Gout is a metabolic condition characterised by high levels of urate within the body. The greater the level and the longer the duration of hyperuricaemia the more likely gout becomes. However, the majority of patients with hyperuricaemia do not develop gout, but the reasons for this are not clear.
Urate sometimes precipitates from blood and forms crystals. These form in and near synovial joints to cause the inflammatory response.
Gout affects about 1 per cent of the population. It is much more common in men, in older patients and in those with higher uric acid levels within the blood. Gout in pre-menopausal women is rare.
The pathophysiology of this condition is not fully understood. Uric acid within the body comes from either the diet or as a by-product of metabolism. Some patients have hyperuricaemia because their kidneys cannot manage the current load of uric acid. Other causes include alcohol, drugs such as diuretics and medical incidents.
Acute gouty arthritis is often a monoarthritis. The pain starts suddenly, often during the night. If the toe joint is affected, often the weight of the bedclothes can be uncomfortable and because of the tenderness, the patient cannot wear socks or shoes.
The affected joint is swollen and tender with the surrounding skin erythematous. The patient may be systemically unwell with pyrexia.
Acute monoarthritic gout can look like a septic arthritis or a cellulitis. However, an infection does not present so explosively and if left untreated infection will get worse. Without treatment, gout will settle in about 10 days.
As the condition is treated, the recovery period may see the skin surface desquamate.
Apart from the first metatarsophalangeal joint, the knees, ankles, hands and wrists can also be affected. After the initial attack some patients have more frequent attacks while others after an initial attack may never have another.
As the condition progresses, multiple joints can be affected. Chronic gouty arthritis can cause significant joint damage resulting in a polyarthritis, which can result in significant disability. Urate crystals deposit in areas such as the hands, feet, elbows and around the Achilles tendon, to produce the characteristic yellow or white nodules. These nodules can ulcerate and discharge.
Kidney stones containing uric acid can cause renal colic and renal disease can be the result of persistent tophaceous gout that is not being treated.
A definitive diagnosis is made by aspirating the joint or tophus and identifying the appropriate crystals using microscopy. However, this is not always practical in primary care and it is reasonable to make a diagnosis based on the history and clinical examination, especially if there is a known history of gout.
If there is no quick response to gout treatment, consider the differential diagnoses, such as septic arthritis. If this is suspected an emergency, same-day referral is indicated.
Gout may be associated with other conditions such as overweight, alcohol excess and renal impairment. Checking FBC after an attack has settled should help rule out a myeloproliferative disease.
NSAIDs can be used to control pain and provide quick symptom relief. Oral colchicine is an alternative, but significant side-effects, particularly on the gastrointestinal tract, can limit its use. A short course of oral steroids may also be effective.
Weight loss, healthy diet and a reduction in alcohol consumption can reduce the uric acid level. Diuretics should be stopped if possible.
Asymptomatic hyperuricaemia does not usually need treatment. It is justifiable to treat an occasional attack of gout symptomatically without the need to resort to prophylactic drugs such as allopurinol.
Allopurinol is a popular choice because it can be used once daily and is relatively free from side-effects.
Initiation of treatment can induce an attack of gout, so it common to co-prescribe an NSAID or colchicine at low dose during the first three months of treatment to overcome this risk.