Evaluation of Musculoskeletal Complaints
Last updated: October 6, 2014
Over 25% of all adult out-patient primary care evaluations are for musculoskeletal complaints and half of all clinic visits will include arthritis or rheumatic disease as comorbid problem. A focused rheumatologic evaluation should be considered for those with focal or widespread musculoskeletal complaints, systemic features, physical or functional limitations, or those with abnormal laboratory or imaging results suggesting a rheumatic disorder. Although the goal is an early and accurate diagnosis, this is not always possible at the first encounter. Many musculoskeletal complaints are self-limited and may only require symptomatic therapy. Many musculoskeletal disorders resemble each other at the outset, and some may take weeks or months (but not years) to evolve into a firm diagnosis.
Evaluation of musculoskeletal complaints should include a comprehensive medical history and physical examination, with particular emphasis on features that establish a rheumatologic process. The primary goals of the patient’s evaluation are to discern whether the complaint reflects an underlying urgent or “red flag” condition that merits a prompt diagnosis. Only a few rheumatologic disorders are urgent and require a prompt diagnosis and therapeutic intervention to minimize pain or serious morbid sequelae. These red flag conditions include fracture, septic arthritis/bursitis and crystal-induced arthritis. These conditions are unified in that they often present as acute monarthritis. In the absence of a red flag condition, the patient evaluation should disclose if the nature of the complaint is:
- Inflammatory or noninflammatory;
- Articular or periarticular;
- Acute or chronic;
- Monarticular, oligoarticular or polyarticular.
By determining the nature of the complaint, the clinician can then categorize the complaint (e.g., acute inflammatory monarthritis or chronic noninflammatory polyarthritis) and begin to establish a differential diagnosis. Identification of other distinctive articular and extra-articular features (see “Essential Clinical History” section) often provides the necessary clues to make a timely and accurate diagnosis. Finally, the clinician should remember to consider common conditions first. Whereas low back pain, fracture, fibromyalgia, overuse syndromes (bursitis, tendinitis), and gout affect many millions, dramatic disorders like systemic lupus erythematosus (SLE), scleroderma, Lyme disease, or vasculitis are 10-100 times less prevalent.
Inflammatory versus Noninflammatory
Musculoskeletal disorders are often classified as being either inflammatory or noninflammatory based on symptoms or signs that reflect the underlying pathologic process. Inflammatory disorders include a variety of infectious (e.g., tuberculosis), crystal-induced (gout), immunologic (SLE) and reactive (Reiter ’s syndrome) disorders. Noninflammatory disorders may be traumatic (e.g., fracture), degenerative (osteoarthritis), neoplastic (osteoid osteoma), or functional (psychogenic) in origin.
Inflammatory and noninflammatory features can be identified during the history and physical examination and may be supported by laboratory data (Table 1). The cardinal signs of inflammation—erythema, warmth, pain, or swelling—should be sought. Inflammatory pain is often maximal with prolonged rest (e.g., in the morning), improved by activity and time, and associated with prolonged morning stiffness (>1 hour) or systemic symptoms. Swelling of soft tissues (i.e., synovium or tenosynovium) with or without synovial effusion should suggest an inflammatory process. Laboratory evidence of inflammation (i.e., elevated erythrocyte sedimentation rate, C-reactive protein, or thrombocytosis) may be seen with inflammation and should normal in uncomplicated noninflammatory disorders.
|Table 1. Distinguishing Inflammatory and Noninflammatory Findings|
|Pain (worse/when?)||Yes (morning)||Yes (night)|
|Swelling||Soft tissue (±effusion)||Bony|
|Morning stiffness||Prominent (>1 hr)||Minor (<45 min)|
|Systemic features||Sometimes present||Absent|
|Elevated ESR or CRP||Frequent||Absent|
|Synovial fluid WBCs||WBCs >2,000/mm3||WBCs <2,000/mm3|
RA, gout, polymyalgia
Articular stiffness commonly accompanies musculoskeletal disorders. Morning stiffness is ascertained by asking, “upon arising from a night’s sleep, how long (minutes or hours) does it take for your stiffness to go away or get as good as it is going to get?” Rheumatologists often emphasize the importance of morning stiffness in distinguishing inflammatory and noninflammatory states. Unfortunately, the specificity of this feature is poor because common noninflammatory disorders like fibromyalgia and osteoarthritis may also be accompanied by >1 hour of morning stiffness. Stiffness brought on by brief periods of rest, lasting minutes rather than hours, is called gel phenomenon. Gel phenomenon is common with noninflammatory conditions such as osteoarthritis, adhesive capsulitis and fibromyalgia.
