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ILLUSTRATED ORTHOPEDIC PHY SICAL ASSE SSMENT. Third Edition Copyright
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DEDICATION
For Linda, Inspiration Everlasting
For PiS, VR, iG, KB, MAB, CG, LA, CR, KR, DR, RM , RS, iC, PS, MLP, DRG NIR ,
,
is, MF, RH, MRN, SAA, EIW, MAN, LLS, FLvw, RMS MRA, SMR, ID, CMC, MC, ADS ... ,
and all other patients, past and present, participating in my continued search for their wellness ...
For iRB ... because many scientific premises first illuminate in eddies of single malts, plumes of Cuban smoke, and at the end of tight lines ...a consummate physician/scientist ...
And finally, For my mother: An Irish woman who bore a Welsh son. I am blessed by her endless creativity and, compassion, and gift of gab. Were it not for her, I would have less to say ... how very dull.
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ABOUT THE A U T H O R Dr. Ronald C. Evans is a Doctor of Chiropractic and a 1976 graduate of Northwestern Health Sciences Univeristy, and Chaired its Chiropractic Orthopedics Residency Program from 1980 to 1984. He is a Diplomate of the American Board of Chiropractic Orthopedists (DABCO) and Examiner Emeritus of that Board. He is a Fellow of the Academy of Chiropractic Orthopedists (FACO) and Examiner Emeritus of that Board. Dr. Evans is a Fellow of the International College of Chiropractors (FICC), and has lectured in orthopedics and neurology for 35 years, speaking extensively throughout the United States, Canada, New Zealand and Australia, and Scotland. Dr. Evans has lectured on the campuses of Northwestern Health Sciences, Drake University, Texas College of Chiropractic, Logan University/College of Chiropractic, Southern California University of Health Sciences, and Palmer College of Chiropractic, Western States Chiropractic College, as well as at the Center for Alternative Medicine Research, Harvard Medical School. Dr. Evans has addressed diverse audiences that include the Association of Trial Lawyers of Iowa, the American Bar Association, the Australian Chiropractor's Association, the Defense Research Institute of the American Bar Association, the American Public Health Association, and the Royal Academy of Physicians and Surgeons. Dr. Evans is retired from an 11-year term of office on the Iowa Board of Chiropractic Examiners, serving as chairperson of the Board for nearly half that term. He maintains a private practice in Des Moines, and is the senior chiropractic orthopedic staff of a multi-provider, multi-disciplinary health care facility specializing in the non-surgical management of orthopedic and neurological disorders. He is a Trustee of the Foundation for Chiropractic Education and Research, and served as Editorial Advisor for its publication "Staying Well" for many years. Dr. Evans is the Vice President of FCER and continues to serve the FCER as the Chairman of its Department of Defense Committee. Dr. Evans is the Chair of the Evidence-Based Resource Center of FCER. He was an appointee to the RAND Consensus Panel for the study of the Appropriateness of Manipulative Care for the Cervical Spine. He is an appointee, by the Secretary of Defense of the United States, to the Oversight Advisory Committee for Chiropractic Health Care, Department of Defense, now serving as a Senior Member of that Committee, as well as its successor committee, the Chiropractic Healthcare Benefits Advisory Committee. Dr. Evans has served as an Editorial Advisor for DC TRACTS, and is a Prepublication Book Reviewer for Lippincott Williams & Wilkins Publishers; Elsevier, and Aspen Publishing. He is an Associate Editor for the Journal of Neuromusculoskeletal
System of the ACA and a Forum Acquisitions Editor for the ACA Press. Dr. Evans was an appointee by Iowa Governor Terry E. Branstad to the Iowa Health Reform Council, the Iowa Health Regulation Review Task Force, and the Iowa Community Health Management Information System (CHMIS). He is the CEO of the Iowa Chiropractic Physicians Clinic, (ICPC) a single-specialty independent provider network for Iowa and surrounding Midwestern states. Dr. Evans is the recipient of the Chiropractic Orthopedist of the Year Award (1984) and the Distinguished Service Award (1994) from the American College of Chiropractic Orthopedists, receiving the ACCO Distinguished Service Award again for 2001-2002. The Council on Chiropractic Orthopedics recognized Dr. Evans for Lifetime Achievement in 1992 and he received the President's Citation for Distinguished Service by the American Board of Chiropractic Orthopedists in 1991. Dr. Evans received the Award of Excellence in 1993-1994, the Presidential Award in 1994, and the Outstanding ICS Member in 1996-1997, all from the Iowa Chiropractic Society. Most recently, he received the Iowa Board of Chiropractic Examiners Service Award: Iowa Chiropractic Society 1990-2001. Dr. Evans received the Distinguished Service Award from the Academy of Chiropractic Orthopedists in March 2003. Dr. Evans' writings include Orthopedic Test and Signs, A Compendium, NWUHS, 1979, third edition, 1984, 1985; Differential Diagnosis of Conditions Presenting Neck and ArmPain,NWCC, 1980, second edition, 1984,1985; Orthopedic Considerations of the Low Back and Lower Extremity, NWUHS, 1980, second edition, 1984, 1985; The Impairment Rating, NWCC, 1981, second edition, 1984; "The Injured Worker: Role of the Chiropractor," Journal of the Australian Chiropractor's Association; 1985; 15(2); "Malingering and Symptom Embellishment," Chapter 15, Chiropractic Family Practice, Williams & Wilkins, 1990; Thoracic Spinal Examination Procedures; audio lecture for DC TRACTS bimonthly publications, 1989, 1990; "Truncal Pain," Chapter 5, as a contribution to Scoliosis, by D. Aspergren, Williams & Wilkins, 1991; "Back School; a statistical correlation to demonstrate efficacy of a Back School Education Program in the therapeutic regimen: a one year study," completed 12/31/82; "CPT/ICD-9 coding and reference glossary" for Iowa Chiropractic Society; The Role of The Doctor of Chiropractic In Health Care Reform in The State of Iowa Within the Context of the Principles of Reform Of the Iowa Health Reform Council; Notice of Intended Action Insurance Division [191], New Chapter 75, "Iowa Individual Health Benefits Plans"; Managed Care In The United
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ABOUT THE A U T H O R ( C O N T I N U E D )
States Perspectives on Chiropractic Health Care Delivery in Total Managed Care Systems, 1995; Noticed Rules, Chapter 110, "Center for Rural Health and Primary Care," New Section. 514c. 11 Patient Access to Types of Physicians Under Managed Care Health Plan or Indemnity Plan With Limited Provider Network; Analysis of the Final Report on the Physician Utilization Study as authorized by Iowa State Senate, Senate File 2470(1996) and completed by Donald G. Hamm, Jr., FS A William M. Mercer, Incorporated, as the Clinical and Cost Effectiveness of Various Types of Physicians for the Iowa Division of Insurance January 6, 1997 by Ronald C. Evans, DC, FACO, FICC, and Anthony I. Rosner, Ph.D. February 10, 1997; Fibromyalgia: A Conservative Perspective on Definition, Diagnosis and Management, a video presentation for FCER 5/95; Identifying and Understanding Lateral Elbow Pain with Emphasis on Lateral Epicondylitis; Alternative Medicine: Implications for Clinical Practice Chiropractic Health Care; Basic Chiropractic Testing and Evaluation Techniques PAIN: "Is it real, or is it
Memorex," Iowa Trial Lawyers Association Medical Damages Seminar June 9, 1995; Testing Methodology and Protocol of the American Board of Chiropractic Orthopedists, Evans RC, Brandt JR; Evans RC, Rosner A L . "Alternatives in Cancer Pain Treatment: The Application of Chiropractic Care," Seminars in Oncology Nursing 2005;21(3):184-189. His textbooks include The Illustrated Essentials in Orthopedic Physical Assessment, 1993; Illustrated Orthopedic Physical Assessment, 2001; and Instant Access to Orthopedic Physical Assessment, 2002; and Iatrogenic Tendinopathy Associated with Levaquin (Levofloxacin); case report, 2008. Dr. Evans holds the copyright and trademark for the Greenfield Babinski Neurological Reflex Hammer; IMPSTAT (a computer program for the Evaluation and Rating of Physical Impairments (coauthored with Logic Unlimited, Inc.); and he is the co-developer of E X A M M A K E R , a computerized exam-making program, based on multi-statistical permutations, with Logic Unlimited, Inc.
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PREFACE The basic observation of a patient's painful stance and aggravating movements usually allows the formulation of the presenting signs and symptoms into a recognizable constellation of a disease syndrome. The essence of orthopedic diagnosis is the clinically demonstrable or reproducible signs of disease or injury. Many physicians associate an aura of mysticism with the ease and speed with which the orthopedic specialist arrives at a diagnosis. In fact, the specialist's development of interviewing, observation, and physical testing skills allows proceeding directly to the heart of the patient's problem. I have been privileged in clinical practice to be challenged by the myriad orthopedic health problems presented by my patients. I believe that my early and fumbling years were well tolerated by these gracious people. They became well in spite of my efforts. They have remained loyal indeed. In these latter years of practice, many of the early patients return with new diseases. These maladies are often much more difficult to diagnose and treat. My skills as an orthopedic specialist have been honed to a fine edge out of necessity. Some of these patients will not outlive me to give me yet another chance to get it right. The perspective of the role of the physician in modern medicine has changed. Physicians are no longer viewed as the omnipotent beings they were formerly thought to be. The physician is expected to recognize personal skill limitations and make appropriate consultations and referrals. Patients expect the correct diagnosis the first time around. At the least, they deserve that. This book is created to alleviate the frustration and discomfort for two parties in their respective quests for health and wellness. First are the physicians and orthopedic specialists, who labor mightily in pushing, pulling, poking, bending, and twisting patients' body parts in the sometimes less than compassionate search for the cause of the suffering. Second are the patients who have been not-so-gently pushed, pulled, poked, bent, and twisted into inhuman configurations as they wait furtively for the discovery of the cause of their anguish. I salute both parties for their endurance in seeking the origin of disease and discomfort. Although the first edition of Instant Access to Orthopedic Physical Assessment was an unqualified success—voted into the 1994-1995 Top 250 Books of the Year by Doody's Health Sciences Book Review Journal—it could be made to be better. Much of what made the first edition so successful succeeded into a second edition, and now a third edition. There are many major changes to the contents: increasing the information on disease assessment, including more illustrations, and creating many more Orthopedic Gamuts.
Readers will enjoy the "At the View Box," contributions of Dr. Timothy Mick, DC, DACBR, as well as the expanded critical thinking elements. Illustrated Orthopedic Physical Assessment, Third Edition, remains clinically relevant and useful for both the student and the practicing clinician. The scope and organization of Illustrated Orthopedic Physical Assessment, Third Edition, makes it a suitable companion for the clinician at all levels of sophistication, progressing from the initial procedures of orthopedic diagnosis to the requirements of the advanced student and the experienced practitioner. Included in the thirteen chapters are diagnostic facts in orthopedics, organized in a manner most likely to be useful during the examination of patients. The book's compact physical dimensions invite constant use as a reference volume on the physician's office desk, in the instrument bag, and in the clinical setting; its functional internal design, with liberal use of Orthopedic Gamuts, offers a convenient vehicle for refreshing one's memory about seldom encountered and easily forgotten clinical orthopedic phenomena. Only the unusual reader and clinician could master the contents of Illustrated Orthopedic Physical Assessment by studying it in sequence from beginning to end. Rather, the student or clinician should digest the principles and procedures in segments as general diagnostic knowledge progresses. First, the reader should become familiar with Chapters 1 and 2 and the descriptions of the "Cardinal Signs and Symptoms". From these chapters, the clinician should explore the regional chapters. As contact with patients increases and specific questions arise, the reader should become familiar with the "Comments" for each diagnostic procedure. The "Comments" section of each test or sign amplifies the knowledge of an underlying pathology that is often discovered with the pertinent test or procedure. Chapter 13 presents rationale and procedures for investigating malingering or non-organically-based complaints. Included with Chapter 13 are numerous medical record forms, outcomes assessment forms, and pain scale analogs. Each chapter of Illustrated Orthopedic Physical Assessment, Third Edition, has a specific format. The format lends to the quick referencing of tests and maneuvers and crossreferencing of associated procedures. Each chapter begins with indexing of the tests found therein. Each chapter also begins with cross-reference tables for the syndrome assessed and by the syndrome suspected. Further, each chapter presents the separate protocols for the regional joint assessment procedures and for assessment of pain in the particular joint or region. These are presented as testing procedural flow charts. These charts
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identify the test procedure(s) used to objectify the symptoms of pain, paralysis, weakness, and loss of sensation. The chart provides a plan of examination and selections of tests for the joint. Each chapter begins with a set of axioms. Axioms are self-evident or universally recognized truths. Axioms are also established rules, principles, or laws. An axiom used in this text is also a principle accepted as true, without proof as the basis for argument. Each chapter introduction addresses the various unique considerations or pathologies of the focal joint. The introductory section contains the index of the tests presented and illustrated in the chapter. Laced throughout a chapter are Orthopedic Gamuts. The various gamuts present a range or spectrum of facts or concepts in assessing orthopedic disease. The gamuts in each chapter may represent universal orthopedic precepts as well as specific regional principles and maxims. The gamuts serve as diagnostic rubric in examining a patient. Essentia] anatomy is presented in each chapter. The essential anatomy section is not all-encompassing, but rather discusses only the typical tissues that can be examined in orthopedic physical procedures. Essential motion assessment for the joint is included. These illustrations depict the expected full ranges of movement for the joint. The discussion further identifies the amount of lost motion that can affect the activities of daily living. Essential muscle function for each joint is also included. This section identifies the musculature that is the prime mover of the joint, the innervation, and the action of the muscle, and limited discussion of the muscular anatomy. Essential imaging elements are addressed in each chapter, specific for the region or joint discussed. Again, not all imaging techniques or modalities are discussed, only those procedures germane to the physical orthopedic testing of a patient. Each test, maneuver, sign, law, or phenomenon is presented separately. The common usage name for the test, as identified in Stedman's, Taber's, Mosby's, Dorland's, or Churchill's medical dictionaries, is the heading for the test. Equally, common synonyms and eponyms follow this name. Eponyms for certain examinations vary from locale to locale or among institutions within the same area. Such observations are a reflection of the training center's influence. This is especially true where the names of prominent local physicians or clinicians or researchers are frequently used for these examinations. On occasion, the same test is given two or more names, or the name can apply to more
than one test or sign. In a problem-oriented situation, eponyms are routinely used in the physical evaluation process. Familiarity with the terms and techniques used in determining regional problems enables the physician and assistant to record and clarify an orthopedic examination. Following the name of the test, maneuver, or sign is identification of the specific pathology the test is suited to elicit. A test is part of the physical examination in which direct contact with the patient is made. It also may be a chemical test, x-ray, or other study. All tests described in his book will relate to the physical examination. A sign is elicited by a test or a particular maneuver. A sign can be simply a visual observation (e.g., antalgia), and it is an indication of the existence of a problem perceived by the examiner. A maneuver is a complex motion or series of movements, used either as a test or treatment. A maneuver is also a method or technique. A phenomenon is any sign or objective symptom or any observable occurrence or fact. A law is a description of a phenomenon that is so thoroughly tested and accepted that it is regarded as a principle governing like phenomena. For each testing procedure in the book, a general comment is presented about the pathologic condition targeted by the test. Numerous citations from current research literature annotate the discussions of underlying pathologies. Following the comment section is a bulleted delineation of how the test is conducted. Each procedure is supported by photo illustrations and legends. Each test is cross-referenced with other supportive tests and procedures as "Next Steps/Procedures". Where pertinent, a "Clinical Pearl" identifies the subtle nuances or finesse of the tests that the author has gleaned from empirical practice. For selected tests or procedures, At the Viewbox case studies are presented. The case studies exemplify the typical and salient diagnostic image findings for the disease pathology discussed. The case studies have been graciously supplied from the teaching library of Dr. Timothy Mick, DC, DACBR. At the close of each chapter, a "critical thinking" section is included. The critical thinking section is a range of questions germane to the specific region or joint of the chapter. The questions pertain largely to information contained in this text, but may occasionally require the reader to crossreference with other pieces of literature or current scientific journals. The answers for each question are contained in this reference as well.
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The references are listed for each chapter. The bibliographic listing is new, updated, and extensive. In some instances, the bibliography reflects older volumes or works than are commonly found in scientific literature today. These older references are the original work of the creators of various tests or procedures in this book. Preserving the books in these reference lists is an attempt to preserve a continuum in the development of orthopedic investigation. In an effort to accurately depict tissues and pathology involved in orthopedic disease and injury, numerous new illustrations are included in Illustrated Orthopedic Physical Assessment, Third Edition. Largely the new illustrations are from the outstanding and benchmark works of selected
authors. Their works are exemplary in great scientific writing, strongly contributing to the fund of knowledge of modern physicians. The artwork and line drawings used in these works are unsurpassed. Although the various tests and procedures in this book are presented in an anatomical or regional format, the application of the tests is accomplished in a more natural flow of examination procedures. The natural flow of the examination usually moves the patient from the standing position, through sitting, supine, and side-lying positions to the prone position. Appendix A is a Listing of Tests, Alphabetically and Anatomically; Appendix B is a Listing of Tests According to the Position of the Patient. A Glossary of Abbreviations is also included.
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ACKNOWLEDGMENTS Many individuals come to mind for their contributions to the continuum of this reference work, and they are indeed too numerous to list. They are, especially, the physicians who attend my lectures and symposia and take the time to tell me about or demonstrate for me various orthopedic tests and signs. I am sure that in many instances the uninformed or casual onlookers thought that grown men were wrestling in public, when, in fact, we were exchanging the latest testing procedures. I will always be grateful to these keepers of the empirical body of medicine and science. Without their thirst for knowledge and scientific evidence and support, this book could not be written or continue in its evolution. More specifically, I must acknowledge three great mentors in chiropractic orthopedics: Dr. Joseph J. Sweere, Dr. Russell G. Hass (dec), and Dr. Robert N. Solheim (dec). It was my fortune to be their student in orthopedic health science. Their challenges kept me advancing in my fundamental knowledge in orthopedic medicine, and their educational excellence caused me to grow. This book is a product of that growth. Their guidance and vitality have been the breath of life for the entity of orthopedic specialization within the scope of chiropractic practice. Perhaps more especially, I acknowledge Dr. John F. Allenberg, former President, Northwestern University of Health Sciences, as the individual responsible for my completion of the arduous, if not overwhelming, residency program at Northwestern. Although I may have had the talent and intellect for the task, he provided the necessary stimulus at the right times to help me see the endeavor to completion. Without that, I would not be a chiropractic orthopedist. It is hard to define the driving force that propels one to aspire to excellence. Samuel C. Evans, DC, my father, and partner in practice, in his life and love of quietly but efficiently caring for people, embodied the greatest attributes in health science and art. His dedication to truth in science and compassion in ministering to the sick and injured inspired me to greater heights as a physician and as a person. This book, the editions before it, and those that will come after, is penned with eternal respect, admiration, and humility for his lifetime work and contribution to the human condition. The greatest man I ever knew. My contemporary, Dr. James R. Brandt, continued to serve in the development of the third edition of this text, as well as for its companion, Instant Access to Orthopedic Physical Assessment, Second Edition. Dr. Brandt remained steadfast in critical assessment of the work and dedicated to making me strive for excellence in my writing. Dr. Kim A. Skibsted contributed to the third edition with astute clinical photography. Dr. Skibsted's keen eye and
sense of photographic composition are unparalleled and add to the advancement of the images used in various chapters. In many instances, the clinical photography of Dr. Skibsted is unsurpassed in depicting important positions and postures. Dr. Skibsted not only grasped the concept and framing issues of the illustrations, he worked tirelessly to perfect the quality of this book. I am ever indebted. For the third edition, Mrs. Linda K. Evans saw to it that manuscripts for both Illustrated Orthopedic Physical Assessment, Third Edition, and Instant Access to Orthopedic Physical Assessment, Second Edition, were ready, accurate, and finished ahead of time. Her zeal to make these editions as successful as the previous ones is unparalleled. She made the task of revision more interesting and less heavy. I will seek her guidance for future works. For the third edition—and to quote, "It takes a village" —to produce the stunning new color images for the various tests and maneuvers. At the outset, Logan University/ College of Chiropractic president Dr. George Goodman, and Dr. Elizabeth Goodman, Ms. Ann Carter, Assistant to Drs. Goodman, and Ms. Kim Sullivan, Graduation & Event Planner at the Purser Center, are commended for their generosity in providing a magnificent location for the author, crew, editorial photographer, and models, in the production of the art. The Purser Center is unparalleled in its beauty and functionality. Certainly, the college administration and staff saw to every need for this project, ensuring its success. I am grateful to the ITC company for providing the set backdrop and carpet, without which, the art would be less charming. Mr. Jim Visser, primary still photographer, and Mr. Chuck Leroi, and his videographic assistants Matt Aiskenen, and Ryan Cannon, could not have worked harder to achieve any higher degree of excellence with the color photos and illustrations and video footage. They both pushed the models to exceed their known abilities, squeezing out every detail of movement or position. Their collective work embodies the constant search for perfection, serving as a guide for me to create prose equal to the illustrations. I look forward to working with both in future endeavors. The primary photographic models include Ms. Kim Alvis, Mr. Sean Brasfleld, Ms. Candyse Burns, Mr. Ryan Collart, Mr. Ochuko Ekpere, Ms. Angela Fain, Dr. LT Faison, Ms. Sheena Gordon, Mr. John Knott, Mr. Patrick Milford, Ms. Julie Mowczuo, Mr. Gary Taylor, and Ms. Annie Walters. Both Mr. Brasfield and Dr. Faison rose far above the call of duty in providing either specialized and critical equipment for the photos, or in helping recruit suitable models for the shoot. Each of the models demonstrated interminable patience in achieving just the right position or
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look of a test or procedure. I am grateful for their stamina and physical pliability. It is worthwhile noting that some of these able models subsequently entered successful practice as chiropractic physicians. Ms. Bailey Schechinger is a superb model for the clinical illustrations. She was tireless, well-poised, and eager to learn the meanings and usefulness of the procedures. Because of this, she helped make this book better. The Mosby/Elsevier staff for this edition included: Ms. Jennifer Watrous, Senior Developmental Editor, Health Professions 1 department of Editorial. I am pleased that Ms. Watrous elected to engage in the work on my new editions. She worked diligently on the second edition of Illustrated Orthopedic Physical Assessment, and it has been exciting to have her working on the third. Her attention to detail previously made the book into a definitive reference. That same perseverance with editing my writing this time pushes the book yet one notch higher. It is always a pleasure to work with people who truly want to see a project succeed. Ms. Watrous exemplifies this trait. Ms. April Falast, Editorial Assistant, Health Professions I department of Editorial. We could not have completed the work on time or in an organized fashion without Ms. Falast's creative work in making the photographic masters from the second edition. The enlarged illustrations were the perfect tool for both the stills and videos. I am sure this was hard work, but the resulting photo catalog is unsurpassed. I am also grateful for her attention to the needs of the models. Without Ms. Falast's leadership, I am certain the freezing models would simply have left the building, along with Elvis. Ms. Kelly Milford, Associate Developmental Editor, Health Professions 1 department of Editorial, is exceptional in her work. Her attention to detail and dedication to completion of the project kept the manuscripts, models, photographers, and the author moving forward. I am ever indebted to her patience in waiting for the final draft(s). Her professionalism is unsurpassed, especially tested in frequent e-mail and tele-conference contact from the beginning until the first bound copy. One could not
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ask for more of an editor. Her activities in compiling the manuscript schedules, arranging the photo shoot, arranging for the models and organizing the video and audio studios, as well as keeping everyone on the same page were invaluable. I could not have done any of the work without her at the "director's table." Ms. Andrea Campbell, Senior Project Manager, juggled communication with numerous staff constantly. She was the last stop before the "work" becomes a book. She is the sous chef for my manuscripts: I gave her the ingredients and she turned them into something everyone will like to look at and want to read. Ms. Campbell helped to sort out the art problems and keep track of what needed to be redrawn and what needed replacing (according to my seemingly interminable corrections). Quite a task. I am ever grateful for her skills. Ms. Kellie White, Senior Acquisitions Editor, Health Professions I department of Editorial. Worked with me from the earliest stages of Illustrated Essentials in Orthopedic Physical Assessment, through to Illustrated Orthopedic Physical Assessment, Second Edition, and Instant Access to Orthopedic Physical Assessment, and now for Illustrated Orthopedic Physical Assessment, Third Edition, and Instant Access to Orthopedic Physical Assessment, Second Edition. Ms. White continues to provide the necessary latitude and unwavering encouragement for the development of both books to evolve them into nationally recognized, definitive works. She embodies the attributes of a senior editor for which every author hopes. She and her excellent staff brought professionalism, interest, and dedication to the project. I have now written two editions under her guidance, with great result. The current revisions will surpass both our expectations, which I attribute to her skills at marshaling all the creative elements, models, photographers, and the author, to their best. Developing a book with her and for her is a joy. Elsevier is both astute and fortunate to have Ms. White in its Editorial leadership, and I am fortunate to enjoy her friendship and creative counsel. I will continue to strive to give her the best manuscripts. I look forward to future collaborations.
