Morrey's The Elbow and Its Disorders, 4th Edition

Dedication As I was preparing the front material for the Fourth Edition of The Elbow and Its Disorders, my father passed away at age 91. It is with great humility as well as a tremendous sense of loss, but also pride that I dedicate this fourth volume to my father, Alfred E. Morrey, Jr. My dad was a chemical engineer and worked in the petroleum industry all of his life. His professional background and skills were instrumental in my formative years in teaching, observation, precision, accuracy, practicality and problem solving. In many ways these features of engineering are not dramatically different from the requirements of the orthopedic surgeon. But, more importantly than this, my father was my role model. He was openminded and objective and strongly believed in the concept of service. He avoided assuming information as being factual unless it had been demonstrated to be so. But probably the most important characteristic was his desire and stimulus for myself and my siblings to contribute to society and to “give a full days measure”. I have thought of my father regularly throughout my career and with his passing on July 13, 2008, it seems fitting to dedicate this effort to him. He had all three prior volumes proudly displayed in his library. Bernard F. Morrey, MD

CONTRIBUTORS

Julie E. Adams, MD Assistant Professor, Department of Orthopaedic Surgery, University of Minnesota School of Medicine, Minneapolis, Minnesota Fractures of the Olecranon

Robert A. Adams, MA, OPA-C Adjunct Faculty Clinical Coordinator, University of Wisconsin-La Crosse, La Crosse, Wisconsin; Assistant Professor, Mayo College of Medicine, Rochester, Minnesota; Physician Assistant, Mayo Clinic, Rochester, Minnesota Linked Total Elbow Arthroplasty in Patients with Rheumatoid Arthritis; Total Elbow Arthroplasty for Primary Osteoarthritis; Wear and Elbow Replacement

Christopher S. Ahmad, MD Associate Professor, Orthopaedic Surgery, Center for Shoulder, Elbow and Sports Medicine, Columbia University College of Physicians and Surgeons; Attending, Orthopaedic Surgeon, New York Orthopaedic Hospital, Columbia University, New York, New York Arthroscopy in the Throwing Athlete; Diagnosis and Treatment of Ulnar Collateral Ligament Injuries in Athletes

Gilberto J. Alvarado, MD Orthopedic Sports Medicine Fellow, Nirschl Orthopaedic Center for Sports Medicine and Joint Reconstruction, Arlington, Virginia Tennis Elbow Tendinosis

Peter C. Amadio, MD Professor of Orthopedics, Mayo Clinic College of Medicine; Consultant in Orthopedic Surgery, Mayo Clinic, Rochester, Minnesota Congenital Abnormalities of the Elbow

Kai-Nan An, PhD Professor, and Director, Biomechanics Laboratory, Mayo Clinic, Rochester, Minnesota Biomechanics of the Elbow; Functional Evaluation of the Elbow

Karen L. Andrews, MD Assistant Professor of Physical Medicine and Rehabilitation, College of Medicine, Mayo Clinic, Rochester, Minnesota Elbow Disarticulation Amputation

Robert D. Beckenbaugh, MD Professor of Orthopedics, Mayo Clinic, Rochester, Minnesota Arthrodesis

Richard A. Berger, MD, PhD Professor of Orthopedic Surgery and Anatomy, Mayo Clinic College of Medicine; Consultant, Division of Hand Surgery, Department of Orthopedic Surgery, Mayo Clinic, Rochester, Minnesota Overuse Syndrome

Thomas H. Berquist, MD, FACR Professor of Diagnostic Radiology, Mayo Clinic College of Medicine, Rochester, Minnesota; Consultant, Mayo Clinic – Jacksonville, Jacksonville, Florida Diagnostic Imaging of the Elbow

Allen T. Bishop, MD Professor of Orthopedic Surgery, Mayo Clinic College of Medicine; Consultant, Department of Orthopedic Surgery, and Chair, Division of Hand Surgery, Mayo Clinic, Rochester, Minnesota Soft Tissue Coverage of the Elbow; Flaccid Dysfunction of the Elbow

Kenneth P. Butters, MD Consultant, Hand Surgery, Department of Orthopedic Surgery, University of Oregon, Eugene, Oregon Septic Arthritis

Andrea Celli, MD Consultant Orthopaedic and Traumatology Surgeon, Orthopaedic and Traumatology Department, University of Modena e Reggio Emilia, Modena, Italy Triceps Insufficiency Following Total Elbow Arthroplasty

Emilie Cheung, MD Assistant Professor, Medical Center Line, and Stanford Hospital and Clinics, Stanford University, Stanford, California Treatment of the Infected Total Elbow Arthroplasty v

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Contributors

Akin Cil, MD Assistant Professor of Orthopaedics, Department of Orthopaedic Surgery, University of Missouri Kansas City; Attending Surgeon, Department of Orthopaedic Surgery, Truman Medical Center, Kansas City, Missouri Synovectomy of the Elbow

Mark S. Cohen, MD Professor, Director, Orthopaedic Education, and Director, Section of Hand and Elbow Surgery, Department of Orthopaedic Surgery, Rush University Medical Center, Chicago, Illinois Advanced Techniques: Arthroscopic Management of Lateral Epicondylitis

Patrick M. Connor, MD Clinical Faculty, Shoulder and Elbow Surgery/Sports Medicine, and Trauma Surgery, Orthopaedic Surgery Residency Program, Carolinas Medical Center, Charlotte, North Carolina Total Elbow Arthroplasty for Juvenile Rheumatoid Arthritis

William P. Cooney, MD Professor of Orthopedics, Mayo Clinic, Rochester, Minnesota Elbow Arthroplasty: Historical Perspective and Emerging Concepts

Ralph W. Coonrad, MD Associate Clinical Professor, Department of Orthopedic Surgery, Duke University; Medical Director Emeritus, Lenox Baker Children’s Hospital, Duke University, Durham, North Carolina Nonunion of the Olecranon and Proximal Ulna

Joshua S. Dines, MD Clinical Instructor, Orthopedic Surgery, Weill Cornell Medical College; Assistant Attending, Sports Medicine and Shoulder Service, The Hospital for Special Surgery, New York, New York Articular Injuries in the Athlete

James H. Dobyns, MD Professor of Orthopedics, and Emeritus Staff, Mayo Clinic College of Medicine, Rochester, Minnesota, and University of Texas San Antonio Health Science Center, San Antonio, Texas Congenital Abnormalities of the Elbow

Neal S. ElAttrache, MD Associate Clinical Professor, Department of Orthopaedics, Keck School of Medicine, University of Southern California; Director, Sports Medicine Fellowship, Kerlan-Jobe Orthopaedic Clinic, Los Angeles, California Arthroscopy in the Throwing Athlete; Diagnosis and Treatment of Ulnar Collateral Ligament Injuries in Athletes; Articular Injuries in the Athlete

Larry D. Field, MD Clinical Instructor, Department of Orthopaedic Surgery, University of Mississippi School of Medicine; Director, Upper Extremity Service, Mississippi Sports Medicine and Orthopaedic Center, Jackson, Mississippi Diagnostic Arthroscopy: Indications, Portals, and Techniques; Management of Loose Bodies and Other Limited Procedures; Arthroscopic Management of the Stiff Elbow

Gerard T. Gabel, MD Clinical Associate Professor, Department of Orthopedic Surgery, Baylor College of Medicine, Houston, Texas Medial Epicondylitis

David R. J. Gill, MD, ChB, FRACS Joondalup Health Campus, Joondalup, Western Australia, Australia Linked Total Elbow Arthroplasty in Patients with Rheumatoid Arthritis

E. Richard Graviss, MD Professor of Radiology, St. Louis University School of Medicine; Pediatric Radiology, Cardinal Glennon Children’s Hospital, St. Louis, Missouri Imaging of the Pediatric Elbow

G. Dean Harter, MD Associate, Department of Orthopaedic Surgery, Chief, Shoulder and Elbow Institute, Program Director, Orthopaedic Surgery Residency, Geisinger Health System, Danville, Pennsylvania Ectopic Ossification About the Elbow

Alan D. Hoffman, MD Associate Professor of Radiology, Mayo Clinic College of Medicine; Consultant in Radiology – Pediatric Radiology, Mayo Clinic, Rochester, Minnesota Imaging of the Pediatric Elbow

Terese T. Horlocker, MD Professor of Anesthesiology and Orthopedics, Mayo Clinic, Rochester, Minnesota General and Regional Anesthesia and Postoperative Pain Control

Jeffery S. Hughes, MB, FRACS Orthopaedic Consultant, North Shore Private Hospital, Sydney, Australia Injury of the Flexors of the Elbow: Biceps Tendon Injury; Unlinked Arthroplasty: Distal Humeral Hemiarthroplasty

Srinath Kamineni, MBBCh, FRCS-Ed, FRCSOrthopaedics and Trauma, PhD Professor of Bioengineering, Brunel University – School of Engineering and Design; Consultant Elbow, Shoulder, Upper Limb Surgeon, and Clinical Lead, Upper Limb Unit, Cromwell Hospital, London, United Kingdom Distal Humeral Fractures–Acute Total Elbow Arthroplasty

Contributors

Graham J. W. King, MD, MSc, FRCSC Professor, Department of Surgery, University of Western Ontario; Chief of Orthopaedic Surgery, St. Joseph’s Health Centre, London, Ontario, Canada Unlinked Arthroplasty: Unlinked Total Elbow Arthroplasty; Unlinked Arthroplasty: Convertible Total Elbow Arthroplasty; Revision of Failed Total Elbow Arthroplasty with Osseous Integrity

Sandra L. Kopp, MD Assistant Professor of Anesthesiology, Mayo Clinic, Rochester, Minnesota General and Regional Anesthesia and Postoperative Pain Control

Tomasz K. W. Kozak, FRACS West Perth, Western Australia, Australia Total Elbow Arthroplasty for Primary Osteoarthritis

Mikko Larsen, MD Research Fellow, Microvascular Research Laboratory, Department of Orthopedic Surgery, Mayo Clinic, Rochester, Minnesota; Resident in Training, Department of Plastic and Reconstructive Surgery, V.U. Medical Center, Amsterdam, The Netherlands Flaccid Dysfunction of the Elbow

A. Noelle Larson, MD Resident in Orthopedics, Department of Orthopedics, Mayo Clinic, Rochester, Minnesota Hinged External Fixators of the Elbow; Interposition Arthroplasy of the Elbow

Susan G. Larson, MS, PhD Professor, Department of Anatomical Sciences, School of Medicine, Stony Brook University Medical Center, Stony Brook, New York Phylogeny

Brian P. Lee, MD Orthopaedic Associates, Singapore, Singapore Wear and Elbow Replacement

Robert L. Lennon, DO Associate Professor of Anesthesiology, Mayo Medical School; Supplemental Consultant, Mayo Clinic, Rochester, Minnesota General and Regional Anesthesia and Postoperative Pain Control

R. Merv Letts, MD, MSc, FRCSC, FACS Consultant Pediatric Orthopaedic Surgeon, Sheikh Khalifa Medical City, Abu Dhabi, United Arab Emirates Dislocations of the Child’s Elbow

Harvinder S. Luthra, MD Professor of Medicine, Department of Rheumatology, Mayo Clinic, Rochester, Minnesota Rheumatoid Arthritis

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Alex A. Malone, MBBS, MRCS (Eng), FRCS (Tr & Orth) Consultant Orthopaedic Surgeon, Christchurch Hospital, Canterbury, New Zealand; Senior Lecturer in Orthopaedics with an interest in Upper Limb Surgery, Christchurch School of Medicine, Otago University, New Zealand; Honorary Consultant, Shoulder and Elbow Unit, The Royal National Orthopaedic Hospital, Stanmore, United Kingdom; Honorary Lecturer, Department of Surgery, University College London, London, United Kingdom Phylogeny

Pierre Mansat, MD, PhD Professor of Orthopedics and Traumatology, Faculté Medecine Toulouse/Purpan, Université Paul Sabatier, and Service d’Orthopedie/Traumatologie, Unité du Membre Superieur, Centre Hospitalier Universitaire Purpan, Toulouse, France Extrinsic Contracture: Lateral and Medial Column Procedures

Thomas G. Mason, MD Associate Professor of Internal Medicine and Pediatrics, Mayo Clinic College of Medicine; Consultant in Adult and Pediatric Rheumatology, Mayo Clinic, Rochester, Minnesota Seronegative Inflammatory Arthritis

Glen A. McClung II, MD Commonwealth Orthopaedic Surgeons, Lexington, Kentucky Diagnostic Arthroscopy: Indications, Portals, and Techniques

Amy L. McIntosh, MD Associate Clinical Professor, Mayo Clinic, Rochester, Minnesota Complications of Supracondylar Fractures of the Elbow

Steven L. Moran, MD Assistant Professor of Orthopedics and Plastic Surgery, Mayo College of Medicine, and Mayo Clinic, Rochester, Minnesota Soft Tissue Coverage of the Elbow

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Contributors

Bernard F. Morrey, MD Professor of Orthopedic Surgery, Mayo Medical School; Department of Orthopedic Surgery, Mayo Clinic, Rochester, Minnesota Anatomy of the Elbow Joint; Biomechanics of the Elbow; Physical Examination of the Elbow; Functional Evaluation of the Elbow; Surgical Exposures of the Elbow; Principles of Elbow Rehabilitation; Splints and Bracing at the Elbow; Proximal Ulnar Fractures in Children; Dislocations of the Child’s Elbow; Post-Traumatic Elbow Stiffness in Children; Radial Head Fracture: General Considerations, Conservative Treatment, and Open Reduction and Internal Fixation; Radial Head Fracture: Prosthetic Radial Head Replacement; Nonunion of the Olecranon and Proximal Ulna; Coronoid Process and Monteggia Fractures; Complex Instability of the Elbow; Chronic Unreduced Elbow Dislocation; Ectopic Ossification About the Elbow; Extrinsic Contracture: Lateral and Medial Column Procedures; Hinged External Fixators of the Elbow; Injury of the Flexors of the Elbow: Biceps Tendon Injury; Rupture of the Triceps Tendon; Complications of Elbow Arthroscopy; The Future of Arthroscopy of the Elbow; Medial Epicondylitis; Surgical Failure of Tennis Elbow; Elbow Arthroplasty: Historical Perspective and Emerging Concepts; Unlinked Arthroplasty: Radiohumeral Arthrosis: Anconeus Arthroplasty and Capitellar Prosthetic Replacement; Linked Elbow Arthroplasty: Rationale, Indications, and Surgical Technique; Linked Total Elbow Arthroplasty in Patients with Rheumatoid Arthritis; Total Elbow Arthroplasty for Juvenile Rheumatoid Arthritis; Semiconstrained Elbow Replacement: Results in Traumatic Conditions; Total Elbow Arthroplasty as a Salvage for the Fused Elbow; Total Elbow Arthroplasty for Primary Osteoarthritis; Complications of Elbow Replacement Arthroplasty; Treatment of the Infected Total Elbow Arthroplasty; Triceps Insufficiency Following Total Elbow Arthroplasty; Wear and Elbow Replacement; Revision of Failed Total Elbow Arthroplasty with Osseous Integrity; Revision of Failed Total Elbow Arthroplasty with Osseous Deficiency; Nonimplantation Salvage of Severe Elbow Dysfunction; Synovectomy of the Elbow; Interposition Arthroplasty of the Elbow; Primary Osteoarthritis: Ulnohumeral Arthroplasty; Septic Arthritis; Neoplasms of the Elbow; Loose Bodies; Bursitis; The Elbow in Metabolic Disease

Matthew Morrey, MD Senior Orthopaedic Resident, Department of Orthopaedic Surgery, Mayo Clinic, Rochester, Minnesota Hinged External Fixators of the Elbow

Scott J. Mubarak, MD Clinical Professor, Department of Orthopedics, University of California, San Diego; Director of Orthopedic Program, Children’s Hospital, San Diego, California Complications of Supracondylar Fractures of the Elbow

Robert P. Nirschl, MD, MS Associate Clinical Professor, Georgetown University School of Medicine, Washington, DC; Director, Sports Medicine Fellowship Programs, Nirschl Orthopaedic Center for Sports Medicine and Joint Reconstruction, Arlington, Virginia; Attending Orthopedic Surgeon, Virginia Hospital Center, Arlington, Virginia Tennis Elbow Tendinosis

Shawn W. O’Driscoll, PhD, MD Professor of Orthopedic Surgery, Mayo Clinic, Rochester, Minnesota Continuous Passive Motion; Current Concepts in Fractures of the Distal Humerus; Elbow Dislocations; Complex Instability of the Elbow

Nicole M. Orzechowski, DO Instructor of Internal Medicine, Mayo Clinic College of Medicine; Mayo Clinic, Rochester, Minnesota Seronegative Inflammatory Arthritis

Panayiotis J. Papagelopoulos, MD, DSc Associate Professor of Orthopaedics, Athens University Medical School; Consultant, First Department of Orthopaedics, Attikon University General Hospital, Athens University Medical School, Athens, Greece Nonunion of the Olecranon and Proximal Ulna

Hamlet A. Peterson, MD, MS Emeritus Professor of Orthopedic Surgery, Mayo Medical School; Emeritus Consultant in Orthopedic Surgery, Mayo Clinic, Rochester, Minnesota Physeal Fractures of the Elbow

Douglas J. Pritchard, AB, MS, MD Orthopedic Surgery, Retired, Mayo Clinic, Rochester, Minnesota Neoplasms of the Elbow

Matthew L. Ramsey, MD Associate Professor of Orthopaedic Surgery, Thomas Jefferson University, and Rothman Institute, Philadelphia, Pennsylvania Total Elbow Arthroplasty for Distal Humerus Nonunion and Dysfunctional Instability

William D. Regan, MD, FRCS(C) Associate Professor, Department of Orthopaedics, University of British Columbia; Associate Head, Department of Orthopaedics, and Head, Division of Upper Extremity Surgery, University Hospital, Vancouver, British Columbia, Canada Physical Examination of the Elbow; Coronoid Process and Monteggia Fractures

Anthony A. Romeo, MD Associate Professor, and Director, Section of Shoulder and Elbow, Department of Orthopaedic Surgery, Rush University Medical Center, Chicago, Illinois Advanced Techniques: Arthroscopic Management of Lateral Epicondylitis

Joaquin Sanchez-Sotelo, MD, PhD Associate Professor of Orthopedics, Mayo Clinic College of Medicine; Consultant in Orthopedic Surgery, Department of Orthopedic Surgery, Mayo Clinic, Rochester, Minnesota Nonunion and Malunion of Distal Humerus Fractures; Lateral Collateral Ligament Insufficiency; Total Elbow Arthroplasty for Distal Humerus Nonunion and Dysfunctional Instability; Revision of Failed Total Elbow Arthroplasty with Osseous Deficiency; Hematologic Arthritis

Contributors

Felix H. Savoie III, MD Lee Schlesinger Professor, Shoulder, Elbow and Sports Surgery, Department of Orthopaedic Surgery, Tulane University; Chair, Division of Sports Medicine, Tulane Institute of Sports Medicine, New Orleans, Louisiana Diagnostic Arthroscopy: Indications, Portals, and Techniques; Management of Loose Bodies and Other Limited Procedures; Arthroscopic Management of the Stiff Elbow; Advanced Techniques: Arthroscopic Radial Ulnohumeral Ligament Reconstruction for Posterolateral Rotatory Instability of the Elbow; The Future of Arthroscopy of the Elbow

Alberto G. Schneeberger, MD Privatdozent, University of Zurich; Consultant, Shoulder and Elbow Surgery, Zurich, Switzerland Semiconstrained Elbow Replacement: Results in Traumatic Conditions

William J. Shaughnessy, MS, MD Associate Professor of Orthopedic Surgery, Mayo Medical School; Member, Division of Pediatric Orthopedics, Mayo Clinic, Rochester, Minnesota Osteochondritis Dissecans

Alexander Y. Shin, MD Professor, Orthopaedic Surgery, Mayo Clinic School of Medicine; Consultant, Orthopaedic Surgery, Mayo Clinic, Rochester, Minnesota Flaccid Dysfunction of the Elbow

Thomas C. Shives, MD Professor of Orthopedics, Mayo Clinic, Rochester, Minnesota Elbow Disarticulation Amputation

Jay Smith, MD Associate Professor of Physical Medicine and Rehabilitation, Mayo Clinic College of Medicine; Consultant, Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, Minnesota Principles of Elbow Rehabilitation

Robert J. Spinner, MD Professor, Departments of Neurosurgery, Orthopedics and Anatomy, Mayo Clinic College of Medicine; Consultant, Department of Neurologic Surgery and Orthopedics, Mayo Clinic, Rochester, Minnesota Nerve Entrapment Syndromes

Anthony A. Stans, MD Assistant Professor, and Chair, Division of Pediatric Orthopedics, Mayo Clinic, Rochester, Minnesota Supracondylar Fractures of the Elbow in Children; Fractures of the Neck of the Radius in Children; Proximal Ulnar Fractures in Children; Post-Traumatic Elbow Stiffness in Children

Scott P. Steinmann, MD Consultant, Professor of Orthopedics Mayo Clinic College of Medicine, Rochester, Minnesota Fractures of the Olecranon

J. Clarke Stevens, MD Professor of Neurology, Mayo Medical School, Rochester, Minnesota Neurotrophic Arthritis

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Kristen B. Thomas, MD Assistant Professor of Radiology, Mayo Clinic College of Medicine; Consultant in Radiology – Pediatric Radiology, Mayo Clinic, Rochester, Minnesota Imaging of the Pediatric Elbow

Nho V. Tran, MD Assistant Professor of Plastic Surgery, Mayo College of Medicine, and Mayo Clinic, Rochester, Minnesota Soft Tissue Coverage of the Elbow

Stephen D. Trigg, MD Associate Professor, Orthopaedics and Hand Surgery, Mayo Clinic Medical School Hand Surgery, Mayo Medical School, Rochester, Minnesota; Hand Surgeon, Department of Orthopaedics, and Medical Director, Outpatient Surgery Center, Mayo Clinic, Jacksonville, Florida Pain Dysfunction Syndrome

K. Krishnan Unni, MD Emeritus Professor of Pathology, Departments of Anatomic Pathology, Orthopedic Oncology, and Orthopedic Surgery, Mayo Clinic, Rochester, Minnesota Neoplasms of the Elbow

Francis Van Glabbeek, MD, PhD Professor of Functional Anatomy and Orthopaedics, University of Antwerp; Vice Chair, Department of Orthopaedics and Traumatology, University Hospital Antwerp, Antwerp, Belgium Radial Head Fracture: General Considerations, Conservative Treatment, and Open Reduction and Internal Fixation

Ann E. Van Heest, MD Professor, Department of Orthopaedic Surgery, University of Minnesota, Minneapolis; Gillette Children’s Specialty Healthcare, St. Paul, Minnesota Spastic Dysfunction of the Elbow

Roger P. van Riet, MD, PhD Orthopaedic Surgeon, Elbow Surgery, Monica Hospital, Deurne, Antwerp, Belgium Radial Head Fracture: General Considerations, Conservative Treatment, and Open Reduction and Internal Fixation

Ilya Voloshin, MD Assistant Professor, University of Rochester; Director, Shoulder and Elbow Service, University of Rochester Medical Center, Rochester, New York Complications of Elbow Replacement Arthroplasty

Ken Yamaguchi, MD Sam and Marilyn Fox Distinguished Professor of Orthopaedic Surgery, and Chief, Shoulder and Elbow Service, Washington University School of Medicine, St. Louis, Missouri Treatment of the Infected Total Elbow Arthroplasty

Mark E. Zobitz, MS Assistant Professor, Biomechanics Laboratory, Mayo Clinic, Rochester, Minnesota Biomechanics of the Elbow

P R E FA C E

Since the first edition of The Elbow and Its Disorders in 1983 I am extremely proud to hear such comments regarding the original and previous efforts such as “the definitive word in elbow surgery”. Such statements and confidence is a source of tremendous pride and also motivation to continue to improve. In the spirit of the original goal of providing a source of reliable information that will improve patient care, we continue to be focused on this initial desire to provide clear, concise, current, accurate, relevant and intelligible information that is easily accessible. I have a simple personal requirement for the timing of subsequent editions of this book. This is to wait until I feel as though there has been sufficient additional information to justify another volume. This requirement has been met with this particular effort. Thus, I am very pleased along with my co-authors to have completed the current volume. The overall organization, hope and effort to be a comprehensive reference has been maintained with an increased emphasis on surgical technique which is an ever growing and relevant need of the orthopedic community. We are, therefore, specifically pleased to offer video clips in a number of chapters that do complement and enhance the practical and useful learning experience.

The exciting advances in elbow arthroscopy are more extensively explored in the current volume. Innovative opportunities with regard to prosthetic joint replacement are also discussed in the current volume, along with nonprosthetic options such as anconeus arthroplasty. In fact we are pleased to observe considerable enhancement in the majority of chapters. As always I am deeply appreciative and humbled by those who have contributed material, thoughts, and insights over the years, particularly Doctors O’Driscoll, Steinmann, SanchezSotelo and my other partners at the Mayo Clinic. Finally, I should note that this edition is an opportunity to introduce my partner and colleague, Joaquin Sanchez-Sotelo, who has assisted me in the preparation of the current volume, and who has shown an insightful and substantive commitment to the practice of elbow surgery. It remains our hope that the reader will continue to find this text relevant both from the perspective of arriving at a diagnosis of a difficult problem, understanding the options and potential outcome of various interventions, as well insight with regard to how surgical techniques might be executed. Bernard F. Morrey, MD

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Acknowledgment I wish to acknowledge with genuine appreciation all the input and insight I received from orthopedic colleagues around the world, especially my colleagues, residents and fellows at the Mayo Clinic. I also wish to express my most sincere appreciation to Professor Gerber for the thoughtful and gracious comments which he made in the “forward” of this edition. The administrative efforts of my associate of 30 years, Bob Adams, to help find that one unique patient or x-ray has always been a tremendous and an essential asset, as is the secretarial and administrative efforts of my secretary, Sherry Koperski, and the numerous details and competencies provided by Donna Riemersma in the preparation of this manuscript. Finally, and as always, I want to expressly acknowledge my wife, Carla, who has now lived through and encouraged me in the preparation of four editions of “Disorders”. I am deeply appreciative of all the support I have received from Carla, our children, and from the profession throughout my career.

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FOREWORD

Via internet we can gain access to almost any medical data within a few mouse clicks. The most recent Journal articles including illustrations are at hand and most data banks allow us to get immediate access to related articles. If ever we decide to review an older publication not yet available in PDF format, it can be ordered within hours or very few days. Details of current surgical techniques are now reviewed in top quality video and DVD productions coming from leading international experts. The question is therefore inevitable whether the concept of a textbook is out of date and in fact, out of place. Unfortunately, many current textbooks are an assiduous compilation of more or less well digested original articles allowing at best for a cookbook approach to orthopaedics. These many textbooks may decorate a bookshelf but add nothing to the impressive number of references they quote and are superfluous. What could the value of a current textbook be and why would we use it? In this period of time, which Kipling characterizes by the probably unassailable lead of knowledge over wisdom, in a time where orthopaedics is taught in “training” programs – although we know that training refers to dogs and education refers to people – we, the upper extremity surgeons who all have a copy of the Third wait for the Fourth (!) Edition of “The Elbow and its Disorders”. Our expectations are living proof that there remains a role for a textbook, because there is a role for education, for educators, as role models who teach medicine based on an immense body of knowledge with wisdom, experience and compassion. There is a role for an instrument which puts scientific knowledge into perspective and helps us to apply knowledge most effectively to our patients. Dr. Morrey has spent decades observing, describing, and defining elbow problems. In a very systematic fashion, he has studied the identified problems with

collaborators and friends in the laboratory, and brought his insight back into clinical practice. Subsequently not only he and his pupils but surgeons throughout the world have validated and do validate the respective contributions in their patients. This textbook incorporates the knowledge gained from these and many other investigations. It discloses details which have taken the authors years to understand and apply. Yes, this textbook is comprehensive andprecise and yes, it certainly is the gold standard for elbow surgery on all continents. But I see the unique value of this book elsewhere. I see it in sharing an approach to clinical problem solving. Dr. Morrey shows how to identify a problem, how to evaluate a problem and finally how to solve it. The text may not be able to impart the human qualities of the editor, which certainly are large contributors of his success with very difficult patient problems. But the text unequivocally clearly states that orthopaedic surgery is not a manual but an intellectual discipline and that excellent orthopaedic care is an art based on science. Bernie, this textbook is a further testimony to you as a physician – scientist, educator and role model. It has been one of the privileges of my lifetime to meet you early in my career and to benefit from your wisdom and advice. For my next elbow problem, I – as many others – will consult this textbook and I am sure it will not only give me data but it will give me understanding. For any other very difficult problem, I hope I can continue to call you. Christian Gerber, MD, FRCS(hon) Professor and Chair Department of Orthopaedics University of Zürich Zürich, Switzerland

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Chapter 1 Phylogeny

CHAPTER

1

Phylogeny Alex A. Malone and Susan G. Larson

INTRODUCTION The human elbow forms the link between brachium and forearm, controlling length of reach and orientation of the hand, and is one of our most distinctive anatomical regions. An appreciation of elbow phylogeny compliments anatomic knowledge in three ways: (1) it demonstrates how the elbow has evolved to facilitate specific functional demands, such as suspensory locomotion and dexterous manipulation; (2) it explains the functional significance of each morphologic feature; and (3) it assists in predicting the consequences of loss of such features through disease, injury, or treatment. Most of the characteristic features of the human elbow significantly predate the appearance of modern Homo sapiens. In fact, current evidence suggests that this morphology can be traced back to the common ancestor of humans and apes, extant about 15 to 20 million years ago (mya).

EVOLUTION OF THE VERTEBRATE ELBOW The distal humerus of pelycosaurs, the late Paleozoic (255 to 235 mya) reptiles that probably gave rise to more advanced mammal-like reptiles, possessed a bulbous capitellum laterally and medially. The articulation with the ulna was formed by two distinct surfaces: a slightly concave ventral surface and a more flat dorsal surface (Fig. 1-1).11 The proximal articular surface of the ulna was similarly divided into two surfaces separated by a low ridge. Reconstruction of the forelimb of these reptiles suggests that they walked with limbs splayed out to the side. The humerus was held more or less horizontal, the elbow flexed to 90 degrees, and the forearm was sagittally oriented. Forward motion was brought about by rotation of the humerus around its long axis, which propelled the body forward relative to the fixed forefoot. Elbow flexion and extension probably were useful only in side-to-side motions. The ulnohumeral joint, with its dual articular surfaces, was well suited to resist the valgus/varus stress produced by humeral

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rotation, and the proximal end of the radius was flat and triangular, precluding pronosupination. It appears, therefore, that stability rather than mobility was the major functional characteristic of the elbow of these late Paleozoic reptiles. Cynodonts, the more immediate ancestors of mammals from the Permo-Triassic period (235 to 160 mya), had their limbs underneath their bodies rather than at the sides. The distal humeral articular surface consisted of radial and ulnar condyles separated by a shallow groove (see Fig. 1-1). The proximal ulnar articular surface was an elongate spoon shape for articulation with the humeroulnar condyle. The lateral flange on the ulna for articulation with the radius was separated from this surface by a low ridge. This ridge articulated with the groove between the radial and ulnar condyles displaying some features in common with the “tongue and groove” (trochleariform) type of humeroulnar articulation characteristic of many modern mammals. Early mammals from the Triassic (210 to 160 mya) and Jurassic (160 to 130 mya) periods also had radial and ulnar condyles. However, the radial condyle was more protuberant than the ulnar, and the ulnar condyle was more linear and obliquely oriented (see Fig. 1-1). The two condyles were separated by an intercondylar groove. The ulnar notch had articular surfaces for both the ulnar and the radial condyles, each matching the configuration of the corresponding humeral surface. The oblique orientation of the humeroulnar joint resembled a spiral configuration, which helped to keep forearm movement in a sagittal plane as the humerus underwent a compound motion involving adduction, elevation, and rotation during propulsion. The trochleariform distal humeral articular surface in modern mammals largely came about by widening the intercondylar groove and the development of a ridge within it (see Fig. 1-1, bear). The articular surface on the proximal ulna is oblique in orientation, and the distal half retains an articulation with the ulnar condyle. This spiral trochlear configuration allows the forearm to move in a sagittal plane while maintaining the stability of ulnohumeral contact through the cam effect of the ulnar condyle during humeral rotation. Most small noncursorial mammals have maintained the spiral configuration of the trochlear articular surface observed in early mammals. In larger and more cursorial mammals, the trochlea displays various ridges and is narrower to improve stability, although at the expense of joint mobility. Only in the hominoid primates, which include humans, chimpanzees, gorillas, orangutans, and gibbons, is the medial aspect of the distal humeral articular surface truly trochleariform. In the next section, we discuss the functional significance of the unique aspects of the hominoid elbow joint.

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Part I Fundamentals and General Considerations

PHYLOGENY Hominoid primate (chimpanzee)

Graviportal mammal (elephant)

Cursorial mammal (gazelle)

Partly terrestrial mammal (bear)

FIGURE 1-1

Generalized mammal (tree shrew)

Prototherian Cretaceous ~100 mya

Jurassic mammal ~155 mya

Late Triassic mammal ~215 mya

Cynodont

Pelycosaur

Early Triassic ~250 mya

Late Paleozoic ~300 mya

COMPARATIVE PRIMATE ANATOMY OF THE ELBOW REGION Much of what follows is taken from the detailed studies of Rose.20,21 The humeral trochlea may be cylindrical, conical, or trochleariform in nonhuman primates.21 The trochlea is conical in some prosimians, but a cylindrical trochlea seems to be the most common shape and is observed in most prosimians and New World monkeys. The trochlea is also cylindrical in most Old World monkeys but with a pronounced medial flange or keel that is best developed anterodistally (Fig. 1-2). Only in apes and humans is the trochlea truly trochleariform, possessing medial and lateral ridges all around the trochlear margins, which contribute to the stability of the ulnohumeral joint, substituting for the radiohumeral joint, which is freed for pronosupination throughout the flexion range.11,20 In most species, the articular surface of

The major evolutionary stages in the development of the elbow joint from pelycosaurs to advanced mammals. The distal ends of the humeri are shown on the left, and the corresponding radius and ulna are on the right. The form of the pelycosaur elbow was designed to maximize stability. Subsequent evolutionary stages show accommodations to increasing mobility. (Adapted from Jenkins, F. A. Jr.: The functional anatomy and evolution of the mammalian humeroulnar articulation. Am. J. Anat. 137:281, 1973.)

the trochlea expands posteriorly to the area behind the capitellum. In larger monkeys, the lateral edge of the posterior trochlear surface projects to form a keel that extends up the lateral wall of the olecranon fossa (see Fig. 1-2). In hominoids, this keel is a continuation of the lateral trochlear ridge and helps form a sharp lateral margin of the olecranon fossa, providing resistance to varus and internal rotation in extension.20.21 The trochlear notch of the ulna generally mirrors the shape of the humeral trochlea. In humans and apes, the notch has medial and lateral surfaces separated by a ridge that articulates with the trochlear groove (Fig. 1-3).20,21 The differences seen in the configuration of the humeroulnar joint across primate species reflect contrasting requirements for stabilization with different forms of limb use. In most monkeys, the humeroulnar joint is in its most stable configuration in a partially

Chapter 1 Phylogeny

BABOON

CHIMPANZEE

5

HUMAN

Anterior

FIGURE 1-2

Lateral trochlear ridge

Zona conoidea

Distal

Posterior keel

Posterior

BABOON

CHIMPANZEE

HUMAN

Long olecranon process

Heavily buttressed coronoid process

FIGURE 1-3

Proximal ulnae of a baboon, a chimpanzee, and a human. The trochlear notch is wider in the chimpanzee and the human and displays a prominent ridge for articulation with the trochlear groove. In addition, the radial notch faces laterally in the chimp and human, unlike in the baboon, in which it faces more anteriorly.

Distal humeri of a baboon, a chimpanzee, and a human from anterior, distal, and posterior aspects. The lateral trochlear ridge is well developed in both the human and the chimpanzee but is largely nonexistent in the baboon. The baboon humerus displays prominent flanges anteromedially and posterolaterally. The lateral epicondyle is placed higher in the chimpanzee than in the human and displays a more strongly developed supracondylar crest.

flexed position owing to the development of the medial trochlear keel anterodistally and the lateral keel posteriorly.20 It is not surprising that this position of maximum stability is the one assumed by the forelimb during the weight-bearing phase of quadrupedal locomotion. The anterior orientation of the trochlear notch is a direct adaptation to weight bearing with a partially flexed limb. However, such an orientation does limit elbow extension to some degree. The great apes (chimpanzees, gorillas, and orangutans) and the lesser apes (gibbons) move about in a much less stereotypical fashion than do monkeys. To accommodate this more varied form of limb use, the hominoid humeroulnar joint, with its deeply socketed articular surfaces and well-developed medial and lateral trochlear ridges all around the joint margins, is designed to provide maximum stability throughout the flexionextension range.20-22 The use of overhead suspensory postures and locomotion in apes has led to the

6

Part I Fundamentals and General Considerations

evolution of the capacity for complete elbow extension. Apes even keep their elbows extended during quadrupedal locomotion. The ideal joint configuration for resistance of transarticular stress with fully extended elbows during quadrupedal postures would be to have a trochlear notch that was proximally directed. It could then act as a cradle to support the humerus during locomotion. However, a proximal orientation of the trochlear notch would severely limit elbow flexion by impingement of the coronoid process within its fossa. The anteroproximal orientation of the trochlear notch in apes thus represents a compromise that safely supports the humerus on the ulna in extended elbow positions during locomotion without unduly sacrificing elbow flexion.1 On the lateral side of the elbow, the articular surface on the capitellum extends farther posteriorly in apes and humans than in monkeys, allowing the radius to move with the ulna into full extension of the elbow. In addition, the capitellum of apes and humans is uniformly rounded, reflecting versatility rather than stereotypy in forelimb usage (Fig. 1-4). The gutter-like region between the trochlea and capitellum—the zona conoidea—is a relatively flat plane that terminates distally in most monkeys. In the hominoids, it continues posteriorly (see Fig. 1-1).20,21 The zona conoidea articulates with the bevel of the radial head, and differences in its configuration reflect differences in the shape of the radial head. The radial head of hominoid primates is nearly circular, and the peripheral rim is symmetrical and beveled all around the circumference of the radial head for articulation with the zona conoidea (Fig. 1-5). This con-

BABOON

CHIMPANZEE

HUMAN

figuration provides good contact to resist dislocation of the radial head from the humerus under the varied loading regimes experienced by the hominoid elbow and can stabilize the radial head in all positions of pronosupination.20,21 In most monkeys and prosimians, the radial head is ovoid and the proximal radioulnar joint articulation is restricted to the anterior and medial surfaces; as a result, the joint becomes close packed for stability in pronation (Fig. 1-6). In apes and humans, on the other hand, this articular surface extends almost all the way around the head, implying a greater range of pronosupination.20 The radial notch of the ulna in most monkeys and prosimians faces either anterolaterally or directly anteriorly, whereas in hominoids, it faces more laterally.20,21 The configuration observed in apes and humans emphasizes a broad range of pronosupination with a nearly equal degree of stability in all positions.20,21 In general terms, most of the differences in elbow joint morphology between quadrupedal monkeys and

Supination

Pronation

Monkey

Ape

Flaring supracondylar crest High lateral epicondyle

FIGURE 1-4

Low and weakly developed lateral epicondyle

Distal humeri of a baboon, a chimpanzee, and a human from the lateral aspect. The articular surface of the capitellum extends further onto the posterior surface of the bone (small arrows) in humans and chimpanzees to permit full extension at the humeroradial joint.

L

FIGURE 1-5

M

Diagrammatic anterior views of the right humeroradial joints of a monkey and an ape in the prone and supine positions. In the monkey, the lateral bevel of the radial head comes into maximum congruence with the zona conoidea (hatched area) in the prone position, thereby creating a maximally stable joint configuration. In the ape, the rim of the more symmetrical radial head maintains good contact with the recessed zona conoidea in all positions of pronosupination. This contributes to a configuration emphasizing universal stability at the ape elbow rather than a position of particular stability, as seen in the monkey. (Adapted from Rose, M. D.: Another look at the anthropoid elbow. J. Hum. Evol. 17:193, 1988.)

Chapter 1 Phylogeny

Supination

7

Pronation

Monkey

Lateral lip

Ape cg

L

M

FIGURE 1-6

Diagrammatic view of the radioulnar joint in pronation and supination in a monkey and an ape. A section through the radius and ulna in the region of the radial notch is superimposed on an outline of the distal humerus. In the monkey, the radial notch faces anterolaterally, whereas in the ape, it faces more directly laterally. The radial head of the monkey with its lateral lip comes into maximum congruence in the pronated position, conferring maximum stability in this position. The ape radioulnar joint, on the other hand, displays no such position of particular stability and instead emphasizes mobility. (Adapted from Rose, M. D.: Another look at the anthropoid elbow. J. Hum. Evol. 17:193, 1988.)

the apes can be related to the development of a position of particular stability in monkeys versus more universal stability in apes. A few additional features of the human elbow are shared with apes, such as a more distal biceps tuberosity (longer radial neck) relative to their body size.21 In apes, this is probably related to the demands for powerful elbow flexion to raise the center of mass of the body during climbing and suspensory postures and locomotion. Although the radial tuberosity faces more or less anteriorly in most primates, it faces more medially in apes and humans, reflecting their greater range of pronosupination.17 Extreme supination is an important component of suspensory locomotion in apes, and the medially placed tuberosity provides maximum supination torque near full supination.14,30 Apes and humans share a relatively short lever arm for triceps compared with that of most other primates, which is generally attributed to the demands for rapid elbow extension during suspensory locomotion. Finally, apes and humans are distinguished from other primate species in possess-

FIGURE 1-7

Frontal view of an arm-swinging gibbon showing the skeletal structure of the forelimb. The carrying angle of the elbow brings the center of mass (i.e., center of gravity [cg]) more nearly directly under the supporting hand. (Adapted from Sarmiento, E. E.: Functional Differences in the Skeleton of Wild and Captive Orang-Utans and Their Adaptive Significance. Ph.D. Thesis, New York University, 1985.)

ing a biomechanical carrying angle at the elbow. Sarmiento22 has argued that the evolution of a carrying angle in apes is related to the need to bring the center of mass of the body beneath the supporting hand during suspensory locomotion in a manner similar to that in which the valgus knee of humans brings the foot nearer the center of mass of the body during the single limb support phase of walking (Fig. 1-7). All of these features have been retained in humans because of their continued advantages for tool use and other behaviors. Powerful flexion is clearly important. The continued importance of the carrying angle is perhaps less obvious, but one advantage that it does offer is that flexion of the elbow is accompanied by adduction of the forearm, thus bringing the hands more in front of the body, where most manipulatory activities are undertaken. The morphology of the modern human elbow is not identical to that of the ape elbow, however. In some cases, the differences are simply a matter of degree. For example, although both apes and humans are

8

Part I Fundamentals and General Considerations

distinguished from other primates in the medial orientation of the radial tuberosity, it is more extreme in position in the ape; in the human it is typically slightly anterior to true medial. In addition, although the olecranon is short in both humans and apes compared with most monkeys, it is slightly longer in humans than in apes and also shaped to maintain this length throughout the range of flexion—both of which are advantageous for powerful manipulatory activities.4 Other differences between the elbow morphology of humans and that of apes can be related to the fact that the human forelimb has no role in locomotion. These differences include a less robust coronoid process and a relatively narrower, proximally oriented trochlear notch in humans, indicating relative stability in flexion rather than the need to support the weight of the body during quadrupedal locomotion in extension.1,13 Humans possess a smaller and more distally placed lateral epicondyle and a less well-developed supracondylar crest than is seen in the apes, reflecting diminished leverage of the wrist extensors and brachioradialis.23-25 Humans have no bowing of the ulna that is related to enhancing the leverage of the forearm pronators and supinators in apes.1 Finally, a diminution in the prominence of the trochlear ridges and steep lateral margin of the olecranon fossa in humans can be related to the overall reduction in stresses at the human elbow and the concomitant relaxation on the demands for strong stabilization in all positions.20,21 When exactly did the basic pattern for the hominoid elbow arise, and how old is the morphology of the modern human elbow? For answers to these questions we must turn to the fossil record.

FOSSIL EVIDENCE Dendropithecus macinnesi, Limnopithecus legetet, and Proconsul heseloni (all from Africa) are among the earliest known hominoid species dated to the early part of the Miocene epoch (23 to 16 mya) for which postcranial material is known. Overall, the distal humeri of the first two of these forms resemble generalized New World monkeys such as Cebus (capuchin monkeys). The trochlea does not display a prominent lateral ridge, and the zona conoidea is relatively flat. The trochlear notch faces anteriorly, and the head of the radius is oval in outline with a well-developed lateral lip. These features generally are considered to be primitive for higher primates (monkeys, apes, and humans).8,9,20 P. heseloni, on the other hand, does display some features characteristic of extant hominoids. It has a globular capitellum, well-developed medial and lateral trochlear ridges, and a deep zona conoidea forming the medial wall of a recessed gutter between the capitellum and

trochlea.20 In general, the elbow region of Proconsul resembles that of extant hominoids in features related to general stability and range of pronosupination; yet full pronation remained a position of particular stability.20 The limited fossil material that is available from the late Miocene epoch (16 to 5 mya) suggests that many hominoid species, including members of the genera Dryopithecus (from Europe), Sivapithecus (from Europe and Asia), and Oreopithecus (from Europe), displayed the features characteristic of the modern hominoid elbow. Although it is possible that these features arose in parallel in different genera, the more parsimonious explanation is that they inherited this morphology from an early to middle Miocene common ancestor, possibly similar to P. heseloni.16,29,31 Assuming that the characteristic features of the hominoid elbow are shared derived traits, that is, traits inherited from a single common ancestor, we can say that the elbow morphology of modern apes and humans can be dated to roughly 15 to 20 mya. The majority of paleoanthropologists agree that humans are most closely related to the African apes (chimpanzees and gorillas) and that the two lineages arose in the late Miocene or earliest Pliocene period (between 10 and 4 mya).8 The earliest known fossils of the human lineage (hominids) date from the early Pliocene era, approximately 4 to 5 mya. There are three genera of these earliest hominids currently recognized, Ardipithecus, Paranthropus, and Australopithecus. The latter is the best known and most widespread genus, and includes the famous “Lucy” skeleton from Hadar, Ethiopia (A. afarensis).5,12 The genus Homo, to which our own species belongs, first appeared about 2.5 to 2 mya in East Africa with its earliest member species, H. habilis. All of the hominids from the Pliocene period were bipedal, although some probably spent significant time climbing trees.23-26,28 The development of bipedalism freed the upper extremity from the requirements of locomotion, placing greater emphasis on increasing mobility. The ability to supinate and pronate was an immense advantage to hominids in caring for their young, defending themselves, and gathering food. It was also critical in efficient tool handling, which developed approximately 2 mya, at about the same time as H. habilis, although there is debate about which species of early hominid was responsible for making them.27 Several distal humeri are known from these early hominid species. All of the early hominid distal humeri lack the steep lateral margin of the olecranon fossa that is characteristic of chimpanzees and gorillas. However, they do show a considerable amount of morphologic variation in other characteristics (Fig. 1-8). On the basis of the contour of the distal end of the humeral shaft,

Chapter 1 Phylogeny

9

PHYLOGENY

AL 288-1m

KNM-ER 739

Gombore IB 7594

FIGURE 1-8

Distal humeri of Plio-Pleistocene hominids. Gombore IB 7594 represents early Homo on the basis of the moderate development of the lateral trochlear ridge and low position of the lateral epicondyle. AL 288-1m (part of the “Lucy” skeleton, Australopithecus afarensis) displays a more prominent lateral trochlear ridge, a recessed, gutter-like zona conoidea, a high position of the lateral epicondyle, and a well-developed supracondylar crest. Therefore, it resembles living apes in many features of its elbow morphology. KNM-ER 739 has been attributed to Paranthropus boisei and, like AL 288-1m, has a lateral epicondyle that is positioned above the articular surfaces. However, it is more like Homo, with the moderate development of the lateral trochlear ridge.

the placement of the epicondyles, and the configuration of the articular surface, the fossil distal humeri have been divided into two groups. The first group is characterized by a weakly projecting lateral epicondyle that is placed low, at about the level of the capitellum, and by a moderately developed lateral trochlear ridge.23,24 These are features shared with modern humans, and consequently, this group generally is referred to as early Homo. The second group includes the Australopithecus and Paranthropus species and is characterized by a well-developed lateral epicondyle that is high relative to the capitellum. These features are similar to those of modern apes. A number of fragments of early hominid proximal radii have been recovered representing each of the currently recognized species. The proximal radial fragments that have been attributed to early Homo display a much narrower bevel around the capitellar fovea than that of the modern apes and the earlier hominin group. This provides for articulation with a more shallow zona conoidea and a more vertical and uniformly wide surface on the side of the head for articulation with the ulna favoring pronosupination over stability. Other primitive hominoid features include thick cortices, a relatively long and angulated radial neck (lower neck shaft angle), and a more anteromedially (rather than medially) placed biceps tuberosity. Many of these features are still present in a small percentage of modern humans, limiting the functional conclusions that can be drawn and suggesting a mosaic pattern of evolution.18,19 Some early hominid ulnae that have been recovered appear to retain many primitive features including a

longer more curved shaft, greater mediolateral width proximally, and a nonprominent interosseous border.1,2,10 However, early human ulnae attributed to the genus Homo are similar to those of modern humans in having a prominent interosseous border, a supinator crest, and a well-marked hollow for the play of the tuberosity of the radius.6,7,15 It appears, therefore, that many of the characteristics that distinguish the human elbow from that of the ape can be found in the earliest members of our genus. In overview, the combination of comparative anatomy and the fossil record indicates that the modern human elbow owes its beginnings to our hominoid ancestry. Current evidence suggests that many of the characteristic features of the human distal humerus and proximal radius and ulna can be projected back approximately 15 to 20 mya to a common ancestor of extant apes and humans. Functional analysis suggests that this morphologic structure arose in hominoid primates in response to the need for stabilization throughout the flexionextension and pronosupination ranges of motion to permit a more versatile form of forelimb use. This morphology was still largely intact following the evolution of upright posture and bipedal locomotion in the earliest known hominids. However, as the forelimb became less and less involved in locomotion, the hominid elbow underwent additional modifications, relaxing some of the emphasis on stabilization and increasing performance throughout the range of movement. The fossil record indicates that the distinct form of the modern human elbow probably first appeared about 2 mya in

10

Part I Fundamentals and General Considerations

our ancestor H. habilis. This morphology has changed only subtly during all subsequent stages of human evolution.

Acknowledgments SGL would like to thank Jack Stern and John Fleagle for helpful comments on earlier versions of this chapter, and Luci Betti-Nash for the preparation of figures.

The references in this chapter which suggest the evolution of the human from a lower form are not accepted by and do not express the views of all of the contributors of this book.

References 1. Aiello, L. C., and Dean, M. C.: An Introduction to Human Evolutionary Anatomy. London, Academic Press, 1990. 2. Churchill, S. E., Pearson, O. M., Grine, F. E., Trinkaus E., and Holliday T. W.: Morphological affinities of the proximal ulna from Klasies River main site: archaic or modern? J. Hum. Evol. 31:213, 1996 3. Conroy, G. C.: Primate Evolution. New York, W. W. Norton & Co., 1990. 4. Drapeau, M. S.: Functional anatomy of the olecranon process in hominoids and Plio-Pleistocene hominins. Am. J. Phys. Anthropol. 124:297, 2004 5. Drapeau, M. S., Ward, C. V., Kimbel, W. H., Johanson, D. C., and Rak, Y.: Associated cranial and forelimb remains attributed to Australopithecus afarensis from Hadar, Ethiopia. J. Hum. Evol. 48:593, 2005. 6. Day, M. H.: Functional interpretations of the morphology of postcranial remains of early African hominids. In Jolly, C. J. (ed): Early Hominids of Africa. London, Duckworth, 1978, p. 311. 7. Day, M. H., and Leakey, R. E. F.: New evidence for the genus Homo from East Rudolf, Kenya III. Am. J. Phys. Anthropol. 39:367, 1974. 8. Fleagle, J. G.: Primate Adaptation and Evolution, 2nd ed. New York, Academic Press, 1999. 9. Harrison, T.: The phylogenetic relationships of the early catarrhine primates: a review of the current evidence. J. Hum. Evol. 16:41, 1987. 10. Howell, F. C., and Wood, B. A.: Early hominid ulna from the Omo Basin, Ethiopia. Nature 249:174, 1974. 11. Jenkins, F. A. Jr.: The functional anatomy and evolution of the mammalian humeroulnar articulation. Am. J. Anat. 137:281, 1973. 12. Johanson, D. C., Lovejoy, C. O., Kimbel, W. H., White, T. D., Ward, S. C., Bush, M. E., Latimer, B. M., and Coppens, Y.: Morphology of the Pliocene partial hominid skeleton (A.L. 288-1) from the Hadar Formation, Ethiopia. Am. J. Phys. Anthropol. 57:403, 1982.

13. Knussmann, R.: Humerus, Ulna and Radius der Simiae. Bibliotheca Primatologica, Vol. 5. Basel, S. Karger, 1967. 14. Larson, S. G.: Subscapularis function in gibbons and chimpanzees: implications for interpretation of humeral head torsion in hominoids. Am. J. Phys. Anthropol. 76:449, 1988. 15. Leakey, R. E. F.: Further evidence of lower Pleistocene hominids from East Rudolf, Northern Kenya. Nature 237:264, 1972. 16. Martin, L., and Andrews, P.: Cladistic relationships of extant and fossil hominoids. J. Hum. Evol. 16:101, 1987. 17. O’Connor, B. L., and Rarey, K. E.: Normal amplitudes of radioulnar pronation and supination in several genera of anthropoid primates. Am. J. Phys. Anthropol. 51:39, 1979. 18. Patel, B. A. The hominoid proximal radius: re-interpreting locomotor behaviors in early hominins. J. Hum. Evol. 48:415, 2005. 19. Pearson, O. M., and Grine, F. E.: Re-analysis of the hominid radii from Cave of Hearths and Klasies River Mouth, South Africa. J. Hum. Evol. 32:577, 1997. 20. Rose, M. D.: Another look at the anthropoid elbow. J. Hum. Evol. 17:193, 1988. 21. Rose, M. D.: Functional anatomy of the elbow and forearm in primates. In Gebo, D. (ed.): Postcranial Adaptation in Nonhuman Primates. DeKalb, IL, Northern Illinois Press, 1993, p. 70. 22. Sarmiento, E. E.: Functional Differences in the Skeleton of Wild and Captive Orang-Utans and Their Adaptive Significance. Ph.D. Thesis, New York University, 1985. 23. Senut, B.: Outlines of the distal humerus in hominoid primates: application to some Plio-Pleistocene hominids. In Chiarelli A. B., and Corruccini, R. (eds.): Primate Evolutionary Biology. Berlin, Springer Verlag, 1981, p. 81. 24. Senut, B.: Humeral outlines in some hominoid primates and in Plio-Pleistocene hominids. Am. J. Phys. Anthropol. 56:275, 1981. 25. Senut, B., and Tardieu, C.: Functional aspects of PlioPleistocene hominid limb bones: implications for taxonomy and phylogeny. In Delson, E. (ed.): Ancestors: The Hard Evidence. New York, A. Liss, 1985, p. 193. 26. Stern, J. T. Jr., and Susman, R. L.: The locomotor anatomy of Australopithecus afarensis. Am. J. Phys. Anthropol. 60:279, 1983. 27. Susman, R. L.: Fossil evidence for early hominid tool use. Science 265:1570, 1994. 28. Susman, R. L., Stern, J. T. Jr., and Jungers, W. L.: Arboreality and bipedality in Hadar hominids. Folia Primatol. 43:113, 1984. 29. Szalay, F. S., and Delson, E.: Evolutionary History of the Primates. New York, Academic Press, 1979. 30. Trinkaus, E, and Churchill, S. E. Neandertal radial tuberosity orientation. Am. J. Phys. Anthropol. 75:15, 1988. 31. Ward, C. V., Walker, A., and Teaford, M. F.: Proconsul did not have a tail. J. Hum. Evol. 21:215, 1991.

Chapter 2 Anatomy of the Elbow Joint

CHAPTER

2

Anatomy of the Elbow Joint Bernard F. Morrey

11

neus, extensor carpi ulnaris, extensor digitorum quinti, and extensor digitorum communis. Dermal innervation about the proximal elbow is rather variable being provided by the lower lateral cutaneous (C5, C6) and medial cutaneous (radial nerve, C8, T1 and T2) nerves of the arm. The forearm skin is innervated by the medial (C8, T1), lateral (musculocutaneous, C5, C6), and posterior (radial nerve, C6-8) cutaneous nerves of the forearm (Fig. 2-4).

OSTEOLOGY This chapter discusses the normal anatomy of the elbow region. Abnormal and surgical anatomy is addressed in subsequent chapters of this book dealing with the pertinent condition.

TOPICAL ANATOMY AND GENERAL SURVEY The contours of the biceps muscle and antecubital fossa are easily observed anteriorly. Laterally, the avascular interval between the brachioradialis and the triceps, the so-called column, is an important palpable landmark for surgical exposures (Fig. 2-1). Laterally, the tip of the olecranon, the lateral epicondyle, and the radial head also form an equilateral triangle and provide an important landmark for joint aspiration and for elbow arthroscopy (see Chapters 37 and 77). The flexion crease of the elbow is in line with the medial and lateral epicondyles and thus is actually 1 to 2 cm proximal to the joint line when the elbow is extended (Fig. 2-2). The inverted triangular depression on the anterior aspect of the extremity distal to the epicondyles is called the cubital (or antecubital) fossa. The superficial cephalic and basilic veins are the most prominent superficial major contributions of the anterior venous system and communicate by way of the median cephalic and median basilic veins to form an “M” pattern over the cubital fossa (Fig. 2-3). The extensor forearm musculature originates from the lateral epicondyle and was termed the mobile wad by Henry.37 This forms the lateral margin of the antecubital fossa and the lateral contour of the forearm and comprises the brachioradialis and the extensor carpi radialis longus and brevis muscles. The muscles comprising the contour of the medial anterior forearm include the pronator teres, flexor carpi radialis, palmaris longus, and flexor carpi ulnaris. Henry has demonstrated that their relationship and location can be approximated by placing the opposing thumb and the index, long, and ring fingers over the anterior medial forearm. The dorsum of the forearm is contoured by the lateral extensor musculature, consisting of the anco-

HUMERUS The distal humerus consists of an arch formed by two condyles that contain the articular surfaces of the trochlea and capitellum (Fig. 2-5). Medial to the trochlea, the prominent medial epicondyle serves as a source of attachment of the medial ulnar collateral ligament and the flexor-pronator group of muscles. Laterally, the lateral epicondyle is located just proximal to the capitellum and is much less prominent than the medial epicondyle. The lateral ulnar collateral ligament and the supinator-extensor muscle group originate from the flat, irregular surface of the lateral epicondyle. Anteriorly, the radial and coronoid fossae accommodate the radial head and coronoid process during flexion. Posteriorly, the olecranon fossa receives the tip of the olecranon. In about 90% of individuals,86 a thin membrane of bone separates the olecranon and coronoid fossae (Fig. 2-6). The medial supracondylar column is smaller than the lateral and explains the vulnerability of the medial column to fracture with trauma and some surgical procedures.56 The posterior aspect of the lateral supracondylar column is flat, allowing ease of application of contoured plates (see Chapter 22). The prominent lateral supracondylar ridge serves as attachment for the brachioradialis and extensor carpi radialis longus muscles anteriorly and for the triceps posteriorly. It is also an important landmark for many lateral surgical approaches especially for the “column procedure” (see Chapters 7 and 32). Proximal to the medial epicondyle, about 5 to 7 cm along the medial intramuscular septum, a supracondylar process is observed in 1% to 3% of individuals45,49,81 (Fig. 2-7). A fibrous band termed the ligament of Strothers may originate from this process and attach to the medial epicondyle.38 When present, this spur serves as an anomalous insertion of the coracobrachialis muscle and an origin of the pronator teres muscle.34 Various pathologic processes have been associated with the supracondylar process, including fracture45 and median4 and ulnar nerve38 entrapment (see Chapter 80).

12

Part I Fundamentals and General Considerations

RADIUS

FIGURE 2-1

The palpable landmarks of the tip of the olecranon and the medial and lateral epicondyles form an inverted triangle posteriorly when the elbow is flexed 90 degrees but are colinear when the elbow is fully extended. (Redrawn from Anson, B. J., and McVay, C. B.: Surgical Anatomy, Vol. 2, 5th ed. Philadelphia, W. B. Saunders Co., 1971.)

The radial head defines the proximal radius and articulates with the capitellum. It exhibits a cylindrical shape with a depression in the midportion to accommodate the capitellum. The disc-shaped head is secured to the ulna by the annular ligament (Fig. 2-8). Distal to the radial head, the bone tapers to form the radial neck, which, along with the head, is vulnerable to fracture.83 The radial tuberosity marks the distal aspect of the neck and has two distinct parts. The anterior surface is covered by a bicipitoradial bursa protecting the biceps tendon during full pronation (Fig. 2-9). However, it is the rough posterior aspect that provides the site of attachment of the biceps tendon. During full pronation the tuberosity is in a dorsal position and allows repair of a ruptured biceps tendon through a posterior approach12 (see Chapter 34) and is helpful to determine axial alignment of proximal radial fractures.26

ULNA The proximal ulna provides the greater sigmoid notch (incisura semilunaris), which serves as the major articulation of the elbow that is responsible for its inherent

FIGURE 2-2

A line placed over the flexion crease (A) is actually situated about 1 cm above the elbow joint line (B).

Chapter 2 Anatomy of the Elbow Joint

13

Fascia brachii V. basilica humeri

V. cephalica humeri

N. cutaneus M. biceps brachii M. pronator teres Lacertus fibrosus M. flexor carpi radialis V. mediana cephalica V. mediana basilica N. cutaneous antibrachii lateralis

M. pronator teres

V. basilica antibrachii

V. mediana antibrachii V. cephalica antibrachii Ramus anastomoticus

M. flexor carpi radialis

Fascia antibrachii

FIGURE 2-3

The superficial venous pattern of the anterior aspect of the elbow demonstrates a rather characteristic inverted M pattern formed by the median cephalic and median basilic veins. (Redrawn from Anson, B. J., and McVay, C. B.: Surgical Anatomy, Vol. 2, 5th ed. Philadelphia, W. B. Saunders Co., 1971.)

Lateral supraclavicular (C. 3 and 4) Axillary (C. 5 and 6)

Lateral supraclavicular (C. 3 and 4)

Medial cutaneous of arm (T. 1 and 2) and intercostobrachial (T. 2)

Medial cutaneous of arm and intercostobrachial (T. 1 and 2)

Lower lateral cutaneous of arm (radial, C. 5 and 6) Lateral cutaneous of forearm (musculocutaneous, C. 5 and 6) Radial (C. 7 and 8)

Axillary (C. 5 and 6) Posterior cutaneous of arm (radial) Lower lateral cutaneous of arm (radial)

Medial cutaneous of forearm Medial cutaneous of forearm (C. 8, T. 1)

Ulnar (C. 7 and 8)

Radial

Posterior cutaneous of forearm (radial) Lateral cutaneous of forearm (musculocutaneous)

Median (C. 6, 7 and 8) Ulnar

A

FIGURE 2-4

B

Median

Typical distribution of the cutaneous nerves of the anterior (A) and posterior (B) aspects of the upper limb. (Redrawn from Cunningham, D. J.: In G. J. Romanes (ed.): Textbook of Anatomy, 12th ed. New York, Oxford University Press, 1981.)

14

Part I Fundamentals and General Considerations

Groove for the radial n.

Lateral supracondylar ridge

Lateral epicondyle

Coronoid fossa Medial epicondyle

Radial fossa Capitellum

FIGURE 2-5

The bony landmarks of the anterior aspect of the distal humerus.

Trochlea

Groove for the radial n.

Lateral supracondylar ridge Medial supracondylar column Lateral supracondylar column Olecranon fossa

FIGURE 2-6 Sulcus for ulnar n.

The prominent medial and lateral supracondylar bony columns as well as other landmarks of the posterior aspect of the distal humerus.

Chapter 2 Anatomy of the Elbow Joint

Radial head

15

Articular margin

Radial neck

Tuberosity

FIGURE 2-8

Proximal aspect of the radius demonstrating the articular margin for articulation with the olecranon, the radial neck, and tuberosity.

FIGURE 2-7

Typical supracondylar process located approximately 5 cm proximal to the medial epicondyle with its characteristic configuration.

Radiohumeral B.

Supinator B. Cubital interosseus B.

Bicipital radial B.

FIGURE 2-9

A deep view of the anterior aspect of the joint revealing the submuscular bursa present about the elbow joint.

16

Part I Fundamentals and General Considerations

Guiding ridge

Greater sigmoid notch Coronoid Radial notch

Transverse groove of greater sigmoid notch Tubercle

Supinator crest and tuberosity

Olecranon

Ulnar tuberosity

B FIGURE 2-10

A stability (Fig. 2-10). The cortical surface of the coronoid process serves as the site of insertion of the brachialis muscle and of the oblique cord. Medially the sublime tubercle serves as insertion site of the medial ulnar collateral ligament. The triceps tendon attaches to the posterior aspect of the olecranon process. On the lateral aspect of the coronoid process, the lesser semilunar or radial notch articulates with the radial head and is oriented roughly perpendicular to the long axis of the bone. Distal to this the supinator crest serves as attachment to the supinator muscle, a tuberosity occurs on this crest, which is the site of insertion of the lateral ulnar collateral ligament.52,56,66

ELBOW JOINT STRUCTURE ARTICULATION The elbow joint articulation is classified as a trochoginglymoid joint.77 The ulnohumeral joint resembles a hinge (ginglymus), allowing flexion and extension. The radiohumeral and proximal radioulnar joint allows axial rotation or a pivoting (trochoid) type of motion.

Humerus The trochlea is the hyperboloid, pulley-like surface that articulates with the semilunar notch of the ulna covered by articular cartilage through an arc of 300 degrees42,73,77 (Fig. 2-11). The medial contour is larger and projects more distally than does the lateral portion of the trochlea (Fig. 2-12). The two surfaces are separated by a groove that courses in a helical manner from an anterolateral to a posteromedial direction. The capitellum is almost spheroidal in shape and is covered with hyaline cartilage, which is about 2 mm thick anteriorly. A groove separates the capitellum from the trochlea, and the rim of the radial head articulates with this groove throughout the arc of flexion and during pronation and supination.

A, Anterior aspect of the proximal ulna demonstrating the greater sigmoid fossa with the central groove. B, Lateral view with landmarks.

In the lateral plane, the orientation of the articular surface of the distal humerus is rotated anteriorly about 30 degrees with respect to the long axis of the humerus (Fig. 2-13). The center of the concentric arc formed by the trochlea and capitellum is on a line that is coplanar to the anterior distal cortex of the humerus.58 In the transverse plane, the articular surface and axis of rotation is rotated inward approximately 5 degrees (Fig. 2-14), and in the frontal plane, it is tilted approximately 6 degrees in valgus43,47,80 (Fig. 2-15).

Proximal Radius Hyaline cartilage covers the depression of the radial head, which has an angular arc of about 40 degrees,77 as well as approximately 240 degrees of articular cartilage that articulates with the ulna, hence approximately 120 degrees of the radial circumference is not articular and amenable to open reduction internal fixation (ORIF) for fracture16 (Fig. 2-16). The lesser sigmoid fossa forms an arc of approximately 60 to 80 degrees,42,77 leaving an excursion of about 180 degrees for pronation and supination. The anterolateral third of the circumference of the radial head is void of cartilage. This part of the radial head lacks subchondral bone and thus is not as strong as the part that supports the articular cartilage; this part has been demonstrated to be the portion most often fractured.83 The head and neck are not co-linear with the rest of the bone and form an angle of approximately 15 degrees, with the shaft of the radius directed away from the radial tuberosity28 (Fig. 2-17).

Proximal Ulna In most individuals, a transverse portion of nonarticular cartilage divides the greater sigmoid notch into an anterior portion comprising the coronoid and the posterior olecranon (Fig. 2-18). In the lateral plane, the sigmoid notch forms an arc of about 190 degrees.74 The contour is not a true hemicircle but rather is elipsoid. This explains the articular void in the midportion.85

Chapter 2 Anatomy of the Elbow Joint

Corpus humeri

M. brachialis M. biceps brachii Lig. anterius Fat pad

M. triceps brachii Lig. posterius

M. pronator teres

Synchondrosis epiphyseos

N. medianus A. et V. brachialis

Trochlea

M. flexor digitorum sublimis Processus coronoideus M. flexor digitorum profundus

Pars fibrosa Pars synovialis Bursa subtendinea olecrani Cavum articulare

Capsula articularis

Incisura semilunaris ulnae Ulna

Olecranon Synchondrosis epiphyseos ulnae Bursa subcutanea olecrani

M. anconaeus

Trochleocapitellar groove

Tubercle of trochlea

17

FIGURE 2-11

Sagittal section through the elbow region, demonstrating the high degree of congruity. (Redrawn from Anson, B. J., and McVay, C. B.: Surgical Anatomy, Vol. 2, 5th ed. Philadelphia, W. B. Saunders Co., 1971.)

Trochlear groove

Medial lip Lateral lip

FIGURE 2-12

Axial view of the distal humerus shows the isometric trochlea as well as the anterior position of the capitellum. The trochlear capitellar groove separates the trochlea from the capitellum.

The orientation of the articulation is oriented approximately 30 degrees posterior to the long axis of the bone (Fig. 2-19). This matches the 30 degrees anterior angulation of the distal humerus, providing stability in full extension (see Chapter 3). In the frontal plane, the shaft is angulated from about 1 to 6 degrees43,47,73 lateral to the articulation (Fig. 2-20). This angle contributes, in part, to the variation of the carrying angle, which is discussed in Chapter 3. The lesser sigmoid notch consists of a depression with an arc of about 70 degrees and is situated just distal to the lateral aspect of the coronoid and articulates with the radial head.

30˚

FIGURE 2-13

Lateral view of the humerus shows the 30degree anterior rotation of the articular condyles with respect to the long axis of the humerus.

CARRYING ANGLE The so-called carrying angle is the angle formed by the long axes of the humerus and the ulna with the elbow fully extended (Fig. 2-21). In men, the mean carrying angle is 11 to 14 degrees, and in women, it is 13 to 16 degrees.3,43,69 Furthermore, the carrying angle is approxi-

Part I Fundamentals and General Considerations

18

Olecranon Articular circumference 5˚

Head of radius Trochlear notch of ulna

FIGURE 2-14

Axial view of the distal humerus demonstrates the 5- to 7-degree internal rotation of the articulation in reference to the line connecting the midportions of the epicondyles.

Coronoid process

Annular ligament Tuberosity of radius

Radius

Ulna

FIGURE 2-16

Hyaline cartilage covers approximately 240 degrees of the outside circumference of the radial head, allowing its articulation with the proximal ulna at the radial notch of the ulna. (Redrawn from Langman, J., and Woerdeman, M. W.: Atlas of Medical Anatomy. Philadelphia, W. B. Saunders Co., 1976.)

15˚

6˚

FIGURE 2-15

There is approximately a 6- to 8-degree valgus tilt of the distal humeral articulation with respect to the long axis of the humerus.

mately 1 degree greater in the dominant than nondominant side.88

JOINT CAPSULE The anterior capsule inserts proximally above the coronoid and radial fossae (Fig. 2-22). Distally, the capsule attaches to the anterior margin of the coronoid medially as well as to the annular ligament laterally. Posteriorly, the capsule attaches just above the olecranon fossa, distally along the supracondylar bony columns. Distally, attachment is along the medial and lateral articular margin of the sigmoid notch. The greatest capacity of

FIGURE 2-17

The neck of the radius makes an angle of approximately 15 degrees with the long axis of the proximal radius.

the elbow occurs at about 80 degrees of flexion40,70 and is 25 to 30 mL.70 The anterior capsule is normally a thin transparent structure but significant strength is provided by transverse and obliquely directed fibrous bands23,56 (Fig. 2-23).

Chapter 2 Anatomy of the Elbow Joint

19

4˚

3

63

32

2

FIGURE 2-18

The relative percentage of hyaline cartilage distribution at the proximal ulna. (Redrawn from Tillmann, B.: A Contribution to the Function Morphology of Articular Surfaces. Translated by G. Konorza. Stuttgart, George Thieme, Publishers; P. S. G. Publishing Co., Littleton, Mass., 1978.)

30˚

FIGURE 2-19

The greater sigmoid notch opens posteriorly with respect to the long axis of the ulna. This matches the 30-degree anterior rotation of the distal humerus, as shown in Figure 2-13.

The anterior structure is, of course, taut in extension but becomes lax in flexion. The joint capsule is innervated by highly variable branches from all major nerves crossing the joint, including the contribution from the musculoskeletal nerve (Fig. 2-24).

LIGAMENTS The collateral ligaments of the elbow are formed by specialized thickenings of the medial and lateral capsules.

FIGURE 2-20

There is a slight (approximately 4 degrees) valgus angulation of the shaft of the ulna with respect to the greater sigmoid notch.

Medial Collateral Ligament Complex The medial collateral ligament consists of three parts: anterior, posterior, and transverse segments (Fig. 2-25). The anterior bundle is the most discrete component, the posterior portion being a thickening of the posterior capsule, and is well defined only in about 90 degrees of flexion. The transverse component (ligament of Cooper) appears to contribute little or nothing to elbow stability. The ligament originates from a broad anteroinferior surface of the epicondyle.65 The ulnar nerve rests on the posterior aspect of the medial epicondyle but is not intimately related to the fibers of the anterior bundle of the medial collateral ligament itself. This has obvious implications with regard to the treatment of ulnar nerve decompression by medial epicondylar ostectomy. A more obliquely oriented excision might be most appropriate to both decompress the ulnar nerve and preserve the collateral ligament origin. On the lateral projection, the origin of the anterior bundle of the medial collateral ligament is precisely at the axis of rotation at the anterior, inferior margins of the medial epicondyle62 (Fig. 2-26). The posterior bundle inserts along the midportion of the medial margin of the semilunar notch. The width of the anterior bundle is approximately 4 to 5 mm compared with 5 to 6 mm at the midportion of the fan-shaped posterior segment.56 Recently ultrasound assessment has proved helpful in further documenting the dimensions of these structures.61

20

Part I Fundamentals and General Considerations

FIGURE 2-21

21

16

10

5

0

Fibrous capsule

The carrying angle is formed by the variable relationship of the orientation of the humeral articulation referable to the long axis of the humerus and the valgus angular relationship of the greater sigmoid fossa referable to the long axis of the ulna. (Redrawn from Lanz, T., and Wachsmuth, W.: Praktische Anatomie. ARM, Berlin, Springer, 1959.)

Medial epicondyle

Lateral epicondyle Ant. part of ulnar collateral ligament

Radial collateral ligament Annular ligament Sacciform recess

Oblique cord

Tuberosity of radius Ulna

A

B

FIGURE 2-22

Distribution of the synovial membrane from the posterior aspect, demonstrating the presence of the synovial recess under the annular ligament and about the proximal ulna. (Redrawn from Beethman, W. P.: Physical Examination of the Joints. Philadelphia, W. B. Saunders Co., 1965.)

The function of the ligamentous structures is discussed in detail below. Clinically and experimentally, the anterior bundle is clearly the major portion of the medial ligament complex59 and has been divided into anterior, posterior and deep medial subcomponents.62

Lateral Ligament Complex Unlike the medial collateral ligament complex, with its rather consistent pattern, the lateral ligaments of the elbow joint are less discrete, and individual variation is

FIGURE 2-23

There is a cruciate orientation of the fibers of the anterior capsule that provides a good deal of its strength. (Redrawn from Langman, J., and Woerdeman, M. W.: Atlas of Medical Anatomy. Philadelphia, W. B. Saunders Co., 1978.)

common.30,31,40,75 Our investigation has suggested that several components make up the lateral ligament complex: (1) the radial collateral ligament, (2) the annular ligament, (3) a variably present accessory lateral collateral ligament, and (4) the lateral ulnar collateral ligament. These observations have now been confirmed by others. The current thinking is to consider the complex to be roughly in the shape “Y,” the arms of which attach to the anterior and posterior aspect of the semilunar notch13,72 (Fig. 2-27).

Chapter 2 Anatomy of the Elbow Joint

21

Musculocutaneous

Median Ulnar

Radial To anconeus

FIGURE 2-24

Left posterior

Left anterior

A typical distribution of the contributions of the musculocutaneous radial median and ulnar nerves to the joint capsule. (Redrawn from Gardner, E.: The innervation of the elbow joint. Anat. Rec. 102:161, 1948.)

Anterior bundle

Posterior bundle

Transverse ligament

FIGURE 2-25

The classic orientation of the medial collateral ligament, including the anterior and posterior bundles, and the transverse ligament. This last structure contributes relatively little to elbow stability.

Radial Collateral Ligament This structure originates from the lateral epicondyle and is actually a complex of several components (Fig. 2-28). Its superficial aspect provides a source of origin for a portion of the supinator muscle. The length averages approximately 20 mm with a width of approximately 8 mm. This portion of the ligament is almost uniformly taut throughout the normal range of flexion and extension, indicating that the origin of the ligament is very near the axis of flexion (Fig. 2-29).

FIGURE 2-26

The origin of the medial complex is at the axis of rotation, which is located at the anterior inferior aspect of the medial epicondyle. This is the projected center of the trochlea.

A strong band of tissue originating and inserting on the anterior and posterior margins of the lesser sigmoid notch forms the annular ligament and maintains the radial head in contact with the ulna. The ligament is tapered distally to give the shape of a funnel

Annular Ligament

22

Part I Fundamentals and General Considerations

FIGURE 2-27

Dissection demonstrating the “Y” orientation of the lateral collateral ligament complex.

FIGURE 2-29

The lateral collateral complex originates at the center of the lateral epicondyle.

Radial collateral ligament

Annular ligament Accessory collateral ligament

Lateral ulnar collateral ligament

FIGURE 2-28

Schematic representation of the radial collateral ligament complex showing several portions, one of which, termed the radial collateral ligament, extends from the humerus to the annular ligament. This is the portion that is implicated in clinical instability.

and contributes about four fifths of the fibro-osseous ring.52 The structure is not as simple as it appears because fibers arc medially and laterally to secure the annular ligament to the ulna.72 A synovial reflection extends distal to the lower margin of the annular ligament, forming the sacciform recess. The radial head is not a pure circular disc76; thus, it has been observed that the anterior insertion becomes taut during supination and the posterior aspect becomes taut during extremes of pronation.88 In 1985 Morrey and An first described the so-called lateral ulnar collateral ligament.56 Before this, however, Martin had

described a lateral ligament complex including “ . . . additional fibers inserting from the tubercle of the supinator crest to the humerus.” This structure subsequently has been demonstrated to be invariably present and critically important clinically. It originates from the lateral epicondyle and blends with the fibers of the annular ligament arching superficial and distal to it.66 The insertion is at the tubercle of the crest of the supinator on the ulna. Although the origin blends with the origin of the lateral collateral ligament complex occupying the posterior portion, the insertion is more discrete at the tubercle (Fig. 2-30). The function of this ligament is to provide stability to the ulnohumeral joint and was shown to be deficient in posterolateral rotatory instability of the joint.64,65 As confirmed by several subsequent assessments, the key factor is that this ligament represents the primary lateral stabilizer of the elbow and is taut in flexion and extension (Fig. 2-31). Accessory Lateral Collateral Ligament This definition has been applied by Martin to the ulnar insertion of discrete fibers on the tubercle of the supinator as described previously. Others have termed this the lateral arm of the “Y” ligament.72 Proximally, the fibers tend to blend with the inferior margin of the annular ligament (see Fig. 2-27). Its function is to further stabilize the annular ligament during varus stress.

Lateral Ulnar Collateral Ligament

A thin, fibrous layer covering the capsule between the inferior margin and the annular Quadrate Ligament

Chapter 2 Anatomy of the Elbow Joint

23

Radial collateral ligament Lateral ulnar collateral ligament

FIGURE 2-30

Artist’s rendition of lateral collateral complex noting the thickening of the lateral ulnar collateral ligament with a more discrete insertion at the tubercle of the supinator. In life, the supinator origin obscures the ligament, making it unnoticeable unless the supinator muscle has been removed. (From Pede.)

ligament and the ulna is referred to as the quadrate ligament20,60 or the ligament of Denucè.76 Spinner and Kaplan have demonstrated a functional role for the structure, describing the anterior part as a stabilizer of the proximal radial ulnar joint during full supination.76 The weaker posterior attachment stabilizes the joint in full pronation. Oblique Cord The oblique cord is a small and inconstant bundle of fibrous tissue formed by the fascia overlying the deep head of the supinator and extending from the lateral side of the tuberosity of the ulna to the radius just below the radial tuberosity (see Fig. 2-23). Although the morphologic significance is debatable53,76 and the structure is not considered to be of great functional consequence,31 it has been noted to become taut in full supination, and contracture of the oblique cord has been implicated in the etiology of idiopathic limitation of forearm supination.10 At this point, we consider this structure as a curiosity. Bursae The bursae were first detailed by Monro in 1788, and several bursae have been described at the elbow joint.55 Lanz recognized seven bursae, including three associated with the triceps.52 On the posterior aspect of the elbow, the superficial olecranon bursa, which develops around age 7 years,18 between the olecranon process and the subcutaneous tissue is well

FIGURE 2-31

The lateral ulnar collateral ligament complex has an origin at the axis of rotation and thus is isometric, being taut both in extension (A) and in flexion (B). Note presence of the accessory ligament.

known33 (Fig. 2-32). A deep subtendinous bursa is present as the triceps inserts on the tip of the olecranon. An occasional deep subtendinous bursa is likewise present between the tendon and the tip of the olecranon. A bursa has also even been described deep to the anconeus muscle in about 12% of subjects by Henle,36 but we have not appreciated such a structure during more than 500 exposures of this region. On the medial and lateral aspects of the joint, the subcutaneous medial epicondylar bursa is frequently present, and the lateral subcutaneous epicondylar bursa occasionally has been observed. The radiohumeral bursa lies deep to the common extensor tendon, below the extensor carpi radialis brevis and superficial to the radiohumeral joint capsule. This entity has been implicated by several authors17,67 in the etiology of lateral epicondylitis but is probably not a major factor. The constant bicipitoradial bursa separates the biceps tendon from the tuberosity

24

Part I Fundamentals and General Considerations

Medial epicondylar B.

Lat. epicondylar B.

Ulnar n. B. Subanconeus B. Subtendinous B. Intratendinous B. Olecranon B.

Sub ext. carpi radialis brevis B. (Radiohumeral B.)

FIGURE 2-32

Posterior view of the elbow demonstrating the superficial and deep bursae that are present about this joint.

of the radius (see Fig. 2-9). Less commonly appreciated is the deep cubital interosseous bursa lying between the lateral aspect of the biceps tendon and the ulna, brachialis, and supinator fascia. This bursa is said to be present in about 20% of individuals.75 The clinical significance of the relevant bursae about the elbow is detailed in Chapter 85.

VESSELS BRACHIAL ARTERY AND ITS BRANCHES The cross-sectional relationship of the vessels, nerves, muscles, and bones is shown in Figure 2-33. The brachial artery descends in the arm, crossing in front of the intramuscular septum to lie anterior to the medial aspect of the brachialis muscle. The median nerve crosses in front of and medial to the artery at this point, near the middle of the arm (Fig. 2-34). The artery continues distally at the medial margin of the biceps muscle and enters the antecubital space medial to the biceps tendon and lateral to the nerve (Fig. 2-35). At the level of the radial head, it gives off its terminal branches, the ulnar and radial arteries, which continue into the forearm. The brachial artery usually is accompanied by medial and lateral brachial veins. Proximally, in addition to its numerous muscular and cutaneous branches, the large,

deep brachial artery courses posteriorly and laterally to bifurcate into the medial and radial collateral arteries. The medial collateral artery continues posteriorly, supplying the medial head of the triceps and ultimately anastomosing with the interosseous recurrent artery at the posterior aspect of the elbow. The radial collateral artery penetrates the lateral intermuscular septum and accompanies the radial nerve into the antecubital space, where it anastomoses with the radial recurrent artery at the level of the lateral epicondyle. The detailed vascular anatomy of the elbow region has been nicely described recently in great detail by Yamaguchi et al.89 The major branches of the brachial artery are the superior and inferior ulnar collateral arteries, which originate medial and distal to the profunda brachial artery. The superior ulnar collateral artery is given off just distal to the midportion of the brachium, penetrates the medial intermuscular septum, and accompanies the ulnar nerve to the medial epicondyle, where it terminates by anastomosing with the posterior ulnar recurrent artery and variably with the inferior ulnar collateral artery (Fig. 2-36). The inferior ulnar collateral artery arises from the medial aspect of the brachial artery about 4 cm proximal to the medial epicondyle. It continues distally for a short course, dividing into and anastomosing with branches of the anterior ulnar recurrent artery, and it supplies a portion of the pronator teres muscle.

Chapter 2 Anatomy of the Elbow Joint

25

57

57

58 59

59 60

61

61

A

B Biceps brachii m. Brachialis m. Radial n. Brachioradialis m. Ext. carpi radialis longus m.

C

D

E

(57)

Lat. intermuscular septum Humerus

Brachial a. and vv. Median n. Basilic v. Ulnar n. Medial intermuscular septum Triceps brachii m.

Medial antebrachial cutan. n. Pronator teres m. Flexor carpi radialis m. Basilic v. Ext. carpi radialis Flexor digitorum superficialis m. longus and brevis mm. Ulnar collateral lig. Dorsal antebrachial Ulnar n. cutan. n. (59) Flexor carpi ulnaris m. Tendon of common ext. digitorum, Flexor digitorum profundus m. carpi ulnaris, and digiti minimi mm. Anconeus m. Pronator teres m. Radial a. and v. Tendon of biceps brachii m. Lat. antebrachial cutan. n. Medial antebrachial cutan. n. Superficial radial n. Flexor carpi radialis m. Brachioradialis m. Palmaris longus m. Ext. carpi radialis Common interosseous a. and median n. longus and brevis mm. Flexor digitorum superficialis m. Antebrachii fascia Ulnar n. Radius Flexor carpi ulnaris m. Deep radial n. Ulnar a. and v. Common ext. digitorum m. Flexor digitorum profundus m. Ext. digiti minimi m. (61) Ulna Ext. carpi ulnaris m. Interosseous membrane Supinator m. Anconeus m.

FIGURE 2-33

Cross-sectional relationships of the muscles (A) and the neurovascular bundles (B). C, The region above the elbow joint. D, View taken across the elbow joint. E, View just distal to the articulation. (Redrawn from Eycleshymer, A. C., and Schoemaker, D. M.: A Cross-Section Anatomy. New York, D. Appleton and Co., 1930.)

26

Part I Fundamentals and General Considerations

Brachialis Radial n. Brachioradialis Radial recurrent a. Deep and superficial branches of radial n. Supinator Extensor carpi radialis longus Flexor digitorum sublimis Pronator teres Radial a.

Biceps and lacertus fibrosus Median n. Brachial a. Pronator teres, humeral head Flexor carpi radialis and palmaris longus Pronator teres, ulnar head Ulnar n. Ant. and post. ulnar recurrent aa. Ulnar a. Common interosseous a. Posterior and anterior interosseous aa. Anterior interosseous n. Flexor carpi ulnaris

Flexor pollicis longus

Flexor digitorum profundus Dorsal branch of ulnar n.

FIGURE 2-34 Ulnar a. and n. Volar interosseous a. and n. Pronator quadratus

Median n.

Abductor pollicis longus

RADIAL ARTERY The radial artery typically originates at the level of the radial head, emerges from the antecubital space between the brachioradialis and the pronator teres muscle, and continues down the forearm under the brachioradialis muscle. A more proximal origin occurs in up to 15% of individuals.54 The radial recurrent artery originates laterally from the radial artery just distal to its origin. It ascends laterally on the supinator muscle to anastomose with the radial collateral artery at the level of the lateral epicondyle, to which it provides circulation. For better visualization, the radial recurrent artery sometimes is sacrificed with the anterior elbow exposure.

ULNAR ARTERY The larger of the two terminal branches of the brachial artery is the ulnar artery. There is relatively little variation in its origin, which is usually at the level of the radial head. The artery traverses the pronator teres between its two heads and continues distally and medially behind the flexor digitorum superficialis muscle. It emerges medially to continue down the medial aspect of the forearm under the cover of the flexor carpi ulnaris. Two

Anterior aspect of the elbow region demonstrating the intricate relationships between the muscles, nerves, and vessels. (Redrawn from Hollinshead, W. H.: The back and limbs. In Anatomy for Surgeons, Vol. 3. New York, Harper & Row, 1969, p. 379.)

recurrent branches originate just distal to the origin of the ulnar artery. The anterior ulnar recurrent artery ascends deep to the humeral head of the pronator teres and deep to the medial aspect of the brachialis muscle to anastomose with the descending superior and inferior ulnar collateral arteries. The posterior ulnar recurrent artery originates with or just distal to the smaller anterior ulnar recurrent artery and passes proximal and posterior between the superficial and deep flexors posterior to the medial epicondyle. This artery continues proximally with the ulnar nerve under the flexor carpi ulnaris to anastomose with the superior ulnar collateral artery. Additional extensive communication with the inferior ulnar and middle collateral branches constitutes the rete articulare cubiti (see Fig. 2-35). The common interosseous artery is a large vessel originating 2.5 cm distal to the origin of the ulnar artery. It passes posteriorly and distally between the flexor pollicis longus and the flexor digitorum profundus just distal to the oblique cord, dividing into anterior and posterior interosseous branches. The interosseous recurrent artery originates from the posterior interosseous branch. This artery runs proximally through the supinator muscle to anastomose with the vascular network of the olecranon (see Fig. 2-36).

Chapter 2 Anatomy of the Elbow Joint

27

RC

MC SUC SUC

IU

C

B

IUC

RR RR

PUR PUR IR

R

FIGURE 2-36

FIGURE 2-35

Illustration of the anterior extraosseous vascular anatomy demonstrating the medial arcade and the relationship of the radial recurrent artery (RR) to the proximal aspect of the radius. The inferior ulnar collateral artery (IUC) provides perforators to the supracondylar region, medial aspect of the trochlea, and medial epicondyle before it courses posteriorly to anastomose with the superior ulnar collateral (SUC) and posterior ulnar recurrent (PUR) arteries. The radial recurrent artery provides an osseous perforator to the radius as it travels proximally and posterior. B, brachial artery; R, radial artery. (Redrawn from Yamaguchi, K., Sweet, F. A., Bindra, R., Morrey, B. F., and Gelberman, R. H.: The extraosseous and intraosseous arterial anatomy of the adult elbow. J. Bone Joint Surg. 79A:1654, 1997.)

NERVES Specific clinical and pertinent anatomic aspects of the nerves in the region of the elbow are discussed in subsequent chapters as appropriate. A general survey of the common anatomic patterns is given here (see Fig. 2-33).

MUSCULOCUTANEOUS NERVE The musculocutaneous nerve originates from C5-8 nerve roots and is a continuation of the lateral cord. It innervates the major elbow flexors, the biceps and brachialis,

Illustration of the posterior collateral circulation of the elbow. There are perforating vessels on the posterior aspect of the lateral epicondyle, in the olecranon fossa, and on the medial aspect of the trochlea. The tip of the olecranon is supplied by perforators from the posterior arcade in the olecranon fossa. The superior ulnar collateral artery (SUC) is seen terminating in the posterior arcade. IUC, inferior ulnar collateral artery; PUR, posterior ulnar recurrent artery; IR, interosseous recurrent artery, RR, radial recurrent artery; RC, radial collateral artery; MC, middle collateral artery. (Redrawn from Yamaguchi, K., Sweet, F. A., Bindra, R., Morrey, B. F., and Gelberman, R. H.: The extraosseous and intraosseous arterial anatomy of the adult elbow. J. Bone Joint Surg. 79A:1655, 1997.)

and continues through the brachial fascia lateral to the biceps tendon, terminating as the lateral antebrachial cutaneous nerve (Fig. 2-37). The motor branch enters the biceps and the brachialis approximately 15 and 20 cm below the tip of the acromion, respectively.48

MEDIAN NERVE Arising from the C5-8 and T1 nerve roots, the median nerve enters the anterior aspect of the brachium, crossing in front of the brachial artery as it passes across the intermuscular septum. It follows a straight course into the medial aspect of the antecubital fossa, medial to the biceps tendon and the brachial artery. It then passes under the bicipital aponeurosis. The first motor branch is provided to the pronator teres, through which it

28

Part I Fundamentals and General Considerations

Musculocutaneous nerve

Coracobrachialis

Median nerve

Long head of biceps

Lat. cutaneous nerve of forearm

Short head of biceps Brachialis

Pronator teres (C6, C7) Flexor carpi radialis (C6-C8) Flexor digitorum superficialis (C6-T1)

Palmaris longus (C7-T1) communicating branch with ulnar nerve

Flexor pollicis longus (C6-C8) Pronator quadratus (C6-T1)

Flexor digitorum profundus (C8, T1)

Opponens pollicis (C7, C8?, T1) Abductor pollicis brevis (C6, C7, C8?)

FIGURE 2-37 The musculocutaneous nerve innervates the flexors of the elbow and continues distal to the joint as the lateral cutaneous nerve of the forearm. (Redrawn from Langman, J., and Woerdeman, M. W.: Atlas of Medical Anatomy. Philadelphia, W. B. Saunders Co., 1976.)

passes.2,39 It enters the forearm and continues distally under the flexor digitorum superficialis within the fascial sheath of this muscle. There are no branches of the median nerve in the arm (Fig. 2-38). In the cubital fossa, a few small articular branches are given off before the motor branches to the pronator teres, the flexor carpi radialis, the palmaris longus, and the flexor digitorum superficialis. Because all branches arise medially, medial retraction of the nerve during exposure of the anterior aspect of the elbow is a safe technique. The anterior interosseous nerve innervates the flexor pollicis longus and the lateral portion of the flexor digitorum profundus. It arises from the median nerve near the inferior border of the pronator teres and travels along the anterior aspect of the interosseous membrane in the company of the anterior interosseous artery.

RADIAL NERVE The radial nerve is a continuation of the posterior cord and originates from the C6, C7, and C8 nerve roots with

Flexor pollicis brevis (C6-C8) Lumbricals 1 and 2 (C7-T1)

FIGURE 2-38 The median nerve innervates the flexor pronator group of muscles about the elbow, but there are no branches above the joint. (Redrawn from Langman, J., and Woerdeman, M. W.: Atlas of Medical Anatomy. Philadelphia, W. B. Saunders Co., 1976.)

variable contributions of the C5 and T1 roots. In the midportion of the arm, the nerve courses laterally just distal to the deltoid insertion to occupy the spiral groove in the humerus that bears its name. Before entering the anterior aspect of the arm, it gives off motor branches to the medial and lateral head of the triceps, accompanied by the deep branch of the brachial artery. It then emerges inferiorly and laterally to penetrate the lateral intermuscular septum. The nerve is at risk for injury from surgery or fracture at this site. Two recent studies have placed the position of the radial nerve as 54% of the acromion/ulnar distance22 or 1.7% of the transcondylar distance.41 After penetrating the lateral intermuscular septum in the distal third of the arm, it descends anterior to the lateral epicondyle behind the brachioradialis. It innervates the brachioradialis with a single branch to this muscle. In the antecubital space, the nerve divides into the superficial and deep branches. The superficial branch is a continuation of the radial nerve

Chapter 2 Anatomy of the Elbow Joint

29

Radial nerve

Triceps (C6-C8, T1) Post. cutaneous nerve of arm Post. cutaneous nerve of forearm Anconeus Deep branch of radial nerve

Brachioradialis (C5, C6) Extensor carpi radialis longus and brevis (C6-C8) Superficial branch of radial nerve

Extensor carpi ulnaris (C6?, C7, C8) Extensor digitorum (C6, C7, C8)

Extensor pollicis longus (C6?, C7, C8) Abductor pollicis longus (C6?, C7, C8) Extensor pollicis brevis

FIGURE 2-39

The muscles innervated by the right radial nerve. (Redrawn from Langman, J., and Woerdeman, M. W.: Atlas of Medical Anatomy. Philadelphia, W. B. Saunders Co., 1976.)

and extends into the forearm to innervate the middorsal cutaneous aspect of the forearm (Fig. 2-39). The motor branches of the radial nerve are given off to the triceps above the spiral groove except for the branch to the medial head of the triceps, which originates at the entry to the spiral groove. This branch continues distally through the medial head to terminate as a muscular branch to the anconeus. This accounts for the variability of the anconeus when rotated or reflected from its origin.11,44,68 In the antecubital space, the recurrent radial nerve curves around the posterolateral aspect of the radius, passing deep to the supinator muscle, which it innervates. During its course through the supinator muscle, the nerve lies over a bare area, which is distal to and opposite to the radial tuberosity.23 The nerve is believed to be at risk at this site with fractures of the proximal radius.79 It emerges from the muscle as the posterior interosseous nerve, and the recurrent branch innervates the extensor digitorum minimi, the extensor carpi ulnaris, and occasionally, the anconeus. The posterior interosseous nerve is accompanied by the posterior interosseous artery and sends further muscle branches distally to supply the abductor pollicis longus, the extensor pollicis longus, the extensor pollicis brevis, and the extensor indicis on the dorsum of the forearm. The nerve is subject to compression as it passes through the supinator muscle15 or from

synovial proliferation.25,28 Compression and entrapment problems are described in detail in Chapter 81.

ULNAR NERVE The ulnar nerve is derived from the medial cord of the brachial plexus from roots C8 and T1. In the midarm, it passes posteriorly through the medial intermuscular septum and continues distally anterior to the septum and under the medial margin of the triceps. It is accompanied by the superior ulnar collateral branch of the brachial artery and the ulnar collateral branch of the radial artery. Although supposedly there are no branches of this nerve in the brachium, an occasional motor branch to the triceps is encountered (Fig. 2-40). The ulnar nerve passes into the cubital tunnel under the medial epicondyle and rests against the posterior portion of the medial collateral ligament, where a groove in the ligament accommodates this structure. The roof of the cubital tunnel recently has been defined and termed the cubital tunnel retinaculum.64 Retinacular absence accounts for congenital subluxation of the ulnar nerve. Furthermore, the structure flattens with elbow flexion, thus decreasing the capacity of the cubital tunnel (Fig. 2-41).64 This accounts for the clinical observation of ulnar nerve paresthesia with elbow flexion. Similarly, elbow instability can cause traction injury to the nerve.51

30

Part I Fundamentals and General Considerations

Ulnar nerve

Flexor digitorum profundus (C8, T1)

Median nerve

Communicating branch Flexor carpi ulnaris (C8, T1)

Deep head of flexor pollicis (C6-C8) Adductor pollicis (C7, C8, T1)

Digiti Minimi

Triceps m.

Abductor flexor opponens (C7, C8?, T1)

Flexion

Lumbricals (C7-C8, T1) Palmar and dorsal interossei (C7?, C8, T1)

FIGURE 2-40

Muscles innervated by the right ulnar nerve. There are no muscular branches of this nerve above the elbow joint. (Redrawn from Langman, J., and Woerdeman, M. W.: Atlas of Medical Anatomy. Philadelphia, W. B. Saunders Co., 1976.)

A few small capsular twigs are given to the elbow joint in this region.8 As the nerve enters the forearm between the two heads of the flexor carpi ulnaris, it gives off a single nerve to the ulnar origin of the pronator and one to the epicondylar head of the flexor carpi ulnaris. Distally, the nerve sends a motor branch to the ulnar half of the flexor digitorum profundus. Two cutaneous nerves arise from the ulnar nerve in the distal half of the forearm and innervate the skin of the wrist and the ulnar two digits of the hand.

MUSCLES Relevant features of the origin, insertion, and function of the muscles of the elbow region are covered in other chapters dealing with surgical exposure, functional examination, and biomechanics. This information also is discussed in various chapters when dealing with specific pathology. The following description will serve as a basic overview.

Ulnar n. OI ME

B

CTR

FIGURE 2-41 With flexion the cubital tunnel flattens, compressing the ulnar nerve (A and B). (Redrawn from O’Driscoll, S. W., Horii, E., Carmichael, S. W., and Morrey, B. F.: The cubital tunnel and ulnar neuropathy. J. Bone Joint Surg. 73B:613, 1991.)

ELBOW FLEXORS Biceps The biceps covers the brachialis muscle in the distal arm and passes into the cubital fossa as the biceps tendon, which attaches to the posterior aspect of the radial tuberosity (Fig. 2-42). The constant bicipitoradial bursa separates the tendon from the anterior aspect of the tuberosity, and the cubital bursa has been described as separating the tendon from the ulna and the muscles covering the radius (see Fig. 2-9). The bicipital aponeurosis, or lacertus fibrosus, is a broad, thin band of tissue that is a continuation of the anterior medial and distal muscle fasciae. It runs obliquely to cover the median nerve and brachial artery and inserts into the deep fasciae of the forearm and possibly into the ulna as well.19 The biceps is a major flexor of the elbow that has a large cross-sectional area but an intermediate mechanical advantage because it passes relatively close to the

Chapter 2 Anatomy of the Elbow Joint

Acromion

Trapezius

31

Clavicular portion of pectoralis major

Groove for cephalic vein Deltoid Sternocostal portion of pectoralis major Subscapularis Coracobrachialis Deltoid tuberosity

Serratus anterior Teres major and latissimus dorsi

Brachialis Lat. head of triceps

Short head of biceps brachii Long head of biceps brachii

Lat. intermuscular septum Brachioradialis Extensor carpi radialis longus

Tendon of biceps brachii Bicipital aponeurosis Pronator teres

axis of rotation. In the pronated position, the biceps is a strong supinator.6 The distal insertion may undergo spontaneous rupture,57,78 and this condition is discussed in detail later (Chapter 34).

Brachialis This muscle has the largest cross-sectional area of any of the elbow flexors but suffers from a poor mechanical advantage because it crosses so close to the axis of rotation. The origin consists of the entire anterior distal half of the humerus, and it extends medially and laterally to the respective intermuscular septa (Fig. 2-43). The muscle crosses the anterior capsule, with some fibers inserting into the capsule that are said to help retract the capsule during elbow flexion. The major attachment is to the coronoid process about 2 mm distal from its articular margin. More than 95% of the cross-sectional area is muscle tissue at the elbow joint,50 a relationship that may account for the high incidence of trauma to this muscle and the development of myositis ossificans with elbow dislocation.84 The muscle is innervated by the musculocutaneous nerve. The lateral portion of the muscle covers the radial nerve as it spirals around the distal humerus. The median nerve and brachial artery are superficial to the brachialis and lie behind the biceps in the distal humerus.

FIGURE 2-42

Anterior aspect of the arm and elbow region demonstrating the major flexors of the joint, the brachialis, and the biceps muscles. (Redrawn from Langman, J., and Woerdeman, M. W.: Atlas of Medical Anatomy. Philadelphia, W. B. Saunders Co., 1976.)

Brachioradialis The brachioradialis has a lengthy origin along the lateral supracondylar bony column that extends proximally to the level of the junction of the mid and distal humerus (see Fig. 2-43). The origin separates the lateral head of the triceps and the brachialis muscle. The lateral border of the cubital fossa is formed by this muscle, which crosses the elbow joint with the greatest mechanical advantage of any elbow flexor. It progresses distally to insert into the base of the radial styloid (Figs. 2-44 and 2-45). The muscle protects and is innervated by the radial nerve (C5, C6) as it emerges from the spiral groove. Its major function is elbow flexion. Rarely, the muscle may be ruptured.35

Extensor Carpi Radialis Longus The extensor carpi radialis longus originates from the supracondylar bony column joint just below the origin of the brachioradialis (see Fig. 2-44). The origin of this muscle is identified as the first fleshy fibers observed proximal to the common extensor tendon. As it continues into the midportion of the dorsum of the forearm, it becomes largely tendinous and inserts into the dorsal base of the second metacarpal. Innervated by the radial nerve (C6, C7), the motor branches arise just distal to those of the brachioradialis muscle.

32

Part I Fundamentals and General Considerations

Supraspinatus

Subscapularis

Pectoralis major

Latissimus dorsi Teres major

Deltoid

Coracobrachialis

Brachialis Brachioradialis Origins Insertions

Extensor carpi radialis longus

Common extensor tendon

Pronator teres Common flexor tendon

FIGURE 2-43

Anterior humeral origin and insertion of muscles that control flexion of the elbow joint.

In addition to wrist extension, its orientation suggests that this muscle might function as an elbow flexor. Clinically, the origin of this muscle and its relationship with that of the extensor carpi radialis brevis have been implicated in the pathologic anatomy of tennis elbow by Nirschl (Chapter 44).

Extensor Carpi Radialis Brevis The extensor carpi radialis brevis originates from the lateral superior aspect of the lateral epicondyle (see Fig. 2-43). Its origin is the most lateral of the extensor group and is covered by the extensor carpi radialis longus. This relationship is important as the most commonly implicated site of lateral epicondylitis. The extensor digitorum communis originates from the common extensor tendon and is just medial or ulnar to the extensor carpi radialis brevis. At its humeral origin, the fibers of the extensor digitorum communis and brevis are grossly and histologically indistinguishable from one another32 (see Fig. 2-44). The longus and brevis shares the same extensor compartment as they cross the wrist under the extensor retinaculum. The brevis inserts into the dorsal base of the third metacarpal. The function of the extensor carpi radialis brevis is pure wrist extension, with little or no radial or ulnar deviation.1 The extensor carpi radialis

brevis is innervated by fibers of the sixth and seventh cervical nerves. The motor branch arises from the radial nerve in the region of its division into deep and superficial branches.

Extensor Digitorum Communis Originating from the anterior distal aspect of the lateral epicondyle, the extensor digitorum communis accounts for most of the contour of the extensor surface of the forearm (see Fig. 2-44). The muscle extends and abducts the fingers. According to Wright, the muscle can assist in elbow flexion when the forearm is pronated. This observation is not, however, supported by our crosssectional studies.1 Innervation is from the deep branch of the radial nerve, with contributions from the sixth through eighth cervical nerves.

Extensor Carpi Ulnaris The extensor carpi ulnaris originates from two heads, one above and the other below the elbow joint. The humeral origin is the most medial of the common extensor group (Fig. 2-46) (see also Fig. 2-43). The ulnar attachment is along the aponeurosis of the anconeus and at the superior border of this muscle. It is a valuable landmark for exposures of the lateral elbow joint. The insertion is on the dorsal base of the fifth metacarpal after crossing the wrist in its own compartment under the extensor retinaculum. The extensor carpi ulnaris is a wrist extensor and ulnar deviator. Fibers of the sixth through eighth cervical nerve routes innervate the muscle from branches of the deep radial nerve.

Supinator This flat muscle is characterized by the virtual absence of tendinous tissue and a complex origin and insertion. It originates from three sites above and below the elbow joint: (1) the lateral anterior aspect of the lateral epicondyle; (2) the lateral collateral ligament; and (3) the proximal anterior crest of the ulna along the crista supinatoris. The form of the muscle is approximately that of a rhomboid, because it runs obliquely, distally, and radially to wrap around and insert diffusely on the proximal radius, beginning lateral and proximal to the radial tuberosity and continuing distal to the insertion of the pronator teres at the junction of the proximal and middle third of the radius (see Fig. 2-46). It is important to note that the radial nerve passes through the supinator to gain access to the extensor surface of the forearm. This anatomic feature is clinically significant with regard to exposure of the lateral aspect of the elbow joint and the proximal radius and in certain entrapment syndromes.76 The muscle obviously supinates the forearm but is a weaker supinator than the biceps.38 Unlike the biceps,

Chapter 2 Anatomy of the Elbow Joint

33

Biceps brachii Triceps brachii Olecranon Lateral epicondyle of humerus

Brachialis Brachioradialis Extensor carpi radialis brevis

Extensor digitorum Extensor digiti minimi Abductor pollicis longus Extensor carpi ulnaris

Head of ulna

Extensor pollicis brevis Tendons of extensor carpi radialis longus and brevis Styloid process of radius

FIGURE 2-44

The musculature of the posterolateral aspect of the right forearm. (Redrawn from Langman, J., and Woerdeman, M. W.: Atlas of Medical Anatomy. Philadelphia, W. B. Saunders Co., 1976.)

ELBOW EXTENSORS Triceps Brachii

FIGURE 2-45

Posterior view of the radius and ulna demonstrating the insertion of the extensors of the elbow as well as the origin of the forearm musculature.

however, the effectiveness of the supinator is not altered by the position of elbow flexion. The innervation is derived from the muscular branch given off by the radial nerve just before and during its course through the muscle with nerve fibers derived primarily from the sixth cervical root.

The entire posterior musculature of the arm is composed of the triceps brachii (see Fig. 2-39). The long head has a discrete origin from the infraglenoid tuberosity of the scapula. The lateral head originates in a linear fashion from the proximal lateral intramuscular septum on the posterior surface of the humerus. The medial head originates from the entire distal half of the posteromedial surface of the humerus bounded laterally by the radial groove and medially by the intramuscular septum. Thus, each head originates distal to the other, with progressively larger areas of origin. The long and lateral heads are superficial to the deep medial head, blending in the midline of the humerus to form a common muscle that then tapers into the triceps tendon and attaches to the tip of the olecranon with Sharpey’s fibers.14 The tendon usually is separated from the olecranon by the subtendinous olecranon bursa. The distal 40% of the triceps mechanism consists of a layer of fascia that blends with the triceps distally. Innervated by the radial nerve, the long and lateral heads are supplied by branches that arise proximal to

34

Part I Fundamentals and General Considerations

Triceps brachii Olecranon

Brachioradialis Lateral epicondyle

Anconeus

Posterior border of ulna

Extensor carpi radialis longus Supinator Extensor carpi radialis brevis

Extensor carpi ulnaris Flexor carpi ulnaris Extensor pollicis longus Extensor indicis Styloid process of ulna

Radius Abductor pollicis longus Extensor pollicis brevis Tendons of extensor radialis longus and brevis

Dorsal interossei Extensor indicis Tendon of extensor digitorum

the entrance of the radial nerve into the groove. The medial head is innervated distal to the groove with a branch that enters proximally and passes through the entire medial head to terminate by innervating the anconeus, an anatomic feature of considerable importance when considering some approaches (e.g., Kocher, BryanMorrey, Boyd, and Pankovitch) to the joint. The function of the triceps is to extend the elbow. Lesions of the nerve in the midportion of the humerus usually do not prevent triceps function that is provided by the more proximally innervated lateral and long heads.

Subanconeus Muscle The attachment of some muscle fibers of the medial head of the triceps to the posteromedial capsule has been termed the subanconeus muscle. This may have some functional relevance of stabilizing the fat pad to help cushion the elbow as it comes into full extension.87

Anconeus This muscle has little tendinous tissue because it originates from a rather broad site on the posterior aspect of the lateral epicondyle and from the lateral triceps

FIGURE 2-46

The extensor aspect of the forearm demonstrating the deep muscle layer after the extensor digitorum and extensor digiti minimi have been removed. (Redrawn from Langman, J., and Woerdeman, M. W.: Atlas of Medical Anatomy. Philadelphia, W. B. Saunders Co., 1976.)

fascia and inserts into the lateral dorsal surface of the proximal ulna (see Fig. 2-46). It is innervated by the terminal branch of the nerve to the medial head of the triceps. Curiously, the function of this muscle has been the subject of considerable speculation. Possibly the most accurate description of function is that proposed by Basmajian and Griffin and by DaHora, who suggest that its primary role is that of a joint stabilizer.5,21 The muscle covers the lateral portion of the annular ligament and the radial head. For the surgeon, the major significance of this muscle is its position as a key landmark in various lateral and posterolateral exposures and is emerging for usefulness reconstruction of the lateral elbow.

FLEXOR PRONATOR MUSCLE GROUP Pronator Teres This is the most proximal of the flexor pronator group. There are two heads of origin: The largest arises from the anterosuperior aspect of the medial epicondyle and the second from the coronoid process of the ulna, an attachment absent in about 10% of individuals39 (see Fig. 2-37). The two origins of the pronator muscle provide an arch through which the median nerve passes to gain

Chapter 2 Anatomy of the Elbow Joint

access to the forearm. This anatomic characteristic is a significant feature in the etiology of the median nerve entrapment syndrome and is discussed in detail in Chapter 80. The common muscle belly proceeds radially and distally under the brachioradialis, inserting at the junction of the proximal and middle portions of the radius by a discrete broad tendinous insertion into a tuberosity on the lateral aspect of the bone. Obviously, a strong pronator of the forearm, it also is considered a weak flexor of the elbow joint.1,7,82 The muscle usually is innervated by two motor branches from the median nerve before the nerve leaves the cubital fossa.

35

wrist flexor. At the elbow no significant flexion moment is present.1,24

Palmaris Longus This muscle, when present, arises from the medial epicondyle, and from the septa it shares with the flexor carpi radialis and flexor carpi ulnaris (see Fig. 2-43). It becomes tendinous in the proximal portion of the forearm and inserts into and becomes continuous with the palmar aponeurosis. It is absent approximately in 10% of extremities.71 Its major function is as a donor tendon for reconstructive surgery, and it is innervated by a branch of the median nerve.

Flexor Carpi Radialis The flexor carpi radialis originates just inferior to the origin of the pronator teres and the common flexor tendon at the anteroinferior aspect of the medial epicondyle (see Fig. 2-43). It continues distally and radially to the wrist, where it can be easily palpated before it inserts into the base of the second and sometimes the third metacarpal. Proximally, the muscle belly partially covers the pronator teres and palmaris longus muscles and shares a common origin from the intermuscular septum, which it shares with these muscles. The innervation is from one or two twigs of the median nerve (C6, C7), and its chief function is as a

Flexor Carpi Ulnaris The flexor carpi ulnaris is the most posterior of the common flexor tendons originating from the medial epicondyle (see Figs. 2-38 and 2-43). A second and larger source of origin is from the medial border of the coronoid and the proximal medial aspect of the ulna. The ulnar nerve enters and innervates (T7-8 and T1) the muscle between these two sites of origin with two or three motor branches given off just after the nerve has entered the muscle. These are the first motor branches of the ulnar nerve, and therefore, they are useful in localizing the level of an ulnar nerve lesion. The muscle

Brachial artery Median nerve Triceps brachii Aponeurosis of biceps brachii

Brachioradialis Radial artery Pronator teres (cut)

Pronator teres (cut) Brachialis Ulnar artery Humeral head Radial head

flexor digitorum superficialis

Superficial branch of radial nerve Extensor carpi radialis longus

Flexor pollicis longus Flexor carpi ulnaris

Abductor pollicis longus Extensor pollicis brevis Flexor carpi radialis (cut) Flexor retinaculum

Ulnar artery and nerve Flexor digitorum profundus Median nerve Deep layer of flexor retinaculum

Tendon of flexor digitorum profundus

FIGURE 2-47 The flexor digitorum superficialis is demonstrated after the palmaris longus and flexor carpi radialis has been removed. The pronator teres has been transected and reflected. The important relationships of the nerves and arteries should be noted. (Redrawn from Langman, J., and Woerdeman, M. W.: Atlas of Medical Anatomy. Philadelphia, W. B. Saunders Co., 1976.)

36

Part I Fundamentals and General Considerations

continues distally to insert into the pisiform, where the tendon is easily palpable, because it serves as a wrist flexor and ulnar deviator. With an origin posterior to the axis of rotation, weak elbow extension also may be provided by the flexor carpi ulnaris.1

Flexor Digitorum Superficialis This muscle is deep to those originating from the common flexor tendon but superficial to the flexor digitorum profundus; thus, it is considered the intermediate muscle layer. This broad muscle has a complex origin (Fig. 2-47). Medially, it arises from the medial epicondyle by way of the common flexor tendon and possibly from the ulnar collateral ligament and the medial aspect of the coronoid.38 The lateral head is smaller and thinner and arises from the proximal two thirds of the radius. The unique origin of the muscle forms a fibrous margin under which the median nerve and the ulnar artery emerge as they exit from the cubital fossa. The muscle is innervated by the median nerve (C7, C8, T1) with branches that originate before the median nerve enters the pronator teres. The action of the flexor digitorum superficialis is flexion of the proximal interphalangeal joints.

References 1. An, K. N., Hui, F. C., Morrey, B. F., Linscheid, R. L., and Chao, E. Y.: Muscles across the elbow joint: a biomechanical analysis. J. Biomechan. 14:659, 1981. 2. Anson, B. J., and McVay, C. B.: Surgical Anatomy, 5th ed., Vol. 2. Philadelphia, W. B. Saunders Co., 1971. 3. Atkinson, W. B., and Elftman, H.: The carrying angle of the human arm as a secondary sex character. Anat. Rec. 91:49, 1945. 4. Barnard, L. B., and McCoy, S. M.: The supracondyloid process of the humerus. J. Bone Joint Surg. 28:845, 1946. 5. Basmajian, J. V., and Griffin, W. R.: Function of anconeus muscle. J. Bone Joint Surg. 54A:1712, 1972. 6. Basmajian, J. V., and Latif, A.: Integrated actions and functions of the two flexors of the elbow: a detailed myographic analysis. J. Bone Joint Surg. 39A:1106, 1957. 7. Basmajian, J. V., and Travell, A.: Electromyography of the pronator muscles in the forearm. Anat. Rec. 139:45, 1961. 8. Bateman, J. E.: Denervation of the elbow joint for the relief of pain: a preliminary report. J. Bone Joint Surg. 30B:635, 1948. 9. Beetham, W. P.: Physical Examination of the Joints. Philadelphia, W. B. Saunders Co., 1965. 10. Bert, J. M., Linscheid, R. L., and McElfresh, E. C.: Rotatory contracture of the forearm. J. Bone Joint Surg. 62A:1163, 1980. 11. Boyd, H. B.: Surgical exposure of the ulna and proximal third of the radius through one incision. Surg. Gynec. Obstet. 71:86, 1940.

12. Boyd, H. D., and Anderson, L. D.: A method for reinsertion of the biceps tendon brachii tendon. J. Bone Joint Surg. 43A:1141, 1961. 13. Bozkurt, M., Acar, H. I., Apaydin, N., Leblebicioglu, G., Elhan, A., Tekdemir, I., and Tonuk, E.: The annular ligament: an anatomical study. Am. J. Sports Med. 33:114, 2005. 14. Bryan, R. S., and Morrey, B. F.: Extensive posterior exposure of the elbow: a triceps-sparing approach. Clin. Orthop. 166:188, 1982. 15. Capener, N.: The vulnerability of the posterior interosseous nerve of the forearm: a case report and anatomic study. J. Bone Joint Surg. 48B:770, 1966. 16. Caputo, A. E., Mazzocca, A. D., and Santoro, V. M.: The nonarticulating portion of the radial head: anatomic and clinical correlations for internal fixation. J. Hand Surg. 23A(6):1082, 1998. 17. Carp, L.: Tennis elbow (epicondylitis) caused by radiohumeral bursitis. Arch. Surg. 24:905, 1932. 18. Chen, J., Alk, D., Eventov, I., and Weintroub, S.: Development of the olecranon bursa: an anatomic cadaver study. Acta Orthop. Scand. 58:408, 1987. 19. Congdon, E. D., and Fish, H. S.: The chief insertion of the biceps after neurosis in the ulna: a study of collagenous bundle patterns of antebrachial fascia and bicepital aponeurosis. Anat. Rec. 116:395, 1953. 20. Cunningham, D. J.: In Romanes, G. J. (ed.): Textbook of Anatomy, 12th ed. New York, Oxford University Press, 1981. 21. DaHora, B.: Musculus Anconeus. Thesis, University of Recife, Recife, Brazil, 1959. Cited by Basmajian, J. V., and Griffin, W. R.: J. Bone Joint Surg. 54A:1712, 1972. 22. D’Alton, E. J., and Mennen, U.: Instructional Course Article: The position of the radial nerve in the upper arm. S. African Orthop. J. August:32-36, 2003. 23. Davies, F., and Laird, M.: The supinator muscle and the deep radial (posterior interosseous nerve). Anat. Rec. 101:243, 1948. 24. Duchenne, G. B.: Physiology of Motion. Translated and edited by E. B. Kaplan. Philadelphia, J. B. Lippincott Co., 1949. 25. El-Hadidi, S., and Burke, F. D.: Posterior interosseous nerve syndrome caused by a bursa in the vicinity of the elbow. J. Hand Surg. 12B:23, 1987. 26. Evans, E. M.: Rotational deformity in the treatment of fractures of both bones of the forearm. J. Bone Joint Surg. 27:373, 1945. 27. Eycleshymer, A. C., and Schoemaker, D. M.: A CrossSection Anatomy. New York, D. Appleton, 1930. 28. Field, J. H.: Posterior interosseous nerve palsy secondary to synovial chondromatosis of the elbow joint. J. Hand Surg. 6:336, 1981. 29. Gardner, E.: The innervation of the elbow joint. Anat. Rec. 102:161, 1948. 30. Grant, J. C. B.: Atlas of Anatomy, 6th ed. Baltimore, Williams & Wilkins, 1972. 31. Gray, H.: In Warwick, R., and Williams, P. L. (eds.): Anatomy, Descriptive and Applied, 35th ed. Philadelphia, W. B. Saunders Co., 1980, p. 429. 32. Greenbaum, B., Itamura, J., Vangsness, C. T., Tibone, J., and Atkinson, R.: Extensor carpi radialis brevis. An

Chapter 2 Anatomy of the Elbow Joint

33. 34.

35. 36.

37. 38. 39.

40. 41.

42. 43.

44.

45.

46. 47. 48.

49. 50.

51.

52. 53. 54.

anatomical analysis of its origin. J. Bone Joint Surg. 81B:926, 1999. Gruber, W.: Monographie der bursae mucosae cubitales. Mem. Acad. Sc. Petersburg VII:10, 1866. Gruber, W.: Monographie Les Canalis Supracondylaideus Humeri. Mem. Acad. Sc. Petersburg. Cited by Morris, H.: Human Anatomy, 3rd ed. Philadelphia, Blakiston, 1953, p. 214. Hamilton, A. T., and Raleigh, N. C.: Subcutaneous rupture of the brachioradialis muscle. Surgery 23:806, 1948. Henle, J.: Handbuch Der Systematischen Anatomie des Menschen Muskellehre. Berlin, Braunschweig, 1866, p. 224. Henry, A. K.: Extensile Exposure, 2nd ed. Baltimore, Williams & Wilkins, 1966. Hollinshead, W. H.: The back and limbs. In Anatomy for Surgeons, Vol. 3. New York, Harper & Row, 1969, p. 379. Jamieson, R. W., and Anson, B. J.: The relation of the median nerve to the heads of origin of the pronator teres muscle: a study of 300 specimens. Q. Bull Northwestern Univ. Med. School 26:34, 1952. Johansson, O.: Capsular and ligament injuries of the elbow joint. Acta Chir. Scand. (Suppl.) 287, 1962. Wadia, F., Kamineni, S., Dhotare, S., and Amis, A: Radiographic measurements of normal elbows: clinical relevance to olecranon fractures. Clin. Anat. 20:407, 2007. Kapandji, I. A.: The Physiology of Joints. Vol. I: Upper Limb, 2nd ed. Baltimore, Williams & Wilkins, 1970. Keats, T. E., Teeslink, R., Diamond, A. E., and Williams, J. H.: Normal axial relationships of the major joints. Radiology 87:904, 1966. Kocher, T.: Textbook of Operative Surgery, 3rd ed. Translated by H. J. Stiles and C. B. Paul. London, A. & C. Black, 1911. Kolb, L. W., and Moore, R. D.: Fractures of the supracondylar process of the humerus. J. Bone Joint Surg. 49A:532, 1967. Langman, J., and Woerdeman, M. W.: Atlas of Medical Anatomy. Philadelphia, W. B. Saunders Co., 1976. Lanz, T., and Wachsmuth, W.: Praktische Anatomie. ARM, Berlin, Springer, 1959. Linell, E. A.: The distribution of nerves in the upper limb, with reference to variables and their clinical significance. J. Anat. 55:79, 1921. Lipmann, K., and Rang, M.: Supracondylar spur of the humerus. J. Bone Joint Surg. 48B:765, 1966. Loomis, L. K.: Reduction and after-treatment of posterior dislocation of the elbow: With special attention to the brachialis muscle and myositis ossificans. Am. J. Surg. 63:56, 1944. Malkawi, H.: Recurent dislocation of the elbow accompanied by ulnar neuropathy: a case report and review of the literature. Clin. Orthop. 161:170, 1981. Martin, B. F.: The annular ligament of the superior radial ulnar joint. J. Anat. 52:473, 1958. Martin, B. F.: The oblique cord of the forearm. J. Anat. 52:609, 1958. McCormick, L. J., Cauldwell, E. W., and Anson, B. J.: Brachial and antebrachial artery patterns: a study of 750 extremities. Surg. Gynecol. Obstet. 96:43, 1953.

37

55. Monro, A.: A Description of All the Bursae Mucosae of the Human Body. London, 1788. Translated into German by J. C. Rosenmutter (Leipzig, 1799). 56. Morrey, B. F., and An, K. N.: Functional anatomy of the elbow ligaments. Clin. Orthop. 201:84, 1985. 57. Morrey, B. F., Askew, L., An, K. N., and Dobyns, J.: Rupture of the distal tendon of the biceps brachii. J. Bone Joint Surg. 67A:418, 1985. 58. Morrey, B. F., and Chao, E. Y.: Passive motion of the elbow joint. A biomechanical analysis. J. Bone Joint Surg. 58A:501, 1976. 59. Morrey, B. F., Tanaka, S., and An, K. N.: Valgus stability of the elbow. A definition of primary and secondary constraints. Clin. Orthop. 265:187, 1991. 60. Morris, H.: In Schaeffer J. P. (ed.): Human Anatomy, 11th ed. Philadelphia, Blakiston, 1953. 61. Nazarian, L. N., McShane, J. M., Ciccotti, M. G., O’Kane, P. L., and Harwood, M. I.: Dynamic US of the anterior band of the ulnar collateral ligament of the elbow in asymptomatic major league baseball pitchers. Radiology 227:149, 2003. 62. Ochi, N., Ogura, T., Hashizume, H., Shigeyama, A. Y., Senda, M., and Inoue, H.: Anatomic relation between the medial collateral ligament of the elbow and the humero-ulnar joint axis. J. Shoulder Elbow Surg. 8:6, 1999. 63. O’Driscoll, S. W., Bell, D. F., and Morrey, B. F.: Posterolateral rotatory instability of the elbow. J. Bone Joint Surg. 73A:440, 1991. 64. O’Driscoll, S. W., Horii, E., Carmichael, S. W., and Morrey, B. F.: The cubital tunnel and ulnar neuropathy. J. Bone Joint Surg. 73B:613, 1991. 65. O’Driscoll, S. W., Horii, E., and Morrey, B. F.: Anatomy of the attachment of the medial ulnar collateral ligament. J. Hand Surg. 17:164, 1992. 66. O’Driscoll, S. W., Horii, E., Morrey, B. F., and Carmichael, S. W.: Anatomy of the ulnar part of the lateral collateral ligament of the elbow. Clin. Anat. 5:296, 1992. 67. Osgood, R. B.: Radiohumeral bursitis, epicondylitis, epicondylalgia (tennis elbow). Arch Surg. 4:420, 1922. 68. Pankovich, A. M.: Anconeus approach to the elbow joint and the proximal part of the radius and ulna. J. Bone Joint Surg. 59A:124, 1977. 69. Paraskevas, G., Papadopoulos, A., Papaziogas, B., Spanidou, S., Argiriadou, H., and Gigis, J.: Study of the carrying angle of the human elbow joint in full extension: a morphometric analysis. Surg. Radiol. Anat. 26:19, 2004. 70. Polonskaja, R.: Zur frage der arterienanastomosen im gobiete der ellenbagenbeuge des menschen. Anat. Anz. 74:303, 1932. 71. Reimann, A. F., Daseler, E. H., Anson, B. J., and Beaton, L. E.: The palmaris longus muscle and tendon: a study of 1600 extremities. Anat. Rec. 89:495, 1944. 72. Seki, A., Olsen, B. S., Jensen, S. L., Eygendaal, D., and Sojbjerg, J. O.: Functional anatomy of the lateral collateral ligament complex of the elbow: configuration of Y and its role. J. Shoulder Elbow Surg. 11:53, 2002. 73. Shiba, R., Siu, D., and Sorbie, C.: Geometric analysis of the elbow joint. J. Orthop. Res. 6:897, 1988.

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74. Sorbie, C., Shiba, R., Siu, D., Saunders, G., and Wevers, H.: The development of a surface arthroplasty for the elbow. Clin. Orthop. 208:100, 1986. 75. Spalteholz, V.: Hand Atlas of Human Anatomy, 2nd ed. Edited and translated by L. F. Baker. Philadelphia, J. B. Lippincott Co., 1861. 76. Spinner, M., and Kaplan, E. B.: The quadrate ligament of the elbow: its relationship to the stability of the proximal radio-ulnar joint. Acta Orthop. Scand. 41:632, 1970. 77. Steindler, A.: Kinesiology of the Human Body, 5th ed. Springfield, IL, Charles C Thomas, 1977. 78. Stimson, H.: Traumatic rupture of the biceps brachii. Am. J. Surg. 29:472, 1935. 79. Strachan, J. H., and Ellis, B. W.: Vulnerability of the posterior interosseous nerve during radial head resection. J. Bone Joint Surg. 53B:320, 1971. 80. Tanaka, S., An, K. N., and Morrey, B. F.: Kinematics of ulnohumeral joint in simulated active elbow motion. Submitted for publication. 81. Terry, R. J.: New data on the incidence of the supracondylar variation. Am. J. Phys. Anthropol. 9:265, 1926.

82. Thepaut-Mathieu, C., and Maton, B.: The flexor function of the m. pronator teres in man: a quantitative electromyographic study. Eur. J. Appl. Physiol. 54:116, 1985. 83. Thomas, T. T.: A contribution to the mechanism of fractures and dislocations in the elbow region. Ann. Surg. 89:108, 1929. 84. Thompson, H. C., III, and Garcia, A.: Myositis ossificans: aftermath of elbow injuries. Clin. Orthop. 50:129, 1967. 85. Tillman, B.: A Contribution to the Function Morphology of Articular Surfaces. Translated by G. Konorza. Stuttgart, Georg Thieme, P. S. G. Publishing, 1978. 86. Trotter, M.: Septal apertures in the humerus of American whites and negros. Am. J. Phys. Anthropol. 19:213, 1934. 87. Tubbs, R. S., Oakes, W. J., and Salter, E. G.: The subanconeus muscle. Folia Morphol. (Warsz.) 65:22, 2006. 88. Yilmaz, E., Karakurt, L., Belhan, O., Bulut, M., Serin, E., and Avci, M.: Variaton of carrying angle with age, sex, and special reference to side. Orthopedics 28:1360, 2005. 89. Yamaguchi, K., Sweet, F. A., Bindra, R., Morrey, B. F., and Gelberman, R. H.: The extraosseous and intraosseous arterial anatomy of the adult elbow. J. Bone Joint Surg. 79A:1653, 1997.

Chapter 3 Biomechanics of the Elbow

CHAPTER

3

Biomechanics of the Elbow Kai-Nan An, Mark E. Zobitz, and Bernard F. Morrey

INTRODUCTION Upper extremity use depends largely on a functional elbow joint. A complex joint, the elbow serves as a link in the lever arm system that positions the hand, as a fulcrum of the forearm lever, and as a load-carrying joint. Mobility and stability of the elbow joint are necessary for daily, recreational, and professional activities. Loss of function in the elbow, possibly more than that in any other joint, can jeopardize individual independence. In our practice, a working knowledge of biomechanics has been extremely important and rewarding. Clinical relevance includes elbow joint design and technique, the rationale and execution of trauma management, and ligament reconstruction. In short, a clear understanding of biomechanics provides a scientific basis for clinical practice.5 From the clinician’s perspective, we have found the topic of elbow mechanics best discussed according to motion (kinematics), stability (constants), and strength (force transmission).

KINEMATICS The elbow is described as a trochoginglymoid joint. That is, it possesses 2 degrees of freedom (motion): flexionextension and supination-pronation. The articular components include the trochlea and capitellum on the medial and lateral aspects of the bifurcated distal humerus, and distally the upper end of the ulna and the head of the radius. Thus, the joint is composed of three articulations: the radiohumeral, the ulnohumeral, and the radioulnar.

FLEXION-EXTENSION Because of the congruity at the ulnohumeral articulation and surrounding soft tissue constraint, elbow joint motion is considered primarily a hinge type. Yet, two

39

separate three-dimensional studies of passive motion at the elbow revealed that the elbow does not function as a simple hinge joint.51,69 The position of the axis of elbow flexion, as measured from the intersection of the instantaneous axis with the sagittal plane, follows an irregular course. A type of helical motion of the flexion axis has been demonstrated.69 This pattern was previously suggested26,50,61 and was attributed to the obliquity of the trochlear groove along which the ulna moves.52 An electromagnetic tracking device that allows a threedimensional measurement of simulated active elbow joint motion reveals the amount of potential varusvalgus and axial laxity that occurs during elbow flexion to average about 3 to 4 degrees. This has been confirmed with more advanced electromagnetic tracking technology.101

CENTER OF ROTATION The axis of motion in flexion and extension has been the subject of many investigations.60 Fischer (1909), using Reuleaux’s technique, found the so-called locus of the instant center of rotation to be an area 2 to 3 mm in diameter at the center of the trochlea (Fig. 3-1).34 Subsequent experiments with the same technique described a much larger locus.32 In a three-dimensional study of passive motion of the elbow joint, the observations of Fischer were confirmed by using the biplanar x-ray technique.69 Based on direct experimental study as well as analytic investigation, Youm and associates109 concluded that the axis does not change during flexionextension. In our study, however, variations of up to 8 degrees in the position of the screw axis from individual to individual have been shown. As seen from below, the axis of rotation is internally rotated 3 to 8 degrees relative to the plane of the epicondyles. In the coronal plane, a line perpendicular to the axis of rotation forms a proximally and laterally opening angle of 4 to 8 degrees with the long axis of the humerus.105 These data, coupled with the clinical information regarding implant loosening, have inspired the development of less constrained but coupled elbow joint replacement designs. It recently has been demonstrated that these designs do function as semiconstrained implants and allow for the normal out-of-plane rotations noted earlier (see Chapter 49).75 From a practical point of view, despite the different findings of various investigators, the deviation of the center of joint rotation is minimal and the reported variation is probably due to limitations in the experimental design. Thus, the ulnohumeral joint could be assumed to move as a uniaxial articulation except at the extremes of flexion and extension. The axis of rotation passes through the center of the arcs formed by the trochlear sulcus and capitellum.56

Part I Fundamentals and General Considerations

40

Y

2.5mm

7.8mm

90 80

110 100 10

70 30 60 50 40

20 120

0

X Z

FIGURE 3-1 Configuration and dimensions of the locus of the instant center of rotation of the elbow. This axis runs through the center of the articular surface, as viewed on both the anteroposterior (AP) and the lateral planes.

The center of rotation can be identified from external landmarks. In the sagittal plane, the axis lies anterior to the midline of the humerus92 and lies on a line that is colinear with the anterior cortex of the distal humerus.69 The coronal orientation is defined by the plane of the posterior cortex of the distal humerus.19 This axis emerges from the center of the projected center of the capitellum and from the anteroinferior aspect of the medial epicondyle (see Fig. 3-1). Similarly, the effect of altering the center of rotation on the kinematics of the forearm has been recently studied. Alterations of as much as 5 mm proximally, distally, anteriorly, or posteriorly have been shown to have only a slight effect on elbow kinematics (Fig. 3-2). This observation has great clinical relevance regarding the design and insertion of prosthetic replacement and articulating external fixation devices.

FOREARM ROTATION The radiohumeral joint, which forms the lateral half of the elbow joint, has a common transverse axis with the elbow joint, which coincides with the ulnohumeral axis during flexion-extension motion. In addition, the radius rotates around the ulna, allowing for forearm rotation or supination-pronation. In general, the longitudinal

axis of the forearm is considered to pass through the convex head of the radius in the proximal radioulnar joint and through the convex articular surface of the ulna at the distal radioulnar joint.34,97 The axis therefore is oblique to the longitudinal axes of both the radius and the ulna (Fig. 3-3), and rotation is independent of elbow position.45 Mori has characterized the axis of forearm rotation as passing through the attachment of the interosseous membrane at the ulna in the distal fourth of the forearm (see Fig. 3-32).62 This may have particular applications with regard to the sensitivity of forearm rotation to angular deformity in this particular portion of the bone. Clinically and experimentally, less than 10% angulation of either the radius or the ulna causes no functionally significant loss of forearm rotation.91 In the past, ulnar rotation was described as being coupled with forearm rotation.106 This observation could not be reproduced in a subsequent study by Youm and associates.108 By using a metal rod introduced transversely into the ulna, extension, lateral rotation, and then flexion of the ulna was described with rotation from pronation to supination. The axial rotational movements of the ulna were also observed by others.14,22,30,43,69,88,108 Ray and associates88 also suggested that varus-valgus movement of the ulna occurs if the forearm rotates on an axis extending from the head of the radius to the index finger. Experiments from our laboratory76 have demonstrated external axial rotation of the ulna with forearm supination. Internal rotation or closure of the lateral ulnohumeral joint occurs with pronation. Finally, the radius has been shown to migrate 1 to 2 mm proximally with pronation.67 This observation had not been reported previously but has been confirmed by observations at the wrist.82

CARRYING ANGLE The carrying angle is defined as that formed by the long axis of the humerus and the long axis of the ulna. It averages 10 to 15 degrees in men and is about 5 degrees greater in women.1,18,53,97 However, uncertainty has arisen over the use of the term carrying angle in the dynamic setting. Dempster27 described an oscillatory pattern during elbow flexion, whereas Morrey and Chao69 reported a linear change, with the valgus angle being the greatest at full extension and diminishing during flexion. The confusion arises because three descriptions based on different reference systems have been adopted for the measurement of carrying angle changes. Definition 1 The carrying angle is the acute angle formed by the long axis of the humerus as the long axis

Chapter 3 Biomechanics of the Elbow

A

= 5mm ANTERIOR AO-OO varus-valgus and axial rotations, Normalized to OO

DO-OO varus-valgus and axial rotations, Normalized to OO 4 2 0 –2 –4 –6

3 2 1 0 –1 –2 –3

B FIGURE 3-2

0

50

100

3 2 1 0 –1 –2 –3

150

20

0

40

60

80

100

Flexion

Flexion

DO-OO/vrvl DO-OO/irer

AO-OO/vrvl AO-OO/irer

120

140

PROXIMAL

POSTERIOR

PRO-OO varus-valgus and axial rotations, Normalized to OO

PO-OO varus-valgus and axial rotations, Normalized to OO

0

50

100 Flexion PRO-OO/vrvl PRO-OO/irer

150

Degrees, Varus, ER(-) /Valgus, IR(+)

Degrees, Varus, ER(-) /Valgus, IR(+)

Degrees, Varus, ER(-) /Valgus, IR(+)

DISTAL

4 2 0 –2 –4 –6

0

50

100

150

Flexion PO-OO/vrvl PO-OO/irer

Experimental data using the electromagnetic tracking system reveals 5-mm changes in the elbow axis site (A) and causes relatively small effects in the kinematics of the forearm (B).

41

42

Part I Fundamentals and General Considerations

of the ulna projects on the plane containing the humerus (Fig. 3-4A).

Proximal radial-ulnar joint

Definition 2 The carrying angle is described as the acute angle formed by the long axis of the ulna and the projection of the long axis of the humerus onto the plane of the ulna (see Fig. 3-4B).

Ulna

Radius

Distal radial-ulnar joint

FIGURE 3-3

The longitudinal axis of pronationsupination runs proximally from the distal end of the ulna to the center of the radial head. The axis is at the ulnar cortex in the distal one third of the forearm.

Definition 3 The carrying angle is defined analytically as the abduction-adduction angle of the ulna with respect to the humerus when eulerian angles are being used to describe arm motion. From an anatomic point of view, it is not difficult to conclude that the existence of the carrying angle is due to the existence of obliquities, or cubital angles, between the proximal humeral shaft, the trochlea, and the distal ulnar shaft. By assuming that the ulnohumeral joint is a pure hinge joint and that the axis of rotation coincides with the axis of the trochlea, the change in the carrying angle during flexion can be defined as a function of anatomic variations of the obliquity of the articulations according to simple trigonometric calculations.8 If the first or second definition is accepted, the carrying angle changes minimally during flexion. The specific varus/ valgus relationship of the forearm to the humerus during flexion therefore depends on the relative angular relationship of the humeral and ulnar articulations (Fig. 3-5).

FIGURE 3-4

A

B

A, Carrying angle between the humerus and the ulna as measured by viewing from the direction perpendicular to the plane containing the humeral and the flexion axes. Conventionally, the acute angle instead of the obtuse angle shown is used as the carrying angle measurement. B, Carrying angle between humerus and ulna as measured by viewing from the direction perpendicular to the plane containing the ulnar and flexion axes. Conventionally, the acute angle instead of the obtuse angle shown is based as the carrying angle measurement. (From An, K. N., Morrey, B. F., and Chao, E. Y. S.: Carrying angle of the human elbow joint. J. Orthop. Res. 1:369, 1984.)

Chapter 3 Biomechanics of the Elbow

30°

43

30°

FIGURE 3-6

The distal humeral forward flexion is complemented by a 30-degree posterior rotation of the opening of the greater sigmoid notch. (With permission, Mayo Foundation.)

A

B

FIGURE 3-5

The positional relationship of the forearm referable to the humerus in the frontal plane of the humerus (carrying angle) is dependent on the relative tilt of the humeral and ulnar articulations referable to their long axes.

RESTRICTION OF MOTION In normal circumstances, elbow flexion ranges from 0 degrees or slightly hyperextended to about 150 degrees in flexion. Forearm rotation averages from about 75 degrees (pronation) to 85 degrees (supination) (see Chapter 2). The cartilage of the trochlea forms an arc of about 320 degrees, whereas the sigmoid notch creates an arc of about 180 degrees. Generally, the arc of the radial head depression is about 40 degrees,97 which articulates with the capitellum, presenting an angle of 180 degrees. The significance of the 30-degree anterior angulation of the trochlea with the 30-degree posterior orientation of the greater sigmoid notch to flexion and extension and stability of the elbow joint is discussed in detail in Chapter 1 (Fig. 3-6). Impact of the olecranon process on the olecranon fossa and the tension of the anterior ligament and the flexor muscles as well as tautness of the anterior bundle of the medial collateral ligament have been described as serving as a check to extension.40,52 The anterior muscle bulk of the arm and forearm, along with contraction of the triceps, is also reported to prevent active flexion beyond 145 degrees.52 However, the factors limiting passive flexion include the impact of the head of the radius against the radial fossa, the impact of the coronoid process against the coronoid fossa, and tension from the capsule and triceps. For pronation and supination, Braune and Flugel20 found that passive resistance of the stretched antagonist

muscle restricts the excursion range more than that of the ligamentous structures. Spinner and Kaplan,96 however, have shown that the quadrate ligament does provide some static constraint to forearm rotation. Impingement of tissue restrains pronation, especially by the flexor pollicis longus, which is forced against the deep finger flexors. The entire range of active excursion in an intact arm is about 150 degrees, whereas when the muscles are removed from a cadaver specimen, the range increases to 185 to 190 degrees. With cutting the ligaments, the range increased up to 205 to 210 degrees.

CAPACITY AND CONTACT AREA OF THE ELBOW JOINT The capacity of the elbow joint recently has been shown to average about 25 mL. The maximum capacity is observed to occur with the elbow at about 80 degrees of flexion.78 This explains the clinical observation that stiff elbows tend to have fixed deformities at about 80 to 90 degrees of flexion.63 Accurate measurement of the contact points of the elbow is extremely difficult, and several techniques have been applied to this highly congruous joint.99 Silicone casting, Fuji Prescale film, and reversible cartilage staining are most commonly used. Each has advantages and disadvantages. The contact area of the articular surface during elbow joint motion has been investigated by Goodfellow and Bullough, using a staining technique.39 They found that the central depression of the radial head articulates with the dome of the capitellum and that the medial triangular facet was always in contact with the ulna. The upper rim of the radial head made no contact at all. At the humeroulnar joint, the articular surfaces were always in contact during some phases of movement. Others have verified these observations.107 The contact areas on the ulna occurred anteriorly and pos-

44

Part I Fundamentals and General Considerations

teriorly and tended to move together and slightly inward from each side from 0 to 90 degrees of flexion and with increasing load.31,74 Using a wax casting technique, in full extension, the contact has been observed to be on the lower medial aspect of the ulna, whereas in other postures, the pressure areas described a strip extending from posterolateral to anteromedial.37 The radiocapitellar joint also revealed contact during flexion without externally applied load. Investigations in our laboratory show that the contact areas of the elbow occur at four facets: two at the coronoid and two at the olecranon (Fig. 3-7). Only a slight increase in total surface area occurred with elbow flexion and with a sevenfold increase in load.99 With a 10-N load, about 9% contact of the articular surfaces occurs, and with 1280 N, the area increased to about 73%.31

Degrees flexion 0° 90° Medial

FIGURE 3-7

Contact in the sigmoid fossa moves toward the center of the fossa during elbow flexion. (Redrawn from Walker, P. S.: Human Joints and Their Artificial Replacements. Springfield, IL, Charles C. Thomas, 1977.)

When varus and valgus loads are applied to the forearm, the contact changes medially and laterally. This implies a pivot point about which the radioulnar articulation rotates on the humerus in the anteroposterior (AP) plane in extension with varus and valgus stress. In vivo experiments have demonstrated the varus-valgus pivot point of the elbow to reside in the midpoint of the lateral face of the trochlea (Fig. 3-8).

ELBOW STABILITY The elbow is one of the most congruous joints of the musculoskeletal system and, as such, is one of the most stable. This feature is the result of an almost equal contribution from the soft tissue constraints and the articular surfaces. The static soft tissue stabilizers include the collateral ligament complexes and the anterior capsule. Studies from our laboratory regarding the anatomy of the lateral collateral ligament68,77 and others36,79,95 have been discussed previously (see Chapter 2). The lateral collateral ligament and the anterior bundle of the medial collateral ligament originate from points through which the axis of rotation passes. Furthermore, the medial collateral ligament has two discrete components.66,93 The anterior bundle has been shown to be taut in extension; the converse is true for the posterior fibers of the anterior bundle. Because elbow joint motion occurs about a nearly perfect hinge axis through the center of the capitellum and trochlea, the posterior bundle of the medial collateral ligament complex will be taut at different positions of elbow flexion (Fig. 3-9). The lateral collateral ligament and the anterior bundle lying on the axis of rotation will assume a rather uniform tension, regardless of elbow position. Furthermore, the lateral ulnar collateral ligament has inserts on the ulna

FIGURE 3-8

The line of action in the muscles produces a compression force at the radial head when situated just lateral to the middle of the lateral face of the trochlea, and a tension force on the radial head is situated just medial to this point. This indicates that the varus-valgus pivot point in the elbow lies at that point on the AP plane. (From Morrey, B. F., An, K. N., and Stormont, T. J.: Force transmission through the radial head. J. Bone Joint Surg. [Am.] 70:250-256, 1988.)

Normalized distance: Origin to insertion

Chapter 3 Biomechanics of the Elbow

2

45

A - MCL

FIGURE 3-9 RCL 0 0

20 40 60 80 100 120 140 Elbow joint flexion angle (deg)

The anterior medial collateral ligament remains more taut during elbow flexion than does the posterior segment of the ligament. The radial collateral ligament originates at the axis of rotation for elbow flexion; hence, the ligament has little length variation during flexion and extension. (With permission, Mayo Foundation.)

Radial collateral ligament Annular ligament

Lateral ulnar collateral ligament

FIGURE 3-10

The orientation and attachment of the lateral collateral ligament stabilizes the ulna to resist varus and rotatory stresses just as the medial ligament resists valgus stress.

and, as such, helps to stabilize the lateral ulnohumeral joint (Fig. 3-10).23,66,77,81 In experiments performed in our laboratory, O’Driscoll and associates have demonstrated that the lateral ulnar collateral ligament is essential to control the pivot shift maneuver (see Chapter 4). Further evidence of the contribution of the lateral ligament complex to elbow stability is offered by Søjbjerg and associates.94 These investigators also attributed a major role in varus and valgus stability to the annular ligament. Although our work suggests that the major component in the varus and rotatory stability is the structure termed the lateral ulnar collateral ligament, the parallel findings of these investigators suggest that

the lateral complex is, in fact, a major valgus stabilizer of the elbow joint and functions with or without the radial head.80

ARTICULAR AND LIGAMENTOUS INTERACTION The influence of the ligamentous and articular components on joint stability are usually studied with the use of the materials testing machine by imparting a given and controlled displacement to the elbow.47,65,87 The relative contribution of each stabilizing structure can be demonstrated by sequentially eliminating each element and observing the load recorded by the load cell for the

46

Part I Fundamentals and General Considerations

Intact Radial heat excised

Moment 3 (N-m) 2 1

Varus 3°

2°

1° 1

Source

UCL-cut 1°

2°

3° 4° Valgus

Sensor

2 RCL = Radial collateral lig UCL = Ulnar collateral lig

3 4

Load Displacement

5

A

6 Moment 4 (N-m) 3

Intact RCL-cut Radial heat excised UCL-cut

2 1

Varus 5°

4°

3°

2°

1°

1

1°

2°

3°

4° 5° Valgus

Valgus

Varus

FIGURE 3-12

The arrangement of the electromagnetic tracking device allows varus-valgus stresses applied to the elbow during simulated motion with the flexor and extensor muscles. Real-time simultaneous threedimensional motion of the forearm may be monitored with reference to the humerus.

2 3 4

B

RCL = Radial collateral lig UCL = Ulnar collateral lig Load Displacement

FIGURE 3-11

Force displacement curves demonstrate relative contribution of elements to elbow stability in extension (A) and flexion (B). (From Morrey, B. F., and An, K. N.: Articular and ligamentous contributions to the stability of the elbow joint. Am. J. Sports Med. 11:315, 1983.)

TABLE 3-1 Percent Contribution of Restraining Varus-Valgus Displacement Position

Component

Varus

Valgus

Extension

MCL

—

30

LCL

15

—

Capsule

30

40

Articulation

55

30

MCL

—

55

LCL

10

—

Articulation

75

35

Flexion

constant displacement imparted, usually 2 to 5 degrees95 (Fig. 3-11). A simplified summary of the observations from such an experiment is shown in Table 3-1. In extension, the anterior capsule provides about 70% of the soft tissue restraint to distraction, whereas the medial collateral ligament assumes this function at 90 degrees of flexion. Varus stress is checked in extension equally by the joint articulation (55%) and the soft tissue, lateral collateral ligament, and capsule. In flexion, the articulation provides 75% of the varus stability. Valgus stress in extension is equally divided between the medial collateral ligament, the capsule, and the joint surface. With flexion, the capsular contribution is assumed by the medial collateral ligament, which is the primary stabilizer (54%) to valgus stress at this position. Furthermore, for all practical purposes, the anterior portion of the medial collateral ligament provides virtually all of the structure’s functional contribution. Limitations of this experimental model have resulted in an overestimation of the role of the radial head in

MCL, medial collateral ligament complex; LCL = lateral collateral ligament complex.

resisting valgus load.47,65,90 This has prompted the development of an experimental technique that allows simultaneous and accurate measurement of three-dimensional angular and translational changes under given loading conditions (Fig. 3-12). Using the electromagnetic tracking device, an accurate technique for measuring the function of the articular and capsuloligamentous structures was developed.70 More accurate and relevant data were generated.70 Valgus stability is resisted primarily by the medial collateral ligament. With an intact medial collateral ligament, the radial head does not offer any significant additional valgus constraint. With a released or compromised medial collateral ligament, the radial head does resist valgus stress. This important experiment documents that the radial head is a secondary stabilizer

Chapter 3 Biomechanics of the Elbow

Abduction - deg

20

15

10

R head - MCL

RH+PMCL+AMCL RH+PMCL RH INTACT

5

0

0

20

40

A

60 80 100 Elbow flexon - deg

120

140

25

Abduction - deg

20 15

Radial head contribution

10

MCL

5 0 0

20

40

60

80

100

120

140

Elbow flexion - deg

B

MCL+RH PMCL+AMCL

PMCL Intact

FIGURE 3-13

The stabilizing role of the radial head to valgus stress with the collateral intact resection of the radial head has little effect on valgus stability (A). However, if the medial collateral ligament (MCL) has been sectioned, the absence of a radial head markedly increases valgus displacement (B). The fact that the radial head is important only when the medial collateral ligament is released defines the radial head as the secondary stabilizer against valgus stress.

for resisting valgus stress, whereas the medial collateral ligament is the primary stabilizer against valgus force (Fig. 3-13). In a laboratory investigation, the hyperextension trauma produces lesions of the anterior capsule, the avulsion of proximal insertions of both medial and lateral collateral ligaments.103 The degree of extension increased by 17 degrees and induced significant joint laxity in forced valgus internal-external rotation, but not varus.103 It has been recently observed that the valgus and varus laxity of the elbow is dependent on forearm rotation.86 Increased valgus/varus laxity with forearm pronation, particularly in medial collateral ligament deficient elbows, implies a possible additional factor in throwing kinematics that might put professional baseball pitchers at risk of medial collateral ligament injury due to chronic

47

valgus overload. The forearm rotation should be considered during the clinical examination of elbow instability. The stabilizing effects of monoblock and bipolar designs of radial head replacements in cadaver elbows with a deficient medial collateral ligament were studied.85 The constraint mechanism inherent in the implant design significantly affected the mean valgus laxity. The implants all performed similarly except in neutral forearm rotation, in which the elbow laxity associated with the Judet implant was significantly greater than that associated with the other two implants. Comminuted radial head fractures associated with an injury of the medial collateral ligament can be treated with a radial head implant. However, lengthening and shortening of the radial neck by 2.5 mm significantly alters the kinematics and contact pressure through the radiocapitellar joint in the medial collateral ligamentdeficient elbow104 (Fig. 3-14). Radial neck lengthening caused a significant decrease in varus-valgus laxity and ulnar rotation, with the ulna tracking in varus and external rotation. Shortening caused a significant increase in varus-valgus laxity and ulnar rotation, with the ulna tracking in valgus and internal rotation. Therefore, a radial head replacement should be performed with the same level of concern for accuracy and reproducibility of component position and orientation as is appropriate with any other prosthesis. Total elbow arthroplasty has been a valuable procedure for treating patients with rheumatoid arthritis, post-traumatic arthritis, osteoarthritis, and failed reconstructive procedures of the elbow. The development of elbow prostheses diverged into two general types: linked and unlinked. The main concern with such development of unlinked elbow replacements is instability, which is attributable to numerous factors including prosthesis design, ligament integrity, and position of the prosthesis. A series of laboratory studies have been performed to examine the intrinsic constraint of various total elbow arthroplasty designs, as well as the joint laxity after implantation in cadaveric specimens6 (Fig. 3-15). The contribution of the articular geometry to elbow stability was further evaluated by serial removal of portions of the proximal ulna, as shown in Figure 3-16.13 Valgus stress, both in extension and at 90 degrees of flexion, was primarily (75% to 85%) resisted by the proximal half of the sigmoid notch, whereas varus stress was resisted primarily by the distal half, or the coronoid portion of the articulation, both in extension (67%) and in flexion (60%). As demonstrated in subsequent chapters, the central role of the coronoid to provide elbow stability is emerging. As serial portions of the coronoid are removed, the elbow becomes progressively more unstable. If the radial head has been resected, as little as 25% resection causes elbow subluxation at about 70 degrees of flexion. Our

48

Part I Fundamentals and General Considerations

FIGURE 3-14 Average varus (-) or valgus (+) position of the ulna under different radial neck shortening and lengthening conditions, with the application of valgus (top line) or varus (bottom line) gravitational stress. (From Van Glabbeek, F., Van Riet, R. P., Baumfeld, J. A., Neale, P. G., O’Driscoll, S. W., Morrey, B. F., and An, K. N.: Detrimental effects of overstuffing or understuffing with a radial head replacement in the medial collateral-ligament deficient elbow. J. Bone Joint Surg. [Am.] 86:2629, 2004.)

Pritchard-ERS Capitello-Condylar Sorbie-Questor Souter GSB Norway Coonrad-Morrey Human 0

2

4

6

8

10

12

14

Valgus-varus laxity (degrees)

FIGURE 3-15

Joint laxity for human elbow and with total elbow replacement including the SouterStrathclyde, Sorbie-Questor, Pritchard ERS, Ewald Capitellocondylar, GSB III, Norway Elbow, and Coonrad Morrey implants. (From An, K. N.: Kinematics and constraint of total elbow arthroplasty. J. Shoulder Elbow Surg. 14:168S, 2005.)

preliminary studies indicate at least 50% of the coronoid is necessary for elbow stability if the radial head is removed (Fig. 3-17).

FORCE ACROSS ELBOW JOINT Study of the force across the elbow joint is not an easy task. The analysis can be performed at various degrees of sophistication. It can be either two-dimensional or three-dimensional, static or dynamic, with or without the hand activities. The clinical implications of these

forces are obvious, but the magnitudes are not common knowledge. Consequently, in this section, the factors that affect the force passing through the elbow joint will first be analyzed in detail based on two-dimensional considerations. Then, more realistic data based on threedimensional analysis will be presented.

TWO-DIMENSIONAL ELBOW FORCE ANALYSIS In sagittal plane motion, the elbow joint is assumed to be a hinge joint. Forces and moments created at the joint, due to the loads applied at the hand, are balanced by

Chapter 3 Biomechanics of the Elbow

49

= components in x and y direction for the unit vector along the line of action of muscle; Rx, Ry = x and y components of the joint contact force; P, Px, Py = magnitude of the applied forces on the forearm and its associated components; and ri, rp = moment arms of the muscle force and the applied force to the elbow joint center, respectively

fxi, fyi

Combined elbow stability (% of intact)

100 80 25 75 50 100

60 40 20

Elbow angle 0 90

0 25

50

75

100

Excision of proximal ulna (% osteotomy)

FIGURE 3-16

Removal of successive portions of the proximal ulna was studied for its effect on various modes of joint stability. A linear decrease of combined stability is observed, with removal of the olecranon. Note a similar effect for both the extended and the 90degree flexed positions. 100 Elbow stability

50% Coronoid resection 90 60 30 Radial head resection

0 0

15

30

45

60

75

90

105

120

Single-Muscle Analysis

Elbow flexion

FIGURE 3-17

Ulnohumeral instability increases as increasing amounts of coronoid are removed. Resection of 50% of the coronoid can still be stable, but not if the radial head is excised.

the muscles, tendons, ligaments, and contact forces on the articular surfaces. The amount of tension in the muscles and the magnitude and direction of the joint forces are determined by the external loading conditions as well as the responses of muscles-that is, force distribution among these muscles. To calculate these forces, a free-body analysis of the forearm and hand isolated at the elbow joint is required. From this analysis, a set of equilibrium equations is obtained: Σ | Fi | fxi + Rx + Px = 0 Σ | Fi | fyi + Ry + Py = 0 Σ | Fi | · ri + P · rp = 0

The lines of action of muscles crossing the joint have been reported.2,8,84 In the sagittal plane, based on the magnitude of moment arms, the major elbow muscles consist of biceps, brachialis, brachioradialis, extensor carpi radialis longus, triceps, and anconeus (Table 3-2). The other forearm muscles for the hand and wrist provide various but limited contributions to elbow flexion-extension. Unfortunately, the contributions of these forearm muscles are not consistently reported in the literature. Assuming that friction and ligament forces are negligible, the resultant joint constraint force vector should be perpendicular to the arc of the articular surface and pass through the center of curvature of this arc. Thus, the problem of elbow force analysis may be reduced to one of solving the unknown variables Rx, Ry, and | Fi | in equation [1]. However, in reality, even for a simple task, multiple muscles are involved, making the force calculation an indeterminate problem. Methods for resolving these indeterminate problems are thus required.

[1]

in which | Fi | = magnitude of the tension in ith muscle;

The simplest case is to consider only one single muscle involved in resisting external force. This type of consideration has been used widely in the literature for twodimensional force analysis of the musculoskeletal system. The magnitude of the muscle force, f, and the magnitude and orientation of the joint reaction force, R, can be obtained by solving equation [1] with i = 1. f=

rp M d = cos ψ + sin ψ P rf rf R 2 = f + 2f cos (θ + ψ ) + 1 P f sin θ − sin ψ φ = tan −1 f cos θ + cos ψ

[2]

where ψ, θ and φ are the angles between the forearm axis and the applied force, P, muscle pull, M, and resultant joint force, R, respectively. Thus, an intimate relationship between the joint force and muscle forces in balancing the externally applied force on the forearm (Table 3-3) exists. The magnitude of muscle force required for balancing the external force reflects the changes of the muscle’s moment arm, or

Part I Fundamentals and General Considerations

50

TABLE 3-2 Physiologic Cross-Sectional Area (PCSA), Unit Force Vector (Fx, Fy), and Moment Arm (r) of Elbow Muscles in Sagittal Plane ELBOW JOINT FLEXION ANGLE (DEGREE) 0 DEGREES Muscle

PCSA*

30 DEGREES

90 DEGREES

120 DEGREES

r†

Fx

Fy

r

Fx

Fy

r

Fx

Fy

r

Fx

Fy

BIC

4.6

20.7

.86

.50

20.7

.86

.50

45.5

.17

.99

40.0

.35

.93

BRA

7.0

15.2

.82

.57

15.2

.82

.57

33.5

.36

.92

33.8

.12

.97

BRD

1.5

30.8

.99

.11

30.8

.99

.04

75.0

.92

.39

79.9

.89

.41

FCR

2.0

2.0

1.0

.04

2.0

1.0

.04

5.0

1.0

.04

5.9

1.0

.04

ECRL

2.4

8.6

.99

.16

8.6

.99

.16

29.3

.97

.25

32.0

.97

.26

FCU

1.6

0.0

1.0

.04

0.0

.99

.04

0.0

1.0

.04

0.0

1.0

.04

TRI

18.8

23.0

1.0

.09

26.0

.81

.59

20.0

.05

1.0

17.0

.05

1.0

ECRB

1.5

1.0

.99

.17

1.0

.99

.17

2.0

.96

2.8

2.5

.96

.28

ECU

1.7

2.0

.99

.16

9.0

.99

.16

9.0

.98

.19

8.0

.98

.19

EDC

3.8

0.0

.99

.17

0.0

.99

.17

2.0

.98

.22

2.0

.99

.23

FDS

3.0

4.0

1.0

.04

3.0

1.0

.05

3.5

1.0

.04

3.5

1.0

.04

BIC, biceps; BRA, brachialis; BRD, brachioradialis; ECRB, extensor carpi radialis brevis; ECRL, extensor carpi radialis longus; ECU, extensor carpi ulnaris; EDC, extensor digitorum communis; FCR, flexor carpi radialis; FCU, flexor carpi ulnaris; FDS, flexor digitorum superficialis; TRI, triceps. *PCSA = cm2. † r = mm. M2

M1

M3

mechanical advantage, with changes of the joint configuration.

Effect of Muscle Moment Arm + P

R1 +

R2 R

3

FIGURE 3-18

Effect on the muscle and joint forces by changing the moment arm of the muscle force. For a given externally applied force, the longer moment arm decreases the muscle and joint forces. Also, the resultant joint force and orientation (R1, R2, R3) are affected by the magnitude of the muscle moment arm.

The effect of a changing muscle moment arm on the resultant joint force is demonstrated graphically in Figure 3-18. If the loading configuration does not change, both the muscle force and the joint reaction force decrease as the muscle moment arm increases. The orientation of the resultant force also changes from the middle portion of the trochlear notch toward the border of the articular cartilage. Clinically, the concept of increasing the moment arm of the biceps muscle by moving the insertion distally has been adopted for increasing weak flexion force of the elbow in patients with brachial plexus injury.72

Effect of Orientation on Muscle Line of Action Under the same loading condition, the effect of changing the orientation of the muscle line of action under a constant moment arm is demonstrated (Fig. 3-19). The applied force is again assumed to be perpendicular to the forearm. Both magnitudes of muscle and joint reaction forces change slightly with the change of the muscle’s line of action. However, the orientation of the resultant joint force is sensitive to changes in the muscle force line. The orientation of the resultant joint force, therefore, moves from the central portion of the trochlea toward

Chapter 3 Biomechanics of the Elbow

51

Muscle and Joint Forces with Single Muscle*

TABLE 3-3

ELBOW JOINT FLEXION ANGLE (DEGREE) 0 DEGREES

30 DEGREES

90 DEGREES F/P

120 DEGREES

F/P

R/P

φ

F/P

R/P

φ

R/P

φ

F/P

R/P

φ

BIC

15.5

15.5

27.0

15.5

15.0

27.0

7.0

6.1

78.7

8.0

7.1

66.4

BRA

21.1

20.5

32.0

21.1

20.5

32.0

9.6

8.6

66.3

9.5

8.5

82.6

BRD

10.4

10.4

3.2

10.4

10.4

3.2

4.3

4.0

9.6

4.0

3.7

10.5

TRI

13.9

14.5

39.3

12.3

12.9

39.7

16.0

17.0

87.3

18.8

19.8

87.2

BIC, biceps; BRA, bracialis; BRD, brachioradialis; F, muscle force; P, applied force; R, resultant joint force TRI, triceps. *rp, 320 mm; D, 15 mm; ψ, 90 degrees for flexion; ψ, 270 degrees for extension. φ, angle between R and long ulnar axis.

M2 M1

+

P

R1 + R2

FIGURE 3-19

Effect of changing the orientation of the muscle line of action on the muscle and joint force under a given load. The magnitudes of both muscle and joint forces are not changed, but their orientations are.

the rim as the direction of muscle pull relative to the forearm changes from vertical to parallel. This is especially true for the resultant joint force in the trochlear notch brought about by the contraction of the upper arm muscles, whose direction relative to the forearm axis changes with the elbow joint flexion angle. On the other hand, the directions of forearm muscles with respect to the resultant joint forces are thus reasonably constant. When considering the direction of resultant joint forces applied on the trochlea, the effects of upper arm and forearm muscles are just reversed. These changes have been confirmed and directly measured with a force transducer at the proximal radius and different orientation of the line of action of the flexors and extensors.67

Effect of the Moment Arm of External Force With the orientations and moment arms of the muscles kept constant, the magnitude of muscle force and joint

force created to resist the externally applied force decrease proportionally, with the decrease of the moment arm of the external force. This is true, simply because the resultant segmental moment created at the elbow joint due to externally applied load decreases when the moment arm decreases. It should be noticed that the direction of resultant joint force also changes slightly. From the aforementioned results, it is also easy to realize that the magnitude of the muscle and joint force increases proportionally with increases in the magnitude of external force. Therefore, in general, these results are usually expressed in terms of ratio to the external load.

Effect of the Direction of the Externally Applied Force When the force applied at the wrist changes direction from vertical to horizontal, the effective moment arm of this applied force changes. The resultant segmental moment about the elbow joint center due to this force changes as well (Fig. 3-20). Furthermore, when the resultant segmental moments change from flexion to extension, the required muscles also change from flexors to extensors.

Effect of Change in Axis of Rotation The sensitivity of the muscle moment arm to the axis of rotation is a critically important consideration in the clinical setting. Altering the axis by 1 cm anterior, posterior, proximal, and distally has a surprisingly small effect on the muscle moments at the elbow. Such axis changes result in less than 10% change in muscle moment arm values (Fig. 3-21). In summary, the parametric analysis demonstrates that the magnitude and orientation of the resultant joint forces in the trochlear notch depend very much on whether the upper arm or forearm muscles are used, as well as the location and orientation of the external load applied on the forearm and the joint flexion angle that alters the moment arm and orientation of the muscle

52

Part I Fundamentals and General Considerations

line of action. However, alterations of the flexion axis have little impact on muscle moment arm.

Multiple Muscle Analysis In reality, when external loads are applied on the forearm, multiple muscles are involved, and this makes the ana-

d = 1.5 cm rm = 4.44 cm rp = 32.0 cm θ = 47.3º

ψ = 0º

0º 12 0º 15

3 6 0º 90 0º º

FIGURE 3-20

Effect of changes in the orientation of the applied force (χ), where 90 degrees is perpendicular to the long axis of the forearm.

lytic determination of muscle and joint forces difficult. Because the magnitude and orientation of the resultant joint force are two unknown variables, if more than one muscle force is involved the number of unknown variables exceeds the number of available equations (three). This makes the problem indeterminate, and a nonunique solution will result. Several methods have been employed to resolve the indeterminate problem. Electromyographic (EMG) data and the physiologic cross-sectional area may be used to provide an additional equation.35,49 The most commonly adopted techniques are analytic reduction and optimization methods. In the reduction method, the redundant unknown variables are systematically eliminated, making the remaining system uniquely solvable. In a two-dimensional analysis, this method is more or less the same as that which considers only one single muscle, as described in the previous section. This method can usually provide the ranges of magnitude and orientation of the resultant joint forces for a given task. However, the technique may give physiologically unreasonable solutions, such as using one single forearm muscle to resist the forearm load. Additional judgment and screening are thus required. With the use of the optimization method, a unique solution to an indeterminate problem is obtained by minimizing a preselected objective function or cost function.11 Although the solution to the problem is still nonunique, each solution generally is associated with some physiologic phenomenon or condition on which the objective function is constructed and selected. This technique has been described in more detail elsewhere.9

TRICEPS Moment arm (m)

0.06 0.04 0.02 0 0

50

100

0

50

100

150

–0.019 –0.023 –0.027 Flexion angle (deg)

BRACHIALIS

BRACHIORADIALIS Moment arm (m)

0.03 0.02 0.01 0 0

50

100

Flexion angle (deg)

FIGURE 3-21

150

–0.015

Flexion angle (deg)

Moment arm (m)

Intact Ant Post Prox Dist Abd Add Int Ext

Moment arm (m)

BICEPS

150

0.12 0.08 0.04 0 0

50

100

Flexion angle (deg)

A 1-cm alteration in the axis of flexion shows little effect on muscle moment arms.

150

Chapter 3 Biomechanics of the Elbow

Recently, the results based on various object functions have been compared with EMG data regarding the muscles. The dependence of muscle coordination is related more to the degree of freedom considered, and less to the cost function selected.21 The most commonly used objective functions for resolving the indeterminate force analysis problem include linear and nonlinear weighted combinations of the unknown variables. An analytic model for the determination of muscle force across the elbow joint during isometric loading has been developed.10 In addition to the equilibrium equations obtained from free-body analysis, constraints for muscle tensions based on the physiologic considerations of muscle length-tension and velocity-tension relationships were included: 0 ≤ F ≤ Fˆ · PCSA · σ [3] in which F is the magnitude of muscle tension, Fˆ is the normalized muscle force as adjusted by the muscle length, PCSA represents the muscle physiologic crosssectional area, and σ is the upper bound of muscle activation level. The maximum stress could be generated by the muscle. The word activation is used to describe both the number of active units (recruitment) and their degree of activity (firing frequency). The muscle force distribution was then determined by using the optimization method of minimizing σ

[4]

in which σ is taken as the upper bound value of overall activation of all muscles. In this analysis, the effects of muscle architecture on the muscle force were examined.

Major Elbow Muscles We are now in a position to consider several muscles in the solution; these include biceps, triceps, brachialis, and brachioradialis. TABLE 3-4

53

For the loading case of force applied nonperpendicularly at the wrist, the solutions of two types of optimization procedures are shown in Table 3-4. The magnitude (R) and direction (φ) of the resultant joint forces correspond to various loads. The resultant joint force shows more variation along the articular surface with changes of joint flexion (Fig. 3-22). This is because the line of action of the upper arm muscle undergoes a tremendous change in direction with respect to the ulnar axis during flexion, as discussed earlier. The maximum elbow flexion strength occurs at 90 degrees59,71 (see Chapter 5). From the measured lifting strength data, the maximal muscle force per unit of cross-sectional area can be calculated to be in the range of 10 to 14 kg/cm2. About one third to one half of the maximum lifting force can be generated with the elbow in the extended or 30-degree flexed position. At these positions, a force almost three times the body weight can be encountered in the elbow joint during strenuous lifting at about 30 degrees of flexion (Table 3-5). During strenuous actions, the maximum tension that could possibly be provided by each individual muscle is usually considered to be proportional to the physiologic cross-sectional area. This has been carefully measured for muscles crossing the elbow.8 The potential moment contribution of each muscle at the elbow joint can thus be estimated by multiplying its moment arm by its physiologic cross-sectional area. The moment contributions for all of the muscles crossing the elbow joint have been calculated (Fig. 3-23). Of note, the potential moment in varus appears to be balanced by the valgus moment under all of the functional configurations. When flexed, the flexion potential moment seems to be balanced by the extension moment. However, the extension moment exceeds the flexion moment when the elbow is extended.

Muscle and Joint Forces in Resisting Flexion Moment by Three Major Flexors* OPTIMIZATION METHODS FOR SOLUTIONS (ELBOW JOINT ANGLE = 90 DEGREES) Obj = S (MUSCLE STRESS)2

ψ†

BIC

BRA

BRD

Obj‡ = s ; MUSCLE STRESS £ s R

φ

BIC

BRA

BRD

R

φ

0 degrees

.13

.22

.02

.17

17.0

.12

.19

.04

1.17

5.6

30 degrees

1.49

2.55

.26

4.14

56.5

1.43

2.18

.47

3.89

53.3

60 degrees

2.46

4.19

.43

6.30

63.3

2.35

3.58

.77

5.86

60.3

90 degrees

2.76

4.71

.49

6.83

67.4

2.65

4.03

.86

6.31

64.6

120 degrees

2.33

3.97

.41

5.56

72.1

2.23

3.39

.73

5.10

69.6

150 degrees

1.27

2.17

.22

2.88

83.2

1.22

1.85

.40

2.60

81.7

BIC, biceps; BRA, brachialis; BRD, brachioradialis. *Muscle and joint forces are expressed in the unit of externally applied force. † Angle between the vector of externally applied force and the long ulnar axis (degree). ‡ Most realistic solution based on experimental and analytic considerations (see text).

Part I Fundamentals and General Considerations

54

In constructing these moment potential diagrams, it is assumed that all muscles simultaneously and maximally contract to their optimal lengths. To apply these data for more general conditions, consideration should be given and adjustment made for length-tension and force-velocity relationships. In addition, when activities involve submaximal contraction, a proper scaling system based on experimental measurements, such as EMG,3,28,33,35,61 is required. In more refined models, the

90120 Flexion angle:

90120 Flexion angle: Muscle: BIC, BRA, BRD Method: Obj = σ Muscle force < σ

Muscle: BIC

+

+ 0 30

0,30 90120 Flexion angle:

0 30 90 120

90120 Flexion angle: Muscle: BIC, BRA, BRD Method: Obj = ∑ (Muscle stress)2

Muscle: BRA

+

+ 0 30 90 120

Flexion angle:

Flexion angle:

Muscle: BRD

Muscle: BIC, BRA, BRD Method: Obj = ∑ (Muscle force)2

Extensors EMG investigations of the elbow extensor muscles were first completed by Travill in 1962.102 The medial head of the triceps and anconeus muscles were found to be active during extension; the lateral and long head of the triceps acted as auxiliaries. The anconeus also was active during resisted pronation and supination. In fact, the anconeus has been demonstrated to be active during flexion and abduction-adduction resisted motions.35,83

FIGURE 3-22

Joint force magnitude and direction from an applied load at the wrist at various elbow flexion angles. Family of solutions by using different muscle combinations and solution techniques.

TABLE 3-5

EMG analysis is used to provide scaling systems for the muscle force calculations during submaximal contraction and to show the phasic distribution of muscular activities for a given task.

Surface electrodes along the belly of the biceps were first used100 to record electrical activity during dynamic flexion and extension, with and without load. This early study showed a decrease in biceps activity in pronation compared with supination, and that the biceps acted in extension to “brake” the forearm. Subsequent studies have presented inconsistent data, but in almost all investigations, the biceps demonstrates no16 or decreased activity when flexion occurs in pronation.35,58,98 As expected, little influence is reflected in the brachialis muscle with forearm rotation.35,98 The brachioradialis demonstrates electrical activity with flexion, especially with the forearm rotated to the neutral position17,29 or in pronation.35,54,98 These data are summarized for the 90-degree flexion position, because this is the position of maximum strength15,54 and of greatest electrical activity of the elbow flexors35 (Fig. 3-25).

0 30

0,30

Electromyographic Activities of Elbow Muscles

Flexors

+

+

muscle physiology, including the length-velocity-tension relationship, should be considered.10,38 In an analytic modeling, the effect of distal humeral shortening on the triceps force production and thus the elbow extension strength has been demonstrated48 (Fig. 3-24).

Muscle and Joint Forces Under Maximum Flexion Forces

Elbow Flexion Angle (degree)

Maximum Flexion* Strength at Wrist (newton)

MUSCLE FORCE (¥ BODY WEIGHT) BIC

BRA

BRD

Resultant Joint Force

0

90-150

0.79-1.19

1.2-1.81

0.29-0.39

2.15-3.2

30

110-190

1.00-1.48

1.5-2.26

0.32-0.49

2.70-4.1

90

220-383

0.90-1.33

1.3-2.02

0.29-0.43

2.10-3.1

120

178-307

0.72-1.08

1.1-1.66

0.24-0.31

1.70-2.6

BIC, biceps; BRA, brachialis; BRD, brachioradialis. *Based on average body weight of 150 lb.

Anterior

BIC BRD 8.938 BRA 4.252 7.099 PRO 7.810

ECR 11.978 EDC Lateral 10.131 ECU 7.532

Anterior

cm x cm2

FCR Medial 5.563

Lateral

ANC 3.789

TRI 53.301 Posterior

B

A

BIC 6.076 ECR BRD 16.516 4.164 Lateral

cm x cm2

cm x cm2

Anterior BRA 13.649 BIC

ECR BRD 20.233 7.920

BRA 7.914 PRO 6.683 Medial FCR 4.712 FCU FDS 7.868 13.552

EDC 13.213 ECU 11.630 ANC 3.110

15.907 PRO 17.273

Lateral

FCR 4.596

EDC 12.479

ECU 9.847

FDS 11.737

ANC 4.664

Posterior

C

TRI 34.553 Posterior

D

Anterior

Anterior

EDC 11.966

cm x cm2

BRD BIC 6.173 BRA 16.532 14.331 ECR 15.279

BIC 12.156 BRD 5.619

BRA 9.006

PRO 7.742 FCR 3.747

Lateral ECU 11.761 ANC 6.899

Medial

FCU 5.577

TRI 45.393

ECR 13.262

FDS Medial 12.947 FCR 3.514

FCU 7.126

TRI 48.520 Posterior

Anterior

BIC 8.045

EDC 15.197

FDS FCU 17.908 8.984

ANC 3.692

PRO 5.690

BRA BRD 4.092 5.328

ECR 11.978

cm x cm2

Medial

Lateral

PRO 7.611 FCR 4.789 FDS 11.614

EDC 7.855 ECU 9.911

FDS FCU 10.892 7.063

cm x cm2

Medial

FCU 6.566

ANC 5.199

TRI 51.088 TRI 38.602

Posterior

E

F FIGURE 3-23

Posterior

The potential moment contribution of each muscle at the elbow joint was estimated by multiplying the moment arm (cm) of the muscle by its physiologic cross-sectional area (cm2). These diagrams show the contributions to flexion-extension and varus-valgus rotation about the joint center at six elbow and forearm configurations. A, Extended/supinated. B, Extended/neutral. C, Extended/pronated. D, Semiflexed/neutral. E, Flexed/neutral. (From An, K. N., Hui, F. C., Morrey, B. F., Linscheid, R. L., and Chao, E. Y.: Muscles across the elbow joint: A biomechanical analysis. J. Biomech. 14:659, 1981.)

Part I Fundamentals and General Considerations

56

Strength % normal

100

Trochlea

Humerus

Capitulum

Elbow at 30°

80 60

145º 120º

145º

40 120º 90º 60º

20 0 0

10

20

30º

30

120º

90º

11 .4N 90º 0º

60º

30º

Shortening: Origin-insertion/mm

FIGURE 3-24

Length-tension relationship for the triceps with the elbow at 30 degrees of flexion. FLEXION MUSCLE ACTIVITY ELBOW 90º

Supination

Neutral

12.6N

60º 23.9N

Pronation

30º

0º

0º

FIGURE 3-26

Orientation and magnitude of forces at the humeral articular surface during flexion, per unit of force at the hand. (From Amis, A. A., Dowson, D., and Wright, V.: Elbow joint force predictions for some strenuous isometric actions. J. Biomech. 13:765, 1980.)

and, hence, is considered a dynamic joint stabilizer; and (5) generally speaking, the different heads of the triceps and biceps are active in the same manner through most motion.

Brachialis Biceps Brachiorad. Flex. carpi rad.

Forearm Muscles

Ext. carpi rad. Ext. carpi ulna. Anconeus Triceps 0

100

0

100

0

100

% electrical activity

FIGURE 3-25

Electrical activity of the major elbow flexors at 90 degrees of flexion in different forearm rotation positions. (From Funk, D. A., An, K. N., Morrey, B. F., and Daube, J. R.: Electromyographic analysis of muscles across the elbow joint. J. Orthop. Res. 5:529, 1987.)

Thus, the anconeus may be considered a stabilizer of the elbow joint, being active with almost all motions. In 1972, Currier studied the same muscles at 60, 90, and 120 degrees of elbow flexion. The greatest electrical activity occurred at the 90-degree and 120-degree positions, consistent with the position of greatest strength.24 Others55 found there was no difference between position and muscular electrical activity. EMG data of the elbow muscles have thus provided the following information: (1) the biceps is generally less active in full pronation of the forearm, probably owing to its secondary role as a supinator; (2) the brachialis is active in most ranges of function and is believed to be the “workhorse” of flexion; (3) there is an increase of electrical activity of the triceps with increased elbow flexion, probably secondary to an increased stretch reflex; (4) the anconeus shows activity in all positions

Some of the forearm muscles originating at the medial and lateral aspects of the distal humerus had been considered in stabilizing the elbow joint. Flexor carpi ulnaris and flexor digitorum superficialis muscles, because of their positions and proximities over the medial collateral ligaments, were potentially the muscles best suited to provide medial elbow support.25 However, in the EMG investigations, no significant activities of these muscles were noted when valgus and varus stresses were applied.35 In a recent study of baseball pitchers with medial collateral ligament insufficiency, the data did not demonstrate increased electrical activity of these muscles.42 These findings suggested that the muscles on the medial side of the elbow do not supplement the role of medial collateral ligaments.42

Distributive Forces on the Articular Surfaces Joint compressive forces on various facets of the elbow joint have been reported in the literature.3,73 During the activities of resisting flexion and extension moments at various elbow joint positions, the components of force along the mediolateral direction, causing varus-valgus stress, are small compared with those acting in the sagittal plane directed anteriorly or posteriorly. The resultant joint forces on the trochlea and capitellum have been described in the sagittal plane for flexion (Fig. 3-26) and extension (Fig. 3-27) isometric loads. With the elbow extended and axially loaded, the distribution of stress across the joint has been calculated to be approximately 40% across the ulnohumeral joint and 60% across the

Chapter 3 Biomechanics of the Elbow

Trochlea

Humerus

57

Capitulum

145º

FIGURE 3-27

120º 90º

145º

120º

90º

0º 30º 60º

21N 120º 90º

60º 30º

0º

Applied force

40%

8.6N

60º

12.5N

145º

60%

FIGURE 3-28

Static compression of the extended elbow places more force on the radiohumeral than the ulnohumeral joint.

radiohumeral articulation (Fig. 3-28).41,107 More recently, based on a cadaveric study,46,57 it has been noted that with the elbow in valgus realignment, only 12% of the axial load is transmitted through the proximal end of the ulna, but with the elbow in varus alignment, 93% of the axial force is transmitted to proximal ulna. Because of the poor mechanical advantage with the elbow in extension, the largest isometric flexion forces occur in this position (see Fig. 3-27).3,49 Isometric extension produces a posterosuperior compressive stress across the distal humerus. These analytic calculations have undergone experimental confirmation. Using a force transducer at the proximal radius, the greatest force was

30º

0º

Orientation and magnitude of forces at the humeral articulating surface during extension, per unit of force at the hand. (From Amis, A. A., Dowson, D., and Wright, V.: Elbow joint force predictions for some strenuous isometric actions. J. Biomech. 13:765, 1980.)

transmitted across the radiohumeral joint in full extension, a position in which the muscles have poor mechanical advantage.68 When the elbow is flexed, inward rotation of the forearm against resistance imposes large torque to the joint. The magnitudes have been calculated as approaching twice body weight tension in the medial collateral ligament and three times body weight at the radiohumeral joint.4 Experimental data from the force transducer study suggest that the analytic estimate is probably too high. The greatest force on the radial head from the transducer data occurs with the forearm in pronation (Fig. 3-29). Even in this position, however, the maximum possible force transmission at the radiohumeral joint was measured as approximately 0.9 times the body weight.67 Considerably less knowledge is available regarding the distributed forces at the elbow during use. Nicol and associates73 have demonstrated significant forces with daily activities that not only occur at the radiohumeral and ulnohumeral joints but also are generated in the collateral ligaments. An example of such a force pattern is shown in Figure 3-30. The actual distributive forces occurring at this joint with daily activity constitute an important avenue of further investigation.

Contact Stress on the Joint Articular Surface With the magnitude, direction, and point of application of the resultant joint force available, the stress on the articular cartilage can now be determined.84 Because the joint is not a simple geometric shape, a method based on the concept of a rigid body spring model was adopted for solution.11 In the results, it was found that if the line of action of the resultant force is at the middle of the articular surface, the stress is almost equally distributed throughout the entire articular surface (Fig. 3-31A). On the other hand, as the resultant force is directed toward the margin of the articulation anteriorly or posteriorly, the weight-bearing surface becomes smaller, the maximum compressive stress becomes elevated, and the stress distribution over the joint surface becomes more

58

Part I Fundamentals and General Considerations

A

FIGURE 3-29

Consistently greater force transmission occurs with the forearm in pronation than in supination. This indicates that a screw-hole mechanism exists with the proximal radial migration occurring during this maneuver. (From Morrey, B. F., An, K. N., and Stormont, T. J.: Force transmission through the radial head. J. Bone Joint Surg. [Am.] 70:250, 1988.)

B FIGURE 3-31

The contact pressure depends on the direction and magnitude of the resultant compressive force. A, When the resultant force is oriented toward the center of the trochlear notch, a more uniform distribution of pressure is observed. B, When the line of action of the resultant joint force is directed to the rim of the trochlear notch, the weight-bearing surface becomes smaller, and maximum compressive stresses increases.

tudes and directions of the resultant joint forces, and thus the articulating pressure distribution and joint stability, were extensively examined (Fig. 3-32).7

Finite Element Analysis of Composite Fixation for Total Elbow Prosthesis

FIGURE 3-30

Distribution of articular and soft tissue forces across the elbow for a selected activity. (From Nicol, A. C., Berme, N., and Paul, J. P.: A biomechanical analysis of elbow joint function. In Joint Replacement in the Upper Limb. London, Institute of Mechanical Engineers, 1977, p. 45.)

uneven (see Fig. 3-31B). It should be further noted that the position of maximum stress does not necessarily correspond with the point of intersection of the resultant joint force through the articular surface. Based on this model, the role of antagonistic muscles on the magni-

In total elbow arthroplasty implant loosening remains a challenging complication. Achieving rigid fixation using a combination of bone ingrowth and cementing should improve the implant longevity. The semiconstrained Coonrad-Morrey elbow prosthesis employs this philosophy. It has shown generally satisfactory clinical results for a variety of cases including inflammatory arthritis and distal humerus fracture.44,89 The humeral component of the implant incorporates an anterior flange that has the theoretical benefit of transferring stress from the elbow to the humeral bone and relieving stress concentrations at the vulnerable distal humerus cement interface. Finite element analysis was used to evaluate the biomechanical effects of bone graft between the anterior flange and the bone cortex. Models were created that consisted of the humeral component of the Coonrad/Morrey elbow prosthesis,

Chapter 3 Biomechanics of the Elbow

59

Fm Fe Ff

Flexo

r

Φ

or

Extens

U Θ R

Pm P

24

12

16

24

Θ

R

A

θ

R 8

36

.2

.3

.4

.5

FIGURE 3-32

.6

Fe/Ff 20

25

0 Φ

Pm

20 Pm 15

Φ

–40

10 .2

B

–20

.3

.4

.5

.6

Fe/Ff

bone cement surrounding the implant stem, simulated distal humerus, and bone graft between the distal humerus and anterior flange of the prosthesis. Material properties were prescribed as linear elastic with Poisson ratio of 0.3 and elastic modulus values of implant (E = 114 GPa), humerus (E = 17 GPa), bone cement (E = 3 GPa), and bone graft (E = 0.65 GPa). Perfect bonding between the bone-cement and cement-implant interfaces was assumed. Permutations of the stem size (4, 6, and 8 inch), graft size (50% of flange length, 100% of flange length, and 150% of flange length), and distal humerus (normal and simulated defect) were evaluated. Loading to the implant was applied for cases of anterior (45 N), posterior (45 N), axial (45 N), 45 degrees posterior (45 N), and torsion (1 N-m) load.

A, Pressure distribution on elbow joint surface as external load P is applied at the distal end of the ulna. Distribution of muscle force, Fe and Ff, influences the magnitude, R, and the direction, F, of resultant force on the elbow joint. F represents the “attempted displacement,” U, of the humerus relative to the direction of the ulna. B, For the given loading condition, resultant joint force increased with increasing involvement of extensor muscle, as represented by the ratio of extension force Fe to flexor force Ff (top). Peak articular pressure and the direction of the attempted displacement of the humerus also are affected by the level of involvement of extensor muscle (bottom). (From An, K. N., Himeno, S., Tsumura, H., Kawai, T., and Chao, E. Y.: Pressure distribution on articular surfaces: Application to joint stability evaluation. J. Biomech. 23:1013, 1990.)

Finite element analysis shows that stress and strain in the distal humerus and distal cement mantle can be reduced 10% to 30% when using a bone graft compared with no bone graft between the anterior flange and the bone cortex (Fig. 3-33). Furthermore, when the distal humerus had a simulated defect of 2 cm, extension of the bone graft more proximally than the anterior flange reduced the stress and strain up to 17% compared with bone graft just under the flange. Finally, when selecting the stem size, there was up to a 15% reduction in distal cement stress and strain when choosing a 6-inch stem over a 4-inch stem or when choosing an 8-inch stem over a 6-inch stem. These findings confirmed the clinical experience that rigid fixation and stress relief due to the anterior flange of the implant reduce the complication rate for primary and revision total elbow arthroplasty.

60

Part I Fundamentals and General Considerations

Cement strain ratio

1.00 0.75 0.50 0.25 0.00 Posterior Anterior

B

Torsion no graft

Axial

45 Deg post

graft

FIGURE 3-33 Stress transmission through finite element model of elbow prosthesis before (A) and after (B) placement of bone graft between anterior flange and distal humerus. The bone graft and humerus are cut away to show the internal stress transmission.

References 1. Amis, A. A., Dowson, D., Unsworth A., Miller, J. H., and Wright, V. An examination of the elbow articulation with particular reference to variation of the carrying angle. Eng. Med. 6:76, 1977. 2. Amis, A. A., Dowson, D., and Wright, V.: Muscle strengths and musculoskeletal geometry of the upper limb. Eng. Med. 8:41, 1979. 3. Amis, A. A., Dowson, D., and Wright, V.: Elbow joint force predictions for some strenuous isometric actions. J. Biomech. 13:765, 1980. 4. Amis, A. A., Miller, J. H., Dowson, D., and Wright, V.: Biomechanical aspects of the elbow: Joint forces related to prosthesis design. IEEE Eng. Med. Biol. Mag. 10:65, 1981. 5. An, K. N.: Biomechanics: Basic relevant concepts. Section 1 basic science. In Morrey, B. F. (ed.): Joint Replacement Arthroplasty. New York, Churchill Livingstone, 1991, p. 7. 6. An, K. N.: Kinematics and constraint of total elbow arthroplasty. J. Shoulder Elbow Surg. 14:168S, 2005. 7. An, K. N., Himeno, S., Tsumura, H., Kawai, T., and Chao, E. Y.: Pressure distribution on articular surfaces: Application to joint stability evaluation. J. Biomech. 23:1013, 1990. 8. An, K. N., Hui, F. C., Morrey, B. F., Linscheid, R. L., and Chao, E. Y.: Muscles across the elbow joint: A biomechanical analysis. J. Biomech. 14:659, 1981. 9. An, K. N., Jacobsen, M. C., Berglund, L. J., and Chao, E. Y.: Application of a magnetic tracking device to kinesiologic studies. J. Biomech. 21:613, 1988. 10. An, K. N., Kaufman, K. R., and Chao, E. Y.: Physiological considerations of muscle force through the elbow joint. J. Biomech. 22:1249, 1989. 11. An, K. N., Kwak, B. M., Chao, E. Y., and Morrey, B. F.: Determination of muscle and joint forces: A new technique to solve the indeterminate problem. J. Biomech. Eng. 106:364, 1984. 12. An, K. N., Morrey, B. F., and Chao, E. Y.: Carrying angle of the human elbow joint. J. Orthop. Res. 1:369, 1984.

13. An, K. N., Morrey, B. F., and Chao, E. Y.: The effect of partial removal of proximal ulna on elbow constraint. Clin. Orthop. 209:270, 1986. 14. Anderson, R.: Rotation of the forearm. Lancet 2:1333, 1901. 15. Askew, L. J., An, K. N., Morrey, B. F., and Chao, E. Y.: Isometric elbow strength in normal individuals. Clin. Orthop. 222:261, 1987. 16. Basmajian, J. V., and Latif, S.: Integrated actions and functions of the chief flexors of the elbow. J. Bone Joint Surg. [Am.] 39:1106, 1957. 17. Basmajian, J. V., and Travill, A. A.: Electromyography of the pronator muscles in the forearm. Anat. Rec. 139:45, 1961. 18. Beals, R. K.: The normal carrying angle of the elbow. A radiographic study of 422 patients. Clin. Orthop. 119:194, 1976. 19. Blewitt, N., and Pooley, J.: An anatomic study of the axis of elbow movement in the coronal plane: Relevance to component alignment in elbow arthroplasty. J. Shoulder Elbow Surg. 3:151, 1994. 20. Braune, W., and Flugel, A.: Uber pronation and supination des menschlichen vorderarms und der hand. Arch. Anat. Physiol. 169-196, 1882. 21. Buchanan, T. S., and Shreeve, D. A.: An evaluation of optimization techniques for the prediction of muscle activation patterns during isometric tasks. J. Biomech. Eng. 118:565, 1996. 22. Capener, N.: The hand in surgery. J. Bone Joint Surg. [Br.] 38:128, 1956. 23. Cohen, M. S., and Hastings, H. Jr.: Rotatory instability of the elbow. The anatomy and role of the lateral stabilizers. J. Bone Joint Surg. [Am.] 79:225, 1997. 24. Currier, D. P.: Maximal isometric tension of the elbow extensors at varied positions. Part II. assessment of extensor components by quantitative electromyography. Phys. Ther. 52:1265, 1972. 25. Davidson, P. A., Pink, M., Perry, J., and Jobe, F. W.: Functional anatomy of the flexor pronator muscle group in relation to the medial collateral ligament of the elbow. Am. J. Sports Med. 23:245, 1995.

Chapter 3 Biomechanics of the Elbow

26. Deland, J. T., Garg, A., and Walker, P. S.: Biomechanical basis for elbow hinge-distractor design. Clin. Orthop. 215:303, 1987. 27. Dempster, W. T.: Space Requirements of the Seated Operator: Geometrical, Kinematic and Mechanical Aspects of the Body with Special Reference to the Limb. Wright Air Development Center, Project No. 7214, Wright-Patterson AFB, Ohio, 1955. 28. Dempster, W. T., and Finerty, J. C.: Relative activity of wristmoving muscles in static support of the wrist joint: An electromyographic study. Am. J. Physiol. 150:596, 1947. 29. De Sousa, O. M., De Moraes, J. L., and Viera, F. L.: Electromyographic study of the brachioradialis muscle. Anat. Rec. 139:125, 1961. 30. Dwight, T.: The movements of the ulna in rotation of the forearm. J. Anat. Physiol. 19:186, 1884. 31. Eckstein, F., Lohe, F., Muller-Gerbl, M., Steinlechner, M., and Putz, R.: Stress distribution in the trochlear notch. A model of bicentric load transmission through joints. J. Bone Joint Surg. [Br.] 76:647, 1994. 32. Ewald, F. C.: Total elbow replacement. Orthop. Clin. North Am. 6:685, 1975. 33. Fidelus, K.: The significance of the stabilizing function in the process of controlling the muscle groups of upper extremities. In Cerquiglin, S., Venerando, A., and Wartenweiler, J. (eds): Medicine and Sports, Vol. 8, Biomechanics III. Basel, Karger, 1973, p. 129. 34. Fischer, G.: Cited by Fick, R.: Handbuch der anatomie und mechanik du gelenke, unter berucksichtigung der bewegenden muskeln. Jena 2:299, 1911. 35. Funk, D. A., An, K. N., Morrey, B. F., and Daube, J. R.: Electromyographic analysis of muscles across the elbow joint. J. Orthop. Res. 5:529, 1987. 36. Fuss, F. K.: The ulnar collateral ligament of the human elbow joint. Anatomy, function and biomechanics. J. Anat. 175:203, 1991. 37. Goel, V. K., Singh, D., and Bijlani, V.: Contact areas in human elbow joints. J. Biomech. Eng. 104:169, 1982. 38. Gonzalez, R. V., Hutchins, E. L., Barr, R. E., and Abraham, L. D.: Development and evaluation of a musculoskeletal model of the elbow joint complex. J. Biomech. Eng. 118:32, 1996. 39. Goodfellow, J. W., and Bullough, P. G.: The pattern of aging of the articular cartilage of the elbow joint. J. Bone Joint Surg. [Br.] 49:175, 1967. 40. Guttierez, L. F.: A contribution to the study of the limiting factors of elbow flexion. Acta Anat. 56:146, 1964. 41. Halls, A. A., and Travill, A. A.: Transmission of pressures across the elbow joint. Anat. Rec. 150:243, 1964. 42. Hamilton, C. D., Glousman, R. E., Jobe, F. W., Brault, J., Pink, M., and Perry, J.: Dynamic stability of the elbow: Electromyographic analyses of the flexor pronator group and the extensor group in pitchers with valgus instability. J. Shoulder Elbow Surg. 5:347, 1996. 43. Heiberg, J.: The movement of the ulna in rotation of the forearm. J. Anat. Physiol. 19:237, 1884. 44. Hildebrand, K. A., Patterson, S. D., Regan, W. D., MacDermid, J. C., and King, G. J.: Functional outcome of semiconstrained total elbow arthroplasty. J. Bone Joint Surg. [Am.] 82:1379, 2000.

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45. Hollister, A. M., Gellman, H., and Waters, R. L.: The relationship of the interosseous membrane to the axis of rotation of the forearm. Clin. Orthop. 298:272, 1994. 46. Hotchkiss, R. N., An, K. N., Sowa, D. T., Basta, S., and Weiland, A. J.: An anatomic and mechanical study of the interosseous membrane of the forearm: Pathomechanics of proximal migration of the radius. J. Hand Surg. [Am.] 14:256, 1989. 47. Hotchkiss, R. N., and Weiland, A. J.: Valgus stability of the elbow. J. Orthop. Res. 5:372, 1987. 48. Hughes, R. E., Schneeberger, A. G., An, K. N., Morrey, B. F., and O’Driscoll, S. W.: Reduction of triceps muscle force after shortening of the distal humerus: A computational model. J. Shoulder Elbow Surg. 6:444, 1997. 49. Hui, F. C., Chao, E. Y., and An, K. N.: Muscle and joint forces at the elbow during isometric lifting. Orthop. Trans. 2:169, 1978. Abstract. 50. Hultkrantz, J. W.: Das ellbogengeleck and seine mechanik. Jena Fisher 1897. 51. Ishizuki, M.: Functional anatomy of the elbow joint and three-dimensional quantitative motion analysis of the elbow joint. J. Jpn. Orthop. Assoc. 53:989, 1979. 52. Kapandji, I. A.: The Physiology of the Joint: The Elbow, Flexion and Extension, 2nd ed, Vol. 1. London, Livingstone, 1970. 53. Keats, T. E., Tuslink, R., Diamond, A. E., and Williams, J. H.: Normal axial relationship of the major joints. Radiology 87:905, 1966. 54. Larson, R. F.: Forearm positioning on maximal elbowflexor force. Phys. Ther. 49:748, 1969. 55. Le Bozec, S., Maton, B., and Cnockaert, J. C.: The synergy of elbow extensor muscles during dynamic work in man. Part I. Elbow extension. Eur. J. Appl. Physiol. 44:255, 1980. 56. London, J. T.: Kinematics of the elbow. J. Bone Joint Surg. [Am.] 63:529, 1981. 57. Markolf, K. L., Lamey, D., Yang, S., Meals, R., and Hotchkiss, R.: Radioulnar load-sharing in the forearm. A study in cadavera. J. Bone Joint Surg. [Am.] 80:879, 1998. 58. Maton, B., and Bouisset, S.: The distribution of activity among the muscles of a single group during isometric contraction. Eur. J. Appl. Physiol. 37:101, 1977. 59. McGarvey, S. R., Morrey, B. F., Askew, L. J., and An, K. N.: Reliability of isometric strength testing. Temporal factors and strength variation. Clin. Orthop. 185:301, 1984. 60. Meissner, G.: Lokomotion des ellbogengelenkes ber ubd. Fortschr. Anat. Physiol. 1856. 61. Messier, R. H., Duffy, J., Litchman, H. M., et al: The electromyogram as a measure of tension in the human biceps and triceps muscles. Int. J. Mech. Sci. 13:585, 1971. 62. Mori K.: Experimental study on rotation of the forearmfunctional anatomy of the interosseous membrane. J. Jpn. Orthop. Assoc. 59:611, 1985. 63. Morrey, B. F.: Post-traumatic contracture of the elbow. Operative treatment, including distraction arthroplasty. J. Bone Joint Surg. [Am.] 72:601, 1990. 64. Morrey, B. F.: Complex instability of the elbow. J. Bone Joint Surg. [Am.] 79:460, 1997.

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Part I Fundamentals and General Considerations

65. Morrey, B. F., and An, K. N.: Articular and ligamentous contributions to the stability of the elbow joint. Am. J. Sports Med. 11:315, 1983. 66. Morrey, B. F., and An, K. N.: Functional anatomy of the ligaments of the elbow. Clin. Orthop. 201:84, 1985. 67. Morrey, B. F., An, K. N., and Stormont, T. J.: Force transmission through the radial head. J. Bone Joint Surg. [Am.] 70:250, 1988. 68. Morrey, B. F., Askew L. J., and An, K. N.: Strength function after elbow arthroplasty. Clin. Orthop. 234:43, 1988. 69. Morrey, B. F., and Chao, E. Y.: Passive motion of the elbow joint. J. Bone Joint Surg. [Am.] 58:501, 1976. 70. Morrey, B. F., Tanaka, S., and An, K. N.: Valgus stability of the elbow. A definition of primary and secondary constraints. Clin. Orthop. 265:187, 1991. 71. Motzkin, N. E., Cahalan, T. D., Morrey, B. F., An, K. N., and Chao, E. Y.: Isometric and isokinetic endurance testing of the forearm complex. Am. J. Sports Med. 19:107, 1991. 72. Nemoto, K., Itoh, Y., Horiuchi, Y., and Sasaki, T.: Advancement of the insertion of the biceps brachii muscle: A technique for increasing elbow flexion force. J. Shoulder Elbow Surg. 5:433, 1996. 73. Nicol, A. C., Berme, N., and Paul, J. P.: A biomechanical analysis of elbow joint function. In Joint Replacement in the Upper Limb. London, Institute of Mechanical Engineers, 1977, p. 45. 74. Nobuta, S.: Pressure distribution on the elbow joint and its change according to positions. J. Jpn. Soc. Clin. Biomech. Res. 13:17, 1991. 75. O’Driscoll, S. W., An, K. N., Korinek, S., and Morrey, B. F.: Kinematics of semi-constrained total elbow arthroplasty. J. Bone Joint Surg. [Br.] 74:297, 1992. 76. O’Driscoll, S. W., Bell, D. F., and Morrey, B. F.: Posterolateral rotatory instability of the elbow. J. Bone Joint Surg. [Am.] 73:440, 1991. 77. O’Driscoll, S. W., Horii, E., Morrey, B. F., and Carmichael, S.: Anatomy of the ulnar part of the lateral collateral ligament of the elbow. Clin. Anat. 5:296, 1992. 78. O’Driscoll, S. W., Morrey, B. F., and An, K. N.: Intraarticular pressure and capacity of the elbow. Arthroscopy 6:100, 1990. 79. Olsen, B. S., Henriksen, M. G., Sojbjerg, J. O., Helmig, P., and Sneppen, O. Elbow joint instability: A kinematic model. J. Shoulder Elbow Surg. 3:143, 1994. 80. Olsen, B. S., Sojbjerg, J. O., Dalstra, M., and Sneppen, O.: Kinematics of the lateral ligamentous constraints of the elbow joint. J. Shoulder Elbow Surg. 5:333, 1996. 81. Olsen, B. S., Vaesel, M. T., Sojbjerg, J. O., Helmig, P., and Sneppen, O.: Lateral collateral ligament of the elbow joint: Anatomy and kinematics. J. Shoulder Elbow Surg. 1996;5:103-112. 82. Palmer, A. K., Glisson, R. R., and Werner, F. W.: Ulnar variance determination. J. Hand Surg. [Am.] 7:376, 1982. 83. Pauly, J. E., Rushing, J. L., and Scheving, L. E.: An electromyographic study of some muscles crossing the elbow joint. Anat. Rec. 159:47, 1967. 84. Pauwels, F.: Biomechanics of locomotor apparatus. Translated by P. Maquet and R. Furlong. Berlin, Springer-Verlag, 1980.

85. Pomianowski, S., Morrey, B. F., Neale, P. G., Park, M. J., O’Driscoll, S. W., and An, K. N.: Contribution of monoblock and bipolar radial head prostheses to valgus stability of the elbow. [see comment]. J. Bone Joint Surg. [Am.] 83:1829, 2001. 86. Pomianowski, S., O’Driscoll, S. W., Neale, P. G., Park, M. J., Morrey, B. F., and An, K. N.: The effect of forearm rotation on laxity and stability of the elbow. Clin. Biomech. 16:401, 2001. 87. Pribyl, C. R., Kester, M. A., Cook, S. D., Edmunds, J. O., and Brunet, M. E.: The effect of the radial head and prosthetic radial head replacement on resisting valgus stress at the elbow. Orthopedics 9:723, 1986. 88. Ray, R. D., Johnson, R. J., and Jameson, R. M.: Rotation of the forearm: An experimental study of pronation and supination. J. Bone Joint Surg. [Am.] 33:993, 1951. 89. Ray, P. S., Kakarlapudi, K., Rajsekhar, C., and Bhamra, M. S.: Total elbow arthroplasty as primary treatment for distal humeral fractures in elderly patients. Injury 31:687, 2000. 90. Regan, W. D., Korinek, S. L., Morrey, B. F., and An, K. N.: Biomechanical study of ligaments around the elbow joint. Clin. Orthop. 271:170, 1991. 91. Sarmiento, A., Ebramzadeh, E., Brys, D., and Tarr, R.: Angular deformities and forearm function. J. Orthop. Res. 10:121, 1992. 92. Schlein, A. P.: Semiconstrained total elbow arthroplasty. Clin. Orthop. 121:222, 1976. 93. Schwab, G. H., Bennett, J. B., Woods, G. W., and Tullos, H. S.: Biomechanics of elbow instability: The role of the medial collateral ligament. Clin. Orthop. 146:42, 1980. 94. Sojbjerg, J. O., Ovesen, J., and Gundorf, C. E.: The stability of the elbow following excision of the radial head and transection of the annular ligament. An experimental study. Arch. Orthop. Trauma Surg. 106:248, 1987. 95. Sojbjerg, J. O., Ovesen, J., and Nielsen, S.: Experimental elbow instability after transection of the medial collateral ligament. Clin. Orthop. 218:186, 1987. 96. Spinner, M., and Kaplan, E. B.: The quadrate ligament of the elbow—its relationship to the stability of the proximal radio-ulnar joint. Acta Orthop. Scand. 41:632, 1970. 97. Steindler, A.: Kinesiology of the Human Body Under Normal and Pathological Conditions. Springfield, IL, Charles C. Thomas, 1955, p. 493. 98. Stevens, A., Stijns, H., Reybrouck, T., Bonte, G., Michels, A., Rosselle, N., Roelandts, P., Krauss, E., and Verheyen, G.: A polyelectromyographical study of the arm muscles at gradual isometric loading. Electromyogr Clin Neurophysiol 1973;13:465-476. 99. Stormont, T. J., An, K. N., Morrey, B. F., and Chao, E. Y.: Elbow joint contact study: Comparison of techniques. J. Biomech. 18:329, 1985. 100. Sullivan, W. E., Mortensen, O. A., Miles, M., and Greene, L. S.: Electromyographic studies of m. biceps brachii during normal voluntary movement at the elbow. Anat. Rec. 107:243, 1950. 101. Tanaka, S., An, K. N., and Morrey, B. F.: Kinematics and laxity of ulnohumeral joint under valgus-varus stress. J. Musculoskel. Res. 2:45, 1998.

Chapter 3 Biomechanics of the Elbow

102. Travill, A. A.: Electromyographic study of the extensor apparatus of the forearm. Anat. Rec. 144:373, 1962. 103. Tyrdal, S., and Olsen, B. S.: Combined hyperextension and supination of the elbow joint induces lateral ligament lesions. An experimental study of the pathoanatomy and kinematics in elbow ligament injuries. Knee Surg. Sports Traumatol. Arthrosc. 6:36, 1998. 104. Van Glabbeek, F., Van Riet, R. P., Baumfeld, J. A., Neale, P. G., O’Driscoll, S. W., Morrey, B. F., and An, K. N.: Detrimental effects of overstuffing or understuffing with a radial head replacement in the medial collateral-ligament deficient elbow. J. Bone Joint Surg. [Am.] 86:2629, 2004.

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105. Von Lanz, T., and Wachsmuth, W.: Praktische Anatomie. Berlin, Springer-Verlag, 1959. 106. Von Meyer, H.: Cited in Steindler, A.: Kinesiology of the Human Body Under Normal and Pathological Conditions. Springfield, IL, Charles C. Thomas, 1955, p. 490. 107. Walker, P. S.: Human Joints and Their Artificial Replacements. Springfield, IL, Charles C. Thomas, 1977. p. 182. 108. Youm, Y., Dryer, R. F., Thambyrajah, K., Flatt, A. E., and Sprague, B. L.: Biomechanical analyses of forearm pronation-supination and elbow flexion-extension. J. Biomech. 12:245, 1979.

Chapter 4 Physical Examination of the Elbow

CHAPTER

4

Physical Examination of the Elbow William D. Regan and Bernard F. Morrey

INTRODUCTION This chapter deals with the basics of a general comprehensive physical examination of the elbow. Specific and focused features of the examination are pictured with the various conditions described below.

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Conditions involving the lateral joint, that is, the radiocapitellar articulation, generally evoke pain that extends over the lateral aspect of the elbow with radiation proximally to the midhumerus or distally over the forearm. The pain may be superficial, directly over the lateral epicondyle or radial head, for example, or deep, localized poorly in the area of the proximal common extensor muscle mass supplied by the posterior interosseous nerve. For reasons that remain unclear, the posterior lateral ulnohumeral joint appears to be a “watershed” referral point for a spectrum of remote conditions. Less commonly, nonspecific symptoms poorly localized to the medial aspect of the elbow can represent ulnar nerve pathology, medial epicondylitis or arthrosis. As is well known, symptoms from cervical radiculopathy can usually be distinguished by a specific radicular distribution of pain and associated neurologic abnormality of the upper extremity. Today, a suspicion of cervical etiology is readily resolved with the magnetic resonance imaging (MRI) scan.

HISTORY Without question the value of a precise history cannot be overstated. Pain is the most common complaint. The severity of the pain and whether it is intermittent or constant, the quantity and type of analgesia used, and the association of night pain are all important characteristics. The functional compromise experienced, whether it be recreational activity or activities of daily living, should be discussed. Frequently, the patient who has lived with chronic pain, such as that accompanying rheumatoid arthritis, has learned certain accommodative activities that have assisted in lessening or eliminating pain from a conscious level. When considering intervention, it is extremely helpful to determine if the pain is getting better, getting worse, or remaining constant. Functionally, the elbow is the most important joint of the upper extremity, because it places the hand in space away from or toward the body. It provides the linkage, allowing the hand to be brought to the torso, head, or mouth. Because of this, the examiner must be aware of the interplay of shoulder and wrist function as they complement the usefulness of the elbow. However, a considerable limitation of elevation and abduction function can exist at the shoulder complex without producing an appreciable compromise in most activities of daily living. This is true because only a relatively small amount of shoulder flexion and rotation is necessary to place the hand about the head or posteriorly about the waist or hip, and scapulothoracic motion can compensate for glenohumeral motion loss. Full pronation and supination can be achieved only when both the proximal and distal radioulnar joints are normal.6,25

PHYSICAL EXAMINATION INSPECTION Considerable information can be ascertained from careful visual inspection of the elbow joint. Because much of the joint is subcutaneous, any appreciable alteration in the skeletal anatomy is usually obvious. Gross soft tissue swelling or muscle atrophy is also easily observed.

AXIAL ALIGNMENT Axial malalignment of the elbow, when compared with the opposite side, suggests prior trauma or a skeletal growth disturbance. To determine the carrying angle, the forearm and hand should be supinated and the elbow extended; the angle formed by the humerus and forearm is then determined (Fig. 4-1A). Although there is considerable variation with race, age, sex, and body weight, an average of 10 degrees for men and 13 degrees for women has been calculated as the mean carrying angle from several reports.3,4,13,14 Angular deformities, such as cubitus varus or valgus, are also easily identifiable (see Fig. 4-1B and C). The elbow moves from a valgus to varus alignment as with flexion. In a post-traumatic condition, however, abnormalities in the carrying angle cannot be accurately assessed in the presence of a significant flexion contracture (see Chapter 3). Rotational deformities following supracondylar or other fractures of the humeral shaft may be difficult to perceive.

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Part II Diagnostic Considerations

FIGURE 4-1

A, The carrying angle is a clinical measurement of the angle formed by the forearm and the humerus with the elbow extended. B and C, The normal 10- to 15-degree carrying angle can be altered by injury about the elbow, causing a varus carrying angle, or so-called gunstock deformity.

LATERAL ASPECT Fullness about the infracondylar recess just inferior to the lateral condyle of the humerus, the “soft spot,” suggests either an increase in synovial fluid, synovial tissue proliferation, or radial head pathology, such as fracture, subluxation, or dislocation (Fig. 4-2). Subtle evidence of effusion can be determined by observing fullness in this area. Thin, taut, adherent skin over the lateral epicondyle may be indicative of excessive cortisone injections in this area for refractory lateral epicondylitis (see Chapter 44). A prominence involving the lateral triangle often indicates a posteriorly dislocated radial head (Fig. 4-3; see Fig. 4-22A and B).

POSTERIOR ASPECT A prominent olecranon suggests a posterior subluxation or migration of the forearm on the ulnohumeral articulation. Occasionally, marked distortion is associated with surprisingly satisfactory function (Fig. 4-4). Rupture of the triceps tendon at its insertion should be suspected if this finding is accompanied by loss of active extension. Loss of terminal passive extension of the elbow is a

sensitive but nonspecific indicator of intra-articular pathology. Loss of active motion with full passive extension suggests either mechanical (triceps avulsion) or neurologic conditions. The prominent subcutaneous olecranon bursa is readily observed posteriorly when it is inflamed or distended (Fig. 4-5). Rheumatoid nodules frequently are found on the subcutaneous border of the ulna (see Chapter 74).

MEDIAL ASPECT On occasion the ulnar nerve may be observed to displace anteriorly during flexion with recurrent subluxation of the ulnar nerve.8 Otherwise, few landmarks are observable from the medial aspect of the joint. The prominent medial epicondyle is evident unless the patient is obese.

ASSOCIATED JOINTS AND NEURAL FUNCTION No examination of the elbow is complete without a review of the cervical spine and all other components of the upper extremity. If the elbow pain has a radicular pattern, it is important to review the patient’s cervical

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FIGURE 4-2

A normal depression in the contour of the skin in the intracondylar recess (arrowhead) (A) becomes obliterated in the presence of synovitis or effusion (B).

FIGURE 4-3

Developmental posterior dislocation of the radial head (A) is associated with obvious prominence (B). Typically, this problem is associated with only minimal limitation of function.

spine alignment and range of motion and perform neurologic testing of the entire upper extremity. The main nerve roots involved with elbow function are C5-7 (Fig. 4-6). There is considerable overlap in the sensory dermatomes of the upper extremity. The general distribution of sensory levels includes C5, the lateral arm; C6, the lateral forearm; C7, the middle finger; and C8 and T1, the medial forearm and arm dermatomes, respectively. Biceps function from innervation of C5-C6 is a flexor of the elbow and forearm supinator. The reflex primarily tests C5 and some C6 competency. The C6 muscle group of most interest is the mobile wad of three, consisting of the extensor carpi radialis longus and brevis and the brachioradialis muscles. These also are known as the radial wrist extensors and should be assessed for strength and reflex integrity. The reflex is primarily a C6 function, with some C5 component. The primary elbow muscle innervated by C7 is the triceps, which should always be assessed for strength and reflex. Wrist flexion and finger extension also are primarily supplied by C7, with some C8 innervation (see Fig. 4-6). Elbow pain may be referred from the shoulder; therefore, a visual inspection of the shoulder for muscle wasting and appearance should be made, followed by an appropriate functional assessment. Specific attention should be directed toward motion and the spectrum of impingement tendinitis or rotator cuff pathology which often is manifested by pain in the brachium.

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FIGURE 4-4

Gross deformity of the elbow from a malunion of a condylar fracture. The excellent function is typical of condylar but not T-Y type malunions.

FIGURE 4-5

An inflamed or enlarged olecranon bursa is one of the more dramatic diagnoses made by observation in the region of the elbow. (From Polley, H. G., and Hunder, G. G.: Rheumatologic Interviewing and Physical Examination of the Joints, 2nd ed. Philadelphia, W.B. Saunders Co., 1978.)

For normal forearm rotation, there must be a normal anatomic relationship between the proximal and distal radioulnar joint. Inflammatory changes involving either the elbow or the wrist or both will cause a loss of forearm rotation. Disruption of the normal relationship

of the distal radioulnar joint will cause dorsal prominence of the distal ulna exaggerated by pronation and is lessened by supination. Because pronation is the common resting position of the hand, dorsal subluxation of the ulna at the wrist is often identifiable by inspection.

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C5 C6

Posterior view

A C7

FIGURE 4-6

The biceps, brachioradialis, and triceps reflexes allow evaluation of the C5, C6, and C7 nerve roots, respectively.

PALPATION OSSEOUS LANDMARKS Inspection and palpation of the medial and lateral epicondyles and the tip of the olecranon form an equilateral triangle when the elbow is flexed (Fig. 4-7). Fracture, malunion, unreduced dislocation, or growth disturbances involving the distal end of the humerus can be assessed clinically in this fashion. FIGURE 4-7

LATERAL ASPECT The lateral supracondylar region, which we call the lateral column, is readily palpable and is a valuable landmark during lateral surgical exposures (Fig. 4-8) (see Chapters 7 and 32). The definition of the location of the extensor carpi radialis brevis is carefully sought and is enhanced by radial wrist and elbow extension. Examination of the radial head is easily performed provided a joint effusion is not present. Digital pressure over the peripheral articular surface of the radial head, when combined with pronation and supination of the forearm in varying degrees of elbow flexion, will offer valuable information about this bony structure and the status of the synovium. If painful, this examination should be performed gently. Radial head or capitellar fracture thus may be suspected even when the radiographic results are negative. An effusion of the elbow is most easily identified by palpation over the lateral border

With the elbow flexed to 90 degrees, the medial and lateral epicondyles and tip of the olecranon form an equilateral triangle when viewed from posterior. When the elbow is extended, this relationship is changed to a straight line connecting these three bony landmarks (A). The relationship is altered with displaced, intra-articular distal humeral fractures (B).

of the radial head or about the posterior recess located just between the radial head and the lateral border of the olecranon (Fig. 4-9). A radio/humeral plica is appreciated by palpating the snapping of the plica with flexion and extension. As with other joints, significant effusions of hemarthrosis will limit extremes of motion, especially extension. If tense, the elbow will assume a position of maximum joint capacity, which is 80 degrees.19 Palpation of the arcade of Froshe, located approximately 2 cm anterior and 3 cm distal to the lateral epicondyle, locates the posterior interosseous nerve.

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MEDIAL ASPECT Because of the tight ligament and capsule present on the medial side of the olecranon, great difficulty is encountered in assessment of the soft tissues in this area. Palpation of the cubital tunnel is easily performed to assess

the status of the ulnar nerve (Fig. 4-10). A subluxing nerve is identified with flexion and extension. Entrapment is assessed by performing a Tinel test proximal to, at, or distal to the cubital tunnel. The flexor-pronator muscles consist of four muscles taking origin from the medial epicondyle. Wrist flexion and pronation against resistance often accentuate the pain and is consistent with a diagnosis of medial epicondylitis. The medial collateral ligament is the elbow’s primary stabilizer to valgus strain. It takes its origin slightly anterior and inferior to the medial epicondyle and fans out to attach along the greater sigmoid fossa of the ulna with both an anterior and a posterior thickening.24 With the elbow in 30 to 60 degrees of flexion, it should be palpated for tenderness along its course. Valgus stress is painful if the ligament is injured.

Ulnar nerve

Medial epicondyle

FIGURE 4-8

The lateral supracondylar interval is an avascular area that can be readily palpated and serves as an important landmark in many surgical exposures to the elbow. (From Hoppenfeld, S.: Physical Examination of the Spine and Extremities. New York, Appleton-CenturyCrofts, 1976.)

Olecranon

FIGURE 4-10

Palpation of the cubital tunnel. The ulnar nerve is identified proximal and distal to the medial epicondyle.

FIGURE 4-9

The radial head may be readily palpated. The contour and integrity of the structure may be further appreciated by pronating and supinating the forearm during this examination.

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POSTERIOR ASPECT The olecranon bursa overlies the triceps aponeurosis, which inserts on the olecranon. This area should be palpated for thickening and pain. On occasion, a spur or bony prominence may be readily palpable at the tip of the olecranon (see Chapter 84). With elbow flexion, the olecranon fossa may be identified in a thin person by careful palpation. A tense effusion is likewise detectable from this aspect. The posteromedial olecranon and ulnohumeral joint should be carefully palpated. This is a common site for olecranon spur formation and is painful with forced extension. To accentuate this pain, the elbow is snapped into full extension. The subcutaneous border of the olecranon and proximal ulna also are readily appreciated by palpation.

Biceps m.

Lacertus fibrosus (Bicipital aponeurosis)

Medial epicondyle

ANTERIOR ASPECT The cubital fossa is bordered laterally by the brachioradialis and medially by the pronator teres muscles. There are four significant structures passing through the cubital fossa from lateral to medial, including (1) the musculocutaneous nerve, (2) the biceps tendon, (3) the brachial artery, and (4) the median nerve. The musculocutaneous nerve supplying lateral forearm sensation is located deep to the brachioradialis between it and the biceps tendon and is not readily palpable. The biceps tendon is readily palpable with resisted forearm supination. The tendon should be assessed for tenderness and for continuity distally. A medial expansion, the lacertus fibrosus, is noted, which covers the common flexor muscle group as well as the brachial artery and median nerve and may be the source of compression of the median nerve. The pulse of the brachial artery is easily located, lying deep to the lacertus fibrosus (Fig. 4-11).

MOTION Perhaps no portion of the physical examination is more important than the assessment of motion. Loss of full extension is the first motion altered by most pathology. As a matter of fact, in a trauma situation, the likelihood of significant joint pathology in the face of normal elbow motion is so small as not to require radiographic analysis!15 Normally, the arc of flexion-extension, although variable, ranges from about 0 to 140 degrees plus or minus 10 degrees (Fig. 4-12).1,7,26 This range exceeds that which is normally required for activities of daily living.17 Pronation-supination may vary to a greater extent than the arc of flexion-extension. Acceptable norms of

FIGURE 4-11

The lacertus fibrosus is easily palpable at its medial margin, and this covers the brachial artery, median nerve, and becomes attenuated with the distal biceps tendon disruption.

pronation and supination are 75 and 85 degrees, respectively (Fig. 4-13). In assessing motion, the examiner should record both active and passive values. The humerus is placed in a vertical position when evaluating the arc of forearm rotation. Patients will tend to accommodate for loss of pronation by abducting the shoulder. Any significant difference between active and passive ranges of motion suggests pain or motor function as the cause. In patients with a flexion or extension contracture, the examiner should concentrate on solid or soft end points, pain or crepitus during the arc and at the end points. The examiner should then make a careful assessment of any compromised motion at the shoulder or wrist. Often, the disability will arise from a combination of factors, but it should be stressed that a full range of motion at the elbow is not essential for performance of the activities of daily living. The essential arc of elbow flexion-extension required for daily activities ranges from about 30 to 130 degrees.17 Because the loss of

74

Part II Diagnostic Considerations

145 130

50

50

80 85 Supination 0

30

Pronation

FIGURE 4-13

Normal pronation and supination is about 80 and 85 degrees, respectively. The functional arc of forearm rotation consists of approximately 50 degrees of pronation and 50 degrees of supination.

FIGURE 4-12

The normal flexion and extension of the elbows is from zero to approximately 145 degrees. The functional arc of flexion and extension about which most daily activities are achieved is 30 to 130 degrees.

Elbow motion 0–145º

Elbow motion

0–90º

0–145º

Fused, 90º

0–90º Fused, 90º

A

B FIGURE 4-14

Illustration of the marked functional limitation associated with an ankylosed elbow at 90 degrees. Notice the shoulder poorly compensates for the overall effect of limited flexion and extension in both the sagittal (A) and the transverse (B) planes.

extension up to a certain degree only shortens the lever arm of the upper extremity, flexion contractures of less than 45 degrees may have little practical significance, although patients sometimes are concerned about the cosmetic appearance (Fig. 4-14). To perform 90% of required daily activity, 50 degrees of pronation and supination are required (see Fig. 413).17 For most individuals, pronation is the most important function on the dominant side for eating and writing, and loss of pronation is compensated by shoulder abduction. On the other hand, a loss of supination of the nondominant side may significantly hinder per-

sonal hygiene needs, accepting objects, and opening of door handles. These tasks are poorly compensated by shoulder or wrist function.

STRENGTH Only gross estimates of strength are attainable in the clinical setting. Flexion and extension strength testing (Fig. 4-15) is conducted against resistance, with the forearm in neutral rotation and the elbow at 90 degrees of flexion. Extension strength is normally 70%

Chapter 4 Physical Examination of the Elbow

INSTABILITY

that of flexion strength2 and is best measured with the elbow at 90 degrees of flexion, and with the forearm in neutral rotation.10,22,23,27 Pronation (Fig. 4-16), supination, and grip strength are also best studied with the elbow at 90 degrees of flexion and the forearm in neutral rotation. Supination strength is normally about 15% greater than pronation strength.2 The dominant extremity is about 5% to 10% stronger than the nondominant side, and women are 50% as strong as men (see Chapter 5).2

In the absence of articular cartilage loss, the mechanical integrity of the radial and ulnar collateral ligaments is difficult to assess because of the intrinsic stability offered by the closely approximated surfaces of the olecranon and trochlea and the buttressing effect of the radial head against the capitellum. However, when articular cartilage has been destroyed, as in rheumatoid arthritis, or removed, as with radial head excision, collateral

A

B

FIGURE 4-15

Flexion strength is best assessed with the elbow flexed to 90 degrees and the forearm in neutral rotation. Flexion resistance is assessed while the examiner attempts to extend the elbow (A). To test extension strength, the examiner applies resistance to the patient’s ability to extend the elbow with the joint in approximately 90 degrees of flexion and the forearm in neutral (or pronated) position (B). (From Hoppenfeld, S.: Orthopedic Neurology. Philadelphia, J. B. Lippincott Co., 1977.)

A FIGURE 4-16

75

B

Pronation strength is evaluated with the patient comfortable and the elbow at 90 degrees of flexion. Pronation strength is usually measured by grasping the wrist or, less commonly, the hand with the forearm in neutral position or in supination-rotation (A). To test supination strength, the forearm is in neutral position or pronation (B).

76

Part II Diagnostic Considerations

ligament stability can be determined by the application of varus and valgus stresses. Medially, the fibers become taut in an ordered sequential fashion, proceeding from anterior to posterior as the elbow is flexed.22 Accordingly, a portion of the complex is always in tension throughout the arc of flexion (see Chapter 3).24 The radial collateral ligament resists varus stress throughout the arc of elbow flexion with varying contributions of the anterior capsule and articular surface in extension (see Chapter 3). The lateral collateral ligament complex consists of the radial collateral ligament (RCL) and the lateral ulnar collateral ligament (LUCL). The RCL maintains consistent patterns of tension throughout the arc of flexion.24 To properly assess collateral ligament integrity, the elbow should be flexed to about 15 degrees. This relaxes the anterior capsule and removes the olecranon from the fossa. Varus stress is best applied with the humerus in full internal rotation. Valgus instability is best measured with the arm in 10 degrees of flexion (Fig. 4-17). In recent years, we have used the fluoroscan routinely to assess all elbows in where a possible instability exists (see Fig. 4-17C).

A

B FIGURE 4-17

ROTATORY INSTABILITY The lateral collateral complex also includes a narrow but stout band of ligamentous tissue blending with the distal and posterior fibers of the capsule to insert distally on the crista supinatoris of the ulna. This is the lateral ulnar collateral ligament.20,24 Insufficiency of the lateral collateral ligament is responsible for posterolateral instability of the elbow.20 Posterolateral instability is elicited in two ways (see Chapter 44). The more sensitive is by flexing the shoulder and elbow 90 degrees, with the patient supine. The patient’s forearm is fully supinated, and the examiner grasps the wrist or forearm and slowly extends the elbow while applying valgus and supination movements and an axial compressive force (Fig. 4-18). This produces a rotatory subluxation of the ulnohumeral joint; that is, the rotation dislocates the radiohumeral joint posterolaterally by a coupled motion. As the elbow approaches extension, a posterior prominence (the dislocated radiohumeral joint) is noted with an obvious dimple in the skin proximal to the radial

C

A, Varus instability of the elbow is measured with the humerus in full internal rotation and a varus stress applied to the slightly flexed joint. B, Valgus instability is evaluated with the humerus in full external rotation while a valgus stress is applied to the slightly flexed joint. C, Examination under fluroscopy readily reveals medial ligament insufficiency.

Chapter 4 Physical Examination of the Elbow

Axial compression

77

Valgus

Supination

Subluxation

FIGURE 4-18

The pivot shift maneuver consists of extending the elbow with a valgus axial stress while the forearm is supinated and the elbow is being extended. The elbow tends to sublux toward full extension. A palpable snap or pop is felt with flexion and represents reduction.

FIGURE 4-19

Gross appearance and radiograph of a patient with the positive pivot shift maneuver. Note the dimple in the skin. (From O’Driscoll, S. W.: Posterolateral rotatory instability of the elbow. J. Bone Joint Surg. 73A:440, 1991.)

FIGURE 4-20

With partial flexion or sometimes simple pronation of the forearm, the elbow is reduced and the dimple is obliterated. (From O’Driscoll, S. W.: Posterolateral rotatory instability of the elbow. J. Bone Joint Surg. 73A:440, 1991.)

FIGURE 4-21

Using the arms to rise from a chair can replicate the instability pattern of posterolateral rotatory instability (PLRI).

78

Part II Diagnostic Considerations

FIGURE 4-22

A, The patient has done a push-up with hands in neutral and his arms wider than shoulder (valgus) and is at a terminal extension (axial load) of his unaffected elbow. He has apprehension in his affected left elbow (axial load + valgus). B, A close-up of the posterolateral dislocation.

head (Fig. 4-19). Additional flexion results in a sudden reduction as radius and ulna visibly snap into place on the humerus (Fig. 4-20). Alternatively, simply asking the patient to rise from a chair may also reproduce the symptomatology (Fig. 4-21). Finally, having the patient do a push-up places the elbow in the at-risk position (Fig. 4-22). These latter two tests are active apprehension signs.

References 1. American Academy of Orthopedic Surgeons: Joint Motion: Method of measuring and recording. Chicago, American Academy of Orthopedic Surgeons, 1965. 2. Askew, L. J., An, K. N., Morrey, B. F., and Chao E. Y.: Functional evaluation of the elbow: normal motion requirements and strength determination. Orthop. Trans. 5:304, 1981. 3. Atkinson, W. B., and Elftman, H.: The carrying angle of the human arm as a secondary symptom character. Anat. Rec. 91:49, 1945. 4. Beals, R. K.: The normal carrying angle of the elbow. Clin. Orthop. 119:194, 1976. 5. Beetham, W. P., Jr., Polley, H. F., Slocumb, C. H., and Weaver, W. F.: Physical Examination of the Joints. Philadelphia, W. B. Saunders Co., 1965. 6. Bert, J. M., Linscheid, R. L., and McElfresh, E. C.: Rotatory contracture of the forearm. J. Bone Joint Surg. 62A:1163, 1980. 7. Boone, D. C., and Azen, S. P.: Normal range of motion of joints in male subjects. J. Bone Joint Surg. 61A:756, 1979. 8. Childress, H. M.: Recurrent ulnar nerve dislocation at the elbow. Clin. Orthop. 108:168, 1975.

9. Daniels, L., Williams, M., and Worthingham, C.: Muscle Testing: Techniques of Manual Examination, 2nd ed. Philadelphia, W. B. Saunders Co., 1946. 10. Elkins, E. C., Ursula, M. L., and Khalil, G. W.: Objective recording of the strength of normal muscles. Arch. Phys. Med. Rehabil. 33:639, 1951. 11. Hoppenfeld, S.: Physical Examination of the Spine and Extremities. New York, Appleton-Century-Crofts, 1976. 12. Johansson, O.: Capsular and ligament injuries of the elbow joint. Acta Chir. Scand. Suppl. 287:1, 1962. 13. Keats, T. E., Teeslink, R., Diamond, A. E., and Williams, J. H.: Normal axial relationships of the major joints. Radiology 87:904, 1966. 14. Lanz, T., and Wachsmuth, W.: Praktische Anatomie. Berlin, ARM, Springer-Verlag, 1959. 15. Lennon, R. I., Riyat, M. S., Hilliam, R., Anathkrishnan, G., and Alderson, G.: Can a normal range of elbow movement predict a normal elbow x-ray? Emerg Med J 24:86, 2007. 16. McRae, R.: Clinical Orthopedic Examination. London, Churchill Livingstone, 1976. 17. Morrey, B. F., Askew, L. J., An, K. N., and Chao, E. Y.: A biomechanical study of normal functional elbow motion. J. Bone Joint Surg. 63A:872, 1981. 18. Morrey, B. F., and Chao, E. Y.: Passive motion of the elbow joint. A biomechanical study. J. Bone Joint Surg. 61A:63, 1979. 19. O’Driscoll, S. W., Morrey, B. F., and An, K. N.: Intra-articular pressuring capacity of the elbow. Arthroscopy 6:100, 1990. 20. O’Driscoll, S. W., Morrey, B. F., and An, K. N.: Intra-articular pressuring capacity of the elbow. J. Bone Joint Surg. 73A:440, 1991.

Chapter 4 Physical Examination of the Elbow

21. O’Neill, O. R., Morrey, B. F., Tanaka, S., and An, K. N.: Compensatory motion in the upper extremity after elbow arthrodesis. Clin. Orthop. 281:89, 1992. 22. Provins, K. A., and Salter N.: Maximum torque exerted about the elbow joint. J. Appl. Physiol. 7:393, 1955. 23. Rasch, P. J.: Effect of position of forearm on strength of elbow flexion. Res. Q. 27:333, 1955. 24. Regan, W. D., Korinek, S. L., Morrey, B. F., and An, K. N.: Biomechanical study of ligaments about the elbow joint. Clin. Orthop. 271:170, 1991.

79

25. Schemitsch, E. H., Richards, R. R., and Kellam, J. F.: Plate fixation of fractures of both bones of the forearm. J. Bone Joint Surg. 71B:345, 1989. 26. Wagner, C.: Determination of the rotary flexibility of the elbow joint. Eur. J. Appl. Physiol. 37:47, 1977. 27. Williams, M., Stutzman, L.: Strength variation through the range of motion. Phys. Ther. Rev. 39:145, 1959. 28. Youm, Y., Dryer, R. F., Thambyrajahk, K., Flatt, A. E., and Sprague, B. L.: Biomechanical analysis of forearm pronation-supination and elbow flexion-extension. J. Biomech. 12:245, 1979.

80

Part II Diagnostic Considerations

CHAPTER

5

Functional Evaluation of the Elbow Bernard F. Morrey and Kai-Nan An

INTRODUCTION Involvement of the upper limb accounts for about 10% of all compensation paid in the United States for disabling work-related injuries.47,67 In addition, dysfunction of the upper extremity cost about 5.5 million lost work days in 1977.66 Elbow function consists of three activities: (1) allows the hand to be positioned in space, (2) provides the power to perform lifting activities, and (3) stabilizes the upper extremity linkage for power and fine work activities. The essential joint functions are motion, strength, and stability. However, ultimately, the final determinant of function and the ability to perform activities of daily living is pain.

ELBOW MOTION NORMAL MOTION Normal flexion and forearm rotation at the elbow are adequately measured clinically with the handheld goniometer. Forearm rotation is measured with the elbow at 90 degrees of flexion, often with the subject holding a linear object, such as a pencil, to make the measurement more objective.79 In spite of obvious limitations, investigators have concluded that a standard handheld goniometric examination by a skilled observer allows measurement of elbow flexion-extension and pronation-supination with a margin of error of less than 5%.35,95 In fact, the flexion-extension intraobserver reliability correlation coefficient is 0.99.78 Different trained observers also provide measurements that are statistically equivalent.30,78 Normal passive elbow flexion ranges between 0 and 140 to 150 degrees.1,11,44,79 Greater variation of normal forearm rotation has been described but averages about 75 degrees pronation and 85 degrees supination.1,11,44,91

INVESTIGATIVE TECHNIQUES OF MEASURING COMPLEX ACTIVE MOTION To measure the three-dimensional joint motion in daily activities, any one of several rather sophisticated experimental techniques can be used.1,95 For experimental studies, the triaxial electrogoniometer2,16,63 can simultaneously measure three-dimensional motion of more than one joint system with a high degree of reproducibility and reliability58,71 (Fig. 5-1). Video telemetry, computer-simulated motion, and electromagnetic sensors have also been developed to study three-dimensional kinematic measurement.2,71,87 Most recently, robotic techniques and miniature accelerometers and gyroscopes have been adopted to study complex upper extremity compensatory motion.49,56 For the elbow, the complex inter-relationship of shoulder and wrist function, both motion and motor activity, remains a complex and poorly understood area of investigation.32

FUNCTIONAL MOTION For most activities, the full potential of elbow motion is not needed or used. Loss of terminal flexion is more disabling than is the same degree of loss of terminal extension.14,70 Using the electrogoniometer just described, a study of 15 activities of daily living established that most functions can be performed using an arc of 100 degrees of flexion between 30 and 130 degrees (Fig. 5-2) and 100 degrees of forearm rotation equally divided between pronation and supination (Fig. 5-3). This has become the accepted standard for functional elbow motion. The motion requirements of the elbow joint needed for daily activities are really a measurement of the reaching ability of the hand. The extent to which this function is impaired by loss of elbow flexion or extension can be estimated analytically (Fig. 5-4). When motion is limited from 30 to 130 degrees, the potential area reached by the hand is reduced by about 20%. Thus, the range of elbow flexion between 30 and 130 degrees corresponds with about 80% of the normal reach capacity of the forearm and hand in a selected plane of shoulder motion. The functional impact of further loss of the flexion arc is also not equally distributed between flexion and extension. Our clinical experience indicates that flexion is of more value than extension in a ratio of about 2 : 1. Hence, a 10-degree further loss of flexion (120 degrees) is roughly equivalent to 20 degrees further loss of extension (Fig. 5-5). The optimal position of elbow fusion to accomplish activities of daily living has been accepted as 90 degrees.86 To further assess this issue, we hypothesized that the optimal position would be associated with a minimal amount of compensatory shoulder motion.71 It was surprising to observe that for discrete and fixed positions

FIGURE 5-1

The elbow electrogoniometer may be used to measure activities of daily living. A, Elbow flexion and forearm rotation to reach the back of the head. B, The subject is sitting at the activities table. (From Morrey, B. F., Askew, L. J., and Chao, E. Y.: A biomechanical study of normal functional elbow motion. J. Bone Joint Surg. 63A:872, 1981.)

140

Elbow flexion, degrees

120

100

80

60

40

FIGURE 5-2

20

0 Door

Pitcher Shoe

Chair

Sacrum

Newspaper

Waist

Knife

Head vertex Chest

Activities of daily living

Fork

Glass

Telephone

Neck Head occiput

Normal elbow flexion positions for activities of hygiene and those requiring arcs of motion are demonstrated. Most functions can be performed between 30 and 130 degrees of elbow flexion.

Part II Diagnostic Considerations

80 60 40

Pronation

20 Degrees

82

Supination

0 20 40 60 80 Glass

Fork

Sacrum

Chair Head vertex

Door Neck

Pitcher Chest

Waist

Knife

TeleNewsphone paper Head Shoe occiput

Activities of daily living

FIGURE 5-3

Routine daily activities requiring pronation and supination or arcs of motion are performed between 50 degrees pronation and 50 degrees supination.

A FIGURE 5-4

B

The reaching area of the hand in the sagittal (A) and transverse (B) planes, with simultaneous movement of the elbow and shoulder. If the elbow is held at approximately 90 degrees of flexion, marked reduction of reach potential occurs. Note also that the circumduction motion of the shoulder does not compensate for the hinged type motion of the elbow joint.

Chapter 5 Functional Evaluation of the Elbow

145° 130°

145° 130°

145° 130° 120°

110° 40°

70° 100° 0°

70°

50°

30°

0°

Functional arc

30°

0°

Optimum 70° arc

83

30° Optimum 40° arc

FIGURE 5-5

The further loss of motion from the ideal 30 to 130 degree arc is better tolerated as extension loss than as flexion loss.

the optimum position or “least worse” for most activities.

STRENGTH To understand the value and limitations of clinical strength assessment, it will be helpful to briefly review the physiology of muscle contraction and major factors affecting strength.15

z

TYPES OF MUSCLE CONTRACTION

y

x

FIGURE 5-6

As the fixed position of elbow fusion increases toward 90 degrees, activities of daily living are accomplished with the humerus less elevated and more laterally circumducted.

of the elbow, increasing the amount of shoulder motion did not provide greater use or increased function. It was also noted that for greater degrees of fixed elbow flexion, efforts to perform daily functions were accompanied by a tendency of the humerus to assume a less elevated and more lateral circumduction position (Fig. 5-6). This is consistent with the mechanical functions of these two joints; a ball-and-socket joint providing rotatory motion does not provide compensatory motion for hinge-type motion that occurs only in a single plane. This investigation did confirm the accepted tenant that 90 degrees is

There are several types of muscle contraction classified according to changes in length, force, and velocity of contraction (Fig. 5-7).5,31,60 If there is no change in muscle length during a contraction, it is called isometric. When the external force exceeds the internal force of a shortened muscle and the muscle lengthens while maintaining tension, the contraction is called an eccentric, or lengthening, contraction. In contrast, if the muscle shortens while maintaining tension, a concentric contraction occurs. For elbow flexion, eccentric force exceeds isometric force by about 20%, and isometric force exceeds concentric force by about 20% (Fig. 5-8).23,85 However, it is known that eccentric exercise is associated with muscle fiber damage. This may lead to alterations in muscle receptors that can alter joint position sense.13

FORCE CONSIDERATIONS If the muscle produces a constant internal force that exceeds the external force of the resistance, the muscle shortens, and the contraction is further characterized as isotonic. Energy use in this case is larger than that required to produce tension, which will balance the load, and the extra energy is used to shorten the muscle. If the speed of rotation of an exercising limb is predetermined and held constant, changes occur in the amount of tension developed in the muscles causing the motion. This is called an isokinetic contraction. This may

Part II Diagnostic Considerations

84

FIGURE 5-7

Isometric

Concentric

Eccentric

Constant Load

Velocity

Isotonic

Isokinetic

60

be of either the concentric or eccentric type defined earlier.

50

Speed of Contraction

40 Force (pounds)

Types of muscle contractions classified according to change in muscle length. An isometric contraction results in no change of muscle length with a constant load and velocity. The concentric contraction is defined as a shortening of the muscle, whereas the eccentric contraction occurs with lengthening of the muscle. These latter two contractions may be subclassified according to whether a constant load (isotonic) or a constant velocity (isokinetic) condition is met.

30

20

*

*

*

10

*

Flexors Extensors Starting angle

Eccentric Isometric Concentric

*

0 50

60

70

80

90 100 110 120 130 140

Elbow angle (degrees)

FIGURE 5-8

A rapidly contracting muscle generates less force than one contracting more slowly. In an isometric contraction, the velocity is zero because the resistance exceeds the ability of the muscle to move the joint. In sports, rates of motion exceeding 300 degrees per second are common. One recent study has shown that isometric training at maximum strength is more effective to increase power production than no load training at maximum velocity.88

Comparison of isometric, concentric, and eccentric flexion and extension contraction strength for different positions of elbow flexion. Note that approximately 20% greater strength may be generated with an eccentric than with an isometric contraction; the isometric contraction, on the other hand, is approximately 20% greater than the concentric type of contraction. (Modified from Singh, M.: Isotonic and isometric forces of forearm flexors and extensors. J. Appl. Physiol. 21:1436, 1966.)

FACTORS AFFECTING MAXIMUM MUSCLE TENSION Muscle Length at Contraction The relationship of muscle tension to muscle length is recognized by most clinicians and is presented graphically in the form of a length tension curve of an isolated muscle (Fig. 5-9).27 Recent studies suggest this concept is applicable to muscle systems at different anatomic sites.89 The exact nature of the relationship varies from muscle to muscle and from joint to joint, depending on the specific function. For example, a study in our laboratory demonstrated the relationship of triceps strength as a function of muscle shortening. A somewhat linear relationship with 1-, 2-, and 3-cm length change associated with 17%, 40%, and 63% strength reduction, respectively39 (Fig.

Chapter 5 Functional Evaluation of the Elbow

5-10). The length of elbow rotators change considerably over the full range of motion. The percent change at the wrist is 8; at the elbow, 55; and at the shoulder, 200.74

TECHNIQUE OF STRENGTH MEASUREMENT

Total tension

Passive tension

FIGURE 5-9

100

Developed tension Contractile tension only

(Minimum)

In the clinic, the most common study is that of static or isometric flexion-extension strength using a simple tensiometer, or spring device (Fig. 5-11).17,52 For more accurate documentation or for investigative purposes, more sophisticated devices such as a strain gauge tensiometer25 and dynamometer21,64,76 also have been used. Isokinetic strength is a more specific measurement of dynamic elbow flexion-extension function and is used more frequently today, especially for the assessment of athletic or occupational injuries. In an isokinetic muscular movement, the speed of rotation of the limb is held constant despite changes in the amount of tension developed. This isokinetic movement can be measured by means of an accommodating resistance dynamometer. Because of the accommodating load cell, the

Length

(Maximum)

An idealized length tension curve during isometric contraction demonstrates the maximal force for active muscle contractility. A greater amount of force may be attained if the muscle is stretched to some optimal point. Excessive stretching, although theoretically increasing the muscle force, in fact reduces the strength of contraction owing to loss of the ability of the contractile elements to function optimally.

Strength % normal

Tension

Rest length

When evaluating strength, either the torque created about the joint or the force generated in the hand and forearm in resisting joint rotation is measured. Either static or dynamic measuring devices may be used.

85

Elbow @ 30°

80 60 40 20 0 0

10

20

30

Shortening: origin-insertion/mm

FIGURE 5-10

Effect of the change in triceps length on extension strength.

FIGURE 5-11

A simple spring tensiometer, which is used in the clinical setting to estimate elbow flexion strength.

86

Part II Diagnostic Considerations

velocity of an exercising limb cannot be increased.60,72 As more force is exerted against the lever arm of the dynamometer, more resistance is encountered by the limb, and rotation occurs only at the predetermined constant speed. These devices accurately measure peak torque, the joint angle position at peak torque, the range of motion, and endurance.6 This technique is becoming increasingly useful for the measurement of elbow strength and endurance, and for more accurate study of the role of fatigue in arriving at disability estimates.84 This has proven particularly useful in assessing patients with biceps tendon reattachment.

about 5% for women and 10% for men.25 Strengths at the neutral forearm position were slightly greater than those at the supinated and pronated positions.25,43,76,80 For elbow extension, the average maximum torque strength is about 4 kg-m for men and 2 kg-m for women (Fig. 5-12).4 Observations for 14 female and 10 male subjects showed a gradual increase in strength as the elbow was extended and the 90 degree position generates the greatest isometric extension force.20,28,53,76 In general, the dominant extremity is about 5% to 10% stronger than the nondominant side, and men are about twice as strong as women in most positions (see Fig. 512). The isometric force of the flexors is about 40 percent greater than the isometric force of the extensors.4,45

ELBOW STRENGTH The greatest supination strength is generated from the pronated position; the converse relationship is also true.17,55 In the majority of shoulder elbow positions, the average torque of supination exceeded that of pronation by about 15 to 20 degrees for males and females. This was particularly marked when the elbow was extended. On the average, isometric pronation and supination strengths for men are 80 kg-cm and 90 kg-cm, respectively, and for women are 35 kg-cm and 55 kg-cm, respectively. The dominant and nondominant strength difference in these two types of function averaged about 10% (see Fig. 5-12). In one study,83 it was found that isometric elbow strengths of rheumatoid arthritis patients decreased in proportion to an increase in the severity of x-ray findings. The flexion and supination strengths after total elbow replacement were about two times greater than before operation.

Supination and Pronation

STATIC MEASUREMENTS Although the general tends are relatively consistent,9 absolute strength measurements are not exactly comparable owing to variations in study technique and even greater differences between individual subjects, especially correlated to body size and age.10,41 On the average, the maximum isometric torque created at the elbow joint is about 7 kg-m for men and 3.5 kg-m for women.4 Isometric muscle power is greatest during flexion at joint positions between 90 and 110 degrees.25,93 At elbow angles of 45 and 135 degrees, only about 75 percent of the maximum elbow flexion strength is generated.43,45,94 Maximum flexion strength is generated in forearm supination; forearm pronation is associated with the weakest flexion strength.18,43 Most of the torque occurs from contributions of the biceps, brachialis, and brachioradialis.28 The mean difference in isometric flexion force among the three forearm positions at various flexion angles is Flexion Extension

DYNAMIC FUNCTION Fatigue is an important consideration in altered function because routine activities require repetitive

125

1000

Torque kg - cm

800 600

100 75

400

50

200

25

0

0 M

F Flex

FIGURE 5-12

Torque kg - cm

Dominant side Nondominant side M = Males, n = 50 F = Females, n = 54

M

F Ext

M

F Pro

M

F Sup

M

F Grip

Mayo Clinic Biomechanics Laboratory study of normal elbow strength. Notice that men are approximately twice as strong as women and that a 5% to 10% difference is noted between the dominant and nondominant extremities.

Chapter 5 Functional Evaluation of the Elbow

actions, some of which may exceed one million cycles per year.22 The relative value of static and dynamic testing modalities is a debated issue. Motzkin and colleagues65 studied the relationship between isometric and isokinetic fatigue and found no consistent relationship. One reason for this is the marked variation even in test-retest studies of the same function.33 The one reliable association is that the eccentric contracture provides the greatest torque strength for both isometric and isokinetic testing modes.33,65 The relationship between strength and speed of movement is undefined.4 Many investigations support the hypothesis that maximum strength and the rate of movement are independent of each other.68,73 In a recent study,29 isokinetic peak torque and work were greater at the slower speed, as opposed to power, which was significantly greater at the faster speed.

ADDITIONAL VARIABLES OF STRENGTH ASSESSMENT In addition to the factors discussed, other confounding variables to strength testing include motivation, the learning effect of repetitive tests,51,59,81 the psychological benefit derived from repetitive testing,37,54 and the influence of the time of day,58 age, and even body size.10,41 The motivation factor is a variable that is well recognized but is difficult to control, quantitate, or eliminate.19,50,85 The rate of attaining maximum strength during repetitive exertion has been suggested as a possible objective criterion for judging whether a subject is voluntarily exerting full muscular strength or is not giving an honest effort.50 The eccentric : concentric strength ratios as well as the difference between these ratios at the high and the low speeds were highly effective in distinguishing maximal from submaximal efforts,24 and we do currently use this information clinically to assess for “functional” behavior.

STABILITY By virtue of the inherent stability afforded by the joint articulation, clinical instability of the elbow may be a perplexing problem (see Chapters 28 through 30). Ligamentous injury most commonly occurs in association with radial head fracture42,82 or elbow dislocation. Recurrent dislocations, however, occur in only 1% to 2% of patients.54 In fact, recurrent instability at the elbow is most commonly a rotatory instability due to insufficiency of the lateral ulnar collateral ligament69 and is discussed at length in Chapter 48. The clinical concept of complex instability is becoming more recognized. The “unhappy triad” refers specifically to fractures of the

87

radial head and coronoid in association with collateral ligament injury. Quantification of instability is difficult; studies are being conducted to understand instability, but no well-defined standard exists to clinically grade this parameter (see Chapter 4).8

FUNCTIONAL EVALUATION OF THE ELBOW PERFORMANCE INDICES An objective and reproducible means of evaluating the elbow by considering all of these features of function is obviously desirable. A tradeoff exists between a complex but detailed assessment protocol and one that is simple but not sufficiently thorough. A complete and comprehensive assessment that might be useful in a research facility is not practical clinically. For a clinician, a meaningful rating system should be both complete and readily amenable to an office practice (Table 5-1). A single parameter or index composed of all pertinent variables should accurately reflect the gradation of objective function, as discussed earlier. To be of further value, the rating system should include consideration of the presence of pain and specific daily functions that serve as surrogates to several functional variables as they apply to a discrete activity. Finally, it is also realized that no index or system is capable of discriminating changes in function of the full spectrum of pathology. A tool to describe the state of an athlete with tennis elbow is not adequate to describe the dysfunction of rheumatoid arthritis. To date, most proposed rating systems consider both objective function and subjective features (motion, strength, stability, pain, and the ability to perform daily activities).77 Most systems have been developed to document the effectiveness of surgical intervention (Table 5-2).26,40,75 TABLE 5-1 Characteristics and Implications of Patient Assessment Tools Trait

Implication

Short

High compliance

Reflects reality

Valid to draw conclusions

Easy

Nonambiguous questions

Reliable

• Accurate for all respondents • Effective in person or by communiqué

Universal

Addresses broad spectrum of conditions

Validated Variation

Believable data

Reliable

Make decisions

Accurate

Based on outcome

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Part II Diagnostic Considerations

Functional Assessment and Rating Schemes for the Elbow

TABLE 5-2 Reference

Inglis and Pellicci40 26

Ewald et al.

Pain

Motion

Strength

Stability

ADL

Deformity

Total

30

28

10

—

20

12 (contracture)

100

50

10

—

—

30

5 (contracture)

100

5 (varus/valgus) 75

50

25

25

—

—

—

13a

20

10

—

10

10

10

50

Broberg and Morrey12

40

25

10

10

15

—

100

JOA40a

30

30

—

10

20

10

100

45

20

—

10

25

—

100

Prichard

Brumfield

62

Morrey (MEPS)

100

ADL, activity of daily living; JOA, Japanese Orthopaedic Association; MEPS, Mayo Elbow Performance Score.

TABLE 5-3 Function

Mayo Elbow Performance Score Points

Definition (Points)

Pain

45

None (45) Mild (30) Moderate (15) Severe (0)

Motion

20

Arc >100 degrees (20) Arc 50-100 degrees (15) Arc <50 degrees (5)

Stability

10

Stable (10) Moderate instability (5) Gross instability (0)

Function

25

Comb hair (5) Feed (5) Perform hygiene (5) Don shirt (5) Don shoe (5)

Total

100

Classification: excellent, >90; good, 75-89; fair, 60-74; poor, <60.

Broberg and Morrey12 first described a system designed to be applicable not only to joint replacement but also to other reconstructive procedures. However, as noted earlier, it is obvious that no single rating system is both simple and also sensitive enough to distinguish the status and change of function of the person crippled by rheumatoid arthritis and of the professional tennis player with epicondylitis. Nonetheless, I (B.F.M.) have found that a modification of the simple system reported by Broberg has met my clinical needs over the last several years. The currently employed system is termed the Mayo Elbow Performance Score (MEPS) (Tables 5-2 and 5-3).62 Any discussion of a system or index to summarize function should be subjected to

(1) test and retest reliability, (2) internal consistency, and (3) validity. Furthermore, it is highly desirable to be able to determine the index from patient input above, either in person or by questionnaire. The characteristics of an effective functional evaluation scheme are shown in Table 5-1. In most systems,26,75 pain accounts for the majority of the overall score. Because pain improvement is the most common outcome of intervention, one can bias the appearance of the success of a procedure by overweighing pain in the index calculation. Furthermore, I believe that it is important for the specific functional index used in a clinical practice to represent all functions of the elbow joint as accurately as possible. Thus, those indexes that do not consider strength and stability, except as how they relate to activities of daily living, may not be as comprehensive as those that consider these specific joint functions.23 The functions of motion, strength, and stability are also tested and, hence, duplicated by the ability to perform activities of daily living. Thus, this latter category is really a surrogate for the other three. The issue of a reliable, comprehensive, and yet simple method of determining functional assessment remains unanswered for the elbow and, at the present time, is the subject of discussion and investigation by the American Shoulder and Elbow Surgeons. Turchin and colleagues90 recently conducted an extensive assessment of the published elbow rating scores. Although there is a lack of agreement in the aggregate scores, there is good correlation with the individual raw aggregate scores. The most important message is that which reinforces the observation made earlier; there is no one system that accurately reflects therapeutic value for all conditions: athletic, arthritic, traumatic, and the like. In fact, a self administered questionnaire to assess ulnar nerve function has recently been demonstrated to be reproducible and valid.61

Chapter 5 Functional Evaluation of the Elbow

OUTCOME MEASURES In recent years, an increased emphasis has been placed on the subjective status or the “outcome” of intervention. The flurry of activity over the last decade has been productive in first producing useful general tools of assessment such as the Short Form-36 43,46,92 and the Western Ontario and McMaster University Osteoarthritis Index (WOMAC). The WOMAC is designed principally to asses hip and knee function.33 More specific to the elbow and upper extremity, the American Shoulder and Elbow Surgeons described a patient- and physicianadministered assessment tool,48 and a global strategy of documenting upper extremity function including the shoulder, elbow and hand (DASH) has been developed38 by the American Academy of Orthopedic Surgeons in conjunction with the Canadian Institute for Work and Health.38 The DASH continues to be assessed and refined to further enhance its relevance.7 Ultimately, the goal is to measure disease and intervention impact on function36 and quality of life.3 The Patient-Related Elbow Evaluation is a short form using the Visual Analogue Scale to describe pain and daily function.57 The goal is to include patient-specific symptoms as well as components of the functional status including physical, social, and psychological aspects to determine the impact of treatment. The value of specific intervention on quality of life has also been undertaken recently.3 As implied earlier, accurately demonstrating this relationship is surprisingly complex, but by carefully using existing metrics, investigators have objectively documented the positive impact of elbow joint replacement.3 What remains is to also demonstrate the cost effectiveness of interventions and ultimately be in a position to compare selection factors, techniques, implants, and the like by objective and subjective outcome standards.

References 1. American Academy of Orthopaedic Surgeons: Joint Motion: Method of Measuring and Recording. Chicago, American Academy of Orthopaedic Surgeons, 1965. 2. An, K.-N., Jacobsen, M. C., Berglund, L. J., and Chao, E. Y.: Application of a magnetic tracking device to kinesiologic studies. J. Biomechan. 21:613, 1988. 3. Angst, F., John, M., Pap, G., Mannion, A. F., Herren, D. B., Flury, M., Aeschlimann, A., Schwyzer, H.-K., and Simmen, B. R.: Comprehensive assessment of clinical outcome and quality of life after total elbow arthroplasty. Arthritis & Rheum. 53(1):73, 2005. 4. Askew, L. J., An, K. N., Morrey, B. F., and Chao, E. Y.: Functional evaluation of the elbow. Normal motion requirements and strength determinations. Orthop. Trans. 5:304, 1981.

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5. Astrand, P. O., and Rodahl, K.: Textbook of Work Physiology. New York, McGraw-Hill, 1970. 6. Barnes, W. S.: The relationship between maximum isokinetic strength and isometric endurance. Res. Q. Exerc. Sport 51:714, 1980. 7. Beaton, D., and Schemitsch E.: Measures of health-related quality of life and physical function. Clin Orthop 413:90105, 2003. 8. Beingessner, D. M., Dunning, C. E., Stacpoole, R. A., Johnson, J A., and King, G. J.: The effect of coronoid fractures on elbow kinematics and stability. Clin. Biomech. 22:183, 2007. 9. Berger, R. A.: Comparison of static and dynamic strength increases. Res. Q. 33:329, 1962. 10. Bilodeau, M., Henderson, T. K., Nolta, B. E., Pursley, P. J., and Sandfort, G. L.: Effect of aging on fatigue characteristics of elbow flexor muscles during sustained submaximal contraction. J. Appl. Physiol. 91:2654, 2001. 11. Boone, D. C., and Azen, S. P.: Normal range of motion of joints in male subjects. J. Bone Joint Surg. 61A:756, 1979. 12. Broberg, M. A., and Morrey, B. F.: Results of treatment of fracture dislocations of the elbow. Clin. Orthop. 216:109, 1987. 13. Brockett, C., Warren, N., Gregory, J. E., Morgan, D. L., and Proske, U.: A comparison of the effects of concentric versus eccentric exercise on force and position sense at the human elbow joint. Brain Res. 771:251, 1997. 13a. Brumfield, R. H. Rancho Los Amigo Functional Test. Contemp. Gerontol. 8:67, 1984. 14. Carstam, N.: Operative treatment of fractures of the head and neck of the radius. Acta Orthop. Scand. 19:502, 1950. 15. Chao, E. Y.: Experimental Methods for Biomechanical Measurements of Joint Kinematics. CRC Handbook of Engineering in Medicine and Biology, Section B: Instruments and Measurements. West Palm Beach, CRC Press, 1978. 16. Chao, E. Y., An, K. N., Askew, L. J., and Morrey, B. F.: Electrogoniometer for the measurement of human elbow joint rotation. J. Biomech. Eng. 102:301, 1980. 17. Clarke, H. H., and Bailey, T. L.: Strength curves for fourteen joint movements. J. Assoc. Phys. Ment. Rehabil. 4:12, 1950. 18. Clarke, H. H., Elkins, E. C., Martin, G. M., et al.: Relationship between body position and the application of muscle power to movements of the joint. Arch. Phys. Med. 31:81, 1950. 19. Cooper, D. F., Grimby, G. F., Jones, D. A., and Edwards, R. H. Perception of effort in isometric and dynamic muscular contraction. Eur. J. Appl. Physiol. 41:173, 1979. 20. Currier, D. P.: Maximal isometric tension of the elbow extensor at various positions, Part I. Assessment by cable tensiometer. Phys. Ther. 52:1043, 1972. 21. Darcus, H. D.: The maximum torques developed in pronation and supination of the right hand. J. Anat. 85:55, 1951. 22. Davis, P. R.: Some Significant Aspect of Normal Upper Limb Functions. Conference on Joint Replacement of the Upper Extremity. London, Institute of Mechanical Engineers, 1977.

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23. Doss, W. S., and Karpovich, P. V.: A comparison of concentric, eccentric, and isometric strength of the elbow flexion. J. Appl. Physiol. 20:351, 1965. 24. Dvir, Z: An isokinetic study of submaximal effort in elbow flexion. Perceptual and Motor Skills 84(3 Pt 2):1431, 1997. 25. Elkins, E. C., Leden, U. M., and Wakim, K. G.: Objective recording of the strength of normal muscles. Arch. Phys. Med. 32:639, 1951. 26. Ewald, F. C., Scheinberg, R. D., Poss, R., Thomas, W. H., Scott, R. D., and Sledge, C. B.: Capitellocondylar total elbow arthroplasty: Two to five year follow up in rheumatoid arthritis. J. Bone Joint Surg. 62A:1259, 1980. 27. Fick, K.: Handbuch der Anatomie und Mechanic der Gelenke, Vol. 3. Jena, 1911. 28. Funk, D.: EMG Investigation of Muscular Contractions About the Human Elbow. MS Thesis, Mayo Graduate School of Medicine, 1984. 29. Gallagher, M. A., Cuomo, F., Polonsky, L., Berliner, K., Zuckerman, J. D.: Effects of age, testing speed, and arm dominance on isokinetic strength of the elbow. J. Shoulder Elbow Surg. 6:340, 1997. 30. Gajdosik, R. L., Bohannon, R. W.: Clinical measurement of range of motion. Review of goniometry emphasizing reliability and validity. Phys. Ther. 67:1867, 1987. 31. Gowitzke, B. A., and Miller, M.: Understanding the Scientific Basis of Movement, 2nd ed. Baltimore, Williams & Wilkins, 1980. 32. Gribble, P. L., and Ostry, D. J.: Independent coactivation of shoulder and elbow muscles. Experimental Brain Res. 123(3):355, 1998. 33. Griffin, J. W.: Differences in elbow flexion torque measured concentrically, eccentrically, and isometrically. Phys. Ther. 67:1205, 1987. 34. Grootendorst, P., Marshall, D., Pericak, D., Bellamy, N., Feeny, D., and Rottance, G. W.: A model to estimate health utilities index mark 3 utility scores from WOMAC index scores in patients with osteoarthritis of the knee. J. Rheumatol. 34:534, 2007. 35. Hellebrandt, F. A., Duvall, E. N., and Moore, M. L.: The measurement of joint motion: part III. Reliability of goniometry. Phys. Ther. Rev. 29:302, 1949. 36. Hildebrand, K. A., Patterson, S. D., Regan, W. D., McDermid, J. C., and King, G. J. W.: Functional outcome of semiconstrained total elbow arthroplasty. J. Bone Joint Surg. 82A:1379-1386, 2000. 37. Hood, L. B., and Forward, E. M. M.: Strength variations in two determinations of maximal isometric contractions. J. Am. Phys. Ther. Assoc. 45:1046, 1965. 38. Hudak, P. L., Amadio, P. C., and Bombardier, C.: Development of an upper extremity outcome measure: the DASH (Disabilities of the Arm, Shoulder, and Hand). The Upper Extremity Collaborative Group (UECG). Am. J. Indust. Med. 29:602, 1996. 39. Hughes, R. E., Schneeberger, A. G., An, K.-N., Morrey, B. F., and O’Driscoll, S. W.: Reduction of triceps muscle force after shortening of the distal humerus: A computational model. J. Shoulder Elbow Surg. 6:444, 1997. 40. Inglis, A. E., and Pellicci, P. M.: Total elbow replacement. J. Bone Joint Surg. 62A:1252, 1980.

40a. Japanese Orthopaedic Association Elbow Evaluation Sheet. Jpn. Orthop. Assoc. 66:596, 1992. 41. Jaric, S., Radosavljevic-Jaric, S., and Johansson, H.: Muscle force and muscle torque in humans require different methods when adjusting for differences in body size. European J. Appl. Physiol. 87:304, 2002. 42. Johansson, O.: Capsular and ligament injuries of the elbow joint. Acta Orthop. Scand. Suppl. 287:1, 1962. 43. Jorgensen, K., and Bankov, S.: Maximum strength of elbow flexors with pronated and supinated forearm. Med. Sport Biomech. 6:174, 1971. 44. Kapandji, I. A.: The Physiology of the Joints. Vol. I: Upper Limb, 2nd ed. Baltimore, Williams & Wilkins, 1970. 45. Karpovich, P. V., and Singh, M.: Isotonic and isometric forces of forearm flexors and extensors. J. Appl. Physiol. 21:1435, 1966. 46. Katz, J. N., Larson, M. G., Phillips, C. B., Fossel, A. H., and Liang, M. H.: Comparative measurement sensitivity of short and longer health status instruments. Med. Care. 30:917, 1992. 47. Kelsey, J. L., Pastides, H., Kreiger, N., Harris, C., and Chernow, R. A.: Upper Extremity Disorders. A Study of Their Frequency and Cost in the United States. St. Louis, C. V. Mosby Co., 1980. 48. King, G. J. W., Richards, R. R., Zuckerman, J. D., Blasier, R., Dillman, C., Friedman, R. J., et al.: Research Committee, American Shoulder and Elbow Surgeons. A standardized method for assessment of elbow function. J. Shoulder Elbow Surg. 8:351, 1999. 49. Kodek, T., Munih, M.: Quantification of shoulder and elbow passive moments in the sagittal plane as a function of adjacent angle fixations. Technol. Health Care. 11:89, 2003. 50. Kroemer, K. H. E., and Marras, W. S.: Towards an objective assessment of the “maximal voluntary contraction” component in routine muscle strength measurements. Eur. J. Appl. Physiol. 45:1, 1980. 51. Kroll, W.: Reliability variations of strength in test-retest situations. Res. Q. 34:50, 1963. 52. Larson, C. L., and Nelson, R. C.: An analysis of strength, speed and acceleration of elbow flexion. Arch. Phys. Med. Rehabil. 50:274, 1969. 53. Liberson, W. T., Dondey, M., and Asa, M. M.: Brief repeated isometric maximal exercises. Am. J. Phys. Med. 41:3, 1962. 54. Linschied, R. L., and Wheeler, D. K.: Elbow dislocations. J. A. M. A. 194:1171, 1965. 55. Little, A. D., and Lehmkuhl, D.: Elbow extension force: measured in three test positions. J. Am. Phys. Ther. Assoc. 46:7, 1966. 56. Luinge, H. J., Veltink, P. H., and Baten, C. T.: Ambulatory measurement of arm orientation. J. Biomechanics 40:78, 2007. 57. MacDermid, J. C.: Outcome evaluation in patients with elbow pathology: issues in instrument development and evaluation. J. Hand Ther. 14:105, 2001. 58. McGarvey, S., Morrey, B. F., Askew, L. J., and An, K. N.: Reliability of isometric strength testing: temporal factors and strength variation. Clin. Orthop. Rel. Res. 185:301, 1984.

Chapter 5 Functional Evaluation of the Elbow

59. Masley, J. W., Hairabedian, A., and Donaldson, D. N.: Training in relation to strength, speed and coordination. Res. Q. 24:308, 1953. 60. Moffroid, M., et al.: Rehabilitation. Monograph 40: Guidelines for Clinical Use of Isokinetic Exercise. New York, Institute of Rehabilitation Medicine, New York University Medical Center, 1969. 61. Mondelli, M., Padua, L., Giannini, F., Bibbo, G., Aprile, I., and Rossi, S.: A self-administered questionnaire of ulnar neuropathy at the elbow. Neurol. Sci. 27:402, 2006. 62. Morrey, B. F.: Functional evaluation of the elbow. In Morrey, B. F. (ed). The Elbow and Its Disorders, 2nd ed. Philadelphia, W.B. Saunders Co, 1993. 63. Morrey, B. F., Askew, L. J., An, K. N., and Chao, E. Y.: A biomechanical study of normal elbow motion. J. Bone Joint Surg. 63A:872, 1981. 64. Morrey, B. F., Chao, E. Y., and Hui, F. C.: Biomechanical study of the elbow following excision of the radial head. J. Bone Joint Surg. 61A:63, 1979. 65. Motzkin, N. E., Cahalan, T. D., Morrey, B. F., An, K. N., and Chao, E. Y.: Isometric and isokinetic endurance testing of the forearm complex. Am. J. Sports Med. 19:107, 1991. 66. National Center for Health Statistics, 1977. Cited by Kelsey et al. (op. cit.). 67. National Safety Council, 1976. Cited by Kelsey et al. (op. cit.). 68. Nelson, R. C., and Fahrney, R. A.: Relationship between strength and speed of elbow flexion. Res. Q. 36:455, 1963. 69. O’Driscoll, S. W., Bell, D. F., and Morrey, B. F.: Posterolateral rotatory instability of the elbow. J. Bone Joint Surg. 73A:440, 1991. 70. Ogilvie, W. H.: Discussion on minor injuries of the elbow joint. Proc. R. Soc. Med. 23:306, 1930. 71. O’Neill, O., Morrey, B. F., Tanaka, S., and An, K. N.: Compensatory motion in the upper extremity following elbow arthrodesis. Clin. Orthop. 281:89, 1992. 72. Osternig, L. R., Bates, B. T., and James, S. L.: Isokinetic and isometric torque force relationships. Arch. Phys. Med. Rehabil. 58:254, 1977. 73. Pierson, W. R., and Rasch, P. J.: Strength and speed. Perceptual motor skills. 14:144, 1962. 74. Pigeon, P., Yahia, L., and Feldman, A. G.: Moment arms and lengths of human upper limb muscles as functions of joint angles. J. Biomechan. 29:1365, 1996. 75. Pritchard, R. W.: Total elbow arthroplasty. In Joint Replacement in the Upper Limb. London, Mechanical Engineering Publications, 1977, p. 67. 76. Provins, K. A., and Salter, N.: Maximum torque exerted about the elbow joint. J. Appl. Physiol. 7:393, 1955. 77. Richards, R. R., An, K. N., Bigliani, L. U., Friedman, R. J., Gartsman, G. M., Gristina, A. G., Iannotti, J. P., Mow, V. C., Sidles, J., and Zuckerman, J. D.: A standarized method of the assessment of shoulder function. J. Shoulder Elbow Surg. 3:347, 1994. 78. Rothstein, J. M., Miller, P. J., and Roettger, R. F.: Goniometric reliability in a clinical setting. Phys. Ther. 63:1611, 1983.

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79. Russe, O.: An Atlas of Examination, Standard Measurements and Diagnosis in Orthopedics and Traumatology. Vienna, Hans Huber, 1972. 80. Salter, N.: The effect on muscle strength of maximum isometric and isotonic contractions at different repetition rates. J. Physiol. (London) 130:109, 1955. 81. Schenck, J. M., and Forward, E. M.: Quantitative strength changes with test repetitions. J. Am. Phys. Ther. Assoc. 45:562, 1965. 82. Schwab, G. H., Bennett, J. B., Woods, G. W., and Tullos, H.: Biomechanics of elbow instability: the role of the medial collateral ligament. Clin. Orthop. 146:42, 1980. 83. Shigeyama, Y., Inoue, H., Hashizume, H., Nagashima, H., and Senda, M.: Muscle strength in rheumatoid elbow: quantitative measurement and comparison to Larsen’s xray grade. Acta Medica Okayama 51:267, 1997. 84. Simmons, J. W., Rath, D., and Merta, R.: Calculation of disability using the Cybex II system. Orthopedics 5:181, 1982. 85. Singh, M., and Karpovich, P. V.: Isotonic and isometric forces of forearm flexors and extensors. J. Appl. Physiol. 21:1435, 1966. 86. Snider, W. J., and Dewitt, H. J.: Functional study for optimum position for elbow arthrodesis on ankylosis. J. Bone Joint Surg. 55A:1305, 1973. 87. Tanaka, S., An, K.-N., and Morrey, B. F.: Kinematics and laxity of ulnohumeral joint under valgus-varus stress. J. Musculoskeletal. Res. 2:45, 1998. 88. Toji, H., Suei, K., and Kaneko, M.: Effects of combined training loads on relations among force, velocity, and power development. Can. J. Appl. Physiol. 22:328, 1997. 89. Tracy, B. L., Mehoudar, P. D., and Ortega, J. D.: The amplitude of force variability is correlated in the knee extensor and elbow flexor muscles. Experimental Brain Res. 176:448, 2007. 90. Turchin, D. C., Beaton, D. E., and Richards, R. R.: Validity of observer-based aggregate scoring systems as descriptors of elbow pain, function, and disability. J. Bone Joint Surg. 80A:154, 1998. 91. Wagner, C.: Determination of the rotatory flexibility of the elbow joint. Eur. J. Appl. Physiol. 37:47, 1977. 92. Ware J. E., Snow, K. K., Kosinski, M., and Gandek, B.: SF-36 health survey: Manual and interpretation guide, 2nd ed. Lincoln, RI, QualityMetric Inc., 2000. 93. Williams, M., and Stutzman, L.: Strength variation through the range of joint motion. Phys. Ther. Rev. 39:145, 1959. 94. Williams, M., Toberlin, J. A., and Robertson, K. J.: Muscle force curves of school children. Phys. Ther. 45:539, 1965. 95. Wilmer, H. A., and Elkins, E. C.: An optical goniometer for observing range of motion of joints. Arch. Phys. Med. 28:695, 1947. 96. Worshal, D.: The reliability of isometric strength gain in therapeutic assessment. Am. Correct. Ther. J. 33:188, 1979.

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CHAPTER

6

Diagnostic Imaging of the Elbow Thomas H. Berquist

INTRODUCTION Imaging technology has expanded dramatically over the past decade (Box 6-1). However, evaluation of the elbow still relies heavily on routine radiographs or computed radiography (CR) images. Optimal hard copy radiographs, or CR images, are essential to properly select additional studies and are required for accurate interpretation of other modalities such as magnetic resonance (MR) imaging.7 Conventional tomography is rarely performed today. However, computed tomography (CT) has increased in utility with new multidetector systems that provide rapid evaluation of numerous bone and soft tissue disorders.3 Arthrography also can be an important tool in the diagnosis of intra-articular disorders of the elbow. Today, conventional, CT, and MR arthrography play important roles for evaluating the articular cartilage, intra-articular anatomy, and supporting structures of the elbow.7 Magnetic resonance imaging (MRI) frequently is used to evaluate subtle osseous and soft tissue abnormalities. Soft tissue contrast is superior to that achieved with CT. MRI scans can be obtained in any plane, which is an additional advantage. Intravenous or intra-articular injection of gadolinium provides additional information in selected cases.23 Within the scope of this chapter, the indications for diagnostic imaging options as well as their utility in given clinical situations are discussed. Sufficient background information to aid in determining the best modality for a given situation also is presented.

RADIOGRAPHY/COMPUTED RADIOGRAPHY IMAGING An understanding of the process by which routine radiographs or CR images are obtained is essential. Factors such as the type of equipment, patient positioning, and radiation dose must be kept in mind when determining the necessary views in a given clinical

setting. In obtaining views of the elbow, we routinely use a 48-inch target film distance with 50 to 60 kVp, 600 ma, and an exposure time of 0.0125 seconds. Reusable CR or regular cassettes measuring 10 × 12 inches are routinely employed.1,4,5 A minimum of two projections is necessary for evaluation of the elbow. Anteroposterior (AP) and lateral views of the elbow are taken at 90-degree angles and fulfill these criteria. In trauma patients, we routinely obtain oblique views as well.1,5 CR uses phosphor plate technology, which is designed to be used in a filmless environment. This technology is replacing conventional screen-film radiography. Regardless of the method of distribution (film or electronic), the techniques for patient positioning and other factors discussed are similar.

ANTEROPOSTERIOR VIEW The AP view (beam enters the patient anteriorly and the film is posterior) is obtained by placing the patient adjacent to the radiographic table in a sitting position (the supine position may be used if the patient is injured). The patient should be positioned with the extended elbow at the same level as the cassette so that the extremity is in contact with the full length of the cassette.1,4 The hand is supinated, and the beam is centered perpendicular to the elbow (Fig. 6-1A). The AP view demonstrates the medial and lateral epicondyles and the radiocapitellar articular surface (Fig. 6-1B). Assessment of the trochlear articular surface and at least a portion of the olecranon fossa is also possible. The normal carrying angle (5 to 20 degrees, average 15 degrees) can be measured on the AP view.1,5

LATERAL VIEW The lateral view is obtained by flexing the elbow 90 degrees and placing it directly on the cassette. The hand is positioned with the thumb up so that the forearm is in the neutral position; the beam is perpendicular to the humerus (Fig. 6-2A). This view provides good detail of the distal humerus, elbow joint, and proximal forearm. The coronoid of the ulna, which cannot be readily seen on the AP view, and the olecranon are well visualized on the lateral view (see Fig. 6-2B). Because the articular surface makes a valgus angle of about 7 degrees to the long axis of the humerus (see Chapter 2), a lateral view of the arm does not provide a lateral view of the joint. If the x-ray beam is parallel to the articular surface, three concentric arcs can be identified (Fig. 6-3A-D).5 The smaller arc is the trochlear sulcus, the intermediate arc represents the capitellum, and the largest arc is the medial aspect of the trochlea. If the arcs are interrupted, a true lateral view has not been obtained. Unfortunately,

Chapter 6 Diagnostic Imaging of the Elbow

Imaging Techniques for Evaluation of the Elbow BOX 6-1

Radiography/CR imaging AP, lateral, oblique, radial head, and axial views Stress views Computed tomography (CT) Arthrography Conventional single- or double-contrast technique CT with coronal and sagittal reformatting MRI with axial, coronal, and sagittal images MRI Ultrasonography Radionuclide scans/PET Angiography AP, anteroposterior; CR, computed radiography; CT, computed tomography; MRI, magnetic resonance imaging; PET, positron emission tomography;

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in patients with acute injury, true AP and lateral views are often difficult to obtain. Patients are frequently unable to extend or flex the elbow fully. In these situations, the tube must be angled and the cassette positioned to simulate these views as closely as possible.1,4,5

OBLIQUE VIEWS Oblique views are obtained by initially positioning the arm as if one were taking the AP view. For the medial oblique projection (Fig. 6-4A and B), the arm is positioned with the forearm and arm internally rotated approximately 45 degrees (see Fig. 6-4A). This view allows improved visualization of the trochlea, olecranon, and coronoid (see Fig. 6-4B). The radial head is obscured by the proximal ulna. The lateral oblique view is taken with the forearm, hand, and arm rotated externally (Fig. 6-5A). This projection provides excellent visualization of

FIGURE 6-1

A, Patient positioned for the anteroposterior (AP) view of the elbow. The arm is level with the cassette, with the hand positioned palm up. The central beam (pointer) is perpendicular to the elbow. B, Radiograph of the elbow in the AP projection with anatomic labels.

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FIGURE 6-2

A, Patient positioned for the lateral view with the elbow flexed 90 degrees and the beam (pointer) perpendicular to the joint. The shoulder is at the same level as the cassette. This position is required to obtain a true lateral view. B, The projected image.

the radiocapitellar joint, medial epicondyle, radioulnar joint, and coronoid tubercle (see Fig. 6-5B).1,4,5

RADIAL HEAD VIEW Radial head fractures are a common clinical problem and are often difficult to visualize on radiographs or CR images. The radial head view may define the fracture more clearly.16,17,28 This view (Fig. 6-6A and B) is easily accomplished by positioning the patient as one would for the routine lateral view. The tube is angled 45 degrees toward the shoulder joint (see Fig. 6-6A). The radial head view projects the radial head away from the ulna, allowing subtle changes to be more easily identified (see Fig. 6-6B), and it also may allow better visualization of the fat pads.1,16,17

AXIAL VIEWS Occasionally, suspected pathology of the olecranon or epicondyles prompts further evaluation with axial views. Figure 6-7A and B demonstrate the axial projection used to evaluate the epicondyles, olecranon fossa, and ulnar

sulcus. The patient’s elbow is flexed approximately 110 degrees, with the forearm on the cassette and the beam directed perpendicular to the cassette. This view is also helpful in detecting subtle calcification in patients with tendonitis. The olecranon process may be better observed on the reverse axial projection (Fig. 6-8A and B).1,4,5 Other views of the elbow also may be used,1,4,5 but those just discussed are usually sufficient. In fact, when questions arise regarding routine AP, lateral, and oblique views, a CT scan with reformatting in the coronal and sagittal planes or an MRI scan is frequently obtained instead of special views.

ASSESSMENT OF RADIOGRAPHS/COMPUTED RADIOGRAPHY IMAGES Assessment of the above-mentioned views should be complete and systematic. Certain findings should be checked consistently and, if necessary, further views or techniques employed. The relationship of the radial head to the capitellum should be constant regardless of the view obtained Text continued on p. 99.

Chapter 6 Diagnostic Imaging of the Elbow

FIGURE 6-3

A, Dried bone specimen demonstrating the points used for the three concentric arcs. A, capitellum; B, trochlear sulcus; C, medial aspect of trochlea. A true lateral view of the joint requires the beam to be directed distally about 7 degrees. B, On the true lateral view, the three arcs are perfectly aligned. C and D, With slight lateral (C) and medial (D) rotation of the elbow, the arcs are no longer aligned, indicating that the view is not a true lateral.

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Part II Diagnostic Considerations

FIGURE 6-4

Medial oblique view. A, The patient’s arm is internally rotated and the hand pronated. The central beam pointer is perpendicular to the elbow. B, Radiograph of the medial oblique view. The radial head is obscured by the ulna. Note the constant relationship of the radial head and the capitellum.

Chapter 6 Diagnostic Imaging of the Elbow

FIGURE 6-5

Lateral oblique view. A, The patient is positioned with the arm externally rotated, the forearm supinated, and the central beam (pointer) perpendicular to the elbow. B, Radiograph of the lateral oblique view. Note the visualization of the radial head and capitellum, medial epicondyle, and radioulnar joint.

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FIGURE 6-6

Radial head view. A, The patient is positioned as if a routine lateral view (see Fig. 6-2A) were to be obtained. The tube is angled 45 degrees toward the humeral head rather than perpendicular to the joint. B, Radial head view projects the radial head (R) clear of the olecranon and clearly demonstrates the capitellum (C) and radiocapitellar joint.

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FIGURE 6-7

A, Patient positioned for the axial view of the distal humerus. The elbow is flexed approximately 110 degrees, with the forearm and elbow on the cassette. The central beam (pointer) is perpendicular to the cassette and centered on the olecranon fossa. B, The radiograph provides excellent visualization of the epicondyles, ulnar sulcus, and radiocapitellar and ulnotrochlear articulations.

(Fig. 6-9A-C).5,26,28 The radius is normally bowed at the level of the tubercle. Therefore, the line should be drawn in the midpoint of the radial head, not extended to include this portion of the radial shaft. Careful evaluation of the fat pads and supinator fat stripe is essential. These structures are best observed on the lateral (see Fig. 6-2) and radial head (see Fig. 6-6) views. The anterior and posterior fat pads are intracapsular but extrasynovial.5,8,10,26,28 The anterior fat pad is normally visible on the lateral view. The posterior fat pad is obscured owing to its position in the olecranon fossa (Fig. 6-10). Displacement of the fat pads, particularly the posterior fat pad, is indicative of an intraarticular fluid collection due to inflammation or hemarthrosis due to trauma.5,8,10,26,28 Norell26 reported

FIGURE 6-8

A, The patient’s arm is placed on the cassette, with the elbow completely flexed. The central beam (pointer) is perpendicular to the cassette. B, The radiograph demonstrates the olecranon, trochlea, and medial epicondyle. Contrast this view with that of Figure 6-7B.

that 90% of children with displaced posterior fat pads had elbow fractures. This finding is less specific in adults, but if present in patients following trauma (see Fig. 6-9C), a fracture is likely. Cross-table lateral views may be more specific. A lipohemarthrosis, which is more specific for an intra-articular fracture, may be evident.5,26,28 The supinator fat stripe lies anterior to the radial head and neck on the surface of the supinator muscle. Fractures of the elbow frequently displace or obliterate this structure, providing a clue to the underlying injury (Fig. 6-11). Rogers and MacEwan28 reported changes in the fat stripe in 100% of fractures of the radial head and neck and in 82% of other elbow fractures.

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FIGURE 6-9

The radiocapitellar relationship is constant regardless of the view. Oblique views (A and B) demonstrating the constant relationship of the radial head (line) to the capitellum (broken circle). Poorly positioned lateral view (C) with a normal radiocapitellar relationship. Positive fat pad (arrowheads) sign due to a subtle fracture.

STRESS VIEWS

Posterior fat pad

Anterior fat pad Anterior recess

Posterior recess

FIGURE 6-10

Lateral illustration of the elbow, demonstrating the anterior and posterior fat pads. These structures are intracapsular but extrasynovial.

The anterior humeral line helps detect subtle supracondylar fractures in children but is not used as frequently for adults. This line, drawn along the anterior humeral cortex, should pass through the middle third of the capitellum (Fig. 6-12).5

In patients with suspected ligament disruption or instability, varus and valgus stress views are desirable and may be diagnostic. Ideally, these examinations should be performed with fluoroscopic guidance. This allows proper positioning of the elbows. Also, visualization of subtle changes in the articular distance may be evident while stress is being applied. Fluoroscopic images should be obtained in the neutral position and during valgus and varus stress. Accuracy may be hindered by guarding and swelling following acute injury. In this situation, anesthetic injection should be performed before the examination. In the normal elbow, the joint should not open when stress is applied. We have arbitrarily chosen an increase in the joint space of greater than 2 mm as being abnormal (Fig. 6-13A and B). The relationship of the tip of the olecranon in the fossa is also helpful in interpreting radiographic instability. The normal elbow carrying angle also may increase significantly if ligament instability is present.5

COMPUTED TOMOGRAPHY Conventional tomography is rarely performed today due to the improved utility of CT and new fast multi-

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FIGURE 6-11

Anteroposterior (A) and lateral (B) radiographs of the elbow, demonstrating displacement of the fat pads (arrows) and supinator fat stripe (open arrow) due to a subtle impacted radial neck fracture.

detector CT systems. CT is useful in the evaluation of bone and soft tissue abnormalities.5,19 Articular deformities, complex fractures with multiple fragments and other conditions can be evaluated quickly and reformatted into coronal and sagittal planes. Three-dimensional reconstructions can also be obtained. Thin sections using 0.5- to 1.0-mm slices can be easily reconstructed (Fig. 6-14A and B).19 We frequently use CT in combination with arthrography to more clearly define articular or capsular abnormalities.5,30

ARTHROGRAPHY

FIGURE 6-12

Lateral view of the elbow in a child with a displaced physeal fracture of the distal humerus. The anterior humeral line passes through the posterior capitellum. Note the fat pads (small arrows) are displaced.

Elbow arthrography provides valuable information about capsule size, the synovial lining, supporting ligaments, and the articular surfaces of the joints. Needle access also permits fluid aspiration for laboratory studies and diagnostic or therapeutic injections.6 The most common indications for this procedure are the detection of possible loose bodies, evaluation of articular cartilage, and the demonstration of capsular/ligament injuries. Loose bodies may be osteocartilaginous, owing to osteochon-

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FIGURE 6-13

Anteroposterior views of the elbow in neural (A) and valgus (B) stress. Note that the joint space (lines) has increased (arrow), indicating the presence of a ligamentous injury.

A FIGURE 6-14

B

Coronal (A) and sagittal (B) reformatted CT images after elbow trauma demonstrating radial head fractures (arrowheads) and a distal humeral avulsion (open arrow).

Chapter 6 Diagnostic Imaging of the Elbow

dromatosis or osteochondral fragments due to acute trauma, or osteochondritis dissecans. Less commonly, arthrograms are performed to evaluate capsule size in patients with adhesive capsulitis.5,7,12,14,20,32

TECHNIQUE To obtain maximum information, arthrography should be performed by an experienced physician with a thorough understanding of the patient’s clinical situation. Review of the routine radiographs or CR images is essential. These images often provide clues that dictate subtle changes that indicate which imaging technique (conventional, CT, MRI) should be employed following the injection of the contrast material. The choice of contrast material and indications for conventional, CT, or MR arthrography are highly dependent on the clinical setting (Table 6-1).7,31 Contrast agents include air, iodinated contrast material, or a combination of the two for conventional or CT arthrography and gadolinium diluted in iodinated contrast and anesthetic for MR arthrography. Radiographs or CR images are obtained immediately following injection of contrast medium to avoid dilution that

TABLE 6-1 Elbow Arthrography: Indications and Techniques Indication

Technique

Loose bodies Osteochondromatosis Osteochondritis dissecans

Conventional or CT arthrography

Fracture fragments from acute trauma

CT arthrography

Ligament and capsule tears

MR arthrography

Synovitis

Indirect or intravenous MR arthrogram with gadolinium

Synovial cysts

MR arthrography

Articular cartilage abnormalities

MR or CT arthrography

Capsule size

Conventional arthrography

Needle position before aspiration or diagnostic/ therapeutic injection

Conventional arthrography

Postoperative

Subtraction technique for total elbow arthroplasty

Total joint replacement Other

Conventional arthrography with subtraction technique

CT, computed tomography; MR, magnetic resonance.

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reduces image quality. CT and MR arthrography should be performed within 30 and 45 minutes following injection, respectively. If longer delays are expected, this dilutional phenomenon can be prevented by combining 0.3 mL of 1 : 1000 epinephrine with the contrast agent.5,7,31,32 The procedure can be performed with the patient positioned either sitting adjacent to the radiographic table or lying prone on the table (Fig. 6-15). Determination of the best position depends on the equipment available and the patient’s condition. In either position, the elbow is flexed 90 degrees, with the lateral aspect toward the examiner. Before the injection of contrast agent, fluoroscopic evaluation of range of motion and evidence of possible ligament stability or loose bodies should be accomplished.5 The elbow is then prepared using sterile technique. One of two injection sites may be used. In most cases, a lateral approach into the radiocapitellar joint is selected. In patients with previous radial head resection or suspected lateral ligament injury, a posterior approach is more suitable. With the posterior approach, the elbow is again flexed 90 degrees, and the medial and lateral epicondyles and olecranon are palpated. The needle is placed an equal distance between these points and is positioned fluoroscopically (Fig. 6-16). If the needle is properly positioned, the contrast medium will flow away from the needle tip as it is injected. If the needle is not properly positioned, the contrast agent collects at the needle tip and significant resistance is encountered. Following the injection, the needle is removed and the elbow is studied fluoroscopically. This step is essential in evaluating stability of the joint and loose bodies. Routine films or CR images include AP, lateral, and both oblique views. Medial and lateral cross-table lateral views provide additional information with double contrast technique.5,32 CT images are obtained using thin sections (1 mm) with reformatting in the coronal and sagittal planes. MRI scans are also obtained in the axial, coronal, and sagittal planes with fat-suppressed T1weighted images and at least one T2-weighted series as periarticular cysts may not communicate with the joint.7,31

NORMAL FINDINGS In the normal conventional arthrogram (Fig. 6-17A-D), the radiocapitellar, ulnotrochlear, and radioulnar joints can be identified. The anterior (coronoid), posterior (olecranon), and annular recesses also are visualized. The normal joint capacity is 10 to 12 mL. This may increase to 18 to 22 mL in patients with chronic instability, or it may be decreased in patients with capsulitis or flexion contracture.5

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Part II Diagnostic Considerations

FIGURE 6-16

Illustration of needle positioned for lateral (A) and posterior (B) approaches.

6-18).5,7,31 Differentiation of a loose body in the olecranon fossa from the normal os supratrochlear dorsale is possible because of the nature of the trabecular pattern and the cortical thickness. Most symptomatic densities in the olecranon fossa have prominent trabeculae and sclerotic cortical margins (Fig. 6-19B). The normal ossicle has sparse trabeculae and a thin cortical rim (see Fig. 6-19A).5,27 MR arthrography is preferred to exclude ligament/ capsular tears, although conventional techniques may demonstrate the tear when they are complete (Figs. 6-20 and 6-21). Extravasation of contrast material on conventional images indicates a tear (see Fig. 6-20). Care must be taken not to mistake extravasation at the needle site for a rent of the capsule. Therefore, the needle should not be placed near the area of suspected injury regardless of the imaging technique selected. If a lateral tear is suspected, a posterior approach should be used.5

COMPLICATIONS FIGURE 6-15

Patient positioned for lateral injection (A) and posterior injection (B), sitting with the elbow flexed and the metal marker over the needle entry sites. Patient positioned prone (C) for radiocapitellar injection.

ABNORMAL FINDINGS “Loose bodies” may be either attached to the synovium or actually free within the joint. If they are free, they can be observed fluoroscopically or demonstrated on images by contrast that completely surrounds the structure (Fig.

Complications due to elbow arthrography are rare. Freiberger13 reports an incidence of infection of approximately 1 in 25,000 cases. Effusions may occur whether contrast material or air is used; they usually occur within 12 hours and may result in pain and joint stiffness.5,13,31 The joint fluid may have a turbid appearance owing to the high eosinophil count.5 The patient should be questioned about possible allergy to the contrast medium (iodinated or gadolinium). Although it is rare (0.1% of patients affected),13 this complication must be kept in mind. Urticaria is the most common reaction experienced, and often no treatment

Chapter 6 Diagnostic Imaging of the Elbow

FIGURE 6-17

Routine projections for single contrast arthrogram with normal anatomy labeled. A, Anteroposterior view. B, Lateral view. C and D, Oblique views.

105

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Part II Diagnostic Considerations

is necessary. In more severe cases, antihistamines may be required. Most allergic reactions occur in the first 30 minutes after the injection. Premedication with an antihistamine may be used in patients with suspected allergy. These patients should be observed for 1 or 2 hours following the procedure.

MAGNETIC RESONANCE IMAGING

FIGURE 6-18

Single-contrast conventional arthrogram image. The contrast medium completely surrounds the lucent loose body (arrow) in the olecranon fossa.

FIGURE 6-19

MRI of the elbow can clearly define numerous types of osseous and soft tissue pathology. Improved soft tissue contrast and numerous image planes provide advantages over CT and other imaging techniques.7,31 Intraarticular contrast injection using gadolinium, as described previously, affords advantages provided with conventional arthrography and additional information regarding subtle synovial and cartilage abnormalities. Intravenous gadolinium is useful for detection of early synovial inflammation and enhancement of other lesions such as osteomyelitis and neoplasms.2,5,7 Surface coils generally are used to improve image quality. For patient comfort, the arm should be placed at the side when possible. When the arm is raised above

Lateral tomograms of the elbow. A, Asymptomatic patient with an os supratrochlear dorsale. Note the thin cortex and lack of trabeculae (arrow). B, Symptomatic patient with a density in the same region with thick cortex (large arrow) representing a loose body. There is a second smaller density in the joint space inferiorly.

Chapter 6 Diagnostic Imaging of the Elbow

107

the head, there is often motion artifact resulting in image degradation.5,7 MR pulse sequences are designed to demonstrate contrast differences between normal and abnormal tissues. Multiple pulse sequences and image planes are required to identify and stage pathology. Often, the axial plane is combined with sagittal (Fig. 6-22) or coronal images for initial screening.5,7 In certain situations, new fast-scan techniques are used to allow motion (pronation-supination or flexion-extension) studies to be performed. Pronation-supination maneuvers (Fig. 6-23) are most easily performed, because MR gantry size limits ranges of flexion and extension. Newer open magnets provide more flexibility for motion.7

ULTRASONOGRAPHY

FIGURE 6-20

Elbow arthrogram in a patient with ligament and capsular tear with contrast extravasation medially.

Ultrasound applications for musculoskeletal imaging have expanded dramatically from the late 1970s. Improved technology and image quality permit more accurate depiction of normal anatomy and pathologic lesions. Ultrasonography is also more readily available and less expensive than MRI.5,21,24,25 Ultrasound uses mechanical vibrations whose frequencies are beyond audible human perception (about 20,000 Hz or cycles per second). Imaging of most musculoskeletal structures is accomplished in the 7- to 12MHz range.21,24 Doppler ultrasonography for peripheral vascular studies is performed in the 8-MHz range.25 New Doppler scanners provide color flow data that allow different flow rates (venous, arterial) to be easily demonstrated.5,25

FIGURE 6-21

Coronal fat suppressed T2weighted MR arthrogram demonstrates a complete tear of the radial collateral ligament (arrow).

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Part II Diagnostic Considerations

FIGURE 6-22

Patient with chronic muscle pain and weakness. (A) Oblique view of the elbow shows several areas of soft tissue ossification or avulsed fragments laterally (arrowheads). Coronal (B) and axial (C) T1-weighted images (SE 500/11) show low signal intensity changes in the fat and muscle (B) (arrows). Axial (D) and coronal (E) T2-weighted images demonstrate increased signal intensity in the muscles due to a muscle tear.

Chapter 6 Diagnostic Imaging of the Elbow

109

FIGURE 6-23

Sagittal gradient echo images in different degrees of supination. A, The biceps tendon (arrow) is in the image plane. B, The tendon is snapping over the ganglion (arrows).

FIGURE 6-24

Longitudinal ultrasonographic image of a normal (right) and ruptured (left) tendon.

The central component of ultrasound instruments is the transducer, which contains a piezoelectric crystal. The transducer serves as a transmitter and receiver of sound waves. By applying the vibrating transducer to the skin surface (through an acoustic coupling medium such as mineral oil or gel), the mechanical energy is transmitted into the underlying tissues as a brief pulse of high-energy sound waves. Sound waves reach different tissue interfaces (acoustic impedances), resulting in reflection or refraction. The reflected sound waves return to the transducer, where they are converted into electrical energy used to produce the image.5,21,24,25

Ultrasound, once limited to evaluating solid and cystic soft tissue lesions, is now commonly employed to evaluate articular and periarticular abnormalities. In the elbow, ultrasonography is well suited for evaluating tendon (Fig. 6-24) and nerve (Fig. 6-25) pathology. Tendon tears are demonstrated as gaps or areas of abnormal echo texture compared with the normal tendon (see Fig. 6-24). Avulsed bone fragments or calcifications are hyperechoic with posterior acoustic shadowing.21 Cost and flexibility of this technique will, no doubt, result in increased orthopedic use.24

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FIGURE 6-25

Ultrasound of ulnar nerve dislocation demonstrated on pre- (A), passive (B) and active (C) resistance. (Courtesy of Gina Hesley, Mayo Clinic, Rochester, Minnesota.)

Chapter 6 Diagnostic Imaging of the Elbow

RADIONUCLIDE SCANS/POSITRON EMISSION TOMOGRAPHY There are numerous isotopes and indications for radionuclide imaging of the musculoskeletal system.5 Bone scans are typically obtained after intravenous injection of 10 to 20 mCi (370-740 MBq) of technetium-99m– labeled methylene diphosphonate. Images are obtained 2 to 4 hours after injection. Common indications include primary or metastatic bone lesions, subtle fractures, non-accidental trauma in children and other causes of suspected osseous related pain.5 Three-phase bone scans use the same isotope and dose, but images are obtained in the initial 60 seconds after injection, followed by blood pool images at 2 to 5 minutes and delayed images at 3 to 4 hours. Indications for three phase scans include differentiation of cellulitis from osteomyelitis, bone infarction, reflex sympathetic dystrophy, and peripheral vascular disease.5,29 Bone marrow scintigraphy is performed using 10 to 15 mCi (370-555MBq) of technetium-labeled sulfur colloid. Images are obtained approximately 15 minutes after injection. Lead shields are placed over the abdomen to delete counts from the liver and spleen. Bone marrow imaging is most often performed to evaluate marrow replacement disorders and patients with joint prostheses.5 Special approaches may be required in patients with suspected infection. A normal bone scan or three-phase bone scan virtually excludes the possibility of infection. These techniques are sensitive but not specific. Therefore, when there is a high index of suspicion, more specific approaches are generally employed. White blood cells labeled with indium-111 or technetium or technetiumlabeled antigranulocyte antibodies provide more specificity.15,22 Indium-111-labeled leukocyte scans are performed 18 to 24 hours after intravenous injection of the isotope. Technetium-labeled leukocytes or antigranulocyte antibody imaging is performed 2 to 4 hours after injection. Technetium is more readily available, and image resolution is superior to Indium-111 studies. Gallium-67 citrate scans can also be used to identify infection. Scanning is performed 24 to 72 hours after injection. This isotope is less commonly used today.9 Combined studies (i.e., technetium and white blood cells or indium-111 and technetium sulfur colloid) may be required in chronic infections or in the presence of orthopedic implants or prostheses.5,9,22 Positron emission tomography (PET) has provided a new physiologic approach to imaging musculoskeletal disorders, specifically infection and neoplasms.11,18 Positron-emitting agents include flourine-18-deoxyglucose, L-methyl-carbon 11, and oxygen 15. Flourine-18 has a half life of 110 minutes compared with the shorter half

111

life of 20 and 21 minutes respectively for the other agents. Therefore, flourine-18 is the clinical agent of choice. Flourine-18-deoxyglucose imaging demonstrates increased glucose use seen with active disease processes. Patients must be fasting for 4 hours before the study. No sugared beverages should be taken, and blood sugar should be normal for optimal studies. Scanning is performed 1 hour after injection. Early studies demonstrate that PET imaging is more accurate than the studies described above for evaluating infection, chronic infection, and infection associated with orthopedic fixation devices or arthroplasty. PET is also more useful than conventional isotopes for detection of tumor activity and metastasis.11,18

References 1. Ballinger, P. W., and Frank, E. D.: Merrill’s Atlas of Radiographic Positions and Radiologic Procedures, Vol. 1, 10th ed. St. Louis, C.V. Mosby Co., 2003, p. 89. 2. Beltran, J., Chandnani, V., and McGhee, R. A.: Gadopentatate dimeglumine-enhanced MR imaging of the musculoskeletal system. A. J. R. 156:457, 1991. 3. Berland, L. L., and Smith, K. L.: Multi-detector array CT. Once again new technology creates new opportunities. Radiology 209:327, 1998. 4. Bernau, A., and Berquist, T. H.: Positioning Techniques in Orthopedic Radiology. Orthopedic Positioning in Diagnostic Radiology. Baltimore, Urban and Schwartzenberg, 1983. 5. Berquist, T. H.: Imaging of Orthopedic Trauma, 2nd ed. New York, Lippincott-Raven Press, 1992. 6. Berquist, T. H.: Diagnostic/therapeutic injections as an aid to musculoskeletal diagnosis. Semin. Intervent. Radiol. 10:326, 1993. 7. Berquist, T. H.: MRI of the Musculoskeletal System, 5th ed. Philadelphia, Lippincott-Williams and Wilkins, 2006. 8. Bohrer, S. P.: The fat pad sign following elbow trauma. Clin. Radiol. 21:90, 1970. 9. Boutin, R. D., Joachim, B., Sartoris, D. J., Reilly, D., and Resnick D.: Update of imaging of orthopedic infections. Orthop. Clin. North Am. 29:41, 1998. 10. Corbett, R. H. Displaced fat pads in trauma to the elbow. Injury. 9:297-298, 1978. 11. De Winter, F., Van de Wiele, C., Vogelaers, D., de Smet, K., Verdonk, R., and Dierckx, R. A.: Flourine-18 fluorodeoxyglucose-positron emission tomography. A highly accurate imaging modality for diagnosis of chronic musculoskeletal infections. J. Bone Joint Surg. 83A:651, 2001. 12. Eto, R. T., Anderson, P. W., and Harley, J. D.: Elbow arthrography with the application of tomography. Radiology 115:283, 1975. 13. Freiberger, R. H., and Kaye, J. J.: Arthrography. New York, Appleton Century Crofts, 1979. 14. Godefroy, G., Pallardy, G., Chevrot, A., and Zenny, J. C.: Arthrography of the elbow: anatomical and radiological considerations and technical considerations. Radiology 62:441, 1981.

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15. Gold, R. H., Hawkins, R. A., and Katz, R. D.: Bacterial osteomyelitis: findings on radiography, CT, MR and scintigraphy. A. J. R. 157:365, 1991. 16. Greenspan, A., and Norman, A.: The radial head, capitellar view. Another example of its usefulness. A. J. R. 139:193, 1982. 17. Greenspan, A., and Norman, A.: The radial head, capitellar view. Useful technique in elbow trauma. A. J. R. 138: 1186-1188, 1982. 18. Guhlmann, A., Brecht-Krause D., Suger, G., Glatting, G., Kotzerke, J., Kinzl, L., and Reske, S. N.: Flourine-FDG PET and technetium-99m labeled antigranulocyte antibody scintigraphy for chronic osteomyelitis. J. Nucl. Med. 39:2145, 1998. 19. Haapamaki, V. V., Kiuru, J. J., and Koskinen, S. K.: Multi-detector computed tomography diagnosis of adult fractures. Acta Radiol. 45:65, 2004. 20. Hudson, T. M.: Elbow arthrography. Radiol. Clin. North Am. 19:227, 1981. 21. Jacobson, J. A., and van Holsbeeck, M. I.: Musculoskeletal ultrasonography. Orthop. Clin. North Am. 29:135, 1998. 22. Kaim, A., Ledermann, H. P., Bongartz, G., Messmer, P., Müller-Brand, J., and Steinbrich, W.: Chronic post-traumatic osteomyelitis of the lower extremity: comparison of magnetic resonance imaging and combined bone scintigraphy with radio labeled monoclonal antigranulocyte antibodies. Skel. Radiol. 29:378, 2000.

23. Kramer, J., Hofmann, S., and Die, M. R.: Magnetic resonance arthrography: benefits and indications. Adv. M. R. I. Contrast 4:104, 1997. 24. Lin, J., Fessell, D. P., Jacobson, J. A., Weadock, W. J., and Hayes, C. W.: An illustrated tutorial of musculoskeletal ultrasound. A. J. R. 175:637, 2000. 25. Merritt, C. R. B.: Doppler color flow imaging. J. Clin. Ultra. 15:591, 1987. 26. Norell, H. G.: Roentgenologic visualization of the extracapsular fat. Its importance in the diagnosis of traumatic injuries to the elbow. Acta Radiol. 42:205, 1954. 27. Obermann, W. R., and Loose, H. W. C.: The os supratrochlear dorsale: a normal variant that may cause symptoms. A. J. R. 141:123, 1983. 28. Rogers, S. L., and MacEwan, D. W.: Changes due to trauma in the fat plane overlying the supinator muscle: a radiographic sign. Radiology 92:954, 1969. 29. Rupani, H. D., Holder, L. E., Espinola, D. A., and Engin, S. I.: Three phase radionuclide bone imaging in sports medicine. Radiology 156:187, 1985. 30. Singson, R. D., Feldman, F., and Rosenberg, Z. S.: The elbow joint: assessment with double contrast CT arthrography. Radiology 160:167, 1986. 31. Steinbach, L. S., Palmer, W. E., and Schweitzer, M. E. MR arthrography. RadioGraphics 22:1223, 2002. 32. Weston, W. J., and Dalinka, M. K.: Arthrography. New York, Springer Verlag, 1980.

Chapter 7 Surgical Exposures of the Elbow

CHAPTER

7

Surgical Exposures of the Elbow Bernard F. Morrey

INTRODUCTION Few joints require familiarity with as many surgical exposures as does the elbow. Depending on the lesion and the surgical goal, the joint and the surrounding region may be approached from the lateral, posterior, medial, or anterior direction. Exposures from the medial and lateral aspects that once allowed the removal of loose bodies and the treatment of certain localized fractures are used less commonly today. Instead, some form of an extensile posterior exposure is used for most complex fractures and joint reconstructive procedures, and this is considered the universal approach to the joint. It is not the purpose of this chapter to discuss all of the approaches to the joint but rather to provide a comprehensive collection and critique of those relevant exposures that should prove helpful to the practicing orthopedic surgeon.33

GENERAL PRINCIPLES Rigorous adherence to the principles of good surgical technique is of no greater importance in any anatomic part than at the elbow.6,8,35 The most appropriate surgical approach depends on the specific goal of the surgical intervention and on the lesion. As for any orthopedic procedure, the choice of the surgical approach should be based on the following criteria (Box 7-1): 1. Potential to be extended to meet unforeseen circumstances. 2. Capability for providing adequate visualization to define and completely correct the problem. 3. Safety: avoidance of vital structures or visualization of these structures to avoid injury during the procedure. 4. Preservation of the normal anatomy as much as possible during the exposure, the procedure, and at closure.

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5. Dissection along natural tissue planes rather than across muscle, tendon, or ligamentous structures. 6. Provision of careful hemostasis and adequate drainage after extensile exposures and dissections. 7. Careful soft tissue closure that reliably heals and ensures rapid and predictable rehabilitation. A thorough understanding of the anatomy of the elbow region and the relationship of the nerves and vessels is particularly important to selecting the exposure that best satisfies these requirements (Fig. 7-1).

LATERAL APPROACHES A lateral exposure, probably the most commonly used approach to the elbow joint, offers many variations. It is used for radial head excision, removal of loose bodies, and repair of lateral ligaments, to fix condylar and Monteggia fractures, to release the joint capsule, and to remove osteophytes. Access to the radiohumeral articulation has been described by several authors.7,18,21,24,36 The techniques differ according to the muscle interval entered and the means of reflecting the muscle mass from the proximal ulna. With any of the lateral exposures to the joint or to the proximal radius, the surgeon must be constantly aware of the possibility of injury to the posterior interosseous or recurrent branch of the radial nerve. Kaplan has described an approach through the interval between the extensor digitorum communis and the extensor carpi radialis longus and brevis muscles. Because of the proximity of the radial nerve, pronation of the forearm during exposure has been recommended to assist in carrying the radial nerve out of the surgical field. The effect of this maneuver has been quantified by Strachan and Ellis, who found that approximately 1 cm of mediolateral radial nerve translation can occur with forearm pronation (Fig. 7-2).42 Even with this maneuver, however, the radial nerve is precariously close to the surgical field, so this approach is used less often than that described by Kocher. Knowledge of Kaplan’s interval24 is useful to expose the posterior interosseous nerve when decompression is performed in conjunction with tennis elbow release (see Chapter 44).41

THE KOCHER APPROACH AND ITS VARIATIONS Some variation of the Kocher exposure is the most frequently used approach to the lateral aspect of the joint. This has the advantage of being extensile, affording a full complement of surgical options as the exposure is extended. This approach enters the joint through the interval of the anconeus and extensor carpi ulnaris, thus

Part III Surgery and Rehabilitation

116

Brachial a. and vv. Biceps brachii m.

Median n.

Brachialis m.

Basilic v.

Radial n.

Ulnar n. Medial intermuscular septum

Brachioradialis m. 57

Ext. carpi radialis longus m.

58

Triceps brachii m.

B (57)

59

Lat. intermuscular septum Humerus

60

Brachial a. and vv. Biceps brachii m.

61

Median n.

Lat. antebrachial cutan. n. Basilic v.

Cephalic v.

Pronator teres m.

Brachialis m.

Medial epicondyle Brachioradialis m. Ulnar n.

Radial n.

C

A

Ulnar recurrent a.

Ext. carpi radialis longus m.

Capsule articularis

(58) Dorsal antebrachial cutan. n.

Triceps brachii m. and tendon

Medial antebrachial cutan. n. Pronator teres m. Flexor carpi radialis m. Basilic v. Flexor digitorum superficialis m. 57

Ext. carpi radialis longus and brevis mm.

58

Dorsal antebrachial cutan. n.

Ulnar collateral lig. Ulnar n. Flexor carpi ulnaris m.

D

59

Flexor digitorum profundus m.

(59) Tendon of common ext. digitorum, carpi ulnaris, and digiti minimi mm.

60

Anconeus m. Ulnar a. and v.

61

Lat. antebrachial cutan. n. Tendon of biceps brachii m.

Median n. Flexor carpi radialis m. Pronator teres m.

Radial recurrent a.

Palmaris longus m.

Radial n. Flexor digitorum superficialis m.

Brachioradialis m.

E (60)

F

Radial n., deep branch

Flexor carpi ulnaris m.

Ext. carpi radialis longus and brevis mm.

Ulnar n. Flexor digitorum profundus m.

Common ext. digitorum m. Ext. digiti minimi m. Ext. carpi ulnaris m.

FIGURE 7-1

Anconeus m. Supinator m.

Cross-sectional anatomy shows the important neurovascular and muscular relationships that must be understood to achieve a complication-free exposure of the elbow. (Modified from Eycleshymer, A. C., and Schoemaker, D. M.: A Cross Section Anatomy. New York, D. Appleton and Co., 1930. In Darrach, W.: Surgical approaches for surgery of the extremities. Am. J. Surg. 67:93, 1945.)

Chapter 7 Surgical Exposures of the Elbow

exposure can be accomplished by extending the posterior lateral skin incision and elevating the lateral skin cutaneous flap.

Principles of Exposure of the Elbow Region BOX 7-1

1. 2. 3. 4. 5.

Flexible—allows extension Adequate—visualization of pathology Safety—especially nerves Preservation—respect anatomy Natural plane—extend along fascial, subcutaneous planes 6. Hemostasis—release tourniquet, drain as necessary 7. Closure—modified by specific features of case.

–4CMS. –3 Medial

Lateral Lateral epicondyle

–2 –1

2.0 1.5 1.0 0.5 –0.5–1.0 –1.5–2.0CMS. Head of radius

1 2 3

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Limited Distal Lateral Approach: Kocher “J” Indication Simple excision of the radial head. Exposure lateral ulnar collateral ligament.24

Lateral epicondyle, radial head, palpate interval between anconeus and extensor carpi ulnaris.

Landmarks

Skin Incision The skin incision is made from the subcutaneous border of the ulna obliquely across the posterolateral aspect of the elbow in line with Kocher’s interval and ends at or just proximal to the lateral epicondyle (Fig. 7-3A). Interval The interval between the anconeus and extensor carpi ulnaris is identified and entered (Fig. 7-3B). For excision of the radial head, the extensor carpi ulnaris and a small portion of the supinator muscle are dissected free of the capsule and retracted anteriorly (see Fig. 7-3C). The annular ligament is then identified and entered. Care should be taken to enter the annular ligament approximately 1 cm above the crista supinatoris to avoid injury to the lateral ulnar collateral ligament (see Fig. 7-3D).

Expanding the Distal Lateral Exposure Radial tubercle

Indication Reconstruction of the lateral ulnar collateral ligament, harvest anconeus for anconeus arthroplasty.31

4

Lateral epicondyle; posterior border of the extensor carpi ulnaris, anterior edge of anconeus, crista supernatoris of ulna.

Landmarks 5 6 7

Skin Incision If the lateral ulnar collateral ligament is to be reconstructed, the skin incision described earlier is simply extended proximally about 3 cm.

FIGURE 7-2

Approximately 1 cm of medial to lateral translation of the posterior interosseous nerve occurs as the forearm is rotated from supination to pronation. (Redrawn from Strachan, J. H., and Ellis, B. W.: Vulnerability of the posterior interosseous nerve during radial head resection. J. Bone Joint Surg. 53B:320, 1971.)

providing protection to the deep radial nerve. The interval is also anterior to the lateral ulnar collateral ligament, which reduces the likelihood of severing it at arthrotomy. In addition to providing a limited exposure for radial head excision and loose body removal, the particular value of this technique is that it may be converted to an extensile posterolateral approach to the entire distal humerus. If an extensile exposure is anticipated, a posterior incision is made. The same deep

Interval After the interval is entered, the anconeus is more completely reflected from its ulnar insertion (Fig. 7-4A). The lateral collateral ligament complex is identified by first elevating the extensor carpi ulnaris from the annular ligament just distal to the lateral epicondyle (see Fig. 7-4B). The fleshy attachment of the extensor carpi radialis longus is identified just above the common extensor tendon. This origin is freed from the supracondylar ridge. The dissection then elevates the common extensor tendon and the posterior edge of the extensor carpi radialis brevis from the lateral ligament complex (see Fig. 7-4D). This is done very carefully to identify and leave intact the lateral collateral ligament complex, and thus, reconstruction of the lateral ulnar collateral ligament can take place (see Chapter 48).

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Triceps

Triceps Lateral epicondyle

Incision

Lateral epicondyle

Anconeus Incision in capsule

Incision Anconeus Extensor carpi ulnaris

A

B

Extensor carpi ulnaris

C

Triceps

Triceps Extension of incision along epicondylar ridge

Capsule

Humerus Capsule

Capitellum

Anconeus

Head of radius

Head of radius

Head of radius

Annular ligament

Supinator

Anconeus

D

Supinator

E

FIGURE 7-3

The distal Kocher approach. A, The incision begins approximately 2 to 3 cm above the lateral epicondyle over the supracondylar bony ridge and extends distally and posteriorly for approximately 4 cm. B, The interval between the anconeus and the extensor carpi ulnaris is identified. C, Development of this interval reveals the capsule. The joint capsule may be entered proximal to the annular ligament (D), and a more extensive exposure may be obtained by extending the capsular incision proximally (E), thus providing adequate exposure of the radiohumeral articulation. (Redrawn from Banks, S. W., and Laufman, H.: An Atlas of Surgical Exposures of the Extremities. Philadelphia, W. B. Saunders Co., 1953.)

The Limited Proximal Lateral Exposure (Column Approach)

Note This may truly be termed a minimally invasive procedure.

Indication Stiff elbow: Anteroposterior capsular release; also termed the column procedure.28,31

Skin Incision and Technique

Extensor carpi radialis longus, lateral epicondyle, radial head, anterior capsule.

Landmarks

This limited exposure of the anterior (and posterior) capsule has been described by Mansat and Morrey.28 The skin incision is over the lateral column, extending distally over the lateral epi-

Chapter 7 Surgical Exposures of the Elbow

119

A

FIGURE 7-4

A, The anconeus is easily reflected posteriorly from its bed to expose the crista supinatoris (arrowheads). B, Lifting the anterior musculature, including the common extensor tendon and the extensor carpi ulnaris, adequately exposes the lateral collateral ligament complex, allowing reconstruction of this structure.

B

condyle to the radial head (Fig. 7-5A). The extensor carpi radialis longus and distal fibers of the brachial radialis are elevated from the lateral column and epicondyle (see Fig. 7-5B). The brachialis muscle is separated from the anterior capsule, which can be safely performed if the joint has been entered at the radiocapitellar articulation. Since the arthrotomy provides accurate spatial orientation across the joint, damage to neurovascular structures is avoided. The procedure then continues as described in Chapter 44.

POSTEROLATERAL EXPOSURES THE BOYD POSTEROLATERAL EXPOSURE7 Exposure of the lateral ulnohumeral and radiohumeral joint is accomplished with several variations of a pos-

terolateral approach described by Boyd. Depending on the need to expose the proximal ulna or the distal humerus, these approaches can be extended and thus provide significant versatility.40 Indications

Monteggia fractures, Mayo type II olecra-

non fractures. Begin the incision just posterior to the lateral epicondyle and lateral to the triceps tendon, and continue the incision distally to the lateral tip of the olecranon and then down the subcutaneous border of the ulna to the junction of its proximal and middle thirds or as necessary in order to expose the fracture (Fig. 7-6A).

Skin Incision

Technique The anconeus and extensor carpi ulnaris are stripped subperiosteally from the ulna, beginning on the lateral subcutaneous crest of the bone and reflecting

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Brachioradialis

Brachioradialis Extensor carpi radialis longus

Intermuscular septum

ECRL

CET

Triceps Triceps

A

Anconeus

Common extensor tendon

FIGURE 7-5

A, The column procedure provides a limited exposure of the anterior capsule. The incision is approximately 3 to 4 cm and extends from the distal aspect of the origin of the brachioradialis across the radiohumeral joint and common extensor tendon. B, The distal fibers of the brachioradialis as well as the extensor carpi radialis longus are elevated from their attachment on the humerus. C, By elevating the brachioradialis a retractor can be placed behind the anterior musculature exposing the capsule. This is facilitated if an arthrotomy has been carried out. Note that the ability to access the posterior joint is readily accomplished through the so-called posterior interval which elevates the triceps attachment from the posterior aspect of the lateral supracondylar ridge.

the muscles volarward. The supinator is released subperiosteally from its ulnar insertion, and the entire muscle mass is reflected anteriorly (see Fig. 7-6B). Be careful not to detach the ulnar attachment of the lateral ulnar collateral ligament. Thus, the lateral surface of the ulna and the proximal portion of the radius are adequately exposed (see Fig. 7-6C). The substance of the reflected supinator protects the deep branch of the radial nerve (see Fig. 7-6D). If greater exposure of the radius is desired, the recurrent interosseous artery (not the dorsal interosseous artery) is divided in the proximal portion of the wound, and the muscle mass is further reflected volarward to expose the interosseous membrane. The deep branch of the radial nerve remains protected.

EXTENSILE POSTEROLATERAL EXPOSURE (KOCHER) This is an extension of the limited exposures described above involving the release of collateral ligament and capsule.24 Indications Extensile exposure to the joint surface for reconstructive procedures including open reduction

B ECRL Brachioradialis

Posterior interval

C

internal fixation, total elbow arthroplasty (resurfacing), and interposition arthroplasty. Landmarks

Proximal: lateral column; distal Kocher

interval. The triceps may be elevated from the posterior aspect of humerus by extending the skin incision proximally up the lateral column (Fig. 7-7A). This may proceed 6 to 7 cm proximal to the lateral epicondyle without fear of violence to the radial nerve. Proceed as shown in Figure 7-7B by completely elevating the anconeus from the ulna. The triceps is easily elevated from the posterior humerus in the normal situation, and even in post-traumatic contractures, the triceps can be elevated with a periosteal elevator without much additional difficulty (see Fig. 7-7C). The lateral collateral ligament is released from the humeral origin as a separate structure or if prior surgery has caused scarring, with the common extensor tendon complex. The anterior capsule is then incised. A varus stress is applied to the elbow, which opens like a book hinging on the medial ulnar collateral ligament and common

Skin Incision and Technique

Chapter 7 Surgical Exposures of the Elbow

Line of incision

Extensor carpi ulnaris muscle

Anconeus muscle

A Triceps tendon

Olecranon

Flexor carpi ulnaris muscle

Reflected portion of supinator muscle from ulna

Flexor digitorum profundus muscle

Reflected portion of supinator muscle from radius Divided portion of supinator muscle

Reflected anconeus muscle

B Recurrent interosseous artery Radial nerve (deep branch) entering supinator muscle

Exodus of nerve from supinator muscle Dorsal interosseous artery

Supinator muscle

59

60

61

62

C FIGURE 7-6

The Boyd approach. A, The incision begins along the lateral border of the triceps approximately 2 to 3 cm above the epicondyle and extends distally over the lateral subcutaneous border of the ulna approximately 6 to 8 cm past the tip of the olecranon. B, The ulnar insertion of the anconeus and the origin of the supinator muscles are elevated subperiosteally. C, More distally, the subperiosteal reflection includes the abductor pollicis longus, the extensor carpi ulnaris, and the extensor pollicis longus muscles. The origin of the supinator at the crista supinatorus of the ulna is released, and the entire muscle flap is retracted radially, exposing the radiohumeral joint.

121

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Part III Surgery and Rehabilitation

Radial nerve

Flexor digitorum profundus muscle Olecranon Line of incision Anconeus muscle

59

Flexor digitorum profundus muscle

Line of incision Anconeus muscle

D

Radial nerve 61

Supinator muscle Extensor carpi ulnaris muscle

FIGURE 7-6, cont’d D, The posterior interosseous nerve is protected in the substance of the supinator, which must be gently retracted. To extend the incision farther distal, the dorsal interosseous artery must be ligated. (Redrawn from Crenshaw, A. H.: Surgical approaches. In Edmonson, A. S., and Crenshaw, A, H. [eds]: Campbell’s Operative Orthopaedics, 6th ed. St. Louis, C. V. Mosby, 1980. A and B modified from Boyd, H. B.: Surgical exposure of the ulna and proximal third of the radius through one incision. Surg. Gynecol. Obstet. 71:86, 1940; D modified from Eycleshymer, A. C., and Schoemaker, D. M.: A Cross Section Anatomy. New York, D. Appleton and Co., 1930.)

flexor muscles (see Fig. 7-7D). The triceps remains attached to the ulna.

MAYO MODIFIED KOCHER EXTENSILE POSTEROLATERAL EXPOSURE The triceps attachment is further released from the olecranon and the triceps mechanism is reflected from lateral to medial (Fig. 7-8A).

Essential Characteristic

Indications Ankylosis release, resurfacing arthroplasty, open reduction with internal fixation (ORIF), lateral column, distal humerus. Landmarks

Triceps insertion at olecranon.

Technique If more extensile exposure is required than has been obtained with the previous steps (see Figs. 7-5 and 7-6), a medial skin flap is elevated and the ulnar nerve identified. It is protected or translocated according to the merits of the case and after the release has proceeded according to the steps shown in Figure 7-6. The triceps and anconeus muscle sleeve is reflected from the tip of the olecranon by releasing Sharpey’s fibers (see Fig. 7-8A). The entire extensor mechanism including anconeus is thus reflected from lateral to medial (see Fig. 7-8B). After the triceps has been reflected and the posterior capsule released, the lateral collateral ligament may be detached from the humerus depending on the goal of the specific procedure and the additional exposure required. By flexing the elbow and removing the tip of the olecranon, the articular surface and the entire posterior humerus can be exposed.

Note We have found that the described surgical exposures to the elbow are sufficient to perform virtually all of the reconstructive procedures we currently employ. All may be executed after a posterior skin incision. The surgeon should be aware that the classic extensile approach described by Kocher does imply that the anterior capsule has been incised and the lateral collateral ligament has been released. When the Mayo modified Kocher release has been performed, the ulnar nerve must be exposed and released as necessary to avoid compression with varus angular forearm manipulation.

POSTERIOR EXPOSURES Extensile posterior exposure implies effective management of the triceps mechanism.5,37 In recent years, there has been a marked increased interest in revisiting and modifying previously described posterior surgical approaches. A posterior exposure of the elbow joint may be used for virtually any surgical indication. In fact, a posterior skin incision is now considered to be the universal approach to any deep structure of the elbow. Because the dissection may be readily extended and tissues mobilized medially and laterally, distal humeral and proximal ulnar fractures, joint reconstruction, tumors, infections, and synovial processes are amenable to treatment through a posterior exposure. Several skin incisions and techniques have been described. Although MacAusland27 used a transverse incision, most posterior skin incisions are longitudinal. The S incision of Ollier today is not as often used as the straighter incision recommended by Langenbeck.25 Probably the most important aspect of any incision is that it should not cross the tip of the olecranon. Smith also

Chapter 7 Surgical Exposures of the Elbow

Triceps m.

123

Brachioradialis m.

Capsule

Anconeus m. Supinator m. Extensor carpi ulnarie m.

A

Anconeus m.

B

C

Extensor carpi ulnarie m. Brachioradialis m.

Radial collateral ligament

Triceps m.

D FIGURE 7-7

A, The incision is made 8 cm proximal to the joint just posterior to the supracondylar bony ridge and extending distally over the anconeus for approximately 6 cm. B, The interval between the anconeus and the extensor carpi ulnaris is identified and entered. C, The anconeus is reflected subperiosteally from the proximal ulna along with its fascial attachment to the triceps, which is likewise reflected medially, exposing the supinator muscle. The insertion of the triceps on the tip of the olecranon is released by sharp dissection, and the supinator muscle is released from the proximal portion of the ulna and the humerus as necessary to expose the capsule, which is entered via a longitudinal incision. D, The release of the radiocollateral ligament at its humeral origin allows joint subluxation to expose the entire distal humerus.

attributed better healing to a medial incision as compared with a lateral one.38 Releasing the triceps transverse section of the triceps mechanism at its musculotendinous junction has been described but does not afford adequate repair for optimal rehabilitation.46 Releasing the triceps at its attach-

ment to the olecranon26 is not advisable, owing to the difficulty of adequate repair and possible disruption during rehabilitation.9 Today we categorize triceps management into four categories: (1) triceps splitting, (2) triceps reflecting, (3) triceps preserving, and (4) olecranon osteotomy (Fig. 7-9). A midline splitting incision was

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Lateral margin of triceps

Anconeus Sharpey’s fibers

A Ext. carpi radialis longus Common extensor muscle mass

Release radial collateral ligament

FIGURE 7-8

The triceps attachment to the tip of the olecranon may be released by sharp dissection (A), allowing complete translation of the extensor mechanism medially and providing more extensile exposure to the joint (B).

B

described as early as 1918 by James Thompson to expose the distal humerus for fractures, but it did not include release from the ulna to provide exposure of the joint itself.44 Splitting the triceps in line with the muscle fibers and at its insertion to expose the humerus and the elbow joint was described by Langenback25 and Campbell.10 This approach has had considerable resurgence of interest in recent years. When contracture is present, Campbell first separated the tendon from the muscle as an inverted V and then released the muscle fibers longitudinally. This technique, recommended later by Van Gorder46 for distal humerus fractures, allows lengthening of the musculotendinous unit, which may be necessary to fully mobilize the ankylosed joint. This triceps torque exposure has also faced a renewed interest and popularity in recent years.

POSTERIOR TRICEPS SPLITTING (CAMPBELL)10 Elbow arthroplasty,1 unreduced elbow dislocation, distal humeral fracture, posterior exposure of the joint for ankylosis, sepsis, synovectomy, and ulnohumeral arthroplasty.

Indications

Note When releasing the triceps attachment from the medial attachment at the olecranon, care must be exercised to maintain continuity of the triceps expansion with the forearm fascia in continuity with the flexor attachment. Laterally, the anconeus and triceps form a more stable composite structure that has less chance of disruption with reflection of the lateral attachment. Technique The skin incision begins in the midline over the triceps, approximately 10 cm above the joint line, curves gently laterally or medially at the tip of the olec-

Chapter 7 Surgical Exposures of the Elbow

125

The ulnar nerve is visualized and protected in the cubital tunnel. Only closure of the triceps fascia is required proximally, but the triceps insertion may be supplemented with a suture passed through the tip of the olecranon. The incision is then closed in layers.

Triceps Release at Osseous Attachment (Gschwend)

Campbell

Campbell (Van Gorder)

Mayo

Mod. Kocher

TRICEPS SPLITTING, REFLECTION OF TRICEPS APONEUROSIS

B REFLECTING

A SPLITTING

MacAusland

D Muller

Alonso liames

Mayo

Gschwend modified the triceps splitting technique by osteotomizing the triceps attachment with flecks of bone medially and laterally. Closure is with circumferential sutures placed through drill holes in the ulna.

E Chevron

C SPARING F FIGURE 7-9

The posterior approach to the elbow may be some form of triceps approach that splits (A) or releases (B) the tendon in continuity with or without a fleck of bone by preserving the triceps tendon attachment (C) or by intra-articular (D), extra-articular oblique osteotomy (E), or chevron (F).

ranon, and continues distally over the lateral aspect of the subcutaneous border of the proximal ulna for a distance of approximately 5 to 6 cm. If the incision is curved medially at the olecranon, the scar may have less tendency to contract.38 The triceps is exposed along with the proximal 6 cm of the ulna. A midline incision is made through the triceps, fascia, and tendon and is continued distally across the insertion of the triceps tendon at the tip of the olecranon and down the subcutaneous crest of the ulna (Fig. 7-10). The muscle is elevated medially and laterally exposing the distal humerus. Sharp dissection releases the triceps and the anconeus, which are reflected subperiosteally laterally. The insertion of the triceps is carefully released from the medial olecranon, leaving the flexor mechanism in continuity with the forearm fascia.

Indications Same as those for the midline-splitting approach described earlier, plus elbow contracture and unreduced elbow dislocations (see Chapter 30).10,47

Note This approach allows lengthening of the triceps mechanism. It has also become more popular for primary elbow replacement in recent years. Technique The skin incision is begun 10 cm proximal to the olecranon and extends over the lateral aspect of the proximal ulna, ending 4 cm distal to the joint (Fig. 7-11). The triceps fascia and aponeurosis are isolated along with the tendinous insertion into the ulna. The aponeurosis is elevated and reflected from the muscle from proximal to distal, freeing the underlying muscle fibers while preserving the tendinous attachment to the olecranon. Proximally, the triceps muscle is then split in the midline, and the distal humerus is exposed subperiosteally. The dissection continues distally to the olecranon fossa, exposing the posterior aspect of the joint. If more extensive exposure is desired, the subperiosteal dissection is extended to the level of the joint, exposing the condyles both medially and laterally. The ulnar nerve should be identified and protected. After the procedure, if an elbow contracture has been corrected, the joint should be flexed to about 110 degrees allowing the tendon to slide distally from its initial position. The proximal muscle and tendon are reapproximated in the lengthened relationship with nonabsorbable No. 0 sutures. The distal part of the triceps is then securely sutured to the fascia of the triceps expansion with the same suture, and the remainder of the wound is closed in layers.

REFLECTION OF THE TRICEPS IN CONTINUITY The triceps mechanism may be preserved in continuity and simply reflected to one side or the other. Three surgical approaches have been described that preserve

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M. triceps brachii Caput longum

Caput laterale

A M. brachialis Humerus Capsula articularis M. brachioradialis M. anconaeus N. ulnaris M. extensor carpi ulnaris M. flexor carpi ulnaris Ulna

B

Olecranon M. supinator M. flexor carpi ulnaris M. extensor carpi ulnaris

C

FIGURE 7-10

The Campbell posterior approach. The original description calls for a curved incision, but we prefer a straight one just lateral to the tip of the olecranon and the subcutaneous border of the ulna. The triceps may be released from its attachment to the ulna by a thin osteotomy at its site of attachment. (Redrawn from Anson, B. J., and Maddock, W. G.: Callander’s Surgical Anatomy, 4th ed. Philadelphia, W. B. Saunders Co., 1958.)

the triceps muscle and tendon in continuity with the distal musculature and forearm fascia and expose the entire joint. These exposures were designed to allow rapid rehabilitation while limiting the risk of triceps disruption.

Mayo Modified Kocher’s Posterolateral, Extensile Triceps-Sparing Approach This technique has been described earlier, along with the family of Kocher exposures (see Fig. 7-7).23

Mayo Triceps Reflection Technique of Bryan and Morrey Indications Ankylosis release, semiconstrained total elbow arthroplasty, ORIF medial column, distal humerus fractures.9 Skin Incision and Technique A 14-cm skin incision is made just medial to the tip of the olecranon. The dis-

section is carried to the medial aspect of the triceps 6 cm proximal and 4 cm distal to the tip of the olecranon. The ulnar nerve is identified, and if a femoral translocation is carried out, it is released from the margin of the triceps and elevated from its bed (Fig. 7-12A). The cubital tunnel retinaculum is split and the nerve released to the first motor branch. A subcutaneous pocket is developed, the intermuscular septum removed (see Fig. 7-12B), and the nerve is translocated anteriorly. The triceps is released from the entire posterior aspect of the distal humerus. Forearm fascia and ulna periosteum are elevated from the medial margin of the ulna. The Sharpey fiber attachment of the triceps to the olecranon is released by sharp dissection (see Fig. 7-12C). The distal forearm fascia and ulnar periosteum is elevated from the ulna. The lateral margin of the proximal ulna is then identified and the anconeus is elevated from its ulnar bed (see Fig. 7-12D). The extensor mechanism and capsule continues to be reflected from the margin of the lateral epicondyle (see

Chapter 7 Surgical Exposures of the Elbow

Ulnar nerve Radial nerve

FIGURE 7-11

The Campbell (Van Gorder) aponeurosis turn-down approach. The triceps aponeurosis is identified and reflected distally. The remaining fibers of the triceps are then split in the midline and reflected from the humerus, and the anconeus is reflected subperiosteally from the ulna to expose the joint. (Redrawn from Campbell, W. C., Edmonson, A. S., and Crenshaw, A. H. (eds.): Campbell’s Operative Orthopedics. In Surgical Approaches, 5th ed., Vol. I. St. Louis, C. V. Mosby Co., 1971, p. 119.)

Fig. 7-12E). If a medial column fracture has occurred, the tip of the olecranon is removed and the fracture may be addressed. For semiconstrained total elbow arthroplasty, the lateral and medial collateral ligaments are released and the extensor mechanism is reflected lateral to the epicondyle. The elbow is flexed and the tip of the olecranon is removed to expose the joint (see Fig. 7-12F). In every instance in which the triceps has been completely reflected either from lateral to medial (see Fig. 7-7) or medial to lateral (see Fig. 7-12), it is always securely reattached to the olecranon with a locked crisscross type of suture. Drill holes about 3 cm in length are placed in a cruciate fashion in the olecranon from proximal to distal (Fig. 7-13). A third transverse hole is drilled through the olecranon to secure a second stabilizing suture. The margin of the triceps is first grasped with an Allis clamp and brought over the olecranon. It is important to over

127

correct the reattachment medially to ensure that the sleeve of tissue does not sublux laterally with flexion. A No. 5 nonabsorbable suture is introduced with a straight needle from distal to proximal for the modified Kocher and from distal medial to proximal lateral for the Mayo exposure. The suture is first brought through the osseous tunnel emerging at the tip of the olecranon and passes through the triceps tissue at its anatomic attachment site with the elbow flexed 70 degrees. The suture is locked at this site. It is then brought across the tendinous portion and locked medially. The suture then enters the medial hole in the olecranon and is passed from proximal medial to distal lateral. After the suture has emerged from the second hole in the olecranon, it is brought back over the top of the ulna through the soft tissue distal expansion of the extensor sleeve. Care is taken to leave the knot off to the side of the subcutaneous border of the ulna to avoid irritation or skin erosion. The second suture, which is very important to hold the triceps tendon securely applied to the olecranon attachment, is placed transversely across the ulna again beginning on the side from which the triceps reflection began. It is simply brought back across the triceps tendon in a transverse fashion and is locked in the midline to snugly stabilize the triceps insertion against the olecranon. All sutures are tied with the elbow in 70 to 90 degrees of flexion, again with the knots off the subcutaneous border. Skin closure is with staples or in some instances, a subcuticular stitch is used, particularly in women. The aftercare varies dramatically depending upon the pathology being addressed, and this is discussed in the appropriate chapter. It is worthy of note, however, that I typically splint the elbow in extension with an anterior splint for 2 to 3 days. This protects the incision and may help reduce the tendency to develop flexion contracture.

OSTEOCUTANEOUS FLAP One variation of the Mayo approach reflects the triceps with a sliver of bone while executing the same basic exposure philosophy.48 An extensile triceps-reflecting procedure similar in concept to the Mayo approach and most often used for joint replacement arthroplasty, it also may be used for distal humeral fractures.

Indications

Triceps Release (Wolfe and Ranawat) Technique The triceps attachment is released from the ulna by osteotomizing the attachment with a thin wafer of bone that continues the attachment of the triceps tendon. This is the essential difference from the Mayo approach. The medial aspect of the triceps is elevated

Ulnar crest

Ulnar n. motor branch Subcutaneous pocket

Ulnar nerve

A B Ulnar periosteum

Intermuscular septum Radial head Anconeus

Triceps attachment Lateral capsule

Ulnar n. translocated

D C

F

E

FIGURE 7-12

The Bryan-Morrey posterior approach. A, Straight posterior skin incision (approximately 14 cm). The triceps has been exposed, as has the superficial forearm fascia originating from the medial epicondyle and olecranon. The line of incision of the distal fascia-periosteum complex is identified. B, The ulnar nerve has been translocated anteriorly into subcutaneous tissue, and the intravascular septum is removed. C, The medial border of the triceps is identified and released, and the superficial forearm fascia is sharply incised to allow reflection of the fascia and periosteum from the proximal ulna. D, The extensor mechanism has been reflected laterally, and the anconeus has been released subperiosteally from the ulna, allowing exposure of the radial head. E, The proximal portion of the olecranon is removed for joint exposure. F, The shoulder is rotated externally, and the forearm is hyperflexed. Release of the collateral ligaments allows the ulna to separate from the humerus, providing excellent exposure for replacement or interposition. (From Bryan, R. S., and Morrey, B. F.: Extensive posterior exposure of the elbow. A triceps-sparing approach. Clin. Orthop. 116:188, 1982.)

Chapter 7 Surgical Exposures of the Elbow

A

B

C FIGURE 7-13

(A) The triceps is reattached by a heavy (No. 5), nonabsorbable suture placed through crossed and transverse holes in the ulna. (B) The stitch is placed from distal to medial through the olecranon tunnel and pierces the triceps tendon at the site of attachment as the elbow is flexed to 70 degrees. (C) This stitch is locked, and a second locked stitch is placed over the medial hole in the olecranon. The stitch is brought through this hole, across the periosteal sleeve to join the free end of the suture. (D) An additional transverse suture placed from medial to lateral is locked at the center of the triceps as it overlies its attachment.

D

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Part III Surgery and Rehabilitation

proximally, and the triceps attachment, with the wafer of bone, is elevated from the lateral aspect of the ulna in continuity with the anconeus muscle and the fascia (see Fig. 7-12). After the surgical procedure, the olecranon osteotomy is secured to its bed by 20 nonabsorbable sutures placed through bone holes. Interrupted sutures are used to repair the remaining distal portion of the extensor mechanism.

first used for nonunions29 to treat acute fractures and type IV rheumatoid arthritis. Because the triceps is not detached from its insertion at the tip of the olecranon, rapid rehabilitation is possible. It is expected that complete sparing of the triceps attachment will be used more frequently in the future and that the indications will increase. The most important caution is to avoid axial traction to the ulnar nerve from forearm manipulation.

Triceps-Preserving Technique

Editor’s Note Special comment is required to place these exposures in context. In all instances, the proponent reveals excellent outcomes. Of course, what is important is to honestly decide what works for you. We developed the Bryan-Morrey exposure specifically because we experienced unreliable strength outcomes after the Campbell splint and aponeurosis take-down, as well as thin osteotomy of the triceps insertion. All of these exposures are described earlier and are all being revisited with some degree of enthusiasm. In the final analysis, do what works for you.

It is possible to elevate the triceps from the medial and lateral intramuscular septae while leaving the triceps attached to the olecranon.2,30 Several variations are included with this description. Indications Absence of distal humerus such as tumor resection, joint reconstruction for resection of humeral nonunion, or revision joint replacement.30 Technique The technique is usually used for failed reconstructive procedures, so the previous skin incision is followed when possible. Otherwise, a posterior incision is made either medial or lateral to the tip of the olecranon. Medial and lateral skin flaps are elevated with as much subcutaneous tissue and fascia as possible. The medial and lateral aspects of the triceps are identified, and the ulnar nerve is isolated unless it was previously translocated anteriorly (Fig. 7-14A). The distal humeral nonunion or acute fracture fragments are sharply mobilized. The lateral collateral attachment to the humerus is severed, along with the common extensor tendon (see Fig. 7-14B). The common flexor tendon and muscle mass are elevated from the medial epicondyle along with the medial collateral ligament, and the distal segment is removed (see Fig. 7-14C). The distal aspect of the humerus usually is buttonholed laterally to the margin of the triceps (see Fig. 7-14D). Occasionally, the humerus is brought through the medial interval between the triceps muscle and the ulnar nerve. Regardless of the side to which the humerus is delivered, distal traction on the forearm must be avoided because it could stretch the ulnar nerve. The ulna is rotated appropriately to allow exposure to prepare and insert the ulnar component. At this point, a portion of the triceps attachment can be released to better expose the ulna (see Fig. 7-14E). After the implant has been inserted, the joint is articulated. There is no need to close or repair the extensor mechanism. Skin closure is routine, and motion is begun immediately and without restriction.

Comment I have employed this exposure since 1989 in cases in which the distal humeral articulation is absent or resected. I have expanded the application, which was

POSTERIOR TRANSOSSEOUS EXPOSURES Worldwide, a transosseous approach is probably the exposure most often used, especially for distal humeral fractures. The oblique osteotomy has almost been abandoned, and the transverse osteotomy has largely been replaced by the chevron.

OBLIQUE OSTEOTOMY Approach Indications

Oblique osteotomy of the olecranon.34 T or Y condylar fracture.

Technique A 14-cm incision is made just lateral to the midline, extending past the tip of the olecranon. The insertion of the triceps tendon to the proximal ulna is carefully identified, and a 3.2-mm hole is drilled through the tip of the olecranon, centered down the medullary canal and on the insertion of the triceps tendon (Fig. 7-15). The triceps attachment is then carefully isolated and osteotomized in an oblique fashion with an oscillating saw. With its attachment to the osteotomized segment, the muscle is reflected proximally. At the completion of the procedure, the osteotomized fragment is reattached with a lag screw and the wound is closed in layers.

CHEVRON TRANSOLECRANON OSTEOTOMY Indications

fracture.27

Ankylosed

joints;

T

or

Y

condylar

Chapter 7 Surgical Exposures of the Elbow

Common extensor tendon

Anconeus Extensor carpi ulnaris

Anconeus

Lateral collateral ligament

Ulnar n.

A

B Triceps

Common flexor tendon

Medial collateral ligament

Ulnar n.

Triceps

C FIGURE 7-14

A, The medial and lateral aspects of the triceps and extensor mechanism are identified along with the ulnar nerve. B, The distal humeral fracture or nonunion is sharply dissected from the lateral aspect. C, Similarly, the distal humerus is freed of its medial soft tissue attachments, including the ligaments. Partial release of the triceps, either medially or laterally, allows the forearm to be more easily displaced and rotated.

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Forearm rotated externally

Forearm rotated internally

Distal fragment

Distal fragment

D

E

FIGURE 7-14, cont’d

D, The loose fragments, tumor, or area of nonunion is removed, and the distal humerus is exposed from the lateral aspect. E, In some circumstances, such as with long-standing valgus deformity, exposure from the medial margin of the triceps is more efficient. Note rotation of the ulna is required to identify the medullary canal.

Comment The intra-articular osteotomy first described by MacAusland was originally recommended for ankylosed joints. It has been adopted by some20 for radial head excision and synovectomy and used or modified by others12 for T and Y condylar fractures. However, in persons with rheumatoid arthritis, this portion of the bone may be thin, and therefore, this is not a suitable exposure for total elbow arthroplasty. The chevron design markedly enhances the repair and thus allows early motion. Technique Originally, a transverse incision across the elbow was described for the transverse osteotomy. At the present time, a straight incision is recommended (Fig. 7-16A). It is made posteriorly just lateral to the midline and measures approximately 14 cm centered on the olecranon. The ulnar nerve is isolated, dissected from the cubital tunnel, and protected. A 3.2-mm drill hole crosses the proposed osteotomy site for anatomic replacement at the completion of the procedure (see Fig. 7-16B). The joint is exposed at the midportion of the greater sigmoid notch. An apex distal chevron, or V, osteotomy initiated with the saw and completed with an osteotomy. By allowing the subchondral bone to “crack” facilitates accurate repositioning with the interdigitated surfaces. The capsular attachments, including the posterior portion of the ulnar collateral ligament, are

released. The triceps tendon, along with the osteotomized portion of the olecranon, may then be retracted proximally, and by flexing the elbow joint, the tendon can be exposed (see Fig. 7-16C). Occasionally, the radial or medial collateral ligament may be released for better exposure, but it must later be reattached to the bone to avoid instability. At the completion of the procedure, the tip of the olecranon is secured with a single cancellous screw. The elbow usually is immobilized for 2 to 3 weeks, at which time a gentle, active rehabilitation program is instituted when clinically indicated.

COMBINED OSTEOTOMY PLUS TRICEPS SPLITTING A recent report14 has suggested the value of combining the chevron osteotomy with a triceps-splitting technique. This would seem to offer little advantage over the chevron osteotomy as described with the associated triceps reflection techniques.

ANCONEUS SPARING OLECRANON OSTEOTOMY (MAYO TECHNIQUE) Comment Concern with regard to transecting the anconeus attachment to the triceps has prompted the devel-

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FIGURE 7-15

A

The Müller posterior oblique olecranon osteotomy. The lateral margin of the triceps is identified and reflected medially to expose the distal humerus. A, The proximal ulna is predrilled for reattachment later. B, An oblique extra-articular osteotomy, including the attachment of the triceps, is made across the proximal ulna. C, The triceps with its attachment to bone is then reflected proximally, and as the elbow is flexed the entire distal humerus and elbow joint may be exposed. D, After the procedure, the triceps is reattached with a malleolar or cancellous-type screw, which provides good compression across the osteotomy site. (Redrawn from Müller, M. E., Allgower, M., and Willenegger, H.: Manual of Internal Fixation: Technique Recommended by the AO Group. New York, SpringerVerlag, 1970.)

B

C

D

opment of an olecranon osteotomy that preserves the anconeus origin and viability. The attractiveness of this exposure is that the anconeus dissection can be done very safely and quickly. This does preserve the anconeus triceps continuity in the event that a later reconstructive procedure may be necessary that uses the anconeus.

TECHNIQUE The patient is supine with the arm across the chest.28 The exposure is as required by the pathology. Deep exposure is at the Kocher’s interval between the extensor carpi ulnaris and anconeus. The interval is entered and the anconeus is identified and isolated (Fig. 7-17A). The anconeus is elevated from its bed by sharp dissection leaving the attachment of its origin at the fascial expansion of the triceps; the mid portion of the sigmoid notch is identified laterally (see Fig. 7-17B).

Medially, the ulnar nerve is identified, and the midportion of the articulation is exposed (see Fig. 7-17C). A V-shaped Chevron osteotomy is carried out as described earlier with an oscillating saw. The osteotomy is completed with an osteotome (see Fig. 7-17D). The osteotomized olecranon, along with the attached anconeus, is elevated proximally. Closure consists of the standard AO reattachment of the olecranon. The anconeus is brought back to its insertion on the ulna, and the fascia over the anconeus is closed with a running 2-0 absorbable suture. Note The ulnar nerve does not need to be mobilized unless dictated by the pathology. Avoid osteotomy in rheumatoid arthritis because the thin olecranon compromises healing if an osteotomy is carried out.31 The transverse osteotomy of McAusland is associated with an approximately 5% nonunion rate.31 Although for distal humeral fractures Pitfalls

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B A

C FIGURE 7-16

Chevron olecranon osteotomy. A, A straight incision is made just lateral to the tip of the olecranon approximately 7 cm proximal and 7 cm distal to the tip of the olecranon. The proximal ulna is predrilled with a 3.2-mm drill, and the margins of the triceps are identified. B, The triceps is released medially and laterally, while the ulnar nerve is protected. The chevron osteotomy with a distal apex is initiated with an oscillating saw and, C, the proximal portion containing the triceps tendon is retracted proximally, exposing the elbow joint.

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135

A

FIGURE 7-17

B

the Chevron osteotomy may improve these results and decrease the nonunion rate, I personally have not had the clinical need to osteotomize the olecranon in the last 14 years, and osteotomy should be avoided if the olecranon is resorbed.

MEDIAL APPROACHES There are relatively few indications for medial exposure of the elbow joint, which has been superseded by arthroscopic approaches. The transcondylar approach described independently by Molesworth and Campbell provides excellent exposure of the joint, but it involves dissection of the ulnar nerve and healing of the osteotomized epicondyle, both of which increase the complexity, and thus limit the use, of this approach. In 1969, Taylor and Scham43 described a medial approach to the proximal ulna that was used for fractures in this region. The most valuable contribution to medial joint exposure is that described by Hotchkiss.21 This extensile exposure provides great flexibility, particularly

A, The anconeus interval is exposed through a mid-line incision of the distal forearm and extended laterally and distally over the anconeus. The muscle is elevated and the midportion of the lateral ulnohumeral joint identified. B, The medial ulnohumeral joint is entered as the ulnar nerve is protected, and a Chevron osteotomy as described in Figure 7-16 is completed. The olecranon and anconeus are reflected proximally.

for exposure of the coronoid and for contracture release.

TRANSEPICONDYLAR APPROACH Indications Medial epicondylar fractures, loose bodies, medial lesions whose symptoms require ulnar nerve exploration, and resurfacing arthroplasty.10,29

Comment This procedure was described independently by Molesworth in England and by Campbell in the United States. Because it requires osteotomy of the medial epicondyle, which causes more concern about reattachment and healing than other exposures, the indications for its use today are limited. With the elbow flexed at 90 degrees, a medial incision is made from 5 cm above to approximately 5 cm below the elbow over the medial epicondyle. The ulnar nerve is identified, released, and retracted from the medial epicondyle, which is freed from soft tissue. It is helpful to make a longitudinal incision in the

Technique

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capsule just anterior to the ulnar collateral ligament and to place a periosteal elevator under the ligament as a landmark before performing the osteotomy. In this way, healing of the osteotomy restores the integrity of the ulnar collateral ligament. With a small osteotome, the epicondyle is freed and turned downward with its muscular attachments. Blunt dissection allows distal retraction of the flexor muscles, and careful technique avoids injury to the innervation of the muscle mass. The medial aspect of the coronoid process is exposed, along with the anterior and posterior capsules, which may be reflected from the humerus as necessary for additional exposure. Valgus stress hinges the joint on the lateral ligament and the remaining portions of the capsule, and provides generous exposure of virtually the entire elbow joint. Care must be taken to protect the median nerve as it passes over the anterior aspect of the joint. The epicondyle is returned to its anatomic position and secured with a small screw or with sutures placed through the bone. This step is important, because the quality of the repair affects the integrity of the ulnar collateral ligament, which is essential to the stability of the elbow joint.

EXTENSILE MEDIAL APPROACH (“OVER-THE-TOP” [HOTCHKISS]) Indications 1. Access to the coronoid and anterior osteophytes with intact radial head22 2. Ulnar nerve exploration required 3. Need to preserve posterolateral ulnohumeral ligament complex 4. Anterior and posterior access to the joint 5. May be converted to triceps-sparing exposure of Bryan-Morrey Limitations 1. Need for excision of heterotopic bone on the lateral side 2. Access to radial head Technique The patient is usually supine and supported by a hand table. It is helpful to bring the patient as far as possible onto the hand table. The patient’s head may require support, and a roll is placed under the scapula. The skin incision can vary between the boundaries of a pure posterior skin incision and a midline medial incision. The key to this exposure is identification of the medial supracondylar ridge of the humerus, the medial intermuscular septum, the origin of the flexor pronator muscle mass, and the ulnar nerve.

The subcutaneous skin is elevated, and the medial intermuscular septum is identified. Anterior to the septum, running just on top of the fascia (and not in the subdermal tissue), the medial antebrachial cutaneous nerve is identified and protected. It is occasionally necessary to divide this nerve to gain full exposure and to adequately mobilize the ulnar nerve, especially in revision surgery. If the patient previously had surgery, the ulnar nerve should be identified proximally before the surgeon proceeds distally. If anterior transposition was performed previously, the nerve should be mobilized carefully before the operation proceeds. The surface of the flexor pronator muscle mass origin is found by sweeping the subcutaneous tissue laterally with the medial antebrachial cutaneous nerve in this flap of subcutaneous tissue. The medial intermuscular septum is excised from the supracondylar ridge about 5 cm proximally (Fig. 7-18A). The ulnar nerve is protected, and the veins at the base of the septum are cauterized. The supracondylar ridge is located, and elevation of the anterior muscle begins with a wide Cobb elevator. Subperiosteally, all of the anterior structures of the distal humeral region are elevated enough to allow placement of a wide Bennett retractor. The median nerve and brachial vein and artery are superficial to the brachialis muscle. Once the septum is excised, the flexor pronator muscle mass should be divided parallel to the fibers, leaving approximately a 1.5-cm span of flexor carpi ulnaris tendon attached to the epicondyle (see Fig. 718B). A small cuff of fibrous tissue of the origin can be left on the supracondylar ridge as the muscle is elevated. This facilitates reattachment when closing. A proximal, transverse incision in the lacertus fibrosus may also be needed to adequately mobilize this layer of muscle. The flexor pronator origin should be dissected down to the level of bone but superficial to the joint capsule. As this plane is developed, the brachialis muscle is encountered from the underside. This muscle should be kept anterior and elevated from the capsule and anterior surface of the distal humerus. Dissection of the capsule proceeds laterally and distally to separate it from the brachialis muscle (see Fig. 7-18C). At this point, it is helpful to feel for the coronoid process by gently flexing and extending the elbow. A deep, narrow retractor is used and, after capsular excision, the radial head and capitellum can be visualized. In the case of contracture, the capsule, once separated from the overlying brachialis and brachioradialis, can be sharply excised (see Fig. 7-18D). The radial nerve is identified running between the brachialis and the brachioradialis. Care should be taken to stay deep to these two muscles when elevating over to the lateral side. In a contracture release, the anteromedial portion of the capsule often requires release. To expose this area, a small narrow retractor can be inserted to pull the

Medial intramuscular septum

Flexor/pronator attachment

Pronator teres

Brachialis

A

Common flexor tendon

Ulnar n.

B

Excised capsule

Flexor/pronator attachment

C

Capsule

E FIGURE 7-18

Lateral column

D

Medial head of triceps

A, After routine medial exposure, and taking care to protect or resect the distal branches of the medial antebrachiocutaneous nerve, the surgeon identifies the intermuscular septum and excises it for approximately 5 cm. B, The pronator and a portion of the common flexor tendon are excised from the medial epicondyle, leaving a cuff of tissue on the medial epicondyle. The muscle mass is split longitudinally leaving the ulnar head of the extensor carpi ulnaris to protect the nerve. The nerve at this point has been isolated but not translocated. C, With the nerve protected, the capsule is identified, and the undersurface of the flexor pronator group is elevated from the capsule identifying the medial aspect of the brachialis muscle. D, The brachialis muscle is elevated and the entire anterior capsule is exposed. If the primary purpose is capsular release, care is taken to transect as much of the capsule as possible rather than simply releasing it. The coronoid is readily identified on completion of the capsular release. E, A posterior exposure may also be necessary; the periosteal elevator lifts the medial aspect of the triceps from the posterior aspect of the medial condyle and medial column. The ulnar nerve is translocated anteriorly.

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attached flexor carpi ulnaris medially. This affords adequate visualization and protection of the anteromedial collateral ligament. The ulnar nerve is mobilized to permit anterior transposition with a dissection carried distally to the first motor branch to allow the nerve to rest in the anterior position without being sharply angled as it enters the flexor carpi ulnaris. With the Cobb elevator, the triceps is elevated from the posterior distal surface of the humerus (see Fig. 7-18E). The posterior capsule can be separated from the triceps as the elevator sweeps from proximal to distal. The flexor pronator mass should be reattached to the supracondylar ridge with nonabsorbable braided 1-0 or 0 suture through holes in bone or to the fibrous cuff, if it is adequate. After being reattached to the medial supracondylar region, the ulnar nerve should be transposed and secured with a fascial sling (or by the surgeon’s preference) to prevent posterior subluxation.

ANTERIOR EXPOSURES Because of the vulnerability of the brachial artery and median nerve, the anterior medial approach to the

V. cephalica

M. biceps brachii

elbow is not recommended (Fig. 7-19). The extensile exposure described by Henry, as modified from Fiolle and Delmas, is the best known and the most useful for anterior exposure of the joint. Minor modifications of the Henry approach have been described,22,39 and a limited anterolateral exposure has been described by Darrach.14 Approach

Extensile anterior exposure of the elbow

region.19 Indications Anteriorly displaced fracture fragments, excision of tumors in this region, reattachment of the biceps tendon to the radial tuberosity, exploration of entrapment syndromes, and anterior capsule release for contracture. Technique The skin incision begins about 5 cm proximal and lateral to the flexor crease of the elbow joint and extends distally along the anterior margin of the brachioradialis muscle (Fig. 7-20A). Below the elbow joint, the incision turns medially to avoid crossing the flexor crease at a right angle, thus discouraging hypertrophic scar formation. The incision continues transversely to the biceps tendon and then turns distally over

V. basilica

Septum intermusculare mediale M. triceps brachii (caput longum)

M. brachialis N. cutaneous antibrachii lateralis N. radialis Lacertus fibrosus

M. brachialis A. brachialis A. collateralis ulnaris inferior N. medianus

M. brachioradialis

M. pronator teres Vv. brachiales

A. recurrens radialis A. radialis

A. ulnaris

FIGURE 7-19

Because the brachial artery and median nerve occupy the anteromedial aspect of the elbow joint, an anterior medial approach to the joint is not an option. (Redrawn from Anson, B. J., and Maddock, W. G.: Callander’s Surgical Anatomy, 4th ed. Philadelphia, W. B. Saunders, 1958.)

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139

Biceps Brachialis

Brachialis

Biceps

Brachioradialis Fascia

Brachioradialis

Deep branch radial nerve

Superficial branch radial nerve

Lacertus fibrosus

Incision

Radial nerve

Radial artery

Supinator

Pronator teres

Pronator teres

A

B

Biceps Brachioradialis Interosseous branch radial nerve Incision

C

Biceps Radial nerve Brachialis Capitellum Biceps tendon

Radial artery

D FIGURE 7-20

Brachioradialis Incision in capsule opened

Radial nerve Brachialis Capitellum Biceps tendon

Supinator reflected

Sensory branch radial nerve

Supinator

Fascia

Fascia

Pronator teres

Annular ligament

Radial artery

Periosteum reflected

E

The anterior Henry approach. A, An incision is made approximately 5 cm proximal to the elbow crease on the lateral margin of the biceps tendon. It extends transversely across the joint line and curves distally over the medial aspect of the forearm. B, The interval between the brachioradialis and brachialis proximally and the biceps tendon and pronator teres in the distal portion of the wound is identified. The radial nerve is protected and retracted along with the brachialis muscle. C, The radial recurrent branches of the radial artery and its muscular branches are identified and sacrificed if more extensive exposure is required. The biceps tendon is retracted medially, along with the brachialis muscle. D, The supinator muscle is released from the anterior aspect of the radius, which is fully supinated. E, This interval may now be developed to expose the entire anterior aspect of the elbow joint, including the capitellum, the proximal radius, and the radial tuberosity. (Redrawn from Banks, S. W., and Laufman, H.: An Atlas of Surgical Exposures of the Extremities. Philadelphia, W. B. Saunders Co., 1953.)

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the medial volar aspect of the forearm, ending approximately 6 or 7 cm distal to the flexion crease. The interval between the brachioradialis laterally and the biceps and brachialis medially is identified and entered. The fascia is released distally between the brachioradialis and the pronator teres (see Fig. 7-20B). The interval then is entered proximally, and gentle, blunt dissection demonstrates the radial nerve coursing on the inner surface of the brachioradialis muscle. Care is taken to avoid injuring the superficial sensory branch of the radial nerve. Because the radial nerve gives off its branches laterally, it can safely be retracted with the brachioradialis muscle. At the level of the elbow joint, as the brachioradialis is retracted laterally and the pronator is gently retracted medially, the radial artery can be observed where it emerges from the medial aspect of the biceps tendon, giving off its muscular and recurrent branches in a mediolateral direction (see Fig. 7-20C). The muscle branch is ligated, but the recurrent radial artery should be sacrificed only if the lesion warrants the more extensive exposure that can be realized with this maneuver. The dorsal interosseous nerve enters the supinator and continues along the dorsum of the forearm distally. The dissection continues distally, exposing the supinator muscle, which covers the proximal aspect of the radius and the anterolateral aspect of the capsule. Muscle attachments to the anterior aspect of the radius and those distal to the supinator include the discrete tendinous insertion of the pronator teres and the origins of the flexor digitorum sublimis and the flexor pollicis longus. The brachialis muscle is identified, elevated, and retracted medially to expose the proximal capsule. If more distal exposure is needed, the forearm is fully supinated, demonstrating the insertion of the supinator muscle on the proximal radius. This insertion is incised, and the supinator is subperiosteally retracted laterally (see Fig. 7-20D). The supinator serves as protection to the deep interosseous branch of the radial nerve, but excessive retraction of the muscle should be avoided. The proximal aspect of the radius and the capitellum are thus exposed. Additional visualization may be obtained both proximally and distally, because the radial nerve has been identified and can be avoided proximally. The posterior interosseous nerve is protected distally by the supinator muscle, and the radial artery is visualized and protected medially if a more extensile exposure is required (see Fig. 7-20E). Note The recurrent and muscular branches of the radial artery and vein should be ligated before the radial artery is released, to avoid hematoma formation that could cause ischemic contracture of the forearm. Retraction of the brachioradialis and the extensor carpi radialis longus

and brevis muscles is facilitated if the elbow is flexed 90 degrees. This affords easier exposure of the supinator muscle. When the supinator muscle is stripped subperiosteally from the radius, the bursa between the biceps tendon and the radius is usually identified and should be entered, facilitating subperiosteal exposure of the muscle. The proximal radius is further exposed by subperiosteal dissection as the forearm is being pronated and supinated.

RESULTS There have been limited attempts to document the efficacy of one or the other of the various types of tricepssparing approaches. In the original description, we compared the clinical result of the Mayo approach to that of the triceps splitting or transverse release of the triceps reattachment.9 There were no triceps disruptions after approximately 75 procedures done with the triceps being released in continuity (Mayo approach) compared with an approximately 20% complication rate when the triceps was released transversely. Wolfe and Ranawat48 have also observed no instances of triceps insufficiency with their modification of this approach. The use of the Mayo medial exposure was also shown to have improved triceps strength after total elbow arthroplasty.32 This manner of exposing the elbow was found to be associated with approximately 20% greater extension strength than with the Campbell (Van Gorder) type of exposure. An additional consideration in those with rheumatoid arthritis is the thin olecranon that compromises healing if an osteotomy is carried out.20 The transverse osteotomy of McAusland is associated with an approximately 5% nonunion rate.31 Although for fractures the chevron osteotomy may improve these results and decrease the nonunion rate, I personally have not had the clinical need for osteotomized the olecranon in the last 20 years and this should be avoided if the olecranon has been thinned.

COMPLICATIONS One advantage of the above-described exposures is their relative freedom from complications. Today most problems are related to the pathology rather than the surgical approach.

WOUND HEALING Difficult ankylosis release procedures are associated with a significant amount of swelling as often occurs in patients undergoing total elbow arthroplasty. Wound

Chapter 7 Surgical Exposures of the Elbow

healing is generally not a problem, however, and is related to the presence of prior incisions and the magnitude of the dissection as is typical for release of the stiff elbow.

INFECTION The infection rate after total elbow arthroplasty has been reduced at our institution from a high of 11% in 1970 to approximately 3% over the last 10 years.32 This reduction is coincident with adopting the Mayo approach to the elbow but other technique changes have occurred in this period, including using antibioticimpregnated cement and splinting the elbow in extension.

ULNAR NERVE INJURY Injury to the ulnar nerve appears to be more common in those instances in which the ulnar nerve is not exposed and the elbow is flexed on the medial collateral ligament such as with the classic extensile Kocher approach.16,45 Simply exposing the ulnar nerve, while decreasing this complication, does not completely obviate it. The theoretical disadvantage of the Mayo approach, which allows translocation of the ulnar nerve, is that this maneuver devascularizes the nerve, and the dissection itself may cause ulnar nerve irritation. Having used this particular exposure in more than 500 cases, the incidence of permanent ulnar nerve injury with motor dysfunction is less than 1%. Therefore, I am comfortable in exposing and moving the ulnar nerve in a subcutaneous pocket as an essential and integral part of the Mayo triceps-sparing approach.

RADIAL NERVE INJURY Although posterior interosseous nerve palsy is known to occur with some approaches to the radial nerve,21 the complication is virtually unheard of when the joint is exposed through Kocher’s interval.

TRICEPS DISRUPTION Triceps disruption is uncommon in our experience with either the Mayo modified extensile Kocher exposure or the Mayo medial to lateral type of approach. The incidence of triceps disruption is less than 1% in our experience. If, however, the triceps should become disrupted after either of the procedures described above, if adequate tissue is present, it may be reattached as described for the primary procedure. If the remaining tissue is inadequate, triceps power is restored either by an anconeus slide or achilles tendon allograft reconstruction (see Chapter 35).

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References 1. Albee, F. H.: Arthroplasty of the elbow. J. Bone Joint Surg. 15:979, 1933. 2. AlonsoLlames, M.: Bilaterotricipital approach to the elbow. Acta Orthop. Scand. 42:479, 1972. 3. Anson, B. J., and Maddock, W. G.: Callander’s Surgical Anatomy, 4th ed. Philadelphia, W. B. Saunders Co., 1958. 4. Banks, S. W., and Laufman, H.: An Atlas of Surgical Exposures of the Extremities. Philadelphia, W. B. Saunders Co., 1953. 5. Boorman, R. S., Page, W. T., Weldon, E. J., Lippitt, S., and Matsen, F. A. III: A triceps-on approach to semiconstrained total elbow arthroplasty. Techniques in Shoulder & Elbow Surgery 4:139, 2003. 6. Bost, F. C., Schottstaedt, E. R., Larsen, L., and Abbott, L.: Surgical approaches to the elbow joint. In American Academy of Orthopaedic Surgeons: Instructional Course Lectures, Vol. 10. Ann Arbor, J. W. Edwards, 1953, p. 180. 7. Boyd, H. B.: Surgical exposure of the ulna and proximal third of the radius through one incision. Surg. Gynecol. Obstet. 71:86, 1940. 8. Boyd, H. B.: Surgical approaches to the elbow joint. Instruct. Course Lect. 4:147, 1947. 9. Bryan, R. S., and Morrey, B. F.: Extensive posterior exposure of the elbow: a triceps sparing approach. Clin. Orthop. 166:188, 1982. 10. Campbell, W. C.: Incision for exposure of the elbow joint. Am. J. Surg. 15:65, 1932. 11. Campbell, W. C., Edmonson, A. S., and Crenshaw, A. H. (eds.): Campbell’s Operative Orthopedics. In Surgical Approaches, 5th ed., Vol. I. St. Louis, C. V. Mosby Co., 1971, p. 119. 12. Casselbaum, W. H.: Operative treatment of T and Y fractures of the lower end of the humerus. Am. J. Surg. 83:265, 1952. 13. Crenshaw, A. H.: Surgical approaches. In Edmonson, A. S., and Crenshaw, A. H. (eds.): Campbell’s Operative Orthopaedics, 6th ed. St. Louis, C. V. Mosby, 1980. 14. Darrach, W.: Surgical approaches for surgery of the extremities. Am. J. Surg. 67:93, 1945. 15. Ebraheim, N. A., Andreshak, T. G., Yeasting, R. A., Saunders, R. C., and Jackson, W. T.: Posterior extensile approach to the elbow joint and distal humerus. Orthop. Rev. 22:578, 1993. 16. Ewald, F. C., and Jacobs, M. A.: Total elbow arthroplasty. Clin. Orthop. 182:137, 1984. 17. Eycleshymer, A. C., and Schoemaker, D. M.: A Cross Section Anatomy. New York, D. Appleton and Co., 1930. 18. Gordon, M. L.: Monteggia fracture. A combined surgical approach employing a single lateral incision. Clin. Orthop. 50:87, 1967. 19. Henry, A. K.: Extensile Exposure, 2nd ed. Baltimore, Williams & Wilkins Co., 1957. 20. Inglis, A. E., Ranawat, C. S., and Straub, L. R.: Synovectomy and debridement of the elbow in rheumatoid arthritis. J. Bone Joint Surg. 53A:652, 1971. 21. Kaplan, E. B.: Surgical approaches to the proximal end of the radius and its use in fractures of the head and neck of the radius. J. Bone Joint Surg. 23:86, 1941.

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22. Kasparyan N. G., and Hotchkiss, R. N.: Dynamic skeletal fixation in the upper extremity. Hand Clin. 13:643, 1997. 23. Kelly, R. P., and Griffin, T. W.: Open reduction of T condylar fractures of the humerus through an anterior approach. J. Trauma 9:901, 1969. 24. Kocher, T.: Textbook of Operative Surgery, 3rd ed. London, A. and C. Black, 1911. 25. Langenbeck (1864): Cited by Alonso Llames, M.: Bilaterotricipital approach to the elbow. Acta Orthop. Scand. 43:479, 1972. 26. Lexer, B.: Cited by Alonso Llames, M.: Bilaterotricipital approach to the elbow. Acta Orthop. Scand. 43:479, 1972. 27. MacAusland, W. R.: Ankylosis of the elbow: with report of four cases treated by arthroplasty. J. A. M. A. 64:312, 1915. 28. Mansat, P., and Morrey, B. F.: The column procedure: a limited lateral approach for extrinsic contracture of the elbow. J. Bone Joint Surg. 80A:1603, 1998. 29. Molesworth, W. H. L.: Operation for complete exposure of the elbow joint. Br. J. Surg. 18:303, 1930. 30. Morrey, B. F.: Revision total elbow arthroplasty. In Morrey, B. F. (ed.): Joint Replacement Arthroplasty. New York, Churchill Livingstone, 1991, pp. 345-360. 31. Morrey, B. F.: Surgical exposures of the elbow. In Morrey, B. F. (ed.): The Elbow and Its Disorders, 3rd ed. Philadelphia: W. B. Saunders Co., 2000, p. 109. 32. Morrey, B. F., Askew, L. J., and An, K. N.: Strength function after elbow arthroplasty. Clin. Orthop. 234:43, 1988. 33. Morrey, B. F., and Morrey, M. C.: Relevant surgical exposures. In Master’s Techniques in Orthopedic Surgery. Philadelphia, Lippincott, Williams & Wilkins, 2008. 34. Muller, M. E., Allgower, M., and Willenegger, H.: Manual of Internal Fixation: Technique Recommended by the AO Group. New York, Springer-Verlag, 1970. 35. Ogilvie, W. H.: Discussion of minor injuries of the elbow joint. Proc. Roy. Soc. Med. 23:306, 1929.

36. Pankovich, A. M.: Anconeus approach to the elbow joint and the proximal part of the radius and ulna. J. Bone Joint Surg. 59A:124, 1977. 37. Schildhauer, T. A., Nork, S. E., Mills, W. J., and Henley, M.B.: Extensor mechanism-sparing paratricipital posterior approach to the distal humerus. J. Orthop. Trauma 17:374, 2003. 38. Smith, F. M.: Surgery of the Elbow, 2nd ed. Philadelphia, W. B. Saunders Co., 1972. 39. Sorrell, E., and Longuet, Y. J.: La voie transbrachiale anterieure dans la chirurgie des fractures supracondyliennes de l’humerus chez l’enfant. Rev. Orthop. 32:117, 1946. 40. Speed, J. S., and Boyd, H. B.: Treatment of fractures of ulna with dislocation of head of radius (Monteggia fracture). J.A.M.A. 115:1699, 1940. 41 Spinner, M. (ed.): The radial nerve. In Injuries to the Major Branches of Peripheral Nerves of the Forearm, 2nd ed. Philadelphia, WB Saunders, 1978, pp. 85-91. 42. Strachan, J. H., and Ellis, B. W.: Vulnerability of the posterior interosseous nerve during radial head reaction. J. Bone Joint Surg. 53B:320, 1971. 43. Taylor, T. K. F., and Scham, S. M.: A posteromedial approach to the proximal end of the ulna for the internal fixation of olecranon fractures. J. Trauma 9:594, 1969. 44. Thompson, J. E.: Anatomical methods of approach in operations on the long bones of the extremities. Ann. Surg. 68:309, 1918. 45. Trancik, T., Wilde, A. H., and Borden, L. S.: Capitellocondylar elbow arthroplasty. Two to eight year experience. Clin. Orthop. 112:175, 1987. 46. Van Gorder, G. W.: Surgical approach in old posterior dislocation of the elbow. J. Bone Joint Surg. 14:127, 1932. 47. Van Gorder, G. W.: Surgical approach in supracondylar “T” fractures of the humerus requiring open reduction. J. Bone Joint Surg. 22:278, 1940. 48. Wolfe, S. W., and Ranawat, C. S.: The osteoanconeus flap: an approach for total elbow arthroplasty. J. Bone Joint Surg. 72A:684, 1990.

Chapter 8 General and Regional Anesthesia and Postoperative Pain Control

CHAPTER

8

General and Regional Anesthesia and Postoperative Pain Control Terese T. Horlocker, Sandra L. Kopp, and Robert L. Lennon

INTRODUCTION Orthopaedic procedures for the elbow are well suited to regional anesthetic techniques. Continuous catheter techniques provide postoperative analgesia and allow early limb mobilization. In addition to intraoperative anesthesia, brachial plexus and peripheral nerve blocks may also be used in the treatment and prevention of reflex sympathetic dystrophy. Conversely, although the benefits of regional anesthesia in this patient population are well established, the operative site may be adjacent to neural structures, as with total elbow arthroplasty or supracondylar fractures. For example, ulnar nerve dysfunction may occur in up to 10% of patients undergoing elbow arthroplasty.17 Early diagnosis and intervention are paramount in reducing the severity of nerve injury; assessment of neurologic function would not be possible in the presence of a regional block. Thus, the anesthetic and analgesic management are based on the patient’s evolving neurologic status (including the need for serial neurologic examinations, the anticipated rehabilitative goals, and history of side effects or interactions to systemic analgesics). Meticulous regional anesthetic technique, careful patient positioning, and serial postoperative neurologic examinations are required to reduce the incidence of neurologic dysfunction while optimizing surgical outcome.

INTRAOPERATIVE ANESTHETIC MANAGEMENT Surgical procedures for the distal humerus, elbow, and proximal radius, and ulna are commonly performed with regional anesthetic techniques.4 The brachial plexus may be blocked using four distinct approaches. Advances in needles, catheters, and nerve stimulator technology

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have facilitated the localization of neural structures and improved success rates. Selection of regional technique is dependent on the surgical site (Table 8-1). For surgery on the elbow, the supraclavicular (Fig. 8-1), infraclavicular, or axillary (Fig. 8-2) approaches are ideal because these approaches provide adequate blockade of the lower trunk, which remains unblocked with the more proximal interscalene technique. Supraclavicular, infraclavicular, and axillary approaches to the brachial plexus are reliable and provide consistent anesthesia to the four major nerves of the brachial plexus: median, ulnar, radial, and musculocutaneous.19 However, the small but definite risk of pneumothorax associated with supraclavicular blocks makes this approach unsuitable for outpatient procedures. Typically, pneumothorax occurs 6 to 12 hours after hospital discharge; therefore, a postoperative chest radiograph is not helpful. Although chest tube placement is advised for pneumothorax greater than 20% of lung volume, the lung may also be re-expanded with a small Teflon catheter under fluoroscopic guidance, eliminating the need for hospital admission. The infraclavicular and axillary approaches to the brachial plexus eliminate the risk of pneumothorax and reliably provide adequate anesthesia for surgery near the elbow.14,19 The infraclavicular approach has the added advantage of not requiring abduction during regional block, which would be painful in the presence of arm/forearm fracture.6 The various approaches to the brachial plexus blockade may be performed before surgical incision or after postoperative upper extremity neurologic function has been determined. Although preoperative brachial plexus block reduces the intraoperative requirement of volatile anesthetic and opioids, and in theory provides pre-emptive analgesia, postoperative evaluation of neurologic function is not possible until block resolution. In addition, few outcome studies exist comparing regional and general anesthesia specifically for surgery about the elbow. However extrapolating the results of forearm and hand procedures under single-injection brachial plexus block versus general anesthesia, a regional technique is associated with improved analgesia, reduced opioid consumption and postoperative nausea and vomiting, and early hospital dismissal.15 Overall, there are early but no longterm benefits with a single-injection regional anesthetic technique compared with a general anesthetic. However, placement of an indwelling perineural catheter results in more substantial and lasting benefits, including avoidance of hospital admission/readmission, decreased opioid-related side effects and sleep disturbance, and improved rehabilitation.11,13,20 Thus, anesthetic management of patients undergoing elbow surgery is focused on postoperative analgesia, rather than intraoperative anesthesia to improve perioperative outcomes.

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Middle and anterior scalene muscle

A Subclavian artery

Brachial plexus

First rib

Brachial plexus

B

FIGURE 8-1

(A) Supraclavicular block. The interscalene groove is identified at the clavicular level, typically 1.5 to 2.0 cm posterior to the midpoint of the clavicle. Palpation of the subclavian artery at this site confirms the landmark. A 22-gauge, 4-cm needle is directed in a caudad, slightly medial and posterior direction until either a paresthesia or motor response is elicited or the first rib is encountered. If the first rib is encountered without elicitation of a paresthesia, the needle can be systematically walked anteriorly and posteriorly along the rib until the plexus or the subclavian artery is located. Location of the artery provides a useful landmark; the needle can be withdrawn and reinserted in a more posterolateral direction that usually results in a paresthesia or motor response. On localization of the brachial plexus, a total volume of 20 to 30 mL of solution. (B) The three trunks are compactly arranged at the level of the first rib. (Redrawn from Wedel, D. J., and Horlocker, T. T.: Nerve blocks. In Miller, R. D. [ed.]: Miller’s Anesthesia, 6th ed. Philadelphia: Elsevier, 2005, p. 1685, with permission.)

TABLE 8-1

Regional Anesthetic Techniques for Elbow Surgery*

Brachial Plexus Technique

Level of Blockade

Peripheral Nerves Blocked

Surgical Applications

Comments

Axillary

Peripheral nerve

Radial, ulnar, median; musculocutaneous unreliably blocked

Surgery to forearm and hand, less used for procedures about the elbow

Unsuitable for surgery proximal to midhumerus; patient must be able to abduct the arm to perform block

Infraclavicular

Cords

Radial, ulnar, median, musculocutaneous, axillary

Surgery to elbow, forearm and hand

Catheter site (near coracoid process) easy to maintain; no risk of hemothorax or pneumothorax

Supraclavicular

Distal trunkproximal cord

Radial, ulnar, median, musculocutaneous, axillary

Surgery of midhumerus, elbow, forearm, and hand

Risk of pneumothoraxunsuitable for outpatient procedures; phrenic nerve paresis in 30% of cases

*Duration of block performed with long-acting local anesthetic (bupivacaine or ropivacaine) is 12 to 20 hours; intermediate-acting agents (lidocaine or mepivacaine) will resolve after 4 to 6 hours.

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and surgical outcomes compared with systemic opioids but with fewer side effects.4,11 These reports suggest that continuous peripheral techniques may be the optimal analgesic method following elbow surgery. Appreciation of the indications, benefits, and side effects associated with both conventional and novel analgesic approaches is paramount to maximizing rehabilitative efforts and improving patient satisfaction.

Pectoral muscle greater Coracobrachia muscle Biceps muscle

MULTIMODAL ANALGESIA AND PERIPHERAL BLOCKADE

FIGURE 8-2

Multimodal analgesia is a multidisciplinary approach to pain management, with the aim of maximizing the positive aspects of the treatment while limiting the associated side effects. Because many of the negative side effects of analgesic therapy are opioid related (and dose dependent), limiting perioperative opioid use is a major principle of multimodal analgesia. Not surprisingly, the efficacy and side effects of analgesic therapy are major determinants of patient satisfaction. In a prospective survey of 10,811 patients, after adjusting for patient and surgical factors, moderate or severe postoperative pain and severe nausea and vomiting were associated with patient dissatisfaction.18 The use of single-injection and continuous brachial plexus techniques and a combination of opioid and nonopioid analgesic agents for breakthrough pain results in superior pain control, attenuation of the stress response, and decreases opioid requirements.

Axillary artery Ulnar nerve Radial nerve Median nerve

Musculocutaneous nerve

Axillary block. The arm is abducted at right angles to the body and the axillary artery identified. Proximal needle placement and maintenance of distal digital pressure facilitate proximal spread of the local anesthetic. Several methods of identifying the brachial plexus (transarterial injection, elicitation of paresthesia or motor response) have been described, all with reportedly good results. Overall, multiple injections (identifying more than one peripheral nerve) may shorten the onset and increase the reliability of blockade. (Redrawn from Wedel, D. J., and Horlocker, T. T.: Nerve blocks. In Miller, R. D. [ed.]: Miller’s Anesthesia, 6th ed. Philadelphia: Elsevier, 2005, p. 1685, with permission.)

CONVENTIONAL ANALGESIC METHODS Parenteral Opioid Analgesics

POSTOPERATIVE ANALGESIA Patients undergoing major upper extremity surgery experience substantial postoperative pain. Indeed, 30% of patients undergoing ambulatory hand and elbow surgery reported moderate to severe pain at 24 hours postoperatively.16 Failure to provide adequate analgesia impedes early physical therapy and rapid rehabilitation, which are important for maintaining joint range of motion, facilitating hospital dismissal and preventing readmission. Traditionally, postoperative analgesia following major upper extremity surgery was provided by intravenous patient-controlled analgesia (PCA). However, opioids do not consistently provide adequate pain relief and often cause sedation, constipation, nausea/vomiting, and pruritus. Recently, clinical series have consistently reported that continuous brachial plexus block provided a superior quality of analgesia

When adequate analgesia is achieved with systemic opioids, side effects, including sedation, nausea, and pruritus, are common. However, despite these well-defined side effects, opioid analgesics remain widely used for postoperative pain relief. Systemic opioids may be administered by intravenous, intramuscular, and oral routes. Current analgesic regimens typically employ intravenous PCA for 24 to 48 hours postoperatively, with subsequent conversion to oral agents. The PCA device may be programmed for several variables including bolus dose, lockout interval, and background infusion. The optimal bolus dose is determined by the relative potency of the opioid; insufficient dosing results in inadequate analgesia, whereas excessive dosing increases the potential for side effects, including respiratory depression. Likewise, the lockout interval is based on the onset of analgesic effects; too short of a lockout interval allows the patient to self-administer additional medication before achieving the full analgesic effect (and may result

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TABLE 8-2

Intravenous Opioids for Patient-Controlled Analgesia

Agent

Bolus

Lockout Interval

4-Hour Maximum Dose

Infusion Rate*

Fentanyl (10 mcg/mL)

10-20 μ

3-5 min

300 μ

20-100 μ/hr

0.1-0.2 mg

5-10 min

3 mg

0.1-0.2 mg/hr

Hydromorphone (Dilaudid) (0.2 mg/mL) Meperidine (10 mg/mL)

†

Morphine sulfate (1 mg/mL)

5-25 mg

5-10 min

200 mg

5-15 mg/hr

0.5-2.5 mg

5-10 min

30 mg

1-10 mg/hr

*A background infusion rate is not recommended for opioid-naïve patients. † Meperidine limit in healthy patients should be 800 mg in first 24 hours, then 600 mg every 24 hours thereafter. From Horlocker, T. T.: Anesthesia and pain management. In Berry, D. J., Trousdale, R. T., Dennis, D., and Paprosky, W. (eds.): Revision Hip and Knee Arthroplasty. Philadelphia: Lippincott Williams & Wilkins (in press). Used with permission.

in accumulation/overdose of the opioid). A prolonged lockout interval will not allow adequate analgesia. The optimal bolus dose and lockout interval are not known, but ranges have been determined (Table 8-2). Varying the settings within these ranges appears to have little effect on analgesia or side effects. Although most PCA devices allow the addition of a background infusion, routine use in adult opioid-naïve patients is not recommended. There may be a role for a background opioid infusion in opioid-tolerant patients, however. Owing to the variation in patient pain tolerance, PCA dosing regimens may need to be adjusted in order to maximize the benefits and minimize the incidence of side effects. Despite the ease of administration and titratability, parenteral opioids may not provide adequate analgesia for major upper extremity surgery, particularly with movement, as evidenced by pain scores in the moderate to severe range in the first 2 days postoperatively.16 The adverse effects of opioid administration can cause serious complications in patients undergoing major orthopedic procedures. In a systematic review, Wheeler et al25 reported gastrointestinal side effects (nausea, vomiting, ileus) in 37%, cognitive effects (somnolence and dizziness) in 34%, pruritus in 15%, urinary retention in 16%, and respiratory depression in 2% of patients receiving PCA opioid analgesia.

Nonopioid Analgesics The addition of nonopioid analgesics reduces opioid use, improves analgesia, and decreases opioid-related side effects (Table 8-3). The multimodal effect is maximized through selection of analgesics that have complementary sites of action. For example, acetaminophen acts predominantly centrally, whereas other nonsteroidal anti-inflammatory drugs (NSAIDs) exert their effects peripherally.

Acetaminophen The mechanism of analgesic action of acetaminophen has not been fully determined. Acetaminophen may act

predominantly by inhibiting prostaglandin synthesis in the central nervous system. Acetaminophen has very few adverse side effects and is an important addition to the multimodal postoperative pain regimen, although the total daily dose must be limited to less than 4000 mg. The administration should be scheduled (not just on an as-needed basis) to maximize the pharmacologic effects. It is also important to note that many oral analgesics are an opioid-acetaminophen combination (Table 8-4). In these preparations, the total dose of opioid will be restricted to the acetaminophen ingested.

Nonsteroidal Anti-inflammatory Drugs The NSAIDs have a mechanism of action through the cyclooxygenase (COX) enzymatic pathway, and ultimately block two individual prostaglandin pathways. The COX-1 pathway is involved in prostaglandin E2– mediated gastric mucosal protection and thromboxane effects on coagulation. The inducible COX-2 pathway is mainly involved in the generation of prostaglandins included in the modulation of pain and fever but has no effect on platelet function or the coagulation system. In general, NSAIDs block both the COX-1 and COX-2 pathways. Advantages of the COX-2 inhibitors are the lack of platelet inhibition and a decreased incidence of gastrointestinal effects. The introduction of selective COX-2 inhibitors represented a breakthrough in perioperative pain management. Because they do not interfere with the coagulation system COX-2 inhibitors may be continued until the time of surgery and also may be administered in the immediate postoperative period. The perioperative administration of rofecoxib has been shown to have a significant opioid-sparing effect after major orthopedic surgery with no significant increase in perioperative bleeding.22,23 However, despite their efficacy, two (rofecoxib [Vioxx, Merck & Co., Whitehouse Station, NJ], valdecoxib [Bextra, Searle, Skokie, IL]) of three COX-2 inhibitors were voluntarily removed from general use because of an increased

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TABLE 8-3

Oral Nonopioid Analgesics

Analgesic

Dose

Dosing Interval

Maximum Daily Dose

Comments

Acetaminophen

500-1000 mg PO

Q 4-6 h

4000 mg

As effective as aspirin; 1000 mg more effective than 650 mg in some patients

Celcoxib (Celebrex)

400 mg initial, then 200 mg PO

Q 12 h

800 mg

Celecoxib is the only cyclooxygenase (COX)-2 inhibitor available in North America.

Aspirin

325-1000 mg PO

Q 4-6 h

4000 mg

Most potent antiplatelet effect

Ibuprofen (Advil, Motrin, Nuprin, others)

200-400 mg PO

Q 4-6 h

3200 mg

200 mg equal to 650 mg of aspirin or acetaminophen

Naproxen (Aleve, Naprosyn, others)

500 mg PO

Q 12 h

1000 mg

250 mg equal to 650 mg of aspirin, but with longer duration

Ketorolac (Toradol)

15-30 mg PO, IM/IV

Q 4-6 h

60 mg (>65 years); 120 mg (≤ 65 years)

Comparable to 10 mg morphine; reduce dose in patients weighing <50 kg or with renal impairment; total duration of administration is 5 days

Tramadol (Ultram)

50-100 mg PO

Q6h

400 mg; less in cases of renal or hepatic disease

Combination product of tramadol/acetaminophen (Ultracet) is also available

IM, intramuscularly; IV, intravenously; PO, orally. Adapted from Mayo Clinic joint pathway, in Lennon, R. L., and Horlocker, T. T. (eds.): Mayo Clinic Analgesic Pathway: Peripheral Blockade for Major Orthopedic Surgery. Florence, KY: Taylor and Francis Group, 2006. By permission Mayo Foundation for Medical Education and Research.

relative risk for confirmed cardiovascular events, such as heart attack and stroke, after 18 months of treatment. The major side effects limiting NSAID use for postoperative pain control (renal failure, platelet dysfunction, and gastric ulcers or bleeding) are related to the nonspecific inhibition of the COX-1 enzyme.24 Advantages of the COX-2 inhibitors are the lack of platelet inhibition and a decreased incidence of gastrointestinal effects. All NSAIDs have the potential to cause serious renal impairment. Inhibition of the COX enzyme may have only minor effects in the healthy kidney, but unfortunately can lead to serious side effects in elderly patients or those with a low-volume condition (blood loss, dehydration, cirrhosis, or heart failure). Therefore, NSAIDs should be used cautiously in patients with underlying renal dysfunction, specifically in the setting of volume depletion due to blood loss.24 The effect of NSAIDs on bone formation and healing is of concern in the orthopedic patient population. Although the data are conflicting, there is evidence from animal studies that COX-2 inhibitors may inhibit bone healing.7 Thus, the adverse effects of COX-2 inhibitors must be weighed against the

benefits. Until definitive human trials are performed, it is reasonable to be cautious with the use of NSAIDs and COX-2 inhibitors, especially when bone healing is critical. To date, however, there is no evidence that COX-2 inhibitors have a clinically important effect on bone ingrowth.

Tramadol Tramadol (Ultram, Ortho McNeil Pharmaceutical, Raritaran, NJ) is a centrally acting analgesic that is structurally related to morphine and codeine. Its analgesic effect is through binding to the opioid receptors as well as blocking the reuptake of both norepinephrine and serotonin. Tramadol has gained popularity because of the low incidence of adverse effects, specifically respiratory depression, constipation, and abuse potential. Tramadol has been shown to provide adequate analgesia, superior to placebo and comparable with various opioid and nonopioid analgesics for the treatment of acute pain. Thus, tramadol may be used as an alternative to opioids in a multimodal approach to postoperative pain, specifically in patients who are intolerant to opioid analgesics.

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TABLE 8-4

Oral Opioid Analgesics

Analgesic

Dose

Dosing Interval

Maximum Daily Dose

Comments

Extended release oxycodone (Oxycontin)

10-20 mg PO

Q 12 h

Limit to total of four doses to avoid accumulation and opioid-related side effects

Extended release morphine (MS Contin)

15-30 mg PO

Q 8-12 h

Limit to total of four doses to avoid accumulation and opioid-related side effects

Oxycodone (Roxicodone)

5-10 mg PO

Q 4-6 h

Combination products* of oxycodone/acetaminophen (Percocet, Tylox) and oxycodone/ aspirin (Percodan) are also available

Hydromorphone (Dilaudid)

2-4 mg PO

Q 4-6 h

Also available as Dilaudid suppository (3 mg) with 6-8 hr effect

Hydrocodone (Lortab,Vicodin, Zydone)

5-10 mg PO

Q 4-6 h

All preparations contain acetaminophen* Combination products* of codeine/ acetaminophen (Tylenol #2®, Tylenol #3®, Tylenol #4®) and codeine/aspirin (Empirin® with codeine) are also available

Codeine

30-60 mg PO

Q4h

Propoxyphene (Darvon)

50-100 mg PO

Q 4-6 h

600 mg propoxyphene

Combination products* of propoxyphen/acetaminophen (Darvocet, Propoxacet, Tylenol #4) and propoxyphene/aspirin are also available

Tramadol (Ultram®)

50-100 mg PO

Q6h

400 mg; less in cases of renal or hepatic disease

Combination product of tramadol/ acetaminophen (Ultracet) is also available

PO, orally. *Dose in combination products limited by total acetaminophen or aspirin ingestion Adapted from: Mayo Clinic joint pathway, in Lennon, R. L., and Horlocker, T. T. (eds.): Mayo Clinic Analgesic Pathway: Peripheral Blockade for Major Orthopedic Surgery. Florence, KY: Taylor and Francis Group, 2006. By permission Mayo Foundation for Medical Education and Research.

Oral Opioids Oral opioids (see Table 8-4) are available in immediaterelease and controlled-release formulations. Although immediate-release oral opioids are effective in relieving moderate to severe pain, they must be administered as often as every 4 hours. When these medications are prescribed “as needed” (prn), there may be a delay in the administration and a subsequent increase in pain. Furthermore, interruption of the dosing schedule, particularly during the night, may lead to an increase in the patient’s pain. The Acute Pain Management Guidelines developed by the Agency for Healthcare Policy and Research1 recommend a fixed dosing schedule for all patients requiring opioid medications for more than 48 hours postoperatively. The adverse effects of oral opioid administration are considerably less compared with that of intravenous administration, and are mainly gastrointestinal in nature.25 A controlled-release formulation of oxycodone (OxyContin, Purdue Pharma, Norwalk, CT) is also available

and has been shown to provide therapeutic opioid concentrations and sustained pain relief over an extended time period. Administration of controlled-release oxycodone for 72 hours postoperatively improves analgesia and is associated with less sedation, vomiting, and sleep disturbances when compared with oxycodone given on either a fixed-dose or an as-needed basis.21 Therefore, a multimodal analgesic approach may include scheduled administration of controlled-release oxycodone combined with prn oxycodone for breakthrough pain to maximize the analgesic effect and decrease the associated side effects.

CONTINUOUS BRACHIAL PLEXUS ANALGESIA As previously discussed, although single-injection brachial plexus techniques have been used, the duration of effect is often not sufficient to result in substantial improvements in analgesia or outcome.15 Recent appli-

Chapter 8 General and Regional Anesthesia and Postoperative Pain Control

cations of peripheral nerve block techniques have allowed prolonged postoperative analgesia (with an indwelling catheter) to assist rehabilitation and facilitate hospital dismissal.3,20 In addition, moderately severe upper extremity procedures, including total elbow arthroplasty, may be performed on an outpatient basis when analgesia is provided with an indwelling brachial plexus catheter.11,13 In all applications, the addition of a continuous brachial plexus catheter results in superior analgesia with fewer side effects than conventional systemic analgesic therapy.4,11 Brachial plexus catheters may be inserted using supraclavicular, infraclavicular, and axillary approaches. Although analgesia is produced in all nerve distributions, the block may not provide satisfactory surgical anesthesia, even with administration of more potent local anesthetic solutions. Therefore, continuous brachial plexus block is more often used to provide postoperative analgesia rather than intraoperative anesthesia. Catheters may be left indwelling for 4 to 7 days without adverse effects.10 A continuous infusion of local anesthetic solution, such as bupivacaine 0.125%, prevents vasospasm and increases circulation after limb/digit replantation or vascular repair. More concentrated solutions (0.2% ropivacaine or bupivacaine) result in complete sensory block and allow early joint mobilization after painful surgical procedures to the elbow.20 Local anesthetic selection is based on the duration and degree of sensory or motor block desired.3,12,20 Because analgesic requirements vary with activity, a basal infusion with intermittent on-demand boluses allows greater flexibility.12 The presence of dense sensory or motor block is not a contraindication to hospital dismissal. However, the patient should be informed of the anticipated duration of analgesia during the preoperative visit and instructed to protect the blocked extremity until block resolution (Box 8-1). Neurologic dysfunction and intravascular injection are the primary concerns associated with peripheral blockade. However, in a large series involving more than 50,000 peripheral blocks, there were six seizures and 12 patients who reported postoperative nerve injury. Most neurologic complications were transient.2 A series of nearly 4000 peripheral blocks, including 1650 axillary blocks, 69 patients (1.7%) developed transient neurologic dysfunction.5 Complete recovery occurred in 4 to 12 weeks in all patients but one, who required 25 weeks. Despite the placement of a continuous catheter and extended exposure to local anesthetics, neurologic complications following indwelling brachial plexus catheters are uncommon, with the frequency similar to that of single-injection techniques.3 Finally, the performance of a regional technique in a patient with a pre-existing neurologic condition remains controversial. Although the data are sparse, several retrospective series suggest

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BOX 8-1 Instructions for At-Home Brachial Plexus Catheter Patients 1. You are receiving local anesthetic through a small catheter near your nerves to help with your pain after surgery. This may not take away all of your pain but should help greatly. You may take your pain medicines as prescribed by your doctor. The nurse will review this with you. The local anesthetic will initially make your arm very numb. Over time, this degree of numbness will decrease, but usually your arm is not normal until the catheter is removed. Because your arm or leg will not function normally, YOU SHOULD NOT DRIVE. 2. The doctors and nurses will review the pump instructions with you. If you have any problems with the pump, call the technical support number or the number the doctor has given you. 3. Complications that could potentially occur include the following: • The catheter may fall out. If this occurs, make sure to take some of your pain medicine and turn the pump off. • Fluid may leak around the catheter. You can change or reinforce the dressing, if necessary. This is usually not a problem. • The catheter may migrate into a blood vessel and cause high levels of local anesthetic. Symptoms of high levels of local anesthetic may include the following: • Drowsiness • Dizziness • Blurred vision • Slurred speech • Poor balance • Tingling around lips/mouth • Other 4. You should keep your arm in a sling unless doing therapy. 5. Call your physician for medical assistance if any of the following symptoms occur: • Unusual drowsiness • Uncontrollable pain • Uncontrollable vomiting

that these patients are not at a significantly increased risk of neurologic complications.8,9

INTRA-ARTICULAR CATHETERS Intra-articular injection of local anesthetics is a wellestablished method of providing short-term analgesia in patients undergoing ambulatory procedures. Often near-complete pain relief is achieved for 4 to 6 hours, at which time the local anesthetic effect resolves and systemic analgesics are required. Recently, the introduction of disposable elastomeric and programmable pumps

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3

2 1

2.

3.

4. 4

5

6

5.

FIGURE 8-3

Disposable pumps for intra-articular and neural sheath infusion at home. Portable infusion pumps (1) Accufuser (McKinley Medical, Wheat Ridge, CO); (2) Sgarlato (Sgarlato Labs, Los Gatos, CA), (3) Stryker PainPump, (Stryker Instruments, Kalamazoo, MI); (4) MedFlo II, (MPS Acacia, Brea, CA); (5), C-Bloc (IFlow Corp, Lake Forest, CO); and (6) Microject PCA (Sorenson Medical, West Jordan, UT). (From Ilfeld, B. M., Morey, T. E., and Enneking, F. K.: The delivery rate accuracy of portable infusion pumps used for continuous regional analgesia. Anesth. Analg. 95:1331, 2002.)

6.

7. 8.

9.

(Fig. 8-3) has allowed extended infusion (2 to 4 days) of local anesthetic.10 Because an intra-articular infusion does not provide complete blockade of the brachial plexus (compared with a neural sheath catheter), analgesia is often incomplete and oral opioids are required, although consumption is reduced. Note that all patients with infusions of local anesthetic solutions must be educated as to the signs and symptoms of local anesthetic toxicity and given instruction on how and when to call their physician for assistance (see Box 8-1). In summary, sustained and substantial outcome improvements, including joint range of motion and decreased hospital stay are dependent on the method or methods used to provide postoperative analgesia in patients undergoing surgery about the elbow. Recent studies have demonstrated that brachial plexus blocks combined with oral analgesics administered on a schedule provide a quality of analgesia and functional outcomes superior to systemic intravenous opioid analgesia and with fewer side effects. Continued collaborations between orthopedic surgeons and anesthesiologists are necessary to further advance the perioperative management of this patient population.

10.

11.

12.

13.

14.

15.

References 1. Acute Pain Management Guideline Panel. Acute pain management: operative or medical procedures and trauma-

16.

clinical practice guideline. AHCPR Pub No 92-0032. Rockville, MD: Agency for Health Care Policy and Research, Public Health Service, U.S. Department of Health and Human Services, 1992, p. 15. Auroy, Y., Benhamou, D., Bargues, L., Ecoffey, C., Falissard, B., Mercier, F. J., Bouaziz, H., and Samii, K.: Major complications of regional anesthesia in France: the SOS regional anesthesia hotline service. Anesthesiology 97:1274, 2002. Bergman, B. D., Hebl, J. R., Kent, J., and Horlocker, T. T.: Neurologic complications of 405 continuous axillary catheters. Anesth. Analg. 96:247, 2003. Brown, A. R.: Anaesthesia for procedures of the hand and elbow. Best Pract. Res. Clin. Anaesthesiol. 16:227, 2002. Fanelli, G., Casati, A., Garancini, P., and Torri, G.: Nerve stimulator and multiple injection technique for upper and lower limb blockade: Failure rate, patient acceptance, and neurologic complications. Study Group on Regional Anesthesia. Anesth. Analg. 88:847, 1999. Fuzier, R., Fuzier, V., Albert, N., Decramer, I., Samii, K., and Olivier, M.: The infraclavicular block is a useful technique for emergency upper extremity analgesia. Can. J. Anaesth. 51:191, 2004. Gajraj, N. M.: Cyclooxygenase-2 inhibitors. Anesth. Analg. 96:1720, 2003. Hebl, J. R., Horlocker, T. T., Sorenson, E. J., and Schroeder, D. R.: Regional anesthesia does not increase the risk of postoperative neuropathy in patients undergoing ulnar nerve transposition. Anesth. Analg. 93:1606, 2001. Hebl, J. R., Kopp, S. L., Schroeder, D. R., and Horlocker, T. T.: Neurologic complications after neuraxial anesthesia or analgesia in patients with preexisting peripheral sensorimotor neuropathy or diabetic polyneuropathy. Anesth. Analg. 103:1294, 2006. Ilfeld, B. M., Enneking, F. K.: A portable mechanical pump providing over four days of patient-controlled analgesia by perineural infusion at home. Reg. Anesth. Pain Med. 27:100, 2002. Ilfeld, B. M., Morey, T. E., and Enneking, F. K.: Continuous infraclavicular brachial plexus block for postoperative pain control at home: a randomized, double-blinded, placebo-controlled study. Anesthesiology 96:1297, 2002. Ilfeld, B. M., Morey, T. E., and Enneking, F. K.: Infraclavicular perineural local anesthetic infusion: a comparison of three dosing regimens for postoperative analgesia. Anesthesiology 100:395, 2004. Ilfeld, B. M., Wright, T. W., Enneking, F. K., and Vandenborne, K.: Total elbow arthroplasty as an outpatient procedure using a continuous infraclavicular nerve block at home: A prospective case report. Reg. Anesth. Pain Med. 31:172, 2006. Koscielniak-Nielsen, Z. J., Rotboll, N. P., and Risby, M. C.: A comparison of coracoid and axillary approaches to the brachial plexus. Acta Anaesthesiol. Scand. 44:274, 2000. McCartney, C. J., Brull, R., Chan, V. W., Katz, J., Abbas, S., Graham, B., Nova, H., Rawson, R., Anastakis, D. J., and von Schroeder, H.: Early but no long-term benefit of regional compared with general anesthesia for ambulatory hand surgery. Anesthesiology 101:461, 2004. McGrath, B., Elgendy, H., Chung, F., Kamming, D., Curti, B. and King, S.: Thirty percent of patients have moderate to

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17. 18.

19.

20.

21.

severe pain 24 hr after ambulatory surgery: a survey of 5,703 patients. Can. J. Anaesth. 51:886, 2004. Morrey, B. F., and Bryan, R. S.: Complications of total elbow arthroplasty. Clin. Orthop. 170:204, 1982. Myles, P. S., Williams, D. L., Hendrata, M., Anderson, H., and Weeks, A. M.: Patient satisfaction after anaesthesia and surgery: results of a prospective survey of 10,811 patients. Br. J. Anaesth. 84:6, 2000. Neal, J. M., Hebl, J. R., Gerancher, J. C., and Hogan, Q. H.: Brachial plexus anesthesia: essentials of our current understanding. Reg. Anesth. Pain Med. 27:402, 2002. ODriscoll, S. W., and Giori, N. J.: Continuous passive motion (CPM): theory and principles of clinical application. J. Rehabil. Res. Dev. 37:179, 2000. Reuben, S. S., Connelly, N. R., and Maciolek, H.: Postoperative analgesia with controlled-release oxycodone for

22.

23.

24.

25.

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outpatient anterior cruciate ligament surgery. Anesth. Analg. 88:1286, 1999. Reuben, S. S., and Connelly, N. R.: Postoperative analgesic effects of celecoxib or rofecoxib after spinal fusion surgery. Anesth. Analg. 91:1221, 2000. Reuben, S. S., Fingeroth, R., Krushell, R., and Maciolek, H.: Evaluation of the safety and efficacy of the perioperative administration of rofecoxib for total knee arthroplasty. J. Arthroplasty 17:26, 2002. Stephens, J. M., Pashos, C. L., Haider, S., and Wong, J. M.: Making progress in the management of postoperative pain: a review of the cyclooxygenase 2-specific inhibitors. Pharmacotherapy 24:1714, 2004. Wheeler, M., Oderda, G. M., Ashburn, M. A., and Lipman, A. G.: Adverse events associated with postoperative opioid analgesia: a systematic review. J. Pain 3:159, 2002.

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CHAPTER

9

Principles of Elbow Rehabilitation Jay Smith and Bernard F. Morrey

INTRODUCTION The goal of elbow rehabilitation is to restore optimal, pain-free function within the anatomic and physiologic limitations of the patient. To achieve this goal, the clinician should adhere to several principles to guide the rehabilitation process: (1) establish a complete and accurate diagnosis, (2) control pain and inflammation, (3) implement early, atraumatic motion, (4) re-establish neuromuscular control about the elbow, and (5) rehabilitate the elbow in context of the kinetic chain. The purpose of this chapter is to review these principles as they apply to a wide variety of atraumatic and atraumatic elbow disorders. For more detailed discussion of specific rehabilitation protocols, readers are referred to the appropriate chapters in this text.

ESTABLISH A COMPLETE AND ACCURATE DIAGNOSIS Successful rehabilitation is predicated on a complete understanding of the anatomic and physiologic factors pertaining to a particular elbow disorder. The elbow joints (humeroulnar, humeroradial, proximal radioulnar), nerves, vessels, capsule and ligaments, and muscles, as well as adjacent articulations (distal radioulnar and shoulder) should be considered. Anatomic alterations in these tissues will define initial motion restrictions as well as the potential for restoration of motion and stability. However, it is ultimately the patient’s physiologic age and biologic healing potential that will determine how much of this potential is realized. Some patients heal poorly and may be prone to ongoing instability, whereas others exhibit a propensity for scar formation and will develop stiffness despite the best efforts of the treatment team.32 From our perspective, this sometimes dramatic individual variation in the healing response assumes a dominant role in the recovery of some patients. Throughout the rehabilitation process, the physiologic stage of healing directly affects the rehabilitation program.50 During the inflammatory stage, the primary

goals are pain and edema control and adherence to stable arcs of motion to protect tissues at risk. During the fibroblastic phase, controlled stresses may be increased to promote more normal collagen formation, and low-level strengthening is implemented to reestablish neuromuscular control. Finally, during the remodeling phase, stretching and strengthening exercises are advanced, and functional restoration is pursued. The clinician must be constantly aware of the physiologic status of the elbow. The elbow is an unforgiving articulation with significant bony congruity and a tendency to develop inflammation and stiffness.32 Overzealous rehabilitation efforts can quickly regress the elbow from the fibroblastic phase back into the inflammatory phase. Consequently, clinicians should constantly monitor the status of the elbow and modify the rehabilitation program accordingly. This process requires appropriate follow-up, patient education, and constant communication between members of the treatment team.

PATIENT PARTICIPATION As with any successful program, but particularly at the elbow, the patient must be made to understand their role in the recovery process. The clinician and therapist must avoid having the patient become dependent on them, or on formal rehabilitation sessions. The key is to successfully transfer responsibility for improvements to the patient. They become their own therapists.

