescent fractures can be approached from the anterior approach; however, in most of these cases, the fracture will be difficult to visualize (ie, the sacral fracture is more medial or the crescent fracture is posterior to the sacroiliac joint). The author prefers in these cases a posterior approach if the soft tissue will allow it. This allows a direct visualization of the fracture site, which is either posterior to the sacroiliac joint or enters the sacroiliac joint. If the posterior ilium fragment remains attached to the sacrum through the sacroiliac joint ligaments, sacroiliac joint fixation is not required. The deformity that is problematic is the internal/external rotation of the hemipelvis, which is somewhat difficult to manipulate from the back. A combination of reduction clamps and half pin joysticks are used to reduce the rotational deformity of the hemipelvis. A commonly used reduction method is to use small screw holding clamps (Farabeuf or Jungbluth) placed just cephalad to the top border of the sciatic notch to allow fixation above and below the clamp. The superior portion of the sciatic notch is excellent bone and allows good fixation of these crescent fractures. If difficulty is encountered in reducing the fracture, an angled Matta reduction clamp is placed through the notch with one point on the sacral ala and the other point on the broken iliac wing. The clamp can internally or externally rotate the hemipelvis depending on its position. Careful clamp placement is important so that key areas for fixation, such as the sciatic buttress, are accessible. After anatomical reduction is achieved, lag screw fixation placed from the PSIS toward the ASIS secures the reduction followed by definitive plate fixation. Once the crescent fracture is reduced, the sacroiliac joint is evaluated for stability. If unstable, supplemental fixation with iliosacral screws is performed. The rehabilitation of patients with completely unstable pelvic injuries involves touchdown weight bearing for a total of 8 weeks. Once 8 weeks have passed, weight bearing as tolerated with range of motion and resistive exercises are started. The patients with bilateral injuries are unfortunately wheelchair transfers for a total of 8 weeks. Most patients mobilize on the intact side and use crutches or walkers.

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COMPLICATION MANAGEMENT: SALVAGE PROCEDURES As mentioned earlier, the best treatment is prevention.2,4,7,15 The problem of malunions and nonunions appears most common after inadequate initial treatment of displaced fractures and unstable pelvic ring injuries.6 From the technical standpoint, late correction is very difficult because the anatomy is altered; thus, the potential for complications is increased. Osteotomies can easily damage adjacent structures, and scarring around nerves prevents fragments from moving freely without causing nerve palsy. Indications for surgery include pain, pelvic ring instability, and clinical problems relating to the pelvic deformity (gait abnormalities, sitting problems, limb shortening, genitourinary symptoms, vaginal wall impingement, etc). A thorough knowledge of pelvic anatomy is required to understand the three-dimensional deformity. Furthermore, extensive preoperative planning is needed to determine the proper order of exposures for release, reduction, and fixation. Because each patient is different, it behooves the surgeon to individualize the treatment. Simple nonunions often do not require extensive anterior and posterior ring releases and reduction, and they respond to in situ fusion.16 In nonunion cases with significant displacement, in situ fusions are unrewarding and leave the patient with complaints related to deformity as well as pain (Figures 16-5, 16-6, and 16-7). For malunions of the pelvis, the surgical technique often involves a three-stage procedure as described by Letournel.2,3,8 The three stages are performed with the patient supine-prone-supine or prone-supine-prone. After each stage, the wound is closed, and the patient is turned to the opposite position. The first stage mobilizes anterior or posterior injuries by an osteotomy of the malunion or release of the nonunion. The second stage involves release and mobilization of the opposite side. The most important part of the second stage is the reduction of the pelvic ring. However, this stage also includes an osteotomy, mobilization, or both of that side of the ring. Following reduction, the second stage is completed by fixation of that particular side of the pelvic ring. The third stage completes the reduction and fixation of the opposite side (relative to the second stage) of the pelvic ring. The key to reduction is to recognize the deformity, adequately release the deformity, and create a force vector to reduce the deformity. Because these reconstructions are very complex with a high risk of complication, they should be referred to surgeons with experience in their management.

SUMMARY The one-, two-, or three-stage pelvic reconstruction for pelvic malunion or displaced nonunion has benefitted most patients. However, the results of surgery in this setting are not as predictable as the results of acute treatment of pelvic ring injuries, and the rate of complications is higher.3,8 Once the deformity has been established and chronic symptoms develop, the probability of surgical reconstruction returning the patient to his or her preinjury status is decreased. Prevention by acute anatomic closed or open reduction and internal fixation of unstable pelvic injuries is the best treatment for pelvic malunions and nonunions.

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Figure 16-5. Patient presented 1-year postinjury with pain, deformity, and feeling as if “walking crooked.” AP, in x-ray of pelvis from the time of injury demonstrating the rotational deformity.

Figure 16-6. Intraoperative photo illustrates the application of femoral distractors to create the necessary force vectors for correction of the deformity. Bilateral sacral osteotomies were performed in conjunction with anterior and posterior pelvic fixation. A wedge of bone was removed from the osteotomy site on one side and was used to graft the opposite side.

Figure 16-7. AP, inlet, and outlet x-rays of pelvis 18 months postoperative.

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REFERENCES 1. Frigon VA, Dickson KF. Open reduction internal fixation of a pelvic malunion through an anterior approach. J Orthop Trauma. 2001;15(7):519-524. 2. Letournel E. Diagnosis and treatment of nonunions and malunions of acetabular fractures. Orthop Clin North Am. 1990;21(4):769-788. 3. Matta JM, Dickson KF, Markovich GD. Surgical treatment of pelvic nonunions and malunions. Clin Orthop Relat Res. 1996;329:199-206. 4. Matta JM, Saucedo T. Internal fixation of pelvic ring fractures. Clin Orthop Relat Res. 1989(242):83-97. 5. Tile M. Fractures of the Pelvis and Acetabulum. Baltimore, MD: Williams & Wilkins; 1984. 6. Kellam JF. The role of external fixation in pelvic disruptions. Clin Orthop Relat Res. 1989;241:66-82. 7. Semba RT, Yasukawa K, Gustilo RB. Critical analysis of results of 53 Malgaigne fractures of the pelvis. J Trauma. 1983;23(6):535-537. 8. Dickson KF, Matta JM. Surgical reduction and stabilization of pelvic nonunions and malunions. Paper presented at the 63rd Annual Meeting of the American Academy of Orthopaedic Surgeons, 1996, Atlanta, Georgia. 9. Dickson KF, Matta JM. Skeletal deformity after anterior external fixation of the pelvis. J Orthop Trauma. 2009;23(5):327-332. 10. Letournel E, Judet R. Fractures of the Acetabulum. Berlin, Germany: Springer-Verlag; 1993. 11. Matta JM, Tornetta PI. Internal fixation of unstable pelvic ring injuries. Clin Orthop Relat Res. 1996;329:129-140. 12. Beebe KS, Reilly MC, Renard RL, Sabitino CT. The effect of sacral fracture malreduction on the initial strength of iliosacral screw fixation for transforaminal sacral fractures. Paper presented at the OTA 19th Annual Meeting, 2003, Salt Lake City, Utah. 13. Matta JM, Yerasimides JG. Table-skeletal fixation as an adjunct to pelvic ring reduction. J Orthop Trauma. 2007;21(9):647-656. 14. Dickson KF, Hsu J, DiFusco J. Sacral fractures: new technique for reduction and results. Paper presented at the American Academy of Orthopaedic Surgeons Annual Meeting, 2005, Washington, DC. 15. Hundley J. Ununited unstable fractures of the pelvis. Proceedings of the 33rd Annual Meeting of the American Academy of Orthopaedic Surgeons. J Bone Joint Surg Am. 1966:46A. 16. Pennal GF, Massiah KA. Nonunion and delayed union of fractures of the pelvis. Clin Orthop Relat Res. 1980;151:124-129.

17 Acetabulum Fractures Malunion Michael Beltran, MD and Cory Collinge, MD

Displaced acetabular fractures involving the critical weight-bearing surface are usually treated with open reduction and internal fixation (ORIF). The primary goal of surgery is anatomical reconstruction of the acetabular dome and articular surface to prevent pain, stiffness, loss of function, and post-traumatic arthrosis. Malunions of the acetabulum are relatively common despite even the best attempts at reduction and internal fixation. The term malunion encompasses both surgical malreductions as well as fracture displacement after loss of fixation. Although not clearly defined, malunion may best be thought of as any malreduction of 2 mm or more involving the weight-bearing portion of the articular dome and/or when persistent joint subluxation exists despite fixation. Surgical malreductions are dependent on several variables, including fracture pattern and severity, patient age, patient body habitus, surgeon experience, and time from injury to surgical intervention (Figures 17-1 and 17-2).1-4 As fracture severity increases, so does the difficulty in obtaining a satisfactory reduction. Compared to elementary fracture patterns, associated fracture patterns have been shown to have lower rates of anatomic reduction in large operative series, with fewer good and excellent outcomes. As patient age increases, bone osteopenia and comminution make obtaining anatomic reduction and optimal fixation difficult. Surgeons’ impressions that elderly patients may be intolerant of extensile approaches may sometimes result in compromised reductions/fixation in this patient group. Marginal impaction (ie, crush injury of articular surface into the underlying bone) remains an unsolved problem even after bone grafting, as reduction is often compromised by settling of the disimpacted articular segment. Increasing experience with acetabular fractures has been shown to improve reduction results, while delays to surgery, particularly beyond 2 weeks, can make the reduction difficult in the setting of evolving fracture hematoma and early callus formation (Table 17-1).1-3,5 165

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Figure 17-1. (A) AP radiograph and (B) CT of a 31-year-old woman with a body mass index of 43 and a transverse-posterior wall acetabular fracture from a motor vehicle collision.

A

Figure 17-2. Coned-down views of AP and oblique radiographs showing extraarticular malreduction of transverse fracture along the anterior column (black arrow [A]) as well as intra-articular malreduction (white arrow [B]). Reduction may have been affected by large body habitus, positioning for Kocher-Langenbeck approach (eg, lateral versus prone), or surgeon experience.