Noninflammatory disorders are typically worsened by activity. Thus, patients typically complain of maximal pain in the evening or at night. Bony hypertrophy (swelling) at distinctive locations (e.g., Heberdens’ nodes) and a lack of systemic features are characteristic of noninflammatory conditions.
Articular versus Periarticular
During the musculoskeletal evaluation, the examiner must determine whether the complaint originates from articular or periarticular structures as both lie in close proximity and are easily confused. A careful history and examination using knowledge of local anatomy and specific maneuvers are necessary to localize the source of pain. Articular structures include the synovium, synovial fluid, articular cartilage, and joint capsule. The extent of articular involvement is defined as monarticular (one joint), oligoarticular or pauciarticular (two to four joints), or polyarticular (more than four joints). When considering children and juvenile idiopathic arthritis (JIA), oligoarticular (also known as pauciarticular) is defined as four or fewer joints. The differential causes of monarticular and oligoarticular complaints are remarkably similar, thus these two are often lumped together (i.e., mono/oligoarticular) when formulating a differential diagnosis (Table 2).
|Table 2. Distinguishing Articular and Periarticular Joint Pain|
|Anatomic structures||Synovium, synovial fluid,
articular cartilage, joint
|Tendon, bursa, ligament,
muscle, bone, fascia, nerve,
|Painful site||Diffuse, deep tenderness||Focal or “point” tenderness|
|Pain on movement||Pain on active and passive
motion in all planes
|Pain on active motion in few,
|Swelling||Common (bony and soft tissue)||Uncommon|
Periarticular structures include tendon, bursa, ligament, muscle, bone, fascia, nerve, or overlying skin. Periarticular complaints may be described as focal or widespread. Arthralgia (complaint of joint pain) may actually arise from articular or periarticular sites. Periarticular complaints are often misconstrued as articular pain because of their proximity. Table 3 details several distinguishing features useful in discriminating between articular and periarticular joint pain. The approach to evaluating regional articular and periarticular pain is also described in the Diseases section: hand and wrist pain, shoulder pain, neck pain, low back pain, hip pain and knee pain.
|Table 3. Differential Diagnosis of Musculoskeletal Complaints|
|Mono/Oligoarticular Disorders||Polyarticular Disorders|
|Acute||Septic arthritis, Gout, Pseugout, Viral arthritis*, Reactive arthritis, Lyme disease, Rheumatic fever, Hemarthrosis, Palindromic rheumatism||Fracture, Trauma, Mechanical derangement, Sickle-cell crisis||Viral arthritis*, Septic arthritis, Rheumatic fever, Serum sickness, Reactive arthritis||Sickle cell crisis|
|Chronic||Tuberculous arthritis, Fungal arthritis, Psoriatic arthritis, Spondyloarthritis, Pseudogout, Sarcoidosis, JIA||Osteoarthritis, Osteonecrosis, Neuropathic arthritis, Hemarthrosis, Pigmented villonodular synovitis, Foreign body synovitis||RA, JIA, SLE, Psoriatic arthritis, Enteropathic arthritis, Crystal arthritis, MCTD, Lyme, Scleroderma||Osteoarthritis, Hemochromatosis, Hypertrophic osteoarthropathy|
Focal Periarticular Disorders
Widespread Periarticular Disorders
|Acute||Bursitis, Septic bursitis, Tendinitis, Tenosynovitis, Costochondritis, Enthesitis, Dactylitis, Periostitis||Fracture, Carpal tunnel syndrome, Entrapment neuropathy, Sickle-cell crisis, Reflex sympathethic dystrophy||Enthesitis, Polymyalgia rheumatica, Relapsing polychondritis||Sickle-cell crisis|
|Chronic||Tendinitis, Tenosynovitis, Costochondritis, Enthesitis, Dactylitis, Periostitis||Carpal tunnel syndrome, Entrapment neuropathy, Myofascial pain syndrome, Fracture, Raynaud’s, Osteoid osteoma||Polymyalgia rheumatica, Polymyositis, Dermatomyositis, Myasthenia gravis, Eosinophilic fasciitis, Enthesitis||Fibromyalgia, Chronic fatigue syndrome, Myxedema, Drug-induced disorders, Osteoporosis, Paget’s disease, Psychogenic rheumatism|
|* Viral arthritis includes Epstein-Barr virus, Parvovirus B19, hepatitis B or C, rubella, human immunodeficiency virus. Abbreviations: JIA – juvenile idiopathic arthritis, SLE – systemic lupus erythematosus, MCTD – mixed connective tissue disease|
Essential Clinical History
The differential diagnosis may be narrowed further by reviewing key historical information. Because some types of arthritis may affect one population more than others, important diagnostic clues can be obtained from basic demographic information such as gender, race, and family history (Table 4). Some disorders preferentially affect particular ethnic groups; polymyalgia rheumatica, giant cell arteritis, and granulomatosus with polyangiitis (Wegener’s granulomatosis) are most common in whites, whereas sarcoid and lupus are more common in African Americans.
