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Some musculoskeletal disorders affect primarily the joints, causing arthritis. Others affect primarily the bones (eg, fractures, Paget's disease, tumors), muscles or other extra-articular soft tissues (eg, polymyalgia rheumatica, fibromyalgia), or periarticular soft tissues (eg, bursitis, tendinitis, sprain). Arthritis has myriad possible causes, including infection, autoimmune disease, crystal-induced inflammation, other kinds of inflammation, and noninflammatory tissue degeneration; systemic diseases may be involved. Arthritis may affect single or multiple joints, in either a symmetric or asymmetric manner.

History

The physician should ask about systemic and extra-articular symptoms as well as joint symptoms. Many symptoms, including fever, chills, malaise, weight loss, Raynaud's phenomenon, mucocutaneous symptoms (eg, rash, eye irritation or pain, photosensitivity), and GI or cardiopulmonary symptoms, can be associated with joint disorders.

Pain is the most common symptom of many joint disorders. The history should address the location, severity, character, and factors that aggravate or relieve pain. The clinician must determine whether pain is worse upon first moving a joint or after prolonged use and whether it is present upon wakening or develops during the day. Usually, pain originating from superficial structures is better localized than pain originating from deeper structures. Pain originating in small distal joints tends to be better localized than pain originating in large proximal joints. Joint pain can be referred from extra-articular structures or from other joints. Arthritis often produces “aching” pain, whereas neuropathies often produce “burning” pain.

“Stiffness” may mean weakness, fatigue, or fixed limitation of motion to patients. The clinician must separate an inability to move a joint from reluctance to move a joint because of pain. Stiffness of importance to rheumatic disease is difficulty in motion that develops when attempting to move a joint after a period of rest. The duration of stiffness after beginning joint motion reflects its severity. Stiffness is more severe in inflammatory joint disorders. Morning stiffness can be an important early symptom of RA.

Fatigue is a desire to rest that reflects exhaustion. It differs from weakness, inability to move, and reluctance to move due to pain with movement.

Instability, or buckling of a joint, may suggest weakness of the ligaments or other structures that stabilize the joint, which are assessed by stress testing. Buckling occurs most often in the knee and most often results from an internal joint derangement.

Physical Examination

Each involved joint is inspected and palpated, and the range of motion is estimated. With polyarticular disease, certain nonarticular signs (eg, fever, wasting, rash) may reflect systemic disorders.

The rest position of joints is noted, along with any erythema, swelling, deformity, and skin abrasions or punctures. Involved joints are compared with their uninvolved opposites or with those of the examiner.

Joints are gently palpated, noting the presence and location of warmth and tenderness. Determining whether tenderness is present along the joint line or over tendon insertions or bursae is particularly important. Soft masses, bulges, or tissues that fill normal concavities or spaces (representing joint effusion or synovial proliferation) are noted. Palpation of swollen joints can sometimes differentiate among joint effusion, synovial thickening, and capsular or bony enlargement. Small joints (eg, the acromioclavicular, tibiofibular, radioulnar) can be the source of pain that was initially believed to arise from a nearby major joint. Bony enlargement (often due to osteophytes) is noted.

Active range of motion (the maximum range through which the patient can move the joint) is recorded first; limitation may reflect weakness, pain, or stiffness as well as mechanical abnormalities. Then passive range of motion (the maximum range through which the examiner can move the joint) is assessed; passive limitation generally reflects mechanical abnormalities (eg, scarring, swelling, deformities) rather than weakness or pain.

Crepitus, a palpable or audible grinding produced by motion, is noted. It may be caused by roughened articular cartilage or from tendons; crepitus-producing motions should be determined and may suggest which structures are involved.

There are specific features that should be sought at various joints.

Elbow: Synovial swelling and thickening caused by joint disease occur in the lateral aspect between the radial head and olecranon, producing a bulge. Full 180° extension of the joint should be attempted. Although full extension is possible with nonarthritic or extra-articular lesions, its loss is an early change in arthritis. The area around the joint is examined for swellings. Rheumatoid nodules are firm, occurring especially along the extensor surface of the forearm. Tophi are sometimes visible under the skin as cream-colored aggregates and indicate gout. Swelling of the olecranon bursa occurs over the tip of the olecranon, is cystic, and does not limit joint motion; infection, trauma, gout, and RA are possible causes. Epitrochlear nodes occur above the medial epicondyle; they can result from inflammation in the hand but can also suggest sarcoidosis or lymphoma.