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Solving a patient's health problem can be a demanding exercise of orthopedic medical detection and logical deduction. Each health problem is a new diagnostic jigsaw puzzle for which the pieces must be found and fitted together in a carefully organized manner. Each examination or investigation should have a plan for including or excluding a specific member of a "short list" of suspected conditions. It is always the failure to have such an organized plan or approach that makes the diagnosis of orthopedic health problems so artificially difficult. Certainly, common or customary steps must be followed, but not blind routine or blunderbuss investigations.
Diagnosis purely by comparison with previous cases is reserved for the physician or orthopedic specialist who is very experienced and very accurately remembers the cases, but this combination is not the norm. The entry level physician or orthopedic specialist will come nearer to diagnostic accuracy by progressing logically through the medical investigation paradigm. Despite all this, however, the right approach will never be achieved until one misconception is laid to rest. This misconception is that the exact solution of an orthopedic problem does not matter very much and that such a solution will be of academic interest only, with no useful nonsurgical treatment. Such a view is nonsense. It is true that health science is frustrated in treating motor neuron disease; no cure exists for hereditary ataxia, and no reliable method exists to prevent relapses in disseminated sclerosis. Contrary to many beliefs, these diseases occupy only a small part of the orthopedist's time. Think for a moment of the transformation in the last 30 years in the treatment of cervical spine trauma, intervertebral disc prolapse, carpal tunnel syndrome, and deficiency neuropathies. Think of the influence of physiologic therapeutics in hypersensitivity states and in acute episodes of soft-tissue disease, of the continuing progress of manipulative therapy in certain facets of the migraine headache process, mechanical lower-back disorders, and in trigeminal neuralgia. Consider the advances of chiropractic orthopedics in treating various forms of benign spinal compression. Finally, the solution of an orthopedic problem takes time. A solution cannot be rushed, and the examiner must never allow the approach to be influenced by the exhortations of optimistic colleagues to "just glance at this case while passing" or to "just run over the musculoskeletal system, it won't take 5 minutes." It will, it always does, and so it should.
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1 Principles in Assessing Musculoskeletal Disorders, 1 2 Assessing Cardinal Musculoskeletal Symptoms and Signs, 48 3 Cervical Spine, 75 4 Shoulder, 205 5 Elbow, 324 6 Forearm, Wrist, and Hand, 375 7 Thoracic Spine, 467 8 Lumbar Spine, 535 9 Pelvis and Sacroiliac Joint, 699 10 Hip, 765 11 Knee, 843 12 Lower Leg, Ankle, and Foot, 929 13 Malingering, 1004 Glossary of Abbreviations, 1141 Appendix A, 1149 Appendix B, 1151 Answers to Critical Thinking Questions, 1153
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l)I�llllll'II)ll
AXIOMS IN ASSESSING MUSCULOSKELETAL DISORDERS
ORTHOPEDlC EVALUATlON PROCESS
Eliciting the patient's history is the quintessential skill in orthopedics. •
An examiner needs to learn about the patient's major
(,\\\l I t I
The orthopedic evaluation process has three phases:
pre enting symptoms, the chronology of the disorder.
I. History taking
and its impact on the patient's activities of daily living,
2. Examination
as well as ancillary information that include history
3. Diagnosis
and involvement of other systems. The orthopedic examination is the focal activity in assessing the patient's musculoskeletal complaint.
l)I�lIllll'II)I(
The orthopedic examination process is adapted to the specific needs of the patient's musculoskeletal system,
l,\\\l I I'
CLlNlCAL ASSESSMENTS
such as inspection, palpation, and observation.
In clinical practice, assessments occur all day, every day, including: I . Elucidating complaints
INTRODUCTION
2. Establishing impact of the complaints
Health care providers assess patients every day in clinical practice. Commonly, clinical practice is impossible wiLhoUl structured assessments and tests. Examination procedures appear to be straightforward: results are either positive or negative. However, all assessment and testing in clinical practice is based on the assumption of uncertainty: Does the patient have a disease? The probability of a particular disease can be established only by performing a test or a chain of test.s. The accuracy of a test for detecting a disease or a condi
3. Checking the complaint consistency with specific diagnoses 4. Performing a general physical examination 5. Performing special physical examinations 6. Performing laboratory and imaging tests 7. Interpreting test results
8. Formulating a diagnosis 9. Commencing lreaunent 10. Evaluating treatment efficacy
I I . Referring to a specialist, as needed
tion is determined by sensitivity and specificity. A high sensitivity (or a high specificity) does not uffice to make a test lIseful in clinical practice: a test should be as sensitive
dependent on how likely the existence of the disease is
as possible. The sensitivity and specificity of examination
before the procedure is actually conducted. This likelihood
procedures and tesLS can often be found in the literature.
is dependent on the prevalence of the disease.
Sensitivity and specificity are important characteristics of
The decision on whether to perform a new test depends
evidence-based physical assessment procedures but only in
on the resu lt of the previous test. Procedures with the lowest burden. risk. and costs for the patient are performed first,
the context of a specific disease or condition. The probability of a disease or condition after having
and those with the highest burden. risk. or costs are reserved
performed a test (Bayes theorem) is dependent on two
for specific patients in which the prior probability is highest.
things: (I) the specificity and sensitivity of the procedure
Examination procedures in the context of a low prior prob
(test characteristics) and (2) the probability of the disease or
ability of disease is rarely, if ever. informative. The yield of
condition before conducting the procedure. Interpretation of
diagnostic testing will increase the prior probability in the
Bayes' theorem is that the probability of having a disease is
range of approximately 50%. Very experienced clinicians
not only dependent on the lest or examination procedure
intuitively apply these rules and arrange rheir diagnostic
result and the characteristics of the procedure, but is also
process in such a way that the highest possible yield (a
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2
CHAPTER
I Principles in Assessing Musculoskeletal Disorders
llRIIIIlJ'1 \lIt t;AM1J I I l
BOX I-I
BAYES THEOREM
PRECIS IN ORTHOPEDIC DIAGNOSIS
Rules of Thumb rationale for use in clinical
I. HistOry
situations:
2. Examination
I. Highly sensilive and specific lest, will not perform very well in the clinical context if the
a
priori prob
3. Determination of disability lPILS): ,F:revcntable causes of disability Independent living
ability is very low,
2, No single diagnostic test exists that tums an a priori risk of disease of less than 10% into a probabil.ity that
hifeslyle SOCial support
makes a clinician sufficiently convinced to establish a diagnosis,
3, lhting is most valuable if the
a
priori probability of
the disease is somewhere in the range of 40% to 60%, 4, Diagnostic tests can turn such a probability into a sufficiently high posttest probability onto which to base further action.
From the moment of the first encounter with a pmient, the examiner is simultaneously observing and examining the movements and mannerisms of the patient. as well as listen ing to what is being said, The diagnostic process is complex; the examiner needs to establish the physical issues that are of greatest imponance to the patient (those most disrupting to the activities of daily living) and try to differentiate the anatomic and pathologic aspects of any disease or injury that
OIU 1101'1 \lIt t;AMlIl I 4
might be present.
PRECIS OF PHYSICAl EXAMINATION
The history provides much information about what dif ficulties the patient is experiencing and the impact of these
•
Sensitivity and speciticity do not exclusively make a
•
Test results that are considered
diagnostic test as appropriate for clinical use,
normal or abnormal
should always be interpreted in the context of the individual patient. The probability of having a disease is not totally dependent on the test result and the characteristics of the test. The probability of having a disease is also dependent on how prevalent the disease is before the test is actu ally conducted, Testing in the context of a low probability of disease is rarely. if ever, informative. •
Highly sophisticated and costly diagnostic techniques may fail
as easily as
simple, cheap,
diagnostic
maneuvers.
difficulties on the patient. Orthopedic examination is essen tial to define the structures involved; together. these pro cesses allow differentiation of orthopedic disorders into various diagnostic cat.egories (Box I-I).
HISTORY TAKING A carefully elicited history is a most crucial element in onhopedic assessment. An experienced examiner can form an idea of the extent and magnitude simply frol11 the patiem's history. I n the modern era of electronic patient medical record keeping, the examiner has new lools and melhods for not only capturing patient infomlation. but also tracking clinically significant changes. Health care providers arc increa�ingly under pressure to deliver efficient and high-quality care. Irnponant reasons for this pressure arc the ageing population. increasing demands and expectations by patients, rbing medical cOst.l.. and a decrea.l.c of full-time cmployed spccialists. Various innova
highly probable diagnosis) will be oblained at the lowest
tions in information technology have been proposed to
possible burden, risk, and costs for the patient. Less experi
enhance the efficiency and quality of health cart.!. Conse
enced clinicians may learn from experienced colleagues by
quences of these innovations are altered health care pro
recalling Bayes theorem and implemcming ils principles in
cesses. as well as a redefinition or responsibilities and a
everyday clinical practice.
change in workload for caregivers and patients involved in
Health care provider� cannot function adequately without
these processes. A health care innovation that is increasingly
physical examination procedures. In the real world, examin
applied in 1l1:;IIlY medical specialties is telcmedicine (TM).
ers accomplish ciinicul practice appropriately witholll a
TM can be defined as "the use of telecommunications tech
deJailed knowledge of the principles of tests, However, the
nology for medica,1 diagnostic. monitoring and therapeutic
benefits from physical testing can be easily increased by
purpoSC!\ when distance andlor time scparmcs the partici
recognizing that Lhese tests do nothing more than increase
pants" (Bcrgholll ct al. 2006).
the probability of a certain condition or diagnosis. Test results are never infallible.
A recent Institute of Medicine (10M) report charactcr
i/cd increased utilization of advances in health care informa-
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CHAPTER I Principles in Assessing Musculoskeletal Disorders
OIU Illll'lllll I;A�Il'1 1 (,
(lRI I I(l I'II) III,A�\lI11 ,
WORKlNG DIAGNOSIS
An integrated electronic patient record (EPR) is essen tial for the future of health care services. The EPR assists in the sharing of patient infomlation and helps promote efficiency. The most important resource for the development of the EPR is the patient. Computer systems can take appropriate directed medical histories from patients based on chief com plaint.
Essential steps in formulating a working diagnosis include: I. History taking
2. Observation 3. Palpation 4. Orthopedic testing 5. Clinical laboratory and imaging procedures
lion technology (IT) (e.g.. automation of clinical, financial. and administrallve transactions)
as
3
llR1 IIlll' Illlt l,\"l'l 17
essential 10 improving
quality and efficiency. preventing errors. and enhancing comumcr confidence in the health care sy�lem. Research shows that IT loo h •. such as computerized clinical decision suppon
OBSERVATION AND INSPECTION Observation and inspection of the patient occur anytime during the examination or history interview, especially when the patient is not aware of the observation. In this way, the examiner notes: I. Antalgia or deformities of poslure
2. Gait disturbances, especially if the patient needs assistance 3. Spinal synunelry, including prominences or eleva tions, flattening or depressions, scoliosis, or abnor malities of the anteroposterior curValure 4. Surface scars and wounds
physician usc and acceptance by st3ndardiLing medical prose or creating templates; acceptance is Mill suboptimal (Benamia. Elinson. Zarnke. 2(07). Bun and Hmg found that although 73Ck of physician offices u..,ecl computer.., for billing. only 17% lIsed them for
CHIEF COMPLAINT
mainw1l1ing medical records and 8ift. for ordering prescrip
Patients who have more than one complaint, such as those
tion.... The proponion of U.S. physicians who have adoptcd
with pain of spinal origin coupled with other body region
electronic health rccords is estimated to be between 20% and
symptoms or extremity problems. must be guided in ranking
25tH (Schleyer. Spallck. Hernandez, 2(07).
the complaints in priority. Although patients occasionally
The complaint history of a musculoskeletal condition
seek attention for stiffness or some other joint-related com
covers certain essential points. History of trauma helps dif
plaint, most patients with musculoskcletal conditions do so
ferentiate between acquired ligamentous (soft-tissue) insuf
for reasons related to pain, especially when it compromises
ficiency, inherent laxity, and past instability. Ii" trauma or
the activities of daily living.
overuse caused t.he problem, the examiner must determinc
The basic elements of examining the patient include
whether the patient stopped the injurious activity immedi
observation and inspection. palpmion. neurologic evalua
ately and self-treated the resulting condition.
tion. vilal signs, range-of-motion studies, clinical laboratory
Finding
lraumali/ed joints and adjacent Mructures neglected. decon
'lUdies. orthopedic tests, and diagnostic imaging.
ditioned. weakened. or atrophied caused by prolonged
Mo ...t examiner� perfonn routine cOll1prehcn�ivc cxal11l1la
periods of protection is common.
tiom, on patients with even minimal initial chief compl:lint�
An accurate description of the traumatic event. including
(Phelps. Rodriguez. 2005).
the exact position of the part at the moment of injury, is essential. The exact site of the pain is also important. Patients
OBSERVATION AND INSPECTION
often identify pain in one location. such as the hip, but
The first impressions-observations made while taking the
point somewhere else, such as the sacroiliac joint. The more
patient's history-are often the most revealing.
distal the pain is, the morc accurately patients detine its
Reasoning within the�c (pain-based dinical) categories
location.
appears LO be useful in helping providers and patients under-
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I
CHAPTER I Principles in Assessing Musculoskeletal Disorders
4
stand and account for c1inicaJ presenwuons of pain. Such
5 questions for an orUmpedic specialist. Once all five ques
reasoning influences planning of phy.!.ical assessments and
tions are answered, a differential diagnosis can usually be
lreatment (Smart. Doody, 2007).
established (Box 1-2).
A useful approach in the clinical examination of the neu
A rapid general screening examination suffices initially.
romusculoskeletal system is to seek answers to the Critical
Abnormal joints are subjected to a more focused regional orthopedic examination procedure. The examiner must detennine the presence of active or current inHammation. the presence of irreversible joint
ORl lllll'llll( (,A�HlI I X
damage from past. injury or inflammation, and existing
PAIN-BASED CLINICAL REASONiNG
mechanical defects. These findings are not mutually exclu sive. The distribution of joint involvement is important in
Five main categories of pain-based clinical
reaching a diagnosis. Certain patterns characterize specific
reasoning are: •
disorders. The number of involved joints may also be of
Biomedical (structural-functional source)
diagnostic significance.
Psychosocial (perception-interpretation of pain)
Learning what exacerbate!> or relieves the symptom
Pain mechanisms (underlying pathophysiologic
pattern is important. Equally important is how long the com
factors) •
plaints have existed (Table I-I) .
Chronicity (temporal aspects of pain)
Several other features may be of diagnostic importance.
Irritability or severity (degree of pain)
Some of these features produce skin signs or nodules. Exam ples include rheumatoid nodules (Fig. I-I), gouty tophi (Fig. 1-2), dermatomyositis (Fig. 1-3), and psoriatic arU"itis (Fig. 1-4).
(lRllltll'l niL (,AMlil I ')
DETERMINING EXTENT OF INJURY
BOX 1-2
Other characteristic features of diagnostic
CR.ITlCAL QJlESTIONS IN OR.THOPEDIC
importance in determining the extent of the disease
PHYSICAL EXAMINATION
or injury:
I. Are any joints abnormal'?
1. Is involvement symmetric or asymmetric?
2. What is the nature of the abnormality?
2. Are large or small joints affected? 3. Is the distribution of the condition peripheral or axial?
3. What is the extent of the involvement'? 4. Are Olher features of diagnostic importance present?
4. Does the condition affect upper versus lower limbs,
5. Do the answers to questions I tJlrough 4 provide sufficient
data?
or vice versa?
fAKlrl·t JOINT PATTERNS IN ORTHOPEDiC/RHEUMATIC DISORDERS
Diagnosis
Symmetry
Number or JOints lnvolved*
Rheumatoid arthritis
Symmetric
M ono-, oli g o-. polyarth rit is
Large/SmaU .Joints
Peripheral! Central Distribution
Upper! Lower Limb
Predilection
Large/sm all
Pe ripheral
Uppe rllow er
MCPs. PIP,. MTPs. DIPs
Ankylosing
Sacroiliac
Cenlral
spondylitis
joints. hip, sh ou lder
Psoriatic arthritis
Asymmetric
PO lyart hri tis
Large/sma ll
Peri pheral
Uppcrllower
DIPs, sacro i li ac
Reactive arthritis
A!iymmctric
01 igoarthri lis/Polyanhri lis
Large
P eriph eral
Lower
Sacroiliac
join ts join L'I. DIPs (toes)
Gou t
As ym me tri c
MonoarthritislOligoarthritis
Large/s ma ll
P eri ph era l
Lower m ore than upper
First MTP, Knee. Hip
DIPs. Distal interphalangeal joints: Mep.\'. mctacarpoph,lIangeal joints: MTP\. mClalarsophalangcills; PIPs. proxirmll interphalangeal joints.
*Monourthritis dellotes inflammation in a single joint. oligoarthritis Jenoles two to four joint1.. lind polyu � 1hrilis
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CHAPTER I Principles in Assessing Musculoskeletal Disorders
5
I
FIG. 1-3 Skin and nail fold lesions seen in dermatomyosi
lis. Patches (A) and periungual edema and nail fold (B). FIG. I-1 A, Rheumatoid nodules. B, Large nodules may
(From Klippel JH. Dicppc PA: Rhe"l/IlllOlog.\; vol 1-2. cd 2, London. 1998.
develop in the olecranon bursa as well as in the subcutane
Mo!.by.)
ous (issue.
(From Klippel JH. Dieppc PA: Rhelllll(l(% gy. 1'0//-2. ed 2.
London. 1998, Mosby.,
F IG. 1-4 Psorialic anhritis, with swelling of the distal inter
phalangeal joint and pitting in the adjacent fingernails.
(From
Klippel HI, Dicppc PA: R"elll/llifOlog.\� vol 1·2. cd 2. London. 1998. Mosby.)
PALPATION Palpation is the process of assessing the physical character F I G. 1-2 Gouty tophi represent deposits of urate crystals. (From Klippel JH. Dicppc PA: Nlli'1I/1I0to/OKI'. '0'011-2. cd 2. London. 1998.
istics of joints and contiguous structures by touching or feeling the palienes body. The purpose of palpation is to locate and substantiate areas of tenderness, swelling, and
Mo�by.)
abnormal muscle LOne. Palpmion allows the examiner to identify a localized increase or decrease in surface tempera
The answers to the Critical 5 questions usually provide
ture and the presence of induration and mass. Palpation is
sufficient information to establish a differential diagnosis.
classically performed with the fingerlips or Wilh the blum
They mu�l. Ir not, the examiner will need 10 retrace each
end of a cotton·lip applicator. However, instruments can be
examination step ullIil a logical and credible diagnosis can
used in percussion (gently tapping with a renex hammer).
be reached.
Wilh vibralion (using a C-128 lUning fork).
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CHAPTER I Principles in Assessing Musculoskeletal Disorders
() I� I I I () 1'1 I ) I ( (, \ \\ I I I III
SPINAL PALPATION Effective spinal palpation can be accomplished with the patient in the silling or kneeling variants of Adam's position: •
In palpating various structures, the examiner assesses the skin and subcutaneous tissue. Rolling of the skin (Kibler's test) can be perfonned. The examiner observes for surface temperature, hypesthesia, hyper hidrosis, and muscle splinting.
•
Tenderness of muscles and tendons and their attach ments is assessed, in both the anatomic resting posi tion and through various ranges of motion.
FIG. 1-5 From top to bottom, the Greenfield Babinski reflex hammer, Taylor reflex hammer, Buck's neurologic hammer, and Babinski reflex hammer.
Tendon sheaths and bursae are palpated for thickness, crepitus (especially silken versus snowball crepitus), and tenderness. The joints are palpated for all anatomic compo nents to include bones, capsule, ligaments, any specialized structures, swelling. a change of shape or defornlity, posi tional deficits, and tenderness. Palpation also aids in estab lishing the integrity of local circulation. Using a stethoscope or similar instrument improves crep itation grading by enhancing the auditory component in con junction with palpation and is especially useful with patients who display mild or moderate crepitation grade subclassifi cations.
NEUROLOGIC EVALUATION The neurologic evaluation involves locating the lesion; testing deep tendon, superficial, and pathologic reftexes (Fig. 1-5); testing cranial nerve and brainstem function; measuring body parts (mensuration); grading muscular strength;
and
testing
the
gross
sensory
modalities
(Fig. 1-6). Cerebral dysfunction is determined during the consulta lion by nOling the patient's mannerisms and orientation to time, space, and body pans (usually noted in the chan as oriented x3). Funher evaluations of lesions in the cerebrum require advanced imaging procedures and electroneurodiag nos tie testing. Cerebellar
lesions
are
characterized
by
repeated
cogwheel-type muscle actions while the patient's eyes arc open. The posterior columns of the spinal cord are the source
FiG. 1-6 Single-tipped cotton applicators are both eco nomical and versatile and can be used in the following set tings: in emergency rooms, examining rooms, outpatient clinics, and laboratories and on dressing cans. Sterile tongue depressors are usually made from white Birchwood that is '/..-inch thick. These tongue depressors are evenly cut and highly polished for smooth and clean edges, ends, and sur faces.
of the dy function when repeated muscle actions are smooth
sign in the second edition of his Lehrbuch der Nen1en·
and occur while the patient's eyes arc open. However, these
kmnkheiten des Metlsc/len (1851). After discussing a reduc
same muscular actions cannot be repeated as smoothly with
tion of the motor power in the lower extremities. Romberg
the eyes closed. Brainstem dysfunction is discerned through
stales, ··The individual keeps his eyes on his feet to prevent
testing of the cranial nerves. The type and quality of paraly
his movements from becoming still morc unsteady. If he is
sis, reflexes, muscle lone, clonus. atrophy, fasciculation, and
ordered to close his eyes while in the erect posture. he at
reaclions of degeneration can differentiate spinal cord lesions
once commences to tolter. The insecurity of his gait also
from lower motor neuron disorders.
exhibits itself more in the dark·' (Romberg. 1853). Romberg
Moritz Heinrich Romberg (1795-1873), the founder of
thought lhe sign was pathognomonic of tabes dorsalis (Cole.
clinical neurology in Germany. described his now famous
Michael. Roben, 2(03).
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7
CHAPTER I Principles in Assessing Musculoskeletal Disorders
(}1�111(} 1 'lll l ( (,\\11 I I I I
(liZ I II(1 1' I Il l( (, \ \\ I I I I 1
DEEP-TENDON REFLEXES
CRANIAL NERVES AND BASIC FUNCTION
I . Scapulohumeml C5-C6 2. Biceps C5-C6
I:
Smell
3. Radial C5-C6
II:
Vision
4. Triceps C7-C8
IJI :
Light accommodation
5. Wrist C7-C8
I I I, IV, V I :
Eye movement
6. Ulnar C8-T I
v:
Sensation (wink)
7. Patellar L2-L4
VII:
Facial muscle (taste)
8. Hamstring L4-S I
VIII:
Auditory (balance)
9. Achilles 51-52
IX:
Taste (gag)
x:
Voice (swallow)
XI:
Shoulder (shrug)
XII:
Tongue (motor)
tlIZIII(lI'l l l l ( (,\\111 1 1'
SU PERFICIAL REFLEXES J . Corneal IJ I, V
lll� I I Illl'l 111(
2. Upper abdominal 17-T9
(,\ \I I I I I,
COMMONLY ACCEPTED DEEP-TENDON REFLEX GRADING SCHEME
3. Lower abdominal T I (}..T 12 4. Cremasteric 5. Gluteal 6. Plantar
0 = Absent
7. T l 2-L2
I
8. L4-LS
2 = Average
9. S I -S2
2+
=
=
Diminished or hyporeactive Slightly exaggerated (hyperreactive)
3 = Exaggerated (hyperreactive) 4
=
Associated with myoclonus
tl l Zllltl l'lllIl (,\\11 I I 1\
PATHOLOGIC REFLEXES
comraction in the opposite upper or lower extremities (Jendrassik maneuver).
J. Hoffmann
lendrassik faci litation is different between age groups
2. Babinski
and weight bearing versus non-weight bearing. Young
3. Chaddock
patients often demonstrate a significant lendrassik facilita·
4. Oppenheim
tion effect in the standing position, whereas. very often, no
5. Bechterew-Mendel
difference is seen in the elderly patients.
6. Rossohmo
Mensuration of body parts is used to determine atrophy
7. Gordon
and functional and anatomic abnormalities (Fig. J.7).
8. Schaeffer
Grip strength testing examines the functjon of the ulnar nerve and can help differentiate myoneural dysfunction from malingering activity ( Fig. \·8). The examiner can use
Deep·tendon renexes help the examiner locate the lower
three methods of grip strength evaluation (one trial, the
motor neuron lesion and differentiate it from an upper motor
mean of three trials. and the best of three trials) when using
neuron lesion.
the Jamar dynamometer. Two different sLHtic grip tests are
Superficial renexes differentiate lower motor neuron lesions from upper motor neuron lesions.
the five-rung test and the maximal static grip test. Thc five-rung tc�t involve� perrorming one repetition (trial)
Pathologic renexes determine the presence of upper molor neuron lesions.
with the handle or the Jamar dynamometer on each of the rive handle sCllings. whereas the ma"imal static grip tc�t
Cranial nerve function is dClcmlined by testing brainslcm activity.
involves performing three repetitions with the handle on either lhe second or third sCILing (Fess. 1992: Joughin el 31.
