Musculoskeletal complaints account for >315 million outpatient visits per year and >20% of all outpatient visits in the United States. The Centers for Disease Control and Prevention estimate that 54.4 million, or 1 in 5 adults) of the U.S. population has physician-diagnosed arthritis. While many patients will have self-limited conditions requiring minimal evaluation, reassurance, and symptomatic therapy, specific musculoskeletal presentations or their persistence may herald a more serious condition that requires further evaluation or laboratory testing to establish a diagnosis. The goal of the musculoskeletal evaluation is to formulate a differential diagnosis that leads to an accurate diagnosis and timely therapy, while avoiding excessive diagnostic testing and unnecessary treatment (Table 363-1). There are several urgent conditions that must be diagnosed promptly to avoid significant morbid or mortal sequelae. These “red flag” diagnoses include septic arthritis, acute crystal-induced arthritis (e.g., gout), and fracture. Each may be suspected by its acute onset and monarticular or focal musculoskeletal pain.
TABLE 363-1Evaluation of Patients with Musculoskeletal Complaints ||Download (.pdf) TABLE 363-1 Evaluation of Patients with Musculoskeletal Complaints
| Accurate diagnosis |
| Timely provision of therapy |
| Avoidance of unnecessary diagnostic testing |
| Identification of acute, focal/monarticular “red flag” conditions |
| Determine the chronology (acute vs chronic) |
| Determine the nature of the pathologic process (inflammatory vs noninflammatory) |
| Determine the extent of involvement (monarticular, polyarticular, focal, widespread) |
| Anatomic localization of complaint (articular vs nonarticular) |
| Consider the most common disorders first |
| Consider the need for diagnostic testing |
| Formulate a differential diagnosis |
The majority of individuals with musculoskeletal complaints can be diagnosed with a thorough history and a comprehensive physical and musculoskeletal examination. The initial encounter should determine whether the musculoskeletal complaint signals a red flag condition (septic arthritis, gout, or fracture) or not. The evaluation should ascertain if the complaint is (1) articular or nonarticular in origin, (2) inflammatory or noninflammatory in nature, (3) acute or chronic in duration, and (4) localized (monarticular) or widespread (polyarticular) in distribution.
With this approach, the musculoskeletal presentation can be characterized (e.g., acute inflammatory monarthritis or a chronic noninflammatory, nonarticular widespread pain) to narrow the diagnostic possibilities. However, some patients will not fit immediately into an established diagnostic category. Many musculoskeletal disorders resemble each other at the outset, and some may take weeks or months (but not years) to evolve into a recognizable diagnostic entity. This consideration should temper the desire to establish a definitive diagnosis at the first encounter.
ARTICULAR VERSUS NONARTICULAR
The musculoskeletal evaluation must discriminate the anatomic origin(s) of the patient’s complaint. For example, ankle pain can result from a variety of pathologic conditions involving disparate anatomic structures, including gouty arthritis, calcaneal fracture, Achilles tendinitis, plantar fasciitis, cellulitis, and peripheral or entrapment neuropathy. Distinguishing between articular and nonarticular conditions requires a careful and detailed examination. Articular structures include the synovium, synovial fluid, articular cartilage, intraarticular ligaments, joint capsule, and juxtaarticular bone. Nonarticular (or periarticular) structures, such as supportive extraarticular ligaments, tendons, bursae, muscle, fascia, bone, nerve, and overlying skin, may be involved in the pathologic process. Although musculoskeletal complaints are often ascribed to the joints, nonarticular disorders more frequently underlie such complaints. Distinguishing between these potential sources of pain may be challenging to the unskilled examiner. Articular disorders may be characterized by deep or diffuse pain, pain or limited range of motion on active and passive movement, and swelling (caused by synovial proliferation, effusion, or bony enlargement), crepitation, instability, “locking,” or deformity. By contrast, nonarticular disorders tend to be painful on active, but not passive (or assisted), range of motion. Periarticular conditions often demonstrate point or focal tenderness in regions adjacent to articular structures, may radiate or be elicited with a specific movement or position, and have physical findings remote from the joint capsule. Moreover, nonarticular disorders seldom demonstrate swelling, crepitus, instability, or deformity of the joint itself.
INFLAMMATORY VERSUS NONINFLAMMATORY DISORDERS
In the course of a musculoskeletal evaluation, the examiner should determine the nature of the underlying pathologic process and whether inflammatory or noninflammatory findings exist. Inflammatory disorders may be infectious (Neisseria gonorrhoeae or Mycobacterium tuberculosis), crystal-induced (gout, pseudogout), immune-related (rheumatoid arthritis [RA], systemic lupus erythematosus [SLE]), reactive (rheumatic fever, reactive arthritis), or idiopathic. Inflammatory disorders may be identified by any of the four cardinal signs of inflammation (erythema, warmth, pain, or swelling), systemic symptoms (fatigue, fever, rash, weight loss), or laboratory evidence of inflammation (elevated erythrocyte sedimentation rate [ESR] or C-reactive protein [CRP], thrombocytosis, anemia of chronic disease, or hypoalbuminemia). Articular stiffness commonly accompanies chronic musculoskeletal disorders. The duration of stiffness may be prolonged (hours) with inflammatory disorders (such as RA or polymyalgia rheumatica) and improves with activity. By contrast, intermittent stiffness (also known as gel phenomenon) is typical of noninflammatory conditions (such as osteoarthritis [OA]), shorter in duration (<60 min), and is exacerbated by activity. Fatigue may be profound with inflammation (as seen in RA and polymyalgia rheumatica) but may also be a consequence of fibromyalgia (a noninflammatory disorder), chronic pain, poor sleep, depression, anemia, cardiac failure, endocrinopathy, or malnutrition.
Noninflammatory disorders may be related to trauma (rotator cuff tear), repetitive use (bursitis, tendinitis), degeneration or ineffective repair (OA), neoplasm (pigmented villonodular synovitis), or pain amplification (fibromyalgia). Noninflammatory disorders are often characterized by pain without synovial swelling or warmth, absence of inflammatory or systemic features, daytime, intermittent gel phenomena rather than prolonged morning stiffness, and normal (for age) or negative laboratory investigations.
Identification of the nature of the underlying process and the site of the complaint will enable the examiner to characterize the musculoskeletal presentation (e.g., acute inflammatory monarthritis, chronic noninflammatory, nonarticular widespread pain). By narrowing the diagnostic considerations, the examiner can assess the need for immediate diagnostic or therapeutic intervention or for continued observation. Figure 363-1 presents an algorithmic approach to the evaluation of patients with musculoskeletal complaints. This approach relies on clinical and historic features, rather than laboratory testing, to diagnose many common rheumatic disorders.
Algorithm for the diagnosis of musculoskeletal complaints. An approach to formulating a differential diagnosis (shown in italics). CMC, carpometacarpal; CRP, C-reactive protein; DIP, distal interphalangeal; ESR, erythrocyte sedimentation rate; JIA, juvenile idiopathic arthritis; MCP, metacarpophalangeal; MTP, metatarsophalangeal; PIP, proximal interphalangeal; PMR, polymyalgia rheumatica; SLE, systemic lupus erythematosus.
