Management of neurologic complications of coagulopathies

Abstract

Coagulopathy is common in intensive care units (ICUs). Many physiologic derangements lead to dysfunctional hemostasis; these may be either congenital or acquired. The most devastating outcome of coagulopathy in the critically ill is major bleeding, defined by transfusion requirement, hemodynamic instability, or intracranial hemorrhage. ICU coagulopathy often poses complex management dilemmas, as bleeding risk must be tempered with thrombotic potential. Coagulopathy associated with intracranial hemorrhage bears directly on prognosis and outcome. There is a paucity of high-quality evidence for the management of coagulopathies in neurocritical care; however, data derived from studies of patients with intraparenchymal hemorrhage may inform treatment decisions. Coagulopathy is often broadly defined as any derangement of hemostasis resulting in either excessive bleeding or clotting, although most typically it is defined as impaired clot formation. Abnormalities in coagulation testing without overt clinical bleeding may also be considered evidence of coagulopathy. This chapter will focus on acquired conditions, such as organ failure, pharmacologic therapies, and platelet dysfunction that are associated with defective clot formation and result in, or exacerbate, intracranial hemorrhage, specifically spontaneous intraparenchymal hemorrhage and traumatic brain injury.

Keywords: bleeding; blood coagulation factors; blood coagulation tests; coagulopathy; coagulopathy of trauma; hemostasis; intracerebral hemorrhage; intracranial hemorrhage; intraparenchymal hemorrhage; thrombelastography.