Primer on Rheumatic Disease

8/19/2019 Primer on Rheumatic Disease

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Primer on theRheumatic DiseasesTHIRTEENTH EDITION


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Primer on theRheumatic DiseasesTHIRTEENTH EDITION

Edited by

John H. Klippel, MDJohn H. Stone, MD, MPHLeslie J. Crofford, MDPatience H. White, MD, MA


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John H. Klippel, MD John H. Stone, MD, MPHPresident and CEO Associate PhysicianArthritis Foundation Massachusetts General HospitalAtlanta, GA, USA Deputy Editor for Rheumatology UpToDateLeslie J. Crofford, MD Boston, MA, USA

Gloria W. Singletary Professor of Internal Medicine Patience H. White, MD, MAChief, Division of Rheumatology & Chief Public Health Ofcer Women’s Health Arthritis FoundationUniversity of Kentucky Atlanta, GA, USALexington, KY, USA

Library of Congress Control Number: 2007925709

ISBN: 978-0-387-35664-8 e-ISBN: 978-0-68566-3

Printed on acid-free paper

© Springer Science + Business Media, LLC. 2008

All rights reserved. This work may not be translated or copied in whole or in part without the writtenpermission of the publisher (Springer Science+Business Media, LLC, 233 Spring Street, New York,NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use inconnection with form of information storage and retrieval, electronic adaptation, computer software,or by similar or dissimilar methodology now known or hereafter developed is forbidden.The use in this publication of trade names, trademarks, service marks, and similar terms, even if theyare not identied as such, is not to be taken as an expression of opinion as to whether or not theyare subject to proprietary rights.While the advice and information in this book are believed to be true and accurate at the date ofgoing to press, neither the authors nor the editors nor the publisher can accept any legal responsibilityfor any errors or omissions that may be made. The publisher makes no warranty, express or implied,with respect to the material contained herein.

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The 13th edition of the Primer on the Rheumatic Diseases is an extraordinary hand-book for clinical care. The Primer will educate trainees, update established clini-cians, and help health care providers from all walks of the profession provide bettercare for patients with arthritis and rheumatic diseases.

In achieving these purposes, the Primer continues a tradition of excellence datingback more than 70 years. The Primer and its precursors have served as a majorlearning tool for medical students, house ofcers, fellows, and allied health profes-sionals since 1934, when the early publications of the American Committee for theControl of Rheumatism included the Primer on Rheumatism: Chronic Arthritis in1934. Since that work, which consisted of a 52-page brochure, the Primer hasevolved into a reference guide of nearly 90 chapters and 4 appendices.

The Primer is designed to provide up-to-date information about the major clini-cal syndromes seen by primary care physicians, rheumatologists, orthopedic sur-geons, as well as physician assistants, nurse practitioners, physical and occupationaltherapists, and allied health professionals whose expertise contributes to patientcare. Emphasis on the evaluation of the patient, the physical examination includingmusculoskeletal signs and symptoms, laboratory and imaging evaluations, andcurrent and novel therapeutic approaches are essential for all who work in this eld.Arthritis and other rheumatic diseases, which affect more than 46 million Ameri-cans (including 300,000 children), remain a leading cause of disability and the mostcommon chronic illness in the United States.

I congratulate the editors on their superb work. In addition, the multiple con-tributors—many of whom are members of the American College of Rheumatology—should be thanked for their scholarly contributions to the Primer . Rheumatologyhas never been more exciting than it is today, and there is no doubt that the 13thedition of the Primer reects this. I join clinicians and patients alike in thanking theArthritis Foundation for the continuing achievements of this book.

Michael E. W einblatt , MD Professor of Medicine Harvard Medical School Brigham and Women’s Hospital Boston, MA, USA

FOREWORD


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Students, residents, and fellows interested in learning about the rheumatic diseasesare faced with the daunting challenge of trying to integrate learning about a multi-tude of fascinating and diverse clinical disorders with an ever-expanding andcomplex body of basic science.

This need encapsulates the principal rationale for the major changes in the 13th

edition of The Primer on the Rheumatic Diseases. Although the rst part of allrecent editions of The Primer have summarized succinctly the physiology of tissuesand cells that mediate inammation and musculoskeletal disease, preparation of thenew edition resulted in the identication of two major problems with this “tried-and-true” formula. First, for readers who really wished to understand the molecularbasis of rheumatic disease to the depth that would facilitate laboratory research andimprove patient care, the initial chapters no longer provided sufcient detail.Second, for readers seeking an introduction or update within the clinical realm ofrheumatic disorders, the rst part of The Primer bore virtually no relation to thediseases described so engagingly in the rest of the book. In short, in this era ofincreasing integration between the basic and clinical sciences, the preliminaryPrimer chapters were at risk for becoming simply the pages thumbed throughquickly to get to the good stuff.

Therefore, in the 13th edition, the clinical descriptions that The Primer hasalways done best have been augmented by including the clinically relevant basicscience components in the same sections. Thus, for each major rheumatic disease—for example, rheumatoid arthritis, osteoarthritis, systemic lupus erythematosus, andidiopathic inammatory myopathies—the chapter describing the clinical and epide-miological features is accompanied by another chapter devoted to “Pathology andPathogenesis.” This second chapter incorporates the appropriate (and updated)elements from previous Primer chapters entitled “Synovium,” “Articular Carti-lage,” “The Complement System,” and “Muscle” that are essential to understandinga particular disease today.

Moreover, this fundamental change in the contents is only the beginning of theimprovements to the 13th edition. Other changes include:

• New chapters on “Clinical Immunology” and “Applied Genetics” designed toheighten the translational nature of the book.

• Color gures that are particularly important for depicting cutaneous ndings andhistopathology.

• An expanded chapter on the cutaneous manifestations of disease, emphasizingthe types of disorders rheumatologists often see in consultation.

• A section devoted entirely to juvenile inammatory arthritis, with individualchapters on “Clinical Features,” “Pathology and Pathogenesis,” “Treatment andAssessment,” and “Special Considerations.”

• Separate chapters on ankylosing spondylitis and the reactive and enteropathicarthropathies, once lumped together (with psoriatic arthritis) as “seronegativespondyloarthopathies.”

Preface


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• A tripling of the text devoted to psoriatic arthritis, an acknowledgement of thesubstantial treatment advances in that disorder.

• Individual chapters (and more than doubling of the text) to the metabolic andinammatory myopathies, once included in the same chapter.

• Reorganization of the vasculitis section along more rational and all-inclusivelines, with a chapter entitled “ANCA-Associated Vasculitis” that addressestogether Wegener’s granulomatosis, microscopic polyangiitis, and the Churg-Strauss syndrome, disorders with striking similarities but important contrasts.

• Now entering its eighth decade, The Primer has rejected strongly the notion that“If it ain’t broke, don’t x it.” In view of the recent remarkable strides in under-standing and treating rheumatic disease, students, trainees, and practicing clini-cians all need a standard textbook that can change with the times and reectthese advances. The Primer continues to ll that need. Read, learn, and enjoy.

John H. Klippel, MD John H. Stone, MD, MPH

Leslie J. Crofford, MDPatience H. White, MD, MA

v i i i PREFACE


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Foreword by Michael E. Weinblatt . . . . . . . . . . . . . . . . . . . . . . . . . . . v

Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . vii

Contributors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xv

1. Public Health and Arthritis: A Growing Imperative . . . . . . . . 1 Patience H. White and Rowland W. Chang

2. Evaluation of the Patient . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

A. History and Physical Examination . . . . . . . . . . . . . . . . . . . 6 David B. Robinson and Hani S. El-Gabalawy

B. Laboratory Assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 Kerstin Morehead

C. Arthrocentesis, Synovial Fluid Analysis,and Synovial Biopsy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

Kenneth H. Fye

D. Imaging of Rheumatologic Diseases . . . . . . . . . . . . . . . . . . 28 William W. Scott, Jr., William J. Didie,

and Laura M. Fayad

3. Musculoskeletal Signs and Symptoms . . . . . . . . . . . . . . . . . . . 42

A. Monarticular Joint Disease . . . . . . . . . . . . . . . . . . . . . . . . . . 42 H. Ralph Schumacher and Lan X. Chen

B. Polyarticular Joint Disease . . . . . . . . . . . . . . . . . . . . . . . . . . 47 Sterling West

C. Neck and Back Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58 David Borenstein

D. Regional Rheumatic Pain Syndromes . . . . . . . . . . . . . . . . 68 Joseph J. Biundo, Jr.

E. The Fibromyalgia Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . 87

Dina Dadabhoy and Daniel J. Clauw

4. Molecular and Cellular Basis of Immunity and Immunological Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94

Kevin Elias, Richard Siegel, and John J. O’Shea

5. Genetics and Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 108 James Kelley and Robert P. Kimberly

6. Rheumatoid Arthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 114

A. Clinical and Laboratory Manifestations . . . . . . . . . . . . . 114 Christopher V. Tehlirian and Joan M. Bathon

CONTENTS


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x C O N T E N T S

B. Epidemiology, Pathology, and Pathogenesis . . . . . . . . . . 122 Jean-Marc Waldburger and Gary S. Firestein

C. Treatment and Assessment . . . . . . . . . . . . . . . . . . . . . . . . 133 Alyce M. Oliver and E. William St. Clair

7. Juvenile Idiopathic Arthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 142

A. Clinical Features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 142 Daniel J. Lovell

B. Pathology and Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . 149 Patricia Woo

C. Treatment and Assessment . . . . . . . . . . . . . . . . . . . . . . . . 154 Philip J. Hashkes and Ronald M. Laxer

D. Special Considerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163 Carol B. Lindsley

8. Psoriatic Arthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 170

A. Clinical Features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 170 Dafna D. Gladman

B. Pathology and Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . 178 Christopher Ritchlin

C. Treatment and Assessment . . . . . . . . . . . . . . . . . . . . . . . . 185 Philip J. Mease

9. Ankylosing Spondylitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 193

A. Clinical Features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 193 Désirée Van der Heijde

B. Pathology and Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . 200 Juergen Braun

C. Treatment and Assessment . . . . . . . . . . . . . . . . . . . . . . . . 209 John C. Davis, Jr.

10. Reactive and Enteropathic Arthritis . . . . . . . . . . . . . . . . . . . . 217 Robert D. Inman

11. Osteoarthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 224

A. Clinical Features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 224 Paul Dieppe

B. Pathology and Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . 229 Francis Berenbaum

C. Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 235 Leena Sharma

12. Gout . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 241

A. Clinical Features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 241 N. Lawrence Edwards


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CONTENTS x i

B. Epidemiology, Pathology, andPathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 250

Hyon K. Choi

C. Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 258 Robert A. Terkeltaub

13. Calcium Pyrophosphate Dihydrate, Hydroxyapatite, and Miscellaneous Crystals . . . . . . . . . . . . 263

Geraldine McCarthy

14. Infectious Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 271

A. Septic Arthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 271 George Ho, Jr.

B. Viral Arthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 277 Leonard H. Calabrese

C. Lyme Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 282 Linda K. Bockenstedt

D. Mycobacterial, Fungal, and ParasiticArthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 290

Steven R. Ytterberg

E. Rheumatic Fever . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 297 Stanford Shulman and Preeti Jaggi

15. Systemic Lupus Erythematosus . . . . . . . . . . . . . . . . . . . . . . . 303

A. Clinical and Laboratory Features . . . . . . . . . . . . . . . . . . . 303

Jill P. Buyon

B. Epidemiology, Pathology, andPathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 319

David S. Pisetsky

C. Treatment and Assessment . . . . . . . . . . . . . . . . . . . . . . . . 327 Susan Manzi and Amy H. Kao

16. Antiphospholipid Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . 339 Michelle Petri

17. Systemic Sclerosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 343

A. Clinical Features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 343 Maureen D. Mayes

B. Epidemiology, Pathology, and Pathogenesis . . . . . . . . 351 John Varga

C. Treatment and Assessment . . . . . . . . . . . . . . . . . . . . . . . . 359 Maya H. Buch and James R. Seibold

18. Idiopathic Inammatory Myopathies . . . . . . . . . . . . . . . . . . 363

A. Clinical Features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 363 Robert L. Wortmann


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x i i CONTENTS

B. Pathology and Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . 368 Lisa G. Rider and Frederick W. Miller

C. Treatment and Assessment . . . . . . . . . . . . . . . . . . . . . . . . 375 Chester V. Oddis

19. Metabolic Myopathies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 381 Alan N. Baer

20. Sjögren’s Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 389 Troy Daniels

21. Vasculitides . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 398

A. Giant Cell Arteritis, Polymyalgia Rheumatica,and Takayasu’s Arteritis . . . . . . . . . . . . . . . . . . . . . . . . . . 398

Cornelia M. Weyand and Jörg J. Goronzy

B. Polyarteritis Nodosa . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 410 Keith T. Rott

C. The Antineutrophil CytoplasmicAntibody–Associated Vasculitides: Wegener’sGranulomatosis, Microscopic Polyangiitis, andthe Churg–Strauss Syndrome . . . . . . . . . . . . . . . . . . . . . . 416

John H. Stone

D. Immune Complex–Mediated Vasculitis . . . . . . . . . . . . . 427 Philip Seo

E. Miscellaneous Vasculitis (Behçet’s Disease, Primary

Angiitis of the Central Nervous System, Cogan’sSyndrome, and Erythema Elevatum Diutinum) . . . . . . 435 Kenneth T. Calamia and Carlo Salvarani

F. Kawasaki’s Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 444 Barry L. Myones

22. Relapsing Polychondritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 451 Harvinder S. Luthra

23. Adult - Onset Still’s Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . 455 John M. Esdaile

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Periodic Syndromes

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 460 John G. Ryan and Daniel L. Kastner

25. Less Common Arthropathies . . . . . . . . . . . . . . . . . . . . . . . . . . 470

A. Hematologic and Malignant Disorders . . . . . . . . . . . . . 470 Adel G. Fam

B. Rheumatic Disease and Endocrinopathies . . . . . . . . . . 479 Peter A. Merkel

C. Hyperlipoproteinemia and Arthritis . . . . . . . . . . . . . . . . 484 Robert F. Spiera


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CONTENT S x i i i

D. Neuropathic Arthropathy . . . . . . . . . . . . . . . . . . . . . . . . . 488 Ann K. Rosenthal

E. Dermatologic Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . 492 Jeffrey P. Callen

F. Hypertrophic Osteoarthropathy . . . . . . . . . . . . . . . . . . . . 504 Manuel Martinez-Lavin

26. Complex Regional Pain Syndrome . . . . . . . . . . . . . . . . . . . . . 509 Geoffrey Littlejohn

27. Sarcoidosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 514 Edward S. Chen

28. Storage and Deposition Diseases . . . . . . . . . . . . . . . . . . . . . . 523 Duncan A. Gordon

29. The Amyloidoses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 533 Pasha Sarraf and Jonathan Kay

30. Neoplasms of the Joint . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 543 Andrew J. Cooper, James D. Reeves, and Sean P. Scully

31. Heritable Disorders of Connective Tissue . . . . . . . . . . . . . . . 549 Reed Edwin Pyeritz

32. Bone and Joint Dysplasias . . . . . . . . . . . . . . . . . . . . . . . . . . . . 559 William A. Horton

33. Osteonecrosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 565 Thorsten M. Seyler, David Marker, and Michael A. Mont

34. Paget’s Disease of Bone . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 573 Roy D. Altman

35. Osteoporosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 576

A. Epidemiology and Clinical Assessment . . . . . . . . . . . . . 576 Kenneth G. Saag

B. Pathology and Pathophysiology . . . . . . . . . . . . . . . . . . . 584 Philip Sambrook

C. Treatment of Postmenopausal Osteoporosis . . . . . . . . 592 Nelson B. Watts

36. Rehabilitation of Patients with RheumaticDiseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 599

Thomas D. Beardmore

37. Psychosocial Factors in Arthritis . . . . . . . . . . . . . . . . . . . . . . . 609 Alex Zautra and Denise Kruszewski

38. Self-Management Strategies . . . . . . . . . . . . . . . . . . . . . . . . . . 614 Teresa J. Brady

39. Pain Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 620 John B. Wineld


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40. Therapeutic Injections of Joints and Soft Tissues . . . . . . . 628 Juan J. Canoso

41. Nonsteroidal Anti-Inammatory Drugs . . . . . . . . . . . . . . . . 634 Leslie J. Crofford

42. Glucocorticoids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 644 Frank Buttgereit and Gerd-Rüdiger Burmester

43. Operative Treatment of Arthritis . . . . . . . . . . . . . . . . . . . . . . 651 Joseph A. Buckwalter and W. Timothy Ballard

44. Complementary and Alternative Therapies . . . . . . . . . . . . 664 Erin L. Arnold and William J. Arnold

Appendix I. Criteria for the Classication and Diagnosis of the Rheumatic Diseases . . . . . . . . . . . . . . . . . . . . 669

Appendix II. Guidelines for the Management of

Rheumatic Diseases . . . . . . . . . . . . . . . . . . . . . . . . . 683Appendix III. Supplement and Vitamin and

Mineral Guide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 691

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 703


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Juan J. Canoso, MD, FACP, MACRAttending, American British Cowdray Medical Center,Mexico City, Mexico

Rowland W. Chang, MD, MPHProfessor of Preventive Medicine, Medicine, and Physical

Medicine and Rehabilitation; Director, Program in PublicHealth, Northwestern University, Feinberg School ofMedicine, Chicago, IL, USA

Edward S. Chen, MDAssistant Professor, Department of Medicine, Division ofPulmonary and Critical Care Medicine, Johns HopkinsUniversity School of Medicine, Baltimore, MD, USA

Lan X. Chen, MD, PhDClinical Assistant Professor, Department of Medicine/Rheumatology, University of Pennsylvania, Philadelphia, PA,USA

Hyon K. Choi, MD, MPH, DrPH, FRCPCAssociate Professor of Medicine and Mary Pack ArthritisSociety Chair in Rheumatology, Department of Medicine,Division of Rheumatology, The University of BritishColumbia, Vancouver, British Columbia, Canada

Daniel J. Clauw, MDProfessor, Department of Internal Medicine, Division ofRheumatology, University of Michigan, Ann Arbor, MI,USA

Andrew J. Cooper, MDResident, Department of Orthopaedic Surgery, University ofMiami, Miami, FL, USA

Leslie J. Crofford, MDGloria W. Singletary Professor of Internal Medicine, Chief,Division of Rheumatology & Women’s Health, University ofKentucky, Lexington, KY, USA

Dina Dadabhoy, MDClinical Lecturer, Department of Internal Medicine, Divisionof Rheumatology, University of Michigan, Ann Arbor, MI,USA

Troy Daniels, DDS, MSProfessor, Schools of Dentistry and Medicine, University ofCalifornia, San Francisco, San Francisco, CA, USA

John C. Davis, Jr., MD, MPHAssociate Professor, Department of Medicine, Division ofRheumatology, University of California San Francisco, SanFrancisco, CA, USA

