The role of hemostatic therapy in anticoagulation-associated intracerebral hemorrhage: intuition versus evidence.

Previous studies have shown that patients with anticoagulation (warfarin)-associated intracerebral hemorrhage (WAICH) have poor outcome and greater mortality. The mechanisms by which warfarin worsens intracerebral hemorrhage (ICH) outcome are not clearly defined and include larger hematoma volumes at presentation, ongoing bleeding leading to greater hematoma expansion, and greater age and burden of medical comorbidities among warfarin users.1 The intuition that hematoma expansion is a consistent predictor of poor outcome after ICH and is potentially modifiable led to the general recommendation that correcting the international normalized ratio (INR) as rapidly as possible to stop ongoing bleeding in these patients should be the goal of therapy. Warfarin reduces the availability of vitamin K and the maturation of its dependent coagulation factors (VKDCF) II, VII, IX, and X and is thought to exert its anticoagulant effects mostly through reductions in factors II (prothrombin) and X levels. Therefore, vitamin K should be given to reverse the effects of warfarin. However, the full effect of vitamin K may take up to 24 hours to develop. Faster reversal requires restoration of VKDCF, in particular factors II and …