PATHOPHYSIOLOGY: In gout, there is an oversecretion of uric acid or a renal defect resulting in decreased excretion of uric acid, or a combination of both. Primary hyperuricemia may be due to severe dieting or starvation, excessive intake of foods high in purines such as shellfish and organ meats, or heredity. In secondary hyperuricemia, the gout is a clinical feature secondary to any of a number of genetic or acquired processes, including conditions with an increase in cell turnover (leukemias, multiple myeloma, psoriasis, some anemias) and an increase in cell breakdown.
CLINICAL MANIFESTATIONS: Gout is characterized by deposits of uric acid in various joints. Four stages of gout can be identified: asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout, and chronic tophaceous gout. Acute arthritis of gout is the most common early sign. The metatarsophalangeal (MTP) joint of the big toe is most commonly affected; the tarsal area, ankle, or knee may also be affected. The acute attack may be triggered by trauma, alcohol ingestion, dieting, medication, surgical stress, or illness. Abrupt onset occurs at night, causing severe pain, redness, swelling, and warmth over the affected joint. Early attacks tend to subside spontaneously over 3 to 10 days without treatment. The next attack may not come for months or years; in time, attacks tend to occur more frequently, involve more joints, and last longer.
ASSESSMENT AND DIAGNOSTIC METHODS: A definitive diagnosis of gouty arthritis is established by polarized light microscopy of the synovial fluid of the involved joint. Uric acid crystals are seen within the polymorphonuclear leukocytes in the fluid.
MEDICAL MANAGEMENT: Colchicine (oral or parenteral), an NSAID such as indomethacin, or a corticosteroid is prescribed to relieve an acute attack of gout. Hyperuricemia, tophi, joint destruction, and renal problems are treated after the acute inflammatory process has subsided. Uricosuric agents, such as probenecid, correct hyperuricemia and dissolve deposited urate. Allopurinol is effective when renal insufficiency or renal calculi are a risk. Corticosteroids may be used in patients who have no response to other therapy. Prophylactic treatment considered if patient experiences several acute episodes or there is evidence of tophi formation.
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