Gout

Published on 02/04/2015 by admin

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Last modified 22/04/2025

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132 Gout

Instruction

Examine this patient’s hands or examine the feet.

Salient features

History

• Usually acute pain at the base of great toe, worse at night and associated with redness

• Occasionally multiple joints involved

• Systemic symptoms, e.g. low grade fever.

Examination

• Chronic tophaceous deposit with asymmetrical joint involvement.

Proceed as follows:

• Tell the examiner that you would like to examine:

• the helices of the ears
• the elbow for olecranon bursae
• the Achilles tendons for tophi
• the feet or hands.

Notes

• Uric acid crystals are negatively birefringent, needle shaped and may be deposited in bursae and bone marrow. They are demonstrable in synovial fluid within leukocytes and free in the fluid during attacks of gouty arthritis. They react with nitric acid and ammonium hydroxide to give a purple colour (murexide test).

• Be prepared to discuss the differences between the clinical features of typical gout and gout in the elderly.

Diagnosis

This patient has a painful great toe with swelling of the joint (lesion) caused by gout (aetiology) and is unable to walk because of the pain (functional status).

Questions

What is the basic pathophysiology of gout?

Gout is a metabolic disorder of purine metabolism. It is characterized by hyperuricaemia caused by either overproduction (75%) or underexcretion (25%) of uric acid.

What are the different clinical manifestations of gout?

• Asymptomatic hyperuricaemia

• Acute arthritis

• Chronic arthritis

• Chronic tophaceous gout (Figs 132.1 and 132.2).

image

Fig. 132.1 Gouty tophi.

image

Fig. 132.2 Painful olecranon bursitis resembling septic bursitis.

(With permission from Roberts, Hedges 2009.)

How would you treat an acute attack of gout?

Prescribe an NSAID such as indomethacin. Selective cyclooxygenase-2 (COX-2) inhibitors (etoricoxib) are an alternative in patients with GI contraindications to the use of NSAIDs. Corticosteroids or subcutaneous injections of ACTH are also options. Refractory gout may require steroids.

What factors may precipitate acute gouty arthritis?

Drugs (diuretics, aspirin), copious consumption of alcohol, dehydration, surgery, fasting food high in purines (sweetbreads, liver, kidney and sardines).

Advanced-level questions

Under what circumstances would you treat hyperuricaemia?

Frequent attacks of acute arthritis, renal damage and consistently raised serum uric acid levels. Before attempting to lower serum uric acid levels, it is prudent to use colchicine to treat acute attacks. Colchicine should be given within 24 h of the onset of symptoms to abort a severe attack.

Remember: The incidence of gouty arthritis has been linked to serum urate level in a cohort of healthy men, the annual incidence being:

4.9% for urate of at least 90 mg/l (535 µmol/l)

0.5% for 70–89 mg/l

0.1% for <70 mg/l.

What is the drug of choice for controlling hyperuricaemia?

Allopurinol (a xanthine oxidase inhibitor). The goal of therapy is to reduce serum uric acid to <60 mg/l (350 µmol/l). At this level, monosodium urate crystals within joints and in soft tissue tophi are reabsorbed. Febuxostat, a novel non-purine xanthine oxidase inhibitor, may be a useful alternative medication in patients with renal insufficiency.

What are the diagnostic criteria for acute gout?

American Rheumatism Association diagnostic criteria (Arthritis Rheum 1977;20:895–900) for acute gout includes the presence of seven or more of the following criteria:

• More than 1 attack of acute arthritis

• Maximum inflammation developed within 1 day

• Attack of monoarthritis

• Redness observed over joints

• First metatarsophalangeal joint painful and swollen

• Unilateral attack of first metatarsophalangeal joint

• Unilateral attack of tarsal joint

• Tophus (proven or suspected)

• Hyperuricaemia

• Asymmetric swelling within a joint on radiograph

• Subcortical cysts without erosions on radiograph

• Monosodium urate monohydrate microcrystals in joint fluid during attack

• Culture of joint fluid negative for organisms during attack.

What drugs would you use if the patient was allergic to allopurinol?

Uricosuric drugs such as probenecid, sulfinpyrazone.

How would you determine whether a patient with elevated uric acid is an overproducer or an underexcretor?

An overproducer is one whose 24-hour urinary uric acid level >750 mg.

What is pseudogout?

Pseudogout is an acute arthritis resulting from the release of calcium pyrophosphate dihydrate crystals (deposited in the bone and cartilage) into the synovial fluid (Fig. 132.3).

image

Fig. 132.3 Radiograph of knee showing typical articular chondrocalcinosis in the areas of the medial and lateral meniscus in pseudogout.

(With permission from Currie, Douglas 2011.)

Gout was recognized as early as the 4th century BC. Two concepts have prevailed: that it occurs mainly in sexually active mature men and that gastronomic and sexual excesses may precipitate acute attacks.

Antonj van Leewenhoeck (1632–1723) described the microscopic appearance of urate crystals from gouty tophus.

In 1847 Alfred Garrod, in London, identified uric acid in the serum of a gouty man.

Michelangelo’s gout has been depicted in a fresco by Raphael (Lancet 1999; 354:2149–52).

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