An acutely painful, swollen or hot joint is septic arthritis until proven otherwise. Joint infection is a medical emergency and is covered in detail in Chapter 28 , Infection and malignancy. This chapter is dedicated to the far less dangerous but much more common causes of a painful joint – in particular, the acute crystal arthropathies gout and pseudogout.

Gout is an inflammatory arthropathy generated by uric acid crystal deposition in the joints and peri-articular structures, e.g. bursae. Uric acid is a product of DNA breakdown (purine nucleotides) but is also present in foods and alcohol. Once a biochemical threshold is reached in a susceptible individual, crystals precipitate into joints, skin and kidneys causing a spectrum of disease.

Clinical picture

Gout is characterised by acute attacks of joint inflammation separated by asymptomatic periods. The commonest joint to be affected is the first metatarsophalangeal joint (podagra), but other common sites include the ankle, knee, wrist and fingers. Attacks are usually monoarticular but may become polyarticular if recurrent attacks are left untreated, and indeed this chronic inflammation can generate a destructive arthritis.

Hyperuricaemia can be generated by two processes.

• Alcohol, red meats and seafood contain high levels of urate.
  
• Increased cell turnover states such as psoriasis, haematological malignancies or chemotherapy produce purines via DNA breakdown.
  
• Enzyme defects can also be responsible, but these are relatively rare.

Frequently an attack of gout is provoked by trauma, surgery or alcohol/dietary excess.

Note that biochemical hyperuricaemia may not produce the clinical syndrome of gout.

Uric acid deposition in the skin produces tophi – well demarcated collections of crystals that may rupture, releasing a chalk-like substance. Classic sites for tophi include the helix of the ear, the olecranon and prepatellar bursae, the ulnar border of the forearm and the tendons. Tophi may break down or ulcerate and occasionally cause diagnostic confusion with rheumatoid nodulosis.

• Renal stones (remember that uric acid stones are radiolucent).
  
• Urate nephropathy (deposition of urate in renal interstitium or collecting tubules).

Thus, gout can both cause and be caused by renal impairment.

Investigations

Urate levels

These may be normal (or even fall) during an acute attack in up to 50% of patients. They are used principally to monitor the success or compliance of urate – lowering therapy.

X-ray

X-rays show soft tissue swelling, and punched-out erosions in persistent disease which may corticate and heal. Osteopaenia is not a feature and joint fusion is rare.

Joint fluid

Joint fluid shows low viscosity, a high white cell count and the presence of intraneutrophilic urate crystals – characteristically needleshaped and negatively birefringent under polarised microscopy.

Management

Acute attack

The priority is to relieve pain and inflammation using non-steroidal anti-inflammatory agents (NSAIDs), colchicine or steroids.

Prophylaxis

Lifestyle modification with stringent avoidance of risk factors should be undertaken and precipitating drug-therapy altered where possible (e.g. reducing frusemide dose). Urate-lowering therapy is commenced under anti – inflammatory cover once the acute attack has settled. Allopurinol (xanthine oxidase inhibitor) is used most commonly. If renal function is impaired, lower doses must be used. Side effects include rashes and a serious drug interaction with azathioprine, risking bone marrow failure. The alternative xanthine oxidase inhibitor, febuxostat, has recently received NICE approval for patients intolerant of allopurinol. Second-line therapy is the uricosuric agent sulfinpyrazone which increases renal excretion of urate. It cannot be used in the presence of renal stones. In gout patients with hypertension and dyslipidaemia, losartan (angiotensin-1 receptor antagonist) and fenofibrate (hypolipidaemic agent) may be used as adjunct therapy as both reduce serum uric acid levels.

Pseudogout is an inflammatory arthropathy due to calcium pyrophosphate deposition, and is frequently associated with chondrocalcinosis (calcification of fibrocartilage and hyaline cartilage). The commonest presentation is an acutely hot, swollen and tender joint, usually the knee or shoulder, but it can present more insidiously as a ‘pseudor-heumatoid’ polyarticular pattern in the hand. Underlying disease states (including haemachromatosis, Wilson’s disease and hyperparathyroidism) may precipitate pseudogout and these should be sought in a young patient with this diagnosis.

Diagnosis relies on the identification of positively birefringent rhomboid-shaped crystals in synovial fluid.

NSAIDs are the mainstay of treatment, in combination with joint aspiration and intra-articular steroid injection. Low-dose colchicine may play a role in prophylaxis.