A simpler, alternative approach would consider the most commonly encountered complaints first, based on frequency in younger versus older populations. The most prevalent causes of musculoskeletal complaints are shown in Fig. 363-2. Because trauma, fracture, overuse syndromes, and fibromyalgia are among the most common causes of musculoskeletal pain, these should be considered during the initial encounter. If excluded, other frequently occurring disorders should be considered according to the patient’s age. Hence, those aged <60 years are commonly affected by repetitive use/strain disorders, gout (men only), RA, spondyloarthritis, and uncommonly, infectious arthritis. Patients aged >60 years are frequently affected by OA, crystal (gout and pseudogout) arthritis, polymyalgia rheumatica, osteoporotic fracture, and uncommonly, septic arthritis. These conditions are between 10 and 100 times more prevalent than other serious autoimmune conditions, such as SLE, scleroderma, polymyositis, and vasculitis.
Algorithm for consideration of the most common musculoskeletal conditions. GC, gonococcal; IBD, inflammatory bowel disease.
Historic features may reveal important clues to the diagnosis. Aspects of the patient profile, complaint chronology, extent of joint involvement, and precipitating factors can provide important information. Certain diagnoses are more frequent in different age groups. SLE and reactive arthritis occur more frequently in the young, whereas fibromyalgia and RA are frequent in middle age, and OA and polymyalgia rheumatica are more prevalent among the elderly. Diagnostic clustering is also evident when sex and race are considered. Gout, spondyloarthritis, and ankylosing spondylitis are more common in men, whereas RA, fibromyalgia, osteoporosis and lupus are more frequent in women. Racial predilections may be evident. Thus, polymyalgia rheumatica, giant cell arteritis, and granulomatosis with polyangiitis (GPA; formerly called Wegener’s granulomatosis) commonly affect whites, whereas sarcoidosis and SLE more commonly affect African Americans. Familial aggregation is most common with ankylosing spondylitis, gout, and Heberden’s nodes of OA.
The chronology of the complaint is an important diagnostic feature and can be divided into the onset, evolution, and duration. The onset of disorders such as septic arthritis or gout tends to be abrupt, whereas OA, RA, and fibromyalgia may have more indolent presentations. The patients’ complaints may evolve differently and be classified as chronic (OA), intermittent (crystal or Lyme arthritis), migratory (rheumatic fever, gonococcal or viral arthritis), or additive (RA, psoriatic arthritis). Musculoskeletal disorders are typically classified as acute or chronic based on a symptom duration that is either <6 weeks or >6 weeks, respectively. Acute arthropathies tend to be infectious, crystal-induced, or reactive. Chronic conditions include noninflammatory or immunologic arthritides (e.g., OA, RA) and nonarticular disorders (e.g., fibromyalgia).
The extent or distribution of articular involvement is often informative. Articular disorders are classified based on the number of joints involved, as either monarticular (one joint), oligoarticular or pauciarticular (two or three joints), or polyarticular (four or more joints). Although crystal and infectious arthritis are often mono- or oligoarticular, OA and RA are polyarticular disorders. Nonarticular disorders may be classified as either focal or widespread. Complaints secondary to tendinitis or carpal tunnel syndrome are typically focal, whereas weakness and myalgia, caused by polymyositis or fibromyalgia, are more widespread in their presentation. Joint involvement in RA tends to be symmetric and polyarticular. By contrast, spondyloarthritis, reactive arthritis, gout, and sarcoid are often asymmetric and oligoarticular. OA and psoriatic arthritis may be either symmetric or asymmetric and oligo- or polyarticular. The upper extremities are frequently involved in RA and OA, whereas lower extremity arthritis is characteristic of reactive arthritis and gout at their onset. Involvement of the axial skeleton is common in OA and ankylosing spondylitis but is infrequent in RA, with the notable exception of the cervical spine.
The clinical history should also identify precipitating events, such as trauma (osteonecrosis, meniscal tear), drug administration (Table 363-2), antecedent or intercurrent infection (rheumatic fever, reactive arthritis, hepatitis), or illnesses that may have contributed to the patient’s complaint. Certain comorbidities may have musculoskeletal consequences. This is especially so for diabetes mellitus (carpal tunnel syndrome), renal insufficiency (gout), depression or insomnia (fibromyalgia), myeloma (low back pain), cancer (myositis), and osteoporosis (fracture) or when using certain drugs such as glucocorticoids (osteonecrosis, septic arthritis), diuretics or chemotherapy (gout) (Table 363-2).
TABLE 363-2Drug-Induced Musculoskeletal Conditions ||Download (.pdf) TABLE 363-2 Drug-Induced Musculoskeletal Conditions
| Quinidine, cimetidine, beta blockers, quinolones, chronic acyclovir, interferons, IL-2, nicardipine, vaccines, rifabutin, aromatase inhibitors, HIV protease inhibitors, DPP-4 inhibitors (sitagliptin, linagliptin, alogliptin), checkpoint inhibitors (ipilimumab, pembrolizumab, nivolumab) |
| Glucocorticoids, penicillamine, hydroxychloroquine, AZT, lovastatin, simvastatin, atorvastatin, pravastatin, clofibrate, amiodarone, interferon, IL-2, alcohol, cocaine, paclitaxel, docetaxel, imatinib mesylate, colchicine, quinolones, cyclosporine, tacrolimus, protease inhibitors, checkpoint inhibitors |
|Tendon rupture/tendinitis |
| Quinolones, glucocorticoids, isotretinoin, statins, aromatase inhibitors, collagenase injections |
| Diuretics, aspirin, cytotoxics, cyclosporine, alcohol, moonshine, ethambutol, fructose-containing soft drinks |
|Drug-induced lupus |
| Hydralazine, procainamide, quinidine, phenytoin, carbamazepine, methyldopa, isoniazid, chlorpromazine, lithium, penicillamine, tetracyclines, TNF inhibitors, ACE inhibitors, ticlopidine, aromatase inhibitors |
|Drug-induced subacute lupus |
| Proton pump inhibitors, calcium channel blockers (diltiazem), ACE inhibitors, TNF inhibitors, terbinafine, interferons (α and β-1a), paclitaxel, docetaxel, gemcitabine, capecitabine, aromatase inhibitors, HCTZ |
|Osteonecrosis/Atypical fractures |
| Glucocorticoids, alcohol, radiation, bisphosphonates |
| Glucocorticoids, chronic heparin, phenytoin, aromatase inhibitors, anti-androgen therapy, thiazolinediones |
| TNF inhibitors, beta blockers, lithium, hydroxychloroquine, chloroquine, minocycline, ACE inhibitors, terbinafine |
| Vinyl chloride, bleomycin, baricitinib, pentazocine, organic solvents, carbidopa, tryptophan, rapeseed oil |
|Raynaud’s phenomenon |
| Cisplatin, bleomycin, beta blockers, clonidine, bromocriptine, ergot alkaloids, cocaine, methylphenidate, dextroamphetamine, phenteramine, interferon therapy |
| Allopurinol, amphetamines, cocaine (often levamisole adulterated), cannabis, thiazides, penicillamine, propylthiouracil, montelukast, TNF inhibitors, hepatitis B vaccine, trimethoprim/sulfamethoxazole, minocycline, hydralazine |
Lastly, a thorough rheumatic review of systems may disclose useful diagnostic information. A variety of musculoskeletal disorders may be associated with systemic features such as fever (SLE, infection), rash (SLE, psoriatic arthritis), nail abnormalities (psoriatic or reactive arthritis), myalgias (fibromyalgia, statin- or drug-induced myopathy), or weakness (polymyositis, neuropathy). In addition, some conditions are associated with involvement of other organ systems including the eyes (Behçet’s disease, sarcoidosis, spondyloarthritis), gastrointestinal tract (scleroderma, inflammatory bowel disease), genitourinary tract (reactive arthritis, gonococcemia), or nervous system (Lyme disease, vasculitis).