A

B

B

Table 17-1

Risk Factors for Acetabular Fracture Malunion RISK FACTOR

IMPLICATION/RESULT

Fracture pattern/ severity

Complex fracture patterns more difficult to reduce anatomically

Patient age

Osteopenia and comminution; co-morbid conditions affecting choice of surgical approach

Body habitus

Morbid obesity can make anatomic reduction more difficult

Surgeon experience

More likely to accept malreduction, choose wrong approach, unfamiliar with reduction techniques

Time to surgery

More difficult to obtain anatomic reduction when surgery delayed, especially 2 weeks

Surgical approach/ patient positioning

Inadequate exposure may result in inability to adequately reduce fractures and apply stable fixation; optimal positioning of patients may minimize deforming forces in some cases

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PREVENTION: PREOPERATIVE PLAN AND SURGICAL APPROACH Anatomic reduction (while avoiding complications) should be the paramount goal when managing fractures of the acetabulum—even 1 mm of displacement has been shown to influence the likelihood for a good or excellent clinical outcome.2 A careful and deliberate preoperative plan should be formulated to ensure that the appropriate surgical approach is chosen and executed properly. Radiographic workup consisting of anteroposterior (AP) and Judet views of the pelvis/acetabulum are supplemented with a thin-cut computed tomography (CT) scan. Three-dimensional reconstructions can now be performed at most medical centers and can be used to better appreciate the injury and deformity, but they should not be seen as taking the place of high-quality plain films or an axial CT. Radiographs should be critically assessed to determine the fracture pattern and major fracture displacements, areas of intra-articular comminution or marginal impaction, and the presence or absence of associated femoral head fracture or depression, which is strongly associated with poor long-term prognosis.1 There are three classic approaches as described and disseminated by Judet and Letournel to manage acetabular fractures; multiple variations have been described to augment approach exposure or limit approach morbidity.6-8 The two most commonly used surgical approaches to the acetabulum are the ilioinguinal (anterior) and KocherLangenbeck (posterior) approaches. If chosen correctly, one of these approaches should allow the surgeon to expose and reduce the vast majority of fractures, although extensile or combined approaches are recommended for some selected cases.9 The ilioinguinal approach is chosen when the major displacement involves the anterior column and includes the following four patterns: anterior wall, anterior column, anterior column-posterior hemitransverse, and both columns. The Kocher-Langenbeck approach is used to expose the posterior wall, posterior column, and combined posterior wall and column fractures. It is also commonly used in transverse and T-type fractures, unless the major fracture displacement involves the anterior column with minimal posterior column displacement. If chosen correctly, a single approach should allow the surgeon to expose and reduce the majority of acetabular fractures.9 A single extensile approach or combined approaches have been recommended in some cases (eg, where a standard approach will not adequately allow for the goals of surgery to be met [as previously described]). The extended iliofemoral approach is the most extensile approach to the acetabulum available, but carries with it significant potential for complications. This approach may be useful in the following situations: segmental posterior column comminution, transtectal transverse fracture patterns with dome comminution or impaction, and fractures that are older than 21 days from injury. Comminuted both column fractures in which anatomic reduction is unlikely to be obtained from a more limited approach might also be managed with the extended iliofemoral exposure, especially if the patient is physiologically young. Combining the Kocher-Langenbeck and ilioinguinal approaches provides access to the posterior and anterior elements of the acetabulum: anteriorly, access to the pelvic brim and quadrilateral surface is good, but direct visualization of the articular socket is markedly limited. Complications associated with both approaches are present, and if performed in one setting, the surgical burden may be sizable. Finally, intraoperative imaging must be optimized and considered preoperatively if the goals of surgery are to be predictably achieved. This includes the imaging of obese patients, or those who have had oral contrast or ileus, among other considerations. The mainstay of intraoperative imaging is C-arm fluoroscopy,

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which for most patients provides adequate data regarding reduction and implant placement. The C-arm is likely the best method for imaging and recording the axis of periarticular screws. Most acetabular surgeons agree that these patients should receive postoperative radiographs (AP and Judet views) in the operating room under a controlled setting and where operative changes can readily be made, if necessary. Critical assessment of radiographs must be used. Figure 17-1 shows injury AP radiograph and transverse CT cut of a transverse-posterior wall acetabular fracture treated via a Kocher-Langenbeck approach. Figure 17-2 demonstrates radiographically obvious nonarticular malreduction (iliopectineal line at black arrow), which correlates to articular malreduction (white arrow) for this and most other fracture patterns.

PREVENTION: REDUCTION TECHNIQUES Consistent accurate acetabular fracture reduction requires knowledge of both direct and indirect techniques; only the extended iliofemoral approach allows direct and complete visualization of the weight-bearing articular surface. From the ilioinguinal approach, one potentially has direct visual access to the inner wall of the ilium, pelvic brim, and quadrilateral plate (which indirectly represents the articular surface); posterior column reduction requires proper clamp choice and positioning through the greater sciatic notch, with reduction judged by finger palpation and fluoroscopy. Even more of the quadrilateral surface and posterior column can be visualized, and implants including buttress plates and screws can be placed via the modified Stoppa approach.6 The Kocher-Langenbeck approach affords direct visual access to the entire posterior wall and column, although indirect clamp placement through the greater sciatic notch with finger palpation and fluoroscopy are required to judge reduction of fractures involving the anterior acetabulum and quadrilateral surface. If it appears unlikely that the surgeon cannot effectively obtain reduction of important elements of the anterior acetabulum with a Kocher-Langenbeck, another or combined approaches should be considered.

MARGINAL IMPACTION AND THE ELDERLY PATIENT WITH COMORBIDITIES Certain fracture patterns represent a unique challenge because of commonly encountered marginal impaction and their propensity for persistent joint subluxation if anatomic reduction is not obtained; both are strongly related to a poor clinical outcome.1,2,10 Typically, this is seen in younger patients with high-energy posterior wall fractures and elderly, osteoporotic patients with anterior column fractures. Marginal impaction should be corrected at the time of surgery to restore the articular surface and maintain joint congruity. Impaction is tamped up or otherwise elevated and buttressed with either bone graft or bone void substitute. Mini-fragment screws and absorbable pins may also be useful for fixation here.11 Due to poor bone quality, elderly patients are uniquely prone to pathologic acetabular fractures after low-energy falls, and clinical series indicate these fractures typically involve the anterior column, wall, and quadrilateral plate.1,12 Because of medical comorbidities, they may be poor candidates for large exposures with heavy blood loss, limiting the choice of approach. Starr and colleagues13 have described limited open techniques combined with percutaneous fixation into the columns,

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which are effective when treatment options are limited. Anatomic reduction is more challenging in this setting, and late displacement is frequent, although clinical results in this less active population have been reasonably good.

COMPLICATION MANAGEMENT: REOPERATION AND SALVAGE PROCEDURES When an acetabular malunion is identified, it can successfully be revised to a more anatomic reduction with revision surgery, but the ability to achieve a good-toexcellent clinical outcome decreases with time to reoperation. In a series of 64 revision acetabular cases for malunion, Mayo and colleagues14 showed that reduction within 2 mm was obtained in 74% of patients when reoperated within 3 weeks of injury; this figure dropped to 36% when revised after 12 weeks. Early reoperation within 21 days also led to more good-to-excellent clinical outcomes than those treated later. This study highlighted that proper surgical approach is critical: nearly 20% of malreductions were deemed to be due to inappropriate approach selection. Clearly, the philosophy of “getting it right the first time” seems appropriate. Salvage of acetabular malunions is necessary when the inevitable post-traumatic osteoarthrosis becomes painful and symptomatic. The most common salvage procedure remains total hip arthroplasty; this can often be performed without the need for acetabular hardware removal. Even in young patients, new bearing materials have made it possible for arthroplasty implants to last decades, leaving the indications for corrective osteotomy and arthrodesis ill-defined, and these procedures are rarely performed today.

SUMMARY Malunion or malreduction of the acetabulum can occur even in the hands of the most skilled acetabular surgeons. Prevention requires a deliberate and well-formulated surgical plan with attention to fracture pattern, severity, and the age of both the patient and the fracture. Although the significance of avoiding malreduction cannot be overstated, when malunion is identified, early reoperation can often lead to an acceptable reduction and good clinical outcome. When faced with post-traumatic osteoarthrosis, total hip arthroplasty using modern techniques and implants represents an acceptable salvage operation with expectations of reasonably good long-term results.

REFERENCES 1. Letournel E, Judet R. Fractures of the Acetabulum. Elson RA, trans, ed. New York, NY: Springer; 1993. 2. Matta JM. Fractures of the acetabulum: accuracy of reduction and clinical results in patients managed operatively within three weeks after the injury. J Bone Joint Surg Am. 1996;78:1632-1645. 3. Mayo KA. Open reduction and internal fixation of fractures of the acetabulum. Results in 163 fractures. Clin Orthop Relat Res. 1994;305:31-37.

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4. Porter SE, Russell GV, Dews RC, Qin Z, Woodall J Jr, Graves ML. Complications of acetabular fracture surgery in morbidly obese patients. J Orthop Trauma. 2008;22:589-594. 5. Johnson EE, Matta JM, Mast JW, Letournel E. Delayed reconstruction of acetabular fractures 21-120 days following injury. Clin Orthop Relat Res. 1994;305:20-30. 6. Cole JD, Bolhofner BR. Acetabular fracture fixation via a modified Stoppa limited intrapelvic approach. Clin Orthop Relat Res. 1994;305:112-123. 7. Karunakar MA, Le TT, Bosse MJ. The modified ilioinguinal approach. J Orthop Trauma. 2004;18:379-383. 8. Siebenrock KA, Gautier E, Ziran BH, Ganz R. Trochanteric flip osteotomy for cranial extension and muscle protection in acetabular fracture fixation using a KocherLangenbeck approach. J Orthop Trauma. 2006;20(1 suppl):S52-S56. 9. Routt ML Jr, Swiontkowski MF. Operative treatment of complex acetabular fractures. Combined anterior and posterior exposures during the same procedure. J Bone Joint Surg Am. 1990;72:897-904. 10. Moed BR, Willson-Carr SE, Watson JT. Results of operative treatment of fractures of the posterior wall of the acetabulum. J Bone Joint Surg Am. 2002;84:752-758. 11. Mast J, Jakob R, Ganz R. Planning and Reduction Technique in Fracture Surgery. Berlin, Germany: Springer; 1989. 12. Mears DC. Surgical treatment of acetabular fractures in elderly patients with osteoporotic bone. J Am Acad Orthop Surg. 1999;7:128-141. 13. Starr AJ, Jones AL, Reinert CM, Borer DS. Preliminary results and complications following limited open reduction and percutaneous screw fixation of displaced fractures of the acetabulum. Injury. 2001;32(suppl 1):SA45-SA50. 14. Mayo KA, Letournel E, Matta JM, Mast JW, Johnson EE, Martimbeau CL. Surgical revision of malreduced acetabular fractures. Clin Orthop Relat Res. 1994;305:47-52.

18 Acetabulum Fractures Nerve Palsy George V. Russell, MD and Scott A. Wingerter, MD, PhD

Nerve palsy associated with acetabular fractures and subsequent treatment can affect the sciatic, femoral, obturator, and lateral femoral cutaneous, although the incidence of sciatic involvement remains the highest. Post-traumatic sciatic nerve injury has been documented as high as 36%, with iatrogenic or postoperative damage as high as 15%.1-5 The sciatic nerve is in close proximity to the posterior acetabulum because it typically exits the pelvis at the sciatic notch adjacent to the piriformis muscle. Thus, the majority of traumatic sciatic injuries are associated with significantly displaced posterior acetabular fractures and/or posterior hip dislocation. Identifiable lesions have included lacerations by bone fragments, stretching of the nerve across fragments, and entrapment of the sciatic nerve within a fracture line or incarcerated in the hip dislocation. However, some cases of post-traumatic sciatic nerve palsy have no apparent injury at the time of surgery.2 The sciatic nerve consists of tibial and peroneal divisions, and injury associated with acetabular fractures involves either the peroneal division alone or both divisions together.5 Iatrogenic sciatic nerve injuries have been associated with direct trauma and excessive retraction during surgery, typically while in the prone position. Figures 18-1 and 18-2 provide an example of an injury that caused a complete post-traumatic sciatic nerve palsy. This 11-year-old girl was involved in an all-terrain vehicle crash. Her orthopedic injuries included a displaced right femoral neck fracture and a left acetabular fracture dislocation associated with a complete left sciatic nerve palsy. In the emergency room, she was noted to have no motor control distal to her knee and decreased perception to light touch. She underwent closed reduction of her left hip without resolution of the sciatic nerve palsy. The patient underwent open reduction and internal fixation (ORIF) of her right femoral neck fracture the night of the injury. During ORIF, the sciatic nerve was identified tented 171

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Figure 18-1. AP (A) and iliac oblique (B) pelvic radiographs and sagittal reconstruction CT scan (C) of an 11-year-old girl involved in an all-terrain vehicle crash. Injuries included a right femoral neck fracture and left acetabular fracture with complete left sciatic nerve palsy. Radiographs of her left acetabular fracture show marked posterior displacement of the retroacetabular surface, which was thought to be displaced into the sciatic nerve. Arrows indicate location of sciatic nerve with displaced posterior column.