REDUCE PAIN AND INFLAMMATION During the acute post-traumatic or postsurgical period, the primary goal is to control pain and inflammation. The elbow tends to get stiff as a result of adhesion formation and muscular cocontraction.32,50 PRRICEMM principles are applied to reduce pain, edema, and inflammation—Protection, relative Rest, Ice, Compression, Elevation, Medications, and Modalities. Protection and Relative Rest Appropriate protection and relative rest require balancing the need to protect healing tissues with the adverse effects of immobility. Total immobility can precipitate rapid deconditioning, whereas tenuous tissues can be easily damaged by aggressive motion.2,4,21,50 Diagnosis-specific safe elbow motion arcs guide early motion and are discussed in the next section. Bracing or splinting is often prescribed to protect healing tissues and are discussed in Chapter 11. Patients can immediately initiate general aerobic fitness programs (e.g., Exercycle) and exercises with their three unaffected limbs. With respect to the affected limb, patients may perform wrist-hand and shoulder motions

Chapter 9 Principles of Elbow Rehabilitation

while avoiding injurious elbow positions or loads. For example, shoulder abduction will produce a varus elbow stress and therefore is contra-indicated in the early post-traumatic/post-operative period after lateral collateral ligament complex injury/reconstruction.41 Ice Physiologically, ice can reduce inflammation, modulate pain and control muscle spasm.10 Ice is applied regularly in the acute post-traumatic/postoperative period, and intermittently postexercise/postactivity in the later phases of healing.50 Caution should be exercised when applying ice over traversing nerves, particularly those that have been surgically transposed.7

Compression wrapping and elevation above heart level promote edema control. Both static and intermittent air-compression devices have been successfully used in the early stages of rehabilitation. Although published scientific investigation is lacking, a case-control pilot study from our institution documented a statistically significant advantage with respect to edema control for a compression cryotherapy device (Aircast) applied following total elbow arthroplasty (Fig. 9-1).1

Compression and Elevation

Medications Medication use is determined by the specific diagnosis, healing stage, and physician preference.

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Narcotics, nonsteroidal anti-inflammatory drugs (NSAIDs), and acetaminophen are used based upon an individualized risk-benefit ratio analysis. Although NSAIDs may provide short-term analgesic benefits in lateral elbow tendinopathy (“tennis elbow”),20 they are typically used with more caution in the post-traumatic/ postsurgical elbow. Some NSAIDs inhibit platelets and may result in hemorrhage, whereas others may actually inhibit the healing response.30,48 Nonetheless, controlling inflammation with medication is an important element of the postinjury/postoperative recovery period. Patients with inflammatory arthropathies may benefit from rheumatologic consultation to optimize systemic medications. In tennis elbow, corticosteroid injections do provide reliable relief for 4 to 6 weeks in most cases but may not affect long-term outcome and often cause temporary symptom exacerbation.27,45 Further investigation is needed to clarify the initial positive results reported for topical nitric oxide,42 platelet-rich plasma injections,31 and botulinum toxin injections24 in tennis elbow. Interested readers are referred to Chapter 44 for a more in depth discussion. Modalities Other than ice, the role of modalities in the acute post-traumatic/postsurgical period remains poorly defined. During periods of muscle inhibition, highvoltage galvanic stimulation (HVGS)–induced muscle contractions have been used to reduce pain and edema.50 As elbow motion improves, electromyographic (EMG)biofeedback can be used to reduce muscle cocontractions, initially inhibiting the antagonists and subsequently cuing on the agonists.13,50 These modalities should be applied carefully in conjunction with constant reassessment. With respect to tennis elbow, iontophoresis appears to offer some short-term benefit,38 the roles of acupuncture and shock wave therapy remain inconclusive,8,11 and pulsed electrical magnetic stimulation47 and laser therapy8 appear to have no role.

IMPLEMENT EARLY ATRAUMATIC MOTION

FIGURE 9-1

Cryocuff (Aircast) provides both compression and cold to the elbow.

The elbow exhibits a marked tendency to rapidly develop intra-articular and periarticular adhesions, resulting in motion loss that may eventually compromise outcome.32 Early motion is desirable to minimize or prevent adhesion formation,32,51 mitigate against the deleterious effects of immobility,2,4,21,50 facilitate lymphatic and venous drainage,13 and modulate pain through proprioceptive mechanisms.4,13,52 These benefits must be weighed against the risk of irritating healing tissues, thereby deleteriously affecting the rehabilitation program. The long-term range-of-motion goals for the patient must be established, and the patient must have a clear

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understanding of this goal. The potential range of motion is defined by the specific diagnosis and any posttraumatic/postsurgical anatomic alterations. Whether this potential is achieved depends on the ability of the rehabilitation program to optimize the patient’s physiology, as well as the patient’s compliance with the program. Normal elbow range of motion is 0 to 5 degrees of hyperextension, 134 to 145 degrees of flexion, 75 degrees pronation, and 85 degrees supination.28,35 Most activities of daily living are performed within 30 to 130 degrees flexion, 50 degrees pronation, and 50 degrees supination.28,35 However, some daily activities (e.g., reaching to the opposite side of the head), as well as many recreational and vocational activities, may require greater motion.17,36 The patient and the treatment team must understand the expected limitations of the elbow in the context of the potential functional needs, thereby defining realistic functional expectations for “success.” To implement early, atraumatic motion, the clinician must completely understand the patient’s anatomy and physiologic healing stage with respect to all tissues involved—joints, capsule, ligaments, muscle-tendon units, nerves, and vessels. In addition, the elbow must be constantly reassessed for increased pain, swelling, or motion loss, and the rehabilitation program modified accordingly. The initial arc of protected elbow motion is diagnosis specific. For example, a dislocated elbow with lateral ulnar collateral ligament (LUCL) insufficiency is most stable in flexion and pronation,15,33,40 whereas a dislocation with bilateral ligament injuries (LUCL and medial ulnar collateral ligament [MUCL]) and a radial head fracture is kept in neutral pronationsupination to modulate humeroradial contact stress while balancing ligamentous tension.13,32 A normally located ulnar nerve may be irritated by excessive or prolonged flexion, whereas a transposed ulnar nerve, particularly if adhered, may be irritated by excessive or prolonged extension.50 Interested readers are referred to Chapters 28, 29, and 48 for more diagnoses-specific indepth discussion. As previously discussed, elbow bracing or splinting may be protective in the postoperative/post-traumatic period by controlling position and forces, as well as providing external stability.9 As healing progresses to the fibroblastic and remodeling phases, braces may be used to restore motion.9 Appropriate prescription, application, and compliance are the keys to success.9,18,26 Specific applications are discussed in Chapter 11.

TIMING Once safe motion arcs have been defined, motion can be prescribed based on the stage of tissue healing.13,50 A complete clinical examination is necessary to determine the healing stage, as well as the specific tissue or tissues

responsible for the motion loss.32 Assessing both the quality and quantity of motion loss is necessary to accurately prescribe range of motion within the restrictions. Bony motion blocks will not respond to rehabilitation efforts, and well-established soft tissue contractures with a hard end-feel will not respond as reliably as those with a springier end-feel.50 During the inflammatory phase, range of motion must not be aggressive, and must strictly adhere to restrictions while monitoring for regression. As the elbow enters the fibroblastic and eventually remodeling phases, range of motion may become more aggressive because tissues have healed sufficiently to absorb additional forces that will be beneficial to promote collagen reformation. During these latter phases, the clinician must constantly monitor for signs of inflammation and modify the program accordingly. Four types of range of motion are typically used during elbow rehabilitation: active assisted, active, passive, and resisted. Regardless of each type, the role of the therapist must never be so aggressive as to aggravate pain or incite inflammation. Active assisted range of motion (AAROM) is typically implemented earliest, including during the inflammatory phase. Goals are prevention of intra-articular and periarticular adhesions, promotion of cartilage healing, edema control, and pain modulation.13 Maintaining low levels of voluntary muscle activation minimizes elbow joint compression and shear forces. Gravity-assisted motion is often used during this phase, as is continuous passive motion (CPM) (see Chapter 10). Although CPM is by definition “passive,” in the early post-traumatic/postoperative period, its benefits parallel those of AAROM. During gravity-assisted flexion, the patient is positioned supine on the table, upper limb flexed to 90 degrees, and the elbow allowed to flex under the pull of gravity, as guided and assisted by the well arm.13 Gravity-assisted extension may be performed sitting with the upper limb supported, and the elbow allowed to extend under the influence of gravity, assisted by the well arm.13 Both exercises may be initiated during the inflammatory phase with diagnosis specific restrictions. As pain and edema subside, the amount of gravity and well arm assistance may be decreased, eventually transitioning to active range of motion. Active Assisted Range of Motion

Active Range of Motion (AROM) Active range of motion (AROM) may initially be performed in gravityeliminated positions (e.g., table top flexion-extension) before transitioning to antigravity positions (e.g., sagittal plane flexion-extension). Benefits of AROM parallel those of AAROM, with added benefit that AROM voluntarily activates the elbow muscles, thus stimulating

Chapter 9 Principles of Elbow Rehabilitation

neuromuscular control. AROM is performed within safe flexion-extension and pronation-supination motion arcs while monitoring loads placed on the elbow due to upper limb positioning (e.g., effect of forearm pronation on humeroradial compression force,34 effect of shoulder abduction on elbow varus force).41 Passive range of motion (PROM) may be initiated as patients enter the fibroblastic phase, or during the remodeling phase. The goal of PROM, in the form of splinting or stretching, is to induce permanent tissue length changes to gain motion.50 Clinical research supports the efficacy of appropriately applied progressive static splinting for elbow contractures19 (see Chapter 11). Although no form of stretching has been proven superior in the elbow, low-load, long-duration (LLLD) stretches are commonly used based upon supportive basic science research22 and clinical experience.50 The LLLD stretch for the anterior elbow is performed with the patient’s elbow supported, forearm held in supination to optimize anterior capsule tension19 and a small weight or low-resistance exercise band held in the hand50 (Fig. 9-2). Patients perform several repetitions of a 20-second to 2- to 3-minute stretch, or one or two repetitions of a 10- to 12-minute stretch.22,46,50 In either case, stretches are followed by AROM to re-establish neuromuscular control within the newly obtained motion arcs. The process is completed by icing the affected area in a lengthened position to reduce inadvertent inflammation produced during the stretch and to allow cooling in a lengthened position.46 During the fibroblastic and remodeling phases, additional modalities may be beneficial to facilitate motion. Use of superficial heat in the form of hot packs, whirlPassive Range of Motion (PROM)

FIGURE 9-2

Low-load long-duration stretch for anterior elbow soft tissue tightness. Elbow supported and forearm supinated to increase anterior capsular stretch. See text for details.

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pool, fluidotherapy, or a heating pad will increase local blood flow and tissue extensibility while decreasing stiffness and muscle spasm.3,49 Therefore, superficial heat may serve an adjunctive role to stretching and splinting, provided that no signs of inflammation are present. There exists a paucity of data investigating the role of ultrasound (US) in specific clinical conditions about the elbow.8,44 Limited data suggest that low-intensity, pulsed US may promote wound healing and increase fibroblastic activity while controlling inflammation,39,48 whereas high-intensity US may increase the extensibility of scar tissue through heating, particularly when accompanied or followed by stretching.8,39,44,46 There are insufficient data to support or refute the role of US in chronic tendinopathies, which can be considered a dysfunctional fibroblastic phase, although the majority of data suggest that phonophoresis (US with corticosteroid) does not offer any additional benefit over US alone.8,45 Resisted Range of Motion (RROM) Resisted range of motion (RROM) is implemented as healing allows and after AROM has been established. Therefore, formal implementation of RROM, other than antigravity AROM, is typically delayed for 8 to 12 weeks. The primary goal of RROM is to restore neuromuscular control about the elbow, a principle discussed in the following section. Joint Mobilization and Neural Gliding This approach has been advocated as an adjunctive technique to increase motion during elbow rehabilitation.12,50 In theory, joint mobilizations may reduce pain, spasm, and stiffness, but supportive scientific data are lacking.13,50 In practice, therapists will initiate low-amplitude oscillatory motions and progress to higher amplitude distraction techniques as tissue healing allows.13,50 Joint mobilizations may be preceded by heat, and are followed by PROM/stretching to gain motion, and thereafter by AROM to control the newly gained motion, as noted above. Neural gliding consists of gentle exercises to promote nerve mobility with respect to surrounding tissues and has been promoted to disperse intraneural edema, optimize axonal transport, reduce nerve adhesions, and relieve nerve-related pain.12 At this time, there is insufficient evidence to support or refute the practice of joint oscillations or neural glide techniques during the elbow rehabilitation process. Consequently, prescription should be based on the assessment of the risk-benefit ratio, availability of qualified practitioners, and financial and time constraints.

RESTORE REGIONAL NEUROMUSCULAR CONTROL Consideration of the status of the joint is essential with this component of rehabilitation. If the joint cartilage is

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compromised or if the joint surface is compromised, this element of rehabilitation should be described primarily to accomplish activities of daily living. If the joint allows, in order to optimize elbow function, neuromuscular control (NMC) must be reestablished. NMC includes strength, endurance, and coordinated muscle contractions. NMC is a prerequisite to capitalize on the functional potential provided by the range-of-motion gains during the rehabilitation program. In addition, NMC about the elbow may provide some ability to compensate for persistent instabilities despite optimal treatment. For example, coordinated muscle contraction can dynamically improve elbow stiffness,5 and at least partially compensate for instability after LUCL15 and MUCL14,43 injury or reconstruction. Early NMC training is achieved through the AAROM exercises, as previously discussed. Positions and motions are chosen based on diagnosis-specific restrictions and modified accordingly over time. As healing allows, RROM (i.e., strengthening) exercises are initiated. Strengthening exercises are prescribed in the context of a graduated program, initially emphasizing low-load, low-repetition exercise sessions performed multiple times per day (e.g., one to two sets of 10 to 20 repetitions three to five times/day). This scheme re-establishes motor control pathways while minimizing edema and overload risk.50 Finger flexion-extension, wrist ulnarradial deviation, forearm pronation-supination, and elbow flexion-extension are included. Initial isometric contractions can minimize atrophy and may provide some strength gains while controlling joint stress. Typically, 3- to 6-second submaximal isometric contractions are followed by 3 to 6 seconds of rest, repeated 10 to 20 times. Isometric exercises are initially completed in the most stable position for the patient, and are repeated two to three times per day. As the clinical situation allows, frequency is increased, less stable positions are included, and external resistance in the form of free weights, cables, or resistance tubing/bands is added. The optimal repetition-load scheme for strengthening about the elbow remains elusive, but frequency should be stressed over load, at least initially.5,13 It is not uncommon to start resisted elbow flexion exercises with a 1/4 or 1/2 kg weight, performing one set of 10 repetitions three to four times per day. As the rehabilitation progresses, loads and repetitions may be adjusted to meet the specific strength-endurance needs of the patient. Although eccentric-biased strengthening may have a role in chronic tennis elbow,29 this strengthening mode has a limited role in general elbow rehabilitation. As NMC is re-established, it is important to continually monitor the status of the elbow to ensure that injury or irritation is not occurring. In addition, the clinician must remain cognizant of safe versus unsafe positions and motion arcs, and modify the rehabilitation program

A

B FIGURE 9-3

A, Resisted wrist flexion exercise with forearm supinated to minimize elbow valgus stress after medial ulnar collateral ligament injury/repair. B, Similar to Figure 9-3A, with resisted ulnar deviation (targeting the flexor carpi ulnaris [FCU]) performed in midprosupination to minimize elbow valgus stress.

accordingly. For example, initially after MUCL reconstruction or injury, the elbow is inherently more stable with the forearm supinated. In this position, resisted finger flexion, wrist flexion (Fig. 9-3A) and ulnar deviation (see Fig. 9-3B) exercises may be safely performed to strengthen the dynamic medial elbow stabilizers as long as valgus loads are avoided by appropriate positioning.5,14,43 After LUCL injury or reconstruction, wrist extensor strengthening may be performed with the forearm pronated and supinator strengthening with the forearm supinated, in both cases to avoid a varus load on the elbow.15 Following elbow dislocation, the elbow is initially exercised in flexion due to the consistent posterior force vectors of the elbow musculature.33

Chapter 9 Principles of Elbow Rehabilitation

INTEGRATION INTO THE KINETIC-KINEMATIC CHAIN Regardless of pathoetiology, the elbow should not be rehabilitated in isolation of other joints. The elbow represents an important part of the kinetic-kinematic chain, whereby forces and motions are generated, transformed, and transferred through multiple body segments to the hand for the purpose of function.25 As a matter of fact, even if little is being done actively for the elbow, the other joints should be addressed during the recovery period. Throughout the rehabilitation process, patients are encouraged to exercise the entire body, including ipsilateral shoulder and wrist. Programs are tailored to each patient’s anticipated needs and generally include both resistance and aerobic exercise modes. As previously mentioned, the clinician should consider the position of the elbow, and consequent direct and indirect forces at all times during this process. As the elbow improves, integrated total body exercises are implemented and advanced with the goal of return to daily life, work, and sport. Research continues to elucidate the affect of proximal kinetic-kinematic chain dysfunction on incurred elbow stress.25 Consequently, clinicians should evaluate the kinetic-kinematic chain for deficits in flexibility, strength, and coordination that may be pathoetiologic in the presenting elbow disorder. A technique coach or occupational medicine specialist may identify and rectify technique flaws that produce inefficient movement and consequently overstress the elbow.16,23 In some cases, it may be necessary to intentionally increase motion or strength, or both, at adjacent body segments to compensate for permanent elbow deficits (e.g., increased shoulder abduction and internal rotation compensating for forearm pronation loss). Finally, a qualified professional should evaluate the patient’s work or sporting environment and relevant equipment to identify modifiable risk factors that may have contributed to the presenting elbow disorder.37 Placing the patient and the elbow back into the same situational stress may lead to symptom recurrence, and may compromise outcome and satisfaction.

SUMMARY Elbow rehabilitation is a challenging and dynamic process. The commitment of the physician, therapists, and patient and understanding their subjective roles is essential for success. A complete understanding of elbow mechanics and pathomechanics, open communication between patients and all members of the rehabilitation team, and patience is essential. By following the general principles outlined in this chapter (Box 9-1), clinicians

BOX 9-1

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1. Establish a Complete and Accurate Diagnosis a. Consider all tissues involved b. Understand anatomic alterations c. Assess physiologic healing stage d. Reassess throughout rehabilitation e. Communication—patient, surgeon, rehabilitation team 2. Control Pain and Inflammation a. PRRICEMM principles 3. Implement Early Atraumatic Motion a. AAROM → AROM → AAROM + PROM → RROM b. CPM (see Chapter 10) c. Monitor elbow for regression 4. Restore Regional Neuromuscular Control a. Frequency >> Intensity b. Isometric exercises initially c. Control elbow position and loads 5. Integration into the Kinetic-Kinematic Chain a. Elbow rehabilitation = total body rehabilitation b. Treat kinetic-kinematic chain deficits c. Evaluate equipment, training, and movement skills

may successfully rehabilitate a wide variety of elbow disorders while minimizing complications.

References 1. Adams, R., and Morrey, B.: The effect of cryocompression on the elbow: a prospective randomized study. AAOS Annual Meeting. Anaheim, CA, Feb 1999. 2. Akeson, W., Amiel, D., and Woo, S.: Immobility effects on synovial joints. The pathomechanics of joint contracture. Biorheology 17:95, 1980. 3. Allen, R.: Physical agents used in the management of chronic pain by physical therapists. Phys. Med. Rehabil. Clin. North Am. 17:315, 2006. 4. Amiel, D., Akeson, W., Harwood, F., and Frank, C. B.: Stress deprivation effect on metabolic turnover of the medial collateral ligament collage–a comparison between 9 and 12 week immobilization. Clin. Orthop. Rel. Res. 172:265, 1983. 5. An, K., Hui, F., Morrey, B., Linscheid, R. L., and Chao, E. Y.: Muscles across the elbow joint: A biomechanical analysis. J. Biomech. 14:659, 1981. 6. An, K.-N., and Morrey, B.: Biomechanics of the elbow. In Morrey, B. (ed.): The Elbow and Its Disorders, 3rd ed. Philadelphia, W. B. Saunders Co., 2000, p. 43. 7. Bassett, F., Kirkpatrick, J., Engelhardt, D., et al. Cryotherapy induced nerve injury. Am. J. Sports Med. 20:516, 1992. 8. Bisset, L., Paungmali, A., Vicenzino, B., and Beller, E.: A systematic review and meta-analysis of clinical trials on physical interventions for lateral epicondylalgia. Br. J. Sports Med. 39:411, 2005.

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9. Blackmore. S.: Splinting for elbow injuries and contractures. Atlas Hand Clin. 2001:21-50 10. Bleakley, D., and McDonough, S.: The use of ice in the treatment of acute soft tissue injury: a systematic review of randomized controlled trials. Am. J. Sports Med. 32:251, 2004. 11. Buchbinder, R., Green, S., Youd, J., Assendelft, W. J. J., Barnsley, L., and Smidt, N.: Shock waves for lateral elbow pain. The Cochrane Library 4:1, 2006. 12. Butler, D.: Mobilization of the nervouse system. Melbourne, Australia, Churchill Livingstone, 1991. 13. Chinchalker, S., and Szekeres, M.: Rehabilitation of elbow trauma. Hand Clin. 20:363, 2004. 14. Davidson, P., Pink, M., Perry, J., and Jobe, F. W.: Functional anatomy of the flexor pronator muscle group in relation to the medial collateral ligament of the elbow. Am. J. Sports Med. 23:245, 1995. 15. Dunning, C., Zarzour, Z. D., Patterson, S. D., Johnson, J. A., and King, G. J.: Muscle forces and pronation stabilize the lateral ligament deficient elbow. Clin. Orthop. Rel. Res. 338:118, 2001. 16. Elliot, B., Fleisig, G., and Escamilla, R.: Technique effects on upper limb loading in the tennis serve. J. Sci. Med. Sport 6:76, 2003. 17. Fleisig, G., Barrentine, S., Escamilla, R., and Andrews, J. R.: Biomechanics of overhand throwing with implications for injuries. Sports Med 1996;21:421-437. 18. Flowers, K., and LaStayo, P.: Effect of total end range time on improving passive range of motion. J. Hand Ther. 7:150, 1994. 19. Green, D., and McCoy, H.: Turnbuckle orthotic correction of elbow-flexion contractures after acute injuries. J. Bone Joint Surg. 61A:1092, 1979. 20. Green, S., Buchbinder, R., Barnsley, L., Nall, S., White, M., Smidt, N., and Assendelft, W. J. Non-steroidal antiinflammatory drugs (NSAIDS) for treating lateral elbow pain in adults. Cochrane Database Systematic Review 2, 2002. 21. Halar, E., and Bell, K.: Immobility. In DeLisa, J., and Gans, B. (eds.): Rehabilitation Medicine: Principles and Practice. Philadelphia, Lippincott-Raven, 1998, p. 1015. 22. Hardy, M., and Woodal, W.: Therapeutic effects of heat, cold, and stretch on connective tissue. J. Hand Ther. 11:148, 1998. 23. Hatch, G., Pink, M., Mohr, K., Sethi, P. M., and Jobe, F. W.: The effect of tennis racket grip size on forearm muscle firing patterns. Am. J. Sports Med. 34:1977, 2006. 24. Keizer, S., Rutten, H., Pilot, P., Moore, N. N., Vos, J. J., and Verburg, A. D. Botulinum toxin injection versus surgical treatment for tennis elbow. Clin. Orthop. Rel. Res. (401):125, 2002. 25. Kibler, W., and Sciasica, A.: Kinetic chain contributions to elbow function and dysfunction in sports. Clin. Sports Med. 23:545, 2004. 26. Lee, M., LaStayo, P., and vonKersburg, A.: A supination splint worn distal to the elbow. J. Hand Ther. 16:190, 2003. 27. Lewis, M., Hay, E., Paterson, S., and Croft, P. Local steroid injections for tennis elbow: does the pain get worse before it gets better? Clin. J. Sports Med. 21:330, 2005.

28. Magermans, D., Chadwick, E., Veeger, H., and van der Helm, F. C.: Requirements for upper extremity motions during activities of daily living. Clin. Biomech. 20:591, 2005. 29. Manias, P., and Stasinopoulos, D.: A controlled clinical pilot trial to study the effectiveness of ice as a supplement to the exercise programme fo rhte management of lateral elbow tendinopathy. Br. J. Sports Med. 40:81, 2006. 30. Mehallo, C., Drezner, J., and Bytomski, J.: Practical management: nonsteroidal antiinflammatory drug (NSAID) use in athletic injuries. Clin. J. Sports Med. 16:170, 2006. 31. Mishra, A., and Pavelko, T.: Treatment of chronic elbow tendinosis with buffered platelet rich plasma. Am. J. Sports Med. 34:1174, 2006. 32. Morrey, B.: The posttraumatic stiff elbow. Clin. Orthop. Rel. Res. 431:26, 2005. 33. Morrey, B., and An, K.-N.: Stability of the elbow: osseous constraints. J. Shoulder Elbow Surg. 14:174S, 2005. 34. Morrey, B., An, K., and Stormont, T.: Force transmission through the radial head. J. Bone Joint Surg. 70A:250, 1988. 35. Morrey, B., Askew, L., and Chao, E. Y.: A biomechanical study of normal functional elbow motion. J. Bone Joint Surg. 63A:872, 1981. 36. Murray, I., and Johnson, G.: A study of the external forces and moments at the shoulder and elbow while performing every day tasks. Clin. Biomech. 19:586, 2004. 37. Nirschl, R.: Prevention and treatment of elbow and shoulder injuries in the tennis player. Clin. Sports Med. 7:289, 1988. 38. Nirschl, R., Rodin, D., Ochiai, D., Maartmann-Moe, C., and DEX-AHE-01-99 Study Group: Iontophoretic administration of dexamethasone sodium phosphate for acute lateral epicondylitis. Am. J. Sports Med. 31:189, 2003. 39. Nussbaum, E.: The influence of ultrasound on healing. J. Hand Ther. 11:140, 1998. 40. O’Driscoll, S.: Classification and spectrum of elbow instability: chronic instability. In Morrey, B. (ed.): The Elbow and Its Disorders. Philadelphia, W.B. Saunders Company, 1993, p. 453. 41. O’Driscoll, S., Bell, D., and Morrey, B.: Posterolateral rotary instability of the elbow. J. Bone Joint Surg. 73A:440, 1991. 42. Paoloni, J., Appleyard, R., Nelson, J., and Murrell, G. A.: Topical nitric oxide application in the treatment of chronic extensor tendinosis at the elbow. Am. J. Sports Med. 31:915, 2003. 43. Park, M., and Ahmad, C.: Dynamic contributions of the flexor-pronator mass to elbow valgus stability. J. Bone Joint Surg. 86A:2268, 2004. 44. Smidt, N., Assendelft, W., Arola, H., Malmiuaara, A., Green, S., Buchbinder, R., van der Windt, D. A., and Bouter, L. M.: Effectiveness of physiotherapy for lateral epicondylitis: a systematic review. Ann. Intern. Med. 35:51, 2003. 45. Smidt, N., Assendelft, W., and van der Windt, D.: Corticosteroid injections for lateral epicondylitis: a systematic review. Pain 96:23, 2002. 46. Taylor, D., Dalton, J., Seaber, A., and Garrett, W. E. Jr.: Viscoelastic properties of muscle-tendon units: the biome-

Chapter 9 Principles of Elbow Rehabilitation

chanical effects of stretching. Am. J. Sports Med. 18:300, 1990. 47. Trudel, D., Duley, J., Zastrow, I., Kerr, E. W., Davidson, R., and MacDermid, J. C.: Rehabilitation for patients with lateral epicondylitis: a systematic review. J. Hand Ther. 17:243, 2004. 48. Warden, S., Avin, K., Beck, E., DeWolf, M. E., Hagemeier, M. A., and Martin, K. M.: Low-intensity pulsed ultrasound accelerates and a non-steroidal anti-inflammatory drug delays knee ligament healing. Am. J. Sports Med. 34:1094, 2006.

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49. Warren, C., Lehman, J., and Koblanski, J.: Heat and stretch procedures: an evaluation using rat tail tendon. Arch. Phys. Med. Rehabil. 57:122, 1976. 50. Wilk, K., Reinold, M., and Andrews, J.: Rehabilitation of the thrower’s elbow. Clin. Sports Med. 23:765, 2004. 51. Dhert, W. J., O’Driscoll, S., van Royen, B., and Salter, R. B.: Effects of immoblization and continuous passive motion on post-operative muscle atrophy in mature rabbits. Can. J. Surg. 31:185, 1988. 52. Wyke, B.: The neurology of joints. Ann. R. Coll. Surg. Engl. 41:25, 1966.

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10

Continuous Passive Motion Shawn W. O’Driscoll

INTRODUCTION In 1960, Salter and Field16 showed that immobilization of a rabbit knee joint under continuous compression, provided by either a compression device or forced position, resulted in pressure necrosis of cartilage. In 1965, Salter and colleagues17 reported the deleterious effects of immobilization on the articular cartilage of rabbit knee joints and the resultant lesion that they termed obliterative degeneration of articular cartilage. Salter15 believed that, “The relative place of rest and of motion is considerably less controversial on the basis of experimental investigation than on the basis of clinical empiricism.” He reasoned that because immobilization is obviously unhealthy for joints, and if intermittent movement is healthier for both normal and injured joints, then perhaps continuous motion would be even better. Because of the fatigability of skeletal muscle, and because a patient could not be expected to move his or her own joint constantly, he concluded that for motion to be continuous, it would also have to be passive. Thus, he invented the concept of continuous passive motion, which has come to be known as simply CPM. Salter also believed that CPM would have an added advantage; namely, that if the movement was reasonably slow, it should be possible to apply it immediately after injury or operation without causing the patient undue pain.

FOUR STAGES OF ELBOW STIFFNESS Because the elbow is so prone to post-traumatic and postsurgical stiffness, CPM should be especially useful in maintaining motion and preventing such stiffness. The rationale for this is much clearer if one understands the stages of stiffness, of which there are four. The first stage, occurring within minutes to hours following surgery or trauma, is caused by bleeding. The second stage, which occurs during the next few hours and days is very similar but progresses more slowly. It is due to edema. Both bleeding and edema result in swell-

ing of the periarticular tissues, thereby diminishing their compliance. The immediate effect is to limit joint motion and make it more painful and, therefore, less acceptable to the patient. Thus, stiffness in these first two stages is avoided by preventing swelling. This can be accomplished by ensuring that the joint is moved through its entire range of motion right from the start, rather than only a portion of its range. CPM is required for this purpose. The third stage is characterized by deposition of extracellular matrix and the formation of granulation tissue commencing near the end of the first week. It continues for days or weeks. The stiffness is still soft but may require the use of splints to regain motion. The fourth stage commencing after about a month results from fibrosis and is often amenable only to splinting or surgical treatment.

PRINCIPLES OF USE Based on an understanding of how stiffness develops, the principles of use of CPM are readily understandable. Until motion is started, it is preferable to elevate the limb with the elbow in full extension and wrapped in a Jones dressing to minimize swelling. It should not be a compressive wrap because of the risk of losing circulation. A drain is usually useful to prevent accumulation of blood. Before starting CPM, all circumferential wrapping (e.g., Jones, cling) should be removed and replaced with a single elastic sleeve. Failure to do this may cause soft tissue injuries due to shear stresses. Once CPM is started, it is optimal that the full potential range of motion of that specific joint be used (Fig. 10-1A and B). Essentially, the tissues are being squeezed alternately in flexion and extension. CPM causes a sinusoidal oscillation in hydraulic pressure within and around the joint.2,9 This not only rids them of excess blood and fluid but prevents further edema from accumulating.8 In the first 24 hours, swelling can develop in minutes (due to bleeding), so CPM should be virtually continuous. This has a beneficial effect on healing soft tissues similar to that seen with compressive therapy after eccentric muscle injury.6 Bathroom privileges are allowed, and the patient is instructed to come out of the CPM device once every hour for 5 minutes. This safety precaution is to reduce the risk of a pressure or stretch related nerve palsy. As the number of days following surgery increases, the amount of time required for swelling to develop increases also, so that longer periods out of the machine are permitted. CPM requires close supervision by someone skilled with its use, so it is mandatory that the patient and family are involved and educated from the beginning regarding the principles of use and how to monitor the

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limb. Frequent checking and slight adjustments of position prevent pressure-related problems. The arm tends to slip out of the machine, so it must frequently be pulled back into it. Nurses do not always have sufficient time, or sometimes the experience, to look after these needs. The patients and their families develop a keen sense of responsibility very quickly and become an invaluable asset. A preoperative instructional video is useful to educate them and should be watched again postoperatively. The CPM should be used long enough to get the patient through the period during which he or she will be unable to accomplish the full range of motion by himself or herself. This can be several days to a month. For most contracture releases, it tends to be used for four weeks.

PAIN CONTROL Such use of CPM immediately raises questions and concerns regarding uncontrollable pain. Pain control in these patients requires that we depart from traditional teaching. Rather than adjusting the motion according to the level of pain, the analgesia is adjusted instead. This is no different from the principles of anesthesia for surgery. Some patients have more pain than others, and appropriate modifications need to be made for them. We favor the use of an indwelling catheter for continuous brachial plexus block anesthesia (see Fig. 10-1C).13-17 This permits a range from analgesia to anesthesia by varying the dose of bupivacaine, a long-acting local anesthetic. The initial bolus dose may be sufficient to cause a complete or near-complete motor and sensory block. Motor blockade requires splinting of the wrist to protect it. Moderate or complete anesthesia, as opposed to analgesia with minimal anesthesia, requires careful attention to the status of the limb overall, because the patient’s protective pain response is no longer present. Insidious development of a nerve palsy during CPM may be less likely to go unnoticed if some motor and sensory function are still present in each nerve during CPM. The catheter is left in place for 3 days in hospital, then removed. At that time, the patient is usually able to maintain the same range of motion with either no or only oral analgesics. The goal is to have the patient leave the hospital capable of moving the elbow from about 10 to 140 degrees of motion actively. Of course, full motion is preferred. A patient-controlled analgesia pump with morphine has also been used effectively if a brachial plexus block is contraindicated, unsuccessful, or not available.

FIGURE 10-1

A to C, The range of motion on continuous passive motion should be full. This permits the tissues to be squeezed alternately in flexion and extension. Analgesia is accomplished with an indwelling catheter for continuous brachial plexus block anesthesia using bupivacaine, a long-acting local anesthetic.

ADVANTAGES There are a number of advantages to the use of CPM. Most surgeons are aware from the total knee experience that analgesic consumption is diminished because the patients are more comfortable (although

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not always during the first day or two). Swelling is diminished. Although most experience with CPM has been in the knees, several studies have documented the efficacy of CPM for the elbow.1,5,11,12 In two separate studies, postoperative CPM was found to improve elbow motion following open reduction internal fixation (ORIF) of distal humeral fractures in children and adolescents.11,12 CPM has been also documented to be effective in assisting with restoration of elbow motion after surgical release1 or resection of heterotopic ossification.5 My personal experience using CPM in strict accordance with the principles just outlined has convinced me that motion is obtained faster and more completely than that obtained without the use of CPM, despite the studies that failed to show such a benefit in the knee (Fig. 10-2A and B).7,8,18,19 This can be explained on the basis of how CPM has been routinely used. Typical protocols involve starting with a small range of motion tolerated by the patient, for example 30 degrees, and gradually increasing the range each day. This pattern of use is not in compliance with the essential principles of CPM. What such a protocol does is to increase swelling and bleeding due to constant tissue irritation. The most astonishing benefit of CPM, however, is how rapidly the patient is capable of pain-free and relatively full function and, therefore, return to work and sport.

COMPLICATIONS In using CPM for the elbow, I have become aware of the protocol for complications. Bleeding is increased but rarely sufficiently to require a transfusion, although

FIGURE 10-2

some patients have been taken back to the operating room for evacuation of a hematoma under such circumstances. Those elbows were treated by being placed back into a well-padded Jones dressing with an anterior plaster slab holding the elbow in extension, then elevating the arm for 2 to 4 days. It is clear to me that in certain settings, CPM can increase the risk of soft tissue and wound healing complications. Hematomas and seromas, as just mentioned, are more likely if CPM is used after having raised a skin flap as part of the exposure. When large skin flaps have been raised and the extent of deep dissection has been extensive, CPM may cause shearing of the soft tissues that is not able to be tolerated. This leads to dark discoloration of the skin, possibly full thickness necrosis, blistering and/or persistent weeping through the wound. If the wound is not closed very securely (subcuticular stitches are insufficient), it may dehisce. I have changed my use of skin incisions and CPM in these types of cases for these reasons. In such circumstances I prefer medial/lateral incisions with no skin flaps rather than a posterior incision. If I am concerned about soft tissues, I delay the use of CPM for 2 to 4 days until I see how the tissues respond to the surgery itself. Despite these concerns, no patients have lost a flap, although a few have had areas of necrosis that healed by secondary intention without further surgery. One patient almost fell out of bed from lying so close to the edge while using the machine. A word of caution is required. No circumferential wrapping (e.g., cling) should be left on the elbow once the CPM is started. A single elastic tube grip sleeve is best. I do not generally use CPM in the presence of ligament injuries or potential joint instability because it is not possible to keep the elbow perfectly aligned

Typical range of motion seen 3 weeks postoperatively (A) and 1 year postoperatively (B) following a distraction interposition arthroplasty treated postoperatively using continuous passive motion.

Chapter 10 Continuous Passive Motion

with the axis of rotation of the machine. Malalignment would stress the ligaments and bony stabilizers of the joint. Neurologic complications of CPM are well recognized for the leg. With the elbow, CPM can permit pressureinduced palsies, which can be prevented as discussed earlier. Delayed-onset ulnar neuropathy is a risk after contracture release. It appears to be due to compression by the cubital tunnel retinaculum and can largely be prevented by prophylactic nerve decompression. Obviously, any nerve can develop a palsy from stretch as well.

INDICATIONS AND CONTRAINDICATIONS CPM is indicated to prevent stiffness and to retain motion obtained at the time of surgery, particularly following contracture release, synovectomy, and excision of heterotopic ossification. I do not generally use it following the replacement of arthritic joints that were stiff preoperatively because of concern about soft tissue complications that would be serious overlying a prosthesis. It is relatively contraindicated if the soft tissue constraints (ligaments) are insufficient, if fixation of fractures has not been rigid, or if the elbow is unstable.

HOME USE I believe that the use of CPM at home is as important as, or perhaps even more than, its use in the hospital. The home rental market for CPM machines is being served by at least two domestic companies at the time of this writing, so home use of CPM is practical. The typical requirement is in the range of 4 weeks for an elbow that has been stiff before surgery, and 1 to 2 weeks for elbows requiring assistance to prevent stiffness from developing.

References 1. Aldridge, J. M. 3rd, Atkins, T. A., Gunneson, E. E., and Urbaniak, J. R.: Anterior release of the elbow for extension loss. J. Bone Joint Surg. Am. 86A:1955, 2004. 2. Breen, T. F., Gelberman R. H., and Ackerman, G. N.: Elbow flexion contractures: Treatment by anterior release and continuous passive motion. J. Hand Surg. Br. 13-B:286, 1988. 3. Brown, A. R., Weiss, R., Greenberg, C., Flatow, E. L., and Bigliani, L. U.: Interscalene block for shoulder arthroscopy: comparison with general anesthesia. Arthroscopy. 9:295, 1993.

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4. Gaumann, D. M., Lennon, R. L., and Wedel, D. J.: Continuous axillary block for postoperative pain management. Reg. Anesth. 13:77, 1988. 5. Ippolito, E., Formisano, R., Caterini, R., Farsetti, P., and Penta, F.: Resection of elbow ossification and continous passive motion in postcomatose patients. J. Hand Surg. Am. 24:546-553, 1999. 6. Kraemer, W. J., Bush, J. A., Wickham, R. B., Denegar, C. R., Gomez, A. L., Gotshalk, L. A., Duncan N. D., Volek, J. S., Putukian, M., and Sebastianelli, W. J.: Influence of compression therapy on symptoms following soft tissue injury from maximal eccentric exercise. J. Orthop. Sports Phys. Ther. 31:282, 2001. 7. O’Driscoll, S. W., and Giori, N. J.: Continuous passive motion (CPM): Theory and principles of clinical application. J. Rehabil. Res. Dev. 37:179, 2000. 8. O’Driscoll, S. W., Kumar, A., and Salter, R. B.: The effect of continuous passive motion on the clearance of a hemarthrosis from a synovial joint: an experimental investigation in the rabbit. Clin. Orthop. 176:305, 1983. 9. O’Driscoll, S. W., Kumar, A., and Salter, R. B.: The effect of the volume of effusion, joint position and continuous passive motion on intra-articular pressure in the rabbit knee. J. Rheumatol. 10:360, 1983. 10. Pope, R. O., Corcoran, S., McCaul, K., and Howie, D. W.: Continuous passive motion after primary total knee arthroplasty. J. Bone Joint Surg. Br. 79:914, 1997. 11. Remia, L. F., Richards, K., and Waters, P. M.: The BryanMorrey triceps-sparing approach to open reduction of Tcondylohumeral fractures in adolescents: Cybex evaluation of triceps function and elbow motion. J. Pediatr. Orthop. 24:615, 2004. 12. Re, P. R., Waters, P. M., and Hreski, T.: T-condylar fractures of the distal humerus in children and adolescents. J. Pediatr. Orthop. 19:313, 1999. 13. Rice, A. S. C.: Prevention of nerve damage in brachial plexus block. XVI Annual European Society of Regional Anaesthesia Congress. London, 1997. 14. Romness, D. W., and Rand, J. A.: The role of continuous passive motion following total knee arthroplasty. Clin. Orthop. 226:34, 1988. 15. Salter, R. B.: Motion vs. rest. Why immobilize joints? J. Bone Joint Surg. 64-B:251, 1982. 16. Salter, R. B., and Field, P.: The effects of continuous compression on living articular cartilage. An experimental investigation. J. Bone Joint Surg. 42-A:31, 1960. 17. Salter, R. B., McNeill, O. R., and Carbin, R.: The pathological changes in articular cartilage associated with persistent joint deformity. An experimental investigation. Studies of the rheumatoid diseases. Third Canadian Conference on Research in Rheumatic Diseases. Toronto, 1965, p. 33. 18. Schroeder, L. E., Horlocker, T. T., and Schroeder, D. R.: The efficacy of axillary block for surgical procedures about the elbow. Anesth. Analg. 83:747, 1996. 19. Stinson, L. J., Lennon, R., Adams, R., and Morrey, B.: The technique and efficacy of axillary catheter analgesia as an adjunct to distraction elbow arthroplasty: a prospective study. J. Shoulder Elbow Surg. 2:182, 1993.

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11

Splints and Bracing at the Elbow

common problem in the orthopedic practice. Unfortunately, in the author’s experience the use of aggressive physical therapy to address post-traumatic stiffness is not always successful and, in fact, as often as not, makes the contracture worse. This justifies the use of splinting in this clinical setting, but to understand the rationale of splinting for this condition, it is necessary to understand the physiology of the process.

Bernard F. Morrey

PATHOLOGY OF ELBOW CONTRACTURE INTRODUCTION Elbow splints are frequently employed at the elbow and function in several capacities: protection both static and dynamic, to deliver flexion or extension torque. Specifically, the four types of braces or splints used in the postoperative and postinjury management of the elbow include resting and hinged splints, and dynamic and static adjustable splints.10

STATIC AND PROTECTIVE SPLINTS Prophylactic bracing is occasionally employed at the elbow, typically to avoid excessive extension in the athlete.9 Further static splinting for the elbow is commonly used for short periods as a protective measure after injury or surgery. Previously used commonly in those with rheumatoid arthritis, largely because of the effectiveness of disease remitting agents, this type of splinting is uncommonly indicated today (Fig. 11-1). For the unstable elbow a hinged splint is used (Fig. 11-2). By initially locking the hinge, the same device can be used as a resting static splint; some designs allow conversion to a movable stabilizing device. Hinged splints allow active motion and are employed primarily for ligament healing. Occasionally, a hinged brace is prescribed for the resected elbow, but compliance is variable, and I rarely use this type of device.

ELBOW STIFFNESS The most common complication of elbow injury, and even in some arthritic conditions, is stiffness. The most important means of avoiding this after a fracture is rigid fixation accompanied by early motion of the joint (see Chapter 22). After fracture dislocation, it has been demonstrated that immobilization lasting for more than 4 weeks resulted in less satisfactory outcome in each patient,2 and despite the recognized value of early motion after injury or surgery stiffness of the elbow remains a

The exact reason that the elbow is so prone to joint contracture is not known with certainty. What is recognized is that the elbow is one of the most congruous joints in the body (see Chapter 2). Normally, the capsule is translucent, but with insult, it undergoes a marked hypertrophy and extensive cross-linking of the fibrils, as demonstrated on scanning electron microscopy (Fig. 11-3). In some instances, a severe elbow contracture has been observed after trivial insult or such as “strain” without fracture or dislocation. Under these circumstances, the elbow may contract rapidly, often within 2 to 3 weeks. An explanation of the rapid development of elbow contracture may be provided by the basic investigations on wound contracture. Experimental data demonstrate that dermal wounds undergo approximately 80% of the anticipated contracture within the first 3 weeks1 (Fig. 11-4). Continuous motion, if properly used, has been shown to be an important adjunct to successfully alter this tendency and hence prevent contracture (see Chapter 10). After trauma, this modality is used with confidence, particularly if rigid fixation has been afforded to the fracture and if pain and inflammation can be controlled. After 3 to 8 weeks of treatment and if the fracture has been rigidly fixed and it is thought that force can safely be applied, the use of splints may be introduced in order to gain further motion. In general, the author’s philosophy is that continuous motion machine maintains motion but does not gain motion. The use of static adjustable splints attains motion both in flexion and in extension. The question then arises as to the best method of providing a force to stretch the periarticular soft tissues. There are four possibilities: physical therapy, continuous passive motion, dynamic splinting, and static adjustable splinting.

MANAGEMENT OF ELBOW STIFFNESS PHYSICAL THERAPY Physical therapy must be executed with extreme caution in the post-traumatic or inflamed elbow. The reason for

Chapter 11 Splints and Bracing at the Elbow

FIGURE 11-1

165

Resting splint rarely used for more than 2

to 3 weeks. FIGURE 11-3

Scanning electron microscopy (×30) showing dense hypertrophy of collagen fibrils with extensive cross-linkage sites.

50

FIGURE 11-2

Hinged splint allows static support when the mechanism is locked, and active motion thereafter as desired.

this is that passive stretch, in and of itself, can introduce the very inflammation that one is trying to treat in the course of the therapy. Inflammation results in contracture and thus is an obstacle to the treatment goal. A well-trained experienced physical therapist who understands this principle can be of value, especially to assist in addressing concurrent shoulder and wrist stiffness. Such expertise is not possible in the author’s practice; therefore, I have never prescribed physical therapy for a patient of mine with elbow stiffness.

Area cm2

40

30

20

10

0 0

10

20

30

40

50

60

Days

FIGURE 11-4

Experimental data showing that the majority of tissue contracture occurs in the first 3 weeks. (With permission from Billingham, R. E., and Russell, P. S.: Studies on wound healing, with special reference to the phenomenon of contracture in experimental wounds in rabbits’ skin. Ann. Surg. 144:961, 1956, p. 964.)

RESTORATIVE SPLINTING Restorative splinting can be used to assist in attaining elbow motion. Splints are designed according to two diverse philosophies: dynamic or static-adjustable. To comprehend the rationale of dynamic or static adjustable splinting, some understanding of the soft tissue about the elbow as viscoelastic tissue is necessary. If the

soft tissue at the elbow can be considered viscoelastic tissue, its response to a constant versus a variable force is different.12 The theoretical response to a constant force is shown in Figure 11-5. This load results in soft tissue deformation, which is called creep.8 However, what is

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Tissue elongation

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Constant force

Time

FIGURE 11-5

Viscoelastic tissue response to a constant force resulting in gradual stretching of the tissue. The potential for inflammation, however, is not demonstrated by this curve but is possible if the force is constantly present, which is the case in dynamic loading.

FIGURE 11-6

Commercially available dynamic splint. The tension and excursion may be adjusted by the patient.

Applied discrete force

not demonstrated in this illustration is the development of inflammation as a biologic response to this constant load. Inflammation can alter this idealized curve, and in the author’s opinion, inflammation is a common byproduct of dynamic splinting. Nonetheless, this remains an attractive option for many11 (Fig. 11-6). The alternate approach to the stiff elbow is the use of static adjustable splints. In this modality, a constant force is applied to the elbow that results in strain being imparted to the tissue. However, the force is not continuously applied, allowing stress relaxation to occur within the soft tissue sleeve over a period of time. This type of treatment has been employed extensively at the knee by serial casting and has also been effectively used at the elbow.14 It is believed that the stress-free relaxation lessens the likelihood of inflammation, and thus, the elbow in our practice and opinion is more amenable to this type of load application (Fig. 11-7). The constant force is applied so as to exceed the elastic limits of the tissue or result in a stretch. But if this load is maintained at a constant and is not further increased, tissue relaxation should occur over time. Finally, to further avoid the likelihood of inflammation, the patient controls the amount and duration of tension being applied. This is done within a very discrete set of recommendations and a very defined program (see Appendix). However, as with all torque generated across the elbow by whatever means, a compressive force is also applied to the system. This joint force can reach considerable proportions and is a function of the direction of the torque and the ankle of the elbow at the time of application13 (Fig. 11-8). Ideally, the splint hinge mechanism absorbs the majority of the force which is primarily compressive in nature whether the application is in flexion or extension.

Constant length

Time

FIGURE 11-7

The tissue response to the application of a single discrete force results in stress relaxation of the viscoelastic tissue.

DYNAMIC SPLINTING Dynamic splinting has been a popular means of treating impending or developing stiffness. The concept has been used in hemophiliacs by employing a system of reverse dynamic slings at both the knee and at the elbow.3 The earliest examples of dynamic splinting employed rubber

Chapter 11 Splints and Bracing at the Elbow

bands to deliver to torque. At the elbow, this has given way to much more sophisticated mechanics and devices. Data has been published to suggest the value of dynamic splinting to assist extension after triceps injury.7 Today, there are several readily available commercial devices that employ this concept (see Fig. 11-6). The splint is well tolerated at least initially but can cause pain and introduce reactive inflammation if used too aggressively.

STATIC ADJUSTABLE SPLINTS The classic static adjustable splint is a turnbuckle type and use was reintroduced several years ago by Green and associates.6 He reported an 80% success rate in treating elbow contractures from various etiologies, especially those with a major flexion contracture. Two problems were identified with the use of these splints.

Force, normalized

1

167

As the contracture decreases to less than 30 degrees, the effectiveness of a turnbuckle to develop an extension torque decreases. Applying an extension load at this angle results in the majority of the force distributed so as to separate the hinge, and less than 25% of the force actually exerts an extension torque on the elbow (Fig. 11-9). The ability of this concept to enhance post-traumatic elbow motion has been recently demonstrated in a clinical trial.4 In another study, 11 of 22 patients gained satisfactory motion after initiating turnbuckle type bracing in a sample of those who no longer were benefiting from physical therapy.5 Hence, to develop a more effective device, a means was developed to apply the force through a gear mechanism at the axis of flexion; by so doing the entire force is then applied as intended: either to extend or to flex. (Fig. 11-10). The brace was designed at our institution and is termed the “Mayo Elbow Brace (Don Joy,

Rotation

.8

.2 Compression

0

40

80

120

160 160 180

120

80

40

0

Flexion angle, degrees

FIGURE 11-8

During flexion and extension variable proportions of the applied load is converted to rotatory or compressive forces at the joints.

FIGURE 11-10 A static adjustable splint currently used by the author in which the extension torque is directly applied at the axis of rotation. Note use of air pads to distribute the local pressure exerted on the skin.

FIGURE 11-9

Sine 45° = 0.70

45°

Force = 70% extension 30% separation

A

15°

B

30°

Sine 15° = 0.25 Force = 25% extension 75% separation

A, With the elbow at 90 degrees, the anteriorly placed turnbuckle provides an effective force, approximately 70% of which is directed at extending the elbow and 30% in separating the joint itself. B, When the elbow is at 30 degrees, the turnbuckle is working through an angle of 15 degrees. The sine function of 15 degrees is .25. This means that 75% of the force is going to separate the hinge and distract the two components of the brace, and only 25% of the force is actually extending the elbow. These types of braces become inefficient as the elbow gets closer toward full extension.

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FIGURE 11-11 The same splint shown in Figure 11-10, but reversed and being used in the flexion mode; hence, the splint is called the universal splint in our practice. For flexion the straps nearest to the hinge are released to avoid impingement.

Flexion* Extension

Out#

Flexion* Extension

Out#

Flexion* Extension

Out#

Flexion* Extension

Rise

Rise 8 am Noon

1 pm Hours

6 pm Hours

Hours

10 pm Sleep

• *Either flexion or extension; circled as needed. • # Hours out of splint.

FIGURE 11-12

BOX 11-1

A sample of the daily program given to the patient at the time of splint prescription.

Basic Instructions for the Use of Static Adjustable Splints

The following general guidelines for the use of turnbuckle splints may be modified, or instructions may be given to you, depending on your individual needs and progress. I. General Goals

• To attain improved motion of your elbow, inflammation must be avoided. This is done with the use of the anti-inflammatory agents, heat and ice, and education of the patient to the signs of inflammation. II. Cardinal Signs of Inflammation

• Increased soreness, increased discomfort, swelling, or commonly a progressive loss of motion, rather than day-to-day improvement. III. Treatment of Inflammation

• Avoid the causative factor. Be less vigorous with the turnbuckle splint, adhere to the heat and ice program, and take anti-inflammatory agents as prescribed. If they are inadequate, they may need to be modified. Check with us or your local doctor. IV. Direction of Improvement

• Often, both increased elbow flexion and extension is being sought. In general, the motion that is needed most is addressed at night. The opposite motion is encouraged during the day.

V. Typical Splint Program

• On rising in the morning, the splint is removed. Gently flex and extend the elbow while taking a hot bath or shower for approximately 15 minutes. Take an antiinflammatory agent. • Apply the splint in a direction opposite to that which was used at night. Apply it to the point where it is recognized that the elbow is being stressed but pain is not present. • The splint may be removed for 1 hour in the morning, 1 hour in the afternoon, and 1 hour in the evening. Reapply the splint in the opposite direction after these rest periods. • Use the elbow when out of the splint, as able, in the evening. If the elbow is sore or seems inflamed, apply ice for 15 minutes. If the elbow is not inflamed but is stiff, apply heat for 15 minutes while gently working the joint in flexion and extension. • On going to bed at night, apply the splint in the direction needed most. Application should be sufficiently strong so you are aware that the elbow is being stressed, and a person should be able to sleep comfortably for about 6 hours without being awakened by elbow pain. After reading these instructions, contact your physician if you have any specific questions.

Chapter 11 Splints and Bracing at the Elbow

Orthopedics) and is able to hyperextend to enhance the ability to completely resolve the contracture (Fig. 11-11). However, with flexion to more than 100 or 110 degrees, the anterior soft tissue tends to bunch up, limiting further flexion. For this reason, the straps closest to the joint may be released to allow unencumbered flexion. Over the 4-year period from the introduction of this device in 2003 through 2006, we have prescribed approximately 200 braces for patients with various expressions of elbow stiffness. This experience has resulted in the application program shown in Box 11-1 and Figure 11-12. It should be noted that an adequate amount of time should be spent with the patient to explain the rationale of the brace and specific use and goals for the specific device being used.

References 1. Billingham, R. E., and Russell, P. S.: Studies on wound healing, with special reference to the phenomenon of contracture in experimental wounds in rabbits’ skin. Ann. Surg. 144:961, 1956. 2. Broberg, M. A., and Morrey, B. F.: Results of treatment of fracture dislocations of the elbow. Clin. Orthop. 216:109, 1987. 3. Dickson, R. A.: Reversed dynamic slings: A new concept in the treatment of post-traumatic elbow flexion contractures. Injury 8:35, 1976. 4. Doornberg, J. N., Ring, D., and Jupiter, J. B.: Static progressive splinting for posttraumatic elbow stiffness. J. Orthop. Trauma. 20:400, 2006.

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5. Gelinas, J. J., Faber, K. J., Patterson, S. D., and King, G. J.: The effectiveness of turnbuckle splinting for elbow contractures. J. Bone Joint Surg. 82B:74, 2000. 6. Green, D. P., and McCoy, H.: Turnbuckle orthotic correction of elbow-flexion contractures after acute injuries. J. Bone Joint Surg. 61A:1092, 1979. 7. Greer, M. A., and Miklos-Essenberg, M. E.: Early mobilization using dynamic splinting with acute triceps tendon avulsion. J. Hand Ther. 18:365, quiz 371, 2005. 8. Kottke, F. J., Pauley, D. L., and Ptak, R. A.: The rationale for prolonged stretching for correction of shortening of connective tissue. Arch. Phys. Med. Rehab. 47:345, 1966. 9. Lake, A. W, Sitler, M. R., Stearne, D. J., Swanik, C. B., and Tierney, R.: Effectiveness of prophylactic hyperextension elbow braces on limiting active and passive elbow extension prephysiological and postphysiological loading. J. Orthop. Sports Phys. Ther. 35:837, 2005. 10. Morrey, B. F.: The use of splints with the stiff elbow. In Heckman, M. D. (ed.): Prospective in Orthopedic Surgery, Vol. I, No. 1. St. Louis, Quality Medical Publishing, 1990, p. 141. 11. Richard, R., Shanesy, C. P., and Miller, S. F.: Dynamic versus static splints: A prospective case for sustained stress. J. Burn Care Rehab. 16:284, 1995. 12. Richards, R. L., and Staley, M. J.: Biophysical aspects of normal skin and burn scar. In Richard, F. L., and Staley, M. J. (eds.): Burn Care and Rehabilitation: Principles and Practice. Philadelphia, F. A. Davis, 1994, p. 65. 13. Szekeres, M.: A biomechanical analysis of static progressive elbow flexion splinting. J. Hand Ther. 19:34, 2006. 14. Zander, C. L., and Healy, N. L.: Elbow flexion contractures treated with serial casts and conservative therapy. J. Hand Surg. 17:694, 1992.

Chapter 12 Imaging of the Pediatric Elbow

CHAPTER

12

Imaging of the Pediatric Elbow Kristen B. Thomas, Alan D. Hoffman, and E. Richard Graviss

INTRODUCTION Radiography is the primary imaging modality for evaluation of the elbow in children, as it is in adults. Although the radiographic views are the same, the pediatric patient is unique. Injury is the primary reason for evaluating the immature elbow. Children’s reactions to the process of imaging vary greatly, although they are usually related to the patient’s age and the nature of the injury sustained. Modern radiographic equipment is a cornerstone for obtaining high-quality imaging studies. However, the most important component is a qualified radiologic technologist who understands the child’s anxieties and who has empathy for the child’s fears. Such a technologist is aware of patient and parent anxiety and that the minor motions of the elbow may cause pain. The assistance of an accompanying parent or guardian may be useful and, occasionally, is mandatory when there is insufficient technical help available for positioning. A gentle, friendly approach that is firm but reassuring will yield optimal radiographic examinations of the pediatric elbow. The basic elbow study consists of anteroposterior and lateral views. The lateral view invariably is obtained first, because the child maintains an injured elbow in the flexed position. The patient is seated beside a radiographic table so that the arm can be elevated parallel to the level of the table top and a 90-degree flexed position can be maintained. The forearm should be supinated gently, with the thumb pointed up, positioning all three bones of the elbow in the lateral projection. The anteroposterior view then is obtained with the forearm positioned up and the elbow extended slowly as much as the injury allows. If necessary, the anteroposterior view can be divided into two segments: one with the humerus parallel to the radiographic film, and the other with the forearm parallel to the radiographic film. This provides better anatomic detail than does a single exposure with the elbow partially flexed and neither component parallel to the film.

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Some unstable fractures and dislocations require splinting such that views obtained at right angles are usually sufficient for the initial diagnosis. The fracture or dislocation with obvious clinical deformity is usually less problematic than is the subtle fracture, which may go undetected. When the patient is examined for subtle fractures, the lateral view is extremely important, and positioning should be flawless. This view provides clues concerning the injured elbow, such as the anterior and posterior fat pad signs. It also allows for visual alignment of the distal humeral ossification segments with the shaft of the humerus and with the radius. In certain instances, a fluoroscopic examination of the elbow may yield valuable information. The examiner can manipulate the elbow to obtain the precise obliquity required to best evaluate a subtle abnormality. Instead of repeating a radiograph multiple times, optimal positioning can be obtained while watching real-time fluoroscopy and then digital fluoroscopic spot radiographs are easily taken. Tomography, using either a simple linear method or a complex motion system, can be used in the evaluation of growth plates that have closed prematurely following trauma. In most practices, computed tomography has completely replaced conventional tomography. Computed tomography examinations now take only seconds to perform, and sedation is usually not necessary, even in very young infants and children. Using current 64slice multidetector computed tomography technology (MDCT), isovoxel images can be obtained in all three planes down to 0.6-mm collimation. This allows detailed imaging, with the bony trabecular pattern well seen. Examinations are obtained with the patient in the prone position, with the affected arm held above the head with about 90 degrees of flexion at the elbow. Sagittal and coronal two-dimensional reformatted images as well as three-dimensional reconstructions are then made from the raw data. MDCT is a sensitive (92%) and specific (79%) method of evaluating for radiographically occult elbow fractures.6 MDCT can also use automated tube current modulation to markedly decrease the radiation dose to the patient compared with fixed-tube current techniques. MDCT can also be performed with no image degradation through a cast.3 MDCT with reformatting can better delineate intra-articular fractures (Fig. 12-1). Three-dimensional imaging can also provide additional information and help define the joint relationships to aid surgical planning (Figs. 12-2 and 12-3). The resulting three-dimensional image can be rotated in all planes with computerized subtraction of the adjacent soft tissues and bones, if needed. Magnetic resonance imaging (MRI) and ultrasonography are increasingly being used to evaluate the elbow. MRI can evaluate cartilage, bone marrow, and soft tissue structures (Fig. 12-4).8 Radiographs do not show bone

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FIGURE 12-1

Computed tomography two-dimensional reformatted coronal image of intra-articular distal humeral intercondylar fracture in a 13-year-old boy who was injured while skateboarding.

FIGURE 12-2

Computed tomography three-dimensional reconstruction of a complex intra-articular distal humeral fracture from the posterior view in a 14-year-old boy injured while playing basketball.

FIGURE 12-3

Magnetic resonance imaging of a 13-year-old boy with elbow pain, coronal (A) and sagittal (B) views. T1-weighted images show a defect in the capitellum. No loose body is seen. The clinical diagnosis was Panner’s disease, and symptoms resolved in a few months without specific therapy.

Chapter 12 Imaging of the Pediatric Elbow

175

FIGURE 12-5 FIGURE 12-4

Computed tomography three-dimensional reconstruction of an 11-year-old boy with the clinical diagnosis of Panner’s disease. Several small loose bodies are seen adjacent to the capitellum.

bruising, or cartilaginous or soft tissue injury and can underestimate physeal injury. MRI is also occasionally used to better define elbow fractures.2 Owing to the length of the MRI examination (at least 20 minutes), children younger than 5 years old will usually need sedation so that optimal MRI images can be obtained. In children with elbow trauma, MRI reveals a broad spectrum of bone and soft tissue injury, including ligamentous injury, beyond that recognized by radiographs. However, the additional information afforded by MRI usually does not change treatment or clinical outcome in acute elbow trauma.9 MRI can be very useful in the evaluation of osteochondritis dissecans (OCD) of the capitellum. MRI provides information about the size, location and stability of the OCD lesion. All of these factors are important when deciding treatment options (see Chapter 20 for more discussion). Unstable OCD lesions in the capitellum have a peripheral rim of high signal or an underlying fluid-filled cyst on T2-weighted images (Fig. 12-5). Stable OCD lesions have no peripheral signal abnormality.12 Loose bodies in the elbow joint can be visualized by MRI or MDCT, but smaller detached bone fragments are usually better visualized using MDCT (Fig 12-6). Ultrasonography has the ability to dynamically delineate soft tissues and cartilage in detail.13 Soft tissue swell-

Magnetic resonance imaging (T2 sagittal image) of a 12-year-old boy demonstrates osteochondritis dessicans (OCD) of the capitellum with increased signal extending to the articular surface consistent with full-thickness cartilage loss. This indicates a potentially unstable OCD bone fragment that has not yet detached. A moderate elbow joint effusion is also present.

FIGURE 12-6

Computed tomography axial image of a 12year-old female gymnast demonstrates a small intraarticular loose body within the posterior elbow joint (arrow) secondary to osteochondritis dissecans of the capitellum. The tiny bone fragment was not visible on radiographs.

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ing, a mass (including vascular masses investigated with duplex Doppler and color flow Doppler), joint effusion, and fractures, particularly in infants and young children with unossified or minimally ossified epiphyses, are studied with this modality.1,7 Ultrasound can detect early changes of medial epicondylar fragmentation and OCD of the capitellum, even in the asymptomatic stage in selected populations such as young baseball players.10 As with other portions of the appendicular and axial skeletons, side-to-side comparison may be helpful when one is presented with an unfamiliar or a rare variant. Comparison views need to be obtained only in selected cases,14,15 such as when consultation with the standard text of normal cases is not helpful.5,11,17

NORMAL DEVELOPMENT The maturation sequence at the elbow is more variable than that of the hand and wrist. Nonetheless, an appreciation of the normal sequence and timing of the appearance of ossification centers and maturation patterns is important for an understanding of the radiographic

FIGURE 12-7

appearances of the elbow in children (Fig. 12-7). Several mnemonics have been suggested to help remember the time of appearance of the ossification of these centers. We find that the cross-connecting ossification centers (see Fig. 12-7B) are particularly helpful in remembering at least the order of ossification of these centers. An atlas entitled Radiology of the Pediatric Elbow5 shows standards for elbow maturation in children. To consistently evaluate the developing elbow, one must analyze each of the secondary centers of ossification, accounting for its appearance, configuration during development, and associated changes as it matures and eventually fuses with the humeral shaft. The descriptions that follow are brief, but they outline the major points of development and maturation of the centers.

CAPITELLUM The capitellum, the first of the elbow’s six centers to ossify, generally becomes radiographically visible during the first and second years of life. Initially spherical, it flattens posteriorly to conform to the adjacent distal end of the humerus. The physis is broader posteriorly than

A, Normal left elbow showing the secondary centers: capitellum (c); medial epicondyle (m); radial head (r); trochlea (t); olecranon (o); and lateral epicondyle (l). B, The approximate age at time of appearance of these centers is indicated in years. The cross connecting the secondary centers of the distal humerus serves as a reminder of the order of ossification of these centers. (Modified from Brodeur, A. E., Silberstein, M. J., Graviss, E. R., and Luisiri, A.: The basic tenets for appropriate evaluation of the elbow in pediatrics. Curr. Probl. Diagn. Radiol. 12:1, 1983.)

Chapter 12 Imaging of the Pediatric Elbow

anteriorly, giving the capitellum the appearance of a downward tilt; however, this appearance gradually disappears during the first decade (Fig. 12-8). During maturation, the capitellum fuses with the trochlea and the lateral epicondyle before it unites with the humeral shaft (Fig. 12-9). The orientation of the capitellum with the humerus can be evaluated with a true lateral projection. The anterior surface of the humerus is gently bowed posteriorly, from the insertion of the deltoid muscle to the superior aspect of the coronoid fossa. A line drawn along the anterior surface of the humerus, from the deltoid insertion to the top of the coronoid fossa, should pass through the middle third of the capitellum. For practical reasons, most lateral examinations of the elbow do not include the deltoid insertion; therefore, one must use the most proximal portion of the humerus included on the radiograph. These two points determine the anterohumeral line, which passes precisely through the posterior half of the middle third of the capitellum. The capitellum is oriented anteriorly to the distal humerus. One also may draw a curvilinear line along the coronoid fossa. The extension of that line inferiorly should touch the anterior portion of the capitellum. These two lines permit the detection of subtle supracondylar fractures, particularly Salter-Harris type I supracondylar fractures, with minimal posterior dis-

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placement of the distal humeral epiphysis with the capitellar ossification center.

RADIOCAPITELLAR LINE The radiocapitellar line is a line drawn through the long axis of the proximal radial shaft that should, in the absence of dislocation, pass through the middle of the capitellum ossification center. This is generally true in anteroposterior, lateral, or any oblique projection. In early development, however, the radial metaphysis is wedged so that on the anteroposterior projection a normal radial shaft line may appear to extend laterally to the capitellum. However, on the lateral projection, the normal radiocapitellar line can be appreciated (Fig. 12-10). In older patients, although it may appear that the radiocapitellar line is normal in one projection in a patient with a radial head dislocation, it invariably will be abnormal in the projection taken at right angles, generally the lateral projection.18

MEDIAL EPICONDYLE The medial epicondyle is the second elbow ossification center to appear in the normal sequence, usually at about 4 years. Lying posteromedially, it is often best appreciated on the lateral projection (Fig. 12-11). Fre-

FIGURE 12-8

Lateral elbow radiograph of a 2.5-year-old girl. A line along the anterior humeral shaft normally intersects the posterior half of the middle third of the capitellum. The continuation of the curved coronoid line just touches the anterior edge of the ossified capitellum. The angle formed by the coronoid line and humeral shaft line should contain the majority of the ossified capitellum.

FIGURE 12-9

A 13-year-old girl in whom the capitellum has joined with the lateral epicondyle and trochlea before fusion with the humeral shaft. Note the normal sclerotic radial epiphysis that is wider than the radial neck.

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ossification center. In a child between 4 and 8 years of age, at the time of appearance of the medial epicondyle and the trochlear ossification centers, a radiograph suggesting a trochlear ossification center, without visualization of a medial epicondyle center, should suggest that fracture and dislocation of the medial epicondyle have in fact occurred.13

RADIAL HEAD EPIPHYSIS The initial ossification of this epiphysis is fairly predictable and usually occurs in the fifth year (see Fig. 12-7B). Although usually beginning as a sphere, the radial head epiphysis often matures as one or more flat sclerotic centers. This pattern may be mistakenly interpreted as a fracture. With maturation, the physis on the anteroposterior radiograph is wider laterally than medially, and this appearance, combined with the medial angulation of the radius at the junction of its shaft and neck, may suggest dislocation on anteroposterior views. Lateral projection of the elbow will not confirm a suspected dislocation. With further maturation of ossification of the proximal radial ossification center, the normal relationship of the radius and capitellum can be seen on anteroposterior radiographs. Notches or clefts of the metaphysis of the proximal radius often are seen as normal variations of ossification during maturation.11,17 Because fractures of the radial neck are extracapsular, they are not associated with hemarthrosis and abnormalities of the humeral fat pads.19

FIGURE 12-10

A, Normal 7-month-old girl with apparent abnormal radiocapitellar line on the anteroposterior radiograph because of wedging of the metaphysis. B, The relationship between the radial shaft and capitellum is normal on the lateral radiograph.

quently, it develops from more than one ossific nucleus. Although it is the second humeral ossification center to appear, its development is slow, and it is usually the last center to unite with the humeral shaft in the normal child, sometimes as late as 15 or 16 years of age.20 This center may fuse with the trochlea before uniting with the humeral shaft. Injuries involving the nonunited medial epicondyle are relatively common and are among the most difficult to evaluate. Consequently, to avoid errors, Rodgers suggests making a habit of identifying the presence and the position of the medial epicondyle ossification center in each case.16 A classic example of the importance of appreciating the sequence of humeral ossification center appearance is avulsion and displacement of the medial epicondyle ossification center. This frequently results in the displacement of the medial epicondyle into the normal position of the trochlear

TROCHLEAR EPIPHYSIS Ossification of the trochlea appears at about 8 years and often is initially multicentric (Figs. 12-12 and 12-13B). The trochlea frequently maintains an irregular contour during its development and should not be confused with abnormal processes such as trauma or avascular necrosis (Fig. 12-14). The trochlea will fuse with the capitellum before fusion with the distal humeral shaft. It is seldom fractured, except when associated with the vertical component of a supracondylar fracture or when its lateral edge is involved with a lateral condylar fracture.

OLECRANON The ossification center of the olecranon usually develops at 9 years of age, shortly after the trochlea and just before the lateral epicondylar epiphysis. The proximal end of the ulna flattens and becomes sclerotic just before the olecranon physis ossifies. Two ossification centers most often develop, and there is great variability in the configuration of the epiphysis. This results in an occasional misdiagnosis of acute fracture. The posterior

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179

FIGURE 12-11 A, A 10-year old boy with a normal posteromedially lying ossification center for the medial epicondyle (arrows) seen posterior to the humeral shaft on the lateral projection. B, Another 10-year-old boy who sustained trauma resulting in avulsion of the medial epicondyle, which is displaced anteriorly (arrows) on the lateral projection, and displaced medially (C), and rotated on the anteroposterior projection.

FIGURE 12-12 Multiple ossification nuclei of developing trochlea (arrow) in a 9-year-old boy.

ossification center is usually bigger than the anterior ossification center (Fig. 12-15), and these separate centers generally unite before fusion with the proximal humerus. This process usually begins at about 14 years of age. The pattern of closure of the olecranon physis is distinct, with fusion occurring first along the joint line and then extending posteriorly. Frequently, fractures are wedged in the opposite direction.21 The olecranon physis has prominent sclerotic margins just before closure. Fusion proceeds posteriorly from the joint side or the anterior surface (Fig. 12-16). During its development, the physeal line remains relatively perpendicular to the ulnar shaft. As a result of differential growth, often with maturation, the olecranon growth plate, which initially is proximal to the elbow joint, comes to lie at a midelbow joint level by the time of fusion. This “wandering physeal line of the olecranon” does not occur in all individuals.4

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Part IV Conditions Affecting the Child’s Elbow

FIGURE 12-13 A, Lateral radiograph with lucent region in the proximal radial shaft (arrows). B, Anteroposterior view shows prominent but normal radial tuberosity (arrow). Residual changes from previous transcondylar fracture of the humerus are seen.

FIGURE 12-15 FIGURE 12-14 A 9-year-old boy with beginning ossification of the lateral epicondyle (arrow) from a thin sliver widely separated from the metaphysis. Note the irregular outline of the developing ossification center of the trochlea.

Although the majority of olecranon fractures are intracapsular and are associated with alterations of fat pads, some are not. The tip of the olecranon is not within the capsule in some individuals. The only other common site of fracture related to the elbow that lies outside the joint capsule is the radial neck (see Chapter 17).4

A 13-year-old boy with double ossification center of the olecranon. The anterior nucleus is smaller.

LATERAL EPICONDYLE The ossification center of the lateral epicondyle is the last of the elbow centers to appear. Usually, this center is first seen at 10 or 11 years of age, and it fuses to the humeral shaft at about 14 years of age. Unlike the other ossification centers of the elbow, the lateral epicondyle appears first as a thin sliver rather than as a round or spherical ossific nucleus (see Fig. 12-14). Ossification commences at the lateral portion of the cartilaginous mold so that the physis appears particu-

Chapter 12 Imaging of the Pediatric Elbow

larly wide. The inferior aspect of the ossification begins at the junction between the distal humerus and the capitellum.5 Because of the relatively short time between the appearance and fusion of this center, it is not always certain in individual cases whether ossification is delayed or fusion to the humerus already has occurred. To avoid confusion about this point, it must be realized that before ossification, the humerus has a sharp, straight, sloping metaphyseal line that changes to a sloping, curving margin at the capitellum. The fused lateral epicondyle, on the other hand, has a smooth, curved margin that is continuous with the capitellum (Fig. 12-17).

FIGURE 12-16 A 14-year-old male in whom closure of the olecranon growth plate has begun anteriorly. Note the sclerotic margin of that portion of the growth plate that remains unfused.

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NORMAL VARIANTS In addition to the confusing appearances caused by the normally developing elbow, there are a few variations from normal or unusual appearances that should be noted. The radial tuberosity lies medially at the junction of the medial shaft and the neck. On lateral views, it may

FIGURE 12-18 A 6-year-old boy with perforated olecranon fossa. There has been a previous supracondylar fracture.

FIGURE 12-17 A, A 9-year-old boy in whom ossification of the lateral epicondyle is about to begin. The metaphysis has a sharp, straight, sloping margin. B, The fusing lateral epicondyle in this 14-year-old boy, in contrast, has a smoother, rounded margin.

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FIGURE 12-19 Supracondylar process in a mature elbow. Anteroposterior (A) and lateral (B) radiographs.

appear as an undermineralized focus and may be misinterpreted as a destructive lesion of the bone (see Fig. 12-13). On the anteroposterior view of the elbow, the thin humeral olecranon fossa occasionally appears to be entirely lucent, the so-called perforated olecranon fossa (Fig. 12-18). In some instances, there is a bridge of bone crossing or a separate ossicle within a perforated olecranon fossa. A rare anatomic anomaly is a bony projection from the anterior medial distal humerus known as the supracondylar process (Fig. 12-19), which is discussed in Chapter 2.

References 1. Barr, L. L.: Elbow. Clin. Diagn. Ultrasound 30:135, 1995. 2. Beltran, J., Rosenberg, Z. S., Kawelblum, M., Montes, L., Bergman, A. G., and Strongwater, A.: Pediatric elbow fractures: MRI evaluation. Skeletal Radiol. 23:277, 1994. 3. Blickman, J. G., Dunlop, R. W., Sanzone, C. F., and Franklin, P. D.: Is CT useful in the traumatized pediatric elbow? Pediatr. Radiol. 20:184, 1990. 4. Brodeur, A. E., Silberstein, M. J., and Graviss, E. R. Radiology of the Pediatric Elbow. Boston, G. K. Hall, 1981. 5. Brodeur, A. E., Silberstein, M. J., Graviss, E. R., and Luisiri, A.: The basic tenets for appropriate evaluation of the elbow in pediatrics. Curr. Probl. Diagn. Radiol. 12:1, 1983. 6. Chapman, V., Grottkau, B., Albright, M., Elaini, A., Halpern, E., and Jaramillo, D.: MDCT of the elbow in pediatric patients with posttraumatic elbow effusion. A. J. R. 187:812, 2006.

7. Davidson, R. S., Markowitz, R. I., Dormans, J., and Drummond, D. S.: Ultrasonographic evaluation of the elbow in infants and young children after suspected trauma. J. Bone Joint Surg. 76A:1804, 1994. 8. Gordon, A. C., Friedman, L., and White, P. G.: Pictorial review: Magnetic resonance imaging of the paediatric elbow. Clin. Radiol. 52:582, 1997. 9. Griffith, J. F., Roebuck, D. J., Cheng, J. C. Y., Chan, Y. L., Rainer, T. H., Ng, B. K., and Metreweli, C.: Acute elbow trauma in children: Spectrum of injury revealed by MR imaging not apparent on radiographs. A. J. R. 176:53, 2001. 10. Harada, M., Takahara, M., Sasaki, J., Mura, N., Ito, T., and Ogino, T.: Using sonography for the early detection of elbow injuries among young baseball players. A. J. R. 187:1436, 2006. 11. Keats, T. E.: An Atlas of Normal Roentgen Variants That May Simulate Disease, 5th ed. St. Louis, Mosby-Year Book, 1992, p. 395. 12. Kijowski, R., and De Smet, A. A.: MRI findings of osteochondritis dissecans of the capitellum with surgical correlation. A. J. R. 185:1453, 2005. 13. Markowitz, R., Davidson, R. S., Harty, M. P., Bellah, R. D., Hubbard, A. M., and Rosenberg, H. K.: Sonography of the elbow in infants and children. A. J. R. 159:829, 1992. 14. McCauley, R. G. K., Schwartz, A. M., Leonidas, J. C., Darling, D. B., Bankoff, M. S., and Swan, C. S. 2nd: Comparison views in extremity injury in children: an efficacy study. Radiology 131:95, 1979. 15. Merten, D. F.: Comparison radiographs in extremity injuries of childhood: current application in radiological practice. Radiology 126:209, 1978. 16. Rodgers, L. F.: Radiology of Skeletal Trauma. New York, Churchill Livingstone, 1982, p. 435.

Chapter 12 Imaging of the Pediatric Elbow

17. Schmidt, H., and Freyschmidt, J.: Köhler/Zimmer Borderlands of Normal and Early Pathologic Findings in Skeletal Radiology, 4th ed. New York, Thieme Medical Publishers, 1993. 18. Silberstein, M. J., Brodeur, A. E., and Graviss, E. R.: Some vagaries of the capitellum. J. Bone Joint Surg. 61A:244, 1979. 19. Silberstein, M. J., Brodeur, A. E., and Graviss, E. R.: Some vagaries of the radial head and neck. J. Bone Joint Surg. 64A:1153, 1982.

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20. Silberstein, M. J., Brodeur, A. E., Graviss, E. R., and Luisiri, A.: Some vagaries of the medial epicondyle. J. Bone Joint Surg. 63A:524, 1981. 21. Silberstein, M. J., Brodeur, A. E., Graviss, E. R., and Luisiri, A.: Some vagaries of the olecranon. J. Bone Joint Surg. 63A:722, 1981.

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CHAPTER

13

Congenital Abnormalities of the Elbow Peter C. Amadio and James H. Dobyns

somal syndromes, from the common dislocation of the radial head69 through fairly well-known syndromes such as trisomy 18, fibrodysplasia ossificans progressiva and the Antley-Bixler syndrome7 to such rarities as the Bruck syndrome (osteogenesis imperfecta with congenital joint contractures) and a congenital mirror movement syndrome. In some cases, the specific gene locus has now been identified; for example, elbow synostosis may also occur in the context of the multiple synostosis syndrome,53 which has been reported in large family groups and is the result of mutations in genes controlling TGF-β synthesis, including noggin, a protein believed to be important in establishing morphogenic gradients.

INTRODUCTION

CLASSIFICATION

Elbow function and configuration are affected by conditions both proximal and distal to the elbow as well as abnormalities at the elbow itself. With this proviso, this chapter discusses congenital anomalies of the region between the shaft-metaphyseal junction of the humerus proximally and the bicipital tuberosity distally, and reviews the current state of knowledge for evaluation and treatment in that region.

A multitissue defect classification can be based on the most obvious and most inhibiting tissue defect known to be present. Some degree of defect in other tissues is also commonly noted. The classification consists of three major categories: (1) bone and joint anomalies, (2) soft tissue anomalies, and (3) anomalies involving all tissues. Bone and joint abnormalities at the elbow may include major absences, but more commonly the skeletal structures are present but malformed. The common bone and joint problems are synostosis (Fig. 13-1), ankylosis (Figs. 13-2 to 13-4), and instability (Fig. 13-5). Soft tissue anomalies include malformations with contractures, control deficiencies, isolated tissue anomalies (Fig. 13-6), and congenital tumors (Fig. 13-7). Complete absence or disorganization of the whole limb, including elbow structures, may occur, as in phocomelia (Fig. 13-8); usually, recognizable though dysplastic structures are present (Fig. 13-9). Similar involvement, although more isolated to the elbow area, occurs in the pterygium syndromes. With reference to the bone and joint deformities only, it has been useful to many authors to classify them as congenital, developmental, or post-traumatic. As noted earlier, there is much confusion and interplay between these diagnoses, particularly with reference to radial head subluxation or dislocation. In this classification, congenital refers to a primary genetic dysplasia of the skeletoarticular structure of the elbow, resulting in an observed deformity. Other congenital anomalies or a familial history of similar anomalies help confirm this as an etiology. Developmental refers to elbow skeletal structures that are relatively normal at birth but that are then secondarily deformed by abnormal stresses (perhaps from a congenital shortening of the ulna); by paralysis or other limited motion (arthrogryposis); neural, metabolic, endocrine or dyscrasia disturbances (hemophilia, loss of pain recognition, hemochromatosis, and so on); tumor or hamartomatous involvement

CAUSES OF CONGENITAL ANOMALIES The causes of congenital elbow anomalies follow the same patterns of genetic or somatic damage to the embryo that are seen in other congenital anomalies. Often the most difficult problem is to decide whether the presenting deformity is entirely congenital or perhaps developmental or possibly even traumatic, and whether one or more of these etiologies are interacting. The most common condition in which this difficulty arises, radial head subluxation or dislocation, may be congenital, developmental, or post-traumatic. If it is not present at birth, it may be induced by a relatively trivial injury or merely by a short ulna from any cause. Because so much of the elbow area is cartilaginous at birth, it is difficult to rule out trauma as a possible agent in some dislocations and deformities. In addition, infections, tumors (congenital or infantile), and diseases (e.g., hemophilia) occasionally involve the elbow and may simulate congenital anomaly. Conditions that commonly involve the elbow are constitutional diseases of bone, metabolic abnormalities, and syndromes featuring limb formation and differentiation failures36,38,43,54,82,90 (Table 13-1). Some of the syndromes can be grouped under broad categories such as osteochondrodysplasia,3,29,33,90 dysostoses,18 primary growth disturbances, primary metabolic abnormalities, and congenital myopathies. Most, however, are chromo-

Text continued on p. 190.

Chapter 13 Congenital Abnormalities of the Elbow

TABLE 13-1

185

Elbow Deformities in Congenital Syndromes Syndrome Characteristics

Catalog Numbers*

Inheritance

Number of Patients†

1. Achondroplasia

O-1

10080

ASD

>100

2. Mesomelic dwarfism

O-1

15623, 24970

ASD, ASR

>100

3. Nievergelt

O-1

16340

ASD

<50

4. Werner

O-1

27770

ASR

>100

5. Ellis—Van Creveld

O-1

22550

ASR

<50

6. Acrodysostosis

O-1

10180

ASD

<50

7. Acromesomelic dwarfism

O-1

20125

ASR

<50

8. Ulna, fibula hypoplasia

O-1

19140

ASD

<25

9. Type 1 acrocephalo-polysyndactyly

O-1

10110, 20100, 10112, 20102, 16420, 10120, 10130, 10140, 10160

ASD

>100

10. Multiple cartilaginous exostoses

O-2

13370

ASD, ASR

>100

11. Metaphyseal chondrodysplasia

O-3

26040, 25401, 20090, 25022, 25023, 25025, 15640, 25030, 15650, 24270, 15640, 15650, 21505, 25022, 25023, 25025, 25030, 25040, 25041

ASD

<100

12. Cranial dysostosis

D-1

12350, 12290, 21835, 30411

ASD

<100

13. Familial radioulnar synostosis

D-3

17930

ASD

<100

14. Pterygium

D-3

26500, 31215, 19100, 11950, 19360, 17820

ASD, ASR

>50

15. Radial aplasia

D-3

21860

ASD, S

>100

26580, 26570, 27795, 25960, 16630

ASD, ASR

<50

Syndrome

16. Idiopathic osteolysis

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TABLE 13-1

Elbow Deformities in Congenital Syndromes—cont’d

Syndrome

Syndrome Characteristics

Catalog Numbers*

17. Mucopolysaccharidoses

PMA

18. Mucolipidoses

19. Lipidoses

Inheritance

Number of Patients†

25270, 23000, 22380, 25280, 30990, 25290, 25292, 25293, 25294, 25300, 25301, 25320, 25322, 25323

ASR

>100

PMA

25240, 25250, 25260, 25265

ASR

>100

PMA

21280, 30150, 24680, 23050, 23060, 23065, 21208, 25010, 25720

ASR

<50

19235, 10748

ASD

<50

19370, 27772

ASD

>50

23100, 27235, 20100, 10120, 10160, 10140, 20155, 31410, 21850, 21853, 21855, 21860, 25922, 12315

ASD

>100

23. De Lange dwarfism

12247

ASD

>100

24. Diastrophic dysplasia

22260

ASR

<50

16120

ASD

<50

26. Otopalatodigital

31130

X

<100

27. Rubenstein-Taybi

26860

ASR

>100

28. Silver-Russell

27005

ASR

>50

29. Klinefelter

27330

ASR

>50

30. Thalidomide embryopathy

27360

T, ASR

31. Holt-Oram

14290

ASD

>100

32. Acrofacial dyostosis (Nager)

15440

S, ASD

>50

33. LADD

14973

ASD, S

<50

20. VATER complex 21. Craniocarpotarsal dystrophy 22. Craniosynostosis

1

25. Nail-patella

D-2

Chapter 13 Congenital Abnormalities of the Elbow

TABLE 13-1

187

Elbow Deformities in Congenital Syndromes—cont’d Catalog Numbers*

Inheritance

Number of Patients†

34. Fanconi’s anemia

22765, 22766

ASR

>100

35. TAR

27400

ASR

>100

36. Auriculo-osteodysplasia

10900

ASD

<25

37. Ehlers-Danlos

13000, 13001, 13002, 13005, 22535, 30520, 22540, 13006, 22541, 13008, 30415, 22531, 14790

ASD, ASR

>100

38. Phocomelia

26900

ASR

<50

39. Larsen’s

15025, 24560

ASD, ASR

>50

40. Oculomelic complexes

16420, 25790, 25792, 16430, 25795, 16431

ASD, ASR

41. Otopalatodigital

31130

X

<50

42. Amelia of arm

10440

S, ASD

<25

43. Peromelia of humerus

10030, 10330

ASD

<25

44. Humeroradial synostosis

14305, 23640

ASD, ASR

>50

45. Femoral-fibula-ulna complex

22820

ASR

>100

46. Focal dermal hypoplasia (Goltz)

30560

X

>50

47. Split hand

18360

ASD

>100

48. Ulnar mammary

19145

ASD

<25

49. Ulnar deficiency

13575, 19140, 20070, 24960, 10790, 31436, 27170, 20060, 20061

ASD, ASR

>100

Syndrome

Syndrome Characteristics

ASD, autosomal dominant; ASR, autosomal recessive; LADD, lacrimo-auriculo-dento-digital syndrome; D-1, dysostosis with cranial and facial involvement; D-2, dysostosis with predominant axial involvement; D-3, dysostosis with predominant extremity involvement; O-1, defects of growth of tubular bones; O-2, disorganized development of cartilage and fibrous skeletal elements; O-3, abnormalities of diaphyseal cortical density or metaphyseal modeling; PMA, primary metabolic abnormalities; PGD, primary growth disturbances; S, sporadic; T, teratogenic; TAR, thrombocytopenia and absent radius; VATER, vertebrae, anus, trachea, esophageal, renal; X, linked to sex chromosome. *Catalog numbers are those used in McKusick, V. A.: Mendelian Inheritance in Man, 6th ed. Baltimore, Johns Hopkins University Press, 1983. † Approximate number so far reported.

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Part IV Conditions Affecting the Child’s Elbow

FIGURE 13-1

A, Lateral and (B) anteroposterior x-ray views of a hypoplastic distal humerus and an apparent radial head subluxation certainly reveal a deformity but probably not a subluxation. Clinically, there was no evidence of a dislocated radial head. C, The opposite elbow showed a radiohumeral synostosis and also a recent fracture just proximal to the synostosis. This case demonstrates the difficulties of differentiation between subluxation, dislocation, and synostosis about the elbow, but the etiology is clearly congenital.

Chapter 13 Congenital Abnormalities of the Elbow

189

FIGURE 13-2

This anteroposterior view of an elbow in congenital ulnar dimelia shows no radiohumeral joint but two ulnohumeral joints. The appearance is unusual as expected, but no dislocation is noted. Motion of the elbow and forearm is limited by more than 50%.

FIGURE 13-3

A, Elbow and forearm function are, to date, nearly normal in this teenage boy in whom the anteroposterior x-ray view shows ulnar hypoplasia and bowing, distortion of the distal ulnar physis-metaphysis, and subluxation of the radial head. B, The lateral x-ray view shows a similar epiphysis-physis-metaphysis distortion of the proximal ulna with associated joint surface irregularity and shaft bowing. No diagnosis has been confirmed, but this is probably an osteochondrodysplasia. The elbow abnormalities are developmental.

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Part IV Conditions Affecting the Child’s Elbow

FIGURE 13-5

This case further demonstrates the overlap between congenital and developmental abnormalities of the elbow. Gradual radial head subluxation due to unequal length of forearm bones is well known in multiple exostosis. These anteroposterior and lateral xrays demonstrate a severe dislocation of the radial head that was present at birth and was associated with a severe osteochondroma deformity of the distal ulna with inhibition of ulnar growth.

FIGURE 13-4

A, This 18-month-old infant with chondrodysplasia punctata has developmental contractures of many joints including the elbows, where broad metaphyses and irregular, calcified epiphyses (B) are seen.

tion, but it often is not. A radial head subluxation or dislocation in an elbow with normal, neural, muscular, and skeletal structures in both elbow and forearm is post-traumatic until proven otherwise; such an elbow with abnormal skeletal forearm structures is probably due to developmental stresses, but additional trauma may play a part. Such an elbow with a synostosis from birth or other skeletal deformity and no evidence of peri-birth trauma is due to congenital causes, but again, trauma may be an additional factor. The confusions highlighted by this classification have been much discussed in the literature.14,20,38,45,51,54,61,70,71,72,79

DIAGNOSIS BONE AND JOINT ANOMALIES

(fibromatosis, osteochondromata, and so on), and disease (sickle cell anemia, Gorham’s disease, infections). The post-traumatic etiologic grouping is included in this chapter only because of the continuing confusion over early radial head dislocations, which are often posttraumatic, either as a variant of Monteggia fracture dislocation or as a pure dislocation of the soft cartilaginous radial head pulling through the annular ligament (see Chapter 20) and its residua. Both early and late, dislocation of the radial head is often diagnosed as a congenital subluxation or disloca-

Synostosis Synostoses may occur between all or any two of the three bones present at the elbow. The most common synostosis is that between the radius and the ulna proximally in the forearm, near the elbow (Fig. 13-10), but these two bones also may be joined at any point in their paired course in the forearm. Mital55 has classified these synostoses as type I, proximal to the proximal radial physis, and type II, distal to the proximal radial physis. Type II synostoses are more likely to be

Chapter 13 Congenital Abnormalities of the Elbow

FIGURE 13-6

A, Congenital aplasia of skin and soft tissues at the elbow and proximal forearm results in (B) developmental bone changes in the forearm and elbow.

FIGURE 13-7

A, The anteroposterior (AP) and lateral x-rays of the elbow and forearm in a patient with juvenile fibromatosis reveal marked enlargement of the ulna, posterolateral subluxation of the radial head, moderate enlargement of the distal humerus, and surface irregularities at all aspects of the joint. The changes in the elbows are developmental. B, A much more typical congenital posterior radial head dislocation is revealed in these AP and lateral views (A) and (B) of the elbow of a 14-year-old male with nail-patella syndrome and restricted elbow-forearm motion: 30 to 155 degrees flexion extension; 45 degrees supination; 60 degrees pronation. His mother has the same diagnosis and the same problem.

191

192

Part IV Conditions Affecting the Child’s Elbow

humeroradial type is most common, followed by humeroradioulnar and humeroulnar types.52 However, anatomy is not the whole story, and McIntyre and Benson52 have proposed an etiologic classification of developmental elbow synostoses, specifically as to whether the synostosis occurs with (class I, or bony type) or without (class II, or joint type) limb hypoplasia. Within each class, the synostosis can be further characterized as occurring in a sporadic or familial pattern and, if familial, with dominant or recessive inheritance. In familial cases, the condition is usually bilateral.12 One of the more dramatic presentations is in the Antley-Bixler syndrome, an autosomal recessive disorder characterized by radiohumeral synostosis, cranial synostosis, midface hypoplasia, and a variety of urogenital and cardiac abnormalities (Fig. 13-10C).7 Distal radioulnar dislocation is a common accompaniment of many of these syndromes.

Ankylosis

FIGURE 13-8

This radiograph of the upper limb of a patient with congenital phocomelia shows a fairly welldeveloped shoulder and arm, a very hypoplastic hand, and fusion of all elbow elements with the short ulna protruding at right angles to the radius and forearm.

associated with congenital dislocation of the radial head.45 Cleary and Omer12 suggested a four-level classification scheme, in which Type I is clinically but not radiographically fused with a reduced normal-appearing radial head; Type II is similar but with a clear, bony synostosis; Type III has a hypoplastic posteriorly dislocated radial head; and Type IV has a hypoplastic anteriorly dislocated radial head. Type III appears to be the most common deformity and the one most likely to be associated with significant rotational deformity (almost always pronation). In addition, radiohumeral synostosis, ulnohumeral synostosis, or synostosis among the radius, humerus, and ulna may be present; often, the synostosis is in association with other limb abnormalities, the most common of which is probably ulnar deficiency.30,31,42,57,84 Synostosis may also be associated with fetal alcohol syndrome.84 Incomplete synostosis may occur, but often, this is a radiologic appearance rather than an actual occurrence, because complete radiographic synostosis is usually present by maturity.27,38,50,82 Cleary and Omer’s five cases of type I synostosis are, however, genuine; all of the patients were skeletally mature at the time of final clinical and radiologic review.12 Synostosis between the humerus and either the radius, ulna, or both is less common. Of these, the

Partial ankylosis of the elbow or the proximal radioulnar joint is often overlooked because limited elbowforearm motion is common in infancy28 and often not remarked in childhood. Causes include failure of complete synostosis, intrinsic abnormalities of the joint or surface formation mechanism, and abnormalities of the surrounding soft tissues, as occurs in pterygium cubitale. The joint must be formed correctly, must have adequate surface material and ligamentous support, and must move soon after its formation, or it will become ankylosed, as occurs, for example, in arthrogryposis, or, far more rarely, in Apert’s syndrome.35,89 There are instances when all or part of the elbow appears to be dislocated but proves to be only malformed and limited in motion (Fig. 13-11). Patients with dysplasia, such as those with Apert’s syndrome, may show a progressive loss of motion over time.89

Instability True congenital elbow instability seldom resembles the post-traumatic condition, but the two are often mistaken for each other. Congenital ulnohumeral dislocation is infrequent except in severe multitissue hypoplasia such as phocomelia, severe ulnar hypoplasia, and severe pterygium syndrome. The most common problem of instability at the elbow is that of radial head subluxation or dislocation.1,2,11,20,22,25,38,47,48,61,64,67,78,79 When subluxation is an isolated phenomenon, there is considerable doubt about whether it is congenital, developmental, or post-traumatic.14,20,38,45,51 The pulled elbow of infancy is a wellknown clinical problem that is associated with trivial trauma and laxity or minor tears of the annular ligament.61,70,72,75 Children have been seen at birth or shortly thereafter with similar problems.14,61,75 Furthermore, such

Chapter 13 Congenital Abnormalities of the Elbow

FIGURE 13-9

A, In another instance of generalized congenital hypoplasia of the upper limb, all segments from the shoulder girdle through the hand are equally and severely affected. B, Synostosis of all components of the elbow is present (C), correlated with a hypoplastic and asymmetric forearm plus a hypoplastic hand. D, Hypoplasia of the arm, shoulder, and shoulder girdle is also obvious on this radiograph.

193

194

Part IV Conditions Affecting the Child’s Elbow

FIGURE 13-10

A, X-ray view of a typical congenital proximal, radioulnar, synostosis. B, The lateral view of the same synostosis is seen but demonstrates no radial head posterior subluxation, although this is commonly seen. C, Oblique view of the typical congenital radiohumeral synostosis of the Antley-Bixler syndrome.

subluxations in the infant, if not treated by closed reduction or other means, may result in deformities similar to those described as indicative of congenital dislocation of the radial head. It has been said that the degree of deformity in the few cases of known infantile dislocation that have been left untreated but followed suggest that the resulting deformity is milder than that seen in definite congenital hypoplasia at the elbow. This may be so but the so-called criteria for classifying a radial head dislocation as congenital (see later) may be seen after any early radial head dislocation regardless of cause (Fig. 13-12). By contrast, when traumatic dislocation is unreduced in the older child, the development of the radial head and the capitellum remains fairly normal, displaying only minimally those radiographic features said to be characteristic of congenital radial head dislocation. These features are (1) a dislocated or subluxed radial head, (2) an underdeveloped radial head, (3) a flat or dome-shaped radial head, (4) a more slender radius than normal, (5) a longer radius than normal, (6) an underdeveloped capitellum humeri, and (7) a lack of anterior angulation of the distal humerus.4,20,56,63,88 Bilaterality, especially symmetric bilateral dislocation, is

usually also considered evidence of a congenital etiology, but this is not an absolute requirement.48 However, many if not all the features of congenital dislocation can also be seen with developmental dislocation, due to mild degrees of ulnar or capitellar hypoplasia. In such cases the radial head may slowly dislocate with growth, as the paired forearm bones continue to grow at dissimilar rates.4 There may be only one absolute criterion of congenital elbow dislocation—dislocation with severe hypoplasia of all the osseous elements of the elbow. Absence of the capitellum is probably an example of congenital aplasia, but hypoplasia of the capitellum may occur after dislocation from any cause, as may a deformity of the radial head (see Chapter 20). When radial head dislocation is familial, bilateral, or seen at birth, or when it occurs with other musculoskeletal anomalies, particularly anomalies in the same upper limb, the evidence is strong that the radial head dislocation is congenital. Cases that are diagnosed later in life may be associated with a discrepancy in length of the paired forearm bones and, therefore, may fall within the “developmental” category. It is well known

Chapter 13 Congenital Abnormalities of the Elbow

195

FIGURE 13-11 A, Anteroposterior (AP) x-ray view of an apparent radiohumeral dislocation similar to that shown in Figure 13-2 is seen preoperatively. B, A postoperative AP x-ray view 4 years later shows repositioning of what was determined to be a congenital displaced radiohumeral joint without a dislocation of the radial head. C, A lateral postoperative view of the same elbow. Repositioning was obtained when the radius was shortened by removing a segment of the radial shaft. This segment of excised radius was then used to block the repositioned lateral condyle in its new position. This surgical procedure improved the x-ray position of the elbow but did not change function, which demonstrated both preoperatively and postoperatively mild loss of extension-flexion and moderate loss of supination-pronation.

that inadequate length of the ulna from any cause will result in increased compressive stresses along the radius, gradually leading to a subluxation and perhaps a dislocation of the radial head.38,47,79 Such subluxations, therefore, also may be a secondary phenomenon.48 Approximately half of all patients with isolated congenital radial head dislocation will have a problem bilaterally.2,48,56 Bell and associates4 have classified isolated

congenital dislocations of the radial head as type I, subluxation; type II, posterior dislocation with minimal displacement; and type III, posterior dislocation with significant proximal migration of the radius. Type I is the least common dislocation but the one most likely to be associated with pain. Types II and III appear to be roughly equally prevalent. Type III is associated with the most loss of motion, usually supination. Deformity

196

Part IV Conditions Affecting the Child’s Elbow

These anomalies have been subdivided into syndromes with contractures (pterygium syndromes, congenital muscular atrophy and myopathy syndromes), control deficiencies, isolated tissue anomalies (triceps absence or contracture), and congenital soft tissue tumors.

Contractures The classic malformation with contracture is pterygium cubitale, in which almost every soft tissue is abnormal and a severe flexion contracture exists.23,24 The condition also has been called cutaneous webs and webbed elbow; it is but one manifestation of a congenital syndrome that may affect the neck, axilla, elbow, knee, or digits. A survey of 240 cases of cutaneous webs reported in the literature included 29 in the region of the elbow.23 The web may be unilateral or bilateral, or symmetric or asymmetric. The condition has been reported to result from both an autosomal dominant and a recessive gene. Associated abnormalities involving almost every body system have been reported.38,82 Other conditions resulting in formidable contractures about the elbow include fibrodysplasia ossificans progressiva and arthrogryposis.

Control Deficiencies

FIGURE 13-12 Anterior dislocation of the radial head is demonstrated at initial diagnosis (age 2 weeks), at age 4 months, and at age 11 years. In addition to the dislocation, there is a reversal of the ulnar curve and some convexity of the radial head. The etiology is probably post-traumatic.

of the radial head without subluxation also has been reported.22 Finally, Wiley and colleagues86 have reported congenital anterior and lateral dislocations.

Other Bony Problems Hypoplasia of the distal humerus may occur; the resulting deformity may cause ulnar neuropathy, either immediately, from synovial cysts, or chronically, due to abnormal elbow growth and nerve traction.74 Congenital pseudarthrosis of the olecranon has been reported but is exceedingly rare.66

SOFT TISSUE ANOMALIES Soft tissue anomalies or absences may interfere with elbow function as much as bone or joint deformities.

Arthrogryposis and its related syndromes are also included in this group but also are discussed elsewhere (see Chapters 71 and 72). Both flaccid and spastic palsies affect elbow control and range of motion. Simple absences or deficiencies of tissue also affect elbow control. Hypoplasia of the elbow includes deficient growth not only of osseous structures but also of the related soft tissue control elements and cover structures.13,58,81 Most characteristic is probably the extension contracture of arthrogryposis.87

Isolated Tissue Anomalies The skin may be deficient or missing, with absence, hypoplasia, or scarring of the underlying tissues. Nerve, vascular, and lymphatic anomalies in the region of the elbow are common.38 The anconeus epitrochlearis occasionally is present as an anomalous muscle and may cover the ulnar nerve in the cubital tunnel area, contributing to the possibility of entrapment. Other anomalous muscles that may cause nerve entrapment problems are (1) Gantzer’s muscle, an anomalous head of the flexor pollicis longus or flexor profundus that usually originates from the medial epicondyle or the coronoid process of the ulna and occasionally is a factor in anterior interosseous nerve compression; (2) a solitary head of the supinator and other anomalies of this muscle; (3) accessory muscles of the anterolateral aspect of the elbow, including the accessory brachialis or accessory brachioradialis; (4) variations in the head, origin, or insertion of the pronator teres; (5) variations of a similar

Chapter 13 Congenital Abnormalities of the Elbow

nature in the flexor carpi radialis, the flexor carpi ulnaris, and the palmaris longus53; and (6) an aberrant medial head of the triceps, which may snap over the medial epicondyle and irritate the ulnar nerve.16

Congenital Soft Tissue Tumors Tumors of the soft tissue are rare but include a wide variety of abnormalities, ranging from overgrowth to neoplasms and from multitissue hamartomas to single tissue entities. Probably the two most common tumors in the infant are the fibromatoses and vascular tumors. If the elbow area is involved, there is usually some limitation of motion.

COMBINED BONE AND SOFT TISSUE ANOMALIES Soft tissue anomalies may coexist with mild osseous anomalies, such as those related to the supracondyloid process.13,53,80 The supracondyloid process is an anomalous bony prominence extending from the anteromedial aspect of the distal third of the humerus. Struthers81 in 1848 described the ligament associated with this process, and since then, various anomalies have been reported in connection with it. These include a more proximal branching of the ulnar artery off the brachial artery above the bony spur, a more proximal insertion of the pronator teres on the bony process, and various relationships of the neurovascular structures with bone and ligament. The symptoms—pain, tingling, numbness, and so on—usually are neuralgic, but they may be vascular. Many of the congenital anomalies already discussed are manifest in both osseous and soft tissues. These abnormalities may be equivalent as in the supracondyloid process syndrome just discussed, or predominantly in one tissue, as in fibromatosis. More severe changes are seen with severe pterygium cubitale and severe forms of ulnar hypoplasia and phocomelia. In pterygium cubitale, or congenital webbed elbow, a skin web extends from the upper arm across the volar elbow to the forearm. Flexion is usually possible, but extension, pronation, and supination are severely limited. The muscles and neurovascular structures are incompletely developed. The bones are hypoplastic and deformed, and the elbow joint often is dislocated or severely hypoplastic. Fibrous strands represent missing muscles or tendons. Muscle hypoplasia is present posteriorly as well as anteriorly. Severe ulnar hypoplasia is marked by radial head dislocation, diminishing segments (ranging from small to nonexistent) of the proximal ulna, variable but seldom normal motion and stability, and muscle and neurovascular abnormalities. Conditions are more normal proximal to the elbow, but distally, more abnormalities are apparent; the ulnar forearm and hand structures are

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particularly dysplastic. Lorea et al46 have proposed a classification of these findings based on a review of their own experience with 46 patients and a literature review. They propose three elbow types: type 1, normal; type 2, radiohumeral synostosis; and type 3, radial head subluxation. They further recommend subclassifying the elbows as having extension (type E) or flexion (type F) contractures. Unfortunately, they do not give the distribution of these types in their series. Phocomelia may present with similar findings, or the elbow may be even more dysplastic or absent altogether (hand, wrist, or forearm may be attached directly to the shoulder or trunk).

TREATMENT OF BONE AND JOINT DYSPLASIAS TREATMENT OF SYNOSTOSIS The treatment of synostosis of the elbow joint, whether radiohumeral60 or ulnohumeral, is dictated by the position of the forearm-wrist-hand unit and the function of the wrist-hand unit. These treatments have changed little over the past few decades. If the hand is absent or nonfunctional, repositioning of a synostotic elbow is clearly less important. If the hand is functional and the elbow is in a “functional” position (i.e., somewhere near midflexion), especially if the contralateral limb is normal, no treatment is likely to be necessary. For bilateral synostoses, some consideration probably should be given to positioning one arm in relative flexion and the other in relative extension. Frequently, only one forearm bone is well represented, and this may be bowed or deformed in some manner as well as short. In addition, there may be a rotational deformity. The forearm-wrist-hand unit may point directly posterior when the upper limb is in its usual dependent position beside the torso. Although simple rotational deformities can be corrected by osteotomy at any level, multiplane deformities should be corrected at the site of maximum deformity—that is, the humeral-forearm junction—perhaps extending the correction distally in the forearm (Fig. 13-13). One such method involves a posterior approach and a multiplesegment corrective osteotomy, making one or more of the segments trapezoidal in shape and rotating it 180 degrees, if necessary, to realign the unit as desired. If only one limb is involved, this desired position is usually at maximum length, with the forearm, wrist, and hand in the midposition. Derotation should be accomplished in the direction that causes the least torsion of the neurovascular structures, commonly from an internally rotated position through a clockwise rotation to a forearm midposition. Hyperextension, if present, is cor-

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FIGURE 13-13 A, Typical congenital radiohumeral synostosis with marked curving of the radial segment. B, A “shish kabob” corrective osteotomy was carried out with temporary internal fixation. Excellent correction resulted, and there were no complications. The elbow synostosis resulted in a posterior pointing forearm, wrist, and hand.

rected simply to neutral or slight flexion, and the osteotomy segments are adjusted to make the best contact in the desired position; a segment may be excised if this is needed for contouring. If both limbs are involved, enough elbow flexion angle should be included on one side to allow one of the limbs to reach the face and the head. Arthroplasty has been attempted30,31,39,57 but with indifferent results; the usual result is recurrence. Proximal forearm synostosis may occur with elbow synostosis, in which case the elbow is derotated as described previously. If, however, proximal radioulnar synostosis occurs in the presence of a functioning elbow joint, derotation of the forearm alone may be required. The indications for this procedure seem limited. Most patients have little functional deficit.12 Compensatory rotation at the wrist appears to be an important factor in minimizing symptoms.62 Although many authors have attempted and a few have claimed success for passive and even active mobilization of the forearm,8,15,19,27,37,55 there is no body of literature that substantiates these results in a significant number of patients who have been followed for an adequate period of time. When attempted, these procedures usually involve excision of the proximal radius, including the synostotic mass; division of the entire length of the interosseous membrane; interposition of some material between the contact areas of the radius and the ulna;

and tendon transfers, such as rerouting the extensor carpi radialis longus to the volar wrist for supination and the flexor carpi radialis to the dorsal wrist for pronation. A similar procedure involving the interposition of a metallic swivel has been described by Kelikian and Doumanian,37 but few long-term results have been reported. A more reliable procedure is that of derotation osteotomy.27,76 This procedure is best outlined by Green and Mital,24,55 who perform the rotational osteotomy through the synostosis itself. It is indicated primarily when the forearm is fused in the extreme of either pronation or supination; forearms synostotic in neutral or close to neutral function well and often are diagnosed only later in infancy or childhood because of this fact. The synostosis is approached through a dorsal incision and is transversely osteotomized. A radioulnar (in the coronal plane) K-wire or Steinmann pin is then placed distal to the osteotomy site and is left protruding externally on both sides. A longitudinal (in the sagittal plane) pin is then placed from the olecranon across the osteotomy site, and corrective rotation is carried out as desired. Because the indication is an extreme pronated or supinated position, in most instances, 70 to 90 degrees of rotation from pronation toward supination is required. If circulatory deficits appear during or after this derotation, less rotation is accepted, although an additional

Chapter 13 Congenital Abnormalities of the Elbow

amount may be carried out 10 to 15 days later. The radioulnar pin may be fixed by either a plaster cast or an external fixation apparatus. Internal fixation should not be used because alteration of forearm rotation may be necessary to diminish circulatory difficulties. Goldner and associates21 claim that these circulatory problems may be minimized by the use of derotation in the distal forearm (radius only in younger patients; radius and ulna in older patients). Their results have yet to appear in the literature except in abstract form, but the rationale seems reasonable and the technique appropriate. They recommend cross-pin fixation in children and plate fixation in adolescents and adults. One new and unusual problem has been reported recently, as an acute sequela of proximal radioulnar synostosis: flexion contracture. Matsuko et al49 have reported five cases in which an acute hyperflexion episode had resulted in the sudden onset of a fixed flexion contracture in teenaged boys (in four of the five cases). In each case, the problem was treated surgically. Through a lateral approach, the anterior elbow capsule was identified. In each case, a thickened band of anterior capsule was identified, under which the hyperflexed, anteriorly displaced radial head had become trapped. A simple excision of the band resulted in complete correction in each case.

TREATMENT OF ANKYLOSIS Ankylosis that does not involve synostosis, subluxation, or dislocation of the elbow may occur. Paralyses, muscle disease, and other soft tissue abnormalities commonly restrict motion; treatment of these abnormalities is discussed elsewhere (see Chapters 71 and 72). Abnormalities of joint shape and joint cartilage occur but are usually treated only by physical therapy. Rotation ankylosis due to soft tissue abnormalities occurs but has minimal effect on the elbow; its treatment requires release not only of the proximal radioulnar area but also in the forearm and wrist.5

TREATMENT OF INSTABILITY Treatment of infantile dislocations of the radial head, whether congenital, developmental, or traumatic, depends on the degree of hypoplasia present in the forearm and elbow area. If in doubt about the configuration of the various components of the elbow joint, an arthrogram should be performed61; this study may show that there is no dislocation at all but merely a deformed elbow joint with the radiocapitellar joint displaced from the usual position (see Fig. 13-12). Attempts at open reduction have been made, but the result is often recurrence unless both annular ligaments and ulnar length/ configuration are restored (Fig. 13-14). Most authors do

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not advise the procedure,4,56,86 although recently Sachar and Mih71 have reported good short-term results (maintenance of reduction and improved forearm rotation) in 10 of 12 children with congenital radial head dislocation operated on between ages 7 months and 6 years. They reported that the most common finding was an interposition of the annular ligament, which they divided and then repaired in its anatomic position. Follow-up was short, however, averaging less than 2 years, with the longest being only 41 months. The alternative to attempted reduction of congenital or infantile radial head dislocation is to accept the imposed disability (some limitation of forearm rotation, ranging from a few degrees to more than 90 degrees; occasional limitation of elbow motion; and infrequent pain) and proceed with radial head excision, if needed, at maturity.19-21,38,48,79 As noted in a long-term follow-up study,4 painful arthritis is typical only of the least common type I deformity. Relief of pain and cosmesis are more likely to be benefited from surgical excision; motion is seldom improved.4

TREATMENT OF SOFT TISSUE DYSPLASIAS Treatment of most soft tissue problems at the elbow level is discussed in other chapters. Arthrogryposis, as well as other flaccid palsies, is covered in Chapter 71. Spastic neurogenic problems are discussed in Chapter 72, and nerve entrapment around the elbow is discussed in Chapter 80. Successful treatment for other soft tissue dysplasias at the elbow is rare. Aplasia cutis congenita has occurred in the elbow area. In the author’s experience, it was associated with scarring and hypoplasia of the regional forearm muscles plus reactive deformity of the underlying bones. Resurfacing with a skin and subcutaneous flap was eventually necessary, followed by tendon transfers, which in this instance were required to provide extensor function of the wrist and hand. Muscle anomalies may result in either mechanical problems (snapping or catching)16 or neurovascular entrapment, as discussed in Chapter 80.

TREATMENT OF COMBINED BONE AND SOFT TISSUE DYSPLASIAS Pterygium cubitale remains an unsolved challenge. Attempts at treatment have included Z-plasty, skin grafts, and release of other tight structures. Improvement has been limited, and risks are high.23,24 Because there is no substantial report in the literature describing a reliable and useful method of treatment, no recommendations for surgical treatment are offered. Techniques of bone shortening to permit a greater safe excursion of the

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FIGURE 13-14 A, Anteroposterior and lateral x-ray views of a radial head dislocation in a limb with other congenital anomalies but with a fairly normal skeleton at the elbow. Although this fulfills the requirements usually listed for congenital dislocation, the dislocation may simply be developmental, related to the unequal length of the two forearm bones. B, Postoperative lateral radiographs after open reduction of the dislocated radial head and internal fixation. A second operation was carried out a year later, at which time the radius was shortened and the annular ligaments were reconstructed; repeat reduction of the radial head also was performed.

neurovascular structures or techniques of vascular and nerve grafting have been attempted, but adequate reporting is not yet available. The lengthening-stretching techniques of Ilizarov have been tried by a few investigators, so far with limited success. The hands in pterygium cubitale are often deficient also, but because limited excursion of the elbow is available in flexion, at least they are usually able to reach the upper trunk, the face, and the head. In severe forms of ulnar dysplasia, the elbow often displays adequate range and stability. Occasionally, the displaced radial head is sufficiently limiting or symptom provoking so that treatment is offered. Although excision of the radial head and a sufficient portion of the shaft to resolve the mechanical block might suffice, the desire to stabilize and lengthen the forearm plus the fear of recurrent encroachment by the radial shaft usually lead to a recommendation for a one-bone forearm procedure (Fig. 13-15).9 This is carried out as follows: 1. Use a long lateral incision that covers the distal half of the arm, the elbow, and the proximal half of the forearm.

2. Mobilize the anterior flap, identify and protect the radial nerve, and identify and mobilize the anteriorly and radially dislocated radius. 3. Mobilize the posterior flap, identify the short ulnar fragment, and uncover the interosseous space. 4. With both bones visualized through both anterior and posterior intervals (obviously, the procedure can be performed through an anterior approach only or through both a proximal anterior and a distal posterior approach, but we have found that access and safety are preferable this way), the maximum forearm length that the soft tissue will accept is judged by manual displacement. 5. The radius then is osteotomized at the length just determined, and the proximal fragment is removed. 6. The distal fragment is aligned with the short ulnar fragment, and contact is maintained by an intramedullary pin drilled through the olecranon, along the ulnar medullary cavity, across the osteotomy site, and along the radial intramedullary space until it penetrates the radial cortex at some point. (The forearm position, usually the midportion, should be set before this distal penetration occurs.)

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FIGURE 13-15 A, A lateral view of an elbow in ulnar agenesis shows an apparent dislocation proximally and anteriorly of the radial head. Although the ulnar agenesis is congenital, the dislocation is probably developmental. Clinical findings suggested that this was a true dislocation. B, There is occasional need for excision of the dislocated radial head and combination of the proximal ulna and distal radius to form a one-bone forearm, as seen here. This changes both the appearance and the function of the elbow as well as the forearm (the range of motion of the elbow is usually improved; the forearm position becomes fixed).

7. The usual support dressings (long arm splint-dressing combination initially, perhaps changed to a long arm cast later for the older child) are used until healing occurs (4 to 6 weeks). The supports are then discontinued, and the pin is removed.

vention. As has been noted, many synostotic forearms function well, even if in a poor position owing to compensatory hyper-rotation at the wrist. Such factors need to be considered carefully before embarking on a surgical adventure.

In phocomelia, the elbow is seldom the site of the infrequent surgical attention given to this condition, but there may be an occasional indication for a one-bone forearm procedure or for simultaneous lengthening and stabilization at an unstable elbow segment.77

Unwarranted Treatment Due to Misdiagnosis

COMPLICATIONS Overtreatment In many cases, the severe upper limb anomaly, particularly if it is of the sporadic variety, is associated with a completely normal contralateral upper limb. In such cases, surgical treatment may have little effect on the long-term functional level of the patient.6 Therefore, it also is important to consider the likely practical gains from therapy before proposing an inter-

This problem, present in any medical management situation, is a particular hazard with congenital anomalies. In the infant, testing of the neurovascular supply, dynamic and static control elements, and structural and support elements is difficult and uncertain. Interpretation of radiographs, when so much of the skeletal tissue is still cartilaginous, is deceptive. Nevertheless, the best review possible is needed if surgery is contemplated. This may require examination under sedation or special radiographic techniques such as arthrography, computed tomography or magnetic resonance imaging studies, cineradiographic motion and stress studies, and others. It should be recalled that “hands-on” examination is particularly valuable in the child because much cartilage is not yet bone and much muscle and tendon can be palpated better than tested.

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Infection This is a serious problem after any surgical procedure, and the usual wound management preventive measures are employed. The ability to apply a splint dressing that will maintain the desired position and stay in place is important in infants, but must not override the need for wound inspection if infection is suspected.

Vascular damage due to direct insults, compartment pressure increase, or indirect damage from stretch or torsion does occur. The stretchtorsion injury is a particular risk in the corrective osteotomies used to treat synostosis. For this reason, circulation should be checked during the osteotomy procedure. For osteotomies in the proximal forearm or elbow, fixation that can be removed or adjusted to decrease vascular stress is necessary. The circulatory pattern in congenitally abnormal arms is almost always abnormal; if further, extensive alteration in anatomy is anticipated, preliminary angiography may be helpful. Doppler assessment before and during surgery is invaluable.

Vascular Compromise

Nerve injury due to dissection or compression at anatomic entrapment points during postoperative reaction, stretch, or torque stress also may occur. Torque stress usually can be monitored by assessing the effect of the stress on the vascular supply. The other possibilities are best controlled by adequate exposure and careful dissection. Regardless, close and skilled postoperative monitoring is essential.

Nerve Damage

Partial or total destruction of the physis may result from bone cutting, pin or other fixation, or damage to the local physis circulation. Care should be taken to avoid physeal damage, particularly because most such limbs are hypoplastic and short already. A pin passing near the center of and at right angles to the physis seems to run the least risk of serious damage.

Physis Damage

Incongruous, malformed, and abnormally surfaced joints are common with congenital problems, and the investing soft tissue, motor units, and even skin also may limit normal joint function. Therefore, careful preservation of the available joint structures is important; this includes avoiding pin breakage in the elbow joint. Many surgeons, for instance, fix the ulna and radius rather than the humerus and radius to minimize the chances of intra-articular pin breakage after radial head reduction. Recurring elbow or forearm stiffness after operations for congenital elbow area anomalies is the most depressingly common complication of all. Pharmacologic suppression of scar formation and early continuous passive motion for these tiny arms

Joint Damage

may help, and both treatments should be available in the future.

CONGENITAL ELBOW REDUX Can a topic be brought to life, or at least reinvigorated? These questions arise as the authors peruse their prior efforts and the literature since those efforts and note that little has changed. There is still uncertainty regarding the relative incidence of the two most common congenital problems at the elbow, radial head subluxation or dislocation versus proximal radio-ulnar synostosis. Treatment for radial head dislocation still runs the gamut from waiting for symptoms/disability, then removing the radial head10 to open reduction, which may vary from removal of the annular ligament from the joint and reconstructing it in normal position to open reduction, corrective osteotomy of the ulna and reconstruction of an annular ligament, similar to the methods used for similar problems in old Monteggia injuries.85 Usually, radioulnar synostosis continues to be treated by corrective osteotomy, although new methods have been designed with osteotomies of both the radius (distally) and the ulna (proximally) with immediate correction if the deformity is not too severe59 or staged correction for the severe deformities.44 The venturesome among us are still, case by case, trying synostosis excision and interposition of various substances, recently using a vascular fascio-fat graft.34 The association of radial head subluxation or dislocation with other conditions continues to be newsworthy with new reports including congenital pseudarthrosis of the forearm41 treated by a one-bone forearm procedure in one case26 and treated by resection and internal fixation plus a vascularized fibular graft in another case.68 There are many reports of radial head subluxation or dislocation with other conditions17,40,73 and with paralyses.65 It is well known that shortening of the ulna from any cause risks of subluxation or dislocation of the radial head, but the association with radial longitudinal deficiency (44% of extremities with type 1 [more than 2 mm. shortening of the radius] radial deficiency32) is not as well known. However, it is certain that there is a familial component to some instances of radial head dislocation.69 So, what has changed in the last decade in this troublesome arena? Very little, and this is also troublesome. The potential for advances is overwhelming. Stem cell manipulation, embryonic and fetal alterations, early and late childhood intervention offer different and, as yet, minimally explored options. Solutions to the unsolved problems will involve both biologic and biotechnology approaches, and probably combinations of the two. The authors believe that this niche area has been dormant long enough and anticipate a need for

Chapter 13 Congenital Abnormalities of the Elbow

both national and international interactions between all interested parties. In the next edition of this text, we hope to report on a tsunami of interactive investigations.

SUMMARY Congenital elbow dysplasia is a more common problem than is generally realized. If it is mild, elbow function is minimally affected; if it is severe, problems of the entire limb or the wrist and hand often take precedence. In the few instances, when the elbow abnormality is isolated and relatively severe, surgical assistance is available but is less than satisfying. The most common and provocative problem is that of radial head subluxation or dislocation, in which the abnormality may be due to one or more of three differing etiologies: congenital, traumatic, or developmental (resulting from congenital, traumatic, infectious, tumor, or other causes). Effective management protocols have been developed, but unsolved problems still abound.

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35. Kasser, J., and Upton, J.: The shoulder, elbow and forearm in Apert syndrome. Clin. Plast. Surg. 18:381, 1991. 36. Kelikian, H.: Congenital Deformities of the Hand and Forearm. Philadelphia: W B Saunders Co., 1974, pp. 310, 714, 902. 37. Kelikian, H., and Doumanian, A.: Swivel for proximal radioulnar synostosis. J. Bone Joint Surg. 39A:945, 1957. 38. Kelly, D. W.: Congenital dislocation of the radial head spectrum and natural history. J. Pediatr. Orthop. 1:245, 1981. 39. K’Iery, L., and Wouters, H. W.: Congenital ankylosis of joints. Arch. Chir. Neerl. 2:173, 1971. 40. Lee, D. Y., Cho, T. J., Choi, I. H., Chung, C. Y., Yoo, W. J., Kim, J. H., and Park, Y. K.: Clinical and radiological manifestations of osteogenesis imperfecta type V. J. Korean Med Sci. 21:709, 2006. 41. Lee, K. S., Lee, S. H., Ha, K. H., and Lee, S. J.: Congenital pseudarthrosis of the ulna treated by free vascularized fibular graft—a case report. Hand Surg. 5:61, 2000. 42. Leisti, J., Lachman, R. S., and Rimoin, D. L.: Humeroradial ankylosis associated with other congenital defects (the boomerang arm sign). Birth Defects Orig. Artic. Ser. 11:306, 1975. 43. Lenz, W.: Genetics and limb deficiencies. Clin. Orthop. 148:9, 1980. 44. Lin, H. H., Strecker, W. B., Manske, P. R., Schoenecker, P. L., and Seyer, D. M.: A surgical technique of radioulnar osteoclasis to correct severe forearm rotation deformities. J. Pediatr. Orthop. 15:53, 1995. 45. Lloyd-Roberts, G. C., and Bucknill, T. M.: Anterior dislocation of the radial head in children: Aetiology, natural history and management. J. Bone Joint Surg. 59B:402, 1977. 46. Lorea, P., Pajardi, G., Medina, J., Szabo, Z., and Foucher, G.: [The ulnar longitudinal deficiency: proposition of a descriptive classification]. Chir. Main. 23:294, 2004. 47. Mann, R. A., Johnston, J. O., and Ford, J.: Developmental posterior dislocation of the radial head: Ten cases resulting from ulnar hypoplasia. In 38th Annual Meeting of the Western Orthopedic Association. 1974. Honolulu, Hawaii. 48. Mardam-Bey, T., and Ger, E.: Congenital radial head dislocation. J. Hand Surg. 4:316, 1979. 49. Masuko, T., Kato, H., Minami, A., Inoue, M., and Hirayama, T.: Surgical treatment of acute elbow flexion contracture in patients with congenital proximal radioulnar synostosis. A report of two cases. J. Bone Joint Surg. Am. 86-A:1528, 2004. 50. McCredie, J.: Congenital fusion of bones: Radiology, embryology, and pathogenesis. Clin. Radiol. 26:47, 1975. 51. McFarland, B.: Congenital dislocation of the head of the radius. Br. J. Surg. 24:41, 1936. 52. McIntyre, J. D., and Benson, M. K.: An aetiological classification for developmental synostoses at the elbow. J. Pediatr. Orthop. 11:313, 2002. 53. McIntyre, J. D., Brooks, A., and Benson, M. K.: Humeroradial synostosis and the multiple synostosis syndrome: case report. J. Pediatr. Orthop. B 12:192, 2003. 54. McKusick, V.: Mendelian Inheritance in Man, 6th ed. Baltimore, Johns Hopkins Press, 1983.

55. Mital, M. A.: Congenital radioulnar synostosis and congenital dislocation of the radial head. Orthop. Clin. North. Am. 7:375, 1976. 56. Miura, T.: Congenital dislocation of the radial head. J. Hand Surg. 15B:377, 1990. 57. Mnaymneh, W. A.: Congenital radiohumeral synostosis. A case report. Clin Orthop. 131:183, 1978. 58. Murakami, Y., and Komiyama, Y.: Hypoplasia of the trochlea and the medial epicondyle of the humerus associated with ulnar neuropathy. J. Bone Joint Surg. 60B:225, 1978. 59. Murase, T., Tada, K., Yoshida, T., and Moritomo, H.: Derotational osteotomy at the shafts of the radius and ulna for congenital radioulnar synostosis. J. Hand Surg. Am. 28:133, 2003. 60. Murphy, H. S., and Hansen, C. G.: Congenital humeroradial synostosis. J. Bone Joint Surg. 27:712, 1945. 61. Ogden, J. A.: Skeletal Injury in the Child. Philadelphia, Lea & Febiger, 1982, p. 319. 62. Ogino, T., and Hikino, K.: Congenital radioulnar synostosis: Compensatory rotation around the wrist and rotation osteotomy. J. Hand Surg. 12B:173, 1987. 63. Pfeiffer, R.: Die angeborene Verrenkung des Speichenkopfchens als Teilerscheinung anderer kongenitaler Ellenbogengelenkmissbildungen. Mensch Vererb Konstitutionslehre 21:530, 1938. 64. Phillips, S.: Congenital dislocation of radii. Br. Med. J. 1:773, 1883. 65. Pletcher, D. F., Hoffer, M. M., and Koffman D. M.: Nontraumatic dislocation of the radial head in cerebral palsy. J. Bone Joint Surg. 58:104, 1976. 66. Pouliquen, J. C., Pauthier, F., Kassis, B., and Glorion, C.: Bilateral congenital pseudarthrosis of the olecranon. J. Pediatr. Orthop. B 6:223, 1997. 67. Powers, C. A.: Congenital dislocations of the radius. J. A. M. A. 41:165, 1903. 68. Ramelli, G. P., Slongo, T., Tschäppeler, H., and Weis, J.: Congenital pseudarthrosis of the ulna and radius in two cases of neurofibromatosis type 1. Pediatr. Surg. Intern. 17:239, 2001. 69. Reichenbach, H., Hormann D., and Theile, H.: Hereditary congenital posterior dislocation of radial heads. Am. J. Med. Genet. 55:101, 1995. 70. Ryan, J. R.: The relationship of the radial head to radial neck diameters in fetuses and adults with reference to radial head subluxation in children. J. Bone Joint Surg. 51A:781, 1969. 71. Sachar, K., and Mih, A. D.: Congenital radial head dislocations. Hand Clin. 14:39, 1998. 72. Salter, R., and Zaltz, C.: Anatomic investigations of the mechanism of injury and pathologic anatomy of “pulled elbow” in children. Clin. Orthop. 77:134, 1971. 73. Sanatkumar, S., Rajagopalan, N., Mallikarjunaswamy, B., Srinivasalu, S., Sudhir, N. P., and Usha, K.: Benign fibrous histiocytoma of the distal radius with congenital dislocation of the radial head: a case report. J. Orthop. Surg. (Hong Kong) 13:83, 2005. 74. Sato, K., and Miura, T.: Hypoplasia of the humeral trochlea. J. Hand Surg. 15A:1004, 1990.

Chapter 13 Congenital Abnormalities of the Elbow

75. Schubert, J. J.: Dislocation of the radial head in the newborn infant. J. Bone Joint Surg. 47A:1019, 1965. 76. Simmons, B. P., Southmayd, W. W., and Riseborough, E. J.: Congenital radioulnar synostosis. J. Hand Surg. 9:829, 1983. 77. Smith, R. J., and Lipke, R. W.: Treatment of congenital deformities of the hand and forearm, Part II. N. Engl. J. Med. 300:402, 1979. 78. Smith, R. W.: Congenital luxations of the radius. Dublin Q. J. Med. Sci. 13:208, 1852. 79. Southmayd, W., and Ehrlich, M. G.: Idiopathic subluxation of the radial head. Clin. Orthop. 121:271, 1976. 80. Stone, C. A.: Subluxation of the head of the radius: Report of a case and anatomical experiments. J. A. M. A. 1:28, 1916. 81. Struthers, J.: A peculiarity of the humerus and humeral artery. Month. J. Med. Sci. 28:264, 1848. 82. Temtamy, S. A., and McKusick, V. A.: Carpal/tarsal synostosis. Birth Defects 14:502, 1978. 83. Tubiana, R.: The Hand. Philadelphia, W. B. Saunders Co., 1981.

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84. Uthoff, K., and Bosch, U.: Die proximale radioulnare synostose im rahmen des fetalen alkoholsyndrom. Unfallchirug 100:678, 1997. 85. Wang, M. N., and Chang, W. N.: Chronic posttraumatic anterior dislocation of the radial head in children: thirteen cases treated by open reduction, ulnar osteotomy, and annular ligament reconstruction through a Boyd incision. J. Orthop. Trauma 20:1-5, 2006. 86. Wiley, J. J., Loehr, J., and McIntyre, W.: Isolated dislocation of the radial head. Orthop. Rev. 20:973, 1991. 87. Williams, P. F.: The elbow in arthrogryposis. J. Bone Joint Surg. 55B:834, 1973. 88. Windfeld, P.: On congenital and acquired luxation of the capitellum radii with discussion of some associated problems. Acta Orthop. Scand. 16:126, 1946. 89. Wood, V. E., Sauser, D. D., and O’Hara, R. C.: The shoulder and elbow in Apert syndrome. J. Pediatr. Orthop. 15:648, 1995. 90. Wynne-Davies, R.: Heritable Disorders in Orthopaedic Practice. Oxford, Blackwell Scientific Publications, 1973.

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CHAPTER

14

Supracondylar Fractures of the Elbow in Children Anthony A. Stans

INTRODUCTION Supracondylar humerus fractures are the most common fracture about the elbow in children and have the highest complication rate for elbow fractures in this age group.8,16,39 These compelling facts continue to pique the interest and hold the attention of orthopedists who treat pediatric patients. Since the last edition of this text, issues that have generated the most discussion regarding supracondylar fracture treatment concern timing of reduction and treatment as well as pin configuration used for fracture stabilization. Both issues are addressed in the body of this chapter.

INCIDENCE AND ETIOLOGY Supracondylar humerus fractures almost exclusively affect the immature skeleton.41,50 Eliason25 reported that 84% of supracondylar fractures occurred in patients younger than 10 years. The peak age for supracondylar humerus fracture has been reported to be between ages 6 and 7 years, and the left arm is injured more frequently than the right.* Previous reports have suggested that supracondylar fractures are common in boys, but more recent studies have documented an equal sex distribution.† Traditional teaching has held that the peak incidence for extension-type supracondylar humerus fractures occurs at approximately age 7 because that is the age of maximum elbow flexibility and hyperextension. This mechanism has been confirmed by research suggesting that a fall on a hyperextended elbow produces a supracondylar humerus fracture, whereas a fall on an outstretched arm without elbow hyperextension is more likely to cause a distal radius fracture.60 Hyperextension converts what would be an axial loading force to the *See references 13,20,22,40,41,50-52,54,59,76. † See references 38,40,56,57,61,70,75,80.

elbow into a bending moment. The tip of the olecranon acts as a fulcrum, causing the fracture to occur through the relatively thin bone of the olecranon fossa (Fig. 14-1). The distinctive shape of the humeral metaphysis with the medial and lateral condyles and columns, and the narrow midpoint of the olecranon fossa, adds to the instability of the fracture, particularly when there is rotation and tilting of the distal fragment.62,63 Knowledge of elbow anatomy is important to understanding the cause of the injury, and to understanding effective treatment principles (see Chapters 2 and 3). The stability of the elbow derives from bony and soft tissue structures.33,61,66 Soft tissue stability on the lateral aspect of the elbow is provided by an expansion of the triceps, anconeus, brachioradialis, and extensor carpi radialis longus. The thickened periosteum of a young child, both medially and laterally, is an important additional stabilizer of the fracture fragment and provides a medial or lateral hinge during attempted reduction (Fig. 14-2). Research by Khare et al45 has confirmed the importance of the triceps tendon’s acting as a tension band to achieve fracture stability in the flexed elbow. Because angular deformity is a common complication of these fractures, the normal variations in pediatric anatomy should be understood. The carrying angle of the elbow joint is the angle formed by the intersection of the longitudinal axis of the arm and the forearm (Fig. 14-3). The normal elbow is usually in slight valgus alignment, but this feature varies among children.1,17,77 Smith77 noted that, of 150 children aged 3 to 11, the carrying angle in boys averaged 5.4 degrees and ranged from 0 to 11 degrees, whereas in girls, it averaged 6 degrees and ranged from 0 to 12 degrees. Aebi1 observed that the measurements were not constant and changed as the child matured, tending to decrease in magnitude and in variation between children. Although not commonly associated with abuse in the past, a recent report found that 36% of patients younger than age 15 months at the time of their supracondylar fracture sustained the fracture as a result of abuse.79 Clinicians must exclude “nonaccidental trauma” as a potential cause of injury whenever an infant presents with a supracondylar humerus fracture.

CLASSIFICATION A classification system should guide treatment, provide information on prognosis, and facilitate research by ensuring that similar injuries are compared in the literature. The vast majority of supracondylar humerus fractures can be classified as either flexion or extension injuries, a distinction based on the radiographic appearance and the mechanism of injury. The distinction is important for treatment because the reduction

Chapter 14 Supracondylar Fractures of the Elbow in Children

FIGURE 14-1

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A, Transverse and sagittal sections of the distal humerus. The shaft diameter is large above the supracondylar foramen. B, However, if a cut is made through the supracondylar foramen, the “bicolumnar” nature of this region becomes evident, looking proximally (C) and distally (D). (From Ogden, J.: Skeletal Injury in the Child. Philadelphia, Lea & Febiger, 1983.)

FIGURE 14-2

An experimentally produced fracture shows the medial periosteal hinge and offers a glimpse of the posterior hinge. After reduction, the soft tissues hold the fragments in place. The better the reduction, the greater the security. (From Rang, M.: Children’s Fractures, 2nd ed. Philadelphia, J. B. Lippincott, 1983.)

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FIGURE 14-3

A, Change in the carrying angle cannot be detected when the flexed elbows are examined from in front. B, Change in the carrying angle is apparent, however, when the flexed elbows are examined posteriorly. On the right, the bone prominences (black dots) can be seen to have tilted medially. C, With the arms extended, a 25-degree varus deformity of the right arm can be seen in a 9-year-old boy 2 years after a supracondylar fracture of the right arm. There is no limitation of motion. Note that the normal carrying angle of the left arm is 0 degrees. D, When the varus elbow is acutely flexed, the hand points laterally, away from the shoulder joint. This view also demonstrates the medial tilt of the bone prominences. (From Smith, L.: Deformity following supracondylar fractures. J. Bone Joint Surg. 42A:236, 1960.)

maneuvers are essentially opposite for the two fracture types and flexion-type fractures are significantly more difficult to reduce by closed means. A small minority of fractures exhibit multidirectional instability and do not fit into either flexion or extension types.49 Recognition of multidirectional instability is helpful in formulating an effective treatment strategy.

FLEXION-TYPE FRACTURES Flexion-type fractures are the result of a direct fall onto a flexed elbow in which a powerful flexion force is applied to the distal humerus, usually through the olecranon. The distal humeral fragment is displaced anteriorly, and the fracture line crosses the humerus from the distal posterior to the proximal anterior aspect (Fig. 14-4). Flexion-type fractures are frequently completely displaced and are difficult to reduce by closed means. The reduction maneuver for flexion-type fractures involves elbow extension or involves using the forearm

to apply a posterior-directed force to the anteriorly displaced distal fracture fragment.

EXTENSION-TYPE FRACTURES Extension-type fractures typically occur as the result of a fall onto an outstretched arm with a hyperextended elbow. The fracture line traverses the distal humerus from the proximal posterior to the distal anterior aspect. Displacement varies from none to marked displacement with fracture fragments separated by interposed soft tissue. Numerous classifications systems have been devised for extension-type supracondylar humerus fractures,10,24,40,41,68 but the classification system attributed to Gartland31 is the most commonly accepted system in use today. As described by Gartland, the classification system is simple, reproducible, helpful in guiding treatment, and provides information on prognosis and potential complications. A very similar fracture classification system was published in the German literature of the early 20th century by Felsenreich.26

Chapter 14 Supracondylar Fractures of the Elbow in Children

209

FIGURE 14-4

A, Flexion-type supracondylar fracture with anterior and medial angulation. B, Lateral view. Note also that what appears to be an avulsion of the medial epicondyle is really due to the rotation of the distal humerus and the oblique orientation of the film.

TYPE I Type I fractures are nondisplaced (Fig. 14-5). In many patients, the fracture line may not be visible on injury radiographs, but the posterior fat pad sign, palpable tenderness in the supracondylar region, and an appropriate mechanism of injury allows the physician to establish a correct diagnosis. The diagnosis is often confirmed when periosteal callus is seen on radiographs taken 3 weeks after the injury. If recognized and treated appropriately, type I fractures should never be associated with neurovascular injury or malunion.

TYPE II In type II fractures, there is displacement or angulation at the fracture site, but a hinge of bone crossing the fracture keeps the fragments in continuity. The distal fragment is most often displaced posteriorly, and apex anterior angulation at the fracture site results in a hyperextension deformity (Fig. 14-6). Variations of type II fractures have also been described that involve medial impaction or rotation, which can result in cubitus varus if unrecognized (Fig. 14-7). Although there are reports

of neurovascular injury associated with type II fractures, such injuries are rare.69

TYPE III Type III fractures are completely displaced fractures in which there is no continuity between fracture fragments (Fig. 14-8). The distal fragment is displaced posteriorly and may be displaced medially or laterally as well. There is a much higher incidence of neurovascular complications with type III fractures, and soft tissue is usually interposed between fracture fragments. The brachialis muscle is most often interposed, but the median nerve, radial nerve, or brachial artery may also be entrapped.

DIAGNOSIS AND RADIOGRAPHIC EVALUATION We define a supracondylar humerus fracture to be a transverse fracture crossing the entire width of the distal humeral metaphysis without involving the distal humeral physis. The primary challenge in establishing this diagnosis is to rule out other fractures of the distal humerus

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FIGURE 14-5

A and B, Type I supracondylar fracture with an indistinct fracture line but markedly positive anterior and posterior fat pad signs. C and D, After 3 weeks of cast immobilization, fracture callus confirms the presence of a nondisplaced fracture.

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211

FIGURE 14-6

A, Type II supracondylar fracture with apex anterior angulation. B, When treated with flexion of the elbow and casting, the injury shows excellent early alignment.

that do not meet these criteria. Fractures that can sometimes be confused with supracondylar humerus fractures include lateral condyle fractures, medial condyle fractures, and transphyseal fractures. Establishing the correct diagnosis is most difficult in patients younger than 4 years, whose ossific nuclei of the distal humerus are yet unossified. Routine anteroposterior and lateral radiographs should be taken at 90 degrees to each other whenever a supracondylar humerus fracture is suspected. If the examiner is certain of the presence of a distal humerus fracture, because of focal point tenderness, mechanism of injury, and positive posterior fat pad sign, but is unable to identify the specific fracture pattern, 45-degree oblique radiographs often provide adequate visualization to establish the definitive diagnosis. On the other hand, if what may be a pathologic abnormality could possibly be a normal variant in a partially ossified distal

FIGURE 14-7

A, Schematic view of greenstick type II fracture that is causing medial trabecular-cortical compression leading to cubitus varus. This condition must be corrected with manipulation. B, Acute cubitus varus in a 5-year-old child with a type II fracture that was not corrected. C, Mild cubitus varus can be seen 2 years later. (From Ogden, J. A.: Skeletal Injury in the Child. Philadelphia, Lea & Febiger, 1982.)

humerus, comparison films of the opposite elbow allow identification of normal anatomy and determination of whether or not a fracture is present. Once a fracture is identified, the radiographic fracture classification system described earlier may be applied.

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FIGURE 14-8

A and B, Severe type III fracture with rotation and posterior and lateral displacement with associated neurovascular compromise.

The anterior and posterior fat pad signs are often helpful in diagnosing intra-articular elbow fractures such as supracondylar humerus fractures (see Chapter 15). Although it is very sensitive, the anterior fat pad sign is not very specific for intra-articular elbow fractures because the coronoid fossa of the humerus (occupied by the anterior fat pad) is much more shallow than the olecranon fossa (occupied by the posterior fat pad). Any insult that causes a joint effusion may cause the anterior fat pad to become visible on the lateral radiograph. A larger intra-articular fluid collection such as fracture hemarthrosis is necessary to displace the posterior fat pad enough for it to become visible on lateral radiographs; therefore, the posterior fat pad sign is much more reliable. Additional radiographic measurements have been described to assess fracture alignment before and after reduction. The most commonly used measurement is Baumann’s angle, the intersection of a line drawn along the longitudinal axis of the humerus and a line drawn along the physis between capitellum and distal lateral humeral metaphysis. The normal angle varies in magnitude but averages approximately 72 degrees, and it should always be compared with the uninjured contralateral elbow (Fig. 14-9).88 A second useful radiographic reference line is the anterior humeral line (Fig. 14-10). If the capitellar ossific nucleus is displaced posterior to the

FIGURE 14-9

Baumann’s angle is the angle formed by a line perpendicular to the axis of the humerus and a line tangential to the straight epiphyseal border of the lateral part of the distal metaphysis. In the case illustrated, Baumann’s angle is 80 degrees on the fractured left side and 70 degrees on the normal right side, indicating varus angulation of 10 degrees. The same holds true for lateral tilt and valgus angulation. (From Dodge, H. S.: Displaced supracondylar fractures of the humerus in children: treatment by dental extraction. J. Bone Joint Surg. 54A:1411, 1972.)

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TYPE I FRACTURES

FIGURE 14-10 The anterior humeral line (AHL). A, A line is drawn down the anterior humeral cortex. B, A second line is drawn perpendicular to the AHL from the anterior to the posterior extent of the capitellum and is divided into thirds. In normal cases, the AHL passes through the middle third of the capitellum. (From Rogers, L. F., Malave, S. Jr., White, H., and Tachdjian, M. O.: Plastic bowing, torus and greenstick supracondylar fractures of the humerus: radiographic clues to obscure fractures of the elbow in children. Radiology 128:146, 1978.)

anterior humeral line, fracture reduction should be considered. Fracture reduction should restore Baumann’s angle to a measurement similar to that of the opposite elbow on the anteroposterior view, and on the lateral view, it should restore the capitellum to a position in which the central third is bisected by the anterior humeral line. For all patients with supracondylar humerus fractures, the entire extremity should be examined and radiographs obtained of all areas where associated injuries might be present. Approximately 15% of patients with supracondylar fractures have an associated fracture in the ipsilateral extremity.86 Supracondylar fracture associated with a Montaggia lesion has also been reported.3,65

TREATMENT The goal of treatment is to obtain and safely maintain anatomic fracture alignment, promote rapid healing, and return to full and unlimited function with minimal risk of complications. Injury severity determines the ease with which this goal is attained and the most appropriate method of treatment. For extension-type supracondylar fractures, Gartland’s radiographic classification system is a helpful guide to injury severity and optimal treatment.

Because type I fractures are truly nondisplaced, there is minimal swelling and no significant risk of neurovascular injury. Immediate application of an above-elbow cast with the elbow at 90 degrees of flexion (and neutral angles of pronation and supination) is safe and is all that is necessary to prevent loss of reduction and to provide pain relief. If future swelling is a concern, the cast may be bivalved, splitting all fiberglass or plaster elements down to—but not through—the cast padding. The two halves of the cast are spread apart to accommodate swelling and held together with three or four circumferential bands of tape. Five to 10 days later, the cast is simply overwrapped with fiberglass. After 3 weeks of immobilization, the cast is removed and elbow rangeof-motion exercises are begun. At 6 weeks, the fracture is essentially healed and the patient may resume full activity.

TYPE II FRACTURES Despite an intact osseous hinge, type II fractures can vary significantly in displacement and injury severity, which determines treatment choice. For fractures in which the anterior humeral line does intersect the capitellum, reduction may not be necessary and immediate cast immobilization in 90 degrees of flexion is appropriate. Closed reduction should be seriously considered for moderately displaced fractures when the anterior humeral line passes anterior to the capitellum. In a cooperative reliable patient with minimal elbow swelling, gentle closed reduction may be performed under regional anesthesia or conscious sedation in the emergency department, and the fracture should be immobilized in an above-elbow cast with enough flexion to maintain fracture reduction (see Fig. 14-6). If any swelling is present, close attention to the neurovascular examination is critical when immobilizing the elbow in more than 100 degrees of flexion. Fluoroscopic observation can be helpful in determining the minimum degree of flexion required to safely maintain fracture reduction. Displaced or angulated type II fractures may be associated with neurovascular injury. Neurologic and vascular examinations, performed and documented meticulously, are essential. Swelling may make it impossible or unsafe to flex the elbow enough so that the fracture reduction can be maintained. In such situations, closed reduction and percutaneous pinning is indicated to maintain fracture reduction without compromising the neurovascular integrity of the limb. Moderately or severely angulated type II fractures may also be associated with medial column impaction, lateral column impaction, or rotation. If unrecognized, any of these

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three variations of a type II fracture can lead to malunion and angular deformity. Medial impaction, lateral impaction, and rotation all necessitate closed reduction, which is most dependably maintained with percutaneous pinning.19 After percutaneous pinning, a splint or bivalved cast is applied, and 5 to 10 days later, the bivalved cast is overwrapped or the splint removed and an above-elbow cast applied.

TYPE III FRACTURES Completely displaced supracondylar humerus fractures are intrinsically unstable, typically cause severe swelling, and are frequently associated with neurovascular injury (Fig. 14-11). These factors make management of type III fractures challenging and anxiety provoking.

CLOSED REDUCTION Type III extension-type fractures have an intact posterior periosteal hinge, which, in addition to the triceps tendon, provides some stability to the fracture when it is immobilized in flexion. Paradoxically, the completely displaced supracondylar fracture is just the fracture that requires elbow flexion greater than 100 degrees to maintain adequate fracture reduction, but it is also the fracture least able to tolerate flexion beyond 100 degrees because of swelling and risk of neurovascular compromise (Fig. 14-12).53 Because of the relatively high incidence of malunion and neurovascular compromise, immobilization in flexion has been replaced by closed or open reduction and pinning.47,59,64,87,89

PERCUTANEOUS PINNING In 1988, Pirone et al64 published a series of 230 displaced supracondylar humerus fractures and analyzed the results of (1) closed reduction and percutaneous pinning, (2) open reduction, (3) skeletal traction, and (4) closed reduction with casting. Pirone and colleagues reported significantly better results in the group treated with closed reduction and percutaneous pinning as compared with the other three groups. Subsequent studies have confirmed these results, and closed reduction with percutaneous pinning has become the most used and most accepted treatment.12,27,35,36,87 In the emergency department, a meticulous neurovascular examination should be performed and properly documented including median, radial, ulnar, and anterior interosseous nerve function. Because it has only motor function, anterior interosseous nerve injury has been underdiagnosed in the past, but separate investigators have provided substantial evidence to suggest that the anterior interosseous nerve is the nerve most fre-

quently injured in association with supracondylar fractures.17,18,21 Because of the severe nature of the injury, the amount of manipulation required for reduction, and the possible need to perform an open reduction, an attempt at closed reduction should not be made in the emergency department. However, severe displacement and deformity may result in a pulseless or dysvascular extremity. In this situation, under adequate analgesia in the emergency department, gently correcting the severe deformity followed by splinting in a relaxed position— usually approximately 30 degrees of elbow flexion—often restores the radial pulse and minimizes further tissue damage caused by severe fracture displacement. If the limb remains dysvascular, emergent transport to the operating room is indicated, where closed reduction restores perfusion to the upper extremity in the vast majority of patients. A question that has generated considerable discussion in recent medical literature concerns whether a neurovascularly intact, displaced, type III fracture should be treated emergently in the middle of the night, or whether such a fracture can be effectively and safely treated the following morning? In a review of 198 patients with a displaced type III fracture and perfused limb, Mehlman et al55 compared urgent treatment with treatment provided the day following injury and reported no statistical difference between groups with regard to perioperative complications or the need to convert to open fracture reduction. Additional authors have published similar results, suggesting that compared with emergent treatment, delay until the following day does not increase the risk of perioperative complication or the need for open reduction, and does not compromise final outcome.37,43 One article did note an increased need to convert to open reduction when treatment was delayed.85 Our opinion is that the fracture is never easier to reduce than the moment after the fracture occurs; each subsequent hour adds to the swelling and difficulty of reduction. However, there does not seem to be any significant difference in clinical outcome between a neurovascularly intact extremity with a fracture that is reduced and pinned at 2:00 AM compared with a fracture in which treatment is delayed until later that same morning. Closed reduction and percutaneous pinning can be performed successfully using a variety of techniques with the patient positioned supine, lateral, or prone.28 We prefer to perform the reduction with the patient positioned supine using the following series of steps. After general anesthesia has been administered, the patient is positioned toward the edge of the operating table with the affected extremity carefully supported over the side. C-arm fluoroscopy is brought in from the foot of the table, parallel to the table, so the patient’s arm can rest on the C-arm.

Chapter 14 Supracondylar Fractures of the Elbow in Children

FIGURE 14-11 A, Five-year-old patient with a markedly displaced supracondylar fracture whose neurovascular supply was intact. B, After closed reduction and pinning, the radial pulse and median nerve function were lost. C, Entrapment of the brachial artery and median nerve necessitated opening of the fracture site and repinning. Intraoperative angiography shows spasm of the brachial artery that resolved.

215

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FIGURE 14-12

Injection of a cadaver arm from an adolescent shows kinking of vessels. A, Vascular relationships at 90 degrees of flexion. B, In extension, the artery may be traumatized by the proximal fragment or kinked by soft tissue attachments. C, In hyperflexion, the vessels may be compressed in the edematous antecubital region. (From Ogden, J. A.: Skeletal Injury in the Child. Philadephia, Lea & Febiger, 1982.)

Before prepping, with the arm less constrained by drapes, closed reduction is attempted. If the metaphyseal spike from the proximal fragment is tenting the skin and subcutaneous tissue, the brachialis is gently “milked” off of the fragment.5 With the arm in a relaxed position at approximately 20 to 30 degrees of elbow flexion, the medial-lateral displacement is corrected. When available, an assistant supports the forearm, and the operating surgeon places a thumb on posterior aspect of the medial and lateral columns of the distal humeral fragment. The final reduction maneuver involves the assistant’s applying gentle longitudinal traction while the operating surgeon uses each thumb to manipulate the distal fragment distally and anteriorly. Simultaneously, the assistant flexes the elbow to maintain the reduction (Fig. 14-13).58 When working alone, the operating surgeon can apply traction to the forearm and flexion to the elbow with one hand while applying distal and anterior pressure to the patient’s olecranon with the other hand (Fig. 14-14). If the initial displacement is posterior and medial, suggesting an intact medial periosteal hinge, the forearm is pronated. If the initial displacement is posterior and lateral, the forearm is supinated. Occasionally, pronation can cause displacement when in theory it should improve the reduction and vice versa with supination. The key is remaining flexible and gently trying several methods until the best and most stable reduction is obtained. The reduction is imaged with fluoroscopy on anteroposterior and lateral views. If the reduction is adequate or if it is clear that an adequate reduction is attainable with a second attempt, the elbow is extended to approximately 20 degrees of flexion, prepared, and draped. We

prepare the hand into the field to allow neurovascular monitoring and prep to the shoulder to allow for the use of a sterile tourniquet if necessary. After draping, the reduction maneuver is repeated, adequate alignment is confirmed fluoroscopically, and the elbow is temporarily held in a hyperflexed position to maintain the reduction. Controversy persists about the optimal pin configuration that maintains adequate fracture reduction and minimizes potential complications.32,34,48,74 Crossed pins provide the greatest biomechanical stability but have the potential to cause ulnar nerve injury90 (Fig. 14-15). Published reports suggest that the biomechanical stability sacrificed by using two or three lateral pins is not clinically significant and avoids iatrogenic ulnar nerve injury.15,82 If two lateral pins are used, great care must be taken to ensure that both pins cross through both fracture fragments with adequate spacing between the pins; otherwise, fracture reduction may be lost. To pin the medial column first, the elbow is externally rotated; to pin the lateral column, internal rotation is used. Sometimes the fracture is more stable in internal or in external rotation, and this determines which column is pinned first. Because internal rotation of the elbow can result in posterior displacement of the medial distal fragment causing varus angulation, when possible, we typically externally rotate the elbow and pin the medial column first.63 The operating surgeon palpates the medial epicondyle and uses a thumb to retract and protect the ulnar nerve posteriorly (see Fig. 14-13). A 0.062 Kirschner wire is then placed just anterior to the thumb on the medial epicondyle. The Kirschner wire is angled cephalad to

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FIGURE 14-13 Closed reduction of type III supracondylar humeral fracture. A, C-arm fluoroscopy is brought in from the foot of the operating table and used as the operating surface. B, Before surgical preparation and draping, and after medial-lateral displacement is corrected, the fracture is reduced. The operating surgeon places a thumb on the medial and lateral columns translating the fragment distally and anteriorly while the assistant flexes the elbow. C, After ensuring that a closed reduction can be obtained, the surgeon repeats the reduction maneuver after the arm has been prepared and draped. D, The operating surgeon retracts and protects the ulnar nerve with a thumb while placing the medial pin.

travel within the medial column of bone and advanced until it just penetrates the opposite cortex. Using fluoroscopy, the position of the Kirschner wire is checked in anteroposterior and lateral planes. This first pin often substantially improves fracture stability, allowing extension past 90 degrees to image the elbow and facilitate placement of the second pin. The second pin is placed within the lateral column of bone, crossing the first pin well above the fracture site (see Fig. 14-15). The pins are left protruding through the skin, bent at a 90-degree angle, cut long, and a foam or gauze dressing placed beneath the ends to ensure that the pins will not become buried beneath the skin while in the postoperative dress-

ing. Literature describing the use of bioabsorbable pins has reported an unacceptable level of implant failure and loss of reduction.11 Occasionally, the elbow is too swollen or the child too young to allow accurate palpation of the medial epicondyle. In such instances there are several options. A 1-cm incision may be made directly over the medial epicondyle. Soft tissues are spread with a small clamp down to the medial condyle, and a small retractor is used to hold the ulnar nerve and all soft tissues posterior to the pin. With the ulnar nerve retracted, the medial column pin can be placed safely. Alternatively, two or three lateral pins may be used. Zionts’ cadaver study90

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Part IV Conditions Affecting the Child’s Elbow

FIGURE 14-14 A, Manipulative reduction is performed by exerting gentle traction in extension and supination. B, Direct pressure is exerted to realign the distal fragment. C, After realignment, the elbow is flexed to 120 degrees and appropriately pronated or supinated. D, Medial displacement of the distal fragment often requires pronation for stability, with the elbow flexed.

Chapter 14 Supracondylar Fractures of the Elbow in Children

FIGURE 14-14, cont’d

E, Lateral displacement of the distal fragment frequently requires supination for stability, with the elbow flexed. (From Micheli, L. J., Skolnick, D., and Hall, J. E.: Supracondylar fractures of the humerus in children. Am. Family Physician 19:100, 1979.)

demonstrated that, after crossed pins, the next strongest configuration used three lateral pins; two pins placed obliquely across the fracture from the distal lateral to the proximal medial aspect and a third through the capitellum directed up the humeral shaft.

OPEN REDUCTION Inability to achieve closed reduction is usually due to soft tissue interposition. Most frequently, the brachialis muscle is interposed and can be “milked” off the distal metaphyseal spike by closed means. Occasionally, the brachial artery, median nerve, or radial nerve can become interposed between the fracture fragments. Inability to achieve an adequate closed reduction warrants open reduction. Fractures displaced posterolaterally are most likely to cause interposition of the median

219

nerve or brachial artery and are approached anteromedially. Conversely, fractures displaced posteromedially are more likely to have interposition of the radial nerve and are approached anterolaterally. Several recent papers have reported excellent success using a small transverse incision in the elbow flexion crease.7,46,80 Through this limited approach, the offending interposed tissue can usually be easily extracted from the fracture site and anatomic reduction confirmed before percutaneous pinning proceeds. Past reluctance to perform open reduction of supracondylar fractures for fear of causing elbow stiffness has been shown to be unfounded: Several studies have demonstrated that open reduction is safe and effective and does not increase the risk of elbow stiffness.4,6,14,30,73 The majority of severely displaced supracondylar fractures without a radial pulse regain the pulse after fracture reduction. If after closed reduction, the radial pulse does not return and the limb is not perfused, immediate exploration of the brachial artery and open reduction is indicated. A more controversial situation is encountered when an adequate reduction is obtained, the limb remains pulseless, and the state of limb perfusion is unclear. In separate reports, Schoenecker and Shaw and their respective associates have formulated similar algorithms that are useful in this situation.71,72 After reduction and pinning, the vascular status of the limb is assessed. If the radial pulse is detectable by Doppler ultrasound and the hand is pink with brisk capillary refill, the elbow is immobilized, the case is completed, and the patient is carefully monitored overnight. If the radial pulse is not detectable by ultrasound, the brachial artery is explored at the fracture site. Using this algorithm, combining numbers from both studies, 10 patients did not have a detectable radial pulse by Doppler ultrasound and were explored immediately. All 10 arteries were found to be obstructed or transected, and in all extremities, blood flow was re-established by freeing the trapped or kinked vessel (five extremities) or by repairing the lesion with vein graft (five extremities). Using Doppler ultrasound to detect a radial pulse appears to be effective at detecting almost all clinically significant vascular injuries without arteriography and with minimal risk of exposing patients to unnecessary vascular exploration.

POSTOPERATIVE CARE After the fracture is reduced and pinned and adequate perfusion of the limb confirmed, the upper extremity is immobilized. Pin stabilization permits immobilization in a position that optimizes perfusion and minimizes swelling. A simple posterior splint or bivalved cast may be used to immobilize the elbow in approximately 80

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Part IV Conditions Affecting the Child’s Elbow

FIGURE 14-15 A, Closed reduction and percutaneous pinning was performed for a markedly displaced type III supracondylar humerus fracture. B, Pins cross well above the fracture site, maintaining excellent alignment at the time of pin removal 3 weeks postoperatively.

degrees of flexion. A fluffed 4-by-4-inch gauze may be placed in the antecubital fossa as great care is taken to prevent constriction from the dressing. A neurologic examination is performed immediately after the patient awakens from anesthesia, and median, radial, and ulnar nerve function is assessed. Patients are admitted overnight for neurovascular monitoring. The elbow is elevated, and ice is applied through the dressing. Most patients are discharged from the hospital on the day after surgery and are seen back in follow-up 5 to 10 days after surgery. At that time, radiographs are taken and the limb is examined. If adequate reduction has been maintained and swelling has decreased, bivalved casts are overwrapped with fiberglass casting material or the posterior splint may be removed and a cast applied. Three weeks after the injury, the cast is removed and radiographs are repeated. If periosteal bone formation across the fracture is present, the pins are removed, immobilization is discontinued, and gentle active range-of-motion exercise is begun. Immobilization longer than 4 weeks increases the risk of permanent elbow stiffness. Vuckov84 reported immobilizing patients for as short as 2 weeks following supracondylar fractures with no untoward consequences.

TRACTION Historically, traction has been used with acceptable results to obtain and maintain supracondylar fracture reduction until healing has progressed enough to permit cast immobilization.* More recently, improved results, *See references 2,9,20,22,23,42,44,47,70,77,78,83.

decreased cost, and decreased time in the hospital after closed reduction and percutaneous pinning have resulted in complete abandonment of traction for supracondylar fracture treatment.29,64,67,81 Rarely, however, traction may be an appropriate treatment for type III supracondylar fractures. The most common indication for traction would be a displaced fracture that presents for treatment longer than 24 hours after injury and with severe swelling that precludes open or closed reduction (Fig. 14-16). Additional indications for traction include patients with a contraindication to general anesthesia or lack of access to adequate imaging or other equipment necessary for pinning. Two forms of traction traditionally have been used: cutaneous or Dunlop’s traction and skeletal traction. Dunlop’s traction is applied in a lateral direction with the patient lying supine. Pronation and supination of the forearm and varus or valgus tilt of the distal fragment are difficult to control and correct with this method of traction. The forearm tends to rotate into supination, resulting in a loss of stability that ordinarily is achieved when the forearm is maintained in the pronated position in most common fractures. This position also places the distal fracture fragment in some extension. Because of these disadvantages, if traction is necessary we prefer to use skeletal traction with the arm held overhead. Under general or regional anesthesia, a Kirschner wire may be inserted through the proximal ulna at the olecranon. An olecranon screw, which is inserted at the same level, is easier to insert and avoids risk to the ulnar nerve. Gross displacement is corrected at this time. The arm is suspended from an overhead frame with a sling under

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FIGURE 14-16 A to C, A 9-year-old patient with a displaced supracondylar fracture presented with severe swelling and fracture blisters that precluded closed reduction and percutaneous pinning. D, Overhead skeletal traction is used to safely obtain and maintain adequate fracture alignment.

the forearm to control its position. Three to five pounds of traction is usually sufficient to reduce and stabilize the fracture. Too much weight elevates the shoulder and twists the thorax causing the child to shift position resulting in loss of control of the fracture fragment. Suspension of the forearm in this position permits rapid reduction of edema and good control of elbow flexion. Rotational deformity can be controlled by placing the arm in either a cephalad or a caudad position. If neces-

sary, a lateral sling around the upper arm also may provide lateral traction to correct anterior displacement of the proximal fragment (Fig. 14-17). Serial radiographs must be taken, and producing adequate films may require some ingenuity on the part of the technician and direction on the part of the physician. The lateral projection usually is obtained without difficulty, but the axial view requires overcoming the obstruction of the overhead frame by some means. Fracture stability is assessed

FIGURE 14-16, cont’d

E and F, Six months after injury, the fracture is completely healed and the

outcome excellent.

FIGURE 14-17

A, Position of patient in bed relative to overhead traction. B, Angulation of the traction controls reduction. (From Ogden, J. A.: Skeletal Injury in the Child. Philadelphia, Lea & Febiger, 1982.)

Chapter 14 Supracondylar Fractures of the Elbow in Children

clinically and radiographically. When the fracture is minimally tender to palpation, swelling has subsided and early callus has developed, a well-molded aboveelbow cast is applied.

COMPLICATIONS Complications are discussed in detail in Chapter 15. The two broad categories of complications most often associated with supracondylar humerus fractures are malunion and neurovascular injury. Even the most skilled surgeons occasionally encounter complications, but adherence to the principles outlined here will help to minimize these unfortunate events.

Acknowledgment The author would like to acknowledge Dr. Rudolph Klassen for his contributions to this chapter. The information presented in this chapter is based on his efforts in previous editions.

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of the humerus in children. J. Bone Joint Surg. 70A:641, 1988. Powell, R. S., and Bowe, J. A.: Ipsilateral supracondylar humerus fracture and Monteggia lesion: a case report. J. Orthop. Trauma. 16:737, 2002. Rang, M.: Children’s Fractures, 2nd ed. Philadelphia, J. B. Lippincott, 1983. Rodriguez Merchan, E. C.: Supracondylar fractures of the humerus in children: treatment by overhead skeletal traction. Orthop. Rev. 21:475, 1992. Rogers, L. F., Malave, S. Jr., White, H., and Tachdjian, M. O.: Plastic bowing, torus and greenstick supracondylar fractures of the humerus: radiographic clues to obscure fractures of the elbow in children. Radiology 128:145, 1978. Sairyo, K., Henmi, T., Kanematsu, Y., Nakano, S., and Kajikawa, T.: Radial nerve palsy associated with slightly angulated pediatric supracondylar humerus fracture. J. Orthop. Trauma 11:227-229, 1997. Schickendanz, H., Schramm, H., Herrmann, K., and Jager, S.: Fractures and dislocations in the elbow in childhood. Am. Family Physician 13:311, 1973. Schoenecker, P. L., Delgado, E., Rotman, M., Sicard, G. A., and Capelli, A. M.: Pulseless arm in association with totally displaced supracondylar fracture. J. Orthop. Trauma 10:410, 1996. Shaw, B. A., Kasser, J. R., Emans, J. B., and Rand, F. F.: Management of vascular injuries in displaced supracondylar humerus fractures without arteriography. J. Orthop. Trauma 4:25, 1990. Sibly, T. F., Briggs, P. J., and Gibson, M. J.: Supracondylar fractures of the humerus in childhood: range of movement following the posterior approach to open reduction. Injury 22:456, 1991. Skaggs, D. L., Hale, J. M., Bassett, J., Kaminsky, C., Kay, R. M., and Tolo, V. T.: Operative treatment of supracondylar fractures of the humerus in children. The consequences of pin placement. J. Bone Joint Surg. 83A:735, 2001. Smith, F. M.: Children’s elbow injuries. Fractures and dislocations. Clin. Orthop. 50:7, 1967. Siris, J. E.: Supracondylar fractures of the humerus analyzed: 330 cases. Surg. Gynecol. Obstet. 68:201, 1939. Smith, L.: Deformity following supracondylar fractures. J. Bone Joint Surg. 42A:235, 1960. Staples, O. S.: Complication of traction treatment of supracondylar fractures of the humerus in children. J. Bone Joint Surg. 41A:369, 1959.

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79. Strait, R. T., Siegel, R. M., and Shapiro, R. A.: Humeral fractures without obvious etiologies in children less than 3 years of age: when is it abuse? Pediatrics 96 (4 pt 1):667671, 1995. 80. Suh, S. W., Oh, C. W., Shingade, V. U., Swapnil, M. K., Park, B. C., Lee, S. H., and Song, H. R.: Minimally invasive surgical techniques for irreducible supracondylar fractures of the humerus in children. Acta Orthop. 76:862, 2005. 81. Sutton, W. R., Green, W. B., Georgopoulos, G., and Dameron, T. B., Jr.: Displaced supracondylar humeral fractures in children. A comparison of results and costs in patients treated by skeletal traction versus percutaneous pinning. Clin. Orthop. 278:81, 1992. 82. Topping, R. E., Blanco, J. S., and Davis, T. J.: Clinical evaluation of crossed-pin versus lateral-pin fixation in displaced supracondylar humerus fractures. J. Pediatr. Orthop. 15:435, 1995. 83. Vahvanen, V., and Aalto, K.: Supracondylar fractures of the humerus in children. A long-term follow-up study of 107 cases. Acta Orthop. Scand. 49:225, 1978. 84. Vuckov, S., Kvesi, A., Rebac, Z., Cuculi, D., Lovasi, F., and Bukvi, N.: Treatment of supracondylar humerus fractures in children: minimal possible duration of immobilization. Coll. Antropol. 25:255, 2001. 85. Walmsley, P. J., Kelly, M. B., Robb, J. E., Annan, I. H., and Porter, D. E.: Delay increases the need for open reduction of type-III supracondylar fractures of the humerus. J. Bone Joint Surg. 88B:528, 2006. 86. Wilkins, K. E.: Residuals of elbow trauma in children. Orthop. Clin. North Am. 21:291, 1990. 87. Wilkins, K. E.: Supracondylar fractures: what’s new? J. Pediatr. Orthop. 6:110, 1997. 88. Williamson, D. M., Coates, C. J., Miller, R. K., and Cole, W. G.: Normal characteristics of the Baumann (humerocapitellar) angle: an aid in assessment of supracondylar fractures. J. Pediatr. Orthop. 12:636, 1992. 89. Williamson, D. M., and Cole, W. G.: Treatment of selected extension supracondylar fractures of the humerus by manipulation and strapping in flexion. Injury 24:249, 1993. 90. Zionts, L. E., McKellop, H. A., and Hathaway, R.: Torsional strength of pin configurations used to fix supracondylar fractures of the humerus in children. J. Bone Joint Surg. 76A:253-256, 1994.

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CHAPTER

15

Complications of Supracondylar Fractures of the Elbow Amy L. McIntosh and Scott J. Mubarak

INTRODUCTION Complications associated with supracondylar humerus fractures can be divided into broad categories. The etiology of a complication may be due to the injury itself or the management of the injury. The complication may be associated with the soft tissues, such as a neurovascular problem (acute), or in the osseous structures, such as malalignment (chronic). In this chapter, we first discuss the anatomy of this area, then neurovascular problems, and finally bony complications of supracondylar humerus fractures in children.

NEUROVASCULAR PROBLEMS ASSOCIATED WITH SUPRACONDYLAR FRACTURES ANATOMY Anterior to the supracondylar area of the distal humerus is the median nerve (Fig. 15-1). In the proximal forearm, the anterior interosseous branch separates to innervate the flexor profundus to the index finger and the flexor pollicis longus and then terminates with the innervation of the pronator quadratus. There is no sensory branch for this nerve. The remainder of the median nerve traverses the forearm and supplies the sensation to the palmar aspect of the thumb, the index finger, the long finger, and the radial aspect of the ring finger. The radial nerve lies posterolateral to the usual location of supracondylar fractures and, thus, is less commonly involved (see Fig. 15-1). The ulnar nerve with its posterior location is uncommonly involved with a typical extension-type supracondylar fracture. The forearm consists of two basic compartments: volar and dorsal (Fig. 15-2). The volar compartment includes the flexors and pronators of the forearm and wrist, which may be further divided into superficial and

deep muscle groups. The superficial muscles include the flexor carpi ulnaris, the palmaris longus, the flexor carpi radialis, and the pronator teres. The deeper group of muscles consists of the flexor digitorum superficialis and profundus, the flexor pollicis longus, and the pronator quadratus. The median and ulnar nerves traverse the forearm between the superficial and deep flexor groups. The major arteries about the elbow include the brachial artery, which bifurcates in the region of the radial head to form the radial and ulnar arteries. The dorsal compartment consists mainly of the wrist and finger extensors. The mobile wad of Henry includes the brachioradialis and the extensor carpi radialis longus and the brevis muscles. This group of muscles is physically and functionally distinct; it lies between the dorsal and volar forearm compartments and probably should be considered a separate compartment. The major nerve of the dorsal compartment is the posterior interosseous nerve, a continuation of the radial nerve. The major artery of the dorsal compartment is the posterior interosseous artery.

ETIOLOGY: NERVE INJURY Most nerve injuries are associated with type III displaced supracondylar fractures. In a recent study by Louahem et al,46 the most commonly injured nerve was the anterior interosseous branch of the median nerve. This is likely due to its anatomic arrangement of the exclusively motor posterior fascicles which are exposed to the zone of injury, and its tight tethering to the proximal forearm musculature. The second-most commonly involved nerve was the ulnar, followed by the radial nerve. Ulnar nerve injury was most commonly associated with posterolateral fracture patterns due to direct contusion and stretching of the nerve from the medially displaced proximal humeral fragment or edema within the cubital tunnel. Radial nerve injury was consistently associated with posteromedial fractures due to contusion and stretching from the laterally displaced proximal humeral fragment. Ulnar nerve injury also occurred iatrogenically in 5% of patients during medial percutaneous pin placement in a recent large series.69 The causes of iatrogenic ulnar nerve injury include (1) direct penetration of the nerve or its sheath by the medial pin; (2) constriction of the cubital tunnel by the pin while the elbow is in flexion; (3) medial pin injury to an unstable ulnar nerve, which subluxates or dislocates anteriorly when the elbow is in flexion; and (4) nerve contusion and edema.63 In 2001, Skaggs et al reported on 345 extension-type supracondylar humerus fractures in children treated with closed reduction and percutaneous pin fixation. The use of a medial pin was associated with an iatrogenic ulnar

Chapter 15 Complications of Supracondylar Fractures of the Elbow

COMPARTMENT STRUCTURES OF UPPER ARM Radial artery and nerve Triceps muscle Brachialis muscle

Biceps muscle Humerus

Radial nerve Cephalic vein

Ulnar nerve Basilic vein Brachial artery

Median nerve

227

TREATMENT After reduction of the fracture and stabilization with percutaneous pinning, re-evaluation of the neurovascular examination is mandatory. On rare occasions, the compromised nerve may recover before the patient’s discharge, but in most incidents, the neurapraxia requires observation and will gradually return over the ensuing months. If after 4 to 6 months, no return of function is noted, electromyelographic and nerve conduction studies to evaluate the status of recovery are recommended. Only rarely have cases been reported of permanent nerve deficits requiring later neurolysis, grafting, or tendon transfer. Nearly all nerves will return to normal function within the first 6 months following the injury.19 Advances in surgical techniques with lateral pin entry fixation have demonstrated significant decreases in iatrogenic ulnar nerve injury and satisfactory mechanical stability in Gartland type II, III and IV fractures.43,69,70 Authors recommend two-pin lateral-entry fixation as the primary mode of percutaneous fixation in all unstable supracondylar humerus fractures with the addition of a third lateral-entry pin or medial pin as needed to achieve fracture stability.

ISCHEMIC INJURIES FIGURE 15-1

Major neurovascular structures of the elbow. (From Mubarak, S. J., and Hargens, A. R.: Compartment Syndromes and Volkmann’s Contracture. Philadelphia, W. B. Saunders, 1981, p. 24.)

nerve injury in 15% of patients in which the pin was placed with the elbow positioned in hyperflexion. Only 4% of patients sustained nerve injury when the medial pin was placed without hyperflexion, and no iatrogenic injuries occurred in patients treated with all lateral entry pin fixation.69 A displaced supracondylar fracture presenting with an absent radial pulse has a 50% to 60% incidence of associated nerve injury at fracture presentation.19

CLINICAL DIAGNOSIS The diagnosis of anterior interosseous nerve injury is easily missed. The inability to flex the distal segment of the thumb and the index fingers is an indication of this nerve being damaged. With a pure anterior interosseous nerve injury, there is no sensory deficit. Sensory examination by light touch and two-point discrimination is recommended for children, especially in the autonomous zones of the median, ulnar, and radial nerve.

Two basic pathologic processes may result from supracondylar fractures or other injuries to the elbow region that can lead to forearm ischemia: (1) arterial injury and (2) compartment syndrome from hemorrhage or postischemic swelling (Fig. 15-3). An arterial injury may result from laceration, thrombus, embolus, intimal tear, or pseudoaneurysm (Fig. 15-4). Such an injury may cause nerve and muscle ischemia directly or may result in postischemic swelling or hemorrhage, thereby causing a compartment syndrome. The muscles of the extremities are grouped into compartments that are enclosed by a relatively noncompliant osteofascial envelope. Muscle swelling causes increased pressure within the compartment that is not easily dissipated owing to the relatively inelastic nature of the surrounding fascia. If the pressure remains sufficiently high for several hours, loss of function of intracompartmental nerves and muscles due to ischemia may result. A compartment syndrome is a condition in which the high pressure within the compartment compromises the circulation to the nerves and the muscles within the involved compartment. In either event, nerve and muscle ischemia may result, possibly leading to a forearm contracture. To prevent permanent loss of nerve and muscle function, this condition must be diagnosed promptly and

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Ulna

Extensor carpi ulnaris m. Radius Supinator m. Extensor digitorum m. Extensor carpi radialis brevis m.

Brachial v. Ulnar n.

Extensor carpi radialis longus m.

Flexor carpi radialis and palmaris longus and flexor digitorum superficialis m. bundle Medial n.

Radial n. (prof.) Radial n. (superf.) Radial v. Medial cubital v.

Ulnar a. Ulnar v.

Posterior interosseous a., v., n.

Flexor digitorum profundus m. Palmaris Flexor carpi longus m. ulnaris m. Ulnar a., v., n.

Extensor carpi ulnaris m. Extensor digitorum m. Extensor digitorum (comm.) m. Extensor carpi radialis brevis and longus m. Pronator teres m. Brachioradialis m. Radial a., v., n. Brachialcephalic v. Flexor pollicis longus m. Flexor carpi radialis m. Median a., v., n.

Extensor carpi radialis longus and brevis m.

Extensor carpi ulnaris m.

Antebrachial cephalic v. Pronator quadratus m. Radial a., v., n. Flexor carpi radialis m.

Flexor carpi ulnaris m. Ulnar n. Ulnar a.

Median n.

treated correctly. Volkmann’s contracture is the popular term that refers to the end stage of an ischemic injury to the muscles and nerves of the limb (Fig. 15-5). Untreated compartment syndromes and arterial injuries are the primary causes of Volkmann’s contracture. The term Volkmann’s ischemia is nonspecific and should not be used.

ETIOLOGY: ISCHEMIA In general, the most common traumatic event that produces a compartment syndrome or an arterial injury about the elbow is the supracondylar fracture of the distal humerus (Fig. 15-6). In 1956, Lipscomb noted that supracondylar fractures were the cause of 48% of Volkmann’s contractures in 92 cases from the Mayo Clinic.45 In 1967, Ehrlich and Lipscomb, in a review of 32 more

FIGURE 15-2

Forearm compartments: transverse sections through the left forearm at various levels. (From Mubarak, S. J., and Hargens, A. R.: Compartment Syndromes and Volkmann’s Contracture. Philadelphia, W. B. Saunders, 1981, p. 28.)

cases of Volkmann’s contracture, reported that 34% were due to supracondylar fractures and 22% were due to forearm fractures.13 In 1979, Mubarak and Carroll, reporting on 58 Volkmann’s contractures in children (Fig. 15-7), found that supracondylar fractures had caused only 16% of these contractures.56 In most recent studies, compartment syndromes are extremely unusual because of the advent of early closed reduction and percutaneous pinning. An arterial injury can produce nerve and muscle ischemia directly or the additional problem of a compartment syndrome by one of two mechanisms (see Fig. 15-3).57 First, if the major vessel is lacerated, hemorrhage into the compartment may produce the syndrome. Second, a compartment syndrome may result from postischemic swelling if there is inadequate collateral circulation or if the vessel is only partially

Chapter 15 Complications of Supracondylar Fractures of the Elbow

TRAUMA Supracondylar fracture

Post-traumatic swelling Hemorrhage Arterial injury

Increased tissue pressure

229

occluded, for example, from an arterial spasm or an intimal tear. In this situation, the decreased perfusion and ischemia of both capillaries and muscles will cause an increase in the permeability of the capillary walls. The resulting edema will then cause more ischemia, and a vicious circle may ensue. When there is complete arterial occlusion, a compartment syndrome may develop from postischemic swelling or reperfusion injury after the circulation is restored (Fig. 15-8). When complete arterial occlusion is secondary to massive emboli or prolonged use of a tourniquet in which the circulation is not restored, gangrene rather than compartment syndrome will likely result.

Post-ischemic swelling

CLINICAL DIAGNOSIS Compartment syndrome

Nerve and muscle infarction

Volkmann’s contracture

FIGURE 15-3

Diagrammatic representation of the possible mechanisms of Volkmann’s contracture.

There is an association between supracondylar fractures, an absent radial pulse, and Volkmann’s contracture. When the concepts of compartment syndrome as a cause for Volkmann’s contracture became popular, forearm fasciotomies became the accepted treatment method to prevent this devastating complication. An absent radial pulse, which is most commonly associated with arterial injury, began to merge with the notion of compartment syndrome. This misconception has no doubt caused many physicians to delay treatment for a compartment syndrome while waiting for the radial pulse to disappear. Owing to these misconceptions, the

Artery

Vein

Venules

Arteriole

Capillary bed

FIGURE 15-5

FIGURE 15-4

An arterial injury is a disease of the large vessels, whereas a compartment syndrome is a disease of small vessels. (From Mubarak, S. J., and Hargens, A. R.: Compartment Syndromes and Volkmann’s Contracture. Philadelphia, W. B. Saunders Co., 1981, p. 22.)

Volkmann’s ischemic contracture of the forearm. The residual of an untreated forearm compartment syndrome in an 8year-old boy.

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usually described as a feeling of increased pressure and is localized to the affected compartment. It is not relieved by immobilization. Pain may be lacking if a central or peripheral sensory nerve deficit is superimposed. Other early symptoms include swelling, numbness, and weakness. The earliest and most objective finding is a tense compartment that is a direct manifestation of the increased intracompartmental pressure. The tenseness should be evident throughout the involved compartments. To evaluate this, all dressings must be removed. Although it is not possible, even with experience, to estimate consistently by palpation the degree to which intracompartmental pressures are elevated, the presence of significant tenseness throughout the compartment boundaries suggests a compartment syndrome. Conversely, if the compartment is palpably soft, the examiner may be reassured that, for the moment, compartment pressures are not elevated. Pain with passive stretch of the muscles in the involved compartment is a common finding that is usually associated with muscle ischemia. However, direct muscle injury or contusion may elicit this clinical finding. The volar compartment of the forearm is traversed by nerves (radial, ulnar, and median) that have a distal sensory distribution in the hand. The first sign of nerve ischemia is alteration of sensation, which is manifest early by subjective paresthesia in the distribution of the involved nerve, followed by hypesthesia and, later, anesthesia. Unless there is a superimposed sensory or peripheral nerve deficit, decreased sensation to light touch or pinprick in the distal sensory distribution is a very reliable sign of ischemia. The dorsal compartment of the forearm is not associated with a specific sensory nerve. Paresis secondary to nerve or neuromuscular junction ischemia and elevated intracompartmental pressure is a common finding. The paresis may be confusing, however, because it may be secondary to proximal nerve injury or guarding secondary to pain rather than to intracompartmental ischemia. Except in the presence of major arterial injury or disease, peripheral pulses and capillary filling are routinely intact in compartment syndrome patients. Although intracompartmental pressures may become high enough to cause ischemia of the muscle and nerve by occluding the microcirculation within the compartment, the pressures are rarely high enough to occlude the major arteries (Fig. 15-9). In our experience, the intracompartmental pressures usually do not exceed 80 mm Hg and are more commonly between 40 and 60 mm Hg. It has been suggested that absent pulses may result from vascular spasm secondary to elevated

Signs of Compartment Syndrome

FIGURE 15-6

A 3-year-old boy who sustained a supracondylar fracture. At the time of cast removal, his forearm had poor sensation and was contracted in the pronated and flexed position. (From Mubarak, S. J., and Hargens, A. R.: Compartment Syndromes and Volkmann’s Contracture. Philadelphia, W. B. Saunders, 1981, p. 88.)

signs and symptoms of arterial injury compared with those of compartment syndrome will be discussed in detail. Symptoms and Signs of Arterial Injury As with a compartment syndrome, pain out of proportion to that expected for the injury is the earliest symptom of arterial ischemia. The earliest clinical sign for an arterial injury is pain with passive stretch of the involved muscles. This usually will be associated with absent or decreased pulses, poor skin color, and decreased skin temperature. Other early findings are weakness and hypesthesia in a glove-like distribution. Symptoms of Compartment Syndrome The early diagnosis of a compartment syndrome depends on recognition of the signs and symptoms of increased intracompartmental pressure. The first and most important symptom of an impending compartment syndrome is pain that is greater than that expected from the primary problem (e.g., the fracture or contusion). The pain is

Chapter 15 Complications of Supracondylar Fractures of the Elbow

231

FIGURE 15-7

Causes of Volkmann’s contracture in 58 limbs (55 children). In this study, the supracondylar fractures accounted for half of these complications in the upper extremity. (From Mubarak, S. J., and Carroll, N. C.: Volkmann’s contracture in children: aetiology and prevention. J. Bone Joint Surg. 61B:285, 1979.)

intracompartmental pressures.12 Mubarak and colleagues have demonstrated that pressurization to as high as 80 mm Hg of the entire anterolateral compartment in a number of dogs produced only occasional transient spasm of the midsize vessels on angiography.

DIFFERENTIAL DIAGNOSIS Many traumatic events that precipitate a compartment syndrome or arterial injury can also produce a painful, swollen extremity. The diagnosis of the underlying problem (e.g., fracture or contusion) is obvious; the diagnosis of a superimposed ischemia is more difficult. Pain out of proportion to that expected for the injury and any sensory deficit must be explained. A compartment syndrome or an arterial injury also must be differentiated from a nerve injury, which is usually a

neurapraxia when it is associated with a closed elbow fracture or dislocation. The clinical findings of these three entities overlap, frequently making the diagnosis difficult, if not impossible, by clinical means. All of these problems may be associated with motor or sensory deficits and pain. Careful clinical evaluation is necessary to differentiate these entities (Table 15-1). As noted earlier, an arterial injury usually results in absent pulses, poor skin color, and decreased skin temperature. In contrast, a compartment syndrome routinely presents with intact peripheral circulation unless the underlying etiology is an arterial injury. A diagnosis of nerve injury is usually made by exclusion of the other two entities. Doppler blood flow studies, arteriography, and pressure measurements are frequently required to aid in the differential diagnosis of these three entities, especially if these problems are present in combination.

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Arterial occlusion

Typical Clinical Findings of Compartment Syndrome, Arterial Occlusion, and Neurapraxia

TABLE 15-1

Compartment Syndrome

Arterial Occlusion

Neurapraxia

Pressure increased in compartment

+

+

−

Pain with stretch

+

+

−

Paresthesia or anesthesia

+

+

+

Paresis or paralysis

+

+

+

Arterial ischemia (X hours)

Restoration

Postischemic swelling

From Mubarak, S. J., and Carroll, N. C.: Volkmann’s contracture in children: aetiology and prevention. J. Bone Surg. 61B:290, 1979. Compartment syndrome

Compartment syndrome ischemia (Y hours)

Fasciotomy Total ischemia = X hours + Y hours

FIGURE 15-8

Pathogenesis of postischemia-initiated compartment syndrome. (From Mubarak, S. J., and Hargens, A. R.: Compartment Syndromes and Volkmann’s Contracture. Philadelphia, W. B. Saunders, 1981.)

FIGURE 15-9

Schematic view of forearm compartment syndrome. Intracompartmental pressures are rarely high enough to occlude the major arteries of the compartment. However, the pressure is sufficient to cause ischemia of muscle and nerve by occluding the microcirculation within the compartment. (From Rang, M.: Children’s Fractures. Philadelphia, J. B. Lippincott Co., 1974.)

Differentiation of these entities is important because therapy for each is radically different. The neurapraxia accompanying a closed fracture is usually best treated by observation. Arterial injuries warrant immediate operative repair of the vessel, and a compartment syndrome necessitates immediate decompressive fasciotomy.

TREATMENT When evaluating a patient with a traumatized limb and a neurocirculatory deficit, the physician should document carefully the time of injury and examination. A thorough examination should include motor, sensory, and circulatory evaluation. In the case of a young child, in which patient cooperation is not possible, observations of finger movement should be documented while the circulation is objectively assessed by palpation of the pulses and by Doppler examination. When a neurologic deficit is observed in a painful, traumatized, and swollen limb, the physician must evaluate and treat the patient promptly. At this stage, one must differentiate the troublesome problems of compartment syndrome, neurapraxia, and arterial injury. Arterial Injury When an arterial injury associated with a supracondylar fracture is suspected, a Doppler examination should be performed. The velocity Doppler is an integral instrument in assessing the presence of peripheral pulses and is very useful for noninvasive documentation of pulses in the presence of a markedly swollen extremity. A quantitative Doppler technique has been described by Schoenecker and colleagues66 to detect significant asymmetry between the injured and an uninjured extremity in children with type III supracondylar humerus fractures. Arteriography is not recommended in an acute situation.67 Shaw and associates noted the risk of arteriography to be the following: (1) prolongation of ischemic time between fracture and reduction;

Chapter 15 Complications of Supracondylar Fractures of the Elbow

(2) arterial damage at the catheter insertion site; and (3) allergy to contrast material.67 After confirmation of distal forearm ischemia, an attempt to better align the fracture fragments should be made immediately in the emergency room. In extensiontype fractures, this is accomplished by extending the elbow, correcting any coronal plane deformity, and reducing the fracture by bringing the proximal fragment posteriorly and the distal fragment anteriorly (Fig. 15-10). Often, this simple maneuver will immediately restore distal circulation.33 If the distal circulation is not restored, a vascular surgeon should be notified, and the patient should be taken immediately to the operating room. All authors agree that the fracture should be reduced and stabilized by percutaneous pinning or, if necessary, open reduction and fixation. If the radial pulse does not return within 30 minutes, and signs of forearm and hand ischemia continue to be evident, then exploration of the brachial artery at the fracture site is recommended. In these circumstances, prophylactic fasciotomy of the forearm should be considered after brachial artery repair if the period of ischemia is more than 4 hours. An algorithm for the treatment of supracondylar humerus fractures associated with forearm and hand ischemia is represented in Figure 15-11.

233

FIGURE 15-10 A and B, Simple realignment of an ischemic limb may reduce the tension on the brachial artery and restore the distal circulation. (From Herring, J. A.: Tachdjian’s Pediatric Orthopedics, 3rd ed., 2002, p. 2148.)

Supracondylar fracture and ischemia

Anesthesia and operating room

Reduce fracture and stabilize

Absent pulse and ischemia

Intact pulse and soft compartment

Arteriogram ± Axillary block ±

Tight forearm compartment

Pressure measurement Observe < 30 mm Hg

Explore: repair artery

Ischemia > 4 hours

Explore: decompress compartment syndrome

≥ 30 mm Hg

FIGURE 15-11 Scheme for management of supracondylar fractures associated with upper extremity ischemia. (From Mubarak, S. J., and Hargens, A. R.: Compartment Syndromes and Volkmann’s Contracture. Philadelphia, W. B. Saunders, 1981, p. 144.)

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Part IV Conditions Affecting the Child’s Elbow

Shaw and colleagues67 explored three cases and documented intimal tears with thrombus obstructing the brachial artery lumen. In two patients, the injured segment was excised and replaced by a saphenous vein graft; and prophylactic fasciotomy was also performed. One patient was noted to have brachial artery entrapment at the fracture site that was appropriately released. Schoenecker and associates66 recommend brachial artery exploration if Doppler-detectable pulses did not return within 30 minutes after fracture reduction. A vascular surgeon assisted with the exploration. Three of seven patients demonstrated interluminal damage or transsection, requiring saphenous vein graft. Four others demonstrated kinking or entrapment of the artery at the fracture site, with re-establishment of the pulses after mobilization. Garbuz and coworkers19 explored five brachial arteries and found a similar ratio of luminal damage, laceration, and entrapment of the arteries. One patient was treated with ligation, and had long-term claudication symptoms. Eight of 11 patients who initially had an absent radial pulse demonstrated a return of the pulse after the closed reduction. In three children, the radial pulse did not return, but no further treatment was required because the forearm and hand remained pink without any further neurologic deficits. This is known in the orthopedic literature as the “pulseless pink hand.” The Vancouver study group reviewed the pulseless pink hand in 13 patients following closed reduction and percutaneous pinning of the supracondylar fracture.65 They recommended color flow duplex scanning and MRA as a noninvasive safe technique for evaluating brachial artery patency and collateral circulation around the elbow. The vascular injuries in the 13 patients were studied; four had a thrombus or intimal tear. These patients underwent vein patch graft angioplasty. Urokinase infusion was used intra-arterially in four patients, and open thrombectomy was used in one. At follow-up, MRA studies of these patients showed a high rate of asymptomatic reocclusion and residual stenosis of the brachial artery. Thus, the investigators called into question the need for vascular reconstruction of intimal tears when the patient has a pink, well-perfused hand and MRA or other noninvasive studies that demonstrate adequate collateral circulation. They strongly recommended observation as the mainstay of treatment for these patients. In a recent survey of pediatric orthopedic surgeons, 60.5% of responding surgeons would monitor a pulseless pink hand for at least 24 hours following reduction and pinning. If the hand remained pulseless after 24 hours, the majority of respondents (61.2%) would continue to observe the extremity and monitor for adequate collateral circulation.49

Compartment Syndrome When the patient is cooperative, most compartment syndromes can be diagnosed clinically, and intracompartmental pressure measurement is only confirmatory. There are three groups of patients in whom difficulties in eliciting or interpreting the physical findings make measurement of intracompartmental pressure particularly valuable as a criterion for decompression:

1. Uncooperative or unreliable patients. A child with a supracondylar fracture will often be so frightened that careful motor and sensory evaluation is not possible. 2. Unresponsive patients. A patient with a head injury or one who is sedated and on a respirator with a swollen limb needs pressure measurement. 3. Patients with nerve deficits. When there is an associated nerve injury or arterial injury at the elbow, intracompartmental pressure measurement frequently is required to differentiate these problems from a compartment syndrome. Mubarak and colleagues recommend that any intracompartmental pressure greater than 30 to 35 mm Hg be considered for fasciotomy if it is combined with the clinical findings of a compartment syndrome. However, one must remember that any threshold pressure is a relative indication for decompression that should be tempered by the patient’s overall condition, blood pressure, and peripheral perfusion; the trend of the symptoms and signs; the trend of the intracompartmental pressures; and the cooperation and reliability of the patient.57 Bardenheuer2 was the first to report on fasciotomy in the forearm. Eichler and Lipscomb13 described an approach to a patient with a forearm compartment syndrome that included a division of forearm skin, subcutaneous tissue, and fascia. In 1972, Eaton and Green11 described a specific operative technique in which the skin incision began distal to the elbow flexion crease and medial to the bicipital tendon, extending distally in the longitudinal axis of the midforearm to the transverse flexion crease at the wrist. The forearm fascia was incised longitudinally along its full length. The epimysium of all poorly vascularized muscles was sectioned. The fascia was left open, and delayed closure with split-thickness skin grafts and relaxing incisions was performed 48 to 72 hours later. Neumeyer and Kilgore’s incision began adjacent to the medial epicondyle, extended obliquely across the antecubital fossa over the volar mobile wad, and returned to the midline in the distal forearm.59 It continued in a curvilinear fashion across the carpal canal to the midpalm. This report recommended wide exposure of all three possible areas of involvement: the volar and

Chapter 15 Complications of Supracondylar Fractures of the Elbow

dorsal compartments of the forearm and the intrinsic compartments of the hand. Closure was accomplished by split-thickness skin grafts after several days. Whitesides and associates77 described another operative approach in which the incision began above the elbow laterally and was carried transversely across the antecubital fossa to the proximal-medial forearm. The incision was continued distally along the ulnar border of the forearm to the wrist, where it curved laterally in the flexor crease of the wrist and extended into the palm in the thenar crease. The fascia was opened from above the elbow to the midpalm. The carpal tunnel and all neurovascular and muscular envelopes were opened fully. They noted that subcutaneous fasciotomy should never be performed in the forearm. The fascia was left open and was closed by split-thickness skin grafts 48 to 72 hours later. Similarly, Matsen and associates used the volar-ulnar approach. They frequently performed carpal tunnel release and epimysiotomy, as recommended by Eaton and Green.11 The advantage of this volar-ulnar approach is that the flexor tendons and median nerve are not left exposed in the distal forearm. The effectiveness of the volar forearm fasciotomy was evaluated initially in a series of cadaver experiments.21 The incisions used were the volar-ulnar incision described by Whitesides and associates77 and the curvilinear midline volar incision. Both incisions were effective in lowering pressures in the volar forearm, and both also lowered pressure within the mobile wad and dorsal regions in approximately half of the limbs. However, the curvilinear incision allowed easier exposure of the arteries and nerves of the forearm and the mobile wad. The volar forearm pressure generally fell to normal values when the antebrachial fascia had been divided from the lacertus fibrosus to the junction of the middle and distal thirds of the forearm. When the dorsal pressures remained elevated following volar fasciotomy, a dorsal fasciotomy was performed. A Volkmann contracture is the major complication of a compartment syndrome. Fortunately, the incidence of that complication following supracondylar fractures, as previously noted, has declined significantly in the past 40 years. With proper treatment of the elbow injury and early recognition and treatment of ischemia, Volkmann’s contracture is a rarely seen sequela of a supracondylar fracture. Many large series on the treatment of supracondylar fractures report no cases of Volkmann’s contracture when treated by Dunlap’s traction,10 overhead pin traction,6 or percutaneous pinning.14,43,69,70 Gelberman and colleagues20 reported no cases of Volkmann’s contracture in a study of supracondylar fractures. However, they noted that crush injuries or severe open injuries, when associated with compartment syndromes, resulted in considerable disability with decreased strength and limitation of forearm and hand

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motion. In these cases, much of the functional loss can be attributed to the crush injury alone; the compartment syndrome is an additional insult.20 A complete discussion of the treatment of an established contracture is covered by Gelberman20,21 and others,57 and is beyond the scope of this discussion. Authors’ Prefered Fasciotomy Technique We prefer a single longitudinal curvilinear incision for decompression of the volar forearm (Fig. 15-12). This incision allows an easy approach to the antebrachial fascia and the transverse carpal ligament, as well as to the neurovascular structures of the forearm and the mobile wad. The incision is nearly identical to McConnell’s combined exposure of the median and ulnar neurovascular bundles, as described by Henry.31 A straight longitudinal incision is used for the dorsal compartment of the

FIGURE 15-12

Dorsal and volar forearm incisions. (From Gelberman, R. H., Garfin, S. R., Hergenroeder, P. T., Mubarak, S. J., and Menon, J.: Compartment syndromes of the forearm: diagnosis and treatment. Clin. Orthop. 161:252, 1981.)

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FIGURE 15-13 Cross-section of left forearm with wick catheter illustrating its position and fasciotomy incision. W, Wick catheter; 1, ulnar nerve; 2, ulna; 3, radius; 4, median nerve; 5, radial artery; 6, forearm fascia. (From Gelberman, R. H., Garfin, S. R., Hergenroeder, P. T., Mubarak, S. J., and Menon, J.: Compartment syndromes of the forearm: Diagnosis and treatment. Clin. Orthop. 161:252, 1981.)

forearm (see Figs. 15-2 and 15-13). Technique and postoperative care are described in detail elsewhere.20,21,57 It is clear that many factors influence the result of a supracondylar fracture associated with ischemia. However, the treating orthopedic surgeon must carefully assess the clinical findings and document them in the medical records. When appropriate, laboratory instruments such as Doppler blood flow studies, MRA (for a possible arterial injury), and intracompartmental pressure measurements (for possible compartment syndrome) should be performed to clarify the diagnosis. Treating these causes for forearm and hand ischemia promptly will result in the best results.

SURGICAL TIMING AND NEUROVASCULAR COMPLICATIONS A number of recent studies have investigated the association between surgical timing and perioperative complications in the treatment of closed, well-perfused,

displaced supracondylar humerus fractures in children.28,51,75 The groups from Cincinnati and Los Angeles were unable to identify any significant differences in the need for open reduction (2% to 13%), or the rates of pin tract infection (1% to 4%), iatrogenic nerve injury (2% to 4%), vascular injury recognized after surgery (2%), and compartment syndrome leading to Volkmann’s ischemic contracture (0%) when comparing patients with closed, well-perfused, displaced supracondylar humerus fractures treated 8 to 12 hours following the initial injury with those treated more than 8 to 12 hours after injury.28,51 More recently, a group from Edinburgh, Scotland, did demonstrate an increased need to perform an open reduction in patients with closed, well-perfused, Gartland type III supracondylar humerus fractures when surgery was delayed more than 8 hours following injury (33%) compared with those treated in less than 8 hours from the time of injury (11.5%), P = 0.05.75 All of these studies specifically excluded two of the most common indications that prompt the emergent treatment of supracondylar humerus fractures: open fracture and extremity ischemia. We do not recommend delayed treatment in those situations. At present, we will allow an 8- to 12-hour delay in the treatment of displaced supracondylar humerus fractures provided that the skin is intact and the neurovascular examination is normal. These patients are splinted in a position of comfort and are admitted for elevation/observation until definitive surgical treatment. Some fractures with marked displacement can be provisionally reduced in the emergency room to improve patient comfort and fracture position before splinting. Patients in whom the skin is compromised, the swelling is severe, or the neurovascular examination is abnormal are treated with closed reduction and pinning emergently.

OSSEOUS COMPLICATIONS Osseous complications of supracondylar humerus fractures include malunion, nonunion of the fracture, avascular necrosis (AVN) of the distal fragment, and myositis ossificans. Techniques for the management of these complications are discussed here. Stiffness after these fractures is discussed at length in Chapter 22. With current management techniques, good to excellent results should be anticipated in more than 90% of patients with supracondylar fractures.1 The most common significant complication is malunion, which is discussed last and in the greatest detail. Nonunion of the supracondylar fracture is virtually never seen, with only a few scattered anecdotal accounts in the literature. The near absence of nonunion with this fracture may be due to the rich vascular supply in the area, as

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well as to the fact that the fracture tends to be more metaphyseal in location and extra-articular. The lateral condyle fracture, in which the incidence of nonunion or delayed union is much higher, is an intra-articular fracture, with synovial fluid bathing the surface of the fragments, a phenomenon absent in the supracondylar fracture.

AVASCULAR NECROSIS Despite the rich vascular supply, AVN has been reported in the distal fragment following a supracondylar humerus fracture.55 AVN of the capitellum as well as the trochlea has been reported, although both are extremely rare. The occurrence of AVN is much more likely to be associated with a condylar fracture, medial or lateral, than with a supracondylar humerus fracture. Condylar fractures require early and accurate diagnosis as well as prompt management to maximize successful osseous healing and minimize the development of future deformity. Even in widely displaced type III supracondylar fractures, Morrissy and Wilkins55 did not find a correlation between severity of the fracture and the extent of avascular changes, which are very rare. Because the capitellar blood supply enters the distal humerus laterally and distally, a fracture that exits the lateral column very distally may lead to avascular changes in this region. Similarly, low fractures exiting medially may be at increased risk for avascularity associated with the trochlea. Distal humeral AVN and the fishtail deformity may be associated with decreased range of motion, the development of a cubitus valgus deformity, and, occasionally, a subsequent tardy ulnar nerve palsy. Depending on which of the two vascular supplies to the growth centers is compromised, different deformities may develop. With elimination of the more lateral trochlear blood supply, such as may occur with a supracondylar humerus fracture with T intercondylar extension, a classic fishtail deformity of the distal humerus may occur (Fig. 15-14). The fishtail deformity is more frequently associated with an inadequately treated lateral condyle fracture. The deformity includes the loss of the normal crista dividing the capitellum from the trochlear groove and central involution of the distal articular surface. The central involution allows the proximal ulna to “settle” into the distal humerus. Clinically, the prominence of the olecranon normally seen during maximal flexion of the elbow is absent (Fig. 15-15). If both vessels feeding the distal humeral fragment have been compromised, complete aplasia of the trochlea may result. This condition will most likely lead to a progressive cubitus varus deformity and potential posterolateral rotatory instability of the ulnohumeral articulation. A tardy ulnar nerve palsy may also develop.

FIGURE 15-14 Trochlear blood supply. Medial and lateral vessels feed the trochlea; the severity of avascular changes as well as the type of resulting deformity is dependent on which vessel is injured. In this illustration, a central deficiency and fishtail deformity of the distal humerus would be expected to develop. (From Rockwood, C. A., Wilkins, K. E., and Beaty, J. H.: Fractures in Children, 4th ed., Vol. 3. Philadelphia, Lippincott-Raven, 1996.)

FIGURE 15-15 Fishtail deformity—loss of the olecranon prominence. Clinical findings of avascular necrosis (AVN) of the distal humerus can include depression of the prominence of the olecranon secondary to a central deficiency as demonstrated in this silhouette of flexed elbows as viewed from the patient’s head. Also cubitus varus or less likely valgus and diminished range of motion may be seen with AVN of the distal humerus.

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Causative factors include instability of the ulnar nerve over a hypoplastic medial condylar region and scarring or tethering as the nerve enters the flexor carpi ulnaris.16 In time, this leads to abnormal traction, stretching, and friction of the ulnar nerve as it moves over the medial epicondyle, producing a gradual progressive ulnar neuropathy.34 Management of the sequelae of distal humeral AVN is rarely satisfying. Surgical intervention for improvement of motion may be indicated in specific cases, if a vigorous physical program is unsuccessful. Cases of tardy ulnar nerve palsy are managed with anterior transposition of the ulnar nerve. Progressive angular deformity of the distal humerus may be attributable to either AVN or physeal injury. Physeal arrest, sporadically reported in conjunction with even mild supracondylar humerus fractures, appears similar to a nonunion but is rare.37,60 If it is detected early and the degree of physeal involvement is limited, physeal bar resection, although technically demanding, may be considered. Although the fishtail deformity itself is not amenable to

surgical correction, cubitus varus or valgus, which may occur in conjunction with either physeal arrest or AVN, can be corrected with a supracondylar osteotomy. Because the restoration of growth potential may not be possible in cases of AVN, as in some cases of physeal arrest, recurrent angular deformity may occur, depending on the age of the child, requiring multiple osteotomies over time. Other potential etiologies for loss of range of motion include myositis ossificans, soft tissue contracture or scar formation, osseous deformity producing a bone block to motion, and angulation at the fracture site. In cases in which the fracture has healed but flexion or extension is believed to be limited structurally by a bony block, excision of the tip of the olecranon with enlargement of the olecranon fossa may occasionally prove beneficial (Fig. 15-16). Osseous impingement is an uncommon cause of motion loss. The technique has been well described for the management of the more common impingement from degenerative changes of the elbow by Morrey.54

FIGURE 15-16 A, Teenage patient with open reduction and internal fixation of left supracondylar humerus fracture with markedly limited motion postoperatively secondary to arthrofibrosis as well as impingement of both the coronoid and olecranon fossae due to healing with collapse of the medial and lateral columns of the distal humerus. B, Three-dimensional computed tomography scan of elbow showing impingement of the olecranon fossa. C, Distal humeral osteoplasty was performed with removal of the tip of the olecranon, foraminotomy of the distal humerus, and débridement of impinging distal humerus proximal to the capitellum. The arc of motion of the elbow increased by 50 degrees postoperatively.

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MYOSITIS OSSIFICANS

ANGULAR DEFORMITY

Myositis ossificans is a potential complication of supracondylar humerus fractures, which if extensive, results in poor elbow motion. The phenomenon is not common and may even be self-limiting, with resolution over a 1- to 2-year course (Fig. 15-17). Siris71 found a 2% incidence in a 1939 review of 330 supracondylar humerus fractures, whereas more recent studies have reported an incidence of less than 1% and 0% by most authors. The occurrence and severity would intuitively be expected to be increased in cases treated with open reduction, particularly if the surgery is delayed from the time of the injury. In supracondylar humerus fractures treated with open reduction acutely, only one report identifies myositis as a postoperative complication.22 Even with delayed open management, Lal and Bhan42 found no cases of myositis ossificans in their report of 20 fractures treated with open reduction 11 to 17 days after injury. Surgical excision of the affected tissue should be performed only if the ectopic bone is clearly demonstrated to be causative of motion loss, conservative attempts to regain motion have failed, and adequate time from that of the injury has transpired such that the lesion is quiescent. Bone scan has been recommended in assessing the metabolic activity level of the lesion, but the editor favors the plain radiographic features of clear marginal delineation and trabecularization. Attempts to prevent heterotopic bone formation with low-dose external beam irradiation, and administration of oral nonsteroidal anti-inflammatory agents or oral disphosphonates are not warranted due to the rarity and self-limiting nature of this complication.30

Angular deformity of the elbow is the most common significant adverse sequela of a supracondylar humerus fracture. This condition may arise from growth disturbances such as a physeal injury or AVN, as outlined previously, or from the position in which the fracture healed. Malunion may result in either a flexion or extension deformity in the sagittal plane; a varus or valgus deformity in the coronal plane; and rotational deformity in the horizontal plane. Deformity may occur in any single plane or in a combination of planes. Although some remodeling of sagittal plane deformity can be expected, no significant improvement in coronal and horizontal deformity should be anticipated.4,15,40,52 Although cubitus valgus has been reported in association with supracondylar fractures of the humerus,8 cubitus varus is far more commonly reported as a complication of the management of these fractures. Cubitus varus has been termed a cosmetic sequela by numerous authors. This characterization may limit indications for corrective surgery, particularly in the modern medical environment. Tardy ulnar nerve palsy has been described in association with cubitus varus, although it is more commonly found secondary to cubitus valgus.17 Functional deficits and a potential increased risk of new injury as well as limitations of motion and discomfort have been well described in patients with cubitus varus. A correlation between residual cubitus varus following supracondylar humerus fractures and subsequent lateral condyle fractures has been noted.7 Thus, although the indications for surgical correction of cubitus varus do include poor cosmesis of

FIGURE 15-17 Myositis ossificans. A, Supracondylar fracture with myositis ossificans and a rigid elbow. B, Spontaneous resorption and remodeling with restoration of motion, lacking 20 degrees of flexion 7 months after injury.

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an unsightly deformity, one must also consider future function of the extremity and the risk for new injuries due to altered biomechanics of the elbow in varus.

INDICATIONS FOR CORRECTIVE SURGERY The goals of corrective surgery are (1) to restore the upper extremity alignment, (2) to restore range of motion, and hence, (3) to improve function to as near the preinjury state as possible. To achieve these goals, understanding of the anatomic nature and functional requirement of the deformity is necessary. Although simple collapse or impaction of the lateral column of the distal humerus will yield a cubitus valgus angular deformity, and the opposite is true for cubitus varus, rotation may contribute to either deformity and should at least be considered in the planning of corrective surgery. Graham24,25 stressed the contribution of rotation to changes in the carrying angle of the arm. Chess and colleagues5 stated that varus malalignment was the most important contributor to postoperative cubitus varus, but that internal rotation combined with varus accentuates the deformity. In apparent contrast, Mahaisavariya and Laupattarakasern48 reviewing anatomic findings at the time of corrective osteotomy concluded that rotation does not contribute to cubitus varus. Mitsunari and coworkers53 found an increased incidence of residual internal rotation deformity in patients with tardy ulnar nerve palsy following a supracondylar humerus fracture. Many techniques have been espoused for the correction of distal humeral malunions. These include closing wedge osteotomies with or without translation of the distal fragment, dome osteotomy, and complex triplane osteotomy, to name a few. The common concept is that each of these techniques addresses the potential components of the deformity to varying degrees.

SURGICAL APPROACH In considering surgical correction of a distal humeral deformity, one of the first steps is deciding on the surgical approach. A medial approach, which allows visualization and protection of the neurovascular bundles, has been advocated by some authors.39 One potential detraction from this approach is that manipulation of the neurovascular structures is necessary to gain access to the distal humerus. Also, particularly for cubitus varus, an osteotomy with lateral closing is difficult from the medial approach. The posterior approach has been advocated by several authors. This can be accomplished through a triceps-splitting, triceps-tendon transecting,27,61 or tricepssparing technique.27,61 Avascularity of the distal fragment has been reported to be associated with this tendon

FIGURE 15-18 Lateral approach to the distal humerus. The lateral approach is used to expose the distal humerus. The triceps is taken posteriorly; the brachioradialis and extensor carpi radialis longus are mobilized anteriorly from lateral supracondylar ridge; and the brachialis is dissected off the anterior distal humerus. The radial nerve passes laterally around the humeral shaft just proximal to this dissection, passing between the brachialis and brachioradialis before entering the supinator to become the posterior interosseous nerve. (Modified from Hoppenfeld, S.: Surgical Exposures in Orthopedic Surgery: The Anatomic Approach, 2nd ed. Philadelphia, J. B. Lippincott, 1984.)

transection.27 The posterior approach, particularly the first two techniques, affords excellent visualization of the distal humerus, being used with some frequency in displaced intercondylar distal humeral fractures. A long incision is necessary, as well as significant dissection, which risks postoperative adhesion formation. In one study of supracondylar humeral fractures, stiffness was noted in 21% of those managed with closed techniques but in 50% of those treated with open reduction through a posterior approach.61 In addition, intraoperative assessment of the magnitude of correction of the carrying angle can be difficult in the prone or lateral position. The lateral approach is the most frequently used and advocated approach to the distal humerus for the correction of cubitus varus.* The dissection is brought to the shaft of the humerus, distal to the area in which the radial nerve exits laterally from around the shaft. A subperiosteal plane is used to expose the humerus, as well as avoid injury to the medial neurovascular structures (Fig. 15-18). * See references 9,16,26,32,44,58,64,68,71,76.

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Valgus Flexion

FIGURE 15-19 Osteotomy templating. Distal humeral closing wedge osteotomy planned to remove more bone anteriorly to correct any extension deformity, as well as more laterally to correct cubitus varus. The magnitude of anterior closing wedge equals the difference in maximal elbow flexion comparing the injured elbow with contralateral. The magnitude of lateral wedge resection needed equals the degrees of ulnohumeral varus plus degrees of carrying angle of the contralateral elbow. (Modified from Hollinshead, W. J.: Anatomy for Surgeons, Vol. 3: The Back and Limbs, 3rd ed. Philadelphia, Harper & Row, 1982.)

OSTEOTOMY TECHNIQUES The next step in planning the correction of a distal humeral deformity is the nature of the osteotomy. As already outlined, there are various techniques to consider. The lateral closing wedge osteotomy is the most widely used and recommended technique. With a lateral closing wedge osteotomy, correction of the three aspects of distal humeral deformity following supracondylar fracture malunion are possible: cubitus varus, hyperextension, and rotation (Fig. 15-19). Some authors advocate a simple laterally based closing wedge, leaving the medial cortex intact as a hinge.3,23,39,50,62 Although this approach may have value in certain cases with limited deformity, flexion and extension are not well addressed, nor is rotational deformity. Wong and Balasubramaniam80 argue that correction of the rotational component is unnecessary. Also, as the size of the wedge required to achieve appropriate valgus alignment increases, so does the prominence of the distal fragment laterally.78 Owing to these constraints, a corrective closing

FIGURE 15-20 Fragment reduction and fixation. In correction of the deformity, the distal fragment is flexed to eliminate hyperextension, rotated to correct varus and provide the planned degree of valgus, and medialized to minimize lateral prominence of the capitellum. Fixation is provided with two to three threaded Steinmann pins, either solely from the lateral aspect of the humerus, or two from the lateral and one from medial, spaced as widely as possible at the osteotomy site for maximal rotational control. (Modified from Hollinshead, W. J.: Anatomy for Surgeons, Vol. 3: The Back and Limbs, 3rd ed. Philadelphia, Harper & Row, 1982.)

wedge osteotomy that is laterally and anteriorly based with medial translation of the distal fragment is preferred to obtain optimal results (Fig. 15-20).* If desired for greater osseous contact, a spike can be left laterally on the distal fragment to interlock with the proximal shaft, similar to a Wiltse distal tibial varus osteotomy.79 Uchida and associates72 described a three-dimensional osteotomy for the correction of cubitus varus. A posterolateral approach is used, and a complex biplane, tridirectional step cut osteotomy is performed, with fixation provided by screws. Although elegant in design and execution, this technically demanding osteotomy differs from a lateral closing wedge flexion osteotomy only in the extent and angle of bone surface contact. If poor postosteotomy healing is a concern, this technique offers extensive surface contact for osseous bridging. A dome osteotomy has been described that involves a posterior approach, marking the planned dome from a reference Kirschner wire, and uses K-wire fixation.38 * See references 9,16,18,26,29,35,36,41,58,61,68,71,73,74,76.

FIGURE 15-21 A, A 6-year-old boy with cubitus varus of the right elbow following supracondylar fracture. B, Anteroposterior (AP) view of his right distal humerus. C, AP view of the patient’s normal left distal humerus. D, AP view following closing wedge valgus and flexion osteotomy to correct cubitus varus. E, Lateral view 4 weeks postoperatively demonstrating restoration of sagittal alignment, distal humerus.

Chapter 15 Complications of Supracondylar Fractures of the Elbow

This technique allows correction of malrotation and avoids a potentially prominent lateral epicondylar region, but it does not address flexion/extension of the distal fragment. Also, this procedure is more technically demanding than that using the laterally based closing wedge osteotomy. In their report of 11 patients, Kanaujia and associates found that the outcome for all was satisfactory.

FIXATION TECHNIQUES The final consideration in surgical correction of the distal humerus malunion is fixation options for the osteotomy fragments. These include smooth Kirschner wires,62,71 threaded Steinmann pins, screws,72 screws with a wire tension band,3,16,45,50 plates and screws,9,32 and external fixation.42 The smooth Kirschner wire fixation has proven to be less than reliable, with a greater incidence of loss of correction compared with threaded fixation (Fig. 15-21). Adequate fixation and maintenance of alignment is reliably obtained and the buried pins can be retrieved in the future, particularly if the physis was crossed for optimal fixation. In the older, larger child, crossed screws may be used, although great care must be exercised to avoid unplanned translation of the fragments. The technique of screws paralleling the osteotomy, connected with a tension band wire, can be used only if good medial cortical integrity remains following the closing wedge osteotomy. Neither medial translation nor derotation is possible if this fixation is chosen. In the older adolescent, one-third tubular or 3.5-mm pelvic reconstruction plates with screws may be necessary to gain adequate fixation, particularly if early range of motion is planned postoperatively. External fixation is another option, although the size of the distal fragment is such that at most two pins could be used. Also, the inherent difficulties with pin tract care exist, which limits the attractiveness of this option. In summary, distal humeral malunion is not an uncommon complication of supracondylar humerus fractures. The most common deformity is cubitus varus, with varying components of extension and rotation of the distal fragment. The deformity is not purely cosmetic, because it alters the biomechanics of the elbow and may increase the risk to the patient of a future lateral condyle fracture. Corrective osteotomy with attention to detail is reliable and safe. An anterolaterally based closing wedge osteotomy with medial translation of the distal fragment is the treatment of choice. Subdermal threaded Steinmann pin fixation has proved adequate for the vast majority of cases, particularly the younger patient. The buried pins may be removed once healing has occurred, often as early as 6 to 8 weeks. Once osseous union is established, physical therapy can be used to maximize the patient’s range of motion.

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References 1. Alburger, P. D., Weidner, P. L., and Betz, R. R.: Supracondylar fractures of the humerus in children. J. Pediatr. Orthop. 12(1):16, 1992. 2. Bardenheuer, L.: Die Entstehung und Behandlung der ischamischen Muskelkontractur und Gangran. Dtsch. Z. Chir. 108:44, 1911. 3. Bellemore, M. C., Barrett, I. R., Middleton, R. W. D., Scougall, J. S., and Whiteway, D. W.: Supracondylar osteotomy of the humerus for correction of cubitus varus. J. Bone Joint Surg. 66B:566, 1984. 4. Blount, W. P.: Fractures in Children. Baltimore, Williams & Wilkins, 1955, pp. 26-42. 5. Chess, D. G., Leahey, J. L., and Hyndman, J. C.: Cubitus varus: significant factors. J. Pediatr. Orthop. 14(2):190, 1994. 6. D’Ambrosia, R. D.: Supracondylar fractures of the humerus: prevention of cubitus varus. J. Bone Joint Surg. 54A:60, 1972. 7. Davids, J. R., Maguire, M. F., Mubarak, S. J., and Wenger, D. R.: Lateral condyle fracture of the humerus following posttraumatic cubitus varus. J. Pediatr. Orthop. 14:466, 1994. 8. De Boeck, H., and De Smet, P.: Valgus deformity following supracondylar elbow fractures in children. Acta Orthop. Belgica 63:240, 1997. 9. Devnani, A. S.: Lateral closing wedge supracondylar osteotomy of the humerus for post-traumatic cubitus varus in children. Injury 28:643, 1997. 10. Dodge, H. S.: Displaced supracondylar fractures of the humerus in children: treatment by Dunlop’s traction. J. Bone Joint Surg. 54A:1408, 1972. 11. Eaton, R. G., and Green, W. T.: Epimysiotomy and fasciotomy in the treatment of Volkmann’s ischemic contracture. Orthop. Clin. North Am. 3:175, 1972. 12. Eaton, R. G., and Green, W. T.: Volkmann’s ischemia. A volar compartment syndrome of the forearm. Clin. Orthop. 113:58, 1975. 13. Eichler, G. R., and Lipscomb, P. R.: The changing treatment of Volkmann’s ischemic contractures from 1955 to 1965 at the Mayo Clinic. Clin. Orthop. 50:215, 1967. 14. Flynn, J. C., Matthews, J. G., and Benoit, R. L.: Blind pinning of displaced supracondylar fractures of the humerus in children. J. Bone Joint Surg. 56A:263, 1974. 15. France, J., and Strong, M.: Deformity and function in the supracondylar fractures of the humerus in children variously treated by closed reduction and splinting, traction, and percutaneous pinning. J. Pediatr. Orthop. 12:494, 1992. 16. French, P. R.: Varus deformity of the elbow following supracondylar fractures of the humerus in children. Lancet 2:439, 1959. 17. Fujioka, H., Nakabayashi, Y., Hirata, S., Go, G., Nishi, S., and Mizuno, K.: Analysis of tardy ulnar nerve palsy associated with cubitus varus deformity after a supracondylar fracture of the humerus: a report of four cases. J. Orthop. Trauma 9:435, 1995. 18. Gaddy, B. C., Manske, P. R., Pruitt, D. L., Schoenecker, P. L., and Rouse, A. M.: Distal humeral osteotomy for correction

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36. 37.

Part IV Conditions Affecting the Child’s Elbow

of posttraumatic cubitus varus. J. Pediatr. Orthop. 14:214, 1994. Garbuz, D. S., Leitch, K., and Wright, J. G.: The treatment of supracondylar fractures in children with an absent radial pulse. J. Pediatr. Orthop. 16:594, 1996. Gelberman, R. H., Garfin, S. R., Hergenroeder, P. T., Mubarak, S. J., and Menon, J.: Compartment syndromes of the forearm: diagnosis and treatment. Clin. Orthop. 161:252, 1981. Gelberman, R. H., Zakaib, G. S., Mubarak, S. J., Hargens, A. R., and Akeson, W. H.: Decompression of forearm compartment syndromes. Clin. Orthop. 134:225, 1978. Godley, D. R., Loeng, J. C. Y., and Yau, A.: Open reduction and internal fixation of supracondylar fractures of the humerus in children in Hong Kong: Long term results. Abbot Proc. 9:30, 1978. Graham, B., Tredwell, S. J., Beauchamp, R. D., and Bell, H. M.: Supracondylar osteotomy of the humerus for correction of cubitus varus. J. Pediatr. Orthop. 11:228, 1990. Graham, H. A.: Supracondylar fractures of the elbow in children. Part 1. Clin. Orthop. 54:85, 1967. Graham, H. A.: Supracondylar fractures of the elbow in children. Part 2. Clin. Orthop. 54:93, 1967. Griffin, P. P.: Supracondylar fractures of the humerus. Pediatr. Clin. North Am. 2:477, 1975. Gruber, M. A., and Healy, W. A.: The posterior approach to the elbow revisited. J. Pediatr. Orthop. 16:215, 1996. Gupta, N., Kay, R. M., Leitch, K., Femino, J. D., Tolo, V. T., and Skaggs, D. L.: Effect of surgical delay on perioperative complications and need for open reduction in supracondylar humerus fractures in children. J. Pediatr. Orthop. 24:245-248, 2004. Harris, I. E.: Supracondylar fractures of the humerus in children. Orthopedics 15:811, 1992. Hartigen, B. J.: Myositis ossificans after a supracondylar fracture of the humerus in a child. Am. J. Orthopedics 30:152, 2001. Henry, A. K.: Extensile Exposure, 2nd ed. Edinburgh, Churchill Livingstone, 1973. Hernandez, M. A., and Roach, J. W.: Corrective osteotomy for cubitus varus deformity. J. Pediatr. Orthop. 14:487, 1994. Herring, J. A.: Tachdijan’s Pediatric Orthopaedics from the Texas Scottish Rite Hospital for Children, 3rd ed. Philadelphia, Elsevier, 2002, p. 2147. Ih, J., Oh, C. W., Kyung, H. S., Park, I. H., and Kim, P. T.: Tardy ulnar nerve palsy in cubitus varus deformity associated with ulnar nerve dislocation in adults. J. Shoulder Elbow Surg. 15:474, 2006. Ippolito, E., Caterini, R., and Scola, E.: Supracondylar fracture of the humerus in children. Analysis at maturity of the fifty-three patients treated conservatively. J. Bone Joint Surg. 68A:333, 1986. Ippolito, E., Moneta, M. R., and D’Arrigo, C.: Post-traumatic cubitus varus. J. Bone Joint Surg. 72A:757, 1990. Kallio, P. E., Foster, B. K., and Paterson, D. C.: Difficult supracondylar elbow fractures in children: analysis of percutaneous pinning technique. J. Pediatr. Orthop. 12:11, 1992.

38. Kanaujia, R. R., Ikuta, Y., Muneshige, H., Higaki, T., and Shimogaki, K.: Dome osteotomy for cubitus varus in children. Acta Orthop. Scand. 59:314, 1988. 39. King, D., and Secor, C.: Bow elbow (cubitus varus). J. Bone Joint Surg. 33A:572, 1951. 40. Kurer, M. H. J., and Regan, M. W.: Completely displaced supracondylar fracture of the humerus in children. A review of 1708 comparable cases. Clin. Orthop. 256:205, 1990. 41. Labelle, H., Bunnell, W. P., Duhaime, M., and Poitras, B.: Cubitus varus deformity following supracondylar fractures of the humerus in children. J. Pediatr. Orthop. 2:539, 1982. 42. Lal, G. M., and Bhan, S.: Delayed open reduction for supracondylar fractures of the humerus. Int. Orthop. 15:189, 1991. 43. Leitch, K. K., Kay, R. M., Femino, J. D., Tolo, V. T., Storer, S. K., and Skaggs, D. L.: Treatment of multidirectionally unstable supracondylar humerus fractures in children. A modified Gartland type-IV fracture. J. Bone Joint Surg. 88A:980, 2006. 44. Levine, M. J., Horn, B. D., and Pizzutillo, P. D.: Treatment of posttraumatic cubitus varus in the pediatric population with humeral osteotomy and external fixation. J. Pediatr. Orthop. 16:597, 1996. 45. Lipscomb, P. R.: The etiology and prevention of Volkmann’s ischemic contracture. Surg. Gynecol. Obstet. 103:353, 1956. 46. Louahem, D. M., Nebunescu, A., Canavese, F., and Dimeglio A.: Neurovascular complications and severe displacement in supracondylar humerus fractures in children: defensive or offensive strategy. J. Pediatr. Orthop. B. 15:51, 2006. 47. Mahaisavariya, B., and Laupattarakasem, W.: Osteotomy for cubitus varus. A simple technique in 10 children. Acta Orthop. Scand. 67:60, 1996. 48. Mahaisavariya, B., and Laupattarakasem, W.: Supracondylar fracture of the humerus: malrotation versus cubitus varus deformity. Injury 24:416, 1993. 49. Malviya, A., Simmons, D., Vallamshetia, R., and Bache, C. E.: Pink pulseless hand following supra-condylar fractures: an audit of British practice. J. Pediatr. Orthop. B. 15:62, 2006. 50. McCoy, G. F., and Piggot, J.: Supracondylar osteotomy for cubitus varus. The value of the straight arm position. J. Bone Joint Surg. 70B:283, 1988. 51. Mehlman, C. T., Strub, W. M., Roy, D. R., Wall, E. J., and Crawford, A. H.: The effect of surgical timing on the perioperative complications of treatment of supracondylar humeral fractures in children. J. Bone Joint Surg. 83A:323, 2001. 52. Mehserle, W. L., and Meehan, P. L.: Treatment of the displaced supracondylar fracture of the humerus (type III) with closed reduction and percutaneous cross-pin fixation. J. Pediatr. Orthop. 11:705, 1991. 53. Mitsunari, A., Muneshige, H., Ikuta, Y., and Murakami, T.: Internal rotation deformity and tardy ulnar nerve palsy after supracondylar humeral fracture. J. Shoulder Elbow Surg. 4:23, 1995. 54. Morrey, B.: Primary degenerative arthritis of the elbow: treatment by ulnohumeral arthroplasty. J. Bone Joint Surg. 74B:409, 1992.

Chapter 15 Complications of Supracondylar Fractures of the Elbow

55. Morrissy, R. T., and Wilkins, K. E.: Deformity following distal humeral fracture in childhood. J. Bone Joint Surg. 66A:557, 1984. 56. Mubarak, S. J., and Carroll, N. C.: Volkmann’s contracture in children: aetiology and prevention. J. Bone Joint Surg. 61B:285, 1979. 57. Mubarak, S. J., and Hargens, A. R.: Compartment Syndromes and Volkmann’s Contracture. Philadelphia, W. B. Saunders, 1981. 58. Nassar, A.: Correction of varus deformity following supracondylar fracture of the humerus. J. Bone Joint Surg. 56B:572, 1974. 59. Neumeyer, W. L., and Kilgore, E. S., Jr.: Volkmann’s ischemic contracture due to soft tissue injury alone. J. Hand Surg. 1:221, 1976. 60. Nwakama, A. C., Peterson, H. A., and Shaughnessy, W. J.: Fishtail deformity following fracture of the distal humerus in children: Historical review, case presentations, discussion of etiology, and thoughts on treatment. J. Pediatr. Orthop. Part B 9:309, 2000. 61. Omer, C., Pestilci, F. I., and Tuzuner, M.: Supracondylar fractures of the humerus in children: analysis of the results in 142 patients. J. Orthop. Trauma 4:265, 1990. 62. Oppenheim, W. L., Clader, T. J., Smith, C., and Bayer, M.: Supracondylar humeral osteotomy for traumatic childhood cubitus varus deformity. Clin. Orthop. 188:324, 1984. 63. Ozcelik, A., Tekcan, A., and Omerolu, H.: Correlation between iatrogenic ulnar nerve injury and angular insertion of the medial pin in supracondylar humerus fractures. J. Pediatr. Orthopaedics, Part B. 15(1):58-61, 2006. 64. Rang, M.: Children’s Fractures, 2nd ed. Philadelphia, J. B. Lippincott, 1983. 65. Sabharwal, S., Tredwell, S. J., Beauchamp, R. D., Mackenzie, W. G., Jakubec, D. M., Cairns, R., and LeBlanc, J. G.: Management of pulseless pink hand in pediatric supracondylar fractures of humerus. J. Pediatr. Orthop. 17:303, 1997. 66. Schoenecker, P. L., Delgado, E., Rotman, M., Sicard, G. A., and Capelli, A. M.: Pulseless arm in association with totally displaced supracondylar fracture. J. Pediatr. Orthop. 10:410, 1996. 67. Shaw, B. A., Kasser, J. R., Emans, J. B., and Rand, F. F.: Management of vascular injuries in displaced supracondylar humerus fractures without arteriography. J. Orthop. Trauma 4:25, 1991.

245

68. Siris, J. E.: Supracondylar fractures of the humerus analyzed; 330 cases. Surg. Gynecol. Obstet. 68:201, 1939. 69. Skaggs, D. L., Hale, J. M., Bassett, J., Kaminsky, C., Kay, R. M., and Tolo, V. T.: Operative treatment of supracondylar fractures of the humerus in children. The consequences of pin placement. J. Bone Joint Surg. 83A:735, 2001. 70. Skaggs, D. L., Cluck, M. W., Mostofi, A., Flynn, J. M., and Kay, R. M.: Lateral-entry pin fixation in the management of supracondylar fractures in children. J. Bone Joint Surg. 85A:702, 2004. 71. Sweeney, J. G.: Osteotomy of the humerus for malunion of supracondylar fractures. J. Bone Joint Surg. 57B:117, 1975. 72. Uchida, Y., Ogata, K., and Sugioka, Y.: A new threedimensional osteotomy for cubitus varus deformity after supracondylar fracture of the humerus in children. J. Pediatr. Orthop. 11:327, 1991. 73. Usui, M., Ishii, S., Miyano, S., Narita, H., and Kura, H.: Three-dimensional corrective osteotomy for the treatment of cubitus varus after supracondylar fracture of the humerus in children. J. Shoulder Elbow Surg. 4:17, 1995. 74. Voss, F. R., Kasser, J. R., Trepman, E., Simmons, E., and Hall, J. E.: Uniplanar supracondylar humeral osteotomy with preset Kirschner wires for posttraumatic cubitus varus. J. Pediatr. Orthop. 14:471, 1994. 75. Walmsley, P. J., Kelly, M. B., Robb, J. E., Annan, I. H., and Porter, D. E.: Delay increases the need for open reduction of type III supracondylar fractures of the humerus. J. Bone Joint Surg. 88B:528, 2006. 76. Weiland, A. J., Meyer, S., Tollo, V. T., Berg, H. L., and Mueller, J.: Surgical treatment of displaced supracondylar fractures of the humerus in children. J. Bone Joint Surg. 60A:657, 1978. 77. Whitesides, T. E., Jr., Hirada, H., and Morimoto, K.: Compartment syndromes and the role of fasciotomy, its parameters and techniques. Instr. Course Lect. 26:179, 1977. 78. Wilkins, K. E.: Residuals of elbow trauma in children. Orthop. Clin. North Am. 21:291, 1990. 79. Wiltse, L. L.: Valgus deformity of the ankle: a sequel to acquired or congenital abnormalities of the fibula. J. Bone Joint Surg. 54A:595, 1972. 80. Wong, H. K., and Balasubramaniam, P.: Humeral torsional deformity after supracondylar osteotomy for cubitus varus: its influence on the postosteotomy carrying angle. J. Pediatr. Orthop. 12:490, 1992.

246

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CHAPTER

16

Physeal Fractures of the Elbow Hamlet A. Peterson

ANATOMY AND GROWTH The elbow joint consists of the articulating surfaces of three epiphyses: the distal humerus, the proximal ulna, and the proximal radius. At birth, each epiphysis is one mass of cartilage, each with its own epiphyseal growth plate (the physis). With growth, the distal humerus develops four ossification centers1,2,4; the proximal ulna, two5; and the proximal radius, one.3 The lateral three distal humeral ossification centers eventually unite into one bony epiphysis; the fourth, the medial epicondyle, gradually separates from the others, becomes an apophysis, and no longer participates in longitudinal growth or joint articulation (Fig. 16-1). The two proximal ulna ossification centers unite to form one articulating epiphysis; its physis provides longitudinal growth, thereby qualifying it as a true epiphysis. Knowledge of the timing and pattern of ossification of these epiphyses, particularly the distal humerus, is essential in treating fractures of the elbow in children. The growth potential of these three physes is approximately 20% of their respective total bone length. This paucity of growth reduces the remodeling potential, requiring that fracture of any of these epiphyses be anatomically reduced.

EPIDEMIOLOGY The incidence of fracture of physes of the elbow is unknown. Of all elbow fractures in children, slightly more than half are supracondylar fractures (Table 16-1). The vast majority of the remaining half are physeal fractures. When studying physeal fractures at all sites, the relative frequency of elbow fractures varies widely in different series.8,9,12,15-20 The only data available from a population-based study were gathered in Olmsted County, Minnesota, from 1979 to 1988.20 This study reported 951 cases of physeal fracture; 47 (5%) were in the elbow. Of these, 37 (3.9%) were in the distal humerus, 6 (0.6%) in the proximal radius, and 4 (0.4%) in the proximal ulna. Because elbow fractures in children

are often referred to tertiary treatment centers, these percentages will be higher in nonpopulation-based studies. Analyzing data of elbow fractures is further complicated by difficulties in separating supracondylar fractures from physeal fractures of the distal humerus; by the vagaries of ossification of the multiple secondary centers of ossification of the distal humerus1,2,4; by the inclusion or exclusion of fractures of the medial epicondyle, which is an apophysis rather than an epiphysis; by imprecise definition between olecranon and physeal fractures of the proximal ulna, and by the difficulty in distinguishing radial neck fractures from those that involve the radial physis. When physeal fractures of the elbow are considered as a separate category (excluding supracondylar fractures), 60 percent occur in the distal humerus. In one series,9 fracture of the distal humeral lateral condyle was 26%; followed by radial head, 23%; medial epicondyle, 22%; proximal ulna, 17%; T-intercondyle, 4%; medial condyle, 3%; lateral epicondyle, 3%; and separation of the entire distal humeral epiphysis (typically occurring only in infants and young children), 2%.

CLASSIFICATION Many classifications of physeal fractures have been proposed.18,22 The classification of Salter-Harris24 has been the most frequently used over the past four decades. There have been no case reports of acute physeal compression injury (Salter-Harris type V) of the distal humerus, proximal radius, or proximal ulna recorded in the literature. Speculation suggests that acute compression injury (type V) of any physis is unlikely and may not exist.23 Supracondylar fractures of the distal humerus often have fracture lines extending distally into the physis, making them type 1 Peterson physeal fractures (Fig. 16-2).18,88 Fractures of the proximal radius metaphysis (neck) (see Fig. 16-7M), and of the olecranon (see Fig. 16-8), frequently extend proximally into the physis,18,184 also making them Peterson type 1 fractures. Therefore, the Peterson classification18,22 is used in the remainder of this chapter.

EVALUATION Any recent abnormality or change in a child’s elbow, with or without a history of injury, deserves careful physical examination, including vascular and neurologic evaluation.49-51 This will avoid the uncomfortable situation of finding a postreduction vascular or neurologic deficit without knowing the prereduction status.

Chapter 16 Physeal Fractures of the Elbow

0–1 yr

2–4 yrs

5–7 yrs

8–9 yrs

10–12 yrs

247

13 yrs

FIGURE 16-1

Distal humerus epiphysis growth centers at various ages. At birth, the physis is transverse and the epiphysis is one cartilaginous mass. By age 2 years, the capitellar ossification center is usually present.1 The physis still is relatively linear and transverse. At ages 5 to 7 years, there is mild obliquity of the epiphyseal growth plate to the longitudinal axis of humerus and beginning ossification of the medial epicondyle.4 Trochlear ossification begins at 8 to 9 years, is irregular with indistinct margins, and often appears as multiple fragments. At ages 10 to 12 years, a projection of metaphyseal bone separates the medial epicondyle from the major distal epiphysis, which now contains three ossification centers—capitellum, trochlea, and lateral epicondyle.2 These three ossification centers unite with each other in the 13th year and to the humeral epiphysis by the 16th year, earlier in girls. There is wide variation of ages of these occurrences between genders and among children, but the sequence is constant. (From Peterson, H. A.: Epiphyseal Growth Plate Fractures. Heidelberg, Springer, 2007, used with permission of Mayo Foundation for Medical Education and Research.)

TABLE 16-1

Relative Frequency of Elbow Fractures in Children*

Year

Author†

SupraCondylar

1960

Fahey7

231

54

320 551

1986 TOTAL

Landin ‡

Percent

11

57.3

Lateral Condyle

Medial Condyle

Epiphyseal Separation

Medial Epicondyle

Lateral Epicondyle

6

1

–

38

3

67

4

–

–

48

121

10

1

–

86

0.1

–

12.6

Inter Condyle

1.0

8.9

Proximal Ulna§

Total

33

20

386

–

95

42

576

3

128

62

962

0.3

Proximal Radius‡

13.3

6.4

99.9

*Articles reporting only one or two of the three elbow bones are not included. † The Fahey data include 300 cases reported by Maylahn and Fahey in 1958,13 which documents the medial condyle and lateral epicondylar fractures. ‡ Includes both radial neck and head (physeal) fractures. § Includes both ulnar olecranon and physeal fractures of the proximal ulna. Adapted from Peterson, H. A.: Epiphyseal Growth Plate Fractures. Heidelberg, Springer, 2007, with kind permission of Springer Science and Business Media.

Imaging possibilities of cartilage and osseous structures are numerous. True anteroposterior and lateral roentgenographs of good quality are essential for evaluation of the injured pediatric elbow. Soft tissue as well as osseous structures must be clearly discernible. An intra-articular hematoma may displace the posterior fat pad of the distal humerus (the fat pad sign), which may be the only demonstrable change in an undisplaced or spontaneously reduced intra-articular fracture.26,47,94 Symmetric views of the contralateral elbow provide a valuable basis for comparison in assessing injury.48 This is particularly true in the pediatric elbow because of the

wide variance in the ages at which the multiple ossification centers appear. Anteroposterior varus and valgus stress views,35,81,143 and oblique views of the injured or of both elbows are also helpful.48 In younger children in whom the cartilaginous proportion of the epiphysis is high, arthrography,25,26,28,36,40,42,52,143 ultrasonography,29,31,32,44,53 and magnetic resonance imaging (MRI)33,34,41,44,46,119 play important roles in defining the injury. In older children, with predominantly osseous epiphyses, tomography37 and computed tomography (CT)27,30 may be of value.

248

Part IV Conditions Affecting the Child’s Elbow

1

2

3

4

5

6

FIGURE 16-2 Peterson classification of distal humeral physeal fractures in children. (From Peterson, H. A.: Epiphyseal Growth Plate Fractures. Heidelberg, Springer, 2007, used with permission of Mayo Foundation for Medical Education and Research.)

TABLE 16-2

Physeal Fractures of the Distal Humerus by Age and Gender in Olmsted County, Minnesota,

1979-198820 Age

0

1

2

3

4

5

6

7

8

9

10

11

12

13

14

15

Total

Boys

1

1

2

2

2

2

5

0

0

1

0

2

1

2

2

3

26

Girls

0

0

0

0

2

2

1

2

0

2

0

1

1

0

0

0

11

Total

1

1

2

2

4

4

6

2

0

3

0

3

2

2

2

3

37

From Peterson, H. A.: Epiphyseal Growth Plate Fractures. Heidelberg, Springer, 2007, with kind permission of Springer Science and Business Media.

Chapters 6 and 12 of this textbook also review imaging techniques that aid in evaluating anatomy, development, and pathology of children’s elbows.

MANAGEMENT In a study of 698 childhood fractures in all bones, only 7.4% were treated operatively.6 However, fractures about the elbow were operated on 50% of the time. It is paramount that physicians both study each elbow fracture carefully and keep abreast of current literature to choose the best treatment for each fracture.

DISTAL HUMERUS EPIDEMIOLOGY Fractures of the distal humeral physes have two peculiarities when compared with injuries to other physes.17 The age distribution for all physeal fractures is a bellshaped curve, with the peak at age 11 to 12 years for girls and age 14 years in boys.17,20 The distal humerus has a bimodal age distribution, with a larger peak occurring at 2 to 7 years and a second smaller peak occurring at 11 to 15 years (Table 16-2). This bimodal age distri-

Physeal Fractures of the Distal Humerus by Type in Olmsted County, Minnesota, 1979-198820 (Peterson Classification)

TABLE 16-3

Type

1

Number

2

Percent

5.4

2

3

5

8

13.5

21.6

4

5

6

Total

1

21

0

37

2.7

56.8

0

100.0

From Peterson, H. A.: Epiphyseal Growth Plate Fractures. Heidelberg, Springer, 2007, with kind permission of Springer Science and Business Media.

bution may be related to the preponderance of supracondylar (actually transcondylar) fractures, which are predominant at ages 5 to 10 years. The second departure from other physes is the type of fracture. At most other sites, type 2 is the most common fracture. In the distal humerus, more than 50% of physeal fractures of the distal humerus are type 5 (Table 16-3), most likely associated with the preponderance of lateral condyle fractures (see Table 16-1). The changing anatomy of the distal humeral physis during growth (see Fig. 16-1) predisposes it to specific fractures at different ages.19 Although any fracture type can occur at any age, from birth to age 2 years, the most

Chapter 16 Physeal Fractures of the Elbow

common fracture is epiphyseal separation (type 3). From age 2 to age 6 years, type 3 fractures become less common and types 2, 4, and 5 become more common. By age 6 to 10 years, shear type 2 and 3 fractures are rare and type 5 fractures, particularly of the lateral condyle, predominate. During ages 10 years to maturity, type 5 fractures and avulsion fractures of the medial epicondyle are the most common. These patterns provide a basis for presenting the fractures by age.19

NEWBORN TO 2 YEARS The epiphysis of the distal end of the humerus is one large cartilaginous mass during the first 2 years of life (see Fig. 16-1). Its interface with the metaphysis is smooth and transverse. Therefore, transverse, shear-type fractures totally within the physis are the most common fracture in the newborn,39,54,55,57,59,61,62,64,67-69,72,74-78 and in infants.36,56,60,63,66,70,73,79 These fractures tend to be reported separately and not in case series (see Table 16-1). They are typically types 2 and 3 (see Fig. 16-2).70 The entire epiphysis usually is displaced posteromedially60,61,67 but may be displaced medially,63,64,75,79 anteriorly,9,65 posteriorly, or laterally, depending on the mechanism of the injury. Rotatory malalignment may accompany displacement or occur alone. This can predispose to cubitus varus.59 Injuries of types 4 and 5 are theoretically possible, but at this age, they are more difficult to diagnose because the epiphysis is primarily cartilaginous in very young children. Injury with mild displacement may go undetected in abused children who present late for medical attention.25 Types 2 and 3 fractures frequently are misdiagnosed as elbow dislocations.56,57,60,64,66,71,75,83,85 Arthrography,25,26,28,36,40,42,52,57,63,71,83 ultrasonography,31,32,44,53,74,76 and MRI44,58,69,74,77 in these young children may aid in establishing the correct diagnosis. Treatment of type 1, 2, and 3 fractures consists of aligning the epiphysis with the metaphysis. Precise anatomic reduction is desirable but not necessary.9 Usually, this can be obtained by closed manipulation or traction.57,64,66,69,75,85 Immobilization with the elbow in 90 degrees of flexion and forearm pronation for 3 weeks is usually adequate.60,66 Because the entire epiphyseal growth plate usually remains with the epiphysis, damage to the growth plate is uncommon, and the potential for resumption of normal growth is good. The prognosis in these cases is favorable; minor malalignment usually corrects itself with normal growth and development, and physeal growth arrest is uncommon. Percutaneous pin fixation or open reduction25,59 is rarely necessary. Only four cases have been reported in which open reduction and internal fixation were performed late because of severe malalignment or interposition of soft tissue.55,71,86

249

AGES 2 TO 6 YEARS In early childhood, the growth plate gradually becomes more oblique distally and medially, from the lateral to the medial epicondyle (see Fig. 16-1). This obliquity of the epiphyseal line may account in part for the frequent lateral displacement of the epiphysis and the difficulty of maintaining accurate reduction. The ossification center of the capitellum may appear as early as 6 months and always by 2 years of age (see Fig. 16-1).1,83 This ossification center is initially oval and provides valuable orientation for alignment of the radial diaphysis. In the normal elbow roentgenograph, a line drawn through the radial diaphysis always passes through the capitellar ossification center in any projection. This aids in differentiating elbow dislocation from fracture. In a distal humeral epiphyseal separation, the capitellar ossification is aligned with the radius, regardless of degree of displacement, but is not properly positioned on the humerus. If the radius does not align with the capitellar ossification, there is radiohumeral subluxation or dislocation. Type 2 and 3 fractures are common.80 As age increases, type 2 and 3 fractures are progressively less common, presumably due to a more irregular and stable physis. Type 4 fractures are not common at this age but are a source of frequent complication, usually nonunion. They may occur on the medial condyle, which when not ossified makes diagnosis by routine roentgenographs very difficult (Fig. 16-3). When there is significant swelling medially and normal osseous contour, supplemental imaging is necessary. Soft tissue enhancement techniques and stress views are valuable, but if they are not diagnostic, ultrasonography, arthrography, or MRI should be considered. Type 5 fractures are common at this age, and their differentiation from type 2 fractures is difficult and important because displaced type 5 fractures frequently develop nonunion if left untreated (Fig. 164).71,75,78,102,107,110,112,123,130,137 Supplemental imaging, such as arthrography, ultrasonography, or MRI, should be considered. A coronal plane transcondylar fracture pattern has been described.98 All displaced type 5 fractures require anatomic reduction and maintenance of reduction. Attempts to accomplish this with immobilization in a cast frequently lead to subsequent displacement of even nondisplaced or minimally displaced fractures of the lateral condyle. This contributes to significant complications. Because so much of the distal humerus is still only cartilage, closed reduction with percutaneous pinning is also not advised. The bone and pins can be visualized roentgenographically, whereas the cartilage cannot. Open reduction and internal fixation (usually smooth wires) should be considered for any displaced fracture at this age.

250

Part IV Conditions Affecting the Child’s Elbow

FIGURE 16-3

A 5-year-and-1-month-old boy with type 4 fracture of right medial condyle (trochlea). A, Anteroposterior roentgenograph of both elbows (the right elbow is the image on the left). Patient had swelling and tenderness medially. There is mild medial displacement of the radius on the capitellum and of the ulna on the humerus on the right as compared with the left. B, Lateral view of both elbows (the right elbow is the image on the left) shows more soft tissue swelling and less joint congruity on the right elbow. The roentgenographs were interpreted as showing no osseous injury, and no treatment was given. C, Anteroposterior and lateral views at age 8 years. The patient had no pain or functional impairment. Note slight cubitus varus and beginning ossification of displaced, nonunited medial condyle.

Chapter 16 Physeal Fractures of the Elbow

FIGURE 16-3 cont’d

251

D, At age 18 years 1 month, the patient continues to have no pain or functional impairment. E, At age 31 years 5 months, 26 years after fracture, the patient returned with ulnar sensory neuropathy. The nonunion persists, and the cubitus varus is unchanged. F, Patient lacks the final 10 degrees extension and 30 degrees flexion. Note overgrowth of the head of the radius. At the time of the original injury, the presenting clinical findings and subtle roentgenographic changes were sufficient to warrant further evaluation. Better quality routine roentgenographs, varus-valgus stress views, or an arthrogram (and today magnetic resonance imaging) should have resulted in a diagnosis. Open reduction and internal fixation would have been indicated.

FIGURE 16-4

A right-dominant boy, age 2 years 7 months, fell off a bunk bed, injuring his left elbow. A, Oblique roentgenograph shows fracture of the lateral metaphysis. This was regarded to be a type 2 injury, with good prognosis for union and subsequent growth. Note, however, that this could be a type 5 injury, with intra-articular fracture and a poor prognosis. The best way to differentiate these injuries is by arthrography or magnetic resonance imaging. B, Lateral view shows excellent alignment. A cast was applied and multiple roentgenographs in the cast over the next month showed maintenance of position. C, Cast removal 6 weeks after injury. Motion was begun. The fragment was displaced. D, Fifteen months after injury: established nonunion. It now is obvious that this was an intra-articular type 5 injury, because the lateral condyle fragment is displaced proximally. E, Two years 9 months after injury, the patient was referred for treatment. The chief complaint is increasing valgus deformity. No pain or functional impairment. F, Five weeks after osteosynthesis. G, Age 6 years 10 months: union with persistent cubitus valgus. H, Three weeks postoperative arcuate varus osteotomy. Note fracture of the proximal two Crowe pins (arrows), probably from stress of pins holding the osteotomy. The pins were removed. A cast was applied for an additional 3 weeks. I, Age 10 years 3 months: union of lateral condyle with physeal closure, and relative overgrowth of medial epicondyle and proximal radius on left. J, Right elbow comparison. K, Lateral normal right elbow. L, Lateral left elbow. Elbow flexion right, 5 degrees hypertension to 145 degrees; left, 5 to 145 degrees.

Chapter 16 Physeal Fractures of the Elbow

An occasional complication of any distal humeral fracture at this age is the fishtail deformity.43,60,84,87 This occurs most commonly after supracondylar, medial, or lateral condylar fractures and consists of an Λ-shaped distal humeral articular surface. It is caused by premature arrest of the central portion of the physis, which may be due to central longitudinal malunion, avascular necrosis, or central physeal arrest without malunion or avascular necrosis. The deformity is often mild, with no functional impairment, but at this age can be marked with significant consequences.18,84

AGES 6 TO 10 YEARS By 6 years of age, the epiphyseal growth plate begins to become irregular and obliquity increases (see Fig. 16-1). A projection of metaphyseal bone begins to separate the medial epicondyle from the trochlea, adding greater stability to the physis. Therefore, shear-type injuries, such as types 2 and 3 fractures, become less common.96 On transverse section, the physis remains irregularly oval, whereas that of the metaphysis becomes elongated in the coronal plane and thin in the sagittal plane. Thus, the strength of the physis is, at this age, greater than the strength of the metaphysis. Most injuries in this age group are, therefore, supracondylar fractures. The decreased area and elongated contour of bone contact in supracondylar fractures make possible rotation and subsequent tilting of the distal fragment (cubitus varus). Because the area of fracture contact is greater with physeal fractures, rotation, tilt, and subsequent cubitus varus are less likely than for supracondylar fractures.60 At this age, fractures of the physis are usually longitudinal or oblique type 5 of either the lateral or the medial condyle.

LATERAL CONDYLE Fractures of the lateral condyle are relatively common, constituting approximately 10% to 15% of all fractures in the region of the elbow (see Table 16-1). They are the most common physeal fracture of the elbow. They occur in children between the ages of 2 and 16 years104 but are most common between 6 and 10 years of age.90,103,117,133,139,142 The mechanism of injury is usually a varus stress with the elbow in extension.122 The lateral condyle may fracture during elbow dislocation.143 Less commonly, pre-existing cubitus varus may predispose to fracture of the lateral condyle.106 The portion of metaphyseal bone attached to the capitellar and lateral epicondylar epiphysis may be large or small. The most important consideration is that this fracture is both intra-articular and transphyseal. The epiphyseal portion of the fracture may traverse the

253

ossification center of the capitellum but is often entirely through cartilage and therefore not visible on roentgenographs. Because this fracture involves both the articular surface and the physis, anatomic reduction is necessary and must be maintained until the fracture has united. If the fracture is undisplaced and stable, external immobilization by a long arm cast with the elbow in 90 degrees of flexion for 4 weeks will suffice.104,105 Frequent roentgenographic follow-up to assess maintenance of reduction is essential. If there is displacement, reduction and internal fixation will prevent redisplacement. If the fracture can be reduced or closed, pins inserted percutaneously may be used for fixation to prevent redisplacement.92,105 Some authors129 recommend arthrography to ensure a congruent joint surface before proceeding with percutaneous pinning. In most instances, however, open reduction and accurate replacement by direct vision is necessary. The reduction must be held by firm internal fixation, preferably metal rather than suture.89,110,113 Smooth pins, small in diameter, are the standard.101,105,115,142 Screws are preferred by some authors126,136 and biodegradable pins by others.93 Insertion of fixation devices from metaphysis to metaphysis and from epiphysis to epiphysis is preferred. However, because the trochlear cartilage is not ossified and not visible on roentgenographs, the pins may necessarily pass from epiphysis to metaphysis, crossing the physis obliquely. These pins should be removed within 3 weeks to prevent premature partial growth arrest. Pins not crossing the physis should remain in situ until there is some roentgenographic evidence of fracture healing, which occurred after approximately 6 weeks in one study.105 Fractures with early pin removal can be protected with additional long arm cast.105 Threaded pins predispose to premature partial physeal arrest and should not be used across a physis. Skeletal traction for elbow physeal fractures should be used only temporarily in children with multiple injuries. In one series of 33 lateral condylar fractures, four untreated cases all developed nonunion, 12 treated by closed reduction and immobilization had six with “poor results,” and 17 treated by open reduction and nailing had three with poor results.14 Untreated and inadequately treated cases are frequently complicated by malunion and nonunion, and these cause deformity, loss of motion, degenerative arthrosis, and tardy ulnar neuropathy.10,14,90,95,99-102,110,116,126,128,131,140,144,147,156,162 There is no agreement on the management of these complications, although many authors recommend osteosynthesis, combined with corrective osteotomy for significant deformity.89,98,99,108,112,121,125,128,134,145 Lateral prominence of the elbow is common after lateral condyle fracture (Table 16-4). This rarely is trou-

254

Part IV Conditions Affecting the Child’s Elbow

blesome or requires treatment. Varus or valgus deformity is also common (Table 16-5) and may be due to malposition of the fragment or to true overgrowth of the capitellum and its physis. Overgrowth is an interesting phenomenon and occasionally occurs even following successful management of a lateral condyle fracture.97,118,146,147 Although this may produce measurable cubitus varus, functional impairment is rare, and treatment is often for cosmetic improvement. Premature physeal closure113,146 has been noted in up to 20% of lateral humeral fractures. The premature Lateral Elbow Prominence Following Lateral Condyle Fracture

TABLE 16-4 Year

Author*

1975

Jacob122

20

2

10.0

1985

Rutherford135

36

8

22.2

32

13

40.6

28

28

100.0

116

51

44.0

2001 2001

No. Cases

114

Hasler Skak

138

Total

No. Prominence

Percent

*All articles have more than one author; see reference list. From Peterson, H. A.: Epiphyseal Growth Plate Fractures. Heidelberg, Springer, 2007, with kind permission of Springer Science and Business Media.

TABLE 16-5

MEDIAL CONDYLE Fractures of the medial condyle83,84,86,87,102,108,109,148-156 are much less frequent (see Table 16-1) perhaps because of normal cubitus valgus and because of the projection of metaphyseal bone between the trochlea and medial epicondyle. They occur in children of all ages, with the peak age between 6 and 10 years in most series. Fractures of the medial condyle may result from a fall on the apex of the flexed elbow or from an avulsion valgus stress injury on an extended elbow.67,153 Marked swelling on the medial side of the elbow is usually present (see Fig. 16-3). Some occur before the trochlea is ossified. Therefore, the displaced fragment consists of a portion of bone from the medial side of the lower humeral

Varus/Valgus Deformity Following Lateral Condyle Fracture

Year

Author*

1942

Kini125

1971

fusion is more often complete than partial. Complete physeal closure causes no angular deformity, and the cessation of growth results in only minor relative shortening compared with the contralateral humerus. This usually results in no functional or cosmetic impairment. Premature partial lateral closure sufficient to cause progressive cubitus valgus is uncommon. Partial closure of the center of the physis, where a fracture crossed the physis and epiphysis, leads to a disturbance of growth referred to as a fishtail deformity.10,84,101,126,142

No. Cases

113

Hardacre

118

Varus (<0 degrees)

Percent

Valgus (>15 degrees)

Percent

7

2

29

1

14

23

1

4

4

17

1974

Holst-Nielsen

39

23

59

4

10

1974

Loyd127

34

4

12

0

0

43

2

5

0

0

26

8

31

0

0

1985 1985

111

Foster

135

Rutherford 140

1985

So

14

5

36

1988

Dhillon108

14

6

43

5

36

40

12

30

6

15

1988

Morin

132 144

–

1988

Van Vugt

10

3

30

1989

Jeffrey

124

24

4

17

1

4

1989

Kröpf126

16

6

38

0

0

21

5

24

2

10

63

9

14

3

5

374

90

2001 2001

Skak

138 141

Thomas Total

24.1

–

–

26

–

7.4†

*Most articles have more than one author; see References. † 26 of 350 cases in articles in which valgus deformity was recorded. From Peterson, H. A.: Epiphyseal Growth Plate Fractures. Heidelberg, Springer, 2007, with kind permission of Springer Science and Business Media.

Chapter 16 Physeal Fractures of the Elbow

metaphysis, along with the cartilaginous trochlea and the ossified medial epicondyle. The unossified portion of the trochlea is not seen on the roentgenograph. Thus, if the fracture occurs before ossification of the trochlea, it may be mistaken for a fracture of the medial epicondyle. If the diagnosis is not made and the injury is treated nonoperatively as an avulsion fracture of the medial epicondyle, a poor functional result can be anticipated.82,151 In addition to the factors of articular congruity and growth plate alignment, fractures of the medial condyle are important because of its proximity to the ulnar nerve. Anatomic reduction, therefore, is mandatory to avoid tardy ulnar palsy as well as nonunion or malunion. These fractures usually require open reduction and rigid internal fixation. Only if the fracture is undisplaced may this fracture be treated by cast immobilization alone.150 The complication rate is high.155 Fractures may involve both condyles, with a split through the center of the articular surface (Fig. 16-5D).161 These fractures are analogous to the adult Tintercondylar fracture, are frequently comminuted, and fortunately, are not common. They are often the result of direct force and therefore may be open fractures. This is an unstable situation that requires open reduction and internal fixation.9

AGE 10 TO MATURITY The growth plate obliquity and irregularity continue to increase (see Fig. 16-1). The medial epicondyle and the trochlea are completely separated by a projection of metaphyseal bone. The medial epicondyle does not articulate with the ulna or contribute to the longitudinal length of the humerus. All four ossification centers are now visible roentgenographically. Trochlear ossification

A FIGURE 16-5

B

255

is frequently irregular and fragmented, simulating fracture. The trochlea, capitellum, and lateral epicondyle fuse to each other in approximately the 13th year (earlier in girls) before uniting with the humerus.1 Transverse shear-type type 2 and 3 physeal fractures are now virtually impossible (only one case has been illustrated in the literature18), except for the medial epicondyle. This conjoined epiphysis later fuses with the shaft, usually by the 16th year. Once fused, growth ceases and growth alteration following fracture is no longer possible. Injuries involving the conjoined epiphysis at this age are nearly always type 5. Lateral and medial condylar fractures both occur in this age group120 (see Fig. 16-5B and C). Medial condylar fractures129,163 are more common than they are at younger ages but are still less common than lateral condylar fractures. Both require open anatomic reduction and internal fixation. The T- or Y-type fracture (see Fig. 16-5D)131,159 is more frequent than at younger ages and usually requires open reduction and internal fixation. A minimally displaced fracture may be treated by reduction and percutaneous screw fixation.157 A posterior surgical approach gives excellent visualization and an opportunity for reduction and fixation of the multiple fragments.158 The triplane fracture is a type 5 fracture variation, usually found in the distal tibia. It has been reported in the distal humerus,160 and, because it involves both articular and physeal cartilage, it should be treated by anatomic reduction and maintenance of reduction. Premature closure of the physis is frequent at this age with any type of injury. The premature closure, however, is nearly always complete, and angular deformity, which would result from partial closure, is rare. Because the distal humerus contributes only 10% of the longitudinal length of the entire arm, early growth arrest at this age rarely causes noticeable arm length discrepancy.

C

D

Common distal humeral physeal fractures at ages 10 years to maturity. Normal distal humerus (A), type 5 injury of the lateral condyle (B), type 5 fracture of the medial condyle (C), type 5 fracture of both medial and lateral condyles (D). (From Peterson, H. A.: Epiphyseal Growth Plate Fractures. Heidelberg, Springer, 2007, used with permission of Mayo Foundation for Medical Education and Research.)

256

Part IV Conditions Affecting the Child’s Elbow

MEDIAL EPICONDYLE The medial epicondylar apophysis is extra-articular and is usually roentgenographically present (ossified) by age 5 years (see Fig. 16-1). Multicentric ossification centers have been demonstrated and give a fragmented appearance. Awareness of this normal variant may obviate misdiagnosis. The medial epicondyle matures slowly and is the last of the six epiphyses of the elbow to unite with its adjacent metaphysis; as late as the 19th year in men.4 The medial epicondyle is located slightly posteriorly, rather than strictly medially, which may cause confusion in roentgenographic interpretation.4 Oblique roentgenographs of both elbows are sometimes necessary to determine whether the epicondyle on the injured side is in an abnormal position. Fractures of the medial epicondyle constitute nearly 10% of all fractures of the elbow region (see Table 161),47 and usually occur between 9 and 15 years of age.6,165,166,173 The injury is unusual in younger children. The mechanism of injury is usually a valgus stress of the joint, which produces traction on the medial epicondyle through the flexor muscles. Arm wrestling is not a common activity among children but may result in this fracture.172,173 The fracture is usually type 3, although types 2, 4, and 5 have been noted.6,9 The epicondyle is always displaced distally because of the pull of the flexor muscle mass origin. It may be dislocated into and entrapped in the elbow joint, associated with opening of the joint by valgus stress. The entrapped epicondyle must be extracted from the joint and reduced. This is best done by open surgery, because manipulative maneuvers are unlikely to remove it from the joint, reduce it, and render it stable. About half of the cases are associated with partial or complete dislocation of the elbow,164,169,170,175 usually posterolateral dislocation. Nowhere in the discussion of physeal injuries of the elbow is there a greater divergence of opinion concerning treatment than in medial epicondylar fractures. Recommendations range from performing open reduction in virtually all cases, to no surgical treatment for any case (other than for intra-articular epicondyle entrapment). The fear of painful pseudarthrosis following nonoperative treatment has been cited for using open reduction and internal fixation in nearly every case, even with minimal (1-mm) separation.9 Conversely, cases treated nonoperatively are reported to do relatively well for many years, despite a high rate of nonunion.168,171 Any hypesthesia, paresthesia, or paralysis in the ulnar nerve distribution is an adequate reason for exploration, inspection of the nerve, and replacement of the fragment. If the ulnar nerve is found to be constricted or contused, it may be transposed anterior to the medial condyle.85,91 This is rarely necessary.153,167

In North America, 2 mm of displacement seems to be a commonly used criterion to determine treatment of physeal fractures in general. If the medial epicondyle is displaced 2 mm or less, the elbow may be immobilized for 3 weeks in a long arm cast, with the elbow in moderate flexion and the forearm in pronation. Oblique roentgenographs or comparison roentgenographs of the normal opposite elbow may be helpful in determining the degree of displacement. If the medial epicondyle is displaced more than 2 mm or rotated, or if the elbow joint is unstable on application of valgus stress, open reduction and internal fixation are indicated. The gravity stress test is a useful diagnostic test for acute medial instability.179 Displaced fractures of the medial epicondyle, if left untreated, frequently progress to malunion or nonunion (Fig. 16-6). Tardy ulnar palsy is a common late problem despite relatively good elbow motion and freedom from symptoms for several years.171 The medial epicondyle can sometimes be reduced by closed means but cannot be held reduced. Percutaneous pinning is hazardous because of the proximity of the ulnar nerve. Therefore, open reduction and internal fixation with two smooth Kirschner wires, one screw, or absorbable rods and screws, is frequently per-

FIGURE 16-6

A 15-year-and-8-month-old boy with tardy ulnar nerve palsy secondary to nonunion of a previous medial epicondyle fracture. Note hypertrophy of the epicondyle but lack of growth of the medial metaphysis.

Chapter 16 Physeal Fractures of the Elbow

formed.168,174,178 It is usually not necessary to mobilize the ulnar nerve, although if the epicondyle is markedly displaced, this maneuver may be helpful in gaining exposure. Kirschner wires should be removed after 3 weeks and active motion begun. Potential complications after pinning, however, include pseudarthrosis, an ulnar sulcus, a double-contoured epicondyle, hypoplasia, or hyperplasia.176 The physis of the epicondyle often closes after fracture, but because it does not contribute to longitudinal length4 and because the epiphysis does not articulate with the ulna, problems due to growth arrest are rare or nonexistent. This is particularly true because most of these children are near maturity and the other physes about the elbow have already closed. Because of the proximity of the ulnar collateral ligament, elbow stability should be examined after fracture healing. Severe chronic medial instability, and even recurrent elbow dislocation, although rare, may occur after fibrous union of a displaced fracture.177,179 Treatment options include osteosynthesis of the fragment to the condyle or excision of the fragment.

LATERAL EPICONDYLE The ossification center of the lateral epicondyle appears at about age 10 years (see Figs. 16-1 and 16-8A) and fuses with the lateral condyle at 14 years of age.2 Its ossification characteristics are prone to misinterpretation as an avulsion or chip fracture of the lateral metaphysis because (1) it ossifies as a smooth, thin, curved sliver of bone; (2) it is well separated from the humerus; and (3) the distal part usually fuses with the capitellum before the proximal part unites with the adjacent humeral shaft. As the epiphysis matures, its outline usually becomes smooth and well defined, but it may be irregular.2 Fracture of the lateral epicondyle is uncommon (see Table 16-1), and is usually associated with other elbow injuries. Separation fracture may accompany elbow dislocation.180 Isolated fracture of the lateral epicondyle is rare.9,65 In most cases, there is relatively little displacement of the fragment. Immobilization of the elbow for 3 to 4 weeks usually is sufficient. Open reduction and internal fixation are usually unnecessary because these injuries tend to occur only in children approaching the age of skeletal maturity. The risk of associated growth arrest is minimal or nonexistent. Tardy ulnar nerve palsy has been reported.91

sphere, ossification soon advances into one or two ovoid, flat, or wedge-shaped nuclei, which may be eccentrically located on the radial metaphysis45 and misinterpreted as an avulsion fracture of the epiphysis. Notches and clefts in the proximal radial metaphysis may closely resemble post-traumatic appearances.3 By definition, radial head fractures in children (age 0 through 16 years) are those that include the physis (Fig. 16-7). If these fractures appear in older children in whom physis is closed, they include the articular surface.18,184 Radial neck fractures are metaphyseal, entirely distal to the physis. Physeal fractures 1, 2, 5, and 6 also involve the metaphysis, but because the major problem is physeal or articular cartilage involvement, they all qualify as fractures of the head. Of all pediatric elbow fractures, 10% to 15% involve the radial head and neck (see Table 16-1).18,191 Of these head and neck fractures, approximately 50% involve the head and 50% the neck (Table 16-6).18 Proximal radial physeal fractures account for only 0.6% of all physeal fractures.18,20 The normal valgus carrying angle of the elbow causes compression laterally during a fall on the outstretched arm. This drives the capitellum against the outer side of the head of the radius, tilting it and displacing it outward. The fracture may be, therefore, type 1, 2, 3, 4, or 5 (see Fig. 16-7), with type 1 being most common (Table 16-7). A second mechanism of injury is associated with posterior dislocation of the elbow with simultaneous compression of the capitellum on the anterior portion of the head of the radius.187 This has the potential to produce the more serious type 4 and 5 fractures. The joint capsule is attached to the radius in continuity with the annular ligament. Because the radial neck lies outside the joint capsule, fracture of the neck may not cause joint effusion or fat pad displacement. Fracture of the radial head, however, usually produces elbow effusion and a positive fat pad sign.3 Fractures of the Proximal Radial Neck and Head in Children*

TABLE 16-6

Open physis

The epiphysis of the radial head begins to ossify at about the age of 5 years. Although it may appear first as a

Radial Neck (Metaphysis)

Radial Head (Physis)

Total

No. (%)

No. (%)

No. (%)

42 (36)

41 (35) †

83 (71)

Closed physis

16 (14)

17 (15)

33 (29)

Total (percent)

58 (50)

58 (50)

116 (100)

*One hundred sixteen fractures, 0 through 16 years.184 All 17 head fractures with closed physes involved the articular surface and were, therefore, similar to type 4 and 5 physeal fractures. From Peterson, H. A.: Epiphyseal Growth Plate Fractures. Heidelberg, Springer, 2007, with kind permission of Springer Science and Business Media.

†

PROXIMAL RADIUS

257

258

Part IV Conditions Affecting the Child’s Elbow

external immobilization and invariably heal without sequelae. If a type 2 or 3 fracture is minimally displaced or can be manually reduced, immobilization for 3 to 4 weeks will suffice.183 A wire or a hook inserted percutaneously can be used to manipulate a mildly or moderately displaced head into position.9,181 Occasionally, with a type 3 fracture, the entire epiphysis will be inverted or even displaced through the joint capsule, and closed reduction is not possible. In this instance, open reduction is necessary. After surgical reduction, the fracture is often stable, and no internal fixation is necessary.9,189 Immobilization, with the elbow in 90 degrees of flexion and the forearm in neutral rotation, is satisfactory. If the surgical reduction is unstable, internal fixation with two crossed Kirschner wires188 or with one longitudinal wire through the capitellum ossification center extending across the radiocapitellar joint into the intramedullary cavity of the radial diaphysis can be considered.9,186,189 Each method of internal fixation should be supplemented with a long arm cast. The wires may be removed in 3 weeks and gentle protected motion using a collar and cuff begun. If a single longitudinal wire is used, it should be stout enough to avoid wire breakage at the joint level.9 If this occurs, removal of the portion of wire embedded in the radius can be difficult, and it may be less damaging to leave the wire permanently in the radius. Introducing a wire in the distal radius and passing it proximally up the intramedullary canal across the fracture site into the proximal fragment is an appropriate method for reducing or fixing a radial neck fracture, but this procedure is difficult to accomplish in a physeal fracture without further displacing the head. Type 4 and 5 injuries require precise anatomic reduction to restore articular congruity. Open reduction and

Differentiating fractures that involve only the neck of the radius (metaphysis) from those that also involve the physis (head) can be difficult. Oblique roentgenographs and occasionally MRI can be helpful in making this differentiation. The type 1 fracture is common (see Table 16-7), but may be difficult to diagnose. It is usually incorrectly called a neck fracture or type 2 fracture (Fig. 16-8). It is distinguished by a transmetaphyseal fracture with fracture extension to the physis. The transmetaphyseal fracture is often only a compression fracture that may not be visible on the initial roentgenographs. Transmetaphyseal sclerosis, however, is always present 3 to 6 weeks after fracture and verifies the compression component. The fracture line extending to the physis is also frequently difficult to visualize on routine anteroposterior and lateral views and is often best seen on oblique views. This may be only a fracture line, but often there is a displaced corner of metaphysis that may be called a “chip” fracture. Most importantly, however, is that there is no fracture transversely within the physis and the epiphysis is not displaced. Therefore, this is not a type 2 fracture. These fractures need only temporary

Proximal Radius Physeal Fractures by Type (Peterson Classification)22

TABLE 16-7

Type

Year 2000

Author 184

Leung Percent

1

2

3

4

5

6

Total

25 61.0

9 22.0

1 2.4

1 2.4

4 9.8

1 2.4

41 100

From Peterson, H. A.: Epiphyseal Growth Plate Fractures. Heidelberg, Springer, 2007, with kind permission of Springer Science and Business Media.

M

Figure 16-7

1

2

3

4

5

6

Peterson classification of proximal radius physeal fractures in children. M, metaphyseal (neck) fracture. Fracture types 1 through 6, all of which involve the physis, are fractures of the head because the physis is part of the head. (From Peterson, H. A.: Epiphyseal Growth Plate Fractures. Heidelberg, Springer, 2007, used with permission of Mayo Foundation for Medical Education and Research.)

Chapter 16 Physeal Fractures of the Elbow

259

FIGURE 16-8

A, An 11-year-and-6-month-old girl fell down six stairs and noted pain and swelling over the left radial head. Anteroposterior (A), lateral (B), and oblique (C) roentgenographs show a small “chip” fracture of the anterolateral proximal radius metaphysis and very slight increased sclerosis of the proximal neck but no displacement of the epiphysis. A posterior splint was applied. Three weeks after fracture (D), there is increased sclerosis of the proximal radial neck and faint new periosteal bone along the lateral border of the neck. Three months after fracture (E), there is mature subperiosteal new bone along the lateral neck, and the epiphysis and physis are normal. The patient is normally active and asymptomatic, and examination is normal. Note normal lateral epicondyle in A, C, D, and E.

internal fixation with tiny transverse or oblique Kirschner wires will help prevent displacement of the fragments during healing. Premature closure of the physis nearly always occurs,184,187,190 but because the proximal radius accounts for only 20% of the growth of the radius and because type 4 and 5 injuries often occur in older children, problems from growth arrest are rare.182 Functional impairment, however, particularly limited forearm rotation, is common after type 4 and 5 injuries.184 The presence of associated fractures in the humerus and ulna reduces the chance of a favorable outcome.185 Type 6 fracture (a part missing) (see Fig. 16-7) is always an open injury and usually results in functional

impairment.18,21 Regardless of how little physis is lost, the remaining physis always stops growing. Late reconstructive surgery is usually necessary. Most radial head physeal fractures result in premature complete physeal closure and eccentric enlargement of the radial head.185 Abnormal cam motion may occur during forearm rotation, and this may be painful. Excision of the radial head in a growing child will result in distal radial-ulnar length variance and should be avoided. After the patient reaches maturity and has joint pain or limited motion, the radial head may be excised with little risk of development of wrist deformity.85 However, excision of the head rarely restores motion.

260

Part IV Conditions Affecting the Child’s Elbow

Thus, the primary indication for excision of the radial head is pain. The radial head blood supply is through the articular capsular and periosteal vessels. Although these structures are frequently damaged at the time of fracture, ischemic necrosis of the head is uncommon. Treatment considerations relate more to the degree of displacement and angulation, than to the fear of ischemic necrosis.

A

PROXIMAL ULNA The proximal ulnar growth apparatus has features of both an epiphysis and an apophysis.195 Because the proximal ulnar physis produces longitudinal growth and has articular involvement, it is included as an epiphysis. The olecranon is the cartilage/bone projection of the proximal ulna. Its anterior aspect forms the articular surface with the humeral trochlea. As such, the olecranon includes the epiphysis, physis, and most of the metaphysis. Early in life, the physis is L-shaped, extending from the transverse metaphyseal-epiphyseal interface anteriorly and distally as part of the thick subchondral articular surface, to beneath the coracoid process (Fig. 16-9A). With growth, the epiphysis becomes a relatively smaller portion of the olecranon (see Fig. 16-9B, and C). In this sense, the physis “migrates” proximally, and has been called the “wandering physeal line.” The extent of this proximal migration varies among children.47 In the majority of children, the physis continues to migrate proximally and obliquely until it is completely extra-articular (see Fig. 16-9C). This usually occurs by age 12 years. In the minority, the physis remains relatively transverse and closes while its anterior edge is still intra-articular (see Fig. 16-9D). The secondary center of ossification first appears at age 9 years in girls and 11 years in boys.47 The epiphysis initially often has two, sometimes three, and occasionally several ossification centers.5 The physis is usually closed by the end of the 16th year.195 Fractures of the proximal ulna account for 5% to 10% of children’s elbow fractures (see Table 16-1), and are often accompanied by other elbow fractures. Most fractures of the olecranon primarily involve metaphyseal bone distal to the physis (Fig. 16-10M).85 Fractures of the proximal ulnar physis account for only 0.3% of all physeal fractures.18,20 When the physis is involved, the fracture is usually a type 2 injury (see Fig. 16-10, 2a and 2b), occasionally a type 3 injury (see Fig. 16-10, 3). In type 2 injuries, the fracture line in the metaphysis may be oblique (as shown) or may enter the ulnar shaft more longitudinally. Because the proximal fragment contains articular surface, these fractures require ana-

B

C

D

FIGURE 16-9 Proximal ulnar anatomy and growth. A, In infancy the physis is transverse and extends anteriorly and proximally beneath the coracoid. Almost the entire articular surface is part of the epiphysis. B, The ossification center first appears at age 9 years and is separated from the metaphysis more widely than in other epiphyses. The physis is now located relatively closer to the proximal end of the bone. This is called the “wandering physeal line.” The physis still extends anteriorly and distally beneath the entire joint surface. C, By age 12 years, the physis has “migrated” proximally to become entirely extra-articular in most people. In this case, the features of an apophysis now predominate. D, In the minority of individuals, the “migration” ceases while the anterior edge of the physis is still intraarticular. In this case, the features of an epiphysis still predominate. (From Peterson, H. A.: Epiphyseal Growth Plate Fractures. Heidelberg, Springer, 2007, used with permission of Mayo Foundation for Medical Education and Research.)

Chapter 16 Physeal Fractures of the Elbow

tomic reduction and maintenance of reduction until the fracture has united. Frequently, this can be accomplished by closed means, immobilizing the elbow in extension. However, if displacement is more than 3 mm, open reduction and internal fixation are advised.193 Fixation may be accomplished by longitudinal Kirschner wire

M

261

or a wire loop, or in older children, a tension band wire. A longitudinal screw should not be used in a young child if significant growth remains.9 However, growth arrest problems are rare.196,199 Excision of the fragment, which is sometimes performed in adults, should be avoided, particularly in young children. In older children, who subject their upper extremities to excessive stress, delayed physeal closure can simulate a nonunion,197,198 sometimes called a stress or chronic type 3 fracture. Fracture of the coronoid apophysis is rare.192 Children with osteogenesis imperfecta are apparently prone to proximal ulnar type 2 anterior fractureavulsions (see Fig. 16-10, 2a). Internal fixation is commonly used, and although fracture union is the rule, refracture can occur.194,199

GROWTH ARREST 1

2a

2b

3

Growth arrest frequently occurs following any elbow physeal fracture. The older the child, the more likely its occurrence. The entire involved physis usually closes. Partial premature closure with resulting angular deformity is rare. Because the elbow physes contribute only 20% of the longitudinal growth of the humerus and forearm, the growth arrest lines that usually occur after any significant bone injury are indistinct at best. Rarely can these lines be used as a measure of growth or as an indication of a growth arrest problem, as they are in other long bones. Because each of the three elbow physes contribute only 10% of the entire upper extremity length, complete closure of any or all of these physes rarely, if ever, causes significant arm length discrepancy. Any resulting discrepancy is mild and causes no functional impairment

FIGURE 16-10 Peterson classification of proximal ulnar physeal fractures in children.22 M, Fracture of the metaphysis. 1, Type 1 fracture with greenstick or longitudinal split fracture. There is a torus or transmetaphyseal fracture with extension of the fracture proximally to the physis. The arrow suggests compression force originates proximally from the epiphyseal side. However, this has not been proven and distally applied pressure could result in compression if the elbow is in full extension at the moment of impact. This fracture has been noted to occur only before ossification of the epiphysis. 2a, Type 2 fracture with anterior metaphyseal fragment. 2b, Type 2 fracture with posterior metaphyseal fragment. 3, Type 3 fracture.38 (From Peterson, H. A.: Epiphyseal Growth Plate Fractures. Heidelberg, Springer, 2007, used with permission of Mayo Foundation for Medical Education and Research.)

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and few, if any, cosmetic or clothes-fitting complaints. Even if complete closure of all physes about the elbow occurred in a young child, surgical lengthening of the involved humerus or forearm bones or surgical arrest of the contralateral elbow physes would rarely, if ever, be indicated. Premature partial closure of the distal humerus, or proximal radius or ulna, is very rare. Premature partial closure of the medial or lateral humeral condyle theoretically may result in progressive cubitus varus or valgus, respectively. This could be determined only after many months of follow-up. In this rare occurrence, surgical closure of the remaining physis might be considered. Of 178 bar excisions for premature partial closure performed at Mayo Clinic between 1968 and 1997, none involved the elbow.18 Supracondylar osteotomy to correct angular growth is rarely necessary. Premature closure of the central physis between the medial and lateral humeral condyles occurs occasionally and has been called a fishtail deformity.18,84 The underlying cause of the arrest is multifactorial and may be due to a gap in reduction of an intracondylar fracture, avascular necrosis of the central or trochlear portion of the epiphysis, or central premature physeal arrest (bar formation) without a gap or avascular necrosis. This usually occurs in younger children and causes no pain and only minimal loss of motion. With growth, the deformity can, however, gradually progress to premature degenerative arthrosis and functional disability. The intercondylar notch may also predispose to subsequent intercondylar fracture. Thus, if the fishtail deformity is identified in a young child, surgical closure of the medial and lateral portions of the physis may prevent the deformity from progressing and result in only minimal additional humeral length discrepancy. An occasional concern is damage to the physeal cells between the medial humeral metaphysis and the trochlea in young children. Because the trochlear ossification center has not ossified at this early age, this damage cannot be diagnosed by routine roentgenographs, tomographs, arthrograms, CT scan, or scintigraphy. In the future, MRI may have the ability to evaluate such an injury early. It is often necessary to observe these cases for months or years in order to make the diagnosis of premature partial physeal arrest.

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99. von Laer, L., Brunner, R., and Lampert, C.: Malunited supracondylar and condylar humeral fractures [German]. Orthopade 20:331, 1991. 100. Wilkins, K. E.: Residuals of elbow trauma in children. Clin. Orthop. 21:291, 1990. LATERAL CONDYLE 101. Amgwerd, M., and Sacher, P.: Treatment of fractures of the radial condyle of the humerus in children [German]. Z. Unfall. Versicherungsmed. 83:49, 1990. 102. Attarian, D. E.: Lateral condyle fractures: Missed diagnoses in pediatric elbow injuries. Mil. Med. 155:433, 1990. 103. Badelon, O., Bensahel, H., and Mazda, K.: Lateral humeral condylar fractures in children: a report of 47 cases. J. Pediatr. Orthop. 8:31, 1988. 104. Bast, S. C., Hoffer, M. M., and Aval, S.: Nonoperative treatment for minimally and nondisplaced lateral humeral condyle fractures in children. J. Pediatr. Orthop. 18:448, 1998. 105. Cardona, J. I., Riddle, E., and Kumar, S. J.: Displaced fractures of the lateral humeral condyle: criteria for implant removal. J. Pediatr. Orthop. 22:194, 2002. 106. Davids, J. R., Maguire, M. F., Mubarek, S. J., and Wenger, D. R.: Lateral condylar fracture of the humerus following posttraumatic cubitus varus. J. Pediatr. Orthop. 14:466, 1994. 107. DeBoeck, H.: Surgery for nonunion of the lateral humeral condyle in children. Six cases followed for 1-9 years. Acta Orthop. Scand. 66:401, 1995. 108. Dhillon, K. S., Sengupta, S., and Singh, B. J.: Delayed management of the lateral humeral condyle in children. Acta Orthop. Scand. 59:419, 1988. 109. Finnbogason, T., Karlsson, G., Lindberg, L., and Mortensson, W.: Nondisplaced and minimally displaced fractures of the lateral humeral condyle in children: a prospective radiographic investigation of fracture stability. J. Pediatr. Orthop. 15:422, 1995. 110. Flynn, J. C., and Richards, J. F.: Nonunion of minimally displaced fractures of the lateral condyle of the humerus in children. J. Bone Joint Surg. 53A:1096, 1971. 111. Foster, D. E., Sullivan, J. A., and Gross, R. H.: Lateral humeral condylar fractures in children. J. Pediatr. Orthop. 5:16, 1985. 112. Gaur, S., Varma, A. N., and Swarup, A.: A new surgical technique for old ununited lateral condyle fractures of the humerus in children. J. Trauma 34:68, 1993. 113. Hardacre, J. A., Nahigian, S. H., Froimson, A. I., and Brown, J. E.: Fractures of the lateral condyle of the humerus in children. J. Bone Joint Surg. 53A:1083, 1971. 114. Hasler, C. C., and von Laer, L.: Prevention of growth disturbances after fractures of the lateral humeral condyle in children. J. Pediatr. Orthop. 10:123, 2001. 115. Hennrikus, W. L., and Millis, M. B.: The dinner fork technique for treating displaced lateral condylar fractures of the humerus in children. Orthop. Rev. 22:1278, 1993. 116. Heyl, J. H.: Fracture of the external condyle of the humerus in children. Ann. Surg. 101:1069, 1935. 117. Holmberg, L.: Fractures in the distal end of the humerus in children. Acta Chir. Scand. 63(Suppl 103):1, 1945.

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118. Holst-Nielsen, F., and Ottsen, P.: Fractures of the lateral condyle of the humerus in children. Acta Orthop. Scand. 45:518, 1974. 119. Horn, B. D., Herman, M. J., Crisci, K., Pizzutillo, P. D., and MacEwen, G. D.: Fractures of the lateral humeral condyle: role of the cartilage hinge in facture stability. J. Pediatr. Orthop. 22:8, 2002. 120. Ingersol, R. E.: Fractures of the humeral condyles in children. Clin. Orthop. 41:32, 1965. 121. Inoue, G., and Tamura, Y.: Osteosynthesis for longstanding nonunion of the lateral humeral condyle. Arch Orthop. Trauma Surg. 112:236, 1993. 122. Jakob, R., Fowels, J. V., and Rang, M.: Observations concerning fractures of the lateral humeral condyle in children. J. Bone Joint Surg. 57B:430, 1975. 123. Jeffrey, C. C.: Nonunion of the epiphysis of the lateral condyle of the humerus. J. Bone Joint Surg. 40B:396, 1958. 124. Jeffrey, R. S.: Injuries of the lateral humeral condyle in children. J. R. Coll. Surg. Edinburg 34:156, 1989. 125. Kini, M. G.: Fractures of the lateral condyle of the lower end of the humerus with complications. J. Bone Joint Surg. 24:270, 1942. 126. Kröpfl, A., Genelin, F., Obrist, J., and Zirniter, J.: Malunions and disturbances of growth after fractures of the lateral humeral condyle in children [German]. Unfallchirurgie 15:113, 1989. 127. Loyd, R. D., and Miller, W. A.: Fractures of the lateral humeral condyle in children (abstr). J. Bone Joint Surg. 56A:1301, 1984. 128. Masada, K., Kawai, H., Kawabata, H., Masatomi, T., Tsuyuguchi, Y., and Yamamoto, K.: Osteosynthesis of old, established nonunion of the lateral condylar of the humerus. J. Bone Joint Surg. 72A:32, 1990. 129. Mintzer, C. M., Waters, P. M., Brown, D. J., and Kasser, J. R.: Percutaneous pinning in the treatment of displaced lateral condyle fractures. J. Pediatr. Orthop. 14:462, 1994. 130. Mirsky, E. C., Karas, E. H., and Weiner, L. S.: Lateral condyle fractures in children: evaluation of classification and treatment. J. Orthop. Trauma 11:117, 1997. 131. Modrzewski, K.: Late ulnar nerve paresis in adults after neglected treatment for fracture of the capitellum with part of the trochlea in children [Polish]. Chir. Narzadow Ruchn. Orthop. Pol. 60:9, 1995. 132. Morin, B. M., Poitras, B. P., Labelle, H., and Fassier, F.: Fractures of the lateral humeral condyle: Long-term results following early open reduction. In Uhthoff, H. K., and Wiley, J. J. (eds.): Behavior of the Growth Plate. New York, Raven Press, 1988, p, 183. 133. Murnahgan, J. M., Thompson, N. S., Taylor, T. C., and Cosgrove, A. P.: Fractured lateral epicondyle with associated elbow dislocation. Int. J. Clin. Pract. 56:475, 2002. 134. Roye, D. P. Jr., Bini, S. A., and Infosino, A.: Late surgical treatment of lateral condylar fractures in children. J. Pediatr. Orthop. 11:195, 1991. 135. Rutherford, A.: Fractures of the lateral humeral condyle in children. J. Bone Joint Surg. 67A:851, 1985. 136. Sharma, J. C., Arora, A., Mathur, N. C., Gupta, S. P., Biyani, A., and Mathur, R.: Lateral condylar fractures of the

266

137.

138.

139.

140.

141.

142.

143.

144.

145.

146. 147.

Part IV Conditions Affecting the Child’s Elbow

humerus in children: fixation with partially threaded 4.0 mm AO cancellous screws. J. Trauma 39:1129, 1995. Shimada, K., Masada, K., Tada, K., and Yamamoto, T.: Osteosynthesis for the treatment of nonunion of the lateral condyle in children. J. Bone Joint Surg. 79A:234, 1997. Skak, S. V., Olsen, S. D., and Smaabrekke, A.: Deformity after fracture of the lateral humeral condyle in children. J. Pediatr. Orthop. 10:142, 2001. Smith, F. J., and Joyce, J. J. III: Fractures of the lateral condyle of the humerus in children. Am. J. Surg. 87:324, 1954. So, Y. C., Fang, D., Leong, J. C. Y., and Bong, S. C.: Varus deformity following lateral humeral condylar fractures in children. J. Pediatr. Orthop. 5:569, 1985. Thomas, D. P., Howard, A. W., Cole, W. G., and Hedden, D. M.: Three weeks of Kirschner wire fixation for diaphyseal lateral condylar fractures of the humerus in children. J. Pediatr. Orthop. 21:565, 2001. Valdisseri, L., Venturi, B., and Busanelli, L.: External humeral condyle fracture in children. A long-term review of 30 cases reported. Chir. Organi. Mov. 78:105, 1993. van Haaren, E. R., van Vugt, A. B., and Bode, P. J.: Posterolateral dislocation of the elbow with concomitant fracture of the lateral humeral condyle: case report. J. Trauma 36:288, 1994. van Vugt, A. B., Severijnen, R. V. S. M., and Festen, C.: Fractures of the lateral humeral condyle in children: late results. Arch. Orthop. Trauma Surg. 107:206, 1988. Vathana, P., and Prosartritha, T.: Repair of nonunion lateral humeral condyle: a case report. J. Med. Assoc. Thai. 81:146, 1998. Wadsworth, T. G.: Injuries of the capitellar (lateral humeral condyle) epiphysis. Clin. Orthop. 85:127, 1972. Wadsworth, T. G.: Premature epiphyseal fusion after injury to the capitellum. J. Bone Joint Surg. 46B:46, 1964.

MEDIAL CONDYLE 148. Bede, W. B., Lefebvre, A. R., and Rosman, M. A.: Fractures of the medial humeral condyle in children. Can. J. Surg. 18:137, 1975. 149. Chacha, P. B.: Fracture of the medial condyle of the humerus with rotational displacement. Report of two cases. J. Bone Joint Surg. 52A:1453, 1970. 150. El Ghawabi, M. H.: Fracture of the medial condyle of the humerus. J. Bone Joint Surg. 57A:677, 1975. 151. Fahey, J. J., and O’Brien, E. T.: Fracture-separation of the medial humeral condyle in a child confused with fracture of the medial epicondyle. J. Bone Joint Surg. 53A:1102, 1971. 152. Fowles, J. V., and Kassab, M. T.: Displaced fractures of the medial humeral condyle in children. J. Bone Joint Surg. 62A:1159, 1980. 153. Kilfoyle, R. M.: Fractures of the medial condyle and epicondyle of the elbow in children. Clin. Orthop. 41:43, 1963. 154. Kim, H. T., Song, M. B., Conjares, J. V., and Yoo, C. I.: Trochlear deformity occurring after distal humeral frac-

tures: magnetic resonance imaging and its natural progression. J. Pediatr. Orthop. 22:188, 2002. 155. Leet, A. I., Young, C., and Hoffer, M. M.: Medial condyle fractures of the humerus in children. J. Pediatr. Orthop. 22:2, 2002. 156. Minami, A., and Sugawara, M.: Humeral trochlear hypoplasia secondary to epiphyseal injury as a cause of ulnar nerve palsy. Clin. Orthop. 228:227, 1988. Ages 10 Years to Maturity 157. Godette, G. A., and Gruel, C. R.: Percutaneous screw fixation of intercondylar fracture of the distal humerus. Orthop. Rev. 22:466, 1993. 158. Kasser, J. R., Richards, K., and Millis, M.: The tricepsdividing approach to open reduction of complex distal humeral fractures in adolescents: a Cybex evaluation of triceps function and motion. J. Pediatr. Orthop. 10:93, 1990. 159. Papavasiliou, V. A., and Beslikas, T. A.: T-Condylar fractures of the distal humeral condyles during childhood: an analysis of six cases. J. Pediatr. Orthop. 6:302, 1986. 160. Peterson, H. A.: Triplane fracture of the distal humeral epiphysis. J. Pediatr. Orthop. 3:81, 1983. 161. Re, P. R., Waters, P. M., and Hresko, T.: T-condylar fractures of the distal humerus in children and adolescents. J. Pediatr Orthop. 19:313, 1999. 162. Royle, S. G., and Burke, D.: Ulnar neuropathy after elbow injury in children. J. Pediatr. Orthop. 10:495, 1990. 163. Saraf, S. K., and Tuli, S. M.: Concomitant medial condyle fracture of the humerus in a childhood posterolateral dislocation of the elbow. J. Orthop. Trauma 3:352, 1989. MEDIAL EPICONDYLE 164. Carlioz, H., and Abols, Y.: Posterior dislocation of the elbow in children. J. Pediatr. Orthop. 4:8, 1981. 165. Case, S. L., and Hennrikus, W. L.: Surgical treatment of displaced medial epicondyle fracture in adolescent athletes. Am. J. Sports Med. 25:682, 1997. 166. Chessare, J. W., Rogers, L. F., White, H., and Tachdjian, M. O.: Injuries of the medial epicondylar ossification center of the humerus. Am. J. Roentgenol. 129:49, 1977. 167. Collins, R., and Lavine, S. A.: Fractures of the medial epicondyle of the humerus with ulnar nerve paralysis. Proc. Child Hosp. DC 20:274, 1964. 168. Dunn, P. S., Ravn, P., Hansen, L. B., and Burph, B.: Osteosynthesis of medial humeral epicondyle fractures in children. 8-Year follow-up of 33 cases. Acta Orthop. Scand. 65:439, 1994. 169. Fowles, J. V., Slimane, N., and Kassab, M. T.: Elbow dislocation with avulsion of the medial humeral epicondyle. J. Bone Joint Surg. 72B:102, 1990. 170. Hendel, D., Aghasi, M., and Halperin, N.: Unusual fracture dislocation of the elbow joint. Arch. Orthop. Trauma Surg. 104:187, 1985. 171. Josefsson, P. O., and Danielson, L. G.: Epicondylar elbow fracture in children. 35-Year follow-up of 56 unreduced cases. Acta Orthop. Scand. 57:313, 1986. 172. Low, B. Y., and Lim, J.: Fracture of humerus during arm wrestling: report of 5 cases. Singapore Med. J. 32:47, 1991.

Chapter 16 Physeal Fractures of the Elbow

173. Ogawa, K., and Ui, M.: Fracture-separation of the medial humeral epicondyle caused by arm wrestling. J. Trauma 41:494, 1996. 174. Partio, E. K., Hirvensalo, E., Bostman, O., and Rokkanen, P.: A prospective controlled trial of the fracture of the humeral medial epicondyle—how to treat? Ann. Chir. Gynaecol. 85:67, 1996. 175. Pritchett, J. W.: Entrapment of the medial nerve after dislocation of the elbow: case report. J. Pediatr. Orthop. 4:752, 1984. 176. Skak, S. V., Grossman, E., and Wagn, P.: Deformity after internal fixation of fracture separation of the medial epicondyle of the humerus. J. Bone Joint Surg. 76B:272, 1994. 177. Sugita, H., Kotani, H., Ueo, T., Miki, T., Senzouku, F., Hara, T., Nagagawa, Y., Sakka, A., Nagagawa, T., and Seki, K.: Recurrent dislocation of the elbow [Japanese]. Nippon Geka Hokan 63:181, 1994. 178. Szymanska, E.: Evaluation of AO kit screw fixation of medial condyle and epicondyle distal humeral epiphyseal fractures in children [Polish]. Ann. Acad. Med. Stetin. 43:239, 1997. 179. Woods, G. W., and Tullos, H. S.: Elbow instability and medial epicondylar fractures. Am. J. Sports 5:23, 1977. LATERAL EPICONDYLE 180. Li, Y. H., and Leong, J. C.: Fractured lateral epicondyle associated with lateral elbow instability. Injury 26:267, 1995. PROXIMAL RADIUS 181. Chotel, F., Sailhan, F., Martin, J., Filipe, G., Pem, R., Garnier, E., and Berard, J.: A specific closed percutaneous technique for reduction of Jeffrey Type II lesion. J. Pediatr. Orthop. B 15:376, 2006. 182. Gaston, S. R., Smith, F. M., and Baab, O. D.: Epiphyseal injuries of the radial head and neck. Am. J. Surg. 85:266, 1953. 183. Jeffery, C. C.: Fractures of the head of the radius in children. J. Bone Joint Surg. 32B:314, 1950. 184. Leung, A. G., and Peterson, H. A.: Fractures of the proximal radial head and neck, with emphasis on those that involve the articular cartilage. J. Pediatr. Orthop. 20:7, 2000. 185. Malmvick, J., Herbertsson, P., Josefsson, P. O., Hasserius, R., Besjakov, J., and Karlsson, M. K.: Fracture of the radial

186.

187. 188.

189. 190.

191.

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head and neck of Mason types II and III during growth: a 14-25 year follow-up. J. Pediatr. Orthop. B 12:63, 2003. McBride, E. E., and Monnet, J. C.: Epiphyseal fractures of the head of the radius in children. Clin. Orthop. 16:264, 1960. O’Brien, P. I.: Fractures involving the proximal radial epiphysis. Clin. Orthop. 41:51, 1965. Osada, D., Tamai, K., Kuramochi, T., and Saotome, K.: Three epiphyseal fractures (distal radius and ulna and proximal radius) and a diaphyseal ulnar fracture in a seven-year-old child’s forearm. J. Orthop. Trauma 15:375, 2001. Payne, J. F., and Earle, J. L.: Fracture dislocation of the proximal radial epiphysis. Minn. Med. 52:479, 1969. Reidy, J. A., and Van Gorder, G. W.: Treatment of displacement of proximal radial epiphysis. J. Bone Joint Surg. 45A:1355, 1963. Sessa, S., Lascombes, P., Prevot, J., and Gagneux, E.: Fractures of the radial head and associated elbow injuries in children. J. Pediatr. Orthop. 5:200, 1996.

PROXIMAL ULNA 192. Bracq, H.: Fracture of the coronoid apophysis. Rev. Chir. Orthop. 73:472, 1987. 193. Burrel, C. G., Strecker, W. B., and Schoenecker, P. L.: Surgical treatment of displaced olecranon fractures in children. J. Pediatr. Orthop. 17:321, 1997. 194. Gwynne-Jones, D. P.: Displaced olecranon apophyseal fractures in children with osteogenesis imperfecta. J. Pediatr. Orthop. 25:154, 2005. 195. Parson, F. G.: Observations on traction epiphyses. J. Anat. Physiol. 38:248, 1904. 196. Rabinovich, A., Adili, A., and Mah, J.: Outcomes of intramedullary nail fixation through the olecranon apophysis in skeletally immature forearm fractures. J. Pediatr. Orthop. 25:565, 2005. 197. Retrum, R. K., Wepfer, J. F., Olsen, D. W., and Laney, W. H.: Case report 355: delayed closure of the right olecranon epiphysis in a right-handed, tournament-class tennis player (post-traumatic). Skeletal Radiol. 15:185, 1986. 198. Schweitzer, G.: Bilateral avulsion fractures of the olecranon apophyses. Arch. Orthop. Trauma Surg. 107:181, 1988. 199. Zionts, L. E., and Moon, C. N.: Olecranon apophysis fractures in children with osteogenesis imperfecta revisited. J. Pediatr. Orthop. 22:745, 2002.

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CHAPTER

17

Fractures of the Neck of the Radius in Children Anthony A. Stans

INTRODUCTION Fractures of the neck and head of the radius in children are relatively uncommon, constituting 4% to 7% of elbow fractures and dislocations.2,6,14,16,21,24 A review of the early literature reveals considerable controversy on the significance, treatment, and late results of this injury.12,23,24 However, as is explained in the body of this chapter, since the last edition of this text there has been a growing body of evidence indicating that open reduction and internal fixation should be avoided whenever possible, and that percutaneous reduction (and fixation if necessary) is much more likely to result in a favorable outcome. Sex frequency varies from series to series, but overall, there seems to be a slight female preponderance. The typical patient age range for radial neck fractures is between 4 and 14 years, with a mean age between 10 and 12 years. Approximately 30% to 50% of patients have associated injuries to the elbow region (Figs. 17-1 and 17-2).10,18,32,39 The prognosis after this fracture seems to depend more on the severity of the injury, the associated injuries about the elbow, and the type of treatment than on the accuracy of the reduction.10,16,23,25 Although emphasis has been placed on the angulation of the radial head, it is actually the displacement of the fracture that is the more important component of the deformity. The classic discussion on this subject was published by Jeffery,10 whose observations in 1950 clarified the nature of the fracture, the mechanism of injury, the radiologic assessment, the method of reduction, and the prognosis. Complete remodeling of a fracture was demonstrated with perfect function after a residual angulation of 50 degrees. Closed reduction consistently produces better results than open reduction, even taking into account that more severe injuries are more likely to require operation.23,25 Recently, significant technical advances

have been made, making possible the percutaneous reduction of even severely displaced or angulated fractures.1,8,20,31,34

MECHANISM OF THE FRACTURE A fall on the outstretched arm produces a valgus thrust on the elbow that fractures the radial neck and often avulses structures on the medial side of the joint. The radial head tilts laterally because the forearm is usually supinated, but the exact direction of the tilt depends on the rotational position of the forearm at impact. This is the most common mechanism, but the fracture can also occur with posterior dislocation of the elbow, resulting in two types of displacement, depending on whether the radial head fractures during spontaneous reduction or in the course of dislocating. The first type of fracture10,11 (reduction injury) leaves the separated proximal radial epiphysis tilted 90 degrees posteriorly beneath the capitellum of the humerus (Figs. 17-3 and 17-4). This mechanism of injury has been confirmed in a report of an iatrogenic radial neck fracture that occurred during closed reduction of a posterior elbow dislocation.36 With the second type of fracture23 (dislocation injury), axial compression on the elbow results in anterior displacement of the radial head as the proximal radial epiphysis moving posteriorly is obstructed by the capitellum and fractures in the process (see Fig. 17-2). Less common injuries include anterior dislocation of the head of the radius with associated fracture of the radial neck; Montaggia equilavent injuries28; shear fracture through the neck of the radius with medial displacement of the shaft, which may become locked medial to the coronoid process of the ulna17; and osteochondral fracture of the epiphysis with an intra-articular loose body. Associated injuries occasionally occurring with radial neck fracture include fracture of the olecranon, avulsion of the medial epicondyle of the humerus, dislocation of the elbow, and avulsion of the medial collateral ligament from the distal humerus.10 Associated injuries are not only important in themselves but also have implications for prognosis and treatment of the radial neck fracture (see Figs. 17-1 and 17-2).16,39

CLASSIFICATION The fracture may be classified by the degree of angulation of the radial head,24,26 the mechanism of injury,10 the type of epiphyseal plate disruption,26,29 the amount of fracture displacement, or combinations of these.23 O’Brien24 divided these fractures into three groups according to the degree of angulation:

Chapter 17 Fractures of the Neck of the Radius in Children

A

B

269

the shaft (see Chapter 2). The radius is not a straight bone, even in its proximal third.16,33 Thus, a measured angulation of 50 degrees may in reality represent only 35 to 40 degrees of true angulation. As in many pediatric injuries, comparison with the uninjured elbow is often helpful, or even essential, for accurate assessment of this feature. The injury also may be classified according to the type of epiphyseal plate injury. Although some authors believe that the fracture may occur entirely through the metaphysis of the neck of the radius,12,38 this is unusual, both in the literature23 and in our experience.39 The pattern of proximal radial physeal injuries, as traditionally classified by Salter and Harris, includes the following types: Type I: Rare and usually associated with dislocation of the radial head or elbow Type II: The most common pattern of fracture through the neck of the radius Type III: Rare Type IV: Second in frequency39 and associated with a poor prognosis owing to marked displacement, irregularity of the radial head, and occasional radioulnar synostosis (Figs. 17-5 and 17-6) We prefer the classification of Wilkins,27 which combines those of Jeffery10 and Newman.23 It is based primarily on the mechanism of injury, but it also describes the deformity to be corrected and suggests the severity of the injury and thus helps in formulating the prognosis.

C

FIGURE 17-1

A, A displaced and angulated fracture of the neck of the radius and fracture of the olecranon (arrow) in an 8-year-old girl. B, Three weeks after closed reduction and immobilization, it is apparent that the capsular attachment has avulsed a portion of the medial epicondyle (arrow). C, Three years later, the patient had perfect function and no pain.

Type I: less than 30 degrees Type II: 30 to 60 degrees Type III: More than 60 degrees

I. Valgus fractures A. Type A: Salter-Harris type I and II injuries of the proximal physis B. Type B: Salter-Harris type III and IV injuries of the proximal radial physis C. Type C: Fractures involving only the proximal radial metaphysis II. Fractures associated with dislocation of the elbow A. Type D: Reduction injuries B. Type E: Dislocation injuries We have added Salter-Harris type III fractures to the type B classification. These may produce an intraarticular loose body consisting of articular cartilage and a portion of the epiphysis.

TREATMENT He also described an impaction fracture of the articular surface of the head, an injury that is more likely to be associated with lesser degrees of angulation. It is important to recognize that the neck of the radius normally subtends an angle of 165 to 170 degrees with

ASSESSMENT OF INJURY The entire extremity should be thoroughly examined for open wounds, other injuries, and neurovascular

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B

FIGURE 17-2

A, An open dislocation of the elbow, fracture of the neck of the radius, and badly displaced fractures of the distal radius and ulna in a 10-year-old girl. Definitive treatment was not rendered until 8 days after the injury. Two years later (B and C), there was synostosis of the radius and ulna and enlargement and irregularity of the head of the radius.

A

C

A FIGURE 17-3

B

A, Radiograph of the elbow of an 8-year-old girl who had fallen 6 weeks earlier. The radial head is tilted 90 degrees posteriorly and is not articulating with the joint surface of the capitellum. The presumed mechanism of this fracture pattern is that (spontaneous or manipulative) reduction of a posteriorly dislocated elbow reduces the dislocation but leaves the radial head displaced. B, In the same patient 22 years after open reduction, note the enlargement and irregularity of the radial head. She had a full range of motion and no pain. This is the only exception in our experience to the rule that stiffness usually follows late open reduction.

Chapter 17 Fractures of the Neck of the Radius in Children

271

A(2)

A(1)

B

C(1)

C(2)

impairment. A fall on the outstretched hand can result in injury at multiple levels. As in adults, injury about the wrist must be specifically excluded, and fracture of the scaphoid has been reported.10,11 Anteroposterior and lateral radiographs of both the elbow and the entire forearm should be examined for other injuries, particularly about the elbow. An estimate should also be made of the degree of angulation of the radial head and the amount of displacement. The precise degree of angulation can be accurately determined only by an anteroposterior radiograph with the forearm in the position of rotation at the moment of impact. Jeffery10 demonstrated that this is best achieved by taking radiographs in varying degrees of forearm rotation so that the radial head will cast shadows of different shapes. When the radial head forms as nearly

FIGURE 17-4 A, Fracture of the neck of the radius in a 13-year-old girl with dislocation of the elbow and marked posterior angulation was treated (B) by open reduction and internal fixation with a wire passed through the capitellum into the radius. The high rate of complications associated with this method of fixation makes it an undesirable method of treatment. C, Three years later, there is deformity of the head of the radius, subluxation, and marked restriction of forearm rotation.

perfect a rectangle as possible, the real degree of angulation can be determined. Oval shapes indicate that the radiographs have not been taken at a right angle to the plane of maximal angulation (Fig. 17-7). Although obtaining these multiple views is not practical or necessary for the majority of fractures, in cases in which it is unclear whether or not fracture reduction is indicated, performing multiple radiographs as described can be very helpful. Comparison views of the uninjured forearm in the same degree of rotation are helpful in assessing the degree of angulation. Also, in children, normal variations in the radiographic appearance of the proximal radius must be considered when assessing injury.30 Again it is a basic principle of treating elbow fractures in children that radiographs of the injury may be compared with films of the opposite (uninjured) side.

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A(2)

A(1)

A(3) 7 yrs

Post injury

FIGURE 17-5

A, A type IV fracture of the radial head and a dislocation of the elbow in an 8-year-old boy. B, The free fragment was excised, along with the radial head (left). Seven years later (right), that patient had very little forearm rotation, limited extension, irregularity of the articular surface, and valgus deformity.

B

FIGURE 17-6

A

B

A, A comminuted fracture of the head of the radius in a 13-year-old boy. Note the free fragment, which consisted of epiphysis, growth plate, and metaphysis, on the medial aspect of the ulna. The radial neck fracture was reduced open and the fragment was excised. B, Four years later, the patient had full flexion, extension, and pronation but no supination. Note the defect on the medial aspect of the head of the radius. The elbow was only occasionally painful.

Chapter 17 Fractures of the Neck of the Radius in Children

A

E

a

b

c

d

e

FIGURE 17-7

Diagram of the radiographic appearance of the head of the radius in varying degrees of rotation, where A = a and E = e. When the film is taken at right angles to the plane of maximum angulation, the radial head is rectangular in shape as in Ee (shaded epiphysis).

INDICATIONS FOR REDUCTION It is generally agreed that a radial neck fracture with angulation of more than 60 degrees or more than 3 mm of displacement will likely produce problems if it is not corrected.2,6,23,24,39 It is also agreed that in radial neck fractures, less than 30 degrees’ angulation can safely be accepted,10,25,33 and there is some support for the position that fractures less than 45 degrees’ angulation do not require open reduction.2,23,24,32,35,39 The proper treatment approach should be individualized based on the clinical circumstances of each patient when angulation is between 30 and 60 degrees. There is support both for and against open reduction of these fractures.6,18,25,26,32,39 Advocates of open reduction believe that, without it, significant loss of forearm rotation will ensue. Those who prefer closed reduction or acceptance of deformity believe that the complications of open reduction do not justify the risks, considering the minimal disability that is the legacy of fractures left with even 50 to 55 degrees of angulation. Recently, two techniques have been developed that provide the benefits of improved fracture alignment yet have not caused the problems associated with open reduction. In several series, percutaneous reduction of radial neck fractures has been associated with fewer complications and less elbow stiffness as compared with open reduction (Fig. 17-8).1,20,31 Originally described using

273

a Steinmann pin, we have also used a small elevator to percutaneously reduce the fracture with excellent success. After percutaneous reduction, fracture stability should be assessed by bringing the elbow through full range of motion including pronation and supination under fluoroscopic imaging. Frequently, the fracture is stable enough that internal fixation is not necessary and casting alone is sufficient. In situations in which redisplacement or angulation occurs, percutaneous pinning or intramedullary stabilization using the Metaizeau technique may be employed. Metaizeau and colleagues20 described a method of reducing and stabilizing displaced or angulated radial neck fractures using an intramedullary K-wire. An intramedullary pin or small-diameter flexible intramedullary nail is used to enter the radius in a retrograde fashion just proximal to the distal radial physis. Before insertion, a 30- to 45-degree bend is placed in the pin approximately 1 cm from the tip. Advancing the intramedullary pin proximally to the fracture site, the intramedullary pin is used to elevate the depressed or angulated fracture (Fig. 17-9). Rotation of the bent tip is then used to correct displacement. The intramedullary pin is cut proximally where it lies beneath the skin, along the surface of the radius. Often, the pin becomes symptomatic at the insertion site and may be removed after the fracture has completely healed, 3 to 9 months following surgery. Occasionally, radial neck fractures cannot be reduced by use of an intramedullary pin alone. Employment of an intramedullary pin in combination with percutaneous reduction techniques described earlier is a very effective means of reducing and stabilizing severely displaced or angulated fractures by minimally invasive methods. Percutaneous and intramedullary reduction and fixation techniques represent a significant advance in the treatment of radial neck fractures, providing the benefits of improved fracture reduction with minimal risk of avascular necrosis (AVN) and stiffness associated with open techniques.8,20 Displacement, rather than angulation, often leads to loss of forearm rotation. Angulation produces a defect at the joint surface and, therefore, does not obstruct rotation. Incomplete contact between articular surfaces is, theoretically, harmful, but enough remodeling usually occurs so that the incomplete contact appears to improve. Displacement, on the other hand, results in radial neck deformity and abutment on the edges of the radial notch (Fig. 17-10). This produces a cam effect during rotation, confirmed in cadaver studies.39 The radial neck was divided with a saw and fixed with Kirschner wires without angulation but with varying degrees of displacement. The observed effect on forearm rotation was that displacement greater than 3 mm resulted in loss of forearm rotation because of abutment of the radial head against the ulna.

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Part IV Conditions Affecting the Child’s Elbow

A

B

FIGURE 17-8

C

D

Because closed or open reduction performed more than 5 to 7 days after injury leads to loss of forearm rotation and radioulnar synostosis,18,23,32,39 a fracture more than 1 week old is a relative contraindication to reduction. It is better to accept deformity.

PRINCIPLES OF TREATMENT Review of the literature indicates that, regardless of the severity of the injury, closed treatment gives better results than open treatment. In addition, fractures treated with internal fixation tend to have poor results compared with those treated without internal fixation. In particular, transcapitellar fixation with a Kirschner wire passed through the capitellum of the humerus and across the joint into the head and medullary canal of the radius is

A, Fracture of the radial neck angulated approximately 45 degrees. B, A Steinmann pin is inserted percutaneously. C, Using fluoroscopic guidance, the Steinmann pin is used to reduce the fracture. D, Normal anatomy is restored without open reduction, and the fracture is stable without internal fixation. (From Green N. E., and Swiontkowski, M. F.: Skeletal Trauma in Children, 2nd ed. Philadelphia, W. B. Saunders, 1998.)

associated with significant complications including septic arthritis, breakage of the wire within the joint, and nonunion (see Figs. 17-4 and 17-11).7,19 Thus, as little internal fixation as possible is recommended.2,39 When necessary, intramedullary fixaton using the Metaizeau technique seems to avoid the undesirable consequences associated with other internal fixation techniques. Finally, immobilization of the elbow for more than 3 to 4 weeks leads to stiffness, even in children. Thus, the following principles apply to treating radial neck fractures: 1. Closed treatment generally gives better results than open reduction. 2. If closed treatment is not acceptable, use percutaneous reduction and fixation technique.

Chapter 17 Fractures of the Neck of the Radius in Children

C

A D

B E FIGURE 17-9 A, Radial neck fracture angulated greater than 45 degrees. B, A 2-mm diameter pin with a slight bend 1 cm from the tip is advanced retrograde to the fracture within the intramedullary canal and used to elevate the depressed and angulated fracture. C, Rotating the intramedullary pin reduces fracture displacement. D, One year postoperatively, immediately before hardware removal, the fracture has completely healed with full elbow motion in all planes E.

275

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Part IV Conditions Affecting the Child’s Elbow

3. When internal fixation is necessary, use intramedullary technique whenever possible. 4. Treat promptly. 5. Do not use transcapitellar wires. 6. Do not immobilize the fracture longer than 4 weeks.

FIGURE 17-10 Diagram illustrates the effect of union with displacement of the fracture. The white circle represents the shaft of the radius just distal to the fracture, and the gray circle represents the head of the radius. The black area represents the radial notch on the ulna. Rotation of the radius after union with persistent displacement results in abutment on the margin of the radial notch of the ulna. The degree of limitation of pronation and supination is proportional to the degree of displacement.

4 yrs. Post injury

RESULTS When assessing the published results of radial neck fractures, it is apparent that pain from this injury is seldom disabling.9,21,32,35,39 Unsatisfactory results consistently are based on the degree of restriction of elbow and forearm motion.6,7,10,23,26 It may be that permanent stiffness develops, not only because of a mechanical block to rotation but also, possibly, because of reflex inhibition to avoid a painful arc of motion. Even when irregularity of the joint surface results in stiffness, there is usually surprisingly little pain. On the other hand, a “successful” open reduction with a perfect anatomic result also may be associated with significant loss of forearm rotation. Series of patients followed as long as 22 years confirms this impression: Pain is not a prominent feature and is not the reason for poor results.39 Loss of 20 degrees of supination or as much as 40 degrees of pronation is not disabling, particularly when it occurs at a young age. “Fair” and “poor” results occur when loss of forearm rotation is greater than 40 degrees. In contrast to the legacy of adults’ radial neck fractures, loss of elbow flexion and extension is less common in children and not as disabling as loss of rotation. When a limitation develops, it is usually extension that is lost and then seldom more than 30 to 35 degrees. AVN of the radial head, radioulnar synostosis,1,18,23,39 and removal of the radial head are associated with poor results.1,22,35 The incidences of radioulnar synostosis and AVN of a substantial portion of the head of the radius are difficult to determine because of the small series of

FIGURE 17-11 Nonunion of the neck of the radius 4 years after open reduction and fixation with a transcapitellar wire in a 12-year-old boy.

Chapter 17 Fractures of the Neck of the Radius in Children

fractures of the neck of the radius in children. The problem is further complicated by the fact that these complications are associated with widely displaced fractures, those treated overenthusiastically, those treated late, and those concomitant with dislocations of the elbow. These injuries, in turn, make up a smaller part of the total number of fractures. It is enough to say that, in almost every reported series, these complications are mentioned. AVN and synostosis complicate 5% to 20% of fractures and usually follow open reduction and fixation. The unanticipated good results subsequent to acceptance of considerable deformity is related to remodeling of the deformity.4,9,10,18 This is surprising, because the plane of the fracture lies at right angles to the plane of motion of both the elbow and the radioulnar joints. This would seem to be an exception to the rule that remodeling in the child can be expected only if the fracture deformity is in the same plane of motion as the nearby joint. This remodeling may explain why younger children do better after fracturing of the neck of the radius than do older children. Premature fusion of the proximal radial epiphysis does occasionally occur, but it does not appear to influence the final result.23,24 It does not lead to significant shortening of the radius nor to valgus deformity at the elbow.10,23 This is because most of the growth occurs at the distal end, and, initially, the fracture stimulates distal radius growth. Thus, the result depends largely on the degree of restriction of motion. Composite loss of pronation, supination, flexion, and extension greater than 90 degrees leads to functional disability and a poor result. Results are directly related to the severity of the injury, concomitant injuries about the elbow, and how much physical intrusion is necessary to reduce the fracture.7,9

COMPLICATIONS COMPLICATIONS RELATED TO THE INJURY Radioulnar Synostosis The dreaded complication of radioulnar synostosis (see Fig. 17-2)1,18,23,24,25,39 is associated with widely displaced fractures and is often associated with dislocation of the elbow.

Premature fusion is common but of little consequence.4,9,10,18,26

Premature Fusion of the Epiphyseal Plate

277

effect is determined by the degree of loss of blood supply. Enlargement of the Head of the Neck of the Radius and Increase in Diameter of the Neck of the Radius This complication, which is often seen, is accom-

panied by compensatory enlargement of the capitellum of the humerus.23,24,26 Because growth is stimulated by the increased vascularity during the healing phase, the event is of little significance. Ectopic Calcification Ectopic calcification is also frequent, but it is usually limited and has little effect on the outcome.23,25,26,33,39 Vascular and Peripheral Nerve Injury Injuries to vessels and to peripheral nerves are unusual after this injury. When vascular injury occurs, it is usually related to dislocation of the elbow. Nerve injury may occur, but permanent paralysis is unusual. Impaction or Shear Injury to the Articular Surface of the Radial Head This complication is difficult to diag-

nose because it occurs in fractures that produce less angulation and because the joint injury is not directly visualized,24 but it can lead to elbow stiffness and premature physeal closure. A shear injury to the head of the radius can produce an intra-articular free osteochondral fragment containing articular cartilage and a “variable amount” of epiphysis.

COMPLICATIONS RELATED TO TREATMENT Avascular Necrosis AVN can complicate not only widely displaced fractures but also those with lesser degrees of displacement treated by open reduction (see Fig. 17-12).12,16,18,23,39 The risk of AVN can be reduced by carefully preserving the soft tissue attachments. It is seldom seen with closed treatment. Radioulnar Synostosis Radioulnar synostosis also may result from less severe injuries that have undergone the trauma of open reduction or late closed reduction (see Fig. 17-2).3,10 If complete dislocation of the radial head or a dislocation of the elbow is initially unrecognized, reduction should probably be attempted up to 3 months after the injury (see Fig. 17-3). In this setting, the parents must be warned that significant stiffness will result.

Postoperative infection39 is always a concern with open procedures and can result in dissolution of the articular surface and ankylosis.

Infection Avascular Necrosis AVN is most common (Fig. 17-12)12,18,23,32,39 after open reduction but can occur with widely displaced fractures treated by closed reduction. Although this complication probably occurs to a certain extent in many of these serious injuries, the eventual

Nonunion is rare, but when it occurs, it is almost always after open reduction (see Fig. 17-11).37

Nonunion

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Part IV Conditions Affecting the Child’s Elbow

B

A

D

C FIGURE 17-12 A, Irreducible fracture angulated 90 degrees. B, Open reduction was performed with two K-wires place at the periphery of the articular surface angled obliquely across the fracture site. C and D, Three years postoperatively, the patient shows signs of avascular necrosis, but the fracture has united and the patient has excellent motion in all planes.

Chapter 17 Fractures of the Neck of the Radius in Children

Poor results are inevitable,4,26,39 but there may be surprisingly little pain, and excision should be deferred until skeletal maturity. Bone grafting should be considered with caution because radioulnar synostosis frequently develops. Healing of the nonunion has not necessarily led to improvement of clinical symptoms. A rare cause of nonunion may be complete reversal of the head of the radius when the fracture surface faces the capitellum of the humerus and the articular surface faces the distal fragment.25 The radial head should be returned to its proper orientation, even if it has lost all its soft tissue attachments. It should not be excised. Damage to the Articular Surface Such damage can result from injury or from breakage of wires inserted across the joint to fix the fracture. This technique also is associated with stiffness, so it should be avoided.

Stiffness has been associated with open treatment, internal fixation, delayed treatment more than 1 week after the injury, and immobilization longer than 4 weeks.

Loss of Motion

AUTHOR’S PREFERRED METHOD OF TREATMENT Selection of the treatment technique depends on the nature of the injury. The sequence and method of treatment preferred by the author is based on his personal zeal for treating these injuries “closed” whenever that is at all possible. 1. Angulation of less than 45 degrees and displacement of less than 3 mm. An above-elbow cast with the elbow flexed 90 degrees and the forearm in neutral rotation for 3 weeks is appropriate (Fig. 17-13). Radiographs should be taken after 4 to 7 days to check the position. After immobilization is discontinued, the patient may gradually resume normal activity. Physiotherapy is not necessary, and patients may be instructed on simple gentle active stretching exercises. The child should be seen in 3 weeks and again in 3 months, by which time full range of motion should have returned. 2. Angulation between 45 and 60 degrees with displacement of less than 3 mm. Gentle closed reduction by the method described later should be attempted. If the reduction cannot be improved by closed means, percutaneous reduction should be considered. However, if percutaneous reduction proves unsuccessful, the deformity should be accepted. 3. Angulation greater than 60 degrees and displacement of more than 3 mm. Every possible attempt should be made to reduce the fracture

279

closed. It is, however, equally important to be gentle in all attempts. With the patient under general anesthesia, the forearm is rotated while the operator palpates for the position of maximal prominence of the head of the radius at different degrees of flexion and pronation/supination. An assistant applies varus stress to the elbow to open the joint laterally and to increase the prominence of the radial head. Firm pressure is applied to the radial head in mediad and craniad directions. Successful reduction is confirmed by radiographs (several views may be necessary). If the elbow region is too swollen to palpate the radial head, an assistant should stabilize the humerus and flex the elbow to 90 degrees. The forearm is rotated to full supination without applying varus strain to the elbow. Thumb pressure is applied to the anterolateral aspect of the head of the radius just lateral and distal to the cubital fossa. At the same time, the forearm is gradually rotated to the neutral position and then into full pronation. A variation on this technique has been recently described by Neher.22 The reduction is verified radiographically, preferably with a C-arm fluoroscope. The patient’s arm is placed in an above-elbow splint or cast for 3 weeks, and a follow-up radiograph is taken after 1 week.13 If this maneuver fails to achieve reduction, an Esmarch bandage is wrapped snugly around the elbow and the radiographic studies are repeated. Occasionally, this results in reduction. If reduction is still inadequate, the arm is prepared and draped, and an attempt is made to achieve a percutaneous reduction.1,5,31,34 Under fluoroscopic control, a Steinmann pin or small elevator is introduced through the skin, and the radial head is pushed into proper position (see Fig. 17-8). If reduction is achieved and is stable, with the elbow flexed 90 degrees and the forearm in a natural position, a long arm cast is applied. Radiographs confirm the maintenance of reduction. If the radial neck fracture reduction cannot be achieved, cannot be maintained, or is unstable, then an intramedullary pin is placed using the Metaizeau technique (see Fig. 17-9). Only in the rare situation in which percutaneous reduction and the Metaizeau technique are not successful should open reduction be performed. A 5-cm incision is made, commencing on the lateral aspect of the capitellum and angling posteriorly over the radial head. This is the central portion of Kocher’s posterolateral incision at the interval between the extensor carpi ulnaris and the anconeus muscles. To avoid damaging the posterior interosseous nerve, no incision should be made distal to the bicipital tuberosity of the radius. The elbow joint is entered anterior to the anconeus muscle. Do not interfere with the orbicular ligament even if torn, or stiffness may result. The radial head is reduced into its

280

Part IV Conditions Affecting the Child’s Elbow

A

B

D C FIGURE 17-13 A and B, The author’s daughter fell from a couch, sustaining this radial neck fracture angulated 40 degrees, and an associated, nondisplaced olecranon fracture. C and D, Two years following cast immobilization without reduction, the fracture alignment has completely remodeled and the patient has full motion in all planes with unlimited function.

proper position and is often sufficiently stable to make internal fixation unnecessary. If the radial head is unstable, the child’s bone is often soft enough to allow use of a heavy absorbable suture on a stout cutting needle to hold it in place, introducing the needle at the articular margin of the radial head and passing it across the fracture into the neck of the radius and through the cortex. If this does not seem feasible, one or two fine, smooth Kirschner wires are inserted at the articular margin of the radial head, across the fracture, and just through the cortex of the radial neck (see Fig. 17-12). They should be bent external to the skin, cut external to the skin, and a dressing sponge or gauze placed beneath the pins to facilitate removal in 3 weeks. A growing child’s radial head must never be excised. Excision results in pain, increased carrying angle, radio-

ulnar synostosis, or distal radioulnar dysfunction (see Fig. 17-5).2,3,15 If stable reduction cannot be achieved, less than optimal reduction should be accepted. Delayed radial head resection is not usually necessary but can be performed at skeletal maturity. The rare Salter-Harris type III or IV injury produces a dilemma. The fracture fragment should be fixed whenever possible, but if the fragment is too small, the fragment should be excised. The prognosis for Salter-Harris type III or IV fractures is guarded. Loss of motion after this fracture may be due to other factors, because the injury is usually produced by considerable forces. Immobilization following open reduction is as described for closed treatment and should be continued for no more than 3 to 4 weeks. If Kirschner wires have been used, they should be removed at this time. Reha-

Chapter 17 Fractures of the Neck of the Radius in Children

bilitation and follow-up are exactly as described for closed treatment.

SUMMARY Fracture of the neck of the radius is a rare but serious injury, particularly when it is associated with marked angulation and displacement or with concomitant injuries to the elbow region. Every possible attempt should be made to treat this injury closed. Even though more serious fractures are treated by open reduction, clinical reports and personal experience suggest that surgical intervention has an adverse effect on the outcome. Percutaneous reduction techniques may permit reduction of more serious fractures without open surgical exposure. When open reduction is necessary, dissection and internal fixation should be kept to a minimum. Treatment later than 1 week after the injury leads to stiffness, as does external immobilization for longer than 4 weeks.

Acknowledgment The author would like to recognize Dr. John H. Wedge. The current chapter is based on the extensive work done by Dr. Wedge as author of this chapter in previous editions of The Elbow and Its Disorders.

References 1. Bernstein, S. M., McKeever, P., and Bernstein, L.: Percutaneous reduction of displaced radial neck fractures in children. J. Pediatr. Orthop. 13:85, 1993. 2. Blount, W. P.: Fractures in Children. Baltimore, Williams & Wilkins, 1955, p. 56. 3. Bohrer, J. V.: Fractures of the head and neck of the radius. Ann. Surg. 97:204, 1933. 4. Conn, J., and Wade, P. A.: Injuries of the elbow. A ten year review. J. Trauma 1:248, 1961. 5. Dormans, J. P., and Rang, M.: Fractures of the olecranon and radial neck in children. Orthop. Clin. North Am. 21:257, 1990. 6. Dougall, A. J.: Severe fracture of the neck of the radius in children. J. R. Coll. Surg. Edinb. 14:220, 1969. 7. Fowles, J. V., and Kassab, M. T.: Observations concerning radial neck fractures in children. J. Pediatr. Orthop. 6:51, 1986. 8. González-Herranz, P., Alvarez-Romera, A., Burgos, J., Rapariz, J. M., and Hevia, E.: Displaced radial neck fractures in children treated by closed intramedullary pinning (Metaizeau technique). J. Pediatr. Orthop. 17:325-331, 1997. 9. Henriksen, B.: Isolated fractures of the proximal end of the radius in children. Epidemiology, treatment and prognosis. Acta Orthop. Scand. 40:246, 1969.

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10. Jeffery, C. C.: Fractures of the radius in children. J. Bone Joint Surg. 32B:314, 1950. 11. Jeffery, C. C.: Fractures of the neck of the radius in children. Mechanism of causation. J. Bone Joint Surg. 54B:717, 1972. 12. Jones, E. R. L., and Esch, M.: Displaced fractures of the neck of the radius in children. J. Bone Joint Surg. 53B:429, 1971. 13. Kaufman, B., Rinott, M. G., and Tangman, M.: Closed reduction of fractures of the proximal radius in children. J. Bone Joint Surg. 71B:66, 1989. 14. Landin, L. A., and Danielsson, L. G.: Elbow fractures in children. An epidemiological analysis of 589 cases. Acta Orthop. Scand. 57:309, 1986. 15. Lewis, R. W., and Thibodeau, A. A.: Deformity of the wrist following resection of the radial head. Surg. Gynecol. Obstet. 64:1079, 1937. 16. Lindham, S., and Hugosson, C.: The significance of associated lesions including dislocation in fractures of the neck of the radius in children. Acta Orthop. Scand. 50:79, 1979. 17. Manoli, A.: Medial displacement of the shaft of the radius with a fracture of the radial neck. Report of a case. J. Bone Joint Surg. 61A:788, 1979. 18. McBride, E. D., and Monnet, J. C.: Epiphyseal fractures of the head of the radius in children. Clin. Orthop. 16:264, 1960. 19. Merchan, E. C. R.: Displaced fractures of the head and neck of the radius in children: open reduction and temporary transarticular internal fixation. Orthopedics 14:697, 1991. 20. Metaizeau, J.-P., Lascombes, P., Lemelle, J.-L., Finlayson, D., and Prevot, J.: Reduction and fixation of displaced radial neck fractures by closed intramedullary pinning. J. Pediatr. Orthop. 13:355, 1993. 21. Murray, R. C.: Fractures of the head and neck of the radius. Br. J. Surg. 9:114, 1977. 22. Neher, C. G., and Torch, M. A.: New reduction technique for severely displaced pediatric radial neck fractures. J. Ped. Orthop. 23:626, 2003. 23. Newman, J. H.: Displaced radial neck fractures in children. Injury 9:114, 1977. 24. O’Brien, P. I.: Injuries involving the proximal radial epiphysis. Clin. Orthop. 41:51, 1965. 25. Rang, M.: Children’s Fractures. Philadelphia, J. B. Lippincott Co., 1974, p. 112. 26. Reidy, J. A., and Van Gorder, G. W.: Treatment of displacement of the proximal radial epiphysis. J. Bone Joint Surg. 45A:1355, 1963. 27. Rockwood, C. A., Jr., Wilkins, K. E., and King, R. E. (eds.): Fractures in Children, Vol. 3. Philadelphia, J. B. Lippincott Co., 1984, p. 510. 28. Ruchelsman, D. E., Klugman, J. A., Madan, S. S., and Chorney, G. S.: Anterior dislocation of the radial head with fracures of the olecranon and raidal neck in a young child: A Monteggia equivalent fracture-dislocation variant. J. Orthop. Trauma 19:425, 2005. 29. Salter, R. B., and Harris, W. R.: Injuries involving the epiphyseal plate. J. Bone Joint Surg. 45A:587, 1963. 30. Silberstein, M. J., Brodeur, A. E., and Graviss, E. R.: Some vagaries of the radial neck and head. J. Bone Joint Surg. 64A:1153, 1982.

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31. Steele, J. A., and Kerr Graham, H.: Angulated radial neck fractures in children. A prospective study of percutaneous reduction. J. Bone Joint Surg. 74B:760, 1992. 32. Tibone, J. E., and Stoltz, M.: Fractures of the radial head and neck in children. J. Bone Joint Surg. 63A:100, 1981. 33. Vahvanen, V., and Gripenberg, L.: Fracture of the radial neck in children. A long-term follow-up study of 43 cases. Acta Orthop. Scand. 49:32, 1978. 34. van Rhijn, L. W., Schuppers, H. A., and van der Eijken, J. W.: Reposition of a radial neck fracture by a percutaneous Kirschner wire. A case report. Acta Orthop. Scand. 66:177, 1995. 35. Vocke, A. K., and Von Laer, L.: Displaced fractures of the radial neck in children: Long-term results and prognosis

36.

37. 38.

39.

of conservative treatment. J. Pediatr. Orthop. Part B. 7:217, 1998. Ward, W. T., and Williams, J. J.: Radial neck fracture complicating closed reduction of a posterior elbow dislocation in a child: case report. J. Trauma 31:1686, 1991. Waters, P. M., and Stewart, S. L.: Radial neck fracture nonunion in children. J. Pediatr. Orthop. 21:570, 2001. Weber, B. G., Brunner, C. H., and Freuler, F.: Treatment of fractures in children and adolescents. Berlin, SpringerVerlag, 1980, p. 172. Wedge, J. H., and Robertson, D. E.: Displaced fractures of the neck of the radius in children. J. Bone Joint Surg. 64B:256, 1982.

Chapter 18 Proximal Ulnar Fractures in Children

CHAPTER

18

Proximal Ulnar Fractures in Children Anthony A. Stans and Bernard F. Morrey

283

review of the literature of the less rare olecranon or proximal ulnar fracture resulted in the identification of 192 cases but no mention of a fracture of the apophysis.17 The fracture may or may not include the coronoid as the fracture line passes between the growth center and the proximal ulna (see Fig. 18-2). This is because the coronoid does not develop from a separate growth center; thus, the fracture line in this rarest of fractures may be rather variable (Fig. 18-3).

TREATMENT

INTRODUCTION Proximal ulnar fractures in children and adolescents are uncommon, accounting for between 4% and 7% of pediatric and adolescent elbow fractures.1,2,6,8 As a result, (1) they are often completely missed, (2) the variation in growth centers makes the radiographic interpretation confusing, (3) the precise fracture line is often not appreciated, and (4) the potential for a poor outcome occurs if the displacement is not appreciated. In this chapter, we review fractures of the physis, metaphysis, and coronoid (Table 18-1).

The extreme rarity of this fracture makes it difficult to make definitive recommendations for treatment. If the fracture is displaced, basic principles apply; that is, reduce the fracture anatomically. Smooth K-wires, possibly supplemented with a figure-of-eight wire as recommended by the Arbeitsgemeinschaft für osteosynthese fragen (AO) technique for olecranon fractures, appears to be adequate, based on the limited reports from the literature. The major challenge, of course, is to diagnose the displacement. Today, computed tomography (CT) scanning, magnetic resonance imaging (MRI), and ultrasonography are useful for this purpose.

GROWTH AND DEVELOPMENT

METAPHYSEAL FRACTURE

As noted in Chapter 1, at birth none of the articular elements of the ulna, including the coronoid and olecranon, are ossified. At age 9, the secondary center of ossification appears at the olecranon (Fig. 18-1). The ossification center may be bipartite and eccentric, and as the proximal ulna grows, the growth plate orientation alters from transverse to oblique. Closure of the physis begins at the articular surface and progresses toward the extensor surface of the bone. Just before fusion of the growth plate, the metaphyseal bone develops a sclerotic margin and may be widely separated from the apophysis, resembling a fracture. These vagaries can make it difficult to recognize a fracture of the olecranon in a child, and comparative views of the opposite side are often valuable.2 Although a secondary center may appear in the olecranon tip, there is no secondary ossification center of the coronoid. This helps explain the fracture pattern observed in the proximal ulna of the various age groups (Fig. 18-2).

Metaphyseal fractures, although more common than fracture of the apophysis, still account for only approximately 5% of elbow injuries.3,11,15 Wilkins17 identified only 230 cases among 4,684 proximal ulnar fractures reported in the child before 1991. It appears that there is a biphasic frequency by age, with the greatest early frequency occurring between 5 and 6 years12 and a second incidence observed in the adolescent. The first peak probably relates to the growth and development of the bone. The second peak relates to the growth and development of the individual participating in activity with increasing propensity for injury. The mechanism of injury is similar to that described for many injuries about the elbow, including supracondylar, condylar fractures, and dislocations. Although proximal ulna fractures may be caused by direct impact, a more common mechanism is a fall onto an outstretched hand with transmission of the force proximally to the elbow. Differences in injury pattern probably relate to the precise degree of elbow flexion, possibly the rotation of the forearm, and the manner in which the muscles contracted at the time of impact. With fracture of the metaphysis, a varus or valgus force often occurs, causing additional fractures about the elbow. In four large series of proximal ulnar fractures, 20% had a documented associated fracture.17 In some reports, as

APOPHYSEAL FRACTURE Apophyseal fractures are extremely rare. Reviewing his experience and that of the literature up to 1991, Wilkins17 identified only 16 such cases. As a matter of fact, a

Part IV Conditions Affecting the Child’s Elbow

284

Types of Proximal Ulnar Fracture in the Pediatric Age Group

TABLE 18-1 Type

Incidence

Apophyseal (physeal, epiphyseal)

Very rare

Metaphyseal

5% of elbow fractures

Coronoid

Less than 1% of elbow fractures

A

associated injury (±4 mm being the limit). Wilkins17 considered these by the mechanism of the fracture: (A) flexion; (B) extension; (1) valgus; (2) varus; and (C) shear injury. More recently, Graves and Canale7 classified the fracture according to (1) displacement greater or less than 5 mm and (2) presence of compounding. This classification was subsequently modified by Gaddy and coworkers,3 with a type I fracture being less than 3 mm and a type II greater than 3 mm. Evans and Graham2 have proposed a classification system based on anatomic site, fracture configuration, intra-articular displacement, and associated injuries, with approximately 18 subtypes. Thus, this fracture has the interesting characteristic of having almost as many classifications as episodes of occurrence. Although metaphyseal fractures are extremely uncommon, as noted, they are more frequent than the physeal injury is, and they account for approximately 5% of all elbow injuries. Of these, only 10% to 20% require surgical management. Rarely, proximal ulna fractures may be associated with ipsilateral fractures in the distal humerus,9 ulnar shaft,13 or radial head.4

DIAGNOSIS

B FIGURE 18-1

Schematic of ossification of the proximal ulna observed at birth (A) and at adolescence (B). This explains the fracture patterns seen in the young and the adolescent age groups.

Because the fracture involves ossified tissue, the metaphyseal fracture is relatively easily identified on the radiograph. Abrasion of the skin or open wound gives some idea of the mechanism; that is, direct or indirect trauma, respectively. A further means of determining the extent of displacement and hence the need for open reduction and internal fixation is to observe whether the fracture separates with flexion and extension under fluoroscopy. If an excessive amount of motion is observed at the fracture site (3 to 4 mm), then open reduction and internal fixation are carried out.

TREATMENT

FIGURE 18-2

Fracture of the apophysis may (open arrow) or may not (closed arrow) include the coronoid process.

many as 50% to 70% had an additional injury, most commonly involving the radial head with a valgus stress at the time of impact (Fig. 18-4).2,14,16

CLASSIFICATION In 1981, Matthews10 offered a classification based on radiographic appearance, degree of displacement, and

As implied from the above-mentioned classification, the approach to treatment is based primarily on fracture displacement. Fortunately, approximately 80% of these fractures are minimally displaced, requiring open reduction and internal fixation in only 15% to 20% of individuals.2 Reduction may be accomplished in most instances by reversing the mechanism, which provides some justification for Wilkins’ mechanistic classification noted earlier. For those fractures that are minimally displaced, simple immobilization for approximately 3 weeks appears to be adequate and is the universal recommendation. For displacement of greater than 3 mm, depending on the classification, surgical treatment is indicated. It is uncommon to have greater than 4 mm displace-

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A

C

FIGURE 18-3

B

ment in patients under the age of 10 years; thus, open reduction and internal fixation are generally observed in the older age group. Several authors have noted that displacement found intraoperatively is often significantly greater than displacement appreciated on plain radiographs.3,7 Typically, the AO technique with smooth Kwire with circumferential tension band wire is adequate (Fig. 18-5). Recently, there have been several reports successfully using heavy absorbable suture in tension band technique instead of wire.2,5 Absorbable suture was prominent, less likely than wire to become symptomatic and did not need to be removed. Metal internal fixation is typically removed 6 to 12 months postoperatively to ensure that premature closure of the proximal ulnar physis does not occur, and to relieve symptoms of proximal hardware. There have been no reported cases

A 13-year-old boy slipped and fell onto his left arm and presents with point tenderness over his olecranon. (A) Lateral radiograph suggests an olecranon apophysis fracture, which is confirmed by comparison with the contralateral uninjured elbow (B). At the time of his olecranon fracture, the patient was using crutches because he had sustained a left femur fracture 1 month earlier in a motor vehicle accident. The decision was made to perform open reduction with tension band internal fixation (C).

of premature proximal ulnar physeal closure using this internal fixation technique.

RESULTS Graves and Canale7 reported the results of 39 fractures treated over 30 years at the Campbell Clinic. Twentyeight of 30 patients treated nonoperatively were classified as satisfactory after closed treatment. Of the nine treated by open reduction and internal fixation, seven (78%) developed a satisfactory result. Gaddy and colleagues3 reported 35 fractures occurring in patients ranging from 2 months to 15 years. Of these, all 23 treated nonoperatively were considered satisfactory. The criterion for nonoperative treatment was displacement of less than 3 mm. Furthermore, 10 of 10 patients with

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greater than 3 mm of displacement underwent open reduction and internal fixation, and all developed a satisfactory outcome. Evans and Graham2 reported the results of 40 proximal ulna fractures treated surgically. In the text of their article a detailed treatment algorithm is provided, outlining their indications for surgical treatment. In summary, fractures greater than 4 mm were always treated surgically, fractures with less than 2 mm of displacement were never treated surgically, and treatment of fractures with displacement between 2 and 4 mm was determined by anatomic site, fracture configuration, and associated injuries. Thirty-six of 40 fractures were managed by tension band technique; 28 using wire and eight using absorbable suture. In the end, following a simple classification based on the degree of displacement appears to be a reliable guide to surgical intervention and good outcome.

COMPLICATIONS

FIGURE 18-4

The metaphyseal fracture involves the ossified proximal ulna. Varus or valgus angulation patterns assist in documenting the mechanism of injury.

As implied by the above-mentioned comments, the complications are uncommon; thus, approximately a 95% satisfactory outcome is observed whether the fracture is managed operatively or nonoperatively. The most common sequela of the fracture is slight limitation of

B

A

FIGURE 18-5

C

A 10-year-old girl fell 3 feet from a desk directly onto her left elbow, sustaining a proximal ulnar fracture (A) and transcondylar humerus fracture associated with an intra-articular loose bone fragment. Four weeks after open reduction and internal fixation of the proximal ulna and distal humerus, anatomic alignment and periosteal healing are demonstrated (B). Two years following her fracture and 18 months following removal of the tension band wire, the fractures have completely healed, elbow motion is full and without limit, and the patient is entirely asymptomatic (C).

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287

References

FIGURE 18-6 Plain film and three-dimensional reconstruction of stress fracture of the coronoid (arrow) observed in a 17-year-old gymnast. The symptoms resolved with rest. (Courtesy of A. Rettig, Indianapolis, IN.)

extension. Ectopic bone does not appear to be a problem.

FRACTURE OF THE CORONOID Because there is no secondary center of ossification, fracture of the coronoid as an isolated fracture is rare. As in the adult, injury to this structure is seen primarily with severe trauma or elbow dislocation. When a coronoid fracture is observed, a high level of suspicion should be aroused that a concurrent elbow dislocation has occurred.15 We have also seen in consultation a stress fracture of the coronoid in a 17-year-old gymnast (Fig. 18-6). Treatment is predicated on the integrity of the ulnohumeral joint; thus, the elbow is reduced and stability is ensured (see Chapters 27 and 29). The coronoid fracture in the child is then treated as a secondary consideration and frequently nothing need be done if the elbow is stable. We have not seen nor reported a large coronoid fracture as an isolated injury requiring open reduction and internal fixation in the child.

1. Dormans, J., and Rang, M.: Fractures of the olecranon and radial neck in children. Orthop. Clin. North Am. 21:257, 1990. 2. Evans, M. C., and Graham, K.: Olecranon fractures in children, part I: a clinical review. Part II: a new classification and management algorithm. J. Pediatr. Orthop. 19:559, 1999. 3. Gaddy, B. C., Strecker, W. B., and Schoenecker, P. L.: Surgical treatment of displaced olecranon fractures in children. J. Pediatr. Orthop. 17:321, 1997. 4. Gicquel, P. H., De Billy, B., Carger, C. S., and Clavert, J. M.: Olecranon fractures in 26 children with mean follow-up of 59 months. J. Pediatr. Orthop. 21:141, 2001. 5. Gortzak, Y., Mercado, E., Atar, D., and Weisel, Y.: Pediatric olecranon fractures: open reduction and internal fixation with removable Kirschner wires and absorbable sutures. J. Pediatr. Orthop. 26:39, 2006. 6. Grantham, S. A., and Kiernan, H. A.: Displaced olecranon fracture in children. J. Trauma 15:197, 1975. 7. Graves, S., and Canale, T.: Fractures of the olecranon in children. Long-term follow-up. J. Pediatr. Orthop. 13:239, 1993. 8. Henrikson, B.: Supracondylar fracture of the humerus in children. Acta Chir. Scand. 369:1, 1966. 9. James, P., and Heinrich, S. D.: Ipsilateral proximal metaphyseal and flexion supracondylar humerus fractures with an associated olecranon avulsion fracture. Orthopedics 14:713, 1991. 10. Matthews, J. G.: Fractures of the olecranon in children. Injury 12:207, 1981. 11. Maylahn, D. J., and Fahey, J. J.: Fractures of the elbow in children. J. A. M. A. 166:220, 1958. 12. Newell, R. L. M.: Olecranon fractures in children. Injury 7:33, 1975. 13. Olney, B. W., and Menelaus, M. B.: Monteggia and equivalent lesions in childhood. J. Pediatr. Orthop. 9:219, 1989. 14. Papavasilou, V. A., Beslikas, T. A., and Nenopoulos, S.: Isolated fractures of the olecranon in children. Injury 18:100, 1987. 15. Regan, W., and Morrey, B. F.: Fractures of the coronoid process of the ulna. J. Bone Joint Surg. 71A:1348, 1989. 16. Theodorou, S. D.: Dislocation of the head of the radius associated with fracture of the upper end of the ulna in children. J. Bone Joint Surg. 51B:700, 1969. 17.Wilkins, K. E.: Fractures involving the proximal apophysis of the olecranon. In Rockwood, C. A., Wilkins, K. E., and King, R. E. (eds.): Fractures in Children. Philadelphia, J. B. Lippincott, 1991, p. 751.

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CHAPTER

19

Osteochondritis Dissecans William J. Shaughnessy

by motion or use, particularly by throwing or other violent motions. It usually occurs in boys and always during the period of active ossification of the capitellar epiphysis (ages 7 to 12, peak at 9 years). Panner’s disease is not seen before age 5 years. In addition to pain, loss of 5 to 20 degrees of elbow extension is common. Local swelling and tenderness over the lateral side of the elbow is not unusual.23 Symptoms resolve over time with few sequelae.

RADIOGRAPHIC CHARACTERISTICS

INTRODUCTION Osteochondral lesions may be the source of chronic elbow pain, swelling, and loss of motion in children or adolescents. The typical presentation is an adolescent gymnast or baseball pitcher.13,34 The dominant arm is usually involved, but may be bilateral in approximately 5% to 20%.34,41 It is important to distinguish between osteochondrosis of the capitellum, or Panner’s disease, and osteochondritis dissecans. The distinction, based on patient age and degree of involvement of the capitellar secondary ossification center, has received only sporadic attention in the literature. It is possible, however, that the two conditions represent different stages of a single process that affects the formation and maturation of the capitellar epiphysis.

OSTEOCHONDROSIS OF THE CAPITELLUM (PANNER’S DISEASE)

Osteochondrosis of the capitellum is a focal or localized avascular lesion of subchondral bone and its overlying articular cartilage.11 Radiographically, there is fragmentation of the capitellar epiphysis. The fragmentation is due to irregular patches of relative sclerosis alternating with areas of rarefaction (Fig. 19-1A and B). The outline of the epiphysis may be slightly irregular and smaller than that of the opposite normal capitellar epiphysis. Despite the radiographic fragmentation, osteochondral loose bodies do not form. As growth progresses, the capitellar epiphysis eventually assumes a normal appearance in size, contour, and internal architecture as clinical symptoms resolve. Residual deformity of the capitellum is rare. Magnetic resonance imaging (MRI) findings include decreased signal intensity of the ossified epiphysis on T1-weighted images. Both plain films and MRI images of osteochondrosis of the capitellum are similar to findings in Legg-Calvé-Perthes disease of the hip.25 Deformity and collapse of the articular surface is less common in osteochondrosis of the capitellum than in Perthes’ disease of the hip.

INTRODUCTION

TREATMENT

Osteochondrosis is defined as a disease of the growth or ossification centers in children that begins as a degeneration or necrosis, followed by regeneration or recalcification. Familiar sites of osteochondrosis in children include the proximal femur (Perthes’ disease) and the tarsal navicular (Kohler’s disease). Osteochondrosis of the capitellum is also called Panner’s disease, or osteochondrosis deformans capitelli humeri. Osteochondrosis of the capitellum and osteochondritis dissecans may represent two manifestations of the same condition in different aged children. The different outcomes and treatments of the two groups makes it more useful to consider them separately.

Because osteochondrosis of the capitellum is a benign, self-limited condition, no active treatment is necessary. Activity modifications and rest for symptomatic relief are usually sufficient. The prognosis is good.

CLINICAL CHARACTERISTICS Osteochondrosis of the capitellum is characterized by dull, aching pain in the elbow that usually is aggravated

OSTEOCHONDRITIS DISSECANS INTRODUCTION Osteochondritis is defined as an inflammation of both bone and cartilage. Osteochondritis dissecans is described as osteochondritis resulting in the splitting of pieces of cartilage into the joint (in Dorland’s Medical Dictionary). The term osteochondritis dissecans was given to this condition by Franz Konig in 1889, who described a knee condition that appeared to suggest a subchondral inflammatory process that dissected a fragment of cartilage from the

Chapter 19 Osteochondritis Dissecans

289

FIGURE 19-1

A, Anteroposterior view of the right elbow of a 9-year-old boy shows involvement of the entire capitellum in alternating irregular areas of sclerosis and patchy rarefaction. B, The lateral view shows osteochondrosis.

femoral condyle, leading to formation of a loose body.20 Although no inflammatory process has ever been shown to produce such lesions, the name has remained. Osteochondritis dissecans of the capitellum is similar to osteochondritis dissecans in other joints, such as the knee. It involves localized avascular necrosis of subchondral bone and subsequent loss of structural support for the adjacent articular cartilage. Compared with the knee, however, osteochondritis of the capitellum is much less common. Only 6% of patients with osteochondritis dissecans have elbow involvement.41 Because osteochondritis dissecans occurs after the capitellum has almost completely ossified (early adolescence), it should not be confused with osteochondrosis of the capitellum, nor is it due to an “inflammation,” in spite of the definition of osteochondritis cited earlier.41 Osteochondrosis dissecans and osteonecrosis of the capitellum have been suggested as more appropriate terms, but are rarely used today. From a practical standpoint, the localized area of osteochondritis, consisting of articular cartilage and underlying bone, either remains in situ and eventually heals or separates from the capitellum and becomes a loose body in the joint. Osteochondritis dissecans is one of several conditions that can cause “Little League elbow” in immature baseball players.38

CLINICAL CHARACTERISTICS Elbow pain, the most common complaint, is usually dull, poorly localized, and aggravated by use, particularly by athletic endeavors that involve throwing or weight bearing on the upper extremity. Use aggravates the condition and rest relieves it. Lateral elbow pain occurs in approximately 79% to 90% of patients.18,41 A second complaint, limitation of elbow motion, particularly extension, affects about 90% of patients. It is often associated with an effusion, and results in 5 to 20 degrees loss of elbow extension.18,41 Limitation of elbow flexion, pronation, and supination of the forearm also occur, but these problems are less common. Local tenderness over the lateral aspect of the elbow and crepitus with motion are other frequent complaints, but they are not as common as the dull pain and limited extension that occur with use. Later in the course of the disease, catching and locking of the elbow joint may be a prominent complaint; this usually represents separation of osseous or cartilage fragments.

RADIOGRAPHIC CHARACTERISTICS Anteroposterior and lateral radiographs of the elbow are useful and should be obtained in every case. Early in the disease, radiographic changes are most often con-

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fined to the capitellum.29 Rarefaction, irregular ossification, and a bony defect adjacent to the articular surface are frequent findings (Fig. 19-2). The crater of rarefaction in the capitellum usually has a sclerotic rim of subchondral bone adjacent to the articular surface. If the central fragment separates, one or more ossific loose bodies may be seen in the joint, and the articular surface of the capitellum may appear to be irregular or flattened, particularly on the lateral view. Only 30% of loose bodies can be seen on plain films.18 Computed tomography (CT) may be necessary to better define the bony anatomy (Fig. 19-3). MRI is the preferred imaging technique for assessing the extent of osteochondritis. MRI is also the best study to assess the integrity of the articular surface and the displacement of osteochondral fragments. Unstable lesions reveal fluid surrounding the osteochondral fragment on T2-weighted images (Fig. 19-4).8 Several other late radiographic changes are worth noting. As degenerative changes occur, the radial head enlarges. Klekamp described seven patients who had developmental dislocations of the radial head as a result of osteochondritis dissecans of the capitellum (Fig. 19-5).15 The cause-and-effect relationship is obscure. In a few instances, premature distal humeral physeal arrest is evident. Late in the course of disease, degenerative changes characterized by irregularity and incongruity of both the capitellar and radial head articular surfaces are evident; these changes are the most important late sequelae of this condition. If sequestration does not occur, the central sclerotic fragment gradually becomes less distinctive, the surrounding area of rarefaction slowly ossifies, and the lesion heals without significant sequelae. This radiographic evidence of healing may take several years to occur and sometimes is not complete until adult life, long after pain, swelling, and limitation of motion have disappeared (Fig. 19-6A and B).

ETIOLOGY Most of the speculation about the cause of osteochondritis dissecans has been directed toward the condition as it occurs in the knee, not in the elbow. There are three possible causes of osteochondritis dissecans: ischemia, trauma, and “genetic predisposition.”

Ischemia Because the initial histologic appearance of the involved segment of subchondral bone is that of avascular necrosis, one of the most popular theories holds that some type of ischemic insult affects a localized area of subchondral bone.23 The ischemic theory is based primarily on the histopathologic characteristics of the lesion and the vascular anatomy of the distal humerus.

FIGURE 19-2

Tomograms of the right elbow of a 16year-old boy with osteochondritis dissecans. Note the rarefied crater adjacent to the capitellar articular surface (type I lesion).

Haraldsson11 has shown that the vascular supply to the distal humerus is limited in persons aged 5 to 19 years. One or two isolated vessels enter the epiphysis posteriorly, traverse the nonossified cartilaginous epiphysis, and supply the capitellum. No vessels from the metaphysis cross the physis. Because these end arteries supplying the capitellum pass through compressible epiphyseal cartilage, repetitive valgus loading of the elbow may injure the vessels and lead to avascular areas within the epiphysis.34 This theory forms the basis for pitching limitations for young baseball pitchers. The microscopic changes in the involved area of subchondral bone are typical of those seen in bone infarction due to interruption of the subchondral terminal arterial vessels. Initially, the articular cartilage is intact, and the cartilage cells of the most superficial layers continue to receive their nutrition from synovial fluid. Early in the course of disease, hyperemia and edema of the synovium and metaphysis contribute to the eventual overgrowth of the capitellum and the proximal radius. Reparative changes characterized by absorption of necrotic bone by vascular granulation tissue occur at the interface between the necrotic subarticular segment and the normal surrounding bone. At this stage, a typical zone of rarefaction can be seen on radiographs, around the periphery of the lesion. If the articular cartilage remains intact and the necrotic segment remains in situ, the avascular segment is eventually absorbed; it is replaced by viable osseous tissue, and the normal architecture of the articular surface is

Chapter 19 Osteochondritis Dissecans

A

291

B

FIGURE 19-3 A, Coronal CT of the left elbow with osteochondritis dissecans. Note the radiolucent defect in the capitellum. Sequestrum within the capitellar defect. B, Lateral CT shows the irregular capitellum, the sclerotic defect and the bony fragment (sequestrum) within the defect. C, Lateral CT shows intraarticular loose body in the olecranon fossa.

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preserved. This healing process may take several years. If, however, the articular cartilage is fractured during the initial stage of the disease, the necrotic segment may become detached and an intra-articular loose body can form.

Trauma

FIGURE 19-4

Lateral magnetic resonance imaging scan of the elbow with osteochondritis dissecans. There is a defect in the capitellum, sequestrum surrounded by joint fluid, posterior loose body, and an elbow effusion.

For nearly 100 years, trauma has been suggested as a cause of osteochondritis dissecans. Unfortunately, no experimental data support this or any other theory.17,27 A history of frequent repetitive overuse of the elbow is common in persons who have osteochondritis dissecans. Several authors have noted a relationship between osteochondritis dissecans and baseball pitching.1,4,37,40 The valgus compressive forces generated across the radiocapitellar joint during throwing are believed to induce changes in the distal humerus that lead to osteochondritis dissecans.14 Repetitive trauma also is thought to play a role in the development of the condition in adolescent gymnasts,13,34 who bear their entire body weight on their arms and thus expose their elbows to repetitive compressive forces. Repetitive trauma, particularly forceful extension and pronation of the elbow, creates compression and shearing forces that are transmitted by the radius to the adjacent articular surface of the capitellum. This trauma results in separation and infarction of an area of subchondral bone and the overlying articular cartilage. From a study of cadaver elbows, Schenck suggested that the mechanical disparity between a stiff radial head articulating with a less stiff capitellum produces strain during compressive stresses that can lead to osteochondritis dissecans.33

Genetic Factors Numerous but sporadic reports describe osteochondritis of the capitellum in one or in several generations of the same family.9,19,25,41 Osteochondritis dissecans has also been reported to occur in more than one joint in a given patient or in more than one family member. Neilson21 reported the incidence of osteochondritis dissecans to be 4.1 per 1000 men. Among male relatives of affected men, he found an incidence of 14.6%. In spite of these reports, there is no convincing evidence that osteochondritis dissecans of the capitellum is a heritable disease. Multiple epiphyseal dysplasia, which is a rare heritable condition, superficially has many features that are similar to those of this condition.7 Multiple epiphyses are involved. The clinical course and prognosis, however, are in no way similar.

TREATMENT FIGURE 19-5

Lateral view of the elbow in a 16-year-old boy with osteochondritis dissecans. Note the posterolateral subluxation of the radial head.

Treatment of osteochondritis dissecans is dictated by the clinical findings and the radiographic appearance of the lesion. Initial treatment is usually nonoperative:

Chapter 19 Osteochondritis Dissecans

293

FIGURE 19-6

A, Anteroposterior view of a type I lesion in a 14year-old boy with osteochondritis dissecans. B, Anteroposterior view made 1 1/2 years later. The zone of rarefaction surrounding the lesion is becoming less distinct, and the patient is asymptomatic.

limitation of activities and nonsteroidal anti-inflammatory medications. Rest and protection is continued for several weeks. If these methods fail, good results have been obtained with surgical management. Functional limitations are common. Routine radiographs, CT, and MRI may be necessary to determine whether the involved segment has been separated from the capitellum. If an osteochondral fragment is loose within the joint, the diagnosis can usually be made by clinical examination and routine radiographs. Arthroscopy is useful for removing loose bodies from the elbow joint and for treating the capitellar defect with curettage or drilling or microfracture. The condition of the articular surfaces can be visualized by arthroscopy as well.

Intact Lesions If the lesion is intact with no evidence of displacement from its normal site or of fracture of the articular cartilage, nonoperative treatment is indicated.27 The elbow should be rested and any vigorous use avoided. Application of ice and the use of a nonsteroidal antiinflammatory medication may relieve symptoms. A hinged elbow brace may be useful to limit activities.28 If pain is a significant complaint, the elbow should be splinted or placed in a cast for 3 to 4 weeks, after which active range-of-motion exercises are prescribed to preserve motion. Activity should be restricted for 6 to 8

weeks after symptoms have resolved. Radiographic changes should be stable or improving before the patient resumes activities. It is unreasonable to restrict all activities until radiographs are normal, because abnormalities can persist for years. When activities are allowed, they should be gradually “advanced” and modified if any symptoms recur. A history of locking or catching should prompt a search for loose or partially attached fragments.34 If symptoms persist but the articular cartilage remains intact, arthroscopic or open antegrade or retrograde subchondral drilling is considered. Patients with intact lesions treated nonoperatively generally do well.34,41 Most athletes can return to sports, with the exception of baseball pitchers and gymnasts, whose prognosis is more guarded.36,37 With longer follow-up, results are not as good. Takahara, with follow-up of 12 years, found that 50% had clinical and radiographic evidence of osteoarthritis.36

Partially Attached Fragments If radiographic evaluation or arthroscopic examination finds evidence of fracture or fissure of the articular cartilage or of partial detachment of the fragment, the surgeon has two choices: (1) to reattach the area of avascular bone surgically or (2) to excise the loose fragment.27 In this situation, as in the knee, a partially detached fragment can be pinned in situ with Kirschner wires,

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Herbert screws, or bioabsorbable implants13,16 under direct vision or arthroscopic control. In situ fixation of large, partially attached or hinged lesions may be useful in preventing complete detachment, loose body formation, and ultimate osteoarthritis.36 The additional value of repeated drilling of the fragment and its bony bed to stimulate revascularization and healing has never been conclusively established. In general, only limited success has been reported from attempts to pin partially attached articular fragments once the underlying bone is exposed.10

Completely Detached Fragments When the area involved with osteochondritis dissecans has completely detached from the capitellum and is lying free in the joint, the most effective treatment is to remove the fragment surgically, by arthroscopy or arthrotomy.2,13,16,27,34,41 Surgical indications include locking, symptomatic loose bodies, and failure of prolonged nonoperative treatment to relieve symptoms.18,37,41 Arthroscopic techniques using standard 4-mm instruments have been shown to be effective in evaluating and treating elbow disorders such as osteochondritis dissecans.2,10,13 Care must be taken to avoid complications such as nerve palsies.2,26 Most authors agree that the best short-term results are obtained with simple excision of the loose body. Removing the loose body is usually effective in relieving the patient’s pain and mechanical symptoms, although the range of motion may not increase. Late degenerative arthritis may still be the ultimate outcome in as many as 50%.36 Because of evidence that large defects can facilitate degenerative changes, many authors have advocated more complex procedures for such defects. These procedures include drilling, microfracture, fixation, autograft replacement, and autologous cell implantation. Unfortunately, there is little evidence and no long-term follow-up to show that these techniques can prevent the development of osteoarthritis. Procedures other than simple excision are commonly reported but not strongly supported by long follow-up in the literature.2,18,26,34,41 Ruch30 treated 12 elbows with arthroscopic débridement and reported 13 degrees more extension and improved symptoms in 11 elbows (92%) at 3-year follow-up. Curettage and drilling of the defect in the capitellar articular surface is advocated by many.5,12,13,18,31,35,37 The benefit of this approach is difficult to document. In at least two series, the results were no better after drilling, curettage, or trimming of the crater than after removal of the loose body and débridement alone.30,4` Results are worst with complex procedures involving open excision of the capitellum, bone grafting, and internal fixation of the loose fragment.37,41 Chondral resurfacing and osteochondral grafting procedures have been reported for osteochondritis dissecans of the elbow,

but numbers are too small and follow-up is too short to draw conclusions.22,32,39 Short-term postoperative results of arthroscopic loose body removal and débridement vary from series to series. The prognosis for returning to sports varies widely by report but is guarded, especially in throwing sports and gymnastics. McManama and colleagues found that 12 of 14 (86%) patients returned to competitive athletics without restrictions and that elbow range of motion increased 18 degrees after surgeons removed loose bodies, shaved chondral defects, and drilled multiple holes to promote revascularization.18 Tivnon and coworkers37 found a similar 21-degree improvement in range of motion after removal of loose bodies and curettage of the capitellum and improved function in 10 of 12 elbows. After removal of loose bodies, shaving, subchondral drilling, or a combination of these, Janarv and colleagues12 reported that all patients had fewer symptoms or no symptoms and improved elbow motion. Rupp and Tempelhof31 reported mixed results in six patients treated with loose body removal, drilling of the lesion, or débridement of the defect. Results were related to the degree of articular cartilage damage. Singer and Roy34 reported on five female gymnasts with osteochondritis dissecans of the capitellum; two required surgery to excise loose fragments. At 3-year follow-up, all but one had been able to return to competition. In a similar study of gymnasts, Jackson and colleagues found that only one of seven patients was able to continue competitive gymnastics.13 Byrd and Jones treated 10 elbows in adolescent baseball pitchers. All had improved pain but only 4 of 10 (40%) returned to their prior level of activity.6 Tivnon and coworkers37 reported similar (guarded) results among 12 baseball pitchers, only one of whom was able to throw at his prior level. The long-term prognosis for patients with osteochondritis dissecans of the capitellum depends on the patient’s age and on the size and extent of the lesion. Young patients have more favorable outcomes. Large defects that require surgery in older adolescents often progress to degenerative arthritis. Woodward and Bianco41 (with an average 12-year follow-up, range 2 to 34 years) suggest that most patients believed that they had normal use of their elbow. Bauer and colleagues3 suggest that osteochondritis dissecans of the capitellum leads to osteoarthritis in the majority of patients at longterm follow-up.

SUMMARY Osteochondritis dissecans of the capitellum is an uncommon problem that affects adolescents, especially those engaged in repetitive throwing and gymnastics.

Chapter 19 Osteochondritis Dissecans

Compressive forces at the radiocapitellar joint, along with a tenuous blood supply to the region, may contribute to the development of this condition. Most affected persons are adolescents, who initially note lateral elbow pain, loss of extension, and swelling. These symptoms are aggravated by activity and improve with 6 to 8 weeks of rest. Plain radiographs are usually sufficient to make the diagnosis, although CT, MRI, and arthroscopy may be necessary. It is important to distinguish osteochondritis dissecans from Panner’s disease, a benign, self-limited condition that affects the capitellum in younger children. Intact osteochondral lesions usually respond well to activity limitations. Many of these lesions heal, and the patients are able to return to activities. Failed nonoperative treatment or a symptomatic loose body is an indication for surgery, which should aim to remove loose fragments. Curettage of the defect or drilling of the subchondral bone may be useful, but this remains to be proved with long-term follow-up. The place for more complex surgical procedures such as internal fixation, osteochondral grafting, and autologous chondrocyte transplantation, remains to be determined. The shortterm prognosis is good, but a return to high-level competitive athletics involving throwing or gymnastic moves is not possible in many cases.

References 1. Albright, J. A., Jokl, P., Shaw, R., and Albright, J. P.: Clinical study of baseball pitchers: correlation of injury to the throwing arm with method of delivery. Am. J. Sports Med. 6:15, 1978. 2. Andrews, J. R., and Carson, W. G.: Arthroscopy of the elbow. Arthroscopy 1:97, 1985. 3. Bauer, M., Jonsson, K., and Josefsson, P. O.: Osteochondritis dissecans of the elbow. A long-term follow-up study. Clin. Orthop. 284:156, 1992. 4. Brown, R., Blazina, M. E., Derlan, R. K., Carter, V. S., Jobe, F. W., and Carlson, G. J.: Osteochondritis of the capitellum. J. Sports Med. 2:27, 1974. 5. Brownlow, H. C., O’Connor-Reid, L. M., and Perko, M.: Arthroscopic treatment of osteochondritis dissecans of the capitellum. Knee Surg. Sports Traumatol. Arthrosc. 14:198, 2006. 6. Byrd, J. W., Elrod, B. F., and Jones, K. S.: Elbow arthroscopy for neglected osteochondritis dissecans of the capitellum. J. Southern Orthop. Assoc. 10:12, 2001. 7. Clanton, T. O., and DeLee, J. E.: Osteochondritis dissecans. Clin. Orthop. 167:50, 1982. 8. Fritz, R. C., Steinbach, L. S., Tirman, P. F., and Martinez, S.: MR imaging of the elbow. An update. Radiol. Clin. North Am. 35:117, 1997. 9. Gardiner, J. B.: Osteochondritis dissecans in three members of one family. J. Bone Joint Surg. 37B:139, 1955. 10. Guhl, J. F.: Arthroscopy and arthroscopic surgery of the elbow. Orthopedics 8:1290, 1985.

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11. Haraldsson, S.: On osteochondrosis deformans juvenitis, capituli humeri including investigation of intraosseous vasculature in distal humerus. Acta Orthop. Scand. Suppl. 38:1, 1959. 12. Janarv, P. M., Hesser, U., and Hirsch, G.: Osteochondral lesions in the radiocapitellar joint in the skeletally immature: radiographic, MRI, and arthroscopic findings in 13 consecutive cases. J. Pediatr. Orthop. 17:311, 1997. 13. Jackson, D. W., Silvino, N., and Reiman, P.: Osteochondritis in the female gymnast’s elbow. Arthroscopy 5:129, 1989. 14. King, J. W., Brelsford, H. S., and Tullos, H. S.: Analysis of the pitching arm of the professional baseball pitcher. Clin. Orthop. 67:116, 1969. 15. Klekamp, J., Green, N. E., and Mencio, G. A.: Osteochondritis dissecans as a cause of developmental dislocation of the radial head. Clin. Orthop. 338:36, 1997. 16. Kuwahata, Y., and Inoue, G.: Osteochondritis dissecans of the elbow managed by Herbert screw fixation. Orthopedics 21:449, 1998. 17. Lindholm, T. S., Osterman, K., and Vankka, E.: Osteochondritis dissecans of elbow, ankle, and hip. Clin. Orthop. 148:245, 1980. 18. McManama, G. B., Michel, L. J., Berry, M. V., and Sohn, R. S.: The surgical treatment of osteochondritis of the capitellum. Am. J. Sports Med. 13:11, 1985. 19. Mitsunaga, M. M., Adishian, D. O., and Bianco, A. J. Jr.: Osteochondritis dissecans of the capitellum. J. Trauma 22:53, 1982. 20. Naguro, S.: The so-called osteochondritis dissecans of Konig. Clin. Orthop. 18:100, 1960. 21. Neilson, N. A.: Osteochondritis dissecans capituli humeri. Acta Orthop. Scand. 4:307, 1933. 22. Oka, Y., and Ikeda, M.: Treatment of severe osteochondritis dissecans of the elbow using osteochondral grafts from a rib. J. Bone Joint Surg. 83B(5):738, 2001. 23. Omer, G. E. J.: Primary articular osteochondroses. Clin. Orthop. 158:33, 1981. 24. Paes, R. A.: Familial osteochondritis dissecans. Clin. Radiol. 40:501, 1989. 25. Panner, H. J.: A peculiar affection of the capitellum humeri, resembling Calve-Perthes disease of the hip. Acta Radiol. 8:617, 1927. 26. Papilion, J. D., Neff, R. S., and Shall, L. M.: Compression neuropathy of the radial nerve as a complication of elbow arthroscopy: a case report and review of the literature. Arthroscopy 4:284, 1988. 27. Pappas, A. M.: Osteochondritis dissecans. Clin. Orthop. 158:59, 1981. 28. Peterson, R. K., Savoiem, F. H. 3rd, and Field, L. D.: Osteochondritis dissecans of the elbow. Instr. Course Lect. 48:393, 1999. 29. Roberts, N., and Hughes, R.: Osteochondritis dissecans of the elbow joint: a clinical study. J. Bone Joint Surg. 32B:348, 1950. 30. Ruch, D. S., Cory, J. W., and Poehling, G. G.: The arthroscopic management of osteochondritis dissecans of the adolescent elbow. Arthroscopy 14:797, 1998. 31. Rupp, S., and Tempelhof, S.: Arthroscopic surgery of the elbow. Therapeutic benefits and hazards. Clin. Orthop. 313:140, 1995.

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32. Sato, M., Ochi, O., Uchio, Y., Agung, M., and Baba, H.: Transplantation of tissue-engineered cartilage for excessive osteochondritis dissecans of the elbow. J. Shoulder Elbow Surg. 13:221, 2004. 33. Schenck, R. C., Athanasiou, K. A., Constantinides, G., and Gomez, E.: A biomechanical analysis of articular cartilage of the human elbow and a potential relationship to osteochondritis dissecans. Clin. Orthop. 299:305, 1994. 34. Singer, K. M., and Roy, S. P.: Osteochondrosis of the humeral capitellum. Am. J. Sports Med. 12:351, 1984. 35. Smillie, I. S.: Osteochondritis Dissecans: Loose Bodies in Joints; Etiology, Pathology, Treatment. Edinburgh, E. & S. Livingstone, 1960. 36. Takahara, M., Ogino, T., Sasaki, I., Kato, H., Minami, A., and Kaneda, K.: Long term outcome of osteochondritis

37.

38. 39.

40.

41.

dissecans of the humeral capitellum. Clin. Orthop. 363:108, 1999. Tivnon, M. C., Anzel, S. H., and Waugh, T. R.: Surgical management of osteochondritis dissecans of the capitellum. Am. J. Sports Med. 4:121, 1976. Torg, J. S.: Little League: the theft of a carefree youth. Physician Sports Med. 1:72, 1973. Tsuda, E., Ishibashi, Y., Sato, H., Yamamoto, Y., and Toh, S.: Osteochondral autograft transplantation for osteochondritis dissecans of the capitellum in non-throwing athletes. Arthroscopy 21:177.e1, 2005. Tullos, H. S., Erwin, W. D., Woods, G. W., Wukasch, D. C., Cooley, D. A., and King, J. W.: Unusual lesions of the pitching arm. Clin. Orthop. 88:169, 1972. Woodward, A. H., and Bianco, A. J. Jr.: Osteochondritis dissecans of the elbow. Clin. Orthop. 110:35, 1975.

Chapter 20 Dislocations of the Child’s Elbow

CHAPTER

20

Dislocations of the Child’s Elbow R. Merv Letts and Bernard F. Morrey

INTRODUCTION Dislocation of the elbow in children is the most common childhood dislocation, constituting about 6% to 8% of elbow injuries.72,118 In general, however, because the attachments of ligaments and muscles are stronger than the adjacent growth plate, forces exerted about most joints tend to result in epiphyseal injury rather than simple dislocation of the adjacent joint. The elbow is unique in children because type I and II fractures through the distal humeral epiphysis are uncommon; hence, the finding for dislocation. The purpose of this chapter is to discuss the practical aspects of the cause, recognition, and the management of dislocations about the elbow joint in children. Because the elbow is the most common joint injured in childhood, the chapter on imaging (see Chapter 12) and chapters dealing with images of other conditions (see Chapters 14 to 18 and 21) should be carefully studied.

ANATOMIC FACTORS PREDISPOSING TO ELBOW DISLOCATION IN CHILDREN Although the anatomy of the elbow joint was thoroughly discussed in Chapter 2, it is important to emphasize some of the anatomic differences that are unique to the pediatric elbow joint.

GROWTH PLATES, APOPHYSIS, AND SECONDARY CENTERS OF OSSIFICATION To a casual observer, the radiograph of a child’s elbow is an enigma—no two ever seem alike. The reason for this, of course, is that because the child is constantly growing, ossification centers are appearing and fusing, and cartilage is calcifying progressively until skeletal maturity is attained. It is important to emphasize that there is usually a normal contralateral control that can be radiographed and compared with the radiograph of the injured

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elbow. This is not recommended as a routine practice, but sometimes it is necessary and useful, especially for those who treat elbow injuries in children only occasionally. In general, the younger the child at the time of injury, the more difficult it is to assess the elbow, owing to the larger percentage of cartilage that is present about the elbow joint. Fortunately, new imaging modalities allow more accurate assessment.7,8 Yet, in the newborn or infant, it may be very difficult to diagnose an elbow injury or to determine whether it is a transcondylar fracture or a dislocation of the elbow (the former being much more common at this age). The ossific nuclei about the elbow joint are helpful in radiologic interpretation of elbow dislocation (see Chapter 12). The capitellum, whose center of ossification should be present by 6 months of age, facilitates the interpretation of radial head alignment, because a line drawn through the radial head should always intersect the capitellum no matter what view is taken (Fig. 20-1). This interpretation is improved even further with the appearance of the radial head secondary center of ossification, at around 5 years of age. The secondary center of ossification of the olecranon, which appears at about 9 years of age, allows a more accurate assessment of the position of the proximal ulna in relation to the distal humerus, an important consideration in the management of dislocations of the elbow in young children. Both the medial and the lateral apophyses of the distal humerus may be injured in dislocations of the elbow in a child. Although many mnemonics have been devised by residents trying to remember the timing of ossification of the various centers about the elbow, the most important center to remember from a practical standpoint is the medial epicondylar apophysis of the distal humerus. This center is usually present by the age of 5 to 6 years, and because it is frequently entrapped within the joint following a dislocation of the elbow, it should always be searched for and identified after this age. Hence, if the center cannot be identified, it should be assumed that it is within the joint itself. In children younger than the age of 5 years, the diagnosis of entrapment must be clinical or by arthrography, because the apophysis is entirely cartilaginous. The lateral epicondylar apophysis is injured less frequently. In posteromedial dislocations, it may suffer avulsion, owing to a severe varus strain on the elbow and may need to be repaired or fixed surgically.5

ELBOW FLEXIBILITY In children younger than 10 years of age, elbow stability is provided almost entirely by cartilage. Because of this, there is considerable flexibility in the elbow joint in children. It is not unusual for a child to be able to

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dromes,111,119 ligamentous laxity is enhanced and stability is accentuated.

OLECRANON The ulnohumeral joint provides the greatest articular stability in the elbow joint. In children, the coronoid process, which provides anterior stability resisting posterior dislocation of the ulna, is not well developed until about 12 years of age. Even at this age, the coronoid process is largely cartilaginous and, when stressed, is yielding and resilient. Similarly, the olecranon itself is a largely cartilaginous structure until the early teenage years. Neither the coronoid nor the olecranon fossa of the distal humerus is well developed until later in childhood, and they do not contribute as effectively to the “locking in” phenomenon in flexion and extension that occurs with well-ossified coronoid and olecranon processes.

RADIAL HEAD AND NECK

FIGURE 20-1

A, A line drawn through the middle of the neck and head of the radius must always pass through the capitellum in every view. B, If it does not, dislocation of the radial head is present.

hyperextend the elbow joint by 10 or 15 degrees and to have a much greater degree of laxity than is seen in an adult or even an adolescent. It is this combination of hyperflexibility and a lack of osseous stability in a joint subjected to considerable trauma that predisposes the elbow joint to dislocation. The major stabilizing ligaments on the medial and lateral sides are attached to the distal humerus through apophyses—structurally weak areas that are prone to avulsion with subsequent loss of joint integrity. In the many syndromes and conditions such as Ehlers-Danlos and cutis laxa syn-

The radial head and neck in children are cartilaginous but have the same relative diameters as the radial head and neck in adults. Dislocation of the radial head, either as an isolated event or in association with a Monteggia fracture, or with dislocation of the elbow joint itself, is facilitated by the resiliency of the cartilaginous component. Children’s bones have plasticity and can be bent like the proverbial greenstick without fracturing. In the type A Monteggia lesion, for instance, it is conceivable that the ulna bends to the point of fracture, whereas the radius only bends to the point at which the radial head slips under the annular ligament and dislocates anteriorly (Fig. 20-2). It is of interest to note that in most cases requiring open reduction of the radial head, the annular ligament is actually intact. A similar situation may be found with the traumatic isolated dislocation of the radial head that occurs in very young children in which the radius bends just enough for the head and neck to slip under the annular ligament (called nursemaid’s elbow). When trauma is less severe, as in a pulled elbow, the head of the radius has simply slipped into the annular ligament, and there is no actual dislocation. A supination maneuver “screws” the radial head out of the annular ligament, usually with no actual damage to the ligament itself. This combination of generalized laxity, the large cartilaginous component, the lack of osseous stability, and the presence of osseous plasticity as well as numerous secondary centers of ossification and apophyses all contribute to the anachronism of a greater tendency of dislocation of the pediatric elbow joint than seen with other joints.

Chapter 20 Dislocations of the Child’s Elbow

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FIGURE 20-2

Annular ligament reconstruction using forearm fascia (Boyd technique).

TYPES OF DISLOCATION OF THE RADIAL HEAD CONGENITAL DISLOCATION Congenital dislocation of the radial head is a controversial lesion, because some maintain this lesion does not exist at all and all such appearances are simply traumatic or developmental dislocations. This subject is discussed in more detail in Chapter 13. Here, I reserve the diagnosis of congenital dislocation for that entity in which congenital malformation of the extremity is obvious (Fig. 20-3). When isolated dislocation of the radial head is not accompanied by other congenital lesions, the congenital basis for the lesion cannot be substantiated. The long-standing nature of the dislocation can be inferred from the marked convexity of the radial head associated with elongation of the radial neck (Fig. 20-4).27,28 Congenital dislocation of the radial head may be associated with radioulnar synostosis, the synostosis almost always occurring between the proximal radius and the ulna.32-36 Hypoplasia of the capitellum associated with dislocation of the radial head strongly suggests that the dislocation is congenital. The radiologic appearance of congenital dislocations of the radial head has been emphasized by Miura.37 In congenital dislocations, the posterior border of the ulna is usually concave rather than slightly convex, with the radial head being dome-shaped with no central depression (see Fig. 20-3). Posterior congenital dislocation, which constitutes about 40% of congenital dislocations of the radial head, is associated with an accentuation of the normal convexity of the posterior

border of the ulna. In fact, because we have not been able to diagnose this pathology, at best, we consider this a developmental problem.28

DEVELOPMENTAL DISLOCATION Many instances of developmental or secondary dislocation of the radial head are misinterpreted as being congenital in origin.28 Developmental dislocation is defined as any dislocation of the radial head that results from maldevelopment of the forearm. There are many inherited and acquired disease processes affecting the growth plate of the forearm bones that result in asymmetric growth between the radius and the ulna and subsequent dislocation of the radial head. These include the nail patella syndrome, Silver syndrome, arthrogryposis, Cornelia de Lange syndrome, and cleidocranial dysostosis. Asymmetric growth also occurs in multiple exostoses or diaphyseal aclasis. The ulna is most frequently affected at the distal ulnar growth plate; the radius then overgrows relative to the ulna (Fig. 20-5). Paralysis of the muscles innervated by the C5-6 nerve root, as in a nerve root palsy, also predisposes to a gradual dislocation of the radial head that occurs over a number of years of growth or occasionally in infancy.17 Cerebral palsy also may produce isolated dislocation of the radial head through marked spasticity of the muscles attached to the radius (Fig. 20-6).21 Trauma to the radius or the ulna, resulting in asymmetric growth, may also produce dislocation of the radial head. Fracture of the neck of the radius that has not been corrected adequately may result in the proximal radial epiphysis growing laterally instead of toward the capitellum (Fig. 20-7).20-26

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FIGURE 20-3

A and B, Congenital dislocation of the radial head associated with other congenital malformations of the forearm. Note the rounded convexity of the radial head.

A detailed developmental posterior study at the Mayo Clinic describes several grades, or types, of radial head dislocation with characteristic radiographic appearance (Fig. 20-8). Types II and III are complete dislocations and are more obvious cosmetically but have relatively little functional loss except forearm rotation.28 Type I dislocations commonly are associated with late degenerative arthrosis and consist more of a subluxation than a frank dislocation. However, consistent with the definition of forearm maldevelopment, all types have a previous proximal ulnar bow. There are few indications for operative treatment of developmental dislocation of the radial head. For example, a malunion of the radius and the ulna that is obviously directing the head of the radius laterally, posteriorly, or anteriorly should be corrected with an osteotomy to redirect the proximal radius or the deformed ulna19; otherwise, excision of the radial head can be effective to improve motion, lessen pain, or to improve cosmesis. In patients with cerebral palsy, if the bicipital tendon appears to be subluxating the radial head anteriorly, lengthening the biceps may prevent future dislocation.

Once the dislocation is well established, attempts to relocate the radial head probably should not be made, and the dislocation should be accepted. Future resection of the radial head at skeletal maturity can be performed if the head is cosmetically or functionally a problem. The gradual nature of the dislocation and adjacent changes in the surrounding tissues and bone make this type of relocation of the radial head much more difficult than the acute traumatic injury.26 Relocation of the radial head by shortening the radius and reconstitution of the annular ligament is ineffective.

RADIOGRAPHIC APPEARANCE The radiographic appearance of a long-standing dislocated radial head is characterized by a rounded contour or convexity in contrast to the normal concave appearance (see Fig. 20-4). The posterior border of the ulna also may be concave rather than slightly convex in anterior dislocations of the radial head. Posterior dislocations result in a longer neck with a typical

Chapter 20 Dislocations of the Child’s Elbow

a. Concave head Recent dislocation

b. Convex head Congenital or longterm dislocation

C FIGURE 20-4 Developmental or long-standing dislocation of the radial head. A, Note the rounded appearance of the head, convexity of the articular surface, and narrow neck typical of this deformity. B, Opposite normal elbow. C, Convexity of head develops if the radius is not in contact with the capitellum.

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FIGURE 20-5

A to D, Dislocation of the radial head posterolaterally in a patient with multiple exostoses.

dome-shaped head. Even an isolated traumatic dislocation of the radial head, when it occurs in a very young child, may take on the appearance of a congenital or developmental dislocation with the passage of time. A relative increase in ulnar length in relation to the radius and the wrist is often noted. With posterior dislocation, proximal ulnar bowing also is prominent, and proximal radial migration of the radius may be present.28 The capitellum may be hypoplastic or, occasionally, even absent.38 Other factors characteristic of congenital or developmental radial head dislocations have been reported to be bilaterality of involvement,28 association with other congenital anomalies, familial occurrence, absence of traumatic history, and the presence of the entity in a patient younger than 6 months of age17-24 (see Chapter 13).

NATURAL HISTORY Developmental dislocation of the radial head seldom causes severe pain with anterior dislocation. Patients may complain of clicking or impingement at the ulnohumeral joint with flexion of the elbow. In our experience, this is not seen until adolescence or adulthood.

Posterior dislocation of the radial head typically creates a cosmetic protuberance that also may be a source of pain with excessive elbow motion.28 Aching in the region of the dislocation is common in the older child. A prominent ulna at the wrist and the resultant radioulnar subluxation at the distal end may result in some limitation of motion at the wrist, but discomfort is uncommon. There does not appear to be any progressive loss of motion with further growth, and the joint limitation, if present, remains static.20,28

TRAUMATIC DISLOCATION Solitary dislocation of the radial head is uncommon but occurs much more frequently in younger children. It is essential to differentiate this entity from a developmental dislocation of the radial head that typically is diagnosed incidentally when assessing a minor elbow injury. The history is of limited value in these cases because these children are often young, prone to frequent elbow injuries, and unable to make a reliable contribution to the history. The radiograph, however, is usually diagnostic because it shows the rounded concave appearance of the radial head in the congenital or developmental dislocation (see Fig. 20-4).1-16

Chapter 20 Dislocations of the Child’s Elbow

C FIGURE 20-6

A and B, Long-standing dislocation of the radial head in a child with cerebral palsy. The elongation of the neck and convexity of the head indicate the presence of a prolonged dislocation. C, Spasticity or contraction of the biceps tendon may contribute to isolated dislocation of the radial head in children.

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TREATMENT OF ACUTE ANTERIOR DISLOCATION CLOSED REDUCTION If the child is seen within 3 weeks of the injury, a closed reduction may be achieved. Direct pressure over the radial head with gradual flexion of the arm and immobilization in a flexed position of more than 100 degrees is usually successful. If the radial head has been dislocated for several weeks and if the annular ligament has become entrapped, preventing adequate reduction, an open reduction may have to be performed. If the radial head can be reduced but is not stable, a Kirschner wire fixation to the ulna may be effective. Driving a pin across the elbow joint through the capitellum and into the radial head is not recommended because these wires often break, making removal difficult. Breakage occurs because it is virtually impossible to immobilize the child’s elbow completely, and minor motion, even when in a cast, may result in a fatigue fracture of the wire. The elbow joint will then have to be opened unnecessarily to remove the fractured pin. FIGURE 20-7

A and B, A child sustained a fracture of the ulna and neck of the radius that healed in malunion. Four years later, the radial head is dislocating laterally owing to malposition of the proximal radial epiphyseal plate.

CLINICAL FEATURES OF ISOLATED ANTERIOR DISLOCATION With trauma, children who have sustained an anterior dislocation of the radial head demonstrate an unwillingness to use the arm. Careful examination of the extremities and the radiograph may reveal some ulnar bowing. This is analogous to a Monteggia fracture-dislocation except that the ulna is simply bowed rather than fractured. Radiographically, a line drawn through the shaft of the radius and the radial head will not intersect the capitellum when the radial head is dislocated (see Fig. 20-1). Children who have been subjected to child abuse may present with this particular injury, and again, the history will be difficult to elicit.

OPEN REDUCTION Triceps Fascial Reconstruction The technique of open reduction of an anterior dislocation of the radial head in children described by LloydRoberts and Bucknill20 is one I have used with success. This consists of using the lateral portion of the tendon of the triceps for reconstruction of the annular ligament (Fig. 20-9A). A posterolateral incision is preferred rather than a posterior incision, which may disorient the surgeon to the position of the radial head. The triceps tendon is identified, and a long (10-cm) strip is removed from the lateral margin, ensuring attachment at the distal ulnar insertion. The tendon is increased in length by continuing the dissection through the periosteum to a point opposite the neck of the radius, where it is then passed around the neck and sutured to itself and the ulnar periosteum with enough tension to hold the radial head in place. A Kirschner wire is then passed through the ulna into the radius to ensure solid fixation until the tendon has healed (see Fig. 20-9B).18 The extremity is kept immobilized in an above-elbow plaster cast for 6 weeks; gradual mobilization is begun at 6 weeks after the Kirschner wire has been removed. If there is any difficulty in reducing the radial head, careful inspection of the joint capsule may reveal some infolding or tissue interposition, which may have to be excised.

Chapter 20 Dislocations of the Child’s Elbow

I

A

II

B

III

C FIGURE 20-8

The Mayo classification of posterior radial head instability. A, Type I is subluxation with characteristic radial head elongation and is associated with a poor functional result. B, Type II is complete dislocation but without subluxation. These patients typically have minimal pain but moderate loss of forearm rotation. Forearm prominence may be noticed C, Dislocation with posterior subluxation, type III, causes a marked cosmetic deformity but little functional impairment. Surgery is performed only for cosmetic reasons.

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X A

B

FIGURE 20-9

A, Repair of radial head dislocation by reconstruction of annular ligament using triceps fascia (Lloyd Roberts-Bucknill technique). B, A Kirschner wire passed through the capitellum into the radial head (left) is not recommended owing to danger of pin fatigue and breakage. The radial head can be safely held in the reduced position by a pin across the radius and ulna (right).

Specific care must be exercised when exposing the neck of the radius in a child. Unlike the adult, the radial nerve may be only a fingerbreadth below the head of the radius rather than the classic two fingerbreadths that is often referenced.

Fascial Reconstruction of the Annular Ligament If inadequate, the annular ligament may be reconstructed. A strip of fascia is dissected from the forearm muscles but is left attached to the proximal ulna. The length of this fascial strip should be about 5 inches by 1/2 inch. It is passed around the neck of the radius, proximal to the tuberosity and distal to the radial notch of the ulna, and is brought around and fastened to itself with nonabsorbable sutures (see Fig. 20-9). Care should be taken to ensure that the length of this fascial strip is adequate. Cross-radioulnar pin fixation for 4 weeks is reassuring.

UNTREATED ANTERIOR DISLOCATION OF THE RADIAL HEAD A child with a long-standing anterior dislocation of the radial head actually may have good elbow function. The range of motion is usually functional, although the extremes of flexion and extension are usually limited by 20 or 30 degrees. In our experience, pain may develop at a later date, usually the fourth decade. The cosmetic deformity is also a concern, and the elbow may appear somewhat deformed, especially in a small, thin arm. Excision of the radial head at skeletal maturity is generally successful, and the radius does not migrate proximally.

COMPLICATIONS Relocation of an acute dislocation of the radial head in a child is usually successful, and recurrence is uncommon. If not reduced, limited motion and cosmetic deformity ensue. The dislocated radial head may also result in a relative shortening of the radius compared with the ulna, with subsequent subluxation at the radioulnar joint at the wrist. As a general rule, the radial head should not be excised in a child because this may further aggravate shortening of the radius by eliminating the proximal radial growth plate, which contributes about 30% of the final radial length. If there is pain or a grotesque appearance when the child is near skeletal maturity, the radial head is easily removed. In neglected patients, excision of the radial head may allow improved flexion and rotation and may alleviate complaints of pain and discomfort.28

PEDIATRIC MONTEGGIA FRACTURE DISLOCATION The Monteggia injury is uncommon in children but by no means rare. In the 5-year period from 1978 to 1982 at the Winnipeg Children’s Hospital, 33 children were treated for a variety of Monteggia lesions. The true incidence of this fracture-dislocation is unknown, but it is more common than is generally appreciated. Olney and Menelaus53 reported 102 children with acute Monteggia lesions over a 25-year period.

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307

ETIOLOGY The most common cause of dislocation of the radial head associated with an ulnar fracture in childhood is a hyperextension injury,44,62 followed by a hyperpronation injury.45 In hyperpronation, Bado39 pointed out that the bicipital tuberosity is posterior, thus predisposing the proximal radius to the greatest force during violent contraction of the bicipital tendon. In young children, the force generated by the biceps is less than that in the adult, and this mechanism probably is significant only in older children. A direct blow over the posterior proximal ulna will produce a Monteggia lesion with anterior dislocation of the radial head, but this is an uncommon mechanism in children. In our experience, this lesion is most frequently produced by a hyperextension injury. Further support for this theory is the observation that, in open type C injuries, the proximal ulnar fragment pierces the skin on the volar ulnar aspect of the forearm. This would not be possible if the arm were in full pronation because of imposition of the radius. Because of the plasticity of the forearm bones, the radial head and neck may slip under the annular ligament and dislocate as the shaft of the radius bends. Indeed, many of the isolated traumatic dislocations of the radial head are undoubtedly variations of the Monteggia46-48 (Monteggia equivalent), in which the ulna has simply bent but not fractured. The radial shaft is bent to the extent that the head and neck are slipped from within the annular ligament, resulting in an apparent isolated dislocation of the radial head.30,43

CLASSIFICATIONS Classifications of the Monteggia lesion are based largely on the injury in adults39 (see Chapter 27). Because of differences in the configuration of the injury in childhood, the following pediatric classification is suggested to include dislocation of the radial head associated with the plasticity of the forearm bones in childhood (Fig. 20-10).

CLASSIFICATION OF PEDIATRIC MONTEGGIA LESIONS Type A: Anterior dislocation of the radial head anterior bowing of the ulna (Fig. 20-11). Type B: Anterior dislocation of the radial head greenstick fracture of the ulna (Fig. 20-12). Type C: Anterior dislocation of the radial head transverse fracture of the ulna (Fig. 20-13). Type D: Posterior dislocation of the radial head bending or fracture of the ulna (Fig. 20-14).

with with with with

A Anterior bend

B Anterior greenstick

C

Anterior complete

E

Lateral

D Posterior

FIGURE 20-10 Classification of the pediatric Monteggia fracture dislocation: types A through E.

Type E: Lateral dislocation of the radial head with fracture of the ulna (Fig. 20-15). Types B and C are the most commonly encountered Monteggia lesions in children.51

CLINICAL DIAGNOSIS Like Monteggia himself, who described this injury initially in a young woman in 1814, long before the advent of radiography, most physicians today should be able to identify the clinical configuration in those seen early, before swelling has occurred (see Fig. 20-15). The dislocation of the radial head is often evident on inspection of the lateral aspect of the elbow joint. Angulation of the ulna, whether fractured or not, necessitates careful appraisal of the position of the radial head. Dislocation of the radial head is frequently missed by those who treat pediatric elbow injuries only occasionally.52-58 A line drawn through the shaft and the neck of the radius should intersect the capitellum in all views taken (see

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FIGURE 20-11 A and B, Ulnar bend with lateral dislocation of the radial head, a type A Monteggia fracture dislocation.

FIGURE 20-12 A and B, Type B Monteggia fracture associated with a greenstick fracture of the ulna and anterior dislocation of the radial head.

Chapter 20 Dislocations of the Child’s Elbow

Fig. 20-1). If it does not, dislocation of the radial head is highly suspect. In contrast to the lesion in adults, overlap of the ulnar fragments is not a prerequisite for dislocation of the radial head in a child. Disruption of the forearm parallelogram may occur as a result of ulnar bend when the radial head slips out of the annular ligament. It is wise

FIGURE 20-13 Anterior dislocation of the radial head with transverse fracture of ulna.

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to obtain anteroposterior and lateral views of the elbow joint in all fractures of the ulna. The apex of the ulnar bend or angulation is always in the direction of the radial head dislocation.51-65

TREATMENT In contrast to the adult, the Monteggia injury in children usually can be treated by closed methods.31 Pressure directed over the dislocated radius usually will result in a stable ulnar reduction, provided that immobilization is imposed with the elbow flexed more than 90 degrees in types A, B, C, and E lesions. Supination assists in minimizing biceps pull. In the uncommon type D Monteggia lesion with posterior dislocation of the radial head, stability is obtained with extension, not flexion, of the elbow. As long as the radial head is reduced and stable, angulation of the ulna of as much as 15 degrees can be accepted. Remodeling of this angulation will occur with further growth. In children, stable reduction of the radial head is the first priority. A supination-pronation maneuver may facilitate repositioning of the annular ligament, which is seldom completely torn. If it is impossible to obtain a stable reduction of the radial head, I approach the radial head through a Kocher incision and reapproximate the annular ligament around

FIGURE 20-14 A and B, Posterior lateral dislocation of the radial head with bending or fracture of the ulna.

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the neck. If stability is still precarious or if the annular ligament has had to be reconstituted, I recommend internal fixation of the radius to the ulna with a Kirschner wire (Fig. 20-16A). As noted earlier, I would caution against maintenance of the reduction by a wire inserted through the capitellum and into the radial head. Fatigue fracture is always a possibility (see Fig. 20-8B). If the ulna is unstable in the older child, an open reduction with plate fixation may be necessary, but in my experience, this is seldom required in those under 10 years of age.58

NERVE INJURY ASSOCIATED WITH MONTEGGIA LESIONS Anterior dislocation of the radial head may result in a traction injury to the posterior interosseous nerve as it passes dorsolaterally around the proximal radius to enter the substance of the supinator muscle mass between the superficial and deep layers (see Fig. 20-16B).46,60 Compression of the posterior interosseous nerve also may be aggravated by the fibrous arcade of Frohse, a firm fibrous band at the proximal edge of the supinator muscle.59 In children, nerve injury is less common than in adults, and recovery is the rule in closed injuries. In a large series of 102 Monteggia fractures, Olney and Menelaus53 found a 10% incidence of nerve injuries, 6% involving the posterior interosseous nerve and 3% involving the radial nerve. All their nerve injuries healed completely within 6 months.

THE MISSED MONTEGGIA LESION

FIGURE 20-15 Monteggia fracture with lateral dislocation of the radial head. A, Clinical appearance. B and C, Radiologic appearance.

The dislocated radial head that is noticed only after the ulna has healed is a common error made by less experienced clinicians and in some instances the initial injury has almost been forgotten (see Fig. 20-16D). Some confusion may occasionally arise in connection with the congenital dislocated radial head, but in general, the contour of the radial head should be diagnostic— the congenital lesion having a rounded convex head whereas the recently dislocated radius usually has a concave appearance. It can be appreciated that the younger the child, the more difficult it will be to make this interpretation, owing to the large cartilaginous component of the proximal radius.40-44,46,50

DISLOCATION-SUBLUXATION OF THE RADIAL HEAD FOLLOWING MALUNION OF A RADIAL NECK FRACTURE Fractures of the radial neck in children that have occurred after the age of 6 or 7 years may, if unreduced, result in

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311

C FIGURE 20-16 A and B, Preferred radioulnar pinning to hold the radial head in place subsequent to late open reduction of a Monteggia fracture dislocation and annular ligament repair. C, Injury to the posterior interosseous nerve may occur in the Monteggia fracture with anterior dislocation of the radial head. D, Missed dislocation of the radial head in an unappreciated Monteggia fracture with greenstick fracture of the ulna.

a subluxation (see Fig. 20-7). When neck angulation is more than 45 to 50 degrees, the growth plate becomes redirected laterally or posterolaterally. If there is not enough remodeling to allow the growth plate to reattain its normal transverse anatomy, increased prominence of the radial head ensues. As the child grows, pain may be experienced, as well as irritation, cosmetic deformity, and, to a lesser extent, limitation of supination and pronation. This can be avoided by ensuring that the angulation of the radial neck is reduced to less than 45 degrees by closed or open reduction.63

When associated with malunion of the ulna radial head, instability may necessitate osteotomy of the ulna and open reduction of the radial head. It is of course always prudent to attempt a closed reduction of the radial head if the injury has occurred recently (i.e., within 2 months) because the ulna may still be straightened. Usually, however, in the missed Monteggia lesion, an open reduction of the radial head will be necessary, and in this instance, it will almost certainly be necessary to reconstitute the annular ligament—with the ligament itself, if possible, with fascia obtained from the triceps,

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or by using the Bell-Tawse procedure.42,44,49 Shortening of the radius may be necessary to permit reduction. Internal fixation with Kirschner wires through the radius to the ulna is advisable. Relocation of the radial head should be attempted in children younger than 6 years of age.18 In older children in whom the lesion has been present for more than 1 year, it may be advisable to accept the dislocation because this is compatible with excellent function in most instances. A modified technique for reconstruction of the annular ligament has been reported by Peterson and Seel,56 which appears effective in patients with long-standing radial head dislocations. If the radial head becomes cosmetically or functionally disabling, excision is performed as needed when skeletally mature. Removal of the radial head is avoided until skeletal maturity since 30% of radial growth occurs at the proximal radial epiphysis.

PULLED ELBOW SYNDROME Nursemaid’s elbow, or pulled elbow syndrome, has been recognized since early in this century.124 Some children seem to be particularly prone to this injury, and for them, even minor pulls on the arm result in the typical pain and failure of elbow motion that is always of concern to parents (Fig. 20-17A).123,124

ETIOLOGY Subsequent to a longitudinal pull on the forearm, the radial head is pulled down into the annular ligament (see Fig. 20-17B). This results in inability to rotate the radial head without considerable discomfort. Usually, the annular ligament is not torn; however, as the child becomes older, the annular ligament is undoubtedly partially torn, which accounts for the persistence of symptoms for several days even after the reduction. At one time, it was thought that the radial head in a child was smaller in relation to the neck than in adults or older children, and thus, subluxation of the radial head into the annular ligament was more common.125 Studies by Salter and Zaltz129 and Mehta127 have shown that, even in infants, the relative proportion of radial head diameter to neck diameter is similar to that of adults. The pulled elbow syndrome is most common between the ages of 6 months and 3 years, becoming less common as the radius grows in size and becomes more ossified.126 A reasonable explanation for pulled elbow is simply the generalized ligamentous laxity of the elbow that exists at this age and the resiliency imparted to the radial head by the almost entirely cartilaginous structure.122,123 A longitudinal pull with accompanying pronation of the forearm screws the radial head down into the annular

ligament, and the larger head then becomes caught as if in a Chinese finger trap (see Fig. 20-17B).

CLINICAL APPEARANCE A child with the pulled elbow syndrome complains primarily of pain and failure to move the elbow, and there may or may not be a typical history of a longitudinal pull. The infant may well go about his or her normal play activities and is comfortable as long as no one attempts to move the elbow. The child keeps the arm in pronation and expresses discomfort and anxiety if anyone attempts to move the elbow or to pronate or supinate the forearm. Radiographs are singularly nondiagnostic and are sometimes misinterpreted because it is impossible to position the limb properly.124-129 However, the technicians, in attempting to obtain good anteroposterior and lateral films of the elbow, may inadvertently reduce the subluxation by supinating the forearm, and the child returns from the Radiology Department content and moving his or her elbow normally.

MANAGEMENT Reduction of the pulled elbow is usually simple, consisting of a supination motion with the elbow flexed. A click is often felt and sometimes even heard. As the radial head is “screwed up” into the annular ligament, the ligament slips down over the head into its normal position around the neck with a snap. In younger children, resumption of normal activity often ensues in minutes; however, in the older child, the elbow may remain tender, probably owing to small tears within the annular ligament. If pain persists, immobilization of the arm in a plaster cast or splint for a week or so is curative. Other than emotional upset, there are no long-term sequelae from the pulled elbow syndrome, because in some children, its frequent recurrence is a cause of concern to patient and family. In such a case, it is often worthwhile to explain precisely what is happening and demonstrate how to reduce the pulled elbow to avoid visits to the emergency department. Seldom is open repair of the annular ligament necessary, because even in the most recalcitrant circumstances, time and growth always cure this type of instability.

TRAUMATIC DISLOCATION OF THE ELBOW MECHANISM OF THE DISLOCATION As discussed earlier, the elbow joint in a child is basically a ligamentous structure in which only a small portion of cartilaginous stability is imparted by the ulna. With a fall on the outstretched hand the downward force on

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313

A

B Normal anatomical reduction

Pronation plus traction

Supination reduction

the fixed forearm is considerable. An associated valgus or varus force created by the body falling over the fixed elbow occurs (Fig. 20-18). The forearm is typically in pronation during this time. The coronoid process may be fractured (Fig. 20-19). The valgus force of the body rotating over the fixed elbow accounts for the frequent

FIGURE 20-17 A, Some causes of pulled elbow syndrome in small children. B, Pathophysiology of the pulled elbow syndrome.

avulsion of the medial epicondylar apophysis (Fig. 20-20).71,83 If the body falls over the elbow medially instead of laterally, a varus force is exerted, and the lateral epicondyle of the humerus or the lateral condyle may be avulsed84 (Fig. 20-21). Occasionally, as in a fall from a height, the forces may be such that the valgus

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DISLOCATION FORCES ABOUT THE ELBOW Varus force

Coronoid process sheared off

Varus rotatory

Valgus rotatory

cal

Lateral epicondyle avulsion

Ver ti

Anteroposterior

Ground reaction force Valgus force Olecranon fracture

Lateral

Coronoid process Medial epicondyle avulsion

FIGURE 20-18

children.

Valgus

Radial neck fracture

Mechanism of dislocation of the elbow in

force may disrupt the medial apophysis, and the posterolateral dislocation may also avulse the lateral epicondyle, resulting in elbow instability on both the ulnar and the radial sides of the joint. The radius and the ulna seldom separate owing to the strong interosseous membrane, although instances of divergent dislocations with tearing of the interosseous membrane have been reported.75,81,86,96 Less commonly, traction injuries may result in elbow dislocation.80 Occasionally, in falls from a height, the valgus force exerted on the elbow joint may result in a fracture of the neck of the radius and the olecranon process (Fig. 20-22). When the arm is in marked extension, the capitellum also may be fractured. Associated fractures of the distal radius and ulna occasionally occur (Fig. 20-23). Along with the other associated trauma, capsular tearing is responsible for the prolonged stiffness that often follows dislocation of the elbow. The capsular attachment to the ulna and humerus is frequently torn.

SPONTANEOUS REDUCTION OF THE DISLOCATED ELBOW Spontaneous reduction of a dislocated elbow in children is common. Often the child will present to the emergency department with a history of a fall, the only

FIGURE 20-19 A and B, Fracture of coronoid process of olecranon associated with posterior dislocation of the elbow.

Chapter 20 Dislocations of the Child’s Elbow

315

FIGURE 20-20 A and B, Fracture of radial neck with avulsion of the medial epicondyle, which has remained intra-articular following spontaneous reduction of the elbow dislocation.

FIGURE 20-21 A and B, Dislocation of the elbow associated with fracture of the lateral condyle of the humerus. The radial head maintains its relationship with the displaced capitellum.

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FIGURE 20-22 A and B, Dislocation of the elbow with valgus force resulting in fracture of the olecranon, radial neck, and medial epicondyle, which has remained intra-articular following spontaneous reduction.

physical findings being a swollen, boggy elbow and no obvious radiographic evidence of any injury. However, if one looks carefully at the radiograph, signs of previous dislocation may be present (Fig. 20-24). Of particular note is fracture of the coronoid process (Fig. 20-25), which indicates that the elbow has been transiently subluxed. Sometimes, at reduction the humerus may cause a type I or II fracture through the epiphyseal plate of the proximal radius, resulting in posterior displacement of the radial epiphysis on reduction (Fig. 20-26).