On presentation, the clinician should determine whether the complaint is acute or chronic, based on whether the complaint has been present 6 weeks or less (acute) or longer than 6 weeks (chronic). The presentation of fracture, gonococcal arthritis and gout is typically acute; fibromyalgia, OA, and rheumatoid arthritis are chronic. Other aspects of the onset and chronology often provide useful clues (Table 4). For example, intermittent complaints (with disease-free intervals) may indicate a crystal-induced arthropathy (e.g., gout, pseudogout). Incremental involvement of new joints describes an additive pattern characteristic of OA and RA. Migratory arthritis is defined as a rapidly changing pattern in which new joint complaints appear, resolve in days, and reappear at another site(s). A migratory pattern may be seen in rheumatic fever and viral (i.e., hepatitis B) or gonococcal arthritis. The number and distribution of involved joints also provide useful information (Table 4). Complaints may be described as monarticular, oligoarticular (or pauciarticular), polyarticular, focal, or widespread. Symmetric joint involvement in the upper extremity is typical of RA, whereas OA, Reiter’s syndrome, and gout often demonstrate asymmetric, lower extremity disease. Axial (spinal) in- volvement is common in OA and ankylosing spondylitis. Finally, the clinician should be aware that drug-induced musculoskeletal side effects or rheumatic disorders are a common and often overlooked cause of musculoskeletal complaints (Table 4).
Table 4. Clinical Associations Based on History and Physical Examination
– Young (<25 y): JIA, SLE, reactive arthritis, gonococcal arthritis, hypermobility syndrome
– Middle (25–65 y): Fibromyalgia, tendinitis, bursitis, low back pain, RA
– Elderly (>65 y): OA, crystal arthritis, polymyalgia rheumatica, septic arthritis, osteoporosis, drug-induced syndromes
– Males: Gout, ankylosing spondylitis, reactive arthritis, OA of the hip
– Females: Fibromyalgia, RA, SLE, OA
– White: Polymyalgia rheumatica, giant cell arteritis, granulomatosus with polyangiitis (Wegener’s)
– African American: SLE, sarcoidosis
– Asian: RA, SLE, Takayasu arteritis, Behçet’s disease, SAPHO syndrome, Kikuchi’s disease
– Mediterranean: FMF, Takayasu arteritis, Behcet’s
Family history Ankylosing spondylitis, gout, Heberden’s nodes of OA
Onset and Chronology
– Acute: Fracture, septic arthritis, gout, rheumatic fever, reactive arthritis
– Chronic: OA, RA, SLE, psoriatic arthritis, fibromyalgia
– Intermittent: Gout, pseudogout, Lyme disease, palindromic rheumatism, Behçet’s disease, FMF
– Additive: OA, RA, psoriatic arthritis
– Migratory: Viral arthritis (e.g., hepatitis B), rheumatic fever, SLE, gonococcal arthritis
Number and Distribution
– Monarthritis (1 joint): Septic arthritis, gout, pseudogout, fracture, OA, osteonecrosis, reactive arthritis
– Oligoarthritis (2–4): OA, psoriatic arthritis, reactive arthritis, spondyloarthritis, pseudogout, gout, Lyme, sarcoid
– Polyarthritis (>4): RA, SLE, OA, viral arthritis, psoriatic arthritis, serum sickness
– Symmetric: RA, OA, psoriasis, tophaceous gout, viral arthritis
– Asymmetric: OA, reactive arthritis, psoriatic arthritis, podagra/early gout, sarcoid, spondyloarthritis
– Axial: OA, ankylosing spondylitis, fibromyalgia, spinal stenosis, diffuse idiopathic skeletal hyperostosis
– Lower extremity: reactive arthritis, gout, sarcoid, OA, diabetes (neuropathic arthritis), tarsal tunnel syndrome
– Upper extremity: RA, OA, psoriatic arthritis, carpal tunnel syndrome
– Sternoclavicular: Septic arthritis (especially with substance abuse), RA, trauma, OA
– Distal interphalangeal (DIP): OA (Heberden’s node), psoriatic arthritis, swan-neck deformity
