musculoskeletal and connective tissue disorders
Gout
Diagnosis of Gout
Clinical criteria Synovial fluid analysis The diagnosis of gout should be suspected in patients with acute Pain in and Around a Single Joint or Calcium Pyrophosphate Arthritis (however, calcium pyrophosphate deposition generally occurs in larger joints, is not associated with tophi, and its clinical course is often milder but protracted) Rheumatic Fever with joint involvement and Rheumatoid Arthritis (RA) (however, RA tends to be symmetrical and persistent, with more affected joints during a flare, flares persisting for longer periods of time, and flares in all joints subsiding together; whereas in gout, inflammation is usually flaring in some joints while subsiding in others) Acute fracture in patients unable to provide a history of injury (particularly metatarsal stress fractures) Acute Infectious Arthritis or Palindromic rheumatism Acute calcific periarthritis caused by Basic Calcium Phosphate Crystal Deposition Disease and Calcium Oxalate Crystal Deposition Disease None Palindromic rheumatismis characterized by acute, recurrent flares of inflammation in or near one or occasionally several joints or tendon sheaths with spontaneous resolution; pain and erythema can be as severe as in gout. Flares often subside spontaneously and completely in 1 to 3 days. Such flares may herald the onset of RA, and rheumatoid factor tests can help in differentiation; they are positive in about 50% of patients (these tests are positive in 10% of gouty patients also). If acute gouty arthritis is suspected, arthrocentesis and synovial fluid analysis should be done at the initial presentation. A typical recurrence in a patient with previously documented gout does not mandate arthrocentesis, but it should be done if there is any question of the diagnosis or if the patient’s risk factors or any clinical characteristics suggest infectious arthritis. In some cases, a diagnosis of gout may be reasonably presumed based on the patient’s history and clinical features or on imaging results in cases when joint fluid cannot be obtained; however, every attempt should be made to document the presence of MSU crystals in synovial fluid from an affected joint. Synovial fluid analysis can confirm the diagnosis by identifying needle-shaped, strongly negatively birefringent urate crystals that are free in the fluid or engulfed by phagocytes. Synovial fluid during flares has inflammatory characteristics (see table), usually 2,000 to 100,000 white blood cells/mcL, with>80% polymorphonuclear white blood cells. These findings overlap considerably with infectious arthritis, which must be excluded by Gram stain (which is insensitive) and culture. An elevated serum urate level supports the diagnosis of gout but is neither specific nor sensitive; at least 30% of patients have a normal serum urate level during an acute flare in part due to the uricosuric properties of the proinflammatory cytokine interleukin-6 (IL-6) or because a sudden lowering of the serum urate precipitated the flare. However, the baseline serum urate level between flares reflects the size of the extracellular miscible urate pool. The level should be measured on 2 or 3 occasions in patients with newly proven gout to establish a baseline. Quantitation of urinary uric acid excretion to differentiate between overproduction and underexcretion is no longer recommended; it does not predict a patient's response toallopurinolorfebuxostat(both of which decrease uric acid production). The serum urate level can be low after initiation of therapy, but flares can continue to occur as long as tissue deposits remain. The dissolution of the urate deposits may take many months after initiating therapy. X-rays of the affected joint may be taken to look for bony erosions or tophi, but they are unnecessary if the diagnosis of acute gout has been established by synovial fluid analysis and rarely show erosions at the time of first flares. In calcium pyrophosphate arthritis, radiopaque deposits may sometimes be present in fibrocartilage, hyaline articular cartilage (particularly the knee), or both, but calcinosis can be seen in the absence of acute flares. Ultrasonography is more sensitive (although operator-dependent) than plain x-rays for the diagnosis of gout. Urate deposition over the articular cartilage (double-contour sign) and clinically inapparent tophi are characteristic changes. These findings may be evident even before the first gout flare. Dual-energy CT scans (DECTs) can also reveal uric acid deposits and can be useful if the diagnosis is unclear based on standard clinical evaluation and testing, particularly if synovial fluid aspiration and analysis cannot be done. Chronic gouty arthritis should be considered in patients with persistent unexplained joint disease or subcutaneous or bony tophi. Plain x-rays of the 1st metatarsophalangeal joint or other affected joint may be useful. These x-rays may show punched-out lesions of subchondral bone with overhanging bony margins, most commonly in the 1st metatarsophalangeal joint; lesions must be≥5 mm in diameter to be visible on x-ray. Joint space is typically preserved until very late in the course of disease. Synovial fluid findings from chronic effusions of affected joints are usually diagnostic. Diagnostic ultrasonography is increasingly used to detect a typical double-contour sign suggesting urate crystal deposition, but sensitivity is operator-dependent and differentiation from calcium pyrophosphate crystal deposits may be more difficult to do conclusively. 