DIFFERENTIAL DIAGNOSIS OF POSTERIOR DISLOCATION

FIGURE 20-23 A and B, Fracture of distal radius associated with dislocation of the elbow.

The child with dislocation of the elbow is severely incapacitated with pain and deformity. The differential diagnosis basically consists of distinguishing a dislocation from a supracondylar fracture, a lateral condylar fracture, and, in the younger child, a transcondylar fracture of the humerus (Fig. 20-27).92 The elbow will be painful and swollen, and depending on how soon the child is seen after the injury, the posterior deformity may be either obvious or masked by swelling if several hours have passed. The child is always extremely apprehensive

Chapter 20 Dislocations of the Child’s Elbow

and will not allow anyone under any circumstances to move the joint. In my experience, the commonly stated rules of lining up the triangular relationship among the medial epicondyle, lateral epicondyle, and olecranon are not of much practical value in this situation. One can sometimes feel a gap superior to the displaced olecranon, indicating that a posterior dislocation has occurred. The humeral condyles can also be palpated anteriorly. The supracondylar

Avulsion of coronoid tip

Intra-articular Type 1 fracture of medial epicondyle radial epiphysis

FIGURE 20-24 Fractures about the elbow in children indicative of spontaneous reduction of an elbow dislocation.

317

fracture is often difficult to differentiate from a posterior dislocation of the elbow, especially if presentation is late and considerable swelling has occurred to obscure the abnormal anatomy. Excessive examination and movement of such an elbow should be avoided because it serves only to make the child more apprehensive and less cooperative. The neuromuscular examination of the extremity may be difficult but often can be performed simply by observation once the confidence and cooperation of the child have been obtained. Sensation then can be gently tested in the three major nerve distributions, including the anterior and posterior interosseous divisions. It is essential, of course, to assess the neurologic and vascular condition of the limb in the Emergency Department. The child should be encouraged to make the “O” sign with the index finger and thumb. If this cannot be done, injury to the anterior interosseous nerve has occurred, causing paralysis of the flexor pollicis longus. Images are diagnostic today. Dislocation of the elbow is very rare in children younger than the age of 2 years, and transcondylar fracture of the humerus should be suspected (see Fig. 20-25). This may be difficult to differentiate from a posterior dislocation, and confirmation may require special images.68-74,76,79,82 Radiographs should be carefully examined for associated fractures aside from the dislocation. A careful

FIGURE 20-25 A and B, Avulsion fracture of tip of coronoid process following dislocation of the elbow. The brachialis muscle often avulses a small portion of the coronoid process; when present, this is pathognomonic of a previous elbow dislocation.

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Part IV Conditions Affecting the Child’s Elbow

A

FIGURE 20-26 A, Type I fracture of the proximal radial epiphysis with posterior displacement occasionally occurs in posterior dislocation of the elbow if reduction is forceful. B, Fracture of neck of radius secondary to dislocation of the elbow with forceful spontaneous reduction.

FIGURE 20-27 Transcondylar fracture of the humerus in infancy may be misdiagnosed as a dislocation of the elbow. Arthrography or computed tomography scan is diagnostic.

Chapter 20 Dislocations of the Child’s Elbow

appraisal of the coronoid process, the radial neck, the olecranon, and the medial and lateral epicondyles should be carried out.67,77,78,84 If the child is over 5 years of age and the medial epicondyle is not present, a radiograph of the other elbow should be inspected to make sure that it is ossified. If the medial epicondyle cannot be found on the radiograph of the dislocated elbow, it must be assumed that it is obscured by its intra-articular position (see Fig. 20-20).66,71,89-95 An injury to the radial epiphysis may occur when the elbow is forcibly reduced. This may even occur at the time of the injury; for example, when a direct blow to the elbow, following the original dislocation that was sustained by a fall on the outstretched hand, causes reduction. The direct force on the radial head results in a type I fracture through the proximal radial epiphysis with posterior displacement (see Fig. 20-26). It is essential to emphasize that many children present to the emergency department with simply a swollen, boggy elbow joint and a history of a fall. In such cases, one can assume, especially if there is radiographic evidence of avulsion of the coronoid process or of the medial epicondyle, that this elbow has been dislocated and has spontaneously reduced.

319

bined with some anterior pressure over the prominent olecranon is usually successful, usually with an audible and palpable clunk (Fig. 20-28). Occasionally, in older children, the coronoid process becomes locked behind the humerus. In this instance, the arm should be put in extension and a muscle relaxant administered; with traction and good firm thumb pressure over the olecranon, the elbow usually can be reduced. Hyperextension to free the coronoid is hazardous, especially if vascular insufficiency is already present, because it places more stress on the brachial artery, which may be tented over the distal end of the humerus. Once the elbow is reduced, the integrity of the medial and lateral collateral ligaments should be tested. Furthermore, a smooth arc of motion should be demonstrated to ensure no fragment, particularly the medial epicondyle, is caught within the joint. If the joint does not move freely or has a spongy feel to it, a mechanical problem with reduction exists. The reduction should always be checked radiographically, especially with any associated fracture.85,94,97 Aspiration of the joint is recommended to assist in resolving the hematoma and improving joint motion after reduction. Using a local anesthetic may be helpful in the older patient.

TREATMENT OF POSTERIOR DISLOCATION Posterior dislocation of the elbow is a painful, terrifying experience for a child, and the limb should be put at rest with a splint as soon as possible in the emergency department with minimal manipulation of the extremity. No child should ever be sent for radiographs without adequate splintage. The dislocation demands early treatment and, of course, if there is any vascular insufficiency, immediate treatment. Occasionally, in a very cooperative older child, the elbow may be reduced in the emergency department. The instillation of local anesthetic into the joint itself often facilitates this maneuver. Turning the child prone with the arm dangling over the stretcher facilitates the application of some pressure over the olecranon, and this, combined with gravity or slight traction on the dangling limb, may allow the dislocation to be quickly and traumatically reduced.87 If there is an associated fracture of the medial epicondyle, the radial neck, or the olecranon, this maneuver should be avoided. In our experience with children younger than age 12, it is best to proceed with a general anesthetic for complete relaxation, ideally within 6 hours of the trauma. It is not appropriate to allow the child to wait overnight because massive edema may occur, which is extremely uncomfortable for the child and leads to stiffness. Once the child has been anesthetized, it is usually a simple matter to reduce an uncomplicated posterior elbow dislocation. Gentle traction on the forearm com-

MEDIAL EPICONDYLAR ENTRAPMENT If it is known that the medial epicondyle is trapped within the joint, then during the reduction, a valgus strain is placed on the elbow. With flexion of the wrist this may allow the attached flexor muscle mass to pull the trapped fragment out of the joint. Occasionally, this

FIGURE 20-28 The author’s preferred technique for reducing a posterior dislocation of the elbow joint in children.

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Part IV Conditions Affecting the Child’s Elbow

may yield an anatomic or nearly anatomic position. If the medial epicondyle is displaced more than 1 cm, it should be pinned back in place because it will add stability to the elbow subsequent to the dislocation and allow stable elbow motion to occur within 3 to 4 weeks. In children younger than the age of 5, when the medial epicondyle is not ossified, any springiness in the elbow joint subsequent to the reduction indicates an intraarticular position of the medial epicondyle. Ultrasonographic evaluation of the elbow might be helpful in confirming the presence of an intra-articular fragment.74 If the medial epicondyle cannot be removed from the joint with manipulation, it must be removed surgically. The elbow is approached through a medial incision. The flexor muscle mass initially appears to be anatomically intact as it disappears into the joint; however, with valgus force and gentle pull on the muscle mass, the attached fragment can be removed from the joint, and the capsule can be repaired. The fragment then should be reattached to the distal medial humerus. Care should be taken not to injure the ulnar nerve. If there is any concern about this, the nerve should be identified and retracted with tapes until the repair has been completed.66,89,95,109

POSTOPERATIVE MANAGEMENT Following reduction of the elbow, the joint should be immobilized at 90 degrees with slight forearm supination. Flexion is especially important if there has been a coronoid process avulsion. This allows the triceps to tighten posteriorly, acting as a dynamic splint for the elbow, and also helps prevent the ulna from slipping backward into the dislocated position.

This is an extremely rare type of dislocation that results from tearing of the interosseous membrane. Although I have never treated one of these dislocations, medial and lateral pressure over the divergent radius and ulna to align the forearm bone before reducing it as a simple posterior dislocation has been described.75,81,96

Divergent Dislocation

COMPLICATIONS OF ELBOW DISLOCATION Complications from simple dislocations of the elbow are uncommon in children, especially when compared with this injury in the adult. Joint Stiffness As in adults, joint stiffness is the most common problem encountered after dislocation of the elbow in children. The child and his or her parents must be advised that joint motion may be lost as a result of the injury. In older children, fully complete extension may never be recovered, although the loss of the last 5 to 10 degrees of extension is not accompanied by any marked functional deficit. Elbows in children should not be immobilized longer than 4 weeks, and exercises after injury should be primarily active; passive motion should be avoided. Seldom is manipulation or passive physiotherapy required for joint stiffness after a dislocation of the elbow; this type of treatment often delays recovery because it is accompanied by further joint irritation, capsular tearing, and hematoma formation. A year may be required to regain full motion in the child’s elbow, the child being his or her own best physiotherapist. Management of the stiff elbow in the child is discussed in detail in Chapter 21.

Myositis ossificans is an uncommon complication of a simple dislocation of the elbow joint in children unless it is accompanied by a crush injury, head injury, major trauma, or multiple manipulations. Myositis ossificans may bridge the joint involving the brachialis muscle. The ossific lesion can be excised once it is mature, however, but recurrence is still possible.110

Myositis Ossificans

OTHER TYPES OF ELBOW DISLOCATION Anterior dislocation of the elbow in children is uncommon and usually is the result of severe direct trauma to the posterior aspect of the proximal forearm. This may be associated with a fracture of the olecranon. Reduction should be accomplished by direct pressure anteriorly over the dislocated radius and ulna, together with gentle traction on the forearm to allow the olecranon to slide beneath the humerus.72,88

Anterior Dislocation

Purely medial or lateral dislocations are extremely rare and probably do not exist without an anterior/posterior injury. Longitudinal traction may be all that is required for reduction. However, if the joint deviates considerably to either side, appropriate pressure over the medial or lateral aspects to align the elbow prior to reduction often facilitates reduction.77,85

Medial or Lateral Dislocation

Nerve injuries are uncommon in simple posterior elbow dislocations in children. The ulnar nerve is most frequently involved.80,117 The common posterolateral dislocation of the elbow results in a stretch on the ulnar nerve. The median and, rarely, the radial nerves also may suffer neuropraxic injuries secondary to posterior dislocation of the elbow. The median nerve may be vulnerable to entrapment within the joint subsequent to reduction of the elbow dislocation. Although rare, this type of entrapment has been reported only in children, and diagnosis is frequently delayed. It should be suspected when signs of Nerve Injuries

Chapter 20 Dislocations of the Child’s Elbow

FIGURE 20-29

Course of median nerve lying entrapped posterior to the medial epicondyle. (Redrawn from Matev, I.: Radiological sign of entrapment of the median nerve in the elbow joint after posterior dislocation. J. Bone Joint Surg. 58:353, 1976.)

median nerve injury or pain accompany avulsion of the medial epicondyle; in such instances, the nerve usually lies “posterior” to the medial epicondyle (Fig. 20-29).98,102,105,108 As emphasized by Green,101 in an excellent review of this subject, persistent pain or increasing median nerve dysfunction should alert one to the possibility of nerve entrapment. A late clinical sign of entrapment is persistent limitation of elbow motion; a late radiologic sign of median nerve entrapment is depression of the cortex of the distal humerus just proximal to the medial epicondyle, where the median nerve passes behind the humerus.105,106 This is termed Matev’s sign (Fig. 20-30). Immediate exploration should be undertaken once the diagnosis of nerve entrapment has been made. If the nerve is functionally intact, as demonstrated by nerve stimulation, simple removal of the nerve from the joint is sufficient treatment. If the nerve is obviously severely damaged, crushed, or scarred and nonfunctional, resection of the damaged section with end-to-end reanastomosis is recommended.99,107

321

FIGURE 20-30 Median nerve entrapment 3 months after injury. The arrow points to a cortical depression with interruption of periosteal reaction. (From Matev, I.: Radiological sign of entrapment of the median nerve in the elbow joint after posterior dislocation. J. Bone Joint Surg. 58:353, 1976.)

Injury to the brachial artery to the extent of complete occlusion is not commonly observed in dislocations of the elbow in children. The brachial artery may be stretched over the distal humerus, and if the force is sufficient, damage to the artery may occur. This is evident by the usual signs of vascular impairment, which then demand exploration of the artery. The elbow should always be reduced before making a final assessment of the vascular status of the limb because it simply may be occluded subsequent to the elbow deformity.100,103,104,106 In assessing vascular integrity in a child’s arm, caution must be advised in putting too much faith in capillary filling. Collateral circulation may be sufficient to provide excellent capillary filling but insufficient to adequately vascularize the extremity. Vascular Injury

Recurrent Dislocation of the Elbow Recurrent dislocation of the elbow in children is very uncommon, as is an unreduced dislocation.69 Today, recurrent dislocation is known to occur with a deficient lateral ulnar

322

Part IV Conditions Affecting the Child’s Elbow

collateral ligament.93 Inadequate treatment, in which the elbow has been kept flexed at less than 90 degrees, especially when associated with a fracture of the coronoid process, may result in redislocation of the elbow and reinjury and recurrent dislocation.111-121 It is uncommon to experience recurrent dislocation. Uncommonly, this may be secondary to severe generalized ligamentous laxity, as occurs in Ehlers-Danlos syndrome. In a review of the Ehlers-Danlos syndrome by Beighton and Horan,111 19 of 100 patients suffered dislocations of one or more joints, with three having dislocation of the elbow. Recurrent dislocations of the elbow were reported by Rames and Strecker120 in a 9year-old girl who subsequently required a repair of the lateral capsule and ligamentous structures with drill holes through the lateral epicondyle to firmly anchor the capsule, as described by Osborn and Cotterill.119 Recurrent subluxation of the elbow recently was described by O’Driscoll and Morrey,118 who noted the etiology as deficiency of the lateral ulnar collateral ligament. Of note, like the shoulder, recurrence of the elbow dislocation is greater in adolescents than in adults. This may be treated successfully with an orthosis designed to block the last 15 degrees of extension associated with muscle strengthening to protect and stabilize the elbow. If this fails, surgery to reconstruct the lateral collateral ligament complex is required.

SUMMARY Dislocations about the elbow are common in children. Because they often accompany fractures in the region of the joint, care must be taken to examine the environs of the elbow systematically for evidence of skeletal injury coexisting with the dislocation. Particular care should be exercised to ensure that the radial head is in its proper relationship with the capitellum. Because most problems encountered in elbow dislocations in children are the result of missed diagnoses of associated injuries, the value of a thorough clinical and radiographic examination of the elbow cannot be overemphasized.

References TRAUMATIC DISLOCATION OF THE RADIAL HEAD 1. Beddow, F. H., and Corckery, P. H.: Lateral dislocation of the radial humeral joint with greenstick fracture of the upper end of the ulna. J. Bone Joint Surg. 42B:782, 1960. 2. De Lee, J. C.: Transverse divergent dislocation of the elbow in a child. J. Bone Joint Surg. 63A:322, 1981. 3. Heidt, R. S., and Stern, P. J.: Isolated posterior dislocation of the radial head. Clin. Orthop. Rel. Res. 168:136, 1982.

4. Hudson, D. A., and DeBeer, De. V.: Isolated traumatic dislocation of the radial head in children. J. Bone Joint Surg. 68B:378, 1986. 5. Kirkos, J. M., Beslikas, T. A., and Papavasiliou, V. A.: Posteromedial dislocation of the elbow with lateral condylar fracture in children. Clin. Orthop. Rel. Res. 408:232, 2003. 6. Lincoln, T. L., and Mubarek, S. J.: “Isolated” traumatic radial head dislocation. J. Pediatr. Orthop. 14:454, 1994. 7. Macias, C. G., Wiebe, R., and Bothner, J.: History and radiographic findings associated with clinically suspected radial head subluxations. Pediatr. Emerg. Care 16:22, 2000. 8. Pudas, T., Hurme, T., Mattila, K., and Svedstrom, E.: Magnetic resonance imaging in pediatric elbow fractures. Acta Radiol. 46:636, 2005. 9. Schubert, J. J.: Dislocation of the radial head in the newborn infant. J. Bone Joint Surg. 47A:1010, 1965. 10. Stelling, F. H., and Cote, R. H.: Traumatic dislocation of the head of the radius in children. J. A. M. A. 160:732, 1956. 11. Storen, G.: Traumatic dislocation of the radial head as an isolated lesion in children. Acta Clin. Scand. 116:144, 1958. 12. Vesely, D. G.: Isolated traumatic dislocation of the radial head in children. Clin. Orthop. Rel. Res. 50:31, 1967. 13. Wiley, J. J., Pegington, J., and Horwich, J. P.: Traumatic dislocation of the radius at the elbow. J. Bone Joint Surg. 56B:501, 1974. 14. Wright, P. R.: Greenstick fractures of the upper end of the ulna with dislocation of the radial humeral joint or displacement of the superior radial epiphysis. J. Bone Joint Surg. 45B:727, 1963. 15. Yates, C., and Sullivan, J. A.: Arthrographic diagnosis of elbow injuries in children. Pediatr. Orthop. 7:54, 1987. 16. Zivkovic, T.: Traumatic dislocation of the radial head in a 5-year-old boy. J. Trauma 18:289, 1978. DEVELOPMENTAL DISLOCATION OF THE RADIAL HEAD 17. Cummings, R. J., Jones, E. T., Reed, F. E., and Mazur, J. M.: Infantile dislocation of the elbow complicating obstetric palsy. J. Pediatr. Orthop. 16:589, 1996. 18. De Boeck, H.: Treatment of chronic isolated radial head dislocation in children. Clin. Orthop. Rel. Res. 380:215, 2000. 19. Hirayama, T., Takemitsu, Y., Yagihara, K., and Mikita, A.: Operation for chronic dislocation of the radial head in children. Reduction by osteotomy of the ulna. J. Bone Joint Surg. 69:639, 1987. 20. Lloyd-Roberts, G. C., and Bucknill, T. M.: Anterior dislocation of the radial head in children-etiology. Natural history and management. J. Bone Joint Surg. 59B:402, 1977. 21. Pletcher, D., Hofer, M. M., and Koffman, D. M.: Nontraumatic dislocation of the radial head in cerebral palsy. J. Bone Joint Surg. 58A:104, 1976. 22. Peeters, R. L. M.: Radiological manifestations of the Cornelia de Lange syndrome. Pediatr. Radiol. 3:41, 1975.

Chapter 20 Dislocations of the Child’s Elbow

23. Salama, R., Weintroub, S., and Weissman, S. L.: Recurrent dislocation of the radial head. Clin. Orthop. Rel. Res. 125:156, 1977. 24. Silberstein, M. J., Brodeur, A. E., and Graviss, E. R.: Some vagaries of the radial head and neck. J. Bone Joint Surg. 64A:1153, 1982. 25. Southmayd, W., and Parks, J. C.: Isolated dislocation of the radial head without fracture of the ulna. Clin. Orthop. Rel. Res. 97:94, 1973. 26. Subbarao, J. V., and Kumar, V. N.: Spontaneous dislocation of the radial head in cerebral palsy. Orthop. Rev. 16:457, 1987. CONGENITAL DISLOCATION OF THE RADIAL HEAD 27. Almquist, E. E., Gordon, L. H., and Blue, A. I.: Congenital dislocation of the head of the radius. J. Bone Joint Surg. 51A:1118, 1969. 28. Bell, S. N., Morrey, B. F., and Bianco, A. J. Jr.: Chronic posterior subluxation and dislocation of the radial head. J. Bone Joint Surg. 73:392, 1991. 29. Carevias, D. E.: Some observations on congenital dislocation of the head of the radius. J. Bone Joint Surg. 39B:86, 1957. 30. Cockshott, W. P., and Omololu, A.: Familial posterior dislocation of both radial heads. J. Bone Joint Surg. 40B:484, 1958. 31. Gattey, P. H., and Wedge, J. H.: Unilateral posterior dislocation of the radial head in identical twins. J. Pediatr. Orthop. 6:220, 1989. 32. Gunn, D. R., and Pilley, V. K.: Congenital dislocation of the head of the radius. Clin. Orthop. Rel. Res. 84:108, 1964. 33. Kelikian, H. (ed): Dislocation of the radial head. In Congenital Deformities of the Hand and Forearm. Philadelphia, W. B. Saunders Co., 1974, p. 902. 34. Kelly, D. W.: Congenital dislocation of the radial head: spectrum and natural history. J. Pediatr. Orthop. 1:295, 1981. 35. Mardam-Bey, T., and Ger, E.: Congenital radial head dislocation. J. Hand Surg. 4:316, 1979. 36. Mital, M. A.: Congenital radial ulnar synostosis and congenital dislocation of the radial head. Orthop. Clin. North Am. 7:375, 1976. 37. Miura, T.: Congenital dislocation of the radial head. J. Hand Surg. 15B:477, 1990. 38. Mizuno, K., Usui, Y., Kohyama, K., and Hirohata, K.: Familial congenital unilateral anterior dislocation of the radial head: differentiation from traumatic dislocation by means of arthrography. J. Bone Joint Surg. 73A:1086, 1991. MONTEGGIA FRACTURE-DISLOCATION OF THE ELBOW IN CHILDREN 39. Bado, J. L.: The Monteggia lesion. Clin. Orthop. Rel. Res. 50:71, 1967. 40. Boyd, H. B., and Boals, J. C.: The Monteggia lesion: a review of 159 cases. Clin Orthop 66:94, 1969. 41. Bruce, H. E., Harvey, J. P. W., and Wilson, J. C., Jr.: Monteggia fractures. J. Bone Joint Surg. 56A:1563, 1974. 42. Bell-Tawse, A. J. F.: The treatment of malunited anterior Monteggia fractures in children. J. Bone Joint Surg. 47B:718, 1965.

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43. Cappellino, A., Wolfe, S. W., and Marsh, J. S.: Use of a modified Bell Tawse procedure for chronic acquired dislocation of the radial head. J. Pediatr. Orthop. 18:410, 1998. 44. Dormans, J. P., and Rang., M.: The problem of Monteggia fracture dislocations in children. Orthop. Clin. North Am. 21:251, 1990. 45. Evans, E. M.: Pronation injuries of the forearm with special reference to the anterior Monteggia fracture. J. Bone Joint Surg. 31B:578, 1949. 46. Fahmy, N. R. M.: Unusual Monteggia lesions in children. Injury 12:399, 1981. 47. Freedman, L., Luk, K., and Leong, J. C.: Radial head reduction after a missed Monteggia fracture: brief report. J. Bone Joint Surg. 70:846, 1988. 48. Hume, A. C.: Anterior dislocation of the head of the radius associated with undisplaced fracture of the olecranon in children. J. Bone Joint Surg. 39B:508, 1957. 49. Hurst, L. C., and Dubrow, E. N.: Surgical treatment of symptomatic chronic radial head dislocation: a neglected Monteggia fracture. J. Pediatr. Orthop. 3:227, 1983. 50. Kalamchi, A.: Monteggia fracture dislocation in children. Late treatment in two cases. J. Bone Joint Surg. 68:615, 1986. 51. Letts, M., Locht, R., and Weins, J.: Monteggia fracture dislocations in children. J. Bone Joint Surg. 67:724, 1985. 52. Mullick, S.: The lateral Monteggia fracture. J. Bone Joint Surg. 59A:543, 1977. 53. Olney, B. W., and Menelaus, M. B.: Monteggia and equivalent lesions in childhood. J. Pediatr. Orthop. 9:219, 1989. 54. Ovesen, O., Brok, K. E., Arreskov, J., and Bellstrom, T.: Monteggia lesions in children and adults: an analysis of etiology and long-term results of treatment. Orthopedics 13:529, 1990. 55. Papavasiliou, V. A., and Nenopoulos, S. P.: Monteggiatype elbow fractures in children. Clin. Orthop. Rel. Res. 233:230, 1988. 56. Peterson, H. A., and Seel, M. J.: Management of posttraumatic chronic radial head dislocation in children. Presented at the 1998 Annual Meeting of the Pediatric Orthopaedic Society of North America, Cleveland, Ohio, May 7, 1998. 57. Ravessoud, F. A.: Lateral condylar fracture and ipsilateral ulnar shaft fracture: Monteggia equivalent lesions. J. Pediatr. Orthop. 5:364, 1985. 58. Ring, D., and Waters, P. M.: Operative fixation of Monteggia fractures in children. J. Bone Joint Surg. 78B:734, 1996. 59. Spinner, M., Freundlich, B. D., and Teicher, J.: Posterior interosseous nerve palsy as a complication of Monteggia fractures in children. Clin. Orthop. Rel. Res. 58:141, 1968. 60. Stein, F., Grabias, S. L., and Deffer, P. A.: Nerve injuries complicating Monteggia lesions. J. Bone Joint Surg. 53A:1432, 1971. 61. Theodorou, S. D.: Dislocation of the head of the radius associated with fractures of the upper end of the ulna in children. J. Bone Joint Surg. 51B:70, 1969.

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62. Tompikins, D. G.: The anterior Monteggia fracture. Observations on etiology and treatment. J. Bone Joint Surg. 53A:1009, 1971. 63. Wang, M. N., and Chang, W. N.: Chronic posttraumatic anterior dislocation of the radial head in children: thirteen cases treated by open reduction, ulnar osteotomy, and annular ligament reconstruction through a Boyd incision. J. Orthop. Trauma 20:1, 2006. 64. Wiley, J. J., and Galey, J. P.: Monteggia injuries in children. J. Bone Joint Surg. 69B:728, 1985. 65. Wright, P. R.: Greenstick fracture of the upper end of the ulna with dislocation of the radiohumeral joint or displacement of the superior radial epiphysis. J. Bone Joint Surg. 45B:727, 1963. ACUTE DISLOCATION OF THE ELBOW IN CHILDREN 66. Aitken, A. P., and Childress, H. M.: Inter-articular displacement of the internal epicondyle following dislocation. J. Bone Joint Surg. 20:161, 1938. 67. Aufranc, O. E., Jones, W. M., Turner, R. H., and Thomas, W. H.: Dislocation of the elbow with fracture of the radial head and distal radius. J. A. M. A. 202:131, 1967. 68. Beghin, J. L., Bucholz, R. W., and Wenger, D. R.: Intracondylar fractures of the humerus in young children. J. Bone Joint Surg. 64A:1083, 1982. 69. Bilett, D. M.: Unreduced posterior dislocation of the elbow. J. Trauma 19:186, 1979. 70. Blatz, D. J.: Anterior dislocation of the elbow in a case of Ehlers-Danlos syndrome. Orthop. Rev. 10:129, 1981. 71. Bulut, G., Erken, H. Y., Tan, E., Ofluolu, O., and Yildiz, M.: Treatment of medial epicondyle fractures accompanying elbow dislocations in children. Acta Orthop. Traumatol. Turc. 39:334, 2005. 72. Caravias, D. E.: Forward dislocation of the elbow without fracture of the olecranon. J. Bone Joint Surg. 39B:334, 1957. 73. D’Ambrosia, R., and Zink, W.: Fractures of the elbow in children. Pediatr. Ann. 11:541, 1982. 74. Davidson, R. S., Markowitz, R. I., Dormans, J., and Drummond, D. S.: Ultrasonographic evaluation of the elbow in infants and young children after suspected trauma. J. Bone Joint Surg. 76A:1804, 1994. 75. De Lee, J. C.: Transverse divergent dislocation of the elbow in a child. J. Bone Joint Surg. 63A:322, 1981. 76. De Lee, J. C., Wilkens, K. E., Rogers, K. F., and Rockwood, C. A.: Fracture separation of the distal humeral epiphysis. J. Bone Joint Surg. 62A:46, 1980. 77. Eppright, R. H., and Wilkins, K. E.: Fractures and dislocations of the elbow. In Rockwood, C. A. Jr., and Green, D. P. (eds.): Fractures, Vol. 1. Philadelphia, J. B. Lippincott Co., 1975, p. 487. 78. Fowles, J. V., Slimane, N., and Kassab, M. T.: Elbow dislocation with avulsion of the medial humeral epicondyle. J. Bone Joint Surg. 72:102, 1990. 79. Grantham, S. A., and Tietjen, R.: Transcondylar fracturedislocation of the elbow. J. Bone Joint Surg. 58A:1030, 1976. 80. Heilbronner, D. M., Manili, A., and Little, R. E.: Elbow dislocation during overhead skeletal traction therapy. Clin. Orthop. Rel. Res. 147:185, 1981.

81. Holbrook, J. L., and Green, N. E.: Divergent pediatric elbow dislocation. A case report. Clin. Orthop. Rel. Res. 234:72, 1988. 82. Kaplan, S. S., and Reckling, R. W.: Fracture separation of the lower humeral epiphysis with medial displacement. J. Bone Joint Surg. 53A:1105, 1971. 83. Lee, H. H., Shen, H. C., Chang, J. H., Lee, C. H., and Wu, S. S.: Operative treatment of displaced medial epicondyle fractures in children and adolescents. J. Shoulder Elbow Surg. 14:178, 2005. 84. Lejman, T., Kowalczyk, B., and Felu, J.: Does coexistent fractures impair the results of treatment of elbow dislocations in children? Chir. Narzadow Ruchu Ortop Pol. 71:137, 2006. 85. Linscheld, R. L., and Wheeler, D. K.: Elbow dislocations. J. A. M. A. 194:1171, 1965. 86. McAuliffe, T. B., and Williams, D.: Transverse divergent dislocation of the elbow. Injury 19:279, 1988. 87. Meyn, M. A., Jr., and Quibley, T. B.: Reduction of posterior dislocation of the elbow by traction on the dangling arm. Clin. Orthop. Rel. Res. 103:106, 1974. 88. Oury, J. H., Roe, R. D., and Laning, R. C.: A case of bilateral anterior dislocations of the elbow. J. Bone Joint Surg. 12:170, 1972. 89. Patrick, J.: Fracture of the medial epicondyle with displacement into the elbow joint. J. Bone Joint Surg. 28:143, 1946. 90. Protzman, R. R.: Dislocation of the elbow joint. J. Bone Joint Surg. 60A:539, 1978. 91. Rang, M.: Children’s Fractures. Philadelphia, J. B. Lippincott Co., 1983. 92. Rasool, M. N.: Dislocations of the elbow in children. J. Bone Joint Surg. 86B:1050, 2004. 93. Schwab, G. H., Bennett, J. B., Woods, G. W., and Tollos, H. S.: Biomechanics of elbow instability—the medial collateral ligament. Clin. Orthop. Rel. Res. 146:42, 1980. 94. Smith, F. M.: Children’s elbow injuries: fractures and dislocations. Clin. Orthop. Rel. Res. 50:7, 1967. 95. Smith, F. M.: Displacement of the medial epicondyle of the humerus into the elbow joint. Ann. Surg. 124:410, 1946. 96. Sovio, O. M., and Tredwell, S. J.: Divergent dislocation of the elbow in a child. J. Pediatr. Orthop. 6:96, 1986. 97. Tachdjian, M. O.: Pediatric Orthopaedics, Vol. 2. Philadelphia, W. B. Saunders Co., 1972, p. 1604. COMPLICATIONS OF DISLOCATION OF THE ELBOW IN CHILDREN 98. Boe, S., and Holst-Neilson, F.: Intra-articular entrapment of the median nerve after dislocation of the elbow. J. Hand Surg. 12:356, 1987. 99. Floyd, W. E., 3rd, Gebhardt, M. C., and Emans, J. B.: Intraarticular entrapment of the median nerve after elbow dislocation in children. J. Hand Surg. 12:704, 1987. 100. Grimer, R. J., and Brooks, S.: Brachial artery damage accompanying closed posterior dislocation of the elbow. J. Bone Joint Surg. 67:378, 1985. 101. Green, N. E.: Entrapment of the median nerve following elbow dislocation. J. Pediatr. Orthop. 3:384, 1983. 102. Hallet, J.: Entrapment of the median nerve after dislocation of the elbow. J. Bone Joint Surg. 63B:408, 1981.

Chapter 20 Dislocations of the Child’s Elbow

103. Kerian, R.: Elbow dislocation and its association with vascular disruption. J. Bone Joint Surg. 51:756, 1969. 104. Louis, D. S., Ricciardi, J., and Sprengler, D. M.: Arterial injuries: a complication of posterior elbow dislocation. J. Bone Joint Surg. 56A:1631, 1974. 105. Matev, I.: A radiological sign of entrapment of the median nerve in the elbow joint after posterior dislocation. J. Bone Joint Surg. 58B:353, 1976. 106. Noonan, K. J., and Blair, W. F.: Chronic median-nerve entrapment after posterior fracture-dislocation of the elbow. J. Bone Joint Surg. 77A:1572, 1995. 107. Rubens, M. K., and Aulicino, P. L.: Open elbow dislocation with brachial artery disruption: a case report and review of the literature. Orthopaedics 9:539, 1986. 108. Stiger, R. N., Larrick, R. D., and Meyer, T. F.: Median nerve entrapment following elbow dislocations in children. J. Bone Joint Surg. 51A:381, 1969. 109. Tayob, A. A., and Shively, R. A.: A bilateral elbow dislocation with inter-articular displacement of medial epicondyle. J. Trauma 20:332, 1980. 110. Thompson, H. C., and Garcia, A.: Myositis ossificans after massive elbow injuries. Clin. Orthop. Rel. Res. 50:129, 1967. RECURRENT DISLOCATION OF THE ELBOW IN CHILDREN 111. Beighton, P., and Horan, F.: Orthopaedic aspects of the Ehlers-Danlos syndrome. J. Bone Joint Surg. 51B:444, 1969. 112. Hall, R. M.: Recurrent posterior dislocation of the elbow joint in a boy. J. Bone Joint Surg. 35B:56, 1953. 113. Hassmann, G. C., Brunn, F., and Neer, C. S.: Recurrent dislocation of the elbow. J. Bone Joint Surg. 57A:1080, 1975. 114. Hening, J. A., and Sullivan, J. A.: Recurrent dislocation of the elbow. J. Pediatr. Orthop. 9:483, 1989. 115. Jacobs, R. L.: Recurrent dislocation of the elbow: a case report and review of the literature. Clin. Orthop. Rel. Res. 74:151, 1971.

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116. Mantle, J.: Recurrent posterior dislocation of the elbow. J. Bone Joint Surg. 48B:590, 1966. 117. Morrey, B. F.: Complex instability of the elbow. J. Bone Joint Surg. 79A:460, 1997. 118. O’Driscoll, S. W., Bell, D. F., and Morrey, B. F.: Posterolateral rotatory instability of the elbow. J. Bone Joint Surg. 73A:440, 1991. 119. Osborne, G., and Cotterill, P.: Recurrent dislocation of the elbow. J. Bone Joint Surg. 48B:340, 1966. 120. Rames, R. D., and Strecker, W. B.: Recurrent elbow dislocations in a patient with Ehlers-Danlos syndrome. Orthopaedics 14:707, 1991. 121. Trias, A., and Comeau, Y.: Recurrent dislocation of the elbow in children. Clin. Orthop. Rel. Res. 100:74, 1974. PULLED ELBOW 122. Amir, D., Frank, J., and Pogrund, H.: Pulled elbow and hypermobility of joints. Clin. Orthop. Rel. Res. 257:94, 1990. 123. Boyette, D. P., Ahoski, H. C., and London, A. H., Jr.: Subluxation of the head of the radius-”nursemaid’s elbow.” J. Pediatr. 32:278, 1948. 124. Choung, W., and Heinrich, S. D.: Acute annular ligament interposition into the radiocapitellar joint in children (nurse maid’s elbow). J. Pediatr. Orthop. 15:454, 1995. 125. Hart, G. M.: Subluxation of the head of the radius in young children. J.A.M.A. 169:1734, 1969. 126. Magill, H. K., and Aitken, A. P.: Pulled elbow. Surg. Gynecol. Obstet. 98:753, 1954. 127. Mehta, L.: Subluxation of radial head in children with reference to radial head and neck diameters. J. Ind. Med. Assoc. 166:220, 1972. 128. Nussbaum, A. J.: The off-profile proximal radial epiphysis: another potential pitfall in the x-ray diagnosis of elbow trauma. J. Trauma. 23:40, 1983. 129. Salter, R. B., and Zaltz, C.: Anatomic investigations of the mechanism of injury and pathologic anatomy of “pulled elbow” in young children. Clin. Orthop. Rel. Res. 77:141, 1971.

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CHAPTER

21

Post-Traumatic Elbow Stiffness in Children Anthony A. Stans and Bernard F. Morrey

ETIOLOGY Elbow stiffness can be categorized as either extraarticular or intra-articular in origin. Heterotopic ossification and soft tissue contracture are two common causes of extrinsic contracture. Early aggressive passive rangeof-motion (ROM) exercises or repeated forceful manipulation during fracture reduction have been associated with heterotopic ossification and elbow stiffness.25,27 Delayed open reduction and internal fixation have also been shown to increase the risk of developing heterotopic ossification.14 Intra-articular T-condylar fractures are rare in children, but when they occur, they frequently are associated with elbow stiffness.9,23 Soft tissue contracture frequently occurs following immobilization or surgical treatment.29 Fracture malunion, callus formation, and degenerative changes are common intra-articular causes of elbow stiffness.30 Anatomic reduction of displaced intraarticular elbow fractures is important to prevent posttraumatic arthritis as well as to maintain the precise anatomic relationships among the three bones that make up the elbow and is required for normal elbow motion.21 If malunion does occur, resulting in articular incongruity or bone impingement, secondary degenerative changes often follow causing intrinsic elbow stiffness (Fig. 21-1).

INCIDENCE Although it is not common, elbow stiffness may occur following almost any form of elbow trauma. Henrikson6 reported stiffness in 3% to 6% of patients treated for supracondylar humerus fractures. Loss of motion following supracondylar humerus fractures may be due to soft tissue contracture or heterotopic ossification. Wedge and Roberson29 reported some loss of elbow motion following radial neck fractures in 33% of patients undergoing open reduction, and in 100% of patients when internal fixation was used. Aside from fractures, patients frequently experience loss of extension following elbow dislocation.11

PRESENTATION Persistent stiffness is the universal presenting chief complaint, but sometimes, particularly in children, it is difficult to know when early stiffness following treatment is appropriate, when the stiffness is a temporary phase of the healing response, and when the stiffness is inappropriate and likely to result in permanent limitation in ROM. After initial treatment of the injury, patients who have not made significant progress toward restoration of normal motion by 2 to 3 months following their injury are at risk for developing permanent elbow stiffness. This is a reasonable period of time to expect stiffness following initial treatment to be significantly improved. Loss of motion accompanied by pain is an infrequent presenting complaint in young patients and was present in only 3 of 28 patients in a series from the Mayo Clinic.26 Symptoms such as catching or locking may be present and suggest the presence of loose bodies within the elbow.

EVALUATION HISTORY A detailed history of the injury and subsequent treatment is typically all that is necessary to determine whether the etiology for the stiffness is extrinsic or intrinsic. Important information to gather includes the mechanism and time of the initial injury, the precise nature of the nonoperative or operative treatment, and the length of the period of immobilization. Knowledge of the nature and duration of any physical therapy is helpful. Information regarding any complication such as a wound healing problem or infection is also useful. Factors commonly seen in the child that strongly suggest an extrinsic etiology include extra-articular fracture, especially supracondylar involvement, simple dislocation without associated fracture, and immobilization lasting longer than 4 weeks. Crush injuries and highenergy injuries with local soft tissue damage also predispose the patients to developing extrinsic contracture. Patients with an associated head injury are at risk for developing an extrinsic contracture due to heterotopic ossification.19 Post-traumatic intrinsic stiffness is most common following an intra-articular fracture. Because these more commonly require open reduction, surgical treatment may contribute to intrinsic etiology, especially if associated with malunion, excess callus formation, or retained hardware. Detailed questioning about the length of time elapsed since the injury and the specific treatment received for the elbow stiffness is

Chapter 21 Post-Traumatic Elbow Stiffness in Children

327

125 degrees of flexion. Extension is the most common portion of the arc affected. Limitation of pronation and supination is observed almost exclusively after radial head and neck fractures and suggests involvement of the radiocapitellar joint or proximal radioulnar synostosis if no rotational motion is present.

Stability Varus or valgus instability is classified by the method of Morrey.20 The elbow is stable if there is no varus or valgus laxity. Mild instability exists if varus or valgus laxity is present but is less than 5 degrees in either direction. Elbows were considered moderately unstable if varus or valgus laxity was considered to be 5 to 10 degrees and associated with mild symptoms. Severely unstable elbows had greater than 10 degrees varus and valgus laxity and caused limitations in daily activities. Varus and valgus instability associated with elbow stiffness is uncommon in children unless bone has been resected.

IMAGING STUDIES Plain Film Radiographs Anteroposterior and lateral radiographs are taken for all patients and provide helpful information regarding fracture union, fracture reduction, elbow alignment, loose bodies, and bone stock.

FIGURE 21-1

A, A 16-year-and-10-month-old boy sustained an injury to his right elbow while playing football, did not seek medical attention, and presented 2 years later with pain, locking, and elbow range of motion from −40 degrees extension to 130 degrees flexion. B, Six months following excision of ectopic bone, excision of loose bodies, anterior capsulotomy, radial head excision, and continuous passive motion with elbow range of motion from −30 degrees extension to 130 degrees flexion.

helpful in determining improvement.

the

likelihood

of

future

EXAMINATION Motion Accurate measurement of elbow range of motion (ROM) with a goniometer is essential. The functional arc of elbow motion is from 30 to 130 degrees.21 Patients with elbow ROM greater than this arc rarely suffer any functional limitation, but it is reasonable to attempt to restore normal ROM through a trial of nonoperative treatment. We have found that the use of splints is helpful and better tolerated than physical therapy (see Chapter 11). Very seldom is surgical treatment indicated for patients with less than 0 degrees of extension loss or greater than

Computed Tomography With the development of high-speed thin slice scanners, in conjunction with software allowing high-resolution two- and three-dimensional reconstruction images, computed tomography (CT) has recently replaced standard tomography as the best means of imaging elbow osseous anatomy. Reconstruction images in the coronal and sagittal planes are the most helpful views in assessing the etiology of elbow stiffness. Lateral reconstruction images are especially helpful in elbows of patients sustaining intra-articular fractures to assess joint congruity and coronal (A-P) plane reconstruction images are most useful when assessing distal humeral anatomy. CT also provides accurate imaging of loose bodies and other osseous pathology impeding elbow ROM, which greatly facilitates preoperative planning and helps ensure that all pathologic conditions contributing to elbow stiffness are identified and addressed at surgery.

Magnetic Resonance Imaging Recent literature has recommended magnetic resonance imaging (MRI) of the stiff elbow.3 However, MRI does not image osseous anatomy as well as other radiographic techniques. For specific indications, MRI can provide helpful information. Evaluation for possible avascular necrosis, physeal injury, and soft tissue lesions

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is often facilitated by MRI. In general, as with CT, transverse images are less helpful in assessing elbow contracture.

TREATMENT: INDICATIONS AND CONTRAINDICATIONS NONOPERATIVE TREATMENT The amount of time transpiring between the injury and the presence of an established contracture affects treatment. Early and aggressive passive ROM exercises have been demonstrated to cause heterotopic ossification in pediatric patients.25 During the first 1 to 3 months following injury; therefore, active ROM is used primarily. We have found swimming to be a very beneficial activity for the treatment of pediatric elbow stiffness. Although the exact mechanism is not clear, it is easy to imagine how swimming or playing in the water is relaxing, soothing, nonthreatening, and safe for children and adolescents. Therefore, we strongly encourage patients to swim regularly as soon as possible following injury or treatment.

Physical Therapy If decreased elbow ROM is present later than 2 to 3 months following injury, passive ROM exercises and stretching may be employed. Passive ROM and stretching should be limited by elbow swelling, pain, and inflammation. Any significant inflammation about the elbow caused by aggressive therapy may worsen elbow stiffness. The use of ice and a scheduled nonsteroidal anti-inflammatory drug (NSAID) often reduces inflammation and improves patient comfort, allowing greater progress to be made with therapy. Ideally, a physical therapist with an interest and competency in upper extremity rehabilitation instructs the patient on a home program of active and gentle passive stretching exercises that the patient performs daily and that are used in combination with ice and NSAIDs. In fact, because the likelihood of the therapist’s being knowledgeable is limited, we prefer splinting to formal physical therapy.

Splinting Previous authors have described the use of static and dynamic splinting to improve elbow ROM. Green and McCoy5 reported the use of a turnbuckle splint for elbow contracture, whereas others have advocated dynamic splinting.7 Our current practice is to use a static splint primarily at night, with an adjustable hinge that can be fixed in any degree of flexion (see Chapter 11). Each night before retiring, the patient applies the brace to the affected elbow. Preferably this is immediately following a session of stretching. Patients with a primary

limitation in extension place the elbow and splint in maximal extension to the point of tolerance and fix the hinge in this position. Conversely, patients with a primary limitation in flexion fix the splint in maximal flexion, again limited by pain. Patients with significant limitation in both planes alternate nights in flexion and extension. This nonoperative regimen of active and passive ROM exercises, NSAIDs, and splinting should be tried for a minimum of 1 and up to 3 months before its effectiveness can be determined.

SURGICAL TREATMENT Patients whose injuries are more than 6 months old and who have failed an adequate trial of nonoperative treatment as described earlier and who experience significant functional limitation due to elbow stiffness may be considered for operative treatment. Successful surgical treatment addresses all extrinsic and intrinsic pathologic elements contributing to stiffness.22 In the pediatric patient, release of the extrinsic soft tissue contracture is typically performed in a manner similar to the technique described by Husband and Hastings8 or Mansat and Morrey.16 Anterior capsulectomy is performed through a lateral Kocher incision for flexion contracture. If the medial capsule cannot be adequately released through the lateral incision, a medial incision is made through which the anterior capsular release is completed.12 Occasionally, the lateral collateral and medial collateral ligaments must also be released to restore adequate motion. Posterior capsulectomy is performed through the same lateral incision if extension contracture is present, hence the term column procedure.16 Thorough inspection of the joint is also performed, and intraarticular pathology causing limitation of elbow motion is treated. The olecranon tip should be excised if it is impinging on the posterior humerus in extension, and the coronoid tip should be excised if it is impinging within the coronoid fossa in flexion (Fig. 21-2). Lysis of adhesions is performed if necessary and any additional pathologic condition, such as loose bodies, addressed. If marked degenerative changes are present at the radiocapitellar joint, causing restricted ROM, radial head excision may be considered in skeletally mature patients (Fig. 21-3). Occasionally, excessive callus formation or malunion results in a bone block to motion, which may be removed deftly using burr or rongeur. We rarely release muscle/tendon units, because these will stretch out after surgery. An important lesson learned is that patients undergoing posterior release for limited elbow flexion frequently develop ulnar neuritis postoperatively. To prevent ulnar neuritis, we are increasingly proactive and in many patients performing in situ decompression of the ulnar nerve within the cubital tunnel, or subcutaneous

Chapter 21 Post-Traumatic Elbow Stiffness in Children

329

FIGURE 21-2

A, A 21-year-old boy sustained a hyperextension injury to his right elbow 6 months previously and presented with elbow range of motion from ±55 degrees extension to 140 degrees flexion. B, Tomographs confirm the presence of a previous olecranon fracture. C, One year following excision of the olecranon tip, anterior capsulotomy, and continuous passive motion, radiographs demonstrate additional ectopic bone formation about the elbow. Range of motion measured −20 degrees extension and 140 degrees flexion.

anterior ulnar nerve transposition at the time of contracture release. This is performed through the medial incision used to complete elbow contracture release. Patients with extensive intra-articular pathology limiting motion, but who have at least 50% of the articular cartilage intact, may benefit from distraction arthroplasty. A recent publication by Mader reported significant elbow motion improvement in 14 pediatric and adolescent patients treated with mechanical distraction.1,15 Patients with intrinsic contracture and less than 50% of the articular cartilage remaining may be considered for fascial interposition arthroplasty.20 It is less common to require these modalities in the pediatric population. Following closure and application of a soft dressing, the patient is allowed to awaken from anesthesia enough to allow neurovascular assessment. If the patient is neurovascularly intact, an indwelling brachial plexus catheter is inserted and continuous passive motion (CPM) is begun immediately. ROM in the CPM machine is rapidly increased to the amount of motion obtainable intraoperatively (see Chapter 10). The brachial plexus

catheter and CPM are continued on an inpatient basis until satisfactory motion is achieved and the patient is able to tolerate continued use of CPM without the brachial plexus catheter. After a total of approximately 3 to 4 days in the hospital, the patient is discharged home with a portable CPM machine to be used for approximately 6 weeks. When not using CPM, the patient typically uses a static adjustable splint. This regimen requires some compliance not readily attainable in the very young patient; as noted earlier, we attempt to defer surgery in those with open physes if possible. If surgery is performed in the younger child, the above-described regimen is modified according to what is attainable by that particular patient.

RESULTS There is a paucity of literature available on the results of treatment for the stiff elbow in pediatric patients. No published results can be found describing nonoperative results in pediatric patients, and only four papers could

330

Part IV Conditions Affecting the Child’s Elbow

FIGURE 21-3

A, Elbow dislocation with an associated radial head fracture was treated nonoperatively in this 19-year-old patient. B, Tomographs taken 2 months following the injury confirmed persistent displacement and radial head fracture nonunion. Six months after the injury, elbow range of motion measured −35 degrees extension to 115 degrees flexion, and the patient underwent excision of the radial head fragment, anterior capsulectomy, and posterior capsulotomy. C, Eighteen months following his surgery, small remnants of ectopic bone are present about the elbow, and elbow range of motion measures −10 degrees extension to 145 degrees flexion.

be identified describing operative results for the treatment of elbow stiffness in pediatric patients.2,15,18,26 Mih and Wolf18 reported a series of nine pediatric patients treated surgically for elbow stiffness. Six of the nine patients had post-traumatic stiffness, and the remaining three patients had stiffness secondary to juvenile rheumatoid arthritis, hemophilia, or avascular necrosis of the capitellum. Preoperatively, patients had a mean total arc of motion of 55 degrees, which improved to 108 degrees at a mean duration of follow-up of 17 months. We have reviewed our experience with patients age 21 or younger who underwent surgical treatment for elbow stiffness at the Mayo Clinic since 1979.26 Thirtynine patients were identified, 28 of whom developed stiffness following trauma. Excluding nontraumatic eti-

ology, eight patients had a complex fracture with associated elbow dislocation, seven sustained an isolated intra-articular elbow fracture, five patients an isolated elbow dislocation, four patients an extra-articular distal humerus fracture, and four patients a soft tissue injury or contusion without an elbow dislocation or fracture. All patients had failed a trial of nonoperative treatment and had functional limitation because of restricted ROM. Surgical procedures performed are listed in Table 21-1; as noted, virtually all underwent anterior release. Mean preoperative and postoperative ROMs are displayed in Table 21-2. The mean arc of motion improved from 66 degrees preoperatively to only 94 degrees after surgery. These results suggest that, at least in our

Chapter 21 Post-Traumatic Elbow Stiffness in Children

experience, pediatric patients tend to regain less motion than adult patients treated for post-traumatic elbow stiffness (Fig. 21-4).4,8,20,28 Also of note is that, unlike in the adult population, three patients regained no motion or even lost motion after surgery.

ARTHROSCOPIC RELEASE Arthroscopic elbow contracture release has gained increasing popularity in the treatment of adult patients with elbow stiffness10,13,24 and has been used with increasing frequency in pediatric and adolescent patients Surgical Procedures Performed in 28 Pediatric Patients with Elbow Stiffness

TABLE 21-1 Procedure

Number of Patients

Anterior capsulotomy

26

Posterior capsulotomy

12

Olecranon tip excision

9

Radial head excision

7

Osteophyte/heterotopic bone excision

6

External fixation

5

Fascial arthroplasty

3

Hardware removal

3

Loose body removal

3

Coronoid tip excision

2

Humeral contouring

2

TABLE 21-2

331

at the Mayo Clinic.17 Between 1997 and 2004, 45 pediatric and adolescent patients underwent arthroscopic elbow contracture release at the Mayo Clinic. In Table 21-3, motion arc improvement following arthroscopic release in pediatric patients is compared with improvement following open surgical treatment in pediatric patients and following open surgical treatment in adult patients from the same institution. The results of arthroscopic pediatric elbow contracture release appear to be slightly better than open contracture release for pediatric patients but not as successful as open contracture release in adult patients. It is unclear at this time if the improved motion following arthroscopic surgery is a consequence of arthroscopic technique or the result of more consistent use of CPM, static adjustable splinting or other factors.

COMPLICATIONS The combination of previous surgery, extensive dissection, external fixation, and immediate ROM following surgery places surgical patients at risk for complications. In the Mayo series, there was one deep wound infection requiring surgical débridement, one transient radial nerve palsy, one postoperative hematoma that required surgical evacuation, and three patients with persistent contracture without improvement following surgery. Patients undergoing distraction arthroplasty or fascial interposition arthroplasty are at greater risk for complications than patients treated with surgical release without external fixation.20

Preoperative and Postoperative Elbow Ranges of Motion Extension

Flexion

Total Arc

Pronation

Supination

Preoperative

−51

117

66

63

64

Postoperative

−32

129

94

73

64

120° 101°

129° 117°

92°

97° 49°

66°

52°

54° 0°

A

0°

32° Pediatric

B

28° Adult

FIGURE 21-4

The mean motion in the pediatric patient averaged about 65 degrees before and 95 degrees after surgery (A). This is less than the 60 degree improvement often seen in the adult (B).

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Part IV Conditions Affecting the Child’s Elbow

Comparison Between Open Adult, Open Pediatric, and Arthroscopic Pediatric Elbow Contracture Release

TABLE 21-3

Motion Arc Improvement

Mansat

45

Stans

28

McIntosh

38

AUTHORS’ CURRENT PRACTICE The assessment and surgical techniques for treating contracture in the child is similar to that of the adult. However, because of compliance issues as well as problems with less predictable response to surgery, we make every effort to avoid surgical release until the physes have closed. In children and adolescents at risk of developing elbow stiffness, we immediately initiate a patient and family directed active and active-assisted home stretching program. Encouraging children to swim early and often is frequently very helpful. The use of splints before surgery is particularly helpful to improve the motion arc to the extent that surgery may be able to be avoided, it allows assessment of compliance, and splints can be used after surgery should this become necessary. A home splint therapy program is preferred to formal physical therapy and is most effective when used within 3 to 6 months after the onset of stiffness. Surgical treatment for elbow stiffness in the pediatric patient is to be avoided whenever possible, and the unpredictable nature of the procedure must be carefully explained to the patient and his or her family before surgery is undertaken. When performing surgical contracture release, we currently have a low threshold for ulnar nerve decompression in patients lacking flexion or in patients with any symptoms of ulnar neuritis. Depending on surgeon experience as well as concomitant factors such as retained hardware, we may perform the release open or arthroscopically. Postoperatively, the use of CPM for approximately 6 weeks following surgery and compliance with a static adjustable splinting program remain essential to preserving the motion improvement achieved at surgery.

References 1. Ayoub, K., Gibbons, P., and Bradish, C. F.: Compass elbow hinge: Short-term results in five adolescents. J. Pediatr. Orthop. Part B 13:395, 2004. 2. Bae, D. S., and Waters, P. M.: Surgical treatment of posttraumatic elbow contracture in adolescents. J. Pediatr. Orthop. 21:580, 2001.

3. Fortier, M. V., Forster, B. B., Pinney, S., and Regan, W.: MR assessment of post-traumatic flexion contracture of the elbow. J. Magnet. Res. Imag. 5:473, 1995. 4. Gates, H. S., Sullivan, F. L., and Urbaniak, J. R.: Anterior capsulotomy and continuous passive motion in the treatment of post-traumatic flexion contracture of the elbow. J. Bone Joint Surg. 74A:1229, 1992. 5. Green, D. P., and McCoy, H.: Turnbuckle orthotic correction of elbow-flexion contractures after acute injuries. J. Bone Joint Surg. 61A:1092, 1979. 6. Henrikson, B.: Supracondylar fracture of the humerus in children. Acta Chir. Scand. 369:1, 1966. 7. Hepburn, G. R., and Crivelli, K. J.: Use of elbow Dynasplint for reduction of elbow flexion contracture. J. Sports Ther. 5:269, 1984. 8. Husband, J. B., and Hastings, H.: The later approach for operative release of post-traumatic contracture of the elbow. J. Bone Joint Surg. 72A:1353, 1990. 9. Jarvis, J. G., and D’Astous, J. L.: The pediatric T-supracondylar fracture. J. Pediatr. Orthop. 4:697, 1984. 10. Jones, G. S., and Savoie, F. H.: Arthroscopic capsular release of flexion contractures (arthrofibrosis) of the elbow. Arthroscopy 9:277, 1993. 11. Josefsson, O., Gentz, C., and Johnell, O.: Surgical versus nonsurgical treatment of ligamentous injuries following dislocations of the elbow joint. A prospective randomized study. J. Bone Joint Surg. 69A:605, 1987. 12. Jupiter, J. B., O’Driscoll, S. W., and Cohen, M. S.: The assessment and management of the stiff elbow. Instruc. Course Lect. 52:93, 2003. 13. Kim, S. J., and Shin, S. J.: Arthroscopic treatment for limitation of motion of the elbow. Clin. Orthop. Rel. Res. 375:140, 2000. 14. Lal, H. M., and Bhan, S.: Delayed open reduction for supracondylar fractures of the humerus. Int. Orthop. 15:189, 1991. 15. Mader, K., Koslowsky, T. C., Gausepohl, T., and Pennig, D.: Mechanical distraction for the treatment of posttraumatic stiffness of the elbow in children and adolescents. Surgical Technique. J. Bone Joint Surg. 89A(Part 1, Suppl 2):26, 2007. 16. Mansat, P., and Morrey, B. F.: The column procedure: a limited lateral approach for extrinsic contracture of the elbow. J. Bone Joint Surg. 80A:1603, 1998. 17. McIntosh, A., and O’Driscoll, S. W.: Arthroscopic treatment of elbow stiffness in pediatric and adolescent patients. Presented at the American Shoulder and Elbow Surgeons Specialty Day, AAOS Annual Meeting, San Diego CA, Feb. 17, 2007. 18. Mih, A. D., and Wolf, F. G.: Surgical release of elbow-capsular contracture in pediatric patients. J. Pediatr. Orthop. 14:458, 1994. 19. Mital, M. A., Barber, J. E., and Stinson, J. T.: Ectopic bone formation in children and adolescent with head injuries: its management. J. Pediatr. Orthop. 7:83, 1987. 20. Morrey, B. F.: Post-traumatic contracture of the elbow. J. Bone Joint Surg. 72A:601, 1990. 21. Morrey, B. F., Askew, L. J., An, K. N., and Chao, E. Y.: A biomechanical study of normal functional elbow motion. J. Bone Joint Surg. 63A:872, 1981.

Chapter 21 Post-Traumatic Elbow Stiffness in Children

22. Papandrea, R., Waters, P. M.: Posttraumatic reconstruction of the elbow in the pediatric patient. Clin. Orthop. (370):115126, 2000. 23. Papvasilious, V. A., and Beslikas, T. A.: T-condylar fractures of the distal humeral condyles during childhood: an analysis of six cases. J. Pediatr. Orthop. 6:302, 1986. 24. Phillips, B. B., and Strasburger, S.: Arthroscopic treatment of arthrofibrosis of the elbow joint. Arthroscopy 14:38, 1998. 25. Pirone, A. M., Graham, H. K., and Krajbich, J. I.: Management of displaced extension-type supracondylar fractures of the humerus in children. J. Bone Joint Surg. 70A:641, 1988. 26. Stans, A. A., Maritz, N. G. J., O’Driscoll, S. W., and Morrey, B. F.: Operative treatment of elbow contracture in patients

27.

28.

29.

30.

333

21 years of age or younger. J. Bone Joint Surg. 84A:382, 2002. Thompson, H. G., and Garcia, A.: Myositis ossificans: aftermath of elbow injuries. Clin. Orthop. Rel. Res. 50:129, 1967. Urbaniak, J. R., Hansen, P. E., Beissinger, S. F., and Aitken, M.: Correction of post-traumatic flexion contracture of the elbow by anterior capsulotomy. J. Bone Joint Surg. 67A:1160, 1985. Wedge, J. H., and Roberson, D. E.: Displaced fractures of the neck of the radius. J. Bone Joint Surg. 64B:256, 1982. Zionts, L. E., and Mirzayan, R.: Fracture of the lateral epicondyle of the humerus in a child: A case report. J. Bone Joint Surg. 84A:818, 2002.

SECTION

A

FRACTURES AND DISLOCATIONS

CHAPTER

22

Current Concepts in Fractures of the Distal Humerus Shawn W. O’Driscoll

INTRODUCTION Dramatic changes have occurred in the treatment of elbow fractures in recent years. This is especially true for distal humerus fractures. Although improvements in fracture-specific fixation devices have occurred, the most important advances can be attributed to a principlebased approach to these fractures. Recovery of painless and satisfactory elbow function after a fracture of the distal humerus requires anatomic reconstruction of the articular surface, restitution of the overall geometry of the distal humerus and stable fixation of the fracture fragments to allow early and full rehabilitation.2,4,5,7-9,14 Although these goals are obvious, the orthopedic community would agree that they may be technically difficult to achieve, especially in the presence of substantial osteoporosis or comminution.14 The techniques proposed by the AO/ASIF group had been standard for fixation of distal humerus fractures in the past.8,14 Their recommended technique included fixation of the articular fragments with screws and column stabilization with two plates at a 90-degree angle to one another.3,8,19 Fracture stability is only as secure as the fixation of the distal fragment to the shaft. Using standard AO/ASIF techniques, different authors

have reported unsatisfactory results in 20% to 25% of patients.2,4,5,7-9 Improvements in the treatment of these fractures recently have been predicated on understanding and overcoming the limitations and reasons for failure of previous techniques. When treatment of severe distal humerus fractures fails, it typically is due to either nonunion at the supracondylar level or stiffness resulting from prolonged immobilization that has been used in an attempt to avoid failure of inadequate fixation.14 Either way, the limiting factor is fixation of the distal fragments to the shaft. In an effort to increase the yield of excellent and satisfactory results obtained after fixation of distal humerus fractures and to reproducibly obtain stable fixation in the presence of osteoporosis or comminution, I recommend (and have used for two decades) an alternative philosophy and technique based on principles that maximize fixation in the distal fragments and compression at the supracondylar level.11-13,15,17 The key to the stability achieved with this fixation construct is that it combines the features and stability of an arch while locking the two columns of the distal humerus together. The stability achieved allows routine commencement of an intensive rehabilitation program postoperatively, including full active motion with no external protection. The following discussion expands on the general principles of our current approach to these fractures, the specific technical details, the postoperative program, and the potential complications.

PRINCIPLE-BASED FIXATION PRINCIPLES AND TECHNICAL OBJECTIVES Before discussing the details of surgical techniques, it is imperative that the treating surgeon understand the principles (Box 22-1) and technical objectives (Box 22-2) that, if followed and achieved respectively, will maximize the likelihood of a successful outcome from treatment of these fractures. 337

338

Part V Adult Trauma

PRINCIPLE-BASED SURGICAL TECHNIQUE BOX 22-1

Principles of Fracture Fixation Surgery The surgical technique is performed in five steps:

The principles by which the earlier mentioned goals are achieved, and the technical objectives at the time of surgery for achieving them, are 1. Maximize fixation in the distal fragment. 2. All fixation in distal fragments should contribute to stability between the distal fragments and the shaft.

BOX 22-2

Technical Objective Checklist

Concerning screws in the distal fragments (articular segment): 1. Each screw should pass through a plate. 2. Each screw should engage a fragment on the opposite side that is also fixed to a plate. 3. An adequate number of screws should be placed in the distal fragments. 4. Each screw should be as long as possible. 5. Each screw should engage as many articular fragments as possible. 6. The screws should lock together by interdigitation, thereby creating a fixed angle structure and linking the columns together. Concerning the plates used for fixation: 7. Plates should be applied such that compression is achieved at the supracondylar level for both columns. 8. Plates used must be strong enough and stiff enough to resist breaking or bending before union occurs at the supracondylar level.

EXPOSURE The operation is performed with the patient in the supine position. A sterile tourniquet is inflated only for dissection of the ulnar nerve, which is transposed anteriorly. The triceps-anconeus reflecting pedicle (TRAP) approach provides adequate exposure for a surgeon experienced with the technique.10 This technique involves combining the Bryan-Morrey and modified Kocher approaches to reflect the triceps in continuity with the anconeus. However, I believe that an olecranon osteotomy provides even greater exposure and is recommended in the setting of intra-articular comminution. The TRAP approach is indicated if total elbow replacement is necessary.

1. 2. 3. 4. 5.

Articular reduction Plate application and provisional fixation Distal fixation Supracondylar compression Final fixation

Stability and function are restored by achieving eight technical objectives (see Box 22-2) derived from the principles of (1) maximizing fixation in the distal fragments, and (2) ensuring that all fixation in the distal segment contributes to stability at the supracondylar level (see Box 22-1) (Fig. 22-1). All eight of these objectives are achieved with the technique of what we term parallel plating. The medial plate is placed on the medial aspect of the medial column, and the lateral plate is placed laterally, rather than posteriorly, on the lateral column. Although we refer to them as parallel, each plate is actually rotated posteriorly slightly out of the sagittal plane such that the angle between them is often in the range of 150 to 160 degrees. This orientation permits insertion of at least four long screws completely through the distal fragments from one side to the other. These screws interdigitate, thereby creating a fixed-angle structure and greatly increasing stability of the construct. Contact between screws is intended to enhance the locking together of the two columns. The plates must be contoured to fit the geometry of the distal humerus if precontoured plates are not available, but the latter facilitate anatomic reconstruction. Interfragmentary compression is obtained between articular fragments as well as at the metaphyseal level through the use of large bone clamps that provide compression during the insertion of the screws attaching the articular segment to the shaft. In the distal fragments, fully threaded screws inserted in this manner provide maximum thread purchase in the distal fragments. Additional compression at the metaphyseal level results from slight undercontouring of the plates and the use of dynamic compression holes in the plates. The specific steps of the surgical technique are detailed below.

STEP 1. ARTICULAR SURFACE REDUCTION Once the fracture is exposed, the first step is reassembly of the articular surface. The proximal ulna and radial head can be used as a template for the reconstruction of the distal humerus. The articular fragments are provisionally fixed with smooth Kirschner wires

Chapter 22 Current Concepts in Fractures of the Distal Humerus

339

FIGURE 22-1

The technical objectives described in this paper are illustrated. The screws in the distal fragments interlock, providing additional stability to the construct by “closing the arch.” Interlocking is best achieved by contact between the screws. The combination of multiple screws crisscrossing in close proximity with bone between them gives a “rebar” (reinforced concrete) type structure.

Fragment rotation

FIGURE 22-2

Step 1

(K wires) (Fig. 22-2). In cases with extensive comminution, fine threaded wires (1 to 1.5 mm) are used, then cut off and left in as definitive adjunctive fixation. K wires permit assembly of the joint surface fragments in a manner that is analogous to the use of dowels

Step 1. Articular reduction. The articular fragments, which tend to be rotated toward each other in the axial plane, are reduced anatomically and provisionally held with 0.035 inches or 0.045 inches smooth Kirchner wires. It is essential that the wires be placed close to the subchondral level, to avoid interference with later screw placement, and away from where the plates will be placed on the lateral and medial columns. One or two strategically placed pins can be used to provisionally hold the distal fragments aligned with the shaft.

in furniture making. It is necessary that these wires be placed close to the subchondral level so as not to interfere with the passage of screws from the plates into the distal fragments; specifically, no screws are placed in the distal fragments until the plates are

340

Part V Adult Trauma

applied. The articular fragments are fixed in the following order: 1.a. Anterior trochlea and capitellum 1.b. Medial trochlea 1.c. Posterior fragments The articular surface of the distal humerus should be reconstructed anatomically unless bone is missing. In the event of absent bone, two important principles should be taken into consideration. First, the anterior aspect of the distal humerus is the critical region that needs to be restored in order to have a functional joint; reconstruction of the posterior articular surface of the distal humerus is less critical. Second, stability of the articulation requires the presence of the medial trochlea in combination with either the lateral half of the trochlea or the capitellum; thus, the medial trochlea is essential to obtain a stable and well-aligned joint.

STEP 2. PLATE APPLICATION AND PROVISIONAL FIXATION We routinely use precontoured medial and lateral plates from the Mayo Congruent Elbow Plate System (Acumed, Hillsboro, OR) (Fig. 22-3). The medial plate can be extended

to the articular margin in very distal or comminuted fractures and is contoured to the shape of the medial epicondyle. The ulnar nerve must be transposed if this extended plate is used. The distal end placed more posteriorly to prevent impinging on, or cutting into, the common extensor tendon and lateral collateral ligament complex. Both plates should be slightly undercontoured to provide additional compression at the metaphyseal region when applied. The length of the plates is selected so that at least three screws are placed both medially and laterally proximal to the metaphyseal component of the fracture. These plates are designed so that in any combination they will end at different levels to avoid the creation of a stress riser proximally. The plates are then provisionally applied according to the following steps: 1. Two smooth Steinmann pins (2.0 to 2.5 mm) are introduced at the medial and lateral epicondyles through holes in the plates while they are held accurately against the bone; the most commonly used holes are the second one laterally and the third medially. These pins are left in place until after step 4 (see later). The pins create pilot holes for later replacement with screws, are easy to drill around, and do not interfere as much with placement of the two distal screws, as would be the case if they were replaced by screws earlier. 2. The appropriate reduction of the distal fragments to the humeral shaft at the supracondylar level is confirmed. 3. One cortical screw is loosely introduced into a slotted hole to hold each plate in place. Use of slotted holes for these screws facilitate later adjustments in plate positioning.

STEP 3. DISTAL FIXATION

Step 2 FIGURE 22-3

Step 2. Plate application and provisional fixation. Medial and lateral precontoured plates are placed and held apposed to the distal humerus, while one smooth 2 or 2.5 mm Steinmann pin is inserted through hole #2 (numbered from distal to proximal) of each plate, through the epicondyles, and across the distal fragments, to maintain provisional fixation of the plates to the distal fragments. A screw is placed in the slotted hole (#5) of each plate, but not fully tightened, leaving some freedom for the plate to move proximally later during compression. Because the undersurface of each plate is tubular in the metaphyseal and diaphyseal regions, the screw in the slotted hole only needs to be tightened slightly to provide excellent provisional fixation of the entire distal humerus.

Once the plates are provisionally applied, medial and lateral screws are introduced distally to provide stable fixation of the intraarticular fragments and rigid anchorage to the plates (Fig. 22-4). 1. Two distal screws, one medial and one lateral, are inserted using a targeted drill guide. As stated earlier, the screws should be as long as possible, pass through as many fragments as possible, and engage in the opposite column. Before screw insertion, a large bone clamp is used to compress the intra-articular fracture lines, unless there is a gap in the articular surface. This ensures interfragmentary compression without the need for lag screws.

STEP 4. SUPRACONDYLAR COMPRESSION The plates are then fixed proximally under maximum compression at the supracondylar level (Fig. 22-5A and B).

Chapter 22 Current Concepts in Fractures of the Distal Humerus

341

Step 3

FIGURE 22-4

Step 3. Screws are inserted through hole #1 of the lateral plate and across the distal articular fragments from lateral to medial, and tightened. This step is repeated on the medial side, using hole #3. In young patients, 3.5-mm cortical screws are used (to prevent breakage), whereas long 2.7-mm screws are used in patients with osteoporotic bone. The distal screws should be as long as possible, passing through as many fragments as possible, and engaging the condyle or epicondyle of the opposite column.

1. The slotted proximal screw on one side is backed out, and a large bone clamp is applied distally on that side and proximally on the opposite cortex to eccentrically load the supracondylar region. A second proximal screw is inserted through the plate in compression mode and then the screw in the slotted hole retightened. Care should be taken not to change the varus-valgus or rotational alignment of the articular surface when the bone clamps are applied. 2. The same steps are followed on the opposite side. Following this step the fixation should be stable. 3. The remaining diaphyseal screws are then introduced, providing additional compression as a result of the undercontoured plates being pulled down to the underlying bone. To avoid having the screws strip the bone, this last step is best performed by squeezing the plates against the bone with a large clamp rather than relying on the screws to deform the plates.

Step 4A

A

B

Step 4B

FIGURE 22-5

Step 4. A, Using a large tenaculum to provide interfragmentary compression across the fracture at the supracondylar level, the lateral column is fixed first. A screw is placed in dynamic compression mode (inset) in hole #4 of the lateral plate. Tightening it further enhances interfragmentary compression at the supracondylar level (converging arrows) to the point of causing some distraction at the medial supracondylar ridge (diverging arrows). B, The medial column is then compressed in a similar manner using the large tenaculum, and a screw is inserted in the medial plate in dynamic compression mode. If the plates are slightly undercontoured, they can be compressed against the metaphysis with a large bone clamp, giving further supracondylar compression.

STEP 5. FINAL FIXATION

DEALING WITH METAPHYSEAL BONE LOSS

The smooth Steinmann pins are removed, and then the remainder of the screws are inserted (Fig. 22-6). The intraoperative elbow motion should be full unless significant swelling has already developed. One deep and one subcutaneous drain are placed during the closure. The skin should be closed with staples or interrupted sutures.

Adequate bony contact with interfragmentary compression in the supracondylar region is necessary to ensure the stability of the construct and eventual fracture union. If metaphyseal bone loss or comminution precludes an anatomic reconstruction with satisfactory bony contact, the humerus can be shortened at the metadiaphyseal fracture site, provided that the overall alignment and

342

Part V Adult Trauma

Step 5

FIGURE 22-6

Step 5. The smooth Steinmann pins are all removed and the remainder of the screws inserted. The distal screws interdigitate for maximum fixation in the distal articular fragments (as described in Fig. 22-1).

geometry of the distal humerus is correct. We refer to this alternative reconstructive technique as supracondylar shortening (Fig. 22-7A to G). This technique is especially useful in cases of combined soft tissue and bone loss. Shortening by 1 cm or less has only a slight effect on triceps strength in terminal extension,6 and in cases of severe soft tissue and bone loss, up to 2 cm of shortening can be tolerated without serious disturbance of elbow biomechanics.6

POSTOPERATIVE MANAGEMENT Immediately after wound closure, the elbow is placed in a bulky noncompressive Jones dressing with an anterior plaster slab to maintain full extension and the upper extremity is kept elevated for 3 days or more, depending on the extent of soft tissue damage. Those fractures with severe soft tissue damage, which include most open fractures and high-energy closed fractures, are immobilized and elevated in elbow extension for 3 to 7 days postoperatively. While elevated, the limb is let down for a few minutes once or twice each hour to permit

shoulder movement, to relieve discomfort, and to prevent perfusion disturbance. Closed fractures without severe swelling or fracture blisters are removed from the Jones dressing after 3 days, and a nonconstrictive elastic sleeve is applied over an absorbent dressing placed on the wound. A physical therapy program including active and passive motion is then initiated. All patients are permitted active use of the hand and instructed not to lift (or push or pull) anything heavier than a glass of water or a telephone receiver for the first 6 weeks. No form of external protection, such as casts or braces is needed if the technical objectives have been achieved. If postoperative motion fails to progress as expected, a program of patient-adjusted static splinting is instituted as soon as the soft tissues are healed. The torque across the elbow applied with such a patient-adjusted splint was low enough to cause discomfort but not pain, and therefore not of concern with regard to the security of the fracture fixation. Continuous passive motion (CPM) is helpful in speeding the recovery of motion if the soft tissues will tolerate CPM. In cases of severe soft tissue trauma, it may be wise to postpone or avoid using CPM.

STRUCTURAL STABILITY VERSUS FRACTURE STABILITY I wish to emphasize that this principle-based technique is not just a different method of fracture fixation. It is a whole new concept based on the idea that stability of the distal humerus is achieved by the creation of an architectural structure. The bone fragments rely on their integration with the whole structure for stability, rather than on fixation of each bone fragment by screw threads. The concept is borrowed from modern architecture and the application of civil engineering principles to surgery. The interdigitation of screws within the distal segment rigidly attaches the articular fragments to the shaft by linking the two columns together. This permits stability to be achieved in such cases as low transcondylar (Fig. 22-8A to D) or severely comminuted (Fig. 22-9A to D) fractures. The concept follows the architectural principles of an arch, in which two columns are anchored at their base (on the shaft of the humerus) and linked together at the top (long screws from the plates on each side interdigitating within the articular segment). The interdigitation is best achieved by contact between the screws. However, multiple screws separated by small gaps within the bone will function as a “rebar” construct (steel rods inside concrete). Fixation of the bone fragments is thus reliant not on screw purchase in the bone, but on the stability of the hardware framework, in just the same way that a modern building derives its stability from the grid

Chapter 22 Current Concepts in Fractures of the Distal Humerus

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Fragment rotation

A

B

C

E

D

H

I

F

G

FIGURE 22-7

In cases of supracondylar bone loss, and in some cases of severe comminution, anatomic placement of the distal humerus with respect to the shaft would leave a large structural defect in one or other column, and only point contact in the other. In such cases when structural bone graft is not an option, a supracondylar shortening osteotomy can be performed. A, This involves reshaping the distal end of the shaft (dark lines) (never the articular segments) to enhance contact between the distal articular segment and the shaft. Usually, only a small amount of bone is resected from the distal end of the shaft, and sometimes from one side of it as well (for side-to-side apposition and compression). B and C, The limb is shortened through the fracture site to permit interfragmentary compression between the trochlea and the distal shaft, between the capitellum and the distal shaft, and side to side on one or both sides. Once these surfaces have been compressed and fixed with the plates, stability is strong enough to permit immediate motion and rehabilitation. It is acceptable to translate the distal segment medially or laterally, and also slightly anteriorly, provided that rotational and valgus alignment is maintained. D to G, Preoperative and most recent radiographs of a severe distal humerus fracture with substantial bone loss that was treated with shortening. H and I, Elbow range of motion at most recent follow-up was 0 to 150 degrees.

work of steel assembled and bolted or welded together inside its walls and columns. The screws in the distal segment are converted into fixed angle screws by two of the technical objectives. First, several long screws in the distal fragments lock together by interdigitation. Second, these screws pass through a plate on one side and into a bone fragment

on the other side that itself is also anchored by a plate. From an engineering perspective, this technique of creating fixed angle screws enhances fixation in the distal fragments. It also permits rigid linkage and compression between the distal segment and the shaft. The combined use of clamps, strong and slightly undercontoured plates, dynamic compression holes, and selected metaphyseal

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C

A

B D FIGURE 22-8

Low supraintercondylar fractures through osteopenic bone (A and B) require placement of the plates distal enough to allow secure fixation. Excellent stability can still be obtained with the technique of parallel plating, employing a medial plate that is contoured around the epicondyle onto the medial side of the trochlea along with a lateral plate (C and D).

Chapter 22 Current Concepts in Fractures of the Distal Humerus

A

345

C

D B FIGURE 22-9

A severely comminuted fracture (A and B) that healed uneventfully after open reduction and internal fixation. C and D, Fine-threaded K-wires, fully embedded in the bone, were used to assemble the articular fragments, just as dowels are used when pieces of wood are glued together to make furniture.

shortening provides interfragmentary compression at the supracondylar level. The stability of the construct is such that a rehabilitation program can be commenced in the immediate postoperative period without fear of hardware failure.

Role of Locking Screws Although fixed angle locking plates are available, I prefer to use variable angle locking screws (TAPLOC Acumed, Hillsboro, OR) for the distal segment to prevent the problem of incorrect screw positioning due to the fixed

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angles predetermined other plate designs. With the use of locking screws, fewer screws are thought necessary. However, based on my experience, and that of colleagues, I do not believe that locking screws are necessary if the principles and technical objectives for structural stability are achieved.

POTENTIAL COMPLICATIONS The main complications that have been reported after internal fixation of distal humerus fractures are residual decreased range of motion, fixation failure with nonunion or malunion, nerve dysfunction, extensor mechanism dysfunction, post-traumatic degenerative changes, wound and skin problems, and avascular necrosis.1,2,4,5,7-9,20 The combination of ischemic skin and a subcutaneous hematoma is an indication for surgical lavage and reclosure of the wound. With the internal fixation technique described earlier, we have experienced only one case of fixation failure in the past two decades. A 3.5 reconstruction plate experienced fatigue fracture 6 months after surgery in a patient with a severe open injury treated by supracondylar shortening and flap coverage. The lateral column had healed, necessitating only refixation and bone grafting of the medial column, which did result in union. His final range of motion was 20 to 120 degrees. Decreased range of motion may occur secondary to heterotopic ossification, intra-articular adhesions, or capsular contracture. If heterotopic ossification prevents recovery of motion, the patient may require excision of the heterotopic bone and a capsular release that can be performed 3 to 6 months after the surgery. If the surgery is performed later, the hardware can be removed if the fracture is completely healed. However, if it is removed too early, refracture may occur. Dysfunction of the extensor mechanism may occur if the triceps tendon fails to heal to the olecranon. Careful attention to reattachment of the extensor mechanism at surgery should help prevent this complication. The reconstruction should be solid enough to allow passive elbow flexion. Weakness does not seem to be a major problem with use of the TRAP approach for distal humerus fractures although it has not been specifically evaluated. Should discontinuity or subluxation of the extensor mechanism occur, it can be surgically treated by primary repair or augmentation with an Achilles tendon allograft. Olecranon nonunion can be treated by plate fixation and bone grafting. Joint deterioration may be secondary to the cartilage damage sustained at the initial injury or the avascular necrosis secondary to the devascularization of some articular fragments in severely comminuted injuries.

We have had one case of severe osteonecrosis in a severe multifragmentary fracture. To minimize the likelihood of this complication, it is necessary to leave all soft tissues attached to the distal fragments during surgery. Some cases of osteonecrosis may actually represent mechanical destruction due to instability of one or more articular fragments. It can be expected that if a fragment is mobile, it will cause progressive bone erosion.

PITFALLS AND TIPS One pitfall to avoid is the placement of a free screw into the distal fragments prior to application of a plate. Such a screw does not contribute to supracondylar stability (principle #2) and is not as secure as it might have been if it had passed through a plate (principle #1). It also potentially interferes with the passage of the screws through the plate into the distal articular segment. Another pitfall is the inappropriate placement of K-wires for provisional fixation. These should be placed in the subchondral region rather than in the center of the articular segments where the screws will go. They also need to be placed where they will not interfere with the plates. Anticipating where the plates will be positioned on the bone before placing the temporary K-wires avoids this problem. Some surgeons experience difficulty with placement of the distal articular screws through the plates and across to the other side without violating the joint or the olecranon fossa. This maneuver is facilitated by the use of a targeted drill guide and by waiting to replace the 2 or 2.5 mm Steinmann pins in the distal articular segments until after having placed at least one screw through a second hole of each plate. These pins reserve a pathway for screws to be placed across the distal segment from each side. They also are easy to drill past and place a screw past, whereas if they are replaced by screws immediately, the subsequent drilling is rendered more difficult by the larger diameter screw. Moreover, when drilling through the distal segment, a drill bit may be prone to hitting a screw and break. This problem can be avoided by drilling with the drill on reverse or by drilling with a smooth Steinmann pin; the pin will tend to deflect off a screw rather than breaking. With respect to the soft tissues, a common pitfall and misunderstanding is the assumption that the technique of parallel plating requires additional soft tissue stripping. Although the lateral skin flap must be raised around to the lateral supracondylar ridge and the lateral epicondyle, there is no additional stripping of the deep soft tissues from the lateral column compared to traditional plating of a distal humerus fracture. In all circumstances, the soft tissues should be retained on the articular fragments.

Chapter 22 Current Concepts in Fractures of the Distal Humerus

Excessive contouring of the distal end of the lateral plate can cause entrapment of the common extensor origin or lateral collateral ligament complex. This can result in loss of motion and even necrosis of the underlying soft tissues. This is avoided by placing the plate such that it stops at the epicondyle rather than distal to it and by ensuring that the plate does not wrap around the epicondyle and compress the soft tissues. This will give the appearance on the postoperative radiograph of the tip of the plate sitting away from the bone, but this

space is required to accommodate the soft tissues under the plate. The single biggest impediment to successful application of this principle-based technique is the misconception that plates must be applied in two perpendicular planes. Although that used to be true when very weak 3.5 one-third tubular plates were used, it most certainly is not true when strong plates are used. The “parallel” double-plate construct has been shown to provide excellent stability even in the presence of supracondylar

A

B

FIGURE 22-10 Lateral column failure (varus). A, Failure fixation often occurs in the lateral column through repetitive gravitational forces that apply repetitive varus stress across the elbow. If the anteroposterior radiograph of the elbow is turned horizontally, one can readily appreciate the way in which varus stresses are applied. B, This mechanism of failure can be minimized by placing the lateral column plate in the sagittal plane on the lateral surface and having the screws pass all the way through to the medial side. C, With the elbow flexed to 90 degrees, varus stresses pull the lateral column and capitellum away from the posterior plate on the lateral column. Screw failure is by direct pullout from the soft and/or comminuted bone.

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C

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gaps.18 In fact, Schemitsch et al.18 showed that the combination of a medial reconstruction and lateral DuPont plate in parallel planes was stronger than two reconstruction plates placed in two planes 90 degrees to each other, as is recommended by the AO/ASIF group and currently employed by most surgeons. When failure occurs, it is likely to start in the lateral column. With only one to three short screws into the capitellum, it can pull away from a posteriorly placed plate (Fig. 22-10A to C). We strongly recommend the use of this technique for comminuted distal humerus fractures, and prefer its use routinely for less complex fractures as well, because the stability is such that intensive rehabilitation is possible. However, for noncomminuted fractures in good quality bone, either technique can be used reliably. The efficacy of this approach to achieving structural stability was conclusively documented in a series of 32 consecutive complex distal humeral fractures.16 Twentysix fractures were AO type C3, and 14 were open. Despite extensive comminution, bone loss, osteoporosis, or open wounds, neither hardware failure nor fracture displacement occurred in any patient. Union of 31 of the 32 fractures was achieved primarily. No patients required surgery to treat elbow stiffness unless heterotopic ossification had formed. There was one deep infection that resolved without hardware removal and did not impede union. At the time of the most recent followup, 28 elbows were either not painful or only mildly painful, and the mean flexion-extension arc was 99 degrees. In summary, this principle-based approach to achieving “structural stability” in distal humerus fractures has many advantages. Complex fractures are able to be fixed with sufficient stability to permit immediate intensive rehabilitation. Some fractures that have been thought to be unfixable have been very satisfactorily fixed by applying the principles outlined herein. More straightforward fractures are easily fixed using the same techniques. In our experience, the stability achieved with this approach is so much greater than that with traditional methods of fixing distal humerus fractures that bone graft has only very rarely been required, despite the severity of injuries so typical of the tertiary referral nature of our practice.

References 1. Ackerman, G., and Jupiter, J. B.: Non-union of fractures of the distal end of the humerus. J. Bone Joint Surg. 70-A:75, 1988. 2. Gabel, G. T., Hanson, G., Bennett, J. B., Noble, P. C., and Tullos, H. S.: Intraarticular fractures of the distal humerus in the adult. Clin. Orthop. Rel. Res. 216:99, 1987.

3. Helfet, D. L., and Hotchkiss, R. N.: Internal fixation of the distal humerus: A biomechanical comparison of methods. J. Orthop. Trauma. 4:260, 1990. 4. Henley, M. B., Bone, L. B., and Parker, B.: Operative management of intra-articular fractures of the distal humerus. J. Orthop. Trauma 1:24, 1987. 5. Holdsworth, B. J., and Mossad, M. M.: Fractures of the adult distal humerus. J. Bone Joint Surg. 72-B:362, 1990. 6. Hughes, R. E., Schneeberger, A. G., An, K. N., Morrey, B. F., and O’Driscoll, S. W.: Reduction of triceps muscle force after shortening of the distal humerus: a computational model. J. Shoulder Elbow Surg. 6:444, 1997. 7. John, H., Rosso, R., Neff, U., Bodoky, A., Regazzoni, P., and Harder, F: Operative treatment of distal humeral fractures in the elderly. J. Bone Joint Surg. 76-B:793, 1994. 8. Jupiter, J. B., Neff, U., Holzach, P., and Allgower, M.: Intercondylar fractures of the humerus. J. Bone Joint Surg. 67A:226, 1985. 9. Letsch, R., Schmit-Neuerburg, K. P., Sturmer, K. M., and Walz, M.: Intraarticular fractures of the distal humerus. Surgical treatment and results. Clin. Orthop. Rel. Res. 241:238, 1989. 10. O’Driscoll, S.: The triceps-reflecting anconeus pedicle (TRAP) approach for distal humeral fractures and nonunions. Orthop. Clin. North Am. 31:91, 2000. 11. O’Driscoll, S. W.: Optimizing stability in distal humeral fracture fixation. J. Shoulder Elbow Surg. 14(1 Suppl S):186S, 2005. 13. O’Driscoll, S. W., Jupiter, J. B., Cohen, M. S., Ring, D., and McKee, M. D.: Difficult elbow fractures: pearls and pitfalls. Instr. Course Lect. 52:113, 2003. 12. O’Driscoll, S. W., Sanchez-Sotelo, J., and Torchia, M. E.: Management of the smashed distal humerus. Orthop. Clin. North Am. 33:19, 2002. 14. Ring, D., and Jupiter, J. B.: Fractures of the distal humerus. Orthop. Clin. North Am. 31:103, 2000. 15. Sanchez-Sotelo, J., Torchia, M., and O’Driscoll, S. W.: Principle-based internal fixation of distal humerus fractures. Tech. Hand Up. Extrem. Surg. 5:179, 2001. 16. Sanchez-Sotelo, J., Torchia, M. E., and O’Driscoll, S. W.: Complex distal humeral fractures: internal fixation with a principle-based parallel-plate technique. J. Bone Joint Surg. Am. 89:961, 2007. 17. Sanchez-Sotelo, J., Torchia, M. E., and O’Driscoll, S. W.: Complex distal humeral fractures: internal fixation with a principle-based parallel-plate technique. J. Bone Joint Surg. Am. 90(Suppl 2):31, 2008. 18. Schemitsch, E. H., Tencer, A. F., and Henley, M. B.: Biomechanical evaluation of methods of internal fixation of the distal humerus. J. Orthop. Trauma 8:468-475, 1994. 19. Self, J., Viegas, S. F., Buford, W. L., and Patterson, R. M.: A comparison of double-plate fixation methods for complex distal humerus fractures. J. Shoulder Elbow Surg. 4:11, 1995. 20. Sodergard, J., Sandelin, J., and Bostman, O.: Postoperative complications of distal humeral fractures. 27/96 adults followed up for 6 (2-10) years. Acta Orthop. Scand. 63:85, 1992.

Chapter 23 Nonunion and Malunion of Distal Humerus Fractures

CHAPTER

23

Nonunion and Malunion of Distal Humerus Fractures Joaquin Sanchez-Sotelo

INTRODUCTION Nonunion and malunion are two of the most common and challenging complications of distal humerus fractures. Newer internal fixation principles and techniques have improved our ability to achieve stable fixation of complex distal humerus fractures18 (see Chapter 22, Current Concepts in Fractures of the Distal Humerus). However, some fractures will fail to unite, leaving the patient with an unstable, dysfunctional, and oftentimes painful upper extremity requiring additional surgery. Distal humeral malunion is well characterized in the pediatric population after supracondylar fractures (see Chapters 14 and 15) but has not been analyzed as extensively in the adult population.4,8 This chapter reviews the prevalence, risk factors, pathology and treatment options for distal humeral nonunions and the clinical relevance and treatment options for distal humeral malunion.

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extensive comminution or when suboptimal fixation techniques are used. Other risk factors for fracture nonunion include smoking, use of immunosuppressive medications, severe associated soft tissue injuries, osteopenia, and poor compliance with postoperative instructions.

PATHOLOGY Distal humeral nonunions share a constellation of pathologic findings that need to be addressed at the time of surgery (Fig. 23-1). The nonunion is usually located at the supracondylar level; most of the time, the distal fragments heal in a more or less anatomic position. Progressive bone reabsorption at the nonunion site may lead to severely compromised bone stock. Previously placed hardware may compromise bone stock even further, especially when screw loosening results in a windshield-wiper effect. Additionally, severe stiffness develops, and when the patient tries to flex and extend the elbow, most motion occurs through the nonunion site, not through the joint.7 Failure to release the associated elbow contracture at the time of fixation of the nonunion may contribute to failure; otherwise, when elbow motion is rehabilitated excessive loads are transmitted through the nonunion site. Not uncommonly, ulnar nerve excursion is compromised by scarring, especially when there has been previous surgery. Excessive motion at the nonunion site may further compromise the function of the ulnar nerve by stretching. Attention should be paid to the ulnar nerve at the time of surgery.

EVALUATION AND TREATMENT OPTIONS History and Physical Examination

DISTAL HUMERAL NONUNION PREVALENCE AND RISK FACTORS Distal humerus nonunion with hardware failure and fracture redisplacement usually presents within the first few months after surgery. The prevalence of hardware failure is difficult to determine, because in some cases, hardware failure may allow ultimate fracture healing with residual secondary displacement. In addition, some potential failures of fixation may be avoided by prolonged postoperative immobilization, leading to fracture healing but very limited motion. Nonunion or hardware failure have been reported in approximately 8% to 25% of recent series on distal humerus fractures.6,9,14,19,20 In our experience, poor initial fracture fixation is the most common risk factor for fracture nonunion. Stable fixation is difficult to achieve, especially in fractures with

The history and physical examination should help delineate the details of the initial injury and subsequent treatment attempts. Risk factors for bone nonunion should be identified, including smoking and use of medications that may inhibit bone formation. It is also important to document the location and status of previous skin incisions, identify the location and ulnar nerve, and examine the neurovascular function of the upper extremity. Patients should be specifically questioned about symptoms or signs of infection after previous surgeries.

Imaging Studies When possible, sequential radiographs should be evaluated to understand the initial fracture pattern, assess the quality of the initial fixation when previously attempted, and determine the amount of bone loss. Recent radiographs will help determine the feasibility of repeated internal fixation versus

Simple Radiographs

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A FIGURE 23-1

Anteroposterior radiograph of a patient with a distal humerus nonunion after failed internal fixation. Bone stock is compromised by the nature of the initial injury and the effects of loose hardware.

arthroplasty and the need for structural bone graft and special tools for hardware removal. Computed tomography with three-dimensional reconstruction is an invaluable tool when repeated internal fixation is planned (Fig. 23-2), because it provides a better understanding of the remaining bone stock and any degree of associated malunion, and facilitates planning of plate and screw placement in order to achieve the maximum anchorage of the fixation devices.

Computed Tomography

Aspiration and Laboratory Studies Every patient presenting with a distal humerus nonunion and previous surgery or suspicious findings in the history or physical examination should be evaluated for infection. An abnormal cell blood count and elevated sedimentation rate and C-reactive protein should raise the possibility of infection. Aspiration of the elbow joint and the nonunion site provide invaluable information; the aspiration may be performed under fluoroscopy when access is difficult. Ideally, patients on antibiotics should discontinue their treatment between 2 and 4 weeks before the aspiration. Samples should be sent for cell count, gram stain, cultures and sensitivities.

B FIGURE 23-2

A, Computed tomography represents an excellent imaging modality for understanding and surgical planning in distal humerus nonunion. B, Threedimensional reconstruction may help understand rotational and angular deformities and assist in proper reduction at the time of surgery.

Chapter 23 Nonunion and Malunion of Distal Humerus Fractures

INTERNAL FIXATION Internal fixation is the treatment of choice for the majority of patients presenting with a distal humerus nonunion. The goals of internal fixation are (1) to achieve an adequate reduction and stable internal fixation, (2) stimulate bone healing with bone graft or substitutes, (3) release the associated joint contracture to help achieve a functional range of motion and decrease the stresses on the fixation, and (4) protect the ulnar nerve.

Surgical Technique Surgical Approach and Ulnar Nerve Decompression Most patients with previous surgery will have a

posterior midline skin scar that may be used for the revision procedure. If the previous fixation was attempted through separate lateral and medial incisions, most of the time, it is better to ignore those and create a new posterior midline skin incision, unless the skin quality is compromised and wound problems are anticipated. Next, the ulnar nerve should be identified; when a previously transposed ulnar nerve is asymptomatic, additional nerve dissection should be avoided as long as the procedure can be performed without further nerve exposure and the ulnar nerve can be protected and reassessed at the end of the procedure. The nerve should be formally isolated and transposed when it was left in situ during previous surgeries.7 Neurolysis should be

considered in patients with a previously transposed symptomatic ulnar nerve. Several deep exposures may be used. A nonunited previous olecranon osteotomy should be used for exposure whenever present. Similarly, when a tricepsreflecting or triceps reflecting anconeus pedicle (TRAP) approach was used for previous surgeries, the same approach should be used if incomplete healing of the extensor mechanism to the olecranon is found at the time of surgery.11 For extra-articular nonunions with an intact extensor mechanism, the so-called bilaterotricipital approach (working on both sides of the triceps without violating the extensor mechanism) provides good exposure while preventing complications such as olecranon nonunion or triceps weakness (Fig. 23-3).2 Olecranon osteotomy provides an excellent exposure and is used by many surgeons for fixation of distal humerus nonunion (Fig. 23-4).15 Alternatively, a tricepsreflecting (Bryan-Morrey or Mayo-modified extensile Köcher) or TRAP approach is selected when the decision to proceed with fixation versus arthroplasty will be taken intraoperatively.3 Once the deep exposure is complete, tissue should be sent routinely for pathology and microbiology. Capsular contracture is a constant feature of distal humerus nonunions. Failure to release the contracture will limit final range of motion and

Capsular Release

FIGURE 23-3

A

B

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A, Anteroposterior radiograph showing an extra-articular distal humerus nonunion. B, These injuries can be fixed working on both sides of the triceps.

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FIGURE 23-4

Most complex distal humerus nonunions require a more extensile approach such as an olecranon osteotomy for fixation.

increase the stress transmitted to the nonunion site, which may contribute to fixation failure. The posterior capsule and posterior band of the medial collateral ligament can been accessed and resected easily through any of the posterior approaches mentioned earlier. The anterior capsule may be released through the nonunion site (Fig. 23-5). Care should be taken to identify and protect the radial and median nerves at the time of the anterior capsular release. The anterior band of the medial collateral ligament and the lateral collateral ligament complexes should be preserved, along with the muscular attachments on the medial and lateral epicondyles, which are responsible for most of the blood supply to the distal segments. The fixation technique that we recommend for internal fixation of distal humerus nonunions follows the same principles, objectives, and steps described for fixation of acute distal humerus fractures in the previous chapter (see Chapter 22).18 However, bone reabsorption at the nonunion site usually makes it difficult to apply compression at the supracondylar level if the reduction is anatomic, and the concept of metaphyseal shortening (see Chapter 22) often needs to be applied.12 Correct orientation of the distal fragment relative to the diaphysis may be difficult, especially in cases with Fixation Technique and Bone Grafting

FIGURE 23-5

The anterior elbow capsule may be resected through the nonunion site to avoid residual stiffness and decrease stress on the fixation construct.

more extensive bone loss. Care should be taken to avoid excessive flexion, extension, valgus, varus, or malrotation when the distal portion is aligned with the diaphysis. After reduction and provisional fixation of the nonunion with Kirschner wires, the quality of the reduction may be assessed under fluoroscopy, if necessary. Correct rotational alignment will place the forearm in roughly symmetrical positions with shoulder internal and external rotation. Excessive flexion or extension will shift the elbow arc into more flexion or more extension respectively. If shortening at the nonunion level is needed to achieve adequate bone contact and compression, the distal segment should be translated anteriorly to provide room for the coronoid and radial head in flexion; extension will be limited until a new olecranon fossa is recreated by excavating bone at the posterior aspect of the diaphysis. Once the reduction is considered satisfactory, the need for structural bone graft should be assessed and dealt with accordingly. Tricortical iliac crest bone graft may be needed to reconstruct large areas of bone loss. Two parallel plates are then applied medially and laterally, and fixed with multiple distal long screws, which most of the time will interdigitate and interlock, increasing the stability of the construct (Fig. 23-6). Compression at the nonunion site is achieved by a combination of maneuvers including the use of a large reduction

Chapter 23 Nonunion and Malunion of Distal Humerus Fractures

FIGURE 23-6

A

Parallel-plating internal fixation provides satisfactory stability even in cases with severe bone loss. Note the posterior to anterior screws on the lateral radiograph to fix iliac crest bone graft.

B

clamp, proximal screw insertion in the compression mode, and slight undercontouring of the plates. Cancellous bone autograft or a bone graft substitute is then placed at the nonunion site to promote bone healing. Our preference is to fashion two thin corticocancellous plates from the iliac crest and fix them with one or more screws across the nonunion site on the medial and lateral columns (Figs. 23-6 and 23-7).

Postoperative Management After closure, the elbow is immobilized with an anterior plaster splint in full extension and kept elevated to minimize postoperative swelling. Motion is initiated as soon as the condition of the soft tissues allows, provided a stable construct has been achieved. However, when fixation of a nonunion is attempted, bone healing takes precedence over motion. If the distal humerus nonunion heals with residual stiffness, contracture release is very reliable; on the contrary, if the new fixation attempt fails, progressive loss of bone stock will compromise treatment options. Continuous passive motion or patientadjusted static splints are commonly used to maintain the motion achieved at the time of surgery. When intraoperative cultures become positive a few days after internal fixation in a patient with a previously unknown infection, the patient should receive 6 weeks of intravenous antibiotic therapy, and consideration should be given to chronic oral antibiotic suppression.

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FIGURE 23-7

Intraoperative photograph showing iliac crest bone graft fixed posteriorly with screws.

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Outcome There are several studies on the results of internal fixation for distal humerus nonunions. Some articles have included a wide spectrum,5 from delayed unions and nonunions affecting one column to infected nonunions with bone loss and associated deep infection. Other authors have studied more specific group of patients, such as flail or osteochondral nonunions.16,17 It is important to understand the information summarized below as it pertains to the particular case presenting for treatment. Early treatment attempts for distal humerus nonunions were somewhat discouraging. Mitsunaga et al10 reported on 25 patients treated with internal fixation; close to 30% of the patients required additional surgery for revision fixation or bone grafting. Ackerman and Jupiter1 published a higher union rate of 94% in a series of 20 patients, but the functional results were fair or poor in 65% of the cases, and only one patient was considered to have an excellent result. The authors noted that most patients continue to have a major long-term disability despite achieving successful union. The results of internal fixation for distal humerus nonunions were improved with the introduction of better fixation constructs and attention to capsular release and the ulnar nerve.7 The more recent literature on the outcome of internal fixation for distal humerus nonunions shows improved overall results,5 but there are some specific subsets of patients in which internal fixation continues to provide suboptimal outcomes.16,17 Helfet et al5 recently published their experience with internal fixation in 52 patients presenting with a delayed union (13 patients) or a nonunion (39 patients) of the distal humerus. Most (39 patients) but not all patients had undergone previous failed surgery. There was a wide range of patterns of nonunion included in this study. Only 13 nonunions were intercondylar; the remaining were supracondylar in 27 patients, transcondylar in 6 patients, and lateral or medial condylar in 6 patients. Union was achieved in all but one patient, and the average final arc of motion was 94 degrees. However, additional surgery was performed in approximately 30% of the patients, mostly to improve motion, address the ulnar nerve, or remove prominent hardware. Ring et al16,17 have analyzed the outcome in two specific subsets of distal humerus nonunions. In their first study, these authors reported on the outcome of so-called unstable nonunions, defined as those in which the hand and the forelimb cannot be supported against gravity. Union was achieved in 12 of the 15 patients included in their study, but additional surgery was performed in six of the 12 elbows with healing, again to improve motion, address the ulnar nerve, or remove hardware. Osteochondral nonunions were addressed in a separate paper including only three patients who all

achieved union and improved motion without evidence of osteonecrosis.16,17 The Mayo Clinic experience with internal fixation and bone grafting for distal humerus nonunion using the parallel-plating technique described in this chapter has been reviewed recently in a subset of patients with low nonunions requiring shortening. Twelve patients with a low distal humerus nonunion and severe bone loss were treated with internal fixation using a parallel-plating technique, shortening of the humerus at the nonunion site, capsular release, and bone grafting. Union was achieved primarily in all cases, but two elbows developed collapse of the articular surface after union and were revised to a total elbow arthroplasty. At an average follow-up of 2.5 years, eight of the remaining patients had no pain, mean flexion was 113 degrees, and mean extension 22 degrees. Complications included deep infection in one case and heterotopic ossification requiring surgical removal in one case. The mean Mayo Elbow Performance Score was 80 points (range, 30 to 100 points); all patients had an excellent result with no complications.

Infected Nonunions The treatment of infected nonunions is challenging and should be approached individually. A staged approach is probably best for most patients with previous surgery and retained hardware or draining wounds. The first procedure should remove all foreign material and infected tissues including bone. Antibiotic-loaded bone cement beads provide a high local dose of antibiotics. In patients with severe bone loss and poor condition of the soft tissues, temporary external fixation provides adequate stability and allows better wound care. The author has no experience with external fixation as a definitive treatment modality for infected distal humerus nonunion, but its use has been reported by others. When external fixation is not used, the elbow should be kept immobilized in a cast or brace until the second procedure, and 6 weeks of intravenous antibiotics usually are recommended based on the results of the cultures and sensitivity studies. Repeat aspiration to identify residual infection is performed between 2 and 4 weeks after the antibiotic therapy is discontinued. The bone stock remaining after the débridement will largely dictate the second procedure. If bone stock is severely compromised, consideration should be given to elbow arthroplasty instead of internal fixation. The relative risk of recurrent infection after fixation or arthroplasty is unknown, but most surgeons would recommend a longer period of time between surgeries if arthroplasty is selected, owing to concerns of periprosthetic deep infection and the more predictable restoration of motion if the joint is replaced after a long period of immobilization.

Chapter 23 Nonunion and Malunion of Distal Humerus Fractures

ELBOW ARTHROPLASTY Elbow arthroplasty has emerged as a safe and effective treatment option for selected patients with distal humerus nonunion. The details regarding total elbow arthroplasty for the salvage of distal humerus nonunion are described in Chapter 59.

DISTAL HUMERAL MALUNION IN THE ADULT PATIENT The clinical features and treatment options for distal humerus malunions have been studied and reported mostly in the pediatric population, as detailed in Chapters 15 and 16. Malunion also occurs in the adult population, but there is limited information on the evaluation and treatment of distal humerus malunion in adults.4,8

EVALUATION Most patients with malunion after a distal humerus fracture present with a combination of pain and stiffness. In the absence of associated degenerative changes or other pathology, stiffness is usually much more

A FIGURE 23-8

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prominent than pain. However, pain and stiffness may be present in patients with a previous distal humerus fracture complicated by capsular contracture, heterotopic ossification, post-traumatic osteoarthritis, infection, or avascular necrosis. The evaluation of patients with a distal humerus malunion should help determine to what extent correction of the malunion is needed in order to improve pain and function. Plain radiographs are useful mostly to assess the status of the articular cartilage and identify associated pathology (Fig. 23-8). In addition, marked deformity is easily identified in plain radiographs, but computed tomography with three-dimensional reconstruction represents the ideal imaging modality to understand the deformity and determine if there is an associated nonunion of part of the articular surface, because some patients will present with a combination of nonunion on one side of the joint and malunion on the other side of the joint.8 The malunion may be mostly extraarticular, mostly intra-articular, or a combination of the two. The evaluation should be completed with studies to identify infection in patients with previous surgery, risk factors or suspicious findings on the history and physical exam.

B

Anteroposterior (A) and lateral (B) radiographs of a patient with pain and decreased motion secondary to distal humerus malunion.

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TREATMENT Patients with symptomatic distal humerus malunion may be offered several alternatives (Box 23-1). Osteotomy for correction of extra-articular and intra-articular deformities is appealing because it provides the potential to preserve the native joint and improve pain and motion. However, some patients may present with severe joint destruction not amenable to osteotomy. Arthroplasty may represent a good alternative for older patients willing to limit their upper extremity use and prevent mechanical failure. When moderate extraarticular deformity limits motion secondary to impingement of the proximal ulna and radius with the deformed distal humerus, recontouring of the distal humerus by selective removal of bone provides a reasonable alternative with relatively low morbidity. Joint fusion may be considered for patients with severe pain who are not candidates for other surgical alternatives, but most patients with limited motion secondary to a distal humerus malunion are reluctant to have their elbow fused.

Osteotomy Patients with an extra-articular malunion of the distal humerus may benefit from extra-articular osteotomy. Correction of the malunion may improve range of motion and cosmesis. In addition, varus malunion may be associated with progressive ulnar neuropathy as well as gradual attrition of the lateral collateral ligament complex and tardy posterolateral rotatory instability.13 Closing-wedge osteotomies are usually preferred because humeral shortening is relatively well tolerated. Medial or lateral translation of the distal fragment should be considered to avoid a serpentine aspect of the distal humerus. Usually, extra-articular osteotomies are performed through a bilaterotricipital approach and fixed with medial and lateral plates (Fig. 23-9). Capsular release and ulnar nerve transposition may be associated as needed.

Treatment Options for Patients with Distal Humerus Malunion

BOX 23-1

• Osteotomy • Extra-articular • Intra-articular • Combined • Arthroplasty • Distal humerus hemiarthroplasty • Total elbow arthroplasty • Recontouring of the distal humerus • Arthrodesis

Intra-articular osteotomies may be indicated when intra-articular malunion is thought to be responsible for pain or limited motion and joint salvage is not compromised by the severity of joint destruction, avascular necrosis or secondary degenerative changes. Intraarticular osteotomies usually require a more ample approach, such as olecranon osteotomy or reflection of the extensor mechanism. Care should be taken to protect the articular cartilage and bone graft is usually required to fill the defects created by correction of the deformity. Whenever an intra-articular osteotomy is performed, an alternative salvage procedure, such as interposition arthroplasty or joint replacement should be available because the degree of joint destruction is difficult to fully appreciate before surgery.

Arthroplasty Elbow arthroplasty may be considered for older patients with intra-articular distal humerus malunion and posttraumatic osteoarthritis. Elbow arthroplasty offers reliable improvements in pain and motion. However, it introduces the potential for implant-related complications, including mechanical failure. Not uncommonly, distal humerus malunion is associated with a substantial deformity; failure to achieve an adequate soft tissue balance at the time of arthroplasty may be associated with eccentric polyethylene loading and excessive early wear.

Bone Recontouring Malunion of the distal humerus into excessive extension limits elbow flexion; similarly, flexion malunion, which is less common, limits elbow extension. Elbow motion may be improved in these circumstances by removing bone from the distal humerus to accommodate the coronoid and radial head in elbow flexion or the olecranon in elbow extension. When performed through an arthroscopic approach, this procedure is associated with much less morbidity than osteotomy or arthroplasty. The technique involves the use of an arthroscopic burr to deepen the supracondylar region of the distal humerus anteriorly or posteriorly. Capsulectomy may be associated if needed to restore motion. Care should be taken not to weaken the distal humerus to the point of facilitating a postoperative fracture.

OUTCOME There is very limited information about the outcome of surgical correction of distal humerus malunion. Cobb et al4 reported on three patients treated with an intraarticular derotational opening-wedge osteotomy for a distal humerus malunion. Motion was improved in all three patients, but one required conversion to interposition arthroplasty.

Chapter 23 Nonunion and Malunion of Distal Humerus Fractures

A

C

357

B

FIGURE 23-9 A, Extra-articular nonunion may be corrected with a supracondylar osteotomy. B, Intra-articular fluoroscopy showing the planned osteotomy. C, Healed osteotomy after internal fixation with two parallel plates.

More recently, McKee et al.8 reported on a heterogeneous group of 13 patients with intraarticular distal humerus malunion or nonunion following fracture. Six fractures had healed in a malunited position, two elbows presented a combination of

lateral malunion and medial nonunion, and the remaining five presented a nonunion. An intra-articular osteotomy was performed in the eight patients with malunion; results were rated as satisfactory in seven patients.

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The results of arthroplasty in patients with distal humerus malunion are difficult to dissect out of the studies analyzing arthroplasty for the sequelae of trauma (see section on arthroplasty). As noted, the main concern is the increased rate of polyethylene wear found in patients with preoperative angular deformity.

References 1. Ackerman, G., and Jupiter, J. B.: Non-union of fractures of the distal end of the humerus. J. Bone Joint Surg. Am. 70:75, 1988. 2. Alonso-Llames, M.: Bilaterotricipital approach to the elbow. Its application in the osteosynthesis of supracondylar fractures of the humerus in children. Acta Orthop. Scand. 43:479, 1972. 3. Bryan, R. S., and Morrey, B. F.: Extensive posterior exposure of the elbow. A triceps-sparing approach. Clin. Orthop. Rel. Res. 166:188, 1982. 4. Cobb, T. K., and Linscheid, R. L.: Late correction of malunited intercondylar humeral fractures. Intra-articular osteotomy and tricortical bone grafting. J. Bone Joint Surg. Br. 76:622, 1994. 5. Helfet, D. L., Kloen, P., Anand, N., and Rosen, H. S.: Open reduction and internal fixation of delayed unions and nonunions of fractures of the distal part of the humerus. J. Bone Joint Surg. Am. 85-A:33, 2003. 6. Henley, M. B.: Intra-articular distal humeral fractures in adults. Orthop. Clin. North Am. 18:11, 1987. 7. Jupiter, J. B., and Goodman, L. J.: The management of complex distal humerus nonunion in the elderly by elbow capsulectomy, triple plating, and ulnar nerve neurolysis. J. Shoulder Elbow Surg. 1:37, 1992. 8. McKee, M., Jupiter, J., Toh, C. L., Wilson, L., Colton, C., and Karras, K. K.: Reconstruction after malunion and nonunion of intra-articular fractures of the distal humerus. Methods and results in 13 adults. J. Bone Joint Surg. Br. 76:614., 1994. 9. McKee, M. D., Wilson, T. L., Winston, L., Schemitsch, E. H., and Richards, R. R.: Functional outcome following

10.

11.

12.

13.

14.

15.

16.

17.

18.

19.

20.

surgical treatment of intra-articular distal humeral fractures through a posterior approach. J. Bone Joint Surg. Am. 82-A:1701, 2000. Mitsunaga, M. M., Bryan, R. S., and Linscheid, R. L.: Condylar nonunions of the elbow. J. Trauma 22:787, 1982. O’Driscoll, S. W.: The triceps-reflecting anconeus pedicle (TRAP) approach for distal humeral fractures and nonunions. Orthop. Clin. North Am. 31:91, 2000. O’Driscoll, S. W., Sanchez-Sotelo, J., and Torchia, M. E.: Management of the smashed distal humerus. Orthop. Clin. North Am. 33:19, vii, 2002. O’Driscoll S. W., Spinner, R. J., McKee, M. D., Kibler, W. B., Hastings, H. 2nd, Morrey, B. F., Kato, H., Takayama, S., Imatani, J., Toh, S., and Graham H. K.: Tardy posterolateral rotatory instability of the elbow due to cubitus varus. J. Bone Joint Surg. Am. 83-A:1358, 2001. Pajarinen, J., and Bjorkenheim, J. M.: Operative treatment of type C intercondylar fractures of the distal humerus: results after a mean follow-up of 2 years in a series of 18 patients. J. Shoulder Elbow Surg. 11:48, 2002. Ring, D., Gulotta, L., Chin, K., and Jupiter, J. B.: Olecranon osteotomy for exposure of fractures and nonunions of the distal humerus. J. Orthop. Trauma 18:446, 2004. Ring, D., Gulotta, L., and Jupiter, J. B.: Unstable nonunions of the distal part of the humerus. J. Bone Joint Surg Am. 85-A:1040, 2003. Ring, D., and Jupiter, J. B.: Operative treatment of osteochondral nonunion of the distal humerus. J. Orthop. Trauma 20:56, 2006. Sanchez-Sotelo, J., Torchia, M. E., and O’Driscoll, S. W.: Complex distal humeral fractures: internal fixation with a principle-based parallel-plate technique. J. Bone Joint Surg. Am. 89:961, 2007. Sanders, R. A., Raney, E. M., and Pipkin, S.: Operative treatment of bicondylar intraarticular fractures of the distal humerus. Orthopedics 15:159, 1992. Soon, J. L., Chan, B. K., and Low, C. O.: Surgical fixation of intra-articular fractures of the distal humerus in adults. Injury 35:44, 2004.

Chapter 24 Radial Head Fracture

CHAPTER

24

Radial Head Fracture PART A General Considerations, Conservative Treatment, and Open Reduction and Internal Fixation Roger P. van Riet, Francis Van Glabbeek, and Bernard F. Morrey

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stances, up to about 90% of body weight can be demonstrated across the radial head.84 The greatest amount of force transmission occurs with the forearm in pronation. This is because of a screw-home mechanism that occurs during pronation with proximal radial migration. Stability Traditional force-displacement studies have attributed 30% of the resistance to valgus stress to the radial head.57,83,96 Our studies have shown no significant resistance to valgus stability when the medial collateral ligament is intact. On the other hand, if the medial collateral ligament is deficient, the radial head is an important secondary stabilizer in preventing the elbow from dislocating.85 Other investigators115 have also shown a complementary relation of the lateral collateral ligament to the competency of the annular ligament. Therefore, the radial head may be considered a secondary stabilizer to valgus stress, and it does provide an important contribution to joint force transmission (Fig. 24-1).

INCIDENCE OF FRACTURE

INTRODUCTION HISTORICAL REVIEW Before 1933,10 the literature has been well summarized by Schwartz and Young.110 The first description was probably made by Paul of Aegina (AD 625-690): “The ulna and radius are sometimes fractured together and sometimes one of them only, either in the middle or at one end as at the elbow or the wrist.”2 Early difficulty in making the diagnosis was encountered because of “thick muscle covering.”33,93 In 1891, Hoffa described two types of radial head fractures, displaced and undisplaced.55 Hoffa55 and Helferich50 recommended resection of the radial head for late deformity. Three to 4 weeks of immobilization,122 passive motion, avoidance of “operative interference,”45 removal of the fracture fragment, and excision of the entire head for severe comminution54 were all recommended in the early 1900s. The first descriptions of a successful osteosynthesis of the fractured radial head was by Albin Lambotte in 1909.71 Other pertinent contributions include the suggestion that surgery is not a matter of election but rather of selection.54 Although much subsequently has been written about this fracture, the focus has changed to the more complex fractures.16,30,67

BIOMECHANICS AND FUNCTION OF THE RADIAL HEAD Force Transmission Studies in our laboratory have shown that, under the most demanding of circum-

Fracture of the radial head and neck has been variously reported as 1.7% to 5.4% of all fractures.27,66,86 Radial head fractures occur in about 17% to 19% of cases of elbow trauma134,137 and account for about 33% of elbow fractures.77 Approximately one in three cases is associated with another injury.127 In general, about 10% to 15% of these fractures involve the neck,86,122,127 usually in children in whom the physis has not closed.15 Recent demographic data127 from our institution suggest some changes when compared with previously published reports.5,22,23,29,30,135 Gender ratio is approximately 1 : 1. The male population has more severe fracture types and more often sustain associated injuries. Compared with the literature,22,23,29,30 the age of patients sustaining radial head fractures has increased to a mean age of 45 years, 48 years old for women and 41 years for men.127 Age and Sex

MECHANISM OF FRACTURE An axial load on the pronated forearm consistently produces a fracture of the radial head similar to that seen in clinical experience (Fig. 24-2).122 Odelberg-Johnsson88 observed precisely the same effect, noting that the fracture (1) occurred with posterior subluxation of the “forearm as far as the ligaments allowed,” and (2) involved the most anterior portion of the radial head when the forearm was pronated. Because the head of the radius is eccentric to the central axis of the neck,118 the posterolateral aspect of the radial head comes into intimate

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RADIAL HEAD REMOVED Valgus instability (%)

100 80 Arc of Injury 60 40 80º

20 0 MCL intact

Fracture

MCL released

35°

FIGURE 24-1

Relative contribution of radial head and medial collateral ligament to resist valgus stress. These data define the radial head as a secondary stabilizer to resist valgus stress.

Component

Arc

Coronoid

0-35º

Radial Head/Neck

0-80º

0º

FIGURE 24-3

Laboratory data reveal that either the coronoid or the radial head may be fractured with an axial load in extension. With increasing flexion, the radial head is selectively fractured. (Modified from Amis, A. A., and Miller, J. H.: The mechanisms of elbow fractures: An investigation using impact tests in vitro. Injury 26:163, 1998.)

ASSOCIATED INJURIES CONCURRENT FRACTURES ABOUT THE ELBOW

FIGURE 24-2

The mechanism of injury of most radial head fractures is a fall on the outstretched hand with the elbow partially flexed and pronated. A variable amount of valgus force accounts for the associated injuries that are occasionally seen.

contact with the capitellum during pronation. The common occurrence of an anterolateral fracture fragment supports this theory.29,66 A direct blow is another uncommon cause of radial head fracture.29,41 Amis and Miller3 recently enhanced our understanding of this and other fractures by correlating the fracture and the angle of flexion (Fig. 24-3). As is seen experimentally, either the coronoid or radial head may be fractured with the elbow in full extension, but the radial head can be fractured at greater degrees of flexion, approaching 80 degrees of the flexion arc.

Based on our assessment of 333 radial head fractures seen at the Mayo Clinic, we observed that the likelihood of associated injuries strongly correlates with the severity of the radial head fracture.127 The incidence of associated injuries increases from 20% in nondisplaced fractures to 80% in comminuted radial head fractures. The vast majority of these injuries (90%) are fractures about the elbow, mostly articular surface lesions. Approximately 20% of these articular injuries include the distal humerus, whereas in more than 90%, the proximal ulna is involved. Fractures or cartilage injuries of the capitellum are common101,133 but not always appreciated.19 The associated fracture of the capitellum has been studied in some detail by Ward and Nunley.132 About one half of capitellar fractures were shown to have associated radial head fractures, whereas approximately 2% of radial head fractures had associated capitellar fractures. Thus, this combination is rather rare.127,132 Fracture of both the olecranon and the radial head is usually considered a variety of the Monteggia fracture and has been analyzed in detail by Scharplatz and Allgower108 and others.44,70,94,112 In 15% of patients, the radial head fracture is complicated by a coronoid fracture.127 Fractures of the coro-

Chapter 24 Radial Head Fracture

noid have been discussed in detail by Regan and Morrey.100 If the fragment is large, significant elbow instability may occur.47,101,112 In our series, an elbow dislocation was found in about 15% of radial head fractures,127 as compared with approximately 10% quoted in the literature.1,7,27,29 Combined radial head and coronoid fractures are commonly seen in elbow dislocations. The coronoid process is involved in 80% of patients that sustain a radial head fracture as part of an elbow dislocation. Bilateral radial head fractures are uncommon and occur in about 2% of patients.29,127

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positive arthrographic findings in 4% of type I, 21% of type II, and 85% of type III injuries. Using magnetic resonance imaging in patients with types II or III radial head fractures, Itamura and associates63 recently found lesions in the medial collateral ligament in 54%, lateral ulnar collateral ligament in 80%, and lesions of both ligaments in 50%. This suggests that many ligamentous lesions remained subclinical. Unless formal examinations are used, associated ligamentous lesions may be undetected immediately and may predispose patients to develop chronic symptoms. The management of ligamentous injuries is discussed separately.

LIGAMENTOUS INJURY AT THE ELBOW Some degree of ligamentous injury often occurs with radial head fracture; this association is not always fully appreciated (Fig. 24-4).17,49,65,88,133 An incompetent ulnar collateral ligament is suggested by an increased valgus position.22,86,109 Approximately 50% of associated lesions to the elbow involve clinically significant ligamentous injuries. About 10% of patients are diagnosed with a lateral or medial collateral ligament rupture, or a combination of both.127 These clinically relevant injuries are markedly less common than previously described. Wagner130 observed 24 patients with calcification in the medial collateral ligament, and Arner and associates5 described a 12% incidence of ulnar collateral ligament calcification. Arvidsson and Johansson6 found ligament or capsular disruption by arthrography with various types of radial head fractures. Johansson65 demonstrated

OTHER INJURIES About 10% of patients with a radial head fracture sustain associated injuries other than elbow injuries. Fractures of the hand or wrist are found in about 6%.127 Conversely, radial head fractures are found in 6% of all scaphoid fractures.136 Shoulder injuries are uncommon (2%) and are usually found in nondisplaced radial head fractures.127 A ligamentous injury sustained at the distal radioulnar joint at the time of the radial head fracture15,28,116 is diagnosed in less than 1% of acute cases128 but is well recognized as the Essex-Lopresti injury and has been the subject of several reports.36,46,124 Shortening of 5 to 10 mm can be anticipated (Fig. 24-5).46 Open reduction and internal fixation to stabilize the proximal radius is recommended. Trousdale and associates125 reviewed Mayo experience with 20 patients. Fifteen had radial

FIGURE 24-4

A, Radial neck fracture that developed nonunion. B, Resection of this fracture unmasked an associated medial collateral ligament disruption with resulting symptomatic unstable elbow.

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FIGURE 24-5 A, Fracture of the radial head treated without surgery. B, Widening of the distal radioulnar joint was present after the fracture had healed. C, The radial head was removed, and 5 mm of proximal migration occurred during the next 2 years (D).

Chapter 24 Radial Head Fracture

head resection without knowledge of the wrist injury. Such late detection was treated by reconstructive procedures, with a success rate of only 14%. Proper initial diagnosis was associated with an 80% satisfactory outcome and early treatment.

NEUROVASCULAR COMPLICATIONS The uncomplicated fracture of the radial head is rarely associated with any neurovascular symptoms. Severe anterior displacement may affect the radial nerve, and a rare case of posterior interosseus nerve injury has been described in the literature.121

MUSCULAR INJURY By definition, elbow dislocation must violate the brachialis muscle, and this factor is thought to be an important variable in the development of myositis ossificans.75,123 The significance and management of this complication are discussed later in this book.

CLASSIFICATION OF FRACTURE The first classifications of radial head fractures were described by Speed in 1924117 and Eliason in 1925.37 A year later, Cutler reported a second classification29 and this presented the basis for all currently used classifications. The most commonly used classification of radial head fracture is that proposed by Mason (Fig. 24-6).77 A fourth type, the fracture dislocation, was added by Johnston.66 In 1962, Johansson65 added the degree of displacement to his classification and this was later combined with the original Mason classification to form the most recent adaptation of the original Mason classification.57

TYPE I

A

MAYO MODIFICATION OF MASON CLASSIFICATION In the previous versions of this book, Morrey added a degree of sophistication to Mason’s classification of radial head fractures by dividing them into simple and complex fractures, depending on associated lesions.81,82 However, the division between simple and complex fractures can sometimes be difficult, for example, when suspected ligamentous lesions are not formally investigated due to the limited clinical implications. Therefore, based on our clinical experience of more than 333 cases, we propose to add a suffix to the original fracture type in order to quantify associated lesions about the elbow.129 A suffix m is used if a medial collateral ligament injury is suspected or proven, but this has questionable impact on elbow stability. A capital M is used if there is an impact on stability, enough to warrant treatment. For lateral ligament injuries, l and L is used respectively. The same is done to document associated fractures to the ulna (U, u) or humerus (H, h). The suffix P is used to indicate that some sort of procedure was performed (Fig. 24-7); x for excision and F for ORIF.

FRACTURE MANAGEMENT In general, the treatment of radial head fractures is based on the fracture type and the presence of any associated injury. These injuries involve the ligaments or articular elements with variable implications to prognosis and management (Fig. 24-8). Associated injuries should be treated on their own merit, and the following discussion will be limited to the treatment of the radial head fracture as such.

TYPE II

B

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TYPE III

C

FIGURE 24-6 A to C, The Mason classification of uncomplicated radial head fractures. The exact definition of the type II fracture is often difficult to determine. Type IV is not included because it represents a complicated fracture.

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CHARACTERISTICS Type II F,m,L Mayo extended classification Definition Fracture type

I II III

Treatment

Associated lesion m l d c o

M L D C O

Radial head treatment

X F P Rx: upper case

A

C Type II m,l

FIGURE 24-7

B

Clinical findings include hemarthrosis and painful rotation of the forearm, especially with palpation of the radial head. Radiographs are not always conclusive, but an elbow fat pad effusion in an otherwise normal radiograph is indicative of an occult radial head fracture in almost 90% of patients89 (Fig. 24-9). Computed tomography scanning may give additional information on the morphology of the fracture57,126 and may aid in planning and assessing the feasibility of a surgical reconstruction (Fig. 24-10).

CONSERVATIVE TREATMENT Conservative treatment of nondisplaced53 or minimally displaced radial head fractures52 has been shown to yield good results at a long-term follow-up of 21 and 19 years, respectively. Results of conservative treatment of displaced radial head fractures are less favorable, and patients have increased pain and decreased strength when compared with surgically managed patients.68,120

A, Mayo classification of radial head fracture, which allows description of associated injuries. B, Hence, this type II fracture of the radial head with dislocation is termed II m,e. C, After treatment with open reduction and internal fixation and LCL repair it is termed II m L F.

Sedation,111 mobilization,* or immobilization with78,98,114 or without111 a plaster cast have been advocated as conservative treatment options. Minor soft tissue injuries rarely need to be addressed.65,78,135 There is little question that the type I fracture (Fig. 24-11), because of its favorable prognosis and lack of concurrent soft tissue or other osseous injury, should be managed with early motion. Mason and Schutkin,76 reporting a military experience, found a mean period of disability of 4 weeks in 18 patients treated with early motion, compared with 7 weeks in seven individuals treated with 3 weeks of immobilization. Immediate mobilization is recommended, but a delay of up to 5 days has no functional implication after a 4-week follow-up.74 The major residuum is loss of extension rather than pain.29 Mason77 reported that about one third of his 62 patients with this fracture lost an average of 7 degrees of extension. This may be associated with hemarthrosis *See references 1, 5, 7, 21, 23, 43, 65, 74, 87, 98, 111, 133, and 135.

Chapter 24 Radial Head Fracture

A

C

B

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of the joint. In a cadaveric study, McGuigan and Bookout80 demonstrated a decrease in the flexion arc of 2 degrees per milliliter fluid injected into the elbow joint. To facilitate immediate motion, aspiration of the joint, is therefore recommended32,34,40,56,97 and pain relief could be increased by infiltrating some local anesthetic into the joint.27 The most frequent complication of conservative treatment of nondisplaced radial head fractures is degeneration of the articular surfaces, which is found at long-term follow-up in about 80% of patients.52,53 Other complications include displacement or nonunion102 (Fig. 24-12).

D

FIGURE 24-8

A, Elbow stability requires articular and ligamentous integrity. B, Absence of the radial head does not cause instability if the ulnar collateral ligament and distal radioulnar joint are intact. C, Proximal migration can occur if distal ligaments are ruptured. D, Valgus laxity may be present if the ulnar ligament is violated.

FIGURE 24-9

The presence of a fat pad sign as seen here suggests an articular fracture and should be further assessed by a computed tomography study.

FIGURE 24-10 The computed tomography scan is extremely helpful to diagnose subtle associated articular injuries.

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FIGURE 24-11 A, Type I fracture involving approximately 50% of the head but with less than 2 mm of displacement. B, Minimally angulated neck fracture is also considered a type I fracture.

Delayed excision of the entire radial head can be considered only if any of these complications become symptomatic (Fig. 24-13).26,52,53,102 Among 21 patients treated with delayed excision at the Mayo Clinic, Broberg and Morrey13 reported 75% with decreased pain and 77% with improved motion. The time to delayed excision ranged from 1 month to 20 years (Fig. 24-14). A rare complication of nondisplaced radial head fractures treated conservatively is arthrofibrosis, which reportedly can be managed successfully with arthroscopic débridement.18,72

RESECTION OF THE RADIAL HEAD

FIGURE 24-12

alone.

This nonunion was asymptomatic and left

The authors consider this issue somewhat controversial and unresolved. In general, resection is reserved for uncomplicated type III fractures (Fig. 24-15). Rochwerger and colleagues104 compared the treatment of 22 type II fractures. With mean surveillance of 5 years (2 to 23 years), osteosynthesis was found to be superior to resection, as the latter had satisfactory results in just more than 50% of cases. Similar results were found in 28 patients with type III, comminuted radial head fractures. Using a meticulous surgical technique, Ikeda et al60,61 found improved results in the group treated with open

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FIGURE 24-13 A, Type I undisplaced fracture of the left nondominant extremity in a 49-year-old man. Treatment by early motion as tolerated resulted in displacement of the fragment (B), which progressed to a nonunion (C). D, Treatment by late excision of the radial head 4 months after the fracture decreased the pain and improved pronation and supination 6 months after the procedure. (Courtesy of E. T. O’Brien, San Antonio, Texas.)

reduction and internal fixation (ORIF) over the group of patients treated with resection of the radial head. Yet, there has been a surprising resurgence of interest in the earlier treatment of choice, which is simple excision.

Janssen et al64 reported 20 of 21 excellent or good results between 16 and 30 years after excision for comminuted radial head fractures. These investigators did exclude known dislocations. On the other hand, SanchezSotelo et al106 described excision in the face of 10 dislo-

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FIGURE 24-14 A, Type II radial head fracture was treated nonoperatively. B, Persistent pain and limitation of motion resulted in a delayed excision of the radial head. The patient had a satisfactory result.

cations, which is consistent with a Mason type IV classification. In this group, nine of 10 were considered satisfactory, similar to that of Janssen. However, they did note a 5-degree increased valgus carrying angle and early asymptomatic degenerative changes of the ulnohumeral joint with a mean of about 4.5 years surveillance (Fig. 24-16). There have been other recent reports regarding excision without radial head replacement that have yielded surprisingly consistent outcomes. A study from Scandinavia of 61 resections noted that the timing of the resection, whether acute or delayed, was much less important than the Mason classification of the lesion. Similar observations were made from Asia by Ikeda, who reported good results at 10 years after 15 patients (four with type II and 11 with type II treated by excision). They did, however, notice that pain was present in about a third of these patients52a and, as noted above, favor fixation.60,61 Wallenbock et al. evaluated radial head resection in 23 instances with a mean follow-up of 17 years with personal evaluation of the entire sample. They demonstrated that 22 of 27 patients had a satisfactory outcome. They observed those with resection after a type III or IV did less well than after a type II fracture. Interestingly, there was no distinction in their group and their observations whether the patients were treated by excision in the early or in the more chronic period.131 Similarly, a report from Italy by Celli of 31 fracture-dislocations noted that only 40%

were satisfactory and 60% were unsatisfactory after various treatment options.24 This is consistent with Herbertsson’s observations that the fracture type has greater prognostic importance than the acuteness of the treatment. The basic treatment rationale, therefore, of simple resection for those fractures that cannot be reduced and fixed does have some merit. This was well summarized by Wallenbock and Potsch,131 who stated that resection is recommended “as long as there are no better longterm results of prosthetic substitution of the radial head.” We hope that prosthetic substitution will prove valuable and effective. However, realistically the long-term followup data of those treated by resection certainly justify consideration of this as a treatment option, particularly in those that do not have an associated injury.

OPEN REDUCTION AND INTERNAL FIXATION Surgical treatment of displaced radial head fractures has evolved from excision of fracture fragments or the entire head of the radius, to several techniques of ORIF and modern types of radial head replacement. ORIF was used sporadically in the past, largely because of the perception that it had “not proved successful in anyone’s hands.”98 The poor earlier results were probably due to an inadequate understanding of anatomy and less refined techniques for effective internal fixation.

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FIGURE 24-15 A, Type III fracture demonstrating comminution. B, With long-term follow-up of 10 years, there is osteophyte formation at the ulnohumeral joint after radial head excision, but symptoms are mild. (C) The patient had no wrist symptoms.

A

B

C

The fracture fragment frequently has a periosteal hinge, indicating that its viability is possible.48 The ideal fracture for fixation is a simple, large (constituting 30% of the head) fragment that involves the anterolateral margin of the head (Fig. 24-17). However, despite the

bigger technical challenge of fixing smaller fragments, biomechanical studies have also shown a benefit of fixation of fragments smaller than one third of the radial head.8,9 The anterolateral margin of the head does not articulate with the lesser sigmoid notch; instrumented

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fixation of this fragment does not result in impingement (Fig. 24-18).20,113 If there are multiple but large fragments, open reduction can still be performed,48 but results can be disappointing.69,103 In general, experience with ORIF is satisfactory in more than 90% of cases.38,91,95,99,103,111

Geel and coworkers42 reported less than a 10-degree loss of extension and a 10-degree loss of pronation and supination in 19 patients who underwent ORIF. A similar outcome was observed by Sanders and French107 in eight patients treated for difficult type III fractures. In a study of 56 patients, Ring and coworkers103 reported excellent results in patients with minimally comminuted fractures with three or fewer articular fragments. However results were unfavorable in patients with more comminuted fractures or if the fracture was associated with an elbow dislocation. Ikeda et al62 reported excellent and good results in nine out of 10 patients, using lowprofile mini-plates for severely comminuted radial head fractures. Nine patients required hardware removal. The Herbert screw has been reported to provide virtually normal function.14 The traditional AO technique using the 2.0 or 2.7 screws has been reported as satisfactory in 100% of patients with Mason type II fractures but in only 33% of those with Mason type III fractures.69 A small buttress plate can be used for radial neck fractures.73 Esser and colleagues38 reported on 26 cases of osteosynthesis, 11 with type II and nine with type III. All were graded as satisfactory after osteosynthesis (Fig. 24-19).

FIGURE 24-16 A comminuted radial head fracture was excised in a patient with elbow dislocation. The patient had a good result 15 years after surgery but had radiographic evidence of arthritis.

LOW-PROFILE FIXATION We have recently compared the outcome of 10 patients with radial neck fracture managed by plate fixation to

FIGURE 24-17 A, Large, single fragment treated with open reduction and internal fixation (B) in a 40-year-old man. The result was classified as good, with 15 to 20 degrees of extension deficit, normal rotation and no pain.

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70º 120º

A

B FIGURE 24-18

A, The mechanism of slice fracture tends to shear the anterolateral portion of the head. B, This constitutes the 70 degrees of the circumference of the radial head that articulates with the lesser sigmoid fossa, which is devoid of articular cartilage. This anatomic feature allows and justifies the use of AO screws with protruding heads if the fracture is through this portion of the radius.

a comparable injury managed by a new “low-profile fixation” technique. In the latter instance, the fracture is fixed by inserting a threaded Kirschner wire (K-wire) or cannulated screw through the margin of the radial head across the fracture and engaging the opposite radial cortex (Fig. 24-20). A statistically significant better forearm arc of motion and elbow flexion arc was documented with the low-profile axial fixation technique.114 Some other technique modifications have been proposed recently. Fibrin adhesive seal was used as early as 1995, but despite excellent short-term results, this has never become a mainstream technique.4 Bioabsorbable polylactic pins have also been used since the early 1990s, for fixation of radial head fractures.51,59,92 In a recent prospective randomized study of 135 patients, results of fixation using polylactic pins have been shown to yield at least comparable results compared to other types of fixation.51 However, despite favorable results, biocompatibility may be an issue unique to this type of fixation.11,92

In comparison to resection or prosthetic replacement of the radial head, ORIF has been shown to be preferable if a stable fixation can be achieved. In a recent cadaveric study, ORIF has biomechanically been shown to be superior to resection or prosthetic radial head replacement.25 In a retrospective study by Parasa and Maffulli90 of 29 patients with radial head fractures managed with different surgical methods, ORIF showed the best results in Mason type II fractures, followed by type III. Comparing different techniques, the best outcome was observed with screw fixation, followed by excision of the radial head, K-wire fixation, partial excision, Silastic implant, and plating. One prospective study by Khalfayan and associates68 compared the results of 16 patients treated by closed reduction and 20 by ORIF. The former had only 44% satisfactory results, compared with 90% in the group treated by ORIF. Boulas and coworkers12 compared results of ORIF with resection, Silastic radial head replacement, and conservative treatment in 36

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A

B

FIGURE 24-19 Comminuted fracture of head and neck (A) fixed with mini plate and screws (B and C).

C

FIGURE 24-20

So-called low-profile fixation employs axially aligned screw fixation from the margin of the head down the shaft of the proximal radius.

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patients. The best clinical scores were found in patients treated with ORIF, and the authors recommended this type of treatment for displaced radial head fractures. Arthroscopically Assisted Reduction and Internal Fixation As has been described in intra-articular frac-

tures in other joints,125 arthroscopic techniques to reduce and fix radial head fractures are currently under development.31,105

AUTHOR’S PREFERRED TREATMENT NONDISPLACED RADIAL HEAD FRACTURES Type I fractures are treated by joint aspiration for immediate pain relief. From the author’s personal experience, the infiltration of a local anesthetic does not provide much additional relief; on the contrary, it was painful to receive a volume of fluid into the joint. A collar and cuff is given, and immediate motion as tolerated is advised. We see the patient in about 7 to 10 days and perform repeat radiographs for the rare event of secondary displacement. If so, ORIF may still be performed at this stage. We do not routinely use physical therapy in these patients.

DISPLACED FRACTURES Depending on the nature of the fracture and the presence or absence of associated injury, we tend to fix these fractures. Radial head replacement is discussed later. Evaluation of the number, size, and displacement of fracture fragments is extremely difficult from plain radiographs. The fracture and associated bony lesions are therefore routinely assessed using computed tomography (CT) scanning of the elbow (Fig. 24-21). If the displacement is more than 2 mm, ORIF is performed with headless screws or occasionally special plates (Fig. 24-22). The distal radioulnar joint injury is treated by ORIF of the radial head and may also require surgical stabilization by an open procedure or percutaneous cross-pinning to maintain radial length. Even with the aid of CT scanning, the severity of the fracture can sometimes be underestimated from imaging studies; therefore, it is our clinical practice to have screws and plates and also a prosthetic device available during surgery (Fig. 24-23). The radial head and other bony injuries are addressed first, and stability of the elbow and wrist is tested following adequate bony reconstruction. If necessary, ligamentous repair is undertaken. If the elbow remains unstable following bony and soft tissue repair, a hinged elbow external fixation device is applied.

FIGURE 24-21 The computed tomography scan accurately depicts subtle fractures and the precise amount of displacement.

Elbow flexion and extension are allowed within the first week, usually on the third or fourth day after surgery. The surgical technique is described below. Surgical Technique An extended lateral incision is made over the lateral margin of the humerus, extending over the lateral epicondyle and the radial head. The incision is carried distally, parallel to the axis of the forearm. A posterior midline incision may also be used.35 This is especially helpful if associated medial-sided injuries need to be addressed surgically. The Kocher approach between the anconeus and the extensor carpi ulnaris is the most frequently used exposure of the radiocapitellar joint. In traumatic situations, however, a musculocapsular rent is often present and should be incorporated in the approach, without further disruption of the soft tissue envelope. Care should be taken, not to disrupt the lateral ulnar collateral ligament (Fig. 24-24). Hematoma is evacuated and the forearm is rotated to expose the fragment. The forearm should be pronated, and the use of retractors behind the radial head and neck should be avoided in order to protect

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A FIGURE 24-22

A

B Fracture seen in figure is fixed with headless screw (A and B).

B

FIGURE 24-23 If the neck is involved, a mini plate may be used (A and B), but the senior author prefers low-profile fixation (see Fig. 24-20).

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375

Capsular incision

Radial collateral lig.

A

Lat. ulnar collateral lig.

C

the posterior interosseus nerve.119 Reduction and provisional fixation can be achieved with a 0.45 K-wire. Depending on the anatomy of the fracture and size of the fragments, one or two 2.0, 2.7 AO, or Herbert screws,14,79,91 bioabsorbable pins,51,59,92 bladeplates,103 or plates and screws62 are inserted in as perpendicular a position to the joint and fracture surface as possible.39,48,61,111 If necessary, the head is counter-sunk and care is taken to ensure that the screw tip has not violated the opposite cortex (Fig. 24-25). The lateral soft tissues, including the annular ligament are repaired, and, if no associated injuries are present, immediate motion is begun. The aim of all types of ORIF is to obtain a stable fixation that allows for immediate mobilization of the elbow joint. In radial neck fractures, plates tend to produce excessive scar formation, necessitating removal in almost all instances.61,62 If possible, we therefore avoid plate fixation and prefer “axial, low-profile” fixation for neck fractures. Our review of 24 fractures revealed a mean forearm rotation of 113 and 160 degrees for the plate plus lowprofile screw, respectively (P < .05).114 Thus, we prefer

B

FIGURE 24-24 Excision through the annular ligament must be performed proximal so as to avoid injury to the lateral ulnar collateral ligament (A). Clinical examples (B and C).

the “low-profile” screw fixation technique. The technique consists of the use of either threaded K-wires or 2.7-mm cannulated screws placed from the margin of the head, across the fracture to engage the opposite cortex (see Fig. 24-20). The development of low-profile plates such as shown in Figure 24-26 may lessen the tendency for scarring and improve forearm rotation after their use. We must await data to determine if this expectation will be realized.

TYPE III FRACTURES—AUTHORS’ PREFERENCE In uncomplicated type III fractures, we prefer complete and early excision (within 24 hours of injury), followed by active motion in 3 to 5 days if ORIF is not possible. However, fractures are (1) almost always (>80%) associated with additional articular or ligamentous injuries,127 (2) are too comminuted for fixation, and hence, are treated most commonly by prosthetic replacement, especially if the fracture consists of more than four

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Non-articular margin Countersink Forearm fully pronated

FIGURE 24-25 The head of the AO screw is countersunk to lessen the likelihood of impingement or soft tissue irritation.

A

B

C

FIGURE 24-26 The low-profile radial head/neck plate with variable angle locking screws may lessen the likelihood of postoperative scarring. (Courtesy of Small Bone Innovations, Morrisville, NJ.)

Chapter 24 Radial Head Fracture

SBI: RADIAL HEAD MANAGEMENT ALGORITHIM Acute injury

Yes

Slice Fx

References Yes

<3 fragments

Yes

No

Neck intact No

rHead (rHead recon)

FIGURE 24-27

Vs

Low profile plate

“Axial fixation”

Treatment logic for acute radial head

fractures.

Chronic injury

Capitellum involved

Yes

No

Radius aligned

Yes

Capitellar rHead Recon Uni Replacement

No Capitellar rHead Recon Uni Replacement

Radius aligned

rHead Recon

Immobilization is continued for only 3 to 5 days, after which a hinged splint is helpful to provide stability as well as early active motion. The overall treatment logic for managing radial head fractures seen acutely or in a delayed time frame is shown in Figures 24-27 and 24-28, respectively.

Screw fixation

No

No

377

Yes rHead rHead Recon

FIGURE 24-28 Treatment logic for radial head fractures treated in a delayed fashion.

fragments. The growing interest and proliferation of implant designs have prompted a separate section to discuss this important topic more fully. Long-term follow-up studies of 50 type IV fractures treated at the Mayo Clinic12,13 has provided our guidelines of treatment. Immobilization never exceeds 1 to 2 weeks. If increased stability is required for early, active rehabilitation, a radial head prosthesis or the dynamic joint distractor (DJD) articulated external fixator is used. Large, single fragments are fixed with small compression screws.

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Chapter 24 Radial Head Fracture

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75. 76.

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94.

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fractures is desirable. A prospective randomised study of two protocols. Injury 33:801, 2002. Loomis, L. K.: Reduction and after-treatment of posterior dislocation of the elbow. Am. J. Surg. 63:56, 1944. Mason, J. A., and Shutkin, N. M.: Immediate active motion treatment of fractures of the head and neck of the radius. Surg. Gynecol. Obstet. 76:731, 1943. Mason, M. L.: Some observations on fractures of the head of the radius with a review of hundred cases. Br. J. Surg. 42:123, 1954. Mathur, N., and Sharma, C. S.: Fracture of the head of the radius treated by elbow cast. Acta. Orthop. Scand. 55:567, 1984. McArthur, R. A.: Herbert screw fixation of fracture of the head of the radius. Clin. Orthop. Relat. Res. 224:79, 1987. McGuigan, F. X., and Bookout, C. B.: Intra-articular fluid volume and restricted motion in the elbow. J. Shoulder Elbow Surg. 12:462, 2003. Morrey, B. F.: Current concepts in the treatment of fractures of the radial head, the olecranon, and the coronoid. Instruct. Course Lect. 44:175, 1995. Morrey, B. F.: Fractures of the distal humerus: role of elbow replacement. Orthop. Clin. North Am. 31:145, 2000. Morrey, B. F., and An, K. N.: Articular and ligamentous contributions to the stability of the elbow joint. Am. J. Sports Med. 11:315, 1983. Morrey, B. F., An, K. N., and Stormont, T. J.: Force transmission through the radial head. J. Bone Joint Surg. 70A:250, 1988. Morrey, B. F., Tanaka, S., and An, K. N.: Valgus stability of the elbow. A definition of primary and secondary constraints. Clin. Orthop. Relat. Res. 265:187, 1991. Murray, R. C.: Fractures of the head and the neck of the radius. Br. J. Surg. 28:106, 1940. Neuwirth, A. A.: Nonsplinting treatment of fractures of the elbow joint. J. A. M. A. 12:971, 1942. Odelberg-Johnson, G.: On fractures of the proximal portion of the radius and their causes. Acta. Radiol. 3:45, 1924. O’Dwyer, H., O’Sullivan, P., Fitzgerald, D., Lee, M. J., McGrath, F., and Logan, P. M.: The fat pad sign following elbow trauma in adults: its usefulness and reliability in suspecting occult fracture. J. Comput. Assist. Tomogr. 28:562, 2004. Parasa, R. B., and Maffulli, N.: Surgical management of radial head fractures. J. R. Coll. Surg. Edinb. 46:76, 2001. Pearce, M. S., and Gallannaugh, S. C.: Mason type II radial head fractures fixed with Herbert bone screws. J. R. Soc. Med. 89:340, 1996. Pelto, K., Hirvensalo, E., Bostman, O., and Rokkanen, P.: Treatment of radial head fractures with absorbable polyglycolide pins: a study on the security of the fixation in 38 cases. J. Orthop. Trauma. 8:94, 1994. Petit, J. L.: A Treatise of the Disease of the Bones; Containing an Extract and Complete Account of All Their Various Kinds, vol. 6. London, T. Woodward, 1720, p. 288. Pierce, R. O., Jr., and Hodurski, D. F.: Fractures of the humerus, radius and ulna in the same extremity. J. Trauma. 19:182, 1979.

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95. Pomianowski, S., Sawicki, G., and Laskowski, J.: [Internal fixation in the treatment of radial head fractures]. Chir. Narzadow. Ruchu. Ortop. Pol. 67:25, 2002. 96. Pribyl, C. R., Kester, M. A., Cook, S. D., Edmunds, J. O., and Brunet, M. E.: The effect of the radial head and prosthetic radial head replacement on resisting valgus stress at the elbow. Orthopedics 9:723, 1986. 97. Quigley, T. B.: Aspiration of the elbow joint in the treatment of fractures of the head of the radius. N. Engl. J. Med. 240:915, 1949. 98. Radin, E. L., Riseborough, E. J.: Fractures of the radial head. A review of eighty-eight cases and analysis of the indications for excision of the radial head and nonoperative treatment. J. Bone Joint Surg. 48A:1055, 1966. 99. Ramon Soler, R., Paz Tarela, J., and Soler Minores, J. M.: Internal fixation of fractures of the proximal end of the radius in adults. Injury 10:268, 1979. 100. Regan, W., and Morrey, B.: Fractures of the coronoid process of the ulna. J. Bone Joint Surg. 71A:1348, 1989. 101. Reith, P. L.: Fractures of the radial head associated with chip fracture of the capitellum in adults: surgical considerations. South Surgeon 14:154, 1948. 102. Ring, D., Psychoyios, V. N., Chin, K. R., and Jupiter, J. B.: Nonunion of nonoperatively treated fractures of the radial head. Clin. Orthop. Relat. Res. 398:235, 2002. 103. Ring, D., Quintero, J., and Jupiter, J. B.: Open reduction and internal fixation of fractures of the radial head. J. Bone Joint Surg. 84A:1811, 2002. 104. Rochwerger, A., Bataille, J. F., Kelberine, F., Curvale, G., and Groulier, P.: Analyse rétrospective d’une série de 78 fractures de la tête radiale opérées. Acta. Orthop. Belg. 62:87, 1996. 105. Rolla, P. R., Surace, M. F., Bini, A., and Pilato, G.: Arthroscopic treatment of fractures of the radial head. Arthroscopy 22:233 e1, 2006. 106. Sanchez-Sotelo, J., Romanillos, O., and Garay, E. G.: Results of acute excision of the radial head in elbow radial head fracture-dislocations. J. Orthop. Trauma. 14:354, 2000. 107. Sanders, R. A., and French, H. G.: Open reduction and internal fixation of comminuted radial head fractures. Am. J. Sports Med. 14:130, 1986. 108. Scharplatz, D., and Allgower, M.: Fracture-dislocations of the elbow. Injury 7:143, 1975. 109. Schwab, G. H., Bennett, J. B., Woods, G. W., and Tullos, H. S.: Biomechanics of elbow instability: the role of the medial collateral ligament. Clin. Orthop. Relat. Res. 146:42, 1980. 110. Schwartz, R. P., and Young, F.: Treatment of fractures of the head and neck of the radius and slipped radial epiphysis in children. Surg. Gynecol. Obstet. 57:258, 1933. 111. Shmueli, G., and Herold, H. Z.: Compression screwing of displaced fractures of the head of the radius. J. Bone Joint Surg. 63B:535, 1981. 112. Simpson, N. S., Goodman, L. A., and Jupiter, J. B.: Contoured LCDC plating of the proximal ulna. Injury 27:411, 1996.

113. Smith, G. R., and Hotchkiss, R. N.: Radial head and neck fractures: anatomic guidelines for proper placement of internal fixation. J. Shoulder Elbow Surg. 5:113, 1996. 114. Smith, A., Morrey, B. F., and Steinmann, S. P.: Low profile fixation of radial head and neck fractures. Surgical technique and clinical experience. J. Orthop. Trauma. 21:718, 2007. 115. Sojbjerg, J. O., Ovesen, J., and Gundorf, C. E.: The stability of the elbow following excision of the radial head and transection of the annular ligament. An experimental study. Arch. Orthop. Trauma. Surg. 106:248, 1987. 116. Speed, K.: Ferrule caps for the head of the radius. Surg. Gynaecol. Obstet. 73:845, 1941. 117. Speed, K.: Traumatic lesions of the head of the radius. Relation to elbow joint dysfunction. Surg. Clin. North Am. 4:651, 1924. 118. Spinner, M., and Kaplan, E. B.: The quadrate ligament of the elbow—its relationship to the stability of the proximal radio-ulnar joint. Acta. Orthop. Scand. 41:632, 1970. 119. Strachan, J. C., and Ellis, B. W.: Vulnerability of the posterior interosseous nerve during radial head resection. J. Bone Joint Surg. 53B:320, 1971. 120. Struijs, P. A., Smit, G., and Steller, E. P.: Radial head fractures: effectiveness of conservative treatment versus surgical intervention: A systematic review. Arch. Orthop. Trauma. Surg. 127:125, 2006. 121. Sudhahar, T. A., and Patel, A. D.: A rare case of partial posterior interosseous nerve injury associated with radial head fracture. Injury 35:543, 2004. 122. Thomas, T. T.: Fractures of the head of the radius. Univ. Pa. Med. Bull. 18:221, 1905. 123. Thompson, H. C. 3rd, and Garcia, A.: Myositis ossificans: aftermath of elbow injuries. Clin. Orthop. Relat. Res. 50:129, 1967. 124. Trousdale, R. T., Amadio, P. C., Cooney, W. P., and Morrey, B. F.: Radio-ulnar dissociation. A review of twenty cases. J. Bone Joint Surg. 74A:1486, 1992. 125. Van Glabbeek, F., van Riet, R., Jansen, N., D’Anvers, J., and Nuyts, R.: Arthroscopically assisted reduction and internal fixation of tibial plateau fractures: report of twenty cases. Acta. Orthop. Belg. 68:258, 2002. 126. Van Glabbeek, F., van Riet, R., and Verstreken, J.: Current concepts in the treatment of radial head fractures in the adult. A clinical and biomechanical approach. Acta. Orthop. Belg. 67:430, 2001. 127. van Riet, R. P., Morrey, B. F., O’Driscoll, S. W., and Van Glabbeek, F.: Associated injuries complicating radial head fractures: a demographic study. Clin. Orthop. Relat. Res. 441:351, 2005. 128. van Riet, R. P., Van Glabbeek, F., Verborgt, O., and Gielen, J.: Capitellar erosion caused by a metal radial head prosthesis: Case report. J. Bone Joint Surg. 86A:1061, 2004. 129. van Riet, R. P., and Morrey, B. F.: Documentation of associated injuries occuring with radial head fractures. Clin. Orthop. Rel. Res. (466):130, 2008. 130. Wagner, C. J.: Fractures of the head of the radius. Am. J. Surg. 89:911, 1955. 131. Wallenbock, F., and Potsch, F.: Resection of the radial head: An alternative to use of a prosthesis. J. Trauma. 43:959, 1997.

Chapter 24 Radial Head Fracture

132. Ward, W. G., and Nunley, J. A.: Concomitant fractures of the capitellum and radial head. J. Orthop. Trauma. 2:110, 1988. 133. Watson-Jones, R.: Discussion of minor injuries of the elbow joint. Proc. R. Soc. Med. 23:323, 1930. 134. Watson-Jones, R.: Fractures and Other Bone and Joint Injuries, 2nd ed. Baltimore, Williams & Wilkins Co., 1941, p. 336. 135. Weseley, M. S., Barenfeld, P. A., and Eisenstein, A. L.: Closed treatment of isolated radial head fractures. J. Trauma. 23:36, 1983. 136. Wildin, C. J., Bhowal, B., and Dias, J. J.: The incidence of simultaneous fractures of the scaphoid and radial head. J. Hand Surg. 26B:25, 2001. 137. Wilson, P. D.: Fracture and dislocation in the region of the elbow. Surg. Gynecol. Obstet. 56:335, 1933.

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earlier, fixation is always preferable, but when this is not possible or not advisable, as in the presence of more than three fragments, then prosthetic replacement should be considered. Specifically, the implant should be used when the secondary stabilizing function of the radial head is required. This occurs when associated injuries have occurred (Table 24-1). Fracture of more than 25% to 50% of the coronoid with radial head fracture is an absolute indication for replacement if fixation of the head is not possible. Deficiency of the medial collateral ligament or disruption of the distal radioulnar joint are additional well-recognized indications for radial head prosthetic replacement. Longitudinal instability of the radius (Essex-Lopresti injury) continues to be an extremely different problem, as noted earlier.16 Acute management may be adequate in up to 80%, but reconstruction is effective in only about 30% percent.4,13 The radial head implant is useful and may be even essential when reconstructing this difficult problem. A Mason III fracture (which is not amenable to ORIF) without any associated injury need not be replaced, but this is a very uncommon clinical circumstance. In general, displaced isolated type II fractures should be fixed; type III, isolated fractures should be replaced.

PART B Prosthetic Radial Head Replacement Bernard F. Morrey

CONTRAINDICATIONS INTRODUCTION

The use of an implant is obviously contraindicated in the presence of sepsis. Malalignment that does not allow correction to allow articulation with the capitellum is a relative contraindication. If this problem cannot be

In general, indications for management of radial head fracture are well understood and accepted. As noted TABLE 24-1

Summary of 15 Years of Literature Involving Prosthetic Radial Head Replacement PROSTHETIC INTERVENTION TOTAL # (% SATISFACTORY)

Author

Year

Type

Knight9

1993

Mono

8

1996

Bipolar

17

1998

Mono

2000

Bipolar

Judet Wick

Smets12 11

Acute

31 (94) 7 (100) — 13 (77)

— 7 (72) — 2 (0)

Total (%)

Follow-up (yr)

31 (94)

4.5

14 (86)

4

30 (73)

—

15 (67)

2

Popovic

2000

Bipolar

Harrington5

2001

Mono

Holmenschlager7

2002

Bipolar

10 (100)

6 (67)

16 (87)

1.5

Alnot

2003

Bipolar

18 (100)

4 (0)

22 (82)

1.5

2

2005

Mono

10 (100)

2007

Mono

27 (82)

1

Bain

Doornberg3 Total (% satisfied)

11 (83)

Delayed

—

127 (92)

—

11 (83)

—

20 (80)

6 (50) None 25 (48)

2.5 12

16 (81)

2.8

27 (82)

3.5

202 (82)

3–4

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addressed or solved with an articulated device, the implant must not be inserted. Articular trauma to the capitellum is a relative contraindication because some patients will do well, even with some degree of capitellar damage. If the resorption of the proximal radius is too extensive to be accommodated by the device, it obviously should not be inserted.

DESIGN CONSIDERATIONS An increasing number of designs have recently appeared on the market (Fig. 24-29). There are three major considerations when selecting a prosthetic radial head implant: (1) sizing; (2) alignment, and (3) stem fixation.

A

B

C

FIGURE 24-29 Current implant designs are characterized by modularity with fixation concepts of noncemented smooth stems (A), textured implants designed for biological fixation (B), or the implant may be cemented if it is believed to be necessary (C). In addition, the rigid versus articular elements are available.

Chapter 24 Radial Head Fracture

The wide variation in the amount of residual proximal radius, as well as considerable individual variation in anatomic sizes, dictates a system with several stem and head diameter and length variations. One of the most important features distinguishing the systems available today is the ability to accommodate significant proximal resection or resorption. The option of allowing for build-up or shim of the radial neck is an important consideration to offer the maximum flexibility of a replacement system. Hence, the system must offer modularity and flexibility to match stem, head diameter, and neck length with individual variations in anatomy and pathology.

STEM FIXATION There are three basic fixation philosophies: (1) smooth, polished uncemented; (2) cemented stems, and (3) textured implants designed to either provide biologic fixation to be secured with cement. The round, smooth stem of the Evolve device (Wright Medical Technology, Inc., Arlington, TN) makes no attempt at achieving rigid fixation, but rather the stem is used only to align the articular disc with the capitellum. Motion of stems designed to be fixed are typically painful and, if loose, tend to cause osteolysis. However, the smooth polished stem is believed to avoid or lessen this problem. This system also allows for some axial motion between the stem and bone. There are favorable published results with this design philosophy to justify its value and consideration.3 There is inadequate clinical experience to date to determine if the short textured stems can be reliably stabilized by biologic fixation. Most stems that allow the potential for biologic fixation may be cemented at the surgeon’s preference. Therefore, no comparative data exist at this time to direct the selection of one fixation type over another. The selection is, however, design specific.

ARTICULATION What appears to be clearly emerging is that the single most important prognostic consideration is whether the implant is used to address the acute fracture or as a reconstruction device. When the radial head is being replaced as a secondary procedure to salvage a previously failed or untreated traumatic or pathologic event, alignment of the proximal radius is altered and difficult to restore. Therefore, the major requirement is that the prosthetic radial head align with and articulate with the capitellum. When pathology alters the radial/humeral

relationship, the fixed articulation implants become vulnerable to subluxation, dislocation, or erosion of the capitellum. It is for this reason that designs that allow a degree of freedom at the stem/articular junction are attractive to address this circumstance. In the author’s opinion and practice, articulated implants may also be used in the acute fracture setting as well, because they provide reliable articulation in both settings. Experimental data suggest both fixed and articulated ligaments offer similar stability to valgus stress10 (Fig. 24-30). The theoretical disadvantage of the articulated radial head implant, of course, is the potential to generate wear debris. Although this has been a theoretical consideration, we are aware of no instances of this having occurred, in fact, to date; however, the clinical experience is quite limited. In summary, we believe the advantages outweigh the disadvantages.

A 40 Varus/valgus

SIZING

383

30 20 10 0 Intact

B

MCL cut

R head Prosth ex

FIGURE 24-30 The experimental data of the three implants shown demonstrate a consistent pattern of improved valgus stability with implants after a medial collateral ligament injury and radial head resection. Note that although valgus stability is improved it does not completely return to normal.10

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Part V Adult Trauma

Annular ligament Alignment rod is aligned to ulnar styloid Lateral collateral ligament

Extensor carpi ulnaris

FIGURE 24-32 By using a resection guide that aligns with the ulnar styloid, a more reliable resection of the plane of the radial neck is obtained. (Courtesy of Small Bone Innovations, Morrisville, NJ.)

Anconeus

FIGURE 24-31 We prefer exposing the elbow through Kocher’s interval. The capsule is incised anterior to the lateral ulnar collateral ligament. (Courtesy of Small Bone Innovations, Morrisville, NJ.)

TECHNIQUE EXPOSURE With the patient supine Kocher’s or Kaplan’s interval is employed (Fig. 24-31). The lateral capsule is entered anterior to the collateral ligament, and the annular ligament and capsule are reflected anteriorly and posteriorly to expose the radial head. A portion of the lateral collateral ligament and anterior capsule can be reflected from the lateral epicondyle and anterior humerus to facilitate exposure, if necessary, but the lateral ulnohumeral ligament is preserved. If greater exposure is required, the ligament is reflected from its humeral origin. If the ligament has been disrupted, then the exposure progresses through the site of disruption to expose the radiohumeral.

RESECTING THE RADIAL HEAD Optimum articulation requires an accurate resection that assures precise implant placement. We employ a resection guide to replicate the anatomic axis of forearm rotation using the capitellum and ulnar styloid as landmarks (Fig. 24-32). During resection, forearm rotation should be assessed to ensure resection perpendicular to the axis of rotation. The distal extent of resection is the minimal amount that is consistent with the restoration of function as dictated by the fracture line or previous

FIGURE 24-33 The medullary canal is prepared in this instance using an off-set rasp. (Courtesy of Small Bone Innovations, Morrisville, NJ.)

radial head resection but still compatible with implant insertion and length restoration options for the design being used.

INTRAMEDULLARY PREPARATION Varus stress and supination of the forearm allows exposure of the medullary canal, especially if the elbow is unstable. If the stability does not allow exposure of the proximal radius, careful reflection of the origin of the collateral ligament from the lateral epicondyle may be necessary. The canal is identified with a starter awl, with final canal preparation performed with curved rasps (Fig. 24-33).

TRIAL REDUCTION I use one size smaller stem than are to be used (Fig. 24-34). The appropriate-sized trial head is then applied (Fig. 24-35). Tracking in flexion and extension and in forearm rotation is carefully assessed.

Chapter 24 Radial Head Fracture

Trial head

385

Trial radial stem

FIGURE 24-35 For ease of trial, one size smaller stem is employed; however, an accurate estimate of the radial head size is applied. We typically use one size smaller than might be suggested by the resected head because these lesions are often deformed by pathology, and the size of the head overestimates the true articular portion. (Courtesy of Small Bone Innovations, Morrisville, NJ.)

appears inadequate, it should be reinforced with a No. 5 nonabsorbable Bunnell or Krackow suture (Fig. 24-36). For reconstruction applications, a formal LUCL substitute with tendon allograft (palmaris) or autograft (plantaris) may be necessary. FIGURE 24-34

This particular design (RHead SBI) employs a curved stem which improves rotatory stability as well as enhances ease of insertion. (Courtesy of Small Bone Innovations, Morrisville, NJ.)

IMPLANTING THE FINAL COMPONENTS Once proper size, alignment, and positioning of the implant have been determined, the prosthetic radial stem is inserted with a rotational motion down the medullary canal and tapped in place with the impactor. Bone cement (polymethylmethacrylate [PMMA]) may occasionally be used if secure press-fit fixation is not attainable. I try to avoid the use of PMMA, if possible. The modular head is next placed over the taper using longitudinal distraction and/or varus stress to distract the radiocapitellar interface sufficiently to permit the radial head to be inserted. The radial head implant is secured using the impactor. Flexion and extension, pronation, and supination are assessed.

CLOSURE Reconstitution of the lateral ulnar collateral ligament (LUCL) is essential at closure. If the ligamentous tissue

AFTERCARE Passive flexion and extension is allowed on the second day, assuming that the elbow is stable. The goal of radial head replacement and soft tissue repair/reconstruction is to achieve elbow stability. Both flexion-extension and pronation-supination arcs are allowed without restriction. Active motion can begin by day 5. Long-term aftercare requires surveillance, as is the case with any prosthetic replacement. If the implant is asymptomatic and tracks well, routine implant removal is not necessary.

TECHNICAL NOTES Overstuffing A careful study performed by van Glabbeek et al14 in our laboratory documented the sensitivity of this articulation to precise longitudinal placement. Overstuffing of more than 2 mm caused measurable alteration of the kinematics of the elbow joint. A useful and simple means of assessing accurate restoration of radial length is to align the device with the lesser sigmoid notch of the ulna.

386

Part V Adult Trauma

possibly predispose to capitellar erosion by a radial head implant. ECU

STEM FIXATION If the stem is not designed to piston and spin in the medullary canal, rigid fixation is necessary for pain relief and long-term durability. If cement is not to be used, caution should be exercised to avoid over reaming because this can lead to a loose, eroded, and painful device. Biologically fixed devices should demonstrate some resistance during insertion.

RESULTS Anconeus

A

B FIGURE 24-36 Secure repair of the lateral collateral ligament is critical. We typically use a running locked stitch for this purpose. (With permission, Mayo Foundation.)

The most useful understanding of anticipated outcomes is realized from reviewing the literature over the past 15 years. However, because of considerable variation in the indications, acuteness of the injury, pathology being addressed, design employed, surveillance period, and tools of outcome assessment, meaningful comparisons or summaries of outcomes are difficult. Nonetheless, an attempt at a high level summary of the relevant literature is shown in Table 24-1. In general, one might anticipate a satisfactory outcome in about 85% of those treated immediately, and at best 50% to 60% of those treated in a delayed fashion (Fig. 24-37). Regarding axial instability, we have assessed our experience with the use of a current generation radial head implant design and a capitellar replacement to stabilize the proximal migration of the radius. At 25, 63, and 175 months, all three are considered satisfactory.6 This appears to represent an important but far from final step forward in the management of this problem.

PROGNOSTIC FACTORS Without question, as identified in the previous edition of this book and confirmed by subsequent experience, this is the most significant determinant of outcome of radial head replacement. This observation has been confirmed in recent studies, such as that of Bain et al.2 These Australian investigators report 10 of 10 satisfactory outcomes a mean of 28 years after acute replacement for a Mason III fracture with dislocation. In contrast, three of six with delayed reconstruction did poorly. In a similar study from France, Alnot et al1 observed satisfactory function in all 18 acutely replaced radial heads but no acceptable outcomes in the four treated as a reconstructive procedure. In an unpublished review of Mayo early experience, we observed similar results. Acute versus Chronic Condition

Malalignment In monoblock articular implants, the accuracy of the articular alignment is directly related to the accuracy of the proximal radial resection. For this reason, it seems wise to employ some form of resection guide and use a design that allows some tolerance or flexibility (bipolar) at the stem/head interface. Capitellar erosion is believed to be due to malalignment or from overstuffing the joint. If the device has caused capitellar erosion, treatment is by removal of the device. In some instances, a capitellar device may solve this problem. Van Riet et al15 have also recently documented the fact that an osteoporotic capitellum may

Chapter 24 Radial Head Fracture

A

387

B

FIGURE 24-37 A rheumatologist sustained a radial head fracture that displaced; medial collateral ligament deficiency is also noted. The reconstruction was carried out using an articulated or bipolar type design in order to ensure proper tracking in this reconstructive mode. (With permission, Mayo Foundation.)

Outcomes Acute fractures were successfully managed in about 85%, but only about 50% were satisfactory after reconstructive procedures (see Table 24-1). Although not demonstrable as yet by objective assessment, our impression is that we are seeing improved results with the articulated prosthetic device, which avoids those failures associated with malalignment of the radiohumeral joint.

6.

7.

8.

References 1. Alnot, J. Y., Katz, V., and Hardy, P.: Guepar radial head prosthesis for recent and old fractures: A series of 22 cases. Rev Chir. Orthop. Reparatrice Appar. Mot. 89:304, 2003. 2. Bain, G. I., Ashwood, N., Baird, R., and Unni, R.: Management of Mason type III radial head fractures with a titanium prosthesis, ligament repair, and early mobilization. Surgical technique. J. Bone Joint Surg. 98A(Suppl 1 [Pt 1]):136, 2005. 3. Doornberg, J. N., Parisien, R., van Duijn, J., and Ring, D.: Radial head arthroplasty with a modular metal spacer to treat acute traumatic elbow instability. J. Bone Joint Surg. 89:1075, 2007. 4. Edwards, G. S. Jr., and Jupiter, J. B.: Radial head fractures with acute distal radioulnar dislocation. Essex-Lopresti revisited. Clin. Orthop. Relat. Res. 234:61, 1988. 5. Harrington, I. J., Sekyi-Out, A., Barrington, T. W., Evans, D. C., and Tuli, V.: The functional outcome with metallic

9.

10.

11.

12.

13.

radial head implants in the treatment of unstable elbow fractures: A long-term review. J. Trauma. 50:46, 2001. Heijink, A., Morrey, B. F., and Cooney, W. P.: Capitellar resurfacing arthroplasty: A case report of three patients. J. Shoulder Elbow Surg. 17:e12, 2007. Holmenschlager, F., Halm, J. P., and Winckler, S.: Les fractures fraîches de la tête radiale. Résultants de la prothèse à cupule flottant de Judet. Rev. Chir. Orthop. Reparatrice Appar. Mot. 88:387, 2002. Judet, T., Garreau de Loubresse, C., Piriou, P., and Charnley, G.: A floating prosthesis for radial head fractures. J. Bone Joint Surg. 78B:244, 1996. Knight, D. J., Rymaszewski, L. A., Amis, A. A., and Miller, J. H.: Primary replacement of the fractured radial head with a metal prosthesis. J. Bone Joint Surg. 75-B:572, 1993. Pomianowski, S., Sawicki, G., and Laskowski, J.: [Internal fixation in the treatment of radial head fractures]. Chir. Narzadow. Ruchu. Ortop. Pol. 67:25, 2002. Popovic, N., Gillet, P., Rodriguez, A., and Lemaire, R.: Fracture of the radial head with associated elbow dislocation: Results of treatment using a floating radial head prosthesis. J. Orthop. Trauma. 14:171, 2000. Smets, S., Govaers, K., Jansen, N., van Riet, R., Schaap, M., and Van Glabbeek, F.: The floating radial head prosthesis for comminuted radial head fractures: A multicentric study. Acta. Orthop. Belg. 66:353, 2000. Trousdale, R. T., Amadio, P. C., Cooney, W. P., and Morrey, B. F.: Radio-ulnar dissociation. A review of twenty cases. J. Bone Joint Surg. Am. 74:1486, 1992.

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14. Van Glabbeek, F., van Riet, R., Jansen, N., D’Anvers, J., and Nuyts, R.: Arthroscopically assisted reduction and internal fixation of tibial plateau fractures: report of twenty cases. Acta. Orthop. Belg. 68:258, 2002. 15. van Riet, R. P., Van Glabbeek, F., Verborgt, O., and Gielen, J.: Capitellar erosion caused by a metal radial head prosthesis: Case report. J. Bone Joint Surg. 86A:1061, 2004.

16. van Riet, R. P., Morrey, B. F., O’Driscoll, S. W., and Van Glabbeek, F.: Associated injuries complicating radial head fractures: a demographic study. Clin. Orthop. Relat. Res. 441:351, 2005. 17. Wick, M., Lies, A., Muller, E. J., Hahn, M. P., and Muhr, G.: Prostheses of the head of the radius. What outcome can be expected? Unfallchirurg 101:817, 1998.

Chapter 25 Fractures of the Olecranon

CHAPTER

25

Fractures of the Olecranon Julie E. Adams and Scott P. Steinmann

INTRODUCTION The subcutaneous location of the olecranon makes it vulnerable to trauma.7 Isolated fractures of the olecranon comprise approximately 10% of fractures about the elbow,26,38 with an estimated incidence of 1.08 per 10,000 person-years.26 Most result from low energy trauma such as a fall from a height of less than 2 meters, a direct blow to the elbow, or from forced hyperextension.1,17,20,26,27,38 A fall on a partially flexed elbow may generate an avulsion fracture of the olecranon from the pull of the triceps.7 Amis et al investigated variable impact mechanisms and the resultant fracture patterns in a cadaveric model.1 A trend was noted in which radial head and coronoid fractures tended to occur with forearm impacts with the elbow in up to 80 degrees of flexion.1 Olecranon fractures occurred with direct blows at 90 degrees of flexion, whereas injuries occurring with the elbow in greater than 110 degrees of flexion tended to result in distal humerus fractures.1 In general, fractures of the olecranon have a favorable prognosis following treatment,7,10,17,20,25,26 with estimates that ninety-six percent of patients have a good to excellent long-term outcome with only rare adverse events.25,26

ANATOMIC CONSIDERATIONS The olecranon, together with the coronoid process, forms the semilunar or greater sigmoid notch of the ulna.7 This articulates with the trochlea of the humerus and confers stability and facilitates motion in the anterior-posterior plane.7 A transverse “bare area” devoid of cartilage is found at the midpoint between the coronoid and the tip of the olecranon. The unwary surgeon may inadvertently discard structurally significant portions of the olecranon if this is not considered when reconstructing the fractured olecranon.7 The ossification center of the olecranon generally appears by 9 to 10 years of age, and fuses to the proximal ulna by age 14 years.7,14 Persistence of the physis in adulthood may occur, and is usually bilateral and familial. In addition, patella cubiti, an accessory ossicle embedded in the distal triceps, may

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be present and likewise should not be confused with a fracture.7

EVALUATION Because the fracture by nature is intra-articular with the exception of some avulsion-type fractures of the olecranon, hemarthrosis is frequently present in conjunction with olecranon fracture.7 Although this sign may be obfuscated by pain due to the injury, inability to actively extend the elbow against gravity may be an important indication of triceps discontinuity.7 Because of the proximity of the ulnar nerve, the first and each subsequent examination should document the status of the ulnar nerve.7 Anteroposterior and true lateral radiographs should be obtained to aid in diagnosis and treatment considerations.7 The true lateral film should be examined to determine the extent and nature of the fracture pattern and to evaluate for the presence of other lesions such as a radial head fracture or dislocation, or distal humerus or coronoid fractures.7

CLASSIFICATION OF OLECRANON FRACTURES Colton9 classified olecranon fractures according to the degree of displacement and fracture pattern. Colton type I fractures are nondisplaced fractures, in which displacement remains less than 2 mm with elbow flexion to 90 degrees or extension against gravity. The patient can actively extend the elbow against gravity.7,9 Type II, displaced fractures, may be further subtyped into avulsion fractures, oblique and transverse fractures, comminuted fractures, and fracture-dislocations.9 Horne et al20 proposed a classification system and treatment algorithm for olecranon fractures based on review of 100 cases. In this system, type I fractures are either transverse intra-articular fractures of the proximal third of the olecranon or extra-articular fractures involving the point of the olecranon.20 Type II fractures are oblique or transverse intra-articular fractures involving the middle third of the olecranon fossa with type IIA representing those with a single fracture line and type IIB representing those with a second more distal and posteriorly oriented fracture line.20 Type III fractures include those intra-articular fractures of the distal third of the olecranon fossa.20 From review of these 100 cases, Horne et al made treatment recommendations, including favoring the use of plate and screw with tension band fixation in cases of delay of greater than 1 week to decrease the risk of nonunion.20 Extra-articular type I fractures were best treated with excision, whereas intraarticular type I and II fractures should be treated with open reduction and internal fixation with tension band

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wiring. Recommendations for type IIB fractures involved elevation of the depressed intra-articular fracture and buttressing with bone graft, followed by tension band wiring.20 Type III fractures were best treated with plate and screw fixation to provide optimum rigidity to the construct as tension band wiring was less effective at this location.20 The AO classification system (Fig. 25-1) accounts for both proximal radius and proximal ulna fractures as fracture site 2 for radius/ulna, and 21 for the proximal segment of the radius and ulna. Type A fractures are extra-articular, type B are intra-articular fractures involving the articular surface of either the radius or the ulna, and type C are those involving the articular surface of both bones. Additional subtypes denote comminution, displacement, and location.32 Although the AO classificaBONE: RADIUS/ULNA (2)

Location: Proximal segment (21)

Types: A. Extra-articular (21-A)

tion may be useful for research purposes, it is not commonly used in clinical practice. Morrey classified olecranon fractures according to criteria regarding stability, comminution, and displacement.8,31 The Mayo Classification (Fig. 25-2) thus divides olecranon fractures into three types, facilitating classification and providing an algorithm for treatment.8,31 Type I, undisplaced fractures as defined by the Colton criteria earlier, may be subdivided into type IA, noncomminuted fractures, and type IB, comminuted fractures.31 These fractures represent approximately 5% of olecranon fractures. Because these fractures are by definition nondisplaced, the practical significance of the degree of comminution is not significant and types IA and IB may essentially be regarded and treated as the same lesion.31 Mayo type II fractures are the most common type, representing about 85% of olecranon fractures.27,31,38 CLASSIFICATION OF OLECRANON FRACTURES (Morrey)

B. Articular fracture involving articular surface of only one of the two bones (21-B)

Type I Undisplaced

Type II Displacedstable C. Articular fracture involving articular surface of two bones (21-C)

A-Noncomminuted

B-Comminuted

A-Noncomminuted

B-Comminuted

Type III Unstable

FIGURE 25-1

The AO classification accounts for fractures of both the proximal radius and ulna as fracture site 2 for radius/ulna, and 21 for the proximal segment of the radius and ulna. Type A fractures are extra-articular, type B fractures are intra-articular fractures involving the articular surface of either the radius or the ulna, and type C fractures are those involving the articular surface of both bones. Additional subtypes denote comminution, displacement, and location. (Redrawn from Marsh, J. L., Slongo, T. F., Agel, J., et al: Fracture and dislocation classification compendium-2007: Orthopaedic Trauma Association classification, database and outcomes committee. J. Orthop. Trauma 21[suppl 10]:S1, 2007.)

FIGURE 25-2

Mayo classification of olecranon fractures. Type I fractures are nondisplaced, noncomminuted (IA) or comminuted (IB) fractures. Type II fractures are stable displaced fractures, and may be noncomminuted (IIA) or comminuted (IIB). Type III fractures are unstable, displaced fractures, and may be noncomminuted (IIIA) or comminuted (IIIB). (Redrawn from Cabanela, M. E., and Morrey, B. F.: Fractures of the olecranon. In Morrey, B. F. (ed.): The Elbow and Its Disorders, 3rd ed. Philadelphia, W. B. Saunders, 2000.)

Chapter 25 Fractures of the Olecranon

These fractures, which are stable fractures with greater than 3 mm of displacement, may be noncomminuted (type IIA) or comminuted (type IIB).31 Because the collateral ligaments are intact, the forearm is stable relative to the humerus.31 Mayo Type III fractures are unstable, displaced fractures and represent a fracture-dislocation. Like types I and II, type III fractures may be subclassified into noncomminuted (IIIA) or comminuted (IIIB) types.8,31

COMPLEX OLECRANON FRACTURE-DISLOCATIONS Olecranon fractures associated with subluxation of the radial head and/or the coronoid process are typically multifragmentary, complex injuries.12,35,37 Anterior fracture dislocations are often referred to transolecranon fracture-dislocations, because the mechanism of injury appears to involve anterior displacement of the forearm, resulting in the trochlea being driven through the olecranon process.12,35,37 The radial head is displaced anteriorly, and this injury is differentiated from the Bado type I Monteggia fracture by the presence of ulnohumeral joint destabilization with preservation of the radioulnar relationship.35,37 Posterior fracture dislocations of the olecranon are more similar to type II Monteggia fractures, with posterior dislocation of the radial head, an apex posterior fracture of the ulna, and similar implications for the stability and function of both the ulnohumeral joint as well as the forearm.12,35 These fractures may be considered a variant of the posterior Monteggia lesion.12 Both posterior and anterior variants are commonly associated with fractures of the coronoid, which are usually basal fractures involving 50% to 100% of the height of the coronoid.35 In anterior olecranon fracturedislocations, reduction of the olecranon and coronoid fracture fragments results in restoration of stability, with little implication for forearm dysfunction. Posterior olecranon fracture-dislocations, in contrast, have important implications, with elbow instability and forearm dysfunction being common despite fracture reduction.35

TREATMENT The Mayo Classification provides a basis for a rational treatment algorithm by fracture type and subtype, and conveys prognostic value.31,38 Nondisplaced fractures (Mayo type I) may be treated symptomatically and nonoperatively with 7 to 10 days of immobilization in midflexion and neutral rotation, followed by initiation of an active range of motion program.6,8,17,31 Restrictions on active resisted elbow extension and weight bearing should be maintained for 6 to 8 weeks, with gradual increases in these activities

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as tolerated.6 Close follow-up with radiographs at 1, 2, and 4 weeks is recommended to assess for displacement and possible need for further intervention.7 Rarely, in select patients, type I fractures may benefit from open reduction and internal fixation to allow immediate motion and stability.8,31 Some type I fractures may be treated with immobilization in a long arm cast at 90 degrees of flexion for 3 to 4 weeks.7 Thereafter, protected range of motion with avoidance of flexion greater than 90 degrees until radiographic evidence of bony healing occurs, usually at 6 to 8 weeks, is recommended.7 Rangeof-motion exercises may be commenced at an earlier time point in select patients, such as the elderly, in whom stiffness occurs more frequently.7 Displaced fractures (Mayo type II and III) usually require surgical intervention.6,8,17 Goals of surgical management include restoring the articular congruity and stability of the elbow, maintaining extension power, and providing stable anatomic fixation such that early range of motion is possible, thereby lessening the risk of stiffness.7,16,17,21 Options include excision or open reduction and internal fixation with a variety of devices including tension band wiring, intramedullary screw placement, plate and screw constructs, or bioabsorbable pins.4,6,15,17,27,31,38

SURGICAL MANAGEMENT OPTIONS Excision Excision of fracture fragments with advancement and reinsertion of the triceps tendon may be indicated in cases of nonunion, patients who are elderly or who have poor soft tissue viability, avulsion-type extra-articular fractures, and in cases with severe comminution as in Mayo type IIB fractures (Fig. 25-3).7,10,11,13,15,31 Disadvantages of excision include subsequent risks of triceps weakness, instability, stiffness, and a theoretical risk for increased arthrosis due to altered contact pressures.2,7,11,24,29 However, excision obviates risk of nonunion, hardware failure, or prominence, and others suggest a decreased risk of post-traumatic arthritis, because the possibility of incongruity of the articular surface reduction is eliminated with excision of the fragment rather than reduction and fixation.11,17,15 McKeever and Buck determined that one may excise up to 80% of the olecranon without sacrificing stability if the coronoid and anterior soft tissues are intact.7,15,28 If anterior damage is present, instability is a sequelae if too much proximal ulna is excised.7 In addition, An et al2 noted increasing instability of the elbow with olecranon excision, and data from the Mayo laboratory suggest that resection should be limited to 30% of the olecranon. Kamineni et al24 investigated the impact of olecranon resection on stability in relation to posteromedial stresses in a cadaveric model. Resection of osteophytes and

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A

C

FIGURE 25-3

B proximal ulna was performed to simulate treatment of posteromedial osteophytes, such as in throwing athletes. The investigators noted a clinically significant level of instability with valgus stresses following resection of as little as 6 mm of posteromedial olecranon.24 The authors speculated that this instability may not be clinically relevant in low-demand, elderly patients, but it may be problematic in higher demand athletes or active patients or laborers.24 The increased instability may place increased stress upon the medial collateral ligament, predisposing to possible failure.24 However, excision is usually used in older, low demand patients who may not place such demands on their elbows. Many authorities recommend reattachment of the triceps at the level of the articular surface.7,11 However,

This type IIA olecranon fracture (A) was treated with excision of fracture fragments and by suturing the triceps down to the remaining distal fragment (B). At 4 years follow-up, the patient had no complaints and no instability, and range of motion was pronation-supination 80-80, full flexion, with a 25-degree extension lag. Radiographs were satisfactory (C). (From Adams, J. E., and Steinmann, S. P.: Fractures of the olecranon. In Celli, L. [ed.]: Treatment of Elbow Lesions—New Aspects in Diagnosis and Surgical Techniques. Milan, Springer-Verlag Italia, 2007.)

one recent study suggests that attachment more posteriorly results in improved extension strength.11 Didonna et al11 studied variable positions for triceps reattachment following partial olecranon (50%) excision for simulated olecranon fracture in a cadaveric model. Loads were applied along the triceps mechanism at 45 degrees, 90 degrees, and 135 degrees, and the resultant forces were recorded. A significant decrease in extension strength with anterior placement of the triceps relative to normal and relative to posterior placement was noted, with the differences greatest with increasing extension. In contrast, posterior reattachment was noted to result in decreased extensor strength only at 90 degrees. Therefore, the authors recommended more posterior reattachment sites to minimize loss of extension strength.11

Chapter 25 Fractures of the Olecranon

Although some authors report less post-traumatic arthritis with excision due to avoiding an incongruent joint, some speculate that excision may lead to increased risk of post-traumatic arthrosis.29 In a cadaveric model with 50% olecranon osteotomy to simulate an olecranon fracture, peak forces across the ulnohumeral joint were measured following either excision of the proximal fragment or open reduction and internal fixation with tension band wiring.29 Elbows fixed with tension band wiring had no significant difference in peak ulnohumeral pressures when compared with the intact elbow joint.28 In contrast, elbows with excision of the proximal fragment were noted to have significant increases in joint forces over the medial and lateral articular surfaces.29 The authors theorized that open reduction and internal fixation with tension band wiring restores the normal biomechanics of the elbow, whereas excision results in abnormal joint forces, which may predispose to arthrosis.29 As such, Moed et al29 favored open reduction and internal fixation in cases in which a large proximal fragment is present. Nevertheless, satisfactory clinical outcomes (see Fig. 25-3A to C) have been described for treatment of olecranon fracture by excision when used in appropriate patient populations.10,13,15,17 Gartsman17 noted equivalent range of motion, functional status, extensor strength, pain, stability, and incidence of degenerative changes in cases of olecranon fracture treated by open reduction and internal fixation or primary excision.17 In addition, local complications (23% versus 4%) and requirements for additional procedures (an additional 23%), such as hardware removal, were more common in the patients treated with open reduction and internal fixation.17 Such studies demonstrate that excision is a good option for treatment of the appropriate fracture in the appropriately selected patient.

INTERNAL FIXATION Goals of internal fixation include anatomic reduction to prevent post-traumatic arthrosis and to facilitate full return of pain-free motion, and stable fixation to allow early use of the arm and early range of motion, thus limiting contractures. Multiple devices have been proposed, and details of the more commonly used techniques and implants are described.

Biomechanics of Internal Fixation Fyfe et al16 investigated rigidity of various methods of fixation of transverse, oblique, and simulated comminuted olecranon fractures in a cadaveric model. Tension band wiring with two knots was the most stable fixation construct for simulated transverse fractures, whereas intramedullary screw fixation with or without tension banding was unreliable in restoring stability.16 Oblique

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osteotomies were best repaired with one-third tubular plate fixation or tension band wiring with two knots; whereas the comminuted fractures were most rigidly fixed with five-hole AO plate and screw fixation. In all cases, either tension band wiring or plate-and-screw fixation yielded fixation sufficiently rigid to withstand forces equivalent to those experienced in vivo with active mobilization of the elbow. For comminuted fractures, plate-and-screw fixation was recommended due to the greater stability noted in this in vitro study.16 Hume et al22 studied outcomes of displaced olecranon fractures treated with either plate or tension band wiring fixation in a prospective randomized trial. Plate fixation was superior with respect to maintenance of reduction without step off or gap (95% versus 47%), radiographic outcomes (86% versus 47% good) and clinical outcomes (63% versus 37% good). Range of motion at 6 months was equivalent.39 Plate fixation required longer operative times but was associated with no increase in complication rates.22 Tension band wiring was complicated with symptomatic hardware prominence in 42%.22 Horner et al21 investigated use of tension band wiring versus one-third tubular plate and screws for fixation of simulated fractures of the most distal portion of the olecranon (Colton type III and Horne type III) in a cadaveric model. These fractures, due to the deforming forces of the forearm flexors, tend to be more unstable than their more proximal counterparts.21 The study demonstrated increased fixation stiffness in those fractures treated with one-third tubular plate fixation (163 N/mm versus 53 N/mm) versus tension band wiring. Therefore, the authors concluded that fixation with plate and screws would better counteract forces exerted by the brachioradialis and the biceps than tension band wiring in this fracture pattern.21

Specific Fixation Techniques Tension Band Wiring Tension band wiring is widely used as treatment for most olecranon fracture types (Fig. 254).31,38 This technique converts tensile forces across the fracture to compressive forces, which with motion, exert compression across the fracture site.7 Also compared with plate and screw fixation, less soft tissue dissection and periosteal stripping is required.18,20 However, this fixation technique may be associated with hardware complications.38 Owing to the subcutaneous nature and location of the elbow, prominent hardware may be problematic, with large numbers of patients in one series reporting hardware-related pain (24%) and functional difficulties (32%) relieved by hardware removal. Also, pain and functional difficulties post removal were reported by 13% and 15% of patients, respectively.38 Nevertheless, up to 97% good to excellent results have been widely reported with use of tension band wiring using proper technique.41

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A

B

C

E

D'

D

F FIGURE 25-4

E'

F'

Optimal AO technique for tension band wiring. Reduction of the fracture is performed with pointed forceps (A), and parallel Kirschner wires are driven obliquely from proximal to distal until the volar cortex is penetrated (B). A 2.5-mm drill is used to create a transverse hole distally to accept the tension wire (B). The 1.0- or 1.2-mm wire with a prefabricated loop is introduced under the triceps and the two K-wires, then through the transverse hole (C). As an alternative, two separate wires may be used (F). The wires are grasped at the base and twisted together and the twists laid down flat on the bony surfaces (D’, F’). Subsequently, the Kwires are pulled back slightly, cut obliquely, and bent into hooks. The hooks are then impacted into bone over the tension band (E, E’, F’). (Redrawn from Heim, U.: Forearm and hand/mini-implants. In Müller, M. E, Allgöwer, M., Schneider, R., and Henegger, H. W. [eds.]: Manual of Internal Fixation: Techniques Recommended by the AOASIF Group, 3rd ed. New York: Springer-Verlag, 1991.)

Although there are several proposed modifications of the AO technique that have been suggested to result in increased load to failure, technically easier insertion, and fewer complications, several studies suggest no benefit over the traditional AO technique. Wu et al42 found no difference in the rate of K-wire extrusion or load to failure in a series of cadaveric simulated transverse olecranon fractures fixed either with the traditional AO technique or new modifications. Furthermore, results suggested that loads less than 5.5 kg could be borne postoperatively during repetitive activities of daily living, with single loads not to exceed 8 kg, without adverse consequences.42 Paremain et al36 investigated biomechanics of tension band wiring for fixation of olecranon fractures in a cadaveric model. Simulated transverse olecranon fractures were repaired using two techniques of tension band wiring: the two tightening knot AO technique espoused by Weber and Vasey,40 and the modification to this technique proposed by Rowland and Burkhart.39 Similar mechanisms of failure occurred in both groups, with no statistical significance in load to failure between the groups.39 Tension band wiring may be performed using the standard AO technique (Fig. 25-4).18 Bone reduction clamps reduce the fracture; superficial drill holes in the distal fragment may provide a useful traction site for the jaws of the bone reduction forceps. Following reduction, two parallel 1.6-mm K wires are introduced from the posterior aspect of the olecranon, aiming anteriorly and obliquely just through the anterior cortex. A 2.5-mm hole is drilled transversely in the distal fragment for placement of a 1.0-mm or 1.2-mm cerclage wire with a prefabricated loop; alternatively, two cerclage wires may be used. The wire is then routed under the triceps tendon and K-wires to create a figure-ofeight construct. Tensioning is performed symmetrically on each side. The K-wires are pulled back slightly, cut and bent, and finally the bend ends are impacted into bone.18 Intramedullary screw fixation involves placement of a screw down the long axis of the ulnar canal. Ideally, the length of the screw and the width of the threads, which may catch the side cortices, confer sufficient stability for this fixation. However, the screw may compress the fragments, or the fragments may be malrotated. Although stability may be an issue, biomechanical studies suggest favorable features of intramedullary screw fixation for olecranon fractures. Molloy et al30 studied biomechanical features of olecranon fracture fixation with tension band wiring or with intramedullary nail in a cadaveric model. Intramedullary nail fixation was stiffer and had a higher maximum load to failure than did tension band wiring fixation. However, the authors note that this in vitro

Intramedullary Screw Fixation

Chapter 25 Fractures of the Olecranon

study fails to replicate important in vivo considerations, such as the potential for damage to the triceps and soft tissues, and the effect of cyclical loading as well as union rate.30 In addition, with intramedullary nailing, the potential for fracture malreduction secondary to off-axis placement of the nail exists.30 Others have reported on unlocked intramedullary screw fixation for olecranon fractures, but higher rates of fixation loss than in tension band wiring have been noted (Fig. 25-5A).19,30 Some have used tension band wiring in conjunction with unlocked intramedullary screws.30 Molloy et al30 investigated biomechanical features of tension band wiring versus intramedullary nail fixation of transverse olecranon fractures. Both tension band wiring and plate-and-screw fixation have high success and union rates; however, owing to painful or prominent hardware, 80% of tension band wiring and 20% of

plate-and-screw constructs require removal.30 Intramedullary screw prominence is rarely problematic.

Plate-and-Screw Fixation Multiple plate-and-screw constructs have been described for the treatment of olecranon fractures (Fig. 25-6).34 Advantages of plate fixation include favorable biomechanics, which can act as a tension band and as a buttress.34 In addition, hardware prominence is less problematic in plate-and-screw constructs relative to tension band wiring fixation.27 Nowinski et al34 described results of treatment of comminuted olecranon fractures with an AO limited contact dynamic compression plate formerly used for wrist fusion. They noted the lowprofile but rigid characteristics of this plate were favorable for adaptation to olecranon fracture fixation, and described satisfactory clinical outcomes.34 Bailey et al4

A

C

B FIGURE 25-5

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A, This 74-year-old man presented with a symptomatic and painful nonunion of the olecranon 6 months following failed treatment with an intramedullary screw. B, He underwent open reduction and internal fixation with autogenous iliac crest bone graft. C, Postoperative radiographs were satisfactory, and the patient experienced complete pain relief and return of function. (From Adams, J. E., and Steinmann, S. P.: Fractures of the olecranon. In Celli, L. [ed]: Treatment of Elbow Lesions— New Aspects in Diagnosis and Surgical Techniques. Milan, Springer-Verlag Italia, 2007.)

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A

C

B FIGURE 25-6

This type IIA olecranon fracture (A) was treated with plate-and-screw osteosynthesis (B and C). At final follow-up, the patient had full range of motion and a pain-free result. (From Adams, J. E., and Steinmann, S. P.: Fractures of the olecranon. In Celli, L. [ed]: Treatment of Elbow Lesions—New Aspects in Diagnosis and Surgical Techniques. Milan, Springer-Verlag Italia, 2007.)

retrospectively reviewed outcomes of plate fixation of olecranon fractures in 25 patients. All of these patients had Mayo type II or III fractures, and satisfactory anatomic reduction was maintained to bony union. Only supination was statistically poorer in the fractured side relative to the normal side; side-to-side differences in range of motion and strength were not statistically significantly different between the fractured and unfractured sides.21 Mayo Elbow Performance Index (MEP) scores were 88% good to excellent, and the DASH scores were consistent with almost normal upper extremities.4 The Short-Form 36 (SF-36) demonstrated no impairment relative to the average American population.4 Twenty percent of patients required hardware removal due to plate prominence, but outcomes were satisfactory with minimal pain and a high degree of patient satisfaction in most cases (see Figs. 25-4 and 25-5).4 Likewise, Anderson et al3 described satisfactory outcomes in 32 patients treated with a congruent elbow plating system following olecranon fracture. At mean 2.2-year follow-

up, union rate was 94%. Nine percent of patients had symptomatic hardware, requiring removal. At final follow-up, MEP scores demonstrated 92% good or excellent results, with average arc of motion of 120 degrees.3

Bioabsorbable Fixation Bioabsorbable fixation may be desirable because of the potential to avoid future operations for hardware removal.5 Patients treated with conventional metal fixation devices have a high likelihood of requiring an additional procedure for removal of bothersome and/or prominent hardware. Bostman et al5 explored costs associated with need for hardware removal. Savings averaged $410 for use of bioabsorbable implants in olecranon fractures when total costs for metallic fixation and subsequent removal were considered. The breakeven point was 46% of fractures requiring removal, so that only at more than a 46% removal rate would use of bioabsorbable implants be financially favorable.5

Chapter 25 Fractures of the Olecranon

Juutilainen et al23 found equivalent outcomes in patients with olecranon fracture treated with either bioabsorbable implants (poly-L-lactide wire with self-reinforced polyglycolide screws or self-reinforced poly-L-lactide plugs) versus metallic implants (tension band wiring or K-wire plus cerclage wire fixation) and noted cost savings due to avoiding a second operation for hardware removal.23 Further clinical experience is needed to determine the role that bioabsorbable fixation techniques will assume in the future.

PREFERRED TECHNIQUES For Mayo type I fractures, conservative nonoperative management is preferred (Box 25-1). The patient is placed in sling immobilization for comfort with early active gentle range-of-motion exercises. Close weekly follow-up with radiographs is essential to rule out displacement and need for alternative treatment. Type II and III fractures are best treated surgically with either excision or open reduction and internal fixa-

Preferred Techniques of Olecranon Fracture Management

BOX 25-1

• Mayo Type IA and IB Fractures: • Undisplaced (<2 mm) fractures with (IB) or without comminution (IA) • Treatment: Sling immobilization, early active range of motion • Mayo Type IIA Fractures: • Stable fractures with >3 mm displacement. Comminution is absent. • Tension band wiring usually adequate. Plate and screw constructs are preferred if the fracture extends distal to coronoid. Excision may be considered in low demand patients or when small fragments are present. • Mayo Type IIB Fractures: • Stable fractures with more than 3-mm displacement; comminution is present. • Plate and screw constructs preferred, especially in patients younger than 60 years old. • Consider excision in low demand patients or those older than age 60 years, fractures with extensive comminution, or when small fragments are present. • Mayo Type IIIA Fractures: • Unstable, displaced fracture with no comminution. • Plate and screw constructs preferred. • Mayo Type IIIB Fractures: • Unstable, displaced fractures. Comminution is present. • Plate and screw constructs preferred. • Avulsion fractures • Tension band wiring or excision may be utilized.

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tion (see Figs. 25-3 and 25-5). For fractures with fragments distal to the coronoid, plate-and-screw osteosynthesis is preferred, because these more distal fragments are usually not adequately fixed by tension band wiring. Likewise, more comminuted fractures or oblique patterns are best treated with plate-and-screw fixation to optimize stability.16,21 Excision of fracture fragments is preferred for elderly, low-demand patients (see Fig. 25-3A to C) or those with extensive fracture comminution, or for treatment of nonunions. Tension band wiring using the standard AO technique may be performed for selected patterns amenable to this fixation technique. Otherwise, plateand-screw osteosynthesis provides the optimal fixation stability with minimal complications (see Fig. 25-4).

Technique for Excision or Open Reduction and Internal Fixation A midline longitudinal incision is curved over the olecranon to avoid placing the incision over the subcutaneous bone.17 Excision may be performed by sharp dissection of fracture fragments from the triceps aponeurosis, and longitudinal drill holes made through the proximal ulna to secure the triceps tendon down to bone.17 Tension band wiring or plate-and-screw osteosynthesis may be performed using the standard AO technique. The wound is then closed in the standard fashion, and a posterior plaster dressing is applied in full extension. The arm should be elevated overnight and the initial dressing changed on the second day. Active and passive motion is then initiated. Alternatively, if for any reason the operative fixation was believed to be less than optimal, splinting may be continued for 3 to 4 weeks to allow for bony healing at the expense of motion. Protected use of the extremity is maintained with minimal weight bearing and no resistance greater than that of gravity for 6 weeks or until radiographic evidence of healing is seen.

OTHER CONSIDERATIONS Olecranon fracture-dislocations require special considerations for treatment. Because of inherent instability of these fracture patterns, they are best treated with plateand-screw osteosynthesis.12,35 One-third tubular plates lack the stiffness necessary to withstand early range of motion and have been associated with early loosening or fatigue fractures.37 Medial and lateral flaps may be raised to access other pathology to bone or ligamentous structures, or concomitant radial head or coronoid fractures may be treated through the window created by the olecranon fracture.35 The plate may be applied over part of the triceps insertion without muscle or periosteal elevation to optimize bone healing, or the triceps may be split longitudinally and mobilized.35 If a concomitant

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anteromedial coronoid fracture fragment is present, it should be fixed to optimize stability of the elbow.35 When comminution is extensive, a skeletal distractor or temporary external fixation device may be helpful to facilitate reduction; after satisfactory reduction is obtained, definitive fracture fixation using plate and screws with or without augmentation with tension band wiring is usually possible.35,37 If extensive comminution is present such that plate-and-screw fixation does not provide sufficient fracture stability, augmentation with tension band wiring through the triceps insertion may facilitate stable fixation.35 Range-of-motion exercises are ideally initiated within the first 1 to 2 days postoperatively if fracture stability allows.35 More tenuous fixation or fractures in osteoporotic bone, particularly the inherently less stable posterior fracture dislocation patterns, may require support with splinting for up to 4 weeks after surgery.35 The integrity of the lateral collateral ligament and the anteromedial coronoid are important factors in stability of the fracture.35 Ring et al37 noted mostly good to excellent elbow scores following fixation of transolecranon fractures and attributed their low incidence of posttraumatic arthrosis to the nature of the articular surface of the olecranon.37 Restoration of the olecranon and coronoid facets is key because the intervening segment, the transverse ridge of the olecranon, contributes little surface contact area to the articular interface.37

RESULTS Complications of olecranon fracture include nonunion (see Fig. 25-4A), infection, loss of motion, ulnar nerve symptoms, arthrosis, and need for additional procedures, such as hardware removal.17,26,27,31,33,38 Contracture, especially loss of the terminal 10 to 15 degrees of extension, is particularly common, and appears to be related to immobilization.31 Radiographic evidence of degenerative changes in the ulnohumeral joint has been documented in 20% to 50% of patients up to 15 to 25 years following olecranon fracture.17,26 The risk of prominent and bothersome hardware following tension band fixation may be diminished if wires are bent 180 degrees and impacted into bone, with the triceps securely sutured over wires.27,31 Mullett et al34 noted the effect of K-wire position on backing out of the wire in a clinical series.33 They described an increased risk of back-out when wires were placed down the long axis of the ulna as opposed to crossing the anterior cortex with a concomitant increase in symptomatic hardware, requiring hardware removal (42% versus 11.4%).33 In addition, Mullett et al found a higher pullout strength in a cadaveric investigation in those K-wires placed according to optimal AO specification with trans-

cortical contact (122.7 N versus 56.3 N).33 These clinical and biomechanical data reinforce the importance of use of proper transcortical rather than shaft K-wire placement and adherence to AO technique to avoid potential hardware complications.33 Rommens et al38 described outcomes of surgical fixation of 95 consecutive olecranon fractures treated from 1992 to 2000.38 By type and subtype, 14% were type IA, 8% type IB, 20% IIA; 29% IIB; 11% IIIA; 19% IIIB.38 About one third of patients had concomitant upper extremity fractures.38 Ninety-five percent were treated with tension band wiring constructs, whereas the remainder were treated with plate osteosynthesis.38 Approximately 10% experienced implant migration, 3.2% had delayed union, 2.1% had infection, and 14.7% required additional surgical procedures for complications.38 In addition, two thirds underwent hardware removal at an average of 12 months postoperatively.38 Radiographic changes included intra-articular stepoff without frank arthrosis in 7%; mild to moderate arthrosis in 20%, severe arthrosis in 12%, and pseudoarthrosis in 1%.38 Most patients experienced little or no limitations in pronation or supination (>90% had normal or less than a 10 degree deficit) or flexion (81% had no or less than 10 degrees of deficit); but 46% of patients had a more than 10-degree extension deficit.38 In addition, many patients experienced decreased strength in extension (50%) or flexion (37%).38 Patients with Mayo type III fractures or coexisting lesions of the ipsilateral upper extremity were more likely to have larger deficits in the flexion extension arc than patients with type I or II lesions.38 Likewise, suboptimal fixation was noted to be a risk factor for development of arthrosis, although this may be a confounding factor because both were more commonly seen in more complex fracture patterns.38 Karlsson et al25 investigated long-term outcomes of tension band wiring and figure-of-eight wiring techniques for fixation of olecranon fractures. With respect to all fractures, 96% of patients had a good or excellent outcome up to 25 years after injury and fracture fixation.25 No significant difference between fracture fixation type and subjective outcome was noted.25 Fractures fixed with figure-of-eight wiring were more likely to have impaired pronation, but contralateral reduced pronation was also noted in this group, indicating a possible difference between the groups unrelated to the surgical technique.25 No significant differences in other parameters of range of motion were noted between the groups.25 Follow-up radiographs demonstrated degenerative changes in most of the injured elbows, with subchondral cysts in 45%, subchondral sclerosis in 73%, osteophyte formation in 45%, and joint incongruity in 36%.25 Frank osteoarthritis was noted in 7%.25 When the two groups were compared, subchondral cyst formation (50% versus 39%), subchondral sclerosis (93% versus

Chapter 25 Fractures of the Olecranon

54%), and radiographic frank arthrosis (16% versus 5%) were more common in the figure-of-eight wiring group, whereas osteophyte formation 61% versus 50% and joint incongruity (43% versus 29%) were more common in the tension band group.25 Hardware removal was performed in 81% of those elbows treated by tension band wiring and 43% of elbows treated with figure-ofeight fixation.25 Because there were no significant clinical differences between the groups regarding outcome, Karlsson et al recommend use of figure-of-eight wiring for fixation of olecranon fractures because the hardware removal rate was half that of elbows treated with tension band wiring.25 In conclusion, olecranon fractures are commonly seen in orthopedic practice, and with appropriate treatment, patients generally have good to excellent outcomes with little adverse sequelae. Decreased range of motion, radiographic evidence of degenerative changes, and requirement for hardware removal are common but generally are not devastating complications, and may be obviated by attention to proper technique, anatomic reduction, and proper postoperative management.

References 1. Amis, A. A., and Miller, J. H.: The mechanisms of elbow fractures: an investigation using impact tests in vitro. Injury 26:163, 1995. 2. An, K. N., Morrey, B. F., and Chao, E. Y.: The effect of partial removal of the proximal ulna on elbow restraint. Clin. Orthop. Relat. Res. 209:270, 1986. 3. Anderson, M. L., Larson, A. N., Merten, S. M., and Steinmann S. P.: Congruent elbow plate fixation of olecranon fractures. J. Orthop. Trauma 21:386, 2007. 4. Bailey, C. S., MacDermid, J., Patterson, S. D., and King, G. J.: Outcome of plate fixation of olecranon fractures. J. Orthop. Trauma. 15:542, 2001. 5. Bostman, O. M.: Metallic or absorbable fracture fixation devices. A cost minimization analysis. Clin. Orthop. Relat. Res. 329:233, 1996. 6. Boyer, M. I., Galatz, L. M., Borrelli, J. Jr., Axelrod, T. S., and Ricci, W. M.: Intra-articular fractures of the upper extremity: new concepts in surgical treatment. Instr. Course Lect. 52:591, 2003. 7. Bucholz, R. W., and Heckman, J. D. (eds.): Rockwood and Green’s Fractures in Adults, 5th ed. Philadelphia, Lippincott, Williams & Wilkins, 2001. 8. Cabenela, M. E., and Morrey, B. F.: Fractures of the olecranon. In Morrey, B. F. (ed.): The Elbow and its Disorders. Philadelphia, W. B. Saunders Co, 2000, p. 365-379. 9. Colton, C. L.: Fractures of the olecranon in adults: classification and management. Injury 5:121, 1973. 10. Compton, R., and Bucknell, A.: Resection arthroplasty for comminuted olecranon fractures. Orthop. Rev. Relat. Res. 18:189, 1989. 11. Didonna, M. L., Fernandez, J. J., Lim, T. H., Hastings, H. 2nd, and Cohen, M. S.: Partial olecranon excision: the relation-

12.

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ship between triceps insertion site and extension strength of the elbow. J. Hand Surg. Am. 28:117, 2003. Doornberg, J., Ring, D., and Jupiter, J. B.: Effective treatment of fracture-dislocations of the olecranon requires a stable trochlear notch. Clin. Orthop. Relat. Res. 429:292, 2004. Estourgie, R. J., and Tinnemans, J. G.: Treatment of grossly comminuted fractures of the olecranon by excision. Neth. J. Surg. 34:127, 1982. Evans, M. C., and Graham, H. K.: Olecranon fractures in children: Part 1: a clinical review; Part 2: a new classification and management algorithm. J. Pediatr. Orthop. 19:559, 1999. Fern, E. D., and Brown, J. N.: Olecranon advancement osteotomy in the management of severely comminuted olecranon fractures. Injury 24:267, 1993. Fyfe, I. S., Mossad, M. M., and Holdsworth, B. J.: Methods of fixation of olecranon fractures. An experimental mechanical study. J. Bone Joint Surg. Br. 67:367, 1985. Gartsman, G. M., Sculco, T. P., and Otis, J. C.: Operative treatment of olecranon fractures. Excision or open reduction with internal fixation. J. Bone Joint Surg. Am. 63:718, 1981. Heim, U.: Forearm and hand/miniimplants. In Mueller, M. E. (ed.): Manual of Internal Fixation: Techniques Recommended by the AO ASIF Group. New York, Springer Verlag, 1991. Helm, R. H., Hornby, R., and Miller, S. W.: The complications of surgical treatment of displaced fractures of the olecranon. Injury 18:48, 1987. Horne, J. G., and Tanzer, T. L.: Olecranon fractures: a review of 100 cases. J. Trauma. 21:469, 1981. Horner, S. R., Sadasivan, K. K., Lipka, J. M., and Saha, S.: Analysis of mechanical factors affecting fixation of olecranon fractures. Orthopedics 12:1469, 1989. Hume, M. C., and Wiss, D. A.: Olecranon fractures. A clinical and radiographic comparison of tension band wiring and plate fixation. Clin. Orthop. Relat. Res. 285:229, 1992. Juutilainen, T., Pätiälä, H., Rokkanen, P., and Törmälä, P.: Biodegradable wire fixation in olecranon and patella fractures combined with biodegradable screws or plugs and compared with metallic fixation. Arch. Orthop. Trauma Surg. 114:319, 1995. Kamineni, S., Hirahara, H., Pomianowski, S., Neale, P. G., O’Driscoll, S. W., ElAttrache, N., An, K. N., and Morrey, B. F.: Partial posteromedial olecranon resection: a kinematic study. J. Bone Joint Surg. Am. 85-A:1005, 2003. Karlsson, M. K., Hasserius, R., Besjakov, J., Karlsson, C., and Josefsson, P. O.: Comparison of tension-band and figureof-eight wiring techniques for treatment of olecranon fractures. J. Shoulder Elbow Surg. 11:377, 2002. Karlsson, M. K., Hasserius, R., Karlsson, C., Besjakov, J., and Josefsson, P. O.: Fractures of the olecranon: a 15- to 25year followup of 73 patients. Clin. Orthop. Relat. Res. 403:205, 2002. McKay, P. L., and Katarincic, J. A.: Fractures of the proximal ulna olecranon and coronoid fractures. Hand Clin. 18:43, 2002. McKeever, F. M., and Buck, R. M.: Fracture of the olecranon process of the ulna: treatment by excision of fragment and repair of triceps tendon. J. A. M. A. 135:1, 1947.

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29. Moed, B. R., Ede, D. E., and Brown, T. D.: Fractures of the olecranon: an in vitro study of elbow joint stresses after tension-band wire fixation versus proximal fracture fragment excision. J. Trauma 53:1088, 2002.. 30. Molloy, S., Jasper, L. E., Elliott, D. S., Brumback, R. J., and Belkoff, S. M.: Biomechanical evaluation of intramedullary nail versus tension band fixation for transverse olecranon fractures. J. Orthop. Trauma. 18:170, 2004. 31. Morrey, B. F.: Current concepts in the treatment of fractures of the radial head, the olecranon, and the coronoid. Instr. Course Lect. 44:175, 1995. 32. Muller, M. E., Allgower, M., Schneider, R., and Willenegger, H.: Comprehensive classification of fractures of long bones. In Manual of Internal Fixation: Techniques Recommended by the AO-ASIF Group, 3rd ed. New York, SpringerVerlag, 1991, p. 118-150. 33. Mullett, J. H., Shannon, F., Noel, J., Lawlor, G., Lee, T. C., and O’Rourke, S. K.: K-wire position in tension band wiring of the olecranon—a comparison of two techniques. Injury 31:427, 2000. 34. Nowinski, R. J., Nork, S. E., Segina, D. N., and Benirschke, S. K.: Comminuted fracture-dislocations of the elbow treated with an AO wrist fusion plate. Clin. Orthop. Relat. Res. 378:238, 2000.

35. O’Driscoll, S. W., et al.: Difficult elbow fractures: pearls and pitfalls. Instr. Course Lect. 52:113, 2003. 36. Paremain, G. P., et al.: Biomechanical evaluation of tension band placement for the repair of olecranon fractures. Clin. Orthop. Relat. Res. 335:325, 1997. 37. Ring, D., Jupiter, J. B., Sanders, R. W., Mast, J., and Simpson, N. S.: Transolecranon fracture-dislocation of the elbow. J. Orthop. Trauma 11:545, 1997. 38. Rommens, P. M., Schneider, R. U., and Reuter M.: Functional results after operative treatment of olecranon fractures. Acta Chir. Belg. 104:191, 2004. 39. Rowland, S. A., and Burkhart, S. S.: Tension band wiring of olecranon fractures. A modification of the AO technique. Clin. Orthop. Relat. Res. 277:238, 1992. 40. Weber, B. G., and Vasey, H.: [Osteosynthesis in olecranon fractures.]. Z. Unfallmed. Berufskr. 56:90, 1963. 41. Wolfgang, G., Burke, F., Bush, D., Parenti, J., Perry, J., LaFollette, B., and Lillmars, S.: Surgical treatment of displaced olecranon fractures by tension band wiring technique. Clin. Orthop. Relat. Res. 224:192, 1987. 42. Wu, C. C., Tai, C. L., and Shih, C. H.: Biomechanical comparison for different configurations of tension band wiring techniques in treating an olecranon fracture. J. Trauma 48:1063, 2000.

Chapter 26 Nonunion of the Olecranon and Proximal Ulna

CHAPTER

26

Nonunion of the Olecranon and Proximal Ulna Panayiotis J. Papagelopoulos, Ralph W. Coonrad, and Bernard F. Morrey

GENERAL CONSIDERATIONS Nonunion of olecranon and proximal ulna fractures is a relatively uncommon complication with the use of current techniques of osteosynthesis.9,35,59 Although this problem is perhaps less common today than in the past, it continues to challenge the orthopedic surgeon. Olecranon and proximal ulna fracture nonunion can result in profound functional disability. Patients consistently report pain.55 Other features typically include some degree of instability or limitation of elbow joint motion. The main predisposing factors for a nonunion of the proximal ulna are inadequate fixation, premature motion, smoking,7 or a combination of all of these.3,4,20,31,32,37,45,63,73,75

INCIDENCE Nonunion of fractures of the proximal ulna and olecranon has been reported to occur in 5% of all olecranon fractures44 and about 5% of all nonunions.10,11,22 Within a 10-year period (1980 to 1990), 196 olecranon fractures were treated at the Mayo Clinic, and there were only two instances of olecranon nonunion (1%).55 Nonunion is also a recognized complication of the proximal osteotomy of the olecranon to expose a fracture of the distal humerus.70 From 1980 to 1990 at the Mayo Clinic, this complication occurred in only one such patient.55 Other authors have reported a high rate of olecranon nonunion in these patients. Gainor and coworkers30 studied 10 patients who had a transverse osteotomy of the olecranon for surgical exposure of a complex distal humerus fracture. Nine of the osteotomies were reconstructed with a large lag screw and tension band wire, and one with smooth pins and a tension band wire. Within an average follow-up period

401

of 24 months, nonunion of the olecranon osteotomy occurred in three of the patients.30

DIAGNOSIS A definitive clinical diagnosis of nonunion cannot be determined until a pseudoarthrosis is evident radiographically. Six months is usually the minimum accepted time before a definite diagnosis of nonunion may be considered. A slow union is an indolent union that maintains the radiographic appearance of the early stages of a healing fracture; the fracture line is visible, and no decalcification or sclerosis is present at the bone ends.44 Delayed union is described as fracture healing in which evidence of attempted union is present radiographically. Reactive hyperemia, early resorption of bone ends, and some widening of the fracture site are usually associated with delayed union. Nonunion is assumed when all evidence of bone healing has ceased. The bone ends and medullary canals are capped, the endosteal blood supply does not extend across the fracture site, and sclerosis of the bone ends is present in at least 25% of patients.32,34 False motion and a varying radiographic defect between the bone ends also are usually present. If a visible fracture line is not present on the plain radiographs, a tomogram is helpful.

CLINICAL PRESENTATION The term “nonunion,” although describing the pathologic condition, misrepresents the clinical problem. The integrity of the ulna plays an important role not only in the function of the joint but also in the articular surfaces and elbow stability. Clinically, tenderness is consistently reported. Some degree of instability and limitation of motion are the other clinical features of the olecranon nonunion.55 Yet it is important to note that a small percentage of patients may function well with the nonunited fracture.38

CAUSES Ossification in the olecranon begins at two or more centers, and the growing epiphysis may be misinterpreted or confused radiographically with a fracture line or nonunion.62,66 Olecranon nonunion rarely occurs in children, but it may result when displaced fractures are unrecognized or when inadequate internal fixation results in loss of reduction.43,53 Bilateral congenital pseudoarthrosis of the olecranon has been reported with radiographic features distinct

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supply,14 (7) defects between the fragments or interposition of soft tissue, (8) abnormalities of the electrochemical or cellular physiologic mechanisms involved in fracture healing resulting from smoking (Box 26-1),1,3,8,14,17,44,66 and (9) adverse events associated with total elbow replacement.42 Technically, the most important factor in the treatment of either fresh fractures or nonunion of the olecranon is the need to convert the tensile forces arising from the forearm flexors and the triceps acting across the fracture or the nonunion site to a compressive force (Fig. 26-1).18,64 In tissue culture experiments, Bassett5,6 has shown that tension forces may prevent osseous precursors from forming cartilage or bone to promote the growth of fibrous tissue. Tension forces tend to produce an osteoclast-induced positive electrical potential that

from the kind of congenital pseudoarthrosis of the forearm previously reported.16 A vascularized fibular graft has been reported as successful in this circumstance.2 Nonunion of the olecranon has been reported in an infant following a birth injury and in adolescent stress fractures.39,40,67,75,76 Fracture separation of a nonunited ossification center in three adults has been reported.38 Primary bone grafting is recommended in these cases because of the high incidence of fibrous nonunion following simple open reduction and internal fixation.38 Walker71 reported a case of painful unilateral physeal nonunion in an adult weight lifter. After failure of conservative treatment, surgical union was achieved, using tension band wiring augmented with autologous iliac crest bone graft. Unilateral olecranon physeal nonunion may have a mechanical etiology as opposed to a genetic etiology in individuals with bilateral physeal persistence.54 These types of fractures heal reliably with fixation.52 Generally children have a higher rate of periosteal response and union. Fracture healing in the older age group of patients is good despite the fact that their fractures tend to heal at a slower rate than those in the younger patient.11 Fracture healing may be slowed in the diabetic patient, in the patient undergoing irradiation treatment,21,33,60 in the adult with a stress fracture,51,52,54 or as a result of smoking.17 There are several predisposing factors to nonunion of olecranon fractures: (1) inadequate fixation or immobilization,23,74 (2) distraction, (3) compounding of fracture, (4) infection, (5) comminution,64,69 (6) loss of blood

Causes or Predisposing Factors Contributing to Nonunion of the Olecranon

BOX 26-1

Inadequate, nonrigid internal fixation Inadequate immobilization Distraction Compounding of fracture Wound infection Comminution Impairment of blood supply Defects between bone fragments Following total elbow replacement42 Smoking

Compresssion force

Compresssion force Compresssion force Tension force

A FIGURE 26-1

B

A, Diagram of the location of compression forces present near the articular surface of the olecranon and tension forces near the posterior surface produced by either an impacting fracture force of the lower end of the humerus or the force of the elbow flexors and extensor force in nonunions. B, The use of tension band wiring (or similar fixation) converts the tension force to a compression or impacting force. Kirschner wires should be placed closer to the posterior surface, when possible.

Chapter 26 Nonunion of the Olecranon and Proximal Ulna

may interfere with bone healing. Compression forces, on the other hand, tend to effect an osteoblast-induced negative electrical potential that produces an enhancing effect on fracture healing.7,8,44

403

Type I Undisplaced

CLASSIFICATION Generally, nonunions have been pathologically classified into two types, according to the biologic activity at the ends of the fracture fragments.36,50 The hypervascular type of nonunion has rich blood supply at the ends of the fragments and may be confirmed by increased technetium Tc-99m uptake. The avascular type has nonviable ends of the fracture fragments and also may be confirmed by a decreased technetium Tc-99m uptake.36,49,72 Nonunion of the proximal ulna distal to the insertion of the medial collateral ligament carries a better prognosis for reconstruction because the articular surface of the trochlear notch is intact.4,47,60 Any reconstruction for nonunion in an unstable injury at this level (Fig. 26-2) may need medial collateral ligament repair or reconstitution in addition to rigid internal fixation.47

TREATMENT OPTIONS FOR OLECRANON NONUNION

Type II Displacedstable

A-Noncomminuted

B-Comminuted

A-Noncomminuted

B-Comminuted

Type III Unstable

FIGURE 26-2

Mayo classification for olecranon fractures. The type IIB and IIIA and IIIB are at risk for developing nonunions.

INDICATIONS Asymptomatic nonunion with adequate elbow joint function requires no active treatment (Fig. 26-3). For symptomatic olecranon nonunion, the goals of treatment are the same as those of primary treatment for any displaced fracture: (1) to restore congruity of the sigmoid notch, (2) to restore or retain ligamentous stability, (3) to restore triceps extensor function, and (4) to restore mobility of the joint. The indications for treatment require separation of olecranon nonunions into four groups: (1) infected nonunion, (2) those in which the articular surface of the sigmoid notch has not been severely damaged and should be salvaged, (3) those in which articular cartilage has been severely damaged by arthritis or traumatic loss of the joint surface, and (4) those with marked resorption or bone loss. Nonunion of Monteggia fracture-dislocations requires special considerations.

Treatment of Infected Nonunion of the Olecranon The principles of treatment for infection of long bones or joints are well established and include (1) the need for adequate débridement, (2) rigid immobilization of the elbow with mobilization of all other joints in

the upper extremity, and (3) appropriate antibiotic therapy. Muscle, myocutaneous, and vascularized fibular bone grafts have been used successfully in the treatment of nonunions.25 Successful use of a flexor carpi ulnaris local muscle flap has been reported by Meals46 and avoids the complications associated with microvascular repairs. The use of an external fixator or distraction arthroplasty is usually the most effective means of immobilization until soft tissue coverage and control of the infection can be achieved.

Treatment of Nonunion in Which Articular Cartilage Has Not Been Severely Damaged Electrical Stimulation If there is minimal displacement and if the overall alignment is acceptable, consideration might be given to electrical stimulation.7,8,13,56,61 A healing effect of electrical stimulation has been noted with coexisting low-grade infections. This noninvasive method can be used on an outpatient basis. However, the expense and the need to immobilize the joint have caused electrical stimulation to lose favor in recent years. The authors believe electrical stimulation is not a viable treatment option for olecranon or proximal ulna nonunions because of prolonged immobilization of the elbow joint,

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TECHNICAL OPTIONS AND CONSIDERATIONS Small avulsion fragments are uncommon. Best results are obtained by simple excision and meticulous repair or advancement of the triceps tendon to the olecranon. Care must be taken to repair the medial and lateral retinacular portions of the triceps tendon using nonabsorbable suture material. Stay sutures should be placed directly through drill holes extending through the posterior cortex of the distal olecranon fragment (Fig. 26-5). The tendon margin is placed adjacent to the articular surface rather than to the posterior cortex. This improves the stability at the expense of a slightly decreased lever arm. Early active motion is permitted and encouraged 5 days after surgery through a range of 0 to 90 degrees, but flexion beyond 90 degrees should not be permitted for 4 to 6 weeks, depending on the extent of tendon advancement. In an older patient with comminution and when the joint is stable with an intact medial collateral ligament, excellent results have been obtained by excising the olecranon fragments, reattaching the triceps tendon with nonabsorbable sutures through drill holes in the posterior cortex, and placing the tendon attachment adjacent to the articular surface. Concurrent repair of the lateral expansion of the triceps to the olecranon periosteum is important and will permit early active motion in 4 to 5 days.

Excision

FIGURE 26-3

A 38-year-old man, 14-year status after injury. Arc of motion is 65 to 125 degrees; pronation is 25 degrees; supination is 55 degrees. The patient had no pain, and no further treatment was recommended. Note the nonunion of olecranon and the amount of displacement with flexion and extension. (Courtesy of Mayo Clinic.)

Clearly, in a younger patient or in the older individual with a nonunion involving more than 50% of the sigmoid notch, osteosynthesis is the preferred treatment.64 There are three requirements for a successful outcome: ulnohumeral reduction, rigid fixation, and augmentation of healing, that is, bone graft and possibly BMP-7. Rigid fixation can be provided by different techniques, depending on the fracture type. Intramedullary screws, low-profile dynamic compression plates (DCP), or locking olecranon plates each have their place. We have relied on a corticocancellous bone plate fixed with cortical screws to augment the healing response.55 Other than this, the technique for osteosynthesis depends on the characteristics of the fracture. The more frequently used techniques are discussed in the following sections.

Osteosynthesis

which is often already compromised by injury and which can lead to elbow stiffness. The introduction of bone morphogenic protein (BMP-7) has been demonstrated to facilitate healing at several anatomic sites, including the olecranon region.26 Most heal within 4 to 5 months. This basic strategy is effective because the technology is becoming more refined, resulting in efficient delivery systems of effective product. Biologic Enhancement

Encouraging early descriptions of the results of proximal fragment excision are available.22,27,29 In 1947, McKeever and Buck reported that 80% of the sigmoid notch could be excised without producing instability of the elbow joint (Fig. 26-4).45 Gartsman and colleagues31 found that restoration of elbow extensor function was equal after excision or fixation, as measured by static and dynamic strength testing. Excision of the proximal fragment with meticulous reattachment of the triceps tendon is an excellent option for treatment of an older patient with nonunion of a small avulsion fragment or a fragment involving less than 50% of the olecranon surface.31,37,45,47,73 Excision of nonunited fracture fragments is, of course, contraindicated in the growing child with an open proximal epiphysis. Excision

Tension Band Wiring Fixation by a tension band wiring technique coupled with bone grafting is an effective technique for treating undisplaced nonunions (Fig. 26-6).55,74 If tension band wiring is to be used for nonunion in which central portions of the sigmoid notch are missing, pin fixation should be avoided, but if it is used, it should always be placed toward the posterior rather than the articular side of the proximal ulna. This will allow more compression toward the posterior surface, and it tends to prevent narrowing of the notch.

Chapter 26 Nonunion of the Olecranon and Proximal Ulna

FIGURE 26-4

405

A, Preoperative radiograph of a nonunion in a 60-year-old woman. The original fracture was treated by a lag screw of inadequate length. B, The elbow after excision of the olecranon fragment (involving 50% of the articular surface). Satisfactory function resulted.

Triceps muscle

Proximal olecranon fragment

No

Fascial flap Double suture line

Ulnar nerve

D

Fascial flap

A FIGURE 26-5

Olecranon

Distal bone fragment

B

C

Yes

E

Type of U-shaped incision made over the proximal avulsion fragment from the olecranon (A). The proximal fragment is elevated with the flap and excised (B). The flap is turned down against the bone defect (C), and heavy sutures of nonabsorbable suture material are used to maintain the tendon reattachment not at the posterior cortex (D) but at the articular level (E).

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FIGURE 26-6

A, Elbow radiograph of a 19-year-old man with olecranon nonunion at 9 months after open reduction and internal fixation with two threaded and one unthreaded Kirschner wires without tension band wiring. Motion was initiated after Kirschner wire removal at 6 weeks. B, Healing of the nonunion 11 months later after noninvasive electrical stimulation. (Courtesy of Dr. Frank Logue.)

When compression is placed close to the articular surface, narrowing of the sigmoid notch may result in subsequent arthritic changes. Comminuted or unstable fragments with anterior subluxation or instability warrant consideration of other treatment options discussed below. Plating Plating with a six-hole plate is useful in instances of oblique or transverse olecranon fracture nonunions. Rigid fixation can be achieved by the use of a tubular DCP or a 3.5-mm AO plate. The recent anatomic plates specifically designed and contoured to fit the olecranon repair are particularly useful. These include the LCP AO plate and the Mayo clinic congruent olecranon plate (Acumed, Hillsboro, OR). In any instance, motion should be started immediately. For nonunion of

the Monteggia fracture, the ulna should be rigidly fixed with plating and bone grafting. In chronic states, no attempt is made to reduce the dislocation and the radial head is resected (Fig. 26-7). Plating may be the only available method of salvaging nonunion of comminuted fractures and achieving rigid stability in unstable fractures that involve the coronoid process with rupture of the medial collateral ligament.69 Anatomic visualization and reconstitution of the joint surface is mandatory. Sufficient bone must be removed to regain not only normal alignment of the olecranon itself but also an adequate contour of the joint surface of the ulna articulating with the trochlea. Repair or reconstruction of the lateral collateral ligament should always be carried out and the medial collateral ligament should be addressed if instability persists at the

Chapter 26 Nonunion of the Olecranon and Proximal Ulna

FIGURE 26-7

407

A, Nonunion of a comminuted fracture-dislocation of the left proximal ulna (Mayo IIIB). B, Open reduction and internal fixation using a sixhole plate medially and corticocancellous bone plate laterally. The radial head was excised. C, Satisfactory result 1 year postoperatively.

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operating table.68 A curve at the end of a tubular plate by design or introduced at the time of surgery can enhance fixation of a proximal fragment.24,58

begins at 4 to 5 days. The extensor mechanism may be protected while allowing motion at the ulnohumeral joint through the use of dynamic extension splints.

Technical Considerations. When comminuted fragments of the olecranon are large enough to permit restoration of the articular surface of the sigmoid notch, and even when dislocation of the proximal ulna and the radial head has occurred with disruption of the medial collateral ligament, best results are obtained with a rigid plate fixation, often with rigid cancellous and bicortical screw fixation. Immobilization should be at 90 degrees, and early active motion should be initiated.

Bone Grafting A corticocancellous bone graft fixed with screws is a particularly useful technique.55 Supplementary intramedullary screw fixation is also particularly useful (Figs. 26-9 and 26-10). We and others58 have used this bone grafting in combination with screw-andplate rigid fixation (Fig. 26-11).

Lag screw fixation with a longitudinal intramedullary screw (AO cancellous lag screw) may be used, but bicortical screw fixation provides better fixation if the nonunion is amenable to this.70 Biomechanical studies by Murphy and associates51 have demonstrated that a lag screw combined with tension band wiring has the greater strength of fixation when compared with tension band wiring with Kirschner wires, lag screws alone, or figure-of-eight wiring alone. In the recent Mayo Clinic series, eight patients had a successful intramedullary screw fixation for olecranon nonunion.55 This type of fixation is viable only for single fragment transverse or oblique nonunions of the olecranon or proximal ulna in which axial compression will effectively stabilize the fracture and not narrow the olecranon-to-coronoid distance. Sufficient length to engage the metaphysis of the ulna adequately and overdrilling of the proximal fragment to achieve compression are required (Fig. 26-8). Nonunion of an oblique or transverse fracture is well suited to bicortical screw fixation, which was described first in 1969 by Taylor and Scham and later reported by Wadsworth in 1976; this is still a reasonable strategy and involves the use of a washer beneath the screw head.65,70

Lag Screw Fixation

Technical Considerations. Nonunion of transverse and oblique fractures are best treated using a large threaded AO-lag screw. Care is taken to ensure that the screw does not cause displacement of the fragment. Avoid overdrilling the proximal fragment and use a sufficiently long screw extending into the diaphyseal canal of the ulna. The length of the screw should be at least two or three times the length of the nonunited fragment. A washer has been used occasionally to improve the compressive force. Particular care should be taken to avoid having the thread cross the nonunion site, which can result in failure of the procedure due to distraction. Satisfactory results may be obtained with combined use of tension band wiring or bicortical screw fixation for more oblique fractures. Postoperative active motion

Technical Considerations: Corticocancellous Bone Plate. A midline incision over the posterior aspect of the elbow is used or the prior incision is re-entered if possible.55 Dissection exposes the proximal ulna. The medial and lateral aspects of the olecranon are identified, and the nonunion site is exposed. The ulnar nerve is identified, dissected, and protected as needed. The surfaces of the proximal ulna both medially and laterally are flattened by removing prominent callus, and the nonunion is entered. The pseudoarthrosis is removed to allow adequate bone grafting. A corticocancellous bone plate, measuring about 60 by 10 mm, is then harvested from the anterior iliac crest (Fig. 26-12). This is carefully placed over the radial aspect of the olecranon and ulna, and is secured with one or two 2.7-mm mini cortical screws on either side of the nonunion. If a large proximal fragment is present, either a spongiosa (cancellous) intramedullary screw (see Fig. 26-12) or a contoured DCP plate placed over the medial ulna cortex is used (Fig. 26-13). Great care is taken to avoid narrowing the coronoid and olecranon distance. Cancellous bone graft is packed around the nonunion site. Note: In all the above-mentioned circumstances, the degree of capsular contracture is assessed and the capsule is released if necessary to ensure functional motion.

Treatment of Nonunions of the Olecranon when Articular Cartilage Has Been Severely Damaged This problem calls for an entirely different approach from any described previously. If the olecranon nonunion is an isolated problem and if the humeroulnar articular surface is destroyed beyond restoration from recent or old trauma, the factors of pain, malalignment, infection, age, and instability become important.57 A salvage situation often precludes lesser procedures and arthrodesis, total joint replacement, and allograft replacement may be considered. If the nonunion is associated with articular distortion or loss of motion, excision of a proximal unstable fragment, if it constitutes less than 50% to 60% of the joint, may be the most reliable option. The postoperative period of rehabilitation is shortened as well.

Excision

Chapter 26 Nonunion of the Olecranon and Proximal Ulna

409

FIGURE 26-8

A and B, Elbow radiograph of a proximal ulnar nonunion with painful ankylosis in a 49-year-old man. C and D, Healed nonunion with 55 degrees of motion (45 to 100 degrees) treated with compression lag screw fixation and overdrilling of the proximal fragment.

Distraction Arthroplasty In cases of nonunion of the olecranon with severe articular destruction, union must be initially achieved before the question of mobilization can be addressed. If imaging shows evidence of articular incongruity and if attempts at mobilization with dynamic splinting and active exercise are unsuccessful, distraction arthroplasty may be a reasonable and possibly the final treatment option (Fig. 26-14). The concept of distraction arthroplasty has been used since the mid-1980s for treating the stiff elbow and has been adapted for the treatment of the olecranon non-

union. Thus, in those patients in whom there is contracture of soft tissue around the olecranon nonunion, the distraction device is an ideal adjunct because this may be combined with soft tissue release.48 The specific technique is well described in Chapter 33. In the initial Mayo series,55 four patients were managed by distraction arthroplasty combined with internal fixation and bone grafting of the olecranon nonunion. In all four patients, union was achieved and the arc of motion improved from a mean of 48 degrees to a mean of 95 degrees.

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FIGURE 26-9

Anteroposterior (A) and lateral radiographs of a 60-year-old woman who was right-hand dominant and presented with a painful nonunion 6 months after a fracture of the left olecranon treated initially with Kirschner wires in a tension band technique. Pins have been removed. Twentythree months after open reduction and internal fixation of the nonunion with an intramedullary cancellous screw and a corticocancellous bone plate fixed with screws medially (B). The patient had a good result with a stable painless elbow and a range of motion from 45 to 145 degrees of flexion and full pronation and supination. (B, With permission from Papagelopoulos, P. J., and Morrey, B. F.: Treatment of nonunion of olecranon fractures. J. Bone Joint Surg. Br. 76:627, 1994.)

Chapter 26 Nonunion of the Olecranon and Proximal Ulna

FIGURE 26-10 A, Anteroposterior and lateral radiographs of a painful olecranon nonunion in a 58year-old woman who was right-hand dominant. She presented 10 months after removal of tension band fixation. B, Three years after successful open reduction and internal fixation of olecranon nonunion with corticocancellous bone plate fixation combined with intramedullary screw fixation. The patient had a good result with a stable elbow, mild pain, flexion from 30 to 140 degrees, and full pronation and supination. (With permission from Papagelopoulos, P. J., and Morrey, B. F.: Treatment of nonunion of olecranon fractures. J. Bone Joint Surg. Br. 76:627, 1994.)

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FIGURE 26-11 A, Anteroposterior and lateral radiographs of a painful proximal ulna nonunion. The patient was treated initially elsewhere with plate-and-screw fixation for a fracture-dislocation of the left elbow. B, Open reduction and internal fixation of olecranon nonunion with corticocancellous bone plate fixation combined with intramedullary screw-and-plate fixation.

Chapter 26 Nonunion of the Olecranon and Proximal Ulna

413

Corticocancellous bone plate

FIGURE 26-12 Corticocancellous bone plate fixation of olecranon nonunion combined with intramedullary screw fixation. Bone plate of about 60 by 10 mm is harvested from the iliac crest. (By permission from Papagelopoulos, P. J., and Morrey, B. F.: Treatment of nonunion of olecranon fractures. J. Bone Joint Surg. Br. 76:627, 1994.)

FIGURE 26-13 Corticocancellous bone plate fixation of olecranon nonunion combined with DCP plate and screw fixation. The plate is contoured and placed laterally. Mini 2.5-mm screws are used medially for bone plate fixation. (With permission from Papagelopoulos, P. J., and Morrey, B. F.: Treatment of nonunion of olecranon fractures. J. Bone Joint Surg. Br. 76:627, 1994.)

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When stressful use of the elbow mandates a stable joint, such as in a manual laborer, arthrodesis is rarely a consideration for proximal ulna nonunions associated with significant articular distortion (see Chapter 70).

Arthrodesis

In a salvage situation, when pain and instability are paramount and only sedentary activity is acceptable, total joint replacement has been successful, using a linked prosthetic replacement. Joint replacement is effective in elderly patients with severe arthrosis, ankylosis, or osteoporosis (Fig. 26-15). In our experience, these patients are treated successfully with joint replacement and the postoperative rehabilitation period averaged 3 months. But this is considered the ultimate salvage procedure. When total replacement is performed in the face or because of the olecranon nonunion, Marra et al42 have shown osteosynthesis occurs only in about 50% of patients. However, of importance, the function of a stable, undisplaced fibrous nonunion is comparable to a solidly united fracture.

Joint Replacement

Allograft Replacement Frozen cadaver bone allograft replacement has also been used successfully on occasion.12 Late Charcot-like degenerative arthritic changes can be anticipated. Infection and non-union are major risks.

Treatment of Nonunion with Monteggia Fracture-Dislocation Nonunion with anterior fracture dislocation is the most severe and most difficult injury of the proximal ulna because the coronoid is involved.10,19,57 Cases are divided

into two treatment groups: injuries with a restorable articular surface, and those in which articular surface damage precludes restoration. In the first group, accurate realignment and restoration of the articular surface is mandatory. After taking down and repositioning or shortening the fragments, rigid internal fixation must be achieved. The subluxed distal ulnar segment is reduced, and the anterior capsule is dissected from the coronoid process and tubercle to protect the vital anterior neurovascular structures. Exposure is generally achieved by the posterior approach described by Bryan and Morrey.15 The medial collateral ligament is identified and repaired or reconstructed. Shortening of the ulna distal to the coronoid may be necessary to prevent pressure of the ulnar articular surface against the trochlea of the humerus. Internal fixation is best achieved with either a long lag screw or a six- to eight-hole tubular AO plate and screws. Early motion is initiated at 3 weeks. When the articular surface of the sigmoid notch is destroyed and dislocation has existed so long that the articular surface of the lower humerus has been destroyed, the age and overall functional level of the patient is determined. If stressful use of the extremity is demanded, arthrodesis is still a consideration, and the technique is determined by the amount of bone stock present. When chronic nonunion is associated with anterior dislocation and joint destruction, when pain or instability warrant reconstruction, and when sedentary use of the extremity is acceptable, total joint replacement with a semiconstrained prosthesis, with an adequate stem for the ulna, has been a satisfactory approach.

FIGURE 26-14 Painful, stiff nonunion of proximal ulna in a 35-year-old man treated with plate and a bone graft screwed to the nonunion (the two smaller screws). The patient developed a union with residual stiffness that was treated secondarily with distraction arthroplasty.

Chapter 26 Nonunion of the Olecranon and Proximal Ulna

FIGURE 26-15 A, Anteroposterior and lateral radiographs of a 75-year-old woman who was righthand dominant at 1 year after right elbow olecranon fracture and failed osteosynthesis. B, Twentyeight months postoperatively, the patient had an excellent result with no pain. (With permission from Papagelopoulos, P. J., and Morrey, B. F.: Treatment of nonunion of olecranon fractures. J. Bone Joint Surg. Br. 76:627, 1994.)

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COMPLICATIONS OF TREATMENT OF NONUNIONS The complications of treatment for nonunion of olecranon fractures include recurrent nonunion, heterotopic ossification, neurapraxia, diminished range of motion, traumatic arthritic changes, pain, reflex sympathetic dystrophy, and infection.41,55 When rigid internal fixation is achieved and early motion can be initiated at 5 to 7 days in the functional range of 30 to 130 degrees, less permanent contracture may be anticipated. Unless ossification occurs in the brachialis muscle or the anterior capsule, ectopic calcification is usually of little consequence. In the Mayo series, there was only one patient with postoperative ulnar nerve paresthesias after operative treatment of olecranon nonunion.55 Eriksson and associates28 reported a higher rate of nerve complications (10%) with fresh olecranon fractures. Isolation and protection of the nerve are warranted for virtually all reconstructive surgeries for nonunion at the elbow. The use of a nerve stimulator and high-power loops is helpful for dissection of scar tissue about the ulnar nerve.

RESULTS Papagelopoulos and Morrey55 reported the Mayo Clinic experience in 24 consecutive patients treated from 1976 to 1991 for nonunion of olecranon fractures. The mean age of these patients was 42 years, and the mean interval from fracture to treatment for nonunion was 19 months. Management was through rehabilitation and activity as tolerated for three patients, continued immobilization for one, and operative treatment for 20. Operations included excision of the olecranon fragment (1), osteosynthesis (16), and joint replacement (3). Four patients also had distraction arthroplasty. At a mean follow-up time of 18 months, no patient had severe residual elbow pain but three had moderate and six had mild symptoms. The mean arc of motion was 98 degrees, representing an average improvement of 11 degrees. Twelve patients had an excellent result, four good, six fair, and two poor. Union had been achieved in 15 of the 16 patients treated through osteosynthesis. Ring et al58 also noted that not all of those that attain union are considered satisfactory due to associated injuries. Danziger and Healy23 reviewed five patients treated surgically for nonunion of the olecranon. Four of the five fractures leading to nonunion were comminuted or oblique. Three nonunions occurred after tension band wiring, one nonunion occurred after open reduction internal fixation with a semitubular plate, and one nonunion occurred after treatment with a cast. The median interval from fracture to treatment of nonunion was 8 months. All nonunions were treated surgically. Four

patients were treated with a tension band plate technique. All nonunions united at a median of 3 months. The median follow-up period was 36 months (range, 12 to 48 months).

CONCLUSIONS Olecranon nonunion is not a common complication, and even today since the last edition of this book, little has been written regarding its management. Treatment depends on patient age, characteristics of the fracture, bone quality, and joint and soft tissue status. Smokers should be encouraged to quit. No surgical treatment is an acceptable option for painless “fibrous nonunion” with 90 degrees or more of flexion. Immobilization can be used in cases of stress nonunion of the olecranon epiphysis of adolescents. Osteosynthesis is the treatment of choice in young patients or in those without severe comminution or instability or deformity. Bone grafting with a corticocancellous bone plate and a DCP plate or cancellous screw fixation is the treatment of choice of the authors. Soft tissue release with adjunctive use of the distraction fixator is helpful when marked loss of motion has occurred. Overall, an acceptable result is to be anticipated in about 70% to 80% of patients. Total elbow arthroplasty is a viable salvage option for treatment in elderly patients with coexisting severe arthritis or osteoporosis.

References 1. Adler, S., Fay, G. F., and McAusland, W. R. Jr.: Treatment of olecranon fractures. J. Trauma 2:597, 1962. 2. Bae, D. S., Waters, P. M., and Sampson, C. E.: Use of free vascularized fibular graft for congenital ulnar pseudarthrosis: surgical decision making in the growing child. J. Pediatr. Orthop. 25:755, 2005. 3. Bakalim, G., and Wilppula, E.: Fractures of the olecranon I, II, III. Ann. Chir. Gynaecol. Fenn. 60:95, 1971. 4. Barford, B.: Quoted in personal communication with drawing by Colton, C. L.: Fracture of the olecranon in adults: classification and management. Injury 5:121, 1973. 5. Bassett, C. A.: Contributions of endosteum, cortex and soft tissue to osteogenesis. Surg. Gynecol. Obstet. 112:145, 1961. 6. Bassett, C.: Pulsing electromagnetic fields: a new method to modify cell behavior in calcified and noncalcified tissues. Calcif. Tissue Int. 34:1, 1982. 7. Bassett, C., Andrew L., Valdes, M. G., and Hernandez, E.: Modification of fracture repair with selected pulsing electromagnetic fields. J. Bone Joint Surg. 64A:888, 1982. 8. Becker, R.: Bioelectric factors controlling bone structure. In Frost, H. M. (ed.): Bone Biodynamics. Boston, Little, Brown & Co., 1964.

Chapter 26 Nonunion of the Olecranon and Proximal Ulna

9. Berger, P.: Le Traitement des Fractures de et Particulièrement la Suture de par un Procédé (Cedarg de ). Ga. 2 Hebd. de Med. 193, 1902. 10. Boyd, H. B., and Boles, J. C.: The Monteggia lesion. A review of 159 cases. Clin. Orthop. Relat. Res. 66:94, 1969. 11. Boyd, H. B., Lipinski, S. W., and Wiley, J. H.: Observations on nonunions of the shafts of the long bones, with a statistical analysis of 842 patients. J. Bone Joint Surg. 43A:159, 1961. 12. Breen, T., Gelberman, R. H., Leffert, R., and Botte, M.: Massive allograft replacement of hemiarticular traumatic defects of the elbow. J. Hand Surg. 13A:6, 1988. 13. Brighton, C. T., Black, J., Friedenberg, Z. B., Esterhai, J. L., Day, L. J., and Connolly, J. F.: A multicenter study of the treatment of nonunion with constant direct current. J. Bone Joint Surg. 63:1, 1981. 14. Brooks, M.: The Blood Supply of Bone. New York, AppletonCentury-Crofts, 1971. 15. Bryan, R. S., and Morrey, B. F.: Extensive posterior exposure of the elbow. Clin. Orthop. 166:188, 1982. 16. Burge, P., and Benson, M.: Bilateral congenital pseudarthrosis of the olecranon. J. Bone Joint Surg. 69:460, 1987. 17. Chen, F., Osterman, A. L., and Mahony, K.: Smoking and bony union after ulna-shortening osteotomy. Am. J. Orthop. 30:486, 2001. 18. Colton, C. L.: Fractures of the olecranon in adults: classification and management. Injury 5:121, 1973. 19. Conn, J., and Wade, P. A.: Injuries of the elbow (a ten-year review). J. Trauma 1:248, 1961. 20. Coughlin, M. J., Slabaugh, P. B., and Smith, T. K.: Experience with the McAtee olecranon device in olecranon fractures. J. Bone Joint Surg. 61A:385, 1979. 21. Cozen, L.: Does diabetes delay fracture healing? Clin. Orthop. Relat. Res. 82:134, 1972. 22. Crenshaw, A. H., and Perez, E. A.: Fractures of the shoulder, arm and forearm. In Canale, S. T., and Beaty, J. H. (eds.): Campbell’s Operative Orthopedics, 11th ed. Philadelphia, Mosby Elsevier, 2008, p. 3371-3459. 23. Danziger, M. B., and Healy, W. L.: Operative treatment of olecranon nonunion. J. Orthop. Trauma 6:290-293, 1992. 24. Davila, S., Mikuli, D., Haiman, M., Zagar, Z., Popovi, L., and Antabak, A.: Treatment of pseudarthroses of the olecranon with the anatomical hook plate. Lijecn. Vjesn. 122:226, 2000. 25. Dell, P. C., and Sheppard, J. E.: Vascularized bone grafts in the treatment of infected forearm nonunions. J. Hand Surg. 9:653, 1984. 26. Dimitriou, R., Dahabreh, Z., Katsoulis, E., Matthews, S. J., Branfoot, T., and Giannoudis, P. V.: Application of recombinant BMP-7 on persistent upper and lower limb nonunions. Injury 36(suppl 4):S51, 2005. 27. Dunn, N.: Operation for fracture of the olecranon. Br. Med. J. 1:214, 1939. 28. Eriksson, E., Sahlen, O., and Sandohl, U.: Late results of conservative and surgical treatment of fracture of the olecranon. Acta Chir. Scand. 113:153, 1957. 29. Foille, D. J.: Note sur les Fractures de l’Olecrane Par Projectiles de Guerre. Marseille Med 55:241, 1918.

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30. Gainor, B. J., Moussa, F., and Schott, T.: Healing rate of transverse osteotomies of the olecranon used in reconstruction of distal humerus fractures. J. South. Orthop. Assoc. 4:263, 1995 31. Gartsman, G. M., Sculco, T. P., and Otis, J. C.: Operative treatment of olecranon fractures. J. Bone Joint Surg. 63A:718, 1981. 32. Green, D. P., and Rockwood, C. A.: Fractures. Philadelphia, J. B. Lippincott Co., 1975. 33. Green, N.: Radiation induced delayed union of fractures. Radiology 93:635, 1969. 34. Heppenstall, R. B.: Fracture Treatment and Healing. Philadelphia, W. B. Saunders Co., 1980, p. 83. 35. Howard, J. L., and Urist, M. R.: Fracture dislocation of radius and ulna at the elbow joint. Clin. Orthop. 12:276, 1958. 36. Judet, J., and Jude, R.: L’Ostéogenèse et les Retards de Consolidation et les Pseudarthroses des Os Longs. Huitième Congres SICOT 1966, p. 315. 37. Kiviluoto, O., and Santauirta, S.: Fractures of the olecranon. Analysis of 37 consecutive cases. Acta Orthop. Scand. 49:28, 1978. 38. Kovach, J., Baker, B. E., and Mosher, J. F.: Fracture separation of the olecranon ossification center in adults. Am. J. Sports Med. 13:2, 1985. 39. Lee, K. S., Lee, S. H., Ha, K. H., and Lee, S. J.: Congenital pseudarthrosis of the ulna treated by free vascularized fibular graft—a case report. Hand Surg. 5:61, 2000. 40. Lehman, M. A.: Nonunion of an olecranon fracture following birth injury. Bull. Hosp. Joint Dis. 26:187, 1965. 41. Levy, R. N., and Sherry, H. S.: Complications of treatment of fractures and dislocations of the elbow. In Epps, C. H. (ed.): Complications in Orthopedic Surgery. Philadelphia, J. B. Lippincott Co., 1975, p. 237. 42. Marra, G., Morrey, B. F., Gallay, S. H., McKee, M. D., and O’Driscoll, S. W.: Fracture and nonunion of the olecranon in total elbow arthroplasty. J. Shoulder Elbow Surg. 15:486, 2006. 43. Mathews, J. G.: Fractures of the olecranon in children. Injury 12:207, 1980. 44. Mayer, P. J., and Evarts, C. M.: Nonunion, delayed union, malunion, and avascular necrosis. In Epps, C. H. (ed.): Complications in Orthopedic Surgery. Philadelphia, J. B. Lippincott, 1975, p. 159. 45. McKeever, F. M., and Buck, R. M.: Fracture of olecranon process of the ulna. J. A. M. A. 135:1, 1947. 46. Meals, R. A.: The use of a flexor carpi ulnaris muscle flap in the treatment of an infected nonunion of the proximal ulna. Clin. Orthop. Relat. Res. 240:168, 1989. 47. Morrey, B. F., and An, K. N.: Functional anatomy of the ligaments of the elbow. Clin. Orthop. Relat. Res. 201:84, 1985. 48. Morrey, B. F.: Distraction arthroplasty. Clinical applications. Clin. Orthop. Relat. Res. 293:46, 1993. 49. Muller, M. E., Allgower, M., and Willenegger, H.: Manual of Internal Fixation. Berlin, Springer-Verlag, 1970. 50. Muller, M. E.: Treatment of nonunion by compression. Clin. Orthop. Relat. Res. 43:83, 1965. 51. Murphy, D. F., Greene, W. B., Gilbert, J. A., and Dameron, T. B.: Displaced olecranon fracture in adults. Clin. Orthop. Relat. Res. 2:224, 1987.

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52. Nakaji, N., Fujioka, H., Tanaka, J., Sugimoto, K., Yoshiya, S., Fujita, K., and Kurosaka, M.: Stress fracture of the olecranon in an adult baseball player. Knee Surg. Sports Traumatol Arthrosc. 14:390, 2006. 53. Newell, R. L. M.: Olecranon fractures in children. Injury 37:33, 1975. 54. Orava, S., and Hulkko, A.: Delayed unions and nonunions of stress fractures in athletes. Am. J. Sports Med. 16:517, 1988. 55. Papagelopoulos, P. J., and Morrey, B. F.: Treatment of nonunion of olecranon fractures. J. Bone Joint Surg. Br. 76:627, 1994. 56. Paterson, D. C., Lewis, G. N., and Cass, C. A.: Treatment of delayed union and nonunion with an implanted direct current stimulator. Clin. Orthop. 148:117, 1980. 57. Regan, W., and Morrey, B. F.: Fractures of the coronoid process of the ulna. J. Bone Joint Surg. 71A:1348, 1989. 58. Ring, D., Jupiter, J. B., and Gulotta, L.: Atrophic nonunions of the proximal ulna. Clin. Orthop. Relat. Res. 409:268, 2003. 59. Rommens, P. M., Kuchle, R., Schneider, R. U., and Reuter, M.: Olecranon fractures in adults: Factors influencing outcome. Injury 35:1149, 2004. 60. Rothman, R.: The effect of iron deficiency anemia on fracture healing. Clin. Orthop. Relat. Res. 77:276, 1971. 61. Sharrard, W. J. W., Sutcliffe, M. S., Robson, M. J., and Maceachern, A. G.: The treatment of fibrous nonunion of fractures by pulsing electromagnetic stimulation. J. Bone Joint Surg. 64B:189, 1982. 62. Silberstein, M. J., Bradeur, A. E., Graviss, E. R., and Luisiri, A.: Some vagaries of the olecranon. J. Bone Joint Surg. 63A:722, 1981. 63. Smith, F. M.: Surgery of the Elbow. Philadelphia, W. B. Saunders Co., 1972, p. 260. 64. Srivastava, K. P., Vyas, O. N., Varshney, A. K., and Singh, C. P.: Compression osteosynthesis in fractures of the olecranon. Int. Surg. 63:20, 1978.

65. Taylor, T. K. F., and Scham, S. M.: A posteromedial approach to the proximal end of the ulna for the internal fixation of olecranon fractures. J. Trauma 9:594, 1969. 66. Tonna, E. A.: The cellular complement on the skeletal system studied autoradiographically with tritiated thymidine (H3 DTR) during growth and aging. J. Biophys. Biochem. Cytol. 9:813, 1961. 67. Torg, J. S., and Moyer, R. A.: Nonunion of a stress fracture through the olecranon epiphyseal plate observed in an adolescent baseball pitcher. J. Bone Joint Surg. 59A:264, 1977. 68. Tullos, H. S., Schwab, G., Bennett, J. B., and Woods, W. G.: Factors influencing elbow instability. Instruc. Course Lect. 30:193, 1981. 69. Waddell, G., and Howat, T. W.: A technique of plating severe olecranon fractures. Injury 5:135, 1973. 70. Wadsworth, T. G.: Screw fixation of the olecranon after fracture of osteotomy. Clin. Orthop. Relat. Res. 119:197, 1976. 71. Walker, L. G.: Painful olecranon physeal nonunion in an adult weight lifter. A case report. Clin. Orthop. 311:125, 1995. 72. Weber, B. G., and Cech, O.: Pseudarthrosis: Pathology, Biomechanics, Therapy, Results. Berne, Hans Huber Medical Pub., 1976. 73. Weber, B., and Vasey, H.: Osteosynthese bei Olecranon Fraktur. Z. Unfallmed. Berufskr. 2:90, 1963. 74. Weisband, I. D.: Tension band wiring technique for treatment of olecranon fractures. J. Am. Osteopath. Assoc. 77:390, 1978. 75. Weseley, M. S., Barnfield, P. A., and Einstein, A. I.: The use of the Zuelzer hook plate in fixation of olecranon fractures. J. Bone Joint Surg. 58A:859, 1976. 76. Wilkerson, R. D., and Johns, J. C.: Nonunion of an olecranon stress fracture in an adolescent gymnast. Am. J. Sports Med. 18:4, 1990.

Chapter 27 Coronoid Process and Monteggia Fractures

CHAPTER

27

Coronoid Process and Monteggia Fractures William D. Regan and Bernard F. Morrey

THE CORONOID As this fracture often occurs in conjunction with radial head fractures and dislocation; it is also discussed in the chapter on complex instability (see Chapter 29).

MECHANISM OF INJURY Isolated coronoid fractures are uncommon and usually occur in association with elbow dislocation.49,59 One recent review of 120 complex elbow injuries identified 21% with coronoid and radial head fractures, 19% with olecranon and radial head fracture and 33% with radial head, olecranon and coronoid fracture.20 One group identified three of eight isolated coronoid fractures.23 Theoretically, the coronoid is fractured with the elbow in 0 to 20 degrees of flexion during an axial load (Fig. 27-1).1 This is a mechanism similar to that in elbow dislocation. With flexion past 30 degrees, radial head fractures occur. The combination of coronoid and radial head fracture has important implications for treatment, as discussed in Chapter 29. Of particular note is the fact that fractures involving more than 50% of the coronoid (Regan/Morrey type II) are associated with marked elbow instability, especially if the radial head has been resected (Fig. 27-2).12,13,36

INCIDENCE Fractures of the coronoid process are uncommon. This may occur with a comminuted olecranon or proximal ulnar fracture (Fig. 27-3). The injury has also been reported in 2% to 10% of patients with dislocation of the elbow. Our review of 293 acute radial head fractures documented 33 (11%) concurrent coronoid fractures (see Chapter 24).64 Since the initial series of 35 patients,49 a few case reports19,61 and small series have appeared.23,31,56

419

CLASSIFICATION Review of Mayo records resulted in a simple classification of coronoid fractures as well as a rationale for treatment (Fig. 27-4). Type I is a fracture of the tip of the coronoid process caused by a shearing force as the coronoid process subluxates or dislocates over the trochlea. A type II injury involves a single or comminuted fragment constituting about half of the coronoid. A type III fracture involves more than half of the coronoid process. The type II or III fracture may be comminuted, and all three may be associated with dislocation of the elbow or with other injuries. Comminution in the sagittal plane, often involving the medial portion of the coronoid and sometimes even involving the sublime tubercle, has been documented58 (Fig. 27-5). Subtle medial coronoid fractures have also been documented. A hint of such an injury is the appearance of the socalled double crescent sign (Fig. 27-6).

ASSOCIATION INJURIES With type I fractures, or any coronoid fracture, one must assume that the elbow has dislocated. Even if dislocation did not occur, some injury to the ligament is present, even if only a strain. Furthermore, 35% of the patients with type I, 56% of the patients with type II, and 80% of the patients with type III coronoid fractures had other identified injuries.49 In fact, today an isolated injury is considered a rarity and other pathology must be sought if it is not obvious. Our current management philosophy is governed by our clinical experience and by basic investigational data (see Chapter 3).26,31,37,46 Simply put, first and foremost, a stable ulnohumeral joint must be attained and maintained. This means 1. All coronoid fractures of greater than 50%, some type II fractures, and all type II fractures are fixed. 2. All associated radial head fractures are fixed if possible (fewer than four fragments) or otherwise replaced. 3. The lateral ulnar collateral ligament is always repaired. 4. An articulated external fixator is applied if any question about fragment fixation or ulnohumeral stability exists.

TREATMENT Authors’ Preference Type I The patient with type I fracture is treated according to the concurrent pathology. The fracture itself indicates that the elbow has dislocated and should be managed on that basis. One recent report has implicated

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420

Fracture Component

Arc

Coronoid

0-20º

20º

0º

FIGURE 27-1

Coronoid fracture occurs with an axial load and between 0 and 20 degrees of flexion.

100

FIGURE 27-3

The Mayo IIIB transolecranon fracture dislocation typically does involve the coronoid.

Elbow stability

90

60

30

0

the fragment as a source of catching or impingement, both responding to arthroscopic excision.29 It does not need to be fixed acutely.

25% 50% 75%

0

15

30

45

A

60 75 Elbow flexon

90

105

120

90

105

120

100

Elbow stability

90 50% coronoid resection

60

Radial head resection 30

0

B

0

15

FIGURE 27-2

30

45

60 75 Elbow flexon

Experimental data depicting the stability of the ulnohumeral joint. With fractures involving 25%, 50%, and 75% of the coronoid, the joint is grossly unstable. The type II, 50% fracture is unstable at 60 degrees of extension (A) with the radial head removed, the elbow is unstable, even with more than 90 degrees of flexion (B).

Type II Type II fractures should be treated with early motion unless the elbow is unstable. Typically involving more than 50% of the coracoid, screw fixation is effective if the fragment is not comminuted. If comminuted, a suture or a buttress plate are both effective options, and a distraction device can be used to provide the initial stability while the soft tissue heals. Fixation of the smaller fragments alone may not stabilize the joint but should be considered if technically feasible. As a useful clinical tool, we have observed that determining the rotational stability is assisted by a line from the tip of the olecranon through the residual coronoid. If this is parallel to the long axis of the ulna, a type II or a 50% fracture has occurred and the joint is potentially unstable (Fig. 27-7). Type III Type III fractures are always associated with elbow instability. If the fracture is comminuted and is not amenable to fixation, the suture or buttress plate options are employed and an external fixation device is mandatory. Failure to stabilize the elbow in type III fractures results in a painful subluxation of the ulnohumeral joint, usually with marked limitation of motion

Chapter 27 Coronoid Process and Monteggia Fractures

A

Type I

A

Type II

B B Type III

C FIGURE 27-4

Regan-Morrey classification of coronoid fractures. Type I is a small shear fragment (A); type II is a single or comminuted portion involving approximately 50% (B); type III is a fracture involving more than half of the articulation (C).

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Type III

MCL

FIGURE 27-5

Comminuted coronoid fractures may include a sagittal element (A) that will frequently contain the attachment of the medial collateral ligament (MCL) (B).

B

(Fig. 27-8). Hence, open reduction and rigid fixation, with or without the distraction device, remains the treatment of choice. Note: The most important point is that the acute injury must be properly managed. Outcomes of acute management are orders of magnitude better than those of delayed reconstruction.23,42,52,56,67

Technique If the radial head is fractured or the elbow is grossly unstable, exposure and fixation of the coronoid is facilitated. We still usually use a straight posterior skin incision. Kocher’s interval is used if the radial head is fractured. If the fracture is an isolated one, a medial approach is used (see Chapter 7). This is mandatory if a sagittal component is present and if the medial collateral ligament is involved. With the use of the posterior incision, the ulnar nerve is exposed but not transferred. The flexor-pronator origin is released with a 1-cm cuff of tendon left on the medial epicondyle (Fig. 27-9). The brachialis muscle is elevated from the capsule, and the joint entered. Fixation is ideally accomplished with one or two compression screws (Fig. 27-10). With comminuted fractures, a heavy No. 5 nonabsorbable suture may be placed through the brachialis tendon, and then through the fracture, and is

secured through drill holes in the ulna through the base of the fracture (Fig. 27-11). A buttress plate is also effective (Fig. 27-12). An absent coronoid may be reconstructed with a well-fashioned bone graft from the ilium. Moritomo and colleagues35 have also described reconstruction with the osteotomized portion of the olecranon. But in general, reconstruction is unreliable. Using an osteochondral graft is successful in only about 50% of cases. More complex reconstruction has also been assessed42 with better outcomes being realized if the coracoid, radial head, and collateral ligaments are all addressed at the time of the injury.42,53,54

Reconstruction

RESULTS The results of 35 patients with acute coronoid fractures treated at Mayo are shown in Table 27-1. Using an elbow performance index, it is obvious that the chance of a satisfactory result directly correlates with the severity of the injury, as reflected by the coronoid fracture type. Pain is uncommon in type I and typical in type III injury. Our impression is that the results have improved over the last decade owing to (1) a better understanding of the implications of associated injury,

Chapter 27 Coronoid Process and Monteggia Fractures

423

B

A

FIGURE 27-6

Sometimes, the medial coronoid fracture may be very subtle (A). The lateral shows the double crescent sign (arrows) representing the normal and fracture contour (B). The three-dimensional CT reconstruction shows the lesion (C).

C

30° 50%

FIGURE 27-7

A line from the tip of the olecranon across the base of the fractured coronoid is roughly parallel to the long axis of the ulna in type II fractures.

(2) more aggressive exposure, and (3) improved design of internal and external fixation systems. Hence, the reports by both Ring et al55 and Pugh et al46 on 80% satisfactory outcomes following the above-mentioned principles when employed for acute fracture management.

Stress Fracture Although reported for the olecranon,30,68 stress fracture has not been reported for the coronoid. We have,

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FIGURE 27-8

Type III fracture developed chronic painful subluxation (A). Successfully treated with distraction device (B). (From Regan, W., and Morrey, B. F.: Fractures of the coronoid process of the ulna. J. Bone Joint Surg. 71A:1348, 1989.) Coronoid

Excised capsule

A

Lateral column

Medial head of triceps

B

FIGURE 27-9 The flexor-pronator muscle group is reflected with a cuff of tissue for reattachment (A). Elevating the brachialis tendon off the capsule and a medial arthrotomy allows adequate exposure of the coronoid (B).

however, documented one instance occurring in a young 17-year-old female gymnast (Fig. 27-13). Symptoms resolved and full activity returned with cessation of activity for 3 months.

MONTEGGIA FRACTURE Giovanni Battista Monteggia of Milan first described the injury that bears his name in 1814,33 the same year that Colles described his fracture. Monteggia initially reported on a fracture of the ulna associated with anterior dis-

location of the radial head, which is today recognized as the most common of the Monteggia lesions, a term coined by Bado4 that includes all ulnar fractures associated with dislocations of the radiocapitellar articulation. These lesions are uncommon (7% of ulnar fractures, 0.7% of elbow injuries5) but are difficult to manage properly.

CLASSIFICATION Depending on the type of dislocation of the radial head (anterior, posterior, and lateral), three distinct types of

Chapter 27 Coronoid Process and Monteggia Fractures

FIGURE 27-10

425

Type III fracture (A) exposed through a medial approach, fixed with two compression screws, and protected with an external fixator (B) (DJD, Howmedica) with excellent 6-month result (C and D).

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426

injuries were recognized early. Bado4 subsequently proposed a classification that encompasses the full spectrum of these injuries and has become universally accepted.

Type I Type I injury is an anterior dislocation of the radial head associated with a fracture of the ulnar diaphysis at any level with anterior angulation (Fig. 27-14). This is the most common type of lesion (55% to 78% of Monteggia fractures, depending on the series) and is most common in children.

Type II

FIGURE 27-11 A suture through the brachialis tendon may be used to secure badly comminuted fracture fragments.

Type II injury is a posterior or posterolateral dislocation of the radial head associated with a fracture of the ulnar diaphysis with posterior angulation (Fig. 27-15). Usually it is more proximal. The lesion occurs most commonly in adults, with a frequency of about 10% to 15% of cases.

Type III Type III injury is a lateral or anterolateral dislocation of the radial head associated with a fracture of the ulnar metaphysis (Fig. 27-16). Athough it is more common in children, it occurs with a frequency of 6.7% to 20% percent of cases.

A

B FIGURE 27-12

A 35-year-old radiologist has a comminuted fracture of the coronoid (A and B).

Chapter 27 Coronoid Process and Monteggia Fractures

C

D

F

FIGURE 27-12, cont’d

Buttress plate fixation and protected with the external fixator (C and D). At 8 weeks, excellent fixation and early healing. Extension (E); flexion (F).

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Results of Treatment According to Coronoid Fracture Type

TABLE 27-1

TYPE OF FRACTURE I

II

III

Pain, none (%)

50

67

20

Motion, mean lag (degrees)

4-136

12-127

39-100

Satisfactory (%)

92

74

20

8

26

80

Unsatisfactory (%)

Type IV Type IV fracture, the rarest type (5% of cases), consists of an anterior dislocation of the radial head associated with a fracture of the proximal third of the radius and a fracture of the ulna at the same level (Fig. 27-17).

Equivalents Bado also described equivalents to type I and II injury (according to him, types III and IV have no equivalents). Unfortunately, these so-called equivalents may have added uncertainty to our thinking, because the scheme

FIGURE 27-13 Plain film of 17-year-old female gymnast with chronic cubital pain, suggesting sclerosis of the coronoid tip (A). Three-dimensional reconstruction confirms stress fixation (B). (Courtesy of Dr. A. Rettig.)

FIGURE 27-14 Monteggia lesion type I. (Redrawn from Reckling, F. W., and Cordell, L. B.: Unstable fracturedislocations of the forearm: The Monteggia and Galeazzi lesions. Arch. Surg. 96:999, 1968.)

FIGURE 27-15 Monteggia lesion type II. (Redrawn from Reckling, F. W., and Cordell, L. B.: Unstable fracturedislocations of the forearm: The Monteggia and Galeazzi lesions. Arch. Surg. 96:999, 1968.)

Chapter 27 Coronoid Process and Monteggia Fractures

429

4. Fracture of the ulnar diaphysis with a more proximal fracture of the radial diaphysis 5. Fracture of the ulnar diaphysis with anterior dislocation of the radial head and fracture of the olecranon (Mayo type III olecranon fracture) 6. Posterior dislocation of the elbow and fracture of the ulnar diaphysis with or without fracture of the proximal radius (complex instability) (see Chapter 29). Type II Equivalents

1. Epiphyseal fractures of the dislocated radial head 2. Fractures of the neck of the radius

MECHANISM OF INJURY FIGURE 27-16 Monteggia lesion type III. (Redrawn from Reckling, F. W., and Cordell, L. B.: Unstable fracturedislocations of the forearm: The Monteggia and Galeazzi lesions. Arch. Surg. 96:999, 1968.)

FIGURE 27-17 Monteggia lesion type IV. (Redrawn from Reckling, F. W.: Unstable fracture-dislocation of the forearm [Monteggia and Galeazzi lesions]. J. Bone Joint Surg. 64A:857, 1982.)

attempts to account for virtually all other proximal ulna-radial fracture dislocations. With expanded classifications of olecranon, coronoid fractures and a better understanding of “complex instability,” the reliability of the so-called variants has become questionable. Type I Equivalents

1. Isolated anterior dislocation of the radial head in children (nursemaid’s elbow) 2. Fracture of the ulnar diaphysis with fracture of the neck of the radius in adults 3. Isolated fracture of the neck of the radius

Different theories have been proposed to explain the mechanism of injury, which varies according to the type of lesion. The greatest controversy concerns the type I lesion. A direct blow to the posterior aspect of the ulna seems to be the probable mechanism in most cases. However, a fall on the outstretched hand with the forearm in pronation may be the most common mechanism. Evans16 postulated that with such a fall, in which the hand is fixed to the ground by the weight of the body, the full pronation of the forearm is exaggerated by external rotation of the arm on the hand, and an oblique fracture of the ulna occurs. At the same time, the radius, forced into extreme pronation, crosses the ulna at the junction of the middle and proximal thirds. This contact acts as a fulcrum, forcing the proximal radius anteriorly to dislocate its head or to fracture, or, exceptionally, to do both (type IV). Evans carried out cadaver experiments that produced Monteggia type I or equivalent lesions in 17 of 18 attempts, confirming his hypothesis. Tompkins,65 on the other hand, postulated that with a fall on the outstretched hand, the radial head is dislocated by a violent reflex contraction of the biceps; this causes all the weight to be borne by the ulna, and, because of the longitudinal compressive force combined with the pull of the interosseous membrane and the simultaneous contracting brachialis, the ulna fractures and angulates anteriorly. Thus, the mechanism is one of hyperextension. This theory, if correct, would have implications for treatment, because flexion of 100 to 110 degrees would seem to be necessary after reduction to avoid redislocation of the radial head. It is likely that all three mechanisms (direct blow to the ulna, hyperpronation, and hyperextension) could cause a type I Monteggia fracture. Type II injuries occur more often among middle-aged women, in whom ligamentous attachments of the proximal ulna are stronger than the ulna itself.45 This explains

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Part V Adult Trauma

the mechanism of injury, which, similar to that in a posterior elbow dislocation, was confirmed by Penrose in cadaver experiments. Bado believed that these injuries are caused by a direct and supination rotational force,4 but that this has not been proved. The mechanism of injury in type III fractures is a direct blow on the inner side of the elbow with or without rotation.4

SYMPTOMS AND SIGNS Pain and marked tenderness and functional incapacity of the elbow are common to all types of Monteggia fractures. In type I and IV lesions, the forearm and hand assume a fixed pronation position. Shortening of the forearm, swelling, and anterior angulation of the fractured ulna are observable, and the radial head can be palpated in the antecubital fossa. If the fracture is compound, the skin lesion is usually anterior. In type II lesions, the ulnar fracture is more proximal, and the angulation is posterior. The radial head (often fractured) is easily palpated posteriorly, and if compounded, the wound is usually posterior. In type III lesions, there is a lateral angulation of the ulna at the level of the fracture, the forearm is usually in midrotation, and the dislocated radial head can be easily palpated.

A

RADIOLOGIC FINDINGS Adequate imaging is essential. Plane radiographs in two planes, including the elbow and wrist joints, are essential. The ulnar fracture is easy to recognize, but the dislocation of the radial head may be missed. This must be avoided, because it directly influences treatment and outcome. This occurs (1) as a result of poor-quality views, (2) particularly if the displacement is mild, (3) if the dislocation has been reduced inadvertently by a previous examiner or at the time of positioning the patient for the x-ray examination,2 or (4) if true biplanar views are not obtained. The Campbell Clinic experience in 1940 revealed that 52% of injuries were not diagnosed until 4 weeks after injury62; this incidence had decreased to 24 percent when Boyd and Boals8 reported on an expanded series of 159 lesions in 1965. Mobley and Janes32 reported that 5 of 15 patients (33%) had old lesions, and Reckling and Cordell48 found that 4 of 25 (16%) had missed lesions. Today, a CT study, especially with three-dimensional reconstruction, readily describes the full extent of the osseous injury and eliminated prior concerns (Fig. 27-18).

B FIGURE 27-18

CT is helpful in defining accuracy of correction (A), after olecranon osteotomy for malunion from Monteggia fracture (B). This is an excellent method to determine accuracy of radio-humeral alignment.

TREATMENT HISTORICAL PERSPECTIVE It is generally agreed that Monteggia lesions can be treated satisfactorily in children by closed methods but require reduction and fixation in adults. Watson-Jones anticipated an unfavorable outcome from this injury, causing permanent disability in 95%. In spite of contrary opinions,4,16 Speed and Boyd62 in 1940 concluded that closed treatment is unsatisfactory and advocated open reduction and internal fixation of the ulna and reconstruction of the annular ligament. In

Chapter 27 Coronoid Process and Monteggia Fractures

1969, Boyd and Boals8 recommended open reduction and internal fixation of the ulna with a compression plate or an intramedullary nail, but they suggested that closed reduction of the radial head was usually adequate and open reduction usually unnecessary. If a fracture of the radial head was present, they suggested excision. They found the Boyd7 approach to the ulna and proximal third of the radius satisfactory and obtained excellent or good results in 77% of acute lesions. As early as 1951, Penrose44 advised open reduction and internal fixation of the ulnar fracture combined with partial or total radial head excision (if the radial head was fractured) for type II injuries. Pavel43 and others,10,47 however, reported poor results after early radial head excisions for these injuries. Bado4 suggested closed treatment for type II injuries with manipulation by gentle traction and pronation to reduce the dislocation. If the ulnar fracture is not reduced, he advised intramedullary nailing. He also mentioned that results of treatment are less satisfactory with this type of injury. Reckling, in a study reported in 196848 and expanded in 1982,47 showed that the results of treatment of Monteggia lesions in adults were uniformly worse than those in children and that the best results were obtained with open anatomic reduction of the ulnar fracture, internal fixation, and complete closed reduction of the radial head dislocation. Yet, only 9 of 40 adult patients obtained excellent results. Type III injuries are almost exclusively found in children. Bryan,10 however, reported three such injuries in adults, two treated surgically with good results and one by closed means with a poor result. Type IV injuries have been and currently are clearly considered surgical lesions. Both fractures should be managed with open reduction and internal fixation, and the radial head dislocation can often be reduced by closed manipulation (supination).

RECENT EXPERIENCE Surprisingly and unfortunately, more recent reports continue to yield disappointing outcomes. One large study of 67 fractures reported only 54% satisfactory results at 1 to 14 years.51 The best results were in types I and III, with poorer outcomes after types II and IV fractures. In contrast, others have found the worse results after type I injury. A study from Israel described 41 patients—14 children and 27 adults—and emphasized that the type I fracture particularly requires careful monitoring and attention to the radial head.18 The principles of early recognition of proximal radioulnar dissociation and open reduction and internal fixation of the ulnar fracture in the adult are well accepted.55 The key is accurate linear, angular, and rotational alignment

431

of the ulna. This is essential to avoid the major problem of radial head malalignment and instability. The worst problem is the undiagnosed or inadequately treated Monteggia lesion that is seen late (after 4 weeks). The radial head has remained subluxated or redislocated, and the ulna usually exhibits a malposition. Minor degrees of angulation of the ulna and minimal subluxation of the radial head may be left alone if adequate function is present. Moderate angulation of the ulna and dislocation of the radial head are best treated with ulnar realignment osteotomy and plating if a malunion is present, or by realignment and plating of a nonunion. The radial head is resected if it cannot be realigned.

COMPLICATIONS Complications with this fracture remain all too common. One comprehensive study documented 43% complications and 46% unsatisfactory results after 67 fractures.51 Radial neuropathy, particularly that involving the posterior interosseous branch, has been reported rather frequently.9,10,24,32,63 Causes of the deficit are direct trauma, compression of the nerve in the arcade of Frohse, or, most commonly, stretching of the nerve by a laterally dislocated radial head (the nerve lesion that is most common with type III Monteggia lesions). Its incidence has been as high as 20% of acute lesions. The prognosis is usually good, with complete recovery by 6 to 8 weeks.24 Exploration of the posterior interosseous nerve is advisable when no evidence of recovery is present by 8 to 10 weeks. Tardy permanent plasy of the radial nerve after a Monteggia fracture is uncommon28 and typically occurs after an old unreduced lesion with long-standing dislocation of the radial head. Improvement has occurred after exploration of the radial nerve and excision of the radial head, which compresses the nerve during movements of pronation and supination. Median24 and ulnar10,32 nerve palsies are uncommon with Monteggia lesions.

UNION AND STABILITY Gross malunion of the ulna is seldom seen today in the adult, but recurrent dislocation or subluxation of the head of the radius is a common problem. This is usually the result of minor imperfections in the reduction of the ulna. In this age group, a properly performed ulnar osteotomy may be successful in allowing radial head reduction and hence restoring function.22 Ectopic bone formation is common and can be extensive (Fig. 27-19) or present as a single cross-union

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Part V Adult Trauma

FIGURE 27-19 Extensive ectopic bone after a poorly treated Monteggia fracture. A, Type I Monteggia lesion in an 18-year-old boy. B and C, Postoperative x-ray view after open reduction of ulna with AO compression plate and closed reduction of radial head. Full recovery occurred in 3 months.

(Fig. 27-20). The Boyd approach has also been implicated in cross-union in some instances. Nonunion of the ulna most commonly is related to infection but is also the result of inadequate internal fixation.2 Compression plating, properly executed, produces the lowest rate of nonunion. We have found external fixation useful in the treatment of one infected ununited Monteggia fracture.

REFRACTURE The incidence of refracture or fracture through a screw hole after forearm fracture is well recognized to occur from 2% to 28%.2,21,34,57 The fracture occurs at the fracture or screw hole with equal frequency.

AVOIDANCE The selection of the plate for distal Monteggia or Galeazzi fractures is most important. The 3.5 low-profile dynamic compression plate (DCP) is effective and has been associated with less clinical failure. Newer preformed plates are also effective. The plate should be applied with meticulous technique to ensure perfect reduction, rigid fixation and compression and should be left in place for at least 1 year. Ideally, a minimum of 6 months should be allowed for protection before any heavy activity, and we recommend a minimum delay of 9 months to, preferably, 1 year. In the interim, after removal we recommend a forearm protective splint for the first 4 to 6 weeks followed by activity as tolerated.

AUTHORS’ PREFERRED METHOD OF TREATMENT OF MONTEGGIA LESIONS Principles of treatment of Monteggia lesions in adults are as follows. Missing the dislocation of the radial head is unacceptable and guarantees a poor outcome. Remember the head may sublux in the early stages so close radiographic surveillance is required.

Accurate Diagnosis

Accurate Reduction of the Ulnar Fracture and Maintenance of the Reduction This essential step is best

achieved by rigid, anatomic plating, supplemented by cancellous bone graft if there is significant comminution (see Fig. 27-19). In type IV injuries, if not comminuted, compression plating of the radial and ulnar shaft fractures is the treatment of choice. Usually, the radial head reduces spontaneously when the ulnar fracture is reduced. In those rare instances in which it fails to do so, open reduction with incision of the annular ligament is necessary. When fracture of the radial head is present, as in some type II injuries, open reduction and internal fixation is preferred, if at all possible. Otherwise, partial or complete excision of the radial head may be necessary and an articulated radial head implant is used. In these instances in which the radial head must be exposed, we prefer the Boyd approach. In type IV injuries, the radial head dislocation usually reduces with closed methods.

Restoration of the Radiohumeral Joint

Chapter 27 Coronoid Process and Monteggia Fractures

433

FIGURE 27-20

A, Type I Monteggia lesion in an 18-year-old boy. B and C, Postoperative x-ray view after open reduction of ulna with AO compression plate and closed reduction of radial head. Full recovery occurred in 3 months.

For type I, III, and IV injuries, flexion of at least 90 degrees in moderate supination for 4 weeks is usually effective. Lateral radiographs should be rechecked at 1 and 2 weeks to assess the position of the radial head. In type II lesions, immobilization should be maintained in about 70 degrees of flexion.

Adequate Postoperative Immobilization

Active Rehabilitation After the immobilization has been discontinued, active range-of-motion exercises are begun. Improvement occurs slowly, but passive stretching is not advisable. The advent of CT imaging and rigid internal fixation methods has improved the prognosis for these potentially treacherous injuries.

References 1. Amis, A. A., and Miller, J. H.: The mechanisms of elbow fractures: An investigation using impact tests in vitro. Injury 26:163, 1995. 2. Anderson, L. D.: Fractures of the shaft of the radius and ulna. In Rockwood, C. A., and Green, D. P. (eds.): Fractures. Philadelphia, J. B. Lippincott Co., 1975. 3. Austin, R.: Tardy palsy of radial nerve from a Monteggia fracture. Injury 7:202, 1976.

4. Bado, J. L.: The Monteggia lesion. Clin. Orthop. Relat. Res. 50:71, 1967. 5. Beck, C., and Dabezies, E. J.: Monteggia fracture-dislocation. Orthopedics 7:329, 1984. 6. Bohler, L.: The Treatment of Fractures. Vienna, Wilhelm Mandrich, 1929. 7. Boyd, H. B.: Surgical exposure of the ulna and proximal third of the radius through one incision. Surg. Gynecol. Obstet. 71:86, 1940. 8. Boyd, H. B., and Boals, J. C.: The Monteggia lesion: A review of 159 cases. Clin. Orthop. 66:94, 1969. 9. Bruce, H. E., Harvey, J. P., and Wilson, J. C.: Monteggia fractures. J. Bone Joint Surg. 56A:1563, 1974. 10. Bryan, R. S.: Monteggia fracture of the forearm. J. Trauma 11:992, 1971. 11. Burghele, H., and Serban, N.: Fractures of the olecranon: Treatment by external fixation. Ital. J. Orthop. Traumatol. 8:159, 1982. 12. Cheng, S., An, K.-N., Morrey, B. F., and O’Driscoll, S. W.: Biomechanical of the coronoid in complex elbow fracturedislocations. J. Shoulder Elbow Surg. 793:304, 1998. 13. Closkey, R. F., Goode, J. R., Kirschenbaum, D., and Cody, R. P.: The role of the coronoid process in elbow instability: A biomechanical analysis of axial loading. J. Bone Joint Surg. 82A:1749, 2000. 14. Cobb, T. K., and Morrey, B. F.: Use of distraction arthroplasty in unstable fracture dislocations of the elbow. Clin. Orthop. Relat. Res. 312:201, 1995.

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15. Conn, J., and Wade, P. A.: Injuries of the elbow: A ten-year review. J. Trauma 1:248, 1961. 16. Evans, E. M.: Pronation injuries of the forearm with special reference to the anterior Monteggia fracture. J. Bone Joint Surg. 31B:578, 1949. 17. Fiolle, D. J.: Note sur les fractures de folecrane par projectiles de guerre. Marseille Med. 55:241, 1918. 18. Givon, U., Pritsch, M., Levy, O., Yosepovich, A., Amit, Y., and Horoszowski, H.: Monteggia and equivalent lesions: A study of 41 cases. Clin. Orthop. Relat. Res. 337:208, 1997. 19. Hanks, G. A., and Kottmeier, S. A.: Isolated fracture of the coronoid process of the ulna: A case report and review of the literature. J. Orthop. Trauma 4:193, 1990. 20. Heim, U.: Combined fractures of the radius and the ulna at the elbow level in the adult. Analysis of 120 cases after more than 1 year. Revue de Chirurgie Orthop et Reparatrice de l Appareil Moteur 84:142, 1998. 21. Hidaka, S., and Gustilo, R. B.: Refracture of bones of the forearm after plate removal. J. Bone Joint Surg. 66A:1241, 1984. 22. Inoue, G., and Shionoya, K.: Corrective ulnar osteotomy for malunited anterior Monteggia lesions in children: 12 patients followed for 1-12 years. Acta Orthop. Scand. 69:73, 1998. 23. Jeon, I. H., Oh, C. W., Kyung, H. S., Park, B. C., Kim, P. T., and Ihn, J. C.: Functional outcome after operative treatment of eight type III coronoid process fractures. J. Trauma 59:418, 2005. 24. Jessing, P.: Monteggia lesions and their complicating nerve damage. Acta Orthop. Scand. 46:601, 1975. 25. Joshi, R. P.: The Hastings experience of the Attenborough springs and Rush nail for fixation of olecranon fractures. Injury 29:455, 1997. 26. Kamineni, S., Hirahara, H., Neale, P., O’Driscoll, S. W., An, K.-N., and Morrey, B. F.: Effectiveness of the lateral unilateral dynamic external fixator after elbow ligament injury. J. Bone Joint Surg. 89A:1802, 2007. 27. Kozin, S. H., Berglund, L. J., Cooney, W. P., Morrey, B. F., and An, K-N.: Biomechanical analysis of tension band fixation for olecranon fracture treatment. J. Shoulder Elbow Surg. 5:442, 1996. 28. Lichter, R. L., and Jacobsen, T.: Tardy palsy of the posterior interosseous nerve with a Monteggia fracture. J. Bone Joint Surg. 57A:124, 1975. 29. Liu, S. H., Henry, M., and Bowen, R.: Complications of type I coronoid fractures in competitive athletes: Report of two cases and review of the literature. J. Shoulder Elbow Surg. 5:223, 1996. 30. Maffulli, N., Chan, D., and Aldridge, M. J.: Overuse injuries of the olecranon in young gymnasts. J. Bone Joint Surg. 74B:305, 1992. 31. McKee, M. D., Bowden, S. H., King, G. J., Patterson, S. D., Jupiter, J. B., Bamberger, H. B., and Paksima, N.: Management of recurrent, complex instability of the elbow with a hinged external fixator. J. Bone Joint Surg. 80B:1031, 1998. 32. Mobley, J. E., and Janes, J. M.: Monteggia fractures. Proc. Staff Meet. Mayo Clin. 30:497, 1955.

33. Monteggia, G. B.: Instituzioni Chirurgiche, Vol. 5. Milan, Maspero, 1814. 34. Moore, T. M., Klein, J. P., Patzakis, M. J., and Harvey, J. B.: Results of compression plating of closed Galeazzi fractures. J. Bone Joint Surg. 67A:1015, 1985. 35. Moritomo, H., Tada, K., Yoshida, T., and Kawatsu, N.: Reconstruction of the coronoid for chronic dislocation of the elbow: Use of a graft from the olecranon in two cases. J. Bone Joint Surg. 80B:490, 1998. 36. Morrey, B. F.: Fractures and dislocations of the elbow. In Gustilo, R. B. (ed.): Fractures and Dislocations. Chicago, Year Book Medical Publishers, 1992. 37. Morrey, B. F.: Current concepts in the treatment of fractures of the radial head, the olecranon, and the coronoid. J. Bone Joint Surg. 77A:316, 1995. 38. Muller, M. E., Allgower, M., Schneider, R., and Willenegger, H.: Manual of Internal Fixation: Techniques Recommended by the AO Group, 2nd ed. New York, Springer-Verlag, 1979. 39. Murphy, D. F., Green, W. B., and Dameron, T. B.: Displaced olecranon fractures in adults: Clinical evaluation. Clin. Orthop. Relat. Res. 224:215, 1987. 40. Murphy, D. F., Green, W. B., Gilbert, J. A., and Dameron, T. B.: Displaced olecranon fractures in adults: Biomechanical analysis of fixation methods. Clin. Orthop. Relat. Res. 224:210, 1987. 41. O’Donoghue, D. H., and Sell, L. S.: Persistent olecranon epiphysis in adults. J. Bone Joint Surg. 24:677, 1942. 42. Papandrea, R. F., Morrey, B. F., and O’Driscoll, S. W.: Reconstruction for persistent instability of the elbow after coronoid fracture-dislocation. J. Shoulder Elbow Surg. 16:68, 2007. (Epub 2006, Oct. 25). 43. Pavel, A., Pitman, J. M., Lance, E. M., and Wade, P. A.: The posterior Monteggia fracture: A clinical study. J. Trauma 5:185, 1965. 44. Penrose, J. H.: The Monteggia fractures with posterior dislocation of the radial head. J. Bone Joint Surg. 33B:65, 1951. 45. Perruelo, N. N., and Platigorsky, H.: Fractura de olecranonolecranectomia. Acta Ortoped. Traumatol. Iberica 3:12, 1955. 46. Pugh, D. M., Wild, L. M., Schemitsch, E. H., King, G. J., and McKee, M. D.: Standard surgical protocol to treat elbow dislocations with radial head and coronoid fractures. J. Bone Joint Surg. 86A:1122, 2004. 47. Reckling, F. W.: Unstable fracture-dislocation of the forearm (Monteggia and Galeazzi lesions). J. Bone Joint Surg. 64A:857, 1982. 48. Reckling, F. W., and Cordell, L. B.: Unstable fracturedislocations of the forearm: The Monteggia and Galeazzi lesions. Arch. Surg. 96:999, 1968. 49. Regan, W., and Morrey, B. F.: Fractures of the coronoid process of the ulna. J. Bone Joint Surg. 71A:1348, 1989. 50. Rettig, A. C., Waugh, T. R., and Evanski, P. M.: Fracture of the olecranon: A problem of management. J. Trauma 19:23, 1979. 51. Reynders, P., De Groote, W., Rondia, J., Govaerts, K., Stoffelen, D., and Broos, P. L.: Monteggia lesions in adults: A multicenter Bota study. Acta Orthop. Belgica 62(suppl 1):78, 1996.

Chapter 27 Coronoid Process and Monteggia Fractures

52. Ring, D., Hannouche, D., and Jupiter, J. B.: Surgical treatment of persistent dislocation or subluxation of the ulnohumeral joint after fracture-dislocation of the elbow. J. Hand Surg. 29A:470, 2004. 53. Ring, D., and Jupiter, J. B.: Reconstruction of posttraumatic elbow instability. Clin. Orthop. Relat. Res. 370:44, 2000. 54. Ring, D., Jupiter, J. B., Sanders, R. W., Mast, J., and Simpson, N. S.: Transolecranon fracture-dislocation of the elbow: J. Orthop. Trauma 11:545, 1997. 55. Ring, D., Jupiter, J. B., and Waters, P. M.: Monteggia fractures in children and adults. J. A. A. O. S. 6:215, 1998. 56. Ring, D., Jupiter, J. B., and Zilberfarb, J.: Posterior dislocation of the elbow with fractures of the radial head and coronoid. J. Bone Joint Surg. 84A:547, 2002. 57. Rosson, J. W., and Shearer, J. R.: Refracture after the removal of plates from the forearm: An avoidable complication. J. Bone Joint Surg. 73B:415, 1991. 58. Sanchez-Sotelo, J., O’Driscoll, S. W., and Morrey, B. F.: Anteromedial fracture of the coronoid process of the ulna. J. Shoulder Elbow Surg. 15:e5, 2006. 59. Scharplatz, D., and Allgower, M.: Fracture dislocation of the elbow. Injury 7:143, 1975. 60. Schmickal, T., and Wentzensen, A.: Treatment of complex elbow injuries by joint spanning articulated fixator. Unfallchirurg 103:191, 2000. 61. Selesnick, F. H., Dolitsky, B., and Haskell, S. S.: Fracture of the coronoid process requiring open reduction with internal fixation. J. Bone Joint Surg. 66A:1304, 1984.

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62. Speed, J. S., and Boyd, H. B.: Treatment of fractures of the ulna with dislocation of head of radius (Monteggia fracture). J.A.M.A. 115:1699, 1940. 63. Spinner, M., Freundlich, B. D., and Teicher, J.: Posterior interosseous nerve palsy as a complication of Monteggia fractures in children. Clin. Orthop. 58:141, 1968. 64. Terada, N., Yamada, H., Seki, T., Urabe, T., and Takayama, S.: The importance of reducing small fractures of the coronoid process in the treatment of unstable elbow dislocation. J. Shoulder Elbow Surg. 9:344, 2000. 65. Tompkins, D. G.: The anterior Monteggia fracture: Observations on etiology and treatment. J. Bone Joint Surg. 53A:1109, 1971. 66. van Riet, R. P., Morrey, B. F., O’Driscoll, S. W., and van Glabbeek F: Associated injuries complicating radial head fractures: A demographic study. Clin. Orthop. Relat. Res. 441:351, 2005. 67. van Riet, R. P., Morrey, B. F., and O’Driscoll, S. W.: Use of osteochondral bone graft in coronoid fractures. J. Shoulder Elbow Surg. 14:519, 2005. 68. Wilkerson, R. D., and Johns, J. C.: Non-union of an olecranon stress fracture in an adolescent gymnast: A case report. Am. J. Sports Med. 18:432, 1990. 69. Yamamoto, K., Yanase, Y., and Tomihara, M.: Posterior interosseous nerve palsy as complication of Monteggia fractures. Arch. Jpn. Chir. 46:46, 1977.

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CHAPTER

28

Elbow Dislocations Shawn W. O’Driscoll

INTRODUCTION The elbow is the second most commonly dislocated joint, after the shoulder, in adults. In the pediatric age group, it is the joint most commonly dislocated. Despite the prevalence of this injury, there are few analyses of series of this dislocation in the literature.7,16,19,25,29,36,46,52,68,76,96 Current treatment strategies are based on our understanding of the basic biomechanics and mechanism of injury.

The forces acting on the joint, besides producing tensile forces that disrupt the ligamentous constraints, also produce substantial compressive and shear forces on the articular surfaces. Therefore, adjunctive fractures, such as those occurring in the radial head and neck or capitellum, are frequent.2,15 There is evidence from reports of dislocations treated by open means that chondral injuries to the capitellar and trochlear surfaces are probably much more common than was previously believed.11,23 In the child, late nucleation and closure of the physes alter the response to dislocation forces and certainly increase the difficulty of radiographic interpretation. This is covered separately in Chapter 16. Understanding the mechanism of injury is obviously important for appreciating a classification, interpreting the clinical and radiographic findings, instituting treatment, anticipating complications, and providing adequate follow-up care.

CLASSIFICATION MECHANISM OF INJURY Although it used to be thought that dislocations occurred by hyperextension, it is now widely accepted that the mechanism of posterolateral rotatory posterior displacement of the elbow is responsible for most posterior dislocations resulting from falls on the outstretched hand. Motor vehicle accidents, direct trauma, and miscellaneous causes that account for the rest can have other mechanisms. The elbow experiences an axial compressive force during flexion as the body approaches the ground. As the body rotates internally on the elbow (forearm rotates externally on the trunk), a supination moment occurs at the elbow. A valgus moment results from the fact that the mechanical axis is lateral to the elbow (Fig. 28-1). This combination of valgus instability and supination with axial compression during flexion is precisely the mechanism that results in a posterolateral rotatory subluxation or dislocation of the elbow and can be reproduced clinically by the lateral pivot-shift test, which is described later.55 We have documented this exact mechanism in two patients whose dislocations were caught on video camera during wrestling matches. Osborne and Cotterill64 first suggested a posterolateral rotational displacement as the mechanism of elbow dislocation. The radial collateral ligament and the lateral capsule are torn. They suggested a method of repair for recurrent dislocation based on this theory of mechanism, which involved imbrication of the lateral soft tissues. The method has been used with success.25

Acute elbow dislocations are classified as posterior, anterior, and divergent.

POSTERIOR DISLOCATIONS By far the most common dislocation occurs posteriorly (Fig. 28-2). Whether the forearm is medially or laterally displaced is irrelevant to the pathologic condition seen or the ultimate treatment.

ANTERIOR DISLOCATIONS Anterior dislocations are extremely rare and are usually seen in younger individuals (Fig. 28-3).5,93 The forearm bones are displaced anterior to the distal humerus. The mechanism of injury is not well understood or proven, but there is a forward rebounding force that allows the olecranon to slide under the trochlea and the radial head to dislocate from the capitellum. In adults, the olecranon is usually fractured.

DIVERGENT DISLOCATIONS Displacement of the radius from the ulna with concomitant dislocation is a rare injury associated with high energy trauma.3,4,9,30,37,40 The interosseous membrane, annular ligament, and distal radioulnar joint capsule are all necessarily torn.

Chapter 28 Elbow Dislocations

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Valgus

Supination Axial compression

FIGURE 28-1

Proposed mechanism of elbow dislocation. A fall on the outstretched hand with the shoulder abducted produces an axial force on the elbow as it flexes. Because the body internally rotates on the hand and approaches the ground, external rotation and valgus moments are applied to the elbow. This is the same combination of forces and moments that are applied to the elbow during the lateral pivot-shift test for posterolateral rotatory instability. (Redrawn from O’Driscoll, S. W., Morrey, B. F., and Korinek, S., and An, K. N.: Elbow subluxation and dislocation: A spectrum of instability. Clin. Orthop. Relat. Res. 280:186, 1992.) FIGURE 28-2

PATHOMECHANICS OF ELBOW INSTABILITY

A, Posterior dislocation of the elbow from a fall on the outstretched hand. Note the shear fracture of coronoid fragment, which is pathognomonic of an elbow subluxation or dislocation. Small “flake” fractures are not avulsion fractures because nothing attaches to the very tip of the coronoid. The brachialis inserts distally. B, Coronoid fragment has healed.

The pathoanatomy can be thought of as a circle of soft tissue disruption from lateral to medial in three stages (Figs. 28-4 and 28-5). In stage 1, the ulnar part of the lateral collateral ligament is disrupted (the remainder of the lateral collateral ligament complex may be intact or disrupted). This results in posterolateral rotatory subluxation of the elbow, which reduces spontaneously.6,55,61 With further disruption anteriorly and posteriorly, the elbow is capable of an incomplete posterolateral dislocation (stage 2). The concave medial edge of the ulna rests on the trochlea in such a way that a lateral radio-

graph gives one the impression that the coronoid is perched on the trochlea.51 Stage 3 has two parts. In stage 3A, all the soft tissues are disrupted around to and including the posterior part of the medial collateral ligament, leaving the important anterior band intact. This permits posterior dislocation by the previously described posterolateral rotatory mechanism. The elbow pivots around on the intact anterior band of the medial collateral ligament. In stage 3B, the entire medial collateral complex is disrupted.

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2

1 LUCL

3 MUCL 2

FIGURE 28-4

FIGURE 28-3

A, Anterior dislocation, elbow. Avulsion olecranon fragment. B, Three weeks after reduction.

0 Reduced

1 PLRI

Soft tissue injury progresses in a circle-like manner, from lateral to medial, in three stages. In stage 1, the lateral ulnar collateral ligament (LUCL) is disrupted. In stage 2, the other lateral ligamentous structures and the anterior and posterior capsule are disrupted. In stage 3, disruption of the medial ulnar collateral ligament (MUCL) can be partial with disruption of the posterior MUCL only (stage 3A), or complete (stage 3B). (Redrawn from O’Driscoll, S. W., Morrey, B. F., Korinek, S., and An, K. N.: Elbow subluxation and dislocation: A spectrum of instability. Clin. Orthop. Rel. Res. 280:186, 1992.)

2 Perched

3 Dislocated

Supination Axial compression Valgus

FIGURE 28-5

Clinical stages of elbow instability correlating with the pathoanatomic stages of capsuloligamentous disruption. Forces and moment responsible for displacements are illustrated. PLRI, posterolateral rotatory instability. (Redrawn from O’Driscoll, S. W., Morrey, B. F., Korinek, S., and An, K. N.: Elbow subluxation and dislocation: A spectrum of instability. Clin. Orthop. Rel. Res. 280:186, 1992.)

Chapter 28 Elbow Dislocations

Gross varus and valgus as well as rotatory instability is present following reduction, owing to the fact that all ligaments and capsules are disrupted. Surgical exploration has established that the anterior medial collateral ligament usually is disrupted by a complete dislocation of the elbow.7,9,11,13 These pathoanatomic stages correlate with clinical degrees of elbow instability. Therefore, dislocation is the final of three sequential stages of elbow instability resulting from posterolateral ulnohumeral rotatory subluxation, with soft tissue disruption progressing from lateral to medial. In each stage, the pathoanatomy is correlated with the pattern and degree of instability. This has been confirmed in studies of cadaver elbows; 12 of 13 of the elbows could be dislocated posteriorly, with the anterior medial collateral ligament intact.21,56 In all 13 elbows, the coronoid could be perched on the trochlea after release of the lateral collateral ligament complex and the lateral half of the anterior capsule. Following reduction, the elbows were clinically stable to valgus stress. This hypothesis explains the spectrum of instability, from posterolateral rotatory instability to perched dislocation to posterior dislocation without or with disruption of the anterior medial collateral ligament, which occurs with further posterior displacement. Such a posterolateral rotatory mechanism of dislocation is compatible with those suggested by Osborne and Cotterill,64 Roberts,76 and others.1,27,63 The injury patterns in the lateral collateral ligament have been documented.47 The overwhelming majority are by detachment of the lateral collateral ligament (LCL) complex from its origin on the lateral condyle. In most cases, the common extensor tendon is also disrupted.

ASSOCIATED INJURIES Associated injuries with elbow dislocation are common.28,32,62,77,80,95,97 Radial head and neck fractures occur in about 5% to 10% of cases secondary to compressive loading at the radiocapitellar joint. Avulsion of fragments from either the medial or the lateral epicondyles occurs in approximately 12% of cases, and fractures of the coronoid process occur in 10% of dislocations (see Fig. 28-2). It is essential to obtain stability following a fracture-dislocation because the treatment of persistent instability following fracture dislocations is unpredictable.65 One should be particularly careful to assess for fractures of the anteromedial facet of the coronoid (computed tomography [CT] scanning with three-dimensional surface rendering is best) because even an apparently minor fragment can be the only sign of a very serious injury with a grave prognosis due to posteromedial rotatory instability from a fracture subluxation.10,57,59,60

439

Displacement of the medial epicondyle in adolescents ranges from minimal to incarceration of the epicondyle within the joint (Fig. 28-6).36,69,79,88,90,98 The latter, if undetected, results in significant traumatic arthrosis (Fig. 28-7). Medial epicondylar fracture can predispose to late secondary dislocation.36 This may be explained by the loss of medial collateral ligament integrity. Intra-articular fracture, as in the capitellum, occurs occasionally, but osteochondral injuries are probably much more common than standard radiographs would lead one to suspect.18 Injuries at other sites are also common with elbow dislocations, occurring in approximately 12% of the cases.36,52,94 Fractures of the distal radius and the ulnar styloid, perilunar dislocations, and shoulder injuries of the same extremity are the most common of these injuries, with multiple injuries of other areas secondary to severe trauma accounting for the rest. Neurovascular injuries occur with elbow dislocations just as with any other joint injury.69 Neurovascular compromise can also develop following the dislocation rather than during it. When the elbow is dislocated, the extensive soft tissue damage results in marked swelling. The intact structures in the area, such as the forearm fascia, the biceps tendon, and the lacertus fibrosus, may exert a marked constricting effect, resulting in increased compartmental pressures. Volkmann’s ischemic contracture may result and must be watched for and differentiated early from neurologic stretch injuries. It is occasionally possible to reduce the elbow without an anesthetic while the elbow region is insensitive to trauma, especially if it is seen before there is marked swelling or the dislocation is not badly displaced. Prudence suggests transport to a suitable facility for anesthetic coverage and support facilities except in unusual circumstances. General or regional block anesthetic is preferable for muscular relaxation and pain relief. Although reduction may be possible with a narcotic tranquilizer combination, the extra force that is occasionally necessary and the possibility of adding complications make this a less desirable method.

ASSESSMENT AND TREATMENT OF ACUTE ELBOW INSTABILITY ASSESSMENT OF STABILITY On the basis of the aforementioned observations and interpretations, it can be recommended that posterior elbow dislocations be reduced in supination to clear the coronoid under the trochlea, thereby minimizing additional trauma to the medial soft tissues that have not yet been disrupted. Following reduction, instability is

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FIGURE 28-6

A and B, Posterolateral dislocation with fragment of medial epicondyle lying at level of joint. C, Following reduction, medial epicondyle is displaced medially at the level of the joint.

best assessed with the patient under general anesthesia, but this is not always practical. It is indicated when there is any clinical or radiographic evidence for suspicion of persistent instability. The elbow is examined for valgus, varus, and posterolateral rotatory instability (Fig. 28-8). Forced pronation prevents instability by using the intact medial soft tissues as a hinge or fulcrum, just as the periosteum is used for this purpose during the reduction of a supracondylar fracture in a child. Both valgus and varus testing are performed with the elbow in full extension and several degrees of flexion up to about 30 degrees to unlock the olecranon from the olecranon fossa. Posterolateral rotatory instability is diagnosed by

the lateral pivot-shift test of the elbow, which is described in the next section on recurrent instability and is described in detail in Chapters 47 and 48. A positive test is manifested by a clunk that is heard and felt when the ulna and the radius reduce on the humerus. With severe soft tissue disruption, the elbow can sometimes remain dislocated even when flexed past 90 degrees. The patient should be followed with sequential radiographs for any radiographic signs of instability. The drop sign is a key radiographic warning sign of elbow instability, and it indicates severe soft tissue disruption both laterally and medially and a propensity for persistent or recurrent instability.8

Chapter 28 Elbow Dislocations

441

FIGURE 28-7

A and B, Undetected medial epicondyle entrapped within joint. After a year’s duration, there is valgus and traumatic arthrosis. C, Clinical appearance at 35 degrees extension lag. (A, From Linscheid, R. I., and Wheeler, D. K.: Elbow dislocations. J. A. M. A. 194:1171, 1965. © 1965 American Medical Association.)

DELAYED TREATMENT Delayed treatment for neglected dislocations41,85 is discussed in detail in Chapter 30. Open reduction may be indicated for a problem that has been neglected for more than 10 days when firm but gentle manipulation fails.35 Rarely, closed reduction is prevented by interposition of the annular ligament or a collateral ligament.24,66,83 A

laterally placed Kocher incison is preferred, especially if there are concomitant intra-articular fractures or loose fragments at the radiocapitellar joint.12 Buttonholing of the radial head through the capsule may be recognized readily with this approach.24 Proximal radioulnar translocation, a rare entity, has been reported and is treated by open reduction.54

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A FIGURE 28-8 Valgus Axial compression

Supination

Subluxation

B Long-standing chronic dislocations should be reduced open, and the joint should be freed of scar tissue and reconstructed as described in the sections on collateral ligament reconstruction. Open reduction is usually used to retrieve an incarcerated medial epicondyle from within the ulnotrochlear joint,69 a situation that usually occurs in the pediatric patient. If this is necessary, the ulnar nerve should be identified beneath the deep fascia posterior to the medial intermuscular septum for protection during the procedure. The medial collateral ligament attached to the epicondyle also may have been avulsed from the proximal area of the medial humeral condyle. It should be reapproximated and tacked into position with sutures as necessary to maintain its position and ensure better medial stability. If there has been obvious ulnar nerve injury or clinical neurapraxia, anterior translocation may be considered simultaneously before reattaching the medial epicondyle. In many instances, moderate displace-

A, The lateral pivot-shift test of the elbow for posterolateral rotatory instability is performed with the patient supine. A supination valgus moment is applied during flexion. This causes the elbow to subluxate and creates apprehension in the patient. Further flexion produces a palpable, audible clunk as the elbow reduces if the patient is able to relax enough to permit that part of the examination. This usually is not possible and requires a general anesthetic. B, Schematic representation of the lateral pivot shift test. (Redrawn from O’Driscoll, S. W., Bell, D. F., and Morrey, B. F.: Posterolateral rotatory instability of the elbow. J. Bone Joint Surg. 73A:440, 1991.)

ment of the epicondyle may be present without significant neurovascular problems. Accurate anatomic reduction and fixation are, however, desirable.

POSTREDUCTION CARE AND REHABILITATION Treatment recommendations following acute soft tissue injuries correspond to the stages outlined in the spectrum of instability. Initially, the elbow is placed in a padded dressing with a posterior plaster splint in full pronation at 90 degrees of flexion, after assessment for stability. Persistent or increasing pain or loss or diminution of the pulse requires wide release of the dressing anteriorly, inspection of the antecubital space, and a check of the neuromuscular status for signs of impending ischemia. Valgus stability following reduction is

Chapter 28 Elbow Dislocations

present in stages 1 to 3A when the forearm is fully pronated. These injuries are permitted unlimited flexion and extension. Protection may be added by the use of a hinged brace, which is applied with the forearm in full pronation. If the elbow feels stable in any position of forearm rotation, a brace is not necessary. Such stability is usually due to the dynamic stabilizing effects of the muscles crossing the elbow joint. In stage 3B, the elbow is unstable in extension, and a hinged brace (usually in pronation, but occasionally in neutral rotation) is applied with an extension block incorporated to prevent extension beyond the point of instability. This is gradually extended during the healing phase. A total of 3 to 6 weeks of protected motion is adequate. If by 6 to 8 weeks full motion has not been attained, special patientadjusted static flexion and extension splints are used to quickly regain the remaining motion. Based on comprehensive research on elbow kinematics, King and associates31 have shown that that LCLdeficient elbow should be rehabilitated by performing flexion/extension with the forearm pronated. The addition of active muscle contraction further stabilizes the joint. This is readily achieved by overhead exercises in the supine position. Forearm rotation is performed actively and only in the flexed position.

ACUTE LIGAMENT REPAIR The indication for surgery, acute ligament repair, or reconstruction is instability that does not permit early protected motion in a hinged brace or with a removable splint. This usually occurs only when there are associated fractures. In such cases, the ligaments may have been avulsed and can be repaired directly to the bone with heavy sutures. If they are torn and cannot be repaired, they can be reconstructed using the techniques described in the chapters on injuries to the medial and lateral collateral ligaments. In some cases, the tissue can be repaired but not strongly enough to stabilize the joint. The alternative to ligament repair is the application of a hinged external fixator,59,73,87 which is particularly appealing in patients with bilateral elbow dislocations, a rather rare condition.33

FRACTURES The presence of fractures often changes the management of the injury.22,26,49,58,72,74 The treatment of these complex instabilities is discussed in Chapter 29.

RESULTS Melhoff and associates48 reviewed the long-term sequelae of simple elbow dislocations in 52 patients. Half of the

443

patients were asymptomatic; one third had some loss of motion, mainly extension. This related to the duration of postreduction immobilization. Those immobilized for longer than 3 weeks were likely to develop contractures, whereas those immobilized for shorter periods were less likely. Uncomplicated dislocations generally have satisfactory results. Excellent results with full range of motion, normal strength, absent pain, and good stability may be expected in half of simple dislocations (Fig. 28-9). Good results with a loss of no more than 15 degrees of either flexion or extension, minimal discomfort, and normal stability are anticipated in an additional one third of cases. Fair or poor results generally are associated with complications (discussed later) and may be expected in 15% of dislocations. Fair or poor results generally are seen in the more severe original injuries.36 Most patients note continuing improvement for at least 6 months and some for as long as 18 months. This may be sped up by an active rehabilitation program. Recurrent instability has not been commonly reported, although symptoms have been noted in up to 35% of patients.31,42,48,86 It has been widely taught that the medial collateral ligament heals predictably following elbow dislocations and that instability is uncommon.11,50,78,98 However, these opinions have been formulated largely in the absence of objective assessments of elbow stability that have been tested and proven reliable. In addition, most reports precede the generalized awareness of posterolateral rotatory instability or how to diagnose it. Egandal and colleagues17 are to be commended for detailed follow-up analysis of 50 patients with posterolateral dislocations of the elbow treated by closed reduction and conservative treatment. A valgus radiographic stress x-ray study was performed on every patient, and in fact, this revealed that half (24 of 50) of the patients had clear radiographic evidence of valgus instability. Furthermore, valgus instability was associated with increased likelihood of radiographic evidence highly statistically significantly increased incidents of worse pain, worse scores according to the Hospital for Special Surgery score, and radiographic post-traumatic arthritis. It is the author’s opinion that the medial collateral ligament does not necessarily heal in a predictable fashion following an elbow dislocation and that the reason this has not been obvious clinically is that relatively few patients with elbow dislocations also subject their elbows to repetitive valgus stresses such as occurs during overhead throwing, tennis, and contact sports. An elbow dislocation should be monitored much more carefully for evidence of instability in such a high-demand patient.

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FIGURE 28-9

A and B, One year following otherwise uncomplicated posterior dislocation. Right elbow extends to neutral, left elbow to +10 degrees. Flexion limited by 5 degrees on right.

COMPLICATIONS NEUROVASCULAR Neurovascular problems have already been discussed in the section on treatment, but they deserve additional emphasis. Stretching and distortion of the anterior structures may result in spasm, intimal damage, thrombosis, or rupture of the brachial artery.14,20,32,36,39,43,44,53,71,81,84,89,92 Neurologic problems occur in approximately 20% of dislocations. The ulnar nerve is the most susceptible major nerve.36 Symptoms vary from transient paresthesias in the ulnar distribution to a rare permanent ulnar palsy. Median nerve symptoms are less common and also range from a transient to a complete palsy. Combined median-ulnar nerve injuries usually are associated with severe injuries that frequently involve the brachial artery as well. Vascular injuries usually

result in significant long-term disabilities35 (see Complications). Because dislocation often is also disruptive of collateral circulation, the forearm is at risk in this instance. Ischemic myositis, impaired vascularity, or later claudication may result (see Chapter 16). Median nerve symptoms are apt to be associated with arterial injury because of the close proximity of nerve and artery in their course between the brachialis and the pronator teres. Stretch injuries to the nerve occur at the time of dislocation.70 These injuries must be differentiated from secondary compressive injuries, which may occur with increased intracompartmental pressure in the flexor space or intra-articular entrapment. The latter may be suspected if median paresthesias occur shortly after reduction, if there is widening of the medial joint space, or if reduction has an “incomplete feel.”78 This complication is more common in children

Chapter 28 Elbow Dislocations

445

COMPARTMENT SYNDROME Humerus Median n.

Medial epicondyle Medial aspect of medial condyle Ulnar head pronator teres

Ulnar

Intramuscular bleeding and edema formation within the flexor compartment of the forearm may lead to ischemic myositis, especially if it is associated with a concomitant vascular injury. Pain on passive finger and wrist extension is out of proportion to the injury. Compartment pressure measurements are indicated when there is doubt regarding the diagnosis, and arteriography is necessary if arterial injury is suspected. Adequate anterior decompression with special emphasis on sectioning of the lacertus fibrosus and the lower brachial and forearm fascia should not be delayed.

OSTEOCHONDRAL INJURIES Radius

FIGURE 28-10 Entrapment of the median nerve within the elbow joint may occur as the nerve slips around the medial condyle and is stretched across the posterior aspect of the trochlea. During reduction, the nerve may be caught in the sulcus of the trochlea and imprisoned by the ulnar articular surface. (Redrawn from Pritchard, D. J., Linscheid, R. L., and Svein, H. J.: Intraarticular median nerve entrapment with dislocation of the elbow. Clin. Orthop. Relat. Res. 90:100, 1975.)

(Fig. 28-10). There have been several explanations of the mechanism of intra-articular entrapment of the median nerve. The nerve may be displaced posteriorly through a space created by avulsion of the medial epicondyle or the common flexor origin.82 Tension of the nerve across the margin of the epicondylar flare may “notch” the bone to produce a late radiographic sign known as Matev’s sign, after the investigator who described it.45 The nerve also has been seen to slip through the space between the medial condyle and the collateral ligament and then become entrapped between the trochlea and the semilunar notch on reduction.67 The ulnar nerve is the nerve most frequently injured in elbow dislocations, primarily because of valgus stretching.35,79 The induration, hypertrophy, and ossification present within the cubital tunnel may compress the nerve and diminish gliding, causing persistent symptoms. For this reason, anterior translocation may be considered if progressive resolution of paresthesias and paresis is not apparent.

Loose flecks of bone within the joint following reduction usually represent inclusion of an avulsed fragment of the medial epicondyle or a fragment of the articular surface.23 In the latter case, the fragment is usually significantly larger than the radiographic appearance suggests, owing to the radiolucent chondral layer. Such fragments should be removed or replaced as indicated by the findings. If the joint is explored, débridement, irrigation, and soft tissue replacement should be accomplished as soon as possible.12

LATE CONTRACTURE Limitation of extension is common following dislocation. Bracing and physical therapy are not useful after 1 year. Until that time, especially in the first 6 months, bracing is helpful in regaining lost motion. Decisive intervention as early after injury as possible gives the best results from bracing. If there is sufficient limitation of 30 degrees or more after an attempt at nonsurgical treatment, contracture release may be considered. The anterior capsule is often thickened and shortened. It can be released through a lateral incision or arthroscopically. In either case, there will likely be scar tissue and adhesions posteriorly that also need to be removed. An ulnar incision to decompress the nerve may be necessary.

HETEROTOPIC BONE FORMATION Heterotopic bone formation occurs at three primary locations following dislocation. Ossification in the lateral and medial collateral ligaments occurs frequently and occasionally may be sufficient to cause marked functional impairment. Obviously it does, however, affect the suppleness of the ligaments. Ossification also occurs in the anterior capsule above the coronoid process (Fig. 28-11). Occasionally, marked heterotopic ossification occurs in the brachialis muscle, seriously impairing flexion and extension of the elbow.34,38,75,91 Excision is

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Part V Adult Trauma

FIGURE 28-11

One year following posterior dislocation. A and B, Anterior and lateral ossification consistent with mild heterotopic ossification. (From Linscheid, R. L., and Wheeler, D. K.: Elbow dislocations. J. A. M. A. 194:1171, 1965. © 1965, American Medical Association.)

delayed until the reactive bone mass is mature, usually at 1 year. Excision may be performed between 4 to 6 months after injury. Excision at that time usually allows substantial improvement in motion after excitation of the osteoblastic response has subsided.

AUTHOR’S PREFERRED TREATMENT METHOD After suitable anesthesia, with the patient supine and the arm in the overhead position, the elbow is reduced by recreating the deformity. The elbow is hypersupinated and extended, and a valgus torque is applied; then while a distally directed pressure is applied on the olecranon, the elbow is distracted, flexed, and moved into varus. This is the gentlest way to reduce the coronoid under the trochlea. If reduction has not been achieved, the joint should be observed again under the image intensifier, or radiographs should be made in several planes with traction maintained. If subsequent manipulations fail, open reduction should be considered. For lateral and medial dislocations, the reduction is the same, except that the first step is to reduce the medial or lateral displacement. Divergent dislocation may require separate reduction of each bone, and because of the disruption of the interosseous membrane and other soft tissue damage, greater instability may be expected.

Under normal special circumstances, postreduction splinting for a few days is recommended. Active overhead range-of-motion exercises in the supine position are then commenced. The elbow is kept in a removable splint or hinged brace in pronation between exercises for the first three weeks. Careful follow-up to prevent redislocation, however, is essential. For all dislocations, special care is taken to inform the patient of the possible loss of motion that frequently occurs as a consequence of this injury.

References 1. Abe, M., Ishizu, T., and Morikawa, J.: Posterolateral rotatory instability of the elbow after posttraumatic cubitus varus. J. Shoulder Elbow Surg. 6:405, 1997. 2. Adler, B., and Shaftan, G. W.: Radial head fractures: is excision necessary? J. Trauma 4:115, 1964. 3. Altuntas, A. O., Balakumar, J., Howells, R. J., and Graham, H. K.: Posterior divergent dislocation of the elbow in children and adolescents: A report of three cases and review of the literature. J. Pediatr. Orthop. 25:317, 2005. 4. Basanagoudar, P., Pace, A., and Ross, D.: Paediatric transverse divergent dislocation of the elbow. Acta Orthop. Belg. 72(3):359-361, 2006. 5. Blatz, D. J.: Anterior dislocation of the elbow. Findings in a case of Ehlers-Danlos syndrome. Orthop. Rev. 10:129, 1981. 6. Cohen, M., Hastings, H.: Rotatory instability of the elbow. J. Bone Joint Surg. 79A:225, 1997.

Chapter 28 Elbow Dislocations

7. Conn, J., and Wade, P.: Injuries of the elbow: a ten year review. J. Trauma 1:248, 1961. 8. Coonrad, R. W., Roush, T. F., Major, N. M., and Basamania, C. J.: The drop sign, a radiographic warning sign of elbow instability. J. Shoulder Elbow Surg. 14:312, 2005. 9. DeLee, J. C.: Transverse divergent dislocation of the elbow in a child. J. Bone Joint Surg. 63A:322, 1981. 10. Doornberg, J. N., and Ring, D. C.: Fracture of the anteromedial facet of the coronoid process. J. Bone Joint Surg. 88:2216, 2006. 11. Dryer, R., Buckwalter, J., and Sprague, B.: Treatment of chronic elbow instability. Clin. Orthop. Relat. Res. 100:254, 1974. 12. Durig, M., Muller, W., Ruedi, T. P., and Gauer, E. F.: The operative treatment of elbow dislocation in the adult. J. Bone Joint Surg. 61A:23, 1979. 13. Edward, G. E., and Rostrup, O.: Radial head prosthesis in the management of radial head fractures. Can. J. Surg. 3:153, 1960. 14. Eliason, E. L., and Brown, R. B.: Posterior dislocation at the elbow with rupture of the radial and ulnar arteries. Ann. Surg. 106:1111, 1937. 15. Eppright, R. H., and Wilkins, K. E.: Fractures and dislocations of the elbow. In Rockwood, C. A., and Green, D. P. (eds.): Fractures, Vol I. Philadelphia, J. B. Lippincott Co., 1975. 16. Exarchou, E. J.: Lateral dislocation of the elbow. Acta Orthop. Scand. 48:151, 1977. 17. Eygendaal, D., Verdegaal, S. H., Obermann, W. R., van Vugt, A. B., Poll, R. G., and Rozing, P. M.: Posterolateral dislocation of the elbow joint. Relationship to medial instability. J. Bone Joint Surg. 82:555, 2000. 18. Faber, K. J., and King, G. J. W.: Posterior capitellum impression fracture: a case report associated with posterolateral rotatory instability of the elbow. J. Shoulder Elbow Surg. 7:157, 1998. 19. Fazzi, U. G., and Rymaszewski, L. A.: Recurrent dislocation of the elbow in identical twins. J. Shoulder Elbow Surg. 5:401, 1996. 20. Galbraith, K. A., and McCullough, C. J.: Acute nerve injury as a complication of closed fractures or dislocations of the elbow. Injury 11:159, 1979. 21. Garland, D. E., and O’Hollaren, R. M.: Fractures and dislocations about the elbow in the head-injured adult. Clin. Orthop. Relat. Res. 168:38, 1982. 22. Graham, T. J., Jacobson, P. A., Bamberger, H. B., and Infante, A.: Contemporary management of complex elbow disorders. Am. J. Orthop. Suppl. 33, 1998. 23. Grant, I. R., and Miller, J. H.: Osteochondral fracture of the trochlea associated with fracture-dislocation of the elbow. Injury 6:257, 1976. 24. Greiss, M., and Messias, R.: Irradiable postolateral elbow dislocation: a case report. Acta Orthop Scand. 58:42, 1987. 25. Heusner, L.: Ein Fall von habitueller Luxation des Ellenbogen. In Festschrift zur Feier des funfzigjahrigen Jubilamus des Vereins der Aertze des Regierungsberzirks Dusseldorf. Weisbaden, 1894. 26. Hotchkiss, R. N.: Fractures and dislocations of the elbow. In Rockwood, C. A., Green, D. P., Bucholz, R. W., and

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Heckman, J. D. (eds.): Fractures in Adults. Philadelphia, Lippincott-Raven, 1996, p. 980. Johanson, O.: Capsular and ligamentous injuries of the elbow joint: A clinical and arthrographic study. Acta Chir. Scand. 287 (Suppl):1, 1962. Johnston, G. W.: Followup of 100 cases of fracture of the head of the radius. Ulster Med. J. 31:51, 1962. Josefsson, P. O., Johnell, O., and Wendeberg, B.: Ligamentous injuries in dislocations of the elbow joint. Clin. Orthop. Relat. Res. 221:221, 1987. Kazuki, K., Miyamoto, T., and Ohzono, K.: A case of traumatic divergent fracture-dislocation of the elbow combined with Essex-Lopresti lesion in an adult. J. Shoulder Elbow Surg. 14:224, 2005. King, T.: Recurrent dislocation of the elbow. J. Bone Joint Surg. 35B:50, 1953. Kini, M. G.: Dislocation of the elbow and its complications. J. Bone Joint Surg. 22:107, 1940. Koslowsky, T. C., Mader, K., Siedek, M., and Pennig, D.: Treatment of bilateral elbow dislocation suing external fixation with motion capacity: A report of two cases. J. Orthop. Trauma 20:499, 2006. Krishan, M.: Myositis ossificans traumatic of the elbow. Int. Surg. 57:475, 1972. Krishnamoorthy, S., Bose, K., and Wong, K. P.: Treatment of old unreduced dislocation of the elbow. Injury 8:39, 1976. Linscheid, R. L., and Wheeler, D. K.: Elbow dislocations. J. A. M. A. 194:1171, 1965. Lippe, C. N., Williams, D. P.: Combined posterior and convergent elbow dislocations in an adult. A case report and review of the literature. J. Bone Joint Surg. 87:1597, 2005. Loomis, L. K.: Reduction and aftertreatment of posterior dislocation of the elbow. With special attention to the brachialis muscle and myositis ossificans. Am. J. Surg. 63:56, 1944. Louis, D., Ricciardi, J., and Spengler, D.: Arterial injury: a complication of posterior elbow dislocation. J. Bone Joint Surg. 56A:1631, 1979. MacSween, W. A.: Transposition of radius and ulna associated with dislocation of the elbow in a child. Injury 10:314, 1979. Mahaisavariya, B., and Laupattarakasem, W.: Neglected dislocation of the elbow. Clin. Orthop. Relat. Res. 431:21, 2005. Mantle, J. A.: Recurrent posterior dislocation of the elbow. J. Bone Joint Surg. 48B:590, 1966. Marcheix, B., Chaufour, X., Avel, J., Hollington, L., Mansat, P., Barret, A., and Bossavy, J.: Transection of the brachial artery after closed posterior elbow dislocation. J. Vasc. Surg. 42:1230, 2005. Martin, D. J., Fazzi, U. G., and Leach, W. J.: Brachial artery transection associated with closed and open dislocation of the elbow. Eur. J. Emerg. Med. 12:30, 2005. Matev, I.: A radiological sign of entrapment of the median nerve in the elbow joint after posterior dislocation: a report of two cases. J. Bone Joint Surg. 58B:353, 1976. Maylahn, D. J., and Fahey, J. J.: Fractures of the elbow in children: review of three hundred consecutive cases. J. A. M. A. 166:220, 1958.

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47. McKee, M. D., Schemitsch, E. H., Sala, M. J., and O’Driscoll, S. W.: The pathoanatomy of lateral ligamentous disruption in complex elbow instability. J. Shoulder Elbow Surg. 12:391, 2003. 48. Melhoff, T. L., Noble, P. C., Bennett, J. B., and Tullos, H. S.: Simple dislocation of the elbow in the adult. J. Bone Joint Surg. 70A:244, 1988. 49. Morrey, B. F.: Complex instability of the elbow. J. Bone Joint Surg. 79A:460, 1997. 50. Morrey, B. F., and An, K. N.: Articular ligamentous contributions to the stability of the elbow joint. Am. J. Sports Med. 11:315, 1983. 51. Morrey, B. F.: Fractures and dislocations of the elbow. In Gustillo, R. (ed.): Preparation, Fractures and Dislocations. Vol. I. Chicago, Year Book Publishers, 1993, pp. 387-499. 52. Neviaser, J. S., and Wickstrom, J.: Dislocation of the elbow: a retrospective study of 115 patients. South. Med. J. 70:172, 1977. 53. Noonan, K. J., and Blair, W. F.: Chronic median-nerve entrapment after posterior fracture-dislocation of the elbow. J. Bone Joint Surg. 77A:1572, 1995. 54. Nybonde, O. E. T., and Karlsson, G.: Luxation of the elbow complicated by proximal radioulnar translocation. Acta Radiol. 31:146, 1990. 55. O’Driscoll, S. W., Bell, D. F., and Morrey, B. F.: Posterolateral rotatory instability of the elbow. J. Bone Joint Surg. 73A:440, 1991. 56. O’Driscoll, S. W.: Classification and evaluation of recurrent instability of the elbow. Clin. Orthop. Relat. Res. 370:34, 2000. 57. O’Driscoll, S. W.: Coronoid fractures. In Norris, T. R. (ed.): Orthopaedic knowledge update: Shoulder and elbow 2. 2nd ed. Rosemont American Academy of Orthopaedic Surgeons; 2002. p. 379. 58. O’Driscoll, S. W.: Instability. Hand Clin. 10:405, 1994. 59. O’Driscoll, S. W., Jupiter, J. B., Cohen, M. S., Ring, D., and McKee, M. D.: Difficult elbow fractures: Pearls and pitfalls. Instr. Course Lect. 52:113, 2003. 60. O’Driscoll, S. W., Jupiter, J. B., Cohen, M. S., Ring, D., and McKee, M. D.: Difficult elbow fractures: pearls and pitfalls. Instruct. Course Lect. 1:465, 2005. 61. O’Driscoll, S. W., Morrey, B. F., Korinek, S., and An, K. N.: Elbow subluxation and dislocation: A spectrum of instability. Clin. Orthop. Relat. Res. 280:186, 1992. 62. O’Hara, J. P., Morrey, B. F., Johnson, E. W., and Johnson, K. A.: Dislocations and fractured dislocations of the elbow. Fracture Conference. Minn. Med. 58:697, 1975. 63. Olsen, B. S., Sojbjerg, J. O., Nielsen, K. K., Vaesel, M. T., Dalstra, M., and Sneppen, O.: Posterolateral elbow joint instability. The basic kinematics. J. Shoulder Elbow Surg. 7:19, 1998. 64. Osborne, G., and Cotterill, P.: Recurrent dislocation of the elbow. J. Bone Joint Surg. 48B:340, 1966. 65. Papandrea, R. F., Morrey, B. F., and O’Driscoll, S. W.: Reconstruction for persistent instability of the elbow after coronoid fracture-dislocation. J. Shoulder Elbow Surg. 16:68, 1997. 66. Pawlowski, R. F., Palumbo, F. C., and Callahan, J. J.: Irreducible posterolateral elbow dislocation: report of a rare case. J. Trauma 10:260, 1970.

67. Pritchard, D. J., Linscheid, R. L., and Svein, H. J.: Intraarticular median nerve entrapment with dislocation of the elbow. Clin. Orthop. Relat. Res. 90:100, 1973. 68. Protzmann, R. R.: Dislocation of the elbow joint. J. Bone Joint Surg. 60:539, 1978. 69. Purser, D. W.: Dislocation of the elbow and inclusion of the medial epicondyle in the adult. J. Bone Joint Surg. 36B:247, 1954. 70. Rana, N. A., Kenwright, J., Taylor R. G., and Rushworth, G.: Complete lesion of the median nerve associated with dislocation of the elbow joint. Acta Orthop. Scand. 45:365, 1974. 71. Rasool, M. N.: Dislocations of the elbow in children. J. Bone Joint Surg. 86B:1050, 2004. 72. Regan, W., and Morrey, B. F.: Fractures of the coronoid process of the ulna. J. Bone Joint Surg. 71A:1348, 1989. 73. Ring, D., and Jupiter, J. B.: Compass hinge fixator for acute and chronic instability of the elbow. Oper. Orthop. Traumatol. 17:143, 2005. 74. Ring, D., and Jupiter, J. B.: Fracture-dislocation of the elbow. J. Bone Joint Surg. 80:566, 1997. 75. Roberts, J. B., and Pankratz, D. G.: The surgical treatment of heterotopic ossification at the elbow following longterm coma. J. Bone Joint Surg. 61A:760, 1979. 76. Roberts, P. H.: Dislocation of the elbow. Br. J. Surg. 56:806, 1969. 77. Scharplatz, D., and Allgower, M.: Fracture dislocations of the elbow. Injury 7:143, 1975. 78. Schwab, G. H., Bennett, J. B., Woods, G. W., and Tullos, H. S.: Biomechanics of elbow instability: The role of the medial collateral ligament. Clin. Orthop. Relat. Res. 146:42, 1980. 79. Scharma, R. K., and Covelle, N. A.: An unusual ulnar nerve injury associated with dislocation of the elbow. Injury 8:145, 1976. 80. Smith, D. N., and Lee, J. R.: The radiological diagnosis of posttraumatic effusion of the elbow joint and its clinical significance: the “displaced fat pad” sign. Injury 10:115, 1978. 81. Spear, H. C., and Janes, J. M.: Rupture of the brachial artery accompanying dislocation of the elbow or supracondylar fracture. J. Bone Joint Surg. 33A:889, 1951. 82. Strange, F. G., St. Clair: Entrapment of the median nerve after dislocation of the elbow. J. Bone Joint Surg. 64B:224, 1982. 83. Strong, M. L.: Irreducible posterolateral dislocation of the elbow without fracture. Report of two cases. Contemp. Orthop. 11:69, 1985. 84. Sturm, J. T., Rothenberger, D. A., and Strate, R. G.: Brachial artery disruption following closed elbow dislocation. Trauma 18:364, 1978. 85. Subasi, M.: Neglected dislocation of the elbow. Clin. Orthop. Relat. Res. 439:292, author reply 292, 2005. 86. Symeonides, P. P., Paschaloglou, C., Stavrou, Z., and Pangalides, T.: Recurrent dislocation of the elbow. J. Bone Joint Surg. 57A:1084, 1975. 87. Tan, V., Daluiski, A., Capo, J., and Hotchkiss, R.: Hinged elbow external fixators: indications and uses. J. Am. Acad. Orthop. Surg. 13:503, 2005.

Chapter 28 Elbow Dislocations

88. Tayob, A. A., and Shively, R. A.: Bilateral elbow dislocations with intraarticular displacement of the medial epicondyles. J. Trauma 20:332, 1980. 89. Trias, A., and Comeau, Y.: Recurrent dislocation of the elbow in children. Clin. Orthop. Relat. Res. 100:74, 1974. 90. Thomas, T. T.: A contribution to the mechanism of fractures and dislocations in the elbow region. Ann. Surg. 89:108, 1929. 91. Thompson, H., and Garcia, A.: Myositis ossificans: aftermath of elbow injuries. Clin. Orthop. Relat. Res. 50:129, 1967. 92. Van Rossum, J., Buruma, O. J. J., Kamphuisen, H. A. C., and Onolee, G. J.: Tennis elbow-a radial tunnel syndrome? J. Bone Joint Surg. 60B:197, 1978. 93. Venkatram, N., Wurm, V., and Houshian, S.: Anterior dislocation of the ulnar-humeral joint in a so-called “pulled elbow.” Emerg. Med. J. 23:e37, 2006.

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94. Walker, R. H., and Tanner, J. B.: Fracture of the proximal shaft of the radius associated with posterior dislocation of the elbow. Clin. Orthop. Relat. Res. 168:35, 1982. 95. Wheeler, D. K., and Linscheid, R. L.: Fracture dislocations of the elbow. Clin. Orthop. Relat. Res. 50:95, 1967. 96. Wiley, J. J., Pegington, J., and Horwich, J. P.: Traumatic dislocation of the radius at the elbow. J. Bone Joint Surg. 56B:501, 1974. 97. Wilson, P. D.: Fractures and dislocations in the region of the elbow. Surg. Gynecol. Obstet. 56:335, 1933. 98. Woods, W., and Tullos, H.: Elbow instability and medial epicondyle fractures. Am. J. Sports Med. 5:23, 1977.

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CHAPTER

29

Complex Instability of the Elbow Bernard F. Morrey and Shawn W. O’Driscoll

INTRODUCTION Since the first edition of this book, improvements in the recognition and treatment of complex instability are among the most significant developments in managing elbow trauma. The coexistence of multiple articular and soft tissue injuries is being increasingly appreciated.9,42

DEFINITION Complex instability of the elbow is defined as an injury that destabilizes the elbow because of damage to the articular surface and to the ligamentous structures.21 Others add soft tissue involvement, including neural and vascular injuries in the diagnosis.36 However, vascular injuries are uncommon in this setting. Over a 10-year period, for example, Moneim and Garst20 documented only two instances of vascular injury among 56 with fracture dislocation injury. The clinical presentation is usually one in which the instability is obvious, but more subtle forms are being recognized.39 In this chapter, the relative contributions of the articulation and the ligaments to normal stability, as well as to their interactions, are first defined. We then offer a rationale for the reliable treatment of a spectrum of these acute injuries.

CONTRIBUTIONS TO NORMAL STABILITY ARTICULAR ELEMENTS Although the distal humerus is sometimes involved, for the purpose of this discussion, it is assumed that the distal humerus is intact. Therefore, the articular elements to be considered are the radial head, olecranon, and coronoid. The relative role of these elements to elbow stability have been recently reviewed.27

Radial Head It is known clinically that the radial head may be resected without altering the stability of the otherwise normal

elbow.27 Therefore, the contribution of the radiohumeral joint to elbow stability is intimately related to and dependent on the integrity of the collateral ligaments. Experimental data have clearly documented that the resistance to valgus stress provided by the radial head is minimal when the medial collateral ligament is intact24,25,40 (Fig. 29-1). However, the radiohumeral joint offers enough resistance to valgus stress to prevent subluxation if the medial collateral ligament is attenuated or torn. The major structure resisting initial valgus displacement, even with an intact radial head, is the medial collateral ligament. If the medial collateral ligament is intact, the radial head offers little resistance to valgus stress, but if the medial collateral ligament is attenuated or torn, the radial head assumes the role of an important stabilizer. Thus, the radial head is an important secondary stabilizer to valgus stability. The relationship of the radial head to the ulnar part of the lateral collateral ligament has been initially defined experimentally by O’Driscoll and associates.30,32 Today, posterolateral rotatory instability is well recognized to be associated with lateral ulnar collateral deficiency5,19,33 and can occur in the presence or absence of the radial head. However, clinical experience suggests that elbows without a radial head do less well after reconstruction of the ulnar part of the lateral collateral ligament than do those in which the radial head is intact.2,29 This provides further evidence of the important role of the radial head to resist posterolateral rotatory instability but, once again, in a secondary capacity.

Olecranon The major determinant of stability of the elbow is clearly the ulnohumeral joint, specifically the coronoid. Although the stabilizing influence of this joint has not been studied to any great extent, the relative contribution of the olecranon in resisting various loading configurations has been shown to be linearly correlated with the extent of resection of the proximal part of the ulna (Fig. 29-2).1 The critical amount of articulation required for maintaining stability is about 50%. These data may be altered by dynamic forces, but this has not been studied.

Coronoid The amount of the coronoid required for stability with or without ligamentous integrity and with and without the radial head is just now emerging. Experimental and clinical experience suggests that at least 50% of the coronoid must be present for the ulnohumeral joint to be functional (Fig. 29-3). Absence of the radial head further and dramatically compromises the elbow with a 50% coronoid deficiency. From a practical perspective, we have found it useful to observe that the typical 30degree angle formed by a line from the intact olecranon and coronoid is reduced to 0 degrees when the critical

Chapter 29 Complex Instability of the Elbow

1

1

2

Stability

2

451

RH

MCL

MCL

RH

FIGURE 29-1

Demonstration of the radial head as a secondary stabilizer when the medial collateral ligament is intact (2) and the radial head may be removed (1). However, if the medial collateral ligament is released after the radial head has been resected, marked instability occurs. The alternative situation is one in which the radial head is left intact. In this setting, when the medial collateral ligament is resected, some instability occurs but the gross instability is seen only when the radial head has been removed-thus the designation of the radial head as a secondary stabilizer.

50% of the coronoid is present (Fig. 29-4). Anatomically and clinically, the coronoid is the subject of intense investigation to better understand fracture patterns, and the “critical portion” needed for stability.4

Combined elbow stability (% of intact)

100

80

LIGAMENTOUS CONTRIBUTIONS 60

25 75 50 100

40 Elbow angle 0° 90°

20

0 25

50

75

100

Excision of proximal ulna (% osteotomy)

FIGURE 29-2

The articular contribution of the proximal ulna in various loading modes and in various flexion positions demonstrates that the articulation contributes to stability to the extent that it is present. Thus, approximately 25% stability is lost when 25% is removed, 50% is lost when 50% is removed. However, the collateral ligaments are contained in the distal 25%; thus, at least 75% and ideally 50% of the olecranon should be present to provide ulnohumeral stability.

The relative contributions of the medial and lateral collateral ligaments to varus-valgus stability with the elbow articulation intact and in flexion and extension have been studied experimentally.23 This investigation has shown that the collateral ligaments provide approximately 50% of the varus-valgus stability of the joint, and the articular surfaces provide an additional 50%. The only exception is with the elbow in full extension: under this condition, the ulnohumeral joint and anterior capsule render the elbow stable to varus-valgus stress, even in the absence of collateral ligaments. The role of the ligaments in conjunction with the articulation is described earlier.

CLINICAL MANAGEMENT: PRINCIPLE A basic principle underlying the treatment of complex instability is simply that a competent ulnohumeral joint

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1.00 Ulnohumeral translation (cm)

0.90 0.80

30°

0.60 0.50 0.40 0.30

Intact, ligaments in place 50% resection 75% resection 100% resection

0.20 0.10 0.00 0.0

A

50.0

100.0

150.0

Flexion angle (degrees) 1.00

Ulnohumeral translation (cm)

0.90 0.80

FIGURE 29-4

When the coronoid is intact, the line between the tip of the olecranon and the coronoid makes approximately a 30-degree angle with the shaft of the humerus. However, when 50% of the coronoid is absent, a line through the remnant and the tip of the olecranon is approximately parallel to the shaft of the ulna. This information is useful to the clinician in assessing the amount of coronoid present, which has direct implications for treatment options and strategy.

level of suspicion that an injury to the ligament might be present when there is a compression fracture with or without comminution of the radial neck. Ecchymosis on the medial side of the elbow should be an obvious clue but is often absent.

0.70 0.60 0.50 0.40 0.30

Intact, ligaments in place 50% resection 75% resection 100% resection

0.20 0.10 0.00 0.0

B

50%

0.70

50.0

100.0

150.0

Flexion angle (degrees)

FIGURE 29-3 Experimental study measuring ulnohumeral translation with resection of various portions of the coronoid demonstrates instability both with (A) and without (B) the radial head. However, when as much as 50% of the coronoid is present, the degree of instability is dramatically reduced and the ulnohumeral joint approaches normal. These data were obtained after releasing the ligaments, common flexor-extensor tendons, and capsule. The testing was performed with the elbow in the neutral (sagittal) plane and no unbalanced varus-valgus moments.

be attained and maintained.21,31 This is the primary overriding principle.

FRACTURE OF THE RADIAL HEAD WITH ATTENUATION OR TEAR OF THE MEDIAL COLLATERAL LIGAMENT The presentation of medial ligament injury can be extremely subtle. The prevalence is difficult to ascertain, but in my experience, as an isolated lesion, it has occurred only in about 1% to 2% of patients who had a fracture of the radial head.22 One should have a high

Treatment Treatment of this difficult structured problem is based on the realization that the medial collateral ligament tends to heal if the ulnohumeral joint is reduced. Furthermore, the radial head is an important secondary stabilizer to valgus stress when the medial collateral ligament has been disrupted. The primary goal of the treatment strategy is to restore ulnohumeral joint stability. However, a reconstructed medial collateral ligament has been observed to stretch in the absence of radial humeral integrity; hence, if it is amenable to fixation, the fracture is fixed; if not, the head is replaced. If the arc is stable within 40 degrees of extension, unrestricted passive motion is allowed after 7 to 10 days of protection. If dislocation occurs with extension of approximately 60 degrees, the elbow is immobilized for 10 days, after which motion in a Mayo Elbow Brace with a 45-degree extension stop, is allowed for 2 weeks. In our practice, the collateral ligament need not be repaired in those with a stable ulnohumeral, radiohumeral joint. Nonetheless, the popularity of suture anchors has prompted a more aggressive attitude toward ligament repair. Rodgers and colleagues38 report 88% satisfactory results in 17 patients treated with suture anchors who had major elbow injuries. If osteosynthesis is not possible, then restoration of the radiohumeral joint with the use of a prosthesis becomes a higher priority. Prostheses of today are considerably more effective than in the past. Therefore, the possibility of use of metal implants has been

Chapter 29 Complex Instability of the Elbow

reintroduced.7,12,15 In some instances in which the medial collateral ligament has been disrupted, replacement of the radial head with an allograft has been performed as an alternative method of providing stabilization (Fig. 29-5A and B). If the radiohumeral joint cannot be effectively reconstructed, it is appropriate to address the injury of the medial collateral ligament directly and to repair it as soon as possible. The ligament may be avulsed from its origin or insertion, allowing direct reattachment. Midsubstance tears are more difficult to repair, and there is less likelihood of achieving immediate stabilization. Finally, a hinged external fixator is applied in those circumstances in which it is desirable to protect a fractured radial head, the coronoid, or to protect a ligament repair (see Chapter 33).3,13,17 There are several articulated fixators available, but for this indication, Kamineni has shown that the simple half-pin configuration of the Dynamic Joint Distractor (DJDII) (Stryker, Mahwah, NJ) is effective to stabilize the joint even in the absence of both collateral ligaments. Hence, because of cost and simplicity, this is our choice of devices (Fig. 29-6).13 If the fixator is not used, patients are fitted with the Mayo Brace in the locked mode for protection for about 2 weeks postoperatively; the brace is then unlocked, and motion is allowed in the brace through the stable arc. The hinged brace is worn for a total of at least 6 weeks or until the joint is considered stable.

FIGURE 29-5

453

FRACTURES OF THE RADIAL HEAD WITH DISLOCATION OF THE ELBOW This lesion is often referred to as a Mason type IV injury, an extension of the original Mason classification of fractures10,27 (see Chapter 24). This association was observed in 59 of the 333 radial head fractures assessed for associated injuries.42 The simple principle defined earlier continues to be relevant. If it is clearly demonstrated that the coronoid is intact, the basic treatment principle is first to reduce the dislocation and then to determine the extent to which the ulnohumeral articulation is inherently stable. Treatment of the radial head is determined according to the type of fracture.27

Type I Fractures In type I injuries, if the elbow is stable to within 45 or 50 degrees of extension, nothing more need be done except to place the elbow in a splint at 60 degrees flexion to be worn for 1 to 2 weeks. Full extension is then allowed as tolerated usually without protection.

Type II Fractures Type II fractures are treated by open reduction and internal fixation. These injuries are the most amenable to such treatment. King and associates14 report a successful outcome in all eight patients so treated. It is

A, Radiograph showing gross valgus instability in a patient who had resection of the radial head in the presence of an unrecognized disruption of the medial collateral ligament. B, Two years after reconstruction with an allograft, the patient had excellent function.

454

Part V Adult Trauma

FIGURE 29-6

A, Radiograph showing a severe fracture-dislocation of the elbow (a Mason type-III fracture of the radial head). The fracture of the radial head was treated with internal fixation. Because of gross instability, additional stabilization was achieved with use of the Dynamic Joint Distractor (B).

essential that elbows with injuries of the collateral ligaments be treated with open reduction and internal fixation, because these injuries result in chronic instability if the radial head is resected.6,7,12,37 Because these fractures are amenable to such treatment, repair of the medial collateral ligament to a great extent becomes personal preference. One of us (BFM) rarely fixes this ligament, whereas the other author (SOD) is more aggressive in this regard. However, if the elbow remains unstable on examination through the arcs described earlier, enhanced stability is obtained by repairing or stabilizing the medial collateral ligament. Josefsson and associates11 reviewed their experience with 19 complex injuries of the elbow and recommended open reduction and internal fixation of the radial head fracture as well as repair of the medial ligament. However, treatment of 4 of 19 coronoid fractures had a poor result, suggesting that this component of the lesion must be specifically addressed. Without question, the lateral ulnar collateral ligament must be formally and securely fixed. If uncertainty as to stability still exists, we then resort to the use of the external fixator.

Type III Fractures These are the most difficult injuries to treat. Experience has suggested that the entire comminuted radial head should be excised acutely if it cannot be fixed.2 Open reduction and internal fixation is technically difficult and was reported to be successful in only two of six instances by King and colleagues.14 We now know those fractures with more than four fragments should be excised, not

fixed. A prosthesis is then used and is considered an essential component of the treatment. A review of the literature regarding treatment with several metallic radial head implants reveal an overall success rate of about 90% when managed acutely (Table 29-1). The elbow is tested according to the scheme described for type I fractures. If the elbow is unstable, then direct repair of the medial collateral ligament might be considered. If stability remains a problem, a hinged external fixator that allows elbow motion is applied. The indication for use of the external fixator is a joint with a healing radial head with a torn medial collateral ligament that remains unstable (see Chapter 33). If use of an implant or open reduction and internal fixation of the radial head does not restore stability, the distraction device allows congruous alignment of the ulnohumeral joint, allowing motion which lessens the likelihood of stiffness or of fracture displacement. The device is removed as early as the third to fourth week and as late as 12 weeks, after which adjustable splints are used to restore motion (see Chapter 12).

FRACTURE OF THE PROXIMAL PART OF THE ULNA Fractures of the proximal part of the ulna, both the olecranon or coronoid, pose major treatment problems.22 As always, management consists of restoring the integrity of the ulnohumeral joint, as just described. Ideally, this is accomplished by reduction and stabilization of the fracture.

Chapter 29 Complex Instability of the Elbow

455

Summary of 15 Years Literature Involving Prosthetic Radial Head Replacement

TABLE 29-1

PROSTHETIC INTERVENTION TOTAL # (% SATISFACTORY) Delayed

Total

FU/yrs

—

31 (94)

4.5

7 (72)

14 (86)

4

30 (73)

—

15 (67)

2

Yr

Knight et al15

1993

Mono

31 (94)

Judet et al12

1996

Bipolar

7 (100)

1998

Mono

—

2000

Bipolar

13 (77) 11 (83)

Wick et al

43 39a

Smets et al

34a

Type

Acute

Author

—

Popovic et al

2000

Bipolar

Harrington et al7a

2001

Mono

—

Holmenschlager et al7b

2002

Bipolar

Arnot

2003

Bain Doornberg et al4

2 (0) —

11 (83)

2.5

—

20 (80)

12

10 (100)

6 (67)

16 (87)

1.5

Bipolar

18 (100)

4 (0)

22 (82)

1.5

2005

Mono

10 (100)

6 (50)

16 (81)

2.8

2006

Mono

27 (82)

None

27 (82)

3.5

127 (92)

25 (48)

202 (82)

3-4 yr

Total (% satisfied)

Type III Unstable

A-Noncomminuted

B-Comminuted

FIGURE 29-7

Left and Right Panels, A Mayo type III ulnar fracture may or may not be comminuted, but it is characterized by attenuation or disruption of the medial collateral ligament or the ulnar part of the lateral collateral ligament, or both. This is characterization by instability of the forearm.

FRACTURE OF THE OLECRANON The Mayo classification scheme for fractures of the olecranon is based on displacement, comminution, and stability22 (see Chapter 25). The injury discussed here is termed type III, meaning that the elbow is unstable because of injury both to a collateral ligament and from a displaced fracture of the olecranon (Fig. 29-7). In fact, some might appropriately consider this a Monteggia variant9 and others have referred to this as a transolecranon anterior fracture dislocation.28,37 The type III fracture of the olecranon is accompanied by ligamentous disruption. The principle is again applied:

stabilize the ulnohumeral joint (Fig. 29-8). If there is minimum comminution of the olecranon, rigid plate fixation restores the ulnohumeral joint. If the olecranon is rigidly fixed, then the unstable injury is converted to a stable one because the ulnohumeral joint is inherently stable. Hence, the technique for rigid fixation of the fracture is of paramount importance (see Fig. 29-8). A 3.5-mm dynamic compression or low-contour dynamic compression plate bent at an 80-degree angle or precontoured plate applied to the posterior surface of the ulna permits excellent fixation on the small proximal fragment.32 Commonly, one fragment may also involve the coronoid. If it does, this is the most important com-

456

Part V Adult Trauma

A

B

C

FIGURE 29-8

When there has been disruption of the collateral ligament and alteration of the ulnohumeral joint, the ulnohumeral joint must be somehow stabilized. This may occur by rigid plate fixation if the fracture allows (A), by rigid fixation of the coronoid if the fracture allows (B), or by neutralization of the ulnohumeral relationship if the fractures do not allow rigid fixation (C).

ponent of the reduction and fixation. If these principles are followed, a success rate of 88% has been reported in series of 828 and 15 patients.37

FRACTURE OF THE CORONOID Without question, the coronoid is the most important portion of the ulnohumeral articulation. This is related to the posteriorly directed forces of both the biceps and the triceps that tend to “drive” the humerus into the coronoid fracture (Fig. 29-9). The base also serves as a site of attachment for the collateral ligaments.

Type I Fracture According to the classification of Regan and Morrey, type I fractures represent a small chip of the tip of the coronoid and serve mainly as an indicator that the elbow has dislocated or at least displaced sufficiently to have sustained an injury of the collateral ligaments.35 The ulnohumeral joint is stable, and rehabilitation is similar to that recommended for type I fracturedislocations of the radial head. Open reduction is not necessary if the elbow is stable. Occasionally, the fragment will become symptomatic as a snapping or catching requiring arthroscopic removal.16

Type II Fracture In type II fractures, as much as 50% of the coronoid is involved and the elbow is usually unstable, especially if the radial head is also fractured. Careful examination with the patient under anesthesia reveals whether the joint is stable after reduction (Fig. 29-10). The threshold for fixation varies with individual surgeons but we are

aggressive with any hint of instability. If the reduction is stable, motion within the stable arc, as described previously, may be allowed (see Fig. 29-10). If posterior displacement occurs with less than 40 to 45 degrees of flexion, the articulation is considered inadequate, and the ulnohumeral joint must be stabilized. If the fracture fragment is large enough for fixation, osteosynthesis with a single screw is performed. We approach the fracture laterally if the radial head is to be removed and medially if the head is intact. If the fragment is too small for fixation, a heavy No. 5 suture is placed through the fragment (or fragments), which is brought to its anatomic location and tied through drill holes placed in the ulna. In the latter situation, or even if osteosynthesis has been carried out but there is concern about stability, the elbow may need to be neutralized by the application of a hinged external fixatora-as the external fixator eliminates the dynamic forces that are applied to the fracture site by the muscles that flex and extend the elbow joint (Fig. 29-11). The device allows motion of the ulnohumeral joint while a distraction force is placed on the ulna, thus protecting the articulation. The device is maintained for 3 to 6 weeks, depending on the nature of the injury.3 Cobb and Morrey3 reported on seven such injuries and documented a successful outcome in six. In that series, the coronoid fracture was treated as described earlier, and a distraction device was applied in each instance.

Type III Fracture These injuries are the most difficult to treat because, by definition, they render the ulnohumeral joint grossly unstable. If the coronoid is a large fragment and has not

Chapter 29 Complex Instability of the Elbow

457

FIGURE 29-9 A, Radiograph showing a Mayo type III ulnar fracture and a fracture of the radial head. B, The fracture was treated with rigid plate fixation, and resection of the radial head was required; stabilization of the joint was supplemented by an external fixator (B). Excellent result at 1 year (C).

BC

BR TR

FIGURE 29-10 The anterior displacement of the humerus into the coronoid is brought about by the posterior directed vector occurring with elbow flexion that is a component of triceps (TR), brachialis (BR), or biceps (BC) contraction. Thus, there is a tendency for posterior ulnar translation with both flexion and extension movements.

458

Part V Adult Trauma

FIGURE 29-11 Radiograph showing a Regan and Morrey type II coronoid fracture with elbow dislocation (A). The fracture was treated with reduction and fixation and buttress plate, further supplemented by the Dynamic Joint Distractor (B). At 2 months, the fracture has healed (C) and the range of motion is between 20 to 120 degrees (D, E).

been comminuted (type IIIA), it may be fixed with one or two screws and the joint will be stable. However, because of the large forces transmitted through this relatively small surface area, as with the type II fractures, these injuries may be further neutralized with the dis-

traction device. Jeon and colleagues8 highlighted the difficulty in the management in eight patients with this fracture. The severely comminuted coronoid fracture (type IIIB) is a very difficult injury. In this setting, I reduce the

Chapter 29 Complex Instability of the Elbow

459

FIGURE 29-12 When there has been internal fixation in the proximal ulna the dynamic joint distractor is applied in such a way as to result in a distal displacement force on the ulna that allows realignment of the ulnohumeral joint. Current design favors half pins and eliminates the axis pin, lessening the likelihood of infection.

elbow and bring the fracture fragments into relative alignment with the use of a heavy suture or a buttress plate is employed if the fracture pattern is amenable to this type of stabilization. I avoid removing any bone fragments because they may serve as a basis for substantive healing and formation of callus. The ulnohumeral relationship is maintained in a reduced position by the distraction device (Fig. 29-12). In every instance, the most important goal is to prevent posterior displacement of the ulna against the trochlea—thus, the concept of neutralization with an external fixator that permits flexion and extension while keeping the articulation aligned and eliminating the disruptive force from muscle contracture (see Fig. 29-12). The principle of restoration and maintenance of the ulnohumeral integrity has been followed. After the fixator is removed, we typically use a hinged brace, which further protects the collateral ligaments for an additional 4 to 8 weeks (Fig. 29-13).

Fracture of the Radial Head and Coronoid with Dislocation These injuries, termed the unhappy triad, are the most difficult to treat. The principle is the same as already discussed: the radial head must be fixed or replaced. The coronoid fracture is fixed, if possible, with use of a direct or retrograde or posigrade screw. In either instance, the elbow may need to be protected by a hinged external fixator. This allows motion but eliminates force on the radial head and the coronoid. Once again, the lateral

ligament is always fixed. We typically use a No. 5 absorbable running locked stitch.18

OVERVIEW OF PRINCIPLES TREATMENT These basic principles of management are becoming well accepted. 1. The first principle for treating the complex injuries of the elbow is to restore the essential element, the ulnohumeral joint (Fig. 29-14). This is done by reduction of the intact joint or, if the coronoid or the olecranon has fractured, by osteosynthesis. 2. The second principle is that the radial head is an important secondary stabilizer, which must be fixed or replaced if the ulnohumeral joint has been compromised. 3. The lateral collateral ligaments should be repaired in all cases. 4. If the medial ligament is deficient, it is repaired or the complex is stabilized by an external fixator. 5. Efforts to restore the ulnohumeral articulation are enhanced by protection with a hinged external fixator that allows motion. The implications for rehabilitation and the exact degree of instability are best determined after the ulnohumeral joint has been reduced

460

Part V Adult Trauma

A

B FIGURE 29-13 The Mayo elbow brace (Don Joy) allows full flexion (A) and extension (B) as well as provides for a flexion/extension torque delivered through the screw mechanism.

No

Can be fixed rigidly

Ulnohumeral intact

Yes

CONSIDER SECONDARY CONSTRAINTS

Yes

Yes

Stable arc

RADIOHUMERAL INTACT

No

ORIF possible

No

Yes

Stable arc No

Yes No

No

Implant/ allograft

Yes

Ligaments repaired

Stable arc

No

Consider ligament repair

No

Stable arc

Yes

Yes Hinged ex fix

Motion in stable arc

Motion in stable arc

Hinged ex fix

Motion in stable arc

FIGURE 29-14 Treatment logic for complex instability. Notice the pre-eminent status of the integrity of the ulnohumeral joint.

Chapter 29 Complex Instability of the Elbow

and the elbow has been moved through an arc of motion. 6. If there is any tendency for the elbow to subluxate or dislocate within 45 degrees of extension, the primary or secondary constraints have not adequately been restored. The situation is reassessed. 7. Finally, without question, the best time for a successful outcome is proper management of the acute fracture. The best times to reconstruct chronic dislocation or to address early arthritis are unpredictable at best.34,41

References 1. An, K. N., Morrey, B. F., and Chao, E. Y. S.: The effect of partial removal of proximal ulna on elbow constraint. Clin. Orthop. Relat. Res. 209:270, 1986. 2. Broberg, M. A., and Morrey, B. F.: Results of treatment of fracture-dislocations of the elbow. Clin. Orthop. Relat. Res. 216:109, 1987. 3. Cobb, T. K., and Morrey B. F.: Use of distraction arthroplasty in unstable fracture dislocations of the elbow. Clin. Orthop. Relat. Res. 312:201, 1995. 4. Doornberg, J. N., van Duijn, J., and Ring, D.: Coronoid fracture height in terrible-triad injuries. J. Hand Surg. 31:794, 2006. 5. Dunning, C. E., Zarzour, Z. D., Patterson, S. D., Johnson, J. A., and King, G. J.: Ligamenotus stabilizers against posterolateral rotatory instability of the elbow. J. Bone Joint Surg. 83:1823, 2001. 6. Geel, C. W., Palmer, A. K., Ruedi, T., and Leutenegger, A. F.: Internal fixation of proximal radial head fractures. J. Orthop. Trauma 4:270, 1990. 7. Harrington, I. J., and Tountas, A. A.: Replacement of the radial head in the treatment of unstable elbow fractures. Injury 12:405, 1981. 7a. Harrington, I. J., Sekyi-Out, A., Barrington, T. W., Evans, D. C., and Tuli, V.: The functional outcome with metallic radial head implants in the treatment of unstable elbow fractures: A long-term review. J. Trauma 50:46, 2001. 7b. Holmenschlager, F., Halm, J. P., and Winckler, S.: Les fractures fraîches de la tête radiale. Résultants de la prothèse à cupule flottant de Judet. Rev. Chir. Orthop. Reparatrice Appar. Mot. 88:387, 2002. 8. Jeon, I. H., Oh, C. W., Kyung, H. S., Park, B. C., Kim, P. T., and Ihn, J. C.: Functional outcome after operative treatment of eight type III coronoid process fractures. J. Trauma 59:418, 2005. 9. Jepegnanam, T. S.: Salvage of the radial head in chronic adult Monteggia fractures. Report of four cases. J. Bone Joint Surg. 88:645, 2006. 10. Johnston, G. W.: A follow-up of 100 cases of fracture of the head of the radius with a review of the literature. Ulster Med. J. 31:51, 1962. 11. Josefsson, P. O., Gentz, C. F., Johnell, O., and Wendeberg, B.: Dislocations of the elbow and intraarticular fractures. Clin. Orthop. 246:126, 1989.

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12. Judet, T., de Loubresse, C. G., Piriou, P., and Charnley, G.: A floating prosthesis for radial-head fractures. J. Bone Joint Surg. 78B:244, 1996. 13. Kamineni, S., Hirahara, H., Neale, P., O’Driscoll, S. W., An, K. N., and Morrey, B. F.: Effectiveness of the lateral unilateral dynamic external fixator after elbow ligament injury. J. Bone Joint Surg. 89A:1802, 2007. 14. King, G. J., Evans, D. C., and Kellam, J. F.: Open reduction and internal fixation of radial head fractures. J. Orthop. Trauma 5:21, 1991. 15. Knight, D. J., Rymaszewski, L. A., Amis, A. A., and Miller, J. H.: Primary replacement of the fractured radial head with a metal prosthesis. J. Bone Joint Surg. 75-B:572, 1993. 16. Liu, S. H., Henry, M., and Bowen, R.: Complications of type I coronoid fractures in competitive athletes: report of two cases and review of the literature. J. Shoulder Elbow Surg. 5:223, 1996. 17. McKee, M. D., Bowden, S. H., King, G. J., Patterson, S. D., Jupiter, J. B., Bamberger, H. B., and Paksima, N.: Management of recurrent, complex instability of the elbow with a hinged external fixator. J. Bone Joint Surg. 80B:1031, 1998. 18. McKee, M. D., Pugh, D. M., Wild, L. M., Schemitsch, E. H., and King, G. J.: Standard surgical protocol to treat elbow dislocations with radial head and coronoid fractures. Surgical Technique. J. Bone Joint Surg. 87A (suppl 1,Pt 1):22, 2005. 19. Mehta, J. A., and Bain, G. I.: Posterolateral rotatory instability of the elbow. J. Am. Acad. Orthop. Surg. 12:405, 2004. 20. Moneim, M. S., and Garst, J. R.: Vascular injuries associated with elbow fractures and dislocations. Int. Angiol. 14:307, 1995. 21. Morrey, B. F.: Complex instability of the elbow. J. Bone Joint Surg. 79A:460, 1997. 22. Morrey, B. F.: Current concepts in the treatment of fractures of the radial head, the olecranon, and the coronoid: Instructional Course Lecture. J. Bone Joint Surg. 77-A:316, 1995. 23. Morrey, B. F.: Fracture of the radial head. In Morrey, B. F. (ed.): The Elbow and Its Disorders, 2nd ed. Philadelphia, W. B. Saunders, 1993, p. 383. 24. Morrey, B. F., Tanaka, S., and An, K.-N.: Valgus stability of the elbow: A definition of primary and secondary constraints. Clin. Orthop. 265:187, 1991. 25. Morrey, B. F.: Acute and chronic instability of the elbow. J. Am. Acad. Orthop. Surg. 4:117, 1996. 26. Morrey, B. F., and An, K.-N.: Articular and ligamentous contributions to the stability of the elbow joint. Am. J. Sports Med. 11:315, 1983. 27. Morrey, B. F., An, K. N.: Stability of the elbow: Osseous constraints. J. Shoulder Elbow Surg. 14(1 suppl S):174S, 2005. 28. Mortazavi, S. M., Asadollahi, S., Tahririan, M. A.: Functional outcome following treatment of transolecranon fracture-dislocation of the elbow. Injury 37:284, 2006. 29. Nestor, B. J., O’Driscoll, S. W., and Morrey, B. F.: Ligamentous reconstruction for posterolateral rotatory instability of the elbow. J. Bone Joint Surg. 74A:8:1235, 1992.

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30. O’Driscoll, S. W.: Technique for unstable olecranon fracture-subluxations. Op Techniques Orthop. 4:49, 1994. 31. O’Driscoll, S. W., Jupiter, J. B., King, G. J., Hotchkiss, R. N., and Morrey, B. F.: The unstable elbow. Instr. Course Lect. 50:892, 2001. 32. O’Driscoll, S. W., Morrey, B. F., Korinek, S., and An, K. N.: Elbow subluxation and dislocation. Clin. Orthop. Relat. Res. 280:186, 1992. 33. Olsen, B. S., Vaesel, M. T., Sojberg, J. O., Helmig, P., and Sneppen, O.: Lateral collateral ligament of the elbow joint: Anatomy and kinematics. J. Shoulder Elbow Surg. 5(2 pt 1):103, 1996. 34. Papandrea, R. F., Morrey, B. F., and O’Driscoll, S. W.: Reconstruction for persistent instability of the elbow after coronoid fracture-dislocation. J. Shoulder Elbow Surg. 16:68, 2007. 34a. Popovic, N., Gillet, P., Rodriguez, A., and Lemaire, R.: Fracture of the radial head with associated elbow dislocation: Results of treatment using a floating radial head prosthesis. J. Orthop. Trauma 14:171, 2000. 35. Regan, W., and Morrey, B. F.: Fracture of the coronoid process of the ulna. J. Bone Joint Surg. 71-A:1348, 1989. 36. Regel, G., Seekamp, A., Blauth, M., Klemme, R., Kuhn, K., and Tscherne, H.: Complex injury of the elbow joint. Unfallchirurg 99:92, 1996.

37. Ring, D., Jupiter, J. B., Sanders, R. W., Mast, J., and Simpson, N. S.: Transolecranon fracture-dislocation of the elbow. J. Orthop. Trauma 11:545, 1997. 38. Rodgers, W. B., Kharrazi, F. D., Waters, P. M., Kennedy, J. G., McKee, M. D., and Lhowe, D. W.: The use of osseous suture anchors in the treatment of severe, complicated elbow dislocations. Am. J. Orthop. 25:794, 1996. 39. Sanchez-Sotelo, J., O’Driscoll, S. W., and Morrey, B. F.: Medial oblique compression fracture of the coronoid process of the ulna. J. Shoulder Elbow Surg. 14:60, 2005. 39a. Smets, S., Govaers, K., Jansen, N., van Riet, R., Schaap, M., and Van Glabbeek, F.: The floating radial head prosthesis for comminuted radial head fractures: A multicentric study. Acta Orthop. Belg. 66:353, 2000. 40. Søjbjerg, J. O., Ovesen, J., and Nielsen, S.: Experimental elbow instability after transection of the medial collateral ligament. Clin. Orthop. Relat. Res. 218:186, 1987. 41. van Riet, R. P., Morrey, B. F., and O’Driscoll, S. W.: Use of osteochondral bone graft in coronoid fractures. J. Shoulder Elbow Surg. 14:519, 2005. 42. van Riet, R. P., Morrey, B. F., O’Driscoll, S. W., and van Glabbeek, F.: Associated injuries complicating radial head fractures. Clin. Orthop. Relat. Res. 441:351, 2005. 43. Wick, M., Lies, A., Muller, E. I., Hahn, M. P., and Muhr, G.: Prostheses of the head of the radius. What outcome can be expected? Unfallchirurg 101:817, 1998.

Chapter 30 Chronic Unreduced Elbow Dislocation

CHAPTER

30

Chronic Unreduced Elbow Dislocation Bernard F. Morrey

INTRODUCTION Elbow instability in one form or another remains one of the most vexing of all expressions of elbow trauma. The spectrum of elbow instability is carefully addressed in the pediatric patient (see Chapter 20), simple and complex instability in the adult (see Chapters 28 and 29), and in the chapter on external fixation for the elbow (see Chapter 33). The instability addressed in this chapter is termed chronic unreduced complete dislocation. A chronic unreduced dislocation is very uncommon in this country and is principally seen in Third World nations. Thus, much of our understanding has come from contributions from South Africa, Thailand, and India.8,10,11,14,17,18

CHRONIC UNREDUCED ELBOW JOINT The simplest way to consider the two major types of chronic unreduced elbow joints is that of subluxation, or complete dislocation. The most common of these is sometimes a subtle chronic posterior subluxation due to fracture of the coronoid. This chronic instability pattern is dealt with in the chapter on complex instability (see Chapter 29). The chronically unreduced complete dislocation is not common, so few have much experience dealing with it. The second is an unreduced complete dislocation, which is rare except, as mentioned earlier, in underdeveloped countries.

PRESENTATION Chronic unreduced complete dislocation has the following characteristics: (1) gross deformity; (2) variable motion from complete ankylosis in approximately one third of cases to a near-functional arc of motion of greater than 40 degrees in one third, and motion between 0 to 40 degrees in the remaining one third13; (3) pain ranges from minimal to significant depending on the

463

duration of the dislocation with marked individual variation.

OCCURRENCE AND CLINICAL PRESENTATION At presentation, about two thirds have unacceptable function due to instability, pain, or both.13 The frequency is highly dependent on the local medical customs dealing with the initial dislocation, experience, expertise, and expectation. The presence of traditional medical care (bone setters3) explains the reports from Africa documenting large series (81 cases over a 10-year period).14 In Thailand, 135 patients were reported in a 15-year period from three hospitals.10 The deformity may occur both in children and in adults. These patients have often sustained an associated fracture as well. Naidoo14 noted that 13 of 23 patients undergoing treatment had an associated fracture. A similar rate of 45% (62 of 135) was reported from a large multicenter study by Mahaisavariya and associates.10 About 50% simply have a posteriorly displaced, complete dislocation. The patients usually do not have neurologic deficit at the time of presentation, but if there is neural impairment, the ulnar nerve is most commonly symptomatic. Vascular compromise is extremely rare.

TREATMENT The choice of treatment has been predicated on the age of the patient, the timing of the intervention, and the likelihood of successful reduction. The full spectrum of reconstructive options has been suggested as a treatment for the neglected dislocation. These options include reduction, reduction and interposition, resection, fusion, and replacement. Resection is not a viable option today. In most practices and circumstances, fusion might be considered, but this is not usually considered in the United States. The techniques of interposition and replacement arthroplasty are discussed elsewhere (see Chapters 69 and 70). An attempt at closed reduction is reasonable at all ages for dislocations of less than 3 weeks’ duration. Today, this is particularly effective with the added stability provided by an external fixation.9,18 Although fusion and resection have both been considered for the chronic condition,2,4,6 by far the most logical and accepted approach is open reduction (Fig. 30-1). Although this recommendation has been somewhat controversial in the past, open reduction outcomes are as good or better than other options and is effective years after injury.5,11 Here we will review only the treatment strategy for open reduction. The use of an external fixation is discussed in Chapter 33. Joint replacement is recommended in patients older than 60 years of age and is discussed in Chapter 59. The surgical approach is predicated on

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FIGURE 30-1

A, Chronic unreduced dislocation of 4 months’ duration. B, Treated in the manner described with external fixator. C and D, Well reduced and functional with a 105-degree arc of motion 1 year later.

an understanding of the pathology and a flexible surgical treatment plan.

PATHOLOGY The rationale and surgical strategy is predicated on recognizing, anticipating, and treating each element of the

pathology encountered. The pattern is rather consistent: (1) a contracted triceps tendon; (2) contracture of the medial and lateral collateral ligaments; (3) variable involvement of the ulnar nerve; (4) contracted anterior and posterior capsules; (5) fibrous membrane covering the articular surface; and (6) commonly, (30% to 40%) an associated fracture of the coronoid or radial head, or both.

Chapter 30 Chronic Unreduced Elbow Dislocation

SURGICAL TECHNIQUE

branch. A subcutaneous pocket is developed (see Fig. 30-2B). 3. The dissection is carried laterally to the lateral epicondyle. Kocher’s interval is entered, and the radial head exposed. The lateral column of the humerus is exposed proximally. 4. The lateral collateral ligament and extensor mass are elevated from the lateral epicondyle (Fig. 30-2C). The dense adhesions that are consistently present are then released from the articular surface between the ulna and humerus, and the radius and the humerus. The lateral contracted tissue is the limiting factor in preventing relocation, so this is aggressively released, including the extension origin, and the distal fibers of the

The surgical technique preferred by the author specifically addresses the pathology according to a defined sequence (Fig. 30-2). 1. A posterior skin incision is made. With gross deformity, the subcutaneous border of the ulna is identified as the distal landmark and the midportion of the humerus as the proximal landmark. An incision over these two landmarks is then joined to provide a straight incision after the deformity has been corrected (see Fig. 30-2A). 2. The dissection is carried medially to the ulnar nerve, which is identified and released to its first motor

Ulnar nerve

A

B

Common extensor origin

B Extensor origin

Flexor pronator origin

Flexor origin

A Contracted capsule

C

D FIGURE 30-2

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A, Posterior incision is employed by using the subcutaneous border of the ulna distally and the midportion of the humerus proximally. The ends of each incision are joined to ensure proper orientation of the final incision for those with gross deformity. B, Medial and lateral flaps are elevated, and the ulnar nerve is released. C, The lateral contracted ligament and extensor mechanism (A) is first released from the humerus followed by medial collateral ligament release (B) from the humerus if necessary. D, The joint is cleared of membrane, and the posterior and anterior capsules are resected. The triceps is elevated from the humerus.

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Collateral ligament repair

E

F

G FIGURE 30-2, cont’d

E, The joint is manipulated and reduced. F, The collateral ligaments are repaired. G, The construct is stabilized with dynamic external fixation, and the axis pin is removed.

5. 6. 7.

8.

9.

brachioradialis muscle. The greater sigmoid notch is cleaned. The posterior capsule is completely released (see Fig. 30-2D). The anterior capsule is excised. The medial collateral ligament is contracted, and if this prevents relocation, it is then completely released from the medial epicondyle. The elbow is gently manipulated so as to reduce the radial humeral and ulnohumeral articulations (see Fig. 30-2E). Note: At this point, it is important that the joint rest in the reduced state without significant external force. If the joint surface is destroyed, we interpose an Achilles allograft tendon. If the collateral tissue is

inadequate for repair, we use a portion of the tendon for ligamentous reconstruction. 10. The lateral collateral ligament and, if necessary, the medial collateral ligaments are repaired with No. 5 Mersilene sutures placed through the ligament in a Bunnell fashion and attached to the anatomic origin through bone holes (see Fig. 30-2F). Note: If the tissue is inadequate, a plantaris allograft is used to reconstruct the deficient tissue. If both ligaments require reconstruction, we use a simple allograft and “sling” the ulna to the humerus by connecting the medial and lateral humeral origins of the medial and lateral ulnar insertion sites. 11. Triceps repair. Management of the triceps is one of the most controversial issues of this treatment.10 The elbow is flexed to assess the influence of the

Chapter 30 Chronic Unreduced Elbow Dislocation

contracted triceps. If the elbow can be flexed to 110 degrees, no triceps reconstruction is performed because it is believed that the musculotendinous complex will stretch out in time. If less than 100 degrees of flexion is possible, a tricepsplasty is performed. The anconeus is elevated from the bed. The anconeus and triceps are then repositioned over the tip of the olecranon, and with the elbow in 90 degrees of flexion, it is reattached with nonabsorbable No. 5 suture. 12. An external fixator is applied because it is essential to allow immediate motion and to preserve the collateral ligament reconstruction (see Chapter 33) (see Fig. 30-2G).

POSTOPERATIVE MANAGEMENT The arm is elevated for 24 hours, after which continuous passive motion (CPM) is used. The patient returns home in a portable CPM with as much motion as tolerated. The external fixator is maintained for 3 to 4 weeks. The patient then returns to the hospital, and under a brief general anesthesia, the external fixator is removed and the elbow examined under fluoroscopy (see Chapter 33). Flexion and extension splints are then used to establish and maintain an arc of functional motion (see Chapter 11).

RESULTS Naidoo14 described a satisfactory result in 23 of 25 patients treated in a manner similar to that just described but without a fixator. Arafiles1 described a satisfactory outcome in 11 of 12 surgical procedures. Open reduction was reported as successful in 72% of 52 patients by Di Schino and associates.5 Interestingly, these investigators also found complete resection of the elbow for the chronic cases to be successful in 80% of cases.4 However, careful interpretation of these two reports suggests that these authors are referring to improvement of motion and admitted that the resected elbow was weak and had marked instability, and hence, they favor reduction over resection.

MOTION The improvement is marked, but a functional status is not always attained. Of the 23 patients reported by Naidoo14 with 13 associated fractures, eight patients remain with less than 60 degrees of motion (33%). Five had an arc of motion between 60 and 90 degrees (20%), and 10 (40%) had an arc of motion greater than 90 degrees. Naidoo also demonstrated that the overall outcome was not a function of age or duration of

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dislocation as had been previously thought. On the other hand, Arafiles1 reports a mean of 105 degrees arc at 2 years in a group of 11 patients. The most recent report from Bangkok documented a final arc of flexion of 82 degrees in 24 patients 4 years after surgery.11 One major discussion in the literature relates to the management of the triceps. If operated on less than 3 months after injury, this generally need not be lengthened or addressed. However, as mentioned earlier, if the triceps is badly contracted and limits flexion, then some form of triceps augmentation and release is appropriate. Mahaisavariya and colleagues10 demonstrated that leaving the triceps intact was associated with increased motion (P > .05) of 115 degrees in those in which the triceps was not altered, compared with 89 degrees in those with triceps release. In addition, they demonstrated that the flexion contracture was markedly greater (by 70 degrees) in those with a tricepsplasty, compared with 45 degrees in patients in whom tricepsplasty was not carried out. If the triceps is addressed, V-Y lengthening as described by VanGorder has been suggested by some; however, as noted earlier, we prefer the anconeus slide technique. Overall, this approach has been effective even in those with considerable joint deformity (Fig. 30-3A to G)

COMPLICATIONS This is difficult surgery, and as might be expected, this type of injury and surgery are associated with significant complications. Transient nerve injury has been reported in 8% to 40% of cases.7,14 Infection occurs in approximately 5%.1 Ectopic bone was reported in none of the 70 cases of Mahaisavariya and associates10 and none of the 23 cases of Naidoo.14 On the other hand, it was observed in 8% of the patients reported by Fowles and colleagues7 and one in four of the patients described by Billett.3 The overall complication rate is approximately 20% to 25%. Complications that significantly affect the outcome occur at a rate of at least 10%.

AUTHOR’S EXPERIENCE We have treated only six patients with complete, chronic dislocation with reduction and stabilization. Five of the six treatments have been successful, leaving patients with an arc of greater than 90 degrees in four and no or mild pain. One treatment was a failure.

ELBOW REPLACEMENT Because of the factors and prognosis noted previously, we prefer the reliable and functional outcome of elbow arthroplasty in patients older than 65 years of age.

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A

B

C D FIGURE 30-3

A, Established chronic elbow dislocation of 5 years’ duration. B, An Achilles tendon allograft fashioned in a way to preserve the margins as “tails” used to reconstruct the collateral ligaments. C, The elbow is reduced and the Achilles allograft is draped over the joint. The tissue to reconstruct the medial and lateral collateral ligaments have been fashioned. D, Each portion of the allograft is brought through a tunnel connecting the sublime tubercle and the supinator crest. This forms a “sling” of reconstruction.

Chapter 30 Chronic Unreduced Elbow Dislocation

E

F

FIGURE 30-3, cont’d

5 yrs

G

469

E, The external fixator has been applied. Note that the elbow is reduced. F, Note that the patient has freedom of flexion and extension in the external fixator. G, One year after surgery the elbow remains reduced with an arc of motion of 35 to 125 degrees and minimal pain. The patient is well pleased with the outcome.

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FIGURE 30-4

A, Chronic instability of 3 years’ duration and after two procedures. B, Excellent flexion and extension with no evidence of implant failures at 11 years.

Experience with joint replacement in patients with gross instability has been reported by Ramsey and associates.16 A success rate of about 90 percent was documented a mean of 6 years after surgery (Fig. 30-4). Elbow replacement with complete ankylosis has been reported by Mansat and by Peden.12,15 Overall, an 80% satisfactory outcome at 6 years was documented.

CONCLUSIONS Ideally, of course, chronic unreduced elbow dislocation is best managed by prevention. In the absence of prevention, most patients with unreduced elbow dislocations should be managed according to the principles and technique described here. If this methodology is followed, it is expected that approximately 60% to 75% of the patients have a satisfactory result, which includes minimal pain and an arc of motion equal or greater than 80 to 90 degrees. If the surgeon reconstructs the collateral ligaments or performs an interposition, an external fixation device is used. The complication rate is significant and varies as a function of the extent of the pathology, surgeon experience, and expertise. Finally, joint replacement is the treatment of choice for patients older than 65 years of age and affords a reliable salvage procedure.

References 1. Arafiles, R. P.: Neglected posterior dislocation of the elbow. A reconstruction operation. J. Bone Joint Surg. 69B:199, 1987. 2. Ashby, M. E.: Old dislocations of the elbow. J. Natl. Med. Assoc. 66:465, 1974. 3. Billett, D. M.: Unreduced posterior dislocation of the elbow. J. Trauma 19:186, 1979. 4. Di Schino, M., Breda, Y., Grimaldi, F. M., Lorthioir, J. M., and Merrien, Y.: Resection of the distal part of the humerus in neglected elbow dislocations. Apropos of 23 case reports. Med. Trop. 49:415, 1989. 5. Di Schino, M., Breda, Y., Grimaldi, F. M., Lorthioir, J. M., and Merrien, Y.: Surgical treatment of neglected elbow dislocations. Report of 81 cases. Rev. Chir. Orthop. Repar. Appareil Moteur 76:303, 1990. 6. Dryer, R. F., Buckwalter, J. A., and Sprague, B. L.: Treatment of chronic elbow instability. Clin. Orthop. 148:254, 1980. 7. Fowles, J. V., Kassab, M. T., and Douik, M.: Untreated posterior dislocation of the elbow in children. J. Bone Joint Surg. 66A:921, 1984. 8. Krishnamoorthy, S., Bose, K., and Wong, K. P.: Treatment of old unreduced dislocation of the elbow. Injury 8:39, 1976. 9. Lo, C. Y., and Chang, Y. P.: Neglected elbow dislocation in a young man: Treatment by open reduction and elbow fixator. J. Shoulder Elbow Surg. 13:101, 2004. 10. Mahaisavariya, B., Laupattarakasem, W., Supachutikul, A., Taesiri, H., and Sujaritbudhungkoon, S.: Late reduction of

Chapter 30 Chronic Unreduced Elbow Dislocation

11.

12.

13.

14.

dislocated elbow. Need triceps be lengthened? J. Bone Joint Surg. 75B:426, 1993. Mahaisavariya B, and Laupattarakasem, W.: Neglected dislocation of the elbow. Clin. Orthop. Relat. Res. 431:21, 2005. Mansat, P., and Morrey, B. F.: Semiconstrained total elbow arthroplasty for ankylosed and stiff elbows. J. Bone Joint Surg. 82A:1260, 2000. Martini, M., Benselama, R., and Daoud, A.: Neglected luxations of the elbow: 25 surgical reductions. Rev. Chir. Orthop. Repar. Appareil Moteur 70:305, 1984. Naidoo, K. S.: Unreduced posterior dislocations of the elbow. J. Bone Joint Surg. 64B:603, 1982.

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15. Peden, J. P., and Morrey, B. F.: Total Elbow Arthroplasty for the Management of the Ankylosed or Fused Elbow. Submitted for publication, Br. J. Surg. 2008. 16. Ramsey, M., Adams, R. A., and Morrey, B. F.: Elbow displacement for gross instability. J. Bone Joint Surg. 81A:3847, 1999. 17. Silva, J. F.: Old dislocations of the elbow. Ann. R. Coll. Surg. Engl. 22:363, 1958. 18. Sunderamoorthy, D., Smith, A., and Woods, D. A.: Recurrent elbow dislocation—an uncommon presentation. Emerg. Med. J. 22:667, 2005.

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CHAPTER

31

Ectopic Ossification About the Elbow Bernard F. Morrey and G. Dean Harter

INTRODUCTION Development of pathologic formation about the elbow takes on several forms including heterotopic ossification, myositis ossificans, and periarticular calcification. Heterotopic ossification refers to the formation of mature lamellar bone in nonosseous tissue. Heterotopic ossification and ectopic bone are terms that are used interchangeably for this type of bone formation. Myositis ossificans refers to abnormal formation of bone in inflammatory muscle.1 Myositis ossificans also consists of mature lamellar bone and is distinguished from ectopic bone only by its location. Calcification about the elbow is distinctly different from ossification. Calcific deposits typically consist of calcium pyrophosphate and do not contain mature bone. These are usually amorphous globular deposits and have no trabecular structure. Calcific deposits may occur in tendon, synovium, capsular tissue, and ligaments. Calcium deposits are most commonly seen in ligamentous tissue after elbow trauma.10,12,51 Elbow motion is rarely affected to any significant degree.

ETIOLOGY TRAUMATIC CONDITIONS THAT MAY LEAD TO ECTOPIC BONE FORMATION Thompson and Garcia84 documented the incidence of ectopic bone formation in a series of more than 1200 traumatic elbow conditions: 3% in simple dislocations, 20% in elbow dislocations associated with radial head fractures, and 16% in elbow dislocations associated with other fractures. Although the definition of what constitutes ectopic bone is not clear, this report does serve as a worthwhile benchmark of the relative incidence among these three injury types.

Elbow Dislocations Patients with simple dislocations without fracture are less likely to develop ectopic bone formation than are

those with associated fractures.72,73 Linscheid and Wheeler51 noted an incidence of some radiographic density in about 30% in a series of 110 elbow dislocations. True ectopic bone formed in the anterior capsule in five patients (4.5%), and most had calcification in the collateral ligaments below the medial and lateral epicondyles (Fig. 31-1). Josefsson and colleagues42 found true ectopic bone formation in only 1 of 52 elbow dislocations (1.6%). Periarticular calcification, however, was noted in 38 patients (76%). Eleven of the 12 patients in whom there was no evidence of periarticular calcification had sustained their dislocations before the age of 16 years. The incidence of ectopic bone formation increases about fivefold when an elbow dislocation is associated with a radial head fracture.84 McLaughlin55 listed several principles to reduce the formation of ectopic bone: (1) excision of the radial head within 24 hours of injury, (2) complete removal of the radial head with all the fracture fragments, (3) avoidance of the formation of bone dust within the operative bed at the time of radial head excision, (4) careful hemostasis, and (5) avoidance of hematoma formation. There is little scientific evidence to support these recommendations, but they seem reasonable.

Radial Head Fractures Ectopic bone formation may also occur following isolated fractures of the radial head. Patients with Mason type III comminuted fractures are probably at the greatest risk.52 In a study of 60 cases, Mikic and Vukadinovic56 noted ossification about the elbow in 32 (56%). In the 18 patients with more extensive amounts of bone, restriction of elbow motion was seen in all. In 31 (52%) of these patients, there was significant regrowth of bone at the level of resection of the radius, as noted by others.48,81 We have observed a rather consistent pattern of ectopic bone emanating from the resected radius in this clinical circumstance (Fig. 31-2).

Timing of Surgical Treatment with Elbow Trauma We have observed that patients with open injuries undergoing several surgical procedures performed during the first 7 to 14 days of injury are at particular risk (Fig. 31-3). In McLaughlin’s series of radial head fractures,55 12% who underwent excision within 24 hours had ectopic bone formation, compared with 38% who had delayed excision. In a study of 14 patients with fracture-dislocations of the elbow treated by either partial or complete resection of the radial head, Broberg and Morrey8 reported an incidence of significant ectopic bone formation of only 9%. The single patient with significant heterotopic ossification had undergone excision of the radial head

Chapter 31 Ectopic Ossification About the Elbow

8 days after injury, and the results of treatment were graded as fair with continued elbow pain. The issue of delay before definitive surgery for fracture dislocation was initially emphasized by McLaughlin.55 This opinion has been recently strengthened by the work of Ilahi and colleagues.41 Among 71 consecutive elbow injuries of various types, none developed significant ectopic bone when operated on within 48 hours.

On the other hand, 8 of 24 (33%) did enounter ectopic bone formation if treatment was delayed more than 48 hours.

Post-Traumatic Radioulnar Synostosis Cross-union from ectopic bone may be caused by fractures,5,11,23,65,75,85 or soft tissue injury7,60,70 of the forearm. When an associated elbow injury has occurred, the synostosis may be extensive (Fig. 31-4). Vince and Miller86 classified synostoses of the forearm by location: type I, distal third; type II, middle third; and type III, proximal third. Two of three patients with proximal synostoses who were treated surgically had unsatisfactory results because of recurrence of the synostosis. Failla and associates22 reported a series of 20 patients from the Mayo Clinic who underwent excision, with only 7 patients achieving good or excellent results and 13 patients achieving fair or poor results. The timing of synostosis excision appeared to be important, with no good or excellent results in patients operated on less than 12 months after injury or more than 3 years after injury. We use the radiographic appearance of discrete margins and mature trabeculation as the basis of when to resect the lesion. Bone scans and serum enzymes are of little value in deciding when to resect the lesion, and hence, we do not obtain these studies. Jupiter and Ring43 subclassified type III forearm synostosis into three types based on the location of the

Ectopic bone

Bone fragments

Ectopic ossification

Bone exostosis

Soft tissue

Muscle “myositis ossificans”

Capsule

Ligaments

FIGURE 31-1

Distribution of possible radiographic densities about the elbow after trauma. (Redrawn from Broberg, M. A., and Morrey, B. F.: Results of treatment of fracture-dislocations of the elbow. Clin. Orthop. Rel. Res. 216:111, 1987.)

Positive RNBI studies 3-phase

Static only

Radiographs positive

Peak Alk φ 359 U/L (3.5 × normal)

Symptom onset Serum calcium Upper limit Alk φ lower limit for Ca++

Serum Alk φ 0

2

4

6

8

10

12

14

16

18

20

22

24

Time in weeks post injury Injury

FIGURE 31-2

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Temporal correlation of radiographic and serum alkaline phosphatase changes with clinical symptoms. (Redrawn from Orzee, J. A., and Rudd, T. G.: Heterotopic bone formation: clinical, laboratory, and imaging correlation. J. Nucl. Med. 26:125, 1985.)

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FIGURE 31-3

This 26-year-old man was involved in a motor vehicle accident and sustained a dislocation of his right elbow with a proximal ulnar fracture. Open reduction and internal fixation of the ulna was done 3 weeks after his injury. He was first seen at the Mayo Clinic 4 months later with extensive ectopic bone (A). The technetium-99m scan showed marked uptake at 4 months (B), which persisted for 18 months (C).

ectopic bone. Type III A ectopic ossification is located at or distal to the bicipital tuberosity, Type III B involves the radial head and/or proximal ulnar joint, and Type III C refers to a proximal radial ulnar synostosis contiguous with ectopic bone extending across the elbow to the distal humerus. Eighteen patients underwent operative excision of post-traumatic proximal radioulnar synostosis. Recurrence was seen in only one patient. The 17 patients who did not experience a recurrence regained an average of 139 degrees of forearm rotation. No significant relationship between postoperative forearm rotation and synostosis size, the use of interpositional fat, or the concomitant use of a hinged elbow distractor was identified.43 The surgical treatment of proximal radioulnar synostosis has traditionally been viewed with pessimism. This view has been based on very little published data. The importance of forearm rotation to patient function is

well established, and recent experience demonstrates that surgical excision is warranted and is likely to be successful.43 Preoperative planning is necessary to choose the correct surgical approach to remove the entire lesion if this is deemed necessary. CT scans or tomograms can be used to define the anatomy of the synostosis. If possible, the entire lesion must be resected, and the radius and ulna in the area of the synostosis must be contoured to allow motion without impingement. The intimate proximity of neurovascular structures may limit this resection. Ideally, a free space of at least 5 mm should be created and maintained throughout the intraoperative arc of motion. We prefer not to interpose Silastic or other foreign material, but we do translocate fat into the defect. Patients can be expected to lose about 50% of the intraoperative motion achieved. Accordingly, the surgeon should attempt to achieve at least 120

Chapter 31 Ectopic Ossification About the Elbow

475

FIGURE 31-4

Comminuted, compound fracture (A). Three débridements and fixation occurred over a 10-day period. Extensive ectopic bone developed (B).

degrees of combined supination and pronation intraoperatively. An alternative surgical approach to improve forearm rotation in this difficult clinical setting is proximal radial resection as described by Kamenini and Morrey44 (Fig. 31-5). Indications include (1) extensive synostosis not amenable to a safe and discrete resection, (2) articular surface involvement, and (3) associated anatomic deformity. A Kocher approach is recommended to explore the synostosis and the radius distal to the synostosis. One centimeter of bone is excised from the radius, and the remaining exposed bone is covered with bone wax. Postoperative arc of forearm rotation averages 98 degrees. Reankylosis occurred at the site of resection in one patient.

CLASSIFICATION There are several discrete clinical circumstances in which ectopic bone develops around the elbow: (1)

trauma, usually fracture; (2) closed head or spinal cord injury; (3) burn injury to the extremity; and (4) genetic conditions (Box 31-1). Recently, the process has also been reported to occur after adult respiratory distress syndrome37 and after orthotopic liver transplant.62 Radiographically, ectopic bone is seldom seen before 3 weeks after injury or surgery, but it usually can be detected if one looks for it critically. The soft density on the radiograph can be visualized under a bright light. The extent of ectopic bone formation usually is evident by 12 weeks (Fig. 31-6). Bressler and colleagues9 studied the maturation process of ectopic bone in 25 CT scans. Persistent, unossified, low-density soft tissue areas were detected adjacent to mineralized areas up to 16 years after injury. In adults, after the maturation process is completed, the bone usually does not resorb. Resorption may occur in children younger than 16 years. Ectopic ossification may be classified by its anatomic formation site or its functional affect on elbow motion and forearm rotation.

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C

D

FIGURE 31-5

A and B, Radial head fracture with dislocation develops a typical pattern of ectopic ossification after excision. Extensive bone formation after dislocation with ligament injury (C) and displaced type II coronoid fracture (D).

ANATOMIC CLASSIFICATION Ectopic bone may develop in essentially any tissue about the elbow. Common anatomic location of the abnormal bone varies with etiology. In post-traumatic situations, posterolateral elbow is most often involved. A bone bridge often develops between the lateral condyle of the humerus and the posterolateral olecranon. Bone may also fill the olecranon fossa. A second common location in traumatic cases involve the anterolateral

compartment of the elbow. Anterior bone may extend from the distal humerus to the radius and ulna at the level of the bicipital tuberosity. The coronoid is frequently enlarged and blocks elbow flexion because the coronoid fossa cannot accept the volume increase.87 Heterotopic ossification of the elbow in the burn patient is most often posteromedial. This can also occur in cases with a traumatic etiology. The cubital tunnel is often obliterated, and the ulnar nerve may be completely encased in bone.

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Patients at Risk for Developing Ectopic Bone About the Elbow

BOX 31-1

I.

Trauma Patients A. Elbow Trauma 1. Open elbow dislocations requiring extensive or multiple débridements 2. Elbow dislocations associated with fractures requiring open reduction with internal fixation 3. Radial head fractures treated with surgery more than 24 hours after injury 4. Failed internal fixation about the elbow requiring revision fixation within 3 months B. Distal biceps tendon repair C. Repeated procedures with an improper exposure in the first 2 weeks II. Patients with Central Nervous System Injury A. Traumatic brain injury B. Elbow trauma in patients with traumatic brain injury III. Burn Patients A. Third-degree burns over 20% of total body area B. Third-degree burns over the elbow C. Long periods of bed confinement IV. Patients with Genetic Conditions A. Fibrodysplasia ossificans progressive B. History of ectopic bone formation

Neurogenic ectopic ossification most commonly develops anteriorly in the flexor muscles or posteriorly in the extensors. Ossification tends to occur with the muscle and follows a single plane. This contrasts to post-traumatic situations in which multiple planes are frequently involved.6,87 The forearm and proximal radioulnar joint may also be involved. Discussion of this classification system is presented in the section on post-traumatic radioulnar synostosis.

FUNCTIONAL CLASSIFICATION 38

Hastings and Graham have developed the classification based on functional range of motion of the elbow and forearm rotation. Class I ectopic bone refers to the radiographic appearance of abnormal bone without any functional limitations. This should be documented because it signifies a patient’s tendency toward heterotopic bone formation. Prophylactic treatment may be warranted in these patients. Class II refers to patients with limited range of motion. Class II is subdivided into three types. Class II A refers to limitation of motion in the flexion/extension arc, class II B is limited forearm rotation, and class II C has limita-

FIGURE 31-6

Proximal radioulnar synostosis from radioulnar fracture.

tion in both planes. Patients with class III ectopic ossification have ankylosis that eliminates either elbow flexion and extension, pronation and supination, or both. This class is subdivided into three types that are identical to class II.

INCIDENCE OF ECTOPIC BONE FORMATION ECTOPIC BONE FORMATION FOLLOWING CENTRAL NERVOUS SYSTEM INJURY First described during the First World War,16 ectopic bone formation may occur after central nervous system (CNS) injury to the brain or spinal cord.29,72 Garland and others29,35,40 extensively studied the orthopedic problems encountered by patients with both traumatic brain injury and spinal cord injury (see Chapter 72).

Traumatic Brain Injury without Elbow Trauma In a review of 496 patients with traumatic brain injury, Garland and colleagues32,33 found an incidence of periarticular bone formation in 100 joints in 57 patients (11%). Patients with spastic quadriparesis have the

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highest incidence of ectopic bone formation. The hip was the most common location, followed by the shoulder, elbow, and knee. Ectopic bone formation developed in 4% of the elbows. Anterior bone formation was deep to the biceps and brachialis muscles and anterior to the joint capsule, occasionally involving the entire brachialis muscle (Fig. 31-7). The posterior ectopic bone was beneath the triceps tendon in close association to the posterior capsule. In Garland’s series,32 the ectopic bone was anterior in six and posterior in 17, and eight of the elbows were completely ankylosed preoperatively. Pos-

FIGURE 31-7

terolateral ectopic bone formation is the most common site of occurrence.30 A major determinant of potential successful surgical treatment is the residual neurologic deficit. Twenty-three patients underwent resection of ectopic bone about the elbow. In general, resection should be delayed until at least 18 months after CNS injury to allow maximum functional recovery. The results of excision correlate with the neurologic classification.32 Complications include soft tissue infections and neurologic injury. Recurrence is closely associated with spasticity.30

Extensive proximal radioulnar synostosis (A) treated by excision of a segment of the radius distal to the synostosis (B).

Chapter 31 Ectopic Ossification About the Elbow

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Traumatic Brain Injury with Associated Elbow Trauma The incidence of heterotopic ossification about the elbow dramatically increases in patients with fracturedislocations of the elbow and concomitant head injury. In one study,46 ectopic bone developed about the elbow in greater than 90% of patients with this injury complex. Routine prophylaxis in this patient population is logical, although studies demonstrate its efficacy.

ECTOPIC BONE FORMATION IN BURN PATIENTS Significant ectopic bone formation in burn patients is a rare occurrence. Evans20,21 listed the following risk factors: (1) the percentage area, (2) the location of the burn, (3) the length of bed confinement, (4) osteoporosis, (5) superimposed trauma, and (6) genetic predisposition. The elbow, shoulder, and hip are the most commonly involved.20,21 In a study of more than 5000 cases at the U.S. Army Institute of Surgical Research, the incidence of ectopic bone formation was only 1.2%, with 82.5% of those cases involving the elbow. This is similar to the recent report of a 1.2% incidence after 1478 burns, of which the elbow is the most commonly involved joint.67 Although several studies have reported an incidence of ectopic bone formation varying from 2 to 35 percent,20,21,63,76,82 the incidence of significant ectopic bone formation at the elbow that requires treatment is probably about 1%.21 The distribution of the ectopic bone about the elbow in the burn patient is posterior and medial along the medial border of the triceps and anterior in the plane of the brachialis from the anterior surface of the humerus to the coronoid (Fig. 31-8).21 Evans21 and others19 have noted that prevention of ectopic bone in the burn patient is best accomplished by reducing the period of bed confinement and the period of postburn hypermetabolic state through the use of early wound excision and grafting. If ectopic bone formation does occur, passive stretching of the joint should be avoided. Active range of motion exercises of the joint within a pain-free arc may continue.15 Results of excision of heterotopic ossification about the elbow in children with burns was recently reported.36 All patients experienced an improvement in their arc of motion (average increase of 57 degrees), and all patients were able to reach the face and perineum after their operative procedure. No recurrent heterotopic bone was noted. Selection criteria for excision include (1) decreased range of motion sufficient to cause functional limitations, (2) maturation of new bone confirmed on the radiograph, (3) no evidence of acute inflammation, and (4) complete healing of the skin in the area of the ectopic

FIGURE 31-8

The entire brachialis muscle has been replaced in this 30-year-old man after head injury without elbow trauma.

bone. After excision, most patients have functional range of motion arcs and recurrence is uncommon.15,39 The most common complication is ulnar nerve irritation.18 Technical factors include anterior transposition of the ulnar nerve, excision of the ectopic bone and collateral ligaments if they are ossified, and excision of the radial head when forearm rotation is limited.20 In the senior author’s (Bernard F. Morrey, MD) experience, however, radial humeral involvement very rarely occurs. If the anterior aspect of the elbow is significantly scarred by third-degree burns, excision of the scarred areas with release of the contractures and excision of the ectopic bone is recommended.17 In these complex situations, plastic surgical consultation and assistance should be considered.

FIBRODYSPLASIA OSSIFICANS PROGRESSIVA Genetic conditions may lead to ectopic ossification about the elbow. Fibrodysplasia ossificans progressiva is a rare genetic disorder characterized by progressive soft tissue ossification. The etiology is a defect in the induction of enchondral osteogenesis.45 More than half of patients

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with this disorder experience ectopic bone formation about the elbow between the third and fourth decades of life. Family history and a history of prior injury causing exuberant heterotopic ossification suggests this diagnosis. Connor and Evans13 and others74 have recommended against surgical treatment. Massive amounts of ectopic bone form after surgical intervention and result in predictably poor outcomes. Avoidable factors for the precipitation of ectopic bone in these patients include local trauma, careless venipuncture, intramuscular injections, biopsy of the lumps, and operations to excise heterotopic bone.

PATHOLOGY The histology of ectopic bone reveals that it resembles normal bone. It is similarly mineralized, and the bone matrix-forming cells produce a highly organized bone containing secondary haversian systems as evidence of bone remodeling.

CLINICAL PRESENTATION Ectopic ossification about the elbow typically begins to develop approximately 2 weeks following the inciting event. Patients will often experience swelling, warmth, and pain.64 Motion loss may also begin to be evident at this time. Early presentation may be confused with cellulitis, deep infection, reflex sympathetic dystrophy, and thrombophlebitis. Infection must be considered and ruled out, especially in patients who have presented with an open injury. As the process continues, the warmth, erythema, and swelling will gradually resolve. This may be accompanied by diminishing elbow motion. Maturation of the ectopic bone is usually associated with pain resolution. Continued pain at extremes of motion is commonly caused by bony impingement, whereas midarc pain is more commonly associated with articular incongruity, arthritis, or even loose bodies. Pain must be clearly delineated because it is not a common feature of mature ectopic bone.

DIAGNOSTIC STUDIES LABORATORY STUDIES Several laboratory variables have been studied in an effort to identify high-risk patients. An increased incidence of the human leukocyte antigen B18 in a group of patients with central nervous system injury and paraosteoarthropathy has been reported.31,40,50,57,78

Unfortunately, the predictive value of serum alkaline phosphatase determinations has not been consistent and the utility of the test in clinical practice is limited.2,28,49,58,64 The test lacks specificity, and, in most cases, the ideal time to initiate prophylactic treatment may have passed. Serum alkaline phosphatase levels are not predictive of bone maturation and are no longer used to determine surgical timing. Complete blood count with differential, erythrocyte sedimentation rate, and C-reactive protein may be helpful in eliminating infection from the differential diagnosis in patients with early presentation. Overall, however, laboratory evaluation has little benefit in the diagnosis, evaluation, and surgical timing in this disease process.

RADIOGRAPHIC EVALUATIONS The technetium bone scan is markedly positive during the formation of ectopic bone and usually remains positive for a prolonged time (Fig. 31-9).27 The temporal relation between positive technetium bone scans, serum alkaline phosphatase determinations, radiographs, and the clinical presentation of ectopic bone formation was well illustrated by Orzel and Rudd64 in a study of 50 patients with a variety of injuries (spinal cord trauma, traumatic brain injury, extremity trauma, and so forth). Both the technetium bone scan and serum alkaline phosphatase determinations were abnormal before either the clinical onset or radiographic detection of ectopic bone formation (see Fig. 31-6). Standard plain radiographs with anteroposterior, lateral, and oblique radiographs are usually sufficient to allow diagnosis, confirm location of abnormal bone, and determine severity. Plain radiographs are also useful in the evaluation of the maturity level of ectopic ossification. In addition, plain radiographs should be carefully evaluated to evaluate elbow joint incongruity, arthritic changes, deformity, and healing of potential associated fractures. Radiographs often will show evidence of heterotopic ossification as early as 2 weeks following an injury. Radiographs must be scrutinized carefully to see the fluffy soft tissue density at this early time frame. During early formation, the heterotopic bone lacks distinct margins and trabeculation is absent. With maturity, margins become sharply defined and trabeculations develop. The typical location of heterotopic bone development in various clinical scenarios is discussed in other sections of this chapter. CT may be helpful to provide improved localization of heterotopic bone. This study is especially helpful in the evaluation of the proximal radioulnar joint. Bone scans and magnetic resonance imaging (MRI) scans are not routinely needed in the evaluation of the stiff elbow. Pittinger68 believed that ectopic ossification

Chapter 31 Ectopic Ossification About the Elbow

481

FIGURE 31-9

A, Third-degree burn associated with extensive ectopic bone but a normal joint. B, Surgical excision reliably restores function.

should not be excised before 12 months after onset. This was based on the belief that excision of active ectopic bone would lead to recurrence. However, more recent studies dispute this claim. Jupiter43 and McAuliffe53 have shown that active ectopic ossification about the elbow can be excised without an increase in recurrence.

GENERAL PRINCIPLES OF TREATMENT Not all ectopic bone formation about the elbow requires surgical treatment. Ectopic ossification that does not produce symptoms or interfere with the functional arc of elbow rotation should be treated without surgery. The goal of treatment is not, and should not be, normal motion. The main indication for surgical management is ectopic bone producing an arc of elbow motion that is less than functional and limits the patient’s activities of daily living or interferes with occupational or recreational pursuits. Morrey et al61 has shown that a functional arc of motion about the elbow includes a flexion-extension arc of 30 to 130 degrees and forearm rotation of 50 degrees of pronation and supination. Ninety percent of activities of daily living can be performed within this motion arc.