Figure 18-2. Postoperative AP pelvis radiograph of the patient noted in Figure 18-1.

over the displaced retroacetabular surface. The nerve was noted to be in continuity, yet ecchymotic and attenuated from the greater sciatic notch, extending distally approximately 6 cm. Fracture reduction and stabilization were performed. Twelve months after surgery, the sciatic nerve palsy had not resolved. Reports of femoral nerve palsy consist primarily of case reports and small case series due to its rarity from both traumatic and iatrogenic injury.2,6,7 The anatomy of the femoral nerve places it in a relatively protected position in regard to acetabular fractures. When femoral nerve injury does occur as a result of trauma, anterior hip dislocation is the usual mechanism. Iatrogenic injury to the femoral nerve typically occurs during anterior surgical approaches (ilioinguinal) via direct trauma.

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Table 18-1

Risk Factors for Nerve Palsy Associated With Acetabular Fracture RISK FACTOR

IMPLICATION/RESULT

High-energy injury

Significant fracture displacement Blunt contusion, laceration, or stretching

Surgical technique

Excessive retraction during surgery Direct trauma and indirect stretch

Hematoma

Progressive compression of nerve Early postoperative neuropathy

Heterotopic ossification

Encasement and tethering of nerve Late postoperative neuropathy

Case reports of obturator nerve injuries associated with acetabular and pelvic ring injuries have also been reported, but remain rare.8,9 The anatomic course of the obturator nerve places it near the anterior wall and quadrilateral surface of the acetabulum. One case report identified entrapment of the obturator nerve in the hip joint with an associated both column acetabular fracture. Intraoperative examination noted trauma to the nerve, but it remained in continuity. The patient recovered most motor and sensory function and had an overall good result.8 Presumably, excessive intraoperative retraction of the obturator nerve during Stoppa surgical exposures may also lead to an obturator nerve injury. Postoperative issues leading to nerve injury include hematoma formation and heterotopic ossification (HO). The increased pressure from an enlarging hematoma can cause progressive compression on any of the nerves about the acetabulum and is typically seen as an early postoperative neuropathy. HO is a later complication resulting from encasement of the nerve within excess bone. Although less common, significant scarring, hardware failure, and wear debris can cause late nerve palsy (Table 18-1).10

PREVENTION: SURGICAL TECHNIQUES Although little can be done to prevent nerve injuries associated with the initial trauma, a goal must be to minimize additional damage to a traumatically injured nerve. One must be vigilant to document a neurological examination after closed reductions of fracture-dislocations. Careful follow-up examinations must be performed to ensure against progression of a nerve injury. If a progressive nerve injury is noted, a cause must be sought and corrected if possible. Most commonly, progressive nerve injuries are the result of nerve entrapment, which must be relieved to produce the best possible outcome. Multiple factors must be considered to prevent iatrogenic nerve palsy associated with the surgical treatment of acetabulum fractures. The sciatic nerve is primarily at risk during posterior surgical exposures. During exposure of fracture fragments, focus must be placed on identifying and protecting the sciatic nerve.

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Due to the traumatized muscle tissues and displacement of fracture fragments, surgical anatomy may be confusing. To prevent inadvertent injury to the sciatic nerve, the sciatic nerve must be identified clearly outside the zone of injury at the quadratus femoris and exposed through the surgical field from the ischial tuberosity to the greater sciatic notch. The surgeon must be aware of a proximal split of the sciatic nerve or other anatomical variants such as a bifid piriformis muscle enveloping the sciatic nerve. Excessive retraction and traction of the sciatic nerve during a posterior surgical exposure must also be avoided. Direct retraction of the sciatic nerve should be avoided. Special Hohman-type retractors have been developed for the lesser sciatic notch (sciatic nerve retractors) to aid in protecting the nerve from direct trauma and are available from most vendors. The sciatic nerve retractor should only be placed in the lesser sciatic notch. After tenotomy of the short external rotator muscles (superior gemellus, obturator internus, and inferior gemellus), they are reflected posteriorly to pad the sciatic nerve from the retractor. Vigilant inspection must be made during surgery to prevent accidental impalement or crush of the sciatic nerve by an edge of the retractor. To minimize excessive traction on the sciatic nerve, the hip should be extended to neutral and the knee flexed to 90 degrees when retracting the sciatic nerve. Flexing of the knee relaxes the sciatic nerve and has shown a decrease in sciatic palsy from 18% to 3.3%.2 The prone position primarily places the sciatic nerve at risk intraoperatively, but positioning errors in the prone position can also lead to femoral nerve palsy. Care must be taken to properly position the chest rolls distally beneath the anterior superior iliac spines. Improper positioning of the chest rolls too distally may cause increased focal pressure on the femoral nerve, leading to a femoral nerve palsy. The lateral femoral cutaneous, femoral, and obturator nerves are at risk during anterior surgical exposures for acetabular fracture fixation. The lateral femoral cutaneous nerve is at risk while dissecting through the inguinal ligament with an ilioinguinal surgical exposure. Excessive retraction of the lateral femoral cutaneous nerve can lead to postoperative meralgia paresthetica. When working around the middle window in the ilioinguinal surgical exposure, the femoral nerve is at risk. A padded bump under the proximal thigh will lessen the traction on the femoral nerve. Care must also be taken to resist excessive traction on the femoral nerve when retracting the iliopsoas muscle to prevent a traction injury to the femoral nerve. The obturator nerve is at risk during deep exposure within the pelvis in proximity of the neurovascular gutter of the obturator foramen. Care must be taken to avoid excessive traction of the obturator nerve while exposing and plating the pelvic brim and/or the quadrilateral surface. Somatosensory evoked potentials (SSEPs) and spontaneous electromyography (EMG) have been studied as possible measures to reduce the incidence of iatrogenic nerve injury, with some support that spontaneous EMG provides improved results.1 However, some believe that monitoring is unnecessary if the preventive measures listed above are followed.11 Intraoperative SSEPs and EMG monitoring are not used routinely in most centers.

COMPLICATION MANAGEMENT With post-traumatic sciatic nerve palsy, recovery to a functional level has been observed in approximately two-thirds of cases without intervention. Results also indicate that maximal recovery is typically reached by 2 years after injury.2 Single case

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reports of femoral nerve injury have identified both full nerve recovery3 and no recovery at 1 year,6 but other studies involving femoral nerve injury, both traumatic and iatrogenic, indicate that recovery of function can be expected without intervention.7 Management of a post-traumatic nerve palsy is supportive initially. Soft boots or braces are provided to patients to prevent equinus contractures. Nerve inspection is performed during operative exposure, and abnormalities are noted. If a partial or complete nerve laceration is noted intraoperatively, consultation is made with surgeons who have experience with nerve repairs and/or nerve grafting. If no obvious nerve injury is noted, then postoperative supportive measures are continued to prevent contractures and injuries, particularly with insensate limbs. Ankle-foot orthoses may be used to help patients with sciatic nerve palsies ambulate. EMG and nerve conduction velocity (NCV) tests are advocated if no improvement is noted 3 to 6 months after injury. If a focal injury is identified, the patient may be referred to a specialist for nerve grafting. With no focal injury and no clinical improvement, tendon transfers can be considered. After an iatrogenic nerve palsy is identified, the decision to observe and monitor or intervene and treat must be made. Observation is most commonly advocated for neurologic injury after surgery for an isolated motor palsy. If sensory and motor palsies are noted, early EMG/NCV is recommended, looking for evidence of complete nerve laceration. If there is evidence suggestive of an injury with a nerve incontinuity, then observation highlighting the principles above is recommended. If neuropathy is severe, medications are available for symptomatic treatment. Carbamazepine has shown successful results,5 and gabapentin (Neurontin) and pregabalin (Lyrica) are commonly used for neuropathic pain. Most pain studies do not focus on neuropathic pain associated with traumatic peripheral nerve injury, but results and clinical experience do indicate improvement in pain following treatment with gabapentin12 and pregabalin.13 Surgical decompression of an affected nerve has shown better results for sensory than motor palsy.14 Late cases of nerve palsy due to postoperative HO may benefit from surgical decompression and neurolysis. In severe HO, excision of the excess bone with direct nerve release can be beneficial. However, identifying heterotopic bone and isolating nerves from within the bony overgrowth may be difficult. Additional injury to the injured nerve is an added risk during excision of ectopic bone. An example of postoperative HO necessitating surgical intervention is provided in Figures 18-3 and 18-4. The initial injuries included multiple lower extremity fractures with a T-type acetabular fracture with a displaced posterior wall. The fractures were treated operatively with ORIF and the patient subsequently developed HO about her hip.

SUMMARY A thorough neurologic examination of sensory and motor function is critical following acetabular fracture. The sciatic, femoral, obturator, and lateral femoral cutaneous nerves are at risk, with acetabular fractures at the time of injury, during surgery, and postoperatively. Nerve palsies associated with acetabular fractures most commonly affect the sciatic nerve, and most occur at the time of injury. Careful, proper surgical technique and prophylactic measures can aid in limiting iatrogenic and postoperative nerve injuries. When encountered, the majority of nerve injuries are managed conservatively and/or pharmacologically.

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Figure 18-3. AP pelvic radiograph demonstrating extensive heterotopic ossification of a morbidly obese 48-year-old woman approximately 1 year after a motor vehicle crash and open reduction and internal fixation of a left acetabular fracture.

Figure 18-4. Axial CT scan of the patient in Figure 18-3 highlighting the extensive heterotopic ossification about the sciatic nerve lateral to the ischial tuberosity.

REFERENCES 1. Helfet DL, Anand N, Malkani AL, et al. Intraoperative monitoring of motor pathways during operative fixation of acute acetabular fractures. J Orthop Trauma. 1997;11(1):2-6. 2. Letournel E, Judet R. Fractures of the Acetabulum. 2nd ed. New York, NY: Springer; 1993. 3. Matta JM, Mehne DK, Roffi R. Fractures of the acetabulum: early results of a prospective study. Clin Orthop. 1986;205:241-250. 4. Matta JM. Operative treatment of acetabular fractures through the ilioinguinal approach: a 10-year perspective. J Orthop Trauma. 2006;20(1 suppl):S20-S29.