William J. Didie, MDFellow, Musculoskeletal Imaging, Department of Radiology,Johns Hopkins University, Baltimore, MD, USA

Paul Dieppe, MDProfessor, Department of Social Medicine, University ofBristol, Bristol, UK

N. Lawrence Edwards, MDProfessor and Vice Chairman, Department of Medicine,University of Florida, Gainesville, FL, USA

Hani S. El-Gabalawy, MD, FRCPCProfessor, Department of Medicine, Arthritis Centre, Univer-

sity of Manitoba, Winnipeg, Manitoba, Canada

Kevin Elias, MDHoward Hughes Medical Institute-National Institute ofHealth Research Scholar, Lymphocyte Cell Biology Section,National Institute of Arthritis, Musculoskeletal, and SkinDiseases, Bethesda, MD, USA

John M. Esdaile, MD, MPHScientic Director, Arthritis Research Centre of Canada;Professor, University of British Columbia, Vancouver, BritishColumbia, Canada

Adel G. Fam, MD, FRCP(C), FACPEmeritus Professor of Medicine, Department of Medicine,Division of Rheumatology, Sunnybrook & Women’s CollegeHealth Sciences Centre, University of Toronto, Toronto,Ontario, Canada

Laura M. Fayad, MDAssistant Professor, The Russell H. Morgan Departmentof Radiology and Radiological Science, Johns HopkinsUniversity School of Medicine, Baltimore, MD, USA

Gary S. Firestein, MDProfessor, Department of Medicine, Chief, Division ofRheumatology, Allergy and Immunology, University ofCalifornia San Diego, School of Medicine, La Jolla, CA, USA

Kenneth H. Fye, MDClinical Professor, Department of Medicine, University ofCalifornia, San Francisco, San Francisco, CA, USA

Dafna D. Gladman, MD, FRCPCProfessor, Department of Medicine/Rheumatology, Universityof Toronto; Senior Scientist, Toronto Western ResearchInstitute; Director, Psoriatic Arthritis Program, UniversityHealth Network, Toronto, Canada

Duncan A. Gordon, MD, FRCPC, MACR

Professor, Department of Medicine, University of Toronto;Rheumatologist, University Health Network, TorontoWestern Hospital, Toronto, Ontario, Canada

Jörg J. Goronzy, MDCo-Director, Department of Medicine, Kathleen B. andMason I. Lowance Center for Human Immunology, EmoryUniversity School of Medicine, Atlanta, GA, USA

Philip J. Hashkes, MD, MScHead, Section of Pediatric Rheumatology, Department ofRheumatic Diseases, Cleveland Clinic Foundation, Cleveland,OH, USA

x v i CONTRIBUTOR S


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George Ho, Jr., MDProfessor, Department of Internal Medicine, Division ofRheumatology, Brody School of Medicine at East CarolinaUniversity, Greenville, NC, USA

William A. Horton, MD

Director, Research Center/Molecular and Medical Genetics,Shriners Hospital for Children; Professor, Oregon Health andScience University, Portland, OR, USA

Robert D. Inman, MDProfessor, Department of Medicine, Division of Rheuma-tology, University of Toronto, Toronto Western Hospital,Toronto, Ontario, Canada

Preeti Jaggi, MDAssistant Professor, Department of Infectious Diseases,Department of Pediatrics, Ohio State University, Columbus,OH, USA

Amy H. Kao, MD, MPHAssistant Professor, Department of Medicine, Division ofRheumatology and Clinical Immunology, University ofPittsburgh School of Medicine, Pittsburgh, PA, USA

Daniel L. Kastner, MD, PhDChief, Genetics and Genomics Branch; Clinical Director andDirector of Translational Research, National Institute ofArthritis and Musculoskeletal and Skin Diseases, Bethesda,MD, USA

Jonathan Kay, MDAssociate Clinical Professor, Department of Medicine,Harvard Medical School; Director of Clinical Trials,

Rheumatology Unit, Massachusetts General Hospital, Boston,MA, USA

James Kelley, PhDPostdoctoral Fellow, Department of Medicine, Division ofClinical Immunology and Rheumatology, University ofAlabama at Birmingham, Birmingham, AL, USA

Robert P. Kimberly, MDHoward L. Holley Professor of Medicine and Director, Divi-sion of Clinical Immunology and Rheumatology, Senior Asso-ciate Dean for Research, Department of Medicine, Universityof Alabama at Birmingham, Birmingham, AL, USA

John H. Klippel, MDPresident and CEO, Arthritis Foundation, Atlanta, GA,USA

Denise Kruszewski, MSGraduate Student/Research Assistant, Department ofPsychology, Arizona State University, Tempe, AZ, USA

Ronald M. Laxer, MD, FRCPCVice President, Education and Quality, The Hospital forSick Children; Professor, Department of Pediatrics andMedicine, The University of Toronto, Toronto, Ontario,Canada

Carol B. Lindsley, MDProfessor, Department of Pediatrics, Director of PediatricRheumatology, University of Kansas Medical Center, KansasCity, KS, USA

Geoffrey Littlejohn, MD, MPH, MBBS[Hon], FRACP,

FRCP(Edin)Director of Rheumatology and Associate Professor ofMedicine, Department of Medicine, Monash University atMonash Medical Centre, Melbourne, Australia

Daniel J. Lovell, MD, MPHJoseph Levinson Professor of Pediatrics, Division ofRheumatology, Cincinnati Children’s Hospital MedicalCenter, Cincinnati, OH, USA

Harvinder S. Luthra, MDJohn Finn Professor of Medicine, Department ofRheumatology, Mayo Clinic College of Medicine, Rochester,MN, USA

Susan Manzi, MD, MPHAssociate Professor, Department of Medicine, Division ofRheumatology and Clinical Immunology, University ofPittsburgh School of Medicine, University of PittsburghGraduate School of Public Health, Pittsburgh, PA, USA

David Marker, BSMedical Student, Rubin Institute for Advanced Orthopedics,Sinai Hospital of Baltimore, Baltimore, MD, USA

Manuel Martinez-Lavin, MDChief, Department of Rheumatology, National Institute ofCardiology, Mexico, DF, Mexico

Maureen D. Mayes, MD, MPHProfessor, Department of Internal Medicine, Division ofRheumatology and Immunogenetics, University of Texas-Houston Medical School, Houston, TX, USA

Geraldine McCarthy, MD, FRCPIAssociate Professor/Consultant Rheumatologist, Division ofRheumatology, Department of Medicine, University CollegeDublin, Dublin/Mater Misericordiae University Hospital,Dublin, Ireland

Philip J. Mease, MDHead, Seattle Rheumatology Associates; Chief, Division ofRheumatology Research, Swedish Medical Center; ClinicalProfessor, University of Washington School of Medicine,Seattle, WA, USA

Peter A. Merkel, MD, MPHAssociate Professor, Department of Medicine, Section ofRheumatology, Boston University School of Medicine,Boston, MA, USA

Frederick W. Miller, MD, PhDChief, Environmental Autoimmunity Group, Ofce ofClinical Research, National Institute of Environmental HealthSciences, National Institutes of Health, Bethesda, MD, USA

CONTRIBUTORS xv i i


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Michael A. Mont, MDDirector, Rubin Institute for Advanced Orthopedics, SinaiHospital of Baltimore, Baltimore, MD, USA

Kerstin Morehead, MDAssistant Clinical Professor, Department of Medicine,

Division of Rheumatology, University of California, SanFrancisco, San Francisco, CA, USA

Barry L. Myones, MDAssociate Professor, Pediatric Rheumatology Center, BaylorCollege of Medicine/Texas Children’s Hospital , Houston, TX,USA

Chester V. Oddis, MDProfessor, Department of Medicine, Division of Rheumato-logy and Clinical Immunology, University of Pittsburgh Schoolof Medicine, Pittsburgh, PA, USA

Alyce M. Oliver, MD, PhD

Fellow in Rheumatology, Department of Medicine, Divisionof Rheumatology and Immunology, Duke University MedicalCenter, Durham, NC, USA

John J. O’Shea, MDScientic Director, National Institute of Arthritis and Muscu-loskeletal and Skin Diseases; Chief, Molecular Immunologyand Inammation Branch; Chief, Lymphocyte Cell BiologySection, National Institutes of Health, Bethesda, MD, USA

Michelle Petri, MD, MPHProfessor, Department of Medicine, Johns Hopkins UniversitySchool of Medicine, Baltimore, MD, USA

David S. Pisetsky, MD, PhDChief, Department of Medicine, Division of Rheumatologyand Immunology, Duke University School of Medicine,Durham, NC, USA

Reed Edwin Pyeritz, MD, PhDProfessor, Department of Medicine and Genetics, Hospital ofthe University of Pennsylvania, Philadelphia, PA, USA

James D. Reeves, MDResident, Department of Orthopaedic Surgery, University ofMiami, Miami, FL, USA

Lisa G. Rider, MDDeputy Chief, Environmental Autoimmunity Group, Ofceof Clinical Research, National Institute of EnvironmentalHealth Sciences, National Institutes of Health, ClinicalResearch Center, Bethesda, MD, USA

Christopher Ritchlin, MDAssociate Professor, Department of Medicine, Division ofAllergy, Immunology and Rheumatology, University ofRochester Medical Center, Rochester, NY, USA

David B. Robinson, MD, MSc, FRCPCAssociate Professor, Department of Medicine, ArthritisCentre, University of Manitoba, Winnipeg, Manitoba,Canada

Ann K. Rosenthal, MDProfessor, Department of Medicine, Division of Rheumato-logy, Medical College of Wisconsin/Zablocki VA MedicalCenter, Milwaukee, WI, USA

