Seminars in thrombosis and hemostasis
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Activation of coagulation frequently occurs in severe infection and sepsis and may contribute to the development of thrombosis. Coagulation abnormalities in sepsis range from a small decrease in platelet count and subclinical prolongation of global clotting times to fulminant disseminated intravascular coagulation (DIC), characterized by simultaneous widespread microvascular thrombosis and profuse bleeding from various sites. ⋯ Hypothetically, patients with thrombophilia may suffer from more severe coagulopathy in case of severe infection or sepsis, which may result in a more serious clinical course and an unfavorable outcome. On the basis of the knowledge of the pathogenesis of thrombosis in severe inflammation and sepsis, strategies aimed at the inhibition of coagulation activation have been developed and have been found favorable in experimental and clinical studies.
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No standard exists for venous thromboembolism (VTE) prophylaxis after traumatic brain injury (TBI). Caregivers agree that there is an early time point after injury in which the chances of spontaneous injury progression are high and the risks of prophylactic anticoagulation are excessive, and that these injuries eventually stabilize to the point that anticoagulation may be safely started. Translating this consensus into an application that can inform bedside decision making has not occurred. ⋯ Although interest in this field has increased of late, many studies are limited by the simple dichotomization of TBI patients as having the presence or absence of intracranial blood. Although methodologically easier, this approach does not account for the heterogeneity of TBI and, consequently, the spectrum of time to stabilization. To address this, our group has created an algorithm which stratifies patients by risk for spontaneous progression and tailors a unique VTE prophylaxis regimen to each arm.