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5. Fassler PR, Swiontkowski MF, Kilroy AW, Routt ML. Injury of the sciatic nerve associated with acetabular fracture. J Bone Joint Surg. 1993;75-A(8):1157-1166. 6. Hardy SL. Femoral nerve palsy associated with an associated posterior wall transverse acetabular fracture. J Orthop Trauma. 1997;11:40-42. 7. Gruson KI, Moed BR. Injury of the femoral nerve associated with acetabular fracture. J Bone Joint Surg. 2003;85-A(3):428-431. 8. Yang KH, Han DY, Park HW, Park SJ. Intraarticular entrapment of the obturator nerve in acetabular fracture. J Orthop Trauma. 2001;15(5):361-363. 9. Barrick EF. Entrapment of the obturator nerve in association with a fracture of the pelvic ring. A case report. J Bone Joint Surg Am. 1998;80(2):258-261. 10. Issack PS, Helfet DL. Sciatic nerve injury associated with acetabular fractures. Hosp Special Surg J. 2009;5:12-18. 11. Middlebrooks ES, Sims SH, Kellam JF. Incidence of sciatic nerve injury in operatively treated acetabular fractures without somatosensory evoked potential monitoring. J Orthop Trauma. 1997;11:327-329. 12. Gordh TE, Stubhaug A, Jensen TS, et al. Gabapentin in traumatic nerve injury pain: a randomized, double-blind, placebo-controlled, cross-over, multi-center study. Pain. 2008;138:255-266. 13. Whitlock EL, Moradzadeh A, Hunter DA, Mackinnon SE. Pregabalin does not impact peripheral nerve regeneration after crush injury. J Recon Microsurg. 2007;23(5):263-268. 14. Issack PS, Toro JB, Buly RL. Sciatic nerve release following fracture or reconstructive surgery of the acetabulum. J Bone Joint Surg Am. 2007;89(7):1432-1437.

19 Acetabulum Fractures Heterotopic Ossification Madhav A. Karunakar, MD

Heterotopic ossification (HO) is a well-recognized complication of operative treatment of acetabular fractures. The incidence varies greatly, with rates up to 90% reported in the literature.1,2 A recent meta-analysis of 2394 patients demonstrated a 25.6% incidence of HO after the operative treatment of acetabular fractures, with a strong association based on surgical approach: 23.6% with extended iliofemoral, 11.6% with Kocher-Langenbeck, and 1.5% with ilioinguinal.3 Large amounts of ectopic bone have been demonstrated to result in severe limitations of the range of movement of the hip with a decreased functional outcome.4,5 These reports have led to extensive literature and debate regarding prevention/prophylaxis of this condition. However, comparison between studies remains difficult because there is no consensus on how to quantify the amount of ectopic bone. Most studies have used plain radiographs to quantify the amount of ectopic bone and grade with the Brooker classification.6 Older studies frequently report HO as significant based on anteroposterior (AP) radiographs with little or no reference to functional limits in range of motion. Moed and colleagues6 proposed using three-view series, AP, and Judet views to fully assess the three-dimensional extent of disease, while others have suggested that computed tomography (CT) may better quantify the nature of the process.1,6 Matta and colleagues1 defined a 20% reduction in range of motion as a significant functional deficit.1 Despite these proposals, no consensus exists, and most published series are limited by a lack of functional data that does not allow accurate comparison across series.

ETIOLOGY The pathophysiology of HO is poorly understood. Histologic analyses performed on retrieved specimens reveal that the process of ectopic bone formation undergoes a 179

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Table 19-1

Risk Factors for Development of Heterotopic Ossification After Acetabular Fractures RISK FACTOR

SUSPECTED ETIOLOGY

Extensile approach

Abductor muscle surgery/injury

Trochanteric osteotomy

Abductor muscle surgery/injury

Fracture type

Abductor muscle surgery/injury

Traumatic brain injury

Systemic

Male gender

Unknown

DISH/AS/burns

Systemic

systematic progression from osteoid to full calcification. This calcified osteoid remodels over subsequent months into well-organized trabecular bone. This heterotopic bone is metabolically active, with a rate of formation three times greater than normal bone and with more than twice the number of osteoclasts seen in normal bone.7 These findings mirror the clinical appearance of HO with the maximum development of bone typically present 3 months postinjury, with little significant progression after that time.1,6,8 Surgical approach and traumatic brain injury are two factors that have commonly been reported to increase the risk of heterotopic bone formation after acetabular fractures.3,9-11 Multiple authors have demonstrated a low risk with the ilioinguinal approach and higher risk with posterior or extensile approaches.3,9,10 Matta,9 in his classic series of 262 acetabular fractures treated operatively within 3 weeks of injury, reported an overall 18% prevalence of HO. Moderate to severe ectopic bone resulting in a 20% loss of motion occurred in 9%. A strong association with operative approach and amount of ectopic bone was demonstrated, with HO developing in 8% KocherLangenbeck, 20% extended iliofemoral, and 2% ilioinguinal approaches. An increased prevalence of ectopic bone has been noted in patients with traumatic brain injuries. This appears to occur regardless of the type of fracture management pursued (operative versus nonoperative treatment) or timing of intervention.7 Symptomatic HO has been reported in up to 20% of uninjured joints in patients with severe head trauma.7 Webb and colleagues12 reviewed their results in 23 patients with a Glasgow Coma Scale score 聿10 and displaced acetabular fractures requiring operative fixation. Symptomatic HO occurred in 14 of the 23 patients. These observations imply that head injury, acetabular fracture, and operative trauma may act synergistically in producing ectopic bone around the hip. Webb and colleagues12 recommended the consideration of an anterior approach, early fixation, and prophylaxis with lowdose irradiation to reduce the incidence of ectopic bone formation. Ghalambor and colleagues4 reviewed 237 operatively treated acetabular fractures and identified four factors that highly correlated with the development of significant heterotopic bone: the extended iliofemoral surgical approach, two or more operative findings indicating severity of injury (femoral head damage, intra-articular fragments, impaction), T-type fractures, and presence of thoracic or abdominal trauma. Other factors associated with HO include male gender, high Injury Severity Score (ISS), and delay in fracture fixation (Table 19-1).4,11,13,14

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PREVENTION: SURGICAL TECHNIQUES Much of the literature on prevention of HO has focused on chemoprophylaxis or radiation. However, the strong association demonstrated in multiple series with surgical approach suggests that surgical technique may play a role in the development of HO. Some authors have recommended the preferential use of the iliolinguinal approach because the incidence of HO is extremely low.12 This is not really practical as certain fracture patterns (posterior wall, transverse posterior wall, T-type) may not be amenable to an anterior approach. Clinically, HO usually presents in the gluteus minimus muscle tissue and, in most severe cases, results in anklyosing bone formation from the greater trochanter to the iliac wing (Figure 19-1). Historically, the use of a trochanteric osteotomy with a Kocher-Langenbeck approach has been associated with increased HO that is likely related to the elevation of the abductor muscles.4,11,13,14 Most authors suggest that surgical techniques to minimize injury to the abductor muscle may reduce the risk of formation of ectopic bone.1,4,8,15 Rath and colleagues15 reported on the incidence of severe HO in a series of 31 patients treated with gluteus minimus débridement. This technique involves excision of all devitalized gluteus minimus tissue at the end of the procedure because this tissue is believed to be at higher risk for ectopic bone formation. The authors report a 10% incidence of severe HO that compares favorably with other series using chemoprophylaxis. Recently, Siebenrock and colleagues16 have proposed a modification of the trochanteric osteotomy, a trochanteric slide that they believe minimizes abductor injury, resulting in a lower rate of HO.

PREVENTION: CHEMOPROPHYLAXIS AND RADIATION Prophylaxis for HO after operative fixation of acetabular fractures remains controversial. This is likely secondary to the difficulty in defining populations at risk and the relatively poor quality of literature available on this subject. The two most frequently cited methods for prophylaxis are indomethacin and radiation. Each has opponents and proponents, and each has purported advantages and disadvantages.

Indomethacin Indomethacin is a member of the nonsteroidal anti-inflammatory drug (NSAID) class of medications. It functions as a nonselective inhibitor of cyclo-oxygenase (COX) -1 and -2, enzymes that participate in prostaglandin synthesis from arachidonic acid. Prostaglandins are hormone-like molecules normally found in the body where they have a wide variety of effects including bone remodeling and potentiating the inflammatory response after injury. The most common side effects are nausea, vomiting, diarrhea, stomach discomfort, heartburn, rash, headache, dizziness, and drowsiness. Because indomethacin inhibits both COX-1 and COX-2, it inhibits the production of prostaglandins in the stomach and intestines, which maintain the mucous lining of the gastrointestinal tract, and as a result can cause peptic ulcers. The drug may also cause elevations of serum creatinine and more serious renal damage, such as acute renal failure, chronic nephritis, and nephritic syndrome. NSAIDs as a class of medications has also been noted to impair fracture healing.17,18 Indomethacin has been used as prophylaxis for HO in several retrospective studies showing a reduction in bone formation of clinical significance.5,15,19 The results

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A

B

Figure 19-1. (A) AP and (B) Judet radiographs demonstrating grade III heterotopic ossification 1 year after open reduction and internal fixation of the right posterior column acetabulum fracture.

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C

D

Figure 19-1 (continued). (C) Judet radiograph demonstrating grade III heterotopic ossification 1 year after open reduction and internal fixation of the right posterior column acetabulum fracture. (D) AP radiograph showing excision of periacetabular heterotopic ossification around the right hip joint. Note the residual asymptomatic heterotopic ossification around the left hip.

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of two prospective series were unable to demonstrate a significant effect from indomethacin. A prospective, randomized, double-blind, placebo-controlled trial comparing indomethacin with a placebo performed by the author was unable to identify a difference between the treatment groups. This study was unique in that it was the first to attempt to measure serum indomethacin levels to assess patient compliance.8 A significant number of patients withdrew from the study secondary to gastrointestinal intolerance, and two patients withdrew secondary to gastrointestinal bleeds. A 4% difference in the incidence of severe HO between the two groups (15% in the indomethacin group and 19% in the placebo group) was identified. The authors note that, while the study was not sufficiently powered to determine whether this observed difference was significant, based on treatment effect, 25 patients would need to be treated for one to benefit. They concluded that the ultimate decision as to whether to use indomethacin as prophylaxis should remain at the discretion of the physician. However, given the potential for serious complications, poor patient compliance, and the large number of patients needed to be treated before obtaining any benefit, the routine use of indomethacin as prophylaxis for HO does not appear to be justified. Matta and colleagues1 performed a prospective randomized trial of indomethacin versus no prophylaxis. This study demonstrated a higher rate of significant HO in patients undergoing a posterior or extensile approach (9.4%) with indomethacin versus a lower rate (4.8%) without prophylaxis. Finally, basic science data have substantiated concerns regarding the negative effect of indomethacin on fracture healing.17 In a clinical series, Burd and colleagues18 reported a higher incidence of long bone nonunion in patients who received indomethacin in a prospective randomized trial comparing indomethacin with localized irradiation.

Localized Irradiation Localized irradiation is believed to prevent pluripotent mesenchymal cells from differentiating into osteoprogenitor cells and has been recommended as effective prophylaxis against ectopic bone formation when administered 24 hours prior or within 72 hours after a surgical procedure.20 The dose has been reduced over time and is currently recommended at 700 to 800 cGy. Questions regarding the use of radiation include concerns for risk of irradiation to the pelvic area in women of childbearing age influencing fertility, logistical issues around transportation to the radiation treatment facility, and long-term risk of malignant transformation. Finally, radiation treatment is expensive (around $2,400 per treatment), and it is unclear whether this regimen is cost effective.21 Burd and colleagues20 reported a prospective randomized trial of 166 patients comparing indomethacin and radiation for HO prophylaxis after operative treatment of acetabular factures. The incidence of severe HO was 4% in the radiation group and 11% in the indomethacin group, a difference that was not found to be significant. The authors conclude that both local irradiation and indomethacin were effective in prophylaxis against HO. This conclusion must be interpreted cautiously because the difference between the two groups with a 63% relative reduction in the incidence of severe HO may in fact be clinically significant in a larger series of patients.22,23 The study is likely underpowered, and, if the trend demonstrated continued, a minimum of 110 patients per group would be needed to demonstrate no difference. The conclusion of bioequivalence is even more difficult and would require significantly more patients.