Shoulder: Because pain can be referred between areas around the shoulder, shoulder palpation should include the glenohumeral, acromioclavicular, and sternoclavicular joints, the coracoid process, clavicle, acromion process, subacromial bursa, biceps tendon, and greater and lesser tuberosities of the humerus, as well as the neck. Glenohumeral joint effusions may produce a bulge between the coracoid process and the humeral head. Possible causes include RA, osteoarthritis, septic arthritis, Milwaukee shoulder (see Crystal-Induced Arthritides: Basic Ca phosphate crystal deposition disease), and other arthropathies.

Limited motion, weakness, pain, and other disturbed mobility from rotator cuff impairment can be quickly screened by having the patient attempt to abduct and raise both arms above the head and then to slowly lower them. Muscle atrophy and neurologic changes should be sought.

Knee: At the knee, gross deformities such as swelling (eg, joint effusion, popliteal cysts), quadriceps muscle atrophy, and joint instability may be obvious when the patient stands and walks. With the patient supine, the examiner should palpate the knee, identifying the patella, femoral condyles, tibial tuberosity, tibial plateau, fibular head, medial and lateral joint lines, popliteal fossa, and quadriceps and patellar tendons. The medial and lateral joint lines correspond to locations of the medial and lateral menisci and can be located by palpation while slowly flexing and extending the knee. Tender extra-articular bursae such as the anserine bursa below the medial joint line should be differentiated from true intra-articular disturbances.

Detection of small knee effusions is often difficult and is best accomplished using the “bulge sign.” The knee is fully extended and the leg slightly externally rotated while the patient is supine with muscles relaxed. The medial aspect of the knee is stroked to express any fluid away from this area. Placement of one hand on the suprapatellar pouch and gentle stroking or pressing on the lateral aspect of the knee can create a fluid wave or bulge, visible medially when an effusion is present. Larger effusions can be identified visually or by balloting the patella. Joint effusion can result from many joint diseases, including RA, osteoarthritis, gout, and trauma.

Full 180° extension of the knee is attempted to detect flexion contractures. The patella is tested for free, painless motion.

Hip: Examination begins with gait evaluation. A limp is common in patients with significant hip arthritis. It may be caused by pain, leg shortening, flexion contracture, or muscle weakness. Loss of internal rotation (often the earliest change in hip osteoarthritis or any hip synovitis), flexion, extension, or abduction can usually be demonstrated. Placement of one hand on the patient's iliac crest detects pelvic movement that might be mistaken for hip movement. Flexion contracture can be identified by attempting leg extension with the opposite hip maximally flexed to stabilize the pelvis. Tenderness over the femoral greater trochanter indicates bursitis (which is extra-articular) rather than an intra-articular disorder. Pain with passive range of motion (assessed by internal and external rotation with the patient supine and the hip and knee flexed to 90°) suggests intra-articular origin.

Other: Hand examination is discussed elsewhere (see Hand Disorders: Evaluation; see Approach to the Patient With Joint Disease: Polyarticular Pain). Foot and ankle examination is discussed in Foot and Ankle Disorders. Examination of the neck and back is discussed in Neck and Back Pain: Evaluation.

Testing

Laboratory testing and imaging studies often provide less information than the history and physical examination. While some testing may be warranted in some patients, extensive testing is often not.

Blood tests: Some tests, although not specific, can be helpful in supporting the possibility of certain systemic rheumatic diseases. These include antinuclear antibodies (ANA) and complement in SLE, rheumatoid factor and anti-citrullinated peptide (CCP) in RA, and antineutrophil cytoplasmic antibodies (ANCA) in the vasculitides. Tests such as WBC count, ESR, and C-reactive protein may help determine the likelihood that arthritis is inflammatory due to infectious or other systemic diseases, but these tests are not highly specific or sensitive. For example, an elevated ESR or C-reactive protein level suggests inflammation or may be due to aging or a large number of nonarticular inflammatory conditions. Also, elevation may not occur in all inflammatory disorders.