– Proximal interphalangeal (PIP): RA, OA (Bouchard’s node), psoriatic, SLE, viral arthritis, boutonnière deformity
– Metacarpophalangeal (MCP): RA, pseudogout, hemochromatosis, psoriatic arthritis
– Wrist: RA, psoriatic arthritis, septic (e.g., gonococcal) arthritis, deQuervain’s tenosynovitis, carpal tunnel, ganglion
– Elbow: RA, gout, olecranon bursitis, septic arthritis or bursitis, epicondylitis
– Shoulder: Rotator cuff tendinitis/tear, subacromial bursitis, bicipital tendinitis, OA, osteonecrosis, septic arthritis
– Hip: OA, RA, osteonecrosis, osteoid osteoma, fracture, iliopsoas bursitis, trochanteric bursitis
– Knee: OA, RA, pseudogout, gout, septic arthritis, sarcoid, Lyme disease, popliteal cyst, anserine bursitis, meniscal tear, chondromalacia patella, hemophilia, sickle cell, osteonecrosis
– Ankle/Tarsus: Gout, septic arthritis, RA, sarcoid, hemophilia, diabetes (neuropathic arthritis)
– Metatarsophalangeal (MCP): RA, OA, gout, reactive arthritis
– Toes: RA, psoriatic arthritis, reactive arthritis, dactylitis, trauma
– Arthralgias: Quinidine, cimetidine, quinolones, beta-blockers, acyclovir, interferons, IL-2, nicardipine, BCG, HIV protease inhibitors
– Myalgias/myopathy: Steroids, penicillamine, hydroxychloroquine, zidovudine, statins, amiodarone, clofibrate, alcohol, cocaine, taxol, docetaxel, imatinib mesylate, interferons, IL-2, colchicine, tryptophan, cyclosporine, tacrolimus
– Tendon rupture: Quinolones, glucocorticoids, isotretinoin, statins, collagenase injections
– Gout: Diuretics, aspirin, cytotoxics, cyclosporine, alcohol, moonshine, ethambutol, fructose-containing soft drinks
– Drug-induced lupus: Hydralazine, procainamide, quinidine, methyldopa, phenytoin, isoniazid, chlorpromazine, lithium, penicillamine, minocycline, TNF inhibitors, ACE inhibitors
– Drug-induced subacute lupus (SCLE): Proton-pump inhibitors, calcium-channel blockers (diltiazem), ACE inhibitors, TNF inhibitors, terbinafine, interferons (alpha and beta-1a), paclitaxel, docetaxel, thiazide diuretics
– Osteonecrosis: Steroids, alcohol, radiation therapy, trauma
– Osteopenia: Steroids, chronic heparin, phenytoin
– Scleroderma/tight skin: Vinyl chloride, bleomycin, balcitinib, pentazocine, solvents, carbidopa, tryptophan, rapeseed oil
– Vasculitis*: Allopurinol, amphetamines, cocaine (often levamisole adulterated), thiazide, penicillamine, propylthiouracil, montelukast, hepatitis B vaccine, TNF inhibitor, trimethoprim/sulfamethoxazole, minocycline, hydralazine
* most of these are small-vessel, leukocytoclastic vasculitis
Abbreviations: JRA: juvenile rheumatoid arthritis; SLE: systemic lupus erythematosus; RA: rheumatoid arthritis; OA: os- teoarthritis; PMR: polymyalgia rheumatica; FMF: familial Mediterranean fever; IL: interleukin; TNF: tumor necrosis factor; ACE: angiotensin converting enzyme
A comprehensive rheumatic review of systems may disclose extraarticular features indicating particular rheumatic disorders. Table 5 details a suggested review of systems and possible clinical associations. For example, the examiner may narrow the diagnostic possibilities by questioning about the presence of fever (suggesting SLE, septic arthritis, or gout), ocular inflammation (Reiter ’s syndrome, sarcoid, Behçet’s disease), rash (dermatomyositis, SLE, psoriatic arthritis), mucosal ulceration (Behçet’s disease, drug induced), nail abnormalities (psoriasis, Reiter ’s syndrome), myalgias (myositis, fibromyalgia, viral arthritis), heel pain (HLA-B27 spondyloarthropathies, fasciitis), nodules (RA, gout, hyperlipidemia), dysphagia (scleroderma, myositis, Sjögren’s syndrome), paresthesias (carpal tunnel syndrome, vasculitis, Lyme disease), and sleep dis- turbance (fibromyalgia, rotator cuff dysfunction).