Historically, syphilis and tuberculosis were labeled as the “great masqueraders” as their protean symptoms and potential for multi-organ involvement may result in delays in diagnosis and treatment. In the modern era, other serious diagnoses (including lupus, sarcoidosis, vasculitis and lymphoma) have also been labeled as great masqueraders. All of these are either uncommon or rare, and are overshadowed by the most common masquerader with musculoskeletal complaints—fibromyalgia. Fibromyalgia (see Chap. 366) is a pain amplification disorder unified by sleep disturbance, exaggerated pain and sensitivity (owing to lowered pain thresholds), and a multiplicity of symptoms with a paucity of abnormalities on clinical examination or laboratory testing. Tender “trigger points” are often found and include tenderness over the epicondyles, trochanteric bursae, anserine bursae, and muscles (gluteal, trapezius, supraspinatus) that often are misdiagnosed as other nonarticular conditions. Although fibromyalgia classically manifests as widespread aches and pains, presenting symptoms tend to be less specific, and only on further evaluation will the widespread noninflammatory features be disclosed. Fibromyalgia has numerous comorbidities including irritable bowel syndrome, dysmenorrhea, migraine, depression, anxiety, memory loss, non-anatomic paresthesia or dysesthesia, fatigue, myalgias, temporomandibular joint pain, and multiple chemical sensitivities. Fibromyalgia patients often see multiple specialists, are twice as likely to be hospitalized, and are plagued by polypharmacy. Fibromyalgia affects nearly 5 million Americans. Yet, fibromyalgia is frequently underrecognized or misdiagnosed as arthritis, lupus, multiple sclerosis, autoimmune disease, etc. Hence, patients are often referred to multiple consultants and are subjected to multiple investigations and even surgical interventions. Early consideration of this very common disorder can avert needless investigation, therapy, and concern for those afflicted (Fig. 363-2).
RHEUMATOLOGIC EVALUATION OF THE ELDERLY
The incidence of rheumatic diseases rises with age, such that 58% of those >65 years will have joint complaints. Musculoskeletal disorders in elderly patients are often not diagnosed because the signs and symptoms may be insidious, overlooked, or overshadowed by comorbidities. These difficulties are compounded by the diminished reliability of laboratory testing in the elderly, who often manifest nonpathologic abnormal results. For example, the ESR may be misleadingly elevated, and low-titer positive tests for rheumatoid factor (RF) and antinuclear antibodies (ANAs) may be seen in up to 15% of elderly patients. Although nearly all rheumatic disorders afflict the elderly, geriatric patients are particularly prone to OA, osteoporosis, osteoporotic fractures, gout, pseudogout, polymyalgia rheumatica, vasculitis, and drug-induced disorders (Table 363-2). The elderly should be approached in the same manner as other patients with musculoskeletal complaints, but with an emphasis on identifying the potential rheumatic consequences of medical comorbidities and therapies. The physical examination should identify the nature of the musculoskeletal complaint as well as coexisting diseases that may influence diagnosis and choice of treatment.
RHEUMATOLOGIC EVALUATION OF THE HOSPITALIZED PATIENT
Evaluation of a hospitalized patient with rheumatic complaints is often more complex owing to greater symptom severity, more acute presentations, and greater interplay of comorbidities. In patients with rheumatic disorders tend to be admitted for one of several reasons: (1) acute onset of inflammatory arthritis (possibly gout or septic arthritis); (2) undiagnosed systemic or febrile illness; (3) musculoskeletal trauma; (4) exacerbation or deterioration of an existing autoimmune disorder (e.g., SLE); or (5) new medical comorbidities (e.g., thrombotic event, lymphoma, infection) arising in patients with an established rheumatic disorder. Notably, rheumatic patients are seldom if ever admitted because of widespread pain or serologic abnormalities or for the initiation of new therapies.
Acute monarticular inflammatory arthritis may be a “red flag” condition (e.g., septic arthritis, gout, pseudogout) that will require arthrocentesis and, on occasion, hospitalization if infection is suspected. However, new-onset inflammatory polyarthritis will have a wider differential diagnosis (e.g., RA, hepatitis-related arthritis, chikungunya arthritis, serum sickness, drug-induced lupus, polyarticular septic arthritis) and may require targeted laboratory investigations rather than synovial fluid analyses. Patients with febrile, multisystem disorders will require exclusion of crystal, infectious, or neoplastic etiologies and an evaluation driven by the dominant symptom/finding with the greatest specificity. Conditions worthy of consideration may include gout or pseudogout, vasculitis (giant cell arteritis in the elderly or polyarteritis nodosa in younger patients), adult-onset Still’s disease, SLE, antiphospholipid antibody syndrome, IgG4-related disease, and sarcoidosis. A preexisting rheumatic diagnosis (e.g., SLE, RA, ankylosing spondylitis) should be confirmed by careful history, examination and review of medical records, as this will influence the ensuing in-patient evaluation. It is important to note that when established rheumatic disease patients are admitted to the hospital, it is usually not for a medical problem related to their autoimmune disease, but rather because of either a comorbid condition or complication of drug therapy. Patients with chronic inflammatory disorders (e.g., RA, SLE, psoriasis) have an augmented risk of infection, cardiovascular events, and neoplasia.
Certain conditions, such as acute gout, can be precipitated in hospitalized patients by surgery, dehydration, or medications and should be considered when hospitalized patients are evaluated for the acute onset of a musculoskeletal condition. Lastly, overly aggressive and unfocused laboratory testing will often yield abnormal findings that are better explained by the patient’s preexisting condition (chronic lung, renal, or liver disease) rather than a new inflammatory or autoimmune disorder (lupus, vasculitis).
The goal of the physical examination is to ascertain the structures involved, the nature of the underlying pathology, the functional consequences of the process, and the presence of systemic or extraarticular manifestations. A knowledge of topographic anatomy is necessary to identify the primary site(s) of involvement and differentiate articular from nonarticular disorders. The musculoskeletal examination depends largely on careful inspection, palpation, and a variety of specific physical maneuvers to elicit diagnostic signs (Table 363-3). Although most articulations of the appendicular skeleton can be examined in this manner, adequate inspection and palpation are not possible for many axial (e.g., zygapophyseal) and inaccessible (e.g., sacroiliac or hip) joints. For such joints, there is a greater reliance on specific maneuvers and imaging for assessment.