On occasion, eliciting a particular renex is difficult; dis·
1993).
lrJclion techniques are helpful in such situations. If Jcss
The main difference between the static grip test and the
than-nannal reactivity is encountered in the upper or lower
rapid exchange grip ( REG) maneuver is the duration of the
extremities, the patient is directed to perfonn an isometric
muscular contraction during gripping.
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8
CHAPTER I Principles in Assessing Musculoskeletal Disorders
FIG. I-750ft linen tape is marked in inches on one side
and centimeters on Ihe other. The fast-read ing clinical ther mometer.
FIG. 1-8 Manin Vigorimetcr aneroid dynamomeler (left)
and Jamar hand grasp mechanical five-position dynamom eter (right). lll: I l Illl'l l ll(
(, \\\1, I I 1(,
COMMON AREAS OF MENSURATION I. Excursion
of
the
chesl
during
inspiralion
tll:!IILlI'1I11( (,\\\1'1117 and
expiration 2. Upper-extremity circumference (brachium and ante
brachium); measured in the noncontracled and con tracted state 3. Lower-extremity circumferences ( thigh and calf); measured in the noncontracted and contracted states 4. Leg length (measured standing versus supine or prone); differentiates a functional shan leg from an anatomic shan leg
CERVICAL SPINE EXTRINSIC MUSCULATURE WITH SPECIFIC NERVE ROOTS NOTED I. Deltoid (CS)
2. Biceps (C6) 3. Wrist extensors (C6) 4. Triceps (C7) 5. Wrist flexors (C7)
6. Finger extensors (C7) 7. Finger flexors (C8) 8. Finger abductors (T1)
During lhe stalic grip lcst, the duration of muscular contrac tion of each hand grip is 3 10 5 seconds. whereas during Lhe REG maneuver. lhe hands alternate rapidly. resulting in a
LlI:!IILlI'1 \ll( (,\\\tI1 11K
�hortcr duration of each grip (Ics� than 1 .5 sccond� per grip)
2000). A positil'e REG
(Taylor c( al.
test i!
arc greater than static grip scores. which indicates a l'!oub· maximal or a feigned effort. A lIeglll;\'e REG test is obtained when slatic grip scores arc greater than REG scores. indical
THORACOLUMBAR EXTRINSIC MUSCULATURE AND SPECIFIC ASSOCIATED NERVE ROOT LEVElS
ing a maximal or a sincere eITon (Shechlman. Taylor.
I. Hip flexors (L2-L3)
2002).
2. Knee extensors (L3-L4)
Cervical intrinsic muscle lesling relates to the cervical spine functions of flexion, extension, lateral flexion, and
3. Ankle extensors (L4--LS) 4. Hip extensors (L4--LS) 5. Knee nexors (L5-5 I)
rotation. Thoracolumbar imrinsic muscle function is associated
6. Ankle flexors ( 5I-52)
with trunk flexion. extension. lateral flexion. and rotation.
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CHAPTER I Principles in Assessing Musculoskeletal Disorders
9
FIG. 1-9 From top to bottom, the Wanenberg pinwheel:
Boley two-point discrimination gauge: von Frey ancsthe ,imctcr: Buck camel hair brush. pin. and neurologic hammer:
FIG. J-IO Aluminum alloy tuning forks. available in C-64.
and
C- 1 28. C-256. C-5 1 2. C- 1 024. C-2048. and C-4096 vibra
u
Serol China marker.
tions. The lower-frequency luning forks are the usual choices for bone vibration conduction studies. Testing of the gross sensory modalities allows for evalu ation of the derl1latomcs involved in superficial and deep sensations and proprioception (Fig. 1 -9). The superficial scnsation� include light touch. pain. and temperature. Light touch is mediated by the dorsal columns
C6
C4
C4
and easily examined with a colton ball. Pilin receptors are mediated by the lateral spinothalamic tracts and are tested by a pinprick and hot and cold temperatures. Temperature. or thermal scnsalian. mediated by the dorsal columns is tested with warm ( not hot) and cool (not cold) tempera tures. The deep sensat ions arc vibration and deep pressure per ception. The do"al columns of the spinal cord (Fig. 1 - 1 0) mediate vibration. tested with a C-128 or lower-rrequency luning rork. Deep pressure is ICMcd by squeezing any mus cular part of the body and is mediated in the dorsal columns. Proprioception. or joint po\ition �en\e. i� mediated by the dorsal columns and can be tc;ted by having the patient point to a particular part of the body while keeping the eyes closed.
PAIN AND PATTERNS OF PAIN Pain thal arises with activity and decreases with rest is l i kely
C7
to ha\'c mechan ical causc�. The pain may be position depcn
DERMATOMES
MYOTOMES
SCLEROTOMES
dent; most case\ of mechanical spinal pain have both a
F I G. 1-1 1 Primary pallern� of pain originating in the �pioe:
provocative and palli:.ni\'e arc of l11otioo.
derma tomes. myotol11e�. and sclerotomes. Demonstrated for
Spinal pain is the most difficult to differentially diagnose.
lhe right upper extremity. (From Saidofl' DC. McDonough A: Cr;lj·
The three primary patterns are dermatogenous. myogenous.
all 1H.lIl/l\'(/n ill therapf'lIlic in/(·n'f''''i(JI/.�, IIpper f'\lI"('milies, 51 Louis.
and sclcratogenous (Fig. I - I I).
1997. Moshy,)
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10
CHAPTER I Principles i n Assessing Musculoskeletal Disorders A dermatome is the area of sensation atlributed to a par
VITAL SIGNS
ticular nerve root level. Dermatomal pain is often described as sharp. stabbing, and well demarcated. It may result from
Vital signs include the brachial blood pressure, peripheral
herniated discs, stretch injuries, or tumors.
pulse rate, respiration rate, height. weight, and vital capac
Pain referral within muscular or fascial tissue is myoge nous pnin. Areas known as (rigger poiflls refer pain 10 distant
stethoscopes, spirometers, scales, tape measures. and blood
sites. Trigger points are evident in patients with myofascial
pressure cuffs (Fig. 1 - 1 4).
ity. The instrumentation for these measurements includes
pain syndromes. Specific sites of tenderness that do not result from referred pain are termed tellder poillfs. Tender points develop in patients wilh varied sort-tissue, rheumatic.
R ANGE OF MOTION
and collagen-vascular disorders, such as systemic lupus ery
Of a l l the orthopedic tests that an examiner can perform on
thematosus and fibromyalgia.
a patient, none is more crucial than range-of-motion (ROM)
Pain referred from somatic structures such as cartil age.
testing of the affected articulation. Range of motion testing
l igament, joint capsule, or bone often does not follow der
often reveals the origin of the patient's discomfort. because
matome patterns, as does nerve root pain. This pain is known
movement may reproduce the pain. The patient is examined
as sclera/agel/otis pain. Patients may describe this type of
symmetrically for aClive ROM of all the joints that may be
pain as dull, achy, diffuse, and difficult to pinpoint. Sclera logenous pain is one of the morc common spinal pain
involved in the dysfunction or injury (Fig. 1 - 1 5). The exam
patterns.
iner then takes the patient through passi,'e ROM, evaluating the e/ldleel (i.e., spri nginess) of the affected joint.
Local Versus Referred Pain
be tested for ROM. ROM is assessed bilaterally by compar
Any movable joint in the body, including the spine. can
Patients with referred pain often point to large generalized
ing findings with a given set of normal values. Normal
areas. whereas patients with localized lesions can be more
values can vary dramatically, depending on the reference
specific. A patient complaining of unrelenting spinal pain.
source used, An examiner must exercise careful professional
demonstrating ful l , pain-free range of motion presents a
judgment to ensure objectivity. Any ROM that is less than
problem. The patient likely has either viscerosomatic pain,
normal may indicale or be the result of muscle spasm, sprain.
which mandates further diagnostic te ting, or pain resulting
strain. joint subluxation, general anhrilic degeneration. post
from a psychosocial cause. If referred pain from a diseased
surgical condition. or obesity.
organ system is mimicking a local orthopedic problem, the examiner should not hesitate to order appropriate tests.
Recenll),. Childs and colleagues found in a clinical trial that spinal stiffness was one of five
Every effort should be made to objectify the patient's
predictors of which patients
wilh low back pain would respond favorably to a particular
report of pain and discomfort. Measurement instruments
physical lherapy manipulation. In their slUdy. they used a
such as the visual analog scale (Fig. 1 - 12) are reliable and
manual assessment to grade the relative stiffness of the L4�
valid for examining a patient's pain. The McGill Short
L5 and L5-S I joints. A palpable difference in the �tiffncs�
Form Questionnaire (Fig. 1 - 13) is helpful for pain mea
at these joints helped predict which patients were more
surement in a clinical setting.
likely
to respond favorably to manipulative therapy. Manual
Pain is associated with a very high disability rate, sig
palpation methods have been notoriousl), difficult to quan
nificantly affecting the three domains evaluated by the Sheehan Disability Scale, which assesses patient functional
liry and suffer from a lack of objectivity. Interexaminer
impairment in three domains: work impairment. social impairment. and impainnent of family l i fe or home respon sibilities. Two further items gather data on patient-perceived stress and social support.
OINT END-FEEL CATEGORIES In passive joint motion assessment, the end-feel is important. The accepted end-feel categories are: Bone-to-bone: an abrupt halt to movement when two hard surfaces meet
-
Capsular end-feel: a lealhery resistance to movement
On Ihe hoe below.
with a slight amount of give at the very end of the
place a mark mdlcalmg your pam le\el
range Springy block: a usually pathologic end-feel, gener ally representing an intraarticular displacement Tissue approximation: no further joint movement
10
o
F IG. 1 - 12 Visual analog scale for objective pain measure ment.
(From Mulone TR. McPoil TG. Nit7. AJ: Orthopedic mill sports
available •
Empty feel : usually pathologic
p/n·Jical ,lteropy. cd 3. SI Loub. 1 997. Mo:.b).)
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1 1__
CHAPTER I Principles in Assessing Musculoskeletal D isorders
Check only one item for each category to describe your pain today.
4
3
2 1 Flickering
1 Jumping
2 Quivering
1 Pricking
2 Flashing
t Sharp
2 Boring
2 Cutting
3 Pulsing
3 Shooting
3 Drilling
3 Lacerating
4 Throbbing
4 Stabbing
5 Beating
5 Lancinating
6 Pounding 5
6
7
8
1 Pinching
1 Tugging
1 Hot
1 Tingling
2 Pressing
2 Pulling
2 Burning
2 Itchy
3 Gnawing
3 Wrenching
4 Cramping
3 Scalding
3 Smarting
4 Saaring
4 Stinging
5 Crushing 9
10
11
12
1 Dull
1 Tender
1 Tiring
1 Sickening
2 Sore
2 Taut
2 Exhausting
2 Suffocating
3 Hurting
3 Rasping
4 Aching
4 Splitting
5 Heavy 13
14
15
16
1 Feartul
1 Punishing
1 Wretched
1 Annoying
2 Frightlul
2 Grueling
2 Blinding
2 Troublesome
3 Terrifying
3 Cruel
3 Miserable
4 Vicious
4 Intense
5 Killing
5 Unbearable
18
17
19
20
1 Spreading
1 Tight
1 Cool
1 Nagging
2 Radiating
2 Numb
2 Cold
2 Nauseating
3 Penetrating
3 Drawing
3 Freezing
3 Agonizing
4 Piercing
4 Squeezing
4 Dreadful
5 Tearing
5 Torturing
F I G . 1 - 1 3 McGill Short Form Pain QuesLionnaire.
(From Malone TR. McPoil TG . Nitl AJ: Ortho·
pe(Jic (Il1d sports phYJiC(l/ ther(/I)): ed 3. S( Louis, 1 997. Mosby: rrom Mel7.acker R: The McGill Pain Quc�tion· naire: major propenics and scoring methods. Pain 1:277. 1975.)
reliability or chiropractic palpation of segmental fixation is
joint and periarticular structures through their respective
typically poor to 5!light. Inlracxaminer reliability iii usually
arcs and end-range motions. Stability lesting involves stress
rated :,omcwhat beuer. in the moderate to !o.ubMantial range.
ing ligamentous tissues and joint capsules (Fig. 1 - 1 6).
depending on the experience of the exami ner. Similarly. Miffness mcasures commonly used by physical therapi5!ts show liulc interex3miner agreement. Childs and colleagues
MUSCULAR ASSESSMENT
were able to achicve acceptable reliability in the lumbar
Movement resLrictions in a joint's passive ROM are nOI
mobility tClit they used by reducing the assc:,sment to three
exclusively articular. Muscular hypertonicity limits passive
level>: ( I ) hypomobilc. (Owen, C(
(2)
normal. and (3) hypcrmobilc
.1. 2(07).
movement and often occurs in association with articular lesions Uoint dysfunction). Chronic joint problems are also commonly associated with myofascilis.
STABILITY TESTING Because clinical examination reveals the degree of ligamen
CLINICAL L ABORATORY
tous or joint sprain, the examiner must be able to Lest accu
For the examiner concemed with musculoskeletal disorders.
rately for joint instability (Table 1 -2). Stability testing moves
differential diagnosb becomes a chal lenge. Complete blood
Copyrighted Material
I
12
CHAPTER I Principles i n Assessing Musculoskeletal Disorders
F I G . 1 - 1 5 From top to bottom, stainless steel goniometer
measures movement or joints rrom 0 to 180 degrees. Bubble inclinometers measure the angular motion from 0 to 360 degrees. Finger or small joint goniometer measures the movement or interphalangeal joints or fingers and toes. Plastic radiographic goniometer provides standard orthope F IG . 1 - 1 4 Wall-mounted sphygmomanometer and stetho
dic measurements of joint mOl ion and neutral position.
scope (Ie[t). Portable blood pressure curr (top right). Most significant heart sounds occur in the frequency range of 200 to 500 Hz. bUl human auditory sensitivity is l i m i ted to those
,ounds below 1000 Hz. Stethoscopes ampliry the lower rre quencies (bollo/ll right).
lAB l 1 1-2 I N J U RED LIGAMENT REst DUAL FUNCTtON
Extent of Failure
Sprain
Mi nimal
Finol degree
Damage·
Joint Motion, Subluxation
Residual Strength
Residual Functional Length
Residual functional Capacity
Less thun onc lhird of
None
RClaincd or
Nonnal
Retained
Increased. still within
Marked
fibers failed:
slightly
includes Illost
decreased
sprains with few to
some fibers failed. Microlcars also exist.
Partial
Second degree
One-third to two-
In geneml. minimal
Marked
lhirds ligament
or no increased
decrease.
functiomll range
damage; significant
motion.
At risk for
but may later act
requires
damage. but pans
Remaining fibers
complete
as
healing to
of the ligament are
in ligament re�ist
failure
sti l l functional .
openi ng.
Microtcars may exist.
Complete
Third degree
More than two-thirds
Depcnw. on
!>CCondary
continuity remains
re\lrainlS
Conti nui ty lost and gross separation
rather than subtle
regai n
control of joint
function
motions
to complete failure: In pan.
a check rein
compromise:
Little to none
Lost
None
Lost
Depcnd� on
Severely
compromised or lost
Lost
.!.econdary restrai nts
between fibers ·E�limate of damnge i� often difficult: however. the different I) pc.. li"led can u,uall) be diffcrentiated. NOle: Antcrior IInci po..tcrior crucimc IC:lr.. commonly c:tiSI with liule 10 no
.Ihnonnlll
laxilY. Thc c:taminalion for medial and Imeral 1igamentou<; injury is u..ually more :lecumte.
From Fcagin JA. edilor: Th(' ("rllcia/ ligaftlenl.\. New York. 1988. Chun:hill Li"ing�tonc.
Copyrighted Material
CHAPTER I Principles in Assessing Musculoskeletal Disorders
13
FIG. 1-16 Lachman (eM of the anterior crucialc l igament. (From Scuderi GR. McCann PD. Bruno PJ: SWJrI\'
medicine: (Jrind/,Ies ofprimary C(l�.
51 Louis. 1 997. Mosby.)
Ll I�I II LlI' I I) I ( (, \\\l I I _'tl
LA BORATORY RESULTS INTERPRETATIONS
RESISTED MUSCLE MOVEMENT In assessing muscle tissue, resisted movements are the most revealing. Standard interpretations of
For laboratory testing in orthopedic evaluations,
resisted muscle tesling movements include:
results interpretation errors usually Involve one or
Painful and strong is equated with a m i nor lesion of
four areas:
muscle or tendon.
False-positive results
Painful and weak equates with a major lesion of the
False-negative results Measurcmcnt error
muscle or tendon. Painless and weak equates with neurologic injury or
•
Differences in groups of patients compared with indi vidual patients
complete rupture of the muscular auachment. Painless and strong is normaL
and urine tests can help determine a diagnosis. Diseases of the heart. liver. kidney. pancreas. and prostate can mimic back pain of spinal origin. Mo" laboratory te;ting has l imited utility for orthopedic diagnosis (Table
INDIVIDUAL BLOOD AND URINE TESTS Acid Phosphates
1 -3)_ As an example, in rheumatoid
Dietary deficiencies in phosphorus arc rare but may be seen
arthritis, the diagnosis is often established from the history
with alcoholism and malnutrition_ Low levels of phosphorus
and physical examination; for systemic lupus erythemato
(hypophosphatemia) may also be caused by or associated
sus, from the laboratory test antinuclear antibody (ANA);
with:
for gout, from a synovial nuid examination; and for anky�
Hypercalcemia (high levels of calcium), especially as
losing spondylitis, from a radiograph. In common disorders
a result of hyperparathyroidism
such as osteoarthritis. fibromyalgia, or muscular strains and
Overuse of diuretics (drugs that encourage urination)
sprains. essentially no diagnostic role exists for laboratory
Severe burns
tests except to exclude other diagnostic possibilities.
Diabctic ketoacidosis ( after treatment)
The simplest orthopedic screen includes rheumatoid
Hypothyroidism
arthritis factor. ANA, and uric acid, although more elaborate
Hypokalemia (low levels of potassium)
screens arc available, which may include erythrocyte sedi
Chronic antacid use
mentation rate. C-reactive protein. antislreptolysin-O liter.
Rickets and osteomalacia (caused by vitamin-D defi
protein clectrophore�is. quantitative immunoglobulins. and
ciencies)
ANA subsets such as anti-Ro and anti-LA. anti-Sm. and anticentromcre antibodics.
Higher-than-nom,,1 levels of phosphorus (hyperphos phatemia) may be caused by or associated with:
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14
CHAPTER I Principles in Assessing Musculoskeletal Disorders
TAIlI
F Ll
LABORATORY STUDIES USEFUL I N DIAGNOSING
low BACK SYNDROMES
Test
Measurement
Low Back Implication
Complete blood count
A measure of volume of circulating red
May be diminished in systemic diseases (e.g.. neoplasm)
blood cells
Hematocrit hemoglobin White blood count and differential
and in chronic spinal infections. Total white blood cell and shifts in differential Illay be
Amount and type of circulating white blood cells
prescnt in spinal infections or occasionally in spondyJoarthropalhics.
Sedimentation rate
NonspecifiC test of inHammation
Increased in spinal infections. may be increased in
Chemistry
A measure of circulating calcium and
Calcium is elevated in hyperp.trathyroidism, may be
neoplasms and spondylo3nhropalhies. elevated with primary and secondary osseous tumors.
phosphorus
Calcium
alterations in the distribution of calcium and phosphorus
Phosphoru�
accompany many metabolic disorder!\: but arc norma.l in osteoporosis. Enzyme associated with bone rannalian;
Alkaline pho�phi1tase
May be elevated in primary or secondary osseous neoplasllls.
therefore: elevation implies increased bone formalion.
Increased in prostatic tumors.
An enzyme associated with tumors
Acid phosphatase
metastatic to bonc Serum proteins (albumin globulin protein electrophoresis) protcin HLA·B27 antigen
Measurement of amount and type
Elevations of one fraction of globulin are associated with
circulating
multiple myeloma. Usually individuals with spondyloarthropaLhies arc HLA·
A circulating antigen
827 positive. NOle 6·8% of men have this antigen and therefore its presence is not confinnaLory of a spondyloarthropathy. fiLA. Human leukocyte antigen. Adaptcd from Pope ML: OCl"II{J(J/;OIUll low back paill. asseSSIllt'/It, IY'I!(I/f1U.'f/I (lnd prcl'elll{(}I/. SI Louis. 1991, Mosby.
•
Kidney failure
Then the amylase values will return to normal in a few days.
Hypoparathyroidism (underactive parathyroid gland)
In chronic pancreatitis, amylase levels will initially be mod
Diabetic ketoacidosis (when first seen)
erately elevated bul often decrease over time with progres
Phosphate supplementation
sive pancreas damage. Amylase levels may also be significantly increased in
Alkaline Phosphatase
patients with pancreatic duct obstruction. cancer of the pan
Increased serum alkaline phosphatase is seen in states of
creas, and gallbladder allacks. Urine and blood amylase
increased osteoblaSlic activity (hyperparathyroidism, osteo
levels may also be elevated wilh a variety of other condi
malacia. primary and mctastatic neoplasms), hepatobiliary
tions, such as ovarian cancer, lung cancer, tubal pregnancy,
diseases charaClCriL.ed by some degree of inlra- or extrahe
mumps, intestinal obstruction, or perforated ulcer, but
patic cholestasis. and in sepsis. chronic inHammatory bowel
amylase tests are not generally used to diagnose or Illonilor
disease, and thyrotoxicosis. Isoenzyme determination may
these disorders. Decreased blood and urine amylase levels
help detennine the organ or tissue responsible for an alkaline
may indicate permanent damage to the amylase-producing
phosphatase elevation.
cells in the pancreas. Increased blood amylase levels with
Decreased serum alkaline phosphatase may not be clini
normal to low urine amylase levels may indicate decreased
cally significant. However, decreased serum levels have
kidney function or the presence of a macroamylase. a benign
been observed in hypothyroidism. scurvy. kwashiorkor.
complex of amylase and other proteins that accumulates in
achondroplastic dwarfism, deposition of radioactive materi
the blood.
als in bone, and in the rare genetic condition hypophospha
Given that reference values for amylase vary from labo ratory to laboratory, depending on the test method used, no
tasia.
universally accepted numberexisls that can be called nornlal
A mylase
or high.
In acute pancreatitis, amylase in the blood increases (often to four to six times higher than the highest reference value,
limit of normal). The
Anti-Nuclear A ntibody
increase
Anti-nuclear antibody (ANA) tests are performed using dif
occurs within 12 hours of injury to the pancreas and gener
ferent assays (indirect immunoHuorescence microscopy or
ally remains elevated until the cause is successfully treated.
by enzyme linked immunoabsorbent assay). and results are
sometimes called the upper
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CHAPTER I Principles in Assessing Musculoskeletal Disorders
15
reported as a liler with a particular type o f immunofluores
the diffuse form is associated with autoantibodies to the
cence pattern (when positive). Low-level titers are consid
anti-ScI-70.
ered negative, whereas increased lilers, such as I : 320, are
A positive result on the ANA may also show up in
positive and indicate an elevated concentration of ANAs. ANA shows up on indirect immunofluorescence as fluo
patients with Raynaud disease. rheumatoid arthritis. der matomyosilis, mixed connective tissue disease. and other
rescent patterns in cells that arc fixed to a slide that is
autoimmune conditions.
evaluated under a microscope. Different patterns are associ
Because symptoms may come and go. months or years
ated with a variety of autoimmune disorders. Some of the
may be required to show a pattent that might suggest SLE
morc common patlems include:
or any of the other autoimmune diseases.
Homogenous (diffuse)-associated with systemic lupus erythematosus
(SLE)
and
mixed
connective
tissue
disease
necessary: however. because of the episodic nature of auto
Speckled-associated
with
sclerodemta. polymyositis.
SLE.
Sjogren syndrome.
rheumatoid arthritis. and
mixed connective tissue disease Nucleolar-associated
with
scleroderma
immune diseases. repeating the ANA test at a future date may be worthwhile. Aside from rare cases. further autoantibody (subset)
and
poly
myositis
testing is not necessary if a patient has a negative ANA result.
Outline pattern (peripheraJ)-associated with SLE An example of a positive resul t might be positive a/
J : 320 ,Ii/wioll
A negative ANA result makes SLE an unlikely diagnosis. Immediately repeating a negative ANA test is not usually
Antislrepto(ysin-O Titer Antistreptolysin-O ( A SO) titer test results can be reported
",i,h a homoge"ous pallem.
A positive ANA test result may suggest an autoimmune
in several different ways: however. the interpretation is gen
disease, but further specific testing is required to assist in
erally the same: The higher the result is. the more antibody
making a final diagnosis. ANA test results can be positive
that is present in the blood (unless a titer is perfonned. which
in people without any known autoimmune disease. Although
is a ratio and therefore is interpreted differently).
this finding is not common. the frequency of a false positive ANA result increases as people get older.