|Table 5. Rheumatic Review of Symptoms and Clinical Associations|
|Fever||Septic arthritis, gout, pseudogout, SLE, viral arthritis, MCTD, reactive arthritis, RA, vasculitis, rheumatic fever, adult-onset Still’s disease, drug fever, Sweet’s syndrome, osteomyelitis, Brucella, enteropathic arthritis, Behçet’s disease, autoinflammatory syndromes (FMF, TRAPS, PAPA, cryopyrinopathies, Schnitzler syndrome)|
|Weight loss||Uncontrolled inflammatory disorders (SLE, RA, polymyalgia rheumatica), vasculitis (temporal arteritis, polyarteritis), NSAID or H. Pylori induced peptic ulcer disease, enteropathic arthritis|
|Fatigue||Iinflammation (seen in active RA, polmyalgia rheumatica), chronic pain, fibromyalgia, poor sleep, depression, anemia, cardiac failure, endocrinopathy, malnutrition|
|Morning stiffness >1h||RA, polymyalgiarheumatica, psoriatic arthritis, ankylosing spondylitis, inflammatory osteoarthritis, fibromyalgia|
|Ocular involvement||Sjögren’s syndrome, Behçet’s disease, reactive arthritis, spondyloarthritis, enteropathic arthritis, juvenile idiopathic arthritis, sarcoid, RA, ganulomatosus with polyangiitis, Kawasaki syndrome, temporal arteritis, relapsing polychondritis|
|Oral ulcers (+painful?)||SLE (-), reactive arthritis (-), enteropathic arthritis (-), syphilis (-), Behçet’s disease(+), herpes (+), methotrexate (+), gold (+)|
|Genital ulcers (+painful?)||Gonococcal (+), Behçet’s disease (+), aphthous stomatitis (+), PFAPA (+), reactive arthritis (-), psoriasis (-), syphilis (-)|
|Rash||SLE, psoriasis, dermatomyositis, vasculitis, cryoglobulinemia, Lyme disease, viral arthritis, rheumatic fever, adult-onset Still’s disease, Sweet’s syndrome, sarcoid, erythema nodosum|
|Tight skin||Scleroderma, CREST syndrome, morphea, linear scleroderma, MCTD, eosinophilic fasciitis, eosinophilia myalgia syndrome, calcinosis, pseudosclerodactyly (e.g., diabetes, hypothy roidism), drugs (bleomycin, vinyl chloride, solvents, carbidopa)|
|Nail abnormalities||Psoriasis, reactive arthritis, spondyloarthritis, onychomycosis, vasculitis, endocarditis, hypertrophic osteoarthropathy (clubbing)|
|Periungual erythema||Dermatomyositis, SLE, scleroderma, MCTD, psoriasis, reactive arthritis|
|Raynaud’s phenomenon||Scleroderma, MCTD, SLE, RA, inflammatory myositis, Buerger’s disease, vasculitis, antiphospholipid syndrome, primary Raynaud’s phenomenon|
|Sausage digits (dactylitis)||Psoriatic arthritis, spondyloarthritis, reactive arthritis, BCG (Poncet’s disease), scleroderma, MCTD, juvenile idiopathic arthritis, sarcoid, sickle cell disease|
|Myalgias||Fibromyalgia ,polymyositis, rhabdomyolysis, vasculitis, SLE, drug-induced lupus, RA, serum sickness, adult-onset Still’s disease, hypothyroidism, viral syndromes, drugs (statins; see Table 4)|
|Spinal pain||Lumbosacral strain, degenerative disc disease, spondyloarthritis (AS, psoriatic arthritis, enteropathic arthritis, reactive arthritis), OA, diffuse idiopathic skeletal hyperostosis (DISH), fibromyalgia, septic disciitis, spondylodiscitis, vertebral compression fracture, osteomyelitis, metastases, spinal stenosis (central or foraminal), tuberculosis (Pott’s disease), brucellosis|
|Heel pain||Spondyloarthritis, ankylosing spondylitis, reactive arthritis, psoriatic arthritis, enteropathic arthritis, osteoarthritis, plantar fasciitis, Achilles tendinitis, calcaneal fracture, plantar neuropathy, heel pad atrophy, fluorosis, retinoid therapy|
