Effects of nonsteroidal anti-inflammatory therapy on platelets

Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) can produce a mild, systemic hemostatic defect by inhibiting normal platelet function. Aspirin acetylates and permanently inactivates cyclooxygenase (COX), while nonaspirin NSAIDs reversibly block COX; thus, all of these drugs cause platelet dysfunction by inhibiting the formation of thromboxane A2, a platelet-activating and vasoconstricting eicosanoid. However, spontaneous bleeding complications outside the gastrointestinal tract very rarely result from the use of aspirin and other NSAIDs in individuals who are otherwise hemostatically normal. Most types of surgery are not usually associated with clinically significant bleeding in patients taking these drugs, making it typically unnecessary to discontinue them and thus delay surgery for the purpose of restoring normal hemostasis. Exceptions may include operations at sites where optimal hemostasis is critical, surgical manipulation of the genitourinary tract and oral cavity, and possibly cardiac surgery. Factors that increase the risk of bleeding with aspirin and other NSAIDs include coexisting coagulation abnormalities and the simultaneous use of alcohol or anticoagulants.