• Monisha A Kumar.
• Departments of Neurology, Neurosurgery, and Anesthesiology and Critical Care, Perelman School of Medicine, Hospital of the University of Pennsylvania, 3 West Gates Building, 3400 Spruce Street, Philadelphia, PA, 19104, USA, monisha.kumar@uphs.upenn.edu.
• Curr Neurol Neurosci Rep. 2013 Nov 1;13(11):391.

AbstractCoagulopathy is often observed after traumatic brain injury (TBI), but the pathogenic mechanisms of this phenomenon remain elusive. Brain injury is the leading cause of trauma deaths, and the development of coagulopathy after TBI is associated with increased morbidity and mortality in these patients. The coagulopathy after TBI comprises a hypocoagulable and a hypercoagulable state with hemorrhagic and thrombotic phenotypes that are both associated with worse outcome. Some theories of its pathogenesis include massive release of tissue factor, altered protein C homeostasis, microparticle upregulation, and platelet hyperactivity. This article aims to examine the coagulopathy associated with blunt head injury, to review its effect on progression of hemorrhagic injury, and to discuss the possible relevant pathophysiological mechanisms.

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