|Subcutaneous nodules||RA, Gout(tophi), rheumatic fever, hyperlipidemia (xanthomas), panniculitis, erythema nodosum, sarcoid, MCTD, polyarteritis, calcinosis, leprosy, multicentric reticulohistiocytosis, ganglion|
|Dysphagia||Lower (substernal): scleroderma, CREST, syndrome, MCTD, Crohn’s disease
Upper (pharyngeal): polymyositis, dermatomyositis, Sjögren’s syndrome, xerostomia
|Gastrointestinal involvement||Scleroderma, MCTD, enterpathic arthritis, vasculitis, polyarteritis nodosa, Behçet’s disease, Whipple’s disease, SLE, hepatitis, familial Mediterranean fever, intestinal bypass (arthritis-dermatitis) syndrome, primary biliary cirrhosis, autoimmune hepatitis, cryoglobulinemia, autoinflammatory syndromes|
|Serositis||SLE, RA, MCTD, drug-induced lupus, rheumatic fever, adult-onset Still’s disease, familial Mediterranean fever, TRAPs,Whipple’s disease|
|Pulmonary involvement||Granulomatosus with polyangiitis, Churg-Strauss angiitis, polymyositis, dermatomyositis, SLE, scleroderma, CREST, MCTD, Sjögren’s syn drome, sarcoidosis, RA, ankylosing spondylitis, Goodpasture’s syndrome, drug-induced lupus, adult-onset Still’s disease|
|Neuropathy||Carpal o rtarsal tunnel syndrome, SLE, vasculitis, Lyme disease, RA, amyloidosis, cryoglobulinemia, amyloidosis, drug-induced|
|Sleep disturbance||Fibromyalgia, myofascial pain syndrome, osteoarthritis, rotator cuff tendinitis/tear, AS, steroid therapy, depression, osteoid osteoma|
|Abbreviations: SLE, systemic lupus erythematosus; MCTD, mixed connective tissue disease; RA, rheumatoid arthritis; AS, ankylosing spondylitis; FMF, familial Mediterranean fever; TRAPS, TNF receptor associated periodic syndrome; PFAPA, periodic fever, aphthous stomatitis, pharyngitis and cervical adenitis syndrome; CREST, calcinosis, Raynaud’s, esophageal dysmotility, sclerodactyly and telangiectasia; OA, osteoarthritis|
The physical examination should confirm or expand on the differential diagnosis established during the medical history. In addition, the physical examination will further establish whether the complaint is articular or periarticular, inflammatory or noninflammatory, focal or widespread, monarticular or polyarticular or associated with systemic findings. Knowledge of anatomy and other historic and exam clues will distinguish articular from periarticular conditions (Table 2). After a general physical examination, the musculoskeletal examination can be performed by careful inspection, palpation, and a variety of physical maneuvers to elicit diagnostic findings.
Table 6. Physical Examination Checklist
The examiner should assess for:
– Signs of inflammation
– Articular or periarticular abnormalities
– Joint swelling
– Range of motion
– Contracture or deformity
– Joint instability, subluxation, dislocation
– Muscle strength
– Gait abnormalities
– Extraarticular manifestations
In each patient, specific aspects of the musculoskeletal examination should be addressed (Table 6). Examination of symptomatic and asymptomatic joints may reveal the presence and extent of inflammation, indicated by warmth, erythema or swelling. Joints should be palpated from all sides and the range of motion passively assessed in all planes. The examination should discern whether the joint complaint involves articular or periarticular structures. Joint swelling may be caused by synovial effusion, proliferation of the synovial membrane (synovitis), or bony hypertrophy; all of which can be identified by careful inspection, palpation and specific maneuvers.