TABLE 363-3Glossary of Musculoskeletal Terms ||Download (.pdf) TABLE 363-3 Glossary of Musculoskeletal Terms
| A palpable (less commonly audible) vibratory or crackling sensation elicited with joint motion; fine joint crepitus is common and often insignificant in large joints; coarse joint crepitus indicates advanced cartilaginous and degenerative changes (as in osteoarthritis) |
| Alteration of joint alignment such that articulating surfaces incompletely approximate each other |
| Abnormal displacement of articulating surfaces such that the surfaces are not in contact |
|Range of motion |
| For diarthrodial joints, the arc of measurable movement through which the joint moves in a single plane |
| Loss of full movement resulting from a fixed resistance caused either by tonic spasm of muscle (reversible) or by fibrosis of periarticular structures (permanent) |
| Abnormal shape or size resulting from bony hypertrophy, malalignment of articulating structures, or damage to periarticular supportive structures |
| Inflammation of the entheses (tendinous or ligamentous insertions on bone) |
| Infection or inflammation involving an epicondyle |
Examination of involved and uninvolved joints will determine whether pain, warmth, erythema, or swelling is present. The locale and level of pain elicited by palpation or movement should be quantified. One standard would be to count the number of tender joints on palpation of 28 easily examined joints (proximal interphalangeals [PIPs], metacarpophalangeals [MCPs], wrists, elbows, shoulders, and knees). Similarly, the number of swollen joints (0–28) can be counted and recorded. Careful examination should distinguish between true articular swelling (caused by bony hypertrophy, synovial effusion or proliferation), and nonarticular (or periarticular) involvement, which usually extends beyond the normal joint margins. Synovial effusion can be distinguished from synovial hypertrophy or bony hypertrophy by palpation or specific maneuvers. For example, small to moderate knee effusions may be identified by the “bulge sign” or “ballottement of the patellae.” Bursal effusions (e.g., effusions of the olecranon or prepatellar bursa) are often focal, periarticular, overlie bony prominences, and are fluctuant with defined borders. Joint stability can be assessed by stabilizing the proximal joint, by palpation, and by the application of manual stress to the distal appendage. Subluxation or dislocation, which may be secondary to traumatic, mechanical, or inflammatory causes, can be assessed by inspection and palpation. Joint swelling or volume can be assessed by palpation. Distention of the articular capsule usually causes pain and evident enlargement or fluctuance. The patient will attempt to minimize the pain by maintaining the joint in the position of least intraarticular pressure and greatest volume, usually partial flexion. For this reason, inflammatory effusions may give rise to flexion contractures. Clinically, this may be detected as fluctuant or “squishy” swelling in larger joints and grape-like compressibility in smaller joints. Inflammation may result in fixed flexion deformities or diminished range of motion—especially on extension, when intraarticular pressure is increased. Active and passive range of motion should be assessed in all planes, with contralateral comparison. A goniometer may be used to quantify the arc of movement. Each joint should be passively manipulated through its full range of motion (including, as appropriate, flexion, extension, rotation, abduction, adduction, lateral bending, inversion, eversion, supination, pronation, medial/lateral deviation, and plantar- or dorsiflexion). Extreme range of motion may be seen with hypermobility syndrome, with joint pain and connective tissue laxity, often associated with Ehlers-Danlos or Marfan’s syndrome. Limitation of motion is frequently caused by inflammation, effusion, pain, deformity, contracture, or restriction from neuromyopathic causes. If passive motion exceeds active motion, a periarticular process (e.g., tendinitis, tendon rupture, or myopathy) should be considered. Contractures may reflect antecedent synovial inflammation or trauma. Minor joint crepitus is common during joint palpation and maneuvers but may indicate significant cartilage degeneration as it becomes coarser (e.g., OA). Joint deformity usually indicates a long-standing or aggressive pathologic process. Deformities may result from ligamentous destruction, soft tissue contracture, bony enlargement, ankylosis, erosive disease, subluxation, trauma, or loss of proprioception. Examination of the musculature will document strength, atrophy, pain, or spasm. Appendicular muscle weakness should be characterized as proximal or distal. Muscle strength should be assessed by observing the patient’s performance (e.g., walking, rising from a chair, grasping, writing). Strength may also be graded on a 5-point scale: 0 for no movement; 1 for trace movement or twitch; 2 for movement with gravity eliminated; 3 for movement against gravity only; 4 for movement against gravity and resistance; and 5 for normal strength. The examiner should assess for often-overlooked nonarticular or periarticular involvement, especially when articular complaints are not supported by objective findings referable to the joint capsule. The identification of soft tissue/nonarticular pain will prevent unwarranted and often expensive additional evaluations. Specific maneuvers may reveal common nonarticular abnormalities, such as a carpal tunnel syndrome (which can be identified by Tinel’s or Phalen’s sign). Other examples of soft tissue abnormalities include olecranon bursitis, epicondylitis (e.g., tennis elbow), enthesitis (e.g., Achilles tendinitis), and tender trigger points associated with fibromyalgia.
APPROACH TO REGIONAL RHEUMATIC COMPLAINTS
Although all patients should be evaluated in a logical and thorough manner, many cases with focal musculoskeletal complaints are caused by commonly encountered disorders that exhibit a predictable pattern of onset, evolution, and localization; they can often be diagnosed immediately on the basis of limited historic information and selected maneuvers or tests. Although nearly every musculoskeletal complaint could be approached in this manner, the evaluation of four common involved anatomic regions—the hand, shoulder, hip, and knee—are reviewed here.
Focal or unilateral hand pain may result from trauma, overuse, infection, or a reactive or crystal-induced arthritis. By contrast, bilateral hand complaints commonly suggest a degenerative (e.g., OA), systemic, or inflammatory/immune (e.g., RA) etiology. The distribution or pattern of joint involvement is highly suggestive of certain disorders (Fig. 363-3). Thus, OA (or degenerative arthritis) may manifest as distal interphalangeal (DIP) and PIP joint pain with bony hypertrophy sufficient to produce Heberden’s and Bouchard’s nodes, respectively. Pain, with or without bony swelling, involving the base of the thumb (first carpometacarpal joint) is also highly suggestive of OA. By contrast, RA tends to cause symmetric, polyarticular involvement of the PIP, MCP, intercarpal, and carpometacarpal joints (wrist) with pain and palpable synovial tissue hypertrophy. Psoriatic arthritis may mimic the pattern of joint involvement seen in OA (DIP and PIP joints), but can be distinguished by the presence of inflammatory signs (erythema, warmth, synovial swelling), with or without carpal involvement, nail pitting, or onycholysis. Whereas lateral or medial subluxations at the PIP or DIP joints are most likely due to inflammatory OA or psoriatic arthritis, dorsal or ventral deformities (swan neck or boutonnière deformities) are typical of RA. Hemochromatosis should be considered when degenerative changes (bony hypertrophy) are seen at the second and third MCP joints with associated radiographic chondrocalcinosis or episodic, inflammatory wrist arthritis.