Keith T. Rott, MD, PhD

Assistant Professor, Department of Medicine, Division ofRheumatology, Emory University School of Medicine,Atlanta, GA, USA

John G. Ryan, MB, MRCPIClinical Fellow, Genetics and Genomics Branch, NationalInstitute of Arthritis and Musculoskeletal and Skin Diseases,National Institutes of Health, Bethesda, MD, USA

Kenneth G. Saag, MD, MScAssociate Professor, Director, Center for Education and Re -search on Therapeutics of Musculoskeletal Disorders, Divisionof Clinical Immunology and Rheumatology, University ofAlabama at Birmingham, Birmingham, AL, USA

Carlo Salvarani, MDDirector, Division of Rheumatology, Hospital S. MariaNuova, Reggio Emilia, Italy

Philip Sambrook, MD, FRACPProfessor, Department of Rheumatology, University ofSydney, Sydney, NSW Australia

Pasha Sarraf, MD, PhDFellow, Department of Medicine, Division of Rheumatology,Allergy and Immunology, Massachusetts General Hospital,Boston, MA, USA

H. Ralph Schumacher, MDProfessor, Department of Medicine/Rheumatology, Univer-sity of Pennsylvania; VA Medical Center, Philadelphia, PA,USA

William W. Scott, Jr., MDAssociate Professor, The Russell H. Morgan Departmentof Radiology and Radiological Science, Johns HopkinsUniversity School of Medicine, Baltimore, MD, USA

Sean P. Scully, MD, PhDProfessor, Department of Orthopaedics, Miller School ofMedicine, University of Miami, Miami, FL, USA

James R. Seibold, MDProfessor, Department of Internal Medicine/Rheumatology,Director, University of Michigan Scleroderma Program,University of Michigan Health System, Ann Arbor, MI, USA

Philip Seo, MD, MHSCo-Director, Johns Hopkins Vasculitis Center, Division ofRheumatology, Johns Hopkins University School of Medi-cine, Baltimore, MD, USA

Thorsten M. Seyler, MDCenter for Joint Preservation and Reconstruction, RubinInstitute for Advanced Orthopedics, Sinai Hospital ofBaltimore, Baltimore, MD, USA

x v i i i CONTRIBUTO R S


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Leena Sharma, MDProfessor, Department of Internal Medicine, Division ofRheumatology, Feinberg School of Medicine at NorthwesternUniversity, Chicago, IL, USA

Stanford Shulman, MD

Chief, Department of Infectious Diseases; Professor,Department of Pediatrics, Northwestern University FeinbergSchool of Medicine/The Children’s Memorial Hospital,Chicago, IL, USA

Richard Siegel, MD, PhDPrincipal Investigator, Immunoregulation Group, NationalInstitute of Arthritis and Musculoskeletal and Skin Diseases,National Institutes of Health, Bethesda, MD, USA

Robert F. Spiera, MDAdjunct Clinical Instructor, Department of Medicine/Rheumatology, Mount Sinai School of Medicine, New York,NY, USA

E. William St. Clair, MDProfessor, Department of Medicine, Division of Rheuma-tology and Immunology, Duke University Medical Center,Durham, NC, USA

John H. Stone, MD, MPHAssociate Physician, Massachusetts General Hospital; DeputyEditor for Rheumatology, UpToDate, Boston, MA, USA

Christopher V. Tehlirian, MDPost-Doctoral Fellow, Department of Medicine, Division ofClinical and Molecular Rheumatology, Johns HopkinsUniversity School of Medicine, Baltimore, MD, USA

Robert A. Terkeltaub, MDChief, Rheumatology Section, Department of Medicine,Veterans Affairs Medical Center San Diego; Professor,Department of Medicine, University of California San DiegoSchool of Medicine, San Diego, CA, USA

Désirée Van der Heijde, MD, PhDProfessor, Department of Rheumatology, University HospitalMaastricht, The Netherlands

John Varga, MDGallagher Professor of Medicine, Department of Medicine,Division of Rheumatology, Northwestern University FeinbergSchool of Medicine, Chicago, IL, USA

Jean-Marc Waldburger, MD, PhDPost-Doctoral Scholar, Department of Medicine, Divisionof Rheumatology, Allergy, and Immunology, University ofCalifornia San Diego School of Medicine, La Jolla, CA,USA

Nelson B. Watts, MDProfessor, Department of Internal Medicine, University ofCincinnati College of Medicine, Cincinnati, OH, USA

Sterling West, MDProfessor, Department of Rheumatology, University ofColorado Health Sciences Center, Denver, CO, USA

Cornelia M. Weyand, MDCo-Director, Kathleen B. and Mason I. Lowance Center forHuman Immunology, Department of Medicine, EmoryUniversity School of Medicine, Atlanta, GA, USA

Patience H. White, MD, MA

Chief Public Health Ofcer, Arthritis Foundation, Atlanta,GA, USA

John B. Wineld, MDSmith Distinguished Professor of Medicine Emeritus,Department of Medicine, University of North Carolina,Chapel Hill, NC, USA

Patricia Woo, BSc, MBBS, PhD, MRCP, FRCP, CBEProfessor, Department of Immunology and MolecularPathology, University College London, London, UK

Robert L. Wortmann, MD, FACP, FACRProfessor and C. S. Lewis, Jr., MD Chair of Medicine,

Department of Internal Medicine, The University ofOklahoma College of Medicine, Tulsa, OK, USA

Steven R. Ytterberg, MDAssociate Professor, Department of Medicine, Division ofRheumatology, Mayo Clinic College of Medicine, Rochester,MN, USA

Alex Zautra, PhDFoundation Professor, Department of Psychology, ArizonaState University, Tempe, AZ, USA

C O N T R I B U TO R S x i x


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1

CHAPTER 1

Public Health and Arthritis:

A Growing ImperativePATIENCE H. WHITE, MD, MAR OWLAND W. C HANG, MD, MPH

Forty-six million people have doctor-diagnosedarthritis and by 2030 it is projected to be 67 million,or 25% of the US population.

Arthritis is the number one cause of disability and coststhe United States an estimated 128 billion annually.

Public health focuses on the assessment andreduction of health burden in the population.

Three types of prevention strategies can be applied

to arthritis.

The Merriam-Webster Dictionary denes public healthas “the art and science dealing with the protection andimprovement of community health by organized com-munity effort and including preventive medicine andsanitary and social science.” Until the mid-20th century,the eld of public health was primarily concernedwith the prevention and control of infectious diseases.

More recently, public health scientists and practitio-ners have also been engaged in the prevention andcontrol of chronic diseases. In the mid-19th century,when the therapeutic armamentarium of physicianswas limited, the relationship between the elds ofpublic health and medicine was very close. Indeed,most public health professionals were physicians.However, as biomedical science led to more and morediagnostic and therapeutic strategies for physiciansin the 20th century, and as separate schools ofmedicine and public health were established in Ameri-can universities, the elds have developed differentapproaches to solving health problems. Medicine hasbeen primarily concerned with the diagnosis and thepalliative and curative treatments of disease and thehealth of the individual patient. Public health has beenprimarily concerned with the prevention and control ofdisease and the health of the population. The goal ofthis chapter is to illustrate the magnitude of the arthri-tis public health problem in the United States and todescribe potential public health approaches to mitigatethis problem. In order to more clearly describe publichealth perspective, science, and intervention, contrastswill be made with the medical approach, but this shouldnot be interpreted to mean that one approach is

superior to the other. In fact, it is likely that arthritispatient–physician encounters will be more effectivewhen arthritis public health efforts are successful andvice versa. It is this synergy for which both elds shouldbe striving.

RATIONALE FOR ARTHRITISPUBLIC HEALTH INITIATIVEArthritis and other rheumatic conditions are the lead-ing cause of disability in the United States (1), makingit a major public health problem. Arthritis is one of themost common chronic diseases in the United States.Forty-six million Americans, or one out of every veadults, has doctor-diagnosed arthritis, and 300,000children have arthritis (http://www.cdc.gov/arthritis/).Between 2003 and 2004, an estimated 19 million USadults reported arthritis-attributable activity limitationand 8 million reported arthritis affected their work (2).Arthritis is a large clinical burden, with 36 millionambulatory visits and 750,000 hospitalizations (3,4). In2030, due to the aging of the population and thegrowing epidemic of obesity, the prevalence of self-reported, doctor-diagnosed arthritis is projected toincrease to nearly 67 million (25% of the adult popula-tion) and 25 million (9.3% of the adult population) willreport arthritis-attributable activity limitations (Table1-1) (5).

In the future, this arthritis-related clinical andhealth care system burden will require a planned


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2 PATIENCE H. WHITE AND ROWLAND W. CHANG

coordinated approach with increased need for morearthritis specialists, increased need for training ofprimary care providers in arthritis management, andincreased availability of public health interventions toimprove quality of life through lifestyle changes anddisease self-management.

THE MEDICAL MODELCOMPARED WITH THE PUBLICHEALTH MODELThere are several differences between medicine and

public health, but perhaps the most important differ-ence is that of perspective. Medicine focuses on thediagnosis and treatment of individuals , whereas publichealth focuses on the assessment and the reduction ofhealth burden in the population . The diagnostic toolsof the physician includes history, physical examination,and a vast array of diagnostic tests including bloodtests, imaging, and tissue sampling, all performed onthe individual patient. Medical treatment includespharmaceuticals, surgery, and rehabilitation. Theassessment tools of the public health professionalinclude surveys and disease registries for dened popu-lations (local, state, and/or national). Public healthintervention includes community health educationand programs and advocacy for public policy reform.Medical research programs emphasize basic science,drilling down to individual abnormalities at themolecular and genomic level, whereas public healthresearch programs emphasize epidemiology and thesocial sciences, searching out risk factors that pertainto a large proportion of the population. While medicalscience has undeniably improved the individual treat-ment of some forms of arthritis (e.g., rheumatoidarthritis), still much more needs to be done to dealwith the coming increases in arthritis prevalence and

arthritis-related disability associated with the aging ofthe US population. This is perhaps the most importantreason to embrace an arthritis public health initiative:to have a greater impact on the health of thepopulation.