Surgical expectation of the patient and surgeon need to coincide. Patients must understand the concept of a functional motion arc as well as the risk-benefit ratio. Each patient must also be committed to a rigorous postoperative therapy and splinting program. Tomograms may be necessary to determine whether the joint surfaces are congruous. In traumatic circumstances, if the joint surfaces are not congruous, total elbow arthroplasty or distraction arthroplasty may be necessary. The maturation is judged with plain radiographs. We do not employ laboratory tests or technetium bone scans because they are of limited value for determining the timing of resection. When considering surgical excision of heterotopic ossification about the elbow the following criteria should be considered: (1) symptomatic limitation of elbow motion; (2) healing of associated fractures; (3) congruent articular surfaces; (4) lack of severe arthritic changes; (5) soft tissue stabilization about the elbow; (6) stabilization of brain injury; (7) patient motivation and understanding of the surgical goals and postoperative regimen. General principles include (1) excision of all motionlimiting heterotopic bone; (2) avoiding articular cartilage damage; (3) atraumatic tissue handling; (4) careful hemostasis; (5) suction drainage of the wound; (6) avoiding

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the creation and deposit of bone dust in the joint by the use of osteotomes rather than saws; (7) meticulous lavage; (8) avoiding neurologic injury; and (9) early postoperative range of motion. Careful preoperative planning is crucial to identify areas to be resected and the appropriate and safe surgical approach to access all involved heterotopic bone.

Timing of Surgical Treatment The appropriate timing of surgical intervention remains controversial; however, the trend is toward earlier surgical excision of function-limiting ectopic ossification about the elbow. As previously discussed, recent articles have demonstrated no evidence of increased recurrence rates when early excision is performed.38,43,53 Various methods of postoperative prophylaxis were used in this study (including no prophylaxis). Long surgical delays are not without risks. Severe limitation of elbow rotation is extremely disabling and persistent contracture may lead to articular cartilage destruction. Many surgeons now consider a 3- to 4-month interval adequate and proceed with surgical excision at that time. The senior author still prefers to wait at least 6 months. A surgical delay in excess of 6 months, however, is appropriate in certain situations. Surgical delays in burn and head injuries etiologies allow soft tissue maturation and maximum neurologic recovery. The pediatric population also may benefit from prolonged observation as spontaneous resolution is known to occur.

Indications to Interpositional Arthroplasty and Total Elbow Arthroplasty Radiographic evaluation of patients with elbow ectopic ossification should include consideration of associated elbow incongruity and arthritic changes. Joint surface incongruity could represent arthritic surface malunion or residual elbow instability. Both can lead to progressive arthritic changes about the elbow and require treatment at the time of ectopic bone excision. Malunions are best treated with osteotomy and residual instability with ligamentous repair or reconstruction as indicated. Concomitant interpositional arthroplasty is indicated in a younger patient with coexisting articular surface damage representing greater than 50% of the joint surface.59 This same scenario in an older patient or more sedentary patient, is probably best managed with total elbow replacement. The age cutoff for these procedures is controversial.66

ULNAR NEUROPATHY IN ASSOCIATION WITH ECTOPIC BONE FORMATION Late ulnar neuropathy may occur as a result of compression in the cubital tunnel from ectopic bone. Sometimes when completely encased in bone, it is further at

risk if elbow motion increases while it remains tethered or compressed by the ectopic ossification. Although ulnar neuropathy from ectopic bone is most often found in the brain-injured adult,32,34,47,89 it occurs after burns88 and trauma as well. In a 5-year period, 2.5% of the adult brain-injured population in one study developed late ulnar neuropathy.47 Fourteen percent had a history of trauma, and 86% were found to have idiopathic heterotopic ossification associated with spasticity. Treatment consisted of ulnar nerve transposition anteriorly, with 85% of the patients having complete recovery. We completely free the nerve from the ectopic bone for a distance of 3 cm with preservation of function. Simple subcutaneous translocation of the nerve is adequate. If completely surrounded by bone, I usually release the nerve, remove the ectopic bone and replace it in its bed, or translocate the nerve if it is stretched by motion.

Indications for Ulnar Nerve Transposition Ulnar nerve transposition is frequently indicated when surgical excision of ectopic ossification is undertaken. Simple subcutaneous transposition is the procedure of choice. Submuscular transposition is undesirable in this clinical scenario due to poor muscular beds, scarring, and prior zones of injury. The most common indication for transposition is associated ulnar nerve symptoms preoperatively. Further indications include preoperative flexion of less than 90 degrees and a preoperative arc of motion less than 60 degrees.

SURGICAL TECHNIQUES In all instances, the basic surgical strategy is to remove the ectopic bone at its narrowest portion, and with the least risk to the articulation. It is often possible to visualize the interface between normal and heterotopic bone. Avoid injury to cartilage by excising enough bone to initiate some motion and define the joint line. Once some motion is initiated, additional bone is resected as necessary. Capsular contracture releases are also often indicated to achieve a functional arc of motion. Both anterior and posterior capsular releases may be required in addition to heterotopic bone resection. The collateral ligaments are preserved, even if calcification is seen in these structures radiographically. Ligamentous calcification is not true heterotopic ossification and rarely limits motion. The operation is not complete until near full range of motion is returned. A flexion-extension arc of 10 degrees to 140 degrees and forearm rotation arc of 60 degrees to 60 degrees should be obtained.

Surgical Approach In most cases, a posterior skin incision is made. Subcutaneous dissection is performed laterally or medially depending on the location of the bridge.

Chapter 31 Ectopic Ossification About the Elbow

For the posterolateral resection, the triceps mechanism is retracted medially without disturbing its insertion, and the ectopic bone is exposed subperiosteally. The central bridge of ectopic bone is resected initially. The elbow is then flexed, and attachments of the ectopic bone to the humerus and olecranon are removed. Anterior capsule release is not necessary. Varying amounts of the olecranon are excised to reduce olecranon impingement. The posterior bar is the easiest to resect and, in our experience, has an excellent prognosis. A medial exposure is employed when (1) posterior ectopic bone extends to the medial aspect of the elbow, (2) ulnar nerve transposition is necessary, and (3) the medial collateral ligament requires resection. The ulnar nerve is always identified first and in some cases is completely surrounded by bone. The triceps expansion is exposed and incised distally to the triceps insertion. The ectopic bone is subperiosteally exposed and resected. When the ectopic bone interferes with ulnar nerve function, the nerve is decompressed or transferred anteriorly if necessary.

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The use of postoperative radiation remains controversial. Gaur et al36 found no recurrence in children with burns as the etiology. Jupiter and Ring43 found no recurrence in 17 patients in whom post-traumatic radioulnar synostoses were excised. No prophylaxis was used in either patient group. However, Jupiter and Ring43 later reported on surgical treatment of complete anklyosis about the elbow and found recurrences in one third of the trauma cohort and one patient in the burn cohort. The authors now use prophylactic radiation routinely. Prospective randomized studies are needed to further define the use of this modality.

Medial Excision

If an anterior excision is necessary, the bone is exposed by elevating the origins of the brachioradialis and common extensor tendons. Occasionally, an anterior approach is used. The interval between the brachioradialis and brachialis muscles is identified. The radial nerve is identified and retracted laterally. The brachialis muscle fibers are split at their most lateral border, and the muscle is elevated off the ectopic bone. The central bridge of bone is resected, allowing motion of the elbow, which further facilitates resection of the ectopic bone off the humerus and coronoid process.

Anterolateral Approach

Closure Bone wax is applied to all exposed bony surfaces. The tourniquet is deflated, and hemostasis is achieved before wound closure. Routine layered closure is then performed over a suction drain. No attempt is made to close the capsule. A soft dressing is applied that will allow immediate postsurgical range of motion.

POSTOPERATIVE MANAGEMENT If the process involves muscle fibers, the surgical field is treated with 700 cGy radiation. Otherwise, 75 mg indomethacin is prescribed 3 weeks before and 8 weeks after surgery. The elbow is managed with continuous motion and splints as described in Chapters 10 and 11. When motion goals are not met, manipulation under anesthesia is performed 6 weeks after surgery.

ADJUVANT TREATMENT TO PREVENT ECTOPIC BONE FORMATION There are three main adjuvants to reduce the likelihood of ectopic bone formation after excision: (1) oral nonsteroidal anti-inflammatory agents, (2) oral diphosphonates, and (3) low-dose external beam irradiation. Several authors have shown that indomethacin is an effective agent54,71,77 that significantly reduces the formation of ectopic bone about the hip. The recommended dosage is 75 mg daily for 6 weeks after surgery.54,71,77 We typically begin the treatment 1 to 2 weeks before the surgery but have no scientific basis for this practice. Oral diphosphonates have been used,24,79,83 and experimental data have shown this class of drug to delay the mineralization of osteoid.69 Unfortunately, when these drugs are discontinued, the osteoid may mineralize.77,80 Low-dose external beam irradiation has been shown to be an effective method of preventing ectopic bone formation about the hip after total hip arthroplasty3,4,14,49 and following acetabular fractures.6 Recent studies noted effective control of ectopic bone with only 700 cGy in a single dose.3,4 External beam irradiation should be delivered to the high-risk patient within 24 hours and no later than 72 hours after surgery. Delay of radiation treatments beyond 72 hours significantly reduces its effectiveness. Potential or theoretical problems of lowdose irradiation include wound healing problems and nonunion. The risk of postirradiation sarcoma is extremely rare. In the past 10 years, we have treated more than 100 patients with low-dose irradiation for control of ectopic bone formation about the elbow and hip, and we have never detected delayed wound healing that was attributable to the low-dose irradiation. When necessary, bone graft fracture sites may be shielded.25 In our experience, there have been no nonunions directly attributable to the low-dose irradiation. There are more than 130 postirradiation sarcomas in the Mayo Clinic files, and none has been caused by the use of low-dose irradiation for the prevention of ectopic bone.26 We have found no instance of sarcoma to have developed after doses of 3000 cGy or less.

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in the setting of neuromuscular blockade. Arthritis Rheum. 40:1619, 1997. Hastings, H., and Graham, T. J.: The classification and treatment of heterotopic ossification about the elbow and forearm. Hand Clinic 102:417-437, 1994. Hoffer, M. M., Brody, G., and Ferlic, F.: Excision of heterotopic ossification about the elbows in patients with thermal injury. J. Trauma 18:667, 1978. Hunter, T., Dubo, H. I. C., Hildahl, C. R., Smith, N. J., and Schroeder, M. L.: Histocompatibility antigens in patients with spinal cord injury or cerebral damage complicated by heterotopic ossifications. Rheum. Rehabil. 19:97, 1980. Ilahi, O. A., Strausser, D. W., and Gabel, G. T.: Post-traumatic heterotopic ossification about the elbow. Orthopedics 21:265, 1998. Josefsson, P. O., Johnell, O., and Gentz, C. F.: Long-term sequelae of simple dislocation of the elbow. J. Bone Joint Surg. 66A:927, 1984. Jupiter, J. B., and Ring, D.: Operative treatment of posttraumatic proximal radioulnar synostosis. J. Bone Joint Surg. 80A:248, 1998. Kamineni, S., Maritz, N. G., and Morrey, B. F.: Proximal radial resection for posttraumatic radial synostosis: A new technique to improve forearm rotation. J. Bone Joint Surg. 84A:745, 2002. Kaplan, F. S., Tabas, J. A., Gannon, F. H., Finkel, G., Hahn, G. V., and Zasloff, M. A.: The histopathology of fibrodysplasia ossifican progressive. An enchondral process. J. Bone Joint Surg. 75A:220, 1993. Keenan, M. A. E., and Haider, T.: The formation of heterotopic ossification after traumatic brain injury: A biopsy study with ultrastructural analysis. J. Head Trauma Rehabil. 11:8-22, 1996. Keenan, M. A., Kauffman, D. L., Garland, D. E., and Smith, C.: Late ulnar neuropathy in the brain-injured adult. J. Hand Surg. 13A:120, 1988. King, B. B.: Resection of the radial head and neck: An end result of thirteen cases. J. Bone Joint Surg. 21:839, 1939. Klein, L., Van Den Noort, S., and Dejak, J. J.: Sequential studies of urinary hydroxyproline and serum alkaline phosphatase in acute paraplegia. Med. Serv. J. Can. 22:524, 1966. Larson, J. M., Michalski, J. P., Collacott, E. A., Eltorai, D., McCombs, C. C., and Madorsky, J. B.: Increased prevalence of HLAB27 in patients with ectopic ossification following traumatic spinal cord injury. Rheum. Rehabil. 20:193, 1981. Linscheid, R. L., and Wheeler, D. K.: Elbow dislocations. J. A. M. A. 194:1171, 1965. Mason, M. L.: Some observations on fractures of the head of the radius with a review of 100 cases. Br. J. Surg. 42:123, 1954. McAuliffe, J. A., and Woitson, A.: Early excision of heterotopic ossification about the elbow followed by radiotherapy. J. Bone Joint Surg. 79A:749-755, 1997. McLaren, A. C.: Prophylaxis with indomethacin for heterotopic bone after open reduction of fractures of the acetabulum. J. Bone Joint Surg. 72A:245, 1990. McLaughlin, H. L.: Some fractures with a time limit. Surg. Clin. North Am. 35:553, 1955.

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56. Mikic, Z. D., and Vukadinovic, S. M.: Late results in fractures of the radial head treated by excision. Clin. Orthop. Rel. Res. 181:220, 1983. 57. Minaire, P., Betuel, H., Girard, R., and Pilonchery, G.: Neurologic injuries, paraosteoarthropathies, and human leukocyte antigens. Arch. Phys. Med. Rehabil. 61:214, 1980. 58. Mollan, R. A. B.: Serum alkaline phosphatase in heterotopic para-articular ossification after total hip replacement. J. Bone Joint Surg. 61B:423, 1979. 59. Morrey, B. F.: Posttraumatic stiffness: Distraction arthroplasty. Orthopedics 15:863-869, 1992. 60. Morrey, B. F., Askew, L. J., An, K. N., and Dobyns, J. H.: Rupture of the distal tendon of the biceps brachii: A biomechanical study. J. Bone Joint Surg. 67A:418, 1985. 61. Morrey, B. F., Askew, L. J., and Chao, E. Y.: A biomedical study of functional elbow motion. J. Bone Joint Surg. 63A:872-877, 1981. 62. Munin, M. C., Balu, G., and Sotereanos, D. G.: Elbow complications after organ transplantation. Case reports. Am. J. Phys. Med. Rehab. 74:672, 1995. 63. Munster, A. M., Bruck, H. M., Johns, L. A., von Prince, K., Kikman, E. M., and Remig, R. L.: Heterotopic calcification following burns: A prospective study. J. Trauma 12:1071, 1973. 64. Orzel, J. A., and Rudd, T. G.: Heterotopic bone formation: Clinical, laboratory, and imaging correlation. J. Nucl. Med. 26:125, 1985. 65. Newman, J. H.: Displaced radial neck fractures in children. Injury 9:114, 1977. 66. Peden, J. P: Total elbow arthroplasty for the management of the ankylosed or fused elbow. J. Bone Joint Surg. [Br.] (Accepted for publication, 2008) 67. Peterson, S. L., Mani, M. M., Crawford, C. M., Neff, J. R., and Hiebert, J. M.: Post burn heterotopic ossification: insights for management decision making. J. Trauma 29:365, 1989. 68. Pittinger, D. E.: Hetertopic ossification. Orthop. Rev. 20:33, 1991. 69. Plasmans, C. M. T., Kuypers, E. I. M., and Sloof, T. J. J. H.: The effect of ethane-1-hydroxy-1, l diphosphonic acid (EHDP) on matrix-induced ectopic bone formation. Clin. Orthop. Rel. Res. 132:233, 1978. 70. Razemon, J. P., Decoulx, J., and Leclair, H. P.: Les synostoses radiocubitales posttraumatiques de l’adulte. Acta Orthop. Belgica 31:5, 1965. 71. Ritter, M. A., and Sieber, J. M.: Prophylactic indomethacin for the prevention of heterotopic bone formation following total hip arthroplasty. Clin. Orthop. Rel. Res. 196:217, 1985. 72. Roberts, P. H.: Heterotopic ossification complicating paralysis of intracranial origin. J. Bone Joint Surg. 50B:70, 1968. 73. Roberts, P. H.: Dislocation of the elbow. Br. J. Surg. 56:806, 1969. 74. Rogers, J. G., and Geho, W. B.: Fibrodysplasia ossificans progressiva: a survey of forty-two cases. J. Bone Joint Surg. 61A:909, 1979. 75. Russell, T. A.: Malunited fractures. In Crenshaw, A. H. (ed.): Campbell’s Operative Orthopaedics, 7th ed., vol. 3. St. Louis, C. V. Mosby, 1987, p. 2041.

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76. Schiele, H. P., Hubbard, R. B., and Bruck, H. M.: Radiographic changes in burns of the upper extremity. Radiology 104:13, 1972. 77. Schmidt, S. A., Kjaersgaard-Andersen, P., Pedersen, N. W., Kristensen, S. S., Pedersen, P., and Neilson, J. B.: The use of indomethacin to prevent the formation of heterotopic bone after total hip arthroplasty. J. Bone Joint Surg. 70A:834, 1988. 78. Seignalet, J., Moulin, M., Pelissier, J., Romain, M., BouffeardVercelli, M., Lapinski, H., and Roquefeuil, B.: HLA and neurogenic paraosteoarthropathies. Tissue Antigens 21:268, 1983. 79. Stover, S. L., Niemann, K. M., and Miller, J. M.: Disodium etidronate in the prevention of postoperative recurrence of heterotopic ossification in spinal cord injury patients. J. Bone Joint Surg. 58A:683, 1976. 80. Stover, S. L., Niemann, K. M., and Tullos, J. R.: Experience with surgical resection of heterotopic bone in spinal cord injury patients. Clin. Orthop Rel. Res. 263:71, 1991. 81. Sutro, C. J.: Regrowth of bone at the proximal end of the radius following resection in this region. J. Bone Joint Surg. 17:867, 1935. 82. Tepperman, P. S., Hilbert, L., Peters, W. J., and Pritzker, K. P. H.: Heterotopic ossification in burns. J. Burn Care Rehabil. 5:283, 1984.

83. Thomas, B. J., and Amstutz, H. C.: Results of the administration of diphosphonate for the prevention of heterotopic ossification after total hip arthroplasty. J. Bone Joint Surg. 67A:400, 1985. 84. Thompson, H. C., and Garcia, A.: Myositis ossificans: Aftermath of elbow injuries. Clin. Orthop. Rel. Res. 50:130, 1967. 85. Tooms, R. E.: Complications of treatment of injuries to the forearm. In Epps, C. H. (ed.): Complications in Orthopaedic Surgery, 2nd ed., vol. 1. Philadelphia, J. B. Lippincott, 1986, p. 325. 86. Vince, K. G., and Miller, J. E.: Cross-union complicating fracture of the forearm. Part 1. Adults. J. Bone Joint Surg. 69A:640, 1987. 87. Viola, R., and Hastings, H.: Treatment of ectopic ossification about the elbow. CORR 370:65-86, 2000. 88. Vorenkamp, S. E., and Nelson, T. L.: Ulnar nerve entrapment due to heterotopic bone formation after a severe burn. J. Hand Surg. 12A:378, 1987. 89. Wainapel, S. F., Rao, P. U., and Schepsis, A. A.: Ulnar nerve compression by heterotopic ossification in a head-injured patient. Arch. Phys. Med. Rehabil. 66:512, 1985.

SECTION

B

SOFT TISSUE CONSIDERATIONS

CHAPTER

32

Extrinsic Contracture: Lateral and Medial Column Procedures Pierre Mansat and Bernard F. Morrey

INTRODUCTION Of the numerous potential causes for elbow stiffness, the causes and pathophysiologic mechanisms dictate treatment and affect prognosis. Extrinsic contracture typically involves only the soft tissues around the elbow, sparing the joint space (Fig. 32-1).45 Post-traumatic stiffness is one of the most frequent causes of this kind of contracture47; however, it can also occur in association with other causes, such as congenital or developmental disease, osteoarthritis or inflammatory arthritis, burns, and head injury. Intrinsic contracture is associated with joint articular involvement and is not discussed here (see Chapters 33 and 69). Several options have been proposed for treatment of elbow contracture. Conservative treatment sometimes gives good results if the contracture is of short duration4,6,13,15,16,21,23,38,46; however, its efficacy is unpredictable. With failure of nonoperative treatment, surgical release may be indicated. Most employ an open procedure, and several have been described.1,3,7,9-12,17,19,22,26,27,31-34,39,43,51,53,55,56,58-64 There is, however, an increasing interest in using an arthroscopic procedure.5,29,35,49,52,54,57

ETIOLOGY AND INCIDENCE An extrinsic contracture usually involves the periarticular soft tissue without involving the articulating surface. Contracture may involve the capsuloligamentous structures or muscle tissue. Ectopic ossification is also considered an extrinsic condition. Bone may form a bridge across the joint or form in the capsule or in the muscle crossing the joint. Trauma is the major cause of extrinsic stiffness, especially elbow dislocation, with or without fracture.30,41 The brachialis muscle that crosses the anterior capsule36 tears with dislocation, developing scar tissue or ectopic bone when healing,49 often associated with contracture of the capsule.25,47,65 Pain, swelling, limited motion, and contracture after this type of elbow trauma then leads to the irreversible changes that constitute extra-articular ankylosis. Collateral injuries can contribute to elbow ankylosis from permanent contracture.8,24,28 In trauma, length of immobilization has also been recognized as a major contributor to postinjury contracture. The precise incidence of elbow stiffness after trauma is difficult to identify and is as much a function of the severity of injury as of the initial treatment. In adults, nontraumatic elbow contractures are usually caused by a primary inflammatory process. With osteoarthritis, a mild inflammatory synovitis occurs with periarticular fibrosis and osteophytic new bone formation.50 The articular surface of the joint is intact, but osteophytes are present at the tip of the olecranon and at the tip of the coronoid process.3 Hemophilia,14 juvenile rheumatoid arthritis, acute or chronic septic arthritis, and periarticular new bone formation after head injury18,37,42 can produce ankylosis of the elbow but often involve the joint space. Congenital stiffness is rare and is often associated with bone malformation or soft tissue dysplasia.2

PRESENTATION AND CLASSIFICATION Post-traumatic contracture of the elbow usually affects young, active patients around 40 years of age, who need 487

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FIGURE 32-1

A, Radiograph of a stiff elbow after dislocation appears normal, but the range of flexion was 70 to 100 degrees. B, An intense reaction in the anterior capsule caused the contracture.

the use of the elbow joint. Although such contractures are often related to intrinsic lesions, they can be associated with extrinsic stiffness. Osteoarthritis, on the other hand, involves patients in their mid-50s, predominantly men. At the beginning, the lesions are periarticular and can be considered an extrinsic condition. Generally, the patient initially notices loss of full extension but no limitation of activity. The first complaint is pain in terminal extension. Concurrent with this is the recognition that midarc motion typically is not painful, a finding that confirms the extrinsic character of the stiffness. Occasionally, full flexion also produces pain. Flexion contracture develops progressively. In addition to classifying elbow contracture according to extrinsic and intrinsic lesions, age of the patient, severity of the stiffness, and distribution of the contracture are also important for evaluating what might be expected from the surgery. Thus, the stiffness may be graded as very severe, severe, moderate, or minimal, depending on data on the amount of residual arc of flexion.1,17,48 The stiffness is considered very severe when the total arc is 30 degrees or less, severe when it is between 31 and 61 degrees, moderate between 61 and 90 degrees, and minimal when it is greater than 90 degrees. Based on the functional arc of motion described by Morrey and colleagues,48 the distribution of the contracture referable to the 30- to 130-degree arc is also considered.

DIAGNOSIS Diagnosis of the contracture is usually made by identifying a characteristic history and performing a physical examination. Joint involvement is confirmed by plain radiographs. The anteroposterior view gives good visualization of the joint line, but the lateral view demonstrates osteophytes on the coronoid and at the tip of the olecranon, even when the joint space is preserved. The details of the extent of the involvement are best observed on tomography. Transverse imaging by magnetic resonance imaging (MRI) or computed tomography (CT) has little use in our practice.

INDICATIONS GENERAL Capsular release is indicated for extrinsic lesions with flexion contracture greater than 60 degrees and flexion less than 100 degrees. Surgical intervention is pursued only after very careful discussion of its risks and benefits. The patient’s specific expectations and functional needs, and an estimate of the likelihood that the procedure will satisfy those needs, are carefully addressed. The potential for improving motion at the expense of stability, strength, and pain is also specifically discussed.

Chapter 32 Extrinsic Contracture: Lateral and Medial Column Procedures

Open Release The procedure described herein is relatively straightforward and may be reliably performed by the well-trained orthopedic surgeon. Arthroscopic release should be considered by those with experience and a fairly high level of competency with both the elbow and with the scope. Furthermore, the presence of ulnar nerve symptoms is an additional indication for an open procedure.

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ADVANTAGES 1. Allows exposure of the anterior and posterior compartment 2. Direct access to the radial head 3. Preserves the lateral collateral ligament 4. Relatively simple to perform.

DISADVANTAGES

CONTRAINDICATIONS Limited involvement and limited soft tissue contracture argue against these procedures. An inadequate period of an appropriate splint program is also a contraindication. Intrinsic lesions are not absolute contraindications, but a lower level of improvement has to be expected in these cases.39

PREOPERATIVE PLANNING Before surgery, the decision must be made to approach the capsule from the lateral or medial aspect. If the ulnar nerve is to be addressed or there is extensive medial or coronoid arthrosis, the medial approach is of value. If the radiohumeral joint is involved or if a simple release is all that is required, the lateral “column” procedure is carried out (Fig. 32-2).

TECHNIQUE: COLUMN PROCEDURE

1. Difficulty in removing heterotopic bone on the medial side of the joint 2. Exploration and mobilization of ulnar nerve requires additional exposure The column procedure consists of open arthrolysis of the elbow through a limited lateral approach, with the aim of releasing the anterior capsule safely but also of releasing the triceps attachment and posterior capsule, if necessary. The exposure employs a limited skin incision of only about 6 cm, but this is sufficient to remove coronoid or olecranon osteophytes (Fig. 32-3). General anesthesia has been used for the majority of patients. The patient is placed supine with a sandbag under the ipsilateral extremity, and the involved arm is freely draped. The proximal half of Kocher’s incision is performed if no previous incision was present and if there are no ulnar nerve symptoms. If, previously, a posterior skin incision was made, it is re-entered and a subcutaneous dissection laterally exposes the lateral column. To release the anterior capsule with minimal disruption of normal tissue, the origin of the distal fibers of

INDICATIONS 1. Treatment of extrinsic elbow contracture 2. Degenerative arthritis with anterior and posterolateral osteophytes

Avascular supracondylar ridge the “column”

THE COLUMN PROCEDURE Lateral column

Posterior capsule release

Anterior capsule release Coronoid osteophyte

Olecranon osteophyte

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FIGURE 32-2

The supracondylar bone immediately proximal to the lateral epicondyle is called the column.

FIGURE 32-3

The concept of the release is to identify the supracondylar ridge and approach the anterior and posterior capsules as necessary. Removal of anterior and posterior osteophytes is readily accomplished.

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the brachioradialis and the extensor carpi radialis longus are identified (Fig. 32-4A). Release of the fleshy origin of the extensor carpi radialis longus and the distal fibers of the brachioradialis from the humerus provides direct access to the superior aspect lateral of the capsule (see Fig. 32-4B). The capsule is entered anteriorly at the radiohumeral joint, an approach that allows identification of the thickness and orientation of the capsule. The brachialis muscle is swept from the anterior capsule with a periosteal elevator. A specially designed retractor protects the brachialis muscle, the median nerve, and the brachial artery (see Fig. 32-4C). The anterior capsule is

Lateral column

Anterior interval

grasped and excised, at least to the level of the coronoid. The medial most aspect of the capsule is often difficult to visualize clearly but can be palpated. It is incised to complete the release (Fig. 32-4D). At this juncture, if extension is full or within 10 degrees of normal and the radiographs reveal no olecranon spur, no additional release is needed and the wound is closed. If scarring is extensive and adhesions involve the posterior capsule, the triceps is elevated from the posterior aspect of the humerus. The posterior capsule is released, and the olecranon fossa is cleaned of soft tissue (see Fig. 32-4E). The tip of the olecranon is excised when osteophytes

Intermuscular septum

Brachioradialis

Common ECRL extensor tendon ECRB

Brachioradialis ECRL

CET

Posterior interval

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Triceps lateral head

A

Triceps Anconeus

B

Brachioradialis

ECRL

C Posterior interval

D FIGURE 32-4

E

A limited Kocher skin incision measuring 6 cm is made over the lateral epicondyle. A, The anterior and posterior aspects of the lateral column are identified. B, The extensor carpi radialis longus (ECRL) and distal fibers of the brachioradialis are elevated. C, A special retractor facilitates exposure and protection of the anterior structures. D, The anterior capsule is isolated from the brachialis and identified by arthrotomy at the anterior radiohumeral joint. E, The lateral capsule is excised as widely as possible, and the remaining medial capsule is incised. The posterior capsule is identified (D) and excised as necessary by elevating the triceps from the lateral osseous column. The posterior aspect of the ulnohumeral joint is exposed and the capsule incised (see Fig. 32-3). ECRB, extensor carpi radialis brevis.

Chapter 32 Extrinsic Contracture: Lateral and Medial Column Procedures

are present. The range of flexion and extension at the elbow is assessed. If flexion is essentially normal, nothing more need be done posteriorly. If there are symptoms of or if the clinical examination has shown ulnar nerve irritation, a posterior incision is used and a medial flap is elevated. The ulnar nerve is inspected—and occasionally translocated—but more often, it is simply decompressed in situ. If the ulnar nerve is known to be a major component of the lesion, the medial approach to the capsule of Hotchkiss is preferred, but the skin incision is posterior. With a simple lateral approach, “anterior only” release has minimal postoperative bleeding and drains are not required. As the complexity of the surgery and the severity increase, however, postoperative hematoma must be avoided. Because retained blood and hematoma causes pain, inflammation, and occasionally temporary nerve dysfunction and retards progress toward improved motion, a drain is appropriate.

MEDIAL RELEASE INDICATIONS 1. Treatment of contracture release and stiff elbow 2. Degenerative arthritis with anterior and posteromedial osteophytes 3. Ulnar nerve symptoms

ADVANTAGES 1. Allows exposure, protection, and transposition of the ulnar nerve 2. Preserves the anterior medial collateral ligament 3. Affords access to the coronoid with intact radial head

DISADVANTAGES 1. Difficulty in removing heterotopic bone on the lateral side of the joint 2. Affords poor access to radial head

DESCRIPTION OF EXPOSURE See also Chapter 7.

PATIENT POSITIONING AND SKIN INCISION The patient is usually positioned supine, supported by an elbow or a hand table. Two folded towels should be placed under the scapula. The author (R.H.) prefers a sterile tourniquet. To expose the posterior joint, the

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patient’s shoulder should have fairly free external rotation; otherwise, the arm should be positioned over the chest. The skin incision may be a posterior skin incision or a midline medial one. The key to this exposure is identification of the medial supracondylar ridge of the humerus. At this level, the surgeon can locate the medial intermuscular septum, the origin of the flexor pronator muscle mass, and the ulnar nerve. This site also serves as the starting point of the anterior and posterior subperiosteal extracapsular dissection of the joint.

EXPOSING THE ULNAR NERVE AND THE MEDIAL FASCIA Once the medial intermuscular septum is identified, the medial antebrachial cutaneous nerve is identified, traced distally, and protected. The branching pattern varies, however, so it is occasionally necessary to divide the nerve to gain full exposure and to adequately mobilize the ulnar nerve, especially in revision surgery. If this is necessary, the nerve is divided as proximally as the skin incision will allow, ensuring that the cut end lies in the subcutaneous fat. If previously anterior transposition was performed, the nerve should be fully identified and mobilized before proceeding. The surgeon must be prepared to extend the previous incision proximally, as necessary. In this setting, the nerve is often flattened over the medial flexor-pronator muscle mass, or it can “subluxate” to a posterior position. This dissection requires patience and may take considerable time. Dissection of the nerve needs to be carried distally far enough to allow the nerve to sit in the anterior position without being kinked distal to the epicondyle. The septum is excised from the insertion on the supracondylar ridge to the proximal extent of the wound, usually about 5 to 8 cm. Many of the veins and perforating arteries at the most distal portion of the septum require cauterization.

EXPOSING THE ANTERIOR CAPSULE FOR EXCISION AND INCISION Once the septum has been excised, the flexor-pronator muscle mass should be divided parallel to the fibers, leaving approximately a 1.5-cm span of flexor carpi ulnaris tendon attached to the epicondyle (Fig. 32-5A). The surgeon then returns the supracondylar ridge and begins elevating the anterior muscle with a Cobb elevator. Subperiosteally, the anterior structures of the distal humeral region proximal to the capsule are elevated, to allow placement of a wide Bennett’s retractor. As the elevator moves from medial to lateral, the handle of the

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Flexor/pronator attachment

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Brachialis

Flexor/pronator attachment Capsule

A

B

Excised capsule

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Medial column

C

D

Medial head of triceps

FIGURE 32-5

A, After the ulnar nerve has been identified and protected and the septum excised, the flexor-pronator muscle mass is divided, leaving a cuff for reattachment. B, After the fibers of the brachialis are swept from the anterior capsule, a special elbow or Bennett retractor is placed across the joint and the interval between the capsule and muscle is developed further. Once the capsule has been adequately exposed, it is excised as far laterally as can be identified. C, The last fibers laterally may be incised if excision cannot be safely done. D, If contracture persists posteriorly, the medial aspect of the triceps is elevated, and the posterior capsule is identified and excised, along with any ectopic bone or spur formation.

elevator is lifted carefully, keeping the blade of the elevator along the surface of the bone. When heterotopic ossification along the lateral distal humerus is profuse, the radial nerve is at risk if it is entrapped in the scar on the surface of the bone. A separate approach to the lateral side is sometimes needed (see section on column procedure). The median nerve, brachial vein, and artery are superficial to the brachialis muscle. A small cuff of fibrous tissue of the origin can be left on the supracondylar ridge as the muscle is elevated. This facilitates reattachment during closing. A proximal, transverse incision in the lacertus fibrosus may also be needed to adequately mobilize this layer of muscle. Once the Bennett retractor is in place and the medial portion of the flexor-pronator has been incised, the

plane between muscle and capsule should be carefully elevated (see Fig. 32-5B). As this plane is developed, the brachialis muscle is encountered from the underside. This muscle should be kept anterior and elevated from the capsule and anterior surface of the distal humerus. Finding this plane requires careful attention. The dissection of the capsule from the brachialis muscle proceeds both laterally and distally. At this point, it is helpful to feel for the coronoid process by gently flexing and extending the elbow. The first few times that this approach is used, the coronoid seems deep and far distal. A deep, narrow retractor is often helpful to allow the operator to see down to the level of the coronoid. The extreme anteromedial corner of the exposure deserves special comment. In a contracture release, the

Chapter 32 Extrinsic Contracture: Lateral and Medial Column Procedures

anteromedial portion often requires release. To see this area, a small, narrow retractor can be inserted to retract the medial collateral ligament, pulling it medially and posteriorly. This affords visualization of the medial capsule and protection of the anterior medial collateral ligament. The anterior capsule should be excised (see Fig. 32-5C) to the extent that that is practical and safe. When first performing this procedure, it is helpful first to incise the capsule from the medial to the lateral aspect along the anterior surface of the joint. Once this edge of the capsule is incised, it can be lifted and excised as far distally as is safe. From this vantage, and after capsule excision, the radial head and capitellum can be visualized and freed of scar, as needed. In cases of primary osteoarthritis of the elbow, removing the large spur from the coronoid is crucial. Using the Cobb elevator, the brachialis muscle can be elevated anteriorly for 2 cm from the coronoid process. With the elevator held in position, protecting the brachialis but anterior to the coronoid, the large osteophyte can be removed with an osteotome. The brachialis insertion is well distal to the tip of the coronoid.

EXPOSING AND EXCISING THE POSTERIOR CAPSULE AND BONE SPURS The posterior capsule of the joint is exposed likewise to the anterior surface. The supracondylar ridge is again identified (see Fig. 32-5D). Using the Cobb elevator, the triceps is elevated from the posterior distal surface of the humerus. The exposure should extend far enough proximal to permit use of a Bennett retractor. The posterior capsule can be separated from the triceps as the elevator sweeps from proximal to distal. The posterior medial joint line should also be identified, as it is often involved by osteophytes or heterotopic bone. In contracture release, the posterior capsule and posteromedial ligaments should be excised. The medial joint line up to the anterior medial ligament should also be exposed and the capsule excised. This area is the floor of the cubital tunnel. In contracture release and in primary osteoarthritis, the tip of the olecranon usually must be excised to achieve full extension. The posteromedial joint line is easily visualized, but the posterolateral side must also be carefully palpated to ensure clearance.

ULNAR NERVE TRANSPOSITION After being reattached to the medial supracondylar region, the ulnar nerve may be transposed and secured with a capacious fascial sling to prevent posterior subluxation. The sling can be fashioned by elevating two overlapping rectangular flaps of fascia or by using a

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medially based flap attached to the underlying subcutaneous tissue. Once this maneuver is completed, the nerve must not be compressed or kinked. The joint should be flexed and extended to ensure that the nerve is free to move. If the release is a simple one of the anterior capsule, the nerve should be observed and protected but need not be mobilized or translocated.

CLOSURE FLEXOR-PRONATOR MUSCLE ORIGIN The flexor-pronator mass should be reattached to the supracondylar ridge with nonabsorbable braided 1-0 or 0 suture. If enough fibrous tissue was left behind, no holes need be drilled in bone. Otherwise, drill holes in the edge of the supracondylar ridge can be made to secure the flexor-pronator mass.

AFTERCARE If the neurologic examination findings in the recovery room are normal, a brachial plexus block is established and maintained with a continuous pump through a percutaneous catheter.20 The arm is elevated as much as possible, and mechanical continuous passive motion exercise is begun the day of surgery and adjusted to provide as much motion as pain or the machine itself allows (see Chapter 10). After 2 days, the plexus block is discontinued, and at day 3, the continuous passive motion machine is stopped. Physical therapy is not used, but a detailed program of splint therapy is prescribed. Adjustable splints are prescribed,46 depending on the motion before and after the procedure (see Chapter 11). The splints include a hyperextension or a hyperflexion brace, or both (Fig. 32-6). A detailed discussion regarding heat, ice, and anti-inflammatory medication, along with a visual schedule for bracing, is provided (see Fig. 32-6). During the first 3 months, the patient sleeps with the splint adjusted to maximize flexion or extension, whichever is more needed, and yet not to be so uncomfortable as to prevent sleeping for at least 6 hours. On rising in the morning, the patient moves the elbow actively in a tub of hot water for 15 minutes and then applies the other splint to hold the elbow at the opposite extreme of motion during the daytime. Between 8:00 in the morning and 12:00 noon, noon and 6:00 in the evening, and 6:00 in the evening and 12:00 midnight, the splint is removed for 1 hour, and the patient is encouraged to move the elbow frequently through a full range of active motion. At bedtime, if the elbow is sore from the activity, ice is applied for 10 to 15 minutes. If the elbow is stiff but not

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Afternoon

Morning Out

Out

AM

Noon II

Evening Out Dinner

III

Sleep Out Bed I

IV

Morning, evening

Night, afternoon

FIGURE 32-6

A printed prescription of the splint use program is provided to patients undergoing splint therapy. Typically the elbow is splinted with a Mayo Elbow Brace in extension at night and at noon; it is placed in flexion in the morning and evening.

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100

100

asked to make tracings of the upper limb with the elbow in maximum flexion and maximum extension and to send them in for review. The angles so formed are measured with a goniometer to document the patient’s progress. After 4 weeks, an arc of about 80 degrees of motion is obtained, and the amount of time that each splint is worn is gradually decreased. Splinting at night is continued for as long as 6 months if flexion contracture tends to recur when the splint is not used. Patients are advised that it may take a year to realize full correction.

RESULTS 55 25

FIGURE 32-7

A functional arc of rotation between 30 and 130 degrees is obtained in more than 50 percent of cases.

sore, heat is applied for the same period. Because the principal objective is to gain motion but to avoid pain, swelling, and inflammation, routine use of an antiinflammatory medication is prescribed. Therapy with splints is continued for about 3 months, during which time the patient is seen at 2- to 4- week intervals, if possible. Because this is not often feasible, the patient is

Recent reports on the results of surgical arthrolysis reveal an absolute gain in the flexion-extension arc between 30 and 60 degrees.1,10,17,26,33,43-45,59 A functional arc of motion between 30 and 130 degrees is obtained in more than 50% of cases, and some improvement in motion in more than 90% of the cases has been reported in the literature (Fig. 32-7).1,10,17,26,33,43-45,51,59 An anterior exposure popularized by Urbaniak produced good results for extrinsic stiffness, but patients with intrinsic stiffness did less well and were not considered ideal candidates for arthrolysis.59 This approach does not address disorders that limit flexion, and requires the identity and protection of the neurovascular structures. The experience was updated additionally with assessment of continuous passive motion (CPM). They concluded that the CPM did improve flexion, but did not considerably improve the amount of elbow extension after surgery.19 In Europe, a combined lateral and medial approach has been used for many years, and gains in flexion arc have averaged between 40 and 72 degrees

Chapter 32 Extrinsic Contracture: Lateral and Medial Column Procedures

150 120 Flexion arc, deg

(in approximately 400 procedures).1,10,11,17,43 Some preferred a posterior extensile approach if medial and lateral exposures are anticipated. The importance of sequential release of tissues has been emphasized based on an experience with 44 of 46 patients (95%) who were satisfied with such an approach.40 The preoperative arc improved from 45 to 99 degrees. The authors emphasize the need to release the exostosis and the collateral ligament when contracted, especially noting the need the posterior portion of the medial collateral ligament and decompress the ulnar nerve when ulnar nerve symptoms exist preoperatively.40 The outcome from different studies using a lateral approach has been gratifying. Husband and Hastings26 reported the results obtained with a lateral approach in seven patients with primarily extrinsic contractures. Range of motion (ROM) for extension contractures improved from 45 to 12 degrees and for flexion contractures from 116 to 129 degrees. The complication rate was low. A recent Scandinavian study reported that, after 5 years, range of motion was acceptable in 11 of the 13 cases.62 Using the same approach, Kessler33 observed improvement in 13 of 14 elbows. Schindler and associates55 employed a lateral approach in 30 patients and obtained a mean improvement of flexion of 35 degrees, and 30% have a normal range of motion. Using a lateral approach, Cohen and Hastings12 obtained an increase of approximately 74 degrees in 22 patients. Similarly, in 12 consecutive patients treated with a lateral exposure, the mean arc before surgery averaged 70 degrees and improved to 117 degrees after surgery, with a mean follow-up of 36 months.34 These authors added a posterior exposure to remove the capsule and osteophytes, when indicated. The Mayo Clinic experience was reported by Mansat and coworkers.39 From 1989 through 1994, 38 elbows were operated on principally for extrinsic stiffness using this limited lateral approach called the column procedure. Trauma was the cause of the contracture in 20 patients (53%). Primary osteoarthritis was responsible for the stiffness in seven patients, heterotopic ossification around the elbow secondary to head trauma or coma in five, a burn in three, congenital stiffness in two, and stiffness due to excessive immobilization after distal biceps repair in one. The mean preoperative arc of total motion was 49 degrees (range 52 to 101 degrees). At an average of 42 months of follow-up, the mean arc of total motion was 92 degrees (range 28 to 120 degrees). The total gain in flexion and extension was 43 degrees, and 33 of 38 patients (87%) enjoyed greater range of motion (Fig. 32-8). Improvement was greater in those with severe or very severe stiffness and with combined flexion-extension contractures. Extrinsic stiffness had better results on improvement of motion. Using a medial approach, Wada and coworkers60 obtained improvement of the mean arc of movement of

495

90 60 30 0 Pre-operative arc

Post-operative arc

FIGURE 32-8.

Clinical results after the initial 38 procedures performed at the Mayo Clinic. Note the considerable individual variation.

64 degrees. A functional arc of flexion/extension (30 to 130 degrees) was obtained in 7 of the 14 elbows. None of the patients developed symptoms related to the ulnar nerve. According to Wada and associates, the medial approach has several advantages over both the anterior and lateral approaches. Pathologic changes in the posterior oblique bundle of the medial collateral ligament can be observed and excised under direct vision. Anterior and posterior exposure is possible through one medial incision, through which a complete soft tissue release and excision of part of the olecranon and coronoid process can be undertaken if necessary. Additional lateral exposure is indicated only if the medial approach has proved to be inadequate.60 In the medial approach, the ulnar nerve is routinely released and protected under direct vision which decreases the risk of damage.

NERVE PALSIES A most important emerging consideration of the proper treatment of the elbow stiffness is the vulnerability of the ulnar nerve. The most common cause of failure of treatment has been those patients in whom the preoperative ulnar nerve symptoms were not appreciated or addressed, or those patients in whom ulnar nerve symptoms developed postoperatively without adequate treatment. This is attributed to traction neuritis caused by the abrupt increase in elbow flexion during the operation. Even in the absence of preoperative neurologic symptoms, the nerve may be compromised subclinically and becomes symptomatic as elbow flexion increases after surgery. Therefore, all patients who have stiff elbows must be evaluated for the presence or absence of ulnar nerve symptoms. Antuna and colleagues3 recommended that elbows with preoperative flexion limited to 90 to 100 degrees in which we expect to improve the

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Part V Adult Trauma

motion by 30 or 40 degrees must be treated with inspection and often prophylactic decompression or translocation of the nerve depending on the appearance of the nerve once the surgical procedure is finished. Furthermore, all patients with preoperative ulnar-nerve symptoms, even if they are mild, are treated with mobilization of the nerve. Manipulation of the elbow in the early postoperative period must be avoided if the nerve has not been decompressed or translocated. In our series, we found that about 10% of patients have dysfunction of the nerve after release. Most of these problems resolve over a period of days or weeks. The radial nerve is also vulnerable, especially if excessive retraction is applied through the lateral approach. The other point of vulnerability is distal at the level of the posterior interosseous nerve.39

COMPLICATIONS In our study,39 complications occurred in 4 of 38 elbows (10%): two cases of intra-articular bleeding, one of which impaired the final outcome; and two transient paresthesias of the ulnar nerve, both of which resolved spontaneously. The typical complication is loss of motion after surgery. Loss of the flexion arc after a period of improvement was seen in 10 patients (26%). Four patients ultimately lost the benefits of the procedure and, on average, had 25 degrees’ less motion than before surgery. The same amount of decreased ROM between the immediate postoperative ROM and the ROM measured at follow-up were reported in the literature. In Cikes’ study, the patients decreased their ROM in flexionextension by 7.77 degrees (range, -35 to 0 degrees).11 Chantelot reported an average decrease between 5 and 15 degrees compared with the mobility obtained just after surgery.10

6.

7.

8. 9.

10.

11.

12.

13.

14.

15.

16.

17.

18.

References 1. Allieu, Y.: Raideurs et arthrolyses du coude. Rev. Chir. Orthop. 75(suppl I):156, 1989. 2. Amadio, P. C., and Dobyns, J. H.: Congenital abnormalities of the elbow. In Morrey, B. F. (ed.): The Elbow and Its Disorders, 3rd ed. Philadelphia, W.B. Saunders, 2000, p. 165. 3. Antuna, S. A., Morrey, B. F., Adams, R. A., and O’Driscoll, S. W.: Ulnohumeral arthroplasty for primary degenerative arthritis of the elbow. Long-term outcome and complications. J. Bone Joint Surg. 84A:2168, 2002. 4. Balay, B., Setiey, L., and Vidalain, J. P.: Les raideurs du coude. Traitement orthopédique et chirurgical. Acta Orthop. Belg. 41:414, 1975. 5. Ball, C. M., Meunier, M., Galatz, L. M., Calfee, R., and Yamaguchi, K.: Arthroscopic treatment of post-traumatic

19.

20.

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22.

23.

elbow contracture. J. Shoulder Elbow Surg. 11:624, 2002. Bonutti, P. M., Windau, J. E., Ables, B. A., and Miller, B. G.: Static progressive, stretch to reestablish elbow range of motion. Clin. Orthop. Relat. Res. 303:128, 1994. Breen, T. F., Gelberman, R. H., and Ackerman, G. N.: Elbow flexion contractures: treatment by anterior release and continuous passive motion. J. Hand Surg. 13B:286, 1988. Buxton, J. D.: Ossification in the ligaments of the elbow. J. Bone Joint Surg. 20:709, 1938. Cauchoix, J., and Deburge, A.: L’Arthrolyse du coude dans les raideurs post traumatiques. Acta Orthop. Belg. 41:385, 1975. Chantelot, C., Fontaine, C., Migaud, H., Remy F, Chapnikoff, D., and Duquennoy, A.: Etude retrospective de 23 arthrolyses du coude pour raideur post-traumatique: facteurs prédictifs du résultat. Rev. Chir. Orthop. 85:823, 1999. Cikes, A., Jolles, B. M., and Farron, A.: Open elbow arthrolysis for posttraumatic elbow stiffness. J. Orthop. Trauma 20:405, 2006. Cohen, M. S., and Hastings, H. II: Posttraumatic contracture of the elbow: Operative release using a lateral collateral ligament sparing approach. J. Bone Joint Surg. 80B:805, 1998. Dickson, R. A.: Reversed dynamic slings. A new concept in the treatment of posttraumatic elbow flexion contractures. Injury 8:35, 1976. Dietrich, S. L.: Rehabilitation and nonsurgical management of musculoskeletal problems in the hemophilic patients. Ann. N. Y. Acad. Sci. 240:328, 1975. Doornberg, J. N., Ring, D., and Jupiter, J. B.: Static progressive splinting for posttraumatic elbow stiffness. J. Orthop. Trauma 20:400, 2006. Duke, J. B., Tessler, R. H., and Dell, P. C.: Manipulation of the stiff elbow with patient under anesthesia. J. Hand Surg. 16A:19, 1991. Esteve, P., Valentin, P., Deburge, A., and Kerboull, M.: Raideurs et ankyloses post-traumatiques du coude. Rev. Chir. Orthop. 57(suppl I):25, 1971. Garland, D. E., and O’Hollarin, R. M.: Fractures and dislocations about the elbow in the head injury adult. Clin. Orthop. Relat. Res. 168:38, 1982. Gates, H. S., Sullivan, R. N., and Urbaniak, J. R.: Anterior capsulotomy and continuous passive motion in the treatment of post-traumatic flexion contracture of the elbow. J. Bone Joint Surg. 74A:1229, 1992. Gaumann, D. M., Lennon, R. L., and Wedel, D. J.: Continuous axillary block for postoperative pain management. Reg. Anesth. 13:77, 1988. Gelinas, J. J., Faber, K. J., Patterson, S. D., and King, G. J. W.: The effectiveness of turnbuckle splinting for elbow contractures. J. Bone Joint Surg. 82B:74, 2000. Glynn, J. J., and Niebauer, J. J.: Flexion and extension contracture of the elbow. Surgical management. Clin. Orthop. Relat. Res. 117:289, 1976. Green, D. P., and McCoy, H.: Turnbuckle orthotic correction of elbow-flexion contractures after acute injuries. J. Bone Joint Surg. 61A:1092, 1979.

Chapter 32 Extrinsic Contracture: Lateral and Medial Column Procedures

24. Gutierrez, L. S.: A contribution to the study of the limiting factors of elbow extension. Acta Anat. 56:146, 1964. 25. Hildebrand, K. A., Zhang, M., and Hart, D. A.: High rate of joint capsule matrix turnover in chronic human elbow contractures. Clin. Orthop. 439:228, 2005. 26. Husband, J. B., and Hastings, H.: The lateral approach for operative release of post-traumatic contracture of the elbow. J. Bone Joint Surg. 72A:1353, 1990. 27. Itoh, Y., Saegusa, K., Ishiguro, T., Horiuchi, Y., Sasaki, T., and Uchinishi, K.: Operation for the stiff elbow. Int. Orthop. 13:263, 1989. 28. Johanson, O.: Capsular and ligament injuries of the elbow joint: clinical and arthrographic study. Acta Chir. Scand. 287(suppl):124, 1962. 29. Jones, G. S., and Savoie, F. H. III: Arthroscopic capsular release of flexion contractures (arthrofibrosis) of the elbow. Arthroscopy 9:277, 1993. 30. Josefsson, P. O., Johnell, O., and Gentz, C. F.: Long-term sequelae of simple dislocation of the elbow. J. Bone Joint Surg. 66A:927, 1984. 31. Judet, J., and Judet, H.: Arthrolyse du coude. Acta Orthop. Belg. 41:412, 1975. 32. Kerboull, M.: Le traitement des raideurs du coude de l’adulte. Acta Orthop. Belg. 41:438, 1975. 33. Kessler, I.: Arthrolysis of the elbow. In Kashiwagi, D. (ed.): Elbow Joint, Proceedings of the International Seminar, Kobe, Japan. International Congress, Series 678. Amsterdam, Excerpta Medica, 1985, p. 77. 34. Kraushaar, B. S., Nirschl, R. P., and Cow, W.: A modified lateral approach for release of posttraumatic elbow contracture. J. Shoulder Elbow Surg. 8:476, 1999. 35. Kim, S. J., and Shin, S. J.: Arthroscopy treatment for limitation of motion of the elbow. Clin. Orthop. Relat. Res. 375:140, 2000. 36. Loomis, J. K.: Reduction and after-treatment of posterior dislocation of the elbow: with special attention to the brachialis muscle and myositis ossificans. Am. J. Surg. 63:56, 1944. 37. Lusskin, R., Grynbaum, B. B., and Dhir, R. S.: Rehabilitation surgery in adult spastic hemiplegia. Clin. Orthop. Relat. Res. 63:132, 1969. 38. MacKay-Lyons, M.: Low-load, prolonged stretch in treatment of elbow flexion contractures secondary to head trauma: a case report. Phys. Ther. 69:292, 1989. 39. Mansat, P., and Morrey, B. F.: The “column procedure”: a limited surgical approach for the treatment of stiff elbows. J. Bone Joint Surg. 80A:1603, 1998. 40. Marti, R. H., Kerkhoffs, G. M., Maas, M., and Blankevoort, L.: Progressive surgical release of a posttraumatic stiff elbow. Technique and outcome after 2-18 years in 46 patients. Acta Orthop. Scand. 73:144, 2002. 41. Mehlhoff, T. L., Noble, P. C., Bennett, J. B., and Tullos, H. S.: Simple dislocation of the elbow in the adult. J. Bone Joint Surg. 70A:244, 1988. 42. Mendelson, L., Grosswassner, Z., Najenson, T., Sandbank, U., and Solzi, P.: Periarticular new bone formation in patients suffering from severe head injuries. Scand. J. Rehab. Med. 7:141, 1975-1976.

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43. Merle D’Aubigne, R., and Kerboul, M.: Les opérations mobilisatrices des raideurs et ankylose du coude. Rev. Chir. Orthop. 52:427, 1966. 44. Morrey, B. F.: Surgical takedown of the ankylosed elbow. Orthop. Trans. 12:734, 1988. 45. Morrey, B. F.: Post-traumatic contracture of the elbow. Operative treatment, including distraction arthroplasty. J. Bone Joint Surg. 72A:601, 1990. 46. Morrey, B. F.: Splints and bracing at the elbow. In Morrey, B. F. (ed.): The Elbow and Its Disorders, 3rd ed. Philadelphia, W. B. Saunders, 2000, p. 150. 47. Morrey, B. F.: The posttraumatic stiff elbow. Clin. Orthop. Relat. Res. 431:26, 2005. 48. Morrey, B. F., and An, K. N.: Functional evaluation of the elbow. In Morrey, B. F. (ed.): The Elbow and Its Disorders, 3rd ed. Philadelphia, W. B. Saunders, 2000, p. 74. 49. Nowicki, K. D., and Shall, L. M.: Arthroscopic release of a posttraumatic flexion contracture in the elbow: a case report and review of the literature. Arthroscopy 8:544, 1992. 50. Oh, I., Smith, J. A., Spencer, G. E. Jr, Frankel, V. H., and Mack, R. P.: Fibrous contracture of muscles following intramuscular injections in adults. Clin. Orthop. 127:214, 1977. 51. Park, M. J., Kim, H. G., and Lee, J. Y.: Surgical treatment of post-traumatic stiffness of the elbow. J. Bone Joint Surg. 86B:1158, 2004. 52. Phillips, B. B., and Strasburger, G.: Arthroscopic treatment of arthrofibrosis of the elbow joint. Arthroscopy 14:38, 1998. 53. Richards, R. R., Beaton, D., and Bechard, M.: Restoration of elbow motion by anterior capsular release of post-traumatic flexion contractures. J. Bone Joint Surg. 73B(suppl II):107, 1991. 54. Savoie, F. H. III, Nunley, P. D., and Field, L. D.: Arthroscopic management of the arthritic elbow: indications, techni-que and results. J. Shoulder Elbow Surg. 8:214, 1999. 55. Schindler, A., Yaffe, B., Chetrit, A., Modan, M., and Engel, J.: Factors influencing elbow arthrolysis. Ann. Chir. Main Memb. Super. 10:237, 1991. 56. Seth, M. K., and Khurana, J. K.: Bony ankylosis of the elbow after burns. J. Bone Joint Surg. 67B:747, 1985. 57. Timmerman, L. A., and Andrews, J. R.: Arthroscopic treatment of posttraumatic elbow pain and stiffness. Am. J. Sports Med. 22:230, 1994. 58. Tsuge, K., and Mizuseki, T.: Débridement arthroplasty for advanced primary osteoarthritis of the elbow. Results of a new technique used for 29 elbows. J. Bone Joint Surg. 76B:641, 1994. 59. Urbaniak, J. R., Hansen, P. E., Beissinger, S. F., and Aitken, M. S.: Correction of post-traumatic flexion contracture of the elbow by anterior capsulotomy. J. Bone Joint Surg. 67A:1160, 1985. 60. Wada, T., Ishii, S., Usui, M., and Miyano, S.: The medial approach for operative release of post-traumatic contracture of the elbow. J. Bone Joint Surg. 82B:68, 2000. 61. Weiss, A. P. C., and Sachar, K.: Soft tissue contractures about the elbow. Hand Clin. 10:439, 1994.

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62. Weizenbluth, M., Eichenblat, M., Lipskeir, E., and Kesslser, I.: Arthrolysis of the elbow: 13 cases of post-traumatic stiffness. Acta Orthop. Scand. 60:642, 1989. 63. Willner, P.: Anterior capsulectomy for contractures of the elbow. J. Int. Coll. Surg. 11:359, 1948.

64. Wilson, P. D.: Capsulectomy for the relief of flexion contractures of the elbow following fracture. J. Bone Joint Surg. 26A:71, 1944. 65. Wheeler, D. K., and Linscheid, R. L.: Fracturedislocations of the elbow. Clin. Orthop. Relat. Res. 50:95, 1967.

Chapter 33 Hinged External Fixators of the Elbow

CHAPTER

33

Hinged External Fixators of the Elbow Bernard F. Morrey, A. Noelle Larson, and Matthew Morrey

INTRODUCTION By definition, a dynamic hinged external fixation allows for an axis of rotation to provide elbow stability and motion following trauma or reconstruction.30 With a properly constructed device, the ulna may be separated or distracted from the humerus and still allow physiologic flexion and extension. The mechanics and anatomic landmarks for the application of several fixator devices have been well defined.6,20,28 The axis of rotation of the distal humerus passes through the tubercle of origin of the lateral collateral ligament and through the anteroinferior aspect of the medial epicondyle (Fig. 33-1). Replication of the axis of rotation is essential to avoid pin loosening, persistent stiffness, or instability. In cadaver models, 5 mm of translation or 5 degrees of angulation results in a fourfold increase in resistance to elbow flexion.15

INDICATIONS External fixation allows for flexion of the elbow to prevent contracture while still maintaining joint space and appropriate coronal alignment (Fig. 33-2).18 The hinged fixator, when properly applied, maintains a reduced and balanced ulnohumeral joint during motion, thereby protecting repaired or reconstructed collateral ligaments. In trauma, fixators may be used to protect operative fixation of unstable fractures and ligament repair in cases of persistent postoperative instability and for longstanding elbow dislocation or recurrent instability.9 In reconstruction of the elbow, hinged fixators can also be used in the treatment of instability, following ligamentous repair, or with interposition arthroplasty.3,19 Although goals of treatment may be attained with relatively simple designs, greater flexibility and broader utility have been introduced by Hotchkiss with a more complex fixation. Although several designs are currently available (Fig. 33-3), only the Mayo dynamic joint dis-

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tractor (DJD)19 and the Hotchkiss Compass Hinge12 are discussed in this chapter because they represent the spectrum from simple to complex.

TRAUMA In many traumatic circumstances, the goal is to “neutralize” the forces across the joint while elbow motion is maintained. The fixator can be applied acutely as an adjunct to operative repair or as a secondary measure in case of reduction failure. The specific indications for dynamic external fixators of the elbow in acute trauma include the following: (1) instability, (2) articular injury, and (3) residual or recurrent subluxation.

Instability Elbow dislocation with extensive soft tissue injury results in gross instability, even after reduction or repair of involved structures.5 Adjunctive management of late untreated elbow dislocations involve the use of an external fixator.9

Articular Injury (Fracture-Dislocation) This category includes instability with fractures of the radial head,17,21 some olecranon fractures (Mayo type III)16 as well as Regan-Morrey type II and III coronoid fractures.13,23 Use of a hinged fixator for complex, unstable distal humerus fractures has also been described.7 Open fixation is the primary treatment modality. When gross instability persists or when fixation is deemed vulnerable, an external fixator can be added to allow for immediate postoperative motion and neutralization or unloading of the stresses placed on the fracture fixation (Fig. 33-4).

Residual or Recurrent Subluxation Residual or recurrent subluxation after simple or complex fracture-dislocation is the third indication for use of a fixator.24 In this setting, percutaneous fixator application can assist in reducing a subluxated joint without having to revert to an open procedure. Maintenance of the device allows for early motion with minimal risk of frank redislocation or continued subluxation. The added stability facilitates proper healing of the capsule and soft tissue restraints.

RECONSTRUCTION The same basic goals obtain for the use of the fixator after reconstructive interventions. When arthrolysis for the post-traumatic joint stiffness is carried out, release of the collateral ligament is sometimes necessary, as well as excision of

Ankylosis

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FIGURE 33-1

On the medial side, placement of the axis pin is at the anteroinferior aspect of the medial epicondyle. On the lateral side, the center of rotation is at the tubercle of the lateral epicondyle, which is at the center of the projection of the curvature of the capitellum.

Interposition Arthroplasty At least one collateral ligament must be released for exposure.3 Hence, the goals in this setting are as follows:

1. To separate the joint surfaces, protecting the interposed tissue from compression and shear forces while it heals to the humerus. 2. To provide motion during the healing phase and prevent contracture. 3. To allow the released or reconstructed ligament to heal without tension (Fig. 33-5).

CONTRAINDICATIONS RELATIVE CONTRAINDICATIONS

FIGURE 33-2 An articulated external fixator (1) allows flexion motion, (2) protects the ligaments from varus and valgus stress, and (3) separates the joint.

capsular and bone restraints.8,19 These releases can result in instability. Application of the device protects the repaired collateral ligaments after the arthrolysis while allowing immediate motion of the stabilized concentric joint.

1. Local sepsis at desired site of pin insertion. The external fixation pins should not be placed through infected bone or skin. They may be placed through areas of exposed tissue, although this is clearly less desirable. In trauma cases, ideally they are placed outside of the zone of injury and ideally should be located away from areas of anticipated hardware or prostheses placement. The fixators can be used to stabilize a septic joint, which on occasion is helpful. However, care must be taken to ensure that the pins of the device are fixed to bone in areas free of infection or local cellulitis. 2. Altered anatomy. When uncertainty exists regarding the anatomic location of the neurovascular structures due to post-traumatic or postoperative disturbance of the anatomy, a careful dissection with protection

Chapter 33 Hinged External Fixators of the Elbow

A

B

C D FIGURE 33-3

A variety of articulated external fixators are currently available. Note: All are based on identity of the axis of rotation with variable means of skeletal attachment and distraction. Illustrated here in increasing order of complexity: DJD II (Stryker, Kalamazoo, MI) (A), Orthofix Inc. (McKinney, Texas) (B), OptiROM (EBI, Parsipanny, New Jersey) (C); and Compass (Smith & Nephew, Mississauga, Ontario, Canada) (D).

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B

A

C FIGURE 33-4

D

Fracture-dislocation in 38-year-old radiologist involving the comminution of the coronoid. Anteroposterior (A), lateral (B). After fixation with screws and a buttress plate the elbow was stabilized and neutralized with the DJD external fixator. Note position of the pins referable to the intercondylar distance. C, Lateral projection with external fixator. Note replication of axis of rotation by the fixator (D).

Chapter 33 Hinged External Fixators of the Elbow

8 wks 5-135 deg

E

F

FIGURE 33-4, cont’d At 8 weeks the patient has virtually extension (E) and full flexion (F) and has returned to work.

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of the vulnerable nerves (usually the ulnar and radial) must be made when fixator placement is necessary. 3. The presence of fracture fixation devices in the humerus or proximal ulna, making pin placement impossible. (There is some flexibility for pin placement. The presence of internal fixation does not absolutely preclude use.) 4. Inexperience with the use of external fixation devices. 5. Patient inability to comply with pin site care or rehabilitation program.

SELECTION OF FIXATOR CONFIGURATION Over the last several years, a number of experiments have been conducted in our laboratory to better understand the function and indications for external fixator

FIGURE 33-5

A patient with post-traumatic ankylosis, subluxation, and arthrosis (A). This was treated with the distraction device and interposition using in this instance fascia lata (B). At 1 year, a satisfactory result was obtained (C).

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configuration. One such assessment demonstrated that compression across the joint with the half-pin lateral application of an external fixator doubles the stiffness of the system in varus load when in extension but had much less effect otherwise. Thus, distraction, one of the recommended applications of the articulated external fixator, does render this system less stable than when the articulation is compressed.27 Of particular importance is the study of Kamineni et al.10 which released the medial and lateral collateral ligaments and assessed the kinematic pattern with a half-pin laterally applied external fixator. In this experiment, it was demonstrated that both varus and valgus stability was restored even with the half-pin lateral configuration and even with up to 7 N out of plane load applied to the forearm (Fig. 33-6). Rotational stability, however, was not as reliably restored (Fig. 33-7). An additional clinical relevant experiment sought to assess the sensitivity of pin placement approximating the axis of rotation. It has been shown that increased energy is needed to move the elbow if a nonoptimum application of the articulated external fixator occurs.15 A subsequent assessment in our laboratory demonstrated that the nonoptimum placement of an external fixator, however, did not alter the kinematics as much as had been anticipated (Fig. 33-8). Based on these data, it was concluded that a slight proximal place-

ment of the axis of the external fixator actually enhances the rigidity of the elbow in a manner that would favor reconstruction of the lateral ulnar collateral ligament. Thus, there may be instances in which slight nonanatomic axis placement is clinically acceptable.2 Hence, based on these experiments, our current practice is to employ the lateral half-pin application of the DJD II in virtually all clinical settings in which the fixator is believed to be necessary.

TECHNIQUE MAYO DYNAMIC JOINT DISTRACTOR Patient Positioning The patient is placed in the position required for proper treatment of the primary pathologic condition. The distraction device itself may be applied with the patient in the prone, supine, or lateral decubitus position. In the practice of one of us (B.F.M.), the supine position is favored for most circumstances.

Author’s Surgical Technique The patient is supine with a sandbag under the scapula, and a nonsterile tourniquet is applied. The arm is draped free and brought across the chest. In most cases of

VARUS VALGUS INJURY DISPLACEMENT WITH MEDIAL OR MEDIAL + LATERAL, AND THE EFFECT OF A LATERAL DJD 20

Angular displacement ( degrees) ( valgus +) ( varus −)

15 10 5

FIGURE 33-6

0 −5 −10 −15 −20 −25 −30 Varus hand

Varus hand + 350g

Varus hand + 700g

Intact Medial injury Medial injury + ExFix Medial + lateral injury Medial + lateral injury + ExFix

Valgus hand

Valgus hand + 350g

Valgus

Analysis of varus/valgus stability in a normal elbow and following medial and lateral collateral ligament disruption. Note that half-pin configuration applied laterally restores stability even when both medial and lateral collateral ligaments have been disrupted and with both varus and valgus loading conditions. (After Kamineni, S., Hirahara, H., Neale, P., O’Driscoll, S. W., An, K-N., and Morrey, B. F.: Effectiveness of the lateral unilateral dynamic external fixator after elbow ligament injury. J. Bone Joint Surg. Am. 89:1802, 2007.) (With permission, Mayo Foundation.)

Chapter 33 Hinged External Fixators of the Elbow

505

Angular displacement ( degrees) ( pronation −) (supination +)

ROTATIONAL DISPLACEMENT WITH LATERAL + MEDIAL INJURY, AND THE EFFECT OF A LATERAL DJD 4 2 0 −2 −4 −6 −8 −10 −12 −14 −16 Varus hand

Varus hand + 350g

Varus hand + 700g

Valgus hand + 350g

Valgus hand

Valgus

Intact Lateral injury Lateral injury + ExFix Lateral + medial injury Lateral + medial injury + ExFix

trauma or reconstruction, a posterior skin incision is used and the elbow joint is exposed either medially or laterally according to the pathologic condition being addressed. If the joint is to be altered or the joint is badly distorted, an extensive exposure is required, and the lateral collateral ligament is typically released from its origin at the lateral condyle. In this instance the ligament must be carefully repaired or reconstructed. Furthermore, when the condition involves the joint surface that requires an extensive dissection, identification and protection of the ulnar nerve is necessary. This is usually accomplished through a posterior skin incision.

Applying the DJD II External Fixator Once the elbow has been exposed and the pathologic condition addressed including collateral ligament repair/ reconstruction, the external fixator is applied. Several possible configurations are available and are used depending on the lesion and surgeon preference (Fig. 33-9). As noted earlier, we employ the lateral half-pin configuration almost exclusively today.

FIGURE 33-7

Unlike the varus/valgus stability, rotational stability is not perfectly restored with the half-pin configuration after both collateral ligaments have been disrupted. (With permission, Mayo Foundation.)

meral joint or reconstructed joint is identified as the axis of rotation. Although not commonly repaired, fluoroscopy may be employed if there is concern about axis stylus placement. On the medial aspect of the distal humerus, the axis of rotation lies just anterior and inferior to the medial epicondyle. This corresponds to the center of curvature of the medial contour of the trochlea and is the locus of the humeral origin of the medial ulnar collateral ligament (Fig. 33-11).

AXIS STYLUS 1. The pointed tip of the humeral axis target guide is placed on the medial side, with the cannulated stylus guide on the lateral side. The reference stylus is tapped in place with a mallet through to lateral cannula of the target device (Fig. 33-12). 2. The DJD II frame is placed on the reference pin and aligns with the anterior humeral cortex (Fig. 33-13).

HUMERAL PIN INSERTION AXIS IDENTIFICATION The essential landmarks of the flexion axis are identified. On the lateral aspect of the capitellum, a tubercle is present at the site of origin of the lateral collateral ligament, which represents the geometric center of curvature of the capitellum (Fig. 33-10). Note: If this anatomic feature has been altered by pathology, then the center of curvature of the ulnohu-

3. The interepicondylar width defines a safe location for placement of the proximal humeral pin. The maximum distance from the reference stylus should not exceed the epicondylar dimension “D” (Fig. 33-14). 4. A cannulated trochar is inserted through the pin guide to engage the lateral humeral cortex (Fig. 33-15). 5. The proximal humeral smooth or self-drilling/selftapping Apex 4-mm (or 3-mm for small bones) pin

506

Part V Adult Trauma

Degrees, Varus, ER (−) /Valgus, IR (+)

VARUS-VALGUS AND AXIAL ROTATIONS, NORMALIZED TO OO

5 mm

4 2

PO-OO/vrvl PO-OO/irer

Rotation

0 −2

50

100

Var/Val 150

−4 −6

C

Flexion

Degrees, Varus, ER (−) /Valgus, IR (+)

VARUS-VALGUS AND AXIAL ROTATIONS, NORMALIZED TO OO PRO-OO/vrvl PRO-OO/irer

3 2 1

Rotation

0 −1

50

150

−2

Var/Val

−3

D

A

100

Flexion VARUS-VALGUS AND AXIAL ROTATIONS, NORMALIZED TO OO

3

Degrees, Varus, ER (−) /Valgus, IR (+)

VARUS-VALGUS AND AXIAL ROTATIONS, NORMALIZED TO OO AO-OO/vrvl AO-OO/irer

2 1

Var/Val

0 −1

20

40

60

80

−2

120

140 Rotation

−3

B

100

E

4 2

PO-OO/vrvl PO-OO/irer

Rotation

0 −2

50

100

Var/Val 150

−4 −6 Flexion

Flexion

FIGURE 33-8

If the center of rotation is not accurately defined, the kinematic pattern of the elbow changes (A). Note, however, that these changes are relatively slight for all variations: anterior (B), posterior (C), proximal (D), and distal (E). The baseline, 0, represents normal kinematics.

Chapter 33 Hinged External Fixators of the Elbow

507

FIGURE 33-9

Several configurations may be employed with the DJD II fixator, including half-pin or transfixing pin constructs.

FIGURE 33-11 Medially, the axis site is defined as the anterior/inferior aspect of the medial epicondyle, which is at the geometric center of the trochlea.

FIGURE 33-10 The axis of rotation is identified at the lateral tubercle which is the projected center of the curvature of the capitellum.

508

Part V Adult Trauma

1.4 d

d

d

FIGURE 33-12 The axis is identified by a target guide, which is then applied with the alignment guide at the anterior/inferior aspect of the medial epicondyle. The stylus is tapped into place to replicate the axis of rotation. Note the smooth pin avoids entry to any reconstruction that may have been performed.

FIGURE 33-14

The proximal-most pin is defined by the so-called safe zone D. If D represents the dimensions from the medial and the lateral epicondyle, the radial nerve is 40% proximal to this distance. Hence, the distance “D” is a safe site for inserting the proximal pin.

is advanced through the lateral cortex of the humerus and penetrates the medial cortex through a trochar, which is placed through a pin guide. 6. The proximal pin is fixed to the humeral rod with a Hoffmann II Compact pin-to-rod coupling (Fig. 33-16). Make a second stab incision and place the pin guide on the humeral rod; the cannulated trochar is placed through the pin guide. 7. The second 4-mm (or 3-mm) self-drilling/self-tapping Apex pin is now inserted more distally through the pin guide and fixed to the humeral rod. Note: The humeral pins need not be parallel. The distal pin is fixed to the humeral rod with a Hoffmann II Compact pin-to-rod coupling, which is then tightened using a Hoffmann II Compact wrench. The pin guide is then removed. 8. The axis of the fixator is now defined and rigidly fixed. The stylus pin is removed with a drill or pliers. FIGURE 33-13 The external fixator is placed over the stylus, which replicates the axis of rotation. Note the side bar is aligned with the anterior cortex of the humerus.

Ulnar Pin Insertion 9. The 3-mm diameter pin is recommended for the ulna. Place the 3-mm pin guide over the ulnar rod,

Chapter 33 Hinged External Fixators of the Elbow

d

509

and insert the 3-mm cannulated trochar through the pin guide and identify the lateral ulnar cortex (Fig. 33-17). 10. The distal ulnar 3-mm self-drilling/self-tapping Apex pin is inserted into the lateral cortex through the trochar and through the pin guide and pierces the medial ulnar cortex. The distal pin is fixed to the ulnar rod with a Hoffmann II Compact pin-to-rod coupling. 11. The second ulnar pin is placed and secured in a similar fashion. Note: As with the humerus, the pins do not necessarily need to be parallel. If a different pin insertion angle is required to access a more adequate pin insertion area, slightly rotate the pin guide over the ulnar rod until such a pin insertion area can be reached. By providing proper pin-rod distance, the system allows an independent pin placement. The trochar and pin guide is then removed.

DISTRACTION 12. If distraction is desired, the amount of separation is determined by the calibrations on the distraction FIGURE 33-15 A cannula is inserted through the pin guide and protects the soft tissue with the placement of the threaded pin.

FIGURE 33-16

The threaded half-pins have been inserted and are attached to the external fixation with the universal coupler. The stylus pin is removed.

FIGURE 33-17 After the stylus pin has been removed the trochar is placed through the ulnar pin guide. The ulnar pin is then placed through the trochlea and pierces the medial cortex of the ulna.

510

Part V Adult Trauma

unit (Fig. 33-18). Typically 2 to 3 mm of distraction is sufficient to accomplish the goals of the procedure. 13. Skin closure is usually deferred until the distraction is applied.

Percutaneous Application For some acute or subacute fractures in which the elbow is unstable due to coronoid deficiency, there is a tendency for the ulna to sublux posteriorly. In these cases, the dynamic joint distractor may sometimes be applied percutaneously under fluoroscopy to neutralize fracture displacement forces (Figs. 33-19 and 33-20). Full motion may be achieved by this slight asymmetric distraction, but a flexion arc of 60 to 90 degrees of motion is usually attainable and this is considered adequate given the specific goals of this application.

When the frame has been assembled and appropriately adjusted, it should slide along the axis pin without significant impingement or resistance (Fig. 33-21). If there is resistance, the components are probably out of alignment. The clinician should make sure to allow for swelling in the postoperative period, allowing at least 2 cm of clearance from the skin to the hinge block at the time of surgery.

THE COMPASS HINGE Frame Assembly The frame should be prebuilt to confirm that proper ring size has been selected. In most adults, the 150-mm ring size is usually the best fit. It is important that the geared component is always medial, with the knob facing posterior. FIGURE 33-19 Percutaneous application may be carried out. This is done by the use of fluoroscopic control. The key is to identify the axis of rotation. The stylus pin is applied percutaneously to replicate the axis of rotation.

FIGURE 33-18 Once the ulnar pins have been attached the desired distraction may be simply introduced through the distracting mechanism.

FIGURE 33-20 In a manner similar to the open condition (see Fig. 33-14), the key is to place the proximal pin at a distance “D” from the axis pin, which is a safe distance from the radial nerve. The use of the trochar further minimizes the likelihood of injury to the radial nerve. The pins are placed distally in the ulna to avoid the plate.

Chapter 33 Hinged External Fixators of the Elbow

511

FIGURE 33-21 Preassemble the frame so that the alignment of the axis elements freely slide on a 4-mm pin. (With permission, Smith & Nephew, Inc.)

Patient Positioning For release of contracture and removal of heterotopic bone, the patient should be placed in the supine position, with the arm on a radiolucent hand table. If the patient first requires a more extensive exposure of the distal humerus for fracture or reconstructive work, it may be useful to begin the operation with the arm over the chest when using one of the more standard posterior approaches to the elbow, either olecranon ostectomy or a triceps sparing exposure (Bryan-Morrey). In cases of gross instability, the prone position can be used, with the added benefit that gravity in this position tends to reduce the joint during hinge placement and operative ligament repair or reconstruction. However, exposure of the coronoid is difficult in the prone position.

FIGURE 33-22 Once the axis pin has been inserted, the preconstructed frame should slide freely medial to lateral on the axis pin. (With permission, Smith & Nephew, Inc.)

As with the dynamic joint distractor, a single temporary axis pin is placed across the joint, or two half-pins can be inserted, one from the medial and the other from the lateral aspect. The alignment of the axis is crucial. It is important to take the time necessary to achieve perfect placement of this pin for alignment of the Compass Hinge at the elbow. Both an anteroposterior and lateral radiograph should be viewed to ensure adequate placement. Once the two pins are coincident, entering at their respective centers of rotation, the frame should still be easy to slide from medial to lateral, back and forth, before securing the axis pin from the medial side (Fig. 33-22).

or jeopardizing any neurovascular structures. If there is internal fixation present, the pin placement can be adjusted to avoid the plates by customizing the frame. In general, two 5-mm half-pins, medial and lateral, are required. In larger elbows, or in cases in which internal fixation precludes use of the described sites, a third humeral pin may be used, usually placed laterally, superior to the spiral groove. The medial pin is usually placed first through a twohole Rancho cube guide on the undersurface of the upper ring. Both cortices should be engaged. The lateral pin is usually placed using a two-hole post and a single-hole Rancho cube. The lateral flare of the humerus is used for placement. The drill guide rests on the lateral supracondylar ridge, directed anterior and distally. The radial nerve, at this level, is anterior to the pin (Fig. 33-23). Humeral fixation and alignment of the axis of the hinge must be achieved before fixation of the ulna.

Humeral Pin Placement

Placement of Ulnar Fixation

The principle is to secure the humerus in two planes, without impaling any of the major muscle-tendon units

One 5-mm and one or two 4-mm pins are used in the ulna. The more proximal pin (5-mm) provides optimal

Axis Pin Placement

512

Part V Adult Trauma

FIGURE 33-23

The correct rotatory orientation of the ring referable to the humerus is perpendicular to the long axis of the humerus. The half-pins are inserted using the Rancho system through the alignment blocks, securing first the humerus, followed by the ulnar components. (With permission, Smith & Nephew, Inc.)

control of the joint and is placed from the dorsal surface through the coronoid. The smaller (4-mm) pins are used more distally in the ulna, again from the dorsal surface. If the elbow is grossly unstable, it is quite important to reduce the elbow by placing it in approximately 90 degrees of flexion when applying the ulnar fixation. Once the joint is reduced and held in position, the first two proximal ulnar pins can be placed. After this, ranging through flexion and extension and ensuring reduction of the joint is important. If there is a tendency for the elbow to subluxate, then alignment has not been achieved and the bolts must be loosened and reduction achieved (see Fig. 33-23).

Application of Distraction After the joint has been reduced and all pins applied, distraction can then be applied to the system through the distraction mechanism. Distraction is achieved by turning the bolts located on the ulnar ring fixation blocks (Fig. 33-24). Both sides of the hinge should be

FIGURE 33-24 Distraction is achieved by rotating the bolts under the ulnar ring. Both sides should be distracted an equal amount. (With permission, Smith & Nephew, Inc.)

distracted an equal amount. Use and extent of distraction should be done at the discretion of the surgeon.

Aftercare For aftercare of the Compass Hinge, passive mobilization is initiated using the gear mechanism. In the early postoperative period, the elbow is incrementally extended to the maximally tolerated position. As swelling subsides over the following days, incremental flexion is initiated. The patient then begins a schedule of maximizing the position of flexion or extension using the gear mechanism on alternating days. The device is usually left on the patient for 4 to 6 weeks. For the DJD II, the patient is placed in a continuous motion machine for 21/24 hours a day (see Chapter 10). After reconstructive procedures, the patient returns approximately 3 weeks after dismissal from the hospital, the distraction device is removed, and the elbow is examined under general anesthesia. The arc of motion obtained at surgery is re-established under anesthesia. Care is taken not to forcefully manipulate the elbow, but some sense of the firmness of the end points of motion

Chapter 33 Hinged External Fixators of the Elbow

is determined, because this is believed to have prognostic value. Joint crepitus and stability are also assessed. We have encountered virtually no problems with this assessment.1 Further evaluation is predicated on the severity of the injury, soft tissue integrity, and stability of the internal fixation. A common program is to see the patient at 1, 3, and 6 weeks. For patients treated for arthrolysis, static adjustable splints are employed when the device is removed, usually at about 3 weeks for stiffness and 4 to 6 weeks after fracture (see Chapter 11). The goal is to attain a degree of soft tissue stretch with a constant force allowing the soft tissue to “relax” under the constant pressure. For the first 3 weeks of application, the patient wears one or the other for approximately 20 to 21 hours a day. After 3 weeks, the program is individualized, with the time in the splint decreasing to 10 to 16 hours, but the basic principles continue to be followed. For release of the stiff elbow, splint usage may be required at night

Splints

TABLE 33-1

513

and to maintain motion for up to 3 months or occasionally even up to 6 months. Fixator Removal and Examination Under Anesthesia

If progress is not being achieved with the splints and there is no concern about fracture displacement, additional examination under anesthesia may be performed. If this is to be done, this is accomplished before 3 months. The most recent radiograph should be available to appreciate the specific pathologic lesion being addressed. We have evaluated the effectiveness of 56 “evaluations,” 30 of which occurred at the time of external fixator removal. A mean of 37 degrees improvement in the flexion arc was documented. There were no fractures or any other notable complications.1

RESULTS A summary of the literature organized by documented indications is shown in Table 33-1. For most surgeons,

Results from External Fixation According to Indication No. of Pts

Indication

Treatment

Morrey, 199019

Ankylosis/contracture

Release ± interposition, DJD

20

95% patients satisfied

66.5

Morrey, 199019

Result

Gain in FlexionExtension (Degrees)

Reference

Ankylosis/contracture

Release, no fixator

6

83% pts satisfied

43

26

Ankylosis/contracture

Release, Compass hinge

23

n/a

89

26

Ring et al., 2005

Ankylosis/contracture

Release, no fixator

19

n/a

78

Cobb and Morrey, 19955

Complex instability

DJD, ORIF, interposition arthroplasty, and so on

7

86% pts satisfied

55º 2 of the 7 did not have preoperative ROM available

McKee et al., 199816

Complex instability

Compass hinge after treatment failure

16

80%

n/a

Ring et al., 200424

Chronic instability after fracture

Compass hinge w/ fixation, reconstruction radial head prosthesis

13

77% good/ excellent MEPs

n/a

Jupiter and Ring, 20029

Persistent elbow dislocation

Open reduction, Compass hinge

5

100% good/ excellent MEPs

n/a

Cheng and Morrey, 20003

Arthritis

Fascial interposition, DJD

13, 5 revised to TEA

54% good/ excellent MEPs

15º (excluding 4 who were revised)

Larson and Morrey, 200814

Arthritis

Achilles interposition, DJD 2

37

29% good/ excellent MEPs

46º

Larson and Morrey, 200814

Arthritis

No fixator, Achilles interposition alone

20

46% good/ excellent MEPs, subjective 89% satisfied

54º

Ring et al., 2005

514

Part V Adult Trauma

the value of these devices is in the management of trauma and its sequelae (Fig. 33-25) (also see Figs. 33-4, 33-19, and 33-20).16,17 Surgical indications for hinged fixator use include ankylosis or elbow contracture, acute or chronic elbow instability, or arthritis. Elbows treated for ankylosis or contracture respond well to release, with mean flexion arc gains of 40 to 80 degrees.19,25 In a series of 26 patients, Morrey initially reported greater patient satisfaction and elbow range of motion following arthrolysis with the use of a hinged external fixator compared with no fixator.18 A retrospec-

tive series of 42 patients reported by Ring et al.,25 however, showed no significant advantage in postoperative range of motion with the use of external fixator and capsular release when compared with capsular release alone for the treatment of elbow contractures. Demographics and injury characteristics were similar between the two groups, but in the latter group, the plan was to specifically use the fixator (Compass) as an adjunct to improving motion. External fixators have also been described in the treatment of complex instability with approximately

FIGURE 33-25 Patient with instability from coronoid and radial head fracture (A). External fixation device applied with half-pins (B). This was well tolerated by the patient (C and D).

Chapter 33 Hinged External Fixators of the Elbow

80% patient satisfaction or satisfactory Mayo Elbow Performance scores.5,16,24,26 Jupiter and Ring report successful results in five out of five patients treated for long-standing unreduced elbow dislocations.9 In a complex patient population with joint subluxation and coronoid deficiency, Papandrea et al.22 were not able to demonstrate the value of the external fixator as an adjunct to the complex management in these complex injuries treated at the Mayo Clinic. For post-traumatic or inflammatory elbow arthritis, the literature contains several reports of external fixators used in conjunction with débridement, capsular release, or interposition arthroplasty.3,14 A series of 13 patients undergoing fascial interposition arthroplasty in conjunction with distraction by the Dynamic Joint Distractor documented in 54% good or excellent Mayo Elbow Performance (MEP) scores.3 Recently, we reported a series of 57 patients undergoing Achilles tendon interposition arthroplasty, 37 with placement of the Dynamic Joint Distractor II and 20 with no use of a fixator. Only 29% of patients in the external fixator group had good or excellent MEP score.14 From the 20 patients without the use of an external fixator, 46% had good/excellent results.14 However, there were strong selection bias to use the fixator in the more difficult cases. Of note, the more unstable elbows were more likely to be placed in an external fixator after operative reconstruction, and instability has independently been shown to be a predictor of poor outcomes following interposition arthroplasty.3,14 Nonetheless, there was no statistical

TABLE 33-2

515

association between clinical outcomes and use of an external fixator. The important point is when treating patients with complex problems and instability such as in the treatment of the above-mentioned indications, the outcome is not attributed to the fixator but to the complexity of the injury. This is particularly true for the management of the stiff or unstable joint. We do, however, believe that the hinged external fixator brings added value to interposition arthroplasty for management of intrinsic pathologic conditions and is essential for the effective management of selected cases of complex instability with articular injury.

COMPLICATIONS This topic has recently been studied by Cheung et al.,4 who reviewed the Mayo experience with 100 consecutive applications of 80 DJD II and 20 Compass fixators. The complications documented to be associated with these respective devices are listed in Table 33-2. These include superficial or deep infection, skin irritation, nerve injury, pin loosening, fracture, and pin breakage. There are statistically significant differences in the complication rate, which is greater with the use of the more complicated Compass device.4 Difference in the frequency of these complications relate to a number of factors, including the indications for application and possibly from technical difficulties encountered. No reoperations were required in any patient for pain-related problems.

Complications by Severity and Type of Fixator Device Used MAYO EXPERIENCE: 100 PATIENTS DJD II

Patients Pins

Compass

80

20

100

320

113

433

DJD II Minor complications:

Total

Per Pin

COMPASS

Per Patient

Per Pin

P VALUE

P VALUE

Per Patient

By Pin

By Patient

<.001

<.02

Serous drainage >5 days

8 (2.5%)

4 (5%)

13 (11.5%)

5 (25%)

Skin release

1 (0.3%)

1 (1.3%)

8 (7.1%)

5 (25%)

<.001

<.001

Minor complications, total

9 (2.8%)

5 (6.3%)

21 (18.6%)

10 (50%)

<0.001

<0.001

2 (0.6%)

1 (1.3%)

12 (10.6%)

3 (15%)

Major complications: Purulent drainage/deep infection Loosening of pins requiring revision of pin placement Malalignment leading to early removal of fixator Major complications, total

<.001

<.02

4 (5%)

0

0

NS

NS

4 (1.3%)

1 (1.3%)

0

0

NS

NS

17 (5.3%)

7 (8.9%)

3 (15%)

<0.05

<0.05

11 (3.4%)

12 (10.6%)

516

Part V Adult Trauma

INFECTION

References

Soft tissue pin site infection or irritation is a minor problem and is readily treated by pin removal. In the Mayo retrospective assessment of 433 pins in 100 patients, 11 pins loosened (2.5%), 13 pin sites resulted in deep (not osseous) infection (3%), and 21 pin sites (5%) had redness and nonpurulent drainage managed with oral antibiotics.3 Transarticular pins used in the early external fixator designs were a concern, because infection at that site can cause a deep infection of the joint, resulting in treatment failure. Although deep infection may occur, it should be noted that these largely occur in the post-traumatic patient population, who is generally at a higher risk of infection due to previous instrumentation or open contamination of the fracture or elbow than the general adult population. Nonetheless, the current designs of external fixators eliminate a permanent articular pin, which should certainly reduce the frequency of intra-articular infection.

1. Araghi, A., Celli, A., Adams, R., and Morrey, B. F.: The effect of examination under anesthesia on the stiff elbow following surgical release. (Submitted for publication). 2. Baumfeld, J. A., Morrey, B. F., van Riet, R. P., Neale, P. G., O’Driscoll, S. W., and An, K. N.: The effect of malpositioning of a hinged elbow external fixation device (In preparation). 3. Cheng, S. L., and Morrey, B. F.: Treatment of the mobile, painful arthritic elbow by distraction interposition arthroplasty. J. Bone Joint Surg. 82B:233, 2000. 4. Cheung, E. V., O’Driscoll, S. W., and Morrey, B. F.: Complications of hinged external fixators of the elbow. J. Shoulder Elbow Surg. 2008 Epub Feb 27. 5. Cobb, T. K., and Morrey, B. F.: Use of distraction arthroplasty in unstable fracture dislocations of the elbow. Clin. Orthop. Rel. Res. 312:201, 1995. 6. Deland, J. T., Gerd, A., and Walker, S. P.: Biomechanical basis for elbow hinge-distractor design. Clin. Orthop. Rel. Res. 215:303, 1987. 7. Hall, J., Schemitsch, E. H., and McKee, M. D.: Use of a hinged external fixator for elbow instability after severe distal humeral fracture. J. Orthop. Trauma 14:442, 2000. 8. Hertel, R., Pisan, M., Lambert, S., and Ballmer, F.: Operative management of the stiff elbow: Sequential arthrolysis based on a transhumeral approach. J. Shoulder Elbow Surg. 6:82, 1997. 9. Jupiter, J. B., and Ring, D.: Treatment of unreduced elbow dislocations with hinged external fixation. J. Bone Joint Surg. 84A(9):1630, 2002. 10. Kamieni, S., Ankem, H., and Amis, A.: A safe normalized parameter for lateral distal humeral pin insertion. (Accepted for publication, Clin Anat, 2007). 11. Kamineni, S., Hirahara, H., Neale, P., O’Driscoll, S. W., An, K-N., and Morrey, B. F.: Effectiveness of the lateral unilateral dynamic external fixator after elbow ligament injury. J. Bone Joint Surg. Am. 89:1802, 2007. 12. Kasparayan, N. G., and Hotchkiss, R. N.: Dynamic skeletal fixation in the upper extremity. Hand Clin. 13:643, 1997. 13. Koslowsky, T. C., Mader, K., Siedek, M., and Pennig, D.: Treatment of bilateral elbow dislocation using external fixation with motion capacity: A report of two cases. J. Orthop Trauma 20:499, 2006. 14. Larson, A. N., and Morrey, B. F.: Interposition arthroplasty with an Achilles tendon allograft. AAOS, San Diego, CA, 2007 (accepted for publication). 15. Madey, S. M., Bottlang, M., Steyers, C. M., Marsh, J. L., and Brown, T. D.: Hinged external fixation of the elbow: optimal axis alignment to minimize motion resistance. J. Orthop Trauma 14:41, 2000. 16. McKee, M. D., Bowden, S. H., King, G. J., Patterson, S. D., Jupiter, J. B., Bamberger, H. B., and Paksima, N.: Management of recurrent, complex instability of the elbow with a hinged external fixator. J. Bone Joint Surg. 80B:1031, 1998. 17. Morrey, B. F.: Complex instability of the elbow. J. Bone Joint Surg. 79A:460, 1997.

NEURAL INJURIES The incidence of neural injury relates to the underlying pathologic condition, to the surgical approach, and to the surgeon’s skill and care in the use of the device. A posterior interosseus nerve palsy that subsequently recovered has been attributed to placement of the proximal ulnar half-pin with the forearm pronated.29 In our experience with 100 applications using 433 pins, there have been no cases of direct nerve injury applicable to the device.4 The ulnar nerve may certainly be irritated from increased motion after arthrolysis. If it is tethered or compressed, the additional motion, especially in flexion, causes nerve entrapment and compression that occasionally requires a decompressive procedure.

SUMMARY The external fixator is an important tool in the elbow surgeon’s armamentarium, although its precise role in a variety of pathologic conditions is still being defined. The protective effect and ability to replicate elbow kinematics has been experimentally verified.2,11 Clinically, the fixator is a useful augment to reconstruction in cases of complex instability and interposition arthroplasty. Several designs of hinged external fixators are currently available, each with strengths and deficits. Although a low rate of significant pin site complications have been reported, meticulous technique and appropriate monitoring of pin sites is essential to achieving safe, successful results from an external fixator.

Chapter 33 Hinged External Fixators of the Elbow

18. Morrey, B. F.: Distraction arthroplasty: Clinical applications. Clin. Orthrop. Rel. Res. 293:46, 1993. 19. Morrey, B. F.: Post-traumatic contracture of the elbow: Operative treatment including distraction arthroplasty. J. Bone Joint Surg. 72A:601, 1990. 20. Morrey, B. F., and Chao, E. Y.: Passive motion of the elbow joint. J. Bone Joint Surg. 58A:501, 1976. 21. Morrey, B. F., Chao, E. Y., and Hui, F. C.: Biomechanical study of the elbow following excision of the radial head. J. Bone Joint Surg. 61A:63, 1979. 22. Papandrea, R. F., Morrey, B. F., and O’Driscoll, S. W.: Reconstruction for persistent instability of the elbow after coronoid fracture-dislocation. J. Shoulder Elbow Surg. 16:68, 2007. 23. Regan, W., and Morrey, B. F.: Fractures of the coronoid process of the ulna. J. Bone Joint Surg. 71A:1348, 1989. 24. Ring, D., Hannouche, D., and Jupiter, J. B.: Surgical treatment of persistent dislocation or subluxation of the ulnohumeral joint after fracture-dislocation of the elbow. J. Hand Surg. 29:470, 2004.

517

25. Ring, D., Hotchkiss, R., Guss, D., and Jupiter, J.: Hinged elbow external fixation for severe elbow contracture. J. Bone Joint Surg. 87A:1293, 2005. 26. Ring, D., Jupiter, J., and Zilberfarb, J.: Posterior dislocation of the elbow with fractures of the radial head and coronoid. J. Bone Joint Surg. 84A:547, 2002. 27. Sekiya, H., Neale, P. G., O’Driscoll, S. W., An, K. N., and Morrey, B. F.: An in vitro biomechanical study of a hinged external fixator applied to an unstable elbow. J. Shoulder Elbow Surg. 14:429, 2005. 28. Tomaino, M. M., Sotereanos, D. G., and Plakseychuk, A.: Technique for ensuring ulnohumeral reduction during application of the Richards compass elbow hinge. Am. J. Orthop. 26:646, 1997. 29. Tomaino, M. M., Sotereanos, D. G., Westkaemper, J., and Plakseychuk, A.: Posterior interosseous nerve palsy following placement of the compass elbow hinge for acute instability: a case report. J. Hand Surg. 24A:554, 1999. 30. Volkov, M. V., and Oganesian, O. V.: Restoration of function in the knee and elbow with a hinge-distractor apparatus. J. Bone Joint Surg. 57A:591, 1975.

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Part V Adult Trauma

CHAPTER

34

Injury of the Flexors of the Elbow: Biceps Tendon Injury Jeffery S. Hughes and Bernard F. Morrey

has been used as a “stent” for the tendon insufficiency with success. Simple plication of the stretched tendon is less effective.

AVULSION By far, the most common injury is tendon avulsion, and complete avulsion is much more common than a partial injury. According to McReynolds,54 the first known diagnosis of a distal rupture was reported by Starks in 1843.

INCIDENCE

INTRODUCTION Except for epicondylitis, injury to the muscles or tendons about the elbow, as an isolated event, is rather uncommon.3,13,16,30,70 Distal biceps tendon injury, usually avulsion from the radial tuberosity, is the most common tendinous injury in this region, and the incidence seems to be increasing. Calcific tendinitis has been observed in the biceps tendon, but it is very uncommon.58

DISTAL BICEPS TENDON INJURY The biceps muscle-tendon complex may be injured at the musculotendinous junction by an incontinuity tear of the tendon and by a complete or partial tear or avulsion from the radial tuberosity (Fig. 34-1).

MUSCULOTENDINOUS JUNCTION This is an uncommon injury and one rarely reported.68 The mechanism is similar for all biceps injuries—an eccentric load against a contracting biceps muscle. It may have a predilection for persons with encephalopathy, a condition present in many who experience triceps rupture.

Treatment Because of the delay in diagnosis, or owing to the frequency of underlying disease, our experience with surgical repair and reconstruction has been unpredictable. I have used a Bunnell-type suture repair and more recently augmentation with an Achilles tendon allgoraft has provided improved clinical outcomes. The elbow is protected in a splint for 3 weeks, with slow stretch and return to function over a 3-month period.

TEAR IN CONTINUITY A tear of the tendon in continuity is very rare. An Achilles tendon allograft from the tuberosity to the muscle

Avulsion of the biceps tendon at its distal insertion was reported in three of 100 patients with biceps tendon rupture who were studied by Gilcreest.25 The European literature suggests that distal avulsion injury accounts for approximately 3% to 10% of all biceps tendon ruptures.35 Only 24 cases were reported in a 43-year period after the original surgical descriptions by Johnson40 in 1897 and Acquaviva1 in 1898. Three hundred and fiftyfive surgeons responded to a questionnaire Dobbie circulated in 1941, and only 51 cases were added.21 In addition, only three of this group had experience with as many as three cases. By 1956, the world literature contained 152 cases.27 At present, the injury is well known; either the incidence may be increasing or the lesion is recognized more often.* More reports in the literature notwithstanding, we have encountered only two instances of involvement in a woman in the English literature.54 In addition, more than 80% of the reported cases have involved the right dominant upper extremity, usually in a well-developed man9,62 whose average age is about 50 years5,21,57 (range 2163 to 7021 years).

MECHANISM OF INJURY In virtually every reported case,8,21,57 a single traumatic insult, often a force of 40 kg or more against resistance from an elbow in about 90 degrees of flexion, has been implicated. This mechanism, along with abuse of anabolic steroids, accounts for its surprisingly common occurrence in well-conditioned, healthy, but competitive weightlifters. Pre-existing degenerative changes in the tendon predispose to rupture.18,19 Acute pain in the antecubital fossa is noted immediately. Rarely, a patient complains of a second episode of acute pain several days later. Such a history suggests the possibility of an initial partial rupture or of secondary failure of the lacertus fibrosus.11,14 Occasionally, forearm pain has been reported, but it is considered rather uncommon. * See references 2, 6, 11, 20, 27, 28, 33, 47, 48, 50, 52, 69, and 73.

Chapter 34 Injury of the Flexors of the Elbow: Biceps Tendon Injury

519

FIGURE 34-2

Irregularity of the biceps tuberosity is frequently observed, suggesting that a degenerative process may be implicated, at least in part, in the causation of this condition.

FIGURE 34-1

The biceps mechanism may be rarely torn at the musculotendinous (large arrow) or tendinous (medium arrow) junction; a complex or partial avulsion is the most common injury (small arrow).

ETIOLOGY

A

The cause of the injury has been discussed by several authors and is considered in detail by Davis and Yassine.18 The histologic pathology is that of a degenerative process, a finding consistent with the radiographic changes of spurring sometimes observed at the radial tuberosity (Fig. 34-2).21,37,62 During pronation and supination, inflammation and subsequent attenuation of the biceps tendon is initiated by irritation from the irregularity of the radial tuberosity (Fig. 34-3) or from chronic cubital bursitis (Fig. 34-4).42 Predisposition to this and other tendon injuries has been associated with anabolic steroid use,51 hyperparathyroidism,15,63 chronic acidosis,59 and systemic diseases such as lupus erythematosus.71 One study has also implicated a hypovascular zone of tendon near its attachment as a cause or contributing factor to the injury.66 More recent studies of the “footprint” and function of the biceps tendon insertion have revealed additional insight into the insertion pattern (Fig. 34-5). The portion oriented more distally is along the line of the short head tendon; the long head portion inserts further from the axis of rotation (see Fig. 34-5).22

FIGURE 34-3

B

Illustration of the pathophysiology of distal biceps rupture. Hypertrophic changes at the radial tuberosity cause irritation of the tendon, predisposing it to degenerative changes and rupture during pronation and supination. (Redrawn from Davis, W. M., and Yassine, Z.: An etiologic factor in the tear of the distal tendon of the biceps brachii. J. Bone Joint Surg. 38A:1368, 1956.)

BT

BT

R R

FIGURE 34-4

U

U

Cubital bursitis may occur in association with degeneration of the distal biceps insertion. BT, biceps tendon. (Redrawn from Karanjia, N. D., and Stiles, P. J.: Cubital bursitis. J. Bone Joint Surg. 70B:832, 1988.)

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Part V Adult Trauma

PRESENTATION Subjective Complaints The common symptom of distal biceps tendon rupture is a sudden, sharp, tearing-type pain, followed by discomfort in the antecubital fossa or in the lower anterior aspect of the brachium. The intense pain usually subsides in several hours, but a dull ache persists for weeks. Immediately after the injury, activity is possible but dif-

ficult. If surgical repair is not performed, chronic pain with activity is common.38 Flexion weakness of about 15 percent inevitably develops but over time some flexion strength returns.46 Loss of supination strength has been reported as the source of variable dysfunction but has been measured as averaging 40 percent,57 and diminution of grip strength also has been recognized.2,46,57

Objective Complaints Ecchymosis is variably present in the antecubital fossa,21,61 and occasionally over the proximal ulnar aspect of the elbow joint.8 Extensive bleeding is uncommon but is seen occasionally (Fig. 34-6). With elbow flexion, the muscle contracts proximally and a visible, palpable defect of the distal biceps muscle is obvious (Fig. 34-7). If the contour is relatively normal, the lacertus fibrosus may be intact or the lesion may be a partial tear. With time, stretch of the lacertus fibrosus14 may occur.

FIGURE 34-5

The “footprint” of the tuberosity reveals the short head tendon inserts more distally (arrows); the long head portion more “ulnarly” from the axial rotation axis. The bursa lies more radially.

A

FIGURE 34-7

Proximal retraction of the biceps muscle is the consistent and obvious finding and should allow the diagnosis to be readily made.

B FIGURE 34-6

A, The forearm ecchymosis is variable and only rarely is extensive.

Chapter 34 Injury of the Flexors of the Elbow: Biceps Tendon Injury

521

FIGURE 34-8

The biceps tendon view consists of the patient lying prone, the elbow flexed over the head, and the forearm supinated.

Assessment of strength alteration is essential to substantiate the diagnosis. Local tenderness is present in the antecubital fossa. The defect may be palpable; if it is not and if symptoms are otherwise consistent with the diagnosis, a partial rupture may have occurred. With partial rupture, an intense peritendinosis or bursitis may develop and crepitus or grinding is noted with forearm rotation.11 Motion is not altered, except possibly as a result of pain at the extremes of flexion, extension, and supination. Flexion weakness usually is detectable by routine clinical examination. The loss of strength may be profound,21 especially on supination immediately after injury. Loss of grip strength is variable in degree but does occur with most injuries.

FIGURE 34-9

The view described earlier nicely demonstrates the length of the biceps tendon as well as the musculotendinous junction (bottom arrow) and its insertion into the tuberosity (top arrow). (Courtesy of Dr. Mark Collins.)

(Fig. 34-10). In addition, the elbow is near the center of the magnet and, thus, fat suppression is optimal, enhancing visualization of small amounts of fluid. Continuing technical advances allow visual reconstruction and enhancements (see Fig. 34-10B).

Imaging of the Distal Biceps Tendon Plain x-ray study is usually normal; however, spurring of the bicipital tuberosity is sometimes seen as being suggestive of a chronic tendon enesiopathy. Magnetic resonance imaging is commonly used to make or to confirm the diagnosis,47 especially when the lacertus fibrosus is intact and the typical retraction deformity is not present or when trying to differentiate complete tears from partial tears. The treatment of complete tears without retraction or partial tears can benefit from precise delineation of the extent of the pathology. Guiffre and Moss26 have described the Flexion Abduction Supination (FABS) view. With the elbow flexed and forearm supinated, the radial tuberosity is directed medially and the distal biceps tendon is almost a direct line from the tuberosity to the muscle belly (Fig. 34-8), allowing a longitudinal view to include the muscle belly, tendon, and the difficult-to-assess bicipital tuberosity insertion (Fig. 34-9). Because the tendon is assessed longitudinally and is at full length and partially unravelled, the differentiation of partial from complete tears is made easier

Surgical Findings If the biceps tendon is explored early, local hemorrhage is present in the antecubital space but usually is not extensive. The tendon may have recoiled into the muscle or may lie loosely curled in the antecubital fossa. Invariably, the separation is clean and from the radial tuberosity,8,21,46,52,57,61 with a bulbous stump of degenerative tendon. This supports our histologic studies and the hypothesis that the underlying lesion is degeneration at the site of attachment.14,18 After several months, typically the tendon has retracted into the substance of the biceps muscle and cannot be retrieved to be reattached. However, this response as well as the status of the lacertus fibrosus is variable.

TREATMENT Acute Disruption Reliance on the older literature is unwise. Nonoperative management has been reported to provide satisfactory

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A

B

FIGURE 34-10 A, Magnetic resonance imaging scan of the arm shown in Figure 34-1, 4 days after the injury. This study was useful for demonstrating distal avulsion with retraction of the tendon and absence of tendon in the cubital fossa. B, Visual reconstruction.

results37; however, the functional superiority of surgical treatment is obvious when the results of cases treated with and without surgical intervention are reviewed.57 The recent literature offers overwhelming documentation of the excellent results of early repair.2,6,50,60 Although tendon strains will heal, true partial rupture does not and chronic pain necessitates surgical repair.

Surgical Repair Reattachment to the radius by any one of several techniques5,9,24,59,69 is clearly the treatment of choice. The difficulty of performing the anterior exposure needed to avoid radial nerve injury has inspired the development of a second incision that is placed over the dorsal aspect of the forearm.12 Curiously, this technique appears first to have been employed in 1937 by Plummer to reattach the biceps tendon to the proximal ulna.21 It is paramount to understand that the two-incision Boyd-Anderson technique originally described has been modified at the Mayo Clinic to reduce the likelihood of the development of ectopic bone between the radius and ulna. This point is explained later. Because of concern over the development of ectopic bone associated with the two-incision technique, and with the advent of suture anchors, the anterior exposure

using these anchors is gaining popularity. If the procedure is performed promptly, the tract of the biceps tendon is still present and is easily identified. Later (more than 2 weeks after injury), the tract may be obliterated, making the exposure more difficult36 and complications more frequent.44

SURGICAL TECHNIQUE Two-Incision Technique (Mayo) This technique has been described in detail elsewhere.56 With the patient in the supine position, a tourniquet is applied to the arm and the extremity is prepared, draped, and placed on an elbow table. A limited 3-cm transverse incision is made in the cubital crease (Fig. 34-11). The brachium is grasped and milked distally to deliver the biceps tendon. In the majority of cases, the tendon is readily retrieved with this maneuver. The tendon is inspected and invariably is found to be cleanly avulsed from the radial tuberosity. The distal 5 to 7 mm of degenerative tendon is resected, and two No. 5 nonabsorbable Bunnell or whipstitch (Krackow) sutures are placed in the torn tendon for a distance of at least 3 cm (see Fig. 34-11). The tuberosity is palpated with the index

Chapter 34 Injury of the Flexors of the Elbow: Biceps Tendon Injury

523

Radius pronated

Limited transverse incision

A

Dorsal lateral incision

B

4 3

3 2

1

a

6

b

4 5

c

C

d

FIGURE 34-11 A, A transverse incision is used to expose the antecubital space proximally. The retracted biceps tendon is milked into the field. B, The tendon is trimmed, and a blunt instrument is introduced in the tract of the biceps tendon, and the skin is indented on the volar aspect of the proximal forearm. An incision is made over this instrument. C, Two Bunnell sutures or a Krachow lock stitch (a to d) are placed in the end of the tendon.

Part V Adult Trauma

524

NO Extensor digitorum communis Ulna Radial tuberosity

Extensor carpi ulnaris Anconeus

Radial nerve Supinator

D

Supinator Extensor carpi ulnaris

Drill holes

YES

Extensor digitorum communis

E

Radial tuberosity 1.5 mm 7 mm

5 mm

F

G

Biceps tendon

H

FIGURE 34-11, cont’d

D, The common extensor and supinator muscles are then split to expose the radial tuberosity. The ulna is not exposed. Full pronation of the forearm brings the tuberosity into the field. E, The radial tuberosity is excavated using a high-speed burr. F, Osseous bridges 5 to 7 mm from the edge and 7 mm between the holes are ideal, and the biceps tendon is then brought through its previous tract (G) and reinserted into the radial tuberosity with two nonabsorbable sutures (H).

fingers, and a blunt, curved hemostat is carefully inserted into the space previously occupied by the biceps tendon. The instrument slips past the tuberosity and is advanced below so its tip may be palpated on the dorsal aspect of the proximal forearm (see Fig. 34-11). A second incision is made over the instrument. The tuberosity is

exposed by a muscle-splitting incision, with the forearm maximally pronated. Note: The ulna is never exposed.24 A high-speed burr is used to evacuate a defect 1.5 cm wide and 1 cm deep in the radial tuberosity (see Fig. 34-11). Three holes are then placed 7 to 8 mm apart and at least 5 mm from

Chapter 34 Injury of the Flexors of the Elbow: Biceps Tendon Injury

the edge of the excavation. The tendon is delivered through the second incision, and No. 5 sutures are brought through the holes in the tuberosity. The tendon is carefully introduced into the excavation formed in the tuberosity, and with the forearm in the neutral position, the sutures are pulled tight and secured. The wounds are closed in layers, and a suction drain is inserted in the depths of the wound, both anteriorly and posteriorly. The elbow is placed in 90 degrees of flexion with the forearm placed in 45 degrees of supination. A compressive dressing is applied.

Single-Incision Technique The patient is prepared as noted earlier. Some use a sterile tourniquet because having exposed the proximal radius, removal of the tourniquet to facilitate mobilization of the biceps muscle belly distally may be required. A longitudinal 5-cm incision is made distal to the cubital crease. The lateral antebrachial cutaneous nerve is specifically identified and followed distally, where it lies deep to the median cephalic vein. It is here that the nerve can be injured if the vein is ligated or divided to obtain exposure. In the acute presentation the residual tendon sheath is usually composed of inflammatory bursa filled with haemoserous fluid.4 This is easily followed down onto the bicipital tuberosity by fully supinating the forearm to orientate the tuberosity volarwise. In the chronic case, the sheath may be scarred and obliterated.36,44 If this is the case, then the anterior aspect of the brachialis muscle is followed distally, between the common flexor and common extensor muscles. Note: The radial nerve is carefully avoided. The bicipital tuberosity is palpated while rotating the forearm, to distinguish the radius from the ulna. Retraction should be with long right-angled retractors rather than bone levers to avoid injury to the posterior interosseous nerve. If the tear is acute, then the tendon stump may be milked into the surgical field, as described earlier. If the tear is a few weeks old, formal dissection may be required because the tendon often recoils and lies in a phlegmonous stump, possibly even tethered to the median or the lateral antebrachial cutaneous nerve. The distal 5 to 7 mm of degenerative tendon is resected. Generally, the lacertus fibrosis is left intact to maintain its function to the transfer flexion forces to the ulna. If there is a marked retraction of the biceps tendon and a tight repair is required, then release and reapposition should be considered as a potential median nerve entrapment has been postulated.4

Tendon Fixation A number of different means of tendon fixation to the bicipital tuberosity have been described either using various suture anchors7 or an endobutton.4

525

Suture Anchor The precise technique depends on three variables: exposure, type of anchor used, and method of reattachment. Usually a limited anterior approach is employed. The use of both the screw and the barb designs has been described (Fig. 34-12). Typically, two or three suture anchors are used, most often placed directly into the tuberosity, which has been débrided but not decorticated. One technique places a hole the diameter of the tendon stump in the bicipital tuberosity, and the anchors are placed proximal and distal on either side of the biceps tuberosity. The tendon suture is placed approximately 1 cm distal to the end of the tendon stump and the suture tensioned on the anchors, thus allowing apposition of the tendon stump into the radius.53 Greenberg and associates29 compared fixation strength with the endobutton and traditional techniques. A mean pullout strength of 253 N for the Mitek G4 Superanchor (barb design), 177 N for a conventional bone grid, and 584 N for the titanium endobutton. The button was three times stronger than the bone bridge (P > .0001) and two times stronger than the Mitek anchor (P > .0007). Note that 19-gauge wire was used to exclude suture properties. Other studies,67 however, have not demonstrated any real differences between barbed anchors and endobutton with No. 2 reinforced polyester suture (Fiberwire; Arthrex Corp., Naples, FL) and cyclic loading. The endobutton did reveal a nonsignificant 16% greater ultimate tensile load to failure than did the suture anchor group (274.77 N versus 230.06 N).

A FIGURE 34-12

B

Both the screw (A) and barbed-tip (B) suture anchor designs have been used for biceps tendon attachment.

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Part V Adult Trauma

Endobutton Technique The endobutton (Acufex; Smith & Nephew, Inc., Andover, MA) technique was first described by Bain and colleagues4 for both primary repair and late reconstruction with a semitendinosis tendon. The advantage of this technique is that the biceps tendon fixation construct is prepared outside the wound (Fig. 34-13A) rather than down a deep tunnel, and the construct is the strongest available to date.29 The bicipital tuberosity is exposed as described earlier. With the forearm fully extended and maximally supinated, an elongated elliptical cortical window (approximately 6 × 12 mm) is made in the most medial portion of the tuberosity to restore the normal anatomic insertion and thus maintain the “windlass effect” of the distal biceps. Although initially described using a burr and lavaging the wound of any bone debris, drilling and dry sucking the wound minimizes the soiling of tissue with bone debris, decreasing the risk of heterotopic ossification. The cortical window is achieved by drilling a 2-mm guidewire into the bicipital tuberosity and just penetrating the far cortex of the radius (all drilling is undertaken with a tissue guard to protect the soft tissues). Using a 6-mm drill, only the radial tuberosity cortex is drilled (not the far cortex). The drill is then lifted on the guidewire, tilted proximally and drilled, lifted and tilted distally and drilled, resulting in an elliptical cortical window. Using the same guidewire, the far cortex of the radius is drilled with 4.5-mm drill to allow passage of the endobutton through the far cortex (see Fig. 34-13B). The degenerated tendon is débrided to healthy tissue and using a nonabsorbable suture (No. 5 ethibond [Ethican Inc., Sommerville, MA] or No. 2 Fiberwire [Arthrex Corp., Naples, FL]), a Bunnell or “whip” stitch is placed in both the medial and lateral margins of the tendon (see Fig. 34-13A). A gap of 2 mm is left between the tendon end and endobutton to allow it to be passed through the dorsal cortex of the radius and to flip in place. Two strong sutures, which can be differentiated from each other, are placed in the leading and trailing holes of the endobutton. These sutures are threaded onto a long-eyed needle. The forearm is maximally supinated and the elbow held flexed to bring the forearm to the tendon in a straight line. The needle is passed through the bicipital cortical window, through the dorsal cortex and out through the extensor compartment and skin. The needle is directed in an ulna direction (but should not touch the ulna) to avoid injury to the posterior interosseous nerve. The leading suture is tractioned to deliver the endobutton through the radius and then the trailing suture is tensioned to flip the endobutton and lock it on the dorsal surface of the radius (see Fig. 34-13C). Intraoperative confirmation of a locked button should be done in all cases (usually with fluoroscopy), because it can appear locked when it is only

partially passed through the volar cortical window (see Fig. 34-13D). The tension of the repair is assessed to ensure that the tendon remains within the radius at all times and to determine the “safe arc” as a guide for rehabilitation. Rehabilitation involves a resting splint for 1 week and a sling for 3 to 6 weeks and gentle flexion/extension and rotation movements encouraged. No heavy lifting is allowed for at least 3 months.

RESULTS Two-Incision Technique Today, few surgeons attach the acutely ruptured tendon to the brachialis, but in the past, this maneuver has been said to produce full function of the forearm,13,45 including adequate supination.10,62 Restoration of normal or nearly normal supination strength without anatomic reinsertion of the biceps tendon is incomprehensible. The result may be surprisingly good, but it is not normal and cannot restore supination strength. We have conducted isometric strength assessment tests on seven patients at least 15 months after the two-incision technique.57 Restoration of strength approached normal in flexion and supination (Table 34-1). Nontreated distal biceps rupture results in loss of about 20% flexion and 40% supination strength.57,65 The objective measurements of restoration of normal strength have been reaffirmed with the use of Cybex testing for strength but also endurance.2 Interestingly, these investigators found restoration of normal strength only if the dominant extremity was involved, and a residual 20% to 30% weakness if the nondominant side was involved. Although this observation of different results by the dominant extremity has also been made by others,48 this certainly has not been our experience with isometric testing. Barbed suture anchors for distal biceps repair were first reported in 1993.7 In one study, using a single limited incision and two barbed suture anchors, 53 patients were evaluated at a mean follow-up of 38.1 months. Using the Andrews-Carson scores, there were 46 excellent and seven good results. Two patients developed ectopic ossification associated with mild loss of forearm rotation and mild arm pain. One patient developed a temporary radial nerve palsy, which resolved completely within 8 weeks.39

Suture Anchors

Endobutton Technique Bain and coworkers4 first reported on 12 patients with endobutton repair. Motion averaged 5 to 146 degrees and 81 degrees supination and 80 degrees pronation. All returned to previous activities and had a grade 5 strength.

Chapter 34 Injury of the Flexors of the Elbow: Biceps Tendon Injury

4 mm

A

B

C FIGURE 34-13

A, The humerus is prepared by using a 2-mm drill through the tuberosity and through the opposite cortex. The proximal hole is enlarged with the burr, the distal hole is enlarged with the 4-mm drill bit to allow the passage of the endobutton. B, A heavy, usually No. 5 nonabsorbable, suture is placed in the distal biceps tendon and tied to the endobutton. Two sutures are then passed through either hole of the endobutton and inserted through the eye of a Keith needle. C, The Keith needle is passed retrograde through the tuberosity and out the hole in the opposite cortex, taking care not to touch the ulna. The suture is then grasped, and the leading edge and one of the sutures is differentially tensioned allowing the endobutton to slide through the hole in the opposite cortex. D, Once the endobutton has been completely deployed, it is tightened against the opposite cortex by opposite tension on the biceps tendon. The leading and trailing sutures are removed. (Modified from Bain, G. I., Prem, H., Heptinstall, R. J., Verhellen, R., and Paix, D.: Repair of distal biceps tendon rupture: A new technique using the endobutton. J. Shoulder Elbow Surg. 9:120, 2000.)

D

527

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Part V Adult Trauma

TABLE 34-1

Strength of Various Functions After Treatments for Distal Biceps Tendon Rupture STRENGTH (%)*

Treatment (No. of Patients)

Follow-Up per Month

Flexion

Extension

Pronation

Supination

Grip

None (2)

15

61

100

93

63

86

Early reattachment (2)

17

97

117

99

95

114

Late reattachment (1)

36

85

74

94

64

77

Insertion into brachialis (1)

20

87

105

113

43

100

*Percentage difference from opposite extremity, corrected for effect of the dominant side.

There was no synostosis, reruptures, or neurologic complications. A subsequent study of 14 patients who had tendons repaired with the endobutton technique revealed recovery of 97% of flexion strength and 82% of supination strength. Patients were able to participate in an aggressive postoperative rehabilitation program and were able to regain strength and function rapidly, with satisfactory return to preinjury activities and occupations.29

COMPLICATIONS As a result of consistent reports of ectopic ossification and neurologic injury associated with distal biceps repair, interest has centered on the surgical exposure and means of fixation as potential factors influencing complications. Only one report in the English literature from the Mayo Clinic specifically deals with the complications of surgical treatment for distal biceps tendon rupture.44 This experience reported 74 tendon repairs using the Mayo modified Boyd-Anderson approach stratified by acute (<10 days), subacute (10-21 days) and chronic (>21 days) repairs. The association between the incidence of complications and the delay to surgery was highly significant. Repairs performed less than 10 days from injury incurred complications in 24% of patients, 10 to 21 days in 38% of patients and greater than 21 days in 41% of patients. This probably represents the greater dissection that is required to identify and reattach the tendon. Eighty-six percent of patients who had a repair at less than 10 days and only 53% in the 10-to-21-day group had a patent tunnel at surgery. Most complications were mild including sensory paresthesias (5), temporary posterior interosseous nerve palsy (1), and persistent pain (6). Heterotopic ossification was observed in four but there were no synostosis. Transient sensory paresthesias especially of the lateral antebrachial cutaneous nerve, are relatively common. This nerve is at risk proximally as it passes from behind the lateral border of the biceps tendon. Distally, it passes deep to the median cephalic vein, where it may be

inadvertently divided or ligated with the vein. In very tight repairs, there may be entrapment of the lateral antebrachial nerve as it passes from behind the tendon. If symptoms occur, then a slower restoration of extension may be indicated. Similarly, the median nerve may be trapped if the tendon is advanced excessively while leaving the lacertus fibrosus intact.4 If this is the case, then consideration to release the lacertus may be indicated. Transient radial or posterior interosseous nerve palsy with reattachment to the tuberosity has been,21,55 and continues to be, noted occasionally.50,60 The lesions have still been seen with both single and double incision exposures. The mechanism of injury is thought to be due to retraction, possibly with the use of bone levers over the lateral border of the radial neck where the nerve lies on the bone and where it can be compressed or stretched by retractors. Long retractors may minimize this risk. Nonanatomic routing of the tendon in relation to the median, radial, and lateral antebrachial cutaneous nerve can result in persistent postoperative palsies.43 Most palsies are temporary.39,44 Reattachment of the tendon through an anterior approach with a pullout suture has received support50,60 but potentially has skin and wound problems. In two recent series of 24 cases in all, this approach produced excellent restoration of function but also one musculocutaneous nerve injury and two temporary radial nerve palsies, complications that are clearly associated with an anterior surgical approach for this condition. The possibility of ectopic bone formation is well known. The formation of ectopic bone has been reported with both single- and double-incision (Fig. 34-14) exposures, and may be associated with pain but generally does not cause a significant restriction of rotation, as noted earlier. Bridging synostosis is most commonly associated with the Boyd-Anderson two-incision technique. The development of proximal radioulnar synostosis is thought to be associated with exposing the periosteum of the lateral ulna, and in our opinion, it can be avoided, or at least minimized, with a muscle-splitting

Chapter 34 Injury of the Flexors of the Elbow: Biceps Tendon Injury

incision (Fig. 34-15).24 The role of nonsteroidal antiinflammatory drugs to prevent ectopic ossification has not been established one way or the other. If an osseous bridge does develop, successful resection can be undertaken about 8 to 9 months after the initial surgery (Fig. 34-16).23 In some cases, extensive involvement of the interosseous space compromises the site of attachment (Fig. 34-17). Removing the osseous bar may thus result in detachment of the biceps tendon,

529

which then must be reattached into the tuberosity (Fig. 34-18). A good result may be anticipated, but rehabilitation must begin anew. If a bridge is excised, irradiation (700 cGy) may be administered, but in my practice, there has been little tendency for recurrence of the ectopic bone. If the surface area of resection is large and recurrence is a concern, a vascularized interposition adipofascial interposition graft may be a useful adjunct to prevent recurrence.41 Recurrence of the avulsion is rarely reported and usually is associated with patient (inappropriate early or abnormal use) or surgeon factors (poor positioning of bone bridges). One of us (BFM) has had one such case in a paralytic man who uses his arms for transfer and local motion sustained a recurrent avulsion less than 1 month after repair. A revision was successfully performed.

AUTHOR’S PREFERRED TREATMENT METHOD When the diagnosis of disruption of the distal biceps tendon is made within the first 7 to 10 days, reattachment to the radial tuberosity is recommended. The surgeon’s experience may affect the success and the incidence of complications when using any of these techniques. If one is comfortable with the anterior exposure, then endobutton fixation is preferred, especially if an accelerated rehabilitation is to be undertaken (JH). Morrey continues to use the two-incision technique.

LATE RECONSTRUCTION FIGURE 34-14

Ectopic bone after employment of suture

anchors.

Supinator

Supinator EDC ECU

A

Muscle splitting– recommended approach

The individual needs of the patient and the goals of any late surgical procedure must be carefully balanced. If the patient’s occupation and residual strength do not require

Anconeus ECU

B

EDC

Anconeus

(Kocher’s interval)

Avoid intervals exposing ulna

FIGURE 34-15 A, The curved hemostat passes close to the radius and past the tuberosity, avoiding the ulna. B, Curving the instrument toward the ulna is to be avoided. ECU, extensor carpi ulnaris; EDC, extensor digitorum communis.

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Part V Adult Trauma

A

B

FIGURE 34-16 A, Proximal radioulnar synostosis resulted from reattachment of an avulsed right biceps tendon to the radial tuberosity using the two-incision technique of Boyd and Anderson, for which the ulna was exposed. B, Three months after it was removed, the radioulnar synostosis had not recurred. The patient had improved pronation and supination strength by 20% to 40%, and the total arc of motion had improved from 5 to 110 degrees.

FIGURE 34-17 The ectopic bone bridges the radius and ulna and has progressed proximally up the repaired tendon, as observed on the plane film (A) and the three-dimensional reconstruction (B).

improvement of supination strength, simple reinsertion into the brachialis muscle is performed. Although it is rarely indicated, this surgical procedure is easy, improves flexion strength, and is essentially free of complications. Postoperative rehabilitation is similar to that described earlier, except that no limitations are placed on pronation and supination in the early postoperative course.

AUGMENTATION PROCEDURES Sometimes, after careful discussion with the patient, improved supination strength is found to be required. Chronic pain, due to tethering of neurovascular struc-

tures or cramping of a chronically retracted biceps muscles, is an indication for intervention. In chronic tears, a graft is usually necessary to restore muscle tendon length. Autologous grafts described include hamstring tendon (semitendinosus),34 fascia lata,37 palmaris longus,64 flexor carpi radialis,49 and Achilles tendon allograft.65 Hallam and Bain31 reported the results of anatomic repair for chronic distal biceps tendon ruptures by use of a semitendinosus autograft with the endobutton. All nine patients were satisfied with their outcome and were able to return to their jobs. The mean pain score was 0.5, and the postoperative flexion arc was from

Chapter 34 Injury of the Flexors of the Elbow: Biceps Tendon Injury

531

FIGURE 34-18 A, Extensive radioulnar bridging after the two-incision technique. B, The repaired tendon embedded in the synostosis required readvancement at the time of osseous excision. At 6 months, the arc of forearm rotation was 100 degrees and strength was 80% of normal.

3 degrees to 147 degrees, with supination to 75 degrees and pronation to 62 degrees. The mean Mayo Clinic Elbow score was 96.3 (range, 85 to 100). Wiley72 reported results with delayed semitendinosus reconstruction compared with nonoperative management. Superior results were documented in the delayed reconstruction group. The autograft reconstruction group was employed with a two-incision technique, and flexion and supination strength were restored to the normal range. The nonoperative group lacked 20% of normal strength. Endurance in both groups was within the normal range. No radial nerve injuries or heterotopic ossification occurred, and all reconstructions remain intact. At the Mayo Clinic, we favor an autologous Achilles tendon graft (Fig. 34-19). This is a very satisfying tissue and one ideally suited to this reconstruction. The fleck of calcaneus bone may be trimmed and embedded into the excavated radial tuberosity. Then, with the elbow flexed to 45 to 60 degrees, the Achilles fascia is draped over the biceps muscle and the bone tendon stump is sewn into the muscle. This offers a very gratifying reconstruction that allows more aggressive rehabilitation.

PARTIAL (INCOMPLETE) DISTAL BICEPS RUPTURE Partial rupture of the distal biceps tendon has been reported since the first edition of this book was published. It is becoming increasingly recognized as a cause of anterior cubital fossa and forearm pain. The history of forced eccentric contracture is typical, and overuse may have preceded this event. Pain subsides but does not completely abate and recurs with reintroduction of heavy activities. Often, the patient is a male manual worker who notes intolerance to repetitive lifting of twisting activities. Occasionally, partial tears were seen in women with an underlying inflammatory arthropathy. Clinically, the patient has an intact lacertus fibrosus associated with anterior elbow pain that is exacerbated with resisted forearm supination or when the arm is placed in full extension and pronated. There may be a palpable fullness to the cubital fossa due to an enlarged cubital bursa. Distinguishing rupture from bicipital tubercle bursitis may be difficult, especially because the two conditions often coexist. Diagnosis of partial or impending rupture of the biceps tendon is becoming

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45°–60°

A

B FIGURE 34-19 The calcaneus is trimmed to a small fleck measuring 1.3 × 0.8 cm that contains the Achilles tendon attachment. A, The calcaneus bone is brought through the tunnel in the cubital space and embedded into the excavated tuberosity. Sutures are placed through the tendon and bone and secured to the tuberosity. B, With the elbow flexed 40 to 60 degrees, the flare of the tendon fascia is secured to the biceps with a Bunnell stitch in the tendon remnant (if one exists).

more common, due to the increased index of suspicion and imaging with magnetic resonance imaging (MRI). MRI using the FABS view allows an assessment of the extent of loss of the footprint attachment of the biceps tendon, the extent of any bursitis, and its relationship to neurologic structures. In a study conducted by Karanjia and Stiles,42 one of the two patients with cubital bursitis was found at surgery to have distal biceps tendon degeneration in association with the bursitis. I (BFM) have observed this finding in one female patient in whom the initial exploration through Henry’s approach revealed extensive “bursitis.” Only after careful inspection of the biceps tendon was it noted that a 50% disruption had occurred.11 My experience suggests that a partial rupture of the biceps tendon occurs first and that the second episode of pain indicates complete rupture. Later, secondary stretch or rupture of the lacertus fibrosus may occur (Fig. 34-20). Rarely, the cubital bursitis can enlarge to produce an insidious compressive neuropathy of the posterior interosseous nerve.

TREATMENT The indication for intervention depends on the patient’s symptoms, including pain and weakness (both the severity and longevity). Today, because of the tendency for radial tuberosity bursitis, we believe that all the partial ruptures (not strain) should be fixed or pain will develop. The treatment of the partial tendon rupture may best be understood by considering the pathology of a

FIGURE 34-20 Surgical photograph shows that some fibers of the biceps tendon had detached (arrow) while others had remained in continuity (arrowheads). Note that the lacertus fibrosus is stretched (open arrow).

Chapter 34 Injury of the Flexors of the Elbow: Biceps Tendon Injury

degenerative tendon. Reimplantation of the remaining portion of the tendon to the radial tuberosity does not reliably relieve pain.16 Complete removal of the remaining fibers (which effectively creates a complete tear), trimming of the distal tendon, and then reattachment as for an acute injury is the treatment of choice.

CALCIFIC TENDINITIS Acute calcific tendinitis does occur in the distal biceps tendon but very rarely.58 Calcification has also been observed in more chronic presentations associated with overuse activities.10 There appears to be no relationship between the acute process and subsequent degeneration and rupture. It is possible for the process to resolve spontaneously and completely. Cortisone injections must be considered very cautiously owing to the proximity of the radial nerve. Supportive treatment includes rest and anti-inflammatory medications.

RUPTURE OF THE BRACHIALIS MUSCLE A single case report describes rupture of the brachialis muscle at the musculotendinous junction after direct trauma to the muscle.32 Diagnosis was made by demonstrating a palpable defect at the musculotendinous junction. Treatment by direct suture was reported to be successful.32 Coonrad and coworkers17 also reported snapping of a brachialis tendon that caused pain and median nerve irritation after a hyperextension injury. Release of the abnormal bone relieved the symptoms.

References 1. Acquaviva, J.: Rupture du tendon inférieur du biceps brachial droit a son insertion sur la tuberosité bicipitale: Tenosuture success operatoire. Marseilles Med. 35:570, 1898. 2. Agins, H. J., Chess, J. L., Hoekstra, D. V., and Teitge, R. A.: Rupture of the distal insertion of the biceps brachii tendon. Clin. Orthop. Relat. Res. 234:34, 1988. 3. Anzel, S. H., Covey, K. W., Weiner, A. D., and Lipscomb, P. R.: Disruption of muscles and tendons: An analysis of 1,014 cases. Surgery 45:406, 1959. 4. Bain, G. I., Prem, H., Heptinstall, R. J., Verhellen, R., and Paix, D.: Repair of distal biceps tendon rupture: A new technique using the Endobutton. J. Shoulder Elbow Surg. 9:120, 2000. 5. Baker, B. E.: Operative vs. nonoperative treatments of disruption of the distal tendon of biceps. Orthop. Rev. 11:71, 1982. 6. Baker, B. E., and Bierwagen, D.: Rupture of the distal tendon of the biceps brachii. J. Bone Joint Surg. 67A:414, 1985.

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7. Barnes, S. J., Coleman, S. G., and Gilpin, D.: Repair of avulsed insertion of biceps: A new technique in 4 cases. J. Bone Joint Surg. 75B:938, 1993. 8. Bauman, B. S.: Triceps tendon rupture. J. Bone Joint Surg. 44A:741, 1962. 9. Bauman, G. I.: Rupture of the biceps tendon. J. Bone Joint Surg. 16:966, 1934. 10. Bell, M. M.: Elbow pain in a cyclist. Physician Sports Med. 25:83, 1997. 11. Bourne, M. H., and Morrey, B. F.: Partial rupture of the distal biceps tendon. Clin. Orthop. Relat. Res. 291:143, 1981. 12. Boyd, H. B., and Anderson, M. D.: A method for reinsertion of the distal biceps brachii tendon. J. Bone Joint Surg. 43A:1041, 1961. 13. Brickner, W. M., and Milch, H.: Ruptures of muscles and tendons. Int. Clin. 2:94, 1928. 14. Chevallier, C. H.: Sur un cas de desinsertion du tendon bicipital inferieur. Mem. Acad. Chir. 79:137, 1953. 15. Cirincione, R. J., and Baker, B. E.: Tendon ruptures with secondary hyperparathyroidism: A case report. J. Bone Joint Surg. 57A:852, 1975. 16. Conwell, H. E., and Alldredge, R. H.: Ruptures and tears of muscles and tendons. Am. J. Surg. 35:22, 1937. 17. Coonrad, R. W., and Spinner, R. J.: Snapping brachialis tendon associated with median neuropathy. A case report. J. Bone Joint Surg. 7:1891, 1995. 18. Davis, W. M., and Yassine, Z.: An etiologic factor in the tear of the distal tendon of the biceps brachii. J. Bone Joint Surg. 38A:1368, 1956. 19. Debeyre, J.: Desinsertion du tendon inferieur du biceps brachial. Mem. Acad. Chir. 74:339, 1948. 20. Delarue, J., and Denoix, P.: L’alteration degenerative des tendons: Cause de rupture-amorce de tumeurs. Presse Med. 54:869, 1946. 21. Dobbie, R. P.: Avulsion of the lower biceps brachii tendon: Analysis of fifty one previously reported cases. Am. J. Surg. 51:661, 1941. 22. Eames, M. H., Bain, G. I., Fogg, Q. A., and van Riet, R. P.: Distal biceps tendon anatomy: A cadaveric study. J. Bone Joint Surg. 89A:1044, 2007. 23. Failla, J. M., Amadio, P. C., and Morrey, B. F.: Posttraumatic proximal radioulnar synostosis: Results of surgical treatment. J. Bone Joint Surg. 71A:1208, 1989. 24. Failla, J. M., Amadio, P. C., Morrey, B. F., and Beckenbaugh, R. D.: Proximal radioulnar synostosis after repair of distal biceps brachii rupture by the two incision technique: Report of four cases. Clin. Orthop. Relat. Res. 253:133, 1990. 25. Gilcreest, E. L.: Rupture of muscles and tendons. J. A. M. A. 84:1819, 1925. 26. Giuffre, B. M., and Moss, M. J.: Optimal position for MRI of the distal biceps brachii tendon: flexed abducted supinated view. Am. J. Radiol. 182:994, 2004. 27. Giugaro, A., and Proscia, N.: Le rotture del tendine distale e del tendine del capo breve del bicipite brachiale. Min. Orthop. 8:57, 1957. 28. Granato, F., and Marcacci, G.: Su tre casi di lacerazione traumatic della inserzione distale del bicipite brachiale. Clin. Orthop. Relat. Res. 9:245, 1957.

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29. Greenberg, J. A., Fernandez, J. J., Wang, T., and Turner, C.: EndoButton-assisted repair of distal biceps tendon ruptures. J. Shoulder Elbow Surg. 12:484, 2003. 30. Haldeman, K. O., and Soto Hall, R.: Injuries to muscles and tendons. J. A. M. A. 104:2319, 1935. 31. Hallam, P., and Bain, G. I.: Repair of chronic distal biceps tendon ruptures using autologous hamstring graft and the endobutton. J. Shoulder Elbow Surg. 13:648, 2004. 32. Hamilton, A. T.: Subcutaneous rupture of the brachioradialis muscle. Surgery 23:806, 1948. 33. Hang, D. W., Bach, B. R. Jr., and Bojchuk, J.: Repair of chronic distal biceps brachii tendon rupture using free autogenous semitendinosus tendon. Clin. Orthop. Relat. Res. 323:188, 1996. 34. Hang, L., and Josefsson, G.: Rupture of the distal biceps tendon. Acta Orthop. Scand. 48:280, 1977. 35. Hempel, K., and Schwenke K.: Uber Abrisse der distalen Bizepssehne. Arch. Orthop. Unfallchir. 79:313, 1974. 36. Hook, F. R., and Mazet, R. Jr.: Avulsion of the biceps tendon from its radial insertion. U.S. Nav. Med. Bull. 40:409, 1942. 37. Hovelius, L., and Josefsson, G.: Rupture of the distal biceps tendon. Acta Orthop. Scand. 48:280, 1977. 38. Jaslow, I. A., and May, V. R.: Avulsion of the distal tendon of the biceps brachii muscle. Guthrie Clin. Bull. 15:124, 1946. 39. John, C. K., Field, L. D., Weiss, K. S., Savoie, F. H., and Roanoke, B. C.: Single incision repair of acute distal biceps ruptures by use of suture anchors. J. Shoulder Elbow Surg. (in press). 40. Johnson, A. B.: Avulsion of biceps tendon from the radius. N. Y. Med. J. 66:261, 1897. 41. Jones, M. E., Rider, M. A., Hughes, J., and Tonkin, M. A.: The use of a proximally based posterior interosseous adipofascial flap to prevent recurrent of synostosis of the elbow joint and forearm. J. Hand Surg. Eur. 32:143, 2007. 42. Karanjia, N. D., and Stiles, P. J.: Cubital bursitis. J. Bone Joint Surg. 70B:832, 1988. 43. Katzman, B. M., Caligiuri, D. A., Klein, D. M., and Gorup, J. M.: Delayed onset of posterior interosseous nerve palsy after distal biceps tendon repair. J. Shoulder Elbow Surg. 6:393, 1997. 44. Kelly, E. W., Morrey, B. F., and O’Driscoll, S. H.: Complications of repair of the distal biceps tendon with modified two-incision technique. J. Bone Joint Surg. 82A:1575, 2000. 45. Kron, S. D., and Satinsky, V. P.: Avulsion of the distal biceps brachii tendon. Am. J. Surg. 88:657, 1954. 46. Lee, H. G.: Traumatic avulsion of tendon of insertion of biceps brachii. Am. J. Surg. 82:290, 1951. 47. Le Huec, J. C., Moinard, M., Liquois, F., Zipolia, B., Chauveaux, D., and Le Rebeller, A.: Distal rupture of the tendon of biceps brachii: Evaluation by MRI and the results of repair. J. Bone Joint Surg. 78B:767, 1996. 48. Leighton, M. M., Bush-Joseph, C. A., and Bach, B. R. Jr.: Distal biceps brachii repair: Results of dominant and nondominant extremities. Clin. Orthop. Relat. Res. 317:114, 1995. 49. Levy, H. J., Mashoof, A. A., and Morgan, D.: Repair of chronic ruptures of the distal biceps tendon using flexor

50.

51. 52.

53.

54.

55.

56.

57.

58.

59.

60. 61. 62.

63.

64.

65.

66.

carpi radialis tendon graft. Am. J Sports Med. 28:538, 2000. Louis, D. S., Hankin, F. M., Eckenrode, J. F., Smith, P. A., and Wojtys, E. M.: Distal biceps brachii tendon avulsion: A simplified method of operative repair. Am. J. Sports Med. 14:234, 1986. Louis, D. S., and Peck, D.: Triceps avulsion fracture in a weightlifter. Orthopedics 15:207, 1992. Maydl, K.: Uber subcutane Muskel und Sehnenzerreissungen, sowie Rissfracturen mir Berucksichtigung der Analogen, durch directe gewalt Enstandenen und offenen Verletzungen. Deut. Zschr. Chir. 17:306, 1882;18:35, 1883. McKee, M. D., Hirji, R., Schemitsch, E. H., Wild, L. M., and Waddell, J. P.: Patient-oriented functional outcome after repair of distal biceps tendon ruptures using a single-incision technique. J. Shoulder Elbow Surg. 14:302, 2005. McReynolds, I. S.: Avulsion of the insertion of the biceps brachii tendon and its surgical treatment. J. Bone Joint Surg. 45A:1780-1781, 1963. Meherin, J. H., and Kilgore, B. S. Jr.: The treatment of rupture of the distal biceps brachii tendon. Am. J. Surg. 99:636, 1960. Morrey, B. F.: Distal biceps tendon injury. In Morrey B. F. (ed.): The Elbow: Master Techniques in Orthopaedic Surgery. 3rd ed. Philadelphia, Lippincott Williams & Wilkins, 2007. Morrey, B. F., Askew, L. J., An, K. H., and Dobyns, J. H.: Rupture of the distal biceps tendon: Biomechanical assessment of different treatment options. J. Bone Joint Surg. 67A:418, 1985. Murase, T., Tsuyuguchi, Y., and Hidaka, N.: Calcific tendinitis at the biceps insertion causing rotatory limitation of the forearm: A case report. J. Hand Surg. 19:266, 1994. Murphy, K. J., and McPhee, I.: Tears of major tendons in chronic acidosis with elastosis. J. Bone Joint Surg. 47A:1253, 1965. Norman, W. H.: Repair of avulsion of insertion of biceps brachii tendon. Clin. Orthop. Relat. Res. 193:189, 1985. Platt, H.: Observations of some tendon ruptures. Br. Med. J. 1:611, 1931. Postacchini, F., and Puddu, G.: Subcutaneous rupture of the distal biceps brachii tendon. J. Sports Med. 15:81, 1975. Preston, F. S., and Adicoff, A.: Hyperparathyroidism with avulsion at three major tendons. N. Engl. J. Med. 266:968, 1961. Rantanen, J., and Orava, S.: Rupture of the distal biceps tendon. A report of 19 patients treated with anatomic reinsertion, and a metaanalysis of 147 cases found in the literature. Am. J. Sports Med. 27:128, 1999. Sanchez-Sotelo, J., Morrey, B. F., and Adams, R. A.: Reconstruction of chronic ruptures of the distal biceps tendon with use of an Achilles tendon allograft. J. Bone Joint Surg. 84:999, 2002. Seiler, J. G., 3rd, Parker, L. M., Chamberland, P. D., Sherbourne, G. M., and Carpenter, W. A.: The distal biceps tendon. Two potential mechanisms involved in its rupture: Arterial supply and mechanical impingement. J. Shoulder Elbow Surg. 4:149, 1995.

Chapter 34 Injury of the Flexors of the Elbow: Biceps Tendon Injury

67. Spang, J. T., Weinhold, P. S., and Karas, S. G.: A biomechanical comparison of EndoButton versus suture anchor repair of distal biceps tendon injuries. J. Shoulder Elbow Surg. 15:509, 2006. 68. Steindler, D.: Traumatic Deformities of the Upper Extremities. Springfield, IL, Charles C Thomas, 1946. 69. Straugh, R. J., Michelson, H., and Rosenwasser, M. P.: Repair of rupture of the distal tendon of the biceps brachii. Review of the literature and report of three cases treated with a single anterior incision and suture anchors. Am. J. Orthop. 26:151, 1997. 70. Waugh, R. L., Hathcock, T. A., and Elliott, J. L.: Ruptures of muscle and tendons. Surgery 25:370, 1949.

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71. Wener, J. A., and Schein, A. J.: Simultaneous bilateral rupture of the patella tendon and quadriceps expansions in systemic lupus erythematosus: a case report. J. Bone Joint Surg. 56A:823, 1974. 72. Wiley, W. B., Noble, J. S., Dunlaney, T. D., Bell, R. H., and Noble, D. D.: Late reconstruction of chronic distal biceps tendon ruptures with a semitendinosus autograft technique. J. Shoulder Elbow Surg. 15:440, 2006. 73. Witvoet, J., Robin, B., and Charbrol, J.: A propos d’une desinsertion de l’extremite inférieur du biceps brachial. Presse Med. 74:389, 1966.

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CHAPTER

35

Rupture of the Triceps Tendon Bernard F. Morrey

INTRODUCTION Rupture of the triceps tendon is rare.1,2,3 Anzel and colleagues2 reported that 85% of the 1015 tendon injuries treated at the Mayo Clinic involved the upper extremity. Of this group of 856, only 8 instances of triceps tendon injury were reported, and 4 of these were due to laceration. Since the first report of Partridge in 1868 as cited by Bennett,5 as of 2000, fewer than 50 instances have been recorded in the English literature.6,9,10,11 Unlike ruptures of the distal biceps tendon, this may occur both in men and women, with a female to male ratio of 2 : 3. The mean age of occurrence is about 33 years, but rupture has been observed in a broader spectrum of ages including children (aged 7) to adolescents in whom the olecranon physes has just closed,14 to individuals in the eighth decade.15

triceps also may occur spontaneously with minimal trauma in individuals who are compromised by a systemic disease process,35 such as renal osteodystrophy and secondary hyperparathyroidism.9,15 Although the pathophysiology of this association has not been completely explained, an increased amount of elastic fibers in the tendons of patients with renal osteodystrophy undergoing dialysis has been reported.29 Calcification due to the chronic hypercalcemia of secondary hyperparathyroidism may be yet another explanation for the associated tendon ruptures in this group of patients.35 Ruptures also have been reported in association with steroid treatment for lupus erythematosus45 and chronic acidosis,29 and in individuals with osteogenesis imperfecta tarda25 or Marfan’s syndrome.38 Diabetes has been recently implicated in a patient with triceps rupture at the musculotendinous junction.44 In spite of the association with debilitating states and conditions, this injury is well recognized in the athletic population as well. Such diverse activities as power weightlifting and handball have been implicated.13,19,24,39 It should be noted that the injury can be associated with localized hematoma, and there are reports of ulnar nerve compression as a result of hematoma compression after triceps rupture in power lifters.13,19 Triceps deficiency occurring after total elbow replacement is obviously a problem of exposure, and repair and is discussed elsewhere.7

DIAGNOSIS MECHANISM OF INJURY Rupture of the triceps tendon may occur either spontaneously, after trauma, or after surgical release and reattachment. Two types of traumatic episodes may be implicated. The most common event is a deceleration force imparted to the arm during extension as the triceps muscle is contracting. This usually occurs during a fall, but avulsion has been reported due to simple, uncoordinated triceps muscle contraction against a flexing elbow.4,26 The association of triceps tendon avulsion39 or tear19 associated with body builders is consistent with the observation of muscle unit damage associated with eccentric contractures in the unconditioned muscle.24,31 The possibility of anabolic steroid usage must also be considered in this type of patient. A direct blow to the posterior aspect of the triceps at its insertion in varying positions also has been reported in several instances1,33,45 but is probably an uncommon mechanism of injury.

PREDISPOSING CONDITIONS An association of olecranon bursitis has been noted to predispose to triceps tendon rupture.10 Disruption of the

Without question, a history of acute pain and weakness in extension or an eccentric loading in flexion against forcible triceps contracture, such as a fall on the outstretched hand, is the most reliable method of making this diagnosis. A palpable defect is present in some instances, depending on the extent of triceps retraction (Fig. 35-1). Injury to the muscular tendinous junction results in pain proximal to the olecranon.3,30 Some loss of extension power is universally observed. Some active elbow extension may be present, but extension against gravity is not possible with a complete rupture. The length/tension relationship of the triceps has been studied by Hughes and associates,20 who found that as little as 2 cm shortening between origin and insertion causes a marked (40%) loss of strength.

IMAGING Today, imaging is a most reliable means of making a definitive diagnosis that more precisely defines the location and nature of the tear. A plain radiograph is extremely useful in that uncommon instance in which the triceps rupture occurs with a fleck of bone readily

Chapter 35 Rupture of the Triceps Tendon

537

FIGURE 35-1

On gross examination of the lateral aspect of the elbow, a depression just proximal to the olecranon is noted (arrow) that demonstrates proximal retraction of the triceps. (From Farrar, E. L., and Lippert, F. G.: Avulsion of the triceps tendon. Clin. Orthop. Rel Res. 161:240, 1981.) FIGURE 35-3

A magnetic resonance imaging scan, revealing triceps rupture from its insertion, is more accurate in making the diagnosis if the bone is not involved. (With permission, Mayo Foundation.)

sonic diagnosis is also emerging as a reliable and less expensive imaging modality.31,34

PATHOLOGY

FIGURE 35-2

Radiograph of a patient with triceps rupture. The fragment is readily viewed on the lateral film.

identified in the lateral film15,35,38 (Fig. 35-2). Without question, however, the advent of the magnetic resonant imaging has provided an accurate and reliable means of not only diagnosing this injury but also localizing the site and the extent of the pathology (Fig. 35-3).16,34 Ultra-

Theoretically, three sites of failure may occur and these have also been observed clinically: the muscle belly, the musculotendinous junction, and the osseous tendon insertion.27 For this particular injury, the failure has occurred almost universally at the site of insertion, although failure at the musculotendinous junction has occasionally been reported.18,28,44 Associated injuries also have been reported. Several instances of concurrent fracture of the radial head have been noted,35,42 and a recent report of six such injuries suggests that the association may be more common than is appreciated.23 I have not diagnosed this combination in my practice. A single report of fracture of the wrist22 along with fracture of the radial head supports the case for the mechanism of injury being a fall on the outstretched hand.

PHYSICAL EXAMINATION The diagnosis of a partial rupture may be difficult. Pain is not dysfunctional; thus, a number of patients present

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several weeks after the acute event.21 Furthermore, some weak residual extension power may be provided by the anconeus/triceps expansion. This effect can be negated by observing the inability to extend overhead against gravity. The radiograph is of considerable benefit for diagnosis of this injury in some patients, because flecks of avulsed bone are apparent on the lateral film (see Fig. 35-2).14,41

TREATMENT Treatment may be simply categorized according to partial or complete and acute or chronic presentations.

place two parallel rows of running locked stitches in the tendinous portion of the triceps mechanism (Fig. 35-4). The suture is then brought through cruciate drill holes in the olecranon. With the elbow extended to 30 degrees, the sutures are tied. To further ensure that the tendon is firmly approximated to its origin and to avoid poor healing from synovial fluid, a second transverse suture may be placed which more securely applies the tendon to its site of attachment. If there has been any delay in the treatment, the adventitial bursa tissue should be removed and the area scarified to ensure healing. Concurrent reconstructive options are not necessary in the acute (i.e., less than 2-week-old) injury.

DELAYED RECONSTRUCTION PARTIAL RUPTURES Incomplete tendon rupture should be initially treated nonoperatively.1 However, a distinction must be made between a true partial insertional rupture and one occurring at the musculotendinous junction. Improved imaging modalities are helpful to make this distinction.16,34 A true partial detachment from the olecranon does not reliably heal. With an acute injury, we do favor protecting the extremity and observing the amount of progress over a 6- to 8-week period. A strain of the attachment or of the musculotendinous junction will improve. Although appearing to heal, partial ruptures will continue to be symptomatic with increased activity. In the event that there is no clinical contraindication, surgical intervention is indicated. If there is evidence of healing by progressive resolution of symptoms, then in our judgment this represents a strain and not a rupture and nonoperative management is recommended.

COMPLETE RUPTURE For complete rupture, immediate surgery is the treatment of choice. At the time of exploration, the tendinous portion of the triceps is usually involved and retracted within the muscle.22,35 However, complete disruption of the entire extension mechanism is uncommon. More than 90% of these injuries occur at the olecranon, with injury of the other sites being reported only occasionally.17,25 In our experience, the tendinous central third is most typically detached both with complete and partial injury.42 Lateral continuity with the anconeus is thus a common finding.

ACUTE Direct attachment with a nonabsorbable suture through drill holes placed in the olecranon or through a subperiosteal flap is effective treatment for the acute injury. We employ a heavy No. 5 nonabsorbable suture and

Several reconstructive procedures have been reported for individual cases. Bennett5 and Farrar and Lippert14 describe a forearm fascial flap to reconstruct the triceps mechanism. The classic triceps fascial turndown procedure is not reliable, in our opinion,10 for those with soft tissue deficiency at the point of attachment. We use two reconstructive procedures: anconeus slide and achilles tendon allograft reconstruction.37 The slide is used for minor defects when the anconeus is intact. Technique The patient is supine and the arm brought across the chest. Kocher’s interval between the anconeus and the extensor carpi ulnaris is entered. The anconeus is mobilized from its humeral and ulnar attachments in continuity with the triceps (Fig. 35-5). The triceps/anconeal sleeve is left attached distally and mobilized sufficiently medial to fully cover the site of triceps attachment (Fig. 35-6). The sleeve of extensor musculature is secured in a manner described earlier with a criss-cross No. 5 nonabsorbable suture. The suture is tied with the elbow at 30 degrees of extension. The tendinous fibers that are displaced medially are rotated under the tendon and sewn to themselves.

Achilles Tendon Allograft. The allograft Achilles tendon has recently proven to be particularly attractive in those with marked deficiency (see Fig. 35-6). The position of patient is the same as that noted earlier. The incision begins distal to the olecranon approximately 4 cm and extends proximally to the extent necessary to identify the distal third of the triceps musculature. The ulnar nerve is identified and protected. The defect is débrided, and the triceps musculature is mobilized and its flexibility is tested. In most instances, a trough is made in the subcutaneous border of the proximal ulna and the tendinous portion of the Achilles graft is inserted into the tendinous trough and secured with a No. 5 nonabsorbable

Chapter 35 Rupture of the Triceps Tendon

FIGURE 35-4

539

For acute triceps tendon avulsion, No. 5 nonabsorbable suture is passed through crossed bone tunnels (A) and into the avulsed tendon with a running locked stitch (B). (With permission from the Mayo Foundation.)

A

B

B

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ECU Anconeus Modified Kocher

A

FCU

Olecranon Triceps reflecting

B

FIGURE 35-5

C

The attachment of the anconeus to the lateral margin of the the triceps allows the anconeus to serve as a reconstructive option for triceps deficiency (A). (With permission, Mayo Foundation.) For modest defects (B) the anconeus may be mobilized and oriented over the tip of the olecranon (C).

Chapter 35 Rupture of the Triceps Tendon

541

Anconeus

FIGURE 35-5, cont’d

The tear or deficiency is repaired or re-enforced with a No. 5 nonabsorbable suture (D). (With permission, Mayo Foundation.)

D

D

A FIGURE 35-6

B

When a gap occurs between the triceps tendon and the attachment at the olecranon, as is seen in A, the deficiency is most effectively managed with allograft tissue. The authors prefer an Achilles tendon allograft. The calcaneus can serve as an osseous graft to olecranon if it were deficient (B).

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Part V Adult Trauma

suture placed through two drill holes in the proximal ulna (Fig. 35-7). The elbow is placed in 30 degrees of extension. The triceps musculature is mobilized as far distally as possible. The fascia is brought as far proximal as possible under tension and secured with a No. 5 suture. Once the No. 5 nonabsorbable suture has been placed and secured, the elbow is brought into full extension relaxing the graft. The triceps tendon is brought distally, and the tendon is secured to the muscle and fascia of the triceps with running absorbable suture. If osseous union is desired, a Chevron resection of the proximal olecranon is performed. A matching preparation of the calcaneal bone allows an osseous union of the distal site. The calcaneus is fashioned in a way to match the preparation of the proximal ulna (Fig. 35-8). The calcaneus is secured as an allograft to the olecranon with a cancellous screw, and the remainder of the repair is performed as described earlier. In all reconstructive options, the construct is secured toward extension, such as about 40 to 60 degrees of flexion. After surgery, the arm is protected at 90 degrees of flexion for 3 weeks. Gentle active motion is begun. We have been impressed that recovery, even for acute repair, is slow, possibly taking 6 months to gain 80% of normal strength. Full function is often not realized for a year. The results of immediate or delayed repair have ultimately been universally good. In most instances, marked improvement in strength and full motion have been restored. A loss of approximately 5 degrees of terminal extension strength has been regularly noted. Suprisingly, good results have been observed with repair or reconstruction that has been delayed for up to 1 year.45 However, as noted earlier, it should be emphasized that recovery may be slow and may take a year for full improvement. Two comprehensive assessments of Mayo’s 20-year experience with 23 triceps deficiencies have been reported by van Riet et al.42 and 14 after total elbow by Celli et al.7 Of the 23 not related to joint replacement, there were 8 partial and 15 complete ruptures. Only 2 (8%) had osseous avulsions. Of these 23, 14 were primary repairs and 9 were reconstructions followed on average of 88 months. At final follow-up, the average arc of motion was 10 to 135 degrees. Isokinetic and dynamic testing in 10 patients showed peak strength of approximately 82% of the uninvolved extremity. The endurance, however, was almost 99% of normal. Of interest, results from repair and reconstruction were comparable but the recovery period was prolonged in those undergoing reconstruction. Overall, 90% were considered to have Results and The Mayo Experience

had a subjective satisfactory outcome and all patients were able to extend against gravity. In the group with deficiencies after total elbow, all but one was allowed to extend against gravity.

COMPLICATIONS AND RESIDUA Few complications have been reported other than delayed recovery, variable loss of extension strength, and olecranon bursitis.32

AUTHOR’S PREFERRED TREATMENT METHOD Immediate repair with a posterior incision just lateral to the midline is the treatment of choice. No. 5 nonabsorbable suture is placed in Bunnell fashion in the torn tendon and then through criss-crossed holes in the proximal ulna (see Fig. 35-4). If the avulsion has occurred with a sufficiently large fleck of bone, however, reattachment with the AO tension band technique is preferred.43 If the lesion has been overlooked or treatment delayed by several weeks or months, one of the two reconstructive procedures described earlier is carried out.

SNAPPING TRICEPS TENDON The perception of a posterior snapping elbow is usually localized posteriorly and medially. The cause of such symptoms may be a subluxating ulnar nerve8 or dislocation of a portion of the triceps mechanism.41 Furthermore, an anomalous slip of the triceps tendon may cause these symptoms, but the most common etiology is subluxation of the medial head of the triceps over the medial epicondyle, usually occurring spontaneously in the second decade of life.12,36,40 A common associated finding with this condition is chronic irritation of the ulnar nerve, causing an ulnar neuritis.12,36 Other than this feature, however, the snapping is generally well tolerated. It is very important to recognize this relationship and be suspicious of a snapping triceps concurrent with a subluxating ulnar nerve. Treatment consists of simply detaching or releasing and rerouting the offending portion from the medial attachment under the triceps mechanism to its lateral attachment (Fig. 35-9). Management of the ulnar nerve is based on its degree of involvement, especially on the stability of the nerve.

Chapter 35 Rupture of the Triceps Tendon

Anconeus Olecranon

Ruptured tendon

A

B

B

C C FIGURE 35-7

If the triceps attachment is deficient of tendinous tissue (A), a trough is made in the proximal ulna (B) and the tendinous portion of the Achilles graft is laid in the trough (C) and secured to the proximal ulna with sutures passing through bone.

543

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Part V Adult Trauma

D

FIGURE 35-7, cont’d

The remainder of the reconstruction consists of attaching the aponeurosis to the remnants of the triceps tendon and muscle (D).

D

A FIGURE 35-8

B

An Achilles tendon allograft with calcaneal bone provides an effective reconstructive unit. The calcaneus attachment is fashioned (A) and screwed to the olecranon and prepared to receive the calcaneal allograft (B).

Chapter 35 Rupture of the Triceps Tendon

545

References

20–30°

C FIGURE 35-8, cont’d

With the elbow at 20 to 30 degrees of flexion, the remnant of the triceps is brought distally and the Achilles fascia is brought proximally and secured. The proximal aspect of the graft is secured with multiple No. 1 interrupted and running sutures (C).

FIGURE 35-9

The most common cause of snapping elbow is dislocation of the medial head of the triceps, which subluxes over the medial epicondyle. (Redrawn from Dreyfuss, U.: Snapping elbow due to dislocation of the medial head of the triceps. J. Bone Joint Surg. 60B:57, 1978.)

1. Anderson, K. J., and LeCoco, J. F.: Rupture of the triceps tendon. J. Bone Joint Surg. 39A:444, 1957. 2. Anzel, S. H., Covey, K. W., Weiner, A. D., and Lipscomb, P. R.: Disruption of muscles and tendons: An analysis of 1,014 cases. Surgery 45:406, 1959. 3. Aso, K., and Torisu, T.: Muscle belly tear of the triceps. Am. J. Sports Med. 12:485, 1984. 4. Bauman, G. I.: Rupture of the biceps tendon. J. Bone Joint Surg. 16:966, 1934. 5. Bennett, B. S.: Triceps tendon rupture. J. Bone Joint Surg. 44A:741, 1962. 6. Brickner, W. M., and Milch, H.: Ruptures of muscles and tendons. Int. Clin. 2:94, 1928. 7. Celli, A., Arash, A., Adams, R. A., and Morrey, B. F.: Triceps insufficiency following total elbow arthroplasty. J. Bone Joint Surg. 87A:1957, 1964. 8. Childress, H. M.: Recurrent ulnar nerve dislocation at the elbow. Clin. Orthop. Relat. Res. 1:168, 1975. 9. Cirincione, R. J., and Baker, B. E.: Tendon ruptures with secondary hyperparathyroidism. A case report. J. Bone Joint Surg. 57A:852, 1975. 10. Clayton, M. L., and Thirupathi, R. G.: Rupture of the triceps tendon with olecranon bursitis: A case report with a new method of repair. Clin. Orthop. Rel. Res. 184:183, 1984. 11. Debeyre, J.: Desinsertion du tendon inferieur du biceps brachial. Mem. Acad. Chir. 74:339, 1948. 12. Dreyfuss, U.: Snapping elbow due to dislocation of the medial head of the triceps. J. Bone Joint Surg. 60B:57, 1978. 13. Duchow, J., Kelm, J., and Kohn, D.: Acute ulnar nerve compression syndrome in a powerlifter with triceps tendon rupture—a case report. Int. J. Sports Med. 21:308, 2000. 14. Farrar, E. L., III, and Lippert, F. G., III: Avulsion of the triceps tendon. Clin. Orthop. Relat. Res. 161:242, 1981. 15. Fery, A., Sommelet, J., Schmitt, D., and Lipp, B.: Avulsion bilaterale simultanée des tendons quadricipital et rotulien et rupture du tendon tricipital chez un hemodialyse hyperparathyroidien. Rev. Chir. Orthop. 64:175, 1978. 16. Fritz, R. C., and Steinbach, L. S.: Magnetic resonance imaging of the musculoskeletal system. Part 3. The elbow. Clin. Orthop. 324:321, 1996. 17. Gerard, F., Marion, A., Garbuio, P., and Tropet, Y.: Distal traumatic avulsion of the triceps brachii. Apropos of a treated case. Chir. Main 17:321, 1998 18. Gilcreest, E. L.: Rupture of muscles and tendons. J. A. M. A. 84:1819, 1925. 19. Herrick, R. T., and Herrick, S.: Ruptured triceps in a powerlifter presenting as cubital tunnel syndrome: A case report. Am. J. Sports Med. 15:514, 1987. 20. Hughes, R. E., Schneeberger, A. G., An, K.-N., Morrey, B. F., and O’Driscoll, S. W.: Reduction of triceps muscle force after shortening of the distal humerus. A computational model. J. Shoulder Elbow Surg. 6:444, 1997. 21. Inhofe, P. D., and Moneim, M. S.: Late presentation of triceps rupture: A case report and review of the literature. Am. J. Orthop. 25:790, 1996. 22. Lee, M. L. H.: Rupture of triceps tendon. Br. Med. J. 2:197, 1960.

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23. Levy, M., Fishel, R. E., and Stern, G. M.: Triceps tendon avulsion with or without fracture of the radial head: A rare injury? J. Trauma 18:677, 1978. 24. Louis, D. S., and Peck, D.: Triceps avulsion fracture in a weightlifter. Orthopedics 15:207, 1992. 25. Match, R. M., and Corrylos, E. V.: Bilateral avulsion fracture of the triceps tendon insertion from skiing with osteogenesis imperfecta tarda. Am. J. Sports Med. 11:99, 1983. 26. Maydl, K.: Ueber subcutane Muskel und Sehnenzerreissungen, sowie Rissfracturen mit Berucksichtigung der Analogen, durch directe Gewalt enstandenen und offenen Verletzungen. Deut. Zschr. Chir. 17:306, 1882, 18:135, 1883. 27. McMaster, P. E.: Tendon and muscle ruptures: clinical and experimental studies on causes and locations of subcutaneous ruptures. J. Bone Joint Surg. 15:705, 1933. 28. Montgomery, A. H.: Two cases of muscle injury. Surg. Clin. Chic. 4:871, 1920. 29. Murphy, K. J., and McPhee, I.: Tears of major tendons in chronic acidosis with elastosis. J. Bone Joint Surg. 47A:1253, 1965. 30. O’Driscoll, S. W.: Intramuscular triceps rupture. Can. J. Surg. 35:203, 1992. 31. O’Reilly, K., Worhal, M., Meredith, C., et al.: Immediate and delayed ultrastructural changes in skeletal muscle following eccentric exercise. Med. Sci. Sports Exerc. 18(Suppl):S42, 1986. 32. Pantazopoulos, T., Exarchou, E., Stavrou, Z., and Hartofilakidis-Garofalidis, G.: Avulsion of the triceps tendon. J. Trauma 15:827, 1975. 33. Penhallow, D. P.: Report of a case of ruptured triceps due to direct violence. N.Y. Med. J. 91:76-77, 1910. 34. Popovic, N., Ferrara, M. A., Daenen, B., Georis, P., and Lemaire, R.: Imaging overuse injury of the elbow in professional team handball players: a bilateral comparison using

35.

36. 37.

38.

39.

40.

41. 42.

43. 44.

45.

plain films, stress radiography, ultrasound, and magnetic resonance imaging. Int. J. Sports Med. 22:60, 2001. Preston, F. S., and Adicoff, A.: Hyperparathyroidism with avulsion at three major tendons. N. Engl. J. Med. 266:968, 1961. Rolfsen, L.: Snapping triceps tendon with ulnar neuritis. Acta Orthop. Scand 41:74, 1970. Sanchez-Sotelo, J., and Morrey, B. F.: Surgical techniques for reconstruction of chronic insufficiency of the triceps— rotation flap using anconeus and tendo Achilles allograft. J. Bone Joint Surg. 84B:1116, 2002. Schutt, R. C., Powell, R. L., and Winter, W. G.: Spontaneous ruptures of large tendons. American Academy of Orthopedic Surgeons Annual Meeting, New Orleans, January 25, 1982. Sherman, O. H., Snyder, S. J., and Fox, J. M.: Triceps tendon avulsion in a professional body builder: A case report. Am. J. Sports Med. 12:328, 1984. Spinner, R. J., and Goldner, R. D.: Snapping of the medial head of the triceps and recurrent dislocation of the ulnar nerve. J. Bone Joint Surg. 80A:239, 1998. Tarsney, F. F.: Rupture and avulsion of the triceps. Clin. Orthop. Relat. Res. 83:177, 1972. van Riet, R. P., Morrey, B. F., Ho, E., and O’Driscoll, S. W.: Surgical treatment of distal triceps ruptures. J. Bone Joint Surg. 85A:1961, 2003. Viegas, S. F.: Avulsion of the triceps tendon. Orthop. Rev. 19:533, 1990. Wagner J. R., and Cooney, W. P.: Rupture of the triceps muscle at the musculotendinous junction: a case report. J. Hand Surg. 22A:341, 1997. Wener, J. A., and Schein, A. J.: Simultaneous bilateral rupture of the patella tendon and quadriceps expansions in systemic lupus erythematosus: a case report. J. Bone Joint Surg. 56A:823, 1974.

Chapter 36 Soft Tissue Coverage of the Elbow

CHAPTER

36

Soft Tissue Coverage of the Elbow Nho V. Tran, Allen T. Bishop, and Steven L. Moran

INTRODUCTION Difficult-to-manage soft tissue defects about the elbow occur as a result of trauma, infection, extravasation of chemotherapeutic agents, cutaneous ulceration or necrosis, and limb-sparing tumor surgery. Treatment options are many, and appropriate management requires careful consideration of all alternatives. Coverage choices may include primary closure, skin grafting, local cutaneous flaps, fasciocutaneous transposition flaps, island fascial or fasciocutaneous flaps, local or distant one-stage muscle or myocutaneous transposition, distant temporary pedicle flaps, and microvascular free tissue transfer. Historically, the reconstructive algorithm for providing elbow coverage has proceeded in a stepladder fashion, with the simplest procedures being used first to obtain coverage; however, with advancements in microsurgical techniques, the reconstructive ladder is often disregarded in preference for the surgical procedure, which provides the patient with the best form and function.

PATIENT ASSESSMENT THE PATIENT In the acute traumatic situation associated lifethreatening injuries must be managed before proceeding with the wound reconstruction. Acute wounds should be thoroughly débrided of all necrotic tissue. If possible, risk factors for flap failure should be minimized before embarking on any reconstructive procedure. Lifethreatening injuries or other medical illness may preclude immediate lengthy complex reconstruction. Extensive crushed injury and prior surgical scars may exclude many local flap options. A thorough assessment of the extremities vascular status should be performed before flap reconstruction. A hand-held Doppler device is useful in planning axial flaps in such cases. Systemic factors such as steroid use, hypoalbuminemia, and diabetes may all negatively affect the body’s

547

potential to heal large wounds; in elective cases, such factors should be medically controlled before surgery. Patients ideally should cease smoking 1 month before surgical reconstruction.

THE WOUND Most soft tissue defects benefit from early coverage. Advantages of expeditious closure include diminished edema, lower rates of wound infection, decreased scar formation and wound contraction, less pain, and enhanced upper limb function.65,69,106,110 Traumatic defects require thorough débridement and irrigation but often may be closed within 24 hours of injury, with salutary results.31,65 In contrast, complex wounds resulting from high-energy injury (electrical burns, crush, avulsion) and grossly contaminated wounds may require serial débridements and a delay to allow adequate assessment of tissue viability. Open packing, temporary coverage with biologic dressings or use of negative pressure therapy devices (vacuum-assisted closure [VAC]) may be required during this phase of management. VAC therapy has become an important adjunct in the management of major soft tissue injuries over the last 10 years. VAC therapy (V.A.C., KCI, San Antonio, TX) uses a polyurethane ether foam with a pore size of 400 to 600 μm, which is cut to size and applied to the wound with a transparent dressing to create an airtight seal. Controlled intermittent or continuous topical negative pressure is then delivered to the wound by incorporating a tube into the seal, and this is provided by a dedicated vacuum pump appliance. Exudate, edema, and bacterial load is reduced and the growth of granulation tissue is encouraged, and these properties make it a useful tool in any algorithm for soft tissue reconstruction because it has the potential to convert a difficult wound into one that may be closed or covered with a simpler technique. Its use is particularly important in two scenarios—when systemic comorbidity precludes a major lengthy reconstructive procedure; and when local wound factors, such as heavy contamination, necessitate multiple wound débridements before the definitive wound closure.3 In these situations, VAC therapy is not usually a substitute for surgery, but it offers a bridge until definitive surgery can proceed safely11 (Fig. 36-1). After appropriate débridement, the size, depth, and location of the defect are determined. Tissue loss may not be limited to skin, and appropriate reconstruction of vessels, nerves, musculotendinous units, and bone and joint may be necessary, either primarily or later. A bed containing exposed vital structures, internal fixation devices, or tissues too poorly vascularized to accept skin grafting must be covered with a flap.

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Part V Adult Trauma

B

A

C FIGURE 36-1

A to C, A patient presented with a rapidly spreading soft tissue infection of the elbow, developing from a chronic elbow bursitis. The wound was radiacally débrided (A) and then temporized with the application of a wound VAC sponge (B and C) until it was safe to proceed with definitive wound closure.

RECONSTRUCTIVE METHODS Reconstructive goals are to obtain optimal wound healing, restore function, and maximize aesthetic outcome, which should always be considered. Historically, the simplest method that provides adequate coverage and meets reconstructive needs is chosen. Thus, tension-free closure of an elbow defect by skin elevation and advancement is often performed. If tension-free closure is not possible, skin grafting can be considered for selected defects with well-vascularized tissue beds. Otherwise, the location, size, and tissue composition of a defect all in part dictate selection of an appropriate flap. Local flaps provide the best tissue match but are limited in size and can devascularize or weaken an already damaged limb. Larger defects and those that require composite tissues for primary reconstruction of tendon, muscle, bone, or sensibility demand consideration of other methods, including local island fasciocutaneous flaps, local or distant pedicle muscle,

myocutaneous transfer, and free tissue transfer. An algorithm for tissue coverage is useful in preoperative planning (Fig. 36-2).

SKIN GRAFTING Indications Skin grafting may be indicated for any defects with an acceptable bed. Exposed structures that will accept a graft include subcutaneous tissue, paratenon, and muscle. Other tissues, such as exposed bone, joint, tendon, and nerve, may be covered temporarily by graft used as a biologic dressing but will not support a graft for permanent coverage. Beds containing tissues of questionable viability, chronic granulation tissue, or frank infection must be appropriately débrided. Bacterial contamination, accumulation of serum, and a small amount of capillary bleeding are not contraindications for grafting. Tidy wounds that contain fewer than 105 bacteria per gram of tissue or that allow xenograft adherence

Chapter 36 Soft Tissue Coverage of the Elbow

Yes

Adequate bed

Yes

Tidy wound

No

No

549

Débride

Exposed vital structures

No

Local tissue available

Yes

Large defect

No

Yes

No

Yes

Skin graft

Local skin flaps Fasciocutaneous flap Local muscle or myocutaneous flap Fasciocutaneous island flap

within 24 hours allow successful skin grafting.27,52,61,93,107 Skin grafts are contraindicated in areas that are exposed to repetitive trauma or that lie over osseous prominences. In addition, skin grafting should be avoided in areas that may require secondary surgery for bone or nerve grafting. All split-thickness grafts will undergo some component of contracture over time; thus, if these grafts are placed over large areas of the antecubital fossa or olecranon, there is a risk of limitation in elbow motion. To improve durability, a collagen-glycoaminoglycan biodegradable matrix (Integra, Plainboro, NJ) can be grafted first to create a neo-dermis, then a splitthickness skin graft can be applied subsequently to improve durability of the graft.18

Technique Small defects in areas where wound contracture is undesirable may be optimally covered with a full-thickness graft harvested from the inguinal crease. The thin, lax skin in this area provides excellent graft material and allows closure of the donor site with an inconspicuous linear scar. Split-thickness grafts that are harvested with a power-driven dermatome are used to cover larger areas. Any area may be used as a donor site; usually the proximal thigh is chosen because of its relatively flat contour and generally concealed location. The thickness of such grafts can range from 0.012 to 0.015 inch. Older adults and children with thin dermis should receive

Latissimus dorsi Other pedicle flap Free tissue transfer

FIGURE 36-2

An algorithm for managing soft tissue defects about the elbow.

0.012-inch thick graft to avoid full thick skin loss at donor site. A meshed graft allows expansion and is indicated for large or draining defects. The donor site is dressed with a plastic vapor-permeable dressing or fine mesh gauze, and exudate is removed from beneath the donor site with a syringe, as needed, or the gauze is dried with a heat lamp.45,96 The graft is secured with chromic sutures or stables and covered with Xeroform or some other form of nonadherent occlusive dressing. Immobilization of the graft during the early stages of healing is essential for complete graft survival and may be accomplished with either the use of a bolster or a VAC sponge. A cotton bolster may be created with gauze and saline-soaked cotton balls. Nylon sutures secured to the margin of the graft are tied over the cotton, firmly compressing the skin to its bed. The elbow is immobilized, and the graft is left undisturbed for 5 to 7 days. If VAC therapy is to be used to promote graft adherence the sponge is set to provide 75 mm Hg of constant suction for 5 days. This method has been shown to significantly improve skin grafting survival in a recent prospective randomized study.81

LOCAL FLAPS Random Cutaneous Flaps Often, small defects unsuitable for grafting may be covered by skin immediately adjacent to the primary

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Part V Adult Trauma

defect. Such random cutaneous flaps carry their own blood supply through the dermal and subdermal plexuses and occasionally through a specific cutaneous artery oriented in the axis of the flap (axial flap). In general, random flap should be designed with a 1 : 1 length-width ratio. Such flaps are further categorized according to motion applied to the flap as it covers the defect; these flaps include transposition or translation flaps, advancement flaps, and rotation flaps.63 Transposition flaps are raised and moved laterally to an adjacent area, and the primary defect is closed by triangulating the defect and closing one angle of the triangle. The flap is then drawn as a parallelogram and raised (Fig. 36-3). Its pivot axis or critical line may be extended by lengthening or widening the flap or extending the cut parallel to the defect side (extension cut) or toward the defect (back cut).63 Closure of the secondary defect generally

requires skin grafting. Other examples of transposition flaps include Z-plasties and rhomboid flaps (i.e., in the shape of an equilateral parallelogram). Rhomboid flaps are occasionally useful about the elbow when the defect may be excised or débrided to a rhomboid shape. A rhombus with 60- and 120-degree angles, the Limberg flap, is optimal, but other angles may be accommodated using Dufourmental’s method (Fig. 36-4).64 Such single rhomboid flaps have the disadvantages of creating tension at the flap tips and at the line of donor site closure, anatomic landmark displacement, and occasionally, cause difficulty in orientation for optimal scar appearance. A double-Z rhomboid may be a superior alternative for some defects (Fig. 36-5).21 Orientation of the long axis of the rhomboid to the relaxed skin tension line produces the least tension and “maximal cosmesis.”

Axial Fasciocutaneous Flaps Z

X

W

V pivot point

Y

FIGURE 36-3

Drawing of a theoretical skin defect (XYZ) that has equal sides. A transposition flap is designed on side XY, this being the common border between the transposition flap and the defect it is to cover. XW is an extension of ZX and is equal in length, although it need not be unless local conditions so dictate. WV is drawn parallel to XY and equal in length. Thus, V becomes the pivot point around which the equilateral parallelogram flap XYWV will rotate to move into the defect XYZ. Therefore, the distance from V to X and its ability to stretch to reach the line VZ is critical and is called the critical line. (From Lister, G.: The theory of the transposition flap and its practical application in the hand. Clin. Plast. Surg. 8:115, 1981.)

The above-mentioned random flaps are limited in their ability to cover large defects due to a poor random blood supply, limited mobility, and inadequate local skin elasticity. In contrast, the axial flap by inclusion of a known axial blood supply can allow safe extension of the length and narrowing of the base to improve coverage.79 The blood supply to the skin of the upper extremity was studied by Manchot71 more than a century ago and most recently by Le Huec and Liquois,59 by Salmon93a and Lamberty,56 and by others.94 A predictable pattern of cutaneous angiosomes exists that can be used in planning local flaps (Fig. 36-6). Blood from the named vessels supplying each of these regions may enter the skin from direct cutaneous vessels, musculocutaneous perforators, or fasciocutaneous vessels.19 These vessels form a plexus both subdermally and in deep fascia.108 Although forearm and elbow transposition flaps containing only subcu-taneous tissue have been reported by Marty and colleagues, inclusion of deep fascia in transposition flaps improves viability.19,29,74,76 The blood

RSTL

a

FIGURE 36-4

b

b

RSTL

a

A single rhomboid flap oriented to minimize skin tension on closure with the long diagonal side of the flap parallel with the relaxed skin tension lines (RSTL). (From Cuono, C. B.: Double Z-plasty repair of large and small rhombic defects: the double-Z rhomboid. Plast. Reconstr. Surg. 71:658, 1983.)

Chapter 36 Soft Tissue Coverage of the Elbow

551

FIGURE 36-5

A double-Z rhomboid flap. The short axis of the defect, all of its sides, and each limb of both Z-plasties are of equal length. Limbs ADE and CBG of the flaps that will resurface the rhomboid defect along its long axis AC are each twice the length of one side of the defect and are mathematically 15% longer than the longer axis AC. (From Cuono, C. B.: Double Z-plasty repair of large and small rhombic defects: the double-Z rhomboid. Plast. Reconstr. Surg. 71:658, 1983.)

7 6 3

2

4 1 3 5

1

TERRITORIES 1 Ulnar artery 2 Median artery 3 Radial artery 4 Posterior interosseous 5 Anterior interosseous 6 Elbow anastomosis 7 Brachial artery

FIGURE 36-6

A reproduction of Manchot’s original diagrams of the forearm angiotomes. (From Lamberty, B. G. H., and Cormack, G. C.: The forearm angiotomes. Br. J. Plast. Surg. 35:420, 1982.)

supply to these areas of skin may come from multiple fasciocutaneous perforators, a single consistent and sizable pedicle, or multiple small branches from an underlying large vessel, the most dominant of which is the superior ulnar collateral artery.59 Fasciocutaneous transposition flaps may be raised from the medial arm based on the medial elbow anastomotic vessels (superior ulnar collateral artery and ulnar recurrent vessels), the lateral arm based on the terminal branches of the profunda brachii and their recurrent interosseous artery anastomoses, as well as forearm fasciocutaneous perforators from radial, ulnar, and anterior and posterior interosseous arteries.50,56,74,99 These perforators, arranged in four parallel rows, enter the forearm skin at regular intervals (Fig. 36-7).74 An example of such a flap is shown in Figure 36-8, based on the posterior interosseous vessels and lateral elbow anastomotic blood vessels. Of all available forearm fasciocutaneous arteries, Lamberty and Cormack found that only the inferior cubital cutaneous artery, a branch

FIGURE 36-7

Location of cutaneous perforating vessels to the forearm. (From Marty, F. M., Montandon, D., Gumener R., and Zbrodowski, A.: The use of subcutaneous tissue flaps in the repair of soft tissue defects of the forearm and hand: an experimental and clinical study of a new technique. Br. J. Plast. Surg. 37:95, 1984.)

of the radial recurrent artery, was sufficiently large and constant to reliably supply a large cutaneous area (most of the territory attributed to the median artery by Manchot) (see Fig. 36-6).56,57 Coverage of the olecranon is achieved reliably and easily with this tissue technique. In case of extensive trauma or reoperative surgery, it is advisable to use a hand-held Doppler device to confirm

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Part V Adult Trauma

FIGURE 36-8

Coverage of an olecranon area defect secondary to olecranon bursitis and mixed connective tissue disease with a lateral forearm fasciocutaneous flap. The donor site is covered by a meshed split-thickness skin graft. A, The flap outlined. B, The flap raised. C, The transposed flap immediately after completion of the flap. D, Final result. (Courtesy of N. B. Meland, M.D.)

the presence and extent of the vascular pedicle before raising the flap. Island flaps are the ultimate application of fasciocutaneous axial transposition flaps. Several upper extremity island flaps have been described in the past decade for use in orthograde or retrograde pedicle transposition or free tissue transfers. Island flaps are raised with a base consisting solely of a fully mobilized vascular pedicle, and they may include fascia, subcutaneous tissue, skin, and segments of vascularized muscle, bone, tendon, and cutaneous nerves, depending on the particular reconstructive needs. Some flaps used for elbow coverage are orthograde antecubital fasciocutaneous flap, radial forearm, ulnar forearm, and posterior interosseous flaps and retrograde medial and lateral arm flaps.* Their orthograde axial vascular pedicle allows the widest possible arc of rotation and present relatively little risk of circulatory embarrassment. Coverage of small and

*See references 12, 20, 24, 26, 35, 37, 41, 47, 48, 50, 51, 62, 66, 77, 82, 83, 87, 98-100, 104-106.

moderate defects on all surfaces of the elbow is possible without microvascular anastomoses and upper extremity mobilization.37

Antecubital Fasciocutaneous Flap Described by Lamberty and Cormack,56,57 the antecubital fasciocutaneous flap is an axial-pattern, fasciocutaneous flap based on the inferior cubital artery. This vessel usually arises from the radial recurrent artery (17.5%) or from the radial artery proper (62.5%) and lies in the intermuscular septum between brachioradialis and flexor carpi radialis.70 It runs distally, paralleling the course of the cephalic vein in the superficial fascia. The vessels origin is 4 cm inferior to the midportion of the anterior interepicondylar line (Fig. 36-9). Venous drainage is provided principally by the cephalic vein.57 A 4 : 1 length-width-ratio flap may safely be raised. Technique The vessel may be identified preoperatively with a handheld Doppler probe. The vessels origin is approximately 2 to 5 cm (average 4 cm) below the interepicondylar line running parallel to the course of

Chapter 36 Soft Tissue Coverage of the Elbow

LATERAL

MEDIAL

Inter-epicondylar line 4 cm Site of origin of inferior cubital artery

Cephalic vein

FIGURE 36-9

The distribution of the inferior cubital artery. (From Lamberty, B. G. H., and Cormack, G. C.: The forearm angiotomes. Br. J. Plast. Surg. 35:420, 1982.)

the radial artery. Flap dissection begins at the distal medial margin of the flap. The deep fascia is identified and then elevated, and includes the intermuscular septum between brachioradialis and the flexor carpi radialis of the forearm. Proximally, the inferior cubital artery is identified as it passes through this septum and then is protected. The flap must include the proximal cephalic vein for outflow, while its distal counterpart is ligated and divided. Sensory innervation to the flap is provided through the lateral antebrachial cutaneous nerve. The flap may be formed into an island flap by isolating the inferior cubital artery and cephalic vein. Its length and relatively narrow base allow it to be rotated to cover many elbow area defects.

Radial Forearm Island Flap The cutaneous territory nourished by the radial artery includes the radial two thirds of the anterior forearm and its lateral aspect.56 A fasciocutaneous flap based on an orthograde (proximal) pedicle provides excellent elbow coverage of moderate-sized defects, including the posterior aspect of the region.2,24,28,35,63 Approximately 9 to 17 cutaneous perforators from the radial artery supply the skin, including musculocutaneous vessels proximally and fasciocutaneous vessels distally by means of a deep prefascial plexus and a subdermal plexus.105 Its chief

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advantages are its reliability, technical simplicity, and versatility, the results of its being a compound flap including fascia only, composite skin and fascia, vascularized brachioradialis, flexor carpi radialis, or palmaris longus tendon segment of the distal radius and its sensibility with lateral and medial antebrachial cutaneous nerves.26,37,82 Its arc of rotation allows coverage of all aspects of the elbow joint but is limited proximally by its point of rotation at the radial artery origin 10 cm below the elbow joint.105 The principal drawback of this method is the unsightly donor site, which requires splitthickness skin grafting unless a small area or fascia only is used.47 Although the size of the radial cutaneous territory may be as large as 15 by 25 cm, flaps generally no larger than 16 by 8 cm (usually smaller) are considered for elbow defects that measure 6 to 8 by 14 to 6 cm.24,26,56,104 A complete deep palmar arch is necessary for adequate perfusion of the hand by the ulnar and, occasionally, median arteries. Other complications following radial forearm flap elevation can include decrease in radial nerve sensation, delayed healing at the skin graft site, decreased range of motion, and fractures of the radius following osteocutaneous flap elevation. Richardson found in a series of 100 patients that 13% experienced exposed tendons, 19% had delayed healing over the donor site and 32% had decrease sensation in the radial nerve distribution.91 Raising the flap with a portion of the radius has been associated with a high incidence of postoperative fractures.9,102,106 Attempts at limiting donor site morbidity have included modifications in flap elevation. The flap may be elevated as a pure facial flap, allowing for primary closure of the donor site.47,89 The flap may also be elevated suprafacially; this allows for fewer donor site complications with enhancement of skin graft take and elimination of tendon exposure.5,15,68 Further improvement to the donor site may be made by placing tissue expands before or following flap transfer to help with primary closure of the donor site.34,36,75 Also ulnar-based skin islands have been used to close the donor site.7,49 Despite donor site complications, the radial forearm flap has remained a workhorse flap for elbow coverage. Technique The course of the radial artery is marked with the help of a Doppler ultrasound probe, and a timed Allen’s test is performed to verify adequate distal circulation with the radial artery occluded. The donor skin area is outlined somewhat larger than the defect and as distal as possible to create a pedicle long enough to reach the elbow defect. It is centered over the radial artery and may include the cephalic vein. The flap is then raised from distal to proximal, protecting the superficial radial nerve distally but including the proximal cephalic vein and lateral antebrachial cutaneous nerve;

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this allows for the creation of a sensate flap. The margins are incised, including the antebrachial fascia. Distally, the radial artery is ligated and the flap, including the lateral intermuscular septum, radial vessels, and fasciocutaneous perforators, is raised as a proximally based island flap transposed to cover the elbow (see Fig. 36-9). Closure of the donor site requires split-thickness skin grafting (Fig. 36-10). Incomplete graft “take” is a common complication, but the risk may be minimized by preserving paratenon over distal tendons and by immobilizing the wrist and digits for several days after surgery.77,106 Further improvement in graft take may be accomplished by mobilization of the superficialis muscle belly over any component of exposed flexor carpi radialis tendon. We use a nonmeshed graft to improve donor site cosmesis.

Retrograde Lateral Arm Flap The lateral arm flaps described by Katsaros and colleagues have been widely used for upper limb reconstruction as a free flap transfer based on its fasciocutaneous supply by means of a terminal branch of the profunda brachii artery, the posterior radial circumflex artery.51 This vessel contributes to the anastomotic blood supply of the elbow through the interosseous recurrent artery. Culbertson and Mutimer have described a retrograde island flap based on this distal circulation with reverseflow venous drainage through venae comitantes in a

fashion analogous to the reverse radial forearm flap (Fig. 36-11).20,62,82 It should be noted that any retrograde island flap may be prone to the development of venous congestion due to inadequate venous outflow. Venous congestion in such cases may require additional microvascular venous anastomosis to prevent partial flap failure.17 The flap may include fascia only, skin up to 8 to 10 cm as well as sensation by neurotization of the posterior brachial cutaneous nerve, triceps tendon, or even a segment of vascularized humerus.51 Recently Kuek and Lanzetta and their respective colleagues revealed that local circulation supports greater distance to the forearm than had been previously described.53,58 This allows a broader indication than previously reported. As a retrograde flap, it covers all surfaces of the elbow and is indicated for burn cicatrix, olecranon area defects secondary to pressure sores, excision of rheumatoid nodules or bursitis, and local skin loss of other causes, provided that the anastomotic circulation is not disturbed. From measurements of the defects in flexion and extension a more accurate estimate of posterior coverage can be made.109 It has the significant advantages of a minimal donor site problem (if donor defect can be closed primarily) and no need to sacrifice a major vessel, which are two problems associated with the radial forearm flap. Yet, one recent study of almost 100 procedures reported concerns for appearance in 27% of patients and

FIGURE 36-10 Coverage of a posterior defect secondary to chronic olecranon bursitis with an orthograde radial forearm flap. Earlier, a brachioradialis flap had failed to cover the defect. A, The donor site with skin graft. B, The flap in place over the olecranon. (Courtesy of M. B. Wood, M.D.)

Chapter 36 Soft Tissue Coverage of the Elbow

555

FIGURE 36-11 Design of a reverse lateral arm flap for elbow coverage. (From Culbertson, J. H., and Mutimer, K.: The reverse lateral upper arm flap for elbow coverage. Ann. Plast. Surg. 18:62, 1987.)

paresthesias in 59%, and the investigators recommended the procedures only for men.33 Technique The axis of the flap is a line from the deltoid insertion to the lateral humeral epicondyle. The course of the posterior radial circumflex artery is located with a Doppler ultrasound probe, and a flap of sufficient size and pedicle length to allow transposition to the elbow is outlined. The flap is elevated from the proximal to the distal aspect, including the biceps and triceps fascia and the lateral intermuscular septum. The vessels are identified and divided proximally and are included with the flap as a distally based pedicle. The flap is then rotated into the recipient site.

Other Fasciocutaneous Flaps From least to most reliable option, the medial arm, posterior interosseous and ulnar forearm flaps also may be used for elbow coverage. The medial arm flap is not used often as a free flap because of its variable cutaneous blood supply through unnamed cutaneous arteries and biceps myocutaneous branches from the brachial artery. The anastomoses these vessels form with the superior ulnar collateral artery are various and not uniform.51,99 Its theoretical potential as a fasciocutaneous transposition flap for elbow coverage has been based on this anastomotic connection, but no clinical cases have been reported.50 The posterior interosseous flap described by Zancolli and Angrigiani in 1986, has been used primarily as a retrograde flap for hand coverage.12,87,112 It also may be used reliably as an orthograde fasciocutaneous flap

FIGURE 36-12

An orthograde posterior interosseous flap for elbow coverage. (From Penteado, C. V., Masquelet, A. C., and Chevrel, J. P.: The anatomic basis of the fasciocutaneous flap of the posterior interosseous artery. Surg. Radiol. Anat. 8:209, 1986.)

based on some of the 7 to 14 fasciocutaneous perforators that arise from the posterior interosseous artery. These vessels run in the interval between the extensor carpi ulnaris and the extensor digiti minimi. The pivot of the flap is the point of emergence of the artery in the posterior forearm at the junction of the proximal and middle thirds of forearm, and the axis lies on a line drawn from the lateral humeral epicondyle to the ulnar head. A flap outlined in the distal third of the forearm will reach the antecubital fossa and olecranon (Fig. 36-12).87 An orthograde ulnar artery forearm flap also may cover the elbow, and it offers the potential for sensibility

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and composite tissue inclusion.66 Its drawbacks are similar to those of the radial forearm flap, and it is seldom indicated.

PEDICLE MUSCLE FLAPS For coverage about the elbow, a number of muscle flaps have been reported, including flexor digitorum superficialis, extensor carpi radialis longus, extensor carpi ulnaris, anconeus, brachioradialis, and latissimus dorsi.10,13,29,41,54,76,84 Indications for muscle rotation to cover a cutaneous defect include infection, dead space that must be filled, and loss of motor function (restored by functional muscle transfer). Muscle flaps have been shown to diminish the bacteria count and to survive better than skin flaps when placed over infected wounds.16 They are preferred in cases of infection. Their bulk is useful to fill defects. In addition, elbow flexion and extension and digit flexion have been restored by pedicled latissimus dorsi transfer.6,42,93,97,101,105,113 Because of significant functional loss with many of the aforementioned muscles or limited coverage secondary to small size and limited arc of rotation, only brachioradialis, anconeus, and latissimus dorsi transfers are used frequently about the elbow.10,41

Anconeus The anconeus muscle was first used for coverage in the elbow region by Cardany et al.14 in 1981. The technique of transfer and vascular anatomy were further delineated by Mathes and Nahai 73 and Parry et al.86 in 1982 and 1988. The muscles size (4 × 8 cm) limits its use to small posterior defects over the radiocapitellar joint, the distal triceps tendon, and the olecranon.95 The anconeus only aids in the terminal 15 degrees of elbow extension and forearm supination and its sacrifice has not been shown to produce any decreased range of motion or strength.95 It receives its major blood supply via the recurrent posterior interosseus and medial collateral arteries43,86,95 (Fig. 36-13A). The medial collateral artery, a branch of the profunda brachii, enters proximally, underneath the muscle and allows an easy and expeditious transposition or rotation of a proximally based flap over the defect (see Fig. 36-13B). Thus, it has the potential of being harvested under regional blockade in patients who cannot support a lengthy procedure under general anesthesia (Fig. 36-13C and D).

Extensor Carpi Radialis Longus The ease of harvest and the extensive arc of rotation have made the extensor carpi radialis longus popular for limited coverage of the anterior aspect of the elbow.46 The minimal functional deficiency and ease of rotation are attractive for limited defects.

Brachioradialis The brachioradialis is an expandable elbow flexor that arises from the upper two thirds of the lateral supracondylar ridge of the humerus and the anterior aspect of the lateral intermuscular septum. The muscle belly extends to the midforearm and ends in a broad, flat tendon that inserts at the radial styloid process. The blood supply to the muscle comes from several arterial pedicles.55 A consistent vascular anatomy includes a major pedicle found near the elbow joint.92 Its major pedicle arises from the radial recurrent artery located between brachioradialis and brachialis muscles, with additional smaller vessels from the radial artery (Fig. 36-14).54 The skin overlying the muscle belly in the distal arm and the proximal forearm may be included. This flap was first described by Lendrum60 and its relevant anatomy by Lai and colleagues.54 It is indicated for small defects in the antecubital and the lateral aspects of the elbow. It will not reach medially and will not reliably cover the olecranon or the posterior soft tissue. Technique The muscle is exposed through a longitudinal anterolateral forearm incision, including overlying skin if the surgeon desires. The tendon of insertion is divided, and the muscle is freed working from proximal to distal until the main pedicle from the radial recurrent vessel is reached. Several secondary pedicles are divided during the exposure. If needed, its origin may also be released to allow full rotation of the muscle about its major pedicle (Fig. 36-15).

Latissimus Dorsi Myocutaneous Pedicle Flap The latissimus dorsi flap, along with the radial forearm flap, are the predominant workhorse flaps for coverage of large defects in the arm and elbow.15 The latissimus dorsi muscle is a broad, fan-shaped muscle with a single dominant thoracodorsal arterial pedicle in the axilla. The muscle originates from the lower six thoracic and lumbar vertebrae, the lower four ribs, and the posterior ilium, and ends in a broad tendon that inserts into the intertubercular groove of the humerus (Fig. 36-16).10 The entire muscle or its anterior half may be rotated on a posterior axillary axis point and tunneled into the arm. Fully mobilized, it extends well into the midforearm and covers all aspects of the elbow.69 A large skin paddle (up to 12 by 35 cm) may be included with primary closure of the recipient site (Fig. 36-17).76 Its use in an elbow flexorplasty or tricepsplasty is beyond the scope of this chapter, but simultaneous skin coverage and functioning muscle transfer occasionally is desirable.88 We have found this to be a major asset in certain instances. Its size, large skin paddle, enormous arc of rotation, simplicity, functional potential, and expendability as a

Chapter 36 Soft Tissue Coverage of the Elbow

Deep brachial artery

Anterior radial collateral artery

Posterior radial collateral artery Medial collateral artery

Recurrent posterior interosseus artery

A

C

B

D

FIGURE 36-13 A, The arterial anatomy surrounding the anconeus muscle. The muscle receives the majority of its blood supply from the recurrent posterior interosseous artery (RPIA) and medial collateral artery (MCA), which may be visualized in (B). The flap may be rapidly elevated and pedicled to cover traumatic defects about the olecranon (C to D). (Figure A from Moran, S. L., and Johnson, C. J.: Skin and soft tissue: Pedicled flaps. In Berger, R. A., and Weis, A. P. C. [eds.]: Hand Surgery. Philadelphia, Lippincott, Williams & Wilkins, 2004, p. 1131.)

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Profunda brachii artery

Brachial artery

Anterior descending branch of profunda brachii artery

Radial recurrent artery Muscular branch Ulnar artery Radial artery

FIGURE 36-14 Location of radial recurrent artery and the muscular branch to brachioradialis. (From Lai, M. F., Krishna, B. V., and Pelly, A. D.: The brachioradialis myocutaneous flap. Br. J. Plast. Surg. 34:431, 1981.)

FIGURE 36-16 The anatomy of the latissimus dorsi muscle and vascular pedicle. A, artery. (From Bostwick, J., Nahai, F., Wallace, J. G., and Vasconez, L. D.: Sixty latissimus dorsi flaps. Plast. Reconstr. Surg. 63:31, 1979.)

shoulder extensor, adductor, and internal rotator are its principal virtues.76

FIGURE 36-15

Coverage of an arthrocutaneous fistula after total elbow arthroplasty with a brachioradialis transposition flap. (Courtesy of M. B. Wood, M.D.)

Technique The patient is positioned in the lateral decubitus position, and the involved extremity and ipsilateral hemithorax are prepared and draped from the iliac crest distally to the midline posteriorly and the nipple line anteriorly. The skin incision parallels the anterior border of the muscle several centimeters posterior to it, and a skin paddle is centered over the anterior muscle if needed. The incision is carried directly to muscle fascia and is directed anteriorly to identify the interval between latissimus and serratus anterior. The dissection then proceeds distally, deep to the latissimus from its free anterior edge at its midpoint. The latissimus is thus freed from its caudal and posterior insertions. It is then mobilized proximally at the scapula from the teres major by blunt dissection, and the neurovascular pedicles are identified. A constant branch of the thoracodorsal artery to the serratus anterior is divided, and proximal dissection is continued as required. The entire subscapular artery may be mobilized, if needed, by dividing the circumflex scapular artery in the axilla. The muscle is then rotated into the arm through a subcutaneous tunnel. If necessary, the humeral insertion may

Chapter 36 Soft Tissue Coverage of the Elbow

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FIGURE 36-17 A, Exposed hardware and avulsed ulnar nerve after fixation of a floating elbow injury. B, Coverage was achieved with a myocutaneous latissimus dorsi transposition flap.

be divided for maximal mobility. Meticulous hemostasis is needed to minimize the risk of a seroma, which can be as high as 30%. The incidence of seroma formation at the donor site can be significantly reduced with the use of postoperative drains and internal quilt suturing, which coapt the deep dermis to the remaining underlying muscles.90

Distant Pedicled Flaps For many years, temporary pedicle flaps raised from the chest or abdominal wall were the mainstay for coverage of large elbow defects.18,102 Today, such distant flaps should be reserved for large defects of skin and subcutaneous tissue when a local flap is not available and free flap transfer is not appropriate because of general medical concerns. Their major drawback is the temporary pedicle itself, which demands a two-stage procedure, a prolonged hospital stay, and the need to splint the extremity to the thorax for at least 2 weeks. Joint stiffness and extremity edema may result.24 Flaps appropriate for emergency or salvage elbow coverage include thoracoepigastric flaps (based on internal mammary perforators), lateral thoracic flaps (thoracodorsal or lateral thoracic artery), external oblique fasciocutaneous flaps (myocutaneous perforators), pectoralis major flaps (muscle used as carrier for skin), and proximally based rectus abdominis pedicle flaps (Hartrampf’s flap).1,4,13,23,25,29,39,67,76,94,110 Several donor sites are illustrated in Figure 36-18. The interested reader is referred to the original salvage reference or to the third edition of this book for details.

FREE TISSUE TRANSFER Free flaps are assuming an ever-increasing role in reconstruction of upper extremity defects. The added

Medial arm flap

Deltopectoral flap Lateral thoracic flap

Groin flap

Thoracoepigastric flap

Hypogastric flap

FIGURE 36-18 Several potential temporary pedicle donor sites for upper extremity coverage. (From Gilbert, D. A.: An overview of flaps for hand and forearm reconstruction. Clin. Plast. Surg. 8:129, 1981.)

operative time, need for microvascular anastomoses must be taken into consideration, but elective flap failure rates are now as low as 3% in most major centers.93 In certain circumstances, free tissue transfer is the procedure of choice, provided that the patient’s health, age,

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E

A

B

C

D

FIGURE 36-19 For large defects free tissue transfer often provides the best option for elbow coverage. A, Large soft tissue defect originally presented in Figure 36-1 was covered with the use of a vertical rectus myocutaneous flap harvested from the patients abdomen (B). The use of a composite flap (including both skin and muscle) allowed for muscle coverage of devacularized and infected tissue, while the skin component of the flap will allow for motion across the elbow joint. Anastomosis is performed just distal to the level of the antecubital fossa (C). D and E, Appearance at final insetting.

Chapter 36 Soft Tissue Coverage of the Elbow

and injuries allow surgery and that a skilled microvascular surgical team is available. In many instances, simpler methods are either inappropriate or less desirable.22,40,111 For example, multiple tissue reconstruction may be possible in a single stage with a composite free flap. Distant pedicle flaps are contraindicated in a recipient site with marginal vascularity or when early limb mobilization is important. A local flap may be precluded by an external fixator, and free tissue transfer may be necessary (Fig. 36-19). The choice of a flap is dictated by the size of the defect, the type of tissue required, donor site morbidity, and the surgeon’s preference. Fasciocutaneous flap choices for the elbow include the anterolateral thigh, scapular or parascapular, and lateral arm flaps.8,28,38,40,44,51,80 Muscle is often preferable when dead space infection, or significant risk of infection is present, either with overlying skin or covered by a split-thickness graft. Manktelow and McKee pioneered free neurotized muscle transfers for functional reconstruction in the upper extremity.72 The large variety of potential donor muscles includes latissimus dorsi, serratus anterior, rectus abdominis, gracilis, and triceps.22,32,78,85,103 A composite lateral arm free flap with triceps tendon or triceps muscle has been possible without significant loss of extension strength.32 Vascularized bone is optimally provided with a composite groin flap based on the deep circumflex iliac vessels or a fibular flap including muscle, skin, or both, as needed. End-to-side arterial anastomosis to the brachial artery and end-to-end venorrhaphy to a vena comitante or cephalic vein is preferred for most elbow defects.30

References 1. Abu Dalu, K., Muggia, M., and Schiller, M.: A bipedicled chest wall flap to cover an open elbow joint in a burned infant. Injury 13:292, 1982. 2. Akpuaka, F. C.: The radial recurrent fasciocutaneous flap for coverage of posterior elbow defects. Injury 22:332, 1991. 3. Argenta, L. C., Morykwas, M. J., Marks, M. W., DeFranzo, A. J., Molnar, J. A., and David, L. R.: Vacuum-assisted closure: State of clinic art. Plast. Reconstr. Surg. 117:127S, 2006. 4. Ariyan, S.: The pectoralis major myocutaneous flap. Plast. Reconstr. Surg. 63:73, 1979. 5. Avery, C. M., Pereira, J., and Brown, A. E.: Suprafascial dissection of the radial forearm flap and donor site morbidity. Int. J. Oral. Maxillofac. Surg. 30:37, 2001. 6. Axer, A., Segal, D., and Elkon, A.: Partial transposition of the latissimus dorsi: a new operative technique to restore elbow and finger flexion. J. Bone Joint Surg. 55A:1259, 1973.

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7. Bardsley, A. F., Soutar, D. S., Elliot, D., and Batchelor, A. G.: Reducing morbidity in the radial forearm flap donor site. Plast. Reconstr. Surg. 86:287, 1990. 8. Bartwick, W. J., Goodkind, D. J., and Serafin, D.: The free scapular flap. Plast. Reconstr. Surg. 69:779, 1982. 9. Boorman, J. G., Brown, J. A., and Sykes, P. J.: Morbidity in the forearm flap donor arm. Br. J. Plast. Surg. 40:207, 1987. 10. Bostwick, J., Nahai, F., Wallace, J. G., and Vasconez, L. D.: Sixty latissimus dorsi flaps. Plast. Reconstr. Surg. 63:31, 1979. 11. Braakenburg, A., Obdeijn, M. C., Feitz, R., van Rooij, I. A., van Griethuysen, A. J., and Klinkenbijl, J. H.: The clinical efficacy and cost effectiveness of the vacuumassisted closure technique in the management of acute and chronic wounds: A randomized controlled trial. Plast. Reconstr. Surg. 118:390; discussion 398, 2006. 12. Büchler, U.: Retrograde posterior interosseous flap. J. Hand Surg. 16A:283, 1991. 13. Burstein, F. D., Salomon, J. C., and Stahl, R. S.: Elbow joint salvage with the transverse rectus island flap: a new application. Plast. Reconstr. Surg. 84:492, 1989. 14. Cardany, C., Maxwell, P., and Gilbert, A.: The antecubital forearm flap. New York, Martin Dunitz, 1992. 15. Chang, L. D., and Goldberg, N. H.: Elbow defect coverage with a one-staged, tunneled latissimus dorsi transposition flap. Ann. Plast. Surg. 32:496, 1994. 16. Chang, N., and Mathes, S.: Comparison of the effect of bacterial inoculation in musculocutaneous and random pattern flaps. Plast. Reconstr. Surg. 70:1, 1982. 17. Chen, H. C., Cheng, M. H., Schneeberger, A. G., Cheng, T. J., Wei, F. C., and Tang, Y. B.: Posterior interosseous flap and its variations for coverage of hand wounds. J. Trauma 45:570, 1998. 18. Chou, T. D., Chen, S. L., Lee, T. W., Chen, S. G., Cheng, T. Y., Lee, C. H., Chen, T. M., and Wang, H. J.: Reconstruction of burn scar of the upper extremities with artificial skin [see comment]. Plast. Reconstr. Surg. 108:378: discussion 385, 2001. 19. Cormack, G. C., and Lamberty, B. G. H.: A classification of fasciocutaneous flaps according to their patterns of vascularization. Br. J. Plast. Surg. 37:80, 1984. 20. Culbertson, J. H., and Mutimer, K.: The reverse lateral upper arm flap for elbow coverage. Ann. Plast. Surg. 18:62, 1987. 21. Cuono, C. B.: Double Z-plasty repair of large and small rhombic defects: the double-Z rhomboid. Plast. Reconstr. Surg. 71:658, 1983. 22. Daniel, R. K., and Weiland, A. J.: Free tissue transfers for upper extremity reconstruction. J. Hand Surg. 7:66, 1982. 23. Davis, W. M., McCraw, J. B., and Carraway, J. H.: Use of a direct, transverse thoracoabdominal flap to close difficult wounds of the thorax and upper extremity. Plast. Reconstr. Surg. 60:526, 1977. 24. Fatah, M. F., and Davies, D. M.: The radial forearm island flap in upper limb reconstruction. J. Hand Surg. 9B:234, 1984. 25. Fisher, J.: External oblique fasciocutaneous flap for elbow coverage. Plast. Reconstr. Surg. 75:51, 1985.

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26. Foucher, G., Genechten, E., Merle, N., and Michon, J.: A compound radial artery forearm flap in hand surgery: an original modification of the Chinese forearm flap. Br. J. Plast. Surg. 37:139, 1984. 27. Freshwater, M. F.: Ten signs for successful skin grafting. Plast. Reconstr. Surg. 72:491, 1983. 28. Gilbert, A., and Teot, L.: The free scapular flap. Plast. Reconstr. Surg. 69:601, 1982. 29. Gilbert, D. A.: An overview of flaps for hand and forearm reconstruction. Clin. Plast. Surg. 8:129, 1981. 30. Godina, M.: Preferential use of end to side arterial anastomoses in free flap transfers. Plast. Reconstr. Surg. 64:673, 1979. 31. Godina, M.: Early microsurgical reconstruction of complex trauma to the extremities. Plast. Reconstr. Surg. 78:285, 1986. 32. Gosain, A. K., and Matloub, H. S.: The composite lateral arm free flap: vascular relationship to triceps tendon and muscle. Ann. Plast. Surg. 29:496, 1992. 33. Graham, B., and Adkins, P.: Complications and morbidity of the donor and recipient sites in 123 lateral arm flaps. J. Hand Surg. 17B:189, 1992. 34. Hallock, G. G.: Free flap donor site refinement using tissue expansion. Ann. Plast. Surg. 20:566, 1988. 35. Hallock, G. G.: Island forearm flap for coverage of the antecubital fossa. Br. J. Plast. Surg. 39:533, 1986. 36. Hallock, G. G.: Refinement of the radial forearm flap donor site using skin expansion. Plast Reconstr Surg 81:21 1988. 37. Hallock, G. G.: Soft tissue coverage of the upper extremity using the ipsilateral radial forearm flap. Contemp. Orthop. 15:15, 1987. 38. Hamilton, S. G., and Morrison, W. A.: The scapular free flap. Br. J. Plast. Surg. 35:2, 1982. 39. Hartrampf, C. R., Scheflan, M., and Black, P. W.: Breast reconstruction with a transverse abdominal island flap. Plast. Reconstr. Surg. 69:216, 1982. 40. Hing, D. N., Buncke, J. H., Alpert, B. S., and Gordon, L.: Free flap coverage of the hand. Hand Clin. 1:741, 1985. 41. Hodgkinson, D. J., and Shepard, G. H.: Muscle musculocutaneous and fasciocutaneous flaps in forearm reconstruction. Ann. Plast. Surg. 10:399, 1983. 42. Hovnanian, A. P.: Latissimus dorsi transplantation for loss of flexion or extension of the elbow. Ann. Surg. 143:493, 1956. 43. Hwang, K., Han, J. Y., and Chung, I. H.: Topographical anatomy of the anconeus muscle for use as a free flap. J. Reconstr. Microsurg. 20:631, 2004. 44. Ikuta, Y., Watari, S., and Kuwamura, K.: Free flap transfers by end-to-side arterial anastomosis. Br. J. Plast. Surg. 28:1, 1975. 45. James, J. H., and Watson, A. C. H.: The use of Opsite, a vapor permeable dressing on skin graft donor sites. Br. J. Plast. Surg. 28:107, 1975. 46. Janevicius, R. V., and Greager, J. A.: The extensor carpi radialis longus muscle flap for anterior elbow coverage. J. Hand Surg. 17A:102, 1992. 47. Jin, Y., Guam, W., Shi, T., Quian, Y., Xu, L., and Change, T.: Reversed island forearm fascial flap in hand surgery. Ann. Plast. Surg. 15:340, 1985.

48. Jones, N. F., Hardesty, R. A., Goldstein, S. A., and Ward, W. T.: Upper limb salvage using a free radial forearm flap. Plast. Reconstr. Surg. 79:468, 1987. 49. Juretic, M., Car, M., and Zambelli, M.: The radial forearm free flap: Our experience in solving donor site problems. J. Craniomaxillofac. Surg. 20:184, 1992. 50. Kaplan, E. N., and Pearl, R. M.: An arterial medial arm flap: vascular anatomy and clinical applications. Ann. Plast. Surg. 4:205, 1980. 51. Katsaros, J., Schusterman, M., Beppu, M., Banis, J. C., and Ackland, R. D.: The lateral upper arm flap: anatomy and clinical applications. Ann. Plast. Surg. 12:489, 1984. 52. Krizek, T. J., Robson, M. C., and Kho, E.: Bacterial growth and skin graft survival. Plast. Surg. Forum 18:518, 1967. 53. Kuek, L. B.: The extended lateral arm flap: a detailed anatomical study. Ann. Acad. Med. Singapore 21:169, 1992. 54. Lai, M. F., Krishna, B. V., and Pelly, A. D.: The brachioradialis myocutaneous flap. Br. J. Plast. Surg. 34:431, 1981. 55. Lalikos, J. F., and Fudem, G. M.: Brachioradialis musculocutaneous flap closure of the elbow utilizing a distal skin island: a case report. Ann. Plast. Surg. 39:201, 1997. 56. Lamberty, B. G. H., and Cormack, G. C.: The forearm angiotomes. Br. J. Plast. Surg. 35:420, 1982. 57. Lamberty, B. G. H., and Cormack, G. C.: The antecubital fasciocutaneous flap. Br. J. Plast. Surg. 36:428, 1983. 58. Lanzetta, M., and Bernier, M.: The lateral forearm flap: an anatomic study. Plast. Reconstr. Surg. 99:460, 1997. 59. Le Huec, J. C., and Liquois, F.: A study of the fasciocutaneous vascularization of the arm. Surgical applications. Surg. Radiol. Anat. 17:121, 1995. 60. Lendrum, J.: Alternatives to amputation. Ann. R. Coll. Surg. Engl. 62:95, 1980. 61. Levine, N. S., Lindberg, R. B., Mason, A. D., and Pruitt, B. A.: The quantitative swab culture and smear: a quick simple method for determining the number of viable aerobic bacteria in open wounds. J. Trauma 16:89, 1976. 62. Lin, S. D., Lai, C. S., and Chin, C. C.: Venous drainage in the reverse forearm flap. Br. J. Plast. Surg. 34:431, 1981. 63. Lister, G.: The theory of the transposition flap and its practical application in the hand. Clin. Plast. Surg. 8:115, 1981. 64. Lister, G. D., and Gibson, T.: Closure of rhomboid skin defects: the flaps of Limberg and Dufourmentel. Br. J. Plast. Surg. 25:300, 1972. 65. Lister, G., and Schecker, L.: Emergency free flaps to the upper extremity. J. Hand Surg. 13A:22, 1988. 66. Lovie, M. J., Duncan, G. M., and Glasson, D. W.: The ulnar artery forearm free flap. Br. J. Plast. Surg. 37:486, 1984. 67. Luce, E. A., and Gottlieb, S. F.: The pectoralis major island flap for coverage in the upper extremity. J. Hand. Surg. 7:156, 1982. 68. Lutz, B. S., Wei, F. C., Chang, S. C., Yang, K. H., and Chen, I. H.: Donor site morbidity after suprafascial elevation of the radial forearm flap: A prospective study in 95 consecutive cases. Plast. Reconstr. Surg. 103:132, 1999. 69. Mackinnon, S. E., Weiland, A. J., and Godina, M.: Immediate forearm reconstruction with a functional latissimus dorsi island pedicle myocutaneous flap. Plast. Reconstr. Surg. 71:700, 1983.

Chapter 36 Soft Tissue Coverage of the Elbow

70. Magden, O., Icke, C., Arman, C., and Atabey, A.: An anatomical study of the inferior cubital artery. Eur. J. Plast. Surg. 20:24, 1997. 71. Manchot, C.: Die Hautarterien des Menschlichen Körpers. Leipzig, F. C. W. Vogel, 1889. 72. Manktelow, R. T., and McKee, N. H.: Free muscle transplantation to provide active finger flexion. J. Hand. Surg. 3:416, 1978. 73. Mathes, S., and Nahai, F.: Clinical Applications for Muscle and Musculocutaneous Flaps. St Louis: CV Mosby; 1982. 74. Marty, F. M., Montandon, D., Gumener R., and Zbrodowski, A.: The use of subcutaneous tissue flaps in the repair of soft tissue defects of the forearm and hand: an experimental and clinical study of a new technique. Br. J. Plast. Surg. 37:95, 1984. 75. Masser, M. R.: The preexpanded radial free flap. Plast. Reconstr. Surg. 86:295, 1990. 76. McCraw, J. B., Dibbell, D. G., and Carraway, J. H.: Clinical definition of independent myocutaneous vascular territories. Plast. Reconstr. Surg. 60:341, 1977. 77. McGregor, A. D.: The free radial forearm flap: the management of the secondary defect. Br. J. Plast. Surg. 40:83, 1987. 78. Milloy, F. J., Anson, B. J., and McAfee, D. K.: The rectus abdominis muscle and the epigastric arteries. Surg. Gynecol. Obstet. 110:293, 1960. 79. Milton, S. H.: Pedicled skin flaps: the fallacy of the lengthwidth ratio. Br. J. Surg. 57:502, 1970. 80. Moffett, T. R., and Madison, S. A.: An extended approach for the vascular pedicle of the lateral arm free flap. Plast. Reconst. Surg. 89:259, 1992. 81. Moisidis, E., Heath, T., Boorer, C., Ho, K., and Deva, A. K.: A prospective, blinded, randomized, controlled clinical trial of topical negative pressure use in skin grafting. Plast. Reconstr. Surg. 15:917, 2004 82. Mühlbauer, W., Herndl, E., and Stock, W.: The forearm flap. Plast. Reconstr. Surg. 70:343, 1982. 83. Mühlbauer, W., Herndl, E., and Stock, W.: The forearm flap. Plast. Reconstr. Surg. 70:336, 1982. 84. Ohtsuka, H., and Imagawa, S.: Reconstruction of a posterior defect of the elbow joint using an extensor carpi radialis longus myocutaneous flap: case report. Br. J. Plast. Surg. 38:238, 1985. 85. Onishi, K., and Yu, M.: Cutaneous and fascial vasculature around the rectus abdominis muscle: anatomic basis of abdominal fasciocutaneous flaps. J. Reconstr. Microsurg. 2:247, 1986. 86. Parry, S. W., Ward, J. W., and Mathes, S. J.: Vascular anatomy of the upper extremity muscles. Plast. Reconstr. Surg. 81:358, 1988. 87. Penteado, C. V., Masquelet, A. C., and Chevrel, J. P.: The anatomic basis of the fasciocutaneous flap of the posterior interosseous artery. Surg. Radiol. Anat. 8:209, 1986. 88. Pruzansky, M., and Kelly, M.: Latissimus dorsi musculocutaneous flap for elbow extension. J. Surg. Oncol. 47:62, 1991. 89. Reyes, F. A., and Burkhalter, W. E.: The fascial radial flap. J. Hand Surg. Am. 13:432, 1988.

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90. Rios, J. L., Pollock, T., Adams, W. P. Jr.: Progressive tension sutures to prevent seroma formation after latissimus dorsi harvest. Plast Reconstr. Surg. 112:1779, 2003. 91. Richardson, D., Fisher, S. E., Vaughan, E. D., and Brown, J. S.: Radial forearm flap donor-site complications and morbidity: A prospective study. Plast. Reconstr. Surg. 99:109, 1997. 92. Rohrich, R. J., and Ingram, A. E. Jr: Brachioradialis muscle flap: clinical anatomy and use in soft tissue reconstruction of the elbow. Ann. Plast. Surg. 35:70, 1995. 93. Romm, S., and Massac, E.: A guide to skin grafting. Contemp. Orthop. 11:35, 1985. 93a. Salmon, M.: Arteres de la Peau. Paris, Masson, 1936. 94. Sbitany, U., and Wray, R. C. Jr.: Use of the rectus abdominis muscle flap to reconstruct an elbow defect. Plast. Reconstr. Surg. 77:988, 1985. 95. Schmidt, C. C., Kohut, G. N., Greenberg, J. A., Kann, S. E., Idler, R. S., and Kiefhaber, T. R.: The anconeus muscle flap: Its anatomy and clinical application. J. Hand Surg. Am. 24:359, 1999. 96. Schoofs, M., Bienfast, B., Calteux, N., Dachy, C., Vandermaeren, C., and de Coninck, A.: Le lambeau aponéurotique de l’avantbras. Ann. Chir. Main 2:197, 1983. 97. Schottstaedt, E. R., Larsen, L. J., and Bost, F. G.: Complete muscle transposition. J. Bone Joint Surg. 37A:897, 1955. 98. Song, R. S., Gao, Y., Song, Y., Yu, Y., and Song, Y.: The forearm flap. Clin. Plast. Surg. 9:21, 1982. 99. Song, R., Song, Y., Yu, Y., and Song, Y.: The upper arm free flap. Clin. Plast. Surg. 9:27, 1982. 100. Soutar, D. S., and Tanner, S. B.: The radial forearm flap in the management of soft tissue injuries of the hand. Br. J. Plast. Surg. 37:18, 1984. 101. Stern, P. J., Neale, H. W., Gregory, R. O., and Kreilein, J. G.: Latissimus dorsi musculocutaneous flap for elbow flexion. J. Hand Surg. 7:25, 1982. 102. Swanson, E., Boyd, J. B., Mulholland, R. S.: The radial forearm flap: A biomechanical study of the osteotomized radius. Plast. Reconstr. Surg. 85:267, 1990. 103. Takayanagi, S., and Tsukie, T.: Free serratus anterior muscle and myocutaneous flaps. Ann. Plast. Surg. 8:277, 1982. 104. Thornton, J. W., Stevenson, T. R., and Vander Kolk, C. A.: Osteoradionecrosis of the olecranon: treatment by radial forearm flap. Plast. Reconstr. Surg. 80:833, 1987. 105. Timmons, M. J.: The vascular basis of the radial forearm flap. Plast. Reconstr. Surg. 77:80, 1986. 106. Timmons, M. J., Missotten, F. E. M., Pode, M. D., and Davies, D. M.: Complications of radial forearm flap donor sites. Br. J. Plast. Surg. 39:176, 1986. 107. Tobin, G. R.: The compromised bed technique. Surg. Clin. North Am. 64:653, 1984. 108. Tolhurst, D. E., Haeseker, B., and Zeeman, R. J.: The development of the fasciocutaneous flap and its clinical applications. Plast. Reconstr. Surg. 71:597, 1983. 109. Tung, T. C., and Wang, K. C.: Reverse pedicled lateral arm flap for reconstruction of posterior soft-tissue defects of the elbow. Ann. Plast. Surg. 38:635, 1997. 110. Winspur, I.: Distant flaps. Hand Clin. 1:729, 1985.

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111. Wood, M. B., and Irons, G. B.: Upper extremity free skin flap transfer: results and utility as compared with conventional distant pedicle skin flaps. Ann. Plast. Surg. 11:523, 1983. 112. Zancolli, E. A., and Angrigiani, C.: Colgajo dorsal de antebrazo (en “isla” con pediculo de vasos interosseos poste-

riores). Rev. Assoc. Arg. Orthop. Traumatol. 51:161, 1986. 113. Zancolli, E., and Mitre, H.: Latissimus dorsi transfer to restore elbow flexion: an appraisal of eight cases. J. Bone Joint Surg. 55A:1265, 1973.

SECTION

A

ARTHROSCOPY Felix H. Savoie III

CHAPTER

37

Diagnostic Arthroscopy: Indications, Portals, and Techniques Glen A. McClung II, Larry D. Field, and Felix H. Savoie III

HISTORY In 1932, Michael Burman concluded in the Journal of Bone and Joint Surgery that the elbow joint was “unsuitable for examination” arthroscopically.8 Since that time, advances in arthroscopy and equipment have made elbow arthroscopy safe and effective in the management of a variety of elbow disorders. Elbow arthroscopy is a technically demanding procedure that requires a thorough knowledge of the neurovascular anatomy of the elbow. The original indications for elbow arthroscopy only included the diagnosis and removal of loose bodies. As techniques have advanced, the indications for elbow arthroscopy have expanded to include the treatment of synovitis, osteochondritis dissecans, capsular contractures, arthritis, fractures, lateral epicondylitis, and instability.28,29,34,48 Elbow arthroscopy was originally performed with the patient in the supine position and the hand suspended to traction. Because of poor access to the posterior aspect of the elbow, Poehling et al.35 popularized the prone position for elbow arthroscopy. The lateral decubitus position has been advocated by O’Driscoll and Morrey.29 The arm is positioned with the involved side up, the elbow flexed at 90 degrees, and the arm

supported by a padded bolster. This position allows better access to both anterior and posterior compartments.

INDICATIONS AND CONTRAINDICATIONS The indications for elbow arthroscopy include the removal of loose bodies,7,18,23,26-28,40 removal of osteophytes secondary to osteoarthritis,25,30 radial head resection,20 release of capsular contractures and adhesions,9,14 and the resection of symptomatic plica.4,11 Other indications include the treatment of osteochondritis dissecans,6,28,37,42 fractures,3,24,28 lateral epicondylitis,5,44 instability,45 septic arthritis,48 synovectomy,3,48 and evaluation of patients with chronic elbow pain.28 Multiple studies have demonstrated the effectiveness of elbow arthroscopy for the diagnosis and treatment of loose bodies. Success rates have been reported in the 90% range.7,18,26,27 Elbow arthroscopy for loose bodies is indicated in symptomatic patients who fail to respond to conservative treatment. The operating surgeon should attempt to determine the etiology of the loose body. Loose bodies are often a result of osteochondritis dissecans. Other causes include trauma, arthritis, or synovial osteochondromatosis. It is essential that the operating surgeon determines the source of loose bodies because the outcome of the patient will be determined by the disease, not just the removal of loose fragments.42

SURGICAL TECHNIQUES ANESTHESIA Elbow arthroscopy can be performed under general or regional anesthesia. General anesthesia allows for complete muscle relaxation and flexibility of the patient.35 In an awake patient with regional anesthesia, the prone or lateral decubitus position may be poorly tolerated.17 Neurologic function can also be monitored postoperatively with general anesthesia alone. 567

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Regional anesthesia with a scalene, axillary, or Beir intravenous regional block may also be used if the patient cannot undergo general anesthesia. The axillary block does not always achieve complete anesthesia about the elbow. Regional anesthesia may limit operative time secondary to longevity of the anesthetic agent or the intolerance of the patient to the tourniquet in a Beir block.

POSITIONING

the elbow joint in a more familiar anatomic orientation. Conversion of an arthroscopic procedure to an open procedure is readily facilitated in the supine position when required. Disadvantages of the supine position include the requirement for a traction device with the assistance of a second person to stabilize the arm during arthroscopy. Manipulation of the elbow is more difficult with the overhead traction device. Finally, this position provides poor access to the posterior compartment of the elbow joint.

Supine Position

Prone Position

In the supine position, first reported by Andrews and Carson3 in 1985, the patient lies supine with the shoulder over the edge of the operating table. The shoulder is abducted to 90 degrees and is in neutral rotation with 90 degrees of elbow flexion. The elbow is suspended by a traction device that is attached to either the hand or forearm (Fig. 37-1). There are several advantages of the supine position in elbow arthroscopy.19,21 The supine position allows the anesthesiologist an easier access to the patient’s airway, and there is more flexibility to the choice of anesthesia. The conceptualization of the intra-articular anatomy is facilitated with the elbow in the supine position with

In response to the disadvantages of the supine position, Poehling and associates35 described the prone position for elbow arthroscopy. The patient is placed prone on the operating table over chest rolls to ensure adequate ventilation. The shoulder is abducted to 90 degrees, and the arm is supported by an arm positioner or an arm board (Fig. 37-2). The arm board is placed parallel to the operating table, centered at the shoulder. A sandbag, foam support, or rolled blankets are placed under the upper arm to elevate the shoulder and allow the elbow to rest in 90 degrees of flexion. Advantages of the prone position are improved access and visualization of the posterior compartment

FIGURE 37-1

FIGURE 37-2

Arthroscopy may be performed in the supine position, as noted with the elbow suspended to overhead traction as noted in this right elbow.

Elbow arthroscopy may be performed in the prone position with a bolster under the upper arm, as noted in this figure.

Chapter 37 Diagnostic Arthroscopy: Indications, Portals, and Techniques

569

of the elbow. Because the forearm hangs freely from the arm board, the elbow is easily manipulated from near full flexion to full extension. In the prone position, the anterior aspect of the elbow is facing inferiorly toward the floor, which allows neurovascular structures to fall anteriorly away from the joint. This provides an additional margin of safety when establishing portals. No special equipment or additional personnel are needed because the elbow position on the arm board is stable. The prone position, like the supine position, allows for easy conversion to an open procedure.39 Disadvantages of the prone position are associated with airway and patient positioning. Chest rolls, protective padded face masks, and pillows are needed to pad all prominences susceptible to pressure sores during the procedure. Regional anesthesia is usually not well tolerated by the patient. If general anesthesia becomes necessary secondary to failure of the block or patient anxiety, repositioning of the patient is required. Open approaches to the medial and lateral side are readily accessible however an anterior approach would require repositioning.

Lateral Decubitus Position The lateral decubitus position, first described by O’Driscoll and Morrey,29 combines the advantages of the supine and prone position while avoiding some of the pitfalls of each position. The patient is placed in the lateral decubitus position, with the arm positioned in an arm holder or over a bolster. The shoulder is flexed to 90 degrees and internally rotated, and the elbow flexed 90 degrees over a padded bolster (Fig. 37-3). The surgical procedure is performed with the elbow in the prone position and thus provides the same advantages of the prone position. The lateral decubitus does allow for easier patient positioning, and patients can tolerate lateral decubitus position better if regional anesthesia is needed. This position allows a better access to the airway and is easier to convert from regional to general anesthesia if required. Disadvantages include the use of a padded bolster and the possibility of needing to reposition if an open procedure is required.

PORTALS A thorough knowledge of the neurovascular anatomy of the elbow and its three-dimensional relationship to the surface anatomy is required to perform elbow arthroscopy. There are eight access portals that are used in elbow arthroscopy. These portals are determined by neurovascular and musculotendinous anatomy about the elbow. Arthroscopic treatment of the elbow may require the use of several of these portals because the

FIGURE 37-3

Prone positioning of the elbow may also be accomplished by placing the patient in the lateral decubitus position and using the elbow support device.

elbow is a highly constrained joint. Because the complexity of arthroscopic procedures of the elbow has increased, the number of portals used has also increased with an emphasis on the proximal anterior portals. Surface landmarks are marked on the skin before creating portals. Important landmarks to outline are the radial head, olecranon, lateral epicondyle, medial epicondyle, and ulnar nerve. Before making portals, the joint must be distended with 20 to 30 mL of sterile saline (see Fig. 37-1). This can be done by placing an 18-gauge spinal needle either in the olecranon fossa or the soft spot bounded by the lateral epicondyle, olecranon, and radial head. Neurovascular structures are displaced away from the joint with distension of the joint, which gives an additional margin of safety.15,16

Proximal Anteromedial Poehling and associates35 first described the proximal anteromedial portal in 1989. This portal is located 2 cm proximal to the medial epicondyle and just anterior to the medial intermuscular septum (Fig. 37-4). The medial intermuscular septum is identified by palpation, and the portal is made anterior to the septum so that the ulnar nerve is not injured. The blunt trocar is introduced into the portal, anterior to the septum, and aimed toward the

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FIGURE 37-5

In this view from the proximal anterior medial portal, multiple loose bodies are noted anterior to the radiocapitellar joint.

FIGURE 37-4

The multiple portals are delineated on the elbow. Surface landmarks, including the ulnar nerve marked by the long, parallel lines, the medial and lateral epicondyles marked by the circles, and the various portals marked by the x’s, are shown in this patient’s left elbow in the prone position.

radial head while maintaining contact with the anterior surface of the humerus. This allows the brachialis muscle to remain anterior and protect the median nerve and brachial artery. The trocar enters the elbow through the tendinous origin of the flexor-pronator group and medial capsule.17 The proximal anteromedial portal has been recommended as the initial portal used with the patient in the prone or lateral decubitus position.15,35 This portal is thought to offer safer access and better visualization of the joint. In addition, fluid extravasation may be less with this portal compared with the anterolateral portal.15 Visualization of the entire aspect of the anterior aspect of the joint including the anterior capsule, trochlea, capitellum, coronoid process, radial head, and medial and lateral gutters can be obtained with this portal. The primary structure at risk with this portal is the posterior branch of the medial antebrachial cutanenous nerve.46 This nerve is located approximately 2.3 mm from the trocar. With the elbow in flexion, the median nerve is relatively safe, protected by the brachialis muscle, being located on average a distance of 12.4 to 22 mm

from the trocar.15,46 The path of the trocar aims distally and is in a parallel orientation to the median nerve making injury to the nerve less likely. The ulnar nerve is located on average a distance of 12 to 23.7 mm from the portal.15,46 The ulnar nerve is not at risk as long as the portal is made anterior to the intermuscular septum. Contraindications to the use of this portal are a history of subluxation or transposition of the ulnar nerve from its groove.15,32,46 Care must be taken to ensure that the ulnar nerve is not subluxed before anteromedial portal placement. This portal may be used in these circumstances only if the nerve is identified prior to trocar entry.

Anteromedial Portal The anteromedial portal, first described by Andrews and Carson,3 is positioned 2 cm distal and 2 cm anterior to the medial epicondyle (Fig. 37-5). With the elbow flexed to 90 degrees, the blunt trocar is aimed at the center of the joint, passing through the flexor-pronator origin and the brachialis muscle before entering the joint capsule anterior to the medial collateral ligament. This portal may also be established by using an inside-out technique, with the arthroscope in the lateral portal.15 The entire anterior compartment of the elbow, especially the lateral structures, can be visualized from this portal. The medial antebrachial cutaneous nerve is at greatest risk of being injured, located on average 1 mm from the portal.22,46 The median nerve is in closer proximity to this portal being located on average a distance of 7 to 14 mm.16,46 Lindenfeld15 reports an average distance of 22 mm from the portal to the median nerve if this portal is established 1 cm anterior to the medial epicondyle.

Chapter 37 Diagnostic Arthroscopy: Indications, Portals, and Techniques

Proximal Anterolateral The proximal anterolateral portal, described by Stothers and associates,46 Field and associates,12 and Savoie and Field41 is positioned 2 cm proximal and 1 to 2 cm anterior to the lateral epicondyle (Fig. 37-6). This portal may be used as the initial portal in elbow arthroscopy. The blunt trocar is aimed towards the center of the joint while maintaining contact with the anterior humerus, and pierces the brachioradialis muscle, brachialis muscle and lateral joint capsule before entering the anterior compartment. This portal allows visualization of the anterior compartment, specifically the lateral and anterior aspects of the radial head and capitellum, lateral gutter, anterior ulnohumeral joint, and anterior elbow capsule. The structures at risk on the lateral side are the posterior branch of the lateral antebrachial cutaneous nerve and the radial nerve. The trocar in the proximal anterolateral portal lies on average 6.1 mm from the posterior branch of the antebrachial cutaneous nerve.46 This portal was developed because of the proximity of the radial nerve to the standard anterolateral portal. With the elbow in 90 degrees of flexion and distended with fluid, the radial nerve is located an average distance of 9.9 to 14.2 mm from the proximal anterolateral portal in contrast to 4.9 to 9.1 mm from the standard anterolateral portal.12,46

Anterolateral Portal The standard anterolateral portal, first described by Andrews and Carson3 in 1985, is located 3 cm distal and

571

1 cm anterior to the lateral epicondyle (see Fig. 37-6). The blunt trocar is aimed toward the center of the joint and passes through the extensor carpi radialis brevis muscle and lateral joint capsule before entering the joint. This portal can also be established with an inside-out technique using the arthroscope in the anteromedial or proximal anteromedial portal. The arthroscope is advanced to the capsule lateral to the radial head. The arthroscope is then removed from the cannula and replaced with a blunt rod that tents the overlying skin. The skin is incised over the rod and a cannula is positioned over the rod and placed into the joint. It is imperative when using this technique that the blunt rod enters the capsule lateral to the radial head rather than anterior to it in order to avoid injury to the radial nerve.15,32,46 The anterolateral portal offers visualization of the anterior medial aspect of the joint including the coronoid process, trochlea, coronoid fossa, and medial aspect of the radial head. Visualization of the lateral joint is better with the proximal anterolateral portal.12 This portal is also useful as a working portal with the arthroscope in the proximal anteromedial portal, especially for procedures on the radial head. Lynch and associates16 have shown the anterolateral portal to be located 2 mm from the posterior antebrachial cutaneous nerve. The radial nerve lies 4.9 to 9.1 mm from this portal with the elbow in 90 degrees of flexion and the joint distended with fluid.12,46 Because of its proximity and increased risk to the radial nerve, most authors recommend a more proximal entry for this portal.

Medial antebrachial cutaneous n.

Median n.

Ulnar n. Brachial a.

FIGURE 37-6

The proximal anterior-medial portal located approximately 2 cm superior and 2 cm anterior to the medial epicondyle is marked along with relevant neurovascular structures.

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Midlateral Portal The midlateral portal is located in the center of the triangular area bordered by the olecranon, lateral epicondyle, and the radial head. This portal is also known as the direct lateral portal or soft spot. The blunt trocar passes through the aconeous muscle and the posterior capsule and into the joint. This is the same path that an 18-gauge needle takes for initial distension of the joint. The midlateral portal offers visualization of the radialulnar joint, as well as the inferior aspect of the radial head and capitellum. Instrumentation of the lateral gutter and posterior radiocapetellar joint may be used with this portal. There is minimal risk to neurovascular structures with this portal. The posterior antebrachial cutaneous nerve, approximately 7 mm away,1 is the only structure at risk. Because of leakage of fluid into the soft tissues, it is advisable to delay this portal until the end of the operation.32,34,46

Straight Posterior Portal The straight posterior or transtriceps portal is located 3 cm proximal to the tip of the olecranon in the midline posteriorly33,34 (Fig. 37-7). This portal allows visualization of the entire posterior compartment, as well as the medial and lateral gutters.17 The blunt trocar is advanced toward the olecranon fossa through the triceps tendon and posterior joint capsule. With the arthroscope in the posterolateral portal, the straight posterior portal can be used for distal humeral fenestration with a drill or burr in ulnohumeral arthroplasty to access the anterior com-

partment of the elbow.32 This portal may also be used for instrumentation in removal of loose bodies and excision of olecranon spurs.17

Posterolateral Portal The posterolateral portal is located 3 cm proximal to the olecranon tip and just lateral to the triceps tendon (see Fig. 37-7). The blunt trocar is advanced toward the olecranon fossa, passing lateral to the triceps tendon to enter the joint through the posterolateral capsule. This is performed with the elbow held in 45 degrees of flexion in order to relax the triceps and posterior capsule.46 Triceps tendon injury can be avoided by remaining close to the posterior humeral cortex with the blunt trocar. This portal is approximately 20 mm from the medial antebrachial cutaneous nerve and 25 mm from the posterior antebrachial cutaneous nerve.16 The posterolateral portal allows excellent visualization of the posterior compartment of the elbow as well as medial and lateral gutters. In examining the medial gutter from this portal, the operating surgeon must be aware of the location of the ulnar nerve, which lies just superficial to the medial capsule.32,35

Posterolateral II Portal Access to the posterolateral aspect of the elbow can be obtained anywhere between the soft spot portal to the standard posterolateral portal, 3 cm proximal to the olecranon tip. This portal is usually placed just lateral to the olecranon process and can be moved proximally or distally as needed. Visualization through this portal usually consists of distally the posterior radiocapitellar

Medial antebrachial cutaneous n.

Median n.

Ulnar n. Brachial a.

FIGURE 37-7

The standard anteromedial portal is delineated being approximately 2 cm distal and 2 cm anterior to the medial epicondyle. Pertinent neurovascular structures are delineated in this illustration well.

Chapter 37 Diagnostic Arthroscopy: Indications, Portals, and Techniques

joint and proximally across the olecranon into the olecranon fossa. It may be used for excision of lateral olecranon spurs, resection of posterolateral plica, and débridement of the radial aspect of the ulnohumeral joint. The triceps tendon and ulnohumeral cartilage are at risk with placement of this portal.41

PROCEDURE Before taking a patient to the operating room for the removal of loose bodies, a careful history and physical examination must be performed. A history of prior surgeries, particularly those involving release or transposition of the ulnar nerve, should be obtained. Physical examination should include range of motion, stability, and a neurovascular examination. The ulnar nerve should be evaluated during elbow flexion to ascertain subluxation or dislocation of the nerve. Loose bodies are commonly located in the coronoid fossa, the olecranon fossa, and the posterior lateral gutter, and access to these sites must be obtainable by the surgeon. A complete and thorough evaluation of the joint is necessary because loose bodies can migrate to any area of the elbow. General anesthesia is administered, and the patient is placed in the prone position on the operating table over chest bolsters to ensure adequate ventilation. All bony prominences are well padded, and the shoulder is abducted to 90 degrees. An arm board is placed parallel to the operating table and a sandbag is positioned under the arm to elevate the shoulder. The forearm is allowed to fall over the arm board with the elbow flexed to 90 degrees. A Mayo stand with the appropriate instruments are placed next to the surgeon and scrub nurse, while the video monitor and equipment are placed on the opposite side of the patient. A tourniquet is placed on the upper part of the arm and an esmarch is used to

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exsanguinate the extremity. Once the arm is prepped and draped, surface landmarks of the elbow are outlined including the medial and lateral epicondyle and the olecranon process (Fig. 37-8). Also the ulnar nerve is specifically palpated to confirm that it remains in the cubital tunnel and is not subluxated. An 18-gauge spinal needle is next placed into the straight posterior or soft spot portal, and 20 to 30 mL of sterile saline is injected into the joint. This usually results in slight extension of the elbow as the joint space is filled. The proximal anteromedial is the initial portal established unless history of ulnar nerve transposition or subluxation prohibits its use. This portal is located 2 cm proximal to the medial epicondyle and anterior to the intermuscular septum. A No. 11 knife blade is used to incise skin only while a hemostat dissects to the joint capsule. With the elbow in 90 degrees of flexion, a small blunt trocar and cannula for the 4.5-mm arthroscope is aimed toward the radial head while maintaining contact with the anterior aspect of the humerus. Once inside the joint, an egress of fluid confirms intra-articular placement. A 4.5-mm, 30-degree arthroscope is introduced into the cannula with the inflow connected to the bridge on the scope. With the arthroscope in the proximal anteromedial portal the entire anterior compartment of the elbow can be evaluated. From lateral to medial this includes examination of the lateral gutter, capitellum, radial head, anterior capsule, trochlea, coronoid process, and if properly placed, medial gutter. The arthroscopic evaluation initially includes inspection of the radiocapitellar joint through a range of motion in pronation and supination. This is performed to ensure that the radial head is congruent with the capitellum and that no subluxation exists and to evaluate the articular cartilage of the radial head. The arthroscope is then advanced anterior to the radiocapitellar joint, and the lens is rotated to visualize the

Radial nerve Anterosuperior lateral portal Proximal anterolateral portal

Anterolateral portal

FIGURE 37-8

Three primary lateral portals being the proximal anterolateral portal, the anterosuperior lateral portal, and the distal anterolateral portal are delineated in this figure, along with their proximity to the radial nerve.

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Medial brachial cutaneous nerve

Triceps muscle

Straight posterior portal

Posterolateral portal

Posterior antebrachial cutaneous nerve Olecranon

Ulnar nerve

FIGURE 37-9

The two standard posterior portals most commonly utilized in the elbow are delineated in this figure.

capsule and undersurface of the extensor muscles. The ulnohumeral articulation is next evaluated by retracting and rotating the arthroscope so that the coronoid process is in view. By rotating the lens superiorly, the attachment of the capsule to the humerus is visible. Loose bodies are commonly found in the anterior compartment in the coronoid fossa (Fig. 37-10). Once the loose body is identified, a lateral portal is established using a spinal needle. For removing loose bodies the proximal anterolateral portal is preferred. The spinal needle is placed 2 cm proximal and 1 to 2 cm anterior to the lateral epicondyle, aiming toward the center of the joint. Once intra-articular placement is confirmed arthroscopically, the spinal needle is removed and a No. 11 blade knife is used to incise skin only in order to avoid damage to cutaneous nerves. A blunt trocar and cannula is then advanced into the joint while maintaining contact with the anterior humerus to avoid injury to the radial nerve. A grasper with teeth is introduced into the proximal anterolateral portal and used to remove the loose bodies. It may be necessary to “pin or stab” the loose body with an 18-gauge spinal needle, inserted through the mid anterolateral or anteromedial portal site, in order to provide resistance for grasping. The loose body should be rotated as it is being brought

FIGURE 37-10 These loose bodies may be removed from an anterolateral portal using a grasping device.

through the soft tissue so that it does not get lost. For larger loose bodies the portal may have to be enlarged in order to accommodate the size of the fragment. Otherwise, the loose body may need to be removed piece by piece.

Chapter 37 Diagnostic Arthroscopy: Indications, Portals, and Techniques

Once the loose bodies in the anterior compartment are removed, the posterior compartment is addressed. The cannula in the proximal anteromedial portal is left in place, and the inflow is attached so that the loose bodies are pushed to the posterior compartment. In the posterior compartment, loose bodies are usually located in the olecranon fossa (Fig. 37-11). The straight posterior portal is established using a No. 11 blade knife 3 cm proximal from the olecranon process and in the midline posteriorly. The blunt trocar and cannula are directed toward the olecranon fossa. Once loose bodies are identified, the posterolateral portal is established by placing a spinal needle 3 cm proximal to olecranon process and lateral to the triceps. Once the spinal needle is determined to be in the appropriate position arthroscopically, a No. 11 blade knife is used to incise only skin and a blunt trocar and cannula are introduced into the posterior compartment. Usually a motorized shaver is necessary to débride soft tissue in order to obtain full access to the olecranon fossa. The loose bodies can be removed from either the straight posterior or posterolateral portal. The tip of the olecranon should be carefully evaluated because this is often a source for loose bodies. The arthroscope is next directed toward the medial gutter. Using the opposite hand, the surgeon applies pressure in an alternating fashion to the soft tissues posterior to the medial epicondyle in a distal to proximal direction. This maneuver should “milk” any loose bodies from the medial gutter. “Hidden” loose bodies are often found in the posterolateral gutter. The scope is then directed down the lateral gutter where the midlateral or soft spot portal is established

FIGURE 37-11 Loose bodies may also be noted in the posterior aspect of the elbow. This loose body is located in the center of the olecranon fossa.

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by first using a spinal needle to confirm placement intraarticularly. Usually, a soft tissue plica or synovium may need to be débrided for adequate visualization. This portal is useful in locating and removing loose bodies as well as locating osteochondritis dissecans. Once all loose bodies have been removed, Steri-Strips are placed over the portals and a compressive dressing is placed on the extremity. Neurovascular checks are performed in the recovery room.

TECHNICAL ALTERNATIVES AND PITFALLS Loose body removal from the elbow is the most successful and ideal indication for elbow arthroscopy. The success of the procedure often depends on the cause of the loose body. Most pitfalls in elbow arthroscopy relate to damage to neurovascular structures with a prevalence ranging from zero to 14%2,13,16,31,33,36,38 in the literature. Most nerve injuries are transient and can be caused from extravasation of fluid or local anesthestic,3 compression from the arthroscopic sheaths, direct injury from the trocar, or overaggressive joint distension. Injury to the radial, median, anterior interosseous, medial antebrachial cutaneous, and ulnar nerves have been reported.3,10,16,31,36,38,43,47 In a review of 473 consecutive elbow arthroscopies, Kelly and associates13 found 10 patients (2.5%) with transient nerve palsies. Many nerve injuries are associated with the use of the anterolateral and anteromedial portals because of their close proximity to neural structures. The radial nerve, posterior interosseous nerve, and superficial branch of the radial nerve have been injured during placement of the anterolateral portal.16,31,47 Injuries of the median and anterior interosseous nerves during placement of the anteromedial portal have been reported.3,16,38 Neuroma formation can result from injury of the superficial cutaneous nerve.16 In order to avoid nerve injuries, knowledge of neurovascular anatomy and careful portal placement are critical. The prone position allows neurovascular structures to fall anteriorly, away from the joint. Fluid distension of the joint and flexing the elbow to 90 degrees have been documented to increase the distance between neurovascular structures and portals.15,16 When making a portal, the knife blade should cut only through skin. The skin should drag across the blade instead of making a stab incision. This prevents injuries to the superficial cutaneous nerves. Other complications in elbow arthroscopy are iatrogenic articular cartilage injury, infection, persistent drainage of portals, synovial fistula formation, and problems associated with the tourniquet. Complications such as arthrofibrosis, reflex sympathetic dystrophy, and thromboembolism are seen less frequently.43

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REHABILITATION Postoperatively, the patient is usually placed in a compressive dressing and may use the extremity as tolerated. On postoperative day one, the patient is started on a home exercise program of active and active assisted range of motion. This program includes flexion, extension, supination, and pronation. The patient is seen in the office 1 week after surgery, and his or her progress is monitored so that full range of motion is attained.

OUTCOMES AND FUTURE DIRECTIONS Probably one of the most successful operations in elbow arthroscopy is removal of symptomatic loose bodies. Several authors have reported on the beneficial effects of removal of loose bodies. As mentioned previously, the physician should attempt to determine the cause of the loose bodies. In many cases, simply removing loose fragments will not improve the outcome of the patient. This point is illustrated by O’Driscoll and Morrey’s28 review of 71 elbow arthroscopies in which 24 elbows had loose bodies. Fourteen patients with a primary diagnosis of loose bodies and another four patients with loose bodies secondary to osteochondritis dissecans improved after arthroscopic removal of their loose bodies. Patients with loose bodies secondary to posttraumatic arthritis, primary degenerative disease, synovial chondromatosis, or idiopathic flexion contracture did not improve with simple removal of loose bodies. The indications of elbow arthroscopy continue to expand as surgical techniques improve. Elbow arthroscopy decreases the morbidity of an open procedure while allowing the operating surgeon a complete evaluation of the joint. With careful attention to detail and meticulous surgical technique, elbow arthroscopy can be performed safely with minimal risk of complications.

References 1. Aldolfsson, L.: Arthroscopy of the elbow joint: A cadaveric study of portal placement. J. Shoulder Elbow Surg. 3:53, 1994. 2. Andrews, J. R., and Baumgarten, T. E.: Arthroscopic anatomy of the elbow. Orthop. Clin. North Am. 26:671, 1995. 3. Andrews, J. R., and Carson, W. G.: Arthroscopy of the elbow. Arthroscopy 1:97, 1985. 4. Antuna, S. A., and O’Driscoll, S. W.: Snapping plicae associated with radiocapitellar chondromalacia. Arthroscopy 17:491, 2001. 5. Baker, C. L. Jr, Murphy, K. P., Gottlob, C. A., and Cuerd, D. T.: Arthroscopic classification and treatment of lateral epicondylitis: two-year clinical results. J. Shoulder Elbow Surg. 9:475, 2000.

6. Baumgarten, T. E., Andrew, J. R., and Satterwhite, Y. E.: The arthroscopic evaluation and treatment of osteochondritis desiccans of the capitellum. Am. J. Sports Med. 26:520, 1998. 7. Boe, S.: Arthroscopy of the elbow: Diagnosis and extraction of loose bodies. Acta Orthop. Scand. 57:52, 1986. 8. Burman, M.: Arthroscopy of the elbow joint: a cadaver study. J. Bone Joint Surg. 14:349, 1932. 9. Byrd, J. W.: Elbow arthroscopy for arthrofibrosis after type I radial head fractures. Arthroscopy 10:162, 1994. 10. Casscells, S. W.: Neurovascular anatomy and elbow arthroscopy: inherent risks [Editor’s comment]. Arthroscopy 2:190, 1986. 11. Clarke, R.: Symptomatic lateral synovial fringe of the elbow joint. Arthroscopy 4:112, 1988. 12. Field, L. D., Altchek, D. W., Warren, R. F., O’Brien, S. J., Skyhar, M. J., and Wickiewicz, T. L.: Arthroscopic anatomy of the lateral elbow: A comparison of three portals. Arthroscopy 10:602, 1994. 13. Kelly, E. W., Morrey, B. F., and O’Driscoll, S. W.: Complications in elbow arthroscopy. J. Bone Joint Surg. Am. 83:25, 2001. 14. Jones, G. S., and Savoie, F. H.: Arthroscopic capsular release of flexion contractures (arthrofibrosis) of the elbow. Arthroscopy 9:277, 1993. 15. Lindenfield, T. N.: Medial approach in elbow arthroscopy. Am. J. Sports Med. 18:413, 1990. 16. Lynch, G. J., Meyers, J. F., Whipple, T. L., and Caspari, R. B.: Neurovascular anatomy and elbow arthroscopy: Inherent risks. Arthroscopy 2:191, 1986. 17. Lyons, T. R., Field, L. D., and Savoie, F. H.: Basics of elbow arthroscopy. Instruct. Course Lect. 49:239, 2000. 18. McGinty, J.: Arthroscopic removal of loose bodies. Orthop. Clin. N. Am. 13:313, 1982. 19. McKenzie, P. J.: Supine position. In Savoie, F. H., and Field, L. D. (eds.): Arthroscopy of the Elbow. New York, Churchill Livingstone, 1996, p. 35. 20. Menth-Chiari, W. A., Ruch, D. S., and Poehling, G. G.: Arthroscopic excision of the radial head: Clinical outcome in 12 patients with post-traumatic arthritis after fracture of the radial head or rheumatoid arthritis. Arthroscopy 17:918, 2001. 21. Meyer, J. F., and Carson, W. G. Jr.: Elbow arthroscopy: Supine technique. In McGinty, J. B., Burkhart, S. S., Jackson, R. W., Johnson, D. H., and Richmond, J. C. (eds.): Operative Arthroscopy, 3rd ed. Philadelphia: Lippencott-Raven, 2003, p. 665. 22. Miller, C. D., Jobe, C. M., and Wright, M. H.: Neuroanatomy in elbow arthroscopy. J. Shoulder Elbow Surg. 4:168, 1995. 23. Morrey, B. F.: Arthroscopy of the elbow. Instruct. Course Lect. 35:102, 1986. 24. Moskal, J. H., Savoie, F. H., and Field, L. D.: Elbow arthroscopy in trauma and reconstruction. Orthop. Clin. North Am. 30:163, 1999 25. O’Driscoll, S. W.: Arthroscopic treatment for osteoarthritis of the elbow. Orthop. Clin North Am. 26:691, 1995. 26. O’Driscoll, S. W.: Elbow arthroscopy for loose bodies. Orthopaedics 15:855, 1992.

Chapter 37 Diagnostic Arthroscopy: Indications, Portals, and Techniques

27. O’Driscoll, S. W.: Elbow arthroscopy: loose bodies. In Morrey, B. F. (ed.): The Elbow and Its Disorders, 3rd ed. Philadelphia, Saunders, 2000, p. 510. 28. O’Driscoll, S. W., and Morrey, B. F.: Arthroscopy of the elbow: Diagnostic and therapeutic benefits and hazards. J. Bone Joint Surg. Am. 74:84, 1992. 29. O’Driscoll, S. W., and Morrey, B. F.: Arthroscopy of the elbow. In Morrey, B. F. (ed.): The Elbow and Its Disorders, 2nd ed. Philadelphia, Saunders, 1993, p. 120. 30. Ogilvie-Harris, D. J., Gordon, R., and MacKay, M.: Arthroscopic treatment for posterior impingement in degenerative arthritis of the elbow. Arthroscopy 11:437, 1995. 31. Papilion, J. D., Neff, R. S., and Shall, L. M.: Compression neuropathy of the radial nerve as a complication of elbow arthroscopy: a case report and review of the literature. Arthroscopy 4:284, 1988. 32. Plancher, K. D., Peterson, R. K., and Breezenoff, L.: Diagnostic arthroscopy of the elbow: Set-up, portals, and technique. Oper. Tech. Sports Med. 6:2, 1998. 33. Poehling, G. G., and Ekman, E. F.: Arthroscopy of the elbow. Instruct. Course Lect. 44:217, 1995. 34. Poehling, G. G., Ekman, E. F., and Ruch, D. S: Elbow arthroscopy: Introduction and overview. In McGinty, J. B., Caspari, R. B., Jackson, R. W., and Poehling, G. G. (eds.): Operative Arthroscopy, 2nd ed. Philadelphia, LippincottRaven, 1996, p. 821. 35. Poehling, G. G., Whipple, T. L., Sisco, L., and Goldman, B.: Elbow arthroscopy: a new technique. Arthroscopy 5:222, 1989. 36. Rodeo, S. A., Forester, R. A., and Weiland, A. J.: Neurologic complications due to arthroscopy. J. Bone Joint Surg Am. 75:917, 1993. 37. Ruch, D. S., Cory, J. W., and Poehling, G. G.: The arthroscopic management of osteochondritis dissecans of the adolescent elbow. Arthroscopy 14:797, 1998.

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38. Ruch, D. S., and Poehling, G. G.: Anterior interosseous nerve injury following elbow arthroscopy. Arthroscopy 13:756, 1997. 39. Rubin, C. J.: Prone or lateral decubitus position. In Savoie, F. H., and Field, L. D. (eds.): Arthroscopy of the Elbow. New York, Churchill Livingstone, 1996, p. 41. 40. Savoie, F. H.: Arthroscopic management of loose bodies of the elbow. Oper. Tech. Sports Med. 9:241, 2001. 41. Savoie, F. H., and Field, L. D.: Anatomy. In Savoie, F. H., and Field, L. D. (eds.): Arthroscopy of the Elbow. New York, Churchill Livingstone, 1996, p. 3. 42. Savoie, F. H., and Field, L. D.: Basics of elbow arthroscopy. Tech. Orthop. 15:138, 2000 43. Small, N. C.: Complications in arthroscopy: the knee and other joints. Arthroscopy 2:253, 1986. 44. Smith, A. M., Castle, J. A., and Ruch, D. S.: Arthroscopic resection of the common extensor origin: anatomic considerations. J. Shoulder Elbow Surg. 12:375, 2003. 45. Smith, J. P. 3rd, Savoie, F. H., and Field, L. D.: Posterolateral rotatory instability of the elbow. Clin. Sports Med. 20:47, 2001. 46. Stothers, K., Day, B., and Reagan, W. R.: Arthroscopy of the elbow: Anatomy, portal sites, and a description of the proximal lateral portal. Arthroscopy 11:449, 1995. 47. Thomas, M. A., Fast, A., and Shapiro, D. L.: Radial nerve damage as a complication of elbow arthroscopy. Clin. Orhop. Relat. Rel. 215:130, 1987. 48. Wiesler, E. R., and Poehling, G. G.: Elbow arthroscopy: introduction, indications, complications, and results. In McGinty, J. B., Burkhart, S. S., Jackson, R. W., Johnson, D. H., and Richmond, J. C. (eds.): Operative Arthroscopy, 3rd ed. Philadelphia: Lippincott-Raven, 2003, p. 661.

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CHAPTER

38

Management of Loose Bodies and Other Limited Procedures Larry D. Field, and Felix H. Savoie III

INTRODUCTION The arthroscope has proven itself to be ideally suited for the removal of elbow loose bodies and is the most common indication for elbow arthroscopy.4,16,26 Other limited procedures such as débridement and synovectomy are also very amenable to arthroscopic management. Elbow arthroscopy has, in fact, proven itself valuable in the treatment of many elbow conditions.1,3,4,8,12,14-16,28,31,34 The potential advantages of elbow arthroscopy in the identification and removal of loose bodies include reduced iatrogenic insult using limited portal site incisions, a more thorough and complete assessment of the anterior and posterior compartments of the elbow, and possibly reduced propensity for scarring postoperatively as a result of limited disruption of the elbow capsule. Disadvantages of elbow arthroscopy center squarely on the technical requirements to safely and effectively perform the procedure due to the close proximity of neurovascular structures. A thorough knowledge of the anatomy of the elbow, particularly from the arthroscopist’s perspective, is critical in reducing the chances of neurovascular injury.33 Preinsufflation of the joint with fluid and maintaining the elbow at approximately 90 degrees of flexion during the procedure increase the distance of the neurovascular structures from the articular surfaces and arthroscopic instruments, decreasing the chance of morbidity from portal placement.17 Also, drawing the anatomic landmarks, including marking the location of the ulnar nerve at the initiation of the procedure, probably serves to reduce the risk of injury to these structures as well.32

LOOSE BODIES Patients with loose bodies usually present with complaints of elbow pain and stiffness and often report

catching, snapping, popping, or locking of the joint (Fig. 38-1) (see Chapter 84). Loose bodies do not cause elbow contracture, but they are often present in patients with elbow contracture. These patients with elbow contractures develop loose bodies as a result of the underlying pathologic condition such as osteochondritis dissecans, posterior impingement, or degenerative arthritis with posterior osteophytes on the olecranon and in the olecranon fossa. On physical examination, patients with loose bodies generally have maintenance of elbow motion but may have mild degrees of flexion and/or extension loss. Also, a mild effusion best identified in the posterolateral gutter of the elbow may be present. Although anteroposterior (AP) and lateral radiographs of the elbow often demonstrate loose bodies (Fig. 38-2), as many as 30% of loose bodies are not detected on plain x-ray studies.26,29,41 Most often, when loose bodies are suspected but not identified on plain radiographs, they will be found in the posterior compartment of the elbow25 (Fig. 38-3). In addition, loose bodies will often migrate within the elbow and even between compartments, making reliable identification more difficult. Computed tomographic arthrography and magnetic resonance imaging may be helpful in diagnosing loose bodies.41 However, even if objective testing fails to demonstrate loose bodies in patients with classic loose body symptoms, elbow arthroscopy may still be indicated because it represents the best diagnostic modality.

SURGICAL INDICATIONS Elbow arthroscopy performed for loose body removal is indicated in symptomatic patients who have failed to respond to nonoperative management. An important adjunct in the management of these patients, however, is a concerted attempt to determine the etiology of the loose bodies. Loose bodies often result from pathologic conditions such as osteochondritis dissecans, trauma, degenerative arthritis, or synovial osteochondromatosis. Determining the source of the loose bodies will allow the surgeon to more effectively treat the underlying cause of the elbow condition. In fact, effective arthroscopic management of the primary cause of the loose bodies may be more important than simple removal of the loose bodies themselves.

SURGICAL TECHNIQUE Originally, elbow arthroscopy was performed with the patient in the supine position and the hand suspended in traction. Poehling et al33 used the prone position for elbow arthroscopy, allowing improved access to the posterior aspect of the elbow and facilitating the conversion to open procedures when necessary. O’Driscoll and Morrey27 have popularized the lateral decubitus posi-

Chapter 38 Management of Loose Bodies and Other Limited Procedures

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FIGURE 38-1

Loose bodies identified in the anterior compartment of the elbow.

tion. In this position, the arm is placed across the chest. All of these positions are acceptable for removal of loose bodies, but the posterior compartment, where loose bodies are more often found, may be more difficult to access with the patient in the supine position. Regardless of patient position, a thorough assessment of both the anterior and posterior elbow compartments is required. In many patients, more loose bodies are identified at arthroscopy than can be seen on preoperative radiographs.27 Once the patient has been properly positioned, careful palpation of the anatomic structures, particularly the ulnar nerve, is imperative. A dislocated or subluxatable ulnar nerve is present in 16% of the population,5 and care should be taken to ensure that the nerve can be identified in its normal anatomic location. Next, 20 to 30 mL of sterile saline is injected into the joint using the straight posterior or soft spot portal location. Insufflation should continue until some resistance to further fluid injection is felt. Complete filling of the joint with fluid ensures a tight elbow capsule, making joint penetration with the arthroscopic trocar and cannula safer and more reliable. A proximal anteromedial portal is established initially, and thorough arthroscopic assessment of the anterior elbow joint is carried out. Next, a proximal anterolateral portal may be established. On identification of loose bodies, they can be removed using a variety of arthroscopic graspers (Fig. 38-4). Loose bodies can be surprisingly large and may require a bigger grasper. In fact, these loose bodies will often be larger than the plastic cannula used in the procedure. Options for removal of large loose bodies include either breaking

A

B FIGURE 38-2

An anteroposterior (A) and lateral (B) radiograph demonstrating elbow loose bodies.

the loose body into more easily removable fragments or grasping the loose body with a large grasper and backing the cannula out of the elbow while keeping this loose body in contact with the tip of the cannula. Additionally, the arthroscopic camera can be used to help push the grasped loose body out of the opposite side of the elbow. Other tips for removal of loose bodies include “pinning” the loose fragment with a spinal needle to provide resistance for grasping the loose body. Débridement of osteophytes or loose articular fragments, and arthroscopic management of other anterior

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FIGURE 38-5 FIGURE 38-3

Multiple loose bodies identified in the olecranon fossa posteriorly. Small loose bodies may be difficult to visualize radiographically in the olecranon fossa.

FIGURE 38-4

Elbow loose body removal with an arthroscopic grasper.

compartment pathologic conditions may be necessary at the time of loose body removal. Also, inflammatory tissue and reactive synovitis may be present, and synovectomy should be carefully performed as well11,13,20 (Fig. 38-5). However, use of motorized shavers around the anterior capsule can lead to perforation of the capsule and put the neurovascular structures at increased risk

Arthroscopic photograph demonstrating marked synovitis in the anterior compartment of the elbow in a patient with rheumatoid arthritis.

for injury. A thorough synovectomy is important, however, to maximize the outcome of arthroscopic treatment and to help identify loose bodies that can sometimes be obscured by the presence of this synovial tissue. The supplemental use of arthroscopic retractors is valuable and effective in improving visualization during procedures such as synovectomy and in providing additional protection of the capsule and the adjacent neurovascular structures. These retractors can be placed either on the same side as the working portal or opposite that portal depending on the areas to be accessed. In fact, retractors are important to use for a variety of arthroscopic procedures (Fig. 38-6). Blunt-tipped switching sticks and smooth freer elevators can also be used effectively as soft tissue retractors. Following loose body removal and débridement of the anterior compartment, attention is turned to the posterior compartment. Loose bodies or attached fragments of bone are often present in the olecranon fossa. Leaving the inflow anteriorly may help to “flush out” posteromedial gutter or posterolateral gutter loose bodies as well. In addition, “milking” the gutters, which is accomplished by manually pressing against the posterolateral and posteromedial capsule, may allow for the identification of additional loose bodies located here. Thorough arthroscopic visualization and assessment of both the posteromedial and posterolateral gutters helps to ensure that all loose bodies posteriorly are identified. Limited arthroscopic débridement of soft tissue, particularly in the posterolateral gutter, is often required to view all of the articulating surfaces and to identify loose bodies in this area. Finally, as is the case for the anterior compartment, débridement and removal of reactive

Chapter 38 Management of Loose Bodies and Other Limited Procedures

FIGURE 38-6

Arthroscopic retractors can improve visualization and protect the capsule and other structures.

tissue and prominent osteophytes posteriorly is important as well.

OUTCOMES Multiple studies have demonstrated the effectiveness of elbow arthroscopy in the diagnosis and treatment of loose bodies, with success rates of 90% reported.4,16,23 In a review by O’Driscoll and colleagues,26 70% of 71 consecutive elbow arthroscopies were therapeutically beneficial, with loose body removal being the most successful procedure. In fact, all patients with isolated loose bodies benefited from the intervention. However, it is also important to recognize that loose body removal without supplemental arthroscopic management of osteoarthritis has not been found to help patients significantly.23,26,29

ARTHROSCOPIC SYNOVECTOMY Synovectomy of the elbow carried out arthroscopically allows for access to the anterior and posterior compartments while minimizing the iatrogenic insult required with an open approach. It can, however, be difficult to accomplish secondary to thickened reactive synovitis that limits visualization and can obscure intra-articular structures such as the articular cartilage and any loose bodies that may be present as well. Complete synovectomy is often important to achieve and involves the removal of the entire synovium of the elbow joint. The most at risk area intra-articularly is the anterolateral

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inferior capsule adjacent to the radial head as the posterior interosseous nerve (PIN) lies adjacent to the capsule in this area. Arthroscopic synovectomy is usually initiated with the shaver in the anterolateral portal and the arthroscope in the proximal anteromedial portal. A complete synovectomy of the lateral aspect of the joint is then performed. As much synovium as possible should be removed, taking care to avoid damage to the capsule itself. A supplemental arthroscopic retractor placed through a proximal anterolateral area can improve visualization and protect the lateral capsule and PIN. The arthroscope is then switched to the lateral portal, and synovectomy of the medial joint is completed using an arthroscopic shaver in the medial portal. Following synovectomy of the anterior elbow compartment, attention is turned to the posterior compartment. A posterior central portal can be established for visualization, and a posterior lateral portal can be placed that allows the olecranon fossa to be débrided. Maintaining the scope in the posterior central portal, the posterolateral gutter may be débrided of all synovium as well. Finally, the arthroscope can be placed in the posterolateral portal and the shaver placed in the posterior central portal to allow for débridement of the posteromedial gutter. Extreme care should be taken in the posteromedial gutter to avoid damage to the posteromedial capsule and the ulnar nerve adjacent to this capsule. Limited suction should be used in the posteromedial gutter, and the shaver itself should be kept facing away from the capsule when performing a synovectomy in the medial gutter. Also, arthroscopic retractors can aid in visualization and protection posteriorly.

SYMPTOMATIC PLICAE The initial description of elbow snapping caused by a synovial plica was by Clarke in 1988.6 Since that time, the presence of a synovial band or plica adjacent to the radiocapitellar joint has become accepted as a pathologic entity. Little, however, has been published regarding this entity. Antuna and O’Driscoll presented a case series of snapping plicae that represented 8.7% of their arthroscopic elbow procedures performed during a given period.2 Moore, Nirschl, and Stack have all described a synovial fringe excision as part of the operative treatment of lateral epicondylitis.18,22,37 Clarke suggests that a symptomatic synovial plica should be included in the differential diagnosis of tennis elbow or lateral elbow pain.6 Patients with soft tissue impingement due to plicae present with a variety of symptoms. The most dramatic involve a painful locking or catching of the elbow that can be resolved with gentle manipulation. These symptoms can be easily confused with a loose body except

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that the pain is reproducible over the radiocapitellar joint. More subtle presentations are often difficult to distinguish from lateral epicondylitis. On physical examination, a band is sometimes palpable over the lateral aspect of the radiocapitellar joint. This point is slightly more distal than the typical lateral epicondylitis pain. A “flexion-pronation test,” described by Antuna and O’Driscoll,2 can reproduce symptoms and often even reproduces snapping. In this test, the forearm is maximally pronated and passively flexed to 90 to 110 degrees. The snapping can be felt during flexion through this limited arc of motion. Another cause of lateral elbow pain that can simulate a snapping plica is posterolateral rotatory instability, but this pathologic condition is usually characterized by pain with supination while under a valgus load at a flexion angle of about 40 degrees.24

A

SURGICAL INDICATIONS Patients suspected to have a snapping plica unresponsive to nonoperative measures such as activity limitations, nonsteroidal medications, and local injection of corticosteroids can often be treated successfully with arthroscopic débridement and excision of this plica. A systematic assessment of the entire elbow joint is important to avoid overlooking associated lesions or loose bodies. The plica is identified either anteriorly while visualizing through an anteromedial portal or posteriorly by viewing through a posterolateral portal (Fig. 38-7A and B). This lesion can vary from a thin synovial fold to a meniscoid-type band of tissue impinging on the radial head articulating surface. Arthroscopic débridement of this plica requires specific portals that improve access to the lesion. A proximal anteromedial portal is key to viewing the radiocapitellar joint and assessing the plica. A lateral working portal can then be established that allows for excision of the plica. Viewing from a posterolateral portal into the posterolateral gutter affords an excellent view of the plica when it is located posteriorly. The radial head should also be carefully inspected for chondromalacia from the abrading plica. A soft spot portal is usually established to excise the plica as necessary. Postoperatively, patients are generally allowed to resume activities as tolerated, and no formal physical therapy is required.

ARTHROSCOPIC ASSESSMENT OF ELBOW INSTABILITY Bennett and Waris were two of the first investigators to identify problems in the dominant elbows of overhead athletes.35,42 Since these early reports, understanding of

B FIGURE 38-7

A and B, Arthroscopic views of snapping

plica.

medial and lateral elbow instability has advanced significantly. A thorough understanding of the relevant ligamentous anatomy about the elbow is important in assessing and treating patients with instability. The diagnosis of the presence and degree of elbow instability can be difficult even for experienced clinicians. A thorough history and careful physical examination can improve the chances of making an accurate diagnosis, but symptoms and signs are often subtle. Arthroscopic evaluation of the elbow for the presence of either valgus instability due to disruption of the medial ulnar collateral ligament or arthroscopic assessment for posterolateral rotatory instability as a consequence of disruption of the lateral ligamentous structures can be helpful in certain clinical situations. Diagnostic elbow arthroscopy performed as an isolated procedure for the purposes of recognizing instability is rarely, if

Chapter 38 Management of Loose Bodies and Other Limited Procedures

ever, indicated. However, as a surgical adjunct performed in concert with other arthroscopic and/or open surgical procedures, arthroscopic elbow instability assessment can provide valuable information.

MEDIAL INSTABILITY The medial ulnar collateral ligament is composed of an anterior bundle, a fan-shaped posterior bundle, and a transverse ligament that does not contribute to elbow stability35,40 (Fig. 38-8). Disruption of this medial ulnar collateral ligament may be caused by acute or chronic stresses. Overhead throwing regularly subjects the elbow to tremendous valgus forces, and these forces are concentrated on the anterior bundle of the medial ulnar collateral ligament. Undersurface tears of the ulnar medial collateral ligament have been reported, and a sudden valgus stress also can lead to acute rupture of the ligament.38 Such patients often complain of medialsided elbow pain and sometimes complain of crepitation as well. Complaints of instability, however, are unusual. Even in the presence of a complete disruption of the anterior bundle of the medial ulnar collateral ligament, valgus opening of the elbow occurs only to a very limited extent. This makes definitive diagnosis of medial ulnar collateral ligament instability sometimes difficult. The arthroscope has proven itself a valuable tool in identifying patients with complete disruptions of this ligament. Rarely would arthroscopic evaluation for instability be indicated simply to make a diagnosis of valgus instability, but arthroscopic assessment may greatly influence intraoperative decision making. In a cadaveric study, the medial ulnar collateral ligament was not able to be visualized arthroscopically.10 This makes

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direct arthroscopic assessment of the anterior bundle’s integrity difficult, if not impossible. Applying a valgus stress to the elbow, however, can provide for effective indirect arthroscopic evidence of medial ulnar collateral ligament insufficiency. This is accomplished through arthroscopic visualization of the most medial aspect of the anterior ulnohumeral articulation from the anterolateral portal with the elbow flexed 60 to 70 degrees. This test, called the arthroscopic valgus instability test, was first described by Timmerman and Andrews.38,39 In a cadaveric study, an evaluation of this arthroscopic valgus instability test demonstrated that opening of the ulnohumeral joint space of as little as 1 mm can represent a complete disruption of the anterior bundle of the medial ulnar collateral ligament.9 In this study, either 1 or 2 mm of ulnohumeral joint opening was seen even after complete transection of the anterior bundle in a cadaveric model while visualizing the ulnohumeral joint arthroscopically. Also, no opening of the medial ulnohumeral joint was seen before complete release of this ligamentous bundle was carried out. This study demonstrates that very little if any ulnohumeral joint opening is demonstrated arthroscopically until complete disruption of the ligament occurs. It also highlights the fact that when the ligament is completely disrupted, a small but reproducibly measurable amount of ulnohumeral joint opening occurs. As a result, the arthroscopic valgus instability test provides a very sensitive measure of the presence and degree of medial joint opening even when clinical examination reveals subtle or no appreciable opening to valgus stress. Finally, it is also important to note that when no ulnohumeral joint opening occurs at the time of arthroscopic assessment, integrity of the medial ulnar collateral ligament is confirmed (Fig. 38-9).

Ulnar collateral ligaments:

Anterior oblique

Posterior oblique

FIGURE 38-8

Transverse oblique

The components of the medial ulnar collateral ligament include the anterior oblique ligament, the posterior oblique ligament, and the transverse oblique ligament.

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humerus humerus

capsule capsule ulna ulna

FIGURE 38-9

This illustration demonstrates opening of the medial ulnohumeral joint occurring when valgus stress is applied in the presence of complete disruption of the medial ulnar collateral ligament. Visualization is from an anterolateral portal.

LATERAL INSTABILITY In 1991, O’Driscoll et al introduced the term posterolateral rotatory instability (PLRI) to describe elbow instability caused by injury to the radial ulnohumeral ligament (RUHL) or lateral ulnar collateral ligament. Since this original description, the concept of posterolateral rotatory instability has gained much attention. The original report was that of a group of patients who presented with symptoms of valgus instability after trauma but that did not show typical clinical signs of a deficient medial collateral ligament complex. They found that the radial head rotated and subluxated posteriorly when the elbow was forced into valgus from a supinated and extended position and attributed this instability to the incompetence of the posterolateral structures, specifically the radial ulnohumeral ligament. Although these patients had responded poorly to the standard treatment for valgus instability, they improved significantly after plication or reconstruction of this ligament.24 The lateral or radial ligament complex is made up of 4 components; the RUHL, the radial collateral ligament, the annular ligament, and the accessory lateral collateral ligament19 (Fig. 38-10). O’Driscoll and associates have shown that deficiencies of the RUHL and laxity of the lateral capsule allows the proximal radioulnar joint to rotate and the radial head to sublux posteriorly when stressed, leading to posterolateral rotatory instability.27 In patients with this instability pattern, the radial head subluxes, and on rare occasion, can dislocate posteriorly depending on the position of the elbow. With the forearm supinated and slightly flexed, valgus stress

applied to the elbow causes rotation of the ulnohumeral joint, compression of the radiocapitellar joint, and posterior subluxation of the radial head.7,21,24 Symptoms vary from obvious instability complaints to reports of mild pain and discomfort. Occasionally, patients will complain of clicking, popping, snapping, or locking. True dislocations tend to be rare. Rather, patients describe the elbow slipping in and out of joint, particularly when the arm is supinated and slightly flexed.21,24,25,30 Posterolateral rotatory instability may be difficult to diagnose on elbow examination. Differential diagnoses include lateral epicondylitis, radial tunnel syndrome, valgus instability, symptomatic elbow plica, and true radial head dislocation. As in the arthroscopic assessment for valgus instability, the arthroscope can also be used to demonstrate posterolateral rotatory instability. In patients in whom PLRI is suspected, the “pivot shift test” described earlier can be performed while arthroscopically viewing the radiocapitellar joint from the anteromedial portal. The radial head will rotate and translate posteriorly if PLRI is present; with a competent ligament, the radial head will rotate but will not translate36 (Fig. 38-11A and B). Also, while viewing from the posterolateral portal, the radial head can be seen to sublux posteriorly when the pivot shift test is applied or often even with maximum forearm supination. Finally, in the presence of significant posterolateral rotatory instability, the arthroscope can often be easily driven through the lateral gutter and into the lateral aspect of the ulnohumeral joint. Arthroscopic visualization of the presence or absence of posterolateral rotatory instability can greatly influence intraoperative

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Annular ligament

Common extensor tendon

Accessory collateral ligament

Lateral ulnar collateral ligament

FIGURE 38-10 Anatomy of the lateral ligament complex of the elbow. (Lateral ulnar collateral ligament = radial ulnohumeral ligament.)

Radial collateral ligament

C

C

RH RH

A

B FIGURE 38-11 Arthroscopic findings in posterolateral rotatory instability. A, Concentric radiocapitellar joint alignment is seen as viewed from the posterolateral gutter when no stress to the lateral ligament complex is applied. B, Posterior subluxation of the radial head is seen in this same patient with posterolateral rotatory instability when the pivot shift test is applied. C, capitellum, RH, radial head

decision making as it pertains to the possibility of repair or reconstruction of the lateral collateral ligament complex.

SUMMARY The most reliably successful elbow arthroscopic procedure in elbow arthroscopy is loose body removal. Thorough and intimate knowledge of elbow anatomy combined with careful surgical technique can be very effective for patients with these symptomatic loose bodies. Arthroscopic management of the underlying

cause leading to the production of loose bodies is important as well with arthroscopic débridement and synovectomy often required. Recognition that more loose bodies are usually present than are represented radiographically and careful use of proper arthroscopic technique will help improve outcomes and minimize surgical complications. Symptomatic snapping plicae can also be effectively managed using arthroscopic techniques. Recognition of the lesion and differentiation from other more common causes of lateral elbow pain, including lateral epicondylitis, is important. Finally, when not otherwise obvious, the arthroscope can also be used to identify the presence and degree of elbow

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instability, including valgus and posterolateral rotatory instability.

References 1. Andrew, J. R., and Carson, W. G.. Arthroscopy of the elbow. Arthroscopy 1:97, 1985. 2. Antuna, S. A., and O’Driscoll, S. W.: Snapping plicae associated with radiocapitellar chondromalacia. Arthroscopy 17:491, 2001. 3. Bennett, G. E.: Shoulder and elbow lesions of the professional baseball pitcher. J. A. M. A. 117:510, 1941. 4. Boe, S.: Arthroscopy of the elbow: diagnosis and extraction of loose bodies. Acta Orthop. Scand. 57:52, 1986. 5. Childress, H. M.: Recurrent ulnar nerve dislocation at the elbow. Clin. Orthop. Relat. Res. 108:168, 1986. 6. Clarke, R.: Symptomatic, lateral synovial fringe (plica) of the elbow joint. Arthroscopy 4:112, 1988. 7. Cohen, M. S., and Hastings, H. II.: Rotatory instability of the elbow: The anatomy and role of the lateral stabilizers. J. Bone Joint Surg. Am. 79:225, 1997. 8. Commandre, F., Taillan, B., Benezis, C., Follacci, F. M., and Hammou, J. C.: Plica synovialis (synovial fringe plica) of the elbow: report of one case. J. Sports Med. Phys. Fit. 28:209, 1988. 9. Field, L. D., and Altchek, D. W.: Evaluation of the arthroscopic valgus instability test of the elbow. Am. J. Sports Med. 24:177, 1996. 10. Field, L. D., Callaway, G. H., O’Brien, J. S., and Altchek, D. W.: Arthroscopic assessment of the medial collateral ligament complex of the elbow. Am. J. Sports Med. 23:396, 1995. 11. Horiuchi, K., Momohara, S., Tomatsu, T., Inoue, K., and Toyama Y.: Arthroscopic synovectomy of the elbow in rheumatoid arthritis. J. Bone Joint Surg. 84A:342, 2002. 12. Jackson, D., Silvino, N., and Reiman, P.: Osteochondritis in the female gymnast’s elbow. Arthroscopy 5:129, 1989. 13. Lee, P. H., and Morrey, B. F.: Arthroscopic synovectomy of the elbow for rheumatoid arthritis. J. Bone Joint Surg. Br. 79B:770, 1997. 14. Lindenfeld, T. N.: Medial approach in elbow arthroscopy. Am. J. Sports Med. 18:413, 1990. 15. Lynch, G., Meyers, J., Whipple, T., and Caspari, R.: Neurovascular anatomy and elbow arthroscopy: inherent risks. Arthroscopy 2:191, 1986. 16. McGinty, J.: Arthroscopic removal of loose bodies. Orthop. Clin. North. Am. 13:313, 1982. 17. Miller, C. D., Jobe, C. M., and Wright, M. H.: Neuroanatomy in elbow arthroscopy. J. Shoulder Elbow Surg. 4:168, 1995. 18. Moore, M. Jr.: Radiohumeral synovitis: a cause of persistent elbow pain. Surg. Clin. North Am. 33:1363, 1953. 19. Morrey, B. F.: Anatomy of the elbow joint. In Morrey, B. F. (ed.): The Elbow and Its Disorders, 3rd ed. Philadelphia, WB Saunders, 2000, p. 43. 20. Nemoto, K., Arino, H., Yoshihara, Y., and Fujikawa, K.: Arthroscopic synovectomy for the rheumatoid elbow: a short-term outcome. J. Shoulder Elbow Surg. 13:652, 2004.

21. Nestor, B. J., O’Driscoll, S. W., and Morrey, B. F.: Ligamentous reconstruction for posterolateral rotatory instability of the elbow. J. Bone Joint Surg. Am. 74:1235, 1992. 22. Nirschl, R. P., and Pettrone, F. A.: Tennis elbow. J. Bone Joint Surg. Am. 61:832, 1979. 23. O’Driscoll, S. W.: Elbow arthroscopy for loose bodies. Orthopaedics 15:855, 1992. 24. O’Driscoll, S. W., Bell, D. F., and Morrey, B. F.: Posterolateral rotatory instability of the elbow. J. Bone Joint Surg. Am. 73:440, 1991. 25. O’Driscoll, S. W., Jupiter, J. B., King, G. J., Hotchkiss, R. N., and Morrey, B. F.: The unstable elbow. Instr. Course Lect. 50:89, 2001. 26. O’Driscoll, S. W., and Morrey, B. F.: Arthroscopy of the elbow: diagnostic and therapeutic benefits and hazards. J. Bone Joint Surg. 74A:84, 1992. 27. O’Driscoll, S. W., and Morrey, B. F.: Loose bodies of the elbow: diagnostic and therapeutic roles of arthroscopy. J. Bone Joint Surg. 74B(suppl III):290, 1992. 28. O’Driscoll, W. S., and Morrey, B. F.: Arthroscopy of the elbow. In Morrey, B. F. (ed.): The Elbow and Its Disorders, 2nd ed. Philadelphia, WB Saunders, 1993, p. 130. 29. Ogilvie-Harris, D. J., and Schemitsch, E.: Arthroscopy of the elbow for removal of loose bodies. Arthroscopy 9:5, 1993. 30. Osborne, G., and Cotterill, P.: Recurrent dislocation of the elbow. J. Bone Joint Surg. Br. 48:340, 1966. 31. Poehling, G. G., and Ekman, E. F.: Arthroscopy of the elbow. J. Bone Joint Surg. 76A:1265, 1994. 32. Poehling, G. G., and Ekman, E. F.: Arthroscopy of the elbow. Instruct. Course Lect. 44:214, 1994. 33. Poehling, G. G., Ekman, F., and Ruch, D. S.: Elbow arthroscopy: introduction and overview. In McGinty, J. B., Caspari, R. B., Jackson, R. W., and Poehling, G. G. (eds.): Operative Arthroscopy, 2nd ed. Philadelphia, Lippincott, 1996, p. 821. 34. Poehling, G., Whipple, T., Sisco, L., and Goldman, B.: Elbow arthroscopy: a new technique. Arthroscopy 5:222, 1989. 35. Schwab, G. H., Bennet, J. B., Woods, G. W., and Tullos, H. S.: Biomechanics of elbow instability: the role of the medial collateral ligament. Clin. Orthop. Relat. Res 146:42, 1980. 36. Smith, J. P. III, Savoiem, F. H. III, and Field, L. D.: Posterolateral rotatory lateral instability of the elbow. Clin. Orthop. Relat. Res. 20:47, 2001. 37. Stack, J. K., and Hunt, W. S.: Radio-humeral synovitis. Q. Bull. Northwestern Univ. 20:394, 1946. 38. Timmerman, L. A., and Andrews, J. R.: Undersurface tear of the ulnar collateral ligament in baseball players. Am. J. Sports Med. 22:33, 1983. 39. Timmerman, L. A., and Andrews, J. R.: Histology and arthroscopic anatomy of the ulnar collateral ligament of the elbow. Am. J. Sports Med. 22:667, 1994 40. Tullow, G. S, Schwab, G., Bennett, J. B., and Woods, G. W.: Factors influencing elbow instability. Instr. Course Lect. 30:185, 1981. 41. Ward, W. G., Belhobek, G. H., and Anderson, T. E.: Arthroscopic elbow findings: correlation with preoperative radiographic studies. Arthroscopy 8:498, 1992. 42. Waris, W.: Elbow injuries of javelin throwers. Acta Chir. Scand. 93:563, 1946.

Chapter 39 Arthroscopy in the Throwing Athlete

CHAPTER

39

Arthroscopy in the Throwing Athlete Christopher S. Ahmad and Neal S. ElAttrache

INTRODUCTION Throwing places unique demands on the elbow, resulting in predictable injury patterns. Many of these injuries are treated successfully with arthroscopy. Appreciation of elbow biomechanics relevant to throwing assists the clinician in accurate diagnosis, nonoperative treatment, surgical indications, and surgical technique. In the acceleration phase of throwing, the elbow reaches an angular velocity of 3000 deg/sec as it extends from 110 to 20 degrees of flexion, which corresponds to 64N-m valgus torque. The combination of the valgus torque and rapid extension generates three major forces on the elbow: a tensile stress along the medial aspect (ulnar collateral ligament [UCL], flexor pronator mass, medial epicondyle), a shear stress in the posterior aspect (posteromedial tip of olecranon and olecranon fossa), and compression forces in the lateral aspect (radiocapitellar joint). On the medial side, the repetitive tensile forces challenge the ultimate strength of the UCL, creating the well known injury risk to the ligament. Patients who develop valgus instability and continue to throw may initiate and exacerbate pathology in the posterior and lateral aspects of the elbow. In the posterior compartment, throwing repeatedly drives the olecranon into the olecranon fossa. The combination of valgus and extension forces creates shear forces on the medial aspect of the olecranon tip and olecranon fossa may cause injury and development of osteophytes (Fig. 39-1). This constellation of injuries has earned the term “valgus extension overload syndrome.” The relationship between the posterior compartment of the elbow and the UCL is evident in a series of professional baseball players who underwent olecranon débridement. Twenty-five percent of these athletes developed valgus instability and eventually required UCL reconstruction. This observation suggests that both the olecranon and the UCL contribute Portions of this text have been reprinted with permission from Yamaguchi, K., King, G. J. W., McKee, M. D., and O’Driscoll, S. W. M. (eds): Advanced Reconstruction Elbow. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2007, pp 179-184.

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to valgus stability, and the authors believed that they may have missed UCL injuries in many of these patients. A cadaver study supports this theory and has demonstrated that UCL injury results in contact pressure alterations in the posterior compartment that explains the formation of osteophytes on the posteromedial olecranon.1 Another cadaver biomechanical study demonstrated that sequential partial resection of the posteromedial aspect of the olecranon increases elbow valgus angulation.14 Another cadaver study confirmed that strain in the UCL is increased with increasing posteromedial olecranon resection beyond 3 mm.15 These last two studies conclude that overaggressive olecranon resection used to treat posteromedial impingement puts the UCL at risk for injury. In summary, patients with posteromedial impingement pain from valgus extension overload should be critically evaluated for suspected concomitant UCL injuries and avoid overaggressive olecranon resection. In the lateral compartment, compression forces calculated as high as 500 N may result in injuries that has been referred to as radiocapitellar overload syndrome. The syndrome occurs often in combination with medial ligament instability and valgus extension overload. Persistent repetitive radiocapitellar compression may eventually result in chondral or osteochondral fracture and the production of intra-articular loose bodies. In skeletally immature athletes, this is in part the proposed etiology of capitellar osteochondritis dissecans.

VALGUS EXTENSION OVERLOAD Patients report posteromedial elbow pain that occurs during the deceleration phase of throwing as the elbow reaches terminal extension. Patients also report limited extension, which results from impinging posterior osteophytes or locking and catching resulting from loose bodies. Physical examination demonstrates crepitus and tenderness over the posteromedial olecranon, and pain is reproduced when forcing the elbow into extension. Valgus stress testing, milking maneuver, and moving valgus stress tests are important to assess the status of the UCL. Anteroposterior, lateral, oblique, and axillary views of the elbow may reveal posteromedial olecranon osteophytes and/or loose bodies (Fig. 39-2). Magnetic resonance imaging (MRI) can further assess osteophytes and soft tissues (Fig. 39-3). Computed tomography with two-dimensional reconstruction and three-dimensional surface rendering may best visualize the bony pathology in addition to MRI. Surgical treatment is indicated for those patients who maintain symptoms of posteromedial impingement despite nonoperative management. A relative contraindication to performing isolated olecranon débridement

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C

B A

FIGURE 39-1

Throwing creates valgus torque on the elbow that results in (A) medial tension, (B) lateral compression, and (C) posterior shear forces.

FIGURE 39-2

Radiograph demonstrating osteophyte on posteromedial aspect of olecranon.

is the presence of UCL insufficiency. UCL insufficiency may become symptomatic following posteromedial decompression. Therefore, careful history, physical examination, and advanced imaging must be performed to avoid missed UCL injuries or valgus instability. Surgical options include arthroscopic débridement or limited incision arthrotomy to decompress the posterior compartment. Arthroscopy offers the advantages of limited morbidity and complete diagnostic assessment of the elbow. The patient may be positioned supine, prone, or lateral decubitus. If concomitant UCL reconstruction is anticipated, the supine position may be preferred to avoid repositioning of the patient following the arthroscopy. Alternatively, the arthroscopy may be

FIGURE 39-3

Magnetic resonance imaging scan demonstrating osteophyte on posteromedial olecranon.

performed in the lateral position, followed by repositioning and repeat prepping and draping for the UCL reconstruction. Evaluation of the posterior compartment uses direct posterior and posterolateral portals. Diagnostic arthroscopy evaluates presence of osteophytes on the posteromedial aspect of the olecranon, loose bodies, and any evidence of chondromalacia. Figure 39-4 illustrates removal of the olecranon osteophyte with a small osteotome placed at the margin of the osteophyte and normal

Chapter 39 Arthroscopy in the Throwing Athlete

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Postoperative rehabilitation consists of early active elbow flexion and extension exercises. Emphasis is placed on restoring flexor-pronator strength. At 6 weeks, a progressive throwing program is begun. During this time, plyometric exercises and neuromuscular training is enhanced. Endurance exercises are progressed and return to competition is typically achieved at 3 to 4 months postoperatively.

OSTEOCHONDRITIS DISSECANS

FIGURE 39-4

Arthroscopic removal of olecranon osteophytes. Note direct posterior and posterolateral portal placement and ulnar nerve. (Redrawn with permission from ElAttrache, N. S., and Ahmad, C. S.: Valgus extension overload and olecranon stress fractures. Sports Med. Arthrosc. Rev. 11:25, 2003.)

olecranon (Fig. 39-5A). The motorized burr introduced through either the direct posterior portal or posterolateral portal may further contour the olecranon tip, as shown in Figure 39-5B. A lateral radiograph may be obtained intraoperatively to ensure adequate bone removal and that no bone debris remains in the soft tissues surrounding the elbow. It is important to remove only the osteophyte and not normal olecranon to prevent increased strain on the UCL during valgus loading.15 Once the osteophyte has been removed from the olecranon, the trochlea and olecranon fossa should be examined for osteophytes or kissing lesions, which should also be removed. It is important to recognize that the osteophytes occur on both the ulna and the humerus. Some nonthrowing athletes have a major component of direct extension overload without significant valgus stress. For these patients, the risk of developing UCL insufficiency following posterior decompression is much less compared with that of the throwing athletes and, therefore, débridement can be more aggressive, if necessary. Care should be taken to avoid injury to the ulnar nerve, which lies in the cubital tunnel, by avoiding suction and use of burrs adjacent to the nerve, which may wrap up soft tissues. If concern exists for ulnar nerve injury, the nerve should be explored through an open incision and protected during the débridement.

Lesions of the capitellum in young athletes must be differentiated as either Panner’s disease or osteochondritis dissecans (OCD). Panner’s disease is an osteochondrosis of the capitellum, which affects individuals younger than 10 years of age.24 Radiographic features include fissuring, irregularity, and fragmentation of the capitellum. Panner’s disease is usually self-limited and resolves spontaneously with radiographic reossification. In adolescent athletes, OCD is believed to be caused by repetitive radiocapitellar joint compression forces that result in cartilage and bone damage.10,13,25,28 Patients with capitellar OCD typically have a history of repetitive activity, such as throwing or gymnastics. Symptoms include lateral elbow pain associated with loss of motion. Locking and catching suggests the presence of intraarticular loose bodies. Physical examination most commonly demonstrates a 15 to 20 degree flexion contracture with crepitus and tenderness localized to the radiocapitellar joint. Plain radiographs demonstrate fragmented subchondral bone with lucencies and irregular ossification of the capitellum. Loose bodies may also be seen in the elbow joint on plain radiographs. MRI further delineates the avascular segment and loose bodies (Fig. 39-6). Capitellar OCD lesions have been classified based on status and stability of the overlying cartilage.4,9 Initial treatment for all lesions consists of activity modification, avoidance of throwing or other related sports, use of nonsteroidal anti-inflammatory drugs, and occasionally a short period of bracing for acute symptoms. For lesions that do not demonstrate detachment or frank loose bodies, throwing and sports are restricted for 4 weeks. Physical therapy is instituted during this time to regain strength and motion. Following return of strength and motion, a progressive throwing program with proper pitching mechanics instruction is begun. Three to four months is typically required to achieve return to preinjury performance. Surgery is indicated for patients with stable intact lesion in whom nonoperative treatment has failed. Surgical treatment includes diagnostic arthroscopy confirming the stability of the overlying cartilage, followed by drilling of the lesion with a 2-mm diameter smooth pin.

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FIGURE 39-5

Posteromedial impingement. A, Osteotome to remove osteophyte, B, Olecranon tip contoured with motorized burr. (From Ahmad, C. S., and ElAttrache, N. S.: Posteromedial decompression of valgus extension overload syndrome. In Yamaguchi, K., O’Driscoll, S., King, G., and McKee, M. [eds.]: Advanced Reconstruction: Elbow. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2007, p. 56.)

For patients with unstable or detached lesions, surgery is indicated immediately, particularly if mechanical symptoms exist. Diagnostic arthroscopy is performed and the overlying cartilage is assessed. Loose bodies are removed and the cartilage is contoured to a stable rim using shavers and curettes. Antegrade drilling of the lesion is then performed with perforations separated by 2 to 3 mm to introduce marrow elements and create a fibrocartilage healing response. Figures 39-6 to 39-9 depict an MRI scan with a displaced OCD lesion treated with loose body removal and drilling. Mosaicplasty is a technique of multiple osteochondral autograft transfer and is an alternative for large OCD lesions of the capitellum. Osteochondral transfer was first introduced as a treatment in the knee and has demonstrated good results.5,11 Advantages of mosaic-

plasty include ready availability of donor cartilage-bone plugs, ability to cover defects of varying size, and use of native hyaline cartilage containing active, mature chondrocytes. Theoretically, the native articular cartilage used for grafting will function superior to fibrocartilage, which has been shown to have inferior biomechanical properties. For mosaicplasty treatment of the capitellum, a case report and two clinical series using an open approach have reported good results.12,23,31 All-arthroscopic mosaicplasty has been performed by the senior author (NSE) and is indicated for large capitellar lesions that allow the radial head to engage the lesion as observed during arthroscopy. These lesions typically involve the lateral aspect of the capitellum with loss of the lateral buttress to the radial head articulation and occupy greater than 50% of the overall capitellar articular

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Capitellum

FIGURE 39-8

Drilling of osteochondritis dissecans lesion.

Loose body

FIGURE 39-6

Sagittal magnetic resonance imaging scan of grade V capitellar osteochondritis dissecans lesion demonstrating defect in capitellum and loose body posterior to capitellum. (From Ahmad, C. S., and ElAttrache, N. S.: Mosaicplasty for capitellar osteochondritis dissecans. In Yamaguchi, K., O’Driscoll, S., King, G., and McKee, M. [eds]: Advanced Reconstruction: Elbow. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2007, p. 184.)

A

B FIGURE 39-7

Loose body removal from posterior compartment of elbow.

surface. Advanced stages of OCD that involve degenerative changes of the radial head and gross deformity of the capitellum are relative contraindications to mosaicplasty. The surgical technique involves initial standard diagnostic arthroscopy and removal of loose bodies.

FIGURE 39-9

Bleeding confirmed from drill sites.

Visualization of the OCD lesion is then achieved through the midlateral portal. A working portal is created adjacent and slightly lateral to the midlateral portal. The lesion is prepared by shaving loose fragments of cartilage to subchondral bone and establishing healthy stable

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Donor plug

FIGURE 39-10 Recipient tunnel for osteochondral autograft drilled. (From Ahmad, C. S., and ElAttrache, N. S.: Mosaicplasty for capitellar osteochondritis dissecans. In Yamaguchi, K., O’Driscoll, S., King, G., and McKee, M. [eds.]: Advanced Reconstruction: Elbow. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2007, p. 182.)

cartilage borders. The size of the recipient site is determined with a calibrated probe or sizing guides (Arthrex, Inc., Naples, FL) and is typically either 4 or 6 mm. Next, the elbow is positioned in 90 to 100 degrees of flexion and a spinal needle is introduced for an exact perpendicular approach to the lesion. This needle entrance is 3 to 4 cm distal from the midlateral portal and penetrates the anconeus. The recipient site is then drilled creating the desired diameter tunnel according to the osteochondral grafting instrumentation used (Fig. 39-10). The donor osteochondral graft is then arthroscopically harvested from the intercondylar notch of the knee. The osteochondral graft is introduced into the recipient site using the harvester/inserter instrumentation and impacted flush with the surrounding cartilage (Fig. 39-11). Care must be taken to avoid either proud or recessed plugs that will create local increased stress and early cartilage degeneration. It is better to error with the plug slightly recessed than proud.17,18 It is also critical to harvest the donor plug and drill the recipient site exactly perpendicular to the surface to avoid a graft that is nonconforming to the surrounding cartilage. Nonconforming grafts have proud regions and opposite side recessed regions relative to the surrounding cartilage that may result in early cartilage degeneration.17 The process of osteochondral grafting is repeated until the lesion is adequately replaced (Figs. 39-12 and 39-13). If the entire lesion is not resurfaced, the remaining uncovered areas are treated with drilling. Typically two to three

FIGURE 39-11 First osteochondral autograft in place and flush with surrounding articular surface. (From Ahmad, C. S., and ElAttrache, N. S.: Mosaicplasty for capitellar osteochondritis dissecans. In Yamaguchi, K., O’Driscoll, S., King, G., and McKee, M. [eds.]: Advanced Reconstruction: Elbow. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2007 p. 182.)

Donor plug Recipient tunnel

FIGURE 39-12 Recipient tunnel for second osteochondral autograft drilled. (From Ahmad, C. S., and ElAttrache, N. S.: Mosaicplasty for capitellar osteochondritis dissecans. In Yamaguchi, K., O’Driscoll, S., King, G., and McKee, M. [eds.]: Advanced Reconstruction: Elbow. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2007, p. 182.)

plugs are used. Synthetic graft substitutes are alternative sources to fill the recipient sites on the capitellum (OsteoBiologics, Inc., San Antonio, TX). Such substitute plugs are composed of polylactide-do-glycolide copolymer and are available in multiple diameters. These graft sub-

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C

P

A

FIGURE 39-13 Completed mosaicplasty with osteochondral graft plugs indicated. (From Ahmad, C. S., and ElAttrache, N. S.: Mosaicplasty for capitellar osteochondritis dissecans. In Yamaguchi, K., O’Driscoll, S., King, G., amd McKee, M. [eds.]: Advanced Reconstruction: Elbow. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2007, p. 182.)

stitutes are currently under investigation for the treatment of capitellar OCD. The elbow is splinted initially for 7 to 10 days until the portals are healed and sutures are removed at the first postoperative visit. Physical therapy is then instituted to regain range of motion while avoiding strengthening that may compromise the healing. Gentle resistance exercises are initiated at 3 months with greater resistance at 4 months. For throwing athletes, a throwing program is started at 5 months and full effort throwing is achieved at 7 months. Several long-term follow-up studies of patients with capitellar OCD indicate impairment of elbow function. Bauer et al.3 reported a 50% incidence of restricted motion, exertional pain, and radiographic degenerative disease at an average follow-up of 23 years. Similar findings have been observed in other long term followup studies.22,29 Ability to return to competitive sports has been variable in some shorter term follow-up studies,20,30 with other studies demonstrating more favorable return to competitive athletics.4,6-8,19,21,26 No reports are available for all arthroscopic mosaicplasty treatments for capitellar OCD. We have performed seven arthroscopic mosaicplasties for elbow OCD with good to excellent patient satisfaction, and six patients were able to return to preinjury activity. There were no complications. The unsatisfied patient had arthritic

C

R

B FIGURE 39-14 Arthroscopic view of radiocapitellar plica. A, Before excision. B, After excision. C, capitellum; P, plicae; R, radial head. (Reproduced from Ahmad, C. S.: Athletic Injuries and the Throwing Athlete: Elbow. In Galatz, L. M. [ed]: Orthopaedic Knowledge Update: Shoulder & Elbow, 3rd ed. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2007.)

changes involving the radial head and significant deformity of the capitellum that contributed to the poor result.

RADIOCAPITELLAR PLICA Lateral synovial plica in the elbow has been identified as a cause of lateral elbow pain most often observed

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in throwers and golfers. Patients report posterolateral elbow pain associated with clicking or catching. Examination with forced flexion with the forearm pronated reproduces symptoms. Diagnostic arthroscopy demonstrates thickened, hypertrophic lateral synovial plicae, often with adjacent synovitis and capsular inflammation. Some patients also have chondromalacia involving the capitellum and/or the radial head. Arthroscopic removal is depicted in Figure 39-14 and has a high success rate in relieving symptoms.2,16,27

References 1. Ahmad, C. S., Park, M. C., and Elattrache, N. S.: Elbow medial ulnar collateral ligament insufficiency alters posteromedial olecranon contact. Am. J. Sports Med. 32:1607, 2004. 2. Antuna, S. A., and O’Driscoll, S. W.: Snapping plicae associated with radiocapitellar chondromalacia. Arthroscopy 17:491, 2001. 3. Bauer, M., Jonsson, K., Josefsson, P. O., and Linden, B.: Osteochondritis dissecans of the elbow. A longterm follow-up study. Clin. Orthop. Relat. Res. 284:156, 1992. 4. Baumgarten, T. E., Andrews, J. R., and Satterwhite, Y. E.: The arthroscopic classification and treatment of osteochondritis dissecans of the capitellum. Am. J. Sports Med. 26:520, 1998. 5. Bobic, V.: Arthroscopic osteochondral autograft transplantation in anterior cruciate ligament reconstruction: a preliminary clinical study. Knee Surg. Sports Traumatol. Arthrosc. 3:262, 1996. 6. Bojanic, I., Ivkovic, A., and Boric, I.: Arthroscopy and microfracture technique in the treatment of osteochondritis dissecans of the humeral capitellum: report of three adolescent gymnasts. Knee Surg. Sports Traumatol. Arthrosc. 14:491, 2005. 7. Brownlow, H. C., O’Connor-Read, L. M., and Perko, M.: Arthroscopic treatment of osteochondritis dissecans of the capitellum. Knee Surg. Sports Traumatol. Arthrosc. 14:198, 2006. 8. Byrd, J. W., and Jones, K. S.: Arthroscopic surgery for isolated capitellar osteochondritis dissecans in adolescent baseball players: minimum three-year follow-up. Am. J. Sports Med. 30:474, 2002. 9. Difelice, G., Meunier, M., and Paletta, G. J.: Elbow injury in the adolescent athlete. In Altchek, D., and Andrews, J. (eds.): The Athlete’s Elbow. Philadelphia: Lippincott Williams & Wilkins, 2001, p. 231. 10. Douglas, G., and Rang, M.: The role of trauma in the pathogenesis of the osteochondroses. Clin. Orthop. Relat. Res. 158:28, 1981. 11. Hangody, L., Kish, G., Karpati, Z., Szerb, I., and Udvarhelyi, I.: Arthroscopic autogenous osteochondral mosaicplasty for the treatment of femoral condylar articular defects. A preliminary report. Knee Surg. Sports Traumatol. Arthrosc. 5:262, 1997.

12. Iwasaki, N., Kato, H., Ishikawa, J., Saitoh, S., and Minami, A.: Autologous osteochondral mosaicplasty for capitellar osteochondritis dissecans in teenaged patients. Am. J. Sports Med. 34:1233, 2006. 13. Jackson, D. W., Silvino, N., and Reiman, P.: Osteochondritis in the female gymnast’s elbow. Arthroscopy 5:129, 1989. 14. Kamineni, S., Hirahara, H., Pomianowski, S., Neale, P. G., O’Driscoll, S. W., ElAttrache, N., An, K. N., and Morrey, B. F.: Partial posteromedial olecranon resection: a kinematic study. J. Bone Joint Surg. Am. 85-A:1005, 2003. 15. Kamineni, S., ElAttrache, N. S., O’Driscoll, S. W., Ahmad, C. S., Hirohara, H., Neale, P. G., An, K. N., and Morrey, B. F.: Medial collateral ligament strain with partial posteromedial olecranon resection. A biomechanical study. J. Bone Joint Surg. Am. 86-A:2424, 2004. 16. Kim, D. H., Gambardella, R. A., Elattrache, N. S., Yocum, L. A., and Jobe, F. W.: Arthroscopic treatment of posterolateral elbow impingement from lateral synovial plicae in throwing athletes and golfers. Am. J. Sports Med. 34:438, 2006. 17. Koh, J. L., Kowalski, A., and Lautenschlager, E.: The effect of angled osteochondral grafting on contact pressure: a biomechanical study. Am. J. Sports Med. 34:116, 2006. 18. Koh, J. L., Wirsing, K., Lautenschlager, E., and Zhang, L. O.: The effect of graft height mismatch on contact pressure following osteochondral grafting: a biomechanical study. Am. J. Sports Med. 32:317, 2004. 19. Krijnen, M. R., Lim, L., and Willems, W. J.: Arthroscopic treatment of osteochondritis dissecans of the capitellum: Report of 5 female athletes. Arthroscopy 19:210, 2003. 20. Maffulli, N., Chan, D., and Aldridge, M. J.: Overuse injuries of the olecranon in young gymnasts. J. Bone Joint Surg. Br. 74:305, 1992. 21. McManama, G. B. Jr., Micheli, L. J., Berry, M. V., and Sohn, R. S.: The surgical treatment of osteochondritis of the capitellum. Am. J. Sports Med. 13:11, 1985. 22. Mitsunaga, M. M., Adishian, D. A., and Bianco, A. J. Jr.: Osteochondritis dissecans of the capitellum. J. Trauma 22:53, 1982. 23. Nakagawa, Y., Matsusue, Y., Ikeda, N., Asada, Y., and Nakamura, T.: Osteochondral grafting and arthroplasty for endstage osteochondritis dissecans of the capitellum. A case report and review of the literature. Am. J. Sports Med. 29:650, 2001. 24. Panner, H.: An affection of the capitulum humeri resembling Calvé-Perthes’ Disease of the hip. Acta Radiol. 8:617, 1927. 25. Ruch, D. S., and Poehling, G. G.: Arthroscopic treatment of Panner’s disease. Clin. Sports Med. 10:629, 1991. 26. Ruch, D. S., Cory, J. W., and Poehling, G. G.: The arthroscopic management of osteochondritis dissecans of the adolescent elbow. Arthroscopy 14(8):797-803, 1998. 27. Ruch, D. S., Papadonikolakis, A., and Campolattaro, R. M.: The posterolateral plica: a cause of refractory lateral elbow pain. J. Shoulder Elbow Surg. 15:367, 2006. 28. Singer, K. M., and Roy, S. P.: Osteochondrosis of the humeral capitellum. Am. J. Sports Med. 12:351, 1984. 29. Takahara, M., Ogino, T., Sasaki, I., Kato, H., Minami, A., and Kaneda, K.: Long term outcome of osteochondritis dissecans of the humeral capitellum. Clin. Orthop. Relat. Res. 363:108, 1999.

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30. Tivnon, M. C., Anzel, S. H., and Waugh, T. R.: Surgical management of osteochondritis dissecans of the capitellum. Am. J. Sports Med. 4:121, 1976. 31. Yamamoto, Y., Ishibashi, Y., Tsuda, E., Sato, H., and Toh, S.: Osteochondral autograft transplantation for osteochon-

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dritis dissecans of the elbow in juvenile baseball players: minimum 2-year follow-up. Am. J. Sports Med. 34:714, 2006.

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CHAPTER

40

Arthroscopic Management of the Stiff Elbow Felix H. Savoie III and Larry D. Field

INTRODUCTION Arthroscopic management of the stiff elbow has now progressed to become the operative treatment of choice in most cases. The stiff elbow includes both the arthritic elbow with ulnohumeral, radiocapitellar, and proximal radioulnar joint deterioration, as well as those with loss of motion due to post-traumatic capsular contracture, intra- and periarticular adhesions and arthrofibrosis. These contractures and adhesions may occur after trauma, surgery, or systemic disease. This chapter addresses both management of the arthritic elbow and the arthrofibrotic elbow. Although each disorder may present as a stiff elbow, the etiology and management is different. Therefore, each disorder is discussed in separate subsections.

THE NONARTHRITIC STIFF ELBOW PATHOLOGY OF ELBOW STIFFNESS (ARTHROFIBROSIS) Arthrofibrosis of the elbow is defined as a loss of both extension and flexion of the elbow due to intrinsic and extrinsic abnormalities produced by fractures, dislocations, arthritic conditions, burns, head injury, or cerebral palsy.5,13,24,49,52,55 Intrinsic factors include intra-articular damage, fractures, loose bodies, synovitis, and foreign bodies whereas extrinsic factors include contractures due to scarring of the capsule or collateral ligaments, flexor or extensor musculature, instability, heterotopic bone, and skin contractures. Peripheral problems including head injuries, cerebral palsy, and neurologic dysfunction may also result in muscular contracture and spasticity with resultant loss of motion. In managing a patient with contracture of the elbow, all etiologies must be considered before treatment. Patients with skin contracture or muscle spasticity must obviously be managed in a different fashion from those

with intra-articular fracture or arthritic conditions. Commonly, more than one problem is involved in producing a stiff elbow. Each should be evaluated and managed appropriately. Arthroscopic treatment of flexion contracture of the elbow allows the surgeon to address the intrinsic intra-articular causes of elbow contracture, as well as those extrinsic causes that may be safely reached by this technique, including capsular and collateral ligament damage as well as problems with the extensor musculature. The risk of nerve injury, including posterior interosseous nerve and ulnar nerve injury, is real in these stiff elbows and should be considered by the operative surgeon before undertaking arthroscopic management of this condition. Additionally, in the most contracted elbows, the restoration of motion may also produce late problems with the surrounding nerves, specifically the ulnar nerve. This complication of tardy ulnar nerve palsy may be prevented by arthroscopic or open ulnar nerve release at the time of the index surgery to restore motion (Box 40-1).

HISTORY OF ARTHROSCOPIC MANAGEMENT OF THE STIFF ELBOW In 1931 and 1932, Burman6,7 described the use of the arthroscope in cadaveric elbow specimens. The use of arthroscopic techniques for the elbow lagged behind the knee and shoulder until the 1980s, during which time Andrews and Carson2 and Poehling et al48 reported on techniques for supine and prone arthroscopy. The 1990s brought about more work in elbow arthroscopy, with pioneering articles presented by O’Driscoll and Morrey, Baker, and McGinty.3,45 The first reports on the arthroscopic treatment of stiff elbows were by Nowicki and Shall,44 Jones and Savoie,27 and Byrd9 in the early 1990s. As techniques evolved, more reports by Kelly et al, Timmerman and Andrews, Ball et al and numerous others were presented.4,29,61 The works of O’Driscoll and Savoie spearheaded the advance of improved safety and surgical techniques that led to both improved results and expanded indications. Sporadic reports of neurologic injuries have occurred, emphasizing the need for caution and experience when dealing with these difficult problems.19,27,39

INDICATIONS FOR TREATMENT Loss of motion of the elbow may cause significant morbidity.16,65 The American Academy of Orthopaedic Surgeons defines normal flexion of the elbow as 0 to 146 degrees of flexion.65 In 1981 Morrey et al42 defined a functional arc of motion of the elbow as 30 to 130 degrees of flexion. This 100-degree arc of motion is the arc in which most activities of daily living (ADLs) are performed, and motion less than this results in an

Chapter 40 Arthroscopic Management of the Stiff Elbow

Indications for Exploration of the Ulnar Nerve (Arthoscopic or Open)

BOX 40-1

1. 2. 3. 4.

Preoperative ulnar nerve symptoms Narrowed cubital tunnel due to spurs/loose bodies. Previous ulnar nerve surgery of unknown type. Preoperative arc of motion of 30 degrees or less or lack of flexion past 90 degrees (increased risk of tardy ulnar nerve palsy once motion is restored).

inability to perform even minimal ADLs. Certain activities may require more motion, including tying shoes, eating, personal hygiene, and sporting activities. Treatment is indicated for those contractures with a loss of extension of 30 degrees of motion, a loss of flexion of similar nature, and in those patients in whom a greater range of motion is required. As in all areas of the body, pain and functional impairment refractory to nonoperative management represent the primary indication for surgical treatment.

ANATOMIC CONSIDERATIONS The altered anatomy of the contracted elbow joint makes a thorough understanding of the pathogenesis of contracture and how the anatomy is altered of paramount importance to the surgeon. Because the contracted joint does not distend normally with inflow, neurovascular structures about the elbow may not be safely displaced from the joint during insufflation. The medial epicondyle and medial intramuscular septum are usually preserved in most cases and are used as a guide to the initial entrance to the elbow joint. The proximal anteromedial portal is generally made in an outside-in manner and kept superiorly and also posterior to the entirety of the brachialis muscle because this approach provides an extra margin of safety that protects the median nerve and brachial artery from possible damage. Distal lateral elbow trauma or contracture may cause hypertrophy or adhesions that may bind the posterior interosseous nerve, increasing the risk of damage from a primary lateral portal. Using the insideout technique with an anterior superior lateral portal decreases the risk of injury to this structure. Unlike a normal elbow, portal establishment in a contracted elbow joint requires cautious and careful placement of the canula, not only through the skin, but during joint entrance to prevent misdirection by the hypertrophied tissue with resultant soft tissue injury. In severe cases, it may be necessary to develop the tissue plane between the brachialis muscle and the capsule, and secondarily incise and then excise the capsule. It is essential that the

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anterior neurovascular structures and brachialis muscle be protected by retractors if this approach is attempted. Posteriorly, an adherent medial capsule or extensive olecranon deformity may displace the ulnar nerve, making the initial insertion through a posterior central portal into the olecranon fossa an increased risk. In these cases, it is essential to insert the canula directly into the olecranon fossa and avoid medial displacement that may put this neurologic structure at risk. During the capsular release and excision, the surgeon must remember the relationship of the capsule to the neurovascular structures. In the anterior procedures, the brachialis muscle lies between the capsule and the anterior neurovascular structures (median nerve, radial nerve, and brachial artery). Thus, arthroscopic capsular release and excision should be continued from within the joint until brachialis muscle fibers are visible but no further. Shaver blades and cutting instruments must be kept in close proximity to the humerus at all times to avoid straying too far anteriorly and potentially into the neurovascular structures by brachialis muscle penetration. Using accessory anterior portals to place protective retractors to hold the brachialis muscle and anterior neurovascular structures away from the operative field is helpful in preventing potential complications. On the lateral aspect of the elbow, the radial nerve courses between the brachioradialis and brachialis muscles. It divides into the superficial radial nerve and the posterior interosseous nerve at the level of the elbow joint. The posterior interosseous nerve courses distally and laterally to the brachialis muscle, and becomes immediately adjacent to the anterior joint capsule in the distal half of the elbow. Scar tissue and hypertrophied joint capsule from injury to this area may tether the posterior interosseous nerve and allow damage to it during release. In these cases, the nerve should be identified by the perineural fat and retracted before continuing the excision distally. Until the location of the nerve is identified, extension of the capsular excision should remain proximal to the radial head. Posteriorly, the ulnar nerve should be identified and protected throughout the procedure. This may be accomplished arthroscopically by incising the capsule under the nerve, locating it, and retracting it, or by a small open incision over the nerve to do the same.

ETIOLOGY The loss of motion in arthrofibrosis centers around soft tissue trauma,62 an injury, or a disease process that produces a synovitic reaction, hemorrhage, and inflammation of the capsule. In arthrofibrosis, the capsular tissues respond to this by thickening and becoming rigid. Attempts to aggressively stretch the capsule produces tearing, creating more hemorrhage and increased stiff-

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ness. The elbow is held in a flexed position to accommodate the hemarthrosis and the painful swelling in the capsular tissues. Physical therapy and splinting in this inflammatory phase may actually result in worsening conditions rather than improvement because of the repeated damage inflicted upon the capsule. Collateral ligament injury can further contribute to elbow contracture by allowing abnormal movement, producing further pressure on the damaged capsule.8,18,40,62 Additional problems occur with the scarring between the triceps tendon and the humerus, restricting flexion and extension by its tethering effect. This effect is more noticeable in the post-traumatic contractures and seems to be especially prevalent after open reduction internal fixation of periarticular fractures of the elbow. Post-traumatic arthrofibrosis of the elbow may also be secondary to other intra-articular causes. Fractures and osteochondral lesions, articular incongruities, loose bodies, and foreign material may stimulate an inflammatory response in the capsule and result in a mechanical limitation to elbow motion. On the lateral side of the joint, this is often caused by residual deformity in the capitellum, radial fossa, or radial head following osteochondritis or trauma.26 On the medial side of the joint, a more congruous relationship of articular surface exists. Less severe injures to the coronoid or olecranon may produce bony incongruity, resulting in a painful arc of motion and subsequent loss of motion. The specific components of arthrofibrosis may vary according to the mechanism of injury and postinjury treatment.50,60 Each factor must be considered in managing the arthrofibrotic elbow.

NONOPERATIVE MANAGEMENT Management options for the contracted elbow include both conservative and surgical management. All patients with this disorder should undergo an extended trial of nonoperative therapy before surgery is considered. Selective Celestone injections, protected range of motion using a double-hinged elbow brace, and physical therapy including gentle stretching, icing, and joint mobilization, may prove to be beneficial.11,17 Static splinting is often helpful in obtaining a function arc of motion in the elbow. Caution should always be exercised during therapy to prevent additional capsular damage and worsening of the arthrofibrotic condition.

INDICATIONS FOR SURGERY Surgical treatment is indicated for those patients who are refractory to conservative management. Both the surgeon and patient should play an active role in the decision to undergo surgical management of the stiff elbow. The etiology of the condition, potential risks,

expected results, and possible complications, including the risk of nerve damage, should be understood by both the surgeon and the patient before undertaking operative intervention. In the past, several authors have described open surgical release techniques for correction of elbow flexion contractures. These techniques include osteotomy of the medial epicondyle with complete anterior capsulectomy and lengthening of the biceps, limited lateral approach with capsulotomy, limited medial approach, and extensive posterior approach.16,65 Urbaniek and associates64 found a decrease in preoperative flexion contracture from 48 to 19 degrees with a lateral approach. Husband and Hastings25 found extension improved from a mean of 45 degrees preoperatively to 12 degrees postoperatively and flexion increased from 116 degrees to 129 degrees. Open surgical release of elbow flexion contracture produces increased soft tissue trauma from the dissection, postoperative scarring of the capsule and anterior structures that may add to the risk of contracture recurrence, and additional elbow trauma above and below the elbow when an external fixator is used. Potentially increased time before physical therapy may be initiated due to surgical pain and scarring. Additionally, it is difficult to address the entire intrinsic joint pathology without a combined approach of the elbow. In contrast to open release techniques, the arthroscopic release allows the surgeon a complete examination and treatment avenue for intrinsic, intra-articular joint pathology. Removal of intra-articular adhesions, release of associated scarring, and capsular resection anteriorly and posteriorly can all be accomplished arthroscopically. Evaluation, management, and release of medial and lateral gutter adhesions, as well as collateral ligament release, can also be accomplished arthroscopically, reducing the risk of recurrence and allowing early initiation of a physical therapy program. The main contraindication to capsular release for arthrofibrosis is a lack of experience with elbow arthroscopy. This procedure can be extremely difficult with a high risk of nerve injury and should be attempted only by experienced arthroscopic surgeons.

SURGICAL TECHNIQUE: AUTHORS’ PREFERRED METHOD The arthroscopic setup for surgical release of the elbow flexion contracture is that of a standard elbow arthroscopy (Box 40-2). A 4.5-mm arthroscope and shaver are used along with standard camera and video recording equipment. We prefer the prone position because it allows better access to both the anterior and posterior capsular structures, but certainly either the lateral decubitus or supine position can be used at the surgeon’s

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Steps in Arthroscopic Management of the Arthrofibrotic Elbow

BOX 40-2

1. Diagnostic arthroscopy 2. Anterior débridement a. Resect coronoid, if necessary b. Remove adhesions 3. Proximal capsular resection a. Medial septum to lateral septum b. Expose brachialis c. Retract brachialis and neurovascular structures d. Complete excision of capsule with nerves and artery protected by both retractors and brachioradialis 4. Olecranon fossa débridement a. Elevate triceps tendon 5. Resect olecranon tip 6. Medial gutter débridement: expose and protect ulnar nerve if necessary 7. Lateral gutter débridement: look for loose bodies 8. Olecranon fossa fenestration, if indicated

preference. In patients in whom there is quite a bit of scarring around the ulnar nerve or the posterior interosseous nerve, each of these may be approached through a small incision and a Penrose drain used to surround the nerve before attempting arthroscopy to protect the nerve from possible intraoperative damage. Indications for doing this include anteriorly displaced radial head fractures and anterior heterotopic bone for the posterior interosseous nerve, and large osteophytes and extraarticular fragments over the ulnar nerve. If this is deemed necessary by the preoperative evaluation, the posterior interosseous nerve (PIN) is approached through the transbrachioradialis approach of Lister with minimal damage to the surrounding musculature. The ulnar nerve is approached through a small incision posterior to the medial epicondyle. In each case, the arthroscopy can still be accomplished but with an increased margin of safety. The author usually prefers to attempt to expose the nerve arthroscopically in most cases but will use one of the above-mentioned approaches immediately if there is any distortion of normal anatomy near the normal course of the nerve. The initial attempt to insufflate the elbow is made through a standard soft spot portal, entering the joint between the radial head, capitellum, and ulna. A proximal anterior medial portal is then established using a blunt trocar only. The arthroscope is introduced through this canula, and the anterior compartment of the elbow is evaluated (Fig. 40-1). A proximal anterolateral portal is then established via an outside-in technique. The use of proximal portals to begin the procedure adds an

FIGURE 40-1

This view from the proximal anterior medial portal demonstrates the anterior compartment of the elbow with the damaged, contracted anterior capsule.

anatomic protective factor to assist in the prevention of inadvertent neurologic damage. The more distal anterior lateral and anterior medial portals may be established once the joint and anatomy are better defined. These are useful for both retraction and for protection. Débridement of the anterior structures is then accomplished and an anterior capsular excision is performed (Fig. 40-2A to D). Excision of the capsule usually begins with the shaver in the medial portal. The capsule is excised beginning with the humeral attachment and continuing distally while remaining on the medial side of the joint until brachialis muscle fibers can be visualized (see Fig. 40-2A and B). The dissection progresses back toward the medial septum until the flexor pronator origin can be seen. The excision then continues laterally to the radial side of the joint. The scope is then placed in the medial portal and similarly from proximal to distal the capsule is excised to the lateral extensor muscle origin (see Fig. 40-2A to D). On completion of the anterior capsulectomy, the brachialis muscle should be visualized from the lateral to the medial intermuscular septum. Extension of the elbow is attempted, and range of motion is evaluated. The bone architecture is then reassessed for the need to restore the radial fossa, excise the radial head or excise part of the coronoid (see section on arthritis for the specifics of these techniques). The arthroscope is then transferred to a posterior central and proximal posterolateral portal (Fig. 40-3A and B). The triceps is elevated off the distal humerus, and the olecranon fossa is débrided (Fig. 40-4). An ulnohumeral arthroplasty may be performed at this

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Anterior capsular release

A

B

C

D

FIGURE 40-2

E

Septum to septum release

Steps in the anterior compartment of the elbow during capsular release. A, The anterior capsule is incised, and the release is begun adjacent to the humerus. B, As the release begins, the brachialis fibers begin to be seen through the capsule. C, As the release continues, the proximal aspect of the anterior capsule is excised. The humerus, brachialis, and capsule can all be well visualized. D, On completion of the release and partial excision of the proximal aspect of the capsule, the brachialis muscle should be well visualized from medial to lateral across the anterior aspect of the elbow. It can then be retracted, protecting the neurovascular structures and the rest of the capsule is removed. E, The radial fossa must be reestablished in the post-fracture elbow. The excess bone above the articular cartilage edge of the capitellum must be removed until the normal cortex or normal contour is restored.

Chapter 40 Arthroscopic Management of the Stiff Elbow

601

A FIGURE 40-4

During the posterior capsular débridement, the triceps muscle is elevated off the humerus proximal to the fossa. This improves visualization of the posterior elbow and also assists in the restoration of elbow flexion.

POSTOPERATIVE MANAGEMENT

B FIGURE 40-3

A, A degenerative olecranon tip producing posterior impingement. B, The tip of the olecranon after débridement and partial resection.

Continuous passive motion (CPM) is initiated in the recovery room and continued for approximately the first 3 weeks. Compressive cryotherapy is used on a daily basis beginning postoperative day 1 as well. Physical therapy is started the day of surgery for aggressive stretching and strengthening of the elbow. The patient is encouraged to use the arm as aggressively as possible in the immediate postoperative period. Physical therapy is performed daily for 3 weeks and three times per week thereafter. Static splints are used beginning in week 1 if full motion is not obtained by the therapist.

RESULTS point, connecting the olecranon and coronoid fossa to allow improved flexion and extension and to diminish the risk of recurrent stiffness (Fig. 40-5). The medial gutter is then débrided of all loose bodies, joint adhesions, and osteophytes while protecting the ulnar nerve (Fig. 40-6A). The more severe the preoperative stiffness, the more necessary it may be to expose the ulnar nerve, either arthroscopically (see Fig. 40-6B) or open. The lateral gutter is then débrided as well, the posterolateral plica excised and synovitis, which is common in this area, also removed (Fig. 40-7A and B). Motion is then attempted again, and at this time, full flexion and extension should have been achieved. A drain is then inserted anteriorly, a pain pump is inserted posteriorly, and the patient is placed in a soft dressing.

The arthroscopic management of arthrofibrosis has continued since the initial report by Jones and Savoie.27 Extension of the elbow increased from 46 degrees to 5 degrees, and flexion increased 96 degrees to 138 degrees. Recent reports by Timmerman et al,61 Lapner et al,31 Ball et al,4 and Nguyen et al43 have described the effectiveness of the arthroscopic management of the stiff elbow. In most cases, it would appear to be an effective tool in the treatment of this disorder.

COMPLICATIONS In the authors’ initial series, there was a single isolated nerve injury, which was case 12. However, reports by Haapaniemi19 and Miller39 have delineated the further

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A

Ulnohumeral arthroplasty

B FIGURE 40-5

An arthroscopic ulnohumeral arthroplasty is performed by drilling a center hole to connect the olecranon and coronoid fossa. The drill hole is then enlarged using an arthroscopic burr to a diameter of 1 to 2 cm.

risk of nerve damage. Morrey et al have also presented the risk of elbow arthroscopy in the Mayo Clinic series. They described no permanent neurologic injuries, and had an overall complication rate of approximately 10%, a level that parallels our own experience.29

THE ARTHRITIC ELBOW NONOPERATIVE MANAGEMENT Nonoperative management includes use of selected Celestone injections and nonsteroidal anti-inflammatory medications and physical therapy. Surgical treatment is indicated only when nonoperative management becomes

A

B FIGURE 40-6

A, The medial gutter of the elbow is débrided with the shaver in the posterior central portal and the scope in the posterolateral portal. B, The ulnar nerve should be carefully protected during arthroscopic posterior medial gutter surgery.

ineffective and the patient’s pain and functional limitations warrant surgical intervention.*

INDICATIONS FOR SURGERY Pain and functional impairment refractory to nonoperative management would indicate surgery for the arthritic elbow. The age, activity level, patient desires, bone stock, and severity of the deformity dictate the choice between arthroscopic management and total elbow arthroplasty.10,22,56,57

* See references 1, 2, 10, 12, 14, 15, 19–23, 27, 29, 30, 32-37, 46, 47, 51, 53, 54, 56-59, 63, 66, and 67.

Chapter 40 Arthroscopic Management of the Stiff Elbow

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C RH

O

A

B FIGURE 40-7

A, In the stiff elbow, the posterolateral plica is often enlarged and fibrotic. This area is also often the site of loose bodies and adhesions. All of this should be removed during surgery. B, These contractures are débrided in the posterolateral gutter using a combination of a posterolateral portal and a soft spot portal.

SURGICAL MANAGEMENT—HISTORY Modern nonprosthetic operative management for arthritis of the elbow dates back to the OuterbridgeKashiwagi procedure.28 Through a triceps-splitting approach, the olecranon is débrided and a clower drill is used to bore a hole between the olecranon and coronoid fossa, improving both flexion and extension and decreasing symptoms of anterior and posterior impingement. In inflammatory arthritis, resection of the radial head has proved to be beneficial, especially in patients with rheumatoid arthritis. Morrey modified the Outerbridge-Kashiwagi procedure by using a Bryan-Morrey approach and elevating the triceps rather than splitting it, believing that this decreased intra-articular adhesions and improved range of motion while allowing transposition of the ulnar nerve.40 Savoie et al54 modified Morrey’s approach to perform the procedure arthroscopically and used the arthroscopic instruments to fenestrate the olecranon and coronoid fossa, resect the radial head as necessary, and remove loose bodies and perform synovectomy with excellent results with a minimum 2-year follow-up. Cohen et al10 reported on 26 patients managed arthoscopically with excellent pain relief and no complications. Phillips and Strasburger47 reported on 25 patients with similar results. McLaughlin et al37 reported on a group of 36 patients with primary radial sided initiation of damage who responded well to arthroscopic management, including radial head excision in all patients. They isolated a group that they thought were more at risk for early progression of the arthritis and suggested the benefit of earlier excision due to deformity and slight instability. These reports seem to indicate the enduring

Steps in the Management of the Arthritic Elbow

BOX 40-3

1. Anterior Compartment Evaluation a. Resect coronoid spurs b. Assess/restore radial fossa c. Radial head excision if necessary 2. Posterior Compartment Evaluation a. Elevate triceps tendon b. Débride olecranon fossa/fenestration of fossa c. Resect olecranon tip 3. Medial Gutter Débridement a. Retract ulnar nerve b. Remove spurs and loose bodies c. Find, explore, and release ulnar nerve, if necessary 4. Lateral Gutter Débridement a. Excise plica b. Remove posterior radiocapitellar spurs c. Re-evaluate radial head excision and proximal radioulnar joint

success of the arthroscopic method for early and midstage arthritis and even late-stage arthritic changes in the more active individual in whom an elbow replacement might be contraindicated.

SURGICAL TECHNIQUE: AUTHORS’ PREFERRED METHOD The elbow is entered through a standard proximal anterior medial portal (Box 40-3). The proximal anterolateral portal is established, and the anterior aspect of the elbow

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joint is evaluated. The tip of the coronoid is evaluated and usually resected (Fig. 40-8A and B). The radial head and radial fossa are evaluated for anterior impingement with flexion. The preoperative evaluation should have formulated a plan as to whether or not the radial head needs to be excised. McLaughlin et al have reported on a subset of post-traumatic arthritic patients in whom the radial column is the initiating factor in the arthritis. In this group, they believed that radial head excision was necessary to prevent progression of the arthritis and also to prevent posterior radiocapitellar impingement that limited extension. In the more common primary arthritic elbow, the radial head may be preserved and only the radial fossa débrided to increase flexion. It is important to make this distinction preoperatively. Radial fossa excision is accomplished with the arthroscope in

A

B FIGURE 40-8

A, In the arthritic elbow, the coronoid may be grossly deformed preventing flexion. B, This gross deformity of the coronoid tip should be excised until impingement on the trochlea that prevents flexion no longer occurs.

the proximal anterior medial portal and the shaver in the proximal anterior lateral portal. The excess bone just above the articular rim of the anterior capitellum is removed until the normal cortex is encountered. Flexion of the elbow determines if enough bone has been resected to allow full excursion of the radio-capitellar joint. If radial head excision is necessary, the anterior aspect of the radial head is resected first in order to avoid penetrating the anterior capsule with possible injury to the posterior interosseous nerve (which lies adjacent to the anterolateral capsule at the level of the radial head and neck). Once the radial head anterior margin has been resected, a protective retractor is placed in the proximal anterior lateral portal to sit between the radial head and the anterior capsule to retract and protect the radial nerve. The burr is then introduced through the soft spot portal, and the radial head is coplaned until a complete resection has been accomplished (Fig. 40-9A and B). In the case of isolated radiocapitellar impingement, the proximal 8 to 10 mm of the radial head may be resected and if the proximal radioulnar joint is involved, the entire radial head can be resected (see Fig. 40-9C). The surgical focus is then moved to the posterior elbow joint. An inflow canula is left anteriorly to ensure that fluid flows through the gutters and into the posterior compartment. A straight posterior viewing portal is established and also an accessory posterior lateral instrument portal. The olecranon fossa is débrided and three 5-mm drill holes are placed in the olecranon fossa, connecting it to the coronoid fossa. These holes are connected using a burr and enlarged until a fenestration of approximately 1 to 3 cm in diameter is made. This should allow visualization of the anterior structures through the fenestration and evaluation of the coronoid resection can be made. If necessary, additional resection can be accomplished while viewing from this portal. The tip of the olecranon is then excised. Care should be taken to plane medially and laterally to prevent impingement of the medial and lateral aspects of the olecranon on the columns of the distal humerus. In most cases, it is this medial and lateral impingement that limits the extension, not the center of the olecranon. The resection for arthritis might include as much as 1 to 2 cm. This is in contrast to cases with instability, in which only minimal bone should be removed to decrease the risk of exacerbating the instability. Medial gutter spurs are then resected with the suction turned off to prevent injury to the ulnar nerve. The presence of significant spurs may require release of the ulnar nerve by either open or arthroscopic (Fig. 40-10) means. If there is any question, the nerve should be exposed and tracked with the arthroscope or via open technique to both decompress the nerve and decrease the risk of tardy ulnar

Chapter 40 Arthroscopic Management of the Stiff Elbow

605

C A

FIGURE 40-9

B

A, In the arthritic elbow, the radial head may be remarkably deformed in both the radiocapitellar joint and the proximal radioulnar joint. B, In cases of radiocapitellar impingement, the radial head can be coplaned and excised for a distance of approximately 6 mm to allow clearance of this joint without affecting the proximal radioulnar joint. C, In cases in which the proximal radial ulnar joint is also involved, the entire radial head can be excised down to the radial neck.

nerve palsy. The lateral gutter is then evaluated and any debris removed. If a symptomatic posterolateral plica is present, it is resected. This area of the posterior radiocapitellar joint and proximal radioulnar joint is a common area for loose bodies and for synovitis. It must be evaluated in every case. The entire elbow joint is then re-evaluated, completing the procedure.

POSTOPERATIVE COURSE

FIGURE 40-10 The arthroscopic view of the ulnar nerve (UN) during its release in a degenerative elbow.

The patient is started on immediate continuous passive motion in the recovery room. Physical therapy is initiated on postoperative day 1, and the patient is allowed to resume activities as tolerated. Early and rapid use for normal ADLs is encouraged. Compressive cryotherapy is used at night to decrease edema and assist with improved function and pain control.

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RESULTS In a previous study, Nunely et al54 delineated approximately 96% good to excellent results and a minimum 2-year follow-up for the arthritic elbow. This is in a degenerative population in which two thirds of the patients required radial head excision, indicating the efficacy of this procedure for the arthritic elbow. McLaughlin and colleagues37 reported a series of degenerative elbows managed by this technique in which the instigating factor for the arthritis was a radial column injury. Satisfactory results were reported in 36 patients, with no significant complications. Cohen et al,10 MenthChiari et al,38 Phillips and Strasburger,47 and Kim and Chin30 reported excellent results with no significant complications in their series of patients. In combining these series, the average arc of motion improved between 41 and 81 degrees, with a significant decrease in pain and improvement in function.

COMPLICATIONS Most complications involve the presence of persistent drainage from the lateral portals. Recent reviews from the Mayo Clinic and the Mississippi Sports Medicine and Orthopaedic Center (MSMOC) of large series of patients fortunately revealed no permanent neurologic injuries. However, in both series, the overall complication rate was 10%, emphasizing the risks inherent in arthroscopy of the elbow.29,53

References 1. Aldridge, J. M. III, Atkins, T. A., Gunneson, E. E., and Urbaniak, J. R.: Anterior release of the elbow for extension loss. J. Bone Joint Surg. Am. 86:1955, 2004. 2. Andrews, J. R., and Carson, W. G.: Arthroscopy of the elbow. Arthroscopy 1:97, 1985. 3. Baker, C. L. Jr, and Jones, G. L.: Arthroscopic of the elbow. Am. J. Sports Med. 27:251, 1999. 4. Ball, C. M., Meunier, M., Galatz, L. M., Calfee, R., and Yamasuchi, K.: Arthroscopic treatment of post traumatic elbow contracture. J. Shoulder Elbow Surg. 11:624, 2002. 5. Bede, W. B., Lefebvre, A. R., and Rosman, M. A.: Fractures of the medial humeral epicondyle in children. Can. J. Surg. 18:137, 1975. 6. Burman, M. S.: Arthroscopy or the direct visualization of joints. A cadaveric study. J. Bone Joint Surg. 13:669, 1931. 7. Burman, M. S.: Arthroscopy of the elbow joint: An experimental cadaveric study. J. Bone Joint Surg. 14:349, 1932. 8. Buxton, J. D.: Ossification in the ligaments of the elbow. J. Bone Joint Surg. 20:709, 1938. 9. Byrd, J. W.: Elbow arthroscopy for arthrofibrosis after Type I radial head fractures. Arthroscopy 10:162, 1994.

10. Cohen, A. P., Redden, J. F., and Stanley, D.: Treatment of osteoarthritis of the elbow: A comparison of open and arthroscopic debridement. Arthroscopy 16:701, 2000. 11. Dickson, R. A.: Reverse dynamic slings. A new concept in the treatment of post-traumatic elbow flexion contractures. Injury 8:35, 1976. 12. Ferlic, D. C., Patchett, C. E., Clayton, M. L., and Freeman, A. C.: Elbow synovectomy in rheumatoid arthritis: Longterm results. Clin. Orthop. Relat. Res. 220:119, 1987. 13. Freehafer, A.: Flexion and supination deformities of the elbow in tetraplegics. Paraplegia 15:221, 1977. 14. Gallay, S. H., Richards, R. R., and O’Driscoll, S. W.: Intraarticular capacity and compliance of stiff and normal elbows. Arthroscopy 9:9, 1993. 15. Gendi, N. S., Axon, J. M., Carr, A. J., Pile, K. D., Burge, P. D., and Mowat, A. G.: Synovectomy of the elbow and radial head excision in rheumatoid arthritis: Predictive factors and long-term outcome. J. Bone Joint Surg. Br. 79:918, 1997. 16. Glynn, J., and Niebauer, J. J.: Flexion and extension contractures of the elbow. Clin. Orthop. Relat. Res. 177:289, 1976. 17. Green, D. P., and McCoy, H.: Turn buckle orthotic correction of elbow flexion contractures after acute injuries. J. Bone Joint Surg. 61A:1092, 1979. 18. Gutierre, L. S.: A contribution to the study of the limiting factors of elbow extension. Acta Anat. 56:146, 1964. 19. Haapaniemi, T., Berggren, M., and Adolfsson, L.: Complete transection of the median and radial nerves during arthroscopic release of post-traumatic elbow contracture. Arthroscopy 10:784, 1999. 20. Hagena, F. W.: Synovectomy of the elbow. In Hama-lainen, M., and Hagena, F. W. (eds.): Rheumatoid Surgery of the Elbow, vol 15. Basel, Switzerland, Karger, 1991, p. 6. 21. Hahn, M., and Grossman, J. A.: Ulnar nerve laceration as a result of elbow arthroscopy. J. Hand Surg. (Br.) 23:109, 1998. 22. Hamalainen, M., Ikavalko, M., Kammonen, M. Epidemiology of the elbow joint involvement in rheumatoid arthritis. In Hamalainen, M., and Hagena, F. W. (eds.): Rheumatoid Surgery of the Elbow, vol 15. Basel, Switzerland, Karger, 1991, p. 1. 23. Horiuchi, K., Momohara, S., Tomatsu, T., Inoue, K., and Toyama, Y.: Arthroscopic synovectomy of the elbow in rheumatoid arthritis. J. Bone Joint Surg. Am. 84:342, 2002. 24. Huang, T. T., Blackwell, S. J., and Louis, S. R.: Ten years of experience in managing patients with burn contractures of the axilla, elbow, wrist and knee joints. Plast. Reconstr. Surg. 61:70, 1978. 25. Husband, J. B., and Hastings, H.: The lateral approach for operative release of post-traumatic contracture of the elbow. J. Bone Joint Surg. 72A:1353, 1990. 26. Jones, G. S., and Geissler, W. B.: Complications of Minimally Displaced Radial Head Fractures. San Francisco, CA, American Academy of Orthopaedie Surgeons, 1993. 27. Jones, G. S., and Savoie, F. H.: Arthroscopic capsular release of flexion contractures (arthrofibrosis) of the elbow. Arthroscopy 9:277, 1993.

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28. Kashiwaga, D.: Osteoarthritis of the elbow joint: intraarticular changes and the special operative procedure. Outerbridge-Kashiwaga method. In Keshiwaga, D. (ed.): Elbow Joint. New York, Elsevier, 1985, p. 177. 29. Kelly, E. W., Morrey, B. F., and O’Driscoll, S. W. Complication of elbow arthroscopy. J. Bone Joint Surg. 83A:25, 2001. 30. Kim, S. J., and Shin, S. J.: Arthroscopic treatment for limitation of motion of the elbow. Clin. Orthop. Relat. Res. 375:140, 2000. 31. Lapner, P. C., Leith, J. M., and Regan, W. D.: Arthroscopic debridement of the elbow for arthrofibrosis resulting from nondisplaced fracture of the radial head. Arthroscopy 12:1492, 2005. 32. Lee, B. P., and Morrey, B. F.: Arthroscopic synovectomy of the elbow for rheumatoid arthritis: A prospective study. J. Bone Joint Surg. Br. 79:770, 1997. 33. Lonner, J. H., and Stuchin, S. A.: Synovectomy, radial head excision, and anterior capsular release in stage III inflammatory arthritis of the elbow. J. Hand Surg. (Am.) 22:279, 1997. 34. Maenpaa, H., Kuusela, P., Lehtinen, J., Savolainen, A., Kautiainen, H., and Belt, E.: Elbow synovectomy on patients with juvenile rheumatoid arthritis. Clin. Orthop. Relat. Res. 412:65, 2003. 35. Maenpaa, H. M., Kuusela, P. P., Kaarela, K., Kautiainen, H. J., Lehtinen, J. T., and Belt, E. A.: Reoperation rate after elbow synovectomy in rheumatoid arthritis. J Shoulder Elbow Surg 12:480, 2003. 36. Makai, F., and Chudacek, J.: Long-term results of synovectomy of the elbow with excision of the radial head in rheumatoid arthritis. In Hamalainen, M., and Hagena, F. W. (eds.): Rheumatoid Surgery of the Elbow, vol 15. Basel, Switzerland, Karger, 1991, p. 22. 37. McLaughlin, R. E., Savoie, F. H. III, Field, L. D., and Ramsey, J. R.: Arthroscopic treatment of the arthritic elbow due to primary radiocapitellar arthritis. Arthroscopy 22:63, 2006. 38. Menth-Chiari, W. A., Ruch, D. S., and Pochling, G. G.: Arthroscopic excision of the radial head: Clinical outcome in 12 patients with post traumatic arthritis after fracture of the radial head and rheumatoid arthritis. Arthroscopy 17:918, 2001. 39. Miller, C. D., Jobe, C. M., and Wright, M. H.: Neuroanatomy in elbow arthroscopy. J. Shoulder Elbow Surg. 4:168, 1995. 40. Morrey, B. F.: Primary degenerative arthritis of the elbow: treatment by ulnohumeral arthroplasty. J. Bone Joint Surg. 74B:409, 1992. 41. Morrey, B. F., and An, K. N.: Articular and ligamentous contributions to the stability of the elbow joint. Am. J. Sports Med. 11:315, 1983. 42. Morrey, B. F., Askew, L. J., and Chao, E. W.: A biomechanical study of normal functional elbow motion. J. Bone Joint Surg. 63A:872, 1981. 43. Nguyen, D., Proper, S. I., MacDermid, J. C., King, G. J., and Faber, K. J.: Functional outcomes of arthroscopic capsular release of the elbow. Arthroscopy 22:842, 2006. 44. Nowicki, K. D., and Shall, L. M.: Arthroscopic release of a posttraumatic flexion contracture in the elbow: a case

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64. Urbaniak, J. R., Hansen, P. E., Beissinger, S. F., and Aitken, M. S.: Correction of post-traumatic flexion contracture of the elbow by anterior capsulotomy. J. Bone Joint Surg. Am. 67A:1160, 1985. 65. Wilner, P.: Anterior capsulectomy for contractures of the elbow. J. Int. Coll. Surg. 11:359, 1948. 66. Woods, D. A., Williams, J. R., Gendi, N. S., Mowat, A. G., Burge, P. D., and Carr, A. J.: Surgery for rheumatoid arthritis

of the elbow: A comparison of radial-head excision and synovectomy with total elbow replacement. J. Shoulder Elbow Surg. 8:291, 1999. 67. Wright, T. W., Glowczewskie, F. Jr, Cowin, D., and Wheeler, D. L.: Ulnar nerve excursion and strain at the elbow and wrist associated with upper extremity motion. J. Hand Surg. (Am.) 26:655, 2001.

Chapter 41 Advanced Techniques

CHAPTER

41

Advanced Techniques PART A Arthroscopic Management of Lateral Epicondylitis Mark S. Cohen and Anthony A. Romeo

INTRODUCTION Lateral epicondylitis, or tennis elbow, is the most common affliction of the elbow. The origin of the extensor carpi radialis brevis (ECRB) has been implicated as the source of pathology in this condition.2,5,7-10,13-16,18 Reported histopathologic findings in the affected tendon origin include vascular proliferation and hyaline degeneration, which are consistent with a chronic, degenerative process.10,14,18,20 Most commonly, surgical treatment is directed at excision of this pathologic tissue through an open approach or more recently arthroscopic methods.1,3,5,6,11,15,17,19,21,22 This chapter covers the anatomy of the extensor tendon origins at the humeral epicondyle based on anatomic dissections.4 The location of the ECRB tendon origin is defined relative to intra-articular landmarks. Using these data, a technique for arthroscopic lateral epicondylitis surgery is presented with early clinical results.

ANATOMY The extensor carpi radialis longus (ECRL) and the ECRB have a unique relationship at the level of the elbow. The ECRL overlies the proximal portion of the ECRB such that the ECRL must be elevated anteriorly in order to visualize the superficial surface of the ECRB. A thin film of areolar connective tissue separates these two structures. The origin of the ECRL is entirely muscular along the lateral supracondylar ridge of the humerus (Fig. 41-1). The muscle origin has a triangular configuration, with the apex pointing proximally. In contrast, the origin of

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the ECRB is entirely tendinous. Although it blends with the origin of the extensor digitorum communis (EDC), when dissected from a distal to proximal direction and using the tendon undersurface, it can be separated from the EDC back to the humerus (Fig. 41-2). The anatomic origin of the ECRB is located just beneath the distal most tip of the lateral supracondylar ridge (Fig. 41-3). The footprint is diamond shaped, measuring approximately 13 by 7 mm (Fig. 41-4). At the level of the radiocapitellar joint, the ECRB is intimate with the underlying anterior capsule of the elbow joint, but it is easily separable at this level.4 In an effort to develop a strategy for arthroscopic identification and release of the tendon origins, we performed a cadaveric study. The ECRB was identified at the level of the radiocapitellar joint by first separating the ECRL anteriorly from the extensor aponeurosis posteriorly (Fig. 41-5). The EDC origin was then dissected from anterior to posterior to expose the underlying ECRB tendon. The anterior and posterior borders of the ECRB were marked with intra-articular 18-gauge needles, and the ECRL/EDC interval and the skin were repaired (Fig. 41-5). The specimens were then mounted, and elbow arthroscopy was performed. Based on pilot studies, a modified lateral portal was established from an insideout technique. This portal was made several millimeters proximal and anterior to the top of the humeral capitellum. Using a monopolar thermal device (Arthrocare, Austin, TX), the tissue between the two needles was released from the humerus, taking care to use the previously determined intra-articular landmarks for the ECRB origin. The joint capsule was first ablated to expose the undersurface of the ECRB tendon. Above the anterior needle, the muscular origin of the ECRL was identified. The ECRB tendon was then released from its humeral origin and allowed to retract distally. Care was taken to release all the tissue located between the two needles and dissect down to the midline of the radiocapitellar joint as visualized arthroscopically. The specimens were then removed from the mounting device and individually dissected. The ECRL/EDC interval was opened, and the origin of the ECRB was evaluated to document complete release. The elbow capsule was identified beneath this plane at the joint level. The origin of the lateral collateral ligament was then exposed by reflecting the remaining extensor tendon origin posteriorly. In addition, the posterior interosseous nerve (PIN) was dissected out to document that it was not compromised by the arthroscopic release procedure. Dissection of the specimens revealed an intact extensor aponeurosis and a complete release of the underlying ECRB in all cases (Fig. 41-6). The capsule was identified as a separate layer beneath the ECRB release.

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The collateral ligament origin was not violated, and the PIN was well distal to the release and not compromised in any case (see Fig. 41-6). Using these data, an arthroscopic technique was designed for lateral epicondylar release.4

TECHNIQUE The patient is positioned prone, with all bony prominences well padded. We favor regional anesthesia. Bony landmarks are drawn out including the path of the ulnar nerve. Once the tourniquet is inflated, the elbow is insufflated with an 18-gauge needle introduced through the soft spot of the elbow (midlateral portal). Next, a standard anteromedial portal is established (Fig. 41-7). This is started several centimeters proximal and anterior to the medial epicondyle and well anterior to the palpable intermuscular septum. Care is taken to slide along the anterior humerus, and the joint is entered with a blunt introducer or a switching stick. This medial portal allows one to view the lateral joint including the radial head, capitellum, and the lateral capsule. It is often helpful at this point to open the inflow to allow distension of the capsule. If visualization is a problem, a retractor can be introduced through a proximal anterolateral portal 2 to 3 cm proximal and just anterior to the lateral supracondylar ridge. A simple freer elevator is useful for this purpose. By tensioning the capsule anteriorly, improved visualization of the lateral capsule and soft tissues can be achieved.

FIGURE 41-1

Anatomic specimen showing the footprint of the extensor carpi radialis lonugs tendon. This origin is principally muscular originating off of the supracondylar ridge of the humerus.

A

B FIGURE 41-2

C

A, Lateral view of cadaveric specimen. The extensor carpi radialis longus (ECRL) has been reflected anteriorly and the extensor carpi ulnaris posteriorly revealing the common extensor tendon origin of the extensor carpi radialis brevis (ECRB) and extensor digitorum communis (EDC). These are indistinguishable when viewed from the outer surface. B, The muscles and tendons have been reflected proximally. The origins of the ECRB anteriorly and the EDC posteriorly are identifiable on the undersurface of the extensor origin. C, Close-up view of the two tendons that can be separated back to their origins. Note the underlying lateral collateral ligament (probe).

Chapter 41 Advanced Techniques

A

B FIGURE 41-3

A, The extensor digitorum communis has been removed allowing better visualization of the bony extensor carpi radialis brevis (ECRB) origin on the humerus. B, The ECRB footprint is identified with elevation of the tendon from the humerus.

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A

B

C FIGURE 41-5

FIGURE 41-4

Schematic diagram depicting the relationship between the extensor carpi radialis brevis (ECRB) origin at the humerus and bony landmarks. Note that the ECRB footprint origin is diamond shaped and located between the midline of the joint and the top of the humeral capitellum beneath the most distal extent of the supracondylar ridge. The tendon does not originate on the epicondyle specifically. Note the relationship between the ECRB origin and the underlying lateral collateral ligament.

A, Cadaveric specimen depicting the junction between the muscular extensor carpi radialis longus (ECRL) anteriorly and the extensor aponeurosis posteriorly, which has been opened. B, The aponeurosis and tendons have been reflected posteriorly off of the ECRL, revealing the undersurface of the extensor carpi radialis brevis (ECRB) tendon. C, The extensor digitorum communis has been dissected off of the underlying ECRB, revealing the anterior and posterior margins of the ECRB tendon.

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A

B

FIGURE 41-6

C

A modified anterolateral portal is established using an inside-out technique. This is started 2 to 3 cm above and anterior to the lateral epicondyle (see Fig. 41-7). The portal is slightly more proximal than a standard anterolateral portal. This allows instrumentation down to the tendon origin rather than entering the joint through the ECRB tendon itself. If lateral synovitis is present, this can be débrided with a resector. The capsule is next released. Occasionally in epicondylitis, one can find a disruption of the underlying capsule from the humerus (Fig. 41-8). Most commonly, the capsule is intact although small linear tears can be present (Fig. 41-9). We have found it easier to release the lateral soft tissues in layers using a monopolar thermal device. In this way, the capsule is first incised or released from the humerus. When it retracts distally, one can appreciate the ECRB tendon posteriorly and the ECRL, which is principally muscular, more anterior. As noted earlier, the ECRB tendon spans from the top of the capitellum to the midline of the radiocapitellar joint. Once the capsule is adequately resected, the ECRB origin is released from the epicondyle (see Figs. 41-7 and 41-9). This is started at the top of the capitellum and carried posteriorly. The lateral collateral ligament is not

A, Following arthroscopic release of the extensor carpi radialis brevis (ECRB), the specimen is opened documenting a complete release of the ECRB. Note the distal retraction of the tendon edge. B, The posterior interosseous nerve has been exposed as it passes from anterior to posterior (arrow). This is well distal and anterior to the tendon origin release. C, The tendinous origin has been elevated posteriorly revealing the intact lateral collateral ligament (LCL). The ligament is safe as long as the release stays anterior to the midline of the radiocapitellar joint.

at risk if the release is kept anterior to the midline of the radiocapitellar joint.19 On average, adequate resection of the ECRB must include approximately 13 mm of tendon origin from anterior to posterior.4 Care is taken to drive the scope in adequately to view the release down to the midline of the radiocapitellar joint. Typically, the entire ECRB retracts distally away from the humerus. Care is taken not to release the extensor aponeurosis, which lies behind the ECRB tendon. This can be visualized as a stripped background of transversely oriented tendon and muscular fibers much less distinct than the ECRB (see Fig. 41-9). It is located posterior to the ECRL, which again is principally muscular in origin. If the aponeurosis is violated, one will débride into the subcutaneous tissue about the lateral elbow.

Discussion In recent years, there has been an interest in arthroscopic treatment of lateral epicondylitis.1,3,6,11,17,19,21,22 A cadaveric study demonstrated that arthroscopic release of the ECRB was a safe, reliable, and reproducible procedure for refractory lateral epicondylitis.11 However, the results of arthroscopic treatment of this condition have been variable. Tseng reported satisfactory results in 9 of 11 patients.22 However, he also had a 33% complication

Chapter 41 Advanced Techniques

A B

C

D

E

F

FIGURE 41-7

A, Diagram depicting the medial portal used in visualization for the arthroscopic lateral epicondylar release. B and C, Field of view from the medial portal. D, Diagram depicting the relationship of the extensor tendon origins when viewed intraarticularly. These are located outside (behind) the elbow capsule. E, Needle used to help establish a modified lateral portal. Note how this is begun slightly proximal and anterior to the proximal margin of the humeral capitellum. F, Cannula used to establish the final lateral portal.

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G H

FIGURE 41-7, cont’d

I

G, Release of the capsule from the lateral humeral margin allowing visualization of the tendinous origins behind. The extensor carpi radialis longus (ECRL) is more anteriorly located and is muscular. The extensor carpi radialis brevis (ECRB) is more posterior. H, The ECRB is released from the top of the capitellum to the (I) midline of the radiocapitellar joint.

FIGURE 41-8

Initial intraoperative view of a patient with recalcitrant lateral epicondylitis. Note the capsular rent. In some cases, the capsule is noted to have torn away from its humeral origin.

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A

B

C

D

615

FIGURE 41-9

A, Initial intraoperative view of a patient treated surgically for lateral epicondylitis. The lateral capsule obstructs the view of the extensor tendon origins. Note the small longitudinal rent in the capsule. B, The capsule has been released revealing the muscular extensor carpi radialis longus (ECRL) anteriorly and the tendinous extensor carpi radialis brevis (ECRB) more posteriorly. Note the capsular layer distally which is deep to the tendon. C, The ECRB has been released. Behind this, one can see the muscular ECRL anteriorly and the extensor aponeurosis which lies behind the ECRB (asterisk). It is characteristically composed of transversely stripped tendinous fibers much less distinct than the ECRB. D, Final close-up view following ECRB release. Using the resector, one can see the thick ECRB origin which has retracted distally following release.

rate. Stapleton and Baker compared five patients treated arthroscopically with 10 patients treated by open débridement.21 They reported similar results and complication rates between the two groups. Later, Baker et al.1 reported on 39 elbows treated arthroscopically, with 37 reporting being “better” or “much better” at follow-up. Peart et al17 reported on 33 arthroscopic procedures for

lateral epicondylitis, with 28% of patients failing to achieve good or excellent outcomes. The variable results reported using various arthroscopic techniques may be related to increased difficulty in identifying the ECRB origin through the arthroscope.6 The tendon is extra-articular, and capsular release is required to visualize its origin. The tendon footprint is

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diamond shaped and located between midline of the radiocapitellar joint and the top of the humeral capitellum averaging 13 by 7 mm (see Fig. 41-4). The posterior interosseous nerve should be well medial and distal to the area of dissection. The lateral collateral ligament is not compromised, as long as the release is kept anterior to the midline of the radiocapitellar joint. Care is taken not to release the extensor aponeurosis, which lies superficial to the ECRB tendon. We reviewed a consecutive series of 36 patients with recalcitrant lateral epicondylitis treated with arthroscopic release using the aforementioned technique.12 There were 24 men and 12 women, with an average age of 42 years at the time of surgery. The cohort had symptoms for an average of 19 months before surgical intervention. Intraoperative findings revealed significant lateral intraarticular synovitis in approximately 30% of patients. Approximately 75% of cases had an intact elbow capsule or a minor linear capsular tear, whereas 25% had a significant proximal capsular disruption. All patients were evaluated by independent examiners for the purposes of this study at a minimum 2-year follow-up. On average, patients required 4 weeks to return to regular activities and 7 weeks to return to full work duties. No major complications were reported. One patient had a neurapraxia of the superficial radial nerve that resolved by 2 weeks postoperatively. The average functional component of the Mayo Elbow Performance Score at follow-up averaged 11.1 out of 12 (range, 5-12). Grip strength averaged 91% of the opposite, uninvolved side. Subjective pain ratings as measured on a visual analog scale improved from 8.5 + 2.4 to 1.9 + 1.3 (P < 0.01). However, 10 patients reported continued pain with strenuous activities and repetitive use of the affected arm. Two patients continued to have significant pain and were considered failures.12 In summary, arthroscopic release of the ECRB appears to be an effective option for the surgical treatment of chronic lateral epicondylitis unresponsive to conservative modalities. Knowledge of the anatomy, including the extensor tendon origins as visualized from an intraarticular perspective, is essential for effective surgical release.

References 1. Baker, C. L., Murphy, K. P., Gottlob, C. A., and Curd, D. T.: Arthroscopic classification and treatment of lateral epicondylitis: two-year clinical results. J. Shoulder Elbow Surg. 9:475, 2000. 2. Bunata, R. E., Brown, D. S., and Capelo, R.: Anatomic factors related to the cause of tennis elbow. J. Bone Joint Surg. 89A:1955, 2007.

3. Cohen, M. S., and Romeo, A. A.: Lateral epicondylitis: open and arthroscopic treatment. J. Am. Soc. Surg. Hand 3:172, 2001. 4. Cohen, M. S., Romeo, A. A., Hennigan, S. P., and Gordon, M.: Lateral epicondylitis: anatomic relationships of the extensor tendon origins and implications for arthroscopic treatment. J. Shoulder Elbow Surg. (in press). 5. Coonrad, R. W., and Hooper, W. R.: Tennis elbow: its course, natural history, conservative and surgical management. J. Bone Joint Surg. 55A:1177, 1973. 6. Cummins, C. A.: Lateral epicondylitis: in vivo assessment of arthroscopic debridment and correlation with patient outcomes. Am. J. Sports Med. 34:1486, 2006. 7. Cyriax, J. H.: The pathology and treatment of tennis elbow. J. Bone Joint Surg. 18:921, 1936. 8. Garden, R. S.: Tennis elbow. J. Bone Joint Surg. 43-B:100, 1961. 9. Gardner, R. C.: Tennis elbow: diagnosis, pathology, and treatment. Clin. Orthop. Relat. Res. 72:248, 1970. 10. Kraushaar, B. S., and Nirschl, R. P.: Tendinosis of the elbow (tennis elbow). Clinical features and findings of histological, immunohistochemical, and electron microscopy studies. J. Bone Joint Surg. 81A:259, 1999. 11. Kuklo, T. R., Taylor, K. F., Murphy, K. P., Islinger, R. B., Heekin, R. D., and Baker, C. L. Jr. Arthroscopic release for lateral epicondylitis: a cadaveric model. Arthroscopy 15:259, 1999. 12. Lattermann, C., Anbari, A., McCarty, L. P., Cole, B. J., Romeo, A. A., and Cohen, M. S.: Three-year follow-up of arthroscopic treatment for recalcitrant lateral epicondylitis, Arthroscopy (under review). 13. Morrey, B. F.: Reoperation for failed surgical treatment of refractory lateral epicondylitis. J. Shoulder Elbow Surg. 1:47, 1992. 14. Nirschl, R. P.: Elbow tendinosis/tennis elbow. Clin. Sports Med. 11:851, 1992. 15. Nirschl, R. P., and Pettrone, F. A.: Tennis elbow. The surgical treatment of lateral epicondylitis. J. Bone Joint Surg. 61A:832, 1979. 16. Organ, S. W., Nirschl, R. P., Kraushaar, B. S., and Guidi, E. J.: Salvage surgery for lateral tennis elbow. Am. J. Sports Med. 25:746, 1997. 17. Peart, R. E., Strickler, S. S., and Schweitzer, K. M. Jr: Lateral epicondylitis: a comparative study of open and arthroscopic lateral release. Am. J. Orthop. 33:565, 2004. 18. Regan, W., Wold, L. E., Coonrad, R., and Morrey, B. F.: Microscopic histopathology of chronic refractory lateral epicondylitis. Am. J. Sports Med. 20:746, 1992. 19. Smith, A. M., Castle, J. A., and Ruch, D. S.: Arthroscopic resection of the common extensor origin: anatomic considerations. J. Shoulder Elbow Surg. 12:375, 2003. 20. Spencer, G. E., and Herndon, C. H.: Surgical treatment of epicondylitis. J. Bone Joint Surg. 35-A:421, 1953. 21. Stapleton, T. R., and Baker, C. L.: Arthroscopic treatment of lateral epicondylitis. Arthroscopy 10:335, 1996. 22. Tseng, V.: Arthroscopic lateral release for treatment of tennis elbow. Arthroscopy 10:335, 1994.

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PART B Arthroscopic Radial Ulnohumeral Ligament Reconstruction for Posterolateral Rotatory Instability of the Elbow Felix H. Savoie, III

INTRODUCTION Since the original description by O’Driscoll and Morrey in 1991, there has been increasing attention and research directed toward the diagnosis and management of posterolateral rotatory instability (PLRI) of the elbow. PLRI has been described as an instability pattern of the elbow that results from an incompetent radial ulnohumeral ligament (RUHL).6 Recent anatomic studies have attempted to further define the involved tissue. Dunning et al. state that both the RUHL and the radial collateral ligament must be sectioned to achieve PLRI. They also state that they could not differentiate visually the two ligaments at their humeral origin. They could only differentiate the RUHL from the radial collateral ligament (RCL) by identifying the distal extent of the RUHL at the supinator crest.2 Seki et al10 were able to show that sectioning just the anterior band of the lateral collateral ligament was insufficient to induce instability. These and other more recent studies demonstrate that the entity of PLRI is, in fact, a spectrum of injury.3-5,8,9,12 Although originally described as either the result of an elbow dislocation or due to extensive tennis elbow surgery, these anatomic studies help support the concept that there is a continuum of injury between mild, grade 1 PLRI and frank elbow dislocation.6,11

EXAMINATION The history is usually one of a minor trauma. The symptoms are vague pain and feelings of minor and inconsistent shifting with certain activities. PLRI is best demonstrated clinically with the pivot shift test of the elbow. This test as first described by O’Driscoll and Morrey may elicit gross instability or simply pain and apprehension.6 Two other very useful clinical tests described by Regan8 include pain when pushing up from an arm chair with the palms facing inward. A second test involves having the patient push up from a

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prone position first with the forearms maximally pronated and with the thumbs pointing toward each other. Repeating the test with the thumbs pointed outward and the forearms maximally supinated causes symptoms that were not present with the forearms pronated. This can alternately be performed standing while performing a wall pushup.12 Imaging studies for PLRI can be helpful. Radiographs may reveal an avulsion fragment from the humeral lateral epicondyle. However, radiographs often are normal. A stress radiograph or fluoroscopy performed while conducting the pivot shift test will show the radial head and proximal ulnar moving together in a subluxed and posterolaterally rotated position. Examination under anesthesia will show similar findings. Contrast-enhanced magnetic resonance imaging of the elbow has been described to identify a lesion in the RUHL.7 It is our experience that the best interpretation occurs when the radiologist and orthopedist interpret the films together. Although much has been written about the pathoanatomy and biomechanics of the lesion, little has been reported on the arthroscopic treatment of these patients. Chapter 40 reports on the management by a conventional open procedure, whereas this chapter section reviews the technique and results of the authors’ arthroscopic technique previously described by Smith et al.11

SURGICAL TECHNIQUE The development of an arthroscopic technique for the treatment of PLRI was described by Smith et al11 in 2001. The instability can be readily seen during arthroscopic evaluation. While viewing from the proximal anteromedial portal, the ulna and radial head can be seen to subluxate posterolaterally during the performance of a pivot shift test. Additionally, an arthroscope in the posterolateral portal placed down the posterolateral gutter can be driven into and across the lateral aspect of the ulnohumeral joint, the arthroscopic “drive through” sign of the elbow, which we believe is analogous to the “drive-through” sign of multidirectional laxity in shoulder instability (Fig. 41-10). This ability to translate the arthroscope through the ulnohumeral joint from lateral to medial is not possible in stable elbows, nor after the instability is corrected in patients with PLRI. The instability from an injured lateral collateral ligament complex can often be effectively treated with an arthroscopic plication. This is performed by placing six to seven absorbable sutures obliquely from the radial border of the ulna to the radial border of the humerus. The sutures are introduced through a spinal needle. The first two sutures are delivered into the joint through the annular ligament (Fig. 41-11A) and retrieved through

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FIGURE 41-10

A

Posterolateral “drive-through” sign.

the humeral attachment of the capsule. Subsequent sutures are brought into the joint in a progressively more proximal position. Each suture is immediately retrieved with a suture retriever that passes into the joint adjacent to the posterior aspect of the lateral epicondyle (Fig. 41-11B). These sutures are then retrieved subcutaneously through the soft spot skin portal and pulled to tension. The arthroscope is driven out of the lateral gutter as the sutures are tensioned. The sutures are then tied individually from distal to proximal either under or over the anconeus muscle. If there is a humeral avulsion, a suture anchor is placed under direct arthroscopic visualization into the normal site of origin of the RUHL from the posterior epicondyle. The suture from the anchor is retrieved under all the transfixing sutures before they are tied and are pulled out of the skin distal to the most distal suture. The sutures are then tied and the anchor suture retrieved

B

FIGURE 41-11

C

A, Inserting first suture through spinal needle. B, Suture in place from ulna to lateral epicondyle. C, Multiple sutures in place plicating radial ulnohumeral ligament.

Chapter 41 Advanced Techniques

subcutaneously over the sutures and then tied, pulling the entire reconstructed ligament back to the normal origin (see Fig. 41-11C). Postoperatively, patients are immediately immobilized in an extension splint with the forearm rotation at neutral and the elbow fully extended. This is progressed in the first week to a hinged elbow brace, with the arc of motion from 0 to 30 degrees for approximately 2 more weeks. At 3 weeks, the patients are allowed to increase the range of motion in the brace to 0 to 60 degrees and then at 5 to 6 weeks to 90 degrees. After eight weeks, the brace is loosened to full range of motion. During the 6th week visit, physical or occupational therapy for wrist, elbow, and shoulder/scapular exercises with the brace in place are initiated. The exercises are increased at the 8-week visit as tolerated with the brace in place. Usually by 10 to 12 weeks postoperatively, the brace may be removed for activities of daily living but continued for sports and aggressive exercises. Depending on individual progression, patients are allowed to start strengthening exercises out of the brace after 12 weeks. They must be able to perform all strengthening exercises pain free in the brace before progression out of the brace.

RESULTS Gurley et al reviewed the results of 17 patients with an arthroscopic PLRI reconstruction. Six of the 17 arthroscopically treated patients had the addition of an anchor to supplement the arthroscopic suture plication (personal communication). The average follow-up was 41 months (range 12-103 months). Overall, Andrews-Carson scores for all repairs improved from 145 to 180 P < 0.0001.1 Subjective scores from 57 to 85 P < 0.0001 and objective scores improved from 88 to 95 P = 0.008. This study, along with that of Smith et al.11 reveals that arthroscopic plication of the RUHL can be as successful as open repair. Arthroscopic suture plication has become a useful technique in shoulder instability, and this report shows that the same ideas can translate to the elbow. The technique is technically demanding and requires a thorough understanding of elbow anatomy. Treating surgeons should be aware of the differential diagnosis of lateral elbow pain. This includes PLRI, lateral epicondylitis, radiocapitellar arthritis, capitellar OCD, posterolateral plica syndrome, and posterior interosseous nerve compression. It is important for surgeons treating elbow pain to be adept at performing the pivot shift test in both the prone and supine position, as well as the additional clinical tests outlined in this chapter to help distinguish PLRI from other causes of lateral elbow pain. We believe PLRI may be an initiating factor in the

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development of refractory lateral epicondylitis, and should be considered as one potential primary cause in this disorder, as described by Cohen et al. Each of these disorders may be managed by arthroscopic measures in addition to the standard open surgical treatments. In most of our patients, arthroscopic repair seemed to be an effective method of managing the instability. One should always be prepared to use either an open technique or a supplemental graft in each of these cases. We have found the number of previous surgeries to be the best predictor of the need for a graft. This chapter describes an arthroscopic variation of the repair technique described by O’Driscoll and Morrey that we believe to be an effective way to correct several varieties of posterolateral elbow instability.

References 1. Andrews, J. R., and Carson, W. G.: Arthroscopy of the elbow. Arthroscopy 1:97, 1985. 2. Dunning, C. E., Zarzour, Z. D., Patterson, S. D., Johnson, J. A., and King, G. J.: Ligamentous stabilizers against posterolateral rotator instability of the elbow. J. Bone Joint Surg. Am. 83-A:1823, 2001. 3. Kalainov, D. M., and Cohen, M. S.: Posterolateral rotatory instability of the elbow in association with lateral epicondylitis. A report of three cases. J. Bone Joint Surg. 87A:1120, 2005. 4. King, G. J., Dunning, C. E., Zarzour, Z. D., Patterson, S. D., and Johnson, J. A.: Single-strand reconstruction of the lateral ulnar collateral ligament restores varus and posterolateral rotatory stability of the elbow J. Shoulder Elbow Surg. 11:60, 2002. 5. Mehta, J. A., and Bain, G. I.: Posterolateral instability of the elbow. J. Am. Acad. Orthop. Surg. 12:405, 2004. 6. O’Driscoll, S. W., Bell, D. F., and Morrey, B. F.: Posterolateral rotatory instability of the elbow. J. Bone Joint Surg. Am. 73:440, 1991. 7. Potter, H. G., Weiland, A. J., Schatz, J. A., Paletta, G. A., and Hotchkiss, R. N.: Posterolateral rotator instability of the elbow: usefulness of MR imaging in diagnosis. Radiology 204:185, 1997. 8. Regan, W., and Lapner, P. C.: Prospective evaluation of two diagnostic apprehension signs for posterolateral instability of the elbow. J. Shoulder Elbow Surg. 15:344, 2006. 9. Sanchez-Sotelo, J., Morrey, B. F., and O’Driscoll, S. W.: Ligamentous repair and reconstruction for posterolateral rotatory instability of the elbow. J. Bone Joint Surg. 87B:54, 2005. 10. Seki, A., Olsen, B. S., Jensen, S. L., Eygendaal, D., and Sojbjerg, J. O.: Functional anatomy of the lateral collateral ligament complex of the elbow: configuration of Y and its role. J. Shoulder Elbow Surg. 11:53, 2002. 11. Smith, J. P., Savoie, F. H., and Field, L. D.: Posterolateral rotatory instability of the elbow. Clin. Sports Med. 20:47, 2001. 12. Yadao, M. A., Savoie, F. H. 3rd, and Field, L. D.: Posterolateral rotatory instability of the elbow. Inst. Course Lect. 53:607, 2004.

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CHAPTER

42

Complications of Elbow Arthroscopy Bernard F. Morrey

INTRODUCTION The potential for complications with elbow arthroscopy is as well known as that of any orthopedic technique. This may explain in part why elbow arthroscopy is still not widely performed by most orthopedic surgeons. Other reasons include (1) relative infrequency of elbow involvement and (2) difficulty of effectively and accurately performing arthroscopy in a very congruent joint, especially when the pathology alters the joint capacity.

INFORMATION AND CLINICAL EXPERIENCE Although suffering from a deserved reputation for significant potential complications, there is still relatively little information in the orthopedic literature regarding the frequency of complications from elbow arthroscopy. With the exception of a Mayo report, what data exist pertain to a single or limited case reports often associated with an anatomic study.1,3,6,19-22 We will consider this complication in the following order: (1) anatomy; (2) pathology being treated; (3) procedures available to the arthroscopist; (4) incidence of reported complications; (5) Mayo’s experience; and (6) recommendations.

ANATOMY The elbow is one of the most congruous joints in the body; hence, the ability to manipulate the joint to separate the articular surfaces and allow better visualization is extremely limited, and multiple portals may be needed.2,9,18 Furthermore, the capacity of the joint is limited in the normal situation and is even further curtailed by most pathology. O’Driscoll and colleagues24 demonstrated an average normal capacity of approximately 30 mL. Post-traumatic and degenerative processes result in contracture of the joint, often allowing less than 10 mL of intra-articular distension. The soft tissue envelope of the elbow is extremely thin, the capsule being separated from the skin Joint Congruence and Capacity

by a thin layer of subcutaneous tissue in some locations. Thus, the tendency for the portals to “seal” is limited. This feature predisposes to chronic drainage and the possibility of infection.15 Neurovascular Structures Without question, the greatest concern regarding elbow anatomy is the proximity of the radial and ulnar nerves that cross the joint in proximity to the capsule. The relationship of the radial, median, and ulnar nerves to the capsule in both the distended and the nondistended positions has been studied extensively.1,3,6,19-22,30,31,33 Furthermore, the vulnerability of cutaneous nerves had also been studied in relationship to the arthroscopic portal sites. These data are summarized in Table 42-1. It is particularly important to note that distension of the joint does alter the relative location of cutaneous nerves as well as the radial and median nerves referable to the portal site. However, a distended joint in no way protects either of these nerves from an intra-articular procedure.20 As a matter of fact, the distended capsule may theoretically render these nerves more, rather than less, vulnerable. The most vulnerable nerve anatomically is the posterior interosseous nerve.10 This nerve may typically be 5 to 10 mm from an anterolateral portal. However, there is significant variation, and in some instances. the nerve can be as close as 2 to 3 mm to the capsule because it lies over the radial neck. Similarly, the median nerve demonstrates a variation of approximately 5 mm between the distended and the nondistended capsule referable to the anteromedial portal. However, once again, the distended capsule approximates the nerve—it does not separate the nerve. Although it is clearly the most protected, median nerve injury has been reported.11 Of great concern is that of a concurrent injury to the brachial artery or vein. Finally, the ulnar nerve actually rests on the medial capsule.30 The greatest risk consists of procedures performed in the posteromedial corner of the elbow.12 However, injury from portal placement has also been reported.7 In general, these nerves are not vulnerable to portal insertion if the portal sites are accurately defined and the joint is distended. The risk of nerve injury is as follows: least risk, the median nerve; moderate risk, the ulnar nerve; greatest risk, the radial nerve.

PATHOLOGY The nature of the pathology influences potential risks of complications22 (Table 42-2). The most common reason for arthroscopy of an elbow involved with rheumatoid arthritis is synovectomy. The capsule is extremely thin in these patients, and therefore, the nerves are at

Rheumatoid Arthritis

Chapter 42 Complications of Elbow Arthroscopy

significant risk of injury with this procedure. One patient developed a temporary ulnar nerve paresthesia owing to the instability associated with rheumatoid synovitis and the vulnerability of the nerve referable to a thin capsule covered by proliferative synovium. The removal of loose bodies is still probably the best and most common indication for elbow arthroscopy in both the degenerative and the post-traumatic elbow.4,23,25,27 The complications are uncommon unless the portal site strays from the recommended positions or débridement is required. Both generally place the radial nerve at risk. Loose Body

Degenerative Arthritis Primary degenerative arthritis is a good indication for elbow arthroscopy.4,14 The selection of a procedure may include removal of loose bodies, débridement of the coronoid and olecranon osteophytes, and anterior and posterior capsular release. The anterior capsular release places the median and, particularly, the radial nerve at risk. The posterior release may place the ulnar nerve at risk. In addition, the multiple portal sites necessary for effectively carrying out this procedure may further add an element of vulnerability to these nerves. In addition to the degenerative as well as the post-traumatic elbow, the capsular capacity is very limited,24 making even a diagnostic procedure something of a risk particularly for articular scuffing. As

Nerve Distances to Capsule and Portals

TABLE 42-1

Distance (mm) Nerve

Portal Site

Portal

Radial

Ant. lat.

Median

Ant. medial

10

15

14 (6-24)

Ulnar

Ant. med.

1-22

1-22

1-2 (?)

Flaccid

TABLE 42-2

5

Capsule

Distended

10 (1-13)

9 (6-16)

621

confidence increases and a greater amount of bone is removed, the potential for ectopic bone has also been reported8 (Fig. 42-1). The potential risks of this complication are similar to those with primary degenerative arthritis. Contracture and altered anatomy make the procedure technically difficult. The articular structures as well as the neural and even the vascular ones may be at risk, depending on the aggressiveness of the procedure, which is typically débridement of bone and soft tissue.

Post-traumatic Elbow

SURGICAL PROCEDURE In addition to variation in pathology as implied previously, different risks are also associated with varying complexities of surgical procedures (Table 42-3).22 The procedure that has the lowest risk is that of loose body removal. However, attention must be paid to the location of the portal with the distended joint.

Loose Body

Osteophyte Removal Removal of an osteophyte can predispose to articular scuffing, but removal of the medial corner of an olecranon space places the ulnar nerve at particular risk, because this osteophyte frequently extends to the medial joint line. This osteophyte may approximate the ulnar nerve. Certainly, any medial osteophytic removal from the humerus should be performed with extreme care, because the ulnar nerve frequently rests on or very near this medial osteophytic process. Capsular Release A capsular release may be the most dangerous arthroscopic procedure.14,22 The capsule is usually thick, and the joint capacity limited. Some débridement may be required to obtain adequate visu-

Authors’ View of the Relative Risk of Complication by Diagnosis* Neural

Diagnosis

Rheumatoid arthritis

Articular Scuff

Radial

Median

Ulnar

NA

Infection

Vascular

+*

P. trauma 䊊

Primary OA Post. u. nerve transfer

NA

OA, osteoarthritis; P, post; u, ulnar. *If anterior medial portal used. Risk: NA, Not applicable; low, 䊊; intermediate, +/−; high, +.

NA

NA

+*

䊊

NA

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Part VI Sports and Overuse Injuries to the Elbow

Medial antebrachial cutaneous n.

Median n.

Ulnar n. Brachial a.

B

FIGURE 42-1

Proximal anteromedial portal. A, Anterosuperior medial portal (proximal anteromedial portal). B, Illustration of gross anatomy.

TABLE 42-3

Authors’ View of the Relative Risk of Complication by Procedure Neural

Procedure

Articular Scuff

Radial

Medial

Ulnar

Infection

䊊

+/−

䊊

䊊

NA

䊊

+/−

䊊

䊊

䊊

䊊

䊊

Loose body Osteophyte

+/−

䊊

+/−

+

䊊

NA

Capsular release

䊊

+

䊊

䊊

䊊

䊊

Synovectomy

䊊

+

+/−

+

䊊

䊊

Diagnostic (portal)

Vascular

Risk: Not applicable, NA; low, 䊊; intermediate, +/−; high, +.

alization. The radial nerve is at particular risk because it is often closely applied to the anterior capsule at the radial head. As noted earlier, the ulnar nerve is valuable to posterior capsular release. Injury to the median nerve may also occur but at a lower risk. Complication from synovectomy is a function of the aggressiveness of the procedure.9 Multiple portals do place the nerves at some risk, even for the diagnostic component. In addition, the thin capsule generally present in the rheumatoid patient may unknowingly be violated, thus immediately placing the anterior nerves at risk. Furthermore, use of low suction may draw the nerve into the débriding instrument. Synovectomy

Finally, the pathology itself frequently makes visualization difficult, and débridement to attain better visualization may violate the capsule, thus increasing the vulnerability to nerve injury. With care, these problems can be avoided. We have recently documented no permanent nerve problems after 83 elbow synovectomies. Of note, however, was that 6 did have some transient paresthesias of the radial (three) and ulnar (three) nerves.5

VASCULAR INSULT To date, we were unable to identify any documentation of vascular injury or compartment syndrome after

Chapter 42 Complications of Elbow Arthroscopy

elbow arthroscopy. The marked swelling that may occur quickly resolves. It has been shown that infusion systems that control both pressure and flow cause less extravasation than systems that control pressure alone.26

INCIDENCE The incidence of complications has been poorly documented. In 1986, the Arthroscopic Association of North America conducted a survey of almost 1600 procedures, and only one radial nerve injury was reported, along with two instances of infection. Obviously, this complication rate (0.2%) grossly understates the actual incidence of these injuries. A review of the literature reveals that the greatest focus is placed on neural injury, documented in about 2.1% of patients, although this is usually transient (Table 42-4). Infection and all other problems are not commonly reported. Overall, a review of more than 600 procedures reveals some form of complication in 5%.4,5,9,13,16,19,23,25,29,32 We consider this an inaccurate estimate of the reality.15 Mayo Clinic Experience Because the potential risk is high and owing to a lack of information in the literature regarding the true incidence of elbow arthroscopy com-

623

plications, we have reviewed our experience with elbow arthroscopy.15 After 449 procedures, 1% of individuals have a significant complication requiring treatment or altering outcome. There were no permanent neural vascular injuries in this series. Furthermore, 10% have a nonpermanent “problem” associated with the procedure. The data in Tables 42-3 and 42-4 reflect this experience.

PREVENTION The recommendations for avoiding complications of elbow arthroscopy are generally well recognized: (1) define landmarks before distension; (2) recognize that distension protects the nerve from portal injury but not from capsular procedures; (3) portals more proximal to the joint tend to be safer30; (4) keep the elbow flexed 90 degrees to increase the distance between the nerves and the capsule; (5) do not use pressurized infusion26; (6) débriding with radius pronated protects the posterior interosseous nerve; (7) always visualize the instrument tip; (8) avoid suction around a nerve; (9) capsular “retraction” may be useful; and (10) use local anesthesia judiciously because this can cause neural anesthesia, which confuses the patient’s postoperative status. Most important, recognize the potential risk and be realistic about your competency.

Complications Reported with Elbow Arthroscopy

TABLE 42-4

Complications Reference

Year

Guhl9 Lynch et al

19

O’Driscoll et al

23

Ward and Anderson32 Ogilvie-Harris and Weisleder Schneider et al

29

Baker and Brooks Kelly et al15 5

Cil et al

28

Savoie et al Micheli

20a

Cohen5a Kim et al Reddy

16

27a

Horiuchi et al

13

4

26

Procedures

Nerve (Transient)

Infection (Drainage)

Other

1985

45

1

0

0

1986

21

3 (2)

0

0

1992

71

3 (3)

3

0

1993

35

0

1

3

1993

34

2 (2)

0

0

1994

67

7 (7)

0

0

1996

200

0

0

1

2001

473

12 (9)

4 (4)

—

2007

83

4 (4)

0

0

1999

24

0

1

1

2001

47

0

0

0

2000

18

0

0

0

2000

63

2000

187

1

0

2

2002

21

3 (3)

0

0

9 (.7%)

7 (.6%)

Totals %

1389

36 (2.1%)

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Part VI Sports and Overuse Injuries to the Elbow

References 1. Adolfsson, L.: Arthroscopy of the elbow joint: A cadaveric study of portal placement. J. Shoulder Elbow Surg. 3:53, 1994. 2. Andrews, R. J., and Carson, W. G.: Arthroscopy of the elbow. Arthroscopy 1:97, 1985. 3. Angelo, R. L.: Advances in elbow arthroscopy. Orthopedics 16:1037, 1993. 4. Baker, C. L., and Brooks, A. A.: Arthroscopy of the elbow. Clin. Sports Med. 15:261, 1996. 5. Cil, A., Veillette, C. J. H., O’Driscoll, S. W., and Morrey, B. F.: Arthroscopic Synovectomy of the Elbow in Inflammatory Arthritis. Submitted for publication, 2007. 5a. Cohen, A. P., Redden, J. F., and Stanley, D.: Treatment of osteoarthritis of the elbow: A comparison of open and arthroscopic debridement. Arthroscopy 16:701, 2000. 6. Drescher, H., Schwering, L., Jerosch, J., and Herzig, M.: The risk of neurovascular damage in elbow joint arthroscopy: Which approach is better: Anteromedial or anterolateral? Z. Orthop. Ihre Grenzgeb. 132:120, 1994. 7. Dumonski, M. L., Arciero, R. A., and Mazzocca, A. D.: Ulnar nerve palsy after elbow arthroscopy. Arthroscopy 22:577. e1, 2006. 8. Gofton, W. T., and King, G. J.: Heterotopic ossification following elbow arthroscopy. Arthroscopy 17:E2, 2001. 9. Guhl, J. F.: Arthroscopy and arthroscopic surgery of the elbow. Orthopedics 8:1290, 1985. 10. Gupta, A., and Sunil, T. M.: Complete division of the posterior interosseous nerve after elbow arthroscopy: A case report. J. Shoulder Elbow Surg. 13:566, 2004. 11. Haapaniemi, T., Berggren, M., and Adolfsson, L.: Com-plete transection of median and radial nerves during arthroscopic release of post-traumatic elbow contracture. Arthroscopy 15:784, 1999. 12. Hahn, M., and Grossman, J. A.: Ulnar nerve laceration as a result of elbow arthroscopy. J. Hand Surg. 23B:109, 1998. 13. Horiuchi, W., Momohara, S., Tomatsu, T., et al.: Arthroscopic synovectomy of the elbow in rheumatoid arthritis. J. Bone Joint Surg. 84A:342, 2002 14. Jones, G. S., and Savoie, F. H.: Arthroscopic capsular release of flexion contractures (arthrofibrosis) of the elbow. Arthroscopy 9:277, 1993. 15. Kelly, E., Morrey, B. F., and O’Driscoll, S.: Complications of elbow arthroscopy. J. Bone Joint Surg. 83A:25, 2001. 16. Kim, S. J., Kim, H. K., and Lee, J. W.: Arthroscopy for limitation of motion of the elbow. Arthroscopy 11:680, 1995. 17. Lee, B. P. H., and Morrey, B. F.: Arthroscopic synovectomy of the elbow for rheumatoid arthritis. J. Bone Joint Surg. 79B:770, 1997. 18. Lindenfeld, T. N.: Medial approach in elbow arthroscopy. Am. J. Sports Med. 18:413, 1990.

19. Lynch, G. J., Myers, J. F., Whipple, T. L., and Caspari, R. B.: Neurovascular anatomy and elbow arthroscopy: Inherent risks. Arthroscopy 2:191, 1986. 20. Marshall, P. D., Fairclough, J. A., Johnson, S. R., and Evans, E. J.: Avoiding nerve damage during elbow arthroscopy. J. Bone Joint Surg. 75B:129, 1993. 20a. Micheli, L. J., Luke, A. C., Mintzer, C. M., and Waters, P. M.: Elbow arthroscopy in the pediatric and adolescent population. Arthroscopy 17:694, 2001. 21. Miller, C. D., Jobe, C. M., and Wright, M. H.: Neuroanatomy in elbow arthroscopy. J. Shoulder Elbow Surg. 4:168, 1995. 22. Morrey, B. F.: Complications of elbow arthroscopy. Instr. Course Lect. 49:255, 2000. 23. O’Driscoll, S. W., Morrey, B. F., and An, K. N.: Intraarticular pressure and capacity of the elbow. Arthroscopy 6:100, 1990. 24. O’Driscoll, S. W., and Morrey, B. F.: Arthroscopy of the elbow: Diagnostic and therapeutic benefits and hazards. J. Bone Joint Surg. 74A:84, 1992. 25. Ogilvie-Harris, D. J., and Schemitsch, E.: Arthroscopy of the elbow for removal of loose bodies. Arthroscopy 9:5, 1993. 26. Ogilvie-Harris, D. J., and Weisleder, L.: Fluid pump systems for arthroscopy: A comparison of pressure control versus pressure and flow control. Arthroscopy 11:591, 1995. 27. Poehling, G. G., and Ekman, E. F.: Arthroscopy of the elbow. Instr. Course Lect. 44:217, 1995. 27a. Reddy, A. S., Kvitne, R. S., Yocum, L. A., Elattrache, N. S., Glousman, R. E., and Jobe, F. W.: Arthroscopy of the elbow: a long-term clinical review. Arthroscopy 16:588, 2000. 28. Savoie, F. H. 3rd, Nunley, P. D., and Field, L. D.: Arthroscopic management of the arthritic elbow: Indications, technique, and results. J. Shoulder Elbow Surg. 8:214, 1999. 29. Schneider, T., Hoffstetter, I., Finnk, B., and Jerosch, J.: Longterm results of elbow arthroscopy in 67 patients. Acta Orthop. Belg. 60:378, 1994. 30. Stothers, K., Day, B., and Regan, W. R.: Arthroscopy of the elbow: Anatomy, portal sites, and a description of the proximal lateral portal. Arthroscopy 11:449, 1995. 31. Verhaar, J., van-Mameren, H., and Brandsma, A.: Risks of neurovascular injury in elbow arthroscopy: Starting anteromedially or anterolaterally? Arthroscopy 7:287, 1991. 32. Ward, W. G., and Anderson, T. E.: Elbow arthroscopy in a mostly athletic population. J. Hand Surg. 18:220, 1993. 33. Unlu, M. C., Kesmezacar, H., Akgun, I., Ogut, T., and Uzun, I.: Anatomic relationship between elbow arthroscopy portals and neurovascular structures in different elbow and forearm positions. J. Shoulder Elbow Surg. 15:457, 2006.

Chapter 43 The Future of Arthroscopy of the Elbow

CHAPTER

43

The Future of Arthroscopy of the Elbow

625

complications and problems with their colleagues, leading to improved results and decreased risk. The key is to advance the investigations and procedures while always operating within one’s own personal “safe zone” of experience and comfort. One of the most comforting advances, popularized by O’Driscoll, is the use of arthroscopic retractors to protect the neurovascular structures. This single advance has allowed the application of elbow arthroscopy to many more complex procedures.

Felix H. Savoie III and Bernard F. Morrey

EXTRA-ARTICULAR DEVELOPMENTS INTRODUCTION As with many joints, arthroscopy of the elbow has become more common. Case reports and anecdotal evidence support the rapid growth of the use of arthroscopy in a variety of disorders of the elbow. The future holds much promise in the expansion of the application of arthroscopic techniques. The success of arthroscopy over open procedures in other areas has pushed both the surgeon and the public to advance the application of these techniques to the elbow. Minimally invasive surgery, with its advantage of causing less surgical damage while achieving the same results, is the current preferred method in all areas of orthopedics. The elbow is no different. The key to the advancement of elbow surgery will be the development of guidelines and teachers to improve the safety of these surgeries. O’Driscoll, in the last edition of this text, detailed the learning curve necessary to allow advancement, using the arthrofibrotic elbow as an example. Although complications occurred during the development of the process, the procedure now is the method of choice for most elbow surgeons in managing this complex problem. These advances were attributable to the honesty of the investigating surgeons and their willingness to share the

Of particular interest are arthroscopy’s potential applications to the management of extra-articular pathology. Recent reports have detailed the use of arthroscopic techniques in the evaluation and management of olecrenon bursitis, distal biceps tears, and triceps tendon tears. The possibility of arthroscopic management of various instability patterns of the elbow, including eventually medial ulnar collateral ligament reconstruction, is also emerging.

INTRA-ARTICULAR OPPORTUNITY There is every expectation that the management of some fractures will be amenable to or assisted by arthroscopy. These include fractures of the radial head, coronoid, olecranon, and distal humerus. The main limitation to the use of these future techniques is imposed by the neurovascular anatomy. Future advances will depend on the increased familiarity with normal and pathologic anatomy of the elbow. Technically, the ability of the surgeon to protect these structures is critical. Localization and retraction of the nerves and arteries while maintaining visualization and safely proceeding with the surgery holds the key to progression of the application of arthroscopy to the elbow.

SECTION

B

MUSCLE AND TENDON TRAUMA

CHAPTER

44

Tennis Elbow Tendinosis Robert P. Nirschl and Gilberto J. Alvarado

INTRODUCTION Tennis elbow is a common term used to describe what was originally introduced as lawn tennis arm in 1883.39 Over the years, it has been used to describe a variety of maladies that occur in and about the elbow.6,10,12,13,19,66 The accurate diagnosis of this entity requires a thorough understanding of the epidemiology and clinical presentation as well as the pathophysiology of this condition. The traditional terms tendinitis and epicondylitis do not accurately reflect the true pathology of this condition. On the basis of clinical and surgical experience,16,25,37,50,51 it can be stated with confidence that the pathology of classic tennis elbow resides primarily in tendon tissue. Associated intra-articular issues such as synovial plica or capsular defects or degeneration, may be noted in a small percentage of patients. Therefore, rather than being inflammatory the demonstrated changes are degenerative (E. R. Stay, personal communication).34,37,63 The absence of inflammatory cells and findings of dysfunctional vascular and fibrous elements with total distortion of collagen has prompted us to describe this pathology as angiofibroblastic tendinosis.34,35,37

this condition is during the fourth and fifth decades of life. A random study of 200 tennis players in three tennis clubs revealed that half of the players older than 30 years of age had experienced symptoms of characteristic tennis elbow at one time or another.47,50 Of this group, half noted minor symptoms with a duration of less than 6 months, and the rest had had major symptoms with an average duration of 21/2 years. A larger statistical analysis of 2500 patients performed by Priest at the Vic Braden Tennis Camps revealed similar data.61,62 A study performed by Gruchow and Pelletier29 correlated playing time with the incidence of tennis elbow in club players. Not restricted to tennis and racquet sports, the incidence of the malady varies among other sports and occupations that require repetitive forearm and wrist movements, including baseball, fencing, and swimming. Stressful repetitive uses of the forearm, such as computer keyboard use, carpentry, plumbing, meat cutting, textile production, and constant handshaking (e.g., politicians) are occupations related to the occurrence of tennis elbow.

CLASSIFICATION Elbow tendinosis may be simply classified on an anatomic basis. Lateral Elbow Tendinosis (Tennis Elbow) The primary structure involved in all cases is the extensor carpi radialis brevis tendon origin. The anterior edge of the extensor digitorum communis may be involved in approximately 50% of the cases as well. Occasionally, the underside of the extensor carpi radialis longus and, rarely, the origin of the extensor carpi ulnaris are also involved.

The flexorpronator mass origin, which is located about the medial epicondyle, includes the structures most commonly related to medial elbow tendinosis. The primary structures involved in the majority of cases are the flexor carpi radialis and the pronator teres origin. The flexor carpi ulnaris origin is involved in 5% of cases.

Medial Elbow Tendinosis (Golfer’s Elbow)

INCIDENCE Lateral tendinosis typically affects approximately 2% of the general population. The dominant arm is affected in more than half of the patients. The peak incidence of 626

Chapter 44 Tennis Elbow Tendinosis

An additional complicating factor associated with medial elbow tendinosis is ulnar nerve compression neuropraxia (cubital tunnel syndrome). This phenomenon is evident in approximately 30% of all cases51-53 (see Chapter 45). “Country Club Elbow” It is common to have combined signs and symptoms of both lateral and medial tennis elbow tendinosis occurring simultaneously. Beause this combination commonly occurs in recreational golfers and tennis players, we have coined the term “country club elbow.”

Tendinosis of the triceps at its attachment to the olecranon is relatively uncommon as an isolated event, but it has been noted in throwers (e.g., baseball players, javelin athletes) in association with olecranon compartment abnormalities, such as synovitis and loose bodies.

Posterior Tennis Elbow

ASSOCIATED ABNORMALITIES AND DIFFERENTIAL DIAGNOSIS A thorough history and physical examination of the neck, shoulder and entire upper extremity is essential. Several associated abnormalities are often found in combination or as separate entities. These abnormalities include: Ulnar Nerve Neuropraxia (Cubital Tunnel Syndrome) Ulnar nerve neuropraxia is commonly as-

sociated with medial elbow tendinosis and is of special note because it has an impact on the prognosis51-53 (see Chapter 45). Carpal Tunnel Syndrome Approximately 10% of elbow tendinosis patients may also have signs and symptoms of carpal tunnel syndrome.46,51-53

The association of carpal tunnel syndrome and trigger finger, as well as the association of rotator cuff tendinosis, bilateral elbow tendinosis and cubital tunnel syndrome, has led me (R. N.) to the conclusion that a constitutional factor may play a significant role in certain patients with elbow tendinosis.46,51,53 This combination of pathology has been coined mesenchymal syndrome (R. P. Nirschl, unpublished data).

Mesenchymal Syndrome

Radial Nerve Entrapment Entrapment of the motor branch of the radial nerve in the radial tunnel at the canal of Froshe (posterior interosseus nerve) may coexist with and can cause symptoms similar to those seen with lateral elbow tendinosis. Diagnosis is confirmed by find-

627

ings of electromyographic abnormality. Roles and Maudsley64 reported a surgical experience with 33 cases in 1972. In the Roles report, specific care was taken to decompress the radial tunnel by releasing the origin of the extensor carpi radialis brevis. Thus, the success of the reported operation may be due to an alteration of the origin of the extensor brevis rather than decompression of the nerve. Entrapment of the posterior interosseous nerve has also been implicated as the cause of lateral elbow pain by Werner,77 Dobyns (personal communication), and others (see Chapter 46). Entrapment of the radial nerve proximal to the sensory-motor bifurcation of the radial tunnel syndrome has also been described. A random sample of 20 electromyographic studies in patients with the classic signs of clinical lateral tennis elbow and suggested radial tunnel symptoms, however, failed to reveal any radial nerve abnormality (R. P. Nirschl, unpublished data). In most instances, if posterior interosseus nerve entrapment does occur, it is not associated in a major statistical way with classic lateral tennis elbow. In his classic study, Werner77 did report that the two coexist in about 5% of patients. When, on occasion, entrapment of the posterior interosseous nerve does occur, it may present as an entirely separate entity with vague aching symptoms that are more diffuse and felt more distally over the extensor muscle mass, tenderness in the same more distal forearm area, and a provocative handshake stress test that elicits symptoms in resisted supination. Most commonly, electromyographic studies tend to be normal in both radial tunnel syndrome and posterior interosseus nerve entrapment, thereby clouding the opportunity for objective laboratory diagnostic clarity. As noted earlier, multiple areas of tendinosis often occur in association with tennis elbow.46,51,53 As noted earlier, the term mesenchymal syndrome has been employed to identify this subset of patients.46 It is the author’s clinical hypothesis, that this entity is hereditarily based and probably represents a slight collagen distortion—perhaps cross-linkage—as it relates to tendons. The practical ramifications of this entity include the necessity of rehabilitative exercise dedicated to the shoulder as well as the elbow when one formulates a treatment plan. Rotator Cuff Tendinosis

Cervical Osteoarthritis and Nerve Root Compression Gunn and Milbrandt30 have reported pain relief

in 53 cases of tennis elbow by directing treatment to osteoarthritis of the cervical spine. Because the greatest incidence of tennis elbow occurs in individuals in the fourth and fifth decades of life, coincidental cervical osteoarthritis is common. Because the findings of lateral tennis elbow are usually specific, including response to local elbow tendon injections, it is unlikely that osteo-

628

Part VI Sports and Overuse Injuries to the Elbow

arthritis in the cervical spine is anything but a coincidental finding. The report, however, reinforces the concept that shoulder and neck problems often occur in combination and must be addressed by rehabilitation. Individuals who use the arm with high torque and shearing forces, as in the aggressive activities of baseball or javelin throwing, are vulnerable to associated intra-articular problems. These generally take the form of synovitis, traumatic osteoarthritis,45 and osteocartilaginous loose bodies present in the lateral or, more rarely, medial elbow compartments, as well as in the posterior olecranon fossa when associated with ligamentous laxity of the medial ulnar collateral ligamentous structures. Ulnar nerve neuropathy (cubital tunnel syndrome) commonly complicates the medial tendinosis clinical picture. Appropriate history, physical, and imaging examinations identify this subset of patients, and treatment should be adjusted accordingly. In a review, Baker and Cummings1 demonstrated that in some, there is arthroscopic evidence of capsular degeneration and synovial plica coexists with degeneration of the extensor carpi radialis brevis.1 In a review of his arthroscopic findings, Cummins16 reported a low incidence of intra-articular pathology, and this report is consistent with my observation (e.g., less than 5%).16 Nonetheless, the intraarticular component does exist. Intra-articular Abnormalities and Joint Laxity

ETIOLOGY Age and Sex The characteristic age at onset of classic uncomplicated tennis elbow is between 35 and 50 years, with a median of 41 years.47,61 Although the condition is most common in the third, fourth, and fifth decades, tennis elbow occurs in patients as young as 12 and as old as 80 years. Depending on a given patient population, the overall male-to-female ratio is usually equal.

The overall intensity and duration of arm use associated in some instances with a constitutional predisposition is the major cause of tendinosis. In this regard, younger patients such as competitive tennis players and professional baseball athletes characteristically place high demands on the upper extremities and are at increased risk. Inadequate, marginal, or compromised musculoskeletal fitness also appears to play a role in the etiology of medial and lateral elbow tendinosis. Lateral tennis elbow is directly related to activities that increase tension loads, and hence the stress, of the wrist and finger extensors and, possibly, the supinator muscles. Funk and associates22 revealed that the extensor carpi radialis brevis is active with flexion, extension, varus, Overuse

and valgus stress, hence, supporting the notion of overuse or overexertion of this anatomic structure. Medial tennis elbow characteristically occurs with wrist flexor activity and active pronation, as in baseball pitching, the tennis serve and overhead strokes, and the pull-through strokes of swimming. Posterior tennis elbow consists of extension overload of the triceps attachment that occurs in sports such as javelin throwing, baseball pitching, and football that incorporate techniques that initiate a sudden forceful elbow extension. The primary overload abuse in tendinosis is caused by intrinsic muscular contraction. These muscular contractile overloads may occur concentrically or eccentrically. Micro tears that occur within the tendon intercellular substance as a consequence of these overloads may be the inciting factor to tendon degeneration. Other forces such as valgus tensile extrinsic overload common in baseball (e.g., valgus instability or macro trauma) are more likely to cause excessive joint torque forces, leading to ligamentous rupture and traumatic osteoarthritis. In these sports activities, therefore, a distinction from classic tendinosis occurs because combination pathologies are present. Therefore, the etiologies in these circumstances also include both intrinsic and extrinsic factors. Traumatic Etiology Repetitive overuse is clearly associated with the development of tennis elbow.50,61,62 A typical sports patient is an active recreational tennis player who plays at least three or four times per week.6,61,62 Less commonly, acute onset may be associated with a direct blow to one of the epicondylar areas or a sudden extreme effort or activity.

PATHOLOGY GROSS ABNORMALITIES Before 1964, defined pathoanatomy was not known precisely. In 1922 Osgood,57 and in 1932 Carp,13 related the condition to radiohumeral bursitis. Goldie,25 in his classic 1964 report, was the first to describe pathology adjacent to the lateral elbow. Goldie used longitudinal incisions and binocular magnification for more thorough assessment of the tissues.25 Before Goldie’s report, previous release techniques described by Bosworth8 and Hohmann31 failed to observe specific pathologic tendon abnormalities. Careful gross surgical inspection of the abnormal tendinosis specimen reveals a characteristically grayish color and homogeneous and generally edematous tissue (Fig. 44-1). This typical gross pathologic appearance is present in lateral, medial, and posterior tendinosis.

Chapter 44 Tennis Elbow Tendinosis

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FIGURE 44-1

Gross pathologic appearance. The brevis origin is exposed by retracting the extensor longus anteriorly (closed arrows). The characteristic visual appearance of angiofibroblastic hyperplasia (open arrow) is a grayish, homogeneous, edematous, and friable tissue. This appearance has led us to coin the phrase thick unhappy gray tendon, weeping with edema.

Indeed, similar visual characteristics are present in tendinosis involving the rotator cuff, and patellar and Achilles tendons, and even in plantar fasciosis (fasciitis). In my original surgical series of lateral tennis elbow, 97% of cases demonstrated varying degrees of this pathologic tissue at the origin of the extensor brevis tendon (which was ruptured in some degree in 35%).53 Observations in these and subsequent surgical cases also revealed that approximately 50% of cases also had associated tendinosis changes in the anteromedial edge of the extensor digitorum communis or extensor aponeurosis (usually 10% to 20% of the volume of the extensor digitorum communis tendon).51-53 Radiographic examination revealed that 22% of patients had some form of bony exostosis at the tip of the lateral epicondyle.51-53 Soft calcification in the substance of the tendon can also occur, but this finding is rare. Today, in some cases, the use of magnetic resonance imaging (MRI) may be helpful in demonstrating pathology at the lateral epicondyle. In the editor’s (B. F. M.) experience, this image is very rarely indicated to diagnose epicondylitis (Fig. 44-2).

