Introduction:
Gout is caused by the deposition of monosodium urate monohydrate (MSUM)
crystals at synovial joints. It has a prevalence of 1–2%, and is more common in
men, in certain ethnic groups and with increasing age. Uric acid mainly comes
from the metabolism of purines within the body but some is ingested with food.
Gout is becoming more common with increased longevity and prevalence of
metabolic syndrome, of which hyperuricaemia is a component.
Clinical features
Acute gout:
This presents with rapid onset of severe pain in a single distal joint, commonly the first metatarsophalangeal joint. Other common sites include the ankle, midfoot, knee, hand, wrist and elbow. Examination reveals marked synovitis with swelling, red shiny skin and extreme tenderness. Periarticular swelling and fever may also be present. Symptoms are usually self-limiting over 5–14 days. The differential diagnosis includes septic arthritis, cellulitis and reactive arthritis.
Recurrent and chronic gout:
Following an acute attack, many patients
go on to experience a second attack within a year. The frequency of attacks
increases with time. Involvement of several joints with continued MSUM
deposition eventually leads to joint damage and chronic pain.
Chronic tophaceous gout:
MSUM crystal deposits produce irregular firm nodules (‘tophi’) around extensor surfaces of fingers, forearms, elbows, Achilles tendons and ears. Tophi are usually a late feature of gout.
Renal and urinary tract manifestations:
Chronic hyperuricaemia may be complicated by renal stone formation and sometimes renal impairment due to interstitial nephritis caused by urate deposition in the kidney. This particularly affects patients with chronic tophaceous gout who are on diuretics.
Investigations
Joint aspiration reveals long, needle-shaped MSUM crystals, which are negatively birefringent under polarised light. Synovial fluid in acute gout appears turbid due to the high neutrophil count (> 90%). Serum uric acid is usually elevated, but hyperuricaemia itself does not confirm gout. Equally, acute inflammation reduces levels, so a normal uric acid level does not exclude gout. Serum creatinine should be checked to exclude renal impairment. There is neutrophilia with a raised CRP in acute gout; FBC and ESR may detect myeloproliferative disorders during remission of the acute episode.
Joint X-rays are usually normal in early gout. Changes of
secondary OA and gouty erosions may develop with chronic disease.
Management
Acute attacks:
Oral NSAIDs are standard treatment. Ice packs provide symptomatic relief. Oral colchicine is also very effective but vomiting and diarrhoea are common side-effects. Joint aspiration and intra-articular corticosteroid injections are effective in more severe cases.
Long-term management:
Allopurinol lowers serum uric acid levels by
inhibiting xanthine oxidase, which reduces conversion of hypoxanthine and
xanthine to uric acid. It is indicated in patients with recurrent attacks of acute
gout, tophi, joint damage or renal impairment. Allopurinol initiation can
trigger an acute attack; it should therefore be initiated after the acute
attack has settled, and should be co-prescribed with an NSAID or colchicine for
the first few weeks.
Predisposing factors should be addressed:
● Weight loss: advised in obese patients.
● Excess beer: avoid.
● Diuretics: stop if possible.
● High-purine
diet (seafood, red meat and offal): avoid.
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