Introduction The high mortality and disability associated with intracerebral hemorrhage (ICH), and especially the potentially preventable damage from rebleeding, have brought hemostatic strategies to the forefront of the medical management of acute ICH. Hemostatic abnormalities are frequent in ICH with evidence for both systemic and local coagulation disturbances involving activation of both fibrinolytic and coagulation systems. A number of pharmacological agents have been reported to reduce bleeding in a variety of clinical settings, while only one to date, recombinant activated factor VII (rFVIIa), has undergone a double-blind randomized controlled study in ICH. This chapter reviews hemostatic abnormalities reported in patients with ICH and discusses pharmacological strategies for prevention of hematoma expansion in both coagulopathic and non-coagulopathic ICH. Hemostatic systems Hemostasis, the physiological response to vascular injury, results from activation of a highly regulated series of procoagulant and anticoagulant zymogens and cofactors. Coagulation factors circulate in the blood as inactive zymogens. In vivo activation of hemostasis requires a combination of endothelial injury and exposure of the subendothelial protein matrix to circulating blood. The process requires two key cell types: tissue factor (TF)-bearing cells and platelets. According to the cell-based model of coagulation, the process of hemostasis begins with the interaction between cell-derived TF and blood-borne FVIIa, the initiation phase [1,2] (Fig. 21.1). The formation of the FVIIa–TF complex permits activation of factors IX and X, a process which generates small amounts of thrombin and is critical to the amplification and propagation phases of coagulation.
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