The ASO antibody is either absent or present in very low concentrations in patients who have not had a recent
Approximately 95% of patients with SLE have a positive
streptococcal (strep) infection. Antibodies are produced
ANA test result. If a patient also has symptoms of SLE. such
approximately a week to a month after the initial slrep infec
as anhritis. a rash. and autoimmune thrombocytopenia. then
tion. ASO levels peak at approximately 4 to 6 weeks after
the patient probably has SLE. In cases such as these. a
the illness and then taper off but may remain at detectible
positive ANA result can be useful to support the SLE diag
levels for several months after the strep infection has
nosis. Two subset tests for specific types of autoantibodies.
resolved.
such as anti-dsDNA and anti-Sm. may be ordered to help confimt that the condition is SLE.
If the test is negative. or if ASO is present in very low concentrations. then the patient 1110St likely has not had a
A positive ANA can also mean that the patient has drug induced lUpus. This condition is associated with the devel
recent strep infection. especially if a sample taken 1 0 to 1 4 days later is also negative or minimal.
opment of aUloanlibodies to histones, which are water-soluble
If the ASO level is high or is rising. then a recent strep
proteins rich in the amino acids lysine and arginine. An anti·
infection has likely occurred. ASO levels that are initially
histone test may be ordered to support the diagnosis of
high and then decline suggest that an infection has occurred
drug-induced lupus.
and may be resolving.
Other conditions in which a positive ANA test result may be seen include:
The ASO test does not predict whether complications will occur after a strep infection, nor do they predict the
Sjogren syndrome: Between 40% and 70% of patients
severity of the disease. If symptoms of rheumatic fever or
with this condition have a positive ANA test result.
glomerulonephritis are present, an elevated ASO level may
Even though this finding supports the diagnosis, a
be used to confirm the diagnosis.
negative result does not rule it out. The examiner may want to test for two subsets of ANA: anti-SS-A (Ro) and
Bence-Jones Protein
anti-SS-B (La). The frequency of autoantibodies to
A Bence-Jones protein is a monoclonal globulin protein
SSA in patients with SjOgren syndrome can be 90% or
found in the blood or urine. The isolated finding of a Bence
greater.
Jones protein is known as monoclonal gammopathy of
Scleroderma: Approximately 60% to 90% of patients
uncertain significance. Finding this protein in the context of
with scleroderma have a positive ANA finding. In patients
end-organ manifestations such as renal failure, lytic bone
who may have this condition. ANA subset tests can help
disease. or anemia. or large numbers of plasma cells in the
distinguish two forms of the disease. l imited versus
bone marrow of patients can be diagnostic of multiple
diffuse. The diffuse form is more severe. Limited disease
myeloma.
is most closely associaled with the anticentromere patlem
The proteins are antibody immunoglobulin-free light
of ANA staining (and the anticentromere test), whereas
chains (paraproteins) and are produced by neoplastic plasma
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16
C HAPTER I Principles i n Assessing M usculoskelelal Disorders
cells. The lighl chains can be delecled by healing or eleclro
Calcium
phoresis of concentrated urine. Light chains precipitate
A nonnal calcium result with other nom13l laboratory results
when heated 10 50· 10 60· C and re-dissolve aI 90· 10 100·
means lhal Ihe patient has no problems with calcium melab·
C. These tests arc essential in patients who may bave Bence
olism (use by the body).
Jones proteins in their urine because these proteins do not
Because approximately one half of the calcium in Ihe
react with the reagents normally used in urinalysis dipsticks.
blood is bound by albumin (a prolein). Ihese IwO lesls are
This circumstance lead� to false-negative results in people
usually ordered logelher. Calcium values musl be inlerpreled
with Bence-Jones proteins in their urine undergoing stan
in combination with albumin 10 delenlline if the calcium
dard urinaly�is. Various rarer conditions can produce Bence
concentration of serum is appropriate. As albumin level�
Jones proteins. such as Waldenstrom macroglobulinemia
rise, calcium rises as well. and vice versa. A high calcium level is called hypercalcemia, requiring
and other mal ignancies.
trearment for the underlying condition. Hypercalcemia is
Bilirubin
usually caused by:
VeM.'boT/u
Hyperparathyroidism
Excessive bilirubin kills developing brain cells in infanls
funclion): This condilion is usually caused by a benign
( i ncrease
in
paralhyroid gland
and may cause mental retardation. physical abnonnalities,
lumor on Ihe paralhyroid gland. This fonn of hypercal
or blindness. Bilirubin in newborns must not become 100
cemia is usually mild and can be present for many years
high. When Ihe level of bilirubin is above a crilical lhresh
before being nOliced.
old, special treatments arc initiated to lower it. An excessive
Cancer: Cancer can cause hypercalccmia when it �preads
bilirubin level may resull from Ihe breakdown of red blood
to the bones, which releases calcium into the blood. or
cells ( R BCs) caused by Rh blood Iyping incompatibililY.
when cancer causes a hormone similar to parathyroid
(The mOlher is Rh negalive I Rh-I. lhe father is Rh posilive
hormone to increase calcium levels.
I Rh+l. and Ihe felUs is Rh+: Ihe mOlher develops antibodies
Olher causes of hypercalcemia include: Hyperthyroidism
again;! Ihe newbom's RBCs. which are destroyed.)
Sarcoidosis
Idl///.\ alld Childrell
Tuberculosis
Bi lirubin level� can be used (0 idcIHify liver damage or
Bone break!>. combined with bed rest or not moving
disease or to monitor the progression of jaundice. A conju
for a long periods
gated bilirubin that is elevated may indicate some kind of
Excess vitamin D intake
blockage of Ihe liver or bile duCI. hepmilis. lrauma 10 lhe
Kidney lransplantation
l iver, a drug reaction. or long-Icnn alcohol abuse. Inherited
High prolein levels (e.g .. if a lourniquel is used for 100
di,orders caused by abnonnal bilirubin melabolism (Gilbert,
long while blood is collecled)
ROlOr. Dubin·Johnson. or Crigler·Najjar syndromes) may
In this case, free or ionized calcium remains normal. High levels of ionized calcium occur with all the conditions previ
also cause increased levels.
ously menlioned. excepl high prolein levels.
Blood Urea Nitrogen
Low calcium levels. called hypocalcemia. mean that the
Increased blood urea nilrogen (BUN) levels suggesl impaired
patient has insufficieJ1l calcium i n the blood or Ihal Ihe
kidney function. This elevation may be caused by acute or
patient has insufficienl prolein in Ihe blood. The moS!
chronic kidney disease. damage. or failure; i t may also be
common cause of low total calcium is low protein levels.
caused by a condilion Ihal resulls in decreased blood How
especially low albumin. When low prolein i< Ihe problem.
(0 the kidneys, slich as congestive heart failure, shock. stress,
the ionized calcium level remains normal.
recent heart attack, or severe bums; to conditions that cause
Low calcium. known as hypocalcemia, is caused by many conditions:
Ob!
Low prolein levels
B U N concentrations may be elevated in the setting of excessive prolein catabolism (breakdown). significanlly
Underaclive paralhyroid gland ( hypoparalhyroidism)
i ncrea!>.ed protein in the diet. or ga!>.lIointestinal bleeding
Decreased dietary imake of calcium
(becau,e of Ihe prolein, presenl in the blood).
Decreased levels of vitamin 0 Magnesium deficiency
Low BUN levels are not common and are not usually a cause for concern. They may be seen in severe liver disease,
Excessive phosphorus
malnutrition. and sometimes when a patient is overhydnlled
Acute inflammation of the pancreajo,
(excessive nuid volume): bUI Ihe B U N lesl is nol normally
Chronic renal failure
used to diagnose or monitor these conditions.
Calcium ions becoming bound 10 prole in (alkalosis)
Both decreased and increased B U N concentrations may
Bone disease Malnutrition
be seen during a normal pregnancy. I f one kidncy is fully funclional, B U N concenlralions may be nonnal even when significant dysfunction is presem in Ihe olher kidney.
Alcoholism Causes of low ionized calcium Icvels include all of these condition except low protein levels.
Copyrighted Material
17
C HAPTER I Principles in Assessing Musculoskeletal Disorde"
Chloride
Glucose
Increased levels of chloride (hyperch/oremia) usually indi
High levels of glucose most frequently indicate diabetes, but
cate dehydration, but high levels can also occur with any
many other diseases and conditions can also cause elevated
other problem that causes high blood sodium. Hyperchlore
glucose. The following information summarizes the meaning
mia also occurs when excessive base is lost from the body
of the test results. These points are based on the clinical
( producing metabolic acidosis) or when a person hyperven
practice recommendations of the American Diabetes Asso
tilates (causing respiratory alkalosis).
ciation (Table 1 -4).
Decreased levels of chloride (hypoch/oremia) occur with any disorder that causes low blood sodium. Hypochloremia also occurs with prolonged vomiting or gastric suction.
Some of the other diseases and conditions that can result in elevated glucose levels include: •
Acromegaly
chronic diarrhea. emphysema or other chronic lung disease
Acute stress (response to trauma, hean attack, and
(causing respiratory acidosis), and with loss of acid from the
stroke for instance)
body (causing metabolic alkalosis).
•
Chronic renal failure Cushing syndrome
Cholesterol
Drugs (e.g., conicosteroids, tricyclic antidepressants. diuretics, epinephrine, estrogens [birth control pills
In a routine setling in which testing is perfonncd to screen for risk factors, the test results arc grouped in three catego
and hormone replacement medications I, lithium, phe
ries of risk:
nytoin [ Dilantin"'" salicylates)
Desirable:
A
cholesterol
level
below
200 mg/dL
Excessive food intake
(5. 1 8 mmol/L) is considered desirable and reflects a low
Hyperthyroidism
risk of heart disease.
Pancreatic cancer
Borderline high: A cholesterol level of 200 to 240 mg/dL (5. 1 8-6.22 mmol/L) is considered 10 reflect moderate risk. High
Pancreatitis Low to nondetectible urine glucose results are considered normal. Anything that raises blood glucose levels also has
risk:
A
cholesterol
level
above
240 mg/dL
(6.22 mmol/L) is considered high risk.
the potential to elevate urine glucose levels. Increased urine glucose levels may be seen with medications such as estro gens and chloral hydrate and with some forms of renal
Creatinine
disease.
Increased creatinine levels in the blood suggest diseases
Moderately increased levels may be seen with prediabe
or conditions that affect kidney function, including the
tes. This condition, if left untreated. often leads to type 2
fol lowing:
diabetes.
Damage to or swelling of blood vessels in the kidneys (glomerulonephritis) caused by. for example, infection or
Low
glucose
levels
(hypoglycemia)
are
also
autoimmune diseases
Adrenal insufficiency
Bacterial infection of the kidneys (pyelonephritis)
Drinking alcohol
Death of cells in the kidneys' small tubes (acute tubular
Drugs (e.g., acetaminophen, anabolic ;tcroids)
necrosis) caused. for example, by drugs or toxins
Extensive liver disease Hypopituitarism
Prostate disease, kidney stone. or other causes of urinary tracl obstruction
•
Reduced blood flow to the kidney caused by shock, dehy
seen
with:
Hypothyroidism Insulin overdose
drmion. congestive hean failure. atherosclerosis, or com
Insulinomas (insulin-producing pancreatic tumors)
plications of diabetes
Starvation
Creatinine can also increase temporarily as a result of muscle injury. Low levels of creatinine are not common and are not usually a cause for concern and can be seen with
Heavy Metal Screens
conditions that result in decreased muscle mass. Creatinine
Heavy metals are increasingly responsible for the produc
levels are generally slightly lower during pregnancy.
tion of free radicals. as well as undermining the illlernal ell v;romnellf and body chemistry. The main concern is not
Creatinine Phosphokinase
so much the type of metal that may be detected but rather if
A high creatinine phosphokinase (CK) level, or one that
metals in their ionic form are present. Chemical analyses can
goes up from the first to the second or later samples, gener
establish the exposure to excessive amounts of toxic sub
ally indicales some damage to the heart or other muscles; it
stances. Many analytical procedures can be performed if the
can also indicate that the patient's muscles have experienced
problem warrants me investment of time and the client is
heavy use. If the patient has experienced a heart allack and
willing to pay for the procedure. Although screening samples
the CK is high, a more specific test (troponin or CK-MB)
for cenain groups of chemicals is possible. analyzing for
should be ordered to determine if the patient's heart is
everything or checking for poisons is not feasible. Heavy
damaged.
metals include arsenic. cadmium. calcium. cobalt, copper,
Copyrighted Material
18
C HAPTER I Principles i n Assessing Musculoskeletal Disorders
TAIl L E 1 -4 SUMMARY or GLUCOSE TOLERANCE TESTS AND I NTERPRETATtONS Fasting Blood Glucose From 70 to 99 rng/dL £3.9 to 5.5 mmol/L)
Normal glucose tolerance
From 1 00 LO 125 OlgldL {5.6 to 6.9 mmoVL)
Impaired fasting glucose (prediabclc..'iI)
1 26 mgldL (7.0 mmol/L) and above on more than one tcsling occasion
Diabetes
Oral Glucose Tolerance Test (OG1T) [except pregnancy] (2 hours after a 75-gram glucose drink) Lc�s Lhan 1 40 mgldL (7.8 mmollL)
Nonllai glucose tolerance
From 140 10 200 mgldL (7.8 10 1 1 . 1 mmollL)
Impaired glucose lo\cram:e (pre-diabetes)
Over 200 mgldL ( 1 1 . 1 Illmul/L) on more limn one testing occasion
Diabetes
Gestational Diabetes Screening: Glucose Challenge Test (1 hour after a 50-gram glucose drink) Less than 140* mg/dL (7.8 mmoVL)
Normal glucose tolerance
1 40· mgldL (7.8 rnmollL) and over
Abnormal. needs OGTI (�ce below)
Gestational Diabetes Diagnoslic: OGT'I' ( I OO-gram glucose drink) Fu!.ting·
95 mg/dL (5.3 mmolfL)
I hour after glucose load
180 mgidL ( 1 0.0 mmollL)
2 hours after glucose load'
155 IllgidL (8.6 mmollL)
3 hours after glucose load'
140 mgidL (7.8 mmol/L)
"'Some use
,\
cUloff of > I JO mg/LIL (7.2 mmollL) bccau..c that identitic!; 901H of women with ge�w.lional diuOOlc.... compureel to SOIk idcmilicd using the
lhreshold or >140 mgldL (7.8 mmoIlL). If two or more val ue...
:u-c
ubove the criteria. gestutionul diabetes is diagnosed.
A 75-gr:lI11 glucose load may be used. although thh method is not as v.cll validated as the IOO-gram OGTI: the 3-hour ..ample b not dr:lV.n iPS gram... is
u�cll.
cyanide.
f1 uoride,
iron,
lead,
magnesium,
manganese.
mercury, molybdenum, phosphorus, potassium, selenium.
Below-normal hemoglobin levels may lead to anemia that can be the result of: Iron deficiency or deficiencies in essential vitamins of
sodium, and zinc.
other elements such as vitamin B 1 2, folate. vitamin
Hematocrit
B6
Decreased hematocrit indicates anemia, such as that caused
•
lnherited hemoglobin defects. such as sickle cell anemia or thalassemias
by iron deficiency or other deficiencies. Further testing Illay be necessary to detennine the exact cause of the
Other inherited derects arfecting the RBCs
anemia.
CilThosis of the liver (during which the liver becomes scarred)
Other conditions that can result in a low hematocrit include vitamin or mineral deficiencies, recent bleeding, cir
Excessive bleeding
rhosis of the liver, and malignancies.
Excessive destruction of RBCs Kidney disease
The 1l10�t common cause of increased hematocrit is dehy dration, and with adequate fluid intake, the hematocrit
•
Other chronic illnesses
returns to normal. However, increased levels may reflect a
Bone marrow failure or aplastic anemia
condition called pol.\'cythemia \Iera-thm is, when a peniOll
Cancers lhat afrect the bone marrow
ha, more than the normal number of RBCs. Increa,ed hema tocrit can be caused by a problem with the bone marrow or.
Human Leukocyte Antigen-B27
more commonly. as compensation for inadequate lung func
Human leukocyte antigen ( H LA)-B27 will be present or
tion (the bone marrow manufacLUres more RBCs to carry
absent. I f it is present. then the HLA-B27 antigen ( protein structure) exists on the surface or the body's while blood
enough oxygen throughout the body).
cell> (WBCs) ,uld nucleated cells. I f a patient has HLA-B27
Hemoglobin
and has symptoms such as chronic pain. innammalion. and
Normal values in an adult nre 1 2 to 1 8 gJdL ( 1 00 mm/dL)
degenerative changes to his bones (as seen on X-ray exam
of blood. Above-nonnal hemoglobin levels may be the result
ination), then it supports a diagnosis of ankylosing spondy
or:
litis (AS), Reiter syndrome. or another autoimmune disorder Dehydration
thal is a'Sociated with the presence or HLA-B27. This cir
Excessive production of RBCs in the bone marrow
cumstance is especially true ir the patient is young. male
Severe lung disease
gender. and ir the patient experienced the first symptoms
Several other conditions
before the age of -10.
Copyrighted Material
19
CHAPTER I Principles in Assessing Musculoskeletal Disorders The presence o f HLA-B27 may also seen w i t h other autoimmune conditions huch as:
and unjaundiced patients. Values under 1 000 units arc of no help in the differential diagnosis of jaundice, but values
Isolated acute anterior uveitis
above 1000 units are highly indicative of b i liary ob;truction.
•
Undifferentiated spondyloarthropathies
The differentiation of intra- from extrahepatic obstruction,
•
Entcropathic synovitis
as well as of malignant from benign jaundice. cannot gener
I f HLA-B27 is not present. then the symptoms arc likely the result of an HLA-B27-associated autoimmune disorder. ( Exceptions to this rule, however. arc approxi mately 10% of
a l l y be e;tablished by this single tesl.
Lipase
patients with AS and 40% to 50% of those with Reiter syn
In acute pancreatitis, l i pase levels are freq uently very high,
drome w i l l be negative for HLA-B27.)
often 5 to 1 0 times higher than the highest reference value
At this time. identifying the presence of HLA-B27 does not predict the likel ihood of developing an autoimmune disease.
If a patient does have an associated disorder. the
(often cal led the upper limit of normal). In acute pancreati tis. l i pase concentrations rise within 24 to 48 hours of an acute pancremic atlack and may remain elevated for approx
presence of HLA-B27 cannot be used to tell which disease
imately 5 to 7 days. Concentrations may also be increased
is present, how quickly it will progress, its severity. prog
with pancreatic duct obstruction. pancreatic cancer. and
nosis. or the degree of organ involvement.
other pancreatic diseases.
Lactic Dehydrogenase Compression Test n
conditions such as kidney disease (caused by decreased
Elevated levels of lactic dehydrogenase (LDH) and changes
clearance from the blood), salivary gland infl ammation, a
Moderately increased l ipa;e values may occur in other
in the ratio of the LDH isocl1tymcs usually indicalc some
bowel obstruction, or peptic ulcer dise,,-,e, although the
type of tissue damage. LDH levels w i l l usually rise as the
l ipase test is not nOnllally lIsed to monitor these conditions.
cellular destruction begins. peak after some time period. and
Decreased li pase levels may indicate pennanent damage to
then begin to fal l . For instance. when someone has a heart
the l i pase-producing cells in the pancreas.
allack, blood levels of total LDH will rise within 24 to 48 hour;, peak in 2 to 3 days, and return to normal in 1 0 to 1 4
lipidS
days.
The lipid profile includes IOtal cholesterol, high-density l ipoprotein ( H D L ) cholesterol (often called good choles
Elevated levels of LDI-I may be seen with: Cerebrovascular accident (CVA. stroke)
terol). low-density l ipoprotein (LDL) cholesterol (often
Drugs (c.g .. anesthetics, aspirin, narcotics. procain
called bad cholesterol). and triglycerides. The report w i l l
amide_ alcohol)
sometimes includc additional calcu lated valucs such a'\
Hemolytic anemia
H DULDL ratio or a risk score based on lipid profile results,
Pernicious anemias ( megaloblastic anemias)
age. sex, and other risk factors.
I nfectiolls mononucleosis
A normal level for fasting triglycerides is less than
I ntestinal and pul monary infarction (tissue deat h )
1 50 mgldL
Kidney disease
without also having high cholesterol is unusual. Most treat
( 1 .70 mmoI/L).
Having
high
triglycerides
Liver disease
ments for heart disease risk will be aimed at lowering LDL
Muscular dystrophy
cholesterol. However, the type of treatment used to lower
Pancreatitis
LDL cholesterol may differ depending on whether triglyc
Some cancers
erides are high or normal.
With .!tome chronic and progressive conditions. and ;ol11e
drugs.
moderately
elevated
LDH
levels
may
per�isl.
Triglycerides that arc very high (greater than 1 000 mgldl 1 1 1 .30 mmol/L]) increases the risk of developing pancreati tis. Treatment to lower trig lycerides should be started a;
Low and normal levels of LDH do not usually indicate a problem. Low levels are sometimes seen when a patient
soon as possible.
ingests large amounts of ascorbic acid (vitamin C).
Lupus Erythematosus Cell Prep
Latex Agglutination
diagnosis of SLE for nearly 50 years. having a sensitivity of
The lupus erythematosus (LE) cell prep was the primary
Various rapid tests identifying bacterial antigen from body
nearly 50%. This test has been replaced by a more sensitive
nuids are becoming increasingly avail able. One of these
test. ANA. which measures the binding of a patient's serum
technique;. latex agglutination. is frequently used 10 test
antibodies to HEp-2 cell nuclei.
cerebrospinal fluid in chi ldren being eval uated for possible
The results of each of the lupus anticoagulant te", lead
meningitis. Early diagnosis of meningitis can lead to prompt
either toward or away from the likeli hood of having a lupus
treatment.
anticoagulant. Although the tests performed may vary. they
Leucine Aminopeptidase
( PTT ) .
u,u,lIly begin with a prolonged panial thromboplastin time
Serum leucine aminopeptidase determination is a useful
If the PTT or lupus anticoagulant (LA)-PTT is prolonged,
screening procedure for hepatobi l iary disease in jaundiced
and mixing it with normal pooled plasma does not correct
Copyrighted Material
20
C HAPTER I Principles in Assessing Musculoskeletal Disorders Chronic antacid use
the result, then an inhibitor is likely present. If the pro longed test corrects when phospholipid is added, then a
Rickets
lupus anticoagulant is likely present. (After heparin con
deficiencies)
tamination. a lupus 3micoagulalll is the most common
and osteomalacia (caused
by
vitamin-D
H igher-than-normal levels of phosphorus ( hyperphos phatemia) may be caused by or associated with:
reason for a prolonged PTr.) If the PTr is not prolonged, a lupus anticoagulant may
Kidney failure
not be present, the test reagents may contain too much
phospholipid. or the test may not be sufficiently sensitive
Hypoparathyroidism (underactive parathyroid gland)
to pick up the lupus anticoagulant. The LA-sensitive PTr may need to be performed. If a dilute Russell viper venom time or modified Russell
Diabetic ketoacidosis (when first seen)
•
Phosphate supplementation
Potassium
viper venom time test is prolonged and does not correct
Increased potassium levels indicate hyperkalemia. Increased
when mixed with normal pooled plasma but does corrCCl
levels may also indicate the following health conditions:
with Ihe addition of phospholipids, then a phospholipid
Excessive dietary potassium intake ( Fruits are par
antibody is likely present.
ticularly
If a thrombin time lest is nonnal, then heparin contamina
intake of fruits or juices may contribute to high
tion is excluded.
potassium.)
high
in
potassium;
therefore,
If a fibrinogen test is nonnal. then fibrinogen is likely
Excessive imrdvenous potassium intake
sufficient for normal clot formation.
Acute or chronic kidney failure
Other tests that may be performed 10 help confinn the
Addison disease
excessive
Hypoaldosteronism
diagnosis of a lupus anticoagulant include:
Injury to tissue
Platelet neutralization (This test uses platelets as a source of phospholipids.)
Infection
Hexagonal ( I I ) phase phospholipid assay (Staclot-LA
Diabetes Dehydration
test)
Cenain drugs can also cause hyperkalemia in a small
Kaolin clotting time Tissue thromboplastin inhibition lest Venereal Disease Research Laboratory (VORL) or
percentage of patients. Among these drugs are nonsteroidal "' untiinnammatory drugs (e.g., Advil"'. MOlIin , Nuprin- ).
rapid plasma reagin (RPR) (These tests are used to
beta-blockers
detect syphilis. Their reagents arc made of cardiolipin
converting enzyme inhibitors (e.g .. captopril. enulapril.
(e.g..
propranolol
atenolol).
angiotensin
and they may give a false positive result for both
lisinopril). and potassium-sparing diuretics (e.g
anlicardiolipin antibodies and for lupus anticoagu
terene. amiloride. spironolactone).