Synovial fluid often produces fluctuant or ballottable soft tissue enlargement. In large joints such as the knee, synovial effusion may be suggested by a “bulge” sign or ballottable patella (Table 7). Proliferation of synovial tissue can be felt as a supple, compressible, squishy, soft tissue swelling within the margins of the joint capsule. Bursitis (i.e., olecranon, prepatellar) may manifest as a localized pain, with or without a well-defined, fluctuant, subcutaneous swelling over bony extensor surfaces and lying adjacent to the joint capsule. Swelling may also be caused by bony hypertrophy that may accompany OA, neuropathic arthritis, or trauma. Such hypertrophic joints often present as asymmetric, bony-hard enlargements of juxtaarticular bone that may or may not be painful.
|Table 7. Physical Examination: Specific Signs and Maneuvers|
|Test/Maneuver (Joint)||Use and Description|
|Bulge sign (knee)||Identifies small to moderate synovial effusions. Starting above the knee, the examiner should manually push or “milk” joint fluid downward and laterally from the suprapatellar pouch; applying pressure lateral to the patella will result in a visible “bulge” (or movement of fluid) to the medial side of the joint.|
|Drawer sign (knee)
||Identifies joint instability and possible cruciate tear; with the patient supine and the knee/leg at a 90-degree angle, the examiner places hands behind the knee and pulls the proximal tibia forward (toward the examiner); excessive laxity or forward excursion may indicate an anterior cruciate ligament tear.|
|McMurray test (knee)||Identifies a meniscal cartilage tear; with the patient supine, the hip and knee flexed and internally rotated, the lower limb is extended while maintaining internal torque to detect a palpable or audible snap or “pop” or intraarticular pain indicating a cartilage tear. The procedure should be repeated with external rotation and torque to assess the contralateral meniscus.|
|Patrick or FABERE test (hip & SI)||Identifies hip and sacroiliac (SI) abnormalities. FABERE stands for Flexion, ABduction, External Rotation and Extension. With the patient lying supine, place the foot on the contralateral knee and externally rotate at the hip by moving the knee downward and laterally; pain in the inguinal region may indicate hip disease; the SI joint may be compressed by simultaneously pushing the flexed ipsilateral knee and contralateral superior iliac crest downward.|
|Straight leg test (lumbar, sciatic nerve)||Identifies abnormalities of the lumbar nerve roots and/or sciatic nerve; with the patient lying supine and the leg straight, elevate (flex at the hip) the limb upward by grabbing the heel. Normally, the leg can be raised to an angle >80 degrees before discomfort is noted; if pain is noted before this point, lower slightly (10-20 degrees) and dorsiflex the foot to put stretch on the sciatic nerve; dorsiflexion-induced pain suggests sciatic nerve or lumbar nerve root abnormalities. If dorsiflexion of the foot does not cause pain, then limitation of motion may be from tight hamstring tendons.|
|Schober test (lumbar, SI)||Identifies limited motion in the SI or lumbar spine. With the patient standing upright, place penmarks at L5 and 10cm cephalad; ask the patient to bend as far forward as possible (without flexing the knees) and measure the distance between marks. Normally the distance between marks will increase by >2cm; minimal change of <2cm indicates limited SI or lumbar mobility.|
|Drop arm test (rotator cuff)||Identifies a complete tear of the rotator cuff, specifically the supraspinatus tendon. With the patient standing or sitting upright, abduct the arm fully to 90 degrees; ask the patient to slowly lower the arm to his or her side; those with a complete tear of the supraspinatus will suddenly drop the arm down in pain or will be unable to lower the arm smoothly.|
|Finkelstein’s sign (wrist)||Identifies deQuervain’s tenosynovitis (involving the abductor pollicis longus or extensor pollicis brevis). Have the patient place the flexed thumb inside a clenched fist; ulnar deviation of the wrist will produce pain over the involved tendons along the radial aspect of the tendons over the wrist joint (positive test).|
|Tinels sign (wrist, ankle)||Identifies carpal tunnel syndrome (median nerve entrapment) by repetitively tapping (thumping) the volar aspect of the wrist to produce an electric-like sensation or numbness in the first lateral 3 and 1/2 digits of the hand (from thumb to middle of the ring finger); tarsal tunnel syndrome (posterior tibial nerve entrapment) may be diagnosed if the same symptoms are elicited by thumping over the flexor retinaculum (posterior to the medial malleolus) of the ankle.|
Range of motion should be assessed with active (patient-initiated) and passive (examiner-assisted) movement in all planes and be quantified using a goniometer and contralateral comparison. Range of motion may include flexion, extension, rotation, abduction, adduction, lateral bending, inversion, eversion, supination, pronation, and ulnar or radial deviation. The expected range of motion for individual joints is shown in Table 8. Findings may be recorded as either the arc of movement (in degrees) or that which is lacking (e.g., “the shoulder lacked 30 degrees of full abduction”).
