CLINICAL CRITERIA FOR DIAGNOSIS

Any two of the following:

At least two attacks of painful joint swelling with complete resolution within 2 weeks.

Clear history of podagra (1st MTP joint). Ankle & knee may also be affected, hip & shoulder rarely so.

Presence of a tophus on helix of ear, fingers, toes, elbows.

Response to colchicine 500µg tds within 48 hours.

In elderly may present as chronic arthritis with tophi.

DEFINITIVE DIAGNOSIS

Needle shaped crystals in synovial fluid or tissue

Hyperuricaemia is common and does not necessarily mean the patient has gout. Normal uric acid during an acute episode does not exclude gout.

MECHANISMS OF GOUT

Under secretion of urate is most common - thiazides, low dose aspirin, alcohol, impaired renal function.

Over production of urate - myeloproliferative disorders especially when treated, psoriasis.

TRIGGERS OF ACUTE ATTACK

Dehydration, trauma, surgical operations, initiation of allopurinol, alcohol, diuretics.

DIFFERENTIAL DIAGNOSIS.

Pseudogout - often presents as hot swollen knee in elderly with OA. Chondrocalcinosis on X-ray & rhomboid crystals of calcium pyrophosphate in synovial fluid.

Septic arthritis - see Acute Monoarthritis.

Leucocytosis and fever may also occur in gout.

MANAGEMENT OF ACUTE ATTACK

• Fast-acting oral NSAIDs at maximum doses are the drugs of choice eg diclofenac 50 mg tds, or Etoricoxib 120 mg daily, unless contraindicated.
• In patients with increased risk of peptic ulcers, bleeds or perforations, co-prescription of gastro-protective agents should follow standard guidelines for the use of NSAIDs and Coxibs
• Colchicine is an alternative but much slower to work. 1mg stat, then 0.5 mg tds until the attack resolves. More frequent dosing is poorly tolerated. Reduce the dose if diarrhoea occurs
• Intra-articular corticosteroids are highly effective in acute gouty monoarthritis and i.a, oral, i.m or i.v corticosteroids can be effective in patients unable to tolerate NSAIDs or refractory to other treatments
• Allopurinol should not be commenced during an acute attack but in patients already established on allopurinol, it should be continued and the acute attack treated conventionally
• Opiate analgesics can be used as adjuncts

PROPHYLAXIS

• The plasma urate should be maintained below 0.30 mmol/l
• Uric acid lowering drug therapy should be started if a second attack occurs within 1 yr and to patients with tophi, uric acid stones and to patients who need to continue treatment with diuretics
• Delay starting uric acid-lowering drug therapy until 1-2 weeks after inflammation has settled
• Initial long-term treatment of recurrent uncomplicated gout normally should be with allopurinol starting in a dose of 50-100 mg/day and increasing by 50-100 mg increments every few weeks, adjusted for renal function (see BNF), until the therapeutic target (SUA 0.30 mmol/l) is reached (maximum dose 900 mg)
• Uricosuric agents can be used as second-line drugs in patients who are under-excretors of uric acid and in those resistant to, or intolerant of, allopurinol. The preferred drugs are sulphinpyrazone (200-800 mg/day) in patients with normal renal function or benzbromarone (50-200 mg/day) in patients with mild/moderate renal insufficiency
• Colchicine 0.5 mg bd should be co-prescribed following initiation of treatment with allopurinol or uricosuric drugs, and continued for up to 6 months. In patients who cannot tolerate colchicine, an NSAID or Coxib can be substituted provided that there are no contraindications, but the duration of NSAID or Coxib cover should be limited to 6 weeks
• Aspirin in low doses (75-150 mg/day) has insignificant effects on the plasma urate, and should be used as required for cardiovascular prophylaxis. However, aspirin in analgesic doses (600-2400 mg/day) interferes with uric acid excretion and should be avoided
• Follow up by rheumatology recommended

BSR Guideline for the Management of Gout (2007) also includes lifestyle and non-pharmacological measures