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Should non-steroidal anti-inflammatory drugs be given to orthopaedic patients with fractures?

Non-steroidal anti-inflammatory drugs (NSAIDs) are useful adjuncts in perioperative pain relief. They act by inhibiting the activity of the enzyme cyclooxygenase (COX) which catalyses the formation of prostaglandins from arachidonic acid (Peck and Williams, 2000). COX exists as two isoenzymes, COX-1 and COX-2. COX-1 is responsible for the production of prostaglandins that form the protective gastric mucosal barrier, help maintain renal perfusion and regulate haemostatic function. COX-2 facilitates the inflammatory response. The beneficial actions of NSAIDs are associated with inhibition of COX-2 while the adverse effects re associated with inhibition of COX-1. NSAIDs are sub-divided into three main groups: non-specific COX inhibitors, preferential COX-2 inhibitors and specific COX-2 inhibitors. COX-2 is also responsible for the production of prostaglandins by osteoblasts which are essential for bone repair (Raisz, 2001). NSAIDs are therefore implicated in delayed fracture healing or non-union of fractures.