.•
triam
Decreased levels of potassium indicate hypokalemia.
lant.) Coagulation factors (These tests may be ordered to
Decreased levels may occur in several conditions. particu
rule out factor deficiencies that may cause a prolonged
larly: Dehydration
PTr and bleeding episodes.) Prothrombin lime
•
Vomiting Diarrhea
Other tests that may be performed in addition to lupus
Deficient potassium intake ( rare)
anticoagulant testing include: Anticardiolipin and anti-beta2-glycoprotein I antibod ies to check for anti phospholipid syndrome
Protein-Bound Iodine
Platelet count (Mild to moderate thrombocytopenia is
Iodine binds to protein. mainly thyroxin. in the plasma. The
often seen a10ng with the lupus anticoagulant and may
thyroid
be caused by anticoagulant I heparinl therapy.)
agents. and the amount of iodine in a protein precipitate
honnone
is precipitated
by
protein-denaturing
generally indicates the amount of thyroid hormone present
Phosphorus
and is thus an index of thyroid activity. Various values are
Dietary deficiencies in phosphorus are rare but may be seen
given for thyroid function: hypothyroidism. 0 to 3.5 mcg!
with alcoholism and malnutrition. Low levels of phosphorus
mL of protein-bound iodine: euthyroidism. 3.5 to 8.0 g!mL:
(hypophosphatemia) may also be caused by or associated
hyperthyroidism, values higher than 8 mcg!mL.
with:
Red Blood Cell Count
•
Hypercalcemia (high levels of calcium) especially as a result of hyperparathyroidism
A high RBC count may indicate congenital heart disease.
•
Overu�e of diuretics (drugs that encourage urination)
dehydration. obstructive lung disease. or bone marrow
Severe bUnls
overproduction. A high RBC count is also seen in bela
Diabetic ketoacidosis (after treatment)
thalassemia trait, a benign condition with little or no anemia.
Hypothyroidism
A low RBC count may indicate anemia. bleeding. kidney
Hypokalemia (low levels of potassium)
disease. bone marrow failure (for instance. from radiation or
Copyrighted Material
CHAPTER I Principles in Assessing Musculoskeletal Disorders a tumor). malnutrition. o r other call�es. A l o w count may
2\
mine whether other deficiencies or excesses exiM. Frequently
abo indicate nutritional deficiencies of iron. foJ:.uc. vitamin
the balance among thcsc different substances. and the
B 12, and vitamin 86.
changes in them. arc just as important as the concemratiolls.
Rheumatoid A rthritis Factor (RA Latex) Test
ents wilh symptoms thai suggest:
Calcium can be used as a diagnostic test jf the patient pres Kidney stones
A mpid latex .Iide agglutination te,t ror the qualitative and semi-quantitative
determ ination
of rheumatoid
arthritis
•
Bone disease eurologic disorders
factor in human serum. The presence of these aUlOalllibodies to human immunoglobu l i n G (IgG ) is a userul diagnostic
The lotal calcium lesl is Ihe leS( mo;! rrequenlly ordered
tool ror aClive rheumHloid arthrilis ( R A J becau,e high li tres
to cvaluatc calcium status. I n most cases. it is a good rencc
indicate severe disease.
tion of the amount of free calcium involved in Il1cLabolism since the balance between free and bound is usually �lable
Serum Glutamate Oxaloacetale Transaminase
and predictable. However. in !'tome patients. the balance
Very high levels or aspanate aminOlransremse (AST) ( more
between bound and free cnlciull1 is disturbed and total
than 10 Lime!' the highcM nOfmal lcvel) are usually the result
calcium is not a good reflection of calcium status. In thoo,e
of acute hepatitis. oflen caw.,cd by a virus infection. In acute
circumstances. measurement of ioniL.cd calcium i!\ neces
hepat ili,. AST level> u,ually stay high ror approx imately I
sary. Some conditions where ionized calciull1 should be the
to 2 months but can take as long as 3 to 6 l110lllhs to return
test of choice include: critically i l l patients who are receiv
to normal. I n chronic hepatitis. AST levels are usually not
ing transfusions or I V fluids. patients undergoing major
a:-. high as they arc in acute hepat itis. often les� than four
surgery, and paticnts with blood protein abnormalities like
time� the highe�t normal level. I n chronic hepatitis. AST
low albumin. Large fluctuations in ionized calcium can
onen varies between nonnal and slightly increased: there
cau!\c the hean to slow down or to beat too rapidly. can cause
fore. examiner.!> w i l l typically order the test frequently to
muscles to go into spasm (tetany). and can causc confusion
determ ine the pattem.
or even coma. In critically i l l patients, it is extremely im por
In '!'ol1le di seases of the liver. especially when the bile
tant to know the ionized calcium levcl to be able to i ntervene
duct� are blocked. or with cirrhosis and cenain cancers of
and prevent serious cOll1p l i cations. These include the fol
the liver. AST may be close to normal. but it i l1crease� more
lowing:
often than alanine aminotnll1,remse (ALT). When liver damage is the result of alcohol, AST often increases much more than A LT. (This pattem is seen with a few Olher liver
I . Kidney di scase. becausc low calcium is especially common i n those wilh kidney failure:
2. Symptoms of too much calcium. such a!\ fatigue.
dise,,,es.) AST i, also increased arter heart anacks and wilh
weakness. loss of appetite. nausea. VOITIltlllg. con
mu�cle injury. usually to a much greater degree than is
stipation. abdominal
A LT.
increased thirM:
pain. urinary frequency. and
3. Symptoms of low calcium. such as cramp� i n your
Serum Ionized Calcium
abdomen. muscle cramps. or tingling fi ngers: or
Blood calcium is tested to screen for. di agnose. and monitor
4. Olher diseases that have been associaled with abnor
a range of conditions relating to the bones. hean, nerves.
mal blood calcium. such as thyroid d isease. inteMinal
kidneys. and leelh. Blood calcium level> do not directly lell
disease. cancer. or poor nutrition.
how much calcium i s in the bones. but ralher, how much
An ion ized calcium test b, ordered when the patient ha� numbness around the mouth and i n the hands and feet and
calcium is circulating i n lhe blood. A total calcium level is often measured as pan of health
muscle spasms in the same areas. These can be symptoms
screen ing. It is incl uded in the comprehensive metabolic
of low levels of ionized calcium. However. when calcium
panel (CMP) and the basic metabolic panel ( B M P)-groups
levels rail slowly. many people have no symploms at a l l . The
of tests that are performed together to di agnose or monitor
patient may need calcium moniLOring when they have cenain
a variety of conditions. When an abnormal total calcium
kinds or cancer (particularly breast. lung. head and neck,
result is obtai ned. it i s viewed as an indicator or some kind
kidney. and multiple myeloma), have kidney disease, or
of underlying problem. To help diagnose the underlying
have had a kidney transplant. Monitoring may also be neces
problem. additional tests are often done to measure ionized
sary when the patient is being treated for abnormal calcium
calcium. urine calcium, phosphorous, magnesium. vitamin
levels to evaluate the effecti veness of treatment� such as
D. and paralhyroid hormone (PTH). Parathyroid hormone
calcium or vitamin D supplements.
and vitamin D arc responsible for maintaining calcium con centrations in the blood within a narrow range of values.
Calcium absorpLion. usc. and excretion are regulated and Slabil iLed by a reedback loop involving PTH and vitamin D.
Measuring calcium and PTH together can help determine
Conditions and diseases that di�rupt calcium regulation can
whether the parathyroid gland is runclioning normally. Mea
cause inappropriate acute or chronic elevmions or decreases
suring urine calcium can hclp determinc whether the kidneys
in calcium and lead to symptoms or hypercalcemia or hypo
are excreting the proper amount of calcium. and testing for
calcemia. In most cases. total calcium is measured because
vitamin D, phosphorus. and/or magnesium can help deler-
the test is more easily performed than the ionized calcium
Copyrighted Material
22
CHAPTER I Principles in Assessing M usculoskeletal Disorders
test and requires no special handling of the blood ample.
proLein is present. The value of protein electrophoresis
TOlal calcium is usually a good reflection of free calcium
lies in the proportions of proLeins and in the pauerns Lhey
since the free and bound forms are typically each about half
creaLe on the elecLrophoresis graph. The value of immuno
of the total. However. because about half the calcium in
fixation electrophoresis is in identifying the presence of
blood is bound to protein . lOlal calcium lest results can be
a panicular Lype of i m munoglobulin. For example. certain
affected by high or low levels of protein. In such cases. it is
conditions or diseases may be associated with decreases
morc useful to measure free calcium directly using an
or i ncreases in various serum proteins, as reflected as
ionized calcium test.
follows: Albumin
Normal Calcium
Decreased:
A normal lOla) or ionized calcium resulL together with
pregnancy. kidney disease (especially nephroLic syn
other normal lab results generally means that calcium
drome), liver disease, inflammatory conditions, and
metabolism is normal and blood levels arc being appropri
proLein-losing syndromes
ately regulated.
with
malnutrition and malabsorption.
II/creased: with dehydration •
Alpha, globulin
IIigil To/al Calcillm-llypercalcemia
Decreased: in congenital emphysema (CII-antitrypsin
Two of the morc common causes of hypercalcemia are:
deficiency, a rare genetic disease) or severe liver
1. Hyperparathyroidism.
an
increase
in
parathyroid
disease Increased: in acute or chronic inflammatory diseases
gland function: This condition is usually caused by a benign tumor of the parathyroid gland. This fonn of
Alpha, globulin
hypercalcemia is usually mild and can be present for
Decreased: WiLh hyperthyroidism or severe liver
many years before being noticed.
disease. hemolysis (RBC breakage)
2. Cancer: Cancer can cause hypercalcemia when iL
•
spreads to the bones, which releases calcium into the blood. or when a cancer produces a honnone similar
II/creased: with kidney disease ( nephrotic syndrome). acute or chronic inflammatory disease
BeLa globulin
to PTH, resulting in increased calcium levels.
Decreased: with malnutrition. cirrhosis
Some oLher causes of hypercalcemia include:
Increased: with hypercholesterolemia, iron deficiency
1 . Hyperthyroidism
anemia, some cases of multiple myeloma. or mono
2. Sarcoidosis
clonal gammopaLhies of undetermined significance
3. Tuberculosis
(MGUS) Gamma globulin
4. Prolonged immobilizaLion 5. Excess Vitamin D i ntake
Decreased: variety of genetic i m mune disorders. and in secondary immune deficiency
6. Kidney LransplanL
Increased: polyclonal-chronic inflammatory disease.
•
Low
Tolal Calciwll-Uypoca[cemia
RA, SLE. cirrhosis. chronic liver disease. aCULe and
The most common cause of low total calcium is:
chronic infection, recent immunization.
I. Low blood proLein levels. especially a low level of
•
low. Ionized calcium remains normal and calcium
Increased: monoclonal-Waldenstrom macroglobu linemia. muhiple myeloma. MGUS
albumin. I n this condiLion. only the bound calcium is
TOLal protein Low total protein levels can suggest a liver disorder, a
metabolism is being regulaLed appropriaLely. Some oLher causes of hypocalcemia include:
kidney disorder. or a disorder i n which protein is nOL digesLed
I . U nderacLive parathyroid gland (hypoparaLhyroid ism)
or absorbed properly. Some laboraLories also report the cal culated raLio of albumin LO globulins ( NG raLio). Normally,
2. InheriLed resistance LO the effecLs of parathyroid hormone
albumin slighLly exceeds globulins. giving a normal A/G raLio of slighLly over I . Because disease SLates affect Lhe
3. Extreme deficiency in dietary calcium
relaLive changes i n albumin and globulins i n differenL ways.
4. Decreased levels of viLamin D
this ratio may provide a clue to the physician as to the cause
5. Magnesium deficiency
of the change in proLein levels. A low NG raLio may renect
6. Increased levels of phosphorus
overproducLion of globulins. such as seen in muhiple
7. Acute i nflammalion of the pancreas ( pancrealitis)
myeloma or autoimmune diseases, or underproduction of
8. Renal failure
albumin. such
9. MalnUlriLion
albumin from the circulaLion, as occurs with nephroLic syn
10. Alcoholism
and
occurs with cirrhosis, or selective loss of
drome. A high NG raLio suggesLs underproducLion of immu noglobulins. as may be seen in some genetic deficiencies
Serum Protein Electrophoresis Protein
as
and in some leukemias. More specific tests, such as albumin.
i m munofixation electrophoresis tests give
the examiner a rough eSlimate of how much of each
liver enzyme tests, and serum protein elecLrophoresis. must be performed to make an accurate diagnosis.
Copyrighted Material
CHAPTER I Principles in Assessing M uscu.loskeletal Disorders
Sodium
23
GII/cose
Hyponatremia is rarely caused by decreased sodium intake
Normally, urine contains no glucose. A poslLJve glucose
(deficient dietary intake or deficient sodium in intravenous
occurs in diabetes. The number of people who have glucose
fluids). Most commonly. hyponatremia is caused by sodium
in their urine with normal blood glucose levels is small;
loss (Addison disease, diarrhea, excessive sweating, diuretic
however, any glucose in the urine would raise the possibility
administration, or kidney disease). In some cases. hypona
of diabetes or glucose intolerance.
tremia is caused by increased water (drinking too much water, heart failure, cirrhosis, kidney diseases that cause
Proteiu
protein loss [ nephrotic syndrome]). In a large number of
Normally no protein is detectable on a urinalysis strip.
diseases (particularly those involving the brain and the
Protein can indicate ki dn ey damage, blood in the urine, or
lungs, many kinds of cancer, and with some drugs), the body
an i n fection. Up to 10% of children can have protein in their
makes too much 3Illidiurclic hormone, causing the patient
urine. Certain diseases require the use of a special. more
to keep too much water in the body.
sensitive (and more expensive) test for protei n called a
A high blood sodium level means the patient has hyper
microalbumin test. A microalbum i n test is useful in screen
natremia, almost always caused by excessive loss of water
ing for early damage to the kidneys from di abetes, for
(dehydration) withollt enough water intake. Symptoms
instance.
include dry mucous membranes. lhirsl, agitation, restless ness, acti ng irrationally, and coma or convulsions if levels
Illood
rise extremely high. In rare cases, hypernatremia may be
NormaJl y, urine comains no blood. Blood can indicate an
caused by increased salt intake without enough water,
i n fection, kidney stones, trauma. or bleeding from a bladder
Cushing syndrome, or insufficient antidiuretic hormone
or kidney tumor and may be hemolyzed (dissolved blood) or nonhemolyzed (intacl RBCs). R are ly, musc le inju ry can
(diabetes insipidus).
Sodium urine concentrations must be evaluated in asso ciation with blood levels. Concentrations may mirror blood
cause myoglobin to appear in the urine, which also causes the reagent pad to indicate blood falsely.
levels or be the opposite. The body normally excretes excess sodium; thus the concentration in the urine may be elevated
Bilirubin
because it is elevated i n the blood . .It may also be elevated
Normally, urine cOlllains no bilirubin or u rob i l inogen. These
in the urine when the body is losing excessive sodium. In
substances are pigments that arc cleared by the l iver. I n livcr
this case. the blood level would be normal to low. I f blood
or ga ll bladder disease, they may appear in the urine as
sodium levels are low as a resull of i nsufficient intake. then
well.
urine concentrations will also be low.
Nitrate
Uric Acid
Normally negative. nitrate i n the urine usually indicates a
Higher-than-normal uric acid levels mean that the body is
urinary tract infection.
not handling the breakdown of purines well. .Increased con centrations of uric acid can cause crystals to form in the
Leukocyte Esterase
joints. which leads to the joint inHammation and pain char
Leukocyte esterase is normally negative. Leukocytes are the
acteristics of gout. Uric acid can also form crystals or kidney
WBCs (or pus cells). WBCs in the urine suggest a urinary
stones lhat can damage the kidneys.
tract infection.
Low levels of uric acid in the blood are seen much less commonl y than high levels and are seldom considered
Sediment
cause for concern. Although low values can be associated
I tems such as mucous cells and squamous cells arc com
with some kinds of liver or kidney diseases, exposure to
monly seen. Abnormal findings would include >15 RBCsl
toxic compounds, and rarely as the result of an i nherited
hpf (hematuria)-additional i nvestigation must be donc to
metabolic defect, these conditions are typically identified by
determi n e the source of the hematuria (renal or postrenal);
other tests and symptoms and not by an isolated low uric
or >10 WBCs/hpf (pyuria)-additional investigation must
acid result.
be done to determine the source of the pyuria (renal or
Urinalysis
cells. or bacteria (bacteria can be presen t if contamination
pH
was present at the time of collection).
postrenal); or the presence of crystals, casts, renal tubular
Acid ity of urine is measllred by the pH.
White Blood Cell Count
.S'pecijil: Grat'ily
An elevated number of white blood cells ( WBCs) is called
Specific gravity (SO) measures how dilute the urine is.
leukocytosis, which can result rrom bacterial infections.
Water has a SG of 1.000 . Most urine is approximately1.0 10,
inflammation, leukemia, trauma, or stress.
but it can vary greatly depending on when the patient drank Iluids last or if the patient is dehydrated.
A decreased WBC cou n t is called leukopenia. which can result from many differen t situations, such as chemo-
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24
CHAPTER I Principles i n Assessing Musculoskeletal Disorders fall below 1 0 mg/L, clinically active inflammation is no
lhcrapy, radiation therapy. or diseases of the Immune system.
longer present.
Blood and serum panels that are lIseful in the differential
•
diagno1'>is include:
RA latex
Liver Function Tests
Bone panel Alkaline phosphatase Calcium
Alkaline phosphatase
Complete blood eOllnt (CBC)
Cholesterol
B i lirubin-total and direct
Table 1 -5 explains whm increases or decreases in ench of
Gamma-giutamyl transpeptidase (GGT) or peptidase
the components of the esc may mean.
Elevated GGT levels indicate that something is going on wiLh the liver but nOI specifically what. In general, the higher
SPEClTIC PROFILES
the level is, the greater the inslI!1 will be to " liver. Elevated
Arthritis Panel
caused by congestive heart failure. alcohol consumption.
levels Illay be caused by liver disease. but they may aho be
ANA screen
and use of many prescription and nonprescription drugs.
C-reactive protein (CRP)
including
A high or increasing amount ofCRP in the blood suggests
lowering drugs. antibiotics. histamine blockers ( used to treat
an acute infection or inflammation. In a healthy person, CRP
excess slOmach acid production), antifungal agents. seizure
nonsteroidal
antiinflammatory
drugs.
lipid
is usually less than 10 mg/L. Most infections and inflamma
control medications. antidepressants. and hormones slich as
tions re>lilt in CRP levels above 1 00 mg/L. l f the CRP level
testosterone. Oral contraceptives (birth control pills) and
drops. it means inflammation is being reduced. When results
clofibrate can decrease GGT levels.
TAB l E 1-5 SUMMARY OF CBC COMPONENTS AND INTERP RETATIONS
Test
Name
IncreascdU1>ecrcased
WBC
White blood cell
May be increased with i nfections, inflammation, cancer. leukemia;
decre;'lscd with some medications (such as methotrexate). some autoimmune conditions, some severe infections. bone marrow fuilurc. and congenital marrow aplasia ( marrow docsn't develop normally) This is a dynamic population that varies somewhat rrom day to day
% Neutrophil
NeutrophillBandfSeg
% Lymph!'>
Lymphocyte
% Mono
Monocyte
panicu lar types are a.s�ociated with di frerent temporary/acute amVor
% Eo!'>
Eosinophi l
chronic conditions. An example or this is lhe increased number or
o/r- Ba�o
Basophil
lymphocytes seen with lymphocytic leukemia. For more informalion,
Neul rophil
Neu troph illBandfSeg
see Blood S mear and WBC.
depending on what is going on in the body. Significant increase!'> in
Lymphs
Ly mphocyte
Mono
Monocyte
Eos
Eosinophi l
Ba'io
Basophil
RBC
Red blood cell
Decreased wil.h anemia: incrcased whcn too many made and with fluid
Hgh
Hcmoglobin
Mirrors RBe resu l�
Het
Hematocri t
Mirrors RBe results
MeV
Mean corpu scular volumc
Increased with BI: and Folate deficiency: dec reased wilh iron deficiency
MCH
Mean corpuscular hemoglobin
Mirrors MCV results
MCHC
Mean corpu !'>cular hemoglobin concentration
May be del'reased when MCV is decrca!'>cd; increases limited to amount
RDW
Red blood cell distribution width
Increased ROW i ndicutc:-. mixed popu lati on of RBCs: immature RBClt
Platelet
Platelet
Decreased or increa�ed with conditions lhat affect platelet production:
loss due 10 di arrhea, dehydration. burns
and thalassemia
of Hgb that will fil in.�ide a RBe tend to be larger
decreased when greater numbers used. a.s with bleeding: decreased with some inherited disorders (such as Wiskott-Aldrich. Bernnrd·Soulicr),
with Systemic lupus erythcmatoslI:', pernicious anemia, hypersplenism (splcen takcs 100 many Olll of circuhuion), leukcmia. and chemotherapy MPV
Mean platelet volu me
Vary with platclet production; younger platelets are larger than older ones
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25__
CHAPTER I Principles in Assessing Musculoskeletal Disorders LDH (See previous discussion.)
such a s temporal arteritis. polymyalgia rheumatica, and
Serum glutamate pyruvate transaminase (SGPT) (See
rheumatoid arthritis� it call also be used as a crude measure
previolls discussion.)
of response in Hodgkin disease. The use of ESR as a screening test in asymptomatic
Serum glutamate oxaloacetate transaminase (SGOT) Total protein-albumin and globulin
persons is limited by its low sensitivity and specificity. When a moderate suspicion of disease exists, the ESR may have
Parathyroid Function and Calcium Metabolism
some value as a sickness index. An elevaled ESR in Ihe absence of other findings should
Alkaline phosphatase Serum calcium
n01
Serum phosphorm.
tion.
Total protein
trigger an extensive laboratory or radiographic evalua
Uric acid
Urine calcium
•
Pancreas function lests
Synovial fluid analysis, including culture Synovial fluid analysis is inexpen:-.ive and may be diag
Amylase
nostic in patients with bacterial infections or crystal-induced
CBC
synovitis. According to lhe American College of Rheuma
Glucose tolerance
lology (ACR) clinical guidelines committee, Ihis analysis
Lipase
should be performed in dle febrile patienl with an acule flare of established arthritis to rule oul superimposed seplic arthri
Joint Pain or Swelling Tests
tis. In other situations. its main value is to permit classifica
ANA screen
tion into an inflammatory or noninflammatory category.
CBC
Thus, synovial fluid analysis should be performed if il is
Heavy metal screen
readily obtainable and the diagnosis is uncertain after history
RA latex
interview. physical examinatioll, und standard laboratory
Scdimclllalion rate
tests (Table 1 -6).
Although it is frequently ordered. the erythrocyte sedi
The WBC count, differential counL. cultures, Gram slain,
mentation rate (ESR) is not a useful screening (eM; it is
and polarized light microscopy are the mosl valuable sludies,
useful only for diagnosing three diseases: ( I ) myeloma, ( 2 )
Noninflammatory fluids generally have fewer than 2000 " with fewer Ihan 75% polymorphonuclear leu
temporal arteritis, and ( 3 ) polymyalgia rheumatica (in which
WBCs/ml11
it may exceed 100 nlln/hour).
kocytes. The ACR commiltee suggests Ihal unexplained
ESR is commonly lIsed for a di fferential diagnosis for
innammutory fluid, panicularly in a febrile patient, is
Kawasaki disease. and it Illay be increased in some chronic
assumed to be inrected until proven otherwise by appropri
infective conditions such as tuberculosis and infective endo
ate culture.
carditis. The ESR is a componenl of the Pediatric Crohn Disease AClivily Index (PDCAI),
an
Normal joints contain a small amount of synovial fluid
index for assessmenl of
with the following characteristics:
severity of innaml11atory bowel disease in children.
Highly viscous
The clinical usefulness of ESR is limited to monitoring
Clear
the response to therapy in certain inflammatory diseases
Essentially acellular
TAB I F 1-6 CATEGORJ[S OF SYNOVIAL F LU I D BASED UPON CLIN ICAL AN D LABORATORY F I N D I NGS
Measure
Normal
Noninflammatory
Inflammatory
Septic
Hemorrhagic
Volume, IllL (knee)
<3.5
Often >3.5
Oflen >3.5
Often >3.5
Usually >3.5
Clurity
Tnmsparenl
Transparent
Translucent-opaque
Opaque
Bloody
Color
Clear
Yellow
Yellow to opalescent
Yellow to green
Red
Viscosity
H igh
High
Low
Variable
Variable
Wac. per mlll3
<200
200-2.000
2000- 1 0.000
>100.000*
200-2.000
PMN<;. percent
<25
<25
;,50
,,75
50-75
Culture
Negative
Negative
Negative
Often positive
Negative
Total protcin. gldl
1-2
1-3
3-5
3-5
4-6
LDH (comp
Vcry low
Very low
High
Variable
Similar
Nearly equal
Nearly equal to blood
>25. lower than blood
<25. much lower
Nearly equal 10 blood
level!. In blood) Glucose. mgldl
10 blood
than blood
LDH, Laclic dehydrogenase: PMN, polymorphonuclear ce tl: WOc, white blood cell.