MICROSCOPIC PATHOLOGY An understanding of the dense connective tissue that makes up the fibrous portion of the tendon is necessary for a better appreciation and definition of the pathologic process that is present in tennis elbow (E. R. Stay, personal communication). In tendons, collagen fibers and primary tendon bundles run parallel courses. In normal tendons, nerves and blood vessels extend through the major connective tissue septa but do not invade the fascicles (E. R. Stay, personal communication).67 On gross

FIGURE 44-2

Altered magnetic resonance imaging signal at the lateral epicondyle in a patient with lateral epicondylitis.

FIGURE 44-3 Angiofibroblastic hyperplasia. The absence of inflammatory cells has resulted in the term tendinosis replacing tendinitis.

examination, the tendon appears firm, taut, and yellowish white or beige.51,53,54 In tendinosis, the abnormal tissue ordinarily can be identified easily by its appearance and is distinct from the normal tendon. Visual examination usually reveals gray, dull, sometimes edematous and friable, immatureappearing tissue that grossly resembles firm granulation tissue.51,53,54 Microscopically, the normal orderly tendon fibers are disrupted by a characteristic invasion of fibroblasts and vascular granulation-like tissue, which may be described as an angiofibroblastic hyperplasiatendinosis34,37,50,51,54,67 (Fig. 44-3). Adjacent to this early proliferating vascular reparative tissue, the tendon appears hypercellular, degenerative, and microfragmented. The degree of angiofibroblastic infiltration appears to correlate generally with the duration of symptoms.47,50,53 In advanced lesions, adipose, connec-

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FIGURE 44-4

Microscopic appearance on hematoxylin and eosin stains may reveal hyaline degeneration as a feature of the surgical pathology of tennis elbow.

FIGURE 44-5

tive, and even musculoskeletal tissue can reveal infiltration by this pathologic proliferative tissue.37 Others have noted the neovascular channels but emphasized that the mesenchymal cell proliferation indicated that the appearance was one of a healing process.67 On the other hand, Regan and colleagues63 compared 12 patients having surgery for lateral epicondylitis with 12 control patients. The unequivocal changes of hyaline degeneration were interpreted as demonstrating that the basic pathologic lesion was one of degeneration, although the increased vascularity noted by others also was reported. These investigators emphasized the fact that there is no microscopic evidence of inflammation associated with tennis elbow (Fig. 44-4).63 Evidence of acute or chronic inflammation is virtually absent in all cases. In cases treated with corticosteroid injection, nonpolarizable amorphous eosinophilic material can be identified, often without any foreign body response and usually without evidence of calcification (Fig. 44-5). Indeed, the proliferating vascular reparative tissue often insinuates itself between normal and abnormal tissues in regions close to the injection site.67

copy of tennis elbow tendinosis in nine surgical resection specimens. The origin of the extensor carpi radialis brevis was compared with 10 cadaveric specimens of the same anatomic region. These studies revealed that myofibroblasts are present in tendinosis material, a cell type with contractive properties not usually found in healthy tendons. Tendinosis material, therefore, contains hyperplasia of nonfunctional vascular elements, active distorted fibroblasts, and a lack of lymphocyte or neutrophilic populations that is clearly distinct from inflammatory tendinitis and/or normal tendon.37 This study reinforces the prior original hematoxylin and eosin (H&E) stain microscopic observations that “tendinosis” or degeneration is the histopathologic lesion in tendon overuse.51,54,67

IMMUNOHISTOLOGY AND ELECTRON MICROSCOPY OF TENDINOSIS In 1999, Kraushaar and Nirschl37 reported a study of the histology, immunohistochemistry, and electron micros-

Cortisone injection site. Microscopic photograph demonstrates nonpolarizable amorphous eosinophilic material.

WHAT CAUSES THE PAIN? We have pondered this question for a matter of years. The initial presumption of causation was that of regional anoxia with a production of noxious chemicals (e.g., soft tissue avascular necrosis). Khan and Cook34,35 have agreed that the histopathology is devoid of inflammatory cells and have suggested that noxious agents including chemical mediators, matrix substances and disrupted collagen may stimulate nociceptors. Voloshin and associates73 have advanced a similar suggestion concerning rotator cuff and bursal pain. Tasto and col-

Chapter 44 Tennis Elbow Tendinosis

leagues,71 in preliminary basic science investigations, report the possibility of free nerve endings, as noted by the identification of immunohistologic markers for nerve. However, the identification of free nerve endings themselves has not been supported by our electron microscopy evaluations.37 The work of Lian and associates38 on patellar tendinopathy identifies the ingrowth of substance P fibers with the presumption that this may play a nociceptive role.

CLINICAL CORRELATIONS OF PATHOLOGY A complete evaluation of the patient includes range of motion and strength testing of the neck, shoulder and wrist. Grip strength and pain rated on a continuous scale as well as forearm circumference should be documented. The area of maximal tenderness in lateral elbow tendinosis typically lies 5 mm distal and anterior to the midpoint of the lateral epicondyle (e.g., the pathoanatomy typically is not at the epicondyle). Provocative stress testing consists of resisted wrist and finger extension with the elbow in flexion with marked accentuation as the elbow is brought into extension (Fig. 44-6). Increased pain with extension is common even with mild tendinosis. When provocative tests are positive in flexion, the need for surgical intervention is more likely in our experience. The following tendinosis pathologic categories, with corresponding clinical and therapeutic implications, are speculated.51

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CATEGORY I Acute, reversible chemical inflammation is likely, but no angiofibroblastic invasion is seen. Comment: Because this category is rarely operated upon, the histopathology absence is speculative.

Pathology

Minor aching pain is evident, usually after heavy activity.

Clinical Signs

Treatment There is a quick response to simple antiinflammatory measures followed by rehabilitative exercise and future avoidance of force overload or overuse.

CATEGORY II There is a partial angiofibroblastic invasion. The pathology is permanent, but some healing response may occur, depending on the biologic maturation of the pathologic process and the extent of involvement.

Pathology

Often, there is intense pain with activity as well as symptoms at rest. After periods of rest, however, most routine activities can be accomplished without significant discomfort. Note: There is no clinical test to determine the quantity of tendinosis, but history including pain phases and clinical evaluation is reasonably reliable in this quantitative assumption. Magnetic resonance imaging (coronal view) will usually reveal a pathological signal.

Clinical Signs

Treatment If less than half of the tendon diameter is involved, treatment concepts that promote healing gradually bring about resolution, and this process can be managed nonoperatively. Occasionally, however, these patients require surgery for a more complete resolution of symptoms.

CATEGORY III Extensive angiofibroblastic invasion degeneration with or without partial or complete rupture of the tendon is present.

Pathology

Clinical Signs Significant functional defects that include pain at rest as well as night pain make routine daily activities difficult or impossible. At this stage, coronal MRI will reveal major signal changes. Again, history and physical examination will indicate this pathological level in most instances, thereby negating the need for MRI in the typical case. FIGURE 44-6

Arthroscopic inspection of the lateral capsule reveals a full-thickness tear, including the capsule in a patient with chronic epicondylitis/ tendinosis.

Treatment The condition invariably requires surgery for pain relief, as this advanced stage usually does not respond to nonoperative measures.

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NONSURGICAL TREATMENT The general concepts of elbow rehabilitation are covered in detail in Chapter 9. A brief overview, however, is appropriate at this time.48-50,55 The patient with elbow tendinosis most commonly presents for evaluation and treatment because of pain, rather than impairment of mechanical function. Therefore, it is important to control pain, but this, in itself, does not necessarily imply enhancement of healing. The time-honored modalities of relative rest (not absence of activity but abstinence from abuse) and application of cold are appropriate. Activity that aggravates the condition should be eliminated. The use of aspirin as an anti-inflammatory agent is the first choice, but nonsteroidal anti-inflammatory medications, including ibuprofen, and naproxyn, seem to be helpful in some patients. The relief offered by the topical medication dimethyl sulfoxide (DMSO) was no greater than that of a placebo.59 The physical therapy modality of high-voltage electrical stimulation has been helpful in relieving pain, and the author’s anecdotal observations suggest the possibility of enhancing a biologic healing response.48,51,55 Paoloni and associates have suggested that nitric oxide patches aid in pain control.58 If the malady does not respond to an appropiate pain control program and the patient is incapable of performing the prescribed rehabilitative exercises, a cortisone injection may be indicated.14 The senior author uses 2.5 mL of 0.5% lidocaine (Xylocaine) mixed with 20 mg of triamcinolone, instilled under the extensor brevis just anterior and slightly distal to the lateral epicondyle into a triangular fatty recess that occupies this area. If the injection is too superficial (e.g., above the extensor carpi radialis brevis at the epicondyle) or is done on a repetitive basis, subdermal atrophy may occur.48,72 The repeated use of cortisone injections (more than a total of three) is inappropriate and harmful with the potential for tenocyte cellular death and weakening of the surrounding normal tissues.72 Indeed, some patients are extremely sensitive to local instillation of cortisone; subcutaneous atrophy (Fig. 44-7), occasionally after only one injection, may be noted, especially when the injection is placed superficial to the tendon. Therefore, we recommend that no more than three injections should be instilled in any one area. In addition to superficial or direct injections, intratendinous injections should be avoided.2,50-52,72

PROMOTION OF HEALING A biologic healing response includes infiltration of healthy neovascular and fibroblastic elements, collagen production, and collagen maturation at the cellular level in addition to the restoration of strength, endurance, and flexibility to the entire extremity, including the upper

FIGURE 44-7

Subcutaneous atrophy from a subdermal cortisone injection.

back, neck, and shoulder. The healing process may be hastened by three general measures: relative rest, highvoltage electrical stimulation, and most importantly, rehabilitation exercises.48,49,55

Relative Rest The injured part may be rested through the use of (1) immobilizing devices to avoid abuse, (2) alteration of inappropriate technique or activity, (3) selection of proper equipment, and (4) counterforce bracing. Rest attained by complete immobilization such as casting often weakens the affected area and has not been effective in controlling pain when activities are resumed. Partial immobilization by wrist extension splints has the limited value of casting except short term use in the early, fully reversible inflammatory phase of category I injuries. Overall, therefore, modification or elimination of abusive activities is a more appropriate and useful interpretation of the term relative rest than is formal immobilization. A graduated activity program for the injured part, coupled with an aggressive activity program for the adjacent normal, uninjured tissues, should be emphasized.

Abstinence from Abuse

Careful history taking and observation are fundamental to the identification of faulty activity technique. Evidence is accumulating that the correct technique of a sport or occupation not only enhances activity performance but also is less likely to cause injury.48-50,55 The sports most likely to be causally related to either lateral or medial tennis elbow include tennis, golf, baseball throwing, squash, racquetball, weightlifting, fly and cast fishing, swimming, and track and field events. The commonly associated occupational activities include meat cutting and handling, Alteration of Training Technique

Chapter 44 Tennis Elbow Tendinosis

carpentry, plumbing, repetitive assembly line activity, computer keyboard and mouse activity, typing, writing, and handshaking (e.g., politicians at campaign time).48,50,55 Equipment (especially in construction occupations and the racquet sports) may play an important role in imparting forces that can result in tendon overuse injury.6,29,47,48,50,51,55 Biomechanically, in tennis as well as other implement ball sports it is most appropriate to strike the ball at the center of percussion (“sweet spot”) because the increased torsion of off-center hits increases the stresses on musculotendon units, especially at or near the tendon epicondylar attachment areas.6,27,46,47,61,62 Activities that cause forearm impact or stress necessitate equipment of the proper size, weight, balance, and grip to avoid excessive forces.6,27,48 In general, the larger the handle of the device, the greater the leverage for torsion control, but the handle size should be matched to hand size.6,48,50,55 The distance from the midpalmar crease to the ring finger is a helpful aid in selecting the proper handle size48,50-52 (Fig. 44-8). Alteration of Equipment

Finally, the weight, dimension, and flexibility of the equipment should match the available strength of the individual. It is better to use a device that is somewhat lighter to ensure proper positioning of the equipment at the time of impact.6,50 In racquet equipment, however, adequate mass is important to absorb the torsion of off-centered ball impacts. The concepts of functional elbow bracing for tennis elbow were initially introduced by Ilfeld and Field in 1965,32 and by Froimson in 1971.20 The term counterforce, introduced by the senior author (R. P. N.) in 1973,47 describes a wide nonelastic support curved for better fit and support of the conical shape of the forearm.48,51,52,55 Simply stated, the counterforce concept supplements tendon origin and constrains full muscular expansion, thereby decreasing intrinsic muscular force to sensitive or vulnerable areas—namely, the forearm extensors for lateral tennis elbow and the forearm flexors for medial tennis elbow (Fig. 44-9). Studies have shown objective improvement in wrist extension and grip strength or positive biomechanical effects with elbow bracing.20,27,32,75 In medial tennis elbow, an additional support just distal to the medial epicondyle is sometimes helpful.48,50,51 Counterforce Bracing

FIGURE 44-9

FIGURE 40-8

Author’s method of determining proper racket grip diameter (see text).

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Lateral elbow counterforce brace. The nonelastic support is curved to fit the conical forearm shape. Dual tension straps extend the width of the brace and allow full brace tension control. Wide balanced support appears to be most effective for clinical pain control.

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More recent focused compression braces (either air or gel pads) offer no observed advantage and may have a theoretical disadvantage if balanced forearm muscle strength is disturbed. As noted previously, rigid types of immobilization at the elbow or wrist relieve pain, but at the price of atrophy and immobility, and thus are not recommended.

High-Voltage Electrical Stimulation High-voltage electrical stimulation in the treatment of both acute and chronic tendinosis is an accepted treatment modality.3,4 In the author’s experience, this modality diminishes pain (presumed chemical inflammation) and may promote healing. Our standard practice for tendinosis is to employ four to six sessions of highvoltage electrical stimulation during a 2- to 3-week period.48,53,55

Rehabilitative Exercise Program This topic is discussed in detail in Chapter 9. It is important to emphasize, again, that rehabilitation should include not only the cardinal forearm exercises but also those for the upper back and shoulder.48,49,55 Once the probable initial adjacent inflammatory response and the pain have been controlled, an orderly progression of the graduated strength and endurance exercise is started.28,48,55 The patient is protected until about 60% of the rehabilitation exercise goals.44,48,51,53 After the patient has reached the early rehabilitative strength and flexibility goals, these functions are monitored by objective testing until strength, endurance, and flexibility have returned to nearly normal levels. Continuation of the strength and endurance exercise program beyond the preinjury level includes either isokinetic or isotonic, interspaced with isoflex exercises.28,48 Before a final return to a sport or an occupational activity, the patient should be capable of anaerobic sprint repetitions to fatigue without major activity pain.28,48,55

Graduated Exercise and Full-Strength Training

ALTERNATIVE NONOPERATIVE APPROACHES Recent reports have suggested that pain control and possibly biologic alteration of tendinosis tissue may be achieved by other approaches. These include shockwave, various forms of prolotherapy injections (autologous blood, platelets, and dilute sugar), cold laser, nitric oxide patches, magnetic and high intensity infrared heat,4 and acupuncture. Of this group, shock-wave, nitric oxide patches, and autologous injections have the most research support, but success has been inconsistent and further research is indicated.58,65,69,76

SURGICAL TREATMENT HISTORICAL REVIEW The popular literature concerning the surgical treatment of tennis elbow is considered to have begun in 1927 with Hohmann,31 who described release of the extensor aponeurosis at the level of the lateral epicondyle. The technique, now commonly referred to as a muscle slide or release procedure,5,8 does not identify the offending pathology.5,8-10,13,68 In 1936, Cyriax17 was the first to correctly identify by intuitive means the origin of the extensor carpi radialis brevis as the major site of pathology. For treatment, Cyriax theorized that the extensor brevis origin was often partially torn, and reported treatment by closed manipulation of passive forceful elbow extension and forearm supination, thereby converting a partial tear to a complete tear, and thus inciting an active biologic healing response while relieving tension overuse. Wadsworth74 described a similar approach in 1972 with approximately a 50% success rate and with an audible or palpable snap or popping associated with the maneuver. In 1955, Bosworth8 reported a series of 27 elbows, in which four different techniques were used. He suggested that his third technique, which included a release of the extensor aponeurosis as well as the orbicular ligament in and about the radial head in four patients, was seemingly curative. Curiously, Bosworth8 performed the Hohmann-type release operation in 17 instances, but “all” still had some complaints. In addition to the concepts of tendon release as advanced by Hohmann and Bosworth, a companion intervention of resection of a portion of the lateral epicondyle has been undertaken by some authors.23,41,57,60 This approach undoubtedly was based on the erroneous premise that the pathology was an inflammation of the lateral epicondyle. In a fascinating application of the conviction that the origin of the extensor carpi radialis brevis was the source of pathology, Garden23 reported 50 instances in which the extensor brevis tendon was lengthened in the distal forearm. He concluded, as had others,15,70 that active muscular contraction with tendon tensioning of the extensor carpi radialis brevis, causes pain. In 44 cases treated with open Z-plasty lengthening at the extensor carpi radialis brevis musculotendinous junction, Garden noted that full pain relief at the elbow was obtained in all cases. However, in 20 cases (40%) strength had not returned to normal, and pain was noted at the distal surgical site in some cases.

Chapter 44 Tennis Elbow Tendinosis

SURGICAL OPTIONS As noted earlier, historical open-surgical options have focused predominantly on the release of the extensor aponeurosis, as originally proposed by Hohmann. More recent versions of this approach have included percutaneous release.5,68,79 The reports to date are shortterm follow-ups but do suggest that this approach can be effective in as many as 90% or more of patients and has a relatively low complication rate.5,68,79 As an adjunct to the surgical release of the common extensor tendon, Cabot11 also recommends the release of the anterior capsule for patients who have a flexion contracture. He indicates an 87% success rate among the 47 cases so treated. In my observation, elbow adhesive capsulitis is rare with the classic tennis elbow. Note: In those with motion limitation, the editor (B. F. M.) carefully assesses the possibility of an intraarticular cause. Several surgical options are available besides release of the extensor aponeurosis from the lateral epicondyle. In 1964, Goldie25 presented a comprehensive thesis of 49 patients that for the first time detailed pathologic changes in the subtendinous tissue in the lateral epicondyle. He described tendinous tissue invading fibroblastic cells, as well as vascular infiltrates. Kaplan36 reported three cases of resection of the radial nerve branches to the lateral epicondyle and lateral articular areas, with no attempt to identify or remove pathologic tendon tissues. He noted excellent pain relief, but denervation of a motor branch to the extensor brevis probably occurred with this technique. Interestingly, his three patients were hospitalized postoperatively for an average of 7 days. Roles and Maudsley64 described 33 patients who responded to surgical decompression of the posterior interosseus nerve and release of the brevis tendon. The surgery was performed by 11 different surgeons over a 10-year period. Posterior interosseous nerve compression continues to be recognized as an entity, with recent reports emphasizing the association of compression of the nerve at the arcade of Frohse.12,33 In one study, 5% of patients were noted to have posterior interosseus nerve entrapment in association with tendinosis.77 In my observation, true posterior interosseous nerve compression syndrome is uncommon in association with lateral elbow tendinosis. More recently, Tasto71 has introduced radiofrequency ablation of tendinosis pathologic tissue and Baker and Cummings1 introduced an arthroscopic release approach as a surgical option for lateral tennis elbow. The arthroscopic approach describes release of the extensor brevis as well as débridement of occasional intraarticular synovitis when present.21 Importantly, in a report of 18 cases in which Cummins did open surgical

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inspection after arthroscopy, he noted significant unresected tendinosis tissue in 14 of the cases.16 Further communication with Cummins reveals that he is no longer certain that arthroscopy adds value to lateral elbow tendinosis surgery.16 Arthroscopy also results in increased instrument costs, set-up time, and operative time. Arthroscopy also risks neurovascular harm and intra-articular scuffing, and results in some flexion contracture via intra-articular transgression for a problem that is extra-articular. For those few cases (5% in our experience) with associated intra-articular pathology45,55 (easily determined preoperatively by accurate history, and physical and imaging examinations), an expanded mini-open approach with a small incision arthrotomy expansion at the time of tendinosis surgery is more compelling than arthroscopy.53 Editors note: I do prefer arthroscopy to expanding the open procedure when concerned about intra-articular pathology (B. F. M.).

SURGICAL PATHOLOGY A basic principle of any orthopedic surgery is that a clear definition of the pathology and its location is essential for a well-conceived surgical procedure. Because the extensor brevis origin is largely covered by the muscle of the extensor carpi radialis longus, extensor digitorum communis (EDC) aponeurosis release operations do not visualize the extensor carpi radialis brevis tendinosis pathology. Release of the common extensor origin, however, may alter the attachment of the brevis, because a significant segment of its origin is derived from the extensor aponeurosis.8,10,26,53 This anatomy helps to explain the instances of success of release techniques, including percutaneous procedures.5,24,68,78 Blazina and colleagues7 suggested that the major pathologic tendon changes in chronic patellar tendinosis occur by moderate but repetitive overload that results in microrupture of the normal tendinous tissue and secondary replacement by a healing process that is pathologic. Although this theory is attractive, I believe an additional more likely hypothesis is related to vascular supply and follows a sequence of events similar to that described by McNab,40 as well as Moseley and Goldie,43 in the rotator cuff region of the shoulder; namely, vascular compromise, an altered nutritional state, and intrinsic mechanical failure that results from force overload (e.g., tension and shear forces). In any event, actual gross disruption of the extensor carpi radialis brevis tendon, usually incomplete, occurs in approximately 35% of my surgical cases. Overall, the extensor carpi radialis brevis is involved by tendinosis in 100% of cases, with additional involvement of the anteromedial aspects of the extensor digitorum communis tendon (e.g., extensor aponeurosis) also in approximately 50%.

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HISTORICAL SURGICAL RESULTS The literature suggests that for lateral tennis elbow, approximately 85% to 90% of patients can expect some pain relief success with the varied surgical techniques discussed.8,9,15,19,41,60,68,78 Conversely, failure of release techniques is fairly common in this author’s experience. The most common cause for continuing pain after the index surgery is failure to identify and resect pain-producing tendinosis tissue (an integral conceptual deficiency in the release approach) (Chapter 46). Fortunately, when release techniques result in failure, revision salvage surgery can still offer an 85% opportunity of surgical success.42,56 Most articles citing release techniques also tend to be limited or silent regarding the logistics and speed of postoperative recovery. Using this author’s preferred technique, 97% of patients can expect pain improvement.51,53,54 In 85%, full return without pain to all prior activities including sport can be expected.54 In 12%, improvement has occurred, with some pain during aggressive activities, but often patients are able to participate in their usual sports, including the racquet and throwing sports. In about 3%, no improvement is obtained, and the surgery is considered a failure. The reasons for failure of the preferred technique are not always clear, but possibilities include misdiagnosis, such as entrapment of the posterior interosseous nerve and nonphysical or secondary gain factors.42,56 In 2006, we reported a 10- to 14-year follow-up of our preferred technique. The results of 97% success were maintained.18

AUTHOR’S PREFERRED SURGICAL TREATMENT METHOD SELECTION FACTORS FOR SURGERY Failure of Rehabilitation and Duration of Symptoms Patients who have undergone a high-quality

resistance-exercise rehabilitation treatment program but have symptoms that linger for more than 1 year are more likely to have category III pathologic changes.53 The success of cortisone injections or the delivery of corticosteroids by other mechanisms generally has been accepted clinically. Clarke and Woodland14 confirmed this clinical impression but emphasize that the improvement is short lived and recurrence is the rule. In my experience, patients who have received three or more cortisone injections in or about the same area are likely surgical candidates (R. P. Nirschl, unpublished data).52,53 There are two considerations in this group of candidates. First, the patient’s symptoms were of such severity that cortisone injection Multiple Cortisone Injections

was warranted and may have indicated a higher initial pathologic category at the time the patient sought clinical help. Second, the studies of Unverferth and Olix72 and others2 suggest that large amounts of cortisone infiltration have a deleterious effect on the quality of the tendon, perhaps increasing the indication for surgery secondary to cortisone induced pathological change. In the author’s observations, bony exostosis at the anteromedial area of the lateral epicondyle is present in approximately 20% of those undergoing surgery, suggesting a more refractory process. Note: The bony exostosis is not the primary pain producer, however. The etiology of the exostosis may be an expression of the degenerative process.

Lateral Epicondylar Bony Exostosis

Pain (Constant) Without Activity Pain at rest and that which alters routine daily function invariably reflects category III tendon pathology, suggesting the need for surgery.53

It has been the author’s experience that if easy injection flow into the triangular recess under the extensor brevis origin, just distal and anterior to the lateral epicondyle, is present, loosened friable, edematous and torn tendinosis tissue is also present. This injection “feel” suggests a category III pathologic change.

Ease of Injection Flow

Tendon Calcification Calcification in the body of the common extensor tendon (extensor aponeurosis) just distal to the lateral epicondyle has been noted on rare occasions. This form of presentation represents a pathologic tendon and is separate and distinct from lateral epicondylar exostosis (Fig. 44-10). Associated Intra-articular Pathology In the author’s experience, approximately 5% of lateral tennis elbow cases have associated intra-articular signs and symptoms (e.g., synovial entrapment or plica, adhesive capsulitis, chondromalacia, occasional loose bodies). Combined tendinosis and intra-articular pathologies should be evident with appropriate preoperative evaluation. Such combined pathologies warrant resection and repair of the tendinosis and a mini-arthrotomy to resolve the intra-articular pathology. Arthroscopy could be an alternative in this circumstance (see earlier). Patient Frustration Those unable or unwilling to modify their activity level are likely candidates for surgical intervention when other appropriate indication is present (e.g., when the malady is a major limitation to the activities of daily living as well as sports and occupational activities).

Chapter 44 Tennis Elbow Tendinosis

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pain. Drilling in the appropriate area encourages hematoma formation with ingrowth of vascular and fibrotendinosis healthy replacement tissue52,53,56 (see Fig. 44-11). Tissue Repair Restoration of the normal extensor anatomic position, by sewing the posterolateral edge of the extensor longus to the anterior edge of the extensor aponeurosis, has been successful without causing loss of motion and is the repair technique of choice.51-53 Because all the incisions are made longitudinally and, in most cases, do not disturb the extensor aponeurosis attachment to the lateral epicondyle, the surgery provides a firm anchoring point for prompt initiation of the postoperative rehabilitative exercises with prompt return to full motion. Imbrication of the extensor longus over the anterior edge of the extensor aponeurosis or sewing remaining extensor brevis is unnecessary and not recommended because it tends to block full elbow extension. FIGURE 44-10

Calcification in and about the lateral epicondyle occurs in 22% of surgical cases.

LATERAL TECHNIQUE (GENERAL CONCEPTS) Identification and excision of all pathologic tendinosis tissue generally includes most of, if not the entire, origin of the extensor carpi radialis brevis (Fig. 44-11). In addition (approximately 50%), excision of pathology also includes the anteromedial aspects of the extensor digitorum communis aponeurosis and, rarely, the removal of pathologic tissue from the underside of the extensor longus. When the extensor brevis origin is excised, the intimate and firm attachments between the fascia of the extensor brevis and the orbicular ligament and insertion into the distal aponeurosis eliminate any distal extensor brevis retraction beyond 1 to 2 mm (e.g., normal muscle-tendon unit length is maintained). Maintenance of normal muscle tendon length ensures normal leverage of the remainder of the musculotendinous unit of the extensor brevis; therefore, return to essentially normal forearm extensor strength can be anticipated.

Identification of Pathology

Healing Once the pathologic tissue has been removed, a tissue defect in the triangular recess is present in varying degrees. It is appropriate to attempt to enhance the blood supply to this area by drilling one or two small holes through the cortical bone to cancellous depth in the triangular recess just distal and anteromedial to the epicondyle. Do not however drill into the epicondyle itself because this will increase postoperative

Postoperative Rehabilitation The postoperative rehabilitation of either lateral or medial tennis elbow for the author’s preferred techniques follows the treatment principles outlined for conservative care48,52 and detailed in Chapter 9. The elbow is maintained in 90 degrees of flexion, with wrist and hand free in an easily removable elbow immobilizer for approximately 6 days.48,52,53 Limbering activities are undertaken, however, on days 2 to 3, generally by working the arm actively in a warm shower, followed by a gradual return to strength training exercises (usually daily) without resistance for the first 3 weeks postoperatively. Starting at 3 weeks postoperatively, gradual strengthening isotonic and isoflex resistances are implemented, with protection by a medial or lateral counterforce brace. Postoperative counterforce bracing usually persists for 2 to 3 months for activities of daily living (ADLs) and thereafter for sports or occupational activity. Strength training and discretionary use of the arm for other activities are individualized to patient needs.48,52,53 For recreational tennis, it is usual to start easy strokes about 6 weeks from the time of surgery. For return to competitive athletics or occupational activities, the increase in intensity should be gradual and gentle, with counterforce brace protection until full strength has returned to the extremity. Some document this stage by Cybex or dynamometer tests and circumferential forearm girth.48,52,53 Satisfactory completion of the rehabilitative process includes transitional performance–type exercise programs for a return to sports or occupational activities. A return to full-strength use of the arm in competitive athletics, including the world class level, averages 5 to 6 months for lateral elbow tendinosis and 6 to 8 months for medial elbow tendinosis.

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Lateral epicondyle

MAYO ©1993

A

Extensor carpi radialis longus

Degeneration-extensor carpi radialis brevis

Extensor aponeurosis Lateral epicondyle

MAYO ©1993

B

Removal - angio-fibroblastic degeneration extensor brevis

Lateral epicondyle

C FIGURE 44-11

MAYO ©1993

A, Skin incision. B, Incision at interface of extensor longus and aponeurosis. C, Excision of diseased tissue, usually of extensor brevis origin. A small incision may be made through the synovium to afford visual inspection of the lateral compartment.

Chapter 44 Tennis Elbow Tendinosis

639

Decortication by drilling anterior lateral epicondyle

MAYO ©1993

D

Closure, extensor longus to extensor aponeurosis MAYO ©1993

E FIGURE 44-11, cont’d

D, Vascular enhancement is accomplished by drilling the epicondyle as shown. E, The extensor aponeurosis is closed without tension.

ASSOCIATED CONSIDERATIONS

SUMMARY

In approximately 20% of cases, the bony exostosis noted at the tip of the lateral epicondyle is removed. When preoperative symptoms (e.g., history and physical examination) suggest an intra-articular component, preoperative bone scanning, computed tomography, or MRI may be ordered (Fig. 44-12). If positive or if intraarticular analgesia relieves the pain, arthroscopy might be considered to address intra-articular pathology. However, my experience with the miniarthrotomy, just anteromedial to the extensor digitorum communis aponeurosis closely reduplicates the postoperative morbidity of arthroscopy and is my preference in the combined surgical intervention of lateral elbow tendinosis and synovial plica (Fig. 44-13). (Editor prefers arthroscopy [B. F. M.].)

The key issue in tennis elbow, whether lateral or medial, is understanding and identification of the tendinosis histopathology (e.g., devoid of inflammatory cells). The nonoperative goals of treatment focus on revitalization of the area of tendinosis by rehabilitation (e.g., neovascularization and collagen production). If the rehabilitative process fails, surgical resection and repair is an appropriate and a highly successful option.

Acknowledgment Appreciation is expressed to E. Russell Stay, M. D., Department of Pathology, Arlington Hospital, for his initial and original histopathologic evaluation and description of tennis elbow (angiofibroblastic hyperplasia).

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FIGURE 44-12 Although the radiograph is normal, a positive 99Tc bone scan was obtained in a patient who had intra- and extra-articular lateral joint symptoms of 2 years’ duration.

A

C

B

FIGURE 44-13 Arthroscopy of the patient in Figure 40-12 shows moderate capsular degeneration (A). After the degenerated capsule was removed arthroscopically (B), the pain decreased (C).

Chapter 44 Tennis Elbow Tendinosis

References 1. Baker, C., and Cummings, P.: Arthroscopic management of miscellaneous elbow disorders. Operative Techniques Sportsmed. 6:16, 1998. 2. Balasubramaniam, P., and Prathap, K.: The effect of injection of hydrocortisone into rabbit calcaneal tendons. J. Bone Joint Surg. 54B:729, 1972. 3. Bassett, C. A. L.: Pulsing electromagnetic fields: A new method to modify cell behavior in calcified and noncalcified tissues. Calcif. Tissue Int. 34:1, 1982. 4. Bassett, C. A. L., Choksh, H. R., Hernandez, E., Pawlik, R. J., and Strap, M.: The effect of pulsing electromagnetic fields on cellular calcium and calcification of nonunions. In Brighton, C. T., Black, J., and Pollack, S. R. (eds.): Electrical Properties of Bone and Cartilage: Experimental Effects and Clinical Applications. New York, Grune & Stratton, 1979. 5. Baumgard, S. H., and Schwartz, D. R.: Percutaneous release of the epicondylar muscles for humeral epicondylitis. Am. J. Sports Med. 10:233, 1982. 6. Bernhang, A. M.: The many causes of tennis elbow. N. Y. State J. Med. 79:1363, 1979. 7. Blazina, H. E., Kerlan, R. K., Jobe, F. W., Carter, J. S., and Carlson, G. J.: Jumper’s knee. Orthop. Clin. North Am. 413:665, 1973. 8. Bosworth, D. H.: The role of the orbicular ligament in tennis elbow. J. Bone Joint Surg. 37A:527, 1955. 9. Boyd, H. B., and McLeod, A. C.: Tennis elbow. J. Bone Joint Surg. 55A:1183, 1973. 10. Briggs, C. A., and Elliott, B. G.: Lateral epicondylitis: A review of structures associated with tennis elbow. Anat. Clin. 7:149, 1985. 11. Cabot, A.: Tennis elbow, a curable affliction. Orthop. Rev. 16:69, 1987. 12. Capener, N.: The vulnerability of the posterior interosseous nerve of the forearm: A case report and an anatomical study. J. Bone Joint Surg. 48B:770, 1966. 13. Carp, L.: Tennis elbow caused by radiohumeral bursitis. Arch. Surg. 24:905, 1932. 14. Clarke, A. K., and Woodland, J.: Comparison of two steroid preparations used to treat tennis elbow, using the hypospray. Rheum. Rehabil. 14:47, 1975. 15. Coonrad, R. W., and Hooper, W. R.: Tennis elbow: Its course, natural history, conservative and surgical management. J. Bone Joint Surg. 55A:1177, 1973. 16. Cummins, C. A.: Lateral epicondylitis: in vivo assessment of arthroscopic debridement and correlation. Am. J. Sports Med. 34:1486, 2006. 17. Cyriax, J. H.: The pathology and treatment of tennis elbow. J. Bone Joint Surg. 18:921, 1936. 18. Dunn, J., Kim, J., Davis, L., and Nirschl, R.: Ten- to 14-year follow-up of the Nirschl surgical technique for lateral epicondylitis. Am. J. Sports Med. 36:261, 2008. 19. Emery, S. E., and Gifford, J. F.: 100 years of tennis elbow. Contemp. Orthop. 12:53, 1986. 20. Froimson, A. I.: Treatment of tennis elbow with forearm support band. J. Bone Joint Surg. 53A:183, 1971. 21. Field, L., Altchek, D., Warren, R., O’Brien, S., Shyhar, M., and Wickiewicz, T.: Arthroscopic anatomy of the lateral elbow. Arthroscopy 10:602, 1994.

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22. Funk, D. A., An, K. N., Morrey, B. F., and Daube, J. R.: Electromyographic analysis of muscles across the elbow joint. J. Orthop. Res. 5:529, 1987. 23. Garden, R. S.: Tennis elbow. J. Bone Joint Surg. 43B:100, 1961. 24. Gardner, R. C.: Tennis elbow: Diagnosis, pathology and treatment: Nine severe cases treated by a new reconstructive operation. Clin. Orthop. Rel. Res. 72:248, 1970. 25. Goldie, I.: Epicondylitis lateralis humeri (epicondylalgia or tennis elbow): A pathogenetical study. Acta Chir. Scand. Suppl. 339, 1964. 26. Greenbaum, B., and Vangsness, T.: Extensor carpi radialis brevis: An anatomic analysis of its origin. Presented to the Interim Meeting, American Orthopedic Society for Sportsmedicine. New Orleans, March 22, 1998. 27. Groppel, J. L., Nirschl, R. P., Pfantsch, E., and Greer, N.: A mechanical and electromyographical analysis of the effects of various joint counterforce braces on the tennis player. Am. J. Sports Med. 14:195, 1986. 28. Groppel, J. L., Nirschl, R. P., Sholes, J., and Sobel, J.: A mechanical comparison of an isoflex exercise device to the use of free weights. Unpublished data, 1984. 29. Gruchow, H. W., and Pelletier, D: An epidemiologic study of tennis elbow. Incidence, recurrence, and effectiveness of prevention strategies. Am. J. Sports Med. 7:234, 1979. 30. Gunn, C. C., and Milbrandt, W. E.: Tennis elbow and the cervical spine. Can. Med. Assoc. J. 114:803, 1976. 31. Hohmann, G.: Das Wesen und die Behandlung des Sogenannten tennissellenbogens. Munch. Med. Wochenschr. 80:250, 1933. 32. Ilfeld, F. W., and Field, S. M.: Treatment of tennis elbow: Use of special brace. J. A. M. A. 195:67, 1966. 33. Jalovaara, P., and Lindholm, R. V.: Decompression of the posterior interosseous nerve for tennis elbow. Arch. Orthop. Trauma Surg. 108:243, 1989. 34. Kahn, K., Cook, B., Mafulli, N., and Kannus, P.: Where is the pain coming from in tendinopathy? Br. J. Sportsmed. 34:81, 2000. 35. Kahn, K., Cook, B., Trunton, J., and Bonnar, F.: Overuse tendinosis, not tendinitis. Physician Sportsmed. 28:38, 2000. 36. Kaplan, E. B.: Treatment of tennis elbow (epicondylitis) by denervation. J. Bone Joint Surg. 41A:147, 1959. 37. Kraushaar, B., and Nirschl, R.: Tendinosis of the elbow (tennis elbow): Clinical features and findings of histological, immunohistochemical, and electron microscopy studies. J. Bone Joint Surg. 81A:259, 1999. 38. Lian, O., Dahl, J., Ackerman, P., Frihagen, F., Engrebetsen, L., and Bahr, R.: Pronociceptive and antinociceptive neuromediators in patellar tendinopathy. Am. J. Sports Med. 34:1801, 2006. 39. Major, H. P.: Lawntennis elbow. B. M. J. 2:557, 1883. 40. McNab, I.: Rotator cuff tendinosis. Ann. R. Coll. Surg. Engl. 53:271, 1973. 41. Michele, A. A., and Krueger, F. J.: Lateral epicondylitis of the elbow treated by fasciotomy. Surgery 39:277, 1956. 42. Morrey, B. F.: Reoperation for failed surgical treatment of refractory lateral epicondylitis. J. Shoulder Elbow Surg. 1:47, 1992.

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43. Moseley, H. F., and Goldie, I.: The arterial pattern of the rotator cuff of the shoulder. J. Bone Joint Surg. 45B:780, 1963. 44. Neviaser, T. J., Neviaser, R. J., Neviaser, J. S., and Ain, B. R.: Lateral epicondylitis: Results of outpatient surgery and immediate motion. Contemp. Orthop. 11:43, 1985. 45. Newman, J. H., and Goodfellow, J. W.: Fibrillation of the head of the radius: One cause of tennis elbow. J. Bone Joint Surg. 57B:115, 1975. 46. Nirschl, R. P.: Mesenchymal syndrome. Virginia Med. M. 96:659, 1969. 47. Nirschl, R. P.: Tennis elbow. Orthop. Clin. North Am. 4:787, 1973. 48. Nirschl, R. P.: Arm Care. Arlington, VA, Medical Sports Publishing, 1996. 49. Nirschl, R. P.: Isoflex exercise system. Arlington, VA, Med. Sports Pub., 1983. 50. Nirschl, R. P.: Prevention and treatment of elbow and shoulder injuries in the tennis player. Clin. Sportsmed. 7:289, 1998. 51. Nirschl, R. P.: Elbow tendinosis/tennis elbow. Clin. Sportsmed. 2:851, 1992. 52. Nirschl, R. P.: Lateral and medial epicondyltis. In Morrey, B. (ed.): Master Techniques in Orthopedic Surgery: The Elbow. New York, Raven Press, 1994, pp. 129-148. 53. Nirschl, R. P., and Ashman, E.: Elbow tendinopathy: Tennis elbow. Clin Sports Med. 22:813-836, 2003. 54. Nirschl, R. P., and Pettrone, F.: Tennis elbow: The surgical treatment of lateral epicondylitis. J. Bone Joint Surg. 61A:832, 1979. 55. Nirschl, R. P., and Sobel, J.: Conservative treatment of tennis elbow. Phys. Sports Med. 9:42, 1981. 56. Organ, S., Nirschl, R., Kraushaar, B., and Guidi, E.: Salvage surgery for lateral tennis elbow. Am. J. Sports Med. 25:746, 1997. 57. Osgood, R. B.: Radiohumeral bursitis, epicondylitis, epicondylalgia (tennis elbow): A personal experience. Arch. Surg. 4:420, 1922. 58. Paoloni, J., Appleyard, R., Nelson, J., and Murrell, G.: Topical nitric oxide application in the treatment of chronic extensor tendinosis at the elbow. Am. J. Sports Med. 31:915, 2003. 59. Percy, C., and Carson, J. D.: Use of DMSO in tennis elbow and rotator cuff tendinosis: Double-blind study. Med. Sci. Sports Exer. 13:215, 1981. 60. Posch, J. N., Goldberg, V. M., and Larrey, R.: Extensor fasciotomy for tennis elbow: A long-term follow-up study. Clin. Orthop. 135:179, 1978. 61. Priest, J. D., Braden, V., and Gerberich, J. G.: The elbow and tennis (part I). Phys. Sports Med. 8:80, 1980. 62. Priest, J. D., Braden, V., and Gerberich, J. G.: The elbow and tennis (part II). Phys. Sports Med. 8:77, 1980. 63. Regan, W., Wold, L. E., Coonrad, R., and Morrey, B. F.: Microscopic histopathology of lateral epicondylitis. Am. J. Sports Med. 20:746, 1992.

64. Roles, N. C., and Maudsley, R. H.: Radial tunnel syndrome, resistant tennis elbow as a nerve entrapment. J. Bone Joint Surg. 54B:499, 1972. 65. Rompe, J., Decking, J., and Nafe, B.: Shock wave application for chronic plantar fasciitis in running athletes. a prospective randomized placebo controlled trial. Am. J. Sports Med. 31:268, 2003. 66. Runge, F.: Zur Genese und Behandlung des Schreibekrampfes. Berl. Klin. Wochenschr. 10:245, 1873. 67. Sarkar, K., and Uhthoff, H. K.: Ultrastructure of the common extensor tendon in tennis elbow. Virchows Arch. Pathol. Anat. Histol. 386:317, 1980. 68. Savoie, F.: Percutaneous release in the release on the surgical treatment of lateral epicondylitis. Presented to the 3rd International Meeting of the Society for Tennis Medicine. New Haven, Conn., June 1997. 69. Sems, A., Dimeff, R., and Iannotti, J.: Extracorporeal shock wave therapy in the treatment of chronic tendinopathies. J. Am. Acad. Orthop. Surg. 14:195, 2006. 70. Stovall, P. B., and Beinfield, M. S.: Treatment of resistant lateral epicondylitis of the elbow by lengthening of the extensor carpi radialis brevis tendon. Surg. Gynecol. Obstet. 149:526, 1979. 71. Tasto, J., Cummings, J., Medlock, J., Harwood, F., Hardesty, R., and Amiel, D.: The Tendon Treatment Center; New horizons in the treatment of tendinosis. Arthroscopy 19(suppl 1):213, 2003. 72. Unverferth, L. J., and Olix, M. L.: The effect of local steroid injection on tendon. J. Sports Med. 1:31, 1973. 73. Voloshin, I., Gelinas, J., Maloney, M. D., O’Keefe, R. J., Bigliani, L. U., and Blaine, T. A.: Pro-inflammatory cytokines and metalloproteases as expressed in the subacromial bursa in patients with rotator cuff disease. Arthroscopy 21:1076, 2005. 74. Wadsworth, T. G.: Lateral epicondylitis. Lancet 1:959, 1972. 75. Wadsworth, C. T., Nielsen, D. H., Burns, L. T., Krull, J. D., and Thompson, C. G.: The effect of the counterforce armband on wrist extension and grip strength and pain in subjects with tennis elbow. J. Orthop. Sports Phys. Ther. 11:192, 1989. 76. Wang, C., Chen, H.: Shock wave therapy for patients with lateral epicondylitis of the elbow: a one- to two-year follow-up study. Am. J. Sports Med. 30:422, 2002. 77. Werner, C. O.: Lateral elbow pain and posterior interosseous nerve entrapment. Acta Orthop. Scand. Suppl. 174:1, 1979. 78. Yerger, B., and Turner, T.: Percutaneous extensor tenotomy for chronic tennis elbow: An office procedure. Orthopaedics 8:1261, 1985.

Chapter 45 Medial Epicondylitis

CHAPTER

45

Medial Epicondylitis Gerard T. Gabel and Bernard F. Morrey

INTRODUCTION Medial epicondylitis is the most common cause of medial elbow pain but is only 15% to 20% as common as lateral epicondylitis. The relative infrequency of medial epicondylitis has resulted in a paucity of information on medial epicondylitis, but work by Vangsness and Jobe,28 Gabel and Morrey,5 Ollivierre and associates,18 and Kurvers and Verhaar11 has clarified the pathology, treatment, and outcomes in medial epicondylitis. The significance of associated ulnar neuropathy at the elbow has also been assessed and is the primary component of the classification of medial epicondylitis. The results of nonoperative management, including corticosteroid injections, have been reported by Stahl and Kaufman.25 The compilation of information in these studies6 has resulted in a clearer understanding of medial epicondylitis and its management, allowing more appropriate patient care.

ANATOMY The anatomy of medial epicondylitis involves musculotendinous, neural, and ligamentous concerns. The flexor pronator origin at the anterior medial epicondyle is the central focus of medial epicondylitis. The pronator teres muscle originates in part off the superoanterior medial epicondyle, but its primary origin is from an intramuscular tendon (the medial conjoint tendon [MCT]) that has been previously described as the accessory anterior oblique ligament (AOL) or anisometropic AOL. Although it has been demonstrated to be a weak valgus stabilizer in near full extension, it is expendable and plays no role in static valgus stability in the presence of an intact AOL. The only clinical circumstance in which this structure plays a role in valgus stability is in elbow dislocations, in which if the flexor pronator mass is minimally disrupted, the MCT may prevent gross instability. The MCT is also the principle active valgus stabilizer, which may be a concern in athletic valgus loads especially throwing athletes. The pronator teres origin off the MCT occupies the proximoradial side of this vertically oriented septum

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(Fig. 45-1). The flexor carpi radialis, which also has a very small direct muscular epicondylar origin, finds its primary origin off the distoulnar aspect of the MCT. Although additional muscular or tendinous origins off the epicondyle are seen, the critical lesion of medial epicondylitis consists of this MCT and its associated pronator teres and flexor carpi radialis origins. This septum bifurcates 2 to 3 cm distal to the epicondyle (Fig. 45-2) with the pronator teres radially, the flexor carpi radialis between the septa and the digital flexors ulnarly. Although it plays a central mechanical role in medial epicondylitis, the MCT serves surgically as a landmark for the pathology of medial epicondylitis as well as a means of identification and avoidance of the AOL proper. The MCT rises off the anterior inferior epicondyle with an oblique parasagittal orientation extending approximately 12 cm into the proximal forearm. Immediately posterior to the proximal 3 to 4 cm of the MCT is the AOL (see Fig. 45-1). There is a surgical interval between the MCT and AOL, but anatomically, they are contiguous over the proximal 50% to 75% of the AOL. The distal 25% to 50% of the AOL is separate from the MCT’s posterior margin, an interval that allows for independent surgical manipulation of MCT and AOL distally. Any surgical elevation of the MCT off the medial epicondyle, posterior to the MCT, by definition, violates the origin of the AOL. The neural concerns in medial epicondylitis consist of the medial antebrachial cutaneous nerve (MABCN) and the ulnar nerve. The MABCN courses in the subcutaneous tissue in the anteromedial arm13 until just proximal to the medial epicondyle, where it divides into an anterior branch, which travels distally, and a posterior branch,2 which travels directly over the flexor pronator mass to the posterior medial forearm. The ulnar nerve rests on the posterior aspect of the medial intermuscular septum in the arm. As it approaches the medial epicondyle, it is covered by a retinaculum,15 which maintains its position preventing subluxation. It enters the forearm through the two heads of the flexor carpi ulnaris at the cubital tunnel. At entry into the cubital tunnel, the ulnar nerve lies immediately adjacent to the posterior margin of the flexor pronator mass.

PRESENTATION Medial epicondylitis presents with medial elbow pain, which is related to activity, especially repetitive or forceful pronation. It has a peak incidence in the third through fifth decade, with a 2 : 1 male-to-female ratio. It occurs in the dominant elbow in 60% of cases and is associated with an acute injury (direct or indirect) in 30%, whereas 70% of cases have a more insidious onset. Associated

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Gravity test X-ray plate

X-ray beam

Lesion

FIGURE 45-3

Valgus stress radiograph for assessment of valgus instability as a cause of medial elbow pain. (From Woods, G. W., and Tullos, H. S.: Elbow instability and medial epicondyle fractures. Am. J. Sports Med. 5:23, 1977.)

Anterior oblique ligament

FIGURE 45-1

Illustration of medial conjoint tendon (MCT). Forceps are on the vertically oriented MCT. Note that the anterior oblique ligament (AOL) lies on the posterior margin of the MCT. Elevation of the MCT should be performed carefully to avoid injury to the AOL.

A

B

ME

FIGURE 45-2

Intraoperative photograph of the two septae of the medial conjoint tendon, 2 cm distal to the epicondyle. Note the muscular attachments have been elevated. The radial septum (B) is bordered by the pronator teres muscle laterally, the flexor carpi radialis muscle resides between the septae, and the digital flexor muscle bellies are medial to the ulnar septum (A).

patients (hence, the eponym golfer’s elbow). The prevalence of medial epicondylitis is approximately one half of 1%, with smoking, obesity, repetitive, and forceful activities being significant risk factors.20 Physical examination demonstrates direct tenderness over the anterior aspect of the medial epicondyle in essentially all cases. Some patients may have maximum tenderness just distal to the epicondyle in the proximal flexor pronator mass. Resisted pronation tenderness is seen in 90% and resisted wrist palmar flexion tenderness in 70% of patients. Range of motion is typically normal. Associated medial collateral ligament insufficiency may be tested with valgus stress testing, as described by Jobe and associates9 (valgus stress at 30 degrees of flexion with palpation of the AOL) or the moving valgus stress test, as described by O’Driscoll and associates.17 The ulnar nerve should be evaluated, including testing for the presence of Tinel’s sign, elbow flexion test, nerve compression test, and ulnar nerve subluxation. Distal objective function (two-point discrimination, intrinsic strength, and dorsal cutaneous nerve status) completes the ulnar nerve examination. The classification of medial epicondylitis5 is based on the presence and severity of concomitant ulnar neuropathy at the elbow. Type I medial epicondylitis includes those patients with no associated ulnar nerve symptoms. Type II medial epicondylitis is divided based on the degree of ulnar nerve involvement. Type IIA has ulnar nerve symptoms with no objective deficit, whereas type IIB has objective deficits on physical exam or electromyography.

EVALUATION ulnar neuropathy is seen in approximately 50% of cases, whereas associated diagnoses at a separate level (lateral epicondylitis, 30%; carpal tunnel syndrome, 25%; rotator cuff pathology, 20%) are also frequently seen on past medical history. A vocational contribution to the patient’s symptoms may be seen in more than 50% of cases; an avocational contribution is seen in 10% to 20% of

Radiographic evaluation should include plain radiographs to rule out associated lesions (e.g., osteoarthritis) as well as valgus stress radiographs23 if medial instability is suspected (Fig. 45-3). Medial epicondylar calcification is seen in 10% to 20% of cases but is not prognostic. Magnetic resonance imaging (MRI) has concentrated on

Chapter 45 Medial Epicondylitis

lateral epicondylitis,12,19 but within these series and medial epicondylitis–specific series,10 it has a high sensitivity and specificity. Because medial epicondylitis is primarily a clinical diagnosis, MRI should be reserved for more complex situations such as reoperation or associated medial collateral ligament concerns. Electrodiagnostic evaluation of the ulnar nerve is indicated in cases of concomitant ulnar neuropathy. Although electromyographic changes are rare except in type IIB cases, nerve conduction slowing either absolutely (less than 50 m per second) or relative (to proximal or distal segments) is usually seen in type IIA cases. The differential diagnosis of medial elbow pain includes proximal neurogenic sources (cervical radiculopathy, thoracic outlet syndrome) as well as shoulderlevel musculoskeletal sources, each of which can be excluded with appropriate evaluation. Local causes of medial elbow discomfort are limited but should be evaluated as well. A snapping medial head of the triceps24 and subluxation of the ulnar nerve usually give a history of a palpable “popping” sensation and may have an associated ulnar neuropathic condition. On examination, tendon and nerve subluxation are found with elbow flexion. Triceps tendinitis presents with more posterior elbow discomfort, reproduced with resisted elbow extension. Radiographs usually reveal an olecranon spur. Medial collateral insufficiency is typically seen in chronic valgus activities and is evaluated as previously mentioned. Medial collateral ligament deficiency may coexist with medial epicondylitis. Isolated ulnar neuropathy may manifest not only with distal neurologic symptoms but also with medial elbow discomfort from the neuro nervorum. Examination demonstrates reproduction of local pain with the elbow flexion and nerve compression tests. Postoperative medial elbow pain may emanate from any of these diagnoses but also may include injury to the MABCN. Hyperesthesia or hypesthesias at the medial forearm along with the presence of Tinel’s sign along the MABCN confirm this diagnosis.

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If ulnar nerve subluxation is present, the injection should be performed with the elbow extended to minimize the risk of ulnar nerve injury. Injection is associated with a more rapid resolution of medial elbow pain but is not a panacea and requires compliance with the complete conservative program. A wrist splint to rest the wrist flexors, as well as a padded counter-force brace is prescribed.27 The pad of the counter-force brace should be anteromedial on the flexor pronator mass, not medial or posteromedial over the ulnar nerve (Fig. 45-4). If ulnar nerve symptoms are increased with appropriate use of the brace, then the brace needs to be discontinued. If the discomfort has subsided, at 3 to 4 weeks, a conditioning program consisting of composite stretching of the flexor pronator mass and incremental strengthening is begun. Provocative activities are avoided until pain-free premorbid strength is restored. Concomitant ulnar neuropathy at the elbow is managed with avoidance of repetitive or prolonged elbow flexion and leaning on the elbow. Nighttime extension splinting, if tolerated, may be useful. Ultrasound, iontophoresis,3 acupuncture,14 laser,29 and extracorporeal shock wave therapy22 have no proven independent efficacy in medial epicondylitis. Blood or platelet-rich plasma injection reportedly has a role in patients in whom other nonoperative measures have failed, but requires further definitive study.26

SURGICAL INTERVENTION The operative treatment of medial epicondylitis is considered in patients who fail to respond to conservative management (one to two injections over a 6- to 9-month period) or in patients who demonstrate a progression of the ulnar neuropathy. The surgical

TREATMENT NONOPERATIVE MANAGEMENT The nonoperative treatment of medial epicondylitis includes patient education, medications, orthoses, therapy, and time. The patient should be educated as to the contributing activities and should modify or avoid them. Oral anti-inflammatory drugs or corticosteroid injections are given. An equal volume of local anesthetic and corticosteroid, total volume 2 to 3 mL, is injected into the point of maximum tenderness, deep to the fascia, on the anterior aspect of the medial epicondyle.

FIGURE 45-4

Medial counter-force brace. Position over anteromedial/proximal forearm distal to the epicondyle, with pad anterior, away from ulnar nerve.

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Medial antebrachial cutaneous nerve

Ulnar nerve Medial epicondyle

Lesion

FIGURE 45-5

Incision for medial epicondylar débridement with or without cubital tunnel release. Note position of medial antebrachial cutaneous nerve posterior branch.

management of medial epicondylitis is guided by the classification. Type I cases require epicondylar débridement. Type IIA cases require epicondylar débridement, and cubital tunnel decompression or transposition. Type IIB cases require débridement with submuscular transposition of the ulnar nerve. The surgical technique of medial epicondylar débridement involves a 3-cm longitudinal incision just anterior to the medial epicondyle (Fig. 45-5). The MABCN is consistently encountered in the subcutaneous tissue and should be protected. The flexor pronator fascia is discretely identified on the medial epicondyle and is incised, leaving a 2-mm rim of the superficial fascia attached to the medial epicondyle for later repair. The underlying muscle is elevated to allow identification of the longitudinally oriented MCT. A nidus is usually found within the origin of the MCT (Fig. 45-6). The proximal MCT is fully exposed, with care taken on its posterior margin to identify and protect the AOL. A 3- to 4-cm section of the MCT including the nidus is then resected, in essence disconnecting the MCT septum within the flexor pronator mass from the epicondyle. The flexor pronator fascia is repaired back to the retained rim of fascia at its original position or in a slightly (1 cm) lengthened position. In Type IIA cases, with limited ulnar nerve involvement, MCT débridement as in type I cases addresses the tendinosis. Although cubital tunnel release may be used for management of ulnar nerve compression, submuscular transposition is more definitive and may yield better results.11 If any anatomic concern relating to the ulnar nerve is encountered (e.g., subluxation or adhesions), submuscular transposition is indicated.

Anterior oblique lig.

FIGURE 45-6

Illustration of operative technique of medial epicondylar débridement. The pronator teres and flexor carpi radialis origins are elevated off the medial epicondyle, exposing the medial conjoint tendon (MCT). The degenerative nidus, if present, is typically found at the MCT origin off the epicondyle.

Cubital tunnel release is accomplished without extension of the débridement incision. Subcutaneous dissection posteriorly allows identification of the fascia overlying the ulnar nerve. The fascia is opened at the inferior tip of the medial epicondyle distal to the cubital tunnel retinaculum and incised distally, releasing the flexor carpi ulnaris (FCU) arcade. There are two components to the arcade, the superficial and the deep epimysium, both of which need to be released. After release of the superficial FCU fascia, the two muscle bellies (humeral and ulnar origin) are bluntly separated. The deep FCU fascia, directed over the ulnar nerve, is released with tenotomy scissors. The ulnar nerve itself is not disturbed. The proximal retinaculum, as described by O’Driscoll and colleagues,15 is preserved if possible to minimize the risk of iatrogenic subluxation. The nerve is assessed with flexion and, if subluxation is induced, transposition is performed.

Chapter 45 Medial Epicondylitis

In type IIA cases that require transposition or type IIB cases, submuscular transposition is preferred. An incision over the ulnar nerve is created. Care is taken to protect the MABCN distally. The flexor pronator mass and ulnar nerve are identified. Flexor pronator elevation and MCT débridement are performed as previously described. Ulnar nerve transposition is accomplished with decompression, mobilization, and transposition of the nerve. Decompression involves proximal release of the arcade of Struthers and brachial fascia for approximately 10 to 12 cm proximal to the epicondyle. The medial intermuscular septum is discretely exposed and the inferior 4 to 6 cm excised. The FCU arcade is released as with a cubital tunnel release and the deep flexor pronator aponeurosis is bluntly released with Metzenbaum scissors. Mobilization of the ulnar nerve requires preservation of the longitudinal blood supply throughout and segmental blood supply where possible. The nerve is mobilized from its bed for approximately 8 to 10 cm proximally and 3 to 4 cm distally. The distal mobilization may be impeded by the first motor branch of the FCU. This branch can be mobilized by dissection within the ulnar head muscle, gaining approximately 2 cm in length, sufficient to allow transposition without angulation. After the MCT has been resected, the flexor pronator mass is further prepared by incising any additional small septae within the muscle. The posterior fascia of the humeral head of the FCU along the posterior margin of the mass is incised distally for 3 to 4 cm to prevent iatrogenic impingement with transposition. The nerve is then brought anteriorly to its submuscular position and examined for any acute angulation or impingement by any residual fascia bands. The prepared flexor pronator mass is then repaired over the nerve in a transposed position. The repair should begin proximally with the proximal margin of the fascia translated 1.5 to 2 cm distally from its original position (Fig. 45-7). A running braided nonabsorbable suture with the initial knot buried is used. The suture runs distally, suturing the FP mass back down to the epicondyle and then closing the FCU release interval to strengthen the FP mass repair. Once transposition is complete, the nerve is again examined with flexion and extension. Percutaneous medial epicondylar release1 is contraindicated because of concerns with the MABCN and ulnar nerve as well as incomplete management of the medial epicondylitis. Formal medial epicondylectomy8 may compromise the AOL origin16 (Fig. 45-8) and is not recommended. Because the pathology in medial epicondylitis is musculotendinous and not osseous, epicondylar removal offers no pathophysiologic advantage. Endoscopic medial epicondylar débridement7 has not been reported. Postoperatively, with débridement alone or submuscular transposition, the arm is immobilized in a single

647

FPM B UNE ME

A

FIGURE 45-7

Operative picture of submuscular transposition with distal translation of the flexor pronator mass repair. The ulnar nerve (UNE) is deep to the flexor pronator mass (FPM) which has been repaired (level B) 2 cm distal to the origin position (level A).

W

C

L

E

13% 67% 20%

FIGURE 45-8

Diagram of anterior oblique ligament origin at medial epicondyle. Formal, full medial epicondylectomy violates this origin, possibly inducing valgus instability. (Redrawn from O’Driscoll, S. W., Horii, E., and Morrey, B. F.: Anatomy of the attachment of the medial ulnar collateral ligament. J. Hand Surg. 17:164, 1992.)

sugar-tong splint or Muenster cast for 3 weeks. Noncomposite range of motion is then initiated, progressing to composite range of motion after 2 more weeks. A flexor pronator stretch and strength program is begun at 6 weeks postoperatively, progressing as tolerated. Impact activities are avoided until pain-free strength is fully restored.

RESULTS Nonoperative measures are successful in the majority of patients with medial epicondylitis. Conservative treatment fails in only 5% to 10% of patients5 owing

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Part VI Sports and Overuse Injuries to the Elbow

to persistent epicondylitis or persistent progressive ulnar neuropathy. Surgical results correlate with the type of medial epicondylitis. Type IA or IIA medial epicondylitis has 95% good or excellent results, as reported in two studies5,28 and slightly lower success rates in two additional series.11,18 The time to attainment of a good or excellent level is approximately 6 months in two thirds of patients and up to 2 years in the remaining one third.5 Type IIB medial epicondylitis, with more involved associated ulnar neuropathy, has a much poorer prognosis. The poorer results in type IIB medial epicondylitis relate primarily to the failure of ulnar neuropathy to respond to surgical management. Cubital tunnel release alone as a means of management of associated ulnar neuropathy in medial epicondylitis has been shown by Kurvers and Verhaar11 to potentially be suboptimal. Failure to quantify the degree of ulnar nerve involvement and treat accordingly results in persistent ulnar nerve symptoms. Ulnar neuropathy in medial epicondylitis may be related to a “mass effect” at the anterior cubital tunnel from the flexor pronator mass. Although this “mass effect” may be treated by medial epicondylar débridement, fixed changes in the ulnar nerve or cubital tunnel may prevent resolution of the ulnar neuropathy. The management of concomitant ulnar neuropathy in medial epicondylitis requires independent management of the ulnar nerve and medial epicondylitis except in select mild cases of ulnar neuropathy.

COMPLICATIONS Complications of nonoperative management of medial epicondylitis are rare. Iatrogenic injury of the ulnar nerve from corticosteroid injection has been reported and can be avoided with injection with the elbow in extension. Injection of the flexor pronator mass should be done cautiously and may be contraindicated in patients with a prior ulnar nerve transposition. Injections should be placed within MCT, avoiding the immediately posteriorly located AOL. Complications of operative treatment are uncommon. Restricted elbow range of motion is minimized by early protected range of motion. Neurologic complications include neurogenic pain from injury to the MABCN and ulnar nerve deficiencies. Identification and protection of the MABCN2 is essential. If the nerve is injured intraoperatively or if recognized postoperatively, this may be surgically addressed by placement of the medial antebrachial cutaneous neuroma into the brachialis muscle belly. Persistent ulnar neuropathy at the elbow can be managed by revision with submuscular transposition, except in cases that have had a prior submuscular

transposition, in which case the results of revision are less predictable.4 The results with a patient specific approach are approximately 80% good or excellent, but appropriate selection criteria are critical and the patient should be advised of the possibility of no improvement in status. Iatrogenic medial elbow instability is a recognized complication of medial epicondylar débridement and can be avoided as described earlier. Reconstruction at the AOL9,21 has a high success rate but requires a prolonged period of recovery. Persistent medial epicondylar pain is not a complication but does complicate patient management. Up to one third of patients have continued medial epicondylar pain at 6 months and should be continued on a conservative treatment program. In the majority of these patients, the condition will resolve but may require up to 2 years to do so.

References 1. Baumgard, S. H., and Schwartz, D. R.: Percutaneous release of the epicondylar muscles for humeral epicondylitis. Am. J. Sports Med. 10:233, 1982. 2. Dellon, A. L., and MacKinnon, S. E.: Injury to the medial antebrachial cutaneous nerve during cubital tunnel surgery. J. Hand Surg. Br. 10:33, 1985. 3. Demirtas, R. N., and Oner, C.: The treatment of lateral epicondylitis by iontophoresis of sodium salicylate and sodium diclofenac. Clin. Rehab. 12:23, 1998. 4. Gabel, G. T., and Amadio, P. C.: Reoperation for failed decompression of the ulnar nerve in the region of the elbow. J. Bone Joint Surg. Am. 72:213, 1990. 5. Gabel, G. T., and Morrey, B. F.: Operative treatment of medial epicondylitis. Influence of concomitant ulnar neuropathy at the elbow. J. Bone Joint Surg. 77A:1065, 1995. 6. Gabel, G. T., and Morrey, B. F.: Tennis elbow. Instruct. Course Lect. 47:165, 1998. 7. Grifka, J., Boenke, S., and Kramer, J.: Endoscopic therapy in epicondylitis radialis humeri. Arthroscopy 11:743, 1995. 8. Heithoff, S. J., Millender, L. H., Nalebuff, E. A., and Petruska, A. J.: Medial epicondylectomy for the treatment of ulnar nerve compression at the elbow. J. Hand Surg. Am. 15:22, 1990. 9. Jobe, F. W., Stark, H., and Lombardo, S. T.: Reconstruction of the ulnar collateral ligament in athletes. J. Bone Joint Surg. 68A:1158, 1986. 10. Kijowski, R., and De Smet, A. A.: Magnetic resonance imaging findings in patients with medial epicondylitis. Skeletal Radiol. 34:196, 2005 11. Kurvers, H., and Verhaar, J.: The results of operative treatment of medial epicondylitis. J. Bone Joint Surg. Am. 77:1374, 1995. 12. Martin, C. D., and Schweitzer, M. E.: MR imaging of epicondylitis. Skel. Radiol. 27:133, 1998.

Chapter 45 Medial Epicondylitis

13. Masear, V. R., Meyer, R. D., and Pichora, D. R.: Surgical anatomy of the medial antebrachial cutaneous nerve. J. Hand Surg. Am. 14:267, 1989. 14. Molsberger, A., and Hille, E.: The analgesic effect of acupuncture in chronic tennis elbow pain. Br. J. Rheum. 33:1162, 1994. 15. O’Driscoll, S. W., Horii, G., Carmichael, S. W., and Morrey, B. F.: The cubital tunnel and ulnar neuropathy. J. Bone Joint Surg. 73B:613, 1991. 16. O’Driscoll, S. W., Horii, E., and Morrey, B. F.: Anatomy of the attachment of the medial ulnar collateral ligament. J. Bone Joint Surg. 17:164, 1992. 17. Shawn, W. M., O’Driscoll, S. W., Lawton, R. L., and Smith, A.: The “moving valgus stress test” for medial collateral ligament tears of the elbow. Am. J. Sports Med. 33:231, 2005. 18. Ollivierre, C. O., Nirschl, R. P., and Pettrone, F. A.: Resection and repair for medial tennis elbow. A prospective analysis. Am. J. Sports Med. 23:214, 1995. 19. Potter, H. G., Hannafin, J. A., Morwessel, R. M., Dicarlo, E. F., O’Brien, S. J., and Altchek, D. W.: Lateral epicondylitis: correlation of MR imaging, surgical, and histopathologic findings. Radiology 196:43, 1995. 20. Rahman, S., Viikari-Juntura, E., Varonen, H., and Heliovaara, M.: Prevalence and determinants of lateral and medial epicondylitis: a population study. Am. J. Epidemiol. 164:1065, 2006 21. Rohrbough, J. T., Altchek, D. W., Hyman, J., Williams, R. J., and Botts, J. D.: Medial collateral ligament reconstruction

22.

23.

24.

25.

26.

27.

28. 29.

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of the elbow using the docking technique. Am. J. Sports Med. 30:541, 2002. Rompe, J. D., Hope, C., Kullmer, K., Heine, J., and Burger, R.: Analgesic effect of extracorporeal shock wave therapy on chronic tennis elbow. J. Bone Joint Surg. 78B:233, 1996. Schwab, G. H., Bennett, J. B., Woods, G. W., and Tullos, M. S.: Biomechanics of elbow instability. The role of the medial collateral ligament. Clin. Orthop. Relat. Res. 146:42, 1980. Spinner, R. J., and Gabel, G. T.: Iatrogenic snapping of the medial head of the triceps after ulnar nerve transposition. J. South. Orthop. Assoc. 10:236, 2001 Stahl, S., and Kaufman, T.: Ulnar nerve injury at the elbow after steroid injection for medial epicondylitis. J. Hand Surg. Br. 21:69, 1997. Suresh, S. P. S., Kaline, E. A., Jones, H., and Connell, D.: Medial epicondylitis: is ultrasound guided autologous blood injection an effective treatment? Br. J. Sports Med. 40:935, 2006 Walther, M., Kirschner, S., Koenig, A., Barthel, T., and Gohlke, F.: Biomechanical evaluation of braces used for the treatment of epicondylitis. J. Shoulder Elbow Surg. 11:265, 2002. Vangsness, C. T., and Jobe, F. W.: Surgical management of medial epicondylitis. J. Bone Joint Surg. 73B:409, 1991. Vassellen, O., Jr., Hoeg, N., Kjeldstad, B., Johnsson, A., and Larsen, S.: Low level laser versus placebo in the treatment of tennis elbow. Scand. J. Rehabil. Med. 24:37, 1992.

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CHAPTER

46

Surgical Failure of Tennis Elbow Bernard F. Morrey

INTRODUCTION Lateral epicondylitis is the most common elbow affliction in adults. Surgical intervention appears to be increasing, in part due to the introduction of orthopedic releases. Failures after surgery are recognized, but the cause and the means of re-evaluation are seldom addressed. Initially, the most frequent explanation for residual symptoms is too brief a period after surgery or inadequate rehabilitation. The latter may be due to noncompliance or an inadequate program of strengthening and stretching exercises.22 This type of problem is readily determined with a careful interview. The reliability of surgical procedures for lateral epicondylitis makes the need for reoperation uncommon. For this reason, few surgeons have extensive experience with the management of patients after failed intervention for epicondylitis, and reports of such experience in the literature are lacking. The intent of this chapter is to share our experience with this problem and to provide a basis for determining the cause of failure and a basis for further management. Specific focus is on determining which patients might benefit from a second surgical procedure. To be perfectly candid, a review of the literature on this subject over the last 10 years has, I feel, obscured rather than clarified this particular problem.

with neovasculature. This represents an aborted effort of healing but is not inflammation. Inappropriate or inaccurate initial diagnoses may occur,32 such as interosseous nerve entrapment,1,6,19,31,33 or even intra-articular plica.29 Regardless of the etiology or underlying pathology, nonoperative management is usually successful in 90% of patients.22 Similarly, when surgery is performed, a 90% success rate is typically reported. The interesting feature of these data is that the success of surgery seems independent of the surgical technique.2,3,6,14,21,22,26,28,34 On the other hand, when surgical intervention is not successful, there are few reports of subsequent management.9,12,18,19,23

PATIENT EVALUATION CAREFUL HISTORY The first step in the evaluation process is to critically assess the patient and motives. Next, determine whether an adequate period has elapsed since surgery, including whether the patient has exhibited adequate compliance with the rehabilitation program. If concern exists about either point, the patient is treated for symptoms and reassessed. If at least 6 to 9 months has passed since surgery and there are no worrisome personality features, litigation, or compensation issues, the problem may be further studied. The most important determination at this point is to determine whether the symptom complex is identical to or different from that for which the original surgery was performed. This allows the failure to be classified as one of three types: type I, inaccurate initial diagnosis; type II, inadequate treatment; type III, introduction of new pathology.

CLASSIFICATION Type I—Inaccurate Initial Diagnosis

ETIOLOGY AND PATHOLOGY Because the treatment of surgical failure in large measure relates to the etiology and pathology of the condition, analysis of treatment failure logically begins with a brief consideration of the pathoanatomy of lateral epicondylitis. This is discussed in detail in Chapter 44. It is well accepted that the pathology involves the extensor carpi radialis brevis tendon.4,6,8,13,15,22,25 Although generally considered an inflammatory lesion, as many as 14 pathologic features are reported in the literature (Box 46-1).26 A careful blinded study of pathologic and control material reported that the material removed at surgery reveals hyaline degeneration

Several other possible causes of lateral elbow pain include degenerative arthrosis,20 anconeus or extensor muscle compartment syndrome,1,25 lateral ligament instability especially with a history of trauma,23 and entrapment of the posterior interosseous nerve (PIN) in the region of the arcade of Frohse17,30,33 (Fig. 46-1), cutaneous nerve entrapment,10 and intra-articular plica.29 The distinction between lateral epicondylitis and PIN entrapment has been well discussed in the literature.5,11,20,27,28,33 The distinction is made even more difficult because PIN entrapment may coexist with lateral epicondylitis in about 5% percent of individuals.33 In one series, a concurrent and unrecognized PIN entrapment

Chapter 46 Surgical Failure of Tennis Elbow

Histopathologic Features Reported to Be Associated with Lateral Epicondylitis

BOX 46-1

Hemorrhage Recent (i.e., pooled red blood cells) Old (i.e., hemosiderin-laden macrophages) Fibrinoid degeneration Hyaline degeneration Vascular proliferation Fibroblastic proliferation Granulation tissue in subtendinous space Necrosis of tendon fascicles Calcific debris Crystalline debris Cellular infiltrate Polymorphonuclear leukocytes Histiocytes Lipid-laden histiocytes Lymphocytes

651

changes, on the other hand, are not usually present, nor are they necessary to diagnose nerve entrapment. If the onset has followed trauma and if catching or locking is an element of the complaint, possible insufficiency of the lateral ligament complex or an intra-articular cause is suspected. It should also be noted that patient selection is a consideration with a type I failure. Issues include adequate motivation, compliance, and consideration of secondary gain.31 The same factors that resulted in a failure of nonoperative treatment are present in the patient undergoing surgery. The best solution for this difficult problem is obvious: avoid the initial surgical procedure in patients known to be at risk for secondary gain. Avoid additional surgery at all costs. Improper Patient Selection

Type II—Inadequate or Incomplete Procedure In some patients, an incomplete release or excision of the pathologic tissue is the cause of persistent symptoms. This was the most common finding in our19 and Nirschl’s experience. In fact, of 35 secondary procedures by Nirschl, the extensor carpi radialis brevis (ECRB) was felt not to have been addressed at all in 27, and inadequately excised in 7.23 By excising this area, 83% experienced a good or excellent result.

Type III—Introduction of New Pathology If symptoms are different from those present before surgery, a type III failure is defined. Features include a different location of pain, local fullness, swelling in the arm, pain that is different in character from that before surgery, laxity, or looseness or catching may be present. The cause of type III failure is surgically introduced pathology. Synovial fistula or herniation, adventitial bursa, and ligament insufficiency are the most likely causes. Synovial fistulas have been identified as occurring as a complication after 4 of 149 percutaneous procedures33 (Fig. 46-2). Instability may be subtle and we often employ a fluoro-scan to assist in making the diagnosis (Fig. 46-3). An algorithm may also be useful here (Fig. 46-4). FIGURE 46-1

PHYSICAL EXAMINATION

also was suspected as the cause of failure in 2 of 15 patients.33 I have found a reliable triad to help make this diagnosis, consisting of: localization of pain at the arcade of Frohse reproduced by direct palpation; pain aggravated by resisted supination; and pain relief by injection of 2 mL of lidocaine (Xylocaine). Electromyographic

The examination focuses on the three categories of failure. All patients should be evaluated by measurement of flexion-extension and pronation-supination motion. Pain from resisted supination suggests PIN symptoms, and pain elicited by resisted wrist extension suggests persistent lateral epicondylitis. In type I failure, palpation is directed specifically at both the lateral epicondyle and the arcade of Frohse. If the original cause was a traumatic event for a type I failure, and in all patients in

A select number of patients have early arthritis presenting as tennis elbow.

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Part VI Sports and Overuse Injuries to the Elbow

FIGURE 46-2

Arthrogram demonstrating incompetence of the lateral capsule as contrast material is seen distal to the radial head. This patient’s major complaint was forearm pain and swelling.

FIGURE 46-4

The anteroposterior arthroscopic view of the elbow showing incompetent lateral collateral ligament; this patient was complaining of instability.

FIGURE 46-3 Varus stress under fluoroscopy reveals gross instability of the lateral collateral ligament. This patient’s symptoms developed after his surgical procedure.

whom symptoms had changed (type III/failure), examination for varus instability24 or posterolateral rotatory instability (PLRI) is performed. Patients with night pain or motion loss are further evaluated for arthrosis, sepsis, or osteochondritis dissecans of the capitellum. In this latter group, arthroscopy is a useful means of further assessment.

Types I and II A local injection of only 1 or 2 mL of lidocaine in the area of maximum tenderness is the first diagnostic maneuver. The early (1 to 3 hours) response is noted. Complete relief represents a positive response that implicates persistent pathology at the lateral epicondyle (type II). Lack of response is consistent with a type I failure. If the injection at the epicondyle is unsuccessful and if the physical examination suggests PIN entrapment, a second injection with lidocaine is performed in the region of the PIN as it enters the supinator muscle at the arcade of Frohse. If most symptoms (70% to 80%)

Chapter 46 Surgical Failure of Tennis Elbow

are relieved, PIN entrapment is diagnosed. Some surgeons believe that the nerve may also be compressed as it exits the supinator, so this also must be considered. The joint is evaluated by intra-articular injection of 4 to 5 mL of lidocaine in patients whose symptoms are suggestive of intra-articular pathology, but the routine radiographs are inconclusive. A technetium-99m bone scan may be used to localize an articular process (Fig.

653

46-5). Increasingly, arthroscopy is helpful in diagnosing synovial or articular pathology. As Baker has correctly observed, a certain percentage of patients will exhibit capsular involvement diagnosed at arthroscopy (personal communication-Champ Baker, Columbus GA) (Fig. 46-6). Symptoms consistent with an unstable elbow are evaluated by stress radiography under fluoroscopy. This diagnosis also may be confirmed by arthroscopy.

FIGURE 46-5

A, Although the patient reported vague pain in the elbow region, the radiograph is unremarkable. B, A technetium-99 scan demonstrates articular changes in the joint, readily distinguishing this condition from lateral epicondylitis.

A

B FIGURE 46-6

Grinding pain, localized to lateral joint. Morning stiffness prompted indication for arthroscopy. Degenerative lesion was identified (A); pain was relived by débridement (B).

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Part VI Sports and Overuse Injuries to the Elbow

Type III Patients in whom the symptom complex was different after the initial surgical procedure uncommonly represent an incorrect initial diagnosis. The diagnosis is more commonly related to the surgical procedure itself. In type III failure, diagnostic possibilities include adventitial bursa, capsular fistula, and instability. Diagnostic studies are directed by the physical examination and again may include injection in the area of maximal local tenderness. Radiographs may reveal ectopic bone causing residual but different symptoms (Fig. 46-7).7 In the past, an arthrogram was helpful in demonstrating capsular herniation or ligamentous insufficiency (see Fig. 46-2). If motion causes pain or if catching is present, instability is assessed by fluoroscopic stress radiography (see Fig. 46-3). In a patient in whom intra-articular pathology is suspected, intra-articular injection with lidocaine, tomography, bone scan, and arthroscopy are performed, in that order, until the diagnosis is made (see Figs. 46-2 and 46-3). Arthroscopy is particularly helpful in demonstrating subtle instability by revealing laxity of the radiohumeral joint (Fig. 46-8).

more than adequate to reveal whether surgical intervention has been successful. Posch and colleagues25 demonstrated that only 1 of 43 patients improved more than 1 year after surgery. All patients with type I failure are treated nonoperatively if the local injection in the region of the lateral epicondyle or in the region of the arcade of Frohse does not relieve the symptoms. Type II, inadequate treatment

TREATMENT The time before subsequent intervention is an important issue. A review of the literature suggests that a successful surgical procedure is evident within the first 3 or 4 months. One year of follow-up assessment is certainly

FIGURE 46-8

FIGURE 46-7

Ectopic bone was the site of localized tenderness different from that for which the procedure was performed.

A, Radiohumeral relationship in a patient with stable elbow. B, Individual with catching and looseness in the elbow after lateral epicondylar release; note the obvious gap between the radiohumeral joint, clearly demonstrating lateral collateral ligament incompetency.

Chapter 46 Surgical Failure of Tennis Elbow

TABLE 46-1

655

Presentation Type and Results of Reoperation for Tennis Elbow After Prior Procedure Failure Pathology

Presentation type

Patients

Etiology: Trauma

CET

PIN

LCL

Bursa Fistula

Success (%)

I

4

2

0

3

1

—

4 (100)

II

4

2

4

—

0

2

3 (75)

III

5

4

3

2

4 (80)

13

8

4

2

11 (85)

Total

4

1

CET, common extensor tendon; LCL, lateral collateral ligament; PIN, posterior interosseous nerve

problems can be reoperated after 6 to 9 months. In the group of patients in whom the symptoms have changed (type III), however, particularly if an instability pattern is diagnosed, surgery may be offered as soon as this diagnosis is made.

SURGICAL TREATMENT If the examination dictates, exploration of the PIN is carried out through the same incision. If a traumatic event preceded the symptoms and if instability has been diagnosed, the lateral collateral ligament is stabilized (see Chapter 47). In type II problems in patients who met the criteria for surgical intervention, the entire extensor mass and specifically the ECRB are carefully explored.19,23 In patients with type III failure, surgical intervention is directed at the specific pathologic condition. Problems with instability are treated as noted earlier.

FIGURE 46-9

Patient with a localized tenderness immediately over the lateral epicondyle following lateral epicondylar surgery. At exploration, an adventitial bursa in the region of the previous common extensor tendon origin was found. The patient has complete relief of symptoms 5 years after excision of the bursa.

RESULTS Mayo Experience

Type III Results

There is limited experience with surgical treatment for failed lateral epicondylitis. Some time ago, I examined the results of the surgical management of 13 patients who were classified and evaluated in the manner described earlier. Four were type I, four type II, and five type III problems.

Those patients with type III pathology represented a different patient population (see Table 46-1). One had successful removal of an adventitial bursa (Fig. 46-9). Four of the five patients in this group now have satisfactory outcomes. The only patient with an unsatisfactory result was improving 6 months after ligament reconstruction, but because of continued pain at the radiohumeral articulation, the radial head was removed by another orthopedic surgeon. Symptoms worsened. Hence, overall, 11 of 13 patients (85%) had a satisfactory outcome after the second surgical procedure in this highly selected patient population. Patients in whom no pathologic findings could be identified in the preoperative evaluation, who did not respond to injection, and in whom a specific probable cause for persistent pain could not be identified were excluded from this patient population.

Type I Failure Four patients were reviewed who met the criteria for additional surgical intervention with type I failure due to inaccurate diagnoses. Data referable to the presentation and results are shown in Table 46-1. All were successfully managed.

Type II Failure Of the four with inadequate initial resection, subsequent localized débridement was successful in three (75%). This is similar to the outcome reported by Nirschl.23

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Part VI Sports and Overuse Injuries to the Elbow

Symptoms the same (6 mo postop) Yes

No

Localize to epicondyle Yes

No

Inject −

Localize to PIN

+ Release extensor tendon

Unstable Yes No

Yes Inject

Stabilize

Unstable Yes

No

Stabilize

+

−

No

Bursal or capsular defect Yes

Release PIN

No

Repair

No surgery

No surgery

No surgery

No surgery

FIGURE 46-10 A logical sequence of assessment for patients with surgical failure for lateral epicondylitis. Notice that the majority of categories indicate that no surgical intervention is necessary. Also note the major distinction between symptoms that are the same (type I) and those that are different (type II).

OTHER REPORTS As noted earlier, the only other study of reoperation is that of Nirschl, who reported a similar rate of success as we had documented.23 For reasons that are obscure to me, several reports document successful relief of pain by an anconeus muscle rotation transfer to the lateral epicondyle.9,18 Even an adipofascial radial forearm flap coverage of the epicondyle has been reported as a successful revision procedure.12

pathology must be considered. The pivot shift test and arthroscopy are useful in revealing ligamentous insufficiency. The MRI usually shows abnormality, but its specificity is not reliable. Arthrography is helpful in identifying capsular and bursal conditions as well. Reoperation, if well planned in carefully selected patients, may be anticipated to be successful in as many as 85% of patients.

References CONCLUSION Our treatment logic is shown in Figure 46-10. Type I failure represents either improper patient selection, or an incorrect initial diagnosis. The type II failure is persistence of the original pathologic condition that has not been corrected by surgery. Type III failure, identified by altered symptoms, may represent a condition associated with the surgical procedure. A careful history leading to studies directed at a specific cause generally isolates the basis of persistent symptoms. In patients with type I failure, pain typically does not localize well to the lateral epicondyle. Overlooking PIN entrapment should also be considered. In type II failure, if the assessment suggests residual pain at the epicondyle, further release of the extensor tendon at the lateral epicondyle is generally successful. In a patient with a type III failure, either instability or bursal or capsular

1. Abrahamsson, S. O., Sollerman, C., Söderberg, T., Lundborg, G., Rydholm, U., and Pettersson, H.: Lateral elbow pain caused by anconeus compartment syndrome: a case report. Acta Orthop. Scand. 58:589, 1987. 2. Bosworth, D. M.: The role of the orbicular ligament in tennis elbow. J. Bone Joint Surg. 37A:527, 1955. 3. Boyd, H. B., and McLeod, A. C.: Tennis elbow. J. Bone Joint Surg. 55A:1183, 1973. 4. Briggs, C. A., and Elliott, B. G.: Lateral epicondylitis: A review of structures associated with tennis elbow. Anat. Clin. 7:149, 1985. 5. Capener, N.: The vulnerability of the posterior interosseous nerve of the forearm: a case report and an anatomical study. J. Bone Joint Surg. 48B:770, 1966. 6. Coonrad, R. W., and Hooper, W. R.: Tennis elbow: its course, natural history, conservative and surgical management. J. Bone Joint Surg. 55A:1177, 1973. 7. Cushing, M., Lourie, G. M., Miller, D. V., and Hohn, J. A.: Heterotopic ossification after lateral epicondylectomy. J. Southern Orthop. Assoc. 10:63, 2001.

Chapter 46 Surgical Failure of Tennis Elbow

8. Cyriax, J. H.: The pathology and treatment of tennis elbow. J. Bone Joint Surg. 18:921, 1936. 9. Degreef, I., Van Raebroeckx, A., De Smet, L.: Anconeus muscle transposition for failed surgical treatment of tennis elbow: preliminary results. Acta Orthop. Belg. 71:154, 2005. 10. Dellon, A. L., Kim, J., and Ducic, I.: Painful neuroma of the posterior cutaneous nerve of the forearm after surgery for lateral humeral epicondylitis. J. Hand Surg. 29A:387, 2004. 11. Dewey, P.: The posterior interosseous nerve and resistant tennis elbow. J. Bone Joint Surg. 55B:435, 1973. 12. Gaede, F.: Adipofascial radial forearm flap after failed surgical treatment of lateral epicondylitis. Acta Orthop. Belg. 72:761, 2006. 13. Garden, R. S.: Tennis elbow. J. Bone Joint Surg. 43B:100, 1961. 14. Gardner, R. C.: Tennis elbow: Diagnosis, pathology and treatment. Nine severe cases treated by a new reconstructive operation. Clin. Orthop. Relat. Res. 72:248, 1970. 15. Goldie, I.: Epicondylitis lateralis humeri. Acta Chir. Scand. 339(suppl):7, 1964. 16. Henry, M., and Stutz, C.: A unified approach to radial tunnel syndrome and lateral tendinosis. Tech. Hand Up. Extrem. Surg. 10:200, 2006. 17. Jalovaara, P., and Lindholmj, R. V.: Decompression of the posterior interosseous nerve for tennis elbow. Arch. Orthop. Trauma Surg. 108:243, 1989. 18. Luchetti, R., Atzei, A., Brunelli, F., and Fairplay, T.: Anconeus muscle transposition for chronic lateral epicondylitis, recurrences, and complications. Tech. Hand Up. Extrem. Surg. 9:105, 2005. 19. Morrey, B. F.: Reoperation for failed surgical treatment of refractory lateral epicondylitis. J. Shoulder Elbow Surg. 1:47, 1992. 20. Morrison, D. L.: Tennis elbow and radial tunnel syndrome: differential diagnosis and treatment. J. Aust. Orthop. Assoc. 80:823, 1981. 21. Neviaser, T. J., Neviaser, R. J., Neviaser, J. S., and Ain, B. R.: Lateral epicondylitis: results of outpatient surgery and immediate motion. Contemp. Orthop. 11:43, 1985.

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22. Nirschl, R. P., and Pettrone, F. A.: Tennis elbow and the surgical treatment of lateral epicondylitis. J. Bone Joint Surg. 61A:832, 1979. 23. Organ, S. W., Nirschl, R. P., Kraushaar, B. S., and Guidi, E. J.: Salvage surgery for lateral tennis elbow. Am. J. Sports Med. 25:746, 1997. 24. O’Driscoll, S. W., Bell, D. F., and Morrey, B. F.: Posterolateral rotatory instability of the elbow. J. Bone Joint Surg. 73A:440, 1991. 25. Posch, J. N., Goldberg, V. M., and Larrey, R.: Extensor fasciotomy for tennis elbow: a long-term follow-up study. Clin. Orthop. 135:179, 1978. 26. Regan, W., Wold, L. E., Coonrad, R., and Morrey, B. F.: Microscopic histopathology of lateral epicondylitis. Presented at the Annual Meeting of the Canadian Orthopaedic Association, Toronto, Ontario, June 3, 1989. 27. Roles, N. C., and Maudsley, R. H.: Radial tunnel syndrome: resistant tennis elbow as a nerve entrapment. J. Bone Joint Surg. 54B:499, 1972. 28. Rossum, J. V., Buruma, J. S., Kamphuisen, H. A. C., and Onvlee, G. J.: Tennis elbow: a radial tunnel syndrome? J. Bone Joint Surg. 60B:197, 1978. 29. Ruch, D. S., Papadonikolakis, A., and Campolattaro, R. M.: The posterolateral plica: a cause of refractory lateral elbow pain. J. Shoulder Elbow Surg. 15:367, 2006. 30. Smola, C.: About the problem of radial tunnel syndrome or “where does the tennis elbow end and where does the radial tunnel syndrome begin”? Handchir. Mikrochir. Plast. Chir. 36:241, 2004. 31. Stovall, P. B., and Beinfield, M. S.: Treatment of resistant lateral epicondylitis of the elbow by lengthening of the extensor carpi radialis brevis tendon. Surg. Gynecol. Obstet. 149:526, 1979. 32. Svernlöv, B., and Adolfsson, L.: Outcome of release of the lateral extensor muscle origin for epicondylitis. Scand. J. Plast. Reconstr. Surg. Hand Surg. 40:161, 2006. 33. Werner, C. O.: Lateral elbow pain and posterior interosseous nerve entrapment. Acta Orthop. Scand. 114(suppl):174, 1979. 34. Yerger, B., and Turner, T. Percutaneous extensor tenotomy for chronic tennis elbow: an office procedure. Orthopedics 8:1261, 1985.

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CHAPTER

47

Diagnosis and Treatment of Ulnar Collateral Ligament Injuries in Athletes Neal S. ElAttrache and Christopher S. Ahmad

INTRODUCTION Injury to the elbow medial ulnar collateral ligament (MUCL) from valgus forces was first recognized in a javelin thrower in 1946.32 The injury has since become well recognized in baseball pitchers and other overhead throwing athletes. Frank W. Jobe developed the original MUCL reconstruction and described the technique with initial results in 1986.17 The technique transected and reflected the flexor-pronator mass, transposed the ulnar nerve to a submuscular position, and created humeral tunnels that penetrated the posterior humeral cortex. Excellent exposure was achieved at the expense of morbidity to the flexor-pronator mass and handling the ulnar nerve. Since that initial report, modifications in the surgical technique have been made to ease technical demands and decrease soft tissue morbidity. A musclesplitting approach has been developed to safely avoid detachment of the flexor-pronator mass with or without subcutaneous transposition of the ulnar nerve.29,30 Modifications in bone tunnel creation have also been made that direct the tunnels anterior on the humeral epicondyle to avoid risk of ulnar nerve injury while still allowing figure-of-eight graft passage and configuration.30 Further changes in bone tunnel configuration have reduced the total number of tunnels and facilitate easier graft tensioning.1,27 Results with these modified techniques have proven effective in returning high-level athletes back to throwing. In addition to advancements in surgical technique, advancements have been made in the pathophysiology and diagnosis of MUCL injuries. This chapter describes MUCL pathophysiology, patient evaluation, and surgical indications, and describes three popular surgical techniques. Significant portions of this text have been reprinted with permission from Journal of the American Academy of Orthopaedic Surgeons, Volume 14 (12), pp. 693-700.

PATHOPHYSIOLOGY The anterior bundle of the MUCL is the strongest component and the primary restraint and stabilizer to valgus stress.5,16,22,25 The AOL is functionally composed of anterior and posterior bands that provide a reciprocal function in resisting valgus stress through the range of flexion-extension motion.20,25 Valgus stress is generated at the elbow during throwing maneuvers in baseball, softball, football, tennis serving, and volleyball spiking. The calculated valgus torque during the acceleration phase of throwing is 64 N-m,14,33 and more than 60 N-m with the tennis serve.11,13 These estimated forces exceed the known ultimate tensile strength of cadaveric MUCL specimens (33 N-m).38 Thus the MUCL is at risk for injury from these repetitive forces. A cadaver model has demonstrated that the flexor carpi ulnaris is the primary dynamic contributor to valgus stability and the flexor digitorum superficialis is a secondary stabilizer.24 Thus, the muscular dynamic stability to the medial elbow is essential and must be included in rehabilitation programs and morbidity from surgical techniques must be minimized.

DIAGNOSIS HISTORY Patients with MUCL injuries complain of medial elbow pain during the acceleration phase of throwing (Fig. 47-1). Chronic injuries present gradually and often with pain occurring only when throwing greater than 50% to 75% of maximal effort. Acute injuries may present suddenly with a pop, sharp pain, and inability to continue throwing. Patients may be affected with valgus extension overload syndrome associated with MUCL insufficiency. Occasionally, the presenting symptoms of VEO overshadow the symptoms of MUCL insufficiency, especially in the setting of chronic slowly progressive ligament attenuation. In these cases, the symptoms of sharp posteromedial elbow pain in both the acceleration (flexion) and more so in deceleration (extension) phases of throwing are also associated with limited extension and mechanical catching resulting from impinging osteophytes, chondromalacia, and loose bodies.

PHYSICAL Physical examination features indicating MUCL injury include point tenderness directly over the MUCL or toward its insertion sites. Valgus instability is tested with the patients’ elbow flexed between 20 and 30 degrees to unlock the olecranon from its fossa as valgus stress is applied (Fig. 47-2). The milking maneuver is performed

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Acceleration

FIGURE 47-1

Symptoms of ulnar collateral ligament insufficiency are noted primarily during the late cocking and early acceleration phases of the throwing motion.

FIGURE 47-3

Moving valgus stress test with arrows indicated examiner applying valgus stress while moving the elbow from flexion to extension. (From Ahmad, C. S.: Elbow injuries and the throwing athlete. In Galatz, L. M. [ed.]: Orthopaedic Knowledge Update: Shoulder and Elbow 3. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2008, pp. 451-460, with permission.)

FIGURE 47-2

Valgus stress is applied to the elbow with the elbow in 25 degrees of flexion. The ulnar collateral ligament is palpated while applying valgus stress. Tenderness and laxity both are assessed during the maneuver.

by either the patient or the examiner pulling on the patient’s thumb to create valgus stress with the patients’ forearm supinated and elbow flexed beyond 90 degrees. The moving valgus stress test is performed by applying valgus torque while the elbow is then flexed and extended and is considered positive if the medial elbow pain is reproduced at the MUCL and is maximum between 70 and 120 degrees (Fig. 47-3). The moving valgus stress test is highly sensitive and specific. Physical examination should also assess the degree of extension loss. Pain may be elicited in the posterior compartment with pronation, valgus, and extension forces indicating valgus extension overload. The presence of a palmaris longus should be ascertained if MUCL reconstruction is anticipated. The ulnar nerve should be palpated for possible subluxation, and Tinel’s

sign should be elicited. Medial epicondylitis can be confused with and may coexist with MCL injury. Patients demonstrate tenderness at the common flexor origin just distal to the medial epicondyle and pain with resisted pronation and/or flexion of the wrist. Flexor-pronator avulsion can also exist with UCL tears and will present with more obvious weakness and a palpable defect just distal to the epicondyle.

IMAGING Anteroposterior, lateral, and axillary views of the elbow are assessed for joint space narrowing, osteophytes, and loose bodies. Valgus stress radiographs may be used to measure medial joint line opening, and an opening greater than 3 mm has been considered diagnostic of valgus instability.6,17,30 However, mild increased valgus elbow laxity has been observed in uninjured, asymptomatic dominant elbows of professional baseball pitchers when compared with their nondominant elbow.10 Computed tomography and magnetic resonance imaging (MRI) may further define loose bodies and osteophytes. Conventional MRI is capable of identifying thickening within the ligament from chronic injury or more obvious full-thickness tears. MR arthrography enhanced with intra-articular gadolinium improves the diagnosis of partial undersurface tears.7,15,21 Therefore the preferred imaging technique is MR enhanced with intra-articular gadolinium contrast, high-field closed magnet, and narrow slice images. Figure 47-4 demonstrates a full

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Ulnar collateral ligament graft reconstruction

FIGURE 47-5

Classic Jobe UCL reconstruction. (Redrawn from Safran, M., Ahmad, C. S., and ElAttrache, N. S.: Ulnar collateral ligament of the elbow. Arthroscopy 21:1381, 2005, with permission.)

FIGURE 47-4

Magnetic resonance imaging scan with arrow indicating ulnar collateral ligament tear. (From Ahmad, C. S.: Elbow injuries and the throwing athlete. In Galatz, L. M. [ed.]: Orthopaedic Knowledge Update: Shoulder and Elbow 3. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2007, with permission.)

thickness tear of the MUCL from its attachment to the medial humeral epicondyle. Dynamic ultrasonography has recently been studied as a means to evaluate the MUCL and is capable of detecting increased laxity with valgus stress.28 Advantages of ultrasound is that it is noninvasive, inexpensive, and dynamic. A disadvantage lies in dependence on operator experience.

TREATMENT

features are predictive for athletes who will respond to nonoperative treatment. Local steroid injections should be avoided because it may risk further injury to the MUCL. Patients who wish to continue throwing, have failed nonoperative treatment, have an accurate diagnosis of MUCL injury, and are willing to participate in the lengthy rehabilitation are indicated for surgical reconstruction. Contraindications to surgical MUCL reconstruction include those athletes with asymptomatic tears that are common to those athletes with little valgus demands on the elbow. Some patients who do not wish to continue throwing or who cannot participate in the extensive rehabilitation are contraindicated. Patients with coexisting ulnohumeral or radiocapitellar arthritis considering MUCL reconstruction should be informed of the possibility of continued or worsening pain following reconstruction.

INDICATIONS AND CONTRAINDICATIONS Treatment decisions require consideration of the patient’s athletic demands and the degree of MUCL injury. Nonoperative treatment includes a 6-week period of rest from throwing and flexor-pronator strengthening.24 If the patient becomes asymptomatic and the physical examination normalizes, then return to throwing with optimizing throwing mechanics is started. Rettig and colleagures26 demonstrated a 42% return to same level of play with an average return at 24.5 weeks with nonoperative treatment. No history or physical examination

SURICAL TECHNIQUES Several surgical techniques have evolved, and each has advantages and disadvantages. The modified Jobe technique has been considered the gold standard and has a reported success rate as high as 93% in returning throwing athletes back to competition (Fig. 47-5). This technique is technically demanding, however, in regard to number of tunnels, exact placement and connecting of tunnels, graft passing, and graft fixation. The docking technique has the advantages of reducing the complex-

Chapter 47 Diagnosis and Treatment of Ulnar Collateral Ligament Injuries in Athletes

ity of tunnel creation, passing and tensioning, and fixation. A potential disadvantage is that the graft is reduced from a triple strand used in the Jobe technique to a double-strand graft. However, a modification of the technique now allows doubling the graft on itself to form a quadruple limb graft. Finally, the hybrid interference screw technique has the advantage of further reducing the number and complexity of tunnel creation. With a single tunnel required on the ulna, there is less manipulating and risk of injury to the ulnar nerve. Furthermore, this technique allows independent tensioning of the anterior and posterior bands of the anterior bundle of the UCL, which is not accomplished with the other described techniques. A disadvantage is potential inflammatory reaction to the bioabsorbable screws.

Jobe Technique The patient is positioned supine with a pneumatic tourniquet on the upper arm. A skin incision centered over the medial epicondyle is extended 5 cm both proximally and distally. Dissection is carried down to the muscle fascia, and sensory branches of the medial antebrachial cutaneous nerve are consistently identified just anterior and distal to the medial epicondyle. These branches are protected to avoid painful neuroma. A muscle-splitting approach is created by incising the raphe of the flexor carpi ulnaris. A periosteal elevator is used to separate the flexor muscle mass from the MUCL. The ligament is inspected and palpated as valgus stress is applied (Fig. 47-6A). A longitudinal split is made in the ligament and valgus stress applied with the elbow at 30 degrees flexion will reveal opening of the ulnohumeral articulation if the MUCL is insufficient (Fig. 47-6B). Tunnels are then

A

created for graft placement (Fig. 47-7). Converging 3.2mm drill holes are made in the ulna anterior and posterior to the sublime tubercle with a minimum 5 mm bridge (Fig. 47-8A). The drill holes are connected with an angled curette. A 4.5 mm drill hole is made at the site of the anatomic origin of the anterior bundle of MUCL on the medial epicondyle that does not penetrate the posterior cortex (Fig. 47-8B). The fascia over the anterior aspect of the epicondyle is split to expose the broad flat surface of the anterosuperior epicondyle. A 3.2-mm drill hole is placed just anterior to the epicondylar attachment of the medial intermuscular septum and directed to communicate with the 4.5-mm drill hole in the epicondyle. A second 3.2-mm drill hole, which is made in the anterosuperior surface of the epicondyle approximately 1 cm from the previous 3.2-mm hole, illustrates the completed humeral bone tunnels. The palmaris longus from the ipsilateral arm is harvested through a series of small transverse incisions beginning at the distal flexor crease of the wrist. Additional skin incisions are made at 7.5 and 15 cm from the wrist, exposing the entire length of the tendon. Alternatively, the palmaris longus may be harvested with a tendon stripper and a single incision in the flexor crease of the wrist. A number 2 nonabsorbable suture is placed at each end of the graft. The graft is passed through the proximal ulna bone tunnel and medial epicondyle in a figure-of-eight configuration (see Fig. 47-5). With the elbow placed with varus stress, 60 degrees of elbow flexion, and the forearm in supination, tension is applied to the graft. The ulnar side of the graft is sutured to the remnants of the ulnar collateral ligament adjacent to the

B FIGURE 47-6

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A, Muscle-splitting approach with retractors in place and medial ulnar collateral ligament well visualized. B, Medial ulnar collateral ligament incised demonstrating ulnohumeral gapping. (From Ahmad, C. S., and ElAttrache, N. S.: Elbow valgus instability in the throwing athlete. J. Am. Acad. Orthop. Surg. 14:693, 2006, with permission. © 2006 American Academy of Orthopaedic Surgeons.)

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Ulnohumeral gapping

Humeral tunnel

FIGURE 47-7

Medial epicondyle Ulnar tunnel

Ulnar nerve

A

Schematic of medial ulnar collateral ligament incised demonstrating ulnohumeral gapping, ulnar tunnel, and humeral tunnels. (Redrawn from Ahmad, C. S., and ElAttrache, N. S.: Elbow valgus instability in the throwing athlete. J. Am. Acad. Orthop. Surg. 14:693, 2006, with permission. © 2006 American Academy of Orthopaedic Surgeons.)

B FIGURE 47-8

A, Ulnar tunnels created anterior and posterior to sublime tubercle. B, Inferior humeral tunnel created at anatomic medial ulnar collateral ligament insertion. (From Ahmad, C. S., and ElAttrache, N. S.: Elbow valgus instability in the throwing athlete. J. Am. Acad. Orthop. Surg. 14:693, 2006, with permission. © 2006 American Academy of Orthopaedic Surgeons.)

sublime tubercle. The proximal limb of the graft is sutured to the medial intermuscular septum outside the drill hole on the superior surface of the epicondyle. The elbow is then brought through a ROM to verify isometry of the ligament reconstruction. Simple sutures are placed in the crossing limbs of the graft, which places additional tension on the graft and enhances fixation. The native ligament is then repaired over the graft with the placement of simple sutures. The muscle fascia is repaired, and the skin is closed.

Docking Technique The docking technique is a modification of the Jobe technique that simplifies graft passage, tensioning, and fixation (Fig. 47-9). The docking technique modification uses the muscle-splitting approach with tunnel creation on the ulna similar to the Jobe technique (see Fig. 47-6A and B). The humeral tunnel position is located in the anterior half of the medial epicondyle at the anatomic insertion of the native MUCL similar to the Jobe technique. This tunnel is created to a depth of 15 mm using

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Blind ended tunnel at humerus

FIGURE 47-11 Final position of the graft with tensioning of sutures. (From Ahmad, C. S., and ElAttrache, N. S.: Elbow valgus instability in the throwing athlete. J. Am. Acad. Orthop. Surg. 2006; 14(12):693-700, with permission.) FIGURE 47-9

The docking technique creates a humeral tunnel that accepts both limbs of the graft with tensioning performed through superior exit holes. (From Safran, M., Ahmad, C. S., and ElAttrache, N. S.: Ulnar collateral ligament of the elbow. Arthroscopy 21:1381, 2005, with permission.)

is passed into the humeral tunnel. The final length of the anterior limb of the graft is determined by placing it adjacent to the humeral tunnel and visually estimating the length of the graft that would allow the graft to be tensioned within the humeral tunnel. A No. 1 braided nonabsorbable suture is placed in a Krackow fashion. The excess graft is excised and the graft limb is passed into the humeral tunnel with the sutures exiting the small tunnels. Final graft tensioning is performed by placing the elbow through a full range of motion with varus stress placed on the elbow (Fig. 47-11). The sutures are then tied over the bony bridge on the humeral epicondyle with the elbow in 60 degrees of flexion, supination, and varus stress applied.

Hybrid Interference Screw Fixation Technique

FIGURE 47-10 Exit holes created on superior aspect of epicondyle. (From Ahmad, C. S., and ElAttrache, N. S.: Elbow valgus instability in the throwing athlete. J. Am. Acad. Orthop. Surg. 14:693, 2006, with permission. © 2006 American Academy of Orthopaedic Surgeons.)

a 4-mm burr or drill. The upper border of the epicondyle is exposed. Two small exit tunnels separated by 5 mm to 1 cm are created to allow suture passage from the primary humeral tunnel (Fig. 47-10). Suture loops are then placed from the primary humeral tunnel through the exit tunnels to facilitate graft passing. With the elbow in forearm supination and mild varus stress, the horizontal incision in the native MUCL is repaired with a 2.0 absorbable suture. The graft is then passed through the ulnar tunnel from anterior to posterior. The posterior limb of the graft

A new technique of MUCL reconstruction has been evaluated in the laboratory that reconstructs the central isometric fibers of the native ligament and achieves ulnar-sided fixation in a single bone tunnel with an interference screw and humeral fixation using the docking technique (Fig. 47-12). This technique is less technically demanding because the required number of drill holes necessary is reduced. Less dissection through a muscle-splitting approach is afforded because only a single central tunnel is required rather than two tunnels with an intervening bony bridge on the ulna. With a single tunnel, the posterior ulnar tunnel, which is in closest proximity to the ulnar nerve, is avoided. Finally, graft passage is less difficult with an interference screw in a single tunnel. After exposing the MUCL through the musclesplitting approach as described for the previous techniques (see Fig. 47-6A and B), the central isometric fiber attachments on the ulna and humeral epicondyle are identified to direct tunnel placement. At the insertion on

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FIGURE 47-12

Interference screw fixation technique. (Redrawn from Conway, J. E.: The DANE TJ procedure for elbow medial ulnar collateral ligament insufficiency. Tech. Shoulder Elbow Surg. 7:36, 2006, with permission.)

FIGURE 47-13 Ulnar tunnel created at sublime tubercle. (From Ahmad, C. S., and ElAttrache, N. S.: Elbow valgus instability in the throwing athlete. J. Am. Acad. Orthop. Surg. 14:693, 2006, with permission. © 2006 American Academy of Orthopaedic Surgeons.)

the sublime tubercle of the ulna, approximately 4.5 mm distal to the joint surface, a 5-mm diameter tunnel is drilled and directed 45 degrees distally to the long axis of the ulna for a depth of 20 mm (Fig. 47-13). The size of the tunnel diameter may be increased for larger graft diameters. The drill is advanced with guidance of the drill sleeve that protects the soft tissue and ulnar nerve. Maintenance of a 2-mm bone bridge from the edge of the tunnel to the joint avoids possible fracture of the tunnel into the ulnohumeral joint.

The palmaris longus tendon is harvested and folded over to create a double strand graft. A standard whipstitch with number 2 nonabsorbable suture is placed in the folded portion of the graft. Graft fixation into the ulnar tunnel with a 4.75 or 5.5 × 15 mm interference screw is then achieved using a unique bio-Tenodesis driver (Arthrex, Inc., Naples, FL). The driver shaft is used to guide the turning screw into the tunnel while providing constant tension on the graft. Sutures controlling the graft are tied over the interference screw, locking the graft to the screw to increase fixation strength. The humeral tunnels are created as described for the docking procedure, as shown in Figure 47-10. The two limbs of the graft are then prepared as described for the docking procedure with the modification that both limbs must be accurately cut to length (Fig. 47-14). The anterior graft limb sutures are then marked with ink for later identification. One suture from the anterior graft limb and posterior graft limb are then passed through the anterior humeral tunnel using a free needle or suture passing wire. The two remaining sutures from each graft limb are passed through the posterior tunnel. The graft is delivered into the humeral tunnel, and the elbow is flexed and extended with tension on the sutures to eliminate any creep. The elbow is positioned at 80 degrees of flexion, varus stress applied, and the posterior limb sutures tied. Then with the elbow positioned at 30 degrees of flexion and varus stress applied, the anterior limb sutures are tied.

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665

valgus stress to the elbow. Before surgery, the ulnar nerve should be palpated in elbow flexion and extension to assess possible anterior subluxation. Symptoms related to ulnar nerve irritation should be ascertained such as numbness in the fourth and fifth digits. We reserve ulnar nerve transposition in patients with ulnar neuritis that involves compromised motor function or ulnar neuritis combined with ulnar nerve subluxation.

Arthroscopy

FIGURE 47-14

Graft fixed in ulna with interference screw.

SURGICAL CONSIDERATIONS Graft Choices The presence or absence of the palmaris longus tendon should be assessed before the procedure. When this tendon is available, it is the tissue of choice for reconstruction for many surgeons; however, absence of the palmaris longus occurs approximately 6% to 25% in the general population.31 When absent, the gracillus, plantaris, Achilles tendon, and toe extensor tendons are alternative options. Our preference is the ipsilateral gracillus when the palmaris is not available because of predictable size and ease of harvest.

Ulnar Nerve Symptoms of ulnar nerve irritation are present in more than 40% of paitents with UCL insufficiency.6 Inflammation involving UCL traction, friction, and compression can secondarily affect the ulnar nerve as it crossed the elbow. Sources of injury to the ulnar nerve have been divided into three basic groups: compression, friction, and traction. Compression neuropathy can develop secondary to space-occupying lesions such as bony spurs, scar tissue, thickening of the arcuate ligament, calcifications of the MCL, or hypertrophy to the medial head of the triceps. The path of the ulnar nerve about the elbow places it at risk for compression at several anatomic sites including the arcade of Struthers, the medial intermuscular septum, the cubitul tunnel itself, the fascial origin of the flexor digitorum superficialis, and the confluence of the two heads of the FCU. Friction neuropathy results from subluxation of the ulnar nerve over the medial epicondyle. Traction that causes neuritis results from medial elbow instability and repetitive

Arthroscopic evaluation of the elbow joint before MUCL reconstruction has been advocated by some.4,27 Arthroscopic assessment of valgus stability may be performed by placing valgus stress to the elbow while positioned at 90 degrees of flexion and the forearm maximally pronated. Normal elbows demonstrate a maximum of 1 to 2 mm of opening, whereas elbows with MUCL insufficiency demonstrate greater than 2 to 3 mm of opening (Fig. 47-15). Although ulnohumeral opening may be appreciated, a cadaveric study demonstrated that the anterior bundle of the MUCL cannot be directly visualized arthroscopically. Arthroscopy does facilitate diagnostic examination of the anterior and posterior compartments, and associated procedures may be performed when necessary such as removal of loose bodies and marginal osteophytes, anterior capsular release, and anterior, posterior, or lateral débridement.12

Valgus Extension Overload Throwing may also result in posterior elbow pain because the olecranon is repeatedly and forcefully driven into the olecranon fossa. Knowledge of the relationship between the posterior compartment contributions to elbow stability from bony articulations and the soft tissue MUCL is an important concept in the pathophysiology of valgus instability. Andrews et al3 reported that in a series of professional baseball players who underwent olecranon débridement, 25% developed valgus instability and eventually required MUCL reconstruction. This observation suggests that both the olecranon and the MUCL contribute to valgus stability. A recent biomechanical study demonstrated that sequential partial resection of the posteromedial aspect of the olecranon resulted in stepwise increases in elbow valgus angulation.19 Kamineni et al18 also confirmed in a cadaver model that strain in the AOL is increased with increasing posteromedial olecranon resection beyond 3 mm. These studies suggest that aggressive olecranon resection put the MUCL at risk for injury. A different concept suggests that subtle valgus instability may lead posteromedial osteophyte formation.2 MUCL injury simulated in a cadaver model results in contact alterations in the posterior compartment that leads to osteophyte formation. This suggests that patients with posteromedial impinge-

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A

and at 6 months, the patient may perform throwing lightly from the wind-up. At 7 months, a graduated program of range of motion, strengthening, and total body conditioning exercises is performed. Throwers and pitchers are limited to throwing at 50% effort, while gradually increasing the duration of their session to 25 to 30 min. Pitchers are permitted to throw from the pitching mound and progress to 70% of maximum velocity during the eighth or ninth month. Over the next 2 to 3 months, the duration of throwing sessions and velocity are slowly increased to simulate a game situation. Throwing in competition is permitted at 1 year if the shoulder, elbow, and forearm are pain free while throwing and full strength and range of motion have returned. Throughout the rehabilitation phase, careful supervision and focus on body and throwing mechanics should be emphasized. Eighteen months may be required to regain preoperative ability and competitive level with accurate ball control. Relatively shorter periods are required for other player positions or overhead sports.

PEARLS

B FIGURE 47-15 A and B, Arthroscopic evaluation demonstrating ulnohumeral gapping with valgus stress applied. (From ElAttrache, N. S., et al [eds.]: Surgical Techniques in Sports Medicine. Philadelphia, Lippincott Williams & Wilkins, 2006, with permission.)

ment pain should be critically evaluated for suspected MUCL pathology.

POSTOPERATIVE REHABILITATION The elbow is immobilized in a splint for 10 days to allow the skin and soft tissues to heal. Then active wrist, elbow, and shoulder range of motion exercises are initiated. After 4 to 6 weeks, strengthening exercises are begun while avoiding valgus stress until 4 months after surgery. At 4 months after surgery, the patient begins a throwing program initially with ball toss of 30 to 40 feet, two to three times a week for about 15 minutes. At 5 months the patient may increase the tossing distance to 60 feet,

Several aspects of MUCL reconstruction enhance success. The location of the inferior humeral tunnel is extremely important to ensure an isometric graft. Limited dissection of the flexor pronator mass is essential to optimize dynamic stability to the elbow. Less handling of the ulnar nerve has been attributed to improved outcome.30 For all reconstruction techniques described, we prefer to repair the native ligament underneath the reconstruction to keep the new graft extrasynovial. The synovial environment may have inflammatory mediators that delay healing and also cause tunnel expansion if access is gained to the drilled tunnels. Cases in which the sublime tubercle is insufficient such as a previous fracture or previous reconstruction may be better managed with the hybrid interference screw technique. The interference screw fixation is also optimized with attention to several details. The ulnar tunnel should be drilled 0.5 to 1 mm larger than the graft diameter to allow easier placement of the interference screw. Typical graft size is 4.5 mm and tunnel diameter 5.5 mm and a 4.75-mm screw is selected. Fixation strength remains excellent by tying the graft controlling sutures over the interference screw to achieve combined interference fixation and suture anchor fixation.

RESULTS MUCL reconstruction is technically demanding with regard to limiting muscular dissection and avoiding

Chapter 47 Diagnosis and Treatment of Ulnar Collateral Ligament Injuries in Athletes

ulnar nerve injury. Furthermore, achieving graft isometry, adequate graft tension, and secure graft fixation remain challenging while optimizing graft healing biology. Reports of clinical outcome for MUCL reconstruction have been variable, with 68% to 93% having good to excellent results. In a recent study using a muscle-splitting approach without ulnar nerve transposition, 93% of patients who had no previous elbow surgery had excellent results at 2-year followup.30 Prognostic factors were related to associated pathology and history of previous surgery such as olecranon resection. Modifications in surgical technique consisting of minimizing dissection of the flexorpronator mass and handling of the ulnar nerve have been attributed to improved outcome. Less dissection of the muscle mass seems to reduce morbidity to the muscles that dynamically stabilize the medial aspect of the elbow. Azar et al4 reported on 78 throwing athletes who underwent MUCL reconstruction with submuscular ulnar nerve transposition. Fifty-nine patients were available for follow-up at 12 to 72 months. Of those patients, 81% returned to the same or higher level of competition. One patient had ulnar nerve symptoms that eventually resolved 10 months after surgery.4 Rohrbough et al27 reported on 36 patients who underwent the docking technique of MUCL reconstruction. At an average follow-up of 3.3 years, 92% returned to or exceeded their previous level of competition for at least 1 year. A review 100 consecutive overhead-throwing athletes who underwent the docking reconstruction technique with a mean follow-up of 36 months found that 90% were able to compete at the same or a higher level for more than 12 months.9 Another modification of the docking technique using a 4-strand palmaris longus graft for reconstruction has been reported in 25 elite professional and collegiate baseball players with a minimum 2-year follow-up.23 Ninety-two percent were able to return to their preinjury level of competition. The technique of interference screw fixation has been biomechanically evaluated in cadavers, and graft fixation strength was 95% that of control intact MUCLs under valgus load.1 Reconstruction of the MUCL also restored valgus stability to within less than one degree of the intact elbow for all flexion angles.1 Clinical results for the hybrid technique with ulnar screw fixation and humeral docking fixation have been encouraging.8 During a 3-year period, 22 athletes were treated with this technique and evaluated at a minimum of 2 years postoperatively. Nineteen of twenty-two patients had excellent results. There were two fair and one poor result. The poor result was in a revision case. The two other revision UCL reconstructions had excellent outcomes. Additionally, when used in two cases of sublime tubercle avulsions, the results were excellent.

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Postoperative complications occurred in four patients: two patients developed ulnar neuritis, and two patients required second surgeries for lysis of adhesions. Three of these four patients went on to have excellent outcomes.

SUMMARY Since the prior edition of this book, great advancements have been made in the understanding of MUCL injury pathophysiology, diagnosis, nonoperative, and operative treatment. Surgical reconstruction of the MUCL is indicated for patients with symptomatic valgus instability in whom nonoperative treatment has failed. Several surgical technique options now exist that ease the technical demands of the surgery. Less handling of the ulnar nerve and limiting morbidity to the flexor pronator mass has optimized patient outcomes.

References 1. Ahmad, C. S., Lee, T. Q., and ElAttrache, N. S.: Biomechanical evaluation of a new ulnar collateral ligament reconstruction technique with interference screw fixation. Am. J. Sports Med. 31:332, 2003. 2. Ahmad, C. S., Park, M. C., and ElAttrache, N. S.: Elbow medial ulnar collateral ligament insufficiency alters posteromedial olecranon contact. Am. J. Sports Med. 32:1607, 2004. 3. Andrews, J. R., and Timmerman, L. A.: Outcome of elbow surgery in professional baseball players. Am. J. Sports Med. 23:407, 1995. 4. Azar, F. M., Andrews, J. R., Wilk, K. E., and Groh, D.: Operative treatment of ulnar collateral ligament injuries of the elbow in athletes. Am. J. Sports Med. 28:16, 2000. 5. Callaway, G. H., Field, L. D., Deng, X. H., Torzilli, P. A., O’Brien, S. J., Altchek, D. W., and Warren, R. F.: Biomechanical evaluation of the medial collateral ligament of the elbow. J. Bone Joint Surg. Am. 79:1223, 1997. 6. Conway, J. E., Jobe, F. W., Glousman, R. E., and Pink, M.: Medial instability of the elbow in throwing athletes. Treatment by repair or reconstruction of the ulnar collateral ligament. J. Bone Joint Surg. Am. 74:67, 1992. 7. Cotton, A., Jacobson, J., Brossmann, J., Pedowitz, R., Haghighi, P., Trudell, D., and Resnick, D.: Collateral ligaments of the elbow: conventional MR imaging and MR arthrography with coronal oblique plane and elbow flexion. Radiology 204:806, 1997. 8. Dines, J. S., ElAttrache, N. S., Conway, W., Ahmad, C. S., and Conway, J. E.: Clinical Outcomes of the Dane TJ Technique to Address Medial Ulnar Collateral Ligament Insufficiency of the Elbow. In American Orthopaedic Society for Sports Medicine Annual Meeting; 2007 July 15, 2007; Calgary, Canada; 2007. 9. Dodson, C. C., Thomas, A., Dines, J. S., Nho, S. J., Williams, R. J. 3rd, and Altchek, D. W.: Medial ulnar collateral liga-

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ment reconstruction of the elbow in throwing athletes. Am. J. Sports Med. 34:1926, 2006. Ellenbecker, T. S., Mattalino, A. J., Elam, E. A., and Caplinger, R. A.: Medial elbow joint laxity in professional baseball pitchers. A bilateral comparison using stress radiography. Am. J. Sports Med. 26:420, 1998. Elliott, B., Fleisig, G., Nicholls, R., and Escamilia, R.: Technique effects on upper limb loading in the tennis serve. J. Sci. Med. Sport 6:76, 2003. Field, L. D., Callaway, G. H., O’Brien, S. J., and Altchek, D. W.: Arthroscopic assessment of the medial collateral ligament complex of the elbow. Am. J. Sports Med. 23:396, 1995. Fleisig, G., Nicholls, R., Elliott, B., and Escamilla, R.: Kinematics used by world class tennis players to produce high-velocity serves. Sports Biomech. 2:51, 2003. Fleisig, G. S., Andrews, J. R., Dillman, C. J., and Escamilla, R. F.: Kinetics of baseball pitching with implications about injury mechanisms. Am. J. Sports Med. 23:233, 1995. Hill, N. B. Jr, Bucchieri, J. S., Shon, F., Miller, T. T., and Rosenwasser, M. P.: Magnetic resonance imaging of injury to the medial collateral ligament of the elbow: a cadaver model. J. Shoulder Elbow Surg. 9:418, 2000. Hotchkiss, R. N., and Weiland, A. J.: Valgus stability of the elbow. J. Orthop. Res. 5:372, 1987. Jobe, F. W., Stark, H., and Lombardo, S. J.: Reconstruction of the ulnar collateral ligament in athletes. J. Bone Joint Surg. Am. 68:1158, 1986. Kamineni, S., ElAttrache, N. S., O’Driscoll, S. W., Ahmad, C. S., Hirohara, H., Neale, P. G., An, K. N., and Morrey, B. F.: Medial collateral ligament strain with partial posteromedial olecranon resection. A biomechanical study. J. Bone Joint Surg. Am. 86-A:2424, 2004. Kamineni, S., Hirahara, H., Pomianowski, S., Neale, P. G., O’Driscoll, S. W., ElAttrache, N., An, K. N., and Morrey, B. F.: Partial posteromedial olecranon resection: a kinematic study. J. Bone Joint Surg. Am. 85-A:1005, 2003. Morrey, B. F., and An, K. N.: Articular and ligamentous contributions to the stability of the elbow joint. Am. J. Sports Med. 11:315, 1983. Munshi, M., Pretterklieber, M. L., Chung, C. B., Haghighi, P., Cho, J. H., Trudell, D. J., and Resnick, D.: Anterior bundle of ulnar collateral ligament: evaluation of anatomic relationships by using MR imaging, MR arthrography, and

22.

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32. 33.

gross anatomic and histologic analysis. Radiology 231:797, 2004. O’Driscoll, S. W., Jaloszynski, R., Morrey, B. F., and An, K. N.: Origin of the medial ulnar collateral ligament. J. Hand Surg. [Am.] 17:164, 1992. Paletta, G. A. Jr., and Wright, R. W.: The modified docking procedure for elbow ulnar collateral ligament reconstruction: 2-year follow-up in elite throwers. Am. J. Sports Med. 34:1594, 2006. Park, M. C., and Ahmad, C. S.: Dynamic contributions of the flexor-pronator mass to elbow valgus stability. J. Bone Joint Surg. Am. 86-A:2268, 2004. Regan, W. D., Korinek, S. L., Morrey, B. F., and An, K. N.: Biomechanical study of ligaments around the elbow joint. Clin. Orthop. 271:170, 1991. Rettig, A. C., Sherrill, C., Snead, D. S., Mendler, J. C., and Mieling, P.: Nonoperative treatment of ulnar collateral ligament injuries in throwing athletes. Am. J. Sports Med. 29:15, 2001. Rohrbough, J. T., Altchek, D. W., Hyman, J., Williams, R. J. 3rd, and Botts, J. D.: Medial collateral ligament reconstruction of the elbow using the docking technique. Am. J. Sports Med. 30:541, 2002. Sasaki, J., Takahara, M., Ogino, T., Kashiwa, H., Ishigaki, D., and Kanauchi, Y.: Ultrasonographic assessment of the ulnar collateral ligament and medial elbow laxity in college baseball players. J. Bone Joint Surg. Am. 84-A:525, 2002. Smith, G. R., Altchek, D. W., Pagnani, M. J., and Keeley, J. R.: A muscle-splitting approach to the ulnar collateral ligament of the elbow. Neuroanatomy and operative technique. Am. J. Sports Med. 24:575, 1996. Thompson, W. H., Jobe, F. W., Yocum, L. A., and Pink, M. M.: Ulnar collateral ligament reconstruction in athletes: Muscle-splitting approach without transposition of the ulnar nerve. J. Shoulder Elbow Surg. 10:152, 2001. Vanderhooft, E.: The frequency of and relationship between the palmaris longus and plantaris tendons. Am. J. Orthop. 25:38, 1996. Waris, W.: Elbow injuries in javelin throwers. Acta Chir. Scand. 93:563, 1946. Werner, S. L., Fleisig, G. S., Dillman, C. J., and Andrews, J. R.: Biomechanics of the elbow during baseball pitching. J. Orthop. Sports Phys. Ther. 17:274, 1993.

Chapter 48 Lateral Collateral Ligament Insufficiency

CHAPTER

48

Lateral Collateral Ligament Insufficiency Joaquin Sanchez-Sotelo

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ment complex has been required in most experimental settings to produce a significant increase in varus and posterolateral displacements.5,8,13,27,29,35 Isolated section of the ulnar insertion of the lateral ulnar collateral ligament has not been shown to promote dramatic elbow instability in all cadaveric studies.5,27-29 However, reconstruction of the lateral ulnar collateral ligament with a tendon graft restores varus and posterolateral stability in the laboratory.17 The overlying common extensor-supinator group has also been shown to play a major role in elbow stability.5,9 There is a complex interplay between the lateral collateral ligament complex and other elbow structures, including the coronoid and radial head.6,7,15,34

INTRODUCTION ETIOLOGY The lateral collateral ligament complex is one of the main structures implicated in the stability of the elbow joint. Insufficiency of the lateral collateral ligament complex is present in many patients with elbow instability. Several basic science and clinical studies have improved our understanding of the contributions of the lateral collateral ligament complex to elbow stability, the etiology of lateral collateral ligament insufficiency, the value of different clinical and imaging tests for identification of this entity, and the outcome of surgical repair or reconstruction. The term posterolateral rotatory instability has been coined to describe the clinical condition that results from lateral collateral ligament complex insufficiency.25

BASIC SCIENCE Several ligamentous structures may be identified on the lateral aspect of the elbow joint (see Chapter 2). The ligamentous fibers connecting the lateral humeral epicondyle with the lateral aspect of the ulna seem to be the most important for elbow stability on the lateral side. These fibers, commonly referred to as lateral ulnar collateral ligament,22 attach distally into the tubercle of the supinator crest (Fig. 48-1). More anterior fibers originated at the lateral humeral epicondyle, named by some as radial collateral ligament, blend with the fibers of the annular ligament. Unlike the medial side of the joint, morphologic and histologic studies have not been able to show distinct ligaments on the lateral side of the joint consistently.5,14 Lateral collateral ligament complex insufficiency allows excessive posterolateral displacement of the proximal forearm relative to the distal humerus. The contribution of the lateral collateral ligament complex to elbow stability has been investigated in several cadaveric models. Release of the whole lateral collateral liga-

TRAUMA The lateral collateral ligament complex may be damaged as a result of trauma to the elbow, resulting in elbow dislocation, fracture-dislocation, subluxation, or ligamentous sprain (Box 48-1). McKee et al.21 reported on the soft tissue injury patterns identified in 10 dislocations and 52 fracture-dislocations treated surgically. The lateral collateral ligament complex was disrupted in all cases; proximal avulsion was the most common failure mode, followed by midsubstance rupture. The common extensor-supinator group was injured in 66% of the cases. The anterior bundle of the medial collateral ligament was injured in approximately 50% of the cases. Less severe injuries causing dislocation or an elbow sprain (usually hyperextension or varus stress) may also damage the lateral collateral ligament complex if they place substantial strain on the ligament fibers. When injured, the medial collateral ligament seems to heal without residual clinically significant medial-sided instability in most patients.10 On the contrary, persistent lateral-sided instability seems to be more frequent, but the reasons are unclear: It may be related to a decreased healing potential, as seen in other anatomic locations such as the lateral side of the knee joint; the constant tensile gravitational loads imposed on the injured lateral side with elbow use; or the more common association with additional injuries such as radial head or coronoid fractures. Lateral collateral ligament insufficiency should be suspected in patients with recurrent dislocation, subjective instability, lateral-sided pain, and a history of elbow trauma.

CHRONIC ATTRITION Chronic attrition secondary to repetitive valgus stress is a well-known mechanism leading to medial collateral

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Annular ligament Radial collateral ligament

Accessory collateral ligament

Lateral ulnar collateral ligament

FIGURE 48-1

From a practical perspective, the lateral collateral ligament complex may be divided into three main components: the lateral ulnar collateral ligament, the annular ligament, and the radial collateral ligament.

Etiology of Lateral Collateral Ligament Insufficiency

BOX 48-1

Trauma

Chronic attrition

Iatrogenic injury

• • • • • • • • •

Elbow dislocation Elbow fracture-dislocation Elbow subluxation Elbow sprain Cubitus varus deformity Lateral epicondylitis Chronic crutch users Inadvertent sectioning in surgery Repeated steroid injections

ligament insufficiency. Chronic attrition of the lateral collateral ligament complex may occur in rare situations such as long-term crutch-walkers (paraplegics, poliomyelitis). Post-traumatic or congenital cubitus varus deformity is recognized as a risk factor for chronic attrition of the lateral collateral ligament complex and tardy posterolateral rotatory instability.1,26 With varus malalignment, triceps contraction has been hypothesized to force posterolateral rotatory subluxation and eventually lead to attenuation of the lateral collateral ligament complex. In addition, one cadaveric study has shown increased strain on the lateral collateral ligament complex with more than 25 degrees of varus deformity and lateral joint line opening with more than 20 degrees of varus deformity.3 In this setting, corrective osteotomy should be considered as an adjunct to lateral collateral ligament reconstruction to prevent failure. Insufficiency of the lateral collateral ligament has also been identified in patients with tennis elbow and no prior surgery16; insufficiency in this setting may be secondary to ligamentous

involvement by the same pathologic process affecting the common extensor group4 or the detrimental side effects on collagen fibers of repeated steroid injections.4,16

IATROGENIC INJURY Inadvertent damage of the lateral collateral ligament may occur during surgical procedures on the lateral side of the joint. Surgical treatment of tennis elbow may compromise the lateral collateral ligament complex if the release or débridement of the common extensor origin are too extensive, especially when the lateral epicondyle is denuded off soft tissues. Exposure of the radial head or capitellum for fracture fixation or chronic reconstruction may also jeopardize the lateral collateral ligament complex, especially when Köcher’s interval is used or the joint needs to be subluxed or dislocated in order to complete the surgical procedure.12,23,33 Special attention is required when performing surgery on the lateral side of the elbow joint to avoid damage to the lateral collateral ligament complex. Formal repair of the damaged ligament should always be part of the wound closure.

DIAGNOSIS PRESENTATION The clinical expression of lateral collateral ligament complex insufficiency varies considerably depending on the etiology, severity, associated pathology, previous surgery, and activity level (Box 48-2). Some patients may complain of recurrent episodes of frank elbow dislocation. However, most commonly patients complain of more subtle symptoms, including lateral-sided elbow pain, mechanical symptoms (clicking, catching, snapping, locking) or subjective instability.33 Patients with ligamentous insufficiency after a fracture-dislocation may present with more severe pain or stiffness secondary to the associated injuries. Commonly, most patients with lateral collateral ligament complex insufficiency report a previous history of trauma or surgery. In patients with previous surgery, it is important to determine if the preoperative symptoms were corrected by the surgery or if on the contrary surgery had no effect or occasioned a whole new constellation of symptoms. Subtle elbow instability is reflected by the inability of the patient to push with the affected upper extremity to stand up from a seat,31 open a heavy door, or similar activities that require active elbow extension against resistance with forearm supination. However, instability episodes are difficult to identify as such by the patient,

Chapter 48 Lateral Collateral Ligament Insufficiency

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Clinical Diagnosis of Lateral Collateral Ligament Complex Insufficiency

BOX 48-2

History

• • • • Physical examination •

• • • • • Imaging studies

• •

•

Examination under anesthesia

• • •

Arthroscopy

• • •

Lateral-sided elbow pain Mechanical symptoms Subjective instability Recurrent dislocation Pain over the location of the lateral collateral ligament complex Apprehension/pain with varus stress Positive results on posterolateral drawer test Positive results on posterolateral pivot-shift test Positive results on chair test Positive results on push-up test Posterolateral subluxation on plain radiographs Lateral collateral ligament discontinuity on magnetic resonance imaging scan Stress radiographs or fluoroscopy • Lateral joint line opening > 2 mm • Posterolateral subluxation Positive results in posterolateral drawer test Positive results in posterolateral pivot-shift test Fluoroscopically proven • Lateral joint line opening > 2 mm • Posterolateral subluxation Excessive lateral joint-line opening (drive-through) Posterolateral subluxation Lateral capsuloligamentous defect

who often reports pain when attempting to perform the above-mentioned activities.

PHYSICAL EXAMINATION A detailed physical examination should help identify basic information such as the specific location of the pain and elbow range of motion (see Chapter 4). The location of previous skin incisions and the presence of deformity should be noted. As mentioned earlier, cubitus varus predisposes to tardy posterolateral rotatory instability. In addition, lateral skin incisions centered posterior to the midcoronal plane may be associated with

FIGURE 48-2

Posterolateral rotatory drawer test.

inadvertent ligamentous damage. The integrity of the medial and lateral collateral ligament complex should be tested in all cases. Examination maneuvers for instability may be masked by associated pathology (stiffness or an absent radial head, for example). In the author’s experience, pure varus stress does not allow reliable assessment of the competency of the lateral structures. Several other physical examination maneuvers have been described to specifically test the lateral collateral ligament complex:

Posterolateral Rotatory Drawer Test This test demonstrates posterolateral subluxation of the proximal radius and ulna with forced supination. It is best performed with the patient laying supine and the upper extremity overhead to lock the shoulder in internal rotation (Fig. 48-2). Forced supination of the forearm in approximately 45 degrees of flexion will induce abnormal excessive posterolateral subluxation of the elbow. The test is best demonstrated when forced supination is combined with valgus torque and axial compression. In some cases, subluxation may not be demonstrated but patients show apprehension with the maneuver.24

Posterolateral Rotatory Pivot-Shift Test This test demonstrates posterolateral subluxation and relocation of the elbow joint with elbow flexion and extension while applying a valgus and supination moment to the forearm. The patient is examined in the same position described earlier (Fig. 48-3). Application of valgus, axial compression, and hypersupination to the elbow in approximately 20 degrees of flexion induces posterolateral subluxation seen as prominence of the radial head and dimpling of the skin between the proximal radius and ulna. Progressive elbow flexion while maintaining the valgus, compression, and supination

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Valgus Axial compression Rotatory subluxation Supination Supination

Extension Valgus Axial compression

A

Subluxation

B

C

D FIGURE 48-3

Posterolateral pivot-shift test.

torque is accompanied by a sudden rotatory shift and clunk as the elbow is reduced with flexion.24 Again, the shift cannot be demonstrated in every patient, but most report apprehension. In patients with an absent radial head, the clunk is less pronounced.

thumb of the examiner to push over the radial head, giving support and preventing posterior subluxation.

IMAGING STUDIES Plain Radiographs

Chair and Push-Up Apprehension The chair sign involves having the patient stand up from a chair while pushing with the upper extremities and keeping the forearms in supination and the arms abducted to greater than the shoulder width.31 The test is considered positive if there is reluctance to extend the elbow fully as the patient raises his body using exclusively upper extremity force or a dislocation occurs. The push-up sign involves having the patient perform an active floor or wall push-up with the forearms supinated and the arms abducted to greater than the shoulder width. The test is considered positive if the patient shows reluctance to fully extend the elbow or a dislocation occurs. A similar test has been described with the patient pushing against the top of a table.2 Patients report apprehension when asked to perform a press-up with the elbow pointing laterally; pain and apprehension occurs as the elbow reaches approximately 40 degrees of flexion. Symptoms improve when the test is repeated using the

Most patients with isolated lateral collateral ligament complex insufficiency present with normal plain radiographs. Rarely, severe insufficiency may present with fixed posterolateral subluxation or dislocation. Recurrent episodes of elbow dislocation documented with radiographs indicate insufficiency of the lateral collateral ligament complex. Most of the time, radiographs are helpful to delineate associated pathology, including post-traumatic changes at the radial head or coronoid, or varus malalignment of the distal humerus.

Stress Radiographs and Fluoroscopy Radiographic or fluoroscopic imaging of the elbow subjected to stress is an invaluable diagnostic tool in patients with posterolateral rotatory instability, especially when the patient is under anesthesia. The status of the medial collateral ligament should be documented first by applying a valgus load to the extended elbow with the forearm in pronation28; more than 2 mm of medial joint line

Chapter 48 Lateral Collateral Ligament Insufficiency

opening on the anteroposterior view indicates medial collateral ligament insufficiency. The forearm is then placed in full supination and a varus load is applied to determine the amount of lateral joint line opening; again, more than a 2-mm of opening usually indicates lateral collateral ligament insufficiency. However, posterolateral rotatory instability is best demonstrated on the lateral views (Fig. 48-4); with forced supination and valgus, the radius and ulna are subluxed posteriorly so that the center of the radial head does no longer align with the center of the capitellum and there is asymmetry and widening of the ulnohumeral joint.

Magnetic Resonance Imaging The different components of the lateral collateral ligament complex may be visualized on magnetic resonance imaging.30 Although insufficiency of this ligament complex is diagnosed in most patients based on the history, physical examination and stress radiographs or fluoroscopy, magnetic resonance may confirm the presence of a torn or attenuated complex. Some studies have identified selective deficiency of the posterior fibers of the complex lateral ulnar collateral ligament.30 However, negative findings on magnetic resonance imaging does not exclude the diagnosis of posterolateral rotatory instability.11 Magnetic resonance imaging may be especially useful in patients with tennis elbow and coexistent ligamentous insufficiency.4

FIGURE 48-4

Lateral radiograph of a patient with posterolateral rotatory instability demonstrates posterolateral subluxation of the elbow; the radial head and neck are no longer aligned with the center of the capitellum and the ulnohumeral joint line is widened.

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Examination Under Anesthesia and Arthroscopy Positive findings on the posterolateral drawer and shift tests may be difficult to demonstrate in the office due to patient apprehension and guarding. The posterolateral rotatory drawer and posterolateral rotatory pivotshift tests are almost universally positive with the patient under anesthesia; fluoroscopic assessment of elbow stability may also be performed under anesthesia. Arthroscopy may be used when the diagnosis is still not clear after examination under anesthesia; arthroscopic findings may include excessive lateral joint line opening (sometimes allowing the arthroscope to be driven between the radial head and the capitellum), demonstration of posterolateral subluxation under direct visualization inside the joint, and various degrees of capsuloligamentous deficiency as visualized from the inside of the joint.

TREATMENT ACUTE INJURIES Injury to the lateral collateral ligament complex is found in most elbow fracture-dislocations that are treated surgically (Fig. 48-5A). In these circumstances, formal repair is recommended. The lateral collateral ligament complex is usually avulsed from the epicondyle or torn in its midsubstance.21 Our preferred technique for surgical repair of acute injuries involves the use of a heavy nonabsorbable suture through the substance of the lateral collateral ligament complex and into the humeral epicondyle. The suture follows the line of tension of the lateral ulnar collateral ligament. One #2 Fiberwire (Arthrex Inc., Naples, FL) or #5 Ethibond (Ethicon Johnson and Johnson, New Brunswick, NJ) suture is placed on the anterior half of the capsuloligamentous fibers in a running locking configuration18 from proximal to distal, and then from distal to proximal, turning at the ulnar supinator crest (see Fig. 48-5B). A second suture is placed in the same fashion on the posterior half of the capsuloligamentous fibers. These sutures may be passed through the overlying common extensor-supinator fibers to augment the repair. The isometric point of humeral attachment is then located at the geometric center of the capitellum and bone tunnels are created starting at that point and aiming anteriorly and posteriorly. The sutures are passed through the tunnels and tied on the proximal aspect of the lateral epicondyle. Postoperative management should follow the same general principles described for reconstruction in the chronic setting.

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A

B FIGURE 48-5

A, Elbow fracture-dislocations usually present with a complete avulsion of the lateral collateral ligament complex off the lateral humeral epicondyle. B, Acute injuries are repaired with two heavy nonabsorbable sutures through the substance of the lateral collateral ligament complex and the lateral humeral epicondyle. The sutures follow the lines of tension of the lateral ulnar collateral ligament. The sutures are partially placed through the common extensor-supinator group to augment the repair. They are then passed through bone tunnels at the isometric point into the humeral epicondyle.

CHRONIC INSUFFICIENCY Symptomatic insufficiency of the lateral collateral ligament complex is best addressed surgically by reconstruction using a tendon graft. Ligament repair or imbrication have been shown to provide inferior results in the chronic setting.19,33

Surgical Technique Placement of the skin incision depends on the need to address associated pathology. The deep exposure is through the Köcher interval. This interval is best identified distally and developed proximally. The raphe

between the anconeus and extensor carpi ulnaris can usually be felt distally; the fascia is then incised from distal to proximal, aiming to the center of the humeral epicondyle. The extensor carpi ulnaris and the anconeus are then elevated off the remaining lateral elbow capsule and lateral collateral ligament complex with sharp dissection. An effort should be made to preserve capsular flaps, because the tendon graft is best left extra-articular by suturing the capsular flaps underneath the graft at the end of the reconstruction. The tunnels for insertion of the tendon graft into the ulna and humerus are created next (Fig. 48-6A). One hole of the ulnar tunnel is centered over the tubercle of the supinator crest, which can easily be felt by palpation. The second hole is placed proximally and posteriorly leaving a bone bridge wide enough to avoid fracture (usually between 1 and 1.5 cm). A towel clip or angled curette may be used to clear the tunnel of bone debris. The site for humeral attachment of the tendon graft is selected so that the reconstruction will be isometric and maintain the same tension throughout the flexionextension arc.22 The first humeral hole is centered slightly proximal and posterior to the point of isometry. Usually, the point of isometry is located at the geometric center of the capitellar articular surface; this is confirmed with a suture placed through the ulnar tunnel and grasped with a point used to select the point on the surface of the humeral epicondyle, where the suture will maintain the same approximate tension with elbow flexion and extension (see Fig. 48-6A). Next, two proximal exit holes are created on the anterior and posterior aspect of the lateral humeral column, and the anterior and posterior humeral tunnels are created (see Fig. 48-6B). Several options exist for tendon graft selection. Palmaris longus autograft was used in the first reports of the technique.23 Tendon allografts seem to be associated with the same outcome and eliminate the morbidity and additional surgical time associated with autograft harvesting. We currently favor the use of plantaris or semitendinosus allograft depending on the size of the patient. Two #2 Fiberwire can be placed at the ends of the tendon graft in a running locking configuration to pull the tendon through the tunnels and assist in graft attachment. The graft may be looped through the tunnels in different ways, which seem to be equally effective as long as they allow adequate tensioning of the reconstruction.17 The tendon graft is passed first through the ulnar tunnel. Depending on the size of the graft as well as surgeon preferences, the two ends of the tendon graft can be then docked into the anterior and posterior humeral tunnels, tying the sutures over the proximal aspect of the humeral epicondyle (see Fig. 48-6C). Alternatively, one end of the tendon graft may be sutured to the opposite limb at the entrance into the humeral

Chapter 48 Lateral Collateral Ligament Insufficiency

675

A

Posterior

Proximal

C

Point of isometry

B

D

FIGURE 48-6 Reconstruction of the lateral collateral ligament complex using a tendon graft. A, The ulnar tunnel is started at the tubercle of the supinator crest and directed proximally and posteriorly. A suture placed through the ulnar tunnel may be used to confirm the isometricity of the point selected for humeral attachment of the tendon graft. B, Two humeral tunnels connect the point of isometry with the anterior and posterior aspects of the lateral humeral column. C, The graft is doubled on itself and passed through the ulnar tunnel. D, The tendon graft ends may be docked into the isometric humeral tunnels and the sutures tied over the humeral epicondyle.

tunnels creating a yoke-like structure. The longer limb is passed though the posterior tunnel, over the top, and into the anterior tunnel. Traction is then placed at the end of the yoke and the end of the longer limb to tension the graft (Fig. 48-7).

Whenever possible, any remaining capsule should be sutured to seal the joint before the graft reconstruction is completed so that the graft remains extra-articular. The graft should be tensioned with the joint in a reduced position, the forearm in full pronation, and the elbow

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in approximately 45 degrees of flexion. Tensioning may be increased by suturing the two limbs of the graft together in one or more points.

Treatment of Associated Pathology Associated pathology is addressed as needed. Commonly, lateral collateral ligament complex insufficiency is associated to radial head nonunion, malunion or

resection, as well as coronoid deficiency. Radial head replacement or coronoid reconstruction may be required to completely restore elbow stability and function.6,7,15,34 Patients with posterolateral rotatory instability and associated tennis elbow require débridement and repair of the area of tendinosis at the time of ligamentous reconstruction. Interestingly, some patients may present with a combination of stiffness and ligamentous insufficiency, and require ligamentous reconstruction and contracture release as a single or staged procedure. It is important to understand the need to consider reconstruction of the radial head to improve the outcome of treatment.

Underlying Deformity

A

As mentioned earlier, posterolateral rotatory instability may be secondary to chronic ligamentous attrition secondary to cubitus varus deformity. Depending on the severity of the deformity and the cosmetics concerns of the patient, a valgus-producing distal humerus osteotomy may need to be associated to the ligamentous reconstruction. Otherwise, the reconstruction may fail by chronic attrition of the tendon graft subjected to abnormal forces. Osteotomy should probably be considered in patients with more than 15 degrees of varus angulation.26 Experimental data in cadavers has shown increased strain on the lateral collateral ligament complex with more than 25 degrees of varus angulation and increased opening of the joint line space with more than 20 degrees of varus angulation.3

Postoperative Management

B

C FIGURE 48-7

A to C, Alternatively, the two limbs of the graft may be sutured together. One end of the graft may be passed through the humeral tunnels, and the reconstruction may be tensioned applying proximal traction to the yoke tendon and distal traction to the longer limb of the graft.

The ligamentous reconstruction needs to be protected for the first few weeks after surgery in order to prevent graft stretching and recurrent instability. Elbow extension and forearm supination increase tension on the graft; pronation5 and active muscle contraction protect the graft.9 Initially after surgery, the elbow is immobilized in 90 degrees of flexion and forearm pronation. Motion may be initiated in a few days, as long as a brace is used to neutralize the forces across the elbow, maintain the forearm in pronation, and block extension beyond 30 degrees. However, cast immobilization for three to six weeks should be considered when compliance with postoperative protection is questionable, and it is recommended by some surgeons for most patients, provided they do not show a tendency to develop stiffness. Neutralization using a dynamic external fixator during 3 to 6 weeks should be considered for those cases in which more protection is needed; external fixation has occasionally been used as the main treatment modality.20,32 Postoperative management may need to be changed to accommodate associated surgical procedures such as contracture release, in which early motion is more critical.

Chapter 48 Lateral Collateral Ligament Insufficiency

The patient should understand the detrimental role of gravitational stresses on the lateral collateral ligament complex. Most activities of daily living place the lateral side of the elbow facing upward; the weight of the forearm and any additional weight held by the hand will result in tensile stresses on the lateral elbow structures. During the first 3 months after surgery, the patient should learn how to protect the elbow against gravitational stresses. Active overhead flexion and extension exercises with the forearm in pronation protect the lateral collateral ligament reconstruction by avoiding gravitational stresses and increasing joint stability through active muscle contraction.9 Exercises to increase the strength of the extensor-supinator group also help stabilize the joint, and they may be initiated during the first few days after surgery. Unrestricted activities are usually allowed 6 months after surgery.

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and the concerns raised by the use of electrothermal shrinkage of the shoulder make arthroscopic surgery less attractive for the treatment of posterolateral rotatory instability. O’Driscoll et al.26 specifically reported on the outcome of surgical treatment for tardy posterolateral rotatory instability associated with cubitus varus. Twenty-one elbows were treated with osteotomy combined with reconstruction of the lateral collateral ligament complex (seven patients), ligament reconstruction alone (10 patients), or osteotomy alone (four patients) and followed for a mean of 3 years. Ulnar nerve transposition with or without triceps transposition was required in five patients. At most recent follow-up, three patients had persistent posterolateral rotatory instability, and two of these were rated as poor due to associated arthritis with severe pain.

Outcome Nestor et al.23 reported the initial experience at the Mayo Clinic with 11 consecutive cases followed for a mean of 3.5 years (range, 2 to 5.6 years). The lateral collateral ligament complex was imbricated in three patients and reconstructed with a tendon graft (seven patients) or triceps fascia (one patient). Stability was obtained in 10 patients, and seven were considered to have an excellent functional result. More recently, Sanchez-Sotelo et al.33 updated the Mayo Clinic experience with 44 cases followed for a mean of 6 years (2 to 15 years). Ligament repair or imbrication was performed in 12 cases and formal ligament reconstruction in 32. Surgery restored stability in all but five patients. Results were considered satisfactory in 73% of the cases, and 86% of the patients were subjectively satisfied with the procedure. Interestingly, the results were better in patients with traumatic etiology and subjective instability. Tendon reconstruction provided a better result than ligament repair. Other authors have reported similar outcomes in the treatment of this condition. Lee et al.19 reported on 10 patients with posterolateral rotatory instability treated with ligament repair (four cases) or reconstruction (six cases). Instability was corrected in all cases, and results were graded as satisfactory in eight patients. All patients with an excellent result had reconstruction with a tendon graft, a finding consistent with the above-mentioned study from the Mayo Clinic. When patients present with posterolateral rotatory instability and a resected radial head, reconstruction of the lateral collateral ligament complex combined with radial head replacement seems to provide satisfactory results.12,23,33 Arthroscopic capsular plication37 and arthroscopic electrothermal shrinkage36 have been reported as an alternative to tendon reconstruction, but the findings of better overall results with tendon reconstruction versus ligament repair19,33

SUMMARY Insufficiency of the lateral collateral ligament complex may be secondary to trauma, chronic attrition, or iatrogenic injury. The resulting posterolateral rotatory instability may present with recurrent dislocations, mechanical symptoms, or lateral-sided elbow pain. Instability may be demonstrated on physical examination in the office or with the patient under anesthesia. Stress radiographs or fluoroscopy may be used to document the instability. Most patients with chronic symptomatic insufficiency improve with surgical reconstruction using a tendon graft. Ligament repair without augmentation does not seem to be as effective in the chronic setting, but the procedure should be an integral part of the surgical treatment of acute elbow fracturedislocations. After surgery, the ligamentous repair or reconstruction should be protected from gravitational stresses and excessive tensile loads. Associated pathology affecting the radial head, coronoid, or the rest of the joint should be addressed as needed. Patients with tardy posterolateral rotatory instability secondary to cubitus varus often require association of a distal humerus osteotomy.

References 1. Abe, M., Ishizu, T., and Morikawa, J.: Posterolateral rotatory instability of the elbow after posttraumatic cubitus varus. J. Shoulder Elbow Surg. 6:405, 1997. 2. Arvind, C. H., and Hargreaves, D. G.: Table top relocation test—New clinical test for posterolateral rotatory instability of the elbow. J. Shoulder Elbow Surg. 15:500, 2006. 3. Beuerlein, M. J., Reid, J. T., Schemitsch, E. H., and McKee, M. D.: Effect of distal humeral varus deformity on strain

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4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

14.

15.

16.

17.

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in the lateral ulnar collateral ligament and ulnohumeral joint stability. J. Bone Joint Surg. Am. 86-A:2235, 2004. Bredella, M. A., Tirman, P. F., Fritz, R. C., Feller, J. F., Wischer, T. K., and Genant, H. K.: MR imaging findings of lateral ulnar collateral ligament abnormalities in patients with lateral epicondylitis. Am. J. Roentgenol. 173:1379, 1999. Cohen, M. S., and Hastings, H., 2nd: Rotatory instability of the elbow. The anatomy and role of the lateral stabilizers. J. Bone Joint Surg. Am. 79:225, 1997. Deutch, S. R., Jensen, S. L., Tyrdal, S., Olsen, B. S., and Sneppen, O.: Elbow joint stability following experimental osteoligamentous injury and reconstruction. J. Shoulder Elbow Surg. 12:466, 2003. Doornberg, J., Ring, D., and Jupiter, J. B.: Effective treatment of fracture-dislocations of the olecranon requires a stable trochlear notch. Clin. Orthop. Relat. Res. 42:292, 2004. Dunning, C. E., Zarzour, Z. D., Patterson, S. D., Johnson, J. A., and King, G. J.: Ligamentous stabilizers against posterolateral rotatory instability of the elbow. J. Bone Joint Surg. Am. 83-A:1823, 2001. Dunning, C. E., Zarzour, Z. D., Patterson, S. D., Johnson, J. A., and King, G. J.: Muscle forces and pronation stabilize the lateral ligament deficient elbow. Clin. Orthop. Relat. Res. 388:118, 2001. Eygendaal, D., Verdegaal, S. H., Obermann, W. R., van Vugt, A. B., Poll, R. G., and Rozing, P. M.: Posterolateral dislocation of the elbow joint. Relationship to medial instability. J. Bone Joint Surg Am. 82:555, 2000. Grafe, M. W., McAdams, T. R., Beaulieu, C. F., and Ladd, A. L.: Magnetic resonance imaging in diagnosis of chronic posterolateral rotatory instability of the elbow. Am. J. Orthop. 32:501; discussion 504, 2003. Hall, J. A., and McKee, M. D.: Posterolateral rotatory instability of the elbow following radial head resection. J. Bone Joint Surg. Am. 87:1571, 2005. Hannouche, D., and Begue, T.: Functional anatomy of the lateral collateral ligament complex of the elbow. Surg. Radiol. Anat. 21:187, 1999. Imatani, J., Ogura, T., Morito, Y., Hashizume, H., and Inoue, H.: Anatomic and histologic studies of lateral collateral ligament complex of the elbow joint. J. Shoulder Elbow Surg. 8:625, 1999. Jensen, S. L., Olsen, B. S., Tyrdal, S., Sojbjerg, J. O., and Sneppen, O.: Elbow joint laxity after experimental radial head excision and lateral collateral ligament rupture: efficacy of prosthetic replacement and ligament repair. J. Shoulder Elbow Surg. 14:78, 2005. Kalainov, D. M., and Cohen, M. S.: Posterolateral rotatory instability of the elbow in association with lateral epicondylitis. A report of three cases. J. Bone Joint Surg. Am. 87:1120, 2005. King, G. J., Dunning, C. E., Zarzour, Z. D., Patterson, S. D., and Johnson, J. A.: Single-strand reconstruction of the lateral ulnar collateral ligament restores varus and posterolateral rotatory stability of the elbow. J. Shoulder Elbow Surg. 11:60, 2002. Krackow, K. A., Thomas, S. C., and Jones, L. C.: Ligamenttendon fixation: analysis of a new stitch and comparison with standard techniques. Orthopedics 11:909, 1988.

19. Lee, B. P., and Teo, L. H.: Surgical reconstruction for posterolateral rotatory instability of the elbow. J. Shoulder Elbow Surg. 12:476, 2003. 20. McKee, M. D., Bowden, S. H., King, G. J., Patterson, S. D., Jupiter, J. B., Bamberger, H. B., and Paksima, N.: Management of recurrent, complex instability of the elbow with a hinged external fixator. J. Bone Joint Surg. Br. 80:1031, 1998. 21. McKee, M. D., Schemitsch, E. H., Sala, M. J., and O’Driscoll, S. W.: The pathoanatomy of lateral ligamentous disruption in complex elbow instability. J. Shoulder Elbow Surg. 12:391, 2003. 22. Morrey, B. F., and An, K. N.: Functional anatomy of the ligaments of the elbow. Clin. Orthop. Relat. Res. 201:84, 1985. 23. Nestor, B. J., O’Driscoll, S. W., and Morrey, B. F.: Ligamentous reconstruction for posterolateral rotatory instability of the elbow. J. Bone Joint Surg. Am. 74:1235, 1992. 24. O’Driscoll, S. W.: Classification and evaluation of recurrent instability of the elbow. Clin. Orthop. Relat. Res. 370:34, 2000. 25. O’Driscoll, S. W., Bell, D. F., and Morrey, B. F.: Posterolateral rotatory instability of the elbow. J. Bone Joint Surg. Am. 73:440, 1991. 26. O’Driscoll, S. W., Spinner, R. J., McKee, M. D., Kibler, W. B., Hastings, H. 2nd, Morrey, B. F., Kato, H., Takayama, S., Imatani, J., Toh, S., and Graham, H. K.: Tardy posterolateral rotatory instability of the elbow due to cubitus varus. J. Bone Joint Surg. Am. 83-A:1358, 2001. 27. Olsen, B. S., Sojbjerg, J. O., Dalstra, M., and Sneppen, O.: Kinematics of the lateral ligamentous constraints of the elbow joint. J. Shoulder Elbow Surg. 5:333, 1996. 28. Olsen, B. S., Sojbjerg, J. O., Nielsen, K. K., Vaesel, M. T., Dalstra, M., and Sneppen, O.: Posterolateral elbow joint instability: the basic kinematics. J. Shoulder Elbow Surg. 7:19, 1998. 29. Olsen, B. S., Vaesel, M. T., Sojbjerg, J. O., Helmig, P., and Sneppen, O.: Lateral collateral ligament of the elbow joint: anatomy and kinematics. J. Shoulder Elbow Surg. 5(2 Pt 1):103, 1996. 30. Potter, H. G., Weiland, A. J., Schatz, J. A., Paletta, G. A., and Hotchkiss, R. N.: Posterolateral rotatory instability of the elbow: usefulness of MR imaging in diagnosis. Radiology 204:185, 1997. 31. Regan, W., and Lapner, P. C.: Prospective evaluation of two diagnostic apprehension signs for posterolateral instability of the elbow. J. Shoulder Elbow Surg. 15:344, 2006. 32. Ring, D., Hannouche, D., and Jupiter, J. B.: Surgical treatment of persistent dislocation or subluxation of the ulnohumeral joint after fracture-dislocation of the elbow. J. Hand Surg. [Am.] 29:470, 2004. 33. Sanchez-Sotelo, J., Morrey, B. F., and O’Driscoll, S. W.: Ligamentous repair and reconstruction for posterolateral rotatory instability of the elbow. J. Bone Joint Surg. Br. 87:54, 2005. 34. Schneeberger, A. G., Sadowski, M. M., and Jacob, H. A.: Coronoid process and radial head as posterolateral rotatory stabilizers of the elbow. J. Bone Joint Surg. Am. 86A:975, 2004.

Chapter 48 Lateral Collateral Ligament Insufficiency

35. Seki, A., Olsen, B. S., Jensen, S. L., Eygendaal, D., and Sojbjerg, J. O.: Functional anatomy of the lateral collateral ligament complex of the elbow: configuration of Y and its role. J. Shoulder Elbow Surg. 11:53, 2002. 36. Spahn, G., Kirschbaum, S., Klinger, H. M., and Wittig, R.: Arthroscopic electrothermal shrinkage of chronic postero-

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lateral elbow instability: good or moderate outcome in 21 patients followed for an average of 2.5 years. Acta Orthop. 77:285, 2006. 37. Yadao, M. A., Savoie, F. H., 3rd, and Field, L. D.: Posterolateral rotatory instability of the elbow. Instr. Course Lect. 53:607, 2004.

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CHAPTER

49

Articular Injuries in the Athlete Joshua S. Dines and Neal S. ElAttrache

INTRODUCTION Activities such as throwing, lifting, and gymnastics cause large stresses across the elbow joint, which can result in a multitude of pathologies.16,21,90 In skeletally immature athletes, these stresses, combined with the developing bony anatomy and unique physeal biomechanics, lead to distinct injury patterns. In the past, macrotrauma, such as fractures and dislocations, were common in this age group; but recently, there has been a paradigm shift. As more children have begun participating in organized athletics at younger ages, and, as sport specialization with a year-round focus has become more common, repetitive microtrauma is causing a prevalence of overuse injuries. These include syndromes affecting the ligaments, capsule, muscles, and articular surfaces of the joint.2,17 Additionally, osseous manifestations may occur, such as stress fractures, osteophytes, loose bodies, osteochondral lesions and epiphyseal or apophyseal hypertrophy, and avulsion, or fragmentation.44 To better understand the injuries suffered in youth athletes, a thorough understanding of the bone and cartilage anatomy and knowledge of the forces associated with different overhead activities is required. Adult throwers may present with loose bodies and stress fractures as well. However, more commonly, patients in this age group present with symptoms consistent with chronic valgus insufficiency, such as valgus extension overload, lateral compression injuries, and medial tension injuries.4,64,117,118 Acute fractures and dislocations may occur in athletes of any age with a frequency comparable to that of the general population, but these injuries are less common than ligamentous instability.32,35

ANATOMY BONE AND CARTILAGE Elbow anatomy, including the ossification centers and pattern of ossification in the elbow, is discussed in detail

in Chapters 1 and 2. Elbow injury patterns in skeletally immature athletes are associated with stages of growth and development; the skeletal developmental stage defines the weakest link. Childhood terminates with the appearance of all secondary centers of ossification, adolescence terminates with the fusion of all secondary ossification centers, and young adulthood is signified by the completion of skeletal growth.90 Injuries during childhood are related to the developing epiphyses. Excessive forces may alter vascularization or ossification. During adolescence, peripheral fragment avulsions, subchondral osteonecrosis, or physeal injury or nonunion may occur. By the time patients reach young adulthood, stress reactions become more typical, as do ligamentous or capsular injuries.90 Accessory ossicles are of particular anatomic concern to physicians treating articular injuries. These may occur extra-articularly (medial epicondyle or tip of the olecranon in the triceps tendon) or intra-articularly (olecranon fossa, coronoid fossa, lateral epicondyle)45 (Figs. 49-1 and 49-2). Persistent apophyses at the medial or lateral epicondyle may be confused with loose bodies. Sesamoid fabella cubiti in the biceps tendon, patella cubiti in the triceps tendon, or accessory ossicles such as the supratrochlear posterius in the olecranon fossa or the os supratrochlear anterius in the coronoid fossa must also be distinguished from pathologic loose bodies.120

LIGAMENTS Ligamentous anatomy in the elbow region is discussed at length in Chapters 2, 47, and 48. A brief review of their functional anatomy as it relates to articular injuries is presented here. The ulnar collateral ligament (UCL) complex consists of three main portions: the anterior band, the posterior band, and the transverse ligament. The anterior band serves as the primary stabilizer to valgus stress, with the radiocapitellar joint providing secondary stability.27,80,97 Repetitive valgus stresses associated with activities such as throwing generate three, well-described forces on the elbow and its articular surfaces: (1) medial tension, (2) lateral compression, and (3) posterior shear (Fig. 49-3).30,107 Microtrauma to the anterior band of the UCL may cause progressive valgus laxity, which causes an alteration of the basic biomechanics of the joint. Shear forces on the olecranon develop, leading to synovitis, osteophytes, and loose bodies in the posterior compartment. Additionally, an increase in compressive forces is transmitted to the radiocapitellar joint. Fragmentation, loose bodies, or both may result. These changes in the elbow articulation may result in well-described clinical findings, such as increased valgus carrying angle, flexion contractures, medial epicondyle hypertrophy or fragmentation, and trochlear or olecranon fragmentation.42,54,90

Chapter 49 Articular Injuries in the Athlete

DIAGNOSIS HISTORY A detailed history helps narrow the extensive differential diagnosis of elbow pain in athletes (Table 49-1). We find it most helpful to classify injuries by mechanism, with

FIGURE 49-1

Accessory ossicles, medial and lateral epicondyle apiphysis about the elbow joint (anteroposterior view). (Redrawn from Bennett, J. B., and Mehlhoff, T. L.: Articular injuries in the athlete. In Morrey, B. F. [ed]: The Elbow and Its Disorders, 3rd ed. Philadelphia, Saunders, 2000, p. 563.)

further subclassification based on anatomic compartment involved (medial, lateral, posterior) and onset of pain (acute, chronic). Pertinent information includes age, sport played, level of competition, position, characterization of pain (location, duration, onset), mechanism of injury, and past medical history. As mentioned earlier, skeletal age can provide the physician with useful information regarding the likely diagnosis. Different sports predispose athletes to different injuries. Gymnasts must lock out their elbows to support their body weight, causing posterior elbow injuries.93 Baseball players, especially pitchers, put large magnitude valgus stresses on the elbow, which can result in myriad

FIGURE 49-2

Lateral view of accessory ossicles with sesamoid fabella cubiti in the biceps tendon and patella cubiti in the triceps tendon. (Redrawn from Bennett, J. B., and Mehlhoff, T. L.: Articular injuries in the athlete. In Morrey, B. F. [ed]: The Elbow and Its Disorders, 3rd ed. Philadelphia, Saunders, 2000, p. 563.)

C

B A

FIGURE 49-3

681

The valgus torque created during the throwing motion results in three forces: (A) medial tension, (B) lateral compression, and (C) posterior shear.

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TABLE 49-1

Differential Diagnosis of Elbow Pain in Athletes

Medial

Lateral

Posterior

Anterior

Avulsion fracture, medial epicondyle

OCD capitellum

Olecranon fracture

Biceps strain

Flexor pronator strain

Avulsion fracture, lateral epicondyle

Olecranon apophysitis

Distal physeal humerus fracture

Acute

Ulnar collateral ligament insufficiency Fracture capitellum

Triceps strain

Ulnar neuritis

Proximal radius fracture

Olecranon bursitis

Ulnar neuropathy

Lateral epicondylitis

Olecranon traction apophysitis Loose bodies

Medial epicondylitis

Radial head hypertrophy

Loose bodies

Adhesions

Valgus extension overload

OCD capitellum, radial head

Synovitis

Synovitis

Ulnar collateral instability

Plica

Posteromedial spurs

Capsular sprain

Chronic

OCD, osteochondritis dissecans.

injuries. For pitchers in particular, effectiveness over their previous outings, numbers of pitches thrown, types of pitches thrown, phase of throwing associated with the pain, and parent’s or coach’s observations of any changes in mechanics are pertinent. A detailed knowledge of the phases of throwing will help the treating physician narrow the differential diagnosis of elbow pain in throwers. This is discussed at length in Chapter 47. It is important to note that number of pitches thrown and not innings pitched is what places throwers at risk for injury.93

PHYSICAL EXAMINATION Bilateral upper extremities should be examined, beginning with inspection to note muscle atrophy or hypertrophy, bony deformities, elbow asymmetry, or flexion contractures.20 Range of motion of both shoulders and elbows is tested, and carrying angles of the elbows should be compared (Fig. 49-4). Palpation should include the medial and lateral epicondyles, the medial and lateral collateral ligaments, the sublime tubercle, the radial head, and the olecranon process. Careful examination of the ulnar nerve may reveal subluxation, tenderness, or both. Lateral ligaments are tested with varus stress and internal rotation of the arm, whereas medial ligament stability is tested with a valgus stress applied to an externally rotated arm. Special maneuvers used to help diagnose elbow medial collateral ligament (MCL) insuffiency include the moving valgus stress test and the milking test, both of which are detailed in Chapters 4 and 46. Pain with forced hyperextension may suggest hyperextension valgus overload syndrome, whereas mechanical locking or catching may indicate loose bodies or osteochondral defects. In throwing athletes, it may help to

FIGURE 49-4

Increased valgus carrying angle and hypertrophy of left arm in a baseball pitcher. (From Bennett, J. B., and Mehlhoff, T. L.: Articular injuries in the athlete. In Morrey, B. F. [ed]: The Elbow and Its Disorders, 3rd ed. Philadelphia, Saunders, 2000, p. 564.)

have them simulate a pitch to reproduce their symptoms. The examination requires a complete neurologic and vascular assessment, with special attention given to the ulnar nerve.

IMAGING Standard anteroposterior (AP), lateral, and reverse axial views of both the affected and contralateral elbow are an essential part of the workup. Stress views may help

Chapter 49 Articular Injuries in the Athlete

detect subtle ligamentous instability; however, negative stress films do not rule out ligamentous pathology. Magnetic resonance imaging (MRI) can be used in these cases to further evaluate the ligament in question. Additionally, MRI is helpful for diagnosing osteochondritis dissecans (OCD) lesions, stress fractures, and other soft tissue pathology. Computed tomographic (CT) scans are also useful to evaluate loose bodies, bone spurs, and articular cartilage lesions.

ARTHROSCOPY Arthroscopy of the elbow can facilitate or confirm diagnosis of both articular and ligamentous injuries (Fig. 49-5). For example, OCD lesions can be inspected and probed at arthroscopy, which can help dictate the appopriate treatment; the arthroscopic valgus stress test can be used to confirm disruption to the medial UCL.8,12 Chapters 38, 39, and 41 detail the expanding role of arthroscopy of the elbow in the treatment cartilage and synovial lesions in the athlete, such as lateral synovial plicas, loose bodies, OCD lesions, and posterior compartment osteophytes.24,31,51

MEDIAL TENSION INJURIES IN ADOLESCENCE

medial tensile forces and lateral compressive stresses in young, developing throwers.17 In these athletes, the repetitive tensile stress on the medial epicondyle caused by valgus stress and the pull of the flexor-pronator muscle mass and the medial UCL leads to microtrauma at the epiphysis.2,3,36,37,88-90 The resulting spectrum of injury at the medial epicondyle includes subtle widening, separation, fragmentation, and hypertrophy (Fig. 49-6). A recent study revealed that up to 63% of little leaguers had soreness at the medial epicondyle, and of these throwers, 70% exhibited separation and 40% had evidence of fragmentation.48 Clinically, patients may present with progressively worsening, medial-sided elbow pain that is exacerbated with throwing. A triad of symptoms has been described, which includes pain in the late cocking and early acceleration phases, loss of velocity and distance, and decreased throwing effectiveness. On examination, there is point tenderness at the medial epicondyle and a flexion contracture. Patients have pain with valgus stress, but no frank instability. Radiographic findings range from subtle widening to separation or fragmentation. Medial epicondylar stress lesions are benign entities that respond well to cessation from throwing and, if flexion contractures are present, physical therapy for stretching. A return to throwing is predicated on complete resolution of symptoms and the absence of tenderness on

MEDIAL EPICONDYLAR STRESS LESIONS (LITTLE LEAGUER’S ELBOW) The term Little League elbow was originally used by Bennett to describe the spectrum of bony changes caused by

FIGURE 49-5

Capitellar osteochondritis dissecans lesion as visualized during arthroscopy.

683

FIGURE 49-6

Radiograph of medial epicondylar stress lesion demonstrating fragmentation and separation.

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Part VI Sports and Overuse Injuries to the Elbow

examination. A gradual return using a strict throwing program emphasizing proper mechanics is critical. It is important to recognize that, at times, the term Little Leaguer’s elbow is used as a “wastebasket diagnosis” to refer to a constellation of injuries including medial epicondylar avulsion fractures, medial epicondyle apophysitis, OCD, Panner’s disease, hypertrophy of the ulna, olecranon apophyseal injury, and medial UCL injury.3,41,45,71,99,102 In this context, the term is nonspecific and not helpful for tailoring treatment. When evaluating young throwers with medial elbow pain, it is important to make a specific diagnosis.

MEDIAL EPICONDYLE AVULSION FRACTURES When a significant, acute, valgus stress is applied through a violent muscle contracture such as during the throwing motion or arm wrestling, an avulsion fracture of the medial epicondyle can result.72,84 Separation classically occurs through the epiphyseal growth plate, because this is the weakest area of the epicondyle. Clinically, this results in tenderness over the epicondyle and, often, a flexion contracture that may be greater than 15 degrees. Assessment of ulnar nerve function is critical, and physicians must maintain a high index of suspicion for a spontaneously reduced elbow dislocation. Radiographs confirm the diagnosis. A view that we have found particularly useful to evaluate the medial epicondylar apophysis in children is the posterior impingement view as described by John Conway (John Conway Personal communication, 2002)34 (Fig. 49-7A and B). It is an axial view with the elbow maximally flexed and the humerus externally rotated 40 degrees. The x-ray beam is directed perpendicular to the humeral axis. Additionally, this

A

view is useful to visualize the posterior medial olecranon margin in cases of valgus extension overload. Woods and colleagues123 have classified the lesions based on patient age and fragment size. Type I injuries occur in younger patients. These are large fragments typically involving the entire apophpysis with the MCL, and the fragments often displace and rotate. Type II fractures occur in adolescents. These fragments are usually smaller, representing an avulsion of the flexor origin. The anterior oblique ligament is usually intact. Treatment depends on the amount of fragment displacement, although the definition of acceptable displacement is controversial. Less than 3 to 5 mm of displacement is typically well tolerated and responds well to splinting for 2 to 3 weeks, followed by conversion to a hinged elbow orthosis.59 Operative indications include displacement greater than 3 to 5 mm, fragment rotation, valgus instability, ulnar nerve dysfunction, and fragment incarceration (Fig. 49-8). An increasing number of authors are advocating more aggressive treatment of these injuries in competitive, skeletally immature overhead athletes using more then 2 mm of displacement as an indication to operate.53 This is based on studies showing that subtle instability after non-operative management causes degenerative radiocapitellar changes.53 Schwab and associates105 described a radiograph using gravity to impart a valgus stress to help diagnose instability. With the patient lying supine, the shoulder is brought into maximum external rotation (Fig. 49-9). At this point, the sagittal plane of the elbow is parallel to the floor, and the weight of the forearm is resisted solely by the flexor forearm mass and anterior oblique ligament. Instability of the elbow, secondary to Gravity Stress Test

B FIGURE 49-7

Radiographs with a smooth pin placed along the posterior medial olecranon margin. Fluoroscopy was used to line the axis of the pin with the beam. (A) Cubital tunnel view with elbow flexed 140° without rotation; (B) posterior impingement view, as described by John Conway, MD, which can be used to show displacement of the medial epicondyle. (Photos courtesy of John Conway, MD.)

Chapter 49 Articular Injuries in the Athlete

A

685

B

FIGURE 49-8

A, Medial epicondyle fracture. B, Medial epicondyle fracture treated with internal

fixation. X-ray plate

X-ray beam GRAVITY TEST

FIGURE 49-9

Gravity stress view. (Redrawn from Woods, G. W., Tullos, H. S., and King, J. W.: Elbow instability and medial epicondyle fractures. Am. J Sports Med. 5:23, 1977.)

loss of MCL continuity, is indicated by movement of the fragment distally. A positive gravity stress test is an indication for surgical treatment.

MEDIAL LIGAMENT INSTABILITY Injuries of the medial UCL are relatively uncommon in younger throwing athletes; however, there has been an alarming trend of increasing numbers of high school– aged athletes being treated for UCL insufficiency.93 The increasing incidence of these throwers requiring UCL reconstruction may be directly related to overuse of the throwing arm and throwing breaking balls at younger

FIGURE 49-10 MR image consistent with medial ulnar collateral ligament tear.

ages.93 Clinically, these patients usually have subtle findings of instability on examination. The previously described gravity stress test is sometimes useful in diagnosing UCL injury, although MRI is usually a better imaging modality (Fig. 49-10).

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Treatment options include direct surgical repair or ligament reconstruction.54,57According to Jobe, direct repair is indicated if stability can be restored; otherwise reconstruction with a tendon graft should be performed. Petty et al.93 found that the results of UCL reconstruction in high school athletes are less successful than the results in older age groups. For a more complete discussion of UCL injury diagnosis and treatment, please refer to Chapter 47.

LATERAL COMPRESSION INJURIES IN ADOLESCENCE OSTEOCHONDRITIS DISSECANS OF THE CAPITELLUM OCD of the capitellum is a disease of unclear etiology that typically affects patients aged 10 to 15 years.71,124 The most commonly accepted theory is that the lesion is secondary to vascular insufficiency.88,124 Several authors have noted the association between throwing and OCD.1,2,6,13 Tullos and King concluded that compressive forces between the capitellum and radial head occur during the throwing motion.118 Schenk and Dalinka104 showed that a biomechanical mismatch between the radial head and capitellum exist. Together, these studies support the theory that compressive forces produce focal arterial injury and subsequent bone death (or OCD lesions). The focal lesions usually occur in the dominant arm and cause pain and a flexion contracture of 15 degrees or more. A joint effusion is often present. Initial radiographs may be normal. As the disease progesses, irregularities of the capitellum or even a defect in the bone can develop. Loose bodies may be present. Takahara described the use of a 45-degree flexion AP elbow radiograph to reveal lesions that may be underestimated by conventional radiographs110,112 (Fig. 49-11A and B). Arthrograms, ultrasound, and MRI are useful imaging modalities.50,112 The sensitivity and specificity of MRI make it particularly valuable in diagnosing capitellar lesions19 (Fig. 49-12). Decreased signal on T1-weighted images and increased signal on T2-weighted and fast spin–echo sequences are consistent with marrow edema, and are often present before similar changes are seen on plain film.66,104 MR arthrograms are helpful to demonstrate unstable lesions that are not loose bodies.104 It is important to note that there is a normal anatomic sulcus between the lateral condyle and capitellum that may be mistaken for an osteochondral fragment.66 This sulcus is located posteriorly, whereas OCD lesions are usually located more anteriorly. It is imperative to differentiate OCD of the capitellum from osteochondrosis of the capitellum, or Panner’s disease. Panner’s disease is characterized by disordered

ossification of the capitellum with degeneration and necrosis, followed by regeneration and ossification.89 The proposed mechanism involves an alteration in the vascularity of the developing capitellum.101 Age, radiographic findings, the presence of loose bodies, and deformity of the capitellum help to distinguish between the two entities (Table 49-2). Panner’s disease most commonly affects children between the ages of 5 to 10 years. Similar to patients with OCD of the capitellum, patients may complain of dull, aching lateral-sided elbow pain that is aggravated by activity. Unlike OCD, however, flexion contractures are not common. Radiographically, the disease is characterized by fragmentation and deformity of the ossific nucleus of the capitellum66 (Fig. 49-13). Unlike OCD, Panner’s disease is a self-limited process that rarely results in loose body formation. It responds well to conservative treatment, and the capitellum usually heals without late deformity or collapse. Young athletes with Panner’s disease should be restricted from throwing and gymnastics to prevent axial loading and valgus stress to the elbow.54 The natural history of OCD is much less predictable. There are no good criteria to predict healing; and late sequelae, such as loose bodies and residual deformity, do occur. Takahara and colleagues111 treated 24 patients with OCD nonoperatively and found that the lesions had a poor tendency to heal, and that if there was any fragment instability, failure was likely. Because of the inherently poor potential for unstable lesions to heal, they are usually treated surgically. Treatment is guided by lesion classification. The most important factor in staging OCD lesions is determining whether or not the fragment has separated. Intact, stable capitellar lesions (Type Ia) respond well to conservative treatment, which includes rest, antiinflammatory medications, early splinting for acute symptoms, and a gradual return to activity when asymptomatic.92 Surgery is indicated for intact, stable lesions that fail conservative measures and for all unstable lesions (Type Ib, II, III).15,49,92,113 Treatment options include removal of loose bodies, microfracture, abrasion chondroplasty, internal fixation of larger lesions, osteochondral autograft transfer, and drilling of lesions.67,70,75,113-115 Most of these techniques are now performed arthroscopically. Baumgarten et al.15 developed an arthroscopic classification system that helps guide which treatment option would be best. Grade 1 lesions have smooth but soft ballotable cartilage, and they respond well to drilling.56 Grade 2 lesions exhibit fibrillation or fissuring of cartilage. In these cases, cartilage should be débrided back to a stable rim, then drilling, microfracture or abrasion chondroplasty should be performed.5,15,18,22,25,69,75 Grade 3 lesions have exposed bone with a fixed fragment, and grade 4 lesions are loose but nondisplaced fragments. These two stages have traditionally been treated with

Chapter 49 Articular Injuries in the Athlete

C

B

A

D

687

E

FIGURE 49-11 A, Anteroposterior radiograph with the elbow in extension. The capitellum appears normal. B, Anteroposterior radiograph with the elbow in 45 degrees of flexion. There is slight flattening and sclerosis of the lateral surface of the capitellum (arrowhead). C, Anteroposterior radiograph 4 months later with the elbow in 45 degrees of flexion. Arrowheads indicate radiolucent bone. D, Anteroposterior radiograph 11 months after initial radiograph in 45 degrees of flexion. Arrow illustrates radiolucent bone fragment. E, Normal appearing capitellum 3.5 years after the initial examination. (Adapted, with permission, from Takahara, M., Shundo, M., Kondo, M., Suzuki, K., Nambu, T., and Ogino, T.: Early detection of osteochondritis dissecans of the capitellum in young baseball players. Report of three cases. J. Bone Joint Surg. Am. 80:892, 1998.)

removal of the fragment, followed by drilling, microfracture, or chondroplasty. Grade 5 lesions are loose bodies, and along with removal of the fragment, they are treated in a similar manner to grade 3 or 4 lesions. In the short-term, the above-mentioned options seem to improve patients’ symptoms.15,18 However, long-term results indicate impairment of elbow function.14,78,111 In one series with an average follow-up of 23 years, 50% of patients had restricted motion, and 61% had degenerative changes on radiographs.14 Mixed results have

also been reported regarding the ability of patients to return to competitive athletics.24,75,115 Newer treatment options aim to improve outcomes. Kiyoshige et al.65 described the use of a lateral closing wedge osteotomy of the capitellum to treat OCD in seven adolescent baseball players. Preliminary results were promising, with 86% having complete relief of symptoms and return to full activity. Osteochondral autograft transplantation and mosaicplasty for grade 3 and 4 lesions have shown promise; however, longer term follow-up is necessary

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FIGURE 49-12 Magnetic resonance imaging scan consistent with osteochondritis dissecans of the capitellum. Arrows, osteochondritis dissecans lesion; arrowheads, joint effusion.

TABLE 49-2

Comparison of OCD of the Capitellum and Panner’s Disease Osteochondritis Dissecans

Panner’s Disease

Age

Teens

~10 years

Onset

Insidious

Acute

Radiographic finding

Island of subchondral bone demarcated by a rarefied zone

Fragmentation of entire capitellar ossific nucleus

Loose bodies

Present

Absent

Residual deformity of capitellum

Present

Minimal

From Bennett, J. B., and Mehlhoff, T. L.: Articular injuries in the athlete. In Morrey, B. F. (ed.): The Elbow and Its Disorders, 3rd ed. Philadelphia, Saunders, 2000, p. 569.

to better elucidate their efficacy in the treatment of OCD of the capitellum (Fig. 49-14).5,55,125 Chappell and ElAttrache28 recently presented their results treating capitellar OCD lesions. Five patients with lesions involving the lateral column of the capitellum with engagement of the radial head were treated with arthroscopic autologous osteochondral allografts. Three out of the five patients had excellent outcomes, and all five returned to their previous level of sports participation. Fifteen patients with OCD lesions were treated with microfracture. Eleven were available for follow-up, of which all returned to previous levels of sports competition. Based on the above-mentioned findings, it may be that the location of the OCD lesion may be more important than lesion size. Lateral OCD lesions compromise lateral column support, which bear a large portion of the valgus forces generated by athletes during overhand motions. Chapter 39 provides an in-depth discussion of the above-mentioned techniques.

POSTERIOR EXTENSION AND SHEAR INJURIES IN ADOLESCENCE OSTEOCHONDROSIS OF THE OLECRANON Olecranon apophyseal injuries are rare, but they can affect young athletes, including divers, gymnasts, hockey players, and throwing athletes.33,73,106 The etiology is unknown, although several theories have been advanced. Some authors implicate repetitive microtrauma to the olecranon apophysis during the acceleration phase of throwing.91,120 Gore et al.44 maintained that a traction apophysitis, similar to what occurs at the medial epicondyle, is the causative mechanism. Others propose a connection to Osgood-Schlatter disease, with rapid growth and musculotendinous imbalance resulting in an apophysitis.53,76 Clinically, patients complain of activity-related pain with swelling and tenderness around the olecranon

Chapter 49 Articular Injuries in the Athlete

689

process. On plain films, fragmentation and irregularity of the apophysis are visible. Widening may occur.26 Opposite elbow films must be obtained, and the contralateral apophysis must be closed to make the diagnosis. Activity restriction or brief immobilization with a gradual return to sports usually provides a successful outcome.82 Indications for operative treatment include the persistence of symptoms despite more than 3 to 6 months of conservative treatment or radiographically documented failure of apophyseal closure despite nonsurgical management.26 In these cases, open reduction and internal fixation using a single cancellous screw, with or without a tension band, can provide excellent results with minimal complications.26,98

OLECRANON STRESS FRACTURES

FIGURE 49-13 Radiograph exhibiting changes consistent with Panner’s disease.

Donor plugs

FIGURE 49-14 Arthroscopic mosaicplasty for osteochondritis dissecans lesion of the capitellum.

Stress fractures of the olecranon have been reported in throwing athletes, gymnasts, and weight lifters.4,13,74,77,87,93,109,121 These injuries result from the persistent abutment of the olecranon into its fossa, traction from the triceps during the deceleration phase of throwing, and from valgus forces causing impaction of the medial olecranon onto the medial wall of the olecranon fossa.4,64 Different predominating forces cause different fracture configurations: Triceps traction and extension forces lead to transverse fractures, whereas valgus and extension forces create oblique fractures.109 In fact, oblique stress fractures have been shown to occur in combination with partial medial UCL injuries.109 On examination, tenderness occurs over the posterior and posteromedial olecranon. Patients often lack extension. Because valgus stress testing may elicit pain in both the olecranon and the medial UCL, Suzuki recommends performing the milking maneuver at 90 degrees of flexion to prevent the olecranon from engaging in the olecranon fossa. This helps differentiate valgus extension overload syndrome from medial UCL injury.109 Radiographs may demonstrate a fracture line or sclerosis (Fig. 49-15). MRI and bone scan have also been used to make or confirm the diagnosis of stress fracture. Initial treatment involves rest from the inciting activity. The early use of a posterior splint may help with pain relief. Stress fractures often heal slower than regular fractures, so restriction from sports for extended periods of time is necessary in some patients. Before returning to sport, radiographs should demonstrate fracture healing; and patients must be asymptomatic. Those in whom nonoperative treatment fails and athletes who cannot tolerate prolonged restriction from play require surgery. Tension band constructs and compression screws have both been used successfully.43,68,95,121 Orava and Hulkko87 recommended screw compression for oblique fractures and tension band constructs for transverse

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Part VI Sports and Overuse Injuries to the Elbow

A

Rt

Posterior

Lt

B

D

C

E

FIGURE 49-15 Olecranon stress fracture in a major league baseball player. (A) Lateral radiograph; (B) bone scan showing increased activity in the region of the olecranon; (C) magnetic resonance imaging scan consistent with a stress fracture of the olecranon; (D) lateral radiograph 10 days postoperatively. (E) Lateral radiograph 3 months postoperatively. The patient returned to his previous level of play 11 months after the surgery.

Chapter 49 Articular Injuries in the Athlete

fracture lines. Arthroscopy can be used with screw fixation to diagnose associated lesions and to view the intra-articular part of the stress fracture.26 Charlton and Chandler29 treated skeletally immature athletes who had persistence of their olecranon physis with operative stabilization and autogenous bone graft. All patients returned to their prior level of play.

ACUTE INSTABILITY IN ADULTS

691

removal of the proximal ulna on elbow stability in the context of comminuted olecranon fractures. They showed that constraint of the ulnohumeral joint was linearly proportional to the area of remaining articulation. More recently, biomechanical studies showed that as the amount of posteromedial olecranon resected increased, more valgus stress was generated.61 This led to increased strain in the medial UCL. These studies imply that all attempts should be made to restore the normal anatomy of the olecranon in throwing athletes.

ELBOW DISLOCATIONS WITH ASSOCIATED FRACTURES The incidence of elbow dislocations is second only to glenohumeral dislocations, with about 10% resulting from athletic activities.23 Successful management of simple elbow dislocations typically consists of minimal immobilization, followed by early, aggressive range of motion.60 However, when associated injuries occur with dislocations, recommended treatment often differs. Fractures associated with elbow dislocations include radial head fractures (5% to 10% frequency), epicondyle avulsions (12%), and coronoid or olecranon fractures (10%).23,52,60,108,119 The radial head serves as an important secondary stabilizer to valgus stress. This is particularly true after elbow dislocations, when the medial UCL is compromised. In nonathletes, reconstruction of the radial head may be sufficient to restore stability and to allow the ligament to heal. In athletes, however, the increased valgus stress that these patients apply to their elbow necessitates repair of the ligament as well.23,79 Arthroscopy can play a role in both the evaluation and management of nondisplaced fractures of the radial head in athletes.31,58 It allows for recognition of associated soft tissue injuries including medial UCL injury, lateral collateral ligament insufficiency, and annular ligament disruption. Osteochondral defects and loose bodies can also be identified and treated. Short-term results show that a satisfactory outcome can be obtained treating minimally displaced fractures with arthroscopic reduction and fixation.100 Contraindications to the use of arthroscopy in the setting of acute trauma include severe soft tissue swelling, previous history of an ulnar nerve transposition, and largely displaced intra-articular fractures.

OLECRANON FRACTURES Olecranon fractures have been classified and discussed in Chapter 25. When discussing the appropriate management of these fractures in athletes, it is important to understand the effect of olecranon resection on elbow stability.7,61,62 An et al.7 looked at the effect of partial

CHRONIC VALGUS INSUFFICIENCY IN ADULTS THROWING INJURIES Throwing places unique stresses on the elbow that can be detrimental to the integrity of the joint.36,40,47 The injury patterns that result in this group of athletes are fairly predictable; however, the radiographic findings and symptoms do worsen with age, so prompt diagnosis and treatment is beneficial (Table 49-3). Slocum classified the typical throwing injuries of the elbow into three groups: (1) medial tension injuries, (2) lateral compression injuries, and (3) extensor overload injuries.107 Medial tension injuries include UCL tears, flexor-pronator tendonitis, and ulnar nerve injuries. These medial-sided injuries are discussed in detail in Chapter 47. Laterally, compressive forces between the radial head and capitellum result in chondromalacia and loose body formation. In the posterior compartment, shear forces result in valgus extension overload.122 In many throwers, valgus instability, as evidenced by UCL insufficiency, and valgus extension overload can coincide. It is critical to detect the presence of both, because a failure to do so results in a failure of treatment.

Effect of Age on Symptoms and Radiographic Findings in Throwing Athletes

TABLE 49-3 Age (Years)

Pitchers

Pathology

Percent

26-33

17

14

83

25-27

21

13

62

18-21

12

5

42

Total

50

32

From Bennett, J. B., and Mehlhoff, T. L.: Articular injuries in the athlete. In Morrey, B. F. (ed.): The Elbow and Its Disorders, 3rd ed. Philadelphia, Saunders, 2000, p. 572.

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LOOSE BODIES Compressive, shear forces may result in anterior compartment loose bodies, whereas extension overload can cause loose bodies in the posterior compartment. Intermittent locking and catching in the elbow is suggestive of a loose body. Typically, a locking episode is complicated by swelling and decreased range of motion, followed by a gradual improvement in both symptoms. Diagnosis is often confirmed through plain radiographs; however, noncalcified osteochondral fragments are not evident on these films. CT and MRI scans may be helpful, but both of these modalities also have the potential for false-negative results. The use of arthroscopy to treat elbow pathology is discussed in detail in Chapters 37 to 39; however, it is worth noting that arthroscopy is a particularly useful diagnostic and treatment tool for loose bodies in the elbow.8,86

VALGUS EXTENSION OVERLOAD Stability in the thrower’s elbow is provided by a combination of ligamentous, articular, and muscular restraints. Initially, valgus torque is primarily resisted by the medial UCL, with secondary stability provided by the radiocapitellar joint and by the olecranon. As the elbow nears full extension, the articular constraints play a more prominent role in ensuring stability.81 With excessive valgus force or increased UCL laxity, olecranon impingement occurs.64 In addition to valgus forces, during the throwing motion, the flexor muscles help resist the large extension force that is generated during the acceleration phase.38,39 If the deceleration force is not well controlled by the muscles, the olecranon traumatically abuts the posterior compartment. The combination of valgus and extension forces causing posterior and posteromedial olecranon osteophytes has been termed valgus extension overload.9,107,122 In cases of isolated valgus extension overload, patients may report pain in the medial aspect of the elbow during both the acceleration and deceleration phases of throwing. Posterior impingement can cause a loss of extension, and osteophytes that fracture may result in loose bodies. Radiographic evaluation, which should include posterior, lateral, and axial views of the elbow, may identify posteromedial osteophytes or loose bodies (Fig. 49-16). In patients with an appropriate history and radiographic findings, diagnosis is confirmed by a positive valgus extension overload test.26 Pain elicited in the posterior compartment with manual pronation, valgus, and extension force applied is consistent with a positive test. A trial of nonoperative treatment consisting of rest, correction of throwing mechanics, and physical therapy emphasizing flexor-pronator mass strengthening may

FIGURE 49-16 Posteromedial osteophyte consistent with valgus extension overload in the elbow of a 22-year-old baseball pitcher.

be warranted; however, Andrews and Timmerman9 noted that posteromedial olecranon impingement is the most common diagnosis requiring surgery in baseball players. Previously, surgical treatment involved osteophyte excision and loose body removal through an arthrotomy.122 This provided successful results; however, given the advantages of decreased morbidity and increased visualization of the entire joint, arthroscopy is becoming the preferred treatment option. Studies have reported that arthroscopic treatment of valgus extension overload can effectively return professional athletes to their previous level of competition.9,51,96 In the study conducted by Reddy et al., athletes with loose bodies or posterior impingement tended to have improved outcomes compared with those with degenerative joint disease.4,96 Andrews and Timmerman believed that arthroscopic osteophyte excision was technically superior to open excision; however, they emphasized that this is a palliative procedure in athletes with a high level of recurrence if they return to play.26

SYNOVIAL LESIONS Synovial plicae are believed to be normal anatomic structures that represent remnants of embryonic septae formed during development.63,85 Repetitive microtrauma can cause thickening and inflammation of these plicae, which can cause pain and mechanical symptoms in the elbow joint. Typically these symptoms occur in throwing athletes and golfers, and although they are rare, hypertrophic synovial plica may be an underdiagnosed condition.10,63 In the previous edition of this text, Bennett

Chapter 49 Articular Injuries in the Athlete

and Melhoff postulated that two types of lateral synovial plicae exist: a plica in the lateral gutter that pops over the olecranon process; and a plica near the radiocapitellar joint that folds over the margins of the capitellum and radial head. The lateral gutter plica is particularly symptomatic in extension, whereas the radial capitellar plica causes mechanical symptoms with forearm rotation when the elbow is flexed. MRI arthrography is very helpful to make the diagnosis. Awaya et al.11 determined that synovial folds of more than 3 mm in thickness were abnormal and correlated with clinical symptoms. Nonoperative management includes antiinflammatory medication, physical therapy, and activity modification. Corticosteroid injection may help to decrease the synovial reaction. For those in whom nonoperative measures have failed, arthroscopy is highly successful at returning athletes to their previous level of play.10,31,63,102

REHABILITATION A structured rehabilitation program is critical to the success of any treatment modality. Collaboration among the surgeon, therapist, patient, and trainer will provide the best outcomes. In many cases, the use of splints, braces, orthoses, and strengthening modalities is beneficial. Although each case is different, if feasible, early motion (by day 7 to 10) should be encouraged. Prolonged immobilization often results in flexion contractures. Morrey and An81 defined the functional range of motion of the elbow as 30 to 130 degrees of flexion. Although most activities of daily living can be performed through this arc of motion; athletes typically have increased demands. In these cases, therapy should be attempted. However, recalcitrant cases require surgical contracture release. Arthroscopic treatment, including anterior capsule release, medial and lateral gutter débridement, and removal of excessive bone when necessary, is technically demanding but can provide excellent results.58,83,94,103

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the capitellum. Knee Surg. Sports Traumatol. Arthrosc. 14:198, 2006. Burra, G., and Andrews, J. R.: Acute shoulder and elbow dislocations in the athlete. Orthop. Clin. North Am. 33:479, 2002. Byrd, J. W., Elrod, B. F., and Jones, K. S.: Elbow arthroscopy for neglected osteochondritis dissecans of the capitellum. J. South. Orthop. Assoc. 10:12, 2001. Byrd, J. W., and Jones, K. S.: Arthroscopic surgery for isolated capitellar osteochondritis dissecans in adolescent baseball players: minimum three-year follow-up. Am. J. Sports Med. 30:474, 2002. Cain, E. L. Jr., Dugas, J. R., Wolf, R. S., and Andrews, J. R.: Elbow injuries in throwing athletes: a current concepts review. Am. J. Sports Med. 31:621, 2003. Callaway, G. F. L., Deng, X. H., Torzilli, P. A., O’Brien, S. J., Altchek, D. W., and Warren, R. F.: Biomechanical evaluation of the medial collateral ligament of the elbow. J. Bone Joint Surg. Am. 79A:1223, 1997. Chappell, J., and ElAttrache, N.: Clinical outcomes of OCD lesions of the capitellum treated with osteochondral autografts. In Open Meeting American Shoulder Elbow Surgeons; 2008; San Francisco; 2008. Charlton, W. P., and Chandler, R. W.: Persistence of the olecranon physis in baseball players: Results following operative management. J. Shoulder Elbow Surg. 12:59, 2003. Chen, F. S., Rokito, A. S., and Jobe, F. W.: Medial elbow problems in the overhead-throwing athlete. J. Am. Acad. Orthop. Surg. 9:993, 2001. Clarke, R. P.: Symptomatic, lateral synovial fringe (plica) of the elbow joint. Arthroscopy 4:112, 1988. Conn, J., and Wade, P.: Injuries of the elbow: ten-year review. J. Trauma 1:248, 1961. Danielsson, L. G., Hedlund, S. T., and Henricson, A. S.: Apophysitis of the olecranon. A report of four cases. Acta Orthop. Scand. 54:777, 1983. David, T. S.: Medial elbow pain in the throwing athlete. Orthopedics 26:94; quiz 104, 2003. Dehaven, K. E., Ferguson, A., Hale, C. J., Larson, R., and Tullos, H.: Symposium: Throwing injuries to the adolescent elbow. Contemp. Surg. 9:65, 1976. Dehaven, K., Evartsm C.: Throwing injuries of the elbow in athletes. Orthop. Clin. North Am. 1:801, 1973. Dunn, N.: Operation for fracture of the olecranon. B. M. J. 1:214, 1939. Fleisig, G. S., Barrentine, S. W., Escamilla, R. F., and Andrews, J. R.: Biomechanics of overhand throwing with implications for injuries. Sports Med. 21:421, 1996. Fleisig, G. S., Barrentine, S. W., Zheng, N., Escamilla, R. F., and Andrews, J. R.: Kinematic and kinetic comparison of baseball pitching among various levels of development. J. Biomech. 32:1371, 1999. Gainor, B., Piotrowski, G., Puhl, J., Allen, W. C., and Hagen, R.: The throw: biomechanics and acute injury. Am. J. Sports Med. 8:114, 1980. Gartsman, G., Sculco, T., and Otis, J.: Operative treatment of olecranon fractures: excision or open reduction with internal fixation. J. Bone Joint Surg. Am. 63A:718, 1981.

42. Gerbino, P. G., and Waters, P.: Elbow injuries in the young athlete. Op. Tech. Sports Med. 6:259, 1998. 43. Gicquel, P., Maximin, M. C., Boutemy, P., Karger, C., Kempf, J. F., and Clavert, J. M.: Biomechanical analysis of olecranon fracture fixation in children. J. Pediatr. Orthop. 22:17, 2002. 44. Gore, R., Rogers, L., Bowerman, J., Suker, J., and Conpere, C.: Osseous manifestations of elbow stress associated with sports pitchers. A. J. R. Am. J. Roentgenol. 134:971, 1980. 45. Gudmundsen, T., and Ostensen, H.: Accessory ossicles in the elbow. Acta Orthop. Scand. 58:130, 1987. 46. Guggenheim, J., Stanley, R., Woods, G. W., and Tullos, H. S.: Little League survey: The Houston Study. Am. J. Sports Med. 4:189, 1976. 47. Hang, V., Lippert, G., Spolek, G., Frankel, V., and Harrington, R.: Biomechanical study of the pitching elbow. Int. Orthop. 3:217, 1979. 48. Hang, D. W., Chao, C. M., and Hang, Y. S. A clinical and roentgenographic study of Little League elbow. Am. J. Sports Med. 32:79, 2004. 49. Harada, M., Ogino, T., Takahara, M., Ishigaki, D., Kashiwa, H., and Kanauchi, Y.: Fragment fixation with a bone graft and dynamic staples for osteochondritis dissecans of the humeral capitellum. J. Shoulder Elbow Surg. 11:368, 2002. 50. Harada, M., Takahara, M., and Sasaki, I.: Using sonography for the early detection of elbow injuries among young baseball players. A. J. R. Am. J. Roentgenol. 187:1436, 2006. 51. Hepler, M., Steinmann, S., and Rosenwasser, M.: Elbow arthroscopy in the treatment of posterior olecranon impingement. Arthroscopy 14:430, 1998. 52. Inoue, G., and Kuwahata, Y.: Surgical repair of traumatic medial disruption of the elbow in competitive athletes. Br. J. Sports Med. 29:139, 1995. 53. Ireland, M. L., and Andrews, J. R.: Shoulder and elbow injuries in the young athlete. Clin. Sports Med. 7:473, 1988. 54. Ireland, M. L., and Hutchinson, M. R.: Upper extremity injuries in young athletes. Clin. Sports Med. 14:533, 1995. 55. Iwasaki, N., Kato, H., Ishikawa, J., Saitoh, S., and Minami, A.: Autologous osteochondral mosaicplasty for capitellar ostechondritis dissecans in teenaged patients. Am. J. Sports Med. 34:1233, 2006. 56. Jackson, D. W., Silvino, N., and Reiman, P.: Osteochondritis in the female gymnast’s elbow. Arthroscopy 5:129, 1989. 57. Jobe, F. W., Stark, H., and Lombardo, S. J.: Reconstruction of the ulnar collateral ligament in athletes. J. Bone Joint Surg. Am. 68:1158, 1986. 58. Jones, G. S., and Savoie, F. H. 3rd.: Arthroscopic capsular release of flexion contractures (arthrofibrosis) of the elbow. Arthroscopy 9:277, 1993. 59. Josefsson, P. O., and Danielsson, L. G.: Epicondylar elbow fracture in children. 35-year follow-up of 56 unreduced cases. Acta Orthop. Scand. 57:313, 1986. 60. Josefsson, P. O., Johnell, O., Gentz, C. F.: Long-term sequelae of simple dislocation of the elbow. J. Bone Joint Surg. 66A:927, 1984.

Chapter 49 Articular Injuries in the Athlete

61. Kamineni, S., ElAttrache, N. S., O’Driscoll, S. W., Ahmad, C. S., Hirohara, H., Neale, P. G., An, K. N., and Morrey, B. F.: Medial collateral ligament strain with partial posteromedial olecranon resection. A biomechanical study. J. Bone Joint Surg. Am. 86-A:2424, 2004. 62. Kamineni, S., Hirahara, H., Pomianowski, S., Neale, P. G., O’Driscoll, S. W., ElAttrache, N., An, K. N., and Morrey, B. F.: Partial posteromedial olecranon resection: a kinematic study. J. Bone Joint Surg. Am. 85-A:1005, 2003. 63. Kim, D. H., Gambardella, R. A., Elattrache, N. S., Yocum, L. A., and Jobe, F. W.: Arthroscopic treatment of posterolateral elbow impingement from lateral synovial plicae in throwing athletes and golfers. Am. J. Sports Med. 34:438, 2006. 64. King, J., Brelsford, H., and Tullos, H. S.: Analysis of the pitching arm of the professional pitcher. Clin. Orthop. Relat. Res. 67:116, 1969. 65. Kiyoshige, Y., Takagi, M., Yuasa, K., and Hamasaki, M.: Closed-wedge osteotomy for osteochondritis dissecans of the capitellum. A 7- to 12-year follow-up. Am. J. Sports Med. 28:534, 2000. 66. Kobayashi, K., Burton, K. J., Rodner, C., Smith, B., and Caputo, A. E.: Lateral compression injuries in the pediatric elbow: Panner’s disease and osteochondritis dissecans of the capitellum. J. Am. Acad. Orthop. Surg. 12:246, 2004. 67. Kondo, M., and Asoh, K.: The treatment of osteochondritis dissecans of the elbow: Pull out wiring method. Jap. Joint Surg. 11:630, 1992. 68. Kovach, J. 2nd, Baker, B. E., and Mosher, J. F.: Fracture separation of the olecranon ossification center in adults. Am. J. Sports Med. 13:105, 1985. 69. Krijnen, M. R., Lim, L., and Willems, W. J.: Arthroscopic treatment of osteochondritis dissecans of the capitellum: Report of 5 female athletes. Arthroscopy 19:210, 2003. 70. Kuwahata, Y., and Inoue, G.: Osteochondritis dissecans of the elbow managed by Herbert screw fixation. Orthopedics 21:449, 1998. 71. Larson, R. L., and McMahan, R.: The epiphysis and the childhood athlete. J. A. M. A. 196:607, 1966. 72. Lokiec, F., Velkes, S., and Engel, J.: Avulsion of the medial epicondyle of the humerus in arm wrestlers: a report of five cases and a review of the literature. Injury 22:69, 1991. 73. Lowery, W. D. Jr., Kurzweil, P. R., Forman, S. K., and Morrison, D. S.: Persistence of the olecranon physis: a cause of “little league elbow.” J. Shoulder Elbow Surg. 4:143, 1995. 74. Maffulli, N., Chan, D., and Aldridge, M. J.: Overuse injuries of the olecranon in young gymnasts. J. Bone Joint Surg. Br. 74:305, 1992. 75. McManama, G. B. Jr., Micheli, L. J., Berry, M. V., and Sohn, R. S.: The surgical treatment of osteochondritis of the capitellum. Am. J. Sports Med. 13:11, 1985. 76. Micheli, L. J.: The traction apophysitises. Clin. Sports Med. 6:389, 1987. 77. Miller, J.: Javelin thrower’s elbow. J. Bone Joint Surg. 42B:788, 1960.

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78. Mitsunaga, M. M., Adishian, D. A., Bianco, A. J. Jr.: Osteochondritis dissecans of the capitellum. J. Trauma 22:53, 1982. 79. Morrey, B. F.: Current concepts in the treatment of fractures of the radial head, the olecranon, and the coronoid. Instr. Course Lect. 44:175, 1995. 80. Morrey, B., and An, K.: Functional anatomy of the ligaments of the elbow. Clin. Orthop. Relat. Res. 201:84, 1985. 81. Morrey, B. F., and An, K. N.: Articular and ligamentous contributions to the stability of the elbow joint. Am. J. Sports Med. 11:315, 1983. 82. Nuber, G. W., and Diment, M. T.: Olecranon stress fractures in throwers. A report of two cases and a review of the literature. Clin. Orthop. Relat. Res. 278:58, 1992. 83. Nguyen, D., Proper, S. I., MacDermid, J. C., King, G. J., and Faber, K. J.: Functional outcomes of arthroscopic capsular release of the elbow. Arthroscopy 22:842, 2006. 84. Nyska, M., Peiser, J., Lukiec, F., Katz, T., and Liberman, N.: Avulsion fracture of the medial epicondyle caused by arm wrestling. Am. J. Sports Med. 20:347, 1992. 85. Ogata, S., and Uhthoff, H. K.: The development of synovial plicae in human knee joints: an embryologic study. Arthroscopy 6:315, 1990. 86. O’Holleran, J. D., and Altchek, D. W.: Elbow arthroscopy: treatment of the thrower’s elbow. Instr. Course Lect. 55:95, 2006. 87. Orava, S., and Hulkko, A.: Delayed unions and nonunions of stress fractures in athletes. Am. J. Sports Med. 16:378, 1988. 88. Panner, H.: A peculiar affection of the capitulum humeri resembling Calve-Perthes disease of the hip. Acta Radiol. 10:234, 1928. 89. Pappas, A. M.: Osteochondrosis dissecans. Clin. Orthop. Relat. Res. 158:59, 1981. 90. Pappas, A. M.: Elbow problems associated with baseball during childhood and adolescence. Clin. Orthop. Relat. Res. 164:30, 1982. 91. Pavlov, H., Torg, J. S., Jacobs, B., and Vigorita, V.: Nonunion of olecranon epiphysis: two cases in adolescent baseball pitchers. A. J. R. Am. J. Roentgenol. 136:819, 1981. 92. Peterson, R. K., Savoie, F. H. 3rd, and Field, L. D.: Osteochondritis dissecans of the elbow. Instr. Course Lect. 48:393, 1999. 93. Petty, D. H., Andrews, J. R., Fleisig, G. S., and Cain, E. L.: Ulnar collateral ligament reconstruction in high school baseball players: clinical results and injury risk factors. Am. J. Sports Med. 32:1158, 2004. 94. Phillips, B. B., and Strasburger, S.: Arthroscopic treatment of arthrofibrosis of the elbow joint. Arthroscopy 14:38, 1998. 95. Rao, P. S., Rao, S. K., and Navadgi, B. C.: Olecranon stress fracture in a weight lifter: a case report. Br. J. Sports Med. 35:72, 2001. 96. Reddy, A. S., Kvitne, R. S., Yocum, L. A., Elattrache, N. S., Glousman, R. E., and Jobe, F. W.: Arthroscopy of the elbow: a long-term clinical review. Arthroscopy 16:588, 2000.

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97. Regan, W. D., Korinek, S. L., Morrey, B. F., and An, K. N.: Biomechanical study of ligaments around the elbow joint. Clin. Orthop. Relat. Res. 271:170, 1991. 98. Rettig, A. C., Wurth, T. R., and Mielingm, P.: Nonunion of olecranon stress fractures in adolescent baseball pitchers: a case series of 5 athletes. Am. J. Sports Med. 34:653, 2006. 99. Roberts, P.: Dislocations of the elbow. Lancet 2:78, 1934. 100. Rolla, P. R., Surace, M. F., Bini, A., and Pilato, G.: Arthroscopic treatment of fractures of the radial head. Arthroscopy 22:233 e1, 2006. 101. Ruch, D. S., and Poehling, G. G.: Arthroscopic treatment of Panner’s disease. Clin. Sports Med. 10:629, 1991. 102. Ruch, D. S., Papadonikolakis, A., and Campolattaro, R. M.: The posterolateral plica: a cause of refractory lateral elbow pain. J. Shoulder Elbow Surg. 15:367, 2006. 103. Savoie, F. H. 3rd, and Field, L. D.: Arthrofibrosis and complications in arthroscopy of the elbow. Clin. Sports Med. 20:123, ix, 2001. 104. Schenk, M., and Dalinka, M. K.: Imaging of the elbow. An update. Orthop. Clin. North Am. 28:517, 1997. 105. Schwab, G. H., Bennett, J. B., Woods, G. W., and Tullos, H. S.: Biomechanics of elbow instability: the role of the medial collateral ligament. Clin. Orthop. Relat. Res. 146:42, 1980. 106. Singer, K., and O’Neill, D.: Update of elbow injuries in the young athlete. In Grana, W. B. (ed.): Advances in Sports Medicine. Chicago, Year Book Medical Publishers, 1990, p. 147. 107. Slocum, D.: Classification of elbow injuries from baseball pitching. Texas Med. 64:48, 1968. 108. Sneed, J., and Boyd, H.: Fractures about the elbow. Am. J. Surg. 38:727, 1937. 109. Suzuki, K., Minami, A., Suenaga, N., and Kondoh, M.: Oblique stress fracture of the olecranon in baseball pitchers. J. Shoulder Elbow Surg. 6:491, 1997. 110. Takahara, M., Shundo, M., Kondo, M., Suzuki, K., Nambu, T., and Ogino, T.: Early detection of osteochondritis dissecans of the capitellum in young baseball players. Report of three cases. J. Bone Joint Surg. Am. 80:892, 1998. 111. Takahara, M., Ogino, T., Fukushima, S., Tsuchida, H., and Kaneda, K.: Nonoperative treatment of osteochondritis dissecans of the humeral capitellum. Am. J Sports Med. 27:728, 1999.

112. Takahara, M., Ogino, T., Sasaki, I., Kato, H., Minami, A., and Kaneda, K.: Long term outcome of osteochondritis dissecans of the humeral capitellum. Clin. Orthop. Relat. Res. 363:108, 1999. 113. Takeda, H., Watarai, K., Matsushita, T., Saito, T., and Terashima, Y.: A surgical treatment for unstable osteochondritis dissecans lesions of the humeral capitellum in adolescent baseball players. Am. J. Sports Med. 30:713, 2002. 114. Thomson, N.: Osteochondritis dissecans and osteochondral fragments managed by herbert compression screw fixation. Clin. Orthop. Rel. Res. 224:71, 1987. 115. Tivnon, M., Anzel, S., and Waugh, T.: Surgical management of osteochondritis dissecans of the capitellum. Am. J. Sports Med. 4:121, 1976. 116. Torg, J. S., and Moyer, R. A.: Non-union of a stress fracture through the olecranon epiphyseal plate observed in an adolescent baseball pitcher. A case report. J. Bone Joint Surg. Am. 59:264, 1977. 117. Tullos, H. S., Erwin, W., and Woods. G. W.: Unusual lesions of the pitching arm. Clin. Orthop. Relat. Res. 88:169, 1972. 118. Tullos, H. S., and King, J.: Lesions of the pitching arm in adolescents. J. A. M. A. 220:264, 1972. 119. Wadsworth, T.: The Elbow. Edinburgh: Churchill Livingstone, 1982. 120. Warwick, R., and Williams, P.: Gray’s Anatomy, 35th ed. Philadelphia, WB Saunders Co., 1973. 121. Wilkerson, R. D., and Johns, J. C.: Nonunion of an olecranon stress fracture in an adolescent gymnast. A case report. Am. J. Sports Med. 18:432, 1990. 122. Wilson, F. D., Andrews, J. R., Blackburn, T. A., and McCluskey, G.: Valgus extension overload in the pitching elbow. Am. J. Sports Med. 11:83, 1983. 123. Woods, G. W., Tullos, H. S., and King, J. W.: The throwing arm: elbow joint injuries. J. Sports Med. 1:43, 1973. 124. Woodward, A., and Bianco, A. J.: Osteochondritis dissecans of the elbow. Clin. Orthop. Relat. Res. 110:35, 1975. 125. Yamamoto, Y., Ishibashi, Y., Tsuda, E., Sato, H., and Toh, S.: Osteochondral autograft transplantation for osteochondritis dissecans of the elbow in juvenile baseball players: minimum 2-year follow-up. Am. J. Sports Med. 34:714, 2006.

Chapter 50 Overuse Syndrome

CHAPTER

50

Overuse Syndrome Richard A. Berger

INTRODUCTION Although many tissues are subject to fatigue injury, especially those of the immature skeleton,17 the concept of “overuse syndrome” has a broader definition. “No pain, no gain,” a cliché promoted in athletic circles for decades, expresses the underlying attitude that the advancement of one’s physical abilities may depend on exceeding the body’s limits far enough to cause pain and that less vigorous activity constitutes suboptimal performance. The pain that results from these activities may be transient, representing little more than a focal accumulation of muscle metabolic byproducts, or it may be longer lasting, indicating tissue injury. One dilemma is where to draw the line between the two extremes. Others are when it is safe to resume the activities that initially led to the noxious episode, whether or not adjustments in those activities are indicated, and at what point persistent pain no longer represents an acute injury state but signals a more ominous and less understood condition of chronic pain. These are only a few of the unknowns that are associated with overuse syndromes.

DEFINITIONS AND SYNONYMS Usually thought to affect muscle or nerve, the overuse syndromes are imprecisely defined and go by a variety of names—repetitive strain injury, repetitive stress syndrome, chronic pain syndrome, cumulative trauma disorder, pain dysfunction syndrome (see Chapter 81), cervicobrachial occupational disorder, fibromyalgia, and a variety of activity-specific conditions such as writer’s cramp and tennis elbow, among others.6,12,16,18,33,40 The multiplicity of terms reflects the fact that the pathophysiologic mechanisms are, at best, poorly understood. It also contributes to confusion in classification, which, in turn, interferes with our learning from outcome studies. Overall, however, the term overuse syndrome is generally understood to reflect a painful condition, and all tissue types are at risk (Table 50-1). In this text, the term applies to a painful condition of the elbow region that results from excessive activity and whose symp-

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toms have been present for an extended period of time.15 Overuse syndrome is a diagnosis of exclusion. No clear history of injury or date of onset is reported. Conditions that involve injury to specific structures, such as lateral epicondylitis and nerve entrapment syndromes (discussed in other chapters), must be ruled out before overuse conditions are considered. Chronicity also plays a role in the diagnosis of overuse syndrome. Pain of traceable onset less than 3 months before presentation for evaluation may be more likely to signify actual tissue injury related to a specific set of circumstances and to respond more favorably to conventional medical intervention. Conversely, pain of more than 6 months’ duration is much more likely (1) to have been affected by numerous nonorganic factors, (2) to present as a regional complaint, and (3) to display resistance to conventional medical intervention.6

EPIDEMIOLOGY The overuse syndromes are most prominent in two groups of patients, performers and workers.5,7,8,11,15,20,27,36,39 Among the former are athletes and musicians, whose professions demand exceptional physical performance and arduous practice sessions. The tissues most often involved in athletes are the musculotendinous units, the ulnar nerve, and the collateral ligaments.38 In practice sessions, an activity is repeated to improve the performance level, often for extended periods. When the performers are called on to use the skills so perfected, an alteration in the performance level caused by pain may be noticeable and possibly may threaten their ability to continue. Any pre-existing injury can further increase the risk of developing an overuse condition. Workers who daily are expected to perform certain job tasks are also at risk. Occupations reported to carry increased risk for overuse syndromes include typist, telephone operator, cash register operator, interpreter for the deaf, and packing plant worker.8,14,19,33 In the most common scenario, workers are stationed for long periods, during which they perform repetitive tasks. The actual number of workers who suffer from overuse syndrome is difficult to determine. Four percent of noninstitutionalized adults could recall at least 1 month of musculoskeletal pain and the nature of the impact of that pain.9 When specific jobs are evaluated, however, the incidence of upper extremity pain related to overuse may approach 30%.29 In both groups, psychosocial influences may play a major role in determining the pattern of functional recovery once a change in performance level is detected. Such factors actually may influence the manner in which the painful condition is presented to the treating physi-

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Overuse-Induced Lesions at the Elbow and Affected Tissue Types

TABLE 50-1

Involved Tissue

Manifestations

Bone

Angular change, hypertrophy

Joint

Degenerative arthrosis, loose body, spur, osteophyte (olecranon), osteochondritis dissecans

Synovium

Reactive synovitis, effusion

Ligament

Collateral ligament tear, stretch, calcification

Tendon

Epicondylitis, distal biceps, triceps detachment

Muscle

Myofasciitis, hypertrophy, compartment syndrome (anconeus)

Bursa

Inflammation, radiobicipital, olecranon

Nerve

Entrapment, cubital tunnel, arcade of Frohse

cian, which, in turn, may alter the diagnosis and generate a self-perpetuating cycle of pain and reinforcement behaviors. It also must be understood that the worker’s condition is not static and that new stresses may enter into the situation over time. Often, the patience of both employee and employer evaporates and mutual mistrust develops. This may prompt the patient subconsciously to exaggerate reports of pain and limitation of function, further frustrating the care of the condition and often ending in confrontation and litigation.

ETIOLOGY The causes of overuse syndrome have been the subject of speculation in many publications and studies.10,24,31,35,37 One of the earliest observations of pain in a worker subjected to “irregular motions and unnatural postures” dates to the early 18th century.37 Generally, overuse conditions are believed to arise from a combination of static and dynamic loads applied to postural muscles beyond the tolerable contraction level or duration.31 Isometric contraction greater than 10% of the maximum contraction level is not recommended35 because circulation in the contracting muscle may be compromised enough to cause tissue ischemia and accumulation of noxious metabolites.24 The noxious stimulus may prompt recruitment of other muscle groups, which, however, may be at a mechanical disadvantage for assuming such a role and may likewise, in the end, suffer muscle strain. The Japanese Association of Industrial Health identified several risk factors for the development of overuse syndrome, including dynamic muscle recruitment for repet-

FIGURE 50-1

A 32-year-old carpenter had pain on elbow motion of 40 to 110 degrees. Primary arthrosis prompted a career change.

itive tasks, static muscle recruitment for postural support, uncomfortable postures, mental stress, and ergonomic factors such as unpleasant working conditions (Fig. 50-1).2 Continued engagement in high-load activities other than occupational tasks, including hobbies, domestic chores, and recreational activities, may perpetuate the condition by reducing recovery time.

PSYCHOLOGICAL FACTORS Historically, the involvement of psychological factors in the initiation and perpetuation of overuse syndrome has been recognized.23,26 For example, stress has been reported to be a pertinent risk in visual display operators.42 Stress, in this instance, may be related to high expectations on the part of the employee and the employer for accuracy and productivity in the face of monotonous tasks, equipment failure, static posture, and so on. Stress also may result from variables in physical surroundings such as lighting, noise, and coworker distractions. Athletes’ competitive bent may mean that stress plays a more prominent role in the development of overuse syndrome, and the unwillingness to rest the affected body part merely exacerbates the condition. Although it is important to identify the psychological

Chapter 50 Overuse Syndrome

and social factors that may contribute to overuse syndrome, it is equally important to avoid the common tendency to ascribe the entire problem to these factors.

HISTORY AND PHYSICAL EXAMINATION History taking is a most important and time-consuming component of the assessment. At first evaluation, several features commonly are evident. First, the degree of perceived impairment from the discomfort is significant, and the patient’s description of the discomfort may be dramatic and graphic.1,6 Some objective measure of pain may be useful, such as a pain thermometer to establish a baseline for future comparisons. Second, the patient typically has received many—and often conflicting—“other opinions” from family members, the popular press, coworkers, trainers, employers, and other physicians. Early in the first meeting, it is important tactfully to direct the patient’s attention away from previous opinions, to minimize learned behavior and bias and to maximize the effectiveness of future treatments. Finally, the patient may have learned to distort or exaggerate the severity and the area of involvement in an attempt to engage medical attention, this being a reaction to earlier incidents when the painful condition was trivialized by supervisors or industrial health care workers. It is critical, while establishing rapport, to assure the patient that all symptoms are important and that an accurate report of those symptoms greatly enhances the process. A complete description of the patient’s condition and the activities he or she was involved in before and after the onset of symptoms is important to record. For the worker, each job and its duration and a description of its specific tasks should also be recorded. Each task should be thoroughly understood, and the record should note the height of the workstation, the frequency of repetitions, the loads applied, the ambient temperature, the job rotation, the frequency of breaks, and any other relevant conditions. For athletes and musicians, a careful history of practice schedules and conditions is desirable. Next, a chronology of painful trends is required because the onset of symptoms, evaluations by physicians and chiropractors, and all treatments instituted and the patient’s response to those treatments should be recorded. The examiner seeks to gain a thorough understanding of the nature of the presenting complaint, in terms of severity, duration, type of pain, exacerbating and relieving factors, sleep patterns, and resultant functional limitations. Finally, in consultation with the worker, it is important to gain insight into his relationship with the employer, whether legal counsel has been obtained, and especially whether the patient is currently receiving worker’s compensation benefits.

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During the physical examination, the key objective is to rule out all other possible causes of similar pain, including nerve entrapment syndromes, tendinitis, arthritis, bursitis, fracture, sprain, and other conditions such as tennis elbow. A systematic examination of the extremity, including musculoskeletal and neurologic function, circulation, and integument, is standard. After the more common processes have been ruled out, the diagnosis of overuse syndrome or of a similar condition begins to emerge.22,44 Generally, the patient has a relatively diffuse region of discomfort, and “trigger points” are not uncommon. One condition that may present as an unexplained overuse syndrome is fibromyalgia, which may demonstrate trigger points just distal to the medial or lateral epicondyle.18 Weakness may be a prominent complaint in overuse syndrome, but specific testing of muscles likely demonstrates neurologically intact neuromuscular pathways and “breakaway” weakness secondary to pain. It is critical to be mindful of the possible existence of the manifestations of pain dysfunction syndrome, because the treatment modalities are unique to that disorder, which generally does not respond to the therapies recommended for overuse syndrome.1,13 It may be useful to observe the athlete performing the activities that produce the discomfort in the field or the musician playing an instrument. An ergonomic evaluation of the worker’s environment, by either the physician or a qualified ergonomist, may be useful for understanding the circumstances surrounding the patient’s complaints. Finally, serial examination to determine the reproducibility of physical findings and to determine whether the nature of the condition “evolves” is extremely informative and useful.

LABORATORY EVALUATION If there is concern that the patient may be describing signs and symptoms of an early inflammatory condition, the erythrocyte sedimentation rate, white blood count with differential, electrolyte assays, rheumatoid factor, and antinuclear antibody levels should be determined. The serum levels of the muscle enzymes creatine phosphokinase and aldolase have been reported to be elevated in some workers with upper extremity overuse syndrome, but it is believed that further investigation is necessary before widespread use of these determinations can be justified.5 Serologic testing for Lyme disease may be considered, especially if exposure risk factors are suggestive, because in the early clinical phases this disease can mimic overuse syndrome.4 Standard radiographs of the elbow are necessary to evaluate the skeletal integrity of the humerus, the radius, and the ulna. It may be necessary to obtain special oblique views such as a radial head view or tomogram

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if a specific lesion is suspected. Magnetic resonance imaging is useful as a means of excluding obvious derangements or pathologic conditions. The usefulness of three-phase bone scintigraphy in the diagnosis of reflex sympathetic dystrophy has been largely accepted, and this study should be considered when evaluating for overuse syndrome.32 In fact, the technetium Tc 99 m bone scan is a useful screen for suspected inflammatory conditions with minimal findings (Fig. 50-2). Thermography, electromyography, quantitative sudomotor and autonomic reflex testing, and plethysmography all require substantially more investigation before they can be recommended for general use.33,36,45

TREATMENT There is no simple or standard treatment for overuse syndrome. Treatment must take into consideration not only improvement of the immediate painful condition but also prevention of future exacerbations. The treatment modalities for acute pain are different from those for chronic symptoms. In the acute setting, standard techniques of pain management are appropriate—rest, thermal therapy (cold versus heat), ultrasound and phonophoresis, friction massage, oral nonsteroidal anti-inflammatory medication, and occasional injections of corticosteroid solutions into regions that are particularly tender and troublesome (see Chapter 9). Rest may be provided by temporary splint immobilization, but full-time immobilization causes stiffness and deconditioning that can quickly compound the original problem. Gentle, progressive, well-supervised physical therapy often enhances the rehabilitation process and maintains the strength and conditioning of body parts not affected by the

overuse syndrome.41 The patient should continue to work when that is at all possible. To that end, the surgeon can define tolerable limits for tasks that will allow the patient to progress to recovery while maintaining a productive posture with the employer. Keeping the patient away from the workplace can affect the patient’s perception of the degree of impairment that the condition may be generating and could constitute negative reinforcement for recovery (see Chapter 44). On the other hand, some conditions are markedly correlated with occupation, and changing jobs may be an important treatment measure (see Fig. 50-1). Treatment of chronic pain, regardless of the cause, is a difficult process that requires a multidisciplinary approach. Generally speaking, the conventional therapeutic approach described earlier is ineffective and in certain circumstances may be counterproductive. Attempts to treat the symptoms with splints, medications, or injections should cease. It must be made clear that the condition will not respond to medical or surgical intervention. This is not to say that it will not improve with some types of therapy; it merely underscores the need for the patient to stop searching for a medical answer to the problem. A survey of 116 therapists revealed that many common educational themes are employed, especially the nature of the disease process, normal and abnormal anatomy, and job modification.25 The patient should have a functional capacity evaluation, which is useful for determining impairment levels and constructing a work-hardening program.41 Referral to a pain management clinic may avail the patient of unconventional modalities such as TENS and biofeedback. Stellate ganglion block, contrast baths, and massage may benefit patients who are believed to have autonomic dysfunction. If the patient has retained legal

FIGURE 50-2

A patient with chronic elbow pain had normal (“negative”) radiographs (A) but a positive 99 Tc bone scan (B).

Chapter 50 Overuse Syndrome

counsel or is pursuing workmen’s compensation independently, the treating physician becomes an important source of information and will be asked to determine if the workplace was responsible for, or substantially contributed to, the onset of symptoms; what level of impairment due to the symptoms has been established; and what if any permanent restrictions will be necessary as a result of these findings. An independent impairment evaluation center can be very helpful in these circumstances. Prevention at the workplace and preconditioning of workers are critical to combating the overuse syndrome epidemic. Reasonable employers are evaluating workplaces with ergonomists to determine what modifications in the workplace and in task rotations will reduce the incidence of overuse syndromes.3,30,43 Additionally, implementation of ergonomic exercise programs, better employee education and orientation, and soliciting employees’ feedback seem to have salutary effects on reducing overuse syndrome.30 There still remains controversy, however, about whether proof exists that ergonomic adjustments and compensations are efficacious.46

SUMMARY Overuse syndrome of the upper extremity is a poorly understood condition that, by some measures, is reaching nearly epidemic proportions. Clear guidelines for classification, diagnosis, and treatment are needed. Until they are established, the physician carries the responsibility of educating patients, employers, and the community at large and the burden of studying the process to educate fellow physicians.21

References 1. Amadio, P. C.: Pain dysfunction syndromes: current concept reviews. J. Bone Joint Surg. 70A:944, 1988. 2. Aoyama, H., Ohara, H., Oze, Y., and Itani, T.: Recent trends in research on occupational cervicobrachial disorder. J. Hum. Ergol. (Tokyo) 8:39, 1979. 3. Armstrong, T. J.: Ergonomics and cumulative trauma disorders. Hand Clin. 2:553, 1986. 4. Arthritis Foundation: Primer on the Rheumatic Diseases, 9th ed. Atlanta, Arthritis Foundation, 1988, p. 188. 5. Bjelle, A., Hagberg, M., and Michaelsson, G.: Clinical and ergonomic factors in prolonged shoulder pain among industrial workers. Scand. J. Work Environ. Health 5(suppl.):205, 1979. 6. Blair, W. F.: Cumulative trauma disorder in the upper extremity. Iowa Orthopedics J. 11:103, 1990. 7. Brooks, P. M.: Occupational pain syndromes. Med. J. Austral. 144:170, 1986.

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8. Cohn, L., Lowry, R. M., and Hart, S.: Overuse syndromes of the upper extremity in interpreters for the deaf. Orthopedics 13:207, 1990. 9. Cunningham, L. S., and Kelsey, J. L.: Epidemiology of musculoskeletal impairments and associated disability. Am. J. Public Health 74:574, 1984. 10. Dennett, X.: Overuse syndrome: a muscle biopsy study. Lancet 23:905, 1988. 11. Dimberg, L., Olafsson, A., Stefansson, E., Aagaard, H., Oden, A., Anderson, G. B., Hansson, T., and Hagert, C. G.: The correlation between work environment and the occurrence of cervicobrachial symptoms. J. Occup. Med. 31:447, 1989. 12. Dobyns, J. H.: Cumulative trauma disorder of the upper limb. Hand Clin. 7:587, 1991. 13. Dobyns, J. H.: Pain dysfunction syndrome. In Gelberman, R. H. (ed.): Operative Nerve Repair and Reconstruction, 2nd ed. Philadelphia, J. B. Lippincott Co., 1991, p. 1489. 14. Ferguson, D.: The “new” industrial epidemic. Med. J. Austral. 142:318, 1984. 15. Fry, H. J. H.: Overuse syndrome of the upper limb in musicians. Med. J. Austral. 144:182, 1986. 16. Fry, H. J. H.: Overuse syndrome, alias tenosynovitis/tendinitis: the terminology hoax. J. Plast. Reconstr. Surg. 78:414, 1986. 17. Gill, T. J. 4th, and Micheli, L. J.: The immature athlete. Common injuries and overuse syndromes of the elbow and wrist. Clin. Sports Med. 15:401-423, 1996. 18. Goldenberg, D. L.: Fibromyalgia syndrome (fibrositis). Mediguide Inflam. Dis. 7:1, 1988. 19. Hadler, N. M.: Work-related disorders of the upper extremity. Part I: Cumulative trauma disorders-a critical review. Occup. Prob. Med. Prac. 4:1, 1989. 20. Hadler, N. M.: Industrial rheumatology: the Australian and New Zealand experiences with arm pain and backache in the work-place. Med. J. Austral. 144:191, 1986. 21. Hadler, N. M.: Cumulative trauma disorders: an iatrogenic concept. J. Occup. Med. 32:38, 1990. 22. Howard, N. J.: Peritendinitis crepitans. J. Bone Joint Surg. 19:447, 1937. 23. Ireland, D. C. R.: Psychological and physical aspects of occupational arm pain. J. Hand Surg. 13B:5, 1988. 24. Karlsson, J., and Ollander, B.: Muscle metabolites with exhaustive static exercises of different durations. Acta Physiol. Scand. 86:309, 1972. 25. Lawler, A. L., James, A. B., and Tomlin G.: Educational techniques used in occupational therapy treatment of cumulative trauma disorders of the elbow, wrist and hand. Am. J. Occup. Ther. 51:113-118, 1997. 26. Linton, S. J., and Kamwendo, K.: Risk factors in the psychosocial work environment for neck and shoulder pain in secretaries. J. Occup. Med. 31:609, 1989. 27. Louis, D. S.: Cumulative trauma disorders. J. Hand Surg. 5:823, 1987. 28. Louis, D. S.: Evolving concerns relating to occupational disorders of the upper extremity. Clin. Orthop. 254:140, 1990. 29. Luopajarvi, T., Kuorinka, I., Virolainen, M., and Holmberg, M.: Prevalence of tenosynovitis and other injuries of the

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30.

31.

32.

33. 34.

35.

36. 37.

38. 39.

Part VI Sports and Overuse Injuries to the Elbow

upper extremities in repetitive work. Scand. J. Work Environ. Health 5(Suppl.):48, 1979. Lutz, G., and Hansford, T.: Cumulative trauma disorder controls: the ergonomic program at Ethicon, Inc. J. Hand Surg. 12A:863, 1987. Maeda, K., Hunting, W., and Grandjean, E.: Factor analysis of localized fatigue complaints of accounting machine operators. J. Hum. Ergol. (Tokyo) 11:37, 1982. Mackinnon, S. E., and Holder, L. E.: The use of three-phase radionuclide bone scanning in the diagnosis of reflex sympathetic dystrophy. J. Hand Surg. 9:556, 1984. McDermott, F. T.: Repetition strain injury: a review of current understanding. Med. J. Austral. 144:196, 1986. McPhee, B., and Worth, D. R.: Neck and upper extremity pain in the work-place. In Grant, R. (ed.): Physical Therapy of the Cervical and Thoracic Spine. New York, Churchill Livingstone, 1988, p. 291. Onishi, N., Sakai, K., and Kogi, K.: Arm and shoulder muscle load in various keyboard operating jobs of women. J. Hum. Ergol. (Tokyo) 11:89, 1982. Pochachevskyl, R.: Thermography in post-traumatic pain. Am. J. Sports Med. 15:243, 1987. Ramazinni, B.: In Wright, W. (trans.): The Diseases of Workers. Chicago, University of Chicago Press, 1940, p. 1717. Rettig, A. C.: Elbow, forearm and wrist injuries in the athlete. Sports Med. 25:115, 1998. Ryan, G. A., and Hampton, M.: Comparison of data process operators with and without upper limb symptoms. Comm. Health Stud. 12:63, 1988.

40. Semple, J. C.: Tenosynovitis, repetitive strain injury, cumulative trauma disorder, and overuse syndrome, et cetera (Editorial). J. Bone Joint Surg. 73B:536, 1991. 41. Schultz-Johnson, K.: Work hardening: a mandate for hand therapy. Hand Clin. 7:597, 1991. 42. Smith, M. J., Cohen, B. G., and Stammerjohn, L. W.: An investigation of health complaints and job stress in visual display operations. Hum. Factors 23:387, 1981. 43. Stock, S. R.: Work-place ergonomic factors and the development of musculoskeletal disorders of the neck and upper limbs: a meta-analysis. Am. J. Indust. Med. 19:87, 1991. 44. Thompson, A. R., Plewes, L. W., and Shaw, E. G.: Peritendinitis crepitans and simple tenosynovitis: a clinical study of 544 cases in industry. Br. J. Industr. Med. 8:150, 1951. 45. Uematsu, S., Hendler, N., Hungerford, D., Long, D., and Ono, N.: Thermography and electromyography in the differential diagnosis of chronic pain syndromes and reflex sympathetic dystrophy. Electromyogr. Clin. Neurophysiol. 21:165, 1981. 46. Verhagen, A. P., Kerels, C., Bierma-Zeinstra, S. M., Feleus, A., Dahaghin, S., Burdorf, A., De Vet, H. C., and Koes, B. W.: Ergonomic and physiotherapeutic interventions for treating work-related complaints in the arm, neck or shoulder in adults. A Cochrane systematic review. Eura. Medicophys. 43:391, 2007.

SECTION

A

JOINT REPLACEMENT ARTHROPLASTY CHAPTER

51

Elbow Arthroplasty: Historical Perspective and Emerging Concepts William P. Cooney and Bernard F. Morrey

INTRODUCTION The first “modern“ total elbow arthroplasty using bone cement was performed by Dee in 1972. However, in the late 1940s and early 1950s, documentation of replacement of the elbow by means of hemiarthroplasties as well as custom distal humerus or proximal ulna articular bearing materials exists. All of these efforts suffered from poor fixation and lack of understanding of the joint kinematics. In 1952, Venable48 and in 1965 Barr and Eaton3 designed endoprostheses for the distal humerus, usually for reconstructing traumatic deficiencies (Fig. 51-1). There were also efforts made to create a custom ulnohumeral joint when the elbow was unstable and fusion was the only alternative.11,28,29 These early elbow designs exhibited various articular and fixation concepts (Fig. 51-2). However, without bone cement, these prostheses usually became loose and unstable (see Fig. 51-1). In the 1970s, the concept of resurfacing emerged. These designs were intended for more limited pathology. Mayo was actively involved with early efforts to design both hemi and articulated devices (Fig. 51-3).23 The socalled “saddle” was a true resurfacing of the olecranon designed at Mayo in the later 1960s, and was successful in some instances38 (Fig. 51-4). Street and Stevens47 are credited with the first use of a convex trochlea and

capitellum replacement of the distal humerus (Fig. 51-5). The goal of these implants was a hemiarthroplasty replacement that required less bone resection and, it was hoped, preservation of the collateral ligaments. Materials such as nylon, acrylic, stainless steel, and even vulcanized rubber were used in these early prostheses. Although some were successful in relieving pain, most had limited motion, were often unstable without adequate ligamentous support and loosened over time. A few long-term successes were reported; but in general, joint function was limited and the clinical experience consisted of only a few patients. The era of total elbow joint prosthetic replacement followed the limited success with these custom-designed and resurfacing hemiarthroplasty. We consider the “modern” era of prosthetic replacement to have begun in the early 1970s with the design of Dee, followed by a number of hinged elbow arthroplasties7,9,19,21,39,46 (Fig. 51-6). This and other prostheses almost uniformly provided pain relief and a reasonable range of elbow motion (20 degrees of extension, to 110 to 120 degrees of flexion). The important features of the Dee prosthesis is that it was the first implant to use cement fixation. However, the lack of understanding the complex anatomy and biomechanics resulted in a particularly high early failure rate that progressed to virtually 100% failure with time. The disadvantage of rigid fixation and predictable failure was recognized worldwide. Some devices were modified to address the initial design flaws such as the GSB from Zurich (Fig. 51-7). Roland Pritchard was one of the first in this country to recognize the value of a “loose hinge” and a polyethylene bushing (Fig. 51-8). Others sought the desirability of stability and flexibility with a “snap-fit” articulation. The design by Volz also incorporated a radial head to better distribute the forces crossing the joint49 (see Fig. 51-8). Unfortunately these design concepts suffered from deficiencies of technique, soft tissue balance and bushing wear. A less constrained articulation was also attained by a snap fit with some systems (see Fig. 51-8). Finally, Coonrad recognized the problem with a medial/lateral articulation and a collared polyethylene bushing was introduced in 1970 (Fig. 51-9). 705

706

Part VII Reconstructive Procedures of the Elbow

FIGURE 51-1

C

Unfortunately, complication rates proved very high from loosening, component fracture, and infection leading to a rate of reoperation of 22% to 30%. Hence, the whole concept was reassessed. Loosening at the bone-cement interfaces was the predicated price paid for rigid-constraint prostheses.7,10,17 Early recognition of this problem prompted interest in and the development of more prostheses that were not mechanically coupled. These so-called resurfacing or uncoupled designs14,16,25,46 (Fig. 51-10) are best termed

A, Vitallium replacement prosthesis for distal humerus. Instability (B) and loosening (C) were common problems.

unlinked implants and prompted various efforts to restore the anatomic contour. The earliest designs also tried, unsuccessfully, to avoid the use of a stemmed implant. These implants intended to lessen stresses on the bone-cement interface, allowing the soft tissue capsule and ligaments to transmit forces and decrease the risk of mechanical loosening. Over the years, these theoretical advantages have proved to be effective, however, only to the extent that the unlinked device is also less constrained at the articulation. We now know

Chapter 51 Elbow Arthroplasty: Historical Perspective and Emerging Concepts

B

A

D

FIGURE 51-2

C

A, Linked devices were employed for devastating bone loss. B to D, Various articular and design concepts were employed.

707

708

Part VII Reconstructive Procedures of the Elbow

FIGURE 51-3

A, Replacement prosthesis for the proximal ulna (designed by EW Johnson and AP Schlein). The original proximal ulna replacement lasted 13 years before requiring revision to a custom Mayo-Coonrad total elbow arthroplasty. B and C, Custom total elbow revision replacement of the elbow.

Chapter 51 Elbow Arthroplasty: Historical Perspective and Emerging Concepts

709

FIGURE 51-5 FIGURE 51-4

A, A vitallium “saddle” designed by Bickel and Peterson to resurface the proximal ulna. B, Fifteenyear follow-up of a patient with post-traumatic arthritis treated with the vitallium “saddle.” There was mild pain and motion from 80 to 135 degrees. (From Peterson, L. F. A., and Jones, J. M.: Surgery of the rheumatoid elbow. Orthop. Clin. North Am. 2:667, 1971.)

that it is the articular constraint, not the linkage per se, that influences loosening. Our clinical experience with the more modern designs at the Mayo Clinic began in 1971 with the original Coonrad hinged prosthesis. This was composed of humeral and ulna components separated by a highdensity polyethylene bushing (see Fig. 51-9).35 Our experience with this design was flawed by poor stem fixation (Fig. 51-11). With a more sophisticated understanding of biomechanics and after studying our own and the clinical experience of others, a three-piece, semiconstrained, flanged device was designed in 1978 (Fig. 51-12). Morrey inserted two of these devices, and the second one dislocated. The design was abandoned, but the value of the flange concept was believed to be sound and it was incorporated into the Coonrad implant.

A, Distal humerus resurfacing prosthesis designed by Street and Stevens. B, Three-year follow-up of a Stevens-Street prosthesis. Note the new cortical bone growth around the prosthesis. (From Street, D. M., and Stevens, P. A.: A humeral replacement prosthesis for the elbow: Results in ten elbows. J. Bone Joint Surg. 56A:1147, 1974.)

In 1981, we36 reported the results of 80 Mayo and Coonrad prostheses in 72 patients. The results were good in 60%, fair in 16%, and poor in 24%.36 Revisions were frequent, however, and were related to the early deficiencies of surgical technique, poor understanding of essential joint design features, and poor knowledge of elbow biomechanics. The complication rate was 55%, including loosening, infection, triceps rupture, ulnar neuropathy, and medial or lateral condyle fracture. Nevertheless, pain relief was excellent and functional motion (24 to 129 degrees) encouraged our group to the further use and development of total elbow joint replacement. Two major developments in the redesign of the Coonrad prosthesis, along with an improved surgical approach and cementing techniques, led to the continued pursuit of the ideal total elbow joint arthroplasty. Under the direction of Dr. Richard Bryan, a study group of Mayo investigators examined the issue of prosthetic loosening and implant failure. It was concluded that the Mayo snap-fit relatively unconstrained implant was

710

Part VII Reconstructive Procedures of the Elbow

FIGURE 51-6

A

A, The Dee prosthesis was a rigid, metal-on-metal implant that required complete resection of the humerus for implementation. B, Unfortunately, these deficiencies of concept could not be overcome by cement fixation.

B

potentially too unstable and the stem design caused a rotational torque to the humeral articulation. Biomechanical studies suggested that humeral loosening, in particular, might be prevented by better force transfer across what is, in effect, a “weight-bearing” joint. The addition of the anterior flange significantly reduced the problems of the “windshield wiper” effect of stem loosening at the humerus (Fig. 51-13). Better intramedullary cavity bone preparation plus cementing techniques provided more secure fixation of both proximal ulna and distal humerus. As a consequence of these changes, implantation of the Mayo-modified Coonrad prosthesis, the Coonrad II, became the procedure of choice at our institution for the majority of patients requiring total elbow arthroplasty from 1978 to 1981. We applied this design not only in advanced rheumatoid disease but also in osteoarthritis, post-traumatic arthritis, distal humerus nonunion, and supracondylar fractures, as noted earlier. The final design change was the addition of the anterior flange in 1981 and altering the surface preparation of the proximal ulna, and distal humerus, to provide further improvement in prosthetic fixation and overall stability. This is termed the Coonrad-Morrey and, with some modifications, is still in use today. In summary, with an appreciation of forces at the elbow, the mode of failure and normal elbow kinematics, the original Coonrad I design was modified. The

Coonrad II implant (1978) had a loose articulation allowing varus/valgus and rotation laxity at the articulation. The Coonrad III was termed the Coonrad-Morrey after introduction of the flange at the humeral stem.

CURRENT DIRECTION As discussed subsequently, especially in Chapter 52, innovation and reassessment continues. The advantages of unlinked devices is being readdressed by considering a radial head to enhance stability. The flange is recognized to stabilize the bone cement interface (Fig. 51-14). Challenges of technique are being recognized by designing more sophisticated instrumentation. The more anatomic designs have also prompted the implantation of the humeral component as a “hemireplacement” when the proximal radial and ulnar articulations are intact (see Chapter 52B). Finally, the ability to convert an unlinked to a linked articulation real time during surgery is also now available in some designs (Acclaim, Lattitude) (see Fig. 51-14).

Complications Complications related to total elbow replacement have also decreased (see Chapter 61) and overall, a safe, functional, and long-term satisfactory outcome to the multiple types of arthritic deformity may be anticipated. Yet,

Chapter 51 Elbow Arthroplasty: Historical Perspective and Emerging Concepts

A

711

B

FIGURE 51-7

C

A, The original GSB was a rigid metal-on-metal articulation. B, Severe osteolysis resulted from this design. C, The current version allows rotation and translation through polyethylene bushing.

B

C

FIGURE 51-8

A, The Pritchard-Walker articulated generation II design provided an 8-degree varus/ valgus laxity of the articulation. B and C, The Arizona design was a snap fit device that also incorporated a radiohumeral element with radial head replacement and capittelar resurfacing.

FIGURE 51-9 Original Coonrad prosthesis consisted of a polyethylene bushing at the humerus and a polyethylene insert at the ulna.

Chapter 51 Elbow Arthroplasty: Historical Perspective and Emerging Concepts

713

A

C

FIGURE 51-10 A, “Anatomic” or “resurfacing” total elbow prosthesis are best termed “unlinked.” Wadsworth’s experience demonstrated the need for a stem. B, The capitellocondylar prosthesis was more anatomic with a humeral design to allow articulation with a radial head component. C, The Souter-Strathclyde metal humeral and polyethylene ulnar component was the most constrained of all unlinked devices. D, Pritchard unconstrained ulnohumeral, with radial head humeral articulation. Technical and design problems rendered this unreliable. E and F, The Questor designed by Sorbie is one of the most sound implants.

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Part VII Reconstructive Procedures of the Elbow

FIGURE 51-10, cont’d

G, The Kudo Elbow System is a cobalt-chrome alloy humeral component articulated with a polyethylene bearing titanium alloy ulnar component. The current humeral stem achieves fixation without cement.

A FIGURE 51-11

B

A, The initial Mayo design was suggested by Dr. James Beckley, a senior resident. The stem proved to be weak, and the articulation was unstable. B, The next effort, designed principally by Linscheid, Dobyns, and Bryan, incorporated a snap-fit type of simulation for the ulnohumeral joint and option for radial head replacement. The off-center stem provided insufficient stabilization and the implant frequently loosened.

Chapter 51 Elbow Arthroplasty: Historical Perspective and Emerging Concepts

715

FIGURE 51-12 The final Mayo design was implanted in 1979. A more refined snap-fit, more anatomic distal humeral replication was achieved. The design included a flange to resist the posterior directed forces. Unfortunately, this implant was unstable and dislocated in only the second patient to be inserted and it was abandoned.

the history of total elbow arthroplasty still has not been fully told because better materials, biomechanical analysis of forces, prosthetic designs, ligament reconstructions, and protection against infection are developed by interested clinical and basic researchers.37,42 The story, to date, has been an interesting and challenging effort of combining anatomy, mechanics, and surgical experience to produce options for total elbow replacement with progress continued to be made.

CHOICE OF JOINT IMPLANT REPLACEMENT

FIGURE 51-13 Mayo modified Coonrad implant (Coonrad-Morrey). A, Disarticulated lateral view of the prosthesis demonstrating changes from the original design, which include sintered proximal ulna and distal humerus components, anterior flange with the humeral component, and polyethylene bushing. B, Anterior view with humeral and ulnar components shown and polyethylene bushings.

Today, given the options available, the choice of a joint implant for elbow reconstructive surgery is usually based on three factors (Table 51-1): (1) the extent and the etiology of the disease process (post-traumatic, degenerative, or rheumatoid process),22,30 (2) the specific needs of the patient, and (3) the experience or preference of the surgeon.30 The disease process is influenced most significantly by the degree of pain, the amount of joint instability, and the limitation of motion that affects the elbow (Table 51-2). Relief of pain is clearly the primary goal of implant arthroplasty.6,10,12,14 In general, with all of the current elbow prostheses, relief of pain can and should be anticipated in 90% to 95% of all patients. The difference between the unlinked and the linked implants is related to the spectrum of pathology that can be successfully addressed by the design. The potential for instability is greater with the unlinked implant,14,16,40 and hence, limits soft tissue release.4,9,30-33,35,39 The complica-

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Part VII Reconstructive Procedures of the Elbow

tions related to neuropathy (ulnar), surgical approach (triceps weakness), and infection are not dissimilar between the design concepts (see Chapters 61 and 63). In the past, elbow surgeons might select different implants based on the primary pathology and potential soft tissue supports requiring treatment. Hence, unlinked implants might be selected for both juvenile- and adultonset rheumatoid disease, provided that collateral ligament stability was reasonably present or could be obtained by implant insertion.1,8,14,15,25,43,45,50 In primary and post-traumatic arthritis, linked implants are generally preferred because there is more clinical experience with their use than with unlinked implants.33 In posttraumatic arthritis cases with bone loss,24 in particular, either the original or, less commonly, a custom-designed semiconstrained implants, loose-hinged articulated implants of Coonrad/Morrey type provide the best option, if not the only solution. In reality, today a surgeon will commonly select a single specific design and employ it for all indications, based on data, preference, or both. Improved motion following elbow arthroplasty is important because after relief of pain, what the patient

A

TABLE 51-1

Elbow Prosthetic Implants Through

the Years Linked

Capitellocondylar19,20

Mayo or Coonrad-Morrey48,53-56

Roper-Tuke2

Trispherical32

London43

Norway63,64

Souter

B FIGURE 51-14 The newer designs include the Discovery (A), a coupled implant with a semiconstrained articulation. This incorporates the flange to resist posterior and rotatory forces. The Latitude (B) employs these characteristics, as well as allows for the incorporation of a radial head implant to better distribute forces. It also has the attractive features of allowing the implant to be stabilized or coupled if the unlinked version appears to be unstable at the time of surgery.

TABLE 51-2

Unlinked

71

Pritchard60

Sorbie*

Arizona74

Kudo38

GSB III (Gschwend)29,30

Pritchard ERS61

Discovery Latitude† Acclaim†

*Personal communication. † May be linked or unlinked.

Stages of Rheumatoid Disease

Mayo Radiographic Stage

Pathology

Radiograph

Operative Treatment and Prosthesis Choice

I

Pathology, mild synovitis

Normal joint surface, osteoporosis

None

II

Moderate synovitis

Joint space narrowed, joint contour maintained

Synovectomy (resurfacing?)

III

Moderate to severe synovitis; mechanical joint contact; loss of joint cartilage

Loss of joint space; mild instability, collateral ligaments intact

Resurfacing implant

IV

Mechanical instability, bone-bone articulation

Complete loss of joint space

Semiconstrained implant

Chapter 51 Elbow Arthroplasty: Historical Perspective and Emerging Concepts

717

Rheumatoid arthritis

Grade I-II

Grade III-IV

Medical management

Success

Yes

No

Synovectomy

Success

Yes No surgery

End

No

Age <50 yrs

No

Yes Interposition arthroplasty

Prosthetic replacement

needs most is the ability to flex the elbow to touch the face and the head and to extend the elbow forward to reach and grasp objects. Unlike the case with the hip or the knee, improved motion at the elbow may be a primary indication for joint replacement. Motion is particularly relevant in patients with concomitant shoulder and wrist disease. Current studies suggest that 30 to 130 degrees will provide a functional arc of motion.34 Unlinked implants13,25,46 reportedly have less extension, 25 to 40 degrees, possibly as a consequence of longer postoperative immobilization to prevent instability. Semiconstrained linked implants average 20 to 130 degrees of motion.18,21,31,36 It is for this reason that a semiconstrained, loose-hinge implant is preferred when the goal is improved motion and stability for the elbow. The unlinked arthroplasty might be preferred by some in the younger patient in whom pain relief is desired and collateral ligaments and joint stability are close to normal, with motion being a secondary consideration. In addition to motion, strength is a relevant consideration.5,10 However, improvement of strength alone is not an indication for elbow replacement. The absence of strength in the triceps and biceps, in itself, is a contraindication to elbow arthroplasty unless muscle transfer (see contraindications) can restore this function. Improvement in strength prompted the development of the triceps-sparing approach of Bryan/Morrey. This has resulted in fewer difficulties with the function and loss of elbow extension strength. Finally, with improved technique and stem designs, reliable fixation is reflected by a lower loosening rate.

FIGURE 51-15 Treatment logic for rheumatoid arthritis—based on Mayo radiographic classification and age of patient.

Traumatic condition

Pain

Yes

Age <60 yrs

Yes

Stable/ Yes aligned

No No Motion <60 degrees

Yes

No

No No surgery

Linked TEA

Interposition arthroplasty

FIGURE 51-16 Treatment logic for traumatic arthritis based on pain, motion, and age.

This, in turn, has resulted in more frequent demonstration of bushing wear, which has been shown to be associated with longevity and correcting longstanding deformity.26 Our current “logic” for the management of rheumatoid arthritis and for post-traumatic conditions including joint replacement is demonstrated in the treatment algorithms depicted in Figures 51-15 and 51-16, respectively.

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Part VII Reconstructive Procedures of the Elbow

References 1. Ackerman, G., and Jupiter, J. B.: Nonunion of fractures of the distal end of the humerus. J. Bone Joint Surg. 70A:75, 1988. 2. Allieu, Y., Meyer zu Reckendorf, G., and Daude, O.: Longterm results of unconstrained Roper-Tuke total hip arthroplasty in patients with rheumatoid arthritis. J. Shoulder Elbow Surg. 7:560, 1998. 3. Barr, J. S., and Eaton, R. G.: Elbow reconstruction with a new prosthesis to replace the distal end of the humerus: A case report. J. Bone Joint Surg. 47A:1408, 1965. 4. Bell, S., Gschwend, N., and Steiger, U.: Arthroplasty of the elbow. Experience with the mark III GSB prosthesis. Aust. N.Z. J. Surg. 56:823, 1986. 5. Bryan, R. S., and Morrey, B. F.: Extensive posterior exposure of the elbow: Triceps sparing approach. Clin. Orthop. 166:199, 1982. 6. Connor, P. M., and Morrey, B. F.: Total elbow arthroplasty in patients who have juvenile rheumatoid arthritis. J. Bone Joint Surg. 80A:678, 1998. 7. Coonrad, R. W.: History of total elbow arthroplasty. In Inglis, A. E. (ed.): Upper Extremity Joint Replacement (Symposium on Total Joint Replacement of the Upper Extremity, 1979. St. Louis, C. V. Mosby Co., 1982. 8. Davis, R. F., Weiland, A. J., Hungerford, D. S., Moore, J. R., and Volenec-Dowling, S.: Nonconstrained total elbow arthroplasty. Clin. Orthop. 171:156, 1982. 9. Dee, R.: Total replacement arthroplasty of the elbow for rheumatoid arthritis. J. Bone Joint Surg. 54B:88, 1972. 10. Dobyns, J. H., Bryan, R. S., Linscheid, R. L., and Peterson, L. F. A.: The special problems of total elbow arthroplasty. Geriatrics 31:57, 1976. 11. Engelbrecht, E., Bucholz, H. W., Rottger, J., and Siegal, A.: Total elbow replacement with a hinge and a nonblocked system. In Joint Replacement of the Upper Limb. London, Mechanical Engineering Publications, 1978. 12. Ewald, F. C.: Total elbow replacement. Orthop. Clin. North Am. 6:685, 1975. 13. Ewald, F. C.: Nonconstrained metal to plastic total elbow arthroplasty. In Inglis, A. E. (ed.): Symposium on Total Joint Replacement of the Upper Extremity. St. Louis, C.V. Mosby Co., 1982, p. 141. 14. Ewald, F. C., Scheinberg, R. D., Poss, R., Thomas, W. H., Scott, R. D., and Sledge, C. B.: Capitellocondylar total elbow arthroplasty: Two- to five-year follow-up in rheumatoid arthritis. J. Bone Joint Surg. 62A:1259, 1980. 15. Ewald, F. C., Simmons, E. D., Sullivan, J. A., Thomas, W. H., Scott, R. D., Poss, R., Thornhill, T. S., and Sledge, C. B.: Capitellocondylar total elbow replacement in rheumatoid arthritis: Long-term results. J. Bone Joint Surg. 75:498, 1993. 16. Friedman, R. J., Lee, D. E., and Ewald, F. C.: Nonconstrained total elbow arthroplasty. J. Arthroplasty 4:31, 1989. 17. Garrett, J. C., Ewald, F. C., Thomas, W. H., and Sledge, C. B.: Loosening associated with GSB hinge total elbow replacement in patients with rheumatoid arthritis. Clin. Orthop. Rel. Res. 127:170, 1977.

18. Gill, D. R., and Morrey, B. F.: The Coonrad-Morrey total elbow arthroplasty in patients who have rheumatoid arthritis: A 10 to 15 year follow-up study. J. Bone Joint Surg. 80A:1327, 1998. 19. Gschwend, N., Loehr, J., Ivosevic-Radovanovic, D., and Scheler, H.: Semiconstrained elbow prostheses with special reference to the GBS III prosthesis. Clin. Orthop. 232:104, 1988. 20. Gschwend, N., Simmen, B. R., and Matejovsky, Z.: Late complications in elbow arthroplasty. J. Shoulder Elbow Surg. 5(2 Pt 1):86, 1996. 21. Inglis, A. E., and Pellicci, P. M.: Total elbow replacement. J. Bone Joint Surg. 62A:1252, 1980. 22. Inglis, A. E., Ranawat, C. S., and Straub, L. R.: Synovectomy and débridement of the elbow in rheumatoid arthritis. J. Bone Joint Surg. 53A:652, 1971. 23. Johnson, E. W., Jr., and Schlein, A. P.: Vitallium prosthesis for the olecranon and proximal part of the ulna: Case report with thirteen-year follow-up. J. Bone Joint Surg. 52A:721, 1970. 24. King, G. J., Itoi, E., Niebur, G. L., Morrey, B. F., and An, K. N.: Kinematics and stability of the Norway elbow. Acta Orthop. Scand. 64:657, 1993. 25. Kudo, H., Iwano, K., and Watanabe, S.: Total replacement of the rheumatoid elbow with a hingeless prosthesis. J. Bone Joint Surg. 62A:277, 1980. 26. Lee, B. P., Adams, R. A., and Morrey, B. F.: Polyethylene wear after total elbow arthroplasty. J. Bone Joint Surg. 87A:1080, 2005. 27. London, J. T.: Endoprosthetic prosthetic replacement of the elbow. In Morrey, B. F. (ed.): The Elbow and Its Disorders. Philadelphia, W. B. Saunders, 1985, p. 540. 28. MacAusland, W. R.: Replacement of the distal end of the humerus with a prosthesis: Report of four cases. West. J. Surg. 65:557, 1954. 29. Mellen, R. H., and Phalen, G. S.: Arthroplasty of the elbow by replacement of the distal end of the humerus with an acrylic prosthesis. J. Bone Joint Surg. 29:348, 1947. 30. Morrey, B. F.: Elbow replacement arthroplasty: Indications and patient selection. In Morrey, B. F. (ed.): Joint Replacement Arthroplasty. New York, Churchill Livingstone, 1991, p. 275. 31. Morrey, B. F., and Adams, R. A.: Semiconstrained total elbow arthroplasty for rheumatoid arthritis. J. Bone Joint Surg. 74A:479, 1992. 32. Morrey, B. F., and Adams, R. A.: Semiconstrained elbow replacement for distal humeral nonunion. J. Bone Joint Surg. 77B:67, 1995. 33. Morrey, B. F., Adams, R. A., and Bryan, R. S.: Total replacement for post-traumatic arthritis of the elbow. J. Bone Joint Surg. 73B:607, 1991. 34. Morrey, B. F., Askew, L. J., An, K. N., and Chao, E. Y.: A biomechanical study of normal functional elbow motion. J. Bone Joint Surg. 63A:87, 1981. 35. Morrey, B. F., and Bryan, R. S.: Total joint arthroplasty: The elbow. Mayo Clin. Proc. 54:507, 1979. 36. Morrey, B. F., Bryan, R. S., Dobyns, J. H., and Linscheid, R. L.: Total elbow arthroplasty: A five-year experience at the Mayo Clinic. J. Bone Joint Surg. 63A:1050, 1981.

Chapter 51 Elbow Arthroplasty: Historical Perspective and Emerging Concepts

37. O’Driscoll, S. W., Tanaka, S., An, K. N., and Morrey, B. F.: The semiconstrained total elbow replacement: A biomechanical analysis. J. Bone Joint Surg. 74B:297, 1992. 38. Peterson, L. F. A., and James, J. A.: Surgery of the rheumatoid elbow. Orthop. Clin. North Am. 2:667, 1971. 39. Pritchard, R. W.: Long-term follow-up study: Semiconstrained elbow prosthesis. Orthopedics 4:151, 1981. 40. Pritchard, R. W.: Anatomic surface elbow arthroplasty: A preliminary report. Clin. Orthop. 179:223, 1983. 41. Risung, F.: The Norway elbow prosthesis system: Six years experience. Presented at the 1993 European Rheumatoid Arthritis Surgery Society, Oslo, Norway. 42. Risung, F.: The Norway elbow replacement: Design, technique and results after nine years. J. Bone Joint Surg. 79B:394, 1997. 43. Ruth, J. T., and Welde, A. H.: Capitellocondylar total elbow arthroplasty. J. Bone Joint Surg. 74A:95, 1992. 44. Schlein, A. P.: Semiconstrained total elbow arthroplasty. Clin. Orthop. Relat. Res. 121:222, 1976.

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45. Schwyzer, H. K., Simmen, B. F., and Gschwend, N.: Infekt nach Schulter-und Ellbogenarthroplastik. Diagnostik Therapie. Orthopade 24:367, 1995. 46. Souter, W. A.: Arthroplasty of the elbow: With particular reference to metallic hinge arthroplasty in rheumatoid patients. Orthop. Clin. North Am. 4:395, 1973. 47. Street, D. M., and Stevens, P. S.: A humeral replacement prosthesis for the elbow: Results in ten elbows. J. Bone Joint Surg. 56A:1147, 1974. 48. Venable, C. S.: An elbow and an elbow prosthesis: Case of complete loss of the lower third of the humerus. Am. J. Surg. 83:271, 1952. 49. Volz, R. G.: Development and clinical analysis of a new semiconstrained total elbow prosthesis. In Inglis, A. E. (ed.): Upper Extremity Joint Replacement Symposium on Total Elbow Joint Replacement of the Upper Extremity, 1979. St. Louis, C. V. Mosby Co., 1982. 50. Weiland, A. J., Weirs, A. P. C., Wells, R. P., and Moore, J. R.: Capitellocondylar total elbow replacement. J. Bone Joint Surg. 71A:217, 1989.

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CHAPTER

52

Unlinked Arthroplasty Jeffery S. Hughes, Bernard F. Morrey, and Graham J. W. King

PART A Distal Humeral Hemiarthroplasty Jeffery S. Hughes

INTRODUCTION Distal humeral hemiarthroplasty (DHH) was first described in 1947, yet over the past 60 years there have been only a few small series reporting on this technique.1,14,17,25-28 Early series reported treatment of a variety of pathologic conditions, including trauma, inflammatory arthritis, and tumor. Prostheses included both custom-made (of various materials) and nonanatomic humeral components from total elbow systems (capitellocondyllar, kudo) and anatomic components (Street). These early surgeries met with mixed results. The past decade has witnessed renewed interest in DHH with advancements in our understanding of elbow biomechanics and with growing experience in the difficulty of achieving effective outcomes in treating complex distal humerus fractures. This technique provides a treatment alternative that bridges the gap between internal fixation and total elbow arthroplasty (TEA) in unsalvageable distal humeral articular surface pathologies.

INDICATIONS AND CONTRAINDICATIONS The indications for DHH are evolving, both in terms of what is achievable and what is appropriate (Table 52-1). Initial experience has been in the younger patient or the physically active older patient with a comminuted intraarticular distal humeral fracture (sometimes combined with a column fracture) that involves both trochlea and

capitellum, where an adequate reduction and internal fixation cannot be achieved. Open reduction internal fixation (ORIF) remains the gold standard of operative treatment; however, patient factors and bone architecture may limit the surgeon’s ability to reconstruct the elbow. Series reporting on ORIF of comminuted intraarticular fractures indicate a substantial rate of unsatisfactory outcomes and a significant complication rate in complex cases.1,14,17,23,24 Total elbow arthroplasty has gained acceptance as a primary treatment option for intra-articular distal humeral fractures in lower demand, elderly patients with osteopenic bone.4,9-11,20,22 Its application to younger active patients is attendant with the risk of early prosthesis failure. Current indications for DDH include (1) acute trauma, (2) salvage of failed internal fixation, (3) chronic malunion or nonunion, (4) avascular necrosis of the trochlea with collapse of subchondral bone, and (5) tumors of the trochlea where resection allows preservation of the epicondyles and collateral ligaments. The use in inflammatory joint disease may need to be revisited. Early use of hemiarthroplasty with rheumatoid arthritis resulted in a stiff painful joint. However, there may be a role in the young patient with “burnt-out” inflammatory joint or the patient on disease-modifying agents in whom the joint is eburnated and the architecture relatively congruent. Contraindications to DHH include overt local or distant foci of infection; inadequate neurovascular status; insufficient bony column support, especially epicondyle or condylar comminution resulting in implant instability; and poor soft tissue coverage. An intact radial head and coronoid are essential for adequate joint stability. Articular cartilage damage of the radial head and sigmoid fossa due to chronic fracture arthrofibrosis or inflammatory arthropathy may lead to inadequate pain relief, less function, and uncertain longevity. This represents a relative contraindication that may favor a linked TEA. Developmental humeral insufficiency resulting in a nonanatomic ulna architecture, such as a “fishtail deformity,” is a contraindication to DHH.

PRINCIPLES OF DISTAL HUMERAL HEMIARTHROPLASTY Stability of the intact elbow joint is provided by ulnohumeral congruity,18 a competent radiocapitellar articulation, and collateral ligament integrity.5 Because DHH is an “unlinked” reconstruction, the prosthesis must have a high degree of congruency with the radius and ulna to provide stable force transmission through both medial and lateral articular columns; therefore, sizing is important. For the DHH to function optimally, the prosthesis

Chapter 52 Unlinked Arthroplasty

TABLE 52-1

721

Indications and Contraindications for Humeral Hemiarthroplasty

Indications

Contraindications

Trauma Acute Chronic (failed ORIF/malunion/nonunion) Avascular necrosis Steroid/trauma Tumors Resection allows preservation of the epicondyles and collateral ligaments Inflammatory Joint Disease The use in inflammatory joint disease may need to be revisited. Early use of hemiarthroplasty with rheumatoid arthritis resulted in a stiff painful joint; however, there may be a role in the “burnt out” inflammatory joint where the joint is eburnated and the architecture relatively congruent.

Infection/poor soft tissue coverage Chronic instability Inadequate neurovascular status Insufficient bony column support, especially epicondyle condylar comminution resulting in instability Radial head resection/coronoid insufficiency Developmental humeral insufficiency Nonanatomic Ulnar Architecture (e.g., Fishtail Deformity)

ORIF, open reduction and internal fixation.

must be oriented such that the elbow rotation axis relative to the insertions of the anterior band of the medial collateral ligament (MCL) and lateral ulnar collateral ligament (LUCL) is restored.3 This ensures that the ligaments remain isometric through a functional range of motion. The proper joint rotation axis can be determined by surface landmarks, medially at the anterior inferior surface of the medial epicondyle and laterally at the center of a circle formed by the articular surface of the capitellum.2,5-8,19,21 Given these considerations, the prerequisites for implantation of a DHH include (1) the ability to reconstruct both medial and lateral columns; (2) intact or stable reconstruction of the radial head and coronoid process; and (3) intact or reparable MCL and LUCL. Good exposure (e.g., olecranon osteotomy) is generally required to achieve all these goals.

IMPLANT CONSIDERATIONS There are currently two systems available (and an additional one, Coonrad/Morrey [Zimmer, Warsaw, IN] under development) that allow DHH with a prosthesis based on normal articular geometry (Fig. 52-1): (1) the Sorbie Questor elbow system (Wright Medical Technologies, Arlington, TN) and (2) the Latitude elbow system (Tornier, Stafford, TX). All require cement fixation and, because they may be subjected to significant forces, optimal cementing techniques should be used.7 The Sorbie Questor humeral component is a monoblock anatomic prosthesis with three sizes (small, medium, and large) that allow a “best fit” in 95% of all elbows.29 It allows fixation of comminuted bone fragments of either supracondylar column. There is no anterior flange or

long-stem option to augment humeral fixation. This system allows conversion only to an unconstrained TEA, which may not address future instability issues. Mechanical studies of the Sorbie humeral component indicate that an intact radial head is necessary for elbow stability despite an intact MCL.13 It is attractive because it removes little bone and is relatively easy to insert. The Latitude system has three stem sizes that articulate with six sizes of modular anatomic spools. The central stem has medial and lateral column extensions that house an axis pin, which facilitates positioning of the component relative to the collateral insertions before insertion. Although reconstruction of the epicondyles with the attached collateral ligaments is the preferred technique, a hole through the central axis of the prosthesis permits suture fixation of the collateral ligaments if stable bony architecture of the ligament insertions is not possible. An anterior flange allows bone grafting to reduce the risk of prosthesis loosening. Added modularity allows conversion to either an unlinked or a linked TEA.

PREOPERATIVE PLANNING Preoperative imaging studies should include anteroposterior (AP) and lateral views of the elbows. Plain radiographs of the contralateral elbow permit additional templating of the distal humerus for appropriate prosthesis sizing. Sizing is based on the direct correlation between the AP dimensions of the normal articular surface and the radii of the capitellum and trochlea (Fig. 52-2).26 Preoperative assessment might also include a fine-cut computed tomography (CT) scan to evaluate articular comminution, column involvement, and asso-

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Part VII Reconstructive Procedures of the Elbow

FIGURE 52-1

A

B

A, Sorbie Questor hemiarthroplasty. B, Latitude prosthesis with anatomic spool.

complex cases, the necessary instruments for both internal fixation and hemiarthroplasty are available in the operating room and the decision to perform DHH is made on surgical inspection of the fracture. In many cases, combined techniques are used if column fixation is necessary to stably implant the humeral prosthesis, including precontoured periarticular plates, threaded Kirschner wires (K-wires), and tension band sutures. Newer locking plates allow insertion of short, unicortical screws to allow passage of the prosthetic stem in the humeral canal. Timing of the procedure is not crucial, as long as the procedure is undertaken in 7 to 10 days after acute fracture to lessen the possibility of heterotopic ossification. FIGURE 52-2

The anteroposterior radiograph is templated to ensure anatomic reconstruction and to avoid mismatch or overstuffing of the joint. The longitudinal axis of the radial neck should align with the center of the capitellum with the sigmoid fossa being congruent with the prosthesis.

ciated injuries to the radial head and coronoid (Fig. 52-3). Except in cases in which a decision has been made to proceed directly to TEA, we approach all distal humerus fractures with the aim of internal fixation. In

OPERATIVE TECHNIQUE The patient is positioned in the lateral decubitus position. A tourniquet is applied and the arm secured to a short arm support. This allows flexion of the arm to 120 degrees, which facilitates insertion of the component. This also places the posterior aspect of the distal humerus parallel to the floor, when the elbow is flexed 90 degrees. A large sterile basin is placed beneath the arm to catch any bone fragments or instruments. The elbow is approached through an extensile posterior incision, and thick subcutaneous flaps are developed to provide

Chapter 52 Unlinked Arthroplasty

723

A

FIGURE 52-3

B C

access to both epicondyles and columns. The ulna nerve is exposed and protected. A Chevron osteotomy of the olecranon is performed at the level of the sigmoid fossa bare area, and the triceps mechanism is reflected sufficiently proximal to expose any supracondylar fracture extension (see Chapter 7). “Triceps-on” exposures provide poorer exposure and are associated with increased joint instability. During exposure, the humeral insertions and origins of the MCL and LUCL must be preserved. Once exposed, the articular surface can be inspected. If the combination of fracture comminution, osteopenia, and patient considerations favors DHH then trial components should be templated with the radial head and anterior sigmoid fossa to confirm proper fit and to avoid overstuffing of the joint. Injury to the radial head, coro-

A, Comminuted fracture of the distal humerus in a 53-year-old woman. Computed tomography scan more accurately defines the degree of comminution and trochlear involvement. B, Posterior exposure via a chevron osteotomy with preservation of the collateral ligaments. The axis of the prosthesis is aligned with the collateral ligament attachments. C, Anteroposterior x-ray study of Latitude hemiarthroplasty.

noid, and collateral ligaments must be identified to proceed with this option and to ensure a stable reconstruction (see Fig. 52-3). We have currently extended the indications even to those with fractured supracondylar columns. This may not be appropriate for all surgeons to consider, but if this type of pathology is undertaken, before any supplemental column fixation, the humeral canal is opened with a burr and broached. Inserting a trial humeral component will help prevent comprising the canal with ORIF implants. Column reduction must be anatomic so that the insertions of the collateral ligaments will allow proper restoration of the rotation axis. After provisional K-wire fixation, the appropriate precontoured plate is applied if fixation is inadequate.

724

Part VII Reconstructive Procedures of the Elbow

Next, the bone cuts must be made so that the prosthesis can be inserted to the proper depth and rotation to recreate the flexion axis. Free-hand cuts are generally preferred because bone loss from fracture comminution complicates accurate placement of the cutting jigs. The trial prosthesis of appropriate size is inserted. Strict attention should be paid to the depth of insertion and rotation when the trial is seated because this determines ligament tension. Once the trial is in place, the ulna is reduced over its articular surface and the joint taken through a range of motion. Difficulty reducing the ulna suggests that the flexion axis is too distal, and the humeral cuts should be revised to prevent an overly tight reconstruction. The tracking of the anterior half of the olecranon during elbow flexion and extension can also provide a sense of the correct prosthesis rotation (Table 52-2). A cement restrictor should be used to provide good pressurization of the antibiotic cement. The final prosthesis is then inserted to the correct position. The ulna is reduced to the distal humeral prosthesis, and the TABLE 52-2

elbow is extended (not cycled) until the cement is cured. The olecranon osteotomy is fixed using a tension band or a periarticular olecranon plate and always grafted with autologous bone from the trochlea (Fig. 52-4). Although the plate provides the best fixation (and therefore allows more aggressive early mobilization), there are times when soft tissue considerations prevent its use. The elbow should then be taken through a range of motion to ensure the following: (1) motion has not been constrained by an overly tight reconstuction; (2) the olecranon osteotomy remains reduced as tension develops in flexion; and (3) the ulna nerve does not develop undue tension or encroachment by neighboring hardware. The nerve is transposed as necessary.

TREATMENT OF NONACUTE INJURIES Hemiarthroplasty may also be used as a salvage reconstruction in cases of malunion, fixation failure, or nonunion after open reduction internal fixation. In these

Pitfalls and Complications of Hemiarthroplasty

Problem

Cause

Solution

Flexion contracture (intraoperative)

Oversized spool

Check template, trial spool directly onto radial head and coronoid Insert implant deeper Anterior capsular release

Prosthetic axis distal to ligament axis Capsular contracture Joint translocation

Undertensioned collateral ligament repair Overtensioned collateral ligament repair

Reassess ligament repair

Rotatory instability

Malrotation of component Incomplete restoration of column length Failed repair LCL

EUA with radiograph Address identifiable causes

Block to flexion

Displaced fracture fragments Bone cement extravasation Heterotopic ossification

Check intraoperative radiograph Await maturation and resect

Radiocapitellar mismatch

Spool size incorrect PLRI

Revise spool See instability

Olecranon osteotomy nonunion

Inadequate fixation Inadequate biology

Accurate reduction Robust ORIF-plate Bone graft all osteotomies

Ulna neuritis

Acute neurapraxia preoperatively Increased neural tension Ulnar instability

Neurolysis? Transposition? Check depth of implant insertion Ulnar transposition

Painful joint

Overstuffed joint Arthrolysis Sepsis (Staph. epi/Prop. acnes) Loose prosthesis Nonunion (condyle/osteotomy)

Downsize spool Revise to TEA Serology/aspirate/staged TEA Serology/aspirate/staged TEA Serology/ORIF+/− bone graft

Stiff elbow

Overstuffed joint Arthrofibrosis Heterotopic ossification

Downsize spool Revise position of joint axis? Surgical release at 6/12

EUA, examination under anesthesia; LCL, lateral collateral ligament; ORIF, open reduction and internal fixation; PLRI, posterolateral rotatory instability; TEA, total elbow arthroplasty.

Chapter 52 Unlinked Arthroplasty

725

POSTOPERATIVE PROTOCOL Patients start passive range of motion from 20 to 100 degrees, using either continuous passive motion or hourly, self-guided flexion, extension, pronation and supination. Night-time extension splinting is commenced early and changed at 6 weeks to a padded turnbuckle in patients with a significant flexion contracture. Active assisted flexibility exercises are begun at 4 to 6 weeks, along with antigravity extension exercises. Active use of the arm for daily functions is discouraged for 6 weeks if a column fixation was performed as part of the reconstruction. Serial radiographs are obtained to follow healing of the olecranon osteotomy and any other internal fracture fixation. Pending adequate healing, resistive strengthening is withheld until 10 to 12 weeks.

PITFALLS AND COMPLICATIONS

FIGURE 52-4

Fixation of the olecranon osteotomy with a contoured plate.

instances, the principles of the reconstruction are the same in terms of restoring the column architecture, preserving the collateral ligaments and recreating the rotation axis (Fig. 52-5). A thorough surgical débridement is essential, and in the case of nonunion, tissue should be sent for histopathology and microbiology assessment to rule out infection. Once tissue is obtained, regional infusion of antibiotics is performed to provide optimal tissue levels in already compromised soft tissues. If supracondylar bone loss is present following débridement, a shortening osteotomy may be required, along with medial and lateral plate fixation. Autologous bone graft is routinely used to promote bony union (Fig. 52-6). The ability to achieve a stable reconstruction should be carefully considered in these complex cases in which bony and soft tissue anatomy may have been significantly altered by prior injury and treatment. If concern exists about this ability then a linked TEA may offer a more reliable reconstructive option. Articular cartilage damage of the radial head and sigmoid fossa due to arthrofibrosis or inflammatory arthropathy may lead to inadequate pain relief, reduced functional outcomes, and uncertain longevity. This represents a relative contraindication that may favor a linked TEA. Thus, if a DHH is planned, it probably should be undertaken early rather than late in a failed ORIF.

Potential pitfalls and corresponding considerations and solutions are listed in Table 52-2. Many of these pitfalls can be addressed by meticulous surgical technique, a thorough understanding of elbow biomechanics, and knowledge of the prosthesis systems as they relate to restoring articular geometry and elbow stability. Joint stiffness may occur despite a properly performed reconstruction and early mobilization. If stiffness remains unresponsive to static night splinting, then dynamic splinting can be considered at 2 to 3 months. Persistent stiffness despite these efforts can be managed with contracture release by a column approach at 6 to 12 months postoperatively. Heterotopic ossification, although not common, may occur in the setting of severe elbow trauma (Fig. 52-7A). This is managed by excision and contracture release when the bone is radiographically mature. Instability appears to be related to triceps on exposures, epicondyle comminution, and incorrect collateral ligament reconstruction (see Fig. 52-7B). Late complications can include the development of arthrosis of the sigmoid notch due to mismatch with the size or orientation of the prosthesis. If these patients have disabling mid-arc pain, conversion to a linked TEA may be necessary. Implant loosening, periprosthetic fracture, and late infection are also possible.

RESULTS Table 52-3 lists the series of DHH to date. Although long-term prospective data are lacking, except in a few anecdotal case reports, early experience has yielded several observations. First, DHH can lead to substantial

726

Part VII Reconstructive Procedures of the Elbow

A

B

FIGURE 52-5

C

pain relief and improvement in function after complex distal humerus fractures. Second, treatment of acute fractures generally results in more favorable outcomes than salvage reconstruction of nonunion, malunion and hardware failure. Third, DHH has proven less effective in chronic conditions such as inflammatory arthritis and hemophilia. Repeat procedures are usually related to hardware removal for fracture or osteotomy fixation. Revision of components is relatively simple especially with the modular systems that can be converted to linked TEA. Future prospective evaluation will better define indications, technique, restrictions and the longterm effectiveness of DHH.

A 26-year-old man with compound traumatic loss of trochlea and capitellum, fractured radial head and coronoid, treated with débridement, internal fixation of radial head and coronoid, and application of external fixator in distraction. At 3 months, a hemiarthroplasty via an olecranon osteotomy was performed. A and B, Initial fixation of the radial head and a external fixator. C, Latitude hemiarthroplasty with united radial head.

CONCLUSION Treatment of complex distal humerus fractures or loss of trochlea architecture can be demanding. Although internal fixation and TEA have proven effective in many cases, there are circumstances for which neither represents an ideal treatment. These circumstances include younger or physically active patients. DHH offers an alternative that can provide immediate stability and early mobilization with less risk of implant failure compared with a linked TEA. This is a technically demanding procedure that requires experience with both distal humeral fracture fixation and TEA. Combined techniques may be

Chapter 52 Unlinked Arthroplasty

A

B

FIGURE 52-6

A, Established nonunion with associated avascular necrosis of the lateral trochlea, requiring column reconstruction with periarticular plates and bone grafting. B, Intraoperative fluoroscopic assessment.

A

B

FIGURE 52-7 Complications. A, Heterotopic ossification following distal humeral hemiarthroplasty in acute fracture. Should it result in functional loss of movement, it can be resected with predictable good results. B, Instabilty due to inadequate lateral column/lateral collateral ligament reconstruction, requiring urgent revision fixation.

727

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Part VII Reconstructive Procedures of the Elbow

Results of Hemiarthroplasty

TABLE 52-3 Author

No.

Mellen and Phalen17 28

Venable

MacAusland

14 1

Implant

Results

1947

4

Acrylic custom

1952

1

Acrylic custom

1954

4

Nylon custom Custom

Fractured 4 years postoperatively

Distal condylar resurfacing with seven sizes

5 post-traumatic, 3 RhA, 2 inflammatory arthritis/ hemophilia Medial approach Trauma patients: 4/5 painless and functional ROM Inflammatory patients: poor movement/instability

Good pain relief

Barr and Eaton

1965

1

Street and Stevens26

1974

10

Schifrin25

1990

1

Custom prosthesis

20-year follow-up with sustained pain relief, ROM and well-fixed prosthesis

1999

7

Capitellocondylar

Variable results

Papandrea et al

2004

22

Sorbie Questor (Wright Med)

Multicenter report Multiple pathology: acute/chronic, AVN

Hughes, Parsons, O’Brien25

2005

8

Sorbie Questor

Acute and chronic distal humeral fractures 4 acute, 4 chronic distal humeral fractures, age 46 to 83 yrs Postoperative ROM: Ext −10 to −45 (average 22 degrees) Flex 115 to 140 (average 126 degrees) Movement slightly better in patients with acute fracture. ASES Score: Acute: 83.5, Chronic 76.6 Patients with acute distal humeral fractures had less pain than those with chronic humeral fractures Patients with chronic distal humeral fractures all had less pain postoperatively Union was achieved in all column and olecranon osteotomy ORIF, no periprostheic lucent lines

Malone et al.15

2006

29

Sorbie Questor, Latitude

ASES score mean 82.4 (range 64-90), acute 84, chronic 74, ROM Acute 22 to 129 degrees, chronic 41 to 128 degrees Satisfaction: acute 8.0, chronic 8.4

Swoboda and Scott27 22

ASES, American shoulder and elbow score; AVN, avascular necrosis; ORIF, open reduction and internal fixation; RhA, rheumatoid arthritis, ROM, range of motion.

necessary to restore column architecture and resurface the joint. All supplemental fixation must be rigid enough to allow early motion so that the postoperative recovery from DHH can be reduced to the management of the olecranon osteotomy. Based on early encouraging results, we believe that this is a valuable technique that merits continued refinement through surgical experience and ongoing prospective studies. Our experience indicates a more reliable outcome in the acute (80%) than in the delayed, reconstructed (50%) elbow.16

References 1. Barr, J. S., and Eaton, R. G.: Elbow reconstruction with a new prosthesis to replace the distal end of the humerus: A case report. J. Bone Joint Surg. Am. 47:1408, 1965.

2. Beckett, K. S., McConnell, P., Lagopoulos, M., and Newman, R. J.: Variations in the normal anatomy of the collateral ligaments of the human elbow joint. J. Anat. 197:507, 2000. 3. Blewitt, N., and Pooley, J.: An anatomic study of the axis of elbow movement in the coronal plane: relevance to component alignment in elbow arthroplasty. J. Shoulder Elbow Surg. 3:151, 1994. 4. Cobb, T. K., and Morrey, B. F.: Total elbow arthroplasty as primary treatment for distal humeral fractures in elderly patients. J. Bone Joint Surg. Am. 79:826, 1997. 5. Cohen, M. S., and Bruno, R. J.: The collateral ligaments of the elbow: anatomy and clinical correlation. Clin. Orthop. Rel. Res. 383:108, 2001. 6. Cohen, M. S., and Hastings, H. N.: Rotatory instability of the elbow. The anatomy and role of the lateral stabilizers. J. Bone Joint Surg. Am. 79:225, 1997.

Chapter 52 Unlinked Arthroplasty

7. Faber, K. J., Cordy, M. E., Milne, A. D., Chess, D. G., King, G. J., and Johnson, J. A.: Advanced cement technique improves fixation in elbow arthroplasty. Clin. Orthop. Rel. Res. 334:150, 1997. 8. Floris, S., Olsen, B. S., Dalstra, M., Sojbjerg, J. O., and Sneppen, O.: The medial collateral ligament of the elbow joint: anatomy and kinematics. J. Shoulder Elbow Surg. 7:345, 1998. 9. Frankle, M. A., Herscovici, D., DiPasquale, T. G., Vasey, M. B., and Sanders, R. W.: 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 66. J. Orthop. Trauma 17:473, 2003. 10. Gambirasio, R., Riand, N., Stern, R., and Hoffmeyer, P.: Total elbow replacement for complex fractures of the distal humerus. An option for the elderly patient. J. Bone Joint Surg. Br. 83:974, 2001. 11. Garcia, J. A., Mykula, R., and Stanley, D.: Complex fractures of the distal humerus in the elderly. The role of total elbow replacement as primary treatment. J. Bone Joint Surg. Br. 84:812, 2002. 12. Gramstad, G. D., King, G. J., O’Driscoll, S. W., and Yamaguchi, K.: Elbow arthroplasty using a convertible implant. Tech. Hand Up. Extrem. Surg. 9:153, 2005. 13. Inagaki, K., O’Driscoll, S. W., Neale, P. G., Uchiyama, E., Morrey, B. F., and An, K. N.: Importance of the radial head component in Sorbie unlinked total elbow arthroplasty. Clin. Orthop. Rel. Res. 400:123, 2002. 14. MacAusland, W. R.: Replacement of the lower end of the humerus with a prosthesis: A report of four cases. Western J. Surg. Gynec. Obstet. 62:557, 1954. 15. Malone, A. A., Zarkadas, P. C., Hughes, J., and Jansen, S.: American Shoulder and Elbow Surgeons Open Meeting on Biologics in Shoulder Surgery, November 2006. 16. Malone, A., and Hughes, J.: Hemiarthroplasty for the treatment of distal humeral pathology. (Submitted for publication, 2008). 17. Mellen, R. H., and Phalen, G. S. Arthroplasty of the elbow by replacement of the distal portion of the humerus with an acrylic prosthesis. J. Bone Joint Surg. Am. 29:348, 1947. 18. Morrey, B. F., and An, K. N.: Stability of the elbow: osseous constraints. J. Shoulder Elbow Surg. 14(suppl S):174S, 2005. 19. O’Driscoll, S. W., Jaloszynski, R., Morrey, B. F., and An, K. N.: Origin of the medial ulnar collateral ligament. J. Hand Surg. 17:164, 1992. 20. Obremskey, W. T., Bhandari, M., Dirschl, D. R., and Shemitsch, E.: Internal fixation versus arthroplasty of comminuted fractures of the distal humerus. J. Orthop. Trauma 17:463, 2003. 21. Ochi, N., Ogura, T., Hashizume, H., Shigeyama, Y., Senda, M., and Inoue, H.: Anatomic relation between the medial collateral ligament of the elbow and the humero-ulnar joint axis. J. Shoulder Elbow Surg. 8:6, 1999. 22. Papandrea, R., Hughes, J., Sorbie, C., et al: Prosthetic Hemiarthroplasty of the Distal Humerus. ASES Meeting, November 2004.

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23. Parsons, M., O’Brien, R., Jason, H., and Jeffery S.: Elbow hemiarthroplasty for acute and salvage reconstruction of intra-articular distal humerus fractures. Tech Shoulder Elbow Surg. 6:87, 2005. 24. Ray, P. S., Kakarlapudi, K., Rajsekhar, C., and Bhamra, M. S.: Total elbow arthroplasty as primary treatment for distal humeral fractures in elderly patients. Injury 31:687, 2000. 25. Shifrin, P. G., and Johnson, D. P.: Elbow hemiarthroplasty with 20-year follow-up study. A case report and literature review. Clin. Orthop. Rel. Res. 254:128, 1990. 26. Street, D. M., and Stevens, P. S.: A humeral replacement prosthesis for the elbow. Results in ten elbows. J. Bone Joint Surg. 56A:1147, 1974. 27. Swoboda, B., and Scott, R. D.: Humeral hemiarthroplasty of the elbow joint in young patients with rheumatoid arthritis: a report on 7 arthroplasties. J. Arthroplasty 14:553, 1999. 28. Venable, C. S.: An elbow and an elbow prosthesis. Am. J. Surg. 51:1590, 1952. 29. Wevers, H. W., Siu, D. W., Broekhoven, L. H., and Sorbie, C.: Resurfacing elbow prosthesis: shape and sizing of the humeral component. J. Biomed Eng. 7:241, 1985.

PART B Radiohumeral Arthrosis: Anconeus Arthroplasty and Capitellar Prosthetic Replacement Bernard F. Morrey

INTRODUCTION Recognition and focused management of radiohumeral joint arthrosis has emerged over the past several years. Herein we describe the concept and the rationale for capitellar replacement, placing this option in the context of other potential nonprosthetic interventions. One feature that characterizes virtually all of these possibilities is the lack of clinical data of outcomes at this point in time. With the next edition of the book, this whole topic will be much better elucidated. The reader should bear in mind that the information offered here is principally to call attention to the process and to highlight emerging options without claiming at this time that this is the ultimate or final solution to the problem.

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ETIOLOGY Like so many other pathologic conditions, it seems as though the process is more frequent once we are attuned to investigate for its presence. In general, as a condition, primarily osteoarthritis at the elbow, generally considered uncommon in the past, is today well recognized in the orthopedic community.3,6,10,11 Pathology of the radiohumeral joint occurs from primary osteoarthritis, as a sequelae to osteochondritis dissecans, following capitellar fracture, or secondarily to radial head fracture either ignored, treated by open reduction and internal fixation, or by prosthetic replacement. Finally, the condition is seen after split T and Y type of fractures of the distal humerus resulting in malalignment (Fig. 52-8). The frequency and impact of these various conditions is not readily available in today’s literature. There has been some interesting studies referable to primary osteoarthritis of the radiohumeral joint that are worth noting. Ortner13 examined the elbow of a population of Eskimos and South American Indians. As a result of this investigation, the authors describe several forms of osteoarthritis at the radiohumeral joint including (1) hypertrophic bone formation peripheral to the articular surface; (2) hypertrophic bone formation in the radial fossa; (3) increased porosity and hypertrophy of the lateral con-

A

dylar ridge; (4) porosity of the capitellum and; (5) eburnation of the capitellum. These authors note interestingly and accurately that the narrowing of the ulnohumeral joint is not a characteristic of primary osteoarthritis but is more frequently seen at the radiohumeral joint. On the other hand, the osteophyte formation is more commonly observed in the margin of the trochlea and at the coronoid and tip of the olecranon. Subsequently, Goodfellow et al11 documented the increasing incidence of osteoarthritis of the radiohumeral joint with aging and emphasized the early development of the process at the posterior medial ridge separating the trochlea and the capitellum (Fig. 52-9).4 Occupation risks in foundry workers was documented. In general, heavy, repetitive use of the extremity places the joint at risk. Typically, this process appears to be relatively asymptomatic, but with enhanced awareness and closer scrutiny, the presence of radiohumeral joint symptoms is being increasingly appreciated. These observations have been confirmed somewhat in the recent documentation of intervention for primary osteoarthritis of the elbow. Kelly et al7 described radiohumeral narrowing and instances in which the ulnohumeral joint was débrided arthroscopically. They noted that the radial humeral involvement often typically appears to be well tolerated and need not be directly assessed. Others emphasize the

B FIGURE 52-8

Radiohumeral arthritis with primary involvement of the capitellum after capitellar fracture is treated by resection (A). The distal T-condylar fracture resulting in isolated radiohumeral involvement (B).

Chapter 52 Unlinked Arthroplasty

Common extensor ECRL tendon

Brachioradialis

ECRB

W = 3 cm

Triceps lateral head

A

L = 9 cm

731

of primary osteoarthritis. These authors perform radial head resection through the arthroscope and, in so doing, document improved motion in both flexion and extension and pronation and supination.9 The long-term impact, however, of removing the radial head in the presence of ulnohumeral joint arthrosis is unknown. This is one of the major issues that prompts one to consider possibly replacing this joint if it is symptomatic enough to deserve treatment on its own merits.

TREATMENT OPTIONS

Anconeus

Right

B FIGURE 52-9

In some instances joint narrowing of the radiohumeral joint is exhibited as shown by the radiograph and CT (A and B).

technical ability to débride the ulnohumeral joint but do not comment to any extent on the radiohumeral joint. Although both closed7-9 and open procedures1,14,16 are well-accepted means of treating primary osteoarthritis of the elbow, few make reference specifically to the management of the radial head.7,9 Radiographically, however, the radial head involvement has been documented by Dalal.2 In this study of 50 patients with primary osteoarthritis, radial head involvement was present in approximately 85% but was not typically symptomatic. Some narrowing of the joint was present in approximately 60% compared with only 15% narrowing of the ulnohumeral joint. Savoie’s group is one group that has addressed the radiohumeral component

Experience to date on the treatment of isolated radiohumeral arthrosis or particularly a capitellar arthritis is limited. In general, the treatment options include débridement versus reconstruction. The reconstructive options have relatively little data, but these consist of resecting the capitellum, analogous to isolated resection of the radial head but with little data regarding its outcome. Débridement is effective in those with symptomatic osteochondritis dissecans, particularly when the fragment is loose and causing mechanical symptoms (see Chapters 19 and 38). Biologic interposition arthroplasty or prosthetic replacement of the capitellum and/or the capitellum and radial head is a consideration. When the capitellum has been destroyed as a result of fracture, often with resorption, a unique problem exists for which there is no good solution. We have performed allograft replacement with or without interposition arthroplasty in a few of these patients. We have also performed an anconeus rotational plasty in patients with deficient or arthritic capitellum and this does seem to be an effective modality. This procedure does not, however, provide axial stability.12 Without question, one of the greatest problems with the radiohumeral joint relates to problems at the articulation after the radial head has been fractured and treated by fixation or prosthetic replacement. Under these circumstances, the radial head is typically excised or the prosthesis is removed. If the medial collateral ligament is stable, this is adequate treatment. If, however, the medial collateral ligament is unstable, then the major indication for consideration of a prosthetic implant exists. This is intended to satisfy the need to stabilize the “lateral column” in instances in which there is deficient medial collateral ligament or axial instability such as an EssexLopresti lesion. There is some, but limited, experience with prosthetic replacement to date (Pooley J, personal communication).

ANCONEUS ARTHROPLASTY Indications In general, this technique is employed in instances when the proximal radial ulnar or ulnohumeral dysfunction

Part VII Reconstructive Procedures of the Elbow

732

occurs following trauma or resection, or after primary osteoarthrosis. This procedure was designed for two clinical circumstances: (1) radiohumeral impingement, in which the goal is to buffer the proximal radiocapitellar articulation; and (2) rotatory radioulnar impingement.

Anatomy It is important to recognize that the mean length of the anconeus is rather significant, averaging 9 to 10 cm, with a mean width of 3 cm (Fig. 52-10).12,15 The neurovascular survival is by way of a continuation of a branch of the distal radial nerve.

The Surgery 1. The patient is supine, and the arm is brought across the chest. Kocher’s interval is entered and extended proximally past the lateral epicondyle for a distance of about 4 cm. The anconeus is exposed, and the fascia investing the anconeus is split.

2. The muscle is then harvested from distal to the proximal, leaving the proximal pedestal for its neurovascular supply (Fig. 52-11). 3. The anconeus for either application is brought under the lateral collateral ligament. 4. If the goal is to provide a space-occupying buffer between the proximal radius and the distal capitellum, drill holes are placed from posterior to anterior through the capitellum. The anconeus is folded several times on itself in an “anchovy” type of fashion (Fig. 52-12). It is inserted between the radius and the capitellum, and the sutures are securely tied. 5. If the goal is to serve as an interposition between the proximal radius and the ulna, the distal portion of the anconeus is brought distally between the radius

Brachioradialis

Common extensor ECRL tendon

ECRB

W = 3 cm

A

Triceps lateral head

L = 9 cm Anconeus

FIGURE 52-11

The anconeus muscle is reflected from distal to proximal by maintaining its attachment to the triceps to maintain its neurovascular integrity.

R

ANC

U

B FIGURE 52-10 The anconeus muscle is of substantial length, frequently measuring 9 to 10 cm, and is innervated by a terminal branch of the radial nerve distally.

FIGURE 52-12 By folding the anconeus on itself and stabilizing with a suture through the capitellum, the muscle serves as a buffer against proximal radial migration.

Chapter 52 Unlinked Arthroplasty

733

and the ulna. A drill hole is placed in the radius, and the anconeus is wrapped around the proximal radius. The fascia is closed with a running suture.

Aftercare The patient is protected in a splint for approximately 5 to 7 days. Passive motion is then allowed for 2 to 3 weeks. Active full motion is encouraged, starting at about 1 month following surgery.

Outcomes We have reported this technique and our experience in 14 patients who had been treated with one of these types of anconeus interposition arthroplasty with surveillance of at least 2 years (mean, 6.1 years). Twelve of 14 rated their outcome as a success. This included 4 of 5 with Essex-Lopresti injuries (Fig. 52-13).12

A

CAPITELLAR PROSTHETIC REPLACEMENT Indications Specific indications are those instances in which the radiohumeral joint is painful and arthritic and when simple excision of the radial head is not adequate owing to the need to stabilize the lateral joint. The most compelling indications are (1) a need to stabilize the lateral column due to deficiency of the medial collateral ligament or (2) in those in whom there is axial radial instability in the face of capitellar arthrosis or deficiency. The capitellum may be replaced to articulate with the native radial head (Fig. 52-14) or in conjunction with a radial head replacement (Fig. 52-15). The latter requires a polyethylene articulation to articulate with the metallic capitellar device (Fig. 52-16).

Surgical Technique Step 1: Incision. The patient is placed under a general or a regional anesthesia, and a tourniquet is employed. An arm table may be used or the arm may be brought across the chest. A classic Kocher skin incision is made, identifying the interval between the anconeus and the extensor carpi ulnaris. The incision extends approximately 6 to 7 cm. The dissection is carried down to the joint capsule. Step 2: Exposure. If the elbow is stable, the capsule is exposed by elevating a portion of the extensor carpi ulnaris sufficiently to allow identification of the lateral collateral ligament complex (Fig. 52-17). Alternatively, the extensor carpi ulnaris may be split longitudinally, with its fibers staying anterior to the humeral attachment of the lateral collateral ligament. The lateral collateral ligament can be refleced off the lateral epicondyle to expose the capitellum. If the ligament has been disrupted, then the exposure pro-

B FIGURE 52-13 This patient with an Essex-Lopresti lesion was managed by an anconeus interposition arthroplasty. At 1 year, the proximal radial migration is still present, and there are minimal wrist symptoms as well as minimal symptoms at the elbow. Anteroposterior (AP) view of the wrist (A); AP view of the elbow (B).

gresses through the site of disruption to expose the radiohumeral joint. The common extensor tendon and elbow joint capsule are retracted as needed to maximize exposure. Note: If the radial head is not replaced, a greater amount of soft tissue release is necessary for adequate exposure. Step 3. Axis of Rotation. Attach the appropriate sized capitellum template to the drill guide, and align the template to the curvature of the capitellum (Fig. 52-18). The curvature of the edge of the template should align with the most distal articular surface of

734

Part VII Reconstructive Procedures of the Elbow

A

C

1 yr

D B FIGURE 52-14 This patient has traumatic arthritis of the capitellum (A and B). Although the radial head is involved, it is maintained because it is believed to be a more reliable articulation than a prosthetic radial head (C and D).

Chapter 52 Unlinked Arthroplasty

A

735

B

FIGURE 52-15 Patient with a medial collateral ligament laxity and lateral column instability due to significant resection of the radial head and neck (A). Patient treated with capitellar implant and an augmented neck radial head prosthetic replacement. Note a normal ulnohumeral relationship has been restored (B).

ECU

Anconeus

FIGURE 52-16 The radiocapitellar replacement includes a metallic articulation of the capitellum and a polyethylene articulation of the radial head.

the original capitellum. Once alignment is achieved, insert a 0.062 K-wire through the drill guide, and advance medially to the midline of the distal humerus (Fig. 52-19). Leaving the K-wire in place, remove the axis of rotation locator clamp and template. Step 4: Capitellar Resection. There are two resection guide sizes: small and large. Based on the size

FIGURE 52-17 The radial head is exposed in a typical fashion. We employ the Kocher’s interval. The capsule is entered and the attachment to the humerus is released sufficiently to provide adequate exposure for the intended surgery.

of the capitellum, place the appropriate resection guide. Align the resection guide handle so that it is parallel with the long axis of the humerus (Fig. 52-20). Insert a sawblade into the chosen slot in the resection guide, and remove the appropriate amount of capitellum surface. The cut should not involve the trochlea.

Part VII Reconstructive Procedures of the Elbow

736

A

B

FIGURE 52-18 The anatomic center of rotation of elbow flexion is identified laterally by the tubercle of the lateral epicondyle (A). The curvature of the capitellum is matched by the template, which corresponds to the axis of rotation (B).

*Use distal resection slots first

FIGURE 52-20 The resection is of a Chevron type. A distal guide is employed initially to avoid excessive resection.

A

B FIGURE 52-19 (A and B) The axis of rotation is replicated by a .062 K-wire, which is inserted by the use of a targeting guide.

Step 5: Capitellum Trial. Place and stabilize the capitellum trial flush against the resected surfaces (Fig. 52-21). Insert the reference K-wire, which serves as the alignment pin for subsequent preparation.

FIGURE 52-21 A trial reduction allows the insertion of a reference pin, which is used with a cannulated drill, followed by a cannulated rasp.

Step 6: Broaching of the Distal Humerus. Remove the trial capitellum leaving the reference Kwire. Pass the cannulated 0.35-mm drill over the center K-wire to create the broach pilot hole into the distal humerus. Align the broach with the apex of the Chevron cut, insert broach into the pilot hole and advance until the teeth are at the same level as the capitellum osteotomy (Fig. 52-22). Care should be

Chapter 52 Unlinked Arthroplasty

737

A

FIGURE 52-22 The cannulated rasp is carefully aligned to match the apex of the Chevron cut. This provides proper orientation for insertion of the capitellar replacement.

taken to ensure proper alignment and not to overbroach the distal humerus. Step 7: Implanting the Final Component. Once broaching is complete, the definitive implant can be inserted (Fig. 52-23). Distraction of the proximal radius as well as flexion of the elbow may be necessary to allow sufficient access for capitellum insertion. Note: The capitellum may be press-fit or cemented according to surgeon preference. Step 8: C Closure. A No. 5 absorbable suture is placed at the humeral origin of the lateral collateral ligament, and a running locked stitch proceeds distally through the ulnar attachment, then back proximally, ending at the humeral origin of the ligament (Fig. 52-24). The forearm is placed in full or partial pronation, a valgus stress is applied, and the suture tied.

B FIGURE 52-23 The capitellum is inserted from distal laterally (A) and is impacted proximal medially (B). ECU

Aftercare Passive flexion and extension is allowed on the second day, assuming the elbow is considered stable. The goal of radial head replacement and soft tissue repair is to achieve elbow stability. Both flexion/extension and pronation/supination arcs are typically allowed without restriction. Active motion can begin by day 5.

CLINICAL RESULTS There is limited data regarding the use of capitellar prosthetic replacements. In our case series,5 we reported effective treatment of chronic Essex-Lopresti lesions in three patients. Otherwise, we have employed a capitellar

Anconeus

FIGURE 52-24 It is important to stabilize the joint following insertion. We typically employ a running locked stitch using a heavy No. 5 nonabsorbable suture.

738

Part VII Reconstructive Procedures of the Elbow

replacement only in eight additional patients as an isolated replacement, and in four with a radial head replacement as well. To date, there have been no capitellar implant revisions. Using a different design, Pooley (personal communication) has also described the technique and use of a capitellar implant. The primary indication is osteoarthritis. Note: We must emphasize a note of caution here because more information is needed to fully understand the long-term outcome of the procedure.

14. Phillips, N. J., Ali, A., and Stanley, D.: Treatment of primary degenerative arthritis of the elbow by ulnohumeral arthroplasty. A long-term follow-up. J. Bone Joint Surg. 85B:347, 2003. 15. Schmidt, C. C., Kohut, G. N., Greenberg, J. A., Kann, S. E., Idler, R. S., and Kiefhaber, T. R.: The anconeus muscle flap: its anatomy and clinical application. J. Hand Surg. 24A:359, 1999. 16. Wada, T., Isogai, S., Ishii, S., and Yamashita, T.: Debridement arthroplasty for primary osteoarthritis of the elbow. Surgical Technique. J. Bone Joint Surg. 87A:95, 2005.

References 1. Antuna, S. A., Morrey, B. F., Adams, R. A., and O’Driscoll, S. W.: Ulnohumeral arthroplasty for primary degenerative arthritis of the elbow: Long-term outcome and complications. J. Bone Joint Surg. 84A:2168, 2002. 2. Dalal, S., Bull, M., and Stanley, D.: Radiographic changes at the elbow in primary osteoarthritis: A comparison with normal aging of the elbow joint. J. Shoulder Elbow Surg. 16(3):358-361, 2007. 3. Doherty, M., Watt, I., and Dieppe, P. A.: Influence of primary generalized osteoarthritis on development of secondary osteoarthritis. Lancet 2:8, 1983. 4. Goodfellow, J. W., and Bullough, P. G.: The pattern of aging of the articular cartilage of the elbow joint. J. Bone Joint Surg. 49B:175, 1967. 5. Heijink, A., Morrey, B. F., van Riet, R. P., O’Driscoll, W., and Cooney, W. P.: Delayed treatment of elbow pain and dysfunction following Essex-Lopresti injury with metallic radial head replacement. Submitted for publication, J. Bone Joint Surg. Am. 2008. 6. Kashiwagi, D.: Intra-articular changes of the osteoarthritic elbow, especially about the fossa olecrani. Jpn. Orthop. Assoc. 52:1367, 1978. 7. Kelly, E. W., Bryce, R., Coghlan, J., and Bell, S.: Arthroscopic debridement without radial head excision of the osteoarthritic elbow. Arthroscopy 23:151, 2007. 8. Krishnan, S. G., Harkins, D. C., Pennington, S. D., Harrison, D. K., and Burkhead, W. Z.: Arthroscopic ulnohumeral arthroplasty for degenerative arthritis of the elbow in patients under fifty years of age. J. Shoulder Elbow Surg. 16:443, 2007. 9. McLaughlin, R. E. 2nd, Savoie, F. H. 3rd, Field, L. D., and Ramsey, J. R.: Arthroscopic treatment of the arthritic elbow due to primary radiocapitellar arthritis. Arthroscopy 22:63, 2006. 10. Minami, N. M.: Roentgenological studies of osteoarthritis of the elbow joint. Jpn. Orthop. Assoc. 51:1223, 1977. 11. Mintz, G., and Fraga, A.: Severe osteoarthritis of the elbow in foundry workers. Arch. Environ. Health 27:78, 1973. 12. Morrey, B. F., and Schneeberger, A. G.: Anconeus arthroplasty: A new technique for reconstruction of the radiocapitellar and/or proximal radioulnar joint. J. Bone Joint Surg. 84A:1960, 2002. 13. Ortner, D. J.: Description and classification of degenerative bone changes in the distal joint surface of the humerus. Am. J. Phys. Anthrop. 28:139, 1968.

PART C Unlinked Total Elbow Arthroplasty Graham J. W. King

INTRODUCTION Total elbow arthroplasty is indicated for pain and functional limitations secondary to inflammatory arthritis, osteoarthritis, post-traumatic arthritis, acute distal humeral fractures, distal humeral nonunions, tumors, osteonecrosis, and dysfunctional instability. Currently available prostheses can be subclassified as linked, unlinked, or convertible implants, which can be interchanged between a linked or unlinked design. This part of the chapter focuses on the design considerations, techniques, and results of unlinked total elbow arthroplasty.

DESIGN CONSIDERATIONS Polyethylene wear and aseptic loosening of linked total elbow arthroplasties is a significant problem with longer follow-up, particularly in younger and more active patients.11 When a linked arthroplasty reaches the limits of its intrinsic laxity, forces are transmitted to the linkage mechanism and thereby to the stems and the bone implant interface, contributing to bearing wear and implant loosening.30 The concept of unlinked total elbow arthroplasty is that there is a sharing of load between the prosthesis and the capsule, ligaments, and muscles in an effort to decrease the stresses in the articulation and the stems. A necessary prerequisite for an unlinked arthroplasty is the presence of adequate ligaments and

Chapter 52 Unlinked Arthroplasty

bone stock with which the implant can be stabilized after insertion. Unlinked total elbows were initially referred to as resurfacing devices primarily because most were designed without a humeral stem. Owing to the high incidence of implant loosening with these early designs, most unlinked prostheses now incorporate stems on the components in an effort to improve implant longevity (Fig. 52-25). Unlinked total elbow arthroplasties are sometimes referred to as unconstrained devices, whereas loosehinge linked devices are often referred to as being semiconstrained; however, this is a misnomer. All joint arthroplasties have some element of intrinsic constraint by virtue of the shape and interaction of their articular surfaces. The intrinsic constraint of the ulnotrochlear joint of five unlinked total elbow arthroplasty designs were compared and found to vary markedly between implant types.15 Surprisingly, the implants that more closely resembled the articular geometry of the native articulation tended to less accurately replicate the intrinsic constraint of the human elbow (Fig. 52-26). In a series of cadaveric studies, the kinematics and stability of unlinked and linked total elbow arthroplasties have been evaluated.1,13,14,18,30,35,43 The mechanical behavior of these prostheses has been found to vary markedly depending on their articular design. In an effort to improve their stability and load transfer, some unlinked designs have incorporated a radial

FIGURE 52-25 Five and a half years after insertion of an unstemmed humeral component, a fracture has occurred across the distal humeral condyles at the site of fixation of a 39-year-old patient with rheumatoid arthritis. (By permission of Mayo Foundation.)

739

head replacement (Fig. 52-27). The radial head component has been shown to improve the stability of both the Sorbie and Pritchard ERS prostheses in in vitro biomechanical studies.13,35 Although theoretically improving soft tissue balance and load transfer across the elbow, the experience with radial head components in total elbow arthroplasty has been variable. For example, the radial head component of the capitellocondylar prosthesis was abandoned owing to concerns about radiolucent lines around the implant stem, but a subsequent study reported that the outcome was better if a radial head component was used.56 One possible explanation of the variable results with radial head prostheses in unlinked implants to date may be that, in many cases, their designs have been suboptimal. Furthermore, the addition of a third component complicates the surgical technique, making it more challenging to perform correctly, particularly because the instrumentation available to position unlinked total elbows has been lacking relative to other joints such as the hip and knee. Incorrect positioning of a radial head component will result in eccentric motions during prosupination and therefore shear forces across the radiocapitellar articulation. These abnormal kinematics and loads may cause polyethylene wear and early loosening of the radial component. A bipolar radial head component may be more forgiving in this setting because it will compensate for some of the eccentric motions through the bipolar articulation. Functional and balanced collateral ligaments are a key feature of a successful unlinked total elbow arthroplasty. Incompetent ligaments result in articular maltracking, joint subluxation, or dislocation. This has been demonstrated in an in-vitro cadaveric study and observed clinically.14,18 Maltracking of the arthroplasty leads to excessive polyethylene wear, osteolysis, and aseptic loosening. During the insertion of most unlinked designs, one or both of the collateral ligaments are usually released to achieve adequate exposure. Careful repair and successful ligament healing are needed if an unlinked arthroplasty is to be stable and articulate normally. Optimal component positioning improves the outcome of an unlinked total elbow arthroplasty.44,54 Replication of the axis of motion to the native state restores the muscle moment arms and the soft tissue tension of the collateral ligaments, which ensures more normal articular tracking and implant loading. Malpositioning of the humeral component has been demonstrated to alter the in vitro kinematics and stability of the capitellocondylar arthroplasty.14 It has also been reported that correct medial-lateral and proximal-distal positioning of the Souter implant had a lower incidence of loosening.44 Another study evaluating the same implant, however, was unable to demonstrate a relationship between humeral component position and aseptic loosening.58 Current techniques to identify and replicate

740

Part VII Reconstructive Procedures of the Elbow

Native

Capitellocondylar

Souter

Pritchard

Sorbie

Kudo

A 300

Valgus

Torque (Ncm)

100 0 –100 –200

B

–300

Human Varus

Souter

Kudo

Capitellocondylar

Sorbie

the flexion-extension axis are prone to error. In one study, the surgeon’s ability to select the flexionextension axis resulted in errors in axis orientation of up to 10 degrees in normal humerii. These errors are likely greater in clinical practice, where the anatomy is more distorted and the exposure of the landmarks is compromised.2 Perhaps the use of computer or imageassisted surgery will improve the accuracy of elbow component placement in the future, such as has been reported for the hip and knee. In summary, the premise of unlinked designs is that much of their stability is afforded by the geometry of the implant and the surrounding soft tissues rather than the intrinsic constraint of the articulation.1 The goal of an unlinked arthroplasty is to divert the forces that are transferred across the articulation away from the bone

Pritchard

Angle displacement (degrees)

200

14 12 10 8 6 4 2 0 –2 –4 –6 –8 –10 –12 –14

FIGURE 52-26 The intrinsic constraint of the ulnohumeral joints of five different unlinked total elbow arthroplasties were compared with that of the native elbow joint in an in vitro biomechanical study (A). The torque (bar graphs) and angular displacement (line graphs) of the Souter and Kudo implants were most similar to the human elbow (B).

implant interface to the surrounding soft tissues. By virtue of their need for adequate ligaments and bone stock, the indications for unlinked designs are narrower than linked arthroplasties and the instability rate is greater. Although the loosening rate should theoretically be lower with unlinked verses linked prostheses, this has yet to be proven in clinical studies.

INDICATIONS The indications for an unlinked total elbow arthroplasty are similar to those for any design of elbow arthroplasty. The necessary prerequisites to choose an unlinked implant are the presence of sufficient bone stock to support the implant and intact medial and lateral col-

Chapter 52 Unlinked Arthroplasty

741

FIGURE 52-27 The theoretical advantages of distributing forces that pass across the elbow through both columns of the humerus are obvious. (By permission of Mayo Foundation.)

lateral ligaments. The presence of functioning elbow flexor and extensor muscles are particularly important with an unlinked design, which requires muscle balance to maintain implant stability. In the absence of sufficient bone stock or ligamentous constraints, a linked arthroplasty should be used. Typical indications include inflammatory arthritis (rheumatoid, psoriatic, hemophilic), primary or post-traumatic osteoarthritis, osteonecrosis, periarticular tumors and comminuted distal humeral articular fractures in elderly patients.

FIGURE 52-28 The capitellocondylar implant employs a metal backed ulnar component and varying humeral angles to accommodate anatomic variation.

with an unlinked arthroplasty. As for any total elbow arthroplasty, patients who are unwilling to live within the activity and weight restrictions which are thought to be needed for implant longevity should be managed with an alternative treatment.

CONTRAINDICATIONS Active infection is an absolute contraindication to elbow arthroplasty. The absence of functioning muscles to move the elbow and a nonfunctional hand are relative contraindications. Poor skin quality must be corrected before or at the same time as the arthroplasty. Unstable elbows with poor ligaments or deficient bone stock should be managed with a linked device. Gross deformity is an indication for a linked device because achieving precise soft tissue balancing is typically not possible

SURGICAL CONSIDERATIONS OF UNLINKED DESIGNS There are a number of unlinked designs that have been developed and employed. The design features and surgical considerations of a few of the more commonly used devices will be reviewed. The capitellocondylar implant designed by Ewald consists of a cobalt-chrome humeral component with 5-, 10-, and 15-degree valgus angulations8 (Fig. 52-28) (Johnson and Johnson, Raynham,

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FIGURE 52-29 Lateral radiograph 2 years after surgery of a patient with rheumatoid arthritis treated with a capitellocondylar implant.

MA). The ulnar component has two polyethylene thicknesses available. A radial head implant was developed for this system but was abandoned owing to concerns about radiolucent lines around the stems.56 The ulnohumeral joint has a low magnitude of intrinsic constraint, making it prone to maltracking and dislocation.15,17 The implant is most commonly inserted through an extended Kocher approach, with elevation of the triceps off the olecranon from lateral to medial. The medial collateral ligament is preserved, whereas the lateral collateral ligament is cut and repaired during closure. Although excellent results were reported by the inventor, the experience of others has been less favorable owing to problems with instability9,31,40,61 (Fig. 52-29). The Pritchard ERS arthroplasty (DePuy, Warsaw, IN) consists of humeral, ulnar, and radial components (Fig. 52-30).34 It can be inserted through either an extended Kocher or a Bryan-Morrey triceps reflecting approach.3,28,32 One or both collateral ligaments are divided during the approach and then carefully repaired during closure. The radial head component is important for elbow stability.35 The clinical outcome of this prosthesis is largely unknown, with little available information provided in the literature34 (Fig. 52-31). The Souter-Strathclyde arthroplasty (Stryker, Mahwah, NJ) consists of a cobalt-chrome humeral and an all polyethylene ulnar component48 (Fig. 52-32). The humeral component aims to replicate the shape of the native trochlea and maintain the integrity of the supracondylar ridges and their attached collateral ligaments.47

FIGURE 52-30 The Pritchard ERS implant allows for replacement of the radial head with a modular system providing for some flexibility with regard to thickness of the implants.

The ulnar component is closely congruous with the humeral component, making the implant relatively constrained when loaded.15,43 The short-stem humeral component has a fin, which is carefully fitted into the medial supracondylar ridge, and a peg that is inserted into the capitellum (Fig. 52-33). The system has long-stem humeral components and long-stem metal-backed ulnar components available to manage bone loss and revision situations. A snap-fit ulnar component is also available that converts the implant into a linked device. The prosthesis is inserted using a posterior approach, typically using a triceps turndown. The medial collateral ligament is preserved, but the lateral ligament is typically divided to obtain sufficient exposure to allow dislocation and radial head excision. Careful repair of the triceps tendon and lateral collateral ligament is essential. Instability of this implant has been less frequent than other unlinked

Chapter 52 Unlinked Arthroplasty

A

B

FIGURE 52-31 Anteroposterior (A) and lateral (B) radiographs of a 44-year-old woman with rheumatoid involvement 1 year after a Pritchard ERS implant demonstrates no pain and an almost normal range of motion. (With permission Mayo Foundation.)

A FIGURE 52-32

B Standard (A) and long-stem (B) Souter humeral and ulnar components.

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Part VII Reconstructive Procedures of the Elbow

A

B

FIGURE 52-33 Anteroposterior (A) and lateral (B) radiographs 1 year after a well-functioning Souter total elbow replacement in a patient with rheumatoid arthritis.

FIGURE 52-34 The original Kudo arthroplasty had a stemless humeral component, an all-polyethelyene ulnar component, which was prone to loosening.

designs; however, loosening of the short-stemmed humeral component has been a common clinical problem.54 The Kudo total elbow arthroplasty (Biomet, Warsaw, IN) has evolved significantly since it was first introduced.21 Initially, the prosthesis had an all-polyethylene ulnar component and an unstemmed humeral component with a cylindrical articulation. Owing to a high incidence of early loosening, both the humeral and ulnar components were redesigned (Fig. 52-34). The current Kudo type 5 prosthesis consists of a 5-degree valgus cobalt-chrome humeral component with a titanium porous coating that is typically inserted uncemented and a metal-backed cemented ulnar component

A

B

FIGURE 52-35 The current Kudo type 5 total elbow arthroplasty has a stemmed component and a metalbacked ulnar component.

Chapter 52 Unlinked Arthroplasty

A

745

B

FIGURE 52-36

Anteroposterior (A) and lateral (B) radiographs of a well functioning Kudo type 5 total elbow arthroplasty.

(Fig. 52-35). The humeral articulation has a saddleshaped design that allows for medial-lateral translation of the ulnar component. The prosthesis is implanted with sectioning of the collateral ligaments and excision of the radial head. The reported results with the current design are favorable, although instability has been problematic owing to the low intrinsic stability relative to other designs19,20,29,33,50-52 (Fig. 52-36). The Sorbie-Questor total elbow arthroplasty (Wright Medical Technology, Arlington, TN) was designed to replicate the normal anatomy of the elbow (Fig. 52-37).45,46 The humeral component has an angled cobalt-chrome stem. A metal-backed ulnar component is available with two polyethylene thicknesses. The radial head component is a stemmed monoblock design. Originally designed without a humeral stem, loosening was a problem until the stem was added. The implant is inserted though an extended Kocher approach with sectioning of the lateral collateral ligament. There are no published results of the outcome of this device (Fig. 52-38).

SURGICAL TECHNIQUE The precise surgical technique and approach depends on the design of the unlinked prosthesis selected and

FIGURE 52-37 The Sorbie-Questor total elbow arthroplasty has a stemmed humeral component and metal-backed radial and ulnar components. (Reproduced with permission Wright Medical Technology, Arlington, TN.)

the surgeons’ preference. It is recommended that a linked implant system be available in the operating room whenever an unlinked prosthesis is planned. This will allow conversion to a linked design if the elbow is unstable or the articulation is maltracking following trial placement of the unlinked components. The surgical technique of the Kudo type 5 total elbow arthroplasty is presented. The patient is positioned supine with the arm across the chest. A sterile tourniquet is employed and placed high on the upper arm. A midline posterior skin incision is used placed just medial to the tip of the olecranon. The ulnar nerve is isolated and transposed anteriorly into a subcutaneous pocket. The management of the triceps is based on surgeon preference. A distally based triceps flap is recommended by the designer. Both the lateral and medial collateral ligaments are divided from their humeral insertions, and the elbow is dislocated. The radial head is excised. The distal humerus is prepared primarily freehand with minimal bone resection (Fig. 52-39). The ulna is prepared using a barrel reamer, burr, and rasps (Fig. 52-40).

746

A

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Part VII Reconstructive Procedures of the Elbow

FIGURE 52-38 Anteroposterior (A) and lateral (B) radiographs of a well-functioning Sorbie total elbow arthroplasty 5 years postoperatively in a patient with rheumatoid arthritis. The bone cement interface is quiet.

B

B

A trial reduction of the prosthesis is performed to evaluate soft tissue balance and articular tracking. Repositioning of one or both components should be performed, if necessary, to achieve soft tissue tensioning and optimal articular congruency. The humeral component is inserted uncemented if a good press fit is achieved, whereas the ulnar component is routinely cemented. After reduction

C

FIGURE 52-39 Humeral preparation for insertion of the Kudo total elbow arthroplasty. Cutting the distal humerus with a double-bladed chisel (A); rasping the humeral canal (B); insertion of the trial component (C).

of the elbow, the triceps and the fascial layers are meticulously repaired. The collateral ligaments are not routinely repaired. The elbow is splinted in 90 degrees of flexion and immobilized for 1 week postoperatively. Active and active-assisted exercises are then commenced as the soft tissues allow.

Chapter 52 Unlinked Arthroplasty

A

747

B

C

D FIGURE 52-40 Ulnar preparation for insertion of the Kudo total elbow arthroplasty. A barrel reamer prepares the greater sigmoid notch (A); a burr opens the medullary canal of the ulna (B); rasping the ulnar canal (C); insertion of the trial component (D).

RESULTS The reported outcome of unlinked total elbow arthroplasty consists primarily of retrospective case series. Typical complications of elbow arthroplasty such as ulnar neuropathy, infection, triceps failure and wound healing problems are discussed in Chapter 61 and will not be highlighted in this chapter. There are no prospective randomized trials comparing the outcome of different unlinked arthroplasties.24 Little et al25 compared the outcome of the Souter, Kudo, and Coonrad-Morrey designs in a nonrandomized prospective cohort study design. The authors were unable to demonstrate a significant difference between the Kudo and Souter designs with respect to outcome or complications. The linked Coonrad-Morrey implant had outcome that was similar to the unlinked designs, with a lower incidence of instability. The loosening rate did not differ between the three designs at an average of 5 years postoperatively.

There have been a number of case series reporting the outcome of the capitellocondylar prosthesis.4,6-10,31,40,42,55,56,61 Collectively, these studies demonstrate a reliable improvement in pain and function, with a modest improvement in motion. The incidence of loosening has been low in most series; however, instability has been a problem, particularly in the hands of surgeons other than the inventor (Fig. 52-41). Ewald, the surgeon inventor, reported a 3% revision rate out of 202 elbows at an average of 6.7 years.9 Only 1.5% of the elbows had sufficient instability to require revision, and 1.5% developed loosening. Schemitsch et al42 reported that the incidence of instability was higher and pain relief was lower in a matched cohort of patients with a prior radial head excision and synovectomy. Trepman and coworkers,56 also from the same center, reported that the presence of a radial head implant lowered the incidence of instability of this design.

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B

A

E C

D FIGURE 52-41 Anteroposterior (A) and lateral (B) radiographs of an unstable capitellocondylar arthroplasty in a 56-year-old patient with rheumatoid arthritis 2 years postoperatively. Wear of the retrieved ulnar component can be seen due to gross instability (C). Anteroposterior (D) and lateral (E) radiographs 1 year following successful revision to a linked Coonrad-Morrey total elbow arthroplasty.

Chapter 52 Unlinked Arthroplasty

749

The experience with the capitellocondylar prosthesis reported by other investigators is less favorable owing to a higher incidence of instability. Weiland et al61 reported a malarticulation rate of 29% in 40 prostheses followed for 7.2 years. Although most of these elbows remained functional, maltracking of the articulation was a cause for concern due to polyethylene wear at longer follow-up. Similarly, studies by Tranik et al55 and Davis et al6 reported instability rates of 9% and 13%, respectively, although most could be managed without revision. Ring et al38 demonstrated that ligament reconstruction was unreliable in restoring stability of this unlinked arthroplasty, whereas revision to a linked prosthesis had a high complication rate. Collectively, the aseptic loosening rates for the capitellocondylar prosthesis in these studies have been low. In the most recent reported experience with this implant, Ovesen et al31 reported that 83% of 51 prostheses were functional at an average of 6.9 years postoperatively. Seven prostheses required revision, with instability and infection being the most frequent cause of failure. The reported experience with the Pritchard ERS total elbow prosthesis has been limited to date.34 The experience at the Mayo Clinic has not been favorable, with a 10-year Kaplan Meier survival of only 54% out of 46 prostheses. Instability, wear, and aseptic loosening were the most common causes for failure (Fig. 52-42). Ulnohumeral component malpositioning was thought to be the most common reason for instability. The failure rate was much greater if the radial head was not replaced; however, technical issues with positioning the radial head component were common. Preservation of the native radial head provided the longest functioning implants. The results of the Souter total elbow arthroplasty have been widely reported from multiple centers other than that of the surgeon inventor.* The outcome has been uniformly favorable, with a high incidence of improvement in pain and function with a modest improvement in elbow flexion but not extension. In general, instability has been less common than reports of other unlinked designs. Humeral component loosening has been more common than the ulnar component when the short-stem humeral stems were employed53 (Fig. 52-43). The most recent series was reported by Landor et al,23 with 58 elbows followed for an average of 9.5 years. The Mayo elbow performance index improved from 30 to 82 points. The revision rate was 22%, with loosening being the most common cause. Only one elbow was revised for instability. The Kaplan-

Meier survival was 70% at 10 years and 53% at 16 years. Van Der Lugt et al59 reported the results of a prospective study of 204 Souter prostheses inserted for rheumatoid arthritis and followed for an average of 6.4 years. Twelve percent of the prostheses were revised, with loosening of the humeral component being the most common indication. The Kaplan-Meier survival was 77% at 10 years and 65% at 18 years. Trail and coworkers53 evaluated the outcome of 186 prostheses and reported a 12-year survival rate of 87%. Seventy-five percent of the revisions were due to humeral loosening. The use of a long-stem humeral component was subsequently reported to have a much lower incidence of loosening than the short-stem design.54 The use of a snap-fit ulnar component that converts the prosthesis from an unlinked to a linked design was shown to result in a higher incidence of aseptic loosening. The outcome of the Kudo total elbow arthroplasty has largely been reported from the surgeon-inventor, and has reflected the evolution of the prosthesis design.† The early type 1 and 2 prostheses used an unstemmed humeral component, which had a high incidence of loosening.22 Experience with the later designs has been more promising with a low incidence of instability and loosening. The uncemented humeral component has been more reliable than the ulnar component, in which cement and metal backing has improved the success. Thillemann and coworkers52 reported 67% survival of 17 Kudo three elbows followed for an average of 9.5 years. Two had been revised due to loosening of the ulnar component and one for instability. Progressive valgus tilting of the elbow at longer follow-up raised concerns regarding polyethylene wear of the ulnar component at longer follow-up (Fig. 52-44). Professor Kudo and his colleagues have reported excellent results, particularly with the current type 5 prosthesis. Tanaka et al demonstrated that the outcome of a metal-backed cemented ulnar component was superior to an all polyethylene design.51 Mori and coworkers29 reported successful outcomes of the type 5 unlinked design at an average of 8 years, even in the presence of mutilating rheumatoid arthritis with bone loss. Tanaka et al50 reported a 90% survival rate at 13 years using the type 3 prosthesis. Preservation of the medial collateral ligament at surgery was not found to influence the long-term outcome. Potter et al33 reported on the outcome of 35 Kudo type 5 prostheses at an average of 6 years. Although none of

* See references 5, 12, 16, 23, 26, 27, 39, 41, 44, 49, 53, 54, 57, and 59.

†

See references 19-22, 29, 33, 36, 37, 50-52, 60, and 62.

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Part VII Reconstructive Procedures of the Elbow

A

B

C FIGURE 52-42

Anteroposterior (A) and lateral (B) radiographs of a loose Pritchard ERS prosthesis in a 73-year-old patient with rheumatoid arthritis 7 years postoperatively. Wear of the ulnar component can be appreciated on the retrieved implant (C).

the prostheses had been revised, two were loose at follow-up with a Kaplan-Meier survival of 89% at 5 years. One postoperative dislocation was successfully treated with a closed reduction. Willems et al62 reported on the outcome of 36 Kudo prostheses at an average of 5 years. Although the clinical outcome was good or excellent in the majority of patients, 17% had been revised, most commonly for aseptic loosening at longer follow-up. There are no peer review studies documenting the outcome of the Sorbie total elbow arthroplasty to date. In a prospective study of 48 elbows, infection has been

the most common complication in the experience of the surgeon inventor (15%) (Personal communication, Dr. Charles Sorbie). The high initial infection rate was attributed to the use of unsterile tourniquets because there have been no further infections since these were replaced by sterile tourniquets in the latter part of the series. Six percent of the patients have needed a revision for loosening and 4% for instability at an average follow-up of 6.8 years (Fig. 52-45). In summary, the outcome of unlinked total elbow arthroplasties are similar to those reported for linked prostheses.25,63 Although the loosening rates of the more

Chapter 52 Unlinked Arthroplasty

751

FIGURE 52-44 Anteroposterior radiograph of an unstable Kudo total elbow arthroplasty.

FIGURE 52-43 Lateral radiograph of a Souter total elbow arthroplasty with aseptic loosening and extension of the short-stem humeral component, the typical mode of failure of this prosthesis.

FIGURE 52-45

A

B

Anteroposterior (A) and lateral (B) radiographs of a loose Sorbie total elbow arthroplasty in a 53-year-old man with rheumatoid arthritis 5 years postoperatively. The patient admitted to chopping firewood and golfing with his prosthetic elbow.

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Part VII Reconstructive Procedures of the Elbow

FIGURE 52-45, cont’d

C

Anteroposterior (C) and lateral (D) radiographs 1 year following revision to a long-stem linked Coonrad-Morrey total elbow arthroplasty.

D

unconstrained devices are low, the incidence of instability has been problematic in some series. It is likely that patient selection and surgeon experience plays a critical role in the outcome of elbow replacement in general and unlinked devices in particular. Unlinked prostheses are less forgiving than linked designs owing to the need to accurately position the components, balance the soft tissues, and achieve ligament healing. Randomized clinical trials are needed to accurately compare the complications and longevity of elbow prostheses.

5.

6.

7.

8.

References 1. An, K. N.: Kinematics and constraint of total elbow arthroplasty. J. Shoulder Elbow Surg. 14(1 Suppl S):168S, 2005. 2. Brownhill, J. R., Furukawa, K., Faber, K. J., Johnson, J. A., and King, G. J.: Surgeon accuracy in the selection of the flexion-extension axis of the elbow: an in vitro study. J. Shoulder Elbow Surg. 15:451, 2006. 3. Bryan, R. S., and Morrey, B. F.: Extensive posterior exposure of the elbow. A triceps-sparing approach. Clin. Orthop. Rel. Res. 166:188, 1982. 4. Chiodo, C. P., Terry, C. L., and Koris, M. J.: Reconstruction of the medial collateral ligament with flexor carpi radialis tendon graft for instability after capitellocondylar total

9.

10.

11.

elbow arthroplasty. J. Shoulder Elbow Surg. 8:284, 1999. Dainton, J. N., and Hutchins, P. M.: A medium-term followup study of 44 Souter-Strathclyde elbow arthroplasties carried out for rheumatoid arthritis. J. Shoulder Elbow Surg. 11:486, 2002. Davis, R. F., Weiland, A. J., Hungerford, D. S., Moore, J. R., and Volenec-Dowling, S.: Nonconstrained total elbow arthroplasty. Clin. Orthop. Relat. Res. 171:156, 1982. Dennis, D. A., Clayton, M. L., Ferlic, D. C., Stringer, E. A., and Bramlett, K. W.: Capitello-condylar total elbow arthroplasty for rheumatoid arthritis. J. Arthroplasty 5(suppl):S83, 1990. Ewald, F. C., Scheinberg, R. D., Poss, R., Thomas, W. H., Scott, R. D., and Sledge, C. B.: Capitellocondylar total elbow arthroplasty. J. Bone Joint Surg. Am. 62:1259, 1980. Ewald, F. C., Simmons, E. D., Jr., Sullivan, J. A., Thomas, W. H., Scott, R. D., Poss, R., Thornhill, T. S., and Sledge, C. B.: Capitellocondylar total elbow replacement in rheumatoid arthritis. Long-term results. J. Bone Joint Surg. Am. 75:498, 1993. Friedman, R. J., Lee, D. E., and Ewald, F. C.: Nonconstrained total elbow arthroplasty. Development and results in patients with functional class IV rheumatoid arthritis. J. Arthroplasty 4:31, 1989. Hildebrand, K. A., Patterson, S. D., Regan, W. D., MacDermid. J. C., and King, G. J.: Functional outcome of semiconstrained total elbow arthroplasty. J. Bone Joint Surg. Am. 82-A:1379, 2000.

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12. Ikavalko, M., Lehto, M. U., Repo, A., Kautiainen, H., and Hamalainen, M.: The Souter-Strathclyde elbow arthroplasty. A clinical and radiological study of 525 consecutive cases. J. Bone Joint Surg. Br. 84:77, 2002. 13. Inagaki, K., O’Driscoll, S. W., Neale, P. G., Uchiyama, E., Morrey, B. F., and An, K. N.: Importance of a radial head component in Sorbie unlinked total elbow arthroplasty. Clin. Orthop. Relat. Res. (400):123-131, 2002. 14. Itoi, E., Niebur, G. L., Morrey, B. F., and An, K. N.: Malrotation of the humeral component of the capitellocondylar total elbow replacement is not the sole cause of dislocation. J. Orthop. Res. 12:665, 1994. 15. Kamineni, S., O’Driscoll, S. W., Urban, M., Garg, A., Berglund, L. J., Morrey, B. F., and An, K. N.: Intrinsic constraint of unlinked total elbow replacements—the ulnotrochlear joint. J. Bone Joint Surg. Am. 87:2019, 2005. 16. Khatri, M., and Stirrat, A. N.: Souter-Strathclyde total elbow arthroplasty in rheumatoid arthritis: medium-term results. J. Bone Joint Surg. Br. 87:950, 2005. 17. King, G. J., Glauser, S. J., Westreich, A., Morrey, B. F., and An, K. N.: In vitro stability of an unconstrained total elbow prosthesis. Influence of axial loading and joint flexion angle. J. Arthroplasty 8:291, 1993. 18. King, G. J., Itoi, E., Niebur, G. L., Morrey, B. F., and An, K. N.: Motion and laxity of the capitellocondylar total elbow prosthesis. J. Bone Joint Surg. Am. 76:1000, 1994. 19. Kudo, H., Iwano, K., and Nishino, J.: Cementless or hybrid total elbow arthroplasty with titanium-alloy implants. A study of interim clinical results and specific complications. J. Arthroplasty 9:269, 1994. 20. Kudo, H., Iwano, K., and Nishino, J.: Total elbow arthroplasty with use of a nonconstrained humeral component inserted without cement in patients who have rheumatoid arthritis. J. Bone Joint Surg. Am. 81:1268, 1999. 21. Kudo, H., Iwano, K., and Watanabe, S.: Total replacement of the rheumatoid elbow with a hingeless prosthesis. J. Bone Joint Surg. Am. 62:277, 1980. 22. Kudo, H., and Iwano, K.: Total elbow arthroplasty with a non-constrained surface-replacement prosthesis in patients who have rheumatoid arthritis. A long-term follow-up study. J. Bone Joint Surg. Am. 72:355, 1990. 23. Landor, I., Vavrik, P., Jahoda, D., Guttler, K., and Sosna, A.: Total elbow replacement with the Souter-Strathclyde prosthesis in rheumatoid arthritis. Long-term follow-up. J. Bone Joint Surg. Br. 88:1460, 2006. 24. Little, C. P., Graham, A. J., and Carr, A. J.: Total elbow arthroplasty: a systematic review of the literature in the English language until the end of 2003. J. Bone Joint Surg. Br. 87:437, 2005. 25. Little, C. P., Graham, A. J., Karatzas, G., Woods, D. A., and Carr, A. J.: Outcomes of total elbow arthroplasty for rheumatoid arthritis: comparative study of three implants. J. Bone Joint Surg. Am. 87:2439, 2005. 26. Lyall, H. A., Cohen, B., Clatworthy, M., and Constant, C. R.: Results of the Souter-Strathclyde total elbow arthroplasty in patients with rheumatoid arthritis. A preliminary report. J. Arthroplasty 9:279, 1994. 27. Malone, A. A., Taylor, A. J., and Fyfe, I. S.: Successful outcome of the Souter-Strathclyde elbow arthroplasty. J. Shoulder Elbow Surg. 13:548, 2004.

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28. Mehta, J. A., and Bain, G. I.: Surgical approaches to the elbow. Hand Clin. 20:375, 2004. 29. Mori, T., Kudo, H., Iwano, K., and Juji, T.: Kudo type-5 total elbow arthroplasty in mutilating rheumatoid arthritis: a 5- to 11-year follow-up. J. Bone Joint Surg. Br. 88:920, 2006. 30. O’Driscoll, S. W., An, K. N., Korinek, S., and Morrey, B. F.: Kinematics of semi-constrained total elbow arthroplasty. J. Bone Joint Surg. Br. 74:297, 1992. 31. Ovesen, J., Olsen, B. S., Johannsen, H. V., and Sojbjerg, J. O.: Capitellocondylar total elbow replacement in late-stage rheumatoid arthritis. J. Shoulder Elbow Surg. 14:414, 2005. 32. Patterson, S. D., Bain, G. I., and Mehta, J. A.: Surgical approaches to the elbow. Clin. Orthop. Relat. Res. 370:19, 2000. 33. Potter, D., Claydon, P., and Stanley, D.: Total elbow replacement using the Kudo prosthesis. Clinical and radiological review with five- to seven-year follow-up. J. Bone Joint Surg. Br. 85:354, 2003. 34. Pritchard, R. W.: Anatomic surface elbow arthroplasty. A preliminary report. Clin. Orthop. Relat. Res. 179:223, 1983. 35. Ramsey, M., Neale, P. G., Morrey, B. F., O’Driscoll, S. W., and An, K. N.: Kinematics and functional characteristics of the Pritchard ERS unlinked total elbow arthroplasty. J. Shoulder Elbow Surg. 12:385, 2003. 36. Rauhaniemi, J., Tiusanen, H., and Kyro, A.: Kudo total elbow arthroplasty in rheumatoid arthritis. Clinical and radiological results. J. Hand Surg. Br. 31:162, 2006. 37. Reinhard, R., van der Hoeven, M., de Vos, M. J., and Eygendaal, D.: Total elbow arthroplasty with the Kudo prosthesis. Int. Orthop. 27:370, 2003. 38. Ring, D., Kocher, M., Koris, M., and Thornhill, T. S.: Revision of unstable capitellocondylar (unlinked) total elbow replacement. J. Bone Joint Surg. Am. 87:1075, 2005. 39. Rozing, P.: Souter-Strathclyde total elbow arthroplasty. J. Bone Joint Surg Br. 82:1129, 2000. 40. Ruth, J. T., and Wilde, A. H.: Capitellocondylar total elbow replacement. A long-term follow-up study. J. Bone Joint Surg. Am. 74:95, 1992. 41. Samijo, S. K., Van den Berg, M. E., Verburg, A. D., and Tonino, A. J.: Souter-Strathclyde total elbow arthroplasty: medium-term results. Acta Orthop. Belg. 69:501, 2003. 42. Schemitsch, E. H., Ewald, F. C., and Thornhill, T. S.: Results of total elbow arthroplasty after excision of the radial head and synovectomy in patients who had rheumatoid arthritis. J. Bone Joint Surg. Am. 78:1541, 1996. 43. Schneeberger, A. G., King, G. J., Song, S. W., O’Driscoll, S. W., Morrey, B. F., and An, K. N.: Kinematics and laxity of the Souter-Strathclyde total elbow prosthesis. J. Shoulder Elbow Surg. 9:127, 2000. 44. Shah, B. M., Trail, I. A., Nuttall, D., and Stanley, J. K.: The effect of epidemiologic and intraoperative factors on survival of the standard Souter-Strathclyde total elbow arthroplasty. J. Arthroplasty 15:994, 2000. 45. Shiba, R., Sorbie, C., Siu, D. W., Bryant, J. T., Cooke, T. D., and Wevers, H. W.: Geometry of the humeroulnar joint. J. Orthop. Res. 6:897, 1988.

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46. Sorbie, C., Shiba, R., Siu, D., Saunders, G., and Wevers, H.: The development of a surface arthroplasty for the elbow. Clin. Orthop. Rel. Res. 208:100, 1986. 47. Souter, W. A.: Anatomical Trochlear Stirrup Arthroplasty of the Rheumatoid Elbow. Elbow Joint Proceedings of the International Seminar, Kobe, Japan Editor: Kashiwagi, D., Excerpta Medica, Elsevier Science Publishers 1985; 305. 48. Souter, W. A.: Total replacement arthroplasty of the elbow. Joint replacement in the upper limb. London, Institution of Mechanical Engineers 5:96, 1977. 49. Talwalkar, S. C., Givissis, P. K., Trail, I. A., Nuttall, D., and Stanley, J. K.: Survivorship of the Souter-Strathclyde elbow replacement in the young inflammatory arthritis elbow. J. Bone Joint Surg. Br. 87:946, 2005. 50. Tanaka, N., Kudo, H., Iwano, K., Sakahashi, H., Sato, E., and Ishii, S.: Kudo total elbow arthroplasty in patients with rheumatoid arthritis: a long-term follow-up study. J. Bone Joint Surg. Am. 83-A:1506, 2001. 51. Tanaka, N., Sakahashi, H., Ishii, S., and Kudo, H.: Comparison of two types of ulnar component in type-5 Kudo total elbow arthroplasty in patients with rheumatoid arthritis: a long-term follow-up. J. Bone Joint Surg. Br. 88:341, 2006. 52. Thillemann, T. M., Olsen, B. S., Johannsen, H. V., and Sojbjerg, J. O.: Long-term results with the Kudo type 3 total elbow arthroplasty. J. Shoulder Elbow Surg. 15:495, 2006. 53. Trail, I. A., Nuttall, D., and Stanley, J. K.: Survivorship and radiological analysis of the standard Souter-Strathclyde total elbow arthroplasty. J. Bone Joint Surg. Br. 81:80, 1999. 54. Trail, L. A., Nuttall, D., and Stanley, J. K.: Comparison of survivorship between standard and long-stem SouterStrathclyde total elbow arthroplasty. J. Shoulder Elbow Surg. 11:373, 2002. 55. Trancik, T., Wilde, A. H., and Borden, L. S.: Capitellocondylar total elbow arthroplasty. Two- to eight-year experience. Clin. Orthop. Relat. Res. 223:175, 1987. 56. Trepman, E., Vella, I. M., and Ewald, F. C.: Radial head replacement in capitellocondylar total elbow arthroplasty. 2- to 6-year follow-up evaluation in rheumatoid arthritis. J. Arthroplasty 6:67, 1991. 57. Valstar, E. R., Garling, E. H., and Rozing, P. M.: Micromotion of the Souter-Strathclyde total elbow prosthesis in patients with rheumatoid arthritis 21 elbows followed for 2 years. Acta Orthop. Scand. 73:264, 2002. 58. van der Lugt, J. C., Geskus, R. B., and Rozing, P. M.: Limited influence of prosthetic position on aseptic loosening of elbow replacements: 125 elbows followed for an average period of 5.6 years. Acta Orthop. 76:654, 2005. 59. van der Lugt, J. C., Geskus, R. B., and Rozing, P. M.: Primary Souter-Strathclyde total elbow prosthesis in rheumatoid arthritis. J. Bone Joint Surg. Am. 86-A:465, 2004. 60. Verstreken, F., De Smet, L., Westhovens, R., and Fabry, G.: Results of the Kudo elbow prosthesis in patients with rheumatoid arthritis: a preliminary report. Clin. Rheumatol. 17:325, 1998. 61. Weiland, A. J., Weiss, A. P., Wills, R. P., and Moore, J. R.: Capitellocondylar total elbow replacement. A long-term follow-up study. J. Bone Joint Surg. Am. 71:217, 1989.

62. Willems, K., and De Smet, L.: The Kudo total elbow arthroplasty in patients with rheumatoid arthritis. J. Shoulder Elbow Surg. 13:542, 2004. 63. Wright, T. W., Wong, A. M., and Jaffe, R.: Functional outcome comparison of semiconstrained and unconstrained total elbow arthroplasties. J. Shoulder Elbow Surg. 9:524, 2000.

PART D Convertible Total Elbow Arthroplasty Graham J. W. King

A convertible total elbow arthroplasty provides the surgeon the option to change between a linked or unlinked articulation, or vice versa, without removing the prosthesis stems. Conversion can be performed at the time of the initial arthroplasty or at a subsequent revision procedure. Some systems also allow conversion between a distal humeral hemiarthroplasty and a total elbow arthroplasty without removing the stem of the humeral component. This section will focus on the design considerations and technique of convertible total elbow arthroplasties.

DESIGN CONSIDERATIONS As has been outlined earlier in this chapter, unlinked total elbow arthroplasties have a theoretical advantage over linked devices owing to a sharing of load across the articulation between the prosthesis and the joint capsule, ligaments, and muscles. Although the majority of patients with elbow arthritis can be managed with an unlinked elbow arthroplasty, there are patients who require a linked prosthesis due to a lack of adequate bone stock or functional collateral ligaments. Although typically this can be predicted preoperatively, it is always desirable to have a linkable implant immediately available in the operating room whenever a surgeon is planning to perform an unlinked total elbow arthroplasty. If an unlinked implant is not stable or is not articulating congruously intraoperatively, then it should be converted to a linked design. If this is recognized before the unlinked components are cemented, then a different design of linked arthroplasty can be used, although repeat bony preparation will be needed, which is time

Chapter 52 Unlinked Arthroplasty

consuming. The advantage of a convertible prosthesis is significant in this setting because rather than changing prosthesis designs, a linkage mechanism can simply be applied to the same prosthesis for which the bony resection has been completed. If the stems have already been cemented, then the ability to couple an unlinked prosthesis without removing the stems makes a convertible implant system even more appealing. The advantage of having one implant system to manage the majority of clinical situations is also helpful for hospitals by reducing inventories and cost. For surgeons, a convertible design means that only one implant system needs to be mastered. Although most patients who undergo an unlinked total elbow arthroplasty have an excellent outcome, there are some patients who develop elbow instability postoperatively, which is often difficult to manage.3,8,10 When this occurs early, a closed reduction and a period of immobilization may allow the ligaments to heal and the prosthesis to function normally. However, when presenting as a chronic problem, attempts at ligament reconstruction have not been reliable. The concept of having an unlinked elbow arthroplasty that can be linked in the setting of postoperative elbow instability is desirable because removal of a well-fixed unlinked elbow arthroplasty to revise it to a linked arthroplasty is technically difficult with a significant risk of complications.10 Hemiarthroplasty of the distal humerus is becoming more popular to manage comminuted articular fractures of the distal humerus, nonunions, and avascular necrosis, as discussed in Chapter 52. Should the patient develop instability or ulnar subsidence, or have persistent pain, the ability to convert a humeral hemiarthroplasty to either a linked or unlinked total elbow arthroplasty without removing a well-fixed humeral component is attractive.

INDICATIONS The indications for a convertible total elbow arthroplasty are similar to those for any design of elbow arthroplasty. Typical indications include inflammatory arthritis, primary or post-traumatic osteoarthritis, osteonecrosis, periarticular tumors, dysfunctional instability, distal humeral nonunions, and comminuted distal humeral articular fractures in the elderly. Because these implant systems are convertible between linked and unlinked configurations, these designs have the ability to deal with a wide spectrum of pathologies ranging from the situation of well-preserved bone stock and ligaments, in which an unlinked arthroplasty might be used, to the situation where there is extensive bone loss or ligamentous insufficiency, where a linked design

755

would be preferable. In some cases, the final decision as to whether to perform an unlinked or linked prosthesis is made intraoperatively—a convertible total elbow design provides the surgeon the option to choose at any time during the procedure.

CONTRAINDICATIONS As for all elbow arthroplasties, the presence of active infection is an absolute contraindication to convertible elbow arthroplasty. Patients who are unwilling or unable to live within the activity and weight restrictions necessary for an elbow arthroplasty should be managed with an alternative treatment such as a synovectomy, débridement, interposition arthroplasty, or arthrodesis. Poor skin coverage, inadequate muscle function of the elbow, and a nonfunctional hand are relative contraindications to elbow arthroplasty.

SURGICAL CONSIDERATIONS OF CONVERTIBLE DESIGNS Two convertible total elbow arthroplasties have been developed and used to date. The Acclaim (Depuy, Warsaw, IN) is a cobalt-chrome implant with humeral and ulnar components. (Fig. 52-46) The humeral component has fins to resist rotation. The articulation is centralized to the long axis of the humeral component, which results in a lateral shift of the ulna with respect to the humerus, thereby tightening the medial collateral ligament. This lateral shift is thought to better balance the forces across the implant because it does not incorporate a radial head replacement. The unlinked articulation can be converted to a linked version by partial removal of the epicondyles, exchange of the bobbin to a polyethylene yoke, replacement of the polyethylene ulnar insert with a hinged component, and insertion of a polyethylene pin mechanism. The Latitude System (Tornier Inc., Stafford, TX) is a modular device with the option to be configured as a humeral hemiarthroplasty and an unlinked or linked total elbow arthroplasty (Fig. 52-47). The cobalt-chrome implant has a modular humeral component, which incorporates fins and an anterior flange to resist axial rotation and posterior displacement. The axis bolt of the humeral component is cannulated to facilitate secure stable collateral ligament repair to the implant and adjacent bone. The ulnar component is metal backed with thick polyethylene and an extended coronoid process to resist dislocation. A bipolar radial head is available for use when the radial head is arthritic and requires excision. The conversion between an unlinked to a linked device can be accomplished easily by adding a locking

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A B FIGURE 52-46

A

Unlinked (A) and linked (B) versions of the Acclaim total elbow arthroplasty.

B

C

FIGURE 52-47 Unlinked (A), linked (B), and hemiarthroplasty (C) versions of the Latitude total elbow arthroplasty. (Courtesy of Tornier Inc., Stafford, TX.)

Chapter 52 Unlinked Arthroplasty

757

cap during the initial surgery or subsequently through a minimally invasive approach to manage postoperative instability.

SURGICAL TECHNIQUE The surgical technique for the Latitude total elbow arthroplasty is outlined here.4 The patient is placed supine, with the arm across the chest. A sterile tourniquet is employed and prophylactic antibiotics administered before tourniquet inflation. A midline posterior elbow incision is placed just medial to the tip of the olecranon, and full-thickness flaps are developed on the deep fascia. The ulnar nerve is identified, mobilized, and transposed anteriorly. Management of the triceps tendon varies according to the preference of the surgeon. The implant can be placed by elevating the triceps from medial to lateral, as in the Bryan-Morrey approach, from lateral to medial, as in the extended Kochler approach, or through a triceps splitting approach, where the triceps is elevated from the olecranon both medially and laterally.1,6,9,12 The design of the instrumentation also allows for the bony preparation to be performed and the implants to be inserted while preserving the attachment of the triceps to the olecranon. The ‘triceps-on’ approach reduces the risk of triceps insufficiency with postoperative weakness and pain that can occur when the triceps tendon is detached to perform an elbow arthroplasty.2,9 Unfortunately, the triceps-on approach does compromise visualization to some extent, but it can be a useful technique, particularly when there is epicondylar bone loss or when the joint is not too tight. The medial and lateral collateral ligaments and their corresponding common flexor and extensor origins are tagged for later repair and then sharply released from the epicondyles as much as necessary to achieve joint dislocation. The correct sizing of the implant is best achieved by matching the anatomical spool size to the articular surfaces of the ulna and radius and the distal humerus. The key to sizing the Latitude system is choosing the correct joint width such that with the anatomic spool sitting in the trochlear groove, the radial head articulates congruously with the capitellum of the spool (Fig. 52-48). This approach will ensure that the native radial head (or a radial head component) will articulate congruously with the capitellum of the humeral component. There are four prosthesis sizes available for the total elbow arthroplasty and six sizes available for the anatomic distal humeral hemiarthroplasty. As for any total elbow arthroplasty, reproduction of the flexion-extension axis is crucial for a successful result.5,11 With the Latitude system, all subsequent steps are based on the accurate determination of this axis.

A

B FIGURE 52-48 The width of the articulation is key to sizing the Latitude prosthesis. This can be judged using the distal humerus (A) or the proximal radius and ulna (B).

Using a circular guide, the lateral point of isometry is determined at the center of the arc of the capitellum when viewed from the lateral side. The anteroinferior aspect of the medial epicondyle is the medial landmark. The intercondylar portion of the distal humerus is removed, with a saw up to the proximal aspect of the olecranon fossa to facilitate central axis pin placement. An axis guide is used to insert the pin, which marks the flexion-extension axis of the elbow (Fig. 52-49A). The medullary canal is opened with a burr, and the offset of the axis of the medullary canal with the flexionextension axis is determined. Anterior, centered, and posterior offset humeral configurations are available. The distal humeral cuts are made using a mechanized series of jigs based off the flexion-extension and medullary axes (see Fig. 52-49B and C). The humeral canal is

Part VII Reconstructive Procedures of the Elbow

758

E AC RF SU

A

G

IN

TT

CU

D

ME

RIGHT

MEDIUM

C

B

FIGURE 52-49 Humeral preparation is shown. A, An axis pin is inserted at the flexion-extension axis of the elbow. The intercondylar portion (B) and (C) distal portion of the distal humerus are prepared using cutting blocks based off this axis. D, The trial humeral component is then inserted.

D

HT

/ RIG IUM

Chapter 52 Unlinked Arthroplasty

rasped and trial placement of the humeral component is performed (see Fig. 52-49D). Preparation of the radius and ulna is accomplished using a cutting guide and the anatomic spool, which is seated into the articular dish of the radial head and the

759

guiding ridge of the olecranon. If the radial head is to be excised, this is done with a sagittal saw and the trochlear cut is made with a bell-shaped saw from lateral to medial (Fig. 52-50A and B). If the native radial head is to be preserved, then the bell-shaped saw is used to

D

C FIGURE 52-50 Ulnar preparation is shown. A, The radial and ulnar cutting jig is oriented using the anatomic spool and secured in place. The radial head is resected, if desired. B, Using the bell saw, the proximal ulnar cut is performed. C, After preparation of the ulnar canal, the trial ulnar component is inserted. The radial neck is rasped. D, The trial bipolar radial head is attached, and the elbow is reduced and evaluated for alignment and articular tracking.

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Part VII Reconstructive Procedures of the Elbow

cut the ulna from medial to lateral. The ulnar canal is then opened with a burr and prepared using flexible reamers and rasps. After inserting the trial ulnar component, the radius is broached and an appropriate sized radial head trial is placed. The bipolar radial head accommodates for ±10 degrees of angular rotation but cannot substitute for malalignment of the proximal radius to the capitellum (see Fig. 52-50C and D). The elbow is moved through a range of motion with the trial components, and the articular tracking and joint stability are evaluated. If there are adequate soft tissue and bony structures and the elbow prosthesis is tracking well, then an unlinked arthroplasty is performed. If the radial head prosthesis is maltracking on the capitellum and repositioning of the components is unable to correct this problem, a radial head replacement should not be performed and the implant should probably be linked. In the setting of significant bone loss or incompetent collateral ligaments, then a linked prosthesis is routinely selected. Cement restrictors are inserted and pulsatile lavage is used to prepare the medullary canals for component insertion. Antibiotic cement is injected into the humerus, ulna, and radius using a cement gun in a retrograde fashion and the components are inserted. A cancellous bone graft is placed behind the anterior flange of the humeral component after the cement is set; similarly linkage of the components, if indicated, is not performed until the cement is cured. Articular tracking of the components and the stability of the elbow is reassessed. If the prosthesis is to be linked, the locking cap is

A

inserted and secured in position with a torque screwdriver. The collateral ligaments are repaired back to the epicondyles using nonabsorbable Krackow sutures passed through the cannulated screw, which is located at the axis of rotation of the implant (Fig. 52-51A). When tied on the contralateral side of the elbow, these sutures securely approximate the ligaments to their attachment sites while avoiding problems with sutures pulling through the often weak bone of the epicondyles. An additional suture can be placed through the cannulated screw of the implant and through a drill hole in the proximal ulna to act as a temporary artificial ligament to prevent instability in the postoperative period while the collateral ligaments are healing (see Fig. 52-51B). The triceps is carefully secured to the olecranon if it was detached. Drains are placed if indicated and the elbow is placed in a well-padded splint in relative extension.

REHABILITATION As soon as the wound allows for safe mobilization, active range of motion is permitted. If the triceps was detached during surgery extension should be performed with gravity assistance only. In most cases, patients can be taught their exercises before discharge; home therapy is typically not required. A nighttime extension splint helps to gain maximum elbow extension. Strengthening should not be instituted for at least 10 weeks postoperatively to ensure secure ligament healing has occurred.

B FIGURE 52-51 A, Sutures are placed in the medial and lateral collateral ligaments and passed through the axis screw of the humeral component to provide for secure initial fixation. B, A suture can also be placed through a drill hole in the ulna and the humeral component to provide for immediate stability in the postoperative period.

Chapter 52 Unlinked Arthroplasty

761

COMPLICATIONS

RESULTS

The complications of a convertible total elbow arthroplasty are similar to any arthroplasty and are discussed in Chapter 53. These include infection, ulnar neuropathy, fractures, triceps avulsion, and problems with soft tissue healing. The complications specific to the unlinked configuration would be similar to those for any unlinked device, most importantly being instability, whereas for a linked device, it would presumably be polyethylene wear of the linkage mechanism.

The initial experience with the Acclaim total elbow has been favorable, with a significant improvement in pain and motion7 (Fig. 52-52). The preliminary experience with 65 prostheses reported four intraoperative fractures and one dislocation. There are no studies available as of yet documenting the survivorship of this prosthesis. There are no reports documenting the results of the Latitude convertible total elbow arthroplasties. The author’s experience with the Latitude system to date has

C A

D

B FIGURE 52-52

Anteroposterior (A) and lateral (B) radiographs of a 39-year-old patient with juvenile rheumatoid arthritis. Anteroposterior (C) and lateral (D) radiographs following an unlinked Acclaim total elbow arthroplasty. (Courtesy of Dr. John Stanley.)

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Part VII Reconstructive Procedures of the Elbow

A

C

D

B FIGURE 52-53

Anteroposterior (A) and lateral radiographs (B) of a 70-year-old patient with rheumatoid arthritis. Anteroposterior (C) and lateral (D) radiographs 2 years following an unlinked Latitude total elbow arthroplasty.

Chapter 52 Unlinked Arthroplasty

A

B

C D FIGURE 52-54

E

Anteroposterior (A) and lateral (B) radiographs of an 82-year-old patient with an articular fracture of the distal humerus. C, CT scan demonstrating the comminuted nature of the fracture. Anteroposterior (D) and lateral (E) radiographs following a linked Latitude total elbow arthroplasty.

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Part VII Reconstructive Procedures of the Elbow

been favorable because the implant has been able to deal with a wide variety of pathologies and patient profiles. The hemiarthroplasty has been used to manage acute distal humeral fractures, nonunions, and avascular necrosis. Patients with relatively well-preserved bone stock and ligaments are typically managed with the unlinked version of the arthroplasty and this is the author’s current preference (Fig. 52-53). Patients with poor bone stock or ligaments, particularly related to previous trauma, are typically managed with a linked arthroplasty (Fig. 52-54). The radial head is replaced if it is damaged by disease, such as in rheumatoid arthritis, but is retained if it is relatively well preserved, for example in post-traumatic arthritis or acute distal humeral fractures.

References 1. Bryan, R. S., and Morrey, B. F.: Extensive posterior exposure of the elbow. A triceps-sparing approach. Clin. Orthop. 166:188, 1982. 2. Celli, A., Arash, A., Adams, R. A., and Morrey, B. F.: Triceps insufficiency following total elbow arthroplasty. J. Bone Joint Surg. Am. 87:1957, 2005. 3. Chiodo, C. P., Terry, C. L., and Koris, M. J.: Reconstruction of the medial collateral ligament with flexor carpi radialis tendon graft for instability after capitellocondylar total elbow arthroplasty. J. Shoulder Elbow Surg. 8:284, 1999.

4. Gramstad, G. D., King, G. J., O’Driscoll, S. W., and Yamaguchi, K.: Elbow arthroplasty using a convertible implant. Tech. Hand Up. Extrem. Surg. 9:153, 2005. 5. Itoi, E., Niebur, G. L., Morrey, B. F., and An, K. N.: Malrotation of the humeral component of the capitellocondylar total elbow replacement is not the sole cause of dislocation. J. Orthop. Res. 12:665, 1994. 6. Joshi, R. P., Yanni, O., and Gallannaugh, S. C.: A modified posterior approach to the elbow for total elbow replacement. J. Shoulder Elbow Surg. 8:606, 1999. 7. Lerch, K., Tingart, M., Trail, I., and Grifka, J.: [Total elbow arthroplasty. Indications, operative technique and results after implantation of an Acclaim elbow prosthesis]. Orthopade 32:730, 2003. 8. O’Driscoll, S. W., and King, G. J.: Treatment of instability after total elbow arthroplasty. Orthop. Clin. North Am. 32:679, ix, 2001. 9. Pierce, T. D., and Herndon, J. H.: The triceps preserving approach to total elbow arthroplasty. Clin. Orthop. Rel. Res. 354:144, 1998. 10. Ring, D., Kocher, M., Koris, M., and Thornhill, T. S.: Revision of unstable capitellocondylar (unlinked) total elbow replacement. J. Bone Joint Surg. Am. 87:1075, 2005. 11. Shah, B. M., Trail, I. A., Nuttall, D., and Stanley, J. K.: The effect of epidemiologic and intraoperative factors on survival of the standard Souter-Strathclyde total elbow arthroplasty. J. Arthroplasty 15:994, 2000. 12. Wolfe, S. W., and Ranawat, C. S.: The osteo-anconeus flap. An approach for total elbow arthroplasty. J. Bone Joint Surg. Am. 72:684, 1990.

Chapter 53 Linked Elbow Arthroplasty: Rationale, Indications, and Surgical Technique

CHAPTER

53

Linked Elbow Arthroplasty: Rationale, Indications, and Surgical Technique Bernard F. Morrey

INTRODUCTION As noted in Chapter 52 and further described in Chapters 54 through 60, the results of total elbow arthroplasty are improving with increased basic knowledge of elbow mechanics,24 better designs, and greater surgical experience.21 The general principles of the surgical technique and improved designs2,9,14,18,24 and a detailed description of my specific method of inserting the Coonrad-Morrey implant are presented. The results of semiconstrained joint replacement arthroplasty emphasize the Mayo Clinic experience with the modified Coonrad device.

RATIONALE The selection and the rationale for unlinked elbow replacement are described in Chapter 52. The reason for continuing to use a semiconstrained linked implant is simple: the current design works well, is reproducible, and can address a broad spectrum of pathology. The Coonrad-Morrey linked device and similar implants are distinctly different, both conceptually and clinically, from the original, fully constrained articulated devices. In today’s linked prostheses, the one feature in common is that the ulnar component is coupled to the humerus with angular and rotatory laxity of 5 to 10 degrees (Fig. 53-1). The theoretical advantage has been confirmed in the laboratory in which it was demonstrated that the articulation tracks within the limits of its tolerance (Fig. 53-2). This decreases stresses on the bone-cement interface.24 Documentation of improved clinical results attests to the effectiveness of the semiconstrained linked design.2,4,13,14,16,18,21 Of particular note is that the linked implant dramatically broadens the indications for recon-

765

structive surgery of the elbow. Whereas unlinked devices may be very effective for rheumatoid arthritis, the potential for instability limits their use when deformity and osseous and ligamentous deficiency is present. The linked implant may be used with equal effectiveness in patients with rheumatoid arthritis,20 for post-traumatic arthrosis,19 and for revision surgery.18 The enhanced stability supplied by the coupling is provided without transmission of excessive stress to the bone-cement interface with the semiconstrained design.24

INDICATIONS The indication for the semiconstrained linked joint replacement design may be summarized in general terms as constituting the full spectrum of elbow pathology. Hence, patients with rheumatoid arthritis can usually be managed regardless of the degree of bone or soft tissue present or destroyed. The stiff, deformed, or unstable elbow may also be effectively managed with linked devices. Primary or revision procedures with minimal or extensive bone loss were also amenable to management by linked devices.

CONTRAINDICATIONS As for any total elbow arthroplasty, the absolute contraindications for a linked arthroplasty are active infection, inadequate soft tissue protection, and the lack of adequate motor muscle power to flex the elbow to ensure proper functioning of the device. Relative contraindications are lack of patient compliance. Primary degenerative joint disease is also a relative contraindication because patients with this disease are usually younger and active, and alternative selections are effective (see Chapter 60). High demand and a dysfunctional hand are also relative contraindications for total elbow arthroplasty.

PRINCIPLES OF SURGICAL TECHNIQUE One of the most important factors in the improved results of elbow joint replacement in the past and particularly with those being developed is improved surgical technique. Here, we describe our current technique.

POSITIONING The patient is placed in the position of the surgeon’s preference. I place the patient supine with sandbags under the hip and the scapula. The arm is draped free, a nonsterile tourniquet is used, and the extremity is brought across the chest.

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Part VII Reconstructive Procedures of the Elbow

NORMAL KINEMATICS Valgus stress

Varus/valgus, °

3

Neutral 0

−3

Varus stress

0

30

A

60

90

TEA KINEMATICS Valgus stress

A semiconstrained implant, whether it be of an axle or a snap-fit design, is characterized by varus-valgus and axial rotation tolerances of several degrees at the articulation.

Varus/valgus, °

6

FIGURE 53-1

0 Neutral Varus stress

−6

0

30

B

SURGICAL INCISION A straight posterior skin incision is preferred. If a previous incision is present it is employed when possible. If the patient is older than 4 or 5 years of age, it may be repaired if it cannot be incorporated. The incision need not and should not be curved.

THE ULNAR NERVE Opinions are divided with respect to the management of the ulnar nerve. Some surgeons believe that it should not be exposed,7,9,12,16,27 whereas today most believe that the ulnar nerve should be directly visualized and moved as an integral part of the surgical approach and procedure.4,10,15,23 We favor the latter philosophy.

THE TRICEPS The fascial tongue exposure of Campbell (Van Gorder) causes a good deal of soft tissue dissection, with a significant amount of dead tissue that provides an environment favorable to infection, which may result in weakness.5,22 Splitting the triceps in the midline is enjoying a resurgence of popularity. In our experience, this tends to cause detachment of the medial insertion.

150

Flexion, °

10°

10°

120

60

90

120

150

Flexion, °

FIGURE 53-2

The semiconstrained articulation provides flexion motion that replicates normal kinematics (A) and constraints of the design and thus reduces stress at the bone-cement interface (B). TEA, total elbow arthroplasty. (With permission from the Mayo Foundation.)

Therefore, I continue to prefer the Mayo technique of reflecting the triceps in continuity with the ulnar periosteum and forearm fascia described by Bryan and Morrey.5 The important point, however, is a meticulous repair (see later).

EXPOSURE Regardless of the technique, adequate visualization of the joint and of the proximal ulnar and distal humeral shafts must be obtained. This should prevent inadvertent supracondylar column fracture or cortical perforation. Reliable orientation of the stemmed implant requires adequate exposure and orientation of landmarks.

AXIS OF ROTATION The philosophy of the Coonrad-Morrey device is to use the most reliable landmark to serve as the basis for

Chapter 53 Linked Elbow Arthroplasty: Rationale, Indications, and Surgical Technique

defining the flexion axis. The landmark selected for this system is the anterior cortex to establish the anterior/ posterior position of the axis. The roof of the coronoid fossa is the anatomic reference for depth of insertion, and the plane of the columns define the rotation of the axis of the humeral component (Fig. 53-3).

TRIAL REDUCTION Trial reduction, of course, is an essential step for a reliable elbow joint replacement of any design. This is particularly important for uncoupled devices in persons who have a moderate or severe flexion contracture. It is the only way to determine if the implant has been adequately seated and to assess whether sufficient soft tissue has been released.

CEMENTING TECHNIQUE The cement should be introduced down the medullary canal for stemmed implants with an injection system. Generally speaking, injector systems have dramatically improved the radiographic appearance of the bonecement interface. It was shown in our early experience20,23 and subsequently Faber,8 that the quality of the cementing technique is inversely related to the presence of lucent lines, and, ultimately, to implant loosening (Fig. 53-4).

TRICEPS REATTACHMENT Triceps reattachment has emerged as a major emphasis for all elbow joint replacement surgery. Whenever the

A

C

M

L

B FIGURE 53-3

767

Locating the axis of rotation. The Coonrad-Morrey device employs the anterior cortex to identify anterior/posterior location (A); the flange seats against the proximal aspect of the coronoid fossa, identifying the level of proximal insertion (B). Rotation is defined by the posterior plane of the medial and lateral columns (C). (C, with permission from the Mayo Foundation.)

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Part VII Reconstructive Procedures of the Elbow

Warsaw, IN). To date, these two implants have not had sufficient use to document outcomes. The GSB III has evolved through the years and has been frequently used in Europe but its use and support is being discontinued (Fig. 53-5). Experience with the GSB III devices is discussed under the appropriate indications in subsequent chapters. Risung25 has also reported favorable outcomes with a rather novel implant designed termed the Norway elbow.

THE COONRAD-MORREY DEVICE FIGURE 53-4

The incidence of prosthesis revision loosening shows an inverse relationship to the technical quality of the cementing. (With permission from the Mayo Foundation.)

triceps is reflected from its attachment, it must be securely reattached to the olecranon by nonabsorbable sutures placed through bone. The sutures should be tied with the elbow in 90 degrees of flexion, but knots are avoided over the subcutaneous border of the ulna. Because the attachment communicates with the joint and motion will allow the synovial fluid to become interposed between the triceps and the olecranon, an attachment may be compromised. The transverse “cinch” suture applies the tendon to the olecranon. To enhance strength and ensure continuity, we also tend to displace the extensor mechanism slightly medially, if possible, bringing the anconeus slightly over the proximal ulna.

POSTOPERATIVE DRESSING We have had virtually no incision problems because we have been routinely placing the elbow in full extension with an anterior splint and elevating the arm for approximately 24 hours. We see no advantage to allowing the elbow to assume 90 degrees of flexion immediately after surgery. Because of continued concern for the variable swelling and occasional blistering that may occur after surgery, I no longer use the Steri-Drape, and I avoid Betadine solution if the barrier drape is used. A prospective, randomized study recently revealed statistically measurable decreases in swelling after surgery with the use of a compression Cryocuff (Aircast Co., Coconut Creek, FL).1

THE SEMICONSTRAINED LINKED IMPLANT Today, in the United States, several semiconstrained elbow replacements are commercially available, including the Coonrad-Morrey (Zimmer, Warsaw, IN), the Latitude (Tornier, Edina, MN), and the Discovery (Biomet,

The Mayo modified Coonrad total elbow prosthesis (Coonrad-Morrey) is a semiconstrained device manufactured from Tivanium Ti-6Al-4V alloy. In 1978, the initial design (Coonrad I) Zimmer Company (Warsaw, IN). was modified by the Mayo Clinic to permit 7 to 10 degrees of hinge laxity, or toggle (Coonrad II), which is consistent with the average laxity of the normal elbow joint (Table 53-1). This change accounts for the semiconstrained designation applied to the device. The effect of this design concept is discussed above (see Figs. 53-1 and 53-2). The implant was designed for use with methylmethacrylate and is manufactured in two sizes: a regular and a small size (15-percent reduction). The current limited version was released in 1981. It currently has a basic hinge articulation with a hollow cobalt chrome pin that passes through the ultra-high-molecular weight polyethylene bushings to capture the ulnar component. A second pin is inserted from the opposite side to secure the articulation (Fig. 53-6). The prosthesis is easily disassembled if desired. A flange was incorporated in this version to resist posterior and torsional forces. Right and left specificity is attained from the contoured quadrangular ulnar stem. The triangular humeral stem is interchangeable right or left. This implant is intended to be used with bone cement for both immediate and long-term fixation. The humeral stem comes in 10-, 15-, and 20-cm stem lengths (Fig. 53-7). The 15-cm stem is most often used in nonrheumatoid patients to ensure adequate mechanical resistance to rotation in the humerus. The 4-inch stem is used when a shoulder involved by rheumatoid arthritis has been or may be replaced with a humeral prosthesis.11,13 The 8-inch stem is used for revision procedures requiring the device to bypass the prior stem tip (see Chapter 66). The ulna implant is made in standard and small dimensions. The small dimension also comes in an extra long size. Finally, for the patient with juvenile rheumatoid arthritis or a very small canal, as is common in those from Asia, a special extra-small implant is available (Fig. 53-8).

Chapter 53 Linked Elbow Arthroplasty: Rationale, Indications, and Surgical Technique

FIGURE 53-5

A, The Pritchard II was an early and widely used semiconstrained elbow replacement. B and C, The coupling mechanism of the triaxial device has been modified several times. The triaxial began as a snap-fit design to provide joint stability, as does the English Stanmore prosthesis (D). E and F, The GSB III is a popular semiconstrained device used in Europe. G, The Norway elbow designed by Risung is a type of snap-fit design, but with a spool-type snap-fit trochlear design. H, Clinical results have been excellent.

769

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Part VII Reconstructive Procedures of the Elbow

TABLE 53-1

Coonrad-Morrey Implant Modifications

1981-1998 Device

Year

Feature/Modification

Coonrad

1971

Rigid hinge

Coonrad II

1978

Semiconstrained loose hinge

Coonrad-Morrey

1981

Flange, surface treatment

1984

Plasma spray replaced with beads

1991

Beads on ulna replaced with polymethyl methacrylate precoat

1993

Titanium articular pin replaced by cobalt-chromium pin

1998

C ring replaced by pin within a pin

FIGURE 53-7

The humeral components are available in 10-, 15-, and 20-cm lengths and in small and standard sizes.

FIGURE 53-6

The current Coonrad-Morrey semiconstrained implant. Note redesigned articulation locking pin and plasma spray treatment of the proixmal ulna.

SURGICAL TECHNIQUE FOR COONRADMORREY TOTAL ELBOW ARTHROPLASTY Author’s Preference Exposure The patient is positioned supine with a sandbag under the scapula, and the arm is draped free with a nonsterile tourniquet and brought across the chest (Fig. 53-9). The Mayo (Bryan-Morrey) approach is used exclusively for this procedure if condyles are present. In the absence of a distal humerus, the triceps attachment to the olecranon is maintained.5 A straight 15-cm incision is centered just lateral to the medial epicondyle and just medial to the tip of the olecranon. The

medial aspect of the triceps is identified, and the ulnar nerve is carefully isolated and translocated using ocular magnification and a bipolar cautery. It is gently protected throughout the remainder of the procedure. Over the medial aspect of the proximal ulna, the ulnar periosteum is elevated along with the forearm fascia (Fig. 53-10). The posterior capsule is incised. The triceps is elevated from the proximal ulna by transecting Sharpey’s fibers at the site of insertion. The extensor mechanism, including the anconeus, is reflected laterally, allowing complete exposure of the distal humerus, the proximal ulna, and the radial head. The radial and ulnar collateral ligament complexes are released from their attachments in persons with rheumatoid arthritis (Fig. 53-11). Failure to do this may facilitate a fracture of the medial column as the forearm is manipulated. The tip of the olecranon is removed. The humerus is externally rotated, the elbow is hyperflexed, the forearm is brought lateral to the humeral shaft, and the hand is flexed behind the patient’s ear.

The Maneuver

Humeral Preparation The midportion of the trochlea is removed with a rongeur or a saw, depending on the softness of the bone. The medullary canal of the humerus is identified by entering it with a rongeur or a burr at

Chapter 53 Linked Elbow Arthroplasty: Rationale, Indications, and Surgical Technique

771

FIGURE 53-8

The ulnar component is available in small (A) and standard sizes. A longer small implant, also available, is commonly used for revision (B). An extrasmall, long device is available and can be shortened for very small canals, as in patients with juvenile rheumatoid arthritis (C).

Ulnar crest

Ulnar nerve

FIGURE 53-9

The preferred supine position with a sandbag under the patient’s shoulder and the arm lying across the chest. (With permission from the Mayo Foundation.)

the roof of the olecranon fossa (Fig. 53-12) and entered with a twist reamer. The medial and lateral aspects of the supracondylar columns should be identified and visualized throughout the preparation of the distal humerus to ensure proper alignment and orientation. The alignment stem is placed down the canal (Fig. 53-13). The handle is removed, and a cutting block is attached, which allows accurate removal of the appropriate amount of the articular surface of the distal humerus. The interchangeable side arm of the cutting block is attached laterally to rest on the capitellum and to provide the appropriate depth of cut (Fig. 53-14).

Note: The flat of the template rests on the posterior columns to ensure accurate replication of the all important rotatory alignment of the humeral implant. With an oscillating saw, the trochlea is removed according to the dimensions of the appropriate cutting block that corresponds to the sizes of the humeral component. Care should be taken to avoid violating either supracondylar bony column because such disruption may cause a stress riser, leading to a fracture. The humerus involved by rheumatoid arthritis is easily prepared with a rasp in such a way as to receive the appropriately sized humeral component. In younger patients and those with post-traumatic conditions, the

772

Part VII Reconstructive Procedures of the Elbow

Sharpey’s fibers

Motor branch of ulnar n.

Flexor carpi ulnaris m.

FIGURE 53-10 In the Mayo approach used for the semiconstrained implant, the ulnar nerve is identified and the triceps is released from the tip of the olecranon in continuity with the forearm fascia and periosteum. (With permission from the Mayo Foundation.)

Medial epicondyle

Released MCL Released LCL

Ulnar n.

Triceps

FIGURE 53-12

The medullary canal is identified by perforating the roof of the olecranon fossa with a burr or a rongeur. (With permission from the Mayo Foundation.)

FIGURE 53-11 The tip of the olecranon is removed along with the medial collateral ligament (MCL) and the lateral collateral ligament (LCL). The ulna is flexed and rotated to expose the humerus. The radial head is resected or débrided, depending on the extent of disease. (With permission from the Mayo Foundation.)

Chapter 53 Linked Elbow Arthroplasty: Rationale, Indications, and Surgical Technique

773

FIGURE 53-13

Sufficient exposure is required to identify the medial and lateral columns. An alignment stem is placed down the canal. (With permission from the Mayo Foundation.)

canal may be tight, or the anterior humeral bow may make preparation more difficult. A burr is effective to remove bone just proximal to the oriface of the olecranon fossa. The medullary canal of the ulna is identified by using a high-speed burr at about a 45degree angle to the base of the coronoid (Fig. 53-15). The tip of the olecranon is removed, notched, or both, to allow identification of the canal by a small reamer. An appropriately sized rasp is then used, and a mallet is generally required to remove the subchondral bone around the coronoid (Fig. 53-16). The rasp handle is maintained at an orientation perpendicular to the plane of the “flat” of the proximal ulna. This corresponds to the flexion axis and serves to accurately orient the ulnar component. If the canal is tight, flexible reamers are available to prepare and expand the medullary cavity. Ulnar Preparation

A trial reduction allows assessment of depth of insertion and soft tissue restriction to extension. The ulna is inserted to the depth that corresponds to the axis of the implant replicating the axes flexion (Fig. 53-17).

Trial Reduction

FIGURE 53-14 The appropriate cutting block depth is adjusted by the outrigger, which rests over the capitellum and allows accurate removal of bone to receive an implant of a given size. (With permission from the Mayo Foundation.)

Implant Insertion The medullary cavities of both bones are cleansed with a pulsating lavage irrigation system and dried. A medullary cement restrictor is used in the humerus to avoid proximal cement delivery when a shoulder replacement is to be performed or is being contemplated. The cement is first injected down the humeral medullary canal to a depth determined by the length of the humeral stem (Fig. 53-18). The cement is then injected down the ulnar canal. A bone graft is prepared from the excised trochlea or from the bone bank for revision surgery. The graft should measure about 3 to 4 mm in thickness and should be about 2 cm long and 1.5 cm wide. The bone graft is placed anterior to the anterior cortex of the distal humerus, and the humeral component is inserted down the canal to a point that allows articulation of the device at a level where the bone graft is partially covered by the flange as well (Fig. 53-19). If the canal is tight, the anterior bow of the humerus is accommodated by

Part VII Reconstructive Procedures of the Elbow

774

45°

A

A

on

f olecran

Plane o

B FIGURE 53-15

The subcutaneous border of the proximal ulna is visualized and palpated so that the medullary canal may be safely entered with a burr oriented at about a 45-degree angle at the base of the coronoid (A). The olecranon is notched to allow direct entry down the canal (B). (With permission from the Mayo Foundation.)

making a slight bow in the humeral stem with the plate bender (Fig. 53-20). The ulnar component is articulated with the humeral device by placing the hollow axis through the humerus and ulna and securing it with the solid pin inserted from the opposite direction (Fig. 53-21). After the prosthesis has been coupled, the ulna is placed at a 90-degree angle, and the humeral component is impacted down the medullary canal (Fig. 53-22). In general, the device is inserted to a point at which the axis of rotation of the prosthesis is at the level of the normal anatomic axis of rotation. This is approximated when the base of the flange is flush to the anterior bone of the olecranon fossa and the distal aspect of the humeral component is flush or slightly proximal to the distal aspect of the capitellum. If the triceps has been reflected, it is secured to the ulna with a heavy (No. 5) nonabsorbable

The Triceps

90°

B FIGURE 53-16 (A) The proximal canal is prepared with an appropriately sized ulnar rasp. (B) The implant rotation is determined by placing the flexion plane perpendicular to the “flat” portion of the proximal ulna. (With permission from the Mayo Foundation.)

FIGURE 53-17 The ulna is inserted until the center of the ulnar component coincides with the center of the greater sigmoid fossa. (With permission from the Mayo Foundation.)

Chapter 53 Linked Elbow Arthroplasty: Rationale, Indications, and Surgical Technique

775

FIGURE 53-19 The bone graft placed simultaneously behind the distal humerus engages the flange before the joint is articulated. This ensures that the bone graft will be positioned accurately when the humeral component is finally seated. (With permission from the Mayo Foundation.)

A

suture. The first stitch penetrates the lateral tendon in the reduced position and is locked. A second locked throw is placed in the medial tendon, the suture then penetrates the tendon in line with the proximal medial tunnel. It passes through the tunnel from proximal medial to distal lateral. It then is brought through the soft tissue there and is tied to itself. An additional transverse suture is placed across the olecranon, locks at the posterior aspect of the olecranon in the center portion of the tendon and is tied to itself (Fig. 53-23). Sutures are tied beneath the tendon because were they subcutaneous, they might irritate or cause stitch abscess. The tourniquet is deflated, the arm is elevated and compressed for 4 to 5 minutes, and hemostasis is obtained. Drains are optional and the wound is closed in layers. A suture closes the subcutaneous tissue over the translocated ulnar nerve at the medial epicondyle. The rest of the closure is routine. A compressive dressing is applied with the elbow in full extension. The plaster splint is no longer used.

Closure

B FIGURE 53-18 The humeral canal is filled with the intramedullary cement injector system to accommodate a 4-, 6-, or 8-inch humeral component (A). The injector nozzle is cut for the appropriate length of the ulnar component (B). (With permission from the Mayo Foundation.)

776

Part VII Reconstructive Procedures of the Elbow

A

B

POSTOPERATIVE MANAGEMENT The arm is elevated postoperatively for 24 hours, with the elbow above shoulder level. If drains are used, they are removed after approximately 24 hours, and the compressive dressing is removed 24 hours later. A light dressing is applied, and elbow flexion and extension are allowed, as tolerated. A collar and cuff are used, and the patient is allowed to begin activities of daily living. No formal physical therapy is required or indicated. Strength exercises are avoided. Typically, the patient leaves the hospital on the third day and is advised not to lift more than 0.5 kg over the next 3 months. We typically recommend that the patient not lift more than 4 to 5 kg with

FIGURE 53-20 When the canal is small, the normal slight anterior bow may require that the 15- or 20-cm implant be bent slightly anteriorly (A) with a plate bender (B). This allows the stem to avoid posterior penetration of the humeral cortex (C). (With permission from the Mayo Foundation.)

the operated arm as a single event, or more than 1 kg repeatedly. If a flexion contracture greater than 45 degrees existed before surgery, an extension turnbuckle splint is regularly used at night for 4 to 12 weeks.

RESULTS Experience with this device for several conditions is discussed in subsequent chapters. The intermediate and long-term experience is emerging for those with rheumatoid arthritis (Fig. 53-24) and for post-traumatic conditions (Fig. 53-25). The results remain gratifying. Text continued on p. 781

Chapter 53 Linked Elbow Arthroplasty: Rationale, Indications, and Surgical Technique

A

777

B FIGURE 53-21 The articulation is coupled by a pin-within-a-pin mechanism (A) that is very easy to apply. Removal is equally easily done with a special device (B). (With permission from the Mayo Foundation.)

FIGURE 53-22 A specially designed instrument allows impaction of the humeral implant down the canal. (With permission from the Mayo Foundation.)

778

Part VII Reconstructive Procedures of the Elbow

A

B

C FIGURE 53-23 Bone tunnels are placed in the proximal ulna (A). The triceps is reattached with a suture that goes through the forearm and the periosteal sleeve and then through one of the diagonal holes placed in the proximal ulna (B). A criss-cross suture is placed on the triceps. The suture is then brought through a second diagonal hole in the forearm and the ulnar periosteum and is tied (C). A second suture is placed through the tip of the olecranon and through the triceps to ensure firm apposition of the triceps at the site of its previous insertion (D). (By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

D

Chapter 53 Linked Elbow Arthroplasty: Rationale, Indications, and Surgical Technique

FIGURE 53-24

A and B, Patient with severe grade III rheumatoid arthritis. C and D, Excellent 8-year result after replacement.

779

780

Part VII Reconstructive Procedures of the Elbow

FIGURE 53-25 Two years after sustaining a supracondylar fracture, the patient had painful nonunion and tapering of the distal humeral shaft, as shown on the anteroposterior (A) and lateral (B) radiographs. C, Gross instability is evidenced by 45 degrees of varus angulation against gravity. The patient was treated with the newer design of elbow arthroplasty that incorporates an anterior flange to control the rotational and posterior displacement stresses. D, Anteroposterior and lateral views 16 years after replacement.

Chapter 53 Linked Elbow Arthroplasty: Rationale, Indications, and Surgical Technique

References 1. Adams, R. A., and Morrey, B. F.: The effectiveness of a compressive Cryocuff after elbow surgery. A prospective randomized study. Presented at the annual meeting of the AAOS, Anaheim, CA, February 1999. 2. Bell, S., Gschwend, N., and Steiger, U.: Arthroplasty of the elbow. Experience with the Mark III GSB prosthesis. Aust. N.Z. J. Surg. 56:823, 1986. 3. Brownhill, J. R., Furukawa, K., Faber, K. J., Johnson, J. A., and King, G. J. W.: Surgeon accuracy in the selection of the flexion-extension axis of the elbow. An in vitro study. J. Shoulder Elbow Surg. 15:451, 2006. 4. Brumfield, R. H., Kuschner, S. H., Gellman, H., Redix, L., and Stevenson, D. V.: Total elbow arthroplasty. J. Arthroplasty 5:359, 1990. 5. Bryan, R. S., and Morrey, B. F.: Extensive posterior exposure of the elbow. A triceps-sparing approach. Clin. Orthop. Relat. Res. 166:188, 1982. 6. Duggal, N., Dunning, C. E., Johnson, J. A., King, G. J. W.: The flat spot of the proximal ulna: a useful anatomic landmark in total elbow arthroplasty. J. Shoulder Elbow Surg. 13:206, 2004. 7. Ewald, F. C., Scheinberg, R. D., Poss, R., Thomas, W. H., Scott, R. D., and Sledge, C. B.: Capitellocondylar total elbow arthroplasty: 2- to 5-year follow-up in rheumatoid arthritis. J. Bone Joint Surg. 62A:125, 1980. 8. Faber, K. Y., Cordy, M. E., Milne, A. D., Chess, D. G., King, G. J., and Johnson, J. A.: Advanced cement technique improves fixation in elbow arthroplasty. Clin. Orthop. 334:150, 1997. 9. Figgie, M. P., Inglis, A. E., Mow, C. S., and Figgie, H. E. III: Salvage of nonunion of supracondylar fracture of the humerus by total elbow arthroplasty. J. Bone Joint Surg. 3:235, 1988. 10. Figgie, H. E. III, Inglis, A. E., Ranawat, C. S., and Rosenberg, G. M.: Results of total elbow arthroplasty as a salvage procedure for failed elbow reconstructive operations. Clin. Orthop. Relat. Res. 219:185, 1987. 11. Friedman, R. J., and Ewald, F. C.: Arthroplasty of the ipsilateral shoulder and elbow in patients who have rheumatoid arthritis. J. Bone Joint Surg. 69A:661, 1987. 12. Friedman, R. J., Lee, D. E., and Ewald, F. C.: Nonconstrained total elbow arthroplasty: development and results in patients with functional class IV rheumatoid arthritis. J. Arthroplasty 4:31, 1989. 13. Gill, D., and Morrey, B. F.: The Coonrad-Morrey total elbow arthroplasty in patients with rheumatoid arthritis:

14.

15.

16.

17. 18.

19.

20.

21.

22.

23.

24.

25.

26.

27.

781

a 10-15 year follow-up study. J. Bone Joint Surg. 80A:1327, 1998. Gschwend, N., Loehr, J., Ivosevic-Radovanovic, D., Scheier, H., and Munzinger, U.: Semiconstrained elbow prostheses with special reference to the GSB III prosthesis. Clin. Orthop. Relat. Res. 232:104, 1988. Johnson, J. R., Getty, C. J. M., and Lettin, A. W. F.: The Stanmore total elbow replacement for rheumatoid arthritis. J. Bone Joint Surg. 66B:732, 1984. Madsen, F., Gudmundson, G. H., Søjbjerg, J. O., and Sneppen, O.: The Pritchard-Mark II elbow prosthesis in rheumatoid arthritis. Acta Orthop. Scand. 60:249, 1989. Morrey, B. F.: The Elbow and Its Disorders. Philadelphia, W. B. Saunders Co., 1985. Morrey, B. F.: Semi-constrained total elbow arthroplasty. In Morrey, B. F. (ed.): Joint Replacement Arthroplasty. New York, Churchill Livingstone, 1991, p. 311. Morrey, B. F., Adams, R. A., and Bryan, R. S.: Total replacement for posttraumatic arthritis of the elbow. J. Bone Joint Surg. 73B:607, 1991. Morrey, B. F., and Adams, R. A.: Semiconstrained elbow replacement for rheumatoid arthritis. J. Bone Joint Surg. 74A:479, 1992. Morrey, B. F., and Adams, R. A.: Semiconstrained elbow replacement for distal humeral nonunion. J. Bone Joint Surg Br. 77:67-72, 1995. Morrey, B. F., Askew, L. J., and An, K. N.: Strength function after elbow arthroplasty. Clin. Orthop. Relat. Res. 234:43, 1988. Morrey, B. F., Bryan, R. S., Dobyns, J. H., and Linscheid, R. L.: Total elbow arthroplasty: a five-year experience at the Mayo Clinic. J. Bone Joint Surg. 63A:1050, 1981. O’Driscoll, S., An, K., and Morrey, B. F.: The kinematics of elbow semiconstrained joint replacement. J. Bone Joint Surg. 74B:297, 1992. Risung, F.: Characteristics, design and preliminary results of the Norway Elbow System. In Hämäläinen, M., and Hagena, F.-W. (eds.): Rheumatoid Arthritis Surgery of the Elbow. Rheumatology. Vol 15. Basel, Karger, 1991, p. 68. Schuind, F., O’Driscoll, S., Korinek, S., An, K. N., and Morrey, B. F.: Loose-hinge total elbow arthroplasty: an experimental study of the effects of implant alignment on threedimensional elbow kinematics. J. Arthroplasty 10:670, 1995. Wolfe, S. W., and Ranawat, C. S.: The osteo-anconeus flap. J. Bone Joint Surg. 72A:684, 1990.

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Part VII Reconstructive Procedures of the Elbow

CHAPTER

54

Linked Total Elbow Arthroplasty in Patients with Rheumatoid Arthritis David R. J. Gill, Bernard F. Morrey, and Robert A. Adams

INTRODUCTION Both coupled and uncoupled elbow replacement prosthetic designs are employed for the management of end-stage rheumatoid arthritis.11,12,43 This chapter reviews the results of the linked, semiconstrained design, primarily that of the Coonrad/Morrey. As noted previously in this text, the clinical and radiologic presentation of inflammatory arthritis in general and rheumatoid arthritis in particular varies considerably (Fig. 54-1). The semiconstrained implant is especially useful in the type III and IV presentations because this design philosophy assesses stability in the face of bone loss and joint laxity2 (Fig 54-2). When considering the outcome of total elbow arthroplasty, it is helpful to define the expectations of the intervention: 1. Relief of pain 2. Attainment of a functional range of motion in flexion, extension, supination, and pronation 3. Stability 4. Adequate strength to perform daily functions To date, several evaluation systems exist that allow a critical assessment of the elbow when affected by disease and after therapeutic intervention (see Chapter 5). In the past, we employed the Mayo Elbow Performance Score (MEPS) as defined in Table 54-126 and are currently incorporating the measurements of the Disabilities of the Arm, Shoulder and Hand (DASH) questionnaire as well. Review of the literature reveals improving and encouraging results with several semiconstrained designs (Table 54-2).16 In this chapter, we review several of these experiences and then focus on Mayo’s perspective and outcomes. The outcome of replacement for rheumatoid is superior to that for traumatic arthritis.3

HISTORICAL PERSPECTIVE Linked, less constrained designs were introduced in the early 1970s to address problems of early stem loosening attributed to the rigid hinge design. For the most part, the results of these devices were encouraging.

THE PRITCHARD PROSTHESIS The Pritchard II prosthesis (Fig. 54-3) was an early design introduced in the 1970s as a linked semiconstrained device.32,38,39 Pritchard’s own experience with 92 patients was reported in 1981 and included 55 with rheumatoid arthritis. The mean follow-up was short (2.5 years). Although the range of motion, stability, and measure of function were not reported, relief of pain was reported as 98%.38 A 15% complication rate and 2% loosening requiring revision were recorded. Subsequently, Madsen and associates32 followed 25 consecutive Pritchard II implants for a mean of 3 years. Twenty-three of 25 patients had relief of pain. The flexion arc averaged 28 to 130 degrees and pronationsupination was 65 to 62 degrees, respectively. Stability was not discussed, but the mean assessment score improved from 40 to 82. However, radiographic loosening occurred in 6 of 24 elbows, and two necessitated revision. These initial reports of the Pritchard II implant were of small numbers, and their findings were regarded as preliminary.32,38,39 The major problem was wear or fracture of the polyethylene bearing. The device was subsequently modified but is not used to any extent today.

THE TRIAXIAL DEVICE There has been a tendency for wear and dislocation over time; however,13 this articulation has undergone numerous modifications but still allows several degrees of varus-valgus and axial rotation “play” (Fig. 54-4). The implant has been used almost exclusively for patients with rheumatoid arthritis. A customized version has been described for various pathologic states other than rheumatoid arthritis.

RESULTS In the past, several reports emanating from the designing institution have documented the use of several variations of this design for rheumatoid arthritis. In general, a 90% satisfactory result is reported with follow-up less than 5 years.21 In one large series, Kraay and associates26 reviewed the outcome of 113 patients. Of these, 86 had rheumatoid arthritis. With surveillance averaging 5 years, five devices had failed owing to sepsis, but only

Chapter 54 Linked Total Elbow Arthroplasty in Patients with Rheumatoid Arthritis

FIGURE 54-1

783

The spectrum of radiographic presentation from grades I to V in patients with rheumatoid arthritis after Connor and Morrey9 and Morrey.33

784

Part VII Reconstructive Procedures of the Elbow

FIGURE 54-2

Severe type IV involvement (A) is unpredictably treated by resurfacing implants but readily managed with a semiconstrained device (B and C).

TABLE 54-1

Mayo Elbow Performance Score*

Function

Point Score

Pain (45 points) None Mild Moderate Severe

45 30 15 0

Motion (20 points) Arc 100 degrees Arc 50 to 100 degrees Arc 2 degrees

20 15 5

Stability (10 points)† Stable Moderate instability Gross instability Daily function (25 points) Combing hair Feeding oneself Hygiene Putting on shirt Putting on shoes Maximum possible total

10 0 5 5 5 5 5 100

*90 points or more = excellent; 75 to 89 points = good; 60 to 74 points = fair; and less than 60 points = poor. † Stable = no apparent varus-valgus laxity clinically; moderate instability = less than 10 degrees of varus-valgus laxity; gross instability = 10 degrees or more of varus-valgus laxity.

two had been revised because of aseptic loosening. The 3- and 5-year survival rates were 92% and 90%, respectively, but the outcome has subsequently deteriorated owing to instability occurring when the bushing wore.

GSB III PROSTHESIS This device has also undergone several design modifications, primarily related to the articulation. Stabilization of the fixation is sought by wrapping the implant around the distal aspect of the medial and lateral condyles. The device also allows 2- to 3-mm axial translation. Virtually all of the GSB experience is from Europe. The current GSB II device provides about 4 degrees of varus-valgus toggle and uniquely some axial translation (Fig. 54-5). The stem is stabilized by medial and lateral flanges that are attached to the condyles. Hence, a requirement of this implant is intact or reconstructed condyles. Experience with the modified implant was reported by Bell and colleagues4 in 1986. Forty-one of 46 patients had relief of pain, and range of motion averaged 29 to 137 degrees. In 1988, Gschwend and associates17 updated this experience, with the majority of patients having rheumatoid arthritis. Fifty-three of 57 patients had relief of pain; extension-flexion improved from 29 to 140 degrees, with pronation-supination increasing 68 to 64 degrees, respectively. In five elbows,

34

28

1

Totals

Cesar et al, 2007

8

Aldridge et al, 2006

Jensen et al, 200622

Lee et al, 2005

Lo et al, 2003

30

GSB III

Coonrad/Morrey

GSB III

Coonrad-Morrey

Coonrad-Morrey

Coonrad-Morrey

Norway

Risung, 199740

Gill and Morrey, 1998

GSB III

Gschwend et al, 199618

15

Triaxial

Coonrad-Morrey

Kraay et al, 199426

Morrey and Adams, 1992

Madsen et al, 1989

Pritchard II

Triaxial

Leber and Melone, 1988

32

GSB III

GSB III

Pritchard I and II

Gschwend, 1988

Bell et al, 1986

4

Rosenberg and Turner, 1982

Bayley, 1981

Stanmore

Pritchard II

Pritchard, 198138

41

Triaxial

Inglis and Pellicci, 198021

1

Implant

818

69

118

118

113

47

25

11

71

45

14

30

92

44

No. Total Patients

83

44

41

16

8

14

100

100

82

76

100

100

100

72

82

100

90

60

64

% with Arthritis

6

6

20

5

3.5

3

12.5

4.3

4.3

30-130

—

—

35-125

28-131

—

—

—

30-135

>5 5

28-130

30-132

29-140

29-137

—

107 arc

—

—

ExtensionFlexion (degrees)

3

4 (est)

4

2.6

2.6

3.5

2.5

3.5

Follow-up (years)

67-63

—

—

68-62

—

—

—

60-65

65-62

75-75

69-64

65-60

—

107 arc

—

—

PronationSupination (degrees)

Results of Approximately 800 Semiconstrained Joint Replacements from 18 Studies

Study

TABLE 54-2

93

—

—

90

100

0

95

95

—

—

90

100

91

93

96

100

67

98

89

Pain Relief (%)

20

—

—

0

18

9

11

2

32

8

36

27

25

53

67

15

36

Complications (%)

20

2

13

3

—

0

3

2

3

—

4

1

—

—

5

—

—

2

2

Revised Loose (%)

89

84

78

75

100

100

93

95

90*

90

92

91

91

87

94

70

85

—

Satisfactory Result (%)

Chapter 54 Linked Total Elbow Arthroplasty in Patients with Rheumatoid Arthritis

785

786

Part VII Reconstructive Procedures of the Elbow

FIGURE 54-4 FIGURE 54-3

The Triaxial device.

The Pritchard II semiconstrained implant.

FIGURE 54-5

The GSB III prosthesis. Note capacity for axial motion.

Chapter 54 Linked Total Elbow Arthroplasty in Patients with Rheumatoid Arthritis

there was a nonprogressive radiolucency. Overall, 27% of the elbows had complications, including four requiring excision arthroplasty. Seven elbows disarticulated during follow-up. Later Gschwend et al18 focused on the late complications of 118 GSB III implants in patients with rheumatoid arthritis, with a mean surveillance time of 4.3 years. The complication rate was only 11%, with a revision rate of 8.4%. The most common complication in rheumatoid patients was radiographic loosening in 3.4% (clinical, 2.8%), infection in 2.8%, and disarticulation in 2.5%. Instability did not occur. More recently, Cesar et al8 reported satisfactory results in 84% of 44 patients followed a mean of 6 years. Similarly Jensen et al22 observed 85% favorable results at 5 years. These outcomes have been reproduced by others with similar samples and comparable periods of surveillance.

COONRAD-MORREY TOTAL ELBOW ARTHROPLASTY The original Coonrad-Morrey design, used since 1971, was modified in 1978 to allow 7 degrees of varus-valgus motion and 7 degrees of axial rotation (see Chapter 51). In 1981, an anterior flange and plasma spray were added to the humeral component (Fig. 54-6).32,33 The plasma spray was replaced with sintered beads in 1985, and in 1993, the beads were replaced with a polymethyl meth-

787

acrylate precoat on the ulna (Table 54-3). This design has emerged as a popular implant for the treatment of rheumatoid arthritis.15,20 In Coonrad’s career experience with 41 joints followed from 10 to 31 years, at final assessment, there were no resections and all were functional joints, although many had been revised for various reasons.1 In contrast, a limited experience from Singapore of just seven implants for rheumatoid arthritis revealed that six (86%) were satisfactory at 2.5 years.27 A clinical experience with 14 replacements for rheumatoid arthritis documented a satisfactory outcome in 97% at 3 years.30

MAYO EXPERIENCE An initial report detailed experience with the CoonradMorrey device documented outcomes of 58 consecutive implants with a mean surveillance time of 3.8 years; 53 patients (91%) had relief of pain (Fig. 54-7). The functional component of the MEPS improved from 8 to 23, and overall, the score increased from 38 to 94. There were no aseptic loosening, and reoperations occurred in six elbows (10%).34 Subsequently, more recently, the results of the first 78 consecutive Coonrad-Morrey total elbow arthroplasties with at least 10 years’ and up to 20 years’ surveillance has been reported15 (Fig. 54-8). This group included 69 patients with rheumatoid arthritis, three with a distal humeral nonunion, and 12 with a previous total elbow arthroplasty of another design that failed because of aseptic loosening. Of the 78 patients, 76 (97%) reported relief of pain. Mean extension-flexion was 28 to 131 degrees, representing a 12-degree increase. Mean pronation was 68 degrees and supination was 62 degrees, an increased arc of 22 degrees. The MEPS preoperatively was 42 but increased to 87 at final review. The minimum 10-year objective (MEPS) outcome for the Coonrad-Morrey total elbow arthroplasty was 67 of 78 good/excellent (86%) and 11 (14%) fair/poor (see

Modifications of the Original CoonradMorrey Total Elbow Arthroplasty

TABLE 54-3 Implant

Modification

Year

Coonrad III (Mayo modified)

Loose hinge “semi-constrained”

1978

Coonrad-Morrey

Flange Plasma spray

1981

Beaded surface

1984

Precoat ulna

1991

Co-Cr pin

1993

FIGURE 54-6

The current Coonrad-Morrey semiconstrained implant. The flange is an essential design construction to decrease stress to the bonecement interface.

Co-Cr, cobalt-chromium.

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Part VII Reconstructive Procedures of the Elbow

8 yrs.

A

8 yrs.

B

FIGURE 54-7 Modest type II (IIIA) rheumatoid involvement (A). At 8 years, the patient is asymptomatic, and the implant is well fixed (B).

100 92.4%

Survival (%)

80 60 40 Hips 20

Elbows

With 95% confidence limits

0 0

1

2

3

4

5

6

7

8

9

10

11

12

Time since surgery (yrs)

FIGURE 54-9

At 15 years, the bone graft is mature and the distal humerus has remodelled.

Survival data for rheumatoid arthritis: Charnley total hip arthroplasty and Coonrad-Morrey total elbow arthroplasty. (Redrawn from Gill, D. R. J., and Morrey, B. F.: The Coonrad-Morrey total elbow arthroplasty in patients with rheumatoid arthritis: 10-15 year follow-up study. J. Bone Joint Surg. 86:1327, 1998, with permission, Mayo Foundation.)

Fig. 54-8). The 5-year survival rate was 94.4% (95 percent confidence interval [CI], 89% to 99%) and the 10-year rate was 92.4% (95% CI, 85% to 99.1%) (Fig. 54-9). Radiographic analysis was undertaken in 76 of 78 elbows. More than 90% had a well-incorporated bone graft (Fig. 50-10). Loosening was defined as a progressive

radiolucency greater than 2 mm that was completely circumferential about the prosthesis. One humeral and three ulnar components were radiographically loose, and two had been revised. Three of 76 elbows (3.9%) had complete bushing wear, and 6 (7.9%) had partial wear (Fig. 54-11). Of note, only limited osteolysis

FIGURE 54-8

Chapter 54 Linked Total Elbow Arthroplasty in Patients with Rheumatoid Arthritis

789

Complications After Coonrad-Morrey Total Elbow Arthroplasty in Rheumatoid Arthritis Requiring Reoperation 10 to 12 Years After Implantation

TABLE 54-4

Complication

Aseptic loosening

3 (4)

Triceps avulsions

3 (4)

Deep infection

2 (2)

Ulnar fracture

1 (1)

Ulnar component fracture

1 (1)

Total

10 yrs.

FIGURE 54-10 At 10 years, the bone graft is mature and bushing wear is minimal.

FIGURE 54-11 At 20 years after surgery, the ulnohumeral angulation shows medial bushing wear. The 10-degree design tolerance by 5 degrees.

