Updated: Aug 26, 2019
Gout is a type of inflammatory arthritis, often termed ‘the disease of kings’, caused by the deposition of uric acid (monosodium urate) crystals in tissues and typically the joint fluid. This occurs as a result of excessive production of uric acid by the body, or under-excretion of uric acid by the renal system.
Gout is characterised by four clinical phases:
1. Phase I – involves the deposition of uric acid with no symptoms
2. Phase II – (further uric acid deposition) involves intermittent acute attacks of pain and inflammation which resolves spontaneously over a period of 7 – 10 days.
3. Phase III – The stage between acute gout attacks and persistent crystal accumulation.
4. Phase IV – If the excessive crystal deposits are not controlled, individuals can transition into phase IV of gout, which is characterised by chronic crystallisation involving numerous joint attacks and the deposition of crystals in joints as well as in soft tissues.
Men are more likely to develop gout and a family history of gout also increases the risk of developing the disease.
Risk factors for gout includes:
Some drugs: e.g thiazide diuretics, cyclosporine, low-dose aspirin
Diet that mainly consist of meat, seafood and refined sugars/drinks or alcohol.
Other factors that are associated with gout include insulin resistance, metabolic syndrome, obesity, renal insufficiency, hypertension, organ transplantation and congestive heart failure.
Recurrent attacks or flares can also be induced by the use of recent diuretics, alcohol intake, surgery or trauma and recent hospitalisation; initial use of uric acid lowering drugs can also trigger gout attacks in the early periods, however reduce the risk of attacks in the long term.
Signs and Symptoms:
Clinical features of gout include spontaneous onset of intense pain, swelling and redness that most commonly affects the big toe joint (known as podagra). It can also affect other joints of the foot, ankle, mid-tarsal, wrist and knee. Other problems that can cause similar symptoms include pseudogout, psoriatic arthritis and septic arthrtis.
The standard for the diagnosis of gout still remains removal of the joint fluid and evaluation to check for monosodium urate crystals under a microscope. As gout and septic arthritis can co-exist it is also essential to analyse the joint fluid for bacteria through culture. Radiographic imaging of the joints can show the changes due to a chronic history of gout. Sometimes, evidence of crystals in the joint may be seen, but not always. Recently, ultrasound, CT and MRI are also emerging techniques for the diagnosis of gout.
Treatment of gout can involve drug therapy as well as support and rehabilitation measures. Pharmacological management aims to treat acute gout attacks and also helps to maintain an appropriate level of uric acid in the blood in order to prevent recurrence. The British rheumatology guidelines prefer the use of NSAIDs at a high dosage (given no contraindications to its use) with a treatment period of 1-2 weeks. Therapy starts with high doses of anti-inflammatory medications for the first few days with a decrease in the dosage as the symptomatology subsides. For acute attacks of gout, another drug called colchicine is also used in addition to anti-inflammatory medicine.
Long-term management for gout consists of managing the urate levels and maintaining the concentration below a certain level. However, urate-lowering drug therapy is only indicated in patients who have experienced multiple gout attacks or chronic joint pathology and extensive crystal deposition.
Chronic gout can be painful and significantly reduce the mobility in the joint due to the crystal deposits, and the inflammation and damage caused by this. Orthotic therapy is often beneficial in order to increase the range of motion of particular joints and protect the foot from further deformity that can be caused by chronic gout.