PUBLIC HEALTH’S EMPHASIS ONPREVENTION AND HOW ITRELATES TO ARTHRITISTraditionally, public health has been concernedwith the prevention of disease and the prevention

of disease consequences (e.g., death and disability).Three types of prevention have been described:primary, secondary, and tertiary. Primary preventionis the prevention of the disease itself. In the infectiousdisease realm, this is made possible by the identica-tion of the etiologic microorganism and the develop-ment of a vaccine that will protect the host fromdeveloping the infection even when the host is exposedto the microorganism. Primary prevention of a chronicdisease requires the identication of an etiologic factorassociated with the disease and the successful inter-vention (lifestyle change and/or pharmacologic treat-ment) on the risk factor. For example, the reductionof weight by dietary and physical activity interventionhas been successful in the primary prevention of dia-betes, and the pharmacologic treatment of hyperten-sion has proven effective in the prevention of coronaryartery disease. An example of a primary arthritisprevention trial showed that a vaccine for the spiro-chete associated with Lyme disease reduced the riskfor this disease in endemic areas (6). While severaletiologic factors associated with knee osteoarthritis(most notably obesity) have been identied, no trialshave been performed to inform public health practiceregarding the primary prevention of this condition,

TABLE 1-1. ESTIMATED US POPULATION AND PROJECTED PREVALENCE OF DOCTOR-DIAGNOSED ARTHRITIS ANDACTIVITY LIMITATION FOR ADULTS AGES 18 AND OLDER IN THE UNITED STATES.

PROJECTED PREVALENCE OF PROJECTED PREVALENCE OF ARTHRITIS- ESTIMATED US POPULATION DOCTOR-DIAGNOSED ARTHRITIS ATTRIBUTABLE ACTIVITY LIMITATIONSYEAR IN THOUSANDS IN THOUSANDS IN THOUSANDS

2005 216,096 47,838 17,610

2015 238,154 55,725 20,601

2030 267,856 66,969 25,043

SOURCE: Hootman JM, Helmick CG, Arthritis Rheum 2006;54:226–229, by permission of Arthritis and Rheumatism .


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although data will hopefully be available in the comingyears.

Secondary prevention involves the detection ofdisease in its preclinical (i.e., asymptomatic) phase toallow for early treatment and the prevention of impor-tant consequences, such as death or disability. Forexample, mammography has been shown to preventbreast cancer–related death by detecting breast cancerbefore clinical signs and symptoms develop such thatearly treatment can be initiated. Similarly, screeningfor osteoporosis with dual-energy x-ray absorptiometry(DXA) scanning has been shown to reduce fracturerates and subsequent disability by allowing for earlydetection and treatment of this common condition.Secondary prevention of rheumatoid arthritis is likelyto be successful because of effective medical treatmentthat limits joint destruction and arthritis-related dis-ability. Studies have shown that the earlier the treat-

ment, the less the ultimate destruction and disability.The challenge here is to identify a suitable screeningtest.

Tertiary prevention involves the treatment of clinicaldisease in order to prevent important consequences,such as death or disability. Thus, tertiary prevention istypically in the realm of medicine. However, publichealth and public policy efforts to make medical, surgi-cal, and rehabilitation treatment more effective andmore accessible are common public health tertiary pre-vention interventions.

ARTHRITIS PUBLIC HEALTHACCOMPLISHMENTSThe Arthritis Foundation has focused its public healthactivities by promoting the health of people with and atrisk for arthritis through its leadership and involvementin the National Arthritis Act, the National ArthritisAction Plan, the arthritis section of Healthy People2010, and the National Committee on Quality Assur-ance (NCQA) to develop an arthritis-related HealthPlan Employer Data and Information Set (HEDIS)

measure (2003).

National Arthritis ActIn 1974, the Arthritis Foundation joined in a partner-ship that pushed the US Congress to pass the NationalArthritis Act, which initiated an expanded response toarthritis through research, training, public education,and treatment. The National Arthritis Act called for along-term strategy to address arthritis in the UnitedStates.

National Arthritis Action PlanThe National Arthritis Action Plan (NAAP) broughttogether over 40 partners to create a blueprint for popu-lation-oriented efforts to combat arthritis. The NAAPemphasizes four public health values: prevention, theuse and expansion of the science base, social equity, and

building partnerships. The NAAP is now widely utilizedby other public health and professional organizationsas a model program for population-oriented efforts tocombat a chronic disease (see Table 1-2 for the aims andactivities of NAAP). In 2000, the federal governmentfunded the Arthritis Program at the Centers for DiseaseControl (CDC) that provides the infrastructure for theprogram at the CDC, implementation of the arthritispublic health plan through the establishment ofarthritis programs in state health departments (seehttp://www.cdc.gov/arthritis/), limited investigator-initi-ated grant program, and a peer-reviewed grant to theArthritis Foundation. With this funding, the CDCArthritis Program and the Arthritis Foundation havecreated effective public education and awareness activi-ties in both English and Spanish and have developedevidence-based programs for people with arthritis,including an arthritis-specic self-help course, an exer-cise program, and a water exercise program (see theLife Improvement Series descriptions at http://www.arthritis.org).

The Arthritis Group at the Center for DiseaseControl have developed arthritis data collectionplans through the Behavioral Risk Factor SurveillanceSystem (BRFSS), the National Health Interview Survey

TABLE 1-2. THE NATIONAL ARTHRITIS ACTIONPLAN.

The overarching aims of the NAAP are:• Increase public awareness of arthritis as the leading cause of

disability and an important public health problem.• Prevent arthritis whenever possible.• Promote early diagnosis and appropriate management for

people with arthritis to ensure the maximum number of years of healthy life.

• Minimize preventable pain and disability due to arthritis.• Support people with arthritis in developing and accessing the

resources they need to cope with their disease.• Ensure that people with arthritis receive the family, peer, and

community support they need.

The aims of the NAAP will be achieved through three majortypes of activities:• Surveillance, epidemiology, and prevention research• Communication and education• Programs, policies, and systems


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4 PATIENCE H. WHITE AND ROWLAND W. CHANG

(NHIS), and the National Health and Nutrition Exami-nation Survey (NHANES), and it has published anannual arthritis data report during Arthritis Monthin May.

Healthy People 2010Healthy People 2010 is the nation’s public healthplan that was created in consultation with the nation’shealth constituencies by the Department of Healthand Human Services. Healthy People 2010 has twogoals: (1) increase quality and years of life and (2)eliminate health dis parities. Healthy People 2010 con-tains a separate chapter on Arthritis and Other Rheu-matic Conditions, including osteoporosis and backpain. The overall goal of this section of Healthy People2010 is to “prevent illness and disability related toarthritis and other rheumatic conditions, osteoporosis,and chronic back conditions” (www.healthypeople.gov).

The general Healthy People 2010 arthritis objectivesare to:

• Reduce the mean level of joint pain among adultswith doctor-diagnosed arthritis.

• Reduce the proportion of adults with doctor-diagnosed arthritis who experience a limitation inactivity due to arthritis or joint symptoms.

• Reduce the proportion of adults with doctor-diagnosed arthritis who have difculty in performing

two or more personal care activities, thereby preserv-ing independence.• Increase health care provider counseling for persons

with doctor-diagnosed arthritis.• Increase health care provider counseling about

weight loss among persons with doctor-diagnosedarthritis.

• Increase health care provider counseling for physicalactivity or exercise for persons with doctor-diagnosedarthritis.

• Reduce the impact of doctor-diagnosed arthritis onemployment.

• Increase the employment rate among adults withdoctor-diagnosed arthritis in the working-agedpopulation.

• Decrease the effect of doctor-diagnosed arthritis onpaid work.

• Eliminate racial differences in the rate of total kneereplacements.

• Increase the proportion of adults who have seen ahealth care provider for their chronic jointsymptoms.

• Increase the proportion of persons with doctor-diagnosed arthritis who have had effective,

evidence-based arthritis education as an integralpart of the management of their condition.

Quality of Care Measures for

People with ArthritisThe Arthritis Foundation Quality Indicators Project(AFQUIP) created indicators for treatment of rheuma-toid arthritis and osteoarthritis, and for analgesics andpain use (7).

These were used by the National Committee forQuality Assurance (NCQA) to develop a HEDISmeasure for disease-modifying antirheumatic drugs(http://www.ncqa.org). The osteoarthritis indicatorshave been used by the American Medical Associa-tion (AMA) Physician Consortium for PerformanceImprovement.

Through a focus on public health goals, severalorganizations are cooperating and collaborating tolessen disability in the aging population, decreasehealth disparities, and increase physical activityand reduce calorie intake in order to mitigate theepidemic of obesity and its serious impacts on health.The Arthritis Foundation and the CDC are activelyforming partnerships with state public health depart-ments, federal government agencies such as theNational Institute of Arthritis and Musculoskeletal andSkin Diseases at the National Institutes of Health, theAgency for Orthopedic Surgery, community healthorganizations, volunteer health organizations, other

volunteer organizations such as Research! America,and professional organizations such as the AmericanCollege of Rheumatology and the American Academyof Healthcare Research and Quality to move thisagenda forward.

