Diagnosis of gout

Graf, 2015Neogi, 2015Sivera, Andres, Carmona, 2014Sivera, Andres, Falzon, 2014

While a suspected diagnosis of gout can be made based on clinical assessment (see Clinical presentations of acute gout), a definitive diagnosis requires the identification of monosodium urate crystals under polarised microscopy in synovial (or bursal) fluid or tophi (see Utility of joint aspiration and synovial fluid analysis for rheumatological diseases).

Confirmation of the diagnosis is important because gout usually requires lifelong urate-lowering therapy. Microscopy and culture of the synovial (or bursal) fluid should also be undertaken to exclude infection. Once a definitive diagnosis of gout has been made, diagnostic aspiration is not required for recurrent attacks unless infection is suspected.

Note: Aspiration of an affected joint or bursa is the gold standard for confirming a diagnosis of gout.

If synovial fluid analysis is not feasible (ie the joint is difficult to aspirate [eg the big toe]), a clinical diagnosis of gout is supported by the following features:

  • monoarticular involvement of the foot or ankle (especially the first metatarsophalangeal [MTP] joint)
  • previous similar acute arthritis episodes
  • rapid onset of severe pain and swelling (reaching a peak in the intensity of pain and swelling within 24 hours)
  • erythema
  • tophi
  • strong family history of gout
  • cardiovascular disease and hyperuricaemia in males or postmenopausal femalesHak, 2010.

These features are highly suggestive of, but not specific to, gout.

Diagnostic certainty is required before starting patients on lifelong urate-lowering therapy. Because allopurinol use can be associated with significant harm, ensure any differential diagnoses have been ruled out. Ideally, urate-lowering therapy should not be started in someone without crystal-proven disease. If a joint is difficult to aspirate, there is often another joint or bursal swelling containing monosodium urate crystals that is suitable for aspiration. If the diagnosis cannot be confirmed, practitioners should keep other diagnoses in mind and look for an opportunity to aspirate a swollen joint.

Note: While clinical context is important, ideally, urate-lowering therapy should not be started in someone without crystal-proven disease.

Serum uric acid concentration should be measured in all patients with suspected gout. However, the presence of hyperuricaemia alone is insufficient to diagnose gout and, in patients with acute gout, serum uric acid concentration may be normal. Other than the presence of tophi, individual clinical features (eg history of painful or swollen big toe) have a low diagnostic utility. Response to colchicine does not replace aspiration in the diagnosis of gout; it can support a diagnosis of crystal arthritis, but does not distinguish between gout and acute calcium pyrophosphate crystal arthritis.

Monosodium urate crystals are not seen on plain X-ray because they are not radiopaque. A plain X-ray is useful to identify joint damage due to gout and the presence of radiographic damage is an indication for urate-lowering therapy. In complex or difficult cases, specialists may use other imaging modalities such as ultrasound or dual energy computed tomography (DECT) in the diagnosis of gout, but their utility is uncertain. Imaging does not replace joint or bursal aspiration.

In patients with suspected gout, kidney function should be measured as impaired kidney function is both a risk factor and a consequence of gout, and can affect treatment choice and dosing. A search for other causes of gout should be undertaken as appropriate (see Pathogenesis of and risk factors for gout).