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Table 19-2

Prevalence of Severe Heterotopic Ossification Reported in Randomized Trials Compared with Historic Data (Letournel) AUTHOR

SEVERE HETEROTOPIC OSSIFICATION NO PROPHYLAXIS INDOMETHACIN RADIATION

Letournel11

11% (31/281)

Karunakar8

19% (12/62)

15% (9/59)

5% ( 1/21)

9% (3/32)

Matta*1 Burd20

11% (8/72)

4% (3/78)

*Only includes patients treated through a posterior or extensile approach.

Summary of Current Evidence The ideal prophylactic regimen for HO should show a significant reduction in the incidence of formation of severe ectopic bone, be easy to use with a high rate of patient compliance, and be cost effective with minimal risk of side effects or complications. Unfortunately, based on current evidence, neither indomethacin nor radiation meets all of these criteria. Table 19-2 lists the patient groups and prevalence of HO from the most rigorous randomized trials currently available and compares them to historic controls. Letournel11 reported an 11% prevalence of severe HO in 281 acetabular fractures treated through a Kocher-Langenbeck approach without any prophylaxis. This prevalence is similar to the 9% to 15% reported for patients receiving indomethacin in randomized trials.1,8,20 Blokhuis and colleagues24 performed a meta-analysis of 384 patients identified from five prospective studies to compare the effectiveness of indomethacin with radiation therapy. Although the studies had methodologic limitations that affect the quality of the meta-analysis, the authors noted a significantly lower incidence of severe HO with radiation therapy. As a result, they concluded that, with current data available, radiation is the preferred method of preventing HO after operative treatment of acetabular fractures. Given the significant cost associated with radiation and the uncertainty of long-term effects of radiation, it seems prudent to recommend selective use in patients with increased risk based on the assessment of the treating surgeon. While the most recent literature does not appear to support the routine use of indomethacin, considerable controversy remains. If a physician elects to use this method of prophylaxis, he or she should be well versed in the risks, including gastrointestinal bleed, renal toxicity, and long bone nonunion.8

COMPLICATION MANAGEMENT: OPERATIVE RESECTION The prevalence of severe heterotopic bone present after operative treatment of acetabular fractures varies from 4% to 20%.3 However, the number of patients in this subset with functional limitations remains more difficult to define. As a result, it is unclear from the current literature how many patients require secondary

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procedures for severe HO. Currently, there are no large series reporting on the treatment of severe HO after acetabular fractures, but rather small series reporting the results of excision of ectopic bone in patients suffering from traumatic brain injury or experiencing neurologic findings related to sciatic nerve compression. Good results have been reported in patients with traumatic brain injuries when excision is performed after the bone has matured and the patient can actively participate in physical therapy (see Figure 19-1).11,25,26 Several authors have also reported the successful treatment of sciatic nerve entrapment in ectopic bone, which improved with excision of bone and neurolysis.25-29 Most authors recommend the administration of localized irradiation after excision is performed to reduce the risk of recurrence.11,25,26

SUMMARY HO is a commonly described complication after operative treatment of fractures of the acetabulum. The reported prevalence and severity of heterotopic bone varies widely and has been associated with extensile or posterior approaches and traumatic brain injury. Large amounts of ectopic bone around the hip can result in severe limitations of range of motion and decreased functional outcome. Identification of patients at risk remains difficult, and prophylaxis is controversial. Disadvantages have been reported with chemoprophylaxis with both indomethacin and radiation. If severe limitations of motion or neurologic symptoms secondary to development of heterotopic bone occur, operative resection is the procedure of choice.

REFERENCES 1. Matta JM, Siebenrock KA. Does indomethacin reduce heterotopic bone formation after operations for acetabular fractures? A prospective randomised study. J Bone Joint Surg Br. 1997;79(6):959-963. 2. Bosse MJ, Poka A, Reinert CM, Ellwanger F, Slawson R, McDevitt ER. Heterotopic ossification as a complication of acetabular fracture. Prophylaxis with low-dose irradiation. J Bone Joint Surg Am. 1988;70(8):1231-1237. 3. Giannoudis PV, Grotz MRW, Papakostidis C, Dinopoulos H. Operative treatment of displaced fractures of the acetabulum. A meta-analysis. J Bone Joint Surg Br. 2005;87(1):2-9. 4. Ghalambor N, Matta JM, Bernstein L. Heterotopic ossification following operative treatment of acetabular fracture. An analysis of risk factors. Clin Orthop Relat Res. 1994;305:96105. 5. Moed BR, Karges DE. Prophylactic indomethacin for the prevention of heterotopic ossification after acetabular fracture surgery in high-risk patients. J Orthop Trauma. 1994;8(1):34-39. 6. Moed BR, Smith ST. Three-view radiographic assessment of heterotopic ossification after acetabular fracture surgery. J Orthop Trauma. 1996;10(2):93-98. 7. Pape HC, Lehmann U, van Griensven M, Gansslen A, von Glinski S, Krettek C. Heterotopic ossifications in patients after severe blunt trauma with and without head trauma: incidence and patterns of distribution. J Orthop Trauma. 2001;15(4):229-237. 8. Karunakar MA, Sen A, Bosse MJ, Sims SH, Goulet JA, Kellam JF. Indomethacin as prophylaxis for heterotopic ossification after the operative treatment of fractures of the acetabulum. J Bone Joint Surg Br. 2006;88(12):1613-1617.

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9. Matta JM. Fractures of the acetabulum: accuracy of reduction and clinical results in patients managed operatively within three weeks after the injury. J Bone Joint Surg Am. 1996;78(11):1632-1645. 10. Matta JM. Operative treatment of acetabular fractures through the ilioinguinal approach: a 10-year perspective. J Orthop Trauma. 2006;20(1 suppl):S20-S29. 11. Letournel E, Judet R. Late complications of operative treatment within three weeks of injury. In: Elson RA, ed. Fractures of the Acetabulum. 2nd ed. Berlin, Germany: SpringerVerlag; 1993:558-563. 12. Webb LX, Bosse MJ, Mayo KA, Lange RH, Miller ME, Swiontkowski MF. Results in patients with craniocerebral trauma and an operatively managed acetabular fracture. J Orthop Trauma. 1990;4(4):376-382. 13. Johnson EE, Kay RM, Dorey FJ. Heterotopic ossification prophylaxis following operative treatment of acetabular fracture. Clin Orthop Relat Res. 1994;305:88-95. 14. Kaempffe FA, Bone LB, Border JR. Open reduction and internal fixation of acetabular fractures: heterotopic ossification and other complications of treatment. J Orthop Trauma. 1991;5(4):439-445. 15. Rath EM, Russell GV Jr, Washington WJ, Routt ML Jr. Gluteus minimus necrotic muscle débridement diminishes heterotopic ossification after acetabular fracture fixation. Injury. 2002;33(9):751-756. 16. Siebenrock KA, Gautier E, Ziran BH, Ganz R. Trochanteric flip osteotomy for cranial extension and muscle protection in acetabular fracture fixation using a KocherLangenbeck approach. J Orthop Trauma. 2006;20(1 suppl):S52-S56. 17. Altman RD, Latta LL, Keer R, Renfree K, Hornicek FJ, Banovac K. Effect of nonsteroidal anti-inflammatory drugs on fracture healing: a laboratory study in rats. J Orthop Trauma. 1995;9(5):392-400. 18. Burd TA, Hughes MS, Anglen JO. Heterotopic ossification prophylaxis with indomethacin increases the risk of long-bone nonunion. J Bone Joint Surg Br. 2003;85(5):700-705. 19. McLaren AC. Prophylaxis with indomethacin for heterotopic bone. After open reduction of fractures of the acetabulum. J Bone Joint Surg Am. 1990;72(2):245-247. 20. Burd TA, Lowry KJ, Anglen JO. Indomethacin compared with localized irradiation for the prevention of heterotopic ossification following surgical treatment of acetabular fractures. J Bone Joint Surg Am. 2001;83-A(12):1783-1788. 21. Moore KD, Goss K, Anglen JO. Indomethacin versus radiation therapy for prophylaxis against heterotopic ossification in acetabular fractures: a randomised, prospective study. J Bone Joint Surg Br. 1998;80(2):259-263. 22. Michalak RE. Prevention of heterotopic bone and type-II errors. J Bone Joint Surg Am. 2002;84(7):1272. 23. Pellegrini VD. Commentary and perspective on: Burd TA, Lowry KJ, Anglen JO. Indomethacin compared with localized irradiation for the prevention of heterotopic ossification following surgical treatment of acetabular fractures. J Bone Joint Surg Am. 2001; 83:1783-1788. Available at www.jbjs.com. 24. Blokhuis TJ, Frolke JP. Is radiation superior to indomethacin to prevent heterotopic ossification in acetabular fractures? A systematic review. Clin Orthop Relat Res. 2009;467(2):526530. 25. Garland DE, Hanscom DA, Keenan MA, Smith C, Moore T. Resection of heterotopic ossification in the adult with head trauma. J Bone Joint Surg Am. 1985;67(8):1261-1269. 26. Moore TJ. Functional outcome following surgical excision of heterotopic ossification in patients with traumatic brain injury. J Orthop Trauma. 1993;7(1):11-14. 27. Issack PS, Toro JB, Buly RL, Helfet DL. Sciatic nerve release following fracture or reconstructive surgery of the acetabulum. J Bone Joint Surg Am. 2007;89(7):1432-1437.

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28. Manidakis N, Kanakaris NK, Nikolaou VS, Giannoudis PV. Early palsy of the sciatic nerve due to heterotopic ossification after surgery for fracture of the posterior wall of the acetabulum. J Bone Joint Surg Br. 2009;91(2):253-257. 29. Thakkar DH, Porter RW. Heterotopic ossification enveloping the sciatic nerve following posterior fracture-dislocation of the hip: a case report. Injury. 1981;13(3):207-209.

IV

Hip

20 Femoral Head Fracture Osteonecrosis and Hip Instability Samuel A. McArthur, MD and Walter W. Virkus, MD

Fractures of the femoral head occur in conjunction with hip dislocations and are the result of high-energy trauma, such as motor vehicle collisions. The position of the hip at the time of injury and the patient’s degree of femoral anteversion determine the direction of dislocation as well as the size and location of associated femoral head or posterior wall acetabulum fractures. Anterior dislocation is frequently complicated by femoral head fracture.1 However, because more than 90% of dislocations are posterior,2,3 the vast majority of femoral head fracture-dislocations are posterior. Increased anteversion4 and positions of hip extension, abduction, and external rotation5 all predispose to fracture-dislocation over simple posterior dislocation. Dislocation has been demonstrated to cause occlusion of femoral head blood flow in both animal6 and cadaveric7 models. Fracture of the femoral head represents an additional insult to its vascularity. As well, fracture-dislocations are frequently treated operatively, leading to the possibility of iatrogenic vascular injury to the femoral head (Table 20-1).8 Osseous anatomy figures prominently in the hip’s inherent stability. The femoral head is normally seated deep within the acetabulum. Hip instability following dislocation is most often the product of associated posterior wall acetabular fracture. There is usually one primary failure point, either the femoral head or the posterior wall, and sizable fracture of both structures is infrequent. Femoral head fracture does compromise joint congruency and osseous stability. Instability can also result from soft tissue injury,9,10 usually the hip capsule, particularly in the setting of decreased femoral anteversion.