No. (%)

10 (12)

occurred, even with extensive bushing wear, but some resorption does occur. During the 10 to 15 years after implantation, 10 of the 78 patients (12.8%) required reoperation for reasons summarized in Table 54-4 (see Chapters 65 and 66). King and associates25 have reported the Mayo experience with revision elbow replacement surgery. This experience is summarized in Chapters 65 and 66. Overall, the success rate approached 90%, with an average MEPS of 87 a mean of 6 years after revision. Overall, patients expressed satisfaction in 74 of 78 (95%) total elbow arthroplasties. These are the only long-term results for the CoonradMorrey total elbow arthroplasty, and they form the basis for comparison for other total elbow arthroplasty experiences. In our opinion, avulsion of the triceps early in the postoperative period reflects the early learning curve for triceps reattachment using the Mayo approach.7 This complication has not been experienced to any extent in our recent practice (see Chapter 63). The two deep infections (2%) in this most recently reported series represent a marked reduction in the rate of infection compared with previously reported series,34-36 but the rate is higher than that experienced for major joint replacement in the lower extremity at the Mayo Clinic.5,19 We perform the Mayo approach for all primary total elbow arthroplasties in patients with rheumatoid arthritis. We reflect the triceps extensor mechanism and transfer the ulnar nerve with 1 g of gentamicin per 40 g of cement. All elbows are splinted in extension overnight, and active and active-assisted range of motion exercises are begun on the first postoperative day. We do not use physical therapists at any time during the rehabilitation process for the elbow. The long-term Kaplan-Meier survivorship data compare very favorably with total hip arthroplasty data at our institution in rheumatoid patients (see Fig. 54-9).5,24

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Part VII Reconstructive Procedures of the Elbow

COMPARATIVE ANALYSIS One comprehensive comparative assessment comparing deficient designs was conducted by Carr et al.29 In this study, the Coonrad/Morrey did outperform the Kudo and Souter Strathclyde by fewer complications and longevity, even though the majority of the Coonrad/Morrey implants had the precoat ulna, known to be vulnerable to osteolysis in a small number of patients.27

CONCLUSION The reported experience with the semiconstrained total elbow arthroplasty is significantly better than that reported for more constrained devices. The experience is also comparable if not better than that reported with the unlinked devices, although the pathologic states that can be addressed are considerably more varied with semiconstrained implants. In fact, the results of the most popular designs now suggest that total elbow arthroplasty approaches the reliability of lower extremity joint arthroplasty.15 Attention to technique remains important, but the success with the full spectrum of pathologic conditions in rheumatoid patients has led to an expansion of the indications for total elbow arthroplasty.32,35,42

References 1. Aldridge, J. M. 3rd, Lightdale, N. R., Mallon, W. J., and Coonrad, R. W.: Total elbow arthroplasty with the Coonrad/ Coonrad-Morrey prosthesis. A 10 to 31 year survival analysis. J. Bone Joint Surg. 88B:509, 2006. 2. An, K.: Kinematics and constraint of total elbow arthroplasty. J. Shoulder Elbow Surg. 14(1 suppl S):168S, 2005. 3. Angst, F., Goldhahn, J., John, M., Herren, D. B., and Simmen, B. R.: Comparison of rheumatic and post-traumatic elbow joints after total elbow arthroplasty. Comprehensive and specific evaluation of clinical picture, function, and quality of life. Orthopade 34:794, 2005. 3a. Bayley, J. L. L.: Elbow replacement in rheumatoid arthritis. Recon. Surg. Traumat. 18:70, 1981. 4. Bell, S., Gschwend, N., and Steiger, U.: Arthroplasty of elbow: Experience with the Mark III 65B prosthesis. Austr. N. Z. J. Surg. 56:823, 1986. 5. Berry, D. J., Harmsen, W. S., Cabanela, M. E., and Morrey, B. F.: Twenty-five year survivorship of 2000 consecutive primary Charnley total hip arthroplasties. Factors affecting survivorship of acetabular and femoral components. J. Bone Joint Surg. 84A:171, 2002. 6. Brumfield, R. H., Kushner, S. H., Gellman, B., Redix, L., and Stevenson, D. V.: Total elbow arthroplasty. J. Arthroplasty 5:359, 1990. 7. Bryan, R. S., and Morrey, B. F.: Extensive posterior exposure of the elbow: A triceps sparing approach. Clin. Orthop. Relat. Res. 166:188, 1982.

8. Cesar, M., Roussanne, Y., Bonnel, F., and Canovas, F.: GSB III total elbow replacement in rheumatoid arthritis. J. Bone Joint Surg. 89B:330, 2007. 9. Connor, P. M., and Morrey, B. F.: Total elbow arthroplasty in patients who have juvenile rheumatoid arthritis. J. Bone Joint Surg. 80A:678, 1998. 10. Davis, R. F., Weiland, A. J., Hungerford, D. S., Moore, J. R., and Volenec-Dowling, S.: Nonconstrained total elbow arthroplasty. Clin. Orthop. Relat. Res. 171:156, 1982. 11. Dennis, D. A., Clayton, M. L., Ferlic, D. C., Stringer, E. A., and Branlett, K. W.: Capitello-condylar total elbow arthroplasty for rheumatoid arthritis. J. Arthroplasty 5(suppl):S83, 1990. 12. Ewald, F. C., Simmons, E. D., Jr., Sullivan, J. A., Thomas, W. H., Scott, R., Poss, R., Thornhill, T. S., and Sledge, C. B.: Capitellocondylar total elbow replacement in rheumatoid arthritis: Long-term results. J. Bone Joint Surg. 75A:498, 1993. 13. Figgie, M. P., Su, E. P., Kahn, B., and Lipman, J.: Locking mechanism failure in semiconstrained total elbow arthroplasty. J. Shoulder Elbow Surg. 15:88, 2006. 14. Garrett, J. C., Ewald, F. C., Thomas, W. H., and Sledge, C. B.: Loosening associated with GSB hinge total elbow replacement in patients with rheumatoid arthritis. Clin. Orthop. Relat. Res. 127:170, 1977. 15. Gill, D. R. J., and Morrey, B. F.: The Coonrad-Morrey total elbow arthroplasty in patients with rheumatoid arthritis: 10-15 year follow-up study. J. Bone Joint Surg. 80A:1327, 1998. 16. Gschwend, N.: Present state of the art in elbow arthroplasty. Acta Orthop. Belg. 68:100, 2002. 17. Gschwend, N., Loehr, J., Ivosevic-Radovanovic, D., Sheier, H., and Munzinger, U.: Semiconstrained elbow prosthesis with special reference to the GSB III prosthesis. Clin. Orthop. Relat. Res. 232:104, 1988. 18. Gschwend, N., Simmen, B. R., and Matejovsky, Z.: Late complications in elbow arthroplasty. J. Shoulder Elbow Surg. 5:86, 1996. 19. Hanssen, A. D., Fitzgerald, R. H., Jr., and Osmon, D. R.: The infected total hip arthroplasty. In Morrey, B. F. (ed.): Reconstructive Surgery of the Joints, 2nd ed. New York, Churchill Livingstone, 1996, p. 1229. 20. Hildebrand, K. A., Patterson, S. D., Regan, W. D., MacDermid, J. C., and King, G. J.: Functional outcome of semiconstrained total elbow arthroplasty. J. Bone Joint Surg. 82A:1379, 2000. 21. Inglis, A. E., and Pellicci, P. M.: Total elbow replacement. J. Bone Joint Surg. 62A:1252, 1980. 22. Jensen, C. H., Jacobsen, S., Ratchke, M., and Sonne-Holm, S.: The GSB III elbow prosthesis in rheumatoid arthritis: a 2-9 year follow-up. Acta Orthop. 77:143, 2006. 23. Kasten, M. D., and Skinner, H. B.: Total elbow arthro-plasty: An 18-year experience. Clin. Orthop. 290:177, 1993. 24. Kavanagh, B. F., Dewitz, M. A., Ilstrup, D. M., Stauffer, R. N., and Coventry, M. B.: Charnley total hip arthroplasty with cement: Fifteen-year results. J Bone Joint Surg 71A:1496, 1989. 25. King, G. J., Adams, R. A., and Morrey, B. F.: Total elbow arthroplasty: Revision with use of a non-custom semiconstrained prosthesis. J. Bone Joint Surg. 79A:394, 1997.

Chapter 54 Linked Total Elbow Arthroplasty in Patients with Rheumatoid Arthritis

26. Kraay, M. J., Figgie, M. P., Inglis, A. E., Wolfe, S. W., and Ranawat, C. S.: Primary semiconstrained total elbow arthroplasty. Survival analysis of 113 consecutive cases. J. Bone Joint Surg. 76B:636, 1994. 26a. Leber, C., and Melone, C. P. Jr.: Total elbow replacement. Orthop. Rev. 17:85, 1988. 27. Lee, B. P., Adams, R. A., and Morrey, B. F.: Polyethylene wear after total elbow arthroplasty. J. Bone Joint Surg. 87A:1080, 2005. 28. Lee, K. T., Singh, S., and Lai, C. H.: Semi-constrained total elbow arthroplasty for the treatment of rheumatoid arthritis of the elbow. Sing. Med. J. 46:718, 2005. 29. Little, C. P., Graham, A. J., Karatzas, G., Woods, D. A., and Carr, A. J.: Outcomes of total elbow arthroplasty for rheumatoid arthritis: Comparative study of three implants. J. Bone Joint Surg. 87A(11):2439-2448, 2005. 30. Lo, C. Y., Lee, K. B., Wong, C. K., and Chang, Y. P.: Semiconstrained total elbow arthroplasty in Chinese rheumatoid patients. Hand Surg. 8(2):187-192, 2003. 31. Loreto, C. A., Rollo, G., Comitini, V., and Rotini, R.: The metal prosthesis in radial head fracture: Indications and preliminary results. Chir. Organi Mov. 90:253, 2005. 32. Madsen, F., Gudmundson, G. H., Søjberg, J. O., and Sneppen, O.: Pritchard Mark II elbow prosthesis in rheumatoid arthritis. Acta Orthop. Scand. 60:249, 1989. 33. Morrey, B. F.: Semiconstrained total elbow replacement. In Morrey, B. F. (ed.); Thompson, R. C. Jr. (series ed.): The Elbow. Master Techniques in Orthopaedic Surgery. New York, Raven Press, 1994, pp. 231-255.

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34. Morrey, B. F., and Adams, R. A.: Semiconstrained arthroplasty for the treatment of rheumatoid arthritis of the elbow. J. Bone Joint Surg. 74A:479, 1992. 35. Morrey, B. F., and Adams, R. A.: Semiconstrained elbow replacement for distal humeral nonunion. J. Bone Joint Surg. 77B:67, 1995. 36. Morrey, B. F., and Bryan, R. S.: Infection after total elbow arthroplasty. J. Bone Joint Surg. 65A:330, 1983. 37. Plausinis, D., Greaves, C., Regan, W. D., and Oxland, T. R.: Ipsilateral shoulder and elbow replacements: on the risk of periprosthetic fracture. Clin. Biomech. 20:1055, 2005. 38. Pritchard, R. W.: Long-term follow-up study: Semiconstrained elbow prosthesis. Orthopaedics 4:151, 1981. 39. Pritchard, R. W.: Total elbow arthroplasty in patients with rheumatoid arthritis. Semin. Arthritis Rheum. 21:24, 1991. 40. Risung, F.: The Norway elbow replacement: design, technique and results after nine years. J. Bone Joint Surg. 79B:394, 1997. 41. Rosenberg, G. M., and Turner, R. H.: Nonconstrained total elbow arthroplasty. Clin. Orthop. Relat. Res. 187:154, 1984. 42. Schneeberger, A. G., Adams, R. A., and Morrey, B. F.: Semiconstrained total elbow replacement for the treatment of post-traumatic osteoarthrosis. J. Bone Joint Surg. 79A:1211, 1997. 43. van der Lugt, J. C., and Rozing, P. M.: Systematic review of primary total elbow prostheses used for the rheumatoid elbow. Clin. Rheum. 23:291, 2004.

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CHAPTER

55

Total Elbow Arthroplasty for Juvenile Rheumatoid Arthritis Patrick M. Connor and Bernard F. Morrey

INTRODUCTION Juvenile rheumatoid arthritis (JRA) is a disabling condition that affects nearly a quarter of a million children in the United States.3,45 It has been defined by the American Rheumatology Association3 as arthritis that has been present in at least one joint for 6 weeks to 3 months when the patient is younger than 16 years old. Patients with this affliction often present with stiff, painful elbows, and some may have disabling elbow ankylosis. This condition has implications regarding treatment. Just as the clinical manifestations of JRA may differ from those of adult rheumatoid arthritis in the hip, knee, and shoulder,26,28,45 the course of this disease process also differs in the elbow.20 Patients often have severe osseous atrophy, deformity, and soft tissue contractures about the elbow that require special consideration and may adversely affect treatment outcomes.8,9,11,14,15,20,21 We have also reconstructed extremely small joints and narrow intramedullary cavities. Most patients with JRA who present with stiff, painful elbows have had prior treatment of other symptomatic joints and are functionally limited to only activities of daily living.6 The painful impairment of elbow function may have been overlooked by the patient or minimized by the physician because of the severity of other joint involvement as well as a general lack of awareness regarding treatment options and results. In one study, 15 of 19 patients with JRA had had an average of five (range, two to eight) previous arthroplasties or arthrodeses of other major joints (e.g., hip, knee, shoulder) before presentation for total elbow arthroplasty.6

EVALUATION As with all inflammatory conditions, clinical assessment of patients with JRA must include a detailed evaluation

of the ipsilateral shoulder, wrist, and hand. The assumption that shoulder motion compensates for loss of elbow flexion and extension is invalid (see Chapter 5). Thus, range of motion of the shoulder and elbow should be carefully and independently assessed. Although some controversy exists regarding the ideal order of surgical management in patients with multiple joint involvement, the most painful and functionally disabled joints should have priority.18 In the event that all joints are equally symptomatic, the next priority is usually given to the hand and wrist, because the function of the shoulder and elbow is to place a functional hand in space. There are differences of opinion if the decision focuses on the priority of shoulder or elbow arthroplasty. Although one study suggests that elbow arthroplasty should have precedence over shoulder arthroplasty,16 others believe that shoulder arthroplasty should be performed first.38 Suggested reasons for proceeding with shoulder arthroplasty before elbow arthroplasty include the following38: 1. Infections occur more commonly after elbow arthroplasty than shoulder arthroplasty and may potentially “burn bridges.” 2. The elbow arthroplasty may be mechanically stressed, either by a stiff, arthritic shoulder or during the actual procedure of a shoulder arthroplasty when the extremes of valgus load are placed on the elbow implant. 3. It is stated, but not our experience, that referred pain from the shoulder to the elbow is relieved by total shoulder arthroplasty. 4. Most importantly, the rotator cuff and glenoid bone stock may become irreversibly damaged with delay, making clinical results of shoulder arthroplasty less reliable.1,2,13,24,31,39 Our opinion has changed since we demonstrated in our surgical practice that greater functional benefit derives from the elbow replacement.18 This is shown by a markedly extended period before a patient requested to replace the shoulder after the elbow compared with requesting the elbow replacement after the shoulder is done first. Therefore, if the elbow had been replaced first, sufficient improvement often exists, so the shoulder operation can be delayed for a larger period than if the shoulder is replaced first. The radiographs that are essential for evaluation of the JRA elbow are the anteroposterior and lateral views. The radiographic presentation of the JRA elbow has five distinct stages6,32: grade I indicates no radiographic changes with the exception of osteopenia associated with active synovitis; grade II, symmetric narrowing of the joint space with the architecture intact; grade III, alteration of the architecture of the joint that may be

Chapter 55 Total Elbow Arthroplasty for Juvenile Rheumatoid Arthritis

relatively mild (type A) or extensive (type B); grade IV, gross destruction of most or all of the articular architecture. A grade V, radiographic change was defined if a review of the JRA radiograph revealed an absence of an identifiable ulnohumeral joint on anteroposterior and lateral radiographs or by mature bony trabeculation crossing the ulnohumeral joint (Fig. 55-1). If severe bony atrophy is present, calibrated markers may be necessary for preoperative templating purposes.

A

793

TREATMENT ALTERNATIVES Open communication between the rheumatologist, orthopedist, and physical therapist helps provide ideal care for these patients. The nonsurgical management of JRA differs little from that of adult rheumatoid arthritis. Improved results appear to be occurring from the use of disease-remitting agents (see Chapter 74). Efforts should be geared toward pain relief and especially maintenance of joint motion. Elbow splinting is unpredictable. Resting or night splints can be helpful. Judicious use of corticosteroid injections in the elbow joint may also be helpful for early symptoms. Gentle exercises should be performed regularly for the all important goal of maintaining mobility and muscle strength. When nonoperative management fails to provide adequate relief of symptoms, surgical treatment alternatives include surgical or clinical synovectomy, interposition arthroplasty, and joint replacement. The relative roles of synovectomy and interposition arthroplasty of the rheumatoid elbow are discussed in Chapters 68 and 69 of this text. As previously emphasized, elbows with JRA have a propensity toward stiffness. Thus, if a synovectomy or interposition arthroplasty is proposed, concomitant anterior and posterior capsular releases may be necessary to re-establish functional range of motion. This was recently reaffirmed by a series of 24 synovectomies for JRA patients. The outcome was considered satisfactory in 72% at 5 years.30 Of importance was that motion did not improve in these patients. On the other hand, a more aggressive approach to débridement and removal of capsule and bony impingement might improve results, as was shown in the Mayo experience.7 If the rather stringent indications for synovectomy and interposition arthroplasty are not met, elbow arthroplasty is recommended.

TOTAL ELBOW ARTHROPLASTY: OPERATIVE TECHNIQUE

FIGURE 55-1

The type V radiographic change with rheumatoid arthritis is one of ankylosis demonstrated by complete trabeculation across the joint. Anteroposterior (A) and lateral (B) views.

The technique of total elbow arthroplasty for the adult rheumatoid elbow is described in Chapter 54 of this text. In this patient in particular, to avoid potential complications, it is essential that the surgeon spend time planning preoperatively for the anatomic deformities and technical challenges that are especially common with elbows affected by JRA. Emphasis is placed on ensuring that the proper sized (small) implant is available to accommodate the small intramedullary canal, especially of the ulna. As mentioned earlier, this may require preoperative radiographs with calibrated templating markers. Be prepared to bend both humeral and ulnar component stems. A posterior incision is used, and the ulnar nerve is routinely transferred anteriorly to a subcutaneous posi-

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Part VII Reconstructive Procedures of the Elbow

tion. The triceps is then released in a subperiosteal manner from the olecranon, in continuity with the ulnar periosteum and the fascia of the forearm along with the anconeus.5 Again, elbows affected by JRA are characterized by stiffness and by very small, fragile bones; thus, care should be taken during the exposure to avoid excessive forces about the elbow, which could cause a fracture. If there is osseous ankylosis (grade V radiographic classification), a curved microsagittal saw or a small osteotome is used to re-establish the joint line after osseous landmarks are identified. Care is taken to restore the proper center of rotation of the ulnohumeral joint

to maximize the biomechanical function of the prosthetic elbow.14,25 With severe soft tissue contracture or osseous ankylosis, or both, circumferential capsular and collateral ligament releases are necessary to maximize postoperative motion and function. For this reason, unlinked prostheses depend on functional collateral ligaments and proper soft tissue balancing; therefore, these prostheses are not typically indicated in this clinical situation. Rather, a linked semiconstrained prosthesis is employed, the collateral ligaments are released, and the anterior capsule is completely excised (Fig. 55-2) and further

Curved osteotome

B

FIGURE 55-2

C

Because of the stiffness and pericapsular adhesions associated with juvenile rheumatoid arthritis, complete release of the collateral ligaments (A) and stripping of the anterior capsule (B) is typically required. Sometimes the implant should be inserted more proximally, but this might compromise the medial epicondyle (C).

Chapter 55 Total Elbow Arthroplasty for Juvenile Rheumatoid Arthritis

795

FIGURE 55-3

A series of cannulated reamers ranging from 5 to 7.5 mm are helpful to prepare the small ulnar canal.

reflected from the distal aspect of the humerus with an osteotome or blunt periosteal elevator. These maneuvers and this prosthesis allow the greatest possible motion and stability for patients who have severe preoperative stiffness. The intramedullary canals of the humerus and the ulna characteristically are very narrow or are completely obliterated in some patients with JRA. Thus, care must be taken in the identification and preparation of these canals. During preparation, it is important to stay centered and to remain within the confines of the cortical bone. We thus employ a small (4-mm) cannulated flexible reamer and intramedullary guide for this purpose (Fig. 55-3). The Coonrad-Morrey implant system now includes an extra small humeral and ulnar component. In the ulnar component, the intramedullary cross-section diameter is only 3 mm (Fig. 55-4). Although the use of individualized custom prostheses has not been necessary in our experience, it is important to have an appropriate inventory of prosthetic sizes available to address the small intramedullary canal. In elbows in which an angular change is needed in the ulnar or humeral component, the Coonrad-Morrey prosthetic ulnar stem may be slightly modified with a cam-lever bending device (Fig. 55-5). The cementing technique used in patients who have JRA differs little from standard techniques. Tobramycinimpregnated cement (1 g/40 g cement) is routinely used in an effort to lessen the likelihood of infection, and cement for both the humeral and ulnar component is inserted with an intramedullary injection system. Because many patients who have JRA have involvement of the ipsilateral shoulder, which has either had or may eventually require prosthetic replacement (Fig. 55-6), a cement restrictor is deployed to limit the level of cement injected in the humerus. The short, 10-cm extra small diameter humeral component is used.

A

B FIGURE 55-4

In some patients, the ulnar canal is almost nonexistent, as seen here in the (A) anteroposterior and (B) lateral 10-year views.

AFTERCARE After repair of the extensor mechanism5 and routine closure, the elbow is placed in a compressive dressing and elevated in a vertical elbow sling for 24 hours. The patient is then allowed to use the extremity as tolerated

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Part VII Reconstructive Procedures of the Elbow

in 19 patients (in 24 elbows) with JRA who had been managed with total elbow arthroplasty at the Mayo Clinic were evaluated. At an average of 7.4 years (range 2 to 14) after the operation, there was an improvement in the average Mayo Elbow Performance Score (MEPS) from 31 points (range, 5 to 55) preoperatively to 90 points (range, 55 to 100) postoperatively.6 In 22 (96%) of the 23 elbows available at the most recent follow-up evaluation, there was little or no pain, but the improvement in the range of motion was not as reliable. The average arc of flexion improved 27 degrees from only 63 degrees preoperatively to 90 degrees postoperatively. The mean postoperative arc of flexion was between 35 to 125 degrees. Examination of the four elbows that had been completely ankylosed before the procedure revealed an average arc of 73 degrees after the operation, and evaluation of the 20 ipsilateral wrists that were not limited by disease revealed that pronation and supination had been maintained. The average functional MEPS improved from 9 points (range, 0 to 25) preoperatively to 23 points (range, 15 to 25) postoperatively (P < .001). Eighteen elbows (78%) were noted by patients to cause no difficulties with standard daily activities. These results with regard to pain relief (6%) compare favorably with or are better than those reported in published series of elbow arthroplasty for adults who had rheumatoid arthritis* and other diagnoses.19,34,35,36 This fact is important when considering other options (see Fig. 55-6).12,22,29,44 Improvements in the range of motion after elbow arthroplasty in these patients are not as reliable as with most other diagnostic categories including the expected improvement in motion following from arthroplasty in the adult with rheumatoid arthritis.11,33

A

B FIGURE 55-5

If the canal is small and bowed, the stem may be bent with a cam-type plate bender (A) to accommodate the bowed canal (B).

for activities of daily living. Patients who have JRA are encouraged to use the elbow to enhance postoperative motion and a Mayo Elbow Brace is typically used. (See Chapter 11.)

OUTCOME Even today, a Medline search reveals only one study that has been published regarding total elbow arthroplasty in patients who have JRA. The long-term results

COMPLICATIONS There were 13 complications that affected 12 of the 24 elbows. Early complications (including a fracture of the olecranon, subluxation of a resurfacing prosthesis, elbow stiffness, and problems with wound healing) that were appropriately diagnosed and treated did not adversely affect the long-term outcome. Late complications include aseptic loosening of a press-fit unlinked prosthesis, instability of an unlinked prosthesis, and a worn bushing of the linked implant led to three poor results. Importantly, none of the 18 semiconstrained prostheses had radiographic evidence of loosening at the most recent follow-up evaluation. The implications of this observation are particularly relevant for patients with JRA who undergo an elbow arthroplasty at a relatively young age. This position is supported by the demonstration that

* See references 4, 10, 11, 17, 23, 26, 27, 33, 37, 41-43, and 46.

Chapter 55 Total Elbow Arthroplasty for Juvenile Rheumatoid Arthritis

797

FIGURE 55-7

Satisfactory long-term results with the limited implant can be anticipated, particularly because these patients are not able to use their arm in an aggressive fashion.

FIGURE 55-6

Commonly, a patient has shoulder, hand, and wrist symptoms, and thus, all three joints will have to be replaced or otherwise addressed surgically.

the functional laxity of the Coonrad-Morrey prosthesis is consistently less than its inherent structural laxity.40 This explains the low rate of aseptic loosening of this implant design.

SUMMARY AND CONCLUSION Total elbow arthroplasty for JRA provides rewarding pain relief and improvements in function. However, the favorable restoration of range of motion that is seen after elbow arthroplasty in patients who have adult rheumatoid arthritis cannot be expected in this patient group. Because many elbows affected by JRA have preexisting anatomic deformities, there are complex and challenging technical considerations, and thorough preoperative planning must be emphasized. This is particularly relevant with regard to determining the size and type of prosthetic implant. Finally, experience with operations on the elbow, and with prosthetic replacement in

particular, will increase the likelihood of a satisfactory outcome (Fig. 55-7). To date, because of the need for aggressive soft tissue release, a semiconstrained linked implant design is recommended.

References 1. Barrett, W. P., Thornhill, T. S., and Thomas, W. H.: Nonconstrained total shoulder arthroplasty in patients with polyarticular rheumatoid arthritis. J. Arthroplasty 4:91, 1989. 2. Boyd, A. D., Jr., Thomas, W. H., Scott, R. D., Sledge, C. B., and Thornhill, T. S.: Total shoulder arthroplasty versus hemiarthroplasty: Indications for glenoid resurfacing. J. Arthroplasty 5:329, 1990. 3. Brewer, E. J.: Criteria for the classification of juvenile rheumatoid arthritis. Bull. Rheum. Dis. 23:712, 1972. 4. Brumfield, R. H., Kuschner, S. H., Gellman, H., Redix, L., and Stevenson, D. V.: Total elbow arthroplasty. J. Arthroplasty 5:359, 1990. 5. Bryan, R. S., and Morrey, B. F.: Extensive posterior exposure of the elbow: A triceps-sparing approach. Clin. Orthop. Relat. Res. 166:188, 1982. 6. Connor, P. M., and Morrey, B. F.: Total elbow arthroplasty in patients who have juvenile rheumatoid arthritis. J. Bone Joint Surg. 80A:678, 1998.

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Part VII Reconstructive Procedures of the Elbow

7. Cill, A., Veillette, C. J. H., O’Driscoll, S. W., and Morrey, B. F.: Arthroscopic synovectomy of the elbow in inflammatory arthritis. (Paper submitted for review 2008) 8. Dee, R.: Total replacement of the elbow joint. Orthop. Clin. North Am. 4:415, 1973. 9. Dennis, D. A., Clayton, M. L., Ferlic, D. C., Stringer, E. A., and Bramlett, K. W.: Capitellocondylar total elbow arthroplasty for rheumatoid arthritis. J. Arthroplasty 5(suppl):S83, 1990. 10. Ewald, F. C., Scheinberg, R. D., Poss, R., Thomas, W. H., Scott, R. D., and Sledge, C. B.: Capitellocondylar total elbow arthroplasty: Two- to five-year follow-up in rheumatoid arthritis. J. Bone Joint Surg. 62A:1259, 1980. 11. Ewald, F. C., Simmons, E. D., Sullivan, J. A., Thomas, W. H., Scott, R. D., Poss, R., Thornhill, T. S., and Sledge, C. B.: Capitellocondylar total elbow replacement in rheumatoid arthritis: Long-term results. J. Bone Joint Surg. 75A:498, 1993. 12. Ferlic, D. C., Patchett, C. E., Clayton, M. L., and Freeman, A. C.: Elbow synovectomy in rheumatoid arthritis: Longterm results. Clin. Orthop. Relat. Res. 220:119, 1987. 13. Figgie, H. E. III, Inglis, A. E., Goldberg, V. M., Ranawat, C. S., Figgie, N. P., and Wile, J. M.: An analysis of factors affecting the long-term results of total shoulder arthroplasty in inflammatory arthritis. J. Arthroplasty 3:123, 1988. 14. Figgie, H. E., Inglis, A. E., and Mow, C.: A critical analysis of biomechanical factors affecting functional outcome in total elbow arthroplasty. J. Arthroplasty 1:169, 1986. 15. Figgie, M. P., Inglis, A. E., Mow, C. S., and Figgie, H. E.: Total elbow arthroplasty for complete ankylosis of the elbow. J. Bone Joint Surg. 71A:513, 1989. 16. Friedman, R. J., and Ewald, F. C.: Arthroplasty of the ipsilateral shoulder and elbow in patients who have rheumatoid arthritis. J. Bone Joint Surg. 69A:661, 1987. 17. Garrett, J. C., Ewald, F. C., Thomas, W. H., and Sledge, C. B.: Loosening associated with G.S.B. hinge total elbow replacement in patients with rheumatoid arthritis. Clin. Orthop. Relat. Res. 127:170, 1977. 18. Gill, D. R. J., and Morrey, D. F.: The Coonrad-Morrey total elbow arthroplasty in patients with rheumatoid arthritis: 10-15 year follow-up study. J. Bone Joint Surg. 80A:1327, 1998. 19. Inglis, A. E.: Revision surgery following a failed total elbow arthroplasty. Clin. Orthop. Relat. Res. 170:213, 1982. 20. Inglis, A. E., and Figgie, M. P.: Septic and nontraumatic conditions of the elbow: Rheumatoid arthritis. In Morrey, B. F. (ed.): The Elbow and Its Disorders, 2nd ed. Philadelphia, W. B. Saunders, 1993, p. 753. 21. Inglis, A. E., and Pellicci, P. M.: Total elbow replacement. J. Bone Joint Surg. 62A:1252, 1980. 22. Jonsson, B., and Larsson, S. E.: Elbow arthroplasty in rheumatoid arthritis: Function after 1-2 years in 20 cases. Acta Orthop. Scand. 61:344, 1990. 23. Kasten, M. D., and Skinner, H. B.: Total elbow arthroplasty: An 18-year experience. Clin. Orthop. Relat. Res. 290:177, 1993. 24. Kelly, I. G., Foster, R. S., and Fisher, W. D.: Neer total shoulder replacement in rheumatoid arthritis. J. Bone Joint Surg. 69B:723, 1987.

25. King, G. J. W., Glauser, S. J., Westreich, A., Morrey, B. F., and An, K. N.: In vitro stability of an unconstrained total elbow prosthesis: Influence of axial loading and joint flexion angle. J. Arthroplasty 8:291, 1993. 26. Kraay, M. J., Figgie, M. P., Inglis, A. E., Wolfe, S. W., and Ranawat, C. S.: Primary semiconstrained total elbow arthroplasty: Survival analysis of 113 consecutive cases. J. Bone Joint Surg. 76B:636, 1994. 27. Kudo, H., Iwano, K., and Prefecture, K.: Total elbow arthroplasty with a non-constrained surface-replacement prosthesis in patients who have rheumatoid arthritis: A long-term follow-up study. J. Bone Joint Surg. 72A:355, 1990. 28. Levine, W. N., Scott, R. D., Sledge, C. B., Thomas, W., and Thornhill, T. S.: Shoulder arthroplasty in juvenile rheumatoid arthritis: Mean 12-year follow-up. Orthop. Trans. 19:365, 1995. 29. Ljung, P., Jonsson, K., Larsson, K., and Rydholm, U.: Interposition arthroplasty of the elbow with rheumatoid arthritis. J. Shoulder Elbow Surg. 5:81, 1996. 30. Maenpaa, H., Kuusela, P., Lehtinen, J., Savolainen, A., Kautiainen, H., and Belt, E.: Elbow synovectomy on patients with juvenile rheumatoid arthritis. Clin. Orthop. Relat. Res. 412:65, 2003. 31. McCoy, S. R., Warren, R. F., Bade, H. A., III, Ranawat, C. S., and Inglis, A. E.: Total shoulder arthroplasty in rheumatoid arthritis. J. Arthroplasty 4:105, 1989. 32. Morrey, B. F., and Adams, R. A.: Semiconstrained devices. In Morrey, B. F. (ed.): Reconstructive Surgery of the Joints, 2nd ed. New York, Churchill Livingstone, 1996, p. 515. 33. Morrey, B. F., and Adams, R. A.: Semiconstrained arthroplasty for the treatment of rheumatoid arthritis of the elbow. J. Bone Joint Surg. 74A:479, 1992. 34. Morrey, B. F., and Adams, R. A.: Semiconstrained elbow replacement for distal humeral nonunion. J. Bone Joint Surg. 77B:67, 1995. 35. Morrey, B. F., Adams, R. A., and Bryan, R. S.: Total replacement for post-traumatic arthritis of the elbow. J. Bone Joint Surg. 73B:607, 1991. 36. Morrey, B. F., and Bryan, R. S.: Revision total elbow arthroplasty. J. Bone Joint Surg. 69A:523, 1987. 37. Morrey, B. F., Bryan, R. S., Dobyns, J. H., and Linscheid, R. C.: Total elbow arthroplasty: A five-year experience at the Mayo Clinic. J. Bone Joint Surg. 63A:1050, 1981. 38. Neer, C. S., II: Glenohumeral arthroplasty. In Neer, C. S., II (ed.): Shoulder Reconstruction. Philadelphia, W. B. Saunders, 1990, p. 167. 39. Neer, C. S., II, Watson, K. C., and Stanton, F. J.: Recent experience in total shoulder replacement. J. Bone Joint Surg. 64A:319, 1982. 40. O’Driscoll, S. W., An, K. N., Korinek, S., and Morrey, B. F.: Kinematics of semi-constrained total elbow arthroplasty. J. Bone Joint Surg. 74B:297, 1992. 41. Rosenberg, G. M., and Turner, R. H.: Nonconstrained total elbow arthroplasty. Clin. Orthop. Relat. Res. 187:154, 1984. 42. Ruth, J. T., and Wilde, A. H.: Capitellocondylar total elbow replacement: A long-term follow-up study. J. Bone Joint Surg. 74A:95, 1992.

Chapter 55 Total Elbow Arthroplasty for Juvenile Rheumatoid Arthritis

43. Rydholm, U., Tjornstrand, B., Pettersson, H., and Lidgren, L.: Surface replacement of the elbow in rheumatoid arthritis: Early results with the Wadsworth prosthesis. J. Bone Joint Surg. 66B:737, 1984. 44. Rymaszewski, L. A., MacKay, I., Ames, A. A., and Miller, J. H.: Long-term effects of excision of the radial head in rheumatoid arthritis. J. Bone Joint Surg. 66B:109, 1984.

799

45. Scott, R. D., and Sledge, C. B.: The surgery of juvenile rheumatoid arthritis. In Kelly, W. N., Harris, E. D., Ruddy, S., and Sledge, C. B. (eds.): Textbook of Rheumatology, 2nd ed. Philadelphia, W. B. Saunders, 1985, p. 1910. 46. Souter, W. A.: Arthroplasty of the elbow: With particular reference to metallic hinge arthroplasty in rheumatoid arthritis. Orthop. Clin. North Am. 4:395, 1973.

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CHAPTER

56

Distal Humeral Fractures—Acute Total Elbow Arthroplasty Srinath Kamineni

INTRODUCTION Distal humeral fractures are infrequent when compared with other fractures and comprise approximately 1% to 2% of all adult fractures and 10% of humeral fractures.27,29,33 The population distribution of such fractures tends to be bimodal, with a peak in the second and third decades, and with a second peak in the sixth to eighth decades.13

NONSURGICAL MANAGEMENT Nonoperative options of soft sling or plaster cast are traditionally used in cases in which reconstruction is not an option, by virtue of patient or surgical factors. Although widely propagated as an acceptable methodology, it is documented that such a strategy does not yield consistent pain relief or consistent joint stability, with unsatisfactory results in approximately 40% of cases.17

FRACTURE FIXATION A prerequisite for reconstruction is to fix the fracture fragments with some form of rigid fixation construct that then synchronously allows stable fixation and joint motion. However, there are three main fracture factors that adversely affect the ability to reconstruct the distal humeral fracture: (1) Comminution: If the distal humeral articular surface is significantly comminuted (Fig. 56-1A), not only is it not possible to fix all the bony fragments, but the cartilage surface would also have undergone considerable injury, leading to a suboptimal bearing surface. (2) Size of fracture fragments: It is straightforward to understand the issues with a large number of small bony fragments, with a significant number made up of small osteochondral fragments. Additionally a transcondylar or very low supracondylar fracture also poses the same problem of the ability to hold the fracture sufficiently rigidly while allowing joint motion (see Fig. 56-1B). (3) Quality of bone stock: Good quality

young bone stock allows better fixation than does osteopenic/osteoporotic older bone.26,31 In a young population with an average age of 35 years, distal humeral articular surface fractures treated with internal fixation achieved good and sustainable results, although 40% required secondary procedures: an average flexion arc of 106 degrees, average foream rotational arc of 165 degrees, and a Mayo Elbow Performance Score (MEPS) of 91.2 A choronologically older group of patients with distal humeral fracture fixation, but without objective proof of osteoporosis, resulted in a 75% good/excellent range of motion and 80% satisfaction,15 although other studies of the older age group found less satisfactory results.27 Helfet et al8 demonstrated that despite good surgical technique and adequate internal fixation, 2-10% of such patients develop non-unions. Furthermore, if early motion is sacrificed, a compromise made for the quality of bone stock, the prediction is a better rate of union with a stiff joint. Pajarinen and Bjorkenheim26 correlated that immobilization greater than 3 weeks was a poor prognostic factor, after open reduction and internal fixation (ORIF), for achieving a good functional score. Thereby, when the principle of rigid internal fixation with early joint mobilization cannot be adhered to, then fracture fixation, joint immobilization to union, and a secondary motion gaining procedure may have to be considered.

ACUTE TOTAL ELBOW ARTHROPLASTY An alternative strategy that has gained a wider acceptance is the acute total elbow replacement, when the fracture is judged to be unreconstructable or reconstructable without the predictability desired to allow early motion. However, the replacement of an unreconstructable fracture involving a joint is not a new concept. Hip7 and shoulder,6,25 and less commonly knee,7,14 surgeons, have an established body of literature regarding the relevance and successful outcomes of this concept. Total elbow replacements have been proven effective in the treatment of distal humeral nonunions,22 posttraumatic arthritis,16,24,30 rheumatoid arthritis,23 and chronic fracture dislocations.20 More recently, a growing literature appears to be favorable regarding this concept in the treatment of the difficult-to-reconstruct distal humeral fracture in the older age group of patients (Table 56-1). The first large series, which was reported by Cobb and Morrey,1 was a retrospective study of 21 distal humeral fractures in patients with an average age of 72 years. Ten of the cases had pre-existing rheumatoid arthritis, and the follow-up period was an average of 3.3 years (Table 56-2). The outcomes, based on the MEPS, were 15 excellent and five good results, with inadequate data in one case. Only one patient required

Chapter 56 Distal Humeral Fractures—Acute Total Elbow Arthroplasty

A

B

C

D

E

801

FIGURE 56-1

A, Distal humeral fracture showing, with a radiograph, computed tomography scan, and intraoperative findings, the extent of comminution and osteopenic state of the bone. Low osteoporotic transcondylar fractures (B, C) have little bone of quality for fixation. This is an example of such a fracture that is malrotated when immobilized in a plaster cast (D, E).

Indications and Contraindications for Acute Elbow Arthroplasty

TABLE 56-1 Indications

Unreconstructable distal humeral fracture Osteoporotic bone stock Relative Indications

Elderly patient Relatively sedentary patient Distal humeral articular fracture in rheumatoid Contraindications

Infection/gross contamination Neurologic compromise Noncomplaint patient Relative Contraindication

Poor bone stock Open fracture Heavy upper limb loader

revision arthroplasty due to a fractured ulna component (Table 56-3). This study was extended by Kamineni et al12 to 43 patients, and re-reported with a seven year follow-up. Nineteen patients in this cohort had pre-existing rheumatoid arthritis. The average flexion arc was 107 degrees, with an average MEPS of 13/100. Five patients required revision arthroplasty due to trauma (n = 3), aseptic loosening (n = 1), and septic loosening (n = 1). This latter study demonstrated that the results were maintained over a longer follow-up period, although the revision rate increased with time, from 5% at 3 years to 12% at 7 years. Ray et al28 reported on seven patients with a mean age of 81 years who underwent acute total elbow arthroplasty without underlying pathology. The functional outcomes were excellent in five and good in two patients, with an average flexion arc greater than 100 degrees. Only one patient had mild pain, with the other six patients being completely pain free. The use of unlinked prosthesis for an acute arthroplasty was reported in only one series, which focused

Part VII Reconstructive Procedures of the Elbow

802

TABLE 56-2

Results of TEA for Acute Trauma

Authors

n

Age

Cobb and Morrey (1997)1

21

72

28

Fracture type

Mean Follow-up Time

Mayo score

ROM (degrees)

3.5 y32

95

105

5 (24%)

1 (5%)

Compl

Rev

7

81.7

4C

2y

5 excellent 2 good

110

1 (14%)

0

Gambirasio et al (2001)5

10

84.6

2B/8C

18 m

94

102

0

0

Garcia et al (2002)5a

16

73

2A/2B/11C

3y

93

101

2 (12%)

0

49

69

6A/5B/38C

7y

93

107

14 (29%)

7

73

4A/1B/2C

25 m

94

89

1 (14%)

25

78

25C

2y

86

107

9

73

9C

3.5 y

95

118

Ray et al (2000)

12

Kamineni and Morrey (2004) Lee et al (2006)

18 32

Veillette et al (2006)

10

Kalogrianitis (2008)

10 (23%) 0 3 (12%)

1 (11%)

0

Compl, complications; Rev, revisions; ROM, range of motion; TEA, total elbow arthroplasty.

Complications Associated with Acute Elbow Arthroplasty

TABLE 56-3 Early

Intraoperative fracture Superficial infection11,28 Wound dehiscence12 Instability (unlinked prosthesis) Late

Deep/hematogenous infection10,12 Aseptic loosening11,12 Periprosthetic fracture12 Prosthesis fracture1,12 Triceps avulsion/failure10 Ulna nerve neurapraxia1,12 Reflex sympathetic dystrophy1 Heterotopic ossification5,12

on a group of patients with an average age of 73 years and a follow-up of 3.5 years.11 The MEPS was 95, and the average arc of flexion was 98 degrees. This helps to corroborate the concept of acute arthroplasty for fractures, independent of the choice of linked or unlinked prostheses. When distal humeral fractures are associated with underlying rheumatoid or other inflammatory arthritides, the indications for an acute arthroplasty are more relaxed.1,11,12,28 Furthermore, fractures in the rheumatoid population should be considered a different pathology than that of a fracture in a joint that was nonpathologic before injury.1,12,28 The generally good results that can be expected in the fractured rheumatoid population was reported by Ikavalko and Lehto.10 A 100-degree arc of flexion was maintained up to a 4-year period. However, due to the low demands of this population, complica-

tions can be dealt with much more conservatively than the non-rheumatoid patient. Whereas the indications for acute elbow joint replacement are being extended, as is expected of any new procedure, caution must be exercised when making the decision between conservative, osteosynthesis, and arthroplasty management. The importance of a correct and timely decision is highlighted by the functional outcomes of a successful osteosynthesis versus an acute arthroplasty, as opposed to a later conversion of a failed osteosynthesis to a secondary arthroplasty. Frankle et al have reported a retrospective comparison of value.4 Patients older than 65 years with C2 or C3 intra-articular distal humeral fractures were treated with either osteosynthesis or acute elbow arthroplasty. In the osteosynthesis group, there were one fair and three poor MEPS outcomes, whereas in the arthroplasty group, only excellent and good results were achieved at a 2-year followup. Veillette and McKee32 corroborated these findings with a multicenter prospective randomized study comparing osteosynthesis with acute elbow arthroplasty in patients older than 65 years. The MEPS revealed a significant improvement with acute arthroplasty (total elbow arthroplasty [TEA] 86 versus ORIF 73) over a 2-year follow-up. However, the Disabilities of the Arm, Shoulder and Hand (DASH) questionnaire showed a significantly better outcome for acute arthroplasty in the first 6 months, but at a longer 2-year follow-up, the results between the two groups showed no statistical difference. However, a finding of note was that the arthroplasty group had a lower reoperation rate (12% versus 26%). When the decision to perform an osteosynthesis is incorrect at the time of injury and the fixation fails, requiring a secondary arthroplasty, the results are generally poorer than if the primary intervention was an acute elbow arthroplasty. Mighell et al21 reported 28

Chapter 56 Distal Humeral Fractures—Acute Total Elbow Arthroplasty

803

FIGURE 56-2

The arm is cleaned and prepared with a tourniquet placed to allow access to a minimum of 10 cm proximal to the olecranon process. Identify and mark all the bony points and the ulna nerve.

cases of failed osteosynthesis converted to total elbow arthroplasty in patients with an average age of 66 years. At a 3-year follow-up, the improvement in functional outcomes (American Shoulder and Elbow Surgeons [ASES] scores) were statistically significant from 36 to 65, with improvements in pain, motion and function. These results could be interpreted as lesser to those results for a primary acute arthroplasty. In addition, 21% (6/28) required revision implant surgery, five patients required revision arthroplasty for aseptic loosening, and one required ultimate arthrodesis for septic loosening. Hence, the wrong decision at the primary intervention appears to result in a lesser functional outcome and a higher complication and revision rate. With an aging population, with more osteoporotic bone stock, the frequency of the distal humeral fracture not amenable to osteosynthesis is predicted to increase. The challenges that the surgeon faces is to better select patients suitable for an acute arthroplasty and for the implant design to allow more normal function for an ever-increasing and active life span.

SURGICAL TECHNIQUE Two commonly used surgical techniques will be described in this section, the Modified Bryan-Morrey (B-M) and the triceps split (TS) approach.

OPERATING ROOM PREPARATION The relevant imaging of the fracture should be displayed for the operating surgeon to reference during the procedure. A torniquet is positioned on the upper arm, and its size should allow surgical access to a minimum of 10 centimeters proximal to the olecranon process for distal humeral fractures (Fig. 56-2). The torniquet should be inflated only when the whole limb is prepared and draped after the limb is elevated for 5 minutes.

Subcutaneous border

Soft-roll Ulnar nerve

Towel roll

FIGURE 56-3

Supine positioning of the patient allows the arm to be draped over a towel roll, which, in turn, allows easy maneuvering of the arm during the procedure, with little restriction to access.

PATIENT POSITIONING The patient is placed supine on the operating table with no other supports to restrict arm motion. The arm is placed across the chest, and rested on a bolster or roll of towels. The towel roll should be sterile in order to reposition during different parts of the procedure (Fig. 56-3).

SKIN INCISION A straight skin incision 5 cm distal to and 10 cm proximal to the olecranon tip is employed (Fig. 56-4). The

804

Part VII Reconstructive Procedures of the Elbow

FIGURE 56-4

The initial skin incision is 5 cm distal to and up to 10 cm proximal to the olecranon process.

FIGURE 56-5

The skin incision is deepened to the level of the triceps central tendon without breaching its surface.

FIGURE 56-6

In the trauma setting, raising a skin flap can often be performed with simple finger dissection, which also allows a tactile assessment of the underlying fracture.

incision should be just medial or lateral to the tip of the olecranon in order to avoid the discomfort of a scar on a weight-bearing part of the elbow, when resting on the arm, with a potential for wound breakdown. Deepen the incision to define the superficial surface of the triceps central tendon, without breaching its surface (Fig. 56-5).

APPROACH A full-thickness skin flap should be first raised up to the level of the border of the triceps muscle belly, which can often be achieved with simple finger dissection (Fig. 56-6). A method of raising the skin flaps, which are more adherent, is the flat blade technique, in which the blade

Chapter 56 Distal Humeral Fractures—Acute Total Elbow Arthroplasty

is pressed against the deeper plane but angled at 45 degrees toward the superficial plane (Fig. 56-7). Because bruising and blood clots may obscure normal anatomy, at this point, the ulna nerve should be palpated gently by digital probing. The nerve should be dissected free of the cubital tunnel and released up to the first motor branch, freeing it from the medial epicondyle fragment. A vessel loop should be placed around the nerve, knotted loosely to allow easy control without an attached artery clip (Fig. 56-8). Once the nerve is protected, the remainder of the medial skin flap can be raised to allow access to the anterior aspect of the medial fragment. Once the fragments are freed, they can be removed either posterior or anterior to the nerve, depending on which situation places the nerve under least tension (Fig. 56-9). The lateral full-thickness skin flap should also be raised. Continuing the dissection distal to the epicondyle allows the anconeus–extensor carpi ulnaris interval to be identified, which will be the continuation for the lateral triceps border mobilization (Fig. 56-10). The lateral

epicondyle is then enucleated of all soft-tissue attachments, and then removed through the lateral exposure (Fig. 56-11). When the fracture is a low supracondylar or transcondylar configuration, the fragment may be more easily removed, once freed medially and laterally, through the TS approach (Fig. 56-12). With the modified B-M approach, the forearm is now rotated toward the head of the patient in order to better expose the implantation surfaces of the humerus and ulna. The triceps, with the ulna nerve, is displaced medially. In order to improve exposure, the triceps is elevated from the medial and lateral aspects of the ulna but not from the posterior aspect. Using a triceps-sparing approach, a split is made from the apex of the olecranon, in line with the central triceps tendon fibers, for 5 to 7 cm proximally. The triceps is elevated from the posterior olecranon, sufficient to allow ulna preparation and implantation. The amount of triceps generally required to be elevated, by Sharpey fiber dissection, is 1 to 2 cm2, but no elevation is required from the medial and lateral

FIGURE 56-7

Raising the medial and lateral skin flaps can be performed with a flat blade technique, where the planes are adherent.

FIGURE 56-8

805

Once the medial border of the triceps muscle belly has been defined, palpate and dissect the ulnar nerve. Release it from the cubital tunnel, and control the position of the nerve during the remainder of the procedure with a vessel loop, without a clip, but simply knotted loosely.

806

Part VII Reconstructive Procedures of the Elbow

Common flexor tendon reflected Common flexor tendon Ulnar n.

FIGURE 56-9

Medial distal fragments

ME

Ulnar n.

A

B

D

C

A, Brian-Morrey approach. The medial fragment is enucleated of its attachments, notably the flexor-pronator mass and medial collateral ligament. B, The medial triceps is elevated and the medial fragments removed. C, Triceps split approach. The ulnar nerve, having been dissected and protected, the medial fragment is enucleated and removed, with assistance of a pushing probe through the triceps split. ME, medial epicondyle. D, The triceps is freed from the underlying humerus by sliding a periosteal elevator in a proximal to distal direction.

FIGURE 56-10 The anconeus–extensor carpi ulnaris interval is often identified by a fat streak that exits between the two muscles. Extending this interval proximally will allow the lateral border of the triceps to be mobilized for lateral fragment and radial head removal.

Chapter 56 Distal Humeral Fractures—Acute Total Elbow Arthroplasty

807

Common extensor tendon reflected

Lateral distal fragments

A

B

C

FIGURE 56-11 The lateral fragment is enucleated from its extensor mass and lateral collateral ligament attachments, and can be removed. A, Comminuted fragments are easily removed from the lateral approach. B, Lateral dissection. C, If the fracture fragment is large, then enucleation is the option via the lateral approach, in preparation for central removal of the fragment.

Olecranon

Fracture fragment

FIGURE 56-13 The triceps split approach commences at the apex of the olecranon process and splits the triceps, in line with its central tendon fibers between 5 to 7 cm proximally. The triceps footprint is elevated off the olecranon posteriorly only, with the medial and lateral ulna triceps insertions remaining intact.

FIGURE 56-12 When the fracture fragment is a low transcondylar, or requires a larger dissection through the medial or lateral dissection, it can be easily removed through the central triceps spilt approach.

aspects of the ulna. The humerus is then exposed through the triceps split, as is the olecranon tip (Fig. 56-13). No additional bony cuts are usually required once the fracture fragments are removed, with no real detriment to forearm/wrist power expected (Fig. 56-14).19 The canal is simply rasped to the

correct size, and the flange of the Coonrad-Morrey humeral component should seat at the level of the coronoid fossa apex. A 6-inch humeral stem is the optimal length, but this also has to take into account the possibility of a pre-existing shoulder prosthesis. Additionally, if the patient has pre-existing shoulder pathology, with the possibility of requiring a prosthesis in the future, it is prudent to implant a 4-inch humeral stem, If the humeral fracture does not allow adequate seating of a trial implant, following canal preparation, resect additional bone.

Humeral Preparation

Ulna Preparation In the B-M approach, adequate exposure of the ulna is achieved by dissecting and protecting the ulnar nerve in an anteriorly displaced

808

Part VII Reconstructive Procedures of the Elbow

T

Olecranon

T Radial head Olecranon

Coronoid

Humerus

FIGURE 56-14 Following fracture fragment removal, no bony cuts are usually necessary. The humeral canal preparation will commence by accessing the humeral intramedullary canal with a rongeur at the apex of the olecranon fossa (triangle). T, triceps insertion.

position and then by elevating the medial 25% of the triceps attachment. The forearm is rotated to help in exposing the medial olecranon and coronoid, and the tip of the olecranon is resected. In the TS approach, the posterior flat area of the olecranon is exposed without elevating the medial and lateral aspects of the triceps insertion. The tip of the olecranon is resected, and a clear view is achieved of the base of the coronoid and radial head when the elbow is hyperflexed (Fig. 56-15). The tip of the coronoid is also commonly resected to avoid anterior flange impingement in flexed positions (Fig. 56-16). A high-speed olive-tipped burr is used to open the base of the coronoid process (Fig. 56-17). Extreme care should be exercised during this procedure to avoid the inadvertent injury to the ulna nerve. Tip: Hold the medial and lateral borders of the ulna between two fingers, which automatically displaces and protects the ulna nerve. When the coronoid base is sufficiently opened, ulna shaft rasping can begin. When rasping the canal, always orient the rasp parallel to the flat spot of the ulna; with the Coonrad-Morrey system, the rasp handle will be perpendicular to the flat spot. Because

FIGURE 56-15 The humeral shaft is prepared in the standard manner, with rasps, and the radial head is resected to prevent abutment with the humeral yolk. With the olecranon tip resected, and the elbow hyperflexed, the coronoid base is easily accessible for ulna canal preparation.

there is a risk of penetrating the cortices during rasping, a useful habit is to grasp or palpate the ulnar shaft with the nonrasping hand to help orient the direction of rasping in line with the rasp/burr (see Fig. 56-17). Trial Implantation In the B-M approach, both trial components are inserted and then the components are reduced. Often, gentle distraction of the joint is prudent to avoid levering the components during the reduction. With the TS approach, the humeral component is inserted first and then, with the elbow flexed to 90 degrees, the ulnar component is inserted through the yolk of the humeral component, without the need for a reduction maneuver. The ulnar component center of rotation should coincide with the center of the greater sigmoid notch of the ulna. Once the components are inserted to the correct depth, the elbow should be examined through a full range of extension and flexion. If there is any suggestion that there is bony abutment of the olecranon process posteriorly or coronoid process anteriorly, these should be sufficiently trimmed. Any radial head abutment can also be visualized and an appropriate depth of radial head can be resected. The

Chapter 56 Distal Humeral Fractures—Acute Total Elbow Arthroplasty

809

1 2 3

5

4

A

B

FIGURE 56-16 Once the humerus and ulna are fully prepared, the ulna and humeral canal trajectory of insertion should be readily accessible; this is an example of the triceps split approach. (1) Triceps insertions site of olecranon, (2) resected olecranon tip surface, (3) ulna medullary canal, (4) humeral medullary canal, and (5) resected distal humeral surface.

45

o

FIGURE 56-17 The coronoid base is opened with a burr, and once the ulna canal is accessible for rasping, the burr is used to fashion a furrow, exiting the olecranon posteriorly.

bone resected from the radius is useful for creating the posterior flange bone graft, and should be stored in a damp swab until humeral component insertion. Once the trials are satisfactory, they are removed and the bony canals are pulse lavaged, a cement restrictor is inserted into the humeral canal to the correct level, and the canal kept dry until cementation commences. In situations in which distal humeral bone loss is greater than that would allow standard seating of the standard flange design, an extended flange may be used to regain humeral length (Fig. 56-18). However, triceps power is well maintained with humeral loss of up to 2 cm.9 A single mix of polymethylmethacylate cement with 1 g of vancomycin is vacuum mixed. Good cementing technique is of great impor-

Implant Insertion

tance.3 The cement is loaded into a cement gun, the nozzle of which was pretrimmed to 1 cm beyond the humeral stem length (Fig. 56-19), and the cement inserted into the humerus followed by the ulna. As the humerus is inserted, the bone graft, which should be gently wedge shaped (2 mm thick at the distal and 4 mm at the proximal ends), should be held on the anterior humeral cortex as the flange engages this region. With the B-M approach, the ulna is inserted first (Fig. 56-20), followed by the humerus. Once inserted to the correct depth, a reduction maneuver is performed and the locking pins are articulated. With the TS approach, the humeral component is inserted first, followed by the ulnar component through the yolk. Once the articulating pin is secure, the humeral component is finally tapped into its final position, and the elbow is extended and maintained in this position until the cement is cured (Fig. 56-21). Before setting, excess cement should be diligently removed to avoid cement particles in the articulation. The B-M approach closure consists of anteriorly isolating the ulnar nerve in the plane between the flexor muscle mass and the skin. Care to adequately resect the medial intermuscular septum should be taken, and the pocket is created with a Vicryl suture across the plane, making sure that the ulna nerve is free to mobilize during elbow motion. The flexor mass is then sutured to the medial triceps and the lateral mass to the lateral triceps margin (Fig. 56-22). With the TS approach, No. 2 ethibond is used to close the triceps tendon split with a running locking stitch, which then secures this central triceps to the olecranon through bone tunnels.

Wound Closure

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Part VII Reconstructive Procedures of the Elbow

4 cm 6 cm 3 cm 2 cm

B 2 cm

A FIGURE 56-18 When bone loss is encountered, of distal humeral length, 2 cm of loss can be tolerated. With greater losses, length can be restored with a longer stem and a longer anterior flange.

FIGURE 56-20 The depth of ulna insertion should not exceed the center of the projected center of the greater sigmoid notch of the ulna.

FIGURE 56-19 The cementation of the humeral and ulna canals should be approximately 1 cm distal to the prosthesis tip.

Chapter 56 Distal Humeral Fractures—Acute Total Elbow Arthroplasty

A

B

811

C

FIGURE 56-21 Following final implantation, the implant balance should be assessed by simply supporting the forearm at 90 degrees of elbow flexion (A). The prosthesis should be balanced with a parallel gap between the yolk and liner on both sides (B). If the implant is imbalanced (C), closure of the soft tissues can be modified, with differential tension, in order to help improve the balance.

Olecranon

Anconeus Common extensor mass

Olecranon Common flexor mass

Ulna nerve

Triceps

A

B

C

FIGURE 56-22 Muscle closure. A, With the Brian-Morrey approach, the flexor and extensor masses are reattached to the triceps. B, If the muscle belly is of good quality, the triceps split can be simply closed with a continuous crossed suture, into olecranon cruciate bone tunnels. C, If the muscle belly is of poorer quality, a running locking stitch offers greater security.

The elbow is dressed with a nonadherent dressing, and a volar thermoplastic removable splint in full extension. The arm is elevated for 24 hours, and the patient is typically discharged on the second or third postoperative day following evaluation

Postoperative Management

of the patient’s radiographs (Fig. 56-23). A night-time volar splint is used for the first 4 weeks to encourage the maintainence of full extension. Active elbow flexion is commenced with gravity extension only for the first 4 weeks. Routine physical therapy is not needed. Normal use of the elbow can be encouraged at week 4 after operation (Fig. 56-24).

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Part VII Reconstructive Procedures of the Elbow

B

FIGURE 56-23

C

D

Postoperative radiographs at 1 week (A, anteroposterior [AP]; B, lateral) and 5 years (C, AP; D, lateral) after an acute total elbow replacement. The latter views demonstrate heterotopic ossification but no evidence of implant loosening or bushing wear. Note the well-maintained balance of the implant.

Active anti-gravity extention

FIGURE 56-24 Postoperative motion following a triceps split approach, including an arc of flexion greater than 100 degrees and active antigravity power with overhead extension.

Chapter 56 Distal Humeral Fractures—Acute Total Elbow Arthroplasty

References 1. Cobb, T. K., and Morrey, B. F.: Total elbow arthroplasty as primary treatment for distal humeral fractures in elderly patients. J. Bone Joint Surg. Am. 79:826, 1997. 2. Doornberg, J. N., 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. 89:1524, 2007. 3. Faber, K. J., et al., Advanced cement technique improves fixation in elbow arthroplasty. Clin. Orthop. Relat. Res. 334:150, 1997. 4. Frankle, M. A., et al.: 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 17:473, 2003. 5. Gambirasio, R., et al.: Total elbow replacement for complex fractures of the distal humerus. An option for the elderly patient. J. Bone Joint Surg Br. 83:974, 2001. 5a. Garcia, J., Mykula, R., and Stanley, D.: Complex fractures of the distal humerus in the elderly. The role of total elbow replacement as primary treatment. J. Bone Joint Surg. Br. 84:812, 2002. 6. Grassi, F. A., and Tajana, M. S.: Partial prosthetic replacement of the shoulder in fractures and fracture-dislocations of the proximal humerus. Chir. Organi Mov. 90:179, 2005. 7. Greenough, C. G., and Jones, J. R.: Primary total hip replacement for displaced subcapital fracture of the femur. J. Bone Joint Surg. Br. 70:639, 1988. 8. Helfet, D. L., Kloen, P., Anand, N., and Rosen, H. S.: Open reduction and internal fixation of delayed unions and nonunions of fractures of the distal part of the humerus. J. Bone Joint Surg. Am. 85-A(1):33, 2003. 9. Hughes, R. E., Schneeberger, A. G., An, K. N., Morrey, B. F., and O’Driscoll, S. W.: Reduction of triceps muscle force after shortening of the distal humerus: a computational model. J. Shoulder Elbow Surg. 6:444, 1997. 10. Ikavalko, M., and Lehto, M. U.: Fractured rheumatoid elbow: treatment with Souter elbow arthroplasty—a clinical and radiologic midterm follow-up study. J. Shoulder Elbow Surg. 10:256, 2001. 11. Kalogrianitis, S., Sinopidis, C., El Meligy, M., Rawal, A., and Frostick, S. P.: Unlinked elbow arthroplasty as primary treatment for fractures of the distal humerus. J. Shoulder Elbow Surg. 17:297, 2008. 12. Kamineni, S., and Morrey, B. F.: Distal humeral fractures treated with noncustom total elbow replacement. J. Bone Joint Surg Am. 86-A:940, 2004. 13. Kasten, P., Krefft, M., Hesselbach, J., and Weinberg, A. M.: Kinematics of the ulna during pronation and supination in a cadaver study: implications for elbow arthroplasty. Clin. Biomech. (Bristol, Avon) 19:31-5, 2004. 14. Keenan, J., Chakrabarty, G., and Newman, J. H.: Treatment of supracondylar femoral fracture above total knee replacement by custom made hinged prosthesis. Knee 7:165, 2000. 15. Kocher, M., Melcher, G. A., Leutenegger, A., and Rüedi, T.: [Elbow fractures in elderly patients]. Swiss Surg. 3:167, 1997. 16. Kozak, T. K., Adams, R. A., and Morrey, B. F.: Total elbow arthroplasty in primary osteoarthritis of the elbow. J. Arthroplasty 13:837, 1998. 17. Lecestre, P., Dupont, J. Y., Lortat Jacob, A., and Ramadier, J. O.: [Severe fractures of the lower end of the humerus in

18.

19.

20.

21.

22.

23.

24.

25.

26.

27.

28.

29.

30.

31.

32.

33.

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adults (author’s transl)]. Rev. Chir. Orthop. Reparatrice Appar. Mot. 65:11, 1979. Lee, K. T., Lai, C. H., and Singh, S.: Results of total elbow arthroplasty in the treatment of distal humerus fractures in elderly Asian patients. J. Trauma 61:889, 2006. McKee, M. D., Pugh, D. M., Richards, R. R., Pedersen, E., Jones, C., and Schemitsch, E. H.: Effect of humeral condylar resection on strength and functional outcome after semiconstrained total elbow arthroplasty. J. Bone Joint Surg. Am. 85-A:802, 2003. Mighell, M. A., Dunham, R. C., Rommel, E. A., and Frankle, M. A.: Primary semi-constrained arthroplasty for chronic fracture-dislocations of the elbow. J. Bone Joint Surg. Br. 87:191, 2005. Mighell, M., Virani, M., Frankle, M., and Pupello, D.: Failed open reduction and internal fixation for elbow fractures converted to total elbow arthroplasty. In American Shoulder and Elbow Surgeons Closed Meeting. Chicago, 2006, p. e52. Morrey, B. F., and Adams, R. A.: Semiconstrained elbow replacement for distal humeral nonunion. J. Bone Joint Surg. Br. 77:67, 1995. Morrey, B. F., and Adams, R. A.: Semiconstrained arthroplasty for the treatment of rheumatoid arthritis of the elbow. J. Bone Joint Surg. Am. 74:479, 1992. Morrey, B. F., Adams, R. A., and Bryan, R. S.: Total replacement for post-traumatic arthritis of the elbow. J. Bone Joint Surg. Br. 73:607, 1991. Movin, T., Sjoden, G. O., and Ahrengart, L.: Poor function after shoulder replacement in fracture patients. A retrospective evaluation of 29 patients followed for 2-12 years. Acta Orthop. Scand. 69:392, 1998. Pajarinen, J., and Bjorkenheim, J. M.: Operative treatment of type C intercondylar fractures of the distal humerus: results after a mean follow-up of 2 years in a series of 18 patients. J. Shoulder Elbow Surg. 11:48, 2002. Pereles, T. R., Koval, K. J., Gallagher, M., and Rosen, H.: Open reduction and internal fixation of the distal humerus: functional outcome in the elderly. J. Trauma 43:578, 1997. Ray, P. S., Kakarlapudi, K., Rajsekhar, C., and Bhamra, M. S.: Total elbow arthroplasty as primary treatment for distal humeral fractures in elderly patients. Injury 31:687, 2000. Riseborough, E. J., and Radin, E. L.: Intercondylar T fractures of the humerus in the adult. A comparison of operative and non-operative treatment in twenty-nine cases. J. Bone Joint Surg. Am. 51:130, 1969. Schneeberger, A. G., Adams, R., and Morrey, B. F.: Semiconstrained total elbow replacement for the treatment of posttraumatic osteoarthrosis. J. Bone Joint Surg. Am. 79:1211, 1997. Sodergard, J., Sandelin, J., and Bostman, O.: Mechanical failures of internal fixation in T and Y fractures of the distal humerus. J. Trauma 33:687, 1992. Viellette, J., and McKee, M.: A multicenter prospective randomized controlled trial of open reduction internal fixation versus total elbow arthroplasty for displaced intra-articular distal humeral fractures in elderly patients. In ASES 23rd Annual Closed Meeting, 2006. Chicago, Illinois. Zagorski, J. B., Jennings, J. J., Burkhalter, W. E., and Uribe, J. W.: Comminuted intraarticular fractures of the distal humeral condyles. Surgical vs. nonsurgical treatment. Clin. Orthop. Relat. Res. 202:197, 1986.

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CHAPTER

57

Semiconstrained Elbow Replacement: Results in Traumatic Conditions Alberto G. Schneeberger and Bernard F. Morrey

INTRODUCTION Damage or loss of the articular cartilage of the elbow joint may occur in comminuted intra-articular fractures. Late osteoarthrosis may develop as a result of traumatic cartilaginous damage or joint incongruence of insufficiently reduced intra-articular fractures or subluxed unstable elbows. The treatment of choice for most displaced intraarticular fractures of the elbow joint is open reduction and internal fixation.28,32,33 In a review of nine studies of osteosynthesis of distal humerus fractures, fair to poor outcomes were reported in 25%, with a high complication rate.28 Secondary procedures were required in 70% of the cases. In the elderly, open reduction and internal fixation can be particularly difficult because of marked osteoporosis and extensive comminution.28,33,68 In elderly patients, the use of hip arthroplasty for fracture of the femoral neck is well accepted.13 Similarly, hinged semiconstrained total elbow replacement got wide acceptance in the recent years as an excellent alternative to open reduction and internal fixation of comminuted fractures of the distal humerus, and might be considered the treatment of first choice in properly selected cases of extensively comminuted fractures in patients older than 65 years of age.* Post-traumatic osteoarthrosis, however, differs from acute traumatic conditions in several aspects and poses greater treatment difficulties. This chronic painful condition is usually characterized by stiffness, joint and bone deformity with extensive soft tissue contractures, bone loss, and instability. Typically, one or more previous procedures have resulted in a poor soft tissue envelope, infection, and nerve injury.59

*See references 2, 9, 18, 20, 21, 27, 34, 35, 45, 52, and 57.

Few options exist for salvage of severe post-traumatic osteoarthrosis. Arthrodesis reliably relieves pain41 but results in great functional impairment,54 and hence, is rarely considered a viable option (see Chapter 70).15,46 Interposition arthroplasty may be considered for a young patient, particularly one who has stiffness. Restoration of motion and relief of pain can be achieved with a reasonable (62% to 70%) but unpredictable rate of success.8,19,37,44,65 However, this procedure has an even higher rate of complications than that associated with semiconstrained total elbow replacement (see Chapter 69).8,50 Interposition arthroplasty also is not considered suitable for patients who perform strenuous physical labor.37 Varying results have been reported for allograft replacement of the entire elbow joint.1,11,14,66 Concern about the complication rate, instability, continued degenerative changes and fragmentation, and neurotrophic changes of the allograft explain why this procedure has not found wide acceptance (see Chapter 67). For all of the aforementioned reasons, total elbow replacement using the semiconstrained Coonrad-Morrey prosthesis has become, in our hands, the treatment of choice in these difficult problems in the elderly patient. Our favorable results with surveillance over 12 years are outlined below.

INDICATIONS ACUTE TRAUMA The treatment of choice for acute fractures of the distal humerus is open reduction and internal fixation, if possible.32,33 The indication for semiconstrained total joint replacement for acute fractures of the distal humerus is mainly limited to patients older than about 65 years of age with an extensively comminuted fracture that is not amenable to an adequate and stable osteosynthesis. The usual findings are as follows: (1) a large number of small fragments, (2) poor mechanical quality of severe osteoporotic bone, (3) significant loss of joint fragments in open injuries, and (4) pre-existing joint damage in patients with rheumatoid arthritis or other inflammatory joint diseases.

TRAUMATIC ARTHROSIS For post-traumatic osteoarthrosis, total joint replacement using the semiconstrained Coonrad-Morrey prosthesis is, in our hands, the treatment of choice in selected cases. These cases include advanced destruction of the ulnohumeral joint with marked narrowing or loss of the joint space. This pathology is believed to preclude other reliable treatment modalities, such as débridement or ulnohumeral arthroplasty, and only for

Chapter 57 Semiconstrained Elbow Replacement: Results in Traumatic Conditions

those patients who are older than 60 years of age. For patients younger than 60 years, total elbow replacement should be performed only with reservation, if no other suitable alternatives of operative treatments are available or for those in whom other reconstructive procedures have failed, such as interposition arthroplasty.5 Furthermore, replacement is reserved only for those patients who do not perform strenuous physical activities. Our experience with the semiconstrained CoonradMorrey prosthesis for the treatment of post-traumatic osteoarthritis revealed mechanical complications of the implant in 17% of the cases, most occurring in patients younger than 60 years of age.59 Hence, membership in this group, participation in heavy physical work, and anticipated noncompliance are considered relative contraindications for this procedure. For young patients with a severe post-traumatic osteoarthrosis, interposition arthroplasty may be considered the treatment of first choice, rather than total joint replacement (see Chapter 69). In cases of failed interposition arthroplasty, total joint replacement is the treatment of choice for most patients.

FURTHER CONSIDERATIONS AGE, OCCUPATION, AND PHYSICAL ACTIVITY Because the total elbow prosthesis is a mechanical device, it is subjected to wear, particularly of the polyethylene bushings.67 In our series, those with post-traumatic osteoarthrosis who were younger than 60 years of age had a higher rate of complications (35% versus 17%) and, accordingly, a lower proportion of satisfactory results (78% compared to 89%).59 The prosthesis does not tolerate the stress of heavy physical work; thus, after a total elbow replacement, we always advise the patient to avoid single-event lifting of objects that weigh more than 5 kg as well as the repetitive lifting of any object that weighs more than 1 kg. We discourage the playing of golf and other impact sports.

INSTABILITY Acute or post-traumatic instability is not a contraindication to elbow replacement that involves the use of the semiconstrained Coonrad-Morrey implant53,59; in fact, the condition is well managed with this device.56 Owing to its hinge design, this implant yields immediate and durable stability. In contrast to certain other semiconstrained implants,25 the Coonrad-Morrey device provides valgus-varus and axial stability without the tendency for the components to disassemble. This topic is discussed further in Chapter 53.

815

BONE LOSS Significant bone stock deficiency was present in 13 of the 41 patients in our series with post-traumatic osteoarthrosis.59 Only the humeral diaphysis is required to obtain secure fixation of the Coonrad-Morrey prosthesis. Rotational and anteroposterior stability is maintained by the anterior flange and bone graft (Fig. 57-1). Thus, this implant does not require the condyles for mechanical support. In acute injuries, the fractured condyles are completely removed, as in the treatment of nonunions (see Chapter 59).48 In post-traumatic osteoarthrosis, loss of the condyles does not require their reconstruction. This enormously facilitates total elbow replacement and constitutes a great advantage over those total elbow prostheses that need the condyles for stability.24,25,64 A loss of the distal humerus up to 6 to 8 cm can easily be managed by the noncustom CoonradMorrey device.35 The length of the condyles is approximately 3 cm. If the bone loss extends into the supracondylar area and into the shaft of the humerus, the Coonrad-Morrey humeral component with the long anterior flange can be used compensating for another 3 cm of bone loss. In addition, the humeral component can be cemented up to 2 cm more proximally into the shaft. This results, however, in shortening of the humerus with potential weakening of the muscles crossing the elbow joint.30 However, in chronic situations, this might not be appreciated by patients because of muscle contracture or preoperative weakness from pain. In a retrospective analysis, Hildebrand and coauthors29 measured the extensor muscle strength in 16 patients after Coonrad-Morrey elbow replacement for traumatic or posttraumatic conditions. Although the patients had approximately a three times weaker extension strength of the replaced compared with the contralateral elbows, the patient satisfaction with the result of elbow arthroplasty was very high, and triceps weakness did not seem to be clinically appreciated by the patients. Similarly, McKee and coauthors42 measured the muscle strength of the elbow, forearm, wrist, and hand muscles in 16 patients with Coonrad-Morrey total elbow replacement that had resection of both condyles and compared the values with 16 cases that had intact condyles. They found no significant differences between the two groups with regard to the various strength measurements and with regard to the Mayo Elbow Performance score. Traumatic loss of the proximal ulna is a difficult problem and requires reconstruction with allograft or autograft from the iliac crest to restore the site of insertion of the extensor mechanisms (see Chapter 66).

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Part VII Reconstructive Procedures of the Elbow

6cm 8cm

3cm 2cm

FIGURE 57-1

2cm

DEFORMITY Deformity is a feature often encountered in post-traumatic osteoarthrosis expressed as angular abnormalities of more than 30 degrees or translational problems (Fig. 57-2; see also Fig. 57-9).59,61 Long-standing deformity results in asymmetrical soft tissue contractures. Unlinked resurfacing total elbow prostheses usually cannot correct this type of deformity, and instability is common. Although hinged semiconstrained prostheses have the major advantage of being able to correct deformity, this correction may be at the expense of persistent or increased asymmetrical loads imparted by the distorted soft tissues, causing an increased wear of the prosthesis. Overall, in our experience, a marked preoperative deformity of the elbows was associated with a significantly higher rate of complications (P = .02).59

The implant sits in the nominal location with the absence of all of the distal humeral articulation, approximately 3 cm of bone loss. Use of the long flange allows engagement of the native bone even in the presence of an additional 3 cm of bone loss by allowing the implant not to be fully seated across the deficient 3 cm of distal humeral bone. A total of 8 cm of distal humeral bone loss can be addressed with a noncustom long-flange version of the implant by allowing shortening of 2 cm.

TECHNIQUE: TRAUMATIC CONDITIONS The operative technique for the implantation of the semiconstrained Coonrad-Morrey prosthesis is described in Chapter 53.47 However, some features are unique to this type of prosthesis and should be emphasized. An open type II or III compound fracture should first be irrigated and débrided to avoid wound infection. Total elbow replacement is then performed in a second stage. A type I wound may be treated in a single stage after careful and thorough débridement. A posterior midline incision is used, including posterior scars from previous procedures. Alternatively, prior medial and lateral incisions can be used for exposure. The ulnar nerve is always identified and transposed anteriorly in a subcutaneous pocket, if the procedure has not already been performed. If condyles are present,

Chapter 57 Semiconstrained Elbow Replacement: Results in Traumatic Conditions

817

FIGURE 57-2

A, Preoperative radiograph showing marked osseous deformity in a 41-year-old man who had sustained a supracondylar fracture in his childhood. He had severe pain and moderate instability. B, Anteroposterior radiograph, made 4 years postoperatively, showing worn bushings with recurrence of the valgus deformity. The patient had returned to his previous job as a construction worker, which involved lifting as much as 150 kg on a regular basis, against the advice of the surgeon. C, Postoperative anteroposterior radiograph made after exchange of the bushings. Both the humeral and the ulnar components were found to be solidly fixed.

the recommended operative technique includes a tricepssparing approach, which is accomplished by the release and lateral reflection of the triceps from the olecranon in continuity with the ulnar periosteum and the fascia of the forearm, along with the anconeus, as described by Bryan and Morrey.7 Alternatively, particularly in acute fractures involving the condyles, the triceps insertion is left intact.35 Overall, triceps strength measurements are not different between the elbows in which the triceps was left on the olecranon and those in which the triceps was reflected and then reattached to the olecranon.29 If contracted soft tissue persists, the humeral component is inserted more proximally after removal of additional humeral bone. All soft tissues are released from the humeral fragments, which are then excised (Fig. 57-3). Cultures are taken if there has been prior surgery. The collateral ligaments are detached from the epicondyles, which allows complete exposure of the elbow joint. The repair of the collateral ligaments is not necessary.

Usually, resection of the tip of the coronoid process is necessary to avoid impingement with the anterior flange, which would cause considerable distraction forces on the ulnar component.61 Too deep insertion of the ulnar component is another potential cause of anterior impingement (Fig. 57-4). An intramedullary injecting system is used for optimal insertion of cement to which 1 g of vancomycin has been added for every 40 g of cement.16 An important element is the placement of a bone graft between the anterior flange and the distal part of the humerus to resist, after ingrowth, posterior displacement and rotational stresses on the humeral component. Ingrowth of this bone graft is consistently observed, confirming its role in absorbing mechanical loads.59 Significant bone stock deficiencies with the lack of one or both epicondyles do not change or complicate the implantation of the humeral component. This device requires only the humeral diaphysis to obtain secure fixation. Therefore, the reconstruction of the condyles is not required.

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Part VII Reconstructive Procedures of the Elbow

Common flexor tendon reflected

Medial distal fragments

Ulnar n.

FIGURE 57-3

A and B, For acute fractures, the fracture fragments are completely excised, allowing implantation without removal of the triceps.

Chapter 57 Semiconstrained Elbow Replacement: Results in Traumatic Conditions

Common extensor tendon reflected

Lateral distal fragments

FIGURE 57-3, cont’d

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Part VII Reconstructive Procedures of the Elbow Chapter 57 Semiconstrained Elbow Replacement: Results in Traumatic Conditions

2

2

820

2 1

1

1

a

b

c

FIGURE 57-4

A, Graph showing correct depth of insertion of the ulnar component. The tip of the coronoid process (1) is resected. There is clearance between the coronoid process and the anterior flange of the humeral component (2). Flexion is unrestricted. B, Too deep insertion of the ulnar component resulting in anterior impingement between the coronoid process (1) and the anterior flange of the humeral component. Flexion is restricted. C, Correct depth of insertion of the ulnar component but the coronoid osteophyte (1) has not been resected resulting in anterior impingement and restricted flexion. (Redrawn from Schneeberger, A. G., Meyer, D. C., and Yian, E. H.: Coonrad-Morrey total elbow replacement for primary and revision surgery: A 2 to 7.5 year follow-up study. J. Shoulder Elbow Surg. 16(3 Suppl):47, 2007.)

The device offers three lengths of humeral component: 10, 15, and 20 cm in standard, small, and extra small sizes with a regular or long anterior flange (Fig. 57-5). In cases of post-traumatic osteoarthrosis, we normally use the 15-cm stem. If the patient needs or may need a shoulder replacement, the shorter 10-cm stem for the elbow prosthesis may be a more appropriate choice to avoid a conflict of the elbow and shoulder implants within the humeral diaphysis. Variable lengths and diameters of the ulna are also available. At the end of the procedure, if the triceps has been reflected, it is reattached to the olecranon with two No. 5 nonabsorbable sutures, allowing the immediate use of the joint. Compression dressings and elevation of the extremity are recommended for about 2 days, followed by gentle range-of-motion exercises as tolerated. Formal physical therapy is not necessary.

RESULTS REVIEW OF EARLY LITERATURE The results of total elbow replacements with highly constrained designs in the 1970s were disappointing

because of high rates of loosening.12,22,51 Although less loosening was reported after the introduction of semiconstrained and unconstrained replacement devices,10,15,24,46,55 those reports dealt almost exclusively with the treatment of rheumatoid arthritis. In the 1980s and early 1990s, there was very little information regarding total elbow replacement with an unconstrained or a semiconstrained device for the treatment of posttraumatic osteoarthrosis.† Most of what has been reported showed unfavorable results.36,38,40,63 In 1980, Inglis and Pellicci,31 reported little improvement in nine patients who had been managed with a semiconstrained Pritchard-Walker triaxial implant. Lowe and colleagues40 reported a satisfactory result in only one of seven trauma patients who had an unconstrained device. In 1984, Soni and Cavendish63 reported a good or excellent result for only three of eight patients who had an unconstrained implant. Other than our own experience, Figgie and associates17 reported the first positive experience with a semiconstrained (triaxial) prosthesis with customdesigned stems for the treatment of post-traumatic conditions. Results in eight of the nine patients reported †

See references 6, 17, 24, 31, 36, 38, 40, 46, and 63.

Chapter 57 Semiconstrained Elbow Replacement: Results in Traumatic Conditions

821

Four of them had been treated for post-traumatic arthrosis. The mean follow-up of the 14 patients was 6 years (range, 2 to 9 years). Overall, 29% of the cases required revision due to gross aseptic loosening.

SEMICONSTRAINED TOTAL ELBOW REPLACEMENT ACUTE FRACTURES

FIGURE 57-5

Three lengths of humeral implants are available. The short stem illustrates the standard diameter; the median and long stems are of the small diameter. Standard, small, and extra small sizes are available for all three lengths.

were satisfactory.17 However, different designs with variable stems, as well as fixation with or without cement, were used. In 1994, Kraay and coworkers38 reported the experience with a linked semiconstrained implant. Of 113 patients, only 18 had been managed for post-traumatic osteoarthrosis, nonunion, or fracture. The results in these patients were disappointing, with a 5-year rate of survival of the implants of only 53%. There were five loose humeral components and two infections among the 18 patients. In 1996, Gschwend and colleagues25 reported their experience in 26 patients with post-traumatic osteoarthrosis of the elbow treated with total joint replacement using the semiconstrained GSB III implant. The mean follow-up was 4.3 years (maximum 14 years). Pain relief was obtained in 82% of cases. The mean arc of flexion was 34 to 126 degrees. However, the revision rate was 31% owing to aseptic loosening in two, disassembly in four, and ectopic bone formation in two elbows. Another series of 14 patients treated with the GSB III prosthesis was presented in the year of 2000.60

The first comprehensive series of total elbow replacement for acute fractures was introduced in 1997 by Cobb and Morrey.9 In 2004, an update of the Mayo experience, and in 2005 particular features of the surgical technique was presented by Kamineni and Morrey.34,35,52 It was a series of 49 semiconstrained Coonrad-Morrey total elbow replacements treated at the Mayo Clinic between 1982 and 2001. Forty-three out of these 49 elbows had a minimum follow-up of 2 years (average 7 years; range, 2 to 15). The main inclusion criteria for treatment with total elbow replacement were a fracture that was not amenable to open reduction and internal fixation because of extensive articular comminution (23 elbows), a fracture that had been treated elsewhere with osteosynthesis and had subsequent failure within one month (3 elbows), articular surface destruction by rheumatoid arthritis (17 elbows), pre-existing arthritis (3 elbows), or substantial osteopenia (3 elbows) (Fig. 57-6). The mean age of the patients at the time of injury was 69 years (34 to 92 years). On the basis of the Mayo elbow performance score, 40 patients had a good or excellent result (93%), and three had a fair outcome. Pain relief was reliably obtained, with 35 patients having no pain and 8 patients having mild pain. The mean arc of flexion-extension was 24 to 131 degrees. Severe osteoporosis was common, but it did not appear to influence the functional result. Later reports confirmed the positive Mayo experience.18,20,21,57,58 Three different series of elderly patients treated with the Coonrad-Morrey total elbow prosthesis for acute distal humeral fractures were presented between 2000 and 2002 from various centers.20,21,57 All patients of these three series uniformly showed excellent or good results according to the Mayo Elbow Performance score, no or only mild pain, and a good range of motion. There were no patients with moderate or severe pain. And after follow-ups of 1 to 5.5 years, there were no loose implants observed. In 2000, Ray and coauthors57 presented a series of seven elderly patients treated with the Coonrad-Morrey total elbow prosthesis for distal humeral fractures and followed for 2 to 4 years. According to the Mayo Elbow Performance Score, five patients had an excellent and two had a good result. Six patients had no pain, and

822

Part VII Reconstructive Procedures of the Elbow

FIGURE 57-6

A 79-year-old woman with a comminuted distal humeral fracture (A). Patient is asymptomatic with essentially normal function after joint replacement (B).

one patient had mild pain. There were no cases of loosening in this series. In 2001, Gambirasio and coauthors20 presented a series of 10 patients with complex fractures of the distal humerus treated with the Coonrad-Morrey prosthesis. After a mean follow-up of 1.5 years (range, 1 to 3) all had a satisfactory outcome. Eight had no pain, and two had mild pain. The mean arc of flexion was from 24 to 126 degrees. In 2002, Garcia and coauthors21 presented a similar series of 16 patients with fractures of the distal humerus treated with the Coonrad-Morrey total elbow prosthesis. After a mean follow-up of 3 years (range, 1 to 5.5), 11 patients had no pain, and four had mild pain. According to the Mayo Elbow Performance score, all patients had an excellent (11 patients) or a good (five patients) outcome. There were no cases of loosening in this series. In a retrospective analysis presented in 2003, Frankle and coauthors18 compared open reduction and internal fixation with primary total elbow replacement using the Coonrad-Morrey device in the treatment of intraarticular distal humerus fractures in women older than 65 years of age. After a mean follow-up of 5 years (range, 2 to 6.5), all 12 patients treated with joint replacement had an excellent (11 patients) or a good outcome

(1 patient) according to the Mayo Elbow Performance score, whereas only eight patients (67%) of the internal fixation group had an excellent or good outcome; one had a fair result, and three had a poor result. Other semiconstrained total elbow prostheses have been introduced in the last few years for the treatment of acute distal humerus fractures. Similarly to the Coonrad-Morrey prosthesis, these devices have an anterior flange to resist posterior and rotational stresses on the humeral component.27 Long-term data, however, are not yet available with these recently introduced devices.

CONCLUSION Semiconstrained Coonrad-Morrey total elbow replacement for acute fractures of the distal aspect of the humerus is a reliable treatment in a specific group of elderly patients but is not an alternative procedure to osteosynthesis in younger patients.

POST-TRAUMATIC ARTHROSIS An in-depth review of the Mayo experience was presented in 1997 by Schneeberger and associates. This is by far the most comprehensive series in the literature

Chapter 57 Semiconstrained Elbow Replacement: Results in Traumatic Conditions

consisting of 41 consecutive patients treated from 1981 to 1993 with semiconstrained Coonrad-Morrey elbow replacement and followed an average of almost 6 years.59 The average age of the patients was 57 years (range, 32 to 82 years). The indication for joint replacement was pain for 36 patients; reduced, painful range of motion for two patients, and dysfunction with a flail elbow for

A

three patients. The average time from the original fracture to the joint replacement was 16 years (range, 3 months to 64 years). This is a very difficult group of patients to manage. All but two patients (95) had had previous surgery (Fig. 57-7), the average being 2.3 procedures (range, 0 to 7 procedures). Significant bone stock deficiency with loss

B

FIGURE 57-7

C

823

A, Severe arthrosis with posterior subluxation after open reduction and internal fixation (ORIF) and hardware removal. Anteroposterior (B) and lateral (C) radiographs 11 years after CoonradMorrey total elbow replacement. Stable implant without signs of loosening. Surgery resulted in functional range of flexion from 20 to 130 degrees and significant improvement of symptoms.

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Part VII Reconstructive Procedures of the Elbow

of at least one condyle was present in 13 patients, and 14 patients had a significant joint or bone deformity (Fig. 57-8). Ten of 41 elbow joints were preoperatively subluxed, and seven were dislocated. Additional complications from prior surgery included mild to moderate ulnar neuropathy in six patients and radial nerve palsy due to a complete traumatic laceration in one patient. At the latest follow-up, objectively 40% were rated excellent and 43% were considered good, for an overall rate of 83% satisfactory objective outcome. Subjectively, 95% of the patients with a functioning implant expressed satisfaction with the operation. Although the rate of pain relief (76%) was considered to be rather high, it was not as high as that reported after the treatment of rheumatoid arthritis (97%).23 At follow-up, the mean arc of flexion-extension was 27 to 131 degrees, and the mean arc of pronation-supination was 66 to 64 degrees. An average of 4.8 of the five activities of daily living could be performed by the patients, and strength improvement averaged approximately 30%.3,49 The radiologic analysis showed all grafts behind the flange to have incorporated. There was not one case of aseptic loosening within the 12 years of follow-up. A review of the patients that had been treated at Balgrist, Department of Orthopaedic Surgery of the Uni-

A FIGURE 57-8

B

versity of Zurich, showed a similar series of 16 patients treated between 1996 and 2001 for post-traumatic arthrosis with the Coonrad-Morrey prosthesis.62 At latest follow-up, or at revision due to loosening (one case) or infection (one case), 12 patients (75%) had an excellent or a good outcome according to the Mayo Elbow Performance Score. If at the latest follow-up also the two patients after revision of their failed implants were included, 88% of the patients had a satisfactory objective outcome. The mean arc of flexion was from 27 to 131 degrees. In 2005, Mighell and coauthors43 presented a series of six elderly women with a chronic fracture dislocation treated with the Coonrad-Morrey total elbow replacement. At a mean follow-up of 6 years (range, 2 to 10 years), three patients had no pain, two had moderate pain, and one had severe pain. The American Shoulder and Elbow Surgeons score was five times better (P < 0.001) and the mean flexion arc increased from 33 to 121 degrees (P < 0.001) after operation.

CONCLUSION Severe post-traumatic osteoarthrosis or dysfunction can be reliably and durably treated with a noncustomized

C

A, Preoperative anteroposterior radiograph of a patient after gunshot wound and bony defect of distal humerus. Anteroposterior (B) and lateral (C) radiographs 14 years after insertion of a Coonrad-Morrey total elbow prosthesis. Stable elbow and implant without signs of loosening.

Chapter 57 Semiconstrained Elbow Replacement: Results in Traumatic Conditions

semiconstrained device. The patients’ satisfaction usually is very high. In all of these series, all implants were stable, and function was reliably restored.

COMPLICATIONS The complications for the Mayo and the Balgrist experience are shown in Table 57-1. Of the 49 patients with an acute fracture, 35% had a surgical complication.34 There were 14 patients with a single complication, and three with two complications; 10 of them required additional procedures. Wound problems occurred in 11 cases: three patients required decompression of a hematoma, two had secondary closure to treat a wound dehiscence, one patient had removal of a prominent Kirschner wire in the olecranon 2 months postoperatively, and in another patient, a wound infection was found to have penetrated into the joint cavity 3 weeks after joint replacement necessitating three débridements and staged exchange revision of the humeral component. There were three (6%) temporary neurologic complications: one sensory and one motoric neuropathy of the ulnar nerve, and one with a reflex sympathetic dystrophy. Two patients had important heterotopic bone formation with abutment of the ectopic bone between

825

the humerus and ulna posteriorly. One ulnar shaft periprosthetic fracture after a fall 1 year after the arthroplasty was successfully treated with a plaster cast. Five patients required revision arthroplasty during the follow-up period. One of them had a septic loosening, as mentioned earlier. Two patients sustained a traumatic fracture of the humeral component (one patient) or the ulnar component (one patient) from a fall that required implant revision at 2 and 4 years after insertion of the prostheses. One woman with rheumatoid arthritis underwent two ulnar component revisions, the first because of a fall and the second because of aseptic loosening 3 years later. The fifth patient required a revision arthroplasty at 9 years following the index arthroplasty because of aseptic loosening of the ulnar component. Overall, two out of 43 patients (5%) had aseptic loosening after a maximum follow-up of 15 years. Of the 41 patients in the post-traumatic group treated at Mayo Clinic, 11 (27%) had at least one major complication, and nine (22%) had an additional operation. This contrasts with the report of Gschwend and colleagues,26 who in 1996, described a complication rate of 43% from a meta-analysis of 22 publications of total elbow replacement. Most of these procedures were performed for rheumatoid arthritis; such cases are usually

Major Complications with Total Elbow Arthroplasty After Acute Fracture and Post-traumatic Arthrosis

TABLE 57-1

ACUTE

POST-TRAUMATIC ARTHROSIS Mayo Experience

Orthopedic Complication

n = 49*,†

n = 41‡

Balgrist Experience n = 16§

Aseptic Loosening

2¶

0

3¶

Infection

1¶

2¶

1¶

Wear

0

2¶

0

Fracture Humeral component Ulnar component Ulna

1¶ 1¶ 1

0 5¶ 0

0 0 0

11¶

1¶

2¶

Wound Neural

3 (all temporary)

1

2¶

Triceps rupture

0

1¶

1¶

Other

0

3¶

1¶

*Kamineni, S., and Morrey, B. F.: Distal humeral fractures treated with noncustom total elbow replacement. J. Bone Joint Surg. 86-A:940, 2004. † Forty-three out of 49 patients had a follow-up. ‡ Schneeberger, A. G., Adams, R., and Morrey, B. F.: Semiconstrained total elbow replacement for the treatment of post-traumatic osteoarthrosis. J. Bone Joint Surg. 79A:1211, 1997. § Schneeberger, A. G., and Morrey, B. F.: Total elbow arthroplasty for posttraumatic arthrosis. In Celli, L. (ed.): The Treatment of the Elbow Lesions. Berlin, Heidelberg, Springer, 2008, p. 263. ¶ Required revision or reoperation.

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Part VII Reconstructive Procedures of the Elbow

associated with fewer complications than those in posttraumatic osteoarthrosis cases. The majority of the complications were of a mechanical cause. Fracture of the ulnar component occurred in five elbows 2 to 9 years (average, 4.3 years) postoperatively. Before breakage, all five patients had an excellent result, with an asymptomatic, essentially normal elbow. The cause of failure was severe noncompliance, such as regular lifting of weights of more than 50 kg in two patients (Fig. 57-9). The revisions involved an average of less than 70 minutes of tourniquet time. There were no operative or delayed complications from the reoperations. The fractures of the ulnar component always occurred at the site of sintered beads. Modification of the surface of the ulnar component from sintered beads to a precoat in 1995 and then to a plasma spray coating in 2000 increased the mechanical properties of the implant, and fractures of the proximal ulna were not observed since then by the authors. There was not one case of loosening in this series of post-traumatic arthrosis of the Mayo Clinic. Two patients presented with a particulate synovitis associated with worn bushings. Both cases also had a significant preoperative deformity, and one excessive use. Treatment of the worn bushing consisted of synovectomy and exchange of the bushings, resulting in a satisfactory outcome. Special concern has been expressed for bushing wear in younger and more active patients.67 To analyze poly-

ethylene wear, all Coonrad-Morrey elbow prostheses performed at the Mayo Clinic from 1981 through 2000 for various indications (34% for trauma-related conditions) were retrospectively reviewed.39 Out of 919 patients, only 12 (1.3%) had undergone an isolated exchange of the articular bushings as a result of polyethylene wear. Seven out of these 12 cases had posttraumatic arthrosis. Nine had extensive deformity. The bushings were revised at an average of 8 years after implantation. Polyethylene wear did not seem to be a major problem at the Mayo Clinic. Newer implants such as the Latitude (Tornier—Zirst, Montbonnot, France, Fig. 57-10) or the Discovery (Biomet, Warsaw, IN) have other polyethylene-metal designs aiming to increase longevity of the polyethylene and to allow higher loads on the prosthesis. Follow-up of these new designs will show whether the different contact surfaces of these new designs will succeed, or if eventually larger amounts of wear debris will result. At Balgrist, there were eight patients (50%) with 10 complications requiring seven revisions. One patient with a prior Pseudomonas aeruginosa infection had recurrence of the infection after a clinical infection-free period of 5 years. He required staged revision, resulting in an excellent result. Two wounds were successfully revised for aseptic, prolonged wound drainage of more than 7 days. Because the soft tissue envelope is thin around the elbow, wound problems probably increase the risk of infection. For this reason, the authors believe that aggressive wound management is important. The two patients

FIGURE57-9 A, A 58-year-old farmer showing extensive preoperative osseous deformity owing to a malunited supracondylar fracture from age 10 years. The patient had moderate pain and marked loss of motion. B, Fracture of the ulnar component 9 years after implantation of the prosthesis. The patient had had no pain and had full function during these 9 years, and he had returned to his previous strenuous activities, regularly lifting weights of more than 50 kg, against the advice of the surgeon.

Chapter 57 Semiconstrained Elbow Replacement: Results in Traumatic Conditions

FIGURE 57-10 Latitude total elbow replacement with semiconstrained design can be used as linked or unlinked implant with optional insertion of a bipolar radial head prosthesis.

with wound revisions had an uneventful recovery without development of an infection. Loosening was found in two humeral and two ulnar components of three patients, resulting in a loosening rate of 19%. Ulnar loosening was attributed to impingement between the anterior flange of the humeral component and a long coronoid process in one patient (see Fig. 57-4). Another case of early loosening occurred in a patient with possible persistence of a previously present low-grade infection. Inadequate cementation was observed in two humeral components in the Balgrist series; one of them was found loose at follow-up. In both cases with inadequate cementing, an anterograde cementing technique was used with direct injection of the cement using a syringe contrary to the recommendations of the manufacturer that advise to use an injecting system with retrograde insertion of the cement. Retrograde insertion of cement improves the degree of cement filling and the holding strength of the implants.16 Since 1998, an advanced cementing technique was used at Balgrist, resulting consistently in adequate cementation, and no cases of loosening were observed since then. In 2000, Hildebrand and coauthors29 reported progressive radiolucent lines after a mean follow-up of 4

827

years in 5 out of 15 patients treated with the CoonradMorrey total elbow prosthesis for traumatic or posttraumatic conditions. These radiolucent lines were found more frequently around methylmetacrylate precoated ulnar components than around those covered with sintered beads. As previously mentioned, the surface of the ulnar component had been modified from sintered beads to a precoat in 1995. Owing to above-mentioned fatigue fractures and some observations of radiolucent lines, the surface treatment was modified in 2000 to the currently used plasma spray coating, improving the cement fixation strength and the mechanical stability. Overall, loosening occurred only twice in the acute fracture group and not in one instance in the group of post-traumatic arthrosis at the Mayo Clinic. Three loose components at the post-traumatic group of the Balgrist Clinic were probably associated with poor cementing technique and anterior coronoid impingement. Totally, only five patients out of 100 reported here had loose implants, indicating the great improvement in total elbow replacement, particularly in this very difficult group of patients. This experience contrasts to that of most other series of post-traumatic osteoarthrosis that are still complicated by a certain rate of loosening despite the use of semiconstrained devices.38 However, no loosening was observed by Figgie and colleagues17 in their series of nine semiconstrained triaxial prostheses with customdesigned stems. Gschwend and associates25 reported that after a mean of 4 years (maximum, 14 years), loosening of the GSB III prosthesis had occurred in two of 26 patients. Baksi4 reported only four loose implants out of 79 cases treated for post-traumatic ankylosis or instability with an own semiconstrained device followed for an average of 9.6 years (range, 2 to 13.5 years).

CONCLUSION Serious traumatic conditions can be reliably and durably treated with a noncustomized semiconstrained device. The patient’s satisfaction is high. The loosening rate is low, and function can reliably be restored. This represents a great improvement compared with the prior constrained implants with high loosening rates considering this very difficult group of patients. Correct cementation and surgical technique seems to be important. The rather high complication rate reflects the limitations of this procedure, although most of the complications do not influence the positive final outcome. Especially the mechanical complications indicate that, in younger patients, total elbow replacement may be performed only with reservation, and only for those who do not perform strenuous physical activities.

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Part VII Reconstructive Procedures of the Elbow

References 1. Allieu, Y., Marck, G., Chammas, M., Desbonnet, P., and Raynaud, J. P.: Allogreffes d’articulation totale du coude dans les pertes de substance ostéo-articulaire posttraumatiques étendues. Résultats à 12 ans de recul. Rev. Chir. Orthop. Reparatrice Appar. Mot. 90:319, 2004. 2. Armstrong, A. D., and Yamaguchi, K.: Total elbow arthroplasty and distal humerus elbow fractures. Hand Clin. 20:475, 2004. 3. Askew, L. J., An, K.-N., Morrey, B. F., and Chao, E. Y. S.: Isometric elbow strength in normal individuals. Clin. Orthop. Relat. Res. 222:261, 1987. 4. Baksi, D. P.: Sloppy hinge prosthetic elbow replacement for post-traumatic ankylosis or instability. J. Bone Joint Surg. 80-B:614, 1998. 5. Blaine, T. A., Adams, R., and Morrey, B. F.: Total elbow arthroplasty after interposition arthroplasty for elbow arthritis. J. Bone Joint Surg. 87-A:286, 2005. 6. Brumfield, R. H., Jr., Kuschner, S. H., Gellman, H., Redix, L., and Stevenson, D. V.: Total elbow arthroplasty. J. Arthroplasty 5:359, 1990. 7. Bryan, R. S., and Morrey, B. F.: Extensive posterior exposure of the elbow: A triceps-sparing approach. Clin. Orthop. Relat. Res. 166:188, 1982. 8. Cheng, S. L., and Morrey, B. F.: Treatment of the mobile, painful arthritic elbow by distraction interposition arthroplasty. J. Bone Joint Surg. 82-B:233, 2000. 9. Cobb, T. K., and Morrey, B. F.: Total elbow replacement as primary treatment for distal humeral fractures in elderly patients. J. Bone Joint Surg. 79A:826, 1997. 10. Davis, R. F., Weiland, A. J., Hungerford, D. S., Moore, J. R., and Volenec-Dowling, S.: Nonconstrained total elbow arthroplasty. Clin. Orthop. Relat. Res. 171:156, 1982. 11. Dee, R.: Nonimplantation salvage of failed reconstructive procedures of the elbow. In Morrey, B. F. (ed.): The Elbow and Its Disorders, 2nd ed. Philadelphia, W. B. Saunders Co., 1993, p. 690. 12. Dee, R.: Total replacement arthroplasty of the elbow for rheumatoid arthritis. J. Bone Joint Surg. 54B:88, 1972. 13. DeLee, J. C.: Fractures and dislocations of the hip. In Rockwoood, C. A. Jr., Green, D. P., Bucholz, R. W., and Heckman, J. D. (eds.): Rockwood and Green’s Fractures in Adults, 4th ed. Philadelphia, Lippincott-Raven, 1996, p. 1687. 14. Delloye, C., Cornu, O., Dubuc, J. E., Vincent, A., and Barbier, O.: Reconstruction du coude par allogreffe massive ostéoarticulaire totale: échec précoce par instabilité. Rev. Chir. Orthop. Reparatrice Appar. Mot. 90:360-4, 2004. 15. Ewald, F. C., and Jacobs, M. A.: Total elbow arthroplasty. Clin. Orthop. Relat. Res. 182:137, 1984. 16. Faber, K. J., Cordy, M. E., Milne, A. D., Chess, D. G., King, G. J., and Johnson, J. A.: Advanced cement technique improves fixation in elbow arthroplasty. Clin. Orthop. Relat. Res. 334:150, 1997. 17. Figgie, H. E., III, Inglis, A. E., Ranawat, C. S., and Rosenberg, G. M.: Results of total elbow arthroplasty as a salvage procedure for failed elbow reconstructive operations. Clin. Orthop. Relat. Res. 219:185, 1987.

18. Frankle, M. A., Herscovici, D. Jr., DiPasquale, T. G., Vasey, M. B., and Sanders, R. W.: 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 17:473, 2003. 19. Froimson, A. I., Silva, J. E., and Richey, D.: Cutis arthroplasty of the elbow joint. J. Bone Joint Surg. 58A:863, 1976. 20. Gambirasio, R., Riand, N., Stern, R., and Hoffmeyer, P.: Total elbow replacement for complex fractures of the distal humerus. An option for the elderly patient. J. Bone Joint Surg. 83-B:974, 2001. 21. Garcia, J. A., Mykula, R., and Stanley, D.: Complex fractures of the distal humerus in the elderly. The role of total elbow replacement as primary treatment. J. Bone Joint Surg. 84B:812, 2002. 22. Garrett, J. C., Ewald, F. C., Thomas, W. H., and Sledge, C. B.: Loosening associated with GSB hinge total elbow replacement in patients with rheumatoid arthritis. Clin. Orthop. Relat. Res. 127:170, 1977. 23. Gill, D. R. J., and Morrey, B. F.: The Coonrad-Morrey total elbow arthroplasty in patients who have rheumatoid arthritis. A ten to fifteen-year follow-up study. J. Bone Joint Surg. 80-A:1327, 1998. 24. Gschwend, N., Loehr, J., Ivosevic-Radovanovic, D., Scheier, H., and Munzinger, U.: Semi-constrained elbow prosthesis with special reference to the GSB III prosthesis. Clin. Orthop. Relat. Res. 232:104, 1988. 25. Gschwend, N., Scheier, H., Bähler, A., and Simmen, B.: GSB III elbow. In Ruther, W. (ed.): The Elbow, Endoprosthetic Replacement and Non-endoprosthetic Procedures. Berlin, Springer Verlag, 1996, p. 83. 26. Gschwend, N., Simmen, B. R., and Matejovsky, Z.: Late complications in elbow arthroplasty. J. Shoulder Elbow Surg. 5:86, 1996. 27. Hastings, H. 2nd, and Theng, C. S.: Total elbow replacement for distal humerus fractures and traumatic deformity: results and complications of semiconstrained implants and design rationale for the Discovery Elbow System. Am. J. Orthop. 32 (9 Suppl.):20, 2003. 28. Helfet, D. L., and Schmerling, G. J.: Bicondylar intraarticular fractures of the distal humerus in adults. Clin. Orthop. Relat. Res. 292:26, 1993. 29. Hildebrand, K. A., Patterson, S. D., Regan, W. D., MacDermid, J. C., and King, G. J. W.: Functional outcome of semiconstrained total elbow arthroplasty. J. Bone Joint Surg. 82-A:1379, 2000. 30. Hughes, R. E., Schneeberger, A. G., An, K.-N., Morrey, B. F., and O’Driscoll, S.: Reduction of triceps muscle force after shortening of the distal humerus: A computational model. J. Shoulder Elbow Surg. 6:444, 1997. 31. Inglis, A. E., and Pellicci, P. M.: Total elbow replacement. J. Bone Joint Surg. 62A:1252, 1980. 32. John, H., Rosso, R., Neff, U., Bodoky, A., Regazzoni, P., and Harder, F.: Operative treatment of distal humeral fractures in the elderly. J. Bone Joint Surg. 76B:793, 1994. 33. Jupiter, J. B., Neff, U., Holzach, P., and Allgöwer, M.: Intercondylar fractures of the humerus. J. Bone Joint Surg. 67-A:226, 1985.

Chapter 57 Semiconstrained Elbow Replacement: Results in Traumatic Conditions

34. Kamineni, S., and Morrey, B. F.: Distal humeral fractures treated with noncustom total elbow replacement. J. Bone Joint Surg. 86-A:940, 2004. 35. Kamineni, S., and Morrey, B. F.: Distal humeral fractures treated with noncustom total elbow replacement. Surgical technique. J. Bone Joint Surg. 87-A Suppl. 1(Pt 1):41, 2005. 36. Kasten, M. D., and Skinner, H. B.: Total elbow arthroplasty. Clin. Orthop. 290:177, 1993. 37. Knight, R. A., and Zandt, L. V.: Arthroplasty of the elbow. J. Bone Joint Surg. 34A:610, 1952. 38. Kraay, M. J., Figgie, M. P., Inglis, A. E., Wolfe, S. W., and Ranawat, C. S.: Primary semiconstrained total elbow arthroplasty. J. Bone Joint Surg. 76B:636, 1994. 39. Lee, B. P., Adams, R. A., and Morrey, B. F.: Polyethylene wear after total elbow arthroplasty. J. Bone Joint Surg. 87A:1080, 2005. 40. Lowe, L. W., Miller, A. J., Allum, R. L., and Higginson, D. W.: The development of an unconstrained elbow arthroplasty. J. Bone Joint Surg. 66B:243, 1984. 41. McAuliffe, J. A., Burkhalter, W. E., Ouellette, E. A., and Carneiro, R. S.: Compression plate arthrodesis of the elbow. J. Bone Joint Surg. 74B:300, 1992. 42. McKee, M. D., Pugh, D. M. W., Richards, R. R., Pedersen, E., Jones, C., and Schemitsch, E. H.: Effect of humeral condylar resection on strength and functional outcome after semiconstrained total elbow arthroplasty. J. Bone Joint Surg. 85-A:802, 2003. 43. Mighell, M. A., Dunham, R. C., Rommel, E. A., and Frankle, M. A.: Primary semi-constrained arthroplasty for chronic fracture-dislocations of the elbow. J. Bone Joint Surg. 87B:191, 2005. 44. Morrey, B. F.: Post-traumatic contracture of the elbow: Operative treatment including distraction arthroplasty. J. Bone Joint Surg. 72A:601, 1990. 45. Morrey, B. F.: Fractures of the distal humerus: role of elbow replacement. Orthop. Clin. North. Am. 31:145, 2000. 46. Morrey, B. F., Adams, R. A., and Bryan, R. S.: Total replacement for post-traumatic arthritis of the elbow. J. Bone Joint Surg. 73B:607, 1991. 47. Morrey, B. F., and Adams, R. A.: Semi-constrained elbow replacement arthroplasty: Rationale, technique, and results. In Morrey, B. F. (ed.): The Elbow and Its Disorders, 2nd ed. Philadelphia, W. B. Saunders Co., 1993, p. 648. 48. Morrey, B. F., and Adams, R. A.: Semi-constrained elbow replacement for distal humeral nonunion. J. Bone Joint Surg. 77B:67, 1995. 49. Morrey, B. F., Askew, L. J., An, K.-N., and Chao, E. Y.: A biomechanical study of normal functional elbow motion. J. Bone Joint Surg. 63A:872, 1981. 50. Morrey, B. F., Askew, L. J., and An, K.-N.: Strength function after elbow arthroplasty. Clin. Orthop. Relat. Res. 234:43, 1988. 51. Morrey, B. F., Bryan, R. S., Dobyns, J. H., and Linscheid, R. L.: Total elbow arthroplasty: A five-year experience at the Mayo Clinic. J. Bone Joint Surg. 63A:1050, 1981.

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52. Muller, L. P., Kamineni, S., Rommens, P. M., and Morrey, B. F.: Primary total elbow replacement for fractures of the distal humerus. Oper. Orthop. Traumatol. 17:119, 2005. 53. O’Driscoll, S. W., An, K.-N., Korinek, S., and Morrey, B. F.: Kinematics of semiconstrained total elbow arthroplasty. J. Bone Joint Surg. 74B:297, 1992. 54. O’Neill, O. R., Morrey, B. F., Tanaka, S., and An, K.-N.: Compensatory motion in the upper extremity after elbow arthrodesis. Clin. Orthop. Relat. Res. 281:89, 1992. 55. Pritchard, R. W.: Anatomic surface elbow arthroplasty: A preliminary report. Clin. Orthop. Relat. Res. 179:223, 1979. 56. Ramsey, M. L., Adams, R. A., and Morrey, B. F.: Instability of the elbow treated with semiconstrained total elbow arthroplasty. J. Bone Joint Surg. 81-A:38, 1999. 57. Ray, P. S., Kakarlapudi, K., Rajsekhar, C., and Bhamra, M. S.: Total elbow arthroplasty as primary treatment for distal humeral fractures in elderly patients. Injury 31:687, 2000. 58. Scalise, J. J., and DeSilva, S. P.: Intraarticular distal humerus fracture complicated by osteogenesis imperfecta treated with primary total elbow arthroplasty: a case report. J. Surg Orthop. Adv. 15:95, 2006. 59. Schneeberger, A. G., Adams, R., and Morrey, B. F.: Semiconstrained total elbow replacement for the treatment of post-traumatic osteoarthrosis. J. Bone Joint Surg. 79A:1211, 1997. 60. Schneeberger, A. G., Hertel, R., and Gerber, C.: Total elbow replacement with the GSB III prosthesis. J. Shoulder Elbow Surg. 9:135, 2000. 61. Schneeberger, A. G., Meyer, D. C., and Yian, E. H.: CoonradMorrey total elbow replacement for primary and revision surgery: A 2 to 7.5 year follow-up study. J. Shoulder Elbow Surg. 16(3 Suppl):47, 2007. 62. Schneeberger, A. G., and Morrey, B. F.: Total elbow arthroplasty for posttraumatic arthrosis. In Celli, L. (ed.): The Treatment of the Elbow Lesions. Berlin, Heidelberg, Springer, 2008, p. 263. 63. Soni, R. K., and Cavendish, M. E.: A review of the Liverpool elbow prosthesis from 1974 to 1982. J. Bone Joint Surg. 66B:248, 1984. 64. Souter, W. A., Nicol, A. C., and Paul, J. P.: Anatomical trochlear stirrup arthroplasty of the rheumatoid elbow. J. Bone Joint Surg. 67B:676, 1985. 65. Tsuge, K., Murakami, T., Yasunaga, Y., and Kanaujia, R. R.: Arthroplasty of the elbow. J. Bone Joint Surg. 69B:116, 1987. 66. Urbaniak, J. R., and Black, K. E., Jr.: Cadaveric elbow allografts: A six-year experience. Clin. Orthop. Relat. Res. 197:131, 1985. 67. Wright, T. W., and Hastings, H.: Total elbow arthroplasty failure due to overuse, C-ring failure, and/or bushing wear. J. Shoulder Elbow Surg. 14:65, 2005. 68. Zuckerman, J. D., and Lubliner, J. A.: Arm, elbow and forearm injuries. In Zuckerman, J. D. (ed.): Orthopaedic Injuries in the Elderly. Baltimore, Urban & Schwarzenberg, 1990, p. 345.

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CHAPTER

58

Total Elbow Arthroplasty as a Salvage for the Fused Elbow

occur in more than 33% of patients (Fig. 58-2).11 The incidence of additional joint involvement in the ipsilateral and contralateral extremities was 77% and 46%, respectively, in our experience. In fact, in our experience, an isolated elbow fusion occurred in less than 10% of patients. Post-traumatic neuropathies are also common and may occur in as many as 40% of patients. As a matter of fact, two patients in our published series had previous Volkmann’s ischemic contracture. These complications mitigate the age factor when considering this procedure.

Bernard F. Morrey

CONTRAINDICATIONS INTRODUCTION The ankylosed elbow occurs spontaneously or after formal intent. In either instance, the functional outcome is usually not well tolerated. The reason for this is, first, there is no “optimum” position for elbow fusion. The joint is designed to position the hand in space and to one’s self. Second, the other joints compensate poorly for loss of elbow motion. Analysis of compensatory motion after an elbow arthrodesis has documented a compromised ability to complete activities, despite a significantly increased dependence on spine and wrist motion (Fig. 58-1).10 Furthermore, the shoulder plays only a modest role in compensation. For these reasons, there is continued value and interest in managing the stiff elbow by prosthetic replacement. The goal is to attain a functional arc of motion.7 Elbow fusion or fibrous ankylosis often is associated with severe osseous deformity and soft tissue contracture. Hence, this most challenging pathology is managed by prosthetic replacement. For this reason, patient selection and technique is of utmost importance.11

Considerations

INDICATIONS AND PATIENT SELECTION The primary goal of total elbow arthroplasty is to restore motion to improvement function. We prefer a patient older than 60 years of age if the pathology follows trauma.8 However, pathologic and functional considerations may prompt replacement at an earlier age, especially in those with inflammatory conditions. Of note is that the extent of comorbidities that tends to exist in these patients further complicates the execution of the procedure. Radioulnar, radiohumeral, or a combination of these synostoses, with complete loss of forearm rotation, may

Subacute sepsis is an absolute contraindication for conversion of a fused to a total elbow replacement. Chronic sepsis must be carefully assessed with a sedimentation rate and C-reactive protein studies. A staged procedure is performed if there is any question about active infection. Poor skin coverage is a relative contraindication that can be addressed by soft tissue procedures before the joint replacement (Fig. 58-3). Unwillingness to comply with the 5-kg single event, 1-kg repetitive weight restriction is a reason not to perform total elbow replacement. This implies those involved with heavy use of the extremity such as construction workers should not be offered this operation.

PREOPERATIVE ASSESSMENT The patient’s functional demands are carefully documented. The precise daily limitations and the impact to one’s daily existence is precisely determined. Presence and ability of the triceps to contract is noted. The examination also specifically evaluates the neurovascular status of the extremity. The quality of the skin is noted. The function of the contralateral elbow and the ipsilateral shoulder, hand, and wrist is documented. The flexibility of the cervical spine is assessed.

RADIOGRAPHIC EVALUATION Usually, plane films are adequate. Size and quality of the bone, and angular deformity is noted. We pay close attention to the presence of the olecranon and determine by physical examination if the triceps is attached. The size of the medullary canal and presence and relevance of fixation devices is considered (Fig. 58-4).

Chapter 58 Total Elbow Arthroplasty as a Salvage for the Fused Elbow

831

FIGURE 58-1

The shoulder functions as a ball and joint, whereas the elbow is a hinge allowing flexion and extension. The conal or circumferential motion of the shoulder does not compensate for the to-and-fro motion of the elbow.

A

B

FIGURE 58-3

Because of poor soft tissue in many patients, a preoperative soft tissue reconstruction is essential in order to avoid wound problems after the surgery.

SURGICAL TECHNIQUE

FIGURE 58-2

Loss of forearm rotation is common in patients with ankylosed elbows following spontaneous fusion from inflammatory conditions.

EXPECTATIONS Before surgery, the goals, limitations, and risks are very carefully explained to the patient. Expected outcomes are described based on our experience with approximately 20 cases.5,11 The high degree of osseous and soft tissue involvement adds a high level of complexity to the procedure. The operative time exceeds 2 hours and, in many instances, requires serial application and release of the tourniquet.

The skin incision is seriously considered because prior surgery is common. Ideally, we incorporate any prior incision. Alternatively, the greatest distance from a prior approach that can not be incorporated is sought. In all instances the ulnar nerve must be identified and protected. If ulnar nerve symptoms are present, the nerve is dissected distally to its motor branches, and placed in a protected subcutaneous environment. Ectopic osseous entrapment can impede decompression. If the ulnar nerve is not asymptomatic, it is identified proximally, and its course is defined. Protecting the nerve from the operative field obviates any further dissection. Management of the triceps muscle depends upon the integrity of the triceps attachment and status of the distal humerus. If the condyles are present, or if significant contracture of the extensor mechanism exists, then a triceps sparing approach is employed via a technique previously described.1 Note: The reattachment occurs with the elbow in 9 degrees of flexion. If the condyles are absent, or if the triceps remains adequately compliant, efforts are made to preserve the existing attachment. Contractures may be released by entering Kocher’s interval and mobilizing the anconeus along with the extensor mechanism. Medially, the flexor pronator mass is elevated to expose the fused joint site.

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Part VII Reconstructive Procedures of the Elbow

A

B FIGURE 58-4 A, Gross angular deformity is common. The presence of internal fixation devices increases the likelihood of infection. B, Ectopic bone is the most common postoperative problem that prevents maintenance of functional motion.

Determining the axis of rotation of the implant is a key technical consideration, and in most instances, the remnant of the radial head is used as the landmark laterally. Medially, the prominence of the coronoid is employed as the landmark. The osteotomy begins at this level and follows a curved trajectory emerging posteriorly at a level that ensures the triceps attachment is maintained. Meticulous care is taken to recreate or preserve an olecranon process, providing a functional lever arm for the triceps and protecting the skin from erosion by the implant. Note: Although all cases will have some loss of architecture to some degree, a custom device is usually not necessary. Preoperative planning will provide insight into appropriate sizing of the stem, which frequently demands modifications such as bending or cutting in order to account for canal deformity. In those instances when the ankylosis or fusion has resulted in malorientation of the forearm referable to the humerus, specific care is taken to release the soft tissue contracture of the flexors and extensors to avoid an imbalance at the articulation (Fig. 58-5). Likewise, accurate positioning of the ulnohumeral implant will avoid excessive wear that otherwise occurs with maloriented components. We have not found a need to perform tenotomy of the biceps or brachialis muscles. In some instances, shortening of the humerus may be required to enhance elbow extension. Two centimeters of shortening generally is adequate to decompress the soft tissue contracture

LCL extensors

MCL flexors

FIGURE 58-5

Aggressive release of the capsule as well as the flexor and pronator muscle mass is essential in order to both balance the elbow and to gain as much motion as possible. (With permission, Mayo Foundation.)

and tends to improve extension by 15 to 20 degrees. Given that these elbows are ankylosed, implications of cosmesis due to shortening are not relevant.

POSTOPERATIVE CARE The elbow is placed in an anterior splint and is elevated overnight. Physical therapists do not participate in the

Chapter 58 Total Elbow Arthroplasty as a Salvage for the Fused Elbow

rehabilitation process. A program of static adjustable splinting employs the Mayo Elbow Brace (AirCast DJO, Vista, CA). A permanent lifting restriction of 5 kg is emphasized, and formal strengthening exercises are discouraged. Prophylaxis for heterotopic ossification in the form of single-beam external radiation of 700 cGy is administered to patients with moderate to severe ectopic bone before surgery without postoperative wound complications or rheumatoid disease. Examination under anesthesia for perioperative elbow stiffness is a common adjuvant to our postoperative management.

RESULTS Small numbers of ankylosed elbows have been included in the reported results of several previous elbow studies. Similar to our experience, Figgie et al.11 reported a mean arc of motion of 80 degrees (35 to 115 degrees) that was maintained for an average of 5 years.2 A 26% complication rate was reported, which was also similar to our experience. The outcomes, particularly those based on our experience as described below, must be placed in the context of alternative procedures. The only viable one is distraction interposition arthroplasty.6 In our practice, the effectiveness of this procedure for patients with an arc of motion averaging approximately 30 degrees before surgery is approximately 80%.6 The complication rate is similar.

833

13 elbows. All were treated with a linked semiconstrained noncustom total elbow implant (CoonradMorrey, Zimmer, Warsaw, IN) (Fig. 58-6). The mean age at the time of the surgery was 54 years (range, 24 to 80 years). The stiffness was a consequence of trauma in 10, juvenile rheumatoid arthritis in one, and rheumatoid arthritis in two elbows. Patients were followed for a mean of more than 11 years, being evaluated clinically and radiographically. An average arc of 81 degrees from 37 degrees extension to 118 degrees of flexion was achieved. Objective outcomes were good or excellent in only seven of 13 elbows (55%) at final surveillance. Subjectively, 10 patients felt better or much better after surgery and would elect to undergo the procedure a second time. Complications required reoperation in more than half of patients. Two elbows developed wound healing problems requiring débridement. Implant revision was required in only one elbow owing to failure of the ulnar component. In spite of prophylactic measures undertaken to prevent heterotopic ossification that were not successful in this series, we could not be certain of the efficiency of this treatment. Only one patient required revision for implant failure due to progressive loosening of a polymethylmethacrylate precoat ulnar component with subsequent fatigue fracture at 5 years, 8 months postoperatively.4 Ectopic ossification was present to varying degrees in four elbows despite the administration of prophylactic external-beam radiation in three of the four.

COMPLICATIONS MAYO EXPERIENCE Initial evaluation of efforts to treat the stiff elbow by total elbow arthroplasty was reported by Mansat and Morrey in 2000.5 Fourteen elbows were evaluated a mean of more than 5 years after surgery. The mean preoperative arc averaged 7 degrees, and nine of the 14 elbows were fused. The other five had less than 30 degrees of motion. After the surgery, the mean arc of motion averaged 67 degrees. These authors emphasized the development of ectopic bone around the joint, which was observed to adversely affect outcomes. We also recorded seven complications in five of the 14 patients. These included superficial infection in three, and a deep infection in two. Overall, approximately 78% of patients indicated they were satisfied with the outcome.

RECENT EXPERIENCE We have recently updated our experience and reported on 13 consecutive patients with complete ankylosis in

The complication rate of total elbow replacement approaches 20% in most series.3,9,12 In our practice, three of the 13 elbows encountered a periprosthetic complication including soft tissue compromise in two and infection in another. One elbow developed skin necrosis requiring débridement and coverage with a myocutaneous latissimus flap. Another elbow required débridement and primary closure for superficial dermal lysis.

CONCLUSION Total elbow replacement as a salvage for a dysfunctional ankylosed elbow should be performed with caution. However, the outcome can be reliable and durable, having a dramatically positive impact on patient function and satisfaction. The high potential for complications, however, must be considered. We consider this an acceptable procedure in select patients with reasonable expectations. Use of a linked implant is essential. Custom devices are unnecessary.

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A

8 yr.

8 yr.

B

C

FIGURE 58-6

A, This patient with a devastating injury demonstrates angular deformity and a onebone forearm. B and C, Eight years after implantation without cement on the humeral side, the implant is well fixed. There is no wear. The arc of motion is 80 degrees.

References 1. Bryan, R. S., and Morrey, B. F.: Extensive posterior exposure of the elbow. A triceps-sparing approach. Clin. Orthop. Relat. Res. 166:188, 1982. 2. Figgie, M. P., Inglis, A. E., Mow, C. S., and Figgie, H. E. 3rd: Total elbow arthroplasty for complete ankylosis of the elbow. J. Bone Joint Surg. [Am.] 71-A:513, 1989. 3. Gschwend, N., Simmen, B. R., and Matejovsky, Z.: Late complications in elbow arthroplasty. J. Shoulder Elbow Surg. 5-2 (Pt 1):86, 1996. 4. Hildebrand, K. A., Patterson, S. D., Regan, W. D., MacDermid, J. C., and King, G. J.: Functional outcome of semiconstrained total elbow arthroplasty. J. Bone Joint Surg. [Am.] 82-A:379, 2000. 5. Mansat, P., and Morrey, B. F.: Semiconstrained total elbow arthroplasty for ankylosed and stiff elbows. J. Bone Joint Surg. [Am.] 82-A:1260, 2000. 6. Morrey, B. F.: Post-traumatic contracture of the elbow. Operative treatment, including distraction arthroplasty. J. Bone Joint Surg. [Am.] 72-A:601, 1990.

7. Morrey, B. F.: Functional evaluation of the elbow. In Morrey, B. F. (ed.): The Elbow and Its Disorders, 3rd ed. Philadelphia, WB Saunders, 2000, p. 74. 8. Morrey, B. F., Adams, R. A., and Bryan, R. S.: Total replacement for post-traumatic arthritis of the elbow. J. Bone Joint Surg. [Br.] 73-B:607, 1991. 9. Morrey, B. F., and Bryan, R. S.: Complications of total elbow arthroplasty. Clin. Orthop. Relat. Res. 170:204, 1982. 10. O’Neill, O. R., Morrey, B. F., Tanaka, S., and An, K. N.: Compensatory motion in the upper extremity after elbow arthrodesis. Clin. Orthop. Rel. Res. 281:89, 1992. 11. Peden, J. P., and Morrey, B. F.: Total elbow arthroplasty for the management of the ankylosed or fused elbow. J. Bone Joint Surg. [Br.] (in press). 12. Voloshin, I., Kakar, S., Kaye, E. K., and Morrey, B. F.: Complications of total elbow replacement: Systematic review of literature in the last decade. (in press).

Chapter 59 Total Elbow Arthroplasty for Distal Humerus Nonunion and Dysfunctional Instability

CHAPTER

59

Total Elbow Arthroplasty for Distal Humerus Nonunion and Dysfunctional Instability Joaquin Sanchez-Sotelo and Matthew L. Ramsey

INTRODUCTION Dysfunctional elbow instability may be defined as a condition in which the elbow joint has lost its fulcrum properties and is no longer able to provide enough support for the hand to be functionally controlled in space (Fig. 59-1).10 In the most extreme circumstances, destruction of the elbow leads to a flail extremity. In less severe cases, stability may be maintained with the arm adducted against the body, but not in other positions (Fig. 59-2). This condition may result from situations such as distal humerus nonunion, severe rheumatoid destruction of the humerus, extensive post-traumatic bone loss, and bone resection for the treatment of deep infection or tumors. Linked elbow arthroplasty provides a dramatic improvement in the function and quality of life of these patients, but the improvements need to be balanced against the risk of complications and mechanical failure. As noted above, distal humerus nonunion is one of the conditions commonly presenting as dysfunctional instability. Even in cases with less severe instability, elbow arthroplasty is a very attractive treatment alternative for the salvage of distal humerus nonunion. This chapter reviews the presentation, surgical technique, and outcomes of total elbow arthroplasty for distal humerus nonunion and dysfunctional elbow instability.

ELBOW ARTHROPLASTY FOR DISTAL HUMERUS NONUNION As noted in Chapter 23, nonunion is one of the most challenging complications of distal humerus fractures.

835

Internal fixation is the treatment of choice whenever possible. Modern series have reported a high union rate when internal fixation is used, but the reoperation rate has remained high and function is not always reestablished.6,11 Total elbow arthroplasty is an excellent surgical alternative for the salvage of distal humerus nonunions when fixation is considered to be impractical or expected to be associated with a high rate of failure. Elbow arthroplasty has emerged as a safe and effective treatment option for selected patients with distal humerus nonunion. Although some theoretical interest has been expressed in the use of distal humerus hemiarthroplasty for nonunions, the associated stiffness and bone loss make it less attractive compared to the acute setting. Most patients requiring arthroplasty for a distal humerus nonunion will benefit from the use of a total elbow arthroplasty. A linked implant is of choice in this situation, as the humeral attachments of the collateral ligaments are removed as part of the procedure.

RATIONALE, INDICATIONS AND CONTRAINDICATIONS Joint replacement is a well-accepted treatment modality for fractures in other locations, such as the femoral neck or the proximal humerus. The good track record of some elbow implants for patients with rheumatoid arthritis and other conditions prompted the use of elbow replacement for distal humerus nonunion.5 Elbow arthroplasty is indicated only in a selective group of elderly patients who present with either preexistent symptomatic pathology (for example, a rheumatoid elbow) or low nonunions with substantial osteopenia and severe damage to the articular surface. It is contraindicated in the presence of infection, as well as in nonunions amenable to stable internal fixation and in patients with anticipated high physical demands. An associated nonunion of an olecranon osteotomy complicates the surgical technique but should not be considered a contraindication for the procedure. When total elbow arthroplasty is used for the treatment of distal humerus nonunion, the procedure offers several advantages: the extensor mechanism may be left undisturbed, no postoperative protection is required, functional range of motion is relatively predictable, and pain and limited motion secondary to nonunion, malunion, or post-traumatic osteoarthritis are avoided. The main disadvantages are the risk of other implant-related complications and the need to limit upper extremity use to minimize polyethylene wear.

SURGICAL TECHNIQUE The elbow is exposed through a posterior midline skin incision and the ulnar nerve is identified and treated

836

Part VII Reconstructive Procedures of the Elbow

FIGURE 59-2

Patients with dysfunctional instability are unable to control the position of the arm in the space.

FIGURE 59-1

Severe destruction of the elbow joint may lead to loss of the articular fulcrum and dysfunctional instability.

according to the location of the nerve and preoperative symptoms as mentioned in Chapter 23 on internal fixation for distal humerus nonunions. The extensor mechanism is left undisturbed and the procedure is performed working on both sides of the triceps unless an associated olecranon nonunion, or triceps detachment provides the opportunity for exposure (Fig. 59-3) (see also Chapter 7, Surgical Exposures). Retained hardware is removed, and the nonunited distal humerus is resected subperiosteally and saved for bone grafting behind the flange of the humeral com-ponent. Tissue samples are sent for pathology and microbiology. The working space created by resection of the distal humerus is ample enough to instrument the canals and

implant the components. The surgical technique for implantation of a linked elbow arthroplasty is detailed in Chapter 52. A capsular release should be associated routinely. Use of a humeral component with an intermediate length stem provides secure fixation. In the presence of severe humeral bone loss, an implant with a longer flange may be cemented proud to make up for part of the lost humeral length (Fig. 59-4). On the contrary, a regular humeral component may be cemented in a deeper position to elevate the joint line and correct flexion contractures. Exposure of the ulnar canal may be improved by partial detachment of the triceps from the olecranon on the medial side. The implants may be fully seated before interlocking, because the articular windows at the medial and lateral side of the elbow after removal of the united distal humerus bone allow interlocking. At the end of the procedure, the common extensor and common flexor muscle groups are sutured to the lateral and medial triceps fascia to seal the joint space and maintain the strength of the forearm muscles.

POSTOPERATIVE MANAGEMENT After surgery, the elbow is placed in full extension in a bulky dressing with an anterior plaster splint and kept elevated to minimize swelling. Active-assisted range of motion may be initiated on postoperative day one or two. Once the surgical wound is healed, no additional

A

B

C

D

FIGURE 59-3

Linked elbow arthroplasty may be performed in patients with distal humerus nonunion working on both sides of the triceps. A, Fragment resection from the medial side. B, Humeral rasping leaving the triceps attached. C, Ulnar preparation with the triceps on. D, Implanted components. E and F, Postoperative radiographs showing adequate component positioning and resected medial and lateral condyles.

F

E

838

Part VII Reconstructive Procedures of the Elbow

FIGURE 59-4

An extended flange provides flexibility for depth of insertion of the humeral component and allows reconstruction with a non-custom implant in the presence of severe bone deficiency.

protection is needed, because the implants are fixed with cement and the extensor mechanism is left completely undisturbed. Usually, patients regain functional elbow motion within the first 3 months after surgery.

OUTCOME Total elbow arthroplasty has been shown in several studies to provide satisfactory results in a large proportion of well-selected patients. Figgie et al4 reported on 14 patients who received an elbow arthroplasty for the treatment of a distal humerus nonunion. Their mean age was 65 years, and 10 of the 14 patients had previous surgery. At a mean follow-up of 5 years, the mean elbow score improved from 17 to 84 points and there were three failures secondary to dislocation, deep infection, and humeral component loosening. Morrey and Adams9 reported on 36 consecutive patients with an average age of 68 years who underwent total elbow arthroplasty for a distal humerus nonunion. At an average follow-up of 4 years, results were satisfactory in 86% of the patients. There was no or mild pain in 91% and motion was improved in most patients. Complications included deep infection in two cases, polyethylene wear or particulate synovitis requiring surgery in three cases, and transient ulnar neuropathy in two cases.

The Mayo Clinic experience with total elbow arthroplasty for distal humerus nonunions has been updated recently.3 Ninety-two consecutive total elbow arthroplasties performed for the treatment of a distal humeral nonunion were reviewed at an average follow-up of 6.5 years (range, 0.5 to 20.3 years). There were 22 men and 69 women with an average age of 65 years at the time of elbow replacement. Seventy-six elbows (83%) had undergone prior surgery, with an average of two previous operations (range, one to 10). Five elbows had had at least one prior operation due to infection. Before surgery, 86% of the patients complained of moderate or severe pain. At most recent follow-up, 79% of the patients had no pain or mild pain. Mean extension was improved from 37 to 22 degrees and average flexion from 106 to 135 degrees. Joint stability was restored in all patients, including nine with a grossly flail elbow (Fig. 59-5). Complications included aseptic loosening in 16 (four with periprosthetic fractures), component fracture in five, deep infection in five (three with previous infection), and bushing wear in one patient. At most recent follow-up, 85% of the patients were satisfied with their outcome. Survivorship free or removal or revision for any reason was 95.7% at 2 years, 82.1% at 5 years, 65.3% at 10 and 15 years. The risk of implant failure was increased in patients younger than 65 years old, with two or more prior surgeries, and a history of previous infection. Some concerns have been raised about the effect of humeral condyle resection on elbow and forearm strength. However, McKee et al8 reported on 32 patients who had undergone total elbow arthroplasty with preservation (16 cases) or resection (16 cases) of the humeral condyles. There were no statistically significant differences in elbow flexion and extension, forearm pronation and supination, or grip strength. Both groups also had similar overall results according to the Mayo elbow performance score. In summary, total elbow arthroplasty provides satisfactory pain relief and large improvements in elbow stability and function when performed for the salvage of distal humerus nonunion. Our preference is to resect the ununited fragments in order to preserve the extensor mechanism intact and replace the elbow joint with a linked implant. Condylar resection does not seem to affect pain, strength or function with the design used by the authors. However, when arthroplasty is indicated in this condition, the potential for complications and implant failure in the long-term should be recognized.

ELBOW ARTHROPLASTY FOR DYSFUNCTIONAL INSTABILITY Patients with dysfunctional instability may be offered several treatment options. Some patients with multiple

Chapter 59 Total Elbow Arthroplasty for Distal Humerus Nonunion and Dysfunctional Instability

839

FIGURE 59-5

A, Radiographs of a patient with distal humerus nonunion and dysfunctional instability. B, Linked elbow arthroplasty provided a successful clinical outcome for 16 years.

previous surgeries may choose to use a hinged brace and avoid additional procedures. However, most patients are dissatisfied with their use of the arm and wish to explore reconstructive surgery. Surgical options include internal fixation with bone grafting for some distal humerus nonunions, elbow arthrodesis, osteoarticular allografts, or elbow arthroplasty. The advantages and disadvantages of internal fixation for distal humerus nonunions have been discussed in Chapter 23; as noted earlier, elbow arthroplasty represents a better option for the salvage of selected nonunions. Elbow arthrodesis will restore stability; however, a solid fusion may be difficult to achieve in the presence of massive bone loss, and most patients find lack of elbow motion very limiting. Osteoarticular allografts are attractive for the younger patient, but they have been associated with a high rate of complications and graft resorption. Elbow arthroplasty is our treatment of choice for many patients with dysfunctional instability. The primary indication for elbow arthroplasty in this group of patients is instability that prevents useful function of the arm secondary to inability to position the hand in the space (see Figs. 59-1 and 59-2).1,10 Interestingly, many of these patients do not complain of severe pain. Ideally, elbow arthroplasty should be restricted to older patients with low functional demands. However, arthroplasty may be considered for the younger patient with severe bone loss, severe dysfunction, and no other treatment alternatives.

TOTAL ELBOW ARTHROPLASTY IN DYSFUNCTIONAL INSTABILITY: TECHNICAL TIPS Many of the technical tips described in the section on elbow arthroplasty for distal humerus nonunion apply to any patient with dysfunctional instability. The challenges of replacement arthroplasty in this category of patients may include dealing with bone loss on either side of the joint, achieving a functional range of motion in the face of soft tissue contractures secondary to prolonged shortening, and balancing the joint medially and laterally to avoid eccentric loads of the polyethylene that could accelerate wear. Humeral bone loss in dysfunctional instability can usually be corrected by modifying the depth of insertion of the humeral component, using components with a longer anterior flange in selected cases, and the occasional use of strut grafts (see Fig. 59-4). Most patients with long-standing instability present with shortening of the limb in combination with humeral bone loss. Deeper insertion of the component compensates for the distal bone loss and, at the same time, facilitates achieving more complete elbow extension. Ulnar bone loss can be managed usually by deeper insertion of the ulnar component and the occasional use of strut grafts to reconstruct the olecranon and provide an insertion point and lever arm for the extensor mechanism. In patients with severe shortening, care should be taken to avoid excessive soft-tissue bulk anteriorly in elbow

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Part VII Reconstructive Procedures of the Elbow

FIGURE 59-6

A, Anteroposterior radiograph of a patient with dysfunctional instability and lateralsided soft-tissue contracture. B, Persistent soft tissue imbalance is appreciated as asymmetric seating of the ulna on the humeral yoke. C, This patient developed severe polyethylene wear during the first postoperative years.

Chapter 59 Total Elbow Arthroplasty for Distal Humerus Nonunion and Dysfunctional Instability

flexion, as this is suspected to facilitate loosening of the ulnar component.2 Adequate balance of the medial and lateral soft tissue structures is necessary to avoid eccentric polyethylene loading. In patients with long-standing dysfunctional instability, the forearm tends to be displaced proximally and to the medial or lateral side of the humerus. When the elbow is realigned and brought to length, the soft tissues on the contracted side may deform the elbow and prevent centralized tracking of the prosthesis. In these circumstances, polyethylene edge-loading may lead to accelerated polyethylene wear (Fig. 59-6).7 Adequate soft tissue releases should be performed whenever possible to achieve a balanced reconstruction. Often, patients with dysfunctional instability have undergone multiple previous surgeries. Infection should always be investigated before surgery; when infection is suspected to be present, consideration should be given to staged surgery combining a surgical débridement, followed by component implantation once all surgical cultures are read as negative. Attention should be paid to the location of the ulnar nerve and the condition of the skin; when the skin is severely scarred to the soft tissues, wound healing may be compromised, and a consultation with a plastic surgeon to explore wound coverage options is highly recommended before the procedure.

841

SUMMARY Total elbow arthroplasty has emerged as a very successful treatment option for patients presenting with dysfunctional instability as their main complaint. This condition may be seen in patients with distal humerus nonunion, severe rheumatoid arthritis, post-traumatic bone loss, and resection for deep infection. Linked elbow arthroplasty improves stability and function in patients with dysfunctional instability. In patients with severe bone loss, the arthroplasty may be performed working on both sides of the triceps. Many of these patients present after one or more previous surgeries; attention should be paid to the location of the ulnar nerve, the quality of the soft tissue envelope, and the possibility of an associated deep infection. Adequate soft tissue balance should be achieved in order to prevent polyethylene edge loading and accelerated wear. Elbow arthroplasty has been shown to provide excellent results for distal humerus nonunion and dysfunctional instability, but this procedure is associated with a modest rate of complications and mechanical failure, partly related to the age and activity of the patients and partly related to the challenge of reconstructive elbow surgery in patients with long-standing soft-tissue imbalance and bone loss.

OUTCOME OF ELBOW ARTHROPLASTY IN DYSFUNCTIONAL INSTABILITY Ramsey et al10 reported the results of elbow arthroplasty for dysfunctional instability at our institution. Nineteen total elbow arthroplasties performed for the treatment of elbow instability were reviewed at a mean follow-up of 6 years. The underlying pathology responsible for dysfunctional instability included an unstable distal humerus nonunion in 14 patients, severe rheumatoid arthritis in three patients, post-traumatic bone loss in one patient, and bone loss after resection of infected distal humerus in one patient. The main indication for surgery was instability, and pain was not the primary indication for any of the arthroplasties. At most recent follow-up, 12 patients had no pain, four had mild pain, and three had moderate pain. Before surgery, all patients had a functionally useless range of motion; at most recent follow-up, the mean arc of motion was from 25 degrees of extension to 128 degrees of flexion. The overall results were graded as satisfactory in 86% of the elbows according to the Mayo Elbow Performance Score. Complications included one intraoperative fracture of the olecranon, two ulnar component fractures, and one case of humeral loosening. There was no evidence of loosening or severe polyethylene wear in the remaining cases.

References 1. Baksi, D. P.: Sloppy hinge prosthetic elbow replacement for post-traumatic ankylosis or instability. J. Bone Joint Surg. Br. 80:614, 1998. 2. Cheung, E. V., and O’Driscoll, S. W.: Total elbow prosthesis loosening caused by ulnar component pistoning. J. Bone Joint Surg. Am. 89:1269, 2007. 3. Cil, A., Veillette, C., Sanchez-Sotelo, J., and Morrey, B. F.: Linked elbow replacement: a salvage procedure for distal humeral nonunion. International Congress on Surgery of the Shoulder (ICSS). Brazil, 2007. 4. Figgie, M. P., Inglis, A. E., Mow, C. S., and Figgie, H. E. 3rd: Salvage of non-union of supracondylar fracture of the humerus by total elbow arthroplasty. J. Bone Joint Surg. Am. 71:1058, 1989. 5. Gill, D. R., and Morrey, B. F.: The Coonrad-Morrey total elbow arthroplasty in patients who have rheumatoid arthritis. A ten to fifteen-year follow-up study. J. Bone Joint Surg. Am. 80:1327, 1998. 6. Helfet, D. L., Kloen, P., Anand, N., and Rosen, H. S.: Open reduction and internal fixation of delayed unions and nonunions of fractures of the distal part of the humerus. J. Bone Joint Surg. Am. 85-A:33, 2003. 7. Lee, B. P., Adams, R. A., and Morrey, B. F.: Polyethylene wear after total elbow arthroplasty. J. Bone Joint Surg. Am. 87:1080, 2005.

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Part VII Reconstructive Procedures of the Elbow

8. McKee, M. D., Pugh, D. M., Richards, R. R., Pedersen, E., Jones, C., and Schemitsch, E. H.: Effect of humeral condylar resection on strength and functional outcome after semiconstrained total elbow arthroplasty. J. Bone Joint Surg. Am. 85-A:802, 2003. 9. Morrey, B. F., and Adams, R. A.: Semiconstrained elbow replacement for distal humeral nonunion. J. Bone Joint Surg. Br. 77(1):67-72, 1995.

10. Ramsey, M. L., Adams, R. A., and Morrey, B. F.: Instability of the elbow treated with semiconstrained total elbow arthroplasty. J. Bone Joint Surg. Am. 81:38, 1999. 11. Ring, D., Gulotta, L., and Jupiter, J. B.: Unstable nonunions of the distal part of the humerus. J. Bone Joint Surg. Am. 85-A:1040, 2003.

Chapter 60 Total Elbow Arthroplasty for Primary Osteoarthritis

CHAPTER

60

Total Elbow Arthroplasty for Primary Osteoarthritis Tomasz K. W. Kozak, Robert A. Adams, and Bernard F. Morrey

INTRODUCTION As discussed in Chapter 76, primary osteoarthritis of the elbow is an uncommon lesion that affects fewer than 2% of the population.18 In recent years, an increased incidence or increased recognition, or both, resulted in a greater experience that has offered an opportunity for a more discrete treatment plan based on the specific features of the presentation. These consist both of subjective reports and objective findings. Based on the features of the presentation, three discrete surgical options have emerged: loose body removal, débridement, and joint replacement. All can be appropriate depending on patient symptoms, expectations and surgeon expertise.2,8 The primary report may be catching from a loose body, loss of extension, or pain on terminal extension from osteolysis and capsular contracture, or ulnar nerve symptoms tend to occur later in the process. The radiographic features are motonous and generally correlate reasonably well with the patient’s symptoms. The primary pathology includes maintenance of joint space in the presence of osteophyte formation in the olecranon, olecranon fossa, coronoid, and coronoid fossa.9,11 Secondary changes include osteophytes at the margin of the radial head and loose bodies. Occasionally the radiohumeral joint is selectively involved. As implied, all of these characteristics are readily discerned by the plane radiograph. Computed tomography (CT) or magnetic resonance imaging (MRI) scans are not needed or indicated to diagnose or treat this patient. Selecting the appropriate procedure depends on the clinical and radiographic presentation (Table 60-1). In the early stages, most patients have mild pain and are treated by nonoperative means,13 such as with anti-inflammatory medication and activity modification. Occasionally, removal of loose bodies or débridement with removal

843

of prominent osteophytes is necessary. This can be achieved by arthrotomy or today, most commonly, by arthroscopy. Formal and more aggressive open débridement procedures are employed for extensive involvement, especially with ulnar nerve symptoms. Total elbow arthroplasty is considered an option only after débridement and loose body excision has failed3 or is not appropriate and for older patients. However, some surgeons believe that replacement rarely, if ever, is indicated for advanced primary osteoarthritis of the elbow,19 particularly if using unlinked implants.4,6,7 Still, there are no published reports or detailed clinical data to substantiate any of these positions. Readers may be surprised to learn that, until 1998, there was no information in the literature documenting either technical difficulties or the functional outcome of total joint replacement for primary arthritis of the elbow.10 Since the report in 1998, only a single additional report of a small series of replacements for degenerative disease has appeared.5 For this reason, we are reassessing our experience.

INDICATIONS Total elbow arthroplasty is rarely indicated for primary osteoarthritis of the elbow, because it typically affects relatively young, active men. For them, several effective options are available to address the various elements of the complaint: locking, stiffness, and impingement pain (see Table 60-1).14 The specific but relative indications for joint replacement for primary arthritis include age older than 65, if possible, and a patient who does not need or expect to make extensive use of the extremity. The other options noted earlier must have failed or have been deemed inappropriate for the lesion. Most important, patients who have pain throughout the arc of motion, especially in the functional range, are the best candidates for joint replacement. Radiographs often show extensive heterotopic changes about the elbow joint (Fig. 60-1). High-grade stiffness in older patients is also a potential setting for joint replacement. The limited arc and hypertrophic changes pose technical challenges to successful replacement.

TECHNICAL CONSIDERATIONS The technical concerns are derived from the foregoing discussion: 1. Olecranon osteotomy must be avoided. We continue to employ the Bryan-Morrey triceps reflection exposure. 2. Joint stiffness makes the exposure more difficult. Capsular or contracture and extensive osteophyte

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Part VII Reconstructive Procedures of the Elbow

TABLE 60-1

Treatment Options Based on Presenting Symptoms and Radiographic Features

Presentation

Clinical

Radiographic

Procedure

1. Extension loss, mild pain

Small olecranon spur

None—activity; medication

2. As for 1, limits activity

Larger olecranon/coronoid spurs

Column, arthroscopic débridement

3. Locks, catches

Loose body

Arthroscopic removal

4. Pain with flexion/extension, motion restricted

Osteophyte: foramina, coronoid/olecranon

Column, arthroscopy, ulnohumeral arthroplasty

5. As for 1-4, with ulnar nerve symptoms

As above

Ulnohumeral arthroplasty, nerve decompression

6. Pain arc, high-grade motion loss

Extensive osteophytic changes, joint narrowing, capsular contracture

Age <65, interposition arthroplasty; age >65, semiconstrained total elbow arthroplasty

7. Symptoms localized to radial/ humeral joint

Radiohumeral arthritis

Radial head replacement, possible capitellar replacement.

FIGURE 60-1

Preoperative anteroposterior (A) and lateral (B) radiographs of primary osteoarthritis show ossification and osteophyte formation in the olecranon fossa and osteophytes on the coronoid and olecranon processes.

formation sometimes make exposure of the joint more challenging. Release of the collateral ligaments is required. 3. The ulnar nerve must be decompressed and translated. 4. The periarticular bone is usually very hard, and cutting it requires a saw rather than a rongeur. Spurs are removed with a rongeur or saw. A burr and a rasp are usually necessary to prepare the medullary canal.

5. Developing heterotopic ossification is possible owing to the hypertrophic response that is characteristic of the process. Furthermore, the procedure may create considerable debris. Both features predispose to the formation of ectopic bone. 6. If aggressive release of the soft tissues is necessary, stability from an unlinked device is a problem; hence, we favor linked devices for pathology. 7. Postoperatively, patients may have considerable swelling, because of the extensive soft tissue dissec-

Chapter 60 Total Elbow Arthroplasty for Primary Osteoarthritis

845

FIGURE 60-2

5 years

A

B

This 68-year-old man had marked motion loss, including pronation and supination of 50 and 20 degrees, respectively (A). The radial head was resected to improve forearm rotation (B).

tion. If swelling is not controlled, motion and healing will both be compromised (Fig. 60-2).

TECHNIQUE: COONRAD-MORREY SEMICONSTRAINED DEVICE

Olecranon spur

The surgical technique is basically that described in Chapters 53 and 57. Several specific features of the “degenerative elbow” are considered. 1. The incision is a straight posterior one that affords medial and lateral exposure. Exposing and decompressing the ulnar nerve as an essential first step. 2. Triceps reflection is difficult if extension is less than 70 degrees. The medial most insertion may have poor continuity with the distal fascia or periosteum. If a significant defect is present, the surgeon must be prepared to mobilize the anconeus to better center the extensor mechanism at closure (see Chapter 63). 3. With contractures greater than 60 to 70 degrees, release of the common flexors with the medial ligament at the humerus and of the common extensor insertion with the lateral ligament is carried out (Fig. 60-3) (see Chapter 58). 4. The elbow is flexed and the anterior capsule excised. 5. To gain extension, the humeral component may need to be seated up to 5 mm farther proximal than usual

Contracted capsule

FIGURE 60-3

Coronoid spur

The surgical technique requires extensive removal of the ulnar osteophytes and release of the collateral ligament and the origins of the flexors and extensors. The anterior capsule is also released.

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Part VII Reconstructive Procedures of the Elbow

to help release the anterior soft tissue envelope in extension. The coronoid prominence is removed. 6. The tourniquet is released and meticulous hemostasis effected. 7. The triceps insertion must be firmly secured. Flexion and extension of the joint is helpful to determine the optimal position for trying the sutures.

result (Fig. 60-4), and results in all three of those with the linked device were graded satisfactory. In the experience of Espag et al,5 a Souter-Strathclyde unlinked device was used in six men and four women with a mean age of 66 (range 56 to 79 years). At a mean of 68 months after surgery, one had loosened and was revised. Two additional patients had radiographic evidence of loosening, but nine of 10 were satisfied with the procedure.

AFTERCARE The arm is elevated in extension with a Cryocuff for compressive cryotherapy for the first 24 hours. If flexion or extension is a problem, splints are used, as described in Chapter 11, and postoperatively, motion is encouraged as tolerated and according to swelling and pain. The patient is usually discharged on day 3.

RESULTS Little has been published on joint replacement for osteoarthritis. Our limited experience with a series of five cases has been reported.10 The mean age of the four men and one woman was 68 years (range 61 to 72 years) with surveillance averaging over 5 years. The mean postoperative arc was 85 degrees (37 to 122 degrees), less than that reported for other diagnoses but better by an average of 20 degrees than the mean 65 degrees (40to 105-degree) arc preoperatively. One of two patients treated with an unlinked device had an unsatisfactory

FIGURE 60-4

COMPLICATIONS Complications are frequent. In our series, there were four major and two minor complications in four elbows, including fracture of the humeral component with particulate synovitis, implant subluxation, heterotopic ossification, and ulnar neuropathy (Fig. 60-5). Patients with primary degenerative arthritis of the elbow tend to be active, and most are involved in manual occupations that place greater demands on the prosthesis. One patient returned to his former occupation of carpentry, heavy lifting, and stonework. The humeral component fractured from overuse (Fig. 60-6). Two of the patients had transient postoperative ulnar neuropathy with altered sensation; both cases resolved spontaneously. Ulnar nerve irritation is associated with the development of primary osteoarthritis of the elbow joint. Two of these elbows required revision of one of the components. In Espag’s report in addition to one revi-

Before (A) and 5 years after (B) unlinked implant for primary osteoarthritis of the elbow.

Chapter 60 Total Elbow Arthroplasty for Primary Osteoarthritis

847

FIGURE 60-5

A, Preoperative lateral radiograph shows marked hypertrophic osteophyte formation as a feature of the degenerative process. B, At 41-month follow-up evaluation, a lateral radiograph shows heterotopic ossification anteriorly and posteriorly. There is marked involvement in the triceps tendon insertion, but the Mayo Elbow Performance Score is 95.

(9%),15 post-traumatic arthritis (18%),17 nonunion of the distal humerus (13%),16 and even revision total arthroplasty (17%). The problems encountered, however, are consistent with the relatively high level of activity typical of persons with this diagnosis.

SUMMARY Primary joint replacement is not usually indicated for osteoarthritis; yet, if the patient is older than 65 years and has aching discomfort most of the time, through the entire arc, and at night that also is worse during use, replacement may be considered. Careful attention to technique and limited postoperative use, however, must be emphasized.

FIGURE 60-6

At 10 years after total elbow arthroplasty, the lateral radiograph shows transverse fracture of the humeral component with surrounding lysis of the bone in a patient who continuously engaged in heavy work against medical advice during those 10 years.

sion, two radiographic loose implants, two were documented with ulnar neuropathies and two surgical infections requiring antibiotics. This is a higher rate than that reported at our institution during the same period for total elbow arthroplasty for rheumatoid arthritis

References 1. Bryan, R. S., and Morrey, B. F.: Extensive posterior exposure of the elbow. A triceps-sparing approach. Clin. Orthop. Relat. Res. 166:188, 1982. 2. Cheung, E. V., Adams, R. A., and Morrey, B. F.: Primary osteoarthritis of the elbow: Current treatment options. J. Am. Acad. Orthop. Surg. 16:77, 2007. 3. Coonrad, R. W.: Comments on the historical milestones in the development of elbow arthroplasty: indications and complications. Instruct. Course Lect. 40:51, 1991.

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Part VII Reconstructive Procedures of the Elbow

4. Dennis, D. A., Clayton, M. L., Ferlic, D. C., Stringer, E. A., and Bramlett, K. W.: Capitello-condylar total elbow arthroplasty for rheumatoid arthritis. J. Arthroplasty 5(suppl):S83, 1990. 5. Espag, M. P., Back, D. L., Clark, D. I., and Lunn, P. G.: Early results of the Souter-Strathclyde unlinked total elbow arthroplasty in patients with osteoarthritis. J. Bone Joint Surg. 85B:351, 2003. 6. Ewald, F. C., Scheinberg, R. D., Poss, R., Thomas, W. H., Scott, R. D., and Sledge, C. B.: Capitellocondylar total elbow arthroplasty. J. Bone Joint Surg. 62A:1259, 1980. 7. Goldberg, V. M., Figgie, H. E., III., Inglis, A. E., and Figgie, M. P.: Total elbow arthroplasty, current concepts review. J. Bone Joint Surg. 70A:778, 1988. 8. Grandstad, G. D., and Galatz, L. M.: Management of elbow osteoarthritis. J. Bone Joint Surg. 88A:421, 2006. 9. Kashiwagi, D.: Intraarticular changes of the osteoarthritic elbow, especially about the fossa olecrani. J. Jpn. Orthop. Assn. 52:1367, 1978. 10. Kozak, T. K. W., Adams, R. A., and Morrey, B. F.: Total elbow arthroplasty in primary osteoarthritis of the elbow. J. Arthroplasty 13:837, 1998. 11. Minami, M., Kato, S., and Kashiwagi, D.: OuterbridgeKashiwagi’s method for arthroplasty of osteoarthritis of

12.

13. 14.

15.

16.

17.

18. 19.

the elbow. 44 elbows followed for 8-16 years. J. Orthop. Sci. 1:11, 1996. Morrey, B. F.: The future of elbow joint replacement. In Morrey, B. F. (ed.): Joint Replacement Arthroplasty. New York, Churchill Livingstone, 1991, p. 375. Morrey, B. F.: Primary degenerative arthritis of the elbow. J. Bone Joint Surg. 74B:409, 1992. Morrey, B. F.: Degenerative arthritis of the elbow. In Morrey, B. F. (ed.): Reconstructive Surgery of the Joints, 2nd ed. New York, Churchill Livingstone, 1996, p. 669. Morrey, B. F., and Adams, R. A.: Semiconstrained arthroplasty for the treatment of rheumatoid arthritis of the elbow. J. Bone Joint Surg. 74A:479, 1992. Morrey, B. F., and Adams, R. A.: Semiconstrained elbow replacement arthroplasty for distal humeral nonunion. J. Bone Joint Surg. 77B:67, 1995. Morrey, B. F., Adams, R. A., and Bryan, R. S.: Total replacement for post-traumatic arthritis of the elbow. J. Bone Joint Surg. 73B:607, 1991. Stanley, D.: Prevalence and etiology of symptomatic elbow osteoarthritis. J. Shoulder Elbow Surg. 3:386, 1994. Tsuge, K., and Mizuseki, T.: Debridement arthroplasty for advanced primary osteoarthritis of the elbow. J. Bone Joint Surg. 76B:641, 1994.

Chapter 61 Complications of Elbow Replacement Arthroplasty

CHAPTER

61

Complications of Elbow Replacement Arthroplasty Bernard F. Morrey and Ilya Voloshin

INTRODUCTION Complications after total elbow arthroplasty (TEA) have been widely publicized and are well recognized. An explanation for the high incidence of complications rests on the fact that the elbow is a complex joint that is poorly covered by soft tissue, is intimately transversed by a major nerve, and is vulnerable to hostcompromising conditions, such as rheumatoid arthritis and previously operated-on post-traumatic arthritis. The majority of these complications neither require surgery nor adversely influence the ultimate result. Thus, these problems might best be discussed according to their management and significance: (1) those that increase the morbidity but do not influence the outcome by requiring additional surgery, removal, or replacement of the implant; and (2) those requiring additional surgery, including revision of the implant. Gschwend and colleagues,21 in their systematic review of the world’s literature from 1986 to 1992, discussed 828 procedures. Of these, 43% had complications (Table 61-1). In the intervening years, there have been many advances in prosthetic design and surgical technique. For example, constrained devices have been eliminated owing to their high rate of loosening. Semiconstrained and unconstrained devices are being used now, and recently, hybrid designs that are unlinked but can be converted to a linked design have been developed. Variations in techniques such as triceps tendon dissection and repair, better cementation techniques, routine antibiotic prophylaxis, and others have emerged. Despite advances in prosthetic design and surgical technique over the past decade, there had been no systematic review of the literature on the complications of TEA since the 1996 report by Gschwend et al.21 We recently conducted a comprehensive review of the literature to determine the complications associated with modernday TEA.56 The review comprised 38 studies that reported on 1981 total elbow replacements. The overall significant complication rate (requiring another surgical procedure or resulting in permanent clinical sequalae) after primary

849

TEA was 27.9% ± 13.3%. The main complications included 4.8% clinical loosening (including symptomatic loosening or revision), 3.8% instability including dislocation and symptomatic subluxation, 2.5% deep infection, and 2.5% ulnar nerve complications56 (Table 61-2). In this edition, the treatment of infection is discussed in detail in Chapter 62, and loosening and periprosthetic fractures are dealt with in the chapters on revision (see Chapters 65 and 66). A detailed summary of the current literature regarding complications is given in Table 61-2.

COMPLICATIONS NOT USUALLY REQUIRING SURGERY MOTION RESTRICTION The goal of elbow replacement surgery is to obtain the functional arc of 30 to 130 degrees of flexion.39 Those rheumatoid arthritic patients who have the ankylosing type of disease tend not to obtain the typical 30 to 130 degrees of flexion-extension after surgery.7 Therefore, we attempt to treat this motion restriction with an aggressive capsular resection at the time of the implantation. If the anterior capsule is contracted, sufficient depth of insertion is most important. A trial reduction is essential to identify this potential problem so that it can be avoided. Often, a static adjustable splint is used to gain or maintain motion. Furthermore, a slight but consistently greater flexion contracture is observed with resurfacing designs (see Chapter 52).

WOUNDS Wounds are much less a problem today19 than the 5% incidence previously reported.9,13,23,34,46 Management Wound healing problems are best avoided. At the Mayo Clinic, we avoid the use of the steri-drape after skin preparation with iodinated solutions, especially in patients with rheumatoid arthritis. I also use a straight incision just medial to the tip of the olecranon and carefully cauterize vessels during surgery. The elbow is placed in full extension with a compression/cryotherapy (Cryocuff Aircast, DJO, Vista, CA) device, which is now used routinely.1 If the wound remains tenuous at 1 week or 10 days, we do not hesitate to place the patient in a cast or anterior splint for 10 to 14 days and then reassess.33 If severe wound necrosis occurs, surgical treatment may involve special soft tissue coverage, which is discussed in Chapter 36.

NEURITIS In patients with rheumatoid arthritis or in a joint that has been subjected to previous surgery, the ulnar nerve

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Part VII Reconstructive Procedures of the Elbow

TABLE 61-1

Complications of Elbow Replacement,

1986-1992 Complication

Incidence (%)*

Aseptic loosening Radiologic Clinical

17.2 6.4

Infections

8.1

Ulnar nerve lesions

10.4

Instability

7-19

Disassembly

—

Dislocation

4.3

Subluxation

2.2-6.5

Intraoperative fractures

3.2

Fractures of prosthesis

0.6

Ectopic bone formation

—

*Total number of cases = 828.

TABLE 61-2

Complications of Elbow Replacement,

1993-200456 Complication

Incidence (%)

Aseptic loosening (clinical) 4.81 Aseptic loosening (clinical and radiographic) Linked Designs 15.92 Unlinked Designs 18.53 Infections

2.51 1

Ulnar nerve lesions

2.5

Disassembly

4.21

Dislocation/Subluxation

3.81

Intraoperative fractures

1.81

Fractures of prosthesis

1.11

Ectopic bone formation

—

Total number of cases = 1981. Total number of cases = 282. 3 Total number of cases = 637.

of approximately 10% after almost 900 procedures.21 We have found 3% subjective symptoms after 700 procedures at the Mayo Clinic. No patient had motor weakness. In our review of literature in the last decade, the rate of ulnar neuropathy was found to be 2.5%.56 In light of the association between TEA and ulnar neuropathy, controversy persists regarding the need for routine ulnar nerve transposition during surgery. Some of the cited advantages of routine nerve transposition include protection of the nerve in a safe location during the exposure and elbow manipulation, decreasing the stretching forces on the nerve with elbow motion postoperatively, and reducing the compression on the nerve in the cubital tunnel. Some of the disadvantages include injury to the blood supply to the nerve and mechanical injury during the dissection. In our meta-analysis,56 the rates of significant ulnar neuropathy were compared between the studies that routinely transposed and the ones that selectively transposed the nerve. The results showed that routine ulnar nerve transposition resulted in lower rates of significant ulnar neuropathy (2.1% ± 3.5%) compared with the studies in which the nerve was not mobilized routinely (4.3% ± 5.2%) (P = 0.17). Even though this difference was not statistically significant, it is believed to be clinically significant. The overall rate of significant ulnar neuropathy was only 2.5%, making it very difficult to detect a statistically significant difference between routine and nonroutine ulnar nerve transposition. Management If profound motor weakness is present immediately after surgery and uncertainty about the neural status exists, the nerve should be explored. We have not yet had to do this. Our technique translocates the nerve; thus, little might be gained by another procedure. Sensory defects, especially if they are incomplete, usually resolve spontaneously, and therefore, reexploration is not warranted.

1 2

TRICEPS INSUFFICIENCY

is particularly vulnerable. The incidence of ulnar nerve involvement has been reported in 2%3 to 26%13,54 of patients and varies in severity from profound neuropathy in less than 5%9,31,49,52 to transient paresthesias in as many as 25%.21 Implicated causes are excessive traction, perineural or epineural hematoma, direct mechanical pressure during the procedure, and irritation by the bandage or from swelling. The possibility of thermal damage from juxtaposed methylmethacrylate may be considered, as well as devitalization during the translocation procedure. Gschwend’s review of the experience in the literature from 1986 to 1992 reveals an incidence

Triceps insufficiency is probably common, but it is not reported very often. The poor quality of the triceps tendon in patients with rheumatoid arthritis is well recognized, but only about 4% of patients with rheumatoid arthritis have been recognized as having significant triceps insufficiency.35,38 The Mayo approach and its modification57 was developed because of this problem.5 We have documented 13 of 700 (2%) since 1981. In our literature review of the last decade,56 triceps-related complications were analyzed after the three most common triceps dissection techniques. No triceps-related complications were found with the V-shaped tongue approach at the musculotendinous junction. Triceps reflection, with or without extra-articular wafers of olec-

Chapter 61 Complications of Elbow Replacement Arthroplasty

851

ranon, was associated with a complication rate of 2.3% ± 4.6%, whereas the triceps split, either with or without extra-articular wafers of olecranon, was associated with a 6.2% ± 14.8% complication rate. The difference in complication rates between the three approaches was not statistically significant.56 Treatment Triceps weakness is expected after any exposure that violates the extensor mechanism.38 Today, most exposures reflect rather than transect the attachment. Reattachment is with heavy nonabsorbable No. 2 or No. 5 suture (Fig. 61-1).

ECTOPIC BONE Ectopic bone has been reported after TEA.15 Although some heterotopic ossification may be seen following elbow replacement, in our experience and opinion, this is a very rare complication that occurs only under unusual circumstances, such as in patients with severe degenerative arthritis.26 We have observed only three cases of this problem after approximately 700 primary and revision total elbow replacements using several implant designs and exposures. In one patient, marked hypertrophic changes existed before surgery, extensive bleeding occurred after surgery, and moderate ectopic bone developed (Fig. 61-2).

FRACTURE

A

Anconeus

As greater experience is gained with elbow replacement, an increased incidence of fracture associated with elbow replacement is being observed. These may be classified in several ways, but for consistency, the topic will be discussed in the next section.

COMPLICATIONS REQUIRING REOPERATION As with all prostheses, reoperations may or may not require implant revision.

B FIGURE 61-1

NONREIMPLANTATION REVISION PROCEDURES

A, Triceps reattachment technique used for both primary and reoperation procedures. B, An anconeus slide is used if the triceps attachment is deficient.

Component Failure At the Mayo Clinic, we have observed an increasing frequency of ulnar component stem fracture, especially associated with traumatic arthritis in which near-normal activity is conducted after replacement (Fig. 61-3).51 An incidence of approximately 1.8% has been observed at the ulna and less than 0.5% at the humerus. The cause of these fractures is due to the success of the Stem

initial replacement, which allows heavy use of the arm, and to the stress riser effect or to sintered titanium. Few cases of this kind of failure have been reported except with use of the Coonrad-Morrey component. Since 1994, this problem has not been observed, because the beaded surface finish has been removed from the ulnar component.

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Part VII Reconstructive Procedures of the Elbow

FIGURE 61-2

A patient with hypertrophic osteoarthritis and motion from 60 to 90 degrees before surgery (A) developed marked hematoma and significant posterior ectopic bone (B).

Articulation Bushing wear has been a major problem with the GSB and triaxial device,53 occurring in frequencies of 12% with the Pritchard II prosthesis,32 and in 5% of 173 GSB implants.21 This is attributed primarily to instability and less to osteolysis. Recent modifications in both designs are hoped to decrease or eliminate this problem. At Mayo, we have had an increasing incidence of displacement of the locking ring (Fig. 61-4), but it is unusual to have the pin back out. In our systematic review, semiconstrained devices had a disassembly rate of 4.2% ±0.8%.56 A modification of a pin within a pin (see Chapter 53), which has been approved by the Food and Drug Administration, should eliminate this problem. Inglis and Pellicci23 reported two of 36 articular bushing failures in the early design of the triaxial semiconstrained prosthesis. Pin backout had been a relatively common problem with the Pritchard-Walker implant in up to 5%.34,46 This is less a problem with the current Pritchard III design and has not occurred with the Coonrad device. Component failure is rare in unlinked implants, usually occurring as deformity, wear, or subluxation of the polyethylene.27–29,55

FIGURE 61-3

Fracture of the ulnar component a full 3 years after surgery.

Treatment Articulation failure is treated by replacement of the bushing. The technique is usually not too demanding because the stable, remaining elements are left intact.14 Replacement of a fractured stem requiring techniques used for failed femoral devices, while difficult, is usually successful.

Chapter 61 Complications of Elbow Replacement Arthroplasty

FIGURE 61-4

853

Pritchard Mark II device with pin failure (A); “C” ring displaced with Coonrad-Morrey

device (B).

Wear Until recently, total elbow implants have not been associated with excessive high-density polyethylene debris. The radial head has shown deformity and subluxation in the Mayo design and, more recently, in the resurfacing device designed by Pritchard. We noted significant problems due to metallic synovitis in the early design of the Mayo-modified Coonrad device. This is caused by particulate titanium being freed from the plasma spray surface as it is exposed to the local environment. With increased longevity, an increased incidence of polyethylene wear was noted, at least for the CoonradMorrey device. This can be measured radiographically (Fig. 61-5). It has been observed in patients with survival in excess of 10 years19 and in those with greater stress of the articulation, as with arthritis and instability underlying the process.44,58 Treatment The treatment for excessive wear of the articulation is simply to remove and replace the articulation. The goal is a complete cleansing of the joint of the particulate debris that elicits the adverse response. If the implant is loose and must be removed, care is taken that the intramedullary pseudomembrane is completely removed. The hallmark of the treatment of such a cir-

cumstance is to meticulously débride all of the metal- or polyethylene-laden soft tissues. Implant exchange is usually not required.

COMPLICATIONS TREATED BY IMPLANT REMOVAL Infection Sepsis after TEA is more common than after any other replacement procedure.40 A review of the literature suggests that infection with TEA occurs in about 7% of cases for both types of implant design. Thus, 22 of 332 (7%) resurfacing implants have been reported as infected9,10,13,31,45,49,52,54; a slightly lower frequency of semiconstrained implants have developed this complication.3,4,23,40,43 However, this is changing. Souter reported only one infection after more than 100 procedures using antibiotic-impregnated cement (Souter, personal communication, 1980). Our infection rate at the Mayo Clinic decreased from about 8%40 to less than 2% over the past 10 years. The systematic review of literature in the last decade demonstrated a 2.5% infection rate in modern literature.56 Although the diagnosis is not difficult (Fig. 61-6), the treatment is more challenging. This topic is a major one and is dealt with in a focused manner in Chapter 62.

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Part VII Reconstructive Procedures of the Elbow

3.5˚ 3.5˚ 5˚ > 5˚

⫹

5˚ ⫺

> 5˚

Normal wear Partial wear

A

Complete wear

FIGURE 61-5

Wear can be measured in semiconstrained total elbow arthroplasty (TEA) when the laxity of the bushing is excluded (A). High demand in man with resected distal humerus at 6 years (B). Particulate synovitis from both metal and ultrahigh molecular-weight polyethylene (UHMWPE) (C).

Reimplantation Reimplantation is required for loosening and implant fracture, and in some cases following deep sepsis.58 If a resection arthroplasty is painful or if resection causes significant functional insufficiency due to gross instability (Fig. 61-7), then reimplantation may be considered. If performed for infection, the technique used is similar to those recommended for reimplantation of the septic knee and hip implant. If an implant fractures, we make no effort to remove all cement, but rather leave the cement mantle, if intact, and enlarge it with a burr to remove the new device. Patients who have had resected joints may show significant shortening and must be

prepared to accept this shortening. With the new longer flanged device, this should be less of an issue in the future. Also, patients should be advised that their extensor mechanism may not actively extend the elbow. We have reimplanted eight fractured ulnar components; all are still functioning without loosening. Experience with the infected joint is discussed in Chapter 62.58

Results

Instability Instability after TEA is a problem that is basically limited to unlinked implants (see Chapter 52C). Elbow instability

Chapter 61 Complications of Elbow Replacement Arthroplasty

FIGURE 61-6

855

Infected elbow (A). Reasonable function of the resection (B).

FIGURE 61-7

A patient with infected total elbow arthroplasty underwent resection 8 years previously (A). Because of persistent and significant dysfunction, revision was performed first by using antibioticimpregnated methylmethacrylate as a spacer and to treat the local tissues and medullary canal (B). Reimplantation was effectively accomplished (C).

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Part VII Reconstructive Procedures of the Elbow

following the use of resurfacing implants, either as frank dislocation or subluxation, occurs in approximately 10% of cases.9,10,12,31,48,49,52,54 All designs are valuable for treating this problem (Fig. 61-8). Subluxation occurs about twice as frequently as frank dislocation. Only about 20% of patients with instability require surgical revision. Thus, instability requiring revision is seen in approximately 1% to 5% of the resurfacing devices. In our systematic review of modern literature, the instability rate was significantly higher with unlinked compared to linked designs, 3.4% ±0.7% and 0.4% ±0.9%, respectively (P = 0.014).56 Attempts have been made to improve the design and the surgical technique and, hence, to minimize this complication. It is disappointing to realize that even current reports continue to relate an instability rate of 7% to 8%.9,54 At the Mayo Clinic, 7 of 49 patients (14%) had instability with the capitellocondylar device (Johnson & Johnson, Warsaw, IN). Attaining the proper balance of the soft tissue envelope is technically very difficult, and it requires a thorough understanding of the anatomy and biomechanics25 and a meticulous surgical technique that preserves or restores the function and balance of both ligaments and muscles. Axial malrotation of either the humerus or the ulna appears to be a crucial pitfall of the surgical technique.25 Treatment A period of immobilization to avoid full extension may help eliminate or decrease the fre-

quency of this problem.45,52 If the elbow has dislocated, immobilization in flexion of 90 degrees or more for 3 to 6 weeks is the most common treatment. If this does not render the joint stable, translatory instability is generally well tolerated. If the patient still has symptoms, soft tissue revision is usually not successful, and revision to a semiconstrained device is required in my practice.

Loosening Loosening after TEA is a well-publicized complication.2,4,18,20,24,41,47 Our initial experience at the Mayo Clinic reveals that approximately 25% of the constrained hinged total elbow arthroplasties will loosen within 5 years.41 In our systematic review of modern literature, the rate of clinically symptomatic nonseptic loosening was 4.8%.56 The three factors that have been identified to account for nonseptic loosening are joint mechanics, implant design, and surgical technique. Biomechanics The resultant force vector of up to three times body weight is directed anteriorly during dynamic flexion and posteriorly during extension of the joint.22,42 A cyclic compression-distraction loading pattern occurs up to 1 million cycles per year8 (Fig. 61-9).

Today, all devices are low-friction metal and polyethylene. In addition, the semiconstrained

Prosthetic Design

FIGURE 61-8

Instability is seen with all resurfacing implants of a London device (A), the three-part ERS device (B),

Chapter 61 Complications of Elbow Replacement Arthroplasty

857

FIGURE 61-8, cont’d

the capitellocondylar device (C), the Souter Strathclyde device (D), and the Kudo device (E).

220°

Force >2 BWt

FIGURE 61-9 75°

Flexion-extension causes a cyclic compression and distraction load directed anteriorly, superiorly, and posteriorly. This severe loading condition accounts for loosening of the early, more constrained elbow replacement.

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Part VII Reconstructive Procedures of the Elbow

design includes some play or laxity at the bushing, which has dramatically lessened the rate of loosening of TEA.3,14,32,35,43,46,50 The anterior flange of the Mayomodified Coonrad device absorbs the load applied to the humerus (Fig. 61-10). From the early experience, it is known that the cementing technique is directly correlated to the incidence of radiolucent lines. A stable interface is now reliably attained with intramedullary injecting systems (Fig. 61-11).

Surgical Technique

As noted earlier, Gschwend and colleagues21 reviewed the literature from 1986 to 1992, collecting 828 cases. From this sample, a loosening rate was defined as radiographic: 17%, clinical: 6%. Our own experience at the Mayo Clinic constitutes a group of approximately 500 semiconstrained implants, of which 60% were for rheumatoid arthritis. The loosening rate at 5 years is, surprisingly, less than 2%. Others have reported similar and improved loosening rates as well.2,3,20,23,32,43,46 In our recent systematic review of modern literature, 28 studies from the list of 38 reported on the rate of clinical and radiographic loosening. Aseptic loosCurrent Data

ening, both clinical and radiographic, was correlated with the prosthetic design. Linked prosthesis and unlinked prosthesis were associated with 15.9% ± 22.1% and 18.5% ± 17.8% of aseptic loosening, respectively. There was no significant difference between these rates (P > 0.5). There is little question that loosening does not appear to be a major problem with the current generation of semiconstrained or resurfacing procedures in the rheumatoid population.21 Following trauma, we have reported a rate of loosening of less than 2% after 101 procedures followed for 5 years.6,36,51 Gschwend and colleagues21 note a loosening rate of 3% for rheumatoid arthritis and a radiographic rate of 6% for post-traumatic arthritis. Treatment Loosening is less a problem, but the treatment remains a challenge (see Chapter 65). With aseptic loosening and bone resorption, revision should be offered. Options include removal of the implant, leaving a resection arthroplasty; revision to a different type of prosthetic replacement; fusion of the resected joint; and possibly, cadaveric replacement of the resected elbow (see Chapter 67).

FIGURE 61-10

The anterior flange absorbs the forces that otherwise cause loosening.

Chapter 61 Complications of Elbow Replacement Arthroplasty

859

B

FIGURE 61-11 Early constrained joint replacement was associated with a poor cementing technique and early loosening (A). Use of an intramedullary injector system (B) results in a reproducible depth and quality interface (C).

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Part VII Reconstructive Procedures of the Elbow

References 1. Adams, R., and Morrey, B. F.: The effect of cold compressive dressings after elbow surgery. AAOS Annual Meeting, Anaheim, CA, Feb. 4-8, 1999. 2. Bayley, J. I. L.: Elbow replacement in rheumatoid arthritis. Reconstr. Surg. Traumatol. 18:70, 1981. 3. Bell, S., Gschwend, N., and Steiger, U.: Arthroplasty of the elbow. Experience with the Mark III GSB prosthesis. Aust. N. Z. J. Surg. 56:823, 1986. 4. Brumfield, R. H., Volz, R. G., and Green, J. F.: Total elbow arthroplasty: a clinical review of 30 cases employing the Mayo and AHSC prostheses. Clin. Orthop. Relat. Res. 158:137, 1981. 5. Bryan, R. S., and Morrey, B. F.: Extensive posterior exposure of the elbow: a triceps-sparing approach. Clin. Orthop. Relat. Res. 166:188, 1982. 6. Cobb, T. K., and Morrey, B. F.: Use of distraction arthroplasty in unstable fracture dislocations of the elbow. Clin. Orthop. Relat. Res. 312:201, 1995. 7. Conner P. M., and Morrey, B. F.: Total elbow arthroplasty in patients who have juvenile rheumatoid arthritis. J. Bone Joint Surg. 80A:678, 1998. 8. Davis, P. R.: Some Significant Aspects of Normal Upper Limb Functions. Conference on Joint Replacement of the Upper Extremity. London, Institute of Mechanical Engineers, 1977. 9. Davis, R. F., Weiland, A. J., Hungerford, D. S., Moore, J. R., and Dowling, S. V.: Nonconstrained total elbow arthroplasty. Clin. Orthop. Relat. Res. 171:156, 1982. 10. Dennis, D. A., Clayton, M. L., Ferlic, D. C., Stringer, E. A., and Bramlett, K. W.: Capitello-condylar total elbow arthroplasty for rheumatoid arthritis. J. Arthroplasty 5(suppl):S83, 1990. 11. Dee R.: Total replacement arthroplasty of the elbow for rheumatoid arthritis. J. Bone Joint Surg. 54B:88, 1972. 12. Ewald, F. C., and Jacobs, M. A.: Total elbow arthroplasty. Clin. Orthop. Relat. Res. 182:137, 1984. 13. Ewald, F. C., Scheinberg, R. D., Poss, R., Thomas, W. H., Scott, R. D., and Sledge, C. B.: Capitellocondylar total elbow arthroplasty: two- to five-year follow-up in rheumatoid arthritis. J. Bone Joint Surg. 62A:125, 1980. 14. Figgie, H. E., III, Inglis, A. E., and Mow, C.: Total elbow arthroplasty in the face of significant bone stock or soft tissue losses. J. Arthroplasty 1:71, 1986. 15. Figgie, M. P., Inglis, A. E., Mow, C. S., and Figgie, H. E., III: Salvage of nonunion of supracondylar fracture of the humerus by total elbow arthroplasty. J. Bone Joint Surg. 71A:1058, 1989. 16. Fitzgerald, R. H. Jr., Nolan, D. R., Ilstrup, D. M., Van Scoy, R. E., Washington, J. A., II, and Coventry, M. B.: Deep wound sepsis following total hip arthroplasty. J. Bone Joint Surg. 59A:847, 1977. 17. Friedman, R. J., Lee, D. E., and Ewald, F. C.: Nonconstrained total elbow arthroplasty. Development and results in patients with functional class IV rheumatoid arthritis. J. Arthroplasty 4:31, 1989. 18. Garrett, J. C., Ewald, F. C., Thomas, W. H., and Sledge, C. B.: Loosening associated with GSB hinge total elbow

19.

20.

21.

22.

23. 24.

25.

26.

27.

28.

29.

30.

31.

32.

33.

34.

35. 36.

37.

replacement in patients with rheumatoid arthritis. Clin. Orthop. Relat. Res. 127:170, 1977. Gill, D. R. J., and Morrey, B. F.: The Coonrad-Morrey total elbow arthroplasty in patients who have rheumatoid arthritis. A ten to fifteen year follow-up study. J. Bone Joint Surg. 80A:1327, 1998. Goldberg, V. M., Figgie, H. E., III, Inglis, A. F., and Figgie, M. P.: Total elbow arthroplasty. J. Bone Joint Surg. 70A:778, 1988. Gschwend, N., Simmen, B. R., and Matejovsky, Z.: Late complications in elbow arthroplasty. J. Shoulder Elbow Surg. 5(2)Part 1:86, 1996. Hui, F. C., Chao, E. Y., and An, K. N.: Muscle and joint forces at the elbow during isometric lifting. [Abstract.] Orthop. Trans. 2:169, 1978. Inglis, A. E., and Pellicci, P. M.: Total elbow replacement. J. Bone Joint Surg. 62A:1252, 1980. Johnsson, J. R., Getty, C. J. M., Lettin, A. W. F., and Glasgow, M. M. S.: The Stanmore total elbow replacement for rheumatoid arthritis. J. Bone Joint Surg. 66B:732, 1984. King, G., Itoi, E., Niebur, G. L., Morrey, B. F., and An, K. N.: Motion and laxity of the capitellocondylar total elbow prosthesis. J. Bone Joint Surg. 76A:1000, 1994. Kozak, T. K. W.: Total elbow arthroplasty in primary osteoarthritis of the elbow: a brief report. J. Arthroplasty 13:837, 1998. Kudo, H., Iwano, K., and Watanabe, S.: Total replacement of the rheumatoid elbow with a hingeless prosthesis. J. Bone Joint Surg. 62A:277, 1980. Linscheid, R. L.: Resurfacing elbow joint replacement. In Morrey, B. F. (ed.): Joint Replacement Arthroplasty. New York, Churchill Livingstone, 1991, p. 293. Ljung, P., Lidgren, L., and Rydholm, U.: Failure of the Wadsworth elbow: 19 cases of rheumatoid arthritis followed for 5 years. Acta Orthop. Scand. 60:254, 1989. London, J. T.: Resurfacing Total Elbow Arthroplasty. Presentation. AAOS Annual Meeting, Atlanta, Georgia, February, 1980. Lowe, L. W., Miller, A. J., Allum, R. L., and Higginson, D. W.: The development of an unconstrained elbow arthroplasty: a clinical review. J. Bone Joint Surg. 66B:243, 1984. Madsen, F., Gudmundson, G. H., Sojbjerg, J. O., and Sneppen, O.: The Pritchard Mark II elbow prosthesis in rheumatoid arthritis. Acta Orthop. Scand. 60:249, 1989. Maloney, W. J., and Schurman, D. J.: Cast immobilization after total elbow arthroplasty. A safe cost-effective method of initial postoperative care. Clin. Orthop. Relat. Res. 245:117, 1989. Morrey, B. F.: Complications of total elbow arthroplasty. In Morrey, B. B. (ed.): The Elbow and Its Disorders, 2nd ed. Philadelphia, W. B. Saunders Co., 1993, p. 665. Morrey, B. F.: The Elbow and Its Disorders. Philadelphia, W. B. Saunders Co., 1985. Morrey, B. F., and Adams, R. A.: Semiconstrained joint replacement arthroplasty for distal humeral nonunion. J. Bone Joint Surg. 77B:67, 1995. Morrey, B. F., and Adams, R.: Semiconstrained total elbow arthroplasty for rheumatoid arthritis. J. Bone Joint Surg. 74A:479, 1992.

Chapter 61 Complications of Elbow Replacement Arthroplasty

38. Morrey, B. F., Askew, L. J., and An, K. N.: Strength function after total elbow arthroplasty. Clin. Orthop. 234:43, 1988. 39. Morrey, B. F., Askew, L. J., An, K. N., and Chao, E. Y.: A biomechanical study of normal functional elbow motion. J. Bone Joint Surg. 63A:872, 1981. 40. Morrey, B. F., and Bryan, R. S.: Infection after total elbow arthroplasty. J. Bone Joint Surg. 65A:330, 1983. 41. Morrey, B. F., Bryan, R. S., Dobyns, J. H., and Linscheid, R. L.: Total elbow arthroplasty: a five-year experience at the Mayo Clinic. J. Bone Joint Surg. 63A:1050, 1981. 42. Pearson, J. R., McGinley, D. R., and Butzel, L. M.: A dynamic analysis of the upper extremity: planar motions. Hum. Factors 5:59, 1963. 43. Pritchard, R. W.: Long-term follow-up study: semiconstrained elbow prosthesis. Orthopedics 4:151, 1981. 44. Ramsey, M. L., and Morrey, B. F.: Instability of the elbow treated with semiconstrained total elbow arthroplasty. J. Bone Joint Surg. 81A:38, 1998. 45. Roper, B. A., Tuke, M., O’Riordan, S. M., and Bulstrode, C. J.: A new constrained elbow. A prospective review of 60 replacements. J. Bone Joint Surg. 68B:566, 1986. 46. Rosenfeld, S. R., and Ansel, S. H.: Evaluation of the Pritchard total elbow arthroplasty. Orthopedics 5:713, 1982. 47. Ross, A. C., Sneath, R. S., and Scales, J. T.: Endoprosthetic replacement of the humerus and elbow joint. J. Bone Joint Surg. 69B:652, 1987. 48. Rozing, P. M., and Poll, R. G.: Use of the Souter-Strathclyde total elbow prosthesis in patients who have rheumatoid arthritis. J. Bone Joint Surg. 73A:1227, 1991.

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49. Rydholm, U., Tjornstrand, B., Pettersson, H., and Lidgren, L.: Surface replacement of the elbow in rheumatoid arthritis. J. Bone Joint Surg. 66B:737, 1984. 50. Schlein, A. P.: Semiconstrained total elbow arthroplasty. Clin. Orthop. 121:222, 1976. 51. Schneeberger, A. G., Adams, R., and Morrey, B. F.: Semiconstrained total elbow replacement for the treatment of posttraumatic arthritis and dysfunction. J. Bone Joint Surg. 79A:1211, 1997. 52. Soni, R. K., and Cavendish, M. E.: A review of the Liverpool elbow prosthesis. J. Bone Joint Surg. 66B:248, 1984. 53. Souter, W. A.: Arthroplasty of the elbow: with particular reference to metallic hinge arthroplasty in rheumatoid patients. Orthop. Clin. North Am. 4:395, 1973. 54. Trancik, T., Wilde, A. H., and Borden, L. S.: Capitellocondylar total elbow arthroplasty. Two- to eight-year experience. Clin. Orthop. Relat. Res. 223:175, 1987. 55. Trepman, E., Vella, I. M., and Ewald, F. C.: Radial head replacement in capitellocondylar total elbow arthroplasty. Two- to six-year follow-up evaluation in rheumatoid arthritis. J. Arthroplasty 6:67, 1991. 56. Voloshin, I., Kakar, S., Krall Kaye, E., and Morrey, B. F.: Complications of total elbow replacement: Systematic review of literature in the last decade. [in press.] 57. Wolfe, S. W., and Ranawat, C. S.: The osteoanconeus flap. An approach for total elbow arthroplasty. J. Bone Joint Surg. 72A:684, 1990. 58. Yamaguchi, K. K., Adams, R. A., and Morrey, B. F.: Infection after total elbow arthroplasty. J. Bone Joint Surg. 80A:481, 1998.

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CHAPTER

62

Treatment of the Infected Total Elbow Arthroplasty Emilie Cheung, Ken Yamaguchi, and Bernard F. Morrey

antibiotics. However, this strategy increases the morbidity from a repeat general anesthetic as well as another surgical insult to the elbow. If the implants are well fixed, removal of the prosthesis may pose technically challenging.28,38 The objective of this chapter is to review the evaluation and treatment of the infected total elbow arthroplasty. In particular, patient presentation including health profile, duration of symptoms, fixation of components, and bacteriology are discussed in relation to indications for various treatment strategies for the infected elbow arthroplasty (Fig. 62-1).

ETIOLOGY AND INCIDENCE INTRODUCTION Despite multiple improvements in total elbow arthroplasty design, infection was a relatively common and potentially catastrophic complication, with reported rates as high as 11% in earlier studies.* The rate had decreased considerably, and was 3% in our practice overall.39 Others have reported similar findings, with a slightly higher infection rate of approximately 8% in the revision setting,32 and 5% in patients with rheumatoid arthritis.1,11,30,35 Although not demonstrated with certainty, the rate seems to have increased since the introduction of the disease-remitting agents (DMARDs) to treat rheumatoid arthritis (see Chapter 54). This difficult complication can be treated with either open débridement with placement of antibiotic beads and staged bushing exchange, removal followed by staged reimplantation of components, or resection arthroplasty, depending on the onset and chronicity of symptoms from the time of index arthroplasty. With little information on which to base treatment decisions, poorly functioning and sometimes painful resection arthroplasty has been the definitive procedure of choice, particularly in elderly patients who have relatively low demands on the elbow.14,27,38 Treatment options that have allowed concurrent eradication of the infection with either prosthetic retention or reimplantation have been explored with relatively good results in the past decade, especially at the knee and hip.15,16,21,22,24 Thus, this treatment strategy has been employed in the treatment of the infected total elbow arthroplasty under certain circumstances.6,39,40 Patients who have clinical evidence of infection but have negative cultures represent a treatment dilemma. Most are treated as if they are infected, with resection of the prosthesis, and staged reimplantation after cultures are followed to completion, with a course of parenteral *See references 3, 8-10, 14, 18, 19, 25-27, 29, 32, 37, and 38.

Since the initial reports on infections of total elbow arthroplasties, the clinical presentation of these prosthetic infections has changed. Increased awareness of this complication has led to a high index of suspicion and hence earlier recognition.14 However, even at 3%, the rate of infection for elbow arthroplasties remains well above that for the lower extremity arthroplasties, in part because of the high prevalence of severe rheumatoid arthritis or post-traumatic arthritis.11,14,27,38 Risk factors for total elbow infections include rheumatoid arthritis,1,11,35 previous surgical procedures,27 previous local infections38,40 and use of tumor necrosis factor (TNF) antagonists.17 The elbow is a subcutaneous joint with a relatively thin soft tissue envelope, which increases its susceptibility to wound healing complications. In addition, patients with rheumatoid arthritis are often immunocompromised and are taking DMARDs, which may increase the incidence of periprosthetic infection.17 Those with post-traumatic arthritis frequently have undergone multiple operations that compromise the vascularity of the soft tissues and thus increase the risk of wound healing complications.14,38 Delayed wound healing, wound drainage longer than 10 days postoperatively, and reoperation are prognostic factors associated with increased infection rates.38 The incidence of infections following total elbow arthroplasties appears to have declined with improvements in surgical techniques but is now possibly increasing because of the use of the DMARDs. Our experience has shown a decrease in infection rate from an initial report of 8% to a more recent incidence of about 3%.25,27,39 In one long-term series of total elbow arthroplasty, there was no reported infections after the institution of routine use of antibiotic impregnated cement.37 It appears that the use of antibiotic-impregnated cement to implant the components, along with meticulous postoperative hematoma control, has been helpful in lowering the incidence of infections. By protocol at the Mayo Clinic,

Chapter 62 Treatment of the Infected Total Elbow Arthroplasty

Treatment of infected total elbow arthroplasty

Good health

Patient health status

Poor health

Cultures of arthroplasty Staph. epidermidis ± gram-negative organism

Staph. aureus ± gram-negative organism

Fixation of arthroplasty components

Unstable or loose

Well fixed

Duration of symptoms

Bone quality

Reconstructable

<30 days Débridement and irrigation of arthroplasty

FIGURE 62-1

>30 days

Staged revision arthroplasty (two-stage)

Nonreconstructable

Excisional arthroplasty

Treatment algorithm for the infected total

elbow.

postoperative elbows are immobilized and elevated in full extension for a period of 24 to 36 hours to allow for edema control and wound epithelialization, before allowing range-of-motion exercises.

PATIENT PROFILE The most important consideration in treating a patient with an infected total elbow arthroplasty is the overall status of the host. The health status comprises both the patient’s medical condition and his or her functional needs and expectations. Many patients with rheumatoid arthritis are medically debilitated owing to immunosuppressive medications, anemia of chronic disease, previous surgery, and, sometimes, poor nutrition. Our protocol for these patients includes cessation of DMARDs,

863

which are TNF antagonists (etanercept, infliximab, or adalimumab) at least 2 weeks before surgery and until 2 weeks postoperatively, because these medications have been shown in some studies to increase the incidence of periprosthetic infection.17 For some low-demand patients, the only goal for surgery may be a noninfected, pain-free elbow. The most appropriate treatment for these people may be resection arthroplasty. For others in relatively good health, preservation of function remains an important goal. Treatment of infection with arthroplasty preservation requires multiple surgical procedures and aggressive treatment associated with a high risk of complications. Thus, any treatment plan should be placed in the context of the patient’s needs and abilities to withstand this treatment. The clinical presentation of an infected total elbow arthroplasty may be subtle and only recognized by maintaining a high index of suspicion.38 Patients with an infected olecranon bursa should be assumed to have a deep infection unless proven otherwise. Systemic signs of sepsis (fever and tachycardia) may be absent,27 with the patient complaining of increased pain or pain at rest. Acute inflammation is usually detectable by local signs such as the presence of warmth, erythema, and tenderness. In some patients, there may be drainage from the wound or soft tissues.6,14,27,38 These points become important in determining the onset and thus chronicity of an infection. Preoperative evaluation is critical to establish range of motion, stability of the elbow, neurologic status, and function of the biceps and triceps muscles. Laboratory data may be of limited value, with most patients having a normal leukocyte count but an elevated neutrophil count on differential analysis.27 The erythrocyte sedimentation rate (ESR) is often elevated but not specific, because many have systemic inflammatory disease. Creactive protein (CRP) is now routinely collected to aid in the sensitivity of detecting occult infection.6 The definite step is to aspirate the joint (Fig. 62-2). Patients are considered infected when there are positive cultures or strong clinical suspicion (based on presence of a draining sinus, high white blood cell count, erythrocyte sedimentation rate, CRP, operative observations, and so on) in the context of supportive microscopic pathology.

DURATION OF SYMPTOMS Traditionally, infections have been classified according to length of time from surgery. An infection is considered acute if it developed within 3 months of the index operation, subacute if presentation was between 3 months and 1 year, and late if it was recognized 1 year after surgery.27,38 The time interval from the index pro-

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Part VII Reconstructive Procedures of the Elbow

BACTERIOLOGY

FIGURE 62-2

Aspiration is readily performed and is the best method of providing an early diagnosis.

cedure to the development of infection has traditionally been thought to correlate with the ability to eradicate the infection, but we were unable to demonstrate this in our most recent assessment.6 The duration of symptoms, as in the experience with total knee arthroplasty, has demonstrated a correlation with successful treatment by irrigation and débridement.21,31 Therefore, delineating the onset of symptoms has correlated better with the onset of infection and has direct implications on the treatment strategy.

FIXATION OF COMPONENTS Component fixation in the context of infection is based on the appearance of the bone cement interface on serial radiographs.6,30 The quality of implant fixation has been enhanced in recent years by the improvement in cement techniques. High-quality and comparison radiographs are necessary for the detection of the progression of radiolucent lines, interval changes in implant position, cortical erosions, and osteolysis, suggesting loosening of the prosthesis. Component retention is, of course, a contraindication with loose or poorly fixed components.

The microorganisms of implant infections, as opposed to soft tissue infections, are often difficult to eradicate and continue to be a significant problem. This has been demonstrated in total elbow infections in which the type of organism has had a profound impact on the treatment methods.6,39 Organisms vary in virulence, adherence, and the elaboration of extracellular components. Many factors influence the adherence of bacteria to the prosthesis, including alterations in host immune competence and the ability of bacteria to produce an extracellular matrix.7,13 Unlike total hip and total knee replacements, the infection rate of elbow replacements with gram-negative microorganisms has been low.6,39 Studies of infected orthopedic implants have shown that up to 76% of the infectious microorganisms produce a significant biofilm extracellular matrix to improve adherence to the implant.7,13 Of these, coagulase-negative staphylococci, particularly Staphylococcus epidermidis, have been the most common and the most problematic biofilm producers.13,36 More virulent microorganisms such as coagulasepositive staphylococci (i.e., Staphylococcus aureus) have the capacity to invade and infect healthy tissues but have a lesser ability to form a significant biofilm. Coagulasenegative staphylococcal organisms, particularly S. epidermidis, have been recognized as the primary pathogen of orthopedic device infections owing to their unusual capacity to attach to and to colonize orthopedic implants.2,36 Although a relatively nonvirulent pathogen that normally exists on the skin, it can form a tenacious bacterial biofilm (“slime”), or polysaccharide glycocalyx (protein plus carbohydrate), that envelopes the bacteria. This biofilm promotes colonization and adherence, and protects the bacteria from desiccation and host defense mechanisms.7 It also protects from antibiotic penetration and can even permit adherence to antibioticimpregnated cement. This accounts for the persistence of S. epidermidis and its resistance to treatment.13 Not surprisingly, the presence of S. epidermidis has thus been associated with high incidence of treatment failure in the setting of infected total elbow arthroplasty,6,39 especially with efforts at reimplantation.6,39 Based on our recent studies,6 in the context of resection arthroplasty for infection followed by reimplantation of total elbow arthroplasty, the most common infecting organism from cultures taken at the time of resection was S. epidermidis (44.8%), followed by methicillin-sensitive S. aureus (24%), and Klebsiella pneumoniae (7%). Negative cultures were found in 10.3%, in which case infection was diagnosed clinically on the basis of wound dehiscence, or a draining wound with an exposed prosthesis. Other organisms accounted for the remaining 14%: group A streptococcus in one elbow, aerobic

Chapter 62 Treatment of the Infected Total Elbow Arthroplasty

diptheroids in one elbow, Propionobacter acnes in one elbow, and methicillin-resistant S. aureus in one elbow (Table 62-1).

TREATMENT OPTIONS Once the diagnosis of an infected total elbow arthroplasty is suspected or confirmed, treatment is focused on surgical intervention. In choosing a particular treatment plan, strong consideration must be given to (1) duration of symptoms, (2) the component fixation, (3) the bacteriology, and (4) the patient’s health status (see Fig. 62-1). Debilitated patients who are unable to withstand the rigors of multiple surgical procedures are best served with a resection arthroplasty. Irrespective of the treatment chosen, the primary objective of treatment remains a long-term cure of the infection, which is dependent on the complete removal of the bacteria and its glycocalyx. A secondary concern is restoration of function. All treatment plans require a minimum 6-week course of intravenous antibiotics.

IRRIGATION AND DÉBRIDEMENT WITH RETENTION OF THE COMPONENTS The initial experience with irrigation and débridement with retention of the components resulted in poor outcomes, with this treatment failing in most patients. Wolfe and coworkers37 reported eight failures in 11 patients with this technique, with the other three elbows deemed successes despite intermittent wound drainage. The Mayo Clinic’s initial experience was similar, with only one of nine patients treated successfully. We are aware of one case of an S. aureus–infected total elbow arthroplasty, successfully treated by arthroscopic irrigation and synovectomy in a patient with acute onset of symptoms at 2 months postoperatively.23 With increased awareness and earlier detection of infection, patients are now often seen acutely with wellfixed components without apparent bone involvement. Distribution of Infectious Organisms in Patients Receiving a Reimplantation Following Management of the Septic Condition

TABLE 62-1

Organism

Percent

Staphylococcus epidermidis

45

Methicillin-resistant Staphylococcus aureus

24

Klebsiella pneumoniae

7

“Other”

14

Negative culture

10

865

In Wolfe’s series,38 three of eight patients sustained fractures of the humerus or ulna with component removal. In aseptic revisions, Morrey and Bryan28 noted fractures in 11 of 33 subjects. These results exemplify the difficulty in removal of the components without compromising the bone structure and have renewed interest in component retention. Prior experience with infected total knee arthroplasty has demonstrated a high correlation between the duration of symptoms of infection (21 days or less) and outcome with component retention.22,31 Using this principle of symptom duration of less than 30 days, a recent study reports a 50% long-term success rate (at a mean 71-month follow-up).39 Furthermore, bacteriology played a significant role, with this treatment protocol failing all four patients infected by S. epidermidis whereas six of eight were successfully eradicated of the S. aureus infection.39 Therefore, traditionally, treatment with débridement and component retention is considered dependent on both the duration of symptoms and the bacteriologic findings. Of note, our recent assessment of the success of reimplantation did not demonstrate a prognostic difference in those with early or delayed diagnosis and treatment.6 The indications for this treatment include (1) the presence of well-fixed surgical components by both radiographic and intraoperative examination; (2) bacteriology suggestive of S. aureus or other pathogen amenable to this form of treatment; (3) a suitable soft tissue envelope, with or without the use of flaps; (4) a patient who is medically fit enough to withstand the required multiple surgical procedures; and (5) duration of symptoms less than 30 days. A contraindication to component retention is an infection caused by S. epidermidis. The technique for irrigation and débridement with component retention in our practice is through a posterior approach using the previous incision.6,39 The stability of the components is confirmed, followed by complete disarticulation of the components, including removal of the bushings (Fig. 62-3). This is an essential component of the procedure. The joint is débrided of all necrotic debris and copiously irrigated with pulsatile saline lavage. Antibiotic-impregnated polymethyl methacrylate (PMMA) beads, with a concentration of 2 g tobramycin per half-package of cement, are placed in the wound before wound closure. Patients often return to the operating room every fourth day for repeat irrigation and débridement with antibiotic PMMA bead exchange until the wound bed appears clean. The patient concurrently receives bacteria-sensitive intravenous antibiotics for a minimum period of 6 weeks (based on serum minimal inhibitory and bactericidal concentrations).6,39 The use of chronic oral suppressive antibiotics after completion of parenteral antibiotics is controversial and surgeon dependent.

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Part VII Reconstructive Procedures of the Elbow

FIGURE 62-3

A and B, Intraoperative radiograph from a representative patient who underwent successful irrigation and débridement. The patient presented with well-fixed components and symptoms of infection of 1 day’s duration. The component was disarticulated with bushings and pin removal as an essential portion of the débridement procedure. Six weeks later, a new bushing was placed and the implant re-articulated with a satisfactory result.

The overall success rate of the Mayo series reported by Yamaguchi and coworkers39 was 50% but increased to 70% when those patients infected with S. epidermidis were eliminated. Outcomes produced good functional results but carried a 43% incidence of complication, including a 21% incidence of wound breakdown or triceps avulsion and 21% with peripheral nerve injury.

STAGED EXCHANGE ARTHROPLASTY With the success of staged exchange arthroplasty for lower extremity infections,16,34 this technique has been successfully used for infected total elbow arthroplasties. We reported an 80% success rate at the Mayo Clinic with staged revision, with the only failures occurring in patients infected with S. epidermidis.39 The procedure’s success is dependent on the complete eradication of the pathogenic microorganism, necessitating the complete removal of all prosthetic components including PMMA.6,39,40 After reimplantation of total elbow arthroplasty following resection arthroplasty for infection reported by Cheung et al,6 there were 52% good to excellent, 10% fair, and 38% poor results at mean 7.4 years follow-up. Overall, there was a 28% rate of failure to eradicate

the infection. The success rate of eradication of infection did not correlate with the chronicity of the infection. A success rate of 80% for eradication of infection was achieved if the duration of symptoms was less than 3 months at the time of resection arthroplasty. By comparison, the success rate decreased to 66% when the onset of symptoms was greater than 3 months from the primary arthroplasty. As in previous studies,39,40 elbows infected with S. epidermidis had a higher likelihood of treatment failure following reimplantation. The most common indications for staged exchange arthroplasty in our practice are (1) radiographic or intraoperative evidence of loose components with sufficient bone stock for reconstruction, (2) duration of symptoms longer than 30 days, and (3) a medically fit patient (Fig. 62-4). A relative contraindication, dependent on the surgeon and the patient, is an infection caused by S. epidermidis. The surgical technique uses the previous posterior incision to expose the joint, with consideration of flaps for soft tissue coverage.28,39 While preserving bone stock (see Fig. 62-4), the components and any remaining cement are removed in a meticulous fashion during resection arthroplasty with the use of small curettes, a

Chapter 62 Treatment of the Infected Total Elbow Arthroplasty

FIGURE 62-4

Radiographs from a representative patient who underwent staged exchange arthroplasty. This 45-year-old man presented with a Staphylococcus aureus infection 68 months after the primary procedure. He had had 56 days of symptoms before presentation. A and B, Anteroposterior and lateral radiographs of the elbow with scalloping of the cortical bone and prosthetic loosening consistent with infection. C, The component was removed, and antibiotic-impregnated cement was placed. Seven weeks later, the patient underwent a reimplantation of a semiconstrained prosthesis with antibiotic-impregnated cement. D, At 64 months of follow-up, there are no signs of persistent infection.

867

868

Part VII Reconstructive Procedures of the Elbow

motorized burr, a router, or an ultrasonic cement removal device. Recently, this has been facilitated at the humerus by removing the posterior cortex of the distal humerus as a cortical window. Care is taken to avoid fracture of the condyle and to preserve the intact humerus so the tip of the reimplanted component is two diameters proximal to the osteotomized cortical window (Fig. 625). Every effort is made to preserve the integrity of the condyles. It is important to preserve the integrity of the condyles because they provide structural stability in case the patient is left with a resection arthroplasty, in which the ulna should articulate within the space between the medial and lateral condyles. The condyles also serve as the origins of the common flexor and extensor muscles of the fore-arm, and loss of their integrity would theoretically further compromise function in cases of resection arthroplasty. Removal of a well-fixed ulnar component is more problematic owing to limited accessibility within the small intramedullary canal. A pencil-tipped burr is used to remove cement from the proximal aspect of the ulnar

1-2 d

d

component in the region of the plasma coating. The process continues distally as needed for removal of the device. Occasionally, we have found it necessary to perform an extended osteotomy down the medial proximal aspect of the ulna. The osteotomy site is later spanned and repaired at the time of reimplantation of a new long-stemmed prosthesis with strut allograft and cerclage wires. Care should be taken to protect the ulnar nerve. Antibiotic-impregnated cement (2 g of tobramycin per 20 g of cement) is placed as a spacer between the humerus and ulna, and the incision is closed. The wound is closed and the limb is placed in a cast or hinged orthosis for 4 weeks. Since 1983 at the Mayo Clinic, antibiotic-impregnated cement has been routinely used for fixation of the implant in both primary and revision total elbow arthroplasties. The patient is placed on a 6-week course of intravenous antibiotics, based on organism sensitivity. At our institution, the orthopedic infectious disease service is consulted at the time of initial diagnosis of a prosthetic infection. Repeat irrigation, débridement, and biopsies of the tissues are performed as necessary. Consideration to longer staging intervals and repeat irrigation and débridement may be given to more resistant infections such as S. epidermidis. Arthroplasty reconstruction is performed at some point after 6 weeks using a longstem semi-constrained arthroplasty with antibioticimpregnated PMMA.6,40 Before reimplantation of total elbow arthroplasty and after completion of the 6-week course of antibiotics and resection arthroplasty, we routinely check that a complete blood count with differential, erythrocyte sedimentation rate, and CRP are within normal limits. An aspiration of the elbow with cell count, culture and sensitivity is also performed to confirm the absence of active infection. Intraoperatively, we send at least three tissue samples for frozen section pathology to confirm the absence of acute inflammation before cementing a new prosthesis. If there is no evidence of acute inflammation, we proceed with reimplantation. No additional antibiotics are typically given after the immediate perioperative period of the reimplantation. The patients are reminded of our lifetime postoperative activity restrictions, which they receive preoperatively: no lifting greater than 10 pounds as a single event, or repetitive lifting of greater than 2 pounds.

IMMEDIATE EXCHANGE ARTHROPLASTY FIGURE 62-5

The technique to remove a well-fixed humeral implant involves a trapezoid-shaped osteotomy of the posterior humerus. Care is taken to preserve the intact humerus so the tip of the reimplanted component is two diameters proximal to the osteotomized cortical window. (With permission, Mayo Foundation.)

There has been very minimal information regarding immediate exchange for infected total elbow arthroplasties. We reported one case in which there was failure to eradicate the infection.40 Recently, Gille and colleagues12 reported successful treatment of S. aureus–infected total

Chapter 62 Treatment of the Infected Total Elbow Arthroplasty

elbow arthroplasties in five of six patients treated with single-stage revision arthroplasty and mean follow-up of 6.8 years. The majority of the lower extremity surgical experience has occurred in Europe, with only anecdotal and early reports in North America. Success rates with immediate exchange arthroplasty for infected total knee replacements vary from 35% to 75%, with suggested improved results with gram-positive non–glycocalyxproducing organisms.16,21,24 The indications for immediate exchange arthroplasty are probably very limited and, at this time, undetermined. The principles of the surgical treatment are similar to those of the staged revision with aggressive débridement with removal of all foreign material, antibioticimpregnated cement fixation, and concomitant 6 to 12 weeks of intravenous antibiotics.

RESECTION ARTHROPLASTY Resection arthroplasty has been the standard of treatment for infected elbow arthroplasty and constitutes the largest treatment experience. Functional results are usually limited but can be associated with a high satisfaction rate. Moreover, because many of these patients are debilitated, it is considered the treatment of choice for those medically frail and unfit for extensive or mul-

869

tiple surgical procedures. If successful, it often provides a relatively pain-free satisfactory range of active motion with reasonable stability (Fig. 62-6). Presentation of both condyles is essential for a functional resection arthroplasty. Factors associated with an unsatisfactory result following resection arthroplasty of the elbow include the loss of the medial and lateral humeral condyles, which results in gross instability of the elbow. Marked shortening of the limb decreases the lever arm on the muscles that move the elbow and alteration of the fulcrum effect of the joint. The weakness can be dysfunctional and ultimately can result in a flail elbow. A hinged elbow brace may be worn for stability in such cases. After eradication of infection, arthrodesis of the elbow may be another option, but subjects the patient to the morbidity of another surgical procedure, and is also functionally disabling. Some patients who function at a higher activity level are dissatisfied with such a result. The technique of elbow resection arthroplasty involves removal of the implant components through the previous incision followed by complete removal of the PMMA. All necrotic and contaminated tissue is excised. If remaining intact, the condyles of the distal humerus are then contoured and deepened to encircle the ulna. The soft tissue coverage is established by primary closure or local rotation flaps. Concurrent treat-

FIGURE 62-6

A chronically infected joint (A) successfully managed by resection arthroplasty (B).

870

Part VII Reconstructive Procedures of the Elbow

B

A

D

C FIGURE 62-7

A and B, Radiographs of a 74-year-old woman who had resection arthroplasty following prior infection of total elbow arthroplasty for post-traumatic arthritis. Three months following a course of intravenous antibiotic therapy, this patient had reimplantation of a Coonrad-Morrey total elbow prosthesis. C and D, Anteroposterior and lateral radiographs taken 2 years postoperatively show satisfactory alignment of the prosthesis, adequate cement mantle, no radiolucent lines, and no evidence of implant loosening. This patient had a good functional result. Postoperative Mayo Elbow Performance Score was 80.

Chapter 62 Treatment of the Infected Total Elbow Arthroplasty

ment with 4 to 6 weeks of appropriate antibiotic therapy is used. The limb is placed in a cast or brace for 3 to 4 weeks to obtain soft tissue stability. We have recently assessed the experience with 40 patients treated by resection arthroplasty for sepsis. At a mean of 6-year surveillance, 78% considered their functional status satisfactory from the perspective of pain relief. On the other hand only 55% considered the salvage to be a functional joint.4 If continued dysfunction and patient dissatisfaction persists, a delayed reimplantation may be considered (Fig. 62-7).

COMPLICATIONS Treatment of the infected elbow requires multiple irrigation and débridement, and complications are not uncommon: intraoperative and postoperative fracture due to loss of bone stock, triceps insufficiency, nerve injury, and skin or wound breakdown. Thus, special attention should be given to protect surrounding neurovascular structures intraoperatively during implant and cement extraction. Care should also be taken to preserve the triceps insertion, and maintain meticulous soft tissue handling. Special consideration should be taken using triceps-on approaches and proactive planning for possible soft tissue coverage procedures with preemptive consultation to plastic surgery. Triceps insufficiency may need to be addressed with anconeus muscle rotation at the time of reimplantation.5 Of course, the high risk of complications and the associated morbidity are significant considerations that have to be discussed with the patient before any prosthetic salvage strategy is attempted in the context of infected elbow arthroplasty.

CONCLUSION Infection remains a significant and severe complication of total elbow arthroplasty with an incidence above that of lower extremity joint replacements. Previously, the only treatment option was resection arthroplasty. Recent reports of this problem suggest that both irrigation and débridement and staged exchange arthroplasty can be successful treatment modalities given the appropriate indications (see Fig. 62-1). Our experience suggests a poorer prognosis in those with a history of S. epidermidis and in settings of increasing chronicity of disease. As with other joints, functional outcome is compromised after reimplantation of the prosthesis, even in those with successful treatment in regard to infection. As such, selected treatment methods may improve both the functional and satisfaction rate of this most devastating complication.

871

References 1. Aldridge, J. M. 3rd, Lightdale, N. R., Mallon, W. J., and Coonrad, R. W.: Total elbow arthroplasty with the Coonrad/Coonrad-Morrey prosthesis. A 10- to 31-year survival analysis. J. Bone Joint Surg. Br. 88:509, 2006. 2. Arciola, C. R., Campoccia, D., Gamberini, S., Donati, M. E., Pirini, V., Visai, L., Speziale, P., and Montanaro, L.: Antibiotic resistance in exopolysaccharide-forming Staphylococcus epidermidis isolates from orthopaedic implant infection. Biomaterials 26:6530, 2005. 3. Brumfield, R. H. Jr., Kuschner, S. H., Gellman, H., Redix, L., and Stevenson, D. V.: Total elbow arthroplasty. J. Arthroplasty 5:359, 1990. 4. Cass, B., Adams, R. A., and Morrey, B. F.: Long-term outcome of resection arthroplasty of the elbow for infection. 2007 (in press). 5. Celli, A., Arash, A., Adams, R. A., and Morrey, B. F.: Triceps insufficiency following total elbow arthroplasty. J. Bone Joint Surg. Am. 87:1957, 2005. 6. Cheung, E. V., Adams, R. A., and Morrey, B. F.: Reimplantation of total elbow arthroplasty following resection arthroplasty for infection J. Bone Joint Surg. Am. 90:589, 2008. 7. Christensen, G. D., Baldassarri, L., and Simpson, W. A.: Colonization of Medical Devices. 2nd ed. Washington DC, American Society for Microbiology, 1994, p. 45. 8. Davis, R. F., Weiland, A. J., Hungerford, D. S., Moore, J. R., and Volenec-Dowling, O. T. R.: Nonconstrained total elbow arthroplasty. Clin. Orthop. Relat. Res. 171:156, 1982. 9. Ewald, F. C., Simmons, E. D. Jr., Sullivan, J. A., Thomas, W. H., Scott, R. D., Poss, R., Thornhill, T. S., and Sledge, C. B.: Capitellocondylar total elbow replacement in rheumatoid arthritis: Long-term results. J. Bone Joint Surg. 75A: 498,1993. 10. Figgie, M. P., Gerwin, M., and Weiland, A. J.: Revision total elbow replacement. Hand Clin. 10:507, 1994. 11. Gill, D. R., and Morrey, B. F.: The Coonrad-Morrey total elbow arthroplasty in patients who have rheumatoid arthritis. A ten to fifteen-year follow-up study. J. Bone Joint Surg. Am. 80:1327-1335, 1998. 12. Gille, J., Ince, A., Gonzalez, O., Katzer, A., and Loehr, J.: Single-stage revision of peri-prosthetic infection following total elbow replacement. J. Bone Joint Surg. Br. 88:1341, 2006. 13. Gristina, A. G.: Biomaterial-centred infection: Microbial adhesion versus tissue integration. Science 237:1588, 1987. 14. Gutow, A. P., and Wolfe, S. W.: Infection following total elbow arthroplasty. Hand Clin. 10:521, 1994. 15. Haleem, A., Berry, D., and Hanssen, A.: Mid-term to longterm follow-up of two stage reimplantation for infected total knee arthroplasty. Clin. Orthop. Rel. Res. 428:35, 2004. 16. Hanssen, A.: Managing the infected knee: as good as it gets. J. Arthroplasty 17:98, 2002. 17. Howe, C. R., Gardner, G. C., and Kadel, N. J.: Perioperative medication management for the patient with rheumatoid arthritis. J. Am. Acad. Orthop. Surg. 14:544, 2006.

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18. Kasten, M. D., and Skinner, H. B.: Total elbow arthroplasty: An 18-year experience. Clin. Orthop. Rel. Res. 290:177, 1993. 19. Kraay, M. J., Figgie, M. P., Inglis, A. E., Wolfe, S. W., and Ranawat, C. S.: Primary semiconstrained total elbow arthroplasty. J. Bone Joint Surg. 76B:636, 1994. 21. Marculescu, C. E., Berbari, E. F., Hanssen, A. D., Steckelberg, J. M., and Osmon, D. R.: Prosthetic joint infection diagnosed postoperatively by intraoperative culture. Clin. Orthop. Relat. Res. 439:38, 2005. 22. Marculescu, C. E., Berbari, E. F., Hanssen, A. D., Steckelberg, J. M., Harmsen, S. W., Mandrekar, J. N., and Osmon, D. R.: Outcome of prosthetic joint infections treated with debridement and retention of components. Clin. Infect. Dis. 42:471, 2006. 23. Mastrokalos, D. S., Zahos, K. A., Korres, D., and Soucacos, P. N.: Arthroscopic debridement and irrigation of periprosthetic total elbow infection. Arthroscopy 22:1140, 2006. 24. Mitchell, P., Masri, B., Garbuz, D., Greidanus, N., and Duncan, C.: Cementless revision for infection following total hip arthroplasty. Instr. Course Lect. 52:323, 2003. 25. Morrey, B. F., and Adams, R. A.: Semiconstrained arthroplasty for the treatment of rheumatoid arthritis of the elbow. J. Bone Joint Surg. 74A:479, 1992 26. Morrey, B. F., and Bryan, R. S.: Complications of total elbow arthroplasty. Clin. Orthop. Rel. Res. 170:204, 1982. 27. Morrey, B. F., and Bryan, R. S.: Infection after total elbow arthroplasty. J. Bone Joint Surg. 65A:330, 1983. 28. Morrey, B. F., and Bryan, R. S.: Revision total elbow arthroplasty. J. Bone Joint Surg. 69A:523, 1987. 29. Ruth, J. T., and Wilde, A. H.: Capitellocondylar total elbow replacement: A long-term follow-up study. J. Bone Joint Surg. 74A:95, 1992. 30. Schneeberger, A. G., Meyer, D. C., and Yian, E. H.: CoonradMorrey total elbow replacement for primary and revision

31.

32.

33.

34.

35.

36.

37.

38.

39.

40.

surgery: A 2- to 7.5-year follow-up study. J. Shoulder Elbow Surg. 16(3 Suppl):S47, 2007. Schoifet, S. D., and Morrey, B. F.: Treatment of infection after total knee arthroplasty by débridement with retention of the components J. Bone Joint Surg. 72A:1383, 1990. Sneftrup, S. B., Jensen, S. L., Johannsen, H. V., and Søjbjerg, J. O.: Revision of failed total elbow arthroplasty with use of a linked implant. J. Bone Joint Surg. Br. 88:78, 2006. Trancik, T., Wilde, A. H., and Borden, L. S.: Capitellocondylar total elbow arthroplasty. Clin. Orthop. Rel. Res. 223:175, 1987. Tsukayama, D., Estrada, R., and Gustilo, R.: Infection after total hip arthroplasty. A study of the treatment of one hundred and six infections. J. Bone Joint Surg. Am. 78:512, 1996. van der Lugt, J. C., Geskus, R. B., and Rozing, P. M.: Primary Souter-Strathclyde total elbow prosthesis in rheumatoid arthritis. J. Bone Joint Surg. Am. 86-A:465, 2004. Van Pett, K., Schurman, D. J., and Smith, R. L.: Quantitation and relative distribution of extracellular matrix in Staphylococcus epidermidis biofilm. J. Orthop. Res. 8:321, 1990. Weiland, A. J., Weiss, A. P. C., Wills, R. P., and Moore, J. R.: Capitellocondylar total elbow replacement. A long-term follow-up study. J. Bone Joint Surg. 71A:217, 1989. Wolfe, S. W., Figgie, M. P., Inglis, A. E., Bohn, W. M., and Ranawat, C. S.: Management of infection about total elbow prostheses. J. Bone Joint Surg. 72A:198, 1990. Yamaguchi, K., Adams, R. A., and Morrey, B. F.: Infection after total elbow arthroplasty. J. Bone Joint Surg. 80A:481, 1998. Yamaguchi, K., Adams, R. A., and Morrey, B. F.: Semiconstrained total elbow arthroplasty in the context of treated previous infection. J. Shoulder Elbow Surg. 8:461, 1999.

Chapter 63 Triceps Insufficiency Following Total Elbow Arthroplasty

CHAPTER

63

Triceps Insufficiency Following Total Elbow Arthroplasty Andrea Celli and Bernard F. Morrey

INTRODUCTION Triceps insufficiency can occur as a result of traumatic rupture of the tendon or, most commonly, following a failed surgical reattachment, particularly when there is poor tendon quality.5,12,15,17,18 As a complication following elbow replacement, this is becoming much more appreciated.4 According to the limited literature available on this topic, the incidence of triceps insufficiency following total elbow arthroplasty ranges from 1% to 29%.7,9,10,14,16,17 A recent report using the Gschwend approach documents four of 28 elbows with triceps insufficiency after a triceps-splitting approach to insert the GSB implant (Center Pulse, Zurich).11 In a recent comprehensive review of the literature, Voloshin et al22 documented an incidence of approximately 1% to 5% of triceps insufficiency associated with total elbow arthroplasty. Typically, literature reviews understate the true incidence of this problem. The key factor in avoiding the development of this problem is the nature and execution of the surgical exposure. In this regard, a number of recent studies23 have examined modifications to existing exposures (see Chapter 7).6,19 Olecranon osteotomy is contraindicated in joint replacement surgery. Hence, some means of dealing with the triceps attachment is necessary. There are several options: 1. Reflection of the triceps in continuity with forearm fascia and periosteum and anconeus from medial to lateral.2 Reflection of the triceps with a wafer of bone is a modification that has also been recommended.24 2. Extensile Mayo Modified Kocher approach: following a posterior lateral exposure reflection of the anconeus and approximately one third of the lateral triceps attachment from the tip of the olecranon (see Chapter 7).

873

3. Campbell’s triceps-splitting approach. This approach may be modified by releasing the triceps with wafer of bone.8 4. Preservation of the triceps attachment and aggressive flexor-extensor release to “skeletonize” and deliver the distal humerus. This approach is modified by excision of humeral condyles.1

PRESENTATION AND SYMPTOMS All patients will report loss of active extension and about 15% to 20% will also report pain.4 The most common problem is the inability to reach above the head and to push through doors. The mean time from initial procedure to revision for triceps insufficiency is about 3 years. In our experience the clinical findings at the time of surgical revision were (1) a change in the posterior contour of the elbow with visual and palpable prominence of the implant and atrophy of the subcutaneous tissue; (2) the presence of an olecranon bursitis; (3) atrophy of the triceps muscle; and (4) discernable lateral subluxation or dislocation of the extensor mechanism.

MANAGEMENT Our recommendations are based on the Mayo Clinic experience with triceps insufficiency for any cause21 and particularly after joint replacement.4 From 887 total elbow arthroplasty operations, we identified 16 elbows that underwent subsequent surgical treatment for triceps insufficiency at our institution. The underyling diagnoses for which the primary total elbow arthroplasty was performed were rheumatoid arthritis in nine cases and post-traumatic conditions in seven cases. Initially, the triceps-sparing approach as described by Bryan and Morrey2 was used in 15; in one patient, the tricepssplitting approach as described by Campbell3 was used.

PATHOLOGY At exploration, a complete rupture was observed in 10 and a partial rupture in six of our patients. Of particular importance is the fact that three patients had resorption of the olecranon process. This is a key factor in determining the strategy for successful reconstruction.

REPAIR OR RECONSTRUCTION The logic we currently employ to determine how these problems should be managed is similar to the algorithm developed for management of triceps insufficiency for any cause13,21 (Fig. 63-1). If the tissue quality is good and the olecranon is preserved, we repeat the direct

Part VII Reconstructive Procedures of the Elbow

874

attachment to bone if the tissue is of adequate quality for this. If the tissue is not of good quality but the anconeus and the olecranon are preserved, then we perform an anconeus rotational flap. Finally, if the tissue is not of good quality and the anconeus is not perserved, then an Achilles tendon allograft is carried out. The calcaneus is used to supplement the olecranon if it is resorbed; otherwise, the tendinous tissue is sewn to the intact olecranon and the calcaneus is removed from the allograft.

Tissue quality

No

Good

Anconeus preserved

Yes

No

Yes

Olecranon preserved

No

Olecranon bone graft

Yes

Direct bone repair

Olecranon preserved

Yes

Anconeus rotational flap

Olecranon preserved

REATTACHMENT

No

Yes

Achilles tendon allograft

Achilles tendon with calcaneal bone graft

ANCONEUS ROTATIONAL FLAP

FIGURE 63-1

The treatment algorithm for managing patients with triceps insufficiency following total elbow arthroplasty. (Redrawn with permission of the Mayo Foundation.)

A FIGURE 63-2

This is not commonly indicated if the tendon was properly reattached initially. The key is to avoid the intervention of synovium between the attachment of the triceps tissue and the olecranon. The way to ensure this is to add a circumferential “cinch” suture to apply or compress the triceps tendon closely to its attachment site (Fig. 63-2).

We prefer this technique when the continuity has been lost between the triceps tendon and the periosteal and forearm fascia.

B

Direct suture to bone. When the triceps tendon has not retracted and is of good quality, cruciate criss-cross drill holes are placed in the proximal ulna along with a transverse tunnel (A). A #5 nonabsorbable locking suture (B)

Chapter 63 Triceps Insufficiency Following Total Elbow Arthroplasty

875

D

C

F

FIGURE 63-2 cont’d

E

is placed through the tendon starting from distal medially. After passing through the tendon portion, it is then brought into the second osseous tunnel and secured to itself (C). A specific transverse tunnel is made (D). A No. 5 nonabsorbable suture passes through this tunnel (E), which serves to firmly secure the tendon to its original attachment site on the olecranon (arrow) (F).

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Part VII Reconstructive Procedures of the Elbow

Technique With the patient supine and the arm brought across the chest, the previous skin incision is entered. The triceps mechanism is carefully explored, and the ulnar nerve is protected. The Kocher interval between the anconeus and extensor carpi ulnaris is identified. The anconeus is

A

elevated from the olecranon insertion, leaving intact the distal 20% (Fig. 63-3A). The humeral attachment is detached, allowing the entire extensor mechanism to be rotated from lateral to medial. The fascial attachment of the anconeus is oriented over the posterior aspect of the olecranon and secured with a criss-cross and transverse

A

FIGURE 63-3

B

B

A, The anconeus rotational triceps reconstruction begins by identifying and entering the interval between the anconeus and the extensor carpi ulnaris. The anconeus is elevated from the ulna and rotated medially. B, The anconeus is in continuity with the triceps. The construct is mobilized and repositioned over the olecranon and secured to the olecranon with a No. 5 nonabsorbable suture placed through bone holes.

Chapter 63 Triceps Insufficiency Following Total Elbow Arthroplasty

suture, as described previously (see Fig. 63-3B). The original triceps attachment is now medially displaced. It is incorporated back into the extensor mechanism in order to enhance extension strength. Note: This is an attractive technique to employ during the primary procedure if the triceps attachment is compromised due to inadequacy of the periosteum and forearm fascia.

ACHILLES TENDON RECONSTRUCTION In instances when the anconeus is no longer functional and there is significant tissue loss, an Achilles tendon allograft procedure is performed.

Technique The patient is supine on the table, and the arm is brought across the chest. The olecranon and triceps are widely exposed. The ulnar nerve is identified and protected or translocated, if appropriate. If the olecranon is intact, the triceps muscle is mobilized and the radial nerve is identified and protected as necessary. The fascial expansion of the allograft tendon is brought around the triceps, and the aponeurosis of the allograft securely fastened to the triceps muscle (Fig. 63-4A). The tendinous portion of the achilles allograft is then attached to the olecranon by creating a groove in the posterior aspect of the olecranon with a high-speed burr (Fig. 63-4A, arrow). The graft is placed in the groove and folds over the tip of the olecranon. It is secured with a No. 5 nonabsorbable suture through drill holes in the proximal ulna. Note: Take care to avoid going too deep and notching the ulnar component. The knots are placed off the subcutaneous border to avoid problems of skin irritation.

A

The arm is placed in 45 degrees of extension, and a No. 5 nonabsorbable suture is used to securely attach the distal aspect of the triceps and its tendinous attachment to the allograft. A No. 1 Ethibond running locked suture is then employed circumferentially to attach the fascia of the allograft to the muscle and fascia of the triceps mechanism (see Fig. 63-4B). Note: If the olecranon is deficient, the calcaneus is left on the Achilles tendon and is fashioned in such a way as to be applied to the proximal ulna (Fig. 63-5). The allograft is secured with two Kirschner wires and a circumferential wire according to the AO method. Once the allograft has been secured, once again the elbow is brought into 40 to 45 degrees of extension and the fascial expansion of the tendon is secured to the triceps mechanism as described above.

Aftercare In most instances, the repair or reconstruction is protected for 3 weeks in a splint placed in approximately 45 degrees of extension. After this, active flexion and extension is begun with the elbow limited to 90 degrees of flexion for approximately 6 to 8 weeks. After this period of time, whole flexion is allowed; active extension is allowed only for daily activities. After 3 months, the patient may increase activity; however, extension is limited to 2 to 3 pounds for 6 months from the time of repair. Patients are routinely assessed to ensure that they are following this protocol.

OUTCOME By employing the above-mentioned logic, we were successful in obtaining extension against gravity in 15 of

B FIGURE 63-4

877

The Achilles tendon allograft is secured to the remnants of the triceps muscle; a groove is prepared in the proximal ulna (yellow arrow) (A). With the elbow at 45 degrees of flexion, the tendon is securely attached to the ulna with No. 5 nonabsorbable sutures placed through bone (B).

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Part VII Reconstructive Procedures of the Elbow

PROGNOSTIC FACTORS The most important prognostic factor is the presence or absence of an olecranon process. This detrimental prognostic feature can be obviated by the use of a bone graft. Otherwise the overall quality of the tissues and the number of previous surgical procedures20 are the most important factors that influence outcome.

References

A

20–30°

B FIGURE 63-5

In patients with deficient triceps tissue, an Achilles tendon allograft may be employed. In those in whom there is a deficient olecranon, the calcaneal portion is first attached to the deficient olecranon with a cancellous screw or using the AO technique in the presence of an ulnar component (A). The elbow is placed in 26 to 30 degrees of flexion, and the fascial portion of the allograft is used to envelope the triceps muscle with a continuous No. 1 absorbable suture (B).

16 elbows. There were no significant complications. The major determinant of the success of the operation is the adequacy of the olecranon process. If the olecranon process is absent, it may be reconstructed with the calcaneus along with the Achilles graft. If the olecranon is resorbed and is deficient, simply attaching or reconstructing the triceps is inadequate to restore function.

1. Boorman, R. S., Page, W. T., Weldon, E. J., Lippitt, S., and Matsen, F. A. III: A triceps-on approach to semiconstrained total elbow arthroplasty. Tech. Shoulder Elbow Surg. 4:139, 2003. 2. Bryan, R. S., and Morrey, B. F.: Extensive posterior exposure of the elbow. A triceps-sparing approach. Clin. Orthop. Rel. Res. 166:188, 1982. 3. Campbell, W. C.: In Crenshaw, A. H. (ed.): Campbell’s Operative Orthopaedics. Surgical Approaches, ed. 5, Vol. 1. St. Louis, C. V. Mosby Co., 1971, p. 119. 4. Celli, A., Arash, A., Adams, R. A., and Morrey, B. F.: Triceps insufficiency following total elbow arthroplasty. J. Bone Joint Surg. 87A:1957, 2005. 5. Clayton, M. L., and Thirupathi, R. G.: Rupture of the triceps tendon with olecranon bursitis. Clin. Orthop. Rel. Res. 184:183, 1984. 6. Ebraheim, N. A., Andreshak, T. G., Yeasting, R. A., Saunders, R. C., and Jackson, W. T.: Posterior extensile approach to the elbow joint and distal humerus. Orthop. Rev. 22:578582, 1993. 7. Gill, D. R. J., and Morrey, B. F.: The Coonrad-Morrey total elbow arthroplasty in patients who have rheumatoid arthritis. J. Bone Joint Surg. 80A:1327, 1998. 8. Gschwend, N., Simmen, B. R., and Matejovsky, Z.: Late complications in elbow arthroplasty. J. Shoulder Elbow Surg. 5(2 Pt 1):86, 1996. 9. Hildebrand, K. A., Patterson, S. D., Regan, W. D., MacDermid, J. C., and King, G. J.: Functional outcome of semiconstrained total elbow arthroplasty. J. Bone Joint Surg. 82A:1379, 2000. 10. Inglis, A. E., and Pellicci, P. M.: Total elbow replacement. J. Bone Joint Surg. 62A:1252, 1980. 11. Kelly, E. W., Coghlan, J., and Bell, S.: Five to thirteen year follow-up of the GSB III total elbow arthroplasty. J. Shoulder Elbow Surg. 13:434, 2004. 12. Morrey, B. F.: Complications of Elbow Replacement Surgery. The Elbow and its Disorders. 3rd ed. Philadelphia, WB Saunders, 2000, p. 667. 13. Morrey, B. F.: Rupture of the triceps tendon. In: Morrey, B. F. (ed.): The Elbow and Its Disorders, 3rd ed. Philadelphia, WB Saunders, 2000, p. 479. 14. Morrey, B. F., and Adams, R. S.: Semiconstrained arthroplasty for the treatment of rheumatoid arthritis of the elbow. J. Bone Joint Surg. 74A:479, 1992. 15. Morrey, B. F., and Bryan, R. S.: Complication of total elbow arthroplasty. Clin. Orthop. Relat. Res. 170:204, 1982. 16. Morrey, B. F., Bryan, R. S., Dobyns, J. H., and Linscheid, R. L.: Total elbow arthroplasty—A five-year experience at the Mayo Clinic. J. Bone Joint Surg. 63A:1050, 1981.

Chapter 63 Triceps Insufficiency Following Total Elbow Arthroplasty

17. Pierce, T. D., and Herndon, F. H. The triceps preserving approach to total elbow arthroplasty. Clin. Orthop. Relat. Res. 354:144, 1998. 18. Sanchez-Sotero, J., and Morrey, B. F.: Surgical techniques for reconstruction of chronic insufficiency of the triceps. J. Bone Joint Surg. 84B:1116, 2002. 19. Schildhauer, T. A., Nork, S. E., Mills, W. J., and Henley, M. B.: Extensor mechanism-sparing paratricipital posterior approach to the distal humerus. J. Orthop. Trauma 17:374, 2003. 20. Schneeberger, A. G., Adams, R., and Morrey, B. F.: Semiconstrained total elbow replacement for the treatment of post-traumatic osteoarthrosis. J. Bone Joint Surg. Am. 79:1211, 1997.

879

21. van Riet, R. P., Morrey, B. F., Ho, E., and O’Driscoll, S. W.: Surgical treatment of distal triceps ruptures. J. Bone Joint Surg. 85A:1961, 2003. 22. Voloshin, I., Kakar, S., Kaye, E. K., and Morrey, B. F.: Complications of total elbow replacement: Systematic review of literature in the last decade. J. Am. Assoc. Orthop. Surg. 2007 (in press). 23. Wilkinson, J. M., and Stanley, D.: Posterior surgical approaches to the elbow: A comparative anatomic study. J. Shoulder Elbow Surg. 10:380, 2001. 24. Wolfe, S. W., Figgie, M. P., Inglis, A. E., Bohn, W. W., and Ranawat, C. S.: Management of infection about total elbow prostheses. J. Bone Joint Surg. 72A:198, 1990.

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Part VII Reconstructive Procedures of the Elbow

CHAPTER

64

Wear and Elbow Replacement Brian P. Lee, Robert A. Adams, and Bernard F. Morrey

INTRODUCTION Over the past decade, the reliability and success of total elbow replacement surgery has become more established. The durability of total elbow arthroplasty (TEA) for rheumatoid arthritis is now similar to that of hip replacement.2 Indications have also expanded to include the full spectrum of traumatic conditions: distal humeral nonunion,9 instability,10 ankylosis,7 established arthritis,11 and acute intra-articular, comminuted fractures in selected older patients.4,5 Until recently, wear of the polyethylene articulating surface had not been recognized as a problem or addressed in the literature. Although this may not be a practical concern in unconstrained and unlinked designs, wear of the articular polyethylene bushings in linked, semiconstrained designs is a potential issue, particularly with the evidence of the increasing longevity and improved function that these designs now have, resulting in increased use of the limb. Until recently, this specific topic has not been considered when complications with TEA are being discussed.3 This chapter focuses on our experience with the problem as the development requires or implies long-term stable fixation. Hence, there has been little in the literature regarding this problem with other designs. To address this issue, we reviewed the Mayo Clinic experience with reoperations to exchange worn bushings in the linked, semiconstrained Coonrad-Morrey TEA. Twelve of 919 TEAs reviewed (1.3%) had undergone isolated bushing exchange for wear.6 An additional six patients were diagnosed as having bushing wear on the basis of an asymmetric anteroposterior orientation of the ulnar component within the humeral yoke, although these patients did not have a revision.

CLINICAL AND RADIOLOGIC FEATURES Pain, crepitus and squeaking sounds are the most common presenting features of articular bushing wear.

Loss of range of motion is not marked, and there are no symptoms of functional instability or weakness. In our experience, the patients with post-traumatic arthritis had a higher prevalence of bushing wear (seven of 294; 2.4%) than did those with rheumatoid arthritis (five of 377; 1.4%).6 Radiographic assessment is conducted before the total elbow replacement to identify deformity and after replacement to identify signs of bushing wear, osteolysis and status of the implant. The criteria for the assessment of wear were described by Ramsey et al.10 Anteroposterior plain radiographs of the elbow in full extension made following the index arthroplasty and at the time of bushing exchange are compared. The prosthesis was designed with 7 to 10 degrees of varus-valgus laxity. A line is drawn parallel to the yoke of the humeral component, and another line is drawn parallel to the medial or lateral surface of the articular surface of the ulnar component. An angle of intersection of more than 7 degrees between these two lines indicates alteration of the bushing due to wear or plastic deformation. An angle of more than 10 degrees is considered to indicate mild to moderate bushing wear (Fig. 64-1). Of importance is that none of our patients experienced loosening of the implant because of wear. It must be emphasized the extensive osteolysis seen in the past around the ulnar component was related to osteolysis caused by loosening of a “precoat” ulnar surfaced component. These devices were implanted between 1994 and 2000. Some have confused this appearance as being caused by wear. As in the hip the proper interpretation is the implant becomes loose and the particulars associated with this are termed accelerated bushing wear (Fig. 64-2). Typically bushing wear, even when excessive, causes local osteolysis, but not implant loosening (Fig. 64-3).

SURGICAL TECHNIQUE The treatment of symptomatic wear is simply to exchange the worn articular bushings. The previous skin incision is used to explore the elbow, and the ulnar nerve is palpated. If the patient has ulnar nerve symptoms, the nerve is explored and decompressed. If the nerve is not symptomatic, it is identified proximally at the medial aspect of the triceps and is protected throughout the procedure. If the distal part of the humerus has been resected or is absent, the triceps is left attached to the ulna, the pseudocapsule is entered medially and laterally, the articulation is disengaged, and the humerus and ulna are separated. If the condyles are intact, the triceps is again reflected from the ulna according to a previously described technique. At this juncture, the anterior aspects of the medial and lateral epicondyles are removed to an extent sufficient to allow the implant locking pin to be

Chapter 64 Wear and Elbow Replacement

881

8 yr.

FIGURE 64-1

Wear of the polyethylene is measured according to the angle formed by the articulating portion of the ulnar component and the medial or lateral aspect of the humeral yoke. Angles in excess of 7 degrees indicate displacement greater than allowed by the design tolerances. When this angle is 10 degrees, mild to moderate wear is present. (With permission, Mayo Foundation.).

7° Normal 10° Partial Wear

Complete Wear > +/− 10°

+

−

FIGURE 64-2

Extensive osteolysis occurs from loose stems usually from a precoat surface, as is the case here. This appearance is not because of worn bushings. FIGURE 64-3

removed both medially and laterally (Fig. 64-4). The posterior aspects of the condyles are left intact. The medial and lateral bushings are removed from the humerus, and the bushing is removed from the ulna. The soft tissue is assessed, and a thorough débridement is carried out. If the wear is sufficient to have resulted in impingement of the metallic ulnar component on the

Extensive bushing wear at 16 years in a patient with gun shot deformity. Note limited osteolysis not involving the stems.

metallic humeral component, then black synovitis is the predominant feature (Fig. 64-5). After débridement, the implant is inspected for the integrity of the fixation and orientation to determine if revision of either implant is necessary. If there has been

882

Part VII Reconstructive Procedures of the Elbow

FIGURE 64-6

The replacement of worn bushings is considered a straightforward procedure.

Similarly, an aggressive extensor tendon release, including the distal fibers of the brachioradialis, is performed to treat a fixed valgus deformity. The triceps is reattached with use of a cruciate and transverse drill pattern, as previously described.1 Lateral

Medial

FIGURE 64-4

The condyles are preserved by removing sufficient anterior condylar bone to expose and remove the pin. (With permission, Mayo Foundation.)

FIGURE 64-5

Metallic debris causes a black discoloration of the synovium.

resorption or osteolysis at the distal aspect of the humerus or the proximal aspect of the ulna, the interface is thoroughly cleaned and is filled with polymethyl methacrylate. Fresh bushings are then inserted in the ulnar and humeral components, and the implant is coupled with the use of the pin-within-pin snap-fit articulation (Fig. 64-6). If the preoperative assessment and intraoperative evaluation indicated a fixed angular deformity that cannot be corrected passively, then the soft tissue is released to allow correction of the deformity. Thus, an extensive flexor release from the humerus is carried out for the treatment of varus deformity.

RESULTS The average age at the time of index TEA of the 12 patients who had bushing exchange was 44 years of age compared with a mean age of 62 years in those who did not undergo bushing exchange. No significant difference in hand dominance, body weight, occupation, or lifestyle was found in this small group. Radiographic assessment before index TEA in this group revealed a markedly distorted joint in nine patients, with severe rheumatoid arthritis in four, marked varus or valgus deformity of more than 10 degrees in nine, and gross dissociation (a flail elbow with loss of the distal humeral condyles) in four (Fig. 64-7). Nine of the elbows had absence of one or both distal humeral condyles. All 12 patients had an excellent or good result immediately following the index arthroplasty. Postoperative anteroposterior radiographs revealed the articulation to be at the limits of the designed angular tolerance in nine of the 12 patients, indicating significant stresses at the articulation from severe pre-existing deformity. At the time of bushing exchange surgery, no significant osteolysis or loss of fixation was present (Fig. 64-8). Isolated bushing exchange was technically successful in all of the patients. At average follow-up of 65 months, three patients underwent a second bushing exchange for wear again. All three had marked initial deformity. Two of the twelve patients had limited success due to persistent pain from ulnar nerve neuropathy. More recently, Wright and Hastings also documented bushing wear in 10 patients with the TEA of the same design.13 They identified post-traumatic arthritis,

Chapter 64 Wear and Elbow Replacement

883

A

A

B FIGURE 64-7

A, Severe elbow deformity of 50 years’ duration secondary to fracture of the humeral condyle as a child. B, Worn bushing 5 years after the surgery. The patient worked as a lumberjack against medical advice.

supracondylar nonunion, male sex, young age, and high activity level as associated factors. Importantly, these investigators also implicated failure of the “O” ring, which allows the axis pin to back out as an addition factor of accelerated bushing wear. In a series of semiconstrained TEAs for chronic dislocation of the elbow, Mighell et al8 documented one in six required bushing exchange. Further information is partly limited by the low incidence and by lack of routine stress radiographs to document the absolute wear rate. However, probably the most significant feature with the greatest prognostic

B 7 yr post exchange

FIGURE 64-8

At 12 years, the humeral bushing is worn. Note osteolysis is limited (A). Seven years after bushing exchange shows minimal wear (B).

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Part VII Reconstructive Procedures of the Elbow

importance is the presence of severe preoperative deformity at the time of index elbow replacement. In some cases, the angular deformity may even exceed the tolerance of the design but it is these very problems that can be addressed only by this type of coupled implant. Therefore, our current practice would be to extensively release soft tissue contractures to eliminate progressive deformity in such cases. It would be more appropriate to resect bone in order to lessen soft tissue tension that can result in an imbalance that differentially loads the polyethylene. When a patient presents with asymptomatic radiographic evidence of wear, the process is discussed with the patient. Typically, the problem is followed up radiographically because, in our experience, the wear debris does not cause fixation-compromising osteolysis. If a patient has pain or mechanical squeaking, then revision is offered.

CONCLUSIONS Despite the increased longevity of semiconstrained linked total elbow prosthesis and the use of these implants to treat an increasingly complex array of pathologic conditions, the prevalence of articular wear requiring reoperation is very low (1.3% in our experience of such implants inserted over a 20-year period). A higher bushing revision rate is associated with a younger patient with traumatic conditions and long established fixed deformity. The presence of substantial malrotation of components at the time of implantation, even without deformity, can also contribute to increased bushing wear.12 Isolated bushing exchange is a successful procedure. The intervention is not extensive, and morbidity is minimal when compared with that associated with the index arthroplasty. This problem is likely to receive more attention with the rapid increase in the number of TEAs performed worldwide, improved longevity of the implant, expanded indications, and increased patient activity. Attempts to mitigate the problem of wear, such as by increasing the thickness of polyethylene bushings and using cross-linked polyethylene, are being studied. At present, the need to perform adequate soft tissue release to balance the elbow alignment in patients with long-standing deformity should be emphasized, as

should cautioning patients against exceeding the recommended activity and lifting restrictions.

References 1. Bryan, R. S., and Morrey, B. F.: Extensive posterior exposure of the elbow. A triceps-sparing approach. Clin. Orthop. Relat. Res. 166:188, 1982. 2. Gill, D. R., and Morrey, B. F.: The Coonrad-Morrey total arthroplasty in patients with rheumatoid arthritis. A ten to fifteen-year follow-up study. J. Bone Joint Surg. Am. 80:1327, 1998. 3. Gschwend, N., Simmen, B. R., and Matejovsky, Z.: Late complications in elbow arthroplasty. J. Shoulder Elbow Surg. 5:86, 1996. 4. Kamineni, S., and Morrey, B. F.: Distal humeral fractures treated with noncustom total elbow replacement. J. Bone Joint Surg. Am. 86:940, 2004. 5. Kraay, M. J., Figgie, M. P., Ingils, A. E., Wolfe, S. W., and Ranawat, C. S.: Primary semiconstrained total elbow arthroplasty. Survival analysis of 113 consecutive cases. J. Bone Joint Surg. Br. 76:636, 1994. 6. Lee, B. P., Adams, R. A., and Morrey, B. F.: Polyethylene wear after total elbow arthroplasty. J. Bone Joint Surg. Am. 87:1080, 2006. 7. Mansat, P., and Morreym, B. F.: Semiconstrained total elbow arthroplasty for ankylosed and stiff elbow. J. Bone Joint Surg. Am. 82:1260, 2000. 8. Mighell, M. A., Dunham, R. C., Rommel, E. A., and Frankle, M. A.: Primary semiconstrained arthroplasty for chronic fracture-dislocations of the elbow. J. Bone Joint Surg. Br. 87:191, 2005. 9. Morrey, B. F., and Adams, R. A.: Semiconstrained elbow replacement for distal humeral nonunion. J. Bone Joint Surg. Br. 77:67, 1995. 10. Ramsey, M. L., Adams, R. A., and Morrey, B. F.: Instability of the elbow treated with semiconstrained total elbow arthroplasty. J. Bone Joint Surg. Am. 81:38, 1999. 11. Schneeberger, A. G., Adams, R. A., and Morrey, B. F.: Semiconstrained total elbow replacement for the treatment of posttraumatic osteoarthritis. J. Bone Joint Surg. Am. 79:1211, 1997. 12. Schuind, F., O’Driscoll, S., Korinek, S., An, K. N., and Morrey, B. F.: Loose-hinge total elbow arthroplasty. An experimental study of the effects of implant alignment on three-dimensional elbow kinematics. J. Arthroplasty 10:670 1995. 13. Wright, T. W., and Hastings, H.: Total elbow arthroplasty failure due to overuse, C-ring failure, and/or bushing wear. J. Shoulder Elbow Surg. 14:65, 2005.

Chapter 65 Revision of Failed Total Elbow Arthroplasty with Osseous Integrity

CHAPTER

65

Revision of Failed Total Elbow Arthroplasty with Osseous Integrity Bernard F. Morrey and Graham J. W. King

885

infection with a specificity and sensitivity of 85% and 90% respectively.11 Radiolucency of the bone-cement interface may be due to either mechanical failure or sepsis, but implant loosening is not usually associated with a septic joint unless the process is a chronic one.21 Infection of a well-fixed device is particularly bothersome, because removing the prosthesis may result in fracture of bone that poses major reconstructive problems for the surgeon, but commonly sepsis is managed with a staged reimplantation. The important consideration is to avoid excessive use of bone graft in this setting. This topic was reviewed recently by Cheung and colleagues, and is discussed in detail in Chapter 62.3

DEVICE FAILURE

INTRODUCTION A number of surgical options are available to treat failed elbow arthroplasty. In this chapter, we emphasize the indications and the surgical techniques for prosthetic reimplantation of the joint not requiring graft augmentation. Revision requiring osseous augmentation is discussed in the subsequent chapter (Chapter 66). The general problems of reimplantation for failed elbow arthroplasty are placed in perspective of alternate treatment possibilities that are more thoroughly reviewed elsewhere (see Chapters 67 and 69).

CLASSIFICATION OF FAILURE There are several ways of categorizing failed prior arthroplasty, each with different implications for treatment (Table 65-1). Failure of a nonimplantation procedure such as interposition or resection arthroplasty is a relatively straightforward matter, and the treatment and characteristics are no different from those of an acute fracture with bone loss (see Chapters 56 and 57). In this chapter, we deal with failed total elbow arthroplasty with adequate osseous integrity for a direct reimplantation and cementation. In Chapter 66, the options for osseous augmentation are discussed.18,20,24

SEPTIC FAILURE This is mentioned here to emphasize the need to exclude a septic process as the cause of implant failure. A high index of suspicion must be developed. The value of preoperative screening as with sedimentation rates and C-reactive protein (CRP) is well accepted. One recent study demonstrated a sedimentation rate over 23 mm/ hr and a CRP in excess of 13.5 mg/L correlates with

Device failure may involve the stem or the articular coupling elements of the device. High-density polyethylene articular components do have a tendency to wear,15 but this typically does not cause loosening of the implant. Because the semiconstrained implant is being used for broader indications and loosening is much less of a problem, articular wear is increasingly being recognized over long-term follow-up.10,15 Lee et al15 assessed the experience of almost 900 linked Coonrad/Morrey devices. Only 1.5% required reoperation for isolated bushing wear. The authors make the distinction between bushing wear that is managed by simply exchanging the bushing and loosening that typically occurs as a result of loosening and osteolysis that was seen principally in the precoat ulnar component design. This design has not been used for more than 7 years (Fig. 65-1). Implant fracture is an uncommon complication that usually follows excessive activity or a single significant trauma. This has occurred with the Coonrad-Morrey device owing to the stress-riser effect of the surface treatment of the titanium implant and in patients with excessive physical demands (Fig. 65-2).25 Athwal et al1 reviewed the Mayo experience with fractured components. The technique of removing wellfixed stems and reinsertion into an expansion of the cement mantle was successful in about 80% of patients. This failure mode has prompted the introduction of the stronger precoat, which, owing to the possibility of osteolysis, has been subsequently replaced in 2000 with the current plasma spray surface.

INSTABILITY With unlinked prostheses, instability is not uncommon (see Chapter 61). Delayed or chronic subluxation is associated with excessive activity, improper initial balance, or implant wear.7,21

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Part VII Reconstructive Procedures of the Elbow

Revision Options as a Function of Initial Arthroplasty Type and Osseous Integrity

TABLE 65-1

Index Arthroplasty

Osseous Integrity

Revision Options

Resection

Variably deficient humerus and/or ulna metaphysis

Insert into mature? bone; may require long flange

Fusion

Adequate

Treat as primary arthroplasty

Interposition

Adequate

Treat as primary arthroplasty

Implant failure

Distal deficiency Mild Moderate Extensive Osteolysis

Treat as primary anterior/posterior strut grafts24 Allograft prosthetic composite*20 Impaction grafting*18

A

*Strut and impaction grafting may be combined in some procedures.

If acute instability is due to ligament insufficiency or improper “balance” and does not respond to a period of immobilization, revision with a linked implant should be considered. If early dislocation is due to malpositioning of the components, immediate revision should be performed. In questionable cases, examination under fluoroscopy may show the cause of the instability and allow the management strategy to be defined (Fig. 65-3). The selection of unlinked implant has been predicated to some extent on the assumption that a reoperation or revision would prove more reliable after this type of design. Until recently, this hypothesis has not been proven. A review of Mayo’s 30-year experience with linked and unlinked implants appears to confirm this assumption but only if the revision was from an unlinked to a linked device (Fig. 65-4).16 Specifically, reoperation of all unlinked implants resulted in a more predictable outcome than did revision after all failed linked implants. However, the linked revisions were to a great extent in patients with post-traumatic arthritis. There was no difference in success of revision when only the rheumatoid patient was considered. Furthermore, it was also demonstrated that the need to revise the unlinked implant occurred at a significantly greater frequency than did the need to reoperate on a linked device (Fig. 65-5).16

B FIGURE 65-1

Osteolysis around the Coonrad/Morrey “precoat” ulnar surface component (A and B). This type of loosening is not due to bushing wear, as some have suggested.

LOOSENING The early experience with total elbow arthroplasty demonstrated loosening of the humeral component about twice as often as loosening of the ulnar component.9,12,21

FIGURE 65-2

Fracture of the ulnar component of a Mayo modified Coonrad device removed from a patient who repeatedly lifted more than 50 pounds.

Chapter 65 Revision of Failed Total Elbow Arthroplasty with Osseous Integrity

887

FIGURE 65-3

Failure of the articulation due to instability of a resurfacing implant, as seen on lateral (left) and anteroposterior (middle) radiographs. The 10-year revision is asymptomatic (right).

FIGURE 65-4

Kaplan-Meier curves of Mayo 30-year experience showing good survival with revision of a variety of unlinked designs to the linked Coonrad/Morrey implant (A). Note the very poor outcome when the unlinked was revised to another unlinked design (B). (From Levy, J. C., and Morrey, B. F.: A survivorship of unlinked and linked total elbow arthroplasty for rheumatoid arthritis: A comparative study. J. Bone Joint Surg. Am. [in press].)

This difference is not observed with the CoonradMorrey device because loosening currently occurs more often at the ulna than at the humerus.4,10,16 Pain is a typical but not a universal feature. Different expressions of failure are recognized. One is a loose implant with pain but few or no x-ray changes and no bone resorp-

tion (Fig. 65-6). The other is gross instability and obvious loosening due to bone destruction, with minimal or no pain. Particulate debris results in cortical thinning or “ballooning” of the humerus or the ulna. Resorption of a significant amount of bone can pose major problems with the reconstructive procedure, especially when the

888

Part VII Reconstructive Procedures of the Elbow

FIGURE 65-5

Kaplan-Meier curve showing markedly superior performance of the linked (A) compared with the unlinked device (B). (From Levy, J. C., and Morrey, B. F.: A survivorship of unlinked and linked total elbow arthroplasty for rheumatoid arthritis: A comparative study. J. Bone Joint Surg. Am. [in press].)

FIGURE 65-6

The patient developed pain 18 years after a Dee total elbow arthroplasty. The radiograph did not suggest loosening of the bone-cement interface; however, at revision gross loosening was observed at the humeral prosthesis-cement interface.

bone loss is complicated by fracture (Fig. 65-7). The fracture may be “silent” due to chronic thinning or acute. The latter fracture is not caused by loosening and may heal without a need for implant revision. The topic of periprosthetic fracture is dealt with in detail in Chapter 66 because strut graft is often employed in its treatment.

FIGURE 65-7

Because the grossly loose Pritchard-Walker II implant was not painful, the patient continued to use it, but marked osseous resorption was due to the foreign body wear.

TREATMENT OPTIONS AND INDICATIONS As noted earlier, if the failure requires removal of components, treatment possibilities may be categorized according to the integrity of the bone (see Chapter 70),

Chapter 65 Revision of Failed Total Elbow Arthroplasty with Osseous Integrity

resection (see Chapter 67) and interposition (see Chapter 69). All of these methods may be used to salvage failed prosthetic arthroplasty and are discussed elsewhere. Both reimplantation and nonreimplantation options depend largely on the amount of bone present (Table 65-2). Management of osseous deficiency has been discussed by Sanchez-Sotelo et al,24 and Mansat et al.,20 and is discussed in detail in Chapter 66.

INTERPOSITION ARTHROPLASTY Several types of interposition arthroplasty are described, which, if they fail, may be revised depending on the amount and quality of available bone, and the presence of sepsis. Chapter 60 discusses interposition arthroplasty, and Chapter 67 reviews nonimplantation salvage procedures for failed elbow replacement. Blaine et al2 reviewed the Mayo experience of revising failed interposition arthroplasty with the linked total elbow implant. The average Mayo elbow performance score increased from 32 to 80.4 points. The authors reported 9 of 12 (75%) satisfactory outcomes with elbow replacement following failed interposition arthroplasty.

889

• Ulnar: (1) presence of olecranon; (2) quality of periprosthetic bone; (3) presence and location of fracture. Furthermore, the revision must overcome the shortcomings of the first prosthesis or technique and the effect of the loose implant noted earlier. This usually requires a stem that bypasses any cortical weakness or fracture, provisions for adequate distal humeral or ulnar fixation, and a reliable articulation. Unless measures are taken to address these considerations, reimplantation will not be successful on a regular basis. It must be reemphasized that if reimplantation is to be considered a viable option, the mechanical or biologic causes of the initial failure must be addressed and solved by the new design and technique. The Coonrad-Morrey implant is made with 6- and 8-inch humeral stems, either of which may be used for the purpose of bypassing a shorter stemmed device, depending on the amount of available bone and the need for long-stemmed fixation (Fig. 65-8). An extended ulnar component is available for problems of proximal ulnar bone deficiency (Fig. 65-9).

REIMPLANTATION PROCEDURES Revision strategies can be predicated according to the characteristics of the failure mode. We have found the thought process used for failed femoral components after total hip replacement to be helpful in this regard. In addition to age, diagnosis, and anticipated level of activity, the factors that determine the pertinent strategy include:

General Considerations

• Humeral: (1) presence of distal humerus referable to the olecranon fossa; (2) quality of periprosthetic bone; (3) presence and location of any fracture; (4) presence of shoulder pathology possibly requiring replacement.

Revision Options as a Function of Bone Stock

TABLE 65-2 Bone Stock

Options

Adequate

Arthrodesis, resection, interposition, total elbow arthroplasty, semiconstrained prosthesis

Inadequate

Resection, allograft, total elbow arthroplasty, semiconstrained (long-flanged) prosthesis composite (total elbow arthroplasty with allograft), custom-made prosthesis

B FIGURE 65-8

A, Coonrad-Morrey implants are made with 10-, 15-, and 20-cm humeral stems. B, The 15- and 20-cm stems also are available with an extended flange (B), so routine use of custom implants is unnecessary (A).

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Part VII Reconstructive Procedures of the Elbow

FIGURE 65-9

A special long-stemmed ulnar component is used as an intramedullary rod when revising failure involving an ulnar fracture.

A

B

C

FIGURE 65-10 A, The axis of rotation of the humeral component is coincident with the anatomic axis of rotation of the normal elbow. B, With loss of all of the distal humerus to the level of the roof of the olecranon, the axis of rotation remains in its usual anatomic location. If the distal humerus is not long enough, a long flanged device is used. C, By not fully inserting the implant, additional bone deficiency may be accommodated.

Indications Reimplantation is indicated when the osseous envelope is of adequate quality to “hold” a cement bond, when circumferential integrity is present and if the prior stem length can be bypassed by two bone diameters. Noncustom Semiconstrained Design The Coonrad-Morrey

Revision

Implant

elbow replacement has in our practice been an ideal noncustom option

for the resected joint after failed total elbow arthroplasty or after trauma. The range of sizes and lengths of the humeral (see Fig. 65-8) and ulnar (see Fig. 65-9) components is a most useful feature. Furthermore, the anatomic axis of rotation is restored even with resection at the level of the roof of the olecranon fossa (Fig. 65-10). Shortening of the humerus of up to 2 cm proximal to the olecranon fossa is accepted without resorting to allograft augmentation or

Chapter 65 Revision of Failed Total Elbow Arthroplasty with Osseous Integrity

the need for a custom implant.8,13,23 Long-flanged implants have been very valuable because they allow various depths of insertion. Overall, up to 8 cm of distal humerus deficiency can be addressed with reimplantation of an off-the-shelf device. If the bone loss is greater than the long flange can accommodate, either a custom implant or a component reconstruction with an interposed distal humeral allograft may be considered (see Chapter 66). The particular value of the design of the Coonrad-Morrey device is that the intramedullary cement fixation is enhanced by an extramedullary bone graft placed behind the flange. This flange design resists forces that tend to displace the implant posteriorly as well as rotatory forces (Fig. 65-11). For most applications of distal deficiency we have resorted to using a longer flange, grafting bone behind the flange, and inserting the implant to less than its full depth (Fig. 65-12).

PREOPERATIVE PLANNING Successful intervention requires careful planning to address deficiencies, to anticipate potential complications, and to make available all the options that may be required to ensure a successful outcome. The

A

B

891

broad scope of preoperative planning includes these considerations: 1. Assessment of bone quality, the potential for injury to the bone at the time of revision, and the contribution of the native bone to fixation of the revised device. We have classified distal humeral osseous deficiency according to involvement of the columns (Fig. 65-13). This is important as a consideration of the viability of a resection salvage procedure; however, more important is the quality of the periprosthetic bone and the presence or absence of fracture. 2. Ensuring availability of the appropriate array of tools necessary to remove both the components and the cement, especially if the device was inserted at another institution. 3. Preparation of the iliac crest or availability of banked bone if bone supplementation is required. 4. Ensuring that external fixation or distraction devices are available, if needed. 5. Having the prosthesis available in several sizes if reimplantation is considered. A long-stemmed device is desirable for many revisions.5,21 6. Assessing the possible need for special soft tissue coverage.

C

FIGURE 65-11 A, An anterior flange is an integral part of the Mayo modified Coonrad implant. B, A bone graft is routinely incorporated between this flange and the humerus. C, Studies have shown this resists posterior, axial and rotatory stresses to the bone cement interface, even after distal humeral resection (B).

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Part VII Reconstructive Procedures of the Elbow

FIGURE 65-12

Distal humeral deficiency (A) can be accommodated by the long-flanged device, which is inserted only to the depth necessary to restore effective muscle contracture (B).

A

B FIGURE 65-13

C

D

A useful classification of bone loss. A, Type I involves the articulation, but excellent bone stock remains. B, In type II, both supracondylar columns are intact. C, In type III, one or the other supracondylar column and articular surface are gone. D, In type IV, the entire articulation and supracondylar columns are deficient at the level of or above the olecranon fossa. (From Morrey, B. F., Adams, R. A., and Bryan, R. S.: Total elbow replacement for post-traumatic arthritis. J. Bone Joint Surg. 73B:607, 1991.)

Chapter 65 Revision of Failed Total Elbow Arthroplasty with Osseous Integrity

SURGICAL TECHNIQUE Exposure Skin coverage in this group of patients is sometimes compromised, even at the time of the initial procedure. Use of the previous incision is recommended, if possible. Skin flaps should be kept to a minimum (see Chapter 36). A local or a remote pedicle flap may be necessary to ensure adequate wound healing. Preoperative discussion with a microsurgeon or a plastic surgeon is particularly helpful if any question exists.

Ulnar and Radial Nerves The ulnar nerve must “always” be identified in the revision procedure. In many instances, it will already have been transferred anteriorly; nevertheless, it must be properly identified and protected during the procedure. If ulnar neuropathy is already present and is a significant problem, decompressing the nerve and freeing it of scar tissue has been rewarding in a number of patients. If it is asymptomatic, simply identifying and avoiding injury is appropriate. The radial nerve is identified in all instances and is exposed and protected when cement is removed from the humerus. The radial nerve is vulnerable if the cortex is violated or even from heat polymerization or ultrasonic removal of polymethyl methacrylate. Zook et al29 emphasized the vulnerability of the radial nerve when revising a humeral component. These authors observed that the radial nerve can erode through osteolytic bone, making it extremely vulnerable when removing the intramedullary membrane.

Lateral

893

Triceps Instead of reflecting the triceps from the olecranon, if at all possible, a true triceps-sparing approach is used and the triceps is not detached from the ulna. This approach is discussed in detail in Chapter 7. The triceps is elevated both medially and laterally from the humerus after the ulnar and radial nerves have been protected. The prosthetic device is identified, and the coupling mechanism is removed (Fig. 65-14). The humerus and the ulna are then dissociated. The humerus is usually delivered through the lateral margin of the triceps, protecting the ulnar nerve. In some instances, the humerus may be easier to expose from the medial margin of the triceps, in which case the ulnar nerve must be carefully released more proximally, protected, and brought either laterally or medially to the humerus. If a triceps-sparing approach has been used, the ulna must be rotated axially with some flexion and extension so that the surgeon can visualize and palpate the humerus and the ulna (Fig. 65-15). We have used this approach successfully for the last 8 years. If, however, there is less experience with elbow exposure in several or the major lesion is at the ulna, or the ulna is angulated, the triceps must be reflected to ensure adequate visualization.

Soft Tissue It is increasingly being recognized that the soft tissue must be “balanced.” The soft tissue envelope about the joint is no less important at the time of the revision. Hence, we do not feel obliged to reattach the flexor or extensor muscle groups to the distal humeral shaft

FIGURE 65-14 By exposing either margin of the triceps mechanism, most artificial implants can be disarticulated to afford adequate exposure for revision of the device without removing the triceps from the ulna. (With permission from the Mayo Foundation.)

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Part VII Reconstructive Procedures of the Elbow

1–2 d

FIGURE 65-15

Exposure of the subcutaneous border of the ulna and the lateral margin of the proximal humerus allows these areas to be palpated and protects against osseous penetration. It is particularly important in the humerus to avoid possible injury to the radial nerve. (With permission from the Mayo Foundation.)

d

FIGURE 65-16 Removing a trapezoid-shaped window from the posterior aspect of the humerus allows access to the cement stabilizing the implant.

FIGURE 65-17 Eccentric reaming of well-fixed cement can cause cortical violation.

during distal humeral resection. Loss of attachment of the flexor or extensor muscle mass goes unnoticed by the patient.

REVISING THE HUMERUS The need for revision of well-fixed implants is uncommon unless osteolyses is present. Nonetheless, well-fixed humeral implants can be reliably removed to date by performing a truncated trapezoid type of osteotomy in the posterior aspect of the cortex (Fig. 65-16). This allows the removal of cement around the implant. The implant is then safely removed without fracturing the humerus. After cement has been removed, bone is reapplied. If the revision device employs a flange, the flange engages the anterior cortex; thus, the removal of the posterior bone is well tolerated. It is important to leave both medial and lateral humeral condyles in any instance in which the humerus is removed because this allows subsequent

resection arthroplasty should the elbow become infected. Cement removal is performed with osteotomes or with an ultrasonic device. Great care must be taken to avoid radial nerve injury in any instance in which the humeral implant is being revised. We personally have had several injuries to this nerve even with efforts to identify and protect it. We have found that one helpful technique is to place a 3-mm drill through well-fixed cement and into the medullary canal. A guide pin is then introduced into the hole made in the cement, and the cement is removed by serial flexor flexible reamers. This may then be further expanded with burrs, ultrasonic devices, or osteotomes. However, if the drill is not placed central through the cement and down the canal, eccentric reaming can still violate the cortex and damage the nerve (Fig. 65-17). In this instance, use of an ultrasonic device is recommended. Once again, great care is made to avoid pene-

Chapter 65 Revision of Failed Total Elbow Arthroplasty with Osseous Integrity

tration of the humeral cortex, particularly in the region of the radial nerve.

LOOSE PROSTHESES A loose prosthesis is easily removed, but all or some cement may be left. If reimplantation is to be performed, the cement must be removed very carefully, or cortical penetration or fracture may occur. In some instances, when well-fixed cement is left, the canal is expanded with a high-speed burr. More recently, an ultrasonic device has proved very effective in removing cement and is less likely to damage bone. In the presence of infection, all cement must be removed; the distal humerus may be fractured intentionally or unintentionally in the process.

895

remove cement and perform the needed reconstruction with less risk of penetrating the cortex (Fig. 65-18).

Fractured Component A specific technique is required in those in which an implant has fractured (see Fig. 65-2). The well-fixed portion of the stem is freed of cement with a high-speed “pencil” burr. If the fractured component cannot be reached with needle-nose type pliers, then a controlled osteotomy as described earlier, is carried out. Once the stem has been removed, if the cement remains well fixed to the bone, the cement is expanded in such a way as to receive the stem. A simple recementing and reinsertion of the implant is carried out. Cerclage wire is employed to stabilize an osteotomy.

Closure Well-Fixed Prostheses If the prosthesis has not become loose, removing it may result in some bone loss or in fracture. To minimize damage to the bone, adequate exposure of the distal humerus should be achieved. Removing a trapezoid shape of cortical bone posteriorly allows access to the cement and removal of the humeral stem (see Fig. 6516). Removing as much cement as possible allows the device to be removed more easily. A pin placed across the yoke allows easy removal with the hip extraction devices. Once the prosthesis is removed, if the cement is firmly fixed to bone, the cemented mantle is expanded to receive the revision device. However, no attempt is made to remove cement that is well fixed and that does not interfere with reinsertion.

REVISING THE ULNA The most important point to make about ulnar component revision is adequate exposure. This is readily accommodated, as the ulna is subcutaneous. Hence, exposure is “free” and the bone should be exposed or extensively as needed. With well-fixed implants, the ulna may also be osteotomized. A linear saw cut is made medially approximately three quarters of the distance of the length of the implant. The blade cuts not only the bone but also the cement. An osteotome is used to pry the cement from the implant. If the ulna fractures, it may be reliably fixed to circlage wires. The canal is prepared as described earlier for the humerus. A drill bit is placed through the intact cement, and the canal is enlarged with serial reaming. Attention is paid to the bowing of the ulna, which occurs about 5 cm distal to the coronoid. It is extremely difficult to avoid a small defect in the ulna, but this is usually of no consequence. Yet, it should be avoided if at all possible. Extensive subcutaneous exposure allows palpation of the cortex, which helps to

Regardless of the particular revision option selected, the triceps should be left attached to the ulna when possible. If it is reflected, it should be attached to bone with the technique described in Chapter 53. The tourniquet is deflated to allow meticulous hemostasis, and the skin is carefully inspected. If there is any question about the adequacy of the cutaneous circulation, the elbow is splinted in extension for 3 to 4 days and then reinspected. The decision to drain the wound turns on the amount of bleeding and the quality of the skin. If necessary, an extension cast or splint may be used for 3 to 4 weeks.

POSTOPERATIVE MANAGEMENT If reimplantation has been performed, careful inspection of the skin after 3 days and initiation of motion is recommended. The elbow is rested in a molded splint when

FIGURE 65-18 The subcutaneous nature of the ulna allows safe and easy exposure for a host of revision techniques.

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Part VII Reconstructive Procedures of the Elbow

not being actively exercised by the patient. If marked swelling is present, motion is deferred. If the bone is cracked or if an allograft has been used, protection in a cast brace for 4 to 8 weeks does not compromise the range of motion eventually achieved. To emphasize, if healing of the soft tissue is in question, the arm is simply rested in an extension splint or a cast for 2 to 4 weeks. No formal therapy is prescribed, but activities of daily living are encouraged.

was a satisfactory device and a fairly reliable procedure.27 Others have documented a short-term follow-up with approximately a 50% satisfactory and 50% unsatisfactory outcomes after 14 revision procedures. These authors also use an unlinked implant to revise the failed unlinked device.6

MAYO EXPERIENCE Initial Experience

RESULTS Several studies have emerged documenting the outcomes of revision procedure. One recent study with the use of a linked device for a revision of both linked and unlinked implants report a 5-year survival rate of 64%. Eleven of the 30 patients in this series ultimately required reoperation.26 The successful revision of the unlinked implant with yet another unlinked implant was reviewed by Van der Lugt et al.28 These authors revealed eight of 24 aseptic failures, with two of 24 becoming infected. Overall, however, the 5-year success rate was considered to be 74%, with the revision implants remaining in situ. A report from the Scandinavian experience of 23 patients revised with a linked implant estimated a 5-year survival of 83% using the Coonrad/Morrey implant. The study concluded that this

A study of 10 years’ experience with 33 consecutive revision elbow arthroplasties at our institution, all of which used some version of the Coonrad implant, was reported in 1987.22 All patients were evaluated at least 3 years after surgery (average follow-up 61 months, range 3 to 13 years). The range of motion averaged 25 to 130 degrees of flexion, 50 degrees of pronation, and 60 degrees of supination. Complications developed in 20 patients (67%). Three patients incurred an infection, and prosthesis loosening occurred in seven. Eleven (33%) required reoperation. At the time of that review, 55% of the initial revision elbows were still in place and were considered to have satisfactory results. During the course of this study, an additional surgical procedure was performed on 11 elbows. At the time of last review, 73% of all of the elbows were considered satisfactory by current radiographic and clinical standards.22

11 yrs.

FIGURE 65-19

A

B

A grossly loose Mayo implant (A) was successfully managed at 11 years by reinsertion of a 150-cm Coonrad/Morrey implant (B).

Chapter 65 Revision of Failed Total Elbow Arthroplasty with Osseous Integrity

Subsequent Experience A subsequent assessment of our 15-year experience using the Coonrad-Morrey device exclusively as a revision implant was reported 10 years ago by King and associates.14 The use of the “noncustom-flanged” device has increased the success rate: 38 of 41 (93%) elbows were functional at an average of 6 years after surgery. Although 14 (35%) had cortical penetration at revision in this series, the advent of ultrasonic cement removal has decreased the frequency of this problem in recent years. Of concern, three patients had injury to the radial nerve, which in two was due to extravasation of cement from a cortical defect and in one occurred during cement removal from the humeral canal with power instruments. Two had revision for bushing wear, each at 6 years, and two others had aseptic loosening due to particulate debris from the plasma-sprayed surface. The mean Mayo Elbow Performance Score improved from 44 ± 17 points preoperatively to 87 ± 16 points at the latest follow-up, results similar to those reported for primary arthroplasty with this implant. The data from this study indicated that when possible, prosthetic reimplantation is a viable option for revision of failed total elbow arthroplasty. If the patient is young, more than one revision may be necessary. The strategies discussed earlier have in general proven to be successful, at least in the short to intermediate term.

CURRENT EXPERIENCE REVISITED We are currently in the process of reassessing the experience with reinsertion of implants with recementing and reinserting the implant in intact bone (Fig. 65-19).19 The preliminary results of 39 procedures indicate just less than a third required another operation within 5 years. In some instances, the failure of this technique is predicated on the poor quality of the bone, which can be anticipated preoperatively. Based on this study, reimplantation in the face of poor quality is associated with both loosening and fracture and should be avoided.

5.

6.

7.

8.

9.

10.

11.

12. 13. 14.

15.

16.

17.

References 1. Athwal, G. S., and Morrey, B. F.: Revision total elbow arthroplasty for prosthetic fracture. J. Bone Joint Surg. 88:2017, 2006. 2. Blaine, T. A., Adams, R., and Morrey, B. F.: Total elbow arthroplasty after interposition arthroplasty for elbow arthritis. J. Bone Joint Surg. 87A:286, 2005. 3. Cheung, E. V., Adams, R. A., and Morrey, B. F.: Reimplantation of a total elbow prosthesis following resection arthroplasty for infection. J. Bone Joint Surg. 90A:589, 2008. 4. Cil, A., Veillette, C. J., Sanchez-Sotelo, J., and Morrey, B. F.: Linked elbow replacement: A salvage procedure for distal

18.

19.

20.

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humeral nonunion. J. Bone Joint Surg. Am. 2008 (in press). Coonrad, R. W.: Seven-year follow-up of Coonrad total elbow replacement. In Inglis, A. E. (ed.): Upper Extremity Joint Replacement (Symposium on Total Joint Replacement of the Upper Extremity, 1979). St. Louis, C.V. Mosby Co., 1982. Ehrendorfer, S.: Elbow revision arthroplasty in the situation of bone loss using an unlinked long-stem prosthesis. J. Hand Surg. 24A:1337, 1999. Ewald, F. C., Scheinberg, R. D., Poss, R., Thomas, W. H., Scott, R. D., and Sledge, C. B.: Capitellocondylar total elbow arthroplasty: two- to five-year follow-up in rheumatoid arthritis. J. Bone Joint Surg. 62A:1259, 1980. Figgie, H. E., Inglis, A. E., and Mow, C.: Total elbow arthroplasty in the face of significant bone stock or soft tissue losses: preliminary results of custom-fit arthroplasty. J. Arthroplasty 1:71, 1986. Figgie, H. E., Inglis, A. E., Ranawat, C. S., and Rosenberg, G. M.: Results of total elbow arthroplasty as a salvage procedure for failed elbow reconstructive operations. Clin. Orthop. Relat. Res. 219:185, 1987. Gill, D., and Morrey, B. F.: The Coonrad-Morrey total elbow arthroplasty in patients who have rheumatoid arthritis: A 10- to 15-year follow-up study. J. Bone Joint Surg. 80:1327, 1998. Greidanus, N. V., Masri, B. A., Garbuz, D. S., Wilson, S. D., McAlinden, M. G., Xu, M., and Duncan, C. P.: Use of erythrocyte sedimentation rate and C-reactive protein level to diagnose infection before revision total knee arthroplasty. A prospective evaluation. J. Bone Joint Surg. 89:1409, 2007. Inglis, A. E.: Revision surgery following a failed total elbow arthroplasty. Clin. Orthop. Relat. Res. 170:213, 1982. Inglis, A. E., and Pellicci, P. M.: Total elbow replacement. J. Bone Joint Surg. 62A:1252, 1980. King, G. J. W., Adams, R. A., and Morrey, B. F.: Total elbow arthroplasty: revision with use of a non-custom semiconstrained prosthesis. J. Bone Joint Surg. 79A:394, 1997. Lee, B. P., Adams, R. A., and Morrey, B. F.: Polyethylene wear after total elbow arthroplasty. J. Bone Joint Surg. 87A:1080, 2005. Levy, J. C., Loeb, M., Chuinard, C., Adams, R. A., and Morrey, B. F.: Effectiveness of revision following linked versus unlinked total elbow arthroplasty. (in press). Levy, J. C., and Morrey, B. F.: A survivorship of unlinked and linked total elbow arthroplasty for rheumatoid arthritis: A comparative study. J. Bone Joint Surg. Am. (in press). Loebenberg, M. I., Adams, R. A., O’Driscoll, S. W., and Morrey, B. F.: Impaction grafting in revision total elbow arthroplasty. J. Bone Joint Surg. 87A:99, 2005. Malone, A., Sanchez-Sotelo, J., Adams, R., and Morrey, B.: Revision of total elbow arthroplasty by exchange cementation. (Submittion for publication, 2008). Mansat, P., Adams, R. A., and Morrey, B. F.: Allograftprosthesis composite for revision of catastrophic failure of total elbow arthroplasty. J. Bone Joint Surg. 86A:724, 2004.

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21. Morrey, B. F., and Bryan, R. S.: Complications of total elbow arthroplasty. Clin. Orthop. Relat. Res. 170:204, 1982. 22. Morrey, B. F., and Bryan, R. S.: Revision total elbow arthroplasty. J. Bone Joint Surg. 69A:523, 1987. 23. Rosenfeld, S. R., and Anzel, S. H.: Evaluation of the Pritchard total elbow arthroplasty. Orthopedics 5:713, 1982. 24. Sanchez-Sotelo, J., O’Driscoll, S., and Morrey, B. F.: Periprosthetic humeral fractures after total elbow arthroplasty: Treatment with implant revision and strut allograft augmentation. J. Bone Joint Surg. 84A:1642, 2002. 25. Schneeberger, A. G., Adams, R., and Morrey, B. F.: Semiconstrained total elbow replacement for the treatment of posttraumatic arthritis and dysfunction. J. Bone Joint Surg. 79A:1211, 1997.

26. Shi, L. L., Zurakowski, D., Jones, D. G., Koris, M. J., and Thornhill, T. S.: Semiconstrained primary and revision total elbow arthroplasty with use of the Coonrad-Morrey prosthesis. J. Bone Joint Surg. 89A:1467, 2007. 27. Sneftrup, S. B., Jensen, S. L., Johannsen, H. V., and Sojbjerg, J. O.: Revision of failed total elbow arthroplasty with use of a linked implant. J. Bone Joint Surg. 88B:78, 2006. 28. van der Lugt, J. C., and Rozing, P. M.: Outcome of revision surgery for failed primary Souter-Strathyclyde total elbow prosthesis. J. Shoulder Elbow Surg. 15:208, 2006. 29. Zook, J., and Ward, W. G. Sr: Intraosseous radial nerve entrapment complicating total elbow revision. J. Arthroplasty 16:919, 2001.

Chapter 66 Revision of Failed Total Elbow Arthroplasty with Osseous Deficiency

CHAPTER

66

899

IMPACTION GRAFTING INDICATIONS

Revision of Failed Total Elbow Arthroplasty with Osseous Deficiency Bernard F. Morrey and Joaquin Sanchez-Sotelo

INTRODUCTION As might be expected, it is clear that the most important distinction to make when planning a revision procedure is the status of bone; that is, is the failure with an intact or compromised osseous structure? If osseous integrity is compromised, what is the extent and nature of this feature? There are several expressions of osseous deficiency. These include (1) deficient length, resulting from absent distal humerus or proximal ulna; (2) compromised bone quality secondary to osteolysis characterized by ballooning of an intact cortex; and (3) periprosthetic fracture. We have classified the periprosthetic fracture as proximal (I) (metaphyseal), with stem involvement (II), or past the stem (III) (Fig. 66-1). From a revision standpoint, the type II fracture involving the stem or a type III fracture proximal or distal to the tip of the stem are of greatest significance. Because the rationale and technique of revision have been covered in detail in Chapter 65, herein we describe three techniques that are used for reimplanation revision following failed total elbow arthroplasty in the face of osseous deficiency. These techniques include impaction grafting, allograft strut grafting, and allograft prosthetic composite. Obviously, impaction grafting and strut grafting can be used in conjunction with these other techniques as well. Implant selection is an important issue. Some have employed unlinked devices in some cases of revision with osseous compromise.4 Others have employed custom designs for such problems.5 We believe that these problems require a linked implant with multiple sizing options.

Osteolysis with or without associated fracture. This technique can be used in conjunction with strut grafting, particularly when fracture or bone distortion is present.

SURGICAL TECHNIQUE The exposure is routine. As in all revisions, it is imperative that the ulnar and radial nerve be identified and protected. Bone preparation follows the same basic steps: 1. All membranous tissue associated with the osteolytic expansion is removed. Note: The radial nerve is vulnerable in those with osteolysis extending to the spiral groove and may be injured when removing the membrane.14 2. The normal medullary canal is identified. 3. A revision system (Zimmer, Warsaw, IN) allows execution of the impaction technique. The “tube with the tube” system is employed (Fig. 66-2). 4. The inner tube is inserted through the outer tube. The smaller tube should extend at least two diameters into normal host bone. The outer tube should extend the length of the osteolytic portion. 5. Allograft or autograft that has been through a bone mill or morcellized bone with fragments measuring 2 to 4 mm are tamped or impacted tightly around the outer tube. Serial tamps have been designed to allow this to be done effectively and efficiently. 6. The cement is mixed in the cartridge and the cartridge is screwed onto the adapter of the inner tube. 7. Cement is delivered into the host bone for the distance (D), which is equal to at least two diameters of the canal width. 8. The inner tube is withdrawn for a distance (D) so as to align with the outer tube and both the inner and outer tubes are then withdrawn while cement is being delivered to the canal formed by the vacated and larger tube. 9. A bone graft is placed behind the flange. This bone graft extends past the expanded osteolytic region if there is a fracture or distortion at the junction between the osteolytic and the host bone interface. 10. The implant is then inserted through the cement channel and into the host bone. Pearl. Care is taken to tightly impact the cancellous bone to avoid collapse of the void left by removing the outer tube. Furthermore, the cement is injected while in a relatively viscus state to allow better intru-

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Part VII Reconstructive Procedures of the Elbow

sion into the cancellous bed and to allow more controlled insertion of the stem.

Type III

RESULTS The value of impaction grafting was described originally for acetabular deficiencies by Schreurs et al.13 A 20-year experience with impaction grafting and cemented acetabular component revealed excellent long-term results as well as biopsy evidence of viability and incorporation of the impacted graft. This provides a rationale and a basis for the application at the elbow. We have recently reviewed our experience with 12 patients undergoing revision elbow arthroplasty using an impaction grafting technique between the years 1993 and 1997.9 The average surveillance period was 6 years, with a minimum 2-year follow-up. Recognizing that this represents a salvagetype revision, at the time of last follow-up, eight were intact after the index procedure (Fig. 66-3). In addition, two other patients underwent revision because of loosening and a third required revision due to a subsequent failure of the unrevised ulnar component. One patient developed an infection. Of the eight remaining patients, marked radiographic improvement was observed. At the

Type II

Type I

Type III

MAYO CLASSIFICATION OF PERIPROSTHETIC FRACTURE

FIGURE 66-1

Mayo Classification of periprosthetic fractures about the elbow. The types II and III are typically managed with strut grafting.

D

D

A

B FIGURE 66-2

C

D

E

The technique of impacting grafting. A, A smaller diameter tube is inserted through a larger diameter tube and extends past the larger diameter tube for a distance (D) by approximately 2 cortical diameters into the normal host bone. The outer diameter tube is inserted to the depth of the osteolytic segment. B, Small chips of cancellous bone are tightly impacted around the outer diameter tube. C, The cement cartridge is attached to the inner diameter tube, which is withdrawn to the level of the larger outer tube while cement is being injected. D, At this point, both tubes are withdrawn together while cement continues to be delivered through the inner tube. E, The implant is inserted through the cement and impacted graft composite and into normal host bone.

Chapter 66 Revision of Failed Total Elbow Arthroplasty with Osseous Deficiency

901

BONE STRUTS We have adopted the excellent experience of strut reconstruction about the hip, as popularized by Gross,6 for application at the elbow. The results have been gratifying.

INDICATIONS In type II or III periprosthetic fractures, bone struts are used to reconstruct distal or proximal bone deficiency and as bone graft to be placed behind the anterior flange.

SURGICAL TECHNIQUE

A

After the appropriate exposure, once again the nerves are identified. For the strut grafting of the humerus, it is particularly important to identify the radial nerve because wires are routinely passed under the nerve in order to provide fixation of this graft more proximally.

TECHNICAL NOTES

B FIGURE 66-3

A, A patient with marked osteolysis of the distal humerus with gross loosening. B, Seven years following impaction, grafting shows a well-fixed implant with no evidence of loosening.

final follow-up after the additional revision in three patients, five were excellent and four were good with three fair results. This suggests that impaction grafting is a viable option as a salvage for the difficult revision with poor bone quality due to osteolysis.

1. The placement of the grafts is made easier by tapering the edges with a burr and allowing them to slide down the anterior and posterior aspects of the humerus. 2. Because patients who have received strut grafts are typically osteoporotic, a second posterior strut graft is often needed to “back up” the anterior strut to avoid the wire cutting through the soft bone (Fig. 66-4). 3. We prefer to use a humeral strut graft, and ideally, a portion of the curvature of the strut is retained because this provides enhanced stability to the construct when placed under compression of a cerclage wire. For periprosthetic fracture, the goal is to bypass the fracture by a sufficient amount to provide stability from the compression of the onlay struts by the circumferential wire. 4. Signficant deficiencies of 8 cm can be accommodated by a strut that is securely fixed to the host bone with a distal extension of up to 4 cm. This allows the long flange to engage the strut and still engage the host bone as well (Fig. 66-5). 5. Care is taken when passing the proximal wires to identify and slide under the radial nerve. Wire knots are always placed posteriorly or posteromedially to avoid the radial and ulnar nerves. 6. We prefer at least two and ideally three cerclage wires proximal and distal to the fracture. Pearl. The cerclage wires are placed loosely around the humerus. The strut grafts are then fashioned and inserted anteriorly and posteriorly. The struts are stabilized by loosely tightening the cerclage wire.

Part VII Reconstructive Procedures of the Elbow

FIGURE 66-4

With osteoporotic bone, the bone strut is best applied as a pair to avoid wire cut through and to enhance stability. To avoid a stress riser effect, care is taken to avoid having the grafts end at the same level of the host bone.

6 cm

3 cm

A

8 cm total

902

2 cm

2 cm

B

FIGURE 66-5 A, Deficiencies up to 8 cm in length can be addressed by a 4-cm extension of graft to span the anterior defect and by accepting a 2-cm shortening of the extremity. B, The distal 3 cm of the humerus is not required for proper position and fixation.

Chapter 66 Revision of Failed Total Elbow Arthroplasty with Osseous Deficiency

D

FIGURE 66-6

The so-called “Shuck” test assists in determining the proper depth of insertion of the humeral component in the absence of distal humerus. The humeral implant is inserted down the canal and is coupled with the ulnar trial. At 90 degrees of flexion the forearm is then displaced distally. The position of the humeral component defines the optimum position for implant insertion.

7. The implant is then inserted into the cemented canal with premeasurement as to the appropriate depth of insertion, which dictates the distal extension of the anterior strut length. Pearl. The depth of insertion of the humerus is determined by the “Shuck” test. The trial implant is inserted and with the elbow at 90 degrees the ulna is separated as much as allowed by the soft tissue. This position determines the correct depth of insertion (Fig. 66-6). 8. The technique with the ulna is similar to that with the humerus. On occasion, a double strut construct is employed. One unique feature of ulnar strut grafting is that this can be used as an extension proximally to provide a lever arm against which the triceps may function more effectively.

RESULTS Some employ bone grafting techniques to reconstruct the distal condylar portion of the humerus, if this bone is required by the implant design.7 Experience using strut grafts at the elbow is relatively limited. The Mayo experience with these strut grafts for periprosthetic fractures of the humerus was reported by Sanchez-Sotelo in 2002.12 Between 1991 and 1999 at the Mayo Clinic, 11 periprosthetic fractures with a loose humeral component were managed by two parallel strut grafts, as described earlier (see Fig. 66-4). The average follow-up was 3 years but ranged from 0.75 years to 8 years. At the time of final assessment,

903

there were no implant failures. Seven of eight patients with an intact reconstruction had a functional arc and no sign of pain (Fig. 66-7). One patient did have limited motion and moderate pain. The complications included one additional undisplaced humeral periprosthetic fracture that failed to heal with closed treatment, one olecranon fracture, one ulnar nerve palsy, and one case of triceps insufficiency. It was concluded that the use of a strut graft can be an effective means of reconstructing the patients with a type II or III periprosthetic fracture. At the ulna, Kamineni et al8 documented the outcome of 22 patients so treated (Fig. 66-8). For the most part, these series represented a salvage procedure because they had an average of two and one-half prior procedures involving the elbow joint. Among 22 patients, the Mayo Elbow Performance score improved from 34 to 79 points. Overall some incorporation of the strut graft occurred in 91%, which reflects the approximate 90% satisfactory rate with the procedure.

ALLOGRAFT PROSTHTETIC COMPOSITE The use of structure allografts is limited at the elbow since the outcomes are considered unreliable.1-3 On the other hand, the allograft prosthetic composite is a wellrecognized technique for massive reconstruction of hip and knee deficiencies often associated with tumor resections.10 At the elbow, the technique of allograft prosthetic composite has changed dramatically. Initially we performed procedures similar to those described for the hip and knee, with a step-cut type of interface between the allograft and the host bone. This experience was reported by Mansat et al11 and is considered our early-phase experience.

INITIAL MAYO EXPERIENCE Thirteen patients were reviewed who underwent allograft prosthetic composite.11 With an average of 42 months’ follow-up, the Mayo Elbow Performance score was excellent for four, good for three, fair for one, and poor for five (Fig. 66-9). Nine of the 13 patients had minimal pain. The mean arc of flexion was 97 degrees. There were seven complications affecting seven elbows. Five of the seven, however, required revision procedures. Deep infection was the most serious complication, occurring in four elbows. There were two nonunions occurring at the allograft-humeral junction. As a result of this experience, we entered a period in which the allograft prosthetic composite was avoided in favor of the strut grafts described earlier. However, a modification of the fixation has provided a new perspective.

904

Part VII Reconstructive Procedures of the Elbow

Preop

A

B

C

1 yr

FIGURE 66-7

A, A Mayo type H2 periprosthetic fracture. Strut grafts applied to the distal humerus are secured with monofilament wire. The anterior strut is used to provide fixation for stability to the anterior flange of the implant. The posterior strut enhances the stability of the construct and avoids the wire from cutting through the osteoporotic bone. Anteroposterior (B) and lateral radiographs (C) at 1 year.

A

B FIGURE 66-8 A, Excessive ulnar deficiency. B, Problem was managed by dual onlay strut grafts. Note that the proximal extension of the ulnar strut provides a lever arm for the extensor mechanism in an attempt to enhance the extension moment.

Chapter 66 Revision of Failed Total Elbow Arthroplasty with Osseous Deficiency

B

C

A

FIGURE 66-9

D

2 yrs.

Traditional allograft prosthetic composite reconstruction. The proximal ulna is deficient (A) and resected (B). The junction of the allograft composite is secured with metallic plates (C and D).

905

906

A

C

Part VII Reconstructive Procedures of the Elbow

B

FIGURE 66-10 A, An example of a side-to-side allograft prosthetic composite. Loss of the proximal one third of the ulna is treated with side-to-side application of fibular allograft (B and C). The broad surfaces of the allografts reliably heal to the broad surface of the host bone.

Chapter 66 Revision of Failed Total Elbow Arthroplasty with Osseous Deficiency

907

B A

C

FIGURE 66-11 Several APC constructs are currently being employed. A, “Side-to-side” anastomosis in which the tubular allograft is secured to the tubular host bone by cerclage wires. B, A tubular allograft secures the implant, but the allograft is altered by removing a portion of the circumferential cortex, allowing a continuation of the remaining cortex to serve as a strut along the host bone. In many instances, a longer implant is employed so that it can traverse the circumferential allograft and then be inserted down the medullary canal of the host bone. C, In some instances, a ballooned cortex that is not felt to be adequate for impaction grafting is filled with circumferential allograft with the host bone securely wired to the allograft with anticipation that the host will heal to the allograft and the allograft will serve as secure stabilization of the cemented implant.

CURRENT MAYO TECHNIQUE

MAYO EXPERIENCE

The difficulty and the time consumption of precise stepcuts prompted the concept of a “side-to-side” application. With this logic, the entire circumferential allograft is applied to the host bone and secured with cerclage wires. This approach has been used effectively in those individuals with marked bone loss and in whom the above-mentioned techniques would not be adequate (Fig. 66-10). Several variations have been developed (Fig. 66-11). One modification of this technique has been developed by employing the circumferential allograft to stabilize the implant, but the distal or proximal extension is modified as a continuation of a strut type graft (Fig. 66-12). There is some concern as to the strength of the interface between the allograft and the host bone but there is a high likelihood of healing of the strut graft. A third and final version of fixation is to telescope the circumferential allograft into the expanded host bone (Fig. 66-13).

We are currently investigating the outcome of these various modifications of the allograft prosthetic composite. Our impression to date is that this is a more reliable method to address these difficult salvage elbows. It is our clinical impression that the outcomes are better and the complication rate is lower with the approach described earlier.

SUMMARY The three methods described earlier do provide a reasonably reliable set of options for difficult salvage situations. However, it should be emphasized that these do not represent routine revisions but salvage-type procedures, and their high complication rates and potential for failure must be appreciated.

908

Part VII Reconstructive Procedures of the Elbow

A

C

B

D

FIGURE 66-12 A and B, Patient with loss of distal humerus and proximal ulna. The problem was resolved with strut grafting on the humerus (C and D). A type II allograft prosthetic composite was employed in which the extended ulnar component traverses the circumferential allograft and then enters the host bone. The allograft continues distally as a strut (see Fig. 66-11B).

Chapter 66 Revision of Failed Total Elbow Arthroplasty with Osseous Deficiency

A

C

909

B

FIGURE 66-13 A, Patient with a loose ulnar component with osteolysis of the entire proximal ulna in a circumferential manner. B, This patient was managed effectively by cementing a long-stemmed implant into a circumferential fibular strut. The implant extends into the host bone. C, The circumferential fibular strut is wired to the proximal ulna with anticipation of osseous incorporation, providing and anticipating a long-term stable construct.

910

Part VII Reconstructive Procedures of the Elbow

References 1. Breen, T., Gelberman, R. H., Leffert, R., and Botte, M.: Massive allograft. Surgery 13A:900, 1988. 2. Dean, G. S., Holliger, E. H., and Urbaniak, J. R.: Elbow allograft for reconstruction of the elbow with massive bone loss. Long term results. Clin. Orthop. Relat. Res. 341:12, 1997. 3. Dee, R.: Reconstructive surgery following total elbow endoprosthesis. Clin. Orthop. Relat. Res. 170:196, 1982. 4. Ehrendorfer, S.: Elbow revision arthroplasty in the situation of bone loss using an unlinked long-stem prosthesis. J. Hand Surg. 24A:1337, 1999. 5. Figgie, H. E., Inglis, A. E., and Mow, C.: Total elbow arthroplasty in the face of significant bone stock or soft tissue losses: preliminary results of custom-fit arthroplasty. J. Arthroplasty 1:71, 1986. 6. Gross, A. E., Wong, P. K., Hutchison, C. R., and King, A. E.: Onlay cortical strut grafting in revision arthroplasty of the hip. J. Arthroplasty 18(3 suppl 1):104, 2003. 7. Gschwend, N.: Salvage procedure in failed elbow prosthesis. Arch. Orthop. Trauma Surg. 101:95, 1983. 8. Kamineni, S., and Morrey, B. F.: Proximal ulnar reconstruction with strut allograft in revision total elbow arthroplasty. J. Bone Joint Surg. Am. 86A:1223, 2004.

9. Loebenberg, M. I., Adams, R. A., O’Driscoll, S. W., and Morrey, B. F.: Impaction grafting in revision total elbow arthroplasty. J. Bone Joint Surg. 87A:99, 2005. 10. Mankin, H. J., Doppelt, S., and Tomford, W.: Clinical experience with allograft implantation: the first ten years. Clin. Orthop. Relat. Res. 174:69, 1983. 11. Mansat, P., Adams, R. A., and Morrey, B. F.: Allograftprosthesis composite for revision of catastrophic failure of total elbow arthroplasty. J. Bone Joint Surg. 86A:724, 2004. 12. Sanchez-Sotelo, J., O’Driscoll, S., and Morrey, B. F.: Periprosthetic humeral fractures after total elbow arthroplasty: Treatment with implant revision and strut allograft augmentation. J. Bone Joint Surg. 84A:1642, 2002. 13. Schreurs, B. W., Sloof, T. J., Gardeniers, J. W. M., and Buma, P.: Acetabular reconstruction with bone impaction grafting and a cemented cup: 20 years’ experience. Clin. Orthop. Relat. Res. 393:202, 2001. 14. Zook, J., and Ward, W. G. Sr: Intraosseous radial nerve entrapment complicating total elbow revision. J. Arthroplasty 16:919, 2001.

Chapter 67 Nonimplantation Salvage of Severe Elbow Dysfunction

CHAPTER

67

Nonimplantation Salvage of Severe Elbow Dysfunction Bernard F. Morrey

INTRODUCTION Today, several salvage options exist for severe elbow dysfunction following trauma or failed prior intervention. If the joint is stiff and destroyed, interposition arthroplasty is recommended (see Chapter 69). If strength is required in a young person, especially if the joint is infected, fusion may be considered (see Chapter 70). If the injury is to the brachial plexus, strategies for management are discussed in Chapter 71. In this chapter, we review resection arthroplasty and allograft reconstruction for massive bone loss.

RESECTION ARTHROPLASTY Removal of articular bone, as a reconstructive strategy, is not an acceptable procedure. Badly comminuted articular fracture fragments may be excised in the setting of extensive soft tissue damage or contamination. In the absence of sepsis, these problems are subsequently addressed by prosthetic or allograft reconstruction.

INDICATIONS We reserve resection arthroplasty for septic total elbow replacements, especially when reimplantation cannot be done.

TECHNIQUE To remove a well-fixed implant, a trapezoidshaped cortical window is removed from the posterior aspect of the distal humerus (Fig. 67-1). Care is taken to preserve the epicondyles (Fig. 67-2). The olecranon is positioned between the two columns. We use a No. 3 PDS suture to help stabilize this relationship.

911

AFTERCARE A cast is applied for 6 weeks. Protected motion is begun using a Mayo Elbow Brace (Donjoy International, Vista, CA) and continued for an additional 6 to 8 weeks (Fig. 67-3).

RESULTS We have just completed an assessment of 59 resected elbows after failed total elbow arthroplasty (TEA) for sepsis at a mean time of 12 years after surgery. Although the study is still under way, preliminary analysis demonstrates a clear distinction between those with “contained” articulation (Fig. 67-4) having medial and lateral condyles doing markedly better than those with more extensive resection preventing any opportunity for a fulcrum effect (Fig. 67-5). Custom orthotic braces are occasionally prescribed, but infrequently worn on a regular basis (Fig. 67-6).

SEGMENTAL BONE LOSS The unstable or “flail” elbow with segmental bone loss, that is, complete loss of articulation and ligament attachments, is difficult to manage. Treatment with a primary replacement is discussed in Chapters 59 and 66. This problem can be a sequel of trauma, infection, failed elbow arthroplasty, or tumor resection. Bone may be lost at the original injury following a severe open fracture, or it may be removed subsequent to infection, particularly if the fragment is avascular. In treating recalcitrant union of supracondylar fractures, surgeons have in the past (and disastrously) succumbed to the temptation to remove the condylar fragment of the humerus and treat the problem by inserting an endoprosthesis. If the problem is limited to just the articular region of the humerus, a hemireplacement may be effective (Fig. 67-7). If, however, all stability and distal contour of the humerus is lost, today, a linked replacement is performed for such patients (see Chapter 59). On the other hand, in the situation of a flail elbow, particularly in a young patient, arthrodesis may be considered (see Chapter 70). However, failure of fusion, even under optimal conditions, has been high in some series2,14,16 and successful arthrodesis is unlikely in patients with large bone stock deficiencies. Reconstruction procedures, such as those involving reattachment of muscles more proximally on the humerus or interposing a tongue of triceps muscle into the gap, are unlikely to be successful. Muscle transfer procedures can improve flexion in cases of flail elbow associated with paralysis, but in these cases, the problem is of a different nature. A successful outcome will occur only if a stable

912

Part VII Reconstructive Procedures of the Elbow

1–2 d

d

FIGURE 67-1

Resecting a well-fixed total elbow arthroplasty can be accomplished by removing a trapezoid-shaped segment of the posterior humerus. This allows access to the medullary canal. The length of this should allow at least two diameters of reinsertion of an implant should that be necessary. Possibly more importantly, this should carefully be done in order to maintain the medial and lateral condyles.

FIGURE 67-2

Patient with resected arthroplasty after an infected total elbow (A and B). Notice that the medial and lateral columns have been maintained (A). This patient has a Mayo Elbow Performance Score of 80 and a functional elbow.

A

B

Chapter 67 Nonimplantation Salvage of Severe Elbow Dysfunction

913

2 yrs.

FIGURE 67-3

The Mayo Elbow Brace is helpful in immobilizing and stabilizing the extremity in the early phases and then allowing flexion and extension in the later phases.

fulcrum is provided and muscles are restored to their normal functioning length.

FIGURE 67-4

Two years after resection arthroplasty, notice the maintenance of the medial and lateral columns.

ALLOGRAFT REPLACEMENT For the younger patient, at this time, allograft replacement of the missing bone segment might be considered.17 Autografts such as vascularized fibula18 and iliac crest8 have been used in the upper limb, but lack of articular surface and donor site morbidity limit their application. Lexer10 is credited with the first report of an allograft transplantation as early as 1908. Renewed interest has been sparked by a series of publications in the late 1960s and 1970s.11-13 Ottolenghi12 believed that partial allograft joint transplantation gave better results than replacement of the whole joint. Considerable success has been documented in replacing isolated segments of the humerus.4 The use of distal humeral allograft or proximal ulnar allograft requires careful stabilization of the joint by reconstructing both the medial and lateral collateral ligament. For bone loss distal to the humeral collateral attachments, we use a hemiprosthetic device (see Fig. 67-7) (see Chapter 52). With more extensive bone loss, a hemiallograft replacement is employed (Fig. 67-8). Animal studies indicate that a major cause of failure in total joint allograft replacement is delayed or incomplete union and failure of revascularization.6 Thus, allograft reconstruction is a viable choice for short-term restoration of function in this difficult group of patients. It provides a stable joint without a requirement for

associated complex soft tissue reconstruction. It is important, if good stability and function are to be achieved, that the allograft match as nearly as possible the size of the lost segment of bone and its articular contour.4,15 Radiographs of the normal side are valuable for planning purposes. When inserting the allograft, we take care to achieve the correct degree of muscle tension. This precaution not only guarantees good functional restoration but also improves joint stability, and ligamentous reconstruction is unnecessary. Before any reconstructive procedure, there must be a careful assessment of the quality of all soft tissues, including the muscle as well as skin and soft tissues. The soft tissues must be able to accommodate a large allograft and still permit closure. Vascularized free flaps of soft tissue may be required (see Chapter 36).

LONG-TERM CONSIDERATIONS The fate of implanted allograft material depends on many factors, some of which are not fully understood. Large segmental allografts must unite with host bone (by a process of osteoconduction) if they are to succeed.7 This union occurs frequently, provided that the fixation to the host is technically satisfactory (Fig. 67-9). The standard AO plating technique is usually effective. Considerable loss of bone is observed to occur with time

914

Part VII Reconstructive Procedures of the Elbow

A A

FIGURE 67-5

B

A, In some instances, a complete resection of the joint may be indicated. This is usually in the case of sepsis. However, the result is dysfunctional instability. B, The use of the extremity is markedly compromised due to a windmill type of global instability.

Chapter 67 Nonimplantation Salvage of Severe Elbow Dysfunction

915

in that portion of the graft remote from the donor host junction. The exact nature of this neurotrophic type response is unknown at this time. One of the advantages of the method is that this gradual loss of allograft over time appears to allow some functional adaptation of muscles so that joint stability sufficient to permit continuing good function remains.3 Subluxation may also occur. Even if further reconstruction is required on some future occasion, it is facilitated, not prejudiced, by the augmentation of the patient’s bone stock that is achieved by the allograft. In fact, if we perform their procedure, it is considered a staged bone augmentation procedure that facilitates elbow replacement should this be necessary.

BICOMPATIBILITY

FIGURE 67-6 A custom-fit prosthesis is sometimes employed after resection arthroplasty. Compliance is low, however.

The immune response is not universally deleterious to the outcome of these transplants because satisfactory and full incorporation of the allograft into the host’s skeleton does occur. Graft incorporation depends on the mechanical environment and the type of graft as well as immune factors that are complicated and poorly understood.7,9 The immunogenicity of allografts is reduced by freezing or freeze drying, which renders

FIGURE 67-7

The instances in which there is loss of articular surface and bone but maintenance of collateral origins allows a hemireplacement of the joint and is an attractive option that has recently emerged.

916

A

Part VII Reconstructive Procedures of the Elbow

B

FIGURE 67-8

C

Patient with a distal humeral infected nonunion (A). An antibiotic spacer was inserted for 6 weeks (B). The distal humerus was replaced with an allograft carefully sized to match the proixmal ulna (A) and radius (C).

Chapter 67 Nonimplantation Salvage of Severe Elbow Dysfunction

FIGURE 67-9

Radiograph of a 20-year-old woman with flail elbow following infected open fracture (A). The elbow soft tissues were augmented with a free vascularized skin flap 6 months before elbow reconstruction (here, seen immediately before allograft implantation surgery) (B). Radiograph immediately following the procedure. In this case, a fresh-frozen graft was used (C). Eight months postoperatively, union has occurred (D). The patient is doing office work. The arm is not braced and the joint is stable (no soft tissue reconstruction or ligamentous support of any kind). Three years postoperatively (E). Five years postoperatively (F and G). Note progressive bone loss. The elbow is braced, but the fulcrum is maintained and the arm is functional. No dislocation is present, but there is some posterior subluxation in extension.

917

918

Part VII Reconstructive Procedures of the Elbow

them more suitable for clinical use. However, even preserved allografts provoke recognizable cellular and humoral antibody responses. Donor-specific anti— human leukocyte antigen (HLA) antibodies and cellular antibodies have been identified in frozen and freezedried grafts.5 The major reactivity appears to be cellular because viable bone marrow cells and, to a lesser extent, bone cells are highly immunogenic and induce both a cell-mediated and a humoral response. Antigens in the extracellular matrix (collagen and the noncollagenous proteins) seem to be of much less significance in the clinically observed allograft response.9 At this time, it has not been possible to identify the specific criteria that define an immune rejection of these grafts, as opposed to failure caused by some other process. Any infection inevitably spells failure for this procedure. As more becomes known of the nature of the rejection phenomenon, it may be possible to favorably manipulate the response, perhaps by tissue typing and immunosuppression of the host. Some anxiety with disease transmission continues to exist concerning the use of these large bone grafts. In spite of improved screening techniques, one cannot offer these patients absolute assurance that one is not

transferring disease from donor to host. Unlike small grafts, such as femoral head grafts, these larger upper limb allografts are inevitably from dead donors. Obviously, this means that the opportunity for donor interrogation is not available. Also, there is no way to identify donors who may convert and become seropositive at a later date.

RESULTS Urbaniak15 found total joint transplantation to be successful in six of eight cases, with a relatively short follow-up period of up to 6 years. Subsequent surveillance has tempered this enthusiasm due to predictable deterioriation of the articulation.3 Others have reported somewhat similar results. A French report described patient satisfaction in five of seven patients with TEA replacements.1 In five of six patients, progressive joint resorption occurred. In our limited experience, ultimate joint deterioration universally occurs, but can be readily managed by a joint replacement (Fig. 67-10). Otherwise, there is little information in the peer-reviewed literature regarding this treatment option.

Allograft TEA

A

B

C

FIGURE 67-10 A, As shown, a 44-year-old patient with an elbow replacement and early loosening with osseous resorption four years after insertion. The patient was found to have a nickel allergy (A and B). A resection of the joint and allograft elbow replacement was carried out (C and D).

Chapter 67 Nonimplantation Salvage of Severe Elbow Dysfunction

Allograft TEA

D

E

G

F

H FIGURE 67-10, cont’d

Sixteen years later, the allograft has undergone a neurotrophic change. The patient’s elbow was unstable and painful (E and F). An elbow replacement was carried out. The allograft provided a structural basis for the total elbow arthroplasty (G and H).

919

920

Part VII Reconstructive Procedures of the Elbow

References 1. Allieu, Y., Marck, G., Chammas, M., Desbonnet, P., and Raynaud, J. P.: Total elbow joint allograft for long-term posttraumatic osteoarticular loss. Follow-up results at 12 years. Rev Chir. Orthop. Reparatrice Appar. Mot. 90:319, 2004. 2. Carnesale, P. G., and Stewart, M. J.: Complications of arthrodesis surgery. In Epps, C. H. (ed.): Complications in Orthopaedic Surgery, Vol. 2. Philadelphia, J. B. Lippincott Co., 1978, p. 1109. 3. Dean, G. S., Holliger, E. H. 4th, and Urbaniak, J. R.: Elbow allograft for reconstruction of the elbow with massive bone loss. Long term results. Clin. Orthop. Relat. Res. 341:12, 1997. 4. Dee, R.: Reconstructive surgery following total elbow endoprosthesis. Clin. Orthop. Relat. Res. 170:196, 1982. 5. Friedlaender, G. E.: Immune responses to osteochondral allografts. Current knowledge and future directions. Clin. Orthop. Relat. Res. 174:58, 1983. 6. Goldberg, V. M., and Heiple, K. G.: Experimental hemijoint and whole-joint transplantation. Clin. Orthop. Relat. Res. 174:43, 1983. 7. Goldberg, V. M., Stephenson, S., and Schaffer, J. W.: Biology of allografts and autografts. In Friedlaender, G. E., and Goldberg, V. M. (eds): Bone and Cartilage Allografts: Biology and Clinical Applications. Chicago, American Academy of Orthopedic Surgery Publications, 1991. 8. Gschwend, N.: Salvage procedure in failed elbow prosthesis. Arch. Orthop. Trauma Surg. 101:95, 1983.

9. Horowitz, M. C., and Friedlaender, G. E.: The immune response to bone grafts. In Friedlaender, G. E., and Goldberg, V. M. (eds): Bone and Cartilage Allografts: Biology and Clinical Applications. Chicago, American Academy of Orthopedic Surgery Publications, 1991. 10. Lexer, E.: Die Verwendung der freien Knochenplastik nebst Versuchen über Gelenkversteifung und Gelenk-transplanation. Arch. Lin. Chir. 86:939, 1908. 11. Mankin, H. J., Doppelt, S., and Tomford, W.: Clinical experience with allograft implantation. Clin. Orthop. Relat. Res. 174:69, 1983. 12. Ottolenghi, C. E.: Massive osteo- and osteo-articular bone grafts. Clin. Orthop. Relat. Res. 87:156, 1972. 13. Parrish, F. F.: Allograft replacement of all or part of the end of a long bone following excision of a tumor. J. Bone Joint Surg. 55A:1, 1973. 14. Stewart, M.: Arthrodesis. In Edmonson, A. S., and Crenshaw, A. (eds.): Campbell’s Operative Orthopaedics. St. Louis, C. V. Mosby Co., 1980, p. 1137. 15. Urbaniak, J. R., and Black, K. E.: Cadaveric elbow allografts: a six-year experience. Clin. Orthop. Relat. Res. 197:131, 1985. 16. Van Gorder, G. W., and Chen, C. M.: The central-graft operation for fusion of tuberculosis of knees, ankles, and elbows. J. Bone Joint Surg. 41A:1029, 1959. 17Wavreille, G., Dos Remedios, C., Chantelot, C., Limousin, M., and Fontaine, C.: Anatomic bases of vascularized elbow joint harvesting to achieve vascularized allograft. Surg. Radiol. Anat. 28:498, 2006. 18. Weiland, A., Moore, J. R., and Daniel, R. K.: Vascularized bone autografts. Clin. Orthop. Relat. Res. 174:87, 1983.

SECTION

B

NONPROSTHETIC RECONSTRUCTION

Synovectomy of the Elbow

management as an initial interventive procedure. Despite this, controversy still remains as to the role and method of execution, especially in advanced stages and in patients with instability and stiffness. This chapter highlights the issues of open versus arthroscopic techniques and the resection versus preservation of the radial head during elbow synovectomy.

Akin Cil and Bernard F. Morrey

INDICATIONS AND PATIENT SELECTION

CHAPTER

68

INTRODUCTION Rheumatoid arthritis affects 1% to 2% of the general population.53 The most common cause of elbow arthritis is rheumatoid arthritis in which the involvement of elbow after an average of at least 10 years can be seen in more than half of the patients clinically or radiologically.17,25,27 Medical management is discussed in detail in Chapters 74 and 75. The mainstays of surgical treatment available for the patient with rheumatoid arthritis of the elbow include synovectomy, interposition arthroplasty, and total elbow replacement, in addition to other treatment options with limited application like arthrodesis and resection arthroplasty. Joint replacements and interposition arthroplasty are considered in Chapters 54, 55, and 69. Synovectomy with or without radial head excision is a well-recognized and accepted form of treatment for the rheumatoid elbow. This procedure reduces the amount of joint fluid and removes proliferative synovitis, and thereby decreases intra-articular pressure, relieves pain, and reduces swelling. After a few months, a new synovial membrane is regenerated in the joint5; however, the lack of villous change, vasculitis, and decreased pathologic enzymatic activity in the new synovial membrane and the joint fluid34 indicates a difference in the inflammatory process after synovectomy.38 Still, the role of synovectomy must be defined in the context of the success of total elbow replacement. The primary indication for elbow synovectomy in a patient with rheumatoid arthritis is persistent painful synovitis that is unresponsive to at least 6 months of appropriate medical

Synovectomy is ideal for the patients who present with uncontrolled synovitis resulting in a painful elbow with limited function. However, a period of nonsurgical treatment including anti-inflammatory agents, steroids, disease-modifying anti-rheumatic drugs in addition to maintaining supple joints with an active range of motion program and splinting for at least 6 months should be attempted before surgery is considered4 (see Chapter 54). Early in the disease, synovitis is a prominent feature (Fig. 68-1). A warm, swollen elbow with a mild flexion contracture and a painful limitation of flexion and extension in addition to pronation and supination characterizes a typical joint. As the disease progresses, the synovitis generally wanes and persistent pain and stiffness results from joint destruction with articular incongruity. Although classically the disease stage employs the Carson system, for our purposes, it is convenient to describe the radiographic appearance into five categories. Type I: synovitis with a normal appearing joint; type II: loss of joint space but maintenance of the subchondral architecture; type IIIA: alteration of the subchondral architecture; type IIIB: alteration of the architecture with deformity; type IV: gross deformity; type V: radiographic appearance of ankylosis (Fig. 68-2). This classification is helpful in providing a basis for treatment options (see Fig. 68-1). Elbow synovectomy is ideally reserved for the early stages of the disease (type I, type II, and early type IIIA) (Fig. 68-3). Synovectomy per se is not effective or reliable in restoring motion. As a result, a functional arc (30 to 130 degrees of flexion) should ideally be present.33 In patients with a long-standing and advanced disease, this arc is 921

922

Part VII Reconstructive Procedures of the Elbow

RHEUMATOID SURGERY OF THE ELBOW Time

Joint involvement

Total joint change Mechanical change Synovitis

! I

II

III

IV

Synovectomy and radial head resection

FIGURE 68-1

Scheme depicting the relationship of synovitis and joint distraction to treatment options. Patients with minimal architectural involvement are the best candidates for synovectomy.

Resurfacing arthroplasty Semiconstrained arthroplasty ! Morrey classification of xray changes

FIGURE 68-2 A, Mayo radiographic classification of rheumatoid involvement of the elbow considers synovitis, articular involvement, and joint distraction (see text). B, A type V radiographic presentation is one of ankylosis, as reported by Connor and associates.6

often not present. Therefore, a total arc of flexion of at least 80 degrees is recommended before the procedure. However, more recently, it has been shown that with anterior and posterior capsular release or capsulectomy, a better outcome may be possible even in those with less than 80 degrees of flexion.28,41

The role of synovectomy in more advanced stages of disease is still debatable in the literature. In advanced stages of the disease, damage to either or both the medial and lateral ligamentous complexes combined with bony and cartilaginous loss in addition to significant erosion and instability of the radial head may result in gross

Chapter 68 Synovectomy of the Elbow

923

FIGURE 68-3

Type IIIA involvement (A). Three years after arthroscopic synovectomy, the patient has less pain and has maintained a 100 degree arc of motion (B).

medial-lateral elbow instability, precluding synovectomy. This is an indication for total elbow arthroplasty, which can be reliable even in the presence of instability.6,14,32 Critical assessment of prior reports reveal a small number of articles that report worsening of the results over the long term, especially due to the development of instability.10,50 On the other hand, the majority of reports agree that advanced radiographic stage of the disease might not influence the ultimate outcome* (Fig. 68-4). Furthermore, although instability can be seen in up to 50% of patients in the advanced stages,40 this generally does not seem to cause symptomatic instability requiring an operation.† As a result, synovectomy might be employed with reservations in advanced stages as well if instability is not one of the major complaints of the patient. Nevertheless, those experienced with the techniques of total elbow replacement as well as synovectomy, and those who are familiar with the results of both, favor total elbow replacement to synovectomy in treating later stages of the disease because patients are more satisfied, functional improvement is greater, and the results are more predictable.6,14,32

when radial head excision is performed. In the series of Rymaszewski and colleagues,40 most of the displeased patients had medial tenderness and pain with attempted valgus stress in the elbow, which was attributed to tension on medial collateral ligaments, mainly due to resection of the radial head. Also, the initial good results may deteriorate with time with increasing instability of the joints due to gradual bone loss.50 Limited elbow motion is the other major contraindication for synovectomy of the elbow, because elbow function cannot predictably be improved, and some patients lose some motion. Severe joint stiffness resulting from inflammatory fibroarthrosis is more commonly seen in juvenile rheumatoid arthritis. Because complete ankylosis can be observed in these patients, grade 5 radiologic classification was added to the original classification of the rheumatoid arthritis6 (see Fig. 68-2). Synovectomy alone cannot be advocated in this subgroup of patients for the sole purpose of improving motion.30 Radiographic involvement of the joint architecture with deformity (type IIIB) is also a relative contraindication.

CONTRAINDICATIONS

TECHNIQUES

One of the major contraindications to synovectomy is severe joint disruption. Synovectomy performed in this situation will not correct instability, and débridement of the joint may actually aggravate instability, particularly

Synovectomy can be performed nonsurgically (chemical or radiation synovectomy)8,15,37,44 or surgically, which can be performed either open or by an arthroscopic technique.‡

*See references 2, 3, 7, 9, 12, 13, 18, 22, 26, 28–30, 35, 39–41, 45, and 49. † See references 2, 7, 9, 10, 18, 21-23, 26, 28, 39, 41, 45, 49, and 54.

‡

See references 2, 3, 7, 9, 10, 12, 13, 18, 19, 21, 22, 24, 26, 28-30, 35, 39-41, 45, 46, and 49.

924

Part VII Reconstructive Procedures of the Elbow

FIGURE 68-4

A 43-year-old woman with late type II changes (A and B), still functioning without pain at 8 years (C and D). Note remodeling on the lateral radiograph (D).

Chapter 68 Synovectomy of the Elbow

925

Triceps

Humerus Capsule

Head of radius Annular ligament Anconeus

Supinator

FIGURE 68-5

A Kocher incision of variable extent is the preferred approach for open synovectomy. The radial head may be readily excised, and if this is done, synovectomy is facilitated. The posterior compartment is also readily accessed through this approach.

NONSURGICAL SYNOVECTOMY

SURGICAL SYNOVECTOMY

Chemical and radiation synovectomy has been advocated as a noninvasive procedure. Owing to the size and subcutaneous surface of the joint, rhenium-186,15 yttrium-90,44 and osmic acid37 have been used with caution at the elbow. Although patients with early radiologic stages of elbow involvement have a better success rate, especially with the addition of triamcinolone to radiosynovectomy, the overall success rate is less than 50% with these agents with a very limited follow-up.15,44 The potential for cartilage necrosis and the subcutaneous location of this joint has limited the use of these agents in the United States.16,31 Also, radial head excision, if needed, is not possible. Besides, in marked synovitis in which synovial swelling is above the effective penetration range of the radionuclide, the lower layers of synovium cannot be reached by radiosynoviorthesis and the destruction process and pain will continue.15 However, this technique can be considered as a more conservative treatment option to surgical synovectomy, especially in patients who are unable to undergo surgery.

ARTHROTOMY Although there are an increasing number of reports on arthroscopic synovectomy, open surgery is still commonly performed for elbow synovectomy. This technique is well established and requires less technical expertise than arthroscopic synovectomy, particularly when radial head excision is performed. However, more remarkable postoperative pain, increased risk of wound breakdown, and increased risk of infection, in addition to loss of ligamentous or muscle and tissue supports require a delay in the initiation of rehabilitation, which might potentially result in elbow stiffness.3,21

Technique An extensile Kocher approach provides excellent visualization of the lateral joint and preserves the medial collateral ligaments (Fig. 68-5). The radial head is removed if there are significant symptoms with pronation and supination or marked radial humeral joint pain with flexion and extension. The synovitis typically involves the sacriform recess of the radial neck and a thorough

926

Part VII Reconstructive Procedures of the Elbow

synovectomy of this region is required. If the radial head is removed, a very thorough synovectomy can be carried out.2,13,18,22,39,50,54 If radial head is preserved anterior compartment exposure is more difficult but can still be adequately achieved. A second medial exposure is not necessary in our experience and that of most of the investigators.§ The triceps is elevated from the lateral column and the joint is extended. The posterior compartment synovectomy can then be carried out. Because a complete synovectomy can be achieved through the extensile Kocher approach, separate lateral and medial approaches have been advocated sporadically.7,39,50 The main advantage of adding a medial incision is that radial head need not be resected for adequate synovectomy.7 However, even in bilateral approach proponents, it has been noted that if an extended lateral approach is used, results do not differ.39 In various reports, a medial incision is also added to an extended lateral approach in several cases because of the need for the decompression and translocation of the ulnar nerve.3,26,49,54 The use of Mayo posteromedial triceps reflecting exposure has also been advocated for synovectomy of the elbow.20 It provides for identification of the ulnar nerve and facilitates subsequent skin incision for total elbow replacement. However, surgery is more extensive than the extensile Kocher approach with the added potential for extensor mechanism complications, and we have not found it necessary to use this approach for routine synovectomy. Synovectomy and débridement through a transolecranon approach is contraindicated.21

Aftercare Following synovectomy, the joint is injected with bupivacaine with epinephrine and a corticosteroid at a 4 : 1 ratio. Closure of the lateral soft tissue and capsule is carried out with a suction drain in situ. The elbow is extended, and a padded Jones dressing with anterior plaster slab is applied. The extremity is elevated by being suspended in a stockinette. The plaster, dressing, and drain are removed the next day. The brachial plexus block is removed after 48 hours, and the patient is discharged the following day. A portable continuous passive motion machine is used for 3 weeks. The sutures are then removed, and the patient is allowed to resume activity as tolerated. A Mayo Elbow Brace is used especially at night if there are concerns about maintaining motion. Increasingly, an immediate continuous passive motion machine can be started immediately postoperatively under the brachial plexus anesthetic block.

§

See references 2, 9, 10, 18, 22, 28–30, 41, and 46.

ARTHROSCOPIC SYNOVECTOMY Arthroscopy is being used with increasing frequency to diagnose and treat elbow disorders. Because elbow arthroscopy has become popular in recent years, concern regarding potential complications, including septic arthritis, superficial skin infection, persistent drainage from portal sites, and most frequently, nerve injuries (transient and permanent), has also risen23 (see Chapters 40 and 41). The risk can be minimized with observation of certain safety precautions. In our series, of all procedures, it was found that two factors were associated with a higher risk of nerve palsy—the performance of capsular release and the diagnosis of rheumatoid arthritis.23 In experienced hands, the advantages of arthroscopic over open synovectomy are obvious. It can be performed on an out-patient basis, causes minimal morbidity (decreased scarring, decreased risk of infection, less postoperative pain), possibly enables a more thorough visualization of the elbow joint than is possible with an arthrotomy during some procedures, results in rapid return of motion, and shortens the recovery period.23 With improved technique and greater experience, a complete synovectomy including excision of the radial head, if necessary, is possible (see Chapter 40).

Technique Several strategies can be used and our technique of elbow arthroscopy has evolved.36 Patients are placed in the lateral decubitus position, with the involved elbow over a padded bolster. The forearm is allowed to swing free, and the elbow is flexed to 90 degrees (Fig. 68-6). The arm is then prepared in the usual fashion. The forearm is exsanguinated by elevating the limb. A soft elastic bandage is then wrapped around the hand and forearm to within 10 cm of the olecranon. The tourniquet, which is used routinely, is inflated to 250 mmHg. The elastic bandage is left on until the end of the procedure, to limit the periarticular swelling to the elbow area. At the end of the procedure, the bandage and the tourniquet are removed and any accumulated edema rapidly dissipates into the tissues of the forearm and arm. The joint is distended with approximately 15 to 25 mm sterile normal saline solution through a needle inserted in the direct midlateral portal (soft spot). Portal placement is determined by the careful palpation of underlying osseous structures. Skin markings are less reliable after swelling occurs. We begin the procedure by visualization through anteromedial portal (Fig. 68-7). Somewhat more proximal than the standard anteromedial portal, this increases nerve-to-portal distance and minimizes the amount of manipulation through the bulky muscles of the flexor pronator origin. An 18-gauge needle helps determine the

Chapter 68 Synovectomy of the Elbow

927

FIGURE 68-6

The arm is draped free. The shoulder is protected with a padded bolster.

optimal site for this portal. Portal placement has been accomplished with both the outside-in and the insideout technique, but over time, the outside-in technique has been preferred. Emphasis is placed on using the retractors through proximal anterolateral and distal anteromedial portals. These portals are primarily used for visualization in the anterior compartments instead of pressurization to accomplish joint distension. This reduces the risk of edema and allows more complex surgical procedures to be performed. The débriding instrument is a 4-mm reciprocating device with outflow to gravity inserted through an anterior/lateral portal. Synovitis can be extensive, and visualization improves as removal of synovium proceeds. The tip of the resector must be in view at all times and closed immediately if muscle fibers are seen or if the cutting head disappears from view. The shaver blade should always point inward and away from the capsule which is often extremely thin in rheumatoid arthritis. With the help of a switch stick, the débriding instrument is introduced to anteromedial portal and an anterior synovectomy is completed (see Fig. 68-7B). Considerable visualization of the posterior compartment can usually be achieved through the midlateral posterior portal. A posterior synovectomy is completed by inserting the débriding instrument through a posterolateral portal (see Fig. 68-7C). The instrument can then be switched (with the arthroscope in the posterolateral and shaver in the midlateral portal) to facilitate removal of synovium in the sacriform recess and removal of radial head when indicated. If a contracture is present, osteophytes are removed from the olecranon and coronoid processes. If motion is still limited, a capsular release is performed: (1) Blunt stripping of the capsule off the humerus is performed

first; (2) the anterior capsule is resected in its midsection starting from the medial and working toward the lateral side. This is best performed with a shaver using no suction, but with the outflow on the shaver simply left open to drainage.

Aftercare The patient is given an axillary block and placed in continuous passive motion (CPM) machine. The block is discontinued after 48 hours. The patient is encouraged to move the joint and discharged on the second or third day to carry on daily activities. Physiotherapy is not necessary.

RESULTS OPEN SYNOVECTOMY Surveillance Considering recognized inconsistencies inherent in summarizing diverse reports using different evaluation standards, 71% to 93% of the procedures can be considered to have a satisfactory outcome in short to intermediate term. The rate of repeat synovectomy, resurfacing arthroplasty, or conversion to total elbow replacement in these patients occurs in up to 10%.2,7,21,22,26,39 The longterm results of open elbow synovectomy are summarized in Table 68-1. Nonetheless, with longer follow-up, the percentage of satisfactory results will decrease to even below 50%, with a rate of reoperation as high as 25%. Some reports suggest that results deteriorate minimally with time.7,8,26,41,49 In a study by Herold and Schroeder18 in 11 patients (12 elbows) at 14 years after the surgery, 83% maintained satisfactory pain relief, however,

928

Shaver

Part VII Reconstructive Procedures of the Elbow

Scope

A

Shaver Scope

B

Scope

Shaver

FIGURE 68-7

C

A, The arthroscopic synovectomy begins with a scope placement through an anterior medial portal. The shaver is introduced through an anterolateral portal. B, After the anterior lateral compartment has been débrided, the scope and shaver portals are reversed and the synovectomy is completed with the shaver introduced through an anteromedial portal. C, Attention to the ulnar nerve is required for posterior placement. Typically the scope is placed near the midline while the shaver is introduced through a posterolateral portal.

Chapter 68 Synovectomy of the Elbow

radiographic progression was noted and reoperation was required in two elbows. In another long-term study with follow-up averaging 10 to 20 years, only 67% of 21 patients were satisfied with the procedure.1 Others with surveillance averaging 7 to 8 years reported initial satisfactory results of 90% had decreased to less than 75% at final assessment.43,50 Gendi and associates13 reported a large series of 113 elbows 5 to 20 years after synovectomy and noted a cumulative survival rate of 81% at 1 year, decreasing an average of 2.6% per year. By final follow-up, 46% of the procedures had failed. There is a tendency toward failure to appear after 3 years of follow-up.39,45 Rymaszewski and colleagues40 noted 25% of the patients with initial good pain relief deteriorated after an average of 6 years of follow-up. Many reoperations occur within the first 5 years3,12,29,40 but failure is seen with increasing frequency after 8 to 9 years.12,18,46,50 Clearly there are no data to suggest that synovectomy arrests the progress of disease process.

RADIAL HEAD The value of radial head resection continues to be debated. Although most series report radial head excision in the majority of their cases,¶ more recent results suggest that its preservation can reliably achieve comparable results with pain relief in 70% to 83% of the patients even at about 9 to 13 years of follow-up.29,43,46,49 The majority maintain or regain a functional arc of motion, with approximately 50% improving flexion and extension, 30 to 35% remaining unchanged, and 15% losing a small amount of motion. When capsular release or capsulectomy is done in addition to open synovectomy, a significant increase in flexion arc, particularly originating from gain in extension had been shown in the vast majority of the patients in two studies.28,41 Although pronation and supination is also a function of wrist joint which is usually involved, gain in forearm rotation is regularly noted.¶

ARTHROSCOPIC SYNOVECTOMY Surveillance There is still a dearth of reports regarding the results of arthroscopic synovectomy (Table 68-2). Horiuchi and colleagues19 reported on 20 patients with a mean followup of 8 years. Similar to the trend seen in open synovectomies and our initial report on arthroscopic synovectomies,24 71% of satisfactory results at 2 years decreased to 43% at the final follow-up. Also, clinically apparent synovitis occurred in 24% of the elbows, with two of them requiring total elbow replacement. However, ¶

See references 1, 3, 9, 10, 12, 18, 28, 40, 43, 47, and 50. See references 3, 7, 9, 10, 12, 18, 28, 40, 43, 45, 46, and 50.

¶

929

these authors did not débride the medial gutter and did not perform osteophyte excision or capsular release. Furthermore, they had reported favorable results mainly in patients with early-stage disease. Tanaka and colleagues46 recently observed similar results with 48% pain relief at an average follow-up of 13 years in 29 elbows. They compared these results with a matched group of open synovectomies and detected no significant difference between the overall clinical results of both procedures. However, especially in elbows with a limited preoperative arc of flexion (<90 degrees), arthroscopic synovectomy provided significantly better function than open surgery after mid-term follow-up, and motion and function continued to be better in those patients at the most recent follow-up evaluation.

MAYO EXPERIENCE We recently updated the results of our initial assessment of arthroscopic synovectomy in 83 elbows with an average follow-up of 6.5 years (2 to 14 years).24 Pain relief was observed in 76%, with a satisfaction rate of 76%. Unlike the techniques employed in the past, we also performed capsular release and/or capsulectomy in two thirds of our patients and osteophyte excision in one half, along with medial gutter synovectomy. This technique required an average of six portals, but the arc of flexion increased from 91 degrees to 119 degrees, with an average gain in flexion of 10 degrees and extension of 18 degrees. Eight patients (10%) required total elbow replacement, leaving 80% free of total elbow replacement at 14 years; this is comparable to open synovectomy (Fig. 68-8).

REPEAT SYNOVECTOMY Repeat synovectomy following an initial failed procedure has occasionally been recommended. The frequency of performing repeat synovectomy has been reported to be between 1% to 20%12,13,18,29,30,43,45,50 after open procedures and 6% to 9%5,35 after arthroscopic synovectomy. Most repeat synovectomies are performed within 3 years after the index operation,5,21 indicating a lack of initial satisfactory response.12,50 Because the results of repeat synovectomy following a return of symptoms is less predictable, other successful alternatives such as total elbow replacement or interposition arthroplasty should be considered in case of a failure6,14,32 (see Chapters 54 and 69).

TOTAL ELBOW REPLACEMENT FOR FAILED SYNOVECTOMY Schemitsch and colleagues42 compared patients undergoing capitellocondylar total elbow replacements with

1984

Rymaszewski et al40

1990

1991

Tanaka et al46

Fuerst et al

12

Mäenpää et al

Mäenpää et al

2006

2006

2003

1997

Gendi et al13

2003

1997

Lonner and Stuchin28

29

1995

30

1993

Herold and Schroder18

Smith et al

43

Vahvanen et al

Alexiades et al

50

1989

1987

1

Tulp and Winia49

Ferlic et al

10

1985

1982

Eichenblat et al9

Brumfeld and Resnic

1976

Taylor et al47

3

Year

29

85

103

24

115

12

12

85

70

21

61

57

42

40

25

44

No. of Procedures

0

72

46

4

113

12

11

0

66

21

41

57

42

40

25

44

No. of Radial Heads Removed

Lateral

Lateral, medial

Lateral

Lateral

—

Lateral (with anterior capsular release)

Lateral

Lateral

Lateral and medial

Lateral, transolecranon

Lateral, bilateral

Lateral

Lateral, medial, transolecranon

Lateral

Lateral

Lateral

Recommended Approach

16

46

71

15

60

10

10

67

55

14

—

—

27

20

22

38

No.

70

75

85

83

54

83

83

79

79

67

—

—

64

50

88

86

%

Pain Relief

—

72

—

—

—

83

—

64

—

54

—

76

64

21

80

0

Gained

—

—

—

—

—

—

—

—

—

18

—

9

14

—

0

0

No Change

Motion %

—

28

—

—

—

17

—

—

—

28

—

15

17

—

20

11

Lost

RESULTS

Results of Elbow Synovectomy for Rheumatoid Arthritis (Open Procedures, Average Follow-up >5 years)

Author

TABLE 68-1

—

71

60

72

54

100

156

104

62

60

78

73

168

108

<75 83

90

173

78

86

84

72

60

60

120-216

32-228

12-96

12-96

60-288

24-132

144-180

60-240

18-264

120-252

48-120

12-240

24-204

12-180

24-132

6-96

Range

Follow-up (Mo)

Mean

71

67

70

77

78

45

100

91

% Satisfactory

930 Part VII Reconstructive Procedures of the Elbow

Chapter 68 Synovectomy of the Elbow

931

Results of Elbow Synovectomy for Rheumatoid Arthritis (Arthroscopic Procedures with at Least 2 Years of Follow-up)

TABLE 68-2

RESULTS

Author

Year

No. of Procedures

Lee and Morrey24

1997

14

—

Horiuchi19

2002

21

4

Tanaka et al46

2006

29

4

2007

83

6 (3-9)

5

Cil et al

No. of Portals

Additional Interventions

Pain Relief

Motion

No Change

Lost

% Satisfactory

Follow-up (Mo)

No.

%

Gained

Mean

Range

No

9

64

43

50

7

57

42

24-84

No

16

76

—

—

—

43

97

42-160

No

11

48

—

—

—

—

156

120-216

Capsular release/ osteophyte removal

57

76

63

27

10

76

79

24-168

A

B

FIGURE 68-8 A, Thirty-eight-year-old patient with grade II rheumatoid arthritis of the right elbow underwent arthroscopic synovectomy. B, Six years later, the patient has osteopenia and mild progression of the process but her pain had increased.

932

Part VII Reconstructive Procedures of the Elbow

FIGURE 68-8 cont’d

C, Ten years after total elbow arthroplasty, the patient is without symptoms with a Mayo Elbow Performance score of 89.

C

patients who had a failed open synovectomy and radial head excision. The rate of complication, reoperations, and postoperative instability was higher in patients with previous synovectomy procedures with an average follow-up of 4 years. Fink and colleagues11 found a higher complication rate as well as a higher rate of loosening, especially in patients with previous distraction interposition arthroplasty in addition to previous open synovectomies. However, van der Lugt and colleagues51 demonstrated no increased rate of complications after a previous radial head resection and open synovectomy and no effect on the long-term functional outcome and survival an unlinked implant. In our assessment of the Coonrad/Morrey replacement after synovectomy and radial head excision, similar outcomes were documented compared with a control group.52 Yet, open synovectomy and radial head excision, although not associated with any increased rate of revision following subsequent arthroplasty of the elbow, do increase slightly the risk of complications.52

COMPLICATIONS Recurrence Recurrence of pain and synovitis is the most common complication following synovectomy and is discussed earlier.

Loss of motion, as noted earlier, can occur in 10% to 20% of patients. These problems are less commonly seen in those with clear indications for the procedure initially. More important, arthroscopic

Motion Loss

synovectomy and early aggressive motion facilitate early motion and appear to eliminate the tendency for motion loss after synovectomy.5 Residual instability has been reported in about 15% of the patients.48 The incidence is higher, up to 50%, in patients with more advanced disease and in those with significant instability before synovectomy.40 This is particularly true if radial head excision is performed in patients with pre-existing instability. Instability is not a common problem, even with radial head excision, if the ulnohumeral joint is reasonably intact and if the medial collateral ligament is also competent.

Instability

Nerve injury is rare after open synovectomy but is a significant potential risk with arthroscopic synovectomy given the fact that the neurovascular structures lie very closely to the joint capsule.23 The risk of neurovascular injury is always a concern and a significant disadvantage especially in patients with rheumatoid arthritis with limited range of motion.19,23,24,35,46 This is particularly true with anterior or posterior capsulectomy. Hence, the operating surgeon must either be able to identify the radial or ulnar nerve at the time of capsulectomy or have sufficient experience with this procedure and knowledge of the neural anatomy in relation to capsule and intra-articular structures so that such visualization of the nerves is not necessary. Temporary ulnar nerve neuropraxia occurred in one patient (7%) in our initial report24; two ulnar nerve neuropraxias and one median nerve neuropraxia accounted for a 4% frequency in the updated series.5 Neuropathy

Chapter 68 Synovectomy of the Elbow

SUMMARY Although traditionally some have reported satisfactory results in patients with significant joint involvement, more recent results suggest that the best outcome is seen when less extensive joint involvement has occurred (type I and II). The current recommendation to avoid synovectomy in those patients with severe type IIIB or type IV disease is based on the predictable outcomes with total elbow arthroplasty and unpredictable results with synovectomy in this type of patient. Capsulectomy and osteophyte excision performed together with synovectomy may facilitate improvement in motion. Improved outcome with arthroscopic synovectomy is observed as the surgical technique improves with continued caution regarding the potential for the injury. The synovectomy may increase the complication rate of subsequent arthroplasty but overall does not have an increased effect on outcome.

12.

References

18.

1. Alexiades, M. M., Stanwyck, T. S., Figgie, M. P., and Inglis, A. E.: Minimum ten-year follow-up of elbow synovectomy for rheumatoid arthritis. Orthop. Trans. 14:255, 1990. 2. Brattstrom, H., and Al Khudairy, H.: Synovectomy of the elbow in rheumatoid arthritis. Acta Orthop. Scand. 46:744, 1975. 3. Brumfield, R. H. Jr, and Resnick, C. T.: Synovectomy of the elbow in rheumatoid arthritis. J. Bone Joint Surg. 67A:16, 1985. 4. Bryan, R. S., and Morrey, B. F.: Rheumatoid arthritis of the elbow. In Evarts, C. M. (ed.): Surgery of the Musculoskeletal System, Vol. 2, 2nd ed. London, Churchill Livingstone, 1990, p. 1759. 5. Cil, A., Morrey, B. F., and O’Driscoll, S.: Arthroscopic synovectomy of the elbow: An update with improved surgical technique. (In press.) 6. Connor, P. M., and Morrey, B. F.: Total elbow arthroplasty in patients who have juvenile rheumatoid arthritis. J. Bone Joint Surg. 80A:678, 1998. 7. Copeland, S. A., and Taylor, J. G.: Synovectomy of the elbow in rheumatoid arthritis. J. Bone Joint Surg. 61B:69, 1979. 8. Dawson, T. M., Ryan, P. F., Street, A. M., Robertson, P. L., Kalff, V., Kelly, M. J., and Cicuttini, F. M.: Yttrium synovectomy in haemophilic arthropathy. Br. J. Rheumatol. 33:351, 1994. 9. Eichenblat, M., Hass, A., Kessler, I., and Israel, R.: Synovectomy of the elbow in rheumatoid arthritis. J. Bone Joint Surg. 64A:1074, 1982. 10. Ferlic, D. C., Patchett, C. E., Clayton, M. L., and Freeman, A. C.: Elbow synovectomy in rheumatoid arthritis: Longterm results. Clin. Orthop. 220:119, 1987. 11. Fink, B., Krey, D., Schmielau, G., Tillmann, K., and Rüther, W.: Results of elbow endoprostheses in patients with rheu-

13.

14.

15.

16.

17.

19.

20.

21.

22.

23.

24.

25.

26.

27.

28.

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matoid arthritis in correlation with previous operations. J. Shoulder Elbow Surg. 11:360, 2002. Fuerst, J., Fink, B., and Futher, W.: Survival analysis and long-term results of elbow synovectomy in rheumatoid arthritis. J. Rheumatol. 33:892, 2006. Gendi, N. S. T., Axon, J. M. C., Carr, A. J., Pile, K. D., Burge, P. D., and Mowat, A. G.: Synovectomy of the elbow and radial head excision in rheumatoid arthritis. Predictive factors and long-term outcome. J. Bone Joint Surg. 79B:918, 1997. Gill, D. R. J., and Morrey, B. F.: The Coonrad-Morrey total elbow arthroplasty in patients who have rheumatoid arthritis. J. Bone Joint Surg. 80A:1327, 1998. Gobel, D., von Rothkirch, G.-T., and Becker, W.: Radiosynoviorthesis with rhenium-186 in rheumatoid arthritis: A prospective study of three treatment regimens. Rheumatol. Int. 17:105, 1997. Goldberg, V. M., Rashbaum, R., and Zika, J.: The role of osmic acid in the treatment of immune synovitis. Arthritis Rheum. 19:737, 1976. Gschwend, N.: Operations in the repair of the elbow joint. In Gschwend, N. (ed.): Surgical Treatment of Rheumatoid Arthritis. New York, Georg Thieme Verlag, 1980, p. 45. Herold, N., and Schroder, H. A.: Synovectomy and radial head excision in rheumatoid arthritis: 11 patients followed for 14 years. Acta Orthop. Scand. 66:252, 1995. Horiuchi, W., Momohara, S., Tomatsu, T., Inoue, K., and Toyama, Y.: Arthroscopic synovectomy of the elbow in rheumatoid arthritis. J. Bone Joint Surg. 84A:342, 2002. Inglis, A. E., and Figgie, M. P.: Septic and non-traumatic conditions of the elbow. In Morrey, B. F. (ed.): The Elbow and Its Disorders, 2nd ed. Philadelphia, W. B. Saunders, 1993, p. 759. Inglis, A. E., Ranawat, C. S., and Straub, L. R.: Synovectomy and debridement of the elbow in rheumatoid arthritis. J. Bone Joint Surg. 53A:652, 1971. Jensen, C. M., Rasmussen, S. W., Haugegaard, M., Melchior, T. M., and Hansen, H.: Elbow synovectomy in rheumatoid arthritis. Acta Orthop. Belg. 62:144, 1996. Kelly, E. W., Morrey, B. F., and O’Driscoll, S. W.: Complications of elbow arthroscopy. J. Bone Joint Surg. 83A:25, 2001. Lee, B. P. H., and Morrey, B. F.: Arthroscopic synovectomy of the elbow for rheumatoid arthritis. A prospective study. J. Bone Joint Surg. 79B:770, 1997. Lehtinen, J. T., Kaarela, K., Ikavälko, M., Kauppi, M. J., Belt, E. A., Kuusela, P. P., Kautiainen, H. J., and Lehto, M. U.: Incidence of elbow involvement in rheumatoid arthritis. A 15 year endpoint study. J. Rheumatol. 28:70, 2001. Linclau, L. A., Winia, W. P., and Korts, J. K.: Synovectomy of the elbow in rheumatoid arthritis. Acta Orthop. Scand. 54:935, 1983. Ljung, P., Jonsson, K., Rydgren, L., and Rydholm, U.: The natural course of rheumatoid elbow arthritis: A radiographic and clinical five-year follow-up. J. Orthop. Rheumatol. 8:32, 1995. Lonner, J. H., and Stuchin, S. A.: Synovectomy, radial head excision, and anterior capsular release in stage III inflammatory arthritis of the elbow. J. Hand Surg. 22A:279, 1997.

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29. Mäenpää, H. M., Kuusela, P. P., Kaarela, K., Kautiainen, H. J., Lehtinen, J. T., and Belt, E. A.: Reoperation rate after elbow synovectomy in rheumatoid arthritis. J. Shoulder Elbow Surg. 12:480, 2003. 30. Mäenpää, H. M., Kuusela, P. P., Lehtinen, J. T., Savolainen, A., Kautiainen, H., and Belt, E.: Elbow synovectomy on patients with juvenile rheumatoid arthritis. Clin. Orthop. Relat. Res. 412:65, 2003. 31. Mitchel, N., Laurin, C., and Shepard, N.: The effect of osmium tetroxide and nitrogen mustard on normal articular cartilage. J. Bone Joint Surg. 55B:814, 1973. 32. Morrey, B. F., and Adams, R. A.: Semiconstrained arthroplasty for the treatment of rheumatoid arthritis of the elbow. J. Bone Joint Surg. 74A:479, 1992. 33. Morrey, B. F., Askew, L. J., An, K. N., and Chao, E. Y.: A biomechanical study of normal functional elbow motion. J. Bone Joint Surg. 63A:872, 1981. 34. Myllyla, T., Peltonen, L., Puranen, J., and Korhonen, L.: Consequences of synovectomy of the knee joint, clinical, histopathological and enzymatic changes and changes in 2 components of complement. Ann. Rheum. Dis. 42:28, 1983. 35. Nemoto, K., Arino, H., Yoshihara, Y., and Fujikawa, K.: Arthroscopic synovectomy for the rheumatoid elbow: A short term outcome. J. Shoulder Elbow Surg. 13:652, 2004. 36. O’Driscoll, S. W., and Morrey, B. F.: Arthroscopy of the elbow: Diagnostic and therapeutic benefits and hazards. J. Bone Joint Surg. 74A:84, 1992. 37. Oka, M., Rekonen, A., and Ruotsi, A.: The rate and distribution of intra-articularly injected osmium tetroxide (os-191). Acta Rheum. 15:35, 1969. 38. Paus, A., Refsum, S., and Forre, O.: Histopathologic changes in arthroscopic synovial biopsies before and after open synovectomy in patients with chronic inflammatory joint diseases. Scand. J Rheumatol. 19:202, 1990. 39. Porter, B. B., Park, N., Richardson, C., and Vainio, K.: Rheumatoid arthritis of the elbow: The results of synovectomy. J. Bone Joint Surg. 56B:427, 1974. 40. Rymaszewski, L. A., Mackay, I., Amis, A. A., and Miller, J. H.: Long-term effects of excision of the radial head in rheumatoid arthritis. J. Bone Joint Surg. 66B:109, 1984. 41. Saito, T., Koshino, T., Okamoto, R., and Horiuchi, S.: Radical synovectomy with muscle release for the rheumatoid elbow. Acta Orthop. Scand. 57:71, 1986.

42. Schemitsch, E. H., Ewald, F. C., and Thornhill, T. S.: Results of total elbow arthroplasty after excision of the radial head and synovectomy in patients who had rheumatoid arthritis. J. Bone Joint Surg. 78A:1541, 1996. 43. Smith, S. R., Pinder, I. M., and Ang, S. C.: Elbow synovectomy in rheumatoid arthritis: Present role and value of repeat synovectomy. J. Orthop Rheumatol. 6:155, 1993. 44. Stucki, G., Bozzone, P., Treuer, E., Wassmer, P., and Felder, M.: Efficacy and safety of radiation synovectomy with yttrium-90: A retrospective long-term analysis of 164 applications in 82 patients. Br. J. Rheumatol. 32:383, 1993. 45. Summers, G. D., Taylor, A. R., and Webley, M.: Elbow synovectomy and excision of the radial head in rheumatoid arthritis: A short term palliative procedure. J. Rheumatol. 15:566, 1988. 46. Tanaka, N., Sakahashi, H., Hirose, K., Ishima, T., and Ishiim, S.: Arthroscopic and open synovectomy of the elbow in rheumatoid arthritis. J. Bone Joint Surg. 88A:521, 2006. 47. Taylor, A. R., Mukerjea, S. K., and Rana, N. A.: Excision of the head of the radius in rheumatoid arthritis. J. Bone Joint Surg. 58B:485, 1976. 48. Torgerson, W. R., and Leach, R. E.: Synovectomy of the elbow in rheumatoid arthritis: Long-term results. J. Bone Joint Surg. 71B:664, 1989. 49. Tulp, J. J. A., and Winia, W. P.: Synovectomy of the elbow in rheumatoid arthritis: Long-term results. J. Bone Joint Surg. 71B:664, 1989. 50. Vahvanen, V., Eskola, A., and Peltonen, J.: Results of synovectomy in rheumatoid arthritis. Arch. Orthop. Trauma Surg. 110:151, 1991. 51. van der Lugt, J. C. T., Geskus, R. B., and Rozing, P. M.: Influence of previous open synovectomy on the outcome of Souter-Strathclyde total elbow prosthesis. Rheumatology 43:1240, 2004. 52. Whaley, A., Morrey, B. F., and Adams, R.: Total elbow arthroplasty after previous resection of the radial head and synovectomy. J. Bone Joint Surg. 87B:47, 2005. 53. Wolfe, A. M.: The epidemiology of rheumatoid arthritis: A review. Bull. Rheum. Dis. 19:518, 1968. 54. Woods, D. A., Williams, J. R., Gendi, N. S. T., Mowat, A. G., Burge, P. D., and Carr, A. J.: Surgery for rheumatoid arthritis of the elbow: A comparison of radial-head excision and synovectomy with total elbow replacement. J. Shoulder Elbow Surg. 8:291, 1999.

Chapter 69 Interposition Arthroplasty of the Elbow

CHAPTER

69

Interposition Arthroplasty of the Elbow Bernard F. Morrey and A. Noelle Larson

INTRODUCTION In my practice, interposition arthroplasty is assuming an ever-increasing relevance as we continue to struggle to develop alternatives to prosthetic replacement in the younger patient. Since the last edition, we have improved our technique, and possibly our results.

HISTORICAL ASPECTS The so-called functional arthroplasty, popularized by Hass (1944),11 might be considered the predecessor of interposition arthroplasty. Functional arthroplasty is actually a variation of resection arthroplasty, except that the distal humerus is fashioned in the shape of a wedge and various types of interposed tissues may be inserted (Fig. 69-1). Hass reported a long-term satisfactory result of 73% in 15 patients, with an average follow-up period of 5.5 years. Because this is a type of resection arthroplasty, it is not surprising that 13 of the 15 procedures were in patients with previous infection. Interposition arthroplasty has been used for treatment of arthritis involving the temporomandibular, shoulder, wrist, knee, and hip joints. Of these, the elbow has been reported as second only to the temporomandibular as the joint most amenable to the technique.13 In Europe, arthroplasty was popularized by Putti30 and by Payr.28 Schüller was the first to recommend the procedure for patients with rheumatoid arthritis.32 Various muscle flaps, pig bladder,2 fascia-fat transplants, skin, and other materials have been used as the interposing agent. In 1902, Murphy introduced and popularized arthroplasty in the United States.26,27 Lexer,21 in 1909, emphasized the value of autogenous tissue and confirmed the impression of Murphy27 that fat and fascia were the best substances for interposition arthroplasty. He reported that fascia remained viable and was replaced by fibrous and fibrocartilaginous tissue. The observation has not been subsequently confirmed,

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rather the joint appears to be comprised primarily of fibrous tissue.29

OUTCOMES Autogenous or xenograft cutis has been used as an interposing membrane in resection arthroplasties (cutis arthroplasty) of various joints since 1913, and successful use in the elbow has been reported by several authors.9,16,24 Cutis is the thick dermal layer of skin that remains after the superficial epidermal layer has been removed. It is a tough, durable, elastic membrane, and it closely adheres to the cut surface of the distal humerus. Fascia lata is easy to harvest and conforms readily to the bony surfaces, but the donor site leaves variable morbidity. Efforts to enhance its effect have been reported by Kita17 using chromicized fascia lata, the so-called J-K membrane. In 1979, Shahriaree and colleagues33 reported that of 30 patients, 90% returned to their previous occupations after excisional arthroplasty with Gelfoam interposition. Smith and associates34 successfully used silicone sheets as interposition material in six patients with hemophilic arthropathy. In recent years, the concept has been reassessed with the addition of three important features to the technique: distraction, motion, and large allograft interposition.

INDICATIONS BASIC CONCEPTS For the young individual who has lost the use of the elbow, avoidance of arthroplasty is desirable. Alternative recommendations include (1) no surgical treatment and altered activity, (2) orthotics for the unstable elbow, (3) arthrodesis, and (4) interposition (distraction) arthroplasty. Resection arthroplasty is rarely, if ever, indicated at this time, the only indication being uncontrollable infection with inadequate bone to allow an ulnohumeral fulcrum. If the elbow is ankylosed in a functional position, no treatment may be required. If it is ankylosed in a poor position, osteotomy with correction of the position may be considered. If the patient has mildly painful motion or a minimally unstable elbow, an orthotic brace may allow continuation of activities until progression dictates definitive treatment. The individual who is required to carry out strenuous activities may not be a suitable candidate for any type of arthroplasty.

INTERPOSITION Specific Indications The basic indications for interposition arthroplasty are either incapacitating pain or loss of motion in an

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Part VII Reconstructive Procedures of the Elbow

Skin graft

FIGURE 69-1

The so-called functional or anatomic arthroplasty resects variable amounts of distal humerus but fashions the bone as a fulcrum against which the proximal ulna pivots. Skin and other substances can be used to cover the humerus and create a new articular surface; hence, the term interposition arthroplasty.

individual younger than 40 years of age with rheumatoid arthritis, and younger than 60 years of age with traumatic arthritis. Loss of motion may follow trauma, sepsis, burns, or degenerative or inflammatory arthritis. However, the most compelling indication for arthroplasty of the elbow is incapacitating functional loss. If the loss of motion and pain are postinfectious, careful evaluation must be done to ensure that the patient has been free of the infection, preferably for at least 1 year. The best indication for this procedure is post-traumatic, painful loss of motion not complicated by sepsis in an individual who does not require long-term heavy demand on the joint.25 In addition to the specific pathology, selection of the proper candidate for interposition arthroplasty largely depends on patient needs and expectations, and whether alternatives exist.

CONTRAINDICATIONS If recent sepsis has occurred, other than débridement, reconstruction should not be considered. If epiphyseal closure has not occurred, arthroplasty should be delayed until growth is complete. In the past, a major contradiction to interposition arthroplasty was inadequate bone stock. Grishin and colleagues,10 however, have reported using interposition arthroplasty in conjunction with reconstructive bone grafts for marked osseous deficiency.

We have found gross instability, deformity, and marked pain, especially at rest, are all associated with poorer outcomes.8,20,25 The patient with a grossly unstable elbow from rheumatoid or post-traumatic arthritis cannot be adequately stabilized by an interposition procedure. Congenital ankylosis of the elbow joint that lacks the necessary ligamentous support may be treated with interposition and ligamentous reconstruction. However, the absence of flexion motor power is an absolute contraindication to this procedure. The need to use the upper extremity in ambulation or for transfer from bed to chair is a relative contraindication because excessive loading of the elbow destabilizes the joint. If the patient is a heavy laborer, interposition arthroplasty may not be as satisfactory as a painless arthrodesis of the elbow in a functional position. Although interposition arthroplasty offers the patient a relatively pain-free durable joint, it cannot guarantee enough stability to allow for the activities of heavy labor. If multiple joints in the same extremity have become ankylosed, it will be more difficult to secure a satisfactory result. Finally, it is of utmost importance that the patient have the motivation and fortitude to participate in a preoperative and postoperative rehabilitation program for proper rehabilitation of the musculature of the upper extremity.

PREFERRED TISSUE Autogenous skin and fascia and achilles tendon allografts have all been used by the senior author. The cutis is very durable and thick, rapidly adheres to the bone, and has generally been successful.4,7,9 The harvest techniques are attractive in those patients in whom primary closure may be carried out. Cutis tissue without the epidermis is somewhat more difficult to harvest. Fascia is also commonly used because it is readily available from the thigh and can be overlapped to ensure adequate bulk.18,25 Recently other processed tissues such as AlloDerm (LifeCell, Branchburg, NJ) are being investigated for this purpose.12 At present, we prefer the achilles tendon allograft because it is readily available. The following anatomic features are required for success of the procedure: absence of donor site morbidity, large size and thickness, sufficient material for ligament reconstruction if necessary, and presence of calcaneus if osseous graft is required.

PREFERRED TECHNIQUE—ACHILLES TENDON ALLOGRAFT Herein we describe our current exposure, preparation, graft insertion, and closure. The technique may be used for any tissue.

Chapter 69 Interposition Arthroplasty of the Elbow

SURGICAL TECHNIQUE The patient is positioned supine with a pneumatic tourniquet in place. A posterior incision is preferred, although a pre-existing incision is reopened if consistent with the needed deep exposure. In all instances, the ulnar nerve is identified, mobilized, and protected throughout the case. The nerve is transposed subcutaneously if it is found to subluxate at the completion of the surgery. Kocher’s interval is developed between the anconeus and extensor carpi ulnaris. The lateral collateral ligament (LCL) complex and the common extensor muscles are released from the lateral condyle of the humerus. Anterior and posterior capsulectomy is performed to obtain useful elbow motion (Fig. 69-2). The tip of the olecranon is removed if it is prominent. The triceps muscle is elevated

Lateral collateral ligament

937

from the lateral distal humerus, and the anconeus mobilized from its ulnar attachment. The lateral one half of the triceps attachment is released from the olecranon, and the extensor mechanism is inserted as the forearm is flexed and supinated. If the cartilage appears beyond salvage, then the decision is made to proceed with interposition arthroplasty. The ulnar and humeral surfaces are prepared with a rongeur, burr, or semicircular saw to obtain a congruent articulation (Fig. 69-3). Care is taken to avoid resection of the subchondral bone, which may lead to excessive bony resorption, although the medial and lateral trochlear ridges are removed if necessary to obtain a smooth articulation. Sufficient bone is resected from the ulnar and humeral articular surfaces to accommodate at least 2 to 3 mm of joint space laxity even after insertion of the tendon to avoid “overstuffing” the joint.

Common extensor tendon

Anconeus

A

Triceps attachment

FIGURE 69-2

B

A, Kocher’s interval is entered through a posterior skin incision. The triceps is elevated posteriorly from the humerus, whereas the extensor mechanism is elevated anteriorly. Typically, approximately a third to a half of the triceps attachment is removed from the olecranon in order to afford adequate exposure for insertion of the interposition tissue. B, The lateral collateral ligament is released along with the anterior and posterior capsules. (A, By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

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Part VII Reconstructive Procedures of the Elbow

FIGURE 69-3

The distal humerus has been exposed. The lateral collateral ligament has been preserved. The ulnar nerve has been anteriorly translocated (left). Preparation of the distal humerus preserves the subcondral bone. Through-and-through drill holes are placed to receive the graft (right). (Right, By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

Graft Application and Ligament Reconstruction A fresh-frozen Achilles tendon allograft is our current preference (Fig. 69-4). Three or four drill holes are made across the distal humerus (see Fig. 69-3). Using a horizontal mattress stitch, the graft is sutured to the distal humerus through the drill holes (Fig. 69-5). The ulnohumeral joint is then reduced, and the integrity of the medial collateral ligament (MCL) is assessed. The smoothness of the articulation and elbow range of motion are determined. If adequate tissue is present, the lateral collateral ligament is repaired primarily. If the tissue is inadequate, reconstruction of the remaining portion of the ligament is carried out with the allograft tendon (Fig. 69-6). In cases in which both lateral and medial collateral ligaments are intraoperatively found to be deficient, a tunnel is drilled through the distal humerus, replicating the axis of rotation at the ulna. A second tunnel connects the sublime tubercle and the tubercle of the crista supinatorus. The distal strands of the allograft are threaded through the humeral tunnel and ulnar tunnels to create a “sling” simultaneously to reconstruct both the MCL and LCL (Fig. 69-7). The sling is hand-tensioned to maintain joint stability but still allow for smooth flexion and extension across the articulation. Following the reconstruction, the elbow is again taken through a range of articulated motion and tested for stability.

FIGURE 69-4

An Achilles tendon allograft with sutures in place ready to be placed over the distal humerus preserves the subchondral bone.

Chapter 69 Interposition Arthroplasty of the Elbow

939

FIGURE 69-5

The Achilles tendon allograft has been placed over the distal humerus. Two of the three sutures that secure the graft are in place.

FIGURE 69-7

In instances in which both collateral ligaments have been deficient, the “tails” of the Achilles tendon graft are harvested to reconstruct the medial and lateral collateral ligaments. A single drill hole connects the ulna attachment of these two ligaments as shown. Under these circumstances, the construct is always protected with the external fixator. (By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

Anatomic origin

Aftercare FIGURE 69-6

An extension of the lateral aspect of the Achilles tendon graft is preserved, brought over the lateral aspect of the distal humerus, and anchored to the anatomic origin of the lateral ulnar collateral ligament.

EXTERNAL FIXATION Standard treatment today involves placement of an external fixator (DJD I or II Dynamic Elbow Joint Distractor, Stryker, Kalamazoo, MI). This device may be applied without damage to any collateral repair or reconstruction (Fig. 69-8). The fixator is intended to maintain stability and to distract or separate the joint, allowing for motion while protecting the interposition and the ligament reconstruction to allow for proper healing. In some instances, because of patient preferences, geographic distances rendering follow-up impractical, or surgeon’s intraoperative judgment, the fixator is not applied.

Patients are treated with continuous passive motion in the hospital for a mean of 2.3 days, typically with an axillary block for regional pain control. Today patients are routinely dismissed home on postoperative day two. At a mean of 30 to 35 days postoperatively, the patient returns for removal of the external fixator under anesthesia. The elbow is gently “examined” for stability and smoothness of the articulation, as well as being taken through a range of motion. No forceful maneuvers were employed, but the flexion and extension limits are stretched at this time. Mean range of motion obtained at the examination under anesthesia is about 115 degrees.1 Patients with persistent stiffness are prescribed static adjustable flexion and extension splints to be worn 23 hours per day for 3 weeks to maintain the range of motion obtained at the examination under anesthesia. Maintenance bracing is continued for 8 to 12 weeks. No dynamic splinting is used, and no patient is treated with formal physical therapy.

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Part VII Reconstructive Procedures of the Elbow

A

B

C D FIGURE 69-8

A, The external fixator is applied using a stylus to simulate the axis of rotation. The stylus prevents injury to the reconstructed collateral tissue. B, The ulna is separated from the humerus in order to allow motion while protecting against shearing forces on the interposed tissue, allowing it to securely heal to the humerus. Excellent flexion (C) and extension (D) motion is expected.

CUTIS ARTHROPLASTY

CUTIS HARVEST—FROIMSON

HARVEST AND APPLICATION

Using a hand-held or motorized dermatome, remove a thin split-thickness skin graft from the patient’s lower abdomen, leaving a standard split-thickness donor site with punctate bleeding. With a sharp knife, remove this deep dermal layer with minimal subcutaneous fat (Fig. 69-10). Secure hemostasis with electrocautery and use the split-thickness graft to cover the donor site.

The senior author uses the cutis for limited interposition such as for radiohumeral arthritis. Froimson and associates9 have described a more extensive harvest and application. If fascia is to be used, we favor folding the graft into a three-ply construct (Fig. 69-9).

Options

Chapter 69 Interposition Arthroplasty of the Elbow

941

FIGURE 69-9

The tissue is attached by throughand-through sutures across the distal humerus. If fascia is used, a three-ply composite is used and is attached as shown.

FIGURE 69-10 Froimson technique for harvesting cutis arthroplasty from the lower abdomen. This does require a skin graft to be placed over the cutis donor site. This graft is usually obtained from the thigh.

LIMITED HARVEST—MORREY An alternative method to harvest a limited graft has been developed. An elliptical pattern is placed in the bikini line (Fig. 69-11). Linear incisions just through the epidermis are made every 3 to 4 mm. The dermis is elevated leaving the cutis, which is sharply excised. The wound is closed primarily. This has the advantage of

being a relatively quick procedure with a more pleasing scar at the donor site.

APPLICATION Attach the cutis graft to the prepared end of the distal humerus as described earlier.

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Part VII Reconstructive Procedures of the Elbow

Cutis

A

B

RESULTS HISTORICAL Early reports of fascial arthroplasty by Campbell,5,6 Henderson,13,14 and MacAusland and MacAusland23 showed that excellent or good pain relief and improvements in motion and function were obtained in about 75% of patients. In 1940, Speed and Smith35 noted that the best results could be obtained in patients between the ages of 18 and 40 years. In 1952, Knight and Van Zandt18 reported 56% good and 22% fair results in 45 patients an average of 14 years after fascial arthroplasty. Their best results were obtained in patients between the ages of 20 and 50 years. Most patients regained motion between 6 months and 6 years after surgery, and maximum strength was obtained at about 1 year. In 1967, Vainio37 reported that more than half of 131

FIGURE 69-11 The Morrey technique harvests a limited amount of cutis tissue in the bikini line (A). Thin strips of dermis are removed, allowing the cutis to then be excised. The donor site is closed primarily (B).

patients undergoing fascial arthroplasty for rheumatoid arthritis were free of pain and had more than 90 degrees of flexion. Subsequent reports have supported the value of fascial arthroplasty of the elbow in well-selected patients.9,16,24,36 Kita17 reported the use of a chromicized fascial interposition material in 31 patients in an attempt to reduce the inflammatory response initiated by fascia lata. At 19-year follow-up, half of his patients had excellent or good results and 20% had poor results. Uuspaa36 reported improved range of motion and decreased contractures after 51 cutis arthroplasties in 48 patients with rheumatoid arthritis; these patients ranged in age from 25 to 69 years. In a recent review of cutis arthroplasties in 14 patients ranging in age from 26 to 51 years, motion and medial-lateral stability were satisfactory in all.21 Although the technique is favored for rheumatoid arthritis in Europe, both rheumatoid and traumatic

Chapter 69 Interposition Arthroplasty of the Elbow

conditions are available to interposition arthroplasty if the proper indications are met (see Figs. 69-7, 69-8, and 69-12). Little correlation between the final radiographic appearance of the elbow and the functional result is accepted. Range of motion and stability of the arthroplasty are best in patients with good periarticular structures and good elbow flexor and extensor musculature.

943

years. Overall, 69% were satisfied and 70% had no or minimal activity restriction. Generally good results were reported in 14 with rheumatoid arthritis and followed 12 years after autogenous triceps fascial interposition.24 Ljung and associates22 described the results of 35 procedures using bovine cutis interposition and followed a mean of 6 years. Although 21 of 28 (75%) were pain free, functional limitation, especially instability, prompted the authors to recommend elbow replacement as the treatment of choice.

CURRENT EXPERIENCE Rüther and colleagues31 recently reported the results of 61 procedures for rheumatoid arthritis and using dura mater, 17 of which were followed for less than 5 years, 52 between 5 and 10 years, and 12 for more than 10

MAYO EXPERIENCE The initial experience was focused on a group of 60 patients with stiffness as the primary diagnosis.25 The concept of an aggressive soft tissue release, interposition

FIGURE 69-12 A, Radiographic appearance of an elbow with post-traumatic arthritis. B, Radiographic appearance following fascial arthroplasty; left, extension; right, flexion. C, Flexion 5 years following surgery. D, Extension 5 years following surgery.

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Part VII Reconstructive Procedures of the Elbow

with fascia lata and protection using an external fixator was introduced. With a follow-up of more than 5 years, more than 80% of patients were satisfied with the procedure. The arc of motion increased from a mean of 30 degrees to 90 degrees (Fig. 69-13). In a subsequent study of 13 patients with traumatic arthritis but good motion (>80 degrees), Cheng and Morrey8 documented 75% satisfactory results using fascia lata, a mean of 5 years (range, 2 to 12 years) after surgery. It is of note that those without pre-existing instability revealed 80% satisfactory outcomes. Those with residual instability had a 50% unsatisfactory outcome (Fig. 69-14).

points postoperativeloy (P < 0.001), matched pairs analysis) (see Fig. 69-14). Only 30% demonstrated a satisfactory MEPS, however, subjectively 88% would repeat the procedure. Despite efforts to reconstruct collateral ligaments, preoperative instability on physical examination was associated with low MEPS (P = 0.03), and high DASH scores15 (P = 0.006, Fisher exact test) postoperatively when compared to patients with no preoperative instability. On the other hand, a well-balanced interposition procedure can last up to 20 years (Fig. 69-15). PRE-OP

MAYO RECENT EXPERIENCE Our experience has recently been updated by Larson et al.20 Between 1996 and 2003, 69 consecutive elbows underwent interposition arthroplasties, all with an achilles tendon allograft. A hinged external fixator was used postoperatively in two thirds of these patients. Overall, the patient population was young, averaging 39 years. About 25% were for inflammatory and 75% had posttraumatic arthritis. Details are available in 45 patients. The mean time to clinical follow-up was 6.0 years (range 2.9 to 10.5 years). Seven patients subsequently underwent revision surgery: two infection cases, two instability cases, one elbow arthrodesis for instability, and two elective total elbow arthroplasties. In the thirty-eight patients with surviving allografts, the flexion-extension arc improved from a preoperative mean of 51 degrees to 97 degrees following surgery (P < 0.001, matched pairs analysis). Mean preoperative MEP score was 42 points, improving to a mean of 65 140

A

B 6.5 YRS. POST-OP

Mean ± SD

Flexion arc (degrees)

120 100 80 60 40

C

D

20

FIGURE 69-14 0 Pre-op

Post-op

FIGURE 69-13 Results after distraction interposition arthroplasty in patients with preoperative stiffness.

A and B, Preoperative radiograph of 32-year-old woman with rheumatoid arthritis. Her preoperative arc of flexion was 45 degrees. C and D, Six and a half years after surgery, the patient has minimal pain with an arc of motion of 30 to 125 degrees. She is satisfied with the procedure.

% surviving

Chapter 69 Interposition Arthroplasty of the Elbow

1.0 0.9 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.1 0.0

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80% at 10 yrs. 89% at 5 yrs.

0

1

2

3

4

5

6

7

8

9

10

11

Years

FIGURE 69-16

The Kaplan-Meier survival curve free of reoperation reveals that in many instances, the fascial interposition arthroplasty, if it is successful early on, may be maintained for many years. 20 yrs

FIGURE 69-15

This long-term 20-year result of a fascial interposition arthroplasty is believed to largely be due to the well-balanced relationship between the ulna and the humerus, and the stability of this construct.

We consider interposition arthroplasty a salvage procedure indicated for young active patients with severe inflammatory or post-traumatic arthritis, especially with limited elbow motion. Caution must be used in patients with primary surgical indication of instability or intense pain. Yet, it can be a reliable salvage in many patients (Fig. 69-16).

COMPLICATIONS Complications of this procedure are considerable and include bone resorption, heterotopic bone formation, triceps rupture, medial and lateral subluxation, infection, and seroma formation in the fascial graft donor site, and long-term failure. Bone resorption occasionally occurs at the distal humeral condyles. It may cause no difficulty, or it may contribute to instability, especially if resorption occurs more on one side than on the other. Subluxation and instability may occur from resorption or because of technical difficulties. Although the joint may function reasonably well in spite of medial or lateral subluxation, usually these patients do not do well, so if the tendency to subluxate is apparent at the time of the interposition arthroplasty, this is addressed by repairing or reconstructing the collateral ligaments and applying a distraction device.10 If this is not successful, then proceed to fusion or prosthetic replacement.

Triceps rupture is an uncommon complication that is related to the surgical exposure and repair rather than to the procedure itself. This can be minimized by using the exposure described above. Infection following fascial arthroplasty should be managed promptly and aggressively. For superficial infections and cellulitis, the part should be placed at rest, elevated, and immobilized in a long arm posterior splint while appropriate antibiotics are administered. If the infection involves the deep structures, open drainage and excision of the graft is required. If bony infection occurs, removal of the implant and osseous débridement are required. Although this will leave the elbow more unstable, a useful limb often can be salvaged. Salvage with prosthetic replacement is out of the question in the short term (<1 year). If a hematoma or seroma forms at the surgical or donor sites, it will usually resolve over a period of weeks. These collections rarely require drainage. If such an accumulation persists or is unusually large, needle aspiration should be adequate.

REVISION Revision of failed interposition arthroplasty is usually due to pain, reankylosis, or instability. The result can deteriorate with time, especially in the active individual. Additional surgery may not be offered because frequently little more can be done to modify the symptoms or attain the expectations of the patient. If the precise cause of failure can be identified, revision is occasionally helpful.19 Larson and associates reported four of six successful re-interposition procedures performed at the Mayo Clinic. Typically, however, prosthetic replacement is the salvage procedure of choice and is readily performed (Fig. 69-17). Blaine et al3 reviewed our experience

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Part VII Reconstructive Procedures of the Elbow

FIGURE 69-17 Rheumatoid arthritis in a 34-year-old woman (A) treated with fascial interposition arthroplasty using the distractor, as discussed in the text (B).

Chapter 69 Interposition Arthroplasty of the Elbow

947

FIGURE 69-17, cont’d

At 3 years, the patient complained of severe pain (C). Three years after elbow replacement, she is again pain free (D).

with 13 revisions of failed interposition to elbow replacement. With a mean surveillance of 9 years (2 to 16 years); 11 of 13 (85%) were classified as satisfactory. Hence, failed interposition can be successfully salvaged with prosthetic replacement.

References 1. Aragi, A., Celli, A., Adams, R. A., and Morrey, B. F.: The effect of examination under anesthesia on the stiff elbow following surgical release. J. Bone Joint Surg. Br. (in press).

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Part VII Reconstructive Procedures of the Elbow

2. Baer, W. S.: Preliminary report of animal membrane in producing mobility in ankylosed joint. Am. J. Orthop. Surg. 7:3, 1909. 3. Blaine, T. A., Adams, R., and Morrey, B. F.: Total elbow arthroplasty after interposition arthroplasty for elbow arthritis. J. Bone Joint Surg. 87A:286, 2005. 4. Brown, J. E., McGraw, W. H., and Shaw, D. T.: Use of cutis as an interposing membrane in arthroplasty of the knee. J. Bone Joint Surg. 40A:1003, 1958. 5. Campbell, W. C.: Mobilization of joints with bony ankylosis: an analysis of 110 cases. J. A. M. A. 93:976, 1924. 6. Campbell, W. C.: Operative Orthopedics. St. Louis, C. V. Mosby Co., 1939. 7. Cannaday, J. E.: Some experiences in the use of the cutis graft in surgery: with case reports. South. Med. J. 41:876, 1948. 8. Cheung, S. L., and Morrey, B. F.: Treatment of the mobile, painful arthritic elbow by distraction interposition arthroplasty. J. Bone Joint Surg. Br. 82B:233, 2000. 9. Froimson, A. I., Silva, J. E., and Richey, D.: Cutis arthroplasty of the elbow. J. Bone Joint Surg. 58A:863, 1976. 10. Grishin, I. G., Goncharenko, I. V., Kozhin, N. P., et al.: Restoration of the function of the cubital joint in extensive defects of bones and soft tissues using endoprosthesis and free skin grafts. Acta Chir. Plast. 31:143, 1989. 11. Hass, J.: Functional arthroplasty. J. Bone Joint Surg. 26:297, 1944. 12. Hausman, M. R., and Birnbaum, P. S.: Interposition elbow arthroplasty. Tech. Hand Up. Extrem. Surg. 8:181, 2004. 13. Henderson, M. S.: What are the real results of arthroplasty? Am. J. Orthop. Surg. 16:30, 1918. 14. Henderson, M. S.: Arthroplasty. Minn. Med. 8:97, 1925. 15. Hudak, P. L., Amadio, P. C., and Bombardier, C.: Development of an upper extremity outcome measure: The DASH (disabilities of the arm, shoulder and hand). The Upper Extremity Collaborative Group (UECG). Am. J. Ind. Med. 29:602, 1996. 16. Hurri, L., Pulkki, T., and Vainio, K.: Arthroplasty of the elbow in rheumatoid arthritis. Acta Chir. Scand. 127:459, 1964. 17. Kita, M.: Arthroplasty of the elbow using J-K membrane. Acta Orthop. Scand. 48:450, 1977. 18. Knight, R. A., and Van Zandt, I. L.: Arthroplasty of the elbow: an end-result study. J. Bone Joint Surg. 34A:610, 1952. 19. Larson, N., and Morrey, B. F.: Revision of failed interposition arthroplasty by re-interposition procedure. (in press).

20. Larson, N., and Morrey, B. F.: Interposition arthroplasty as a salvage procedure of the elbow using an achilles tendon allograft. Accepted for publication, J. Bone Joint Surg. Am. (in press), 2008. 21. Lexer, E.: Über Gelenktransplantationen. Arch. Klink. Chir. 90:263, 1909. 22. Ljung, P., Jonsson, K., Larsson, K., and Rydholm, U.: Interposition arthroplasty of the elbow with rheumatoid arthritis. J. Shoulder Elbow Surg. 5(2)Part I:81, 1996. 23. MacAusland, W. R., and MacAusland, A. R.: The Mobilization of Ankylosed Joints by Arthroplasty. Philadelphia, Lea & Febiger, 1929. 24. Mills, K., and Rush, J.: Skin arthroplasty of the elbow. Aust. N. Z. J. Surg. 41:179, 1971. 25. Morrey, B. F.: Post-traumatic contracture of the elbow: operative treatment, including distraction arthroplasty. J. Bone Joint Surg. 72A:601, 1990. 26. Murphy, J. B.: Ankylosis: Arthroplasty-clinical and experimental. Trans. Am. Surg. Assoc. 22:215, 1904. 27. Murphy, J. B.: Ankylosis: Arthroplasty, clinical and experimental. J. A. M. A. 44:1573, 1671, 1794, 1905. 28. Payr, E.: Über die operative Mobilizierung ankylosierter Gelenke. Munch. Med. Wchnschr. 37:1921, 1910. 29. Phemister, D. B., and Miller, E. M.: The method of new joint formation in arthroplasty. Surg. Gynecol. Obstet. 26:406, 1924. 30. Putti, V.: Arthroplasty. Am. J. Orthop. Surg. 3:421, 1921. 31. Rüther, W., Tillmann, K., and Backenhöhler, G.: Resection interposition arthroplasty of the elbow in rheumatoid arthritis. J. Orthop. Rheum. 5:31, 1992. 32. Schüller, M.: Chirungische mittheilungen über die chronish rheumatischen gelenkentzundungen. Arch. Klin. Chir. 45:153, 1893. 33. Shahriaree, H., Sajadi, K., Silver, C. M., and Sheikholeslamzadeh, S.: Excisional arthroplasty of the elbow. J. Bone Joint Surg. 61A:922, 1979. 34. Smith, M. A., Savidge, G. F., and Fountain, E. J.: Interposition arthroplasty in the management of advanced haemophilic arthropathy of the elbow. J. Bone Joint Surg. 65B:436, 1983. 35. Speed, J. S., and Smith, H.: Arthroplasty: a review of the past ten years. Int. Abst. Surg. Gynecol. Obstet. 70:224, 1940. 36. Uuspaa, V.: Anatomical interposition arthroplasty with dermal graft: a study of 51 elbow arthroplasties on 48 rheumatoid patients. Z. Rheumatol. 46:132, 1987. 37. Vainio, K.: Arthroplasty of the elbow and hand in rheumatoid arthritis: a study of 131 operations. In Chapchal, G. (ed.): Synovectomy and Arthroplasty in Rheumatoid Arthritis. Stuttgart, Georg Thieme Verlag, 1967, p. 66.

Chapter 70 Arthrodesis

CHAPTER

70

Arthrodesis Robert D. Beckenbaugh

INTRODUCTION Experience with elbow arthrodesis is often related to injuries seen from military conflict.2 Most civilian experience with elbow fusion has come from spontaneous arthrodesis subsequent to infection, trauma, or rheumatic disease of the elbow (Fig. 70-1). One of the prerequisites for elbow fusion is satisfactory function of the shoulder; yet, studies from our laboratory have clearly shown that the increased shoulder motion cannot compensate for loss of elbow motion (Fig. 70-2).17 Biomechanical and clinical studies have demonstrated that compensatory spinal column and wrist motions are used to improve function after elbow arthrodesis.17 Thus, limited function (motion) in these areas may be a relative contraindication to elbow arthrodesis. When disease involves both the elbow and the shoulder, arthroplasty must, therefore, be selected. In addition, arthrodesis is not indicated for bilateral elbow disease because the functional limitations are too great. If bilateral arthrodesis is performed, one elbow should be fused in 90 degrees of flexion for personal care and hygiene functions and the other in 45 to 65 degrees of flexion for other uses.9,17 Functionally, a limited range of 100 degrees in midposition is enough for most daily activities, but removing all elbow motion restricts the majority of necessary daily functions.14 Hence, some patients request fusion take-down and total elbow even after many years (see Chapter 58).

POSITION The optimal position for fusion depends on associated joint involvement, gender, the patient’s occupation, or specific functional requirements. Traditionally, 110 degrees is a more functional position.26 For men, 90 degrees of flexion is probably the best position of arthrodesis in a dominant arm that has good shoulder and wrist motion.16 In this position, the hand can reach the mouth with adaptive neck, shoulder, and wrist motion, and writing may be done comfortably. This has recently been challenged by one recent study suggesting special needs for the nondominant arm may prompt

949

fusion in 30 degrees or 60 degrees of flexion, if, for example, bench work or assistive movements are required.17,22 If power is not an issue, a position of 70 degrees may be desirable.

INDICATIONS Because of the limitations mentioned earlier, arthrodesis of the elbow is not often indicated. In fact, although shoulder fusion was employed in 23 of 144 patients with brachial plexus injury, elbow fusion was not preferred in a single patient.21 If it has a place in the surgeon’s armamentarium, it is for younger patients with post-traumatic unilateral arthrosis of the elbow who require a strong and stable joint.2 In patients older than 45 years who have bilateral disease and limited shoulder or wrist motion, arthroplasty, with or without joint replacement, is preferable. For unilateral postinfectious arthrosis, Rashkoff and Burkhalter proposed plate fixation of contaminated traumatic injuries of the elbow with chronic sepsis.13,20 Arthrodesis may be difficult to achieve after failed total elbow arthroplasty and is rarely indicated.11,27 It has yet to be performed at the Mayo Clinic after more than 1700 elbow replacements.

TECHNIQUE Most of the limited reports on arthrodesis deal with the various techniques.1,3,11,15,18 The elbow is one of the most difficult joints to fuse surgically. The hand and the forearm act as a long lever arm that produces strong bending forces across the potential fusion site. Success rates have improved considerably with adjunctive internal fixation and intramedullary bone grafting.11

HISTORICAL SURGICAL TECHNIQUES Steindler 25 described a single posterior tibial cortical graft keyed into the olecranon for fusion (Fig. 70-3A). Brittain developed a technique of crossed grafts through the elbow joint5,7 (see Fig. 70-3B). Noting that gravitational forces tended to compress the ends of the graft, he believed that the crossing of the grafts was important. Koch and Lipscomb12 have described a modification of this technique in which a tibial graft is placed through a large drill hole in the humerus and ulna, and other cancellous bone grafts are added to the joint. Staples24 uses a corticocancellous iliac graft through the posterior portion of the elbow and oblique humeral and olecranon intra-articular resection (see Fig. 70-3C).

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Part VII Reconstructive Procedures of the Elbow

A

B

FIGURE 70-1 Spontaneous arthrodesis (A) is more common than surgically performed fusion (B) in a civilian population.

STABILIZATION

FIGURE 70-2

Loss of elbow motion cannot be effectively compensated for by increased shoulder motion, as illustrated by the crescent-shaped space lost by a flexion contracture of the elbow, with normal shoulder motion.

RECENT SURGICAL TECHNIQUES Today, fusion is achieved through rigid plate fixation, transfusion fixation screws, an external fixator, or a combination of the last two.

Today, rigid fixation with supplemental autogenous or allograft bone is preferred. In the presence of active infection, external skeletal fixation has been preferred; however, fusion with plate stabilization, antibiotics, and an open wound can also succeed.13,20 In the presence of long-standing sepsis or arthrosis with limited motion and minimal deformity, arthrodesis may be achieved with limited internal fixation (screws), with or without bone grafts.11 If significant instability or deformity is present preoperatively, internal fixation with screws and supplemented with external skeletal fixation or plates should be used. Today, data clearly favor use of internal fixation.10 External fixation alone was successful in only five of nine in a recent series from Germany.

TECHNICAL OPTIONS Plate Fixation

PRINCIPLES: JOINT PREPARATION In some instances, the joint may be fixed after minimal removal or fashioning of the joint surfaces. This is preferable if articular bone is present.

Spier23 and Plank19 have described a compression arthrodesis that makes use of a bent plate and an external compression device (Fig. 70-4). This is also the method favored by Burkhalter13 and is probably most commonly used today.18

Chapter 70 Arthrodesis

Sagittal section showing position of graft

A

B

951

nally and detached distally for 5 cm with medial and lateral periosteal sleeves. The radial head and both humeral condyles are resected. Complete synovectomy and removal of the articular cartilage is performed. The proximal ulna and the olecranon fossa are shaped into matching triangular sets. After the olecranon is inserted into the trochlea, a single cortical screw is placed from the posterior olecranon and humerus obliquely into the ulna. The flexor and extensor origins are sutured to the triceps fascia, and the triceps is repaired anatomically; the ulnar nerve is transposed anteriorly. Postoperatively, the patient wears a long-arm cast for 3 months, and then mobilization is allowed. Appropriate drug therapy is initiated preoperatively and continued as necessary through 18 months. In 13 patients with tuberculosis, he achieved healing within 3 months in all.

EXTERNAL SKELETAL FIXATION

C FIGURE 70-3

A, Steindler technique of elbow fusion. B, Crossed tibial graft technique of Brittain. C, Staples’ technique of elbow arthrodesis. (A redrawn from Steindler, A.: Reconstructive Surgery of the Upper Extremity. New York, D. Appleton & Co., 1923; B redrawn from Brittain, H. A.: Architectural Principles in Arthrodesis, 2nd ed. Edinburgh, E. & S. Livingstone, Ltd., 1952; C from Staples, O. S.: Arthrodesis of the elbow joint. J. Bone Surg. 34A:207, 1952.)

Compression Screws For post-traumatic arthrosis of the elbow with minimal motion that causes significant pain, we have used compression fixation of the elbow with screws. The procedure involves partial débridement of remaining articular surfaces and compression screw fixation without grafts (Fig. 70-5). Others have subsequently reported on similar techniques.11,18 For active draining sinuses due to tuberculosis, Arafiles1 has described a technique that locks the olecranon in the humeral fossa and stabilizes it by screw fixation.

Technique A straight longitudinal incision is made over the posterior elbow. The triceps tendon is split longitudi-

Bonnel3 reported a successful case of elbow arthrodesis (for failed arthroplasty) in which external skeletal fixation was combined with bone grafting (Fig. 70-6). In the presence of active sepsis, synovectomy and débridement of the radial head and articular surfaces, followed by external skeletal fixation allows spontaneous arthrodesis to occur in the desired position. Fixation has also been described with a bilateral trapezoidal frame. Two transfixing pins are placed in the midportion of the humerus and in the proximal ulna. Care must be taken to avoid the radial and ulnar nerves. Three nontransfixing pins are placed in the midportions of the radius and ulna, and the trapezoidal configuration is completed.6 There is, however, no single arrangement that must be followed; rather, the design is dictated by the lesion, especially by the amount of bone fusion (Fig. 70-7).

Combination: AO Compression When possible, axial compression with external fixation coupled with a cancellous lag screw placed into the humeral shaft is an attractive blend of concepts (Fig. 70-8). Through a posterior approach, the surfaces of the distal humerus and olecranon are resected to provide a wedge fit. The radial head is excised, and a Kirschner wire is passed from the olecranon up the humeral shaft. Transverse pins are inserted through the olecranon and humerus, the Kirschner wire is removed, and a long, cancellous screw is inserted with a washer up the shaft of the humerus. External compression clamps are then applied.

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Part VII Reconstructive Procedures of the Elbow

FIGURE 70-4

A contoured plate applied posteriorly is the most common technique of elbow arthrodesis today (A). Distal humeral nonunion (B) treated with the posterior plate (Spier’s technique) (C). (B and C from Spier, W.: Beitrag zur Technik der Druckarthrodese des Ellenbogengelenks. Monatsschr. Unfallheilkd. 76:274, 1973.)

FIGURE 70-5 A, Post-traumatic elbow arthrosis. Patient has 10 degrees of painful motion. B, Solid fusion after compression screw application across elbow without bone graft.

Chapter 70 Arthrodesis

953

FIGURE 70-6

Fixation of humerus, radius, and ulna with Hoffmann’s device for arthrodesis of elbow. (From Bonnel, F.: Technique d’arthrodese du coude par fixateur externe. J Chir. [Paris] 107:79, 1974.)

FIGURE 70-7

A, Unstable elbow after débridement for chronic draining Pseudomonas osteomyelitis in a steroid-dependent rheumatoid arthritis patient. B, Two months after application of a bilateral triangular frame. Wounds were left open and healed per primum. Bony arthrodesis is occurring. C, Bilateral triangular frame of the type seen in A and B for an unstable and infected elbow.

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Part VII Reconstructive Procedures of the Elbow

FIGURE 70-8

The AO technique of axial fixation and external skeletal fixation for arthrodesis of the elbow. (Redrawn from Muller, M. E., Allgower, M., Schneider, R., and Willenegger, H.: Manual of Internal Fixation: Techniques Recommended by the AO-Group, 2nd ed. Berlin, Springer-Verlag, 1979.)

FIGURE 70-9

A, Fracture below elbow arthrodesis. B, Rapid healing with simple immobilization.

AUTHOR’S PREFERRED METHOD OF TREATMENT FOR UNSTABLE ELBOWS Without Sepsis Application of internal fixation with screws to an unstable elbow not involved by sepsis will achieve immediate stability and allow additional bone grafting, if necessary. This, in conjunction with cast fixation, should produce simplified and more rapid union.

In the presence of infection and an unstable elbow, however, I prefer to use simple external skeletal fixation with cancellous grafting, if necessary. There is often a hypertrophic bony response to infection. Thus, external skeletal fixation with the bilateral or uni-

With Infection

lateral triangular configuration can achieve compression and good immobilization and allow the wounds to be left open and to close gradually in anticipation of spontaneous union (see Fig. 70-7).

FOR STABLE ELBOWS For a stable elbow without infection, internal fixation with cancellous compression screws is a very simple method that promotes more rapid union and earlier mobilization. Grafts generally are not necessary, and minimal débridement of cortical surfaces is required to allow the fusion to mature. Again, in the presence of infection, external skeletal fixation with articular débridement and open wound packing promotes union.

Chapter 70 Arthrodesis

COMPLICATIONS Few data are available about success rates for primary arthrodesis. Koch and Lipscomb reported that primary arthrodesis failed in nine of 17 patients treated at the Mayo Clinic.12 Six of 11 elbows treated for tuberculosis failed to unite. Extensive joint destruction and unavailability of chemotherapy were cited as contributory factors to this poor rate of fusion. A recent updating of the Mayo Clinic experience has demonstrated a significant decrease in nonunion rates with internal fixation. Hahn documented six of six fusions with a combination of internal and external fixation but only five of nine fused when external fixation alone was used.10 Nonunion

The long lever arm created by elbow fusion increases stress along the entire extremity. Fracture through or proximal to the fused or ankylosed joint is not uncommon and was reported in four of 17 patients by Koch and Lipscomb.12 Conservative treatment, however, usually results in union (Fig. 70-9).

Fracture

References 1. Arafiles, R. P.: A new technique of fusion for tuberculous arthritis of the elbow. J. Bone Joint Surg. 63A:1396, 1981. 2. Bilic, R., Kolundzic, R., Bicanic, G., and Korzinek, K.: Elbow arthrodesis after war injuries. Mil Med. 170:164, 2005. 3. Bonnel, F.: Technique d’arthrodese du coude par fixateur externe. J. Chir. (Paris) 107:79, 1974. 4. Boyd, A. D. Jr., and Thornhill, T. S.: Surgical treatment of the elbow in rheumatoid arthritis. Hand Clin. 5:645, 1989. 5. Brittain, H. A.: Architectural Principles in Arthrodesis, 2nd ed. Edinburgh, E. & S. Livingstone, 1952, p. 161. 6. Connes, H.: Hoffmann’s External Anchorage: Techniques, Indications and Results. Paris, Editions GEAD, 1977, p. 118. 7. Crenshaw, A. H. (ed.): Campbell’s Operative Orthopaedics, 5th ed. St. Louis, C. V. Mosby Co., 1971, p. 1191. 8. Dahl, H. K.: AO Metoden ved Osteotomi og Arthrodese. Nord. Med. 85:599, 1971. 9. Figgie, M. P., Inglis, A. E., Mow, C. S., Wolfe, S. W., Sculco, T. P., and Figgie, H. E., III: Results of reconstruction for failed total elbow arthroplasty. Clin. Orthop. 253:123, 1990.

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10. Hahn, M. P., Ostermann, P. A., Richter, D., and Muhr, G.: Elbow arthrodesis and its alternative. Orhtopade 25:112, 1996. 11. Irvine, G. B., and Gregg, P. J.: A method of elbow arthrodesis: brief report. J. Bone Joint Surg. 71B:145, 1989. 12. Koch, M., and Lipscomb, P. R.: Arthrodesis of the elbow. Clin. Orthop. 50:151, 1967. 13. McAuliffe, J., and Burkhalter, W.: Post-traumatic elbow infection and fixation failure. Orthop. Consultation 12:1, 1991. 14. Morrey, B. F., Askew, L. J., An, K. N., and Chao, E. Y.: A biomechanical study of normal functional elbow motion. J. Bone Joint Surg. 63A:872, 1981. 15. Muller, M. E., Allgower, M., Schneider, R., and Willenegger, H.: Manual of Internal Fixation: Techniques Recommended by the AO-Group, 2nd ed. Berlin, Springer-Verlag, 1979, p. 387. 16. Nagy, S. M. 3rd, Szabo, R. M., and Sharkey, N. A.: Unilateral elbow arthrodesis: The preferred position. J. Southern Orthop. Assoc. 8:80, 1999. 17. O’Neill, O. R., Morrey, B. F., Tanaka, S., and An, K. N.: Compensatory motion in the upper extremity after elbow arthrodesis. Clin. Orthop. 281:89-96, 1992. 18. Orozco, R., Giros, J., Sales, J. M., and Videla, M.: A new technique of elbow arthrodesis. A case report. Int. Orthop. 20:92, 1996. 19. Plank, E., and Spier, W.: Die Arthrodese des Ellenbogens. Aktuel Probl. Chir. Orthop. 2:41, 1977. 20. Rashkoff, E., and Burkhalter, W. E.: Arthrodesis of the salvaged elbow. Orthopedics 9:733, 1986. 21. Ruhmann, O., Schmolke, S., Bohnsack, M., Carls, J., Flamme, C., and Wirth, C. J.: Reconstructive operations for the upper limb after brachial plexus palsy. Am. J. Orthop. 33:351, 2004. 22. Snider, W. J., and De Witt, H. J.: Functional study for optimum position for elbow arthrodesis or ankylosis. In Proceedings of the American Academy of Orthopedic Surgeons. J. Bone Joint Surg. 55A:1305, 1973. 23. Spier, W.: Beitrag zur Technik der Druckarthrodese des Ellenbogengelenks. Monatsschr. Unfallheilkd. 76:274, 1973. 24. Staples, O. S.: Arthrodesis of the elbow joint. J. Bone Joint Surg. 34A:207, 1952. 25. Steindler, A.: Reconstructive Surgery of the Upper Extremity. New York, D. Appleton & Co., 1923. 26. Tang, C., Roidis, N., Itamura, J., Vaishnau, S., Shean, C., and Stevanovic, M.: The effect of simulated elbow arthrodesis on the ability to perform activities of daily living. J. Hand Surg. 26A:1146, 2001. 27. Wolfe, S. W., Figgie, M. P., Inglis, A. E., Bohn, W. W., and Ranawat, C. S.: Management of infection about total elbow prostheses. J. Bone Joint Surg. 72A:198, 1990.

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71

Flaccid Dysfunction of the Elbow Mikko Larsen, Allen T. Bishop, and Alexander Y. Shin

INTRODUCTION Flaccid paralysis of the elbow severely limits a patient’s ability to position and stabilize the hand so that it can function. The patient with paralysis of the elbow flexors (biceps, brachialis, and brachioradialis) is unable to reach the face to eat, shave, wash, and comb the hair. Most jobs require the hand to be held at frequently changing levels for lifting and carrying, and this is impossible when the elbow flexors are paralyzed. Paralysis of the elbow extensors results in loss of ability to work with the extremity held above the horizontal position, for example, to reach for an object on a high shelf. Stabilizing an object in space or on a surface, as when holding a loaf of bread while slicing it, is also impossible. Without active elbow extension, a patient who needs to transfer or use crutches is unable to do so. Supination of the forearm is necessary for lifting and carrying and for using the hand around the face. Pronation is important for positioning the hand for activities such as writing, working at a bench, typing on a computer, or driving a car. Most of the operations described before the microsurgical era that were designed to restore elbow flexion were developed for patients paralyzed as a result of poliomyelitis. Another group of injuries that results in loss of elbow flexion are traumatic brachial plexus injuries. Most often, the injury is the result of high-speed motorcycle or automobile accidents, and results in a varying degree of injury to the brachial plexus. With irreparable lesions of the C5 and C6 nerve roots, known as upper trunk injuries, there is flaccid paralysis of the elbow flexors in addition to the shoulder girdle musculature with preservation of nearly normal hand function. Obstetric birth palsy also can affect elbow function in the infant and typically involves the upper portion of the brachial plexus (Erb’s palsy) resulting in paralysis or weakness on elbow flexion that may require reconstructive surgery. Traumatic irreparable damage directly or indirectly to the musculocutaneous and radial nerves proximal to the muscles innervated by them results in

flaccid paralysis of the elbow. Extensive direct muscle injury occasionally necessitates tendon and muscle transfer to replace lost function. Restoration of elbow extension is essential in patients with tetraplegia. By increasing reachable workspace, the ability to relieve pressure, better wheelchair propulsion, and independent transfer, the lives of tetraplegics can be significantly improved. Upper extremity surgery generally has a positive impact on quality of life through an increased ability to perform activities of daily living (ADLs) and independence for people with tetraplegia. It is essential to realize that the hand is useless unless it can be maintained in a useful position by the elbow. Therefore, the first goal in the treatment of the flaccid elbow is to restore elbow flexion by direct nerve surgery or secondary reconstructive surgery whenever possible. The basic types of reconstructive procedures available for restoration of elbow function include nerve transfers, tendon transfers, and free functioning muscle transfers. Combinations of nerve transfers and novel uses of free functioning muscle transfers have offered more function in patients with devastating injuries. Each of the basic types of reconstructive procedures, the timing, principles, anatomy, outcome and our overall recommendations will be detailed in this chapter.

GENERAL PRINCIPLES TIMING Timing of surgical reconstruction varies depending on the etiology of the injury that caused loss of elbow flexion. Historically, the literature is often confusing with respect to timing of surgical procedures. Older literature is often in direct conflict with the newer literature. For example, for traumatic brachial plexus injuries, the recommendation was to wait at least 12 months for spontaneous return of function before embarking on tendon transfer. Often a locking-hinge elbow brace was applied, particularly for patients who have good hand function.249 However, with the advent of microsurgical reconstructive techniques, intervention before 6 months from injury is now recommended.7,54,73,176,214 In tetraplegic patients, reconstructive surgery to replace triceps function should not be undertaken less than a year after the injury. In a child with arthrogryposis, transfers to gain elbow flexion can be done after the age of 5 years. Usually, reconstruction should be performed on one side only so that one extremity can be used for activities that require flexion, while the unoperated elbow is used for those that require extension. After the traumatic loss of a flexor or extensor muscle compartment, it is advisable to wait until the

Chapter 71 Flaccid Dysfunction of the Elbow

tissues about the elbow joint are supple before proceeding with tendon transfer or free muscle transfers. Any use of the hand will be wasted without elbow function to maintain it in a useful position. Therefore, the first goal in the treatment of a flail arm is the restoration of elbow flexion by primary direct nerve surgery or secondary reconstructive surgery.17,172,176 An exception is in polio-type brachial plexus paralysis, in which priority should be given to restoration of shoulder abduction rather than elbow flexion. In these cases, early nerve transfers within 1 year of paralysis achieve significantly more shoulder abduction than late nerve transfer or palliative reconstruction with muscle/tendon transfer or shoulder arthrodesis, whereas elbow flexion may spontaneously recover in up to 90% of cases.142 In obstetric brachial plexus palsy, timing of surgical intervention is highly controversial. Although most authors agree that surgical intervention is indicated when no recovery of biceps function occurs, some have recommended intervention at 3 months92 or as late as 9 months.60 In all timing of reconstructive procedures for neurologically disabled patients, achieving stability of neurologic status, mental status (acceptance of the permanency of the disorder), and social status (clearly established goals of rehabilitation) is an essential prerequisite before any surgery is undertaken that is not itself concerned with stability.110 Conditions that interfere with progression toward the goals of rehabilitation before neurologic stability has been achieved include flexion contractures of the elbow and supination contractures of the forearm, which must be corrected before further reconstruction is undertaken.

CORRECTION OF PRE-EXISTING JOINT CONTRACTURE Reasonably functional passive motion of the elbow must be obtained before nerve, tendon, or muscle transfers are performed. This often requires the joint and muscle contractures to be stretched, and as a result, the functioning muscles are strengthened by progressive resistance exercises. Passive flexion of at least 120 degrees is desirable before tendon transfer is carried out. Static adjustable splints (see Chapter 11) are useful in regaining passive extension.95 Occasionally, surgery is required to release a severely damaged elbow flexor, extensor muscle, or joint capsule before the joint can be mobilized. A preliminary or concurrent V to Y release of a contracted triceps, in conjunction with flexorplasty, may be necessary to correct an extension contracture in an arthrogrypotic child. If soft tissue cover is necessary, it usually can be provided as a skin paddle on the transposed latissimus dorsi flap. When contractures are greater than 60 degrees and interfere with or are exaggerated during ADLs, surgical

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release is indicated.126 The contracture correction can consist of combinations of Z-lengthening of the biceps tendon, myofascial release of the brachialis, and release at the origin of the wrist flexor-pronators. Capsular release is necessary only in severe, long-standing contracture. The contracture that occurs in Erb’s palsy is paradoxical in nature, given the normal triceps function in the face of weak or absent biceps function. A dynamic splint126 or serial casting, followed by biceps tenotomy with further casting,84 may also be used. The latter method is associated with improved joint range of motion without loss of elbow flexion strength in 80% of cases. Drawbacks of this treatment are pressure sores and stiffness, and the limitations in correcting pronation as the elbow reaches full extension. When an upper motor neuron unit is involved in the contracture, botulism toxin or selective crush of the musculocutaneous nerve is used with success concurrent with casting, especially in contractures developing early after spinal cord injury. These patients are especially prone to developing a pronation contracture due to biceps weakness. Pronation and supination contractures should also be addressed before fixed bony changes occur in the radius and ulna.

CHOOSING AN APPROPRIATE MUSCLE FOR TENDON TRANSFER The type of muscle transfer depends on the muscle groups that are available.172 The original functional properties between the donor and recipient muscles must be matched.86 A transferred muscle must provide both adequate strength and excursion in its new role. Clinical and electromyographic testing of various muscles should be performed before transfer. A muscle to be transferred should show an adequate electromygraphic trace and have appropriate strength. The extent of a brachial plexus lesion dictates which muscles will have retained their innervation. The most common cause of failure in tendon transfers about the elbow, as elsewhere, is overestimating the strength of the transferred muscle. The muscle to be transferred should contract against gravity resistance (grade 4, ”M4“) if significant function is to be anticipated (Table 71-1). Preoperative electromyography (EMG) of the muscle proposed for transfer is a good idea, but mild denervation changes do not preclude the transfer.226 In addition to muscle strength, which is determined by clinical examination, it is helpful to consider the comparative work capacities of the various muscles available for transfer.245 The work capacity is determined by multiplying the power of the muscle (3.65 kg/cm2 of physiologic cross section) by its amplitude (the distance through which the tendon moves when its muscle contracts). The work capacity of the biceps for elbow flexion

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Muscle Strength Grading System According to the British Medical Research Council161

TABLE 71-1

Grade

Definition

Explanation

0

Absent

No function

1

Trace

Slight contraction, no motion

2

Poor

Complete motion, gravity eliminated

3

Fair

Complete motion against gravity

4

Good

Complete motion against gravity and some resistance

5

Normal

Apparently normal strength

is 4.8 kg/m, and for forearm supination, it is 1.1 kg/m. The sternocostal head of the pectoralis major muscle has nearly three times as much work capacity at 10.4 kg/m. By contrast, the work capacity of all forearm flexors1 (pronator teres, flexor carpi radialis and ulnaris, and palmaris longus) is 3.8 kg/m.116 The dispensability of the transferred muscle must be considered when a muscle is chosen for transfer around the elbow. Triceps transfer for elbow flexion is not often indicated because the triceps is not really expendable. The latissimus dorsi is not expendable in polio patients, who rely on it to elevate the pelvis when the other pelvic elevators are paralyzed. Finally, cosmesis may be a consideration. The bowstringing of the sternocleidomastoid transfer across the side of the neck makes it an undesirable transfer, even though, theoretically, it is one of the most mechanically efficient ones. Restoration of nearly normal bulk of the arm in a patient with loss of flexor or extensor muscle mass is a nice cosmetic byproduct of the bipolar transplant of the latissimus or pectoralis muscle.

