Hemostatic Therapy Should Be Used for Acute Treatment of Anticoagulation-Related Intracerebral Hemorrhage

Abstract

Not only does warfarin increase the risk of intracerebral hemorrhage (ICH), but it leads to more severe hemorrhages and worse outcome. This poor prognosis is primarily a function of ongoing bleeding from the warfarin-induced hemostatic defects. Use of warfarin is a strong and independent determinant of hematoma expansion1—a major risk factor for poor outcome in spontaneous ICH2—and prolongs the window during which expansion occurs.1 Warfarin-associated ICH therefore represents a true emergency requiring rapid and sustained reversal of anticoagulation to normal or near-normal values, a position endorsed by consensus guidelines from multiple organizations. This strategy makes intuitive sense; earlier international normalized ratio (INR) correction is associated with improved outcome in warfarin users with spontaneous3 and traumatic4 ICH. If warfarin reversal is the goal how should it be accomplished? Vitamin K, even if given intravenously, is incapable of rapidly reversing warfarin-induced coagulopathy during the peak time for hematoma growth. Still, it should be administered to achieve sustained warfarin reversal because the other agents used have relatively short half-lives. Despite a common misperception, allergic and anaphylactic reactions to intravenous vitamin K are quite rare (approximately 3 per 10 000 doses).5 There …