Gout

Gout is a form of inflammatory arthritis characterised by recurrent attacks of joint pain, swelling, and redness. It is caused by the deposition of needle-like crystals of uric acid, known as monosodium urate crystals, in the joints. These attacks often reach their peak intensity within 12 hours.

The joint at the base of the big toe (podagra) is most commonly affected, but other joints such as heels, knees, wrists, and fingers can also be involved. Long-term elevated uric acid levels can lead to tophi, kidney stones, or kidney damage.

Signs and Symptoms

Gout typically presents as a red, tender, hot, and swollen joint. The pain usually begins at night and peaks within 24 hours. Symptoms may include fatigue and fever, although these are rare. Chronic hyperuricaemia may result in hard, painless deposits of uric acid crystals called tophi, which can lead to chronic arthritis due to bone erosion. Elevated uric acid levels may also precipitate in the kidneys, causing kidney stones.

Causes

The crystallisation of uric acid due to high levels in the blood is the primary cause of gout. This can result from diet, genetic predisposition, or underexcretion of urate by the kidneys. Dietary factors include alcohol, sugar-sweetened beverages, meat, and seafood. Other triggers include physical trauma and surgery.

Pathophysiology

Gout arises from a disorder in purine metabolism, leading to uric acid crystallisation in joints and surrounding tissues. These deposits, or tophi, may be walled off by a ring of proteins, preventing inflammation. However, naked crystals can trigger an immune-mediated inflammatory reaction, especially in cooler temperatures or rapid changes in uric acid levels.

Diagnosis

Diagnosis of gout can often be made based on clinical presentation and hyperuricaemia. However, synovial fluid analysis is definitive, identifying needle-like monosodium urate crystals under polarised light microscopy. Blood tests may show hyperuricaemia, but elevated uric acid levels are not always present during an attack.

Treatment

The initial aim of treatment is to alleviate the symptoms of an acute attack. NSAIDs, glucocorticoids, and colchicine are commonly used. Long-term prevention involves lowering uric acid levels through lifestyle changes and medications such as allopurinol or probenecid.

NSAIDs

NSAIDs are the first-line treatment for gout, offering rapid relief of pain and inflammation. Indometacin and ibuprofen are commonly used, with the latter preferred due to a better side effect profile.

Colchicine

Colchicine is an alternative for those who cannot tolerate NSAIDs. It is effective at lower doses and well-tolerated but may cause gastrointestinal upset at higher doses.

Glucocorticoids

Glucocorticoids are as effective as NSAIDs and can be used if NSAIDs are contraindicated. They can be administered orally or through intra-articular injection, but joint infection must be excluded first.

Prognosis

Without treatment, an acute gout attack usually resolves within a week, but recurrent attacks are common. Long-term complications include chronic gout, joint deformity, and kidney stones. Effective management of uric acid levels can prevent these complications.

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Self-assessment MCQs (single best answer)

What is the primary cause of gout?

Which joint is most commonly affected by gout?

What is the term used for gout affecting the joint at the base of the big toe?

Which of the following is NOT a common dietary factor that can trigger gout?

What is the definitive diagnostic test for gout?

Which medication is typically the first-line treatment for an acute gout attack?

What are tophi?

Which of the following is a long-term medication used to lower uric acid levels in gout patients?

What is the characteristic appearance of uric acid crystals under polarised light microscopy?

Which symptom is rare but may accompany a gout attack?