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Table 20-1

Risk Factors for Femoral Head Osteonecrosis RISK FACTOR

IMPLICATION/RESULT

Dislocation

Occlusion of retinacular vessels Duration correlates with osteonecrosis

Femoral neck fracture

Displacement of femoral neck fragments Injury to retinacular vessels

Incautious exposure

Disruption of vessels, loss of tissue attachment to fragments No retained vascularity to head or fragments

Inadequate reduction

Increased shear across femoral head Expanded fracture gap and synovial fluid within fracture Impaired revascularization/healing of fragment

PREVENTION: SURGICAL TECHNIQUES/REDUCTION The most critical factor in successful treatment of femoral head fracture-dislocations is early hip reduction. Multiple series have demonstrated that the duration of hip dislocation correlates with the incidence of osteonecrosis.11-13 Though the critical window for reduction remains controversial, improved outcomes have been noted with an interval as brief as 6 hours. Initial radiographs (anteroposterior [AP] pelvis, AP and lateral hip) should be evaluated for femoral neck fracture (Figure 20-1). If none is present, an emergent attempt at closed reduction should be performed. Adequate sedation is required, and the reduction method should employ continuous traction rather than abrupt movements or forceful torsion, which can lead to iatrogenic fracture of the femoral neck.14 A computed tomography (CT) scan should be performed following reduction to evaluate femoral-acetabular congruency in addition to size and location of associated fractures. Irreducible dislocations can be addressed operatively from a posterior, Kocher approach. If needed, the patient can be positioned laterally to allow for subsequent treatment of femoral head fracture. A CT scan can assist with preoperative planning by identifying interposed structures and fractures and should be obtained if it can be completed in a reasonable time frame. Care should be taken during the posterior exposure to protect the medial femoral circumflex artery (MFCA) by leaving the quadratus femoris insertion intact and dividing the conjoint tendon a minimum of 1.5-cm medial to the intertrochanteric crest.8 Additionally, sutures used to repair the short rotators should not penetrate their deep surface to avoid piercing the MFCA. With posterior dislocation, fracture of the femoral head is most often anteromedial (Figure 20-2). The trajectory is characteristically between 25 and 45 degrees from the sagittal.15 The location of the principal fracture line and fragments should be confirmed on CT; however, typically they are inadequately visualized from a posterior approach. Alternative exposures, such as an anterior, Smith-Petersen approach,16 or digastric (trochanteric flip) approach,17 provide superior visualization. The Smith-Petersen has the advantage of familiarity; it provides excellent exposure of the femoral head and anterior neck, allowing for reduction of both if needed. There is an increased incidence of heterotopic ossification (HO) with this approach,16

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Figure 20-1. AP radiograph demonstrating posterior hip dislocation. A large femoral head fracture fragment extending from just above the fovea remains within the acetabulum.

Figure 20-2. Axial CT image following closed reduction of the right hip. The primary fracture is in the typical, anteromedial location.

and prophylaxis should be considered, particularly in those with head injury or prior history of HO. Elevation of the abductors from the ilium is believed to be contributory and should be avoided. Posterior pathology cannot be addressed from this exposure. A Kocher approach through a separate incision can be performed if there is an irreducible dislocation or significant posterior wall acetabular fracture. The digastric or trochanteric flip approach allows exposure of both the posterior and anterior hip through a single skin incision. It does, however, necessitate trochanteric osteotomy with the potential complications of trochanteric bursitis and nonunion. The posterior portion of the approach carries similar risks to the femoral circulation as the Kocher approach. Neither the Smith-Petersen16,18 nor the digastric approach17,19 has been shown to result in increased osteonecrosis. Though risk to the femoral circulation is less

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Figure 20-3. (A) Intraoperative photograph of right femoral head fixation with subchondral standard screws via the trochanteric flip approach. Note the wide zone of cartilaginous injury adjacent to the primary fracture line. (B) AP fluoroscopic image following placement of two countersunk standard screws perpendicular to the anteromedial fragment.

anteriorly, caution should still be employed along the superior femoral neck to avoid disruption of retinacular vessels. Surgical dislocation, when required, does not appear to lead to a significant increase in osteonecrosis. Small fracture fragments below the level of the fovea can be discarded. Though not in the weight-bearing surface, larger infrafoveal fragments assist in maintaining stability and can be used to obtain reduction of associated posterior wall fracture. Frequently, the ligamentum teres or capsule will insert into fracture fragments, and every attempt at maintaining soft tissue attachments for retained pieces should be made. In addition to providing vascularity, soft tissue can assist with determining the correct orientation of fragments. Reduction can be built from the fovea or other clear capsular or fracture keys, provisionally fixated, and evaluated fluoroscopically (Figure 20-3). Correct rotational alignment may be difficult to gauge visually, and multiple radiographic views (AP, Judet) should be assessed for subtle loss of head sphericity. Inadequate reduction can lead to shear across the fragment or increased gaping at the fracture site, resulting in additional exposure to synovial fluid. In either case, healing potential is diminished. Once fixation of the femoral head has been accomplished, hip stability should be assessed. Posterior wall fracture of less than 20% to 25% is typically considered predictive of stability20,21; however, smaller fractures of the posterior wall or injury to the labrum and capsule can also lead to recurrent dislocation.9,10 Reduction and fixation of acetabular fractures is discussed further in Chapter 17. With posterior exposure or instability on examination, an attempt at primary capsular repair should be made. If a large defect persists, the piriformis can be used to reinforce it. Capsular avulsions from the acetabular rim can be addressed by tying over drill holes or with suture anchors. Tears or detachment of the labrum can also frequently be repaired primarily. Care should be taken to retain as much labrum as possible to maintain acetabular depth.

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Table 20-2

Implants for Femoral Head Fracture IMPLANT

CRITICAL FACTORS

Traditional (headed) screws

Require countersinking Greatest variability of available diameter and length

Headless screws

Cannulation assists with provisional fixation and fluoroscopic evaluation prior to insertion Differential thread pitch creates compression

Resorbable pins

Location or migration cannot be evaluated radiographically Decreased need for removal or interference with revision procedures

Suture

Low relative strength of fixation May allow fixation of very small fragments that will not accommodate screws/pins

PREVENTION: IMPLANT SELECTION AND APPLICATION Femoral head fracture fragments are often quite thin, with only a few millimeters of subchondral bone underlying the articular surface. There are multiple acceptable fixation devices available; however, the surgeon should ensure that the device is inserted below the level of the cartilage. Prominent hardware can damage the articular surface of the acetabulum, causing arthrosis and complicating secondary interventions. The fracture plane should be determined by CT and confirmed intraoperatively. Frequently, there is little space within the fragment for fixation, and the desired trajectory and location of screws must be planned carefully. Screws/pins perpendicular to the fracture allow for ease of compression and subchondral placement but may limit length. Suture anchors used to repair the capsule should be directed peripherally to avoid inadvertent entry into the joint (Table 20-2).

COMPLICATION MANAGEMENT: SALVAGE PROCEDURES The long-term prognosis for patients with traumatic osteonecrosis is less clear than those suffering from osteonecrosis due to other causes. Progression of collapse is not certain.22 If the acetabular articular surface is well maintained, a segmental collapse due to traumatic osteonecrosis may, therefore, be more responsive to focal salvage measures. Durable improvement has been demonstrated following vascularized fibular grafting for osteonecrosis resulting from hip dislocation23; however, there is little evidence to support its use in the setting of fracture dislocation. Intertrochanteric osteotomy is used more commonly and results in patients under 40 with traumatic osteonecrosis are typically better than for idiopathic/systemic etiology.24 Varus or valgus osteotomy can be performed depending on the location of collapse. With a medial femoral head defect, varus femoral osteotomy with blade plate is performed to shift load bearing to the lateral femoral head. Twenty degrees is

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considered sufficient intact lateral articular arc to allow for varus osteotomy. Lateral femoral head osteonecrosis can be treated with valgus femoral osteotomy. Data for hip arthrodesis and arthroplasty are more robust, and performance of these procedures is potentially complicated by prior grafting or osteotomy. For patients with recurrent hip instability, repair of soft tissue, capsular imbrication, or labral repair may be sufficient. Use of bulk allograft or autologous iliac crest to create a posterior buttress for the labrum has also been described.9,10 An internalrotation intertrochanteric femoral osteotomy can be performed if decreased anteversion is determined to be contributory.25 Few patients require secondary operations for hip laxity; however, limited reports following labral reinforcing bone block and rotational osteotomy reflect resolution of instability.

SUMMARY Osteonecrosis is a frequent complication of hip dislocation and is more common with associated femoral head fracture. Emergent hip reduction is critical to decrease the incidence of osteonecrosis. Careful surgical exposure prevents compromise of femoral head vascularity and provides adequate visualization for reduction and stable fixation. Appropriate reduction decreases mechanical and biologic stress on fracture fragments and should decrease fragment necrosis. Limited, traumatic osteonecrosis can be addressed with intertrochanteric osteotomy; however, alteration of femoral anatomy and retained implants can complicate other salvage treatments. Instability after hip dislocation is most often the result of posterior wall acetabular fracture. Accurate reduction of the femoral head improves congruency and stability of the hip and can assist with fixation of associated posterior wall fracture. Intraoperatively, the capsule and labrum should be repaired if the posterior hip is exposed or if instability is noted following femoral head fixation. Osseous labral reinforcement and rotational femoral osteotomy can resolve recurrent instability.

REFERENCES 1. DeLee JC, Evans JA, Thomas J. Anterior dislocation of the hip and associated femoral head fractures. J Bone Joint Surg Am. 1980;62(6):960-964. 2. Yang RS, Tsuang YH, Hang YS, Liu TK. Traumatic dislocation of the hip. Clin Orthop Relat Res. 1991;265:218-227. 3. Sahin V, Karakas ES, Aksu S, Atlihan D, Turk CY, Halici M. Traumatic dislocation and fracture dislocation of the hip: a long term follow up study. J Trauma. 2003;54(3):520-529. 4. Upadhyay SS, Moulton A, Burwell RG. Biological factors predisposing to traumatic posterior dislocation of the hip. A selection process in the mechanism of injury. J Bone Joint Surg Br. 1985;67(2):232-236. 5. Letournel E, Judet R. Fractures of the Acetabulum. 2nd ed. New York, NY: Springer-Verlag; 1993. 6. Shim SS. Circulatory and vascular changes in the hip following traumatic hip dislocation. Clin Orthop Relat Res. 1979;140:255-261. 7. Yue JJ, Wilber JH, Lipuma JP, et al. Posterior hip dislocations a cadaveric angiographic study. J Orthop Trauma. 1996;10(7):447-454. 8. Gautier E, Ganz K, Krügel N, Gill T, Ganz R. Anatomy of the medial femoral circumflex artery and its surgical implications. J Bone Joint Surg Br. 2000;82(5):679-683.

