What causes the chronic inflammation characteristic of rheumatoid arthritis isn’t known, but infectious (viral or bacterial) or hormonal factors and lifestyle may influence disease onset. In some patients, immunoglobulin (Ig) M antibody develops against their body’s IgG, which is called RF.

The cartilage damage that results from the inflammation triggers further immune system responses, including complement activation. Complement, in turn, attracts polymorphonuclear leukocytes and stimulates the release of inflammatory mediators, which exacerbates joint destruction.

If unarrested, joint inflammation occurs in four stages. First, synovitis develops from congestion and edema of the synovial membrane and joint capsule. Formation of pannus—thickened layers of granulation
tissue—marks the onset of the second stage. Pannus covers and invades cartilage and eventually destroys the joint capsule and bone.

Progression to the third stage is characterized by fibrous ankylosis—fibrous invasion of the pannus and scar formation that occludes the joint space. Bone atrophy and misalignment cause visible deformities and disrupt the articulation of opposing bones, causing muscle atrophy and imbalance and, possibly, partial dislocations or subluxations. In the fourth stage, fibrous tissue calcifies, resulting in bony ankylosis and total immobility.

Pain associated with movement may restrict active joint use and cause fibrous or bony ankylosis, soft-tissue contractures, and joint deformities. Vasculitis can lead to skin lesions, leg ulcers, and multisystem complications.

Between 15% and 20% of patients develop Sjögren’s syndrome with keratoconjunctivitis sicca. Rheumatoid arthritis can also destroy the odontoid process, part of the second cervical vertebra. Rarely, spinal cord compression may occur, particularly in patients with long-standing deforming rheumatoid arthritis.

Other complications include subluxations, carpal tunnel syndrome, popliteal (Baker’s) cysts, osteoporosis, vasculitis, amyloidosis, recurrent infections, anemia, necrosis of the hip joint, cardiac and pulmonary disorders, renal insufficiency, GI disturbances, and pleural effusions.

The patient’s history may reveal an insidious onset of nonspecific symptoms, including fatigue, malaise, anorexia, persistent low-grade fever, weight loss, and vague articular symptoms.

Later, more specific localized articular symptoms develop, frequently in the fingers at the proximal interphalangeal, metacarpophalangeal, and metatarsophalangeal joints. These symptoms usually occur bilaterally and symmetrically and may extend to the wrists, elbows, knees, and ankles.

The patient may report that affected joints stiffen after inactivity, especially on rising in the morning. She may complain that joints are tender and painful, at first only when she moves them, but eventually even at rest. Ultimately, joint function is diminished. She may also experience tingling paresthesia in the fingers, the result of synovial pressure on the median nerve from carpal tunnel syndrome.

Other complaints include stiff, weak, or painful muscles. If the patient has peripheral neuropathy, she may report numbness or tingling in the feet or weakness or loss of sensation in the fingers. If pleuritis develops, she may complain of pain on inspiration (although pleuritis often causes no symptoms). The patient with pulmonary nodules or fibrosis may complain of shortness of breath.

Inspection of the patient’s joints may show deformities and contractures, especially if active disease continues. The fingers may appear spindle shaped from marked edema and congestion in the joints. Proximal interphalangeal joints may develop flexion deformities or become hyperextended. Metacarpophalangeal joints may swell dorsally, and volar subluxation and stretching of tendons may pull the fingers to the ulnar side (ulnar drift). The fingers may become fixed in a characteristic swan-neck deformity or in a boutonnière deformity. The hands appear foreshortened, and the wrists boggy. Inspection of pressure areas such as the elbows may reveal rheumatoid nodules—subcutaneous, round or oval, nontender masses—the most common extra-articular finding.

If the patient has vasculitis, you may observe such extra-articular signs as lesions, leg ulcers, and multiple systemic complications. If she has scleritis or episcleritis, you may observe redness of the eye.

Palpation may reveal joints that are hot to the touch. If the patient has pericarditis, auscultation may reveal pericardial friction rub (although pericarditis may cause no signs).

If spinal cord compression occurs, your assessment may also reveal signs of upper motor neuron disorder, such as a positive Babinski’s sign and weakness. You may also detect signs of other extra-articular findings, including temporomandibular
joint disease, infection, osteoporosis, myositis, cardiopulmonary lesions, lymphadenopathy, and peripheral neuritis.

The criteria developed by the American Rheumatism Association can serve as guidelines to establish a diagnosis. Butkeep in mind that failure to meet these criteria—particularly early in the disease—doesn’t exclude the diagnosis. (See Criteria for classifying rheumatoid arthritis.)

Although no test definitively diagnoses rheumatoid arthritis, the following are useful: