Acetylsalicylic acid (ASA) irreversibly blocks the platelet cyclo-oxygenase enzyme system, preventing formation of thromboxane A2 and inhibiting platelet aggregation for the life of the affected platelet (approximately 10 days).
This block occurs even at the lowest therapeutic/prophylactic ASA dose usually prescribed, 81 mg/day (10%/24 h). Because the ASA effect on individual platelets is complete, it cannot be reversed.
Based upon the customary rate of platelet production, approximately 5–6 days are required after cessation of ASA to replace approximately 50% of the circulating platelets
Perioperative low dose use was not associated with increased risk of perioperative complications 1).
Aspirin increased the risk of rehaemorrhagia after surgery of hypertensive cerebral hemorrhage (HCH) 2).
Preinjury use of warfarin, but not antiplatelet medications, influences survival and need for neurosurgical intervention in elderly TBI patients with intracranial hemorrhage; hemorrhage progression and morbidity are not affected. The importance of antithrombotic therapy may lie in its impact on initial injury severity 3).
Various medicamentous methods of counteracting aspirin-induced platelet dysfunction and excessive bleeding in this context are revaluated. In this context, platelet infusion and the administration of Desmopressin seems to be an effective and accepted as well as frequently adopted measure to antagonize the aspirin effect on platelet function during various major surgical procedures 4)