REFERENCES 1. Centers for Disease Control and Prevention. Prevalence of

disabilities and associated health conditions among adults:United States 1999. Morb Mortal Wkly Rep 2001;50:120–125.

2. Centers for Disease Control and Prevention. Racial/ethnicdifferences in the prevalence and impact of doctor diag-nosed arthritis: United States, 2002. Morb Mortal WklyRep 2005;54:119–121.

3. Hootman JM, Helmick CG, Schappert SM. Magnitude andcharacteristics of arthritis and other rheumatic conditionson ambulatory medical visits, United States 1997. ArthritisRheum 2002;47:571–581.

4. Lethbridge-Cejku M, Helmick CG, Popovic JR. Hospital-izations for arthritis and other rheumatic conditions: datafrom the 1997 National Hospital Discharge Survey. MedCare 2003;41:1367–1373.


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5. Hootman JM, Helmick CG. Projections of US prevalenceof arthritis and associated activity limitations. ArthritisRheum 2006;54:226–229.

6. Steere AC, Sikand VK, Meurice F, et al. Vaccinationagainst Lyme disease with recombinant Borrelia burg-dorferi outer-surface lipoprotein A with adjuvant. Lyme

Disease Vaccine Study Group. N Engl J Med 1998;339:209–215.

7. MacLean CH, Saag KG, Solomon DH, Morton SC, SampselS, Klippel JH. Measuring quality in arthritis care: methodsfor developing the Arthritis Foundation’s quality indicatorset. Arthritis Rheum 2004;51:193–202.


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CHAPTER 2

Evaluation of the Patient

A. History and Physical ExaminationDAVID B. R OBINSON, MD, MSC, FRCPCHANI S. EL-GABALAWY, MD, FRCPC

The patient history and physical examination formthe basis of diagnosis and monitoring the course ofrheumatic and musculoskeletal diseases.

Attention is focused on signs and symptoms of both joint and extra-articular features.

The joint examination must include pattern, range ofmotion, signs of inammation, stability, weakness,and deformity.

Musculoskeletal complaints are among the mostcommon problems in clinical medicine. It is thereforeimportant that all physicians are able to conducta basic screening evaluation that identies the pres-ence of pathology or dysfunction of musculoskeletalstructures.

RHEUMATOLOGICALHISTORYA thoughtful and detailed history plays a critical role indetermining the nature of the complaint and helps tofocus the clinical evaluation (1). The history should bestructured to answer specic questions.

Questions for the Clinicianto Address 1. Is the problem regional or generalized, symmetric or

asymmetric, peripheral or central? 2. Is it an acute, subacute, or chronic problem? Is it

progressive? 3. Do the symptoms suggest inammation or damage

to musculoskeletal structures? 4. Is there evidence of a systemic process? Are there

associated extra-articular features? 5. Is there an underlying medical disorder which may

predispose to a specic rheumatologic problem? 6. Has there been functional loss and disability? 7. Is there a family history of a similar or related

problem?

Location and SymmetryThe location of a musculoskeletal problem is often themost important clue in identifying the specic cause.Musculoskeletal problems can broadly be categorizedas regional or generalized, although there is often con-siderable overlap between these two categories.Regional syndromes typically affect a single joint or

periarticular structure, or an entire extremity or bodyregion. A regional pain syndrome can be on a referredbasis, and have little to do with the area where the painis experienced. Joints both immediately above andbelow the painful area should be routinely examined forpathology.

Specic arthropathies have a predilection for involv-ing specic joint areas (2). Involvement of the wrists andthe proximal small joints of the hands and feet is animportant feature of rheumatoid arthritis (RA). In con-trast, psoriatic arthritis (PsA) often involves the distal

joints of the hands and feet. An acutely painful andswollen great toe is most likely caused by a gouty attack.An important aspect of the articular pattern of involve-ment is symmetry. Rheumatoid arthritis tends to involve

joint groups symmetrically, whereas the seronegativespondyloarthropathies and osteoarthritis (OA) tend tobe asymmetrical in their articular patterns.

Onset and ChronologyThe mode of onset and evolution of musculoskeletalsymptoms over time is very helpful in establishing adiagnosis. For most chronic arthropathies such as RA,the onset is typically subacute, occurring over weeks to


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CHAPTER 2 • EVALUATION OF THE PATIENT 7

months rather than hours to days. Attacks of gout andseptic arthritis, on the other hand, have an acute onset,reaching a crescendo within hours. The pain of bromy-algia is often reported as being present for years withepisodic exacerbations. A temporally associated trau-matic event or history of repetitive use of a joint can bea particularly good clue to diagnosing a regional mus-culoskeletal syndrome.

Inammation and WeaknessArticular pain and swelling can be on an inammatoryor non-inammatory basis. When intra-articular inam-mation is present, the process involves the synovialmembrane, and is termed synovitis . The swelling isusually due to accumulation of uid in the articularcavity and/or inltration and enlargement of thesynovium. Pain and swelling associated with the pres-

ence of synovitis often occur at rest, whereas in degen-erative disorders such as OA, these symptoms becomemore evident with joint use. In the presence of synovitis,the patient may also complain of difculty moving the

joints after a period of immobility, a symptom referredto as stiffness . In inammatory disorders such as RA,this stiffness is most evident in the early morning.Indeed, the duration of morning stiffness, typicallyestablished by asking the patient, “How long does ittake you before you are moving as well as you are goingto move for the day?” is a semiquantitative measure ofthe degree of articular inammation.

Complaints of limitation in joint motion, deformity,and joint instability are usually caused by damage toarticular and periarticular structures. The patient shouldbe carefully questioned to establish the circumstancesaround which these symptoms were initiated, and thetypes of movements that aggravate them.

Patients with musculoskeletal pathology often com-plain of muscle weakness. This feeling of weakness maybe associated with pain, stiffness, and, in some cases,parasthesia or other neurological symptoms. General-ized weakness may be in response to pain from articularor periarticular inammation, as in the case of RA andpolymyalgia rheumatica. Alternatively, weakness maybe caused by a primary neuropathic or myopathicprocess. In the case of myopathies, the weakness is typi-cally symmetrical and involves proximal muscles mostseverely, whereas neuropathies more commonly affectthe distal musculature.

Systemic and Extra-ArticularFeaturesConstitutional symptoms of fatigue, weight loss,anorexia, and low grade fever can be associated with anysystemic inammatory process, and their presence is an

important diagnostic clue. In addition, systemic rheu-matic diseases are commonly associated with nonarticu-lar features that are of value in diagnosis. For example,a history of recent genitourinary symptoms in associa-tion with lower extremity asymmetric oligoarthritis ishighly suggestive of reactive arthritis, whereas this samearticular pattern in association with recurrent abdomi-nal pain and bloody diarrhea is more suggestive of thearthropathy of inammatory bowel disease. It is thusimportant that the clinician perform a complete reviewof systems and directly question the patient regardingthe presence of specic symptoms, such as rashes or skinchanges, photosensitivity, Raynaud’s phenomenon,mouth ulcers, and dryness in the eyes and mouth.

Functional LossesQuestioning regarding functional loss is essential for

understanding the impact of a musculoskeletal disorderand, in turn, developing a plan of management. Thequestioning should span the spectrum of activities, fromsimple activities of daily living such as dressing andgrooming to more physically demanding activities suchas sports. In some cases, the functional loss may be quitesevere, impairing basic activities such as stair climbingand gripping, while in others it may be quite subtle,detectable only as a reduction in strenuous activitiessuch as jogging.

Family HistoryA number of rheumatic diseases have a strong geneticbasis. Disorders such as ankylosing spondylitis are muchmore common in HLA-B27–positive families than inthe general population. Questioning regarding familyhistory should not be restricted only to ascertainingwhether other family members have a similar arthritis,but should be as complete as possible regarding autoim-mune diseases, many of which (e.g., RA, thyroid disease,and diabetes) tend to cluster in families.

PRINCIPLES OF

RHEUMATOLOGICALEXAMINATIONEvaluation of musculoskeletal complaints involvesexamination of the joints and their soft tissue supportstructures, the bony skeleton, and the muscle groups thatmove the skeletal structures (3). The joints, bones, andmuscles can be directly accessible to examination, as inthe extremities, or they may be inaccessible to directexamination, as in the case of the spine and hip joints.

All joint areas should be inspected from multipleangles to assess for deformity (sometimes seen as loss

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8 DAVID B. ROBINSON AND HANI S . EL-GABALAWY

of symmetry with the contralateral side), muscularatrophy, swelling, erythema, or surgical scars. Extremity

joints should be palpated for warmth using the dorsumof the hand. Supercial joints are normally slightlycooler than the surrounding soft tissue. The joint lineand major bony and soft tissue structures should bepalpated for tenderness.

Functional joint motion should be tested both byhaving the patient actively move the joint to its extremesand by having the examiner passively move the jointthrough its range. Tenderness elicited by gentle stresson the joint at its end range of motion (stress tender-ness) is characteristic of joint pathology and may beabsent in pain syndromes such as bromyalgia. Loss ofrange of motion is seen both with acute articular inam-mation and with chronic arthritis and damage. Jointsshould be assessed for the presence of swelling. Thecardinal signs of articular inammation are warmth,

joint line tenderness, pain on motion (particularly at theextremes of the range of motion), and intra-articularswelling or effusion.

Deformity caused by loss of alignment is a conse-quence of destructive arthropathies such as RA. Thedamage is commonly associated with loosening of thesoft tissue support structures surrounding the joints. Insome cases, the joint may not exhibit any obvious defor-mity, but may be unstable when put through its rangeof motion or is mechanically stressed.