Sites of hand or wrist involvement and their potential disease associations. CMC, carpometacarpal; DIP, distal interphalangeal; MCP, metacarpophalangeal; OA, osteoarthritis; PIP, proximal interphalangeal; RA, rheumatoid arthritis; SLE, systemic lupus erythematosus. (From JJ Cush et al: Evaluation of musculoskeletal complaints, in Rheumatology: Diagnosis and Therapeutics, 2nd ed, JJ Cush et al [eds]. Philadelphia, Lippincott Williams & Wilkins, 2005, pp 3–20. Used with permission from Dr. John J. Cush.)
Dactylitis manifests as soft tissue swelling of the whole digit and may have a sausage-like appearance. Common causes of dactylitis include psoriatic arthritis, spondyloarthritis, juvenile spondylitis, mixed connective tissue disease, scleroderma, sarcoidosis, and sickle cell disease. Soft tissue swelling over the dorsum of the hand and wrist may suggest an inflammatory extensor tendon tenosynovitis possibly caused by gonococcal infection, gout, or inflammatory arthritis (e.g., RA). Tenosynovitis is suggested by localized warmth, swelling, or pitting edema and may be confirmed when the soft tissue swelling tracks with tendon movement during flexion and extension of fingers, or when pain is induced while stretching the extensor tendon sheaths (flexing the digits distal to the MCP joints and maintaining the wrist in a fixed, neutral position).
Focal wrist pain localized to the radial aspect may be caused by de Quervain’s tenosynovitis resulting from inflammation of the tendon sheath(s) involving the abductor pollicis longus or extensor pollicis brevis (Fig. 363-3). This commonly results from overuse or follows pregnancy and may be diagnosed with Finkelstein’s test. A positive result is present when radial wrist pain is induced after the thumb is flexed and placed inside a clenched fist and the patient actively deviates the hand downward with ulnar deviation at the wrist. Carpal tunnel syndrome is another common disorder of the upper extremity and results from compression of the median nerve within the carpal tunnel. Manifestations include pain in the wrist that may radiate with paresthesia to the thumb, second and third fingers, and radial half of the fourth finger and, at times, atrophy of thenar musculature. Carpal tunnel syndrome is commonly associated with pregnancy, edema, trauma, OA, inflammatory arthritis, and infiltrative disorders (e.g., amyloidosis). The diagnosis may be suggested by a positive Tinel’s or Phalen’s sign. With each test, paresthesia in a median nerve distribution is induced or increased by either “thumping” the volar aspect of the wrist (Tinel’s sign) or pressing the extensor surfaces of both flexed wrists against each other (Phalen’s sign). The low sensitivity and moderate specificity of these tests may require nerve conduction velocity testing to confirm a suspected diagnosis.
During the evaluation of shoulder disorders, the examiner should carefully note any history of trauma, fibromyalgia, infection, inflammatory disease, occupational hazards, or previous cervical disease. In addition, the patient should be questioned as to the activities or movement(s) that elicit shoulder pain. While arthritis is suggested by pain on movement in all planes, pain with specific active motion suggests a periarticular (nonarticular) process. Shoulder pain may originate in the glenohumeral or acromioclavicular joints, subacromial (subdeltoid) bursa, periarticular soft tissues (e.g., fibromyalgia, rotator cuff tear/tendinitis), or cervical spine (Fig. 363-4). Shoulder pain is referred frequently from the cervical spine but may also be referred from intrathoracic lesions (e.g., a Pancoast tumor) or from gallbladder, hepatic, or diaphragmatic disease. These same visceral causes may also manifest as focal scapular pain. Fibromyalgia should be suspected when glenohumeral pain is accompanied by diffuse periarticular (i.e., subacromial, bicipital) pain, tender points (i.e., trapezius or supraspinatus), and a sleep disturbance. The shoulder should be put through its full range of motion both actively and passively (with examiner assistance): forward flexion, extension, abduction, adduction, and internal and external rotation. Manual inspection of the periarticular structures will often provide important diagnostic information. Glenohumeral involvement is best detected by placing the thumb over the glenohumeral joint just medial and inferior to the coracoid process and applying pressure anteriorly while internally and externally rotating the humeral head. Pain localized to this region is indicative of glenohumeral pathology. Synovial effusion or tissue is seldom palpable but, if present, may suggest infection, RA, amyloidosis, or an acute tear of the rotator cuff. The examiner should apply direct manual pressure over the subacromial bursa that lies lateral to and immediately beneath the acromion (Fig. 363-4). Subacromial bursitis is a frequent cause of shoulder pain. Anterior to the subacromial bursa, the bicipital tendon traverses the bicipital groove. This tendon is best identified by palpating it in its groove as the patient rotates the humerus internally and externally. Direct pressure over the tendon may reveal pain indicative of bicipital tendinitis. Palpation of the acromioclavicular joint may disclose local pain, bony hypertrophy, or, uncommonly, synovial swelling. Whereas OA and RA commonly affect the acromioclavicular joint, OA seldom involves the glenohumeral joint, unless there is a traumatic or occupational cause.
Origins of shoulder pain. The schematic diagram of the shoulder indicates, with arrows, the anatomic origins of shoulder pain.
Rotator cuff tendinitis or tear is a very common cause of shoulder pain. Nearly 30% of the elderly will have shoulder pain, with rotator cuff tendinitis or tear as a primary cause. The rotator cuff is formed by four tendons that attach the scapula to the proximal humerus (supraspinatus, infraspinatus, teres minor, and subscapularis tendons). Of these, the supraspinatus muscle is the most commonly damaged. Rotator cuff tendinitis is suggested by pain on active abduction (but not passive abduction), pain over the lateral deltoid muscle, night pain, and evidence of the impingement signs (pain with overhead arm activities). The Neer test for impingement is performed by the examiner raising the patient’s arm into forced flexion while stabilizing and preventing rotation of the scapula. A positive sign is present if pain develops before 180° of forward flexion. Tear of the rotator cuff is common in the elderly and often results from trauma; it may manifest in the same manner as tendinitis. The drop arm test is abnormal with supraspinatus pathology and is demonstrated by passive abduction of the arm to 90° by the examiner. If the patient is unable to hold the arm up actively or unable to lower the arm slowly without dropping, the test is positive. Tendinitis or tear of the rotator cuff is best confirmed by magnetic resonance imaging (MRI) or ultrasound.
Knee pain may result from intraarticular (OA, RA) or periarticular (anserine bursitis, collateral ligament strain) processes or be referred from hip pathology. A careful history should delineate the chronology of the knee complaint and whether there are predisposing conditions, trauma, or medications that might underlie the complaint. For example, patellofemoral disease (e.g., OA) may cause anterior knee pain that worsens with climbing stairs. Observation of the patient’s gait is also important. The knee should be carefully inspected in the upright (weight-bearing) and supine positions for swelling, erythema, malalignment, visible trauma, muscle wasting, and leg length discrepancy. The most common malalignment in the knee is genu varum (bowlegs) or genu valgum (knock-knees) resulting from asymmetric cartilage loss medially or laterally. Bony swelling of the knee joint commonly results from hypertrophic osseous changes seen with disorders such as OA and neuropathic arthropathy. Swelling caused by hypertrophy of the synovium or synovial effusion may manifest as a fluctuant, ballotable, or soft tissue enlargement in the suprapatellar pouch (suprapatellar reflection of the synovial cavity) or regions lateral and medial to the patella. Synovial effusions may also be detected by balloting the patella downward toward the femoral groove or by eliciting a “bulge sign.” With the knee extended, the examiner should manually compress, or “milk,” synovial fluid down from the suprapatellar pouch and lateral to the patellae. The application of manual pressure lateral to the patella may cause an observable shift in synovial fluid (bulge) to the medial aspect. The examiner should note that this maneuver is only effective in detecting small to moderate effusions (<100 mL). Inflammatory disorders such as RA, gout, pseudogout, and psoriatic arthritis may involve the knee joint and produce significant pain, stiffness, swelling, or warmth. A popliteal or Baker’s cyst may be palpated with the knee partially flexed and is best viewed posteriorly with the patient standing and knees fully extended to visualize isolated or unilateral popliteal swelling or fullness.
Anserine bursitis is an often missed periarticular cause of knee pain in adults. The pes anserine bursa underlies the insertion of the conjoined tendons (sartorius, gracilis, semitendinosus) on the anteromedial proximal tibia and may be painful following trauma, overuse, or inflammation. It is often tender in patients with fibromyalgia, obesity, and knee OA. Other forms of bursitis may also present as knee pain. The prepatellar bursa is superficial and is located over the inferior portion of the patella. The infrapatellar bursa is deeper and lies beneath the patellar ligament before its insertion on the tibial tubercle.
Internal derangement of the knee may result from trauma or degenerative processes. Damage to the meniscal cartilage (medial or lateral) frequently presents as chronic or intermittent knee pain. Such an injury should be suspected when there is a history of trauma, athletic activity, or chronic knee arthritis, and when the patient relates symptoms of “locking” or “giving way” of the knee. With the knee flexed 90° and the patient’s foot on the table, pain elicited during palpation over the joint line or when the knee is stressed laterally or medially may suggest a meniscal tear. A positive McMurray test may also indicate a meniscal tear. To perform this test, the knee is first flexed at 90°, and the leg is then extended while the lower extremity is simultaneously torqued medially or laterally. A painful click during inward rotation may indicate a lateral meniscus tear, and pain during outward rotation may indicate a tear in the medial meniscus. Lastly, damage to the cruciate ligaments should be suspected with acute onset of pain, possibly with swelling, a history of trauma, or a synovial fluid aspirate that is grossly bloody. Examination of the cruciate ligaments is best accomplished by eliciting a drawer sign. With the patient recumbent, the knee should be partially flexed and the foot stabilized on the examining surface. The examiner should manually attempt to displace the tibia anteriorly or posteriorly with respect to the femur. If anterior movement is detected, then anterior cruciate ligament damage is likely. Conversely, significant posterior movement may indicate posterior cruciate damage. Contralateral comparison will assist the examiner in detecting significant anterior or posterior movement.
The hip is best evaluated by observing the patient’s gait and assessing range of motion. The vast majority of patients reporting “hip pain” localize their pain unilaterally to the posterior gluteal musculature (Fig. 363-5). Such pain tends to radiate down the posterolateral aspect of the thigh and may or may not be associated with complaints of low back pain. This presentation frequently results from degenerative arthritis of the lumbosacral spine or disks and commonly follows a dermatomal distribution with involvement of nerve roots between L4 and S1. Sciatica is caused by impingement of the L4, L5, or S1 nerve (i.e., from a herniated disk) and manifests as unilateral neuropathic pain extending from the gluteal region down the posterolateral leg to the foot. Some individuals instead localize their “hip pain” laterally to the area overlying the trochanteric bursa. Because of the depth of this bursa, swelling and warmth are usually absent. Diagnosis of trochanteric bursitis or enthesitis can be confirmed by inducing point tenderness over the trochanteric bursa. Gluteal and trochanteric pain are common findings in fibromyalgia. Range of movement may be limited by pain. Pain in the hip joint is less common and tends to be located anteriorly, over the inguinal ligament; it may radiate medially to the groin. Uncommonly, iliopsoas bursitis may mimic true hip joint pain. Diagnosis of iliopsoas bursitis may be suggested by a history of trauma or inflammatory arthritis. Pain associated with iliopsoas bursitis is localized to the groin or anterior thigh and tends to worsen with hyperextension of the hip; many patients prefer to flex and externally rotate the hip to reduce the pain from a distended bursa.
Origins of hip pain and dysesthesias. (From JJ Cush et al: Evaluation of musculoskeletal complaints, in Rheumatology: Diagnosis and Therapeutics, 2nd ed, JJ Cush et al [eds]. Philadelphia, Lippincott Williams & Wilkins, 2005, pp 3–20. Used with permission from Dr. John J. Cush.)
The vast majority of musculoskeletal disorders can be logically diagnosed by a complete history and physical examination. An additional objective of the initial encounter is to determine whether additional investigations or immediate therapy is required. Additional evaluation is indicated with: (1) monarticular conditions; (2) traumatic or inflammatory conditions; (3) the presence of neurologic findings; (4) systemic manifestations; or (5) chronic symptoms (>6 weeks) and a lack of response to symptomatic measures. The extent and nature of the additional investigation should be dictated by the clinical features and suspected pathologic process. Laboratory tests should be used to confirm a specific clinical diagnosis and not be used to screen or evaluate patients with vague rheumatic complaints. Indiscriminate use of broad batteries of diagnostic tests and radiographic procedures is rarely a useful or cost-effective means to establish a diagnosis.
Besides a complete blood count, including a white blood cell (WBC) and differential count, the routine evaluation should include a determination of an acute-phase reactant such as the ESR or CRP, which can be useful in discriminating inflammatory from noninflammatory disorders. Both are inexpensive, easily obtained, and may be elevated with infection, inflammation, autoimmune disorders, neoplasia, pregnancy, renal insufficiency, advanced age, or hyperlipidemia. Extreme elevation of the acute-phase reactants (CRP, ESR) is seldom seen without evidence of serious illness (e.g., sepsis, pleuropericarditis, polymyalgia rheumatica, giant cell arteritis, adult Still’s disease).
Serum uric acid determinations are useful in the diagnosis of gout and in monitoring the response to urate-lowering therapy. Uric acid, the end product of purine metabolism, is primarily excreted in the urine. Serum values range from 238 to 516 μmol/L (4.0–8.6 mg/dL) in men; the lower values (178–351 μmol/L [3.0–5.9 mg/dL]) seen in women are caused by the uricosuric effects of estrogen. Urinary uric acid levels are normally <750 mg per 24 h. Although hyperuricemia (especially levels >535 μmol/L [>9 mg/dL]) is associated with an increased incidence of gout and nephrolithiasis, levels may not correlate with the severity of articular disease. Uric acid levels (and the risk of gout) may be increased by inborn errors of metabolism (Lesch-Nyhan syndrome), disease states (renal insufficiency, myeloproliferative disease, psoriasis), or drugs (alcohol, cytotoxic therapy, thiazides). Although nearly all patients with gout will demonstrate hyperuricemia at some time during their illness, up to 50% of patients with an acute gouty attack will have normal serum uric acid levels. Monitoring serum uric acid is useful in assessing the response to urate-lowering therapy or chemotherapy, with the target goal being a serum urate <6 mg/dL.
