Treatment of oral anticoagulant-associated cerebral hemorrhage The incidence of cerebral hemorrhage in patients taking oral anticoagulants with an INR between 2.0 and 4.5 ranged from 0.3% to 3.7% per year. The incidence in the placebo group was 0.1% per year. for every 0.5 increase in INR, the risk of bleeding increased by 1.4. patients without oral anticoagulants had a higher incidence of embolism, up to 5% to 10% per year, and patients at high risk with mechanical valves had a relatively low risk of embolism of 0.2% to 0.4% within two weeks. In contrast, patients on oral anticoagulants have a very high risk of early rebleeding. The incidence of rebleeding within 7 d was 16% (9/75) in patients without oral anticoagulants and 54% in patients on oral anticoagulants. Several studies support the idea below that the incidence of embolic events remains low even in high-risk patients who discontinue oral anticoagulants for 10 to 14 d. Other studies have shown that patients with cerebral hemorrhage on oral anticoagulants have greater bleeding, higher mortality, and a worse prognosis compared with patients without oral anticoagulants. Warfarin use is associated with poor prognosis in patients with cerebral hemorrhage. flibotte et al. found that after controlling for baseline levels of cerebral hemorrhage and the volume of intraventricular hemorrhage, warfarin use still resulted in a significant increase in mortality. In addition, warfarin use and increased anticoagulation intensity were independent predictors of 3-month mortality. Based on these trials, it is recommended that INR should be urgently controlled to normal limits in patients with oral anticoagulant-associated cerebral hemorrhage. INR can theoretically be corrected by administration of prothrombin complex (PCC), fresh frozen plasma (FFP), or vitamin K, but there are no randomized trials comparing these different approaches. PCC, FFP, and vitamin K can be combined if necessary, as the half-lives of warfarin and phenprocoumarin (24 h and 7 d, respectively) are significantly longer than those of vitamin K-dependent coagulation factors. The exact dose depends on the clinical situation. In the acute phase, the status of anticoagulation should be repeatedly evaluated and the opinion of a hematologist should be sought. rFVIIa is used to reduce INR in volunteers receiving vinblastine coumarin and is focused on increasing INRs in patients on warfarin . However, it should be remembered that INR does not reflect the actual status of all vitamin K-dependent coagulation factors. The interest in using rFVIIa has been fuelled by the lack of alternative pharmacological treatments. In 2 small retrospective studies in patients with cerebral hemorrhage, this drug has been used alone or in combination with FFP. Although there are no RCTs on oral anticoagulant-associated cerebral hemorrhage, treatment guidelines on oral anticoagulant-associated cerebral hemorrhage are still available. When considering whether and when to resume anticoagulation in patients with oral anticoagulant-associated cerebral hemorrhage, it is important to consider whether the cerebral hemorrhage has been fully controlled, the estimated risk of thrombosis, and the pathophysiologic characteristics of the cerebral hemorrhage, as these will determine the risk of recurrence of the hemorrhage. The indications for the use of oral anticoagulants for secondary prophylaxis after cerebral hemorrhage should be re-evaluated. The EUSI currently recommends that anticoagulants should be used prophylactically in patients who have already experienced cardiogenic embolism caused by atrial fibrillation, heart valve repair, and other proven causes. Stratification of the bleeding model revealed that patients with atrial fibrillation and patients with lobar hemorrhage do not benefit from restarting anticoagulation because the high risk of rebleeding and death outweighs the risk of recurrent cerebral ischemia. This is in contrast to deep bleeding. A recent meta-analysis showed that antiplatelet therapy-associated cerebral hemorrhage occurs less frequently in primary prevention of cardiovascular events . However, there is a net benefit to the use of aspirin for primary prevention of cardiovascular events. There is no evidence to support any other antiplatelet agent as a substitute for aspirin. For patients with oral anticoagulant-associated cerebral hemorrhage and INR >1.4 the following recommendations are available: oral anticoagulants should be discontinued, PCC or FFP should be used, and intravenous vitamin K should be used to normalize INR (level IV evidence); oral anticoagulants can be reintroduced after 10-14 d after reassessment of thromboembolic risk and risk of recurrent cerebral hemorrhage (as recommended by the European Stroke Council). guidelines on ischaemic line stroke) (evidence IV).