Imaging studies: Imaging studies are often unnecessary. Plain x‑rays in particular reveal mainly bony abnormalities, and most joint disorders do not affect bone primarily. However, imaging may help in the initial evaluation of relatively localized, unexplained persistent or severe joint and particularly spine abnormalities; they may reveal primary or metastatic tumors, osteomyelitis, bone infarctions, periarticular calcifications (as in calcific tendinitis), or other changes in deep structures that may escape physical examination. If chronic RA, gout, or osteoarthritis is suspected, erosions, cysts, and joint space narrowing with osteophytes may be visible. In pseudogout, Ca pyrophosphate deposition may be visible in intra-articular cartilage.

For musculoskeletal imaging, plain x‑rays may be obtained first, but these are often less accurate than CT or MRI. MRI is the most accurate study for fractures not visible on plain x‑rays, particularly in the hip and pelvis, and for soft tissues and internal derangements of the knee. CT is useful if MRI is contraindicated or unavailable. Ultrasound, arthrography, and bone scanning may help in certain conditions, as can biopsy of bone, synovium, or other tissues.

Arthrocentesis: Arthrocentesis is the process of puncturing the joint with a needle. If there is an effusion and arthrocentesis is performed correctly, fluid can generally be withdrawn. Examination of synovial fluid is the most accurate way to determine the cause of joint effusions and is indicated in all patients with severe or unexplained monarticular joint effusions and in patients with unexplained polyarticular effusions.

Arthrocentesis is performed using strictly sterile technique. Infection or other rash over the site used to enter the joint is a contraindication. Preparations for collecting samples should be made before performing the procedure. Local anesthesia, with lidocaine Some Trade Names
XYLOCAINE
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or difluoroethane spray, is often used. To avoid nerves, arteries, and veins, which are usually on the joint's flexor surface, many joints are punctured on the extensor surface. A 20-gauge needle can be used for most joints, removing as much fluid as possible. Specific anatomic landmarks are used (s ee Fig. 1: Approach to the Patient With Joint Disease: Arthrocentesis of the shoulder., Fig. 2: Approach to the Patient With Joint Disease: Arthrocentesis of the elbow., and Fig. 3: Approach to the Patient With Joint Disease: Arthrocentesis of the knee.).

Fig. 1
Arthrocentesis of the shoulder. The glenohumeral joint is punctured while the patient sits with the arm at the side and hand on the lap. The needle is inserted anteriorly, slightly inferior and lateral to the coracoid process, aiming posteriorly toward the glenoid fossa. A posterior approach is also possible.

Fig. 2
Arthrocentesis of the elbow. The ulnohumeral joint is entered while the patient's elbow is flexed at 60 and the wrist is pronated. The needle enters the joint's lateral surface, between the lateral humeral epicondyle and the ulna.

Fig. 3
Arthrocentesis of the knee. The knee and connecting suprapatellar pouch can be punctured while the patient is supine and knee is extended. The needle, usually 20-gauge, can be inserted laterally, just under the cephalad edge of the patella. Alternatively, the needle can be inserted medially, under the cephalad half of the patella.

Metacarpophalangeal joints, metatarsophalangeal joints, and interphalangeal joints of the hands and feet are punctured similarly to each other, using a 20- or 22-gauge needle. The needle is inserted dorsally, to either side of the extensor tendon.

Synovial fluid examination: At the bedside, gross characteristics of the fluid are assessed, such as its color, turbidity, and viscosity. Viscosity can be assessed using the “string” sign. The length of a viscous string of joint fluid dropped from the syringe is normally > 3 cm. Inflammation decreases viscosity, decreasing the length of the string.

Gross characteristics allow many effusions to be tentatively classified as noninflammatory, inflammatory, or infectious (see Table 1: Approach to the Patient With Joint Disease: Classification of Synovial Effusions). Effusions can also be hemorrhagic. Each type of effusion suggests certain joint diseases (see Table 2: Approach to the Patient With Joint Disease: Differential Diagnosis Based on Synovial Fluid Classification*†). So-called noninflammatory effusions are actually mildly inflammatory but tend to suggest diseases such as osteoarthritis, in which inflammation is not severe.