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9. Lieberman JR, Altchek DW, Salvati EA. Recurrent dislocation of a hip with a labral lesion: treatment with a modified Bankart-type repair. Case report. J Bone Joint Surg Am. 1993;75(10):1524-1527. 10. Rashleigh-Belcher HJ, Cannon SR. Recurrent dislocation of the hip with a “Bankart-type” lesion. J Bone Joint Surg Br. 1986;68(3):398-399. 11. Brav EA. Traumatic dislocation of the hip. Army experience and results over a twelve year period. J Bone Joint Surg Am. 1962;44:1115-1134. 12. Hougaard K, Thomsen PB. Traumatic posterior dislocation of the hip: prognostic factors influencing the incidence of avascular necrosis of the femoral head. Arch Orthop Trauma Surg. 1986;106(1):32-35. 13. Reigstad A. Traumatic dislocation of the hip. J Trauma. 1980;20(7):603-606. 14. Sy MH, Kinkpé CV, Dakouré PW, et al. [Femoral neck fracture complicating orthopedic reposition of a dislocated hip: four cases]. Rev Chir Orthop Reparatrice Appar Mot. 2005;91(2):173-179. 15. Moed BR, Maxey JW. Evaluation of fractures of the femoral head using the CT-directed pelvic oblique radiograph. Clin Orthop Relat Res. 1993;296:161-167. 16. Swiontkowski MF, Thorpe M, Seiler JG, Hansen ST. Operative management of displaced femoral head fractures: case-matched comparison of anterior versus posterior approaches for Pipkin I and Pipkin II fractures. J Orthop Trauma. 1992;6(4):437-442. 17. Solberg BD, Moon CN, Franco DP. Use of a trochanteric flip osteotomy improves outcomes in Pipkin IV fractures. Clin Orthop Relat Res. 2009;467(4):929-933. 18. Stannard JP, Harris HW, Volgas DA, Alonso JE. Functional outcome of patients with femoral head fractures associated with hip dislocations. Clin Orthop Relat Res. 2000;377:44-56. 19. Siebenrock KA, Gautier E, Woo AK, Ganz R. Surgical dislocation of the femoral head for joint débridement and accurate reduction of fractures of the acetabulum. J Orthop Trauma. 2002;16(8):543-552. 20. Vailas, JC, Hurwitz S, Wiesel SW. Posterior acetabular fracture-dislocations: fragment size, joint capsule, and stability. J Trauma. 1989;29(11):1494-1496. 21. Keith JE, Brashear HR, Guilford WB. Stability of posterior fracture-dislocations of the hip. Quantitative assessment using computed tomography. J Bone Joint Surg Am. 1988;70(5):711714. 22. Glimcher MJ, Kenzora JE. The biology of osteonecrosis of the human femoral head and its clinical implications. II. The pathologic changes in the femoral head as an organ and in the hip joint. Clin Orthop Relat Res. 1979;139:283-312. 23. Garrigues GE, Aldridge JM , Friend JK, Urbaniak JR. Free vascularized fibular grafting for treatment of osteonecrosis of the femoral head secondary to hip dislocation. Microsurgery. 2009;29(5):342-345. 24. Maistrelli G, Fusco U, Avai A, Bombelli R. Osteonecrosis of the hip treated by intertrochanteric osteotomy. A four- to 15-year follow-up. J Bone Joint Surg Br. 1988;70(5):761-766. 25. Marti RK, Kloen P. Chronic recurrent posterior dislocation of the hip after a Pipkin fracture treated with intertrochanteric osteotomy and acetabuloplasty: a case report. J Bone Joint Surg Am. 2000;82(6):867-872.

21 Femoral Neck Fracture Nonunion Michael T. Archdeacon, MD, MSE

Femoral neck nonunion is most frequently associated with displaced femoral neck fractures in young patients.1 A high-energy injury, significant fracture displacement, an unstable shear force environment, poor reduction, and inadequate fixation all increase the risk of nonunion (Table 21-1 and Figure 21-1). In more senior patients, where hemiarthroplasty or total hip arthroplasty are more common, nonunion is not an issue.

PREVENTION: SURGICAL TECHNIQUES/REDUCTION Successful treatment of a displaced femoral neck fracture requires an anatomic reduction with stable internal fixation. The fracture orientation must be determined using preoperative radiographs, computed tomography (CT) scans, and/or magnetic resonance imaging (MRI). Intraoperative fluoroscopic imaging is critical in order to ensure an anatomic reduction as well as appropriate implant placement. True anteroposterior (AP) and lateral hip radiographs are needed, which often requires 15 to 20 degrees of overrotation of the C-arm to account for femoral neck anteversion. An alternative imaging technique is intraoperative CT scanning. This allows for excellent visualization of the fracture reduction and implant position; however, it is not universally available. An anatomic closed reduction must be confirmed through radiographic imaging in two planes, with recognition that failure is more likely if an anatomic reduction is not achieved. To facilitate reduction, a fracture table with either distal femoral traction or boot traction can assist with obtaining length and rotation. A thigh support or crutch can help correct posterior sag at the fracture site. An alternative is 199

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Table 21-1

Risk Factors For Femoral Neck Fracture Nonunion RISK FACTOR

IMPLICATION/RESULT

High-energy injury

Significant fracture displacement Damage to retinacular vessels

Vertically oriented fracture pattern

Predispose to varus angulation Inferior fracture translation frequent

Reduction not anatomic

Increases shear forces across fracture site Higher risk of fixation failure

Implant position not adequate

Implant unable to resist deforming forces Varus collapse and shortening occur Shear forces increase at fracture

Figure 21-1. An AP radiograph demonstrating a displaced, vertically oriented femoral neck fracture with a nonanatomic reduction and less than ideal hardware placement. This resulted in a failure of fixation with varus collapse and inferior translation. Ultimately, a femoral neck nonunion was the outcome.

a radiolucent table with the patient in the supine position with slight knee flexion. This is particularly useful in an anterior approach. The standard surgical approaches include the traditional Watson-Jones anterolateral approach, which can facilitate implant placement. However, exposure and reduction of the fracture can be difficult in a large or obese patient. The anterior Smith-Petersen approach provides excellent exposure of the fracture and allows clamp placement directly perpendicular to the fracture plane. However, placement of hardware along the lateral border of the femur can be challenging (Figure 21-2A). A recently described modification of the anterior approach consists of adding a percutaneous or limited open lateral approach for hardware placement (Figures 21-2B and C).2 This combined approach technique is recommended because it allows an anatomic reduction under direct visualization as well as hardware placement through an accessory approach.

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A

C

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B

Figures 21-2. (A) A depiction of the anterior Smith-Petersen approach for femoral neck fracture reduction. (B) An accessory lateral incision for placement of cannulated screws or (C) a sliding hip screw.

PREVENTION: IMPLANT SELECTION AND APPLICATION The appropriate implant is critical for maintaining an anatomic reduction. Acceptable implants include a sliding hip screw construct, with or without a derotation screw, cannulated screws, and a locking proximal femoral plate/screw construct (Table 21-2).3

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Table 21-2

Implants for Femoral Neck Fracture Fixation IMPLANT

CRITICAL FACTORS

Sliding hip screw ± derotation screw

May prevent fracture displacement Tip apex distance ideally less than 25 mm May need to position inferior in order to place derotation screw superior (usually a cannulated 6.5- to 8.0-mm screw) Requires more invasive approach than cannulated screws

Cannulated screws (Figure 21-3)

Placed using a percutaneous approach Inferior calcar and posterior femoral neck screws Unstable unless the fixation buttresses the inferior and posterior femoral neck4 Supplemented with accessory lag screw from lateral trochanter perpendicular across vertical femoral neck fracture

Locking proximal femur plate/ screw construct (Figure 21-4)

Provide rigid fixation for anatomic reduction Potential fixation failure because implant does not allow controlled collapse No published data to support technique

COMPLICATION MANAGEMENT: SALVAGE PROCEDURES If nonunion and hardware failure have not resulted in necrosis or degeneration of the hip, an ideal salvage procedure is to convert the shear forces at the vertical femoral neck fracture into compressive forces. This goal is best achieved using a valgus intertrochanteric osteotomy. The use of this osteotomy converts the vertical femoral neck fracture into a more horizontal orientation (Figure 21-5).5 This procedure is frequently approached via an extensile, vastus elevating lateral approach in either the supine or lateral decubitus position. The author prefers the lateral decubitus position because it improves exposure in morbidly obese patients by allowing adipose tissue to “fall away” during the exposure. Additionally, the lateral position facilitates osteotomy reduction and implant placement. A proximal femoral blade plate is often used in such osteotomies to achieve stable fixation. This salvage technique generally results in fracture union, even for chronic femoral neck nonunion. However, in patients that develop osteonecrosis after osteotomy, the proximal femoral deformity can make arthroplasty difficult.

SUMMARY Femoral neck nonunion is predictable after open reduction and internal fixation if an anatomic reduction is not obtained or if appropriate implants are not chosen or placed correctly. Appropriate surgical technique for reduction and implant positioning is paramount to a successful outcome. Anatomic reduction with placement of a sliding hip screw with or without a derotation screw, cannulated screws

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A

203

Figures 21-3. (A) AP and (B) lateral radiographs of a femoral neck fracture with anatomic reduction stabilized with an inferior calcar buttress screw, as well as a supplemental perpendicular lag screw.

B

inferiorly along the calcar and posteriorly along the femoral neck with or without a supplementary perpendicular lag screw, or a locking proximal femoral plate can minimize the risk of femoral neck nonunion. If a complication occurs, a thorough appreciation of salvage procedures is necessary, and this includes valgus intertrochanteric osteotomy.

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B

Figures 21-4. (A) AP and (B) lateral radiographs of a femoral neck fracture with anatomic reduction stabilized via a locking proximal femoral plate and screws.

Figure 21-5. An AP radiograph of the proximal femur demonstrating a valgus intertrochanteric osteotomy stabilized with an osteotomy blade plate, which has converted the shear force of the vertical femoral neck nonunion into a compressive force. This technique resulted in a healed femoral neck nonunion with restoration of femoral neck height.

REFERENCES 1. Swiontkowski MF, Winquist RA, Hansen ST. Fracture of the femoral neck in patients between the ages of twelve and forty-nine years. J Bone Joint Surg Am. 1984;66:837-846. 2. Molnar RB, Routt ML Jr. Open reduction of intracapsular hip fractures using a modified Smith-Petersen surgical exposure. J Orthop Trauma. 2007;21:490-494. 3. Ruedi TP, Murphy WM. AO Principles of Fracture Management. New York, NY: AO Publishing Thieme; 2000.

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4. Lindequist S, Tornkvist H. Quality of reduction and cortical screw support in femoral neck fractures: an analysis of 72 fractures with a new computerized measuring method. J Orthop Trauma. 1995;9:215-221. 5. Marti RK, Schuller HM, Raaymakers EL. Intertrochanteric osteotomy for non-unions of the femoral neck. J Bone Joint Surg Br. 1989;71:782-787.