A key part of the musculoskeletal evaluation involvesexamination of the ligaments, tendons, menisci, andmuscles. These structures may be the primary source ofthe pathology, or may be involved secondary to thearticular pathology. Examination of individual musclegroups requires a basic knowledge of the origin, inser-tion, and primary action of each muscle. Atrophy andweakness of the muscles surrounding a particular joint isan important indicator of chronic articular pathology.

A Screening MusculoskeletalExamThe GALS (Gait, Arms, Leg, Spine) system has beendevised to screen rapidly for musculoskeletal disease(4). Initially, the patient is asked three basic questions:“Have you any pain or stiffness in your muscles, joints,or back?”; “Can you dress yourself completely without

any difculty?”; “Can you walk up and down stairswithout any difculty?”. Depending on the answers tothe questions, further questioning is undertaken toexplore specic areas.

The examiner then systematically inspects thepatient’s gait, arms, legs, and spine, rst with the patientstanding still and then responding to instructions (Table2A-1). Abnormalities detected on this screening are fol-lowed up with a more detailed regional or generalizedmusculoskeletal examination.

TABLE 2A-1. MAIN FEATURES OF THE GAIT, ARMS, LEG, SPINE (GALS) SCREENING INSPECTION.POSITION/ACTIVITY NORMAL FINDINGS

Gait Symmetry, smoothness of movement; normal stride length; normal heelstrike, stance, toe-off, swing through; able to turn quickly

Inspection from behind Straight spine, normal symmetric paraspinal muscles, normal shoulder andgluteal muscle bulk, level iliac crests, no popliteal cysts, no poplitealswelling, no hindfoot swelling/deformity

Inspection from the side Normal cervical and lumbar lordosis, normal thoracic kyphosis

“Touch your toes.” Normal lumbar spine (and hip) exion

Inspection from the front Arms “Place your hands behind your head, elbows out.” Normal glenohumeral, sternoclavicular, and acromioclavicular joint

movement “Place your hands by your side, elbows straight.” Full elbow extension “Place your hands in front, palms down.” No wrist/nger swelling or deformity, able to fully exend ngers “Turn your hands over.” Normal supination/pronation, normal palms “Make a st.” Normal grip power “Place the tip of each nger on the tip of the thumb.” Normal ne precision, pinch Legs Normal quadriceps bulk/symmetry, no knee swelling or deformity, no

forefoot/midfoot deformity, normal arches, no abnormal callousformation

Spine “Place your ear on your shoulder.” Normal cervical lateral exion

SOURCE: Modied from Doherty et al., Ann Rheum Dis 1992;51:1165–1169, with permission of Annals of Rheumatic Diseases .


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EXAMINATION OF SPECIFICJOINT AREAS

The Hand and Wrist

A number of generalized arthropathies have distinctivepatterns of hand involvement, and the recognition ofthese patterns is highly valuable diagnostically. Exami-nation of the hands should be initiated with the patientsitting comfortably with the hands open and the palmsfacing down. In this position, the examiner can inspectthe alignment of the digits relative to the wrist andforearm. Atrophy of the intrinsic muscles of the handscan readily be appreciated as a hollowing out of thespaces between the metacarpals. The nails should beinspected for evidence of onycolysis or pitting sugges-tive of psoriasis. Redness and telangiectasia of the nail

fold capillaries can by detected on close inspection, andis often indicative of a connective tissue disease such assystemic lupus erythematosus (SLE), scleroderma, ordermatomyositis. Tightening of the skin around thedigits, or sclerodactyly, is typical of scleroderma and isusually both visible and palpable. The pulp of the digitsshould be examined for the presence of digital ulcers,also seen most commonly in scleroderma.

Articular swelling of the distal interphalangeal (DIP)and proximal interphalangeal (PIP) joints can representbony osteophytes as in the case of Heberden’s andBouchard’s nodes in the DIP and PIP joints, respec-tively, or can represent an intra-articular effusion

associated with synovitis in the joint. Palpation willhelp in differentiating these. Swelling and redness ofan entire digit, termed dactylitis , is highly suggestive ofa spondylarthropathy such as psoriatic arthritis or reac-tive arthritis.

Swelling of the metacarpophalangeal (MCP) jointscan be visually appreciated as a fullness in the valleysnormally found between the knuckles (heads of themetacarpal bones). In cases of RA where the MCPsynovitis has been longstanding, it is often associatedwith ulnar subluxation of the extensor tendons, result-ing in the ulnar drift of the digits that is typical of thisdiagnosis. Swelling on the dorsum of the wrist area canresult from synovitis of the wrist or tenosynovitis of theextensor tendons. Getting the patients to gently wigglethe ngers helps differentiate these two ndings in thatthe swelling will tend to move with the tendons if it is aresult of tenosynovitis. Inspection of the palmar aspectof the hands is important for identifying atrophy of thethenar or hypothenar eminences, which can result eitherfrom disuse due to articular involvement of the wristor, in the case of the thenar eminence, carpal tunnelsyndrome.

Global function of the hand should be evaluated byasking the patient to make a full st and to fully extend

and spread out the digits. Pincer function of the thumband ngers should be tested. The grip strength can beestimated by having the patient squeeze two of theexaminer’s ngers. Individual hand joints should be pal-pated to determine the presence of joint line tendernessand effusion, these being the most important indicatorsof synovitis. The technique for palpating the DIP andPIP joints is similar. The thumb and index nder of onehand palpates in the vertical plane, while the thumb andindex nder of the other hand palpates in the horizontalplane (Figure 2A-1). Alternating gentle pressurebetween the two planes will displace small amounts ofsynovial uid back and forth, allowing the examiner todetect effusions in these small joints. Likewise, tender-ness suggestive of synovitis can be elicited by this tech-nique. The technique for palpating the MCP joints issomewhat modied because of the inability to directlypalpate these joints from the horizontal plane. The

thumbs are used to palpate the dorsolateral aspects ofthe joint, while the index ngers palpate the palmaraspect.

Palpation of the wrist involves a similar technique tothat used for the MCPs. The thumbs are used to palpatethe dorsum of the joint, while the index ngers palpatethe volar aspect (Figure 2A-2). Synovial thickening andtenderness suggestive of wrist joint synovitis can usuallybe palpated on the dorsum of the joint. Particular atten-tion should be paid to swelling and tenderness in thearea just distal to the ulnar styloid, where the extensorand exor carpi ulnaris tendons are directly palpable.This area is very commonly involved in early RA. Pain

and tenderness conned to the radial aspect of the wristare most commonly due to either OA of the rst carpo-

FIGURE 2A-1

Technique for examining the small joints of the hands and feet.The thumb and index nger of the examiner’s hands are usedto gently ballot small amounts of intra-articular uid back andforth to elicit evidence of joint line tenderness.


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metacarpal joint, or to DeQuervain’s tenosynovitis. Allthe joints of the hand and wrist should be evaluated forstress tenderness.

The ElbowFlexion and extension of the forearm occur exclusively

at the elbow joint and involve the hinge type of articula-tion between the proximal ulna and distal humerus. Inexamining the elbow, a number of surface landmarksneed to be identied. These are the olecranon process,the medial and lateral epicondyles of the humerus, andthe radial head. A triangular recess is formed in thelateral aspect of the joint between the olecranon process,the lateral epicondyle, and the radial head. This recessis the point where the synovial cavity of the elbow ismost accessible to inspection and palpation.

Examination of the elbow should be undertaken withthe patient sitting comfortably and the entire arm beingwell supported in order to eliminate muscle tension.Initially the joint should be inspected with forearmexed to 90°. Particular attention should be paid to thelateral recess described above. Obvious bulging in thisarea is highly suggestive of an effusion and synovitis. Incontrast, swelling directly over the olecranon processis more suggestive of olecranon bursitis. Any processthat causes true synovitis of the elbow is typically associ-ated with a reduction in the range of motion of the joint,both in exion–extension and in supination–pronation.Having the patient extend the forearm as much as pos-sible will detect the presence of a exion contracture,this being an almost invariant feature of elbow synovi-

tis. With this maneuver, the bulge in the lateral recesswill tend to enlarge, becoming more tense due thereduction in the internal dimension of the elbow in theposition of extension.

The synovial cavity and joint line can best be pal-pated for swelling and tenderness in the area of thelateral recess. This is also the site where arthrocentensisof the elbow is performed. It should be noted that painin the lateral aspect of the elbow area is a common clini-cal problem, and is usually due to lateral epicondylitisor tennis elbow rather than elbow joint pathology. Ten-derness directly palpable over the lateral epicondyleand with stressing the wrist and nger extensors is sug-gestive of this diagnosis.

The ShoulderProper examination of the shoulder should always begin

with appropriate visualization of the entire shouldergirdle area, both from the front and the back. Thisincludes the sternoclavicular, glenohumeral, and acro-mioclavicular joints as well as the scapulothoracicarticulation. Comparison should be made with the con-tralateral shoulder. Any asymmetry between the twosides should be noted. For example, patients with rotatorcuff tears often hold the affected shoulder higher thanthe other side. Atrophy of the shoulder girdle muscula-ture is an important sign of chronic glenohumeral jointpathology, as occurs in RA. This is most evident assquaring of the shoulder due to deltoid atrophy andscooping out of the upper scapular area due to super-

spinatus atrophy. Effusions in the shoulder joint arevisible anteriorly just medial to the area of the bicipitalgroove, and if large enough are also evident laterallybelow the acromion. It should be noted that largeamounts of uid can accumulate in the glenohumeral

joint space without much visible evidence due to con-siderable redundancy in the joint capsule.

