A 65-year-old man presents with acute onset of severe pain in the right big toe for two days following a binge of alcohol. Most probable …

The diagnosis is acute gout — podagra of the first metatarsophalangeal joint. Gout is characterised by intra-articular monosodium urate crystals and generally presents as acute, affecting the first metatarsophalangeal joint, mid foot or ankle, although the knee, elbow or wrist can also be involved. The features that make it near-certain here are the abrupt onset reaching maximum severity within 6–24 hours, the site, the male sex and age, and the alcohol binge. Beer and spirits raise urate by increasing purine load and by lactate-mediated inhibition of renal urate excretion; dehydration after a binge concentrates urate further.

Examine and exclude the one diagnosis that would kill him. The joint will be exquisitely tender, hot, red and swollen with overlying desquamation, and even bedclothes may be intolerable. Look for tophi — subcutaneous urate deposits on extensor surfaces, which can develop in later phases and are sometimes confused with rheumatoid arthritis and its nodules. The critical differential is septic arthritis, which can be indistinguishable and may coexist; also consider pseudogout, cellulitis, trauma or fracture, reactive arthritis and acute osteoarthritic flare. Fever, rigors, a portal of entry, immunosuppression, diabetes or a prosthetic joint mandate urgent aspiration.

Investigations. The definitive diagnosis of gout is established by observing the presence of needle-shaped crystals in the involved joint — negatively birefringent under polarised light, and intracellular within neutrophils during an attack. Send the same aspirate for Gram stain, culture and cell count. Some patients will have elevated uric acid levels — note the wording: serum urate is often normal or low during an acute attack and does not confirm or exclude the diagnosis; repeat it two weeks after the flare settles. Radiographs may reveal well-defined gouty erosions in or around joints — punched-out, with overhanging sclerotic margins and preserved joint space — but these are features of chronic disease. Also check renal function, glucose, lipids, full blood count and liver function, both to find comorbidity and to choose the safest drug.

Treat the acute attack — the choice is dictated by comorbidity, not by efficacy. The goal of treatment is to terminate the acute attack and then to prevent future attacks by considering underlying causes. The acute phase should be managed using short-term NSAIDs, colchicine, corticotrophin or corticosteroids, and treatment choices should be based on patient comorbidities such as renal function and gastrointestinal disease. All three first-line options are of similar efficacy, so choose on safety: NSAIDs — effective but hazardous in the older adult with renal impairment, heart failure, hypertension, anticoagulation or peptic ulcer; colchicine — low-dose regimens (1.2 mg then 0.6 mg one hour later, then 0.5–0.6 mg once or twice daily) are as effective as and far better tolerated than the old high-dose regimen, but reduce the dose in renal impairment and avoid with clarithromycin, ciclosporin, verapamil, diltiazem and statins because of myopathy and marrow suppression; corticosteroids — intra-articular injection is ideal for a single joint, or oral prednisolone 30–35 mg daily for 5 days, and this is often the safest choice in an older patient with chronic kidney disease. Add rest, elevation and ice.

Do not start urate-lowering therapy during the attack — but do plan it. Treatment to decrease uric acid levels should not be initiated during the acute phase, because drugs such as allopurinol or probenecid may exacerbate the acute attack by mobilising crystals. If the patient is already established on allopurinol, continue it — never stop it during a flare. Plan to start urate-lowering therapy 2–4 weeks after the flare has fully settled, under anti-inflammatory cover.

Address the cause and the man, not just the toe. Review alcohol — advise reduction and screen for alcohol-use disorder, since a "binge" in a 65-year-old may signal a wider problem. Review drugs that raise urate: thiazide and loop diuretics, low-dose aspirin, ciclosporin, tacrolimus, pyrazinamide and ethambutol — substituting a diuretic is often curative. Advise reduction of red meat, organ meat, shellfish and fructose-sweetened drinks, adequate hydration, and weight loss. Screen for the associated conditions that make gout a cardiovascular marker: hypertension, chronic kidney disease, obesity, diabetes, dyslipidaemia and ischaemic heart disease.

Current guidance has reversed the old rule that urate-lowering therapy must never be started during or soon after a flare. The ACR gout guideline and subsequent practice hold that starting urate-lowering therapy during a flare does not increase or prolong symptoms as long as anti-inflammatory treatment is given concurrently, and the ACR explicitly notes that patients are most motivated for treatment during an exacerbation — so the pragmatic modern approach in a patient likely to be lost to follow-up is to start allopurinol at a low dose under colchicine or NSAID cover rather than wait. Two further current points: anti-inflammatory prophylaxis should be continued for 3–6 months rather than less than 3 months after starting urate-lowering therapy, with ongoing evaluation; and HLA-B*5801 testing should be offered before starting allopurinol in people of Southeast Asian or African descent, in whom the allele — carried by about 7% of those of Southeast Asian descent — predicts severe allopurinol hypersensitivity. The examination-safe formulation is to state the textbook rule first, then note that current guidance permits concurrent initiation under anti-inflammatory cover.