22 Intertrochanteric Fractures Lag Screw Cut Out and Failure of Fixation Brian D. Solberg, MD

Intertrochanteric fractures are commonly treated with surgical stabilization using a fixed-angle lag screw device that is attached to either an intramedullary (IM) nail or a side plate and screws. There has been a significant trend toward the use of an IM device over the past decade, despite a lack of data suggesting significant clinical benefit.1 The main etiology of mechanical failure of intertrochanteric fracture repair is a lag screw cut out (Figure 22-1), fracture of an IM implant, or failure of fixation with varus collapse (Table 22-1). Lag screw cut out is related to two independent factors: quality of reduction of the intertrochanteric segment and errant placement of the lag screw within the femoral head. Other factors that are less common include active infection and neoplasm. Loss of fixation is commonly a result of varus malreduction of an unstable fracture pattern. Hip screw cut out through the superior femoral head has been reported as the most common mode of failure for fixed-angle hip screw devices, both IM and extramedullary, with an overall rate of 4% to 20% in larger series (Figure 22-2).2 The use of the tip-apex distance (TAD) allows for accurate assessment of the position of the screw within the femoral head. If the hip screw is placed more than 25 mm from the apex of the femoral head, the likelihood of hip screw cut out increases exponentially, with a nearly 80% rate of cut out if the TAD is more than 40 mm regardless of the type of implant used (Figure 22-3).3 The results of this study were observed in relatively higher angle devices (130- to 140-degree devices) in which the most common error was placement of the lag screw too high in the femoral head. There are some preliminary data to suggest that the use of lower angle nails and plates (115 to 125 degrees), which are widely used, now place the tip of the nail inferiorly within the femoral head and reduce implant cut out despite a relatively high TAD. These data have not been widely corroborated. Other causes include excessive fracture collapse 207

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Figure 22-1. Varus collapse of an intertrochanteric fracture with lag screw cut out.

Table 22-1

Complications of Intertrochanteric Fractures COMPLICATION

RISK FACTORS

SOLUTION

Lag screw cut out

High TAD Excessive fracture collapse Static locking of sliding mechanism

TAD less than 25 mm Consider an intramedullary nail for unstable fractures Never lock dynamic screw

Loss of fixation

Varus malreduction

Correct residual varus malreduction

Figure 22-2. Calculation of tipapex distance. (Reprinted with permission from Baumgaertner MA, Curtin SL, Lindskog DL, Keggi JM. The value of the tipapex distance in predicting failure of fixation of peritrochanteric fractures of the hip. J Bone Joint Surg. 1995;77A:10581064.)

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Figure 22-3. Probability of lag screw cut out versus tip-apex distance. (Reprinted with permission from Baumgaertner MA, Curtin SL, Lindskog DL, Keggi JM. The value of the tipapex distance in predicting failure of fixation of peritrochanteric fractures of the hip. J Bone Joint Surg. 1995;77A:10581064.)

Figure 22-4. Uncoupling of the lag screw from the side plate with varus collapse.

exceeding the sliding capacity of the sliding screw, locking the sliding mechanism of the lag screw, and inadequate screw-barrel engagement. Loss of fixation is a generic term, but it generally applies to non-cut out forms of implant failure. These are a result of two types of failure: implant related and nonunion. Implant-related loss of fixation can occur with the use of a short barrel, highangle hip screw combination with a varus malreduction. In this case, the lag screw uncouples from the short barrel of the side plate, and the varus collapse of the intertrochanteric fracture leads to rapid loss of fixation and shortening (Figure 22-4). This complication has largely been obviated by the use of IM devices and lower angle side plate designs; however, a recent study failed to demonstrate a statistically significant difference in outcome between IM and extramedullary implants in the treatment of unstable fracture patterns.4 Nonunion of intertrochanteric fractures is an uncommon complication, occurring in less than 2% of cases, and is largely due to the fact that the fracture occurs through well-vascularized cancellous bone. The exception is the use

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Table 22-2

Three Key Principles of Intertrochanteric Fracture Repair PRINCIPLE

EFFECT

Keep TAD below 25 mm

Minimizes likelihood of lag screw cut out

Avoid varus malreduction

Allows controlled collapse of lag screw in barrel and prevents implant failure

Always dynamize lag screw

Allows controlled collapse of lag screw in barrel and prevents lag screw cut out

Figure 22-5. Failure of the intramedullary nail secondary to varus malreduction.

of fixed-angle, nondynamizing locking plates in the management of unstable pertrochanteric fractures in which the plate prevents controlled collapse of the fracture and may have a higher rate of nonunion and plate fracture. Because of this, the use of these devices for intertrochanteric fractures has been discouraged.

AVOIDANCE OF COMPLICATIONS Although the implant used to repair these types of fractures has largely changed to IM implants over the past decade, the principles of appropriate fracture management have not changed and can be used to avoid complications.5,6 The three main principles are adequate reduction of the fracture, deep and central placement of the lag screw in the femoral head, and adequate dynamization of the lag screw in the nail or plate (Table 22-2). Failure to correct varus deformity, lateral wall displacement, and posterior trochanteric sag are the most common technical errors leading to implant failure (Figure 22-5).7 Residual varus deformity prevents proper engagement of the sliding mechanism of the hip screw and prevents controlled collapse. This, in turn, keeps the fracture distracted and is the most common cause of IM implant failure, which typically occurs at the barrel of the IM nail. Proper correction of residual varus deformity is the single most important aspect of the reduction of intertrochanteric

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Figure 22-6. Correction of varus deformity with a subtrochanteric osteotomy using a 95-degree blade plate.

fractures. Correct placement of the lag screw into the deep, central portion of the femoral head minimizes the TAD and, therefore, minimizes the risk of lag screw cut out. Awareness of the TAD concept reduces errant screw placement and subsequent cut out. This is the single most important aspect of implant placement. Finally, failure to adequately dynamize the lag screw is the last principle of implant placement that is critical in avoiding implant failure. Hip screw side plates have a passive sliding mechanism, while IM nails generally have a dynamization screw within the nail that engages the lag screw to prevent rotation but is loose enough to allow the lag screw to slide freely within the barrel. Failure to adequately loosen the dynamization screw can lock the lag screw in a fixed position and prevent dynamization and controlled collapse, which can lead to lag screw cut out.6

SALVAGE Lag screw cut out is a devastating complication because the lag screw cores a hole in the weight-bearing portion of the femoral head and often erodes corresponding areas of the acetabular articular surface. Prosthetic replacement of the hip joint is the only salvage once this complication occurs. The use of a revision-type calcar substituting implant is often required because this complication usually occurs in unstable fracture patterns with loss of the posteromedial calcar segment. Varus collapse and nonunion-related implant failures are generally salvaged with removal of the implant and revision with a subtrochanteric valgus osteotomy, provided the femoral head is intact and viable (Figure 22-6). This technique has generally been described using a higher angle (120 degrees+) blade plate and is a technically demanding procedure. In cases with osteonecrosis of the femoral head or implant cut out, conversion to a calcar substitution total hip prosthesis is recommended.

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SUMMARY The most common cause of complications with intertrochanteric fractures is lag screw cut out in the femoral head and varus malreduction leading to implant failure. Correct placement of the lag screw in the femoral head (deep and central) and prevention of residual varus malreduction are the two most important elements in preventing loss of fixation or implant failure. The use of IM implants in unstable fractures may prevent excessive collapse, but the lag screw should never be locked to avoid cut out in the femoral head.

REFERENCES 1. Anglen JO, Weinstein JN, American Board of Orthopaedic Surgery Research Committee. Nail or plate fixation of intertrochanteric hip fractures: changing pattern of practice. A review of the American Board of Orthopaedic Surgery Database. J Bone Joint Surg Am. 2008;90(4):700-707. 2. Baumgaertner MR, Chrostowski JH, Levy RN. Intertrochanteric hip fractures. In Browner BD, Levine AM, Jupiter JB, et al, eds. Skeletal Trauma. Vol 2. Philadelphia, PA: WB Saunders; 1992:1833-1881. 3. Baumgaertner MR, Curtin SL, Lindskog DM, Keggi JM. The value of the tip-apex distance in predicting failure of fixation of peritrochanteric fractures of the hip. J Bone Joint Surg Am. 1995;77(7):1058-1064. 4. Barton TM, Gleeson R, Topliss C, Greenwood R, Harries WJ, Chesser TJ. A comparison of the long gamma nail with the sliding hip screw for the treatment of AO/OTA 31-A2 fractures of the proximal part of the femur: a prospective randomized trial. J Bone Joint Surg Am. 2010;92(4):792-798. 5. Templeman D, Baumgaertner MR, Leighton RK, Lindsey RW, Moed BR. Reducing complications in the surgical treatment of intertrochanteric fractures. Instr Course Lect. 2005;54:409-415. Review. 6. Haidukewych GJ. Intertrochanteric fractures: ten tips to improve results. Instr Course Lect. 2010;59:503-509. 7. Carr JB. The anterior and medial reduction of intertrochanteric fractures: a simple method to obtain a stable reduction. J Orthop Trauma. 2007;21:7.

23 Intertrochanteric Fractures Lateral Wall Fractures Bradley Merk, MD and Erik Eller, MD

The status of the lateral femoral cortex in an intertrochanteric fracture is a significant determinant of postreduction fracture stability. The lateral cortex provides a buttress that allows for interfragmentary compression. Recently, it has been demonstrated that lateral wall fractures are a potential intraoperative iatrogenic complication that can lead to a prolonged, painful recovery.1 The etiology of these fractures is related to the initial fracture pattern, implant selection, surgical technique, and patient characteristics (Table 23-1). The incidence of lateral wall fractures has been reported to be 3% in AO/OTA type A1-A2.1 fractures and 31% in AO/OTA type A2.2 or A2.3 (Figure 23-1).2 These higher grade fractures have more comminution and less lateral wall bone stock. The status of the lateral wall largely determines the modality of fixation that may be employed (ie, sliding hip screw with side plate versus a fixed-angle device). Finally, fractures of the lateral cortex can occur with improper surgical technique, including poor entry angle of drill, improper screw alignment in the predrilled path, large bore screws, and multiple perforations of cortex during reaming (see Table 23-1).2

PREVENTION: SURGICAL TECHNIQUES/REDUCTION The key to preventing lateral wall fractures is first to recognize those intertrochanteric fractures at risk (AO/OTA A2.2 and A2.3) and select the appropriate implant. Adequate preoperative radiographs should be obtained, including a pelvis x-ray, dedicated hip films, and a cross-table lateral. Second, the insult to the lateral cortex must be minimized. This can be done by obtaining an anatomic reduction, ensuring that the sliding screw follows the reamed pathway precisely, achieving a 213

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Table 23-1

Risk Factors for Lateral Wall Fractures RISK FACTOR

IMPLICATION/RESULT

Large-diameter screw

Significant bone violation of fragile lateral wall

AO/OTA type A2.2 or A2.3 fracture

Increased comminution of greater trochanter leads to diminished lateral wall bone stock

Improper entry angle

Levering of the screw on the lateral cortex

Multiple lateral cortex perforations

Compromised lateral cortex integrity

Age

Diminished bone quality in the elderly

Figure 23-1. Diagram of AO/OTA type 31-A fractures. 31-A1 fractures are simple fractures. 31-A2 fractures extend into the lesser trochanter with increasing degrees of comminution. 31-A3 fractures involve a violation of the lateral cortex.

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center-center head position of the screw to reduce forces on lateral cortex (a tip-apex distance of