RESTORATION OF ELBOW FLEXION INTRODUCTION Neurotization or brachial plexus reconstruction is the treatment of choice in early cases of the flail upper extremity.* In chronic cases or failed early reconstruction, several tendon transfer procedures to restore elbow flexion are available49: Steindler flexorplasty and its modifications,28,36,40,76,146,158,222 anterior transposition of the triceps tendon,43 pectoralis-to-biceps transfer, with or without the pectoralis minor,† pectoralis minor alone,200 *See references 25, 31, 53, 58, 128, 174, 175, 181, 201, 204-206, 212, and 233. † See references 34, 46, 58, 90, 101, 207, 209, 218, and 219.

sternomastoid-to-biceps transfer with or without shoulder arthrodesis,40,44 transfer of the flexor carpi ulnaris,1 and unipolar or bipolar transposition of the latissimus dorsi muscle.11,15,33,48,117,207,237,255 Free muscle transfer‡ is fast becoming a mainstay of the armamentarium of upper extremity reconstructive surgeons and has proved useful in both early and chronic cases of brachial plexus and traumatic injuries. Each of these treatment modalities has its advocates, and knowledge of a number of different options will allow treatment to be tailored to the needs and expectations of the patient. The muscle groups chosen for tendon transfer depend on those that are available. Triceps-to-biceps transfer is advocated when there are biceps-triceps co-contractions, and Steindler’s procedure when the elbow flexors reach only grade 2.7 The latter may be contraindicated when the elbow flexors are grade 0, when the wrist flexors are weak, or when wrist and finger extensors are paralyzed.172 The Steindler flexorplasty can also be augmented by a pectoralis minor transfer. In children with obstetric brachial plexus palsy at the C5, C6 level, flexorplasties are indicated when there is a functional hand but with weak elbow flexion and inability to position the hand.113 In these patients, the Steindler procedure is reserved for elbows with excellent forearm muscles for wrist and digit flexion. When these are not all M5, the triceps-to-biceps transfer is advocated, by some authors using only a normal triceps,113 and by others,202 even with a weak triceps. When neither the triceps nor the forearm flexors are judged as being of sufficient strength, the pectoralis major or minor transfer can be used, or preferably, a free-functioning muscle transfer can be performed.

NEUROTIZATION Neurotization is the technique of nerve transfer used to restore motor or sensory function after brachial plexus injuries when the nerve damage is too far proximal for standard nerve-grafting techniques to be feasible. In 1903, Harris and Low104 inserted half of the distal fascicles of the C5 root, which was damaged at the foramen, into the healthy spinal nerve C6 or C7 in three cases of Erb’s palsy. No results were recorded. In 1913, Tuttle241 mentioned one case of neurotization using the spinal accessory nerve. In 1963, Seddon211 first reported neurotization of the musculocutaneous nerve using intercostal nerves in two patients, both times obtaining active elbow flexion. Subsequently, many early cases of neurotization using intercostal nerves have reported a modicum of success.§ Early reports on neurotization of the muscu‡

See references 3, 51–53, 55, 69, 70, 152, 155, and 218. See references 73, 88, 121, 122, 164, 165, 176, 178-181, 212, 215, 216, 228, and 238. §

Chapter 71 Flaccid Dysfunction of the Elbow

locutaneous nerve using parts of the cervical plexus35 and spinal accessory nerve5,122,181 also mention some limited success.98 Later series report satisfactory restoration of elbow flexion after intercostal nerve transfer to the musculocutaneous nerve without intercalated grafts.68,128,174 The goal is to provide the musculocutaneous nerve with the best motor donors.233 This can be achieved by reconstruction using intraplexus donors such as nerve grafts from the proximal stumps of avulsed C5 roots. It must be stressed, however, that nerve transpositions are effective only when they are performed within 6 to 9 months of injury.5,24,51,128,163,181,201,217 Currently used extraplexus transpositions for elbow flexion, in general order of decreasing frequency, are the intercostal nerve,88,179 spinal accessory nerve,6 thoracodorsal nerve,204 pectoral nerve,31 phrenic nerve,53,98 hypoglossal nerve,177 platysma motor branch,22 and high cervical nerve roots.252 The ulnar186 and median nerves148,150,151 can be used as intraplexus donors, with their vascular supply left intact. This is recommended only for global plexopathy or tetraplegia involving C7, C8 and T1 so as not to sacrifice any remaining or potential nerve function.139,186 Other intraplexus donors can be obtained by the selective contralateral C7 method56,97,235 or by transfer of the medial pectoral nerve.205,246 Crosschest radial nerve transfer has been proposed and is feasible anatomically but requires tendon transfer reconstruction of radial nerve innervated muscles in the contralateral arm.21 Another rarely used intraplexus donor is the long thoracic nerve,177 which provides the sole innervation for the serratus anterior, causes scapular winging after transfer, and therefore, is not recommended.144 The phrenic nerve can be transferred without pulmonary complications,98 even with concurrent intercostal nerve transfer,101 although the risk of reduced vital capacity is greater when the right phrenic nerve is used.149 Its full length can be harvested using videoassisted thoracic surgery techniques.251 Transfer of intercostal nerves alone have been associated with a nonsignificant mild decline in pulmonary function, without a subjective effect on respiratory status or stamina.128 Intraoperative somatosensory evoked potential (SEP) recording is mandatory to ascertain the level of injury— even when a root appears to have sustained a posganglionic injury, nerve grafting is never indicated in a root with a negative SEP.175

TECHNIQUE The exposure of the brachial plexus as performed by Sedel is described in this section.19 The patient, under general anesthesia, is given no neuromuscular blocking

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agents. An incision is made parallel to the clavicle, with an extension parallel to the sternocleidomastoid muscle. The skin flaps are elevated, and the external jugular vein is ligated. The sternocleidomastoid is retracted, allowing dissection to proceed in the prescalene area. The phrenic nerve is identified on the scalenus anterior. The fifth cervical root is identified at the point where the phrenic nerve crosses the lateral aspect of the scalenus anterior proximally. The sixth cervical root is more distal and medial with a more horizontal direction. The seventh cranial nerve root is more horizontal still and more posterior; more posteriorly and medially lie the more difficult to identify eighth cervical and first thoracic nerve roots. The scalenus anterior is divided, the subclavian artery is retracted ventrally, and the pleural dome is retracted dorsally. The infraclavicular incision is extended onto the deltopectoral groove, sometimes extending over the arm. The axillary artery is dissected and the lateral, posterior and medial cords of the brachial plexus are identified. If exposure is required behind the clavicle, this is divided and repaired with an AO plate later. A supraclavicular or infraclavicular approach can be used. In accordance with the goals of reconstruction of the flail upper limb, the first priority in neurotization is to attach a motor nerve donor to the musculocutaneous nerve. Grafts used for this purpose include the suprascapular and spinal accessory nerve, alone or in conjunction with two or three intercostal nerves (Fig. 71-1). In decreasing order of priority, the radial nerve (after dissection and removal of the triceps or posterior cord branch), median nerve, and axillary nerves are reconstructed in a similar fashion. The operative strategy depends on the type and extent of the lesion and the number, quality and length of available grafts, as well as the aspect of the proximal neuroma. If there is a neuroma in continuity, there is controversy as to whether it should be resected or treated by simple neurolysis.250 In any case, conduction across the neuroma is best assessed using nerve action potential rather than muscle action potential, because the former requires 40 to 50 times as many fibers of reasonable caliber to elicit a response. There is discussion as to the advantage of using interposition nerve grafting when performing intercostal nerve transfers. It has been demonstrated that intercostal nerves lose up to 10% of motor axons per 10 cm measured from the midaxillary line to the sternum.163 Coaptation of the transfer closer to the motor endplates, avoidance of tension on the nerve repair, and earlier shoulder mobilization are other theoretical advantages. This includes coaptation directly to the dominant motor branch of the biceps muscle rather than to the musculocutaneous nerve.31,128 There is no consensus on the optimum number of intercostal nerves to be transferred to the musculocutaneous nerve to obtain optimal

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Part VII Reconstructive Procedures of the Elbow

Intercostal motor nerves 3 4 Motor branch musculocutaneous N.

FIGURE 71-2

FIGURE 71-1

Intercostal nerve neurotization of the musculocutaneous nerve. (By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

biceps function. Also, there is no consensus on using the spinal accessory nerve over intercostal nerves. A theoretical advantage of the spinal accessory nerve for transfer is the high number and ratio of motor fibers (1500-3000) compared with an intercostal nerve (500700 motor fibers per nerve).5,88,244 However, a clear disadvantage cited by most authors is the need for an interpositional graft when using the spinal accessory nerve. If necessary, the spinal accessory nerve can be harvested through a posterior approach.12,99,194 An average extra length of 12 cm can be gained compared with the standard anterior approach, allowing the terminal branches of the brachial plexus to be neurotized without the need for an interposition graft (Fig. 71-2).244 Vathana et al.244 measured an average of 817 myelinated axons at the most distal level; however, these authors warn that the size mismatch with terminal branches in the brachial plexus (varying between 5000 and 14000 axons) may predict poorer outcome and that this approach may be more suitable for reinnervation of the suprascapular nerve at the level of the supraclavicular notch. When interposition grafts are unavoidable, results may be improved with the use of vascularized nerve grafts.53 The vascularized ulnar nerve graft has been shown to maintain its blood supply and viability even in a scarred bed.235 Pedicled on the superior ulnar col-

The posteriorly harvested spinal accessory nerve can be used to reach distal anterior targets in the brachial plexus. (By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

lateral vessels and ulnar vessels, this yields better results than including the superior ulnar collateral vessels alone.97 This intraplexus donor has a greater number of axons than any extraplexus donor, potentially increasing the probability for successful neurotization.235 Distal nerve-to-nerve transfers are possible, however, only when the lower plexus is intact. Possible transfers include ulnar nerve to the biceps branch of the musculocutaneous nerve or to biceps and brachialis, medial pectoral, and thoracodorsal nerves (Fig. 71-3).147,150,151,187 A shorter distance and time to reinnervation is provided by these transfers.

RESULTS Intraplexus donors provide better results than extraplexus donors, although direct neurotization of the musculocutaneous nerve from ipsilateral intercostal nerves produces results comparable to intraplexus neurotizations,233 as does direct neurotization of the suprascapular nerve with the spinal accessory nerve for shoulder function.235 A meta-analysis of the English literature (26 studies, 965 nerve transfers) showed M3 biceps strength in 72% of direct intercostal-to-musculocutaneous transfers versus 47% with interposition grafts (P < 0.001), with a trend observed at ≥M4 biceps strength (41% vs 32%).163 Spinal accessory nerve–to–musculocutaneous nerve transfers for elbow flexion were comparable to intercostal nerves without interposition grafts at

Chapter 71 Flaccid Dysfunction of the Elbow

Motor branch musculocutaneous n.

961

fer from the ulnar and median nerves to biceps and brachialis branches of the musculocutaneous nerves.147,151 Several nerve transfers may be combined to decrease the time to functional return and provide better results. Leechavengvongs and colleagues140 reported the results of 15 combined spinal accessory–to–suprascapular nerve, ulnar nerve–to–biceps motor branch, and long head of the triceps branch–to–the axillary nerve transfers for C5 and C6 avulsion injuries. Elbow flexion strength was M4 in 13 patients and M3 in two patients at an average follow-up of 24 months.

Ulnar nerve

TENDON TRANSFERS FIGURE 71-3

Oberlin187 transfer of the ulnar nerve to the musculocutaneous nerve. When the ulnar nerve is intact, a fascicle can be transferred to the biceps motor branch to restore elbow flexion. (By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

≥M3 strength (77% vs 72%). Intercostal nerves, however, were significantly better at providing ≥M4 biceps strength relative to spinal accessory nerve (41% vs 29%; P < 0.001). The same authors were unable to demonstrate a difference when two versus three or four intercostal nerves were used for restoration of elbow flexion to ≥M3 strength. This contrasts with a prospective study involving 205 patients performed by Waikakul et al.,247 comparing spinal accessory to intercostal nerve transfer. These authors found that spinal accessory nerve transfers produced significantly better motor outcomes, but patients with intercostal nerve transfers had significantly better protective sensation and pain relief. Also, the shoulder subluxation in the spinal accessory group required more frequent shoulder fusion. Spinal accessory nerve transfer is preferred by these authors in isolated biceps paralysis, whereas intercostal transfer is recommended for global plexus palsy, particularly those with deafferentation pain.247 A beneficial effect of neurotization that frequently precedes functional return by months is the alleviation of deafferentation pain and an improvement in protective sensation.181 A lack of pain allows patients to concentrate on rehabilitation and improve their function and dexterity.235 The contrasting results between different studies may be due to the use of an interposition graft with the spinal accessory nerve that may offset the advantage of containing more motor fibers.163 Oberlin’s method of transfer of two ulnar nerve fascicles show promising results for restoration of elbow flexion,139,186,232 as does the double fascicular nerve trans-

Steindler’s Flexorplasty Steindler first described his simple but ingenious concept of proximally shifting the origin of the flexor-pronator muscle group to increase its lever arm in flexing the elbow in 1918.220,221 His technique consisted of the subperiosteal dissection of the origin of the flexor-pronator muscles of the forearm from the medial epicondyle. The muscle flap was then transposed proximally between the brachialis and the triceps, and was sutured to the medial epicondylar ridge through two drill holes 2 inches above the epicondyle. Steindler recommended the procedure only if the wrist flexors were normal or only slightly weakened. Subsequent authors differed on the prerequisites for Steindler’s flexorplasty. Mayer and Green158 believed that the epicondylar muscle group strength should be grade 3 or better, and they re-emphasized the need for strong wrist flexors if the operation is to succeed. They described this simple test: The arm is abducted to 90 degrees to eliminate gravity. Any patient who can flex the elbow in this position (using the epicondylar muscle group) is a candidate for the operation. Nyholm believed that the criteria for forearm muscle strength should be liberalized because all of his patients achieved 90 degrees of elbow flexion, even though a relatively large number had forearm muscles that were “primarily paretic.”183 Dutton and Dawson76 performed the operation if the strength of the forearm flexor-pronator group was rated fair or better. Alnot7 believed that the shoulder flexorplasty was most indicated to reinforce a biceps that had recovered to M2 strength. It seems that there is considerable variability in the preoperative muscle strength needed for active flexion, and the axiom that the muscle loses a grade in transferring it does not necessarily apply in this particular situation. Others have modified and refined Steindler’s original concept to increase flexor strength and decrease the tendency toward development of a pronation deformity. Bunnell40 described extending the common tendon of

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Part VII Reconstructive Procedures of the Elbow

origin with a fascia lata graft that would reach 2 inches up the lateral border of the humerus. This resulted in moderate but not complete correction of the pronation tendency. Mayer and Green158 detached the flexorpronator origin with a portion of the medial epicondyle and attached it through a window cut in the anterior cortex of the humerus 5 to 7.5 cm proximal to the joint. Their description of the technical details of the Steindler flexorplasty, which includes careful dissection of the ulnar and median motor branches, is the best in the literature. Lindholm and Einola145 used a screw to fix the epicondylar fragment to the humerus in two cases. Eyler79 advocated omitting the flexor carpi ulnaris to allow the surgeon to work in the “internervous plane” between the flexor sublimis, anteriorly, and the flexor profundus and flexor carpi ulnaris, dorsally. Efforts have been made to augment the strength of elbow flexion, especially in patients who have weakness of the flexor-pronator muscle group. Initially, Steindler recommended proximal transfer of the radial wrist extensor muscle origins off the lateral epicondyle in conjunction with the medial transfer, but he did not comment on it in his later communications.222 Mayer and Green reported having difficulty mobilizing the lateral epicondylar muscle group without damaging the nerve supply158 and gave up the procedure after two unsatisfactory results. Lindholm and Einola146 were unable to detect any increase in flexion strength in the six patients who had the additional lateral transfer.

FIGURE 71-4

The pronator teres arises from two heads. The humeral head originates from the medial supracondylar ridge, the medial intermuscular septum, and the common flexor tendon. The smaller ulnar head arises from the coronoid process of the ulna. The median nerve enters the forearm between the two heads of the pronator teres. The flexor carpi radialis, palmaris longus, and humeral head of the flexor superficialis all originate from the common flexor tendon. The flexor carpi ulnaris arises from two heads: the humeral head originates from the common flexor tendon, and the ulnar head originates along the medial border of the olecranon and posterior border of the upper three fifths of the ulna. Branches originating from the medial surface of the median nerve supply the pronator teres (C6, C7), the flexor carpi radialis (C6, C7), the palmaris longus (C7, C8), and the humeral head of the flexor superficialis (C8 and T1). The flexor carpi ulnaris (C8 and T1) is innervated by two or three branches of the ulnar nerve, the first of which usually leaves the nerve just as it passes between the two heads of the muscle.

Anatomy

A sandbag is placed under the opposite hip (Fig. 71-4). A tourniquet usually is not used. The incision begins on the anterior aspect of the arm about 7.5 cm above the elbow and swings gently in a medial direction. At the elbow, it runs just posterior to the epicondyle. It then curves anteriorly, following the direction of the pronator teres, ending about 10 cm below the elbow. The ulnar

Technique (modified from Mayer and Green)

Steindler’s flexorplasty.221 A, The incision. B, The ulnar nerve is mobilized proximally and distally, and its motor branches to the flexor carpi ulnaris are identified and protected. C, The common flexor-pronator origin is detached with a flake of medial epicondyle. The motor branches of the median nerve to the flexor-pronator group are identified and protected. D, The detached flexorpronator group is mobilized distally as far as the motor branches of the medial and ulnar nerves will permit. The brachialis muscle is divided. E, The distal humerus is prepared, and a prolene pull-out suture is used to anchor the transferred muscles to the anterolateral surface of the humerus 5 to 7.5 cm above the elbow. (After Mayer, L., and Green, W.: Experiences with Steindler flexorplasty of the elbow. J. Bone Joint Surg. 36A:775, 1954.)

Chapter 71 Flaccid Dysfunction of the Elbow

nerve is isolated and freed distally to the branches of the flexor carpi ulnaris. Preserving these motor branches, the surgeon continues the dissection distally for 5 cm. The lacertus fibrosus is divided, and the median nerve is exposed above the elbow and dissected distally, exposing the motor branches (all of which leave the medial aspect of the nerve) to the common flexorpronator muscle group. The common flexor-pronator muscle origin is then detached with a flake of epicondyle (cartilage in children and bone in adults). The flake of bone or cartilage is then grasped with a clamp, and while traction is exerted in distal and anterior directions, the muscles are stripped from the anterior surface of the joint and from the coronoid process of the ulna. As the ulnar head of the flexor carpi ulnaris is detached from the ulna with an elevator, the assistant puts gentle traction on the median and ulnar nerves, demonstrating the motor twigs that must be carefully avoided. Dissection is continued distally as far as the anatomic distribution of the nerves permits. The common tendon is then transfixed with a modified pull-out suture of No. 1 prolene. The elbow is flexed to 120 degrees, and traction is exerted on the transfer to determine how far above the elbow the transfer will reach. This is usually between 5 and 7.5 cm. The ulnar nerve often seems to have less tension on it if it is transferred anterior to the epicondyle. The atrophic fibers of the brachialis are slit longitudinally, the periosteum is incised, and the anterior humerus is exposed subperiosteally. An opening in the anterior cortex of the humerus nearer to the lateral than to the medial border is made at the point to which the transplant reaches when the elbow is flexed. Two small drill holes are made from anterior to posterior through this cortical window. The prolene suture ends are then threaded through the holes and out through the triceps muscle and skin. To be sure that they are not subjected to undue tension on twisting, the nerves are inspected as the transfer is pulled into the cortical window. The distal portion of the wound is closed, up to the bend in the elbow. The sutured ends are drawn tight with the elbow in maximal flexion and tied over a button under which a thick piece of felt has been placed. Several auxiliary sutures between the periosteum and the transplanted epicondylar tissues are placed, and the wound is closed with a drain. A posterior splint is then applied with the elbow in about 120 degrees’ flexion and the forearm in full supination. Four weeks after surgery, the pull-out suture is removed. A removable Orthoplast splint is applied, and active flexion and supination and extension exercises are begun. No special retraining is required because the muscles transferred functioned as an accessory elbow flexor before transfer.58 Splinting is discontinued 6 to 8 weeks after surgery, the longer time being necessary for patients with normal triceps function. A dynamic exten-

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sion splint is often useful if the patient has no triceps function (Fig. 71-5). In patients with C5-7 palsy in which the wrist and finger extensors are weakened or paralyzed, the forearm flexor-pronators are strong but the triceps is not available or co-contracts with the biceps, the Steindler procedure should be complemented with wrist arthrodesis.172 Furthermore, success of the procedure relies on sufficient power of the flexor-pronator muscles.76,124,145,146,155,158 Published results of the Steindler flexorplasty reflect a high degree of success in achieving a functional range of elbow flexion against gravity. Most transfers reported have been performed for poliomyelitis. Steindler achieved 79.5% good results (flexion against gravity of not less than 90 degrees) in 39 cases.224 Fifteen good results (useful range of flexion with good to fair power) in 27 flexorplasties were reported by Carroll and Gartland.42 Using strict criteria for success, including subtracting from the total score for flexion contracture of more than 15 degrees and for supination of less than 45 degrees, Mayer and Green recorded 11 excellent results, five good, four fair, and two poor results among the 22 flexorplasties they followed up (Fig. 71-6).158 Segal and associates compared the results of 13 Steindler flexorplasties (transplantation of both flexor and Results

A

B FIGURE 71-5

A and B, A dynamic flexion and extension elbow splint. The dynamic extension is particularly useful in patients who have Steindler’s flexorplasty but lack triceps function.

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Part VII Reconstructive Procedures of the Elbow

A

B FIGURE 71-6

A, A 21-year-old man sustained a brachial plexus injury in a motorcycle accident. Steindler’s flexorplasty performed 16 months after injury restored excellent elbow flexion. Subsequent transfer of the flexor carpi ulnaris into the extensor carpi radialis brevis restored wrist extension, and finger and thumb extension were restored using the superficialis muscle of the middle and ring fingers. Shoulder arthrodesis was also performed. B, Fixed flexion deformity of 35 degrees was present after Steindler’s flexorplasty.

extensor origins) and 17 Clark pectoralis major transfers.213 The flexorplasty results were better than the pectoralis transfers, but the average flexion contracture in the flexorplasty group was 60 degrees, whereas it rarely exceeded 15 degrees in the Clark transfer group. Kettelkamp and Larson, evaluating 15 flexorplasties using Mayer and Green’s scoring system, noted eight excellent or good results, six fair results, and one poor one.124 They also measured the carry-lift strength (flexion against gravity, plus weight in 1-pound increments) and found that nine of the 14 patients who were able to flex the elbow 110 degrees or more against gravity were able to flex through this range with 1 pound or more. The maximum weight lifted was 6 pounds by one patient. Nyholm183 reported on 24 patients, six of whom achieved a normal degree of elbow flexion after flexorplasty. Five patients (three who had brachial plexus trauma and two polio) recovered some biceps function, which did not seem to be compromised by the previous flexorplasty. Nyholm noted that all of the patients except

two preferred to flex the elbow with the forearm pronated and hand clenched. Hoffer and Phipps113 reported on three Steindler flexorplasties in children with obstetric brachial plexus palsies (C5, C6). They achieved flexion strength M4 with 20 to 30 degrees of extension deficit. One of the largest series of flexorplasties was reported by Lindholm and Einola,145 who found that 50 of their 61 patients achieved a range of flexion of at least 90 degrees. Eleven were able to lift a weight heavier than 1 kg at right angles. Dutton and Dawson76 noted that 20 patients had excellent or good function of the transferred muscles. Eighteen could lift at least 1 to 2 kg through an arc of full elbow motion. Finally, several investigators have noted the beneficial effect of arthrodesis of the flail shoulder in patients who have had flexorplasties.76,124,145,223 Shoulder arthrodesis permits abduction at the scapulothoracic joint that decreases the gravitational forces that must be overcome by the transferred flexor-pronator muscle group. Stabilizing the humerus also maximizes the power of the transfer in preventing backward movement of the elbow, which diminishes the advantage of the flexion contracture by increasing the length of the arc through which the reconstructed flexor muscle must move the weight against gravity.124 A retrospective review of 12 patients with C5-7 brachial plexus palsy and extremely weak elbow flexion (M2 or less) were treated by Steindler flexorplasty and wrist arthrodesis. Eleven patients were found to have good or very good outcomes based on the criteria established by Alnot and Abols,8 and one patient had mild active flexion of the elbow.172 These results emphasize that despite recent advances in neurolysis nerve grafting and neurotization procedures, a direct approach to the neurologic lesion can give incomplete results, and for this reason, tendon transfers still play an important role. Chen49 reported results in eight patients, in four of whom one or several flexor-pronator tendons had been used in tendon transfer procedures to restore wrist and finger extension. The results after modified Steindler flexorplasty were not negatively affected by these previous procedures. Liu and associates146 reported on the largest cohort of 71 patients with a follow-up of 4 to 15 years. The mean range of motion during active flexion against gravity was 114 degrees (range: 80 to 140 degrees). A mean extension lag of 28 degrees (range: 0 to 50 degrees) was created. Fourteen patients (20%) had significant loss of supination, for 11 of whom flexor carpi ulnaris–to– extensor carpi radialis brevis tendon transfers were performed to regain supination. Using Mayer and Green’s scoring system,158 results were excellent in 32%, good in 47%, fair in 13%, and poor in 8%. A clear improvement was seen over time; the results in operations performed

Chapter 71 Flaccid Dysfunction of the Elbow

between 1981 and 1987 were significantly better than those performed between 1970 and 1980 (57% versus 16% excellent results). This difference was attributed by the authors to the addition of shoulder arthrodesis as a stabilizing supplementary procedure in 45 cases, and the aforementioned tendon transfers in patients without active supination. Andrisano9 reported on the long-term follow up (313 years, average 8.6 years) in 22 patients. These authors found good results in 50%, fair in 19% and poor results in 38%. These results were independent of the etiology of the elbow paralysis and the patient’s age, but were strongly dependent on surgical factors, such as the correct tension and placement of the epitrochlear mass. Brunelli and coworkers36 have modified the procedure such that during transfer of the flexor carpi ulnaris, flexor carpi radialis, and palmaris longus, they are carefully separated from the flexor digitorum superficialis, which is left in place. Together with placement of the transfer on the anterior aspect of the humerus, the socalled Steindler effect (pronation and simultaneous elbow and finger flexion) could be avoided in 28 of 32 cases. The main complications of Steindler’s transfer are pronation and flexion contractures. Pronation contractures are related to (1) preoperative absence of active supination in most of these patients and (2) tightening of the pronator teres as a result of its proximal shift. Inserting the transfer more anteriorly and laterally on the humerus diminishes this tendency, but if no active supination is present, pronation deformity still may be a problem. Segal and associates213 and Nyholm183 did not notice any great change in passive supination after Steindler flexorplasty in their patients. Carroll and Gartland42 noted that approximately half of the 23 patients who were improved by the flexorplasty had pronation defects. Lindholm and Einola145 encountered pronation contracture in 17 of 61 patients who had had a flexorplasty, but 14 of them had had no active supination preoperatively. Dutton and Dawson noted an average loss of supination of 39 degrees in the 25 patients on whom they reported.76 The strength of the transferred muscles, the duration of immobilization, and the strength of the opposing triceps muscle affect the extent of the flexion contracture. A flexion contracture of the elbow does increase the mechanical advantage of the transferred muscle, and this is especially important in patients who have significant weakness of the transferred muscle group. The degree of fixed flexion contracture of the elbow that is considered acceptable varies a good deal among surgeons. Steindler believed that a 60-degree flexion contracture was acceptable,223 and Carroll and Gartland accepted 40 Complications

965

degrees.42 Kettlekamp and Larson124 observed that, when strength rather than appearance was important (typically for men and patients with severe paralysis of the contralateral arm), flexorplasties are more satisfactory with a flexion contracture between 30 and 60 degrees. Mayer and Green158 were not satisfied if the flexion contracture exceeded 15 degrees, and they used turnbuckle splints postoperatively to minimize the flexion deformity. Dutton and Dawson76 preferred a flexion contracture of 15 to 30 degrees, which allows the arm to “hang at the side” more normally in patients concerned with appearance, and a 30- to 45-degree contracture in patients who were more concerned with function. Dutton and Dawson76 reported transient ulnar nerve paresthesias in two patients. Lindholm and Einola145 reported on two patients with postoperative ulnar nerve paresthesias, one of whom was still having symptoms at follow-up. Description of the transferred muscle occasionally occurs with variable impact. Steindler reported an excellent result after reinsertion,223 whereas Kettelkamp and Larson recorded a poor result in a patient with an untreated description.124 Inherent in the Steindler flexorplasty is the increased pronatory effect on the forearm and the associated risk of pronation deformity (Steindler effect). The incidence in the literature varies from 28% to 50%.42,76,145 Theoretically, inserting the flexor mass more anteriorly and laterally on the humerus will decrease this effect.146 The flexor carpi ulnaris can be transferred to the flexor carpi radialis40 or extensor carpi radialis brevis146 primarily or secondarily, or the flexor digitorum superficialis origin can be left in place.36

Latissimus Dorsi Transfer Schottstaedt and colleagues207 were the first investigators to report successful restoration of elbow flexion by rotating the entire latissimus dorsi muscle on its neurovascular pedicle, reattaching its insertion to the coracoid and its origin to the distal biceps muscle and tendon. One patient could lift 4 pounds. They noted that the procedure was contraindicated when the latissimus dorsi was the only muscle capable of elevating the pelvis for a forward step. Zancolli and Mitre refined the technique described by Schottstaedt and associates and coined the term bipolar transfer.254 Brones and colleagues33 reported that the bipolar myocutaneous latissimus dorsi flap restored contour and function in a post-traumatic condition. Restoration of elbow flexion by transferring only the origin of the latissimus dorsi to the biceps insertion (unipolar transfer) was reported by Hovnanian in 1956.117 He noted that the cross-sectional area, fiber length, and excursion of the latissimus dorsi muscle History

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Part VII Reconstructive Procedures of the Elbow

compared favorably with those of the biceps and brachialis. Axer11 and others modified the unipolar technique by using only the upper third of the latissimus dorsi, transferring its origin off several spinous processes to the biceps tendon. Excursion of 7 cm was obtained by stimulating this part of the muscle. According to these authors, transferring only a portion of the muscle avoids the sometimes bulky enlargement of the arm that results when the whole muscle is used. Preservation of some function in the undisturbed portion of the latissimus dorsi was noted in one of the patients. Botte and Wood28 decided whether to do bipolar or unipolar transfer at the time of surgery. If the line of pull stabilized in the plane of elbow motion and there was no tension on its neurovascular pedicle, the transfer was completed as a unipolar transfer. If the line of pull deviated outside the plane of elbow flexion or there was tension on the neurovascular pedicle, the transfer was converted to a bipolar transfer. The latissimus muscle flap is widely used as a pedicled muscle flap for restoration of elbow flexion.53,55,155,182 The latissimus dorsi is a broad, thin muscle (Fig. 71-7) with a wide origin from the lower six thoracic vertebrae, from the spinous processes of the lumbar and sacral vertebrae by an aponeurosis from the iliac crest, and by muscle slips from the lower four ribs. It inserts into the medial wall and floor of the intertubercular groove of the humerus. The major vascular pedicle of the muscle is the thoracodorsal artery, a terminal branch of the subscapular artery. In 94% of the 114 specimens, a bifurcation of the common neurovascular trunk into

Anatomy

lateral (parallel to the lateral border of the muscle) and medial (parallel to the upper border) branches has been documented.237 Bartlett and coworkers15 studied 50 latissimus dorsi muscles and noted the same bifurcation in 56% of the dissections. These studies provide the anatomic basis for the clinical findings noted by Axer and colleagues.11 The thoracodorsal nerve (C6-8) is derived from the posterior cord, and enters the muscle with the artery and its vein on its deep surface about 10 cm from its insertion. There are one to three branches from the thoracodorsal artery to the serratus muscle that have to be ligated to allow complete mobilization of the latissimus during a bipolar transfer. In the study by Bartlett and coworkers,15 the vascular pedicle to the latissimus dorsi had an average length of 11 cm and the thoracodorsal nerve a mean length of 12.3 cm. Technique The bipolar transplantation is preferable to the unipolar transfer for several reasons. The mechanical efficiency of the transplant is increased by the more anterior placement of the origin into the coracoid process, the proper length is easier to determine when the distal insertion is completed first, and there is less chance for kinking the neurovascular pedicle.

Bipolar Transplantation This description follows that of Zancolli and Mitre (Fig. 71-8).254 The operation is carried out in four steps: 1. Division of the latissimus dorsi muscle origin and insertion while preserving its neurovascular pedicle. 2. Exposure of both ends of the biceps muscle through separate incisions.

C5 C6 C7 C8 T1

Thoracodorsal artery and nerve

FIGURE 71-7

A

B

A and B, The anatomy of the latissimus dorsi. Shortly after entering the muscle, the single neurovascular pedicle (thoracodorsal nerve and artery) divides into lateral and medial branches.

Chapter 71 Flaccid Dysfunction of the Elbow

C

967

D

FIGURE 71-8

Bipolar transplantation of latissimus dorsi. A, Incisions used for this procedure. B, The origin and insertion of the latissimus dorsi are divided, and the muscle is mobilized on its neurovascular pedicle. C, Transplantation of the muscle under a cutaneous bridge in the axilla; the origin is redirected through a subcutaneous tunnel in the arm to the biceps tendon. D, The distal anastomosis is completed first, and the proximal attachment to the coracoid process and its conjoined tendon is used to set the tension. (After Zancolli, E. A., and Mitre, H.: Latissimus dorsi transfer to restore elbow flexion. J. Bone Joint Surg. 55A:1265, 1973.)

3. Transplantation of the latissimus dorsi muscle under a cutaneous bridge in the axilla to the bed of the paralyzed biceps and brachialis, resecting the biceps muscle, if need be, to provide room for the latissimus dorsi. 4. Fixation of the transposed muscle to the coracoid process and biceps tendon. The patient is in the lateral position, and the upper extremity is draped free. A longitudinal incision is made parallel to the lateral border of the latissimus dorsi muscle, extending from the posterior border of the axilla to the iliac crest. The dissection of the muscle is begun along its lateral border and leads from distal to proximal. The neurovascular pedicle must be freed up to its origin in the axilla, and this requires the ligation of any branches of the thoracodorsal artery that enter the serratus anterior. Once the neurovascular pedicle is freed, the origin

and insertion of the latissimus dorsi are sectioned. When the muscle is small, it is transplanted completely, but when it is entirely normal, it may be necessary to transplant only its lateral half. It is also possible to fold over the vertebral border of the muscle to make it more tubular in shape. Initially, a pocket is created in the anterior aspect of the upper arm, big enough to fit the muscle. Then the muscle is dissected from its origin to its insertion and transferred to the anterior arm based on its neurovascular pedicle. The muscle is shaped to simulate a biceps muscle and is fixed proximally at the clavicle and distally to the radial tuberosity.218 A deltopectoral incision is used to expose the coracoid process and free the tendon of the pectoralis major, behind which the transposed latissimus dorsi will be routed. The insertion of the biceps is then exposed through a bayonet incision over the anterior aspect of the elbow. If the paralyzed biceps is to be resected, the

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Part VII Reconstructive Procedures of the Elbow

resection is carried out through these two incisions and care is taken to protect the neurovascular bundle of the arm and to preserve a long segment of distal biceps tendon. The latissimus dorsi muscle is then passed under the skin bridge of the axilla, protecting its neurovascular pedicle from any kinking or tension. The insertion of the transposed muscle is passed deep to the pectoralis major tendon and up to the coracoid process while its distal end is passed downward toward the elbow beneath the skin of the arm. It is convenient at this time to close the thoracic incision over several drains. The distal biceps aponeurosis is opened up and spread out so that it can be wrapped around the distal end of the latissimus dorsi. A significant amount of distal latissimus muscle usually has to be excised because it is too long. After the distal anastomosis is completed, the distal skin incision is closed. The proximal end is then fixed at the junction of the conjoined tendon with the coracoid process, the length of the transplant being adjusted so that the elbow remains spontaneously at 90 to 100 degrees of flexion with some trial sutures in place. When the proper length has been determined, the final suturing of the proximal end is carried out and the shoulder wound is closed. A plaster Velpeau bandage is then applied with the elbow flexed and the forearm supinated. The drains are removed at 48 hours. Postoperative immobilization is maintained for 6 weeks. Flexion exercises are then permitted (with gravity eliminated) with gradually decreasing extension block splinting over the next 2 weeks. At 8 weeks, flexion against gravity begins. Four to 6 months is required before the transplant attains maximum strength. Myocutaneous transplantation of the latissimus dorsi is performed using the same technique, except that an appropriately sized segment of skin is left attached to the muscle (Fig. 71-9).

Unipolar Transfer This description is based on that of Hovnanian (Fig. 71-10).117 The patient is positioned as for the bipolar transfer. The incision begins in the loin, extends along the lateral margin of the latissimus to the posterior axillary fold, and continues across the axilla and downward along the medial arm to the elbow. The muscle is detached from its origin, preserving part of the aponeurosis with it, and is freed up proximally. Branches from the thoracodorsal artery to the serratus anterior muscle are ligated. The muscle is then transferred to the anterior arm, where it is attached to the biceps tendon and periosteal tissues of the bicipital tuberosity. The arm is bandaged to the thorax for 3 to 4 weeks, at which time active and passive exercises are started. The posterosuperior muscle fibers are shorter than the anteroinferior muscles; therefore, one must ensure

A

B FIGURE 71-9

Technique used for myocutaneous latissimus dorsi transplantation.

that all muscle fibers are anchored caudally as well as cranially.70,153 Experience is with small patient samples.11,27,117 Zancolli and Mitre254 observed eight patients who had had bipolar transplantation of the latissimus dorsi for more than 4 years. Active range of flexion was 105 to 140 degrees, and flexion strength varied from 0.7 to 5 kg. Flexion contractures of 10 degrees and 15 degrees occurred in two, and active supination of 20 to 50

Results

Chapter 71 Flaccid Dysfunction of the Elbow

A

969

B

FIGURE 71-10 Unipolar transfer of the latissimus dorsi for elbow flexion. A, Incisions employed. B, The detached origin, rotated on its neurovascular pedicle, is attached to the biceps tendon and aponeurosis.

degrees was achieved in six. Takami and others230 reported on two patients. One obtained elbow motion from 0 to 125 degrees and supination of 30 degrees and could lift 3 kg; the other had motion from 0 to 130 degrees with 60 degrees of supination and could lift 2 kg. Moneim and Omer171 achieved satisfactory flexion (100 degrees or more) in three of five patients. The two others achieved 65 to 70 degrees of flexion and initially had paralysis of the latissimus dorsi, so they were advised that the procedure should not be done unless the muscle was normal. Preoperative EMG evaluation of the muscle was recommended. Hirayama and associates111 reported four excellent results, three good results, and one failure among eight patients who had transfers of the latissimus dorsi. Botte and Wood28 noted satisfactory function in four of five patients treated with unipolar or bipolar latissimus dorsi transfer, and flexion that averaged 87 degrees (range 35 to 130). Chen48 achieved satisfactory function with average motion from 32 degrees of extension to 126 degrees of flexion in six patients who had bipolar transfers of the latissimus dorsi. They could lift only 1.5 to 2.5 kg, which was sufficient for most activities of daily living but not for heavy manual work. Concurrent skin coverage with restoration of elbow flexion is accomplished nicely with a latissimus dorsi myocutaneous flap.33,112,199,225 Clinical evidence of a functional deficit after transfer or transplantation of the latissimus dorsi is unusual. Russell and coworkers203 did document some minimal changes in shoulder strength and range of motion after transfer or transplantation of the latissimus dorsi in 24 patients.

A

B

FIGURE 71-11 A and B, This 36-year-old man who had C5-C6 paralysis following a closed brachial plexus injury underwent a bipolar transfer of the latissimus dorsi 3 years after the injury. Good elbow flexion was restored (A), and nearly full extension of the elbow was maintained (B). Shoulder arthrodesis was also performed.

Patients are able to hold weights between 8 and 15 kg,18 and up to 115 degrees of elbow flexion can be achieved (Fig. 71-11).171 Haninec and Smrcka102 reported M3 flexion up to 120 degrees at 16 months, unchanged from 5 months, in two patients.

Pectoralis Muscle Transfer The first use of the pectoralis major muscle to restore elbow flexion was reported in the European lit-

History

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Part VII Reconstructive Procedures of the Elbow

erature in 1917 by Schulze-Berge,209 who transferred its tendon of insertion directly into the belly of the biceps. Subsequent modifications of the method of insertion of the pectoralis major included the use of fascia lata or strands of silk to form tendons of insertion, either into the biceps tendon or directly into the ulna.115,137,138,198 Clark59 reported the first really successful physiologic transfer of the pectoralis major in 1946. In his procedure, the sternocostal origin of the muscle with its separate nerve (medial pectoral) and blood supply was mobilized, passed subcutaneously down the upper arm, and attached to the biceps tendon. Seddon modified Clark’s operation by elevating a segment of rectus abdominis sheath in continuity with the distal end of the transplant to act as a tendon.210 Brooks and Seddon34 described a unipolar transfer of the entire pectoralis major muscle, employing the devascularized long head of the biceps as its tendon of insertion. They recommended this operation instead of a Clark transfer when either the lower part of the pectoralis major was paralyzed but the clavicular head strong, or the whole muscle was weak.213 In 1955, Schottstaedt and others first reported bipolar transplantation of the chondrosternal portion (lower two thirds) of the pectoralis major on its neurovascular pedicle to restore elbow flexion.207 The humeral insertion was detached and shifted to the coracoid process, and the origin was transplanted to the biceps tendon. Carroll and Kleinman46 transplanted the entire pectoralis major muscle on both of its neurovascular pedicles. The muscle origin with its attached anterior rectus abdominis sheath was attached to the biceps tendon, and its tendon of insertion was secured to the anterior aspect of the acromion. With bipolar transplantation of the entire muscle, they noted increased shoulder stability, which obviated shoulder arthrodesis and improved mechanical efficiency for elbow flexion as compared with the unipolar transfer. Matory and coworkers157 transferred the lower sternocostal portion of the muscle with a 4-cm portion of rectus sheath mobilized with the medial and lateral pectoral nerves and accompanying vessels. The muscle was “tubularized” and woven through the biceps tendon, and the transverse aponeurosis was repaired to restore a pulley. Separate midline and deltopectoral incisions were used to avoid the undesirable scar from the standard pectoralis transfer approach. Tsai and associates239 added unipolar transfer of the pectoralis minor muscle to a bipolar pectoralis major transplant, noting excellent strength of elbow flexion without endangering the two muscles’ common neurovascular bundles. The lateral half of the clavicular origin of the pectoralis major was left intact to preserve shoulder adduction. The first transfer of the pectoralis minor to the paralyzed biceps to restore elbow flexion was done in 1910

by Bradford.30 Spira219 reported on one patient who had complete paralysis of the pectoralis major secondary to poliomyelitis who enjoyed excellent function after the transfer of the origin of the pectoralis minor into the distal biceps. Alnot7 recommended transferring the pectoralis minor to the biceps at the time of plexus exploration and nerve repair. Concerns such as diminished excursion, the obligatory supination of the forearm, and the oblique scar on the chest have been the focus of several modifications to the technique. Especially in women, there are cosmetic concerns because the procedure may create breast asymmetry.155 Another concern has been that the pectoralis major muscle is not strong enough to substitute for the biceps in cases of complete absence of elbow flexion.218 Phylogenetically, the pectoralis major muscle evolved from three separate ones, and today it has a segmental configuration with an independent neurovascular supply (Fig. 71-12). The pectoralis major muscle has two constant (clavicular and sternocostal) subunits, and in about half of humans, an abdominal subunit.236 The clavicular portion of the muscle originates from the medial third of the clavicle. The sternocostal portion arises from the anterior surface of the manubrium and the body of the sternum and cartilage of the first six ribs. The abdominal portion, when present, arises from the aponeurosis of the external oblique muscle and is found posterior to the axillary border of the sternocostal portion. The lateral pectoral nerve, derived from the lateral cord and containing fibers from nerve roots C5, C6, and C7, supplies the clavicular and upper portions of the sternocostal parts of the muscle. The medial pectoral nerve, derived from the medial cord and containing fibers from C8 and T1, innervates the lower sternocostal and abdominal parts of the pectoralis major after piercing the pectoralis minor or passing around its lateral edge as it also innervates this muscle. The clavicular and upper sternocostal portions of the pectoralis major are supplied by the pectoral branch of the thoracoacromial artery. The lower sternocostal portion and the abdominal portion, when present, receive their blood supply from the lateral thoracic artery.

Anatomy

Technique Prerequisites to this technique are that the sternocostal part of the pectoralis major muscle is of normal strength, and the elbow has full passive range of motion.218

Unipolar Transfer The unipolar transfer approach is based on that of Clark59 and Holtmann and associates116 (see Fig. 71-12). The patient is supine with a sandbag behind the shoulder. The arm is draped free and supported on a hand

Chapter 71 Flaccid Dysfunction of the Elbow

971

Lateral pectoral nerve Pectoral branch: thoracoacromial artery Medial pectoral nerve Lateral thoracic artery

A

B

C

D

FIGURE 71-12 Unipolar transfer of the pectoralis major for elbow flexion. A, The anatomy of the pectoralis major muscle. The lateral pectoral nerve and pectoral branch of the thoracoacromial artery supply the clavicular portion and the upper part of the sternocostal portion of the muscle. The medial pectoral nerve and branches from the lateral thoracic artery supply the lower part of the sternocostal portion and the abdominal portion (when present) of the pectoralis major. B, Incisions employed in performing a unipolar transfer of the lower sternocostal portion of the pectoralis major (Clark’s transfer). C, The lower third of the pectoralis major, detached with a 6-cm segment of anterior rectus abdominis sheath, is mobilized proximally on its neurovascular pedicle. D, The detached origin with the attached rectus abdominis sheath is passed through a subcutaneous tunnel and attached to the biceps tendon.

table or Mayo stand. An incision is made parallel to the lateral border of the pectoralis major muscle from the axilla to the seventh rib. The origin of the lower third of the muscle is detached from the sternum and fifth and sixth costal cartilages in continuity with a 6-cm segment of anterior rectus abdominis sheath. The sternocostal segment is carefully freed from the rest of the pectoralis major muscle to protect its nerve (medial pectoral) and vascular (lateral thoracic branches) supplies. The biceps tendon is exposed through an oblique incision over the anterior aspect of the distal arm and

elbow. Large forceps are then thrust upward from this distal incision to create a subcutaneous tunnel continuous with the upper end of the other incision. The muscle is pulled through the tunnel, and its rectus sheath segment is woven through the biceps tendon with the elbow in 125 degrees’ flexion and the forearm fully supinated. With the shoulder in adduction and internally rotated, the elbow and forearm are immobilized in acute flexion and supination for 6 weeks. Isometric contractions are begun at 3 weeks, followed by active elbow flexion from an initial position of 90 degrees of elbow flexion.

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Partial Bipolar Transplantation of Pectoralis Major This description follows that of Schottstaedt and colleagues.207 The muscle is exposed through an incision extending from 2.5 cm distal to the margin of the axilla along the lateral border of the pectoralis major muscle to within 5 cm of the midline. The lower half of the pectoralis major muscle is detached from its sternocostal origin and separated from the underlying pectoralis minor, care being taken to protect its nerve (medial pectoral) and vascular supply (lateral thoracic arterial branches). Through a separate 10-cm deltopectoral incision, the pectoralis major tendon of insertion is detached. The clavicular fibers of insertion should be detached from the freed tendon. The lower portion of the muscle is detached from the upper portion in line with its fibers; it is now completely free on its neurovascular pedicle. The biceps tendon is exposed in the distal arm and antecubital space through an oblique 12-cm incision extending from the proximal medial to the distal lateral aspect. A subcutaneous tunnel is created upward to the deltopectoral incision, and the sternocostal origin of the muscle is drawn through the tunnel so that it overlies the paralyzed biceps. The pectoralis muscle is then sewn to the biceps tendon, and the aponeurosis is closed with heavy, nonabsorbable sutures. The distal wound is closed, and the pectoralis major insertion is attached to the conjoined tendon at the coracoid by weaving it through several times. While the proximal suturing is

A

B

performed, the muscle tension should be maximal with the elbow in about 125 degrees of flexion. At this point, it can be noticed that the pedicle is made more lax by relieving some of the downward pull placed on it initially when the muscle was sutured to the distal biceps. According to Schottstaedt and others, an extension of length using rectus abdominis sheath is usually unnecessary. The postoperative position of immobilization and the exercise program are as described earlier.

Complete Bipolar Transplantation of Pectoralis Major This procedure is based on that of Carroll and Kleinman46 (Fig. 71-13). The patient is placed in the supine position, with a flat bolster under the blade of the scapula and the upper extremity draped free. A long, curvilinear incision is made from the seventh sternocostal joint proximally to two fingerbreadths inferior to the clavicle. The incision continues laterally to the coracoid process, then distally along the anteromedial aspect of the arm to the level of the axilla. With the acromion and the entire pectoralis major muscle exposed, a second curvilinear incision is made over the antecubital fossa with its transverse limb across the fossa and the longitudinal limb extending medially and distally 6 cm. The entire pectoralis major muscle is then detached from its origin along the medial half of the clavicle and its sternocostal border with a 10- by 4-cm strip of attached rectus abdominis fascia. In the

FIGURE 71-13 Bipolar transplantation of the pectoralis major muscle for elbow flexion. A, The incisions. Solid lines indicate skin incisions and dotted lines indicate the extent of detachment of the pectoralis major and rectus abdominis sheath. B, The completely detached pectoralis major is rotated on its two neurovascular pedicles. Its origin is attached to the biceps tendon, and its insertion is attached to the acromion through drill holes.

Chapter 71 Flaccid Dysfunction of the Elbow

process of freeing the pectoralis major from the chest wall and the underlying pectoralis minor, meticulous care is given to preserving its two neurovascular pedicles. Care must be taken during dissection because the muscle’s neurovascular bundle can easily be avulsed.218 The entire muscle mass is then rotated 90 degrees on its two neurovascular pedicles. The clavicular and sternocostal origins with the attached rectus sheath are rolled into a tube and directed through the subcutaneous tunnel, exiting through the second incision. With the elbow flexed 135 degrees, the fascial tube is enclosed under maximal tension to the biceps tendon with nonabsorbable sutures, including a transcutaneous stay suture tied over a bolster. The tendon of insertion is then detached, directed proximally, and anchored securely to the anterior acromion by nonabsorbable sutures through drill holes. Before exercises are commenced, the elbow is immobilized for 6 weeks, with the joint flexed 135 degrees using a collar and cuff with a swathe. Results The original description was of only one patient, who had flexion limited by only 15 degrees, extension limited by 5 degrees, and flexion power 40% of normal 16 weeks after a partial bipolar transfer of the pectoralis major.59 Seddon noted excellent results (powerful flexion against gravity and resistance) in seven of 16 Clark’s transfer patients on whom he reported.210 In the remainder, the elbow could be flexed against gravity and slight resistance. Seven patients regained supination against resistance (from 10 to 90 degrees). In four cases in which the pectoralis major power was subnormal, the pectoralis minor was used in addition. D’Aubigne reported excellent active flexion, independent of shoulder adduction, in two patients who had Clark’s transfer.62 Using the unipolar transfer of the pectoralis major into the devascularized long head of the biceps, Brooks and Seddon34 achieved three excellent, three good, and two fair results (less active flexion than passive or flexion against gravity but not against resistance), and two complete failures. Two of the good results, however, required second operations (triceps to biceps) because of simultaneous action of the pectoralis major and the triceps, a phenomenon they ascribed to axonal confusion during regeneration after brachial plexus lesions. Holtmann and associates116 noted useful active elbow flexion through a mean range of 96 degrees, accompanied by supination of the forearm, in all seven of Clark’s transfers on which they reported. Four of the patients had arthrogryposis, and, in all cases, the transfer was extended with a 6-cm segment of anterior rectus sheath. Leffert and Pess141 reported the results of 15 pectoralis transfers: good result in eight, improvement in four, and no improvement in three cases. They recommended that shoulder fusion be

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carried out several months before the transfer in patients who have a paralyzed shoulder. Botte and Wood28 recorded satisfactory results in all five patients who had bipolar pectoralis major transfers but cautioned against using it in women because of the cosmetic disfigurement. Matory and associates157 transferred the lower sternocostal segment of the pectoralis major in seven patients and achieved a functional range of elbow flexion (mean 98 degrees) in all. Extension loss was only 15 to 25 degrees, and sustained flexion strength averaged 8 pounds. Tsai and others used modified bipolar transplantation of the pectoralis major (leaving the lateral half of the clavicular origin intact), supplemented with a unipolar transfer of the pectoralis minor, in four patients.239 Three of the four achieved excellent results (full extension with at least 60 degrees of flexion), and the other patient required a secondary Steindler’s flexorplasty. Spira achieved strong flexion through a range of 135 degrees with virtually full extension in a patient with total paralysis of the pectoralis major and elbow flexors secondary to poliomyelitis whose pectoralis minor origin he transferred to the biceps tendon.219

Arthrogryposis In arthrogrypotic children, Lloyd-Roberts and Lettin149 observed that preliminary posterior release and triceps lengthening may be necessary to secure passive flexion. They modified Clark’s transfer by obtaining a longer anterior rectus abdominis sheath and inserting the transfer into the ulna, because the biceps tendon frequently is absent. All seven patients who had the modified transfer could get their hands to their mouth against gravity and some resistance. Atkins and coworkers10 transferred the pectoralis major by detaching its clavicular origin to allow its insertion to be tied into the biceps tendon remnant in six children, five of whom were arthrogrypotic. The operations achieved good results in three, three others were fair, and one was poor. Doyle and coworkers74 reported on seven cases of arthrogryposis in which a bipolar transfer of the entire sternal head of the pectoralis major with a generous tongue of anterior rectus abdominis sheath was performed. All seven patients achieved improved elbow motion, and six were able to feed themselves using only one hand. Three of the four patients reported on by Carroll and Kleinman46 who had bipolar transfers of the entire pectoralis major muscle achieved excellent results. Because of the increased shoulder stability achieved with this operation, shoulder arthrodesis was not necessary.

Comparative Studies Segal and associates, using combined objective and subjective evaluations, compared the results of 13 flexorplasties, three triceps transfers, 17 Clark’s transfers, and

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Part VII Reconstructive Procedures of the Elbow

eight Brooks-Seddon transfers.213 Fifty-three percent of Clark’s transfers and 75% of Brooks-Seddon transfers either had fair results or failed, whereas only 31% of the flexorplasties had a fair result and there were no failures. The decreased flexion contracture of the elbow, simultaneous contraction of the triceps when the pectoralis transfer flexed the elbow, and undesirable shoulder adduction and internal rotation movements accompanying elbow flexion all contributed to less satisfactory results in the pectoralis transfer group. These authors, and Clark himself, advised against using the pectoralis transfer when some biceps activity was present or could be anticipated.61 Rostoucher200 reported the results in 15 cases of pectoralis minor transfer, with good (M4, <120 degrees flexion) results in 53%. Six failures were salvaged by a secondary Steindler flexorplasty, improving the results to 80% good. The results were good or very good in seven of the nine C5-6 lesions. One good result and three failures were reported in the patients with C5-7 lesions, possibly owing to the lower strength of power of the transferred muscle in these combined lesions. Doyle and associates74 reported on two patients who developed transient nerve palsy, one medial and one radial, after pectoralis major transfer. Both problems resolved completely after several weeks. Simultaneous contraction of the triceps when the elbow is flexed by the transfixed pectoralis major was noted in three cases by Segal and coworkers.213 All three had brachial plexus injuries and initially had had paralysis of the triceps and elbow flexors. Axonal confusion after regeneration seems to be the likely explanation, but the complication cannot be predicted, because in six other cases in which the triceps initially was paralyzed and later recovered, no simultaneous flexor-extensor action developed. Complications

15 patients.45 They advised against performing triceps transfer bilaterally or in a patient who uses crutches. Botte and Wood28 also advised against the procedure in patients who use a cane or a wheelchair and those who have to work with their hands overhead. Several authors have recommended triceps-to-biceps transfer with poorly functioning biceps when there is co-contraction of a reinnervated triceps.7,28,202 This may yield a favorable result even when there is insufficient triceps strength. Otherwise this would be a contraindication. A clear disadvantage is the loss of active extension but when compared with transfers of the hand flexors and extensors, the power of elbow extension is greater, with fewer extension deficits.202 The triceps muscle arises from three heads— one from the scapula (long head) and two from the posterior humerus (lateral and medial heads). The medial head has an extensive origin from the posterior shaft of the humerus, extending from the insertion of the teres major to within 2.5 cm of the trochlea of the humerus. The muscle is supplied by the radial nerve (C7 and C8, with a smaller contribution from C6) through multiple branches that arise above the spiral groove. An exception is the posterior branch to the medial head, which leaves the radial nerve just as it enters the groove.32

Anatomy

Technique This description is based on that of Carroll (Fig. 71-14). The patient is placed in the distal decubitus position and the extremity is draped free. A posterior

Triceps Transfer Biesalski and Mayer23 and later Vulpius and Stoffel were the first to describe the transfer of part of the triceps muscle to compensate for the loss of elbow flexion. Since that time, it has been used in the treatment of the flaccid elbow in brachial plexus palsy to a varying degree.7,28,43 Use of the triceps muscle to restore elbow flexion was condemned by Steindler in 1939 because, he felt, “Loss of the normal function of the triceps is too great a sacrifice.”223 Bunnell, however, described a successful triceps transfer.39 In his opinion, “It is more important to flex than to extend the elbow.”40 Some modern authors have again abandoned this technique because the concurrent loss of elbow extension, critical for joint stabilization, is considered too disadvantageous.233 In 1955, Carroll described the technical details43 and, in 1970, reported the results of triceps transfer in History

246

FIGURE 71-14 Transfer of triceps insertion around the lateral side of the elbow to the biceps tendon.

Chapter 71 Flaccid Dysfunction of the Elbow

midline incision is made that extends over the distal two thirds of the arm and then curves laterally to the olecranon, extending distally over the subcutaneous border of the ulna for 5 cm. The skin flaps are widely undermined so that the ulnar nerve can be exposed medially and the lateral intermuscular septum laterally. A tail of periosteum as long as possible is raised from the ulna in continuity with the triceps insertion, and the medial head is mobilized from the distal third of the shaft of the humerus. The radial motor nerves enter the muscle in the interval between the lateral and medial heads as the radial nerve enters the spiral groove. The raw surface of the stripped medial head is then covered by suturing its two edges together into a tube. The biceps tendon is exposed through a curvilinear incision in the antecubital fossa, and the tendon is dissected free to its insertion onto the radius. The biceps tendon is split longitudinally. The triceps tendon is passed through a laterally placed subcutaneous tunnel between the two incisions, superficial to the radial nerve. The triceps tendon is then passed through the split biceps tendon and sutured in place under maximum tension with the elbow at 90 degrees of flexion and the forearm in full supination. As an alternative, the triceps tendon can be attached to the radial tuberosity using a pull-out wire technique, as described by Bunnell.40 The elbow is immobilized in a posterior splint at 90 degrees of flexion and full supination for 4 weeks, at which time active exercises are begun.

or paralysis patients. Among the eight patients with arthrogryposis, there were five successes, one limited result, and two failures. The average range of motion was 116 degrees and average flexion contracture 24 degrees in the first group, whereas in the arthrogrypotic group motion averaged only 43 degrees and the average fixed flexion deformity was 59 degrees (Fig. 71-15). Seven of the eight arthrogrypotic patients required adjunctive procedures such as excision of a dislocated radial head or modified elbow arthroplasty to achieve an acceptable passive range of motion before triceps transfer. Williams reported improvement measured by flexion against gravity in all 19 arthrogrypotic elbows submitted to triceps transfer, and he did not hesitate to perform the procedure bilaterally.248 However, extension was usually restricted to approximately a right angle because of the tenodesis effect of the triceps. Other authors have reported variable improvement, if any, after triceps transfer in arthrogrypotic patients.74,96,169 Leffert and Pess141 recorded four good and three improved results in seven patients who underwent triceps-to-biceps transfers. Botte and Wood28 reported mean flexion of 125 degrees in three patients who had triceps-to-biceps transfers. No effort was made to mobilize elbow extension past a 30-degree flexion contracture, because this was thought to be mechanically advantageous for elbow flexion. Alnot7 achieved 10 good and one acceptable result in 11 triceps-to-biceps transfers. Three were done after spontaneous triceps recovery, two in patients with co-contraction, and eight after nerve grafting. The investigators noted that 36% of their patients had a dominant triceps innervation from C8 and T1, making it available for transfer in C5, C6, and C7 lesions in these patients. Rühmann202 reported

Results Carroll and Hill recorded the results of 15 triceps transfers.45 Five successes (flexion against gravity with ability to bring the hand to the mouth), one limited result, and one failure were noted in the seven trauma

A

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B

C

FIGURE 71-15 A, A 5-year-old boy with arthrogryposis multiplex congenita underwent triceps transfer on the right extremity. B, Six months after surgery, he was able to flex the elbow to 95 degrees and gravity extension was possible to 50 degrees. C, The opposite elbow was left in extension.

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Part VII Reconstructive Procedures of the Elbow

on a series of three patients, resulting in active elbow function in all patients (mean flexion 113 degrees, range 90 to 30 degrees) with function against resistance (M4-5) and no passive stretching deficit. Loss of active elbow extension was not considered of great importance to these patients. Complications have not been reported for any of these series.

Miscellaneous Transfers for Elbow Flexion Sternocleidomastoid transfer In 1951, Bunnell reported on a single patient with a paralyzed upper extremity secondary to poliomyelitis who gained elbow flexion from transfer of the insertion of the sternocleidomastoid muscle, extended with a strip of fascia lata, into the bicipital tuberosity.44 Carroll reported 80% satisfactory results in 15 cases with this technique.40 Kumar et al130 described a modification to Bunnell’s40 original technique, whereby the sternocleidomastoid muscle is sutured to a fascia lata tube under the clavicle to eliminate the bow-stringing and unsightly skin fold that would otherwise occur during flexion. Flexor Carpi Ulnaris Transfer In 1975, Ahmad published a single case report of a patient with a brachial plexus palsy who achieved 130 degrees of elbow flexion after the transfer of the insertion of the flexor carpi ulnaris, turned back on itself, into the distal humerus.1 No subsequent reports of this transfer have appeared in the literature.

Free-Functioning Muscle Transfers History Free muscle transfer for elbow reanimation is indicated when there are no available local donor muscles,59,155 due to trauma, tumor resection, or chronic denervation. Microneurovascular muscle transfer for recovery of motor function in cases of severely injured extremities has grown from successful experimental studies81,129,231,234 into a clinical reality119,120,152,184 and is now a useful reconstructive option in these difficult cases.50,52,69 Despite requiring meticulous technique and microsurgical skills, overall survival and reinnervation of transplanted muscles are consistently successful in large series.14,52,69 Although reconstruction of elbow function alone with a free-functioning muscle transfer in acute cases of brachial plexus palsy is inferior to direct neurotization of the musculocutaneous nerve when performed within 6 months of injury,3,181 it is indicated to restore elbow flexion in chronic cases,69 when there is irreparable injury to the biceps or distal portion of the musculocutaneous nerve, or when used for a dual purpose combining elbow flexion with animation of the wrist or hand.14,19,67,68,71 Important prerequisites for free muscle transfer include adequate skin cover; a normal or at least functional arc of passive elbow motion; a compliant, stable soft tissue bed permitting

tendon gliding; and available motor nerves and blood vessels. The presence of vascular bypass grafts at the planned site of vessel repair, for example, is in general a contraindication to functioning free muscle transfer. In cases of flaccid elbow paralysis resulting from a brachial plexus injury or lesion, innervation may be provided, even when the limb is flail and all nerve roots avulsed, by direct nerve transfer of two to four intercostal motor nerves or spinal accessory nerve, or following regeneration across a banked nerve graft from the contralateral C7 root.3,52,69,70,153,218 In more favorable circumstances, intraplexal nerve transfer using two to three fascicles of the ulnar nerve supplying flexor carpi ulnaris motor branches,186 median nerve fascicles supplying flexor carpi radialis,147,151,157 or direct repair/graft of the musculocutaneous nerve itself will provide superior results and minimal donor morbidity. In chronic cases requiring free functioning muscle transfer, neurotization of the motor nerve can also be performed using an ulnar nerve fascicle.105,229 In any of the abovementioned nerve procedures, efforts should be made to place the nerve transfer or repair in close proximity to the transferred muscle motor point, thus minimizing the reinnervation time. An accurate epineural repair using microsurgical methods is important. Intercostal nerve transfer is performed with the shoulder in maximal external rotation and 90 degrees of abduction, to allow postoperative shoulder motion up to this positioning limit.66 At surgery, certain principles must be followed to optimize results. It is desirable to place the transferred muscle at its optimal resting tension, with a straight line of pull and anatomic insertion, avoiding crossing of a flail or unstable shoulder when possible, and no bowstringing.66 Best results are seen when antagonistic (triceps) function is either present or reconstructed through direct reinnervation, tendon transfer, tenodesis, or the addition of another free-functioning muscle transfer. Use of the muscle for a second purpose has been demonstrated to weaken elbow flexion.16

Selection of Donor Muscle To be useful as a biceps substitute, the free muscle must have adequate strength and excursion, be expendable, and have a neurovascular pedicle permitting microsurgical transfer and nerve repair.66 Strength is roughly proportional to the cross-sectional area and weight of the muscle, whereas excursion is most directly related to fiber length but is also affected by fiber orientation relative to the muscle long axis (pennate vs. strap muscle) and fascial connections. The points of origin and insertion, and distance from the joint center are further factors to be considered.66 Tendon quality (both proximal and distal) affects the ease and quality of muscle

Chapter 71 Flaccid Dysfunction of the Elbow

insertion through tendinous and neurovascular connections. Volitional control should be provided through a single motor nerve to allow reinnervation by direct nerve transfer. The pattern of blood supply must maintain muscle perfusion following transfer. Mathes and Nahai156 have classified muscles based upon blood vessel pattern, and have determined that their type I (single vascular pedicle), type II (one dominant and minor pedicles) and type V (one dominant and segmental pedicles) groups may serve as functioning free muscle donors. Examples of each include rectus femoris (type I), gracilis and biceps femoris (type II), and latissimus dorsi (type V). A comparison of available donor parameters to biceps has led to recommendations including latissimus dorsi or vastus lateralis,218 or rectus femoris3 muscles. The rectus femoris muscle, for example, being bipennate and having a short muscle fascicle length of 6 to 7 cm, has a relatively low contractile capacity.153 Therefore, it is not a good choice to reconstruct two functions and is prone to create an elbow flexion contracture.69 On review, the gracilis muscle would seem ill-suited to biceps replacement because it is too weak. However, gracilis transfers have become the preferred choice of most authors because of its exceptional length, proximal neurovascular pedicle, and excellent distal tendon.24,142 There is a defined but low level of donor-site morbidity, with a nonsubjective loss of hip adduction of 11%, hypesthesia or dysesthesia of the cutaneous territory of the obturator nerve in 50%, and aesthetic changes to the thigh.64 The satisfactory results reported using the gracilis muscle for elbow function belie the anatomic measurements that would seem to render it inferior as a biceps replacement.24

Patient Considerations Free muscle transfer is a lengthy procedure, and careful preparation of the patient is important. Adequate positioning and protection of bony prominences as well as maintenance of body core temperature (that facilitates peripheral perfusion) are critical aspects of preparation. The surgical procedure requires meticulous planning. An adequate or reconstructible skin cover and bed for tendon gliding are important considerations before a free-functioning muscle is transferred. When a muscle is used for both soft tissue coverage and functional restoration of elbow function, as is often the case in large post-traumatic reconstructions, the resultant excursion may be insufficient for a functional range of motion.26 An expendable motor nerve must be in the vicinity of the muscle neurovascular pedicle. Preoperative assessments should also include a magnetic resonance or conventional angiogram to prepare for vascular physiologic or post-traumatic variations. The rate of subcla-

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vian or axillary artery avulsion, especially associated with first rib and upper extremity fractures, has been reported to be as high as 10% to 25% in brachial plexus injury.100,227 In gracilis transfer, the donor thigh should be the contralateral side, due to the resulting optimal placement of the neurovascular pedicle.

Gracilis Transfer For Elbow Flexion Preparation of the Recipient Site Initial dissection is performed at the recipient site, before any dissection of the donor muscle is performed. A deltopectoral approach is used, with a supraclavicular transverse component needed to expose the lateral clavicle and acromion for proximal tendon fixation, as well as the thoracoacromial trunk. Initially, the cephalic vein is identified and protected. When performed within 6 months of a brachial plexus injury, a surgical exploration of the brachial plexus is performed and intraoperative electrophysiologic studies performed. This commonly includes SEPs and motor evoked potentials (MEPs) to evaluate nerve roots, and neuromuscular stimulation of ulnar and/or median nerves if intraplexal nerve transfers are considered. If the surgical plan includes use of spinal accessory or intercostal nerve transfer, these nerves are next prepared. The spinal accessory nerve is identified through the same incision on the deep anterior surface of the trapezius muscle. A nerve stimulator demonstrates its motor function, and dissection is used to spare two branches, those to the sternocleidomastoid muscle and to the upper part of the trapezius. This preserves muscle function that provides scapulohumeral movement. This is especially important if the shoulder is to be arthrodesed.2 In order to avoid needing a nerve graft, a dorsal approach can be used to dissect more distally, as described by Vathana.244 This provides nerve length reaching to the terminal branches of the brachial plexus and certainly to the motor nerve supplying the free functioning muscle. Another option is to harvest the obturator nerve from the level of the obturator foramen, permitting its length to reach 10 cm. The phrenic nerve remains an alternative choice when no plexal nerves are available, and staged reconstruction with contralateral C7 has also been described, although few results have been reported.56 For hand reanimation, contralateral cross-chest C7 donors have been associated with inferior outcome in some hands,235 whereas others report more encouraging preliminary results.50 Should intercostal nerves be required, the deltopectoral incision is extended across the anterior wall of the axilla, curving beneath the nipple to allow elevation of the pectoralis muscles caudally to expose the ribs. Generally, two intercostal nerves will be sufficient to satisfy the obturator branch fascicles. Usually the third and fourth intercostal nerves are used (T3 and T4), easily

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Part VII Reconstructive Procedures of the Elbow

transferred to lie next to the thoracoacromial trunk. The periosteum is dissected free circumferentially from ribs from the costochondral junction anteriorly to the axilla. By incising the deep (osseous) surface of the reflected interior periosteum, the motor branch is identified at the nipple line and dissected to the costochondral junction. Meticulous dissection is needed to avoid injury to the pleura. Simultaneous biceps reinnervation with the T5 and T6 motor nerves may also be performed. For each transfer, the shoulder is positioned in 90 degrees of abduction and maximal external rotation to ensure adequate nerve length. When the surgical plan is to use ulnar or median nerve fascicles, the muscle is positioned somewhat more distally, and the thoracodorsal vessels are used instead; these muscles are identified lying on the anterior surface of the latissimus dorsi. Next, an antecubital incision exposes the biceps tendon, and subcutaneous tunneling connects the shoulder and elbow incisions. The thoracoacromial trunk is the most commonly used pedicle for arterial anastomosis. It is exposed most readily by caudal dissection of the clavicular head of the pectoralis major, and is facilitated with limited release of the more lateral clavicular origin of the muscle and release of the pectoralis minor from the coracoid process. The latter is tagged for later repair. The muscle will be placed to overlie the distal clavicle and acromion, allowing adjustment of its position proximally or distally to center the vascular pedicle over the thoracoacromial trunk. Three or four suture anchors are placed for securing the muscle before its harvest. The gracilis muscle is a superficial muscle of the medial aspect of the thigh. It is supplied by the obturator nerve, entering the muscle obliquely, cephalad to the main vascular pedicle, at 6 to 12 cm from its origin. The vascular supply is from a 4 to 6 cm long branch of the profunda femoris artery located 8 to 12 cm from the muscle origin and passing between the adductor longus anteriorly and the adductor magnus posteriorly. The gracilis may be harvested to include a paddle of skin serving as a buoy flap centered at this location (Fig. 71-16).154 Three small incisions are sufficient, beginning with exposure of the distal tendon medial and proximal to the tibial tubercle, then a second posteromedially overlying the tendon in the distal thigh to visualize the distal musculotendinous junction. A more proximal incision is made including the skin paddle at the location of the proximal neuromuscular junction. The position of the skin, centered over the muscle, is facilitated by palpation with traction on the distal tendon previously exposed. The skin paddle base includes fascia overlying both the adductor longus anteriorly and the adductor magnus posteriorly. The dissection then converges on the intermuscular plane Harvest of the Gracilis Muscle

FIGURE 71-16

Gracilis muscle during harvest. The monitor skin paddle is shown to the left; the vascular pedicle (not shown) is marked by vessel loops. Distally, the tendon is released from its insertion on the lateral aspect of the tibial tubercle. (By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

FIGURE 71-17 Gracilis muscle after harvest. (By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

between the adductor muscles, at which time the neurovascular pedicle is easily identified. The motor nerve lies cephalad, aligned roughly 45 degrees to the muscle, whereas the vessels pass perpendicularly toward the gracilis muslce. Dissection of the vessels requires careful elevation of the adductor longus and ligation of multiple small muscular branches from the pedicle to it. The nerve is dissected as far cephalad as feasible, often aided with fiberoptic-illuminated retractors, and then divided. The muscle is next released from the pubic symphysis proximally and from the pes anserinus distally. Use of lighted retractors permits tunneling between the three incisions to harvest the muscle. One or more secondary pedicles distally require ligation. Only when the recipient site is fully prepared and the operating microscope positioned is the vascular pedicle divided and the muscle immediately transferred (Fig. 71-17). Free Muscle Transfer When all is ready, the gracilis muscle is brought to the arm, and the proximal tendon connections made and the distal tendon tunneled into the antecubital incision, but not yet fixed. The microarterial anastomosis is made next, most frequently performed end to end to an appropriately sized arterial

Chapter 71 Flaccid Dysfunction of the Elbow

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branch of the thoracoacromial trunk or thoracodorsal artery. A single venous connection to the cephalic vein is made. The nerve transfer is next performed, followed by repair of the distal tendon to the biceps tendon (Fig. 71-18). Tension is adjusted to produce a 30-degree flexion contracture at the elbow. We have found this method to provide reliable postoperative arc of motion without use of marking sutures, as described by Manktelow and Zuker, which require more extensive incisions for muscle exposure in the thigh before harvest.153 The distal end can also be sutured to more distal targets, if needed. In our brachial plexus practice, for example, a single gracilis muscle transfer is sometimes used to provide finger flexion in addition to elbow flexion (Fig. 71-19). The distal gracilis tendon is prolonged with a forearm tendon graft (usually the paralyzed flexor carpi radialis) to reach the flexor digitorum profundus and flexor pollicis longus tendons. To avoid bow-stringing, an antecubital pulley is used, which is either the intact lacertus fibrosis or a fabricated antecubital pulley using the flexor carpi ulnaris (Fig. 71-20). In such a procedure, we also reinnervate the biceps with two additional inter-

FIGURE 71-19

Reconstruction of elbow and finger flexion with a single free gracilis muscle flap. The distal gracilis tendon is prolonged with a forearm tendon graft (usually the paralyzed flexor carpi radialis) to reach the flexor digitorum profundus and flexor pollicis longus tendons. (By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

FCU

FIGURE 71-18

Single-stage reconstruction of elbow flexion with a free-functioning gracilis myocutaneous flap neurotized with the spinal accessory nerve. The muscle is attached proximally to the lateral clavicle and acromion using suture anchors, and is woven into the biceps tendon distally. (By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

FIGURE 71-20 Occasionally, there is bow-stringing of the gracilis muscle when using it as an elbow flexor and finger flexor. In this case, a pulley can be created using the flexor carpi ulnaris (FCU). The FCU can be released from its distal insertion and looped under the forearm extensor origin to create a more effective pulley at the antecubital fossa. (By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

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Part VII Reconstructive Procedures of the Elbow

costal nerves to improve elbow flexion strength and reconstruct antagonist triceps function with nerve transfer or grafting. Aftercare consists of close monitoring of the buoy flap by skin color, turgor and capillary refill, and Doppler examination of myocutaneous perforators for the first 48 hours postoperatively, preferably in an intensive care unit. Passive range of motion exercises in uninvolved joints and edema control are begun immediately, after which patients are progressively mobilized. The shoulder and joints in the operated arm are immobilized for up to 3 weeks, after which gentle passive range of motion exercises are begun. Early recovery is recognized by a “squeeze test” of the muscle, producing a painful sensation, electromyographic evidence of muscle activation using the original function of the transferred nerve (e.g., cough or Valsalva firing intercostal nerves), or visible muscle contraction. This generally occurs 4 to 6 months after surgery. Once reinnervation is documented, biofeedback and re-education techniques with gravity-eliminated motion are used until muscle power has reached antigravity stage. Maximum return of strength requires up to 2 years from the date of surgery. Optimal results are obtained through active participation in rehabilitation programs. Noncompliance with these programs, possibly due to socioeconomic factors in some western countries, may affect the long-term outcomes when these are compared with Asian countries, for example.

Aftercare

Doi et al66,67,71 have described a method of double gracilis transfer combined with neurotization of the triceps and sensory neurotization of the hand to provide patients with four or five brachial plexus root avulsions with shoulder stability and function, as well as active elbow flexion and extension, protective hand sensibility, and rudimentary hand grasp and release. Simple nerve transfers, such as intercostal to musculocutaneous nerve to reconstruct elbow function alone, is not included in this procedure, even in acute cases. In the first stage, the gracilis muscle attached to the clavicle is neurotized with the spinal accessory nerve and an available C5 root, phrenic nerve, or contralateral hemi-C7 transfer is used for shoulder motor reconstruction. The gracilis tendon is sutured to the extensor digitorum communis tendon in the proximal forearm (Fig. 71-21). The applied tension is such that full finger flexion is permitted with the elbow flexed. Using wrist extensors as the distal insertion instead of the finger extensors may improve finger flexion through a tenodesis effect.24 Originally, the brachioradialis muscle was used as a pulley to prevent bow-stringing of the gracilis muscle transfer at the elbow. However, bowTechnique—Two-Stage Reconstruction

FIGURE 71-21

Doi stage I procedure.71 Free muscle transfer is used for restoration of elbow flexion and wrist extension. This procedure is usually combined with neurotization of shoulder girdle musculature (not shown). (By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

stringing would still sometimes occur, prompting the use of a distal portion of the flexor carpi ulnaris, which is detached and used to create a pulley at the level of the proximal forearm (see Fig. 71-20) (David Khoo, personal communication). Alternatively, the flexor carpi radialis has been used for the same purpose.20 The second-stage gracilis transfer, used for finger flexion, is neurotized by two or three intercostal nerves, and is attached to the second rib with multiple drill holes proximally (Fig. 71-22). Vascular connections are to the thoracodorsal vessels. Through a separate incision in the forearm, the flexor digitorum profundus and flexor pollicis longus tendons are sutured in such a way as to create a key pinch and grasp on traction. The gracilis tendon is tunneled under the pronator teres muscle, which serves as the pulley for this transfer, and is secured to the flexor digitorum profundus and flexor

Chapter 71 Flaccid Dysfunction of the Elbow

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2 3 3

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FIGURE 71-23 Neurotization of the triceps branch of the radial nerve with motor branches of the third and fourth intercostal nerves, and transfer of the fifth and sixth intercostal nerve motor branches to the freefunctioning muscle motor nerve. The third to sixth intercostal sensory branches are transferred to the lateral cord of the median nerve to provide protective hand sensation. (By permission of Mayo Foundation for Medical Education and Research. All rights reserved.) FIGURE 71-22

Doi stage II procedure.71 A second free-functioning gracilis transfer for finger flexion is performed, neurotized with two intercostal motor nerves. Additional nerve transfers for protective hand sensibility and triceps motor function are also performed (see Fig. 71-23). (By permission of Mayo Foundation for Medical Education and Research. All rights reserved.)

pollicis longus tendons using a Pulvertaft weave. Tension is set such that the fingers can extend with elbow flexion and such that the fingers and thumb can close with elbow extension. The second stage is completed by neurotization of the motor branch of the triceps brachii muscle with two intercostal motor nerves and the neurotization of the lateral portion of the median nerve with intercostal nerve sensory branches to restore protective hand sensibility (Figs. 71-23 and 71-24). The supraclavicular nerve sensory rami may also be used for this purpose.

FIGURE 71-24 Intercostal nerves can be divided into sensory and motor branches under the operating microscope.

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Shoulder function and stability are important prerequisites for prehension, and for this reason, Doi has augmented his double free-muscle transfer technique with neurotization of the suprascapular nerve with the C5 or C6 nerve root via a nerve graft. If these are not available, neurotization can be performed from a contralateral C7 nerve donor and a vascularized ulnar nerve graft.65

Latissimus Dorsi Transfer The latissimus dorsi as a free vascularized muscle flap offers the advantages of a large and long vascular pedicle (diameter 2-3 mm, length 8-12 cm), a single motor nerve, and the relatively large area of skin that can be carried as an island. For this reason, some authors prefer it as a first choice for restoration of elbow flexion.218 Adequate muscle innervation must be determined preoperatively, because C5, C6, and C7 may also be involved in the injury and not provide reliable latissimus function after transfer. Results Early results of free-functioning muscle reconstruction for elbow flexion were variable. Gilbert reported an excellent result in a 5-year-old child treated with free transplantation of the gracilis, using the musculocutaneous nerve as the recipient nerve, after traumatic destruction of the biceps muscle.91 Five other patients (two with poliomyelitis and three with brachial plexus palsies), however, achieved no useful flexion after a gracilis transplantation that was innervated through a long nerve graft connected to the sternocleidomastoid nerve. O’Brien and colleagues also recorded a failure in one patient 8 years after a free gracilis transplant that was innervated by the second and third intercostal nerves.184 Hirayama and others111 used a free latissimus dorsi muscle flap innervated by the intercostal nerve in a 35year-old man with a complete brachial plexus palsy and disuse atrophy of the biceps. Three years later, he had 90 degrees of flexion and a 30-degree flexion contracture. Botte and Wood28 achieved no useful flexion in three patients who had free latissimus dorsi transfers (two had distant neurotization) and recommended against the procedure. Manktelow152 reported on one patient who had a free gracilis transfer that was innervated by the musculocutaneous nerve to replace crushed biceps and brachialis muscles. Eighteen months after surgery, the patient could flex to 120 degrees from the fully extended position with a 15-pound weight. More recently, Chuang and associates52 reported on the results of 38 cases of brachial plexus injury treated with free-functioning gracilis muscle transfer for elbow flexion. Thirty-one muscle transfers were reinnervated by intercostal nerves; three cases with traumatic loss of the biceps treated at an interval of 6 to 12 months were reinnervated by the original musculocutaneous nerve;

the remaining four cases were reinnervated by the spinal accessory nerve. All 38 patients were followed for at least 2 years. All three patients with traumatic biceps loss regained M4 flexion power within 1 year of rehabilitation. Where three intercostal nerves were used for reinnervation, 78% regained M4 strength. Failures (M3 or less) in the intercostal nerve neurotization group were attributed to the site of proximal muscle insertion, with 1 of 5 failures where attachment was to the coracoid process of the scapula (N = 20), and 4 of 5 failures where attachment was to the second rib or the clavicle (N = 11). Transfer for combined elbow flexion and finger flexion yielded only a limited range of motion (0 to 90 degrees) but M4 strength. Finger flexion was attributed to a tenodesis effect rather than to actual muscle excursion. Rehabilitation for patients reinnervated with two instead of three intercostal nerves was longer (more than 2 years) and yielded less power. After a shorter delay to treatment (6-12 months), reinnervation of a free-functioning muscle by two intercostal nerves supplemented by two intercostal nerve transfers to the musculocutaneous nerve yielded M4 power from both the free-functioning muscle and the brachialis muscles. Last, the group reinnervated by the spinal accessory nerve achieved only M2 to M3 elbow flexion strength even after 3 years’ rehabilitation. Barrie et al14 reported our results at least 1 year after gracilis muscle transfer for elbow flexion and found ≥M4 strength in 79% of single-function transfers, and in 63% of muscles transferred for combined motion (P > 0.05). Comparing results between the two stages of the double gracilis transfer, 75% of stage I transfers (elbow flexion and wrist extension) achieved ≥M4 strength, whereas only one of seven procedures for finger flexion yielded ≥M4 strength. Protective sensation returned in two of seven patients who underwent a two-stage reconstruction.14 After double gracilis transfer, Doi et al68 restored excellent to good elbow flexion in 96%, and 65% achieved more than 30 degrees of total active finger motion with the second stage. Other authors have not been able to consistently restore prehension, although in general, some active flexion is achieved.24 Active motion may be improved by a tenolysis68 or improving the gliding surface of the muscle transfer with silicone sheeting,24 although some authors144 believe that weak muscle excursion is usually due to a lack of muscle recovery as opposed to tendon or muscle adhesion. The number of patients achieving M4 strength is slightly diminished when a single free muscle transfer is used for two functions, and it seems the results are more predictable when a single muscle is used for a single function.24 Shoulder stability and triceps recovery are important added functions that improve outcome after free muscle transfer.65,72 Results in children seem to be superior to those in

Chapter 71 Flaccid Dysfunction of the Elbow

adults, presumably due to the increased potential for nerve recovery.13,106 In a group of 58 single or double free muscle transfers, Doi et al69 found significantly shorter times to reinnervation by the spinal accessory nerve (mean 3.3 months) as opposed to the intercostal nerves (mean 5.25 months) (P < 0.002), with no difference in motor nerve length. These authors found no difference in time to reinnervation between gracilis, latissimus dorsi, and rectus femoris muscles. The power of elbow flexion was equally excellent in these muscles, and no significant difference in the means was found. The rectus femoris muscle, however, had a significantly lower range of motion (mean 34 degrees) and a flexion contracture at the elbow, compared with the gracilis muscle (mean 74 degrees) and latissimus dorsi (mean 78 degrees). When reinnervated with the spinal accessory nerve, the latissimus dorsi transfer gave the most powerful contraction and the greatest range of joint motion. No statistical relationship could be found in brachial plexus patients younger than 50 years of age between patient age and functional recovery or time to reinnervation. Those patients treated after oncologic resection and requiring postoperative chemotherapy showed no significant difference in time to reinnervation. Patients whose shoulder function was augmented by ipsilateral suprascapular nerve neurotization demonstrated statistically better ranges of motion for shoulder flexion and abduction.65

RESTORATION OF ELBOW EXTENSION INTRODUCTION For all persons with tetraplegia, the restoration of elbow extension is uniformly considered essential.¶ In tetraplegia, the deltoid, biceps, brachialis, brachioradialis, and supinator muscles are often spared because of their high-level innervation (C5-C6).127 The triceps muscle (C7) is usually paralyzed, however, and requires reconstruction.80,131,166,190 In large series of tetraplegic patients, the percentages of triceps muscles achieving less that M3 grade strength vary from 59%78 to 73%.167 Active elbow extension is required to reach against gravity, for wheelchair propulsion, pressure relief, independent transfer, and to adequately position the hand for useful ADL function.86 Active elbow extension improves hand positioning by providing an antagonist to elbow flexion, and improves elbow stability after tendon transfer of the brachioradialis and extensor carpi radialis longus muscles.110,131 Because these muscles have a 32-mm and 19-mm excursion on elbow extension (tenodesis effect), ¶

See references 37, 63, 82, 107-109, 135, 159, 170, and 173.

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respectively, active restoration of elbow extension should be achieved before hand rehabilitation is undertaken.29 Additionally, the presence of an active elbow extensor facilitates prehension movements with the arm in pronation, probably by stabilization of the elbow during the transport of objects.114,133 The posterior deltoid-to-triceps transfer and the biceps-to-triceps transfer are two frequently used transfers for elbow extension. The posterior deltoid-to-triceps transfer has several disadvantages,131 including the need for a free tendon graft,166 long immobilization,159 and decreased strength in time, possibly due to stretching.159,190 Early mobilization is associated with poor results after this transfer.63,134 The biceps-to-triceps transfer can be used when the supinator and brachialis muscles are strong enough to replace the function of the transferred biceps. There are several advantages to this procedure, including the ability to simultaneously correct flexion-supination deformities, no need for a tendon graft, earlier time to mobilization, and less extension power loss over time.

NEUROTIZATION History Neurotization of both triceps and biceps muscles with intercostals in adults will result in crippling cocontraction and should be avoided.233 If biceps neurotization has been carried out by intraplexus donors, the triceps may be neurotized by three intercostal nerves. However, because some authors prefer to sacrifice the triceps and use it for biceps function, many do not attempt neurotization. Many patients suffering from cocontraction between the biceps and triceps have cocontraction between the deltoid and the biceps, giving musculocutaneous nerve neurotization cases the advantage of separate motion of the shoulder and elbow.123 Neurotizations for elbow extension in brachial plexus injuries with root avulsions have been performed with the suprascapular nerve, phrenic nerve, contralateral C7 root, partial median or ulnar nerves, and intercostal nerves.94,97,140,149 Early series, especially those using intercalated grafts, reported poor results.212 Later series report satisfactory restoration of elbow extension after intercostal nerve transfer to the long head of the triceps branch without intercalated grafts.72,93

Technique Intercostal nerve to the nerve of the long head of the triceps branch was described by Goubier and Teboul in 2007.93 The technique involves exposing the third to fifth intercostal nerves and mobilizing the motor branches after their isolation by electrical stimulation. The radial nerve is accessed through a brachial and axillary

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Part VII Reconstructive Procedures of the Elbow

approach and usually found behind the brachial vein. Dissection is facilitated through partial or total division of the pectoralis major tendon. The long head of the triceps branch is found at the level of the latissimus dorsi and teres major tendons, and the nerve is followed into the radial nerve and split to increase its length before being sutured to the intercostal nerve endings using microsurgical technique. The three intercostal nerves can be glued together with fibrin before microneural suture. The pectoralis muscle tendon is repaired before skin closure.

Bipolar transplantation of the latissimus dorsi was first reported by Schottstaedt and coworkers in 1955.207 The origin was sutured to the triceps tendon, and the insertion was moved to the acromion. DuToit and Levy75 emphasized the necessity for discarding the distal 3 inches of the latissimus dorsi to get the transplant tight enough. Technique

Unipolar Transfer This description is based on that of Hovnanian (Fig. 71-25). The patient is placed on the side, with the arm draped free. The technique of

Results At an average follow-up of 23 months, intercostal nerve transfer to long head of the triceps branch performed in 10 patients yielded M4 strength in seven patients, M3 in one patient, and M1 and M2 strength in two patients. The average time to recover extension against resistance was 15 months.93 Doi et al. described the results of third and fourth intercostal nerve transfer to the triceps motor branch during the second stage of their double free muscle technique to restore elbow and finger flexion and extension in 32 patients with complete brachial plexus avulsion.68 They found elbow extension postoperatively to be limited by contracture. Positioning of the hand in space was possible in 50% of cases, of which two patients were able to stabilize the elbow while moving the fingers. Recovery of even weak triceps function proved useful in his patients, permitting the double free muscle transfers to provide grasp function independent of elbow position in many cases. On failure of all triceps recovery from intercostal nerve neurotization, some elbow stabilization could be achieved from transfer of the reinnervated infraspinatus muscle, at least with the aid of gravity and its tenodesis effect.72

A

MUSCLE TENDON TRANSFERS Latissimus Dorsi Transfer or Transplant History This technique is not mentioned in the literature of the past decade, and most authors now mention only the options of the biceps and deltoid transfers for elbow extension. Several authors have proposed unipolar transfer of the latissimus dorsi insertion into the extensor mechanism to restore elbow extension.103,115,137 Harmon103 added the teres major to the latissimus dorsi transfer in one case report. Hovnanian118 devised a unipolar transfer of the latissimus dorsi in which its origin was transferred to the triceps tendon. Myocutaneous unipolar transfer of the latissimus dorsi was reported by Landra to provide skin coverage and elbow extension at the same time.136 Tobin and associates performed a similar procedure but used only the lateral segment of the latissimus dorsi with an attached island of skin.237

B FIGURE 71-25 Unipolar transfer of the latissimus dorsi for elbow extension. A, The incisions. The solid line indicates skin incisions, and the dotted line indicates the muscle incision. B, The insertion is undisturbed, and the muscle is rotated on its long neurovascular pedicle. Its origin (after appropriate shortening) is attached to the triceps tendon and olecranon periosteum under maximum tension with the elbow fully extended.

Chapter 71 Flaccid Dysfunction of the Elbow

exposing, detaching, and mobilizing the latissimus dorsi on its neurovascular pedicle is the same as that described for flexor replacement. The incision on the arm, however, is carried over from the posterior axillary fold onto the posteromedial aspect without crossing the neurovascular bundle. Distally, the incision is carried over the medial epicondyle onto the posterior aspect of the proximal ulna. The aponeurotic fascia at the free end of the latissimus dorsi muscle is then sutured under tension to the triceps tendon, the periosteum over the olecranon, and the connective tissue and muscle septa on the extensor surface of the forearm, keeping the elbow in full extension. A considerable amount of muscle usually has to be excised to make the transfer as tight as possible. The elbow is immobilized in extension and bandaged to the side of the body. Passive and active elbow movements are begun after 3 to 4 weeks.

Bipolar Transplantation This description is based on the technique of Schottstaedt and coworkers (Fig. 71-26). The latissimus dorsi muscle is exposed, freed, and completely detached on its neurovascular pedicle through an incision extending from the posterior axillary fold along the muscle’s lateral margin to within 5 to 7.5 cm of the iliac crest. The lower triceps and olecranon are exposed through a posterior incision. A subcutaneous tunnel is then created between this incision and the dorsolateral incision, and the origin of the latissimus dorsi is drawn through it. This portion of the muscle is then attached to the triceps tendon and adjacent soft tissue around the olecranon. The acromion

A

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is exposed through a 5-cm transverse incision over its posterior edge. The insertion of the latissimus dorsi is then drawn up over the deltoid and sutured securely through drill holes to the acromion and the adjacent soft tissues under maximal tension with the elbow fully extended. The elbow is maintained in full extension for 3 to 4 weeks before flexion is allowed. Results

Unipolar Hovnanian117 reported satisfactory results in two patients who had a unipolar latissimus transfer. Tobin and colleagues237 used a unipolar transfer of the lateral portion of the latissimus dorsi with a large island of attached skin to restore extension and to cover a large ulcer involving the elbow joint in a 58-year-old man with syringomyelia. Active elbow extension was achieved. The wound was covered, and latissimus dorsi muscle function in the donor site was said to have been preserved by the innervated medial muscle branch retained in situ. Prudzansky and others193 reported on a 48-year-old man with a recurrent extra-abdominal desmoid tumor that required excision of the entire deltoid-end three fourths of the triceps with the overlying skin. Reconstruction using a large latissimus dorsi myocutaneous flap restored normal elbow extension power with a range from full extension to 95 degrees of flexion. Bipolar Schottstaedt and associates207 achieved full extension of the elbow against gravity after bipolar transplantation of the latissimus dorsi in a 5-year-old child with poliomyelitis. DuToit and Levy75 reported on

FIGURE 71-26 Bipolar transfer of the latissimus dorsi for elbow extension. A, Both the origin and insertion of the latissimus dorsi are detached in this procedure. B, The latissimus dorsi is mobilized on its neurovascular pedicle, and its origin is attached to the triceps tendon and olecranon periosteum and the insertion to the acromion and adjacent soft tissues. (After Schottstaedt, E. R., Larsen, L. J., and Bost, F. C.: Complete muscle transposition. J. Bone Joint Surg. 37A:897, 1955.)

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Part VII Reconstructive Procedures of the Elbow

a 44-year-old man who was able to do push-ups after bipolar transplantation of the latissimus dorsi. They noted that the distal 3 inches of muscle had to be discarded to secure the proper tension in the transplant, and they made the proximal acromial attachment before the distal attachment. No complications have been reported. An illustrative case is shown in Figure 71-27.

Posterior Deltoid Transfer In 1949, d’Aubigne62 mentioned the possibility of transferring the posterior part of the deltoid into the triceps as a method of restoring active extension of the elbow. The first procedure was carried out in a tetraplegic patient in 1975 by Moberg, who mobilized the separately innervated posterior part of the deltoid, extending it with multiple toe extensor tendon grafts inserted into the triceps aponeurosis.166 Converting the transferred deltoid from a one-joint to a two-joint muscle achieved

History

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elbow extension without creating any detectable shoulder dysfunction. Since this communication, there have been several other reports of tetraplegic patients in whom posterior deltoid transfer has been used to achieve elbow extension.37,107 Hentz and colleagues’ communication108 indicates that the deltoid transfer is now being attached directly to the triceps aponeurosis without any intervening graft material. Castro-Sierra and Lopez-Pita47 used two opposing periosteal flaps, one from the deltoid insertion and one turned backward from the triceps insertion into the olecranon, to join the deltoid and triceps. Freehafer and associates82 advised using the anterior tibial tendon as an interposition graft. If the patient can walk or might later be able to, they recommended using fascia lata to connect the deltoid to the triceps insertion. The deltoid-to-triceps transfer is the most frequently used method to restore elbow extension173 and has

B

D

FIGURE 71-27 A, This 19-year-old airman sustained a severe posterior compartment soft tissue injury and an open comminuted fracture of the humerus in a half-track accident. There was complex loss of elbow extension. B, The humeral fracture united after two bone-grafting procedures, and passive extension of the elbow was obtained with a turnbuckle splint. C, Bipolar transplantation of the latissimus dorsi restored satisfactory elbow extension, and full flexion of the elbow was maintained (D).

Chapter 71 Flaccid Dysfunction of the Elbow

become the standard method of treatment over the past 10 years when the deltoid has a minimum of M4 strength.78 The varying techniques differ in the type of material used to attach the deltoid to the triceps.84 Most surgeons prefer lower extremity tendon graft or fascia lata, although a consensus has not been reached on the optimum interpositional graft.127 A new technique described by Mennen and Boonzaier162 involves the use of the bony insertion of the deltoid, which is attached by steel wires to the bony insertion of the triceps into the olecranon reflected cranially with a 10-mm wide central section of the triceps tendon and aponeurosis. No subsequent use of this technique has been described in the literature. A number of investigators have found adequate strength and excursion for elbow extension from this transfer.83,134,167 This procedure is indicated in tetraplegic patients with a good passive range of motion (to within 30 degrees of full extension) at the elbow and with sufficient strength in the posterior deltoid. Inadequate strength on manual muscle testing of the deltoid is an absolute contraindication, and fixed contracture greater than 30 to 45 degrees is a relative contraindication to this procedure.78,110 The deltoid muscle is supplied by two terminal branches of the circumflex nerve, which divides about 6 cm below the level of the acromion. The posterior branch is short and runs almost horizontally to supply the portion of the deltoid arising from the spine of the scapula. The anterior branch is longer and runs horizontally to supply the acromial and clavicular portions of the deltoid.32

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The architectural properties of the posterior deltoid and triceps muscle were studied by Fridén et al86 to determine whether triceps function is appropriately matched by that of the posterior deltoid. It was found that the cross-sectional area of the posterior deltoid was significantly less than that of the three heads of the triceps and that only 20% of the maximum isometric tension could be provided. Despite this factor, the posterior deltoid muscle fiber length was significantly greater, allowing its force to be generated over a much wider range of muscle length, which would explain the relative independence of perioperative posterior deltoid tension on the functional results after transfer.86 The large fiber excursion approaches 25 mm and can potentially offset the potential tendon stretch.118 Technique This procedure is based on that of Moberg (Fig. 71-28). Through a slightly curved incision along the posterior border of the deltoid, the posterior half of the muscle is exposed to its insertion. There is usually a natural cleavage between the two parts of the deltoid where the separation can be accomplished by blunt dissection. Because the deltoid muscle lacks a large tendon of insertion, the tendon of insertion and the surrounding periosteum and a rectangular strip of fascia from the adjacent brachialis muscle should remain attached to the deltoid muscle. The posterior deltoid is mobilized proximally, attaining 3 cm of amplitude, the amount necessary for elbow extension. Care is taken to avoid injury to the axillary nerve branches. The triceps aponeurosis is exposed through separate, slightly curved, longitudinal incisions proximal to the

Fascia lata

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Bone tunnel

FIGURE 71-28 A, Transplantation of the posterior third of the deltoid, extended with toe extensor grafts, to the triceps tendon. This transfer is used to restore extension in a tetraplegic patient. (Courtesy of Mikki Senkarik.) B, Transplantation of the posterior third of the deltoid using fascia lata rather than tendon grafts. (Courtesy of Elizabeth Roselius.)

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Part VII Reconstructive Procedures of the Elbow

olecranon. The conjoined extensor tendons to the second, third, and fourth toes (nonfunctioning in tetraplegic patients) are removed with the aid of a Brand tendon stripper. The graft is attached to the deltoid muscle by at least twice looping the end of the graft through the deltoid tendon and adjacent fascia and periosteum and suturing the graft to the adjacent structures. The graft is then passed distally through a subcutaneous tunnel created between the two incisions. The tendon graft is looped twice through and sutured to the triceps aponeurosis, passed again subcutaneously in a proximal direction and again attached to the deltoid muscle. Suturing of the graft should be done with the elbow extended fully and the shoulder abducted 30 degrees. Fascia lata is an alternative of comparable effectiveness. This graft is applied and attached as shown in Figure 71-28B. The posterior deltoid muscle is infiltrated with 20 mL of 1% lidocaine with epinephrine 1 : 200,000 to prevent disruption of the anastomosis during recovery from anesthesia. The central third portion of the triceps tendon is used as the interposition graft.173 The procedure can be performed simultaneously with other tendon transfers for hand reanimation, such as a brachioradialis-to-flexor pollicis longus transfer for key pinch.190 Also, the procedure is possible with the patient in supine position under axillary block and a block of the axillary nerve with or without local anesthesia.78 A long-arm cast, applied from the upper humerus to just proximal to the wrist with the elbow in 10 degrees of flexion, is worn for 6 weeks. Then the patient begins active extension exercises. To prevent stretching of the newly transferred muscle-tendon unit, however, elbow flexion is increased only 10 degrees per week. A polycentric adjustable elbow splint that allows full extension but blocks flexion at whatever position is desired is useful.107 During the rehabilitation period, elbow extension power must be closely monitored. If a temporary decrease in extension power is observed, reimmobilization in the extended position is carried out until active full extension is regained. Bryan postulated that late stretching originates in the central portion of the grafts secondary to revascularization and advised protecting the arm from flexion past 90 degrees for 3 months after surgery.37 Some authors, after seeing unpredictable results and the considerable elongation that takes place in the two junctions with immediate wheelchair use, have altered their aftercare regimen to include an electric wheelchair and initial casting (4 weeks) and treatment with hinged splints permitting increasing levels of flexion (6 weeks).78 Aftercare

Only one failure is reported by Moberg’s experience with posterior deltoid transfers.167 In general,

Results

elbow extension power was noted to be several times stronger with the extremity at the side in the position for lifting the body than with the limb extended over the head. Bryan37 reported satisfactory results in 10 of 14 deltoid transfers performed in seven tetraplegic patients. In all but one, bilateral deltoid-to-triceps transfers were performed in single operations. De Bendetti63 evaluated 13 tetraplegic patients with 14 deltoid-totriceps transfers. He noted a mean function of 5, as compared with a preoperative mean of 0.5. Castro-Sierra and Lopez-Pita47 noted 10 satisfactory results in 13 tetraplegic patients using Moberg’s technique but were able to shorten the postoperative immobilization period to 35 days. A proximally based flap of triceps tendon with an attached flap of olecranon periosteum is turned back on itself and sutured to the deltoid insertion with the attached periosteum. Lamb and Chan134 reported satisfactory results after 16 Moberg transfers in 10 tetraplegic patients. Hentz and others used a tubed fascia lata strip inserted through drill holes in the olecranon and allowed up to 30 degrees of immediate flexion postoperatively,107 but no follow-up results were given.107,108 Significant preoperative flexion contracture was believed to compromise the result of deltoid-to-triceps transfer. Under these circumstances, they recommend biceps-to-triceps transfer. Freehafer and others82 reported successful results in all 15 cases of triceps paralysis treated by deltoidto-triceps transfer using the anterior tibial tendon as an interposition graft. All of the patients could reach above their heads and noted significant improvement in performing depressor push-ups and transfers from bed to chair. Lacey and associates132 performed a similar procedure in 16 elbows. At surgery, they documented excursion of the posterior deltoid of 7.31 cm. They believed that optimal tension was achieved by suturing the graft with the deltoid pulled to its original insertion length and with the elbow at 90 degrees of flexion. All but one transfer achieved muscle strength of 3 or better. Ejeskar77 recorded the results of deltoid-to-triceps transfer in 40 elbows of 32 patients. Ten of the 30 procedures performed using Moberg’s technique and 1 of the 10 procedures using the method of Castro-Sierra and Lopez-Pita produced full extension of the elbow. Twenty elbows showed no extension beyond 60 degrees, but most had enough extension to maintain elbow control in daily activities. Most of the patients did not have significant use of the elbow extensor when moving between bed and chair, and stretching of some of the transfers was documented.159 Vanden Berghe and colleagues242 initially used the Moberg technique for deltoid-to-triceps transfer. After the first two cases, they changed to the Castro-Sierra and Lopez-Pita technique for the next six cases because of the shorter immobilization time. All eight elbows gained extensor

Chapter 71 Flaccid Dysfunction of the Elbow

power of 3 or better. One patient ruptured a transfer in a fall. Twenty-four transfers were evaluated at an average follow-up of 37 months.170 These authors report M4 strength in 42% and M3 in 29%. Even M2 strength provided some useful increase in hand function, allowing hand positioning at eye level or above. Lamb and Chan reported M5 power in 50% of their posterior deltoid-to-triceps transfers,134 but the discrepancy may be explained by the difference in patient positioning during evaluation. When the patient is supine, the contribution from the pectoral girdle muscles is eliminated in raising the arm above the head, thereby giving true elbow extension strength evaluation.170 The short-term versus long-term comparative results after 11 deltoid-to-triceps procedures in six patients were evaluated with a mean follow-up of 3 years and 24 years after surgery by Vastamäki.243 The study group originally consisted of 27 patients with tetraplegia, but many were lost due to death before they could be evaluated, but the functional results showed an average decrease in extension strength of approximately 1% per year, which may be due mostly to patient aging. This study showed the permanency of results obtained with this procedure. A study using motion analysis methods found increased speed and stability of elbow flexion and extension, and a parallel increase in the speed of shoulder flexion and extension.195 Another biomechanically oriented study found that the posterior deltoid was predicted to operate exclusively on the ascending limb of the length-tension curve, that it generated only 65% of its predicted force, and that the elbow extension moment did not change significantly after rehabilitation.143 Other biomechanical studies have shown that the strength of extension depends on the position of the upper arm relative to the shoulder.125 When the shoulder is weak, as is often the case in C5 or C6 tetraplegia, the upper arm is elevated to shoulder level, which unfortunately corresponds to the position in which the posterior deltoid-to-triceps transfer is the weakest. Stretching and disruption of the proximal or distal anastomosis may require reoperation. In these instances, Moberg has advanced the triceps tendon by osteotomizing the olecranon, advancing the bone, and reattaching the tendon distally with a screw.159 Spasticity of the elbow flexors may compromise the result. Complications adversely affecting results have included elongation of the tendon transfer caused by rapid and early mobilization and attenuation over time,173 as well as graft failure, elbow flexion contractures,168 biceps spacicity,82 and the difficulties associated with the tolerance of a long post-operative course of immobilization.109,168-170 There are multiple reasons why a tendon transfer can fail, including incorrect tension, Complications

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scar formation, disruption or attenuation of the interposition graft or tendon weave, and progressive weakness of the donor muscle.127,131,190

Biceps-to-Triceps Transfer History In 1954, Friedenberg reported a patient with poliomyelitis who had difficulty arising from a chair and walking with crutches because of bilateral absence of triceps function.87 After lateral subcutaneous transfer of the biceps tendon into the triceps aponeurosis, the patient was able to support 7.5 pounds in extension on the right and 8.5 pounds on the left. He was able to transfer independently and to use crutches without difficulty. Friedenberg,87 Hentz and associates,107 and Lamb and Chan134 recorded cases of tetraplegic patients for whom this procedure was unsuccessful. Zancolli255 believes that elbow extension is the most important function one could add for tetraplegic patients. He uses Friedenberg’s method87 after establishing that the supinator is functioning. If there is no supinator muscle function, he transfers the posterior deltoid. Zancolli noted only 24% reduction in elbow flexion power after biceps transfer. Falconer80 has described Zancolli’s technique of biceps transfer. The biceps is exposed through a Z incision along its lateral border, placing the horizontal limb of the Z in the flexion crease. The incision extends 10 cm proximally to the flexion crease and 5 cm distally. The musculocutaneous nerve is identified and mobilized from the undersurface of the biceps muscle 5 cm proximally. The muscle is detached at the radial tubercle and mobilized 10 cm proximally to the elbow, care being taken to protect the radial nerve. A second incision is made over the olecranon, and a flap of triceps aponeurosis is developed. The biceps is passed subcutaneously into the posterior wound and sutured under tension to the aponeurosis flap. The elbow is immobilized in extension for 4 weeks. Ejeskar,77 noting that biceps-to-triceps transfer was the procedure of choice for restoring elbow extension when there is a flexion contracture, reported his results in six cases. One patient died of other causes, two regained full extension, one lacked 80 degrees of extension, and two achieved no extension. One patient sustained a radial nerve palsy that was recovering at 5 months. Some authors have recently reported better results with biceps-to-triceps than with posterior deltoid-totriceps transfer.16,173 Before transfer, an elbow contracture of more than 30 degrees is corrected by some authors, because this degree of biceps contracture would prevent the rerouted tendon from reaching the olecranon.16 However, this technique is better suited to alleviate a mild elbow flexion contracture than the posterior deltoid transfer,118 and as such, an elbow flexion contracture of 30 degrees or more is seen by some authors

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as an indication for biceps-to-triceps transfer over deltoid-to-triceps transfer.78 Also, the need for tendon augmentation is obviated because a direct transfer is possible, and the operation generally takes less time. Active supinator and brachialis muscles must be present (on electromyography) to maintain forearm supination and elbow flexion. If there is doubt about this, the musculocutaneous nerve can be blocked to temporarily paralyze the biceps.110 Some authors4,159,196 argue that paralysis of the pectoralis muscle is an indication for the biceps-to-triceps procedure to avoid the potential for further weakening of the shoulder, although others disagree that this should be taken into account.78 The biceps tendon can be routed around the lateral or medial side of the humerus. Lateral routing techniques have been complicated by radial nerve injuries and consequent diminished function of the brachioradialis and extensor carpi radialis longus.77,131,196 The medial approach, in contrast, has yielded excellent results.77,107,127,131,196 There remains the potential for ulnar nerve injury, but in tetraplegic patients with injury at level C6 or above, the ulnar nerve is nonfunctional. Also, the medial route is a more direct one, with less potential risk of adhesions.131 Even under maximal tension, no median nerve injuries or vascular compression have been observed.197 This procedure is generally associated with a 4078 to 47%196 loss in elbow flexion force, but most authors report that their patients to not register any significant complaints related to this loss110,196 even in contrast to the 24% reduction noted with the lateral route.159,255 Technique Preoperative clinical examination is essential to ensure the presence of an active supinator and brachialis muscle. Ulnar innervated muscles must be assessed to determine if there is any remaining function that could be reduced. This procedure can also be performed with the patient in supine position under axillary block.79 The medial approach is clearly established.131,196 This requires a longitudinal incision along the medial intermuscular septum, through which the ulnar nerve is identified. The biceps tendon is released from the radial tuberosity anteriorly through an incision in the antecubital fossa, passed over the ulnar nerve, and attached to the olecranon via a bony tunnel posteriorly with the elbow in full extension. Fixation is performed by drilling a unicortical hole from the tip of the olecranon to the posterior cortex with a small drill bit. This hole is enlarged sequentially by drilling until it can accommodate the biceps tendon. Two small drill holes are placed through the opposite posterior cortex through which nonabsorbable braided suture, also placed within the tendon, is passed. The sutures are used to pull the tendon into the unicortical hole, and then tied over the bone with the elbow in extension.

General protocols have been established for the postoperative care.109,159,173 The arm is usually immobilized for 3 weeks, after which a brace is fitted with the elbow in extension. Active flexion and extension develops at 15 degrees per week, and movement is integrated into daily activities in a graded fashion. More rigorous precaution can be afforded through added protection as described by Fridén and Lieber88 and Kuz et al.131 Results Results of the medial approach have been encouraging, with consistent restoration of elbow extension. Kuz et al131 reported on the outcome in four transfers, and Revol et al196 in 13 cases, with all patients achieving M4 elbow extension strength 18 months postoperatively. Loss of elbow flexion strength was significant (47% on average), but subclinical in all cases. The lateral routing technique has been associated with a 24% reduction in elbow flexion power.159 Mulcahey et al,173 in a prospective study comparing eight deltoidto-triceps and eight biceps-to-triceps transfers, found M3 or better strength in 7 of 8 biceps transfers compared with 1 of 8 deltoid transfers. Impressive loss in elbow flexion torque was seen (52%), which persisted through the 24-month follow-up period despite some clinical improvement. Kozin and Schloth127 reported a case in which bilateral biceps-to-triceps transfer was successfully used to salvage a failed bilateral deltoidto-triceps transfer. Furthermore, the technique has been shown to increase the pinch strength from a previous brachioradialis transfer.38 The learning time to activate the biceps as an elbow extensor takes from 3 to 6 months.196

Miscellaneous Transfers for Elbow Extension In 1938, Ober and Barr185 described the posterior transfer of the freed anterior margin of the brachioradialis into the proximal ulna, olecranon, and triceps tendon to restore active elbow extension. The addition of the extensor carpi radialis to strengthen the brachioradialis was advised if its power was insufficient. Immobilization of the elbow in full extension and supination was advised, and exercises were started at 10 days. Extension of the elbow against gravity was possible in all six cases. No subsequent reports of the procedure have appeared in the literature. The technique was modified in 2005 by Ozkan et al189 to include a bipolar transfer of the brachioradialis muscle. The short-term results showed slight improvement postoperatively, depending on shoulder abduction. The relative weakness of the brachioradialis muscle was cited as a possible reason for this finding. It is a radial nerve innervated muscle but may be available for transfer due to possible mixed lesions or the higher likelihood of cross-innervation from multiple roots.

Brachioradialis Transfer

Chapter 71 Flaccid Dysfunction of the Elbow

A teres major to triceps transfer has been postulated to be strong enough to keep the forearm positioned on a table but not strong enough to lift the body from a chair in paraplegia.182 No cases have been reported in the literature to date.

Teres Major-To-Triceps Transfer

Free-Functioning Muscle Transfers Transfers for Restoration of Forearm Rotation Children with posterior cord or mixed palsies that develop a supination contracture not permitting any active pronation past neutral in a patient with a functional hand are generally considered for operative management.113

Transfers for Pronation History Paralytic supination contracture of the forearm can occur as a result of brachial plexus palsy and poliomyelitis,41,188,253 or in tetraplegia levels below C5.89 Secondary partial or complete paralysis of the flexor-pronator muscles in the presence of unopposed biceps and supinator muscles is the underlying common denominator. The deformity not only is cosmetically displeasing but also seriously limits the function of the hand for grasping and two-handed activities. Patients with this deformity cannot perform tasks that require pronation, such as controlling a wheelchair joystick, as well as most personal hygiene functions. In children, this is especially cumbersome because it prevents the use of a computer keyboard.192 Patients presenting with supination contracture concurrent with an anterior dislocation of the radial head can be treated by transfer of the biceps insertion to the ulna. Nondynamic correction of the supination deformity by closed osteoclasis26,41 or open osteotomy of the forearm bones256 was advised by earlier authors. Schottstaedt and colleagues208 suggested changing the biceps from a supinator to a pronator by transferring its tendon to the side of the radial tuberosity opposite its normal insertion, but they did not report their results. Zancolli performed a long Z lengthening of the tendon, rerouting the distal strip of the tendon around the neck of the radius.253 All 14 of his patients also required release of the contracted soft tissues, particularly the interosseous membrane, to obtain passive correction of the supination deformity before the biceps rerouting. Manske and coworkers believed that soft tissue releases could be avoided by performing the biceps rerouting earlier; if correction was unsatisfactory, a secondary percutaneous osteoclasis of the radius and ulna was recommended.154 The goal for any surgery is active elbow flexion, with the forearm positioned in neutral rotation or slight pronation.113,191 If the radial head is not dislocated, the forearm can be pronated passively, and there is active supination (on electromyography), then a Zancolli-type biceps rerouting can be carried out, with or without

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release of the contracture.253 Here the goal is to achieve active pronation, and this is the most frequently used corrective procedure. Finally, Hoyen and colleagues119 prefer to perform a radius pronation osteotomy, which allows full correction past that offered by bicepspronator plasty and interosseous membrane and distal radioulnar joint release. The osteotomy is made just distal to the pronator insertion, and fixation is performed after the radius is rotated a desired amount to position the forearm more optimally. This allows more rapid rehabilitation, and offers reliable results.110 Although biceps rerouting has been found to give the best forearm motion, afterward it will not be available for tendon transfer, leaving elbow extension to be achieved by posterior deltoid-to-triceps transfer in most cases. Elbow extension strength may be improved in patients who undergo forearm osteotomy and a biceps-to-triceps transfer, but at this time, the choice of procedure seems to depend in some degree on surgeon preference. This description is based on those of Zancolli253 and Manske and coworkers154 (Fig. 71-29). A high tourniquet is employed, and the biceps tendon is exposed through an incision starting on the medial aspect of the distal arm and extending across the flexion crease of the elbow and distally on the lateral aspect of the forearm. The lacertus fibrosus is incised, and the median nerve and brachial artery are retracted medially. The biceps tendon is exposed to its insertion into the bicipital tuberosity, and the radial recurrent leash of vessels is divided. The tendon is divided by a long Z-plasty to its insertion, and the distal segment is passed posteriorly around the radial neck at the level of the tuberosity using a ligature carrier. The tendons are reattached by side-to-side suture, effectively lengthening the tendon by about 1.5 cm. A long-arm cast is applied with the forearm in the neutral position and the elbow at a right angle for 4 to 6 weeks. If the deformity is long standing and the patient is older, soft tissue releases often are required to obtain passive forearm rotation. The interosseous membrane and supinator muscle can be released through a long dorsal incision overlying the ulna. The extensor muscles are retracted toward the radius, and this protects the interosseous nerve. Owings and colleagues188 suggested releasing the supinator from the volar lateral surfaces of the radius through the anterior incision. Biceps Rerouting: Technique

Results Zancolli performed soft tissue releases and biceps tendon rerouting in 14 patients with paralytic supination contracture of the forearm (four had poliomyelitis, eight birth palsies, and two tetraplegia).253 Correction to the neutral position or some pronation was maintained in all patients, and eight had 10 to 60 degrees of active pronation. Owings and others reported nine

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A

B C

FIGURE 71-29 Biceps tendon rerouting to restore pronation. A, The biceps tendon is divided by a long Z-plasty extended to its insertion. B and C, The distal end of the divided tendon is passed around the neck of the radius using a ligature passer. The two layers of the tendon are reattached side to side, effectively lengthening the tendon by about 1.5 cm. (After Zancolli, E. A., and Mitre, H. Latissimus dorsi transfer to restore elbow flexion. J. Bone Joint Surg. 55A:1265, 1973.)

good results, 11 satisfactory results, and two poor results in 26 patients who had biceps tendon rerouting using the Z-plasty technique.188 The two poor results were related to problems with stability of the proximal radius. Manske and associates154 reported the results of Zancolli’s biceps tendon rerouting in 11 patients with supination deformity secondary to obstetric paralysis. The neutral position was obtained in nine, and six had active supination-pronation movement averaging 42 degrees (range 15 to 65 degrees). Two patients, neither of whom had preoperative passive pronation to neutral, obtained satisfactory results after a secondary percutaneous osteoclasis of the radius and ulna. The authors recommended that surgical correction of paralytic supination deformity of the forearm be done between 3 and 6 years of age. Leffert and Pess141 reported four good and two improved results among six patients using Zancolli’s method of biceps rerouting. More than 2 years’ follow-up was reported on five patients with C5, C6 obstetric brachial plexus palsy, and biceps-to-ulna transfers for correction of supination contractures concurrent with dislocation of the radial head.113 No pronation past neutral was possible preoperatively in each case. Postoperatively, there was full active flexion with no rotation and muscle grades from M3 to M5, with passive pro- and supination from 60 to 75 degrees, respectively. The transfer did not affect active rotation. These authors also reported on eight children with supination contracture and located the radial head where biceps rerouting was performed and

evaluated after more than 2 years. In all cases, no passive pronation was possible. Postoperatively, more effective flexion was possible in neutral rotation, with active pronation against gravity possible in all, ranging from 30 to 90 degrees.113 Eleven of 14 flexion-supination contractures in Freehafer’s group were corrected by cast treatment alone, but five elbows in three patients went on to undergo biceps tendon tenotomy. There were no complications, one patient required six tenotomies due to bilateral recurrence, and all elbows achieved acceptable ADL function and regained M4 flexion and supination.86 However, biceps tendon tenotomy in tetraplegia is not found in other current literature. Zancolli253 reported on two patients who had overcorrection, presumably because the biceps tendon suture was under excessive tension. Owings and colleagues188 reported on one patient who had persistent weakness of thumb extension, two who had proximal radial instability, and one who developed excessive pronation. Complications

Transfers for Supination History Because it is infrequently indicated, muscle transfer to regain supination in the paralyzed upper extremity has received scant attention in the literature. Steindler223 described transferring the flexor carpi ulnaris tendon into the dorsal aspect of the distal radius. Tubby240 described transferring the flexor carpi radialis and pronator teres through the interosseous space to the back

Chapter 71 Flaccid Dysfunction of the Elbow

of the radius to achieve supination in the spastic upper extremity. Schottstaedt and associates208 noted that providing active supination using the flexor carpi ulnaris or palmaris longus redirected dorsally into the radial shaft was often necessary after Steindler’s flexorplasty. Technique—Flexor Carpi Ulnaris Transposition to the Radius This technique is based on Steindler’s method

(Fig. 71-30).223 The flexor carpi ulnaris tendon is detached, and its distal half is mobilized through a 12-cm incision along the volar-ulnar aspect of the forearm. The dorsolateral surface of the distal radius is exposed between the extensor pollicis brevis and the extensor carpi radialis longus tendons using a 5-cm longitudinal incision. A subcutaneous tunnel is created between this incision and the proximal end of the first incision, and the flexor carpi ulnaris tendon is pulled through. A hole is drilled through the distal radius, and the tendon is fed through the hole from the dorsal to the volar aspect. Its end is reflected back and sutured to itself under tension with the forearm supinated and the elbow flexed. A long-arm cast, with the wrist in slight dorsiflexion, the forearm in full supination, and the elbow at a right angle, is worn for 3 weeks. Part-time splinting is continued for 2 months.

Steindler224 reported 11 good and 5 poor results from 16 flexor carpi ulnaris transfers to the radius. A good transfer functioned actively through a useful arc with at least 40 degrees of pronation-supination movement. Results

AUTHOR’S PREFERRED METHOD OF TREATMENT The primary goal in treatment of the flail upper limb should be the restoration of elbow flexion. The second is to restore shoulder external rotation and abduction, or at least glenohumeral stability, followed by grasp function and finally intrinsic motor function. Grasp itself is a complex function requiring sensibility, finger flexion and extension, and stability or active control of the wrist for tenodesis effect. Restoration of elbow extension is important in grasp function at times as well, particularly when powered by free muscle transfers crossing the elbow that would otherwise produce an elbow flexion moment. It is in fact certainly true that the major function of the shoulder and elbow in normal extremities is to position the hand in space for manipulation. More limited use of the proximal extremity, to function as a

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B

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C

FIGURE 71-30 Transfer of the flexor carpi ulnaris to restore supination. A, The flexor carpi ulnaris tendon is detached distally, mobilized proximally, and brought out through the proximal incision. B and C, The dorsoradial aspect of the distal radius is exposed. The flexor carpi ulnaris is redirected through a subcutaneous tunnel and attached to the radius through a drill hole. (After Steindler, A.: Muscle and tendon transplantation at the elbow. In AAOS: Instructional Course Lectures on Reconstruction Surgery. Ann Arbor, JW Edwards, 1944, p. 276.)

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paper weight, perform arm-to-trunk prehension, or support a tray become important more limited goals in flaccid paralysis. For restoration of elbow flexion, understanding the importance of elapsed time from injury on treatment of elbow paralysis is critical. Recovery of elbow flexion by reanimation of paralyzed muscle requires intervention by 6 months from injury, preferably, with steadily decreasing results over the ensuing 6 months. No recovery is to be expected when nerve surgery is performed after 1 year. It is also true, as in general experience, that more is better. That is, two muscles are often better than one for this critical function. This is certainly the case for the Steindler flexorplasty, which works best to augment a weak biceps rather than serve as a replacement.18,52,53 Chuang found that although Steindler’s flexorplasty is effective in increasing elbow flexion function from M2 to M3 or M4, it is less useful in upgrading from M0 or M1 to M3. Similarly, free muscle transplantation alone is less effective than free muscle transfer combined with direct biceps neurotization, particularly when elapsed time from injury does not favor full biceps recovery (6-12 months after trauma). Double nerve transfers to both biceps and brachialis produce reliable M4 recovery of elbow flexion, for patients with isolated upper trunk, or upper and middle trunk injury in whom both ulnar and median nerve fascicle transfers are possible.147,151,187 Late reconstruction should be performed with a freefunctioning muscle supplied by two or three intercostal nerves. Flexion strength can be increased by a stable shoulder, either resulting from nerve recovery, tendon transfers or shoulder arthrodesis. In plexus injury, shoulder joint stability is usually obtained by reinnervation of the suprascapular nerve and the axillary nerve with nerve graft or transfer. Targeting either nerve alone resulted in 30 degrees of shoulder abduction in one study.57 Transfers to both suprascapular and axillary nerves yielded 70 to 115 degrees of shoulder abduction.57,140 As a general rule, in cervical nerve rupture or traction injury, initial treatment to restore elbow flexion consists of brachial plexus reconstruction, using neurolysis and nerve grafts when necessary, and converting to local muscle tendon transfer in chronic cases or when brachial plexus reconstruction has failed. When no strong local muscle is available, this is an indication for freefunctioning muscle transfer. In brachial plexus root avulsion, acute cases (<9 months) can be treated with neurotizations, otherwise converting to local or free muscle transfer when this is not possible in chronic cases or when little or no improvement is seen. In our experience and that of others,235 in global avulsions, delayed cases, and for hand reanimation, free muscle transfer and other secondary procedures are necessary for satisfactory outcome. Early and aggressive

nerve reconstruction usually yields more satisfactory function than the various muscle transfers, and this early surgery should be combined with secondary procedures such as pedicled and free muscle transfers to reach the best possible functional outcome for the upper extremity.

References 1. Ahmad, I.: Restoration of elbow flexion by a new operative method. Clin. Orthop. Relat. Res. 106:186, 1975. 2. Akasaka, Y., Hara, T., and Takahashi, M.: Restoration of elbow flexion and wrist extension in brachial plexus paralyses by means of free muscle transplantation innervated by intercostal nerve. Ann. Chir. Main. Memb. Super. 9:341, 1990. 3. Akasaka, Y., Hara, T., and Takahashi, M.: Free muscle transplantation combined with intercostal nerve crossing for reconstruction of elbow flexion and wrist extension in brachial plexus injuries. Microsurgery 12:346, 1991. 4. Allieu, Y., Benichou, M., Ohanna, F., Bousquet, P., and Chammas, M.: [Surgical classification of the upper limb in tetraplegic patients]. Ann. Chir. Plast. Esthet. 38:180, 1993. 5. Allieu, Y., and Cenac, P.: Neurotization via the spinal accessory nerve in complete paralysis due to multiple avulsion injuries of the brachial plexus. Clin. Orthop. Relat. Res. 237:67, 1988. 6. Allieu, Y., Privat, J. M., and Bonnel, F.: [Neurotization with the spinal nerve (nervus accessorius) in avulsions of roots of the brachial plexus]. Neurochirurgie 28:115, 1982. 7. Alnot, J. Y.: Elbow flexion palsy after traumatic lesions of the brachial plexus in adults. Hand Clin. 5:15, 1989. 8. Alnot, J. Y., and Abols, Y.: [Restoration of elbow flexion by tendon transfer in traumatic paralysis of the brachial plexus in adults. Apropos of 44 injured patients]. Rev. Chir. Orthop. Reparatrice Appar. Mot. 70:313, 1984. 9. Andrisano, A., Porcellini, G., Stilli, S., and Libri, R.: The Steindler method in the treatment of paralytic elbow flexion. Ital. J. Orthop. Traumatol. 16:235, 1990. 10. Atkins, R. M., Bell, M. F., and Sharrard, W. J. W.: Pectoralis major transfer for paralysis of elbow flexion in children. J. Bone Joint Surg. 67B:640, 1985. 11. Axer, A., Segal, D., and Elkon, A.: Partial transposition of the latissimus dorsi. J. Bone Joint Surg. 55A:1259, 1973. 12. Bahm, J., Noaman, H., and Becker, M.: The dorsal approach to the suprascapular nerve in neuromuscular reanimation for obstetric brachial plexus lesions. Plast. Reconstr. Surg. 115:240, 2005. 13. Baliarsing, A. S., Doi, K., and Hattori, Y.: Bilateral elbow flexion reconstruction with functioning free muscle transfer for obstetric brachial plexus palsy. J. Hand Surg. [Br.] 27:484, 2002. 14. Barrie, K. A., Steinmann, S. P., Shin, A. Y., Spinner, R. J., and Bishop, A. T.: Gracilis free muscle transfer for restoration of function after complete brachial plexus avulsion. Neurosurg. Focus 16:E8, 2004. 15. Bartlett, S. P., May, J. W., and Yaremchuk, M. J.: The latissimus dorsi muscle: a fresh cadaver study of the primary

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34. Brooks, D. M., and Seddon, H. J.: Pectoral transplantation for paralysis of the flexors of the elbow: a new technique. J. Bone Joint Surg. 41B:36, 1959. 35. Brunnelli, G., and Monini, L.: Neurotization of avulsed roots of brachial plexus by means of anterior nerves of cervical plexus. Clin. Plast. Surg. 11:149, 1984. 36. Brunelli, G. A., Vigasio, A., and Brunelli, G. R.: Modified Steindler procedure for elbow flexion restoration. J. Hand Surg. [Am.] 20:743, 1995. 37. Bryan, R. S.: The Moberg deltoid-triceps replacement and key pinch operations in quadriplegia: preliminary experiences. Hand 9:207, 1977. 38. Brys, D., and Waters, R. L.: Effect of triceps function on the brachioradialis transfer in quadriplegia. J. Hand Surg. [Am.] 12:237, 1987. 39. Bunnell, S.: Surgery of the Hand. 2nd ed. Philadelphia, J. B. Lippincott Co., 1948. 40. Bunnell, S.: Restoring flexion to the paralytic elbow. J. Bone Joint Surg. 33A:566, 1951. 41. Burman, M.: Paralytic supination contracture of the forearm. J. Bone Joint Surg. Am. 38A:303, 1956. 42. Carroll, R. E., and Gartland, J. J.: Flexorplasty of the elbow. J. Bone Joint Surg. 35A:706, 1953. 43. Carroll, R. E.: Restoration of flexor power to the flail elbow by transplantation of the triceps tendon. Surg. Gynecol. Obstet. 95:685, 1955. 44. Carroll, R. E.: Restoration of elbow flexion by transplantation of sternocleidomastoid muscle. J. Bone Joint Surg. 44A:1039, 1962. 45. Carroll, R. E., and Hill, N. A.: Triceps transfer to restore elbow flexion. J. Bone Joint Surg. 52A:23, 1970. 46. Carroll, R. E., and Kleinman, W. B.: Pectoralis major transplantation to restore elbow flexion to the paralytic limb. J. Hand Surg. 4:501, 1979. 47. Castro-Sierra, A., and Lopez-Pita, A.: A new surgical technique to correct triceps paralysis. Hand 15:42, 1983. 48. Chen, W. S.: Restoration of elbow flexion by latissimus dorsi myocutaneous or muscle flap. Arch. Orthop. Trauma Surg. 109:117, 1990. 49. Chen, W. S.: Restoration of elbow flexion by modified Steindler flexorplasty. Int. Orthop. 24:43, 2000. 50. Chuang, D. C.: Functioning free muscle transplantation for brachial plexus injury. Clin. Orthop. Relat Res. 314:104, 1995. 51. Chuang, D. C.: Neurotization procedures for brachial plexus injuries. Hand Clin. 11:633, 1995. 52. Chuang, D. C., Carver, N., and Wei, F. C.: Results of functioning free muscle transplantation for elbow flexion. J. Hand Surg. [Am.] 21:1071, 1996. 53. Chuang, D. C., Epstein, M. D., Yeh, M. C., and Wei, F. C.: Functional restoration of elbow flexion in brachial plexus injuries: results in 167 patients (excluding obstetric brachial plexus injury). J. Hand Surg. [Am.] 18:285, 1993. 54. Chuang, D. C., Hattori, Y., Ma, H. S., and Chen, H. C.: The reconstructive strategy for improving elbow function in late obstetric brachial plexus palsy. Plast. Reconstr. Surg. 109:116; discussion 27, 2002. 55. Chuang, D. C., Ma, H. S., Borud, L. J., and Chen, H. C.: Surgical strategy for improving forearm and hand func-

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218.

219. 220. 221.

paralysis of the brachial plexus in adults. Int. Orthop. 22:255, 1998. Ruch, D. S., Friedman, A., and Nunley, J. A.: The restoration of elbow flexion with intercostal nerve transfers. Clin. Orthop. Relat. Res. 314:95, 1995. Rühmann, O., Wirth, C. J., and Gosse, F.: Triceps to biceps transfer to restore elbow flexion in three patients with brachial plexus palsy. Scand. J. Plast. Reconstr. Surg. Hand Surg. 34:355, 2000. Russell, R. C., Pribaz, J., Zook, E. G., Leighton, W. D., Eriksson, E., and Smith, C. J.: Functional evaluation of latissimus dorsi donor site. Plast. Reconstr. Surg. 78:336, 1986. Samardzic, M., Grujicic, D., and Antunovic, V.: Nerve transfer in brachial plexus traction injuries. J. Neurosurg. 76:191, 1992. Samardzic, M., Grujicic, D., Rasulic, L., and Bacetic, D.: Transfer of the medial pectoral nerve: myth or reality? Neurosurgery 50:1277, 2002. Samardzic, M., Rasulic, L., Grujicic, D., and Milicic, B.: Results of nerve transfers to the musculocutaneous and axillary nerves. Neurosurgery 46:93; discussion, 3, 2000. Schottstaedt, E. R., Larsen, L. J., and Bost, F. C.: Complete muscle transposition. J. Bone Joint Surg. 37A:897, 1955. Schottstaedt, E. R., Larsen, L. J., and Bost, F. C.: The surgical reconstruction of the upper extremity paralyzed by poliomyelitis. J. Bone Joint Surg. 40A:633, 1958. Schulze-Berge, R.: Ersatz der Benger des Voderarames (Bizeps und Brachialis) durch den Pectoralis major. Dtsch. Med. Wochenschr. 43:433, 1917. Seddon, H. J.: Transplantation of pectoralis major for paralysis of the flexors of the elbow. Proc. R. Soc. Med. 43:837, 1949. Seddon, H. J.: Nerve grafting. J. Bone Joint Surg. 45B:447, 1963. Sedel, L.: The results of surgical repair of brachial plexus injuries. J. Bone Joint Surg. 64B:54, 1982. Segal, A., Seddon, H. J., and Brooks, D. M.: Treatment of paralysis of the flexors of the elbow. J. Bone Joint Surg. 41B:44, 1959. Shin, A. Y., Spinner, R. J., Steinmann, S. P., and Bishop, A. T.: Adult traumatic brachial plexus injuries. J. Am. Acad. Orthop. Surg. 13:382, 2005. Simesen, K., and Haase, J.: Microsurgery in brachial plexus lesions. Acta Orthop. Scand. 56:238, 1985. Solonen, K. A., Vastamaki, M., and Strom, B.: Surgery of the brachial plexus. Acta Orthop. Scand. 55:436, 1984. Songcharoen, P., Mahaisavariya, B., and Chotigavanich, C.: Spinal accessory neurotization for restoration of elbow flexion in avulsion injuries of the brachial plexus. J. Hand Surg. [Am.] 21:387, 1996. Soucacos, P. N., Vekris, M. D., Zoubos, A. B., and Johnson, E. O.: Secondary reanimation procedures in late obstetrical brachial plexus palsy patients. Microsurgery 26:343, 2006. Spira, E.: Replacement of biceps brachii by pectoralis minor transplant. J. Bone Joint Surg. 39B:126, 1957. Steindler, A.: Orthopaedic reconstruction work on hand and forearm. N. Y. Med. J. 108:1117, 1918. Steindler, A.: A muscle plasty for the relief of flail elbow in infantile paralysis. Interstate Med. J. 25:235, 1918.

222. Steindler, A.: Operative treatment of paralytic conditions of the upper extremity. J. Orthop. Surg. 1:608, 1919. 223. Steindler, A.: Tendon transplantation in the upper extremity. Am. J. Surg. 44:260, 1939. 224. Steindler, A.: Muscle and tendon transplantation at the elbow. In AAOS: Instructional Course Lectures on Reconstruction Surgery. Ann Arbor, JW Edwards, 1944, p. 276. 225. Stern, P. J., Neale, H. W., Gregory, R. O., and Kreilein, J. G.: Latissimus dorsi musculocutaneous flap for elbow flexion. J. Hand Surg. 7:25, 1982. 226. Stern, P. J., and Caudle, R. J.: Tendon transfers for elbow flexion. Hand Clin. 4:297, 1988. 227. Sturm, J. T., and Perry, J. F. Jr.: Brachial plexus injuries from blunt trauma—a harbinger of vascular and thoracic injury. Ann. Emerg. Med. 16:404, 1987. 228. Sunderlund, S.: Repair of the brachial plexus directed to restoring elbow flexion. Bull. Hosp. Joint Dis. Orthop. Inst. 44:485, 1984. 229. Sungpet, A., Suphachatwong, C., and Kawinwonggowit, V.: Transfer of one fascicle of ulnar nerve to functioning free gracilis muscle transplantation for elbow flexion. A. N. Z. J. Surg. 73:133, 2003. 230. Takami, H., Takahashi, S., and Ando, M.: Latissimus dorsi transplantation to restore elbow flexion to the paralysed limb. J. Hand Surg. 9B:61, 1984. 231. Tamai, S., Komatsu, S., Sakamoto, H., Sano, S., and Sasauchi, N.: Free muscle transplants in dogs, with microsurgical neurovascular anastomoses. Plast. Reconstr. Surg. 46:219, 1970. 232. Teboul, F., Kakkar, R., Ameur, N., Beaulieu, J. Y., and Oberlin, C.: Transfer of fascicles from the ulnar nerve to the nerve to the biceps in the treatment of upper brachial plexus palsy. J. Bone Joint Surg. Am. 86-A:1485, 2004. 233. Terzis, J. K., and Kostopoulos, V. K.: The surgical treatment of brachial plexus injuries in adults. Plast. Reconstr. Surg. 119:73e, 2007. 234. Terzis, J. K., Sweet, R. C., Dykes, R. W., and Williams, H. B.: Recovery of function in free muscle transplants using microneurovascular anastomoses. J. Hand Surg. [Am.] 3:37, 1978. 235. Terzis, J. K., Vekris, M. D., and Soucacos, P. N.: Outcomes of brachial plexus reconstruction in 204 patients with devastating paralysis. Plast. Reconstr. Surg. 104:1221, 1999. 236. Tobin, G. R., Bland, K. I., and Adcock, R.: Surgical anatomy of the musculus pectoralis major and neurovascular supply. Am. Coll. Surg. Forum 32:574, 1981. 237. Tobin, G. R., Shusterman, B. A., Peterson, G. H., Nichols, G., and Bland, K. I.: The intramuscular neurovascular anatomy of the latissimus dorsi muscle: the basis for splitting the flap. Plast. Reconstr. Surg. 67:637, 1981. 238. Tomita, Y., Tsai, T., Burns, J. T., Karaoguz, A., and Ogden, L. L.: Intercostal nerve transfers in brachial plexus injuries: an experimental study. Microsurgery 4:95, 1983. 239. Tsai, T., Kalisman, M., Burns, J., and Kleinert, H. E.: Restoration of elbow flexion by pectoralis major and pectoralis minor transfer. J. Hand Surg. 8:186, 1983. 240. Tubby, A. H.: Deformities Including Diseases of the Bones and Joints. London, MacMillan, 1912.

Chapter 71 Flaccid Dysfunction of the Elbow 1001

241. Tuttle, H.: Exposure of the brachial plexus with nerve transplantation. J. A. M. A. 61:15, 1913. 242. Vanden Berghe, A., Van Laere, M., Hellings, S., and Vercauteren, M.: Reconstruction of the upper extremity in tetraplegia: functional assessment, surgical procedures and rehabilitation. Paraplegia 29:103, 1991. 243. Vastamaki, M.: Short-term versus long-term com-parative results after reconstructive upper-limb surgery in tetraplegic patients. J. Hand Surg. [Am.] 31:1490, 2006. 244. Vathana, T., Larsen, M., de Ruiter, G. C., Bishop, A. T., Spinner, R. J., and Shin, A. Y.: An anatomic study of the spinal accessory nerve: extended harvest permits direct nerve transfer to distal plexus targets. Clin. Anat. 20:899, 2007. 245. VonLanz, T., and Wachsmuth, W.: Praktische Anatomie. 2nd ed. Berlin, Springer-Verlag, 1959. 246. Vulpius, O., and Stoffel, A.: Muskel- und Sehnentransplantation. Überpflanzungen an der oberen Extremität. In Vulpius, O., and Stoffel, A. (eds.): Orthopädische Operationslehre. 2nd ed. Stuttgart, Ferdinand Enke, 1920, p. 266. 247. Waikakul, S., Wongtragul, S., and Vanadurongwan, V.: Restoration of elbow flexion in brachial plexus avulsion injury: comparing spinal accessory nerve transfer with intercostal nerve transfer. J. Hand Surg. [Am.] 24:571, 1999.

248. Williams, P. F.: The elbow in arthrogryposis. J. Bone Joint Surg. 55B:834, 1973. 249. Wynn Parry, C. B.: Brachial plexus injuries. Br. J. Hosp. Med. 32:130, 1984. 250. Xu, J., Cheng, X., and Gu, Y.: Different methods and results in the treatment of obstetrical brachial plexus palsy. J. Reconstr. Microsurg. 16:417; discussion 20, 2000. 251. Xu, W. D., Gu, Y. D., Xu, J. G., and Tan. L. J.: Full-length phrenic nerve transfer by means of video-assisted thoracic surgery in treating brachial plexus avulsion injury. Plast. Reconstr. Surg. 110:104; discussion 10, 2002. 252. Yamada, S., Peterson, G. W., Soloniuk, D. S., and Will, A. D.: Coaptation of the anterior rami of C-3 and C-4 to the upper trunk of the brachial plexus for cervical nerve root avulsion. J. Neurosurg. 74:171, 1991. 253. Zancolli, E. A.: Paralytic supination contracture of the forearm. J. Bone Joint Surg. 49A:1275, 1967. 254. Zancolli, E. A., and Mitre, H.: Latissimus dorsi transfer to restore elbow flexion. J. Bone Joint Surg. 55A:1265, 1973. 255. Zancolli, E. A.: Structural and Dynamic Bases of Hand Surgery. 2nd ed. Philadelphia, J. B. Lippincott Co., 1979. 256. Zaoussis, A. L.: Osteotomy of the proximal end of the radius for paralytic supination deformity in children. J. Bone Joint Surg. 45B:523, 1963.

1002 Part VII Reconstructive Procedures of the Elbow

CHAPTER

72

Spastic Dysfunction of the Elbow Ann E. Van Heest

CEREBRAL PALSY Cerebral palsy (CP) is a nonprogressive perinatal injury to the developing central nervous system (CNS). CP produces motor dysfunction, movement disorders, weakness, and impaired function.36 The incidence of CP is 1 to 7 per 1000 children worldwide, and 2 to 3 per 1000 in developed countries.33 The incidence has been fairly constant over the past 40 years; a lesser incidence due to improved prenatal and perinatal care, balanced with a greater incidence of enhanced survival of the very preterm births, has lead to a net constant incidence over time.7 The etiology of CP has been described as a causal pathway with a sequence of conditions culminating in injury to the CNS. A recent 15-year review of the incidence of CP determined that risk factors for preterm infants were periventricular leukomalacia (magnetic resonance imaging evidence of brain structural changes), prolonged rupture of membranes, and patent ductus arteriosus. Risk factors for infants with a gestational age of greater than 34 weeks included size small for gestational age, neonatal transfer (patient transfer at birth from the hospital where they were delivered to a hospital with higher levels of care), and a history of sepsis or meningitis.39 CP is most commonly classified by its anatomic distribution (Box 72-1). Diplegic refers to involvement of both lower extremities. Hemiplegic is involvement of one upper and one lower extremity on the same side. Triplegic is involvement of one upper and both lower extremities. Quadriplegic is involvement of all four limbs. The type of muscle tone is attributed to manifestations of CNS dysfunction and further classifies the disorder to include spasticity, dystonia (athetosis), flaccidity, or mixed patterns. Life priorities for individuals with CP differ due to their motor system disabilities. According to Bleck, the top four self-reported life priorities for individuals with CP were, in order of importance, (1) communication with others; (2) ability to perform activities of daily living, particularly personal hygiene; (3) mobility in the

community; and (4) walking.2 As our society becomes more technologically sophisticated, use of the upper extremities becomes more critical. Care of the patient with CP has shifted toward an increased emphasis on improved upper extremity use.

DIAGNOSIS CP is most commonly diagnosed at around 1 year of age due to delayed development of normal pinch motor milestones. Normal children develop two-handed activity and bilateral grasp, and progress from two-handed manipulation of objects to one hand at the age of 18 to 24 months. Early hand dominance is often a presenting sign in children with CP. In this scenario, a complete neurologic evaluation is necessary, including evaluation of their lower extremities, before a diagnosis of CP can be made. CP is a disorder of the CNS that manifests itself in peripheral motor dysfunction and joint malpositioning. In spastic hemiplegia due to CP, the most common peripheral manifestations in the upper limb are shoulder internal rotation, elbow flexion, forearm pronation, wrist flexion/ulnar deviation, finger clenching (flexor spasticity), swan-necking, and thumb-in-palm deformity, as shown in Figure 72-1. Increased muscle spasticity causes muscle imbalance across joints, which initially leads to impaired function and eventually causes joint contractures with skeletal deformity. The typical elbow deformity of CP is elbow flexion and forearm pronation. Occasionally, it results in posterior dislocation of the radial head,32 which requires no treatment unless in adult life it results in a painful bursa; then the radial head may be excised. Flexion-supination contractures of the elbow can occur but are rare in CP.

CLINICAL ASSESSMENT Assessment of the patient with spastic CP starts with the history and physical examination. Because CP is associated with low birth weight and prematurity, associated medical problems should be noted, particularly seizures and mental retardation, which are indicators of more global CNS involvement. Physical examination includes assessment of passive range of motion, active range of motion, muscle tone/ control, and overall function of the limb (including hand function assessment). The limb is first examined for passive range of motion of the shoulder, elbow, forearm, wrist, and hand, evaluating for joint and muscle contractures. Even if only the elbow is to be treated, the shoulder, forearm, wrist, and hand need to be assessed because they are essential for the individual to effectively use the upper limb. Muscle tone is noted through the passive evaluation of joint mobility. Passive range of

Chapter 72 Spastic Dysfunction of the Elbow 1003

BOX 72-1

Simple Classification of Cerebral Palsy

Geographic Distribution

*Hemiplegia: principally one-sided (one arm, one leg) Diplegia: principally lower extremity involvement (two legs) Triplegia: one arm and both legs involvement Quadriplegia: all four extremities involvement

ticularly of elbow flexion/extension as well as pronation/supination. Overall use of the upper extremity should be characterized both from history obtained from the parents as well as by direct physician observation. The dynamic positioning of the shoulder, elbow, forearm, wrist, fingers, and thumb are noted, particularly for grasp and release, as well as pinch function. Ageappropriate tasks or toys that require two-handed use are helpful in this assessment.

Type

*Spastic: increased stretch reaction Dystonic: ataxias, athetosis, chorea Flaccid: lack of movement Mixed: spastic and dystonic *Most elbow problems occur in spastic hemiplegia, although occasionally those with quadriplegia develop fixed contracture.

FIGURE 72-1

Typical posturing of a spastic upper extremity in a patient with right hemiplegia due to cerebral palsy. The elbow is flexed, with forearm pronation, wrist flexion and ulnar deviation, and thumb-in-palm deformity.

motion needs to be done slowly to overcome muscle spasticity with gentle sustained resistance. Assessment for muscle and joint contracture by passive mobility of the joint and passive stretch of the muscle is performed. The tightness and contracture of some of the muscles around the elbow can be easily palpated, particularly the biceps, brachialis, brachioradialis, and pronator teres. Active range of motion is assessed next, including specific muscle testing for voluntary motor control, par-

DEFINITION OF GOALS Functional tasks that should be tested in every child are dressing, toileting, feeding, two-handed assisted work, grasp and release, and pinch. The functional goals for the limb should be established so that it can be determined whether the anticipated function is being accomplished by the patient. Goals for elbow surgery are different for a highly functioning hemiplegic versus a lower functioning quadriplegic. In a higher functioning child, common goals for elbow surgery include improved arm swing with gait, improved positioning of the hand in space, and improved cosmesis. For the lower functioning child or adolescent patient, common goals are decreased elbow contracture for better joint positioning and better hygiene. In the past, sensory deficiencies of the hand were believed to be a contraindication to surgery in CP. If tested carefully, sensory deficiencies are present in nearly all children with CP.42 Several recent studies have shown that impaired sensation is not a contraindication to surgical intervention in the patient with CP.6,8,42 Appropriate consultation or multispecialty approach to care should be considered before considering surgical intervention. Several alternatives to surgical intervention exist and should be considered. Exploration of the treatment pros and cons may require discussions that include the rehabilitation physicians, neurologists, and neurosurgeons to adequately explore the options of tone reducing medications (diazepam [Valium], baclofen), tone-reducing injections (botulinum toxin, phenol), tone-reducing neurosurgery interventions (selective dorsal rhizotomy), or therapy interventions (splinting, stretching programs). At many institutions, a spasticity management team of specialists is involved with patient evaluation for tone-reducing interventions, and helps guide the orthopedic surgeon as to other treatment alternatives.

TRAUMATIC BRAIN INJURY Most often, brain damage acquired in childhood is the result of trauma. The associated spasticity usually does not reach its maximum point until 1 to 2 months after

1004 Part VII Reconstructive Procedures of the Elbow

the incident; then muscle tone may gradually decrease during the next 2 years.22,23 Irreversible surgical procedures should not be performed in children with acquired brain damage in the first 2 years after the insult. During this period, serial casting or splinting can be combined with botulinum toxin or phenol injections to deal with elbows with significant flexor tone. Another problem in children with acquired brain injury is heterotopic bone formation, usually about the anterior aspect of the elbow.35 Unlike adults, most children eventually resorb the heterotopic bone. Therefore, we recommend gentle motion and reevaluation at least 6 months before any attempt is made at excision.

STROKE AND HEAD TRAUMA IN ADULTS Stroke and head trauma produce permanent impairment in approximately 3 million adults in the United States. Abnormal elbow function due to spasticity and loss of motor control is a common disability. The surgeon treating these conditions must be fully cognizant of the complex rehabilitation process after CNS illness, particularly hand rehabilitation. Surgery is undertaken only after careful assessment of the many factors that determine the patient’s potential to use the limb.3 Cerebral vascular accidents commonly involve the middle cerebral artery or its branches in the region of the cerebral cortex supplying the upper extremity. Consequently, the upper extremity usually is affected more frequently—and more severely—than the lower extremity. Elbow flexion contractures are nearly always preventable in stroke patients if standard preventive measures are instituted early. In contrast, head injury is often associated with excessive elbow flexor tone because of decerebrate or decorticates rigidity. The spasticity may be so severe that nonoperative measures alone may not prevent elbow deformity. Substantial neurologic recovery generally follows strokes and head injury. In stroke patients, most neurologic recovery is completed in the first 6 months; in head trauma, patients’ substantial recovery extends over the first year and a half.17 Definitive surgical procedures to improve function are deferred until after the patient’s neurologic condition has stabilized and he or she has learned to cope with the disability and has received appropriate nonoperative therapy. Prevention of elbow muscle and joint contractures is paramount. Nonoperative therapy should include passive range of motion, splints, and serial casts; if progressive elbow flexion deformity develops before neurologic recovery, then botulinum toxin of the biceps and brachialis or phenol injection of the musculocutaneous nerve is performed.13 Elbow flexion contracture due to

spasticity is the most common problem that ultimately requires surgical attention, because it commonly affects patients with nonfunctional hands. Surgery is indicated to correct contracture deformities that interfere with hygiene or cause pain; rarely, it is used to improve cosmesis. Operative intervention is usually deferred until neurologic recovery is complete, which is in 6 to 18 months.

PREOPERATIVE EVALUATION After a thorough medical history investigating the etiology of the elbow spasticity and a documentation of related medical conditions, a physical examination is documented. Range of motion is determined by quickly and slowly extending the elbow. Quick stretch excites the velocity-sensitive components of the muscle spindle and may elicit clonus if spasticity is severe. Consequently, a greater range of extension often can be obtained by slow extension (often over 1 or 2 minutes) with the patient relaxed. Even with excellent patient cooperation, definitive differentiation of muscle tone versus muscle contracture is difficult. Ultimately, spasticity can be differentiated from fixed contracture only by preoperative nerve block or examination under general anesthesia. Dynamic electromyography19,38,41 is becoming increasingly useful because it enables surgeons to determine more precisely which flexor muscles are responsible for a deformity (Fig. 72-2) or whether surgical ablation of a given muscle will be effective.26 Kozin et al reports its use in distinguishing spasticity patterns of the brachioradialis, biceps, and brachialis. This information is particularly valuable for patients with functional elbow motion because it enables the surgeon to release or lengthen only the muscles most involved and to preserve those that are less involved. Slow and fast volitional elbow flexion and extension are assessed. Attempts to move the elbow rapidly enhance an abnormal flexor response. Anterior and posterior radiographs of the elbow are taken before any surgical procedure. Arthritis and other conditions common in the adult patients may be responsible for intrinsic joint restriction and can decrease the probability of a successful surgical outcome. For patients with traumatic brain injury, skeletal trauma to the elbow needs assessment. Presence of heterotopic ossification should also be assessed as this is a known complication of head injury. Last, preoperative evaluation always includes a detailed assessment by a therapist and/or cooperation with a spasticity management team: evaluation of motor and perceptual function of the elbow, hand, and shoulder and examination of cognitive, vocational, and social

Chapter 72 Spastic Dysfunction of the Elbow 1005

Lateral pectoral nerve Pectoral branch: thoracoacromial artery Medial pectoral nerve Lateral thoracic artery

A

B

C

D

FIGURE 72-2

Dynamic electromyogram of head-injured patient with spasticity during slow elbow extension-flexion-extension-flexion cycle. The triceps displays normal bursts of activity during the extension phase. The brachialis is also normally active in flexion. Note that both the long and the short heads of the biceps are inappropriately active during attempted elbow extension, indicating obstructive tone.

factors that are important determinants of arm function and treatment goals.

TREATMENT OPTIONS Treatment of the spastic elbow includes several options. If the deformity is not fixed, and the major goal is reduced muscle tone to improve joint position and function, the elbow flexor tone can be diminished by several methods. Tone-reducing medications (Valium, baclofen) would be indicated if the overall global tone is severely affected; consultation with a neurologist or rehabilitation specialist to initiate this treatment would

be indicated. Mild elbow contractures can be diminished by range-of-motion stretches and elbow splinting; referral to a physical or occupational therapist to initiate this treatment would be indicated.1 Tone reduction specifically localized to the elbow can be achieved through the use of botulinum toxin injections, and phenol injections; a more permanent tone reduction can be achieved with neurectomy or musclelengthening procedures. Muscle-lengthening procedures are the most common surgical procedure performed in the elbow for CP. In order to reduce the flexion posturing of the elbow, lengthening of the biceps and brachialis would be indicated. If the flexion posturing includes pronation deformity of the forearm with wrist flexion

1006 Part VII Reconstructive Procedures of the Elbow

and finger flexion posturing, then a flexor pronator slide would be indicated. If the deformity is fixed, and the contracture of the elbow is long standing, a biceps tenotomy, brachialis lengthening, and brachioradialis release may be indicated with the goal of achieving improved, but not complete, elbow extension. Muscle and elbow joint releases will be limited by the length of the neurovascular bundle; care to avoid neurovascular injury is paramount. If the muscle release is inadequate, a distal humeral extension osteotomy can be performed. As shown in Figure 72-3, timing of surgical intervention is critical and depends on the presenting diagnosis. Because spasticity develops as a consequence of an upper motor neuron dysfunction in the CNS, it is imperative that neurologic recovery is complete before definitive surgical interventions are performed. Botulinum toxin injections and phenol injections are often recommended as temporary measures during neurologic return, or as interventions in the growing child with worsening contractures. Definitive surgical procedures include musculocutaneous neurectomy or elbow muscle lengthenings of the biceps, brachialis, or brachioradialis muscles or flexor pronator slide. Heterotopic

ossification of the elbow can occur with traumatic brain injury or stroke, and is discussed as well.

BOTULINUM TOXIN INJECTIONS Botulinum toxins (Botox, Allergan Pharmaceuticals, Irvine, CA) are protein products of Clostridium botulinum, and are potent neuromuscular paralyzing agents. Botulinum toxin type A is a related protein that can be used therapeutically in minute doses to block the release of acetylcholine to functionally denervate portions of the muscle causing a localized, dose-related weakness, with little or no systemic absorption of the toxin.30,40 Botulinum toxin has been used to control tone in upper extremities.5 It gives temporary benefits that may help therapists and may be most beneficial to head-injured children.38

TECHNIQUE Clinical application for decreasing elbow tone spasticity has been described using doses of 5 to 10 units/kg for all muscles injected, using 3 to 5 units/kg for the biceps

Spastic elbow deformity TBI children *wait 2 years Reversible CNS etiology

TBI adults *wait 18 months

Static CNS etiology

CVA adults *wait 6 months Physiotherapy: PROM splints, serial casting

1 Mild

2 Moderate

3 Severe

Biceps/ brachialis muscle lengthening

• Musculocutaneous neurectomy • Biceps tenotomy • Brachialis lengthening • Brachioradius release • Limited extension goals

If progressive Botulinum toxin injection (biceps, brachialis) Phenol injection (musculocutaneous nerve) If recurrent Musculocutaneous neurectomy 1 Mild elbow contracture in the highly-functioning child can include 0–30º flexion contracture, but impaired arm swing during gait, poor positioning of hand in space, difficulty dressing, and poor appearance. 2 Moderate elbow contracture includes 30–75º flexion contracture, with similar impairments as a mild contracture. 3 Severe elbow contracture includes >75º flexion contracture with impaired hygiene, difficulty dressing, and poor appearance. *or until neurologic status has stabilized

FIGURE 72-3

Decision algorithm for treatment of the spastic elbow.

Chapter 72 Spastic Dysfunction of the Elbow 1007

and brachialis.44 Dilution of the medication in 1 to 5 mL of normal saline helps spread the medication through the muscle belly. Most commonly, a neuromuscular stimulator is used to localize the injection close to motor endplates.25

RESULTS For patients with more focal muscle tone imbalance, botulinum toxin type A injections has been shown to be effective in reducing spasticity in the muscles injected and in improving elbow function. The effects of the injection last approximately 4–6 months. During this period, assessment of the antagonist muscles can be made and possible surgical benefits can be assessed. In addition, antagonist muscles can be strengthened and spastic muscles can be stretched with the benefits lasting beyond the direct effects of the medication. For the mildly involved child, treatment with Botox injections may obviate the need for surgical intervention. Wallen et al44 reported improved goals (dressing, arm at side), decreased elbow tone, and good parent/patient satisfaction in 16 children, with a return to baseline by 6 months in most measures. Chen4 measured decreased elbow flexor spasticity within 2 weeks after injection. A recent meta-analysis45 of 12 studies (three randomized controlled and nine uncontrolled) showed that, although some reports measured decreased spasticity, increased range of motion, or increased functional activities, there was either insufficient evidence or insufficient tools to predictably measure reduced spasticity or increased range of motion or improved upper limb function after treatment with botulinum toxin type A injections.

PHENOL INJECTIONS Acquired spasticity may be effectively controlled by open or percutaneous phenol nerve injections. The purpose of phenol injection is to provide a temporary reduction in spasticity, in order to allow improved limb function and rehabilitation, as well as to prevent joint contracture. Open nerve injections are selected over percutaneous injections if the nerve contains both sensory and motor components. Open technique allows for isolation of the motor branches for injection, and prevents postblock dysasthesias or loss of sensation. In patients with traumatic brain injury or stroke, phenol is a common treatment used. Because the effects of the block are not permanent, no functional loss will occur if central neurologic recovery is complete. If central recovery is incomplete and spasticity recurs, then definitive surgery (neurectomy or tendon lengthening) may be safely performed at that point.

RESULTS Garland et al13 described 13 phenol injections in 12 patients for treatment of elbow spasticity at 4.5 months after closed head trauma. The preinjection elbow flexion contractures averaging 55 degrees improved on average 43 degrees when combined with serial casting; all elbows had less than a 20-degree contracture. After neurologic recovery was complete, two elbows went on to other elbow surgical procedures for spasticity. Keenan et al21 reported on 23 elbows in 17 braininjured adults treated with percutaneous phenol blocks of the musculocutaneous nerve to control elbow spasticity. Ninety-three percent of patients responded with an improvement of resting elbow flexion from 120 degrees of flexion to 69 degrees of flexion. The mean duration of the block was 5 months.

NEURECTOMY Musculocutaneous neurectomy is performed only in nonfunctional upper extremities with an elbow flexion contracture interfering with positioning or hygiene. Even when minimal or no fixed myostatic or joint contracture is present, spasticity may force the elbow into a flexed posture that interferes with function. When hemiplegics walk, it is common for the elbow to assume a flexed posture and it may bounce up and down because of clonus. The patient may purposely walk slowly to decrease clonus. Musculocutaneous neurectomy improves cosmesis and eliminates clonus.16 After musculocutaneous neurectomy, the loss of elbow flexion strength is not important, because most stroke patients with excessive elbow flexion have nonfunctional hands. Because the brachioradialis is innervated by the radial nerve, which is left intact, some elbow flexion persists after surgery if this muscle was active preoperatively, and the loss of musculocutaneous sensation is not bothersome. In a patient who has no brachioradialis control or spasticity, this procedure should not be performed, because musculocutaneous neurectomy leaves a completely flail elbow because a neurectomy irreversibly eliminates all motor input to the biceps and brachialis muscles. If the patient has effective control of the brachioradialis or flexor pronator muscles, these muscles may continue to provide elbow flexion. If elbow contracture exists due to tone alone (usually less than 30 degrees), then partial neurectomy would most commonly improve elbow positioning. If contracture exists in the muscle or joint, then additional serial casting or muscle-lengthening procedures may be necessary to improve elbow extension. A lidocaine (Xylocaine) block of the musculocutaneous nerve along the medial proximal border of the biceps is helpful for

1008 Part VII Reconstructive Procedures of the Elbow

separating the effects of flexor tone from those of contracture. Contracture should be expected to ensue when the spastic posture has been present for years. The lidocaine block also predicts brachioradialis elbow flexion capability after neurectomy.

TECHNIQUE A longitudinal incision is made beginning at the insertion of the pectoralis major muscle in the interval between the biceps (short head) and the coracobrachialis, as shown in Figure 72-4. The biceps and lateral cord of the brachial plexus are located. The musculocutaneous nerve arises from the lateral cord and needs to be identified separate from the median nerve. The nerve is identified before it enters the biceps and confirmed by nerve stimulation. A 1-cm section of the nerve is excised. The wound is closed. The elbow is then splinted in maximum extension.16

fasciculotomy of the musculocutaneous nerve reports follow-up at 1.5 years.34 Total relief of spasticity was achieved in 63% of patients and partial relief in 37%. The authors recommend the procedure as safe, effective, and long lasting. Garland et al16 report on 30 musculocutaneous neurectomies in 29 patients with a nonfunctional upper extremity due to cerbrovascular accident (59%) or head injury (24%). The goals of the surgery were to improve personal hygiene, ambulation (arm swing), and appearance. Patients with a 30-degree contracture preoperatively did not require postoperative casting; patients with a 30 to 75 degree flexion contracture preoperatively required postoperative casting; and patients with greater than 75-degree flexion contracture preoperatively required concomitant muscle releases with postoperative casting. Twenty-eight patients were successfully treated. Other studies have reported similar results.27,37

BICEPS-BRACHIALIS LENGTHENING

RESULTS A large series of 75 elbows in 52 patients treated at an average age of 9.5 years old using a selective motor

Biceps-brachialis lengthening is the most common surgical procedure used in the treatment of elbow spasticity.

Deltoid m. Musculocutaneous n. Lateral cord

Short head of biceps m.

B

Median n.

FIGURE 72-4

A, Axillary exposure provides access to the musculocutaneous nerve, which usually branches from the brachial plexus high in the axilla and is isolated between the biceps and the coracobrachialis (B). The nerve may be injected with phenol or surgically released, as desired. (From Garland, D. E., Lucie, R. S., and Waters, R. L.: Current uses of open phenol nerve block for adult acquired spasticity. Clin. Orthop. Relat. Res. 165:217, 1982 [B redrawn].)

Chapter 72 Spastic Dysfunction of the Elbow 1009

Goals of the surgery are to improve passive and active elbow extension. In the highly functional patient with 30- to 60-degree contracture, this procedure improves gait by allowing the arm to come to the side for swing, improves ease of dressing, and improves cosmesis. In the low-functioning patient with greater than 60 degree contracture, this procedure is done primarily for hygiene; in this case, achievement of full extension is not necessary.24 When deformity is long standing and myostatic contracture considerable, biceps tenotomy can be performed.

A

TECHNIQUE Mital29 performs biceps-brachialis lengthenings through a curved antecubital approach (Fig. 72-5). The lacertus fibrosus is excised, and Z-plasty of the biceps tendon and release of the brachialis aponeurosis are performed. Most commonly, a correction of 30 to 40 degrees is obtained. If near–full extension is achieved, as shown in Figure 72-6, then no further release is necessary. Further correction can be obtained by release of the origin of the brachioradialis, and/or partial myotomy of the

B

FIGURE 72-5

C

D

Diagrams of the sequential steps of the elbow flexor Mital lengthening procedure. A, The initial incision. B, The exposure of the tendon of the biceps, and the excision of the lacertus fibrosus. C, Third step of the elbow flexor-lengthening procedure: the Z-lengthening of the biceps tendon. D, The incision of the aponeurotic fibers covering the brachialis. (Redrawn from Mital, M. A.: Lengthening of the elbow flexors in cerebral palsy. J. Bone Joint Surg. 61A:515, 1979.)

1010 Part VII Reconstructive Procedures of the Elbow

A

B

C

D FIGURE 72-6

E

Clinical case of the sequential steps of the elbow flexor lengthening procedure, the most common procedure for elbow spasticity. A, A curvilinear antecubital incision is made with a sterile tourniquet in place, with the arm positioned on an arm board. B, The lateral antebrachial cutaneous nerve is identified and protected as it courses laterally from under the biceps tendon. C, After the lacertus fibrosis has been excised, the biceps tendon is cut in a Z-lengthening manner with each end of the tendon tagged with suture. D, The fascial investment of the brachialis muscle is incision several times transversely. E, After the tourniquet has been deflated, the biceps tendons are woven back into each other in a lengthened position. The wound is then closed and the patient’s elbow is splinted in full extension.

Chapter 72 Spastic Dysfunction of the Elbow 1011

brachialis. In long-standing contractures of greater than 60 degrees, further elbow extension is blocked by contracture of the neurovascular structures and skin. Excessive tension on the neurovascular elements is unnecessary and can lead to vascular compromise. It is not usually necessary to release the anterior capsule. If this procedure is performed on nonfunctional limbs, full extension is not necessary and surgery in combination with postoperative serial casting provides adequate correction. A period of 4 weeks of postoperative immobilization, followed by bivalved elbow splinting, is recommended.

RESULTS Mital29 has the largest series in the literature, reporting on 32 elbows in 26 patients. Preoperative flexion contracture averaged 48 degrees (range 30 to 60 degrees); postoperative flexion contracture averaged 10 degrees (range 0 to 15 degrees). Average age at the time of surgery was 12 (range 6 to 19 years). Eleven of his patients were quadriplegic, and 15 were hemiplegic. He describes preoperative complaints of excessive dynamic elbow flexion that occurred with excitement or gait, and was a source of frustration and embarrassment. He describes improved gait, improved positioning of the arm, and improved cosmesis in these highly functioning patients. Koman24 describes use of this procedure for more severely involved patients with greater than a 60 degree elbow flexion contracture without specific results reported. Manske28 describes a similar procedure with incision of the lacertus fibrosis, lengthening of the brachialis fascia, and stripping of the biceps tendon (without Zlengthening). For 42 elbows in 40 patients, he reports improved dynamic posturing of the elbow from 104 degrees preoperatively to 55 degrees postoperatively. Functional use, as well as aesthetics of the limb, was improved.

FLEXOR-PRONATOR SLIDE Although flexor pronator slide does provide improved elbow extension, the primary indication for this procedure is for treatment of the forearm, wrist, and hand. If the patient has elbow flexion combined with forearm pronation, wrist flexion, and difficulty with simultaneous wrist and finger extension, then the procedure may be indicated. Volitional control of wrist and finger extension, which is diminished due to overpowering wrist and finger flexor tone, can be improved by this operation. Preoperatively, assessment of the balance of tone may be assisted by diagnostic botulinum toxin injections into the flexor pronator wad.

TECHNIQUE The origin of the pronator-flexor group is released through a medial incision, extending from the medial epicondyle to the proximal forearm. The ulnar and median nerves are identified and protected, and all the structures between them are released, including the pronator teres, flexor carpi radialis and ulnaris, and the flexor digitorum superficialis and profundus. The muscle origins are allowed to slide distally from the medial epicondyle, ulna, and radius. During the release, the medial collateral ligament of the elbow is identified deep to the muscle origin and left intact; the joint capsule is not violated. The slide of the muscles’ common origin should allow improved passive wrist and finger extension primarily, with secondary improved elbow extension. A postoperative long arm splint or cast is used for 4 weeks, holding the elbow in maximum extension, the forearm in supination, and the wrist and fingers in extension. With spasticity in the cast, the muscle length tension heals in an optimum position. After casting, orthoses are used as necessary.

RESULTS Pinzur31 reports on the use of the flexor pronator slide in combination with a Z-lengthening of the flexor pollicus longus tendon for treatment of the spastic hand in the adult after stroke. All patients improved two functional levels following the surgery. White46 described the use of the flexor pronator slide in 27 patients, using a concomitant wrist arthrodesis in 12 patients. No comment was made regarding effect on elbow function; wrist and hand function was good in 10, fair in 11, and poor in 11. Poor results were seen in the patients with poor drive, poor intelligence, and poor motor control. Inglis et al18 reported on 18 patients treated at an average age of 19 (range 12 to 45 years old) for severe spastic contractures of the wrist and hand that were not actively or passively correctable. At an average of 17 months after surgery, there were no recurrences of flexion deformities of the wrist and hand. The patients with mild contractures of the elbow were noted to be “improved,” and in the six patients with severe elbow contractures, release of the brachialis fascia was performed concomitantly. Use of the flexor pronator slide is focused primarily on treatment of the hand spastic dysfunction, with gains in elbow spasticity seen only as a secondary effect.

HETEROTOPIC OSSIFICATION Heterotopic ossification of the elbow, a severe complication that occurs in about 3% of head-injured patients,

1012 Part VII Reconstructive Procedures of the Elbow

is discussed in detail in Chapter 31, but is also relevant in the context of this chapter. It most commonly occurs when hypertonus at the elbow is severe because of rigidity from decorticate or decerebrate posturing or spastic hemiplegia (Fig. 72-7). In general, heterotopic ossification is apparent within the first 6 months after head trauma (peak occurrence 2 months). The typical stroke patient infrequently develops heterotopic ossification. With head injury, the complication occurs more often posterior than anterior.11 The incidence of traumatic heterotopic ossification in combined head and elbow injuries is 90%.14 Heterotopic ossification most often affects the collateral ligaments but can form in any planes about the elbow. Bone formation in the ulnar collateral ligament may contribute to an acute ulnar palsy from the localized swelling or delayed ulnar palsy resulting from long-standing pressure.20 Heterotopic ossification is heralded by swelling, pain, and limitation of motion at the elbow. Evidence of heterotopic ossification on bone scans is apparent 2 to 3

weeks before radiographic evidence of calcification appears. Alkaline phosphatase may not be elevated if only a small amount of new bone is present. Muscle hypertonus exerts continuous forces across the inflamed joint, which intensifies the pain. Pain, in turn, increases spasticity, completing the vicious circle. If the patient’s neurologic condition improves rapidly, the amount of heterotopic ossification is lessened, and no significant impairment may result if an adequate range of elbow motion is maintained. On the other hand, extremity function may be affected if elbow motion becomes severely restricted or ankylosis develops, even if neurologic recovery has occurred. Even in a nonfunctional arm, hygiene of the elbow flexor crease and limb positioning are difficult in a patient with severe limb flexion deformity and ankylosis. Treatment of heterotopic ossification begins with prompt recognition of the condition. Joint motion is preserved by range-of-motion exercises. Movement should be slow to minimize pain. Elbow splints are

FIGURE 72-7

Decerebrate rigidity may be associated with myositis ossificans in the anterior muscles (A) but even more often in the posterior aspect of the elbow (B). (From Garland, D. E., Blum, C. E., and Waters, R. L.: Periarticular heterotopic ossification in headinjured adults. J. Bone Joint Surg. 62A:143, 1980.)

Chapter 72 Spastic Dysfunction of the Elbow 1013

useful to position the elbow in maximal extension. Diphosphonate therapy is controversial. Indocin, for 3 months, may be used alone or in combination with diphosphonates.9 Oral spasmolytic agents or phenol injection of the musculocutaneous nerve may help to reduce muscle tone in the biceps and brachialis muscles. Temporary reduction of elbow flexor tone permits the therapist to perform range-of-motion exercises more easily to maintain elbow extension. Forceful manipulation of the elbow under anesthesia also may help to maintain or increase elbow range.15 Because heterotopic ossification is so prevalent with combined head and elbow injuries, some type of prophylaxis seems warranted. This type of heterotopic ossification is not related to the severity of the head injury, and joint spasticity may not be present. Resection of heterotopic ossification is performed after the bone is skeletally mature.10–12,35 Active motion is essential to maintaining joint range after surgery. Indocin or radiation may be used for prophylaxis.9

Acknowledgment I would like to acknowledge Drs. M. Mark Hoffer, Robert L. Waters, and Douglas E. Garland who wrote this chapter in the prior edition.

References 1. Barus, D., and Kozin, S. H.: The evaluation and treatment of elbow dysfunction secondary to spasticity and paralysis. J. Hand Ther. 19:192, 2006. 2. Bleck, E. E.: Orthopedic Management of Cerebral Palsy. London, Mac Keith Press, 1987. 3. Caldwell, C., and Braun, R. M.: Spasticity in the upper extremity. Clin. Orthop. Relat. Res. 1974:80-91. 4. Chen, J. J., Wu, Y. N., Huang, S. C., Lee, H. M., and Wang, Y. L.: The use of a portable muscle tone measurement device to measure the effects of botulinum toxin type a on elbow flexor spasticity. Arch. Phys. Med. Rehabil. 86:1655, 2005. 5. Corry, I. S., Cosgrove, A. P., Walsh, E. G., McClean, D., and Graham, H. K.: Botulinum toxin A in the hemiplegic upper limb: a double-blind trial. Dev. Med. Child. Neurol. 39:185, 1997. 6. Dahlin, L. B., Komoto-Tufvesson, Y., and Salgeback, S.: Surgery of the spastic hand in cerebral palsy. Improvement in stereognosis and hand function after surgery. J. Hand Surg. [Br.] 23:334, 1998. 7. Drougia, A., Giapros, V., Krallis, N., Theocharis, P., Nikaki, A., Tzoufi, M., and Andronikou, S.: Incidence and risk factors for cerebral palsy in infants with perinatal problems: a 15-year review. Early Hum. Dev. 83:541, 2007. 8. Eliasson, A. C., Ekholm, C., and Carlstedt, T.: Hand function in children with cerebral palsy after upper-limb tendon transfer and muscle release. Dev. Med. Child. Neurol. 40:612, 1998.

9. Garland, D. E.: A clinical perspective on common forms of acquired heterotopic ossification. Clin. Orthop. Relat. Res. 263:13, 1991. 10. Garland, D. E.: Surgical approaches for resection of heterotopic ossification in traumatic brain-injured adults. Clin. Orthop. Relat. Res. 263:59-70, 1991. 11. Garland, D. E., Blum, C. E., and Waters, R. L.: Periarticular heterotopic ossification in head-injured adults. Incidence and location. J. Bone Joint Surg. Am. 62:1143, 1980. 12. Garland, D. E., Hanscom, D. A., Keenan, M. A., Smith, C., and Moore, T.: Resection of heterotopic ossification in the adult with head trauma. J. Bone Joint Surg. Am. 67:1261, 1985. 13. Garland, D. E., Lucie, R. S., and Waters, R. L.: Current uses of open phenol nerve block for adult acquired spasticity. Clin. Orthop. Relat. Res. 165:217, 1982. 14. Garland, D. E., and O’Hollaren, R. M.: Fractures and dislocations about the elbow in the head-injured adult. Clin. Orthop. Relat. Res. 168:38-41, 1982. 15. Garland, D. E., Razza, B. E., and Waters, R. L.: Forceful joint manipulation in head-injured adults with heterotopic ossification. Clin. Orthop. Relat. Res. 169:133, 1982. 16. Garland, D. E., Thompson, R., and Waters, R. L.: Musculocutaneous neurectomy for spastic elbow flexion in nonfunctional upper extremities in adults. J. Bone Joint Surg. Am. 62:108, 1980. 17. Garland, D. E., and Waters, R. L.: Orthopedic evaluation in hemiplegic stroke. Orthop. Clin. North Am. 9:291, 1978. 18. Inglis, A. E., and Cooper, W.: Release of the flexor-pronator origin for flexion deformities of the hand and wrist in spastic paralysis. J. Bone Joint Surg. [Am.] 48:847, 1966. 19. Keenan, M. A., Haider, T. T., and Stone, L. R.: Dynamic electromyography to assess elbow spasticity. J. Hand Surg. [Am.] 15:607, 1990. 20. Keenan, M. A., Kauffman, D. L., Garland, D. E., and Smith, C.: Late ulnar neuropathy in the brain-injured adult. J. Hand Surg. [Am.] 13:120, 1988. 21. Keenan, M. A. E., Thomas, E., and Stone, L.: Percutaneous phenol block of musculocutaneous deformity in cerebral palsy. J. Bone Joint Surg. [Am.] 15:236, 1990. 22. Klonoff, H., Clark, C., and Klonoff, P. S.: Long-term outcome of head injuries: a 23 year follow up study of children with head injuries. J. Neurol. Neurosurg. Psychiatry 56:410, 1993. 23. Koelfen, W., Freund, M., Dinter, D., Schmidt, B., Koenig, S., and Schultze, C.: Long-term follow up of children with head injuries classified as “good recovery” using the Glasgow Outcome Scale: neurological, neuropsychological and magnetic resonance imaging results. Eur. J. Pediatr. 156:230, 1997. 24. Koman, L. A., Gelberman, R. H., Toby, E. B., and Poehling, G. G.: Cerebral palsy. Management of the upper extremity. Clin. Orthop. Relat. Res. 253:62, 1990. 25. Koman, L. A., Mooney, J. F., Smith, B. P., Goodman, A., and Mulvaney, T.: Management of spasticity in cerebral palsy with Botulinum-A toxin: Report of a preliminary randomized double-blind trial. J. Pediatr. Orthop. 14:299, 1994. 26. Kozin, S. H., and Keenan, M. H.: Using dynamic electromyography to guide surgical treatment of the spastic upper

1014 Part VII Reconstructive Procedures of the Elbow

27.

28.

29. 30.

31.

32.

33.

34.

35.

extremity in the brain-injured patient. Clin. Orthop. Rel. Res. 288:109, 1993. Maarrawi, J., Mertens, P., Luaute, J., Vial, C., Chardonnet, N., Cosson, M., and Sindou, M.: Long-term functional results of selective peripheral neurotomy for the treatment of spastic upper limb: prospective study in 31 patients. J. Neurosurg. 104:215, 2006. Manske, P. R., Langewisch, K. R., Strecker, W. B., and Albrecht, M. M.: Anterior elbow release of spastic elbow deformity in children with cerebral palsy. J. Pediatr. Orthop. 21:772, 2001. Mital, M. A.: Lengthening of the elbow flexors in cerebral palsy. J. Bone Joint Surg. [Am.] 61:515, 1979. National Institutes of Health: Clinical use of botulinum toxin. National Institutes of Health Consensus Development Conference Statement, November 12-14, 1990. Arch. Neurol. 48:1294, 1991. Pinzur, M. S.: Flexor origin release and functional prehension in adult spastic hand deformity. J. Hand Surg. [Br.] 16:133, 1991. Pletcher, D. F., Hoffer, M. M., and Koffman, D. M.: Nontraumatic dislocation of the radial head in cerebral palsy. J. Bone Joint Surg. Am. 58:104, 1976. Praemer, A., Furner, S., and Rice, D. P.: Musculoskeletal Conditions in the United States. Rosemont, IL, American Academy of Orthopaedic Surgeons, 1999. Purohit, A. K., Raju, B. S., Kumar, K. S., and Mallikarjun, K. D.: Selective musculocutaneous fasciculotomy for spastic elbow in cerebral palsy: A preliminary study. Acta Neurochir. (Wien) 140:473, 1998. Roberts, J. B., and Pankratz, D. G.: The surgical treatment of heterotopic ossification at the elbow following long-term coma. J. Bone Joint Surg. Am. 61:760, 1979.

36. Samilson, R. L.: Principles of assessment of the upper limb in cerebral palsy. Clin. Orthop. Relat. Res. 47:105, 1966. 37. Sindou, M. P., Simon, F., Mertens, P., and Decq, P.: Selective peripheral neurotomy (SPN) for spasticity in childhood. Childs. Nerv. Syst. 23:957, 2007. 38. Spaulding, S. J., White, S. C., McPherson, J. J., Schild, R., Transon, C., and Barsamian, P.: Electromyographic analysis of reach in individuals with cerebral palsy. Electromyogr. Clin. Neurophysiol. 30:109, 1990. 39. Stanley, F., Blair, E., and Alberman, E.: Cerebral Palsies: Epidemiology and Causal Pathways. London, Mac Keith Press, 2000. 40. Van Heest, A. E.: Applications of Botulinum toxin in orthopaedics and upper extremity surgery. Tech. Hand Up. Extrem. Surg. 1:27, 1997. 41. Van Heest, A.: Functional assessment aided by laboratory studies. Hand Clin. 19:565, 2003. 42. Van Heest, A. E., House, J. H., and Cariellol, C.: Upper extremity surgical treatment of cerebral palsy. J. Hand Surg. [Am.] 24:323, 1999. 43. Van Heest, A. E., House, J., and Putnam, M.: Sensibility deficiencies in the hands of children with spastic hemiplegia. J. Hand Surg. [Am.] 18:278, 1993. 44. Wallen, M. A., O’Flaherty, S. J., and Waugh, M. C.: Functional outcomes of intramuscular botulinum toxin type A in the upper limbs of children with cerebral palsy: a phase II trial. Arch. Phys. Med. Rehabil. 85:192, 2004. 45. Wasiak, J., Hoare, B., and Wallen, M.: Botulinum toxin A as an adjunct to treatment in the management of the upper limb in children with spastic cerebral palsy. Cochrane Database Syst. Rev. CD003469, 2004. 46. White, W. F.: Flexor muscle slide in the spastic hand: the Max Page operation. J. Bone Joint Surg. [Br.] 54:453, 1972.

Chapter 73 Elbow Disarticulation Amputation 1015

CHAPTER

73

Elbow Disarticulation Amputation Thomas C. Shives and Karen L. Andrews

INTRODUCTION Over the years, advances in upper extremity prosthetics have included improved surgical techniques, preoperative management, postoperative management, and advances in prosthetic technology. In the past decade, the greatest advances have occurred in prosthetic technologies, fabrication techniques, and components to more effectively replace the lost function of the extremity.7

DEMOGRAPHICS Trauma is the leading cause of upper extremity limb loss, accounting for 80% of upper extremity amputations. Tumor is the most common cause of upper extremity amputation in children. From 1988 to 1996, the rate of trauma and cancer-related amputations declined. This decline was likely due to improved surgical reconstruction, advances in limb-sparing techniques, and prevention through improved occupational safety awareness.6 Following trauma, the decision to attempt limb salvage or proceed with amputation is complex. There is a bias toward limb salvage in upper extremity trauma surgery. The functional demands of the upper extremity are different from the lower extremity. Lack of weight bearing forces, the ability to function with partial sensation, and limited function of upper extremity prostheses are reasons sited for limb salvage and reimplantation.8

nents. The external hinge elbow mechanisms for elbow disarticulations are not very cosmetically pleasing. In children with upper limb deficiency or amputation, growth and development, bony overgrowth and more rigorous use of a prosthetic device need to be considered. An elbow disarticulation amputation level for this population optimizes residual limb length and avoids bony overgrowth. The slowed humeral growth after elbow disarticulation results in a humeral length at maturity that allows the use of a prosthetic elbow while retaining the suspension and rotational control of an elbow disarticulation.1 In children, transhumeral amputation results in a high incidence of bony overgrowth. An elbow disarticulation preserves the epiphysis, prevents bony overgrowth, and maintains growth potential; therefore, elbow disarticulation is the level of choice.2

AMPUTATION SURGERY Controversy exists whether to perform a long transhumeral amputation or an elbow disarticulation. Amputation surgery should be viewed as a reconstructive procedure. The basic principle of all upper limb amputations is preservation of maximal length consistent with optimal function, control of disease, and satisfactory surgical wound management. Adherent scarred distal tissues or redundant soft tissue should be avoided.

SKIN There is no particular type of skin flap configuration that is better than another. When the soft tissues are normal, equal anterior and posterior flaps are generally preferred. However, skin flaps for traumatic amputations should be fashioned in any manner possible that preserves length. The nature of the trauma, including burns, may require extensive modification of the classic equal flap closure. Skin grafts are not a contraindication to prosthetic fit. Their use may be indicated, particularly in burn amputations. Skin on upper limb amputations is far less subject to pressure, shear, and stretching than it is in the weight-bearing lower limb. The skin that is used to close an amputation should be sensate and well vascularized.

ELBOW DISARTICULATION AMPUTATION Elbow disarticulation has advantages and disadvantages when compared with the transhumeral level of amputation. An elbow disarticulation amputation allows anatomic suspension, rotational control of the prosthesis, and reduces rotation of the socket on the residual limb. The major disadvantages are the suboptimal cosmetic appearance and limited availability of elbow compo-

NERVES AND BLOOD VESSELS Major nerves about the elbow are transected sharply under tension. The transected nerve is allowed to retract into the adjacent soft tissues, away from the amputation site and away from the areas where it could become adherent and a source of pressure irritation from the socket.

1016 Part VII Reconstructive Procedures of the Elbow

Meticulous hemostasis is mandatory to avoid postoperative hematoma formation. All wounds are drained for 48 hours postoperatively.

BONE Through-elbow amputation is carried out as a true disarticulation (Fig. 73-1). Minor contouring of the margins of the distal humerus is usually required to eliminate sharp condylar prominences. For above-elbow amputations, the bone edges should be slightly beveled so that there are no sharp prominences or rough bone edges.

MUSCLE STABILIZATION Whenever possible, the sectioned muscles and tendons are sewn to each other over the end of the humerus at the amputation site (Fig. 73-2). If possible, the triceps tendon and aponeurosis is retained and brought forward through and over the trochlea to be sewn under minimal tension to the brachialis muscles. The biceps tendon also can be interwoven into the brachialis muscle near the amputation site, giving excellent residual limb muscle control. Muscle stabilization requires firm fixation to the distal bone. When opposing muscles are sewn to each other over the bone or joint end without firm distal fixation, a “sling-like” effect can develop that causes bursa formation, reduces effectiveness of the muscles, and can be painful. A myodesis with two or four small 1/8-inch drill holes through the distal humerus may be necessary to accomplish good muscle stabilization.

NERVE TRANSFERS In an attempt to improve functional control of myoelectric prostheses, the possibility of transferring residual nerves to spare muscles in or near the residual limb has been studied. Using nerves to reinnervate targeted muscle, the surface myoelectric signals from these muscles have been used to simultaneously control multiple degrees of freedom in a prosthesis.13 Research into this concept has been promising. Studies have shown that when large nerves (such as the brachial plexus nerves) are transferred onto relatively small muscle areas, the recovery of the muscle is very good.12 With targeted reinnervation, control of a prosthesis will be easier and more natural because the myoelectric signals are physiologically correlated to the movements of the lost arm. Although targeted reinnervation shows exciting potential, ongoing research is needed.13

ACUTE POST-AMPUTATION MANAGEMENT Following surgery, the goals of the preprosthetic period are to 1. Promote residual limb shrinkage and shaping 2. Establish a home exercise program of range of motion (ROM), stretching, strengthening and conditioning 3. Increase upper extremity function 4. Review joint protection principles, energy conservation, and one-handed techniques 5. Optimize tasks required for daily living.

Biceps tendon Brachialis artery & vein Median nerve Brachialis muscle

Ulnar nerve End of humerus Triceps tendon Radial nerve

FIGURE 73-1

Cross-section of the elbow disarticulation before closure of the myoplasty. The myoplastic flaps must be sectioned with sufficient length to permit closure without tension.

Chapter 73 Elbow Disarticulation Amputation 1017

Biceps tendon

Brachialis muscle

Triceps muscle

FIGURE 73-2

Muscle stabilization using anteroposterior myofascial flaps over the contoured distal humerus at the elbow level. The flaps must be stabilized directly to the periosteum or bone.

6. Evaluate adaptive and durable medical equipment needs 7. Determine the electrical potential provided by various muscles in the event myoelectric prosthetic components are prescribed. 8. Review the patient’s specific daily living, leisure, and work needs to determine possible prosthetic components and options. Immediate and early postsurgical prosthetic fitting provides edema control, pain reduction, and protects the surgical incision.14 Successful prosthetic use is higher when fitting is completed within a “golden period” of 30 days after surgery.14 If prosthetic fitting and training are delayed, the patient can become adept at one-handed techniques, making it difficult to incorporate a prosthesis in their daily living activities. A second study has shown that even delayed fitting can be successful.22 Common reasons for rejecting a prosthetic limb include the perception of limited usefulness, excessive weight, and residual limb pain. An early postoperative prosthesis using a plaster cast or a high temperature thermoplastic socket typically can be fit by the third day after surgery. Prepositioned or self-positioned locking elbows are used to avoid excess elbow motion and shearing along the surgical incision. If there is concern about healing of the surgical incision, a stump protector (rigid removable dressing), compressive dressing, or soft dressing can be used until the incision has healed and the patient is ready to be fit for their first definitive prosthesis.

PROSTHETIC MANAGEMENT Successful rehabilitation and effective use of an elbow disarticulation prosthesis depends on many factors. Key elements that influence prosthetic outcomes include 1. Quality and nature of the skin and soft tissue coverage of the limb 2. Muscle function in the residual limb 3. Pain control 4. Joint ROM and strength of the residual limb and upper body 5. Rehabilitation support19 Careful surgery, evaluation, prosthetic fitting, and training are critical to successful outcome and optimal prosthetic function. The long-term rate of prosthetic wear for transhumeral and elbow disarticulation amputations is less than 50%.16 Although a prosthesis is not necessary for an amputee to function, recent studies suggest that overuse in the remaining hand and arm occurs in up to 50% of persons with upper limb amputations.10 Active use of a prosthesis is believed to reduce this risk. The typical sequence of prosthetic rehabilitation involves initial fitting and training with a body-powered prosthesis, followed by a second prosthesis when the residual limb volume has stabilized 3 to 6 months following surgery. Prostheses can be divided into three groups:

1018 Part VII Reconstructive Procedures of the Elbow

1. Conventional or body powered 2. External powered or electric 3. Passive or cosmetic Advantages of using a body-powered prosthesis for the first definitive prosthesis include the greater ease of fitting, greater ability to adapt to changes in residual limb volume, early training in daily living activities, and lower cost compared to external powered devices. Because it is difficult to predict long-term acceptance of an upper limb prosthesis or an individual’s preferred type of prosthetic system (body or external powered), the initial definitive prosthesis should be used to explore prosthetic options. Individuals with a recent upper extremity amputation should be allowed time to explore advantages and disadvantages using a prosthesis and different terminal devices in a variety of home, work, and social settings.6 Prosthetic fitting should be initiated during the first month after upper limb amputation to maximize acceptance and use. Every person with an upper limb amputation should be given the opportunity to use a prosthesis, recognizing that it is ultimately the person’s choice whether a prosthesis becomes part of his or her daily life. Body-powered cable systems offer the advantage of being low cost, light weight, and highly reliable because of their mechanical simplicity. Body-powered control systems also have significant disadvantages. The harness required to transmit muscle forces inevitably restricts the amputee’s work envelop and encumbers the unaffected side. The amputee often exerts significant effort with exaggerated body movements to generate sufficient force and excursion to operate a body-powered cable system. Higher level amputees may be physically unable to generate sufficient motion or force because of the limited leverage. A patient must understand that successful prosthetic and physical rehabilitation is a prerequisite for optimal performance. A state-of-the-art prosthesis will not provide optimal performance to a user who is not physically capable of taking advantage of its features. Conversely, optimal performance will not be achieved with a prosthesis that does not provide a level of technical sophistication that matches or challenges the user’s physical capabilities. The difference between body-powered and electric components should be reviewed. Advantages of a bodypowered prosthesis with a hook terminal device include lighter weight, better durability, increased sensory feedback, less expense, and greater ease in seeing the manipulated object. Advantages of a myoelectric prosthesis include better appearance, moderate or no harnessing, less body movement to operate the prosthesis, the ability to reach overhead, better grip strength, and the ability

to grasp larger objects.3 If the patient’s workplace has magnetic fields or large electrical currents, a myoelectric prostheses may not function unless special shielding materials are used during fabrication to prevent interference. If force or excursion is inadequate for full bodypowered control of a prosthesis, then external power will be needed to control the prosthesis. Myoelectric or Servo controls are available that provide proportional speed and force control. It is common to use a bodypowered elbow and a switch or myoelectric control terminal device. This arrangement simplifies harnessing and reduces weight. The amputee should be actively involved in the discussion of prosthetic options and given an objective, comprehensive overview of the advantages and disadvantages of available socket designs, suspensions, and components (elbow, forearm, wrist, and hand). Each of the components should be reviewed again whenever a patient returns to be cast for a new prosthesis. A careful inventory of the person’s lifestyle and future goals should be discussed. Early following amputation, people frequently have the unrealistic expectation that a prosthesis will simply replace their lost arm and hand. It is important to explain that a prosthesis will serve as a tool and discuss realistic functional expectations. With this knowledge, the patient is less likely to reject the device. During fitting and training with a prosthesis, the initial wearing period should be no longer than 15 to 30 minutes three times daily, with frequent examination of the skin for evidence of redness, increased warmth, or breakdown. If redness persists for more than 20 minutes after the prosthesis is removed, the prosthetist should adjust the socket. If no skin problems are present, wearing periods can be increased in 30-minute increments. When a patient is able to tolerate wear for 3-hour intervals, he or she can advance to all-day wearing. The patient should continue to inspect the skin of the residual limb on a daily basis.

TERMINAL DEVICE The human hand is a very complex anatomic and physiologic structure whose function cannot be replaced by the current level of prosthetic technology. A variety of prosthetic terminal devices are available including passive, body powered, and externally powered hooks and hands. The most commonly prescribed passive terminal device is the passive hand. Many passive hands have bendable or spring loaded fingers that can provide a static grasp for objects. Passive hands do not require cables or batteries for operation; they are light in weight and have a socially acceptable appearance. Prosthetic hands provide a three-jaw chuck pinch.

Chapter 73 Elbow Disarticulation Amputation 1019

Prosthetic hooks provide the equivalent of lateral or tip pinch. Body-powered terminal devices can be opened or closed voluntarily. A voluntary opening device is maintained in the closed position by rubber bands. The patient opens the device by the pull of the cable on the harness system. The rubber bands provide the prehensile force. The maximal prehensile force is predetermined by the number of rubber bands (typically a maximum of six). Voluntary closing terminal devices require a patient to close the device by pulling the cable on the harness system to grasp an object. Voluntary closing devices are held open and closed when the control cable is pulled. Pinch is regulated by the amount of force the user supplies to the control cable. Full range of pronation and supination are important to allow the terminal device to be positioned in the most functional position for a specific task. Body-powered terminal devices transmit grasping forces and proprioception (hand positioning) from the harness and cables used to operate the hand.17 Externally powered devices can have a digital or proportional (stronger signal/faster action) control system. Traditional myoelectric prosthetic hands do not provide feedback regarding the force exerted on a grasped object. The degree of control is imprecise; often more force is applied than necessary.17 Although the kinematics of currently available hand systems have not changed a great deal, significant progress has been made in control options to allow greater precision and ease of operation. A new feedback system with a miniature vibration motor, a piezoresistive force sensor, and control electronics has improved the ability to regulate grasping without the help of vision. The results suggest that more precise control and grasping force are possible with a feedback system.17 Multiple control options are now available, allowing better customization of prosthetic systems to the demands of individual users. Using a computer, a prosthetist can modify the parameters of every component integrated into the prosthesis. State-of-the-art hands have integrated sensors that reduce the user’s need to concentrate on controlling the grasping action.4 Onboard sensors for hand control can signal when to adjust grasping force (magnitude and direction), opening width, and speed of movement.

PROSTHETIC WRIST A quick-disconnect wrist allows the patient to exchange terminal devices more easily. If the patient plans to only use one terminal device, a lighter weight constant friction wrist should be considered.

PROSTHETIC ELBOW Prosthetic elbow joints can be passive, body powered, or externally powered. These devices are controlled by mechanical cables, external switches, or myoelectric signals. Mechanical elbows have a locking mechanism that is manually applied using the contralateral hand, the chin, or a cable system. The traditional body-powered locking elbow with harness control lock is generally preferred if the patient can operate it well. The flexion force across a mechanical elbow is dependent on the wearer’s strength, the comfort of the socket fit, and the ability to efficiently transfer the power from the residual limb to the prosthesis. The elbow disarticulation level requires external locking elbow joints, adjacent to the humeral condyles, to achieve optimal length of the arm. These joints are larger and protrude on the medial aspect reducing the durability and cosmesis of the prosthesis. Limited flexion strength and increased maintenance are additional problems with this type of joint. Outside locking hinges are available in standard and heavy duty models. Standard units provide seven different locking positions throughout the range of flexion. The heavy duty models provide five locking positions. Replacement of the anatomic elbow joint requires a substitute joint that permits flexion and extension to a range of approximately 135 degrees. The unit must permit locking of the elbow at various points throughout the 135-degree ROM. Amputations through the humerus (approximately 5 cm proximal to the elbow joint) provide adequate space to accommodate inside locking elbow mechanisms. Use of a standard prosthetic elbow unit for a person with an elbow disarticulation, however, results in excessively long humeral and shortened forearm segments and creates an unnatural appearance. Elbow center discrepancies also make tabletop activities difficult.

PROSTHETIC SOCKET Traditionally, upper extremity prostheses have used a dual-wall socket design fabricated from lightweight plastic or graphite composite materials. With a dual-wall design, a rigid inner socket fabricated from a custom mold of the residual limb is the primary interface between the user and the prosthesis. Comfort and function are directly related to the quality of the fit of the inner socket. The outer socket wall has the shape and contour of the normal arm. This serves both a cosmetic function and supplies the foundation for the attachment of the suspension and control systems. This type of socket is durable. Variations in residual limb volume are easily accommodated using filler socks to adjust the fit.

1020 Part VII Reconstructive Procedures of the Elbow

Advances in prosthetic materials such as acrylic laminates, carbon graphite, and flexible thermoplastics allow prostheses to be more comfortable, lighter, and more durable. An elbow disarticulation socket is broad and flat distally to conform to the anatomic configuration of the distal humerus (Fig. 73-3). A total contact interface should be attempted at the elbow disarticulation level to allow efficient energy transfer from the residual limb to the prosthetic device. This design provides some selfsuspension and allows active rotation of the prosthesis (internal and external rotation of the humerus). Recent use of silicone materials for the fabrication of prosthetic sockets has expanded the fitting options for upper limb amputees. Silicone suction technology allows suction suspension. Material thickness, stiffness, and color can be precisely controlled.20

The goal of suspension systems is to secure a prosthesis to the body. The elbow disarticulation prosthesis can be suspended by a harness, suction, anatomic, or a silicone sleeve suspension. The traditional figure-of-eight chest strap and shoulder saddle harnesses provide suspension

and control of body-powered prostheses (Fig. 73-4). A figure-of-eight harness provides the greatest available excursion, but it can create pressure problems in the contralateral axilla. A shoulder saddle and chest strap suspension/control system reduces axillary forces and provides better lifting capability but does not harness contralateral shoulder excursion. Typically, a split Pelite insert, a windowed socket, or a flexible wall socket is used to provide entry and anatomic suspension at the elbow disarticulation level. Newer suspension systems include a silicone sleeve, suction, or seal-in liner suspension. These provide improved suspension and decrease pistoning and shear within the socket. These suspensions also simplify donning and allow independent donning of the prosthesis with one hand. Silicone liners accommodate mild to moderate volume changes in the residual limb and can be used successfully with both body-powered and externally powered components. The shape and pressure tolerance of the condyles determine the best suspension for the elbow disarticulation level. Suction suspension is often used in conjunction with externally powered components to eliminate or reduce the amount of harnessing necessary. If the patient has

FIGURE 73-3

FIGURE 73-4

SUSPENSION SYSTEM

An elbow disarticulation prosthesis with a broad and flat distal socket to conform to the anatomic configuration of the distal humerus. (Courtesy of Mike Gozola, C.P., Prosthetic Laboratories, Rochester, MN.)

Body-powered elbow disarticulation prostheses with a figure-of-eight suspension and control system. (Courtesy of Mike Gozola, C.P., Prosthetic Laboratories, Rochester, MN.)

Chapter 73 Elbow Disarticulation Amputation 1021

a great deal of scarring or decreased skin integrity, a thicker liner can be used to enhance soft tissue supplementation. Liner thicknesses range from 3 to 9 mm. These suspensions also provide excellent skin protection and suspension for patients who are very active users.

PROSTHETIC TRAINING Prosthetic training is integral to the rehabilitation process. An occupational therapist works closely with the patient’s prosthetist to review donning, carefully monitor the skin, gradually increase wear time, and optimize bimanual activities, prosthetic function, upper extremity function, and daily living activities.

FUNCTIONAL OUTCOMES Independence in all functional activities is the goal for persons with an upper limb amputation. Following an elbow disarticulation, a person should be independent in all activities of daily living, driving, and work. Some work restrictions with regard to handling delicate, heavy, or voluminous objects may be necessary. Following an elbow disarticulation, a patient should typically be able to lift 10 to 15 pounds. The permanent partial impairment for this level of amputation according to the AMA Guides to Permanent Partial Disability is 57% of the whole person. Prosthetic-specific, adult functional status measures need to be developed and validated. Building a core set of outcome measures will provide a comprehensive picture of different aspects of hand function and prosthetic use.21

SUMMARY The rehabilitation process for a person with an elbow disarticulation is best accomplished with a comprehensive, multidisciplinary, specialized treatment team. A well-fitting prosthesis with appropriate components, supervised training, and ongoing follow-up optimizes prosthetic use and function. Targeted reinnervation and other research on the control of upper limb prostheses hold promise to allow more agile, intuitive control systems to increase prosthetic function, use, and quality of life for persons with limb loss.13

References 1. Abraham, E., Pellicor, J. R., Hamilton, R. C., Hallman, D. W., and Ghosh, L.: Stump overgrowth in juvenile amputees. J. Pediatr. Orthop. 6:66, 1986.

2. Atkin, G. T.: Surgical amputation in children. J. Bone Joint Surg. Am. 45:1735, 1963. 3. Atkins, D.: Managing self-care in adults with upper extremity amputations. In Christian, C. (ed.): Ways of Living: Self-Care Strategies for Special Needs, 2nd ed. Bethesda, MD, American Occupational Therapy Association. 2000, p. 221. 4. Chappell, P. H., and Kyberd, P. J.: Prehensile control of a hand prosthesis by microcontroller. J. Biomed. Eng. 13:363, 1991. 5. Daly, W.: Clinical applications of roll-on sleeves for myoelectrically-controlled transradial and transhumeral prostheses. J. Prosthet. Orthot. 12:88, 2000. 6. DeLisa, J. A.: Physical Medicine and Rehabilitation Principles and Practices, 4th ed. Philadelphia, Lippincott Williams & Wilkins, 2005. 7. Dillingham, T. R., Pezzin, L. E., and MacKenzie, E. J.: Limb amputations and limb deficiency—epidemiology and most recent trends in the United States. South. Med. J. 95:75, 2002. 8. Graham, B., Adtkins, P., and Tsai, T. M.: Major reimplantation versus revision amputation and prosthetic fitting in the upper extremity—a late functional outcome study. J. Hand Surg. 23:783, 1998. 9. Hoffer, J. A., and Loeb, G. E.: Implantable electrical and mechanical interfaces with nerve and muscle. Ann. Biomed. Eng. 8:351, 1980. 10. Jones, L. E., and Davidson, J. H.: Save that arm: a study of problems in the remaining arm of unilateral upper limb amputees. Prosthet. Orthot. Int. 23:55, 1999. 11. Kuiken, T. A.: Use of nerve-muscle grafts to improve the control of artificial limbs. J. Technol. Disabil. 15:105, 2003. 12. Kuiken, T. A., Rymer, W. Z., and Childress, D. S.: The hyperreinnervation of rat skeletal muscles. Brain Res. 1676:113, 1995. 13. Lipschutz, R. D., Kuiken, T. A., Miller, L. A., Dumanian, G. A., and Stubblefield, K. A.: Shoulder disarticulation externally powered prosthetic fitting following targeted muscle reinnervation for improved myoelectric control. J. Prosthet. Orthot. 18:28, 2006. 14. Malone, J. M., Fleming, L. L., Roberson, J., Whitesides, T. E. Jr, Leal, J. M., Poole, J. U., and Grodin, R. S.: Immediate, early, and late post-surgical management of upper limb amputation. J. Rehabil. Res. Dev. 21:33, 1984. 15. Michael, J. W., and Bowker, J. H.: Atlas of Amputations and Limb Deficiencies - Surgical, Prosthetic, and Rehabilitation Principles, 2nd ed. St. Louis, Mosby-Year Book, Inc, 1992. 16. Pinzur, M. S., Angeltas, J., Light, T. R., Izuierdor, R., and Pluthat, T.: Functional outcome following traumatic upper limb amputation and prosthetic limb fitting. J. Hand Surg. 19:836, 1994. 17. Pylatiuk, C., Kargov, A., and Schulz, S.: Design and evaluation of a low-cost force feedback system for myoelectric prosthetic hands. J. Prosthet. Orthot. 18:57, 2006. 18. Salam, Y.: The use of silicone suspension sleeves with myoelectric fitting. J. Prosthet. Orthop. 6:119, 1994.

1022 Part VII Reconstructive Procedures of the Elbow

19. Smith, D. G., Michael, J. W., and Bowker, J. H. (eds.): Atlas of Amputations and Limb Deficiencies—Surgical, Prosthetic, and Rehabilitation Principles, 3rd ed. Rosemont, IL, American Academy of Orthopedic Surgeons, 2004. 20. Uellendahl, J. E., Mandacina, S., and Ramdial, S.: Custom silicone sockets for myoelectric prostheses. J. Prosthet. Orthot. 18:35, 2006.

21. Wright, F. V.: Measurement of functional outcome with individuals who use upper extremity prosthetic devices: current and future directions. J. Prosthet. Orthot. 18:46, 2006. 22. Wright, T. W., Hagen, A. D., and Wood, M. B.: Prosthetic usage in major upper extremity amputations. J. Hand Surg. 28:619, 1995.

Chapter 74 Rheumatoid Arthritis 1025

CHAPTER

74

Rheumatoid Arthritis Harvinder S. Luthra

INTRODUCTION Rheumatoid arthritis (RA) is an inflammatory disease of unknown etiology that has been known to exist since at least the 1800s,75,109 when the first detailed description was reported. Indirect evidence that it may have existed as far back as 4000 to 5000 years ago has been reported.100,102,103 Despite extensive research into its etiology and many theories about its pathogenesis, no uniform idea explains its many presentations and clinical course.17,64 In this chapter, the issue is discussed in general terms. The surgical management of the elbow is discussed in Chapters 54 and 55.

EPIDEMIOLOGY This disease occurs worldwide and has a prevalence of about 0.5% to 2%.112 There is a female preponderance of 2 to 4 in most studies. The etiology of this disease is unknown. The presence of HLA-DR4, the gene for the major histocompatibility complex (MHC), in an increased frequency in patients with RA was a landmark observation,120 and several studies reconfirmed this and showed an increased risk of developing RA in individuals positive for the MHC class II DR-4 gene. Several studies show a strong correlation with the presence of HLA-Dw4 and Dw14 (HLA alleles DRB1*0401 and HLA-DRB1*0404).81,87 This, however, explains only a part of the genetic risk.2,52 The fact that only 1 : 20 to 1 : 35 individuals in the general white population who inherit these genes are at risk for developing RA suggests that other genetic and nongenetic factors3,86,110,133 are involved. Several investigators are currently trying to perform microsatellite mapping to identify other genes that may influence the disease. This approach has led to several likely candidates in animal studies using the rat collagen–induced model of RA.48,95 It would be of interest to see whether these can be confirmed in human studies also. Nongenetic factors that have been suggested include infections,28 pregnancy,111 and smoking,113 and others. These factors continue to be investigated.

PATHOPHYSIOLOGY The etiology of RA is unknown. The genetic predisposition, the involvement of activated immune cells, the clonal expansion of the cells in the pathologic lesions, and the response to immunosuppressive therapy suggest that this disease is immune mediated. The observation that MHC gene HLA-DR4 was associated with RA120 directly linked the antigen-presenting cells with the immune response and suggested that antigen-induced activation was central to the pathogenesis of this disease.134 Soon, however, it was observed that other HLA-DR antigens (HLA-DR9, HLA-DR3, and HLADw16) were similarly associated in different populations.66,106,138 Some of the initial differences were explained by Gregersen and colleagues’ proposal of the shared epitope hypothesis,46,87 which suggested the significance of the shared sequence in the third hypervariable region. Further studies have led to the observation that multiple genes contribute to the genetic component of susceptibility.121,135 Synovial membrane biopsies of recent-onset disease reveal inflammatory cells, including macrophages, T cells, B cells, occasionally plasma cells, and fair number of polymorphonuclear leukocytes, along with edema and increased vascular permeability. As the disease progresses, the inflammatory process intensifies, with macrophages and lymphocytes either developing into nodular aggregates or as diffuse infiltrates. Increased angiogenesis is evident. This inflammatory process progresses and starts to invade normal tissue, leading to erosions, joint space narrowing, and ultimately, destruction of the joint. Interest in recognizing the putative antigen is high, and several candidate antigens have been and are being investigated. These include type II collagen,79 proteoglycans,60 cartilage link protein,92 Epstein-Barr virus,6 65kDa heat shock protein,141 and Proteus mirabilis.31 Some evidence exists for each of them, and yet no one antigen explains the whole picture. This suggests that several different antigens can trigger the disease, with crossreactivity to a self-antigen leading to a self-perpetuating autoimmune process. Local production and release of cytokines, including interleukin-1 (IL-1), tumor necrosis factor-α (TNF-α), IL-8, fibroblast growth factor (FGF), and platelet-derived growth factor (PDGF), and increased expression of intercellular adhesion molecular (ICAM) and lymphocyte function-associated molecules (LFA) and others, contribute to the enhancement of the inflammatory process.119 Of the various cytokines released, TNF-α, a proinflammatory cytokine, is thought to play a prominent role in the pathogenesis of this disease and this has led to development of various new therapeutic agents that are capable of blocking TNF (see below under treatment). B cells are activated and may be involved in antigen presentation.45 They also help plasma

1026 Part VIII Septic and Nontraumatic Conditions

BOX 74-1

Unusual Modes of Presentation

Fever of unknown origin Still’s disease Palindromic rheumatism Polymyalgia rheumatica Paraneoplastic syndrome

cells to produce increased amounts of immunoglobulins, particularly rheumatoid factors (RF). These form immune complexes, which are capable of activating the complement system, leading to enhanced local inflammation. Local release of enzymes capable of damaging the joint (e.g., stromelysin, gelatinase, collagenase) has been demonstrated. These contribute to the ongoing damage.49,143

CLINICAL FEATURES The presentation of RA can be variable. Obviously, when patients present with a symmetric polyarthritis, the diagnosis of RA is very high on the list of possibilities. On the other hand, when patients present with systemic symptoms, the diagnosis is more uncertain. Subacute bacterial endocarditis, a paraneoplastic syndrome, malignancy,33 hepatitis C,99 or other connective tissue disease should be kept in mind. Patients have been known to present with fever of unknown origin and a clinical picture of Still’s disease, prominent fibrositis that can be mistaken for polymyalgia rheumatica, and episodic oligoarthritis (palindromic rheumatism). All of these conditions can be presenting features of RA (Box 74-1). Even when the joint symptoms are dominant, the pattern of presentation can be variable. Patients can present with a single joint swelling (21%), few swollen joints (44%), or a more typical polyarthritis (35%). The onset may be acute (days or weeks) in about half of the patients, whereas an insidious presentation is seen in the other half. About 32% of the patients present with disease of the small joint, whereas 16% present with medium-sized joints involved. Twenty-nine percent have large joints involved at onset, and 26% have a combination.36 Although the American College of Rheumatology revised the criteria for RA (Box 74-2), it is important to remember that these are for classification of groups of patients who are entered into studies and should not be used as diagnostic criteria in individual patients.8 The joint reacts to an insult in a limited number of ways. It is stiff, painful, tender, and swells. Loss of function may result. If the process continues, the joint sustains damage, which may lead to deformity and

American College of Rheumatology Classification Criteria for Rheumatoid Arthritis

BOX 74-2

1. Morning stiffness—in and around joints lasting at least 1 hour 2. Arthritis of three or more joint areas—PIP, MCP, wrist, elbow, knee, ankle, and MTP joints of either or same side 3. Arthritis of joints of the hands—at least one joint area involved 4. Symmetric arthritis—symmetric involvement of the two sides (PIP, MCP, and MTP joint involvement does not require absolute symmetry) 5. Rheumatoid nodules—observed by a physician 6. Serum rheumatoid factor in levels above the normal population 7. X-ray changes should include typical erosions and/ or periarticular osteoporosis When four of seven criteria are present, with one to four present for at least 6 weeks, the patient can be classified as having rheumatoid arthritis. MCP, metacarpophalangeal; MTP, metatarsophalangeal; PIP, proximal interphalangeal. Modified from Arnett, F. C., Edworthy, S. M., Bloch, D. A., McShane, D. J., Fries, J. F., Cooper, N. S., Healey, L. A., Kaplan, S. R., Liang, M. H., Luthra, H. S., et al.: The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum. 31:315, 1988.

permanent compromise in function. Inflammation affects all the joints in the same way, and one can observe these changes in various diarthroidal joints in the patient with RA. Stiffness that improves with use lasting more than 30 minutes is considered significant. It is thought to be due to swelling of the joint and periarticular tissues, leading to redistribution of interstitial fluid when the joint is in one position for several hours (e.g., overnight). Some of these patients also experience a generalized stiffness involving the trunk, shoulder girdles, and hip girdles. This also improves with physical activity21 but recurs with rest and inactivity. The mechanism of this systemic stiffness is not clear but correlates with the activity of disease and can be used as a measure of response to treatment. Pain experienced by the patients is due to the ongoing inflammation. This leads to local (intra-articular) fluid accumulation and swelling of the synovial lining. Typically, the swelling observed is symmetric in a joint in contrast to the swelling seen in degenerative osteoarthritis, which is asymmetric. The cause of predominant bilateral symmetry is not known, but local innervation and release of inflammatory neuropeptides have been suggested as factors.61,90,105 The presence of synovial

Chapter 74 Rheumatoid Arthritis 1027

swelling and synovial fluid is characteristic evidence of inflammation in the joint, as pain and decreased function can be present owing to extra-articular disease. Motion must contribute to the damage, since joints spared from this are spared by the disease.14,44,124 The diarthrodial joints of the thoracic and lumber spine are very rarely involved, and motion may play a role in this also.96,115 The inflammation in RA goes through intermittent exacerbations and remissions. This cycle leads to stretching and damage of the joint capsule and ligaments. Disuse and inflammation lead to weakness of the supporting muscles.108,123 These factors, and recurring mechanical forces that change as the stability of the supporting tissues is compromised, lead to development of deformities that gradually increase with time (Figs. 74-1 and 74-2). The hands and wrist are the most common joints involved in this disease and cause the most disability. Elbow involvement has been reported in 20% to 65% of patients with RA. The earliest change noted in the elbow is loss of extension. In most cases, this occurs imperceptibly, because the patient has involvement of the hands and wrist at the same time, and these deformities are usually more disabling. Loss of the groove on either side of the olecranon is usually good evidence of elbow involvement.91 Disease progression is similar to that with other joints; occasionally, large cystic swellings can occur (Fig. 74-3).

EXTRA-ARTICULAR MANIFESTATIONS Rheumatoid Nodules Nodules occur in about 20% of patients with progressive seropositive disease. These nodules are most commonly subcutaneous and occur along the extensor surfaces of the arms, elbows, olecranon bursae, spine, occiput (Fig. 74-4), and other areas exposed to mechanical pressure. They can be very small, for example, ranging from less than 1.00 mm in size to several centimeters in diameter. The latter usually are collections of many nodules

FIGURE 74-1

Typical symmetric swelling of the wrists, metacarpophalangeal joints (MCPs), and the proximal interphalangeal joints (PIPs) of a patient with rheumatoid arthritis. The distal interphalangeal joint (DIP) changes are due to degenerative osteoarthritis; one can appreciate the prominent Heberden’s nodes. The lateral marginal swelling of the right third and fourth PIPs is due to rheumatoid nodules.

FIGURE 74-2

The hands of a rheumatoid arthritis patient who has developed typical deformities (A). Ulnar deviation (B), swan-neck deformities, and boutonnière (C) deformity of the fingers.

1028 Part VIII Septic and Nontraumatic Conditions

FIGURE 74-4

The forearm of a patient with rheumatoid arthritis showing multiple rheumatoid nodules.

Hematologic Manifestations FIGURE 74-3

A, The forearm of a patient with aggressive and advanced rheumatoid arthritis. In addition to the swelling and deformity of the proximal interphalangeal joints (PIPs), this patient has cystic swellings around the elbow. The forearm swelling is due to elbow synovial cysts dissecting into the forearm. B, Cystic swelling of the elbow joint in a rheumatoid arthritis patient.

occurring together. These nodules have a very characteristic histology in that they are made up of a central area of fibrinoid necrosis surrounded by an area of palisading epithelial cells and fibrocytes. Surrounding this is an area of lymphocytes, plasma cells, and fibrocytes tissue. Detailed study of the early lesion suggests small vessel vasculitis as the initiating event,118 with deposition of immune complexes,88 and localization of HLA-DR-positive cells.9 These nodules can be observed in tendon sheaths, heart, lungs, liver, eyes, and the meninges.54 The presence of multiple nodules should alert the physician to the presence of vasculitis, and ulcerated nodules can be a source of bacteremia.

Anemia is a very common presentation of RA. The prevalence depends on the stage and duration of disease, and the severity on disease activity. The cause of the anemia is multifactorial, resulting from several factors, including subclinical hemolysis, chronic blood loss as a side effect of prolonged use of nonsteroidal antiinflammatory drugs (NSAIDs). The most common cause of the anemia is poor iron utilization from stores in the reticuloendothelial system and reduced erythropoietin levels. The increased production of proinflammatory cytokines in the bone marrow contributes to the anemia of chronic disease.53,69 The anemia is usually normocytic normochromic, although the picture can change depending on other complicating factors. Usually, these patients are not iron deficient, unless they have significant blood loss, and it is not always easy to distinguish between these conditions.77 When these patients schedule surgery, they may not be able to donate autologous blood for use during surgery. Recent experience with the use of synthetic erythropoietin suggests that this may be an option for some selected patients.70,71 This needs more study, because there are patients who may not respond to synthetic erythropoietin.10 Usually, the white blood cells are normal in these patients; however, about 1% of patients with RA develop

Chapter 74 Rheumatoid Arthritis 1029

a neutropenia, and splenomegaly. These patients do have an increased risk of bacterial infections and skin ulcerations. Therapy with agents used to treat RA (e.g., intramuscular gold, D-penicillamine, corticosteroids, and methotrexate) have been successful, although recently, granulocyte-macrophage colony-stimulating factor (GM-CSF) has also been used in small numbers of patients.13,32,63 Surgery should be avoided until the granulocytopenia has resolved. Splenectomy may help, but usually for that episode only, and is best avoided unless a life-threatening situation exists.97

Pulmonary Involvement Pulmonary involvement in this disease is very common, with many patients with this condition being unrecognized and found to have involvement only at autopsy. In most cases, pleural involvement is asymptomatic and may be noted on incidental chest radiographs taken for other reasons (Fig. 74-5). The effusions may require aspiration, mostly for diagnostic reasons. These effusions are exudates with increased cells, protein, and lactate dehydrogenase (LDH). Complement levels are low, and characteristically these patients have very low glucose in the effusion compared with the concomitant blood glucose. These effusions resolve with treatment of the systemic disease, leaving behind fibrosed pleura. Rheumatoid nodules occur in the lungs in patients who are RF positive and have subcutaneous nodules.

These can be single or multiple, unilateral or bilateral, or small or large. The nodules can be particularly large in patients with pneumoconiosis. Malignancy is always a consideration when a new nodule appears in the setting of a stable pulmonary picture. Without a biopsy, this possibility cannot be ruled out.127 Lungs are involved in RA patients in many different ways, although clinically, the patients may present with radiographic changes before symptoms develop. Interstitial fibrosis usually affecting the bases and spreading to the other areas of the lungs can be observed. The clinical picture is similar to that in idiopathic pulmonary fibrosis or the picture of interstitial fibrosis seen in connective tissue diseases. Although as many as 50% of RA patients may develop interstitial disease, only 5% are symptomatic. Pulmonary function tests and highresolution computed tomography can aid in the recognition of small airway disease.30,43,51,68,144 Smoking has been found to be a risk factor for developing interstitial lung disease.104

Cardiac Conditions Pericarditis, similar to pleuritis, can be found in almost 50% of the patients with RA at autopsy. The patients may be asymptomatic or may have moderate to large effusions. Fluid removed shows characteristics similar to those of pleural effusions; that is, they are exudates with increased cell counts, increased protein, LDH, low complement levels, and low glucose. Some patients present with pericardial tamponade that requires emergency aspiration or surgery. Recurrent episodes with resulting fibrosis lead to the development of constrictive pericarditis. Pericardiectomy, pericardial window, or repeated pericardial aspirations can be life-saving; without these, the mortality rates are very high.56,126 Myocarditis and endocarditis can occur in RA patients. Myocarditis is usually found at biopsy or autopsy, and rarely does it lead to congestive heart failure. More often, it presents with cardiac conduction abnormalities, as does the presence of rheumatoid nodules when localized to the conduction system, leading to first-degree, seconddegree, and in some patients, third-degree heart block. Rheumatoid nodules involving the valves have been reported.16,23 Coronary vasculitis has been observed in rare cases.

Vasculitis

FIGURE 74-5

A rheumatoid arthritis patient with a left pleural effusion.

Necrotizing vasculitis of the medium-sized vessels occurs in patients who have progressive uncontrolled disease. These patients have polyarticular, nodular, erosive disease, with fever, recurrent pericarditis, cutaneous ulcerations, scleritis, and digital infarcts (Figs. 74-6 and 74-7). Laboratory studies show that these patients are anemic, and have leukocytosis, eosinophilia, and high titers of RF. The manifestations of vasculitis depend on

1030 Part VIII Septic and Nontraumatic Conditions

FIGURE 74-8

The pannus-rheumatoid inflammatory process invading the cartilage and subchondral bone. This lesion causes the erosions seen on radiographs.

FIGURE 74-6

The periungual infarcts seen in patients with rheumatoid arthritis.

peptide antibody, antinuclear antibodies, liver enzymes, and renal function. Special circumstances may require specific tests, depending on the patient’s condition. Radiologic changes (Fig. 74-8) are an important measure of disease progression, and plain radiographs and magnetic resonance imaging are necessary.50 Although RF tests are positive in about 80% of patients with RA, 20% of patients with this disease are rheumatoid factor negative. Anti-IgG antibodies can also be seen in several other connective tissue diseases, with infections and malignancies, and in other states (Box 74-3); thus, one needs to interpret the results with some caution.

MANAGEMENT AND COMPLICATIONS

FIGURE 74-7

The digital infarcts seen in rheumatoid

vasculitis.

the organ system involved. Cutaneous infarcts, ulcerations, neuropathy, bowel infarcts, digital infarcts, and, gangrene of the gallbladder, brain, heart, and peripheral nerves all can be observed.67,82 These patients are not good candidates for surgery, and it is best to delay any surgical procedures.

LABORATORY STUDIES Laboratory studies are done to aid in diagnosis, monitor the progress and complications of disease, and assess the side effects of drugs. These tests include measuring hemoglobin, white blood cell count, differential white blood cell counts, platelet counts, erythrocyte sedimentation rate, rheumatoid factor, anticyclic citrullinated

In the past, the treatment of RA has been based on anecdotal observations, a few small short-term studies, and personal experiences.98 For many years, researchers have been proposing, trying, and then modifying different ways of approaching this disease, mainly because of a lack of curative agents. These endeavors have helped us understand the disease, the drugs we have used, and the limitations of these approaches.117,139,140 Work during the past two decades, and particularly the last decade, has led to a more scientific approach that is bearing fruit, and we are on the threshold of an era of many new agents,85 which have changed our approach as well as the outlook for patients with this disease. Because, at present, we do not have a cure for this disease, the goal of management is to reduce inflammation, prevent or delay disease progression, and maintain function of the joints and other organs as best as we can and for as long as possible. Although our treatments are aimed at affecting the short-term effects on the patient, the fact that RA is a chronic disease makes it very important that we keep the long-range outcome in

Chapter 74 Rheumatoid Arthritis 1031

SCHEMA OF ARTICULAR COURSE PATTERNS IN RA

Conditions in Which Rheumatoid Factors May Be Positive

BOX 74-3

Progressive 10%

Diagnosis

Rheumatoid arthritis Systemic lupus erythematosus Sjögren’s syndrome Scleroderma Polymyositis Other Inflammatory Diseases

Autoimmune liver disease Cryoglobulinemia—mixed Idiopathic pulmonary fibrosis Sarcoidosis Bacterial Infections

Subacute bacterial endocarditis Leprosy Syphilis Tuberculosis

Polycyclic 70% Articular involvement

Connective Tissue Diseases

Monocyclic 20%

0

1

2

3

4

5

Years from onset of arthritis

FIGURE 74-9

The articular patterns seen in a prospective study of patients with early-onset rheumatoid arthritis. (Redrawn from Masi, A. T.: Articular patterns in the early course of rheumatoid arthritis. Am. J. Med. 75:16, 1983.)

Viral Infections

Hepatitis C Infectious mononucleosis Influenza Acquired immunodeficiency syndrome (AIDS) Miscellaneous

Postimmunization conditions Malignancies Parasitic infections Healthy elderly population

mind. Masi65 followed a group of patients with disease of recent onset and observed that they follow several different patterns. A small group of patients (about 20%) have a monocyclic course. In these patients, the disease usually lasts less than 2 years. A small number of patients (approximately 10%) have progressive aggressive disease that does not respond to the therapies available to us today. The majority of the patients have a polycyclic course, with few actually having periods of remission, whereas others mostly go through cycles of exacerbations and partial remissions (Fig. 74-9). The presence of features described in Box 74-4 have been shown to predict more aggressive disease, and these patients should be treated more aggressively.59 For years, it was believed that RA was a benign disease, but several studies have shown that the mortality of these patients is increased.7,72,78,125 Studies have shown that bony erosions occur early in this disease.37 Thus, aggressive management should be the norm rather than the exception. The management of these patients is best with the help of a rheumatologist,128,129 and such collaboration will become more important as new immunomodulators become available.

Circumstances in Which a More Aggressive Clinical Course of Rheumatoid Arthritis Should Be Suspected

BOX 74-4

Positive rheumatoid factor and anti-CCP antibodies in high titer Elevated inflammatory markers (ESR and CRP) Presence of shared epitope alleles (HLA-DRB1*0401 and HLA-DRB1*0404) Presence of bony erosions (Plain x-rays or MRI) Degree of functional disability (HAQ) anti-CCP, anticyclic citrullinated peptide; CRP, C-reactive protein; ESR, erythrocyte sedimentation rate; HAQ, Health Assessment Questionnaire; HLA, human leukocyte antigen; MRI, magnetic resonance imaging.

It has been shown that rest is beneficial for patients with RA.51,116 It is also clear that rest without any physical activity can lead to further deconditioning and disuse atrophy of the muscles. Thus, a proper balance between physical activity and rest is very important. A physical therapy and occupational therapy26,39,40,121 program with regular monitoring should become part of the management in every case. NSAIDs are analgesics with anti-inflammatory and antipyretic properties that have been traditionally used as initial therapy in these patients.42,47,117 Sodium salicylate was the first drug used for RA, and acetylsalicylic acid was developed for use in RA to avoid the gastrointestinal toxicity. Its mechanism of action was unknown, but later it was found to inhibit cyclooxygenase, a critical enzyme in the production of inflammatory

1032 Part VIII Septic and Nontraumatic Conditions

mediators, including prostglandin E2 and F1a and thromboxane A2. It has been shown that these compounds are capable of inhibiting the activation of transcriptional nuclear factor-κB (NF-κB).57 This affects the transcription of genes of multiple molecules, including IL-1, TNF-α, IL-6, and IL-8. NSAIDs have many common effects, which include, in addition to cyclooxygenase inhibition, inhibition of the production of leukotrienes, superoxide, lysosomal enzyme release, lymphocyte function, and cartilage metabolism. These drugs have a mild antiinflammatory effect on RA. They also share many of the toxicities seen with these agents, the most prominent of which are gastrointestinal. These side effects include epigastric pain, nausea, and vomiting. Patients who have a history of peptic ulcer disease may experience exacerbation, with dyspepsia, indigestion, gastritis, and bleeding.89 These effects are due to suppression of prostaglandin synthesis. Misoprostol, a prostaglandin analogue, has been shown to be beneficial in these patients.114 Other side effects include liver enzyme elevations, skin rashes, headaches, drowsiness, and rarely, confusion. Two isoenzymes of cyclooxygenase, COX-1 and COX-2, have been characterized. COX-1 is constitutively expressed in most tissues and is thought to be important for physiologic homeostasis and function of different organ systems, including the kidney, and platelets. In contrast, COX-2 is absent in most tissues and is expressed in increased amounts in inflammatory states.62,73,80,107 Although several COX-2 inhibitors were developed, currently only celecoxib is approved for use. The main issue that led to their withdrawal was concern for increased cardiovascular events occurring in patients on these drugs.11 These drugs are thought to have considerably less gastrointestinal toxicity and can be used in patients with increased risk of NSAID-induced gastrointestinal bleeding. They are also thought to have no effect on platelet function. Celecoxib is contraindicated in patients with known hypersensitivity to sulfonamides and in patients with known asthma, urticaria or allergic reactions to aspirin or other NSAIDs. Hydrochloroquine has been used for the treatment of this disease for a long time. It is useful in patients with mild to moderate disease.27 Its mechanism of action is believed to be interference with antigen processing. This drug has been found to be safe as long as the daily dose does not exceed 6.5 mg/kg body weight. Annual eye examinations to check for retinal toxicity should be performed. Hydrochloroquine has been found to be of no additional benefit when used in combination,93 to be potentially deleterious,22 or to be beneficial.83,84 D-Penicillamine was used for years and did benefit patients22 but, because of its toxicity, has fallen out of favor. D-Penicillamine inhibits T-lymphocyte activation and decreases the formation of immune complexes. The major side effects, in addition to bone marrow toxicity,

include the development of autoimmune diseases, such as myasthenia gravis, polymyositis, and Goodpasture’s syndrome. Similarly, parenteral gold has been a favorite1 until the past 10 years, when the use of methotrexate has overshadowed it. Parenteral gold has many in vitro and in vivo effects on the cellular and humoral immune response, including inhibition of antigen presentation.25 Parenteral gold use, in addition to the inconvenience of the injections, required patients to have weekly blood and urine monitoring and also exposed the patients to many side effects, some of which were serious, including bone marrow suppression, proteinuria, and skin rashes. Methotrexate has become the standard disease-modifying agent in the treatment of RA. Several studies have shown that this drug is effective136,137 and well tolerated,94,130 and delays radiologic progression.4,131 The mechanism of action is thought to comprise both an anti-inflammatory effect and inhibition of dihydrofolate reductase. The concomitant use of folic acid has not reduced its efficacy but has decreased the frequency and severity of side effects. The concern about liver toxicity has proved not to be as serious as was the experience with psoriatic arthritis, but regular monitoring of liver function is nonetheless required.58 The issue of increased risk of infection in RA patients receiving methotrexate at the time of surgery has been controversial, because reports of both an increased risk19,24 and the lack thereof55 have been published. It has been proposed that stopping methotrexate therapy for 2 weeks before surgery is reasonable.20 Several drugs have been used successfully in combination.83,84 Corticosteroids have been prescribed for patients with RA for several decades. We have gone through the period of excessive use after the first observations were made and the toxicity was not realized. This did put a damper on the use of these drugs, although the current use seems to be more reasonable. High doses of corticosteroids are used for patients who have serious complications, including mononeuritis multiplex, necrotizing vasculitis of medium-sized vessels, vasculitis ulcers, necrotizing scleritis, and corneal melt. More commonly, these drugs are used in low doses (e.g., 10 mg or less of prednisone daily). These patients are at risk for complications including osteoporosis, diabetes mellitus, accelerated atherosclerosis, hypertension, cataracts, and delayed wound healing. These patients require corticosteroids in stress doses before surgery. Leflunomide inhibits the enzyme dihydro-orotate dehydrogenase, thus leading to inhibition of pyrimidine synthesis. This inhibition, in turn, inhibits both T- and B-cell function.38,74 This oral drug has a long half-life of 7 to 8 days, which can increase over a longer time of dosing to as much as 28 days. It is excreted via the kidneys and in the feces in a 1 : 1 ratio. Biliary excretion

Chapter 74 Rheumatoid Arthritis 1033

and reabsorption are major reasons for the prolonged half-life, and female patients planning to have children need treatment with cholestyramine to rid the leflunomide from the body. Leflunomide has been shown to be effective in patients with RA and can be used alone or in combination with methotrexate. It seems to be well tolerated, with the major side effects being gastrointestinal disturbances, skin rashes, weight loss, and alopecia. Gastrointestinal disturbances include abdominal pain, anorexia, nausea, diarrhea, gastritis, and occasionally, vomiting. The past 10 years have seen a revolution in the management of RA.135 New biologic agents targeting various inflammatory molecules have been shown to successfully control this disease and to retard the damage that accompanies it. Several new products aim at blocking tumor necrosis factor (TNF), one of the proinflammatory cytokines produced during the inflammatory process in the joints. Etanercept is a dimeric recombinant fusion protein that consists of the human 75-kd tumor necrosis factor receptor (TNFR) fused with the Fc portion of human IgG1. It binds to TNF, blocking its ability to bind to cell surface TNFRs. It is given parenterally once or twice a week and is one of the few drugs that shows a response within a couple of weeks.76,132 Infliximab122 and adalimumab18 are monoclonal antibodies capable of binding TNF in solution as well as on the cell surface. The former is a chimeric molecule given as an intravenous infusion at 6- to 8-week intervals while the latter is a wholely human molecule and given subcutaneously at weekly or biweekly intervals. All of these agents can be used along with methotrexate. This combination does not have any increased toxicity and, in fact, may have additional benefit than when given alone. They are generally well tolerated. Etanercept and adalimumab can be associated with local injection site reactions; most of these require no treatment. Other side effects have included upper respiratory infections, headaches, rhinitis, dizziness, cough, and dyspepsia, in descending order of frequency. Infliximab is associated with infusion reactions including rash, urticaria, fever, chest heaviness, and rarely, anaphylactic reactions. They are contraindicated in patients with sepsis and during pregnancy. All of these conditions carry a risk of infections including reactivation of tuberculosis and fungal diseases. Because of this problem, all patients are screened for exposure to tuberculosis before therapy is initiated. It has also been observed that patients on these drugs do have a slightly higher risk of lymphoproliferative malignancies.15 This is in the background of increased lymphoproliferative malignancies in patients with RA, as well as treatment with methotrexate. Other rare side effects include demyelinating diseases in rare patients.

Other immunomodulators that are approved for treatment of RA include anakinra, a human recombinant anti-IL-1 receptor antagonist, which is given by daily subcutaneous injections. The benefits on the disease are modest.29 Abatacept is a recombinant fusion protein made up of the extracellular domain of CTLA-4 and Fc portion of human IgG1. This prevents the antigenpresenting cells from activating the T cells. Like antiTNF agents, abatacept has been shown to be effective in RA including patients refractory to methotrexate and anti-TNF agents.41 Rituximab, a chimeric anti-CD20 monoclonal antibody long used for the treatment of non-Hodgkin’s lymphoma, has been found to be effective in treating RA and has been approved for use. This is the only biologic agent approved for treatment of RA that targets the B cells.34,35 It should be pointed out that although these agents are very good in controlling the disease, we are not at a point of putting patients in remission. Thus, the disease flares when they are discontinued. In addition, we still encounter patients in whom these therapies fail. Several other immunomodulators are under study and likely will be available for use in the near future. These drugs have changed the outlook of this disease, and we are seeing a major change in the patient’s suffering and disability. This change will affect the need for surgical procedures, and ultimately, the economic impact on the individual as well as society.

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1034 Part VIII Septic and Nontraumatic Conditions

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Chapter 74 Rheumatoid Arthritis 1035

37. Fuchs, H. A., Kaye, J. J., Callahan, L. F., Nance, E. P., and Pincus, T.: Evidence of significant radiographic damage in rheumatoid arthritis within the first 2 years of disease. J. Rheum. 16:585, 1989. 38. Furst, D.: Cyclosporine, leflunomide and nitrogen mustard. Bull. Clin. Rheumatol. 9:711, 1995. 39. Furst, G. P., Gerber, L. H., Smith, C. C., Fisher, S., and Shulman, B.: A program for improving energy conservation behaviors in adults with rheumatoid arthritis. Am. J. Occup. Ther. 41:102, 1987. 40. Ganz, S. B., and Harris, L. L.: General overview of rehabilitation in the rheumatoid patient. Rheum. Dis. Clin. North Am. 24:181, 1998. 41. Genovese, M. C., Becker, J. C., Schiff, M., Luggen, M., Sherrer, Y., Kremer, J., Birbara, C., Box, J., Natarajan, K., Nuamah, I., Li, T., Aranda, R., Hagerty, D. T., and Dougados, M.: Abatacept for rheumatoid arthritis refractory to tumor necrosis factor alpha inhibition. N. Engl. J. Med. 353:1114, 2005. 42. Gibson, T.: Nonsteroidal anti-inflammatory drugs: Another look. Br. J. Rheumatol. 27:87, 1988. 43. Gilligan, D. M., O’Connor, C. M., Ward, K., Moloney, D., Bresnihan, B., and FitzGerald, M. X.: Bronchoalveolar lavage in patients with mild and severe rheumatoid lung disease. Thorax 45:591, 1990. 44. Glick, E. N.: Asymmetrical rheumatoid arthritis after poliomyelitis. B. M. J. 3:26, 1967. 45. Goronzy, J. J., and Weyand, C. M.: Interplay of T lymphocytes and HLA-DR molecules in rheumatoid arthritis. Curr. Opin. Rheumatol. 5:169, 1993. 46. Gregersen, P. K., Silver, J., and Winchester, R. J.: The shared epitope hypothesis: An approach to understanding the molecular genetics of susceptibility to rheumatoid arthritis. Arthritis Rheum. 30:1205, 1987. 47. Guidelines for the Management of Rheumatoid Arthritis. American College of Rheumatology Ad Hoc Committee on Clinical Guidelines. Arthritis Rheum. 39:713, 1996. 48. Gulko, P. S., Kawahito Y., Remmers E. F., Reese, V. R., Wang, J., Dracheva, S. V., Ge, L., Longman, R. E., Shepard, J. S., Cannon, G. W., Sawitzke, A. D., Wilder, R. L., and Griffiths, M. M.: Identification of a new non-major histocompatibility complex genetic locus on chromosome 2 that controls disease severity in collagen-induced arthritis in rats. Arthritis Rheum. 41:2122, 1998. 49. Hasty, K. A., Reife, P. A., Kang, A. H., and Stuart, J. M.: The role of stromelysin in the cartilage destruction that accompanies inflammatory arthritis. Arthritis Rheum. 33:388, 1990. 50. Ho. C. P., and Sartoris, D. J.: Magnetic resonance imaging of the elbow. Rheum. Dis. Clin. North Am. 17:705, 1991. 51. Ippolito, J. A., Palmer, L., Spector, S., Kane, P. B., and Gorevic, P. D.: Bronchiolitis obliterans organizing pneumonia and rheumatoid arthritis. Semin. Arthritis Rheum. 23:70, 1993. 52. Jawaheer, D., Thomson, W., MacGregor, A. J., Carthy, D., Davidson, J., Dyer, P. A., Silman, A. J., and Ollier, W. E.: “Homozygosity” for the HLA-DR shared epitope contributes the highest risk for rheumatoid arthritis concordance in identical twins. Arthritis Rheum. 37:681, 1994.

53. Jongen-Lavrencic, M., Peeters, H. R., Wognum, A., Vreugdenhil, G., Breedreld, F. C., and Swaak, A. J.: Elevated levels of inflammatory cytokines in bone marrow of patients with rheumatoid arthritis and anemia of chronic disease. J. Rheumatol. 24:1504, 1997. 54. Kamio, N., Kuramochi, S., Wang, R. J., Hirose, S., and Hosoda, Y.: Rheumatoid arthritis complicated by pachy- and leptomeningeal rheumatoid nodule-like granulomas and systemic vasculitis. Pathol. Int. 46:526, 1996. 55. Kasdan, M. L., and June, L.: Postoperative results of rheumatoid arthritis patients on methotrexate at the time of reconstructive surgery of the hand. Orthopedics 16:1233, 1993. 56. Kennedy, W. P., Partridge, R. E., and Matthews, M. B.: Rheumatoid pericarditis with cardiac failure treated by pericardiectomy. Br. Heart J. 28:602, 1966. 57. Kopp, E., and Ghosh, S.: Inhibition of NF-kB by sodium salicylate and aspirin. Science 265:956, 1994. 58. Kremer, J. M., Alarcon, G. S., Lightfoot, R. W., Jr., Willkens, R. F., Furst, D. E., Williams, H. J., Dent, P. B., and Weinblatt, M. E.: Methotrexate for rheumatoid arthritis: Suggested guidelines for monitoring liver toxicity. American College of Rheumatology [see comments]. Arthritis Rheum. 37:316, 1994. 59. Lard, L. R., Visser, H., Speyer, I., vander Horst-Bruinsma, I. E., Zwinderman, A. H., Breedveld, F. C., and Hazes, J. M.: Early versus delayed treatment in patients with recent-onset rheumatoid arthritis: comparision of two cohorts who received different treatment strategies. Am. J. Med. 111:446, 2001. 60. Leroux, J. Y., Poole, A. R., Webber, C., Vipparti, V., Choi, H. U., Rosenberg, L. C., and Bannerjee, S.: Characterization of proteoglycan-reactive T cell lines and hybridomas from mice with proteoglycan-induced arthritis. J. Immunol. 148:2090, 1992. 61. Levine, J. D., Goetzl, E. J., and Basbaum, A. I.: Contribution of the nervous system to the pathophysiology of rheumatoid arthritis and other polyarthritides. Rheum. Dis. Clin. North Am. 13:369, 1987. 62. Lipsky, P. E.: Progress toward a new class of therapeutics: Selective COX-2 inhibition. J. Rheumatol. 24(Suppl. 49):1, 1997. 63. Luthra, H. S.: Felty’s syndrome: A therapeutic dilemma? [editorial] [see comments]. J. Rheumatol. 16:864, 1989. 64. Maini, R., and Feldman, M.: Immunopathogenesis of rheumatoid arthritis. In Maddison, P. J., Isenberg, D. A., Woo, P., and Glass, D. N. (eds.): Oxford Textbook of Rheumatology. Oxford, Oxford University Press, 1998, p. 983. 65. Masi, A. T.: Articular patterns in the early course of rheumatoid arthritis. Am. J. Med. 75:16, 1983. 66. Massardo, L., Jacobelli, S., Rodriguez, L., River, S., Gonzalez, A., and Naschetti, R.: Weak association between HLADR4 and rheumatoid arthritis in Chilean patients. Ann. Rheum. Dis. 49:290, 1990. 67. McCurley, T. L., and Collins, R. D.: Intestinal infarction in rheumatoid arthritis: Three cases due to unusual obliterative vascular lesions. Arch. Pathol. Lab. Med. 108:125, 1984.

1036 Part VIII Septic and Nontraumatic Conditions

68. McDonagh, J., Greaves, M., Wright, A. R., Heycock, C., Owen, J. P., and Kelly, C.: High-resolution computed tomography of the lungs in patients with rheumatoid arthritis and interstitial lung disease [see comments]. Br. J. Rheumatol. 33:118, 1994. 69. Means, R. T., and Krantz, S. B.: Progress in understanding the pathogenesis of the anemia of chronic disease. Blood 80:1639, 1992. 70. Mercuriali, F., Gualtieri, G., Sinigaglia, L., Inghilleri, G., Biffi, E., Vinci, A., Colotti, M. T., Barosi, G., and Lambertengh Deliliers, G.: Use of recombinant human erythropoietin to assist autologous blood donation by anemic rheumatoid arthritis patients undergoing major orthopedic surgery. Transfusion 34:501, 1994. 71. Mercuriali, F.: Epotein alfa for autologous blood donation in patients with rheumatoid arthritis and concomitant anemia. Semin. Hematol. 33(2 Suppl 2):18, discussion 21, 1997. 72. Mitchell, D. M., Spitz, P. W., Young, D. Y., Bloch, D. A., McShane, D. J., and Fries, J. F.: Survival, prognosis, and causes of death in rheumatoid arthritis. Arthritis Rheum. 29:706, 1986. 73. Mitchell, J. A., Akarasereenont, P., Thiemermann, C., Flower, R. J., and Vane, J. R.: Selectivity of non-steroidal anti-inflammatory drugs as inhibitors of constitutive and inducible cyclooxygenase. Proc. Natl. Acad. Sci. U. S. A. 90:11693, 1994. 74. Mladenovic, V., Domljan, Z., Rozman, B., Jajic, I., Mihajlovic, D., Dordevic, J., Popovic, M., Dimitrijevic, M., Zivkovic, M., Campion, G., et al.: Safety and effectiveness of leflunomide in the treatment of patients with active rheumatoid arthritis. Arthritis Rheum. 38:1595, 1995. 75. Morales-Torres, J.: Antiquity of rheumatoid arthritis. In Hochberg, M. C., Silman, A. J., Smolen, J. S., Weinblatt, M. E., and Weissman, M. H. (eds.): Rheumatology, 4th ed. St. Louis, Mosby Elsevier, 2008. 76. Moreland, L. W., Baumgartner, S. W., Schiff, M. H., Tindall, E. A., Fleischmann, R. M., Weaver, A. L., Ettlinger, R. E., Cohen, S., Koopman, W. J., Mohler, K., Widmer, M. B., and Blosch, C. M.: Treatment of rheumatoid arthritis with a recombinant human tumor necrosis factor receptor (p75) fusion protein. N. Engl. J. Med. 337:141, 1997. 77. Mulherin, D., Skelly, M., Saunders, A., McCarthy, D., O’Donoghue, D., Fitzgerald, O., Bresnihan, B., and Mulcahy, H.: The diagnosis of iron deficiency in patients with rheumatoid arthritis and anemia: An algorithm using simple laboratory measures [see comments]. J. Rheumatol. 23:237, 1996. 78. Myllykangas-Luosujarvi, R. A., Aho, K., and Isomaki, H. A.: Mortality in rheumatoid arthritis. Semin. Arthritis Rheum. 25:193, 1995. 79. Nabozny, G. H., Baisch, J. M., Cheng, S., Cosgrove, D., Griffiths, M. M., Luthra, H. S., and David, C. S.: HLA-DQ8 transgenic mice are highly susceptible to collagen-induced arthritis: A novel model for human polyarthritis. J. Exp. Med. 183:27, 1996. 80. Needleman, P., and Isakson, P. C.: The discovery and function of COX-2. J. Rheumatol. 24(Suppl 49):6, 1997. 81. Nepom, G. T., Byers, P., Seyfried, C., Healey, L. A., Wilske, K. R., Stage, D., and Nepom, B. S.: HLA genes associated

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98. Rodnan, G. P., and Benedek, T. G.: The early history of antirheumatic drugs. Arthritis Rheum. 13:145, 1970. 99. Rosner, I.: Rheumatoid-like arthritis associated with hepatitis. C. J. Clin. Rheumat. 1:182, 1995. 100. Rothschild, B. M., and Woods, R. J.: Does rheumatoid polyarthritis come from the New World? Rev. Rhum. Maladies Osteo-Articulaires. 57:271, 1990. 101. Rothschild, B. M., and Woods, R. J.: Symmetrical erosive disease in Archaic Indians: The origin of rheumatoid arthritis in the New World? Semin. Arthritis Rheum. 19:278, 1990. 102. Rothschild, B. M., Turner, K. R., and DeLuca, M. A.: Symmetrical erosive peripheral polyarthritis in the Late Archaic Period of Alabama. Science 241:1498, 1988. 103. Rothschild, B. M., Woods, R. J., Rothschild, C., and Sebes, J. I.: Geographic distribution of rheumatoid arthritis in ancient North America: Implications for pathogenesis [see comments]. Semin. Arthritis Rheum. 22:181, 1992. 104. Saag, K. G., Kolluri, S., Koehnke, R. K., Georgou, T. A., Rachow, J. W., Hunninghake, G. W., and Schwartz, D. A.: Rheumatoid arthritis lung disease: Determinants of radiographic and physiologic abnormalities. Arthritis Rheum. 39:1711, 1996. 105. Sakai, K., Matsuno, H., Tsuji, H., and Tohyama, M.: Substance P receptor (NK1) gene expression in synovial tissue in rheumatoid arthritis and osteoarthritis. Scand. J. Rheumatol. 27:135, 1998. 106. Sattar, M. A., al-Saffar, M., Guindi, R. T., Sugathan, T. N., White, A. G., and Behloehari, K.: Histocompatibility antigens (A, B, C, and DR) in Arabs with rheumatoid arthritis. Dis. Markers 8:11, 1990. 107. Seibert, K., Zhang, Y, Leahy, K., Hauser, S., Masferrer, J., Perkins, W., Lee, L., and Isakson, P.: Pharmacological and biochemical demonstration of the role of cyclooxygenase 2 in inflammation and pain. Proc. Natl. Acad. Sci. U. S. A. 91:12013, 1994. 108. Shapiro, J. S.: A new factor in the etiology of ulnar drift. Clin. Orthoped. Rel. Res. 68:32, 1970. 109. Short, C. L.: The antiquity of rheumatoid arthritis. Arthritis Rheum. 17:193, 1974. 110. Silman, A. J.: Epidemiology of rheumatoid arthritis. Apmis 102:721, 1994. 111. Silman, A. J.: Parity status and the development of rheumatoid arthritis. Am. J. Reprod. Immunol. (Copenhagen) 28:228, 1992. 112. Silman, A. J., and Hochberg, M. C.: Epidemiology of the Rheumatic Diseases. Oxford, Oxford University Press, 1993. 113. Silman, A. J., Newman, J., and MacGregor, A. J.: Cigarette smoking increases the risk of rheumatoid arthritis: Results from a nationwide study of disease-discordant twins [see comments]. Arthritis Rheum. 39:732, 1996. 114. Silverstein, F. E., Graham, D. Y., Senior, J. R., Davies, H. W., Struthers, B. J., Bittman, R. M., and Geis, G. S.: Misoprostol reduces serious gastrointestinal complications in patients with rheumatoid arthritis receiving nonsteroidal anti-inflammatory drugs. Ann. Intern. Med. 123:241, 1995. 115. Sims-Williams, H., Jayson, M. I., and Baddeley, H.: Rheumatoid involvement of the lumbar spine. Ann. Rheum. Dis. 36:524, 1977.

116. Smith, R. D., and Polley, H. F.: Rest therapy for rheumatoid arthritis. Mayo Clin. Proc. 53:141, 1978. 117. Smyth, C. J.: Therapy of rheumatoid arthritis: A pyramidal plan. Postgrad. Med. 51:31, 1972. 118. Sokoloff, L., McCluskey, R., and Bunim, J.: Vascularity of the early subcutaneous nodule of rheumatoid arthritis. Arch. Pathol. Lab. Med. 355:475, 1953. 119. Starkebaum, G.: Role of cytokines in rheumatoid arthritis. Science Med. 5:6, 1998. 120. Stastny, P.: The association of B-cell alloantigen DRw4 with rheumatoid arthritis. N. Engl. J. Med. 298:869, 1978. 121. Stastny, P., Ball, E. J., Khan, M. A., Olsen, N. J., Pincus, T., and Gao, X.: HLA-DR4 and other genetic markers in rheumatoid arthritis. Br. J. Rheumatol. 27(Suppl 2):132, 1988. 122. St. Clair, E. W., van der Heijde, D. M., Smolen, J. S., Maini, R. N., Bathon, J. M., Emery, P., Keystone, E., Schiff, M., Kalden, J. R., Wang, B., Dewoody, K., Weiss, R., and Baker, D.; Active-Controlled Study of Patients Receiving Infliximab for the Treatment of Rheumatoid Arthritis of Early Onset Study Group: Combination of infliximab and methotrexate therapy for early rheumatoid arthritis: a randomized, controlled trial. Arthritis Rheum 50:3432, 2004. 123. Swezey, R. L., and Fiegenberg, D. S.: Inappropriate intrinsic muscle action in the rheumatoid hand. Ann. Rheum. Dis. 30:619, 1971. 124. Thompson, M., and Bywaters, E. G. L.: Unilateral rheumatoid arthritis following hemiplegia. Ann. Rheum. Dis. 21:370, 1962. 125. Vandenbroucke, J. P., Hazevoet, H. M., and Cats, A.: Survival and cause of death in rheumatoid arthritis: A 25-year prospective follow-up. J. Rheumatol. 11:158, 1984. 126. Wallberg-Jonsson, S., Ohman, M. L., and Dahlqvist, S. R.: Cardiovascular morbidity and mortality in patients with seropositive rheumatoid arthritis in Northern Sweden. J. Rheumatol. 24:445, 1997. 127. Walters, M. N., and Ojeda, V. J.: Pleuropulmonary necrobiotic rheumatoid nodules: A review and clinicopathological study of six patients. Med. J. Austral. 144:648, 1986. 128. Ward, M. M., Leigh, P., and Fries, J. F.: Progression of functional disability in patients with rheumatoid arthritis: Associations with rheumatology subspeciality care. Arch. Intern. Med. 153:2229, 1993. 129. Ward, M. M., Lubeck, D., and Leigh, J. P.: Long-term health outcomes of patients with rheumatoid arthritis treated in managed care and fee-for-service practice settings [see comments]. J. Rheumatol. 25:641, 1998. 130. Weinblatt, M. E., Maier, A. L., Fraser, P. A., Coblyn, J. S.: Long-term prospective study of methotrexate in rheumatoid arthritis: Conclusion after 132 months of therapy. J. Rheumatol. 25:238, 1998. 131. Weinblatt, M. E., Polisson R., Blotner, S. D., Sosman, J. L., Aliabadi, P., Baker, N., and Weissman, B. N.: The effects of drug therapy on radiographic progression of rheumatoid arthritis: Results of a 36-week randomized trial comparing methotrexate and auranofin [published erratum

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138. Willkens, R. F., Nepom, G. T., Marks, C. R., Nettles, J. W., and Nepom, B. S.: Associations of HLA-Dw 16 with rheumatoid arthritis in Yakima Indians. Arthritis Rheum. 34:43, 1991. 139. Wilske, K. R.: Inverting the therapeutic pyramid: Observations and recommendations on new directions in rheumatoid arthritis therapy based on the author’s experience. Semin. Arthritis Rheum. 23(2 Suppl 1):11, 1993. 140. Wilske, K. R., and Healey, L. A.: Remodeling the pyramid: A concept whose time has come. J. Rheumatol. 16:565, 1989. 141. Winrow, V. R., Ragno, S., Morris, C. J., Colston, M. J., Mascagni, P., Leosi, F., Gromo, G., Coates, A. R., and Blake, D. R.: Arthritogenic potential of the 65 kDa stress protein: An experimental model. Ann. Rheum. Dis. 53:197, 1994. 142. Wollheim, F.: Rheumatoid arthritis: The clinical picture. In Maddison, P. J., Isenberg, D. A., Woo, P., and Glass, D. N. (eds.): Oxford Textbook of Rheumatology. 1998, Oxford, Oxford University Press, p. 1004. 143. Woolley, D. E., Crossley, M. J., and Evanson, J. M.: Collagenase at sites of cartilage erosion in the rheumatoid joint. Arthritis Rheum. 20:1231, 1977. 144. Yousem, S. A., Colby, T. V., and Carrington, C. B.: Lung biopsy in rheumatoid arthritis. Am. Rev. Respir. Dis. 131:770, 1985.

Chapter 75 Seronegative Inflammatory Arthritis 1039

CHAPTER

75

Seronegative Inflammatory Arthritis Nicole M. Orzechowski and Thomas G. Mason

INTRODUCTION Seronegative inflammatory arthritis refers to a group of conditions in which clinical evidence of noninfectious, active inflammation (Box 75-1) is noted in the joints, but serum autoantibodies, such as rheumatoid factor (RF) or anticyclic citrullinated peptide antibodies (antiCCP), are absent. RF is widely used as a diagnostic marker for rheumatoid arthritis (RA), despite its presence in other inflammatory and infectious conditions. RF can also be detected in some healthy individuals. In recent years, anti-CCP antibodies have been shown to be as sensitive as RF in the diagnosis of RA, but with greater specificity.9 Seventy-five to eighty percent of patients with RA are seropositive for these autoantibodies.9 Therefore, the term seronegative inflammatory arthritis excludes RA. Besides their distinction from RA, the seronegative inflammatory arthridites have several clinical features in common. They present with pain, limited motion and swelling of the affected joint, in the absence of trauma. When only one joint such as the elbow is initially involved, infection needs to be excluded. However, the elbow is often not the only diarthrodial joint involved in these conditions. For the purposes of this discussion, the seronegative inflammatory arthridites will include spondyloarthropathies, crystalline arthropathies, and adult Still’s disease (Box 75-2).

SPONDYLOARTHROPATHIES Spondyloarthropathies (SpA) are a group of inflammatory disorders that includes ankylosing spondylitis (AS), psoriatic arthritis, inflammatory bowel disease, and reactive arthritis, also known as Reiter’s syndrome. They share an increased prevalence of the human leukocyte antigen class I molecule B-27. Classically, the

spondyloarthropathies manifest as an inflammatory arthritis of the spine and sacroiliac joints, but an asymmetric peripheral arthritis can occur as well. A key clinical feature distinguishing SpA from RA is the presence of enthesitis. Enthesitis refers to inflammation that is located at the sites of ligamentous insertion into bone, such as the Achilles tendon or plantar fascia. Table 75-1 illustrates several clinical differences between the SpA and RA. The relative frequency of elbow involvement in the SpA is shown in Table 75-2. Aspiration of the elbow and subsequent synovial fluid (SF) analysis may be necessary to exclude infection in some cases, especially in monoarthritis. The injection of corticosteroids, such as triamcinolone and local anesthetic, into the joint space may also offer pain relief, and facilitate improvements in range of motion and overall joint function for patients with SpA. Nonsteroidal anti-inflammatory drugs (NSAIDs) are the cornerstone of medical management of spondyloarthropathies. They reduce inflammatory features, and reduce joint pain and stiffness. The most common adverse events with the use of NSAIDs are gastrointestinal, and range from dyspepsia in 10% to 20% of patients to serious bleeding or gastroduodenal perforation in 7.3 to 13/1000 patients per year.10 If patients with SpA do not tolerate NSAIDs, are refractory to therapy, or have evidence of active disease or radiographic progression, the use of additional or alternative medications is indicated. These include sulfasalazine (SUSP) and methotrexate (MTX), which down-regulate the inflammatory activity that is associated with these conditions. Such medications require careful monitoring for potential adverse events, including increased risk for infection, hematologic abnormalities, and hepatotoxicity. For this reason, they should be prescribed and monitored only by physicians experienced in their administration. If desired clinical outcomes are not achieved with NSAIDs, SUSP, or MTX, patients with spondyloarthropathies may be candidates for a new class of medications commonly referred to as biologics. Recently developed, they are monoclonal antibodies that bind to tumor necrosis factor-α, an important cytokine in the inflammatory pathway. These powerful medications can be associated with dramatic clinical improvements in patients with refractory spondyloarthropathies. Again, these medications should be administered and monitored under the guidance of a rheumatologist.

CRYSTALLINE ARTHROPATHIES Crystalline arthropathies are a group of inflammatory arthritides associated with crystal deposition in the synovial space. The primary conditions included in this

1040 Part VIII Septic and Nontraumatic Conditions

BOX 75-1 • • • •

Features of Inflammation

BOX 75-2

Pain Erythema Swelling Warmth

TABLE 75-1

Seronegative Inflammatory Arthritis

• Spondyloarthropathies a. Ankylosing spondylitis b. Inflammatory bowel disease c. Psoriatic arthritis d. Reactive arthritis • Crystalline arthropathies a. Gout b. Pseudogout • Adult Still’s disease

Clinical Differences Between Spondyloarthropathies and Rheumatoid Arthritis

Feature

Spondyloarthropathies

Rheumatoid Arthritis

Pattern of peripheral joint involvement

Asymmetric

Symmetric

Sacroiliac joint involvement

Very common

Rare

Lumbar spine involvement

Very common

Rare

Rheumatoid factor and CCP antibody

Rare

Very common

Predominant inflammation

Enthesitis

Synovitis

HLA association

HLA B-27

HLA DR

Extra-articular features

Mucositis, uveitis, IBD, psoriasis, dysuria

Nodules, vasculitis, lung disease, Sjögren’s syndrome

CCP, cyclic citrullinated peptide; HLA, human leukocyte antigen; IBD, irritable bowel disease.

TABLE 75-2

Elbow Involvement in Spondyloarthropathies

Spondyloarthropathy

Frequency of Elbow Involvement

Radiographic Appearance

Ankylosing spondylitis

12%7

Joint space narrowing, demineralization and periostitis

Psoriatic arthritis

25%

5

Erosive disease common

6

Inflammatory bowel disease

35%

Nonerosive, nondeforming

Reactive arthritis

Uncommon

Similar to psoriatic arthritis

group are gout and pseudogout. Patients frequently present with an acute painful monoarthritis, which often is indistinguishable from septic arthritis. Timely aspiration to rule out infection and SF analysis to confirm the diagnosis is essential. The relative frequency of elbow involvement in crystalline arthropathies is shown in Table 75-3. Gout is a common condition associated with the deposition of monosodium urate (MSU) crystals in the SF and synovial tissue. MSU crystals are by-products of an aberrant uric acid metabolism. Risk factors for gout include hypertension, renal insufficiency, obesity, type 2 diabetes mellitus, ethanol intake, lead exposure, and the use of diuretics, particularly thiazide diuretics.2 The diagnosis is confirmed by finding the presence of the MSU crystals in SF under polarizing microscopy. Frequently,

Elbow Involvement in Crystalline Arthropathies

TABLE 75-3

Crystalline Arthropathy

Frequency of Elbow Involvement

Gout

17-33%1,4

Often accompanied by olecranon bursitis or tophi

Pseudogout

16%8

Usually post-traumatic

Comments

but not always, serum uric acid levels may be elevated during an acute gout attack. MSU crystals are long, needle-shaped, and demonstrate strong negative birefringence under compensated polarized light. That is, they appear bright yellow under

Chapter 75 Seronegative Inflammatory Arthritis 1041

the polarizing microscope. During an attack of gout, MSU crystals are often found within white blood cells from synovial fluid. If a tophus is aspirated and examined, the crystals are often found outside the cells as well. Pseudogout is another crystalline arthropathy characterized by an acute monoarthritis, similar to, but often more insidious, than acute gout. The diagnosis of pseudogout is made when calcium pyrophosphate (CPPD) crystals are deposited in the joint. Most CPPD crystal formation is associated with degenerative joint disease. In contrast to MSU crystals, CPPD crystals are rhomboid shaped and exhibit positive birefringence under compensated polarized light, appearing blue. They also can be intracellular or extracellular but are more difficult to identify than MSU crystals because they are smaller and much less bright. In addition, low concentration of CPPD crystals in synovial fluid can lead to a falsenegative report. Treatment of acute gout focuses on excluding infection and confirming the diagnosis. Acute medical therapies include NSAIDs, a brief course of oral corticosteroid (<10 days), intra-articular corticosteroid injection, or oral colchicine. Often the treatment for acute gout depends on minimizing risk of adverse events because one treatment is not clearly superior to another. A key principle is to avoid a rapid change in the serum uric acid level during an acute attack. Management of chronic gout focuses on carefully lowering serum uric acid levels. Medications that facilitate the excretion of uric acid, such as probenecid, may be used. More often, medications that decrease uric acid production, such as allopurinol are used. Consistent with the principle of not changing the uric acid level during an acute attack, the initiation of allopurinol is not indicated during an acute attack of gout. Rather, it should be started at least 2 months, if possible, after an acute attack has resolved, and dosed according to the patient’s creatinine clearance. As with the treatment of SpA, these medications should be administered and monitored by a physician familiar with them. Patients with chronic gout may develop tophi. Tophi are deposits of MSU crystals in the subcutaneous tissues, which are often very painful. The olecranon bursa is a frequent location for tophi in patients with chronic gout. Figure 75-1 depicts such an example. A radiograph of a patient with tophaceous gout is seen in Figure 75-2. As mentioned previously, an acute pseudogout attack presents clinically in a similar manner to an acute gout attack. It is not surprising then, that the treatment is almost identical and includes NSAIDs, a short course of oral corticosteroid or an intra-articular corticosteroid injection. In the workup after an initial pseudogout episode, metabolic abnormalities of calcium metabolism should be excluded. Between acute episodes, physicians

FIGURE 75-1

Olecranon bursitis with tophi in a 68-yearold man. Acute olecranon bursitis is a very common clinical manifestation of gout. Often this presentation is rather dramatic and may be a common location for tophi as well.

FIGURE 75-2

Radiograph of right elbow demonstrating soft tissue swelling and erosion of the olecranon consistent with gout. (Courtesy of R.G. Swee, M.D.)

should address degenerative joint disease that is often associated with pseudogout.

ADULT STILL’S DISEASE Adult Still’s disease (ASD) is a rare form of seronegative inflammatory arthritis. It shares many clinical features with systemic-onset juvenile RA, which accounts for

1042 Part VIII Septic and Nontraumatic Conditions

about 10% of the cases of juvenile RA. Hallmarks of ASD are its extra-articular features including high fever, rash, adenopathy and serositis, and the absence of autoantibodies. ASD can potentially cause a destructive arthritis. The frequency of elbow involvement in chronic ASD ranges from 4% to 44%.3,11 The diagnosis of ASD is frequently made in the clinical setting of a fever of unknown origin. Clinical and exclusion criteria are described in Table 75-4.12 The characteristic salmon-colored evanescent maculopapular rash of ASD is frequently observed at the time of the fever spikes and tends to be located on the trunk. The fevers are more prominent during the afternoon and evening hours as depicted in Figure 75-3. Treatment of the arthritis of ASD resembles the treatment of RA. Typically NSAIDs and oral corticosteroids are used to treat arthritis, fever, and constitutional Criteria for Diagnosing Adult Still’s Disease (ASD)

TABLE 75-4

Major Criteria

Minor Criteria

Exclusion Criteria

Arthralgia >2 weeks

Sore throat

Infection

Temperature >39°C, intermittent, ≤1 week

Lymphadenopathy and/or splenomegaly

Malignancy Rheumatic diseases

Typical rash

Abnormal liver function tests

WBCs >10,000/L (>80% granulocytes)

Negative ANA and RF

ANA, antinuclear antibody text; RF, rheumatoid factor; WBC, white blood cells. *Diagnosis of ASD requires five criteria, at least two major. Data from Yamaguchi, M., Ohta, A., Tsunematsu, T., Kasukawa, R., Mizushima, Y., Kashiwagi, H., Kashiwazaki, S., Tanimoto, K., Matsumoto, Y., Ota, T., and Akizuki, M.: Preliminary criteria for classification of adult Still’s disease. J. Rheumatol. 19:424, 1992. 40

Temperature (C)

39 38 37 36 35 8a 4p mn 8a 4p mn 8a 4p mn 8a 4p mn 8a 4p mn 8a Time

FIGURE 75-3

Fever curve in adult Still’s disease demonstrating late afternoon and evening peaks.

symptoms. MTX may be used to help reduce the need for systemic steroids.

SUMMARY Seronegative inflammatory arthritides are common conditions that can involve the elbow. Frequently, arthrocentesis and synovial fluid analysis are needed to exclude the possibility of infection. Once infection is excluded, a specific diagnosis is confirmed either by documenting the presence of crystals in synovial fluid or by recognition of characteristic clinical features. Medical therapies are based on careful assessment of prognosis and riskbenefit ratio.

References 1. Barthelemy, C. R., Nakayama, D. A., Carrera, G. F., Lightfoot, R. W. Jr., and Wortmann, R. L.: Gouty arthritis: a prospective radiographic evaluation of sixty patients. Skeletal Radiol 11:1, 1984. 2. Choi, H.: Epidemiology of crystal arthropathy. Rheum. Dis. Clin. N. Am. 32:255, 2006. 3. Efthimiou, P., Paik, P. K., and Bielory, L.: Diagnosis and management of adult onset Still’s disease. Ann. Rheum. Dis. 65:564, 2006. 4. Hadler, N. M., Franck, W. A., Bress, N. M., and Robinson, D. R.: Acute polyarticular gout. Am. J. Med. 56:715, 1974. 5. McHugh, N. J., Balachrishnan, C, and Jones, S. M.: Progression of peripheral joint disease in psoriatic arthritis: a 5-yr prospective study. Rheumatology (Oxford) 42:778, 2003. 6. Orchard, T. R., Wordsworth, B. P., and Jewell, D. P.: Peripheral arthropathies in inflammatory bowel disease: their articular distribution and natural history. Gut 42:387, 1998. 7. Resnick, D.: Patterns of peripheral joint disease in ankylosing spondylitis. Radiology 110:523, 1974. 8. Resnick, D., Niwayama, G., Goergen, T. G., Utsinger, P. D., Shapiro, R. F., Haselwood, D. H., and Wiesner, K. B.: Clinical, radiographic and pathologic abnormalities in calcium pyrophosphate dihydrate deposition disease (CPPD): pseudogout. Radiology 122:1, 1977. 9. van Boekel, M. A., Vossenaar, E. R., van den Hoogen, F. H., and van Venrooij, W. J.: Autoantibody systems in rheumatoid arthritis: specificity, sensitivity and diagnostic value. Arthritis Res 4:87, 2002. 10. Wolfe, M. M., Lichtenstein, D. R., and Singh, G.: Gastrointestinal toxicity of nonsteroidal antiinflammatory drugs. N. Engl. J. Med. 340:1888, 1999. 11. Wouters, J. M., and van de Putte, L. B.: Adult-onset Still’s disease; clinical and laboratory features, treatment and progress of 45 cases. Q. J. Med. 61:1055, 1986. 12. Yamaguchi, M., Ohta, A., Tsunematsu, T., Kasukawa, R., Mizushima, Y., Kashiwagi, H., Kashiwazaki, S., Tanimoto, K., Matsumoto, Y., Ota, T., and Akizuki, M.: Preliminary criteria for classification of adult Still’s disease. J. Rheumatol. 19:424, 1992.

Chapter 76 Primary Osteoarthritis: Ulnohumeral Arthroplasty 1043

Primary Osteoarthritis: Ulnohumeral Arthroplasty

Primary osteoarthritis of the elbow has been reported as accounting for 1% to 2% of patients presenting with elbow arthritis.7,18 This is consistent with the observation that less than 5% of joint replacement is performed in patients with this diagnosis.24,37 Doherty and Preston10 reported an incidence of about 7% from a typical rheumatologic practice and was shown to be associated with other sites of involvement, especially of the hand (Fig. 76-1). Because of these features, recognition of the entity is still sometimes overlooked or misinterpreted as a post-traumatic condition.11

Bernard F. Morrey

CLINICAL PRESENTATION

CHAPTER

76

INTRODUCTION Primary degenerative arthritis of the elbow is now well recognized and readily treated. Even today, the studies to better understand the condition are limited. Articular cartilage changes at the distal humerus40 and proximal radius with aging have been observed and studied.15 More recent experience with this condition has clarified to some extent the etiology and presentation, but the greatest advances are in the treatment of this disease.*

INCIDENCE AND ETIOLOGY The existence of degenerative arthritis of the elbow has been recognized by orthopedic surgeons in the past, but the etiology was generally believed to be secondary to unrecognized or repetitive trauma. The radiographic characteristics have, however, been carefully delineated by Mianami et al in 1977.29 Furthermore, demographic studies have shown dramatic differences in the incidence of elbow arthritis in different races, but it is unclear if this is due to a genetic or an environmental influence.43 Smith50 clearly identified a condition that he termed osteoarthritis as a sequelae to trauma such as fracturedislocation or “hard usage.” In fact, the condition as an overuse manifestation is rather well recognized,3,17,32 yet only brief references to the condition are noted in the standard texts.33,50 In addition to an increased awareness, there is some evidence that the actual incidence of the disease may be increasing.8 When discussed, it is thought to be related to a single or repetitive traumatic event or other predisposing conditions such as osteochondritis dissecans.21,50,57 We concur with this opinion as a cause, at least in some.

*See references 4, 8, 10, 11, 19, 26, 29, 31, 34, 36, 38, 47, and 51.

Men are, by far, more commonly affected with this condition than women at a ratio of about 4 to 1.11,19,29,31,38 The age at initial presentation is about 50 years,10 but I and others have observed a surprising variation ranging from 20 to 65 years.31,38 Occupations or avocations involving the repetitive use of an extremity are the most common factors, being present in about 60% of patients. We have diagnosed this problem in persons with neuropathic conditions causing impaired ambulation and requiring continued use of crutches or a wheelchair. The dominant extremity is involved in about 80% to 90% of patients, and bilateral involvement is present in 25% to 60%.10,38 The radiohumeral joint is involved in about 85%, but it may not be symptomatic.8 Stiffness may be a dominant feature.10 Loss of extension is the most common problem prompting medical attention, but mild to occasional moderate pain is also commonly present. The characteristic pain is of terminal extension in almost all patients and of terminal flexion in about 50%. Less commonly, symptoms are present throughout the arc. The intensity of pain is mild to moderate, and only occasionally is the process described as severe. The radiohumeral joint may be symptomatic in flexion, extension, and rotation. Consistent with these features, examination reveals an arc of motion that averages about 30 to 120 degrees (Fig. 76-2). Forearm rotation is not restricted or only minimally so because the radiohumeral joint is typically not severely involved. Because of excessive osteophyte formation, ulnar nerve irritation is observed in at least 10%31 and we suspect in a higher number if carefully examined. Ulnar nerve involvement should be specifically sought in the examination because it may influence treatment decisions and even long-term outcome.1

LABORATORY STUDIES Because the diagnosis is not obvious owing to its relative infrequent occurrence, arthrocentesis, synovial biopsy,

1044 Part VIII Septic and Nontraumatic Conditions

SYMPTOMS

and arthroscopy have all been performed to diagnose this condition.11,39 When one is familiar with the disease, it comes as no surprise that all three of these diagnostic studies offer little if any added value.10,38 The roentgenographic study is diagnostic, and typically no other assessment is indicated or required. The sedimentation rate is normal.

RADIOGRAPHS 1

16

16

RADIOGRAPHIC FEATURES 4

1

5 CMCJ

5

10 MPJ 2 IPJ

7

3

6

1

5

FIGURE 76-1

3

Relative incidence of primary osteoarthritis of the elbow referable to the other joints. (Redrawn from Doherty, M.: Primary osteoarthritis of the elbow. Ann. Rheum. Dis. 48:743, 1989.)

FIGURE 76-2

The roentgenographic features of this condition are classic and characteristic, maybe even monotonous. The characteristic of primary osteoarthritis of the elbow is “marginal osteophyte formation.” Hence, the consistent routine anteroposterior and lateral roentgenograms reveal an anterior osteophyte of the coronoid and a posterior osteophyte of the olecranon process (Fig. 76-3).29 The anteroposterior view also shows a consistent finding of ossification and osteophyte formation in the olecranon or coronoid fossa (Fig. 76-4). In the later stages, no other study is required to make this diagnosis. However, tomography may show subtle osteophyte formation, the presence and location of loose bodies, and the size and extent of the osteophytes on the humerus and ulna (Fig. 76-5). Involvement of the radial head has been documented in about 85%.8 Bell and Minami et al2,31 have characterized the development of loose bodies as an integral feature of primary arthritis of the elbow. Special imaging studies are not needed and are of no value to diagnose this condition. A cubital tunnel view is sometimes obtained if the ulnar nerve shows signs of

A and B, Primary elbow arthrosis usually presents with loss of extension in men older than 40 years of age. Most often flexion and extension are in the functional range.

Chapter 76 Primary Osteoarthritis: Ulnohumeral Arthroplasty 1045

FIGURE 76-3

Typical lateral roentgenogram of primary osteoarthritis of the elbow demonstrating the almost monotonous pattern of osteophytes of the coronoid and olecranon processes.

FIGURE 76-5

Lateral tomogram showing minimal hypertrophic radiographic changes, with a loose body both anteriorly and posteriorly.

ulnar neuritis. These features do reflect the clinical expression and provide a guideline to treatment.

TREATMENT NONOPERATIVE TREATMENT

FIGURE 76-4

Anteroposterior roentgenogram of the elbow demonstrating ossification of the olecranon fossa.

Symptomatic treatment is appropriate, especially in the early stages because symptoms are slowly progressive and well tolerated. Although anti-inflammatory agents may be of use, by the time the patient sees a surgeon, the clinical findings and functional limitations usually justify some intervention. This is in contrast with the experience of others in which nonoperative treatment appears appropriate and adequate.10 In addition to anti-inflammatory agents, in some instances a cortisone injection may be of value. One study, however, demonstrated that the use of hyaluronic acid was not effective in 18 patients treated with hyaluronic acid with the diagnosis of primary osteoarthritis of the elbow.54 The mean time to surgery from symptom onset is about 5 years. The most important feature of the initial treatment is to explain to the patient the cause of the pain and the natural history of the process, and to recommend activity modification. However, because this disorder is so often associated with one’s occupation, this advice usually goes unheeded or cannot be acted on. Avoiding pressure to the cubital tunnel is recommended if there are ulnar nerve symptoms.

1046 Part VIII Septic and Nontraumatic Conditions

the sample is relatively small (60 patients) with a mean follow-up of just more than 3 years, it is impressive that more than 90% of patients expressed satisfaction with relief of pain and the improved arc of motion in these recent studies is greater than 60 degrees. Hence,

OPERATIVE TREATMENT Several surgical options exist and are evoked depending on the dominant symptoms and radiographic change (Table 76-1). For the most part, débridement by arthroscopy or by arthrotomy is the treatment of choice, with or without ulnar nerve decompression. In some instances, symptomatic loose bodies will be the primary pathology or at least the primary complaint. Under these circumstances, simple arthroscopic removal of the loose bodies relieves the patient of their symptoms5,44 and, in some instances, may even improve motion up to 15 degrees.44

General Relationship of Major Symptoms with Preferred Treatment

TABLE 76-1

ARTHROSCOPY Arthroscopic Management Arthroscopic débridement of the elbow is discussed in Chapters 38 to 40; however, there have been a number of reports specifically discussing arthroscopic débridement in the face of primary osteoarthritis (Fig. 76-6).16,23,28 These studies are summarized in Table 76-2. Although

Dominant Symptom

Surgical Technique

Loose body

Arthroscopy

Extension loss Mild Moderate

Arthroscopy*/Column Column

Flexion loss

Column

Impingement Ulnar nerve symptoms

Ulnohumeral arthroplasty

Extensive motion loss Pain full arc; age >60

Total elbow replacement

*Based on experience.

Scope: Summary of the Recent Literature Regarding Arthroscopic Treatment for Primary Osteoarthritis

TABLE 76-2

Author

Savoie49 Krishnan Kelly

22

Total*

25

Yr

No

Radial Head Removed

1999

24

18

2007

11

2007

25

Pain %

Motion Improvement

Follow-up (mo)

Satisfaction (%)

All improved

81

32

100

?

All improved

73

26

100

0

100

10

21

67

90

100

<10

65 degrees

42 mo

97%

60

Pre

Post

*Not all primary degenerative joint disease.

FIGURE 76-6

Arthroscopic appearance of primary arthrosis of the radiohumeral joint.

Chapter 76 Primary Osteoarthritis: Ulnohumeral Arthroplasty 1047

arthroscopic débridement for primary osteoarthritis is emerging as a viable treatment option. In our opinion, the key elements to consider this option are 1. Expertise with arthroscopic surgery; 2. Familiarity with elbow pathology, specifically the pathology of primary osteoarthritis; 3. The extent the disease should not be too extensive, specifically the capacity of the joint should be such that a great deal of effort should not be expended in order to enter the joint and obtain visual landmarks; 4. The ulnar nerve should be asymptomatic; if it is not, arthroscopy can still be done but the ulnar nerve should be dealt with, in our opinion, with a specific open procedure, usually simple decompression is adequate and translocation is not necessary. 5. The postoperative regimen is important in these patients, just as it is for open procedures. 6. The ever-present potential for injury.

débridement procedure was originally described by Outerbridge and popularized and first reported by Kashiwagi in 1978. Simply stated, this débridement procedure removes bone from the ulnar and humeral articular margins, altering the joint and justifying the term arthroplasty. Modification of this technique by exposure, and trephine débridement, descriptively termed ulnohumeral arthroplasty (UHA), is my preferred treatment for the selected patient.38 Subsequently, there have been a number of articles from several sources documenting satisfactory outcomes of various débridement procedures. Most of these are termed the UHA, which is our preference or the O-K arthroplasty after the originators Outerbridge and Kashiwagi. I have also combined the UHA with the column procedure when an anterior débridement and capsular release is desirable (Fig. 76-7). In any event, Table 76-3 summarizes the outcomes of six studies comprising more than 160 patients.

Ulnohumeral Arthroplasty Both the radial and the ulnar nerve must be discussed with the patient and deciduously avoided during the procedure. Indication The indication for this procedure is a loose body or modest osteophye formation. Note: It requires expertise.

The contraindications for this procedure are prior ulnar nerve translocation in the patient and limited experience on the part of the surgeon.

Contraindication

Indications The indications for UHA are extensive ulnohumeral osteophytes, capsular contracture, and impingement pain, especially with ulnar nerve symptoms. Technique The patient is placed in the supine position, with a sandbag under the scapula. The arm is prepped and draped to allow free motion and brought across the chest with the patient rotated about 35 degrees.

Technique The technique for removal of loose bodies and for osseous and capsular débridement are described in detail in Chapters 38 to 40.

Results A summary of arthroscopic intervention is shown in Table 76-2. Two early reports by Redden and Stanley46 and Ogilvie-Harris et al40 provide the results of 12 and 21 patients, respectively. Overall, a successful result from a similar débridement technique is reported for all 33 patients with adequate surveillance. Improved results are observed in the more recent studies. The benefits include universal relief of most or some pain, elimination of locking, and slight improvement in motion at about 2 years.40,46 A rapid recovery was noted in both studies with minimal complications. However, the potential for significant nerve injury, especially with adjunctive débridement must be considered.

Open Joint Débridement A “house cleaning” procedure has long been recommended for arthritic elbow disease.50 A safe and effective

Anterior capsule release Coronoid osteophyte Posterior capsule release

Olecranon osteophyte

FIGURE 76-7

The concept of the column procedure. The anterior and posterior capsules are released. The anterior and posterior osteophytes are removed.

1048 Part VIII Septic and Nontraumatic Conditions

UHA: Summary of the Recent Literature Regarding the Intermediate Outcomes of Open Débridement for Osteoarthritis of the Elbow

TABLE 76-3

Pain

Yr

No

Radial Head

2004

17

No

100

12

32

>36 mo

94

2006

18

No

100

17

16

85

83

2004

16

No

100

6

20

20

87

Phillips

2003

20

No

—

—

20

75

85

Antuna1

2002

46

No

100

24

22

80

76

2001

36

—

—

—

—

39

81

100

15%

22 degrees

60 mo

83%

Author

Sarris48 Tashjian

52

Vingerhoeds 45

13

Foster

Total*

55

15

Pre

Post

Motion Improvement

Change T/Mo

Satisfaction (%)

A straight incision 4 cm distal and 8 cm proximal to the olecranon is made over the posterior aspect of the elbow. A medial flap is elevated and the ulnar nerve decompressed in situ. We only rarely translocate the nerve in this circumstance. The medial one half of the triceps attachment is elevated or the triceps is simply split in the mid line (Fig. 76-8). The tip of the olecranon and its osteophyte is removed. The olecranon fossa is opened with a trephine because this causes less debris and provides a more predictable and cleaner resection of the osteophytes than does a burr. The trephine is placed in the olecranon fossa with the curvature coincident with the concavity of the proximal aspect of the trochlea. The osteophytes, which are universally present in the olecranon fossa and which constitute an essential feature of the disease process, are removed, and the entire core of bone is removed from the olecranon to the coronoid fossa. This causes a through-and-through opening to the anterior joint. Note: The placement of the trephine is worthy of emphasis. If the trephine is placed too distal, the competence of the trochlea may be impaired (Fig. 76-9); if it is placed too lateral, the capitellum may be violated; and if it is placed too medial, the medial column may be weakened. The elbow is then flexed, and the coronoid osteophyte is brought into the foraminectomized coronoid fossa. A curved 7-mm osteotome is used to remove the anterior osteophyte from the coronoid. Any loose bodies are removed. The index finger is introduced through the defect, and the anterior compartment is inspected for any remaining loose bodies. A contracted anterior capsule can only be partially released. A Gelfoam sponge is rolled and placed in the defect of the foramen to avoid osteophyte recurrence.

If greater than 50% of the triceps has been detached, it is reattached with a nonabsorbable suture placed through bone, and the wound is closed. I have yet to remove the radial head as an adjunct to this procedure and agree with Tsuge and Mizuseki53 that this is to be avoided if at all possible. Postoperative Management The postsurgical treatment program is similar to that for those undergoing release for a post-traumatic stiff joint33 (see Chapter 32). On the day of surgery, the patient is given a brachial plexus block with a constant infusion of local analgesic14 (see Chapter 8). The extremity is placed in a continuous motion machine and is elevated, and a passive arc of motion is aggressively established. The analgesic block is discontinued after approximately 24 hours, and continuous passive motion is monitored for a second day. Active motion is allowed to the greatest extent possible. A hinged splint is applied, and the patient is given detailed instructions with regard to the use of the splint to maintain both flexion and extension (see Chapter 11).35

RESULTS Minami et al31 updated the results of the original O-K arthroplasty in 44 elbows that were observed for 8 to 16 years. With a mean surveillance of more than 10 years, 55% had no or minimal pain. Appropriately, 10% deteriorated since the original report with a mean surveillance of about 5 years.30 An additional 61% had partial relief of pain. Overall, 76% of patients had improved flexion and 55% had improved extension after surgery. With subsequent assessment,

Chapter 76 Primary Osteoarthritis: Ulnohumeral Arthroplasty 1049

Reflected triceps

Olecranon osteophyte

A

Trephine

B

FIGURE 76-8

Technique of ulnohumeral arthroplasty. The patient is supine and a straight incision is placed just medial to the olecranon. The ulnar nerve is inspected and decompressed if needed. The medial half of the triceps is reflected from the insertion on the olecranon. A, The tip of the olecranon is removed along with the olecranon osteophyte. The olecranon fossa is foraminectomized with a trephine. B, This crucial maneuver is made by following the contour of the trochlea and the trephine is oriented slightly proximal since the distal articulation of the humerus is anteriorly rotated. The humeral core is removed. C, The humerus is flexed, any anterior loose bodies that may be present are removed, and the osteophyte of the coronoid is removed with an osteotome through the foramen. (By permission, Mayo Foundation, 1987.)

the mean arc had decreased to 32 to 122 degrees, representing a 17-degree loss over time (Fig. 76-10). More recent reports are summarized in Table 76-3. Residual pain is present in about 15% of patients. Only a modest improvement in the arc of approximately 20 degrees of motion was observed. At a mean follow-up of 5 years, approximately 85% of patients were satisfied with the procedure. Furthermore, there has been one specific comparison of 18 patients with the open débridement and 26 patients undergoing arthroscopic joint débridement.6 At approximately 3 years’ follow-up, these investigators conclude interestingly that the pain relief seems to be superior after the arthroscopic procedure; however, at least in their hands, the postoperative arc of motion had increased more in the open than in the arthroscopic patients. We would conclude by saying

C

that both techniques are viable, but the abovementioned principles should be kept in mind for the arthroscopic intervention.

MAYO EXPERIENCE: ULNOHUMERAL ARTHROPLASTY Initial results of Minami and Ishii parallel my preliminary and current experience.38 Mansat et al27 have reviewed the Mayo experience using this procedure in seven patients with osteoarthritis. A mean arc of 43 to 108 degrees improved postoperatively to 21 to 124 degrees, a 38-degree improvement. Pain relief was reliably achieved in all (Fig. 76-11). This technique can be an additional feature to the ulnohumeral débridement described below.

1050 Part VIII Septic and Nontraumatic Conditions

RECENT UPDATE

1

2 3

In 2002 our experience with 46 elbows was reviewed by Antuna et al1 with a mean follow-up of 80 months (2-14 years). It was documented that an improvement of 22 degrees occurred in the flexion arc, with an average arc at follow up of 30 to 135 degrees. Seventy-five percent of the elbows were not painful, reflecting the 75% that were considered satisfactory, a mean follow-up of 7 years. One major finding in this group was that the presence of ulnar nerve symptoms that was not addressed at the time of the débridement significantly and adversely affected the outcome. As a result of this experience, we have aggressively evaluated patients for the presence of ulnar neuropathy and have addressed this appropriately at the time of surgery.

Complications

FIGURE 76-9

Care should be taken to avoid too distal placement that will thin the trochlea (1), too medial displacement that may cause weakness of the medial column (2), or too lateral placement that can involve the capitellum on the anterior aspect (3). (By permission, Mayo Foundation, 1987.)

If the technical points are understood and followed, the complication rate is very low, which is uncommon for most reconstructive procedures at the elbow. The ulnar nerve is at greatest risk. Recurrence of symptoms occur in 20% at 10 years.31 Recurrence of the radiographic changes may develop in as many as 50% of patients after 5 years.19,20,29,30 (Fig. 76-12).

FIGURE 76-10 A, Anteroposterior roentgenogram of patient 3 months after ulnohumeral arthroplasty. B, After 3 years, some of the ectopic bone has re-formed in the fossa. Note osteophyte medially that was the source of ulnar nerve irritation. The result is rated as fair.

Chapter 76 Primary Osteoarthritis: Ulnohumeral Arthroplasty 1051

FIGURE 76-11 Typical features of primary elbow arthritis on the anteroposterior (A) and lateral (B) roentgenograms. Appearance 1 year (C) and 5 years (D) later.

EXTENDED DÉBRIDEMENT In addition to the classic O-K or UHA, other authors have employed variations of an open débridement procedure.42,56 If the patient is too young to undergo prosthetic replacement, an aggressive extensile débridement as recommended by Tsuge,53 Oka,41 and others may be considered.

Procedure Extensile Débridement (Tsuge Technique)

Indication. The indications for extensile débridement include extensive hypertrophic changes, motion arc of less than 45 degrees, ulnar nerve symptoms, and age of younger than 65 years.

1052 Part VIII Septic and Nontraumatic Conditions

Technique. This débridement is essentially that performed with interposition arthroplasty (see Chapter 69) but is limited to release and débridement. The patient is supine, and a posterior incision is performed. The nerve is decompressed and the triceps reflected, generally from medial to lateral. We prefer not

to release the ligaments but this is done by Tsuge (Fig. 76-13). The capsule is released, and the osteophytes are removed. The marginal osteophyte of the radial head is removed only if symptomatic. Removal of the entire radial head is avoided. The postoperative course is that of the ulnohumeral arthroplasty described earlier.

Aftercare

Results Our experience is limited because the set of circumstances justifying this aggressive approach is uncommon. Approximately 80% have improved motion and relief of pain in our series. Tsuge reported improved motion and lessening of pain in most of the 29 patients at a mean of 64 months. The outcome of these procedures is very similar to that which is reported for the UHA, with satisfaction rates ranging from 85% to 95% at 5 to 10 years. The increase of motion averages around 20 to 25 degrees, and less than 10 percent of patients had residual pain.

Complications The ulnar nerve can be symptomatic if not addressed. Tsuge reported a reoperation in two of 29 patients. Otherwise complications have been few.

15 yrs

ULNAR NERVE FIGURE 76-12 Redevelopment of osteophytes in the olecranon fossa and progression of osteophytes around the radial head are noted 15 years after ulnohumeral arthroplasty. The patient lost 10 degrees of extension and has recurrence of extension pain. An arthroscopic débridement was successful in relieving the patient of the posterior impingement pain.

PROSTHETIC REPLACEMENT Kozak et al24 reported our experience of five patients with primary osteoarthritis treated by joint replacement (Fig. 76-14). The mean age was 68 years. All five were doing well at final assessment, with a mean flexion arc of 30 to 125 degrees averaging 5 years after surgery. Yet,

Osteophytes

Matching erosions of capitellum and radial head

Divided radial collateral ligament Osteophytes and loose body

Skirt-like osteophyte Cord-like band of anterior capsule

FIGURE 76-13

Extensile release described by Tsuge and associates.

Chapter 76 Primary Osteoarthritis: Ulnohumeral Arthroplasty 1053

FIGURE 76-14

A, Severe hyptertrophic arthritis in a 67-year-old man. B, Three years after elbow replacement the patient has no pain but motion is only from 50 to 120 degrees (C). Note presence of ectopic bone.

four had significant complications, such as fracture of the implant, ectopic bone, implant wear debris, and transient ulnar nerve symptoms. This topic is reviewed in detail in Chapter 60. Since the last edition, there have been few indications for replacement in our practice. Espag et al. did report 11 instances of primary degenerative arthritis treated by the Souter-Strathclyde implant with a mean surveillance of 68 months. Evidence of loosening was present in three humeral and two ulnar components, one of which was revised during the preparation of the manuscript. These authors also noted two neuropraxias of the ulnar nerve and overall believed that this was a satisfactory outcome in nine of the 11 cases.12

References 1. Antuna, S. A., Morrey, B. F., Adams, R. A., and O’Driscoll, S. W.: Ulnohumeral arthroplasty for primary degenerative arthritis of the elbow: Long-term outcome and complications. J. Bone Joint Surg. 84A:2168, 2002. 2. Bell, M. S.: Loose bodies in the elbow. Br. J. Surg. 62:921, 1975. 3. Bovenzi, M., Fiorito, A., and Volpe, C.: Bone and joint disorders in the upper extremities of chipping and grinding operators. Int. Arch. Occup. Environ. Health 59:189, 1987.

4. Cheung, E. V., Adams, R., and Morrey, B. F.: Primary osteoarthritis of the elbow: Current treatment options. J. Am. Acad. Orthop. Surg. 16:77, 2008. 5. Clasper, J. C., Carr, A. J.: Arthroscopy of the elbow for loose bodies. Ann. R. Coll. Surg. Engl. 83:34, 2001. 6. Cohen, A. P., Redden, J. F., and Stanley, D.: Treatment of osteoarthritis of the elbow. A comparison of open and arthroscopic debridement. Arthroscopy 16:701, 2000. 7. Collins, D. H.: The Pathology of Articular Cartilage in Spinal Disease. London, Edward Arnold Co., 1949. 8. Delal, S., Bull, M., and Stanley, D.: Radiographic changes at the elbow in primary osteoarthritis: A comparison with normal aging of the elbow joint. J. Shoulder Elbow Surg. 16:358, 2007. 9. Debono, L., Mafart, B., Jeusel, E., and Guipert, G.: Is the incidence of elbow osteoarthritis underestimated? Insights from paleopathology. Joint Bone Spine 71:397, 2004. 10. Doherty, M., and Preston, B.: Primary osteoarthritis of the elbow. Ann. Rheum. Dis. 48:743, 1989. 11. Doherty, M., Watt, I., and Dieppe, P. A.: Influence of primary generalized osteoarthritis on development of secondary osteoarthritis. Lancet 2:8, 1983. 12. Espag, M. P., Back, D. L., Clark, D. I., and Lunn, P. G.: Early results of the Souter-Strathclyde unlinked total elbow arthroplasty in patients with osteoarthritis. J. Bone Joint Surg. 85B:351, 2003. 13. Forster, M. C., Clark, D. I., and Lunn, P. G.: Elbow osteoarthritis: Prognostic indicators in ulnohumeral debride-

1054 Part VIII Septic and Nontraumatic Conditions

14.

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16. 17.

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29. 30.

31.

ment—the Outerbridge-Kashiwagi procedure. J. Shoulder Elbow Surg. 10:557, 2001. Gaumann, D. M., Lennon, R. L., and Wodel, D. J.: Continuous axillary block for postoperative pain management. Reg. Anesth. 13:77, 1988. Goodfellow, J. W., and Bullough, D. G.: The pattern and aging of articular cartilage in the elbow. J. Bone Joint Surg. 49B:175, 1967. Gramstad, G. D., and Galatz, L. M.: Management of elbow osteoarthritis. J. Bone Joint Surg. 88A:421, 2006. Hellmann, D. B., Helms, C. A., and Genant, H. K.: Chronic repetitive trauma: A cause of atypical degenerative joint disease. Skeletal Radiol. 10:236, 1983. Huskisson, E. C., Dieppe, P. A., Tucker, A. K., and Cannell, L. B.: Another look at osteoarthritis. Ann. Rheum. Dis. 38:423, 1979. Kashiwagi, D.: Intra-articular changes of the osteoarthritic elbow, especially about the fossa olecrani. Jpn. Orthop. Assoc. 52:1367, 1978. Kashiwagi, D.: Outerbridge Kashiwagi arthroplasty for osteoarthritis of the elbow in the elbow joint. In Kashiwagi, D. (ed.): Proceedings of the International Congress, Kobi, Japan. Amsterdam, Excerpta Medica, 1986. Kelley, W. N., Harris, E. D., Ruddy, S., and Sledge, C. P. (eds.): Textbook of Rheumatology, 3rd ed. Philadelphia, W. B. Saunders Co., 1989. Kelly, E. W., Bryce, R., Coghlan, J., and Simon, B.: Arthroscopic debridement without radial head excision of the osteoarthritic elbow. Arthroscopy 23:151, 2007. Kim, S. J., and Shin, S. J.: Arthroscopic treatment for limitation of motion of the elbow. Clin. Orthop. 375:140, 2000. Kosak, K., and Morrey, B. F.: Prosthetic replacement for primary degenerative arthritis of the elbow. J. Arthroplasty 13:837, 1998. Krishnan, S. G., Harkins, D. C., Pennington, S. D., Harrison, D. K., and Burkhead, W. Z.: Arthroscopic ulnohumeral arthroplasty for degenerative arthritis of the elbow in patients under 50 years of age. J. Shoulder Elbow Surg. 16:443, 2007. Lo, G. H., LaValley, M., McAlindon, T., and Felson, D. T.: Intraarticular hyaluronic acid in treatment of knee osteoarthritis: A meta-analysis. J. A. M. A. 290:3115, 2003. Mansat, P., and Morrey, B. F.: The “column procedure” a limited surgical approach for the treatment of stiff elbows. J. Bone Joint Surg. 80A:1603, 1998. McLaughlin, R. E. 2nd, Savoie, F. H. 3rd, Field, L. D., and Ramsey, J. R.: Arthroscopic treatment of the arthritic elbow due to primary radiocapitellar arthritis. Arthroscopy 22:63, 2006. Minami, N. M.: Roentgenological studies of osteoarthritis of the elbow joint. Jpn. Orthop. Assoc. 51:1223, 1977. Minami, N. M., and Ishii, S.: Outerbridge Kashiwagi arthroplasty for osteoarthritis of the elbow joint. In Kashiwagi, D. (ed.): Proceedings of the International Congress, Kobi, Japan. Amsterdam, Excerpta Medica, 1986. Minami, M., Kato, S., and Kashiwagi, D.: OuterbridgeKashiwagi’s method for arthroplasty of osteoarthritis of the elbow. 44 elbows followed for 8-16 years. J. Orthop. Sci. 1:11, 1996.

32. Mintz, G., and Fraga, A.: Severe osteoarthritis of the elbow in foundry workers. Arch. Environ. Health 27:78, 1973. 33. Morrey, B. F. (ed.): The Elbow and Its Disorders. Philadelphia, W. B. Saunders Co., 1985. 34. Morrey, B. F.: Arthroscopy of the elbow. Instr. Course Lect. 35:102, 1986. 35. Morrey, B. F.: Post-traumatic contracture of the elbow: Operative treatment including distraction arthroplasty. J. Bone Joint Surg. 72A:601, 1990. 36. Morrey, B. F.: Post-traumatic contracture of the elbow: Operative treatment, including distraction arthroplasty. J. Bone Joint Surg. 72A:601, 1990. 37. Morrey, B. F.: Elbow replacement arthroplasty: Patient selection. In Morrey, B. F. (ed.): Joint Replacement Arthroplasty. New York, Churchill Livingstone, 1991, p. 669. 38. Morrey, B. F.: Primary arthritis of the elbow treated by ulno-humeral arthroplasty. J. Bone Joint Surg. (Br). 74B:409, 1992. 39. O’Driscoll, S., and Morrey, B. F.: Elbow arthroscopy: A critical assessment. J. Bone Joint Surg. 74A:84, 1992. 40. Ogilvie-Harris, D. J., Gordon, R., and MacKay, M.: Arthroscopic treatment for posterior impingement in degenerative arthritis of the elbow. Arthroscopy 11:437, 1995. 41. Oka, Y.: Debridement arthroplasty for osteoarthrosis of the elbow: 50 patients followed a mean of 5 years. Acta Orthop. Scand. 71:185, 2000. 42. Oka, Y., Ohta, K., and Saitoh, I.: Debridement arthroplasty for osteoarthritis of the elbow. Clin. Orthop. 351:127, 1998. 43. Ortner, D. J.: Description and classification of degenerative bone changes in the distal joint surface of the humerus. Am. J. Phys. Anthrop. 28:139, 1968. 44. Ozbaydar, M. U., Tonbul, M., Altan, E., and Yalaman, O.: Arthroscopic treatment of symptomatic loose bodies in osteoarthritic elbows. Acta Orthop. Traumatol. Turc. 40:371, 2006. 45. Phillips, N. J., Ali, A., and Stanley, D.: Treatment of primary degenerative arthritis of the elbow by ulnohumeral arthroplasty. A long-term follow-up. J. Bone Joint Surg. 85B:347, 2003. 46. Redden, J. F., and Stanley, D.: Arthroscopic fenestration of the olecranon fossa in the treatment of osteoarthritis of the elbow. Arthroscopy 9:14, 1993. 47. Salk, R. S., Chang, T. J., D’Costa, W. F., Soomekh, D. J., and Grogan, K. A.: Sodium hyaluronate in the treatment of osteoarthritis of the ankle: A controlled, randomized, double blind pilot study. J. Bone Joint Surg. 88A:295, 2006. 48. Sarris, I., Riano, F. A., Goebel, F., Goitz, R. J., and Sotereanos, D. G.: Ulnohumeral arthroplasty: results in primary degenerative arthritis of the elbow. Clin. Orthop. 420:190, 2004. 49. Savoie, F. H. 3rd, Nunley, P. D., and Field, L. D.: Arthroscopic management of the arthritic elbow: indications, technique, and results. J. Shoulder Elbow Surg. 8:214, 1999. 50. Smith, F. M.: The Elbow, 2nd ed. Philadelphia, W. B. Saunders Co., 1972. 51. Stanley, D., and Winsor, G.: A surgical approach to the elbow. J. Bone Joint Surg. 72B:728, 1990. 52. Tashjian, R. Z., Wolf, J. M., Ritter, M., Weiss, A. P., and Green, A.: Functional outcomes and general health status

Chapter 76 Primary Osteoarthritis: Ulnohumeral Arthroplasty 1055

after ulnohumeral arthroplasty for primary degenerative arthritis of the elbow. J. Shoulder Elbow Surg. 15:357, 2006. 53. Tsuge, K., and Mizuseki, T.: Debridement arthroplasty for advanced primary osteoarthritis of the elbow. Results of a new technique used for 29 elbows. J. Bone Joint Surg. 76B:641, 1994. 54. van Brakel, R. W., and Eygendaal, D.: Intra-articular injection of hyaluronic acid is not effective for the treatment of post-traumatic osteoarthritis of the elbow. Arthroscopy 22:1199, 2006.

55. Vingerhoeds, B., Degreef, I., and De Smet, L.: Debridement arthroplasty for osteoarthritis of the elbow (OuterbridgeKashiwagi procedure). Acta Orthop. Belg. 70:306, 2004. 56. Wada, T., Isogai, S., Ishii, S., and Yamashita, T.: Debridement arthroplasty for primary osteoarthritis of the elbow. J. Bone Joint Surg. 86A:233, 2004. 57. Wadsworth, T. G.: The Elbow. Edinburgh, Churchill Livingstone, 1982.

1056 Part VIII Septic and Nontraumatic Conditions

CHAPTER

77

Septic Arthritis Kenneth P. Butters and Bernard F. Morrey

INTRODUCTION Since the last edition of this text, a MedLine search revealed very few contributions specifically dealing with elbow sepsis other than that associated with prosthetic replacement and disease-modifying antirheumatic drugs (DMARDs). There is great interest and emerging data regarding the increased sepsis associated with the administration of DMARDs.

GENERAL CONSIDERATIONS An infection can be defined as the clinical manifestation of a host response to a given inoculum. Aspects of the inoculum include the amount of bacteria, the type of entry, and the nature or virulence of the pathogen. Host factors can be classified as congenital or acquired. Congenital immunoincompetence syndromes are associated with deficiencies of the humeral or bursal immunologic systems and have been well described in standard medical textbooks. Acquired failures or alteration of immunocompetence can be either generalized or localized. Generalized processes include diabetes mellitus, corticosteroid therapy, cancer with or without immunosuppressive therapy, human immunodeficiency virus (HIV) infection, and alcohol or other chemical addiction or abuse. Local processes that alter normal host resistance include anatomic site of involvement, scar formation from previous surgery, burns, radiation, or prior infection. In applying these observations specifically to the elbow, it should be noted that this is a subcutaneous joint. Hence, the elbow is vulnerable to direct inoculation of a pathogen, particularly because host resistance is compromised. In fact, a recent analytic assessment of a 10-year study of infections in England documented an 11% incidence of death with joint sepsis. Of great interest is that a multivariant analysis documented risk factors for mortality to be confusion at presentation, age greater than 65 years of age, multiple joint involvement, and interestingly, involvement of the elbow joint.78

DISEASE-MODIFYING ANTIRHEUMATIC DRUGS Infection and DMARDS are well known to have dramatically changed the life and prognosis of patients suffering from rheumatoid arthritis. Yet, the orthopedic surgeon is very well aware of the potential adverse effects, both with regard to increased risk in surgical infection, as well as the potential for managing patients with spontaneous sepsis related to this type of medication. In spite of the opinion or perception of the orthopedic community that these agents are responsible for an increased infection rate, the literature is somewhat controversial in this regard.7 One can find as many references that fail to support the relationship between DMARDs and infection as exists to demonstrate that this relationship does exist.7,14,18,19,25 One recent study does reveal that treatment with the tumor necrosis factor (TNF) inhibitors does significantly increase the risk of infection in orthopedic surgery (<0.04). Our review of the current literature leaves us to conclude that without any question, DMARDs do increase the potential for infection about the elbow. Although this may not be demonstrable for the hip, a fivefold increased risk for elbow infection has been documented.18 Interestingly it has also been noticed that the skin and soft tissues are also potentially at greatest risk.19 Thus, increased problems with wound healing around the elbow supports the increased incidence of infection. The biggest question that remains unanswered is whether or not withholding the medication in advance subsequently has an effect on this phenomenon. There is evidence that methotrexate need not be withheld,29 whereas others have demonstrated that there is merit in withholding methotrexate therapy in the perioperative period.14

EXPERIENCE AT THE MAYO CLINIC We are currently in the process of analyzing our experience with infected total elbow arthroplasty and the use of DMARDs. The difficulty of our and all such studies is knowing whether medications behave the same in different patients. To what extent is the drugs effect dose dependent, as appears to be the case in some instances? A study from the Mayo Clinic did demonstrate that the dose itself can be a very significant variable that influences the development of an infection with TNF antibody therapy.7

AUTHOR’S RECOMMENDATION Based on our review of the literature and our clinical experience, there is little question in our mind that the

Chapter 77 Septic Arthritis 1057

anti-TNF agents are associated with increased orthopedic infections. For this reason, we do withhold treatment for at least a month before and a month after our surgical intervention. Although we believe that the increased incidence of sepsis is becoming well documented, what is less well known is whether or not all agents have the same adverse impact and whether withholding these agents is of value. What is the “safe period” both before and after surgery? It is hoped that this issue will be resolved over the next several years, but as mentioned earlier, because of the numerous variables that pertain to the issue, it is likely to be debated for many years to come.

OSTEOMYELITIS Bone infection occurs (1) hematogenously, (2) by direct inoculation after surgery or open fracture, or (3) by contiguous spread from a local process.77

HEMATOGENOUS INFECTION

this way, even before radiographic changes are apparent. 2. Gentle passive motion of the joint should be done. With joint infections, all motion is resisted; with metaphyseal osteomyelitis, gentle, supported passive motion is possible. Except in the very acute stages, an elevated leukocyte count is variably present,15,53 and the differential count tends to demonstrate a shift to the left in two thirds of the cases. The erythrocyte sedimentation rate has been the most sensitive blood test; it is elevated in the early stages of infection in about 80 percent of persons.15,52 Therefore, it is very sensitive, but not specific. Interestingly, the rate is statistically higher in joint infections than in bone infections and is a valuable means of following the treatment and resolution of the infection.15,41,50 Early radiographs are not helpful. After 7 to 14 days, osteoporosis may be present, followed by periosteal elevation or erosions. The classic appearance of osteomyelitis by bone scan is a well-defined focal area of increased uptake at the site of active infection (Fig. 77-1). The 99mTc scan may

Hematogenous infection is the most common type of osteomyelitis and has been reported to occur at the elbow in about 4% of such cases.77 In the growing child, the end-arterial loop of the metaphyseal bone causes sluggish bone blood flow. The lack of phagocytic activity in these loops allows maturation of a septic thrombus at the arterial site.37 The abscess spreads through the haversian system into the subperiosteal space. If the metaphysis is intra-articular, as at the hip or shoulder, a septic joint will then result,75 but this is not the case at the elbow. As at other sites, acute hematogenous osteomyelitis is most common in children younger than 3 and older than 7 years of age. The first group is vulnerable owing to the lack of acquired host immunity; the second age group corresponds to the time of rapid growth.51 Our recent study reported 85% septic joints in children were of the knee, hip and ankle; only 8% involved the elbow.11

Presentation and Diagnosis The clinical presentation is typical and includes local pain, warmth, and swelling. The patient may be afebrile but is not necessarily systemically ill. In children, a predisposing, traumatic event is common,50,83 but identity of a remote focus is less frequent. The elbow is held in flexion and pseudoparalysis, or reflex inhibition may be present. The physical examination includes the following: 1. The specific point of maximal tenderness should be determined by gentle palpation. The focus of the septic process can often be accurately localized in

FIGURE 77-1

Technetium bone scan of a rheumatoid patient (note uptake in the shoulder) with an infected total elbow arthroplasty. Notice the increased uptake on the humeral side of the joint.

1058 Part VIII Septic and Nontraumatic Conditions

be positive as early as 24 hours after the onset of symptoms in a patient with osteomyelitis.24 The increased activity of equal intensity on both sides of the joint indicates joint disease, arthritis, or synovitis but is not a reliable indicator in the neonate. Nonspecific inflammatory arthritides of rheumatoid arthritis or gout limits the value of the Ga scan.34 False-negative results are also common.72 At the present time, we recommend first a 99m Tc scan as a low-cost screening test to provide immediate results and localization. The 111In-labeled leukocyte scan may be useful primarily for more acute suppurative infection. More recently, Erdman states that magnetic resonance imaging (MRI) has 100% sensitivity and 0% specificity in a mixed group of acute and chronic osteomyelitis.17 With the continuing advances being made with imaging techniques, it is currently believed that the MRI and nuclear medicine are the most sensitive and specific modalities for detection of the septic process. MRI is most helpful to determine the extent of damage, and ultrasound is an effective, noninvasive method to assess soft tissue involvement. Computed tomography (CT) helps document sequestra. The newer positron emission tomography (PET) and single photon emission computed tomography (SPECT) are emerging as useful to evaluate chronic conditions.59,71 The T1-weighted images of the MRI are also very useful to detect concurrent osteomyelitis in the presence of the septic joint.38 Ongoing efforts to refine short time inversion recovery (STIR) and T1 spin echo (T1 SE) imaging techniques reveal enhanced sensitivity, specifically for osteomyelitis.45 Joint aspiration remains the most simple and reliable means of making the diagnosis of elbow joint sepsis, but even this is positive in only about 85% of cases.78

DIRECT INOCULATION Direct inoculation is a relatively common cause of infection of the elbow joint. The thin soft tissue coverage predisposes to compound fractures that may become secondarily infected. Elective nonprosthetic surgery of the elbow region has been associated with an infection rate of about 2% to 4%, significantly greater than the commonly quoted 1% for elective orthopedic procedures.

SPREAD FROM A CONTIGUOUS FOCUS Infection by spread from a contiguous focus occurs at the elbow from a septic joint or from an infected olecranon bursa. A recent survey of a 10-year experience with septic bursae from Spain documented that three of 69 patients (7.7%) developed osteomyelitis.21 These circumstances are most commonly noted in a patient with rheumatoid arthritis, and the management is the same as that for a septic joint. Because a sympathetic sterile

effusion may occur with metaphyseal osteomyelitis, even though the metaphysis is extra-articular, the joint should be aspirated to exclude septic arthritis in the presence of an effusion.

MICROORGANISMS The most common pathogen causing acute hematogenous osteomyelitis is Staphylococcus aureus. Opportunistic organisms are isolated in the debilitated patient, and Pseudomonas aeruginosa is most commonly associated with drug addiction or chronic, draining wounds. Organisms not generally considered pathogenic must be viewed as such when isolated on several occasions, particularly in patients with compromised resistance. In one report, two of the three cases of diphtheroid osteomyelitis involved the elbow, and both patients had altered local immunocompetency.52 Serratia infection of open fractures has also been reported in the humerus and forearm in about one third of such cases.40 The infected prosthesis is discussed in Chapter 62.

TREATMENT For the elbow, there are no unique management features of acute hematogenous osteomyelitis, except that prolonged immobilization is to be strictly avoided. In cases that are diagnosed early, antibiotics alone may be adequate.6,53 Surgery is indicated when there is no response to parenteral antibiotic therapy after 36 to 48 hours. It has been our experience that acute hematogenous osteomyelitis in which symptoms have been present for less than 10 days may be treated with specific intravenous antibiotics for 2 to 3 weeks. If symptoms have been present for more than 10 days, a discrete soft tissue or bone abscess may have developed and must be surgically decompressed. Subperiosteal needle aspiration is sometimes helpful in accurately defining metaphyseal infection. Today we rely on the MRI to assist in the early diagnosis of bone involvement.20 Intravenous antibiotics should be continued for about 3 weeks. Oral agents can be used for an additional 4 weeks, but bactericidal levels should be attained and monitored.43 Infection involving bone may become subacute or chronic, and in this instance, incision and drainage with limited bone débridement and secondary soft tissue healing may be necessary. An extensive débridement of bone severely impairs function because the joint becomes dysfunctionally unstable and is difficult to fuse (Fig. 77-2). Burkhalter and colleagues60 have discussed the upper extremity restrictions of function created by elbow fusion and the common complications of failure of union and secondary fracture (see Chapter 70). They recommended a posterior compression plate and pointed out that often the hardware is exposed

Chapter 77 Septic Arthritis 1059

RESULTS In the preantibiotic area, Wilensky80 reported that three of 18 patients developed spontaneous ankylosed elbows owing to immobilization for osteomyelitis of the elbow region. Other long-term residual effects include sinus tract formation, recurrent infection, pathologic fracture, growth disturbances, and development of chronic osteomyelitis. West and associates79 observed that chronic osteomyelitis of the humerus appears to have a better prognosis than chronic infection of the tibia or femur. The duration of the septic process is the most important prognostic feature.53,57 Today, it is anticipated that better function will be realized with better techniques for early detection.

SEPTIC ARTHRITIS OF THE ELBOW

FIGURE 77-2

For chronic infection, although both resection (A) and fusion (B) are definitive treatments, both result in a dysfunctional elbow. (From Morrey, B. F., Fitzgerald, R. H., Kelly, P. J., Dohyns, J. H., and Washington, J. A., III: Diphtheroid osteomyelitis. J. Bone Joint Surg. 59A:527, 1977.)

during the process of healing of the fusion. They also accurately emphasize the limited indications for and the occurrence of forearm motion loss after arthrodesis.60 Occasionally, spontaneous arthrodesis occurs after débridement, but extensive removal of bone causes gross instability (Fig. 77-3). If soft tissue coverage is a problem, the flexor carpi ulnaris muscle pedicle flap may be used for coverage of the proximal ulna and elbow. Fourteen centimeters of muscle is available from the pedicle entering 5 cm distal to the elbow joint line. Such a flap brings improved blood supply as well as soft tissue coverage.49 In the acute phase of treatment, the joint should be splinted, elevated, and put to rest. As the process resolves, gentle active motion is encouraged as soon as possible. Continuous passive motion may prove to be beneficial in some patients to avoid ankylosis or adhesions.64

Septic arthritis after joint replacement51 is discussed in Chapter 62. In the experience at the Mayo Clinic, septic arthritis of the elbow occurred in 6% of adults39 and 3% of children diagnosed with septic joints.50 Other investigators report an incidence of 9% to 13%,3,26,78 noting that the ages at risk were those “at the extremes of life.”3 The frequent association of septic arthritis with rheumatoid arthritis is well recognized.30,31,42,61,68 This association is believed to be even more likely in those treated with DMARDs. Kellgren and colleagues42 reported that 33% of septic joints in patients with rheumatoid arthritis involved the elbow. Also noted were the multiple sites of involvement and the high incidence of Staphylococcus aureus organisms (83%). Skeletal infections, including septic arthritis, are more common in patients with HIV, probably related to risk factors such as intravenous drug abuse. HIV-positive hemophiliac patients with fevers, swollen joints, and poor response to factor replacement should prompt a high index of suspicion for septic arthritis.

DIAGNOSIS An incorrect or delayed initial diagnosis is common.39 The clinical examination and an index of suspicion are crucial for a prompt and correct diagnosis. The maximum capacity of the joint is at about 80 degrees of flexion,55 so the patient will present with the joint held in this position. Pain and swelling about the elbow are invariably present, and gentle, passive motion is painful. Differential diagnosis of an infected elbow in the child includes juvenile rheumatoid arthritis, unrecognized trauma, acute rheumatic fever (which affects the elbow in about 15% of cases), and transient synovitis. In the adult, 5% of patients with gout or pseudogout will have

1060 Part VIII Septic and Nontraumatic Conditions

FIGURE 77-3

B

involvement of the elbow. The occurrence of elbow sepsis in those with immunodeficiency is also becoming recognized.10,22,60 Differentiation from osteoarthritis or post-traumatic arthritis should not be a difficult problem. An additional differential diagnosis is nonsuppurative infectious arthritis; such as that associated with Lyme disease and hepatitis or from mycobacterium.87 Gonococcal arthritis is suspected with appropriate sexual history. Rheumatoid arthritis with a secondary infection is, of course, a difficult clinical diagnosis that is usually resolved only with aspiration. Systemic symptoms are variably present. A leukocytosis is often present early, but the shift to the left of the differential leukocyte count is more reliable. The sedimentation rate is invariably increased, but this does not distinguish the patient with active rheumatoid arthritis.15 Even the infected joint replacement shows elevated sedimentation rates, but the effect of the surgery itself is sometimes a source of confusion.66 As with any joint infection, the key to the diagnosis is joint aspiration. The distended joint is easy to enter either from the lateral “triangle” or at the posterior olecranon fossa (Fig. 77-4). Joint aspiration must be done under sterile conditions, because inoculation of the sterile joint is possible with aspiration and has been reported.3 In addition to joint aspiration for culture and cell count, gas-liquid chromatography may be helpful in

Sepsis occurred in fracture dislocation of the elbow leading to spontaneous arthrodesis (A). In some, the débridement and resorptive process causes gross destruction and dysfunctional instability (B).

differentiating a bacterial from a nonseptic inflammatory process.8 The radiographic assessment is not helpful in the early diagnosis of elbow infection, but an increased amount of synovial fluid may show an anterior or posterior fat pad sign.9,46 In this setting, the 99mTc scan is invariably positive (Fig. 77-5). Gallium or labeled white cell scans may be more specific than technetium scans, but they have the disadvantage of a 24- to 72-hour delay in diagnosis and have fallen into disfavor in recent years. An MRI lacks the specificity of distinguishing septic from nonseptic fluid20 but can assist in the diagnosis of a contiguous osteomyelitis. Later, osteopenia and subtle bone erosion at the synovial attachment occur, progressing to uniform thinning of the articular cartilage and then more extensive erosions and subchondral disruption. Additional laboratory investigations include blood cultures, which are positive in about 40% to 70% of patients3,28,53 and in up to 90% if multiple joints are involved. We have observed that the limited use of oral antibiotics will tend to result in a negative blood culture, but the joint aspirate will still reveal the organism.53 Staphylococcus aureus is isolated in about two thirds of cases of bacterial arthritis in adults39 and in at least half of those in children.50 In the neonatal age group, coliform and gram-positive organisms are not uncommon.54

Chapter 77 Septic Arthritis 1061

B FIGURE 77-4

A, Aspiration of the elbow (1) is carried out through the lateral portal between the radial head, lateral epicondyle, and tip of the olecranon. Alternatively, with significant joint distension, a posterolateral approach (2) into the olecranon fossa may be used. The landmarks designating the soft spot are easily identified (B).

At ages 3 months to 3 years, the child is at risk for Haemophilus influenzae, but in children older than 3 years, S. aureus is the predominant organism.50

TREATMENT Initial specific antibiotic treatment is first based on the Gram stain. If infection is suspected and no organism is isolated, initial antibiotic treatment should be based on

age and presentation. This should include penicillin in the young healthy patient, Staphylococcus and gram-negative coverage in the older patient with underlying disease, and drugs for H. influenzae in the young child. Mayo Clinic treatment consists of 3 to 4 weeks of intravenous administration of antibiotics, but this may be somewhat conservative, and the duration should be tailored to the clinical setting. Others have begun an appropriate oral antibiotic approximately 1 week after serum bactericidal levels have been obtained.43 Serial monitoring of the serum antibiotic levels is continued on an outpatient basis. In addition to systemic antibiotics, the treatment, as in any diarthrodial joint, requires removal of accumulated cellular debris and pus. Cartilage is destroyed by digestion from enzymes elaborated from neutrophils, synovium, and bacteria.16 When there is capsular distension, aspiration is easily accomplished (see Fig. 77-5). Rather than simple aspiration for diagnosis, we strongly recommend that the joint be lavaged with sterile saline at the time of aspiration. Lavage has been clearly shown to be effective in preventing collagen loss in the rabbit.15 Hence, we perform a saline lavage at the time of the initial operation and inject 0.5 to 1 g of cefazolin sodium after lavage. Successively decreasing cell counts from the joint aspirate may also be used as an indicator of recovery.26,27 Intermittent joint distension-suction through percutaneous catheters35 has given way to arthroscopic débridement in those not responding immediately to the initial aspiration, lavage and antibiotic deposition. It should be noted that intra-articular administration of antibiotics is controversial in the treatment of septic arthritis. Adequate levels of antibiotics occur in the synovial fluid from parenteral treatment, and postinfection synovitis lasting up to 8 weeks in as many as 40% of the cases has been related to the intra-articular use of penicillin.3 Yet experimental evidence indicates that the joint can be sterilized more rapidly by intra-articular injection of an antibiotic.5 Lacking evidence that the chemical synovitis is harmful to the joint, if there has been a delay in diagnosis of 4 to 5 days, we may inject 0.5 g of cefazolin sodium diluted in 10 mL of sterile water, particularly if a gram-positive organism is suspected. For infections that are subacute, postoperative, or due to direct inoculation, adequate clearance by aspiration is not reliable, and drainage by arthroscopy is preferred. Arthroscopy of the elbow allows inspection, clearance of loculations and adhesions, thorough irrigation, and synovial tissue culture as well as insertion of drainage catheters. Hence, this has emerged as the treatment of choice for most cases that do not respond to aspiration or in those patients requiring synovectomy.74 Aggressive synovectomy and débridement is an

1062 Part VIII Septic and Nontraumatic Conditions

FIGURE 77-5

A, Normal-appearing radiograph in a patient with acute onset of a painful effusion. B, An area of markedly increased uptake demonstrated by the technetium-99m scan was subsequently found to be septic arthritis.

important concept in treating the infected prosthesis65 (see Chapter 38). If extra-articular involvement is present, arthrotomy may be necessary and early motion is begun. Early active motion after incision and drainage was recommended as early as 1919 by Willems,81 who along with others4 reported good results with both knee and elbow infections. The basis of the beneficial effect of early motion has been carefully studied by Salter and associates,64 who found protection of articular cartilage and concluded that this technique (1) prevents adhesions and pannus, (2) improves nutrition of cartilage, (3) enhances clearance of exudate including lysosomal enzymes, and (4) stimulates the living chondrocytes.

RESULTS Delay in diagnosis and treatment is probably the most important factor affecting prognosis.27,42,50 A normal joint is unlikely if treatment is delayed for more than 1 week after the onset of symptoms.50,57 The degeneration of articular cartilage and the development of fibrous

adhesions50 are responsible for the poor results after an infection. Virulence of the organism is also an important prognostic variable.26 In one series, complete recovery occurred in 90% of those infected with Streptococcus, 60% of those infected with Staphylococcus, and less than one third of patients infected with a gram-negative organism.27 Gram-negative infection has a poor prognosis and is often associated with compromised host resistance. Gonococcal arthritis also involves the elbow in about 10% of cases,48 and treatment offers predictably good results. Nongonococcal Neisseria infections have also been reported to involve the elbow, again often with compromised host resistance or in association with a crystalline-induced arthritis.17 Loss of function, not recurrence, is the most common sequela of this infection (Fig. 77-6). In the Mayo series of 103 septic joints, acute infection was eradicated in all but one, with only four recurrences. Argen and associates3 found no evidence of reinfection or chronic osteomyelitis in any of the elbow infections, and no secondary procedures were necessary.50 The ultimate result depends on the state of the joint before the infection.

Chapter 77 Septic Arthritis 1063

C FIGURE 77-6

A 60-year-old patient with rheumatoid arthritis was treated with joint resection for an infected elbow and did well for 2 1/2 years. He had significant loss of bone, but the resection-type arthroplasty (A) functioned reasonably well. The arc of motion of the elbow was between 15 and 135 degrees, with no significant discomfort (B). If the condyles are not preserved, gross instability and poor function ensues (C).

NONBACTERIAL INFECTIONS The elbow joint is also somewhat prone to nonbacterial infection and is involved in approximately 10% of all skeletal infections from tuberculosis.47 Unlike suppurative arthritis, the adjacent bone may also be involved. A tuberculous infection of the elbow is diagnosed by aspiration in 25% to 75% of instances, but most consistently (95%), it results from biopsy of the synovial tissue. Pulmonary tuberculosis is present in only about half of the cases.85 Atypical Mycobacterium infection, for example, M. kansasii,77 may also occur, both from direct inoculation and from lung involvement, and may be slowly progressive over many years. The articular cartilage is preserved well into the course of the disease. The radiographic stages seen in the elbow include: soft tissue involvement, localized cystic lesions in the bone (Fig. 77-7), or resorption with cystic subchondral changes (Fig. 77-8). Wilson pointed out that coronoid lesions are associated with joint space loss, and, as expected, massive lesions of the joint have a poor prognosis for function despite synovectomy.82 In a study of 29 joints involved with tuberculosis, 28 attained a useful joint after 12 months of treatment with chemotherapy alone.47 At present, chemotherapy with

early motion is the treatment of choice, with surgery being used only to make the diagnosis. For residual dysfunction, a synovectomy and radial head resection might be considered, as well as excisional arthroplasty. Arthrodesis may be difficult2 and is recognized as a poor salvage procedure that should be used only if the infection cannot be controlled. Coccidioidomycosis caused by Coccidioides immitis has been reported in the elbow in three of 25 joint infections.84 The treatment recommended is synovectomy with intravenous amphotericin B for the disseminated disease. Kumar44 recently reported a case of elbow sepsis occurring from Chryseobacterium meningosepticum.

SEPTIC OLECRANON BURSITIS Olecranon bursitis has been the topic of several reports10,21,58,62,69,86 and is discussed in Chapter 84. The superficial location of the extensor surface of the elbow places the olecranon bursa at increased risk of trauma,21,63 especially in certain occupations.10 A pre-existing local infection or associated conditions such as diabetes mellitus or alcoholism have also been noted. Infection of the olecranon bursa does not necessarily indicate elbow

1064 Part VIII Septic and Nontraumatic Conditions

FIGURE 77-7

Tuberculosis of the elbow may present as a cystic and sclerotic type of osteomyelitis. In this instance, extensive involvement of the proximal ulna is present. (Courtesy of Dr. Richard Marks, Cape Town, South Africa.)

joint infection, because normally the two structures do not communicate. However, the bursa may communicate with the elbow in rheumatoid arthritis76 and after total elbow replacement. The association with immunoincompetent states, including HIV infection, is also recognized.10 Elbow joint aspiration and sinography may be necessary to determine this association. Of those who do develop a septic olecranon bursa, about one third give a history of a previous noninfected olecranon bursitis.1 Septic olecranon bursitis is rare in children, because this bursa develops around ages 7 to 10 years. The presentation varies widely from acute onset of cellulitis (Fig. 77-9) to a low-grade subacute process of 2 or more weeks’ duration. Importantly, pain and erythema are suggestive of a septic rather than a mechanical process. The range of motion is restricted at the extremes only, aiding the differentiation of bursal from elbow joint sepsis. The differential diagnosis includes septic, traumatic, or inflammatory bursitis, and in patients with rheumatoid arthritis, septic elbow.10,12,23,32,63 The relationship with septic arthritis in the patient with rheumatoid arthritis is particularly important. The coexistence of the two is well established, and septic arthritis may occasionally present as an infected olecranon bursitis.76 Fluid aspirate yields S. aureus in 90% of cases.13,33 Other less

FIGURE 77-8

Classic radiographic picture of tuberculosis involving both sides of the elbow joint with subchondral cyst formation. Subchondral sclerosis is variably present.

FIGURE 77-9

Septic olecranon bursitis in this patient presented with marked cellulitis, swelling, and pain over the entire posterior aspect of the elbow region. Staphylococcus aureus was isolated at the time of aspiration. The process resolved with 5 days of intravenous antibiotic therapy and 10 days of oral antibiotic therapy.

Chapter 77 Septic Arthritis 1065

common organisms include group A Streptococcus31 and anaerobic,73 tuberculous,67 and even parasitic and yeast organisms.1,56 In the series of Pien and colleagues58 that evaluated 34 cases, 41% of septic olecranon bursitis presented as associated cellulitis and lymphadenitis. Sterile hemodialysis olecranon bursitis is now a wellknown entity (see Chapter 84).36 If the bursa becomes secondarily infected, usually with S. aureus, the condition may appear to be indistinguishable from noninfected bursitis and the diagnosis must be confirmed by aspiration. Examination for crystals should be done because gout may coexist with or even predispose to bursal sepsis (see Chapter 84).23 A key point is that aspiration with cell count, crystal determination, and Gram stain probably should be done before corticosteroid injection into the bursa in instances in which underlying diagnosis is uncertain. Rheumatoid and gouty fluid may appear purulent, and infective fluid may be only slightly turbid. Crystal examination with a polarizing microscope should confirm the diagnosis of gout and pseudogout, but the birefringent crystals of a long-acting steroid may confuse the diagnosis. Cell counts below 1000/mm3 are not worrisome, but those above this level are at least suspicious. White cell counts are generally less in the bursa than in joint infection, so a low white count should be cautiously interpreted.

TREATMENT Initially, a single aspiration and oral antibiotic treatment may suffice in the patient with a mild case without systemic symptoms or cellulitis. Intravenous antibiotics and a second aspiration may be required if fever or leukocytosis is present. Early incision and drainage is discouraged. The length of treatment with antibiotics is based on the clinical response and the duration of symptoms. A sterile aspiration serves as an appropriate end point, but usually the clinical course is an adequate indicator. Other factors that may influence the duration of treatment include the underlying disease, the completeness of bursal drainage, the appropriateness of antibiotic treatment, and most important, the duration of infection before the initiation of treatment. Ho and Su32 recommend continued treatment for 5 days after a sterile aspirate has been obtained. Roschman and Bell62 found in immunocompromised patients with olecranon bursitis a mean of 11 days of antibiotic therapy before bursal fluid cultures were negative. Surgical drainage is performed for (1) failed aspiration and antibiotic treatment, (2) chronic, recurrent infection, (3) an infected bursa that has been altered by a prior inflammatory process or surgery, (4) infection with a resistant organism not responding to treatment, and

(5) exploration for extent of infection or foreign body including accessory bursae about the triceps.33 However, surgical drainage may result in a chronic fistula. Hence, arthroscopic débridement, as recently suggested, may emerge as a viable or even preferred treatment option. Indications for excision of the olecranon bursa include prolonged drainage after surgical incision or rupture, recurrent septic bursitis, and chronic bursitis with contiguous osteomyelitis. Ablation is difficult, especially in the patient with rheumatoid arthritis. We have found that meticulous dissection under magnification with preliminary staining of the bursal wall using methylene blue and hydrogen peroxide is helpful.70 The incision should be lateral to the midline, not over the center of the bursa. In order to decrease the likelihood of recurrence, we lavage with a dilute solution of doxycycline, known as tissue-sclerosing agent. This approach seems to be effective in lessening the likelihood of a recurrence.

References 1. Ahbel, D. E., Alexander, A. H., Kleine, M. L., and Lichtman, D. M.: Protothecal olecranon bursitis. J. Bone Joint Surg. 62A:835, 1980. 2. Arafiles, R.: A new technique of fusion for THERABAND arthritis of the elbow. J. Bone Joint Surg. 63A:1396, 1981. 3. Argen, R. J., Wilson, C. H., and Wood, P.: Suppurative arthritis. Arch. Intern. Med. 117:661, 1966. 4. Ballard, A., Burkhalter, W. E., Mayfield, G. W., Dehne, E., and Brown, P. W.: The functional treatment of pyogenic arthritis of the adult knee. J. Bone Joint Surg. 57A:1119, 1975. 5. Bardenheier, J. A., Morgan, H. C., and Stamp, W. G.: Treatment and sequelae of experimentally produced septic arthritis. Surg. Gynecol. Obstet. 122:249, 1966. 6. Blockey, N. J., and McAllister, T. H.: Antibiotics in acute osteomyelitis in children. J. Bone Joint Surg. 54B:299, 1972. 7. Bongartz, T., Sutton, A. J., Sweeting, M. J., Buchan, I., Matteson, E. L., and Montori, V.: Anti-TNF antibody therapy in rheumatoid arthritis and the risk of serious infections and malignancies. Systematic review and metaanalysis of rare harmful effects in randomized controlled trials. J. A. M. A. 295:2275, 2006. 8. Brook, I., Reza, M., Bricknell, K. S., Bluestone, R., and Finegold, S. M.: Abnormalities in synovial fluid of patients with septic arthritis detected by gas-liquid chromatography. Ann. Rheum. Dis. 39:168, 1980. 9. Brower, A. C.: Septic arthritis. Radiol. Clin. North Am. 34:293, 1996. 10. Buskila, D., and Tenenbaum, J.: Septic bursitis in human immunodeficiency virus infection. J. Rheumatol. 16:1374, 1989. 11. Caksen, H., Ozturk, M. K., Uzum, K., Yuksel, S., Ustunba, H. B., and Per, H.: Septic arthritis in childhood. Pediatr Int. 42:534, 2000.

1066 Part VIII Septic and Nontraumatic Conditions

12. Canoso, J. J.: Idiopathic or traumatic olecranon bursitis. Arthritis Rheum. 20:1213, 1977. 13. Canoso, J. J., and Sheckman, P. R.: Septic subcutaneous bursitis: report of sixteen cases. J. Rheumatol. 6:1, 1979. 14. Carpenter, M. T., West, S. G., Vogelgesang, S. A., and Casey Jones, D. E.: Postoperative joint infections in rheumatoid arthritis patients on methotrexate therapy. Orthopedics 19:207, 1996. 15. Covey, D. C., and Albright, J. A.: Clinical significance of the erythrocyte sedimentation rate in orthopaedic surgery. J. Bone Joint Surg. 69A:148, 1987. 16. Daniel, D., Akeson, W., Amiel, D., Ryder, M., and Boyer, J.: Lavage of septic joints in rabbits: effects of chondrolysis. J. Bone Joint Surg. 58A:393, 1976. 17. Degan, T. J., Rand, J. A., and Morrey, B. F.: Musculoskeletal infection with nongonococcal Neisseria species not associated with meningitis. Clin. Orthop. 176:206, 1983. 18. den Broeder, A. A., Creemers, M. C. W., Fransen, J., de Jong, E., de Rooij, D.-J. R., Wymenga, A., de Waal-Malefijt, M., and van den Hoogen, F. H. J.: Risk factors for surgical site infections and other complications in elective surgery in patients with rheumatoid arthritis with special attention for anti-tumor necrosis factor: A large retrospective study. J. Rheumatol. 34:689, 2007. 19. Dixon, W. G., Watson, K., Lunt, M., Hyrich, K. L., Silman, A. J., and Symmons, D. P.: Rates of serious infection, including site-specific and bacterial intracellular infection, in rheumatoid arthritis patients receiving anti-tumor necrosis factor therapy: Results from the British Society for Rheumatology Biologics Register. Arthritis Rheum. 54:2368, 2006. 20. Erdman, W. A., Tamburro, F., Jayson, H. T., Weatherall, P. T., Ferry, K. B., and Peshock, R. M.: Osteomyelitis: characteristics and pitfalls of diagnosis with MR imaging. Radiology 180:533, 1991. 21. Garcia-Porrua, C., Gonzalez-Gay, M. A., Ibanez, D., and Garcia-Pais, M. J.: The clinical spectrum of severe septic bursitis in northwestern Spain: A 10 year study. J. Rheum. 26:663, 1999. 22. Gardner, G. C., and Weisman, M. H.: Pyarthrosis in patients with rheumatoid arthritis: a report of 13 cases and a review of the literature from the past 40 years. Am. J. Med. 88:503, 1990. 23. Gerster, J. C., Lagier, R., and Boivin, G.: Olecranon bursitis related to calcium pyrophosphate dihydrate crystal deposition disease. Arthritis Rheum. 25:989, 1982. 24. Gilday, D. L., Eng, B., Paul, D. J., and Paterson, J.: Diagnosis of osteomyelitis in children by combined blood pool and bone imaging. Radiology 117:331, 1975. 25. Giles, J. T., Bartlett, S. J., Gelberg, A. C., Nanda, S., Fontaine, K., Ruffing, V., and Bathon, J. M.: Tumor necrosis factor inhibitor therapy and risk of serious postoperative orthopedic infection in rheumatoid arthritis. Arthritis Rheum. 55:333, 2006. 26. Goldenberg, D. L., Brandt, K. D., Cohen, A. S., and Cathcart, E. S.: Treatment of septic arthritis. Arthritis Rheum. 18:83, 1975. 27. Goldenberg, D. L., and Cohen, A. S.: Acute infectious arthritis. Am. J. Med. 60:369, 1976.

28. Goldenberg, D. L., and Cohen, A. S.: Synovial membrane histopathology in differential diagnosis of arthritis. Medicine 57:239, 1978. 29. Grennan, D. M., Gray, J., Loudon, J., and Fear, S.: Methotrexate and early postoperative complications in patients with rheumatoid arthritis undergoing elective orthopaedic surgery. Ann. Rheum. Dis. 60:214, 2001. 30. Gristina, H.: Spontaneous septic arthritis in rheumatoid arthritics. J. Bone Joint Surg. 56A:1180, 1974. 31. Ho, G.: Bacterial arthritis. Curr. Opin. Rheum. 4:509, 1992. 32. Ho, G., and Su, E. Y.: Antibiotic therapy of septic bursitis. Arthritis Rheum. 24:905, 1981. 33. Ho, G., Tice, A. D., and Kaplan, S. R.: Septic bursitis in the prepatellar and olecranon bursae. Ann. Intern. Med. 89:21, 1978. 34. Hughes, S.: Radionuclides in orthopedic surgery. J. Bone Joint Surg. 62B:141, 1980. 35. Jackson, R. W., and Parsons, C. J.: Distension-irrigation treatment of major joint sepsis. Clin. Orthop. 96:160, 1973. 36. Jain, V. K., Cestero, R. V. M., and Baum, J.: Septic and aseptic olecranon bursitis in patients on maintenance dialysis. Clin. Exp. Dialysis Apheresis 5:4, 1981. 37. Kahn, D. S., and Pritzker, K.: The pathophysiology of bone infection. Clin. Orthop. 96:12, 1973. 38. Karchevsky, M., Schweitzer, M. E., Morrison, W. B., and Parellada, J. A.: MRI findings of septic arthritis and associated osteomyelitis in adults. Am. J. Radiol. 182:119, 2004. 39. Kelley, P. J., Martin, W. J., and Coventry, M. B.: Bacterial (suppurative) arthritis in the adult. J. Bone Joint Surg. 52A:1595, 1970. 40. Kelley, P. J.: Musculoskeletal infections due to Serratia. Clin. Orthop. 96:76, 1973. 41. Kelley, P. J.: Bacterial arthritis in the adult. Orthop. Clin. North Am. 6:973, 1975. 42. Kellgren, J. H., Ball, J., Fairbrother, R. W., and Barns, K. L.: Suppurative arthritis complicating rheumatoid arthritis. B.M.J. 1:1193, 1958. 43. Kolyvas, E., Ahroneim, G., Marks, M. I., Gledhill, R., Owen, H., and Rosenthal, L.: Oral antibiotic therapy of skeletal infections in children. Pediatrics 65:867, 1980. 44. Kumar, R., and Stephens, J. L.: Septic arthritis caused by Chryseobacterium meningosepticum in an elbow joint prosthesis. South. Med. J. 97:74, 2004. 45. Mahnken, A. H., Bucker, A., Adam, G., and Gunther, R. W.: MRI of osteomyelitis: Sensitivity and specificity of STIR sequences in comparison with contrast-enhanced T1 spin echo sequences. Rofo: Fortschritte auf dem Gebiete der Rontgenstrahlen und der Nuklearmedizin 172:1016, 2000. 46. Markowitz, R. I., Davidson, R. S., Harty, P. M., Bellah, R. D., Hubbard, A. M., and Rosenberg, H. K.: Sonography of the elbow in infants and children. Am. J. Rheum. 159:829, 1992. 47. Martini, M., and Gottesman, H.: Results of conservative treatment of TB of the elbow. Int. Orthop. 4:83, 1980. 48. Masi, A. T., and Eisenstein, B. I.: Disseminated gonococcal infection and gonococcal arthritis. Semin. Arthritis Rheum. 10:173, 1981.

Chapter 77 Septic Arthritis 1067

49. Meals, R. A.: The use of flexor carpi ulnaris muscle flap in treatment of infected non-union of the proximal ulna: A case report. Clin. Orthop. 240:168, 1989. 50. Morrey, B. F., and Bianco, A. J.: Septic arthritis in children. Orthop. Clin. North Am. 6:923, 1975. 51. Morrey, B. F., and Bryan, R. S.: Infection after total elbow arthroplasty. J. Bone Joint Surg. 65A:330, 1983. 52. Morrey, B. F., Fitzgerald, R. H., Kelly, P. J., Dobyns, J. H., and Washington, J. A., III: Diphtheroid osteomyelitis. J. Bone Joint Surg. 59A:527, 1977. 53. Morrey, B. F., and Peterson, H. A.: Hemotogenous pyogenic osteomyelitis in children. Orthop. Clin. North Am. 6:935, 1975. 54. Nelson, J. D.: The bacterial etiology and antibiotic management of septic arthritis in infants and children. Pediatrics 50:437, 1972. 55. O’Driscoll, S. W., Morrey, B. F., and An, K. N.: Intraarticular pressure and capacity of the elbow. Arthroscopy 6:100, 1990. 56. Ornvold, K., and Paepke, J.: Aspergillus terreus as a cause of septic olecranon bursitis. Am. J. Clin. Pathol. 97:114, 1992. 57. Peterson, S., Knudsen, F. U., Andersen, E. A., and Egebald, M.: Acute hematogenous osteomyelitis and septic arthritis in children. Acta Orthop. Scand. 51:451, 1980. 58. Pien, F. D., Ching, D., and Kim, E.: Septic bursitis: Experience in a community practice. J. Orthop. 14:981, 1991. 59. Pineda, C., Vargas, A., Rodriguez, A. V.: Imaging of osteomyelitis: Current concepts. Infect. Dis. Clin. N. A. 20:789, 2006. 60. Rashkoff, E., and Burkhalter, W. E.: Arthrodesis of the salvage elbow. Orthopedics 9:733, 1986. 61. Rimoin, D. L., and Wennberg, J. F.: Acute septic arthritis complicating chronic rheumatoid arthritis. J. A. M. A. 196:109, 1966. 62. Roschmann, R. A., and Bell, C. L.: Septic bursitis in immunocompromised patients. Am. J. Med. 83:661, 1987. 63. Saini, M., and Canoso, J. J.: Traumatic olecranon bursitis. Acta Radiol. Diagn. 23:255, 1982. 64. Salter, R. B., Bell, R. S., and Kelley, F. W.: The protective effect of continuous passive motion on living articular cartilage in acute septic arthritis. Clin. Orthop. 159:223, 1981. 65. Schoifet, S. D., and Morrey, B. F.: Treatment of infection after total knee arthroplasty by debridement with retention of components. J. Bone Joint Surg. 72A:1383, 1990. 66. Schulak, D. J., Rayhack, J. M., Lippert, F. G., III, and Convery, F. R.: The erythrocyte sedimentation rate in orthopaedic patients. Clin. Orthop. 167:197, 1982. 67. Sharma, S. V., Varma, B. P., and Khanna, S.: Dystrophic calcification in tubercular lesions of bursae. Acta Orthop. Scand. 49:445, 1978. 68. Shulman, G., and Waugh, T. R.: Acute bacterial arthritis in the adult. Orthop. Rev. 17:955, 1988.

69. Soderquist, B., and Hedstom, S. A.: Predisposing factors, bacteriology and antibiotic therapy in thirty-five cases of septic bursitis. Scand. J. Infect. Dis. 18:305, 1986. 70. Stewart, N. J., Manzanares, J. B., and Morrey, B. F.: Surgical treatment of aseptic olecranon bursitis. J. Shoulder Elbow Surg. 6:49, 1997. 71. Stumpe, K. D. M., and Strobel, K.: 18F FDG-PET imaging in musculoskeletal infection. The Q. J. Nucl. Med. Mol. Imaging 50:131, 2006. 72. Sullivan, D. C., Rosenfield, N. S., Ogden, J., and Gottschalk, A.: Problems in the scintigraphic detection of osteomyelitis in children. Radiology 135:731, 1980. 73. Tollerud, A.: Anaerobic septic bursitis [obletter]. Ann. Intern. Med. 91:494, 1979. 74. Törholm, C., Hedström, S. A., Sundén, G., and Lidgren, L.: Synovectomy in bacterial arthritis. Acta Orthop. Scand. 54:748, 1983. 75. Trueta, J.: Three types of acute hematogenous osteomyelitis. J. Bone Joint Surg. 41B:671, 1959. 76. Viggiano, D. A.: Septic arthritis presenting as olecranon bursitis in patients with rheumatoid arthritis. J. Bone Joint Surg. 62A:1011, 1980. 77. Waldvogel, F. A., Medoff, G., and Swartz, M. D.: Osteomyelitis: A review of clinical features, therapeutic considerations and unusual aspects. N. Engl. J. Med. 282:198, 260, 316, 1970. 78. Weston, V. C., Jones, A. C., Bradbury, N., Fawthrop, F., and Doherty, M.: Clinical features and outcome of septic arthritis in a single UK Health District 1982-1991. Ann. Rheum. Dis. 58:214, 1999. 79. West, W. F., Kelley, P. J., and Martin, W. J.: Chronic osteomyelitis. J. A. M. A. 213:1837, 1970. 80. Wilensky, A. O.: Osteomyelitis. Its Pathogenesis, Symptomatology, and Treatment. New York, Macmillan, 1934. 81. Willems, C.: Treatment of purulent arthritis by wide arthrotomy followed by immediate active mobilization. Surg. Gynecol. Obstet. 28:546, 1919. 82. Wilson, J. N.: Tuberculosis of the elbow. J. Bone Joint Surg. 35B:558, 1953. 83. Winroth, G., Hedström, S. A., and Lidgren, L.: Posttraumatic bacterial arthritis with luxation of the elbow: A case report. Arch Orthop. Trauma Surg. 103:227, 1984. 84. Winter, W. G., Larson, R. K., Honeggar, M. M., Jacobsen, D. T., Pappagianis, D., and Huntington, R. W.: Coccidioidal arthritis and its treatment. J. Bone Joint Surg. 57A:1152, 1975. 85. Wolfgang, G. L.: Tuberculous joint infection. Clin. Orthop. 136:257, 1978. 86. Zimmermann III, B., Mikolich, D. C., and Ho, G.: Septic bursitis. Semin. Arthritis Rheum. 24:391, 1995. 87. Zretina, J. R., Foster, J., and Reyes, C. V.: Mycobacterium kansasii infection of the elbow joint. J. Bone Joint Surg. 61A:1099, 1979.

1068 Part VIII Septic and Nontraumatic Conditions

CHAPTER

78

Hematologic Arthritis Joaquin Sanchez-Sotelo

INTRODUCTION This chapter reviews the elbow pathology associated with some hematologic conditions characterized by joint involvement. The symptoms and radiographic changes of hematologic arthritis resemble inflammatory conditions such as rheumatoid arthritis. The medical treatment of the underlying process plays an important role in the management of elbow symptoms. Hemophilia and sickle cell disease represent the most common examples of hematologic arthritis. The elbow may also be affected in other conditions such as leukemia and other myeloproliferative disorders. The management of elbow problems in patients with underlying hematologic conditions requires a multidisciplinary approach.

HEMOPHILIC ARTHROPATHY Recurrent hemarthrosis and subsequent hemophilic arthropathy are seen only in patients with hemophilia A (classic hemophilia, factor VIII deficiency) or hemophilia B (Christmas disease, factor IX deficiency) and a moderate (plasma factor level between 1% and 5%) or severe (plasma level less than 1%) coagulation deficiency. Rarely, hemophilic arthropathy may develop in patients with Von Willebrand’s disease (reduced levels of the Von Willebrand cofactor, needed for factor VIII activity). The elbow is frequently involved with acute hemarthrosis.14 In addition, the elbow is the second most common site of arthropathy in the hemophilic patient after the knee joint. A 1965 report from Sweden surveyed 114 patients with hemophilia A and 43 patients with hemophilia B.1 Sixty-six of the 95 severely affected and 20 of the 38 moderately affected patients had elbow involvement; 59 patients had bilateral elbow involvement. The severity of the arthropathy in all joints increased with age and disease severity.

PATHOGENESIS Hemophilia is an X-chromosome–linked disease characterized by a deficiency or functional defect of

coagulation factors VIII or IX, which results in an increased bleeding tendency. Hemophilic arthropathy is believed to be the consequence of repeated episodes of intra-articular bleeding, which can occur spontaneously or as a result of trauma.21 Joint destruction is the result of the direct deleterious effect of joint hematoma on the metabolism of the articular cartilage and the secondary hypertrophic synovitis, which leads to cartilage and bone destruction as well as soft tissue contractures (Box 78-1). Increases in intra-articular pressure may also play a role in producing the degenerative changes.39 The growth plates may be affected in children, which may result in associated angular deformity. The pathogenesis and management of hemophilic arthropathy may be further complicated by the presence of a coexistent human immunodeficiency virus (HIV) infection.10

EVALUATION Patients with hemophilic arthropathy of the elbow may present in various stages of the disease. The first episodes of acute elbow hemarthrosis present with severe pain, effusion, and limited motion. As joint degeneration progresses, patients develop various grades of pain, stiffness, and deformity. Gamble et al18 measured elbow motion in 48 patients with hemophilia followed for an average of 10.8 years. Patients older than 25 years had decreased motion in all planes compared with patients younger than 15 years. Pronation was the first motion to be restricted, and extension was the motion most affected at the end of follow-up. Interestingly, many patients with hemophilic arthropathy are more limited by their lack of pronation and supination than by limited flexion and extension. Hemophilic arthropathy commonly affects other joints including the knees and ankles. In the upper extremity, the elbow is more commonly affected than the shoulder or the wrist; in a series of 23 moderate and severe hemophiliacs, the elbow joints were the site of recognizable arthropathy in 87% of the cases, whereas the shoulder and wrist were affected in a small proportion of patients.21 When surgery is contemplated, attention should be paid to the order in which the different joints need to be addressed. Hemophilic pseudotumors are an uncommon but well-known musculoskeletal complication of hemophilia.29 Pseudotumors occur in approximately 1% to 2% of patients with bleeding disorders. They present usually as an enlarging mass secondary to intraosseous, subperiosteal or intramuscular bleeding with various degrees of bone and soft tissue compromise. They can compress adjacent neurovascular structures and be misdiagnosed as true malignancies based on their clinical and radiographic features.

Chapter 78 Hematologic Arthritis 1069

Imaging Studies Hemophilic arthropathy usually presents with joint line narrowing, spurs, subperiosteal new bone formation, and occasionally, bone loss or deformity. A number of classification systems have been developed to rate the severity of the radiographic changes in hemophilic arthropathy. The system published by Arnold and Hilgarter3 has been extensively used in the literature and includes five stages as detailed in Box 78-2 (see Figs. 78-1 through 78-4). More recently, the World Federation of Hemophilia has adopted the radiographic scoring and classification system proposed by Peterson et al32 and based on the

BOX 78-1

Pathogenesis of Hemophilic Arthropathy

• Direct deleterious effect of joint hematoma on • Articular cartilage • Bone • Capsule and ligaments • Secondary hypertrophic synovitis • Cartilage, bone and soft tissue damage • Contracture • Growth plate abnormalities • Growth deformities (angular, others) • HIV infection • Arthropathy • Opportunistic infections • Extensive localized bleeding leading to pseudotumor

FIGURE 78-1

following eight aspects: osteoporosis, hypertrophy of the endplate, loss of joint space, irregular subchondral surface, subchondral cysts, erosion of the joint surface, incongruity of the joint surfaces, and deformity of the joint. The score ranges from 0 (no radiographic abnormalities) to 13 (severe arthropathy). Some authors have identified three main patterns of joint involvement.19,43 Patients with involvement of predominantly the medial side of the joint present with ulnohumeral joint narrowing and medial spurring, which may irritate the ulnar nerve. Involvement of the lateral side of the joint is associated with radial head enlargement, posterolateral elbow pain, and restriction

Radiographic Classification of Hemophilic Arthropathy3

BOX 78-2

Stage

I II

III

IV V

Features

No skeletal abnormalities Soft issue swelling present Osteoporosis, epiphyseal overgrowth Normal joint line No bone cysts Subchondral joint changes Subchondral cysts visible Trochlear notch widened Joint space narrowing Loss of joint space Joint contracture Enlargement of epiphyses or architectural changes

A and B, Stage II hemophilic arthropathy with overgrowth of the ends of the bones, particularly the radial head. The joint space is maintained.

1070 Part VIII Septic and Nontraumatic Conditions

FIGURE 78-2

A, An example of stage III arthropathy demonstrating subchondral cysts in the distal humerus, the capitellum, and the trochlea. B, The joint spaces are fairly well preserved in the lateral view; however, there is some narrowing of the ulnohumeral joint space and opacification of the synovium (arrow).

FIGURE 78-3

A, Radiographs of the same patient shown in Figure 78-2 taken 5 years later show progressive changes with loss of the joint space narrowing and loss of cartilage (stage IV). B, Again the arrow shows opacification of the synovium.

of pronation and supination. Finally, global involvement of the joint is associated usually with more severe stiffness affecting all planes of motion. As with other inflammatory conditions, magnetic resonance imaging has been used to more precisely evaluate abnormalities of the articular cartilage, soft tissues, and synovium and to monitor the progression of the arthropathy.46 Several scoring systems based on

magnetic resonance findings have been developed to identify patients at risk for the development of severe arthropathy and to prevent articular changes by the use of more intensive medical treatment.25,26

Laboratory Studies The evaluation of patients with hemophilic arthropathy should be completed with coagulation studies and

Chapter 78 Hematologic Arthritis 1071

FIGURE 78-4

A and B, Stage V arthropathy showing marked loss of joint space with extensive enlargement of the epiphysis. Some degree of contracture is evident by the incomplete extension visible on the anteroposterior film.

laboratory tests to detect HIV or hepatitis C infections, when indicated.

TREATMENT Medical Management The treatment of hemophilia requires correction of the coagulation defect by replacement of the deficient factor. Patients with mild hemophilia A or Von Willebrand’s disease may benefit from treatment with desmopressin, which releases factor VIII from endothelial storage sites. At present, recombinant concentrates of factors VIII and IX are the products of choice for factor replacement. The regular administration of replacement therapy with the object of reducing spontaneous bleeding is a logical approach. The goal is to maintain the factor VIII or IX level above 1%. This can be achieved by factor concentrate administration two or three times a week. Some physicians recommend factor replacement for all patients, whereas others favor treating only those patients with frequent bleeding episodes. Starting treatment at a younger age seems to protect against later development of hemophilic arthropathy.17 Replacement therapy is also the treatment of choice of bleeding episodes. The desired factor level is a function of the severity and location of the bleeding episode. Joint or muscle bleeding episodes are treated to achieve factor levels of 30% to 50%. Replacement therapy is also critical when surgery is considered.10 Most orthopedic surgery can be managed with initial levels of 80% to

100%, followed in a few days by minimum levels of at least 30%. Joint manipulation under anesthesia requires levels of at least 50%. The number of units required to obtain these titers is calculated based on the body weight and the volume of distribution, which is 1.5 for factor VIII and 1.2 for factor IX. Factor levels should be checked to ensure the effectiveness of the calculated dose. Patients with factor VIII inhibitor require a specific approach; if the inhibitor titer is below 5 BU, recombinant VII factor is administered. If the inhibitor titer is greater than 5 BU, there are three treatment options: porcine factor VIII, factor VIII inhibitor bypassing activity (FEIBA), or recombinant factor VIIa. Intra-articular injections with steroids may help control some of the inflammatory symptoms of hemophilic arthropathy. Oral steroids may be considered in patients with severe inflammatory symptoms. Physical therapy should also be recommended to preserve elbow flexion and extension as well as forearm pronation and supination. Self-adjustable static elbow splints may be beneficial to improve motion after acute hemarthrosis or in patients with chronic arthropathy.

Acute Hemarthrosis The treatment of acute hemarthrosis is mostly medical, and includes factor replacement and analgesia. The goal of replacement therapy is to maintain levels of 50% to 100% (or increase the plasma level between 20% and 50%) until the bleeding stops. Prompt replacement therapy is advised at the earliest sign of bleeding,

1072 Part VIII Septic and Nontraumatic Conditions

especially in younger patients, in order to prevent joint degeneration. Well-trained patients and families are able to administer their replacement therapy at home without examination by a physician, which might delay treatment. As mentioned earlier, for patients with mild hemophilia A or type I Von Willebrand disease, intravenous or intranasal desmopressin acetate may help control the bleeding episode. Treatment of acute hemarthrosis with desmopressin should only be considered if a previous trial dose has demonstrated a reasonable rise in the missing factor. Desmopressin doses cannot be repeated more frequently than every 48 to 72 hours to avoid the development of tachyphylaxis. Tense painful hemarthrosis may be aspirated under factor replacement coverage. The needle is introduced into the joint usually in the soft spot centered between the radial head, the tip of the olecranon, and the lateral epicondyle. Aspiration should not be performed until the clotting factor has been raised to at least 50%. Uncontrolled massive joint bleeding may be controlled through selective angiographic embolization of the affected blood vessels.30 Acute ulnar nerve compression requiring surgical intervention has been reported as a complication of acute elbow hemarthrosis.27

Established Arthropathy Synoviorthesis involves injecting a pharmacologic agent into the joint with the aim of stabilizing the synovial membrane. Several agents may be used for this process, including radioactive gold, yttrium90, phosphorus-32, rifampicin, osmic acid, and hyaluronic acid.9,16,34,37 Phosphorus-32 (chromic phosphate) is the agent approved by the U.S. Food and Drug Administration for synoviorthesis in hemophiliacs.12 When injected into the joint, these agents remove inflamed synovium, which decreases the frequency and severity of intra-articular bleeding episodes.9 Synoviorthesis is considered usually when the synovitis and recurrent bleeding are not controlled with factor replacement, anti-inflammatory medications, and physical therapy used for 3 to 6 months. It is especially recommended in patients with inhibitors to the clotting factor, advanced HIV infection or hepatitis, or multiple joint involvement. The results are somewhat unpredictable: in a series of 29 elbows treated with synoviorthesis using radioactive gold, results were satisfactory in eight cases at an average follow-up of 14 years.34 In this study, synoviorthesis decreased the frequency of bleeding but did not prevent joint degeneration.

Synoviorthesis

synoviorthesis attempts or when limited motion impairs elbow function but the joint may still be salvaged.24 The procedure involves synovectomy, resection of any contracted capsule, removal of osteophytes, recreation of the humeral fossae, and occasionally, radial head resection. This procedure is most commonly performed through an open lateral approach or arthroscopically. Arthroscopic synovectomy has the potential of decreasing the rate of recurrent hemarthrosis and improving joint function while being associated with lower postoperative morbidity and fewer hospitalizations compared to open surgery (Fig. 78-5).45 Several studies have confirmed these findings in the adult as well as the pediatric population.13,22 In some series, the median bleeding frequency decline approached 85%.13 The indications of radial head resection are controversial; it should be considered when radial head deformity and degeneration are believed to interfere with forearm rotation and responsible for lateral-sided elbow pain. Radial head resection may also allow a more complete synovectomy, and probably was one of the reasons for radial head resection before the advent of arthroscopic synovectomy. There is some published information on the results of joint débridement for hemophilic arthropathy of the elbow. Kay et al24 reported on 12 elbows treated with synovectomy and followed between 1 and 5 years. The average number of bleeding episodes over a 12-month period was decreased from 24 to 3. Five patients lost an average 28 degrees and six improved an average of 11 degrees of motion. Complications occurred in 25% of the cases. Le Balc’h et al28 reported on 23 elbows

Synovectomy, Radial Head Resection, and Contracture Release Surgical débridement and synovectomy of the

elbow joint is indicated when the hemophilic arthropathy fails to respond to replacement therapy and three

FIGURE 78-5

At present, arthroscopic synovectomy is effective in removing the diseased synovium.

Chapter 78 Hematologic Arthritis 1073

followed for 18 to 70 months after synovectomy. Patient age ranged from 8 to 25 years of age. Moderate pain persisted in only three, pronation and supination improved in nine, and flexion-extension improved in 14 elbows. Four elbows presented recurrent bleeding. Interestingly, arthroscopic synovectomy has been shown to be cost effective in a small series of 11 patients who required arthroscopy of the ankle (seven cases), elbow (three cases) or knee (one case). In this group of patients, the average cost per month was $7500 before surgery and decreased to $900 after surgery.42 Total elbow arthroplasty is considered for patients with severe joint destruction, provided they understand and are willing to comply with postoperative weight restrictions. Ideally, this procedure should be reserved for older patients. The results of total elbow arthroplasty for hemophilic arthropathy in two separate institutions have been reported recently. Five patients underwent seven elbow arthroplasties at Oxford using several designs, including the Kudo, Souter, and Coonrad-Morrey prostheses.7,23 There were significant improvements in pain and function at an average follow-up of 2 years. Complications included deep infection requiring resection, ulnar nerve palsy, and axillary vein thrombosis. Kamineni et al23 recently reviewed the results of five total elbow arthroplasties performed at the Mayo Clinic for hemophilic arthropathy. The mean age of the patients was 39 years (range, 25 to 58 years). All patients had concurrent HIV infection. At a mean follow-up of 5.8 years (range, 1 to 11 years), one patient developed uncontrollable hemorrhage and was eventually diagnosed with a deep infection requiring implant removal. One additional late hematogenous deep infection could be controlled by joint débridement and polyethylene exchange. At most recent follow-up, pain and motion were improved significantly in all four patients with a surviving implant (Fig. 78-6). Radiographic loosening was evident in one of the four cases. Arthroplasty

Pseudotumors The treatment of pseudotumors is somewhat controversial and depends on the location and severity of the symptoms. Rapidly growing lesions in the distal part of the skeleton in children usually respond better to nonoperative treatment, whereas slowly growing lesions in the proximal part of the skeleton in adults usually leads to bone erosions and fail to respond to nonoperative treatment.2,36 Hemophilic pseudotumors are initially treated with intensive replacement therapy during 6 weeks. If the pseudotumor regresses by 25% to 50%, nonoperative treatment may be continued. Otherwise, consideration should be given to percutaneous drainage or surgical

FIGURE 78-6

Lateral radiograph 18 months after total elbow arthroplasty for hemophilic arthropathy.

removal. Small pseudotumors may be drained and injected with fibrin glue.6 Surgical resection if larger pseudotumors is associated with good results.36

SICKLE CELL DISEASE The term sickle cell disease is used to include various inherited diseases characterized by the presence of hemoglobin S (sickle hemoglobin). Hemoglobin S imparts a sickle shape to deoxygenated erythrocytes. Sickle cell heterozygosis results in sickle cell trait (hemoglobin AS), whereas sickle cell homozygosity results in sickle cell disease (hemoglobin SS). Bone and joint involvement is exceedingly rare in patients with sickle cell trait. A study of 94 patients with sickle cell trait found no significant difference in the frequency of joint symptoms or objectively demonstrable joint disease when compared with 114 black people with normal hemoglobin electrophoretic patterns.11 In contrast, most if not all patients with homozygous sickle cell anemia experience bone or joint crisis, and bone and joint problems are the most common manifestations (Box 78-3). In a prospective study of 56 adults with SS disease, 31 individuals suffered a total of 61 separate episodes of joint involvement during a 6- to 18-month observation period.15 The elbow was affected

1074 Part VIII Septic and Nontraumatic Conditions

Musculoskeletal Manifestations of Sickle Cell Disease

BOX 78-3

• • • • •

Vaso-occlusive crises Osteomyelitis and septic arthritis Osteonecrosis Sickle cell synovitis and arthropathy Associated inflammatory conditions

at one time or another in 13 patients (42%) usually in association with involvement of other large joints.

PATHOGENESIS Hemoglobin S results from the inherited substitution of valine for glutamic acid as the sixth amino acid of the beta globin chain. This minor change produces profound alterations in the stability and solubility of the hemoglobin molecule.5 Hemoglobin S molecules polymerize in hypoxic and acidic environments, imparting a sickle shape to erythrocytes. Sickle erythrocytes show increased adhesion. Interaction of sickle cells with adhesion proteins of the vascular endothelium initiates an inflammatory response, which further increases cellular adhesiveness. Increased adhesion and inflammation decrease blood flow, leading to further sickling. Repeated episodes of decreased blood flow may lead to impaired nourishment of critical structures. Vascular occlusion is responsible for the bone and joint manifestations of sickle cell disease, including avascular necrosis and increased risk for infection. Synovial biopsy specimens generally reveal microvascular thrombosis, with occasional intraluminal sickled cells, perivascular fibrosis, and mononuclear inflammatory cell infiltration.35

mild (i.e., barely interfering with normal lifestyle) to excruciating. The long bones are affected most commonly, but virtually any bony structure may be affected. In a study of 192 children with sickle cell disease, the bones more commonly affected were the humerus (38%), tibia (23%), and femur (19%).

Septic Arthritis and Osteomyelitis The risk of bacterial infection is increased in children with sickle cell disease due to an early decrease in splenic function, genetic polymorphisms of binding proteins, and human leukocyte antigen (HLA) class II alleles.41 Areas of infarcted bone or bone marrow are typical sites for infections.4 Osteomyelitis is usually due to Salmonella or other gram-negative organisms such as Escherichia coli.4 Staphylococcus aureus, the most common cause of osteomyelitis in normal hosts, probably accounts for only one fourth of all cases in sickle cell disease. Septic arthritis is less common than osteomyelitis. The clinical presentation of osteomyelitis and septic arthritis often is similar to a vaso-occlusive crisis, and the exact diagnosis is often difficult to make. In general, infectious episodes are more likely to be associated with fever, longer lasting pain, and decreased range of motion.

Avascular Necrosis and Arthropathy Joint osteonecrosis is a well-described complication of sickle cell disease.20 The femoral and humeral head are most commonly affected, but the distal humerus may also develop avascular necrosis. It usually presents with elbow pain and stiffness, which usually worsen as secondary degenerative changes ensue. Joint degeneration may also be secondary to microvascular and inflammatory changes in the synovium.35 Finally, inflammatory conditions, such as rheumatoid or gouty arthritis, may coexist with sickle cell disease and contribute to degenerative articular changes.31

Imaging Studies

CLINICAL EVALUATION Vaso-occlusive Crisis Repeated painful vaso-occlusive crises are the hallmark of sickle cell disease. However, their prevalence is highly variable. In a prospective observational study of 3578 patients, the average rate of painful crises per patientyear was 0.8; however, almost 40% of all patients had no episodes of pain, whereas 5% of the patients accounted for one third of all episodes.33 The clinical presentation of a vaso-occlusive episode in a bony structure is dominated by an acute onset of deep-seated pain, often described by the patient as “typical sickle cell pain.” Mild erythema and warmth, as well as local tenderness, usually are present, and many patients have a low-grade fever. Pain may vary from

Plain radiographs may show various degrees of bone and joint involvement. Vaso-occlusive episodes may be associated with negative radiographs initially, but increased radiographic density is not uncommon in 1 or 2 weeks. Osteomyelitis may have a similar radiographic appearance. Avascular necrosis is characterized by increased density followed by subchondral fracturing and collapse with secondary degenerative changes. The radiographic appearance of sickle cell arthropathy with or without avascular necrosis may be indistinguishable from other inflammatory arthritis. Magnetic resonance imaging helps diagnose avascular necrosis in the early stages and may play a role in differentiating osteomyelitis from areas of bone infarction or osteonecrosis.35 Bone scans have also been used to identify infection with variable success.38

Chapter 78 Hematologic Arthritis 1075

Microbiologic studies are needed to confirm the diagnosis of osteomyelitis or septic arthritis and guide treatment based on the results of the cultures and sensitivities. When septic arthritis is suspected, joint aspiration should be performed. The diagnosis of osteomyelitis may require culture of surgical biopsies.

MANAGEMENT Vaso-occlusive Crises Treatment of vaso-occlusive crises consists of hydration (100% to 150% of normal daily fluids), warm packs to the affected area, analgesics, and anti-inflammatory medication. Narcotics are usually needed to control the pain associated with vaso-occlusive crises. Patients with HbSS or HbS-beta(0) thalassemia and repeated episodes of vaso-occlusive crises should be considered for therapy with hydroxyurea, which may decrease the frequency of painful episodes in children and adults.8 The possible beneficial effects of other drugs such as azatidicine, magnesium pidolate, and clotrimazole derivatives is under investigation.

Septic Arthritis and Osteomyelitis The treatment of septic arthritis and osteomyelitis is not different from treatment in normal hosts. Septic arthritis is best treated with open or arthroscopic débridement followed by the appropriate antibiotic medication. When open débridement is performed, our preferred approach is the same described for the so-called lateral column procedure, because it requires a relatively small incision and relatively minimal deep soft tissue dissection, preserves the lateral collateral ligament complex, and provides good exposure for débridement. However, arthroscopic débridement is our treatment of choice, although it requires experience with arthroscopic elbow surgery. Postoperatively, antibiotics are usually administered intravenously for a minimum of 6 weeks. Osteomyelitis may also require surgery, especially when extensive or associated with draining fistulas; however, osteomyelitis may respond to antibiotic therapy.

considered in younger patients when higher physical demands are expected.

Surgery in Patients with Sickle Cell Disease Caution is needed whenever a patient with sickle cell disease needs to undergo anesthesia and surgery. Any surgical procedure may be associated with changes in body temperature, oxygen tension, and pH, which may precipitate hemolysis and vaso-occlusive phenomenons. Care should be taken to maintain optimal oxygenation and pH and to avoid a decrease in either central or peripheral body temperature.

LEUKEMIA AND OTHER MYELOPROLIFERATIVE DISORDERS Leukemia and other myeloproliferative disorders may present with symptoms at the elbow secondary to (1) bone involvement with the myeloproliferative disorders or (2) distal humerus osteonecrosis associated with chemotherapy and treatment with steroids.40 These disorders are also known to be associated with a higher incidence of fractures,40 but they rarely affect the elbow joint. Joint involvement is more common in acute than chronic leukemia and in children compared with adults (Fig. 78-7).44 Surgical treatment is only required for patients with osteonecrosis.

Synovitis, Avascular Necrosis, and Arthropathy Early synovitis without extensive joint damage may respond to arthroscopic débridement. Avascular necrosis and end-stage arthropathy may require reconstructive surgery. Elbow arthroplasty is the treatment of choice for end-stage disease, provided that the patient understands and is willing to comply with postoperative restrictions to decrease the risk of mechanical failure. Distal humerus hemiarthroplasty is a very attractive option for patients without secondary degenerative changes at the proximal ulna and radius. Other reconstructive options, such as interposition arthroplasty or arthrodesis, are less attractive but may need to be

FIGURE 78-7

Myeloid metaplasia shows a mottled radiographic appearance with demineralization on both sides of the joint.

1076 Part VIII Septic and Nontraumatic Conditions

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39.

cell disease. Rates and risk factors. N. Engl. J. Med. 325:11, 1991. Rodriguez-Merchan, E. C., Magallon, M., Galindo, E., and Lopez-Cabarcos, C.: Hemophilic synovitis of the knee and the elbow. Clin. Orthop. Relat. Res. 343:47, 1997. Schumacher, H. R., Andrews, R., and McLaughlin, G.: Arthropathy in sickle-cell disease. Ann. Intern. Med. 78:203, 1973. Shaheen, S., and Alasha, E.: Hemophilic pseudotumor of the distal parts of the radius and ulna. A case report. J. Bone Joint Surg. Am. 87:2546, 2005. Siegel, H. J., Luck, J. V., Jr., Siegel, M. E., Quines, C., and Anderson, E.: Hemarthrosis and synovitis associated with hemophilia: clinical use of P-32 chromic phosphate synoviorthesis for treatment. Radiology 190:257, 1994. Skaggs, D. L., Kim, S. K., Greene, N. W., Harris, D., and Miller, J. H.: Differentiation between bone infarction and acute osteomyelitis in children with sickle-cell disease with use of sequential radionuclide bone-marrow and bone scans. J. Bone Joint Surg. Am. 83-A:1810, 2001. Sokoloff, L.: Biochemical and physiological aspects of degenerative joint diseases with special reference to hemophilic arthropathy. Ann. N. Y. Acad. Sci. 240:285, 1975.

40. Strauss, A. J., Su, J. T., Dalton, V. M., Gelber, R. D., Sallan, S. E., and Silverman, L. B.: Bony morbidity in children treated for acute lymphoblastic leukemia. J. Clin. Oncol. 19:3066, 2001. 41. Tamouza, R., Neonato, M. G., Busson, M., Marzais, F., Girot, R., Labie, D., Elion, J., and Charron, D.: Infectious complications in sickle cell disease are influenced by HLA class II alleles. Hum. Immunol. 63:194, 2002. 42. Tamurian, R. M., Spencer, E. E., and Wojtys, E. M.: The role of arthroscopic synovectomy in the management of hemarthrosis in hemophilia patients: financial perspectives. Arthroscopy 18:789, 2002. 43. Utukuri, M. M., and Goddard, N. J.: Haemophilic arthropathy of the elbow. Haemophilia 11:565, 2005. 44. Weinberger, A., Schumacher, H. R., Schimmer, B. M., Myers, A. R., and Brogadir, S. P.: Arthritis in acute leukemia. Clinical and histopathological observations. Arch. Intern. Med. 141:1183, 1981. 45. Wiedel, J. D.: Arthroscopic synovectomy: state of the art. Haemophilia 8:372, 2002. 46. Yulish, B. S., Lieberman, J. M., Strandjord, S. E., Bryan, P. J., Mulopulos, G. P., and Modic, M. T.: Hemophilic arthropathy: assessment with MR imaging. Radiology 164:759, 1987.

1078 Part VIII Septic and Nontraumatic Conditions

CHAPTER

79

Neurotrophic Arthritis J. Clarke Stevens

INTRODUCTION As noted in prior editions of this book, little has occurred in recent years to change the fact that neurotrophic arthritis of the elbow is distinctly unusual, and poorly understood and treated. Although a large number of causes of neurotrophic arthritis are recognized (Box 79-1), diagnosis is made simpler by the fact that only five or six of these causes affect the upper extremity joints, and only three occur with any frequency at all. In fact, a Medline literature search has revealed that only two case reports have appeared in the literature since 1996.48,69,73 In this section, the causes and pathogenesis of neurogenic arthropathy of the elbow are discussed, along with laboratory investigations and differential diagnosis. Arthropathy of lower limb joints and the spine will not be considered, but references cited in Box 79-1 are provided to direct the interested reader to other sources of information. A recent excellent review of the subject is available.56

PATHOGENESIS Debate about the pathogenesis of neurotrophic arthritis began with Charcot’s paper in 1868,14 and today our understanding of the pathophysiology remains incomplete. Charcot, observing the posterior column demyelination of tabes dorsalis, suggested the loss of a trophic function protecting joints as a pathophysiologic mechanism. This view was soon challenged by those who believed that the disorder resulted from trauma. A major advance in our understanding followed the often-quoted work of Eloesser,26 who sectioned the posterior roots of the hindlimb of cats. Deafferentation combined with thermocautery of the joint cartilage led to the rapid development of neurogenic arthropathy, bone fractures, and dislocations, emphasizing the role of insensitivity and trauma. The results of chemical analysis and tests of bone strength and elasticity were normal—evidence against Charcot’s view that the joints and bones wasted from an abnormality of trophic nerves. The roles of

insensitivity, activity, and trauma were further emphasized by Corbin and Hinsey,19 who found that cats with loss of sensation developed a Charcot joint only if they were allowed to roam freely in the cage, whereas those kept in a restricted space did not. These researchers were impressed by the importance of proprioceptive loss, which allowed an abnormal range of joint movement. It is also recognized that limbs rendered immobile by spasticity rarely develop an arthropathy. An important observation of Harris and Brand36 was that joint breakdown in the neuropathy of leprosy can be minimized or prevented by proper protection. Johnson37 emphasized the importance of unrecognized and untreated fractures, especially stress fractures, in the development of neurogenic arthropathy.

LOSS OF NOCICEPTION The most widely held view on the pathogenesis of Charcot joints, then, involves a loss of protective joint nociception and position sense that subjects the joint to repeated trauma that is not recognized by the affected individual. The neurologically normal patient with an injured joint presents quickly with development of pain and loss of function, leading to immobilization and the search for appropriate medical treatment. In the neurologically impaired person, on the other hand, unrecognized injury is untreated and leads to a vicious circle of compounding injuries. This explanation is intuitively reasonable, particularly in the presence of severe superficial and deep loss of pain perception. It is more difficult to invoke when joint destruction evolves, but sensory loss is minimal or difficult to demonstrate. For example, the author has studied patients with subclinical inherited neuropathy with severe neurotrophic arthropathy of various joints and recurring fractures who had no sensory symptoms or findings on clinical examination.24 Even with sophisticated tests, including computerassisted sensory examination, periosteal nociception, and morphometric and graded teased fiber evaluation of cutaneous nerves, only a mild neuropathic abnormality was found. Methods of measuring joint capsule and articular bone pain perception are not available; however, cortical bone is known to contain both unmyelinated and myelinated fibers, and presumably some of these subserve nociception.18 Joint capsules, particularly in their external layers, contain several types of formed corpuscles and naked nerve endings. Synovium has not been observed to contain nerve endings. Although pain sense is carried by both small myelinated and unmyelinated fibers, the relative importance of these two systems in normal protective joint sensation is unknown. In those puzzling patients in whom sensation appears to be normal, a new method of measuring joint pain perception or afferent nerve fiber activity is needed.

Chapter 79 Neurotrophic Arthritis 1079

BOX 79-1

Etiology of Neurogenic Arthropathy

I.

Brain A. Congenital indifference (asymbolia) to pain29,50,58 B. “Stoic” individual37 C. Functional abnormality of enkephalins, endorphins, or opiate receptors?24 II. Spinal Cord A. Tabes dorsalis16,40,54,62,64,67,71 B. Syringomyelia31,34 C. Paraplegia65 D. Radiation myelopathy71 E. Myelomeningocele12,73 F. Subacute combined degeneration35 G. Arachnoiditis—tubercle bacillus,47 spinal anesthetic72 H. Multiple sclerosis72 I. Idiopathic?5,43 J. Spinal cord tumor K. Traumatic syringohydromyelia51 III. Peripheral Nerve A. Metabolic neuropathy 1. Diabetes mellitus6,11,17,28,46,52,59 2. Amyloidosis49,55 3. Gigantism21 B. Inherited neuropathies 1. Hereditary motor and sensory neuropathy22 a. Type I—Charcot-Marie-Tooth disease7,9 b. Type II—Dejerine-Sottas syndrome53 2. Hereditary sensory and autonomic neuropathy22,23 a. Type I b. Type II c. Type III10,32 d. Type IV e. Type V 3. Subclinical neuropathy with neurogenic arthropathy and recurring fractures24 C. Infection—leprosy27 D. Nutritional—alcoholism54 E. Traumatic—sciatic and other peripheral nerves39,57 F. Surgical denervation45 IV. Corticosteroids—Charcot-like neuropathy2,13,25,63

NEUROVASCULAR THEORY With this said, there are a number of situations in which the neurotraumatic hypothesis seems inadequate for explaining joint destruction entirely, even in the neurologically impaired person, and the additional factor of a trophic vascular mechanism becomes attractive. The neurovascular theory suggests that neurologic disease triggers increased bone blood flow and active bone resorption by osteoclasts, and that fractures and joint damage follow. The arguments in favor of the hypothesis are enumerated below.

First, a proportion of patients with Charcot joints are said to have no neurologic disease when joint destruction develops, making it difficult to blame joint insensitivity. Second, there are instances in which neurotrophic joints develop in bedridden patients in whom weight bearing is impossible and repeated severe joint trauma unlikely. Third, a few patients suffer joint destruction and resorption of articular structures in a matter of weeks to a few months, making pure mechanical destruction hard to accept as the sole mechanism.18 Fourth, some neurotrophic arthropathies are associated with long bone fractures that seemingly occur spontaneously or without unusual trauma. Although histologic examination is reported to show pathologically increased vascularity, it is also a fact that acutely damaged joints become hot and swollen from increased blood flow and exudation as part of the body’s normal repair process, making pathologic vascularity difficult to prove. Hindlimb sympathectomy might be expected to increase blood flow; however, in experimental animals, at least, it does not lead to joint damage or abnormalities in the chemical composition of bone.19 It is still possible, however, that local hyperemia is exaggerated in some patients, leading to rapid bony softening and resorption, and it is not possible to discard this hypothesis out of hand (Fig. 79-1).

INFECTION Although infection may coexist but cannot be offered as a cause of this problem, tuberculosis of the elbow, on the other hand, can cause resorptive and destructive changes similar to those in a neurotrophic joint (Fig. 79-2).

ENVIRONMENT Environmental factors can adversely add to the effect of nociceptive loss in a number of ways. Neurotrophic arthropathy is more common in weightbearing joints and in joints in men, perhaps because men often have occupations involving manual labor and physical activity. Additional factors include the presence of mental retardation, psychosis, the metabolic effect of diabetes, and rheumatoid arthritis or metabolic bone disease. The so-called stoic personality, while admitting pain, seems to be able to ignore it and continue to walk and work unimpeded. There are also those who, although experiencing considerable pain, may cling to a job out of economic necessity despite deforming arthritis. As is being more commonly recognized today, intraarticular administration of local anesthetic is associated with chondrocyte cell death.15,33 For some, it is occasionally followed by rapid joint disintegration. Patients reported with this complication have not had any

1080 Part VIII Septic and Nontraumatic Conditions

FIGURE 79-2

FIGURE 79-1

Gross resorption destruction of the elbow joint due to rheumatoid arthritis, although no hypertrophic changes are present as in the typical neurotrophic joint. This seems to represent an example of hyperemic arthropathy, one of the etiologic considerations of neurotrophic joints.

neurologic disease, and therefore, the joint destruction cannot be called a neurotrophic arthropathy. The interplay of multiple factors in the genesis of bone and joint complications is emphasized in Figure 79-3.

CONDITIONS CAUSING NEUROTROPHIC ARTHROPATHY OF THE ELBOW SYRINGOMYELIA In contrast to tabes dorsalis, 80% of the joints involved in syringomyelia are in the upper extremities.30 It is estimated that approximately 25% of these affected joints will develop joint breakdown. Neuropathic disease involves the shoulder most commonly, followed by the elbow and wrist. Degenerative changes in the cervical spine are not uncommon. The process evolves gradually with paresthesias of the hands, followed by progressive weakness and wasting of the small hand muscles and then atrophy of arm and shoulder muscles. Loss of pain and temperature sense affects the arms and upper

Gross destruction of an elbow joint involved with tuberculous arthritis. Note that both sides of the joint are involved. A distinction between this entity and a neurotrophic arthropathy in the early stages is complicated by the possibility that the two conditions coexist.47 (Courtesy of Dr. Richard Marks, Cape Town, South Africa.)

thoracic segments, often in a cape distribution. As the syrinx enlarges, long tract signs appear, and a Horner syndrome is noted. The Arnold-Chiari malformation is commonly associated and is related to the development of syringomyelia. Post-traumatic syringohydromyelia presenting as a neuropathic arthropathy of the elbow and of the shoulder has been reported.51 Morrey has seen one additional instance of an acquired neurotrophic elbow joint after injury to the cervical spine (Fig. 79-4). The mechanism is also presumably that of a traumatic syringohydromyelia. Electromyography and somatosensory evoked potentials can indicate the presence of a spinal cord lesion and the need for an imaging study.70 Radiographic examination of the cervical spine may show widening of the spinal canal, but the diagnostic procedure of choice is magnetic resonance imaging, which demonstrates both the syrinx and any associated malformation.41 Computed tomography with metrizamide contrast enhancement of the cerebrospinal fluid may also demonstrate spinal cord enlargement and cavitations in some instances. Elbow arthropathy may follow neurologic symptoms but is sometimes a presenting complaint.4 A history of trauma is usually lacking. Joint swelling due to effusion may be marked, and pain is experienced in some cases.

Chapter 79 Neurotrophic Arthritis 1081

Tabes dorsalis, diabetes, leprosy, syringomyelia, HSN I, II, III, IV, and V, HMSN, amyloidosis, focal spinal cord and peripheral nerve lesions

Personality, mental retardation, psychosis, ?opiate receptor and/or system dysfunction

Insensitivity

Indifference

of superficial nociception

Anhidrosis, bony abn.

of deep nociception

Mutilating acropathy • Plantar ulcer • Paronychia • Lymphangitis • Cellulitis

Nonrecognition

Loose bodies, inflammation, instability

Osteomyelitis

Tissue damage

Prednisone, rheumatic or rheumatoid arthritis, metabolic bone disease

Abuse

Trauma, excess use, ataxia, overweight, other ?Loss of protective reflexes

Broken bones Neurogenic arthropathy

FIGURE 79-3

Schematic representation of the interrelationship between the etiology and pathophysiology of neurotrophic arthropathy.24

Atrophic changes in the bone, particularly of the shoulder, are more common than in tabes dorsalis.67 Although extremely rapid destruction of the shoulder may occur with resorption of the humeral head, the elbow seems less likely to be affected in this fashion.51,68 The radiograph of the elbow shows resorption of bone ends and often of the entire joint (Fig. 79-5). Reparative callus is evident, along with gross deformity and instability. The youngest patient documented with elbow involvement was recently reported related to a myelomeningocele.73

DIABETES MELLITUS Today the rate of diabetes mellitus as the leading cause of neurotrophic arthropathy in the lower extremity is well recognized. The arthropathy usually develops in diabetics who have had the disease for some time and

who have suffered the additional complication of a symmetrical sensorimotor polyneuropathy. In diabetic “pseudotabes,” severe sensory and autonomic impairment leads to an ataxic gait, pupillary abnormalities, neurogenic bladder, and lightning pains reminiscent of tabes dorsalis. Diabetic arthropathy affects primarily the joints of the feet, with less frequent involvement of the ankles and knees.6,17,46,52,59 The distal predominance of the arthropathy is in keeping with the stocking pattern of sensory loss, which is maximal in the feet. Bony abnormalities in the upper extremities of diabetics are uncommon, but involvement of the shoulder, elbow, and wrist has been recorded.28 Campbell and Feldman11 presented a radiograph of the elbow in a 59-year-old patient that showed marked disorganization of the joint with destruction of the articular surfaces, numerous bone fragments, and periosteal new bone formation typical of a Charcot joint.

1082 Part VIII Septic and Nontraumatic Conditions

FIGURE 79-5

Gross destruction of an elbow joint in a patient with syringomyelia.

FIGURE 79-4

A brachial plexus injury occurred in a 47year-old man in 1986. Five years later, instability and effusion were noted in the ipsilateral elbow (A). Rapid destruction occurred in the next 3 months (B).

TABES DORSALIS Although syphilis used to be responsible for up to 90% of neurotrophic joints, tabes dorsalis is now a rare disease. Approximately 10% of all tabetics are said to develop a Charcot joint, the majority occurring between the ages of 40 and 60 years, approximately 20 years or more after the primary infection. In approximately 78% of cases, the lower limbs are affected,30 with the knee most frequently involved. In the upper limbs, the shoulder, elbow, hands, and wrists are affected.3,20,61,66,69 Polyarticular involvement occurs in up to 40%. Clinical features include the presence of lightning pains, neuro-

genic bladder disturbances, optic neuritis, and visceral crises. Most patients have pupillary abnormalities, and loss of pupillary reflexes to light (Argyll Robertson pupils) occurs in up to 62%. Vibration and position senses are reduced, and deep pain sensation may be absent. Pain perception may be delayed. Although the Venereal Disease Research Laboratory (VDRL) test may be negative, rapid plasma reagin (RPR) and fluorescent treponemal antibody absorption (FTA-ABS) test results are usually positive. Elbow movement may be restricted, or the elbow may be subluxed and hypermobile with marked instability (Fig. 79-6). Spontaneous fractures can occur. Radiographic examination may show extensive destruction of the bone ends, disintegration of the joint, abundant periosteal callus formation, valgus deformity, and free bodies in the articulation.

CONGENITAL INDIFFERENCE AND INSENSITIVITY TO PAIN The concept of indifference to pain implies that these patients perceive pain stimuli in a normal fashion but fail to react in the usual defensive manner, a kind of asymbolia for pain, whereas insensitivity denotes an inability to receive a painful stimulus because of a neurologic deficit. Most patients with the former disorder have not had detailed electrophysiologic, biomechanical, and pathologic examinations, and it is likely that previously reported patients have had a congenital sensory and autonomic neuropathy of type IV or V.23 Nevertheless, occasionally patients in this group may develop a neurotrophic arthropathy or fracture that

Chapter 79 Neurotrophic Arthritis 1083

FIGURE 79-6

The deformity associated with this Charcot joint from tabes dorsalis is obvious by inspection, and the joint is grossly unstable. (From Beetham, W. P., Kaye, R. L., and Polley, H. F.: Charcot’s joints. Ann. Intern. Med. 58:1002, 1963.)

may affect the elbow.29,44,58 Involvement of the elbow in Charcot-Marie-Tooth disease has also been recorded.8

HEREDITARY SENSORY AND AUTONOMIC NEUROPATHY TYPE II Hereditary sensory and autonomic neuropathy type II has not been reported as a cause of neurogenic arthropathy of the elbow. The author has evaluated a remarkable patient with this disorder, who had severe acral mutilation.

Case Report The patient was a 34-year-old white woman referred by the editor for evaluation of a left elbow effusion and flail joint. At age 2 years, she was found to have a peripheral neuropathy, and her first operation was for a bump on the foot. This was followed by approximately 100 operations on the distal extremities for nonhealing ulcers and infections. At age 18, her right leg was amputated below the knee. At about this time, she had an infection of the left foot. Eventually, a left above-knee amputation was performed when the patient was 34 years old. Beginning at age 12, she began to lose fingers to sepsis and she required distal and middle interphalangeal amputations of the hand. Left elbow symptoms began 6 months before evaluation, when she had surgery for an olecranon bursitis and removal of loose bone fragments. This was followed by an infection that required hospitalization for 3 months. She stated that she could feel temperature and deep pain, but was unable to appreciate textures. The hands felt swollen and ached. There was no history of diabetes or other

family members with a peripheral neuropathy. The patient had an unaffected 6-year-old son. She ambulated with a wheelchair and easily scooted along the floor and examining table or bed using her arms. The left elbow was swollen and flail. The upper forearm had migrated proximally and posteriorly in reference to the distal humerus. There were right below-knee and left aboveknee amputations. On the right, there was an open draining wound of the patella and distal stump. Muscle strength was normal, but the upper extremity reflexes were absent. Nerve conduction studies showed no response with stimulation of the superficial radial nerves bilaterally, median sensory fibers, and the lateral antebrachial cutaneous nerve. Median and radial motor nerve conduction studies were normal. The needle electrode examination showed large motor units and reduced recruitment in the abductor pollicis brevis and first dorsal interosseous muscles. The patient did not feel pain during the needle examination of the thenar muscle. These findings were consistent with a severe axonal sensorimotor peripheral neuropathy with more prominent involvement of sensory than motor fibers. Radiographs showed medial subluxation of the left ulna and radius, with marked destructive joint changes and osseous debris in the periarticular soft tissues (Fig. 79-7). There was marked soft tissue swelling about the elbow, especially in the region of the olecranon bursa. The findings were consistent with a neuropathic joint. Efforts to stabilize the joint failed.

Commercial testing to define genetic abnormality is now available for many varieties of inherited neuropathy.40a

SURGICAL DENERVATION In recent years, there is evidence that aggressive surgical release of contracted elbow joints that causes marked stripping of the bone may cause severance of joint innervation. Two of Morrey’s patients have developed destructive resorption of the elbow after fascial arthroplasty following an aggressive surgical release of the soft tissue around the joint (Fig. 79-8).45 Several years later, one was diagnosed with congenital indifference to pain. The other appears to have occurred possibly from the aggressive soft tissue release.

MISCELLANEOUS A case of idiopathic arthropathy of the elbow was reported by Meyn and Yablon43 in 1973; however, syringomyelia was not excluded because the patient refused myelography. A second example of “idiopathic” arthropathy of the elbow may also have been syringomyelia.5 In a poorly studied patient reported by Karten38 with the CRST* variant of systemic sclerosis and multiple neuropathic joints including the elbows, hysterical indifference to pain was suggested to be a major factor. This *Calcinosis cutis, Raynaud’s phenomenon, sclerodactyly, telangiectasia.

1084 Part VIII Septic and Nontraumatic Conditions

FIGURE 79-7

A, Gross destruction as described in the case report. B, An effort to restore function by arthroplasty was completely unsuccessful after two procedures.

seems an unlikely explanation, however, because muscle weakness and atrophy and absence of deep pain were present. Another unusual patient, described by Alajouanine and Boudin,1 had elbow arthropathy associated with distal muscular atrophy, subcutaneous and vascular calcification, and abnormal calcium and phosphorus metabolism. There were no sensory changes, and the cause of the arthropathy is obscure.

INVESTIGATION AND DIAGNOSIS The examination of a patient with a neurotrophic arthropathy of the elbow should focus on a search for evidence of syringomyelia, diabetes, and tabes dorsalis because almost all patients will be found to harbor one of these disorders. When physical signs of these diseases are lacking, the patient should be examined carefully for evidence of pes cavus, hammer toes, enlargement of peripheral nerves, and distal sensory loss, which may suggest the presence of a peripheral neuropathy. A dissociated sensory loss is found in syringomyelia but may also be present in amyloid neuropathy, familial dysautonomia, hereditary sensory and autonomic neuropathy type II, and Tangier disease. Evidence of an autonomic neuropathy is important because small myelinated and unmyelinated pain afferents that provide joint nociception are often involved as well. Loss of sweating, orthostatic hypotension, urinary incontinence, and impotence are the most important symptoms of the autonomic dysfunction seen in a variety of small fiber

neuropathies. Other neuropathies may have a more generalized sensory disturbance that affects both large and small fibers. A profound loss of pain sense, however, is not a necessary prerequisite for the development of neurogenic arthropathy, and the patient’s complaint of pain and the presence of normal or nearly normal nociception should not deter further investigation. It is often helpful to interview and examine family members, even when no apparent disease is known to kin. This is particularly necessary in patients with a peripheral neuropathy or only slight neurologic abnormalities, in whom the hereditary nature of the disorder may become evident only after intensive investigation of relatives. The clinician should also look for wasting of small hand muscles and ulnar sensory loss because the nerve may be compromised behind the medial epicondyle by the deformity associated with the Charcot joint. Laboratory investigations that my colleagues and I have found useful in the investigation of neurogenic arthropathy, in addition to “routine tests,” are listed in Box 79-2. We have found the computer-assisted sensory examination and electromyography and nerve conduction studies helpful in detecting disease in minimally affected patients and family members. In a few patients, nerve biopsy, including teased fiber preparations, quantitative morphometry, electron microscopy, histochemistry, analysis of myelin lipids, the in vitro nerve action potential, and studies of axonal transport may be needed for complete evaluation of the specimen. The differential diagnosis of neurogenic arthropathy is listed in Box 79-3.

Chapter 79 Neurotrophic Arthritis 1085

FIGURE 79-8

Traumatic arthritis of the right elbow in a 33-yearold man (A). Interposition arthroplasty was performed (B), and the joint developed aseptic resorption in less than 18 months (C).

C

1086 Part VIII Septic and Nontraumatic Conditions

TREATMENT Two stages of the disease process should be identified for treatment. During the early stages of development, the neurotrophic joint should be protected with a longarm cast or molded splint. The appropriate diagnosis

BOX 79-2

Laboratory Investigations

Differential Diagnosis of Neurogenic Arthropathy

BOX 79-3

1. Serologic tests for syphilis (blood and cerebrospinal fluid) 2. Fasting blood glucose and glycosylated hemoglobin 3. Serum vitamin B12 4. Serum and urine immunoelectrophoresis for monoclonal protein 5. Genetic tests for inherited neuropathy 6. Nerve conduction studies and needle electromyography 7. Somatosensory evoked potentials 8. Computer-assisted sensory examination 9. Autonomic reflex screen 10. Thermoregulatory sweat test 11. Magnetic resonance imaging 12. Computed tomography 13. Sural nerve biopsy 14. Psychological and psychometric assessment

A FIGURE 79-9

is obviously important during this stage. Thus, some knowledge of the existence of this entity as well as the etiologic factors is important (see Box 79-1). As the active process resolves, the residual dysfunction should be assessed. Pain is rare. Hence, stability is the primary consideration in most clinical settings. This residual is

B

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

Osteoarthritis Traumatic arthritis Acute infectious arthritis* Avascular necrosis Rheumatoid arthritis Gout Malignant disease Osteoblastic metastases and Paget disease (spine) Hemophilia Tuberculosis arthritis* Thrombophlebitis, cellulitis

*Note: These two conditions may coexist.

C

Early changes in a patient with diabetes and lack of joint proprioception or pain (A). Anteroposterior and lateral radiographs at 3 months (B and C) show a well-fixed implant;

Chapter 79 Neurotrophic Arthritis 1087

D

E

FIGURE 79-9, cont’d

at 3 years, loosening is evident of the humeral and ulnar components (D and E).

usually treated with an orthoplast splint with hinges to retain function. Surgical fusion is extremely difficult and should be considered rarely only as a procedure of last resort.60

MAYO EXPERIENCE We have recently reviewed the management of six patients treated at Mayo and followed a mean of 51 months. All three treated by efforts to stabilize the joint failed, and the treatment failed miserably in two (see Fig. 79-8C). There is little experience with prosthetic replacement. We have concerns about this as a long-term option (Fig. 79-9). Today, our recommendation is to reaffirm the classic: protect and splint; do not operate.

References 1. Alajouanine, T., and Boudin, G.: Sur un complexus clinique caractérisé par une atrophie musculaire, myelopathique de type distal avec grosses déformations des pieds, arthropathies du caude et de la colonne vertébrale nodosités calcaires sous-cutanées et artérité calcaire avec perturbation du métabolisme phosphocalcique. Rev. Neurol. 77:193, 1945. 2. Alarcon-Segovia, D., and Ward, L. E.: Charcot-like arthropathy in rheumatoid arthritis: Consequences of overuse of a joint repeatedly injected with hydrocortisone. J. A. M. A. 193:1052, 1965.

3. Beetham, W. P., Kaye, R. L., and Polley, H. F.: Charcot’s joints: A case of extensive polyarticular involvement, and discussion of certain clinical and pathologic features. Ann. Intern. Med. 58:1002, 1963. 4. Bhaskaran, R. K., Suresh, K., and Iyer, G. V.: Charcot’s elbow. J. Postgrad. Med. 27:194, 1981. 5. Blanford, A. T., Keane, S. P., McCarty, D. J., and Albers, J. W.: Idiopathic Charcot joint of the elbow. Arthritis Rheum. 21: 923, 1978. 6. Boehm, H. J.: Diabetic Charcot joint: Report of a case and review of the literature. N. Engl. J. Med. 267:185, 1962. 7. Bruckner, F. E.: Double Charcot’s disease. Br. Med. J. 2:603, 1968. 8. Bruckner, F. E., and Howell, A.: Neuropathic joints. Semin. Arthritis Rheum. 2:47, 1972. 9. Bruckner, F. E., and Kendall, B. E.: Neuroarthropathy in Charcot-Marie-Tooth disease. Ann. Rheum. 28:577, 1969. 10. Brunt, P. W.: Unusual cause of Charcot joints in early adolescence (Riley-Day syndrome). Br. Med. J. 4:277, 1967. 11. Campbell, W. L., and Feldman, F.: Bone and soft tissue abnormalities of the upper extremity in diabetes mellitus. A.J.R. 124:7, 1975. 12. Carr, T. L.: The orthopaedic aspects of one hundred cases of spina bifida. Postgrad. Med. J. 32:201, 1956. 13. Chandler, G. N., Jones, D. T., Wright, V., and Hartfall, S. J.: Charcot’s arthropathy following intra-articular hydrocortisone. Br. Med. J. 1:952, 1959. 14. Charcot, J. M.: Sur quelques arthropathies qui paraissent dépendre d’une lesion cerveau ou de la moelle épinieère. Arch. Physiol. Normale Pathol. 1:161, 1868. 15. Chu, C. R., Izzo, N. J., Papas, N. E., and Fu, F. H.: In vitro expsoure to 0.5% bupivacaine is cytotoxic to bovine articular chondrocytes. Arthroscopy 22:693, 2006. 16. Cleveland, M., and Smith, A.: Fusion of the knee in cases of Charcot’s disease: Report of four cases. J. Bone Joint Surg. 13:849, 1931. 17. Clouse, M. E., Gramm, H. F., Legg, M., and Floyd, T.: Diabetic osteoarthropathy: Clinical and roentgenographic observations in 90 cases. A.J.R. 121:22, 1974. 18. Cooper, R. R.: Nerves in cortical bone. Science 160:327, 1968. 19. Corbin, K. B., and Hinsey, J. C.: Influence of the nervous system on bone and joints. Anat. Rec. 75:307, 1939. 20. Das, P. C., Banerji, A., Roy, A., and Basu, S.: Neurogenic arthropathies (Charcot’s joints). J. Indian Med. Assoc. 54:368, 1979. 21. Daughaday, W. H.: Extreme gigantism. N. Engl. J. Med. 297:1267, 1977. 22. Dyck, P. J.: Neuronal atrophy and degeneration predominantly affecting peripheral sensory and autonomic neurons. In Dyck, P. J., Thomas, P. K., Griffin, J. W., Low, P. A., and Poduslo, J. F. (eds.): Peripheral Neuropathy, 3rd ed. Philadelphia: W. B. Saunders, 1993, p. 1065. 23. Dyck, P. J., Mellinger, J. F., Reagan, T. J., Horwitz, S. J., McDonald, J. W., Litch, W. J., Daube, J. R., Fealey, R. D., Gio, V. L., Kao, P. C., Brimijoin, W. S., and Lambert, E. H.: Not “indifference to pain,” but varieties of hereditary sensory and autonomic neuropathy. Brain 106:373, 1983.

1088 Part VIII Septic and Nontraumatic Conditions

24. Dyck, P. J., Stevens, J. C., O’Brien, P. C., Oviatt, K. F., Lais, A. C., Coventry, M. B., and Beabout, J. W.: Neurogenic arthropathy and recurring fractures with subclinical inherited neuropathy. Neurology 33:357, 1983. 25. Eibel, P.: Painless arthropathy complicated by massive hemorrhagic effusion. Clin. Orthop. 60:149, 1968. 26. Eloesser, L.: On the nature of neuropathic affections of the joints. Ann. Surg. 66:201, 1917. 27. Faget, G. H., and Mayoral, A.: Bone changes in leprosy: A clinical and roentgenologic study of 505 cases. Radiology 42:1, 1944. 28. Feldman, M. J., Becker, K. L., Reefe, W. E., and Longo, A.: Multiple neuropathic joints including the wrist, in a patient with diabetes mellitus. J. A. M. A. 209:1690, 1969. 29. Fitzgerald, J. A. W.: Neuropathic arthropathy secondary to atypical congenital indifference to pain. Proc. R. Soc. Med. 61:663, 1968. 30. Floyd, W., Lowell, W., and King, R. E.: The neuropathic joint. South. Med. J. 52:563, 1959. 31. Foster, J. B., and Hudgson, P.: Syringomyelia. In Barnett, H. J. M., Foster, J. B., and Hudgson, P. (eds.): Traditional Concepts of Syringomyelia. Philadelphia, W. B. Saunders, 1973. 32. Goldberg, M. F., Payne, J. W., and Brunt, P. W.: Ophthalmologic studies of familial dysautonomia: The Riley-Day syndrome. Arch. Ophthalmol. 80:732, 1968. 33. Gomoll, A. H., Kang, R. W., Williams, J. M., Bach, B. R., and Cole, B. J.: Chondrolysis after continuous intra-articular bupivacaine infusion: an experimental model investigating chondrotoxicity in the rabbit shoulder. Arthroscopy 22:813, 2006. 34. Greitemann, B., Schuling, S., and Baumgartner, R.: CharcotEllenbogengelenk bei syringomyelie. Seitschrift Fur Orthopadie Und Ihre Grenzgebiete. 130:5515, 1992. 35. Halonen, P. I., and Jarvinen, A. J.: On the occurrence of neuropathic arthropathies in pernicious anemia. Ann. Rheum. Dis. 7:152, 1948. 36. Harris, J. R., and Brand, P. W.: Patterns of disintegration of the tarsus in the anaesthetic foot. J. Bone Joint Surg. 48B:4, 1966. 37. Johnson, J. T. H.: Neuropathic fractures and joint injuries. J. Bone Joint Surg. 49A:1, 1967. 38. Karten, I.: CRST syndrome and “neuropathic” arthropathy. Arthritis Rheum. 12:636, 1969. 39. Kernwein, G., and Lyon, W. F.: Neuropathic arthropathy of the ankle joint resulting from complete severance of the sciatic nerve. Ann. Surg. 115:261, 1942. 40. Key, J. A.: The treatment of tabetic arthropathies. Urol. Cutan. Rev. 49:161, 1945. 40a. Klein, C. J.: The inherited neuropathies. Neurol. Clin. 25: 173, 2007. 41. Kokmen, E., Marsh, W. R., and Baker, H. L. Jr.: Magnetic resonance imaging in syringomyelia. Neurosurgery 17: 267, 1985. 42. Kwon, Y. W., and Morrey, B. F.: Neuropathic elbow arthropathy: A review of six cases. J. Shoulder Elbow Surg. 15:378, 2006. 43. Meyn, M., and Yablon, I. G.: Idiopathic arthropathy of the elbow. Clin. Orthop. 97:90, 1973.

44. Mooney, V. M. H. J.: A case of congenital insensitivity to pain with neuropathic arthropathy. Arthritis Rheum. 9:820, 1966. 45. Morrey, B. F.: Post-traumatic contracture of the elbow: Operative treatment including distraction arthroplasty. J. Bone Joint Surg. 72A:601, 1990. 46. Muggia, F. M.: Neuropathic fracture: Unusual complication in a patient with advanced diabetic neuropathy. J. A. M. A. 191:336, 1965. 47. Nissenbaum, M.: Neurotrophic arthropathy of the shoulder secondary to tuberculous arachnoiditis. Clin. Orthop. Relat. Res. 118:169, 1976. 48. Nozawa, S., Miyamoto, K., Nishimoto, H., Sakaguchi, Y., Hosoe, H., and Shimizu, K.: Charcot joint in the elbow associated with syringomyelia. Orthopedics 26: 731, 2003. 49. Peitzman, S. J., Miller, J. L., Ortega, L., Schumacher, H. R., and Fernandez, P. C.: Charcot arthropathy secondary to amyloid neuropathy. J. A. M. A. 235:1345, 1976. 50. Petrie, J. G.: A case of progressive joint disorders caused by insensitivity to pain. J. Bone Joint Surg. 35B:399, 1953. 51. Rhoades, C. E., Neff, J. R., Rengachary, S. S., Batnitsky, S., Ketcherside, J., Price, H. I., and Jacobs, R. R.: Diagnosis of post-traumatic syringohydromyelia presenting as neuropathic joints: Report of two cases and review of the literature. Clin. Orthop. Relat. Res. 180:182, 1983. 52. Robillard, R., and Gagnon, P. A.: Diabetic neuroarthropathy: Report of four cases. Can. Med. Assoc. J. 91:795, 1964. 53. Russell, W. R., and Garland, H. G.: Progressive hypertrophic polyneuritis with case reports. Brain 53:376, 1930. 54. Samilson, R. L., Sankaran, B., Bersani, F. A., and Smith, A.: Orthopedic management of neuropathic joints. Arch. Surg. 78:115, 1959. 55. Scott, R. B., Elmore, S., Brackett, N. C., Harris, W. O., and Still, W. J. S.: Neuropathic joint disease (Charcot joints) in Waldenström’s macroglobulinemia with amyloidosis. Am. J. Med. 54:535, 1973. 56. Sequeira, W.: The neuropathic joint. Clin. Exp. Rheumatol. 12:325, 1994. 57. Shands, A. R.: Neuropathies of the bones and joints: Report of a case of an arthropathy of the ankle due to a peripheral nerve lesion. Arch. Surg. 20:615, 1930. 58. Silverman, F. N., and Gilden, J. J.: Congenital insensitivity to pain: A neurologic syndrome with bizarre skeletal lesions. Radiology 72:176, 1959. 59. Sinha, S., Munichoodappa, C. S., and Kozak, G. P.: Neuroarthopathy (Charcot joints) in diabetes mellitus. Medicine 51:191, 1972. 60. Smith, F. M.: Surgery of the Elbow. Philadelphia: W. B. Saunders, 1972. 61. Soto-Hall, R., and Haldeman, K. O.: The diagnosis of neuropathic joint disease (Charcot joint). J. A. M. A. 114:2076, 1940. 62. Sprenger, H. R., and Foley, C. J.: Hip replacement in a Charcot joint. Clin. Orthop. Relat. Res. 82:191, 1982. 63. Steinberg, C., Duthie, R. B., and Piva, A. E.: Charcot-like arthropathy following intra-articular hydrocortisone. J. A. M. A. 181:851, 1962.

Chapter 79 Neurotrophic Arthritis 1089

64. Steindler, A.: The tabetic arthropathies. J. A. M. A. 29:250, 1931. 65. Stepanek, V., and Stepanek, P.: Changes in the bones and joints of paraplegics. Radiol. Clin. North Am. 29:28, 1960. 66. Storey, G.: Charcot joints. Br. J. Vener. Dis. 40:109, 1964. 67. Storey, G.: Charcot joints. Ann. Rheum. Phys. Med. 10:312, 1970. 68. Storey, G. A., Stein, J., and Poppel, M. H.: Rapid osseous changes in syringomyelia. Radiology 69:415, 1957. 69. Unnanuntana, A., and Saranatra, W.: Neuropathic arthropathy of the elbow. A report of two cases. J. Med. Assoc. Thailand 89:533, 2006.

