Acute Monoarticular Arthritis

Brian F. Mandell

RAPID BOARD REVIEW—KEY POINTS TO REMEMBER:

The distinction between crystal-induced and bacterial arthritis cannot be made reliably with studies from peripheral blood or from clinical presentation alone. Synovial fluid analysis, with cell count, polarized microscopy, and culture, is the gold standard diagnostic test.

Gouty Arthritis

Attacks of acute gout can be elicited by abrupt changes in serum urate levels, whether up or down. Serum urate may be normal at the time of an attack, but if checked repeatedly, in the absence of hypouricemic therapy, chronic gout patients will almost invariably have serum levels >6.7 mg/dL, the saturation point for urate.

Non-urate Crystalline Arthritis

Calcium pyrophosphate crystals can cause attacks that totally mimic gout (pseudogout), but they can also cause chronic arthritis syndromes. Radiographic finding of calcium deposition within menisci and other intra-articular cartilage has been termed chondrocalcinosis and may be asymptomatic or associated with inflammatory arthritis. Systemic diseases associated include hyperparathyroidism, hypothyroidism, hypophosphatasia, hypomagnesemia, gout, amyloidosis, prior joint trauma or surgery, hemochromatosis.
Oxalate-induced arthritis, in patients on dialysis.
Hydroxyapatite-induced arthritis, in patients with Milwaukee shoulder.

Treatment of Crystalline Arthritis

Hyperuricemia develops in the overwhelming majority of patients because of insufficient renal excretion rather than overproduction. Therapy includes xanthine oxidase inhibitors, such as allopurinol, and uricosuric agents, such as probenecid.
Colchicine or NSAIDs should be used as initial simultaneous prophylactic antiinflammatory medications because drug-induced hypouricemia frequently precipitates an attack of gout.
Acute attacks can be treated with NSAIDs at high doses (not aspirin), corticosteroids, ACTH, intra-articular corticosteroids, IL1 antagonists (off label), or colchicine.

Septic Arthritis