·Lower with infcctiol1\ caused by partially treated or low virulence organi!'!tns
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26
CHAPTER I Principles in Assessing Musculoskeletal Disorders •
Protein conccnLration approximately one-third thaL of plasma
TAB L E 1 -7 SUMMARY OF THYRO I D-STIMUlATING HORMONE
Glucose concentration similar to that in plasma If a synovial effu�ion is present and anhrocentesi� is indicated, joint nuid should be routinely analyzed for volume, clarity, color, viscosity, crystals cell counL differ ential. Gram stain. and culture. In certain circumstances. the presence and type of crystals should also be assessed. Syno vial fluid is subsequently categorized as either normal. non inflammatory. inflammatory, septic, or hemorrhagic based on the clinical and labonuory analysis. The differential diag
TEST RESULTS AND INTERPRETATIONS
TSH
T4
T3
Interpretation
High
Normal
NOnllal
Mild (subclinical)
High
Low
Hypothyroidi"m
Low
Nonnal
Low or normal Normal
Low
High or normal
High or
Hyperthyroidism
Low
Low or normal
Low or normal
hypothyroidism
hypcnhyroidi!im normal
nosis of each of these specific calegories is broad and nOI necessarily exclusive:
hypothyroidism
tive joint disease (osteoarthritis). trauma. osteochondritis innammation, hypertrophic oSleoarthropathy. and pig
Rare pilUitury (secondary)
NOllinjfallllJl(l[ory effusions may be caused by degenera
dissecans. neuropathic arthropathy, subsiding or early
Mild ( ..ubclinical)
n. Triiodothyronine: T-I. thyroxinc� TSN. lhyroiu-\timul;lling hurmone.
mented villonodular synovitis. Illfiall/II/atory effusions may be caused by RA, acule
hormone medication in patients who are being treated for an
crystal-induced synovitis. reactive arthritis (formerly
underactive (or removed) thyroid gland. In rare cases. a low
Reiler
TSH resuh may indicale damage 10 the piluilary gland that
syndrome),
ankylosing
spondylilis,
psoriatic
arlhriti�. arthritis associated wilh inflammatory bowel
prevents it from producing adequate amounts of TSH.
disease, rheumatic fever, SLE. hyperuophic osteoar
Whelher high or low, an abnormal TSI I indicates an
thropathy, and scleroderma. Rheumalic fever, SLE, and
excess or deficiency in the amount of thyroid hormone avail·
scleroderma can also cause a noninflammatory effusion.
able 10 the body, bUI il does nOI indicate Ihe reason why. An
Septic effusions may be caused by bacleria. mycobacte
abnormal TSH lest result is usually followed by additional
ria, or fungus.
testing to investigate the cause of the increase or decrease.
Hemorrhagic effusions may be caused by hemophilia or
other hemorrhagic dimhesis, scurvy, trauma with or
Table 1 -7 summarizes test results and their potelllial meaning.
withoul fraclure, neuropalhic arthropathy, pigmenled vil lonodular synovitis. synovioma, hemangioma. and other benign neoplnsms.
Thyroxille
In general. high free or tOlal T4 results may indicale an overaclive thyroid gland (hyperthyroidism). and low free or
Thyroid Profile
10lal T4 resulls may indicale an underactive thyroid gland
Free Thyroxine Jilt/ex
(hypothyroidism). The test resuils alone are nOI diagnoslic
The free thyroxine index ( Ff l or T7) is a mathematical
but will prompt t.he examiner to perform additional teMing
computation thm allows lhe laboratory to estimate the free
10 invesligale the cause of Ihe excess or deficiency. Both
Ihyroxine index from Ihe Ihyroxine (T4) and lriiodOlhyro
decreased and increased T4 results are associated with a
nine (T3) uplake leSls. The resuhs lell how much thyroid
variety of temporary and chronic thyroid conditions. Low
hormone is free in the blood stream 10 work on the body.
T4 resuils in conjunction wilh a low TSH level. or high T4
Unlike Ihe T4 alone, Ffl
is not affected by estrogen
resuils along wilh a high TSH, may indicate a piluitary gland
levels.
condition.
Thyroid·Stimulating Hormoll('
meaning.
Table 1 ·8 summarizes lest results and their potential A high Ihyroid-stimulaling hormone (TSH) resuh often means an underactive thyroid gland that is not responding
T,.iiodot"yrollille
adequalely 10 the slimulalion of TSH because of some IYpe
Increased or decreased thyroid hormone results indicate an
of acute or chronic thyroid dysfunction. In rare instances, a
imbalance bel ween Ihe body's requiremenls and supply, bUI
high TSH resuh can indicate a problem wilh Ihe pituilary
they do not lell the examiner specifically whal i s cau,ing Ihe
gland. such as a tumor that produces unregulated levels
excess or deficiency.
of TSH, in what is known as secondary hyperThyroidism. A high TSH value can also occur when palienls wilh a
Table 1 -9 summarizes test results and their potential meaning.
known thyroid disorder (or those who have had their thyroid
If a patient is being treated with antithyroid medication
gland removed) are receiving inadequate thyroid hormone
for hyperthyroidism and Ihe T3 (or, morc frequeJ1lly, the T4
medicatioll.
or TSH) is normal, then the medication is likely controlling
A low TSti resull can indicate an overactive thyroid
the condition. If the T3 (or T4) is elevaled, Ihen Ihe medica
gland (hyperthyroidism) or excessive amOUI1lS of dlyroid
lion is not sufficient to control the condition, and the palient
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27
CHAPTER I Principles in Assessing Musculoskeletal Disorders
the most useful in this range. When patients in Ihe gray lone
TAB L E 1·8
have decrea\ed levels of free "SA. lhey have a higher prob
SUMMARY OF THYROX I N E (T4) TFST RESULTS
ability of proslate cancer; when Ihey have elevated levels o f
AND I NTERPRETATIONS
free PSA. the risk is dimin ished. The ratio of free to total
T4
T8H
T3
Interpretation
Nannal
HIgh
NOnllal
Mild (�ubcJinic
Low
High
Low or nonna1
Ilypothyroidi..m
Nannal
Low
Nonnni
Mild huOclinicnl)
High or normal
Low
High or nomlal
Hypcnhyroidi"m
Low or normal
Low
Low or nonna!
Rare pituitary
hyperthyroidism
PSA can help the examiner decide whelher a proslate biopsy should be performed. When the complexed PSA (cPSA) test is used as a screen ing tool. increa.\cd leyels may indicate an increased ri\k of prostate C�1J1cer. whereas lower Icvels indicate a decreu\cd risk. In addition to lhe inlroduction of the free PSA and cPSA tests. efforts have been made to increase the u"iefulnes!o. of
(!ooccondary ) hypothyroidi..m n. Triiuollihyronlllc; 14. thyroxine; TW/, thyroill-..llIl1ulallllg hormone.
the total PSA as a screening 100\. A l lhough none of these efforts have been widely accepted yet. researchers are study ing them. and some examiners are using them. These factors include: PSA velocilY. This tesl mea,ures the change In PSA con centrations over time. If the PSA continues 10 risc sig nificantly over time. such as 3 or more years. then proslatc
TABLE I ·') SUMMARY Of TRIIODOTHYRO N I N E
canccr is morc l i kely present. I f it climbs rapidly. then lhe
(D) TEST
patient may have a morc aggre...sive form of cancer.
RESULTS AND INTERPRETATIONS
T4
T3
T8H
Nannal
Nonnal
High
•
Interpretation Mild bubclimcal) hypothyroidi..m
LO\I, or nc.mnal
Lo"
High
Hypothyroidism
r\onnal
Nonnal
Low
Mild (..ubclinical) hyperthymidi..m
PSA doubling lime. This leM i!o. another version of the PSA velocity. 11 measures how rapidly Ihe PSA concen tration doubles. PSA densilY. This te'l is a comparison o f Ihe PSA con· centration and the volume o f the prostate (as metlsurcd by ultrasound). Paliel11S with larger prostates tend to produce morc PSA; thus. thi'i factor is an adjuslment to
High or nonnal
High or 00011al
Low
Hypcnhyroidh,m
compensate for the SilC.
Low or normal
Low or 110mlal
Lo"
Rare pituita!)
Age-specific PSA ranges. Given Ihat PSA le,e1s nalurally
7J, Triiodulh)roninc;
hccondaryl
increase as a man ages. experts have proposed thal nonnal
hypolhyroidi'im
ranges be tai lored to a man's age.
T.J, Ihyro'(illl:: TSH. Ih)roji.J-_�lillluJaling hormone.
During trealment for prostale cancer. the PSA level should begin to fall. At the end of treatment. it should be al very low or undetectable levels i n the blood. I f concentra tions do not fall to very low levels. Ihen lhe trcalment ha,
may be experiencing symptoms associated with hyperthy
not been fully effective. After Ireatment. Ihe PSA lesl is perfonned at regular intervals to monitor the patient for
roidi!o.ITI.
recurrence. Because even tiny increases can be signi ficant.
Prostate Profile
patients may want to have their monitoring PSA tests per fonned by the same laboralory each time so Ihal testing
I'ro.\llIl(·.Sp(·ciji(' \ IIli/.:(·11
The normal value for lOWI proslale·specific anligen (PSA)
\'arialion is kept to a minimum.
has heen ScI at less Ihan 4.0 ng/mL blood. Some experls believe lhat Ihis level should be lowered to 2.5 ng/mL to
IJro.\ltItil- \cill Phmpllllla.\"l!
detect more C3SC!o. of pro"tate cancer. Other" argue that this
Pro'tatic acid phosphatase (PAP) is an enlyme produced by
change would exacerbate overdiagnosing and overtreating
the prostate. It may be found in increased amount.s in mcn
cancers that are not clinically signilicant.
who have prostate cancer or other diseases. This same
Mosl experls agree thai palients with a total PSA level grealer than 10.0 ng/mL are aI an increased risk for pros laiC
enzyme is also found in significant amounts in female ejaculate.
cancer (more than a 67CJr chance. according to the American
The highesl levels of PAP are found in melaslasized pros·
Cancer SocielY). Levels belween 4.0 and 1 0.0 ng/mL may
tate cancer. Diseases of the bone (e.g .. Pagel di,ease. hyper
indicate pro'itatc cnncer (approx imntcly a 25% chance.
parathyroidism). diseases of blood cells (e.g
according to the Americnn Cancer Society). benign prm,tntc
disease. multiple myeloma). or lysosomal storage disease,
hyperplasia.
(e.g .. Gaucher disease) will sho\\ moderalely increased
or
pro'itutitis.
Thc'ie conditions
are more
common in older adult males. as is a general increase in
.•
sickle-cell
levels.
PSA levels. Concentrations of total PSA between 4.0 and
Certain medicmioJ1!o. can cau-,e temporary increa!o.c!o. or
10.0 ng/mL arc often called the gra\" :olle. The free PSA is
decreases ill PA P levels. Manipulation of the prostate gland
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28
CHAPTER I Principles in Assessing M usculoskeletal D isorders
through massage. biopsy. or rectal examination before a tcst
lligll-Dellsity Lipoproteill Cilolesterill
can increase the level.
LDL cholesterol •
Hypertension ( Coronary Risk Profile)
Health Screen
Cholesterol •
Triglycerides
Coronary risk indicator
•
This is a group of tests and health faclOrs have been
Albumin Low albumin levels can suggest liver di\ease. Other liver
proven to indicate a patient's chance of having a coronary
enlYme tests are ordered to detemline exactly which type of
evenl. They havc been refined to indicate the degree of risk:
liver disease. Low albumin levels can also reflect diseases in which the kidneys cannot prevent albumin from leaking
slight, moderate, or high. Perhap� the most important indicators for cardiac risk are
from the blood into the urine and being losl. In this case. the
those of the personal health history. Age, hereditary factors.
amount of albumin (or protein) in the urine also may be
weight. smoking. blood pre sure, exercise h istory, and dia
measured. Low albumin levels can ;]Iso be seen in inflam
betes arc all important in determining risk. The lipid profile
mation. shock. and malnutri tion. Low albumin levels may
is the most important blood test for risk assessmenl. Other
also suggest conditions in which the body does nOl properly
tests, bOlh invasive and noninvasive, may be used in cardiac
ab,orb and digest protein (e.g
risk assessment. Noninvasive tests may include an electro
which large volumes of protein are 10M from the intes
cardiographic stress lest, thallium SlrcSS lest. electrocardio
tines.
.•
Crohn di,ea,e. 'prue) or in
gram, computed tomographic scan. and echocardiogram.
High albumin levels usually reflect dehydration.
I nva�ivc tests include an arteriogram and cardiac catheter
NG ratio (See previous discussion.)
ization.
Alkaline phosphatase
The lipid profile measures cholesterol. triglycerides. HDL
Anion gap
(good cholesterol), and LDL (bad cholesterol). Triglycerides
Anion gap can be classified as high. normal. or. in
are the major form of fat found in the body. and their func
rare cases, low. A high anion gap indicates a lo�s of bicar
tion is to provide energy for the cells. The de,irable ranges
bonate without a subsequent increase in chloride. Electro
for the components of the lipid profile include the follow
neutrality is mail1lained by the increased production of
ing:
anions such as ketones, lactate. phosphate. and sulfate; lhese anions are not part of the anion-gap calculation. and there
Cholesterol <200 mg/dL (5. 1 8 mmollL) HDL cholesterol >40 mg/dL ( 1 .04 mmollL)
fore a high anion gnp results. In patiel1l� with a normal
LDL cholesterol < 1 00 mg/dL* (2.59 mmol/L)
anion gap. the drop in bicarbonate is compensated for by
Triglycerides < 1 50 mg/dL ( 1 .70 mmollL)
an increase in chloride and hence i ... also known til., hyper
If any or all of the results arc significantly outside these
chlorcmic acidosis.
ranges, the risk of a cardiac event is increased. If they are only slightly outside the desirable level. diet, exercise, med ication. or any combination of these treatments may be suf
Higtt Illiol/ Gap
ficient to reduce the abnormal levels. thereby reducing
The bicarbonate 10M is replaced by an lInmea�ured anion.
ri�k.
and thus a high anion gap will be present in the following
Another test gaining importance is serum homocysteine.
disorders:
Homocysteine is un amino acid that comes from the normal
Lactic acido�is
breakdown of proteins in the body and appears to be a beller
Ketoacidosis
test than cholesterol testing for predicting heart disease,
Diabetic ketoacidosis
stroke. and reduced blood now to the hands and feel. Lipo
Alcohol abuse
protein A (Lpl a J ) is a lipoprotein consisting of an LDL
Toxins:
molecule with another protein (apolipoprotein A) attached
Ethanol
to il. Lp(a) is similar to LDL but does not respond to typical
Ethylene glycol
strategies to lower LDL such as dict. exercise, or most lipid
Lactic acid
lowering drugs. Given that the level of Lp(a) appears to be
Methanol
genetically determined and not easily altered. the presence
Paraldehyde
of a high level of Lp(a) may be used to identify individuals
Aspirin
who might benefit from more aggressive treatment of other
Cyanide. coupled with elevated venous oxygenation
risk factors. A fairly new test, high-sensitivity (hsCRP), may
Iron
be measured on apparently healthy patients to detemline if
Isoniazid
they are at risk for a coronary event. evcn if their lipid levels
The mnemonic MUDPILES is used to remember the causes of a high anion gap.
are normal or borderline elevated.
Methanol/metformin *Oplim:tl le'o'cl, will depend on the number and type of ri-;k facloN prcsclll and whether testing i.. being used in primary or secondary intervention
Uremia I!iabetic ketoacidosis
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CHAPTER I Principles i n Assessing Musculoskeletal Disorders faraldehyde/propylene g l yco l
29
Blood, which consists largely of the protein hemoglobin,
In reClion/ischcl11i vi .. son i azid
is broken down by digestive enzymes of the upper GI
Lactate
tract into amino acids.
Ethylene glycol/ethanol
The amino acids. which origimlte from the hemoglobin,
S.al icylate,/starvation
are reabsorbed by the lower G I tracl.
Some people. especi al ly those not in the emergency
Urea is a break-down product of amino acid catabolism;
room. find the mnemonic KILU easier to remember and also
therefore, the protein meal from an upper GI bleed shows
more useful cli ni cal ly :
lip in the blood as urea.
Ketone;
Because of decreased muscle mass. elderly patients may
Ingestion
have an e le vated B U N/creatinine ratio at baseline.
,Lactic acid
Calcium
Uremia
Calculated LDL CBC
All of lhe componeJ1ls of M UDPILES are also covered
with the KILU device. with the added imperative that these
Chloride
th ings can kill a patie nt
Cholesterol
.
Ketones: morc slraigillfofward than remembering dia
CholeslCrol-HDL ratio
betic ketosis, starvation ketosis, and so forth.
Creatinine
Ingeslion: methanol. metfonnin. paraldehyde, propylene
GGT (Sec earlier discussion.)
glycol. i;oniazid. ethylene glycol. ethanol. and sal icy
G lobul i n
lales are covered by i ngestion. These substances can
Globulins are roughly divided into alpha. beta. and
be considered as a single group-illgesliolls-during
gamma globulins. These values can be separtlled and mea
the initial con�idcration. especially when nOt triaging
sured in the laboratory by techniques called electrophoresis
a patient in the emergency room.
and densitometry. The gamma fraction includes the variou�
LaclicAcid: including that caused by infection and shock
types of alllibodies ( immunoglobulins M, G, and A).
(U,ually the bicarbonate lost is replaced by a chloride
Normal values are:
anion. and thus the anion gap is normaL)
Serum globulin: 2.0 to 3.5 g/dL
Gastrointestinal loss of bicarbonate (e.g., diarrhea) (
IgM component: 75 10 300 mgldL IgG component: 650 to 1 850 mgldL
ote: Vomiting causes hypochloremic alkalosis.)
Renal loss of bicarbonate (e.g.. proximal renal tubular
IgA component: 90 to 350 mgldL
acidosis)
I ncreased gamma globu l i n proteins may i ndicate:
Uremia: Renal dysfunction (e.g .. renal failure. hypoal
Multiple myeloma
doslcronism, distal renal tubular acidosis)
Chronic inflammatory disease (e.g., RA, SLE)
A low anion gap i� re l at ive ly rare but may occur from the
Hyperimmun ization
presence of abnormal positively charged proteins. as in mul
Acute infection
tipl e myelom a or in the settin g of a low serum albumin
Waldenstrom macroglobulinemia
,
level.
Glucose
Bilirubin (IOtal)
HDL
BUN (See earlier discussion.)
•
BUN-creatinine ratio
The B UN/creatinine ratio is
Ionized calcium LDH
a
rmio of two laboratory test
Phosphorus
values: the BUN and serum creatinine. It is used in the United States. Elsewhere (Canada. Europe). urea is used
Potas� i U 111 •
Serum glutamate ox aloaccta te transaminase
instead of BUN; thus. it is the urea-lo-creatinine ratio, also
Serum glutamate pyruvate transaminase
urea-creatinine ratio. and urea/creatinine ratio.
Sod i um T4 radioimmunoassay ( R I A )
The BUN/creatinine ratio is predictive of prerenal failure, if the BUN-to-creatinine r'Jtio is greater than 20 or the
T4 b y RIA i s the most widely used thyroid test of a l l . I t
urea-Io-creatinine ratio of marc than 0. 1 0 and urea of more
i s frequently called a T7, which means that a resin T3 uptake
than 1 0. I n prerenal fai lure, urea rises out of proportion
(RT3u) has been accomplished 10 correc t for certain medica
to the creatinine because of enhanced proximal tubular
tions such as birth control pills, other hormones. seizure
reabsorption
medication. cardiac dru gs, or even aspirin that may alter the
.
The BUN/creatinine ratio is useful for the diagnosis of
routine T4 tesl. The T4 renects the amount of T4 in
upper gastrointestinal ( G I ) bleeding in patients who do not
the blood. If the patient does not take any type of thyroid
exhibit overt vomiting of blood. In children. a B U N/cremi
medication. this test is u su al ly a good measure of thyroid
nine ratio of 30 or above has a sens i tivity of 68.80/0 for upper
functi on
GI b leeding and a specificity of 98%.
•
The reason the urea concentration increases in upper GI bleeds is as follows:
.
Total carbon dioxide Carbon dioxide levels that arc higher or lower than
nonnal suggest that the body is having troublc mainwining
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30
CHAPTER I Principles in AssessLng Musculoskeletal Disorders Normal synovial nuid is a hypocellular. avascular con nective tissue. In disease, the synovial Huid increases i n
SYNOVIAL FLUID
volume and can b e aspirated. Synovial Auld is a transudate
For three significant aspects, analysis of synovial fluid differs from other body fluids: I . Neoplastic processes rarely arfect synovial joints.
2. Recognition of noncellular paniculate material, such microorganisms and crystals and cartilage frag
as
ments. is essential for defining the disease process affecting the joint.
3. Diagnostic information comes not only from recogni tion of cell types but also from their quantification.
of plasma supplemented with high molecular weight. sac charide-rich
1110lecules. The
1110st notable of these
is
hyal uronan (hyaluronic acid). which is produced by fibro blast-derived type B synoviocyte ( Box 1-3). Variation in the volume and composition of synoviai lluid reRects pathologic processes within the joint.
ORTHOPEDIC TESTS In the orthopedic physical examination, a test is positive or a sign is present when the procedure dupl icates the patient's complaint or symptom. Tests are based on joint, muscle, or
its acid-base balance or that the electrolyte balance is upset,
nerve function. If testing causes different pain or symptoms,
perhaps by losing or retaining fluid. Both of these imbal
it may indeed be significant, but the result is nOI positive for
ances may be the result of a wide range of dysfunctions.
the findings that Ihe test was designed to elicit.
•
Total protein
During an examination, the examiner must use techniques
Triglycerides
that defeat the human tendency of exaggeration. The exam
Uric acid
iner must conduct several tests and multiples of similar tests
Synovial fluid
so that the patient is not aware of which specific tissue func tion is being examined. Wilh lime and exposure to a myriad of orthopedic disorders. examiners develop the skill and
IIOX
accuracy necessary to reach diagnoses efficiently. However.
1-3
interpreting the results of examination processes in a clini
N O RMAL SYNOVIAL F L U I D
caJly meaningful way requires the examiner to consider the reliability of the clinical measurements and tests.
OsmOlarity
296 mO,mIL
pH
7.44
Carbon dioxide pressure
6.0 kPa (range 4.7-7.3)
Oxygen prc�surt!
<4.0 kPa
sures, bUI also on the sensitivity and specificity of the signs
Potassium
4.0 mmoJIL
Sodium
136 mmoUL
elicited by the test procedures.
Calcium
1 .8 mmollL
Urea
2.5 mmoUL
Uric acid
0.23 mmollL
Glucose
tOO mmollL
Chondroitin sulfate
40 "'gIL
Hyaluronate
2. t 4 gIL
Interpretation and analysis of examination procedures depend not only on Ule reliability and validity of such mea
DIAGNOSTIC IMAGING MODALITIES IN ORTHOPEDICS I maging procedures are important to the diagnosis and man agement of an orthopedic condition. The decision to use any
Cholesterol
Small amounts
diagnostic imaging procedure, especially ionizing imaging
TOl..lI prolein
procedures, should be based on a demonstrated need and
Albumin
-25 gIL -8 gIL
(Xt-antitrypsin
0.78 mcglL
CcnllopJasmin
obtained and a physical examination is conducted. The deci
Haptoglobin
-43 I1lgIL -90 mgIL
(X.:z-macroglobin
0.31 gIL
Laclofcrrill
0.44 mglL
IgG
2.62 gIL
IgA
0.85 gIL
IgM
0. 1 4 gIL
lL-I�
20 pglmL
IL-2
1 5 . t U/mL
TNF-ct
1 .38 hglmL
INF-ct
350 U/mL
INI'-o
13.7 U/mL
should be used only after an adequate medical history is sion to use any imaging procedure must also be based on the assumption lhat the results of the eXIDllination. even if negative, will significantly affect the treatment of the patient. The value of the information gained from the imaging exam ination must be worth the possible detrimental effects of the procedure. In imaging modalities tJlat use ionizing radiation (plain-film radiography, fluoroscopy, and considered (Fig. 1 - 1 7 ).
Plain-Film Radiography (Conventional Radiography)
IgA. Imml.lll/)gfo/JII/ifl A; IgG. imfllllllog/oi>u/ifl G; IgM. imlllllllog!obllUn M: IL. imerle"k;lI: INF. illft:ljI!l"Ofl: TNF. tulllor-necrosis/aclor:
Adapted from Klippel lH. Dieppe PA: RlwulI/lIw/agy. \'0/ /·2. ed 2. London. 1998. Mosby.