Serologic tests for RF, cyclic anticitrullinated peptide (CCP or ACPA) antibodies, ANAs, complement levels, Lyme and antineutrophil cytoplasmic antibodies (ANCA), or antistreptolysin O (ASO) titer should be carried out only when there is clinical evidence to specifically suggest an associated diagnosis because these have poor predictive value when used for screening, especially when the pretest probability is low. For most of these, there is no value to repeated or serial serologic testing. Although 4–5% of a healthy population will have positive tests for RF and ANAs, only 1% and <0.4% of the population will have RA or SLE, respectively. IgM RF (autoantibodies against the Fc portion of IgG) is found in 80% of patients with RA and may also be seen in low titers in patients with chronic infections (tuberculosis, leprosy, hepatitis); other autoimmune diseases (SLE, Sjögren’s syndrome); and chronic pulmonary, hepatic, or renal diseases. When considering RA, both serum RF and anti-CCP antibodies should be obtained as these are complementary. Both are comparably sensitive, but CCP antibodies are more specific than RF. In RA, the presence of anti-CCP and RF antibodies may indicate a greater risk for more severe, erosive polyarthritis. ANAs are found in nearly all patients with SLE and may also be seen in patients with other autoimmune diseases (polymyositis, scleroderma, antiphospholipid syndrome, Sjögren’s syndrome), drug-induced lupus (Table 363-2), chronic liver or renal disorders, and advanced age. Positive ANAs are found in 5% of adults and in up to 14% of elderly or chronically ill individuals. The ANA test is very sensitive but poorly specific for lupus, as only 1–2% of all positive results will be caused by lupus alone. The interpretation of a positive ANA test may depend on the magnitude of the titer and the pattern observed by immunofluorescence microscopy (Table 363-4). Diffuse and speckled patterns are least specific, whereas a peripheral, or rim, pattern (related to autoantibodies against double-strand [native] DNA) is highly specific and suggestive of lupus. Centromeric patterns are seen in patients with limited scleroderma (calcinosis, Raynaud’s phenomenon, esophageal involvement, sclerodactyly, telangiectasia [CREST] syndrome), primary biliary sclerosis, Sjögren’s syndrome or thyroiditis and nucleolar patterns may be seen in patients with diffuse systemic sclerosis or inflammatory myositis.
TABLE 363-4Antinuclear Antibody (ANA) Patterns and Clinical Associations ||Download (.pdf) TABLE 363-4 Antinuclear Antibody (ANA) Patterns and Clinical Associations
|ANA Pattern ||Antigen Identified ||Clinical Correlate |
|Diffuse ||Deoxyribonucleoprotein ||Nonspecific |
|Histones ||Drug-induced lupus, lupus |
|Peripheral (rim) ||ds-DNA ||50% of SLE (specific) |
|Speckled ||U1-RNP ||>90% of MCTD |
|Sm ||30% of SLE (specific) |
|Ro (SS-A) ||Sjögren’s 60%, SCLE, neonatal lupus, ANA(–) lupus |
|La (SS-B) ||50% of Sjögren’s, 15% lupus |
|Scl-70 ||40% of diffuse scleroderma |
|PM-1 ||Polymyositis (PM), dermatomyositis |
|Jo-1 ||PM w/pneumonitis + arthritis |
|Nucleolar ||RNA polymerase I, others ||40% of PSS |
|Centromere ||Kinetochore ||75% CREST (limited scleroderma), PBC, Sjogren’s, thyroiditis |
Aspiration and analysis of synovial fluid are always indicated in acute monarthritis or when an infectious or crystal-induced arthropathy is suspected. Synovial fluid may distinguish between noninflammatory and inflammatory processes by analysis of the appearance, viscosity, and cell count. Tests for synovial fluid glucose, protein, lactate dehydrogenase, lactic acid, or autoantibodies are not recommended because they have no diagnostic value. Normal synovial fluid is clear or a pale straw color and is viscous, primarily because of the high levels of hyaluronate. Noninflammatory synovial fluid is clear, viscous, and amber-colored, with a WBC count of <2000/μL and a predominance of mononuclear cells. The viscosity of synovial fluid is assessed by expressing fluid from the syringe one drop at a time. Normally, there is a stringing effect, with a long tail behind each synovial drop. Effusions caused by OA or trauma will have normal viscosity. Inflammatory fluid is turbid and yellow, with an increased WBC count (2000–50,000/μL) and a polymorphonuclear leukocyte predominance. Inflammatory fluid has reduced viscosity (no stringing), diminished hyaluronate, and little or no tail following each drop of synovial fluid. Such effusions are found in RA, gout, and other inflammatory arthritides. Septic fluid is opaque and purulent, with a WBC count usually >50,000/μL, a predominance of polymorphonuclear leukocytes (>75%), and low viscosity. Such effusions are typical of septic arthritis but may also occur with RA or gout. In addition, hemorrhagic synovial fluid may be seen with trauma, hemarthrosis, or neuropathic arthritis. An algorithm for synovial fluid aspiration and analysis is shown in Fig. 363-6. Synovial fluid should be analyzed immediately for appearance, viscosity, and cell count. Monosodium urate crystals (observed in gout) are seen by polarized microscopy and are long, needle-shaped, negatively birefringent, and usually intracellular. In chondrocalcinosis and pseudogout, calcium pyrophosphate dihydrate crystals are usually short, rhomboid-shaped, and positively birefringent. Whenever infection is suspected, synovial fluid should be Gram stained and cultured appropriately. If gonococcal arthritis is suspected, nucleic acid amplification tests should be used to detect either Chlamydia trachomatis or N. gonorrhoeae infection. Synovial fluid from patients with chronic monarthritis should also be cultured for M. tuberculosis and fungi. Last, it should be noted that crystal-induced arthritis and septic arthritis occasionally occur together in the same joint.
Algorithmic approach to the use and interpretation of synovial fluid aspiration and analysis. PMNs, polymorphonuclear (leukocytes); WBC, white blood cell count.
DIAGNOSTIC IMAGING IN JOINT DISEASES
Conventional radiography has been a valuable tool in the diagnosis and staging of articular disorders. Plain x-rays are most appropriate and cost effective when there is a history of trauma, suspected chronic infection, progressive disability, or monarticular involvement; when therapeutic alterations are considered; or when a baseline assessment is desired for what appears to be a chronic process. However, in acute inflammatory arthritis, early radiography is rarely helpful in establishing a diagnosis and may only reveal soft tissue swelling or juxtaarticular demineralization. As the disease progresses, calcification (of soft tissues, cartilage, or bone), joint space narrowing, erosions, bony ankylosis, new bone formation (sclerosis, osteophytes, or periostitis), or subchondral cysts may develop and suggest specific clinical entities. Consultation with a radiologist will help define the optimal imaging modality, technique, or positioning and prevent the need for further studies.