Table 1
Classification of Synovial Effusions Normal Hemorrhagic Infectious Inflam-matory Noninflammatory Gross examination            Appearance Clear Bloody Turbid or purulent Yellow, cloudy Straw-colored, clear   Viscosity High Variable Variable Low High Routine laboratory examination             Culture Negative Negative Often positive Negative Negative   PMN %* < 25 — Usually > 85 > 50 < 25   WBC count* < 200/µL Affected by amount of blood 5000 to > 100,000/μL 1000 to 50,000/μL 200 to 1000/μL *WBC count and PMN % in infectious arthritis are lower if organism is less virulent (eg, gonococcal, Lyme, tuberculous, or fungal arthritis) or partially treated. Some effusions in SLE and other connective tissue diseases are only equivocally inflammatory, with a WBC count of 500 to 2000/μL. Noninfectious effusions rarely have up to 100,000 WBC/μL.

Table 2
Differential Diagnosis Based on Synovial Fluid Classification*† Hemorrhagic INFECTIOUS Inflammatory Noninflammatory Anticoagulant treatment Hemangioma Coagulopathy Neurogenic (neuropathic) arthropathy Pigmented villonodular synovitis Scurvy Thrombocytopenia Trauma with or without fracture Tumor Various organisms depending on patient characteristics (see Table 2: Infections of Joints and Bones: Organisms That Commonly Cause Acute Infectious Arthritis  in Infections of Joints and Bones:Acute Infectious Arthritis) Acute crystal synovitis (gout and pseudogout) Ankylosing spondylitis Crohn's disease Lyme disease Partially treated or less virulent bacterial infections Progressive systemic sclerosis Psoriatic arthritis Reactive arthritis Reiter's syndrome RA Rheumatic fever SLE Ulcerative colitis Amyloidosis Ehlers-Danlos syndrome Hypertrophic pulmonary osteoarthropathy Metabolic diseases causing osteoarthritis Neurogenic (neuropathic) arthropathy Osteoarthritis Osteochondritis dissecans Osteochondromatosis Progressive systemic sclerosis Rheumatic fever Sickle cell disease SLE Subsiding or early inflammation Trauma *See Table 1: Approach to the Patient With Joint Disease: Classification of Synovial Effusions for classification. This differential diagnosis is only a partial listing. †Some disorders span classifications (eg, neuropathic arthropathy can be hemorrhagic or noninflammatory; progressive systemic sclerosis can be inflammatory or noninflammatory).

Laboratory tests commonly performed on joint fluid include cell count, leukocyte differential, culture (if infection is a concern—see Infections of Joints and Bones), and wet drop examination for cells and crystals. However, the exact tests often depend upon what diagnoses are suspected.

Microscopic examination of a wet drop preparation of synovial fluid for crystals (only a few drops of fluid from a joint are needed), using polarized light, is essential for definitive diagnosis of gout, pseudogout, and other crystal-induced arthritides (see Crystal-Induced Arthritides). A polarizer over the light source and another between the specimen and the examiner's eye allow visualization of crystals with a shiny white birefringence. Compensated polarized light is provided by inserting a first-order red plate, as is found in commercially available microscopes. The effects of a compensator can be reproduced by placing two strips of clear adhesive tape on a glass slide and placing this slide over the lower polarizer. Such a homemade system should be tested against a commercial polarizing microscope. If a wet drop reveals crystals that are not typical of monosodium urate (gout) or Ca pyrophosphate (pseudogout), several less common crystals (cholesterol, liquid lipid crystals, oxalate, cryoglobulins) or artifacts (eg, depot corticosteroid crystals) should be considered.

Other synovial fluid findings that occasionally make or suggest a specific diagnosis include the presence of specific organisms (identifiable by Gram or acid-fast stain); LE cells; marrow spicules or fat globules (caused by fracture); “Reiter's cells” (monocytes on Wright's stained smears that have phagocytized PMNs), present most often in reactive arthritis; amyloid fragments (identifiable by Congo red stain); and sickled RBCs (caused by sickle cell hemoglobinopathies).

Measurements of rheumatoid factor in synovial fluid can give false-positive or false-negative results and, thus, should not be performed. Extremely low synovial fluid glucose levels in specimens carefully handled in fluoride tubes may suggest infection.

Last full review/revision November 2005

Content last modified November 2005