CT), the possible
effect of radiation on the patient or future offspring must be
Plain-film radiography. or conventional radiography. pro vides a wide and di verse array of diagnostic data about musculoskeletal problems. such as soft-tissue injury. bony
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31
CHAPTER I Principles in Assessing Musculoskeletal Disorders malalignment, loss of integrity of the osseous structures. and
The patienl's history and clinical evaluation are guides that help determine which portion or portions of the body
joint space abnormality. Plain-film X-ray examination is an efficient way to dis cover dislocations, fracLUres, the static component of ana
requires plain-film imaging and how many different views should be produced (Fig. 1 - 1 8 ) .
tomic subluxations. certain types of stress injuries. metastatic
Radiography i s a useful tool in the initial assessment
disease, some types of primary tumors, metabolic disease,
of rheumatologic disorders because it may providc specific
degenerative arthropathic diseases (Table 1 - 10). and abnor
infomlalion thaI contributes to establishing a diagnosis.
malities in the growth plate.
Various rhcumatologic disorders have unique fealUres that
Soft-tissue structures require careful scrutiny on film
can be easily detcclCd with plain-film radiographs. Abnor
because they may offer subtle clues to serious or underlying
malities on plain-film radiographs can be detected with a
pathologic abnormalities.
high degree of sensitivity. Serial radiography is useful in
A radiologic evaluation of the traumatized sites should
measuring structural damage, and features such as erosions.
include films of the adjacent joints. If a need exists for
joint space narrowing. and disease-specific findings can hclp
special projections, other radiologic investigation may be
gauge response to therapy (Dry. 2003).
necessary (Table I - I I ). Care must be taken to investigate the possibility of asso ciated injuries in trauma victims (Table 1 - 1 2). Patients may not realize that such injuries have occurred.
Tomography Conventional tomography is also known as thill-section radiography, planigraphy, and linear tomography. Conven
tional tomography is largely replaced by CT. However, some circumstances. such as evaluating sublle alteralions of bone density and ruling out fracture, necessitate conventional
lA I\ L E 1 · 1 0
tomography. CT scans are used for more detailed apprecia
PLAtN- F t LM EVALUATION t N DEGENERATIVE
tion of skeletal pathologic processes, which can help evalu
ARTH ROPATHIC DISORDERS
ate suspected intervertebral disc protrusions or herniations,
Diagnosis
Site of Plain-Film findings
Psoriatic anhritis
Hand. sacroiliac joints (common):
facet disease. or central canal and lateral recess stenosis. I f spinal disease is suspected and is not well idenlified o n plain films and the patient is not responding to care, a CT scan is
pubis symphysis, hip, knee (less
indicated. A CT scan is especially useful for the appreciation
common) Rheumatoid arthritis
of bone and caJcifications and surpasses magnetic resonance
Wrist and hand, shoulder. knee.
imaging ( M R I ) in this regard.
cervical spine. hip Spondyloarthropathy
Sacroiliac joints. thoracolumbar spine
Osteoarthritis
Lumbosacral spine, hip, knee. foot
CT has been useful in a wide variely of musculoskeletal disorders, including those related 10 trauma (Fig. 1 - 1 9), back pain (e.g., herniated nucleus pulposus) (Fig. 1 -20), and met
and ankle, hand
abolic bone disease (e.g .. osteoporosis, tumor and soft-tissue masses). Two thirds of patients with multiple injuries suffer from blunt chest trauma. and severe thoracic trauma is associated with multiple injuries in 70% lO 90% of cases (LoCicero J 3rd. MallO •. 1989; Pinilla. 1982).
f i G . 1 - 1 7 From left to right and top 10 bottom, An arias of I/ormal roelllgell variants fhat may simulate disease (by
Theodore E. Keats). gonadal shielding, sandbag, DuPont
F I G . 1-18 Displacemenl of fat pads in the elbow by joint
Quanta Delail Rare Earth X-ray casselle screens, and com
effusion. (From Klippel JH. Dieppe
patible film.
London. 1 998. Mosby.)
Copyrighted Material
PA: RheumatOlogy. vol 1-2.
ed 2.
32
C HAPTER I Principles in Assessing Musculoskeletal Disorders
O R1 1101'1 \l I L GAMli r I 2\
ARTHRITIDES: D IAGNOSIS AND CLINICAL PROGRESSION ASS.ESSMENT STEPS IN RHEUMATOID ARTHRITIS, PSORIATlC ARTHRITlS, ANKYLOSIS SPONDYLITlS, AND OSTEOARTHRITIS radiographs of pelvis, sacroiliac joints, and axial spine
Rheumatoid arthritis Serial radiographs (posteroanterior [PAl view) of hands,
•
annually or every other year
wrists, and feet at baseline and at 6-month intervals for
Serial radiographs ( l ateral and AP views) of cervical,
a minimum of 2 years after onset
thoracic, and lumbar spine annually or every other year
Monitoring frequency decreased after 2 years in patients
Radiographs (PA view) of hands and feet at baseline;
without erosions at 2 years
fol low-up radiographs based on clinical features
Distinguishing radiographic features: bilateral symmetri
Distinguishing radiographic features: cervical lesions not
cal involvement of the small joints ( hands, wrists, and
typically associated with instability and subluxations of
feel),juxtaanicular osteopenia, lack of proliferative bone
the lower five vertebrae as in rheumatoid arthritis, less
response, marginal erosions. joint space narrowing.
severe hip lesions than in rheumatoid arthritis without protrusions, osteophytcs along the margin of articular
Psoriatic arthritis •
•
(and spine and other joints if symptoms are present) at
in consecutive vertebrae. sacroiliilis. 'bamboo spine,'
baseline and at 6-month intervals for a minimum of 2
smaller and more localized erosions, and less frequent
years after onsel
joint space narrowing and osteopenia compared with rheumatoid arthritis
Distinguishing radiographic features: asymmetric and possibly oligoarticular joint involvement, initially mar
Osteoarthritis
ginal erosions lhat become irregular and ill defined, distal
•
interphalangeal joint involvement, abnormalities in pha
•
Radiographs (PA view) of the hrulds and fect annually Radiographs of the hips (AP pelvic in supine position)
langeal tufts and at sites of uuachmcnts of tendons and
and knees (standing, weight-bearing AP with full knee
ligaments to the bone, possible spondylitis, paramarginal
extension) annually
syndesmophytes in nonconsecutive vertebrae, sausage
Distinguishing radiographic features of osteoanhritis:
digits, proliferative bone changes, and ankylosis
osteophytes, subchondral sclerosis Distinguishing radiographic features of erosive osteoar
Ankylosing spondylitis
•
canilage of the femoral head, marginal syndesmophytes
Serial radiographs (PA view) of hands, wrists. and feet
Serial radiographs (anteroposterior IAPI view) of pelvis.
thritis: distribution in distal joints of fingers similar to
sacroiliac joints. and axial spine
that of psoriatic anhritis; centrally located erosions; ero
If early ankylosing spondylitis is suspected, repeat pelvic
sions typically absent i n metacarpophalrulgeal joints
radiographs 6 months from baseline; otherwise, serial Adapted from Ory PA: Radiography in the aSSCS\IllC'llt of mu,>culoskeletal condj(ion�, Ik�/ Prtlc/ R('\ Clin Rlll'lflll 17(�1:495·5 1 2 . 2003.
Among hlum injuril!!oi 10 the chest. lung contllsion is con!'lidcred one of the mo�t important factors contrihuting to
Discography Although effective, discography has been a controversial
the incre"lsed morbidity and mortality of patients with mlll�
imaging modality for spinal disc disease. Clinicians use
riple injuries (Johnson. Cogbi ll. Winga, 1986: Schild el al.
discography for specific cases of spinal pain that arc recal
1 986).
citrant to conventional therapy. emergency
Discography is an important diagno�tic procedure in which
department for blunt injuries to the chest includes a routine
disc pressure comrolled by need le injection is correlated
chest x-ray taken in the supine position m ; d an ultrasound.
with degree of lumbar pain rcp<Jrred by the patient. Although
Despite this approach. significam injuries such as pneumo
imaging studic'i. such MRI. call be used to document paLho
The
usual
diagnostic
work-up
in
rhe
thoraces. hemothoraces. and lung contusions can be missed
logic changes in the disc. some studies have 'ihown a poor
during the initial trauma assessmem (W:'lgner, Jamieson,
con'e1ation between MRI findings and clinical symptoms
(989).
because di!'lc degeneration and hernimion incrc<'lsc wil.h
CT scanning is accurate in visualizing intrathoracic inju
normal aging (Boden el at. 1990).
ries. In addilion, the availabil i ty, reliability, and low com
The high incidence of asymptollliltic findings on MRI
plication rate of CT scans has led to its widespread use in
makes imcrprelalion of patienl ,,(udies morc difficult becau\c
the evaluation of blunt trauma.
each imaging finding must be closely correlated 10 symp
Clinicians often use the noninvasive technique of quan litatjvc CT to mea�ure bone mineral density.
LOIllS Ihat can be relatively nonspecific in mallY palicllls.
MRI alone is not able 10 differentiate \ymplOmatic from
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33
CHAPTER I Princi ples in Assess ing Musculoskeletal Disorders
TA B l E I- I I PREFFRR£D RADIOGRAP HIC VI EWS I N SKE LETAL TRAUMA
Arca
Specific Views
Area
Specific Views
Skull
POSlCroanlerior or anteroposterior Caldwell
Sternum.
Posteroanterior
Townes
sternoclavicular joinLS
Uilcral (one lateral should be upright)
Right and left anterior obliques with cephalad angle of lube Lateral
Facial bones
Elbow
Waters
Anteroposterior
Modified Waters
Lateral
Caldwell
Capitellum
Lateml Cervical spi nc
Anteroposterior
Radioulnar joims (forearm)
Coned odontoid or oflhopanlogram
A meroposlerior or posteroanterior Lateral
Odontoid Lateral (cross�table or upright) Swimmer latem! (cross-table) BOlh obliques, when possible Thomcic spine
Wrist and hand
Anteroposterior
Posteroanterior
Lateral (cross-table or routine)
Oblique imerna!. ex.temal. or both
Swimmer (coned to upper thoracic spine)
Lateral Navicular views. if needed
Lumbar spine
Pelvis, acetabulum
Anteroposterior
Anl.eroposterior Obliques (Judet)
L
Hip. proximal part
Anteroposterior (tube-angled cephalad)
of femur
Lateral
Anteroposterior pelvis Frog·leg or cross-table lateral Obliques
Chest
Femur
Posteroanterior or anteroposterior
Anterol>osterior (to include hip and knee) Lateral (to include hip and knee)
Left lateral (may not be possible in Lrauma) Lateral decubitus (pneumothorax.. pleur'c11 Ouid) Ribs
Distal part of femur
Anteroposterior or posteroanterior Oblique
and knee
Anteroposterior Latcml Tunncl Internal oblique
Shoulder
Tibia. fibula
Anteroposterior (internal rOlation)
Antcroposterior (to include ankle and knec) Lateral (to include both joints)
Anteroposterior (ncutml) Transscapular lat.eral (NeeI') Axi llary Humerus
Anteroposterior (to include elbow and shoulder)
Ankle
Latcml (10 include both joints)
Anteroposterior Oblique (mortise) Lateral
Clavicle
Anteroposterior or posteroanterior (to include
Calcancus
Tangential Lateral
both joints with and without weight bearing) FOOl
Laternl Anteroposterior Oblique Lateral
From Gu:;tilo RB. Kyle RF. Templeman DC: Fr(lCfU"e� ami (/islocmio//'\', 1'01 I. 51 Louis. 1993. Mosby,
asymptOmatic degenerative disc Changes (Scuderi et al. in
Lhe sagittal, coronal, o r axial planes, a s well a s a n y other
pres:;).
oblique plane desired. The MRI can i mage neuro logi c struc tures and other soft tissues and can reveal disc degeneration
Magnetic Resonance Imaging
before any other imagi ng method. Indications for MRI are
M R I is a computerized, thin-section imaging proced ure that
similar 10 those for CT. M R I is superior to CT for the
uses a magnetic field and radio·frequency waves rather than
evaluation of suspected spinal cord tumors or damage intra
ionizing radiation. M R I can produce thin-section images in
cranial disease. and various types of central nervous system
.
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34
CHAPTER I Principles in A"essing Musculoskelelal Disorders
" IZI II"I' I I) l l (,\\\1 1 1 ' j
ASSESSMENT ABILITIES AND LIMITATIONS OF PLAIN-FILM RADIOGRAPHY
r------
I . Plain- if lm radiography is Ihe leasl expensive and mosl widely ..vailable imaging lechnique.
2. Radiography offers higher spalial resolulion than any other modalily, providing exlremely high contrast for cortical and trabecular bone. 3. Radiography affords only a projectional viewing per spective.
4. Projeclion of three-dimensional anatomy onlo a 1\\'0dimensional film results in morphologic distortion and superimposilion of overlapping struclures.
5. The sensitivily for trabecular bone los> is relalively poor.
6. As much as 30% 10 50% of lrabecular bone must be removed before Ihe change becomes perceplible on convenlional radiographs.
7. The contrast for soft lissues Ihal are not calcified or fauy is relatively poor.
8. Radiography cannOI directly visual ize Ihe articular cartilage, inflamed synovial lissue, joint effusion, bone marrow edema, or intraanicular fat pads.
(1IZIII " I' I I) I (
(,\\\1 I I "
ASSESSMENT A B I LITIES AND LIMITATIONS OF COMPUTED TOMOGRAPHY I . The grealeS! advantage of CT over convenlional radi ography is its lomographic nalure.
2. CT provides high contrast belween bone and adjacem
F I G.
1-19 Complex acetabular fraclure. A, Anlcropo,lerior
tissues and is excellent for evaluating osseous struc
plain film. B, Axial computed tomography scan. (hum GU'lilo
lures.
R H . Kyle RF. T�mplcman DC· rraC"lIln.'\ mul di,hlnllimu. \01 I Sl l.oui,
3. CT offers slightly grealer SOh-lissue contra>! than
1993. M
radiography.
4. Image contrasl is insufficienl lo visual ile the articular canilage or synovial tissue or to discrimjnate between cilha diagnmm. or operative planning. A "'OfHiv..ue rna..... In
lendonilis and tendon ruplure.
5. CT reveals only Ihe surfaces of these struclures; il does nOI disclose intra substance changes that may precede gross morphologic disruption.
the hand may be a manifc..tallon of ncopla...m. congenital malformation. infection. other inOammalory proce ...... or trauma. Infcctiou... and traumallc cau ..c... arc more prc\alcOi
111 pediatric palicllI!'I than ncopla,ia or congcmtal malfonnalion. The evaluation of the...e ma,...c!'l ...hould IIlclude an a....e . .... menl
di «asc (e.g .. multiple sclerosis). M R I is especially lIseful in
of the extent of the ...oft-u......ue.
m...cou....
and
ncurova,cular II1volvement. Of all Ihe lIunging ImxJalllle"
identifying small di fferences among similar soft tissues and
MRI i ... he..., ..uiled for ,hi... role (Jimene/. Jaramillo. Con
surpa"es CT in Ihis regard.
nolly. 2(05 ).
The evaluation of a child with a \uspccted ..oft ti"..uc mass
In Ihe management of low back pain and lumbar degen
III the hand i.., . 1 chal lenge. Imagmg evaluation ... houkl t>egin
erative kyphosis disorder!'!, paraspinal muscles are subjected
with radiograph... that l11a) reveal the diagno..i!'!. Further
to many slUdies using ultrasound, CT. needle eleclromyog
· ith uhra...ound. CT. or MRI is often required for imaging ....
raphy (EMG). and histopalhologic analysis. MRI can evalu-
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35
CHAPTER I Principles in Assessing Musculoskeletal Disorders fA 1l 1 E 1- 1 2 I N I U RI ES ASSOCIATW WITH SKELETAL TRAUMA
Fracture
Associated Injury
Bone and bone
Remote additional spinal fracture
Spine
Scapula fracture
Chest wall
Sacrum fracture or dislocated
Anterior pelvic arch Femoral shaft
sacroiliac joint Fracture or fraclUrc-dislocation of hip
Tibia (severe) Calcaneus
Dislocated hip Fractured thoracolumbar spine
Bone and viscera
Ruptured mcscnlcry or small bowel
Chance fracture of spine
Laceration of liver. spleen. kidney. or diaphragm
Lower ribs Pelvis
Ruptured bladder or urethra
Pelvis
Ruptured diaphmgm
Bone and vascular
F I G . 1-20 Axial image showing a right paracentral hernia
lion of the nucleus pulposus.
Ruptured aona
(From Brier SR: Prim(lr" {"(Ire orOw
/u'lJicl. 51 Lou i )l. 1 999. Mo�by.)
Ribs I . 2. or 3
Myocardial contusion
Sternum
Laceration of pelvic arterial lree
Pelvis
Laceration of femoral artery
Obtai third femur
Popliteal ancl)' laceration
Knee dislocation Adapted from Roger� IF. Hendrix RW: Evaluating the multiple injured patient radiographically. Orillop CIi" Norlll Am 2 1 (3):444. 1990.
O RI II O I' I Il I ( (,,\ �1l1 1 1 '>(,
OIU 1101'1 J) I ( (, ·\ M ll I I 2 7
fOR CERTAIN PATHOLOG [ C COND [ TlONS, MAGNETIC RESONANCE IMAG[NG [ S THE D LAGNOSTIC PROCEDURE O f CHOICE I . Spinal disc disease
USES Of DISCOGRAPHY
2. Medullary tumor
To rule out disc involvement. especially as a cause of postoperative pain To detennine the appropriate level for spinal fusion To test the potential effectiveness of chemonucleoly sis
3. Mulliple sclerosis
4. Cerebral edema 5. Spinal stenosis 6. Metastatic disease 7. Hemiated disc 8. Discilis (or infection)
To visualize internal disc anatomy
9. Meniscal lear ( fibrocartilage abnormalities) 10. Central nervous system tumor
I I . Soft-tissue tumor ate fatly infiltration in the muscles and the fascia status overlying the muscles. The MRI enables the examiner to distinguish between muscle and fibrous tissue. The ratigue or the lumbar muscles is probably one or the
(l JU II () I' I J) I (
mO!
a
cause. of low back pain. whereby pain limits
(, \\\11 I I .> H
ASSESSMENT A B [ L 1 T 1 ES NO L 1 M [ TATIONS O F MAGNETIC RESONANCE [ MAG[NG
movement and muscle atrophy OCCUf!
I . Diarthrodial joints are panicularly suitable for MRI.
1984).
2. MRI is unparalleled in its ability to depict soft-tissue
For patients who have sustained head trauma with skull fractures. MRI is an efficient way to identify the early signs of cerebral edema. The test procedure of choice for diagnos ing metaslalic disease is an M R I scan (Table 1 - 1 3 ).
detail. 3. MRI is the only modality lhat can examine all com
ponents of the joint simultaneously.
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36
CHAPTER I Principles in Assessing Musculoskeletal Disorders
TA l\! [:
1 - 13
MAGNETIC RESONANCE IMAGING VERSUS COMPUTED TOMOGRAPHY
Anatomic Area Brain (including brainslcm)
Ear, nose. throat, and eye
Musculoskeletal spine
Indications
Recommended Procedure
Inilial evaluation (e.g., demyelination disease seizures)
MRt
Previous normal cr
MRI
Previous abnormal CT
CT or MRI*
Unchanged abnormal CT with increase in symptoms
MRI
Contrast aJ lergy
MRI
Acute trauma
CT
Pituitary tumors
MRI
Neurosensory hearing loss (e.g., \0 rule out acoustic neuroma)
CT
Conductive hearing loss
CT
Cancer staging (including laryngeal cancer)
CT or MRI'"
CholeMealOTna of temporal bone
CT
Fractures of facial bones
CT
Thyroid or parathyroid dysfunction (artcr US)
MRI
Sinus conditions
CTor MRI*
Orbital disease
MRl or CT*
Disease of optic t:racLS and chiasm
MRI
Internal derangement of lemporonmndibu,lar joint
MRt
Lower back or radicular pain in younger person
MRI
Lower back or radicular pain in older person
MRI or CT*
Cervical disk disease
MRt
Spinal stenosis
MRt
Cervical
CTor MRI*
Lumbar
MRI
Tumors
MRt
Metaslalic disease Hips Extremities Chest
Abdomen and pelvis
Early detection or aseptic necrosis
MRt
Congenital hip dislocation or reduction
US
Tumors, disease. or injury to muscle. ligaments. or c
MRI
Confirmation or calcificution or rracture
CT
Diseases or the hi la
MRI
Diseases or the mediastinum
MRI or CT*
Lung disease
CT
General survey (e.g., to rule oul !Ulnar)
CT
Li\'er disease
CTor MRI*
Renal cell cancer staging
MRI
Prostate disease
MRI. CT. or US
B ladder disease
MRl orCT
Abdominal aortic aneurysm
MRJ*
Other
cr. Computed tomography: MRI. mugnctlc resonunce imaging: US. ultrasonography. *Consult r.ldiologiSi for imaging options. From Brier SR: Primary eMf! ortlwpedicx. 51 Loui!l. 1 999, Mosby; originally councsy of Roben Goodman. MD. Soulh Sun·olk MRI. Pc. Bayshore. New York.
The guideline ror using the imaging modalities 10 best advaIHagc can be summaril.cd as follows: Using slate
of IIle
Contrast A rthrography
art M R techniques with high resolulion, at lcasi lwo plancs,
The conventional usc of arthrography in musculoskeletal
fast sequences, phaSed-array coils, and established technical
disease involves the use of air to distend a synovial joint and
parameters. M R I can answer all clillical questions. This
a radiopaque contrast agent to outline anatomic structures,
guidelinc applies 10 conditions treated conservatively or sur
The injection of contrast material into the joint space results
gically, as well as to all manifestations of degenerative spine
in a radiographic outline of the cartilage. menisci, ligaments.
disense. In particul;u. only MRI can identiry abnormalities
or synovium. Conventional arthrography is used in diagnos
within the spinal cord as syringomyelia or myelopathy
ing the scope and magnitude of orthopedic trauma to the
(Krcu :schmar, 1 998),
shoulder, wrist. knee. and ankle (Table 1 - 1 4).
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37
CHAPTER I Principles in Assessing Musculoskeletal Disorders
TA B l
E 1-14
JOI NTS TYPICALLY STUDIED WITH COMPUTED TOMOG RAPHIC ARTHROGRAPHY FOLLOWING TRAUMA
Joint
To Observe
Knee
Meniscus. cruciate and colhlleral ligaments. hYlilinc cartilage tears, osteochondral delects
Shoulder
ROlator cuff, glenoid labrum disruption
Hip
Hyaline cartilage integrity and teurs.
Wrist
Triangular fibrocartilage, intercarpal
Elbow
Hyaline cartilage integrity.
A n kle
LigamenLous lears. osteochondral
Temporomandibular
Disc and condylar integrity
pro!!lhctic joint loosening ligament imcgrilY osteochondral defects defects
Adapted from GUl>lil(} RB. Kyle RF. Templeman DC: FraclI!res allli (Ii:.!oCll/iol1:'i, 1'01 I. 5t Loui .... 1993. Mosby.
0 1( 1 1 1 0 1' 1 Il l l
A
l,,\MIII I 2<)
ASSESSMENT ABILITlES AND LIMITATlONS OF RADlONUCLIDE SCANNING
•
I , The principal advantage of scintigraphy over oLher imaging modalities is its ability to help in identifying tissues or organs with abnormal physiologic Or bio chemica.l properties. 2, Increased skeletal uptake can be seen at sites of ele vated blood flow or increased bone metabolism, 3, Scintigraphy is a convenient way of surveying the enlire skeleton for multifocal processes,
COl1lra�l-cnhanccd cartilage imaging can visualize early degenerative cartilage lesions before substantial morpho lugic changes occur. The application or contrast agent can
he performed a� either direct or indirect M R arthrography. Despite the advantages of indirect MR arthrography using intravenolllo. contrast material. direct M R arthrography has gained increasing popularity
il:-;
B F I G.
1-2 1 Normal bone scans.
(From Earl), PJ, Sodcl DB: Prin
dples (lml practice of mtl.·lea,. IIU!tiicifll!. Sl Louis. 1 995. Mosby.)
a safe diagnmaic 1001 in
assessing subtle illlraanicuiar derangements. including the evalu�lIion of articular cartilage especially in the shoulder, the hip, the ankle. ilnd the postoperative knee (Guntern
lomography ( SPECT) scans, are valuable in diagnostic
C\ a1. 2003: Kassarjian CI al. 2005: McCauley. 2005: Schmid
imaging because of their highly sensitive and noninvasive
CI ul. 2003),
nature. Whole-body scanning for metastatic and infectious di seases, as well as in flammatory and ischemic processes. is
Radionuclide Scanning
possible with scintigraphy (Fig. 1 -2 1 ),
Examinations conducLed wiLh the use of nuclear medicine
Highly active individuals (e.g.. competitive athletes) are
techniques, including bone scans. posiLron emission LOmog
prime candidates for bone scanning when the diagnosis
raphy (PET) scans. and single-photon emission computed
is uncertain. A bone scan may show increased uptake or
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38
CHAPTER I Principles in Assessing Musculoskeletal Disorders
the radioactive isotope consistent with a Slfess fracture (Fig. 1 -22). Because of the high incidence of falsc-ncgalivc radiographs early in the course of stress fractures, additional diagnostic imaging is oftcn indicted. Radionuclide bone scanning has traditionally been the Lest of choice in this situation but is being supplanted by M R I . An increased uptake observed on a bone scan correlates with increased bone activity caused by fatigue failure and confinns the diagnosis of stress frac ture (Sehils et al . 1 992). Despite being sen�itivc. bone scanning is nOI specific and can yield false-positive rates between 1 3% and 24%. Additionally. localiJ.ing the precise anatomic location of injury can be difficult (Steinbronn. Bennet!. Kay. 1994).
