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)
Between January 2006 and December 2016, 941 patients without continuous antithrombotic or anticoagulant medication were treated due to SAH in the Department of Neurosurgery, Goethe University, Frankfurt am Main, Germany. Fourteen of them (1.5%) had taken ASA as a single dose because of headache within 24 h before hospital admission. A matched pair analysis was performed. Admission status was good in 93% of patients with one-time use of ASA (OTA), but only in 59% of all other patients (p < 0.01). Bleeding pattern did not differ, but half of the patients with OTA had no identifiable bleeding source; this rate was significantly lower in the rest of the patients (p < 0.005). Aneurysm treatment and related complications did not differ between both groups. Cerebral vasospasm was more often only mild and rates of cerebral infarctions were lower in the OTA group but not on a significant level. Eighty-six percent of the OTA group and 84% (p = 0.8) of the matched pair control group reached favorable outcome according to mRS 6 months after SAH. Patients with OTA in case of SAH are usually in good clinical condition and bleeding pattern does not differ. In half of the patients with OTA, no bleeding source was detectable. In the case of aneurysm treatment, related complications did not differ and most of the patients reached favorable outcome. In the case of aneurysm treatment procedure, OTA does not influence treatment course and should not influence treatment decisions 5).