Gout as a consequence of bone healing: A diagnostic dilemma

Abstract

Diagnosis of acute gout remains a diagnostic challenge if associated with trauma, and may easily be mistaken as cellulitis or septic arthritis. Gout is an inflammatory arthritis that is triggered by the deposition of sodium urate crystals within the joints and soft tissues, and is frequently associated with hyperuricemia. Hyperuricemia may arise in a wide range of clinical situations that cause overproduction or under-excretion of uric acid, or a combination of both. As uric acid is the ultimate breakdown product of purine nucleotide degradation in humans, any increase in purine production due to accelerated cell turnover may precipitate an acute attack of gout. Gout may be precipitated by conditions such a trauma, surgery, diuretic therapy, or ethanol intake. All predisposed individuals such as those with hypreuricemia, hypothyroid etc. with trauma and bone fractures should be observed for precipitation of acute gouty arthritis. Bone healing after a fracture may also lead to acute gout. Healing of a fractured bone, through multiple mechanisms, can precipitate acute gout, particularly in the presence of certain predisposing factors such as hypothyroidism, pre-existing hyperuricemia or tissue hypoxia. Acute inflammation and pain, if resistant to non-steroidal anti-inflammatory drugs, may necessitate treatment with colchicine.