Additional imaging techniques may possess greater diagnostic sensitivity and facilitate early diagnosis in a limited number of articular disorders and in selected circumstances and are indicated when conventional radiography is inadequate or nondiagnostic (Table 363-5). Ultrasonography is useful in the detection of soft tissue abnormalities, such as tendinitis, tenosynovitis, enthesitis, bursitis, and entrapment neuropathies. Wider use, lower cost, better technology, and enhanced site-specific transducers now allow for wider use in outpatient care, especially for the evaluation of synovial (Baker’s) cysts, rotator cuff tears, tendinitis and tendon injury, and crystal deposition on cartilage. Use of power Doppler allows for early detection of synovitis and bony erosions. Radionuclide scintigraphy is a very sensitive, but poorly specific, means of detecting inflammatory or metabolic alterations in bone or periarticular soft tissue structures (Table 363-5). Scintigraphy is best suited for total-body assessment (extent and distribution) of skeletal involvement (neoplasia, Paget’s disease) and the assessment of patients with undiagnosed polyarthralgias, looking for occult arthritis. The use of scintigraphy has declined with greater use and declining cost of ultrasound and MRI. MRI has largely replaced scintigraphy in diagnosing osseous infection, neoplasia, inflammation, increased blood flow, bone remodeling, heterotopic bone formation, or avascular necrosis. Gallium scanning uses 67Ga, which binds serum and cellular transferrin and lactoferrin and is preferentially taken up by neutrophils, macrophages, bacteria, and tumor tissue (e.g., lymphoma). As such, it is primarily used in the identification of occult infection or malignancy. Scanning with 111In-labeled WBCs has been used to detect osteomyelitis and infectious or inflammatory arthritis. Despite their utility, 111In-labeled WBC or 67Ga scanning has largely been replaced by MRI, except when there is a suspicion of septic joint or prosthetic joint infections.
TABLE 363-5Diagnostic Imaging Techniques for Musculoskeletal Disorders ||Download (.pdf) TABLE 363-5 Diagnostic Imaging Techniques for Musculoskeletal Disorders
|Method ||Imaging Time, h ||Costa ||Current Indications |
|Ultrasound ||<1 ||++ ||Synovial (Baker’s) cysts |
| || || || |
Rotator cuff tears
Bursitis, tendinitis, tendon injury
Carpal tunnel syndrome
Urate or calcium pyrophosphate deposition on cartilage
Early detection of synovial inflammation or erosions
|Radionuclide scintigraphy || || || |
Metastatic bone survey
Evaluation of Paget’s disease
| 99mTc ||1–4 ||++ || |
Identifying occult arthritis in patients with undiagnosed polyarthralgia
| 111In-WBC ||24 ||+++ || |
| 67Ga ||24–48 ||++++ || |
Acute and chronic infection
|Computed tomography (CT) ||<1 ||+++ || |
Herniated intervertebral disk
|Dual-energy CT ||<1 ||NA || |
Uric acid deposition
|Magnetic resonance imaging ||1/2–2 ||++++ ||Avascular necrosis |
Septic arthritis, infected prosthetic joints
Intraarticular derangement and soft tissue injury
Derangements of axial skeleton and spinal cord
Herniated intervertebral disk
Pigmented villonodular synovitis
Inflammatory and metabolic muscle pathology
Computed tomography (CT) provides detailed visualization of the axial skeleton. Articulations previously considered difficult to visualize by radiography (e.g., zygapophyseal, sacroiliac, sternoclavicular, hip joints) can be effectively evaluated using CT. CT has been demonstrated to be useful in the diagnosis of low back pain syndromes (e.g., spinal stenosis vs herniated disk), sacroiliitis, osteoid osteoma, and stress fractures. Helical or spiral CT (with or without contrast angiography) is a novel technique that is rapid, cost effective, and sensitive in diagnosing pulmonary embolism or obscure fractures, often in the setting of initially equivocal findings. High-resolution CT can be advocated in the evaluation of suspected or established infiltrative lung disease (e.g., scleroderma or rheumatoid lung). The recent use of hybrid (positron emission tomography [PET] or single-photon emission CT [SPECT]) CT scans in metastatic evaluations has incorporated CT to provide better anatomic localization of scintigraphic abnormalities.
18F-Fluorodeoxyglucose (FDG) is the most commonly used radiopharmaceutical in PET scanning. FDG-PET/CT scans have been seldom used in the evaluation of septic or inflammatory arthritis, but have also been useful in the evaluation of patients with fever of unknown origin or suspected large vessel vasculitis. Dual-energy CT (DECT) scanning, developed in urology to identify urinary calculi, has been a highly sensitive and specific method used to identify and quantify uric acid deposition in tissues (Fig. 363-7).
Dual-energy computed tomography (DECT) scan from a 45-year-old woman with right ankle swelling around the lateral malleolus. Three-dimensional volume-rendered coronal reformatted DECT image shows that the mass is composed of monosodium urate (red) in keeping with tophus (arrow). (Used with permission from S Nicolaou et al: AJR 194:1072, 2010.)
MRI has significantly advanced the ability to image musculoskeletal structures. MRI has the advantages of providing multiplanar images with fine anatomic detail and contrast resolution (Fig. 363-8) that allows for the superior ability to visualize bone marrow and soft tissue periarticular structures. Although more costly with a longer procedural time than CT, the MRI has become the preferred technique when evaluating complex musculoskeletal disorders.
Superior sensitivity of magnetic resonance imaging (MRI) in the diagnosis of osteonecrosis of the femoral head. A 45-year-old woman receiving high-dose glucocorticoids developed right hip pain. Conventional x-rays (top) demonstrated only mild sclerosis of the right femoral head. T1-weighted MRI (bottom) demonstrated low-density signal in the right femoral head, diagnostic of osteonecrosis.
MRI can image fascia, vessels, nerve, muscle, cartilage, ligaments, tendons, pannus, synovial effusions, and bone marrow. Visualization of particular structures can be enhanced by altering the pulse sequence to produce either T1- or T2-weighted spin echo, gradient echo, or inversion recovery (including short tau inversion recovery [STIR]) images. Because of its sensitivity to changes in marrow fat, MRI is a sensitive but nonspecific means of detecting osteonecrosis, osteomyelitis, and marrow inflammation indicating overlying synovitis or osteitis (Fig. 363-8). Because of its enhanced soft tissue resolution, MRI is more sensitive than arthrography or CT in the diagnosis of soft tissue injuries (e.g., meniscal and rotator cuff tears); intraarticular derangements; marrow abnormalities (osteonecrosis, myeloma); and spinal cord or nerve root damage, synovitis, or cartilage damage or loss.
The author acknowledges the insightful contributions of Dr. Peter E. Lipsky to this chapter in previous editions.
et al: Utility of immunologic testing in suspected rheumatologic disease. Curr Allergy Asthma Rep 14:405, 2014.
M: Serology of lupus erythematosus: Correlation between immunopathological features and clinical aspects. Autoimmune Dis 2014:321359, 2014.
et al: Differentiating radiculopathy from lower extremity arthropathy. Am J Med 129:1124. e1, 2016.
et al: How to diagnose axial spondyloarthritis early. Ann Rheum Dis 63:535, 2004.
CS: Radiologic approach to musculoskeletal infections. Infect Dis Clin North Am 31:299, 2017.