|Table 8. Range of Motion – Normal Values|
|Joint||Flexion (deg)||Extension (deg)||Other|
|Neck||45°||>50°||Lateral bend 45°, rotation>60°|
|Shoulder||180°||>40°||Abduction 90°, rotation 90°|
|Elbow||>150°||0–5°||Pronation 80°, supination 90°|
|Wrist||>80°||>60°||Deviation: ulnar 60°, radial 25°|
|Lumbosacral||90°||30°||Lateral bend 40°, rotation 45°|
|Hip||120°||>15°||Abduction >45°, IR/ER >45°|
|Knee||>135°||0–15°||Inversion 30°, eversion 20°|
|Abbreviations: IR/ER, inversion and eversion; MCP, metacarpophalangeal; PIP, proximal interphalangeal; DIP, distal interphalangeal; MTP, metatarsophalangeal.|
Joint crepitus may be felt during these maneuvers. Whereas fine crepitus is common and insignificant in most large joints, coarse crepitus indicates advanced cartilaginous and degenerative changes. Joint motion may be limited by effusion, pain, deformity, or contracture. Contractures often indicate antecedent synovial inflammation or trauma. Joint deformity suggests chronic joint pathology that may result from ligamentous destruction, soft tissue contracture, bony enlargement, ankylosis, erosive disease or subluxation.
Joint stability can be assessed by palpation and by application of manual stress and maneuvers such as the “drawer” sign (also known as the Lachman test) may be used to diagnose cruciate ligament damage (Table 7). Subluxation or dislocation can be assessed by inspection and palpation.
The muscle examination should document strength and the presence of pain, spasm, atrophy or weakness. Muscle strength testing should assess the musculature of the neck, trunk, and distal and proximal extremities and be quantified as shown in Table 9. Typically the limb or muscle group is graded and expressed on a 0-5 scale (e.g., “right hip flexor motor strength was 4/5 “). The clinician should observe the patient rising from the chair and walking forward. The gait should be observed and recorded if abnormal.
Table 9. The Medical Research Council Grading Scale for Muscle Strength
0 = No movement
1 = Trace (flicker) movement
2 = Able to move with gravity eliminated
3 = Able to move against gravity, but not resistance
4 = Able to oppose gravity and resistance
5 = Normal strength
The clinician should carefully examine for periarticular (nonarticular) involvement, especially when articular complaints are not supported by objective findings referable to the joint capsule. Identification of periarticular pain helps prevent unwarranted and often expensive additional evaluations. Examples of periarticular abnormalities include olecranon bursitis, epicondylitis (i.e., tennis elbow), enthesitis (i.e., Achilles tendinitis), and trigger points associated with fibromyalgia. In selected instances, specific maneuvers may be used (Table 7) to identify extraarticular abnormalities, such as a carpal tunnel syndrome (identified by the Tinel sign).
The vast majority of rheumatic conditions can be easily diagnosed by a complete history and physical examination. Further investigations are infrequently required to establish the correct diagnosis. The clinician should avoid the temptation to use screening tests or broad batteries (rheumatic panels) of tests as an aid to diagnosis. Indiscriminate testing is expensive and often yields results with low predictive value. The utility and predictive value of rheumatic tests are disappointingly low when the pretest probability of an anticipated diagnosis is low. Primary indications for further testing include any monarticular presentation (consider arthrocentesis), systemic features (e.g., fever, rash), neurologic manifestations, antecedent trauma (consider radiographs, appropriate imaging), or chronic symptoms that are undiagnosed after an appropriate evaluation, symptomatic therapy, and observation over time (> 6 weeks).
Any history of recent trauma should prompt a careful examination and consideration of appropriate imaging. If necessary, laboratory investigations may include a complete blood count, selected blood chemistries, an acute-phase reactant (e.g., erythrocyte sedimentation rate or C-reactive protein) or possibly a serum uric acid level (if gout is clinically suspected). Routine serologic testing for antinuclear antibodies or rheumatoid factor should be discouraged unless clearly warranted by the clinical picture. Advanced serologic testing (e.g., anti-neutrophil cytoplasmic antibodies, HLA-B27, anti-streptolysin [ASO] antibodies) is only indicated in select clinical situations and are of little value when searching for possible diagnoses. Finally, arthrocentesis and synovial fluid analysis should be considered for patients with monarthritis, suspected infection, or crystal-induced arthritis or when the diagnosis is uncertain. The following chapters will review the use, indications, and interpretation of synovial fluid testing, the use and performance of arthrocentesis and the use and interpretation of many commonly used diagnostic tests and imaging modalities.
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