70. Veilleux, M., and Stevens, J. C.: Syringomyelia: Electrophysiologic aspects. Muscle Nerve 10:449, 1987. 71. Wirth, C. R., Jacobs, R. L., and Rolander, S. D.: Neuropathic spinal arthropathy: A review of the Charcot spine. Spine 5:558, 1980. 72. Wolfgang, G. L.: Neurotrophic arthropathy of the shoulder: A complication of progressive adhesive arachnoiditis. Clin. Orthop. Relat. Res. 87:217, 1972. 73. Zimmerman, A., Law, C., Blount, J., and Gilbert, S.: Neuropathic arthropathy of the elbow in a pediatric patient with myelomeningocele. Dev. Neurorehabil. 10:261, 2007.

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CHAPTER

80

Nerve Entrapment Syndromes Robert J. Spinner

INTRODUCTION The diagnosis of a nerve entrapment lesion arising at the elbow can be relatively straightforward if the history, physical examination, electromyographic (EMG), and imaging studies, when indicated, all confirm the diagnosis and the localization of the lesion.12,32,47,87,93,138 However, when the history and physical examination do not correspond or the electrophysiologic or imaging studies do not support a specific clinical diagnosis, then problems can arise. Therefore, one must apply the same systematic, thoughtful approach to the care of every patient. One can then put all of the data of the clinical puzzle together to offer appropriate treatment. Sometimes, historical information can be misleading. For example, it is not uncommon for an elderly patient to say that his or her fingers are “stiff” when in reality the fingers are numb. Stiffness suggests an arthritic process, whereas numbness suggests involvement of the peripheral neurologic system in the pathologic process. Other times, physical findings may be difficult to interpret. Persistent pain about the lateral aspect of the elbow that is resistant to all forms of conservative treatment as well as operative treatment directed to the lateral epicondyle may represent resistant lateral epicondylitis, entrapment of the posterior interosseous nerve alone, or both entities. In this instance, EMG studies, more commonly than not, do not help establish the diagnosis of resistant “tennis elbow” due to posterior interosseous nerve compression or localize the pathologic process. If both conditions are believed to be present on clinical grounds, then management of both lesions needs to be addressed simultaneously to relieve the patient’s symptoms. Other issues may confound the clinical picture and the treating physician: 1. Simultaneous peripheral nerve compressions may occur, whether from related or unrelated causes.25 For example, a diabetic patient may present with symptoms related to concurrent carpal tunnel syndrome and cubital tunnel syndrome. An active individual

may present with well-defined symptoms of ulnar nerve compression at the elbow; electrical studies, however, may have normal results in the ulnar nerve but reveal changes of carpal tunnel syndrome (which may be either subclinical or less symptomatic to the patient). Post-traumatic thickening of the brachial fascia in the distal arm can produce a simultaneous median and lateral antebrachial nerve compression. When more than one nerve is suspected in the neural compression process, a more proximal lesion such as the brachial plexus, must be ruled out as the site of the pathologic process. 2. A nerve can be compressed at more than one level; that is, a “double crush” lesion may exist. This most commonly occurs at the neck and the wrist but can also occur at other locations such as the thoracic outlet and the cubital tunnel. 3. Two separate neurologic processes may coexist. For example, a patient who is wheelchair-bound from a syrinx may develop hand atrophy, which represents new bilateral ulnar nerve compression rather than progression of the syrinx. Thus, on occasion, it is necessary to direct one’s conservative or surgical attention to two nerves, two sites on one nerve, or even two neurologic conditions to address the patient’s presenting symptoms and new neurologic findings. Some patients are prone or predisposed to sequential neural compression lesions. There are predisposing factors for multiple neural entrapment lesions. A group of substances, such as sorbitol, can cause an increase in intrafascicular pressure, which can predispose a patient with diabetes mellitus to a neural compression lesion. Hereditary neuropathies also occur; despite genetic advances, the mechanism of dysfunction is not fully understood. Congenital anomalies of the elbow, such as from a lacertus fibrosus variant or a ligament of Struthers, may result in nerve compression lesions. Developmental changes from hypertrophied muscles may lead to compressive neuropathies, such as a pronator syndrome in an athlete. Trauma may induce a nerve compression syndrome either acutely or chronically, either from bony or associated soft tissue changes. Recurrent neural compression lesions also occur. A physician may successfully care for an individual’s neural compression only for another nerve compression to arise a few months or years later that affects the same peripheral nerve or another nerve.132,139,198 Usually, technical factors at surgery can prevent recurrent lesions. Free gliding of the nerve with elbow flexion and extension and forearm rotation helps prevent late postoperative symptoms. If a nerve is fixed by adhesions or scarring or at a fracture site, it is not just a matter of entrapment. A traction neuritis can exist as well. As the joint moves, the nerve is tethered and can be stretched.

Chapter 80 Nerve Entrapment Syndromes 1091

If the ulnar nerve is transposed anteriorly (especially if it has not been transposed in a straight line), ulnar neuritis can develop at a later date. Similarly, if the medial epicondyle is resected and the nerve becomes adherent to the medial epicondylectomy site, resistant ulnar nerve neuritis can develop after the primary surgery. Certain principles apply to the surgical management of entrapment lesions. Wide exposure is often necessary to define the normal anatomy and the pathologic region. The nerve should be identified in a healthy region proximally and distally both grossly and microscopically; only then should the nerve be traced to the pathologic region. Surgery should be guided by the use of internervous planes, and gentle handling of the nerve is critical. During the wide decompression, care must be given to the cutaneous nerves. Patients who have entrapment lesions are prone to develop symptomatic postoperative skin neuromata; their initial symptoms related to the nerve compression lesion may disappear postoperatively to be replaced by a different type of neuromatous pain. In particular, at the elbow level, the medial cutaneous nerve of the forearm is susceptible

Brachialis Radial n. Brachioradialis Radial recurrent a. Deep and superficial branches of radial n. Supinator Extensor carpi radialis longus Flexor digitorum superficialis Pronator teres Radial a.

during ulnar nerve transposition and median nerve decompression, and the posterior cutaneous nerve of the forearm is at risk with posterior interosseous nerve neurolysis. In the majority of cases of nerve compression, external neurolysis is the usual operative intervention. Internal neurolysis, when indicated, should be limited to the neural segment and the internal region clinically involved. The perineurium should rarely, if ever, be violated. Nerves should be placed in healthy beds away from scar tissue. Intraoperative nerve action potentials may help in the management of more advanced lesions. Postoperative care should emphasize early mobilization. Early motion can improve neural gliding. The development of a stiff joint can undo an otherwise successful nerve decompression. A detailed understanding of the complex normal anatomy of this region and the “common” variants is essential for proper diagnosis and treatment of these conditions (Fig. 80-1). Careful history, serial examinations and EMG studies, and at times, imaging modalities can usually localize the lesion or lesions. Early, accurate diagnosis and treatment are important for effective overall management of nerve compression lesions.

Biceps and bicipital aponeurosis Median n. Brachial a. Pronator teres, humeral head Flexor carpi radialis and palmaris longus Pronator teres, ulnar head Ulnar n. Ant. and post. ulnar recurrent aa. Ulnar a. Common interosseous a. Posterior and anterior interosseous aa. Anterior interosseous n. Flexor carpi ulnaris

Flexor pollicis longus

Flexor digitorum profundus Dorsal branch of ulnar n.

Ant. interosseous a. and n. Pronator quadratus Abductor pollicis longus

Ulnar a. and n. Median n.

FIGURE 80-1

Major neurovascular and muscular relationships of the elbow region. (Redrawn from Hollinshead, W. H.: Anatomy for Surgeons, 3rd ed. Vol. 3. New York, Harper & Row, 1982.)

1092 Part VIII Septic and Nontraumatic Conditions

Understanding the degree of nerve injury can help a physician predict recovery patterns and guide management.

NEUROPHYSIOLOGY OF NERVE COMPRESSION LESIONS Nerve compression may be categorized as first-, second-, third-, or fourth-degree neural lesions. This method was first described by Sir Sydney Sunderland.184 The earlier classification of Sir Herbert Seddon (1943)157 uses the terms neurapraxia, axonotmesis, and neurotmesis and can be correlated with Sunderland’s classification in the following manner. A first-degree lesion is a neurapractic lesion. A second-degree or mild third-degree lesion is an axonotmetic lesion. The neurotmetic lesion encompasses all of the fourth-degree lesions (the neuroma in continuity) and the advanced third-degree lesions. I prefer using Sunderland’s classification when correlating clinical problems with the underlying nerve fiber pathologic condition present (Table 80-1).139 With neural compression lesions, it is rare to have a pure first-, second-, or third-degree lesion. Most often, these lesions are mixed. One of the degrees of injury usually predominates in a particular case.138 The lesion mix can be determined by serial physical examinations, preoperative and postoperative serial EMG studies, and knowledge of the duration of the partial or complete nerve compression lesions. A fourth-degree nerve compression lesion is found most often when motor and sensory complete paralysis of a particular nerve has existed for more than 18 months. The factors that affect return of nerve function following entrapment lesions are (1) the nerve fiber pathology, (2) the duration of the lesion and whether it is complete or partial, (3) the status of the end organs (i.e., motor and sensory), and (4) the level of the lesion.120 When a nerve is entrapped, it is the peripheral fibers that are the most vulnerable to the pathologic process. Similarly, the heavy myelinated fibers are more susceptible to compressive forces. Correlation of Seddon and Sunderland Classification of Nerve Injuries*

TABLE 80-1

SUNDERLAND (DEGREE) Seddon

First

Second

Neurapraxia Axonotmesis Neurotmesis *Shaded areas indicate equivalent terms.

Third

Fourth

There appear to be several types of first-degree injury. These lesions are correlated best when both the nerve fiber pathologic processes and the clinical recovery following neurolysis are analyzed temporally. There are ionic96 and vascular40,109,117 lesions of nerve fibers that respond to release by prompt recovery within, at times, hours of surgery. There is a structural first-degree lesion, described by Gilliatt and colleagues64 and Ochoa,136 in which there is segmental injury to the nerve fiber consisting of segmental demyelination and remyelinization of just a few nodal segments of the fibers. In this instance, the entire recovery process takes 30 to 60 days. The clinical implications of this particular lesion are as follows: whether the lesion is high or low in the nerve, it takes 30 to 60 days for neural function to be restored. In contrast, in the second-degree lesion of nerve compression, there is degeneration from the point of injury distally. Regeneration of the nerve fibers occurs within the intact basement membrane. This usually progresses at the rate of 1 mm or more a day from the site of the lesion. A low second-degree lesion recovers much more rapidly than a high lesion with second-degree compression. A second-degree brachial plexus injury often takes at least 15 months before the intrinsic muscles in the hand recover, and they often do not recover fully. The more proximal extrinsic muscles of the forearm recover function at about the ninth to the 12th month following a second-degree entrapment lesion of the brachial plexus. Third-degree injury due to neural entrapment occurs most frequently when other mechanical factors affecting nerves, such as traction and friction, are superimposed on the compression neuropathologic process. In the third-degree lesion, there is increased fibrosis in and about the nerve fibers that causes further structural change and neural dysfunction. Nerves move with motion of the limb. If their mobility is restricted by adherence of the nerve about a joint, as for example at the site of a supracondylar fracture in which the ulnar nerve adheres to the posterior aspect of the distal humerus, movement of the joint without movement of the nerve can cause traction neuritis of the ulnar nerve, which, in turn, can produce a stovepipe appearance of the nerve. A markedly thickened ulnar nerve can be the source of chronic pain even when it is intact and functioning.

Fifth

RADIAL NERVE The radial nerve and its major branches, the posterior interosseous nerve and the superficial radial nerve, are vulnerable to compression forces from the level of the lateral head of the triceps through the region of the elbow, proximal forearm, and even into the distal

Chapter 80 Nerve Entrapment Syndromes 1093

forearm.27,53,133 Depending on which branch of the nerve is involved at the elbow, either pure motor (posterior interosseous nerve) or sensory (superficial radial nerve) paralysis can occur; rarely, motor and sensory involvement can be due to a process in the proximal forearm affecting both branches rather than the radial nerve itself.

Relevant Anatomy The radial nerve in the distal arm passes anteriorly, 10 cm proximal to the lateral epicondyle (Fig. 80-2).80 At the level of the radiocapitellar joint, it divides into its major branches, the deep and the superficial radial nerves. In this passage, the radial nerve passes just deep to the fascia of the brachioradialis. Above the elbow, the radial nerve innervates the brachioradialis and the extensor carpi radialis longus. The motor branch to the

Radial n.

extensor carpi radialis brevis arises from the superficial radial nerve in 58% of the population.155 It frequently arises as a separate terminal branch of the radial nerve with the posterior interosseous and superficial radial nerves. At the elbow, the deep branch passes between the two heads of the supinator muscle, where it becomes the posterior interosseous nerve.31 The proximal edge of the supinator forms an arch for the posterior interosseous nerve, the arcade of Frohse. The superficial radial nerve passes superficial to the supinator muscle. It is covered anteriorly by the brachioradialis. Recurrent vessels of the radial artery cross superficial and deep to these radial nerve branches. The posterior interosseous nerve courses in a dorsoradial direction in the proximal forearm. As it passes through the supinator, it innervates this muscle by multiple branches. Approximately 6 to

Brachial a. Median n. Medial epicondyle

Brachioradialis

Radial recurrent a. Palmaris longus

Arcade of Frohse Supinator

Flexor carpi ulnaris

Extensor carpi radialis longus and brevis Pronator teres

A

Flexor carpi radialis

Recurrent radial a. Deep radial n. Nerve to supinator Arcade of Frohse

Supinator (superficial head) Superficial radial n.

Extensor carpi radialis brevis n. Posterior interosseous n.

B

FIGURE 80-2

A, Dissection of the anterior aspect of the elbow demonstrating the anatomic relationship with the radial nerve. B, An enlarged view of the antecubital fossa shows the relationship of the posterior interosseous nerve to the supinator muscle and the arcade of Frohse. Note how the proximal superficial radial nerve is spared from compression by the arcade. (Redrawn from Spinner, M.: Injuries to the Major Branches of Peripheral Nerves of the Forearm, 2nd ed. Philadelphia, W. B. Saunders, 1978.)

1094 Part VIII Septic and Nontraumatic Conditions

8 cm below the elbow joint, this nerve emerges from the supinator muscle, where it divides into its terminal motor branches to the extensor digitorum communis, extensor digiti minimi, extensor carpi ulnaris, abductor pollicis longus, extensor pollicis longus and brevis, and extensor indicis proprius.

Posterior Interosseous Nerve Syndrome In cases of a high bifurcation, the deep branch may be compressed at the lateral intermuscular septum, 4 cm proximal to the lateral epicondyle. There is focal tenderness and often wrist and finger extensor weakness. In these rare cases, the superficial radial nerve lies anterior to the lateral intermuscular septum. The deep branch can be compressed by a fibrous band or thickened proliferating rheumatoid synovium from the radiocapitellar joint,18,114,116 the radial recurrent artery, or the leading tendinous edge of the extensor carpi radialis brevis.119 Next, the posterior interosseous nerve can be compressed at the arcade of Frohse,54,118,134,152,163,168,196 the most common site of compression. It may also be compressed by fibrotic bands within the midportion of the supinator26 and its distal end. Other causes of compression include adhesions at the anterior aspect of the distal humerus, muscular anomalies, vascular aberrations,41 bursae,2 inflammatory thickening, and adherence of the extensor carpi radialis brevis119 tendinous origin to the proximal edge of the supinator on its radial side.19,20 Some have identified focal constriction within the posterior interosseous nerve.71,94 Posterior interosseous nerve palsy may result from fractures124,179 or fracture-dislocations (Fig. 803).122,171 Tardy posterior interosseous nerve palsy may also occur years after unreduced Monteggia fracturedislocations73,105 or after radial osteomyelitis (Fig. 80-4).176 Tumors may compress the nerve primarily, which can be secondarily compressed by a structure such as the arcade of Frohse.7,11,17,151,178,200 Classically, the clinical presentation of this nerve paralysis is thought to be typically motor because the posterior interosseous nerve basically carries motor fibers destined to innervate the extensor digitorum communis, extensor digiti minimi, extensor carpi ulnaris, abductor pollicis longus, extensor pollicis longus and brevis, and extensor indicis proprius. However, pain simulating lateral epicondylitis is also recognized as a common early presentation (see later discussion).19 Because of the segmental innervation of the supinator, the proximal or distal location of the compression of this nerve in the supinator can be determined by evaluating the electromyogram occasionally. Fibrillations in the supinator muscle suggest that the compression is proximal, at the arcade of Frohse. The pattern of involvement of this nerve varies depending on whether the entire nerve is compressed or whether there is a partial

FIGURE 80-3

Fractures of the proximal radius often demonstrate posterior angulation, which places the posterior interosseous nerve in jeopardy. (Redrawn from Spinner, M., and Spinner, R. J.: Management of nerve compression lesions of the upper extremity. In Omer, G. E., Spinner, M., and Van Beek, A. L. [eds.]: Management of Peripheral Nerve Problems, 2nd ed. Philadelphia, W. B. Saunders, 1998.)

FIGURE 80-4

This patient presented with a partial posterior interosseous nerve palsy. Plain films showed thickened cortices and a widened radial metaphysis, bony changes from an old osteomyelitis. (From Spinner, R. J., and Spinner, M.: Tardy posterior interosseous nerve palsy due to childhood osteomyelitis: A case report. J. Hand Surg. 22A:1049, 1997.)

paralysis. When the entire posterior interosseous nerve is compressed, the fingers and thumb cannot extend at the metacarpophalangeal level and the wrist deviates in a radial direction with wrist extension (because the branches to the extensor carpi radialis longus and brevis

Chapter 80 Nerve Entrapment Syndromes 1095

FIGURE 80-5

Patient with a complete posterior interosseous nerve paralysis showing inability to extend the fingers at the metacarpophalangeal joints as well as an inability to extend the thumb. The patient can dorsiflex his wrist. Wrist dorsiflexion is in a radial direction through the intact extensor carpi radialis longus, which is innervated at or above the elbow. Sensation in the hand is intact. (From Spinner, M.: Injuries to the Major Branches of Peripheral Nerves of the Forearm, 2nd ed. Philadelphia, W. B. Saunders, 1978.)

FIGURE 80-7

FIGURE 80-6

This patient has a complete radial nerve paralysis at the mid-arm level. Note the wristdrop with loss of finger extension at the metacarpophalangeal joints. The brachioradialis is paralyzed. Sensory loss is present in the autonomous zone of the radial nerve, that is, the dorsum of the thumb and first web space. In addition there is sensory loss in the distributions of the posterior cutaneous nerve of the forearm and the lower lateral cutaneous nerve of the arm.

usually take off more proximally) (Fig. 80-5).15,197 An untreated partial paralysis commonly evolves into a complete paralysis. Wristdrop signifies a lesion proximal to the posterior interosseous nerve branch (Fig. 80-6). With partial paralysis, some of the digits, for example the fourth and fifth fingers at the metacarpophalangeal joints, do not extend but the others do.41,66,78,126 This attitude looks like a “pseudoulnar” claw hand. In reality, there is no clawing but only a drop at the metacarpo-

This patient has a complete low ulnar nerve palsy of the right hand with typical ulnar nerve clawing of the ring and little fingers. Note in this type of ulnar nerve palsy that there is hyperextension at the metacarpophalangeal joint typically seen with a claw finger. If a digit cannot be passively hyperextended at the metacarpophalangeal joint, a claw finger would not develop in the event of a low ulnar nerve paralysis. Sensation is absent in the palmar aspect of the little finger and ulnar half of the ring finger. Sensibility on the dorsal side is intact. (From Spinner, M., and Spinner, R. J.: Management of nerve compression lesions of the upper extremity. In Omer, G. E., Spinner, M., and Van Beek, A. L. [eds.]: Management of Peripheral Nerve Problems, 2nd ed. Philadelphia, W. B. Saunders, 1998.)

phalangeal joint and no true hyperextension of the metacarpophalangeal joints of the fourth and fifth fingers, as is present in a typical ulnar nerve palsy (Fig. 80-7). Understanding the branching pattern of the posterior interosseous nerve can assist in further localization of partial lesions. Different patterns of presentation have been described and localized.72,77,173,181 These include dropped finger (all) and thumb deformity; dropped long-ring, and little finger (and extensor carpi ulnaris) deformity; dropped thumb (abductor pollicis longus,

1096 Part VIII Septic and Nontraumatic Conditions

extensor pollicis brevis and longus, and extensor indicis proprius) deformity; and dropped long and ring fingers only (“sign of the horns”). If surgery is entertained for incomplete lesions, the exit of the supinator should also be explored. In both partial and complete posterior interosseous nerve paralysis, sensation in the autonomous region on the dorsum of the first web space of the hand is uninvolved. On occasion, isolated superficial radial nerve entrapment may occur in the elbow or proximal forearm region, but it is more commonly involved in the distal forearm or wrist. Isolated radial sensory paresthesias are usually secondary to irritations to the nerve in the region of the radial styloid. A compression neuropathy may occur in which this nerve penetrates the deep fascia in the midforearm between the brachioradialis and extensor carpi radialis longus.37 Focal tenderness usually identifies the involved site. Plain radiographs may be helpful in showing a fat stripe of a lipoma or a bony lesion in the vicinity of the radial neck (see Fig. 80-4). Ultrasound or magnetic resonance imaging (MRI) may demonstrate an occult ganglion or elucidate a palpable mass by its imaging characteristics (Fig. 80-8).178 MRI is helpful in demonstrating denervation atrophy and hyperintensity in the nerve, which may help confirm a diagnosis or localization of nerve compression, or both. Electrical studies

FIGURE 80-8

This patient had a near complete posterior interosseous nerve palsy associated with a 2.5 cm mass. Plain radiographs were unremarkable. Sagittal T1 (a)weighted MR images show a mass (*) iso-intense to muscle in the region of the radial neck and the supinator muscle (S). (From Spinner, R. J., Lins, R. E., Collins, A. J., and Spinner, M.: Posterior interosseous nerve compression due to an enlarged bicipital bursa confirmed by MRI. J. Hand Surg. 18B:753, 1993.)

typically demonstrate denervational changes in the muscles innervated by the posterior interosseous nerve. If there are no EMG abnormalities in the supinator, then one should have a suspicion that the compression lesion of the posterior interosseous nerve is at the distal end of this muscle rather than at its proximal end. The brachioradialis and the extensor carpi radialis longus and brevis should not reveal any abnormalities in the typical posterior interosseous nerve syndrome because these muscles are innervated by the radial nerve proximal to the arcade of Frohse. Because of the overlap of posterior interosseous nerve syndrome with many cases of Parsonage-Turner syndrome, EMG should examine other muscles (e.g., shoulder muscles) to identify a more diffuse neurologic process that would favor the diagnosis of an inflammatory disease. The favorable response of operative decompression in some patients with posterior interosseous nerve “entrapment” may well be due to a favorable natural history of Parsonage-Turner syndrome. I believe that Parsonage-Turner syndrome is underrecognized. For this reason, I recommend performing decompression after 6 months of observation in patients with spontaneous onset of symptoms in whom mass lesions are not discovered and there has not been any clinical recovery.

Resistant Tennis Elbow (Radial Tunnel Syndrome) For the most part, resistant tennis elbow is caused by degeneration or fascial tears at the lateral epicondyle. On occasion, persistent complaints have been attributed to either compression of the posterior interosseous nerve or to a combination of nerve compression and persistent localized epicondylitis.20,153,165 Resistant pain localized to the proximal forearm should suggest that entrapment of the adjacent posterior interosseous nerve may be an unrecognized factor. Physical findings frequently reveal tenderness, both over the lateral epicondyle and anteriorly over the course of the nerve as it passes through both heads of the supinator. On occasion, pain can be localized to the distal end of the supinator posteriorly at the junction of the middle and upper thirds of the proximal forearm. Pain may be increased with resisted active supination of the forearm or with resisted extension of the long finger with the elbow extended. There are no sensory abnormalities in the hand. EMG studies in cases of resistant tennis elbow due to entrapment of the posterior interosseous nerve are often normal, even if the condition has been present for months and with definite clinical findings. Conduction delays are observed rarely. Stress testing as described by Werner193 has sometimes been helpful in confirming the diagnosis. Fibrillations in the muscles innervated by the posterior interosseous nerve are usually sparse, but if

Chapter 80 Nerve Entrapment Syndromes 1097

present, they are most likely in the extensor indicis proprius. If fibrillations are widespread in the more severe lesions, weakness of the finger extensors and extensor carpi ulnaris is also usually evident. Patients suspected of having coexisting lateral epicondylitis and posterior interosseous nerve compression, who fail conservative treatment, should have both conditions treated simultaneously. Patients with persistent pain after surgery for lateral epicondylitis should be suspected of having posterior interosseous nerve compression.121

Triceps

Preferred Operative Exposure for the Entire Course of the Posterior Interosseous Nerve When exposure of the entire posterior interosseous nerve is needed, the plane between the extensor carpi radialis brevis and the extensor digitorum communis (Fig. 80-9) is developed. The incision begins 5 cm proximal to the lateral epicondyle and passes over the lateral epicondyle down to the region of the origin of the outcropping muscles (abductor pollicis longus, extensors pollicis longus and brevis). The aponeurotic plane between the extensor carpi radialis brevis and the exten-

Biceps Brachialis

Brachioradialis

Extensor digitorum communis

Extensor carpi radialis longus Extensor carpi radialis brevis Abductor pollicis longus

A

Brachialis

Brachialis Radial n.

Biceps Median n.

Median n. Brachioradialis Posterior interosseous n.

Brachioradialis

Supinator Pronator teres Superficial radial n.

Flexor carpi radialis

B

C

FIGURE 80-9

A, Incision for extensile exploration of the radial nerve is helpful for exploring the radial nerve, the proximal half of the posterior interosseous nerve, and the superficial radial nerve. B, The interval between the brachioradialis and the brachialis and pronator teres is developed. C, The radial nerve and its major forearm branches, the posterior interosseous and the superficial branches are exposed. (Redrawn from Spinner, M.: Injuries to the Major Branches of Peripheral Nerves of the Forearm, 2nd ed. Philadelphia, W. B. Saunders, 1978.)

1098 Part VIII Septic and Nontraumatic Conditions

sor digitorum communis is developed from distal to proximal (Fig. 80-10). Identification of the plane is facilitated by passive motion of the fingers while the wrist is held steady, and the plane can be developed by blunt dissection. The supinator muscle is seen in the depth of the wound as these muscles are liberated. To gain complete exposure to the proximal end of the supinator, the extensor carpi radialis brevis tendon can be detached from its origin at the lateral epicondyle. At times, the distal portion of the origin of the extensor carpi radialis longus is detached, if necessary, for complete exposure of the underlying arcade of Frohse. This is facilitated with elbow flexion. Adherence of the tendinous origin of this muscle to the lateral portion of the supinator muscle is frequently found and is freed to give exposure to the proximal end of the supinator. One can identify the posterior interosseous nerve by flexing the elbow and by palpating the nerve’s course as it passes obliquely through the supinator in a dorsoradial direction. By gently spreading longitudinally through the fat on both sides of the nerve with a right-angled hemostat, the

Radial n.

Posterior interosseous n.

BR ECRL ECRB Supinator

Arcade of Frohse Extensor digitorum communis ECU EDC

FIGURE 80-10 Details of the innervation provided by the posterior interosseous nerve. The nerve may be traced to the supinator showing the terminal branches (BR, brachioradialis; ECRB, extensor carpi radialis brevis; ECRL, extensor carpi radialis longus; ECU, extensor carpi ulnaris). (Redrawn from Spinner, M.: Injuries to the Major Branches of Peripheral Nerves of the Forearm, 2nd ed. Philadelphia, W. B. Saunders, 1978.)

nerve can be isolated. Because there are recurrent vessels in the vicinity, dissection must be gentle. Any vessels crossing the nerve should be clamped and tied individually. When the posterior interosseous nerve is identified proximal to the arcade of Frohse, a vasoloop is passed about it so that its identity and continuity are maintained. The arcade of Frohse may be found to be thickened. A hemostat is placed deep to the arcade but superficial to the nerve, and the arcade is incised, liberating the most proximal portion of the nerve. If further surgery is necessary, the entire posterior interosseous nerve can be traced and brought into direct view. Compression of the proximal and distal region has been described, as well as compression of the nerve in its midportion.177 Epineurotomy of the posterior interosseous nerve at the site of its compression on occasion may be deemed necessary. Microsurgical technique should be used when this is indicated. The detailed anatomy of the nerve supply to the extensor digitorum communis is important because this muscle obtains its innervation from branches of the terminal portion of the posterior interosseous nerve that run at right angles to the plane of the forearm in the distal portion of the proximal third of the forearm (see Fig. 80-10).173 The operating surgeon should not sweep the planes between the extensor digitorum communis and the supinator because these branches are vulnerable. Furthermore, strong retraction posteriorly of the extensor digitorum communis in this area could damage the nerve supply to this important muscle. The tendinous origin of the extensor carpi radialis brevis tendon is not reattached. Increasingly it has been recognized that the thick tendon of origin of this muscle in its distal prolongation passes directly over the arcade of Frohse. The combination of frictional and compressive irritation from this structure may be a major factor in the development of the radial tunnel syndrome. For this reason, a 3- to 4-cm portion of its most proximal tendinous origin may be excised. The tourniquet is released, and hemostasis is obtained. If the patient had lateral epicondylar pain and tenderness preoperatively, then at this time, the lateral epicondyle can be drilled or a small portion excised. The skin is closed, and the arm is immobilized in long arm plaster splints with the elbow at 90 degrees, the forearm in mid-position, and the wrist in a functional position. The immobilization is continued for 2 weeks, and the limb is gradually mobilized. If a limited approach to the proximal portion of the supinator is needed, I prefer an anterior exposure of the posterior interosseous nerve. The lesion localized to the arcade of Frohse is approached by developing the plane proximal to the elbow between the brachialis and brachioradialis (see Fig. 80-9). Distal to the elbow, the anatomic dissection is continued, and the plane between the brachioradialis and the pronator teres is developed.

Chapter 80 Nerve Entrapment Syndromes 1099

Brachioradialis m. Cut tendon of origin of the ECRB

Radial n. Post. interosseous n. Ulnar n.

Superficial radial n.

Arcade of Frohse FCU

Lister’s approach

FIGURE 80-11 An extensile exposure of the forearm to demonstrate the radial nerve may be accomplished by the surgical excisions shown here. The data outlined by Lister may be used to aid in performing an extensile exposure to the radial tunnel.

If the dissection is difficult because of scarring or muscle anomalies, the superficial radial nerve can be identified distally and traced proximally to the main radial nerve and then to the deep branch. Any obstructing collateral vessels are ligated. The proximal third of the posterior interosseous nerve can be best visualized with this exposure. If necessary, the rest of the nerve can be followed by a separate posterior approach. A longitudinal transmuscular approach through the brachioradialis has been popularized by Lister and associates.107 It provides direct access to the nerve from the radiohumeral level to the midsupinator (Fig. 80-11). When there has been prior surgery in the region, an anterior and separate posterior incision may be necessary to expose the radial nerve and its branches safely.

ULNAR NERVE

Cubital tunnel retinaculum

FIGURE 80-12 The cubital tunnel retinaculum seems to be the predominant site of pathology for patients with primary ulnar nerve symptoms at the elbow. (Redrawn from O’Driscoll, S. W., Horii, E., Carmichael, S. W., and Morrey, B. F.: The cubital tunnel and ulnar neuropathy. J. Bone Joint Surg. 73B:613, 1991.)

Struthers, is controversial.164 The ulnar nerve, similarly, passes from posterior to the medial epicondyle to the anterior compartment of the forearm a few centimeters distal to the medial epicondyle and the cubital tunnel. In the arm, there usually are no branches of the ulnar nerve of significance. Occasionally there is a variant high take-off of a motor branch to the flexor carpi ulnaris in the distal arm. The dorsal cutaneous nerve of the forearm, the sensory branch to the dorsoulnar aspect of the hand, rarely has been observed to arise in the proximal rather than the distal forearm. At the elbow level, the first branch is usually an expendable articular branch that arises just distal to the medial epicondyle; next are usually varying branches of the flexor carpi ulnaris and the motor branch to the fourth and fifth flexor digitorum profundus muscles. Stimulation of these branches can help the physician in deciphering whether the branch is a motor branch to an end organ or an articular branch. In addition, fascicular mobilization of these branches can be performed safely for a distance up to 6 cm to facilitate ulnar nerve transposition.192

Relevant Anatomy At the elbow, the ulnar nerve90 passes posterior to the medial epicondyle through the cubital tunnel. The cubital tunnel retinaculum137 (Fig. 80-12) seems to be the predominant site of pathology for patients with primary symptoms. In the proximal arm, the nerve descends in the anterior compartment. In the majority of upper extremities, the ulnar nerve crosses from the anterior to the posterior compartment in the distal arm. The anatomy of the region (about 8 cm proximal to the medial epicondyle), corresponding to the so-called arcade of

Etiology Ulnar nerve compression lesions may be due to many factors.4,69,110,140,141,189,190 At the elbow level, spontaneous compression neuritis is well known as the cubital tunnel syndrome.49 It is second only to carpal tunnel syndrome in its frequency. Ulnar nerve lesions may be due to compression, stretch, traction, friction, or a combination of these. Direct pressure on the posterior aspect of the elbow can compress the nerve and is seen in patients follow-

1100 Part VIII Septic and Nontraumatic Conditions

ing coma, in surgical cases, or even in those who use wheelchairs. Flexion of the elbow may exacerbate symptoms, because it causes tightening and narrowing of the cubital tunnel and traction-related deformation of the nerve.60 The tendinous origin of the flexor carpi ulnaris can compress this nerve between its ulnar and humeral heads with elbow flexion.6 Extrinsic pressure on the nerve may result from the anconeus epitrochlearis,29,102 a variant muscle crossing the ulnar nerve in the region of the medial epicondyle, or from adhesions. Tumors130 such as ganglia14,89 may also be a causative factor. A hypermobile ulnar nerve can produce symptoms.23 This usually occurs during elbow flexion, as the nerve dislocates from the undersurface of the medial epicondyle to a position anterior to the epicondyle. Snapping of the medial triceps43,75,149,154,175 may be found in association with a dislocating ulnar nerve, and this can result in elbow pain, snapping, and ulnar nerve symptoms (Figs. 80-13 and 80-14). Persistent pain after an otherwise successful ulnar nerve transposition may represent unrecognized snapping of the triceps. Bony changes at the elbow, whether acute or chronic, can result in ulnar nerve symptoms. Fracturedislocations, medial epicondylar fractures, arthritic changes from osteoarthritis or rheumatoid arthritis,45,104 callus, heterotopic bone, and spurs have been implicated. Both cubitus valgus and varus deformities1,56,188 may produce late ulnar nerve symptoms at the elbow. Iatrogenic causes of secondary ulnar nerve compression are numerous and related to technical factors.57 Compression may occur when the ulnar nerve is trans-

posed anteriorly and is insufficiently mobilized, proximally or distally.169,170 After a previous transposition, secondary compression can be found proximally at the level of the so-called arcade of Struthers or distally where the ulnar nerve passes in the region of the common aponeurosis for the humeral head of the flexor carpi ulnaris and the origin of the flexor digitorum superficialis.86 If these aponeurotic areas are not released sufficiently both proximally and distally (Fig. 80-15), then potential secondary sites of entrapment are created, which can produce symptoms.172 The medial intermuscular septum should be excised because it, too, is a common cause of secondary ulnar nerve entrapment. However and whenever, the ulnar nerve is transposed, it should be transposed anteriorly without kinking. Tight slings used to maintain the nerve in an anterior position may result in secondary compression.103,108 Furthermore, traction neuritis can result when the nerve is transposed into a groove in the flexor-pronator group of muscles. When the nerve heals in the muscular groove, the longitudinal fibrotic aponeuroses of flexor muscles of the medial aspect of the elbow can produce secondary traction neuritis.

Clinical Presentation A patient with an ulnar nerve lesion at the elbow typically presents with a combination of elbow pain and sensory and motor complaints. It usually begins with intermittent paresthesias in the ring and little fingers that are aggravated by elbow flexion and frequently awaken the patient. Sensory loss in the ring and little fingers of the hand usually occurs later, but sensory loss in the

Medial epicondyle Ulnar n.

Medial head of triceps

First snap– Ulnar n.

Second snap– Medial head of triceps

FIGURE 80-13 The ulnar nerve can be palpated within the cubital tunnel with the elbow in extension. Then with passive or active flexion of the elbow, the examiner can assess whether the ulnar nerve or another structure, such as a portion of the medial head of the triceps or an anomalous triceps tendon, moves anterior to the medial epicondyle. (Redrawn from Spinner, R. J., and Goldner, R. D.: Snapping of the medial head of the triceps and recurrent dislocation of the ulnar nerve: Anatomical and dynamic factors. J. Bone Joint Surg. 80A:239, 1998.)

Chapter 80 Nerve Entrapment Syndromes 1101

E O

Full extension

1 2 T

R

U R

1 2

U

1 O

E T

A

E

130° flexion

2

B FIGURE 80-14 A, Magnetic resonance imaging can demonstrate a snapping triceps and dislocating ulnar nerve. Here the ulnar nerve (1) and a portion of the medial head of the triceps (2) are anterior to the medial epicondyle (E) with the elbow fully flexed. Computed tomography or real-time ultrasonography can also confirm the diagnosis. Imaging, however, is not necessary for confirmation of a diagnosis. Patients undergoing ulnar nerve surgery should be examined preoperatively and intraoperatively, with the elbow in flexion and extension, so that the surgeon can evaluate whether the medial head of the triceps snaps over the medial epicondyle. R, radius; U, ulna. B, Corresponding artist drawing shows the position of the ulnar nerve and the medial head of the triceps to the medial epicondyle in full extension and flexion. O, olecranon; T, triceps. (A from Spinner, R. J., Hayden, F. R., Jr., Hipps, C. T., and Goldner, R. D.: Imaging the snapping triceps. A.J.R. Am. J. Roentgenol. 167:1550, 1996; B redrawn from Khoo, D., Carmichael, S. W., and Spinner, R. J.: Ulnar nerve anatomy and compression. Orthop. Clin. North Am. 27:317, 1996.) Traction-compression type mechanical neuropathy of ulnar nerve

Intact arcade

dorsoulnar aspect of the hand is a classic localizing sign. Usually, there are no sensory abnormalities in the forearm. The sensory fibers and the intrinsic motor fibers lie more peripherally than the fibers of the flexor digitorum profundus or the flexor carpi ulnaris and may explain their vulnerability early on. Motor weakness

FIGURE 80-15 Tethering of the ulnar nerve may result from a previous (incomplete) decompression. (From Spinner, M., and Spinner, R. J.: Nerve decompression. In Morrey, B. F. [ed.]: Master Techniques in Orthopaedic Surgery: The Elbow, 2nd ed. Philadelphia, Lippincott Williams & Wilkins, 2002.)

may be progressive in both the extrinsics and the intrinsics; at times, significant motor findings can be present with minimal sensory symptoms. With paralysis of the flexor digitorum profundus to the ring and little fingers, there is usually minimal clawing or no clawing of the ring and little fingers. With partial lesions, clawing may

1102 Part VIII Septic and Nontraumatic Conditions

be more pronounced if the flexor digitorum profundus muscles are intact and the intrinsic muscles are atrophic.113,182 However, if the metacarpophalangeal joints of the ring and little fingers cannot hyperextend because of innate tightness of the volar plates, then clawing will also not be observed. A mechanical lesion of the ulnar nerve at the elbow may present with different clinical patterns in different patients because of the presence or absence of neural anomalies and the extent of involvement of the nerve. There are numerous variations in fibers carried within the ulnar nerve at the elbow level.169 In 15% of upper extremities, the median nerve will carry many of the intrinsic motor fibers to pass from the median nerve or the anterior interosseous nerve branch of the median nerve to the ulnar nerve in the midforearm. The sensory pattern typical of an ulnar nerve lesion at the elbow with diminished or absent sensation on the dorsoulnar aspect of the hand100 may not be observed. This may occur when other sensory nerves take over the area usually supplied by the dorsal cutaneous branch of the forearm. One variant sensory pattern is observed when the superficial radial nerve not only innervates the dorsal radial aspect of the hand but also extends to supply the dorsoulnar aspect. Furthermore, sensation in all of the ring and middle fingers can be affected in some complete ulnar nerve lesions.

syndrome) have normal EMG studies. The absence of ulnar F-wave abnormalities and cervical paravertebral fibrillations and the presence of an ulnar nerve conduction delay distally across the elbow can be suggestive findings of a lesion at the elbow. However, double crush lesions can occur and patients who have persistent symptoms after elbow surgery may have a more proximal lesion. Entrapment in the hand is much less common than entrapment at the elbow; entrapment in the forearm is even rarer. Depending on the level of nerve involvement, varying clinical signs and symptoms become manifest. In a full-blown lesion in Guyon’s canal, there is usually more significant (“paradoxical”) clawing of these digits because the flexor digitorum profundus is functioning (see Fig. 80-7). The sensation on the dorsoulnar aspect of the hand is intact, whereas the palmar aspect of the hand may have some hypesthesia. Lesions of the ulnar nerve in the proximal forearm have findings similar to those at the elbow, whereas in the middle and distal forearm, symptoms depend on the relationship of the lesion to the motor branch of the flexor digitorum profundus and the dorsal cutaneous branch of the forearm. A lesion distal to the take-off of the motor branch of the flexor digitorum profundus is usually seen in patients with clawing. A lesion proximal to the dorsal cutaneous branch presents with numbness in the dorsoulnar aspect of the hand.

Differential Diagnosis In the differential diagnosis, a nerve lesion that involves the cervical foramina, as in cervical arthritis, can present with ulnar nerve type symptoms. Restriction and pain on movement of the neck, positive foraminal compression maneuvers, arthritic changes seen radiographically, and cervical paravertebral muscle electrical abnormalities are usually noted. Short segment stimulation may be effective in isolating the level of the compression to the ulnar nerve at the elbow.46 Another frequent site for exclusion is the thoracic outlet. The medial components of the plexus (lower trunk, or C8 and T1) are most frequently involved. Radiation of paresthesias along the inner aspect of the arm with symptoms extending to the ring and little fingers is a common neural presentation. Clinical signs characteristic of thoracic outlet syndrome, including a positive percussion sign, or a positive Adson or Wright test, or hyperabduction maneuver, or the presence of an arterial bruit with abduction or extension, may help localize the pathologic process to the thoracic outlet, but one should also be aware of the presence of falsepositive physical examination findings in the normal population. EMG studies in patients with neurogenic (or true) thoracic outlet syndrome have abnormalites beyond the ulnar nerve territory, whereas those with thoracic outlet symptoms (or disputed thoracic outlet

Conservative Treatment In the milder cases, a trial of conservative treatment is often helpful. Avoidance of prolonged elbow flexion, especially at night, is helped by an elbow splint with the elbow maintained in a semiflexed position of about 60 degrees. During the day, resting the elbow on a table should be avoided. A 4- to 6-week trial of these measures is worthwhile.

Operative Treatment There are several different approaches for the surgical intervention of the ulnar nerve: simple decompression, medial epicondylectomy, subcutaneous, intramuscular and submuscular transposition and endoscopic or arthroscopic techniques. Many surgeons over the years have passionately advocated a particular technique under all circumstances, whereas others have suggested that the choice of operative procedure52 should be fitted to the patient’s symptoms and the EMG findings. Despite these opinions, recent prospective studies performed in primary cases have not demonstrated any statistical differences between simple decompression and the different types of anterior transposition.8,10,61,128,202 As a result, simple decompression in these cases is becoming more commonly performed. In secondary cases, submuscular transposition is the procedure of choice.

Chapter 80 Nerve Entrapment Syndromes 1103

For mild and moderate ulnar nerve compression, I perform a simple release of the cubital tunnel.24 If the nerve is noted to dislocate intraoperatively after release, I perform an anterior subcutaneous translocation, the same procedure that I perform currently in most patients with severe ulnar neuropathy. If the patient has no fat in the subcutaneous tissue, or in revision surgery, I prefer the Learmonth procedure, the submuscular anterior translocation of the ulnar nerve.101,103 I do not perform submuscular transposition in patients with rheumatoid arthritis or in those with post-traumatic medial bony changes.

Preferred Operative Exposure for Simple Decompression of the Ulnar Nerve Under monitered anesthetic care, the ulnar nerve is exposed through a 4- to 5-cm posteromedial incision to the elbow centered at the level of the olecranon groove. The ulnar nerve is identified just proximal to the elbow. A vasoloop is placed around the ulnar nerve. With the nerve protected, it is traced through the cubital tunnel retinaculum and a portion of the flexor carpi ulnaris. An occult lesion, such as a joint-related ganglion is looked for posterior to the nerve without circumferential mobilization of the nerve. The medial intermuscular septum is not resected. Proximal release is not done. The stability of the nerve and the position of the medial triceps is assessed with passive elbow range of motion.

Preferred Operative Exposure for Anterior Transposition of the Ulnar Nerve The incision extends 5 cm proximal to the medial epicondyle and 4 cm distal to the medial epicondyle on the

posteromedial side of the elbow (Fig. 80-16A). The Vshaped flap formed at the elbow level is undermined subcutaneously and is retracted medially. The medial cutaneous nerves of the forearm and arm are identified and preserved by vasoloops about them. Avoidance of injury to them is important because patients afflicted with ulnar entrapment lesions are vulnerable to symptomatic postoperative skin neuromata.38 The plane between the subcutaneous fat and the brachial and antebrachial fascia in the distal arm is delineated and undermined. The medial intermuscular septum is seen, and the ulnar nerve is identified just posterior to the medial intermusclar septum in the distal third of the arm. In approximately 70% of limbs, muscular fibers of the medial head of the triceps have been reported to cross the ulnar nerve and attach to the so-called arcade of Struthers, 8 cm proximal to the medial epicondyle. If these muscular fibers of the medial head of the triceps are noted, it is a clear indication that the ulnar nerve must be liberated in this area (see Fig. 80-16B). The medial intermuscular septum is cleared posteriorly of muscular fibers to the level of the humerus. Anteriorly, the medial intermuscular septum is separated with care from the neurovascular bundle. The inferior ulnar collateral vessels, which penetrate the intermuscular septum, can be preserved, and the medial intermuscular septum is excised (see Fig. 80-16C). The ulnar nerve is mobilized. Its external longitudinal vessels are kept in continuity with the nerve. The transverse components of the vascular supply can be cauterized, preferably with a bipolar unit, keeping the external and internal vascular supply intact. At the level of the posterior aspect of the medial epicondyle, the ulnar nerve is liberated and an articular branch to the adjoined surface is sacrificed. One or two

Arcade of Struthers Median n.

Ulnar n.

Medial intermuscular septum

A

B

C

FIGURE 80-16 A, Anterior translocation of the ulnar nerve requires exposure of the medial intermuscular septum and the so-called arcade of Struthers. B, The arcade has been released. C, A portion of the medial intermuscular septum is then removed, and the ulnar nerve is brought forward anterior to the flexion axis of the elbow. (Redrawn from Spinner, M.: Injuries to the Major Branches of Peripheral Nerves of the Forearm, 2nd ed. Philadelphia. W. B. Saunders, 1978.)

1104 Part VIII Septic and Nontraumatic Conditions

rubber bands are placed about the ulnar nerve to aid in the dissection. Distal to the medial epicondyle, the ulnar nerve is identified as it passes through the cubital tunnel. The tendinous arch for the origin of the flexor carpi ulnaris of the humerus and ulna in the proximal region is identified. The humeral attachment is detached, and the interval between the common aponeurosis of the flexor carpi ulnaris humeral head and the flexor digitorum superficialis is defined. The ulnar nerve is identified distally, deep to the flexor carpi ulnaris. Its common fibrous aponeurosis is liberated to free the ulnar nerve in the proximal forearm. The multiple branches of the flexor carpi ulnaris are preserved. The motor branch to the flexor digitorum profundus of the ring and little fingers is also identified and preserved. The ulnar nerve is mobilized in the proximal third of the forearm with the use of loupe magnification and microsurgical technique to permit nontethered anterior translocation.67 At this point, the nerve can be placed in a subcutaneous plane or placed in a submuscular position. A loose fasciodermal sling44 or the medial intermuscular septum145 may be used to stabilize the ulnar nerve; before wound closure, the elbow should be passively flexed and extended to ensure that ulnar nerve compression has been eliminated and to check that snapping of the medial portion of the triceps is not present.175 If snapping of the medial triceps is identified either preoperatively or intraoperatively, one can trans-

pose laterally or excise the offending dislocating portion of the medial triceps. To proceed with the Learmonth procedure, the median nerve is identified proximal to the lacertus fibrosus in the distal arm and a rubber band is placed around it (Fig. 80-17). The median nerve is found deep to the brachial fascia at the elbow level medial to the brachial artery. The lacertus fibrosus in the proximal forearm is incised longitudinally. The next step in the dissection is to detach the muscles of the flexor-pronator group 1 cm distal to the medial epicondyle. To accomplish this, a tonsillar clamp is placed from the radial side of the flexor-pronator group of muscles 1 cm distal to the medial epicondyle and passed medially deep to the flexor-pronator group of muscles to exit in the region of the cubital tunnel. The tonsillar clamp is passed superficial to the ulnar collateral vessels on the anterior aspect of the medial side of the forearm. The flexorpronator origin is incised sharply. The brachial fascia is identified. By a combination of sharp dissection and periosteal stripping, the flexor-pronator group of muscles is stripped distally. The tourniquet is released. Any additional bleeding is brought under control either by ties or with the bipolar electrocautery. The ulnar nerve is translocated anteriorly adjacent to the median nerve, and the flexor-pronator origin is repaired (Fig. 80-17B). Z-lengthening or advancement of the flexor-pronator origin can also be performed.33-35,135 The subcutaneous

Median n. Ulnar n. Flexorpronator mass

A

B

FIGURE 80-17 A, Extensive skin incision is employed for translocation of the ulnar nerve. This allows exposure of the proximal aspect of the medial intermusuclar septum and the so-called arcade of Struthers. B, Submuscular translocation (Learmonth) technique requires proximal dissection of the ulnar nerve and release of the medial intermuscular septum approximately 8 cm proximal to the flexor-pronator muscle group, which is elevated from the medial epicondyle. The ulnar nerve is brought forward to lie next to the median nerve. The flexor-pronator group is then reattached to the medial epicondyle. Particular care is taken not to injure the anterior interosseous branch of the median nerve, which arises in this region. (Redrawn from Spinner, M.: Injuries to the Major Branches of Peripheral Nerves of the Forearm, 2nd ed. Philadelphia. W. B. Saunders, 1978.)

Chapter 80 Nerve Entrapment Syndromes 1105

tissues and skin are closed with either interrupted or subcuticular sutures. After a submuscular transposition, the elbow is immobilized in a semiflexed position with the forearm in midposition and the wrist in neutral; the fingers and thumb are free. The immobilization is continued for 7 days followed by progressive active extension in a blocking splint. I do not have direct experience with medial epicondylectomy28,55,63,84,85,158 and do not like intramuscular transposition for ulnar nerve neuritis, although other surgeons have reported success with these techniques. Endoscopic and arthroscopic techniques are being employed by some surgeons.79,95,144,187

MEDIAN NERVE The median nerve at the level of the elbow may on occasion be susceptible to a compressive neuropathy from the level of the supracondylar process proximally to the flexor superficialis arch distally. Between these

levels, the ligament of Struthers, the lacertus fibrosus, the deep head of the pronator teres, variant muscles, distended bursae, or vascular malformations may produce symptomatic median nerve compression.

Relevant Anatomy The median nerve lies beneath the brachial fascia on the medial aspect of the arm resting on the brachialis muscle (Fig. 80-18).80 The brachial artery and veins lie laterally in close proximity and adjacent to the biceps tendon. The medial intermuscular septum lies posteriorly and attaches to the medial epicondylar flare. The median nerve passes first alongside the humeral origin of the pronator teres and then beneath it to lie on the deep surface. It most often passes between the humeral head and the ulnar head of the pronator muscle but may pass deep to both heads, or the ulnar head may be absent. Fibrous arches may play a role in the nerve compression.39 The motor branches of the pronator teres usually arise from the medial aspect of the nerve beneath the Median n. Pronator teres Flexor carpi radialis Palmaris longus

Brachialis

Flexor digitorum superficialis Brachioradialis

Median n. Humeral Ulnar heads of pronator teres Flexor carpi radialis Palmaris longus Flexor carpi ulnaris

A

Brachioradialis

Flexor carpi ulnaris Flexor digitorum profundus Flexor pollicis longus Flexor carpi radialis

B

Median n. Palmar branch Palmaris longus Ulnar n.

FIGURE 80-18 A, As the median nerve enters the forearm, it gives off branches to the humeral and ulnar heads of the pronator teres, which originate from the medial aspect of the nerve. B, The median nerve is followed deeper into the forearm. The anterior interosseous nerve is shown entering the forearm under the flexor digitorum superficialis. The nerves to the flexor-pronator group are demonstrated. (Redrawn from Hollinshead, W. H.: Anatomy for Surgeons, 2nd ed, Vol. 3. New York, Harper & Row, 1969.)

1106 Part VIII Septic and Nontraumatic Conditions

upper margin of the muscle but variably arise above the antecubital area. The branch to the ulnar head may arise from the main branch or as a separate branch from the median nerve. The anterior interosseous branch arises deep and usually laterally at the level of the deep head of the pronator teres and in close approximation to the bifurcation of the radial and ulnar arteries from the brachial artery.68,81 The main branch of the median nerve next passes beneath the tendinous arch of origin of the flexor digitorum superficialis and lies in close approximation to the deep surface of this muscle (see Fig. 8018B). The anterior interosseous nerve runs onto the index flexor digitorum profundus muscle and the flexor pollicis longus.112 The pronator teres usually arises from the common origin of the medial epicondyle but may extend proximally along the medial epicondylar flare. The lacertus fibrosus passes from the biceps tendon to the antebrachial fascia obliquely over the flexor-pronator group of muscles. Altered anatomy, whether from anatomic variation or a pathologic condition, may play an important part in causing nerve compression syndromes.51,98 The most important for median nerve compression about the elbow are the supracondylar process and ligament of Struthers,180 the Gantzer muscle,3,59 the palmaris profundus,169 the flexor carpi radialis brevis,169 a variant lacertus fibrosus (Fig. 80-19),174 and vascular perforation or tethering of the nerve.13 Distal humeral fracture or dislocation is well known to cause median nerve injury.106,146

Supracondylar Process Compression of the median nerve at the level of the distal humerus may occur when the nerve passes beneath the osseous process,115 which extends obliquely midanteriorly and continues to the medial epicondyle as the ligament of Struthers.62 (Ulnar nerve compression may rarely occur in association with a supracondylar process and the ligament of Struthers.) Muscle hypertrophy or strenuous use may facilitate the irritant effect of this structure.80 The supracondylar process has been a compressive factor in approximately 40 case reports. The supracondylar spur may be associated with proximal extension of the humeral head of the pronator teres, which may also be a factor in compression of the median nerve.

Pronator Syndromes The pronator syndrome has been described as a neural compression syndrome within the proximal forearm.70,82,83,92,123,161,194 It is a controversial disorder. The symptoms are often vague, consisting of discomfort in the forearm with occasional proximal radiation into the arm. A fatigue-like pain description may be elicited. Numbness of the hand in the median distribution is

Biceps brachii m.

Third head of biceps brachii m. Median n. Site of compression Accessory bicipital aponeurosis

Anterior interosseous branch of the median n.

Primary bicipital aponeurosis

FIGURE 80-19 An accessory bicipital aponeurosis from the third head of the biceps has compressed the median nerve, resulting in both anterior interosseous and main branch motor weakness without sensory symptoms. (From Spinner, R. J., Carmichael, S. W., and Spinner, M.: Partial median nerve entrapment in the distal arm because of an accessory bicipital aponeurosis. J. Hand Surg. 16A:236, 1991.)

often secondary. Repetitive strenuous motions, such as industrial activities, weight training, or driving, often provoke the symptoms. Nocturnal symptoms are infrequent. Numbness may affect all or part of the median distribution. Occasionally, patients may insist on emphasizing numbness of the little finger or the “whole hand.” Women seem to be at greater risk than men of developing these symptoms, especially if they are exposed to highly repetitive, moderately strenuous industrial occupations in which alternate pronosupinatory motions are required. The symptoms usually develop insidiously, but occasionally a specific event or sudden onset of pain in the forearm is associated with heightened susceptibility to muscular stress. Acute symptoms should be distinguished from the typical pattern of a more chronic “pain syndrome.” An expanding hematoma such as following venipuncture can result in acute compression of the median nerve by the lacertus fibrosus. Renal dialysis patients with arteriovenous fistulae have been reported to develop median

Chapter 80 Nerve Entrapment Syndromes 1107

nerve symptoms suddenly that localize to the elbow level. Pronator syndrome may also occur following crushing or contusion of the proximal forearm or stretching of the spastic musculature by casting in patients with cerebral palsy. Diagnosis is often delayed because of the vague, poorly related history, lack of easily observed findings, and association with workers’ compensation evaluation. At times, the patient seems more interested in recriminatory action against his or her employer than with resolution of the problem. Physical Examination Physical findings are often subtle, and several observations have been suggested to help to make the diagnosis:

1. An indentation of the flexor-pronator muscle mass below the medial epicondyle suggests that the lacertus fibrosus exerts a constrictive effect at that level.70,97,117,185 The indentation may be increased by active or passive pronation of the forearm. This should be compared with the opposite arm (Fig. 80-20).

Supination

Median n.

Median n.

Lacertus fibrosus

Constriction of pronator m. by lacertus fibrosus

Pronation

FIGURE 80-20 When the arm pronates, contraction of the pronator muscle may result in indentation of this structure by the lacertus fibrosus. Such a process may give rise to entrapment of the median nerve and the socalled pronator syndrome.

2. The flexor-pronator musculature feels indurated or tense in comparison with the opposite arm or with resisted pronation. Most patients with this syndrome have well-developed forearm musculature.70 3. Resisted pronation for 60 seconds may initiate the symptoms by contracting the flexor-pronator muscle (Fig. 80-21). 4. Resisted elbow flexion and forearm supination may elicit similar symptoms, also presumably by tensing the lacertus fibrosus. Variations in the lacertus fibrosus may be recognized by a separate protrusion in the medial aspect of the antecubital space during resisted flexion. An accessory lacertus fibrosus has shown a tendency to invoke weakness affecting the anterior interosseous nerve fibers within the median nerve.174 5. Resisted flexion of the middle finger proximal interphalangeal joint by tightening the fibrous arch of the origin of the superficialis muscle may also induce symptoms, although this test seems to be positive far less frequently than the previous two. 6. Direct pressure by the examiner’s hand over the proximal portion of the pronator teres approximately 4 cm distal to the antebrachial crease while exerting moderate resistance to pronation has also been useful. It should be compared with results of a similar test on the asymptomatic forearm. 7. The median nerve is sensitive to direct pressure, tapping, or rolling beneath the finger in the antecubital space. 8. Occasionally, passive stretching of the finger and wrist flexors will accentuate the symptoms, but this is unlikely to be positive before the preceding tests. 9. Weakness of the median innervated muscles is infrequent, but careful comparison of strength between the two hands is indicated. The flexor pollicis longus and index finger flexor digitorum profundus are the most likely to show weakness. It is important to verify whether these tests mimic or reproduce exactly the symptoms that brought the patient to the physician. This syndrome is most likely to be confused with carpal tunnel syndrome, and unfortunately, the two conditions may occur simultaneously, or one may antedate the other, suggesting a susceptibility factor. Some factors that may help to differentiate between the two syndromes are indicated in Table 80-2. Obviously, careful clinical judgment is required to ensure the correct diagnosis. Indications for surgery depend largely on the severity of the patient’s symptoms. Aside from avoidance of the activities associated with aggravation of the symptoms, there is little available nonoperative treatment. A mixture of lidocaine and hydrocortisone instilled near the nerve may produce temporary beneficial effect and provide an additional diagnostic aid if

1108 Part VIII Septic and Nontraumatic Conditions

A

B

C

FIGURE 80-21 Described features of the physical examination that help to demonstrate the so-called pronator syndrome. A, Proximal forearm pain is increased by resistance to pronation and elbow flexion as well as to flexion of the wrist. B, Pain in the proximal forearm that is increased by resistance to supination is also suggestive of compression by the lacertus fibrosus. C, Resistance of the middle finger flexor produces pain in the proximal forearm when compression of the median nerve occurs at the flexor digitorum superficialis arch. (Redrawn from Spinner, M.: Injuries to the Major Branches of Peripheral Nerves of the Forearm, 2nd ed. Philadelphia, W. B. Saunders Co., 1978.)

Comparison of Findings Between the Carpal Tunnel Syndrome and the Pronator Syndrome

TABLE 80-2

Carpal Tunnel Syndrome

Pronator Syndrome

Nocturnal symptoms

+

−

Muscular fatigue

−

+

Proximal radiation

±

+

Thumb paresthesias

±

+

Thenar atrophy

+

−

Phalen’s sign

+

−

Pronator signs

−

+

Electromyography

+

−

effective. An increasing number of surgeons have advocated carpal tunnel release before pronator release,5 whereas others are releasing both areas simultaneously.125 EMG findings as an aid in the diagnosis of the pronator syndrome have been disappointing.16 Findings that adequately supported the diagElectromyography

nosis were found in only 10% of patients with the diagnosis of pronator syndrome. Slowed conduction velocity across the median nerve below the elbow is seldom detected. The best explanation for this is the size and complexity of the nerve, which is insufficiently compressed to prevent a stimulus progressing at normal velocities down a significant number of fascicles of the nerve. The slowed impulses in affected fascicles are blurred and dampened in the recording. Muscle studies are seldom specific. Isolated fibrillations, particularly in the pronator teres, have been observed. Insertional changes are often nonspecific. Electrical studies are useful in ruling out the presence of another entrapment site or underlying peripheral neuropathy. Intraoperative studies of conduction velocities and voltages were carried out before and after median nerve release in 10 forearms in the early part of one series.70 Significant increases in recorded velocities or voltages at the distal electrodes were noted in only five instances after decompression. Newer techniques may improve the diagnostic acuity of EMG, but at this time, the history and physical examination must be relied on for the diagnosis. Operative Findings The median nerve seldom shows the flattening, indentation, or pseudoneuroma formation so common at the carpal tunnel. The lacertus fibrosus is usually apparent in its course from the biceps tendon

Chapter 80 Nerve Entrapment Syndromes 1109

to its interdigitations with the longitudinally directed fibers of the antebrachial fascia over the proximal third of the flexor-pronator muscle group. An indentation of the pronator teres is apparent with passive pronation (see Fig. 80-20). At times, this finding may be dramatic. The compression may even be due to an accessory bicipital aponeurosis. After release of the lacertus fibrosus and antebrachial fascia, the median nerve is apparent lying adjacent to the humeral head of the pronator teres (Fig. 80-22). The median nerve is followed under the humeral head of the pronator teres, where it encounters the ulnar head of the muscle, which varies considerably in size. It may be primarily a fleshy head, but usually the tendon of origin of the muscle arises laterally and crosses the nerve. It may vary from a structure measuring 1 or 2 mm in diameter to a band of 1 or 2 cm in width. This structure lies just distal to the overlying lacertus fibrosus. Occasionally, the tendon arises medially, thus allowing the nerve to pass under rather than through the prona-

tor teres. Sometimes no ulnar head is discernible, and forearms with this arrangement may be less susceptible to the condition. In the majority of patients with the pronator syndrome, the combination of a tight tendinous band of the ulnar head associated with hypertrophy of the flexor-pronator musculature, which is constricted by the enveloping antebrachial fascia and lacertus fibrosus, produce the combination of pressure and tension on the nerve that induces symptoms. The fibrous arch of origin of the flexor digitorum superficialis lies 1 to 2 cm distal to the deep head of the pronator teres (see Fig. 80-22B). This, too, may be a constriction, especially when there is a large sharp edge to the band and hypertrophy of both the deep flexors and overlying muscle groups. This structure can be a cause of pronator syndrome. In a similar fashion, variant or vestigial muscles such as the Gantzer muscle, palmaris profundus, or flexor carpi radialis brevis may act to produce constriction. Less common factors that act to compress the median nerve are vascular malformations or distention of the bicipital bursa. The nerve may be perforated by a branch of the radial artery and accompanying veins or overlain by a taut vascular bridge. Some authors74,129 have recommended microsurgical interfascicular dissection of the median nerve in the distal arm and elbow region in suspected cases of pronator or anterior interosseous nerve syndromes where no obvious sign of median nerve compression is identified.

Anterior Interosseous Nerve Syndrome

Pronator teres (ulnar head)

Median n.

A Median n.

C B

Brachioradialis m.

Tendinous arch of Flexor digitorum superficialis m. (cut)

FIGURE 80-22

A, Release of the lacertus fibrosus reveals the median nerve as it enters the pronator teres muscle. B, Release of the ulnar head sometimes reveals a tight arch of the flexor digitorum superficialis muscle. C, If the ulnar head of the pronator teres is the offending part, it is released.

Isolated paresis or paralysis of the anterior interosseous nerve gained modern acceptance following the report of Kiloh and Nevin in 1952 and is often referred to as the Kiloh-Nevin syndrome.91 It was perhaps originally described by Tinel in 1918,186 and a number of authors have cited case reports or small series.48,99,111,131,148,162,167 Several larger series have recently been reported.156,159,166 Both complete and incomplete presentations have been described.76 The cause of this problem may be an acute demyelination episode similar to those seen in the brachial plexus as in Parsonage-Turner syndrome or brachial plexitis.142,199 An initial period of nonoperative therapy is therefore warranted, to allow time for improvement of symptoms which would be characteristic of ParsonageTurner syndrome, or the development of other neurologic findings, which might suggest another diagnosis. Commonly, a deep unremitting pain in the proximal forearm initiates the symptoms, which subside within 8 to 12 hours. The patient may then note a lack of dexterity or weakness of pinch that fails to resolve. If the patient was seen previously, diagnoses from tendinous rupture to multiple sclerosis may have been

Symptoms

1110 Part VIII Septic and Nontraumatic Conditions

entertained, particularly if the onset has been insidiously painless. Spontaneous improvement has been reported in some instances in which the patient had an apparently demyelinating etiology.58,195 Physical Findings In complete cases, the findings are those associated with denervation of the classic distribution of the anterior interosseous nerve to the flexor pollicis longus, the index and middle finger flexor digitorum profundus, and the pronator quadratus. The stance of the thumb and index finger when attempting to pinch is characteristic (Fig. 80-23). Because of an inability to flex the distal joints, they are approximated in hyperextension along their distal phalanges. Pinch is weak, and manipulative facility is impaired. Isolated testing shows marked weakness or paralysis of the flexor pollicis longus and index finger flexor digitorum profundus (see Fig. 80-23B). The middle finger is usually less affected, depending on the relative contributions of the ulnar and median nerves to the profundi. Thumb to little finger opposition is unaffected. In incomplete cases, usually the flexor pollicis longus or the index finger profundus is affected. Incomplete lesions are frequently misdiagnosed as a tendon rupture and electrodiagnosis is especially helpful both in establishing neural dysfunction but also excluding polyneuropathy or wider median nerve dysfunction. They may occur spontaneously or follow fracture fixation.88 Special care must be taken in all cases to rule out Parsonage-Turner syndrome. As with posterior interos-

seous nerve palsy, patients with anterior interosseous nerve syndrome may demonstrate subtle features suggestive of an inflammatory type disorder. Inciting events may be blamed for causation of the neurologic deficit, when in fact they may be “innocent bystanders.” Other findings elicited on history (periscapular pain), clinical examination (shoulder muscle weakness), electrophysiologic testing (patchy fibrillations in muscles beyond the anterior interosseous nerve territory) and MRI studies (denervation in other muscles) may be helpful in identifying more widespread neural involvement. These features should be sought out which would be suggestive of a diagnosis of Parsonage-Turner syndrome. Weakness in pronation is seldom a recognizable complaint of the patient because it is submerged in the general discomforts of weakness and clumsiness of the extremity. The pronator quadratus is tested by placing both elbows against the side and resisting pronation with the elbow flexed to a right angle. This effectively reduces the strength contribution of the pronator teres humeral head, allowing relative isolated testing of the pronator quadratus. Tenderness over the proximal forearm is usually absent, and sensory disturbance is not apparent. EMG findings of fibrillations are present in the affected muscles. In one study, all patients had electrical changes; the pronator quadratus was most consistently affected.159 Nerve variations such as the Martin-Gruber anastomosis may occur between the anterior interosseous nerve and the ulnar nerve, as well as between the

FIGURE 80-23 A, Anterior interosseous nerve syndrome demonstrating the characteristic pinch attitude. B, The patient is unable to flex the terminal phalanx of the thumb or index finger. Sensation is intact. There is some weakness of the flexor digitorum profundus of the middle finger, which in this patient is supplied and motored enough to flex the distal joint through a branch of the ulnar nerve in the proximal forearm. (A from Spinner, M.: Injuries to the Major Branches of Peripheral Nerves of the Forearm, 2nd ed. Philadelphia. W. B. Saunders Co., 1978.)

Chapter 80 Nerve Entrapment Syndromes 1111

median and ulnar nerves. These fibers are likely to innervate intrinsic muscle on the radial aspect of the hand. Therefore, it is necessary to differentiate partial apparent ulnar paralysis from the anterior interosseous nerve syndrome. An observation period of at least 6 months is indicated in most instances before surgical exploration is considered. Operative Findings The operative findings reported are similar to those described earlier for the pronator syndrome. The usual finding is a constriction due to the tendon or origin of the ulnar head of the pronator teres across the posterolateral aspect of the anterior interosseous nerve as it separates from the median nerve (Fig. 80-24). There may be a fibrous reaction in the area that is probably associated with the acute episode of pain, suggesting a localized vascular reaction such as thrombosis or ischemia.

Preferred Treatment for Exposure of the Median Nerve The spectrum of median nerve problems at the elbow suggests that the initial incision should be adaptable to unsuspected findings. A longitudinally oriented incision is curved at the antecubital crease or zigzagged to increase exposure and decrease tension on the scar line during healing. The medial antebrachial cutaneous nerve should be sought and protected. Major veins are retracted after ligating communicating veins. The plane over the brachial and antebrachial fascia is cleared to observe the effect of the lacertus fibrosus on passive pronation. A deep indentation of the flexor-pronator group is significant. If the pronator teres is prolonged proximally, the muscle often covers the median nerve above the elbow. The medial intermuscular septum and the brachial fascia tend to envelop the nerve in this situation. A true ligament of Struthers may be present if there is a supracon-

Deep head of pronator teres compressing ant. interosseous n.

A

Kiloh Nevin syndrome ant. interosseous n. compression

B FIGURE 80-24 Compression of the anterior interosseous nerve can occur at its entrance to the pronator muscle near its origin. A, Cadaveric specimen demonstrates a thin tendinous origin of the deep head of the pronator teres as it crosses over the take-off of the anterior interosseous nerve branch from the median nerve. B, Artistic rendition. (A from Spinner, M.: Injuries to the Major Branches of Peripheral Nerves of the Forearm, 2nd ed. Philadelphia, W. B. Saunders Co., 1978.)

1112 Part VIII Septic and Nontraumatic Conditions

dylar process. Although such a diagnosis is usually made radiographically, palpation of the lower humerus through this incision may indicate an unsuspected supracondylar process. The median nerve is identified proximal to the lacertus fibrosus in the distal arm. The lacertus is incised, and the median nerve is traced distally. The tendinous origin of the pronator teres should be detached. Arches over the pronator teres and the flexor digitorum superficialis are released. The plane between the pronator teres and the flexor carpi radialis is used. This plane can be identified distally and the median nerve can then be traced in a distal to proximal direction. All of these potential sites of entrapment should be explored, because multiple sites of entrapment could be present. It may be important to extend the incision proximally in certain instances; hence, draping to the axilla and the use of a sterile tourniquet are wise precautions.

Margin of biceps aponeurosis

Lat. antebrachialcutaneous n.

CUTANEOUS NERVES Lateral Antebrachial Nerve Compression neuropathy of the lateral antebrachial cutaneous nerve is a recently recognized syndrome.9,30,50,65,143 This cutaneous branch may also be injured at surgery or with injections.201 Relevant Anatomy The musculocutaneous nerve, after supplying the coracobrachialis, biceps, and brachialis muscles, continues in the interval between the last two muscles as a sensory nerve to supply the skin over the anterolateral aspect of the forearm, often as far as the thenar eminence. It emerges from beneath the biceps tendon laterally and penetrates the brachial fascia just above the elbow crease to course down the forearm (Fig. 80-25).

Bassett and Nunley describe both acute and chronic problems.9 A distinct mechanism of injury consisting of elbow hyperextension and pronation or resisted elbow flexion and pronation was elicited from their patients; presumably, the nerve was compressed between the biceps tendon and the brachialis fascia because both the nerve and the tendon were rendered taut by the forearm position. Burning dysesthesia in the distribution of the nerve is seen acutely. In chronic phases, the patient complains of a vague discomfort in the forearm with some dysesthetic qualities that are sometimes made worse by supinopronatory activities with the elbow extended. On physical examination, a dysesthetic area on the anterolateral aspect of the forearm can be elicited by gently stroking across the skin transversely with a blunt point. Tenderness to direct pressure on the lateral aspect

Clinical Findings

FIGURE 80-25 The lateral antebrachial cutaneous nerve has been reported to be compressed at the lateral margin of the biceps aponeurosis at the level of the lateral epicondyle.

of the bicipital tendon just proximal to the elbow crease is characteristic127; loss of extension and pronation is often exhibited with this maneuver. The sensory action potential may exhibit a prolonged latency or diminished amplitude.50 Treatment For the acute injury, rest, splinting, avoidance of extension-pronation, and anti-inflammatory medication are indicated. Corticosteroidal injections at the area of tenderness may help if exacerbation occurs. In chronic syndromes or those failing to respond to nonoperative measures, surgical decompression is appropriate. Under tourniquet control, a zigzag incision across the lateral aspect of the elbow crease allows exposure of the lateral antebrachial nerve. The site of compression usually occurs where the nerve emerges beneath the bicipital tendon. A tight band of antebrachial fascia at the elbow crease has been noted to alter the course of the nerve to an acute angle. Release of the brachial fascia and excision of a triangular portion of the bicipital tendon at the point of impingement is recommended. Obliteration of vascular markings at the site of compression may be noted. A neuroma, if present, can be excised and allowed to retract.

Chapter 80 Nerve Entrapment Syndromes 1113

Results Symptoms may subside after an acute episode, but the nerve thereafter is apparently more susceptible to further irritation. Surgical decompression can often produce relief of pain, improvement in sensibility, and restoration of motion.

8.

Medial Antebrachial Cutaneous Nerve The posterior branch of the medial antebrachial cutaneous nerve has received some attention because of its course near the medial epicondyle. This has obvious clinical significance. Neuromata occur relatively frequently after ulnar nerve surgery38 but may also occur following treatment of medial epicondylitis.150 A recent anatomic study147 describes the course of this cutaneous nerve and its variations. Rare cases of compressive lesions have also been reported.21,160 Patients present with sensory disturbance in the posteromedial forearm or pain at the medial aspect of the elbow or both.

9.

10.

11.

12. 13.

Posterior Antebrachial Cutaneous Nerve Nerve lesions of the posterior antebrachial cutaneous branch (a branch of the radial nerve at or near the spiral groove) do occur. Patients may present with isolated sensory abnormalities in the dorsolateral forearm or lateral elbow pain, or both. Several cases22,36,42 have been reported, occurring either spontaneously or following surgery. The nerve emerges from the lateral triceps and has a variable relationship with the lateral intermuscular septum. It then courses over the brachioradialis near the lateral epicondyle. Its course makes it particularly vulnerable in surgery for lateral epicondylitis or posterior interosseous nerve releases, and even following humeral fracture reduction and fixation, demonstrating the nerve’s vulnerability more proximally. Excision of the neuroma or decompression of the nerve branch can relieve the symptoms.

References 1. Abe, M., Ishizu, T., Okamoto, M., and Onomura, T.: Tardy ulnar nerve palsy caused by cubitus varus deformity. J. Hand Surg. 20A:5, 1995. 2. Agnew, D. H.: Bursal tumor producing loss of power of forearm. Am. J. Med. Sci. 46:404, 1863. 3. Al-Qattan, M. M.: Gantzer’s muscle. An anatomical study of the accessory head of the flexor pollicis longus muscle. J. Hand Surg. 21B:269, 1996. 4. Amadio, P. C.: Anatomical basis for a technique of ulnar nerve transposition. Surg. Radiol. Anat. 8:155, 1986. 5. Amadio, P. C.: Operations I no longer do (well, hardly ever). J. Hand Surg. 27B:155, 2002. 6. Apfelberg, D. B., and Larson, S. J.: Dynamic anatomy of the ulnar nerve at the elbow. Plast. Reconst. Surg. 51:76, 1973. 7. Barber, K. W., Jr., Bianco, A. J., Jr., Soule, E. H., and MacCarty, C. S.: Benign extramural soft tissue tumors of the

14. 15.

16.

17.

18.

19.

20.

21.

22.

23. 24. 25. 26.

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1114 Part VIII Septic and Nontraumatic Conditions

27. Comtet, J. J., Chambaud, D., and Genety, J.: La compression de la branche posterier du nerf radial. Une etiologie meconnue de certaines paralysies et de certaines spicondylalgies rebelles. Nouv. Presse Med. 5:1111, 1976. 28. Craven, P. R., Jr., and Green, D. P.: Cubital tunnel syndrome. J. Bone Joint Surg. 62A:986, 1980. 29. Dahners, L. E., and Wood, F. M.: Anconeus epitrochlearis, a rare cause of cubital tunnel syndrome: a case report. J. Hand Surg. 9A:579, 1984. 30. Davidson, J. J., Bassett, F. H. III, and Nunley, J. A.: Musculocutaneous nerve entrapment revisited. J. Shoulder Elbow Surg. 7:250, 1998. 31. Davies, F., and Laird, M.: The supinator muscle and the deep radial (posterior interosseous) nerve. Anat. Rec. 101:243, 1948. 32. Dawson, D. M., Hallett, M., and Millender, L. H.: Entrapment Neuropathies, 2nd ed. Boston, Little, Brown & Co., 1990. 33. Dellon, A. L.: Techniques for successful management of ulnar nerve entrapment at the elbow. Neurosurg. Clin. North Am. 2:57, 1991. 34. Dellon, A. L., and Coert, J. H.: Results of the musculofascial lengthening technique for submuscular transposition of the ulnar nerve at the elbow. J. Bone Joint Surg. 85A:1314, 2003. 35. Dellon, A. L., and Coert, J. H.: Results of the musculofascial lengthening technique for submuscular transposition of the ulnar nerve at the elbow. J. Bone Joint Surg. 86A(suppl 1 Pt 2):169, 2004. 36. Dellon, A. L., Kim, J., and Ducic, I.: Painful neuroma of the posterior cutaneous nerve of the forearm after surgery for lateral humeral epicondylitis. J. Hand Surg. 29A:387, 2004. 37. Dellon, A. L., and Mackinnon, S. E.: Radial-sensory nerve entrapment in the forearm. J. Hand Surg. 11A:199, 1986. 38. Dellon, A. L., and Mackinnon, S. E.: Injury to the medial antebrachial cutaneous nerve during cubital tunnel surgery. J. Hand Surg. 10B:33, 1985. 39. Dellon, A. L., and Mackinnon, S. E.: Musculoaponeurotic variations along the course of the median nerve in the proximal forearm. J. Hand Surg. 12B:359, 1987. 40. Dennny-Brown, D., and Brenner, C.: Paralysis of nerve induced by direct pressure and by tourniquet. Arch. Neurol. Psychiatry 51:1, 1944. 41. Dharapak, C., and Nimberg, G. A.: Posterior interosseous nerve compression. Report of a case caused by traumatic aneurysm. Clin. Orthop. 101:225, 1974. 42. Doyle, J. J., and David, W. S.: Posterior antebrachial cutaneous neuropathy associated with lateral elbow pain. Muscle Nerve 16:1417, 1993. 43. Dreyfuss, U., and Kessler, I.: Snapping elbow due to dislocation of the medial head of the triceps. A report of two cases. J. Bone Joint Surg. 60B:56, 1978. 44. Eaton, R. G., Crowe, J. F., and Parkes, J. C., III.: Anterior transposition of the ulnar nerve using a non-compressing fasciodermal sling. J. Bone Joint Surg. 62A:820, 1980. 45. Erhlich, G. E.: Antecubital cysts in rheumatoid arthritis: a corollary to popliteal (Baker’s) cysts. J. Bone Joint Surg. 54A:165, 1972.

46. Escobar, P. L.: Short segment stimulations in ulnar nerve lesions around elbow. Orthop. Rev. 12:65, 1983. 47. Eversmann, W. W., Jr.: Entrapment and compression neuropathies. In Green, D. P. (ed.): Operative Hand Surgery, 2nd ed. New York, Churchill Livingstone, 1988, p. 1423. 48. Farber, J. S., and Bryan, R. S.: The anterior interosseous nerve syndrome. J. Bone Joint Surg. 50A:521, 1968. 49. Feindel, W., and Stratford, J.: The role of the cubital tunnel in tardy ulnar palsy. Can. J. Surg. 1:296, 1958. 50. Felsenthal, G., Mondell, D. L., Reischer, M. A., and Mack, R. H.: Forearm pain secondary to compression syndrome of the lateral cutaneous nerve of the forearm. Arch. Phys. Med. Rehabil. 65:139, 1984. 51. Flory, P. J., and Berger, A.: Die akzessorische brachialissehneselten Ursache des Pronator Teres-Syndroms. Handchir. 17:270, 1985. 52. Foster, R. J., and Edshage, S.: Factors related to outcome of surgically managed compressive ulnar neuropathy at the elbow level. J. Hand Surg. 6:181, 1981. 53. Freundlich, B. D., and Spinner, M.: Nerve compression syndrome in derangements of the proximal and distal radioulnar joints. Bull. Hosp. Joint Dis. 19:38, 1968. 54. Frohse, F., and Frankel, M.: Die Muskeln des menschlichen Ames. In Bardelenbens Handbuch der Anatomie des Nenschlichen. Jena, Fisher, 1908. 55. Froimson, A. I., and Zahrawi, F.: Treatment of compression neuropathy of the ulnar nerve at the elbow by epicondylectomy and neurolysis. J. Hand Surg. 5:391, 1980. 56. Fujioka, H., Nakabayashi, Y., Hirata, S., Go, G., Nishi, S., and Mizuno, K.: Analysis of tardy ulnar nerve palsy associated with cubitus varus deformity after a supracondylar fracture of the humerus: a report of four cases. J. Orthop. Trauma 9:435, 1995. 57. Gabel, G. T., and Amadio, P. C.: Reoperation for failed decompression of the ulnar nerve in the region of the elbow. J. Bone Joint Surg. 72A:213, 1990. 58. Gaitzsch, G., and Chamay, A.: Paralytic brachial neuritis or Parsonage-Turner syndrome anterior interosseous nerve involvement. Report of three cases. Ann. Chir. Main 5:288, 1986. 59. Gantzers, C. F. L.: De Musculorum Varietates, thesis. Berlioni, J. F. Starckie, 1813. 60. Gelberman, R. H., Yamaguchi, K., Hollstien, S. B., Winn, S. S., Heidenreich, F. P., Jr., Bindra, R. R., Hsieh, P., and Silva, M. J.: Changes in interstitial pressure and crosssectional area of the cubital tunnel of the ulnar nerve with flexion of the elbow. An experimental study in human cadavera. J. Bone Joint Surg. 80A:492, 1998. 61. Gervasio, O., Gambardella, G., Zaccone, C., and Branca, D.: Simple decompression versus anterior submuscular transposition of the ulnar nerve in severe cubital tunnel syndrome: a prospective randomized study. Neurosurgery 56:108, 2005. 62. Gessini, L., Jandolo, B., and Pietrangeli, A.: Entrapment neuropathies of the median nerve at and above the elbow. Surg. Neurol. 19:112, 1983. 63. Geutjens, G. G., Langstaff, R. J., Smith, N. J., Jefferson, D., Howell, C. J., and Barton, N. J.: Medial epicondylectomy or ulnar nerve transposition for ulnar neuropathy at the elbow? J. Bone Joint Surg. 78B:777, 1996.

Chapter 80 Nerve Entrapment Syndromes 1115

64. Gilliatt, B. W., Ochoa, J., Rudge, P., and Neary, D.: The cause of nerve damage in acute compression. Trans. Am. Neurol. Assoc. 99:71, 1974. 65. Gillingham, B. L., and Mack, G. R.: Compression of the lateral antebrachial cutaneous nerve by the biceps tendon. J. Shoulder Elbow Surg. 5:330, 1996. 66. Goldman, S., Honet, J. C., Sobel, R., and Goldstein, A. S.: Posterior interosseous nerve palsy in the absence of trauma. Arch. Neurol. 21:435, 1969. 67. Graf, P., Hawe, W., and Biemer, E.: Gefabversorgung des n. ulnaris nach Neurolyse im Ellenbogenbereich. Handchir. 18:204, 1986. 68. Gunther, S. F., DiPasquale, D., and Martin, R.: The internal anatomy of the median nerve in the region of the elbow. J. Hand Surg. 17A:648, 1992. 69. Harrelson, J. M., and Newman, M.: Hypertrophy of the flexor carpi ulnaris as a cause of ulnar-nerve compression in the distal part of the forearm. Case report. J. Bone Joint Surg. 57A:554, 1975. 70. Hartz, C. R., Linscheid, R. L., Gramse, R. R., and Daube, J. R.: Pronator teres syndrome: compressive neuropathy of the median nerve. J. Bone Joint Surg. 63A:885, 1981. 71. Hashizume, H., Inoue, H., Nagashima, K., and Hamaya, K.: Posterior interosseous nerve paralysis related to focal radial nerve constriction secondary to vasculitis. J. Hand Surg. 18B:757, 1993. 72. Hashizume, H., Nishida, K., Nanba, Y., Shigeyama, Y., Inoue, H., and Morito, Y.: Non-traumatic paralysis of the posterior interosseous nerve. J. Bone Joint Surg. 78B:771, 1996. 73. Hashizume, H., Nishida, K., Yamamoto, K., Hirooka, T., and Inoue, H.: Delayed posterior interosseous nerve palsy. J. Hand Surg. 20B:655, 1995. 74. Haussmann, P., and Patel, M. R.: Intraepineurial constriction of nerve fascicles in pronator syndrome and anterior interosseous nerve syndrome. Orthop. Clin. North Am. 27:339, 1996. 75. Haws, M., and Brown, R. E.: Bilateral snapping triceps tendon after bilateral ulnar nerve transposition for ulnar nerve subluxation. Ann. Plast. Surg. 34:550, 1995. 76. Hill, H. A., Howard, F. M., and Huffer, B. R.: The incomplete anterior interosseous nerve syndrome. J. Hand Surg. 10A:4, 1985. 77. Hirachi, K., Kato, H., Minami, A., Kasashima, T., and Kaneda, K.: Clinical features and management of posterior interosseous nerve palsy. J. Hand Surg. 23B:413, 1998. 78. Hobhouse, N., and Heald, C. B.: A case of posterior interosseous paralysis. Br. Med. J. 1:841, 1936. 79. Hoffmann, R., and Siemionow, M.: The endoscopic management of cubital tunnel syndrome. J. Hand Surg. 31B:23, 2006. 80. Hollinshead, W. H.: Anatomy for Surgeons, Vol. 3, The Back and Limbs, 3rd ed. New York, Harper and Row, 1982. 81. Jabaley, M. E., Wallace, W. H., and Heckler, F. R.: Internal topography of major nerves of the forearm and hand: a current view. J. Hand Surg. 5:1, 1980. 82. Jebson, P. J. L., and Engber, W. D.: Radial tunnel syndrome: long-term results of surgical decompression. J. Hand Surg. 22A:889, 1997.

83. Johnson, R. K., Spinner, M., and Shrewsbury, M. M.: Median nerve entrapment syndrome in the proximal forearm. J. Hand Surg. 4:48, 1979. 84. Jones, R. E.: Medial epicondylectomy for ulnar nerve compression syndrome at the elbow. Clin. Orthop. 139:174, 1979. 85. Kaempffe, F. A., and Farbach, J.: A modified surgical procedure for cubital tunnel syndrome: partial medial epicondylectomy. J. Hand Surg. 23A:492, 1998. 86. Kane, E., Kaplan, E. B., and Spinner, M.: Observations of the course of the ulnar nerve in the arm. Ann. Chir. 27:487, 1973. 87. Kaplan, E. B.: Functional and Surgical Anatomy of the Hand, 2nd ed. Philadelphia, J.B. Lippincott Co., 1965. 88. Keogh, P., Khan, H., Cooke, E., and McCoy, G.: Loss of flexor pollicis longus function after plating of the radius. J. Hand Surg. 22B:375, 1997. 89. Keret, D., and Porter, K. M.: Synovial cyst and ulnar nerve entrapment: a case report. Clin. Orthop. 188:213, 1984. 90. Khoo, D., Carmichael, S. W., and Spinner, R. J.: Ulnar nerve anatomy and compression. Orthop. Clin. North Am. 27:317, 1996. 91. Kiloh, L. G., and Nevin, S.: Isolated neuritis of the anterior interosseous nerve. Br. Med. J. 1:859, 1952. 92. Kopell, H. P., and Thompson, W. A. I.: Pronator syndrome. N. Engl. J. Med. 259:713, 1958. 93. Kopell, H. P., and Thompson, W. A.: Peripheral Entrapment Neuropathies. Baltimore, Williams & Wilkins, 1963. 94. Kotani, H., Miki, T., Senzoku, F., Nakagawa, Y., and Ueo, T.: Posterior interosseous nerve paralysis with multiple constrictions. J. Hand Surg. 20A:15, 1995. 95. Krishnan, K. G., Pinzer, T., and Schackert, G.: A novel endoscopic technique in treating single nerve entrapment syndromes with special attention to ulnar nerve transposition and tarsal tunnel release: clinical application. Neurosurgery 59(1 Suppl 1):ONS89, 2006. 96. Kuszynski, K.: Functional micro-anatomy of the peripheral nerve trunks. Hand 6:1, 1974. 97. Laha, R. K., Lunsford, L. D., and Dujovny, M.: Lacertus fibrosus compression of the median nerve. A case report. J. Neurosurg. 48:838, 1978. 98. Lahey, M. D., and Aulicino, P. L.: Anomalous muscles associated with compression neuropathies. Orthop. Rev. 15:19, 1986. 99. Lake, P. A.: Anterior interosseous nerve syndrome. J. Neurosurg. 41:306, 1974. 100. Learmonth, J. R.: A variation of the radial branch of the musculo-spiral nerve. J. Anat. 53:371, 1919. 101. Learmonth, J. R.: Technique for transplanting the ulnar nerve. Surg. Gynecol. Obstet. 75:792, 1942. 102. LeDouble, A. F.: Traite des Variations du Systeme Musculaire de l Homme. Paris, Schleicher, 1897. 103. Leffert, R. D.: Anterior submuscular transposition of the ulnar nerves by the Learmonth technique. J. Hand Surg. 7:147, 1982. 104. Leffert, R. D., and Dorfman, H. D.: Antecubital cyst in rheumatoid arthritis. Surgical findings. J. Bone Joint Surg. 54A:1555, 1972.

1116 Part VIII Septic and Nontraumatic Conditions

105. Lichter, R. L., and Jacobsen, T.: Tardy palsy of the posterior interosseous nerve with a Monteggia fracture. J. Bone Joint Surg. 57A:124, 1975. 106. Lipscomb, P. R., and Burleson, R. J.: Vascular and neural complications in supracondylar fractures in children. J. Bone Joint Surg. 37A:487, 1955. 107. Lister, G. D., Belsole, R. B., and Kleinert, H. E.: The radial tunnel syndrome. J. Hand Surg. 4:52, 1979. 108. Lluch, A. L.: Ulnar nerve entrapment after anterior transposition at elbow. N. Y. State J. Med. 75:75, 1975. 109. Lundborg, G.: Ischemic nerve injury. Experimental studies on intraneural microvascular pathophysiology and nerve function in a limb subjected to temporary circulatory arrest. Scand. J. Plast. Reconstr. Surg. [Suppl.] 6:1, 1970. 110. Macnicol, M. F.: Extraneural pressures affecting the nerve at the elbow. Hand 14:5, 1982. 111. Maeda, K., Miura, T., Komada, T., and Chiba, A.: Anterior interosseous nerve paralysis. Report of 13 cases and review of Japanese literature. Hand 9:165, 1977. 112. Mangini, U.: Flexor pollicis longus muscle. Its morphology and clinical significance. J. Bone Joint Surg. 42A:467, 1960. 113. Mannerfelt, L.: Studies on the hand in ulnar nerve paralysis. A clinical-experimental investigation in normal and anomalous innervation. Acta Orthop. Scand. Suppl. 87:1966. 114. Marmor, L., Lawrence, J. F., and Dubois, E.: Posterior interosseous nerve paralysis due to rheumatoid arthritis. J. Bone Joint Surg. 49A:381, 1967. 115. Marquis, J. W., Bruwer, A. J., and Keith, H. M.: Suparcondyloid process of the humerus. Proc. Staff Meeting Mayo Clin. 37:691, 1957. 116. Marshall, S. C., and Murray, W. R.: Deep radial nerve palsy associated with rheumatoid arthritis. Clin. Orthop. Relat. Res. 103:157, 1974. 117. Martinelli, P., Gabellini, A. S., Poppi, M., Gallassi, R., and Pozzatti, E.: Pronator syndrome due to thickened bicipital aponeurosis. J. Neurol. Neurosurg. Psychiatry 45:181, 1982. 118. Mayer, J. H., and Mayfield, P. H.: Surgery of the posterior interosseous branch of the radial nerve. Surg. Gynecol. Obstet. 84:979, 1947. 119. Millender, L. H., Nalebuff, E. A., and Holdsworth, D. E.: Posterior interosseous nerve syndrome secondary to rheumatoid synovitis. J. Bone Joint Surg. 55A:753, 1973. 120. Miller, R. G.: Acute versus chronic compressive neuropathy. Muscle Nerve 7:427, 1984. 121. Morrey, B. F.: Reoperation for failed surgical treatment of refractory lateral epicondylitis. J. Shoulder Elbow Surg. 1:47, 1992. 122. Morris, A. H.: Irreducible Monteggia lesion with radialnerve entrapment. J. Bone Joint Surg. 46A:608, 1964. 123. Morris, H. H., and Peters, B. H.: Pronator syndrome: Clinical and electrophysiological features in seven cases. J. Neurol. Neurosurg. Psychiatry 39:461, 1976. 124. Mowell, J. W.: Posterior interosseous nerve injury. Int. Clin. 2:188, 1921. 125. Mujadzic, M., Papanicolaou, G., Young, H., and Tsai, T. M.: Simultaneous surgical releases of ipsilateral pronator

126.

127.

128.

129.

130.

131.

132.

133. 134.

135.

136.

137.

138.

139.

140. 141. 142. 143.

144.

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Chapter 80 Nerve Entrapment Syndromes 1117

145. Pribyl, C. R.: Use of the medial intermuscular septum as a fascial sling during anterior transposition of the ulnar nerve. J. Hand Surg. 23A:500, 1998. 146. Pritchard, D. J., Linscheid, R. L., and Svien, H. J.: Intraarticular median nerve entrapment with dislocation of the elbow. Clin. Orthop. 90:100, 1973. 147. Race, C. M., and Saldana, M. J.: Anatomic course of the medial cutaneous nerves of the arm. J. Hand Surg. 16A:48, 1991. 148. Rask, M. R.: Anterior interosseous nerve entrapment: report of seven cases. Clin. Orthop. 142:176, 1979. 149. Reis, N. D.: Anomalous triceps tendon as a cause for snapping elbow and ulnar neuritis: a case report. J. Hand Surg. 5:361, 1980. 150. Richards, R. R., and Regan, W. D.: Medial epicondylitis caused by injury to the medial antebrachial cutaneous nerve: a case report. Can. J. Surg. 32:366, 1989. 151. Richmond, D. A.: Lipoma causing a posterior nerve lesion. J. Bone Joint Surg. 35B:83, 1953. 152. Riordan, D. C.: Radial nerve paralysis. Orthop. Clin. N. Am. 5:283, 1974. 153. Roles, N. C., and Maudsley, R. H.: Radial tunnel syndrome. Resistant tennis elbow as a nerve entrapment. J. Bone Joint Surg. 54B:499, 1972. 154. Rolfsen, L.: Snapping triceps tendon with ulnar neuritis. Report on a case. Acta Orthop. Scand. 41:74, 1970. 155. Salsbury, C. R.: The nerve to the extensor carpi radialis brevis. J. Surg. 26:95, 1938. 156. Schantz, K., and Riegels-Nielsen, P. R.: The anterior interosseous nerve syndrome. J. Hand Surg. 17B:510, 1992. 157. Seddon, H. J.: Three types of nerve injury. Brain 66:237, 1943. 158. Seradge, H., and Owen, H.: Cubital tunnel release with medial epicondylectomy factors influencing the outcome. J. Hand Surg. 23A:483, 1998. 159. Seror, P.: Anterior interosseous nerve lesions. Clinical and electrophysiological features. J. Bone Joint Surg. 78B:238, 1996. 160. Seror, P.: Forearm pain secondary to compression of the medial antebrachial cutaneous nerve at the elbow. Arch. Phys. Med. Rehab. 74:540, 1993. 161. Seyfarth, H.: Primary myoses in the m. pronator teres as cause of lesion of the n. medianus (the pronator syndrome). Acta Psychiatr. Neurol. Scand. Suppl. 74:251, 1951. 162. Sharrard, W. J. W.: Anterior interosseous neuritis. Report of a case. J. Bone Joint. Surg. 50B:804, 1968. 163. Sharrard, W. J. W.: Posterior interosseous neuritis. J. Bone Joint Surg. 48B:777, 1966. 164. Siqueira, M. G., Martin, R. S.: The controversial arcade of Struthers. Surg. Neurol. 64(S1):17, 2005. 165. Somerville, E. W.: Pain in the upper limb. Proceedings of the British Orthopaedic Association. J. Bone Joint Surg. 45B:621, 1963. 166. Sood, M. K., and Burke, F. D.: Anterior interosseous nerve palsy. A review of 16 cases. J. Hand Surg. 22B:64, 1997. 167. Spinner, M.: The anterior interosseous nerve syndrome: with special attention to its variations. J. Bone Joint Surg. 52A:84, 1970.

168. Spinner, M.: The arcade of Frohse and its relationship to posterior interosseous nerve paralysis. J. Bone Joint Surg. 50B:809, 1968. 169. Spinner, M.: Injuries to the Major Branches of Peripheral Nerves of the Forearm, 2nd ed. Philadelphia, W. B. Saunders Co., 1978. 170. Spinner, M.: Nerve decompression. In Morrey, B. F. (ed.): Master Techniques in Orthopedic Surgery. The Elbow. New York, Raven Press, 1994. 171. Spinner, M., Freundlich, B. D., and Teicher, J.: Posterior interosseous nerve palsy as a complication of Monteggia fracture in children. Clin. Orthop. Relat. Res. 58:141, 1968. 172. Spinner, M., and Kaplan, E. B.: The relationship of the ulnar nerve to the medial intermuscular septum in the arm and its clinical significance. Hand 8:239, 1976. 173. Spinner, R. J., Berger, R. A., Dyck, P. J., Carmichael, S. W., and Nunley, J. A.: Isolated paralysis of the extensor digitorum communis associated with the posterior (Thompson) approach to the proximal radius. J. Hand Surg. 23A: 135, 1998. 174. Spinner, R. J., Carmichael, S. W., and Spinner, M.: Partial median nerve entrapment in the distal arm because of an accessory bicipital aponeurosis. J. Hand Surg. 16A:236, 1991. 175. Spinner, R. J., and Goldner, R. D.: Snapping of the medial head of the triceps and recurrent dislocation of the ulnar nerve. Anatomical and dynamic factors. J. Bone Joint Surg. 80A:239, 1998. 176. Spinner, R. J., and Spinner, M.: Tardy posterior interosseous nerve palsy due to childhood osteomyelitis: a case report. J. Hand Surg. 22A:1049, 1997. 177. Sponseller, P. D., and Engber, W. D.: Double-entrapment radial tunnel syndrome. J. Hand Surg. 8A:420, 1983. 178. Steiger, R., and Vogelin, E.: Compression of the radial nerve by an occult ganglion. Three case reports. J Hand Surg. 23B:420, 1998. 179. Strachan, J. C. H., and Ellis, B. W.: Vulnerability of the posterior interosseous nerve during radial head resection. J. Bone Joint Surg. 53B:320, 1971. 180. Struthers, J.: On a peculiarity of the humerus and humeral artery. Monthly J. Med. Sci. 8:264, 1848. 181. Suematsu, N., and Hirayama, T.: Posterior interosseous nerve palsy. J. Hand Surg. 23B:104, 1998. 182. Sunderland, S.: The innervation of the flexor digitorum profundus and lumbrical muscles. Anat. Rec. 83:317, 1945. 183. Sunderland, S.: Nerve lesions in the carpal tunnel syndrome. J. Neurol. Neurosurg. Psychiatry 39:615, 1976. 184. Sunderland, S.: Nerves and Nerve Injuries. Baltimore, Williams & Wilkins Co, 1968, p. 749. 185. Swiggett, R., and Ruby, L. K.: Median nerve compression neuropathy of the lacertus fibrosus: report of three cases. J. Hand Surg. 11A:700, 1986. 186. Tinel, J.: Nerve Wounds. New York, William Wood, 1918, p. 183. 187. Tsai, T. M., Chen, I. C., Majd, M. E., and Lim, B. H.: Cubital tunnel release with endoscopic assistance: results of a new technique. J. Hand Surg. 24A:21, 1999.

1118 Part VIII Septic and Nontraumatic Conditions

188. Uchida, Y., and Sugioka, Y.: Ulnar nerve palsy after supracondylar humerus fracture. Acta Orthop. Scand. 61:118, 1990. 189. Vanderpool, D. W., Chalmers, J., Lamb, D. W., and Whiston, T. B.: Peripheral compression lesions of the ulnar nerve. J. Bone Joint Surg. 50B:792, 1968. 190. Wadsworth, T. G.: The external compression syndrome of the ulnar nerve at the cubital tunnel. Clin. Orthop. Relat. Res. 124:189, 1977. 191. Wartenberg, R.: Cheiralgia paresthetica (isolierte Neuritis des Ramus superficialis nervi radialis). Z. Neurol. Psychiatry 141:145, 1932. 192. Watchmaker, G. P., Lee, G., and Mackinnon, S. E.: Intraneural topography of the ulnar nerve in the cubital tunnel facilitates anterior transposition. J. Hand Surg. 19A:915, 1994. 193. Werner, C. O.: Lateral elbow pain and posterior interosseous nerve entrapment. Acta Orthop. Scand. [Suppl] 174:1, 1979. 194. Wertsch, J. J., and Melvin, J.: Median nerve anatomy and entrapment syndromes: A review. Arch. Phys. Med. Rehabil. 63:623, 1982. 195. Wertsch, J. J., Sanger, J. R., and Matloub, H. S.: Pseudoanterior interosseous nerve syndrome. Muscle Nerve 8:68, 1985.

196. Whitely, W. H., and Alpers, B. J.: Posterior interosseous palsy with spontaneous neuroma formation. Arch. Neurol. 1:226, 1959. 197. Woltman, H. W., and Learmonth, J. R.: Progressive paralysis of the nervus interosseous dorsalis. Brain 57:25, 1934. 198. Wood, V. E., and Biondi, J.: Double-crush nerve compression in thoracic-outlet syndrome. J. Bone Joint Surg. 72A:85, 1990. 199. Wong, L., and Dellon, A. L.: Brachial neuritis presenting as anterior interosseous nerve compression-implications for diagnosis and treatment: a case report. J. Hand Surg. 22A:536, 1997. 200. Wu, K. T., Jordan, F. R., and Eckert, C.: Lipoma. A cause of paralysis of deep radial (posterior interosseous) nerve. Report of a case and review of the literature. Surgery 75:790, 1974. 201. Yuan, R. T., and Cohen, M. J.: Lateral antebrachial cutaneous nerve injury as a complication of phlebotomy. Plast. Reconstr. Surg. 76:299, 1985. 202. Zlowodzki, M., Chan, S., Bhandari, M., Kalliainen, L., and Schubert, W.: Anterior transposition compared with simple decompression for treatment of cubital tunnel syndrome. A meta-analysis of randomized, controlled trials. J. Bone Joint Surg. 89:2591, 2007.

Chapter 81 Pain Dysfunction Syndrome 1119

CHAPTER

81

Pain Dysfunction Syndrome Stephen D. Trigg

INTRODUCTION Previous chapters of this book have dealt largely with the management of specific traumatic conditions and surgical reconstructive principles involved in the treatment of disorders of the elbow articulation. Necessarily, inferred but often understated in the discussion of these subjects is the inherent and inseparable consequence of some degree of pain experienced by normal individuals. Pain is defined as the perception of an unpleasant sensation that is generally localized to a specific anatomic region in response to a noxious stimulus (trigger) capable of producing potential or actual tissue damage.19,59,73 Although unpleasant, the perception of acute pain serves an important physiologic function because it elicits a protective behavioral response outwardly noted as retraction from the noxious stimulus, followed by a transitory period of protection and guarding of the injured part.37 Inseparable from the experience of acute pain is an individually variable emotional response that is dependent on the physiologic, psychological, cultural, and socioeconomic state of the person.3,29,141 Both postoperative pain and the temporary residual pain of recent injury are physiologic (functional) variants of acute pain.63,141 Orthopedic surgeons generally have considerable clinical experience in dealing with a normal acute pain response and its variants by proceeding first with proper care of the injured part, administration of appropriate analgesics, and offering of emotional support and counseling. However, if during the course of initial treatment or the rehabilitation period a patient’s complaint of reported pain is judged to be extreme with respect to the known degree of tissue damage, or if the pain is abnormally prolonged, or the location and quality are poorly defined or nonspecific, then the possibility of a dysfunctional pain disorder must be considered when all plausible functional causes (e.g., compartment syndrome) have been eliminated.89 The presentation of a patient’s dysfunctional pain response is most assuredly an unwelcome and worrisome complication, and often poses considerable challenges to the

subsequent successful treatment and resolution of the presenting musculoskeletal problem. Moreover, following the recognition of dysfunctional pain, there is often a reasonable degree of consternation and possible indecision regarding the implementation of appropriate measures of management. Reasons for such indecision are well founded, because often the historical details, nature, and presentation of any patient’s dysfunctional pain pattern are individually variable, and clinical expertise is difficult to achieve in normal practice. Furthermore, until relatively recently, the amount of clinically relevant information on abnormal pain disorders within the musculoskeletal literature has been sparse, most often made up of anecdotal case studies.29 The more detailed descriptive reports that are present in the literature have unfortunately been collectively categorized under a confusing array of terms (Box 81-1).

HISTORICAL PERSPECTIVE The first of the terms in Box 81-1, causalgia (Gk., “burning”), was initially defined by S. Weir Mitchell, a Union surgeon during the Civil War.96 Mitchell eloquently described a syndrome characterized by the onset of unrelenting intense, often burning, pain of an affected extremity, hypersensitivity, vasomotor disturbances, and the overzealous guarding of the injured part. Mitchell also described the consistent and profound psychological changes noted in affected patients, most of whom had sustained direct rifle ball wounds to major peripheral nerves of the upper extremity.1,2,96,124,142 After the war, Mitchell, Bernard, Leriche, and other noted physicians of the time, continued investigation of this and related pain disorders, primarily focused on the pathophysiologic basis for the observed autonomic nervous system disturbances, whereas other researchers proposed theories for a psychogenic basis of causalgia.* Most of the early investigative information from the study of causalgia and related disorders was derived from the evaluation of patients who had often sustained major injuries to the involved extremity. In 1953, Bonica proposed the term reflex sympathetic dystrophy (RSD) to define an abnormal pain syndrome clinically similar to causalgia that required sympathetic autonomic dysfunction as a major feature but was associated with an extremely varied range of etiologic factors.1,10,115,135 Associated events included both major and minor trauma, multiple types of surgical procedures, and repetitive occupational activities, and a collection of physiologically unrelated systemic diseases and idiopathic case examples.1,2,10,11,109,115,118 *See references 1, 22-25, 71, 73, 74, 77, 96, 99, 123, 141, and 143.

1120 Part VIII Septic and Nontraumatic Conditions

Various Terms Used to Describe the Clinical Condition Referred to as Pain Dysfunction Syndrome

BOX 81-1

Causalgia Mimo-causalgia Sympathetic dystrophy Algoneurodystrophy Chronic traumatic edema Post-traumatic edema Post-traumatic pain syndrome Shoulder-hand syndrome Sudeck’s atrophy Sympathalgia Post-traumatic spreading neuralgia Post-traumatic osteoporosis Neurodystrophy Reflex sympathetic dystrophy

DEFINITION AND TERMINOLOGY It is perhaps largely due to the confusing diversity of precipitating etiologic factors proposed by Bonica, as well as his prominent role in research in this area and the lack of any reproducible laboratory models to explain either a pathophysiologic relationship or the relative importance of these factors to the clinical development of RSD, that the term has been badly misused in the literature.2,4,29,120,141 Indeed, the term RSD has unfortunately evolved both in general clinical correspondence and in the medical literature to stand as a generic term for the presentation of any abnormal pain presentation or prolonged extremity dysfunction whether or not autonomic dysfunction exists.29 The unfortunate end result of the continued clinical confusion and the generic use of the term RSD with respect to treatment implementation is that currently no consistent agreement exists regarding diagnostic criteria, natural history, and psychological factors involved in the syndromes listed in Box 81-1. These unresolved issues have often resulted in arbitrary clinical evaluation and anecdotal treatment protocols.29,141 More recently, several authors have stressed the importance of distinguishing whether the sympathetic nervous system is involved by subcategorizing abnormal pain syndromes as sympathetically maintained pain or as sympathetically independent pain.94,114 When a critical review of the literature is undertaken comparing the diagnostic criteria of each of the syndromes listed in Box 81-1 irrespective of the proposed etiologies or pathophysiologic factors, all clearly have two common denominators: an abnormal pain response and dysfunction of the affected extremity.3,29 From the

recognition of this commonality of abnormal pain and extremity dysfunction among all the various pain syndromes and with the intent to rectify the perpetuation of the use of RSD as a generic label, Dobyns29 and Amadio3 have recently recommended a more general term, pain dysfunction syndrome (PDS), to define such disorders. The use of the term PDS has several advantages. First, it is both clinically descriptive and sufficiently broad so as to encompass the diversity of possible precipitating factors and removes the contingency that sympathetic nervous system dysfunction exists in all cases of an abnormal pain presentation, which was necessarily implicit in the generic use of the term RSD.29 By using PDS as a clinically descriptive label, the treating physician may then proceed without any nosologic hindrances to objectively differentiate, order, and subcategorize all the involved factors of a PDS into specific components.29 These components include the physiologic characteristics of the injury and other sources of pain, any psychological manifestations, and the presence or absence of autonomic dysfunction.3 By proceeding in this logical fashion, the design of an effective and nonarbitrary treatment protocol can then be implemented (Fig. 81-1).

PHYSIOLOGY AND PATHOPHYSIOLOGY OF PAIN Before any further meaningful discussion on the clinical aspects of an abnormal pain response as a component of PDS can proceed, it is necessary to have an understanding of normal pain physiology. The sensation of normal acute pain begins with the interaction of a physical trigger (mechanical, thermal, and chemical) on a region of the body. Peripheral sensory nociceptors and mechanoreceptors are activated by the triggering event and transduce the physical energy into an electrochemical stimulus, which is then relayed proximally along the peripheral nerve via myelinated (Ad and Aβ) and unmyelinated (C) fibers to synapse on wide dynamic range neurons of the dorsal horn of the spinal cord.4,53,81,93,114,136,140,141 Further proximal propagation of the stimulus is then transmitted through the spinothalamic and spinoreticular pain pathways to central pain centers, which are located primarily within the midbrain, thalamus, and frontal cortex.37,140 Modulation of nociceptive stimulation occurs via central descending pathways and peripheral chemical factors.14 At the site of injury, should the physical trigger be of sufficient magnitude to produce tissue damage, local chemical modulators (hydrogen, potassium, bradykinin, serotonin, prostaglandins,16 substance P) are released from the damaged cells, which further activate and sensitize the peripheral receptors and focally produce the character-

Chapter 81 Pain Dysfunction Syndrome 1121

Abnormal presentation of pain that is prolonged and/or poorly defined or localized that results in extremity dysfunction

Pain dysfunction syndrome (PDS) Clinical suspicion of autonomic dysfunction? Yes

No

Positive

Negative Proceed to C

Pain clinic referral for pharmacologic intervention

Physiotherapy

• Regional sympathetic chain blockers • Oral medications

C. Identify possible functional causes for perpetuation of pain (e.g., nonunions, compressive neuropathy, offending hardware) trigger points

B. Psychological manifestations of PDS?

A. Appropriate diagnostic studies to confirm autonomic nervous system dysfunction (sympathetically maintained pain, RSD)

Yes

No

Positive

Emotional support vs referral to psychologist/psychiatrist for psychometric testing, counseling, and possible psychotropic medications

Proceed to A or C

Surgical intervention or diagnostic/therapeutic injections

Negative Malingering or financial/legal disincentives to recover?

Physiotherapy Reasonable attempts to correct • Social work referral

Resolution of PDS

• Legal consultation

FIGURE 81-1

Treatment protocol for pain dysfunction syndrome.

istic signs of edema, vasodilation, hyperpathia, and allodynia.111,141 Provided that no ongoing or irreversible tissue damage occurs, both the cognitive perception of pain and the physiologic signs and symptoms of the acute pain dystrophic response subside.37,53,140 The failure of any feature of the acute pain dystrophic response to resolve normally becomes a matter of clinical concern. In some cases, the abnormal persistence of pain may have a functional etiology, as when an unrecognized infection, synovial inflammation, ischemia, or nerve entrapment exists.3 Systemic factors such as rheumatologic disorders, endocrine or metabolic disorders (e.g., diabetic neuropathy), and the collagen vascular diseases can alter normal pain sensation as well as prolong the natural resolution process.3,26,27,37 When all functional causes have been excluded, of particular concern is any reported change in the intensity, quality, and location of the pain sensation and the persistence or dissemination of focal edema, color changes, and thermoregulatory adaptations that are seen initially as part of the acute pain dystrophic response. It has been well established both clinically and experimentally that the sympathetic nervous system can contribute to the pathogenesis of RSD and other related pain syndromes.2,10,11,77,78,130,131 Evidence for this has been demonstrated by the fact that regional anesthetic blockade or interruption of the sympathetic nervous system pro-

duces relief of the pain of RSD and that electrical stimulation of the sympathetic chain exacerbates the pain in many patients suspected of having a sympathetically maintained pain.37 Further evidence that the sympathetic nervous system contribution to the genesis and maintenance of certain abnormal pain syndromes is indeed a pathologic process is demonstrated by the observation that in normal persons when sympathetic outflow is electrically stimulated, no painful sensation is produced, nor does regional sympathetic blockade alter normal pain sensation.37 Despite these and other clinical and experimental observations, there as yet exists no definitive laboratory model that explains fully how the sympathetic nervous system alters, produces, or maintains the pain of RSD and related disorders, although numerous plausible hypotheses have been proposed.1,2,33,67,77,101,111,114,127 Collectively, these hypotheses can be grouped into either adaptive central nervous system dysfunction processes or peripheral end organ and receptor abnormalities.13

CLASSIFICATION Several classification schemes for RSD have been described in the literature.1,74 In general terms, the more accepted classification schemes have been based on

1122 Part VIII Septic and Nontraumatic Conditions

Lankford’s Classification of Reflex Sympathetic Dystrophy by Cause

BOX 81-2

BOX 81-3 Type I

Causalgia Major: motor-sensory involvement Minor: sensory involvement Traumatic Major: fracture, crush Minor: sprain, contusion

Type II

Type III

Classification of Reflex Sympathetic Dystrophy by Temporal Factors (Steinbrocker)

TABLE 81-1 Type

Duration (months)

Acute

<3

Dystrophic

3-6

Atrophic

>6

either the natural history of signs and symptoms of the disorder or on the type and magnitude of the precipitating injury.71-74,103 Lankford’s classification, based on injury type, proposes two distinct forms of sympathetic dysfunction (Box 81-2). The first, causalgia, results from direct nerve injury and is further subcategorized into either major or minor causalgia depending on whether the injury is due to a mixed motor/sensory or a sensory nerve, respectively. Traumatic dystrophy, the second type, is similarly subcategorized into major and minor subtypes. A minor traumatic dystrophy generally results from a less severe injury such as a sprain or contusion, whereas a major traumatic dystrophy results from a more extensive injury such as a fracture.3,34,73,74 Amadio and others have pointed out that the use of this type of classification scheme can be both confusing and imprecise, because some examples of RSD have no clear traumatic etiology and some minor causalgia may prove to be more disabling than a major causalgia.3 The second type of classification scheme for RSD is based on the natural history of the clinically observed physiologic, morphologic, and functional changes observed in untreated RSD.115,128 The Steinbrocker classification recognizes three distinct stages: (1) the acute stage (0 to 3 months), (2) the dystrophic stage (3 to 6 months), and (3) the atrophic stage (6 months and beyond) (Table 81-1).128 In the earlier phases, the pain is often burning and more focal than diffuse, and the associated edema, vasomotor, and thermoregulatory dysfunction are usually prevalent. In the later stages, the pain is more constant and poorly localized. Muscle atrophy, joint stiffness, or contractures may develop,

Complex Regional Pain Syndrome Reflex sympathetic dystrophy Abnormal pain, dysfunction of the extremity, autonomic nervous system abnormalitites, and recognizable dystrophic clinical features without direct nerve injury Causalgia Abnormal pain, dysfunction of the extremity, autonomic nervous system abnormalities, and recognizable dystrophic clinical features with a known nerve injury? Other pain dysfunction syndromes

along with subcutaneous fibromatous organization and cyanosis of the skin. End-stage RSD is characterized by the appearance of more permanent changes of the skin, blood vessels, and joints (ankylosis).37,115 It is important to recognize that RSD is a dynamic process, and although the previously mentioned stages accurately describe the symptomatic and pathophysiologic changes in general, in any individual a considerable temporal variability may occur in the development of the characteristic signs and symptoms, and subtle and partial manifestations are generally the rule rather than the exception. Therefore, no classification scheme is wholly satisfactory.3,37 In view of this, recently (similar to Dobyns) Boas8 has recognized the importance of a clinically descriptive classification scheme, and the term has been proposed and is gaining wider acceptance in the literature (Box 81-3).

PSYCHOLOGY OF PAIN AND DYSFUNCTION In the previous section, the sensorineural mechanisms involved in the sensation of acute pain were outlined. These mechanisms, however, do not exist in isolation. The perception of a painful stimulus always yields an affective or emotional component that is individually variable and complex.27,29,50 In the treatment of patients with PDS, the psychological component of the disorder may be pronounced and may evolve into the dominant clinical feature.29

The Psyche Although it is beyond the scope of this chapter to discuss at length the multiple theories of how the psyche may produce changes on the soma, in the past, considerable clinical emphasis has been placed on the probability that there are definite psychogenic causes for some chronic pain disorders, particularly RSD.† Supporting the †

See references 11, 25, 29, 58, 71-74, 88, 96, 99, 103, 106, and 121.

Chapter 81 Pain Dysfunction Syndrome 1123

notion of a psychogenic basis for these disorders (even in less overt PDS) is that commonly a considerable disparity exists between the physical examination and the patient’s degree of fear, anxiety, and the reported degree of discomfort.37,50,51,118 In the past, patients were variously described as “hysterical,” “emotionally labile,” “dependent,” “unstable,” “depressed,” and having “vulnerable, brittle autonomic nervous systems.”24,30,58,71,95,99 Such descriptive psychological assessments imply that a premorbid personality or even psychoses may exist. What is clear from review of these early accounts is that these psychological assessments were largely the result of opinion rather than based on psychological testing.50,88,126 Several studies on RSD and other chronic pain syndromes, however, convincingly conclude that the observed personality and behavior changes are likely the consequence of the state of prolonged suffering rather than a manifestation of a pre-existing personality or psychological disorder.50,118,120,126,129,139 This is not to imply that some understandable emotional and psychological disturbances can occur in any individual living with chronic pain.29,32,37,41,50 Most frequently reported are persistent anxiety, reactive depression, dependency, and somatic preoccupation, all of which can impede the resolution of a PDS.29,37 In the process of identifying the psychological components of a PDS, one must differentiate from certain bona fide psychopathologic syndromes that often have as common features decreased pain tolerance or increased pain susceptibility or both; these are somatization disorder, conversion disorder, malingering, and factitious injury disorder.3,4,29,37,38,40 Patients with a somatization disorder often present with chronic pain as well as a history of recurrent multiple somatic complaints (at least 12) of long duration but for which no physical diagnosable disorder can be found.4,37,38 These patients are convinced that they are seriously ill and are not deterred by the evidence of normal test results. The disorder is generally more common in women and usually begins during adolescence. Common complaints are chronic pain and weakness of the extremities, nausea, amnesia, shortness of breath, and fainting spells.3,4,38 Conversion disorder, formerly called hysterical neurosis, like somatization disorder is also more common in women and usually presents with a history of chronic intermittent pain, the source of which is not medically identifiable.4,38 Other common symptoms are pseudoparalysis, nonanatomic sensory loss, and blindness.145 Posturing of the hand and upper extremity is frequently observed, the persistence of which may result in contracture.4,29 Differing from somatization disorder, the onset of a conversion disorder is usually more sudden and, when identifiable, the physical manifestations of the disorder occur unconsciously in reaction to a disturbing psychological conflict.4,29,38

Other identifiable syndromes in which complaints of pain are commonly associated include major depression (endogenous depression), hypochondriasis, factitious injury, and malingering.4,38 Major depression may be suspected by the characteristic dysphoric mood, sense of hopelessness, and vegetative symptoms (sleep alterations, poor appetite, fatigue), and often there is a preoccupation with pain, disease, and death.4,37,38,61,62 Hypochondriasis may be a symptom of major depression or may exist as a separate disorder characterized by a pervasive conviction that various imagined symptoms including pain are indicative of impending disease.3,4,38,61,62 Malingering is the conscious willful act of misrepresentation of symptoms of illness to avoid obligation or is contrived for secondary monetary gain. Factitious injury when secondary gain is identifiable represents a form of malingering.3,4

OTHER CONSIDERATIONS Finally, in the process of distinguishing the psychic components of a PDS, we, as orthopedic surgeons, are perhaps especially aware of our society’s current socioeconomic and legal factors that may both produce and perpetuate the development of the various psychological components. Workers’ compensation laws, disability programs, and pending accident litigation all provide convincingly powerful disincentives to recover from injury.37,50,52,146 Nonetheless, we must remain cognizant that most patients present initially with legitimate claims of an injury and thus have functional reasons for their pain. Oftentimes our clinical suspicions of a contrived disincentive to return to useful activity may be the manifestation of the patient’s unwitting learned behavior that develops during the course of a prolonged rehabilitation from serious injury because there may be significant emotional, familial, legal, and financial rewards for the continuance of disability.33,144 These factors over time may then eventually overshadow some previously held good intentions to return to employment or obligation.18,37,39 Early settlement of compensation claims in such instances has been shown to have a positive effect on the overall recovery from a PDS.50,141,146 In recent years, a growing awareness of fibromyalgia is occurring in the orthopedic community. This syndrome, characterized by upper and lower extremity symptoms, may well present with the major focus on the elbow or shoulder. The most important consideration for the orthopedic surgeon is to beware when multiple additional musculoskeletal complaints are present. Although the optimal treatment is unclear, patient education and the exploration of psychogenic factors are usually entertained.

Fibromyalgia

1124 Part VIII Septic and Nontraumatic Conditions

PATIENT PRESENTATION Patients with a suspected PDS may present initially to any number of medical practitioners, but in most cases, the task of making the diagnosis and proceeding with a plan of treatment will be placed in the domain of orthopedic surgeons.

HISTORY The historical details of the events of the initial injury, if one is identifiable, including the mechanism and site of injury as well as the patient’s recollection of the intensity and subjective quality of the initial pain and extent of extremity dysfunction, are important facts.29 Details of the initial treatment and all subsequent treatment regimens are noted so as to establish the patient’s assessment of the effectiveness of previous treatment and should be compared with information in the medical records. Moreover, the patient’s recollection of any signs or symptoms suggestive of autonomic dysfunction or a sympathetically maintained pain are noted and compared with the recorded data. A thorough investigation of the patient’s work history, family setting, and job satisfaction is necessary to fully investigate the patient’s assessment of how the injury and present dysfunction has affected his or her family life, employment, and future goals to gain insight into the emotional and psychological manifestations of the PDS.5,37,50 In related terms, documentation of any past or ongoing psychiatric treatment or present substance abuse, including use of prescribed medications, may be relevant.50 Finally, details of past medical history are taken to determine the existence of any systemic diseases that may contribute to the presentation or prolongation of chronic pain.3

evaluated. When pertinent, assessment of fracture reduction and healing is noted, along with any associated joint swelling or synovitis as possible sources of ongoing pain (triggers). Provocative maneuvers are performed to document any signs of a peripheral nerve injury or presence of a compressive neuropathy. After both extremities have been allowed to equilibrate to room temperature, a gross estimation of any thermal abnormality about the affected extremity can be compared with the contralateral side to assess for thermoregulatory dysfunction. When thermal differences are noted, a more precise measurement can be made with special skin thermometers.64,65 Trigger Points Dobyns has observed that musculoskeletal trigger points and irritability about peripheral nerves (particularly sensory cutaneous branches) are commonly found during the physical examination of patients with a PDS.3,29 Musculoskeletal trigger points are infrequently discussed in the orthopedic literature but are described often in those medical fields dealing with the treatment of chronic pain.29,37,41,47,54,90,91 Their etiology, however, remains controversial.37,42 Trigger points can be recognized as localized areas of tenderness that are most often found about the origin and insertion of muscles, tendons, and ligaments and along fascial planes and about capsular structures. They may or may not be anatomically related to the site of the original injury and often persist after the injury has healed and thus may perpetuate dysfunction.3,29,37 Irritability along cutaneous nerves is another common clinical problem found in the evaluation of PDS and is often secondary to trauma, surgical procedures, and improper application of casts and is associated with prolonged focal edema. Like musculoskeletal trigger points, nerve irritability can persist for long periods and thus act as a continued source of pain.84

PHYSICAL EXAMINATION Often the physical examination of a patient with a PDS is difficult to perform secondary to the patient’s degree of discomfort and level of anxiety. The physical examination begins with the observation of any pertinent visible signs. If an injury was sustained, the examiner should note the patient’s posture and degree of protection of the injured part, the nature and extent of any wounds or surgical scars, the degree of edema, the presence of atrophy, and the presence of any characteristic signs of autonomic dysfunction, including circulatory differences, abnormal sweat patterns, alterations of hair growth and skin trophic changes. Following this, an orderly physical examination of the extremity is undertaken: the location of the pain along with the presence of any spasm or cocontraction is recorded, and range of motion, reflexes, motor strength, and sensibility are

DIAGNOSTIC STUDIES In addition to the findings obtained from the physical examination, certain diagnostic tests should be ordered to provide further objective information. Current plain radiographs of the involved extremity are obtained, often with comparison views of the contralateral extremity, to detect any differences in radiographic bone density.15,43,46,56,64,68-70 When indicated, other studies including arthrograms, tomograms, computed tomography, magnetic resonance imaging, electromyography, and nerve conduction studies may yield useful information.3,35,43,84 Radionuclide imaging may confirm a previous diagnosis or can reveal previously unforeseen problems, as noted by localized increased radioisotope uptake.3,29,64,66,68-70 The three-phase bone scan technique has proven to be a particularly useful diagnostic tool in

Chapter 81 Pain Dysfunction Syndrome 1125

the evaluation of RSD, with a reported high degree of specificity in untreated cases.3,67-70,85 Other diagnostic tests for RSD and autonomic dysfunction have been described, including quantitative sweat production (Q-SART Low), dynamic vasomotor reflex assessment, and cold stress thermoregulatory capacity, all of which may add diagnostic information.3,36,48,64,83 The usefulness of thermography (infrared telethermometry) as a diagnostic test for RSD is controversial.75,105-107,119,135 Although all of these ancillary diagnostic tests may be necessary in certain case examples, the response to sympathetic blockade remains the single most useful and preferred test for the establishment of the diagnosis of RSD.3,76,78,97,102,104,116,117 As previously stated, the psychological aspects of a PDS are variable both in degree and in presentation. To objectively assess the psychic manifestations of the disorder, examiners have traditionally used several standard personality, psychometric, and pain quantitation tests to evaluate patients suffering from chronic pain and RSD.3,17,122 These tests include the Minnesota Multiphasic Personality Inventory, the McGill Pain Questionnaire, the Visual Analogue Scale, and the Dartmouth Pain Questionnaire.17,20,49-51,141 When properly interpreted, the Minnesota Multiphasic Personality Inventory can provide some useful evaluative information of the personality profiles for some chronic pain states, although some argue its importance as a predictor of treatment success.17,20,41,50,51,87 The McGill Pain Questionnaire is widely used as a method of quantitating subjective pain intensity, and this study, along with other visual quantitation methods, is often useful to assess individual treatment progress.50,51 In some cases, precise localization of a source of pain between several contiguous anatomic structures may be aided by a selective diagnostic local anesthetic injection of small amounts of 1% lidocaine. This simple diagnostic procedure can also be used as an aid in the localization of multiple adjacent trigger points.

specific problem-oriented treatment regimens may be begun (see Fig. 81-1). In most cases of PDS, the treatment of certain components is outside the domain of orthopedic surgery, and therefore, consultation of other medical associates to assist in the overall treatment plan is required. Pain control specialists (anesthesiologists), physiatrists, physical therapists, and psychiatrists are most often consulted, owing to their particular expertise in dealing with some of the more common problems involved in recovery from chronic pain and dysfunction.3,29,37 Associates in internal medicine for the treatment of certain systemic disorders, as well as rheumatologists, neurologists, and endocrinologists, may be required in specific instances. By consulting these medical specialists, the primary physician generally yields to their recommendations for specific treatment; however, the patient rightly expects that one physician will remain in overall charge of his or her care. Failure to do so can often result in disastrous failures in treatment stemming from misunderstanding, disillusionment, and distrust. The treatment of the physical components of a PDS in most cases will come under the direction and care of the orthopedic surgeon, particularly when an injury has occurred. It is obligatory from the outset of treatment to identify any physical and anatomic problems that act as sources of continued pain and dysfunction. Fracture nonunions and malunions, offending internal fixation hardware, postimmobilization joint stiffness, neuromas, painful constrictive scars, and traumatic arthritis are all common examples of continued painful foci that are potentially correctable with surgical intervention. Reluctance on the part of the surgeon to proceed with corrective operative procedures should be dismissed even in cases in which there are recognizable extenuating problems (e.g., previous surgical failures, active psychological dysfunction) because avoidance of recognized treatable problems will ensure perpetuation of the disorder.3

PHYSIOTHERAPY

TREATMENT After obtaining a thorough historic investigation and physical examination as well as additional objective data from appropriate diagnostic studies, the treating physician should be able to accurately identify those specific components involved in any PDS. All involved components of a PDS must be addressed in the design of a treatment plan if a complete and expeditious recovery from the disorder is to be expected.29,117 Dobyns29 recommends that all components be ordered so that the most predominant problems are listed first. This process results in a prioritized outline from which

In addition to the decision for further surgical treatment, the form and direction of a physical therapy program will most often initially come under the direction and control of the orthopedic surgeon. A close association with the therapist should be established early and maintained through completion of rehabilitation. All involved components of a PDS should be discussed with the therapist to delineate the specific physical problems necessitating the referral and to identify any potential impediments to the success of subsequent treatment. Restoration of normal functional activity involves both active and passive modalities, but the design of any physical therapy program for PDS should allow direct

1126 Part VIII Septic and Nontraumatic Conditions

patient involvement, along with establishment of clearly defined treatment goals.3,39,125 In the earlier phases of therapy, the degree of pain is usually the determining factor as to which modalities are to be employed. However, active and active-assistive programs are generally most effective because they allow the patient to have some control of his or her level of pain.138 In addition to specific physiotherapy modalities directed toward the site of injury or obvious sources of pain and dysfunction, it is also important to recognize and treat any secondary adaptive physical problems that evolve in adjacent joints and anatomic structures. Examples of a secondary problem would be decreased range of motion of the shoulder and cocontraction of parascapular muscles following a prolonged period of immobilization.29

PHARMACOLOGIC TREATMENT Pharmacologic pain management may initially be instituted by the musculoskeletal physician. Aside from the need for immediate postoperative narcotic medications, narcotics as a class of drugs in pain management should be avoided in the treatment of a PDS, because drug dependency is often associated with this disorder and identification of such dependency requires early referral for treatment.3,50,108 Nonsteroidal anti-inflammatory medications and other non-narcotic drugs may be particularly beneficial during the acute phases of the normal dystrophic response and, therefore, may facilitate participation in physical therapy and resumption of normal activities of daily living.3,111 When indicated, anesthetic injections of trigger points and corticosteroid solution injections of joints and about inflamed musculotendinous structures are also effective and easily administered methods to control pain.28,92 Beyond these initial measures in pain management, the consultation of a pain control specialist is recommended for the treatment of refractory functional causes of pain and in all cases in which autonomic dysfunction and sympathetically maintained pain exist. Pain control specialists may use oral, intravenous, and regional nerve blocks as well as adaptive therapeutic measures such as transcutaneous electric stimulation for the control and treatment of chronic functional pain.‡

Sympathetic Blockade The pharmacologic treatment of the sympathetic nervous system dysfunction of RSD involves blockade of abnormal sympathetic efferent activity by multiple or continuous stellate ganglion blocks; continuous axillary blockade; end organ blockade by intravenous guanethidine, bretylium, or reserpine; and use of systemic calcium channel ‡

See references 3, 7, 28, 31, 32, 42, 45, 60, 80, 86, 98, 100, 113, and 132.

blockers.§ Pharmacologic treatment alone often is only partially successful in the treatment of sympathetically maintained pain, and an interdisciplinary approach using physical therapy and psychiatry may be initiated by the pain control specialist to successfully treat all the manifestations of the disorder.

THE PSYCHE The treatment of any recognizable psychic disturbances begins with initiation of any and all measures to resolve the patient’s pain, because as previously mentioned, relief from prolonged pain alone may result in a significant diminishment of any existing psychological and emotional abnormalities.74,75 However, consultation with a psychotherapist should be considered, even for the more situationally induced psychological disturbances described earlier, when such problems are identified as a major feature of a PDS. Depending on the patient, there may be considerable reluctance, denial, and even anger when mention is made of the possibility of any associated psychological factors, and particularly so when a recommendation is made for psychiatric referral. Nothing should be disclosed in a confrontational manner, and prior discussion with the psychotherapist may circumvent any potential negative consequences.3,37 Relaxation therapy, hypnosis, biofeedback, distraction techniques, supportive psychotherapy, and psychotrophic medications have all been shown to be effective in the management of the psychological disturbances associated with chronic pain syndromes.3,29,37,50,82,112,133,134 Likewise, the psychotherapist may assist in resolving familial, economic, and workers’ compensation issues.2,8,12,29,37 Formal psychoanalysis is necessary when somatization disorder, conversion disorder, major depression, malingering, and factitious injury disorders have been identified.37,50,61,62 The early detection and prompt referral to psychotherapists for treatment of these disorders are important to protect the patient from unnecessary surgery, possibly harmful diagnostic tests, the potential for self-inflicted injury, and unnecessary hospitalization and incurred medical costs.3,37,51

CONCLUSION Pain dysfunction syndrome is unlike most other complications encountered in the treatment of disorders of the upper extremity. The syndrome is a confluence of numerous possible precipitating factors, which may then involve a diversity of physiologic, psychological, and systemic components, yielding an individually variable § References 6, 9, 16, 21, 42, 44, 55, 57, 76, 79, 86, 88, 90, 110, 111, 127, 131, and 137.

Chapter 81 Pain Dysfunction Syndrome 1127

presentation of pain and extremity dysfunction. Perhaps no other clinical complication is looked on with more consternation, and from this there has historically been an overall reluctance to accept and treat the many problems of this disorder. Dobyns’ approach to PDS solves many of the clinical challenges this syndrome presents by first clarifying the involved components, eliminating nosologic hindrances, and providing guidelines for an effective nonarbitrary treatment program.29 Fortunately, with proper management, all components of a PDS can be alleviated, but treatment always becomes more difficult and protracted the longer the components of the syndrome are allowed to progress before care is initiated. Therefore, the willingness to accept responsibility for treatment remains perhaps the last and most difficult obstacle to overcome.

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107.

108.

nificance to other chronic musculoskeletal pain syndromes. Pain 37:273, 1988. McKain, C. W., Urban, B. J., and Goldner, J. L.: The effects of intravenous regional guanethidine and reserpine. J. Bone Joint Surg. 65A:808, 1983. Melzack, R.: Prolonged relief of pain by brief, intense transcutaneous somatic stimulation. Pain 1:357, 1975. Melzack, R., Stillwell, D. M., and Fox, E. J.: Trigger points and acupuncture points for pain: Correlations and implications. Pain 3:3, 1977. Melzack, R., and Wall, P. D.: Pain mechanisms: A new theory. Science 150:971, 1965. Mershey, H., and Bogdeuk, N.: Classification of chronic pain. Descriptions of chronic pain syndromes and definitions of pain terms. Prog. Pain Res. Manage 1:39, 1994. Miller, D. S., and de Takats, G.: Post-traumatic dystrophy of the extremities: Sudeck’s atrophy. Surg. Gynecol. Obstet. 75:558, 1942. Mitchell, S. W.: Injuries of Nerves and Their Consequences. London, Smith Elder, 1872. Mockus, M. B., Rutherford, R. B., Rosales, C., and Pearce, W. H.: Sympathectomy for causalgia: Patient selection and long-term results. Arch. Surg. 122:668, 1987. Nashold, B. S., Jr., Goldner, J. L., Mullen, J. B., and Bright, D. S.: Long-term pain control by direct peripheral-nerve stimulation. J. Bone Joint Surg. 64A:1, 1982. Omer, G.: Management of pain syndromes in the upper extremity. In Hunter, J. M., Schneider, L. H., Macklin, E. J., and Bell, J. A. (eds.): Rehabilitation of the Hand. St. Louis, C. V. Mosby, 1978. Omer, G., and Thomas, S.: Treatment of causalgia: review of cases at Brooke General Hospital. Tex. Med. 67:93, 1971. Oschoa, J. L., Yainitsky, D., Marchettini, P., Dotso, R., Dotson, R., and Cline, M.: Interactions between sympathetic vasoconstrictor outflow and C noceceptor-induced antidromic vasodilatation. Pain 54:191, 1993. Owitz, S., and Koppolu, S.: Sympathetic blockade as a diagnostic and therapeutic technique. Mt. Sinai J. Med. 49:282, 1982. Pak, T. J., Martin, G. M., Magness, J. L., and Kavanaugh, G. J.: Reflex sympathetic dystrophy: Review of 140 cases. Minn. Med. 53:507, 1970. Payne, R.: Neuropathic Pain Syndromes, With Special Reference to Causalgia and Reflex Sympathetic Dystrophy. New York, Raven Press, 1986. Perelman, R. B., Adler, D., and Humphreys, M.: Reflex sympathetic dystrophy: Electronic thermography as an aid in diagnosis. Orthop. Rev. 16:561, 1987. Pochaczevsky, R., Wexler, C. E., Meyers, P. H., Epstein, J. A., and Marc, J. A.: Liquid crystal thermography of the spine and extremities: Its value in the diagnosis of spinal root syndromes. J. Neurosurg. 56:386, 1982. Pollock, F. E., Jr., Koman, L. A., Toby, E. B., Barden, A., and Poehling, G. C.: Thermoregulatory patterns associated with reflex sympathetic dystrophy of the hand and wrist. Orthop. Trans. 14:156, 1990. Portenoy, R. K., and Foley, K. M.: Chronic use of opioid analgesics in non-malignant pain: Report of 38 cases. Pain 25:171, 1986.

1130 Part VIII Septic and Nontraumatic Conditions

109. Procacci, P., and Maresca, M.: Reflex sympathetic dystrophies and algodystrophies: Historical and pathogenic considerations. Pain 31:137, 1987. 110. Prough, D. S., McLeskey, C. H., Poehling, G. G., Koman, L. A., Weeks, D. B., Whitworth, T., and Semble, E. L.: Efficacy of oral nifedipine in the treatment of reflex sympathetic dystrophy. Anesthesiology 62:796, 1985. 111. Raja, S. N., Meyer, R. A., and Campbell, J. N.: Peripheral mechanisms of somatic pain. Anesthesiology 68:571, 1988. 112. Reuler, J. B., Girard, D. E., and Nardone, D. A.: The chronic pain syndrome: Misconceptions and management. Ann. Intern. Med. 93:588, 1980. 113. Rizzi, R., Visentin, M., and Mazzetti, G.: Reflex sympathetic dystrophy. In Benedetti, C., Chapman, C. R., and Moricca, G. (eds.): Advances in Pain Research and Therapy, Vol. 7. New York, Raven Press, 1984. 114. Roberts, W. J.: A hypothesis on the physiological basis for causalgia and related pains. Pain 24:297, 1986. 115. Rowlingson, J. C.: The sympathetic dystrophies. In Stem, J. M., and Wakefield, C. A. (eds.): Pain Management. Boston, Little, Brown, 1983, p. 117. 116. Schott, G. D.: Mechanisms of causalgia and related clinical conditions: The role of the central and of the sympathetic nervous system. Brain 109:717, 1986. 117. Schutzer, S. F., and Gossling, H. R.: The treatment of reflex sympathetic dystrophy syndrome. J. Bone Joint Surg. 66A:625, 1984. 118. Schwartzman, R. J., and McLellan, T. L.: Reflex sympathetic dystrophy, a review. Arch. Neurol. 44:555, 1987. 119. Sherman, R. A., Barja, R. H., and Bruno, G. M.: Thermographic correlates of chronic pain: Analysis of 125 patients incorporating evaluations by a blind panel. Arch. Phys. Med. Rehab. 68:273, 1987. 120. Shumacker, H. B., Jr.: A personal overview of causalgia and other reflex dystrophies. Ann. Surg. 201:278, 1985. 121. Smith, R. J., Monson, R. A., and Ray, D. C.: Patients with multiple unexplained symptoms: Their characteristics, functional health, and health care utilization. Arch. Intern. Med. 146:69, 1986. 122. Southwick, S. M., and White, A. A.: Current concepts review: The use of psychological tests in the evaluation of low-back pain. J. Bone Joint Surg. 65A:560, 1983. 123. Spebar, M. J., Rosenthal, D., Collins, G. J., Jarstfer, B. S., and Walters, M. J.: Changing trends in causalgia. Am. J. Surg. 142:744, 1981. 124. Speigel, I. J., and Milowsky, J. L.: Causalgia. J. A. M. A. 127:9, 1945. 125. Spero, M. W., and Schwartz, E.: Psychiatric aspects of foot problems. In Jahss, M. H. (ed.): Disorders of the Foot. Philadelphia, W. B. Saunders Co., 1982. 126. Spiegel, D., and Chase, R. A.: The treatment of contractures of the hand using self-hypnosis. J. Hand Surg. [Am] 5:428, 1980. 127. Spurling, R. G.: Causalgia of the upper extremity: Treatment by dorsal sympathetic ganglionectomy. Arch. Neurol. Psychiatry 23:784, 1930.

128. Steinbrocker, O.: The shoulder-hand syndrome: Present status as a diagnostic and therapeutic entity. Med. Clin. North Am. 42:1537, 1958. 129. Sternbach, R. A., and Timmermans, G.: Personality changes associated with the reduction of pain. Pain 1:1771, 1975. 130. Sunderland, S.: The painful sequelae of injuries to peripheral nerves. In Sunderland, S. (ed.): Nerves and Nerve Injuries. London, Churchill Livingstone, 1978, p. 377. 131. Sunderland, S.: Pain mechanisms in causalgia. J. Neurol. Neurosurg. Psychiatry 39:471, 1976. 132. Tabira, T., Shibasaki, H., and Kuroiwa, Y.: Reflex sympathetic dystrophy (causalgia) treatment with guanethidine. Arch. Neurol. 40:430, 1983. 133. Thompson, R. L., II.: Chronic pain. In Kaplan, H. I., and Sadock, B. J. (eds.): Comprehensive Textbook of Psychiatry. Baltimore, Williams & Wilkins, 1985. 134. Turner, J. A., and Chapman, C. R.: Psychological interventions for chronic pain: A critical review. II. Operant conditioning, hypnosis and cognitive-behavioral therapy. Pain 12:23, 1982. 135. Uematsu, S., Hendler, N., Hungerford, D., Long, D., and Ono, N.: Thermography and electromyography in the differential diagnosis of chronic pain syndromes and reflex sympathetic dystrophy. Electromyogr. Clin. Neurophysiol. 21:165, 1981. 136. Wall, P. D.: Stability and instability of central pain mechanisms. In Dubner, R., Gebhart, G. F., and Bond, M. R. (eds.): Proceedings of the Fifth World Congress on Pain. Amsterdam, Elsevier, 1988, p. 13. 137. Wang, J. K., Erickson, R. P., and Ilstrup, D. M.: Repeated stellate ganglion blocks for upper extremity reflex sympathetic dystrophy. Reg. Anaesth. 10:125, 1985. 138. Watson, H. K., Carlson, L., and Brenner, L. H.: The “dystrophile” treatment of reflex dystrophy of the hand with an active stress loading program. Orthop. Trans. 10:188, 1986. 139. White, J. C., and Sweet, W. H.: Pain and the Neurosurgeon. Springfield, IL, Charles C. Thomas, 1969. 140. Willis, W. D., Jr.: Ascending somatosensory systems. In Yaksh, T. L. (ed.): Spinal afferent processing. New York, Plenum Press, 1986, p. 243. 141. Wilson, P. R.: Sympathetically maintained pain: Diagnosis, measurement, and efficacy of treatment. In Hicks, M. S. (ed.): Pain and the Sympathetic Nervous System. Norwell, MA, Kluwer Academic Publishers, 1982, p. 91. 142. Wilson, R. L.: Management of pain following peripheral nerve injuries. Orthop. Clin. North Am. 12:343, 1981. 143. Wirth, F. P., and Rutherford, R. B.: A civilian experience with causalgia. Arch. Surg. 100:637, 1970. 144. Withrington, R. M., and Wynn-Parry, C. B.: The management of painful peripheral nerve disorders. J. Hand Surg. 9B:24, 1984. 145. Withrington, R. M., and Wynn-Parry, C. B.: Rehabilitation of conversion paralysis. J. Bone Joint Surg. 67B:635, 1985. 146. Woodyard, J. E.: Diagnosis and prognosis in compensation claims. Ann. R. Coll. Surg. Engl. 64:191, 1984.

Chapter 82 Neoplasms of the Elbow 1131

CHAPTER

82

Neoplasms of the Elbow Douglas J. Pritchard, K. Krishnan Unni, and Bernard F. Morrey

INTRODUCTION Most benign and malignant tumors of bone and soft tissue are relatively rare, and their occurrence in the region of the elbow is even more unusual. Although there are no valid statistics on soft tissue tumors, compilation of data from the files of the Mayo Clinic until December 2003 indicates that only 1% or so of bone tumors occur at the elbow (Table 82-1). Hence, no single entity is likely to be encountered very often at this site. Unfortunately, comparable figures are not available for benign and malignant soft tissue tumors, although our impression is that the most common benign soft tissue tumor in the elbow region is the lipoma. Ganglia and myxomas are also occasionally seen in this region. Of the malignant soft tissue tumors, epithelioid sarcoma and synovial sarcoma are probably the most frequently encountered at this joint. The locally aggressive desmoid tumor may also occur at or near the elbow. Metastatic disease usually originates from the breast or kidneys.55 Tumors that occur in the region of the elbow are unique in that because there are a relatively large number of important structures in a relatively small and confined area, there is little normal tissue that can be spared; and it may be difficult or impossible to remove a tumor with a margin of normal tissue on all sides without severely compromising the function of the forearm and hand. In this respect, tumors that occur at the elbow, particularly those in the antecubital fossa, are comparable with tumors that occur in the region of the knee. However, the upper extremity is probably considered more important by most patients and their physicians; hence, amputation surgery is probably less likely to be carried out for these tumors than for those of the lower extremity. In addition, it is generally considered difficult to fit a patient with an upper limb prosthesis; and even if upper limb prosthetic devices are prescribed, patients are often reluctant to use them. In contrast, most patients readily accept the use of a lower limb prosthesis. An

amputation may be required for aggressive or malignant tumors to achieve adequate surgical margins, and yet both the patient and the physician may be reluctant to accept this radical treatment. Finally, as with traumatic conditions, the tumor or its treatment often renders the elbow stiff and restricts function.27,54

CLINICAL PRESENTATION As with mesenchymal tumors arising in other locations, patients usually complain of a lump or pain, or perhaps both. Lesions in the region of the elbow may cause some limitation of motion, and this may be the first symptom that the patient notices. In addition, swelling or increased warmth may be noted by either the patient or the physician. Dilated veins may be the first indication that there is an underlying tumefaction. Symptoms may occur as a result of localized compression of one or more of the nerves that cross the elbow joint, causing local or referred pain, numbness, or paresthesia. A long history suggests that the lesion is benign. If the patient describes a mass that seems to fluctuate in size, a ganglion or hemangioma may be considered.

PREOPERATIVE EVALUATION In addition to the usual history and physical examination, the physician should pay particular attention to the palpation of any tumor mass that may be encountered. The consistency of the mass may give a clue to its nature. As with soft tissue masses in other locations, a stethoscope should be used to listen for the presence of a bruit. Pain or paresthesias referred to the forearm or the hand at the time of palpation of the tumorous mass may suggest the presence of a neurogenic tumor, such as a neurofibroma. Following the clinical examination, radiographs in at least two planes should be obtained.22 Computed tomography (CT), with a comparison of the opposite elbow joint, may yield useful information, particularly in terms of planning for the surgical procedure. The authors have not found the performance of routine arteriography to be particularly helpful in this or any other site; however, if one needs to know the relationship of the tumor to the adjacent major vessels, contrast material can be used when CT is performed, thereby supplying this information more simply and safely than by performing routine arteriography. Magnetic resonance imaging has proved to be particularly valuable in the assessment of both bone and soft tissue tumors in most areas, including the elbow. Soft tissue tumors can be defined as to the extent of disease and their relationships with major neurovascular

1132 Part VIII Septic and Nontraumatic Conditions

Bone Tumors—Mayo Experience: Updated, 2003

TABLE 82-1

Type of Tumor

Number at Elbows

Total

Benign Osteoid osteoma Osteochondroma Giant cell tumor Chondromyxoid fibroma Osteoblastoma

25 16 13 2 1

397 884 682 50 108

Malignant Malignant lymphoma Ewing sarcoma Osteosarcoma Fibrosarcoma Angiosarcoma Chondrosarcoma Malignancy in giant cell tumor Malignant fibrous histiocytoma Myeloma

38 15 16 3 1 6 2 1 19

905 611 1984 285 109 1080 39 98 1069

*Does not include patients with multiple exostoses.

structures. Information about the extent of medullary involvement can be ascertained for bone tumors. Radioisotopic bone scans may be useful not only in defining the extent of the lesion in the elbow but also in ruling out additional disease in other sites. Although it is unusual for tumors of any type to metastasize to the elbow, it is possible and should be considered whenever a primary mesenchymal neoplasm is being considered. In addition, all other modalities used in the evaluation of mesenchymal tumors in other locations should be employed as well. Routine blood chemistries and hematologic studies should be obtained. The relevance of these tests to certain specific entities will be discussed later, as these entities are considered in more detail. Certainly, a routine chest radiograph should be obtained in every patient. It should be stressed that as much information as possible should be obtained about the patient and the tumor before any surgical procedure is performed.

BIOPSY As with musculoskeletal tumors in other locations, the biopsy procedure should be considered at least as important as the definitive surgical procedure. It should be planned with the definitive surgery in mind and should probably not be undertaken unless one is willing and prepared to proceed with whatever surgery may be indicated, depending on the results of the histologic examination and whether the pathologist can render a judgment on the basis of the frozen section. If one is

approaching a lipoma or a ganglion cyst, for example, this usually becomes readily apparent to the surgeon so that he or she can perform a simple excisional biopsy as a one-stage procedure. If subsequent histologic examination of the permanent section should reveal something unexpected, definitive surgery can be performed later. The biopsy procedure itself should be done meticulously. Very careful hemostasis should be obtained to prevent the dissemination of tumor cells in the hematoma. If the tumor lies under a muscle belly, it is usually better to go straight through the muscle, rather than to dissect around the muscle, which may contaminate additional tissue planes. The general principle that incisions on extremities should be made vertically, rather than transversely, holds for the region of the elbow, although for lesions in the region of the antecubital fossa, it may be desirable to make an S-shaped incision with the transverse portion crossing the crease of the elbow. Fine-needle aspirates are becoming an acceptable way of making a diagnosis in bone and soft tissue tumors. At the Mayo Clinic, fine-needle aspirates are performed by radiologists under CT or ultrasonographic guidance. A 16- or 18-gauge needle is employed. In addition to cytologic material, the radiologist also obtains tiny fragments of tissue. The cytologic smears are stained immediately with the Papanicolaou technique, and if the smears are positive the tissue is held over for permanent sections. If the smears, however, are negative, there is an option to do frozen sections on the tissue. A diagnosis of malignancy can usually be made on the smears. However, the tissue fragments are extremely helpful in subclassifying the neoplasm. Fine-needle aspirates are very useful in the diagnosis of malignant tumors. They are less useful in the diagnosis of benign lesions and even less useful in non-neoplastic conditions.

STAGING The staging system of Enneking and colleagues,24 which includes both soft tissue and bone sarcomas, is useful. This system has two main factors, the first of which is the biologic potential of the lesion. If the lesion is benign, it is labeled G0. If it is malignant, it is judged to be either a low-grade (G1) or a high-grade (G2) lesion; the highgrade lesions have a greater potential for metastatic spread. The second factor is the anatomic site of the lesion; that is, whether it is entirely within a surgical compartment (T1) or whether it extends outside the compartment (T2). With these classifications, a low-grade malignant tumor that is entirely within a single compartment is a 1A lesion; a low-grade lesion that extends into a second compartment is a 1B lesion; a high-grade

Chapter 82 Neoplasms of the Elbow 1133

replacement for both primary and metastatic diseases.3,54 The majority (90%) were treated for metastatic diseases. Satisfactory outcomes may be expected given that the overall prognosis of these patients is guarded, with a mean survival time of only 3 years3 (Fig. 82-1).

malignant tumor that is confined to a single compartment is a 2A lesion; and a high-grade tumor that extends into a second compartment is a 2B lesion. Any tumor that shows evidence of metastatic spread is considered a stage 3 lesion. The terminology suggested by Enneking23 describing surgical procedures is now generally accepted. Thus, if a lesion is entered at surgery, the procedure should be considered an intralesional resection; if a tumor is “shelled out,” the procedure should be considered a marginal resection; and if there is a margin of normal tissue on all aspects of the resected specimen, the operation should be considered a wide excision. For the procedure to be judged a radical resection, all the structures within the involved compartment must be resected. When the lesion involves bone, the entire bone must be removed if the procedure is to be considered a radical resection. The same terminology is applicable to amputation surgery. With these general principles in mind, we will now discuss some of the entities that are likely to be encountered in the region of the elbow.

BONE TUMORS BENIGN BONE TUMORS Osteoid Osteoma and Osteoblastoma Osteoid osteoma arising in an intra-articular location is relatively uncommon; however, it may occur in the region of the elbow. It is relatively common at the elbow, but only a few reports on the presentation,36 diagnosis,33 and management41 have appeared. This small benign bone tumor occurs in patients of any age, most commonly children and young adults. As with most bone tumors, boys and men are more commonly affected than girls and women. Unremitting pain is the usual symptom for which the patient seeks medical attention; however, progressive loss of motion may also be a characteristic feature. Pain during the night is particularly prominent. Aspirin may afford very dramatic relief of pain, a fact that may even suggest the diagnosis of osteoid osteoma. Occasionally, the pain may be experienced at a site remote from the lesion. Another peculiar

PROSTHETIC REPLACEMENT With improved designs and techniques, we have improved our outcomes with the use of prosthetic

A

B FIGURE 82-1

C

Pathologic fracture and failed effort at open reduction and internal fixation of a metastatic lesion (A). Effective palliation 1 year later with joint replacement employing a long flange and cortical allograft strut graft (B and C).

1134 Part VIII Septic and Nontraumatic Conditions

2 8

2 2

FIGURE 82-2

Distribution of 14 osteoid osteomas treated at the Mayo Clinic.

feature of this tumor is its occasional association with atrophy of the adjacent soft tissues. In the Mayo Clinic’s experience with 14 such cases, eight have occurred in the distal humerus, four in the ulna (two coronoid, two olecranon), and two in the radial head–neck region60 (Fig. 82-2). As noted previously, when osteoid osteoma occurs at or near the elbow joint, there is characteristically loss of some flexion or extension, but pronation and supination are preserved. In addition, there may be a synovial reaction that may further confuse the diagnosis. The most striking feature of these tumors is the prolonged average time required for making the diagnosis. In the Mayo Clinic’s experience, the delay to diagnosis averaged almost 2 years.60 The osteoid osteoma, by definition, is small, usually no more than 1.5 cm in diameter. Lesions that are clinically and histologically similar but are 2 cm or more in diameter are referred to as osteoblastomas; these lesions have clinical features somewhat different from those of osteoid osteoma,48 but loss of motion is a common feature.8,27 Osteoid osteoma is small when first encountered and remains small,30 further complicating the diagnosis. An extensive diagnostic evaluation is usually required in determining the precise location of the osteoid osteoma.12,34 When the patient complains of unremitting pain in the elbow, plain radiographs are obtained (Fig. 82-3). These may or may not reveal the presence of the tumor. The lesion typically appears as a central small nidus, which is a radiolucent area usually surrounded by an area of sclerosis. It is this sclerosis that is usually seen38; the central area of the nidus is more difficult to identify. When the lesion is located on the surface of the bone, there may be periosteal new bone formation that

FIGURE 82-3

Osteoid osteoma in a 10-year-old boy, upper radial shaft. Rarefied nidus with central sclerotic area and surrounding bone formation (arrow).

further obscures the nidus.36 Cronemeyer and colleagues13 described an unusual radiographic feature of osteoid osteoma in the elbow joint—subperiosteal new bone formation in adjacent bones; for example, an osteoid osteoma in the distal end of the humerus that exhibits periosteal new bone formation in the proximal radius and ulna.13 These authors concluded that “awareness of this association will prevent misdiagnosis of the benign neoplasm as an inflammatory arthritis.” Technetium-99m scintigraphy has been helpful in locating these lesions.33 If technetium-99m scintigraphy reveals no abnormality, an osteoid osteoma is unlikely; however, if the bone scan is positive, further diagnostic studies of the involved area should be undertaken (Fig. 82-4). If there is any significant synovial reaction, there may be increased uptake owing to the synovitis as well as to the lesion itself.51,52 Sometimes, multiple radiographs must be taken before the lesion can be identified. Today, CT is the diagnostic standard, however, if the tumor is so small it may be missed on this examination.55 Grossly, there is usually some sclerotic bone surrounding a central nidus. This nidus may be somewhat redder than the surrounding cortical bone and has been described as having the appearance of a small cherry. It is sometimes helpful to obtain radiographs of the excised block of tissue before the pathologist cuts into the block. Microscopic examination of the

Chapter 82 Neoplasms of the Elbow 1135

FIGURE 82-4

Patient presented with a chronic painful elbow of almost 1 year’s duration. A, Plain film was read as negative, although a generalized increased density of the olecranon might be appreciated. B, Technetium bone scan indicates intense uptake in the olecranon region. C, The patient was found to have an osteoid osteoma in the coronoid portion of the proximal ulna.

C

1136 Part VIII Septic and Nontraumatic Conditions

surrounding bone shows no unusual features; the nidus itself consists of a network of osteoid trabeculae (see Fig. 82-3). Treatment. In the past, the treatment of osteoid osteoma was surgical excision of the nidus. It is not necessary to remove all of the sclerotic bone. The main problem with this type of surgery is identification of the lesion and confirmation of its removal by the pathologist, which may be difficult. Ghelman and associates26 have described a method for localizing an osteoid osteoma intraoperatively using a scintillation probe. This technique may simplify the localization of the lesion at the time of surgery. Patients whose lesions are not completely excised will probably continue to have the same pain and will probably require a second operation.50 The authors have observed that the loss of motion so characteristic of this lesion at the elbow resolves with removal of the nidus. Hence, capsular release is not necessary as an adjunctive procedure.60 At present, the treatment of choice for most lesions is radiofrequency obliteration performed under CT direction.

Osteochondroma Osteochondroma is probably the most common benign bone tumor, but it is not very commonly encountered in the elbow. The incidence may be somewhat higher than that reflected in our surgical experience, however, because many osteochondromas in other locations are asymptomatic and presumably may also be in the region of the elbow. The osteochondroma is not inherently painful but causes symptoms by pressure on adjacent structures. The tumor may be found in a patient of any age, but it usually stops growing when skeletal maturity is reached. An osteochondroma may arise from the surface of any bone but most commonly does so in the metaphyseal region of long bones (Fig. 82-5). The tumor tends to project away from the joint along the direction of attached muscles. The tumor may be pedunculated on a stalk or may be sessile and have a broad base (Fig. 82-6). The tumor is covered by a cartilage cap, which, if it becomes markedly thickened, suggests the possibility of sarcomatous transformation. If it is more than 1 cm thick, the risk of secondary chondrosarcoma is relatively high. In children, the cartilage cap is normally thicker than in adults. Probably fewer than 1% of osteochondromas ever become malignant.29 Multiple osteochondromas sometimes occur, a condition that tends to be familial. When multiple bones are involved, there may be some element of dysplasia with the deformity and the elbow can be severely involved. Because of the possibility of sarcomatous change, probably near 10%, patients with multiple osteochondromas need to be carefully observed through periodic followup examination.

FIGURE 82-5

Osteochondroma in a 23-year-old woman. Radial shaft with cortical and medullary bone extending into tumor.

FIGURE 82-6

Osteochondroma of the distal humerus in a 41-year-old man. Note the soft tissue reaction.

Chapter 82 Neoplasms of the Elbow 1137

Osteochondromas in the region of the elbow may cause mechanical difficulties; specifically, interference with the motion of the elbow joint. In addition, the cartilage cap may impinge on important neurovascular structures. If there are symptoms or mechanical or cosmetic difficulties, complete excision of the osteochondroma, together with the overlying cartilage cap, is performed. Excision commonly involves the use of an osteotome to shave the lesion level with the underlying cortical bone. Such simple excision generally results in cure, although local recurrence may occasionally be noted, indicating that part of the cartilaginous cap was left behind. If the cap is thicker than 1 cm in an adult, the lesion must be carefully studied histologically to exclude the possibility of a sarcoma.

Giant Cell Tumor Benign giant cell tumors are occasionally encountered in the region of the elbow. In general, giant cell tumors more commonly affect women than men, contrary to the situation with most benign and malignant bone tumors. About 80% of giant cell tumors occur in persons who are older than 20 years of age. This point may be helpful in differentiating a giant cell tumor from an aneurysmal bone cyst, which may be radiographically similar but tends to occur in persons who are younger than 20 years of age. Giant cell tumors nearly always occur in the epiphyseal region and may extend to the articular surface of the bone. Campanacci and coworkers10 have attempted to grade giant cell tumors according to radiographic criteria; thus, grade 1 lesions are radiographically indolent, and grade 3 tumors are radiographically aggressive. Unfortunately, the majority of giant cell tumors are probably what Campanacci and colleagues refer to as grade 2, in which the radiographic appearance is aggressive but the tumor has not yet broken through cortical bone. Radiographic grading may be important in helping the surgeon decide on the appropriate treatment. Grossly, the tumor consists of a red, soft tissue that typically extends up the subchondral bone at the articular surface. Microscopically, a giant cell tumor shows a combination of giant cells and mononuclear cells, with a more or less uniform distribution of the giant cells. Giant cell tumors that appear to be more aggressive histologically do not necessarily behave more aggressively clinically.17 The extent of surgery required to eradicate giant cell tumors is somewhat controversial. In the region of the elbow, particularly difficult problems may be encountered. The distal end of the humerus does not lend itself well to surgical excision by curettage unless the lesion is radiographically a grade 1 lesion. Total excision of the distal end of the humerus, although it would probably be curative and prevent local recurrence, creates a very

serious problem for the reconstructive surgeon. Allograft replacement might be considered in this setting, but the decision about the method of treatment is often exceedingly difficult. Excision by curettage in other locations results in a local recurrence rate of approximately 25%. It is probably reasonable to accept this risk and to try curettage for the first treatment because the alternative of resection of the distal end of the humerus is so drastic (Fig. 82-7). However, if the tumor has already broken through the cortex into the surrounding soft structures, curettage is unlikely to be effective. For tumors of the proximal end of the ulna, curettage might be more reasonable because there is more bone to work with; hence, a larger margin of normal bone can be included in the resected specimen, whether resection is done by curettage or actual excision. Whenever possible, the treatment of choice is to pack the tumor cavity with methylmethacrylate (Fig. 82-8). This method of reconstruction has, in other locations, proved to be effective. If the proximal radial head is involved with a reasonably small tumor, it is probably best treated with simple excision.28,32 Radiation therapy for benign giant cell tumors should be avoided, if possible. In our previous experience, irradiation of benign giant cell tumors was accompanied by a significant risk of subsequent malignant transformation.

Aneurysmal Bone Cyst An aneurysmal bone cyst typically contains abundant benign giant cells in scattered zones and formerly was included among the giant cell tumors. It is different, however, because it nearly always contains blood-filled spaces, is somewhat fibrogenic, and usually has zones with osteoid formation and trabeculae of bone. An aneurysmal bone cyst may arise de novo, or a similar reactive change may be seen in various benign and even in malignant tumors of bone. It is necessary to rule out any associated pathology, because the clinical behavior of the lesion depends on the nature of the underlying pathology. In the Mayo Clinic’s experience with 134 aneurysmal bone cysts unrelated to pre-existing disease, 43% occurred in men. In contrast to the age of predilection for giant cell tumors, 78% of the patients were younger than 20 years of age. Only eight examples of aneurysmal bone cysts were found in the region of the elbow. Pain and swelling are the most common features.14 Radiographically, the diseased area is sometimes confusingly like that of a malignant tumor, but the zone of rarefaction is usually well circumscribed, eccentric, and associated with an obvious soft tissue extension of the process (Fig. 82-9). Classically, the soft tissue extension is produced by bulging of the periosteum and a resultant layer of radiographically visible new bone that delimits the periphery of the tumor. Fusiform expansion may be

1138 Part VIII Septic and Nontraumatic Conditions

FIGURE 82-7

A, Gross destruction of the distal humerus due to a locally aggressive giant cell tumor. The patient was treated by resection of the distal humerus and replacement with joint replacement arthroplasty. B, The arc of motion is 15 to 140 degrees with no pain, and there is no evidence of implant loosening at 3 years.

FIGURE 82-8

Giant cell tumor involving the lateral condyle in a 25-year-old patient. The lesion was curetted, and the defect was filled with methylmethacrylate.

FIGURE 82-9

Aneurysmal bone cyst of the ulna in a 5year-old boy. Note circumscription of the mass, which is associated with destruction of the shaft and the end of the bone.

Chapter 82 Neoplasms of the Elbow 1139

produced, especially when small bones such as a fibula or a rib are affected. The lesion is usually metaphyseal in location.6,18 Pathologically, an aneurysmal bone cyst contains anastomosing cavernous spaces that usually constitute the bulk of the lesion. The spaces are usually filled with unclotted blood, which may well up into, but does not spurt from, the tumor when it is unroofed. The most important factor to recognize histologically is the benign quality of the constituent cells.16,46 Telangiectatic osteo-

sarcoma may simulate aneurysmal bone cyst when viewed at low magnification. Treatment is essentially the same as that for benign giant cell tumors. Curettage and bone grafting are usually required, and the majority of lesions treated in this way will be cured. Perhaps 25% of these cases will recur and require additional surgery.

OTHER BENIGN BONE TUMORS AND TUMOR SIMULATORS Benign tumors of bone at the elbow other than those previously discussed may rarely be encountered (Fig. 82-10). In addition, a number of lesions may occur in any bone and may simulate or mimic a primary bone tumor (Figs. 82-11 through 82-13). Benign cartilage

FIGURE 82-10

Histiocytosis X producing a well-defined rarefaction of the humeral shaft. This completely benign lesion is associated with a good prognosis, especially if it is solitary.

FIGURE 82-12 Fibrous dysplasia producing extensive changes on both sides of the joint.

FIGURE 82-11 Paget’s disease of the proximal two thirds of the ulna. This classic lesion is associated with pathologic fracture and extends to the end of the bone. Paget’s disease of bone is very rare in patients younger than 40 years of age.

1140 Part VIII Septic and Nontraumatic Conditions

tumors are very rare at the elbow; nevertheless, they do occasionally occur (Fig. 82-14).

MALIGNANT BONE TUMORS Lymphoma Currently, the term malignant lymphoma is used for those small round cell tumors of bone that

previously were referred to as reticulum cell sarcoma.42 Lymphoma tends to occur in middle-aged or elderly adults; young persons are uncommonly affected. Patients with lymphoma generally present with pain and perhaps swelling in the region of the lesion. The tumor may arise primarily in any bone, including bones in the region of the elbow (Fig. 82-15).

FIGURE 82-13 A and B, Cyst of upper part of the ulna secondary to degenerative joint disease at the elbow.

FIGURE 82-14 A and B, Benign chondroblastoma of the distal end of the humerus in a 25-year-old man. Note the discrete zone of rarefaction. Such lesions are more innocuous than giant cell tumors.

Chapter 82 Neoplasms of the Elbow 1141

FIGURE 82-15 Radiograph of assumed “avascular necrosis” of distal humerus (A); lymphoma found eroding the posterior portion of the trochlea was excised (B).

A

B

The radiographic features of lymphoma are nonspecific (Fig. 82-16). There is usually a diffuse, destructive, mottled appearance with indistinct margins. Variable degrees of sclerosis may be present in the lesion; the cortical bone is usually eroded, and the tumor may extend into the adjacent soft tissues. Periosteal new bone formation usually is not a prominent feature. Grossly, lymphoma tissue is usually gray or white and very soft. Microscopically, malignant lymphomas fit into the group of small round cell tumors. Under low power, the tumor shows a permeative pattern. The infiltrate tends to fill up the marrow cavity without destroying medullary bone. When a diagnosis of lymphoma in bone is made, it is important to stage the disease process. If the disease is localized to one site, the prognosis is excellent.40 About a fourth of patients will have multiple bones involved. Even these patients do well. However, if there are other sites, such as liver, spleen, or lymph nodes, the survival rate decreases dramatically. Lymphoma is generally treated with radiation therapy if there is only a solitary lesion of bone. For lymphoma in the region of the elbow joint, some morbidity can probably be expected from the radiation therapy. Radiation therapists generally try to avoid circumferential treatment of an extremity to allow some normal lymphatic channels to remain open. Failure to do so may result in significant swelling distal to the treatment area.

B

FIGURE 82-16 Malignant lymphoma producing malignant-appearing destruction of the distal part of the humerus in a 60-year-old woman.

It may be difficult or impossible to avoid treating the entire circumference of the extremity in the region of the elbow. In addition, when radiation exceeds approximately 4000 rad, radiation therapists generally try to direct treatment away from the articular surface.

1142 Part VIII Septic and Nontraumatic Conditions

FIGURE 82-17 Recurrent Ewing’s sarcoma with a cyst-like lesion of the upper half of the ulna in a 21-year-old woman. The original tumor had been treated 10 years previously.

There is no clear-cut or obvious advantage to the use of adjunctive chemotherapy at the time of initial treatment if only a solitary lesion is present.49 In general, lymphoma presenting primarily in bone has a long-term survival of about 60%.7 However, no figures are available for the occurrence of lymphoma of bone specifically at the elbow.

Ewing’s Sarcoma Ewing’s sarcoma may arise in any bone, including those in the region of the elbow. Ewing’s sarcoma is more frequently found in children than adults; very young infants, however, very rarely have this tumor. The usual radiographic appearance of Ewing’s sarcoma is that of a mottled or moth-eaten destructive lesion that may contain both lytic and blastic areas (Fig. 82-17). Although not pathognomonic, there is frequently periosteal reactive new bone, which may form layers, forming the “onion skin” appearance that is reported to be typical of this disease. The radiographic appearance combined with the presence of fever and an elevated erythrocyte sedimentation rate may lead to the erroneous diagnosis of osteomyelitis.2 Grossly, Ewing’s sarcoma may be very soft or even semiliquid; indeed, the appearance may simulate the purulence of infection. Microscopically, Ewing’s sarcoma is very cellular, composed of small round cells that are remarkably similar to one another. Periosteal new bone formation, if present, may complicate the histologic interpretation.47 Treatment of Ewing’s sarcoma of bone in the region of the elbow is similar to that for other sites. The local lesion is generally treated with radiation therapy, and systemic combination chemotherapy is generally used in an attempt to prevent micrometastases. Although there is a growing trend toward considering a larger role for surgery in the treatment of the primary lesion, there is little enthusiasm for resecting malignant tumors in the region of the elbow because it is difficult to achieve adequate margins in this region without damaging important normal structures.44 Even if an adequate resection could be achieved, satisfactory reconstruction would be difficult or impossible. This is particularly true when one deals with children with open physes. The

FIGURE 82-18 Grade 4 osteosarcoma of the distal end of the humerus in a patient with Paget’s disease of the entire bone.

treatment for Ewing’s sarcoma is the same as that for lymphoma in the region of the elbow.5,31 A major side effect is soft tissue fibrosis causing a stiff joint.

Osteosarcoma Osteosarcoma is the most common bone malignancy except for myeloma. Radiographically, osteosarcoma usually appears to be aggressive, with evidence of cortical destruction and reactive periosteal new bone formation. In the distal humerus, the classic “sunburst” appearance may be evident. The precise extent of the lesion may not be apparent on plain radiographs (Fig. 82-18). The tumor can usually be more accurately assessed with a technetium or gallium bone scan. Other

Chapter 82 Neoplasms of the Elbow 1143

studies, such as CT, may be used to help determine the extent of soft tissue involvement if it is present. Magnetic resonance imaging may be helpful in further defining both the extent of soft tissue involvement and the extent of intramedullary involvement. The reactive new bone formation at the periphery of the lesion should not be sampled for biopsy because this will simply lead to confusion in the interpretation of the histologic findings. If there is a soft tissue extension of the tumor, this is the area that is best to biopsy because it is usually the most malignant and the easiest to process in the pathology laboratory. About one half of these tumors are predominantly fibrous or cartilaginous, and the remainder are predominantly bone forming. Because any one of these three types of differentiation may predominate, the lesions may be subtyped into fibroblastic, chondroblastic, or osteoblastic osteosarcoma. This subclassification may be important because the osteoblastic subtype appears to have a worse prognosis than the other two subtypes.9,15,19,35,56-58 Malignant fibrous histiocytoma can also show areas of matrix production.20 Yet, only one of the 83 tumors listed as malignant fibrous histiocytoma in the Mayo Clinic files occurred in the elbow region. From a practical standpoint, the clinical management of this malignancy is essentially identical with that of osteosarcoma (Fig. 82-19). In the author’s own experience, 8% to 10% of patients with newly diagnosed osteosarcoma are found

FIGURE 82-19 Grade 4 malignant fibrous histiocytoma producing malignant-appearing destruction of the upper part of the ulna in a 45-year-old man.

to have metastatic disease, either by plain radiography or CT.53 The usual treatment of osteosarcoma, as of other radioresistant malignant bone tumors, is surgical ablation. For many years, amputation was required. However, today the majority of patients with osteosarcoma can be managed with various limb salvage procedures. Neoadjuvant chemotherapy is generally employed before one proceeds with surgery, and additional chemotherapy is usually offered after surgery. The prognosis for patients with osteosarcoma today is much improved; 70% to 90% of such patients may be long-term survivors.

METASTATIC TUMORS There is no particular predilection for metastatic disease to involve the elbow. Yet extensive destruction is observed on occasion from several tumor types. Treatment is most commonly joint replacement (Fig. 82-20). In the editor’s experience, 18 of 20 conditions treated with joint replacement were metastatic. Patients do well in general with this palliative treatment. Complications relate to nerve dysfunction and stiffness.3

SOFT TISSUE TUMORS Mesenchymal soft tissue tumors, especially the malignant types, are probably the least understood of all tumors. There are numerous varieties of mesenchymal tumors, but most of them are rarely encountered. A full discussion of all of these tumors is well beyond the scope of this chapter. Many benign soft tissue tumors are commonly encountered; however, because some soft tissue sarcomas may grow very slowly, both the patient and the physician may be misled into thinking that a soft tissue mass is benign. When this happens, a definitive diagnosis may be delayed, sometimes for years. When the patient does seek medical attention, it is common for the physician to perform a biopsy procedure that may jeopardize subsequent surgical care. As with bone tumors, proper placement of the biopsy incision is critical, and any subsequent resection surgery for malignant tumors demands that the biopsy site be included in the resected specimen. If the biopsy incision is not well placed, inclusion of the site at surgery may be difficult or impossible to achieve. If the mass is small and is situated in a favorable location, it is far preferable to perform an excisional biopsy, leaving a margin of normal tissue on all aspects of the suspected lesion. If an incisional biopsy is performed, sufficient tissue must be removed to allow adequate representative sampling of the tumor so that

1144 Part VIII Septic and Nontraumatic Conditions

FIGURE 82-20 A, Metastatic adenocarcinoma involving the lateral aspect of the left elbow, including the capitellum and radial head. B, The extent of involvement is revealed most dramatically by technetium bone scan. C, Complete resection of the distal humerus and proximal radius and insertion of a Mayo modified Coonrad implant was effective in restoring function within 3 weeks of surgery.

Chapter 82 Neoplasms of the Elbow 1145

the pathologist can arrive at the correct diagnosis. Perhaps no other factor is as important in the management of patients with soft tissue tumors as the proper performance of the biopsy procedure. Patients may complain of a lump or pain, or both. Small painful lumps may represent benign tumorsneurilemoma (schwannoma), neurofibroma, vascular myoma, glomus tumor, or fat necrosis. Sometimes, these lesions may be occult, particularly when they are small and buried in the deep soft tissues. When the patient complains of well-localized pain, these entities should be considered. The presence of a slowly growing mass that has been present perhaps for several years should lead to a suspicion of sarcomas such as synovial sarcoma, clear-cell sarcoma, or even a well-differentiated sarcoma of a more common histologic type, such as a liposarcoma or malignant fibrous histiocytoma. When the lesion is located in the upper extremity, epithelioid sarcoma should be considered. Some of the commonly encountered soft tissue lumps may be reasonably diagnosed on the basis of the history and physical examination alone. This is particularly true for lipomas, which are commonly encountered by all physicians. When the lesion is asymptomatic and has characteristic features on the clinical examination, biopsy is probably not necessary. However, caution is needed and follow-up assessment is appropriate because even the most benign-appearing soft tissue tumor may be malignant. If a sarcoma is suspected, then a full battery of routine laboratory tests should be obtained. Plain radiographs may be helpful, particularly if the radiologist uses special soft tissue techniques. Calcium or even ossification may be present within the lesion. In addition, the relationship of the lesion to the surrounding structures may be ascertained. This is particularly true if there is erosion of the underlying skeleton. If the lesion is totally lucent and has very sharply circumscribed margins, it may be a lipoma. If, however, the lesion has irregular margins and a nonhomogeneous density, sarcomatous change must be suspected. Magnetic resonance imaging is particularly valuable in the assessment of soft tissue tumors. In summary, for soft tissue tumors, when the diagnosis is in doubt, as much information as possible should be obtained before the performance of the biopsy procedure.

multiple lipomas have occurred. The tumor is simply a localized collection of adipose tissue that is histologically and chemically similar to ordinary fat. Most lipomas are small, asymptomatic, and relatively dormant in that they seem to remain approximately the same size. Occasionally, however, the tumor may grow and become symptomatic. If there is trauma to the area, necrosis may develop within the lipoma, and this is usually symptomatic. Most lipomas consist almost entirely of adipose tissue; however, there may be increased vascularity, in which case the lesion is referred to as angiolipoma.21 Most of these lesions can be easily and confidently diagnosed on the basis of the clinical examination alone; however, some lipomas may not have the clinical characteristics of the usual subcutaneous lipoma and may require further diagnostic modalities. Surgical excision should be considered for lipomas that increase in size, are symptomatic or cosmetically undesirable, or interfere with function and in situations when the diagnosis is not certain (Fig. 82-21). For most such tumors, a simple marginal excision is all that is

BENIGN SOFT TISSUE TUMORS Lipoma Lipoma is probably the most frequently encountered benign soft tissue neoplasm and is the most common tumor in the elbow region. It is usually solitary, but

FIGURE 82-21 Expanding, prominent soft tissue mass in the cubital space (A) was found to be a benign lipoma (B).

1146 Part VIII Septic and Nontraumatic Conditions

indicated. The vulnerability of the neurovascular structures is of particular concern for lipoma of the antecubital space. When a lipoma is located within the belly of a muscle, it may be necessary to sacrifice some normal muscle tissue on all aspects to minimize the risk of local recurrence. At the elbow, this can cause permanent stiffness.

Glioma The editor has encountered an instance of a glioma in the anticubital space. Diagnosis was delayed 2 years, although the pain was “unbearable.” Complete relief of symptoms was effected with resection.

Ganglion A ganglion is a cystic lesion generally found in the hands, wrists, and feet, but it may be found less commonly in the region of the elbow. A true ganglion has no or only a poorly defined synovial lining. Although the ganglion may connect with the joint, it does not always do so; indeed, the lesion may occur within a tendon, in a muscle, or even on occasion in bone. Treatment is simple excision, ensuring that the entire lesion has been removed and, as with the lipoma, that the neurovascular elements are carefully protected. Not all ganglia require excision, however, and most patients may be treated symptomatically.

Myxoma A myxoma occasionally occurs in the soft tissues at the elbow. This lesion is soft, well circumscribed, and myxoidal. Histologically, the lesion is hypocellular and contains stellate cells in a myxoid stream. A myxoma is relatively small and is usually encountered in the superficial soft tissues. It is not uncommon for this tumor to arise within the substance of a major muscle. The treatment for myxoma is excision; however, a wide excision, rather than a marginal resection, is probably indicated because this tumor tends to recur if it is marginally excised.

most frequently encountered in the small joints of the fingers, whereas the diffuse form is most commonly found in the knee joint. At the elbow, swelling, with a suggestion of increased thickening of the synovium, may be present, but motion loss is always present. Radiographs may reveal cystic erosions on either side of the joint (Fig. 82-22). When erosions are found and there is no loss of joint space and no demineralization of the surrounding bone, the diagnosis should be suspected. In most cases of pigmented villonodular synovitis, however, there is no bony erosion but there is evidence of lobular swelling of the soft tissues.4 Microscopic study shows a stromal background of reticulin and collagen fibers, in which various different cells may be found. The firm, nodular lesions have more collagenous stroma, whereas the soft villous lesions have less stroma. In the nodular form, the nodule may be simply excised with the expectation that a cure will be achieved in most cases. However, the results of treatment of the diffuse form are likely to be followed by local recurrence, which is more frequent when there is evidence of bony erosion. Even multiple synovectomies have not always been curative; because of this, various alternative treatments have been attempted. Radiation therapy has been used, but there is no convincing evidence that such treatment will actually eliminate the disease and prevent local recurrences. High doses of radiation are avoided at the elbow joint. Synovectomy is the treatment of choice, but the incidence of recurrence is at least 33% with open procedure.43 This may be less with arthroscopic procedures (Fig. 82-23). If synovectomy leads to symptomatic local recurrence, arthrodesis is considered in most joints. At the elbow, however, because this joint

Pigmented Villonodular Synovitis In the past, pigmented villonodular synovitis had various names, including xanthoma, xanthogranuloma, giant cell tumor of the tendon sheath, and myeloplaxoma. This disease probably belongs in the middle of the spectrum of diseases, within the general category of fibrous histiocytoma. It involves the synovium, bursae, or tendon sheaths. The knee is the most common site of involvement. In the authors’ experience, only two cases occurred in the elbow joint.43 This is not surprising, because Pimpalnerkar43 reports that only 18 cases have been cited in the literature through 1998. Clinically, there are two forms of the disease: nodular and diffuse. The nodular or localized form is probably

FIGURE 82-22 Pigmented villonodular synovitis in a 17year-old girl, with a 3-year history of pain and swelling. Note cystic erosions.

Chapter 82 Neoplasms of the Elbow 1147

FIGURE 82-23 Arthroscopic synovectomy is now the treatment of choice for pigmented villonodular synovitis.

does poorly with an arthrodesis, replacement arthroplasty would appear to be the treatment of choice.

Synovial Chondromatosis Chondromatosis is a benign, tumorous, multifocal, chondromatous, or chondro-osseous metaplastic proliferation involving the subsynovial connective tissue of joints, tendon sheaths, or bursae (see Chapter 83). The process can involve any joint. The average age of the patients is about 40 years; men are affected more often than women. Symptoms include pain and limited motion. The duration of symptoms may be long or relatively short before diagnosis is made. In the Mayo Clinic series, only two thirds of the radiographs showed radiopaque masses (Fig. 82-24).37 Diagnosis is difficult because the radiograph may not reveal ossified bodies even when they are present. When the radiographic diagnosis is indefinite and symptoms persist without any other obvious cause, diagnostic arthrotomy or arthroscopy is indicated. Because osteochondromatosis may be sharply localized and may not be a diffuse condition of the entire synovium, careful inspection of the whole synovial lining is important. Generally, diagnosis can be made by the gross appearance and confirmed by biopsy. Grossly, nodules of cartilage of varying sizes are seen embedded in the synovium that may be markedly thickened. Histologically, nodules of cartilage are found within the synovium. The authors have seen one example of synovial chondromatosis of the elbow undergo malignant change to chondrosarcoma.

FIGURE 82-24 Synovial chondromatosis of the elbow. Note that a small mineralized focus is evident in the antecubital fossa.

The treatment of osteochondromatosis consists of removing any loose osteochondromatous bodies and the involved synovium from which they arise. In general, complete synovectomy is necessary and today is done arthroscopically. The condition may recur because nests of synovium may be left behind. If this happens, a second procedure, maybe even an arthrotomy, is necessary. Long-standing synovial osteochondromatosis creates secondary osteoarthritis (see Chapters 83 and 85).

Myositis Ossifications (Heterotopic or Ectopic Ossification) Heterotopic ossification, often erroneously called myositis ossificans, may occur near the elbow, either in muscle or in other soft tissue. In its early, or “florid,” stage, there may be such pronounced cellular activity that it may be mistaken for sarcoma.1 The relative rarity of this disease has delayed understanding of the peculiar tissue reaction associated with it. The topic has been thoroughly reviewed in Chapter 31. A similar non-neoplastic benign, reactive process may occur in the deeper portions of the skin. The poorly defined small mass that is found may also show prominent mitotic activity. The lesion is called proliferative fasciitis and has been mistaken for entities such as liposarcoma or fibrosarcoma.11 The rapidly proliferating cells again do not show true anaplasia. Another related entity is proliferative myositis.25 In this condition, there is a tumefactive, intramuscular proliferation of benign fibroblastic cells, but no discernible osseous metaplasia. Mitotic activity may be pronounced, making it possible to mistake this lesion for a malignant tumor.

1148 Part VIII Septic and Nontraumatic Conditions

MALIGNANT SOFT TISSUE TUMORS Synovial Sarcoma Synovial sarcoma, or synovioma, is a malignant soft tissue tumor that usually arises in the extremities or limb girdles; about 70% of lesions involve the lower extremity, most commonly the thigh, but this tumor does occur in the region of the elbow. In the Mayo Clinic experience, only the tumors of about 20% of patients had suggestive evidence of origin from anatomic synovium.61 This tumor can be found in patients of any age, but young or middle-aged adults seem to be most commonly affected. Symptoms may be present for many years before diagnosis. In the Mayo Clinic experience, the average duration of symptoms before diagnosis was 21/2 years. The radiographic examination may be particularly helpful because about a third of patients with synovial sarcoma show evidence of calcification. When calcification is found in a soft tissue tumor, synovial sarcoma should be included in the differential diagnosis. This tumor can invade the bone on a rare occasion.39 The tumor is lobular, circumscribed, and gray and may contain areas of calcification, hemorrhage, necrosis, or cyst formation. Classically, synovial sarcoma has a bimorphic histologic pattern; that is, a combination of slender spindle cells and larger epithelial-appearing cells that may form glands or even show squamous change. Close cooperation between the pathologist and the surgeon is essential if the diagnosis is to be made at surgery. Local excision of the tumor generally results in a local recurrence; with local recurrence, the prognosis for survival is lessened. In the Mayo Clinic experience, the overall 5-year survival rate was 23%, with a median survival time of 39 months.59 However, for patients treated after 1960, the 5-year survival rate has been 55% and the 10-year rate has been 38%. Patients who had the best prognosis were those treated with wide excision or radical surgery. Today, the authors usually combine radiation therapy and surgery; with this approach local recurrence occurs in only about 5% of cases. We do not routinely employ lymphadenectomy unless the regional nodes are clinically involved.

Liposarcoma The pathologic diagnosis of liposarcoma may be difficult, especially when the lesion is histologically of low grade. A lipoma that shows evidence of growth should be suspected of being malignant. Roentgenograms are not as diagnostic for liposarcoma as they are for lipoma, but the combination of more dense and less dense tissues may be characteristic of liposarcoma. CT is very helpful not only in defining the extent of the lesion but

also in showing relative densities. Histologically, liposarcomas are recognized because of their component of malignant lipoblasts. Liposarcomas may arise in any part of the body and are occasionally found at the elbow. Older adults are more commonly affected than younger persons. The extent of treatment depends, at least in part, on both the size and the grade of the tumor. Lesions that are grade 1 or grade 2 probably can be safely excised with a margin of normal tissue on all aspects, but this can be very difficult at the elbow. If the lesion recurs, it can probably be excised without the need for radical surgery. However, the higher grade lesion should probably be treated with wide resection and perhaps with radical resection unless the tumor can be totally and widely removed without sacrifice of limb function. This is difficult to do with tumors in the region of the elbow, and amputation may be necessary. As with other soft tissue sarcomas, the authors usually combine radiation therapy and surgery. In the Mayo Clinic experience, more than 50% of all patients treated for liposarcoma may expect to survive for 5 years and be free from evidence of disease progression.45

Malignant Fibrous Histiocytoma Malignant fibrous histiocytoma is now the most commonly encountered malignant soft tissue tumor of the extremities and, as noted earlier, may also occur in the bone. The upper extremity and, more specifically, the region of the elbow are not uncommonly affected by this tumor. This tumor can arise in any age group. As with other malignant soft tissue tumors, there are no unique clinical or radiographic features characteristic of this lesion. Both CT and magnetic resonance imaging have been used to define the extent and relationship of the tumor with surrounding structures. Grossly, this tumor is usually soft and pink or yellow. It may vary in consistency and color from patient to patient and, indeed, even in different areas of the same tumor. There may also be an area of firm, white tumor adjacent to a yellow, mucoid, necrotic area. Tumors arising in the upper extremity in general tend to be smaller than those arising in the buttock or lower extremity, probably because they are noticed by the patient earlier in their evolution. Microscopically, the lesion may vary from the most benign-appearing spindle cells with small nuclei and relatively few mitotic figures, such as those seen in a grade 1 lesion, to the wildly anaplastic, bizarre histiocytic cells found in grade 4 lesions. There is growing evidence that the grade of the lesion as manifested by anaplasia is a more important predictor of behavior than are the histologic subtypes. There is no one universally acceptable treatment for this lesion. Relatively small tumors may be excised with

Chapter 82 Neoplasms of the Elbow 1149

FIGURE 82-25 A and B, Epithelioid sarcoma that has eroded into and destroyed much of the distal part of the humerus in a 27-year-old woman.

a margin of normal tissue on all aspects. Larger lesions or those that are histologically higher grade require a more aggressive approach. In this situation, the authors now favor a course of preoperative radiation therapy using approximately 5000 rad, followed after several weeks by excision of the lesion with a margin of normal tissue on all aspects. Adjunctive chemotherapy has not been helpful in our experience.

Epithelioid Sarcoma Epithelioid sarcoma is a rare, slowly growing malignant tumor that usually begins in the superficial tissues of the hand or forearm and may occur at the elbow. The tumor is made up of small, poorly defined tumor nodules composed of epithelioid cells or histiocytic aggregates. Sometimes, central necrosis in these aggregates of cells suggests that the disease is a granulomatous infection. There is often a delay in recognition of the malignant nature of the disease, and the long-term prognosis for life is poor. Rarely, the tumor erodes into underlying bones (Figs. 82-25 and 82-26). Lymphatic or hematogenous metastasis is common, especially in the later stages of this disease. Treatment for cure requires wide excision. Marginal or intralesional excision almost always results in tumor recurrence and subsequent disease progression. The relatively slow growth of the tumor and the unusual nature of the histology may tend to dissuade the surgeon from performing adequate surgery.

FIGURE 82-26 Another epithelioid sarcoma that has caused osseous destruction at the elbow.

HEMOPOETIC INVOLVEMENT Although certainly not characteristic, the elbow may be involved from hemopoetic neoplastic processes. The key feature is having a level of suspicion. A history of pain, often at night, without an easily identified or explained cause is almost always present for infection or neoplasm. Treatment is as for the underlying pathology. Diagnosis may be made by open biopsy or arthroscopy.

1150 Part VIII Septic and Nontraumatic Conditions

References 1. Ackerman, L. N.: Extra-osseous localized non-neoplastic bone and cartilage formation (so-called myositis ossificans): Clinical and pathologic confusion with malignant neoplasms. J. Bone Joint Surg. 40A:279, 1958. 2. Angervall, L., and Enzinger, F. M.: Extraskeletal neoplasm resembling Ewing’s sarcoma. Cancer 36:240, 1975. 3. Athwal, G. S., Chin, P. Y., Adams, R. A., and Morrey, B. F.: Coonrad-Morrey total elbow arthroplasty for tumours of the distal humerus and elbow. J. Bone Joint Surg. 87B:1369, 2005. 4. Atmore, W. G., Dahlin, D. C., and Ghormley, R. K.: Pigmented villonodular synovitis: A clinical and pathologic study. Minn. Med. 39:196, 1956. 5. Bacci, G., Picci, P., Gitelis, S., Borghi, A., and Campanacci, M.: The treatment of localized Ewing’s sarcoma: The experience at the Istituto Ortopedico Rizzoli in 163 cases treated with and without adjuvant chemotherapy. Cancer 49:1561, 1982. 6. Bonaledarpeun, A., Levy, W. M., and Aegerter, E.: Primary and secondary aneurysmal bone cyst: A radiologic study of 75 cases. Radiology 126:75, 1978. 7. Boston, H. C., Jr., Dahlin, D. C., Ivins, J. C., and Cupps, R. E.: Malignant lymphomas (so-called reticulum cell sarcoma) of bone. Cancer 34:1131, 1974. 8. Brabants, K., Geens, S., and van Damme, B.: Subperiosteal juxta-articular osteoid osteoma. J. Bone Joint Surg. 68:320, 1986. 9. Campanacci, M., and Cervelatti, G.: Osteosarcoma: A review of 345 cases. Ital. J. Orthop. Traumatol. 1:5, 1975. 10. Campanacci, M., Giunti, A., and Olmi, R.: Giant cell tumors of bone: A study of 209 cases with long-term follow-up in 130. Ital. J. Orthop. Traumatol. 1:249, 1975. 11. Chung, E. B., and Enzinger, F. M.: Proliferative fasciitis. Cancer 36:1450, 1975. 12. Corbett, J. M., Wilde, A. H., McCormick, L. J., and Evarts, C. M.: Intra-articular osteoid osteoma, a diagnostic problem. Clin. Orthop. Relat. Res. 98:225, 1974. 13. Cronemeyer, R., Kirchmer, N. A., Desmet, A. A., and Neff, J. R.: Intra-articular osteoid osteoma of the humerus simulating synovitis of the elbow: A case report. J. Bone Joint Surg. 63A:1172, 1981. 14. Dahlin, D. C.: Bone Tumors: General Aspects and Data on 6221 Cases. Springfield, IL, Charles C Thomas, 1978, p. 445. 15. Dahlin, D. C.: Pathology of osteosarcoma. Clin. Orthop. Relat. Res. 111:23, 1975. 16. Dahlin, D. C., Besse, B. E., Jr., Pugh, D. G., and Ghormley, R. K.: Aneurysmal bone cysts. Radiology 64:56, 1955. 17. Dahlin, D. C., Cupps, R. E., and Johnson, E. W., Jr.: Giant cell tumor: A study of 195 cases. Cancer 25:1061, 1970. 18. Dahlin, D. C., and McLeod, R. A.: Aneurysmal bone cyst and other non-neoplastic conditions. Skeletal Radiol. 8:243, 1982. 19. Dahlin, D. C., and Unni, K. K.: Osteosarcoma of bone and its important recognizable varieties. Am. J. Surg. Pathol. 1:61, 1977.

20. Dahlin, D. C., Unni, K. K., and Matsuno, T.: Malignant (fibrous) histiocytoma of bone—fact or fancy? Cancer 39:1508, 1977. 21. Dionne, G. P., and Seemayer, T. A.: Infiltrating lipomas and angiolipomas revisited. Cancer 33:732, 1974. 22. Edeiken, J., and Hodes, P. J.: Roentgen Diagnosis of Diseases of Bone, Vols. 1 and 2, 2nd ed. Baltimore, Williams & Wilkins, 1973. 23. Enneking, W. F.: Musculoskeletal Tumor Surgery, Vol. 1. New York, Churchill Livingstone, 1983. 24. Enneking, W. F., Spanier, S. S., and Goodman, M. A.: A system for the surgical staging of musculoskeletal sarcoma. Clin. Orthop. Relat. Res. 153:106, 1980. 25. Enzinger, F. M., and Dulcey, F.: Proliferative myositis: Report of thirty-three cases. Cancer 20:2213, 1967. 26. Ghelman, B., Francesca, M., Thompson, F. M., William, D., and Arnold, W. D.: Intra-operative radioactive localization of an osteoid osteoma: Case report. J. Bone Joint Surg. 63A:826, 1981. 27. Gil-Albarova, J., and Amillo, S.: Osteoblastoma causing rigidity of the elbow: A case report. Acta Orthop. Scand. 62:602, 1991. 28. Goldenberg, R. R., Campbell, C. J., and Bonfiglio, M.: Giant cell tumor of bone: An analysis of 218 cases. J. Bone Joint Surg. 52A:621, 1970. 29. Harsha, W. N.: The natural history of osteocartilaginous exostoses (osteochondroma). Am. Surg. 20:65, 1954. 30. Jaffe, H. L., and Lichtenstein, L.: Osteoid-osteoma: Further experience with this benign tumor of bone; with special reference to cases showing the lesion in relation to shaft cortices and commonly misclassified as instances of sclerosing non-suppurative osteomyelitis or cortical-bone abscess. J. Bone Joint Surg. 22:645, 1940. 31. Johnson, R. E., and Pomeroy, T. C.: Evaluation of therapeutic results in Ewing’s sarcoma. A.J.R. 123:583, 1975. 32. Larsson, S. E., Lorentzon, R., and Boquist, L.: Giant-cell tumor of bone: A demographic, clinical, and histopathological study of all cases recorded in the Swedish Cancer Registry for the years 1958 through 1968. J. Bone Joint Surg. 57A:167, 1975. 33. Lenoble, E., Sergent, A., and Goutallier, D.: Preoperative, intraoperative, and immediate postoperative skeletal scintigraphy to locate and facilitate excision of an osteoid osteoma of the coronoid process. J. Shoulder Elbow Surg. Sept./Oct.:323, 1994. 34. Marcove, R. C., and Freiberger, R. H.: Osteoid osteoma of the elbow: A diagnostic problem. Report of four cases. J. Bone Joint Surg. 48A:1185, 1966. 35. Matsuno, T., Unni, K. K., McLeod, R. A., and Dahlin, D. C.: Telangiectatic osteogenic sarcoma. Cancer 38:2538, 1976. 36. Moser, R. P., Jr., Kransdorf, M. J., Brower, A. C., Hudson, T., Aoki, J., Berrey, B. H., and Sweet, D. E.: Osteoid osteoma of the elbow: A review of six cases. Skeletal Radiol. 19:181, 1990. 37. Murphy, F. P., Dahlin, D. C., and Sullivan, C. R.: Articular synovial chondromatosis. J. Bone Joint Surg. 44A:77, 1962. 38. Norman, A., and Dorfman, H. D.: Osteoid osteoma inducing pronounced overgrowth and deformity of bone. Clin. Orthop. Relat. Res. 110:223, 1975.

Chapter 82 Neoplasms of the Elbow 1151

39. O’Donnell, P., Diss, T. C., Whelan, J., and Flanagan, A. M.: Synovial sarcoma with radiological appearances of primitive neuroectodermal tumour-Ewing sarcoma: Differentiation by molecular genetic studies. Skeletal Radiol. 35:233, 2006. 40. Ostrowski, M. L., Unni, K. K., Banks, P. M., Shives, T. C., Evans, R. G., O’Connell, M. J., and Taylor, W. F.: Malignant lymphoma of bone. Cancer 58:2646, 1986. 41. Otsuka, N. Y., Hastings, D. E., and Fornasier, V. L.: Osteoid osteoma of the elbow: A report of six cases. J. Hand Surg. 17:458, 1992. 42. Parker, F., Jr., and Jackson, H., Jr.: Primary reticulum cell sarcoma of bone. Surg. Gynecol. Obstet. 68:45, 1939. 43. Pimpalnerkar, A., Barton, E., and Sibly, T. F.: Pigmented villonodular synovitis of the elbow. J. Shoulder Elbow Surg. 7:71, 1998. 44. Pritchard, D. J., Dahlin, D. C., Dauphine, R. T., Taylor, W. E., and Beabout, J. W.: Ewing’s sarcoma: A clinicopathological and statistical analysis of patients surviving five years or longer. J. Bone Joint Surg. 57A:10, 1975. 45. Reszel, P. A., Soule, E. H., and Coventry, M. B.: Liposarcoma of the extremities and limb girdles: A study of two hundred twenty-two cases. J. Bone Joint Surg. 48A:229, 1966. 46. Sanerkin, N. G., Mott, M. G., and Roylance, J.: An unusual intraosseous lesion with fibroblastic, osteoclastic, osteoblastic, aneurysmal, and fibromyxoid elements: “Solid” variant of aneurysmal bone cyst. Cancer 51:2278, 1983. 47. Schajowicz, F.: Tumors and Tumor-like Lesions of Bones and Joints. New York, Springer-Verlag, 1981, p. 581. 48. Schajowicz, F., and Lemos, C.: Osteoid osteoma and osteoblastoma: Closely related entities of osteoblastic derivation. Acta Orthop. Scand. 41:272, 1970. 49. Schwartz, H. S., Unni, K. K., and Pritchard, D. J.: Pigmented villonodular synovitis. Clin. Orthop. Relat. Res. 247:243, 1989.

50. Shoji, H., and Miller, T. R.: Primary reticulum cell sarcoma of bone: Significance of clinical features upon the prognosis. Cancer 28:1234, 1971. 51. Sim, F. H., Dahlin, D. C., and Beabout, J. W.: Osteoid osteoma: Diagnostic problems. J. Bone Joint Surg. 57A:154, 1975. 52. Snarr, J. W., Abell, M. R., and Martel, W.: Lymphofollicular synovitis with osteoid osteoma. Radiology 106:557, 1973. 53. Spanos, P. K., Payne, W. S., Ivins, J. C., and Pritchard, D. J.: Pulmonary resection for metastatic osteogenic sarcoma. J. Bone Joint Surg. 58A:624, 1976. 54. Sperling, J. W., Pritchard, D. J., and Morrey, B. F.: Total elbow arthroplasty following resection of tumors at the elbow. Clin. Orthop. Relat. Res. 367:256, 1999. 55. Swee, R. G., McLeod, R. A., and Beabout, J. W.: Osteoid osteoma: Detection, diagnosis, and localization. Radiology 130:117, 1979. 56. Taylor, W. F., Ivins, D. C., Edmonson, J. H., and Pritchard, D. J.: Trends and variability in survival from osteosarcoma. Mayo Clin. Proc. 53:695, 1978. 57. Unni, K. K., Dahlin, D. C., and Beabout, J. W.: Periosteal osteogenic sarcoma. Cancer 37:2476, 1976. 58. Unni, K. K., Dahlin, D. C., Beabout, J. W., and Ivins, J. C.: Parosteal osteogenic sarcoma. Cancer 37:2466, 1976. 59. Weatherby, R. P., Dahlin, D. C., and Ivins, J. C.: Postradiation sarcoma of bone: Review of 78 Mayo Clinic cases. Mayo Clin. Proc. 56:294, 1981. 60. Weber, K., and Morrey, B. F.: Osteoid osteoma of the elbow: A diagnostic challenge. J. Bone Joint Surg. 81A:1111, 1999. 61. Wright, P. H., Sim, F. H., Soule, E. H., and Taylor, W. F.: Synovial sarcoma. J. Bone Joint Surg. 64A:112, 1982.

1152 Part VIII Septic and Nontraumatic Conditions

CHAPTER

83

Loose Bodies Bernard F. Morrey

INTRODUCTION First described in the knee by Ambroise Paré32 in 1558, loose bodies occur in the elbow with a frequency second only to that in the knee.33 As in other joints, it is sometimes difficult to distinguish with certainty between ossification centers and acquired lesions (Box 83-1).5

ACCESSORY OSSIFICATION Confusion with acquired processes is caused by accessory ossicles that occur at the elbow as normal variations. Three sites for accessory ossicles about the elbow have been described: distal to the medial epicondyle; proximal to the tip of the olecranon (the patella cubiti); and in the olecranon fossa (the os supratrochleare dorsale8) (Fig. 83-1). Some ossicles show fragmentation, possibly secondary to trauma. This is sometimes mistaken for a manifestation of osteochondritis dissecans. Even though accessory ossicles may be considered a normal variation, they may well cause symptoms after trauma and require treatment.

MEDIAL EPICONDYLE ACCESSORY OSSICLE An accessory ossicle to the medial epicondyle19 is sometimes seen as a smooth, rounded ossification just distal to this structure. Because calcification can follow injury to the medial collateral ligament, whether the radiographic lesion reflects a traumatic or a congenital insult is often confusing,40 possibly more than at any other site. However, a discrete, rounded, smooth ossicle in patients who have no history of injury to this region suggests an accessory structure (Fig. 83-2). An irregular or misshapen medial epicondyle suggests a traumatic origin. Nevertheless, the formation of a fully developed medial epicondyle does not necessarily prove the diagnosis, because in a child, the medial epicondyle can remodel and appear normal in later years.

PATELLA CUBITI The so-called patella cubiti is rare but has been thoroughly described in earlier literature,16,20,37 and a thorough review has been presented by Habbe.16 This ossicle occurs in the triceps tendon near its insertion and is considered a true sesamoid bone.21 The proximal position is so characteristic in appearance that there should be little doubt about its origin (Fig. 83-3A). This structure should be distinguished from an avulsed olecranon apophysis, which appears farther distal (see Fig. 83-3B), and from a calcified olecranon bursa. Because of its superficial location, this ossicle may be subject to direct trauma and even fracture,4 but the injury generally responds to symptomatic treatment. Confusion with a fractured olecranon spur may exist.

OS SUPRATROCHLEARE DORSALE The radiographic density observed in the olecranon fossa has been a source of controversy. Characteristically, the ossicle has a smooth and round or oval shape that is often best seen in the lateral projection but is also demonstrated in the anteroposterior view (Fig. 83-4). In early descriptions of this entity it was considered to be a form of osteochondritis dissecans of the trochlea.29 The precise origin of this osseous structure is still the subject of some discussion, and trauma is often blamed.2 The supposed mechanism of injury is that with hyperextension, impaction of the tip of the olecranon into the olecranon fossa may cause a spur to develop at the tip of the olecranon. Conceivably it can be dislodged, form a nidus and grow into the characteristic os supratrochleare. Certainly, this mechanism has been implicated in the formation of loose bodies in the olecranon fossa (Fig. 83-5).39 The problem has been discussed in detail and clarified by Obermann and Loose, who concluded that the os supratrochleare dorsale is most likely a congenital accessory bone.30 Rather than being caused by trauma, it is subject to injury that produces secondary chondrometaplasia and resulting symptoms. When this occurs, the ossicle may look damaged and have an irregular margin. Thus, the distinction between an ossicle caused by trauma and an existing one subjected to trauma remains obscure (see Fig. 83-5). Regardless of the source, the treatment is obvious. Mere radiographic evidence of the osseous density does not imply that it needs to be removed. If it is painful owing to injury caused by hyperextension or a direct blow, symptomatic treatment should resolve the pain. If catching, locking, or persistent pain is present, the ossicle is easily excised through a limited posterolateral incision or, preferably, arthroscopically (see Chapter 38).31

Chapter 83 Loose Bodies 1153

ACQUIRED LOOSE BODIES Loose or pedunculated cartilaginous or osseocartilaginous bodies are believed to originate from a small nidus.33 The sequence of morphologic alterations that ensue is common to all free bodies, regardless of their origin.25 Surface proliferation of chondroblasts and osteoblasts nourished by the synovial fluid creates a laminar or layered effect that is seen in about 87% of such bodies that are predominantly cartilaginous and in 80% of those that are predominantly osseous (Fig.

BOX 83-1

83-6).25 The growth process continues as long as the free or pedunculated body is exposed to the synovial fluid.

ETIOLOGY Our understanding of intra-articular loose bodies has been much enhanced by the work of Milgram.24-26 By clinical findings and presentation, acquired free or pedunculated bodies can be divided into three groups:

A, B, D

Classification of Loose Bodies

A

B D

E

Congenital (developmental) Medial epicondyle—accessory ossification Olecranon—os patella cubiti Olecranon fossa—os supratrochleare dorsale Acquired Articular fracture—osteochondritis dissecans Degenerative Synovial proliferation—synovial chondromatosis From Broberg, M. A., and Morrey, B. F.: Results of treatment of fracture dislocations of the elbow. Clin. Orthop. Relat. Res. 216:109, 1987.

FIGURE 83-2

C

FIGURE 83-1 Identification of accessory ossicles: A, Anterior supratrochleare; B, posterior supratrochleare; C, radial epicondyle; D, of the olecranon; and E, medial epicondyle. (Redrawn from Gudmundsen, T. E., and Ostensen, H.: Accessory ossicles in the elbow. Acta Orthop. Scand. 58:132, 1987.)

A, The occurrence of a smooth ossicle at the inferior aspect of the medial epicondyle without a history of injury represents an accessory ossicle. B, An earlier medial epicondyle fracture may have the same appearance, but the epicondyle may remodel in young patients (see Chapter 16). Note the loose bodies in the olecranon fossa.

1154 Part VIII Septic and Nontraumatic Conditions

(1) osteochondral fractures, (2) degenerative disease of the articular surface, and (3) a proliferative disorder of the synovium, synovial chondromatosis. Milgram25 defines three types of cartilage associated with loose bodies based on their supposed site of origin: (1) articu-

lar cartilage cells, (2) osteophytic cells from a proliferating osteophyte in a degenerative joint, and (3) lobular cartilage from the synovial lining cell. Pathologically, these loose bodies can originate from a joint fracture, from degenerative osteophytes, or de novo as a proliferative disease of the synovium.

OSTEOCHONDRAL FRACTURE

FIGURE 83-3

The os patella cubiti is present in the triceps tendon; the proximal location helps to distinguish this lesion from a variation of the olecranon ossification center.

FIGURE 83-4

Fracture of the joint surface may be acute or the result of a chronic process such as osteochondritis dissecans. A shear fracture of the capitellum may involve little osseous substance, as in type II lesions (see Chapter 19). If in the acute stage, this fracture is missed, an intraarticular loose body may develop (Fig. 83-7). Elbow dislocation often leads to fractures of the coronoid, capitellum, or radial head and subsequent development of loose or attached intra-articular osseous bodies. Postreduction ossification of collateral ligaments is common, even without fracture. Avulsion of the medial epicondyle at the time of dislocation can also cause entrapment of the loose body in the joint with reduction. This complication is usually obvious (Fig. 83-8) and requires open treatment and fixation. The development of osteochondritis dissecans of the capitellum is discussed thoroughly in Chapters 19 and 49. It can progress to fragment detachment, with formation of a loose body in the joint (Fig. 83-9). Clinical

A smooth, rounded ossicle in the olecranon fossa, observed on the anteroposterior (A) radiograph (black arrow) and sometimes more obvious (arrow) on the lateral one (B), is consistent with the diagnosis of os supratrochleare. Other small densities are present on the anteroposterior view (white arrows).

Chapter 83 Loose Bodies 1155

FIGURE 83-5

A and B, Subject to trauma, this ossicle may sometimes take on an irregular shape, which can mislead the examiner to suspect that the cause is trauma, or even osteochondritis dissecans of the trochlea. Hyperextension of the elbow may cause spur formation on the tip of the olecranon and multiple loose bodies in the olecranon fossa, a condition that should be distinguished from the os supratrochleare. Coronoid osteophytosis suggests primary arthrosis as another possible cause.

surface or margin (Fig. 83-10). In fact, because trauma has become the accepted cause for loose bodies in the elbow joint, some researchers attribute all extraneous ossific densities, even accessory ossicles, to trauma.1,27,29,40 Although the clinical features and precise causes vary, a bony nidus is the common pathologic finding in each of these traumatic lesions.24

LOOSE BODIES OF DEGENERATIVE ORIGIN

FIGURE 83-6

Classic demonstration of the laminar effect of a cartilaginous loose body, which is responsible for the growth of these structures. (From Milgram, J. W.: The development of loose bodies in human joints. Clin. Orthop. Relat. Res. 124:295, 1977.)

manifestations include the occurrence of subtle pain, loss of extension, grating, snapping, and frank locking of the joint that is due to separation of a loose osteocartilaginous fragment of osteochondritis dissecans or a lesion of the capitellum or other portions of the articular

Degenerative joint disease can induce loose body formation by creating a nidus from a fragmented joint surface, from a degenerative osteophyte, or from the synovium of a joint involved with degenerative cartilaginous changes.25 Primary degenerative arthritis is discussed in detail in Chapter 76. Bullock and Goodfellow7 have studied primary articular changes of the radiohumeral joint; this process could certainly give rise to the formation of a nidus and the subsequent development of a loose body. Bell3 reviewed 52 instances of loose bodies in the elbow and concluded that most were related to primary or secondary osteoarthritis. He observed that most occurred in the anterior aspect of the joint (Fig. 83-11), but we cannot confirm this from our experience. With degenerative disease, small osteophytes may be observed at the tips of both the olecranon and the coronoid process, either of which could eventually give rise

1156 Part VIII Septic and Nontraumatic Conditions

FIGURE 83-7

Post-traumatic loose body originating from fracture of the capitellum (A) and radial head (B). The potential for osteophytic loose bodies exists even without frank fracture (C).

FIGURE 83-8

Entrapment of the medial epicondyle in the ulnohumeral joint after fracture-dislocation of the elbow.

Chapter 83 Loose Bodies 1157

to the development of an intra-articular loose body (see Fig. 83-7C). In fact, the presence of loose bodies is recognized to be an integral pathologic feature of primary osteoarthritis (Fig. 83-12).28

(see Chapter 38). Arthroscopic removal is the treatment of choice for symptomatic loose bodies.31,35 I prefer replacement of a large fragment of the capitellum in osteochondritis dissecans by a suture technique, and the topic is discussed in Chapter 39.

TREATMENT SYNOVIAL CHONDROMATOSIS The use of the arthroscope has enhanced the diagnosis, localization, and removal of loose bodies (Fig. 83-13)

FIGURE 83-9

Osteochondritis dissecans of the capitellum has caused an osteocartilaginous loose body in the joint.

Since the initial description of the entity in 1558,32 much has been written about synovial chondromatosis or osteochondromatosis, and we have recently reviewed our experience with this condition at the elbow.18 In this review, an 80% expectation of successful management with arthroscopic or open débridement was documented. The topic is discussed further in Chapter 76.9 Henderson and Jones reviewed the literature and reported the initial Mayo Clinic experience of 25 cases in 1923.17 They concluded that this entity was separate from traumatic or degenerative loose body formation and that the nidus originated from the synovial tissue (Fig. 83-14). More specifically, the condition is believed to be a proliferative disorder of the subsynovial soft tissue.14 Thus, some risk of malignant transformation is recognized, possibly as high as 5%.9 Milgram has identified three phases of the process.26 In the active initial phase, no free or loose bodies are present. In the transitional phase, osteochondral nodules form in the synovial membrane and nonossified free bodies are found in the joint (Fig. 83-15). In the final phase, free, sometimes very extensive ossified, osteochondral bodies apparently herald the quiescent phase of the disease (Fig. 83-16). In the second phase, the cartilaginous component becomes symptomatic before it ossifies, producing

FIGURE 83-10 A fragment of capitellum from a 24-year-old man with a 7-year history of intermittent restricted range of motion. No viable blood supply is present even though the surgeon had to cut through the articular cartilage to excise the underlying osseous defect. The articular cartilage chondrocytes exhibit no reactive change even though this fragment has fractured. The bone does show reactive changes, however, although the articular cartilage does not. (From Milgram, J. W.: Radiologic and Histologic Pathology of Nontumorous Diseases of Bones and Joints. Vol. 1. Northbrook, Ill., Northbrook Publishing Co., 1990.)

1158 Part VIII Septic and Nontraumatic Conditions

B FIGURE 83-11 A, Anterior loose bodies of the elbow joint in a patient with no history of trauma. B, Lateral radiograph revealing multiple loose bodies in patient with primary osteoarthritis.

FIGURE 83-12 Anteroposterior radiograph of primary degenerative arthritis of the elbow demonstrates a loose body in the olecranon fossa.

symptoms of elbow pain and loss of motion even in the presence of a relatively normal radiograph (see Fig. 83-16). Enchondral bone formation replaces the cartilaginous component, and this gives rise to the obvious radiographic demonstration of multiple loose bodies (see Fig. 83-16). Thus, the condition may present with multiple (as many as 100) radiolucent cartilaginous (see Fig. 83-15) or radiopaque ossified (see Fig. 83-16) loose bodies. When the bodies are ossified, a possible cartilaginous neoplasm may be considered, but as discussed in Chapter 82, with the exception of the experience reported by Davis and coworkers,10 the occurrence of cartilaginous sarcomas about the elbow is extremely rare. Yet the distinction can be difficult and may be resolved only by histologic examination of the tissue.11 More recently, computed tomography has been demonstrated to be effective in confirming this diagnosis in the nonossified phase.34 The disease is usually considered a self-limiting process that runs a rather predictable course, but this is not always the case and the process may be very aggressive.26 More recent reports have emphasized the development of nerve compression from capsular distension.36,38 The large volume occupied by the chondromatous tissue has been shown to cause anterior distension and compression of the radial nerve at the arcade of Frohse, which results in partial paralysis of the posterior interosseous nerve.13 A

Chapter 83 Loose Bodies 1159

FIGURE 83-13 Lateral radiograph demonstrates anterior and posterior loose bodies (A) that were localized arthroscopically (B). Multiple loose bodies may be removed with this technique (C).

FIGURE 83-14 Microradiograph of a pedunculated body in a patient with osteochondromatosis. Note the presence of a vascular supply (arrowheads) and mature bone nidus. (From Henderson, M. S., and Jones, H. T.: Loose bodies in joints and bursae due to synovial osteochondromatosis. J. Bone Joint Surg. 5:400, 1923.)

1160 Part VIII Septic and Nontraumatic Conditions

FIGURE 83-15 A and B, The patient presented with grating and limitation of motion and radiographic evidence of only minimal hypertrophic changes. C, Arthrotomy demonstrated erosion of the radial head with multiple radiolucent cartilaginous loose bodies. The presumptive diagnosis was osteochondromatosis.

similar mechanism might be attributed to the ulnar neuropathy reported by Roth and others12,23 and even the cutaneous branch of this nerve has been involved.38

SIGNS AND SYMPTOMS Loose bodies are more common in men than in women, regardless of the etiology, traumatic, degenerative, or proliferative.17 Among Bell’s 52 cases and in our experience, most patients present with loss of motion, usually extension.3 Symptoms may be of catching but rarely are disabling. Pain may or may not be a finding and usually occurs with a sensation of locking or grating. The discomfort is usually generalized. Radiography is helpful for large lesions but can be

deceptive if it fails to demonstrate loose bodies that have not yet calcified, if small ossicles are present in the ulnohumeral joint (see Fig. 83-5B), if the location is obscured by surrounding structures, or if the traumatic lesion contains little osseous tissue. These difficulties in diagnosis have been solved with magnetic resonance imaging.6,22

TREATMENT Regardless of the stage of presentation, arthroscopy, and synovectomy, if required, is now clearly the treatment of choice for removal of the loose bodies (Fig. 83-17). If the process extends beyond the capsule, an open procedure is of course required.

Chapter 83 Loose Bodies 1161

FIGURE 83-16

A and B, Radiographs from an early case treated at the Mayo Clinic by Dr. M. S. Henderson in 1918 show the ossified form of osteochondromatosis. C, Arthrotomy allowed removal of more than 100 loose bodies.

1162 Part VIII Septic and Nontraumatic Conditions

B

FIGURE 83-17 A clinical presentation of limited extension and pain in a 36-year-old woman (A) that was diagnosed as osteochondromatosis and confirmed with magnetic resonance imaging (B), which was treated by removal of loose bodies under arthroscopic guidance (C and D).

D

Chapter 83 Loose Bodies 1163

References 1. Atsatt, S.: Loose bodies of the elbow joint: An unusual location and form. J. Bone Joint Surg. 15:1008, 1933. 2. Bassett, L. W., Mirra, J. M., Forrester, D. M., Gold, R. H., Bernstein, M. L., and Rollins, J. S.: Post-traumatic osteochondral “loose body” of the olecranon fossa. Radiology 141:635, 1981. 3. Bell, M. S.: Loose bodies in the elbow. Br. J. Surg. 62:921, 1975. 4. Birsner, J. W., and DeSmet, D. H.: Patella cubiti with fracture. Ann. West. Med. Surg. 4:744, 1950. 5. Broberg, M. A., and Morrey, B. F.: Results of treatment of fracture dislocations of the elbow. Clin. Orthop. Relat. Res. 216:109, 1987. 6. Brunton, L. M., Anderson, M. W., Pannunzio, M. E., Khanna, A. J., and Chhabra, A. B.: Magnetic resonance imaging of the elbow: Update on current techniques and indications. J. Hand Surg. 31A:1001, 2006. 7. Bullock, P. G., and Goodfellow, J. W.: Pattern of aging of the articular cartilage of the elbow joint. J. Bone Joint Surg. 49B:175, 1967. 8. Burman, M. S.: Unusual locking of the elbow joint by the sesamum cubiti and a free joint body. Am. J. Radiol. 45:731, 1941. 9. Christensen, J. H., and Poulsen, J. O.: Synovial chondromatosis. Acta Orthop. Scand. 46:919, 1975. 10. Davis, R. I., Hamilton, A., and Biggart, J. D.: Primary synovial chondromatosis: A clinicopathologic review and assessment of malignant potential. Hum. Pathol. 79:683, 1998. 11. Dufour, J. P., Hamels, J., Maldague, B., Noel, H., and Pestiaux, B.: Unusual aspects of synovial chondromatosis of the elbow. Clin. Rheumatol. 3:247, 1984. 12. Fahmy, N. R. M., and Noble, J.: Ulnar nerve palsy as a complication of synovial osteochondromatosis of the elbow. Hand 13:308, 1981. 13. Field, J. H.: Posterior interosseous nerve palsy secondary to synovial chondromatosis of the elbow joint. J. Hand Surg. 6:336, 1981. 14. Fisher, A. G. T.: A study of loose bodies composed of cartilage or of cartilage and bone occurring in joints. Br. J. Surg. 8:493, 1931. 15. Gudmundsen, T. E., and Ostensen, H.: Accessory ossicles in the elbow. Acta Orthop. Scand. 58:130, 1987. 16. Habbe, J. E.: Patella cubiti, a report of four cases. A. J. R. 48:513, 1942. 17. Henderson, M. S., and Jones, H. T.: Loose bodies in joints and bursae due to synovial osteochondromatosis. J. Bone Joint Surg. 5:400, 1923. 18. Kamineni, S., O’Driscoll, S. W., Morrey, B. F.: Synovial osteochondromatosis of the elbow. J. Bone Joint Surg. 84B(7):961-966, 2002. 19. Keates, T. E.: An Atlas of Normal Roentgen Variants That May Simulate Disease. Chicago, Year Book Medical Publishers, 1979.

20. Kienbock, R., and Desenfans. G.: Uber Anomalien am Ellbogengelenk Patella cubiti. Beitr. Klin. Chir. 165:524, 1937. 21. Kohler, A., and Zimmer, E. A.: Borderlands of the Normal and Early Pathologic in Skeletal Anatomy, 3rd ed. New York, Grune & Stratton, 1968. 22. Martinoli, C., Bianchi, S., Zamorani, M. P., Zunzunegui, J. L., and Derchi, L. E.: Ultrasound of the elbow. Europ. J. Ultrasound 14:21, 2001. 23. Lister, J. R., Day, A. L., and Ballinger, W.: Ulnar palsy caused by synovial chondromatosis. Surg. Neurol. 15:428, 1981. 24. Milgram, J. W.: The classification of loose bodies in human joints. Clin. Orthop. Relat. Res. 124:282, 1977. 25. Milgram, J. W.: The development of loose bodies in human joints. Clin. Orthop. Relat. Res. 124:292, 1977. 26. Milgram, J. W.: Synovial osteochondromatosis. J. Bone Joint Surg. 59B:492, 1977. 27. Morgan, P. W.: Osteochondritis dissecans of the supratrochlear septum. Radiology 60:241, 1953. 28. Morrey, B. F.: Primary osteoarthritis of the elbow: Ulno-humeral arthroplasty. J. Bone Joint Surg. 74B:409, 1992. 29. Morton, H. S., and Crysler, W. E.: Osteochondritis dissecans of the supratrochlear septum. J. Bone Joint Surg. 27:12, 1945. 30. Obermann, W. R., and Loose, H. W. C.: The os supratrochleare dorsale: A normal variant that may cause symptoms. A.J.R. 141:123, 1963. 31. O’Driscoll, S. W., and Morrey, B. F.: Arthroscopy of the elbow: A critical analysis. J. Bone Joint Surg. 74A:84, 1992. 32. Paré, A.: As quoted by Henderson, M. S., and Jones, H. T.: J. Bone Joint Surg. 5:400, 1923. 33. Phemister, D. B.: The causes and changes in loose bodies arising from the articular surface of the joint. J. Bone Joint Surg. 6:278, 1924. 34. Rao, J. P., Spingola, C., Mastromonaco, E., and Villacin, A.: Synovial osteochondromatosis: Computerized axial tomography, frozen section and arthrography in diagnosis and management. Orthop. Rev. 15:94, 1986. 35. Rupp, S., and Tempelhof, S.: Arthroscopic surgery of the elbow. Therapeutic benefits and hazards. Clin. Orthop. Relat. Res. 313:140-145, 1995. 36. Ruth, R. M., and Groves, R. J.: Synovial osteochondromatosis of the elbow presenting with ulnar nerve neuropathy. Am. J. Orthop. 25:843, 1996. 37. Sachs, J., and Degenskein, G.: Patella cubiti. Arch. Surg. 57:675, 1948. 38. Slater, R. N. S., Koka, S. R., and Ross, K. R.: Cheiralgia paraesthetica secondary to synovial osteochondromatosis of the elbow. J. Orthop. Rheumatol. 6:179-181, 1993. 39. Tullos, H. S., and King, J. W.: Lesions of the pitching arm in adolescents. J. A. M. A. 220:264, 1972. 40. Zietlin, A.: The traumatic origin of accessory bones at the elbow. J. Bone Joint Surg. 17:933, 1935.

1164 Part VIII Septic and Nontraumatic Conditions

CHAPTER

84

Bursitis Bernard F. Morrey

INTRODUCTION It is unlikely that the following discussion will do a great deal to alter the rather menial significance attributed to the bursae: Ensuring the smooth and frictionless working of the body corporate, usually uncomplaining, inconspicuous, hardworking, and very modest in their requirements, the bursae have been so neglected that, even when one of them misbehaves, this is usually misattributed to some more important structure.30

Recent advances in the surgical management of soft tissue problems about the olecranon have mitigated somewhat our prior indication. Olecranon bursitis is the most commonly involved site followed by the bicipital radial bursa. The latter is particularly involved in partial ruptures of the biceps tendon insertion. The presence of these structures is even variable and is probably developmental, because not all bursae are present at birth.43

ANATOMY As early as 1788, Monro described several deep bursae about the elbow (Fig. 84-1). Through the years, additional bursae have been described. They may be divided into deep and superficial types (Fig. 84-2). Anatomically, the deep bursae are situated between muscles or between muscle and bone, which makes anatomic recognition somewhat difficult and clinical involvement almost impossible to diagnose. The superficial bursae consist only of those over the epicondyles and that over the olecranon, which is by far the most important one.

DEEP BURSAE Pathologic involvement of any of the deep bursal structures is rather uncommon. This fact, coupled with the difficulty of identifying some of these structures by anatomic dissection, brings into question the very exis-

tence of certain structures. The most significant of the deep bursae is the bicipital radial bursa, which occurs at the radial tuberosity (Fig. 84-3). Owing to its anatomic site, inflammation of the bursa may occur with pronation and supination and can be confused with distal biceps tendinitis.20 Distinguishing between impending distal biceps tendon rupture and bicipital radial bursitis is not simple.1 In fact, one of the few cases of cubital bursitis reported by Karanjia and Stiles showed degeneration of the biceps tendon insertion.20 Crepitus on pronation and supination suggests impending rupture. Fullness or swelling of the cubital space that is accentuated on pronation is more consistent with bicipital radial bursitis.20 I have used selective lidocaine injections to help localize the lesion to the tuberosity, but this does not distinguish between the two processes. Usually the diagnosis is presumptive and the treatment is symptomatic—rest, ice or heat, and anti-inflammatory agents. Tennis elbow and irritation of the radial nerve have been reported to result from inflammation of the radiohumeral bursa, which lies under the extensor carpi radialis brevis.5 Although bursitis was once thought to be a common cause of tennis elbow, according to our current understanding of lateral epicondylitis the association seems to be uncommon. Yet this structure does exist and has been demonstrated in anatomic dissections.30,31 I have had one patient who developed adventitial epicondylar bursitis after a common extensor tendon slide. Symptoms resolved after excision. Deep bursae have been associated with the triceps tendon. The significance of the two deep bursae around the triceps (Fig. 84-4) is a matter of speculation, because no recognizable clinical presentation has been documented for these structures. It is possible that inflammation of either the intratendinous or subtendinous bursae could be mistaken for tendinitis or that of the subtendinous bursae for tendinitis, synovitis, or capsulitis. Idiopathic calcific involvement of the subtendinous bursae has been described.41 Yet calcification of bursae around the elbow is distinctly unusual, in contrast to calcific tendinitis in the region of the shoulder. Calcium appears to form in response to anoxia, which causes a cellular response with giant cell reaction. The result is an inflamed, “hot”-looking joint or bursa.

SUPERFICIAL BURSAE The olecranon and the medial and lateral epicondylar bursae are the only superficial bursae about the elbow. I have occasionally observed an inflamed medial epicondylar bursa associated with chronic subluxation of the ulnar nerve. This probably rather uncommon lesion is treated by attending to the primary pathologic process involving the ulnar nerve. It is interesting to note that

Chapter 84 Bursitis 1165

FIGURE 84-1

A, The existence of the radiohumeral bursa and the bicipital radial bursa (X) has been recognized for more than 200 years, as demonstrated by this original 1788 illustration from Monro. B, Similarly, the subtendinous olecranon bursa was well illustrated in this monograph.

Medial epicondylar B. Radiohumeral B.

Lat. epicondylar B.

Cubital interosseous B. Ulnar n. B. Subanconeus B.

Supinator B.

Bicipital radial B.

Subtendinous B. Intratendinous B.

Sub ext. carpi radialis brevis B. (Radiohumeral B.)

Olecranon B.

A B FIGURE 84-2

A, Many deep bursae have been reported to exist in the region of the elbow, usually interposed between muscle and muscle or tendon and bone. B, The subcutaneous bursa of the olecranon is the most recognized and clinically important of these bursae.

1166 Part VIII Septic and Nontraumatic Conditions

BT BT R R

U

A

U

B

FIGURE 84-3

Because the bicipital radial bursa is situated between the tuberosity and tendon (A), symptoms are exaggerated with pronation, as the bursa impinges between tendon and bone (B). BT, bicipital tendon; R, radius; U, ulna.

FIGURE 84-5

Development of olecranon bursitis after elbow joint replacement. Note the well-healed posterior incision. This was an aseptic process.

Subtendinous bursa Intratendinous bursa

Olecranon bursa

FIGURE 84-4

Lateral illustration of the elbow demonstrates the superficial subcutaneous olecranon bursa, the intratendinous bursa found in the substance of the tendon, and the subtendinous bursa lying between the tip of the olecranon and the triceps tendon.

the olecranon bursa is not present at birth and has been shown to develop after the 7th year.6 This is consistent with others’ observations that bursae increase in size with age. Spontaneous rupture of the triceps tendon (see Chapter 35) may be related to tendon degeneration, as has been documented with disruptions of the insertion of the bicipital tendon.10 This process could masquerade as bursitis.

OLECRANON BURSITIS The olecranon is the site of the most common type of superficial bursitis.33 Olecranon bursitis is caused by a

number of pathologic conditions that are traumatic (overuse or direct impact), inflammatory, infectious, or noninfectious. Since 1975, it has been associated with dialysis in the ipsilateral extremity.17 I have also observed olecranon bursitis after reconstructive procedures when a posterior approach was used (Fig. 84-5). Inflammation of the superficial olecranon bursa can also result from direct trauma or repetitive stress, the so-called miner’s elbow or student’s elbow. Larson and Osternig have also shown that olecranon bursitis is a common football injury and is often associated with artificial turf.24 Involvement with systemic inflammatory processes such as rheumatoid arthritis,27 gout, chondrocalcinosis,12 or hydroxyapatite crystal deposition29 has been reported. Diffuse pigmented villonodular synovitis has also been shown to give rise to olecranon synovitis,28 and xanthoma has been reported to involve this region.38 In lesions due to chronic overuse—for example, coal miner’s bursitis—the synovial cells that are least subject to mechanical stress have been shown to be those that elaborate the synovial fluid.26 The distinction between septic and aseptic olecranon bursitis can be somewhat difficult to make. About 20% of cases of acute bursitis have a septic cause.18,38 Distinguishing between a septic and an aseptic inflammatory bursitis has been the subject of a detailed study by Ho and Tice15 and is discussed in Chapter 68. Fever, tenderness, and parabursal cellulitis are common with septic

Chapter 84 Bursitis 1167

bursitis; however, these findings are not specific, and a more detailed study by Smith and associates revealed that the skin over a septic bursa is almost 4ºC warmer than that over the nonseptic contralateral extremity.37 The sepsis causes pain in approximately 80%, whereas nonseptic bursitis is tender in only about 20%. It should be noted that Gram stain results are positive in only about 50% of patients. Approximately 80% are caused by Staphylococcus aureus or another gram-positive organism.44 Particular care must be exercised in evaluating dialysis patients because they may present with a sterile inflammatory process but have pain and warmth that suggest an infection.17 The problem is compounded by the fact that about 20% of these patients are also found to have a septic process.19 The correct diagnosis is suggested when aspirate from the bursa demonstrates a high leukocyte count. Thus, a presumptive diagnosis can usually be made before the culture results have been obtained. Contiguous spread of septic olecranon bursitis leading to osteomyelitis of the olecranon has been thought to be possible, although it is probably rare. Excision of the olecranon has been recommended to avoid this possibility.25

CLINICAL PRESENTATION A distended olecranon bursa is usually painless unless it is associated with a septic or crystalline inflammatory process. The two inflammatory conditions most frequently associated with olecranon bursitis are rheumatoid arthritis and gouty arthritis, in that order (Fig. 84-6).2 In patients with rheumatoid arthritis, the presentation can be variable. The bursa may rupture and dissect proximally, presenting as triceps swelling.32 In patients with rheumatoid arthritis, the bursa may also commu-

FIGURE 84-6

Gouty olecranon bursitis with tophi noted in the subcutaneous tissue.

nicate with the joint, dissect anteriorly and distally into the forearm, or even rupture and present as a subcutaneous fullness over the subcutaneous border of the ulna,11,14,34 all complications that are usually relatively painful. The association of triceps tendon rupture with olecranon bursitis after trauma has been cited.7 I have seen a bursa-type reaction after subacute or partial distal biceps rupture and suspect that the bursal reaction was an effect of biceps tendon injury and partial rupture, rather than a cause of rupture. On the other hand, traumatic bursitis is surprisingly painless after the initial event. When the bursitis is symptomatic, flexing the elbow to more than 90 degrees causes most symptoms. In fact, positions between 60 and 90 degrees have been shown in the laboratory to produce considerably greater pressure in the bursa than elbow extension.4 Canoso noted no pain with flexion, even when the bursa was distended, and speculated that discomfort probably originated in nerve endings in the osseous tendinous attachment, rather than in the roof of the bursa. Loss of motion has been reported, but this must be uncommon. I have not yet observed this in my practice. This phenomenon was first described by Irby and colleagues in 1975.17 Another clinical setting in which olecranon bursitis is becoming an increasingly recognized complication is hemodialysis.8,17,19 As many as 7% of dialysis patients may be affected.17,19 The pathophysiology of this manifestation has not been demonstrated conclusively. It is possible that direct pressure or low-grade trauma from posturing of the elbow may be the principal insult. Use of anticoagulants increases the possibility of hemobursitis (Fig. 84-7). It has also been proposed that it may represent uremic serositis, but none of these possibilities has been confirmed.19 A septic cause has been reported in about 25 percent of cases.19 Canoso has also characterized the clinical features of 30 cases of noninflammatory olecranon bursitis.3 Repetitive trauma was reported in 14 cases and a discrete, single traumatic event in seven. The nine other cases might be considered idiopathic. An olecranon spur was observed in 10 of 30 patients (Fig. 84-8). When symptoms had been present more than 2 weeks, the bursa appeared discretely swollen; when symptoms had been present less than 2 weeks, parabursal edema was observed in the arm and forearm in half of the patients (Fig. 84-9).8 Aspiration showed evidence of hemorrhage in cases of post-traumatic bursitis. The synovial fluid was further characterized by a low leukocyte count (average only 878 cells per high-power field, with 84% monocytes). This contrasts with the high leukocyte counts and predominance of polymorphonuclear cells in septic bursitis.

1168 Part VIII Septic and Nontraumatic Conditions

TREATMENT ACUTE BURSITIS Control of any underlying systemic or inflammatory process is the obvious first step in treatment. Sometimes the olecranon bursa communicates with the joint in rheumatoid arthritis, and the inflammation is generally

FIGURE 84-7

Acute hemobursitis developed in a patient receiving anticoagulation therapy after coronary bypass surgery. The inflammation was very refractory to treatment but eventually resolved with compressive dressing and protection.

FIGURE 84-8

considered a secondary process.16 If the bursa is not painful, local measures to prevent injury are all that is required.12 A resting splint and compression may be necessary, and this is the usual treatment in the early stages. Acute traumatic or idiopathic bursitis is also treated symptomatically with elbow pads (Fig. 84-10). If pain in the bursa prevents daily or occupational activity, aspiration and cortisone injection are indicated. Weinstein and colleagues42 reviewed 47 patients with nonseptic bursitis who were followed for 6 months to 5 years. Aspiration with and without corticosteroids demonstrated that adding corticosteroids did reduce the chance of recurrence but was associated with a significantly greater complication rate. Infection developed in three of 25 patients, and subdermal atrophy in five of 25 (Fig. 84-11). The orthopedic surgeon must be particularly vigilant here. “Nonsurgeons” tend to treat the septic process for a long time before they consider intervention.44 If the process does not rapidly resolve, if pain persists, and if parabursal swelling or erythema is present and is not resolving, septic bursitis is likely and the bursa must be aspirated. If this has already been done and the initial aspirate revealed no bacteria, repeat aspiration is indicated; at this time, culture is occasionally “positive.”

CHRONIC BURSITIS Chronic recurrent or painful olecranon bursitis may require more definitive measures. A 16-gauge indwelling needle that maintains drainage with a compressive dressing for about 3 days has been cited as being effec-

Lateral radiograph of the elbow of a patient with long-standing recurrent olecranon bursitis (A). Occasionally, this prominence fractures, but with few long-term consequences (B).

Chapter 84 Bursitis 1169

FIGURE 84-9

In acute septic olecranon bursitis, rather diffuse swelling is noted about the distal brachium and the proximal forearm.

FIGURE 84-10 Traumatic olecranon bursitis from artificial turf treated by protection with an elbow pad. The ideal pad should be relieved somewhat over the olecranon. (From Larson, R. L., and Osternig, L. R.: Traumatic bursitis and artificial turf. J. Sports Med. 2:183, 1974.)

Percentage of patients with bursal effusion

100 Aspiration alone N = 22 Corticosteroid injection N = 25

90 80 70 60 50 40 30 20 10 0 0

1

2

3

4

8

16

24

Weeks after treatment

FIGURE 84-11

Temporal resolution of bursitis associated with treatment by aspiration with and without cortisone injection. (Redrawn from Weinstein, P. S., Canoso, J. J., and Wohlgethan, J. R.: Long-term follow-up of corticosteroid injection for traumatic olecranon bursitis. Ann. Rheum. Dis. 43:45, 1984.)

tive in reducing recurrence of bursal swelling.12 Knight and colleagues,21 who refined this technique using percutaneous placement of a suction irrigation system, reported the results of 10 cases of septic olecranon bursitis. The average time in the hospital was approximately 12 days.42 Today, because increasing pressure for patient dismissal compromises this form of treatment, it is uncommon. Surgery is not commonly indicated; however, when the process is refractory to nonoperative measures and is interfering with occupational or daily activities, operative intervention should be considered.

OPERATIVE INTERVENTION Endoscopic Procedures Not surprisingly, endoscopic management of chronic olecranon bursitis has now been described.36 Nine patients were successfully treated by this technique with more rapid return to work than a control group treated in the traditional manner. This technique may be of value; time will tell.

1170 Part VIII Septic and Nontraumatic Conditions

Open Procedure 39

A longitudinal incision medial to the midline or a transverse incision has been recommended.38 All bursal tissue is removed, and the joint is immobilized in flexion or extreme flexion for approximately 2 weeks. Freeing the bursa from the skin can devitalize the skin over the olecranon process or cause problems with healing. Thus, I recommend a compressive dressing on the elbow placed in about 45 degrees of flexion. To avoid this, a rather unusual approach has been reported by Quayle

and Robinson35 (Fig. 84-12). The concern about wound healing attendant to the subdermal dissection of the bursa is avoided by reflecting the skin with the bursal tissue from the tip of the olecranon in a lateral to medial or a medial to lateral direction. At this point, the tip of the olecranon is obliquely osteotomized, leaving the bursal tissue intact. The triceps mechanism is then reflected back over the olecranon, and the wound is closed with a drain. Eleven patients treated with this technique have had no recurrences.35

Posterior approach Triceps reflected

Inflamed olecranon bursa

Ulnar n.

Humerus

Olecranon

A

B

FIGURE 84-12 Surgical treatment for chronic olecranon bursitis recommended by Quayle and Robinson. A, A straight medial incision is preferred. The skin flap that includes the bursa is reflected laterally. B, The triceps is reflected laterally, revealing the tip of the olecranon. C, A generous osteotomy is recommended. D, Most chronic bursae have a fibrous band through the bursal sac that appears to prevent healing leading to chronicity.

C

D

Plane of excision

Chapter 84 Bursitis 1171

RECONSTRUCTIVE OPTIONS In the last several years, a fasciocutaneous flap technique has been described by Lamberty and Cormack23 to cover defects around the olecranon process of the ulna. The flap involves a single stage local transport of tissue from the forearm (Fig. 84-13). The viability of the transfer rests on the circulation of the fascia for viability. The donor site over the forearm is closed primarily as well as with a split-thickness skin graft as needed. Several authors have recently documented the effectiveness of this or a modification of this procedure.9,23,40 Alternatively, a more proximal flap may be elevated based on a single local perforator vessel and medialized distally.13

RESULTS Stewart and associates39 reviewed the Mayo Clinic experience with 21 cases of surgical excision of the olecranon

bursa. Not surprisingly, only two of five patients with rheumatoid arthritis (40%) enjoyed complete relief. Fortunately, 15 of 16 (94%) in the nonrheumatoid group were free of recurrence an average of 5 years after surgery.39

COMPLICATIONS Complications of wound healing are the most common ones associated with incision and drainage or with excision of the olecranon bursa (Fig. 84-14). We had no recurrent drainage after the 21 resections reported by Stewart and associates. Should coverage be a problem, however, muscle flap transfers, either free or local, have been used with success for this application. Lai and colleagues recently described a more limited adipofascial flap to cover this area.22 Indiscriminate incision or removal of the olecranon bursa must be seriously questioned in light of the possibility and magnitude of this complication.

FIGURE 84-13 A, Chronic right olecranon ulcer with the outline of the fasciocutaneous flap. B, The flap has been elevated on a single vessel originating from the deep fascia. C, Local rotation of the flap covers the defect of the olecranon. The deficiency created in the forearm is covered with a split thickness skin graft. (Courtesy of N. B. Meland, M.D.)

1172 Part VIII Septic and Nontraumatic Conditions

FIGURE 84-14 A chronic draining sinus after incision and drainage of an infected olecranon bursa. Note the absence of swelling and local reaction.

References 1. Bourne, M., and Morrey, B. F.: Partial rupture of the distal biceps tendon. Clin. Orthop. Relat. Res. 271:143, 1991. 2. Bywaters, E. G.: The bursae of the body. Ann. Rheum. Dis. 24:215, 1965. 3. Canoso, J. J.: Idiopathic or traumatic olecranon bursitis. Clinical features and bursal fluid analysis. Arthritis Rheum. 20:1213, 1977. 4. Canoso, J. J.: Intrabursal pressures in the olecranon and prepatellar bursae. J. Rheumatol. 7:570, 1980. 5. Carp, L.: Tennis elbow. Arch. Surg. 24:905, 1932. 6. Chen, J., Alk, D., Eventov, I., and Weintroub, S.: Development of the olecranon bursa: An anatomic cadaver study. Acta Orthop. Scand. 58:408, 1987. 7. Clayton, M. C., and Thirupathi, R. G.: Rupture of the triceps tendon with olecranon bursitis. Clin. Orthop. 184:183, 1984. 8. Cruz, C., and Shah, S. V.: Dialysis elbow: Olecranon bursitis from long-term hemodialysis. J. A. M. A. 238:238, 1977. 9. Davalbhakta, A. V., and Niranjan, N. S.: Fasciocutaneous flaps based on fascial feeding vessels for defects in the periolecranon area. Br. J. Plast. Surg. 52:60, 1999. 10. Davis, W. M., and Yassine, Z.: An etiologic factor in tear of the distal tendon of the biceps brachii. J. Bone Joint Surg. 38A:1365, 1956. 11. Ehrlich, G. E.: Antecubital cysts in rheumatoid arthritis: A corollary to popliteal (Baker’s) cysts. J. Bone Joint Surg. 54A:165, 1972.

12. Fisher, R. H.: Conservative treatment of disturbed patellae and olecranon bursae. Clin. Orthop. Relat. Res. 123:98, 1977. 13. Frost-Arner, L., and Bjorgell, O.: Local perforator flap for reconstruction of deep tissue defects in the elbow area. Ann. Plast. Surg. 50:491, 2003. 14. Goode, J. D.: Synovial rupture of the elbow joint. Ann. Rheum. Dis. 27:604, 1968. 15. Ho, G., and Tice, A. D.: Comparison of nonseptic and septic bursitis. Arch. Intern. Med. 139:1269, 1979. 16. Hollinshead, W. H.: Anatomy for Surgeons, 2nd ed. Vol. 3. New York, Hoeber, 1969. 17. Irby, R., Edwards, W. M., and Gatter, R. J.: Articular complications of hemotransplantation and chronic renal hemodialysis. Rheumatology 2:91, 1975. 18. Jaffe, L., and Fetto, J. F.: Olecranon bursitis. Contemp. Orthop. 8:51, 1984. 19. Jain, V. K., Cestero, R. V. M., and Baum, J.: Septic and aseptic olecranon bursitis in patients on maintenance hemodialysis. Clin. Exp. Dial. Apheresis 5:405, 1981. 20. Karanjia, N. D., and Stiles, P. J.: Cubital bursitis. J. Bone Joint Surg. 70B:832, 1988. 21. Knight, J. M., Thomas, J. C., and Maurer, R. C.: Treatment of septic olecranon and prepatellar bursitis with percutaneous placement of a suction-irrigation system: A report of 12 cases. Clin. Orthop. Relat. Res. 206:90, 1986. 22. Lai, C. S., Tsai, C. C., Liao, K. B., and Lin, S. D.: The reverse lateral arm adipofascial flap for elbow coverage. Ann. Plast. Surg. 39:196, 1997. 23. Lamberty, B. G., and Cormack, G. C.: Fasciocutaneous flaps. Clin. Plast. Surg. 17:713, 1990. 24. Larson, R. L., and Osternig, L. R.: Traumatic bursitis and artificial turf. J. Sports Med. 2:183, 1974. 25. Lasher, W. W., and Mathewson, L. M.: Olecranon bursitis. J. A. M. A. 90:1030, 1928. 26. Letizia, G., Piccione, F., Ridola, C., and Zummo, G.: Ultrastructural comparisons of human synovial membrane in joints exposed to varying stresses. Ital. J. Orthop. Traumatol. 6:279, 1980. 27. MacFarlane, J. D., and van der Linden, S. J.: Leaking rheumatoid olecranon bursitis as a cause of forearm swelling. Ann. Rheum. Dis. 40:309, 1981. 28. Mathews, R. E., Gould, J. S., and Kashlan, M. B.: Diffuse pigmented villonodular tenosynovitis of the ulnar bursa: A case report. J. Hand Surg. 6:64, 1981. 29. McCarty, D. J., and Gatter, R. A.: Recurrent acute inflammation associated with focal apatite crystal deposition. Arthritis Rheum. 9:84, 1966. 30. Monro, A.: A Description of All the Bursae Mucosae of the Human Body. Edinburgh, Elliot, 1788. 31. Osgood, R. B.: Radiohumeral bursitis, epicondylitis, epicondylalgia (tennis elbow). Arch. Surg. 4:420, 1922. 32. Petrie, J. P., and Wigley, R. D.: Proximal dissection of the olecranon bursa in rheumatoid arthritis. Rheumatol. Int. 4:139, 1984. 33. Pien, F. D., Ching, D., and Kim, E.: Septic bursitis: Experience in a community practice. Orthopaedics 14:981, 1991. 34. Pirani, M., Lange-Mechlen, I., and Cockshott, W. P.: Rupture of a posterior synovial cyst of the elbow. J. Rheumatol. 9:94, 1982.

Chapter 84 Bursitis 1173

35. Quayle, J. B., and Robinson, M. P.: A useful procedure in the treatment of chronic olecranon bursitis. Injury 9:299, 1976. 36. Schulze, J., Czaja, S., and Linder, P. E.: Comparative results after endoscopic synovectomy and open bursectomy in chronic bursitis olecrani. Swiss Surg. 6:323, 2000. 37. Smith, D. L.: Septic and nonseptic olecranon bursitis. Arch. Intern. Med. 149:1581, 1989. 38. Smith, F. M.: Surgery of the Elbow, 2nd ed. Philadelphia, W. B. Saunders Co., 1972. 39. Stewart, N. J., Manzanares, J. B., and Morrey, B. F.: Surgical treatment of aseptic olecranon bursitis. J. Shoulder Elbow Surg. 6:49-53, 1997. 40. Van Landuyt, K., De Cordier, B. C., Monstrey, S. J., Bondeel, P. N., Tonnard, P., Verpaele, A., and Matton, G.: The ante-

41. 42.

43.

44.

cubital fasciocutaneous island flap for elbow coverage. Ann Plast. Surg. 41:252, 1998. Vizkelety, T., and Aszodi, K.: Bilateral calcareous bursitis at the elbow. J. Bone Joint Surg. 50B:644, 1968. Weinstein, P. S., Canoso, J. J., and Wohlgethan, J. R.: Longterm follow-up of corticosteroid injection for traumatic olecranon bursitis. Ann. Rheum. Dis. 43:44, 1984. Whittaker, C. R.: The arrangement of the bursae in the superior extremities of the full-term fetus. J. Anat. Physiol. 44:133, 1910. Zimmerman, B., 3rd, Mikolich, D. J., and Ho, G., Jr.: Septic bursitis. Semin. Arthritis Rheum. 24:391-410, 1995.

1174 Part VIII Septic and Nontraumatic Conditions

CHAPTER

85

The Elbow in Metabolic Disease Bernard F. Morrey

INTRODUCTION With the possible exception of tumoral calcinosis, no metabolic diseases have a special predilection for or a characteristic presentation at or about the elbow joint.1,6,19 Therefore, information is rather limited on the effects of metabolic bone disease of the elbow joint. In fact, at the Mayo Clinic, the radiographic bone survey routinely taken to assess the extent of involvement of these diseases does not include the elbow region. A MEDLINE review of all the conditions discussed herein from 1996 to 2007 revealed only one citation of any of these conditions related to the elbow.12 No attempt will be made here to mention all the conditions that might incidentally involve the elbow. However, several conditions are regularly manifested at this joint: gout, pseudogout, and inborn errors of metabolism that cause congenital anomalies (see Chapters 13 and 75). Paget’s disease may, of course, involve any part of the body, including the elbow (see Chapter 82). Synovial chondromatosis is mentioned here and in the section on arthroscopic management of loose bodies (see Chapter 38). It seems appropriate to discuss the appearance of and the effect of several of the more common or characteristic metabolic disorders that involve the elbow region and the impact of exogenous treatment with corticosteroid.

RICKETS In the immature skeleton, vitamin D deficiency typically causes widening of the physis and cupping of the metaphysis, which are well represented at the wrist. Interestingly, although it has not been emphasized in the literature, rather dramatic widening of the radiohumeral joint is typical of this disease (Fig. 85-1). The deficiency will obviously be better demonstrated in the faster growing bones, and the physes of the distal humerus and proximal forearm are relatively slow growing.6 Thus, the manifestations of rickets in the region of the elbow are usually not dramatic.

OSTEOMALACIA Classically, vitamin D deficiency of the mature skeleton resulting in the production of uncalcified osteoid may be due to one of several mechanisms—nutritional intake deficiencies, absorption abnormalities, and utilization abnormalities.15,16 Dialysis is one of the most common causes for this condition today. Radiographically, marked loss of bone density is usually observed along with coarsening of the trabecular pattern. There are no characteristic features at the elbow (Fig. 85-2). The lack of structural integrity causes bowing deformities of the weight-bearing extremities, but this is uncommon in the upper limbs.

TUMORAL CALCINOSIS Extensive para-articular calcification, so-called tumoral calcinosis, does have a certain predilection for the elbow region, although it is more common at the hips and shoulders.7 The differential diagnosis includes hyperparathyroidism, hypervitaminosis D, calcinosis universalis, and calcinosis circumscripta.4 Tumoral calcinosis characteristically occurs in young persons who have normal serum calcium concentrations, but a predilection has been noted in black persons and a familial tendency has also been reported.7,12 First described by Inclan and colleagues in 1943,9 the association with hyperphosphatemia has suggested a metabolic cause for this disease.2,13 Chemical assessment reveals hyperphosphatemia but normal levels of serum calcium, parathyroid hormone, and alkaline phosphatase. The exact cause of the condition is obscure, but calcium salts are deposited in the posterior or anterior extra-articular regions of the elbow. The calcium salt is usually calcium phosphate or carbonate. A well-circumscribed capsule may be present around the firm to soft, discrete masses. Sinus drainage may be seen as well.12 In one report, a similar radiographic appearance was demonstrated that was attributed to the deposition of hydroxyapatite crystals.8 The intra-articular nature of this deposition serves to distinguish it from true tumoral calcinoses (Fig. 85-3). Surgical treatment can be successful, particularly if the tumor masses are relatively small. Large areas of involvement, however, often cause difficulty with wound healing, and scarring in the skin and subcutaneous tissue (see Fig. 85-3). Recurrences are common even if excision appears to have been complete.

HYPERPARATHYROIDISM Primary hyperparathyroidism may be due to an adenoma, hyperplasia, carcinoma, or an aberrant tumor

Chapter 85 The Elbow in Metabolic Disease 1175

FIGURE 85-1

A 6-month-old infant was slow to roll over or attempt sitting. The diagnosis was rickets. This radiograph demonstrates the marked widening of the radiohumeral growth region.

FIGURE 85-2

that secretes the parathyroid hormone22 or to type II multiple endocrine neoplasia. Secondary hyperparathyroidism is the result of a chronic hypocalcemic state that stimulates the production of parathyroid hormone. The classic radiographic appearance of hyperparathyroidism is subperiosteal resorption, especially along the radial margin of the middle phalanges of the hand. More advanced but less common changes involve resorption of large amounts of bone, a phenomenon that results in the radiographic appearance of the so-called brown tumor. Hyperparathyroidism rarely demonstrates any features in the region of the elbow, but occasionally periosteal resorption or a brown tumor may be observed. A careful radiographic analysis of the manifestations of renal osteodystrophy at the elbow was published by Kricun and Resnick.11 Subtendinous bone resorption tends to occur at the origin and insertion of the tendinous attachments about the elbow (Figs. 85-4 and 85-5). Possibly the most dramatic change is resorption of the subcutaneous border around the olecranon. Resorption at the ulnar site of the origin of the anconeus is such a prominent feature in this disease that it is believed to be pathognomonic for hyperparathyroidism.11 Additional radiographic characteristics include the subchondral cystic erosions often noted at the ulnohumeral articulation, which are thought to be one of the characteristic manifestations of the disease.3

A and B, Blurred trabecular pattern and mottled decrease in bone density typical of osteomalacia without distinguishing features at the elbow joint. Primary disease was renal tubular dysfunction.

1176 Part VIII Septic and Nontraumatic Conditions

FIGURE 85-3

A, Extensive periarticular calcification in the region of the posterior aspect of the elbow was diagnosed as tumoral calcinosis. There was a history of familial hyperphosphatemia. B, This problem is not easily treated by surgery.

Triceps (I)

Anconeus (I)

Common extensor (O)

Pronator teres (O) Common flexor (O)

Anconeus (O) Radius

A

Ulna

Humerus (anterior)

B

Humerus (posterior)

C

FIGURE 85-4

In persons who have renal osteodystrophy, radiographic resorption is noted at the sites of tendinous origin (O) and insertion (I) about the elbow. The most common anatomic sites of involvement are shown. (Redrawn from Kricun, M. E., and Resnick, D.: Elbow abnormalities in renal osteodystrophy. A. J. R. 140:577, 1983.)

ACROMEGALY The skeletal manifestations of acromegaly have been well described.5 The elbow is affected in fewer than 10% of patients, 74% of whom have skeletal manifestations of the disease. Approximately 75% of patients have some

skeletal manifestation, about 10% of which involve the elbow. The manifestation is a hypertrophic osteophytic reaction, especially of the coronoid process and olecranon.24 Thus, the appearance and treatment are similar to those for primary degenerative arthritis (see Chapter 67).

Chapter 85 The Elbow in Metabolic Disease 1177

WILSON’S DISEASE (HEPATOLENTICULAR DEGENERATION) Caused by an inborn error of copper metabolism, Wilson’s disease is best known for renal, hepatic, and neurologic symptoms; however, its effect on the bones and joints is well known.18,21,22 Osteoporosis occurs in about 75% of patients,18 and osteomalacia is also common.21 Joint involvement includes degenerative changes, sclerosis, fragmentation, and periarticular calcification (Fig. 85-6). The radiographic appearance often correlates poorly with the clinical findings. The goal of treatment with penicillamine is to decrease the accumulation of copper in the body. On occasion, the severity of the joint involvement requires surgical intervention. I have replaced the knee joint in some patients with this condition but have not surgically treated the elbow joint.

FIGURE 85-5

Hyperparathyroidism secondary to renal failure is manifested in the region of the elbow by resorption and osteoporosis of the anterior proximal ulna, the so-called brown tumor. Subperiosteal resorption of the tip of the olecranon is also demonstrated.

HYPERLIPOPROTEINEMIA TYPE II (FAMILIAL ESSENTIAL HYPERCHOLESTEROLEMIA) Periosteal xanthomatosis and tendon xanthomas result from increased serum cholesterol levels, which promote accumulation of cholesterol crystals. Typically, the olec-

FIGURE 85-6

Wilson’s disease involving the elbow has the classic appearance of fragmentation and periarticular calcification. A, Anteroposterior view; B, lateral view.

1178 Part VIII Septic and Nontraumatic Conditions

ranon bursa and the triceps tendon are susceptible to this disorder.23 If the process is symptomatic in the olecranon bursa, excision may be indicated. Care should be taken, however, before excising these deposits in the triceps tendon, because this can weaken the extensor mechanism. The usual approach is to treat the underlying disease, as with diet and clofibrate (Atromid-S).

The effects at the elbow are most often manifested as type III radial head fractures or comminuted olecranon fractures in older persons and are associated with relatively little trauma. Unlike the spine and hip, the elbow region exhibits no characteristic radiographic features of osteoporosis.

STEROID-INDUCED AVASCULAR NECROSIS OSTEOPOROSIS In the broadest sense, osteoporosis may be defined as a decrease of bone substance so extreme as to be pathologic and to result in spontaneous fractures.10 Although these usually occur in the spine, distal radius, and hip, proximal humeral20 and pelvic fractures17 associated with minimal trauma have been linked to osteoporosis.

Although recognized complications are known to involve the hip, shoulder, knee, and ankle, steroidinduced avascular necrosis is uncommon.14 The diagnosis is easily made by magnetic resonance imaging (Fig. 85-7). This has been the subject of only a few case reports, and we, personally, have seen less than 10 such cases. Although this experience is hardly definitive, we

FIGURE 85-7

A 47-year-old man receiving chronic corticosteroid treatment had marked elbow pain (A). Avascular necrosis was confirmed by magnetic resonance imaging (B). Treatment was arthroscopically guided decompression (C).

Chapter 85 The Elbow in Metabolic Disease 1179

have had some success with arthroscopic dissected drilling/decompression of the involved portion of the joint.

References 1. Aegerter, E., and Kirkpatrick, J. A.: Orthopedic Diseases, 4th ed. Philadelphia, W. B. Saunders Co., 1975. 2. Baldursson, H., Evans, E. B., Dodge, W. F., and Jackson, W. T.: Tumoral calcinosis with hyperphosphatemia. J. Bone Joint Surg. 51A:913, 1969. 3. Bywaters, E. G. L., Dixon, A. S. J., and Scott, J. T.: Joint lesions in hyperparathyroidism. Ann. Rheum. Dis. 22:171, 1963. 4. Destouet, J. M., and Gilula, L. A.: Painful nodules of the right forearm and elbow. Orthop. Rev. 14:99, 1985. 5. Dettenbeck, L. C., Tressler, H. A., O’Duffy, J. D., and Randall, R. V.: Peripheral joint manifestations of acromegaly. Clin. Orthop. Relat. Res. 91:119-127, 1973. 6. Greenfield, G. B.: Radiology of Bone Diseases, 2nd ed. Philadelphia, J. B. Lippincott Co., 1975. 7. Hensley, D. C., and Lin, J. J.: Massive intra-synovial deposition of calcium pyrophosphate in the elbow. J. Bone Joint Surg. 66A:133, 1984. 8. Hartofilakidis-Garofalidis, G., Theodossiou, A., Matsoukas, J., Rigopoulos, C., and Papathanassiou, B.: Tumoral lipocalcinosis. Ann. Intern. Med. 41:387, 1970. 9. Inclan, A., Leon, P., and Gomez, C. M.: Tumoral calcinosis. J. A. M. A. 121:490, 1943. 10. Jowsey, J.: Metabolic Diseases of Bone. Philadelphia, W. B. Saunders Co., 1977. 11. Kricun, M. E., and Resnick, D.: Elbow abnormalities in renal osteodystrophy. A. J. R. 140:577, 1983. 12. Kumaran, M. S., Bhadada, S., Bhansali, A., Shiriram, M., and Kumar, B.: Young boy with multiple periarticular

13.

14.

15.

16.

17.

18.

19. 20.

21.

22.

23. 24.

swellings and discharging sinuses: Tumoral calcinosis. Indian J. Pediatr. 71:e74, 2004. Lafferty, F. W., Reynolds, E. S., and Pearson, O. H.: Tumoral calcinosis: a metabolic disease of obscure etiology. Am. J. Med. 38:105, 1965. Madsen, P. V., and Andersen, G.: Multifocal osteonecrosis related to steroid treatment in a patient with ulcerative colitis. Gut 35:132, 1994. Mankin, H. J.: Rickets, osteomalacia, and renal osteodystrophy, Part I (review article). J. Bone Joint Surg. 56A:101, 1974. Mankin, H. J.: Rickets, osteomalacia, and renal osteodystrophy, Part II (review article). J. Bone Joint Surg. 56A:352, 1974. Melton, L. J., Sampson, J. M., Morrey, B. F., and Ilstrup, D. M.: Epidemiologic features of pelvic fractures. Clin. Orthop. 155:43, 1981. Mindelzun, R., Elkin, M., Scheinberg, I. H., and Sternlieb, I.: Skeletal changes in Wilson’s disease. A radiological study. Radiology 94:127, 1970. Pugh, D. G.: Radiographic Diagnosis of Diseases of the Bone. New York, Thomas Nelson, 1951. Rose, S. H., Melton, L. J., Morrey, B. F., Ilstrup, D. M., and Riggs, B. L.: Epidemiologic features of humeral fractures. Clin. Orthop. Relat. Res. 168:24, 1982. Rosenoer, V. M., and Mitchell, R. C.: Skeletal changes in Wilson’s disease (hepatolenticular degeneration). Br. J. Radiol. 32:805, 1959. Salassa, R. M., Jowsey, J., and Arnaud, C. D.: Hypophosphatemic osteomalacia associated with “non-endocrine tumors.” N. Engl. J. Med. 283:65, 1970. Smith, F. M.: Surgery of the Elbow, 2nd ed. Philadelphia, W. B. Saunders, 1972. Tsai, E., Freiberg, A. A., and Louis, D. S.: Elbow arthrosis as an initial presentation of acromegaly. Orthopedics 21:901-902, 1998.

INDEX Note: Page numbers followed by f refer to figures; those followed by t refer to tables.

A Abuse, supracondylar fractures and, 206 Accelerometers, 80 Accessory lateral collateral ligament, 22, 22f Accessory ossicles, 680, 681f Acclaim total elbow arthroplasty clinical results, 761–764, 761f surgical considerations and, 755, 756f Acetaminophen, 146, 147t Achilles tendon allografts. See also Interposition arthroplasty aftercare and, 939 chronic tears and, 531, 532f external fixation and, 939, 940f graft application and, 938, 938f–939f ligament reconstruction and, 938 Mayo recent experience and, 944– 945, 944f–945f surgical technique and, 937–938, 937f–938f triceps insufficiency and, 468f, 877, 877f–878f, 936–939 triceps tendon rupture and, 538, 541f, 542 Active assisted range of motion, 154 Active range of motion, 154–155 Acupuncture, 153 Acute anterior dislocation closed reduction and, 304 open reduction and, 304–306 Acute hemarthrosis, 1071–1072 Acute Pain Management Guidelines, 148 Adult Still’s disease, 1041–1042, 1042f, 1042t AlloDerm, 936 Allograft replacement, 913–919. See also Achilles tendon allografts; Interposition arthroplasty biocompatibility and, 915–918 cellular and humoral antibody responses and, 918 disease transmission and, 918 hemiallograft replacement, 916f hemiprosthetic devices and, 915f joint deterioration and, 918f–919f long-term considerations and, 913–915

Allograft replacement (Continued) olecranon and proximal ulna nonunion and, 414, 415f prosthetic composite reconstruction, 903–905, 905f, 906f results and, 918 union and, 913–915, 917f Amputation. See Disarticulation amputation; Transhumeral amputation Analgesics, postoperative, 145–150 acetaminophen, 146, 147t continuous brachial plexus analgesia, 144t, 148–149 control-released Oxycodone, 148 COX-2 inhibitors, 146–147 intravenous opioids for patientcontrolled analgesia, 146t multimodal, 145 nonsteroidal anti-inflammatory drugs, 146–147 oral nonopioid analgesics, 146, 147t oral opioids, 146, 147t, 148, 148t parenteral opioid analgesics, 145–146 peripheral blockade and, 145 Tramadol, 148, 148t Anatomic (functional) arthroplasty, 935, 936f. See also Interpositional arthroplasty Anatomy, 11–36. See also pertinent conditions accessory lateral collateral ligament, 22 anconeus muscle, 34 annular ligament, 21–22 anterior aspect, 26f anterior capsule fibers, 20f anterior extraosseous vascular anatomy, 27f articulation, 15f, 16–17 biceps, 30–31 brachial artery, 24–25 brachialis, 31 brachioradialis, 31 bursae, 23–24, 24f carrying angle, 17–18, 20f cross-sectional relationships, 25f cutaneous nerves, 13f distal humerus, 14f, 17f, 18f elbow joint structure, 16–17

Anatomy (Continued) extensor carpi radialis longus, 31–32 extensor carpi ulnaris, 32 extensor digitorum communis, 32 flexion crease, 12f flexor carpi radialis, 35 flexor carpi ulnaris, 35–36 flexor digitorum superficialis, 35f, 36 forearm compartments, 228f forearm musculature, 33f–34f general survey, 11 humerus, 11, 14f, 16, 17f hyaline cartilage, 18f, 19f inverted M pattern, 13f joint capsule, 18–19, 20f–21f lateral epicondylitis and, 609–610 lateral ligament complex, 20–24, 22f, 23f, 585f lateral ulnar collateral ligament, 22, 23f ligaments, 19–24 major flexors, 31f medial collateral ligament, 21f median nerve, 27–28, 28f middle collateral ligament complex, 19–24, 21f muscles, 30–36 musculocutaneous nerve, 27, 28f neck of radius, 18f nerves, 27–30 oblique cord, 23 osteology, 11–16 palmaris longus, 35 posterior collateral circulation, 27f pronator teres, 34–35 proximal radius, 16 proximal ulna, 16–17, 16f quadrate ligament, 22–23 radial artery, 26 radial collateral ligament, 21, 22f radial nerve, 28–29, 29f radius, 12, 15f sagittal section, 17f sigmoid notch, 19f subanconeus muscle, 34 submuscular bursa, 15f supinator, 32 supracondylar process, 15f synovial recess, 20f 1181

1182 Index

Anatomy (Continued) topical, 11, 12f–13f triceps brachii, 33–34 ulna, 12, 16, 16f ulnar artery, 26 ulnar nerve, 29–30, 30f vessels, 24–27 Anconeus arthroplasty aftercare and, 733 anatomy and, 732, 732f Essex-Lopresti lesions and, 733, 733f indications for, 731–732 outcomes and, 733 radiohumeral arthrosis and, 731–733 surgical procedure and, 732–734, 733f Anconeus epitrochlearis, 196 Anconeus muscle anatomy, 34, 34f Anconeus muscle flap, 556, 557f Anconeus rotational triceps reconstruction, 874–877, 876f Anesthesia. See also Analgesics, postoperative arthroscopy and, 567–568 intra-articular catheters, 149–150, 150f intraoperative anesthetic management, 143, 144f–145f regional anesthetic techniques, 144t Aneurysmal bone cyst, 1137–1139, 1138f Angiofibroblastic hyperplasia, 629, 629f Angulation deformity identification and, 67, 68f radial neck fractures and, 279 supracondylar fractures and, 206 Ankylosing spondylitis, 1040t Ankylosis, 189f–190f, 830–834 congenital, 936 diagnosis of, 192, 195f functional limitation and, 74f hinged external fixation and, 499–500 treatment of, 199 Annular ligament anatomy of, 21–22 reconstruction of, 299f, 306 Antecubital fasciocutaneous flaps, 552– 553, 553f Anterior aspect palpation, 73, 73f Anterior capsule column procedure and, 491–493, 492f fibers of, 20f Anterior capsulectomy, 328 Anterior Henry approach, 138–140, 139f Anterior humeral line, supracondylar fractures and, 212–213

Anterior interosseous nerve syndrome, 1109–1112 characteristic pinch attitude, 1110f median nerve exposure and, 1111–1112 operative findings and, 1111, 1111f physical findings and, 1110–1111, 1110f symptoms and, 1109–1110 Anterior oblique ligament, 643, 644f Anterior surgical exposures, 138–140, 138f–139f Anterior translocation of ulnar nerve, 1103–1105, 1103f–1104f Anterolateral portal, 570, 570f Antibiotic-impregnated cement, 868 Antibiotic treatment osteomyelitis and, 1058 septic arthritis and, 1061 septic olecranon bursitis and, 1065 Antley-Bixler syndrome, 192 AO classification system, 390, 390f AO technique, 951, 954f Apert’s syndrome, 192 Aplasia cutis congenita, 199 Aponeurosis turn-down approach, 125, 127f Apophyseal fracture, 283, 285f Apophysis, dislocations in children and, 297 Arnold-Chiari malformation, 1080 Arterial injuries schematic of, 229f simple realignment and, 233, 233f symptoms and signs of, 230 treatment of, 232–234 Arterial occlusion, 232t Arthritic stiff elbow management, 602–606 complications and, 605–606 history and, 603 nonoperative management and, 602 postoperative course and, 605 preferred surgical technique, 603– 605, 604f–605f steps in, 603 surgical indications and, 602 surgical results and, 605 Arthritis. See also Osteoarthritis; Rheumatoid arthritis arthroscopic complications and, 620–621 gouty, 1167, 1167f hematologic, 1068–1075 hypertrophic, 1053f juvenile rheumatoid arthritis, 792–797 neurotrophic, 1078–1087 post-traumatic, 717f, 734f, 942–943, 943f psoriatic, 1040f septic, 1056–1063

Arthritis (Continued) seronegative inflammatory, 1039–1042 sickle cell disease and, 1074–1075 tennis elbow and, 651f Arthrodesis AO compression and, 951, 954f bilateral elbow disease and, 949 chronic infection and, 1059, 1060f compression screws and, 951, 952f crossed tibial graft technique and, 951f external skeletal fixation and, 951, 953f–954f fracture and, 954f, 955 historical surgical techniques and, 949–950, 951f Hoffman’s device and, 953f indications for, 949 with infection, 954 joint preparation and, 950 loss of motion and, 949, 950f nonunion and, 414, 955 optimal position and, 949 plate fixation and, 950, 952f preferred treatment method, 954 recent surgical techniques and, 950 spontaneous, 949, 950f stabilization and, 950 stable elbows and, 954 Staples’ technique and, 951f Steindler technique and, 951f techniques and, 951, 951f unstable elbows and, 954 without sepsis, 954 Arthrofibrosis, 596–602 Arthrography, 101–106 abnormal findings, 104, 106f–107f complications and, 104–106 normal findings, 103, 105f technique, 103, 103t Arthrogryposis developmental dislocation and, 299 muscle transfer and, 973 tendon transfer and, 975, 975f Arthropathy hemophilic, 1068–1073 hyperemic, 1080f idiopathic, 1083–1084 neurotrophic, 1078–1087 Arthroplasty. See also Convertible total elbow arthroplasty; Distal humeral hemiarthroplasty; Linked arthroplasty; Total elbow arthroplasty; Unlinked total elbow arthroplasty anconeus, 731–733, 732f–733f Arizona design, 712f Bickel and Peterson design, 709f capitellocondylar prosthesis, 713f complications of, 849–859

Index 1183

Arthroplasty (Continued) convertible total elbow arthroplasty, 755–764 Coonrad prosthesis, 712f current directions and, 710–715 cutis arthroplasty, 940, 941f, 942 Dee prosthesis, 710f devastating bone loss and, 707f Discovery model and, 716f distal humeral fractures and, 800–812 distal humeral hemiarthroplasty, 720–728 distal humeral malunion and, 356 distal humeral nonunion and, 354, 835–838 dysfunctional instability and, 835–842 early elbow designs and, 705, 706f–707f ectopic ossification and, 482 functional, 935, 936f fused elbow and, 830–834 GSB design, 711f historical perspective and, 705–710 immediate exchange arthroplasty, 868–869 infection and, 141, 862–871 interposition arthroplasty, 500, 503f, 889, 935–947 joint implant replacement choice, 715–717 juvenile rheumatoid arthritis and, 792–797 Kudo elbow system, 714f Latitude elbow system, 716f linked arthroplasty, 765–780 Mayo designs, 714f–715f modern era of prosthetic replacement and, 705–710 modified Coonrad implant, 715f primary osteoarthritis and, 843–847 Pritchard unconstrained ulnohumeral, 713f Pritchard-Walker generation II design, 712f prosthetic implants through the years, 716t proximal ulna replacement, 708f radiohumeral arthrosis and, 729–738 resection arthroplasty, 869–871, 869f–870f, 911 resurfacing concept emergence and, 705, 708f–709f revision with osseous integrity, 885–897 rheumatoid arthritis and, 782–790 semiconstrained joint replacements and, 785t Souter-Strathclyde component, 713f

Arthroplasty (Continued) staged exchange arthroplasty, 866– 868, 867f–868f Street and Stevens design, 709f treatment logic and, 717f triceps insufficiency and, 873–878 ulnohumeral, 1047–1050 unlinked total elbow arthroplasty, 738–754 value of, 47 Vitallium replacement prosthesis, 706f wear and, 880–884 Arthroscopic complications, 620–623. See also Arthroscopy capsular release and, 621–622 degenerative arthritis and, 621 incidence of, 623, 623t joint congruence and capacity and, 620 loose bodies and, 621 nerve distances to capsule and portals, 621t neurovascular structures and, 620 osteophyte removal and, 621 post-traumatic elbow and, 621 prevention of, 623 relative risk by diagnosis, 621t relative risk by procedure, 622t rheumatoid arthritis and, 620–621 synovectomy and, 622 vascular insult and, 622–623 Arthroscopic synovectomy aftercare and, 927 results and, 929 technique, 926–927, 927f–928f Arthroscopy. See also Arthroscopic complications; Loose bodies advantages of, 578 anesthesia and, 567–568 anterolateral portal and, 570, 570f arthritic stiff elbow management and, 602–606 arthrofibrosis and, 596–602 arthroscopic retractors and, 580– 581, 581f articular injuries and, 683, 683f capitellar prosthetic replacement and, 733–738 contraindications and, 567 débridement and, 579–580, 582 disadvantages of, 578 elbow dislocations and, 691 elbow instability and, 582–583 elbow stiffness and, 331, 596–606 extra-articular developments and, 625 future of, 625 history and, 567 indications and, 567 intra-articular opportunity and, 625

Arthroscopy (Continued) lateral collateral ligament insufficiency and, 673 lateral decubitus position and, 569, 569f lateral epicondylitis and, 609–616 lateral instability and, 584–585, 584f–585f loose bodies and, 574–575, 574f– 575f, 578–581 medial instability and, 583, 583f–584f midlateral portal and, 572 nerve injuries and, 575 nonarthritic stiff elbow management and, 596–602 olecranon stress fractures and, 690 osteoarthritis and, 1046–1047, 1046f, 1046t pitfalls and, 575 pivot shift test and, 584, 585f portals and, 569–573 positioning and, 568–569 posterior medial gutter surgery, 602f posterolateral portals and, 572–573 primary lateral portals and, 573f procedures and, 573–575 prone position and, 568–569, 569f proximal anteromedial portal and, 569–570, 570f radial ulnohumeral ligament reconstruction and, 617–619, 618f reduction and internal fixation and, 373 septic arthritis and, 1061 standard posterior portals and, 574f straight posterior portal and, 572, 572f supine position and, 568, 568f surgical techniques and, 567–575 symptomatic plicae and, 581–582, 582f synovectomy and, 581 technical alternatives and, 575 tennis elbow and, 639, 640f, 651, 654 in throwing athlete, 587–594 ulnar collateral ligament injuries and, 665, 666f Arthrosis. See also Semiconstrained elbow replacement radiohumeral, 729–738 traumatic, 439, 441f, 814–827 Arthrotomy aftercare and, 926 Kocher approach and, 925–926, 925f technique, 925–926, 925f Articular bushing wear, 880–884 Articular fixation, distal humerus fractures and, 340, 341f

1184 Index

Articular forces for selected activity, 58f Articular injuries accessory ossicles and, 680, 681f acute instability in adults, 691 arthroscopy and, 683, 683f bone and cartilage anatomy and, 680 carrying angle and, 682f cartilage damage and, 403–404, 408–414 chronic valgus insufficiency in adults, 691–693 detailed history and, 681–682 differential diagnosis and, 682t elbow dislocations with associated fractures, 691 fragment displacement and, 684 gravity stress test and, 684–685, 685f hinged external fixation and, 499, 502f–503f imaging and, 682–683 lateral compression injuries in adolescence, 686–688 ligamentous anatomy and, 680 loose bodies and, 692 medial epicondylar stress lesions, 683–684, 683f medial epicondyle avulsion fractures, 684–685, 684f–685f medial ligament instability and, 685–686, 685f medial tension injuries in adolescence, 683–686 olecranon stress fractures and, 689– 690, 689f, 690f osteochondritis dissecans of the capitellum, 686–688, 687f–689f, 688t osteochondrosis of the olecranon, 688–689 Panner’s disease and, 686, 688t, 689f physical examination and, 682 posterior impingement view and, 684 rehabilitation and, 693 shear injuries in adolescence and, 688–689 synovial lesions and, 692–693 throwing injuries and, 691 valgus extension overload and, 692 Articular interaction with ligaments, 45–48, 46f–49f Articular margin, 15f Articular patterns, rheumatoid arthritis and, 1031f Articular surfaces. See also Articular injuries contact stress and, 57–58, 58f, 59f distal humerus fractures and, 338– 340, 339f

Articular surfaces (Continued) distributive forces and, 56–57, 56f–58f radial head fractures and, 365–366, 366f radial neck fractures and, 279 Articulated external fixators. See Hinged external fixation Articulation, 16–17 humerus, 16, 17f–18f proximal radius, 16, 18f proximal ulna, 16–17, 19f total elbow arthroplasty and, 852, 853f Aspiration acute bursitis and, 1168, 1169f distal humeral nonunion and, 350 early diagnosis and, 863, 864f septic arthritis and, 1060, 1061f Aspirin, 147t Atraumatic motion implementation, 153–155 active assisted range of motion, 154 active range of motion and, 154–155 joint mobilizations and, 155 neural gliding and, 155 passive range of motion and, 155, 155f resisted range of motion and, 155 timing of, 154–155 Augmentation procedures, biceps tendon injury and, 530–531 Autografts, osteochondral, 592, 592f–593f Avascular necrosis, 237–238, 1141f fishtail deformity and, 237–238, 237f management of, 238 motion loss and, 238, 238f radial head fractures and, 273, 276–277 radial neck fractures and, 277, 278f sickle cell disease and, 1074 trochlear blood supply and, 237f Avulsion, biceps tendon. See Distal biceps tendon injury Avulsion fracture, 317f Axial alignment, physical examination and, 67, 68f Axial fasciocutaneous flaps, 550–552, 551f Axial load coronoid process fractures and, 420f radial head fracture and, 359–360, 360f Axillary block, 143, 145f Axis of rotation linked elbow arthroplasty and, 766– 767, 767f muscle moment arm and, 51–52, 52f

B Baumann’s angle, 212, 212f Bell-Tawse procedure, 312 Benign bone tumors aneurysmal bone cyst, 1137–1139, 1138f benign cartilage tumors, 1139–1140, 1140f cyst of the ulna, 1140f fibrous dysplasia, 1139f giant cell tumors, 1137, 1138f osteochondroma, 1136–1137, 1136f osteoid osteoma, 1133–1136, 1134f–1135f Paget’s disease, 1139f Benign soft tissue tumors ganglion, 1146 glioma, 1146 lipoma, 1145–1146, 1145f myositis ossifications, 1147 myxoma, 1146 pigmented villonodular synovitis, 1146–1147, 1146f–1147f synovial chondromatosis, 1147, 1147f Biceps. See also Distal biceps tendon injury anatomy of, 30–31, 31f rerouting of, 991, 992f tenotomy, 1006 Biceps-brachialis lengthening, 1008– 1011, 1009f–1010f Biceps-to-triceps transfer, 980–990 Bicipital radial bursa, 1164, 1166f Bilateral congenital pseudoarthrosis, 401–402 Bilateral elbow disease, 949 Bioabsorbable fixation, 396–397 Biocompatibility, allograft replacement and, 915–918 Biofeedback, 1126 Biologic enhancement. See Bone morphogenic protein (BMP-7) Biomechanics, 39–60. See also Elbow force analysis articular and ligamentous interaction, 45–48, 46f–49f capacity of elbow joint, 43 carrying angle, 40–43, 42f, 43f center of rotation, 39–40, 41f, 42f contact area, 43–44, 44f elbow force analysis, 48–60 elbow stability, 44–45, 45f flexion-extension, 39 force across elbow joint, 48 forearm rotation, 40, 42f kinematics, 39 radial head, 359 restriction of motion, 43, 43f Biopsy procedures, 1132 Bipolar transfer, 965

Index 1185

Bipolar transplantation for elbow extension restoration, 985–986, 985f–986f for flexion restoration, 966–968, 967f, 969f, 972–973, 972f Blood vessels, disarticulation amputation and, 1015–1016 Bone. See also Bone and joint anomalies; Bone loss; Osseous complications disarticulation amputation and, 1016 recontouring, 356 resorption, 945 Bone and joint anomalies ankylosis, 189f–190f, 192, 195f, 199 combined with soft tissue anomalies, 197 instability, 190f, 192–196, 196f, 199, 200f synostosis, 188f, 190–192, 194f, 197– 199, 198f Bone grafting distal humeral nonunion and, 352– 353, 353f olecranon and proximal ulna nonunion and, 408, 410f–413f Bone loss classification of, 892f segmental, 911–913, 915f semiconstrained elbow replacement and, 815, 816f Bone morphogenic protein (BMP-7), 404 Bone spurs, 493 Bone struts applying in pairs, 901, 902f indications for, 901 results and, 903, 904f “shuck” test and, 903, 903f significant deficiencies and, 901, 902f surgical technique and, 901 technical notes and, 901–903 ulnar deficiency and, 904f Bone tumors. See Benign bone tumors; Malignant bone tumors Botulinum toxin injections, 1005–1007 Boutonnière deformity, 1027f Boyd-Anderson technique, 528, 530f Boyd postlateral exposure, 119–120, 121f–122f Brachial artery anatomy, 24, 25f–27f Brachial plexus blocks and, 143, 145 catheters and, 148–149 paralysis and, 976 Steindler’s flexorplasty and, 964f Brachialis anatomy of, 31, 32f lengthening of, 1006 rupture of, 533

Brachioradialis anatomy of, 31, 32f–33f flaps, 556, 558f transfer and, 990 Bracing and splinting, 164–169. See also Ulnar collateral ligament injuries achilles tendon allograft and, 939 daily program sample, 168f dynamic splinting, 166–167, 166f elbow contracture pathology and, 164, 165f elbow stiffness and, 164, 328 extrinsic contracture and, 493–494, 494f fused elbow and, 833 medial epicondylitis and, 645, 645f posterior deltoid transfer and, 988 restorative splinting, 165–166, 166f, 167f static adjustable splints, 167–169, 167f–168f static and protective splints, 164, 165f Steindler’s flexorplasty and, 963, 963f tennis elbow tendinosis and, 633– 634, 633f Brain injury, traumatic, 477–479, 478f Brushing exchange, isolated, 880–882 Brushing replacement, 852 Brushing wear, total elbow arthroplasty and, 852 Bryan-Morrey approach, 17f, 126–127, 757, 806f Burn patients, ectopic bone formation in, 479, 479f Bursae anatomy, 23–24, 24f Bursitis acute bursitis treatment, 1168, 1169f anatomy and, 1164, 1165f aspiration and cortisone injections and, 1168, 1169f bicipital radial bursa, 1164, 1166f chronic bursitis treatment, 1168–1169 clinical presentation and, 1167 complications and, 1171, 1172f deep bursae, 1164, 1166f elbow pads and, 1169f endoscopic procedures and, 1169–1170 gouty arthritis and, 1167, 1167f hemodialysis and, 1167 olecranon bursitis, 1166–1167, 1166f olecranon spur and, 1167, 1168f open procedure and, 1170, 1170f operative intervention and, 1169–1170 reconstructive options and, 1171, 1171f rheumatoid arthritis and, 1167

Bursitis (Continued) superficial bursae, 1164–1166 surgical results and, 1171 swelling and, 1167, 1169f triceps and, 1164, 1166f triceps tendon rupture and, 1167, 1167f

C Calcific tendinitis, 533 Calcification, tennis elbow tendinosis and, 636 Campbell posterior approach, 124–125, 126f Cannulated reamers, 795f Capacity, elbow joint, 43 Capitellar prosthetic replacement, 733–738 aftercare, 737 broaching distal humerus, 736–737, 737f capitellum trial, 736, 736f clinical results and, 737–738 closure and, 737, 737f exposure and, 733, 735f implanting final component, 737, 737f incision and, 733 indications for, 733, 734f–735f surgical technique and, 733–737 Capitellocondylar arthroplasty, unstable, 748f–749f Capitellocondylar device, 857f Capitellum fractures, 360, 730, 730f imaging of, 176–177, 177f lesions, 589–590, 686, 688f osteochondritis dissecans of, 687– 688, 687f–689f, 688t osteochondrosis of, 288, 289f resection, 735, 736f traumatic arthritis of, 734f Capsular release arthroscopic complications and, 621–622 distal humeral nonunion and, 351– 352, 352f extrinsic contracture and, 488 Capsular tears, 107f Capsulectomy, 328 Cardiac conditions, rheumatoid arthritis and, 1029 Carrying angle anatomy and, 17–18, 20f angular deformities and, 67, 68f supracondylar fractures and, 208f uncertainty regarding, 40–43, 42f, 43f Catheters brachial plexus, 148–149 intra-articular, 149–150, 150f Celcoxib, 147t

1186 Index

Cellulitis, 1064, 1064f Cement, eccentric reaming of, 894f Center of rotation, 39–40, 41f, 42f Cerebral palsy, 1002–1003 clinical assessment and, 1002–1003 diagnosis and, 1002, 1003f dislocations in children and, 299, 300, 303f goal definition and, 1003 simple classification of, 1003 Cervical nerve rupture, 994 Cervical osteoarthritis, 627–628 Cervical radiculopathy, 67 Chair sign, 672 Charcot joints. See Neurotrophic arthritis Charcot-Marie-Tooth disease, 1083 Chevron transolecranon osteotomy, 130–132, 134f Child’s elbow. See Pediatric elbow Chip fractures, 258 Chronic unreduced dislocations, 463– 470. See also Dislocations achilles tendon allografts and, 468f complications and, 467 continuous passive motion and, 467 elbow joint and, 463 motion and, 467 occurrence and, 463 pathology of, 464 postoperative management and, 467 presentation and, 463 success rate treating, 470, 470f surgical technique and, 465–467, 465f–466f treatment of, 463–464, 464f treatment results, 467 triceps management and, 467 Chronic valgus insufficiency in adults, 691–693 Chryseobacterium meningosepticum, 1063 Circumduction motion, 81f Circumferential wrapping, continuous passive motion and, 162 Clark’s transfers, 973–974 Cleidocranial dysostosis, 299 Closed reduction acute anterior dislocation and, 304 supracondylar fractures and, 214, 216f Coccidiodes immitis, 1063 Coccidioidomycosis, 1063 Codeine, 148t Collateral ligament insufficiency. See Lateral collateral ligament insufficiency Column procedures, 489–496 advantages of, 489 aftercare, 493–494 clinical results and, 494–495, 495f closure and, 493

Column procedures (Continued) complications and, 496 disadvantages of, 470–472, 470f–472f exposing and excising posterior capsule and bone spurs, 493 exposing anterior capsule for excision and incision, 491– 493, 492f exposing ulnar nerve and medial fascia, 491 indications for, 489 lateral approach, 491 medial release, 491–493 osteoarthritis and, 1047, 1047f patient positioning and skin incision, 491 post-traumatic elbow stiffness in children and, 328 ulnar nerve transposition and, 493 Combined bone and soft tissue anomalies, 197, 199–201 Comminuted fractures of distal humerus, 345f, 723f Compartment syndrome dislocations and, 445 postischemia-initiated, 232f schematic view of, 232f supracondylar fracture and, 227–228 symptoms and signs of, 230–231 treatment of, 234–235 typical findings in, 232t Volkmann contracture and, 229f, 235 Compass fixators, 501f Compass Hinge, 510–513. See also Hinged external fixation application of distraction, 512, 512f axis pin placement, 511, 511f frame assembly, 510, 511f humeral pin placement, 511, 512f patient positioning and, 511 ulnar fixation placement, 511–512, 512f Complex instability. See also Stability, elbow clinical management of, 451–452 coronoid fracture and, 456–459, 457f–458f definition of, 450 Dynamic Joint Distractor and, 453, 454f, 459, 459f elbow dislocation and, 453–454, 454f fixation and, 453, 454f gross valgus instability and, 453, 453f Mayo elbow brace and, 460f medial ligament injury and, 452–453 olecranon fracture and, 455–456, 455f, 456f

Complex instability (Continued) proximal fracture of ulna and, 454, 455f radial head and coronoid fracture with dislocation and, 459 radial head fractures and, 452–454 radiohumeral joint restoration and, 452–453 treatment of, 459–461, 460f Compression screws, arthrodesis and, 951, 952f Computed tomography, 101–102, 102f. See also Diagnostic imaging; Imaging of pediatric elbow; pertinent conditions Computer-simulated motion, 80 Concentric contractions, 82, 83f Concomitant ulnar neuropathy, 645 Condylar fracture, malunion of, 70f Congenital abnormalities, 184–203 bone and joint anomalies, 190–199 causes of, 184 classification of, 184–190 combined bone and soft tissue anomalies, 197, 199–200 dislocations, 299, 300f, 301f webbed elbow, 197 historical perspective and, 202–203 infection and, 202 joint damage, 202 nerve damage, 202 overtreatment and, 201 physis damage, 202 soft tissue anomalies, 196–197, 199 soft tissue tumors, 197 syndromes, 185t–187t ulnohumeral dislocation, 192 unwarranted treatment and, 201 vascular compromise and, 202 Contact area, 43–44, 44f Continuous brachial plexus analgesia, 144t, 148–149 Continuous passive motion (CPM), 160–163 advantages of, 161–162 chronic unreduced dislocations and, 467 complications and, 162–163 distal humerus fractures and, 342 elbow stiffness and, 160, 329 indications and contraindications and, 163 pain control and, 161, 161f principles of use and, 160–161 range of motion and, 162, 162f Contract stress on joint articular surface, 57–58, 58f, 59f Contraction correction, pre-existing, 957 Contraction speed, 83 Contractures, malformations and, 196 Control deficiencies, 196

Index 1187

Conversion disorder, 1123 Convertible total elbow arthroplasty. See also Arthroplasty; Total elbow arthroplasty Acclaim system, 755, 756f, 761–764, 761f clinical results and, 761–764, 761f–763f complications and, 761 contraindications for, 755 design considerations and, 754 humeral preparation and, 757, 758f indications for, 755 Latitude system, 755–757, 756f, 761– 764, 762f–763f rehabilitation and, 760 surgical considerations and, 755–757 surgical technique and, 757–760 suturing and, 760, 760f ulnar preparation and, 757–760, 759f Coonrad-Morrey implants. See also Linked elbow arthroplasty; Semiconstrained elbow replacement axis of rotation and, 766–767, 767f bone tunnels and, 778f clinical results and, 747, 749f, 752f closure and, 775 complications and, 789t composite fixation and, 58–59, 60f current implant, 768, 770f, 787f cutting block depth and, 773f exposure and, 770, 771f–772f, 773f humeral implant impaction and, 777f humeral preparation and, 770–773, 772f–773f humeral stems and, 889, 889f implant insertion and, 773–774, 775f–777f juvenile rheumatoid arthritis and, 795 loosening and, 887–888, 889f maneuver and, 770 modifications 1981-1998, 770t, 787t osteoarthritis and, 845–846 osteolysis and, 886f pin-within-a-pin mechanism, 777f polyethylene wear and, 853, 854f post-traumatic osteoarthrosis and, 814–827 preferred supine position and, 771f rationale and, 765 replacement arthroplasty and, 890–891 rheumatoid arthritis and, 787–790, 787f, 787t stem fracture and, 851 surgical technique for, 770–775 survival data and, 887f

Coonrad-Morrey implants (Continued) trial reduction and, 773, 774f triceps and, 774–775, 778f ulnar component and, 771f, 886f ulnar preparation and, 773, 774f Cornelia de Lange syndrome, 299 Coronoid elbow stability and, 450–451, 452f lateral collateral ligament insufficiency and, 676 Coronoid process fractures, 419–424 association injuries and, 419 avulsion fracture and, 317f axial load and, 420f chronic painful subluxation and, 424f classification of, 419, 421f comminuted coronoid fractures, 422f complex instability and, 456–459, 457f–458f incidence of, 419 injury mechanism and, 419 medial coronoid fracture, 423f radial head fracture and, 360–361 radial head fracture with dislocation and, 459 reconstruction and, 422 Regan-Morrey classification and, 421f stress fixation and, 428f stress fractures and, 287, 287f, 423–424 surgical technique and, 422, 424f–427f treatment of, 419–422 type I fracture, 419–420 type II fracture, 419, 420 type III fracture, 419, 420–422 ulnohumeral joint stability and, 420f Corticosteroids, rheumatoid arthritis and, 1032 Cortisone injections acute bursitis and, 1168, 1169f tennis elbow tendinosis and, 636 Cosmoses, 958 Counterforce bracing. See also Bracing and splinting medial epicondylitis and, 645, 645f tennis elbow tendinosis and, 633–634, 633f Country club elbow, 627 Cross-sectional anatomy, surgical exposures and, 116f Crossed tibial graft technique, 951f Crutch walkers, lateral collateral ligament insufficiency and, 670 Cryocuff (Aircast), 153, 153f Crystal examination, olecranon bursitis and, 1065

Crystalline arthropathies, 1039–1041, 1040t Cubital artery distribution, 553f Cubital bursitis, 519f Cubital fossa, “M” pattern over, 11, 13f Cubital tunnel, palpation and, 72f Cubital tunnel syndrome, 627 Cubitus varus deformity and, 670 supracondylar fractures and, 239– 240, 242f Cutaneous nerve entrapment, 1112–1113 Cutaneous nerves, upper limb, 11, 14f Cutis arthroplasty, 935, 936, 940, 941f, 942 Cutis laxa syndrome, 298 Cyclooxygenase (COX), 146–147 Cystic swelling, rheumatoid arthritis and, 1028f

D D-Penicillamine, 1032 Dartmouth Pain Questionnaire, 1125 Débridement arthropathy and, 1072–1073 arthroscopic, 579–580, 582 articular bushing wear and, 881 for chronic draining Pseudomonas osteomyelitis, 953f extended, 1051–1052, 1052f infected prosthesis and, 1061–1062 irrigation and, 865–866, 866f medial epicondylar, 646–647, 646f open joint, 1047 posterior capsular, 599–601, 601f radiohumeral joint, 730–731 soft tissue coverage and, 547, 548f Dee total elbow arthroplasty, 888f Deep bursae, 1164, 1166f Deformity angulation and, 67, 68f avascular necrosis and, 237–238, 237f Boutonnière deformity, 1027f cubitus varus deformity, 670 fishtail deformity, 237–238, 237f fused elbow and, 834f lateral collateral ligament insufficiency and, 676 post-traumatic osteoarthrosis and, 816, 817f pronation deformity, 965 rheumatoid arthritis and, 1027f semiconstrained elbow replacement and, 816, 817f supracondylar fractures and, 239–240 varus/valgus deformity, 254t Degenerative arthritis, arthroscopic complications and, 621 Delayed union, 401

1188 Index

Deltoid-to-triceps transfer. See Posterior deltoid transfer Denervation, surgical, 1083, 1085f Depression, 1123 Derotation osteotomy, 198–199 Detached fragments, osteochondritis dissecans, 293–294 Developmental dislocation, 299–300, 302f–304f Diabetes mellitus, neurotrophic arthropathy and, 1081 Diagnostic imaging, 92–111. See also Imaging of pediatric elbow; pertinent conditions anteroposterior view, 92, 93f arthrography, 101–106 assessment of, 94, 99–100, 100f–101f axial views, 94, 99f computed tomography, 100–101, 102f lateral view, 92–93, 94f–95f magnetic resonance imaging, 106–107 oblique views, 93–94, 96f–97f positron emission tomography, 111 radial head view, 94, 98f radionuclide scans, 111 stress views, 100, 102f ultrasonography, 107–109 Dimple, obliterated, 77f Direct inoculation, infection and, 1058 Disabilities of the Arm, Shoulder and Hand (DASH) questionnaire, 88, 782, 802 Disarticulation amputation surgery advantages and disadvantages of, 1015 bone and, 1016 children and, 1015 cross-section of, 1016f demographics and, 1015 early prosthesis and, 1017 functional outcomes and, 1021 muscle stabilization and, 1016, 1017f myoelectric prosthetic hands and, 1019 nerve transfers and, 1016 nerves and blood vessels and, 1015–1016 post-amputation management and, 1016–1017 prosthetic elbows and, 1019, 1020f prosthetic fitting and, 1017–1018 prosthetic management and, 1017–1018 prosthetic sockets and, 1019–1020 prosthetic training and, 1021 prosthetic wrists and, 1019 skin flap configuration and, 1015 suspension systems and, 1020–1021, 1020f terminal devices and, 1018–1019

Discovery implants, 826 Disease-modifying antirheumatic drugs (DMARDS), 862, 1056 Dislocations. See also Chronic unreduced dislocations; Dislocations in children acute ligament repair and, 443 anesthetics and, 439 anterior dislocations, 306, 320, 436, 438f associated injuries and, 439, 440f, 691 chronic unreduced, 463–470 classification of, 436 compartment syndrome and, 445 complex instability and, 452–454, 454f complications and, 444–446 coronoid fractures and, 459 delayed treatment and, 441–442 divergent dislocations, 436 ectopic ossification and, 472 elbow instability and, 437–439, 437f exercise and, 156 fractures and, 443 heterotopic bone formation and, 445–446, 446f hinged external fixation and, 499 injury mechanisms, 436, 437f late contracture and, 445 long-standing chronic, 442 medial epicondyle displacement and, 439, 440f–441f median nerve entrapment and, 444–445, 445f neurovascular complications and, 444–445, 445f osteochondral injuries and, 445 pivot-shift test and, 442f posterior dislocations, 436, 437f postreduction care, 442–443 radial head and, 69f, 361, 459 recurrent instability and, 443 rehabilitation and, 442–443 soft tissue damage and, 439 stability assessment and, 439–440, 442f treatment results, 443 ulnar nerve injury and, 445 valgus instability and, 443 Dislocations in children, 297–322 acute anterior dislocation treatment, 304–306 anatomic factors and, 297–300 anterior dislocation, 320 complications of, 320–322 congenital dislocation, 299, 300f, 301f developmental dislocation, 299–300, 302f–304f differential diagnosis and, 316–319

Dislocations in children (Continued) divergent dislocation, 320 elbow flexibility and, 297–298 fascial reconstruction of annular ligament, 306 isolated anterior dislocation, 304 joint stiffness and, 320 lateral dislocation, 320 mechanisms of, 312–314, 314f–315f medial dislocation, 320 medial epicondylar entrapment and, 319–320 Monteggia fracture-dislocation, 306–312 myositis ossificans and, 320 natural history and, 302 nerve injuries and, 320–321, 321f olecranon and, 298 posterior dislocation, 316–319 postoperative management and, 320 pulled elbow syndrome, 312 radial head and, 298, 298f, 299f, 306 radiographic appearance and, 300– 301, 301f recurrent dislocation and, 321–322 spontaneous reduction and, 314–316 traumatic dislocations, 302, 312–320 triceps fascial reconstruction and, 304–305 vascular injury and, 321 Displacement medial epicondyle fractures and, 256 metaphyseal fractures and, 284–285 radial head fractures and, 373–375, 373f–374f radial neck fractures and, 273, 276f, 279 Disposable anesthetic pumps, 149–150, 150f Distal biceps tendon injury Achilles tendon graft and, 531, 532f acute disruption and, 521–522 augmentation procedures and, 530–531 avulsion and, 518 brachialis muscle rupture and, 533 calcific tendinitis and, 533 complications and, 528–529, 529f cubital bursitis and, 519f ectopic bone formation and, 528– 529, 529f–531f endobutton technique and, 526– 528, 527f etiology and, 519 forearm ecchymosis and, 520f imaging of, 521, 521f–522f incidence of, 518 injury mechanisms, 518 interosseous nerve palsy and, 528

Index 1189

Distal biceps tendon injury (Continued) late reconstruction and, 529–530 musculotendinous junction and, 518 objective complaints and, 520–521 partial (incomplete) distal biceps rupture, 531–532, 532f pathophysiology of, 519f preferred treatment method and, 529 presentation and, 520–521 proximal retraction and, 520f radioulnar bridging and, 531f single-incision technique and, 525 subjective complaints and, 520 surgical findings and, 521 surgical repair and, 522 surgical results and, 526–528, 528t surgical technique and, 522–526 suture anchors and, 525, 526, 536f tear in continuity and, 518 tendon fixation and, 525–526 transient sensory paresthesias and, 528 treatment and, 521–522, 532–533 tuberosity and, 519f–520f two-incision technique (Mayo) and, 522–525, 524f, 526 Distal humeral fractures, 337–348 acute total elbow arthroplasty and, 800–803 anconeus-extensor carpi ulnaris interval and, 806f arthroplasty indications and contraindications, 801t arthroplasty technique and, 803–812 articular fixation and, 340, 341f articular surface reduction and, 338–340, 339f bone stock quality and, 800 Bryan-Morrey approach and, 806f comminution and, 800, 801f exposure and, 338 final fixation and, 341, 342f fracture fixation and, 800 fracture size and, 800, 801f fragments and, 807f humeral preparation and, 807, 808f implant insertion and, 809, 810f–811f joint deterioration and, 346 lateral column failure and, 347f locking screws role and, 345–346 metaphyseal bone loss and, 341– 342, 343f nonsurgical management and, 800 nonunion and, 349–354 operating room preparation and, 803, 803f patient positioning and, 803, 803f pediatric physeal fractures, 248–253

Distal humeral fractures (Continued) pitfalls and tips, 346–348 plate placement and, 340, 340f postoperative management and, 342–346, 811, 812f potential complications and, 346 principle-based fixation and, 337– 338, 338t principle-based surgical technique and, 338–341 provisional fixation and, 340, 340f range of motion and, 346 skin incision and, 803–804, 804f structural vs. fracture stability, 342– 346, 344f–345f supracondylar compression and, 340–341, 341f surgical approach and, 804–812, 805f technical objectives and, 338t, 339f treatment results and, 802t trial implantation and, 808–809 triceps split approach and, 807f ulnar preparation and, 807–808, 808f–809f wound closure and, 809, 811f Distal humeral hemiarthroplasty contraindications for, 720, 721t established nonunion and, 727f heterotopic ossification and, 727f implant considerations and, 721 indications for, 720, 721t instability and, 727f Latitude elbow system, 721, 722f nonacute injuries and, 724–725, 726f–727f olecranon osteotomy fixation, 724, 725f operative technique and, 722–724 pitfalls and complications of, 724t, 725, 727f preoperative imaging studies, 721–722, 722f–723f preoperative planning and, 721–722 principles of, 720–721 results of, 728t Sorbie Questor elbow system, 721, 722f Distal humerus achilles tendon allograft and, 938f–939f axial view of, 17f–18f bony landmarks of, 14f comminuted fracture of, 723f deficiency in, 892f hypoplasia of, 196 lateral view of, 17f posterior aspect of, 14f primate anatomy and, 6, 6f Steindler’s flexorplasty and, 962f valgus tilt of, 18f

Distal humerus malunion, 355–358 arthroplasty and, 356 bone recontouring and, 356 evaluation and, 355, 355f osteotomy and, 356, 357f treatment options and, 356, 356t treatment outcomes and, 356–358 Distal humerus nonunion, 349–354. See also Dysfunctional instability aspiration and laboratory studies and, 350 bone grafting and, 352–353, 353f capsular release and, 351–352, 352f computed tomography and, 349– 350, 350f elbow arthroplasty and, 355 evaluation and treatment options, 349–350 extra-articular nonunions, 351, 351f fixation technique and, 352–353 history and physical examination and, 349 imaging studies and, 349–350 infected nonunions and, 354 internal fixation and, 351–354, 353f joint replacement rationale and, 835 linked elbow arthroplasty and, 837f olecranon osteotomy and, 351, 352f pathology and, 349, 350f postoperative management and, 353, 836–838 prevalence and risk factors and, 349 simple radiographs and, 349 surgical indications and contraindications and, 835 surgical outcome and, 354, 838 surgical technique and, 351–353, 835–836, 837f–838f total elbow arthroplasty and, 835–838 ulnar nerve decompression and, 351 Distal lateral exposures, 117, 118f, 119f Distal nerve-to-nerve transfers, 960 Distant pedicled flaps, 559, 559f Distraction arthroplasty, 409, 414f Distraction techniques, 1126 Distributive forces, on articular surfaces, 56–57, 56f–58f Divergent dislocation, 320 DJD II fixator. See Mayo Dynamic Joint Distractor Docking technique, ulnar collateral ligament injuries and, 662– 663, 663f Doi procedure, 980–981, 980f–981f Donor muscle selection, 976–977 Dorsal forearm incisions, 235f Double gracilis transfer, 982 Double-Z rhomboid, 550, 551f Dufourmental’s method, 550, 550f Dunlop’s traction, 220

1190 Index

Dynamic electromyography, 1004, 1005f Dynamic function, strength assessment and, 85–86 Dynamic Joint Distractor, 453, 454f, 459, 459f Dynamic splinting, 166–167, 166f. See also Bracing and splinting Dynamometer, 84–85 Dysfunctional instability. See also Distal humerus nonunion arm position and, 835, 836f flail extremity and, 841f fulcrum property loss and, 835, 836f humeral bone loss and, 839 linked elbow arthroplasty and, 839f polyethylene wear and, 840f, 841 radiographs of, 839f–840f soft tissue imbalance and, 840f surgical outcomes and, 841 technical tips and, 839–841 total elbow arthroplasty and, 838–842 ulnar bone loss and, 839–841

E Eccentric contractions, 82, 82f Ectopic bone biceps tendon injury and, 528–529, 529f–531f calcification and, 277 total elbow arthroplasty and, 851, 852f Ectopic ossification. See also Heterotopic ossification adjuvant treatment and, 483 anatomic classification and, 476–477 burn patients and, 479, 479f classification of, 475–477 diagnostic studies and, 480 elbow dislocations and, 472 etiology of, 472–475 fibrodysplasia ossificans progressiva, 479–480 functional classification and, 477 incidence of, 477–479 interpositional arthroplasty and, 482 laboratory studies and, 480 neoplasms and, 1147 pathology and, 480 post-traumatic radioulnar synostosis, 473–475, 475f postoperative management and, 483 proximal radioulnar synostosis and, 477f, 478f radial head fractures and, 472 radiographic evaluations and, 480– 481, 481f at risk patients and, 477t surgical techniques and, 482–483

Ectopic ossification (Continued) surgical timing with elbow trauma, 472–473, 474f total elbow arthroplasty and, 482 traumatic brain injury and, 477– 479, 478f traumatic conditions and, 472–475 treatment principles and, 481–482 ulnar nerve transposition and, 482 ulnar neuropathy and, 482 Ehlers-Danlos syndrome, 298, 322 Elbow contracture pathology, 164, 164f Elbow dislocations. See Dislocations Elbow extension restoration biceps-to-triceps transfer, 989–990 brachioradialis transfer, 990 forearm restoration and, 991 free-functioning muscle transfers and, 991 latissimus dorsi transfer or transplant, 984–986, 984f muscle tendon transfers, 984–993 neurotization, 983–984 posterior deltoid transfer and, 986–989 preferred treatment and, 993–994 teres major-to-triceps transfer, 991 transfers for pronation, 991–992, 992f transfers for supination, 992–993 Elbow extensors, 33–34 anconeus, 34, 34f electromyographic studies of, 54–56 subanconeus muscle, 34 triceps brachii, 33–34, 34f Elbow flexion restoration. See also Flaccid dysfunction; specific procedure arthrogryposis and, 973 bipolar transplantation, 966–968 complete bipolar transportation of pectoris major, 972–973 flexor carpi ulnaris transfer, 976 free-functioning muscle transfers, 976–983 gracilis transfer, 977–982 latissimus dorsi transfer, 965–966, 982–983 neurotization, 958–961 partial bipolar transplantation of pectoralis major, 972 pectoris muscle transfer, 969–970 preferred treatment and, 993–994 Steindler’s flexorplasty, 961–965 sternocleidomastoid transfer, 976 triceps transfer, 974–976 ulnar transfer, 968–969 unipolar transfer, 970–971 Elbow flexors, 30–36 biceps, 30–31, 31f brachialis, 31, 32f

Elbow flexors (Continued) brachioradialis, 31, 32f–33f electromyographic studies of, 54, 56f extensor carpi radialis brevis, 32, 32f–33f extensor carpi radialis longus, 31–32, 33f extensor carpi ulnaris, 32, 34f extensor digitorum communis, 32, 33f flexor carpi radialis, 35 flexor carpi ulnaris, 35–36 flexor digitorum superficialis, 36 palmaris longus, 35 pronator teres, 34–35 supinator, 32–33, 34f Elbow force analysis, 48–60 axis of rotation change and, 51–52, 52f contact stress on joint articular surface, 57–58, 58f, 59f direction of externally applied force and, 51, 52f distributive forces on articular surfaces, 56–57, 56f–58f elbow joint flexion angle and, 49, 50t electromyographic activities of elbow muscles, 54–56 extensors and, 54–56 flexors and, 54, 56f force across elbow joint, 48 forearm muscles, 56 major elbow muscles and, 53–54, 53t, 54f, 54t, 55f multiple muscle analysis, 52–53 muscle moment arm effects, 50, 50f, 50t orientation and muscle line of action, 50–51, 51f single-muscle analysis, 49–50, 50f, 51t total elbow prosthesis and, 58–59, 60f Elbow function. See Functional evaluation Elbow morphology, human vs. ape, 7–8 Elbow motion, 80–82 complex active motion, 80, 80f functional motion, 80–82, 80f–82f normal motion, 80 Elbow stability, 44–45, 45f, 190f. See also Complex instability; Dysfunctional instability acute instability, 691 arthroplasty and, 835–842 arthroscopic assessment and, 582–585 articular elements and, 450–451 coronoid and, 450–451, 452f

Index 1191

Elbow stability (Continued) coronoid process fractures and, 456–459, 457f–458f diagnosis and, 192–196, 196f dislocations and, 437–440, 442f, 443, 452–454 dysfunctional instability, 835–842 elbow stiffness and, 327 humeral bone loss and, 839 iatrogenic medial elbow instability, 648 implant failure classification and, 885–886 implant removal and, 854–856, 856f instability treatment, 199, 200f lateral collateral ligament insufficiency and, 670–671 lateral instability, 584–585, 584f– 585f, 735f ligamentous contributions and, 451 linked elbow arthroplasty and, 837f, 839f medial instability, 583, 583f–584f olecranon and, 450, 451f, 455–456, 455f, 456f physical examination and, 75–76, 76f posterior radial head instability, 305f posterolateral instability, 76, 584– 585, 584f–585f radial head and, 359, 360f, 450, 451f rotatory instability, 76–77, 77f–78f, 724t semiconstrained elbow replacement and, 815 synovectomy and, 932 tennis elbow surgical failure and, 651, 652f total elbow arthroplasty and, 835– 842, 854–856, 856f, 885–886, 887f–888f ulnar bone loss and, 839–841 ulnar fracture and, 454, 455f ulnohumeral instability, 47–48, 49f valgus instability, 76, 76f, 443, 453, 453f varus instability, 76, 76f Elbow strength, 85–86 Electrical stimulation, 403–404, 634 Electromagnetic sensors, 80 Electromyographic activities, elbow muscles and, 54–56 Electromyographic biofeedback, 153 Embryonic alterations, 202 Endobutton technique, 526–528, 527f English Stanmore prosthesis, 769f Entrapment, nerve. See Nerve entrapment syndromes Epicondylitis, 72 Epiphyseal growth, physeal fractures and, 246, 247f

Epiphyseal plate fusion, radial neck fractures and, 277 Epithelioid sarcoma, 1149, 1149f Erb’s palsy, 957 ERS device, 856f Escherichia coli, 1074 Esmarch bandage, 279 Essex-Lopresti injury, 361 Essex-Lopresti lesions, 733, 733f Etanercept, 1033 Evolution of elbow development. See Phylogeny Ewald arthroplasty, 741–742, 741f, 747 Ewing’s sarcoma, 1142, 1142f Extended débridement, osteoarthritis and, 1051–1052, 1052f Extensile medial approach, 136–138, 137f Extensile postlateral exposure, 120–122, 123f Extension. See also Elbow extension restoration functional arc of, 74f loss of, 82f normal, 74f strength assessment and, 74, 75f triceps length and, 84f Extension-type fractures, in children, 208 Extensor carpi radialis brevis anatomy, 32, 32f–33f tennis elbow and, 609–616, 610f– 612f, 615f Extensor carpi radialis longus anatomy, 31–32, 33f flaps, 556 tennis elbow and, 609, 611f, 612 Extensor carpi ulnaris anatomy, 32, 34f Extensor digitorum communis anatomy, 32, 33f tennis elbow and, 609, 610f Extensors. See Elbow extensors External fixation. See also Hinged external fixation achilles tendon allograft and, 939, 940f skeletal, 951, 953f–954f Extra-articular involvement, septic arthritis and, 1062 Extra-articular nonunions, 351, 351f Extraplexus transpositions, 959 Extrinsic contracture. See also Column procedures capsular release and, 488 classification of, 474–475 column procedures and, 489–496 complications and, 496 contraindications and, 489 diagnosis of, 488 etiology of, 474 incidence of, 474 indications and, 488–489

Extrinsic contracture (Continued) nerve palsies and, 495–496 open release and, 489 preoperative planning and, 489, 489f presentation of, 474–475 radiograph showing, 488f splint therapy and, 493–494, 494f treatment options, 474

F Factitious injury, 1123 Failure classification, implant, 885–888. See also Revision arthroplasty device failure, 885 instability, 885–886 loosening, 886–888 septic failure, 885 Fascia lata, interposition arthroplasty and, 935, 936 Fascial arthroplasty. See Interposition arthroplasty Fascial reconstruction of annular ligament, 306 Fasciocutaneous flaps antecubital, 552–553, 553f axial, 550–552, 551f transposition, 551–552 Fasciotomy, forearm, 234–236 Fasciotomy incisions, 235–236, 235f–236f Fat pad sign, 364, 365f Fentanyl, 146t Fetal alterations, 202 Fibrodysplasia ossificans progressiva, 479–480 Fibromyalgia, 699, 1123 Fibrosis, 160 Fibrous dysplasia, 1139f Figure-of-eight wiring, olecranon fractures and, 398 Fine-needle aspirates, 1132 Fishtail deformity, 237–238, 237f, 253, 262 Fixation. See also Distal humeral fractures; Hinged external fixation; Internal fixation; Olecranon fractures; Radial head fractures achilles tendon allografts and, 939, 940f ankylosis and, 499–500 articular, 340, 341f, 499, 502f–503f bioabsorbable, 396–397 complex stability and, 453, 454f Coonrad-Morrey implants and, 58– 59, 60f coronoid process fractures and, 428f distal humerus nonunion and, 351– 354, 353f hybrid interference screw fixation technique, 663–665, 664f–665f

1192 Index

Fixation (Continued) infected total elbow arthroplasty and, 864 intermedullary screw fixation, 394– 395, 395f Kirschner wire fixation, 243 lag screw fixation, 408, 409f neural injuries and, 516 open reduction and internal fixation (ORIF), 367–370, 370f, 371–375 plate-and-screw fixation, 395–396, 396f skeletal, 951, 953f–954f supracondylar fractures and, 242f, 243 threaded fixation, 243 two-pin lateral-entry fixation, 227 Fixed elbow flexion, 82f Flaccid dysfunction arthrogryposis and, 973 biceps-to-triceps transfer and, 989–990 brachioradialis transfer and, 990 donor muscle selection, 976–977 flail arm and, 957 flexion restoration and, 958–961 flexor carpi ulnaris transfer and, 976 free-functioning muscle transfers and, 976–977, 991 general principles and, 956–958 gracilis transfer and, 977–982 injury types and, 956 latissimus dorsi transfer and, 965– 969, 984–986, 984f muscle choice for tendon transfer and, 957–958 muscle strength grading system and, 958t neurotization and, 958–961, 983–984 paralysis and, 956 pectoralis major and, 972–973, 972f pectoralis muscle transfer and, 969–974 posterior deltoid transfer and, 986–989 pre-existing joint contracture and, 957 preferred treatment method and, 993–994 pronation and, 991–992, 992f reconstructive procedures and, 956 Steindler’s flexorplasty and, 958, 961–965 sternocleidomastoid transfer and, 976 supination and, 992–993 teres major-to-triceps transfer, 991 tetraplegic patients and, 956–957 timing of reconstruction and, 956–957

Flaccid dysfunction (Continued) triceps-to-biceps transfer and, 958 triceps transfer and, 974–976 Flaccid elbow paralysis, 976 Flail arm, 956–957. See also Flaccid dysfunction Flail elbow, 917f Flexion. See also Elbow flexion restoration contractures, 199, 965 functional arc of, 74f hemiarthroplasty and, 724t loss of, 82f maximum force and, 53, 54t muscle and joint forces in resisting, 53, 53t normal, 74f, 80f strength assessment and, 74, 75f, 85, 85f Flexion crease anatomy, 12f Flexion-pronation test, 582 Flexion-type fractures, in children, 208 Flexor carpi radialis anatomy, 35 Flexor carpi ulnaris anatomy, 35–36 arcade, 646–647 transposition to radius, 993, 993f Flexor digitorum superficialis, 35f, 36 Flexor-pronator mass, 647, 647f Flexor-pronator muscle group, 34–36, 962f Flexor-pronator slide, 1011 Flexorplasty, Steindler’s. See Steindler’s flexorplasty Flexors. See Elbow flexors Force analysis. See Elbow force analysis Forearm. See also Forearm rotation compartments, 228f ecchymosis, 520f fasciotomy, 234–236 incisions, 235–236, 235f–236f muscles, electromyographic studies of, 56 Forearm ischemia. See Ischemic injuries Forearm rotation, 40, 42f functional arc of, 74f fused elbow and, 830, 831f inflammatory changes and, 70 restoration of, 991 valgus and varus laxity and, 47 Forelimb, skeletal structure of, 7, 7f Fossil evidence, elbow evolution and, 8–10 Fractures. See specific fracture type Fragment displacement, articular injuries and, 684 Free flaps, 559–561, 560f Free-functioning muscle transfers donor muscle selection and, 976–977 elbow extension restoration and, 991

Free-functioning muscle transfers (Continued) flexion restoration and, 976–977 forearm rotation restoration and, 991 gracilis transfer and, 977–982 latissimus dorsi transfer and, 982–983 patient considerations and, 977 Free-tissue transfers, 559–561, 560f Froimson harvesting technique, 940, 941f Functional arthroplasty, 935, 936f. See also Interpositional arthroplasty Functional evaluation, 80–88 effective scheme characteristics, 86t, 87 elbow motion, 80–82 elbow strength, 85–86 muscle contraction types, 82, 83f muscle length at contraction, 83–84 outcome measures, 88 performance indices and, 86–87 stability, 86 strength, 82–85 Fused elbow angular deformity and, 834f axis of rotation and, 832 clinical results and, 833 compensatory motion and, 830, 831f complications and, 833 contraindications for arthroplasty, 830 forearm rotation and, 830, 831f indications for arthroplasty, 830 one-bone forearm and, 834f patient selection and, 830 postoperative care and, 832–833 preoperative assessment, 830 preoperative soft tissue reconstruction and, 830, 831f radiographic evaluation and, 830, 832f recent experiences and, 833 reoperation and, 833 soft tissue contracture and, 832, 832f surgical expectations and, 831 surgical technique and, 831–832, 832f total arthroplasty for, 830–834 Fusion. See Arthrodesis; Fused elbow

G Gantzer’s muscle, nerve entrapment and, 196 Genetic factors, osteochondritis dissecans and, 292 Giant cell tumors, 1137, 1138f Gliomas, 1146

Index 1193

Global avulsions, 994 Golfer’s elbow. See Medial elbow tendinosis Gout, 1040–1041, 1041f Gouty arthritis, 1167, 1167f Gracilis muscle transfer aftercare and, 980 bow-stringing and, 979f harvesting and, 978, 978f neurotization and, 981, 981f recipient site preparation, 977–978 single-stage reconstruction and, 978–980, 979f–980f two-stage reconstruction and, 980–982, 981f Granulation tissue, formation of, 160 Gravity-assisted motion, 154 Gravity stress test, 684–685, 685f Growth arrest, physeal fractures and, 261–262 Growth plates, dislocations in children and, 297 GSB III prosthesis, 769f, 784, 786f, 787, 852 Gschwend modified triceps splitting technique, 125 Gyroscopes, 80

H Haemophilus influenzae, 1060 Hand, reaching area of, 81f Hand reanimation, 994 Harvesting, gracilis muscle, 978, 978f Head trauma, 1004 Heberden’s nodes, 1027f Hemarthrosis, 1071–1072 Hematogenous infection, 1057–1058 Hematologic arthritis hemophilic arthropathy and, 1068–1073 leukemia and, 1075 myeloproliferative disorders and, 1075, 1075f sickle cell disease and, 1073–1075 Hemiallograft replacement, 916f Hemiarthroplasty. See Distal humeral hemiarthroplasty Hemiprosthetic device, 915f Hemodialysis, bursitis and, 1167 Hemophilia. See Hemophilic arthropathy Hemophilic arthropathy, 1068–1073 acute hemarthrosis and, 1071–1072 arthroplasty and, 1073, 1073f established arthropathy, 1072–1073 evaluation and, 1068–1071 imaging studies and, 1069–1070, 1069f–1071f laboratory studies and, 1070–1071 medical management and, 1071 pathogenesis and, 1068–1069

Hemophilic arthropathy (Continued) patterns of joint involvement, 1069–1070 pseudotumors and, 1073 radial head resection and, 1072–1073 radiographic classification of, 1069 replacement therapy and, 1071 stage II, 1069f stage III, 1070f stage IV, 1069f stage V, 1071f steroids and, 1071 synovectomy and, 1072, 1072f synoviorthesis and, 1072 Hemopoietic involvement, 1149 Henry approach, 138–140, 139f Hepatolenticular degeneration, 1177, 1177f Herbert screw, 370 Hereditary sensory and autonomic neuropathy type II, 1083 Heterotopic ossification. See also Ectopic ossification dislocations and, 445–446, 446f following distal humeral hemiarthroplasty, 727f interposition arthroplasty and, 945 lesions and, 1147 total elbow arthroplasty and, 844 trauma and, 1011–1013, 1012f High-voltage galvanic stimulation (HVGS), 153 Hinged external fixation. See also Compass Hinge; Mayo Dynamic Joint Distractor aftercare and, 512–513 anatomic landmarks and, 500f ankylosis and, 499–500 articular injury and, 499, 502f–503f articulated external fixators, 500f–501f Compass Hinge, 510–513 complications and, 515–516, 515t contraindications and, 500–503 dislocation and, 499 fixator configuration selection, 503– 504, 504f–505f fixator removal and, 512–513 indications for, 499 infection and, 516 interposition arthroplasty and, 500, 503f Mayo Dynamic Joint Distractor and, 504–510 neural injuries and, 516 reconstruction and, 499–500 residual or recurrent subluxation and, 499 results according to indication, 513– 515, 513t, 514f rotational stability and, 505f

Hinged external fixation (Continued) splints and, 512–513 traumatic circumstances and, 499 varus/valgus stability and, 504f Hinged splints, 165f Hinged type motion, 81f History taking, physical examination and, 67 Horner syndrome, 1080 Hotchkiss approach, 136–138, 137f Human immunodeficiency virus (HIV) hemophilic arthropathy and, 1068 septic arthritis and, 1059 septic olecranon bursitis and, 1064 Humeral articulating surface, extension and, 57f Humeral bone loss, dysfunctional instability and, 839 Humeral fractures, displaced, 71f Humeral implants removal of, 868, 868f revision of, 894–895 Humeral preparation convertible total elbow arthroplasty and, 757, 758f Coonrad-Morrey device and, 770– 773, 772f–773f distal humeral fractures and, 807, 808f total elbow arthroplasty and, 746f Humerus. See also Distal humerus anatomy of, 11, 14f anterior displacement of, 457f articulation of, 16, 17f–18f Hyaline cartilage anatomy of, 18f–19f tennis elbow tendinosis and, 630, 630f Hybrid interference screw fixation technique, 663–665, 664f–665f Hydrochloroquine, 1032 Hydrocodone, 148t Hydromorphone, 146t, 148t Hyperemic arthropathy, 1080f Hyperlipoproteinemia type II, 1177–1178 Hyperparathyroidism, 1174–1175, 1176f–1177f Hyperplasia, angiofibroblastic, 629, 629f Hypertrophic arthritis, 1053f Hypertrophic osteophyte formation, 847f Hypnosis, 1126 Hypochondriasis, 1123 Hypoplasia, 196–197

I Iatrogenic injury, lateral collateral ligament insufficiency and, 670 Iatrogenic medial elbow instability, 648

1194 Index

Iatrogenic ulnar nerve injury, 226 Ibuprofen, 147t Idiopathic arthropathy, 1083–1084 Imaging of pediatric elbow, 173–182. See also Diagnostic imaging basic elbow study, 173–175 capitellum and, 176–177, 177f lateral epicondyle and, 180–181, 181f magnetic resonance imaging and, 175, 175f medial epicondyle and, 177–178, 179f multidetector computed tomography technology and, 173, 174f normal development and, 175–181, 176f normal variants and, 181–182, 181f–182f olecranon and, 178–180, 180f–181f radial head epiphysis and, 178 radiocapitellar line and, 177, 178f trochlear epiphysis and, 178, 179f–180f ultrasonography and, 175–176 Immediate exchange arthroplasty, 868–869 Impact grafting indications for, 899 results and, 900–901, 901f surgical technique and, 899–900, 900f Implant removal. See also Revision arthroplasty infection and, 853, 855f instability and, 854–856, 856f loosening and, 856–859 reimplantation and, 854, 855f total elbow arthroplasty and, 853–859 Incisions. See Surgical exposures Infected total elbow arthroplasty aspiration and, 863, 864f bacteriology and, 864–865 clinical presentation of, 863 complications and, 871 component fixation and, 864 distal humeral, 354 etiology and, 862–863 immediate exchange arthroplasty and, 868–869 incidence and, 862–863 irrigation and débridement and, 865–866, 866f patient profiles and, 863 preoperative evaluation and, 863 resection arthroplasty and, 869–871, 869f–870f risk factors and, 862 staged exchange arthroplasty and, 866–868, 867f–868f

Infected total elbow arthroplasty (Continued) symptom duration and, 863–864 treatment options and, 862, 863t, 865–871 Infections. See also Infected total elbow arthroplasty; Septic arthritis arthrodesis and, 954, 1059, 1060f component fixation and, 864 hematogenous, 1057–1058 hinged external fixation and, 516 implant removal and, 853, 855f inoculations and, 1061 interposition arthroplasty and, 945 microorganisms and, 864–865, 865f, 1058 neurotrophic arthritis and, 1079, 1080f nonbacterial infections, 1063, 1064f nonunion of olecranon and proximal ulna and, 403 osteomyelitis, 1057–1059 radial neck fractures and, 277 resection and, 1058, 1058f septic arthritis, 1056–1063 septic olecranon bursitis, 1063–1065 surgical procedures and, 202 Inferior ulnar collateral artery, 27f Inflammation reduction of, 152–153 rheumatoid arthritis and, 1026–1027 stress-free relaxation and, 166 Inflammatory bowel disease, 1040t Infraclavicular block, 143 Inoculation, infection and, 1058 Instability, elbow. See Complex instability; Dysfunctional instability; Elbow stability Intercostal nerve neurotization, 960f transfer, 959 Internal fixation bioabsorbable fixation, 396–397 biomechanics of, 393 distal humeral nonunion and, 351– 354, 353f intramedullary screw fixation, 394– 395, 395f olecranon fractures and, 393–397 plate-and-screw fixation, 395–396, 396f specific flexion techniques and, 393–395 tension band wiring and, 393–395, 394f Interposition arthroplasty. See also Achilles tendon allograft achilles tendon allograft and, 936–939 basic concepts and, 935 complications and, 945

Interposition arthroplasty (Continued) contraindications for, 936 current experience and, 943 cutis arthroplasty, 940, 941f cutis harvest and, 940, 941f ectopic ossification and, 482 Froimson technique and, 940, 941f hinged external fixation and, 500, 503f historical aspects of, 935 historical results and, 942–943 indications for, 935–936 limited harvest and, 941, 942f Mayo experience and, 943–945 Morrey technique and, 941, 942f outcomes and, 935 preferred tissue and, 936 revision and, 945–947, 946f–947f specific indications and, 935–936 Intra-articular abnormalities, tennis elbow tendinosis and, 628 Intra-articular catheters, 149–150, 150f Intra-articular fracture, elbow dislocation and, 439 Intracondylar recess, 69f Intramedullary pins, radial neck fractures and, 273 Intramedullary screw fixation, olecranon fractures and, 394– 395, 395f Intraoperative anesthetic management, 143, 144f–145f Intraoperative somatosensory evoked potential (SEP), 961 Intraplexus donors, 959 Irrigation, infected total elbow arthroplasty and, 865–866, 866f Ischemia. See also Volkmann’s contracture arterial injury symptoms and signs, 230 arterial injury treatment, 232–234 clinical diagnosis and, 229–231 compartment syndrome symptoms and signs, 230–231 compartment syndrome treatment, 234–235 differential diagnosis and, 231–232, 232t etiology of, 228–229 osteochondritis dissecans and, 290–292 supracondylar fractures and, 227– 236, 233f Island flaps, 552 Isokinetic contractions, 82 Isokinetic strength, 84–85 Isolated anterior dislocation in children, 306 Isolated brushing exchange, 880–882 Isolated tissue anomalies, 191f, 196–197

Index 1195

Isometric contractions, 82, 83f Isotonic contractions, 82

J J-K membrane, 935 Jobe technique, 660f, 661–662, 661f–662f Joint capsule anatomy, 18–19, 20f–21f Joint congruence, arthroscopic complications and, 620 Joint damage, 202 Joint deterioration, distal humerus fractures and, 346 Joint laxity, tennis elbow tendinosis and, 628 Joint mobilizations, 155 Joint narrowing, radiohumeral, 730, 731f Joint stiffness. See Stiff elbow Joint translocation, hemiarthroplasty and, 724t Juvenile rheumatoid arthritis aftercare and, 795–796 cannulated reamers and, 795f cementing technique and, 795 clinical outcome and, 796 complications and, 796–797 Coonrad-Morrey device and, 795 evaluation and, 792–793 joint replacement and, 797f long-term results and, 797f operative technique and, 793–795, 794f osseous ankylosis and, 794 presentation and, 792 radiographs and, 792–793, 793f severe soft tissue contracture and, 794 shoulder arthroplasty and, 792 total elbow arthroplasty and, 792–797 treatment alternatives and, 793 ulnar canal and, 795f

K Kaplan-Meier survivorship analysis for fascial interposition arthroplasty, 945f for primary linked total elbow arthroplasty, 888f for revision of unlinked to linked prosthesis, 887f Keith needle, 527f Ketorolac (Toradol), 147t Kinematics, 39 Kinetic-kinematic chain, 157 Klebsiella pneumoniae, 864 Kocher approach displaced fractures and, 373–375 Mayo modified, 126 reconstructive procedures and, 757 synovectomy and, 925–926, 925f

Kocher exposures, 115–119 expanding distal lateral exposure, 117, 119f extensile postlateral exposure, 120– 122, 123f limited distal lateral approach, 117, 118f limited proximal lateral exposure, 118–119, 120f Mayo modified, 122, 124f Kohler’s disease, 288 Kudo arthroplasty, 740, 740f, 744–745, 744f–745f, 857f clinical results and, 747, 749–750, 751f humeral preparation and, 746f surgical technique and, 745 ulnar preparation and, 747f

L Laboratory studies. See pertinent conditions Lacertus fibrosus, palpation and, 73f Lag screw fixation, 408, 409f Late contracture dislocations and, 445 preferred treatment method, 446 Lateral antebrachial nerve entrapment, 1112–1113, 1112f Lateral approach to distal humerus, 240f Lateral aspect palpation and, 71, 72f physical examination and, 68, 69f Lateral closing wedge osteotomy of the capitellum, 687 Lateral collateral ligament insufficiency achilles tendon allograft and, 939f acute injuries and, 673, 674f arthroscopy and, 673 associated pathology treatment and, 676 basic science and, 669 chair and push-up apprehension and, 672 chronic attrition and, 669–670 chronic insufficiency and, 674–677 clinical diagnosis and, 670–673 cubitus varus deformity and, 670 etiology of, 669–670 examination under anesthesia and, 673 gravitational stresses and, 677 iatrogenic injury and, 670 imaging studies and, 672–673 instability episodes and, 670–671 ligament reconstruction and, 674– 676, 675f–676f long-term crutch walkers and, 670 magnetic resonance imaging and, 673 osteotomy and, 676 physical examination and, 671–672

Lateral collateral ligament insufficiency (Continued) plain radiographs and, 672 posterolateral rotatory drawer test and, 671, 671f postlateral rotatory pivot-shift test and, 671–672, 672f postoperative management and, 676–677 presentation and, 670–671 radial head replacement and, 676 stress radiography and fluoroscopy and, 672–673, 673f surgery and, 674–676, 675f–676f surgical outcome and, 676 suture repair and, 673, 674f tendon graft and, 674–676, 675f–676f tennis elbow and, 670 three main components in, 670f trauma and, 669–670 treatment and, 673–677 underlying deformity and, 676 Lateral column failure, distal humerus fractures and, 347f Lateral column instability, 735f Lateral compression injuries in adolescence, 686–688 Lateral condylar fractures, 253–254, 254t Lateral decubitus position, arthroscopy and, 569, 569f Lateral dislocation, 320 Lateral elbow prominence, following lateral condyle fracture, 254t Lateral elbow tendinosis. See Tennis elbow tendinosis Lateral epicondyle bony exostosis, 636 fractures, 257, 259f imaging of, 180–181, 181f Lateral epicondylitis. See Tennis elbow Lateral exposures, 115, 117f Lateral ligament complex, 20–24, 22f– 23f, 585f Lateral supracondylar interval, palpation and, 72f Lateral trochlear ridge, primate anatomy and, 4, 5f Lateral ulnar collateral ligament, 22, 23f, 45, 45f Latissimus dorsi myocutaneous pedicle flap, 556–559, 558f–559f Latissimus dorsi transfer elbow extension restoration and, 984–986, 984f bipolar transplantation and, 985–986, 985f–986f history and, 984 results and, 985–986 unipolar transfer and, 984–985, 984f, 985

1196 Index

Latissimus dorsi transfer (Continued) flexion restoration and, 965–969 anatomy and, 966, 966f bipolar transplantation and, 966–968, 967f, 969f free functioning, 982–983 history and, 965–966 myocutaneous transplantation and, 968, 968f unipolar transfer and, 968–969, 969f Latitude System clinical results and, 761, 762f–763f convertible designs and, 755–757, 756f reconstructive procedures and, 721, 722f surgical technique and, 757–760 traumatic conditions and, 826, 827f Learmonth procedure, 1104, 1104f Leflunomide, 1032–1033 Length tension curves, 84f Leukemia, 1075 Ligament anatomy, 19–24 accessory lateral collateral ligament, 22, 22f annular ligament, 21–22 bursae, 23–24, 24f lateral ligament complex, 20–24, 22f–23f lateral ulnar collateral ligament, 22, 23f medial collateral ligament complex, 19–24, 21f oblique cord, 23 quadrate ligament, 22–23 radial collateral ligament, 21, 22f Ligaments. See also Lateral collateral ligament insufficiency; Ligament anatomy; Ulnar collateral ligament injuries achilles tendon allografts and, 938 annular ligament, 306 anterior oblique ligament, 643, 644f articular interaction with, 45–48, 46f–49f continuous passive motion and, 162–163 dislocations and, 306, 443 docking technique and, 662–663, 663f medial ligament injury, 452–454 medial ligament instability, 685– 686, 685f medial ligament insufficiency, 76, 76f postlateral rotatory drawer test and, 671, 671f postlateral rotatory pivot-shift test and, 671–672, 672f push-up sign and, 672 radial head fractures and, 361, 361f

Ligaments (Continued) radial head replacement and, 676 radial ulnohumeral ligament reconstruction, 617–619, 618f ulnar collateral ligament injuries, 665, 666f unlinked total elbow arthroplasty and, 739 valgus extension overload and, 665–666 valgus stress and, 72, 658–659, 659f Limited harvesting, 941, 942f Linked elbow arthroplasty, 765–780. See also Coonrad-Morrey implants angular and rotatory laxity and, 765, 766f cementing technique and, 767, 768f clinical results and, 776, 779f–780f commercial availability and, 768, 769f contraindications for, 765 Coonrad-Morrey device and, 768–775 dysfunctional instability and, 837f, 839f exposure and, 766 flexion motion and, 766f indications for, 765 positioning and, 765 postoperative dressing and, 768 postoperative management and, 776 rationale for, 765 rheumatoid arthritis and, 779f rotation axis and, 766–767, 767f semiconstrained linked implant and, 768 supracondylar fracture and, 780f surgical incision and, 766 surgical technique and, 765–768 trial reduction and, 767 triceps reattachment and, 767–768 ulnar nerve and, 766 Lipoma, 1145–1146, 1145f Liposarcomas, 1148 Little Leaguer’s elbow. See Medial epicondylar stress lesions Local flaps. See Soft tissue coverage Locking ring displacement, 852 Locking screws, 345–346 London device, 856f Loose bodies, 578–581 arthroscopic complications and, 621 arthroscopic graspers and, 579, 580f arthroscopic retractors and, 580– 581, 581f arthroscopy and, 574–575, 574f–575f, 581 compression shear forces and, 693 débridement and, 579–580 extension overload and, 693

Loose bodies (Continued) identification of, 578, 579f radiographs and, 578, 579f–581f surgical indications and, 578 surgical technique and, 578–581 synovitis and, 580, 580f Loosening, implant. See also Arthroplasty; Complete elbow arthroplasty; Revision arthroplasty biomechanics and, 846f–858f, 856 current data regarding, 858 prosthetic design and, 856–858, 858f revision and, 886–888, 895 surgical technique and, 858, 859f total elbow arthroplasty and, 856–859 treatment of, 858 Low-load, long-duration (LLLD) stretches, 155, 155f Low-profile fixation, radial head fracture and, 370–373, 372f Lymphoma, 1140–1142, 1141f

M Magnetic resonance imaging (MRI), 106–107, 108f–109f. See also Diagnostic imaging; Imaging of pediatric elbow; pertinent conditions Malignant bone tumors Ewing’s sarcoma, 1142, 1142f lymphoma, 1140–1142, 1141f osteosarcoma, 1142–1143, 1142f–1143f Malignant soft tissue tumors epithelioid sarcoma, 1149, 1149f liposarcoma, 1148 malignant fibrous histiocytoma, 1143, 1148–1149 synovial sarcoma, 1148 Malingering, 1123 Malunion, distal humeral, 355–358 Martin-Gruber anastomosis, 1110–1111 Mason classification, radial head fractures and, 363, 363f Mason type IV injury, 452–454 Matev’s sign, 321 Mayo Congruent Elbow Plate System, 340 Mayo Dynamic Joint Distractor, 501f, 505, 507f. See also Hinged external fixation applying, 505, 507f axis identification and, 505, 507f axis stylus and, 505, 508f distraction and, 509–510, 510f humeral pin insertion and, 505–508, 508f–509f patient positioning and, 504 percutaneous application and, 510, 510f

Index 1197

Mayo Dynamic Joint Distractor (Continued) surgical technique and, 504–505 ulnar pin insertion and, 508–509, 509f Mayo Elbow Brace development of, 167–169, 167f–168f extrinsic contracture and, 494f flexion and extension and, 460f nonimplantation salvage and, 913f static adjustable splinting program and, 833 Mayo Elbow Performance Scores (MEPS), 87, 87t, 784t Mayo triceps reflection technique, 126–127, 128f McGill Pain Questionnaire, 1125 Medial antebrachial cutaneous nerve entrapment and, 1113 medial epicondylitis and, 643 Medial arm flap, 555 Medial aspect palpation and, 72, 72f posterior aspect and, 68 Medial collateral ligament anatomy of, 19–24, 21f laxity and, 735f Medial condyle fractures, 254–255, 255f Medial conjoint tendon, medial epicondylitis and, 643, 644f Medial coronoid fracture, 423f Medial dislocation, 320 Medial elbow tendinosis, 626–627 Medial epicondyle. See also Medial epicondylitis avulsion fractures and, 684–685, 684f–685f débridement and, 646–647, 646f elbow dislocation and, 439, 440f–441f entrapment and, 319–320 fracture and, 256–257, 256f imaging of, 177–178, 179f postoperative pain and, 648 stress lesions and, 683–684, 683f Medial epicondylectomy, 647, 647f Medial epicondylitis anatomy and, 643, 644f complications and, 648 counterforce brace and, 645, 645f differential diagnosis and, 645 electrodiagnostic evaluation and, 645 nonoperative management and, 645 physical examination and, 644 presentation of, 643–644 radiographic evaluation and, 644– 645, 644f surgery and, 645–647, 646f–647f surgical intervention and, 645–647, 646f–647f

Medial epicondylitis (Continued) surgical results and, 647–648 valgus stress radiographs and, 644, 644f Medial fascia exposure, column procedure and, 491 Medial instability, arthroscopic assessment of, 583, 583f–584f Medial ligament injury, complex stability and, 452–454 Medial ligament instability, 685–686, 685f Medial ligament insufficiency, 76, 76f Medial periosteal hinge, supracondylar fractures and, 207f Medial release. See Column procedures Medial surgical approaches, 135–138 extensile medial approach, 136–138, 137f transepicondylar approach, 135–136 Medial tension injuries in adolescence, 683–686 Medial ulnar collateral ligament injury. See Ulnar collateral ligament injuries Median nerve anatomy, 27–28, 28f Median nerve entrapment, 1105–1112 anatomy and, 1105–1106, 1105f anterior interosseous nerve syndrome, 1109–1112, 1110f–1111f dislocations and, 444–445, 445f preferred treatment for exposure, 1111–1112 pronator syndromes and, 1106–1109 supracondylar process and, 1106 Meperidine, 146t Mesenchymal soft tissue tumors, 1143 Mesenchymal syndrome, tennis elbow tendinosis and, 627 Metabolic disease acromegaly, 1176 hyperlipoproteinemia type II, 1177–1178 hyperparathyroidism, 1174–1175, 1176f–1177f osteomalacia, 1174, 1175f osteoporosis, 1178 rickets, 1174, 1175f steroid-induced avascular necrosis, 1178–1179, 1178f tumoral calcinosis, 1174, 1176f Wilson’s disease, 1177, 1177f Metaizeau technique, 273, 274, 279 Metaphyseal bone loss, distal humerus fractures and, 341–342, 343f Metaphyseal fractures, 283–287 angulation patterns and, 286 classification and, 284 complications and, 286–287

Metaphyseal fractures (Continued) diagnosis and, 284 displacement and, 284–285 results and, 285–286 treatment and, 284–285, 286f Methotrexate, 1032 Microneurovascular muscle transfer, 976 Microorganisms implant infections and, 864–865, 865t septic arthritis and, 1058 Midlateral portal, 572 Minnesota Multiphase Personality Inventory, 1125 Moberg technique, 987–989 Mobile wad, 11 Moment arm of external force, 51 Monteggia fractures/dislocations, 424–433 accurate reduction of ulnar fracture and, 432 active rehabilitation and, 433 avoidance and, 432 classifications of, 307, 307f–309f, 424–429 clinical diagnosis of, 307–309, 310f complications and, 431 equivalent injuries and, 428–429 etiology of, 307 historical perspective and, 430–431 injury mechanisms and, 429–430 missed lesions and, 310 nerve injury and, 310 nerve palsies and, 1094 olecranon and proximal ulna nonunion and, 414 pediatric, 306–312 postoperative immobilization and, 433 preferred treatment and, 432–433 radial neck fractures and, 310–312 radiohumeral joint restoration and, 432 radiologic findings and, 430, 430f recent experiences and, 431 refracture and, 432 symptoms and signs and, 430 treatment and, 309–310, 430–431 type I injury, 426, 428f type II injury, 426, 428f type III injury, 426, 429f type IV injury, 428, 429f union and stability and, 431–432, 432f–433f Morphine, postoperative pain control and, 146t, 148t Morrey limited harvesting technique, 941, 942f Mosaicplasty, 590–593, 687

1198 Index

Motion. See also Bracing and splinting arthrodesis and, 949, 950f assessment of, 73–74, 74f elbow stiffness and, 327 radial neck fractures and, 279 restriction of, 43, 43f total elbow arthroplasty and, 849 Müller posterior oblique olecranon osteotomy, 130, 133f Multidetector computed tomography technology (MDCT), 173, 174f Multimodal analgesia, 145 Musculature. See also Elbow force analysis; Free-functioning muscle transfer; Gracilis muscle transfer; Pectoralis muscle transfer aconeus muscle, 34, 34f aconeus muscle flap, 556, 557f anatomy of, 30–36 arthrogryposis and, 973 axis of rotation and, 51–52, 52f contraction types and, 82, 83f disarticulation amputation surgery and, 1016, 1017f distal biceps tendon injury and, 533 donor muscle selection, 976–977 elbow extension restoration and, 984–993 elbow extensors, 33–34 elbow flexion restoration and, 969– 970, 976–983 elbow flexors, 30–33 electromyographic activities and, 54–56 flaccid dysfunction and, 957–958, 958f, 969–974, 976–977, 991 flexor-pronator muscle group, 34– 36, 962f forearm, 56 functional evaluation of, 82–84, 83f Gantzer’s muscle, 196 length at contraction, 83–84, 84f lines of action, 49–51, 50t, 51f microneurovascular muscle transfer, 976 paralysis and dislocations in children, 299 relationship with nerves and vessels, 26f relationship with neurovascular bundles, 25f single-muscle force analysis, 49–50, 50f, 51t strength grading system, 958t subconeus muscle, 34 tendon transfer and, 957–958 Musculocutaneous nerve anatomy, 27, 28f Musculotendinous junction injury. See Distal biceps tendon injury Mycobacterium infections, 1063

Myeloproliferative disorders, 1075, 1075f Myocutaneous transplantation, 968, 968f Myoelectric prosthetic hands, 1019 Myositis ossificans, 239, 239f, 320, 472, 1147 Myxomas, 1146

N Nail patella syndrome, 299 Naproxen, 147t Neoplasms. See also Bone tumors; Soft tissue tumors biopsy and, 1132 bone tumors, 1132, 1133–1143 clinical presentation and, 1131 hemopoietic involvement and, 1149 imaging studies and, 1131–1132 metastatic tumors, 1143, 1144f preoperative evaluation and, 1129–1130 prosthetic replacement and, 1133, 1133f soft tissue tumors, 1143–1149 staging and, 1132–1133 Nerve anatomy, 27–30 median nerve, 27–28, 28f musculocutaneous nerve, 27, 28f radial nerve, 28–29, 29f ulnar nerve, 29–30, 30f Nerve compression. See Nerve entrapment syndromes Nerve entrapment syndromes. See also Median nerve entrapment; Radial nerve entrapment; Ulnar nerve entrapment anatomy and, 1091–1092, 1091f anterior interosseous nerve syndrome, 1109–1112, 1110f–1111f categorization of, 1092 cutaneous nerves and, 1112–1113 diagnosis of, 1090–1091 lateral antebrachial nerve and, 1112–1113, 1112f medial antebrachial cutaneous nerve, 1113 median nerve and, 1105–1112 neurophysiology and, 1092 posterior antebrachial cutaneous nerve, 1113 posterior interosseous nerve syndrome, 1094–1096, 1094f–1096f pronator syndromes, 1106–1109 radial nerve and, 1092–1099 recurrent neural compression lesions and, 1090–1091 sequential neural compression lesions and, 1090

Nerve entrapment syndromes (Continued) supracondylar process and, 1106 surgical management and, 1091 ulnar nerve and, 1099–1105 Nerve injuries anatomy and, 226, 227f–228f arthroscopy and, 575 clinical diagnosis and, 227 elbow dislocation and, 320–321, 321f etiology of, 226–227 Monteggia fracture-dislocation and, 310 outcomes and future directions and, 576 rehabilitation and, 576 supracondylar fractures and, 226–227 treatment of, 227 Nerve palsies elbow stiffness and, 495–496 fractures-dislocations and, 1094, 1094f interosseous, 528 Nerve paralysis. See Nerve entrapment syndromes Nerve root compression, tennis elbow tendinosis and, 627–628 Nerve roots, elbow function and, 69, 71f Nerve transfers. See Flaccid dysfunction; Neurotization Nerves disarticulation amputation and, 1015–1016 relationship with muscles and vessels, 26f Neural gliding, 155 Neural injuries, hinged external fixation and, 516 Neurapraxia, typical findings in, 232t Neurectomy, 1007–1008, 1008f Neuritis, total elbow arthroplasty and, 849–850 Neurologic complications, continuous passive motion and, 163 Neurologic dysfunction, peripheral blockade and, 149 Neuromuscular control, restoration of, 155–157 Neurotization elbow extension restoration and, 983–984 history, 983 results and, 984 technique, 983–984 elbow flexus restoration and, 958–961 currently used transpositions and, 959

Index 1199

Neurotization (Continued) gracilis muscle transfer and, 981, 981f historical aspects of, 958–959 intercostal nerve, 960f Oberlin transfer and, 961, 961f results and, 960–961 spinal accessory nerve and, 960f technique and, 959–960, 960f–961f Neurotrophic arthritis congenital indifference to pain and, 1082–1083 diabetes mellitus and, 1081 differential diagnosis and, 1086 environmental factors and, 1079–1080 etiology of, 1079 hereditary sensory and autonomic neuropathy type II, 1083 hyperemic arthropathy and, 1080f idiopathic arthropathy and, 1083–1084 infection and, 1078f, 1079 interplay of multiple factors and, 1081f investigation and diagnosis and, 1084 laboratory investigations and, 1086 Mayo experience and, 1086f–1087f, 1087 neurovascular theory and, 1079 nociception and, 1078 pathogenesis and, 1078 surgical denervation and, 1083, 1085f syringomyelia and, 1080–1081, 1082f tabes dorsalis and, 1082, 1083f treatment of, 1084–1087 Neurovascular bundles, relationship with muscles, 25f Neurovascular injury arthroscopic complications and, 620 dislocations and, 444–445, 445f radial head fractures and, 363 supracondylar fractures and, 214, 215f, 226–227 surgical timing and, 236 Neurovascular structures, 227f Nociception, neurotrophic arthritis and, 1078 Nonarthritic stiff elbow management, 596–606 anatomic considerations and, 597 arthroscopic management of, 596–602 complications and, 601–602 etiology and, 597–598 history of, 596 indications for surgery, 598 postoperative management, 601

Nonarthritic stiff elbow management (Continued) preferred surgical method and, 598–601, 599f–603f steps in, 599 surgical results and, 601 treatment indications, 596–597 Nonbacterial infections, 1063, 1064f Nonimplantation salvage allograft replacement and, 913–919 resection arthroplasty and, 911, 912f–915f segmental bone loss and, 911–913, 915f Nonopioid analgesics, 146, 147t Nonpolarizable amorphous eosinophilic material, 630, 630f Nonreimplantation revision procedures, 851–853 articulation and, 852, 853f component failure and, 851–852 stem fracture and, 851 Nonsteroidal anti-inflammatory drugs (NSAIDs), 146–147, 153 Nonunion. See also Olecranon and proximal ulna nonunion arthrodesis and, 955 distal humeral, 349–354 lateral condyle fractures and, 253 radial neck fractures and, 276f, 277–278 Norway elbow device, 769f

O Oberlin transfer, 961, 961f Oblique cord anatomy, 23 Oblique osteotomy, 130, 133f Obstetric brachial plexus palsy, 957 Olecranon. See also Olecranon fractures bilateral congenital pseudoarthrosis and, 401–402 bursitis and, 1041f, 1063–1065, 1064f, 1166–1167, 1166f dislocations in children and, 298 elbow stability and, 450, 451f imaging of, 178–180, 180f–181f inflamed or enlarged bursa and, 70f ossification and, 401 osteochondrosis and, 688–689 perforated fossa and, 181–182, 181f posterior impingement and, 601f pseudoarthrosis and, 196 spur formation and, 73, 1167, 1167f ulcers and, 1171f Olecranon and proximal ulna nonunion allograft replacement and, 414 arthrodesis and, 414 biologic enhancement and, 404 bone grafting and, 408, 410f–413f causes of, 401–403

Olecranon and proximal ulna nonunion (Continued) children and, 402 classification of, 403, 403f clinical presentation and, 401 compression forces and, 402–403, 402f diagnosis of, 401 distraction arthroplasty and, 409, 414f electrical stimulation and, 403–404 excision and, 404, 405f, 408 general considerations and, 401 incidence of, 401 joint replacement and, 414, 415f lag screw fixation and, 408, 409f Monteggia fracture-dislocation and, 414 nonserious articular cartilage damage and, 403–404 osteosynthesis and, 404 plating and, 406–408, 407f predisposing factors and, 402, 402f severely damaged articular cartilage and, 408–414 technical options and considerations and, 404–415 tension band wiring and, 404–406, 406f treatment complications and, 416 treatment of infection and, 403 treatment options and, 403–404 Olecranon fractures anatomic considerations and, 389 AO classification system and, 390, 390f bioabsorbable fixation and, 396–397 classification and, 389–391 complex fracture-dislocations, 391 complex instability and, 455–456, 455f, 456f complications of, 398–399 coronoid process and, 314f evaluation and, 389 excision and, 391–393, 392f, 397 figure-of-eight wiring and, 398 incidence of, 389 internal fixation and, 393–397 intramedullary screw fixation and, 394–395, 395f Mayo classification and, 390–391, 390f, 403f plate-and-screw fixation and, 395– 396, 396f plate-and-screw osteosynthesis and, 397–398 preferred techniques and, 397, 397t prognosis following, 389 radial head fractures and, 360 range-of-motion exercises and, 398 stress fractures, 689–690, 689f, 690f

1200 Index

Olecranon fractures (Continued) surgical management options and, 391–393 tension band wiring and, 393–395, 394f treatment of, 391 Olecranon osteotomy distal humerus nonunion and, 351, 352f fixation and, 724, 725f hemiarthroplasty and, 724t osteoarthritis and, 843 Open joint débridement, 1047, 1048t Open reduction acute anterior dislocation and, 304– 306, 306f supracondylar fractures and, 219 Open reduction and internal fixation (ORIF) proximal radius and, 16 radial head fracture and, 367, 368– 370, 370f, 371–375 Open release, extrinsic contracture and, 489 Opioids intravenous, 146t oral opioid analgesics, 146, 148, 148t parenteral opioid analgesics, 145–146 OptiROM, 501f Orientation effects, muscle line of action and, 50–51, 51f Orthofix Inc., 501f Osseous attachment, triceps release at, 125 Osseous complications. See also Heterotopic ossification angular deformity and, 239–240 avascular necrosis and, 237–238 dislocations in children and, 297 heterotopic, 727f juvenile rheumatoid arthritis and, 794 myositis ossificans and, 239, 239f olecranon and, 401 proximal ulnar fractures and, 283, 284f revision arthroplasty and, 885–897, 899–910 supracondylar fractures and, 236–240 Osseous landmarks, 71, 71f Osteoarthritis aftercare and, 846 arc of motion and, 1043, 1044f arthroplasty indications and, 843 arthroscopic management and, 1046–1047, 1046f, 1046t clinical presentation and, 1043 column procedure and, 1047, 1047f complications and, 846–847

Osteoarthritis (Continued) Coonrad-Morrey device and, 845–846 etiology of, 1043 extended débridement and, 1051–1052 heterotopic ossification and, 844 hypertrophic osteophyte formation and, 847f incidence of, 1043 joint stiffness and, 843 laboratory studies and, 1043–1044 nonoperative treatment and, 1045 olecranon osteotomy and, 843 open joint débridement and, 1047, 1048t periarticular bone and, 844 postoperative swelling and, 844–845 presenting symptoms and, 843, 844t radiographic features and, 843, 844f, 1044–1045, 1045f relative incidence of, 1044f soft tissue release and, 844 surgical results and, 846 surgical technique and, 845–846, 845f symptoms and preferred treatment, 1046t technical considerations and, 843–845 total elbow arthroplasty and, 843–847 transverse fracture and, 847f treatment options and, 843, 844t ulnar nerve and, 844, 1052–1053, 1053f ulnohumeral arthroplasty and, 1047–1050 Osteoarthrosis, post-traumatic, 814–827 Osteochondral autograft transplantation, 687 Osteochondral injuries, dislocations and, 445 Osteochondritis dissecans, 288–293 arthroscopy and, 589–593, 591f–593f of the capitellum, 686–688, 687f– 689f, 688t clinical characteristics and, 289 completely detached fragments and, 294 computed tomography and, 290, 291f description of, 288–289 genetic factors, 292 intact lesions and, 293 ischemia and, 290–292 magnetic resonance imaging and, 175f, 290, 292f partially attached fragments and, 293–294 posterolateral subluxation and, 292f

Osteochondritis dissecans (Continued) radiographic characteristics and, 289–290 rarefied crater and, 285f trauma and, 292 treatment and, 292–294 zone of rarefaction and, 293f Osteochondroma, 1136–1137, 1136f Osteochondrosis of capitellum, 288, 289f Osteocutaneous flap, 127–130, 131f–132f Osteogenesis imperfecta, 261 Osteoid osteoma, 1133–1136, 1134f–1135f Osteolysis, articular bushing wear and, 880, 881f, 883f Osteomalacia, 1174, 1175f Osteomyelitis, 1057–1059. See also Septic arthritis antibiotics and, 1058 arthrodesis and, 1059, 1060f bone scan and, 1057–1058, 1057f contiguous focus and, 1058 direct inoculation and, 1058 fusion and, 1058–1059, 1058f hematogenous infection and, 1057–1058 imaging and, 1058 microorganisms and, 1058 presentation and diagnosis, 1057– 1058, 1057f resection and, 1058, 1058f sickle cell disease and, 1074, 1075 treatment of, 1058–1059 treatment results and, 1059 Osteophyte redevelopment, 1050, 1052f removal, 621 Osteoporosis, 1178 Osteosarcoma, 1142–1143, 1142f–1143f Osteosynthesis, olecranon and proximal ulna nonunion and, 404 Osteotomy anconeus sparing olecranon, 132– 133, 135f Chevron transolecranon, 130–132, 134f combined with triceps splitting, 132 distal humeral malunion and, 356, 357f fragment reduction and fixation, 241f lateral collateral ligament insufficiency and, 676 oblique, 130, 133f osteoarthritis and, 843 supracondylar fractures and, 241– 243, 241f templating, 241f

Index 1201

Outcome measures, functional assessment and, 88 Outerbridge-Kashiwagi procedure, 603 “Over-the-top” surgical approach, 136– 138, 137f Overload abuse, tendinosis and, 628 Overtreatment, 201 Overuse syndrome affected tissue types and, 698t definitions and synonyms and, 697 diagnosis of, 697 epidemiology and, 697–698 etiology of, 698 history taking and, 699 laboratory evaluation and, 699–700 pain management and, 700 physical examination and, 699 primary arthrosis and, 698f prominent groups and, 697 psychological factors and, 698–699 psychosocial factors and, 697–698 risk factors and, 698 99 TC bone scan and, 690, 690f three-phase bone scintigraphy and, 690 treatment and, 700–701 workplace prevention and, 701 Oxycodone, 148, 148t

P Paget’s disease, 1139f Pain. See also Analgesics; Pain dysfunction syndrome; Rehabilitation acute pain management guidelines, 148 congenital indifference to, 1082–1083 continuous passive motion and, 161, 161f coronoid process fracture and, 424f Dartmouth Pain Questionnaire, 1125 hemiarthroplasty and, 152–153 McGill Pain Questionnaire, 1125 morphine and, 146t, 148t neurotrophic arthritis and, 1082–1083 overuse syndrome and, 700 physical examination and, 67 physiotherapy and, 1125–1126 rehabilitation and, 152–153 rheumatoid arthritis and, 1026 tennis elbow tendinosis and, 630– 631, 636 Pain dysfunction syndrome classification and, 1121–1122 complex regional pain syndrome, 1122 definition and terminology and, 1120 diagnostic studies and, 1124–1125

Pain dysfunction syndrome (Continued) fibromyalgia and, 1123 historical perspective and, 1119 history details and, 1124 imaging studies and, 1124–1125 pathophysiology and, 1120–1121 patient presentation and, 1123–1125 personality, psychometric, and pain quantitation tests and, 1125 pharmacologic treatment and, 1126 physical examination and, 1124 physiology and, 1120–1121 physiotherapy and, 1125–1126 psychic disturbances and, 1126 psychology and, 1122–1123 sympathetic blockade and, 1126 temporal factors and, 1122t treatment and, 1121f, 1125–1126 trigger points and, 1124 Palmaris longus, anatomy, 35 Palpation, 71–73 anterior aspect and, 73, 73f lateral aspect and, 71, 72f medial aspect and, 72, 72f osseous landmarks and, 71, 71f posterior aspect and, 73 Panner’s disease, 164f, 288, 289f, 589, 686, 688t, 689f Paralysis. See Flaccid dysfunction Parenteral opioid analgesics, 145–146 Parsonage-Turner syndrome, 1096, 1110 Partial bipolar transplantation, 972 Partial (incomplete) distal biceps rupture, 531–532, 532f Passive range of motion (PROM), 155, 155f Patient-controlled analgesia, 145, 146, 146t Patient participation, rehabilitation and, 152 Patient-Related Elbow Evaluation, 88 Pectoralis muscle transfer, 969–974 anatomy and, 970, 971f arthrogryposis and, 973 comparative studies and, 974 complete bipolar transplantation and, 972–973, 972f complications and, 974 history and, 969–970 partial bipolar transfer and, 972 results and, 973 unipolar transfer and, 970–971 Pectoris major complete bipolar transplantation of, 972–973, 972f partial bipolar transplantation of, 972 Pediatric elbow computed tomography of, 173 congenital abnormalities and, 184–203

Pediatric elbow (Continued) imaging of, 173–182 osteochondritis dissecans and, 288–293 periosteal response and union, 402 physeal fractures and, 246–262 proximal ulnar fractures and, 283–287 radial neck fractures and, 268–281 supracondylar fractures and, 206–223 Pedicle muscle flaps. See Soft tissue coverage Percutaneous pinning, supracondylar fractures and, 214–219, 217f–220f Performance indices, functional evaluation and, 86–87, 86t–87t Periarticular bone, osteoarthritis and, 844 Peripheral nerve injury, radial neck fractures and, 277 Periprosthetic fracture classification, 900f Periungual infarcts, rheumatoid arthritis and, 1030f Peterson classification of distal humeral physeal fractures, 248f of proximal radius physeal fractures, 258, 258f, 258t of proximal ulnar physeal fractures, 261f Phenol injections, 1005, 1007 Phocomelia, 192f, 197, 201 Phrenic nerve transfer, 959 Phylogeny, 3–10 comparative primate anatomy, 4–8, 4f–7f fossil evidence and, 8–10 major evolutionary stages of elbow, 4f vertebrate elbow evolution, 3 Physeal fractures in children, 246–262 ages 2 to 6 years, 249–253 ages 6 to 10 years, 253 ages 10 to maturity, 255 anatomy and growth, 246, 247f classification of, 246, 248f distal humerus, 248–253 epidemiology, 246, 247t evaluation of, 246–248 growth arrest and, 261–262 lateral condyle, 253–254 lateral epicondyle, 257 management of, 248 medial condyle, 254–255 medial epicondyle, 256–257 newborn to 2 years, 249 proximal radius, 257–260 proximal ulna, 260–261

1202 Index

Physical examination, 67–78. See also Palpation associated joints and neural function, 68–70 axial alignment and, 67, 68f history taking and, 67 inspection and, 67 instability and, 75–76, 76f lateral aspect and, 68, 69f medial aspect and, 68 motion assessment and, 73–74, 74f palpation and, 71–73 posterior aspect and, 68, 70f rotatory instability and, 76–77, 77f–78f strength assessment and, 74–75, 75f Physical therapy. See Rehabilitation Physiological cross-sectional area, 50t Physiotherapy, pain dysfunction and, 1125–1126 Physis damage, 202 Pigmented villonodular synovitis, 1146–1147, 1146f–1147f Pin backout, 852 Pivot-shift test, 77f, 442f, 584, 585f Plate-and-screw fixation, 395–396, 396f Plate placement, distal humerus fractures and, 340, 340f Plating, olecranon and proximal ulna nonunion and, 406–408, 407f Plicae, symptomatic, 581–582, 582f Plio-Pleistocene hominids, 9, 9f Pneumothorax, 143 Polio-type brachial plexus paralysis, 957 Polyethylene surface wear, 853, 854f, 880–884 Polymethyl methacrylate (PMMA) beads, 865 Portals, access. See Arthroscopy Positron emission tomography, 111. See also Diagnostic imaging; Imaging of pediatric elbow; pertinent conditions Posterior antebrachial cutaneous nerve entrapment, 1113 Posterior aspect diagnostic considerations and, 68, 70f palpation and, 73 Posterior capsulectomy, 328 Posterior collateral circulation, 27f Posterior deltoid transfer aftercare and, 988 anatomy and, 987 complications and, 989 history and, 986–987 results and, 988–989 technique and, 987–988, 987f

Posterior dislocation differential diagnosis of, 316–319, 318f postoperative management, 320 reduction technique and, 319f treatment and, 319 Posterior exposures, 122–124, 125f. See also Posterior transosseous exposures; Posterior triceps splitting Posterior extension injuries in adolescence, 688–689 Posterior impingement view, articular injuries and, 684 Posterior interosseous flap, 555, 555f Posterior interosseous nerve nerve entrapment and, 650–651, 651f operative exposure for, 1097–1099, 1097f–1099f syndrome, 1094–1096, 1094f–1096f Posterior tennis elbow. See Tennis elbow tendinosis Posterior transosseous exposures, 130–135 anconeus sparing olecranon osteotomy, 132–133, 135f Chevron transolecranon osteotomy, 130–132, 134f combined osteotomy plus triceps splitting, 132 oblique osteotomy, 130, 133f Posterior triceps splitting (Campbell), 124–125, 126f Posterior ulnar recurrent arteries, 27f Posterolateral II portal, 572–573 Posterolateral instability, 76 Posterolateral plica, in stiff elbow, 601, 603f Posterolateral rotatory instability, 584– 585, 584f–585f arthroscopic surgical technique and, 617–619, 618f examination and, 617 physical examination and, 77f Posteromedial impingement, 589, 590f Postlateral dislocation, 78f Postlateral exposures, 119–120, 121f–122f Postlateral rotatory drawer test, 671, 671f Postlateral rotatory pivot-shift test, 671–672, 672f Postoperative analgesia. See Analgesics, postoperative Pre-existing joint contracture, 957 Primate anatomy, comparative, 4–8 Pritchard implants articulation and, 852, 853f clinical results and, 749, 750f coupling mechanism and, 769f initial reports on, 782, 786f

Pritchard implants (Continued) intrinsic constraint and, 740, 740f surgical considerations and, 742, 742f–743f Pritchard-Walker implant, 852, 888f Pronation daily routine activities and, 81f deformity and, 965 normal, 74f reconstructive procedures and, 965 strength and, 75, 75f, 85 Pronation transfers biceps rerouting, 991 complications and, 992 history and, 991 results and, 991–992 Pronator syndromes, 1106–1109 carpal tunnel syndrome compared, 1108t electromyography and, 1108 operative findings and, 1108–1109, 1109f physical examination and, 1107, 1107f–1108f Pronator teres anatomy, 34–35 Prone position, arthroscopy and, 568– 569, 569f Propionbacter acnes, 865 Propoxyphene, 148t Prosthesis disarticulation amputation and, 1017–1018 infected, 1061–1062 metastatic diseases and, 1133, 1133f prosthetic sockets, 1019–1020 prosthetic training, 1021 prosthetic wrists, 1019 Prosthetic implants. See Arthroplasty; specific implant type Prosthetic radial head replacement, 381–387, 454, 455f active vs. chronic conditions and, 386 aftercare and, 385 articulation and, 383, 383f closure and, 385, 386f contraindications for, 381–391 current implant designs, 382f design considerations, 382–383 exposure and, 384, 384f final component implanting, 385 intramedullary preparation, 384, 384f literature summary regarding, 381t malalignment and, 386 outcome results and, 386, 387, 387f overstuffing and, 385 prognostic factors and, 386–387 resecting radial head, 384, 384f sizing and, 383 stem fixation and, 383, 386 technical notes, 385–386

Index 1203

Prosthetic radial head replacement (Continued) technique and, 384–385, 384f–386f trial reduction and, 384, 385f Protective splints. See Bracing and splinting Provisional fixation, distal humerus fractures and, 340, 340f Proximal anteromedial portal, 569–570, 570f, 622f Proximal forearm synostosis, 198 Proximal lateral exposure, 118–119, 120f Proximal radial epiphysis fracture, 318f Proximal radioulnar synostosis, 477f, 478f Proximal radius articulation of, 16, 18f fractures, 257–260, 257t, 258f–259f, 258t Proximal retraction, biceps muscle, 520f Proximal ulna. See also Olecranon and proximal ulna nonunion; Proximal ulnar fractures anatomy and growth, 260f articulation of, 16–17, 19f Proximal ulnar fractures, 260–261, 261f apophyseal fracture, 283 in children, 283–287, 284t fracture pattern and, 283, 284f growth and development, 283 metaphyseal fracture, 283–287 ossification and, 283, 284f Pseudogout, 1040–1041 Pseudomonas aeruginosa, 1058 Pseudotumors, 1068, 1073 Psoriatic arthritis, 1040t Psychological factors, overuse syndrome and, 698–699 Psychotherapy, 1126 Psychotropic medications, 1126 Pterygium cubitale, 197, 199–200 Pulled elbow syndrome, 312, 313f Pulmonary involvement, rheumatoid arthritis and, 1029 Push-up sign, lateral collateral ligament insufficiency and, 672

Q Quadrate ligament anatomy, 22–23

R Radial artery anatomy, 26, 27f Radial collateral ligament, 21, 22f, 669 Radial epiphysis fracture of, 318f injury to, 319 Radial forearm island flap, 553–554, 554f

Radial head. See also Radial head fractures arthritic elbow and, 604, 605f arthropathy and, 1072–1073 dislocation and, 69f, 192–195, 196f, 199, 298, 299f elbow stability and, 450, 451f imaging of, 178 lateral collateral ligament insufficiency and, 676 palpation and, 72f resection, 929 stabilizing role of, 47, 47f unlinked total elbow arthroplasty and, 739, 741f untreated anterior dislocation of, 306 Radial head fractures age and sex data, 359 arthroscopically assisted reduction and internal fixation, 373 articular surface degeneration and, 365–366, 366f associated injuries, 360–363 biomechanics and function, 359 in children, 257–260, 257t classification and, 363, 363f complex stability and, 452–453 computed tomography and, 102f, 365f concurrent fractures about the elbow and, 360–361 conservative treatment and, 364–366 coronoid fracture with dislocation and, 459 displaced fractures and, 373–375, 373f–374f ectopic ossification and, 472 elbow dislocation and, 439 fat pad sign and, 364, 365f force transmission and, 359 fracture incidence and, 359 historical review and, 359 ligamentous injury and, 361, 361f low-profile fixation and, 370–373, 372f management of, 363–373, 365f Mason classification and, 363, 363f Mayo classification and, 363, 364f mechanism of, 359–360, 360f muscular injury and, 363 neurovascular complications and, 363 nondisplaced fractures, 373 open reduction and internal fixation and, 367, 368–370, 370f overall treatment logic and, 377f preferred treatment and, 373–377 prosthetic replacement and, 381– 387, 381t, 382f

Radial head fractures (Continued) radial head implants and, 47 radioulnar joint widening and, 361, 362f resection and, 366–368, 369f stability and, 359, 360f surgical technique and, 373–375, 375f–376f treatment by motion and, 366, 367f type I fracture, 364, 366f type II fracture, 366, 368f type III fracture, 366–367, 369f, 375–377 Radial neck. See also Radial neck fractures dislocations in children and, 298, 299f lengthening, 47, 48f shortening, 47, 48f Radial neck fractures, 257–260, 257t in children, 268–281 classification of, 268–269, 272f complications related to injury, 277 complications related to treatment, 277–278 elbow dislocation and, 439 epidemiology of, 268, 269f–270f injury assessment and, 269, 273f mechanism of fracture, 268, 270f–271f Monteggia lesion and, 310–312 preferred treatment method and, 279–281 prognosis and, 268 radiographic appearance and, 273f reduction indications and, 273–274, 274f–276f results and, 276–277 treatment principles, 274–276, 276f Radial nerve. See also Radial nerve entrapment anatomy and, 28–29, 29f, 1093–1094, 1093f compression forces and, 1092–1093 fractures and, 1094, 1094f palsy and, 1094, 1094f posterior interosseous nerve syndrome and, 1094–1096, 1094f–1096f revision surgery and, 893 supracondylar fractures and, 226 Radial nerve entrapment paralysis and, 1094–1095, 1095f preferred operative exposure and, 1097–1099, 1097f–1099f resistant tennis elbow and, 1096–1097 tennis elbow tendinosis and, 627 Radial osteomyelitis, 1094 Radial recurrent artery anatomy, 27f Radial tunnel syndrome, 1096–1097

1204 Index

Radial ulnohumeral ligament reconstruction, 617–619, 618f Radiocapitellar impingement, 604, 605f Radiocapitellar line, 177, 178f Radiocapitellar mismatch, 724t Radiocapitellar plica, 593–594, 593f Radiographic appearance. See Diagnostic imaging; Imaging for pediatric elbow; pertinent conditions Radiohumeral arthrosis anconeus arthroplasty and, 731– 733, 732f–733f arthroplasty and, 729–738 capitellar fracture and, 730, 730f capitellar prosthetic replacement and, 733–738 etiology of, 730–731, 730f joint narrowing and, 730, 731f treatment options and, 731 Radiohumeral joint restoration, 432, 452–453 Radiohumeral synostosis, 197, 198f Radionuclide scans, 111. See also Diagnostic imaging; Imaging for pediatric elbow; pertinent conditions Radioulnar joint biceps tendon injury and, 531f primate anatomy and, 6, 7f radial head fractures and, 361, 362f radial neck fractures and, 277 synostosis and, 198, 473–475, 475f, 477f, 530f Radius anatomy of, 12, 15f articulation of, 16, 18f Random cutaneous flaps, 549–550, 550f Range of motion. See also Atraumatic motion implementation active, 154–155 active assisted, 154 continuous passive motion and, 162, 162f distal humerus fractures and, 346 elbow rehabilitation and, 154–155 passive, 155, 155f restricted, 155 Rating schemes, functional assessment and, 87t Reactive arthritis, 1040t Recurrent dislocation, 321–322 Recurrent neural compression lesions, 1090–1091 Recurrent subluxation, hinged external fixators and, 499 Reduction acute anterior dislocation and, 304–306 arthroscopy and, 373 closed reduction, 214, 216f, 304

Reduction (Continued) Coonrad-Morrey implants and, 773, 774f dislocated elbow and, 314–316, 317f distal humerus fracture and, 249 lateral condyle fracture and, 253 linked elbow arthroplasty and, 767 medial condyle fracture and, 255 medial epicondyle fracture and, 256 metaphyseal fracture and, 284 Monteggia fracture-dislocation and, 309–310 open reduction, 219, 304–306, 306f open reduction and internal fixation (ORIF), 367–375, 370f posterior dislocation and, 319f radial head fracture and, 367–370, 370f, 373 radial head replacement and, 384, 385f radial neck fracture and, 273–274, 274f–276f, 279 ulnar fracture and, 432 Reflex sympathetic dystrophy. See Pain dysfunction syndrome Regional anesthetic techniques, 144t Regional neuromuscular control, restoration of, 155–157 Rehabilitation, 152–157 articular injuries and, 693 compression and elevation and, 153 convertible total elbow arthroplasty and, 760 dislocations and, 442–443 early atraumatic motion and, 153–155 elbow stiffness and, 164–165, 328 establishing diagnosis and, 152 ice use and, 153 kinetic-kinematic chain and, 157 medications and, 153 modalities and, 153 Monteggia fractures/dislocations and, 433 nerve injuries and, 576 patient participation and, 152 principles of, 157 protection and relative rest and, 152–153 range of motion and, 154–155 reducing pain and inflammation, 152–153 regional neuromuscular control and, 155–157 relaxation therapy, 1126 tennis elbow tendinosis and, 634, 637 ulnar collateral ligament injuries and, 666 ultrasound and, 155

Reimplantation procedures, 889–891 axis of rotation and, 890, 890f extended ulnar component and, 890f flange design and, 891, 891f general considerations, 889 humeral stems and, 889f indications for, 890 noncustom semiconstrained revision implant design and, 890–891 reconstructive procedures and, 854, 855f Relaxation therapy, 1126 Resection arthroplasty, 869–871, 869f–870f aftercare and, 911 chronic infection and, 1058, 1058f custom-fit prosthesis and, 915f dysfunctional instability and, 914f indications for, 911 radial head fracture and, 366–368, 369f results and, 911 technique and, 911 Residual subluxation, hinged external fixators and, 499 Resistant tennis elbow, 1096–1097 Resisted range of motion (RROM), 155 Resting splints, 165f Restorative splinting, 165–166, 166f, 167f. See also Bracing and splinting Restriction of motion, 43, 43f Retrograde lateral arm flap, 554–555, 555f Reverse lateral arm flap, 555f Revision arthroplasty with osseous deficiency allograft prosthetic composite reconstruction and, 903–905 bone struts and, 901–903 impact grafting and, 899–901 periprosthetic fracture classification, 900f Revision arthroplasty with osseous integrity bone loss classification and, 892f bone stock and, 889f clinical results and, 896 closure and, 895 current experiences revisited, 897 exposure and, 893 fractured components and, 895 humeral revisions and, 894–895, 894f interposition arthroplasty and, 889 loose prostheses and, 895, 896f Mayo experience and, 896–897 postoperative management and, 895–896

Index 1205

Revision arthroplasty with osseous integrity (Continued) preoperative planning and, 891 reimplantation procedures and, 889–891 soft tissue and, 893–894 surgical technique and, 893–894 triceps and, 893, 893f–894f ulna revisions and, 895, 895f ulnar and radial nerves and, 893 well-fixed prostheses and, 895 Rheumatoid arthritis. See also Juvenile rheumatoid arthritis aggressive clinical course and, 1031 allografts and, 944, 944f arthroplasty complications and, 789t arthroplasty results and, 782–784 arthroscopic complications and, 620–621 articular patterns and, 1031f bone graft and, 788f–789f boutonnière deformity and, 1027f bursitis and, 1167 cardiac conditions and, 1029 classification criteria for, 1026 clinical features and, 1026–1027 complications and, 1030–1033 conditions and positive rheumatoid factors, 1031 Coonrad-Morrey device and, 787– 790, 787f, 787t, 789t cystic swelling and, 1028f epidemiology and, 1025 extra-articular manifestations and, 1027–1030 GSB III prosthesis and, 784, 786f, 787 hematologic manifestations and, 1028–1029 inflammation and, 1026–1027 interposition arthroplasty and, 946f–947f laboratory studies and, 1030, 1030f linked elbow arthroplasty and, 779f management and, 1030–1033 modest type II involvement and, 788f neuritis and, 849–850 pain and, 1026 pathophysiology and, 1025–1026 periungual infarcts and, 1030f pleural effusion and, 1029f Pritchard II prosthesis and, 782, 786f pulmonary involvement and, 1029 radiographic presentation and, 783f rheumatoid nodules and, 1027– 1028, 1028f septic arthritis and, 1059 severe type IV involvement and, 784f

Rheumatoid arthritis (Continued) survival data and, 788f swan-neck deformities and, 1027f synovectomy and, 921–933 total elbow arthroplasty and, 782–790 treatment logic for, 717f triaxial device and, 782, 786f triceps insufficiency and, 850, 851f typical symmetric swelling and, 1027f ulnar deviation and, 1027f unusual presentation modes and, 1026 vasculitis and, 1029–1030, 1030f Rheumatoid nodules, 1027–1028, 1028f Rickets, 1174, 1175f Rotation ankylosis, 199 Rotation axis, linked elbow arthroplasty and, 766–767, 767f Rotation center, 39–40, 41f, 42f Rotational deformities, identification of, 67 Rotator cuff tendinosis, 627 Rotatory instability hemiarthroplasty and, 724t physical examination and, 76–77, 77f–78f Rupture. See also Triceps tendon rupture of brachialis muscle, 533 of cervical nerve, 994 partial distal biceps rupture, 531– 532, 532f ultrasonographic image of, 109f

S Salter-Harris type injury, 280 Screw compression, 689 Segmental bone loss, 911–913, 915f Semiconstrained elbow replacement acute fractures and, 821–822 acute trauma and, 814 age and, 815 bone loss and, 815, 816f clinical results and, 820–821 complications and, 825–827, 825t deformity and, 816, 817f fragments and, 818f–819f humeral implant lengths and, 821f indications for, 814–816 loosening and, 826–827 occupation and, 815 physical activity and, 815 post-traumatic arthrosis and, 822– 824, 823f–824f post-traumatic instability and, 815 surgical technique and, 816–820, 818f–820f traumatic arthrosis and, 814–815

Semiconstrained elbow replacement (Continued) ulnar component fracture and, 826, 826f ulnar component insertion and, 820f Sepsis. See Infection; Septic arthritis Septic arthritis. See also Osteomyelitis antibiotic treatment and, 1061 arthroscopy and, 1061 aspiration and, 1060, 1061f diagnosis of, 1059–1061 disease-modifying antirheumatic drugs and, 1056 extra-articular involvement and, 1062 general considerations and, 1056 HIV-positive patients and, 1059 radiographic assessment and, 1060, 1062f rheumatoid arthritis and, 1059 sickle cell disease and, 1074, 1075 systematic symptoms and, 1060, 1061f treatment and, 1056–1057, 1061–1062 treatment results and, 1062, 1063f Septic failure, revision arthroplasty and, 885 Septic olecranon bursitis, 1063–1065, 1064f Sequential neural compression lesions, 1090 Seroma formation, interposition arthroplasty and, 945 Seronegative inflammatory arthritis adult Still’s disease and, 1041–1042, 1042f, 1042t crystalline arthropathies and, 1039– 1041, 1040t features of, 1040 gout and, 1040–1041, 1041f pseudogout and, 1040–1041 spondyloarthropathies and, 1039, 1040t Serratia infection, 1058 Shear injuries in adolescence, 688–689 radial neck fractures and, 277 “Shish kabob” corrective osteotomy, 198f Shock wave therapy, 153 Short Form-36, 88 Shuck test, 903, 903f Sickle cell disease, 1073–1075 avascular necrosis and, 1074, 1075 clinical evaluation and, 1074–1075 imaging studies and, 1074–1075 management of, 1075 musculoskeletal manifestations of, 1074

1206 Index

Sickle cell disease (Continued) osteomyelitis and, 1074, 1075 pathogenesis of, 1074 septic arthritis and, 1074, 1075 surgery and, 1075 synovitis and, 1075 vaso-occlusive crisis and, 1074, 1075 Sigmoid notch anatomy, 19f Silver syndrome, 299 Single-muscle force analysis, 49–50, 50f, 51t Skeletal traction, 220, 221f Skin flap configuration, disarticulation amputation and, 1015 Skin grafting, 548–549 Skin incisions. See Surgical exposures Slow union, 401 Snapping elbow, 542, 545f, 581–582, 582f Soft tissue anomalies. See also Soft tissue tumors combined with bone anomalies, 197 continuous passive motion and, 162 contractures, 196, 794 control deficiencies, 196 isolated tissue anomalies, 191f, 196–197 phocomelia, 192f treatment of, 199 Soft tissue coverage anconeus muscle flaps, 556, 557f antecubital fasciocutaneous flaps, 552–553, 553f axial fasciocutaneous flaps, 550–552, 551f brachioradialis flaps, 556, 558f débridements and, 547, 548f distant pedicled flaps, 559, 559f extensor carpi radialis longus flaps, 556 free tissue transfer and, 559–561, 560f latissimus dorsi flaps, 556–559, 558f–559f local flaps and, 549–556 management algorithm, 549f medial arm flap, 555 patient assessment and, 547 pedicle muscle flaps, 556–559 posterior interosseous flaps, 555, 555f radial forearm island flaps, 553–554, 554f random cutaneous flaps, 549–550, 550f reconstructive goals and, 548 retrograde lateral arm flaps, 554–555, 555f skin grafting and, 548–549 ulnar artery forearm flaps, 555–556 wounds and, 547

Soft tissue reconstruction, fused elbow and, 830, 831f Soft tissue release, osteoarthritis and, 844 Soft tissue revision surgery, 893–894 Soft tissue tumors. See Benign soft tissue tumors; Malignant soft tissue tumors Sorbie-Questor total elbow arthroplasty biomechanical study, 740f design of, 745, 745f–746f implant considerations and, 721, 722f outcomes and, 750, 751f Souter-Strathclyde arthroplasty articular geometry and, 739, 740f design of, 742, 743f–744f instability and, 857f outcomes and, 747, 749, 751f Spastic dysfunction biceps-brachialis lengthening and, 1008–1011, 1009f–1010f botulinum toxin injections and, 1006–1007 cerebral palsy and, 1002–1003 decision algorithm and, 1006f dynamic electromyogram and, 1004, 1005f flexor-pronator slide and, 1011 heterotopic ossification and, 1011– 1013, 1012f neurectomy and, 1007–1008, 1008f phenol injections and, 1007 preoperative evaluation and, 1004–1005 stroke and head trauma and, 1004 tone-reducing medications and, 1005 traumatic brain injury and, 1003–1004 treatment options and, 1005–1006 Spinal accessory nerve, neurotization and, 960f Splinting. See Bracing and splinting Spondyloarthropathies, 1039, 1040t Spontaneous reduction, of dislocated elbow, 314–316, 317f Stability, elbow. See Elbow stability Staged exchange arthroplasty, 866–868, 867f–868f Staging systems, tumors, 1132–1133 Staphylococcus aureus, 864, 865, 867f, 1058, 1060, 1074 Staphylococcus epidermidis, 864, 865–866 Staples’ technique, 951f Static adjustable splints, 167–169, 167f– 168f. See also Bracing and splinting Static compression, 57f Static measurements, elbow strength and, 85, 85f

Static splints, 164, 165f Steindler’s flexorplasty, 958, 961–965. See also Flaccid dysfunction anatomy and, 962 complications and, 965 results and, 963–965, 964f splinting and, 963, 963f technique (modified from Mayer and Green), 951, 962–963, 962f Steinmann pin, radial neck fractures and, 273, 274f Stem cell manipulation, 202 Sterile hemodialysis olecranon bursitis, 1065 Steroid-induced avascular necrosis, 1178–1179, 1178f Stiff elbow, 326–332. See also Arthritic stiff elbow management; Nonarthritic stiff elbow management arthritic elbow management, 602–606 arthroscopic release and, 331 author’s current practice, 332 complications and, 331 computed tomography and, 327 contracture release comparison, 332t elbow dislocation and, 320 etiology of, 326, 326f evaluation of, 326–328 examination and, 327 four stages of, 160 hemiarthroplasty and, 724t history taking and, 326–327 imaging studies and, 327–328 incidence of, 326 magnetic resonance imaging and, 327–328 motion evaluation, 327 nonarthritic elbow management, 596–602 nonoperative treatment and, 328 osteoarthritis and, 843 physical therapy and, 164–165, 328 plain film radiographs and, 327 presentation of, 326 ranges of motion and, 331t restorative splinting and, 164–166, 166f, 167f, 328 stability evaluation and, 327 surgical treatment and, 328–329, 329f–330f, 331t treatment results and, 329–331 Straight posterior portal, 572, 572f Strain gauge tensiometer, 84 Strength evaluation, 74–75, 75f, 82–85 contraction speed and, 83 dynamic function and, 85–86 flexion extension and, 85 force considerations and, 82–83 men vs. women, 85f

Index 1207

Strength evaluation (Continued) muscle length at contraction, 83–84 pronation and, 85 static measurements and, 85 strength measurement techniques, 84–85 supination and, 85 variables in, 86 Strengthening exercises, 156 Stress fractures of coronoid, 287, 287f of olecranon, 689–690, 689f, 690f Stress-free relaxation, inflammation and, 166 Stroke, 1004 Subanconeus muscle, 34 Subchondral bone, achilles tendon allograft and, 938f Sublime tubercle insufficiency, 666 Subluxating nerve, 72 Subluxation, 192–194 hinged external fixators and, 499 interposition arthroplasty and, 945 Submuscular bursa, 15f Superficial bursae, 1164–1166 Superior ulnar collateral artery, 27f Supination contracture, 991 normal, 74f routine daily activities and, 81f strength, 75, 75f, 85 transfers, 992–993, 993f Supinator anatomy, 32–33, 34f Supine position, arthroscopy and, 568, 568f Supraclavicular block, 143, 144f Supracondylar bone loss, 343f Supracondylar compression, 340–341, 341f Supracondylar fractures anatomy and, 206 anterior humeral line and, 212–213, 213f Baumann’s angle and, 212, 212f bicolumnar nature of region and, 207f carrying angle and, 208f in children, 206–223 classification of, 206–208 closed reduction and, 214, 216f complications and, 223 corrective surgery indications, 240–243 diagnosis and, 209–213 extension-type fractures, 208 fixation techniques and, 242f, 243 flexion-type fractures, 208, 209f incidence and etiology, 206 ischemic injuries and, 227–236 linked elbow arthroplasty and, 780f medial periosteal hinge and, 207f nerve injuries and, 226–227

Supracondylar fractures (Continued) neurovascular injury and, 214, 215f, 226–227 neurovascular surgery and, 236 open reduction and, 219 osseous complications and, 236–243 osteotomy techniques and, 241–243, 241f percutaneous pinning and, 214–219, 217f–220f postoperative care and, 219–223 radiographic evaluation and, 209–213 surgery and, 240–243, 240f traction and, 220–223, 221f–222f treatment of, 213–219 type I fractures, 209, 210f, 213 type II fractures, 209, 211f, 213–214 type III fractures, 209, 212f, 214 Supracondylar process imaging, 15f, 182, 182f Supracondylar shortening, 342, 343f Supraintercondylar fractures, through osteopenic bone, 344f Surgery. See pertinent conditions; Surgical exposures Surgical exposures anterior exposures, 138–140, 138f–139f aponeurosis turn-down approach, 125, 127f Boyd postlateral exposure, 119–120, 121f–122f complications and, 140–141 cross-sectional anatomy and, 116f extensile postlateral exposure, 120– 122, 123f general principles, 115 Kocher approach and variations, 115–119 lateral approaches, 115 Mayo-modified Kocher exposure, 122, 124f Mayo triceps reflection technique and, 126–127 medial approaches, 135–138 osteocutaneous flap and, 127–130, 131f–132f posterior exposures, 122–124 posterior transosseous exposures, 130–135 posterior triceps splitting, 124–125, 126f posterolateral exposures, 119–120, 121f–122f principles of, 117 radial nerve injury and, 140–141 triceps disruption and, 140–141 triceps-sparing approaches, 125– 127, 128f, 130, 131f ulnar nerve injury and, 140–141 wound healing and, 140–141

Suspension systems, disarticulation amputation and, 1020–1021, 1020f Suture anchors, 525, 526, 536f Swan-neck deformities, rheumatoid arthritis and, 1027f Symmetric swelling, rheumatoid arthritis and, 1027f Symptomatic plicae, 581–582, 582f Synostosis diagnosis of, 190–192, 194f proximal radioulnar, 530f radiohumeral, 188f treatment of, 197–199, 198f Synovectomy arthroscopic complications and, 622 arthroscopic synovectomy, 581, 926–927, 927f–928f, 929 arthrotomy and, 925–926, 925f contraindications for, 923 elbow motion and, 923 indications for, 921–923, 1072, 1072f infected prosthesis and, 1061–1062 instability and, 932 Mayo experience and, 929, 931f–932f motion loss and, 932 neuropathy and, 932 nonsurgical synovectomy, 925 open synovectomy, 927–929 patient selection and, 921–923 radial head resection and, 929 radiographic classification and, 921, 922f recurrence and, 932 repeat synovectomy, 929 results of, 927–932, 930t–931t severe joint disruption and, 923 synovitis and, 921, 921f total elbow replacement for failed, 929–932 type II involvement and, 924f type IIIA involvement and, 923f Synovial chondromatosis, 1147, 1147f Synovial fistulas, 651, 652f Synovial lesions, 692–693 Synovial membrane distribution, 20f Synovial sarcoma, 1148 Synoviorthesis, 1072 Synovitis, 69f, 580, 580f Syringomyelia, 1080–1081, 1082f

T Tabes dorsalis, 1082, 1083f Technetium-99 scan, 653, 654f, 690, 690f Tendon calcification, tennis elbow tendinosis and, 636 Tendon graft, lateral collateral ligament insufficiency and, 674–676, 675f–676f

1208 Index

Tendon injury. See Distal biceps tendon injury Tendon transfer, choosing muscle for, 957–958. See also Flaccid dysfunction Tennis elbow. See also Tennis elbow surgical failure; Tennis elbow tendinosis anatomy and, 609–610, 610f–612f arthroscopic technique and, 610– 616, 613f–615f intraoperative views of, 614f–615f iontophoresis and, 153 lateral collateral ligament insufficiency and, 670 medications and, 153 resistant, 1096–1097 Tennis elbow surgical failure algorithm and, 651, 652f arthritis and, 651f arthroscopy and, 653, 654f careful history and, 650 classification and, 650–651 etiology and pathology and, 650 histopathologic features and, 651 improper patient selection and, 651 incomplete or improper diagnosis and, 650–651 patient evaluation and, 650 physical examination and, 651–654 presentation type and reoperation results, 655t reoperation and, 655 subtle instability and, 651, 652f synovial fistulas and, 651, 652f technetium-99 scan and, 653, 654f treatment and, 654–655, 656f type I failure and, 652–655 type II failure and, 650–653, 655 type III failure and, 651, 654–655 Tennis elbow tendinosis abuse abstinence and, 632 age and, 628 alternative nonoperative approaches, 634 angiofibroblastic hyperplasia and, 629, 629f arthroscopy and, 639, 640f associated intra-articular pathology and, 636 carpal tunnel syndrome and, 627 category I, 631 category II, 631 category III, 631 cervical osteoarthritis and, 627–628 classification of, 626–627 clinical correlations of pathology, 631 counterforce bracing and, 633–634, 633f country club elbow, 627 electron microscopy and, 630

Tennis elbow tendinosis (Continued) equipment alteration and, 633, 633f etiology and, 628 full-thickness tear and, 631f gender and, 628 graduated exercise and full-strength testing and, 634 gross abnormalities and, 628–629, 629f healing promotion and, 632–634 high-voltage electrical stimulation and, 634 historical surgical results and, 636 hyaline degeneration and, 630, 630f imaging and, 639, 640f immunohistology and, 630 incidence of, 626 injection flow ease and, 636 intra-articular abnormalities and joint laxity and, 628 lateral elbow tendinosis, 626 lateral epicondylar bony exostosis and, 636 lateral technique and, 637–639, 638f–639f medial elbow tendinosis, 626–627 mesenchymal syndrome and, 627 microscopic pathology and, 629– 630, 629f–630f multiple cortisone injections and, 636 nerve root compression and, 627–628 nonsurgical treatment and, 632 overuse and, 628 pain causes and, 630–631 pain (constant) without activity and, 636 pathology and, 628–629 patient frustration and, 636 posterior tennis elbow, 627 postoperative rehabilitation and, 637 postsurgical healing and, 637 preferred surgical treatment method and, 636–639 radial nerve entrapment and, 627 rehabilitation failure and, 636 rehabilitative exercise program and, 634 relative rest and, 632–634 rotator cuff tendinosis and, 627 subcutaneous atrophy and, 632f surgery and, 634–636 tendon calcification and, 636, 637f tissue repair and, 637 training technique and, 632–633 traumatic etiology and, 628 ulnar nerve neurapraxia and, 627 Tensiometers, 84, 84f Tension band constructs, 689–690

Tension band wiring olecranon and proximal ulna nonunion and, 404–406, 406f olecranon fractures and, 393–395, 394f, 398 Teres major-to-triceps transfer, 991 Terminal devices, disarticulation amputation and, 1018–1019 Tetraplegia elbow extension restoration and, 983 flaccid dysfunction and, 956–957 Threaded fixation, 243 Thrombectomy, ischemic injuries and, 234 Throwing injuries age effects on, 691t arthroscopy in, 587–594 compression forces and, 587 imaging and, 587, 588f mosaicplasty and, 590–593 olecranon osteophytes and, 587, 588f, 589f osteochondral autografts and, 592, 592f–593f osteochondritis dissecans and, 589–593, 591f–593f posteromedial impingement and, 589, 590f radiocapitellar plica and, 593–594, 593f valgus extension overload and, 587–589 valgus torque and, 587, 588f Tinel test, 72 Tissue contracture time line, 165f Tissue healing stage, atraumatic motion and, 154 Tissue preference, interposition arthroplasty and, 936 Tissue repair, tennis elbow tendinosis and, 637 Tone-reducing medications, 1005 Total elbow arthroplasty. See also Arthroplasty; specific arthroplasty type articulation and, 852, 853f, 887f brushing wear and, 852 complications and, 849–859, 860t component failure and, 851–852 convertible arthroplasty, 755–764 device failure and, 885, 886f distal humeral fractures and, 800–812 distal humerus nonunion and, 835–838 dysfunctional instability and, 835–842 ectopic bone and, 851, 852f failed synovectomy and, 929–932 failure classification and, 885, 886t

Index 1209

Total elbow arthroplasty (Continued) finite element analysis of fixation, 58–59, 60f fracture and, 851 fused elbow and, 830–834 hemophilic arthropathy and, 1073, 1073f implant removal and, 853–859 infection and, 853, 855f, 862–871 instability and, 854–856, 856f, 885– 886, 887f–888f joint laxity and, 47, 48f juvenile rheumatoid arthritis and, 792–797 Kaplan-Meier curves and, 887f linked arthroplasty, 765–780 loosening and, 856–859, 886–888 motion restriction and, 849 neuritis and, 849–850 nonreimplantation revision procedures, 851–853 osteolysis and, 886f primary osteoarthritis and, 843–847 reimplantation and, 854, 855f resection and, 911, 912f–915f revision with osseous integrity, 885–897 rheumatoid arthritis and, 782–790 septic failure and, 885 stem fracture and, 851, 852f triceps insufficiency and, 850–851, 873–878 unlinked arthroplasty, 748–754 wear and, 853, 880–884 wound healing problems and, 849 Traction, supracondylar fractures and, 220–223, 221f–222f Traction injury, 994 Tramadol, 138, 147t Transcondylar fracture, 318f Transepicondylar approach, 135–136 Transhumeral amputation, 1015 Transient sensory paresthesias, 528 Transient ulnar nerve paresthesias, 965 Translocation of ulnar nerve, 1103– 1105, 1103f–1104f Trauma. See also Semiconstrained elbow replacement arthroscopic complications and, 621 arthrosis and, 952f brain injury and, 477–479, 478f disarticulation amputation and, 1015 dislocations in children and, 302 ectopic ossification and, 472–475, 474f hinged external fixation and, 499 interpositional arthroplasty and, 936 lateral collateral ligament insufficiency and, 669, 670 osteochondritis dissecans and, 292

Trauma (Continued) post-traumatic arthritis, 942–943, 943f post-traumatic osteoarthrosis, 814–827 post-traumatic radioulnar synostosis, 473–475, 475f radiographic densities about elbow and, 473f radioulnar synostosis and, 473–475, 475f semiconstrained elbow replacement and, 814–827 syringomyelia and, 1080 tennis elbow tendinosis and, 628 traumatic arthritis, 717f, 734f traumatic brain injury, 1003–1004 Trephine placement, ulnohumeral arthroplasty and, 1048, 1049f Triaxial electrogoniometer, 80, 80f Triceps. See also Triceps insufficiency; Triceps tendon rupture; Triceps transfer bursae around, 1164, 1166f chronic unreduced dislocations and, 467 Coonrad-Morrey device and, 774– 775, 778f disruption, 141 fascial reconstruction and, 304–305, 305f length, extension strength and, 84f linked elbow arthroplasty and, 766, 767–768 reattachment and, 851f reconstruction and, 874–877, 876f revision surgery and, 893 rupture and, 945 Triceps-anconeus reflecting pedicle approach, 338 Triceps brachii anatomy, 33–34, 34f Triceps insufficiency achilles tendon reconstruction and, 877, 877f anconeus rotational flap and, 874– 877, 876f avoiding, 873 incidence of, 873 management of, 873–878 pathology and, 972 presentation and symptoms and, 873 prognostic factors and, 878 reattachment and, 851f, 874, 874f–876f repair or reconstruction and, 873–874 total elbow arthroplasty and, 850–851 treatment algorithm for, 874f Triceps release technique (Wolfe and Ranawat), 127–130

Triceps-sparing surgical approaches, 125–127, 128f Triceps splitting combined with osteotomy, 132 technique, 124–125, 126f Triceps tendon rupture achilles tendon allograft and, 538, 541f, 542 acute injury and, 538, 539f bursitis and, 1167, 1167f complete ruptures and, 538 complications and, 542 delayed reconstruction and, 538– 542, 540f–542f diagnosis and, 536 imaging and, 536–537, 537f injury mechanism and, 536 olecranon bursitis and, 1167 partial ruptures and, 538 pathology and, 537 physical examination and, 537–538 predisposing conditions and, 536 preferred treatment method and, 542 proximal retraction and, 537f snapping triceps tendon and, 542, 545f treatment and, 538–545 treatment results and, 542 Triceps transfer anatomy and, 974 arthrogryposis and, 975, 975f flaccid dysfunction and, 974–976 history and, 974 results and, 975–976, 975f technique and, 974–975, 974f triceps-to-biceps transfer, 958, 974 Tricepsplasty, 467, 470 Trigger points, musculoskeletal, 1124 Trochlear blood supply, avascular necrosis and, 237f Trochlear epiphysis, imaging of, 178, 179f–180f Trochlear notch, primate anatomy and, 4, 5f Tsunge technique, 1050f, 1051–1052 Tuberculosis, 1063, 1064f Tuberosity, biceps, 519f–520f Tumor necrosis factor inhibitors, 1056 Tumoral calcinosis, 1174, 1176f Tumors. See Bone tumors; Soft tissue tumors Two-pin lateral-entry fixation, supracondylar fractures and, 227

U Ulna. See also Ulnar collateral ligament injuries; Ulnar nerve; Ulnar nerve entrapment anatomy of, 12, 16, 16f articulation of, 16–17, 19f

1210 Index

Ulna (Continued) bone loss and, 839–841 bone struts and, 904f cysts and, 1140f deviation exercises and, 156f dorsal subluxation of, 70 dysplasia and, 200–201, 201f ectopic bone formation and, 482 hypoplasia and, 197 implant removal and, 868 implant revision and, 895 neuritis and, 724t neuropathy and, 645, 648, 850 rheumatoid arthritis and, 1027f varus-valgus movement of, 40 Ulnar artery anatomy of, 26, 27f forearm flap, 555–556 Ulnar collateral ligament injuries arthroscopy and, 665, 666f diagnosis and, 658–660 docking technique and, 662–663, 663f history and, 658 hybrid interference screw fixation technique and, 663–665, 664f–665f imaging and, 659–660 inferior humeral tunnel location and, 666 Jobe technique and, 660f, 661–662, 661f–662f magnetic resonance imaging and, 659–660, 660f muscle-splitting approach and, 661f nonoperative treatment, 660 pathophysiology and, 658 physical examination and, 658–659 postoperative rehabilitation and, 666 postsurgery throwing program and, 666 schematic of incised ligament, 662f sublime tubercle insufficiency and, 666 surgical considerations and, 665–666 surgical results and, 666–667 surgical techniques and, 660–664 throwing motion and, 658, 658f treatment indications and contraindications and, 660 ulnar nerve irritation and, 665 ulnar tunnel creation and, 662f, 664f valgus extension overload and, 665–666 valgus stress testing and, 658–659, 659f Ulnar fracture accurate reduction of, 432 complex instability and, 454, 455f

Ulnar nerve. See also Ulnar nerve entrapment anatomy of, 29–30, 30f arthroscopic view of, 605f decompression and, 351–353 dislocations and, 110f, 445 ectopic bone formation and, 482 exposure, column procedure and, 491 iatrogenic injury of, 648 irritation and, 665 linked elbow arthroplasty and, 766 medial epicondylitis and, 643 neurapraxia and, 627 Oberlin transfer of, 961, 961f osteoarthritis and, 844 palsy, 256f, 1095, 1095f prosthetic replacement and, 1052– 1053, 1053f revision surgery and, 893 Steindler’s flexorplasty and, 962f supracondylar fractures and, 226 transposition, 493 Ulnar nerve entrapment anatomy and, 1099, 1099f clinical presentation and, 1100–1102 conservative treatment and, 1102 differential diagnosis and, 1102 etiology and, 1099–1100, 1100f–1101f hypermobility and, 1100 iatrogenic causes and, 1100 operative exposure for anterior transposition, 1103–1105, 1103f–1104f operative exposure for simple decompression, 1103 operative treatment and, 1102–1103 snapping triceps and, 1101f tethering and, 1101f Ulnar preparation convertible total elbow arthroplasty and, 757–760, 759f Coonrad-Morrey device and, 773, 774f distal humeral fractures and, 807– 808, 808f–809f total elbow arthroplasty and, 747f Ulnar rotation, 40 Ulnar stem fracture, total elbow arthroplasty and, 851, 852f Ulnohumeral arthroplasty, 602f, 1047–1050 complications and, 1050, 1052f indications for, 1047 Mayo experience and, 1049–1050, 1051f osteophyte redevelopment and, 1050, 1052f postoperative management and, 1048

Ulnohumeral arthroplasty (Continued) results and, 1048–1049, 1050f technique and, 1047–1048, 1049f trephine placement and, 1048, 1049f Ulnohumeral dislocation, 192 Ulnohumeral stability, 47–48, 49f, 420f Ultrasonography, 107–109, 109f–110f. See also Diagnostic imaging; Imaging of pediatric elbow; pertinent conditions Ultrasound in rehabilitation, 155 Unipolar transfer for elbow extension restoration, 984–985, 984f for flexion restoration, 968–969, 969f, 970–971 Unit force vector, 50t Unlinked total elbow arthroplasty, 728–754 clinical results and, 746–752 component positioning and, 739 contraindications for, 741 convertible total elbow arthroplasty, 754–764 design considerations and, 738–740 distal humeral hemiarthroplasty, 720–728 Ewald design and, 741–742, 741f functional and balanced collateral ligaments and, 739 implant longevity and, 739, 739f indications for, 740–741 intrinsic constraint of human elbow and, 739, 740f Kudo arthroplasty and, 744–745, 744f–745f Pritchard arthroplasty and, 742, 742f–743f radial head replacement and, 739, 741f radiohumeral arthrosis and, 729–738 Sorbie-Questor arthroplasty and, 745, 745f–746f Souter arthroplasty and, 742, 743f–744f surgical considerations and, 741–745 surgical technique and, 745–746, 746f–747f Unwarranted treatment due to misdiagnosis, 201 Urokinase infusion, 234

V Valgus extension overload, 587–589, 589f–590f, 665–666, 692, 692f Valgus instability, 76, 76f, 443, 453, 453f Valgus stress articular injuries and, 680, 681f ligament injuries and, 72

Index 1211

Valgus stress (Continued) radiographs, 644, 644f ulnar collateral ligament injuries and, 658–659, 659f Valgus tilt, of distal humerus, 18f Varus instability, 76, 76f Varus-valgus deformity, 254t Varus-valgus displacement, 46–47, 46t Varus-valgus stresses, 46, 46f Vascular compromise, 202 Vascularized bone, 561 Vasculitis, rheumatoid arthritis and, 1029–1030, 1030f Vaso-occlusive crisis, 1074, 1075 Vein patch graft angioplasty, 234 Vertebrate elbow evolution, 3 Vessel anatomy, 24–27 brachial artery and branches, 24, 25f–27f radial artery, 26 ulnar artery, 26, 27f Video telemetry, 80

Viscoelastic tissue response, 166f Visual Analogue Scale, 88, 1125 Volar forearm fasciotomy, 235 Volar forearm incisions, 235f Volkmann’s contracture causes of, 231f compartment syndrome and, 235 etiology of, 228–229 schematic view of, 229f untreated compartment syndrome and, 229f Von Willebrand disease. See Hemophilic arthropathy

W Wear and elbow replacement, 880–884. See also Replacement arthroplasty angle of intersection and, 880, 881f clinical and radiologic features and, 880 clinical results and, 882–884

Wear and elbow replacemen (Continued) condyle preservation and, 882f metallic debris and, 882f osteolysis and, 880, 881f, 883f surgical technique and, 880–882 worn bushings replacement, 882f Webbed elbow. See Contractures Western Ontario and McMaster University Osteoarthritis Index (WOMAC), 88 Wilson’s disease, 1177, 1177f Wound healing continuous passive motion and, 162 total elbow arthroplasty and, 140– 141, 849 Wrist flexion exercise, 156f

X Xenograft cutis, 935

Y “Y” ligament, 22, 22f