After inspecting the shoulder area in the resting posi-tion, the patient is asked to demonstrate the activerange of motion of the shoulder. Abduction is observedas the patient moves both outstretched arms from theirside in the lateral plane until the palms meet overhead.The movement is evaluated for discomfort, symmetry,and uid scapulohumeral coordination. Patients withshoulder pathology will usually move the arm forwardsomewhat in order to complete the maneuver. Externalrotation can then be tested by having the patient attemptto touch the back of their head with the palm of thehand from the fully abducted position. If abduction isabnormal, active exion should be tested by having thepatient lift the outstretched arm from their side directlyup in front of them. Active internal rotation and exten-sion is observed by having the patient reach behindtheir back and attempt to have their ngertips touch thehighest point possible on their scapula.

FIGURE 2A-2

The dorsum of the wrist joint is palpated for tenderness and

swelling using the examiner’s thumbs. The wrist should beexamined in slight exion to allow the joint line of the radiocar-pal, intercarpal, and carpometacarpal joints to be optimallypalpated.


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Palpation should include the entire shoulder girdlearea. The sternoclavicular joint is palpated, then thengers are walked laterally over the clavicle to the acro-mioclavicular joint, which is palpated for tenderness andswelling. The subacromial space, containing the supra-spinatus tendon and subacromial bursa, lies directlybelow the acromion. Immediately below the acromio-clavicular joint, the coracoid process should be identi-ed. The short head of the biceps inserts on this process.The long head of the biceps can be palpated lateral tothis in the bicipital groove. The anterior aspect of theglenohumeral joint can be palpated between the cora-coid process and the long head of the biceps and followsthe contour on the rounded anterior aspect of thehumeral head. Shoulder synovitis can be palpated in thisarea as joint line tenderness and/or boggy effusion.

Passive range of shoulder motion is then evaluated.The most informative parts of the range of motion are

internal/external rotation and abduction. When testingthese movements it is very important to immobilize thescapula to prevent rotation at the scapulothoracic area.In this way, glenohumeral motion can be isolated andappropriately evaluated. One effective technique toachieve this is to rmly press down on the top of theshoulder area with the palm of one hand, while the otherhand moves the arm through the range of motion (Figure2A-3). Internal/external rotation should be tested withthe arm by the patient’s side and with the arm abductedto 90°. Examination of the patient in the supine positionmay aid in relaxing musculature in patients who areunable to fully relax during this maneuver.

A large number of special maneuvers have beendescribed that suggest specic clinical syndromes in the

shoulder. The predictive value of these maneuvers ismodest (5). Forced supination of the hand with theelbow exed at 90° will cause pain in the area of thelong head of the biceps in patients with bicipital tendi-nitis. Impingement of the subacromial bursa or supra-spinatus tendon is suggested by pain with forced internalrotation and exion of the glenohumeral joint from aposition of 90° exion with the elbow exed at 90°.Supraspinatus tendinitis can be detected by having thepatient position their outstretched arm at 90° of abduc-tion while maximally internally rotating the glenohu-meral joint such that the thumb is pointing downward.The examiner then asks the patient to resist attempts topush the arm down. In patients with superspinatus ten-dinitis, the maneuver will be associated with pain, andmay result in the patient suddenly dropping the arm.

The HipPain resulting from hip arthritis is typically experiencedin the groin or, less commonly, the buttock. It tends toradiate down the anteromedial aspect of the thigh, occa-sionally down to the knee. Pain in the lateral trochan-teric area is most often indicative of bursitis involvingthe trochanteric bursa.

Because the hip joint cannot be directly examined,the examiner needs to glean important diagnostic cluesfrom observing the patient’s gait, buttock and thighmusculature, and from evaluating passive range ofmotion of the hip joint. As with all load bearing joints,evaluation of functional joint motion needs to be

assessed under load with the patient walking and stand-ing. Subtle hip pathology may be detected by havingthe patient perform a squat. The patient with true hipdisease often walks with a coxalgic gait, tending toquickly swing the pelvis forward on the affected side inorder to avoid weight bearing on the hip affected byarthritis. If the hip arthritis is prolonged and severe, thebuttock musculature tends to atrophy, as does the thighmusculature. In severe cases, the abductor muscles areunable to hold the pelvis in a horizontal position whenthe patient is asked to stand only on the affected hip.This forms the basis of the Trendelenburg test, wherethe patient’s pelvis tends to sag down on the contralat-eral side when the patient is asked to hold their entireweight on the affected leg.

With the patient in the supine position, passive rangeof motion should initially be screened by log rolling theentire extended leg. The leg is then exed maximally toassess completeness of this motion. With the knee exedto 90° and the hip exed to 90°, internal and externalrotation of the hip are then tested. Care should be takenthat the hip movements are isolated, and that thepatient’s pelvis is not rotating to compensate for lostrange of motion. Pain and loss of motion on internalrotation are particularly sensitive indicators of hip

FIGURE 2A-3

Glenohumeral joint motion is best examined with the elbowexed to 90° and the upper arm in partial abduction. Internaland external rotation of the shoulder are then examined in thisposition. Care should be taken to immobilize the scapula using atechnique such as that shown.


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pathology. Flexion contracture of the hip tends toaccompany longstanding severe hip arthritis.

The Sacroiliac JointPalpation of the sacroiliac (SI) joint is undertaken withthe patient lying at on their abdomen. With the palmof the examiner’s hand held around the iliac crest, thethumb tends to fall directly over the joint which extendsdown below the dimples in the posterior pelvic area. Toelicit tenderness in the SI joint, direct pressure is appliedwith the thumb in this area. In addition to direct palpa-tion, the examiner can perform other maneuvers tofurther establish the presence of sacroiliitis. Direct pres-sure over the sacrum will produce pain in an inamedSI joint. Gaenslen’s maneuver is performed by havingthe patient hyperextend their leg over the edge of theexamining table, thereby stressing the ipsilateral SI

joint.

The SpineThe spine should be examined initially with the patientstanding and the entire spine well visualized. The normalcurvature of the spine, lumbar lordosis, thoracic kypho-sis, and cervical lordosis should be evaluated by observ-ing the patient from the both the back and the side, andany loss or accentuation of these curves noted. If scolio-sis is noted with the patient standing upright, they shouldbe asked to bend forward and ex the spine to evaluatethe effects of this movement on the scoliosis. True sco-

liosis will be present irrespective of the state of spinalexion, while a functional scoliosis due to leg lengthdiscrepancy will tend to decrease with spinal exion.The level of the iliac crests relative to the spine shouldalso be evaluated by observing the patient from theback, and the examiner sitting with their eyes at approxi-mately the level of the iliac crests. A tilted pelvis can bedue to compensation for a primary scoliosis in the spineor, alternatively, due to a leg length discrepancy.

The range of motion of the entire spine should beexamined in segments. The lumbar spine is assessed byhaving the patient attempt to touch their toes and thenextend their back. Lateral exion is assessed by havingthe patient reach their ngertips as far as possible downthe lateral aspect of their leg. Lateral rotation, whichinvolves both the lumbar and thoracic spine, is testedby having the patient turn their upper body with theexaminer holding the pelvis stable.

The Schober test is performed to specically assessmovement in the lumbar spine. With the patient stand-ing, a distance of 10 cm is measured up the lumbar spinefrom the lumbosacral junction at the level of the sacraldimples. Marks are placed at both ends of this 10 cmsegment. The patient is then asked to ex forward as faras possible, attempting to touch their toes. With this

motion, the marks identifying this 10 cm segment nor-mally expand to 15 cm or more, indicative of distractionbetween the vertebrae. While reduction in this mea-surement is not specic for any particular pathology, itcan be used over time to follow disorders with progres-sive loss of motion, such as ankylosing spondylitis.

Patients presenting with symptoms suggestive of alumbar radiculopathy, such as pain and parasthesiashooting down the leg, need to undergo an examinationof the lumbosacral area and a detailed neurologicalexamination of the leg. Maneuvers that put traction onthe lumbar spinal roots are used to provide further evi-dence of a radiculopathy. The most commonly used ofthese maneuvers is the straight leg raising test, wherethe patient lies in the supine position and the leg is pas-sively raised by the examiner with the knee fullyextended. A positive test requires that the patient expe-rience pain and parasthesia shooting down the leg to the

level of the foot.Cervical range of motion begins with the patientupright and the examiner in front. The patient is askedto ex, extend, laterally ex (patient attempts to touchtheir ear to their shoulder), and laterally rotate (patientattempts to touch their chin to their shoulder) theirhead. Movements should be evaluated for symmetry,fullness of motion, and discomfort. Gentle passive rangeof motion may be attempted with the patient supine.Spinous processes and surrounding musculature shouldbe palpated for spasm or tenderness. It should be notedthat pain in the neck area often radiates down the arm,up the occiput, or down to the scapular area. The pain

may be aggravated by particular parts of the range ofmotion.

The KneeExamination of the knee starts with inspection of thepatient’s gait and with the patient standing. Wheninspecting from the front, attention should rst be paidto the areas above and below the knee. Atrophy of thequadriceps usually indicates chronic knee pathology.Swelling due to synovial uid accumulation or synovialinltration and thickening is most readily appreciatedin the suprapatellar bursa. When a large effusion ispresent, it can be seen to also cause bulging of both thelateral and medial compartments of the knee. Inspec-tion of the knee from the back with the patient standingup is the best way to evaluate the alignment of thefemur relative to the tibia. Varus deformities of theknee causing a bow-legged appearance most commonlyre

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Primer on Rheumatic Disease