Seminars in thrombosis and hemostasis
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Polytraumatic injury results in tissue factor (TF) release from damaged cells. The acute coagulopathy of trauma (ACT) occurs early and results from significant tissue injury and tissue hypoperfusion. ACT is augmented by therapies resulting in acidemia, hypothermia, and hemodilution contributing to trauma-induced coagulopathy. ⋯ TBI has also recently been shown to cause platelet dysfunction. Platelet receptor inhibition prevents cellular initiation and amplification of the clotting cascade, limiting thrombin incorporation, and stabilization of clot to stop hemorrhage. Therefore, head injury in the presence of polytrauma does appear to augment ACT and warrants close monitoring and appropriate intervention.
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Semin. Thromb. Hemost. · Nov 2013
ReviewIntracerebral bleeding in patients on antithrombotic agents.
Patients treated with oral anticoagulants (OAC) carry a 7- to 10-fold higher risk of intracerebral hemorrhage (ICH) than patients without OAC. ICH related to oral anticoagulation (OAC-ICH) is a particularly severe form of stroke. The overall incidence of OAC-ICH ranges between 2 and 9 per 100,000 population/year and is expected to increase as the number of patients treated with OAC rises. ⋯ Factors that mediate worse outcome in OAC-ICH are more frequent and prolonged secondary hematoma enlargement and intraventricular hemorrhage, The current concept of emergency treatment in OAC-ICH is rapid restoration of effective coagulation using hemostatic factors such as prothrombin complex concentrate, fresh frozen plasma, factor IX concentrates, and recombinant factor VIIa in addition to vitamin K. Emergency management of ICH under treatment with the new direct OAC is a major challenge. In the absence of specific antidotes, prothrombin concentrates are recommended mainly on the basis of preclinical data.