Bone scanning has become common in the evaluation of child abuse. Very young chi ldren typically do not develop stress fractures of multiple fracture sites in normal living situations (Fig. 1 -23).
Video Fluoroscopy Video fluoroscopy is used when a function study of the joint is warranted. Video fluoroscopy should be used when a biomechanical abnormality is present but is not adequately demonstrated by plain-film stress surveys or other examina tion methods. Three-dimensional mOlion visualization in the context of clinical and biomechanical analyses of the musculoskeletal �ystcl1l is becoming a key instrument for investigating its complex mechani�rnJ, and the
awkward
characteristics
(Lcardini cl al. 2006). Conventional
inslrumented
gait
analysis
with
skin
mounted markers has the disadvantage of measuring arte facts because of skin movement relative to the underlying bones. Video fiuoro!'ocoPY i!'o a well-established mcthod of marc accurately mca\uring knee joint kinematics by avoid ing the usc of skin markers. The small field of view of the image intensifier and thc ability only to gain kinematic data are lhe two main dbadvantagcs of this system (Zihlmann ct .1. 2006).
Diagnostic Ultrasound Diagnostic ultra ound, a sound wave echo study. is particu larly useful for evalualing soft tissues. The diagnostic ultra sound does not provide the same quality of image as CT or MRI. Diagnostic ultrasound requires high-resolution equip
B
ment. including a high-frequency transducer. Diagnostic ultrasound perfomls well in the detection of rotator cuff tears and other tendon abnormalities, as well as in identifying some metabolic disease. In cases of suspected pediatric hip disease. diagnostic u ltrasound is the recommended primary imaging technique.
FIG. 1-22 Radiographic film (A) and bone scan (B) dem onstrating Slress fracture. (From Nichola... JA, Hen-hm:!n EB: lower exm'mity mul .fpillt' in
Mosby.)
Preoperative ultrasound-guided marking of calcium dcposits significa11lly enhances the clinical re�ults of arthroscopic removul of calciulll deposits. The success of this type of surgery is largely dependcnl on the exact localil.ation and removal of calcium deposits. Complete removal of calcium
Copyrighted Material
.�/}()rtf
The
meliil'illt!, cd 4. St Louis, 1995.
CHAPTER I Principles in Assessing Musculoskeletal Disorder.
39 _ _ .....
___
IIOX 1·4 STRENGTHS AN D L IM ITATIONS O F MYElOGRAPH I C ST U D I E S
Strengths Studies 01" the subarachnoid space arc poss.ible. Inlraarachnoid lesions are shown. Demarcation of multi-disc levels is shown. Information on surgical scars is provided. AS'icssment of ftexion and extension dynamic
•
arc
possihle,
Limitations Lesions removed from outside of the thecal sac can be missed. Study variations are problematic. Detail shown in the dorsal spine is poor.
•
Postoperative studies arc impossihle to read with accur.J.cy. Testing. procedure is invasive. From Brier SR: Primlln- cart' onho/H·t!in. St Loui�, 1999. Mosh)'.
A FI G
Myelography
B
Traditional myelographic techniques involve Ihe inlroduc
1-23 A, Whole-body scintigraphy. B, Normal bone
scan is shown for comparison. (Fmm Klippel JH. Dieppc
PA
lion of 'imall amounts of water-soluble contrast medium into the subarachnoid space, either through a lumbar approach below the level of the conus medullaris or at the level of
Rht'lIInuw!og\', "01 1·2. eel 2. London. 1 998. Mo�by.)
C I -C2 through a posterolateral approach. Standard films of the spinal canal are made to determine the presence or absence of a filling defect. In cases of acute spinal trauma,
1l1�l l l ll l' I I) 1 1 (,\\\1 I 1 ,(I
myelography may be used in conjunction with CT (Fig. 1 -24).
ASSESSMENT A BILIT I ES AND L I MITATIONS OF ULTRASONOGR APHY
Myelography remains valuable in evaluating intrinsic spinal cord lesions, nerve root lesiom and dural tear!) asso • .
ciated with severe trauma ( Box 1-4).
I . U ltrJsonography offers direct multiplanar tomogra
phy without any need for image reformatting.
Depending on patient selcction and therapeutic strategy. the role of plain CT and MRI. as well as myelography comhlncd
2. U ltrasonography can also provide i mages in real time, without any exposure to ionizing radiation.
with myclo-CT. in the diagnmtic evaluation of dcgenerative change\ of the ,;pinc is judged diffcrently ( Krcl.t\chmar.
3. The modality is inexpensive and widely available.
1 998).
4. Ultrasonography offers relatively good soft-tissue
In paticnt, with di\k dlsca\c. plain-film cr for initial
contrast and is panicularly effective at helping
diagnmtic examination is rccommcnded. if the complaints
to identify fluid collections such as bursitis and
are non\pccific (Thornbury ct al. 1 99 1 . 1 993).
abscesses.
If the clinical finding:o, \uggest a herniated dis�. MRI
5. Ultrasound waves cannot penetrate bone.
should he given prcfcrence ovcr myclog.raphy comhined with myclo-CT. Thc U\C of non ionic contrast media without meningeal irritation or neurotoxicity ha� reduced the mor bidity of myelography < Krett...chmar. 199K).
dcro�lt... correlatc!'! with good or excellent clinical rcsult\ c Porccllini cl ::II. 2()().l: Rupp. Scil. Kohn. 2(00 ).
Thermography
Identlrying the COUI"\C of the calcium dCPQI;it i\ therefore
Using temperature differentials of the body. Ihermography
extremely importanl. The prescnce of a calcium dcpo\lI with
illustrates neurovascular changes in injury or dh�ease. Ther
an atypical cour\c and location more proximal 10 the joint
mograms do not provide speci ic f information regarding the
complicates the opcmlion c\'cn further Failure to locate the
cause of nerve fiber irritation (e.g .. herniated disc. scar
calcium dcpo.. 11 can make the ...urgical process extremely
tissue_ myospasm).
fnlslratmg and may rcsult in a vcry long operativc time ( Kayscr ct al. :W(7).
Reflex sympathetic dywophy is pan of a spectrum of sympathetically mediated pain syndromes that usually occur
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CHAPTER I Principle> in As;essing Musculoskeletal D i sorders
(\1(l 11(l1' 1 1) 1 ( (,\\\ 1 ' 1 I ; )
ASSESSMENT A BILITIES AND LIMITATIONS OF T RMOG RA!'.H_ Y_ --= ....:. H .:...: .E ::..:. ..:
I-
_ _
I . The thermographic examination
is conducted with the
use of contact liquid cl)'slal detectors or electronic infrared sensors. 2. Thennography is extremely scnsiti\'c to
Ill
icro\'ascu
lar changes in the skin. 3 . ThemlOgraphy IS excellent f"r differentiati ng between
a neurologic and vascular abnormality. 4. Thennography has a greater degree of 'cns l l l \ lIy in
documenling neurovascular abnormality than any other imaging sy\lcm.
5. Thermography has a greater degree of spec i ficity of image than mdionuclide hone scan.
6. Thermography has a lesser degree of speci licity of Image resolution than CT or ,\1RI.
Motor and trophic \ymptom.... ho\\c\cr. characlcri/c mmplex regional pam ,yndromc, hut arc not found after acute trauma. Thc\c latter 'ymptom, ob\iou,l) need time to de\cJop. and the durallon of d .. ,ea,e clear!} "::panuc" complex regional pam ,,)ndrome' (\\ccb) ,\Ild trJlllna (da)" (811-)"'lell1 ct al. 2000 ).
Electrodiagnostic Testing Although electrodiagnostic testing provides valuahle infor mation. it docs not stand alone as a diagnostic entity (Table
I - I S). The data obtained must be correlated
w
i lh the phySi
cal examination findings and case hi\lory. Electrodiagnostic testing can potentially dliTerent i ate asymptomatic dh , k hcmialions rrom symptomatic ones. A minimal amount of dencn'aLion can occur in asymptomat ic ..,pines. With �urface measurement of motor nerve conduction. velocity provides a "aluable anci llary procedure In the diag no�is of various pcriphcral nerve lesions in both thc upper and lowcr extrcmities. This form of testing involves stimu F I G . 1-24 Lumbar myelogram ( A ). with computed tomog raphy aX1i.I1 imuge (8) through the T 1 2 body. (hom GU... lilo RB. Kyle RF Fm('tllrt'\' rllld d/\lowtfOlI\, vol 1. SI l.oui ... 1�J3. �10,hy. )
lating a peripheral ncrve at two ...eparatc po...itions along it ... COUfl)C and recording the action potentials obscrved on an
oscilloscopic scrcen. Slow conduction time'> indicate nCf\'C entrapment syndromes across the poi III HI whir h thc il11puhc� are delayed. Thc electrical rcsponses of nCf\OllS system sensory trad"
in an extremity after a \ccm i ngly minor injury or
\
urgical
are SOIl1l11o.\ellsory-e\'okl'l1 potentials (SSEPs). SSEPs evalu atc varioul) pathologic variation!) from the peripheral nene
procedure . Even Lhough certain ...imilarilic... cxi--I helwccn aculccomplcx
through the spinal cord to the \omatoscll..,ory region of the
regional pmn \yndromc\ (n:tlcx \yrnpathclic dy\lrophyJ and
brain. SSEPs assess discascs of thc "'pinal cord. trauma
patient...
to thc spine. ncuromuscular diseasc. and demyelinating
\\ IIh
acule trauma. detailed illvc\tigauol1 or the.....:
...ign ... n!\ic.lh ...lriking di fference... . The dinical ... imi lnril) compn ...c\ pam. hypcralgc...ia. and ..,ome prc... umahly auto· nomic di,turhancc\ (edema and ,kill tcmpcnllurc change..,),
disorders. U,ing needle electrodes, needle EMG is
\\
idely u,ed to
diagnosc nCf\'C root le... ions at the level of the 'pille. EMG
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CHAPTER I Principles in Assessing Musculoskeletal Disorders
lAll L I I 1 5 STRENGTHS A N D liMITATIONS O F ELECfRODIAGNOSTIC TESTING
Testing Modality
Strengths
Limitations
Nerve conduction velocity
Helpful in ruling OUI peripheral cntrapmcni neuropathic
Provides imperfect sensitivity; limiled locali/..alion
conditions (c.g., prolonged latencies exhibited in
and determination of injury severity; Liming of
carpal tunnel syndrome, tarsal tunnel syndrome) lind
study an imponant factor
ulnar neuropathic variations F waves
Evaluates motor reflex only: possibly evailimes
Provides screening for lale mOlor response with distal sweeps staning at the fool
abnonnal findings only in lhe presence of multiple-level injury
l-I reflex
Provides assessment of S I nerve root only
Equivalent of ankle join! reflex: evaluates monosynaptic reflex with sensory and mOlor S I function Helpful in documenting sensory pathway dislUrbances
SSEP,
Offers imperfect localization: findings arc rarely
in proximal neural injury and central conduction
abnonnal if results of other electrodiagnostic
delays, as in myopathies and multiple sclerosis Needle EMG
tests within nomlal limits
Useful in assessing conductivity of ncuntl tissues:
Unable to detect denervation potentiab for 14 to 28 days aftcr injury: provides imperfect
helpful in determining sile and severity of lesion; may be helpful in carly assessment of recovery.
5.Cnsitivity: study timing an imponant factor:
screening for fibrillation potentiab. and signs of
proxinu11 lesions sometimes inaccessible
denervation from nerve rOOI compre�sion disorders
anatomically: effectiveness reduced after surgery
EMG. Eh..'Ctmmyography: SSEPs. .;omutoscmory-c\lokcd potential!..
Adapted from Brier 5R: Priman' ('lirt' ortl/Of1l'dic.�, 5t Loui!., 1 999. Mo<,hy.
llltl l llll'l nil l,,\'\\ ll l I \2
ASSESSMENT A BILlTlES AND LIMITATIONS OF NERVE CONDUCTlON VELOCITY I . Studies of nerve conduction velocity (NCV) can rule out peripheral neuropathic conditions. 2. Routine NCV tests are not specific for conditions
such as radiculopathy, but they may be helpful i n cases o f chronic pain that have a questionable spinal origin.
F I G . 1-25 The IMEX portable Doppler
(righl).
audibly
lllU IIll l' l llIl t, " I ll I I II
monitors pulses in noisy environments when palpation is
ASSESSMENT A BILITIES AND L1 MlTATlONS OF ELECTROMYOGRAPHY
queslionable or not possible or when the pulse is especially weak or rapid. The Doppler also aids in the assessment of circulation distal to fractures, burns. and other injuries Lo quickly determine the extent of injury. Transmission
I. Electromyography (EM G) shows fibrillation poten
gel
(Iefl)
is used to couple the Doppler head to the skin
tials and possible motor unit changes in denervated
surface and eliminate air gaps that can degrade sound
muscles.
transmission.
2. Denervation of paraspinal muscle, indicates that the
patient has a lesion at the nerve root level. 3. The usual finding of needle EMG in a palient who has dorsal root disease is normal.
4. It does not provide any information with respect to the locus of injury (e.g., root, nerve, muscle) and, in fact, often rcneclS associated tissue injury rather than neurovascular dysfunction.
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CHAPTER I Principles in Assessing Musculoskeletal Disorders
differentiates a central spinal lesion from a peripheral neu
Laser Doppler flowmetry is a valuable noninvasive method
ropathic condition. Resuhs of the procedure are accurate i n
for investigation of the very early skin vcnoartcriolar dys
differentiating disease o f a neuromuscular origin.
functions. for evaluation of focal autonomic dysrcgulation and skin vasomotor abnormalities in patients with Raynaud
Doppler Ultrasonic Vascular Testing
phenomenon. Laser Doppler-recorded vcnoartcriolar reflex
Doppler vascular testing allows the assessment of pulses in
testing i� a simple procedure and an adequatc addilional
noisy environments or when pulses are weak. This lest is
diagnostic 1001. which contribute� to diagno�c Raynaud phe·
efticient when palpation of a pulse is questionable or not
nomcnon and differentiate primary frolll secondary Raynaud
possible. The Doppler instrument aids in the assessment of
phenomenon (Stoyncva.
circulation distal to fracture sites. burns, and other injuries lhal potentially compromise vascular tissue, quickly deter mining the extent of injury (Fig. 1 -25).
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200�).
CHAPTER I Principles in Assessing Musculoskeletal Disorders
43
C R I I I CA L 1 11 1 N 1\.1 N (; I . In the complaint history of a musculoskeletal condi-
lion, what essential points
hould be included for
proper history taking by an experienced examiner?
2. Name the five essential steps in drawing a working diagnosis for your patient.
3. Name the Cr;t;cal 5 questions in orthopedics.
S. How are the two tests penormed?
9. How would you describe the presentation of a patient with scleralogenous pain?
10. Why is serial radiography useful i n a patient with rheumatoid arthritis? I I . What area or areas would you monitor?
4. Describe lendrassik maneuver.
1 2. How Frequent should radiography be used?
5. You have a patient who is complaining of unrelenting
1 3. You have just diagnosed a case of AS. How frequent
spinal pain who demonstrates full and pain-free range
should you penorm serial studies of this patient?
of motion. What two problems should you consider
14. What areas should be monitored? 1 5. A question of causation arises in a child with multiple
with this presentation? 6. Describe the difference and what information can be obtained from the five rung test and the max;mal stalic grip when using a Jamar dynamometer.
om mend for this child? 1 6. SSEPs are useful in the evaluation of various patho-
7. What are the significances of the clinical findings of the static grip test and the REG test?
complaints. What imaging procedure would you rec-
logic conditions. What part of the nervous system is evaluated with this process?
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CHAPTER I Principles in Assessing Musculoskeletal Disorders
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C H A PTER 2 Assess ing Cardi nal Musculoske letal Sym ptoms and S ig n s
69
TA B U 2- 1 2 TREMOR C LAS S I F I CAT I O N
Cause
Type and Rate of Movement
Anxiety
Fine, rapid. I () to 12/scl' Fine, regular. or coarse. 2 t o 5/sec
Parkinsonism
Description I rregular, variahle I ncreased by attempts to move part; decreased by relaxation of part Occurs at rest May be i n h i bited by mov e me nt
Involves flexion of fi nger and thumb pill rollillg
Accompanied by rigidity. cogwheel phe n ome n a , brady k i nesia
Cen:hcllar tremor
Variable rate
Evident o n l y
on
mo ve m c n t (most prom i nent on linger-to-nose test)
Dysmetria (seen when patient i s asked to pat rapi d l y ; pats are of unequal force Essential
or
Coarse. 3 to 7/sec
seni Ie
Metabolil'
and do not all arri ve at same point)
I n volves the jaw. sometimes the lOngue, and sometimes the entire head Disappears on complete relaxation
or
in re s pon se to a lcoho l
Yariahle Patient is obv iously i l l ; if i l l ness i s a res u l t of hepatic fai' l u rc, patiel1l w i l l have other signs, such as palpable l i ver, spider nevi
From Barkauskas YH et al: Health & physical assessmefl/. ed 2 , St Louis.
1 998. M osby.
Cramps and Spasm Muscu lar spasm, or tremor (Table 2- 1 2), may occur at rest or with movement. S pasms and tremors occur in the normal ind i vidual with metabo l ic and electrolyte a l terations. Cramp ing is a common complaint after excessive sweati ng and subsequent hyponatremia, hypocalcemia, hypomagnese mia, or hyperuricemia. Exercise-associ ated muscle c ram pin g is a pai n fu l . involun tary contraction of skeletal muscle that occurs i mmed i a tel y
after e x e rc i se . Any athlete who e x h i bi t s repeated epi sodes of muscle spas ms should u n d ergo a comprehensive h is lOry
and p h y s ic al e x a m i n ation and. in most cases, l aborato ry
studies to evaluate e l ectro l y te s . Athl etes should a l so have a
O RI H O P I D l l' ( ; ;\ , \HJ r 2 I I
GAIT Gait impairments of predominant neurologic origin include the following (in descending order of frequency): I . Di sorders of the corticospinal pathways (spasticity ) 2. Basal gangl ia ( parki nsonism) 3 . Cerebel l u m and connections ( ataxia) 4. Cerebral cortex (gai t aprax ia) 5 . Neuromuscul ar system ( weakness) 6. Sensation (atax ia)
u r i n a l y s i s to c h ec k for blood or myoglob i n . The i n i ti a l
history shou l d i ncl ude questions pertai n i ng t o h ydra t io n status, frequency of s t ret ch i n g . and the use of ergogenic
s upp l eme n t s s uc h
as
stero id s
or
creat i ne . Questions to define
the athlete's me d i c a l h i story should i n q u i re about how the
muscle crampi ng relates to temperature, d iet. fa m i l y history,
u r i ne color changes (myog l o b i nuria), and how l o ng the symptom� last
( Nad l er et
ai,
2004).
Tetany Hypocalcemia and hypomagnesemia often cause the invo l untary spasms of s keletal m uscle, which resemble cramping. Tetan ic cramps can be el icited by repeatedly per c u ss i ng the motor nerve, which leads to a muscle gro u p contraction-cramp-spasm at frequenc ies o f 1 5 t o 20 per second. Chvostek s ign is the spasm of fac ial muscles pro duced by tapping over the facial nerve near i t s foraminal ex it. Chvostek s ign may also occur w i th normocalcemia, as wel l as w i th h y pocalcem ia. Patients w i th hypocalcemic seizures demonstrate marked Chvostek sign, positive Trousseau sign, sweaty hands, and hyperreflexia (Ahmed et ai, 2004).
Trousseau sign i s demonstrated by i nflating a sphygmo manometer around the wrist area of the left hand to above systolic blood pressure for 3 mi n u tes while observ i ng the hand. Typ ical carpal spasm, which relaxes approxi mately 5 seconds after the cuff is released, is considered a positive Trousseau sign. Tetany i s m o s t c ommo n l y caused by h ypoca l c e m i a . Low levels of free or ion ized e x trace l l u lar c a l c i u m reduce the normal transmembrane pote n t i a l of the nerve by i ncreasing
so d i u m conductance, thus red u c i n g the threshold req u ired to cause depolarization. Normal serum ion ized c a l c i u m l evels range from
5.9
to
6.5
mg/d l . Levels fa l l i n g be l o w 4.3 mgldl
can cause tetany. H y poca l cem ia i s observed in h y poparathy roid i s m , v i ta m i n - D deficiency, m a l ab s orpt i o n s y n dromes. acute pancrea t i t i s .
m a l i g n ancy,
sep s i s .
and
drug effect.
Hyper venti lat i o n lead i n g to respiratory a l k a l o s i s and sec ondary reduction of ionized c a l c i u m may prec i p i tate tetany
(Freeman, M ichae l . R ob e rt .
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70
CHAPTER 2 Assessing Cardinal Muscu loskeletal Symptoms and S i gns
Impairment of Gait Finding a spinal or lower ex tremity orthopedic or neurologic
O RI I I O I' I D I C l,A,\\ lJl 1- 1 -1-
di sorder that does not produce abnormal i ties of gait a t some
IMPAIRED MICTURIT I ON
time during i ts course i s d ifficult. Gait disturbances a fter a stroke a r e multifaceted a n d hence
Localization of impaired micturition depends on the
must be studied from multiple perspectives. B iomechanical
following:
measurements such as temporal distance parameters, kine matics, kinetics, mechanical energy, and energy costs, as
1 . Loss of bladder sensation
2. Perineal sensory loss
well as electromyography, can evaluate the behavioral
3. Patulous anal sph i ncter
profile of gait and reflect CNS adaptation with respect to
4. Absence of the bulbocavernous and anocutaneous reflexes
internal and external demands. Electrophysiologic measure ments such as stretch reflex, H-reflex, and cutaneous reflexes
5 . Sensory, motor, and reflex changes in the lower extrem ities
can evaluate the integrity of spinal cord functions during gait and indirectly assess the integrity of the descending control system (Lamontagne, Stephen son, Fung, 2007).
B1adder Control Incontinence and other disturbances of urinary bladder fu nc
bilateral-needle
tion are occasion al l y the fi rst man ifestation of d isease of the
externaI anal sphincter and sometimes of the bulbocaverno
e1ectromyographic
examination
of
the
spinal cord, as well as the rest of the nervous system. The
sus muscle needs to be considered first. Detection of spon
physiologic mechanism of micturition is complex. The terms
taneous denervation activity, most appropriately in the bul
atonic bladder and spastic bladder are no longer useful i n
bocavernosus muscle, is common in the interval from 3
descri bing
different
levels
of
neurologic
i n v olvement
because they are related mainly to l ocal factors i n the bladder
weeks to several months after a lower motor neuron i njury ( Podnar, in press).
A n associated history of erectile dysfunction or rectal
wall. Compressive lesions to the cauda equina or conus medullaris
incontinence should c learly
are a common cause of neurogenic lower urinary tract dys
common neurogenic cause for urinary i n continence. The
suggest the presence of a
function, although more peripheral lesions may also cause
additional presence of sacral pain should suggest tumor in
sacral disease. [n patients with suspected focal sacral disease,
the sacral region.
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71
CHAPTER 2 Assessing Cardinal Musculoskeletal Symptoms and S igns
CRt n e A L T H t N Kt N C I . What are the five groups of signs and symptoms dif
9. What are the two most common tumors of the dig its of the hand and on the dorsum of the foot?
ferentiating muscu loskeletal complaints?
2. Why can articular or periarticular pain radiate widely
1 0 . A hel iotropic rash and Gottron papules are character
and be fe lt in a spot di stant from its originating
istic and possibly pathognomonic cutaneous feature
tissue?
of what condition?
3 . What typical sensations differentiate pain with nerve
I I . Where
entrapment, vascular compromise, and articular or
found?
joint involvement?
can
Gottron
papules
most commonly
be
1 2 . The Leeds Assessment of Neuropathic Symptoms
4 . In listening to a patient's description of pai n , i . e . , when present, what relieves i t , what makes i t worse, and what improves it, pain at rest, night, or with u se suggests what kinds of problems?
and S igns i s used in the assessment of what type of conditions? 1 3 . You have a very athletic patient with reoccurring episodes of muscle cramping with exercise . What
5 . What is the leading cause of accidental death in older adults?
would be your immed iate action steps for this case presentation?
6. What subgroup of patients is at high risk of develop ing chronic lower back pain ?
1 4 . Gait impairments from d isorders of the corticosp inal pathways are mani fested by what?
7. What four issues are important in assessing a patient's disability?
1 5 . Gait
i m pairments
from
the
cerebe l l u m
connections are c haracterized by what?
8. After thoroughly examining the patient's painful part, you have doubt of the source of the symptoms. What would your next step be?
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its
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CHAPTER 2 Assessing Cardinal Musculoskeletal S),mptoms and Signs
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